Give cvs ms, mr, as ,ar short case positive history and examination findings difference between the conditions and diagnostic features
Reading File
Finding Sources
Finding Sources
Finding Sources
Finding Sources
Reading File
Reading File
Reading File
Reading File
Reading File
Reading File
Reading File
I now have all the content I need. Let me compose the comprehensive clinical answer.
CVS Valvular Heart Disease: Short Case Guide
MS | MR | AS | AR - History, Examination, Differences & Diagnostics
1. MITRAL STENOSIS (MS)
Short Case - Positive History
- Young to middle-aged woman (20-50 yrs), often with history of rheumatic fever in childhood
- Progressive exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea (PND)
- Palpitations (atrial fibrillation is common)
- Haemoptysis (pink frothy sputum)
- Recurrent chest infections / bronchitis
- Embolic episodes - stroke, limb ischaemia (clot from dilated LA or LA appendage)
- Fatigue, reduced exercise tolerance
- Hoarseness (Ortner syndrome - left recurrent laryngeal nerve compression by enlarged LA)
- May have history of RHD in family or community
Examination Findings
| Feature | Finding |
|---|---|
| General | Mitral facies (malar flush - dusky pinkish-red cheeks), thin, AF on pulse |
| Pulse | Irregularly irregular (AF), low volume |
| JVP | Raised if RHF has developed |
| Apex beat | Tapping (non-displaced, palpable S1), diastolic thrill at apex |
| Auscultation | Loud S1, Opening snap (OS) after S2, Mid-diastolic rumbling murmur at apex (best in left lateral position, low-pitched, heard with bell) |
| Other signs | Signs of pulmonary hypertension (loud P2, RV heave), signs of RHF (oedema, hepatomegaly) |
Key murmur character: Low-pitched, rumbling mid-diastolic murmur at apex, increases with exercise (turn patient to left lateral decubitus, use bell of stethoscope)
2. MITRAL REGURGITATION (MR)
Short Case - Positive History
- Myxomatous degeneration (most common in developed countries) or rheumatic fever history
- Insidious onset; often asymptomatic for years
- Gradual exertional dyspnea, fatigue, reduced effort tolerance
- Palpitations (AF)
- History of mitral valve prolapse, ischaemic heart disease, infective endocarditis, or dilated cardiomyopathy
- Acute MR: sudden onset pulmonary oedema (chordal rupture, papillary muscle infarction - always ask about recent MI)
- Symptoms worsen when LV function eventually declines
Examination Findings
| Feature | Finding |
|---|---|
| General | May look well chronically, or acutely unwell (acute MR) |
| Pulse | AF if chronic, tachycardia in acute |
| Apex beat | Displaced laterally (LV volume overload, cardiomegaly), hyperdynamic |
| Auscultation | Soft/absent S1, Pansystolic (holosystolic) murmur at apex, high-pitched, blowing, radiates to axilla and left scapula, S3 gallop present (volume overload) |
| Other signs | Mid-systolic click if MVP (Barlow's), signs of pulmonary congestion |
Key murmur character: High-pitched, blowing pansystolic murmur maximal at apex, radiates to left axilla, does not decrease with inspiration
3. AORTIC STENOSIS (AS)
Short Case - Positive History
- Elderly patient (calcific/degenerative AS, most common valvular lesion in adults >65 yrs) or middle-aged with bicuspid aortic valve
- Classic triad of symptoms (all brought on by exertion):
- Angina (increased O2 demand with LVH; may occur without CAD)
- Syncope or pre-syncope (exertional - inability to increase cardiac output)
- Exertional dyspnea / heart failure (most ominous - LV decompensation)
- Symptoms indicate severe disease and drastically shorten prognosis without intervention
- May report progressive reduction in exercise tolerance over years
Examination Findings
| Feature | Finding |
|---|---|
| General | May appear well initially |
| Pulse | Slow-rising, low-volume, narrow pulse pressure (pulsus parvus et tardus) - Note: may be absent in elderly due to arterial stiffness |
