PLABABLE MOCKS

Question 1

A patient with long-standing GORD presents with progressive dysphagia to solids first, then liquids. Endoscopy shows smooth, concentric narrowing of the distal oesophagus.
➡️ What is the most likely diagnosis?

Answer 1

✅ Diagnosis: Peptic oesophageal stricture
✅ Cause: Chronic gastro-oesophageal reflux disease (GORD)
✅ Endoscopy: Smooth, concentric distal narrowing
✅ Symptom Pattern:

Solids → Liquids (progressive mechanical obstruction)
🧠 Mnemonic

“GORD → Scarring → STRICture”

Question 2

🟦 FRONT:
Cirrhotic patient presents with hypotension, haematemesis, and melaena. Most appropriate initial management?

Answer 2

🟩 BACK:
✅ IV octreotide + urgent endoscopic band ligation
✅ Give IV antibiotics (ceftriaxone)
✅ Resuscitate with fluids + blood
✅ TIPS only if bleeding refractory
Mnemonic: “VARIX = OCT + SCOPE + ABX”

Question 3

🔍 Key Clues from the Stem

Sudden worst-ever headache → SAH

Young (36 years)

Hypertension

Recurrent UTIs

Right-sided abdominal discomfort

Family history of early stroke

CT shows subarachnoid haemorrhage

🔎 Other Possible Clues That Could Lead to the SAME Answer

Palpable bilateral renal masses

Flank pain

Haematuria

Progressive renal failure

Berry aneurysm on angiography

Family members with kidney disease

Answer 3

Autosomal dominant mutation (PKD1/PKD2)

Progressive formation of renal cysts

Causes:

✅ Hypertension

✅ UTIs

✅ Flank/abdominal discomfort

Also causes berry aneurysms in Circle of Willis

Aneurysm rupture → subarachnoid haemorrhage

💊 Management (NICE / BNF Level)
✅ Acute SAH

Admit to neurosurgical ICU

Nimodipine to prevent vasospasm

BP control

Definitive aneurysm treatment:

Endovascular coiling or surgical clipping

✅ Long-Term ADPKD Management

Aggressive BP control (ACE inhibitors)

Renal function monitoring

Family screening

Question 4

make the main points bold

🔍 Key Clues from the Stem

Sudden-onset palpitations

Shortness of breath + lightheadedness

Heart rate = 160 bpm

Regular, narrow-complex tachycardia

No visible P waves

Haemodynamically stable

🔎 Other Possible Clues That Could Lead to the SAME Answer

“Sudden racing heart that stops abruptly”

Young patient with no structural heart disease

“Neck pounding” (AVNRT)

Valsalva partially slows the rhythm

History of previous similar brief episodes

Answer 4

🧠 Pathophysiology

AV nodal re-entry tachycardia (AVNRT)

Re-entrant electrical circuit within AV node

Causes:

Rapid regular ventricular rate

Narrow QRS (normal ventricular conduction)

Absent visible P waves

Adenosine → transient AV node block → terminates re-entry loop

💊 Management (NICE / BNF Level)
✅ Stepwise Acute SVT Management

Vagal manoeuvres

If unsuccessful:

IV Adenosine 6 mg rapid bolus

If no effect → 12 mg IV

Continuous ECG monitoring required

✅ If unstable → synchronized DC cardioversion

A. IV beta-blockers → Used for rate control in AF/flutter

C. Oral calcium channel blockers → Not used acutely in ED

D. Electrical cardioversion → Reserved for haemodynamically UNSTABLE patients

E. IV digoxin → Chronic rate control in AF, not acute SVT termination

Question 5

What is the first step in managing a stable patient with regular narrow-complex tachycardia at 160 bpm and absent P waves?

Answer 5

Vagal manoeuvres

If unsuccessful, proceed to IV Adenosine.

Question 6

What medication is used to terminate AV nodal re-entry tachycardia (AVNRT)?

Answer 6

IV Adenosine

Administer 6 mg rapid bolus, followed by 12 mg if no effect.

Question 7

True or false: Electrical cardioversion is used for stable patients with SVT.

Answer 7

FALSE

Cardioversion is reserved for haemodynamically unstable patients.

Question 8

What are the key ECG findings in AV nodal re-entry tachycardia (AVNRT)?

Answer 8

• Regular narrow QRS
• Absent visible P waves

Indicates a re-entrant electrical circuit within the AV node.

Question 9

What is the pathophysiology of AV nodal re-entry tachycardia (AVNRT)?

Answer 9

Re-entrant electrical circuit within AV node

Causes rapid regular ventricular rate and narrow QRS.

Question 10

List the steps in acute SVT management.

Answer 10

• Vagal manoeuvres
• IV Adenosine 6 mg rapid bolus
• If no effect, 12 mg IV
• Continuous ECG monitoring

If unstable, synchronized DC cardioversion is required.

Question 11

What is a common trap in managing true SVT?

Answer 11

Giving beta-blockers first

This is incorrect; beta-blockers are used for rate control in AF/flutter.

Question 12

What mnemonic can help remember the management of stable SVT?

Answer 12

Regular + Narrow + No P = ADENOSINE

This highlights the key ECG features leading to the use of adenosine.

Question 13

What is the haemodynamic status of a patient with stable SVT?

Answer 13

Haemodynamically stable

This indicates that the patient does not require immediate cardioversion.

Question 14

What should be monitored continuously during the administration of IV Adenosine?

Answer 14

ECG monitoring

Essential to observe the patient’s response and any potential complications.

Question 16

What are the key clues for suspected Diabetes Insipidus?

Answer 16

• Excessive thirst
• Polyuria
• Drinking 8 litres/day
• Nocturia
• Sodium = 148 mmol/L (high-normal to raised)

Other possible clues include dry mucous membranes, low urine specific gravity, and a history of head injury or pituitary disease.

Question 17

What is the pathophysiology of Diabetes Insipidus?

Answer 17

• Failure of ADH
• Central DI: ↓ ADH production
• Nephrogenic DI: kidneys unresponsive to ADH
• Inability to concentrate urine
• Dilute urine → dehydration → hypernatraemia

Urine osmolality distinguishes primary polydipsia from DI.

Question 18

What is the best next investigation for a patient suspected of having Diabetes Insipidus?

Answer 18

Urine osmolality

This test confirms diabetes insipidus vs psychogenic polydipsia.

Question 19

What is the management for Central Diabetes Insipidus if confirmed?

Answer 19

Desmopressin

For Nephrogenic DI, treatment includes thiazide diuretics and a low-salt diet.

Question 20

True or false: Hyperglycaemia is a key feature of Diabetes Insipidus.

Answer 20

FALSE

Diabetes Insipidus is confused with diabetes mellitus, but it does not present with hyperglycaemia.

Question 21

What are the common traps to avoid when diagnosing Diabetes Insipidus?

Answer 21

• Confusing with diabetes mellitus
• Choosing CT head too early
• Forgetting sodium points toward water loss, not sugar

These traps can lead to misdiagnosis and inappropriate management.

Question 22

Fill in the blank: The mnemonic for remembering the signs of Diabetes Insipidus is __________.

Answer 22

THIRST + TANKING Na

This mnemonic helps recall the key features associated with Diabetes Insipidus.

Question 23

What are the clinical clues indicating Diabetes Insipidus?

Answer 23

• Polyuria
• Polydipsia
• High sodium levels

These clues help in the initial assessment of the condition.

Question 24

What is the first-line treatment for Benign Paroxysmal Positional Vertigo (BPPV)?

Answer 24

Epley manoeuvre

The Epley manoeuvre is used to reposition dislodged otolith crystals in the posterior semicircular canal.

Question 25

What triggers the **vertigo episodes** in BPPV?

Answer 25

Head movement ## Footnote Vertigo episodes are recurrent and triggered by movements such as turning in bed.

Question 26

How long do the **vertigo episodes** in BPPV typically last?

