🇬🇧 Professional and Linguistic Assessments Board (PLAB) · subject

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

The Medicine and Acute Care syllabus for Professional and Linguistic Assessments Board (PLAB) in full: 5 chapters, 30 topics and 80 sub-topics, every one listed below, plus 65 Medicine and Acute Care flashcards with answers.

5Chapters
30Topics
80Sub-topics
65Flashcards

Medicine and Acute Care syllabus: all 5 chapters

Expand any chapter to see its topics and sub-topics.

  1. Cardiovascular Medicine

    6 topics
    • Acute Coronary Syndromes
      • STEMI recognition and immediate management
      • NSTEMI and unstable angina risk stratification (GRACE)
      • Antiplatelet and anticoagulation therapy
      • Post-MI complications and secondary prevention
    • Heart Failure
      • Acute pulmonary oedema management
      • Chronic heart failure with reduced ejection fraction
      • Diuretics, ACE inhibitors and beta-blockers
    • Arrhythmias
      • Atrial fibrillation rate vs rhythm control
      • CHA2DS2-VASc and HAS-BLED anticoagulation decisions
      • Bradyarrhythmias and heart block
      • Tachyarrhythmias and ALS algorithms
    • Hypertension
      • NICE staging and ambulatory monitoring
      • Stepwise pharmacological management
      • Hypertensive emergencies
    • Valvular Heart Disease
      • Murmur interpretation
      • Aortic stenosis and mitral regurgitation
      • Infective endocarditis and prophylaxis
    • Venous Thromboembolism
      • DVT diagnosis and Wells score
      • Pulmonary embolism assessment and PERC
      • Anticoagulation duration
  2. Respiratory Medicine

    6 topics
    • Asthma
      • Acute severe and life-threatening asthma
      • Chronic stepwise management
      • Inhaler technique and adherence
    • Chronic Obstructive Pulmonary Disease
      • Acute exacerbation management
      • Long-term oxygen therapy criteria
      • Spirometry interpretation
    • Pneumonia
      • CURB-65 severity scoring
      • Community vs hospital-acquired pathogens
      • Empirical antibiotic selection
    • Pulmonary Embolism and Pleural Disease
      • Pneumothorax classification and management
      • Pleural effusion and Light's criteria
    • Lung Cancer
      • Red flag presentations and two-week wait referral
      • Staging principles
    • Interstitial and Occupational Lung Disease
      • Idiopathic pulmonary fibrosis
      • Sarcoidosis
  3. Gastroenterology and Hepatology

    6 topics
    • Upper GI Bleeding
      • Glasgow-Blatchford and Rockall scores
      • Variceal vs non-variceal management
      • Resuscitation and endoscopy timing
    • Inflammatory Bowel Disease
      • Crohn's vs ulcerative colitis distinction
      • Acute severe colitis and toxic megacolon
    • Liver Disease
      • Cirrhosis and decompensation
      • Hepatic encephalopathy and ascites
      • Viral hepatitis serology
    • Pancreatic and Biliary Disease
      • Acute pancreatitis and Glasgow score
      • Gallstone disease and cholangitis
    • Functional and Common GI Disorders
      • Irritable bowel syndrome
      • GORD and peptic ulcer disease
      • Coeliac disease
    • Colorectal Cancer
      • Screening programme and referral criteria
      • Iron deficiency anaemia workup
  4. Renal, Endocrine and Metabolic Medicine

    6 topics
    • Acute Kidney Injury
      • Pre-renal, intrinsic and post-renal causes
      • Staging and fluid management
      • Hyperkalaemia emergency treatment
    • Chronic Kidney Disease
      • eGFR staging and complications
      • Renal anaemia and bone disease
    • Diabetes Mellitus
      • Diabetic ketoacidosis management
      • Hyperosmolar hyperglycaemic state
      • Type 2 diabetes pharmacological ladder
      • Diabetic complications screening
    • Thyroid Disorders
      • Hyperthyroidism and thyroid storm
      • Hypothyroidism and myxoedema
    • Adrenal and Pituitary Disorders
      • Addisonian crisis
      • Cushing's syndrome
    • Fluid, Electrolyte and Acid-Base Balance
      • Hyponatraemia assessment
      • Arterial blood gas interpretation
  5. Neurology and Acute Presentations