| BP | Normal or low systolic, narrow pulse pressure |
| Apex beat | Sustained, heaving, non-displaced (concentric LVH, not dilated) |
| Auscultation | Harsh, ejection systolic murmur (ESM) in aortic area (right 2nd intercostal space), radiates to carotids, peaks in mid-late systole; soft or absent A2 (calcified valve) |
| Other signs | Ejection click in younger patients (bicuspid valve); S4 gallop (stiff LV) |
Key murmur character: Harsh, crescendo-decrescendo ejection systolic murmur at aortic area, radiates to neck; the later the murmur peaks = more severe
4. AORTIC REGURGITATION (AR)
Short Case - Positive History
- Young adult with bicuspid aortic valve, or older patient with rheumatic disease, infective endocarditis, aortic root dilation (Marfan's, hypertension, syphilis, ankylosing spondylitis)
- Chronic AR: long asymptomatic phase, then dyspnea, exertional intolerance, palpitations (awareness of forceful heartbeat), angina (wide pulse pressure reduces diastolic coronary filling)
- Acute AR (endocarditis, aortic dissection): sudden onset acute pulmonary oedema, cardiogenic shock - this is a surgical emergency
- Symptom onset indicates LV dysfunction and mandates surgery
Examination Findings
| Feature | Finding |
|---|---|
| General | Young patient with hyperdynamic circulation |
| Pulse | Collapsing/water-hammer pulse (Corrigan's pulse) - rapidly rising and falling; wide pulse pressure (high systolic, low diastolic) |
| BP | Wide pulse pressure (e.g., 160/50 mmHg) |
| Apex beat | Displaced laterally and inferiorly (eccentric LVH - volume overload, LV dilates) |
| Auscultation | Early high-pitched, blowing diastolic murmur at left sternal border (3rd/4th ICS), best heard in sitting forward, expiration; Austin-Flint murmur (low-pitched mid-diastolic rumble at apex, functional MS due to AR jet hitting mitral leaflet); Soft S1 |
| Peripheral signs | Corrigan's pulse, Quincke's sign (capillary pulsation in nailbed), de Musset's sign (head nodding), Traube's sign (pistol shot femorals), Duroziez's sign (femoral bruit with pressure), Müller's sign (uvular pulsation) |
Key murmur character: High-pitched, blowing early diastolic murmur at left sternal border; patient sitting forward, breath held in expiration
KEY DIFFERENTIATING FEATURES AT A GLANCE
| Feature | MS | MR | AS | AR |
|---|---|---|---|---|
| Aetiology | Rheumatic fever (main) | Myxomatous/RHD/IHD/IE | Calcific (elderly)/Bicuspid/RHD | Bicuspid/RHD/IE/Aortic root dilation |
| Murmur timing | Mid-diastolic | Pansystolic | Ejection systolic | Early diastolic |
| Murmur character | Low-pitched rumble | High-pitched blowing | Harsh, crescendo-decrescendo | High-pitched blowing |
| Location | Apex | Apex | Aortic area (R 2nd ICS) | Left sternal border (3rd ICS) |
| Radiation | None | Left axilla/scapula | Carotids | None |
| Best heard | Left lateral, bell | Any position | Sitting up, leaning forward | Sitting forward, expiration |
| S1 | Loud | Soft/absent | Normal | Soft |
| S2 | Normal | Normal | Soft/absent A2 | Normal |
| Extra sounds | Opening snap, S3 in pulm HTN | S3 gallop | S4 gallop, ejection click | Austin-Flint murmur |
| Apex beat | Tapping, non-displaced | Displaced, hyperdynamic | Heaving, non-displaced (sustained) | Displaced L+D, hyperdynamic |
| Pulse | Low volume, AF | AF in chronic | Pulsus parvus et tardus | Collapsing/waterhammer |
| Pulse pressure | Narrow | Normal/narrow | Narrow | Wide |
| Main symptom | Dyspnea, haemoptysis, AF | Exertional dyspnea, fatigue | Angina, syncope, dyspnea (SAD triad) | Dyspnea, angina, palpitations |
| Cardiac chamber | LA dilates, LV small | LA + LV dilate | LV hypertrophy (concentric) | LV dilates (eccentric hypertrophy) |
| AF risk | Very high | High | Low-moderate | Low |
| Embolic risk | High (LA thrombus) | Moderate | Low | Low |