Answer 26

1–5 minutes ## Footnote Episodes are brief and can be accompanied by severe nausea and retching.

Question 27

True or false: **Hearing loss** is a symptom of BPPV.

Answer 27

FALSE ## Footnote BPPV does not involve hearing loss or tinnitus.

Question 28

What test is positive in BPPV?

Answer 28

Dix–Hallpike test ## Footnote This test helps confirm the diagnosis of BPPV.

Question 29

What is the **pathophysiology** of BPPV?

Answer 29

Dislodged otolith crystals in posterior semicircular canal ## Footnote Head movement causes abnormal endolymph flow, leading to false motion signals and vertigo.

Question 30

What should be avoided in the management of BPPV?

Answer 30

Long-term vestibular suppressants ## Footnote These should be avoided as they do not address the underlying issue.

Question 31

What is a common **trap** in the management of BPPV?

Answer 31

Treating BPPV like Ménière’s ## Footnote This can lead to inappropriate treatment choices.

Question 32

Fill in the blank: **BPPV = Bed → Position → __________ → EPLEY**.

Answer 32

Positional Vertigo ## Footnote This mnemonic helps remember the key aspects of BPPV.

Question 33

What is the **duration** of vertigo in BPPV?

Answer 33

Seconds–minutes ## Footnote The episodes are brief, typically lasting only a few minutes.

Question 34

What is the **management** step if symptoms persist after the Epley manoeuvre?

Answer 34

Repeated canalith repositioning ## Footnote This may be necessary if initial treatment does not resolve symptoms.

Question 35

What is the diagnosis for an **elderly woman** who has a mechanical fall at home, is unable to bear weight, and has severe hip pain?

Answer 35

Neck of femur fracture ## Footnote Key clues include age, fall mechanism, and inability to bear weight.

Question 36

List the **key clues** from the case that indicate a neck of femur fracture.

Answer 36

* 78-year-old woman * Mechanical fall at home * Unable to bear weight * Severe hip pain * X-ray shows clearly displaced proximal femoral fracture ## Footnote These clues help in identifying the fracture type.

Question 37

True or false: A **hip dislocation** typically occurs after high-energy trauma.

Answer 37

TRUE ## Footnote This distinguishes it from the mechanism of injury for a neck of femur fracture.

Question 38

What are the **other possible clues** that could lead to the diagnosis of a neck of femur fracture?

Answer 38

* Shortened, externally rotated leg * Groin pain after minor fall * Osteoporosis history * Pain worsened with passive movement * Inability to straight-leg raise ## Footnote These clues further support the diagnosis.

Question 39

Why is a **pubic ramus fracture** not the correct diagnosis in this case?

Answer 39

Pain but often still weight-bearing ## Footnote This contrasts with the inability to bear weight seen in neck of femur fractures.

Question 40

What is the **management** for a displaced intracapsular neck of femur fracture?

Answer 40

* Immediate analgesia (IV opioids + paracetamol) * IV fluids * Pressure sore prevention * Definitive surgical management: Hemiarthroplasty within 24–48 hours ## Footnote Urgent surgical intervention is crucial to prevent complications.

Question 41

What is the **pathophysiology** behind a neck of femur fracture in the elderly?

Answer 41

* Elderly + osteoporosis → fragile bone * Fall → fracture through femoral neck * Disrupts blood supply → high AVN risk * Leads to immobility → ↑ pneumonia, DVT, mortality ## Footnote Understanding the pathophysiology helps in managing and preventing complications.

Question 42

What is a common **trap** when diagnosing neck of femur fractures?

Answer 42

* Confusing with pubic ramus fracture * Delaying surgery unnecessarily * Missing AVN risk ## Footnote Awareness of these traps is essential for timely and effective treatment.

Question 43

Fill in the blank: The mnemonic for remembering the signs of a neck of femur fracture is **OLD + FALL + CAN’T STAND = ______**.

Answer 43

NOF FRACTURE ## Footnote This mnemonic aids in recalling key indicators for diagnosis.

Question 44

What is the diagnosis for a **young patient** with **eye pain on movement** and **reduced colour vision**? Prior transient neurological symptoms?

Answer 44

Optic neuritis ## Footnote Associated with MS; treat with IV methylprednisolone if severe.

Question 45

What is the **common mnemonic** for remembering the signs of **optic neuritis**?

Answer 45

PAIN + PALE RED + MS = OPTIC NEURITIS ## Footnote Helps recall symptoms and associations.

Question 46

What medication is associated with **thiazide-induced hyponatraemia** in an elderly patient with confusion and sodium level of 122 mmol/L?

Answer 46

Indapamide ## Footnote Causes renal sodium loss and dilutional hyponatraemia.

Question 47

What is the **management** for thiazide-induced hyponatraemia?

Answer 47

* Stop indapamide * Fluid restriction * Slow sodium correction ## Footnote Severe symptoms may require hypertonic saline in HDU.

Question 48

True or false: **Indapamide** can cause confusion and lethargy due to hyponatraemia.

Answer 48

TRUE ## Footnote It leads to confusion, falls, and lethargy due to sodium levels.

Question 49

What are the **key clues** for diagnosing **optic neuritis**?

Answer 49

* Sudden onset blurred vision * Eye pain worse on movement * Loss of colour vision * Previous neurological weakness ## Footnote These clues suggest demyelination and possible MS association.

Question 50

What is the **pathophysiology** of **optic neuritis**?

Answer 50

* Immune-mediated demyelination * Slows conduction * Visual loss + pain on eye movement ## Footnote Strongly associated with Multiple Sclerosis.

Question 51

What are the **common traps** to avoid when diagnosing **optic neuritis**?

Answer 51

* Choosing retinal detachment due to vision loss * Missing eye-movement pain clue * Forgetting MS association ## Footnote Important to consider all symptoms and history.

Question 52

What are the **symptoms** of **thiazide-induced hyponatraemia**?

Answer 52

* Confusion * Lethargy * Falls * Urge incontinence ## Footnote Symptoms arise from low sodium levels affecting brain function.

Question 53

What is the **diagnosis** for a patient with AF and sudden limb pain requiring immediate surgery?

Answer 53

Acute embolic limb ischaemia ## Footnote The condition is characterized by acute arterial occlusion due to an embolus.

Question 54

What should be done with **warfarin** in the case of acute limb ischaemia requiring urgent surgery?

Answer 54

Withhold warfarin ## Footnote Continuing warfarin increases the risk of surgical bleeding.

Question 55

List the **symptoms** of acute arterial occlusion.

Answer 55

* Painful * Pale * Pulseless * Paraesthetic * Paralysed * Perishing cold ## Footnote These symptoms indicate severe limb ischaemia.

Question 56

True or false: It is appropriate to **add DOAC** for a patient on warfarin before emergency surgery.

Answer 56

FALSE ## Footnote Switching to DOAC in an acute pre-op setting is inappropriate.

Question 57

What is the **urgent management** step for acute limb ischaemia after withholding warfarin?

Answer 57

Urgent embolectomy ## Footnote This procedure is necessary to restore blood flow to the affected limb.

Question 58

What is the **INR level** mentioned for the patient on warfarin?

Answer 58

INR 2.8 ## Footnote This level is considered therapeutic but poses a risk for surgery.

Question 59

What is a common trap in managing patients on warfarin before emergency surgery?

Answer 59

Continuing warfarin into emergency surgery ## Footnote This can lead to increased bleeding risk during the procedure.

Question 60

What is the **pathophysiology** leading to acute limb ischaemia in patients with AF?

Answer 60

AF → embolus → acute arterial occlusion ## Footnote Atrial fibrillation can lead to the formation of emboli that occlude arteries.

Question 61

What should be administered after the **embolectomy** if indicated?

Answer 61

IV unfractionated heparin ## Footnote This may be necessary to manage anticoagulation post-procedure.

Question 62

What are the **incorrect management options** for acute limb ischaemia?

