Clinical Medicine Flashcards

24 sample cards from the Medicine deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. How do gastric and duodenal ulcer pain typically relate to eating?

   Duodenal ulcer pain is classically relieved by eating and worsens 2–5 hours later / at night (hunger pain). Gastric ulcer pain is typically worsened by eating, often leading to weight loss/food avoidance.

2. What is the standard first-line eradication regimen for Helicobacter pylori (triple therapy)?

   A proton pump inhibitor plus two antibiotics for 7 days: typically a PPI + amoxicillin + clarithromycin (or metronidazole if penicillin-allergic). Bismuth-based quadruple therapy is used where clarithromycin resistance is high or as second-line.

3. Compare Crohn's disease and ulcerative colitis by location, depth, and histology.

   Crohn's: any part of the GI tract (mouth to anus), 'skip lesions', transmural inflammation, non-caseating granulomas, cobblestoning, fistulae. Ulcerative colitis: continuous from the rectum, limited to colon, mucosal/submucosal only, crypt abscesses, no granulomas, pseudopolyps.

4. Which extra-intestinal feature and smoking association distinguish Crohn's from ulcerative colitis?

   Smoking worsens Crohn's disease but is protective in ulcerative colitis. Primary sclerosing cholangitis is strongly associated with UC. Both share arthritis, erythema nodosum, uveitis; UC has a higher colorectal cancer risk with extensive long-standing disease.

5. What are the three most common causes of liver cirrhosis worldwide?

   Chronic alcohol-related liver disease, chronic viral hepatitis (hepatitis B and C), and non-alcoholic/metabolic-associated fatty liver disease (NAFLD/MASLD). Cirrhosis is irreversible fibrosis with regenerative nodules replacing normal liver architecture.

6. What parameters make up the Child-Pugh score for cirrhosis severity?

   Bilirubin, Albumin, Prothrombin time/INR, Ascites, and Encephalopathy ('BAP-AE'). Each scored 1–3; totals give class A (5–6), B (7–9), C (10–15), predicting mortality and surgical risk.

7. List key complications of decompensated liver cirrhosis.

   Portal hypertension leading to oesophageal varices (variceal bleeding), ascites and spontaneous bacterial peritonitis, hepatic encephalopathy, hepatorenal syndrome, coagulopathy, and hepatocellular carcinoma.

8. How are the routes of transmission of hepatitis A/E compared with B/C/D?

   Hepatitis A and E: faecal-oral (contaminated food/water), typically self-limiting acute infection. Hepatitis B, C, and D: blood-borne/parenteral, sexual, and vertical transmission; B and C can become chronic. Hepatitis D requires co-existing hepatitis B (uses HBsAg).

9. Interpret hepatitis B serology: HBsAg positive, anti-HBc IgG positive, HBeAg positive.

   HBsAg positive indicates active infection (>6 months = chronic). Anti-HBc IgG indicates past/ongoing exposure (not vaccination). HBeAg positive indicates high viral replication and high infectivity. Anti-HBs alone (with negative HBsAg) indicates immunity from vaccination or cleared infection.

10. What distinguishes an ischaemic from a haemorrhagic stroke, and why is imaging mandatory before treatment?

    Ischaemic stroke (~85%) is due to arterial occlusion (thrombus/embolus); haemorrhagic (~15%) is due to vessel rupture. A non-contrast CT head is mandatory to exclude haemorrhage before giving thrombolysis or antiplatelets, which would be dangerous in a bleed.

11. What is the treatment time window for IV thrombolysis (alteplase) and for mechanical thrombectomy in acute ischaemic stroke?

    IV thrombolysis: within 4.5 hours of symptom onset (if no contraindications). Mechanical thrombectomy: up to 6 hours for large-vessel occlusion, extendable to 24 hours in selected patients with favourable perfusion imaging. 'Time is brain'.

12. Give the ABCD² score components used to assess stroke risk after a TIA.

    Age $\geq 60$ (1), Blood pressure $\geq 140/90$ (1), Clinical features (unilateral weakness 2, speech disturbance without weakness 1), Duration ($\geq 60$ min 2, 10–59 min 1), Diabetes (1). Higher scores predict higher early stroke risk.

