BoardQBank monogram BoardQBankCONO-II Clinical Sciences
A. Circulatory flow Lymphedema Central edema Peripheral edema Pulmonary edema Raynaud disease / primary Raynaud phenomenon Chronic arterial / chronic venous insufficiency Stasis dermatitis Peripheral vascular disease / peripheral artery disease Hyperlipidemia Intermittent claudication Cluster headache Migraine headache
B. Blood vessels Varicose veins Esophageal varices Hemorrhoids Aortic aneurysm Cerebral aneurysm
C. Blood pressure Primary hypertension Secondary hypertension Hypertensive crisis Pulmonary hypertension Hypotension
D. Ischemic conditions Ischemic heart disease Myocardial infarction Cardiac arrest Cerebrovascular accident / stroke Transient ischemic attack Avascular necrosis of femoral head Gangrene Embolism Pulmonary infarction Pulmonary embolism
E. Blood Aplastic anemia Hemolytic anemia Macrocytic anemia Microcytic anemia Normocytic anemia Anemia of chronic disease Neutropenia Eosinophilia Basophilia Thrombocytopenia Henoch-Schonlein purpura / IgA vasculitis Disseminated intravascular coagulation Thrombosis
F. Cardiac arrhythmias Atrial fibrillation Atrial premature beats Ventricular premature beats / PVCs Heart block Sinus bradycardia Sinus tachycardia Supraventricular tachyarrhythmias Ventricular fibrillation Ventricular tachycardia
G. Pregnancy-specific vascular conditions Gestational hypertension Antepartum anemia Placenta previa Abruptio placenta Pre-eclampsia

CONO-II Clinical Sciences · Vascular System

Vascular course for clinical recognition, red flags, and exam-style practice.

Study circulatory flow, blood vessel disease, blood pressure, ischemia, thrombosis, bleeding patterns, and vascular risk reduction in a clean BoardQBank course page.

Start studying Practice 36 MCQs
6vascular modules
36practice questions
A&Dprimary domain
9–11%condition weighting

Course map

Click a topic to open the vascular module. Use the one-by-one disease topic bars for all tested vascular groups. Click a condition name to open that condition separately in the window.

Circulatory Flow5 MCQs Blood Vessels6 MCQs Blood Pressure6 MCQs Ischemic Conditions7 MCQs Inflammation, Thrombosis & Bleeding6 MCQs Risk Reduction & Chronic Complications6 MCQs

A. Circulatory Flow disease topic bar

Click one Circulatory Flow condition at a time. The disease window opens definition, full description, key history, physical examination, red flags, investigations or management, and exam trap for that condition.

Lymphedema

Chronic limb swelling caused by impaired lymphatic drainage.

Lymphatic obstruction
Full description

Lymphedema is protein-rich interstitial swelling due to reduced lymph transport. Primary lymphedema results from congenital or inherited lymphatic abnormality. Secondary lymphedema may follow cancer surgery, lymph node dissection, radiation, infection, trauma, obesity, malignancy, or chronic venous disease. Early swelling may pit; chronic disease becomes firm, fibrotic, and non-pitting with skin thickening and recurrent cellulitis risk.

Key history
  • Onset, progression, unilateral or bilateral swelling.
  • Cancer surgery, radiation, lymph node removal, trauma, obesity, venous disease, or recurrent cellulitis.
  • Limb heaviness, tight skin, infection episodes, fever, pain, or rapid change.
Physical examination
  • Pitting early and firm non-pitting edema later.
  • Skin thickening, fibrosis, asymmetry, heaviness.
  • Positive Stemmer sign: inability to pinch skin at the base of the second toe or finger.
  • Check pulses and signs of cellulitis.
Red flags
  • Sudden unilateral swelling.
  • Painful swelling with fever.
  • Rapid progression or new swelling with cancer history.
  • Ulceration, necrosis, or systemic infection signs.
Investigations / management
  • Assess for secondary causes when swelling is new, progressive, or asymmetric.
  • Compression when appropriate, manual lymph drainage, exercise, skin care, weight management.
  • Treat cellulitis promptly.
Exam trap

Established lymphedema is not simple water retention. Diuretics usually do not correct protein-rich lymphatic swelling.

Central edema

Generalized edema driven by systemic fluid overload, low oncotic pressure, or venous congestion.

Systemic fluid balance
Full description

Central edema reflects a systemic cause rather than an isolated limb problem. Important causes include congestive heart failure, kidney disease, nephrotic-range protein loss, liver disease, hypoalbuminemia, hypothyroidism, pregnancy-related disorders, and medication-related fluid retention. The clinical task is to identify the organ system producing fluid retention and recognize cardiopulmonary or renal danger signs.

Key history
  • Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, exercise intolerance.
  • Oliguria, foamy urine, abdominal distension, liver disease symptoms, fatigue, cold intolerance.
  • Medication review: calcium channel blockers, NSAIDs, corticosteroids, hormones.
Physical examination
  • Bilateral dependent edema or sacral edema in bedbound patients.
  • Jugular venous pressure, lung crackles, S3, hepatomegaly, ascites.
  • Blood pressure, weight trend, pulses, skin changes, renal or liver disease signs.
Red flags
  • Edema with shortness of breath, orthopnea, chest pain, hypoxia, or syncope.
  • New edema with oliguria or severe hypertension.
  • Pregnancy with severe headache, visual symptoms, or hypertension.
Investigations / management
  • CBC, creatinine/eGFR, electrolytes, albumin, liver enzymes, urinalysis, urine albumin-to-creatinine ratio.
  • BNP/NT-proBNP, ECG, chest imaging, or echocardiography when heart failure is suspected.
  • Management depends on the underlying cause and severity.
Exam trap

Do not label bilateral edema as venous insufficiency before assessing heart, kidney, liver, thyroid, albumin, medication, and pregnancy-related causes.

Peripheral edema

Abnormal fluid accumulation in interstitial tissues, commonly feet, ankles, and legs.

Leg swelling pattern
Full description

Peripheral edema may be bilateral or unilateral. Bilateral causes include heart failure, chronic venous insufficiency, kidney disease, liver disease, hypoalbuminemia, hypothyroidism, and medication-related edema. Unilateral causes include deep vein thrombosis, lymphedema, cellulitis, trauma, venous obstruction, or a local mass. The key distinction is local versus systemic disease and pitting versus non-pitting pattern.

Key history
  • Onset, duration, unilateral versus bilateral swelling.
  • Pain, redness, warmth, immobility, travel, surgery, pregnancy.
  • Shortness of breath, orthopnea, chest pain, oliguria, medication changes.
Physical examination
  • Pitting versus non-pitting edema.
  • Skin temperature, erythema, tenderness, calf circumference.
  • Varicose veins, pulses, JVP, lung crackles, hepatomegaly, cellulitis signs.
Red flags
  • Sudden unilateral painful leg swelling.
  • Chest pain or shortness of breath.
  • New edema with oliguria, severe hypertension, or heart failure signs.
  • Fever with spreading erythema.
Investigations / management
  • Venous ultrasound for suspected DVT; renal, liver, thyroid, albumin, and urine testing for systemic causes.
  • Compression may help venous edema after arterial circulation is assessed.
  • Urgent assessment when DVT, PE, heart failure, kidney injury, or cellulitis is suspected.
Exam trap

New unilateral painful leg swelling should be considered possible deep vein thrombosis until assessed.

Pulmonary edema

Fluid accumulation in lung interstitium and alveoli causing dyspnea and impaired oxygenation.

Alveolar fluid overload
Full description

Pulmonary edema is commonly cardiogenic from left-sided heart failure, ischemia, valvular disease, arrhythmia, hypertensive emergency, or volume overload. Non-cardiogenic causes include acute respiratory distress syndrome, sepsis, inhalational injury, high altitude, renal failure, and toxins. In vascular questions, pulmonary edema can signal hypertensive emergency, myocardial infarction, or acute heart failure.

Key history
  • Acute dyspnea, orthopnea, pink frothy sputum, chest pain, palpitations.
  • Hypertension, coronary disease, valve disease, renal failure, medication nonadherence.
  • Recent infection, toxin exposure, sepsis symptoms, fluid overload.
Physical examination
  • Respiratory distress, hypoxemia, tachypnea, crackles.
  • Elevated JVP, S3, peripheral edema, hypertension or hypotension.
  • Cyanosis, diaphoresis, altered mental status in severe cases.
Red flags
  • Oxygen saturation low or rapidly worsening dyspnea.
  • Chest pain, new neurologic symptoms, severe hypertension, syncope.
  • Hypotension, confusion, or signs of shock.
Investigations / management
  • Oxygen saturation, ECG, chest X-ray, BNP/NT-proBNP, troponin when ischemia is suspected.
  • Creatinine/electrolytes; echocardiography when structural heart disease is suspected.
  • Emergency care is required when acute respiratory distress or hypoxemia is present.
Exam trap

Pulmonary edema with severe BP elevation is target-organ damage; that pattern is hypertensive emergency, not a simple high BP reading.

Raynaud disease / primary Raynaud phenomenon

Episodic vasospasm of fingers or toes triggered by cold or emotional stress.

Small-vessel vasospasm
Full description

Raynaud phenomenon produces episodic digital colour change from vasospasm. The typical sequence is white to blue to red, although every patient may not show all phases. Primary Raynaud is more likely when symptoms are symmetric, begin at a younger age, cause no tissue injury, and occur without autoimmune features. Secondary Raynaud is associated with systemic sclerosis, lupus, rheumatoid arthritis, Sjogren syndrome, mixed connective tissue disease, vibration exposure, smoking, and vasoconstrictive medications.

Key history
  • Cold or stress trigger, colour sequence, pain or numbness.
  • Symmetric versus unilateral symptoms; age at onset.
  • Digital ulcers, skin thickening, dysphagia, joint swelling, rash, autoimmune symptoms, smoking, medication triggers.
Physical examination
  • Digits for pallor, cyanosis, erythema, ulcers, pitting scars, necrosis.
  • Nailfold capillaries if available.
  • Skin thickening, joint swelling, rash, pulses, and signs of connective tissue disease.
Red flags
  • Onset after age 30-40.
  • Unilateral symptoms, severe pain, digital ulceration, tissue necrosis.
  • Abnormal nailfold capillaries, skin thickening, dysphagia, rash, joint swelling, systemic symptoms.
Investigations / management
  • Avoid cold, use warming strategies, stop smoking, avoid vasoconstrictive medications when possible.
  • Investigate autoimmune disease when secondary Raynaud is suspected.
  • Medical management may be needed for persistent or severe symptoms.
Exam trap

Raynaud with ulcers, necrosis, or systemic symptoms should not be classified as uncomplicated primary Raynaud.

Chronic arterial / chronic venous insufficiency

Chronic arterial insufficiency reduces tissue perfusion; chronic venous insufficiency causes venous pooling and hypertension.

Perfusion versus pooling
Full description

Chronic arterial insufficiency is usually atherosclerotic and causes reduced oxygen delivery to distal tissues. Chronic venous insufficiency results from incompetent valves and venous hypertension. Arterial disease causes cold skin, weak pulses, exertional pain, distal ulcers, rest pain, and possible gangrene. Venous disease causes heaviness, edema, varicose veins, hyperpigmentation, stasis dermatitis, lipodermatosclerosis, and venous ulcers near the medial malleolus.

Key history
  • Arterial: exertional pain, rest pain, cold feet, poor wound healing, smoking, diabetes.
  • Venous: heaviness after standing, swelling worse later in day, relief with elevation, itching, varicose veins.
  • Prior DVT, pregnancy, occupation standing, cardiovascular risk factors.
Physical examination
  • Arterial: pulses, capillary refill, cool limb, shiny skin, hair loss, toe/foot ulcers.
  • Venous: pitting edema, varicosities, pigmentation, dermatitis, medial malleolar ulcer.
  • Assess ABI before strong compression when PAD is suspected.
Red flags
  • Rest pain, non-healing ulcer, gangrene, sudden cold pulseless limb.
  • Sudden unilateral painful swelling or PE symptoms.
  • Bleeding ulcer, rapidly worsening skin breakdown, infection signs.
Investigations / management
  • ABI for suspected arterial disease; duplex ultrasound for venous reflux or DVT assessment.
  • Arterial management: smoking cessation, risk-factor control, exercise therapy, vascular assessment for severe disease.
  • Venous management: elevation, calf exercise, compression when arterial circulation is adequate, skin and wound care.
Exam trap

Compression helps venous disease, but high-pressure compression is unsafe if severe arterial disease has not been excluded.

Stasis dermatitis

Eczematous inflammation of the lower legs caused by chronic venous hypertension.

Venous skin inflammation
Full description

Stasis dermatitis develops when chronic venous insufficiency produces edema, capillary leakage, hemosiderin deposition, and skin inflammation. It often occurs around the ankles with itching, scaling, erythema, brown pigmentation, and can progress to lipodermatosclerosis or venous ulceration. It is commonly associated with varicose veins, obesity, prolonged standing, and prior DVT.

Key history
  • Leg heaviness, swelling worse with standing, improvement with elevation.
  • Itching, scaling, skin discoloration, ulcer history, varicose veins.
  • Prior DVT, pregnancy, obesity, prolonged standing, skin infection symptoms.
Physical examination
  • Bilateral or asymmetric lower-leg dermatitis, hyperpigmentation, edema.
  • Varicose veins, lipodermatosclerosis, venous ulcer near medial malleolus.
  • Check pulses and look for cellulitis or arterial insufficiency.
Red flags
  • Rapidly spreading erythema, fever, severe pain.
  • Non-healing ulcer, bleeding, necrosis.
  • Absent/reduced foot pulses or acute unilateral swelling.
Investigations / management
  • Clinical diagnosis; duplex venous ultrasound when venous reflux, ulcer, or DVT is suspected.
  • Compression after arterial assessment, leg elevation, walking, calf exercise, skin care, wound care.
  • Treat secondary infection or cellulitis when present.
Exam trap

Stasis dermatitis may mimic cellulitis. Fever, rapid spread, unilateral warmth, and systemic illness shift concern toward infection.