Answer 62

* Add DOAC * Add clopidogrel * Continue warfarin * Switch to DOAC ## Footnote Each of these options poses risks or provides no benefit in this acute setting.

Question 63

What is the **best investigation** for suspected Zenker’s diverticulum?

Answer 63

Barium swallow ## Footnote Confirms Zenker’s diverticulum and is the gold standard for diagnosis.

Question 64

True or false: **OGD** is the best investigation for Zenker’s diverticulum.

Answer 64

FALSE ## Footnote OGD risks perforation and can miss Zenker’s diverticulum.

Question 65

What are the **key clues** for diagnosing Zenker’s diverticulum?

Answer 65

* Regurgitation of undigested food * Halitosis * Nocturnal cough * Gurgling sound on swallowing ## Footnote These symptoms are classic indicators of Zenker’s diverticulum.

Question 66

What is the **pathophysiology** of Zenker’s diverticulum?

Answer 66

False diverticulum due to cricopharyngeal muscle dysfunction ## Footnote This leads to outpouching above the upper oesophageal sphincter, causing food to get trapped.

Question 67

What is the **management** for symptomatic patients with Zenker’s diverticulum?

Answer 67

* Endoscopic stapling * Open diverticulectomy * Aspiration precautions while awaiting surgery ## Footnote These treatments are recommended for symptomatic relief.

Question 68

Fill in the blank: The best investigation for suspected Zenker’s diverticulum is _______.

Answer 68

barium swallow ## Footnote This is the gold standard for diagnosis.

Question 69

What mnemonic can help remember the symptoms of Zenker’s diverticulum?

Answer 69

HALITOSIS + REGURG = ZENKER ## Footnote This mnemonic highlights the key symptoms associated with the condition.

Question 70

What are the **common traps** when diagnosing Zenker’s diverticulum?

Answer 70

* Choosing OGD instead of barium swallow * Assuming this is reflux or cancer * Missing halitosis + regurgitation as Zenker’s red flags ## Footnote These misconceptions can lead to misdiagnosis.

Question 71

What is the **diagnosis** for a patient with widespread pain, normal exam, normal blood tests, and repeated healthcare visits?

Answer 71

Somatoform disorder ## Footnote This condition features real symptoms without an organic disease.

Question 72

What are the **features** of Somatoform disorder?

Answer 72

* Real pain * No organic disease ## Footnote Symptoms manifest as physical but lack a structural cause.

Question 73

What is the **first line management** for Somatoform disorder?

Answer 73

* Reassurance * Structured follow-up with one GP * CBT ## Footnote Avoid excessive investigations and provide continuity of care.

Question 74

Fill in the blank: **SOMA** stands for Symptoms without _______.

Answer 74

Objects (disease) ## Footnote This mnemonic helps remember the essence of Somatoform disorder.

Question 75

What are the **common traps** in diagnosing Somatoform disorder?

Answer 75

* Confusing with fibromyalgia * Ordering endless scans * Labeling as 'imaginary' ## Footnote Symptoms are real and should not be dismissed.

Question 76

What is the **most likely diagnosis** for bilateral painful parotid swelling in an 18-year-old with fever and pain on chewing?

Answer 76

Mumps ## Footnote Viral paramyxovirus causes bilateral parotitis with supportive treatment. Complications include orchitis, meningitis, and pancreatitis.

Question 77

What imaging is required for **cauda equina syndrome**?

Answer 77

MRI lumbar spine ## Footnote Urgent MRI is needed to assess for nerve root compression due to conditions like disc prolapse.

Question 78

True or false: **Mumps** can cause orchitis in post-pubertal males.

Answer 78

TRUE ## Footnote Orchitis is a known complication of mumps, particularly in males after puberty.

Question 79

What are the **common complications** of mumps?

Answer 79

* Orchitis * Meningitis * Pancreatitis ## Footnote These complications can arise from the viral infection affecting various organs.

Question 80

Fill in the blank: The **incubation period** for mumps is approximately _______.

Answer 80

2–3 weeks ## Footnote This is the time it takes for symptoms to appear after exposure to the virus.

Question 81

What are the **key symptoms** of cauda equina syndrome?

Answer 81

* Faecal incontinence * Urinary retention * Bilateral weakness * Saddle anaesthesia * Hyporeflexia ## Footnote These symptoms indicate significant nerve root compression and require urgent intervention.

Question 82

What is the **urgent management** for cauda equina syndrome?

Answer 82

* Urgent MRI * Urgent neurosurgical decompression * Catheterisation for retention ## Footnote Timely intervention is crucial to preserve function and prevent permanent damage.

Question 83

What is the **pathophysiology** of mumps?

Answer 83

Paramyxovirus infection → replicates in salivary gland ducts ## Footnote This leads to inflammation and obstruction, causing painful bilateral parotid swelling.

Question 84

What is the **main reason** for not moving a victim suspected of having a spinal injury?

Answer 84

Risk of spinal cord laceration ## Footnote Moving the victim could exacerbate injuries and lead to permanent paralyzation.

Question 85

True or false: **Bacterial parotitis** typically presents with bilateral swelling.

Answer 85

FALSE ## Footnote Bacterial parotitis usually presents unilaterally with severe pain and purulent discharge.

Question 86

What is the **incubation period** for mumps?

Answer 86

2–3 weeks ## Footnote This is the time frame from exposure to the onset of symptoms.

Question 87

What serological marker indicates **immunity after hepatitis B vaccination**?

Answer 87

Hepatitis B surface antibody (anti-HBs) ## Footnote This marker confirms immunity following vaccination, as no natural infection occurred.

Question 88

True or false: **Anti-HBc** is a marker of immunity after vaccination.

Answer 88

FALSE ## Footnote Anti-HBc indicates previous infection and is never positive after vaccination.

Question 89

What is the **correct management** if anti-HBs titre is low?

Answer 89

Offer booster dose according to UK guidelines ## Footnote Especially important for healthcare workers.

Question 90

What type of carcinoma is indicated by a **pearly, translucent nodule** with rolled edges?

Answer 90

Basal Cell Carcinoma (BCC) ## Footnote Classic presentation includes slow growth and no itching or pain.

Question 91

List two **key characteristics** of Basal Cell Carcinoma (BCC).

Answer 91

* Slowly growing lesion * Pearly, translucent nodule with rolled edges ## Footnote Often found in sun-exposed areas and may have telangiectasia.

Question 92

What is the **first-line management** for Basal Cell Carcinoma (BCC)?

Answer 92

Excision with clear margins ## Footnote Alternatives include Mohs micrographic surgery for high-risk areas.

Question 93

Fill in the blank: Chronic **UV exposure** leads to DNA damage and mutations in the _______ gene, resulting in BCC.

Answer 93

PTCH1 ## Footnote This gene is a tumor-suppressor gene involved in the development of BCC.

Question 94

True or false: **Cherry angiomas** can be confused with Basal Cell Carcinoma due to their appearance.

Answer 94

FALSE ## Footnote Cherry angiomas are small red papules and do not have the pearly appearance of BCC.

Question 95

What is a common misconception about **non-pigmented lesions**?

Answer 95

They cannot be cancer ## Footnote Non-pigmented lesions can still be malignant, such as BCC.

Question 96

What is the **pathophysiology** of Basal Cell Carcinoma?

Answer 96

Chronic UV exposure leads to DNA damage and mutations in PTCH1 gene ## Footnote This results in uncontrolled basal cell proliferation.

Question 97

What is the **first-line antibiotic** for a penicillin-allergic woman with **community-acquired pneumonia (CAP)**?

Answer 97

Azithromycin ## Footnote Azithromycin is preferred for patients with penicillin allergy according to primary care guidelines.

Question 98

What are the **key symptoms** indicating pneumonia in the case presented?

Answer 98

* Productive cough * Fever * Shortness of breath * Crackles * Bronchial breathing in right lower zone ## Footnote These symptoms suggest consolidation in the lungs.

Question 99

True or false: A **history of asthma** changes the antibiotic choice for a patient with pneumonia.