    6 topics
    • Stroke and TIA
      • ROSIER and FAST assessment
      • Thrombolysis and thrombectomy windows
      • Secondary prevention
    • Headache Disorders
      • Subarachnoid haemorrhage red flags
      • Migraine, cluster and tension headache
      • Giant cell arteritis
    • Seizures and Epilepsy
      • Status epilepticus management
      • First seizure assessment and driving advice
    • Neuromuscular and Movement Disorders
      • Parkinson's disease
      • Guillain-Barre syndrome
      • Myasthenia gravis
    • Altered Consciousness and Meningitis
      • Glasgow Coma Scale assessment
      • Bacterial meningitis and sepsis
    • Sepsis and Acute Deterioration
      • Sepsis Six and NEWS2 escalation
      • Recognition of the deteriorating patient

Professional and Linguistic Assessments Board (PLAB) Medicine and Acute Care flashcards — 65 questions with answers

  1. What ECG changes distinguish STEMI from NSTEMI in acute coronary syndrome?

    STEMI: ST elevation $\geq 1$ mm in $\geq 2$ contiguous limb leads or $\geq 2$ mm in chest leads, or new LBBB. NSTEMI: ST depression, T-wave inversion, or no ECG changes, but with raised troponin. Unstable angina has the ischaemic symptoms but a normal troponin.

  2. What is the immediate initial management (first-line drug therapy) for a patient with suspected acute coronary syndrome?

    MONA + dual antiplatelet: Morphine (if in pain), Oxygen (only if $\text{SaO}_2 < 94\%$), Nitrates (GTN), Aspirin 300 mg, plus a second antiplatelet (e.g. ticagrelor/clopidogrel). STEMI requires primary PCI within 120 minutes, or thrombolysis if PCI unavailable.

  3. Which coronary artery territory corresponds to ECG leads II, III and aVF, and what is a key complication to watch for?

    Inferior MI, usually from the right coronary artery (RCA). Watch for bradycardia/heart block and right ventricular infarction — give nitrates cautiously as RV infarcts are preload-dependent and can cause profound hypotension.

  4. How are the four New York Heart Association (NYHA) functional classes of heart failure defined?

    Class I: no limitation of activity. Class II: slight limitation, comfortable at rest, ordinary activity causes symptoms. Class III: marked limitation, comfortable only at rest. Class IV: symptoms at rest, unable to carry out any activity without discomfort.

  5. What is the first-line pharmacological management of chronic heart failure with reduced ejection fraction (HFrEF)?

    An ACE inhibitor (or ARB if intolerant) PLUS a beta-blocker, titrated to maximally tolerated doses. Add a mineralocorticoid receptor antagonist (e.g. spironolactone) if symptoms persist. Loop diuretics (furosemide) are used for congestion/symptom relief but do not improve prognosis.

  6. What blood test is used to help diagnose and risk-stratify heart failure, and what does a high value indicate?

    BNP (B-type natriuretic peptide) or NT-proBNP. It is released by ventricular myocytes under stretch; a raised level suggests heart failure and prompts echocardiography. NICE: NT-proBNP $> 2000$ ng/L warrants urgent (2-week) specialist assessment and echo.

  7. What is the CHA₂DS₂-VASc score used for, and what does each component represent?

    It estimates stroke risk in atrial fibrillation to guide anticoagulation. Congestive HF (1), Hypertension (1), Age $\geq 75$ (2), Diabetes (1), prior Stroke/TIA/thromboembolism (2), Vascular disease (1), Age 65-74 (1), Sex category female (1). Anticoagulate if score $\geq 2$ (or $\geq 1$ in men).

  8. How is the management of haemodynamically unstable atrial fibrillation different from stable AF?

    Unstable AF (shock, syncope, myocardial ischaemia, severe heart failure) requires immediate synchronised DC cardioversion. Stable AF is managed with rate control (beta-blocker or rate-limiting calcium channel blocker) and a decision on rhythm control plus anticoagulation based on CHA₂DS₂-VASc.

  9. What is the ECG hallmark of complete (third-degree) heart block, and what is the definitive treatment?

    Complete AV dissociation — P waves and QRS complexes occur independently with no relationship, and the ventricular rate is slow (escape rhythm). Definitive treatment is a permanent pacemaker; atropine or transcutaneous pacing is used acutely if symptomatic.

  10. What are the UK (NICE) thresholds defining Stage 1 and Stage 2 hypertension by clinic and ambulatory/home readings?

    Stage 1: clinic $\geq 140/90$ mmHg and ABPM/HBPM average $\geq 135/85$ mmHg. Stage 2: clinic $\geq 160/100$ mmHg and ABPM/HBPM $\geq 150/95$ mmHg. Severe (stage 3): clinic systolic $\geq 180$ or diastolic $\geq 120$ mmHg.

