IMT Flashcards

Question

What about D in ABCDE?

Answer 1

1. Glucose (particularly important in seizure, stroke, drowsy or confused patient) - also mention ketones here 2. AVPU/GCS (?any confusion/orientation) formally - continue to check/monitor this (in real life nurses to continue to check) and if becomes drowsy with dropping gcs - escalation to ITU (monitor GCS throughout admission) *The consciousness of patients with meningitis can deteriorate alarmingly quickly 3. Pupils + any focal neurological signs/neurological exam (?meningism) 4. Meds incl pain 5. CT brain

Answer 2

Ensure adequate exposure for a full examination (head to toe), whilst maintaining their dignity. This may provide further information about the cause of the presenting complaint. Expose maintaining dignity and warmth/minimise heat loss to fully examine him, to look for bleeds/blood loss, rashes, trauma esp head/injuries importantly head/trauma, wounds, lines, drains, devices, track marks Examine abdomen (?hepatomegaly or ascites or bladder distension) + limbs for signs of infection (?synovitis) or cause of the presenting complaint Flank tenderness!!! Peritonism? Sacral oedema Hydration status Can do DVT check here Temperature if not done To check for any alternative cause of their presentation/which may explain their presentation It would also be an important consideration when assessing this patient to be mindful of what her escalation status is likely to be. Although this would not be my immediate concern - as the first priority is to stabilise her medically - this is something that is important to establish promptly, as will affect subsequent management. ?Mention calculate clinical frailty score at baseline if relevant. A patient with a background of cognitive impairment may already have some advanced care planning in place, and so I would ensure that the details of this are established. Another good sentence - It would also be important to establish a social history when later considering escalation status. THEN..... Having completed my initial assessment..... I would go back to reassess ABC (and review any investigations that were available - LOVE UP TO HERE) while waiting for investigations/adjust to investigations or management, discuss my findings with a senior, and re-escalate accordingly if the patient deteriorates or develops another episode of seizure or airway compromise. I would also review the patient’s notes and take a more detailed history and collateral if appropriate. Throughout, I’d continuously reassess his stability and call for the medical or anaesthetic registrar immediately if he showed any signs of acute deterioration. If there is any suggestion the patient is deteriorating, or failing to respond to initial management measures, I would escalate immediately to my registrar, and critical care if necessary.

Answer 3

1. Obs 2. My number one differential would be sepsis, secondary to pneumonia or HAP but need to rule out other common sources such as urinary sepsis 3. Could also be viral - flu/COVID 4. PMH and hospital course/progress since admission will help me narrow down my differential

Answer 4

1. Having completed my initial assessment -> History / collateral 2. Notes to see progress during admission 3. Reassess ABCDE - adjust management in response to investigations + arrange other investigations 4. If any concerned about any aspect - escalate it appropriately to my registrar but in sepsis immediate escalate to senior - young pt, in shock and high risk for sepsis - if this is delayed or the patient deteriorating before possible I I would discuss with ITU - may need NIIV or in extreme cases intubation 5. If rapid deterioration 2222 adult cardiac arrest call to get immediate assistance 6. Explain the plan to the patient and update any next of kin with consent if this was required

Answer 5

1. Bedside: full obs, ABG (low sats), lactate (sepsis), blood glucose, CXR + urine dip/analysis/sample (source) or urine tox or preg, ECG (tacky), viral swabs, peak flow 2. Bloods + VBG: FBC, CRP, U&E, LFTs, amylase and coagulation screen + blood cultures if sepsis suspected (if poss before antibiotics) 3. Scans - depending on findings of my full history and A to E assessment maybe CXR or CT Head

Answer 6

Sepsis 6 - give fluids (bolus and monitor to see if any response), broad spectrum IV antibiotics and oxygen (aim >94%, 15L then titrate down) then take cultures, urine output (along with BP and HR gives response to fluids, should be >0.5ml/kg/hour) and lactate Paracetamol to help temperature If pt is having abdominal pain - keep NBM and get surgical review

Answer 7

Investigate for opportunistic infections e.g., TB, PJP and be cautious for parapneumonic effusions/empyema Re-examine to ensure no systemic features of infection I have missed Intraabdominal collections - examine his abdomen closely - low threshold for CT abdomen if any cancern Micro input - does the antibiotic I have prescribed provide suitable cover for immunocompromised patient Greater risk of rapid deterioration so I could ensure my seniors/ITU aware of this new information

Answer 8

1. Supportive - sats >94%, adequate fluid balance and good nutrition 2. If can't maintain oxygen - NIV in ITU, may also require intubation and proning 3. Dexamethasone 4. Antivirals - trusts have criteria and discussed with ID and micro teams 5. Antibiotics only when suspected superimposed bacterial pneumonia

Answer 9

Vertigo (false sensation of movement, usually spinning, either of oneself or the surroundings) Lightheaded/faint Unsteady

Answer 10

Hypoglycaemia Anxiety Cardio (arrhythmia, ACS, AS) incl meds (bp lowering, bbs, diuretics) - do they have chest pain/palps/SOB, do they have triggers (carotid sinus) or do they have a postural drop (dehydration via vom/diarrhoea or bleeding or PD or diabetes) Do they ever faint? Does their visual go dark? Do they feel they have to sit or lie down? Nausea/sweat/pallor?

Answer 11

Alcohol. Cerebellar disease incl stroke. Peripheral neuropathy.

Answer 12

Describe it - onset and pattern and exacerbating/relieving. Ever happened before? PMH? Meds?

Answer 13

Cardio and neuro exam incl cerebellar and gait w in line walking and rombergs and dix hall pike. *Mention key findings e.g., would be concerned if the patient had direction changing nystagmus or vertical*

Answer 14

Inner ear and vestibular nerve. BPPV, VN/L, Menieres, acoustic neurona.

Answer 15

Brainstem and cerebellum. MS, tumour, PCS (or bleed), vestibular migraine.

Answer 16

BPPV - seconds, associated with head movements Menieres - mins to hours episodic, fullness, fluctuating hearing loss, tinnitus VN/L (hearing loss) - hours to days

Answer 17

Progressive/worsening or has features suggesting central causes of vertigo

Answer 18

Dysdiadokinesia Ataxia - limb, truncal, gait Nystagmus - direction changing or vertical Intention tremor Slurred speech Hypotonia Also: Diplopia Headache Sudden weakness (facial droop) or numbness High vascular risk - HTN, diabetes, AF, hyperlipidemia, previous TIA/stroke (CV hx) makes suspicious for another stroke Cerebellar stroke actually often causes imbalance not spinning - feel pulled to one side Sudden onset inability to stand unaided or severe gait instability is stroke until proven otherwise Other symptoms of POCS: Dysphagia, ptosis, reduced consciousness and visual field defects (may actually only have visual symptoms by themselves)

Answer 19

1. Supportive - protection and monitoring of the patients airway, breathing and circulation as required 2. Give the reduced respiratory rate I would give a STAT dose of Naloxone 3. If present within 1-2 hours of taking the overdose, some local guidelines support the use of activated charcoal 4. If medicines were identified I would review the information on Toxbase or consult toxicology advice for specific management 5. I would escalate this patient to my seniors/ITU colleagues if I felt they were unstable or required immediate escalation of care

Answer 20

I would consult local guidelines regarding the management of Paracetamol toxicity and review whether this level is above the treatment line necessitating intervention. If this was the case I would initiate ?urgent treatment with NAC infusion as per the hospital guidance and recheck blood tests as per the protocol. (and further supportive measures as needed) I would continue to perform any required supportive management measures and continue close observation of the patient for any deterioration. I would discuss the patient with my colleagues in ITU so that they were aware of him in case of any further deterioration. I would explain the plan to the patient and update any next of kin with consent if this was required. At this point I would also consider any mental health team input that may be required both now and further down the line and conduct a basic risk assessment for the possibility of further suicidal intent. I would also consider a referral to any alcohol or substance misuse services, if this was identified as a concern.

Answer 21

Small proportion of Paracetamol is metabolised by CYP450 system enzymes to form NAPQI (toxic) This gets conjugated by glutathione to form a non-toxic compound which gets excreted in the urine In overdose the supply of glutathione is eventually depleted which allows NAPQI to exert hepatotoxic effects NAC replenishes glutathione stores and prevents hepatotoxicity This needs to be administered within 8 hours of ingestion to ensure maximum efficacy

Answer 22

This patient has evidence of hepatotoxicity and subsequent liver failure and therefore requires urgent discussion with a local transplant centre for advice and consideration of transfer. The King’s College Criteria is used to guide referral for transplant, with the main clinical metrics being a pH of <7.3 OR INR > 6.5 + creatinine > 300 + the presence of grade 3/4 hepatic encephalopathy I would also like to seek further support from seniors locally and consider specialist input as needed from local toxicology or gastroenterology services. There may be supportive measures we can perform initially to ensure the best patient outcome and they may require admission to the intensive care unit in order to facilitate this.

Answer 23

I would start by asking the nurse whether they feel the patient’s condition is immediately life-threatening/whether they feel the patient’s life is at immediate risk. If so I would advise them to put out a 2222 cardiac arrest call and I am on my way. Then: A = is the patient independently maintaining the airway? can they speak? is there any stridor or wheeze? B = what are the saturations and respiratory rate? are they on oxygen? C = what is the heart rate and blood pressure? Lastly: 1. What admitted with? 2. What treatments have they had? Do they have any allergies? 3. Was this acute event or have they been progressively deteriorating? 4. Any another symptoms - chest pain, sweating, dizziness? If they are continuing to deteriorate quickly -> call the crash team and get help!

Answer 24

This is potentially an anaphylactic reaction to the antibiotic that has been given and the patient needs to be treated as such -> inform the nurse to put out a 2222 call immediately. STOP the IV infusion. The patient will need treatment with adrenaline - 0.5mg IM. If the nurse is not going to give this then advise them to get the drug ready and you will come immediately to administer it. Advise that if patient has a cardiac arrest then CPR should be started immediately.

Answer 25

Given the history and events I am aware of, anaphylaxis sounds like the most likely cause for this presentation. However, given the PMH my differential list would include: 1. Sepsis - given the initial presentation with infection 2. Not responded to initial treatment 3. Pulmonary oedema - sig cardiac hx and given IVF 4. Pneumothorax 5. PE 6. Cardiac cause - sig cardiac hx and given she has diabetes she may not have chest pain

Answer 26

1. Monitoring obs - sats, HR and BP 2. Perform perform 12 lead ECG (any ischaemic change) then attach continuous 3 lead cardiac monitoring 3. Bloods (urgent) + VBG to check for markers of infection, such as the patient’s white cell count and CRP, if the patient has a temperature I would also send blood cultures 4. ABG 5. CXR

Answer 27

I would contact my seniors and ensure make sure the nurses have put out a 2222 call. If there was any life threatening features of anaphylactic reaction present, namely: A = swelling, hoarseness, stridor B = rapid breathing, wheeze, fatigue, cyanosis, SpO2 < 92%, confusion C = pale, clammy, low blood pressure, faintness, drowsy/coma I would give IM adrenaline. I would give high flow oxygen and maintain the patient’s airway. If there is no response I would give another IM adrenaline dose after 5 minutes along with IV fluids. I would recall for help if none had arrived. Adrenaline can be repeated every 5 mins. Oxygen. Salbutamol neb. Give further IV fluid boluses. Lie flat + elevate legs. Send tryptase. After: Prescribe adrenaline auto-injectors, refer to allergy clinic and provide written anaphylaxis action plan

Answer 28

(Na+ + K+) - (Cl- + HCO-3). The normal range = 10-18 mmol/L.

Answer 29

Lactate - shock, sepsis, hypoxia Urate - renal failure Ketones - diabetic ketoacidosis, alcohol Acid poisoning - salicylates (late), methanol

Answer 30

Lower GI loss - prolonged diarrhoea Addisons disease RTA Acetazolamide or ammonium chloride injection

Answer 31

Bedside: ECG (tachy ?AF), glucose, L/S BP if dizziness presenting Bloods: FBC (platelets), U&E (kidney function), coagulation screen, G&S (in case FFP is needed to reverse a coagulopathy in the case of ICH) Imaging (ALWAYS DISCUSS SCANS WITH REG): non contact CT Brain (rule out if ICH), MRI Head (when stable, best imaging modality for confirming ischaemic stroke) More longer term: Investigations to try and establish the cause of any stroke e.g., HBA1c, lipids

Answer 32

1. Present within 4.5 hours of onset of symptoms = thrombolysed with IV alteplase (risk benefit diminishes after this) 2. Thrombectomy in patients with large vessel occlusion, can be effective when undertaken in first 24 hours after presentation but can only be carried out in some centres 3. Aspirin 300mg ANYONE WITH SUSPECTED STROKE SHOULD BE DISCUSSED WITH THEIR LOCAL STROKE TEAM WHEN CONSIDERING INITIATING TREATMENT for 2 weeks (unless haemorrhage) followed by clopidogrel 75mg OD 4. Atorvastatin 80mg OD 5. Only give BP lowering treatment if >185/110 or complications eg encephalopathy

Answer 33

Delay anticoagulation to 14 days. If given straight away increases risk of intracranial haemorrhage, including haemorrhagic transformation of the infarct. Any decision to start anticoagulation earlier than this should be led by the patient’s stroke consultant.

Answer 34

Not every hospital has a HASU. Provide 24/7 hyperacute care including rapid imaging, IV thrombolysis and monitoring during the first 72 hours. Some HASUs also perform mechanical thrombectomy onsite while others transfer eligible patients to a regional theombectomy centre (as part of the integrated stroke network). Care is delivered by specialist stroke teams - cons, reg, stroke nurses - enabling immediate expert assessment. After hyper acute phase patients are repatriated to a local acute stroke unit.

Answer 35

Delivered through regional integrated care networks. These are regional structures linking hospitals, specialist centres and community services to provide rapid/time critical patient centred coordinated care across a defined population. Patients with suspected stroke are taken directly to a hyper acute stroke unit - time is brain. Not every hospital has a HASU. Provide 24/7 hyperacute care including rapid imaging, IV thrombolysis and monitoring during the first 72 hours. Some HASUs also perform mechanical thrombectomy onsite while others transfer eligible patients to a regional theombectomy centre (as part of the integrated stroke network). Care is delivered by specialist stroke teams including cons, reg, stroke nurses - enabling immediate expert assessment. After hyper acute phase patients are repatriated to a local acute stroke unit which focus on ongoing IP care, secondary prevention and rehabilitation.

Answer 36

Focus on ongoing IP care, secondary prevention and rehabilitation.

Answer 37

If the patient is within a thrombolysis window, and your site is not that with a stroke service, then they should be transferred prior to arranging a CT head and other investigations. This is because you should act on clinical suspicion so that they are transferred to a centre with thrombolysis facilities as soon as possible, before radiological confirmation. If they are outside the thrombolysis window then there is less time urgency, and a CT scan could be done locally. If you were uncertain on how stroke services are managed at your hospital, you should urgently contact the medical registrar for advice.

Answer 38

These are regional structures linking hospitals, specialist centres and community services to provide rapid/time critical patient centred coordinated care across a defined population. Patients with suspected stroke are taken directly to a hyper acute stroke unit - time is brain.

Answer 39

The management of suspected STEMIs (i.e. referral to primary PCI centres). Primary PCI services are delivered through regional integrated care networks for patients with suspected STEMI. Ambulance crews use ECG + bypass local hospitals and take patients direct to the regional primary PCI centre for intervention. After the procedure, patients are repatriated to their local hospital for ongoing medical management and rehab. If patients are in a hospital without PCI they are stabilised locally and then urgently transferred to a regional PCI centre for intervention.

Answer 40

A to E assessment (including glucose... obviously... as you do for everyone!) My main concern is acute stroke so I would contact my local stroke service which may not be at my hospital. If stable - arrange transfer without delay as time is brain. This may mean calling 999 from your hospital ward and arranging an urgent transfer. Don't need to wait for referral accepted - but courteous to let them know heading their way. If the patient is within a thrombolysis window, and your site is not that with a stroke service, then they should be transferred prior to arranging a CT head and other investigations. This is because you should act on clinical suspicion so that they are transferred to a centre with thrombolysis facilities as soon as possible, before radiological confirmation. If they are outside the thrombolysis window then there is less time urgency, and a CT scan could be done locally. If you were uncertain on how stroke services are managed at your hospital, you should urgently contact the medical registrar for advice.

Answer 41

1. I would start by empathising with them and make sure they feel I have acknowledged their concerns 2. I would not try to resolve it myself but I would explain what steps have been taken since establishing the diagnosis of stroke with regards to the treatments given so far (as making sure the patient is safe and receiving the right treatment is the most important thing) 3. Acknowledge their right to complain (if unhappy with the medical care they have received) and explain to them the process for this in hospital 4. I would direct patients or relatives to the Patient Advice and Liaison Service (PALS) for which I would give them a leaflet or written information PALS is the Patient Advice and Liaison Service, which helps patients, families, and carers with confidential advice, support, or concerns about care. 5. I would ask them if they wanted to speak to one of the senior clinicians on my team who may be able to further address their concerns 6. To finish our conversation, I would again empathise with them with regards to the situation that they find themselves in and let them know that I am available to speak to again in case they have any further questions or issues with the complaints process

Answer 42

1. Pick a diagnosis 2. Make a differential list and why not likely other things 3. Prep handover

Answer 43

This is a young patient who has been !admitted with breathlessness and !presumed exacerbation of their asthma. However, differentials I would want to rule out include: PE Pnuemothorax Pneumonia HF due to cardiomyopathy or pulmonary arterial hypertension Anaphylaxis!

Answer 44

When assessing a patient with an exacerbation of asthma it is essential to identify the severity of the asthma attack: Moderate Severe Life-threatening Near fatal

Answer 45

Raised CO2 or requiring mechanical ventilation with raised inflation pressures

Answer 46

1. PEFR 2. RR 3. HR 4. Sentences

Answer 47

Moderate = 50-75% best or predicted Severe = 33-50% Life threatening = <33%

Answer 48

Moderate = <25 Severe = >25 Life threatening = poor resp effort/silent chest/cyanosis *Sats <92% and normal CO2*

Answer 49

Moderate = <100 Severe = >100 Life threatening = brady/arrythamia or low BP

Answer 50

Moderate = speech normal Severe = can't complete sentences Life threatening = exhaustion/confusion/reduced consciousness/coma

Answer 51

I would assess the patient using an A to E approach, making sure to also establish the metrics of severity recommended by the British Thoracic Society for the assessment of an acute asthma exacerbation. Specifically mention in B - assess for cyanosis, silent chest, and a poor respiratory effort as these are all signs of a life threatening asthma exacerbation Specifically mention in C - low BP life threatening, as is arrhythmia so 12 lead ECG followed by continuous 3 lead cardiac monitoring PEF expressed as a % of the patient’s previous best value is most useful clinically – but an estimate of their predicted PEF can also be used as a rough guide. An ABG is essential to providing information about oxygenation. CXR may be required especially when I consider my differentials and would be helpful to rule out suspected pneumothorax or consolidation. CXR would also be important in a patient not responding to initial treatment, as well as consideration of further investigations like a CTPA, as acute PE is an important differential for any patient presenting with acute breathlessness.

Answer 52

This patient needs urgent treatment, delivered in an acute hospital setting. Therefore, I would administer supplemental oxygen immediately to maintain saturations between 94-98%. First line treatment is with a nebulised β₂ agonist via an oxygen driven nebuliser. If there is no initial response, then I would ask the nurses to give nebulised ipratropium bromide back-to-back. Steroids should be given to all patients suffering an exacerbation of asthma, and in a life-threatening situation, these could be given IV as hydrocortisone or IM methylprednisolone if the patient cannot take an oral steroid. IV magnesium can be given to patients with a severe asthma attack or worse and I would consider this for this patient, particularly if there has not been a good response to initial treatment. However, before commencing this I would discuss this with my senior team.

Answer 53

As per the British Thoracic Guidelines, I would refer any patient that is: 1. Requiring ventilatory support - ignore 2. Acute severe or life-threatening asthma, who is failing to respond to therapy, as evidenced by: Deteriorating PEF Persisting or worsening hypoxia Hypercapnia ABG analysis showing decreasing pH or increasing H+ Exhaustion, feeble respiration Drowsiness, confusion, altered conscious state Respiratory arrest

Answer 54

I would immediately put out a ‘2222’ adult cardiac arrest call and call for help in the ward. I would start my assessment as per the ALS guidelines, checking for a pulse and signs of life, and start CPR if the patient has arrested. When considering a cardiac arrest in a patient with asthma it is important to consider the following: 1. I would make sure high flow oxygen continues to be administered – hypoxaemia is likely the cause of the arrest 2. Ventilate with respiratory rate (8-10 min) and sufficient tidal volume to cause the chest to rise 3. Aim to intubate early once your anaesthetic team arrive 4. I would check for reversible causes of CPR, particularly a tension pneumothorax 5. Disconnect from positive pressure ventilation if this has been started 6. Consider ECPR in accordance with local protocols if initial resuscitation efforts are unsuccessful

Answer 55

Before speaking with the patient's relative I would discuss the case with my consultant or senior registrar to be clear on the information I was going to communicate with them and so that I did not set unrealistic expectations or speak without fully understanding the situation. Before speaking I would try and find a quiet space on the ward with chairs, to minimise interruptions, and hand over my bleep to one of my colleagues. I would ask the patient's sister if there is anyone else they would like to be with them. I would start our conversation by asking the sister what they already know and what they understand has happened. I would be clear about the order of events. When delivering bad news, I would ensure that I gave warning shots before, particularly when talking about cardiac arrest. I would make sure that I give appropriate pauses in my consultation for the relative to ask questions or take on board the information I am delivering. I would minimise my use of medical jargon and keep things simple. When ending the consultation, I would check with the sister again if there is anyone else I need to speak to. I would offer her the chance to come to ITU and see her brother, once I had spoken to the ITU team. I would make sure that she is aware of other people on the ward she can speak with or how to get hold of me once we have finished, in case she has further questions. Frameworks like the “SPIKES” tool can be useful to structure breaking bad news conversations. This is also something you could mention in your answer, if asked about difficult communication skills scenarios.

Answer 56

Based on the history and the observations I would be most concerned that this patient has sepsis. She is hypotensive, tachypnoeic and has an altered mental state. Based on these observations she meets the new criteria for sepsis. Her other observations also support this diagnosis and my assessment and management would be based on this. Based on hypotension, tachypnoea, and altered mental state, this patient meets ≥2 qSOFA criteria and therefore fulfils the Sepsis-3 criteria for suspected sepsis. She meets 3/3 qSOFA criteria, which is very concerning for sepsis. Acute organ dysfunction. qSOFA criteria (quick SOFA) is a bedside screening tool, ≥2 = high risk of sepsis. Respiratory rate ≥22 / min Systolic BP ≤100 mmHg Altered mental state GCS <15 / new confusion ➡ 2 or more = sepsis likely and requires urgent escalation.

Answer 57

Sepsis = life-threatening organ dysfunction caused by a dysregulated host response to infection.

Answer 58

Septic shock is a subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality. Clinically, it is defined by all of the following despite adequate fluid resuscitation: 1️⃣ Persistent hypotension requiring vasopressors to maintain MAP ≥65 mmHg 2️⃣ Elevated serum lactate Lactate >2 mmol/L 3️⃣ Suspected or confirmed infection with features of sepsis (organ dysfunction)

Answer 59

Give 3 Take 3 1. Titrate oxygen to a saturation target of 94% 2. Lactate and other bloods 3. IVF + commence accurate urine output measurement 4. Administer empiric intravenous antibiotics with blood cultures prior if possible

Answer 60

Follows sepsis 6 1. Start broad-spectrum IV antibiotics - these should be started within one hour of sepsis being suspected AND should be (daily assessed and) adjusted in response to micro/previous sensitivities, abx therapy should be guided by clinical response and normally lasts 7-10 days 2. I would give a bolus of IV Fluid and monitor the blood pressure to see if there is any response. Urine output should also be measured in response to IV fluids and output should be greater than 0.5mL/kg/h 3. High flow oxygen should be given unless there is a known contraindication 4. Once initial steps done need to identify the source and control it

Answer 61

Underlying malignancy Age older than 65 years Immunocompromise Haemodialysis Alcoholism Diabetes mellitus

Answer 62

These represent signs of septic shock as defined earlier. I would continue to resuscitate with IV fluids. As the patient is deteriorating despite initial management, I at this point would be considering escalation to a HDU or ITU for consideration of vasopressors and other organ support. At this point, I would also be discussing the patient with my registrar, and seeking their support - and if it was agreed that the patient is for escalation, would refer to the critical care team.

Answer 63

The prognosis in patients with sepsis and septic shock is guarded at best. The mortality rate from sepsis has been estimated in a number of studies to be between 28% and 50%. The SOAP study in Europe observed an overall hospital mortality of 36%.

Answer 64

In background and its good to say something like she has a known history of cognitive impairment but at baseline she is alert and independently mobile. Also make sure to use the information you get along the way for SBAR esp. assessment section.

Answer 65

1. Senior clinical review 2. Jobs I need you to follow up on e.g. bloods for hyponat every 4 hours to ensure under 8 moll in 24 hours and review cause maybe fluid restrict/review diuretic dosing with endo help/chase pleural fluid aspirate results and depending on results may need further antibiotic treatment, chest tube drainage or further imaging to determine the further course of management 3. ITU escalation (done or if...)/discuss with specialty + discussion with family/NOK/POA (update and escalation of treatment/resuscitation)

Answer 66

If the patient is alert enough I can do this with oral glucose. In the unconscious patient, IV 20% (or 10%) glucose or IM glucagon can be used.

Answer 67

Adrenal insufficiency - send cortisol! Also send TFTs (plus Mg Phos and Ca) + paired serum and urine osmo plus urine sodium Also lipids Given the initial investigations showing hyponatraemia and hypoglycaemia and the history of weight loss and lethargy, I would be concerned about an adrenal crisis causing this presentation and so would ensure to manage this.

Answer 68

Amylase Also surgical review +/- CT abdomen (this would need to be discussed with my registrar)

Answer 69

FBC CRP U&E LFTs Bone profile Mg

Answer 70

Tissue hypoxia / poor perfusion Acute mesenteric ischaemia Severe hypoxia / respiratory failure – inadequate oxygen delivery to tissues Medications / toxins – e.g., metformin, β-agonists, cyanide, ethanol

Answer 71

My first suspicion would be septic shock and I would initially look to manage them as this. Could also be acute pancreatitis or acute liver failure or history of abdominal pathology or trauma.

Answer 72

Adrenal crisis is a life-threatening condition caused by insufficient cortisol (and sometimes aldosterone), leading to hypotension, shock, hyponatraemia, hyperkalaemia and hypoglycaemia, often presenting with dizziness, vomiting, and in severe cases altered consciousness. It usually occurs when the body is unable to produce sufficient cortisol in response to acute stressors such as infection, surgery, trauma, or sudden steroid withdrawal, and requires urgent treatment with IV hydrocortisone and fluids.

Answer 73

Adrenocortical insufficiency may be subclinical for days and months in otherwise well individuals. Stress precipitates the adrenal crisis due to the body’s inability to produce Cortisol in response to it. Common stressors include infection (the most common precipitating factor), surgery, anaesthesia, trauma, exogenous steroid withdrawal (for example in a patient who has been treated for an exacerbation of asthma).

Answer 74

Treatment may be required before the diagnosis is confirmed. General measures such as giving oxygen, broad spectrum antibiotics for infection and fluid balance monitoring should be started. The patient may require a catheter. Shock should be treated with IV fluids such as normal saline 0.9%. 1L should be given stat and then subsequent bags titrated to response. I would make sure that the patient’s sodium is repeated at 4 hours to make sure its correction is not too rapid. Finally, the most important treatment for this patient is administration of glucocorticoids. Hydrocortisone should be given intravenously. (It is worth noting that commencing hydrocortisone can do little harm and may be life saving!). Continue with IV hydrocortisone before switching to oral steroids at 72 hours. Mineralocorticoid replacement once the patient is stable is achieved with fludrocortisone. If you suspect adrenal crisis, you should usually give antibiotics as well, unless there is a clear non-infective cause. Infection is the most common precipitating factor for adrenal crisis Adrenal crisis and sepsis look very similar: Hypotension Shock Confusion Raised lactate You cannot safely distinguish them early, and they often co-exist

Answer 75

Autoimmune destruction of the adrenal cortex is the most common cause of primary adrenal insufficiency in the UK, accounting for 80% of cases. This is termed Addison's disease and results in reduced cortisol and aldosterone being produced. The symptoms of Addison’s disease are often vague and most frequently encompass weakness, fatigue, nausea, vomiting and weight loss (low BMI). The most common physical sign is hyperpigmentation of the skin and mucous membranes. Patients will typically be hypotensive with significant orthostatic hypotension.

Answer 76

Addison’s disease is typically associated with other autoimmune disorders such as autoimmune thyroid disease, premature ovarian failure, type 1 diabetes mellitus, vitiligo, alopecia and coeliac disease. This spectrum of disorders is also referred to as autoimmune polyendocrine syndrome - condition characterised by autoimmune destruction of two or more endocrine organs, leading to multiple hormone deficiencies.

Answer 77

Patients should be told to wear a medical alert bracelet. During times of stress (e.g. minor surgery, infections) patients should be instructed to double or triple their usual maintenance dose of steroid. Patients should know to contact their GP or seek medical help in times of severe stress when oral uptake of steroids may be compromised – for example in severe vomiting or diarrhoea. Patients should also be given instruction on how to administer IM injections in these scenarios.

Answer 78

The short Synacthen test is a test of adrenal insufficiency that can be used as a screening procedure in the non-critically ill patient. The test is based on a measurement of serum cortisol before and after an injection of synthetic ACTH. In acute adrenal crises, where delaying treatment could be life threatening, a blood sample for a random cortisol should be taken prior to starting hydrocortisone. A random plasma cortisol of greater than 25 mcg/dL effectively excludes adrenal insufficiency.

Answer 79

The correction in sodium concentration must not exceed 10 mmol/L in the first 24 hours and 18 mmol/L in the first 48 hours. Rapid correction of hyponatraemia must be avoided as it can result in osmotic demyelination known as central pontine myelinolysis.

Answer 80

Yes - warrants HDU care also if hypovolaemic shock ITU review also contacting the on-call endocrine team to discuss this patient and his further management and continuous fluid balance monitoring, regular sodium, potassium, and glucose monitoring as we commence fluid resuscitation

Answer 81

The patient in the scenario has a seizure episode likely secondary to severe symptomatic hyponatraemia. This will require prompt assessment and correction of sodium and further monitoring and management in an HDU/ITU setting.