Answer 99

FALSE ## Footnote The antibiotic choice remains the same regardless of asthma history.

Question 100

What is the **most common organism** associated with mild community-acquired pneumonia?

Answer 100

Streptococcus pneumoniae ## Footnote This bacterium is the most frequently identified pathogen in mild CAP cases.

Question 101

List the **common organisms** in mild CAP.

Answer 101

* Strep pneumoniae * H. influenzae * Mycoplasma pneumoniae ## Footnote These organisms are typically responsible for mild cases of community-acquired pneumonia.

Question 102

What is the **CURB-65 score** for mild pneumonia in the case presented?

Answer 102

0 ## Footnote A CURB-65 score of 0 indicates mild severity and supports outpatient management.

Question 103

Fill in the blank: If a patient is allergic to penicillin, the first-line treatment for mild CAP is _______.

Answer 103

azithromycin ## Footnote Azithromycin is recommended for patients with a penicillin allergy.

Question 104

Why is **co-amoxiclav** contraindicated for the patient in this case?

Answer 104

It is penicillin-based ## Footnote Patients with a penicillin allergy should avoid all penicillin-based antibiotics.

Question 105

What are the **safety netting** measures for patients with mild CAP?

Answer 105

* Worsening breathlessness * Fever lasting >48 hours * Confusion * Chest pain ## Footnote These measures help identify patients who may need further medical attention.

Question 106

What should be avoided in the treatment of pneumonia unless it is severe or atypicals are resistant?

Answer 106

Fluoroquinolones ## Footnote Fluoroquinolones have significant side effects and are not first-line treatments for mild CAP.

Question 107

What is the **pathophysiology** of community-acquired pneumonia?

Answer 107

Bacterial infection causing inflammation of lung parenchyma leading to consolidation ## Footnote This results in crackles and bronchial breathing sounds.

Question 108

What is the **risk** associated with choosing **clarithromycin** over azithromycin for patients with asthma?

Answer 108

Can prolong QT and interact ## Footnote Azithromycin is preferred to avoid these risks.

Question 109

What is the **significance** of a urticarial rash in relation to penicillin allergy?

Answer 109

Counts as a penicillin allergy ## Footnote Patients with urticarial rash should avoid penicillin-based antibiotics.

Question 110

What is the **correct answer** for the chronic alcohol use leading to severe anterograde amnesia and confabulation?

Answer 110

E – Korsakoff’s syndrome ## Footnote Key clues include chronic alcohol use, severe anterograde amnesia, and confabulation.

Question 111

What are the **key signs** of Korsakoff’s syndrome?

Answer 111

* Chronic alcohol use * Severe anterograde amnesia * Confabulation * Other cognition intact early * Signs of chronic liver disease * Anosognosia ## Footnote These signs indicate a long-standing memory disorder following Wernicke’s encephalopathy.

Question 112

What is the **pathophysiology** of Korsakoff’s syndrome?

Answer 112

* Chronic alcohol use * Thiamine deficiency * Damage to mammillary bodies * Damage to thalamus * Damage to limbic system ## Footnote This leads to Korsakoff’s syndrome, a chronic amnestic disorder.

Question 113

What is the **management** for Korsakoff’s syndrome?

Answer 113

* High-dose IV thiamine (Pabrinex) * Abstinence from alcohol * Nutritional support * Long-term cognitive therapy ## Footnote Korsakoff’s syndrome is often only partially reversible.

Question 114

True or false: **Wernicke’s encephalopathy** is a chronic memory disorder.

Answer 114

FALSE ## Footnote Wernicke’s encephalopathy is characterized by an acute triad: confusion, ataxia, and ophthalmoplegia.

Question 115

What distinguishes **Korsakoff’s syndrome** from **Alzheimer’s disease**?

Answer 115

* Korsakoff’s: selective memory dysfunction * Alzheimer’s: progressive global cognitive decline ## Footnote Confabulation is much more characteristic of Korsakoff’s syndrome.

Question 116

What are the **common traps** in diagnosing Korsakoff’s syndrome?

Answer 116

* Confusing Wernicke’s (acute) vs Korsakoff’s (chronic) * Thinking confabulation = Alzheimer’s * Assuming alcoholic dementia = global impairment ## Footnote Korsakoff’s syndrome is characterized by selective memory loss.

Question 117

Fill in the blank: **Chronic alcohol use + amnesia + confabulation = _______.**

Answer 117

Korsakoff’s syndrome ## Footnote This condition is associated with thiamine deficiency.

Question 118

What mnemonic can help remember the differences between **Wernicke’s** and **Korsakoff’s**?

Answer 118

WERnicke is WAR → acute chaos; Korsakoff is ‘KONstructed stories’ → confabulation ## Footnote This mnemonic highlights the acute vs chronic nature of the conditions.

Question 119

What causes **thiamine deficiency** in chronic alcohol use?

Answer 119

* Malnutrition * Malabsorption * Impaired hepatic activation ## Footnote Thiamine deficiency is a significant consequence of chronic alcohol consumption.

Question 120

Which enzymes are disabled by **thiamine deficiency**?

Answer 120

* Pyruvate dehydrogenase * α-ketoglutarate dehydrogenase * Transketolase ## Footnote The inhibition of these enzymes leads to metabolic disturbances.

Question 121

What are the consequences of thiamine deficiency on cerebral metabolism?

Answer 121

* Cerebral ATP failure * Lactate accumulation * Oxidative stress * Blood–brain barrier breakdown ## Footnote These consequences contribute to neurological damage.

Question 122

What type of brain injury is caused by acute thiamine deficiency?

Answer 122

Wernicke’s encephalopathy ## Footnote This condition can lead to severe neurological symptoms if untreated.

Question 123

What evolves from untreated Wernicke’s encephalopathy?

Answer 123

Korsakoff amnestic syndrome ## Footnote This syndrome is characterized by profound anterograde amnesia and confabulation.

Question 124

What are the key features of **Korsakoff amnestic syndrome**?

Answer 124

* Profound anterograde amnesia * Confabulation ## Footnote Korsakoff syndrome results from untreated Wernicke’s encephalopathy.

Question 125

What areas of the brain are affected by **symmetrical hemorrhagic necrosis** due to thiamine deficiency?

Answer 125

* Mammillary bodies * Medial thalamus * Limbic structures ## Footnote Damage to these areas is associated with memory and emotional processing.

Question 126

Positional inspiratory stridor in a thriving neonate is caused by {{c1::______}} affecting the {{c2::______}}.

Answer 126

laryngomalacia ## Footnote Stridor that worsens supine and improves upright is classic for laryngomalacia.

Question 127

What is the **first-line antihypertensive** for a 58-year-old African-Caribbean man with persistent hypertension?

Answer 127

Amlodipine ## Footnote Ethnicity drives drug choice; calcium channel blockers are preferred for Black patients.

Question 128

True or false: **Beta-blockers** are considered first-line treatment for hypertension in African-Caribbean patients.

Answer 128

FALSE ## Footnote Beta-blockers are not first-line; calcium channel blockers are preferred.

Question 129

In the management of hypertension, what is the preferred treatment for patients aged **≥55** or of **Black ethnicity**?

Answer 129

Calcium channel blocker (Amlodipine) ## Footnote This is part of NICE Hypertension Step 1 guidelines.

Question 130

What condition is characterized by **immature, soft supraglottic cartilage** collapsing inward during inspiration?

Answer 130

Laryngomalacia ## Footnote This condition leads to narrowing of the airway and positional stridor.

Question 131

Fill in the blank: **Stridor** that worsens when lying flat and improves when upright is classic for _______.

Answer 131

laryngomalacia ## Footnote This condition typically resolves spontaneously by 18–24 months.

Question 132

What are the **indications for referral** to ENT in cases of laryngomalacia?

Answer 132

* Poor feeding * Failure to thrive * Apnoea or cyanosis * Severe cases ## Footnote Severe cases may require supraglottoplasty.

