Plab1Keys - For PLAB 1, UKMLA & USMLE Step 2 CK

PLAB 1 & UKMLA AKT eye, dermatology, orthopaedics, and cardiology questions often test pattern recognition rather than memorized definitions.

• Herpes simplex labialis (HSV-1 / cold sores).
✓ Painful vesicles on lips or around mouth.
✓ Prodromal tingling or burning before lesions appear.
✓ Mainly transmitted by direct saliva contact.
✓ Main answer in most questions → supportive treatment and pain relief.
✓ Severe, recurrent, or first severe episode → oral aciclovir.

• Achilles tendon rupture.
✓ Sudden “pop” during sport.
✓ “Someone kicked me from behind” = classic clue.
✓ Calf and heel pain.
✓ Positive Thompson test → absent plantar flexion after calf squeeze.
✓ Refer to orthopaedics.

• Cardiac tamponade.
✓ Beck’s triad:
→ Hypotension.
→ Muffled heart sounds.
→ Raised JVP.
✓ Diagnosis → Echocardiography.
✓ Treatment → urgent pericardiocentesis.
✓ Trauma is an important cause.

• Conjunctivitis exam differentiation:
✓ Bacterial → purulent discharge + eyes stuck together.
✓ Viral → watery discharge + recent URTI + preauricular nodes.
✓ Allergic → bilateral itching + chemosis + atopy history.

• High-yield exam trap:
Painful vesicles outside mouth → HSV-1.
Painful red eye with visual loss → think beyond simple conjunctivitis.

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USMLE Step 2 CK cardiovascular questions frequently test preload, afterload, and hemodynamic logic rather than simple memorization. The pattern behind the physiology is usually the key.

• HFpEF (diastolic dysfunction).
– HF symptoms with preserved EF (>50%).
– Common clues: obesity, HTN, edema, left atrial enlargement.
– Stiff ventricle → impaired filling, not impaired contraction.
– Symptom control = loop diuretics + treat comorbidities.

• HFpEF pearl.
– Normal EF does not exclude heart failure.
– Think preserved squeeze but poor filling.

• Right ventricular MI (RVMI).
– Inferior STEMI + hypotension + JVD + clear lungs.
– RV becomes preload dependent.
– Treatment = IV normal saline bolus.

• RVMI trap.
– Avoid nitrates and diuretics.
– Dropping preload can worsen shock.

• AV fistula physiology.
– AV fistula bypasses high-resistance arterioles.
– ↓ SVR + ↑ venous return → high-output state.
– May eventually cause high-output heart failure.

• ASD with reversible pulmonary hypertension.
– Normal PCWP + elevated pulmonary pressure that improves with vasodilators.
– Indicates precapillary pulmonary hypertension with reversibility.
– Reversible disease → ASD closure may be beneficial.

• High-yield rapid associations.
– Inferior STEMI + clear lungs → RV infarction.
– Normal EF + HF symptoms → HFpEF.
– AV fistula → high output + low SVR.
– ASD + reversible pulmonary pressure → consider closure.

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Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a classic PLAB 1 & UKMLA AKT nephrology diagnosis — and the exam commonly tests the association between hematuria, hypertension, family history, and intracranial aneurysm.

High-yield pattern recognition:

• Hematuria + hypertension + loin/flank pain → Think ADPKD.

Classic presentation:
Adults presenting with:
• Hypertension.
• Microscopic or gross hematuria.
• Flank or loin pain.
• Progressive renal impairment.

Major PLAB / UKMLA association:
ADPKD + intracranial (berry) aneurysm.

This is one of the highest-yield associations and is frequently tested.

Important inheritance clue:
ADPKD is autosomal dominant.

Exam pearl:
Affected parent → approximately 50% risk for offspring.

Diagnostic investigation:

First-line investigation:
• Ultrasound of kidneys (KUB/renal ultrasound).

Why?
Ultrasound can detect multiple renal cysts and is the common exam answer.

Common complications:

• Progressive chronic kidney disease (CKD).
• Hypertension.
• Intracranial aneurysm.
• Hematuria.
• Recurrent UTIs.
• Renal stones.

Major PLAB traps:

• Missing family history clues.
• Forgetting intracranial aneurysm association.
• Choosing CT before ultrasound in straightforward diagnosis questions.

Pattern recognition shortcut:
Adult + hypertension + hematuria + flank pain + family history = ADPKD.

Memory anchor:
ADPKD = Adult + Dominant + Aneurysm.

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PLAB 1 & UKMLA AKT renal questions commonly test the classic triad and associations of ADPKD. Family history is often the biggest clue.

• Think of ADPKD when you see:
Hematuria.
Hypertension.
Loin or flank pain.

• Important inheritance pattern:
Autosomal dominant.
→ 50% chance of transmission to offspring.

• High-yield association:
Intracranial (berry) aneurysm.