  11. According to NICE, how does first-line antihypertensive choice depend on age and ethnicity?

    Age $< 55$ and not of Black African/Caribbean origin: ACE inhibitor or ARB (A). Age $\geq 55$ OR Black African/Caribbean of any age: calcium channel blocker (C). Step 2 combines A + C; step 3 adds a thiazide-like diuretic (D).

  12. What is the most common cause of secondary hypertension, and what biochemical clue suggests it?

    Primary hyperaldosteronism (Conn's syndrome). Suspect it with hypertension plus hypokalaemia (or refractory hypertension); screen with the aldosterone-to-renin ratio (raised aldosterone with suppressed renin).

  13. What is the classic auscultation finding of aortic stenosis, and where does the murmur radiate?

    An ejection-systolic (crescendo-decrescendo) murmur loudest at the right second intercostal space (aortic area), radiating to the carotids. Severe AS features: slow-rising pulse, narrow pulse pressure, soft/absent S2, and symptoms of syncope, angina or dyspnoea.

  14. Contrast the murmurs of mitral regurgitation and mitral stenosis.

    Mitral regurgitation: pansystolic murmur loudest at the apex, radiating to the axilla. Mitral stenosis: mid-diastolic rumbling murmur with an opening snap, best heard at the apex in the left lateral position, often associated with a malar flush and AF.

  15. What are the components of the Wells score for DVT, and how does the result guide investigation?

    Items include active cancer, paralysis/immobilisation, recent bedridden/surgery, localised tenderness, entire leg swollen, calf swelling $> 3$ cm, pitting oedema, collateral veins, and prior DVT (each scoring); alternative diagnosis subtracts 2. Score $\geq 2$ = DVT likely $\to$ proximal leg vein ultrasound; $\leq 1$ = unlikely $\to$ D-dimer.

  16. What is the first-line anticoagulant treatment for confirmed DVT or PE, and the standard treatment durations?

    A DOAC (e.g. apixaban or rivaroxaban) is first-line. Duration: 3 months if provoked by a transient reversible factor; at least 3-6 months and often long-term/indefinite if unprovoked or due to active cancer or ongoing risk factors.

  17. List the features used to assess acute asthma severity, distinguishing moderate, severe and life-threatening attacks.

    Moderate: PEF 50-75% predicted, no severe features. Severe: PEF 33-50%, RR $\geq 25$, HR $\geq 110$, unable to complete sentences. Life-threatening: PEF $< 33\%$, $\text{SpO}_2 < 92\%$, silent chest, cyanosis, poor effort, exhaustion, hypotension, arrhythmia, altered consciousness, or a normal/rising $\text{PaCO}_2$.

  18. Outline the stepwise acute drug management of a severe asthma attack in the emergency setting.

    Oxygen to keep $\text{SpO}_2$ 94-98%; nebulised salbutamol (back-to-back); oral prednisolone or IV hydrocortisone; nebulised ipratropium bromide if severe/life-threatening; consider IV magnesium sulfate; escalate to senior/ICU for aminophylline or ventilation if not responding.

  19. What spirometry result confirms airflow obstruction in COPD, and how is severity graded?

    Post-bronchodilator $\text{FEV}_1/\text{FVC} < 0.7$ confirms obstruction. Severity by FEV₁ % predicted: Stage 1 (mild) $\geq 80\%$, Stage 2 (moderate) 50-79%, Stage 3 (severe) 30-49%, Stage 4 (very severe) $< 30\%$.

  20. What is the target oxygen saturation range when giving controlled oxygen to a patient with a COPD exacerbation, and why?

    88-92%, delivered via a controlled (e.g. 24-28% Venturi) mask. This avoids loss of hypoxic respiratory drive and worsening type 2 respiratory failure (hypercapnia) in CO₂ retainers; adjust based on ABG.

Show the other 45 Medicine and Acute Care flashcards
  1. What scoring system is used to assess severity of community-acquired pneumonia, and what do the components stand for?

    CURB-65: Confusion (AMT $\leq 8$/new disorientation), Urea $> 7$ mmol/L, Respiratory rate $\geq 30$, Blood pressure ($< 90$ systolic or $\leq 60$ diastolic), age $\geq 65$. Each scores 1; 0-1 home treatment, 2 consider hospital, $\geq 3$ severe/consider ICU.

  2. What are the most common causative organisms of community-acquired pneumonia, and which is most common overall?

    Streptococcus pneumoniae is the most common overall. Others: Haemophilus influenzae, Mycoplasma pneumoniae (atypical, younger patients), Staphylococcus aureus (often post-influenza), Legionella pneumophila (hyponatraemia, recent travel), and Chlamydophila species.