Answer 82

Chest X-ray to assess for infection/aspiration (post seizure) or fluid overload for volume status

Answer 83

I would DISCUSS WITH MY SENIORS RE giving 150 mL of 3% hypertonic saline over 20 minutes and re‐check sodium to target an initial rise of ~5 mmol/L (in first hour) (repeat once if needed), then limit correction to ≤8–10 mmol/L in 24 hours with serum sodium checks every 4–6 hours (using 5% dextrose or desmopressin if it’s climbing too fast after discussion with endocrine), ?all the while watching for new or worsening neurological signs such as headache, confusion, dysarthria, dysphagia or limb weakness that could point out towards osmotic demyelination and escalating to senior or the endocrine team immediately if correction exceeds safe limits, symptoms develop ?or the underlying cause remains unclear.

Answer 84

The duration of hyponatraemia is determined by careful history and review of previous sodium measurements; when onset is unknown, assume chronic. In acute severe hyponatraemia (onset < 48 h with neurological symptoms), a 100–150 mL bolus of 3% saline to achieve a rapid 4–6 mmol/L sodium rise is given to halt cerebral oedema. In contrast, chronic or mild cases warrant slow correction using isotonic saline, ?low‐dose hypertonic saline or fluid restriction, aiming for a total increase of ≤ 8 mmol/L over 24 h. Overcorrection is guarded against by checking serum sodium every 4–6 hours and by performing neurological observations hourly, and hypotonic fluids or desmopressin are employed if sodium rises too rapidly.

Answer 85

Start with Possible differentials in this case, depending upon history and examination findings, include: Hypovolaemic: Gastrointestinal losses (vomiting, diarrhoea) Furosemide-induced renal salt and water loss Third-space fluid losses (e.g. pancreatitis, burns) Haemorrhage Thiazide diuretic use Addison’s disease (primary adrenal insufficiency) Euvolaemic: SSRI-induced SIADH Adrenal insufficiency Hypothyroidism Primary polydipsia Beer-potomania or “tea-and-toast” diet Post-operative or pain/nausea-induced ADH release CNS pathology (e.g. subarachnoid haemorrhage, stroke) Malignancy-associated SIADH (e.g. small-cell lung cancer) Drug-induced SIADH (e.g. carbamazepine, cyclophosphamide) Hypervolaemic: Dilutional hyponatraemia from chronic heart failure Cirrhosis of the liver Nephrotic syndrome Advanced chronic kidney disease Acute decompensated heart failure beyond NYHA II

Answer 86

SIADH‑inducing drugs: Selective serotonin reuptake inhibitors (e.g., sertraline, fluoxetine) Serotonin–noradrenaline reuptake inhibitors (e.g., venlafaxine) Carbamazepine and oxcarbazepine Tricyclic antidepressants (e.g., amitriptyline) Cyclophosphamide Certain antipsychotics (e.g., haloperidol) Proton‑pump inhibitors (e.g., omeprazole) NSAIDs (by potentiating ADH action) Renal salt‑wasting agents: Thiazide diuretics (e.g., hydrochlorothiazide) Loop diuretics (e.g., furosemide) Altered renal water handling: ACE inhibitors and ARBs (may enhance water retention) - euvolaemia in SIADH section Desmopressin (exogenous ADH analogue) Each group lowers serum sodium either by inappropriate water retention (SIADH or ADH potentiation) or by excess renal sodium loss.

Answer 87

I would define mild–moderate hyponatraemia as a serum sodium of 120–130 mmol/L in a patient who is only mildly symptomatic, such as experiencing nausea, headache or lethargy without seizures or significant neurological deficit. But regardless of Na level if the patient has severe symptoms - seizures, reduced consciousness, severe N/V, confusion or resp compromise (slow/hypoventilating/irregular) - discussion with seniors/HDU for hypertonic saline. Management depends entirely on volume status. CHECK SODIUM EVERY 4 HOURS TO ENSURE NOT RISING TO FAST. In hypervolaemic patients, I would treat the underlying cause, e.g., optimising heart failure, cirrhosis or nephrotic syndrome and impose fluid restriction with strict input/output charts, daily weights and regular renal and electrolyte monitoring. Furosemide if needed. In hypovolaemic patients I would address the precipitant (for example stopping diuretics or treating GI losses) and give 0.9 % saline if the sodium is ≥ 125 mmol/L ?or Hartmann’s solution (or 500 mL normal saline followed by 1 L 5 % dextrose) if it is < 125 mmol/L, checking sodium after each 1.5 L and aiming for a rise of < 8 mmol/L per 24 hours in high-risk patients. In euvolaemic patients, I would treat the underlying cause, restrict fluids to 1–2 L/day, and if sodium remains low after 48 hours, investigate for SIADH; if SIADH is confirmed, I would commence fluid restriction of < 1 L/day with endocrinology input and if it is excluded I would consider a trial of oral sodium chloride replacement.

Answer 88

Pseudohyponatraemia is defined as a laboratory artefact in which serum sodium appears low because an abnormally high burden of lipids or proteins, such as in severe hypertriglyceridaemia, paraproteinaemia in multiple myeloma or following large‐volume IV immunoglobulins. The excessive lipids and proteins displace the plasma water fraction and result in incorrect serum sodium measurement while the serum osmolality remains normal. To manage it, ?I would request plasma osmolality?, ?avoid any unnecessary hypertonic saline?, and focus on treating the underlying cause of the lipaemia or protein excess.

Answer 89

It is often caused by rapid correction of chronic hyponatremia. It leads to irreversible demyelination in central pons. Prevent by correcting chronic hyponatremia slowly <8-10mmol/L per 14 hours (<8 rise in high risk or chronic hyponatreamic patients). Everyone is <8 per 24 hours thereafter. Doesn't matter if acute or chronic. It occurs 2-6 days after rapid correction - slurred speech, diplopia, increased tone, locked in syndrome/coma. Umbrella term is osmotic demyelination syndrome.

Answer 90

Severe symptomatic hyponatraemia DISCUSSING WITH SENIORS/ITU due to risk of cerebral oedema. Seizures, reduced consciousness, severe N/V, confusion, resp compromise: Bradypnoea or irregular breathing Hypoxia (low SpO₂) or rising CO₂ Reduced GCS (stupor/coma) Apnoeic episodes or need for assisted ventilation

Answer 91

Nausea Headache Mild confusion Lethargy

Answer 92

150ml 3% hypertonic saline in ITU/HDU over 20 mins

Answer 93

Aim for acute rise in serum sodium around 5 mmol/L in the first hour to reduce immediate risk from cerebral oedema / prevent further seizures If symptoms persist or sodium has not risen by 5 mmol/L after the first hour (re check after 30 mins) repeat bolus UNDER SENIOR MX

Answer 94

Cause specific treatment - fluid restrict or isotonic saline Close supervision is needed to avoid over correction (ODS) - Na checked every 4 hours

Answer 95

Onset of symptoms and review of previous sodium measurements In acute brain cannot adapt do risk of cerebral oedema is high Whereas in chronic, brain adapts to low sodium over time this is why don't routinely use 3% saline UNLESS SYMPTOMATIC AFTER DISCUSSION WITH SENIORS, instead correct slowly using isotonic saline or fluid restrict

Answer 96

M = malignancy e.g. SCLC I = infection e.g. TB or pneumonia N = neuro e.g. SAH D = drugs e.g. SSRI

Answer 97

BP and postural change Armpits Mucous membranes and skin turgor JVP and oedema Weight change and history

Answer 98

Increase salt intake (salty foods) Increase protein e.g. meat/dairy/eggs (needed for kidneys to excrete free water effectively) Usually no restriction needed, unless also overloaded Oral Na replacement if diet alone is insufficient

Answer 99

Hyperglycaemia Alcohol Mannitol 2xNa+glucose+urea If gap>10 suspect ethanol/methanol (visual disturbance)/ethylene glycol/isopropanol/glycerol/radiographic contrast

Answer 100

Antagonises ADH Approved for hyponatremia due to SIADH when restriction to 1L/day fails and hypervolaemic hyponatraemia under specialist supervision if hyponataremia and fluid overload persists

Answer 101

Hypo = low BP, high HR, postural drop and dry MM Eu = normal Hyper = often high BP, pitting oedema, raised JVP, crackles and weight gain

Answer 102

Hypo = NaCl and correct cause Eu = fluid restrict Hyper = fluid restrict and diuretic

Answer 103

Urine Na<20 extra renal = diarrhoea/vomiting Urine Na>20 renal loss = Addisons, diurectic, nephropathies and CSWS

Answer 104

Urine osmo<100 = water intoxication, beer and tea and toast syndrome (diet low in salt and protein) Urine osmo>100 = SIADH and hypothyroid

Answer 105

Urine Na<20 = oedematous state (heart failure, cirrhosis, low albumin, nephrotic syndrome or hypotonic saline) Urine >20 = renal failure Interestingly, heart failure and cirrhosis have a low urine sodium but high urine osmo - opposites

Answer 106

Mild–moderate renal impairmen: Yes, loop diuretics help mobilize fluid, correct edema, and improve sodium concentration Severe renal failure/oliguric: Often limited response; may require high-dose loop diuretics or combination therapy (e.g., thiazide + loop) End-stage/anuric: Diuretics usually ineffective; renal replacement therapy (dialysis) may be required to remove fluid and correct sodium Combine with fluid restriction Diurese if kidneys can; dialyze if they can’t!

Answer 107

Loops lose everything (Na, K, Cl, Ca, Mg), thiazides lose K but hold Ca, K sparing keeps K in. Loop = furosemide and bumetanide Thiazide = bendroflumethiazide (common for hypertension) Thiazide like = indapamide K sparing = spironolactone and eplerenone (aka aldosterone antagonists)

Answer 108

The patient has hypercalcemia with mild/moderate symptoms, I would start by carrying out an A to E assessment followed by fluid replacement to correct the calcium levels FBC, U&Es, renal and liver function, calcium (with parathyroid hormone (PTH) and parathyroid hormone related peptide (PTHrP)), phosphate, magnesium, vitamin D, TFTs and a myeloma screen 0.9 % saline at around 150–200 mL/hr to restore intravascular volume and promote calciuresis - STRICT FLUID BALANCE WITH CATHETER Loop diuretics may be used if fluid overload develop - discuss with senior After rehydration (once euvolaemic) - IV bisphosphonates (also discuss with senior) Examine him for signs of hypercalcaemic complications

Answer 109

If his serum calcium rose above 3.5 mmol/L, if he became confused or drowsy, if his urine output dropped despite fluids (or renal function drop), if the ECG showed arrhythmias or marked QT changes, or if his creatinine rose further despite resuscitation, I would escalate immediately to my registrar and consider ITU input.

Answer 110

STONES: I would ask about any symptoms of kidney stones such as pain or blood in the urine or any change in thirst or urinary frequency (polydipsia/polydipsia) BONES: Any bone pain or fractures GROANS: N/V, constipation, indigestion or abdo pain MOANS: confusion or mood changes or fatigue or insomnia Then review all medications—especially thiazides, or calcium/vitamin D supplements—any changes? Finally ask about weight loss, night sweats or cough that might suggest an underlying cancer.

Answer 111

ALWAYS SPEAK SLOWLY (LOOKS GOOD AND GIVES ME TIME TO RELAX AND THINK). I would tell her that her father’s blood calcium level is higher than normal, which can make him feel tired and sick, and can affect his heart and kidneys. We are giving him fluids through a drip to help his body get rid of the extra calcium, checking his heart with a monitor, and running tests to find out why the calcium is high. I have involved my senior doctor to decide on further medication that will lower the calcium more effectively once it is safe.

Answer 112

1. Primary hyperparathyroidism 2. Malignancy-associated hypercalcaemia (such as PTHrP-secreting tumours or osteolytic metastases/myeloma) 3. Drug-induced, such as due to thiazide diuretics 4. Vitamin D mediated either due to granulomatous diseases, such as sarcoidosis, or exogenous overconsumption of vitamin D supplements 5. Other endocrine causes, such as thyrotoxicosis or adrenal insufficiency For investigations: Bedside = full obs, urine dip and CONTINOUS ECG Bloods = FBC, U&E, LFT, CRP, bone profile including calcium and phosphate, Mg then PTH, PTHrP, vitamin D, TFTs and a myeloma screen including serum protein electrophoresis and free light chains Imaging = CXR, neck US (if parathyroid adenoma suspected) or CT CAP if malignancy suspected after discussing with senior

Answer 113

This confirms malignancy-driven hypercalcaemia. I would continue IV fluids and discuss with my senior regarding the use of IV bisphosphonates or denosumab (if renal failure or bisphos don't work), liaise urgently with Oncology and Respiratory teams to arrange biopsy and staging and maintain symptom control with antiemetics.

Answer 114

Cardiac causes: !!!Acute coronary syndrome, pericarditis, coronary spasm Respiratory causes: !!!Pulmonary Embolism, !!!Pneumothorax, Pneumonia and subsequent pleurisy Musculoskeletal Chest Pain Gastrointestinal system: Oesophagitis, Pancreatitis, Cholecystitis, !!!Boerhaave’s perforation of the Oesophagus, Peptic Ulcer Disease Vascular causes: !!!Aortic dissection, Aortic aneurysm Psychiatric Causes: Anxiety Explain to the examiner what your most likely differential is – this man has risk factors for ischaemic heart disease and is the right age group for an MI. The examiners will be most interested in the way you structure the answer. Make sure it is clear to the examiner that in the acute setting you are thinking about the conditions that are potentially life threatening to the patient.

Answer 115

Classic structure PLUS RISK FACTORS FOR WHAT YOU ARE WORRIED ABOUT AND DIRECTLY ASK QUESTIONS LIKE IS THE CHEST PAIN TEARING IN NATURE, IF THEY HAVE A COUGH, DO THEY HAVE HEMOPTYSIS? SOCRATES is always used for pain including chest pain Make sure you ask about artherosclerosis risk factors: older age, male (don't say these two in your questions though), smoking, hypertension, hypercholesterolaemia, diabetes and family history. Use this question again to reiterate that you are thinking about life threatening conditions. You should ask specifically about chest pain that is ‘tearing in nature’ and radiating to the back (aortic dissection); sudden onset pleuritic chest pain with breathlessness (Pneumothorax, PE), ask about haemoptysis and risk factors for PE.

Answer 116

Bedside: full observations should be the first line investigations, ECG Blood tests: FBC, U+Es, inflammatory markers, troponin – this should be measured on admission and then again 6-12 hours after the onset of pain. Remember there are other causes of a raised Troponin. Should you send a D-Dimer? In general no, unless a PE is suspected and the Modified Wells Score suggests PE is unlikely. ?Different hospital trusts will have different criteria for when a D-Dimer should be sent. Imaging: CXR, they will also need an ECHO, however, this will not be part of your acute investigations

Answer 117

Condition where air comes trapped in the SC tissue - swelling under skin/puffy but not red nor inflamed. Characteristic crackling or popping sensation when the area is pressed - this is called crepitus. Locations = chest wall, neck or face. It can spread quite far due to fascial planes.

Answer 118

It is benign/self limiting but is a clue to serious pathology underlying Air escapes from resp or GI tract and tracts under skin: Pneumothorax - often tension/traumatic Rib fractures Boerhaave syndrome Mechanical ventilation with high pressures Post surgical - thoracic/neck/dentist Severe asthma/coughing fits

Answer 119

Not usually chest pain. Most often presented with sudden, severe abdominal pain, back pain or flank pain, often with hypotension or collapse in thoracic AA where chest pain is common.

Answer 120

1. Acute aortic syndrome - aortic dissection or ruptured thoracic aortic aneurysm (both cause widened mediastinum) 2. MI 3. PE 4. Tension pneumothorax 5. Cardiac tamponade (raised JVP, muffled heart sounds, low BP) Clinically, ruptured TAA and acute aortic dissection overlap heavily

Answer 121

Sudden severe chest pain Tearing in nature Stanford A (ascending aorta meaning risk of cardiac tamponade) - anterior chest pain into neck or jaw Stanford B (descending aorta) - back between shoulder blades into neck or abdomen Sweating/SOB/N+V/syncope Limb ischaemia or AKI Neuro deficits BP difference between arms

Answer 122

Stabilise - IV access, oxygen Morphine BP 100-120, HR <60 - 1st line is IV labetalol Investigate = CT aorta, TTE does detect type A or pericardial effusion/tamponade Type A = surgical emergency Type B = medical if uncomplicated, surgery if complicated

Answer 123

70-90 Because if higher can disrupt the contained haematoma (tamponade) - let the hameatoma tamponade Emergency surgical repair

Answer 124

Cardiac (heart-related) causes (most common and important): Acute coronary syndrome / Myocardial infarction (heart attack) Myocarditis (inflammation of the heart muscle, often viral) Heart failure (acute or chronic) Tachyarrhythmias or bradyarrhythmias (very fast or very slow heart rates) Hypertensive emergency Cardiac contusion (blunt chest trauma) Aortic dissection Cardiac procedures (PCI, ablation, cardioversion, surgery) Supply–demand mismatch (Type 2 MI) - troponin rises due to stress on the heart rather than plaque rupture: Sepsis Severe anemia Hypotension or shock Hypoxia / respiratory failure Pulmonary embolism Severe hypertension Prolonged tachycardia Non-cardiac causes: Pulmonary embolism Stroke or subarachnoid hemorrhage Chronic kidney disease (reduced clearance and chronic myocardial injury) Severe burns Extreme exertion (e.g., marathon running) Rhabdomyolysis Infiltrative diseases (e.g., amyloidosis) Chronic low-level elevation in stable heart failure or CKD Key points: Troponin = myocardial injury, not automatically a heart attack Rising and/or falling levels + clinical context determine significance Diagnosis of MI requires symptoms, ECG changes, or imaging, not troponin alone 1️⃣ Type 1 MI – Primary coronary event (Plaque rupture / thrombosis) STEMI NSTEMI 👉 True acute coronary syndrome 2️⃣ Type 2 MI – Supply–demand mismatch (No acute plaque rupture) Sepsis Tachyarrhythmias / bradyarrhythmias Severe anaemia Hypotension / shock Hypertension with LVH Hypoxia / respiratory failure 👉 Common in ICU and medical wards 3️⃣ Non-ischaemic myocardial injury (Direct myocardial damage) Inflammatory / infiltrative Myocarditis (viral, autoimmune) Sarcoidosis Amyloidosis Mechanical / structural Heart failure (acute or chronic) Cardiac contusion Post–cardiac surgery or cardioversion Toxic Chemotherapy (e.g. anthracyclines) Cocaine Carbon monoxide 4️⃣ Cardiac strain / pressure overload Pulmonary embolism Pulmonary hypertension Right heart strain Severe aortic stenosis 5️⃣ Systemic / critical illness Sepsis Stroke / subarachnoid haemorrhage Burns Severe renal failure (reduced clearance + chronic injury) 6️⃣ Chronic troponin elevation Chronic kidney disease Stable heart failure Structural heart disease 👉 Usually stable, non-dynamic levels

Answer 125

A spontaneous full thickness perforation of the oesophagus, usually after a sudden rise in intraoesophageal pressure (often from forceful vomiting, usually binge eating or alcohol). It is a surgical emergency.

Answer 126

1. Vomiting (violent) then sudden chest pain 2. The chest pain is retrosternal/upper abdomen radiating to the back or neck or shoulder 3. Subcutaneous emphysema - crepitus in neck or chest from mediastinal air SOB Fever later due to infection Shock when sepsis develops

Answer 127

CXR Contrast swallow will show leak (gastrographin) CT thorax Early repair IVF, abx broad spectrum, NBM and analgesia Drainage of mediastinal/pleural collections

Answer 128

Inferior wall - may cause heart block Leads: II, III, aVF and check right-sided leads, V4R elevation means RV infarct Artery: RCA V4R elevation is a crucial sign of right ventricular (RV) involvement or infarction during an inferior heart attack (MI) - V4 electrode is moved to the right side of the chest, to the fifth intercostal space in the midclavicular line when a standard ECG suggests an inferior MI Anterior wall - large infarcts, cardiogenic shock (septal is V1-V2) Leads: V1–V4 Artery: LAD Lateral wall Leads: I, aVL, V5–V6 Artery: LCx Anterolateral Leads: V3–V6, I, aVL Artery: LAD Posterior wall - often missed on standard ECG Clues: ST depression in V1–V3 Tall R waves in V1–V3 Confirm with: Posterior leads V7–V9 (ST elevation) Artery: RCA or LCx

Answer 129

First say this ECG shows ... e.g., widespread ST segment depression most obvious in which leads e.g., anterolateral leads - this is consistent with a NSTEMI ABCDE approach and I would base my management on the results of the ABCDE assessment, correcting any urgent findings MONABASH... If hypoxic, I would administer oxygen (15L, via non-rebreather mask, if necessary) to target sats of 94-98% or 88-92% if they were at risk of CO2 retention I would commence medical management with a stat dose of antiplatelets - 300mg aspirin Nitrates relieve pain but do not improve survival in STEMI and are contraindicated in RV infarction (inferior STEMI ± V4R elevation) and hypotension (SBP <90 mmHg or >30 mmHg drop from baseline) and recent PDE-5 inhibitor use Nitrates are first line for pain management in STEMI, if pain is not relieved by nitrates or if nitrates cannot be given, give morphine (co-prescribe antiemetics) Nitrates are given in the form of sublingual GTN spray then IV GTN infusion if chest pain or hypertension persists Use with loop diuretics for pulmonary edema if needed (three uses chest pain, hypertension, pulmonary oedema) If there are no contraindications, I would prescribe anticoagulation in the form of a heparin-based drug (age and renal function can influence) Further medical management would include beta blockers, ACE-inhibitors and high dose statins, which I would ensure are started

Answer 130

All get 300mg aspirin immediately then differs depending on ST elevation or not (always check trust protocol for everything esp. antiplatelets/enox vs fonda choice but...) STEMI - if PCI not poss within 120 mins, thrombolysis, give clopidogrel and treatment dose enox (for ongoing pain/ischaemic go for PCI i.e., if the patient's ECG taken 90 minutes after fibrinolysis failed to show resolution of the ST elevation) STEMI - if PCI poss, given clopidogrel (no prasugrel/ticag) but no enox as will get UFH pre lab NSTEMI/UA - calculate GRACE if low risk, give P2Y12 and treatment dose enox or fondaparinux (if ongoing symptoms - early angiography and revascularization just like those with high risk features, see below for more) NSTEMI - if GRACE high or intermediate go for PCI (immediately if unstable, 72 hours if not), if immediate P2Y12 is questionable, depends on CABG possibility - chat to cardio, they will get UFH pre lab so no enox required, if not immediate i.e., stable, given P2Y12 + treatment dose Enox (1mg/kg BD, also fondaparinux is an alternative) until it happens “Only maintenance? → Load for ACS!” “Already on DAPT? → Maintain, don’t reload!” PCI can be immediate after angiography (common in STEMI) or delayed after diagnostic angiography in NSTEMI Angiography = see the problem (“look at the sculpture”) PCI = fix the problem (“put the stent in”)

Answer 131

This depends on the severity and clinical stability of the patient. However, in general current evidence supports early angiography and revascularization in patients who present with either high-risk features, or patients with low risk features who have ongoing symptoms. Even in those patients who are low risk and settle with medical management, early angiography and revascularization is still the recommended treatment following non-invasive stress testing. Risk factors include: Poor LV systolic function Previous CABG/PCI (in last 6/12) Patients with other comorbidities Patients with high-risk features of NSTEMI/UA -Recurrent angina -Recurrent ischaemic ECG changes despite optimal medical therapy -Elevated troponin -Tachyarrythmias post MI Again, you don’t need to know all of these but it will look good if you can come up with a few features that suggest a patient is high risk and will be a candidate for inpatient angiography.

Answer 132

Age - Higher age → higher risk Heart rate - Tachycardia increases risk Systolic blood pressure - Hypotension increases risk Creatinine - Renal dysfunction increases risk Killip class - Reflects heart failure: I–IV Cardiac arrest at admission - Present → higher risk ST-segment deviation - ST depression or elevation on ECG Elevated cardiac enzymes - Troponin/CK-MB positive

Answer 133

A history of sustained acute chest pain typical of AMI, accompanied by acute ST segment elevation or new left bundle branch block (LBBB) on a 12-lead ECG is the basis for diagnosis of STEMI / All patients with chest pain and ST elevation or new left bundle branch block (LBBB) fulfil primary percutaneous coronary intervention (PC) criteria. If this is suspected when you see a patient they should be discussed immediately with the on call cardiology team - cardiology may not be based at the hospital you are working in. Explain that in these patients, if they are haemodynamically stable they should be sent via a blue light ambulance to a hospital that can provide primary PCI. If unstable STEMI → stabilize first (oxygen, IV fluids cautiously, inotropes if needed, consider temporary pacing for bradyarrhythmias, treat arrhythmias immediately) then transfer for PCI, sometimes with adjunct support (airway support or ICU transfer, mechanical circulatory support (IABP / ECMO) in select cases). If PCI delay is inevitable and patient unstable may require rescue thrombolysis if no immediate PCI possible. This is a good opportunity to show the examiners that you are safe. If you suspect a STEMI then it should be immediately discussed with a senior, as the time to PCI is an important factor in subsequent prognosis.

Answer 134

DARTH VADER D = Death (cardiac arrest) A = Arrhythmia - VT or VF, heart block following inferior MI R = Rupture - left ventricular free wall rupture 1-2 weeks after (AHF secondary to cardiac tamponade) ALSO IV septum rupture in the first week (AHF with a pan-systolic murmur, ECHO diagnostic and will exclude acute mitral regurgitation which presents in a similar fashion, urgent surgical correction is needed) T = Tamponade ABOVE H = Heart failure (cariogenic shock or CHF) V = Valve disease - infero-posterior infarction and may be due to ischaemia or rupture of the papillary muscle - acute hypotension and pulmonary oedema may occur, an early-to-mid systolic murmur is typically heard, patients are treated with vasodilator therapy but often require emergency surgical repair A = Aneurysm - ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation, this is typically associated with persistent ST elevation and left ventricular failure. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated. D = Dressler’s syndrome (pericarditis in first 48 hours, Dressler's 2-6 weeks later) E = Embolism ABOVE R = Re-infarction

Answer 135

Also described as autoimmune pericarditis, occurs 2-10 weeks post MI In fact, simple pericarditis post-MI is more common than Dressler’s syndrome and presents within 2-4 days post MI The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers. It is characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs. You would manage this patient as you would any with acute chest pain. Remember the ABCDE approach. An ECG will be important and may show widespread diffuse saddle-shaped ST elevation across multiple leads. An echocardiogram may show pericardial effusion. The management of this condition is with non-steroidal anti-inflammatory medication. If there is a significant effusion it can be aspirated.

Answer 136

For consideration of PCI. If not eligible then medical management should be completed, with further antiplatelets, anticoagulation, and ACE-inhibitors, beta-blockers and statins for secondary prevention. (if high risk get PCI within 72 hours, if not later, delayed/early invasive PCI in NSTEMI performed within 24–72 hours depending on risk stratification (GRACE score) - this is secondary PCI) Primary PCI is PCI performed immediately (emergently) as the first reperfusion strategy in STEMI, without prior fibrinolysis Rescue PCI is also secondary PCI - done urgently after failed thrombolysis, indicated if patient remains symptomatic or has persistent ST elevation NSTEMI unstable that goes for immediate PCI is not primary PCI - it is urgent PCI for NSTEMI. NSTEMI do not get fibrinolysis. Timing: High-risk NSTEMI: PCI within 24 hours Very high-risk / unstable: PCI immediately

Answer 137

Primary PCI workflow: Patient arrives at PCI-capable center Immediate coronary angiography in cath lab Culprit artery identified PCI performed — balloon angioplasty and stent placement Often, angiography and PCI happen in the same session, so it may seem simultaneous, but the angiogram is always done first.

Answer 138

I would continue to monitor the patient’s saturations and respiratory rate (also sats). If there are signs of hypoxia/became hypoxic I would start high flow oxygen (15L via non re breath). Monitoring BP and HR - ask for eCG to check rhythm If looks intravascualary deplete e.g., dry tongue/MM (esp diarrhoea) I would give IVF and monitor UO using catheter. Baseline GCS and monitor throughout admission.

Answer 139

I would like to know more about the patient’s history. Has she had any abdominal pain? Has she travelled anywhere recently? (This is particularly important). Has she noticed any PR bleeding? Has she had any recent weight loss or night sweats? Has she had any obstructive symptoms (vomiting)? Has she ever had this before or similar symptoms? Has she eaten anything different or new prior to the onset of these symptoms? Is there any FH of note and does she know of any !!!close contacts with the same symptoms?

Answer 140

SOFA (Sequential [Sepsis-related] Organ Failure Assessment) Purpose: Quantifies organ dysfunction in ICU patients Used to track severity and predict mortality in sepsis Variables (6 organ systems, scored 0–4 each) qSOFA (quick SOFA) Purpose: Rapid bedside screening for sepsis outside ICU Predicts poor outcomes, not full organ assessment

Answer 141

VBG (on the spot e.g., K) and blood cultures!!!

Answer 142

MC&S and C. difficile Also consider empirical antibiotics if sepsis is suspected Early escalation to senior colleagues is essential if the patient fails to respond to initial resuscitation

Answer 143

For this 24-year-old male with persistent diarrhoea, hemodynamic instability, and bloody stools, consider: Infectious gastroenteritis: Bacterial (Campylobacter, Salmonella, Shigella, E. coli), especially with blood and mucus; C. difficile if antibiotic history; parasitic infections (Entamoeba histolytica); viral. The most common cause for a young person presenting with diarrhoea is infection! Could be viral or bacterial gastroenteritis. Inflammatory bowel disease: Ulcerative colitis or Crohn's disease - suggested by blood, mucus, abdominal pain, and weight loss. Irritable bowel syndrome (IBS) (or anxiety): Though less likely given the acute presentation with hemodynamic compromise and bloody stools, IBS should remain in the differential, especially if other causes are ruled out and symptoms persist or recur. Malabsorption - coeliac disease, pancreatic insufficiency Metabolic - hyperthyroidism causing increased bowel motility Other considerations: Ischemic colitis, food poisoning with toxin-producing bacteria, or medication-induced diarrhea. Given the hypotension, tachycardia, and tachypnea, infectious gastroenteritis with impending septic shock requires immediate attention while also keeping IBD as an important differential.