Peripheral vascular disease / peripheral artery disease

Atherosclerotic narrowing of peripheral arteries, most often the lower limbs.

Arterial atherosclerosis
Full description

Peripheral artery disease causes reduced limb perfusion and is a marker of systemic atherosclerosis. It can present with claudication, cold feet, numbness, poor wound healing, rest pain in advanced disease, and arterial ulcers. Major risk factors include smoking, diabetes mellitus, hypertension, hyperlipidemia, chronic kidney disease, older age, and family history of premature cardiovascular disease.

Key history
  • Exertional calf, thigh, buttock, or foot pain relieved by rest.
  • Cold feet, numbness, tingling, poor wound healing, rest pain.
  • Smoking, diabetes, hypertension, hyperlipidemia, CKD, family history.
Physical examination
  • Reduced or absent pulses, cool limb, pallor, delayed capillary refill.
  • Shiny skin, hair loss, thick nails.
  • Arterial ulcers on toes, feet, or pressure areas.
Red flags
  • Rest pain, non-healing ulcer, gangrene.
  • Sudden painful cold pulseless limb.
  • New sensory or motor deficit in the limb.
Investigations / management
  • Ankle-brachial index is the usual initial non-invasive test.
  • ABI less than 0.90 supports PAD; diabetes and CKD may falsely elevate ABI from calcified vessels.
  • Smoking cessation, exercise therapy, lipid/BP/diabetes control, antiplatelet therapy when medically indicated, vascular assessment for severe disease.
Exam trap

Arterial ulcers are often distal, painful, punched-out, and associated with reduced pulses; venous ulcers usually occur near the medial malleolus with edema and pigmentation.

Hyperlipidemia

Elevation of LDL cholesterol, triglycerides, or both.

Atherosclerotic risk
Full description

Hyperlipidemia increases the risk of atherosclerosis, coronary artery disease, stroke, and peripheral artery disease. Very high triglycerides also increase pancreatitis risk. Secondary causes include diet pattern, obesity, diabetes, hypothyroidism, kidney disease, liver disease, alcohol excess, family history, and medications.

Key history
  • Family history of premature cardiovascular disease.
  • Diet, alcohol, physical activity, smoking, obesity.
  • Diabetes, hypothyroidism, kidney/liver disease, medication contributors.
Physical examination
  • Blood pressure, BMI/waist circumference, cardiovascular exam.
  • Signs of hypothyroidism, xanthomas or xanthelasma when present.
  • Peripheral pulses when vascular disease is suspected.
Red flags
  • Very high triglycerides with abdominal pain.
  • Chest pain, stroke/TIA symptoms, claudication, or non-healing ulcers.
  • Strong family history of early cardiovascular disease.
Investigations / management
  • Lipid panel, diabetes assessment, thyroid testing when indicated, kidney/liver function, medication review.
  • Mediterranean-style dietary pattern, reduce trans fats and excess saturated fats, increase soluble fibre, exercise, weight management, smoking cessation.
  • Limit alcohol when triglycerides are elevated.
Exam trap

Very high triglycerides are not just a cardiovascular risk issue; they increase pancreatitis risk.

Intermittent claudication

Reproducible muscle pain during exertion caused by inadequate arterial blood flow that improves with rest.

Exertional ischemia
Full description

Intermittent claudication is the symptomatic exertional pain pattern of PAD. Calf pain suggests superficial femoral or popliteal disease, thigh/buttock pain suggests aortoiliac disease, and foot pain suggests distal arterial disease. Vascular claudication is triggered by walking and relieved by rest; neurogenic claudication is often relieved by sitting or lumbar flexion.

Key history
  • Walking distance that reliably triggers pain and rest interval needed for relief.
  • Risk factors: smoking, diabetes, hypertension, dyslipidemia, CKD.
  • Ask whether sitting or leaning forward relieves symptoms, suggesting spinal stenosis.
Physical examination
  • Peripheral pulses, capillary refill, limb temperature, skin and nail changes.
  • Foot ulcers, hair loss, shiny skin, neurologic screen.
  • Back posture and neurologic signs if neurogenic claudication is possible.
Red flags
  • Rest pain, non-healing ulcer, gangrene.
  • Sudden severe limb pain with coldness or pulselessness.
  • New motor or sensory deficit.
Investigations / management
  • ABI; vascular imaging when severe, progressive, or procedural planning is needed.
  • Smoking cessation, supervised exercise therapy, lipid/BP/diabetes control.
  • Vascular assessment for severe, progressive, or limb-threatening disease.
Exam trap

Pain relieved by sitting or leaning forward suggests neurogenic claudication from lumbar spinal stenosis rather than vascular claudication.

Cluster headache

Severe unilateral orbital, supraorbital, or temporal headache with ipsilateral autonomic signs.

Trigeminal autonomic headache
Full description

Cluster headache causes excruciating unilateral pain in short attacks, usually 15-180 minutes, recurring over weeks or months. Patients are often restless or agitated during attacks. Ipsilateral autonomic features include lacrimation, conjunctival injection, nasal congestion, rhinorrhea, eyelid edema, facial sweating, miosis, or ptosis.

Key history
  • Attack duration, frequency, strict side, orbital/temporal location.
  • Tearing, conjunctival injection, nasal symptoms, eyelid edema, sweating, ptosis/miosis.
  • Restlessness during attacks and pattern over weeks or months.
Physical examination
  • Neurologic exam and cranial nerves.
  • Autonomic signs during an attack.
  • Assess for persistent Horner syndrome, neurologic deficit, fever, meningismus, altered mental status.
Red flags
  • First or worst headache.
  • Neurologic deficit.
  • Horner syndrome outside an attack.
  • New headache pattern, fever, neck stiffness, or altered mental status.
Investigations / management
  • Clinical diagnosis when classic; urgent evaluation or imaging when red flags/atypical features are present.
  • Differentiate from migraine, sinusitis, temporal arteritis, and intracranial pathology.
  • Acute and preventive treatment follows appropriate medical pathway.
Exam trap

Cluster headache patients are often restless during attacks; migraine patients often prefer lying still in a dark room.

Migraine headache

Recurrent headache with moderate to severe pain, nausea, photophobia, phonophobia, and disability.

Primary headache disorder
Full description

Migraine may be unilateral or bilateral and is often throbbing, worsened by activity, and associated with nausea, vomiting, light sensitivity, or sound sensitivity. Aura can include visual, sensory, or speech symptoms that usually develop gradually and resolve completely. Trigger recognition and red flag screening are essential.

Key history
  • Onset, duration, frequency, disability, associated nausea, photophobia, phonophobia.
  • Aura timing, gradual development, reversibility.
  • Triggers: sleep disruption, stress, dehydration, missed meals, alcohol, hormones, bright light, smells, foods.
  • Medication frequency to detect medication-overuse headache.
Physical examination
  • Neurologic examination and vital signs.
  • Fundoscopy when raised intracranial pressure is suspected.
  • Check for neck stiffness, fever, focal deficits, temporal artery tenderness when relevant.
Red flags
  • Thunderclap onset, neurologic deficit, new headache after age 50.
  • Fever or neck stiffness, cancer or immunosuppression, pregnancy/postpartum state.
  • Head trauma, progressive worsening, papilledema, altered mental status.
Investigations / management
  • Clinical diagnosis when recurrent and typical; image/evaluate when red flags are present.
  • Trigger control, sleep regularity, hydration, regular meals.
  • Acute and preventive treatment when appropriate; avoid medication-overuse headache.
Exam trap

Migraine aura is usually gradual and reversible. Sudden focal neurologic deficit must be assessed as possible TIA or stroke.

B. Blood Vessels disease topic bar

Each blood-vessel topic opens separately so candidates can compare venous dilation, portal hypertension, aneurysm rupture, and hemorrhage patterns.

Varicose veins

Dilated, tortuous superficial veins caused by venous valve incompetence and venous hypertension.

Superficial venous dilation
Full description

Varicose veins commonly affect the lower limbs and are part of the chronic venous disease spectrum. Risk factors include age, pregnancy, obesity, prolonged standing, family history, prior DVT, chronic venous insufficiency, and reduced calf-muscle pump activity. Symptoms are often heaviness, aching after standing, edema later in the day, itching, and relief with elevation.

Key history
  • Leg heaviness, aching after standing, swelling later in the day, relief with elevation.
  • Itching, skin discoloration, ulcer history.
  • Prior DVT, pregnancy history, occupation with prolonged standing.
Physical examination
  • Visible tortuous superficial veins.
  • Pitting edema, hyperpigmentation, stasis dermatitis, lipodermatosclerosis.
  • Venous ulcer near the medial malleolus; check peripheral pulses before compression advice.
  • Calf tenderness or asymmetry when thrombosis is possible.
Red flags
  • Sudden unilateral painful swelling, calf warmth/tenderness.
  • Shortness of breath or chest pain.
  • Non-healing ulcer, rapid skin breakdown, bleeding varicose vein.
  • Absent or reduced foot pulses.
Investigations / management
  • Usually clinical diagnosis.
  • Duplex venous ultrasound when symptoms are significant, surgery is considered, reflux needs confirmation, or DVT must be excluded.
  • ABI before strong compression when arterial disease is suspected.
  • Elevation, walking/calf exercise, weight management, compression when arterial circulation is adequate, skin care, vascular assessment for severe symptoms or ulceration.
Exam trap

A painful swollen leg with varicose veins is not automatically uncomplicated venous disease; acute unilateral swelling and pain require DVT assessment.

Esophageal varices

Dilated submucosal esophageal veins caused by portal hypertension, most commonly from cirrhosis.

Portal hypertension bleeding
Full description

Esophageal varices can rupture and cause life-threatening upper gastrointestinal bleeding. Risk factors include cirrhosis, chronic viral hepatitis, alcohol-associated liver disease, non-alcoholic steatohepatitis, portal vein thrombosis, splenomegaly, and other signs of portal hypertension. Hematemesis in liver disease should be treated as possible variceal bleeding until proven otherwise.

Key history
  • Vomiting blood, black tarry stool, dizziness, syncope.
  • Known liver disease, alcohol use, viral hepatitis, abdominal swelling, easy bruising, confusion.
  • Medication review: NSAIDs, anticoagulants, antiplatelets.
Physical examination
  • Vital signs, orthostatic hypotension, pallor, signs of shock.
  • Jaundice, ascites, spider angiomas, palmar erythema, hepatosplenomegaly.
  • Asterixis and mental status for hepatic encephalopathy.
Red flags
  • Hematemesis, melena with dizziness, hypotension, tachycardia, syncope.
  • Confusion in liver disease, severe abdominal distension.
  • Known cirrhosis with gastrointestinal bleeding.
Investigations / management
  • CBC, INR/PT/coagulation profile, liver enzymes/bilirubin, albumin, renal function/electrolytes, type and screen/crossmatch.
  • Upper endoscopy for diagnosis and treatment; abdominal ultrasound for liver disease and portal hypertension assessment.
  • Active bleeding needs emergency department care, hemodynamic stabilization, blood product management when indicated, vasoactive medication, antibiotics, and urgent endoscopic therapy.
Exam trap

Hematemesis in a patient with cirrhosis should be treated as possible variceal bleeding until proven otherwise.

Hemorrhoids

Enlarged vascular cushions in the anal canal, internal above the dentate line and external below it.

Anorectal vascular cushions
Full description

Internal hemorrhoids are usually painless unless prolapsed, strangulated, or thrombosed. External hemorrhoids can be painful, especially when thrombosed. Risk factors include constipation, straining, pregnancy, prolonged sitting, low-fibre diet, obesity, chronic diarrhea, and portal hypertension in selected patients. Rectal bleeding must be assessed carefully because hemorrhoids can coexist with colorectal disease.

Key history
  • Bright red blood on toilet paper or stool surface.
  • Pain with defecation, anal itching, prolapse, mucus discharge.
  • Constipation, straining, change in bowel habits, weight loss, family history of colorectal cancer, anticoagulant/antiplatelet use.
Physical examination
  • External hemorrhoids, thrombosed external hemorrhoid, anal fissure.
  • Rectal mass; digital rectal examination when appropriate.
  • Anoscopy or proctoscopy when available and clinically appropriate.
Red flags
  • Melena, large-volume rectal bleeding, iron-deficiency anemia.
  • Unintentional weight loss, bowel habit change, rectal mass, family history of colorectal cancer.
  • New rectal bleeding in an older adult; severe pain with fever/systemic illness.
Investigations / management
  • CBC if recurrent or significant bleeding.
  • Colonoscopy or gastroenterology assessment when red flags are present.
  • Anoscopy for local anorectal disease; stool testing may be used for screening but does not replace evaluation of concerning bleeding.
  • Fibre, fluids, avoid straining, stool softening when appropriate, sitz baths, topical symptom relief.
Exam trap

Bright red rectal bleeding is not automatically hemorrhoids. Red flags require colorectal assessment.

Aortic aneurysm

Abnormal dilation of the aorta from arterial wall weakening, involving thoracic or abdominal aorta.

Large artery dilation
Full description

Abdominal aortic aneurysm usually occurs below the renal arteries and is associated with atherosclerosis, smoking, older age, and male sex. Thoracic aneurysm may be associated with hypertension, connective tissue disorders, bicuspid aortic valve, or genetic aortopathy. Rupture can cause rapid hemorrhagic shock and death.