DIAGNOSTIC FEATURES
ECG
| Condition | ECG Features |
|---|---|
| MS | P mitrale (broad, bifid P wave in II), AF, RVH + right axis deviation if pulmonary HTN |
| MR | P mitrale, LVH (large QRS complexes, Sokolow criteria), AF, inferior Q waves if ischaemic MR |
| AS | LVH (dominant R in V5/V6, S in V1/V2), left axis deviation, ST-T strain pattern, LBBB in advanced disease |
| AR | LVH (volume overload pattern - tall R waves), possible LBBB, ST-T changes |
CXR
| Condition | CXR Features |
|---|---|
| MS | Enlarged LA (double shadow right heart border, splaying of carina), pulmonary venous congestion, Kerley B lines, upper lobe diversion, calcified mitral valve |
| MR | Cardiomegaly (LA + LV), pulmonary congestion, calcified valve |
| AS | Normal heart size (LVH is concentric - no cardiomegaly until late), calcified aortic valve, post-stenotic aortic dilatation |
| AR | Cardiomegaly (LV enlargement), aortic root dilatation, boot-shaped heart (apex displaced down-left) |
Echocardiography (Gold Standard)
| Condition | Echo Features |
|---|---|
| MS | Thickened, calcified mitral leaflets, "fish-mouth" orifice on parasternal short axis, decreased E-F slope on M-mode, reduced MVA (<1.5 cm² mild, <1 cm² severe), LA enlargement, elevated transmitral gradient |
| MR | Colour Doppler jet into LA, LA + LV dilatation, reduced LVEF in decompensation, identify cause (prolapse, flail leaflet, annular dilation) |
| AS | Thickened, calcified AV with restricted leaflets, LVH, elevated mean gradient (severe ≥40 mmHg), peak velocity ≥4 m/s, valve area ≤1 cm² |
| AR | Colour Doppler regurgitant jet into LV in diastole, LV dilatation, Austin-Flint murmur can be seen, vena contracta >6 mm = severe, pressure half-time <200 ms = severe |
Cardiac Catheterisation
| Condition | Catheterisation |
|---|---|
| MS | Elevated PCWP, transmitral gradient; useful before PMV/surgery |
| MR | Elevated PCWP + LA 'V' waves; cineventriculography shows LA opacification in systole |
| AS | Aortic valve gradient; LV-aortic pull-back shows pressure gradient; before AVR if CAD suspected |
| AR | Aortography shows regurgitation into LV; aortic root dilation; LV end-diastolic pressure; before AVR |
MEMORY ANCHORS
- MS: "Rumble in the jungle" - young rheumatic woman, mitral facies, tapping apex, OS + rumble
- MR: "Blowing in the wind" - pansystolic, axilla radiation, displaced hyperdynamic apex, S3
- AS: "SAD triad" - Syncope, Angina, Dyspnea + slow pulse + heaving non-displaced apex + ESM to carotids
- AR: "Big heart, bounding pulse" - collapsing pulse, wide PP, displaced apex, blowing early diastolic murmur, many eponymous peripheral signs
Sources: Textbook of Family Medicine 9e, Braunwald's Heart Disease (Cardiovascular Medicine), Pfenninger & Fowler's Procedures for Primary Care
PICCLE and other general examination findings causes and DDs and viva questions and answers
Finding Sources
Finding Sources
Finding Sources
Finding Sources
Finding Sources
Finding Sources
Finding Sources
Reading File
Finding Sources
Finding Sources
Reading File
I now have enough from the textbooks. Let me now compose the comprehensive answer entirely from my knowledge base and textbook content - this is a classic clinical examination topic that I can deliver comprehensively.
PICCLE - General Examination Findings
P-I-C-C-L-E: Causes, DDs, and Viva Q&A
PICCLE stands for the standard general examination acronym used at the bedside:
P - Pallor | I - Icterus (Jaundice) | C - Cyanosis | C - Clubbing | L - Lymphadenopathy | E - Oedema
(Some schools extend this to PICCLED - adding Dehydration, or use JACCOL - Jaundice, Anaemia, Clubbing, Cyanosis, Oedema, Lymphadenopathy)
P - PALLOR
What it is
Pallor is paleness of the skin, conjunctiva, mucous membranes, and palmar creases due to reduced haemoglobin, reduced blood flow, or vasoconstriction.
