General

Question 1

INR

Answer 1

The international normalised ratio (INR) is a laboratory measurement of how long it takes blood to form a clot. It is used to determine the effects of oral anticoagulants on the clotting system.

Question 2

Oxygen saturation

Answer 2

Oxygen saturation is the fraction of oxygen-saturated hemoglobin relative to total hemoglobin (unsaturated + saturated) in the blood. The human body requires and regulates a very precise and specific balance of oxygen in the blood. Normal arterial blood oxygen saturation levels in humans are 95–100 percent.

Question 3

Sinus tachycardia

Answer 3

Sinus tachycardia (also colloquially known as sinus tach or sinus tachy) is an elevated sinus rhythm characterized by an increase in the rate of electrical impulses arising from the sinoatrial node. In adults, sinus tachycardia is defined as a heart rate greater than 100 beats/min (bpm).

Question 4

Clinical diaagnosis

Answer 4

clinical diagnosis (countable and uncountable, plural clinical diagnoses) The estimated identification of the disease underlying a patient’s complaints based merely on signs, symptoms and medical history of the patient rather than on laboratory examination or medical imaging

Question 5

Parenteral vs enteral

Answer 5

utrition can be provided either through a feeding tube (enteral nutrition) or, when the digestive tract cannot be used, through an intravenous tube called a catheter that is inserted directly into the veins (parenteral nutrition).

Question 6

sentinel lymph node biopsy

Answer 6

A sentinel lymph node is defined as the first lymph node to which cancer cells are most likely to spread from a primary tumor. Sometimes, there can be more than one sentinel lymph node.
Sentinel node biopsy is a surgical procedure used to determine whether cancer has spread beyond a primary tumor into your lymphatic system. It’s used most commonly in evaluating breast cancer and melanoma. The sentinel nodes are the first few lymph nodes into which a tumor drains.

Question 7

Invasive carcinoma vs metastatic

Answer 7

• Invasive: cancer cells moving to local or nearby tissue.
• Metastatic: cells that have broken free from the primary site and migrated to other parts of the body. This isn’t just invasive cancer, it is also metastatic.

• For cancer, invasion is the direct extension and penetration by cancer cells into neighboring tissues. It is generally distinguished from metastasis, which is the spread of cancer cells through the circulatory system or the lymphatic system to more distant

Question 8

Risk factors of laryngeal cancer

Answer 8

• Tobacco and alcohol use
• Poor nutrition: vitamin deficiencies. It has been suggested that eating fewer fried foods and processed foods and eating more plan-based foods might help reduce laryngeal cancer risk.
• Human papillomavirus (HPV): infection seems to be a factor in some throat cancers eg. tonsils, but it is still a rare factor for laryngeal cancer.
• Genetic syndromes: dyskeratosis congenita: this can cause aplastic anemia, skin rashes and abnormala fingernails and toenails. People with this genetic syndrome and inherited gene are at a high risk of developing cancer of the mouth and throat when they are young.
• Workplace exposure: exposure to paint fumes, chemicals, petroleum, plastics and textile industries can increase risk of laryngeal and hypopharyngeal cancers. Some studies are debating whethere asbestos (linked to lung cancer) is also a risk factor for laryngeal cancer.
• Gender: x4 more common in men than women (because men smoke and drink more?)
• Age: above 65 years, more likely to find this cancer.
• Race: more common amongst African Americans and whites, than Asian and latinos.
• Gatroesophageal reflux disease: still being studied on whether it is linked to laryngeal cancer.
• Low immunity: increased risk if you have HIV or AIDS, are taking medication to suppress your immune system adter an organ transplant.

Question 9

1. Difference in appearance between bone/cartilage/soft tissue on CT

Answer 9

Firstly- what is a CT scan? A computed tomography scan is a non-invasive diagnostic procedure used to create computerized axial images of the body. X-rays are fired at the body in a circle and the computer collects this information and displays it as a 2-d image on the monitor. It is useful as it shows detailed pictures of the bones, organs, muscles and fat.
On the CT scans, the bones appear white as the calcium within blocks the photons from the x-ray, whereas calcium actually doesn’t emit a signal in MRI scans, appearing black.

Cartilage is simply shown as black on the X-rays, as when osteoarthritis is shown on CT scans, it is shown as a reduction in gaps between the bones. It is also likely to be shown as completely black, as there is no calcium, or any other types of molecules – which can block out the X-rays

Soft tissue mostly appears to be grey on CT scans,

Question 10

2. Well differentiated vs poorly differentiated carcinomas

Answer 10

Well-differentiated cancer cells look and behave more like the normal cells in the tissue they started to grow in. Tumours that have well-differentiated cancer cells tend to be less aggressive. This means they tend to grow and spread slowly. Well-differentiated cancers are low grade.

Undifferentiated or poorly differentiated cancer cells look and behave very differently from normal cells in the tissue they started to grow in. These cells look immature, undeveloped or aggressive and aren’t organized in the same pattern as normal cells. Tumours that are undifferentiated or poorly differentiated tend to be more aggressive. They tend to grow more quickly, spread more often and have a worse prognosis than tumours with well-differentiated cancer cells. Cancers that are undifferentiated or poorly differentiated are high grade.

Question 11

What type of drug increases risk of peptic gastric/duodenal ulcers?

Answer 11

NSAIDS

Question 12

What is the most likely sign of peritonitis? 
Swelling 
Involuntary guarding? 
Pain on rebound percussion 
pain on percussion of right iliac fossa

Answer 12

Involuntary guarding.
Pain on rebound percussion also however suggests peritonitis. So does pain on percussion of right iliac fossa, maybe something you see on acute appendicitis. So it is better you go for percussion rather than rebound.

