Professional and Linguistic Assessments Board (PLAB) Medicine and Acute Care Flashcards

24 sample cards from the Medicine and Acute Care deck

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

1. What are the diagnostic glucose thresholds for diabetes mellitus and the role of HbA1c?

   Diabetes: fasting glucose $\geq 7.0$ mmol/L, random/2-hour OGTT glucose $\geq 11.1$ mmol/L, or $\text{HbA1c} \geq 48$ mmol/mol (6.5%). In asymptomatic patients two abnormal results are required. HbA1c reflects average glycaemia over $\approx$ 2-3 months.

2. What biochemical features define diabetic ketoacidosis (DKA) and its key management steps?

   Diagnostic triad: blood glucose $> 11$ mmol/L (or known diabetes), ketonaemia $\geq 3$ mmol/L (or ketonuria $\geq 2+$), and acidosis with $\text{pH} < 7.3$ or bicarbonate $< 15$ mmol/L. Management: IV 0.9% saline fluid resuscitation first, then fixed-rate insulin infusion, careful potassium replacement, and treat the precipitant.

3. Contrast the typical thyroid function test results in primary hypothyroidism and primary hyperthyroidism.

   Primary hypothyroidism: high TSH with low free T4 (e.g. Hashimoto's, anti-TPO antibodies). Primary hyperthyroidism: low/suppressed TSH with high free T4 and/or T3 (e.g. Graves' disease, TSH-receptor antibodies). In secondary (pituitary) disease TSH is inappropriately normal/low with low T4.

4. What is the classic biochemistry of Addison's disease (primary adrenal insufficiency), and what test confirms it?

   Hyponatraemia, hyperkalaemia, hypoglycaemia, and metabolic acidosis, often with raised ACTH and skin hyperpigmentation. The short Synacthen (ACTH stimulation) test confirms it: cortisol fails to rise adequately after synthetic ACTH. An Addisonian crisis is treated with IV hydrocortisone and fluids.

5. How are the causes of hyponatraemia classified by volume status?

   Hypovolaemic: D&V, diuretics, Addison's (renal/extra-renal sodium loss). Euvolaemic: SIADH (urine osmolality high, urine sodium $> 20$), hypothyroidism, glucocorticoid deficiency. Hypervolaemic: heart failure, cirrhosis, nephrotic syndrome, renal failure. Urine osmolality and urine sodium help localise the cause.

6. How do you classify a metabolic acidosis using the anion gap, and what is the formula?

   Anion gap $= [\text{Na}^+] - ([\text{Cl}^-] + [\text{HCO}_3^-])$ (normal $\approx 8-12$ mmol/L). Raised anion gap acidosis (MUDPILES: methanol, uraemia, DKA, lactate etc.) reflects added acid; normal anion gap (hyperchloraemic) acidosis reflects bicarbonate loss (diarrhoea, renal tubular acidosis).

7. What time-critical assessment tool is used in suspected acute stroke, and what is the thrombolysis window?

   FAST (Face, Arm, Speech, Time) in the community and ROSIER in hospital. After excluding haemorrhage with a non-contrast CT head, IV thrombolysis (alteplase/tenecteplase) is given within 4.5 hours of symptom onset; mechanical thrombectomy is considered for large-vessel occlusion up to 24 hours in selected patients.

8. What features differentiate the most common primary headache disorders: migraine, tension-type and cluster headache?

   Migraine: unilateral, throbbing, 4-72 hours, with nausea, photophobia/phonophobia $\pm$ aura. Tension-type: bilateral, pressing/tight, non-pulsatile, no significant nausea. Cluster: severe unilateral periorbital pain in clusters, 15-180 minutes, with ipsilateral autonomic features (lacrimation, rhinorrhoea, ptosis) and restlessness.

9. What is the definition of status epilepticus and its first-line emergency management?

   A seizure lasting $\geq 5$ minutes, or repeated seizures without recovery of consciousness in between. Management: ABCDE, oxygen, check glucose; first-line is IV lorazepam (or buccal midazolam/PR diazepam in the community), repeated once; second-line IV levetiracetam, phenytoin or valproate; then general anaesthesia/ICU if refractory.

10. What are the key clinical and CSF findings that distinguish bacterial from viral meningitis?

    Bacterial: cloudy/turbid CSF, high neutrophils (polymorphs), high protein, low glucose (CSF:serum ratio $< 0.4$ to $0.6$), high opening pressure. Viral: clear CSF, lymphocytosis, normal/mildly raised protein, and normal glucose. Give empirical IV ceftriaxone immediately for suspected bacterial meningitis (plus dexamethasone).

11. What are the components of the Glasgow Coma Scale and the score that defines the need for airway protection?

    Eye opening (max 4), Verbal response (max 5), Motor response (max 6); total range 3-15. A GCS $\leq 8$ indicates a significantly reduced conscious level and usually warrants definitive airway protection (intubation).

12. What is the qSOFA score, and what threshold indicates a high risk of poor outcome in suspected sepsis?

    qSOFA (quick SOFA) uses: respiratory rate $\geq 22$/min, altered mentation (GCS $< 15$), and systolic BP $\leq 100$ mmHg. A score $\geq 2$ identifies patients at higher risk of mortality and prompts escalation. Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection.