Where to look (examination)
- Conjunctival pallor - lower palpebral conjunctiva (most reliable)
- Palmar crease pallor - creases same colour as surrounding skin = significant pallor
- Nail bed pallor
- Tongue and buccal mucosa
- General skin pallor (less reliable, especially in dark-skinned patients)
Grading
- Mild: pallor visible on conjunctiva only
- Moderate: conjunctiva + palmar creases
- Severe: all of the above + tongue, extreme pallor
Causes (by mechanism)
| Mechanism | Causes |
|---|---|
| Decreased Hb (anaemia) | Iron deficiency, B12/folate deficiency, haemolytic anaemia, aplastic anaemia, thalassaemia, anaemia of chronic disease, CKD |
| Blood loss | GI bleed, trauma, menorrhagia, haemorrhage |
| Decreased circulation | Shock (hypovolaemic, cardiogenic, septic), peripheral vascular disease, Raynaud's |
| Bone marrow failure | Leukaemia, lymphoma, myeloma, aplastic anaemia |
| Chronic disease | Malignancy, CKD, hypothyroidism, SLE |
Differentials from pallor
- Normal fair skin (no conjunctival pallor)
- Hypopituitarism (loss of secondary sexual pigmentation)
- Vitiligo (patchy depigmentation)
- Albinism
CVS-specific causes of pallor
MS, MR with low output, severe AS (low cardiac output), acute AR, infective endocarditis with anaemia
I - ICTERUS (JAUNDICE)
What it is
Yellow discolouration of the sclerae, skin, and mucous membranes due to hyperbilirubinaemia (>35 µmol/L or >2 mg/dL). Sclerae turn yellow first (elastic tissue has high affinity for bilirubin).
Where to look
- Sclerae - best seen in natural daylight; look at outer angle of eye
- Under the tongue / frenulum
- Hard palate
- Skin (hands, face)
Classification and Causes
| Type | Bilirubin | Urine | Stool | Causes |
|---|---|---|---|---|
| Pre-hepatic (haemolytic) | Unconjugated ↑ | Normal (no bilirubin) | Dark (↑ urobilinogen) | Haemolytic anaemia (sickle cell, spherocytosis, G6PD, thalassaemia), malaria, transfusion reaction |
| Hepatic (hepatocellular) | Both ↑ | Dark (conjugated) + urobilinogen | Pale-normal | Viral hepatitis (A,B,C), alcoholic hepatitis, cirrhosis, drug-induced liver injury, leptospirosis, yellow fever, Wilson's disease |
| Post-hepatic (obstructive/cholestatic) | Conjugated ↑ | Dark (bilirubinuria), no urobilinogen | Pale/clay-coloured, steatorrhoea | CBD stone, carcinoma head of pancreas, cholangiocarcinoma, stricture, primary sclerosing cholangitis, biliary atresia |
CVS causes of jaundice
- Cardiac jaundice: right heart failure causes hepatic congestion → hepatocellular jaundice (mild, green-tinged tinge with tender hepatomegaly)
- Haemolytic jaundice: prosthetic heart valve haemolysis, infective endocarditis
- Post-cardiac surgery: transfusion jaundice
DD of Yellow Discolouration
- Jaundice (sclerae yellow) vs Carotenaemia (sclerae spared - yellow palms/soles only from excess carotene intake)
- Quinacrine drug ingestion
C1 - CYANOSIS
What it is
Blue-purple discolouration of skin and mucous membranes due to >5 g/dL of deoxygenated haemoglobin in capillaries (absolute amount, not percentage - hence polycythaemia patients cyanose easily; severe anaemics may not).