Question 13

Upper abdomen pain

Answer 13

Where you will feel pain as a result of pathology in structures of the foregut. Eg, lower oesophagus to ligament of trites. Structures in this distribution will give pain in upper third of abdomen.

Question 14

Midgut pain

Answer 14

Structures within ligament of trites to the ilio-coecal valve will characteristically give pain across the middle of the abdomen.

Question 15

Hindgut

Answer 15

Structures associated with the hindgut: iliocoecal valve to rectum will characteristically cause pain in lower part of abdomen.

Question 16

Generalised abdominal pain indicates

Answer 16

Peritonitis –> symptom of something.
Perforation, leads to peritonitis
Acute pancreatitis.
Diabetes

Question 17

Central AP

Answer 17

Early appendicitis 
Small bowel obstruction 
AAcute gastritis 
Acute pancreaatitis 
Ruptured AAA. 
Mesenteric thrombosis

Question 18

Most important investigation in abdominal pain

Answer 18

ABG–> if raised lactate and deragnged base excess, that person is sick.

Question 19

nitrates in urine are indicative of what?

Answer 19

infection

Question 20

High amylase indicitive of what

Answer 20

pancreatitis

Question 21

Rhinorrhea

Answer 21

The production of mucoid, watery, nasal discharge.

Question 22

Cardiac output at rest

Answer 22

4-6L

70bpm* 70ml = litres per min

Question 23

Preload

Answer 23

Preload is the amount of blood entering ventricle during diastole.
Stretching of left ventricle on filling.
Stretching of the heart at rest, increases stroke volume due to Starling’s law.
Increase preload increases stroke volume.

Question 24

Afterload

Answer 24

Afterload is the resistance the ventricles must overcome to circulate the blood. Things that increase afterload increase resistance: hypertension, atherosclerosis, and vasoconstriction.
Afterload is resistance to ejection.

Afterload occurs during systole, when ventricles are contracting, ejecting blood out of aorta and into pulmonary trunk.

Increased afterload decreases/ opposes stroke volume.

Afterload opposes ejection, reduces stroke volume due to Laplaces law.

Question 25

Starling's law

Answer 25

Greater stretch of ventricle in diastole (blood entering). …then greater energy of contraction. …and greater stroke volume achieved in systole • The ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return is called the Frank-Starling mechanism • The Frank-Starling Law states that the stroke volume of the left ventricle will increase as the left ventricular volume increases due to the myocyte stretch causing a more forceful systolic contraction. • increased filling pressure stretches the heart and increases its force of contraction. Increasing the force of contraction expels more blood from the left ventricle, so that cardiac output increases when the preload increases. • The normal ventricle, therefore, is capable of increasing its stroke volume to match physiological increases in venous return