Key history
  • Deep abdominal, back, flank, chest, or tearing pain.
  • Pulsatile abdominal mass, syncope, known aneurysm.
  • Smoking, hypertension, family history, connective tissue disease, bicuspid aortic valve, prior aneurysm.
Physical examination
  • Vital signs and shock signs.
  • Abdominal pulsatile mass, abdominal/back/flank tenderness.
  • Peripheral pulses, limb perfusion, neurologic symptoms.
  • Cardiac murmur when thoracic aneurysm or aortic valve disease is suspected.
Red flags
  • Sudden severe abdominal, back, chest, or flank pain.
  • Syncope, hypotension, pulsatile abdominal mass, known aneurysm with new pain.
  • Signs of limb ischemia, neurologic deficit, shock.
Investigations / management
  • Abdominal ultrasound for screening or stable aneurysm assessment.
  • CT angiography for symptomatic aneurysm or surgical planning.
  • CBC, renal function, type and screen/crossmatch if rupture suspected, ECG/cardiac assessment when relevant.
  • Symptomatic or ruptured aneurysm requires emergency department and vascular surgery care.
Exam trap

The classic triad of pain, hypotension, and pulsatile mass may be incomplete. Do not wait for all signs before considering rupture.

Cerebral aneurysm

Focal dilation of an intracranial artery; rupture can cause subarachnoid hemorrhage.

Intracranial artery dilation
Full description

A cerebral aneurysm may be asymptomatic until rupture. Rupture causes a life-threatening hemorrhagic stroke pattern, often thunderclap headache with meningismus, vomiting, photophobia, loss of consciousness, seizure, or focal neurologic findings. Risk factors include family history, smoking, hypertension, polycystic kidney disease, connective tissue disorders, prior aneurysm, and vascular malformations.

Key history
  • Sudden severe headache or worst headache description.
  • Neck stiffness, vomiting, photophobia, loss of consciousness, seizure, focal neurologic symptoms.
  • Family history, hypertension, smoking, anticoagulant use.
Physical examination
  • Vital signs, level of consciousness, neck stiffness.
  • Cranial nerves, motor/sensory function, speech, coordination.
  • Fundoscopy when indicated; signs of raised intracranial pressure or meningismus.
Red flags
  • Thunderclap headache, worst headache of life.
  • Headache with syncope, seizure, neck stiffness, neurologic deficit, or altered mental status.
  • New severe headache during exertion, pregnancy, or postpartum.
Investigations / management
  • Non-contrast CT head, CT angiography when vascular lesion is suspected.
  • Lumbar puncture in selected cases when CT is negative but suspicion remains.
  • CBC, coagulation profile, electrolytes, ECG when acute neurologic event suspected.
  • Emergency neurology/neurosurgery pathway for suspected aneurysmal subarachnoid hemorrhage.
Exam trap

Thunderclap headache is subarachnoid hemorrhage until proven otherwise. Do not diagnose migraine first when onset is sudden and maximal at the beginning.

C. Blood Pressure disease topic bar

Open each blood-pressure topic separately: primary hypertension, secondary causes, crisis patterns, pulmonary hypertension, hypotension, and orthostatic changes from the vascular course.

Primary hypertension

Persistently elevated blood pressure without a single identifiable secondary cause.

Common adult hypertension
Full description

Primary hypertension is the most common form of adult hypertension and is usually asymptomatic. Risk factors include age, family history, high sodium intake, obesity, sedentary lifestyle, alcohol excess, smoking, diabetes, chronic kidney disease, obstructive sleep apnea, and dyslipidemia. Diagnosis requires repeated properly measured readings and assessment of cardiovascular risk.

Key history
  • Previous and home BP readings.
  • Cardiovascular, stroke/TIA, kidney disease, diabetes, sleep apnea symptoms.
  • Smoking, alcohol, diet/sodium, exercise, medication/supplement use, family history.
Physical examination
  • Proper BP measurement; both arms when appropriate.
  • Heart rate, BMI/waist circumference.
  • Fundoscopy when indicated, cardiac exam, carotid bruits, peripheral pulses, abdominal bruit, edema.
  • Neurologic exam when symptoms suggest target-organ involvement.
Red flags
  • Chest pain, dyspnea, neurologic deficit, confusion, seizure, papilledema.
  • Acute kidney injury signs, severe headache with neurologic features, pregnancy with severe BP.
  • Severe tearing chest/back pain suggesting aortic dissection.
Investigations / management
  • Creatinine/eGFR, electrolytes, fasting glucose or HbA1c, lipid profile, urinalysis, urine ACR when indicated, ECG.
  • Lifestyle foundations: sodium reduction, weight management, physical activity, moderation of alcohol, smoking cessation, dietary improvement.
  • Pharmacotherapy when medically indicated based on BP and risk.
Exam trap

Do not diagnose chronic hypertension from a single mildly elevated reading taken during pain, anxiety, acute illness, or poor technique.

Secondary hypertension

Elevated BP due to an underlying condition, medication, substance, endocrine disorder, renal disease, or vascular cause.

Identifiable cause
Full description

Secondary hypertension should be suspected when hypertension is atypical, severe, resistant, sudden in onset, young onset, or associated with clinical clues. Causes include chronic kidney disease, renal artery stenosis, polycystic kidney disease, glomerulonephritis, primary aldosteronism, pheochromocytoma, Cushing syndrome, thyroid disease, hyperparathyroidism, obstructive sleep apnea, coarctation, medications, stimulants, licorice, and excess alcohol.

Key history
  • Young onset, sudden worsening, resistant hypertension.
  • Episodic headache/sweating/palpitations, muscle cramps or weakness, snoring/daytime sleepiness.
  • Kidney disease, urinary abnormalities, medication/supplement/substance use, family history of early hypertension or kidney disease.
Physical examination
  • BP both arms, radiofemoral delay when coarctation suspected.
  • Abdominal bruit, pulses, fundoscopy when indicated.
  • Cushingoid features, thyroid enlargement/tremor, OSA features, CKD signs.
Red flags
  • Onset before 30 without obesity/family history.
  • Resistant or severe hypertension, hypokalemia, abdominal bruit.
  • Episodic headache/sweating/palpitations, kidney dysfunction, flash pulmonary edema, weak femoral pulses.
Investigations / management
  • Creatinine/eGFR, electrolytes, urinalysis, urine ACR.
  • Renal ultrasound, aldosterone-renin ratio, plasma or urinary metanephrines, TSH, sleep study, renal artery imaging based on suspected cause.
  • Treat underlying cause and control BP; use specialty pathway when needed.
Exam trap

Hypokalemia with hypertension should raise suspicion for primary aldosteronism, especially without potassium-wasting diuretic use.

Hypertensive crisis

Severe blood pressure elevation where the key distinction is acute target-organ damage.

Severe BP elevation
Full description

Hypertensive emergency is severe BP elevation with acute target-organ damage such as stroke, intracranial hemorrhage, hypertensive encephalopathy, acute coronary syndrome, acute heart failure or pulmonary edema, aortic dissection, acute kidney injury, eclampsia, severe preeclampsia, or papilledema with neurologic symptoms. Severe asymptomatic hypertension is markedly elevated BP without acute organ damage and is not managed the same way.

Key history
  • Chest pain, dyspnea, severe headache, confusion, visual change, neurologic deficit, seizure.
  • Reduced urine output, pregnancy/postpartum state, stimulant/cocaine use, medication nonadherence.
  • Known aneurysm or aortic disease.
Physical examination
  • Repeat BP with proper technique; both arms if dissection suspected.
  • Neurologic status and fundoscopy when indicated.
  • Heart/lung exam, pulses, pulmonary edema signs, pregnancy-related assessment when relevant.
Red flags
  • Chest pain, neurologic deficit, confusion, seizure, papilledema.
  • Acute dyspnea, pulmonary edema, severe tearing chest/back pain.
  • Pregnancy with severe hypertension, acute kidney injury signs.
Investigations / management
  • ECG, troponin when chest pain/ischemia suspected, creatinine/electrolytes, urinalysis, CBC.
  • Chest imaging for pulmonary edema or aortic disease, CT head for neurologic symptoms, pregnancy testing when relevant.
  • Hypertensive emergency requires emergency care, monitored BP reduction, and treatment of the specific organ injury.
Exam trap

Hypertensive emergency is defined by acute target-organ damage, not by the BP number by itself.

Pulmonary hypertension

Elevated pressure in the pulmonary circulation that increases right ventricular workload.

Pulmonary arterial pressure
Full description

Pulmonary hypertension can result from pulmonary arterial disease, left heart disease, chronic lung disease or hypoxia, chronic thromboembolic disease, or multifactorial mechanisms. It may progress to right heart failure. Associated conditions include left heart failure, valvular disease, COPD, interstitial lung disease, obstructive sleep apnea, prior PE, connective tissue disease, congenital heart disease, portal hypertension, HIV, and certain drugs or toxins.

Key history
  • Progressive exertional dyspnea, fatigue, chest pressure.
  • Syncope/presyncope, palpitations, leg swelling, reduced exercise tolerance.
  • PE history, lung disease, sleep apnea symptoms, connective tissue disease symptoms, liver disease, family history.
Physical examination
  • Oxygen saturation, respiratory disease signs.
  • Loud pulmonary component of S2, right ventricular heave.
  • JVP, peripheral edema, hepatomegaly, ascites, cyanosis, clubbing when lung disease present.
Red flags
  • Syncope with exertion, resting hypoxemia.
  • Chest pain with dyspnea, right heart failure signs, hemoptysis.
  • Rapidly worsening dyspnea, PE history, severe pregnancy-related dyspnea/syncope.
Investigations / management
  • Oxygen saturation, ECG, chest X-ray, echocardiography, BNP/NT-proBNP when heart failure suspected.
  • Pulmonary function tests, CT pulmonary angiography or V/Q scan for thromboembolic disease, sleep study, autoimmune testing when indicated.
  • Right heart catheterization confirms and classifies pulmonary hypertension.
Exam trap

Pulmonary hypertension may be misread as asthma, anxiety, or deconditioning. Exertional syncope, loud P2, elevated JVP, and right-sided failure signs should raise suspicion.

Hypotension

Abnormally low BP causing symptoms or inadequate tissue perfusion.

Low perfusion pressure
Full description

Hypotension may be acute or chronic. Causes include dehydration, vomiting/diarrhea, hemorrhage, diuretic excess, myocardial infarction, arrhythmia, heart failure, valvular disease, sepsis, anaphylaxis, neurogenic shock, adrenal insufficiency, severe hypothyroidism, antihypertensives, nitrates, alpha blockers, tricyclics, opioids, and alcohol. The priority is perfusion and shock assessment.

Key history
  • Dizziness, syncope, weakness, chest pain, palpitations, dyspnea.
  • Fever, bleeding, vomiting/diarrhea, reduced intake, medication changes.
  • Allergic exposure, diabetes/autonomic symptoms, adrenal disease risk.
Physical examination
  • BP and pulse, orthostatic vitals when safe, temperature.
  • Mental status, capillary refill, skin temperature, mucous membranes, JVP.
  • Heart/lung exam, abdominal tenderness, bleeding signs, peripheral perfusion.
Red flags
  • Syncope with injury, chest pain, shortness of breath, altered mental status.
  • Fever with hypotension, shock signs, severe allergic reaction, active bleeding.
  • Pregnancy with hypotension, new hypotension with cardiac disease.
Investigations / management
  • CBC, electrolytes, creatinine, glucose, ECG.
  • Troponin when cardiac ischemia suspected, lactate/blood cultures when sepsis or shock suspected.
  • Pregnancy test when relevant, chest imaging or urinalysis based on presentation.
  • Acute symptomatic hypotension, shock, sepsis, anaphylaxis, MI, arrhythmia, or active bleeding requires urgent care.
Exam trap

A low BP number is less important than perfusion. Confusion, cold clammy skin, syncope, oliguria, chest pain, or dyspnea makes hypotension dangerous.

Orthostatic changes

Drop in BP after standing due to failure to maintain cerebral perfusion during position change.

Position-related BP drop
Full description

Orthostatic hypotension is commonly defined as a systolic BP drop of at least 20 mmHg or diastolic drop of at least 10 mmHg within 3 minutes of standing. Causes include dehydration, blood loss, diuretics, antihypertensives, alpha blockers, diabetic autonomic neuropathy, Parkinson disease/autonomic failure, prolonged bed rest, alcohol, and adrenal insufficiency. Pulse response helps interpret mechanism.

Key history
  • Dizziness on standing, near-syncope, syncope, falls.
  • Medication timing, fluid intake, vomiting/diarrhea, blood loss.
  • Diabetes, neurologic disease, palpitations, chest pain, meal-related symptoms.
Physical examination
  • Supine and standing BP and pulse.
  • Hydration status, cardiac rhythm, neurologic signs, peripheral neuropathy.
  • Gait/fall risk, anemia or bleeding signs.
Red flags
  • Syncope during exertion or while supine.
  • Palpitations before syncope, chest pain, dyspnea, new neurologic deficit.
  • Severe anemia signs, GI bleeding, recurrent falls in an older adult.
Investigations / management
  • CBC, electrolytes, creatinine, glucose, ECG, medication review.
  • Additional testing based on suspected bleeding, cardiac, endocrine, or neurologic disease.
  • Correct dehydration/blood loss, review medications, gradual position changes, compression garments when appropriate, physical counter-maneuvers, treat cause.
Exam trap

Orthostatic dizziness in diabetes may reflect autonomic neuropathy, but medication effect and volume depletion must still be assessed.