Central vs Peripheral Cyanosis
| Feature | Central Cyanosis | Peripheral Cyanosis |
|---|---|---|
| Site | Tongue, lips, mucous membranes | Fingertips, toes, earlobes, nose tip |
| Tongue | Blue/purple | Normal/pink |
| Mechanism | Desaturated arterial blood | Excess O2 extraction from normal/reduced flow |
| Warmth test | Does NOT improve with warming | Improves with warming/rubbing |
| Causes | Respiratory: COPD, pneumonia, ILD, PE; Cardiac: R→L shunt (cyanotic CHD, Eisenmenger), pulmonary oedema; High altitude; Methaemoglobinaemia | Low cardiac output, cold exposure, Raynaud's, PVD, DVT |
Causes of Central Cyanosis (CVS)
- Congenital cyanotic heart disease: ToF, TGA, Eisenmenger syndrome, TAPVC, tricuspid atresia
- Pulmonary oedema (severe left heart failure - MS, MR, AS decompensation)
- Pulmonary arteriovenous fistula
Causes of Peripheral Cyanosis (CVS)
- Low cardiac output states (cardiogenic shock, severe AS, end-stage HF)
- Mitral stenosis (low output + pulmonary HTN)
- Raynaud's phenomenon
Key Point for Viva
Cyanosis requires 5 g/dL of deoxygenated Hb. In severe anaemia (Hb 5 g/dL), you cannot become cyanosed even with 100% desaturation. In polycythaemia, cyanosis appears at SpO2 levels that would be safe in normal patients.
C2 - CLUBBING
What it is
Loss of the normal angle between the nail and nail fold (Lovibond angle >180°), with softening of the nail bed (fluctuation), increased curvature of the nail in both AP and lateral planes, and eventually drumstick fingers with periosteal new bone formation.
Grading (Schamroth's sign)
Place two corresponding fingers dorsum-to-dorsum: normally a diamond-shaped window is visible. In clubbing, this window is obliterated.
| Grade | Features |
|---|---|
| 1 | Fluctuation of nail bed (soft, ballotable) |
| 2 | Loss of Lovibond angle (normally ~160°, now ≥180°) |
| 3 | Increased curvature of nail (beaking) |
| 4 | Drumstick appearance (bulbous fingertips) |
| 5 | Hypertrophic osteoarthropathy (periosteal new bone, wrist/ankle pain) |
Causes - Mnemonic: "CLUBBING"
| System | Causes |
|---|---|
| Cardiac | Cyanotic congenital heart disease (ToF, TGA, Eisenmenger), infective endocarditis (subacute bacterial endocarditis - SBE) |
| Respiratory | Bronchogenic carcinoma (most common cause overall), bronchiectasis, lung abscess, empyema, cystic fibrosis, ILD/cryptogenic fibrosing alveolitis, mesothelioma |
| Liver/GI | Cirrhosis, IBD (Crohn's, UC), GI lymphoma, coeliac disease |
| Others | Thyroid acropachy (Graves'), congenital (familial), idiopathic |
Conditions that do NOT cause clubbing (important for viva!)
- Simple COPD/asthma (no clubbing - if present, think malignancy)
- Pulmonary TB (usually no clubbing)
- Uncomplicated CHD without cyanosis
CVS-specific clubbing causes
- Infective endocarditis (SBE) - classic cause; acute IE rarely causes clubbing
- Cyanotic CHD - ToF, Eisenmenger, TGA
- Cardiac cirrhosis (secondary hepatic cirrhosis from RHF)
L - LYMPHADENOPATHY
What it is
Enlargement of lymph nodes (>1 cm in most areas; >1.5 cm in groin is upper limit of normal).