  3. How does Light's criteria differentiate an exudative from a transudative pleural effusion?

    An effusion is an exudate if any one applies: pleural/serum protein ratio $> 0.5$; pleural/serum LDH ratio $> 0.6$; or pleural LDH $>$ two-thirds the upper limit of normal serum LDH. Transudates (e.g. heart failure, hypoalbuminaemia) fail all criteria; exudates suggest infection, malignancy or inflammation.

  4. What are the components of the Wells score for PE outcome categories, and how do PERC and D-dimer fit in?

    Wells $> 4$ (PE likely) $\to$ CTPA; Wells $\leq 4$ (PE unlikely) $\to$ D-dimer, with CTPA only if positive. Items include clinical DVT signs, PE most likely diagnosis, HR $> 100$, immobilisation/surgery, prior DVT/PE, haemoptysis, and malignancy. The classic ECG finding $S_1Q_3T_3$ is uncommon; sinus tachycardia is most frequent.

  5. What is the most common type of lung cancer overall, and which type is most strongly associated with paraneoplastic syndromes such as SIADH and ectopic ACTH?

    Adenocarcinoma is the most common type overall (and commonest in non-smokers). Small cell lung cancer (SCLC) is most associated with paraneoplastic syndromes: SIADH, ectopic ACTH (Cushing's), and Lambert-Eaton myasthenic syndrome.

  6. Which lung cancer is classically associated with hypercalcaemia via PTH-related peptide secretion?

    Squamous cell carcinoma of the lung — it secretes parathyroid hormone-related peptide (PTHrP), causing hypercalcaemia. It is also associated with cavitating lesions and is typically central.

  7. Name the occupational lung disease associated with asbestos exposure that affects the pleura, and its hallmark.

    Mesothelioma — a malignancy of the pleura with a long latency (often 30-40 years) after asbestos exposure. It presents with chest pain, dyspnoea and a unilateral pleural effusion; asbestos also causes pleural plaques and asbestosis (interstitial fibrosis).

  8. What is the characteristic HRCT and spirometry pattern of idiopathic pulmonary fibrosis (interstitial lung disease)?

    HRCT shows a usual interstitial pneumonia pattern: bibasal, peripheral, subpleural reticulation with honeycombing and traction bronchiectasis. Spirometry shows a restrictive pattern: reduced FEV₁ and FVC with a preserved or increased $\text{FEV}_1/\text{FVC}$ ratio ($> 0.7$) and reduced transfer factor (TLCO).

  9. What is the immediate management of a haemodynamically unstable patient with an acute upper GI bleed?

    ABCDE resuscitation: two large-bore cannulae, fluid/blood resuscitation, correct coagulopathy, and use the Blatchford score to assess risk. Urgent endoscopy within 24 hours (immediately after resuscitation if unstable). For variceal bleeds add terlipressin and prophylactic antibiotics.

  10. What scoring systems are used before and after endoscopy in upper GI bleeding?

    Glasgow-Blatchford score (pre-endoscopy) assesses need for intervention/admission — a score of 0 may allow outpatient management. The full Rockall score (post-endoscopy) estimates the risk of rebleeding and mortality.

  11. Compare the typical distribution and histological features of ulcerative colitis versus Crohn's disease.

    Ulcerative colitis: continuous inflammation from the rectum proximally, limited to the colon, mucosa/submucosa only, with crypt abscesses and no granulomas. Crohn's disease: skip lesions anywhere mouth-to-anus, transmural inflammation, non-caseating granulomas, and a cobblestone appearance; associated with fistulae and strictures.

  12. What is the first-line investigation and a characteristic blood finding in autoimmune (chronic) liver disease screening?

    Liver screen autoantibodies: anti-mitochondrial antibody (AMA) for primary biliary cholangitis; anti-smooth muscle and anti-LKM antibodies for autoimmune hepatitis; raised IgG in autoimmune hepatitis and raised IgM with AMA in PBC. ANCA (pANCA) and MRCP (beaded ducts) suggest primary sclerosing cholangitis.

  13. What scoring systems quantify the severity and prognosis of liver cirrhosis?

    Child-Pugh score uses bilirubin, albumin, INR, ascites and encephalopathy to grade A-C. MELD score uses bilirubin, INR and creatinine (and sodium in MELD-Na) to predict mortality and prioritise transplantation.