Question 26

Molecular basis of Starling's law

Answer 26

``` Un-stretched fibre Overlapping actin/myosin - Mechanical inference - Less cross-bridge formation available for contraction ``` ``` Stretched fibre Less overlapping actin/myosin Less mechanical inference - Potential for more cross-bridge formation Increased sensitivity to Ca2+ ions ```

Question 27

Preload roles and effects of Starling's law.

Answer 27

Balances outputs of the right ventricle and left ventricle – important. Responsible for fall in CO during a drop in blood volume or vasodilation (e.g. haemorrhage, sepsis). Restores CO in response to intravenous fluid transfusions. Responsible for fall in CO during orthostasis (standing for a long time) leading to postural hypotension & dizziness as blood pools in legs.. Contributes to increased SV & CO during upright exercise.

Question 28

Laplace's law

Answer 28

Opposes Starling’s law at rest Increased preload gives increased stretch of chamber (Starling’s law) This increases chamber radius (decreases curvature) – increase afterload In a healthy heart, Starling’s Law overcomes Laplace’s – so good ejection. Facilitates ejection during contraction Contraction reduces chamber radius so less afterload in ‘emptying’ chamber. This aids expulsion and increases stroke volume. Contributes to a failing heart at rest and during contraction In a failing heart the chambers are often dilated - so increased afterload opposing ejection. Laplace’s Law is good ejection with small radius, bad with large radius.

Question 29

Decompensatory mechanisms

Answer 29

If compensatory mechanisms are unable to sufficiently restore arterial pressure, irreversible shock can occur. Circulatory decompensation is defined as failure of neurohumoral compensatory mechanisms and resuscitation to maintain a critical level of arterial pressure sufficient to perfuse vital organs, which leads to irreversible shock and death. This is observed when prolonged shock leads to resuscitation failure even when blood volume is completely restored by blood transfusions. Cardiogenic shock Impaired coronary blood flow resulting from hypotension causes myocardial hypoxia and acidosis, which depress cardiac function and cause arrhythmias Sympathetic escape Accumulation of tissue metabolic vasodilator substances impairs sympathetic-mediated vasoconstriction, which leads to loss of vascular tone, progressive hypotension and organ hypoperfusion Loss of precapillary vascular tone increases capillary hydrostatic pressure and capillary fluid filtration, which reduces plasma volume Cerebral ischemia/hypoxia Loss of sympathetic outflow from a hypoxic medulla leads to vasodilation, which further reduces arterial pressure and cerebral perfusion Metabolic acidosis Acidosis depresses cardiac muscle and vascular smooth muscle contraction, which further decreases arterial pressure Rheological factors Reduced microcirculatory flow causes blood viscosity within tissues to increase, which further reduces perfusion Plugging of the microcirculation by leukocytes and platelets, and intravascular coagulation reduce organ perfusion Systemic inflammatory response Endotoxins released into systemic circulation from the ischemic gastrointestinal tract lead to cytokine production, and enhanced formation of nitric oxide and oxygen free radicals, which cause vasodilation, cardiac depression, and organ injury

Question 30

How to write micro grams in prescription document

Answer 30

Don’t use Greek letters or abbreviate as can be marked down As it can be confusing and lead to wrong dosages which is very dangerous. Write micrograms or microg so it is clear.

Question 31

Dyspnea

Answer 31

is the medical term for shortness of breath, sometimes described as “air hunger.

Question 32

AAA

Answer 32

Abdominal Aortic Aneurysm Focal dilatation of the abdominal aorta. Two-thirds of patients with ruptured AAAs die before reaching hospital. Of those who make it to emergency surgery, half die. Ultrasound used for diagnosis and screening. CT used for suspected leak, but this must not delay emergency surgery. Screening for AAA is offered to all men when they turn 65. It is a quick ultrasound scan to measure the abdominal aorta, done in the community. If the test is negative (< 3 cm), there will be no further recall scans, unlike other screening programmes If the test is positive (> 3 cm), further action depends on the diameter of the aneurysm: 3.0 - 4.4 cm = repeat in 1 year; 4.5 - 5.4 cm = repeat in 3 months; > 5.5 cm = immediate referral to vascular surgeons to consider elective repair

Question 33

AAA risk factor and patient presentation

Answer 33

Risk factors • Risk factors include • Smoking (strongest risk factor) • Hypertension • Older age (peak incidence at age 70 to 80) • Family history (in 15 to 25%) • Race (more common in whites than in blacks) • Male sex • Patient presentation • DEPENDS! • Often incidental findings • Clinical skills – sometimes able to see Pulsative and expansile mass on abdominal examinations • Bruising around the umbilicus and flanks (cullens sign & grey turners) – potential slow leaking aneurysm (look these up)

Question 34

BCG vaccine

Answer 34

BCG-vaccination Children with a negative TST and continued high-risk exposure (e.g., drug-resistant TB) Health-care workers on an individual basis Notification: Any health care worker that knows of a case of suspected or confirmed tuberculosis in a patient should notify the TB program in their department within 24 hours Postexposure management: after recent contact with a person who has active TB Perform PPD test or IGRAs and a chest x-ray Positive results and/or clinical symptoms of active TB → sputum stain and culture Sputum stain and/or culture positive: start treatment for active TB (see ”Treatment of active disease” above) Sputum stain and/or culture negative but interferon-γ and/or PPD test positive: start treatment for LTBI (see “Treatment of LTBI” above) If tests are negative in infants, children, and HIV-positive or other severely immunocompromised patients → LTBI treatment

Question 35

Atheroma, atherosclerosis, aneurysm

Answer 35

Atheroma: hard plaque formed by build up and oxidation of cholesterol. It is found in atherosclerosis. Atherosclerosis: hardening of the arterial wall. Aneurysm: dilation of arterial wall, not as a result of atherosclerosis however the two may co-exist.

Question 36

Airway

Answer 36

A compromised airway is the most time critical problem, with any small reduction in airway radius significantly affecting air flow Remember that halving airway radius leads to a 16 fold increase in resistance (Poiseuille’s law) Examining the oropharynx will afford the opportunity to suction liquid material which may otherwise descend into the airway lungs and exacerbate existing problems. Use of the ‘jaw thrust’ to protrude the jaw and open the airway is more appropriate for these patients in whom a simple manoeuvre is required. Airway adjuncts should be used as and when necessary Nasopharyngeal airways are a useful place to start, as they are relatively well tolerated and can be placed in patients that are biting down, such as those during a seizure. Oropharyngeal airways are only tolerated well in patients who are obtunded and no longer have a functional gag reflex. Supraglottic airway devices are relatively simple to insert with training and can provide more reliable, temporary support in the patient with airway compromise.