D. Ischemic Conditions disease topic bar

Open each ischemic condition separately. The focus is time-sensitive recognition of reduced blood flow, organ injury, embolism, infarction, and necrosis.

Ischemic heart disease

Reduced myocardial oxygen supply from coronary atherosclerosis or spasm causing stable angina, unstable angina, or infarction.

Coronary perfusion mismatch
Full description

Ischemic heart disease ranges from exertional stable angina to acute coronary syndrome. Coronary plaque, thrombosis, vasospasm, anemia, hypoxia, tachyarrhythmia, severe hypertension, or hypotension can create oxygen supply-demand mismatch. Risk is higher with diabetes, smoking, hypertension, dyslipidemia, CKD, older age, and family history.

Key history
  • Chest pressure, tightness, heaviness, burning, exertional pattern, rest symptoms.
  • Radiation to arm, jaw, neck, back, or epigastrium; dyspnea, diaphoresis, nausea, syncope.
  • CAD history, diabetes, CKD, hypertension, dyslipidemia, smoking, stimulant use.
Physical examination
  • Vital signs, oxygen saturation, cardiovascular and lung exam.
  • Signs of heart failure, new murmur, arrhythmia, shock.
  • Peripheral perfusion and signs of alternative diagnoses.
Red flags
  • Chest pain at rest or prolonged pain.
  • Dyspnea, diaphoresis, syncope, hypotension, heart failure signs.
  • Neurologic deficit or severe tearing pain suggesting dissection.
Investigations / management
  • ECG promptly when ACS suspected; serial troponins.
  • CBC, electrolytes, creatinine, glucose/lipids when appropriate; chest imaging when alternate causes considered.
  • Acute coronary syndrome requires emergency department/cardiology assessment.
Exam trap

Diabetic, older, and female patients may have atypical ischemic symptoms such as dyspnea, nausea, fatigue, or epigastric discomfort.

Myocardial infarction

Myocardial injury and necrosis from insufficient coronary blood supply, usually acute thrombosis after plaque rupture.

Cardiac muscle necrosis
Full description

ST-elevation myocardial infarction usually reflects acute coronary artery occlusion and requires urgent reperfusion assessment. Non-ST-elevation myocardial infarction has elevated troponin without diagnostic ST elevation. Unstable angina causes ischemic symptoms without troponin elevation. Rapid recognition is vital because myocardium is time-sensitive tissue.

Key history
  • Chest pressure, heaviness, burning, or tightness; radiation to arm/jaw/neck/back/epigastrium.
  • Dyspnea, diaphoresis, nausea/vomiting, syncope, palpitations.
  • Exertional pattern, prior CAD, diabetes, CKD, hypertension, dyslipidemia, smoking, stimulant use.
Physical examination
  • Vitals, oxygen saturation, distress level.
  • Heart sounds, new murmur, S3, lung crackles, peripheral perfusion.
  • Signs of cardiogenic shock, heart failure, arrhythmia.
Red flags
  • Persistent chest pain, STEMI pattern, hemodynamic instability.
  • Pulmonary edema, syncope, ventricular arrhythmia.
  • New neurologic symptoms or signs of shock.
Investigations / management
  • ECG, serial troponins, CBC, electrolytes, creatinine, glucose.
  • Chest imaging when differential diagnosis includes pulmonary or aortic disease.
  • Emergency department/cardiology pathway for suspected MI; urgent reperfusion assessment for STEMI.
Exam trap

A normal early troponin does not rule out MI. Serial testing and ECG interpretation are needed when suspicion persists.

Cardiac arrest

Abrupt loss of effective cardiac mechanical activity causing unresponsiveness, absent normal breathing, and absent pulse.

Loss of effective circulation
Full description

Cardiac arrest may result from ventricular fibrillation, pulseless ventricular tachycardia, asystole, pulseless electrical activity, acute myocardial infarction, severe hypoxia, massive pulmonary embolism, electrolyte disturbance, tamponade, tension pneumothorax, toxins, or severe shock. Immediate basic life support and defibrillation when indicated are time-critical.

Key history
  • Collapse, unresponsiveness, witnessed event, chest pain before collapse.
  • Dyspnea, syncope, seizure-like activity, medication/toxin exposure.
  • Known CAD, arrhythmia, heart failure, electrolyte disorder, PE risk.
Physical examination
  • Check responsiveness, breathing, pulse according to BLS principles.
  • Assess for airway obstruction, trauma, shockable rhythm when AED/monitor available.
  • After return of circulation: vitals, neurologic status, cardiac and pulmonary findings.
Red flags
  • Unresponsive patient with absent normal breathing or pulse.
  • Agonal breathing should not be mistaken for normal breathing.
  • Post-arrest chest pain, shock, hypoxia, neurologic deficit.
Investigations / management
  • Immediate CPR and AED/defibrillation pathway.
  • Emergency medical services activation.
  • After stabilization: ECG, troponin, electrolytes, glucose, blood gas/lactate, imaging/testing based on suspected cause.
Exam trap

Do not delay CPR while searching for a perfect diagnosis. Recognition and immediate resuscitation are the tested priorities.

Cerebrovascular accident / stroke

Acute neurologic deficit from ischemic or hemorrhagic injury to brain tissue.

Brain infarction or hemorrhage
Full description

Cerebrovascular accident can be ischemic from thrombosis or embolism, or hemorrhagic from vessel rupture. Symptoms reflect affected brain territory. Time of onset, last-known-well time, severity, anticoagulant use, BP, glucose, and stroke mimics must be assessed quickly. Stroke is time-sensitive and requires hospital-based stroke pathway.

Key history
  • Sudden weakness, facial droop, speech difficulty, vision loss, numbness, ataxia, vertigo.
  • Headache, seizure, altered mental status, last-known-well time.
  • Atrial fibrillation, hypertension, diabetes, smoking, anticoagulants, prior TIA/stroke.
Physical examination
  • Focused neurologic exam: face, arm/leg strength, speech, visual fields, coordination, gait when safe.
  • Vitals, glucose, cardiac rhythm, carotid/cardiovascular exam.
  • Assess swallowing and level of consciousness when appropriate.
Red flags
  • Any sudden focal neurologic deficit.
  • Decreased consciousness, severe headache, seizure, very high BP with neurologic symptoms.
  • Symptoms in pregnancy/postpartum or while anticoagulated.
Investigations / management
  • Emergency stroke assessment, non-contrast CT head to distinguish hemorrhage from ischemia.
  • CTA/vascular imaging when indicated, glucose, CBC, electrolytes/creatinine, coagulation profile, ECG.
  • Stroke prevention assessment after acute phase: AF, carotid disease, lipids, diabetes, BP, smoking.
Exam trap

Do not diagnose migraine or Bell palsy before excluding stroke when symptoms are sudden, focal, or involve speech/vision/limb weakness.

Transient ischemic attack

Brief focal neurologic dysfunction from temporary cerebral or retinal ischemia without persistent infarction.

Transient focal ischemia
Full description

TIA symptoms resolve, but the event is a warning sign for future stroke. Symptoms include transient unilateral weakness/numbness, speech disturbance, monocular vision loss, diplopia, or ataxia. Even if the patient feels normal, urgent stroke-prevention evaluation is required.

Key history
  • Exact symptom type, start time, duration, full resolution.
  • Weakness, numbness, speech disturbance, monocular blindness, visual field loss, ataxia.
  • AF, carotid disease, hypertension, diabetes, smoking, prior stroke/TIA, antithrombotic use.
Physical examination
  • Neurologic exam may be normal after resolution.
  • Cardiac rhythm, carotid bruits, BP, pulse, vascular risk assessment.
  • Look for residual deficits and stroke mimics.
Red flags
  • Recurrent or crescendo events.
  • Motor weakness, speech disturbance, symptoms lasting longer, AF, carotid bruit.
  • Symptoms with headache, seizure, altered mental status, or anticoagulant use.
Investigations / management
  • Urgent stroke/TIA assessment pathway.
  • Brain imaging, vascular imaging, ECG/monitoring for AF, labs including glucose, CBC, electrolytes/creatinine, lipids/HbA1c.
  • Secondary prevention: antithrombotic decisions, risk factor control, carotid/cardiac assessment when indicated.
Exam trap

TIA is not benign because symptoms resolved. It is a high-yield warning event requiring urgent stroke prevention assessment.

Avascular necrosis of femoral head

Death of bone tissue due to impaired blood supply, commonly affecting the femoral head.

Bone ischemia
Full description

Avascular necrosis of the femoral head can follow corticosteroid use, alcohol use, trauma/fracture/dislocation, sickle cell disease, autoimmune disease, clotting disorders, and other causes. It produces deep groin or hip pain, often worse with weight-bearing. Early X-rays may be normal, and MRI is the most sensitive early test.

Key history
  • Deep groin, hip, buttock, or thigh pain; weight-bearing pain.
  • Steroid exposure, alcohol use, trauma, sickle cell disease, lupus, thrombophilia, prior hip injury.
  • Functional limitation, limp, night pain, progression.
Physical examination
  • Gait, hip range of motion, pain with internal rotation.
  • Assess for trauma findings, leg length, neurologic and vascular status when relevant.
  • Look for bilateral hip involvement in high-risk patients.
Red flags
  • Severe pain after trauma, inability to bear weight.
  • Fever or systemic illness suggesting septic joint.
  • Rapid progression, neurologic deficit, or suspected fracture/dislocation.
Investigations / management
  • Hip X-ray initially, but early disease can be missed.
  • MRI is most sensitive for early avascular necrosis.
  • Orthopedic assessment when suspected or progressive; management depends on stage and cause.
Exam trap

A normal early X-ray does not exclude avascular necrosis when risk factors and deep groin pain are present.

Gangrene

Tissue death from critically reduced blood supply, infection, or both.

Tissue necrosis
Full description

Gangrene can be dry, wet, or gas-forming. Dry gangrene is ischemic necrosis often in PAD/diabetes. Wet gangrene includes infection with swelling, discharge, odor, systemic illness, and sepsis risk. Gas gangrene is a rapidly progressive necrotizing infection. In vascular exam questions, gangrene indicates limb-threatening disease and urgent care needs.

Key history
  • Black discoloration, pain or numbness, wound progression, foul drainage.
  • Diabetes, PAD, smoking, trauma, frostbite, infection symptoms.
  • Fever, chills, rapidly worsening pain, reduced pulses.
Physical examination
  • Colour, temperature, capillary refill, pulses, sensation, motor function.
  • Wound depth, drainage, odor, surrounding cellulitis, crepitus.
  • Vitals for sepsis and shock.
Red flags
  • Fever, tachycardia, hypotension, confusion.
  • Rapidly spreading infection, crepitus, severe pain out of proportion.
  • Absent pulses, motor/sensory loss, black necrosis with wet discharge.
Investigations / management
  • Urgent vascular/surgical assessment.
  • CBC, inflammatory markers, renal function, glucose, blood cultures when systemic illness, wound imaging as needed.
  • Vascular imaging, antibiotics for infected gangrene, debridement/amputation decisions under specialist care.
Exam trap

Dry black tissue with poor pulses may become infected. Wet gangrene and systemic illness are emergency patterns.

Embolism

Occlusion of a vessel by thrombus, plaque, air, fat, septic material, or other material traveling from another site.

Vascular obstruction by traveling material
Full description

Embolism causes sudden ischemia in the destination organ. Arterial embolism may cause acute limb ischemia, stroke, mesenteric ischemia, renal/splenic infarction, or myocardial ischemia. Venous thromboembolism can lodge in pulmonary arteries. Important sources include atrial fibrillation, valvular disease, mural thrombus after MI, DVT, endocarditis, atherosclerotic plaque, and trauma.

Key history
  • Sudden onset pain, neurologic deficit, dyspnea, chest pain, or organ-specific symptoms.
  • AF, recent surgery/immobility, DVT symptoms, cancer, pregnancy/postpartum, endocarditis symptoms.
  • Prior embolic event, anticoagulation use, vascular disease.
Physical examination
  • Pulse deficits, limb temperature, capillary refill, neurologic status.
  • Cardiac rhythm for AF; signs of DVT or PE.
  • Abdominal tenderness for mesenteric ischemia; skin findings for septic emboli.
Red flags
  • Sudden cold painful pulseless limb.
  • Sudden neurologic deficit, syncope, hypoxemia, pleuritic chest pain.
  • Severe abdominal pain out of proportion to exam.
Investigations / management
  • Testing depends on site: ECG, vascular ultrasound/CTA, CT head/CTA, CTPA, D-dimer in selected PE/DVT probability settings.
  • CBC, creatinine, coagulation profile before anticoagulation when appropriate.
  • Urgent specialty pathway based on organ threatened.
Exam trap

Embolic ischemia is often sudden. A normal limb exam hours earlier does not reduce concern when the current limb is cold, painful, and pulseless.

Pulmonary infarction

Ischemic injury to lung tissue, usually from pulmonary embolism blocking pulmonary arterial flow.

Lung tissue ischemia
Full description

Pulmonary infarction occurs when a pulmonary embolus compromises lung tissue perfusion, particularly in peripheral wedge-shaped areas. It may cause pleuritic chest pain, hemoptysis, dyspnea, tachycardia, fever, and pleural rub. It is closely linked to pulmonary embolism and should be approached through PE risk assessment.