  14. What is the gold-standard scoring system for acute pancreatitis severity, and name common causes via the mnemonic.

    The Glasgow (or modified Glasgow/Imrie) and APACHE II scores assess severity. Causes — 'I GET SMASHED': Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion sting, Hypercalcaemia/Hypertriglyceridaemia, ERCP, Drugs. Gallstones and alcohol are the two commonest.

  15. What constitutes Charcot's triad and Reynolds' pentad in biliary disease?

    Charcot's triad (ascending cholangitis): right upper quadrant pain, fever/rigors, and jaundice. Reynolds' pentad adds hypotension (shock) and confusion (altered mental status), indicating severe suppurative cholangitis requiring urgent biliary decompression.

  16. What are the Rome IV diagnostic criteria principles for irritable bowel syndrome (functional GI disorder)?

    Recurrent abdominal pain on average $\geq 1$ day/week in the last 3 months (onset $\geq 6$ months prior), associated with $\geq 2$ of: pain related to defecation, change in stool frequency, or change in stool form/appearance. It is a positive diagnosis after excluding red flags (weight loss, bleeding, anaemia).

  17. Which gene mutations and screening pathway are central to hereditary colorectal cancer syndromes?

    Familial adenomatous polyposis (FAP): APC gene mutation, hundreds of polyps, near-100% cancer risk. Lynch syndrome (HNPCC): DNA mismatch repair gene mutations (MLH1, MSH2 etc.) causing microsatellite instability and right-sided tumours. The UK uses faecal immunochemical testing (FIT) for screening/symptomatic triage.

  18. How does the typical presentation of right-sided versus left-sided colorectal cancer differ?

    Right-sided (caecum/ascending): iron-deficiency anaemia, weight loss, occult bleeding, and a palpable mass — often presents late. Left-sided (descending/sigmoid/rectum): change in bowel habit, PR bleeding/blood mixed with stool, tenesmus, and obstruction.

  19. What are the KDIGO criteria for diagnosing acute kidney injury (AKI)?

    Any of: rise in serum creatinine $\geq 26 \, \mu\text{mol/L}$ within 48 hours; rise in creatinine $\geq 1.5\times$ baseline within 7 days; or urine output $< 0.5 \, \text{mL/kg/h}$ for $> 6$ hours. Causes are classified as pre-renal, intrinsic (renal), and post-renal (obstructive).

  20. What ECG changes and emergency treatment are associated with severe hyperkalaemia in AKI?

    ECG: tall tented T waves, then flattened/absent P waves, broad QRS, and eventually a sine-wave pattern. Emergency treatment: IV calcium gluconate (cardiac membrane stabilisation), then insulin with dextrose and nebulised salbutamol to shift potassium into cells; treat the underlying cause.

  21. How is chronic kidney disease staged using eGFR and albuminuria (the G and A categories)?

    G stages by eGFR (mL/min/1.73m²): G1 $\geq 90$, G2 60-89, G3a 45-59, G3b 30-44, G4 15-29, G5 $< 15$. A stages by albumin:creatinine ratio (mg/mmol): A1 $< 3$, A2 3-30, A3 $> 30$. CKD requires abnormalities present for $> 3$ months.

  22. 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.

  23. 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.

  24. 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.

  25. 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.

  26. 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.

  27. 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).

  28. 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.

  29. 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.

  30. 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.

  31. 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).

  32. 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).

  33. 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.

  34. 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.

  35. 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.

  36. 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.

  37. 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.

  38. 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.

  39. 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.

  40. 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.

  41. 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.

  42. 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).

  43. 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).

  44. 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.

  45. 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.

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

What is in the Professional and Linguistic Assessments Board (PLAB) Medicine and Acute Care syllabus?

Professional and Linguistic Assessments Board (PLAB) Medicine and Acute Care is split into 5 chapters: Cardiovascular Medicine, Respiratory Medicine, Gastroenterology and Hepatology, Renal, Endocrine and Metabolic Medicine and Neurology and Acute Presentations. Together they contain 30 topics and 80 sub-topics.

How many chapters are in Professional and Linguistic Assessments Board (PLAB) Medicine and Acute Care?

5 chapters, containing 30 topics and 80 sub-topics. The largest chapter is Cardiovascular Medicine, with 6 topics.

Are there flashcards for Professional and Linguistic Assessments Board (PLAB) Medicine and Acute Care?

Yes — a 65-card Medicine and Acute Care deck, printed in full in the flashcards section of this page and available in the Examius app with spaced repetition. The free plan covers one exam of your choice, including its flashcards; Examius Pro, a one-time purchase, unlocks every other exam and deck.