Question 133

What common mistake involves confusing **tracheomalacia** with laryngomalacia?

Answer 133

Confusing expiratory stridor with inspiratory stridor ## Footnote Tracheomalacia causes expiratory stridor, while laryngomalacia causes inspiratory stridor.

Question 134

What mnemonic can help remember that **Black patients** should start with a calcium channel blocker for hypertension?

Answer 134

'BLACK → BLOCK the calcium!' ## Footnote This emphasizes that Black patients should receive calcium channel blockers first-line.

Question 135

Live head lice infestation is first-line treated with {{c1::______}}.

Answer 135

permethrin 5% ## Footnote White oval eggs stuck to hair shafts are called nits.

Question 136

The classic triad of **Haemolytic uraemic syndrome (HUS)** includes ______, ______, and ______.

Answer 136

* Bloody diarrhoea * Thrombocytopenia * Acute kidney injury ## Footnote This condition often follows an infection with E. coli O157.

Question 137

True or false: **Antibiotics** should be given to a child with HUS.

Answer 137

FALSE ## Footnote Antibiotics can worsen the condition.

Question 138

What are the **key symptoms** of HUS in a child?

Answer 138

* Bloody diarrhoea * Abdominal pain * Vomiting * Low haemoglobin * Thrombocytopenia * Raised urea and creatinine ## Footnote These symptoms indicate a classic presentation of HUS.

Question 139

In the management of HUS, what is the primary treatment approach?

Answer 139

Supportive care ## Footnote This includes IV fluids and electrolyte monitoring, with dialysis if severe renal failure occurs.

Question 140

What is the **pathophysiology** of HUS?

Answer 140

Shiga toxin from E. coli O157 causes endothelial damage leading to microangiopathic haemolytic anaemia, thrombocytopenia, and acute kidney injury ## Footnote This sequence of events is critical in understanding HUS.

Question 141

What is a common mistake when treating HUS?

Answer 141

Giving antibiotics ## Footnote This can exacerbate the condition and lead to worse outcomes.

Question 142

The mnemonic for remembering HUS is **HUS = Hamburger → Urea ↑ → Small platelets**. What does this represent?

Answer 142

HUS is associated with undercooked meat leading to increased urea and low platelet count ## Footnote This helps in recalling the condition's association with E. coli O157.

Question 143

The **smoking cessation drug** contraindicated in epilepsy is __________.

Answer 143

bupropion ## Footnote Best alternative after NRT failure is varenicline.

Question 144

In a patient with hair thinning and microcytic anaemia, the most likely diagnosis is __________.

Answer 144

iron deficiency anaemia ## Footnote Confirmed by low ferritin and low Hb.

Question 145

The **first-line options** for smoking cessation include __________.

Answer 145

* Nicotine Replacement Therapy (NRT) * Varenicline ## Footnote If NRT fails and epilepsy is present, varenicline is the safest effective next step.

Question 146

True or false: Varenicline is contraindicated in patients with a history of seizures.

Answer 146

FALSE ## Footnote Varenicline is safe for smoking cessation in patients with epilepsy.

Question 147

The **most common side effect** of varenicline is __________.

Answer 147

nausea ## Footnote Monitoring for mood changes and sleep disturbances is also important.

Question 148

In the context of iron deficiency anaemia, low ferritin indicates __________.

Answer 148

iron deficiency ## Footnote It is the most sensitive early marker for iron deficiency.

Question 149

The **pathophysiology** of iron deficiency leads to __________.

Answer 149

* Microcytic, hypochromic RBCs * Reduced oxygen delivery ## Footnote This results in symptoms like fatigue and hair thinning.

Question 150

What are the **key symptoms** of ADHD in children? List at least three.

Answer 150

* Unable to sit still * Poor concentration * Impulsivity ## Footnote Symptoms must be present at school and home for diagnosis.

Question 151

The **first-line drug** for moderate–severe ADHD is __________.

Answer 151

methylphenidate ## Footnote It is important to monitor BP, heart rate, weight, and growth.

Question 152

The **pathophysiology** of ADHD involves dysregulation of __________.

Answer 152

* dopamine * noradrenaline ## Footnote This affects impulse control and attention regulation.

Question 153

What is the **correct answer** for the condition described as diplopia and inability to abduct the eye?

Answer 153

E – Cranial nerve VI palsy (Abducens nerve palsy) ## Footnote This condition is characterized by double vision and inability to move the eye laterally.

Question 154

What type of **diplopia** is indicated by two identical images side-by-side?

Answer 154

Horizontal diplopia ## Footnote This occurs when the lateral rectus muscle is affected.

Question 155

What muscle is responsible for **abduction** of the eye?

Answer 155

Lateral rectus muscle ## Footnote Innervated by cranial nerve VI (Abducens nerve).

Question 156

What are the **key clues** indicating CN VI palsy?

Answer 156

* Double vision (diplopia) * Unable to abduct the left eye past midline * Worse diplopia when looking toward affected side ## Footnote These clues help differentiate CN VI palsy from other cranial nerve palsies.

Question 157

What are some **common causes** of CN VI palsy?

Answer 157

* Diabetes * Hypertension * Raised intracranial pressure (ICP) ## Footnote CN VI palsy is commonly affected in cases of raised ICP due to its long intracranial course.

Question 158

True or false: A **CN II palsy** causes diplopia.

Answer 158

FALSE ## Footnote CN II palsy causes vision loss, not diplopia.

Question 159

What are the **characteristics** of a CN III palsy?

Answer 159

* 'Down and out' eye * Ptosis * Dilated pupil ## Footnote These symptoms are distinct from CN VI palsy.

Question 160

What type of diplopia is associated with **CN IV palsy**?

Answer 160

Vertical diplopia ## Footnote This type of diplopia is worse on stairs.

Question 161

What is the **management** for CN VI palsy due to raised ICP?

Answer 161

* Identify and treat underlying cause * Urgent neuroimaging ## Footnote Management may also include temporary measures like an eye patch or prisms for diplopia.

Question 162

What is a common **trap** when diagnosing CN VI palsy?

Answer 162

Confusing CN VI (horizontal diplopia) with CN IV (vertical diplopia) ## Footnote It's important to remember that raised ICP commonly causes CN VI palsy first.

Question 163

What is the mnemonic for remembering the function of CN VI?

Answer 163

Six lets your eye go to the SIDE ## Footnote This helps recall that CN VI is responsible for lateral eye movement.

Question 164

What is the **first-line treatment** of hyperthyroidism in the **1st trimester**?

Answer 164

Propylthiouracil (PTU) ## Footnote Carbimazole is avoided early due to aplasia cutis.

Question 165

True or false: **Carbimazole** is safe to use in the **1st trimester** of pregnancy.

Answer 165

FALSE ## Footnote Carbimazole is associated with fetal scalp defects (aplasia cutis) in the 1st trimester.

Question 166

What is the **most common cause** of hyperthyroidism in early pregnancy?

Answer 166

Graves disease ## Footnote hCG crosses the placenta and stimulates TSH receptors.

Question 167

List the **risks** associated with excess T3/T4 in maternal health during pregnancy.

Answer 167

* Miscarriage * Pre-eclampsia ## Footnote Excessive thyroid hormones can lead to serious complications for the mother.

Question 168

What is the **gold-standard investigation** for assessing fragility fracture risk in postmenopausal women?

Answer 168

DEXA scan ## Footnote A T-score ≤ –2.5 confirms osteoporosis.

Question 169

Fill in the blank: A **T-score** of ≤ _______ indicates osteoporosis.

Answer 169

-2.5 ## Footnote This measurement is obtained through a DEXA scan.

Question 170

What are the **common traps** in managing hyperthyroidism during pregnancy?

Answer 170

* Giving carbimazole in 1st trimester * Choosing radioiodine * Reassuring despite elevated free T3/T4 ## Footnote These mistakes can lead to serious complications for both mother and fetus.