Key history
  • Pleuritic chest pain, dyspnea, hemoptysis, cough, fever.
  • DVT symptoms, recent surgery, immobilization, cancer, estrogen therapy, pregnancy/postpartum, prior VTE.
  • Anticoagulant use or bleeding risk.
Physical examination
  • Vitals, oxygen saturation, respiratory rate, heart rate.
  • Chest exam for pleural rub, signs of DVT in legs.
  • Assess for shock, right heart strain, hypoxemia.
Red flags
  • Syncope, hypotension, hypoxemia, tachycardia.
  • Hemoptysis with dyspnea and pleuritic pain.
  • Pregnancy/postpartum state, cancer, recent surgery, or massive PE signs.
Investigations / management
  • Clinical probability assessment for PE.
  • D-dimer in selected low-probability cases; CTPA or V/Q scan when imaging indicated.
  • CBC, creatinine, coagulation profile before anticoagulation; ECG/chest imaging as needed.
Exam trap

Pulmonary infarction symptoms can mimic pneumonia or pleurisy, but hemoptysis with pleuritic pain and VTE risk should trigger PE assessment.

Pulmonary embolism

Obstruction of pulmonary arterial circulation, usually from thrombus arising in deep veins.

Pulmonary artery obstruction
Full description

Pulmonary embolism ranges from small peripheral emboli to massive PE with shock. Risk factors include DVT, surgery, immobility, cancer, pregnancy/postpartum, estrogen therapy, thrombophilia, prior VTE, and major trauma. Symptoms include sudden dyspnea, pleuritic chest pain, hemoptysis, syncope, tachycardia, and hypoxemia.

Key history
  • Dyspnea, pleuritic chest pain, cough, hemoptysis, syncope, palpitations.
  • Unilateral leg swelling/pain, surgery, immobility, travel, cancer, pregnancy/postpartum, estrogen, prior VTE.
Physical examination
  • Respiratory rate, oxygen saturation, heart rate, BP.
  • Signs of DVT: calf swelling, tenderness, warmth, erythema.
  • Signs of right heart strain or shock.
Red flags
  • Hypotension, syncope, severe hypoxemia, altered mental status.
  • Pleuritic chest pain with dyspnea and tachycardia.
  • Pregnancy/postpartum, cancer, recent surgery, unilateral leg swelling.
Investigations / management
  • Clinical probability assessment, D-dimer when appropriate, CTPA or V/Q scan.
  • Compression venous ultrasound when DVT suspected.
  • CBC, creatinine, coagulation profile; anticoagulation decisions and emergency care based on severity.
Exam trap

A swollen painful calf plus shortness of breath is possible PE, not uncomplicated venous disease.

E. Blood disease topic bar

Open each blood topic separately. This bar covers anemia patterns, white-cell abnormalities, platelet disorders, purpura, DIC, and thrombosis.

Aplastic anemia

Pancytopenia due to marrow failure with reduced red cells, white cells, and platelets.

Bone marrow failure
Full description

Aplastic anemia can be idiopathic or related to drugs, toxins, radiation, viral infections, autoimmune mechanisms, pregnancy, or inherited marrow failure syndromes. It presents with anemia symptoms, infections from neutropenia, and bleeding from thrombocytopenia. The exam task is to recognize pancytopenia rather than isolated iron deficiency.

Key history
  • Fatigue, dyspnea, pallor, infections, fever, easy bruising, nosebleeds, gum bleeding.
  • Medication/toxin/radiation exposure, viral illness, autoimmune disease, pregnancy.
  • Family history or congenital features when young.
Physical examination
  • Pallor, petechiae/purpura, mucosal bleeding, fever/infection signs.
  • Usually no splenomegaly; lymphadenopathy or splenomegaly suggests alternate diagnoses.
  • Vital signs and sepsis assessment when febrile.
Red flags
  • Fever with neutropenia symptoms.
  • Mucosal bleeding, severe anemia symptoms, syncope, chest pain.
  • Pancytopenia on CBC.
Investigations / management
  • CBC with differential, reticulocyte count, peripheral smear.
  • B12/folate/iron studies as indicated; viral/autoimmune testing based on context.
  • Bone marrow evaluation through hematology when marrow failure suspected.
Exam trap

Pancytopenia with low reticulocytes suggests marrow production failure; do not treat as simple iron deficiency.

Hemolytic anemia

Anemia caused by accelerated destruction of red blood cells.

Red cell destruction
Full description

Hemolytic anemia may be immune-mediated, hereditary, mechanical, microangiopathic, drug-induced, infectious, or related to G6PD deficiency or hemoglobinopathies. It presents with fatigue, jaundice, dark urine, splenomegaly, and elevated reticulocytes. Severe hemolysis can cause renal injury and hemodynamic instability.

Key history
  • Fatigue, dyspnea, jaundice, dark urine, abdominal pain.
  • New medications, infections, autoimmune disease, transfusion history, family history, G6PD triggers.
  • Gallstones or splenomegaly symptoms.
Physical examination
  • Pallor, jaundice, scleral icterus, splenomegaly.
  • Signs of severe anemia: tachycardia, flow murmur, hypotension.
  • Petechiae or neurologic signs if microangiopathic process suspected.
Red flags
  • Rapid drop in hemoglobin, dark urine, severe jaundice.
  • Neurologic symptoms, renal dysfunction, thrombocytopenia, fever.
  • Transfusion reaction symptoms.
Investigations / management
  • CBC, reticulocyte count, bilirubin, LDH, haptoglobin, peripheral smear.
  • Direct antiglobulin test when immune hemolysis suspected; G6PD testing when indicated.
  • Urgent care for severe anemia, hemolytic crisis, or microangiopathy.
Exam trap

High MCV can occur from reticulocytosis in hemolysis; macrocytosis is not always B12/folate deficiency.

Macrocytic anemia

Anemia with elevated mean corpuscular volume, commonly from B12/folate deficiency, alcohol/liver disease, hypothyroidism, medications, reticulocytosis, or marrow disease.

Large red cells
Full description

Macrocytic anemia is divided into megaloblastic and non-megaloblastic causes. B12 deficiency may cause neurologic symptoms and can occur with pernicious anemia, malabsorption, metformin or acid-suppressing medications, vegan diet, or GI surgery. Folate deficiency can occur with poor intake, alcoholism, pregnancy, hemolysis, or medications.

Key history
  • Fatigue, glossitis, paresthesias, gait changes, cognitive symptoms.
  • Diet, alcohol use, GI surgery, malabsorption, medications, thyroid/liver disease.
  • Bleeding, hemolysis, pregnancy, neurologic complaints.
Physical examination
  • Pallor, glossitis, jaundice if ineffective erythropoiesis/hemolysis.
  • Neurologic exam: vibration/proprioception, gait, reflexes.
  • Signs of liver disease, hypothyroidism, malnutrition.
Red flags
  • Neurologic deficits with suspected B12 deficiency.
  • Severe anemia, syncope, chest pain, pregnancy.
  • Pancytopenia or abnormal smear suggesting marrow disease.
Investigations / management
  • CBC with indices, reticulocyte count, B12, folate, TSH, liver enzymes.
  • Peripheral smear; methylmalonic acid/homocysteine when needed.
  • Treat cause; do not give folate without addressing possible B12 deficiency.
Exam trap

Folate can improve anemia while B12-related neurologic injury progresses. Check B12 when macrocytosis has neurologic features.

Microcytic anemia

Anemia with low MCV, commonly iron deficiency, thalassemia, anemia of chronic disease, sideroblastic anemia, or lead toxicity.

Small red cells
Full description

Iron deficiency is the most common microcytic anemia and should prompt evaluation of blood loss, diet, malabsorption, menstruation, pregnancy, or gastrointestinal bleeding. Thalassemia may show disproportionate microcytosis with normal/high RBC count. Anemia of chronic disease can be microcytic or normocytic.

Key history
  • Fatigue, pica, restless legs, dyspnea.
  • Menstrual bleeding, GI bleeding, diet, pregnancy, NSAID/aspirin use, malabsorption.
  • Family/ethnic history suggesting thalassemia.
Physical examination
  • Pallor, tachycardia, koilonychia, glossitis/angular cheilitis.
  • Abdominal/rectal exam when bleeding suspected and appropriate.
  • Signs of chronic inflammatory disease.
Red flags
  • Iron-deficiency anemia in an adult with GI symptoms or occult bleeding.
  • Melena, weight loss, bowel habit change.
  • Severe anemia symptoms, syncope, chest pain.
Investigations / management
  • CBC, ferritin, transferrin saturation, iron/TIBC, reticulocyte count.
  • Stool/GI evaluation when blood loss suspected; hemoglobin electrophoresis when thalassemia suspected.
  • Treat iron deficiency and underlying cause.
Exam trap

Do not give iron indefinitely without identifying the reason for iron deficiency, especially in adults with possible GI blood loss.

Normocytic anemia

Anemia with normal MCV from blood loss, early deficiency, chronic disease, kidney disease, hemolysis, marrow disease, or mixed causes.

Normal-sized red cells
Full description

Normocytic anemia requires reticulocyte interpretation. A high reticulocyte count suggests blood loss or hemolysis. A low reticulocyte count suggests underproduction from chronic kidney disease, inflammation, endocrine disease, marrow suppression, or early nutritional deficiency. Mixed deficiencies can normalize MCV.

Key history
  • Bleeding symptoms, fatigue, dyspnea, chronic disease, kidney disease.
  • Medication use, inflammatory disease, infection, cancer symptoms.
  • Dark urine or jaundice suggesting hemolysis.
Physical examination
  • Pallor, tachycardia, orthostatic changes.
  • Signs of bleeding, jaundice/splenomegaly, renal disease, inflammatory disease.
  • Lymphadenopathy or hepatosplenomegaly when marrow/malignancy possible.
Red flags
  • Acute bleeding, syncope, chest pain, severe dyspnea.
  • Pancytopenia, hemolysis signs, renal failure.
  • Weight loss, night sweats, abnormal smear.
Investigations / management
  • CBC, reticulocyte count, smear, creatinine/eGFR, ferritin/iron studies, B12/folate when mixed disease possible.
  • Hemolysis labs when indicated; inflammatory markers or malignancy evaluation based on clinical context.
  • Treat underlying cause.
Exam trap

Normal MCV does not mean benign anemia; mixed iron and B12 deficiency or kidney disease can produce normocytic anemia.

Anemia of chronic disease

Anemia due to chronic inflammation, infection, autoimmune disease, kidney disease, or malignancy affecting iron handling and erythropoiesis.

Inflammatory iron restriction
Full description

Anemia of chronic disease is often normocytic and sometimes microcytic. Inflammation increases hepcidin, reducing iron availability despite normal or increased ferritin. It can overlap with true iron deficiency, so interpretation of ferritin and transferrin saturation must consider inflammation and kidney function.

Key history
  • Chronic inflammatory disease, infection, malignancy symptoms, kidney disease.
  • Fatigue, reduced exercise tolerance, bleeding symptoms.
  • Medication use and nutritional history.
Physical examination
  • Signs of the underlying inflammatory, renal, infectious, autoimmune, or neoplastic process.
  • Pallor, edema/CKD signs, lymph nodes, organomegaly when indicated.
  • Assess for GI blood loss when iron deficiency remains possible.
Red flags
  • Unintentional weight loss, fever, night sweats.
  • Severe anemia symptoms or rapid hemoglobin drop.
  • Iron deficiency markers in an adult without clear cause.
Investigations / management
  • CBC, reticulocyte count, ferritin, iron/TIBC/transferrin saturation, CRP/ESR, creatinine/eGFR.
  • Evaluate underlying disease; distinguish from coexisting iron deficiency.
  • Management centers on treating the cause; hematology/nephrology input in complex disease.
Exam trap

Ferritin may be normal or high in inflammation even when functional iron availability is low; interpret iron studies in context.

Neutropenia

Reduced absolute neutrophil count causing increased bacterial and fungal infection risk.

Low neutrophils
Full description

Neutropenia may result from viral infections, medications, chemotherapy, autoimmune disease, nutritional deficiency, bone marrow disorders, severe infection, hypersplenism, or congenital causes. Severity and fever determine urgency. Febrile neutropenia is a medical emergency because infection may progress rapidly.

Key history
  • Fever, chills, sore throat, oral ulcers, skin infections, recurrent infections.
  • Medication/chemotherapy exposure, viral illness, autoimmune symptoms, nutritional risk.
  • Prior CBC trends and ethnicity/family history when benign neutropenia possible.
Physical examination
  • Temperature and sepsis signs.
  • Oral mucosa, throat, skin, perianal area, lungs.
  • Lymphadenopathy, hepatosplenomegaly, signs of marrow disease.
Red flags
  • Fever with neutropenia.
  • Hypotension, tachycardia, altered mental status.
  • Severe or rapidly worsening neutropenia, pancytopenia.
Investigations / management
  • CBC with differential, repeat CBC, peripheral smear.
  • Cultures and infection workup when febrile; B12/folate/copper, viral/autoimmune testing based on context.
  • Urgent hospital-based care for febrile neutropenia.
Exam trap

A neutropenic patient may have serious infection with subtle local signs because inflammatory response is blunted.

Eosinophilia

Elevated eosinophil count linked to allergy, asthma, parasites, drug reactions, autoimmune disease, adrenal insufficiency, or malignancy.

High eosinophils
Full description

Eosinophilia may be mild and reactive or severe with organ involvement. Common causes include atopy, asthma, eczema, helminth infection, medication reactions, eosinophilic gastrointestinal disease, connective tissue disease, adrenal insufficiency, and hematologic malignancy. Organ damage can involve lung, heart, skin, nervous system, and GI tract.