Question 37

Breathing

Answer 37

Oxygen therapy: Put on 15 litres per minute via a non-rebreathe mask if in any doubt and titrate down oxygen levels from there. Do not be tempted to leave a patient in a hypoxic state, prior to oxygen, in order to get an arterial blood gas on air. An arterial blood gas (ABG) sample is key to appreciating the clinical state and subsequent efficacy of treatment in patients with respiratory compromise. It is worth being aware of the risks of hypercapnia in patients with COPD but these patients are a subcohort of COPD patients and oxygenation must be prioritised in the immediate phase. A chest radiograph (CXR) may be essential in your initial diagnosis for a patient If you feel you patient may be too unwell to be transferred to the X- ray department, then ask for a portable radiograph Any wheeze can be treated with nebulised salbutamol 5mg and ipratropium 500micrograms, back to back if needed. Remember that wheeze can be heart failure related among other conditions so consider the patient’s fluid status. Treat any suspected infection post-cultures being taken, yet you should not delay administration if any significant delay to cultures is anticipated. You need to consider the volume status of this patient as well as their electrolyte status and renal function before diuresis. However if there are no contraindications, IV furosemide 40mg can be a good place to start or if it is severe pulmonary oedema, a glyceryl trinitrate infusion can be started. You must be sure to recheck your patient to avoid adverse effects like hypotension and renal failure. A patient who is this unwell should be discussed with your team and potentially the medical registrar on call.If you think your patient is not breathing effectively or at all but still has a pulse, then this is a respiratory arrest and immediate help in the form of a cardiac arrest team should be sought while you and a colleague use a bag-valve-mask to oxygenate the patient.

Question 38

Circulation

Answer 38

Shock means that organs are hypoperfused and that means they will begin to fail without aggressive intervention. It is likely that hypovolaemia and sepsis will be responsible for the majority of the shock you deal with as an inpatient, but do remember that other types of shock are possible (the management for sepsis, hypovolaemia, and anaphylaxis can be found elsewhere on the site) If the patient is deteriorating, ensure early access and insert a wide bore cannula (ideally a grey or orange) in each antecubital to allow the most prompt fluid resuscitation. Start IV fluid replacement in an attempt to increase the intravascular volume, to increase the blood pressure and the perfusion of the organs but the constituents of the fluid are important. Try to give the same fluid that you are losing such as blood in haemorrhage and keep the electrolytes balanced (these can become depleted in nausea and diarrhoea in particular). A good start is using crystalloids in rapid 250ml bolus, reassessing after each bag.* *Be careful not to run through bags with added potassium chloride ‘stat’, as rapid boluses of potassium can cause cardiac arrest.Autotransfusion Raising the patient’s legs can be a good initial step while fluids are being made up as it delivers an ‘autotransfusion’ (uses gravity to redistribute the patient’s own blood more centrally to increase the blood pressure.) Any sick patient should have concurrent blood samples taken for full blood count, urea and electrolytes, coagulation, liver biomarkers, troponins, venous gas samples for lactate and cultures as required and they should also undergo a 12 lead ECG to explore whether the shock is of cardiac origin If you suspect post-operative complications, including internal haemorrhage which would not be amenable to simple compression, then you need to notify your team urgently for further assessment and potentially returning to theatre to explore and manage. Blood (rather than just serosanguinous fluid) in drains, disproportionate pain, and signs of peritonism can all be clues to support any suspected pathology.

Question 39

Disability

Answer 39

There is a wide variety of potential pupil changes that can occur, yet typical changes may include: ‘Pinpoint’ or bilaterally constricted pupils (miosis) may indicate opioid toxicity Anisocoria (a unilaterally dilated (mydriasis) pupil) can occur with rising intracranial pressure (including from intracranial haemorrhage), affecting CN III Any nausea and vomiting in the patient with a head injury may not be simple post-operative nausea and vomiting, but again may a sign of rising intracranial pressure. Any significant changes in input and output of fluids can alter the blood’s electrolyte content, most commonly hyponatraemia. This may be treated with electrolyte replacement with sodium chloride, yet further advice may be beneficial from your own team or medical teams, due to potential side effects from this electrolyte disturbance. Check the blood glucose levels and manage accordingly (results may be transient so careful monitoring is required) Concentrated glucose solutions include buccal agents or oral drinks, intravenous preparations (ranging from 5 to 50% glucose), or IM glucagon. Any opioid induced respiratory depression, bradypnoea, or coma will require naloxone reversal (results may be transient so careful monitoring is required) If required, you probably need extra help from your seniors, the critical care outreach team, or the on call medical team, as administration requires (quite specific) increasing dosage (as described in the BNF). Be aware that naloxone will reverse any analgesic effects too and as such your patient may experience a lot of pain. Any seizures require treatment with benzodiazepines. 10-20mg PR diazepam is typically advised as first line, before 4mg IV lorazepam as second line. If IV is not an option, then 10mg buccal midazolam should be trialled. Any failure to respond within a few minutes should prompt you to seek urgent senior help from your own team or the on call medical team.

Question 40

Exposure

Answer 40

t may be necessary to fully expose the patient for a full assessment. Remember to prioritise patient dignity and conservation of body heat. Assessment Ask again: Is the patient in any pain? This can help to guide your assessment. Inspection Check skin for rashes (adverse drug reaction, meningococcal sepsis), other signs of infection, and bruising (coagulation disorders) Calves: Are they red, tender or swollen? (e.g. DVT) Lines in: Are there any signs of phlebitis or infection? Replace and remove any concerning lines- consider line tip culture Catheter output: Is there pus or blood suggestive of infection or injury? Surgical wounds: Are there signs of bleeding or infection? There could be concealed internal bleeding into (e.g. peritoneum, pelvis or thoracic cavity) Drains: What is the output? Worrying signs include pus, blood, or high/low output