Examination approach
Examine all accessible nodal groups:
- Cervical: submental, submandibular, anterior/posterior cervical chain, preauricular, postauricular, occipital
- Supraclavicular: especially left supraclavicular (Virchow's node = Troisier's sign) - GI malignancy
- Axillary: apical, pectoral, subscapular, lateral
- Inguinal: horizontal (superficial), vertical
Character of nodes (examine for)
| Feature | Likely Cause |
|---|---|
| Soft, tender, mobile | Reactive (infection) |
| Firm, rubbery, discrete, mobile | Lymphoma |
| Hard, fixed, irregular | Metastatic carcinoma |
| Matted (nodes stuck together), firm | TB, lymphoma |
| Fluctuant | TB (cold abscess), pyogenic |
Causes of Generalised Lymphadenopathy
| Category | Causes |
|---|---|
| Infections | EBV (infectious mononucleosis), HIV, CMV, toxoplasmosis, TB, brucellosis, secondary syphilis, viral URTI |
| Haematological malignancy | Leukaemia (ALL, CLL, AML, CML), Hodgkin's lymphoma, Non-Hodgkin's lymphoma |
| Autoimmune | SLE, RA, sarcoidosis |
| Drugs | Phenytoin, allopurinol, carbamazepine |
Causes of Localised Lymphadenopathy
| Site | Likely cause |
|---|---|
| Cervical | URTI, EBV, oral/pharyngeal cancer, TB, lymphoma |
| Left supraclavicular | Abdominal/thoracic malignancy (Troisier's sign) |
| Right supraclavicular | Pulmonary/mediastinal malignancy, lymphoma |
| Axillary | Breast cancer, melanoma, lymphoma, UL infection |
| Inguinal | LL infection/STI, lymphoma, pelvic/anorectal malignancy |
CVS relevance
- Infective endocarditis (rare associated lymphadenopathy)
- Cardiac sarcoidosis (generalised LAD)
- Systemic causes of cardiomyopathy (lymphoma, SLE)
E - OEDEMA
What it is
Abnormal accumulation of fluid in interstitial tissue spaces. Pitting oedema: finger pressure leaves a temporary pit (indicates free fluid in interstitium). Non-pitting oedema: no pitting (lymphoedema, myxoedema).
Examination
- Press firmly for 30 seconds over bony prominences (tibia, sacrum, malleoli)
- Grading: 1+ (2mm) to 4+ (8mm)
- Dependent distribution: ankles/feet in ambulant patients; sacrum in bed-bound
- Check for bilateral vs unilateral (bilateral = systemic cause; unilateral = local cause)
Starling's Forces - Pathophysiology
Oedema occurs when:
- Capillary hydrostatic pressure ↑ (HF, DVT, venous obstruction)
- Plasma oncotic pressure ↓ (hypoalbuminaemia)
- Lymphatic obstruction
- Increased capillary permeability (inflammation, allergy, sepsis)
Causes of Bilateral Pitting Oedema
| Category | Causes |
|---|---|
| Cardiac | Congestive heart failure (RHF or biventricular), constrictive pericarditis, tricuspid regurgitation |
| Hepatic | Cirrhosis (low albumin + portal hypertension) |
| Renal | Nephrotic syndrome (massive proteinuria → low albumin), CKD, acute nephritic syndrome |
| Nutritional | Protein-energy malnutrition (kwashiorkor) |
| Endocrine | Hypothyroidism (non-pitting myxoedema), Cushing's syndrome |
| Drugs | Amlodipine (CCBs), NSAIDs, steroids, thiazolidinediones, minoxidil |
| Venous | Bilateral DVT, inferior vena cava obstruction |
| Physiological | Pregnancy, prolonged sitting/standing |
Causes of Unilateral Oedema
DVT, cellulitis, lymphoedema (filariasis, post-mastectomy), venous insufficiency, Baker's cyst rupture, compartment syndrome
CVS-specific oedema features
| Condition | Oedema features |
|---|---|
| Right heart failure | Bilateral pitting oedema (ankles → ascites → anasarca), raised JVP, hepatomegaly |
| Constrictive pericarditis | Gross oedema + ascites disproportionate to peripheral oedema, raised JVP with Kussmaul's sign |
| Tricuspid regurgitation | Pulsatile hepatomegaly + oedema |
| Nephrotic syndrome | Periorbital oedema (especially morning) + anasarca, no raised JVP |
| Hypothyroid myxoedema | Non-pitting, periorbital, hands/face, cool dry skin, bradycardia |
ADDITIONAL GENERAL EXAMINATION FINDINGS