Key history
  • Allergy/asthma/eczema history, travel, parasite exposure, new medications/supplements.
  • Rash, fever, wheeze, abdominal pain/diarrhea, weight loss.
  • Cardiac symptoms, neuropathy, sinus disease, autoimmune symptoms.
Physical examination
  • Skin rash, wheeze, nasal polyps/sinus disease.
  • Cardiac exam, neurologic exam, abdominal tenderness, lymph nodes.
  • Signs of drug hypersensitivity or systemic illness.
Red flags
  • Eosinophilia with fever, rash, organ dysfunction, or new medication exposure.
  • Chest pain, dyspnea, neurologic symptoms.
  • Marked persistent eosinophilia or weight loss/night sweats.
Investigations / management
  • CBC differential trend, smear, medication review.
  • Stool/parasite testing or serology based on exposure; liver/kidney tests; chest imaging when pulmonary symptoms.
  • Target workup to suspected cause; specialist care for marked/persistent or organ-involving eosinophilia.
Exam trap

Do not assume eosinophilia is allergy when there is drug exposure, travel, systemic symptoms, or organ involvement.

Basophilia

Elevated basophils, often reactive but classically associated with myeloproliferative neoplasms such as chronic myeloid leukemia.

High basophils
Full description

Basophilia can occur with allergy, inflammation, infection, hypothyroidism, iron deficiency, and myeloproliferative disorders. Persistent basophilia with leukocytosis, splenomegaly, constitutional symptoms, or abnormal smear should raise concern for hematologic disease.

Key history
  • Allergy/inflammation symptoms, thyroid symptoms, infection symptoms.
  • Weight loss, night sweats, early satiety, abdominal fullness.
  • Prior CBC abnormalities or myeloproliferative history.
Physical examination
  • Lymphadenopathy, splenomegaly, hepatomegaly.
  • Skin/allergic findings, thyroid exam.
  • Pallor, bruising, infection signs if other cell lines abnormal.
Red flags
  • Persistent basophilia with high WBC.
  • Splenomegaly, weight loss, night sweats.
  • Abnormal smear or other cytopenias/cytoses.
Investigations / management
  • Repeat CBC with differential, peripheral smear.
  • TSH/iron studies or inflammatory/infectious workup if clinically indicated.
  • Hematology assessment when persistent, marked, or associated with abnormal smear or splenomegaly.
Exam trap

Basophilia is uncommon; persistent basophilia with leukocytosis should not be dismissed as simple allergy.

Thrombocytopenia

Reduced platelet count causing mucocutaneous bleeding risk and sometimes signaling serious systemic disease.

Low platelets
Full description

Thrombocytopenia can arise from decreased production, increased destruction, splenic sequestration, dilution, medications, immune thrombocytopenia, infection, liver disease, marrow disease, DIC, thrombotic microangiopathy, or pregnancy-related disorders. Bleeding pattern is often petechiae, purpura, bruising, epistaxis, gum bleeding, heavy menstrual bleeding, or GI/GU bleeding.

Key history
  • Easy bruising, petechiae, nosebleeds, gum bleeding, heavy menstrual bleeding.
  • Medication exposure, alcohol/liver disease, infection, autoimmune disease, pregnancy, recent heparin.
  • Neurologic symptoms, fever, abdominal pain, hematuria, melena.
Physical examination
  • Petechiae/purpura, mucosal bleeding, large bruises.
  • Hepatosplenomegaly, lymph nodes, fever, neurologic findings.
  • Blood pressure and shock signs if bleeding is significant.
Red flags
  • Severe headache or neurologic symptoms.
  • Fever, hypotension, rapidly progressive purpura.
  • Mucosal bleeding, GI bleeding, hematuria, pregnancy with hypertension.
  • Thrombocytopenia with anemia/renal dysfunction.
Investigations / management
  • CBC with platelet count, repeat CBC to exclude clumping, peripheral smear.
  • PT/INR, aPTT, fibrinogen/D-dimer when DIC suspected; liver/renal tests, viral/autoimmune testing as indicated.
  • Urgent care for severe bleeding, neurologic symptoms, DIC/TMA pattern, or very low platelets.
Exam trap

Platelet clumping can falsely lower automated platelet counts; confirm unexpected thrombocytopenia with smear or repeat testing.

Henoch-Schonlein purpura / IgA vasculitis

IgA-mediated small-vessel vasculitis causing palpable purpura, arthralgia, abdominal pain, and renal involvement.

Small-vessel vasculitis
Full description

Henoch-Schonlein purpura, now commonly called IgA vasculitis, is classically seen in children but can occur in adults. It often follows an upper respiratory infection. Palpable purpura on lower limbs/buttocks, joint pain, abdominal pain, GI bleeding, hematuria, and proteinuria are key features. Renal monitoring is essential.

Key history
  • Recent infection, rash, abdominal pain, vomiting, GI bleeding.
  • Joint pain/swelling, hematuria, edema, hypertension.
  • Medication exposure and systemic symptoms.
Physical examination
  • Palpable non-blanching purpura, especially legs/buttocks.
  • Abdominal tenderness, joint swelling, edema.
  • Blood pressure and urinalysis findings for renal involvement.
Red flags
  • Severe abdominal pain or GI bleeding.
  • Hematuria/proteinuria, hypertension, edema.
  • Neurologic symptoms or rapidly progressive purpura.
Investigations / management
  • CBC/platelets, urinalysis, creatinine/eGFR, urine protein assessment, inflammatory markers.
  • Stool blood testing if GI bleeding suspected; skin or renal biopsy in selected cases.
  • Monitor kidney involvement and use appropriate medical/specialist pathway when severe.
Exam trap

Palpable purpura with abdominal pain and hematuria is systemic vasculitis until proven otherwise, not simple bruising.

Disseminated intravascular coagulation

Widespread activation of coagulation causing microthrombi, consumption of platelets/clotting factors, and bleeding.

Systemic clotting and bleeding
Full description

DIC occurs secondary to severe illness such as sepsis, major trauma, malignancy, obstetric complications, severe transfusion reaction, pancreatitis, or shock. It produces simultaneous thrombosis and bleeding with falling platelets, prolonged PT/aPTT, low fibrinogen, elevated D-dimer, organ dysfunction, petechiae, purpura, oozing from lines, and shock.

Key history
  • Sepsis, trauma, cancer, obstetric complication, pancreatitis, transfusion reaction.
  • Bleeding, bruising, oozing from IV sites, shortness of breath, confusion, oliguria.
  • Fever, hypotension, severe systemic illness.
Physical examination
  • Vital signs and shock assessment.
  • Petechiae, purpura, ecchymoses, mucosal bleeding, line-site oozing.
  • Neurologic status, respiratory status, renal perfusion, limb ischemia signs.
Red flags
  • Fever with purpura and hypotension.
  • Bleeding plus thrombosis signs.
  • Altered mental status, oliguria, respiratory failure, rapidly progressive purpura.
Investigations / management
  • CBC/platelets, PT/INR, aPTT, fibrinogen, D-dimer, smear.
  • Renal/liver tests, lactate, blood cultures when sepsis suspected.
  • Emergency hospital-based care; treat underlying cause and provide blood product support when indicated.
Exam trap

DIC is not a primary diagnosis to treat in isolation. The underlying trigger, often sepsis or obstetric catastrophe, must be identified and managed.

Thrombosis

Formation of a clot inside a blood vessel causing venous or arterial obstruction.

Intravascular clot formation
Full description

Thrombosis may be venous, such as DVT, or arterial, such as stroke, MI, or acute limb ischemia. Causes include stasis, endothelial injury, hypercoagulability, cancer, antiphospholipid syndrome, pregnancy/postpartum state, estrogen therapy, surgery, immobilization, inflammatory disease, nephrotic syndrome, myeloproliferative disorders, and inherited thrombophilia.

Key history
  • Location-specific symptoms: unilateral leg swelling, chest pain/dyspnea, neurologic deficit, limb pain/coldness.
  • Recent surgery/immobility, cancer, pregnancy/postpartum, estrogen, family history, autoimmune disease.
  • Recurrent thrombosis, young age, unusual clot location, pregnancy losses.
Physical examination
  • Affected limb: swelling, tenderness, pulses, temperature, capillary refill.
  • Respiratory rate/oxygen saturation and heart rate for PE.
  • Neurologic/cardiac exam depending on thrombotic site.
Red flags
  • Sudden dyspnea, pleuritic chest pain, hemoptysis, syncope, hypoxemia.
  • Cold painful pulseless limb, neurologic deficit, chest pain.
  • Thrombosis with thrombocytopenia, unusual site, cancer symptoms.
Investigations / management
  • Clinical probability assessment, D-dimer when appropriate, venous ultrasound, CTPA, CTA, ECG/troponin based on site.
  • CBC, creatinine, coagulation profile when anticoagulation considered.
  • Treat the thrombotic event and prevent embolic complications; thrombophilia testing is selective.
Exam trap

A negative Homans sign does not exclude DVT. Use clinical probability and appropriate testing.

F. Cardiac Arrhythmias disease topic bar

Open each rhythm topic separately. This bar emphasizes pulse pattern, ECG recognition, instability, stroke risk, and urgent rhythm danger signs.

Atrial fibrillation

Supraventricular tachyarrhythmia with disorganized atrial activity and irregular ventricular response.

Irregularly irregular rhythm
Full description

Atrial fibrillation increases risk of stroke, heart failure, tachycardia-mediated cardiomyopathy, and hemodynamic instability. It may be paroxysmal, persistent, or permanent. Triggers and associations include age, hypertension, valvular disease, heart failure, hyperthyroidism, alcohol, infection, pulmonary disease, sleep apnea, and postoperative states.

Key history
  • Palpitations, dyspnea, fatigue, chest discomfort, dizziness, syncope.
  • Stroke/TIA symptoms, heart failure symptoms, thyroid symptoms, alcohol use, sleep apnea.
  • Medication use and anticoagulation history.
Physical examination
  • Irregularly irregular pulse, variable S1, rate assessment.
  • Blood pressure, oxygen saturation, heart failure signs, murmurs.
  • Neurologic screen for stroke/TIA.
Red flags
  • Chest pain, hypotension, pulmonary edema, syncope.
  • Neurologic deficit, very rapid rate with instability.
  • New AF in severe infection, PE, thyrotoxicosis, or MI pattern.
Investigations / management
  • ECG confirmation, electrolytes, TSH when indicated, CBC, renal function.
  • Echocardiography when structural disease suspected; stroke risk and bleeding risk assessment.
  • Unstable patients need urgent emergency/cardiology pathway; stable care involves rate/rhythm strategy and anticoagulation decisions when indicated.
Exam trap

AF can present as stroke or heart failure rather than palpitations. Always assess neurologic symptoms and hemodynamic stability.

Atrial premature beats

Premature atrial contractions producing early P waves and irregular pulse sensations.

Early atrial beats
Full description

Atrial premature beats are common and often benign, but frequent ectopy can be associated with stimulants, stress, sleep deprivation, alcohol, hyperthyroidism, electrolyte abnormalities, pulmonary disease, or structural heart disease. They may trigger supraventricular tachyarrhythmias in susceptible patients.

Key history
  • Skipped beats, fluttering, palpitations, triggers such as caffeine/alcohol/stimulants.
  • Chest pain, dyspnea, syncope, thyroid symptoms, medication use.
  • Frequency, exertional symptoms, known heart disease.
Physical examination
  • Pulse irregularity, BP, cardiac exam.
  • Signs of thyroid disease, heart failure, pulmonary disease.
  • Look for sustained tachyarrhythmia rather than isolated ectopy.
Red flags
  • Syncope, chest pain, dyspnea, sustained rapid rhythm.
  • Known structural heart disease or heart failure.
  • Neurologic symptoms or hemodynamic instability.
Investigations / management
  • ECG; ambulatory monitoring if intermittent or frequent symptoms.
  • Electrolytes, TSH when indicated, review stimulants and medications.
  • Reassurance and trigger reduction when benign; medical assessment when frequent, symptomatic, or associated with heart disease.
Exam trap

Do not diagnose anxiety before checking pulse and ECG when palpitations are recurrent or associated with red flags.

Ventricular premature beats / PVCs

Premature ventricular complexes arising from ventricular myocardium.

Early ventricular beats
Full description

PVCs may be benign in structurally normal hearts but can indicate ischemia, electrolyte imbalance, stimulant/toxin exposure, cardiomyopathy, myocarditis, hypoxia, or medication effect. Frequent PVCs may cause symptoms or contribute to cardiomyopathy. PVCs after MI or with structural heart disease require careful assessment.

Key history
  • Skipped beats, thumps, palpitations, dizziness.
  • Chest pain, dyspnea, syncope, stimulant use, electrolyte-loss history.
  • Known CAD, heart failure, myocarditis symptoms, family sudden death.
Physical examination
  • Pulse with premature beats and compensatory pause.
  • BP, cardiac exam, heart failure signs.
  • Assess for ischemia, hypoxia, and instability.
Red flags
  • Syncope, chest pain, sustained ventricular tachycardia.
  • PVCs with structural heart disease, MI symptoms, electrolyte disturbance.
  • Family history of sudden cardiac death.
Investigations / management
  • ECG, electrolytes including potassium/magnesium when appropriate, troponin if ischemia suspected.
  • Ambulatory monitoring for burden; echocardiography when structural disease suspected.
  • Urgency depends on symptoms, burden, and underlying heart disease.
Exam trap

PVCs in a healthy person differ from PVCs with chest pain, syncope, cardiomyopathy, or post-MI context.

Heart block

Impaired conduction from atria to ventricles, ranging from first-degree block to complete heart block.

AV conduction delay
Full description

Heart block may be due to aging conduction disease, ischemia/MI, medications such as beta blockers or calcium channel blockers, digoxin, electrolyte disturbances, Lyme disease, myocarditis, infiltrative disease, or post-procedure causes. Higher-grade block can cause bradycardia, syncope, heart failure, or sudden deterioration.