13. What are the elements of the 'Sepsis Six' bundle to be delivered within the first hour?

    Three IN: high-flow oxygen, IV broad-spectrum antibiotics, IV fluid resuscitation. Three OUT (measure): blood cultures (before antibiotics), serum lactate, and urine output (monitor hourly). The bundle aims to be completed within 1 hour of recognising sepsis.

14. What movement disorder features define Parkinson's disease, and what is the underlying pathology?

    The classic triad: bradykinesia, resting (pill-rolling) tremor at $\approx 4-6$ Hz, and rigidity (cogwheel/lead-pipe), often with postural instability and asymmetric onset. Pathology: loss of dopaminergic neurones in the substantia nigra pars compacta with Lewy bodies; treated with levodopa/carbidopa.

15. What distinguishes a transient ischaemic attack (TIA) from a stroke, and how is early stroke risk managed?

    A TIA is a transient neurological deficit of vascular origin without acute infarction (clinically resolves, typically within minutes-hours, fully within 24 hours); a stroke causes infarction/permanent injury. Give aspirin 300 mg immediately and refer for specialist assessment within 24 hours; the ABCD2 score historically estimated short-term stroke risk.

16. What antibody and electrophysiological features characterise myasthenia gravis (a neuromuscular disorder)?

    Anti-acetylcholine receptor antibodies (anti-AChR), or anti-MuSK antibodies in seronegative cases. It causes fatigable weakness worsening with activity (ptosis, diplopia, bulbar/limb weakness). Repetitive nerve stimulation shows a decremental response; treated with pyridostigmine and immunosuppression. Associated with thymoma/thymic hyperplasia.

17. How is the severity and reversibility of asthma versus COPD distinguished on spirometry and clinical features?

    Asthma: variable, reversible obstruction — $\text{FEV}_1$ improves $\geq 12\%$ (and $\geq 200$ mL) after bronchodilator, with diurnal PEF variability and atopy; often younger, non-smokers. COPD: largely fixed/irreversible obstruction ($\text{FEV}_1/\text{FVC} < 0.7$ post-bronchodilator), in older smokers with progressive dyspnoea and minimal reversibility.

18. What ECG features and management define ventricular fibrillation in a peri-arrest arrhythmia setting?

    VF: chaotic, irregular waveform with no identifiable QRS complexes and no cardiac output — a shockable rhythm. Management per ALS: immediate unsynchronised defibrillation, high-quality CPR (30:2 or continuous with advanced airway), adrenaline 1 mg every 3-5 minutes, and amiodarone 300 mg after the third shock.

19. What is the cardiac biomarker of choice in ACS, and how should serial troponin be interpreted?

    High-sensitivity cardiac troponin (T or I). A rise and/or fall on serial sampling (e.g. at 0 and 3 hours) above the 99th percentile, in an appropriate clinical context, supports myocardial infarction. Troponin can be chronically elevated in CKD, sepsis, PE and heart failure, so the dynamic change is key.

20. What clinical and biochemical features characterise a thyroid storm (thyrotoxic crisis), and its initial management?

    Severe hyperthyroidism with fever, tachyarrhythmia/AF, agitation/delirium, heart failure and GI upset. Management: beta-blocker (propranolol) for symptoms, a thionamide (propylthiouracil/carbimazole) to block synthesis, Lugol's iodine $\geq 1$ hour later to block release, and hydrocortisone (blocks T4$\to$T3 conversion); treat the precipitant.

21. What is the difference between type 1 and type 2 respiratory failure on arterial blood gas?

    Type 1: hypoxaemia ($\text{PaO}_2 < 8$ kPa) with normal or low $\text{PaCO}_2$ — a V/Q mismatch problem (e.g. pneumonia, PE, pulmonary oedema). Type 2: hypoxaemia with hypercapnia ($\text{PaCO}_2 > 6$ kPa) — alveolar hypoventilation (e.g. COPD, neuromuscular disease, opioid toxicity).

22. What features suggest a subarachnoid haemorrhage as a cause of headache, and how is it investigated?

    Sudden-onset 'thunderclap' headache peaking within seconds ('worst headache of life'), $\pm$ neck stiffness, photophobia, vomiting and reduced consciousness. Investigate with urgent non-contrast CT head; if negative and done $> 6$ hours after onset, perform a lumbar puncture looking for xanthochromia (bilirubin from RBC breakdown).

23. How is the cause of jaundice classified, and what bilirubin/urine findings localise it?

    Pre-hepatic (haemolysis): unconjugated hyperbilirubinaemia, normal urine, raised LDH/reticulocytes. Hepatic: mixed picture with raised transaminases. Post-hepatic (obstructive/cholestatic): conjugated hyperbilirubinaemia, dark urine, pale stools, raised ALP and GGT, and pruritus.

24. What is the corrected calcium formula, and what symptoms and ECG change accompany hypercalcaemia?

    Corrected calcium $= \text{measured Ca}^{2+} + 0.02 \times (40 - \text{albumin in g/L})$. Symptoms: 'stones, bones, groans, and psychic moans' — renal stones, bone pain, abdominal pain/constipation, polyuria, confusion. ECG shows a shortened QT interval; managed with IV fluids $\pm$ bisphosphonates.

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