Question 41

6. How does the RAAS system influence blood pressure?

Answer 41

The Renin-Angiotensin-Aldosterone System (RAAS) is a hormone system within the body which is essential for the regulation of blood pressure. The first part of the system involves the enzyme renin, which is released from the Juxtaglomerular Cells Apparatus (JGA) that are found in the kidney. Renin is released due to 3 possible different events: • A reduction in Sodium being delivered to the macula densa cells • Reduction in blood pressure, detected by baroceptors I the afferent renal arteriole • Sympathetic stimulation of the JGA via Beta1 adrenoceptors Renin released is directly inhibited by ANP (atrial natriuretic peptide) which is released due to atrial stretching, as a result of an increase in blood pressure Angiotensin II Angiotensinogen is the pre-cursor protein which is produced in the liver, and cleaved by renin to form angiotensin I. Angiotensin I is then converted to angiotensin II by angiotensin converting enzyme (ACE). This conversion occurs mainly in the lungs where ACE is produced by vascular endothelial cells, although ACE is also generated in smaller quantities within the renal endothelium. Angiotensin II exerts its action by binding to various receptors throughout the body. It binds to one of two G-protein coupled receptors, the AT1 and AT2 receptors. Most actions occur via the AT1 receptor. Finally, angiotensin II acts on the adrenal cortex to stimulate the release of aldosterone. Aldosterone is a mineralocorticoid, a steroid hormone released from the zona glomerulosa of the adrenal cortex. Aldosterone acts on the principal cells of the collecting ducts in the nephron. It increases the expression of apical epithelial Na+ channels (ENaC) to reabsorb urinary sodium. Furthermore, the activity of the basolateral Na+/K+/ATPase is increased. This causes the additional sodium reabsorbed through ENaC to be pumped into the blood by the sodium/potassium pump. In exchange, potassium is moved from the blood into the principal cell of the nephron. This potassium then exits the cell into the renal tubule to be excreted into the urine. As a result, increased levels of aldosterone cause reduced levels of potassium in the blood.

Question 42

How do we use volume expanders and blood products in the treatment of shock?

Answer 42

Plasma volume expanders are used for the treatment of circulatory shock. They restore vascular volume, stabilising circulatory haemodynamics and maintaining tissue perfusion. Two general categories of expander are used: crystalloids or colloids, or a mixture of both . Albumin is normally present in the blood and constitutes 50-60% of the plasma proteins and 80-85%of the oncotic pressure. Plasma protein fraction consists of 88% albumin and 12% globulins. Plasma protein fraction is effective in maintaining blood volume but does not increase oncotic pressure. Hartmans got near physiological concentration of crystalloids, but don’t use in people with potassium. Know difference between colloids and crystalloids: Colloids stay in plasma, crystalloids stay out more. How do plasma volume expanders work? Plasma volume expanders increase the oncotic pressure in the intravascular space. Water moves from the interstitial spaces into the intravascular space, increasing the circulating blood volume. This increased volume leads to an increase in central venous pressure, cardiac output, stroke volume, blood pressure, urinary output and capillary perfusion, and a decrease in heart rate, peripheral resistance and blood viscosity.

Question 43

Oopen abdominal surgery vs evar

Answer 43

Treatment depends on several factors, including location and size of the aneurysm, your age, and other conditions you have, repair options include: Medical Monitoring: Your doctor might recommend this option if your abdominal aortic aneurysm is small and you do not have symptoms. You will have regular appointments to check if your aneurysm is growing, and treatment to manage other medical conditions, such as high blood pressure, that could worsen your aneurysm. It's likely you'll need regular imaging tests to check on the size of your aneurysm. Expect to have an abdominal ultrasound at least six months after your aneurysm is diagnosed and at regular follow-up exams. Open abdominal surgery. This involves removing the damaged section of the aorta and replacing it with a synthetic tube (graft), which is sewn into place. Full recovery is likely to take a month or more. This is the more likely option, if the aneurysm is very large, or has already ruptured. Most aneurysms formed at renal artery. More durable after. Endovascular aneurysm repair (EVAR) of the abdominal aorta is performed using an abdominal aortic aneurysm (AAA) stent graft. The AAA stent is placed within the aneurysm to provide a permanent, alternative conduit for blood flow within the patient’s vasculature, thereby excluding the aneurysmal sac from blood flow and pressure and preventing the walls of the aneurysm from rupturing. Endovascular aneurysm repair (EVAR) involves inserting a graft within the aneurysm through small groin incisions using X-rays to guide the graft into place. The advantage of this type of repair is that there is no abdominal surgery. This technique is therefore safer than the traditional operation, and you need to spend less time in hospital. A disadvantage is that some patients have to undergo a further operation at a later stage to refine the initial procedure. Abdominal aorta aneurysm (weakening of the aortic wall). -Aneurysms typically represent dilation of all layers of the arterial wall • True aneurysm: all 3 layers of the arterial wall involved • False: single layer of fibrous tissue forms the aneurysm wall. Causes of AAA: - common in groups of those who suffer from standard arterial disease: are hypertensive, have diabetes, are or have been smokers. - patients suffering from connective tissue disorders such as Marfan’s. - In patients with abdominal aortic aneurysms the extracellular matrix becomes disrupted with a change in the balance of collagen and elastic fibres. Pathophysiology - Occur primarily as a result of the failure of elastic proteins within the extracellular matrix. There is infiltration of vessel wall by lymphocytes and macrophages. - Loss of smooth muscle cells and thinning of tunica media. - destruction of elastin in tunica media. -Most aneurysms are caused by degenerative disease. The pathophysiology involved in the development of aneurysms is complex and the primary event is loss of the intima with loss of elastic fibres from the media. This process is associated with, and potentiated by, increased proteolytic activity and lymphocytic infiltration.