Answer 144

Bloods: FBC (to check for anaemia and to look at the WCC), U&Es, CRP to check for inflammation, calcium, phosphate, Mg, and TFTs to screen for thyroid disease. VBG: lactate and on the spot measurement of K Bedside: ECG, stool sample and send it for microscopy, culture and sensitivities + C. diff. Imaging: erect CXR (also check free air under diaphragm), AXR to check for colonic dilatation If the patient’s symptoms persist then further investigations could include a faecal calprotectin to assess further for inflammatory causes, and a FIT test, to screen for malignancy. Endoscopy may also be required if there was suspicion of colitis (not acutely) or malignancy – I would discuss this with a specialist team.

Answer 145

Mild: < 4 stools/day, only a small amount of blood Moderate: 4-6 stools/day, varying amounts of blood, no systemic upset Severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers) Mild-moderate = topical (rectal) aminosalicyate mesalazine +/- oral +/- oral steroid Severe = IV steroids

Answer 146

Glucocorticoids (oral, topical or intravenous) are generally used to induce remission Enteral feeding with an elemental diet may be used in addition to or instead of other measures to induce remission, particularly if there is concern regarding the side-effects of steroids (for example in young children)

Answer 147

Supportive treatment is the main therapy goal. Her initial fluid management will depend on the outcome of her blood tests above. If she has signs of dehydration or an AKI on her bloods then she will need IVF. If she has been having severe diarrhoea for several days with minimal oral intake then she may be severely fluid deplete. Her potassium may be low as a result of the diarrhoea and I would look to replace this along with the IV Fluids. Antibiotics are only indicated following advice with micro after a positive culture result and would not be routinely started in patients presenting with diarrhoea.

Answer 148

I would look for extra-intestinal manifestations of IBD: Aphthous ulcers Erythema nodosum Pyoderma gangrenosum Peripheral arthropathy Sacroiliitis Ankylosing spondylitis Eye complications – uveitis, conjunctivitis, episcleritis

Answer 149

There are numerous clinical and biochemical markers of severity in IBD, these include: Markers of a severe attack of IBD include: Severe diarrhoea (more than 6–8 stools a day). Systemically unwell: e.g. dehydration, pyrexia, tachycardia and hypotension (?and raised inflammatory markers) Complications (?especially in Crohn’s) like suspected intestinal obstruction, toxic megacolon, or intra-abdominal or perianal abscess Anaemia Additionally, tools such as the Truelove and Witts’ Severity Index for Ulcerative Colitis are also available, which can be used to quantify severity.

Answer 150

Fluid resuscitation is till the key point of treatment. It is also important to monitor for acute electrolyte derangements. I would discuss the patient with my surgical colleagues if I thought there were any signs of severe disease activity. I would send samples to exclude infective colitis and other tests to exclude systemic infection. If the diagnosis is more certain (for instance if there is a history of IBD) then corticosteroids can be used. NICE recommends that IV corticosteroids should be considered for people admitted to hospitals with severe IBD. If I were considering this, I would discuss this decision with my senior registrar or the gastroenterology team. If not known IBD - escalate to my senior about steroids (just as you would do for known IBD)

Answer 151

Ulcerative colitis only affects the large bowel. There is variation in which parts of the large bowel are affected although the rectum is always affected. Inflammation is uniform (no skip lesions like Crohn's) and confined to the mucosa. On histology, granulomas are absent. Meanwhile, Crohn’s disease can affect any part of the gastric tract. Inflammation is not continuous (skip lesions) and the rectum is frequently spared. The bowel wall is thickened and has a cobblestone appearance due to deep ulcers and swelling of the tissue. Histology confirms the presence of granulomas with inflammation extending through the mucosa and muscle of the bowel. Four layers of bowel wall: mucosa, submucosa, muscularis propria and serosa/adventitia. UC affects mucosa only; Crohn’s affects all layers (transmural).

Answer 152

Around 30% of patients with UC will require a colectomy at some stage. Colonic perforation, uncontrollable bleeding, toxic megacolon and fulminating disease (also patient choice) require urgent proctocolectomy. Surgery in Crohn’s disease is not curative and is only indicated for perforation, obstruction, abscess formation and fistulae. There is a high recurrence rate after surgery.

Answer 153

S – I am handing over a 24 year old woman with a likely first presentation of inflammatory bowel disease. B – She has a history of 5 days of bloody diarrhoea with no other features of infection and a family history of inflammatory bowel disease. A – I have sent investigations to check for electrolyte imbalance and dehydration. I have started fluid resuscitation. I have sent stool cultures to rule out infection but have not started antibiotics pending the results of this. R – I would recommend admitting this patient and an urgent referral to the gastroenterology team (or review by the rheumatology team if neutropenic sepsis due to methotrexate)!!!!!to give advice on further management and investigations which may include starting steroids and arranging a sigmoidoscopy. !!!!!In the hepatic encephalopathy one - to discuss treatment with rifaximin which may be indicated if there is no response to initial treatment

Answer 154

Once the patient is stable and the stroke pathway has been activated, I would aim to complete an NIHSS either while the patient is being prepared for CT or immediately after imaging, ensuring it does not delay CT.

Answer 155

HPC: Gradually getting worse or sudden deterioration? How are they feeling systemically? Weight loss, fever and night sweats could indicate malignancy Right upper quadrant pain/N+V/pruritis? Fever? Diarrhoea? Steatorrhea? Dark urine + pruritis + pale stools are typically seen in obstruction of biliary flow or post hepatic (obstructive) jaundice Bronzed skin and signs of diabetes are suggestive of haemochromatosis PMH: Gallstones History of liver disease - fatty liver disease, Hep B/C, alpha-1 antitrypsin deficiency, PBC and PSC Recent blood transfusion or surgery Diabetes Ulcerative colitis Medication: Changes? New meds e.g., antibiotics? Regular OTC meds e.g., paracetamol overdose can lead to hepatitis Family history: There are various familial conditions that cause jaundice. Gilbert’s Haemochromatosis Wilson’s disease Sickle cell disease Hereditary spherocytosis Social history: Alcohol - quantify number of units IVDU Unprotected sex or multiple partners Recent foreign travel - exposure to malaria, Hep A, Hep E Tattoos Vaccination history including Hep B

Answer 156

Finger clubbing Leukonychia Palmar erythema Ecchymosis!!! Jaundice Spider naevi Gynaecomastica Testicular atrophy Hepatomegaly - the cirrhotic liver may be small or enlarged, in most cases a cirrhotic liver is small and shrunken, but in cases where it is due to alcohol or NAFLD, hepatomegaly may be present

Answer 157

1. Alcohol 2. Hep B and C 3. Autoimmune hepatitis, PBC, PSC 4. Wilsons disease, haemachromatosis, MASLD, alpha 1 antitrypsin deficiency 5. Amiodarone, methotrexate

Answer 158

Bedside: If evidence of ascites = arrange ascitic tap (culture and microscopy and WCC) Bloods: FBC - anaemia? infection? platelet count? CRP U&E - hepatorenal syndrome/baseline LFTs... AST, ALT - hepatocellular injury (very high in acute viral hepatitis) ALP - cholestasis (bile flow obstruction) GGT - confirms hepatic source of ALP (or raised in isolation after recent alcohol consumption) Albumin - synthetic function Bilirubin - conjugated vs unconjugated Clotting studies (PT / INR) – synthetic function (clotting factors, deranged PT is an early marker of compromised liver function) Amylase - rouge but suggestive of pancreatic pathology Blood film Then liver screen vibes for the causes... 1. Hep B/C 2. Autoimmune - ANA/ASMA for autoimmune hepatitis and AMA for PBC 3. Ferritin + transferrin saturation and serum copper + caeruloplasmin for Haemochromatosis or Wilson’s disease, also α-1 antitrypsin level in case of A1AT deficiency, also lipids & HbA1c (MASLD risk) Imaging: US abdomen ?pancreatic to biliary tree pathology also any liver cirrhosis or malignancy Biopsy

Answer 159

This is a sudden deterioration which likely represents decompensation of chronic liver failure with hepatic encephalopathy. Cause also be infection ?SBP - confusion + hypotension represent 2 of qSOFA meaning this patient is high risk of sepsis, could also have pneumonia Head injury

Answer 160

1. Infection - SBP or pneumonia or acute viral hepatitis 2. Acute GI haemorrhage 3. Alcoholic binge 4. Drugs - hepatotoxic drugs, diuretics, narcotics 5. Hypoglycaemia or electrolyte disturbance

Answer 161

This is a neuropsychiatric disturbance of cognitive function in a patient with acute on chronic liver disease. Clinically there is altered conscious level, asterixis, abnormal EEG, impaired psychometric tests, and an elevated arterial ammonia concentration.

Answer 162

Grade 1 – Insomnia/reversal of day/night sleep pattern Grade 2 – Lethargy/disorientation Grade 3 – Confusion Grade 4 - Coma Asterixis may be present at any stage. Hepatic encephalopathy carries a high risk of mortality

Answer 163

Exclude other causes of confusion e.g. CT Head Identify and correct the precipitating cause e.g., treat infection Give lactulose. This alters faecal pH and nitrogen utilisation by bowel flora. Phosphate enemas help to purge the large bowel. Also give thiamine (crucially before glucose if needed) Stop offending medications e.g., diuretics/hepatotoxic drugs Correct electrolytes Treatment with rifaximin may be indicated if there is no response to initial treatment, but this should be discussed with the gastroenterology team. Rifaximin = secondary prevention (most common), prevents recurrent episodes of HE, typically given after at least one overt HE episode, often combined with lactulose IT IS ALSO USED AS adjunct therapy in overt HE, it is used with lactulose if HE is not fully controlled by lactulose alone

Answer 164

Treatment depends on the underlying disease: Abstinence in alcoholic liver disease; antiviral therapy in viral hepatitis; and immunosuppression in autoimmune hepatitis, all improve liver fibrosis. Abstinence from alcohol improves prognosis in viral hepatitis and chronic liver disease. To screen for complications, 6 monthly abdominal ultrasounds and alpha-fetoprotein measurements help in surveillance for hepatoma (hepatocellular carcinoma - primary malignant tumor of the liver). All patients should undergo endoscopy as surveillance for oesophageal varices. Following an episode of spontaneous bacterial peritonitis, prophylactic antibiotics are indicated.

Answer 165

A transplant centre should take this decision. The selection for transplantation is taken based on the severity of the underlying liver disease against the presence of any co-morbidities. MELD score is used with exceptions - hepatocellular carcinoma extra points or acute liver failure even if low MELD. Also a patient be must abstinent from alcohol. Some conditions should be considered for transplant irrespective of disease severity such as PBC or recurrent cholangitis in PSC.

Answer 166

The examiners want to hear you articulate risk factors that you would want to elicit from a history. Risk Factors for upper GI bleed: 1. Previous upper GI bleed 2. Known atrophic gastritis, GI metaplasia/dysplasia; liver disease; oesophageal disease; known varices 3. Use of antiplatelets, NSAIDs, SSRIs (if the patient has OA they may be using NSAIDs for pain!) PMH: including any underlying cardiac or renal disease will be important to know for my assessment. Drug history: In addition to the above medications, I would want to know if the patient is taking any anticoagulants. I would also want to know if the patient is taking any iron tablets as this could be the cause of the black stool. SH: The patient’s alcohol history will be very important so don’t forget to tell the examiners you will ask for it! Quantify units. Smoking history is also important.

Answer 167

1. Peptic ulcer disease (35-50%) 2. Gastroduodenal ulcerations 3. Oesophagitis or gastritis (alcoholic, drug induced) 4. Varices 5. Malory-Weiss tear 6. Upper GI malignancy ?or benign tumour 7. AV malformations ???8. Vomiting of swallowed blood from a nasal bleed

Answer 168

1. Diverticulosis – most common cause in older adults 2. Angiodysplasia / vascular malformations 3. Colorectal cancer / polyps 4. Inflammatory bowel disease – Crohn’s or ulcerative colitis 5. Ischemic colitis 6. Hemorrhoids / anal fissures – usually minor bleeding 7. Post-polypectomy or post-surgical bleeding

Answer 169

Bedside: PR exam with consent to see if there is any evidence of melaena Bloods: FBC, U&E, CRP, LFTs, Ca, phos, Mg, coagulation screen, G&S (VBG will be useful to quickly see Hb and lactate) Imaging: OGD/endoscopy (will identify cause in >90% of patients and can also administer treatment - THE SEVERITY OF THE UGIB WILL DETERMINE HOW QUICKLY THIS SHOULD BE DONE) + biopsy

Answer 170

The Glasgow Blatchford score is for predicting the need for urgent intervention, like transfusion or endoscopy and identifying lower-risk patients who can be managed as an outpatient. It is applied before interventions. The Rockall score is used to assess the risk of mortality and re-bleeding. It can be used before or after interventions. Both tools use a combination of clinical and laboratory variables. For the GBS, a score of 0 indicates a patient who may be managed as an outpatient, whereas 1 or more indicates a patient who needs inpatient management. Greater than 7 necessitates an urgent conversation with the on call gastro team, as the patient may need an immediate endoscopy. For the Rockall score, less than 3 carries good prognosis but a total score more than 8 carries high risk of mortality.

Answer 171

I would call for help immediately, and perform an A to E assessment, of which the following steps would be most important The patient is likely developing hypovolaemic shock! I would activate the Major Haemorrhage Policy (if patient already has 2 G&S can get the cross matched units in 15 mins?), if MHP taking too long can get O neg from theatres or ED (in the event of a further deterioration she should be given O-negative blood from the transfusion fridge pending her formal cross-matched sample) Large bore IV access x2 – this is essential as you will be aggressively fluid resuscitating this patient. I will send bloods for G+S and urgent cross match 4-8 units. 0.9% saline to maintain SBP > 110 mmHg (100 mmHg if variceal) Correct coagulopathy using vitamin K +/- FFP if required Transfuse platelets if < 50 If a variceal bleed is suspected then terlipressin is indicated in addition to broad spectrum antibiotics. Terlipressin should only be used if the patient has a known history of varices. Terlipressin should not be given in patients with a history of ischaemic heart disease. IV PPIs have not been shown to reduce mortality in UGIBs. Their use will be dependent on your local trust guidelines. Consider early ITU involvement. The patient may require a CVP line and in severe UGIB that cannot be controlled, a Sengstaken tube may be considered (ONLY in ventilated patients (kept on ITU)) I will keep the patient NBM and discuss with the on-call gastroenterology team as the patient will need urgent endoscopy.

Answer 172

Infection with H. pylori is common in patients with peptic ulceration. A “urea breath test" (production of radiolabeled CO2 from swallowed urea – the most accurate test for H. pylori) or a stool antigen test are the most common ways of testing for H. pylori. If the patient is undergoing endoscopy then biopsies of the ulcer can be taken.

Answer 173

Triple therapy, using a PPI and two antibiotics (often amoxicillin and clarithromycin) is the standard treatment for gastric ulceration with confirmed or suspected H. pylori infection. Treatment would be based on local antimicrobial guidelines.

Answer 174

Advice around alcohol and smoking cessation will be important in this patient (if indicated in the history) Advice regarding medication – he should avoid NSAIDs ?and antiplatelet medication (balance of risks!). He should continue on PPIs for a minimum of six weeks, after which a repeat OGD is indicated to further assess for ulceration. It is always important to safety-net and the patient should be advised to return or seek medical help if there is any recurrence of symptoms.

Answer 175

Urgently discuss with the on-call gastroenterology team as he needs an urgent endoscopy to identify the site of bleeding.

Answer 176

Local = haemorrhoids, anal fissures and fistulas Could be on anticoagulants Mesenteric ischaemia (very concerned about this given AF)/ischaemic colitis Gastroenteritis Colorectal/anal cancer Diverticulitis Crohn’s disease/Ulcerative colitis

Answer 177

PC: onset, nature (colour, volume, etc) which may provide an indication as to the severity and aetiology HPC: I would also ask how the patient has been in herself recent (recent infection, systemic symptoms such as weight loss, fever, lethargy) or any previous similar episodes. !!!If concerned about gastroenteritis I may also enquire about infective contacts (i.e. other residents), any potential food sources or recent antibiotics courses (clostridium difficile). PMH: I would ask specifically about past gastrointestinal conditions such as previous diagnoses of diverticulitis or IBD. Dx: I would check if she takes antiplatelets or anticoagulants especially as these may be indicated from the PMH. Family history: clotting disorders or colorectal cancer or IBD Social history: smoking history, diet/lifestyle, these are all risk factors for malignancy, ALSO BASELINE FUNCTIONAL STATUS - this is important because she is at risk of becoming critically unwell, and if so there may need to be conversations with the critical care team about escalation to ITU, and whether this would be appropriate.

Answer 178

Bedside: PR exam (inspect the anal passage for potential causes such as fissures and feel for any masses, also to assess the volume of the bleeding), ECG to assess for cardiac arrythmias, especially given her past medical history. Bloods: Whilst gaining venous access I would obtain blood samples. I would request a full blood count (to assess for anaemia and signs of infection), CRP (to assess for inflammation), clotting profile (to assess for coagulopathy) as well as urea and electrolytes and liver function tests. Given the bleeding it may also be prudent to obtain a group and save sample (with multiple samples at different times if indicated by the trust policy), should blood products be required. VBG give instant Hb and lactate. Also do ABG as sats low and assess acid-base status. Imaging: If anything in the history has lead me to be concerned over either intestinal obstruction or toxic megacolon (ulcerative colitis or clostridium difficle), I would perform an abdominal x ray, an erect chest x ray can also help look for signs of visceral perforation if there was anything in the history or examination which lead me to be concerned about this. The British Society of Gastroenterologists recommends an urgent CT angiogram for haemodynamically unstable patients once the patient has been successfully resuscitated and active bleeding is suspected - I would discuss this decision with my seniors and make sure the patient has been effectively managed before this.

Answer 179

The fact that I have sent bloods e.g., G&S

Answer 180

Senior colleagues: immediately inform and ask them to come and review her ED doctors looking after her: make aware of results so far and ask the ED seniors to get her moved into resus where she can be closely monitored Surgical team: whilst the aetiology is uncertain (medical or surgical), I would also discuss the patient with the surgical team Haematology: if she is on anticoagulation for her AF she may need a reversal agent or discussion ITU: involve if she did not respond to treatment e.g., BP not improving/dropping with IVF and this was appropriate with her escalation status. It may also be worth making them aware of her early and at this stage now, so they are aware of her if she deteriorates to facilitate rapid escalation of care if required. If she were to deteriorate rapidly I would send out a MET team call or involve the crash team by dialling 2222 and immediately involving staff in the area by pressing the emergency buzzer

Answer 181

The arterial blood gas shows a metabolic acidosis with a raised lactate. There is acid base disturbance with signs of hypoperfusion. This is immediately concerning. I would begin the patient on fluids if she is not already on fluids. Providing there are no contraindications I would initiate a fluid challenge starting with 500ml of a crystalloid fluid such as Normal Saline 0.9% ran STAT and would then reassess, continuing as necessary. If the patient was anticoagulated, I would also discuss with the haematologist on call about reversing this if appropriate.

Answer 182

Resp acidosis - COPD, opioids, neuromuscular Resp alkalosis - PE, sepsis (early), anxiety Met acidosis (HAGMA) - DKA, lactate, renal failure, methanol Met acidosis (NAGMA): diarrhoea, Addisons, RTA Met alkalosis - vomiting, diuretics, prolonged predinisolone

Answer 183

Same criteria as DKA (ketones >3 and pH <7.3) but BG<11 (looks like starvation of alcoholic but treated same way as DKA) Common causes: 1️⃣ SGLT2 inhibitors (most important) Empagliflozin, dapagliflozin, canagliflozin Promote urinary glucose loss → normal serum glucose Reduce insulin, increase glucagon → ketogenesis 2️⃣ Reduced carbohydrate intake Prolonged fasting Vomiting Low-carb / ketogenic diets Post bariatric surgery 3️⃣ Partial insulin treatment Insulin taken but insufficient Early DKA 4️⃣ Pregnancy Increased insulin resistance Lower glucose threshold for ketogenesis euDKA compared to alcoholic/starvation: Diabetes - Yes (often T1DM or T2DM on SGLT2) vs usually No Feel like this is important to put in here - IV thiamine MUST BE GIVEN BEFORE glucose if ANY concern that alcoholic, so basically give 0.9% saline first then glucose containing fluids then correct electrolytes (K⁺, Mg²⁺, PO₄³⁻) and treat precipitating cause (infection, pancreatitis) - the thiamine first prevents Wernicke’s encephalopathy In alcoholic and starvation giving glucose stimulates insulin which suppresses ketogenesis

Answer 184

GLUCOSE IS MOST IMPORTANT Very high → DKA Normal/low → AKA or starvation HISTORY OFTEN GIVES ANSWER Alcohol binge +/- vomiting + starvation → AKA Known T1DM? Missed insulin? Infection? → DKA Prolonged fasting / illness / eating disorder? → starvation DKA: high ketones AKA: very high β-hydroxybutyrate (urine ketones may be misleading) Starvation: mild–moderate ketones GIVE FLUIDS Rapid improvement without insulin → AKA If the patient is unconscious and you’re unsure, it is safest to treat as DKA initially

Answer 185

Classic clinical sign of severe metabolic acidosis Deep, rapid, laboured (working harder to breath than normal/increased resp effort) respirations seen in metabolic acidosis It’s a compensatory mechanism by the body to blow off CO₂ (respiratory compensation)

Answer 186

Acute respiratory acidosis → HCO₃⁻ rises slightly as compensation BE may remain normal, indicating no primary metabolic disorder

Answer 187

I suspect that the patient has diabetic ketoacidosis (DKA). She is an insulin dependent diabetic and presents with acidosis. I would need a positive ?urinary or plasma ketone to confirm the diagnosis. Criteria for diagnosis is BG >11, ketones >3 and pH <7.3 (if they already have two just mention the other one you need). ?Don't mention level needed, just say positive? Common precipitants of DKA include (secondary to): 1. Infections (possible in this patient based on the history) 2. Non-compliance with treatment 3. Newly diagnosed diabetes

Answer 188

Dx Differentials Prep handover Think of some investigations and management

Answer 189

Remember 4Ts! 1. Polyuria and polydipsia: patients become dehydrated over a few days 2. Weight loss; weakness 3. Hyperventilation or breathlessness; the acidosis causes Kussmaul’s respiration 4. Abdominal pain (DKA may present as an acute abdomen) 5. Vomiting (exacerbates dehydration) 6. Confusion – coma occurs in 10% of patients

Answer 190

I would continue to monitor the patient’s saturations and respiratory rate, if there are signs of hypoxia I would start high flow oxygen

Answer 191

I would START IVF ?(in line with the DKA protocol and contact my registrar) Based on the severity of the presentation it may be necessary to have a central line – ?this will be helpful in monitoring bloods and giving fluids during treatment, I would contact ITU if these are required.

Answer 192

Bedside: blood glucose, urine dip and MC+S as part of a septic screen Bloods: ABG, FBC (infection), U&Es to measure Na, K and urea, serum osmo AND BLOOD CULTURES (signs of underlying infection) Imaging: CXR

Answer 193

I would follow my local DKA protocol and contact my registrar Step 1: Fluid replacement In my current hospital we would give 1L normal saline over an hour, 500mL boluses if hypotensive such as in this case Step 2: Insulin replacement A FIXED RATE insulin infusion (FRIII) should be started after the first hour of IVF at an initial rate of 0.1unit/kg/hour. IVF are adjusted with K from the time of insulin. 2L NaCl +/- K over 4 hours then over 8 hours. Note K falls rapidly as it shifts into cells under the action of insulin. Close monitoring of K is essential - baseline, 1 hour, 2 hours then 2 hourly thereafter (using VBG) - 0.9% saline is infused alongside IV K at the same time as the FRIII. If K <3.5 = HDU referral for central line as high conc K infusion. The response is reviewed hourly. If blood glucose is not dropping by 3mmol/L/hour, capillary ketones by 0.5mmol/L/hour and bicarb increasing by 3mmol/L/hour the infusion is increased by 1 unit/hour. This is continued until capillary ketones <0.6, venous pH >7.3 and venous bicarbonate >18 (criteria for resolution). At this point switch to a VRIII (SC insulin regimen) until eating and drinking regularly. If the patient is on long-acting insulin this should be continued at their usual dose from the point of admission along with DKA IV insulin protocol (should never be held). Step 3: Glucose If blood glucose <14 add 10% glucose at 125ml/hour along with DKA fluids Step 4: Broad spectrum antibiotics if infection is suspected Step 5: Thromboprophylaxis Step 6: NG tube if vomiting and airway protection if obtunded/GCS reduced

Answer 194

An early referral to ITU is recommended for patients with any of the following features: 1. pH <7.1 2. Severe DKA by the following criteria: Ketones >6 mmol/L or Bicarbonate <5 mmol/L 3. Hypokalaemia on admission (below 3.5) 4. GCS <12 5. Systolic BP <90 mmHg!!!!!! They could put this in question 6. Significant co-morbidity 7. Pregnant

Answer 195

These can be categorised into treatment complications and complications from DKA Secondary to treatment: 1. Hypokalaemia 2. Hypophosphataemia – phosphate moves intra-cellularly in the same way as potassium (check/treat only if respiratory weakness) 3. Cerebral oedema - may be precipitated by sudden shifts in plasma osmolality during treatment, symptoms include drowsiness/confusion and severe headache, mortality is around 70% 4. Hypoglycaemia – from overzealous insulin replacement Secondary to DKA: 1. Tissue hypoperfusion may result from dehydration 2. Hypercoagulable state may result in thromboembolism

Answer 196

Provide education so that re-admission can be avoided I would sit down and talk to the patient. It is important for the patient to understand what precipitates DKA. The most common is non-compliance with medication. Sometimes this may be accidental and sometimes it may be out of choice. I would also explain to the patient that she should seek early medical advice if she feels she is becoming unwell in the future, as early treatment of underlying infection may stop the progression to DKA. We could discuss their HbA1c level. DSN and dietician for education once stable and out of DKA (Hospital diabetic team to discuss treatment and compliance). I would make sure I have written to the GP to arrange early follow up +/- diabetes consultant and I would also make she is under regular review for complications of diabetes.

Answer 197

HHS is a complication of diabetes mellitus, most often seen in type 2 diabetes. It is potentially life-threatening, and requires urgent identification and treatment. HHS most commonly presents in type 2 diabetics who have a concomitant illness that causes reduced fluid intake. It is characterised by the triad of hyperglycaemia, hyperosmolarity and dehydration, without significant ketoacidosis - which distinguishes it from DKA. Dehydration is usually severe, and often the hallmark feature. Any unwell type 2 diabetic should have HHS considered as a differential. The diagnostic criteria is: Lab glucose >30mmol/L Serum osmolality >320mosmol/kg Venous bicarbonate >15mmol/L Capillary blood ketones <3mmol/L (urine ketones <3+)

Answer 198

The most important aspect of management in HHS is fluid resuscitation. This is to avoid cardiovascular collapse and to perfuse vital organs. The average fluid loss is typically 8-10L and so aggressive fluid resuscitation is required. Osmolality should be reduced by 3-8 mOsm/kg/hr (if you work in a hospital where serum osmo takes ages you can calculate manually using MDCalc). Insulin is not required initially and blood glucose will fall with IV fluids alone. Initiation of IV insulin should be based on local hospital guidelines thereafter.

Answer 199

Hourly glucose and ketones, VBG 2 hourly to monitor pH, bicarb and potassium then U&E 4 hourly for Na and urea. ALSO do they meet any criteria for ITU e.g., SBP <90.

Answer 200

Firstly the examiners want to hear you say that this is a potential emergency and you need to go and see the patient urgently. The patient should then be assessed using an ABCDE approach. This will allow for rapid detection of any problems. ABCDE is the same as for everything else A - alert? C - pale or clammy? ask nurse to continue cycling BP and HR to make sure not deteriorating -> start patient on cardiac monitor which continuously tracks heart rhythm and rate, IV access ensure they have it, if not insert large bore cannula E - specifically mention urticarial rash

Answer 201

1. Anaphylaxis - secondary to antibiotics is number 1 concern 2. Asthma 3. Bronchitis 4. Cardiac wheeze (secondary to pulmonary oedema)

Answer 202

In situations of anaphylaxis I would call for help and put out a 2222 call and fast bleep anaesthetics ?intubation. The most important aspect here is maintaining the patient’s airway. I would stop the antibiotic infusion (remove the trigger), give IM adrenaline, start high flow oxygen 100%, commence IV fluids and maintain the patients airway. If there is no response I would give another IM adrenaline dose after 5 minutes along with IV fluids. Signs of anaphylaxis: A = ? airway obstruction (swelling, hoarse voice, stridor) B = ? breathing difficulty (falling sats, cyanosis, fatigue, wheeze, increased work of breathing) C = low BP/signs of shock D = confusion/reduced consciousness

Answer 203

Failure to respond after two doses of IM adrenaline is considered refractory anaphylaxis. The patient needs to be intubated (and admitted to ITU) urgently (due to risk of cardiac arrest). I SHOULD HAVE ALREADY MENTIONED THIS BEFORE: This should now prompt you to put out an arrest call (this is what the examiners need to hear if you have not already said it). However, it is essential to also continue treatment whilst emergency help arrives. The emergency treatment of refractory anaphylaxis that you can immediately give includes: 1. 500ml IV fluid 0.9% as a bolus 2. Maintenance adrenaline – start an infusion as per local protocol, and give further IM adrenaline until this can be initiated If cardiorespiratory arrest occurs then CPR and the ALS resuscitation pathway should be started. There is no further role for IM adrenaline once cardiorespiratory arrest has occurred.

Answer 204

THIS IS THE SAME AS WHAT IS LISTED ABOVE Airway: swelling, hoarse voice, stridor Breathing: wheeze, shortness of breath, respiratory arrest Circulation: pale, clammy, tachycardia, shock, cardiac arrest

Answer 205

Drugs and IV infusions – this can include antibiotics, IV infusions (blood products, IV immunoglobulins, contrast mediums also anaesthetic agents!) Insect bites Food – e.g. nuts, sea food Other common causes: latex, hair dye

Answer 206

An emergency cricothyroidotomy can be performed in an emergency setting where intubation fails or cannot be undertaken. A 14G needle and insufflation with 100% oxygen can be used as a temporary measure until a definitive airway can be achieved.