Key history
  • Dizziness, syncope, fatigue, exercise intolerance, dyspnea, chest pain.
  • Medication review, recent MI symptoms, tick exposure/Lyme symptoms, myocarditis symptoms.
  • Known conduction disease or pacemaker history.
Physical examination
  • Bradycardia, irregular pulse, cannon A waves in complete block sometimes.
  • BP, perfusion, mental status, heart failure signs.
  • Look for ischemia, medication toxicity, and neurologic injury from syncope.
Red flags
  • Syncope, hypotension, chest pain, pulmonary edema, altered mental status.
  • Second-degree Mobitz II or third-degree block.
  • Bradycardia with ischemia or medication toxicity.
Investigations / management
  • ECG is essential; electrolytes, renal function, medication/drug levels when relevant.
  • Troponin if ischemia suspected; Lyme testing when clinically indicated.
  • Unstable high-grade block needs urgent emergency/cardiology pathway and possible pacing.
Exam trap

First-degree block may be observed; Mobitz II and complete heart block are high-risk patterns.

Sinus bradycardia

Sinus rhythm with a low heart rate, sometimes physiologic and sometimes pathologic.

Slow sinus rhythm
Full description

Sinus bradycardia can be normal in athletes or during sleep. Pathologic causes include medications, hypothyroidism, hypothermia, increased intracranial pressure, inferior MI, sick sinus syndrome, electrolyte abnormalities, and vagal states. Symptoms and perfusion determine urgency.

Key history
  • Dizziness, syncope, fatigue, weakness, chest pain, dyspnea.
  • Medication review: beta blockers, calcium channel blockers, digoxin, antiarrhythmics, opioids.
  • Athletic conditioning, hypothyroid symptoms, cold exposure, MI symptoms.
Physical examination
  • Pulse rate and regularity, BP, perfusion, mental status.
  • Cardiac exam, heart failure signs, neurologic signs when ICP concern.
  • Temperature and thyroid signs.
Red flags
  • Hypotension, syncope, chest pain, altered mental status.
  • Pulmonary edema, shock, inferior MI symptoms.
  • Severe bradycardia with poor perfusion.
Investigations / management
  • ECG, electrolytes, glucose, TSH when indicated, medication review.
  • Troponin if ischemia suspected; renal function for drug accumulation.
  • Management depends on symptoms and cause; unstable bradycardia requires urgent care.
Exam trap

A low heart rate in an athlete can be normal, but bradycardia with syncope, chest pain, hypotension, or confusion is dangerous.

Sinus tachycardia

Sinus rhythm with elevated rate, often a physiologic response to stress or disease.

Fast sinus rhythm
Full description

Sinus tachycardia is commonly caused by fever, pain, anxiety, dehydration, anemia, hypoxia, sepsis, hyperthyroidism, pregnancy, stimulant use, withdrawal, pulmonary embolism, heart failure, or shock. The key exam task is to find the cause, not simply slow the rate.

Key history
  • Fever, pain, dehydration, vomiting/diarrhea, bleeding, infection symptoms.
  • Dyspnea, chest pain, palpitations, syncope, stimulant/substance use.
  • Thyroid symptoms, pregnancy, medication changes.
Physical examination
  • Vitals including temperature and oxygen saturation.
  • Hydration, bleeding signs, infection focus, lung and heart exam.
  • Signs of shock, anemia, PE, heart failure, thyroid disease.
Red flags
  • Hypotension, hypoxemia, chest pain, syncope, altered mental status.
  • Fever with sepsis signs, active bleeding, PE symptoms.
  • Persistent unexplained tachycardia.
Investigations / management
  • ECG to confirm sinus rhythm; CBC, electrolytes/creatinine, glucose, TSH, pregnancy test, infection workup as indicated.
  • D-dimer/CTPA or imaging based on PE probability; troponin when ischemia suspected.
  • Treat underlying cause.
Exam trap

Sinus tachycardia is a sign, not the final diagnosis. Look for sepsis, hemorrhage, PE, hypoxia, pain, and hyperthyroidism.

Supraventricular tachyarrhythmias

Rapid tachyarrhythmias originating above the ventricles, including AVNRT, AVRT, atrial tachycardia, atrial flutter, and related rhythms.

Rapid rhythm above ventricles
Full description

SVT often presents with sudden-onset regular palpitations, chest discomfort, dyspnea, anxiety, dizziness, or presyncope. It may be triggered by caffeine, alcohol, stimulants, stress, sleep deprivation, hyperthyroidism, infection, or structural heart disease. Atrial flutter may have stroke-risk implications similar to AF depending on context.

Key history
  • Abrupt onset/offset palpitations, rate, duration, triggers.
  • Chest pain, dyspnea, dizziness, syncope.
  • Known pre-excitation, structural heart disease, thyroid symptoms, stimulant use.
Physical examination
  • Heart rate/rhythm regularity, BP, perfusion.
  • Signs of heart failure, ischemia, hypoxia.
  • Assess for wide-complex tachycardia features.
Red flags
  • Hypotension, syncope, chest pain, pulmonary edema, altered mental status.
  • Wide-complex tachycardia until proven otherwise.
  • Pre-excitation with AF pattern.
Investigations / management
  • ECG during rhythm; electrolytes, TSH when indicated.
  • Ambulatory/event monitor if intermittent.
  • Unstable tachyarrhythmia requires urgent emergency/cardiology pathway; stable management depends on rhythm type.
Exam trap

A regular narrow-complex SVT is different from irregular wide-complex tachycardia. Treat unstable rhythms as emergencies.

Ventricular fibrillation

Chaotic ventricular electrical activity causing no effective cardiac output.

Shockable cardiac arrest rhythm
Full description

Ventricular fibrillation causes sudden cardiac arrest. Common causes include acute MI, ischemia, cardiomyopathy, electrolyte disturbance, QT prolongation, drug toxicity, hypoxia, and inherited channelopathies. Immediate CPR and defibrillation are required.

Key history
  • Collapse, unresponsiveness, no normal breathing, no pulse.
  • Preceding chest pain, syncope, palpitations, stimulant/toxin exposure.
  • History of CAD, cardiomyopathy, long QT, family sudden death.
Physical examination
  • Assess responsiveness, breathing, and pulse.
  • AED/monitor rhythm when available.
  • After return of circulation: neurologic, cardiac, pulmonary, perfusion status.
Red flags
  • Any suspected cardiac arrest.
  • Agonal breathing, pulselessness, cyanosis.
  • Recurrent VF or shock after ROSC.
Investigations / management
  • Immediate CPR and defibrillation/AED.
  • Emergency medical services and advanced cardiac life support pathway.
  • After stabilization: ECG, troponin, electrolytes, blood gas, toxicology when relevant, coronary evaluation when indicated.
Exam trap

Ventricular fibrillation is not a rhythm for pulse-check debate. Start CPR and defibrillate as soon as possible.

Ventricular tachycardia

Rapid ventricular rhythm that may be stable, unstable, or pulseless.

Wide-complex tachycardia
Full description

Ventricular tachycardia often occurs with structural heart disease, prior MI, cardiomyopathy, myocarditis, electrolyte disturbance, QT prolongation, drug toxicity, hypoxia, or inherited arrhythmia syndromes. It can deteriorate into ventricular fibrillation and cardiac arrest. Wide-complex tachycardia should be treated as VT until proven otherwise in many clinical settings.

Key history
  • Palpitations, chest pain, dyspnea, dizziness, syncope.
  • Prior MI/CAD, cardiomyopathy, heart failure, ICD, medications, electrolyte losses.
  • Family history of sudden cardiac death.
Physical examination
  • Rate, rhythm, BP, perfusion, mental status.
  • Heart failure signs, ischemia signs, oxygen saturation.
  • Pulse present versus pulseless.
Red flags
  • Hypotension, syncope, chest pain, pulmonary edema, altered mental status.
  • Pulseless VT.
  • Recurrent episodes, post-MI context, electrolyte abnormality.
Investigations / management
  • ECG, electrolytes including potassium/magnesium, creatinine, troponin when ischemia suspected.
  • Emergency/cardiology pathway for unstable or sustained VT.
  • Assess structural heart disease and reversible triggers.
Exam trap

Do not assume wide-complex tachycardia is SVT with aberrancy in an unstable patient; VT is the safer working diagnosis.

G. Pregnancy-specific vascular conditions topic bar

Open each pregnancy-specific vascular condition separately. The focus is maternal-fetal danger signs, bleeding patterns, hypertension, anemia, and urgent obstetric pathways.

Gestational hypertension

New hypertension after 20 weeks of pregnancy without proteinuria or severe features of pre-eclampsia at diagnosis.

Pregnancy BP elevation
Full description

Gestational hypertension can progress to pre-eclampsia and requires careful monitoring of BP, symptoms, urine protein, platelets, liver enzymes, renal function, fetal growth, and maternal symptoms. Risk factors overlap with pre-eclampsia, including prior hypertensive disorder of pregnancy, chronic hypertension, kidney disease, diabetes, autoimmune disease, multifetal pregnancy, obesity, and advanced maternal age.

Key history
  • Gestational age, prior BP, headache, visual symptoms, RUQ/epigastric pain.
  • Dyspnea, edema, reduced fetal movement, prior pre-eclampsia.
  • Chronic hypertension, kidney disease, diabetes, autoimmune disease, medications.
Physical examination
  • Accurate BP measurement, repeat BP, reflexes/clonus when indicated.
  • Edema, RUQ tenderness, lung exam for pulmonary edema.
  • Fetal assessment pathway depending on setting.
Red flags
  • Severe-range BP, headache, visual symptoms, RUQ/epigastric pain.
  • Dyspnea/pulmonary edema, neurologic symptoms, decreased fetal movement.
  • Abnormal platelets, liver enzymes, creatinine, or proteinuria.
Investigations / management
  • Urinalysis/protein assessment, CBC/platelets, creatinine, liver enzymes.
  • Fetal monitoring/growth assessment under obstetric care.
  • Obstetric assessment and close follow-up; urgent care when severe features appear.
Exam trap

Gestational hypertension is not harmless; it can evolve into pre-eclampsia even when initial urine protein is absent.

Antepartum anemia

Anemia during pregnancy, most often iron deficiency but also folate/B12 deficiency, hemoglobinopathy, bleeding, or chronic disease.

Pregnancy anemia
Full description

Antepartum anemia increases maternal fatigue, dyspnea, palpitations, reduced reserve during bleeding, and adverse pregnancy outcomes depending on severity and cause. Iron requirements rise during pregnancy. Macrocytosis, hemoglobinopathy risk, bleeding symptoms, and poor response to iron require broader evaluation.

Key history
  • Fatigue, dyspnea, dizziness, palpitations, pica.
  • Diet, nausea/vomiting, prior anemia, heavy bleeding, interpregnancy interval.
  • Family/ethnic history of hemoglobinopathy, GI symptoms, medications.
Physical examination
  • Pallor, tachycardia, orthostatic changes, flow murmur.
  • Signs of bleeding, nutritional deficiency, glossitis, neurologic signs if B12 deficiency suspected.
  • Assess gestational age and obstetric context.
Red flags
  • Syncope, chest pain, severe dyspnea, hemodynamic instability.
  • Anemia with vaginal bleeding, abdominal pain, or suspected abruption/previa.
  • Macrocytosis with neurologic symptoms; hemoglobinopathy concern.
Investigations / management
  • CBC with indices, ferritin/iron studies, reticulocyte count.
  • B12/folate when macrocytic or risk factors; hemoglobin electrophoresis when indicated.
  • Treat cause and coordinate with obstetric care; urgent care for unstable bleeding or severe symptoms.
Exam trap

Do not assume every pregnancy anemia is simple iron deficiency when MCV is high, neurologic symptoms are present, or hemoglobinopathy risk exists.

Placenta previa

Placenta partially or completely covering the cervical os, causing risk of painless vaginal bleeding.

Painless antepartum bleeding
Full description

Placenta previa typically presents with painless bright-red vaginal bleeding in the second half of pregnancy. Risk factors include prior cesarean delivery, prior placenta previa, multiple gestation, multiparity, advanced maternal age, smoking, and uterine surgery. Digital vaginal examination can provoke severe bleeding if previa is present.

Key history
  • Gestational age, bleeding amount, pain, contractions, fetal movement.
  • Prior ultrasound placental location, prior cesarean/uterine surgery, prior previa.
  • Dizziness, syncope, anticoagulant use, Rh status when known.
Physical examination
  • Maternal vitals and hemodynamic status.
  • Abdominal exam for tenderness/contractions; fetal assessment under obstetric pathway.
  • Avoid digital vaginal exam until placenta previa excluded.
Red flags
  • Any significant vaginal bleeding in pregnancy.
  • Bleeding with hypotension, tachycardia, syncope, or decreased fetal movement.
  • Recurrent bleeding or preterm contractions.
Investigations / management
  • Urgent obstetric assessment.
  • Ultrasound to confirm placental location; CBC, blood type/Rh, crossmatch when significant bleeding.
  • Management depends on gestational age, bleeding severity, maternal/fetal stability, and obstetric plan.
Exam trap

Painless antepartum bleeding is placenta previa until excluded. Avoid digital vaginal exam before placental location is known.

Abruptio placenta

Premature separation of placenta from uterine wall causing painful bleeding and maternal-fetal risk.

Painful placental separation
Full description

Placental abruption often presents with painful vaginal bleeding, abdominal or back pain, uterine tenderness, contractions, hypertonic uterus, fetal distress, and sometimes concealed bleeding. Risk factors include hypertension/pre-eclampsia, trauma, cocaine use, smoking, prior abruption, multifetal pregnancy, and premature rupture of membranes.