13. Define epilepsy and distinguish focal from generalized seizures.

    Epilepsy is a tendency to recurrent, unprovoked seizures (typically $\geq 2$ seizures >24h apart, or one with high recurrence risk). Focal seizures start in one hemisphere (with/without impaired awareness). Generalized seizures involve both hemispheres from onset (e.g. tonic-clonic, absence, myoclonic).

14. What is status epilepticus, and what is its first-line pharmacological treatment?

    Status epilepticus: a seizure lasting $\geq 5$ minutes, or recurrent seizures without recovery of consciousness between them. First-line: a benzodiazepine (IV lorazepam, or buccal midazolam/rectal diazepam); second-line IV levetiracetam, phenytoin, or valproate.

15. Which first-line antiepileptic drugs are preferred for focal versus generalized tonic-clonic seizures, and which is teratogenic?

    Focal seizures: lamotrigine or levetiracetam first-line. Generalized tonic-clonic: sodium valproate (males) or lamotrigine/levetiracetam. Sodium valproate is highly teratogenic and avoided in women of childbearing potential. Carbamazepine can worsen absence/myoclonic seizures.

16. What is the pathological hallmark and neurotransmitter deficit in Parkinson's disease?

    Progressive loss of dopaminergic neurons in the substantia nigra pars compacta, with intracytoplasmic Lewy bodies (α-synuclein aggregates). This causes a dopamine deficit in the nigrostriatal pathway of the basal ganglia.

17. State the classic motor triad of Parkinson's disease and its characteristic tremor.

    Bradykinesia, rigidity ('cogwheel' / 'lead-pipe'), and a resting tremor (classically 4–6 Hz 'pill-rolling', asymmetrical, worse at rest, improved by movement). Postural instability is a fourth cardinal feature. The syndrome is typically asymmetrical at onset.

18. What is the first-line and most effective medical treatment for Parkinson's disease, and a key long-term complication?

    Levodopa (with a peripheral dopa-decarboxylase inhibitor such as carbidopa or benserazide) is most effective for motor symptoms. Long-term use causes motor fluctuations ('wearing off', 'on-off' phenomena) and dyskinesias.

19. Define multiple sclerosis and the concept of dissemination in time and space.

    MS is a chronic autoimmune, T-cell-mediated demyelinating disease of the CNS. Diagnosis requires demonstrating lesions disseminated in space (different CNS locations) and in time (occurring at different times), reflecting relapsing episodes of neurological dysfunction.

20. Name two classic clinical signs of multiple sclerosis and the key CSF finding.

    Optic neuritis (painful visual loss), internuclear ophthalmoplegia, Lhermitte's sign (electric-shock sensation on neck flexion), and Uhthoff's phenomenon (symptoms worse with heat). CSF shows oligoclonal IgG bands not present in serum. MRI shows periventricular white-matter plaques.

21. How is acute kidney injury (AKI) defined by KDIGO criteria?

    Any of: a rise in serum creatinine $\geq 26.5\,\mu mol/L$ within 48 hours; a rise in creatinine $\geq 1.5\times$ baseline within 7 days; or urine output $< 0.5\,mL/kg/h$ for $\geq 6$ hours. It is an abrupt decline in renal function.

22. Classify the causes of AKI into pre-renal, intrinsic (renal), and post-renal with an example of each.

    Pre-renal: reduced perfusion (hypovolaemia, sepsis, heart failure). Intrinsic/renal: acute tubular necrosis, glomerulonephritis, interstitial nephritis, nephrotoxins. Post-renal: obstruction (stones, prostatic enlargement, tumour). Pre-renal is the most common cause.

23. How is chronic kidney disease staged by eGFR, and what defines the diagnosis?

    CKD = reduced kidney function ($eGFR < 60\,mL/min/1.73m^2$) and/or markers of damage (e.g. albuminuria) for $\geq 3$ months. G1 $\geq 90$; G2 60–89; G3a 45–59; G3b 30–44; G4 15–29; G5 $< 15$ (kidney failure). Staged also by albuminuria (A1–A3).

24. What are the emergency indications for dialysis in kidney failure (mnemonic 'AEIOU')?

    Acidosis (severe metabolic, refractory), Electrolyte disturbance (refractory hyperkalaemia), Intoxication (dialysable toxins, e.g. lithium, salicylates), Overload (refractory fluid/pulmonary oedema), Uraemia (encephalopathy, pericarditis). These represent life-threatening complications unresponsive to medical therapy.

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