Answer 207

In the first instance there is duty of candour towards the patient. The patient should be made aware of the error and apologised to. (PLUS EXPLAINED WHAT WE ARE DOING FOR THEM AND WHAT IT MEANS FOR THEM E.G., LONGER STAY). The most appropriate team member to do this may be the lead or accountable physician, but in some instances you may be the appropriate person to deliver this. In addition, the error should be highlighted to the team (immediate). A clinical incident form should be logged as serious harm came to the patient. This should then be fed back to the members of the disciplinary team involved in the incident (the outcome of the investigation / lessons learned from the incident should be communicated to staff involved).

Answer 208

Anaphylaxis, along with atopy and asthma attacks is classed as a type 1 hypersensitivity reaction. IgE mediates it. It is a fast response that occurs in minutes, rather than hours or days. Activated mast cells degranulate and result in the secretion of pharmacologically active mediators such as histamine, leukotrienes and prostaglandins that act on the surrounding tissue. These mediators cause vasodilation in the circulation, bronchial smooth muscle contraction in the lungs, and tissue oedema in the airways, which can lead to hypotension, bronchospasm, and stridor.

Answer 209

Stage 1: Increase of ≥26.5 µmol/L within 48 h or 1.5–1.9 × baseline AND/OR <0.5 mL/kg/h for 6–12 h (mild injury, often reversible) Stage 2: 2.0–2.9 × baseline AND/OR <0.5 mL/kg/h for ≥12 h (moderate AKI, risk of complications increases) Stage 3: ≥3 × baseline or increase in creatinine to ≥353.6 µmol/L or initiation of renal replacement therapy AND/OR <0.3 mL/kg/h for ≥24 h or anuria for ≥12 h (severe AKI, high risk of morbidity/mortality)

Answer 210

FBC (blood loss, infection) CRP (infection) U&E (serum potassium, renal failure) LFT (drowsy patient) Magnesium (as you may need to correct potassium) ALSO COAG - ?INTRACEREBRAL BLEED VBG (for immediate potassium, acidosis, haemoglobin and lactate)

Answer 211

GCS (<8 call anaesthetist) Check pupils (pinpoint suggests opioid toxicity) Glucose (would be on VBG) Any focal neurological deficit? Temperature

Answer 212

This patient has severe hyperkalaemia. I would call for help and treat them in line with my local hospital policy. Send serum potassium (U&E) but this must not delay treatment. 1 = STOP further potassium sources (IVF and meds) 2 = START continuous cardiac monitoring and give calcium gluconate to stabilise cardiac membrane and reduce arrhythmia risk (does NOT lower K) 3 = SHIFT potassium into cells using insulin + dextrose IV infusion AND salbutamol nebs* 4 = REMOVE potassium from body using oral Lokelma or dialysis if needed The hyperkalaemia kit is only a stabilising/temporary measure - investigate and treat underlying cause e.g., reduced renal excretion (AKI or ACEi), increased potassium release from cells (TLS, rhabdomyolysis, severe burns, trauma, massive transfusion, haemolytic anaemia), increased potassium intake (IV potassium). Stop K raising drugs, check kidney function, Addisons?, correct dehydration, check for tissue breakdown or hemolysis (CK, LDH, blood smear). Loop diuretics may be used, calcium calcium resonium (orally or enema) is not required for immediate management, note enemas are more effective than oral as potassium is secreted by the rectum Dialysis if refractory, in renal failure or very high levels not responding. Dialysis should be considered for patients with AKI with persistent hyperkalaemia. After treatment - frequent K⁺ and glucose checks and observe for rebound hyperkalaemia. *There is also evidence to suggest the benefit of using sodium bicarbonate in the management of acute hyperkalaemia, when there is a significant associated metabolic acidosis. This would be something I would discuss with a senior before initiating. (Sometimes bicarbonate if severe acidosis; less commonly first‑line). IF PATIENT WAS ACIDOTIC I WOULD BE INVOLVING ITU AND REG. Sodium Zirconium Cyclosilicate (SZC) brand name is Lokelma.

Answer 213

Causes of AKI can be split into pre-renal, renal and post-renal. Pre-renal (reduced renal perfusion): volume depletion (most common), low BP, heart failure, liver failure BUN:Creatinine ratio >20:1 (pre-renal azotemia) Urine sodium <20 mmol/L ?Fractional excretion of sodium (FENa) <1% Urine osmolality high (>500 mOsm/kg) Renal (direct damage to the kidney tissue): ATN (ischemic or nephrotoxic e.g., aminoglycosides, contrast, rhabdomyolysis), AIN (antibiotics e.g., penicillin, infection e.g., EBV or immune e.g., sarcoidosis), glomerulonephritis, trauma BUN:Creatinine ratio ~10–15:1 Urine sodium >40 mmol/L ?FENa >2% Urine sediment may show muddy brown casts (ATN) or WBC casts (AIN) Post-renal (obstruction of urine flow anywhere from the renal pelvis to the urethra): stones, BPH, malignancy, BOO, catheter problems

Answer 214

This is a question not only about treating a refractory hyperkalaemia, but also about who else in the hospital you would want to involve at this point. Refractory hyperkalaemia = hyperkalaemia that persists or recurs despite initial treatment with: calcium gluconate, insulin/dextrose, salbutamol nebs and potassium binders. Typically, this is persistent K⁺ >6.5 mmol/L or rising K⁺ despite treatment, especially if accompanied by ECG changes. State your recognition of the refractory hyperkalaemia. Say you would reassess the patient A to E. Has treatment been given? Is the cannula working? Is there any exogenous potassium being given to the patient? Send repeat serum sample to confirm diagnosis. Involve medical registrar and ITU registrar – seeking senior support is essential as this patient is not improving but also is at risk of further deterioration. Move patient to HDU/resus setting.

Answer 215

Sodium zirconium cyclosilicate is a cation-exchange crystalline compound. Binds potassium ions (K⁺) in the gastrointestinal tract, especially in the small and large intestine. Exchanges potassium for sodium and hydrogen in the gut → traps K⁺ in the stool. Potassium is excreted in feces, lowering serum potassium over hours.

Answer 216

A = Metabolic acidosis E = Refractory hyperkalaemia I = CKD Stage 5 (or need to remove toxic substances e.g., lithium, methanol, ethylene glycol, certain drugs) O = Fluid overload unresponsive to treatment U = Symptoms of uraemia

Answer 217

Situation: This is a 65 year old gentleman with refractory hyperkalaemia and metabolic acidosis. Background: He was admitted in AKI and has no other known past medical history. Assessment: The potassium is 7.1 and there are changes on the ECG consistent with hyperkalaemia. The patient is drowsy. Recommendations: I would like an urgent review of this patient by the ITU registrar as he may need emergency dialysis given the lack of response to treatment so far. I will commence cardiac monitoring and continue treatment for the hyperkalaemia pending your review (i.e., do the kit again).

Answer 218

I am worried about sepsis in this patient. Can mention qSOFA. Read out the patients obs e.g., this patient is hypotensive, tachycardic... Based on my initial review I would want to initiate treatment quickly in line with the sepsis guidelines. A to E assessment. Broad spectrum antibiotics as I am not clear on the source at this point for which I would consult my local antimicrobial prescribing guidelines concerning antibiotic choice ensuring I have checked the patients allergy status. Given the high mortality associated with sepsis, I would urgently speak with my senior following my assessment to make sure she is seen quickly by my registrar or consultant.

Answer 219

A raised lactate of more than 4 mmol/L would make me urgently discuss this case with the on call ITU team and my senior team. Additionally, other factors that would make me quickly escalate this case include: 1. A low systolic blood pressure of less than 90 mmHg, despite fluid resuscitation 2. Reduced level of consciousness 3. A respiratory rate of more than 25 4. An unresponsive or rising lactate despite treatment These should all prompt discussion with the ITU team. Any evidence of end organ damage would also make me quickly escalate this patient to my seniors. End organ damage: Reducing consciousness Respiratory failure/increasing oxygen requirement Oliguria (<0.5 mL/kg/hr) Hypotension despite adequate fluid resuscitation - need for vasopressors Liver dysfunction - irising bilirubin (also contributes to coagulopathy) Coagulopathy - DIC DIC: Pathological activation of coagulation → widespread microthrombi Leads to: Bleeding (factor/platelet consumption) Thrombosis (organ ischemia) Typical DIC findings: ↓ Platelets ↑ INR / APTT ↓ Fibrinogen ↑ D-dimer Clinical bleeding (oozing from lines, mucosa)

Answer 220

Think about what the important factors are when considering sepsis in a patient. Also, think about any other information you were given in the scenario. It is likely there for a reason! Do they have any of the risk factors for poor outcome in sepsis I would like to know more about the onset of the symptoms, and symptoms that might point to a source – for example, a cough, diarrhoea or dysuria. Has the patient had any recent contact history with someone who has been unwell? Has the patient travelled recently? Have they previously had any infections or similar admissions? This patient has a history of rheumatoid arthritis. This may be important with regard to the presentation. I would like to know how this is managed and where, as I may need to contact the team after her admission. Is the patient on any medications, including disease-modifying agents or biologics? I would want a full drug history as well as knowing exactly when any medications were taken. In addition, I would like to know if there is any other past medical history that may also be influencing this admission.

Answer 221

Methotrexate can cause bone marrow suppression which can lead to a drop in circulating white cells. This is a rare complication of the medication, but in a person presenting with an unspecified fever, I would be worried about neutropenic sepsis and would manage this according to local trust antimicrobial guidelines. I would also make sure that I have sent blood cultures and requested a chest x-ray and urine sample to be sent to complete my septic screen, and help identify any potential source of infection. Methotrexate more commonly can cause hepatotoxicity. I would make sure that I have sent urgent blood samples for an FBC and LFTs. Methotrexate is excreted renally and therefore an urgent U&Es would be important too. Methotrexate is known to interact with many drugs in a serious way, so I would ensure a thorough drug history is taken.

Answer 222

The main cause of a sudden deterioration in patients taking methotrexate, who have previously been stable, is secondary to drug interactions and anything that might affect the excretion of methotrexate resulting in elevated drug levels. This is the likely cause of this presentation given the new AKI. My bit = Methotrexate toxicity often occurs acutely in stable patients when renal excretion is impaired by dehydration, ?AKI (I think this is implied with dehydration), or interacting drugs. The most common drug interaction which can lead to methotrexate toxicity is with NSAIDs which are commonly used in rheumatoid arthritis to manage flares of pain, inflammation and swelling. NSAIDs and methotrexate in combination can result in nephrotoxicity which reduces the excretion of methotrexate, leading to toxicity. (NSAIDs impair methotrexate clearance thereby increasing the risk of toxicity). Other common medications that would be important to ask about in the drug history would include recent penicillin use or proton pump inhibitor use. Additionally, I would like to know if the patient has been taking folic acid regularly. Folic acid is given in combination with methotrexate to reduce the toxic effects of methotrexate. Methotrexate inhibits the enzyme which converts folic acid into its active form, which is necessary for the synthesis of both DNA and RNA. Even though MTX blocks DHFR (the enzyme), folic acid supplementation raises the overall folate pool as some folic acid is converted by residual DHFR activity as MTX is a competitive inhibitor, not absolute; some DHFR activity remains at low-dose MTX. If the patient has recently stopped taking folic acid, this may be a reason for the onset of myelosuppression for someone who has previously been stable.

Answer 223

1️⃣ Blood cultures Usually two sets from separate sites Helps identify bacteraemia or fungemia Do before antibiotics if possible, but do not delay treatment 2️⃣ Urine Urine culture + urinalysis Detect urinary tract infection, common in elderly or catheterised patients 3️⃣ Respiratory Sputum culture if productive cough Tracheal aspirate / BAL if intubated or ventilated 4️⃣ Wound / device cultures Wound swab or pus if skin/soft tissue infection suspected Line or catheter tip cultures if indwelling devices are present 5️⃣ Imaging Chest X-ray (pneumonia, pulmonary source) Other imaging guided by clinical suspicion (CT abdomen for intra-abdominal sepsis, ultrasound for abscess) 6️⃣ Other targeted tests Stool cultures if GI infection suspected CSF if meningitis suspected

Answer 224

I would stop the methotrexate during the acute admission given this presentation is likely secondary to it. Given the patient has been well-maintained on the methotrexate previously, identifying a precipitating factor would be important. In this case, there is a new AKI and identifying the cause for this will be important before restarting the medication. I would liaise with the patient's Rheumatology team to advise them of the admission and that methotrexate has been stopped. They may want to consider whether restarting the methotrexate is the correct decision or whether another agent would be safer.

Answer 225

I have commenced broad spectrum antibiotics in line with the trust guidelines, pending further investigations including blood cultures, urine cultures and a chest x-ray. Also make sure to say that repeat lactate and clinical review are needed to assess response to fluid resuscitation. If she does not respond to the initial treatment I would recommend an urgent review by the ITU team.

Answer 226

Acute symptomatic relief = NSAIDs or steroids Long term to control disease progression and prevent flares = DMARDs (methotrexate or sulfasalazine) and if ineffective, biologics

Answer 227

Typically oncology setting for ALL, non-hodgkin lymphoma or osteosarcoma.

Answer 228

Methotrexate is renally excreted. Usually due to anything that increases Methotrexate levels: 1. Drug interactions (drugs that impair methotrexate clearance or compete for renal excretion) = NSAIDs, ACEi, penicillin or co-trimox 2. Anything affecting excretion - most commonly dehydration (diarrhoea/vomiting)/acute illness (infection) causing reduced kidney function/pre-existing CKD Common theme = Reduced methotrexate clearance = increased drug levels = toxicity

Answer 229

Bone marrow suppression = pancytopenia GI = mucositis/N+V/diarrhoea Liver = raised LFTs Derm = rash, photosensitve skin Pulmonary = methotrexate pneumonitis (dry cough, dyspnoea, fever - can progress to respiratory failure) THIS IS USUALLY IDIOSYNCRATIC I.E. NOT DOSE DEPENDENT

Answer 230

Methotrexate toxicity is almost always related to elevated drug levels because the drug is normally well tolerated at stable therapeutic doses BUT even at normal low dose therapy, methotrexate can cause mild toxic effects because of its mechanism of action - mild stomatitis, nausea, small drops in WCC/platelets FOLIC ACID rescues normal cells from these minor toxic effects At low doses, methotrexate’s anti-inflammatory effect is mainly due to increased adenosine signalling, with folate antagonism (prevents folate becoming its active form) contributing mainly to toxicity.

Answer 231

I would initially start my history-taking by asking open questions before moving on to more detailed closed questions. From my history, I would want to know: S = Where the pain is O = How long Mr Pine has had the pain Is it getting worse over time C = How would he describe the pain (aching, burning, sharp) R = Is it confined to the joint or does it radiate T = Is it constant or intermittent E = Does anything exacerbate the pain Does anything relieve the pain A = I would then want to know any associated features: Any history of red, hot joints in combination with the pain Any joint stiffness – and if so beginning or end of the day Any history of rashes, lesions or nail changes Any IBD? ?Any back issues Any recent infections? Any recent fatigue/malaise/weight loss Any fevers or night sweats I want to know the impact this is having on Mr Pine. How does it affect his daily living activities? I would then want to take a detailed past medical history and list of current medications and any treatments he may have previously tried for pain. I would like to know his allergy status. A family history of any joint or musculoskeletal disease will be important to know from the history. Social history: I would want to know about his home life and whether the pain is impacting his quality of life. I would also ask for a detailed alcohol and smoking history.

Answer 232

Rheumatoid arthritis Psoriatic arthritis Reactive arthritis SLE-associated arthritis IBD-associated arthritis

Answer 233

Red flag for inflammatory or infective joint disease 1. Inflammatory arthritis Rheumatoid arthritis Psoriatic arthritis Reactive arthritis SLE-associated arthritis IBD-associated arthritis 2. Crystal arthritis Gout (monosodium urate) - 1st MTP joint (acute gout is treated with NSAIDs, colchicine, or corticosteroids; urate-lowering therapy should not be initiated during an acute attack) Pseudogout (CPPD) - knee 3. Septic arthritis 4. Inflammatory flare on background disease

Answer 234

Observation of the hands demonstrates relatively normal alignment of all digits with potential loss of range at the distal interphalangeal joints. There is swelling of the distal interphalangeal joint of the 2nd, 3rd,4th and digits of the right hand. In the left hand there appears to be some swelling of the 3rd proximal interphalangeal joint. The swellings are not erythematous or have any evidence of tophi. There is no evidence of nail pitting or onycholysis. On further examination, I would check the small joints of the hand to assess if the swelling is hard or boggy, if there is any heat associated with the joint, or if there is any tenderness on direct joint palpation. I would then assess the MCP joints and joints of the wrist. I would inspect the forearm and the scalp for any signs of psoriatic plaques or scalp psoriasis. To complete my upper limb examination I would explore the active movement that Mr Pine has in the hand and fingers by getting him to flex and extend at the affected joints. I would then ask him to complete some functional tasks such as picking up a coin off the table. I would also complete a lower limb musculoskeletal exam specifically examining the knees (as these were painful on presentation) and assessing Mr Pine’s gait.

Answer 235

The hands demonstrate changes that would be consistent with Heberden’s nodes which are commonly found in patients with osteoarthritis. These signs along with his age and history of work would make me feel that osteoarthritis affecting the hands and knees is the most likely diagnosis. However, my differential would also include rheumatoid arthritis, psoriatic arthritis and gout.

Answer 236

Bedside: routine observations including blood pressure given his history. Bloods: helpful excluding differential diagnoses and I would request FBC, U&E, CRP snd ESR, LFTs, rheumatoid factor, anti-CCP (RA), urate (gout) and ANA (SLE). Imaging: plain films of the hands and knees which may identify signs consistent with either degenerative arthritis or inflammatory arthropathies.

Answer 237

For this scenario, you will be assessed on your communication skills. Speak clearly and without using medical jargon. Look at the patient when talking to them. Ask them questions to check that they are listening and understand what you are saying. Give them time to speak and only talk when they have finished. Make sure you answer any questions at the end. Answer: Mr Pine, we have discussed your images at the Rheumatology MDT and based on these and the negative tests in addition to the distribution of joint involvement, the pain and swelling in your hands and knees are secondary to what we call osteoarthritis. Have you heard of this before? Osteoarthritis is a type of degenerative arthritis that is extremely common and is associated with aging. Osteoarthritis occurs when the cartilage between our joints wears down. This can be exacerbated from overuse (such as in jobs with lots of manual tasks) and may be worse in patients who are overweight. The good news is this is not an inflammatory type of arthritis, such as rheumatoid arthritis, which is classed as an autoimmune disorder and requires medication to manage the immune response that causes the joint destruction. The mainstay of treatment for osteoarthritis is physical management and pain relief. Questions? Is Osteoarthritis hereditary? Should my children be worried? Osteoarthritis in this case is not hereditary. This is a disease of overuse of the affected joints and is normal as we age. Would surgery help me? Surgery can be a good treatment for osteoarthritis of the large joints, such as the knees. However, physical management undertaken with a physiotherapist would be the first line management. Strengthening muscles helps to support the joints and in many cases can reduce pain. Simple analgesic agents may also be helpful to you and in some cases intra articular injections (steroids/hyaluronic acid) can help. If the pain is not improving, then I would be happy to refer you to see one of my surgical colleagues. Do you have any further questions? I will provide you with written information on Osteoarthritis which will go over everything that we have discussed today.

Answer 238

The first steps in pain management would be reviewing the joint with a physiotherapist or occupational therapist to assess the strength and conditioning of the affected joints and if there are any mitigating factors that may help to relieve pain such as splinting. For example, knee pain can be well managed with quadriceps strengthening for most patients presenting with knee pain. I would give advice to the patient with regard to analgesia that follows a stepwise manner in a pattern akin to the WHO Analgesic Ladder. This would mean starting with non-opioid analgesics such as NSAIDs or paracetamol (if clinically appropriate for the patient) before escalating to weak opioids and then more potent if needed. If I were considering this, I would seek the help of a senior clinician before starting a patient on a potent opioid such as morphine given the risks to the patient associated with such medications. Additionally, there may be other analgesic options that may prove helpful and carry less risk such as topical analgesic ointments and cream (topical NSAIDs or capsaicin). Targeted therapies such as ultrasound-guided joint injections with local anaesthetic and steroid and in some cases hyaluronic acid may prove effective in providing short-term pain relief that allows completion of a home exercise program. All analgesic options should be used in conjunction with physical therapy and not as an alternative. All medication started for pain should have a review date to make sure they are effective and if not, then they should be stopped.

Answer 239

I would take the history to differentiate between transudative vs exudative causes of pleural effusion. I would ask for: Systemic features: “Any fevers, night sweats, weight loss or appetite change?” Infection risk: “Recent chest infections or TB exposure?” Malignancy: “Any personal or family history of cancer?” Heart failure symptoms: “New or worsening ankle swelling, orthopnoea or paroxysmal nocturnal dyspnoea?” Thromboembolism risk: “Leg pain/swelling, recent immobility or prior DVT/PE?” Autoimmune signs: “Joint pains, rashes or dry eyes/mouth?” Occupational/exposure history: “Asbestos, silica or other dust/chemical exposure?” Drug history: “Particularly amiodarone, methotrexate, nitrofurantoin or other drugs known to cause pulmonary or pleural toxicity?” Any frothy urine?????? Based on this, I would narrow my differentials as follows: Exudative causes: Infection (parapneumonic effusion), malignancy, autoimmune conditions, pulmonary embolism, oesophageal rupture, chylothorax or haemothorax. Transudative causes: Congestive heart failure, cirrhosis, nephrotic syndrome

Answer 240

I would organise my approach into four categories, following any local hospital protocol and BTS guidelines: A. Bedside Continuous observations (HR, BP, RR, SpO₂) and a strict fluid-balance chart ECG to exclude ischaemia or arrhythmia Urine dipstick for proteinuria B. Blood Tests FBC, U&Es, LFTs, CRP, coagulation profile Blood cultures if suspicion of sepsis/bacteraemia BNP if I suspect decompensated heart failure D-dimer if pulmonary embolism remains in my differential C. Pleural Fluid Analysis Biochemistry: pleural and serum protein and LDH Microbiology: MCS (including blood culture if infection suspected), AFB if TB suspected. Cytology & cell count: For malignant cells (Yes — cytology specifically refers to the examination of cells in a fluid or tissue sample to look for abnormal or malignant cells AND cell count/differential counts and classifies the types of cells present in the pleural fluid e.g., neutrophils, lymphocytes, eosinophils, mesothelial cells pH: If a parapneumonic effusion is a possibility Amylase: only if I suspect oesophageal rupture or pancreatitis Haematocrit: if there’s any concern for haemothorax D. Advanced Imaging CT thorax with contrast: request via my consultant or respiratory colleagues, ideally after partial drainage, to characterise pleural thickening, nodules or parenchymal disease

Answer 241

Identifying infection / complicated effusion Pleural fluid pH <7.20 → suggests acidic, infected or complicated effusion Causes: 1. Empyema (pus in pleural space) 2. Complicated parapneumonic effusion 3. Malignant effusions (some cases, especially with tumor metabolism) Low pH indicates: High lactate from bacteria or leukocytes Poor buffering (due to protein, CO₂ accumulation) Likely need for drainage Empyema or complicated parapneumonic effusion: pH <7.20, glucose <3.3 mmol/L → prompt chest tube drainage + antibiotics Higher pH → may be treated conservatively Complicated parapneumonic effusion = pleural fluid associated with pneumonia that requires drainage due to bacterial invasion or inflammation, but pus may not be grossly visible Empyema = grossly purulent pleural fluid in the pleural space; infection is advanced

Answer 242

A pleural effusion is considered an exudate if any one of the following is true: Pleural fluid protein / serum protein > 0.5 Pleural fluid LDH / serum LDH > 0.6 Pleural fluid LDH > 2/3 of the upper limit of normal serum LDH If none of these are met → transudate

Answer 243

I would follow the British Thoracic Society Pleural Disease Guideline to determine when to perform or defer a pleural fluid aspiration: Perform diagnostic aspiration if: -The effusion is unilateral and of unknown cause -It measures ≥ 1 cm on ultrasound or blunts the costophrenic angle on CXR -The patient is symptomatic (e.g. significant breathlessness) -There are no clear transudative features (for example, heart failure already responding to diuretics) Defer aspiration if: -The effusion is small (< 10 mm on ultrasound), asymptomatic, and there is an obvious transudative cause (e.g. known decompensated heart failure improving with therapy) -The patient has contraindications (uncorrected coagulopathy, skin infection at the entry site) -It’s a bilateral effusion with an obvious cardiac or renal cause and the patient is clinically stable

Answer 244

1. Identify 5th intercostal space, anterior axillary line (or mid-axillary line) essentially in the triangle of safety. 2. Insert large-bore cannula (14–16G) perpendicular to the chest wall 3. Listen/feel for air escape, then attach to syringe or allow passive decompression If inaccessible, 2nd ICS MCL

Answer 245

I would sit with the patient and begin by explaining in plain language that we’ve identified fluid around their lung on the X-ray. I’d say this fluid is making it harder for them to breathe, and that by taking a small sample with a fine needle, we can both relieve their breathlessness and send the fluid to the laboratory to find out exactly what’s causing the problem. I would then outline the benefits: that the procedure often eases symptoms immediately and that the analysis of the fluid helps guide the right treatment, whether antibiotics for infection, further tests for cancer or other therapies. I’d explain the main risks: a small chance of minor bleeding around the puncture site, a roughly 5–6% risk of a pneumothorax (air entering the space around the lung), a low risk of infection at the site, and an even smaller risk of re-expansion pulmonary oedema (where you develop fluid within the lung tissue) if a large volume is removed too quickly -to prevent limit fluid removal per session to ~1–1.5 L at a time. I would note that severe complications are very rare. I’d then check their understanding by asking them to tell me in their own words what they expect will happen, invite any questions or concerns they have, and reassure them that we can stop at any time if they feel too uncomfortable. Finally, I’d confirm their verbal agreement before documenting the discussion and proceeding with the plan.

Answer 246

Pleural protein >35 g/L suggests an exudate Pleural LDH >2/3 upper limit (>167 U/L) suggests an exudate I recognise that the protein of 45 g/L exceeds the 35 g/L exudate cut–off, so this is an exudative effusion without needing Light’s criteria. The normal pH, glucose ?and modest LDH rule out a complicated parapneumonic effusion or empyema. A neutrophil predominance with sterile cultures fits an uncomplicated parapneumonic process. Negative cytology, ADA and mycobacterial tests exclude malignancy and tuberculosis, and normal amylase rules out pancreatitis (in acute pancreatitis very high, often >1000 IU/L, also raised in Boerhaave’s), confirming a simple exudative parapneumonic effusion.

Answer 247

Clear or slight cloudy Cloudy / turbid Grossly purulent / frank pus Normal pH pH <7.20 pH <7.20 Glucose normal Glucose <3.3 mmol/L Glucose very low (<1–2 mmol/L) Slightly elevated LDH Elevated LDH Very high LDH Microbiology usually negative Microbiology may show bacteria Usually positive culture Cell count predominately neutrophils, moderate Cell count predominately neutrophils, high Cell count predominately neutrophils, very high

Answer 248

"Parapneumonic" means occurring alongside pneumonia. After or during pneumonia, fluid can accumulate in the pleural space. These effusions are classified as: Uncomplicated – clear fluid, free-flowing, usually resolves with antibiotics alone. Complicated – more serious; may require drainage. Empyema – frank pus in the pleural space.

Answer 249

A chest drain is required when the pleural fluid meets the criteria for a complicated parapneumonic effusion or empyema: for example, if the pH is below 7.2, glucose under 2.2 mmol/L, LDH above 1,000 IU/L, or if frank pus is aspirated. A drain is also indicated for large, symptomatic effusions that don’t respond to simple aspiration, or if imaging shows loculations suggesting the fluid won’t drain adequately with needle aspiration alone.

Answer 250

Diagnostic or small drainage vs therapeutic (large effusion, empyema, pneumothorax). Posterior/posterolateral chest wall, 7th–9th intercostal space, midscapular or posterior axillary line (USS guided). Lateral chest wall 5th intercostal space, mid-axillary line or anterior axillary line (triangle of safety) for pleural fluid (pleural effusion or empyema) or pneumothorax. Insert just above upper border of rib to avoid neurovascular bundle.

Answer 251

I would involve the thoracic surgeons when there is evidence of a trapped or non-expandable lung—such as persistent pleural space on imaging after drainage—or a thick pleural peel on CT suggesting fibrinous organisation (need surgery to remove). I would also refer if repeated drainage or an indwelling catheter fails to control the effusion, or when a patient with a malignant effusion is a candidate for surgical pleurodesis, decortication (surgery to remove fibrin) or video-assisted thoracoscopic surgery for pleural biopsy and definitive management. Surgical pleurodesis fuses the pleural layers (visceral and parietal pleura) to prevent fluid from re-accumulating usually done via video-assisted thoracoscopic surgery (VATS). VATS allows the surgeon to see the pleural space directly, take pleural tissue biopsies to confirm malignancy or type of cancer and can also perform pleurodesis or decortication at the same time if needed. VATS allows the surgeon to directly visualize the pleural space, take pleural tissue biopsies to confirm malignancy or determine the type of cancer, and, if needed, perform pleurodesis or decortication at the same time. In summary = refer to thoracic surgery when the effusion doesn’t go away with standard drainage, the lung won’t expand, or surgery could help control recurrent or malignant effusions.

Answer 252

1. Toxic/metabolic states -Hypoxia/hypercapnic/sepsis/ hypotension -CO poisoning -Drug intoxication (sedatives e.g., benzos, opioids, alcohol) -Renal or liver failure -Encephalitis or meningitis -Hypoglycaemia -Ketoacidosis 2. Seizures 3. Causes of raised ICP/herniation -Tumour -Stroke (ischaemic or haemorrhage brainstem) -Severe head trauma/TBI/DAI -EDH -SDH -SAH -Hydrocephalus

Answer 253

SPLIT THE DIFFERENTIALS into time of onset of symptoms: 1. Seconds to minutes – Acute asthma attack, anaphylaxis, Pneumothorax (+ Tension), Inhaled foreign body, Pulmonary Embolism 2.Hours to Days – Pneumonia, Heart Failure, Pleural Effusion 3.Weeks to Months – Worsening COPD, Chronic Asthma, Heart Failure, Pulmonary Fibrosis, Anaemia, Pulmonary HTN, Obesity

Answer 254

Start with questions around the presenting complaint that will help narrow your differential above: Time of onset of symptoms Alleviating or aggravating factors – worse when lying flat? Worse on exertion? Any associated features? – Cough, wheeze, chest pain – pleuritic pain?, weight loss or night sweats? Move onto Past Medical History and Drug History – particularly any recent drug changes or new drugs. Do they have any allergies? Have they ever been admitted to hospital before? Have they ever been to ITU before. Does the patient smoke? Is there any family history of respiratory disease? Social History: Does the patient smoke? Occupational history? Try to keep social history short and only go for point scoring answers. You do not need to say everything you would ask but certainly there will be key things that the examiners want to hear you say – the two listed above. PC/HPC: Onset, progression or episodic, any triggers, anything makes better or worse e.g., lying down or exertion, how bad is it/how long can you walk/how is it affecting your functioning, cough/chest pain/wheeze, how would you describe the pain - sharp, worse when you breath in, does it wake you from sleep, how have you been feeling, any fever/night sweats/weight loss, anything like this before? What do you think it could be/are concerned about?