Question 44

Types of back pain

Answer 44

Pain described as “burning” in nature is typically neuropathic in origin (e.g. nerve root compression) Tearing/ripping thoracic back pain is typically associated with aortic dissection Crushing thoracic back pain is associated with myocardial infarction Sharp pain is less specific but is associated with acute spinal fracture, muscular spasm and pulmonary embolism (pleuritic)

Question 45

How does blood clot?

Answer 45

1. The vascular phase: Damage to the blood vessel wall will cause contraction in that particular area of the blood vessel. This vasoconstriction can last from 30 minutes to a few hours and can completely occlude the vessel. It occurs as a result of damage to the endothelial cells. This damage causes them to release various factors, including: ADP Tissue Factor – aka factor III – required for the activation of thrombin from prothrombin Prostacyclin – kind of a feedback mechanism; thisprotein actually causes vasodilation and prevents formation of the platelet plug Endothelins – these are the primary hormones involved in the vascular phase. They stimulate smooth muscle contraction and stimulate cell division of endothelial cells, smooth muscle cells and fibroblasts, thus aiding repair of the damaged site. Endothelial cells also become ‘sticky’ and will express surface proteins that allow them to ‘stick’ to other endothelial cells, in an attempt to close of the damaged area. 2. The platelet phase: If the damage to a blood vessel is small enough, it can be ‘plugged’ by a platelet plug. Platelets – aka thrombocytes: • Contain actin and myosin, Produce plenty of prostaglandins and fibrin-stabilising factor  Produce platelet derived growth factor (PDGF) – which helps vascular repair  Produce thromboxane A2 – which is a prominent vasoconstrictor  They are actually cell fragments rather than actual cells – as during their development, their precursors break down to form them  Have a special glycoprotein membrane that prevents adhesion to normal epithelium, but that promotes adhesion to damaged epithelium. they are particularly adherent to collagen – which will only be present when deep areas of the cell wall are exposed  About 1/3 of platelets are stored in the spleen and other vascular organs at any one time – waiting to be mobilised  Low platelet count – thrombocytopaenia – this is a process either of high platelet destruction, or low platelet production.  High platelet count – thrombocytosis – this is usually a result of increased platelet formation, most commonly seen in response to infection, inflammation, and cases of cancer. The platelet phase begins as soon as platelets begin to attach themselves to damaged areas of endothelium – normally collagen. This process begins within 15 seconds of injury. The attachment of platelets to exposed surfaces is called platelet adhesion. As more and more platelets arrive, we get platelet aggregation, and finally, once a certain mass of platelets is reached, we have platelet plug formation. This is a totally normally process, and will occur thousands of times a day. People with problems with platelet formation may get thousands of tiny haemorrhages, and problems bruising easily. When a platelet becomes attached to a damaged endothelial surface, it will actually changes it own size and shape: It will swell, and become large and irregular The contractile proteins contract causing the release of granules… ADP, thromboxane and Ca2+ ions are all released – these can act on nearby platelets, and attract them to the site, causing them to adhere to the platelets already present. This creates a positive feedback loop, causing aggregation of more and more platelets. Negative feedback of the plug formation is controlled by prostacyclin released by the endothelium. This reduces platelet aggregation. White cells in the area also release proteins that prevent the clot getting out of control. Plasma enzymes will also break down ATP that is found circulating near the plug, and thus reduce the amount of energy available to the platelets. 3. The coagulation phase: This begins about 30 seconds after the initial injury. It involves a complex sequence of events, that ultimately lead to the activation of fibrin from fibrinogen. The intrinsic pathway: Begins in the blood stream. It is basically activated when blood is exposed to collagen (or other damaged surfaces, but collagen is the main thing involved). Factor XII is activated to XIIa by exposed collagen XIIa, with the help of HMW kininogen,activates XI to XIa. This can proceed more quickly in the presence of prekallikrein. XIa combines with calcium, and activates IX to IXa Simultanesouly, platelets will release PF3, and also simultaneously, VIII will be activated to VIIIa. IXa, (with the help of PF3) will join together with VIIIa and form factor X activating factor (‘tenase’). The extrinsic pathway Begins in the vessel wall. Damaged endothelial cells will release factor III (tissue factor), and the greater the amount of damage, the more is released. This combines with calcium, and activates factor VII and turns it into factor VIIa. This VIIa-tissue factor complex is quickly inactivated by antithrombin III! The Common Pathway X is activated, either by VIIa or tenase , to form Xa – aka prothrombinase Xa, with the help of calcium ions, and Va will turn prothrombin into thrombin! Thrombin is factor IIa Factor V is not activated until it has come into contact with thrombin itself. Thus V is not required for this step, but when present will increase the rate. Thrombin will then activate fibrinogen to fibrin. Fibrin strands will begin to join together, and with the help of XIIIa this will cause the cross-linking of fibrin strands. XIII is also activated by thrombin. XIII is also known as fibrin stabilising factor. Note that – once activated, thrombin can act as a ‘catalyst’ in other areas of the cascade to speed up the process: It can activate factor VII directly It activates factor V The extrinsic pathway produces thrombin very quickly, but in small amounts, the intrinsic pathway produces a large amount of thrombin, but takes a while to get going.

Question 46

Meningitis DR DEAC PIMP

Answer 46