Key history
  • Bleeding amount, abdominal/back pain, contractions, trauma, decreased fetal movement.
  • Hypertension/pre-eclampsia symptoms, cocaine/smoking, prior abruption.
  • Dizziness/syncope and gestational age.
Physical examination
  • Maternal vitals, shock signs, uterine tenderness/rigidity, abdominal pain.
  • Assess bleeding and fetal status through obstetric pathway.
  • Look for DIC signs in severe abruption.
Red flags
  • Painful bleeding with uterine tenderness or rigidity.
  • Decreased fetal movement, fetal distress, maternal hypotension/tachycardia.
  • Trauma, severe hypertension, coagulopathy/DIC signs.
Investigations / management
  • Emergency obstetric assessment.
  • CBC, coagulation profile, fibrinogen, blood type/Rh, crossmatch.
  • Ultrasound can help but does not exclude abruption; management depends on maternal/fetal stability and gestational age.
Exam trap

Abruption may have concealed bleeding. Shock can be worse than visible blood loss suggests.

Pre-eclampsia

New hypertension after 20 weeks with proteinuria or maternal organ dysfunction, with risk of seizures, stroke, organ injury, and fetal compromise.

Hypertensive pregnancy disorder
Full description

Pre-eclampsia can involve kidney injury, liver injury, thrombocytopenia, neurologic symptoms, pulmonary edema, fetal growth restriction, and placental dysfunction. Severe features include severe-range BP, headache, visual symptoms, RUQ/epigastric pain, low platelets, elevated liver enzymes, renal dysfunction, pulmonary edema, or neurologic symptoms. Eclampsia is seizures in this disease context.

Key history
  • Headache, visual symptoms, RUQ/epigastric pain, dyspnea, swelling.
  • Reduced fetal movement, prior pre-eclampsia, chronic hypertension, kidney disease, diabetes, autoimmune disease.
  • Gestational age and BP history.
Physical examination
  • Accurate repeat BP, neurologic status, reflexes/clonus when indicated.
  • Lung exam for pulmonary edema, RUQ tenderness, edema.
  • Fetal assessment via obstetric care pathway.
Red flags
  • Severe BP, persistent headache, visual symptoms.
  • RUQ/epigastric pain, dyspnea/pulmonary edema, neurologic symptoms, seizure.
  • Low platelets, elevated liver enzymes, renal dysfunction, decreased fetal movement.
Investigations / management
  • Urine protein assessment, CBC/platelets, creatinine, liver enzymes.
  • Fetal monitoring/growth assessment; additional tests under obstetric care.
  • Urgent obstetric assessment for severe features; management may include antihypertensives, magnesium sulfate, and delivery planning depending on severity/gestational age.
Exam trap

Pre-eclampsia is systemic vascular-endothelial disease, not just high BP. Symptoms and organ injury determine urgency.

Conditions tested in the vascular system

The vascular course is organized around the condition groups that a CONO-II candidate needs to recognize in clinical vignettes.

Circulatory flow

Lymphedema, central edema, peripheral edema, pulmonary edema, Raynaud’s disease [primary Raynaud’s phenomenon], chronic arterial insufficiency/chronic venous insufficiency, stasis dermatitis, peripheral vascular disease, hyperlipidemia, intermittent claudication, cluster headache, and migraine headache.

Blood vessels

Varicose veins, esophageal varices, hemorrhoids, aortic aneurysm, and cerebral aneurysm.

Blood pressure

Primary hypertension, secondary hypertension, hypertensive crisis, pulmonary hypertension, hypotension, and orthostatic changes from the vascular course.

Ischemic conditions

Ischemic heart disease, myocardial infarction, cardiac arrest, cerebrovascular accident, transient ischemic attack, avascular necrosis, gangrene, embolism, pulmonary infarction, and pulmonary embolism.

Blood

Aplastic, hemolytic, macrocytic, microcytic, normocytic, and chronic-disease anemia; neutropenia, eosinophilia, basophilia, thrombocytopenia, purpura, disseminated intravascular coagulation, and thrombosis.

Arrhythmias

Atrial fibrillation, atrial and ventricular premature beats, heart block, premature ventricular contractions/ventricular ectopic beats, sinus bradycardia, sinus tachycardia, supraventricular tachyarrhythmias, ventricular fibrillation, and ventricular tachycardia.

Pregnancy-specific vascular conditions

Gestational hypertension, antepartum anemia, placenta previa, abruptio placenta, and pre-eclampsia.

30–34%Assessment & Diagnosis

History, physical examination, lab/imaging selection, differential diagnosis, and interpretation.

55–59%Modalities

Applied management principles appear when risk reduction, lifestyle counselling, nutrition, and exercise are tested.

9–13%Critical Care & Public Health

Used when chest pain, stroke symptoms, pulmonary embolism, shock, severe bleeding, or limb-threatening ischemia appears.

Vascular lessons

Use these blocks for quick review before entering practice mode. The wording is rewritten for BoardQBank course navigation and active recall.

01

Circulatory Flow

Differentiate arterial, venous, lymphatic, lipid, and headache patterns.

Blueprint: Assessment & DiagnosisCritical care recognitionCase-based reasoning
Covered conditions

Lymphedema, central edema, peripheral edema, pulmonary edema, Raynaud’s disease [primary Raynaud’s phenomenon], chronic arterial insufficiency/chronic venous insufficiency, stasis dermatitis, peripheral vascular disease, hyperlipidemia, intermittent claudication, cluster headache, and migraine headache.

Recognition checklist
  • Unilateral painful swelling requires DVT consideration.
  • Venous disease: edema, heaviness, pigmentation, medial malleolar ulcer.
  • Arterial disease: weak pulses, exertional pain, cold limb, distal ulcer.
  • Cluster headache: unilateral orbital pain with autonomic signs and restlessness.
Red flags
  • Sudden unilateral painful leg swelling
  • Chest pain or shortness of breath
  • Rest pain or non-healing ulcer
  • Digital ulcers or necrosis in Raynaud
  • Thunderclap or focal neurologic headache features
Exam traps
  • Compression helps venous disease, but severe arterial disease must be excluded.
  • Migraine aura develops gradually; sudden focal deficit is stroke/TIA until proven otherwise.
  • Very high triglycerides can increase pancreatitis risk.
Practice Topic 01 Back to course map
02

Blood Vessels

Recognize venous dilation, portal hypertension, aneurysm, rupture, and thrombotic danger patterns.

Blueprint: Assessment & DiagnosisCritical care recognitionCase-based reasoning
Covered conditions

Varicose veins, hemorrhoids, esophageal varices, aortic aneurysm, cerebral aneurysm, venous thrombosis, arterial occlusion.

Recognition checklist
  • Varicose veins: tortuous superficial veins with heaviness after standing.
  • Hemorrhoids: bright red bleeding but red flags require colorectal assessment.
  • Esophageal varices: hematemesis in cirrhosis.
  • Aortic aneurysm: sudden abdominal/back pain with hypotension or pulsatile mass.
  • Cerebral aneurysm rupture: thunderclap headache with vomiting/neck stiffness.
Red flags
  • Hematemesis in cirrhosis
  • Thunderclap headache
  • Pulsatile abdominal mass with pain
  • Bright red bleeding with anemia/weight loss/bowel habit change
  • Acute cold pulseless limb
Exam traps
  • Do not attribute all rectal bleeding to hemorrhoids.
  • The classic ruptured AAA triad may be incomplete.
  • Upper GI bleeding in cirrhosis is variceal bleeding until proven otherwise.
Practice Topic 02 Back to course map
03

Blood Pressure

Confirm accurate measurement, separate primary from secondary causes, and identify target-organ damage.

Blueprint: Assessment & DiagnosisCritical care recognitionCase-based reasoning
Covered conditions

Primary hypertension, secondary hypertension, hypertensive emergency, severe asymptomatic hypertension, hypotension, orthostatic hypotension, pulmonary hypertension.

Recognition checklist
  • A single mildly elevated office reading does not diagnose chronic hypertension.
  • Hypokalemia with hypertension suggests primary aldosteronism.
  • Severe BP with acute organ damage is hypertensive emergency.
  • Orthostatic hypotension requires BP and pulse interpretation.
  • Pulmonary hypertension causes exertional dyspnea, syncope, loud P2, and right-sided strain.
Red flags
  • Chest pain
  • Neurologic deficit
  • Confusion or seizure
  • Pulmonary edema
  • Severe tearing chest/back pain
  • Pregnancy with severe hypertension
  • Syncope with exertional dyspnea
Exam traps
  • The emergency is target-organ damage, not the BP number itself.
  • Do not rapidly lower severe asymptomatic hypertension without organ damage.
  • Pulmonary hypertension can be mistaken for asthma, anxiety, or deconditioning.
Practice Topic 03 Back to course map
04

Ischemic Conditions

Identify reduced blood flow, infarction, embolism, and tissue necrosis before irreversible damage occurs.

Blueprint: Assessment & DiagnosisCritical care recognitionCase-based reasoning
Covered conditions

Myocardial infarction, stroke, transient ischemic attack, pulmonary embolism, acute limb ischemia, gangrene, avascular necrosis.

Recognition checklist
  • MI may present with chest pressure, dyspnea, diaphoresis, nausea, epigastric pain, or weakness.
  • Stroke/TIA causes sudden focal neurologic deficit.
  • PE may present with dyspnea, pleuritic chest pain, tachycardia, syncope, or hemoptysis.
  • Acute limb ischemia: pain, pallor, pulselessness, paresthesia, paralysis, poikilothermia.
  • Wet/gas gangrene is a systemic infection risk.
Red flags
  • Chest pain with diaphoresis or dyspnea
  • Sudden unilateral weakness or speech change
  • Syncope with dyspnea
  • Cold pulseless limb
  • Motor deficit in limb ischemia
  • Fever with necrotic tissue
Exam traps
  • A normal initial ECG does not exclude acute coronary syndrome.
  • TIA is a warning event and needs urgent stroke prevention assessment.
  • Pulmonary embolism may have normal lung auscultation.
Practice Topic 04 Back to course map
05

Inflammation, Thrombosis & Bleeding

Connect rash, vessel pain, clot risk, bleeding signs, and systemic illness.

Blueprint: Assessment & DiagnosisCritical care recognitionCase-based reasoning
Covered conditions

Vasculitis, superficial thrombophlebitis, deep vein thrombosis, hypercoagulability, petechiae, purpura, ecchymosis, anticoagulant complications.

Recognition checklist
  • Vasculitis can involve skin, kidneys, lungs, nerves, joints, or GI tract.
  • Tender superficial vein does not exclude DVT.
  • DVT with dyspnea or chest pain suggests pulmonary embolism.
  • Petechiae/purpura with fever is a medical red flag.
  • Broad thrombophilia testing is not always useful during acute clotting events.
Red flags
  • Vision loss with new headache after age 50
  • Hemoptysis
  • Hematuria with systemic symptoms
  • Neurologic deficit
  • Digital ischemia
  • Fever with petechiae or purpura
  • Head trauma on anticoagulation
Exam traps
  • Palpable purpura plus hematuria suggests systemic vasculitis.
  • Homans sign is not reliable for excluding DVT.
  • Anticoagulated patients with head trauma need careful assessment even if symptoms are mild.
Practice Topic 05 Back to course map
06

Risk Reduction & Chronic Complications

Use vascular prevention, screening, and follow-up logic in long-term care.

Blueprint: Assessment & DiagnosisCritical care recognitionCase-based reasoning
Covered conditions

Atherosclerosis prevention, smoking, diabetes, dyslipidemia, hypertension, obesity, sedentary lifestyle, chronic kidney disease, diabetic foot risk, vascular follow-up.

Recognition checklist
  • Atherosclerosis is systemic; PAD increases MI and stroke risk.
  • Smoking is a major risk factor for PAD, aneurysm, MI, and stroke.
  • Diabetic foot wounds require vascular, neuropathy, and infection assessment.
  • Albuminuria increases kidney and vascular risk.
  • High ABI in diabetes can reflect calcified vessels, not normal circulation.
Red flags
  • Rest pain in the foot
  • Non-healing foot ulcer
  • Gangrene
  • New claudication with weak pulses
  • Syncope with exertion
  • Acute cold pulseless limb
  • Exertional chest tightness before vigorous exercise
Exam traps
  • Very high triglycerides can increase pancreatitis risk.
  • A prior TIA requires secondary prevention even if symptoms resolved.
  • Exercise advice must be modified when red-flag cardiac symptoms are present.
Practice Topic 06 Back to course map

Practice mode

Select an answer to reveal the correct answer and explanation. This mode is designed for active recall and immediate feedback.

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Reference foundation

Selected standard clinical references used to support the vascular review and BoardQBank-style explanations.

  1. Bickley LS, Szilagyi PG, Hoffman RM, Soriano RP. Bates’ Guide to Physical Examination and History Taking. 13th ed. Philadelphia: Wolters Kluwer; 2021.
  2. Jarvis C. Physical Examination and Health Assessment. 9th ed. St. Louis: Elsevier; 2023.
  3. LeBlond RF, Brown DD, Suneja M, Szot JF. DeGowin’s Diagnostic Examination. 11th ed. New York: McGraw Hill; 2020.
  4. Porter RS, Kaplan JL, editors. The Merck Manual of Diagnosis and Therapy. 20th ed. Kenilworth: Merck Sharp & Dohme Corp.; 2018.
  5. Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J, editors. Harrison’s Principles of Internal Medicine. 21st ed. New York: McGraw Hill; 2022.
  6. Goldman L, Schafer AI, editors. Goldman-Cecil Medicine. 26th ed. Philadelphia: Elsevier; 2020.

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