Answer 255

Again, the examiners want to know that you are methodically thinking about your investigations. Start with bedside investigations and go from there. The most likely diagnosis here is an acute asthma attack. Bedside (first investigations): monitor obs to ensure oxygen is helping sats, peak flow, ECG and ABG to assess the level of oxygen and carbon dioxide. Bloods: FBC (anaemia or raised WCC), CRP (infection) and U&E (K levels will be affected by the treatment you are going to give) Imaging: CXR

Answer 256

1. Sit the patient up in bed 2. High flow oxygen 3. Salbutamol Nebulisers – these can be given back to back. 4. Steroids. These can be given IV initially in the form of hydrocortisone, depending on the severity of the patient in front of you. They can then be continued IV or switched to oral prednisolone. 5. Add nebulised ipratropium bromide if initial response to Beta-2 agonist is poor. 6. Monitor the patient with serial Peak Flows before and after Nebulisers. Repeat the ABG if no signs of improvement. SERIAL PEAK FLOWS + REPEAT ABG IS SO IMPORTANT 7. IV antibiotics if there is any sign of infection and IV hydration are also essential. 8. Administer IV Magnesium Sulphate if no response to above - SENIOR HELP. 9. You could then consider IV aminophylline – although it is not used as regularly and if you are getting to this point it may be best to call for help 10. If the patient continues to make no progress and is getting worse then you should contact ITU as the patient's airway may become compromised. !!!!!!!!!!!If this is happening quickly inform the examiners that you would put out a 2222 call.

Answer 257

This is a chance for you to show the examiners that you know your stuff. Explain that acute asthma attacks can be split into acute severe asthma and life-threatening asthma. The markers for a life-threatening asthma attack include: -PEF <33% best or predicted -Soft breath sounds or silent chest or feeble respiratory effort -Exhaustion, drowsiness, decreasing GCS -Hypotension SBP <100 -Arrhythmia – suggest haemodynamic compromise -Signs of cyanosis -Hypoxia SpO2 <90% or PaO2 <8kPa despite 60% FiO2 -Rising PaCO2 – this is the most important as it indicates ‘near-fatal’ asthma You do not need to remember all of these. Having some of them to hand will be enough to impress the examiners. Reiterating that any of the signs above would prompt you to put out an arrest call is important, as they all suggest the patient is approaching respiratory arrest.

Answer 258

-Reduced tidal volume – taking shallow breaths -Slow respiratory rate – or sometimes irregular breathing -Fatigue of respiratory muscles – patient may struggle to breathe or use accessory muscles excessively -Signs of hypoventilation: Low oxygen levels (hypoxemia) High CO₂ (hypercapnia) → may lead to drowsiness or confusion -Silent chest in asthma – may indicate very poor airflow, a form of inadequate effort

Answer 259

You do not need to go into detail about all the different potential drug combinations when answering this question. However, you should have a basic understanding of what long term asthma treatment involves. The patient would initially be managed on a short course of oral prednisolone. Patients asthma meds should be reviewed. Step 1: low-dose ICS/formoterol combination inhaler to be taken as needed for symptom relief - called AIR therapy Step 2: if the patient presents highly symptomatic (for example, regular nocturnal waking) or with a severe exacerbation start low-dose MART +/- course oral steroids Step 3: moderate-dose MART Then add in LTRA or LAMA trial/specialist in asthma care. MART describes using an ICS/formoterol combination inhaler for daily maintenance therapy and the relief of symptoms as needed, i.e. regularly and as required They can be safely discharged once they are off of regular nebulisers and PEF is >75% of best. Criteria for discharge: 1. Been stable on their discharge medication (i.e. no nebulisers or oxygen) for 12-24 hours 2. Inhaler technique checked and recorded 3. PEF >75% of best or predicted Patient education is always important prior to discharge and should include observation of inhaler technique and PEF record keeping. Follow up should be arranged with the patient's GP – ideally this should happen in 48 hours! Finally, in this particular patient smoking cessation is very important! Fractional exhaled nitric oxide (FeNO) and blood eosinophil count can be elevated in asthma but normal values do not exclude asthma because not all asthma is eosinophilic, could be neutrophilic or paucigranulocytic. Can both be low because not all asthma is driven by type 2 (eosinophilic) inflammation. If asthma is driven by non–type 2 pathways (e.g. neutrophilic or paucigranulocytic inflammation), then eosinophils and FeNO will be normal. If either FeNO or blood eosinophil count is raised need to refer straight to asthma specialist. Note - neutrophilic asthma may respond better to macrolides or biologics targeting non-type 2 pathways, not standard inhaled steroids alone. Also exercise induced asthma might only need pre-exercise SABA (e.g., salbutamol 2 puffs 5–15 min before exercise) - this is all getting too complicated though and is an asthma specialists problem!

Answer 260

I have started initial treatment for this including high flow oxygen, salbutamol nebulisers and steroids. I have asked the staff to commence serial peak flows and to repeat the ABG. I would recommend that this patient is reviewed urgently by the ITU team as they are at risk of further deterioration and may need to be admitted to ITU if they do not show signs of responding to initial treatments.

Answer 261

The onset is quick as the patient was able to discharge themselves from hospital this morning and also had a similar presentation several days ago. I would be considering: 1. Toxic causes such as opiate use, alcohol, anxiolytics, antidepressants 2. Metabolic causes such as hypoglycaemia or electrolyte disturbance 3. Trauma - i.e. head injury 4. A vascular event – such as an intracranial haemorrhage or large territory infarct 5. Infective causes such as meningitis or encephalitis. Given there is evidence of vomiting he is also at risk of aspiration pneumonia 6. Neurological causes - the patient could be post-ictal following a seizure

Answer 262

A to E - airway is CRUCIAL I would start by looking for signs of airway obstruction. In the critically ill patient, depressed consciousness often leads to airway obstruction. This patient’s GCS is low and so I would be concerned about the airway as a priority. If the airway is compromised, I would start by using airway adjuncts available to me at the bedside, such as an oropharyngeal airway or nasopharyngeal airway. If the patient can tolerate these then I would become even more concerned about the on-going patency of the airway. I would fast-bleep the ITU registrar or failing this put out a crash call, as I will need immediate assistance. This is the most important thing you can tell the examiners! Remember – GCS 8 = intubate!! The rest of your assessment is important but the examiner may stop you once you have said the above as they will have heard what they want to hear.

Answer 263

Massive bleeding is managed by: 1. Early activation of the major haemorrhage protocol - IF YOU'RE GIVING BLOOD, THINK CALCIUM, correcting clotting without calcium is like trying to clot without glue 2. Tranexamic acid is not routinely used in all medical bleeding - NOT GI bleed, only in PPH and trauma-related bleeding 3. Correction of coagulopathy Stabilise the patient AND simultaneous identification and control of the bleeding source. Reverse anticoagulation: Warfarin → vitamin K + PCC DOACs → specific reversal agents or PCC Platelets if thrombocytopenic FFP / cryo (Fibrinogen low) if clotting factor deficiency Examples: Upper GI bleed = urgent endoscopy and if variceal bleed → terlipressin + antibiotics Haemoptysis = treat infection, malignancy or vasculitis Anticoagulant-related bleed = immediate drug reversal e.g., intracranial or haemothorax Why calcium matters in bleeding... Calcium (Ca²⁺) is essential for: Activation of multiple clotting factors (II, VII, IX, X) Platelet function Myocardial contractility and vascular tone =>Low calcium → poor clotting + hypotension + arrhythmias. Why hypocalcaemia happens in bleeding, especially during massive transfusion: Citrate in blood products binds calcium => more transfusions → greater calcium chelation Can occur in: Trauma Massive GI bleeds Postpartum haemorrhage Liver disease Medical bleeding contexts where calcium is important: ✅ Massive GI bleed Large volumes of blood products → citrate load Hypocalcaemia worsens coagulopathy ✅ Anticoagulant-related bleeding Correction of clotting factors won’t work properly if calcium is low ✅ Liver disease / variceal bleeding Baseline coagulopathy + transfusions → high risk of hypocalcaemia Give calcium during major haemorrhage protocol if ionised calcium is: <1.1 mmol/L (or lab-specific lower limit) or empirically during massive transfusion How it’s given (UK practice): Calcium gluconate (peripheral line) Calcium chloride (central line only — more potent) Typical dosing (local protocols vary): Calcium gluconate 10 mL of 10% IV Re-check ionised calcium Exam-ready summary: Calcium is a critical cofactor in the coagulation cascade and should be monitored and replaced during major medical bleeding, particularly in the setting of massive transfusion.

Answer 264

Give IV thiamine before glucose if any concern that alcohol dependency BUT if glucose is very low (e.g. 1.2 mmol/L) - give IV glucose immediately e.g. 150–200 mL of 10% glucose IV AND give IV thiamine as soon as possible - ideally at the same time or immediately after Because that level if immediately life threatening - severe hypoglycaemia causes immediate brain injury whereas Wernicke’s encephalopathy is serious but not immediate If glucose ~2.5–3.0 mmol/L and patient is stable = give thiamine first, then glucose as you have time and the risk of Wernicke’s matters

Answer 265

Calcium is given in hypocalcaemia (can cause muscle weakness, tetany, seizures and hypotension due to poor myocardial contractility), life-threatening hyperkalaemia to stabilise the myocardium and during massive haemorrhage to enable coagulation - check ionised calcium (ABG/VBG) and administer calcium according to protocol, also if doing MHP inform reg esp if BP isn't picking up. Also calcium channel blocker overdose

Answer 266

The cause of the patient’s presentation is hypoglycaemia. I would make sure bloods have been taken and then start 100mls of 20% glucose intravenously. If IV access is impossible, I would give 1mg of glucagon IM. Alternatively 150mls of 10% glucose can be used. 50% glucose is no longer recommended due to the high risk of extravasation injury. If hypoglycaemia is the cause of the unconsciousness then the patient should start to show signs of improvement within 10 minutes. Further IV glucose should not be given before repeating the blood glucose. Once the patient is alert enough, I would give them a carbohydrate rich food. There is a suggestion that the patient has been using alcohol. I would make sure that I have given the patient IV Pabrinex to reduce the risk of precipitating Wernicke’s encephalopathy. Once the patient is stable, I would need to try and establish the cause of the hypoglycaemia.

Answer 267

Medications and alcohol use are the most common causes of hypoglycaemia. The most common meds that result in hypoglycaemia are insulin and sulfonylureas (esp in renal/hepatic impairment). Rarer medications resulting in hypoglycaemia are salicylates, beta-blockers, quinine and pentamidine. In addition to the above, hypoglycaemia can be as a result of organ failure, acute liver failure, adrenal failure, myxoedema or hypopituitarism, as well as due to infection (for example malaria). The high potassium and low sodium on the blood gas results would in particular raise suspicion of an acute adrenal crisis. I would ensure in this case to check the patient’s medical records for any history of adrenal insufficiency, if possible, and discuss with a senior as to whether a stat dose of IV steroids should also be given. Other causes = inadequate oral intake/excessive exercise also gastroparesis. Finally, in very rare circumstances hypoglycaemia can be due to tumours such as insulinomas. Do not jump straight to tumours when answering this question in the exam. It is an answer that lots of people will give, however, they are incredibly rare. Medication use is the most common cause along with alcohol.

Answer 268

Glucagon is a hormone that induces conversion of glycogen to glucose in the liver, thereby raising the blood glucose level. The fact that glucagon has not worked would suggest that the process of glycogenolysis is not working. This would indicate that the cause of the hypoglycaemia is due to the inhibition of liver cells, most likely due to acute excessive alcohol consumption. This is the likely cause for the patient’s presentation. In alcohol-induced hypoglycemia, glucagon may fail because glycogen stores are depleted and hepatic gluconeogenesis is inhibited by alcohol metabolism. Also chronic alcohol/severe liver disease (also impairs gluconeogenesis) → glycogen depletion. Route hierarchy for hypoglycaemia: Oral glucose (4 tablets or 2 gels) — if patient is conscious and able to swallow IV dextrose (100ml 20%) — preferred for rapid correction IM (1mg) or SC glucagon — if IV access is not available and patient is unconscious IO glucose (same as IV) — if IV cannot be established and glucagon fails

Answer 269

Patients should be informed that alcohol can increase the risk of hypoglycaemic episodes. Despite containing carbohydrates and initially raising blood sugars on consumption, alcohol inhibits the liver’s ability to release glucose into the blood*. This impairment can last for several hours after drinking alcohol. *Excessive alcohol consumption can impair glycogenolysis and gluconeogenesis, which are the two main ways the body maintains blood glucose during fasting. Not drinking on an empty stomach can decrease the risk of hypoglycaemia. It is also important to take additional carbohydrates before going to sleep at night after drinking alcohol, to avoid overnight hypoglycaemia.

Answer 270

Diabetic patients with episodes of hypoglycaemia need education in nutrition, checking glucose levels at home, and early signs and symptoms of hypoglycaemia. Recognition of early symptoms is paramount for self-treatment (anxiety, palpitations, sweating, tremor, confusion). Patients must inform the DVLA if they drive and take insulin or sulphonylureas. Information about driving and diabetes is available online to patients. Patients should always be encouraged to check their blood glucose before driving and take regular breaks to test their blood sugar. If the blood sugar is less than 5.0 mmol/L then patients should not drive. If they have a hypo they should treat it and not drive for at least 45 minutes, until blood sugars have returned to above 5.0 mmol/L.

Answer 271

Rate: 100–150 bpm vs Often >150 bpm Rhythm: Regular vs Regular P waves: Present, normal vs Often absent/retrograde PR interval: Normal vs Short/not measurable QRS: Narrow vs Narrow (usually) Onset: Gradual vs Abrupt Termination: Gradual vs Abrupt (vagal/adenosine) Cause: Physiological / secondary vs Primary arrhythmia P waves often absent or hidden in preceding T wave (retrograde)

Answer 272

ARIBAR! Are there any ischaemic changes present? ST depression or elevation? Check all leads. If you are presented with an obvious ST elevation MI the examiners will not be impressed if you don’t pick it up. If there is make sure to say the leads and if inferior/anterior and what artery. What is the rate? 150 bpm (300/2) Is this regular or irregular? This a regular rhythm. Is the QRS complex narrow or wide? It is a narrow complex tachycardia. Are there P waves? P waves are not visible in this ECG – this is likely due to the rate – check carefully. You may see them buried in the preceding T wave. Not being able to reliably see P waves indicates it is SVT, rather than sinus tachycardia. Relationship to QRS complexes.

Answer 273

This is a good chance to show off. A structured answer will win more marks then an unorganised list of causes. Split your answer into categories with the most common causes higher up your list of differentials Cardiac causes – MI, Heart Failure, Cardiomyopathy – anything which interferes with the conduction systems in the heart, valvular heart disease or pos-ablation Respiratory causes – the most common presentation of PE is tachycardia! Should be high on your initial differentials, however, normal sats point against this. Infection – the most common cause of SVT presenting to hospital. You will want to look for other symptoms and signs. Lack of temperature reduces this possibility Metabolic causes – Thyroid problems can cause arrhythmias HYPERTHYROID!!!!!!!! Volume loss – anaemia or volume loss secondary to increased GI loss Electrolyte imbalance – Hypo/Hyperkalaemia (although there are no specific signs in this ECG, it should still be included), Hypomagnesaemia Drugs and alcohol – caffeine, alcohol, beta-agonists (salbutamol), amphetamines Pain and stress – A differential that should not be forgotten as it can be easily treated. May be linked with one above – e.g. MI

Answer 274

My management of tachycardia would then be determined by whether the patient is stable or unstable, the type of tachycardia, and the likely cause. I would use an ABCDE approach to first establish this, and ensure the following key parts of the management are enacted i.e., identify and treat reversible causes e.g., give IVF/oxygen/?low Mg. Monitor oxygen, ECG (continuous cardiac monitor) and BP. I am aware of the risk of a patient potentially becoming unstable, and the urgent escalation required in this case (i.e. a crash call). If the rhythm is SVT and the patient is stable, I would attempt to reverse this using vagal manoeuvres, if the patient was able to perform them. Safe, non-invasive, can terminate the arrhythmia. If these are not successful, I would proceed to medical management of the arrhythmia, using the ALS algorithms as guidance (adenosine). I would also escalate to my senior if initial measures were unsuccessful. It would be crucial to continue to reassess the patient using the A to E approach, as if at any point they become unstable I would escalate urgently with a crash call.

Answer 275

When oxygen helps: Hypoxemic patients (low oxygen saturation, SpO₂ <94% in most adults) When oxygen may not help SOB: Normoxic patients (normal SpO₂) Shortness of breath is often subjective or due to other mechanisms: Anxiety / panic attacks Metabolic acidosis Hypercapnia Anemia (oxygen delivery affected by hemoglobin, not saturation) In these cases, oxygen won’t relieve the sensation of breathlessness unless hypoxemia is present => correct the cause. Special caution in COPD: High-flow oxygen in COPD patients with chronic CO₂ retention can worsen hypercapnia → respiratory acidosis Target SpO₂ is usually 88–92% Over-oxygenation can cause CO₂ retention (V/Q mismatch, haldane effect and mild hypoventilation)] Why CO₂ still rises with V/Q mismatch in COPD: Blood shunted to poorly ventilated alveoli Even though CO₂ diffuses easily, these alveoli are very poorly ventilated due to obstruction, mucus, or collapse. The combination of poor alveolar ventilation + increased blood flow makes CO₂ removal less efficient. Worsened V/Q mismatch globally Normally, HPV diverts blood to well-ventilated alveoli → CO₂ efficiently removed. High O₂ reverses HPV → more blood flows to bad alveoli → total CO₂ elimination decreases. Minor contributors add up Haldane effect and slight hypoventilation further raise PaCO₂. Airways are narrowed by inflammation and mucus, ventilation impairment means CO2 cannot be effectively removed. Pulmonary embolism: perfusion blocked, alveoli ventilated → high V/Q regions (dead space) Pneumonia / pulmonary edema: alveoli filled with fluid → low V/Q regions (shunt) COPD / asthma: airway obstruction → some alveoli ventilated poorly → low V/Q Atelectasis: collapsed alveoli → low V/Q or shunt Look at lecture on this! And aesthetics lecture about arterial lines use.

Answer 276

Preparation: Use a large-bore IV (ideally antecubital / proximal vein) Have resuscitation equipment ready ECG monitoring throughout Administration: Rapid IV push (“bolus”) over 1–2 seconds Follow immediately with a 20 mL saline flush — this pushes the drug into central circulation quickly Typical adult dose: First dose: 6 mg IV If no response after 1–2 minutes: 12 mg IV May repeat 12 mg once more if needed Why a rapid bolus is required: Adenosine’s half-life is <10 seconds If infused slowly, it metabolizes before reaching the AV node → ineffective Rapid push ensures a high concentration reaches the AV node → transiently blocks AV nodal conduction → terminates AVNRT (most common cause of PVST) / PSVT Patient experience: Transient flushing, chest pressure, or dyspnea common (lasts a few seconds) Heart may briefly stop (asystole) on ECG — normal, resolves immediately

Answer 277

Adenosine is safe in narrow-complex SVT without signs of pre-excitation, if present and adenosine given can degenerate into VF. If you see broad QRS, irregular rhythm, or delta waves (or can’t check), treat as pre-excited SVT and avoid adenosine (give IV procainamide WITH EXPERT ADVICE). IV procainamide also. The thing is though if broad complex tachycardia I will be choosing amiodarone in line with ALS.

Answer 278

1. Assess stability first: hypotension/shock, chest pain/myocardial ischaemia, altered consciousness/syncope, SOB/low sats (severe heart failure) → unstable → synchronised cardioversion (Midazolam 0.05–0.1 mg/kg IV over 1–2 minutes) 2. Identify QRS morphology: narrow vs broad → guides drug choice 3. Check for pre-excitation: avoid AV nodal blockers or adenosine if present

Answer 279

Very fast, ?irregular(both), broad-complex AF (>200 bpm) → strongly suggests pre-excited AF (WPW) Typical BBB morphology with moderately fast irregular AF → probably AF with BBB History of delta waves / short PR in sinus rhythm → suggests WPW / accessory pathway AV nodal blockers (CCBs, beta-blockers, digoxin, adenosine) are dangerous in pre-excitation → err on the side of caution if uncertain If uncertain: Unstable → DC cardioversion Stable → IV procainamide with cardiology input

Answer 280

Bedside: ECG, ABG/VBG (quickly alert you to electrolyte imbalance, an ABG would be more useful if underlying respiratory cause is suspected), Blood pressure/full set obs. Bloods: FBC (anaemia and infection markers); U+Es + Mg (electrolyte imbalances and kidney function – may have AKI if hypovolemic); TFTs; LFTs (if alcohol or medications are suspected); CRP (infection); Troponin (If MI is being considered) Imaging: CXR – underlying chest infection. Signs of cardiomegaly. Signs of heart failure ALSO ECHO – to look for structural heart disease 24 hour tape – this is more of a long-term investigation if SVTs are thought to be secondary to cardiac arrhythmias or paroxysmal. Secondary to acute illness OR paroxysmal (recurrent primary arrhythmia) A 24-hour ECG is useful if SVT episodes are intermittent (paroxysmal) or if recurrent symptoms suggest an underlying rhythm disorder rather than a one-off secondary cause.

Answer 281

Again, you should stress the importance of identifying and treating the underlying cause. It gets across that you understand that most tachycardias will resolve with treatment of the underlying problem. IV fluids, antibiotics, ACS protocol are also important things to mention at this point. However, at this point in the interview the examiners want you to go further and start talking about specific medications you might use to slow down the heart rate. It would also be sensible to state that if you had reached the point where you were having to chemically cardiovert (Adenosine/Amiodarone) a patient, you would escalate to your senior. Adenosine – works on the AV node by blocking conduction. It causes TRANSIENT heart block (impaired conduction of electrical impulses from the atria to the ventricles). Mediated by the A1 receptor. It is used to identify the underlying rhythm. It has a short half-life. /Adenosine can be used diagnostically because it transiently blocks AV node conduction, unmasking atrial activity on the ECG and allowing differentiation between AVNRT, AVRT, and atrial tachycardias or atrial flutter. (These are the 3 mechanisms for the clinical presentation (sudden tachycardia) PSVT (umbrella term))./ Things you may be asked by the examiners: Contraindications = 1. Long QT syndrome 2. 2nd or 3rd degree heart block without a pacemaker 4 (wink wink). Decompensated heart failure 5. Asthma What you should explain to a patient before giving = they may experience flushing, nausea, light-headedness associated with a ‘sense of impending doom’. This is secondary to TRANSIENT asystole following IV administration. How much = 6mg, followed by a further 12mg if no initial effect. Did they convert? If so the tachycardia can be considered NODAL in origin If it is atrial in origin, adenosine will only transiently block it. It can self terminate but often reverts back We need to watch and monitor for recurrence. /In focal atrial tachycardia episodes start and stop spontaneously, treat the underlying cause first e.g., infection or electrolytes or thyrotoxicosis, multifocal most commonly occurs in COPD - treat hypoxia and hypercapnia./ /Adenosine is not just therapeutic — it’s diagnostic: it can terminate AVNRT/AVRT but reveals atrial tachycardia (or flutter, could also think under same umbrella term) without terminating it./ If tachycardia terminates after adenosine but recurs, we can treat with longer-acting AV node blockers: beta-blockers (first line, use cautiously in asthma/heart failure) or CCBs (second line/alternative if BBs CI e.g., diltiazem). If on identifying the rhythm the patient appears to be in ventricular tachycardia or rhythm is uncertain, amiodarone can be considered. However, for exam purposes it is enough to say you would consider it but would want to discuss it with a senior! /// Remember: Adenosine is diagnostic and acute therapy, not long-term prevention. Longer-acting AV node blockers like beta-blockers or non-dihydropyridine calcium channel blockers are used to prevent recurrence. You do not give adenosine repeatedly indefinitely. The idea is to prevent recurrence in patients with recurrent SVT, using longer-acting AV node blockers rather than relying on repeated adenosine boluses. Management for FAT or MAT is down below.

Answer 282

Severe hyponatremia that may require hypertonic saline (3% NaCl) is generally when serum sodium falls below 120 mmol/L. 130–135 - Often asymptomatic 125–129 - Nausea, malaise, headache 120–124 - Vomiting, confusion, lethargy <120 - Seizures, coma, respiratory arrest, cerebral edema

Answer 283

Acute unstable AF: immediate cardioversion → anticoagulate afterward based on stroke risk (CHA₂DS₂-VASc). Stable AF / elective cardioversion: If AF ≤48 hours: can usually cardiovert without prior anticoagulation (risk is lower) If AF >48 hours or unknown duration: Start anticoagulation for ≥3 weeks before cardioversion, OR Perform transesophageal echocardiography (TEE) to rule out atrial thrombus before urgent cardioversion. Electrical cardioversion is done using synchronized DC shock - stable patient for urgent rhythm control. Pharmacologic cardioversion can be done with flecainide in normal hearts or amiodarone in patients with structural heart disease. Anticoagulation rules same as electrical cardioversion (AF >48h or unknown duration → anticoagulate ≥3 weeks or TEE-guided). In stable atrial fibrillation (AF), the default approach is often rate control, but there are specific reasons why you might opt for rhythm control instead. But remember if unsure about time of onset you have to do 3 weeks of anticoagulation Apixaban (or TTE). In a stable patient, rhythm control is preferred if the patient is symptomatic despite rate control, has underlying heart failure or impaired ventricular function or if AF is recent-onset => likely to convert easily. It can improve symptoms, cardiac output (heart failure ones), and prevent tachycardia-mediated cardiomyopathy. Patients may also prefer sinus rhythm to avoid long-term medications or symptoms, can allow more exercise tolerance and improve quality of life. Recent-Onset AF: Early cardioversion is often more successful in AF <48 hours Minimizes atrial remodeling that makes AF more persistent Avoiding Tachycardia-Mediated Cardiomyopathy: Persistent rapid ventricular response may cause left ventricular dysfunction over time Rhythm control can prevent long-term structural damage

Answer 284

NSAIDs Beta blockers Adenosine

Answer 285

SVT with aberrant conduction is a supraventricular tachycardia that appears wide on ECG because of abnormal intraventricular conduction, often due to rate-dependent bundle branch block. It is important to distinguish from VT because management differs. SVT with aberrant conduction refers to a supraventricular tachycardia (SVT) in which the QRS complex appears wide because of abnormal intraventricular conduction, not because the rhythm originates in the ventricles. SVT: tachycardia originating above the ventricles (atria or AV node) Aberrant conduction: the impulse is conducted through the ventricles abnormally, often due to: Pre-existing bundle branch block (usually right bundle branch block) Rate-dependent bundle branch block (e.g., right bundle fails to repolarize at high rates) Result: wide QRS (>120 ms) even though the origin is supraventricular Rate-dependent RBBB is the most common cause of SVT with aberrancy. If you cannot confidently distinguish SVT with aberrancy from VT, you should treat it as ventricular tachycardia (VT). Also antidromic AVRT (wide-complex) can look very similar to SVT with aberrant conduction on ECG - if uncertain, treat as VT. Don't have time right now to look into IV procainamide. What do you do after given the amiodarone? After giving amiodarone for (suspected) VT 1️⃣ Continuous monitoring Cardiac monitor (rhythm, rate) Blood pressure Oxygen saturation Conscious level 👉 You are watching for: Conversion to sinus rhythm Deterioration → shock / hypotension / unconsciousness 2️⃣ Did it terminate? ✅ If rhythm terminates / stabilises Continue amiodarone infusion UK ALS: 300 mg IV over 20–60 min then 900 mg over 24 hours Arrange: Cardiology review 12-lead ECG Bloods: U&Es, Mg²⁺, troponin Look for reversible causes Ischaemia Electrolyte abnormalities Drug toxicity ❌ If VT persists but patient remains stable Escalate early to senior / cardiology Consider: Further antiarrhythmic strategy Electrical cardioversion if concern increases 3️⃣ If the patient becomes unstable at any point 🚨 Immediate synchronized DC cardioversion Do not wait for drugs to work Follow ALS unstable tachycardia pathway Key safety principle Drugs are for stable VT — electricity is for unstable VT. IMT interview one-liner (memorise this) “After giving amiodarone for a wide-complex tachycardia, I would closely monitor the patient, assess for rhythm conversion and hemodynamic stability, start a maintenance infusion if successful, investigate and correct reversible causes, and escalate to synchronized cardioversion immediately if the patient becomes unstable.” Do you always give the second bag? No What “second bag” means You’re referring to the amiodarone maintenance infusion: After the initial 300 mg IV loading dose The “second bag” = 900 mg over 24 hours When you DO give the second bag ✅ If: The rhythm terminates or stabilises VT is suppressed but risk of recurrence remains Patient is admitted under cardiology / CCU Rationale: Amiodarone has a long onset and long half-life — the infusion helps maintain rhythm stability. When you DO NOT automatically give it ❌ If: VT did not respond and patient proceeds to DC cardioversion Diagnosis changes (e.g. clearly SVT with aberrancy) Significant adverse effects occur (hypotension, bradycardia) Cardiology advises against it

Answer 286

Long-term prevention of SVT recurrences: AVNRT/AVRT = bisoprolol/metoprolol or diltiazem FAT = treat underlying cause first then BBs/CCBs if symptomatic and persistent MAT = treat underlying cause, drugs usually not effective for rhythm control Catheter ablation is curative option for recurrent SVT, especially AVNRT or AVRT How is WPW treated long term? Asymptomatic WPW: Often no treatment if truly asymptomatic and low-risk pathway Symptomatic WPW (tachyarrhythmias): First line = catheter ablation of the accessory pathway So in your orthodromic - no delta, no wide. if irregular (AF) no adenosine. Adenosine is safe in AV node–dependent SVTs, including narrow-complex orthodromic AVRT. It is contraindicated in pre-excited SVT or AF because blocking the AV node may force conduction down the accessory pathway, risking ventricular fibrillation.” Orthodromic AVRT is narrow-complex and AV node–dependent, so adenosine can be used. Antidromic AVRT or pre-excited AF is wide-complex and AV node–independent, so adenosine is contraindicated.” ECG features of pre-excitation (WPW) Short PR interval (<120 ms) Delta wave (slurred upstroke of QRS) Widened QRS (>110 ms) In orthodromic AVRT, the impulse travels down the AV node to the ventricles (anterograde) and then back up the accessory pathway to the atria (retrograde), forming a re-entry loop. The AV node is part of this circuit, so adenosine can terminate it. you usually do NOT see a delta wave in orthodromic AVRT. Distinguishing regular AF from pre-excited AF (AF in WPW) on ECG is critical - Wide QRS and can be over 200 AF (normal): rate control (beta-blocker, CCB), anticoagulation Pre-excited AF: AV nodal blockers (adenosine, beta-blockers, verapamil) are contraindicated Use IV procainamide or electrical cardioversion if unstable “Pre-excited AF in WPW is an irregularly irregular, often very fast, wide-complex rhythm due to conduction over an accessory pathway, whereas regular AF usually has a narrow QRS. Pre-excited AF is dangerous because AV node blockers can precipitate ventricular fibrillation.” If a patient with WPW has atrial fibrillation, you do NOT give adenosine, even if they have had orthodromic AVRT in the past. In a patient with WPW and atrial fibrillation, AV nodal blockers including adenosine are contraindicated due to the risk of ventricular fibrillation. Management is with synchronized cardioversion if unstable, or procainamide if stable.” One-sentence rule to lock this in Adenosine is safe in AV node-dependent SVT, but never in AF with WPW. => its not safe in AV node-independent SVT shown by wide QRS or delta wave (or irregular/AF) AVRT vs WPW WPW = structural predisposition Accessory pathway exists all the time (may show delta wave on ECG) AVRT = arrhythmia Occurs when a re-entry circuit develops using the accessory pathway + AV node Not all WPW patients are in tachycardia, but all WPW tachycardias are technically AVRT (orthodromic or antidromic) AVRT vs AVNRT Re-entry circuit Within or around AV node (dual pathways: fast and slow) Between atria ↔ AV node ↔ accessory pathway ↔ ventricles AV node dependence Yes (critical for re-entry) Yes for orthodromic, retrograde for antidromic In antidromic AVRT, the ventricles are activated via the accessory pathway (anterograde), and the AV node conducts the impulse backward to the atria (retrograde). This means the AV node is not essential for the tachycardia, so AV node blockers like adenosine are ineffective and potentially dangerous. AVNRT is a re-entry tachycardia confined to the AV node using dual pathways, usually narrow-complex, with hidden retrograde P waves, and is AV node–dependent. AVRT involves a re-entry circuit between the atria, AV node, ventricles, and an accessory pathway; orthodromic AVRT is narrow-complex and AV node–dependent, while antidromic AVRT is wide-complex and AV node–independent for antegrade conduction. AVRT always involves the AV node… but the dependence differs by type: (look at phone image 28th December) Type Antegrade conduction AV node role QRS Orthodromic AVRT AV node → ventricles AV node–dependent for antegrade conduction Narrow QRS Antidromic AVRT Accessory pathway → ventricles AV node conducts retrograde only; not essential for the tachycardia Wide QRS so does retrograde mean opposite direction Yes — exactly. Retrograde conduction means that the electrical impulse travels opposite to the normal physiological direction. Antidromic AVRT circuit: Atria → accessory pathway → ventricles → AV node → atria → accessory pathway → ventricles…

Answer 287

This patient is now UNSTABLE. At this point you should call a senior for help and put out a 2222 call. This shows to the examiners you have identified early that this patient could deteriorate further! Following this you should start IV fluid resuscitation and give oxygen (ABCDE - don't think I would give fluids here because feel due to acute heart failure i.e., low sats may reflect acute pulmonary oedema). As per ALS guidelines, since this patient has an SVT and is haemodynamically unstable, he should be considered for immediate DC cardioversion.