Meningitis is a serious infection of the meninges in the brain or spinal cord that is most commonly viral or bacterial in origin, although fungal, parasitic, and noninfectious causes are also possible. Enteroviruses and herpes simplex virus are the leading causes of viral meningitis, while Neisseria meningitidis and Streptococcus pneumoniae are the pathogens most commonly responsible for bacterial meningitis. Rarer forms of bacterial meningitis include tuberculous meningitis and Lyme-associated meningitis. The classic triad of meningitis is fever, headache, and neck stiffness. In infants and young children, the presentation is often nonspecific. Patients may also present with neurological deficits, altered mental status, and seizures, indicating increased intracranial pressure (ICP). The diagnosis is confirmed with lumbar puncture (LP) and CSF analysis. If increased ICP is suspected, a CT of the head should be performed first. Bacterial meningitis requires rapid initiation of empiric treatment. A life-threatening complication of bacterial meningitis (especially meningococcal meningitis) is Waterhouse-Friderichsen syndrome, which is characterized by disseminated intravascular coagulation and acute adrenal gland insufficiency. Viral meningitis typically resolves on its own and has a far less severe course than bacterial meningitis, which is generally fatal if left untreated. When N. meningitidis or S. pneumoniae are identified as the pathogen, the CDC should be notified and preventative measures taken to prevent dissemination of the infection. Epidemiology: In the pediatric population, meningitis most often occurs in children < 1 year of age. [1] The median age of adult patients with meningitis is 43 years. [2] Worldwide, the incidence of meningitis caused by N. meningitidis is highest in sub-Saharan Africa, collectively referred to as the “meningitis belt.” Aetiology: Common causes Otitis media Sinusitis CSF leak after head trauma or neurosurgery Maternal group B streptococcal infection during birth Sepsis Risk factors: Immunocompromise (e.g., due to AIDS, asplenia, heavy alcohol use disorder, chronic illness, cancer, sickle cell anemia, old age, pregnancy) Crowded occupational or living conditions (e.g., college dormitories, military barracks, retirement homes, kindergartens) Close contact with an infected person Aetiology: Common causes Otitis media Sinusitis CSF leak after head trauma or neurosurgery Maternal group B streptococcal infection during birth Sepsis Viral meningitis, fungal meningitis, parasitic meningitis, noninfectious meningitis. Pathways of infection: Most pathogens that cause meningitis colonize the nasopharynx or the upper airways before entering the CNS via: Hematogenous dissemination . Contiguous spread of infections in nose, eyes, and ears Retrograde transport along or within peripheral or cranial nerves Direct infection (e.g., due to trauma or head surgery) [26] Incubation periods Bacterial meningitis: usually 3–7 days. Viral meningitis: usually 2–14 day, depending on the type of virus. Clinical features: Clinical features of bacterial and viral meningitis are similar, although viral meningitis is less acute and usually self-limiting within 7–10 days. -Neonates: In neonates, meningitis often manifests with nonspecific symptoms and without the classic triad of meningitis. Early symptoms Lethargy Muscle hypotonia Irritability Poor appetite, vomiting Hyperthermia or hypothermia Dyspnea, abnormal breathing patterns (e.g., Biot respiration) [28] Late symptoms Fontanelle bulging High-pitched crying Seizures. -Children and adults: Classic triad of meningitis: fever, headache, and neck stiffness (this triad is often not present in neonates and infants) [29][30] Altered mental status Photophobia Nausea, vomiting Malaise Seizures Possibly cranial nerve palsies In the case of N. meningitidis Myalgia and, possibly, petechial or purpuric rash (especially in children) Possibly Waterhouse-Friderichsen syndrome Common symptoms of viral meningitis Prodrome with flu-like symptoms Low-grade fever Malaise, fatigue Myalgia Upper respiratory symptoms (e.g., sore throat) Pharyngitis, herpangina, and/or rash. Signs of meningeal irritation Neck stiffness Kernig sign Brudzinski sign Systemic signs of inflammation Fever Hypotension Tachycardia Signs of increased intracranial pressure: e.g., papilledema (< 5% of cases) [32] Signs of underlying infections Bulging and redness of tympanic membrane: acute otitis media Skin manifestations [33] Cutaneous petechiae in meningococcal meningitis: suggestive of meningococcemia Maculopapular rash in some viral meningitis (e.g., West Nile virus, enterovirus) Nonblanching rash: should raise suspicion for meningococcal meningitis or Rocky Mountain spotted fever (see “Subtypes and variants”) Features suggestive of meningoencephalitis [34][35] In addition to the features of meningitis, meningoencephalitis is characterized by signs of inflammation of the brain parenchyma (encephalitis). Focal neurological signs (e.g., paresis, extrapyramidal symptoms, aphasia) Seizures (focal-onset or generalized) Behavioral changes, psychosis Altered consciousness. DDx: Subarachnoid hemorrhage can manifest with the classic triad of meningitis but has a more sudden onset and patients often lose consciousness. The classical features of acute bacterial meningitis are fever, neck stiffness, and headache. However, this triad of symptoms only manifests in approx. 50% of cases. Management: Bacterial meningitis is a medical emergency and requires immediate treatment. Diagnostic and treatment steps should be initiated simultaneously and empiric treatment should not be delayed for diagnostic steps. If the patient is stable and has no contraindications: Perform LP as soon as possible before starting empiric antibiotics. If the patient is unstable, requires neuroimaging (see criteria for imaging prior to LP in suspected meningitis), or has relative contraindications to LP (e.g., coagulopathy): Defer LP and start empiric antibiotic treatment (see empiric antibiotic therapy for bacterial meningitis). [5] Management of meningitis Do not delay empiric antibiotic therapy in patients suspected of having bacterial meningitis. Investigations: Approach Obtain samples immediately for blood cultures, routine laboratory tests, and screening for organ dysfunction. Confirm the diagnosis with LP and CSF analysis (if no contraindications are present). Routine tests would be: -Blood cultures -CBC -BMP -CRP -Additional tests: coagulation panel, blood gas. Lumbar puncture is indicated in all patients with suspected meningitis (see “Lumbar puncture” for details on indications, contraindications, procedural steps, and complications). Atypical pathogen testing Atypical pathogen testing is not necessary for all patients and should be performed as directed by clinical suspicion.. Treatment: Approach Apply appropriate isolation precautions. Stabilize the patient as needed. Administer empiric antibiotics as soon as possible, preferably within 1 hour (see empiric antibiotic therapy for bacterial meningitis). If LP can be performed rapidly, administer antibiotics and adjuvant therapy (e.g., dexamethasone) after obtaining CSF. If LP is delayed (e.g., because neuroimaging is required), administer antibiotics and adjuvant therapy (e.g., dexamethasone) immediately. Add other antimicrobial therapy (e.g., antivirals, antifungals) as needed (see “Subtypes and variants” for details). Tailor antimicrobial therapy once the pathogen is identified. Provide postexposure prophylaxis for close contacts if indicated (see postexposure chemoprophylaxis for bacterial meningitis). Patient stabilization Airway management: Secure the airway (e.g., intubate) if GCS < 8, the patient has intractable seizures, or there are signs of cerebral herniation. Hemodynamic support with fluids and/or vasopressors (see fluid resuscitation and sepsis). Identify and reverse any coagulopathy (see disseminated intravascular coagulation). Identify and treat elevated ICP. Antimicrobial therapy. Corticosteroids Corticosteroids [39][49] Indication: suspected or proven meningitis due to S. pneumoniae or H. influenzae in adults and children Mechanism: reduces the local and systemic inflammation seen in bacterial meningitis and improves outcomes Recommended agent: dexamethasone Should be administered before or concomitant to antibiotics for optimal results [39] Discontinue if a pathogen other than S. pneumoniae or H. influenzae is identified. Disadvantages: side effects, e.g., hyperglycemia, GI bleeding [49]. Complications: Neurologic Most common: sensorineural hearing loss (transient or permanent) Focal neurological deficits [61] Seizures Cognitive impairment Spasticity or paresis Cerebral edema and elevated ICP Communicating hydrocephalus Cerebrovascular disease Rare: brain abscess, subdural empyema, arteritis (risk of cerebral infarction and cerebral venous sinus thrombosis), ventriculitis, cerebritis Waterhouse-Friderichsen syndrome Epidemiology: predominantly affects small children and asplenic individuals Description: acute primary insufficiency of the adrenal gland most commonly caused by adrenal hemorrhage Dangerous complication of a number of diseases but most commonly associated with meningococcal meningitis Rarer causes include DIC, endotoxic shock, and septicemia due to other pathogens (e.g., S. pneumoniae) Pathophysiology: coagulopathy triggered by endotoxins, which often leads to hemorrhagic necrosis of the adrenal glands Clinical features Fever Myalgia Nonblanching, petechial rash (mostly on trunk and legs); in severe cases, even purpura fulminans with extensive necrosis of the skin Severe malaise Hypotension or even shock Findings of disseminated intravascular coagulation Findings of acute adrenal gland failure Respiratory failure Treatment Treatment of the underlying cause (see empiric antibiotic therapy for bacterial meningitis and pathogen-specific therapy in meningitis) Parenteral fluid therapy and management of disorders of sodium balance Coagulopathy treatment Prognosis: fatal without treatment and often fatal even with treatment, particularly if associated with meningococcal infection (> 40% mortality rate) Prognosis: Bacterial meningitis Fatal if left untreated Prognosis in treated patients depends on age, overall condition, immune status and the pathogen(s) involved. Viral meningitis Resolves spontaneously in the majority of cases Residual symptoms such as sensorineural hearing loss, epilepsy, and cognitive deficits are rare. Fungal meningitis Associated with neurological sequelae and a high mortality rate Treatment adherence is very important to avoid relapse.

Question 47

Blood culture

Answer 47

A blood culture is a test that checks for foreign invaders like bacteria, yeast, and other microorganisms in your blood. Having these pathogens in your bloodstream can be a sign of a blood infection, a condition known as bacteremia. A positive blood culture means that you have bacteria in your blood.

Question 48

Non-blanching rash

Answer 48

Non-blanching rashes are caused by bleeding under the skin. Petechiae are small (< 3mm), non blanching, red spots on the skin caused by burst capillaries. Purpura are larger (3 – 10mm) non-blanching, red-purple, macules or papules created by leaking of blood from vessels under the skin. Any child presenting with a non-blanching rash needs immediate investigation for the underlying cause. The most concerning differential is meningococcal septicaemia. Patients with features of sepsis need immediate management for life threatening meningococcal sepsis.

Question 49

Tonsils

Answer 49

Palatine tonsils at back of mouth between palatoglossal and palatopharyngeal arches. Enlargement: most often due to infection (tonsilitis), in which case there is also erythema and often exudate. Tonsillar enlargement may also be a chronic condition (e.g. tonsillar hypertrophy). Asymmetry: tonsilitis can cause asymmetrical tonsillar swelling, however other causes of unilateral tonsillar swelling include tonsillar stones and malignancy. Tonsillar ulceration: may be caused by viral infections (e.g. herpes simplex), however, malignancy should also be considered. Tonsillar stones: caused by mineralisation of debris trapped within the tonsils. The stones may be visible on inspection of the tonsils and are usually asymptomatic.

Question 50

Uvula

Answer 50

Uvula deviation: may be caused by a peritonsillar abscess, with the uvula deviating away from the abscess. A glossopharyngeal nerve lesion can also cause uvula deviation away from the side of the lesion. If there are no other symptoms or signs, uvula deviation is likely a normal finding.

Question 51

what cream is used to anaesthetise an area of skin?

Answer 51

Ametop

Question 52

What is a hernia?

Answer 52

The often recited surgical definition of a hernia is ‘the protrusion of a viscus into an abnormal space’. In simple terms, a hernia describes a structure that passes through a space or defect, into an abnormal location.

Question 53

Reducible hernia

Answer 53

Reducible – when the contents of the hernia can be manipulated back into its original position through the defect from which it emerges

Question 54

Incarcerated hernia

Answer 54

Incarcerated hernia (irreducible) – the hernia is compressed by the defect causing it to be irreducible (i.e. unable to be pushed back into its original position)

Question 55

Obstructed hernia

Answer 55

Obstructed hernia – refers mainly to hernias containing bowel, where the contents of the hernia are compressed to the extent that the bowel lumen is no longer patent and causes bowel obstruction

Question 56

Strangulated hernia

Answer 56

Strangulated hernia – the compression around the hernia prevents blood flow into the hernial contents causing ischaemia to the tissues and pain

Question 57

labrynthitis

Answer 57

Labyrinthitis, as the name suggests, involves the labyrinth, as well as the eight cranial nerve (vestibular nerve), which gives rise to the hearing impairment and vertiginous giddiness respectively.

Question 58

68 Year old male presents to the GP to discuss his test results. His recent CT scan showed an incidental finding of a AAA at 4.3cm in length. He is currently symptomatic but is concerned regarding potential rupture. What is the minimum size the AAA is suitable for surgery, providing he is asymptomatic and hasn't grown more than 1cm per year?

Answer 58

5.5cm

Question 59

left and right coronary arteries

Answer 59

The left coronary artery - branches into circumflex, main LAD and marginal branches. Think to the ECG and remember the zones that these branches supply - it will help you in interpreting ECGS with suspected pathologies Right coronary - supplies posterior and inferior aspects of the heart - noted as leads 2,3 and AVF (elevated in Infarction and depressed in ischaemia - generally)