Question 171

What are the **key factors** in assessing fragility fracture risk?

Answer 171

* Age (67 years) * Postmenopausal status * Low-impact fractures * Long-term corticosteroid use * Low BMI ## Footnote These factors significantly increase the risk of secondary osteoporosis.

Question 172

What is the **pathophysiology** behind post-menopausal osteoporosis?

Answer 172

* Estrogen loss increases osteoclast activity * Steroids decrease osteoblast function and calcium absorption ## Footnote This results in decreased bone mineral density and increased fragility fractures.

Question 173

What should be avoided in the management of hyperthyroidism during pregnancy?

Answer 173

* Block-and-replace regimens * Radioiodine at all stages ## Footnote These approaches can pose significant risks to the developing fetus.

Question 174

What is the **first-line treatment** for **Prinzmetal (vasospastic) angina**?

Answer 174

Calcium channel blockers (diltiazem, verapamil, or long-acting nifedipine). Avoid beta-blockers. ## Footnote Management includes nitrates for acute relief and smoking cessation.

Question 175

What are the **key clues** from the stem indicating Prinzmetal angina?

Answer 175

* Recurrent rest pain, especially at night * Transient ST-elevation during pain * Normal ECG when asymptomatic * Normal troponin * Pain resolves spontaneously * Occurs both at rest and exertion ## Footnote Often triggered by cold, stress, cocaine, or hyperventilation.

Question 176

True or false: **Beta-blockers** are recommended for the treatment of Prinzmetal angina.

Answer 176

FALSE ## Footnote Beta-blockers can worsen vasospasm due to unopposed alpha activity.

Question 177

What is the **pathophysiology** of Prinzmetal angina?

Answer 177

Transient coronary artery smooth muscle spasm → temporary myocardial ischemia. ## Footnote Causes ST-elevation but no myocyte necrosis, thus troponins remain normal.

Question 178

What are the **common traps** associated with Prinzmetal angina?

Answer 178

* ST-elevation does NOT always indicate MI * Normal troponin differentiates from MI * Beta blockers worsen vasospasm ## Footnote Prinzmetal angina causes transient ST elevation.

Question 179

What is the **key symptom** of a **Pancoast tumour**?

Answer 179

Progressive shoulder + arm pain ## Footnote Ulnar nerve distribution involvement and Horner’s syndrome are also key indicators.

Question 180

What are the **key clues** from the stem indicating a Pancoast tumour?

Answer 180

* Heavy smoker * Ulnar nerve distribution (C8–T1 involvement) * Ptosis + miosis + anhidrosis → Horner’s syndrome * Weak hand muscles * CXR shows apical mass ## Footnote Symptoms may worsen at night and may include weight loss.

Question 181

What is the **management** for a Pancoast tumour?

Answer 181

* CT chest and MRI apex for staging * Biopsy (CT-guided) * Treatment = combined radiotherapy + chemotherapy * Possible surgical resection in selected cases ## Footnote Most Pancoast tumours are non-small cell lung cancer, typically squamous cell.

Question 182

True or false: **Thoracic outlet syndrome** causes Horner’s syndrome.

Answer 182

FALSE ## Footnote Thoracic outlet syndrome does not cause Horner’s syndrome, which is a key differentiator.

Question 183

What does the mnemonic **'SPASM'** stand for in relation to Prinzmetal angina?

Answer 183

* S – ST elevation transient * P – Pain at rest, esp. night * A – Avoid beta-blockers * S – Smoking associated * M – Managed with calcium channel blockers ## Footnote This mnemonic helps remember the key features of Prinzmetal angina.

Question 184

What does the mnemonic **'PANCOAST'** represent?

Answer 184

* P – Pain * A – Anhidrosis (Horner’s syndrome) * N – Nerve (ulnar nerve symptoms) * C – Cancer (lung cancer) * O – Onset (progressive) * A – Apical mass on CXR * S – Smoking history * T – Treatment (radiotherapy + chemotherapy) ## Footnote This mnemonic aids in recalling the characteristics of a Pancoast tumour.

Question 185

What is the **correct next step** for a patient with severe pneumonia, confusion, SpO₂ 87%, and BP 88/59?

Answer 185

Admit into a medical ward ## Footnote This is severe community-acquired pneumonia with sepsis and delirium.

Question 186

List the **key clues** from the stem indicating severe pneumonia.

Answer 186

* Fever 39.7°C * Productive cough + pleuritic chest pain * RR 33, SpO₂ 87%, BP 88/59 * Confused and agitated * Crackles on auscultation * Threatening statement about arson * Hypotension + hypoxia + tachycardia ## Footnote These clues suggest a serious medical condition requiring immediate attention.

Question 187

What does a **CURB-65 score** of ≥ 2 indicate?

Answer 187

Severe pneumonia ## Footnote It is a clinical prediction rule used to assess the severity of pneumonia.

Question 188

Fill in the blank: **Pneumonia** leads to _______ due to alveoli filled with inflammatory exudate.

Answer 188

impaired gas exchange ## Footnote This impairment results in hypoxia and subsequent confusion.

Question 189

What is the **management** protocol for severe pneumonia with sepsis?

Answer 189

* Immediate hospital admission * A–E assessment * High-flow oxygen * IV antibiotics within 1 hour * IV fluids for shock * Blood cultures, ABG, lactate * Consider ICU if not improving ## Footnote These steps are critical for managing severe pneumonia effectively.

Question 190

True or false: **Hypoxic delirium** can be mistaken for primary psychiatric illness.

Answer 190

TRUE ## Footnote It is important to treat the medical cause before addressing psychiatric symptoms.

Question 191

What is the **correct next step** for a diabetic patient with a QRISK of 15% and no prior cardiovascular disease?

Answer 191

Start atorvastatin 20 mg daily ## Footnote This is primary prevention in diabetes with QRISK > 10%.

Question 192

List the **indications** for starting a statin in a diabetic patient.

Answer 192

* Smoker with diabetes * Total cholesterol > 5 * Family history of early MI * Metabolic syndrome ## Footnote These factors increase cardiovascular risk and justify statin therapy.

Question 193

Fill in the blank: **Diabetes** leads to _______ dysfunction and increased risk of MI and stroke.

Answer 193

endothelial ## Footnote This dysfunction accelerates atherosclerosis.

Question 194

What is the **common trap** in managing diabetes and cardiovascular risk?

Answer 194

Treating BP before lipid risk ## Footnote Statins should be prioritized in patients with diabetes and elevated cardiovascular risk.

Question 195

What mnemonic can help remember the management steps for a patient with diabetes and QRISK ≥ 10%?

Answer 195

DIABETES + 10% = STATIN AGAIN ## Footnote This highlights the importance of starting statin therapy in these patients.

Question 196

What is the most likely diagnosis for a **painful penile ulcer** with a red inflamed base and burning sensation?

Answer 196

Herpes simplex virus infection ## Footnote Key clues include a single shallow ulcer, mild dysuria, and the ulcer appearing 3 days ago.

Question 197

List the **key clues** from the stem for the painful penile ulcer.

Answer 197

* Painful genital ulcer * Burning sensation * Single shallow ulcer * Red inflamed base * Appeared 3 days ago * Mild dysuria * No induration * No purulent discharge ## Footnote These clues help in diagnosing the condition.

Question 198

What are the **common traps** when diagnosing a painful penile ulcer?

Answer 198

* Assuming syphilis because of ulcer * Confusing chancroid with HSV * Thinking single ulcer excludes HSV ## Footnote Syphilis is classically painless, and early HSV lesions can be single.

Question 199

What is the **first line management** for herpes simplex virus infection?

Answer 199

Oral Aciclovir ## Footnote Management includes partner notification and counseling on recurrence.

Question 200

What does the mnemonic **HURT = HERPES** stand for?

Answer 200

* H – Hurts * E – Erythema * R – Recurrent * P – Prodrome * E – Epithelial ulcer * S – Sexually transmitted ## Footnote This mnemonic helps remember key features of herpes simplex virus infection.