Answer 288

To differentiate SVTs, I approach them systematically. First, I confirm it is a supraventricular rhythm, excluding sinus tachycardia and ventricular tachycardia. Then I ask two key questions: is the rhythm atrial in origin or atrioventricular/AV node–dependent, and is it regular or irregular? This allows me to narrow the differential and guide acute management. Regular, narrow-complex tachycardias that are AV node–dependent suggest AVNRT or orthodromic AVRT, whereas antidromic AVRT is wide-complex and not AV node–dependent, while regular atrial rhythms may indicate focal atrial tachycardias or flutter with regular block. /Identifying AV node dependence is important because it determines whether adenosine (remember will only show the atrial tachys not stop them like AVNRT or AVRT) or AV node blockers are safe./ Irregular rhythms suggest atrial fibrillation, multifocal atrial tachycardia, or atrial flutter with variable block. SVTs are usually narrow-complex, but they can present as broad-complex tachycardias either due to aberrant conduction (like rate-dependent bundle branch block) or an accessory pathway (pre-excitation/WPW). If the patient is unstable = DC shock and if stable, if there is any uncertainty, the tachycardia should be managed as ventricular tachycardia to be safe. /// Additional clues include P wave morphology, response to vagal maneuvers or adenosine, and QRS width, which help guide both diagnosis and acute management.

Answer 289

Situation: This is a 72 year old man who is in SVT and has now become unstable with hypotension. Background: The gentleman initially presented to A+E with chest pain and was tachycardic but initially maintaining his blood pressure. He has not received any other medications. Assessment: A full ABCDE assessment has been carried out and investigations have been sent for common causes of SVT. Recommendations: I have put out a 2222 cardiac arrest call. I need urgent medical assistance. As per the resuscitation guidelines this gentleman is likely to need DC cardioversion and I will need support from my senior colleagues to carry this out. Due to the hypotension this would now be the preferred management of the SVT rather than medical management.

Answer 290

VIVID Vascular: subarachnoid haemorrhage (SAH); subdural haematoma; cerebral venous sinus thrombosis (non-septic, headache, seizures, focal deficits, anticoagulation) Infection: Meningitis, encephalitis Vision-threatening: temporal arteritis, cavernous sinus thrombosis (septic from facial/sinus infection, periorbital edema, proptosis, cranial nerve palsies, fever, IV antibiotics +/- anticoagulation) Intracranial pressure: space occupying lesion (tumour, abscess, cyst, aneurysm), hydrocephalus, cerebral oedema Dissection: carotid dissection Of that list, some are unlikely given the speed of onset and the age of the patient. Infective causes are much more likely and so should be offered first in any given list of differentials. Vascular causes, though rarer, could also present in the given time course. As well as the above sinister causes, think of tension headache and migraine, although these are unlikely to present with the observations above. It is important that you stress to the examiners that your main concern here is investigating and treating the patient for bacterial meningitis. This should be your number one differential.

Answer 291

In a patient presenting with a headache, a neurological examination of the upper limbs, lower limbs, cranial nerves and cerebellum would also be necessary in order to identify any localising signs or focal neurology. Also say in E - I would look for any evidence of a petechial rash but this is a late sign.

Answer 292

Bloods: FBC (infection), CRP (inflammation), U+Es (dehydration), Mg and calcium given the patient is tachycardic (to check for electrolyte imbalances), coagulation screen (may need invasive procedures as part of her diagnostic work up), blood cultures, preferably before giving antibiotics although if this is not possible I would not delay giving antibiotics. I would also take a VBG as this will give me a bedside lactate. Bedside: urine sample (check for any signs of urinary infection or blood) Imaging: CXR (sepsis work up), urgent CT Head if evidence of any confusion or increasing drowsiness - I would discuss this with my registrar first given the age of the patient, but it is important given the presentation. Finally, I would perform a lumbar puncture. Send the sample for: 1. MC+S includes a gram stain 2. Cell count 3. Biochemistry (glucose and protein) 4. Viral PCR 5. Paired serum glucose 6. If concerned about TB from the history I would also send the sample to be tested for acid fast bacilli

Answer 293

1. Headache, fever and neck stiffness are the most common symptoms (although they are absent in 18% of patients). ?Also photophobia 2. Rash – meningococcal meningitis is most commonly associated with a macular rash progressing to petechiae or purpura. 3. Confusion or altered level of consciousness. In the elderly and the immunocompromised this may be the only symptoms. Mortality increases as consciousness decreases. 4. Focal neurological signs complicate meningitis in at least 15% of cases. It suggests cerebral damage. A brain abscess or encephalitis should be considered if focal neurological signs of seizures predominate. 5. Seizures are a presenting feature in up to 30% of cases.

Answer 294

Common bacteria in adults include Neisseria meningitidis and strep. pneumonia. Rarer causes such as Listeria and Gram negative bacilli should be considered in elderly patients or those patients who are immunocompromised.

Answer 295

If available to me I would follow my local hospital guidelines with regards to the correct antibiotic to use. However if these were not available to me, the empirical first line treatment for suspected bacterial meningitis is IV ceftriaxone or cefotaxime. If meningococcus is suspected (i.e. due to a rash) I would also consider adding benzylpenicillin. If the patient had a definite anaphylaxis or near anaphylaxis to penicillin I would discuss this urgently with the on-call microbiologist. These patients may require IV chloramphenicol or vancomycin, but I would await specialist advice before commencing this. Consider adding amoxicillin/ampicillin in patients >50 years or immunocompromised to cover Listeria monocytogenes

Answer 296

Lumbar puncture should be delayed in patients with severe sepsis or a rapidly evolving rash because the procedure may worsen hemodynamic instability, and immediate empiric antibiotics take priority over diagnostic CSF sampling. LP can be safely performed once the patient is stabilized. In a stable patient without red flags, lumbar puncture should ideally be performed before starting antibiotics to maximize culture yield. However, if the patient is unstable, has raised ICP, or fulminant sepsis, antibiotics should be given immediately, and LP delayed until it is safe. Antibiotics are given before LP only if the patient is very ill or unstable, because immediate treatment takes priority over culture yield. Otherwise, LP should ideally precede antibiotics. If meningococcal meningitis is suspected — particularly with purpuric rash or fulminant sepsis — antibiotics should be given immediately and LP delayed until stabilization. In stable patients with suspected pneumococcal meningitis, LP can be performed first to maximize culture yield before starting antibiotics. In suspected meningococcal meningitis, antibiotics are given immediately if the patient is unstable, and lumbar puncture is delayed until stabilization. There is no strict timing, but LP is usually performed within a few hours after starting antibiotics once it is safe (also must ensure that coag is okay), recognizing that culture yield may be reduced but Gram stain can still be diagnostic.

Answer 297

Benzylpenicillin (penicillin G) is licensed for IM or IV use in the community in the UK Benzylpenicillin is highly effective against Neisseria meningitidis, the most common cause in community cases GPs have limited emergency drugs, Ceftriaxone is less commonly stocked in GP practices Ceftriaxone requires reconstitution, larger dose, or refrigeration Ceftriaxone IM if penicillin allergic

Answer 298

Guidelines from the British Infection Association (previously British Infection Society) recommend that an LP can be performed in patients with suspected meningitis without a CT head. However, this is only advised in cases of simple meningitis – i.e. not obviously septicaemic (I think because straight to IV abx), no focal neurological signs (raised ICP) and NO decrease in consciousness. A CT scan should be performed in all patients with low consciousness. Antibiotics should be given before a CT scan.

Answer 299

Bacterial meningitis: 1. CSF cloudy or turbid 2. Elevated WCC (cells 5-2000 per mm3), main cell type = neutrophils 3. Glucose very low (compared with serum, <40% of serum glucose) 4. Protein elevated (>0.1 g/L/>50mg/L) 5. High opening pressure I would ask the lab to do a gram stain, as this can be positive in 15% of negative culture cases.

Answer 300

1. CSF generally clear 2. Fewer cells, typically no more than 500 per mm3, main cell type = lymphocytes. 3. Glucose normal (often elevated >60% serum) 4. Protein is only slightly raised (0.5-0.9 g/L) 5. Opening pressure normal or mildly raised Viral PCR may identify the offending pathogen. Encephalitis is the same but the protein tends to be slightly higher and HSV PCR positive. Also may see RBCs (temporal lobe necrosis).

Answer 301

Opening pressure: Raised Cells: Lymphocytes Protein: High Glucose: Low

Answer 302

Public health services should be notified in any case of bacterial meningitis. They can then advise on current prophylactic treatment and vaccination, and will assist in contact tracing. The local microbiology team should also be informed of any case of suspected or confirmed bacterial meningitis. /Public health should be notified in all cases of bacterial meningitis so they can identify and manage close contacts, including arranging chemoprophylaxis and vaccination where indicated, to prevent secondary cases./ Contact tracing will be important, especially in high population density settings, for example university halls.

Answer 303

1. Gonococcaemia 2. Sepsis with DIC - the meningitis textbook rash is a sign of DIC (you’ve got a coagulopathy), so its not really a sign of meningitis, you’ve got a sepsis… you can have a sepsis picture without meningitis and have that rash, horrible purpuric rash 3. Haematologic malignancy with septicaemia 4. Henoch-Schonlein purpura 5. Viral haemorrhagic fevers

Answer 304

Full investigations as part of the sepsis work up have been sent, including blood cultures and also has been started on brand spectrum antibiotics as per local guidelines In meningitis can mention that abx were given prior to LP as very unwell/?septic better word and senior clinical review needed as she could deteriorate quickly and if bacterial meningitis is confirmed then local public health services need to be informed.

Answer 305

PINCH ME - but pick the things you feel relevant to your patient, if they have signs of systematic upset e.g., RR then unlikely to be e.g., just fracture Pain - fracture, pressure sore, urinary retention Infection/sepsis (do they have fever?) - UTI, pneumonia, skin or soft tissue, C. diff (if recent antibiotics) or meningitis/encephalitis Nutrition - malnutrition, dehydration, electrolyte disturbances (high or low Na and Ca, consider addisons/adrenal crisis), high or low glucose, thyroid, vitamin deficiencies eg B12 Constipation/faecal impaction Hypoxia/heart/head - pneumonia, COPD exacerbation, PE, intracerebral bleed, stroke, seizure, SOL, MI, arrhythmia, HF exacerbation Meds - new (eg abx, steroids, anti-psychotic), polypharmacy (esp. benzodiazepines, opioids, ACB), overdose, alcohol withdrawal, renal drug toxicity Environment - change, sleep disturbance, sensory deprivation

Answer 306

Bedside: full obs, urine dip, drug chart (?new meds or changes) Bloods + VBG (metabolic state of the patient as well as the patient’s lactate): FBC (to check for anaemia and raised WCC), U&E to look for any impairment in kidney function (discussed in the question) as well as look at any electrolyte imbalance, CRP, Ca, B12, folate, thiamine and thyroid function tests would also be important in anyone presenting with worsening confusion. Blood Cultures!!! I would request drug levels on any medications I was concerned about. Imaging: CXR to look for any signs of lung infection, CT Head acutely to look for any evidence of intracranial haemorrhage, space occupying lesion or subdural haemorrhage that could be contributing to the patient’s symptoms. If I suspected a CNS infection then I would perform a lumbar puncture.

Answer 307

1. In the first instance it is important to identify the cause and treat it. This may include starting antibiotics if there is an infection, withdrawing precipitating medications, correcting electrolyte imbalances, correcting hypoxia or dehydration, treat pain, constipation or retention. 2. If the patient is agitated then sedation may be necessary. Benzodiazepines may exacerbate confusion so should not be used acutely. Medications such as Haloperidol and Chlorpromazine may be better. It should first be discussed with a senior. Should only be given for severe agitation or distress after non-pharmacological measures have failed AND patient is a risk to themselves or others and not to those with Parkinson’s disease, Lewy body dementia or Prolonged QT. 3. Non-pharmacological treatments include nursing in a moderately lit room/calm environment with repeated reassurance. Regular orientation of patient to time, place and person. See if a family member can stay with the patient as this may be reassuring to them and may avoid the need for sedatives. Making sure that the patient has their appropriate sensory aids (glasses, hearing aids etc.).

Answer 308

Cognitive function can be assessed quickly using the abbreviated mental test score (AMTS). The benefit of this test is that it can then be repeated during the admission, giving an indication of response to treatment. Does not diagnose delirium. Rapid screening for dementia or delirium (cognition). The Confusion Assessment Method (CAM) is a specific set of 4 questions designed for the diagnosis of delirium. Looks at: 1. Acute onset (acute change from baseline mental status over hours–days) & fluctuating course e.g., worse in evenings 2. Inattention (months of the year backwards or 3-5 digit span forwards then backwards) 3. Disorganised thinking (Will a stone float on water?) 4. Altered level of consciousness Delirium = 1 + 2 + (3 or 4)

Answer 309

Delirium is a sudden onset and fluctuating impairment in cognitive function and consciousness. It is transient and reversible. Dementia is the progressive and irreversible decline in global function from a premorbid level, without any impairment in consciousness.

Answer 310

Age >65 Dementia Multiple co-morbidities Visual and hearing impairment Recent surgery Polypharmacy Drugs and alcohol dependence

Answer 311

PRIMARY Neurodegenerative: Alzheimer’s disease Frontotemporal dementia Lewy body dementia Parkinson’s disease dementia Parkinson-plus syndromes (PSP, CBD, MSA) Prion diseases (e.g. Creutzfeldt–Jakob disease) Vascular: Vascular dementia (multi-infarct, small-vessel disease) Mixed dementia (Alzheimer’s + vascular) SECONDARY (POTENTIALLY REVERSIBLE IF IDENTIFIED AND TREATED) Metabolic / endocrine: Vitamin B12 deficiency* Folate deficiency* Thiamine deficiency* Hypothyroidism* Cushing’s syndrome* Wilson’s disease* Structural: Normal pressure hydrocephalus* Subdural haematoma* Brain tumours Infective: HIV Neurosyphilis Inflammatory / autoimmune: CNS vasculitis Autoimmune encephalitis Drugs and toxins: Alcohol Heavy metal exposure Medications (e.g. anticholinergics, benzodiazepines) *These have a degree of reversibility, if identified and treated, unlike other forms of dementia causes.

Answer 312

This answer is about how dementia is diagnosed in a hospital setting. In most cases the diagnosis of dementia is made in the memory clinic as an outpatient rather than in hospital. Your role as an acute medical SHO is recognising when dementia may be a possibility and making the appropriate investigations and referrals. I would arrange for investigations that are used to rule out reversible causes of dementia. This includes blood tests for B12 and folate, as well as thyroid function tests. More specialist tests should only be considered if there are indications from the patient’s history and after discussion with senior members of the team e.g. serum ceruloplasmin. A CT head is important for anyone with a possible diagnosis of dementia to rule out reversible causes. On discharge from hospital, the discharge summary should include instructions to the GP to refer the patient to the memory clinic. I would discuss the possible diagnosis with the patient if appropriate, or with the patient’s family so they understand why the memory clinic will be contacting them.

Answer 313

Acetylcholinesterase inhibitors such as Donepezil may be considered in patients with mild to moderate Alzheimer’s disease. Treatment should be initiated by a specialist in dementia. Memantine (an NMDA receptor antagonist) is licensed for use in severe Alzheimer’s disease (MMSE 3-14).

Answer 314

Daily weights and fluid balance (needs catheter and urine output monitored closely)

Answer 315

The likely diagnosis is pulmonary oedema secondary to decompensated heart failure. Your differential for acute presentation of shortness of breath is broad. However, the stem has given you several clues. To answer this question, show the examiners how you are thinking. For example you could split the differential into time of onset of the shortness of breath. 1. Seconds to minutes – Acute asthma attack, anaphylaxis, Pneumothorax (+ Tension), Inhaled foreign body, Pulmonary Embolism 2.Hours to Days – Pneumonia, Heart Failure, Pleural Effusion (also PE) 3.Weeks to Months – Worsening COPD, Chronic Asthma, Heart Failure, Pulmonary Fibrosis, Anaemia, Pulmonary HTN, Obesity

Answer 316

Bedside: urgent ECG to assess for any cardiac arrhythmia - especially as the patient has a history of AF - as well as any evidence of acute ischemic changes; ABG will be useful to assess the PaO₂ and PaCO₂ Bloods: FBC, U+Es, CRP as well as a troponin if it is indicated from the history - acute coronary syndrome (ACS) may be the cause of the decompensated HF If there are signs of sepsis I would send off a septic screen – sputum, urine, blood cultures. Imaging: CXR will be important to look for signs of pulmonary oedema. A CXR will also exclude pneumothorax and consolidation. When the patient is more stable I will need to arrange an ECHO to assess the cardiac function. I would continue to monitor the patient’s saturations. However, this may be inaccurate if the patient is peripherally shut down.

Answer 317

O - obs P - peak flow or PR A - ABG U - urine analysis/tox/preg/monitoring S - swabs (resp or skin) or sputum E - ECG L - lactate or L/S BP G - glucose Sepsis - urine/blood/sputum cultures

Answer 318

A = alveolar edema - patchy opacities often bilateral and perihilar (“bat wing” distribution) B = Kerley B lines / interstitial oedema C = cardiomegaly may or may not be present D = diversion of blood to upper lobes (upper lobe vessels more prominent than normal) E = pleural effusion Interstitial edema Fluid accumulates in the interstitium — the connective tissue around alveoli, bronchi, and pulmonary vessels. Alveolar edema: Fluid fills the alveolar spaces themselves. More severe; often follows interstitial edema if hydrostatic pressure or injury persists.

Answer 319

Acute pulmonary oedema should initially be continuously monitored and managed where full resuscitation facilities are available. I would make sure the patient is sitting upright and start high flow oxygen (unless contraindicated). I would secure venous access and give a stat dose of IV furosemide. This is for symptomatic relief. I would insert a urinary catheter to monitor urine output and start the patient on a fluid restriction. If there is little or no response to the initial dose, the dose should be doubled at two-hour intervals as needed up to the maximum recommended doses. Vasodilator therapy is recommended for patients with urgent need for afterload reduction (eg, severe hypertension). It is also recommended as an adjunct to diuretic therapy for patients without adequate response to diuretics. Therefore, based on the response to the above and if the SBP is >90 mmHg and the patient does not have aortic stenosis, then I could start an IV infusion of GTN and titrate the dose against the BP. I would try to establish the underlying cause of the patient’s decompensation. The patient should be continually monitored. If there is any suggestion of worsening respiratory function I would contact ITU. The patient may benefit from non-invasive ventilation. Additionally if the patient has an SBP of <90 mmHg on presentation then I would also contact ITU as the patient may end up requiring inotropic support. Inotropes may be required as a temporizing measure in patients with severe left ventricular systolic dysfunction and low output syndrome. /If the patient has an SBP <90 mmHg on presentation, I would contact ITU, as inotropes may be required as a temporizing measure in severe LV systolic dysfunction with low output syndrome.

Answer 320

Chronic stable heart failure may easily decompensate. This most commonly results from an intercurrent illness (such as pneumonia), acute coronary syndrome, cardiac arrhythmias (such as AF), uncontrolled hypertension, or the person's failure to maintain an adequate fluid restriction, diet, or a lack of compliance with medication.

Answer 321

The New York Heart Association (NYHA) functional classification provides a simple way of classifying the extent of heart failure. I Cardiac disease, but no symptoms and no limitation in ordinary physical activity, e.g. no shortness of breath when walking, climbing stairs, etc. II Mild symptoms (mild shortness of breath and/or angina) and slight limitation during ordinary activity. III Marked limitation in activity due to symptoms, even during less-than-ordinary activity, e.g. walking short distances (20–100 m). Comfortable only at rest. IV Severe limitations. Experiences symptoms even while at rest. Mostly bedbound patients. Because functional capacity is such a powerful determinant of outcome it remains arguably the most important prognostic marker in routine clinical use in heart failure today.

Answer 322

For patients with heart failure with reduced ejection fraction (HFrEF), the four pillars of therapy are an ACE inhibitor (ramipril) or ARNI (sacubitril/valsartan), a beta-blocker (bisoprolol), a mineralocorticoid receptor antagonist (MRA) (spironolactone) , and an SGLT2 inhibitor (dapagliflozin - only start on specialist advice). These medications have been shown to reduce morbidity and mortality. It is important to initiate these treatments once patients have been stabilised following their acute admission (i.e., get dry!!!). Each should be started at a low dose and titrated to the highest tolerated dose, with careful monitoring of blood pressure, renal function, and electrolytes, to achieve maximal benefit. /In HFpEF SGLT2 inhibitors reduce hospitalizations and may improve quality of life. The evidence for mortality benefit is emerging but modest. Mineralocorticoid receptor antagonists such as spironolactone may reduce hospitalizations in symptomatic HFpEF patients but mortality benefit is limited.

Answer 323

I would calculate the patient's CHADS2-VASC score before considering anticoagulation. This is a score that calculates the risk of thromboembolic stroke in patients that have AF. A score of two and above would indicate anticoagulation is appropriate. This would need discussion with the patient about the risks and benefits of anticoagulation. Using the ORBIT tool to assess bleeding risk would also be indicated, to help quantify this.

Answer 324

I would discuss with the patient the importance of adherence to the medication and it needs to be taken regularly every day to maintain its effects. I would explain that it has a rapid onset of action so once started the patient will be anticoagulated, compared to warfarin which requires a loading period. I would explain to them that no monitoring is required whilst on the treatment. I would ensure that the patient is aware of the signs and symptoms of unusual bleeding and the need to seek urgent medical attention. I would explain to them that they are more at risk of bruising from small innocuous events now they are taking an anticoagulant. I would tell them about the need to inform their doctor or dentist that you are taking a DOAC well before any planned procedure. Patients should be advised to carry a patient alert card with them at all times.

Answer 325

If initial management is not helpful in relieving her symptoms, I would recommend initiating a vasodilator, such as a GTN infusion, if her BP remained elevated. (or CPAP if unable to maintain sats). If the BP is dropping or persistently low then the patient may need inotropic support and ITU should be involved early. Investigations will be needed to establish the cause of the decompensation.

Answer 326

I would start by asking general questions. For example: How long has she had these symptoms? Have they changed over time? For example, are they getting worse? Have they been associated with infection or any episodes where these symptoms have deteriorated significantly? I would then specifically ask questions about each presenting complaint: Cough: Is the cough productive or dry? What colour is the sputum? Is the cough persistent or intermittent? Any time of day? Any history of haemoptysis? Any chest pain when coughing? Wheeze: Does the wheeze occur spontaneously or with triggers (exercise, dust, smoke). What does the wheeze sound like? How long does the wheeze last? Has it ever been managed with medications? Dyspnoea: Does the shortness of breath occur at rest or with exertion? Is there any positional dyspnoea? How long do the episodes last and how does the patient manage it?

Answer 327

I would want to know specifically about her history of weight loss as it is mentioned in her referral. Has this been intentional or not? Has this been associated with any other symptoms? I would want a detailed past medical history and list of medications. Her social history (ALWAYS DO LOST!!!) will also be extremely important in this consultation. I would want a detailed smoking history. Does she smoke cigarettes and what type? Does she smoke anything else? I would want to know about her living situation and where she lives – for example inner city vs out of the city – thinking specifically about pollution. Does she have any pets at home? I would want to know her occupation and any exposure history to specific agents such as asbestos. Finally, I would want to know about her history when growing up. Has she always lived in the UK? Is there any history of TB exposure? I would also want to know a detailed family history. Specifically, is there any history of respiratory or cardiac disorders? For example, is there any history of alpha-1 antitrypsin disorder? Finally, as part of my consultation, I would ask for a detailed systems review which may pick up anything that I may have missed. I would also finish by asking the patient about their ideas, concerns and expectations.

Answer 328

In clinic it slightly differs cause good to have investigations that could be done on the day. Bedside: pulse oximetry and a sputum sample (if the patient can provide this), ECG (given the presentation could still be cardiac). Bloods: FBC (raised Hb in response to chronic hypoxia), U&E and a CRP. Imaging: CXR would be important (although seldom diagnostic) in the diagnosis of COPD as well as assessing for the presence of significant comorbidities e.g. consolidation, masses or effusions suggesting HF. Signs suggestive of COPD on x ray would include hyperinflated lungs and flattened diaphragm. Other investigations that may be useful would include pulmonary function tests and serial peak flow measurement. An echocardiogram would also be useful. Given this is likely a respiratory issue a CT chest would also give more information on any underlying pathology (esp since weight loss). However, given these are more specialised tests I would be keen to discuss these requests with my clinical supervisor in the clinic.

Answer 329

I suspect that this is a respiratory issue. Top differential = COPD (given smoking hx) However, my investigations would be useful to help determine the remaining differentials that would include: Asthma Bronchiectasis Lung cancer Tuberculosis Other non-respiratory causes of persistent cough and dyspnoea would be: Congestive heart failure Medication induced Gastro-oesophageal reflux disease

Answer 330

You can start your answer by explaining that you would set the scene in your clinic. Ask if she needs anyone else with her. Remember to use straightforward language and avoid medical jargon. Keep the answer simple – remember you are not being asked to list the treatment steps of COPD. Hi Mrs Bruth. I wanted to talk to you about the results of the investigations that we have ordered. These have come back and shown the reason for your cough, wheeze and shortness of breath. The scans have confirmed a diagnosis of Chronic Obstructive Pulmonary Disorder. Have you ever heard of this before? Some people will also refer to this as emphysema or chronic bronchitis (It is worth giving the patient time – they may want to respond or will indicate time for you to keep going. Pausing and giving the patient time to take in your words is an important part of communication). Would you like me to explain a little bit about what this diagnosis means? Chronic Obstructive Pulmonary disorder (or COPD for short) is a disease of the lungs which results in damage and inflammation to the airways that makes it harder for you to get air in and out which results in feeling short of breath. It is a progressive disorder /and the inflammation of the airways is not reversible (such as in asthma). COPD is common in the UK. The majority of cases are caused by long term smoking, although air pollution is also a common causative factor. Symptoms can be managed with a combination of inhalers which we will start today and I will ask the respiratory CNS to talk to you in more detail about inhaler technique. The main thing that you can do which will help with slowing the progression of disease is to stop smoking. Exercise and losing weight will also help the condition. COPD is a chronic condition, but you can experience exacerbations of your symptoms which may be prompted by viral infections for example. Exacerbations may require management with antibiotics and in extreme cases oxygen. Explain the importance of managing exacerbations by seeing her GP. Does what I have told you make sense? Do you have any questions? Depending on what you have said, you may be asked various follow up questions. These could range from treatment advice to asking about cancer to long term prognosis. Remember, you are not expected to know everything. All you are being judged on is your ability to communicate, so stay calm and answer in a polite way. Anything you don’t know you can say and demonstrate how you would go about finding the answer. Finally: I will provide you with written information on COPD. I will be referring you to the community respiratory team who will be responsible for your ongoing management of COPD and they along with your GP will be good points of contact moving forward. For the questions... Treatment = Inhaler to open the airways, offered vaccinations, pulmonary rehabilitation in some cases. Prognosis = The main thing that you can do which will help with slowing the progression (and improving symptoms/improve QOL) of disease is to stop smoking. Can use NRT. Exercise and losing weight will also help the condition. Prognosis is never the same for everyone; it depends on: disease severity/stage (test/symptoms/exacerbations), other conditions you have and lifestyle factors (e.g., smoking cessation in COPD). Cancer = Having COPD does increase your risk of lung cancer, especially if you smoke or have smoked in the past. The good news is that stopping smoking significantly lowers this risk. We also keep a close eye on symptoms and you should seek help if you feel that sometimes not right. ?Maybe should say we will provide education on symptoms to be aware of that you should inform you should seek help for e.g. from GP.