• Common PLAB clue:
Family history of cerebral aneurysm or sudden death + kidney symptoms.

• Common complications:
Progressive chronic kidney disease.
Recurrent UTIs.
Kidney stones.
Liver cysts.

• Investigation of choice for diagnosis:
Ultrasound of kidneys, ureters, and bladder (KUB).
Useful for detecting multiple renal cysts.

• Common exam trap:
Adult with hypertension + hematuria + positive family history → think ADPKD before considering isolated CKD causes.

• Red flag:
Sudden severe headache in ADPKD → suspect subarachnoid hemorrhage from ruptured berry aneurysm.

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USMLE Step 2 CK high-yield allergy/immunology emergency: Anaphylaxis is epinephrine until proven otherwise.

A patient who rapidly develops facial swelling, urticaria, throat tightness, wheezing, GI symptoms, or multisystem involvement after antibiotic exposure should immediately trigger anaphylaxis—not delayed treatment with antihistamines alone.

Classic board clues:
• Recent beta-lactam exposure (eg, amoxicillin).
• Rapid onset after trigger.
• Symptoms involving ≥2 systems.
• Facial swelling/angioedema.
• Wheals or urticaria.
• Respiratory or GI symptoms.

Why this matters for Step 2 CK:
USMLE frequently tests recognition of anaphylaxis and whether you know the immediate life-saving next step. The most common mistake is delaying epinephrine.

High-yield pathophysiology:
IgE-mediated mast cell activation → release of histamine, leukotrienes, and prostaglandins → systemic vasodilation and multisystem effects.

Key distinction:
Anaphylaxis:
• Multisystem involvement.
• Airway risk.
• Immediate treatment required.

Simple allergic reaction:
• Localized rash only.
• No airway or systemic compromise.

Best next step:
• Immediate intramuscular epinephrine.
• Support airway, breathing, circulation.
• IV fluids if hypotensive.
• Observe for biphasic reaction.
• Avoid future trigger exposure.

Classic exam trap:
Do not start with antihistamines or steroids alone in true anaphylaxis.

USMLE memory anchor:
“Airway + Skin + GI symptoms after exposure = Epinephrine now.”

Critical board pearl:
Epinephrine is first-line therapy. Delayed treatment increases mortality risk.

Step 2 CK emergency pearl:
When multiple organ systems become involved after a trigger, stop thinking allergy and start thinking anaphylaxis.

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USMLE Step 2 CK allergy/immunology questions commonly test rapid differentiation between histamine-mediated reactions and bradykinin-mediated disease. Missing that distinction can completely change management.

• Mast cell–mediated anaphylaxis.
– Rapid onset after exposure (commonly beta-lactams, foods, stings).
– Involves ≥2 systems: skin + respiratory/GI symptoms.
– Wheals, facial swelling, throat tightness, abdominal symptoms.
– First-line treatment = immediate IM epinephrine.

• High-yield anaphylaxis trap.
– Antihistamines and steroids are supportive only.
– Epinephrine is the first step.

• Hereditary angioedema (HAE).
– Recurrent nonpruritic swelling.
– No urticaria or itching.
– Family history commonly present.
– Caused by C1 inhibitor deficiency → bradykinin accumulation.

• HAE board clues.
– Measure serum C4 level.
– Low C4 strongly supports diagnosis.
– Episodes often triggered by stress, trauma, or procedures.

• Treatment logic.
– Acute HAE attack → C1 inhibitor concentrate or icatibant.
– Epinephrine and antihistamines generally do not fix the underlying problem.

• Rapid differentiation.
– Anaphylaxis → histamine + wheals + multisystem symptoms.
– HAE → bradykinin + isolated swelling + no urticaria.

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PLAB 1 & UKMLA AKT endocrine questions commonly test the classic electrolyte and acid–base associations linked to adrenal disorders and pheochromocytoma.

• Addison’s disease:
Low cortisol + low aldosterone.
→ Hyperkalemia.
→ Hypotension.
→ Metabolic acidosis.

• Conn’s syndrome (Primary hyperaldosteronism):
High aldosterone.
→ Hypokalemia.
→ Hypertension.
→ Metabolic alkalosis.

• High-yield comparison:
Addison’s = low aldosterone → potassium retained.
Conn’s = high aldosterone → potassium loss.

• Pheochromocytoma:
Catecholamine-secreting tumor.

• Classic symptom pattern:
PHE + F.
→ Palpitations.
→ Headache.
→ Hypertension.
→ Flushing/sweating.

• Common PLAB trap:
Episodes are usually paroxysmal with sudden attacks of headache, sweating, and tachycardia.

• Important exam clue:
Resistant hypertension + episodic symptoms → think pheochromocytoma.

• Quick recall:
Addison’s → Hyperkalemia.
Conn’s → Hypokalemia.

────────────────────
• PLAB1Keys.Com – Full PLAB 1 & UKMLA AKT High-Yield Preparation.

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