Question 201

What is the most likely diagnosis for **chronic steroid use** with progressive weight-bearing hip pain?

Answer 201

Avascular necrosis of the femoral head ## Footnote Key clues include long-term oral prednisolone use and improvement of pain with rest.

Question 202

List the **key clues** from the stem for avascular necrosis of the femoral head.

Answer 202

* Long-term oral prednisolone (18 months) * Progressive hip pain * Worse with weight-bearing * Improves with rest * Reduced range of motion * No trauma history ## Footnote These clues indicate the likelihood of avascular necrosis.

Question 203

What are the **common traps** when diagnosing avascular necrosis?

Answer 203

* Confusing with osteoarthritis due to age * Missing steroid risk factor * Thinking improvement with rest excludes serious disease ## Footnote Improvement with rest does not rule out serious conditions.

Question 204

What is the **diagnostic gold standard** for avascular necrosis?

Answer 204

MRI ## Footnote MRI is essential for confirming the diagnosis.

Question 205

What does the mnemonic **STEROIDS KILL THE HIP** stand for?

Answer 205

* S – Steroids * T – Trauma absent * H – Hip pain * I – Ischemia * P – Prosthetic joint eventually needed ## Footnote This mnemonic helps remember key aspects of avascular necrosis related to steroid use.

Question 206

What is the **next step** in management for a patient with **fall + flank bruising + visible haematuria**?

Answer 206

CT abdomen & pelvis with contrast ## Footnote This is the **gold standard** for assessing renal or retroperitoneal injury.

Question 207

What does **macroscopic haematuria** suggest in the context of trauma?

Answer 207

Renal or retroperitoneal injury ## Footnote It indicates potential bleeding into the collecting system due to blunt trauma.

Question 208

List the **common traps** in trauma management regarding imaging.

Answer 208

* Ordering ultrasound first in trauma * Choosing IVP (obsolete) * Assuming haematuria always comes from bladder ## Footnote These misconceptions can lead to inappropriate management decisions.

Question 209

What is the **pathophysiology** of macroscopic haematuria following blunt trauma?

Answer 209

* Renal parenchymal or vascular injury * Bleeding into collecting system * Resulting in macroscopic haematuria ## Footnote This sequence is critical for understanding the injury mechanism.

Question 210

What is the **correct diagnosis** for a 65-year-old vegan with **macrocytic anaemia + neuropathy + anti-intrinsic factor positive**?

Answer 210

Autoimmune destruction of gastric parietal cells ## Footnote This condition is known as **pernicious anaemia**.

Question 211

What are the **key clues** indicating pernicious anaemia?

Answer 211

* Fatigue * Paraesthesia * Difficulty walking * Sore tongue * Macrocytic anaemia (MCV 110) * Very low B12 * Anti-intrinsic factor antibodies positive ## Footnote These symptoms and lab findings are characteristic of the disease.

Question 212

Why is **dietary deficiency** not the cause of macrocytic anaemia in this patient?

Answer 212

Would not have anti-IF antibodies ## Footnote The presence of anti-intrinsic factor antibodies indicates an autoimmune process rather than a simple dietary issue.

Question 213

What is the **management** for pernicious anaemia?

Answer 213

* Lifelong IM hydroxocobalamin * 1 mg IM every 3 months (maintenance) * Treat before folate * Screen for autoimmune conditions ## Footnote Proper management is crucial to prevent neurological complications.

Question 214

What is the **mnemonic** for remembering the management of pernicious anaemia?

Answer 214

IF IS GONE → B12 IS DONE ## Footnote This helps recall the importance of intrinsic factor in vitamin B12 absorption.

Question 215

What is the **correct answer** for lateral elbow pain when gripping or lifting?

Answer 215

B. Tennis elbow (Lateral epicondylitis) ## Footnote Key clues include pain over the lateral epicondyle and pain worse with gripping/lifting tools.

Question 216

What age and profession is associated with the **key clues** for tennis elbow?

Answer 216

42-year-old carpenter ## Footnote This demographic often experiences repetitive gripping/forearm strain.

Question 217

What are the **pathognomonic** signs for lateral epicondylitis?

Answer 217

* Pain over lateral epicondyle * Pain worse with gripping/lifting tools * Pain reproduced with resisted wrist extension ## Footnote These signs are indicative of lateral epicondylitis.

Question 218

List some **other clues** that could appear in different stems for tennis elbow.

Answer 218

* Pain when shaking hands * Pain holding a coffee cup * Pain when lifting a kettle * Tenderness over extensor carpi radialis brevis insertion * Grip weakness ## Footnote These symptoms can help differentiate tennis elbow from other conditions.

Question 219

Why is **Golfer’s elbow** not the correct diagnosis?

Answer 219

Pain at medial epicondyle ## Footnote Golfer's elbow is characterized by pain on the inner side of the elbow, unlike tennis elbow.

Question 220

What is the distinguishing feature of **Olecranon bursitis**?

Answer 220

Swelling at posterior elbow ## Footnote This condition does not present with lateral pain.

Question 221

What symptoms are associated with **Radial nerve entrapment**?

Answer 221

Causes sensory changes + weakness ## Footnote It does not typically cause isolated lateral epicondyle tenderness.

Question 222

What type of pain is associated with an **Ulnar collateral ligament injury**?

Answer 222

Medial elbow pain; valgus stress pain ## Footnote This injury is common in throwing athletes.

Question 223

What is the **pathophysiology** of tennis elbow?

Answer 223

Overuse of wrist extensors → microtears of extensor carpi radialis brevis tendon at lateral epicondyle ## Footnote Repetitive strain leads to tendinopathy, not inflammation.

Question 224

What are the **management** strategies for tennis elbow?

Answer 224

* Activity modification – reduce gripping/lifting * Topical or oral NSAIDs * Physiotherapy – eccentric strengthening exercises * Counterforce brace * Steroid injection only if persistent * Surgery rarely needed ## Footnote These strategies are recommended by NICE / BNF.

Question 225

What is a **common trap** when diagnosing tennis elbow?

Answer 225

Confusing with golfer’s elbow (medial) ## Footnote This misdiagnosis can lead to inappropriate treatment.

Question 226

What should not be assumed about a patient who is a **manual worker**?

Answer 226

Assuming nerve entrapment ## Footnote This assumption can lead to misdiagnosis.

Question 227

Is **ordering imaging** necessary for tennis elbow?

Answer 227

Rarely needed ## Footnote Imaging is not typically required for diagnosis.

Question 228

What is the **mnemonic** for remembering tennis elbow?

Answer 228

Tennis = racquet backhand → wrist extension strain → lateral pain ## Footnote This mnemonic helps recall the mechanism of injury.

Question 229

What is the **flashcard** for tennis elbow?

Answer 229

Pain at lateral epicondyle + worse with resisted wrist extension ## Footnote This summarizes the key symptoms of tennis elbow.

Question 230

What is the **diagnostic test** for a low-pitched diastolic murmur at the apex with a history of rheumatic fever?

Answer 230

Echocardiogram ## Footnote This test is crucial for diagnosing **mitral stenosis**, characterized by a low-pitched rumbling diastolic murmur.

Question 231

What are the **key clues** from the stem indicating mitral stenosis?

Answer 231

* 68-year-old woman * Breathlessness on exertion * Fatigue * Recurrent palpitations * Persistent cough worse at night * Low-pitched rumbling diastolic murmur at the apex ## Footnote These symptoms suggest pulmonary congestion due to mitral stenosis.

Question 232

True or false: A **chest X-ray** is diagnostic for mitral stenosis.

Answer 232

FALSE ## Footnote A chest X-ray may show changes but is not diagnostic for mitral stenosis.

Question 233

What is the **pathophysiology** of mitral stenosis?