Answer 331

Provided with written information and I would want to arrange suitable follow up for her again in this clinic!!!!!!!!!!! to review these tests

Answer 332

I would attach oxygen saturation monitoring. This patient is hypoxic, with evidence of type 1 respiratory failure on their ABG, so I would immediately start 15L oxygen via a non-rebreather mask.

Answer 333

Repeat ABG to monitor response/evaluate effects of my treatment

Answer 334

Give broad spectrum IV abx (AFTER CHECKING ALLERGY STATUS) prior to getting blood cultures but do not delay abx

Answer 335

You need to keep an open mind and consider a wide range of differentials (within reason) that could cause a young female patient such as this to have an acute pleuritic chest pain and SOB. 1. Pulmonary embolism 2. Pneumothorax 3. Infection - LRTI/CAP 4. Acute asthma attack 5. Aortic dissection (unlikely) 6. Musculoskeletal chest pain (diagnosis of exclusion) 7. Cardiac e.g. pericarditis. (ACS is very unlikely in this patient but worth considering)

Answer 336

Definition: Amount of acid or base that must be added to blood to return pH to 7.40 at normal PaCO₂ (5.3 kPa / 40 mmHg). Key point: BE is calculated assuming normal CO₂, so it reflects the metabolic component of an acid-base disorder.

Answer 337

The ABG provided shows a type 1 respiratory failure with a low pO2. The patient may be hyperventilating which would explain the low pCO2. The electrolytes given and lactate are normal with the pH and acid/base balance within normal limits.

Answer 338

Bedside: full obs, ABG (to ensure improving), urine PREGNANCY test, viral (COVID/flu) swabs, ECG Bloods + VBG: I would like to send an FBC, U&Es, LFTs, CRP, coagulation screen. I would consider a D-dimer depending on their Wells Score. I would consider blood cultures and a VBG if I suspected sepsis. Imaging - I would like to perform an urgent chest x-ray. Depending on the findings of this and clinical presentation, I would consider further imaging if appropriate with a CTPA.

Answer 339

In reality in this scenario you would likely be seeking help from a senior (e.g. medical SPR) prior to any intervention and it is appropriate to mention this. Remember, the interviewers want to know that you are a safe doctor who they can rely on. Jumping straight into management may be right but may not be safe if you are not trained on how to do it. Chest drains are one of the core competencies of IMT so you can demonstrate your knowledge of what’s expected of you as a trainee by mentioning this. Following the update to Thoracic Society (BTS) 2023, the size of the pneumothorax is no longer an indication for invasive management. The decision to intervene is based on the clinical presentation of the patient. Conservative management should be considered in patients who are minimally symptomatic. However, in this scenario, the patient presents with breathlessness, chest pain and oxygen saturations of 93%, and a low Pa02. I would therefore consider intervention. The choice would be between needle aspiration or intercostal chest drain. Given that the patient is relatively young with no underlying chest disease, a needle aspiration in the first instance may be appropriate, but the type 1 respiratory failure means she is a higher risk - so a chest drain may be indicated. I would first discuss this with my seniors. The patient can be safely discharged following complete resolution of the pneumothorax, and symptoms. They must be counselled about the risk of recurrence and I would safety net by telling her to return to the hospital in the event of any further symptoms e.g., SOB or chest pain, as well as providing a supporting patient information leaflet to reinforce this advice. They should be told not to fly for seven days post resolution (confirmed on chest x-ray), and warned that scuba diving is permanently not advised, due to the risk of recurrence. She will need a repeat chest x-ray and review in OPD two to four weeks following discharge.

Answer 340

This question is likely to be seen increasingly at interviews given the current bed pressures experienced by the NHS. Admissions must be for the right reason. At the same time, the consultants interviewing you don’t want a dangerous IMT trainee on their team, so be measured in your answer. It is important to impress that you would be cautious with this decision, and explain that you would discuss with a registrar or consultant first and also safetynet the patient. As per the BTS guidelines, successful resolution of symptoms following needle aspiration in patients presenting with a primary spontaneous pneumothorax could be considered for discharge. I would safety net the patient, advising them to seek immediate medical advice if they develop any further breathlessness, chest pain or haemoptysis. I would also ensure they are appropriately counselled on not flying for at least a week following discharge, and advised on a safe return to sports and physical activity and warned that scuba diving is permanently not advised, due to the risk of recurrence. It would be important to support this advice with a patient information leaflet. I would also arrange a follow up and repeat x-ray in two to four weeks /in the Respiratory Clinic or Ambulatory Care Unit depending on the hospital policy.

Answer 341

CXR is done after aspiration/chest drain removal to confirm re-expansion and procedural success/lungs remain fully re-expanded. Follow up CXR in 2 weeks to confirm full resolution - then wait 7 days for flying

Answer 342

PSP: Conservative = same day home, short observation period and safety netting + DISCUSS WITH SENIOR Aspiration = same day home if resolves and stable for short observation period and safety netting + DISCUSS WITH SENIOR Chest drain = long admit, need to ensure lung remains fully expanded and stable/symptom free SSP: Conservative = admit Aspiration = admit at least 24 hours Chest drain = long admit, need to ensure lung remains fully expanded and stable/symptom free EVERY OPTION GETS CXR AND REVIEW IN 2-4 WEEKS

Answer 343

If its primary or secondary

Answer 344

Primary = occurs in patients without underlying lung disease Secondary = occurs in patients with known lung disease (COPD, cystic fibrosis, interstitial lung disease, etc.) Also get traumatic, iatrogenic and tension subtype which can occur with any!

Answer 345

From the history it sounds likely that this patient has had a TIA, and he has several comorbidities which would also support this. My questions would be around understanding the event. I would initially start with open questions followed by more closed questioning to help me narrow my differential diagnosis. I would make sure that I use appropriate language and try to avoid medical jargon in my questions. I would start by asking Mr Adene about the event: 1. When did the event happen (time of day) and for how long did the symptoms last 2. What symptoms occurred: weakness (and distribution), difficulty with speech, slurring of words, change in sensation (and distribution), any visual impairment incl. diplopia, impaired mobility, or balance issues 3. Have they completely resolved or any residual change? 4. Any warning symptoms e.g. aura, or events preceding the onset of symptoms. What was the patient doing before the event? Any history of trauma? 5. Was there any change in conscious level or confusion? 6. Any associated pain e.g. headache? 7. Any previous similar episodes or diagnosis of stroke or TIA? 8. Any jerking movements? Brief systems review: 1. Fevers/sweating/shaking/weight loss/skin changes 2. Chest pain/palpitations 3. SOB/cough 4. Abdominal pain/vomiting/nausea/pain when passing urine The presence of fever might suggest an underlying infection and would point me away from a TIA, or any associated aura symptoms may suggest hemiplegic migraine. I would then take a detailed past medical history. I am aware of his background of hypertension, diabetes, and COPD. I would like to know if hypertension and diabetes are well controlled. How long has he been on treatment for this? I would want to know what medications he is currently taking for the above conditions and his compliance with medications. Is there any family history of stroke? If so, were the causes of the stroke ever known – particularly if this was in a young patient? Social history: L = What is his home set-up? O = Is the patient working? S = Does he have a smoking history and is he still smoking? It would also be important to take an alcohol history and history of any substance misuse as these are risk factors for vascular events T = Does the patient drive? At the end of the history taking, I would ask the patient about their ideas, concerns and expectations and give them the opportunity to ask questions.

Answer 346

TACS – Total Anterior Circulation Stroke All 3 of: * Higher cortical dysfunction (dysphasia, neglect) * Homonymous visual field defect * Motor and/or sensory deficit of (at least 2 of) face, arm, leg PACS – Partial Anterior Circulation Stroke Any 2 of the 3 TACS features, or isolated higher cortical dysfunction LACS – Lacunar Stroke Pure motor, pure sensory, or sensorimotor, or dysarthria–clumsy hand syndrome or weakness + limb ataxia on same side (ataxic hemiparesis) POCS – Posterior Circulation Stroke Brainstem/cerebellar signs ± homonymous hemianopia (POCS may actually only have visual symptoms by themselves i.e., isolated visual symptoms)

Answer 347

This would ultimately be determined by my history taking which would point me towards appropriate investigations to arrange. With my main differential of TIA, within the clinic, I would ask for several quick baseline investigations to help me work out the potential cause of the presentation. Bedside: obs (BP), L/S BP, ECG (AND PROLONGED ECG MONITORING) and glucose Bloods: FBC, U&E, CRP, HbA1c and lipid profile Imaging: ECHO, carotid USS, MRI Head - prior to ordering these investigations, I would discuss the presentation with my consultant

Answer 348

Many conditions (sometimes known as stroke mimics) can present with similar clinical features to stroke and TIA. These account for at least 20–25% of acute presentations and include: 1. Hypoglycaemia/drug or alcohol toxicity 2. Syncope/vertigo (Menieres/labyrinthitis) 3. Trauma 4. Seizure/migraine/MS/peripheral neuropathies/spinal epidural haematoma 5. SOL (tumour or SDH) 6. Local (CNS abscess or encephalitis) or systemic (sepsis) infection 7. Hypertensive/Wernickes encephalopathy (confusion, nystagmus, ophthalmoplegia meaning limited eye movement or squint, ataxia both gait and limb) 8. Acute confusional state, dementia, vasculitis, somatoform or conversion disorder

Answer 349

I would begin by explaining to the patient what a TIA is. I would explain that a transient ischaemic attack (TIA) is often a herald of a stroke. The mainstay of treatment is about prevention of a stroke following the TIA. The patient should be advised on lifestyle measures including encouraging physical activity; advice around stopping smoking and referral to smoking cessation services if indicated; advice on a healthy diet – low salt, reduced intake of saturated fats. Advice should be given about drinking alcohol with consumption limited to less than 14 units a week. With regards to treatment, antiplatelet therapy should be started if the patient is not already on it. For TIAs, monotherapy is recommended with clopidogrel. If contraindicated, aspirin and dipyridamole combinations can be used instead. Dual therapy with aspirin plus clopidogrel or aspirin plus ticagrelor may be initiated in secondary care for some high risk patients,followed by antiplatelet monotherapy. Unless contraindicated, treatment with a high intensity statin should be initiated, such as atorvastatin 80mg OD. Cholesterol should be checked three months after initiating this to check the response to medication. The patient is likely already on anti-hypertensive medication but if not this should be considered in the clinic with a target systolic blood pressure of below 130 mmHg (unless there is severe bilateral carotid stenosis). Making sure his diabetes is well managed will also be an important part of his stroke prevention. I would make sure that I discuss all medication decisions with my clinical supervisor in the clinic.

Answer 350

Anticoagulation should be initiated in patients who present with TIA who are found to have persistent or paroxysmal atrial fibrillation. Treatment can start as soon as imaging has confirmed no presence of haemorrhage or factors that may be contraindicated – for example the presence of microhaemorrhages in cerebral amyloid angiopathy. The risk of bleeding when considering starting anticoagulation can be assessed using the ORBIT bleeding risk tool. The choice of anticoagulant is likely to be determined by local policy and I would discuss this with my clinical supervisor in the clinic.

Answer 351

Make sure that during this consultation you are speaking clearly and slowly, using appropriate language, and avoiding medical jargon. Make sure you listen to the patient and leave time for questions. Make sure that you end the consultation by saying you will provide written information on everything you have discussed. The medication is taken each day and it is important to take the medication at the same time each day to maintain its effects. If you miss a dose, you should take the medication as soon as you remember if on the same day, however, you should not take two tablets on the same day. I would explain that it has a rapid onset of action so once started the patient will be anticoagulated, compared to warfarin which requires a loading period. I would explain to them that no monitoring is required whilst on the treatment like with warfarin. However, kidney function should be checked prior to starting the medication and may need to be reviewed if there is any change in this. Direct oral anticoagulants (DOACs) are drugs which prevent harmful blood clots from forming in your blood vessels. They do this by slowing down the clotting process. They have a similar effect on thinning the blood as warfarin. There are several side effects associated with a DOAC that it is important for you to be aware of. If you experience these, you should seek medical attention: prolonged nosebleed; bleeding from cuts; blood in your stool/vomit/sputum/urine; spontaneous bruising; persistent headache. You should seek emergency medical attention if you suffer any major trauma or head injury. I would tell them about the need to inform their doctor or dentist that you are taking a DOAC well before any planned procedure. Patients should be advised to carry a patient alert card with them at all times. DOACs do not interact with alcohol. However, I would advise minimal alcohol intake when taking a DOAC because of alcohol on your balance/walking and the increased likelihood of head injury when intoxicated. I’m happy to provide you with written information on the drug so that you can read it at your own pace prior to starting the medication so that you can make an informed choice. If you choose not to take the medication the risk of further cerebrovascular events because of the atrial fibrillation will be higher - taking blood thinners reduces your risk by as much of two-thirds. Use of the DOAC tablets in patients with AF reduces the risk of a severe stroke by about 50% compared to those taking warfarin, which is the older drug.

Answer 352

People who have had a TIA must not drive for one month, but they do not need to inform the DVLA. If the patient has a further TIA, then they should stop driving for 3 months and inform the DVLA at this point.

Answer 353

Check response to the medications initiated today and to review the outcome of further investigations arranged. I have made sure to safety net and informed Mr Adene to present back to hospital should he have any recurrence of his presenting symptoms.

Answer 354

Say EVERYTHING YOU have done

Answer 355

This young patient appears to be septic and without further clinical information it is important to maintain a wide differential diagnosis in order to investigate further. 1. Pyelonephritis 2. Acute Cholecystitis 3. Ruptured Ectopic Pregnancy 4. Gastroenteritis 5. Diabetic Ketoacidosis 6. Bowel Obstruction 7. Community Acquired Pneumonia 8. Acute Pancreatitis 9. Acute Hepatitis

Answer 356

Remember to include any investigations that would form part of your initial A-E assessment. Bedside: ECG, check a pregnancy test, and also send a urine sample for microscopy & culture. I would also send COVID swabs. Bloods: full bloods including cultures, VBG (FOR LACTATE), FBC, U&E, LFT, Bone prof Coag, CRP, amylase Imaging: erect CXR, consider an ultrasound of abdomen / kidneys or transvaginal ultrasound if concerned for ectopic pregnancy. If concerned about surgical pathology such as bowel obstruction may consider a CT abdomen & pelvis under specialist guidance. My management for this patient would depend on the findings of the above but would most likely require treatment with IV antibiotics for possible pyelonephritis as per local hospital guidelines. I would make sure that I re-check the patient's allergy status before making a decision on antibiotics. I would also make sure the patient is appropriately fluid resuscitated. I would administer analgesia and antipyretics such as paracetamol initially, as well as antiemetics. I would escalate the patient early to involve my seniors and if deteriorating despite initial management would consider involving the ITU team.

Answer 357

This VBG result indicates a high lactate, measurement of which forms part of the sepsis 6. This is a non-specific marker but may indicate a significant endogenous catecholamine response to infection and be used to monitor treatment in sepsis. The VBG however does not show signs of acidosis. Early management with fluid bolus(es) and antibiotics is therefore crucial along with completing a sepsis 6 bundle.

Answer 358

This result indicates both that the patient’s condition is likely due to a urinary tract infection / pyelonephritis and also that it is being caused by a resistant organism. Antimicrobial resistance is very common in urinary tract infections and this may well require the team to change the antibiotic cover to a different choice to ensure resolution of infection. I would take advice from the microbiology team regarding the most appropriate option. The patient is also likely to require isolation due to the ESBL, so I would speak to the nurse in charge of the ward about this.

Answer 359

Antimicrobial resistance is a growing challenge worldwide. According to a recent Lancet analysis of the impact of antimicrobial resistance worldwide there were nearly 5 million global deaths related to antimicrobial resistance in 2019. This disproportionately affects developing countries where the problem is more severe and it tends to have a lower proportional impact in developed countries such as the UK. Inappropriate antibiotic prescribing is a major contributor to the problem. Antimicrobial stewardship and ensuring judicious prescribing practices for antibiotics is therefore vital for worldwide health systems as part of a range of measures to tackle the issue. Antimicrobial stewardship key principles: Right drug (choose the most appropriate drug for the pathogen and infection site), dose (ensure adequate drug levels to effectively treat the infection), route, duration (avoid unnecessarily long courses that promote resistance) and avoid unnecessary antibiotics (do not treat viral infections or colonization without infection). Start broad empirically if needed, but de-escalate once culture results are available.

Answer 360

Situation: Hello, I’m ‘x’, the IMT1 on the acute medical take. I need to hand over a 27 year old female who has presented with suspected pyelonephritis. Background: She presented with a 1 day history of flank pain and vomiting following recent treatment for a urinary tract infection by her GP. Assessment: I have performed an A-E assessment in which she was found to be febrile, tachycardic and hypotensive. I have initiated treatment with IV fluids and broad spectrum antibiotics. Her VBG revealed a raised lactate and urine cultures have demonstrated a resistant E.coli organism. Recommendation: I would greatly appreciate senior input for this patient in order to guide further investigation & management for suspected pyelonephritis. I plan to consult the microbiology team to ensure appropriate antimicrobial coverage and consider any imaging.

Answer 361

The Bamford classification splits ischaemic strokes into the following: Total Anterior Circulation Stroke (TACS) - 3/3 features of weakness, hemianopia, cognitive Partial Anterior Circulation Stroke (PACS) - ⅔ features or higher cognitive dysfunction alone Posterior Circulation Syndrome (POCS) - posterior/cerebellar signs Lacunar Syndrome (LACS) - pure motor/sensory without higher cognitive dysfunction This remains important in prognostication. The NIHSS can also be used to quantify stroke severity based on the signs elicited.

Answer 362

My main concern is acute stroke. I would carry out an A to E and put out an emergency ‘stroke call’ to ensure timely specialist review and investigations within the essential management time window. I recognise that I may be in a hospital in which the local stroke service may be at a different hospital - they would be contacted immediately. My primary concern would be an acute stroke. I would begin with an immediate A–E assessment to ensure airway protection, adequate breathing, circulation, and to identify any immediately reversible problems such as hypoglycaemia. In parallel, I would activate the emergency stroke pathway to ensure urgent specialist review and timely imaging within the treatment window. If the on-site stroke service is based at another hospital, I would contact them immediately in line with local protocol. Then describe A to E... You can mention in D that you would do the FAST screen or complete the NIHSS like when say that you would do a neurological exam to determine the presence of any focal neurological signs Also after A to E mention the whole would reassess ABC and review any investigations that were available then about history make sure you want to establish onset time //If a patient presents with acute stroke and our hospital does not have a hyperacute stroke unit, I would immediately contact the nearest stroke service to ensure timely specialist review, imaging, and potential thrombolysis or thrombectomy, in line with local protocols.

Answer 363

Whilst the most likely diagnosis in this age group assuming this is an acute onset event is an ischaemic stroke, it is important to keep a range of differentials in mind. 1. Ischaemic stroke (thrombotic & embolic) 2. Haemorrhagic stroke / intracranial bleed 3. Space occupying lesion - e.g. malignancy (primary/secondary) 4. Dissection (aortic / carotid) 5. CNS infection 6. Delirium / infection / other stroke mimics e.g. hypoglycaemia LOOK AT LIST 1-8 I MADE WHEN DOING TIA BIT

Answer 364

Remember to include any investigations that would form part of your initial A-E assessment. Split them into bedside, bloods and imaging: Bedside: I would like to obtain a 12 lead ECG, monitor BP, blood glucose, and an MSU as an infection screen Bloods: VBG, FBC, U&E, LFT, Bone profile, Coagulation screen, CRP - as “stroke bloods” and an infection screen (could also do G&S, BNP, lipid profile and HbA1c) In young person - Antiphospholipid antibodies, ANA, HIV, pregnancy, toxicology (urine) Imaging: Urgent CT head as soon as possible to rule out ICB. Consider imaging vascular systems (e.g. aorta/carotids) under specialist advice if concerns re dissection. Consider CXR as part of an infection screen. Further investigations after the acute phase are likely to include an MRI head, echocardiogram and carotid dopplers depending on initial findings.

Answer 365

I would like to escalate this patient to my seniors and local specialist stroke team if not already involved. This may require discussion and/or transfer to the local hyper acute stroke unit. The patient is likely to also require a loading dose of 300mg aspirin if not yet given. DO NOT LOAD IF GETTING THROMBOLYSED. If this patient has presented within 4.5 hours and no contraindications to thrombolysis exist, then the patient should be considered for thrombolysis under specialist guidance with alteplase. This would need to be balanced against potential bleeding risks and the patient / their next of kin counselled with regards to the treatment options. In some cases outside the initial 4.5 hour thrombolysis window mechanical thrombectomy may be appropriate after discussion with the specialist team. This may be performed up to 24 hours with certain clinical and radiological findings. I would also like to maintain normal blood glucose, consider oxygen therapy if the patient is hypoxic and consider supportive nutrition. Blood pressure control is not usually indicated in acute ischaemic stroke unless very high/encephalopathy or for thrombolysis must be lowered to <185/110mmHg. Considering escalation status may also be important in this 84 year old patient if there is a significant deterioration in his clinical state. It would also be important to communicate the diagnosis with the patient and any next of kin in order to explain to them what is going on and involve them in management decisions. I would also ensure an urgent SLT review is arranged to assess the patient’s swallow, and consider an NG tube. Moving forward, the patient will need the input of the stroke MDT, including SLT, physiotherapy and occupational therapy. Blood glucose, hydration, oxygen saturation and temperature should be maintained within normal limits. If the cholesterol is > 3.5 mmol/l patients should be commenced on a statin. Many physicians will delay treatment until after at least 48 hours due to the risk of haemorrhagic transformation. DON'T THINK IT ACTUALLY MATTERS ABOUT LEVEL. Aspirin can be given rectal if not able to be given oral.

Answer 366

Explain what AF was to patient and risk of it so need for anticoagulation (I would calculate CHADVASC before) CHA₂DS₂-VASc Score 2 in men or 3 in women = anticoagulant, 1 below means consider and 1 below means no, any patient with prior stroke or TIA automatically scores 2 points → anticoagulation is indicated unless CI. Atrial fibrillation increased the risk of ischaemic stroke by approximately 5x when compared to population controls and reducing this risk is therefore important in both paroxysmal and permanent AF. I would use the CHA₂DS₂-VASc and ORBIT scoring tools to assess the patient's stroke and bleeding risk, and if appropriate suggest long term anticoagulation. This patient would score a 2 for age and 1 for hypertension, even without the acute stroke. However, anticoagulation is not recommended in the acute phase for ischaemic stroke due to the risk of haemorrhagic transformation and therefore I would wait at least two weeks prior to starting anticoagulation in this patient, during which time aspirin 300mg OD can be continued. As well as anticoagulation, rate control with a beta blocker or calcium channel blocker should also be started, providing there are no contraindications.

Answer 367

If this is not something you are familiar with then be honest and say you would ask for senior / specialist input. You will have done well to answer the previous questions and get this far and the most important thing is to convey that you would be a safe IMT trainee. In an acute ischemic stroke, generally speaking anti-hypertensive treatment is not recommended regardless of the BP reading as per NICE unless: 1. Candidates for thrombolysis BP must be <185/110 mmHg before IV thrombolysis (alteplase) - BP is lowered carefully with IV agents if above this threshold 2. Hypertensive emergency - very high BP (SBP >220 mmHg or DBP >120 mmHg) with end-organ damage (e.g., encephalopathy, acute heart failure, aortic dissection, renal failure, MI) - requires controlled gradual IV BP reduction In a haemorrhagic stroke current guidance is to control BP more aggressively on a case-by-case basis which may require intravenous treatment (for example with labetalol or GTN infusions). This should be done under specialist guidance with the following aims as per NICE: When rapidly lowering blood pressure in people with acute intracerebral haemorrhage, aim to reach a systolic blood pressure of 140 mmHg or lower while ensuring that the magnitude drop does not exceed 60 mmHg within 1 hour of starting treatment.

Answer 368

I would in particular like to examine the patient’s knee to assess for erythema, joint effusion, any tenderness and whether this could be a septic joint as a source of infection. I would also look for any skin rashes or other joint involvements.

Answer 369

1. Septic Arthritis 2. Cellulitis / Skin infection 3. Trauma - e.g., fracture or haemarthrosis (+/- another infectious source e.g. UTI/LRTI) 4. Gout / Pseudogout 5. Other Inflammatory Arthropathy 6. DVT

Answer 370

Risk factors for it Questions about differentials

Answer 371

Remember to include any investigations that would form part of your initial A-E assessment. Split them into bedside, bloods and imaging: Bedside: I would like to obtain a joint aspirate with aseptic technique if an effusion was present (provided this is a native joint not a prosthetic replacement, due to the high risk of periprosthetic infection) in order to send samples for urgent gram stain and culture (also sensitivity and cell count + differential and crystal analysis) I would perform an ECG, and also send a urine sample for microscopy & culture as part of my infection screening. Bloods: full bloods including cultures, VBG, FBC, UE, LFT, Bone profile, Coag, CRP. Imaging: consider knee XR if any history of trauma or other imaging (such as ultrasound/MRI) under specialist guidance. Arrange a chest XR to rule out a respiratory source. My management for this patient would depend on the findings of the above but would most likely require treatment with IV antibiotics and IV fluids for a possible joint infection and involvement of the orthopaedic team. I would administer analgesia and anti-pyretics. I would consult my local hospital guidelines with regards to suitable antibiotic choice. If this was not clear, I would consult with the on-call microbiology team. I would also re-check that the patient has no allergies. I would also like to escalate to my seniors if I had any concerns regarding the patient’s management in order to provide further support. In prosthetic joint - Instead, I would involve the orthopaedic team, arrange appropriate imaging, and, if needed, have the joint aspirated in a sterile theatre or under imaging guidance.

Answer 372

This indicates septic arthritis as the most likely diagnosis which requires urgent treatment with IV antibiotics as per local hospital guidelines (e.g. IV Flucloxacillin for gram positive cover). I would also like to urgently discuss the patient with the orthopaedics team who may be required to take over the patient’s care to ensure joint aspirations and washout is performed when needed. If this patient became increasingly septic and unwell then I would also escalate to my seniors in case of the need for HDU/ITU support.

Answer 373

Gout would be associated with urate crystals which appear under polarised light microscopy as strongly negatively birefringent needle-shaped crystals. Pseudogout in contrast is caused by calcium pyrophosphate crystals which appear as positively birefringent rhomboid-shaped crystals.

Answer 374

Risk factors include: 1. Age over 80 years 2. Diabetes mellitus 3. Previous joint prosthesis 4. Rheumatoid arthritis 5. Immunosuppression / HIV infection 6. IV drug use

Answer 375

The most common microorganism responsible for septic arthritis is Staph Aureus. Other staphylococci and streptococci can also cause septic arthritis. In young sexually active patients Neisseria gonorrhoeae is also an important possible cause. Rarely, other gram negative organisms, TB, and even fungal or viral infections can cause septic arthritis. The most common route of infection is via haematogenous spread, but it can also result from direct local infectious spread or recent instrumentation.

Answer 376

That you will adjust antibiotics once cultures return

Answer 377

I would greatly appreciate senior input for this patient in order to guide further investigation & management.

Answer 378

I would initially shout for help. If there is no one I would pull the crash bell at the end of the bed. Once help arrives I would ask them to put out a cardiac arrest call and come back with the crash trolley. I would start CPR and follow the resuscitation council algorithm. Once the crash team arrive I would make sure that I hand over to someone to continue adequate chest compressions and would get the defibrillation pads on. I would make sure the attending team know that this is likely an anaphylactic reaction that has resulted in Cardiac Arrest.

Answer 379

It is important to be aware of systems in hospital for reporting serious events, especially where patients have come to harm. In this instance the examiners will want you to describe the Datix process and why this is important. Datix allow for proper investigation of serious events in hospital and looks at ways that they could have been avoided. Incidents are reported via DATIX and a RCA would be undertaken to identify what went wrong, why it happened (contributory factors) and implement system changes to prevent recurrence e.g., employ checklist

Answer 380

Acknowledge immediately Ensure patient safety Inform senior DATIX the incident Reflect and learn No blame behaviour

Answer 381

These questions have been coming up more frequently in the most recent rounds of interviews. The examiners want to see your ‘human side.’ How you communicate with patients and relatives is a big part of that. In this scenario you have to be careful as you are speaking with a patient’s relative and there will always be potential confidentiality issues. However, this is the patient’s next of kin as far as you are aware and you could start by explaining to the examiners that you would want to find out from ward staff if they have met him before. You are obviously about to deliver bad news so explaining to the examiner that you would take the husband to a quiet space and turn off your bleep is important. Then demonstrate how you would break bad news. Remember to lead with a warning shot but then be direct and explain what has happened and where his wife is now. Explain to the examiners that you understand that the husband may be angry and upset, and you would give him time to process the information. You may offer to call another family member. Make sure you finish by saying you will personally take him to see his wife on ITU. During this discussion it is important to discuss with the husband that his wife may have reacted to an antibiotic given incorrectly. Tell the husband that if he would like to speak to your registrar or consultant you can arrange this. S = P = I = K = I'm afraid I have some very serious news about your wife - then be direct (given abx allergic to and she suffered a very severe reaction then resulted in her having a cardiac arrest. She was successfully resuscitated and she is now being treated in intensive care_ E = I am so sorry that this has happened S = She is in ICU getting monitored closely, they are providing the best care possible. If you have any questions to concerns please let me know, I can answer what I can and involve others as needed.

Answer 382

We must be open and honest with patients when something goes wrong in their care and causes or has the potential to cause harm. We must explain what happened and what steps are being taken to ensure safety, apologise, short and long term implications e.g., longer stay and lastly, reassure that the incident has been reported through our internal safety systems so that learning can occur and recurrence is prevent. Healthcare professionals must also be open and honest with their colleagues, employers and relevant organisations, and take part in reviews and investigations when requested (I would also be happy to contribute to root cause analyses and attend Morbidity & Mortality meetings if asked, to help translate lessons learned into safer patient care). They must also be open and honest with their regulators, raising concerns where appropriate. They must support and encourage each other to be open and honest, and not stop someone from raising concerns. //Risk prevention is achieved through strong use of checklists (e.g., WHO Surgical Safety Checklist), guideline adherence, staff education, escalation pathways and learning from Morbidity & Mortality meetings in a no-blame culture. In my role, I support staff education to ensure guidelines and trust protocols are followed correctly, use checklists to guide safe practice and continually update my own knowledge.

Answer 383

Situation: This 68-year-old lady has had an anaphylactic reaction to penicillin and subsequent cardiac arrest. Background: She was initially admitted today because of an infective exacerbation of her COPD. She was started on an IV penicillin-based drug which she is known to be allergic to. Assessment: She was initially given IM adrenaline but continued to deteriorate. She was urgently seen by the cardiac arrest team and has had a return of spontaneous circulation. She has been intubated and taken to ITU. Recommendations: Her husband has come into hospital and I have spoken with him already about what has happened, but he would benefit from speaking with a senior clinician to further explain the situation. An incident report will need to be completed given her history of penicillin allergy was known prior to receiving it.

Answer 384

The MCA says a person is unable to make a decision if they cannot do 1 or more of these things: 1. Understand the information relevant to the decision 2. Retain that information for long enough to make the decision 3. Use or weigh up that information as part of the process of making the decision (pros and cons) 4. Communicate their decision in any way

Answer 385

To me, professionalism means consistently putting patients first — providing safe, up-to-date high-quality care, respecting confidentiality, making sure their voice is heard and always acting in their best interests. It also means acting with integrity, doing the right thing even when it feels daunting, for example being honest with patients if an error occurs. Professionalism involves being reliable, organised and committed to continual learning, following through on tasks safely, working collaboratively within the multidisciplinary team and communicating effectively with both patients and colleagues. It extends to how we treat colleagues too — supporting them, communicating respectfully, and not condoning bullying, harassment or microaggressions of any kind.

Answer 386

Probity means acting with honesty and integrity at all times — being trustworthy, upstanding, and respectful of the trust placed in you by patients, colleagues, and the public. The GMC takes dishonest or inappropriate behaviour very seriously and in their eyes, probity is central to medical professionalism. Probity is important because trust is the foundation of the doctor-patient relationship. Patients share personal and intimate information, which requires confidence that doctors will act honestly and in their best interests. Probity underpins effective teamwork - being transparent and accountable allows multidisciplinary teams to function well, which in turn improves patient safety.

Answer 387

Talk about how you assess it, that it can fluctuate and you can delay the decision if appropriate.

Answer 388

In E look for lines AND take cultures from skin and line AND remove line. Catheter needed for strict I/O. ABG shows acidotic - discuss with ITU (check for advance directive/DNACPR).

Answer 389

tonic-clonic (grand mal) tonic clonic typical absence (petit mal) atonic

Answer 390

Focal aware and impaired awareness Further to this: Motor - Jacksonian march Sensory - paraesthesia Visual - floaters/flashes Temporal - aura occurs in most patients, typically a rising epigastric sensation, also psychic or experiential phenomena, such as deja vu, less commonly hallucinations (auditory/gustatory/olfactory), seizures typically last around one minute, automatisms (e.g. lip smacking/grabbing/plucking) are common

Answer 391

Convulsions lasting more than 5 minutes or repeated convulsions without recovery of consciousness between Emergency - can cause irreversible brain injury

Answer 392

1. START TIMER A = ensure patency, gently turn onto left side to help secretions/saliva drain, protect head, head tilt/chin lift and suction if needed B = high flow oxygen if hypoxic via non-rebreathe mask and start continuous sats monitoring, if sats dropping or signs of cyanosis, immediately put out a 2222 call C = large vein IV access, monitor BP and HR (fluids if needed), VBG and bloods - treat glucose and electrolytes incl. Ca/Mg straight away (can abort and avoid unnecessary intervention) I would send urgent bloods including the big 6, toxicology, anticonvulsant levels, pregnancy and blood cultures D = glucose, lateralising signs, pupils E = trauma, rash, safe from external injury THEN CALL REGISTRAR FOR SUPPORT AND CRITICAL CARE TO INFORM + GTE RESUS TROLLEY (?2222/peri arrest/medical emergency team call) I would continuously reassess ABCDE to ensure airway protection, oxygenation, effective respirations and haemodynamic stability. Ask to review the notes and medication chart to see if there is any history of seizure or if the patient is on any anti-epileptic medication. You want to know how the patient has been over the last 24 hours and if there were any obvious precipitating factors. Tongue can fall back, vomiting or saliva - if any concern about A, fast bleep anaesthetics and support in interim as with others.

Answer 393

At 5 mins give 4mg IV Loraz over 2 mins (2mg if <40kg) - GET SENIOR HELP If not available give 10mg buccal midaz or rectal diaze Ask the nurses to prepare second line anti epileptic treatments After 5 mins give further 4mg IV Loraz Then do not delay - give IV Keppra 60mg/kg (max dose 4.5g) over 15 mins (would check hospital protocol) Anti epileptic is chosen based on comorbidities/allergies/pregnancy status/interactions If still going this is refractory status - patient gets transferred to ICU where they would be intubated/ventilated for continuous IV sedation with anaesthetic agents under continuous monitoring

Answer 394

1. Monitor resp - benzos reduce airway reflexes/post ictal confusion/reduced consciousness (if GCS<8 = intubation), also O2 requirement 2. Document + neuro input for planning maintenance long term anti epileptic if required and individual rescue plan/driving 3. Investigate cause CT/MRI (structural), bloods including alcohol, urine drug screen, LP, EEG, ECG

Answer 395

If patient has a diagnosis of epilepsy - this could be the usual presentation of her seizures, however, I think the most likely cause for this seizure is anti-epileptic non-compliance or withdrawal of medication. Hypoxaemia Drug withdrawal e.g., alcohol Overdose e.g., tricyclics Electrolyte disturbance Head injury Hypoglycaemia Infections e.g., meningitis Cerebral tumours Following stroke - less likely in younger patients

Answer 396

Bloods: FBC, U&Es, Glucose, Calcium, Magnesium, Liver enzymes, toxicology screen, anticonvulsant levels. Bedside: ECG, regular monitoring of observations including HR, BP and temperature. Imaging: urgent CT head should be considered if head injury is suspected to be the precipitant. MRI will be important once the patient is more stable to identify structural abnormalities. LP will be necessary to exclude CNS infection. I would also arrange am EEG to determine seizure type and epilepsy syndrome.

Answer 397

My main concern initially is to stabilise the patient. Most seizures terminate without intervention within two minutes. I would therefore provide supportive treatment with high flow oxygen, IV fluids and administration of IV glucose if hypoglycaemia is thought to be the cause. A seizure lasting beyond 5 minutes will need treatment. First line treatment should be with benzodiazepines. This could be rectal diazepam or IV lorazepam. This is usually enough to terminate a seizure. Because lorazepam has strong cerebral binding, a long duration of action and does not accumulate in lipid stores, it has distinct advantages over diazepam in early status epilepticus. If the seizure is continuing despite initial treatment with benzodiazepines I would contact the ITU team, as this patient may need admission for status epilepticus. I would inform my registrar as the patient will need to be started on an IV ANTI EPILEPTIC infusion/ of phenytoin. Phenytoin can cause cardiac dysrhythmias and so the patient should be attached to a cardiac monitor.

Answer 398

Status epilepticus is a single epileptic seizure lasting more than five minutes, or two or more seizures within a five minute period, without the person returning to normal in between them. Status epilepticus can be divided into both convulsive and non-convulsive. Non-convulsive status can be difficult to diagnose.

Answer 399

Refractory status is where seizures continue beyond 60 minutes after initial therapy. Refractory status should be treated by transferring the patient to ITU as they will require general anaesthesia (either propofol or thiopental). EEG monitoring should be commenced.

Answer 400

1. Respiratory failure 2. Brain injury 3. Aspiration and subsequent pneumonia 4. Cardiac arrhythmia - tachy, brady, arrest 5. Rhabdomyolysis and subsequent AKI 5. Lactic acidosis

Answer 401

Patients should be advised to stop driving and inform the DVLA and their motor insurance company of their seizure. Private car or motorcycle drivers should stop driving for six months from the date of the seizure. LGV drivers or passenger carrying vehicle drivers should not drive for five years after the date of the seizure. They should only return to driving if they have undergone recent assessment by a neurologist and there are no clinical factors or investigation results (eg, EEG, brain scan) which indicate that the risk of a further seizure is greater than 2% per annum. (N.B. – Driving rules are different for a patient with confirmed Epilepsy! More strict) Advice should be given about risks such as bathing – they should shower instead. A patient should be advised not to swim alone.

Answer 402

The responsibility for informing the DVLA rests with the patient. However, GMC guidance states that: ‘if a patient does pose a risk of serious harm to the public by continuing to drive when they are not fit to do so, the doctor should contact the DVLA or DVA, even if they do not have the patient’s consent to do so. These steps should only be taken as a last resort, if efforts to encourage the patient to act responsibly fail.’

Answer 403

Treatment is usually not recommended until after a second epileptic seizure. However it may be indicated after a first seizure if the individual has a neurological deficit, brain imaging shows a structural abnormality or the electroencephalograph (EEG) shows unequivocal epileptic activity.

Answer 404

Say about reassess ABC and adjust to investigations back Then history incl. social (for escalation purposes), collateral if needed, or notes If there is any suggestion the patient is deteriorating, or failing to respond to initial management measures, I would escalate immediately to my registrar, and critical care if necessary.

Answer 405

Remember in this instance not to overreach yourself. Do simple things first, oxygen initiation correction of obvious precipitants (eg glucose). Understanding about medications used in the treatment of seizures in hospital will be important and you should have some idea based on your experience, but you will not have to give specifics. Talking about benzodiazepines as first line is enough in this instance. The last point of the answer below is also important to emphasise to your interviewers. Make sure you show them that you are thinking about patient safety. Start the patient on high flow oxygen and start continuous saturation monitoring. Obtain IV access and monitor for signs of hypotension (which are less likely with seizures initially). Hypotension may require management with IV fluid boluses. Make sure that the patient is safe and remove obstacles from around the bedside which could cause harm. Check for obvious reversible causes and correct hypoglycaemia or metabolic derangements. For example, if hypoglycaemia were the cause of the seizure, IM glucagon can be given. If this is not suitable or not effective, glucose 10% intravenous infusion, or alternatively glucose 20% intravenous infusion should be given. Glucose 50% intravenous infusion is not recommended as it is hypertonic, thus increases the risk of extravasation injury, and is viscous, making administration difficult. If the seizure continues beyond 5 minutes, consider first line medical therapy with benzodiazepines. Whether IV access has been obtained will be helpful in making a decision on treatment. In the first instance, treatment with buccal midazolam or rectal diazepam may be more straightforward if IV access is proving difficult. Lorazepam would be the medication of choice if IV access had been obtained. As you are considering giving medications which could sedate the patient and potentially cause problems of their own, make sure that a cardiac arrest or Medical Emergency Team MET call is put out so that you can get further assistance with this patient. You are likely to need airway support and senior intervention at this point.

Answer 406

Remember as before, start simple and build up. Don’t rush to the CT scan. Show your interviewers how you work through an answer demonstrating the structure in your approach to the situation. Bedside: obs (monitoring of heart rate, blood pressure and saturations, also temp as may indicate an underlying infection) to give you real time feedback on interventions. Urine for MC+S to check for infection and base other tests on the presence of further signs. Blood cultures or CXR indicated if there is a suggestion of sepsis. Bloods: VBG in addition to a full set of blood tests (FBC, U&E, Ca, Phos, Mg, LFTs). The blood gas will quickly identify if there are any obvious things that can be corrected: sodium/potassium/glucose. It may also identify a raised lactate which is common in patients having a seizure. A raised lactate could also suggest at hypoperfusion and underlying infection. Imaging: CT Head and EEG may be useful but not acutely and can be undertaken once management of the seizure has been initiated and there has been a senior review.

Answer 407

There is a wide differential here so go through the different causes systematically. Think about common things, but then also think about what is specific to the scenario that was presented to you! That will bump your answer from a good one to a great one. The patient has been admitted to hospital following an acquired brain injury. The risk of seizures in this patient group is already increased compared to other patients. The amount of subarachnoid bleeding is a big risk factor for development of seizures post insult. The seizure threshold is likely to be lower and therefore common stressors occurring in hospital patients may easily tip this patient into seizure. The most common cause would be infection, most likely chest given the history presented to us. However, the patient has had multiple chest infections and not had issues with seizures in the past, that we are aware of. It would be important to rule out infection as a cause. Hypoglycaemia is another common cause of seizure in hospital, and this would be important to exclude early. If the patient is diabetic and on insulin this would be even more likely the cause. Electrolyte disturbances are also common in hospital patients. This patient has had a stroke and we should consider the possibility that they may have issues with feeding and thus could be dehydrated leading to electrolyte disturbances resulting in seizure. Other triggers for the seizure could be the initiation of new medications. Some medications will lower the seizure threshold further and checking the drug chart would be important to review this. Finally, it would be important to consider further acute intracranial pathology including the possibility of a further bleed or ischaemic insult (for example due to vasospasm) in this patient group.

Answer 408

Its worth remembering that at this point in the interview if you have gotten this far in the time provided you have done very well! You have managed the patient as appropriately and safely as you can. If help has not arrived, now is the time to call for it! At this point, put out a resuscitation call or MET call if senior help has not arrived. The drop in saturations on 100% oxygen would suggest that the patient may be tiring, and they have not responded to medication thus far. They may require IV medication and second line therapies may be required including loading of levetiracetam and phenytoin. This patient is likely going to need airway support and you would need the ITU SpRs assistance for managing this. Once the seizure has been stopped this patient will likely need close monitoring either on ITU or a high dependency unit as further seizures are likely. A repeat full neurological examination will be needed and further investigations as previously described including a CT head will be needed.

Answer 409

I would first start by asking about the falls. This would initially be with open questions – for example, how would the patient describe the fall? Any recent falls or near-falls? A general structure would then be to ask about “before, during and after” the fall. I would use specific questions for this: BEFORE: 1. Were there any proceeding symptoms? For example, lightheadedness/dizziness/feeling faint, palpitations, chest pain, shortness of breath OR any neurological symptoms (weakness, numbness, vision changes, slurred speech) which could suggest stroke/TIA? 2. What was she doing in the moments prior to the fall? For example – standing up, walking, climbing stairs. DURING: 3. How did you fall? (direction, position, stumbling vs collapse) - helps distinguish mechanical trip vs sudden loss of consciousness 4. Did you lose consciousness or retain consciousness and recall the whole event? 5. Did you hit your head? 6. Any unusual movements or incontinence of stool/urine? (jerking, stiffening) 7. Did anyone witness the fall? AFTER: 8. Did she suffer any injuries/any pains (fractures, bruises, lacerations)? 9. Any symptoms after it and how are you feeling now ? For example headache, visual disturbance, neurological deficits, confusion or drowsiness? Or dizzy/nauseated? 10. Were you able to get up from the floor immediately? Or require assistance? Any prior similar episodes? Are all your falls the same? THEN Next, I would ask for a detailed past medical history and medication list. I would be sure to ask specifically about antihypertensive medication and whether anything new had been started in the days/weeks prior to the fall. I would like to know specifically about her diabetic control and whether she uses insulin. I would also explore her social history. Where does she live, accommodation type, who with, any care in place? What is her mobility like at baseline – any aids or independent? I would also ask about alcohol use at this point. Finally, to complete my questioning I would undertake a quick systems review - a brief screen for symptoms in other body systems which may or may not be relevant to the primary presenting complaint. A systemic enquiry may also identify symptoms that the patient has forgotten to mention in the presenting complaint. To complete my history, I would conduct a quick cognitive screening assessment.

Answer 410

Could indicate arrhythmia or dehydration (cardio)

Answer 411

Bedside: L/S BP (postural drop), ECG to make sure there is no obvious cardiac cause of the fall, blood glucose would be important given her history of diabetes. Bloods: FBC to rule out anaemia, U&E, CRP (infection can be a cause of falls), a bone profile and vitamin D (to rule out hypercalcaemia in addition to about bone protection in the elderly who are falling), LFTs if there is any history of high alcohol intake. Imaging: if concern that hit head. Based on my initial investigations I may consider ordering a prolonged ECG (24-72 hours) and serial blood pressure monitoring. If there is a suggestion of any vestibular cause of the fall I would perform the Dix-Hallpike test or ask one of my senior colleagues to assist with this.

Answer 412

This would be based on my history, examination and investigation conducted in clinic. If there is a history of head injury associated with loss of consciousness or change in cognitive function, I would consider a CT head. If the patient is on any anticoagulant medication this would also change my thinking. I would discuss this request with my senior colleagues before ordering it.

Answer 413

Yes I would order an urgent CT head that day to be performed whilst Mrs Redbridge is in clinic. I would be concerned about her having a subdural haematoma or intracranial bleed which could have occurred when she hit her head when falling with an increased risk due to her use of a direct-acting oral anticoagulant. She would meet the NICE criteria for arranging a CT head given her change in cognitive function.

Answer 414

I would start by making sure that we are in a quiet room where we will not be disturbed. I would ask the patient and daughter if there is anyone else that needs to be present. I would start by explaining that the CT head scan has shown a cause for the worsening confusion. (This is the warning shot). I would then explain that the scan has shown a bleed around the outside of her brain. Explain that the blood is likely exerting some pressure on the brain which is why Mrs Redbridge is more confused. The bleeding is likely secondary to her use of rivaroxaban which increases her risk of haematoma formation after head injury. I would explain that the scans have been reviewed by my surgical colleagues who do not think that surgery is required. Explain that Mrs Redbridge will be admitted for a short period to monitor and assess the impact of the bleed before being discharged home. I would then make sure that the patient and family had time to ask questions.

Answer 415

The surgeons have reviewed the scans. Decisions on surgery are made based on the presentation of the patient (is the bleed causing a threat to life), the success of surgery balanced against the risks. In this case, the risks of surgery would be high. The subdural haematoma will be resorbed slowly. We are monitoring to make sure that Mrs Redbridge remains stable.

Answer 416

Yes, we will stop the rivaroxaban today. This will reduce the likelihood of the bleed getting any bigger. A decision on restarting the rivaroxaban will be made with the senior clinician based on the risks and benefits of continuing to take it.

Answer 417

Your mother will be assessed by our inpatient therapy team (PT/OT/nurse/SLT/social work) during the admission to assess her current level of mobility and self-care. Based on this we make recommendations about her safety to go home on her own. She may need a reablement package of care for example depending on the outcome of the assessment.

Answer 418

MDT I would recommend that she is seen by the acute medical therapy team to assess her ongoing falls risks and put a plan in place to help her once she is at home.

Answer 419

Document everything in patients notes (or keep a personal record for non patient related things).

Answer 420

I am concerned that this patient may be septic. I would therefore ensure a sepsis six is completed. This includes checking a lactate, and taking blood cultures. I would also ensure urine output is monitored (with a catheter if necessary), and that fluids, IV antibiotics and oxygen are administered. To complete my investigations, I would begin with blood tests: FBC (for white cell count and differential, as well as anaemia), U&E (for kidney injury and baseline for antibiotics), LFTs, CRP and blood cultures (as previously mentioned). Although the patient is on contraception, it would also be important to do a pregnancy test, especially as she is likely to require radiological imaging. Bedside: ABG (to assess oxygenation + ventilation and to obtain a lactate), ECG (as tachycardic), sputum sample (if productive cough), urine dip for pneumococcal or legionella antigen. Imaging: CXR (to look for consolidation, pleural effusion or other abnormalities given her chest symptoms).

Answer 421

The bloods demonstrated a high white cell count which is predominantly a neutrophilia, supporting the diagnosis of a bacterial infection such as community acquired pneumonia. Both platelets and CRP are elevated, also indicating an inflammatory response. The elevated urea suggests a catabolic stress response and reduced renal perfusion secondary to hypotension. The D-dimer is elevated, which can suggest DVT or PE however can be elevated for several reasons and may be in keeping with pneumonia. CXR is again supportive of pneumonia.

Answer 422

A D-dimer has low specificity (around 45%) and may be raised in many conditions other than PE, including infection, inflammatory disease, malignancy, pregnancy, peripheral vascular disease, and increasing age; therefore, it may not be helpful initially. However, it can be used in conjunction with the modified Wells’ score (for PE or DVT). A patient can be scored and if they are low risk a (negative) D-dimer may be used to rule out a pulmonary embolism. Patients at higher risk of PE should not have a D-dimer and a CTPA should be performed as the first line investigation. In this case I would therefore consider performing a CTPA to rule out a pulmonary embolism.

Answer 423

The results are supportive of community acquired pneumonia so I would continue to treat this, and continue fluid resuscitation. The elevated D-dimer is non-specific and may reflect infection, but given the clinical context I would discuss with my registrar whether further imaging such as CTPA is required to exclude PE.

Answer 424

If a PE is 'likely' (more than 4 points) - arrange an immediate computed tomography pulmonary angiogram (CTPA) If a PE is 'unlikely' (4 points or less) - arranged a D-dimer test, if positive arrange an immediate computed tomography pulmonary angiogram (CTPA)

Answer 425

The most likely diagnosis here is sepsis, secondary to community acquired pneumonia. /Given the patient's age/ I would also want to rule out atypical pneumonias, and would consider this when taking a history (extrapulmonary symptoms, dry cough, headache). Given the patient's history and presentation with haemoptysis, I would want to rule out a pulmonary embolism, although this is less likely then pneumonia overall.

Answer 426

I would inform my registrar and ask for their urgent input, whilst also contacting ITU to ask for their review and input. It may be that the patient would require admission to ITU. Thrombolysis would need to be considered if there are any signs of haemodynamic instability.

Answer 427

Intensive care would be able to provide a higher level of care with intensive nursing and closer monitoring and management from clinicians. In the acute phase ITU may be able to provide an arterial line to facilitate frequent arterial gas sampling for oxygenation + ventilation and lactate monitoring, and venous lines for intensive fluid replacement and monitoring. If required they would be able to facilitate use of vasopressors or intubation and ventilation. //Intensive care would provide advanced monitoring, titratable vasoactive and inotropic support, and multi-organ support including respiratory, renal, and cardiovascular management.

Answer 428

This patient is unwell, demonstrated by their physiology and investigation results. The risk of mortality from community acquired pneumonia can be estimated using a scoring criteria- CURB-65. This patient is not confused but scores a point for urea, respiratory rate, and blood pressure therefore scores 3, this indicates a severe illness with elevated risk of mortality (more than 10% mortality risk). This quick score indicates she needs admission and potentially higher level care.

Answer 429

I would first ensure privacy if I could by drawing curtains. I would introduce myself and my role. I would ask the patient if there was anyone else she wanted to be there such as family over friends. I would ask her what she understood so far of what had been happening in hospital and what we were treating her for. I would then explain in simple language that we were treating her for a bad chest infection and that she needs to stay in hospital, and possibly go to ITU for more intensive care. I would explain that she should start to feel better in the coming days. We would be treating her with antibiotics and fluids through the vein to help treat the infection. I would ask if she wanted me to call anyone to inform them. I would ask her to explain this back to me and ask if she had any questions. I would ensure she felt comfortable to ask questions of staff at any point during the admission.

Answer 430

Attend straight away. A to E. Simultaneously I would sent bloods: TFTs (TSH, free T4, free T3), U&Es, LFTs, bone profile and Mg, FBC, CRP, a random cortisol and a venous blood gas (including lactate and glucose). Given her history of dysuria and suspected urinary sepsis, I would also send blood cultures and a midstream urine sample for culture. Lastly, I would rapidly re-measure her core temperature and look for features of thyroid storm—fever, marked tachycardia often with atrial fibrillation, agitation or confusion—and ask the nurse to contact the on-call endocrinologist and HDU team without delay. Also remember to say that you are worried about neutropenic sepsis: Fever or sore throat in these patients = medical emergency (neutropenic sepsis)

Answer 431

Bedside: continuous ECG (to guide rate control in atrial fibrillation), non‐invasive blood pressure every 5 minutes, SpO₂, core temperature and hourly urine output via a catheter to assess perfusion and response to fluids, midstream urine cultures (identify and treat urinary sepsis precipitant). Bloods: TSH, free T4, free T3 (severity and treatment response); U&Es + Mg + Ca and LFTs (electrolyte, metabolic and hepatic status); FBC + CRP (infection); random cortisol (adrenal reserve); venous blood gas with lactate and glucose (tissue perfusion, exclude hypoglycaemia). Blood cultures. Imaging & special tests: CXR (pneumonia or pulmonary oedema)

Answer 432

I would use the Burch–Wartofsky Point Scale, looking at key parameters: degree of fever, presence of CNS effects (agitation, delirium), cardiovascular dysfunction (heart rate, atrial fibrillation, signs of heart failure), gastrointestinal-hepatic involvement (nausea, diarrhoea, elevated LFTs) and identification of a precipitant (e.g. infection). A total score above 45 indicates thyroid storm, while 25–45 suggests an impending storm that requires the same aggressive management.

Answer 433

Once thyroid storm is confirmed, I would call for senior support—alert the on-call endocrine consultant, the ward registrar and arrange HDU/ICU transfer—so that I’m managing this with appropriate senior oversight. First, I would optimise general measures: assess her volume status and give cautious crystalloid boluses if dehydrated (or limit fluids if there are signs of overload), administer paracetamol and request cooling measures for fever control, and ensure empiric broad-spectrum antibiotics are running for suspected urinary sepsis. Once the basics are in hand, I would start specific thyroid storm therapy: propranolol (80 mg PO TDS, or 2 mg IV over ten minutes if she cannot swallow) to control her rate and inhibit peripheral T4 to T3 conversion; propylthiouracil 200 mg TDS by the most reliable route to block new hormone synthesis and conversion; exactly one hour later, Lugol’s iodine (five drops QDS) to prevent release of stored hormone (thyroid stops releasing stored T3 and T4 for a short period (~24 hours)); and hydrocortisone 200 mg IV followed by prednisolone 20 mg TDS to further reduce conversion and support adrenal reserves. Throughout this, I would liaise closely with the endocrine team for dose adjustments and ask the nursing staff to continue close monitoring of her vitals, urine output and cooling

Answer 434

I would look for and treat her urinary tract infection (sending cultures and starting targeted antibiotics) while correcting dehydration from any vomiting or diarrhoea. I’d ask about recent iodine exposure (for example, contrast studies), any intercurrent illnesses or surgeries and ensure she restarts her antithyroid medication as soon as she can safely swallow.

Answer 435

I would counsel her to report any fever, sore throat or mouth ulcers immediately, as these could signal agranulocytosis from PTU or carbimazole. If her white cell count fell below 1 × 10⁹/L or she developed neutropenic sepsis, I would stop the thionamide at once, isolate her, start broad-spectrum antibiotics and arrange urgent haematology review. I’d also monitor her liver enzymes twice weekly during the acute phase, since hepatotoxicity is a recognised complication; if transaminases rose above three times the upper limit of normal or she developed jaundice, I’d discontinue PTU and consider switching to carbimazole under specialist guidance.

Answer 436

Thyroid storm–related complications: 1. High-output cardiac failure, arrhythmias (AF, atrial flutter, ventricular ectopy) 2. Pulmonary oedema 3. Delirium, seizures or coma 4. Severe hyperthermia with rhabdomyolysis Medication-related complications: 1. Agranulocytosis (fever, sore throat) from thionamides (PTU and carbimazole) 2. Hepatotoxicity (transaminase rise, cholestatic picture) from PTU or carbimazole 3. Hypoglycaemia or adrenal insufficiency during steroid taper 4. Beta-blocker induced hypotension or bronchospasm

Answer 437

Once her thyroid function is stable, I would explain the three main options: continued antithyroid medication for 12–18 months with periodic TFT checks (noting relapse rates of 50 percent and small proportion can become hypothyroid requiring levothyroxine), radioactive iodine ablation to make her hypothyroid and start lifelong thyroxine replacement, or total thyroidectomy; particularly if she has a large goitre or ophthalmopathy. I’d involve the endocrine surgeon and radiology teams to outline risks and benefits, ensure she understands the need for levothyroxine if she becomes hypothyroid and arrange a multidisciplinary review in the outpatient setting.

Answer 438

Purpose: Protects and empowers adults who may lack capacity to make decisions for themselves. Provides a legal framework for assessing capacity and making decisions in the person’s best interests. Key principles (the 5 statutory principles): Presume capacity unless proven otherwise Support people to make decisions where possible People have the right to make unwise decisions Best-interests decisions when a person lacks capacity Least restrictive option should be chosen LPA has to be for health Safeguards: IMCA if no family/friends are available for serious decisions DoLS if the person is deprived of liberty Documentation of capacity assessment and best-interests decisions

Answer 439

Mental capacity means being able to make your own decisions. It is specific to the decision and time of assessment. When considering capacity, we start from the presumption that every adult has capacity. Age, diagnosis, behaviour, limits on communication (e.g stroke), beliefs or a patient making, what you believe, is an unwise decision, are not reasons to assume a patient lacks capacity. A patient who lacks capacity may have capacity again in the future or for a different decision and so must be assessed for each decision being made. Capacity is assessed and demonstrated if they: understand information relevant to the decision in question retain that information use the information to make their decision communicate a decision Patients should be given all reasonable help and time to demonstrate that they have capacity.

Answer 440

Volume status, distended bladder? Baseline creatinine? Use to stage Pre renal - fluids, hold DAMN drugs and adjust drug doses, consider catheter Intra-renal - renal input, urine dip, urine electrolytes and ACR, active urine sediment on urine dip ± microscopy, stop offending drugs, consider steroids, connective tissue disease screen/myeloma/vasculitis, renal screen Post-renal - bladder scan, catheter, urology input, US urinary tract

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