Answer 233

* Rheumatic fever causes scarring and fusion of mitral valve leaflets * Narrowed valve increases left atrial pressure * Leads to pulmonary congestion and dyspnea * Atrial fibrillation develops due to left atrial dilation ## Footnote Understanding the pathophysiology helps in managing the condition effectively.

Question 234

What are the **management options** for mitral stenosis?

Answer 234

* Echocardiogram for diagnosis * Rate control in AF: beta-blockers or rate-limiting CCB * Anticoagulate if AF * Consider percutaneous balloon valvotomy if symptomatic * Surgery for severe cases ## Footnote Management strategies depend on the severity and symptoms of mitral stenosis.

Question 235

What are the **common traps** in diagnosing mitral stenosis?

Answer 235

* Confusing diastolic murmur with aortic regurgitation * Assuming palpitations indicate arrhythmia without confirming valve disease * Ordering chest X-ray before echocardiogram ## Footnote Awareness of these traps can prevent misdiagnosis.

Question 236

What is the **diagnosis** for a 55-year-old man with acute symptoms, pancytopenia, elevated WCC, and blast cells?

Answer 236

Acute Myeloid Leukemia (AML) ## Footnote This diagnosis is supported by the presence of blast cells and acute presentation.

Question 237

What are the **key clues** indicating Acute Myeloid Leukemia (AML)?

Answer 237

* 55-year-old man * 2-week history of fatigue, fever, easy bruising * Pale with multiple bruises * Nosebleeds * High WCC with blast cells present ## Footnote These symptoms are classic for AML, indicating rapid clonal expansion of immature myeloid blasts.

Question 238

What is the **pathophysiology** of Acute Myeloid Leukemia (AML)?

Answer 238

* Rapid clonal expansion of immature myeloid blasts * Bone marrow failure leads to anemia, neutropenia, thrombocytopenia * Circulating blasts replace normal cells ## Footnote Understanding the pathophysiology is essential for effective treatment.

Question 239

What are the **management steps** for Acute Myeloid Leukemia (AML)?

Answer 239

* Immediate hematology referral * Confirm with bone marrow biopsy * Induction chemotherapy: Cytarabine + anthracycline * Consolidation therapy * Stem cell transplant in eligible patients ## Footnote Supportive care includes platelet transfusions and aggressive treatment of infections.

Question 240

True or false: **Aplastic anemia** can be mistaken for acute leukemia.

Answer 240

TRUE ## Footnote The presence of blasts differentiates acute leukemia from aplastic anemia.

Question 241

What is the **classic triad** of Multiple Myeloma?

Answer 241

* Hypercalcaemia * Renal impairment * Anaemia ## Footnote This triad is often referred to as CRAB.

Question 242

What does a **bone marrow biopsy** finding of excess plasma cells indicate?

Answer 242

Multiple Myeloma ## Footnote A diagnosis is confirmed when plasma cells exceed 10%.

Question 243

True or false: **Hypercalcaemia** is a symptom of Multiple Myeloma.

Answer 243

TRUE ## Footnote Hypercalcaemia occurs due to cytokines stimulating osteoclasts.

Question 244

What are the **common management** strategies for Multiple Myeloma?

Answer 244

* Chemotherapy: Bortezomib + lenalidomide + dexamethasone * Bisphosphonates for bone disease * Hydration + steroids for hypercalcaemia * Consider autologous stem cell transplant ## Footnote Management follows NICE/BNF guidelines.

Question 245

What is the **pathophysiology** of ACE-Inhibitor Angio-oedema?

Answer 245

ACE inhibitors prevent breakdown of bradykinin ## Footnote Increased bradykinin leads to increased vascular permeability and swelling.

Question 246

What is the **first step** in managing ACE-Inhibitor Angio-oedema?

Answer 246

Immediate cessation of ACE inhibitor ## Footnote Airway protection is crucial as the condition can deteriorate quickly.

Question 247

Fill in the blank: **ACE-inhibitor angio-oedema** is mediated by _______.

Answer 247

bradykinin ## Footnote This condition is non-allergic and non-IgE mediated.

Question 248

What are the **key symptoms** of ACE-Inhibitor Angio-oedema?

Answer 248

* Lip swelling * Tongue swelling * Difficulty speaking * No rash or itching ## Footnote Symptoms can progress to airway obstruction.

Question 249

Why is **adrenaline** not effective in treating ACE-Inhibitor Angio-oedema?

Answer 249

It is not histamine-mediated ## Footnote This condition requires different management strategies.

Question 250

What is the **common trap** regarding the timing of ACE-Inhibitor Angio-oedema?

Answer 250

Assuming it occurs immediately after starting medication ## Footnote ACE-induced angio-oedema can appear weeks to years later.

Question 251

What is the **most likely diagnosis** for a young man with recurrent visible haematuria 1–2 days after an upper respiratory tract infection and mild proteinuria?

Answer 251

IgA nephropathy ## Footnote Key clues include synpharyngitic haematuria, young adults, normal complement levels, and recurrent episodes. This condition is not post-streptococcal glomerulonephritis, which occurs weeks later.

Question 252

What are the **key clues** from the case stem for IgA nephropathy?

Answer 252

* 25-year-old male * Recurrent visible haematuria * Occurs 1–2 days after URTI * Mild proteinuria * Normal-ish BP (135/85) * Well between episodes ## Footnote The timing of symptoms is classic for IgA nephropathy.

Question 253

What is the **pathophysiology** of IgA nephropathy?

Answer 253

Immune dysregulation → IgA deposition in the glomerular mesangium ## Footnote This condition is often triggered by mucosal infections, such as upper respiratory tract infections, leading to recurrent, self-limited haematuria episodes.

Question 254

What management strategies are recommended for IgA nephropathy?

Answer 254

* BP control (ACE inhibitor/ARB) if proteinuria * Monitor renal function * Immunosuppression if rapidly progressive or nephrotic-range proteinuria * Refer to nephrology if: * Persistent proteinuria * Decline in eGFR * Diagnostic uncertainty ## Footnote Most patients have a benign course.

Question 255

True or false: **IgA nephropathy** typically presents with high blood pressure.

Answer 255

FALSE ## Footnote Early IgA nephropathy may not present with high blood pressure, which can lead to confusion with other forms of glomerulonephritis.

Question 256

What are the **common traps** when diagnosing IgA nephropathy?

Answer 256

* Confusing with post-streptococcal GN (occurs weeks later) * Assuming all glomerulonephritis causes high BP * Over-investigating with biopsy in mild, classic presentations ## Footnote These misconceptions can lead to misdiagnosis or unnecessary procedures.

Question 257

What is the **mnemonic** to remember the timing of IgA nephropathy symptoms?

Answer 257

IgA = Immediately after infection ## Footnote This highlights that symptoms occur 1–2 days after infection, not weeks.

Question 258

What are the **other clues** that might appear in a different question regarding IgA nephropathy?

Answer 258

* Synpharyngitic haematuria * Raised serum IgA * Episodes triggered by exercise * Normal complement levels * Possible Henoch–Schönlein purpura equivalent in children * Mesangial IgA deposition on biopsy ## Footnote These clues can help in identifying the condition in various clinical scenarios.

Question 259

What distinguishes **Goodpasture’s syndrome** from IgA nephropathy?

Answer 259

* Pulmonary haemorrhage * Rapidly progressive renal failure * Not episodic haematuria * Not infection-associated ## Footnote Goodpasture’s syndrome presents with more severe symptoms and is not linked to infections.

Question 260

What are the key features that differentiate **Alport syndrome** from IgA nephropathy?

Answer 260

* X-linked inheritance * Presents with hearing loss * Renal decline in childhood–adolescence * Not isolated recurrent haematuria ## Footnote Alport syndrome has distinct genetic and clinical features.

Question 261

What characterizes **membranous nephropathy** compared to IgA nephropathy?

Answer 261

* Nephrotic syndrome picture * Heavy proteinuria * Oedema * Not episodic haematuria ## Footnote Membranous nephropathy presents differently, with significant proteinuria and edema.