Hands (complete the examination)
| Sign | What it means |
|---|---|
| Koilonychia (spoon-shaped nails) | Iron deficiency anaemia |
| Leukonychia (white nails) | Hypoalbuminaemia (chronic liver disease, nephrotic) |
| Lindsay's nails (half-and-half) | CKD |
| Splinter haemorrhages | Infective endocarditis, vasculitis, trauma |
| Osler's nodes (tender nodules on finger pads) | Infective endocarditis (immune complex deposition) |
| Janeway lesions (painless erythematous macules on palm/sole) | Infective endocarditis (septic emboli) |
| Palmar erythema | Cirrhosis, RA, pregnancy, hyperthyroidism |
| Dupuytren's contracture | Alcoholic liver disease, idiopathic, DM |
| Thenar wasting | Carpal tunnel, T1 lesion, old age |
| Tar staining | Smoking → COPD, lung ca, IHD |
Eyes
| Sign | Meaning |
|---|---|
| Xanthelasma | Hyperlipidaemia (dyslipidaemia) |
| Arcus senilis (<50 yrs) | Hyperlipidaemia |
| Kayser-Fleischer rings | Wilson's disease |
| Anaemic conjunctiva | Anaemia |
| Icteric sclerae | Jaundice |
| Roth's spots (retinal haemorrhages with pale centres) | IE, anaemia, leukaemia |
Face/Neck
| Sign | Meaning |
|---|---|
| Malar flush (mitral facies) | Mitral stenosis |
| Moon face | Cushing's |
| Butterfly rash | SLE |
| Goitre | Thyroid disease |
| Raised JVP | Right heart failure, SVC obstruction, SVCO, cardiac tamponade |
| Carotid bruit | Carotid artery stenosis, aortic stenosis (transmitted) |
VIVA QUESTIONS AND ANSWERS
PALLOR
Q1. What is the most common cause of pallor in clinical practice?
A: Iron deficiency anaemia - the commonest cause of anaemia worldwide, typically from nutritional deficiency, occult GI blood loss, or menorrhagia.
Q2. How do you differentiate pallor of anaemia from normal fair skin?
A: Check the conjunctival mucosa - always pale in anaemia regardless of skin pigmentation. Also check palmar crease pallor: creases the same colour as surrounding skin indicates significant anaemia (Hb typically <7-8 g/dL).
Q3. What are causes of pallor WITHOUT anaemia?
A: Vasovagal syncope (acute peripheral vasoconstriction), cardiogenic shock, Raynaud's phenomenon, hypothyroidism, hypopituitarism, and simply fair complexion.
Q4. In a CVS patient, what would cause pallor?
A: Low cardiac output state (severe AS, HF), haemolysis from prosthetic valve or endocarditis, anaemia of chronic disease in long-standing cardiac conditions.
ICTERUS / JAUNDICE
Q5. What is the bilirubin level at which jaundice becomes clinically detectable?
A: Approximately 35 µmol/L (2 mg/dL). At levels below this, jaundice is termed latent or sub-clinical.
Q6. How do you differentiate pre-hepatic from post-hepatic jaundice clinically?
A: Pre-hepatic (haemolytic): mild jaundice, lemon-yellow tinge, dark urine (urobilinogen), normal/dark stool, splenomegaly, no pruritis, no bilirubin in urine. Post-hepatic (obstructive): deep green-yellow jaundice, dark urine (bilirubin), pale clay-coloured stool, pruritis (bile salt deposition), bilirubin in urine, no urobilinogen.
Q7. What is Courvoisier's law?
A: "In the presence of jaundice, if the gallbladder is palpable and non-tender, the cause is unlikely to be gallstones." (Because chronic stone disease causes a shrunken fibrotic GB; painless obstructive jaundice + palpable GB = carcinoma of head of pancreas until proven otherwise.)
Q8. What causes cardiac jaundice?
A: Right heart failure causes hepatic venous congestion (nutmeg liver), impairing hepatocyte function → mild conjugated hyperbilirubinaemia. Also, haemolysis from mechanical prosthetic heart valves or endocarditis causes unconjugated hyperbilirubinaemia.
CYANOSIS
Q9. Define cyanosis and state the threshold.
A: Cyanosis is blue-purple discolouration of skin and mucous membranes due to >5 g/dL of deoxygenated (reduced) haemoglobin in the capillaries. This is an absolute amount, not a percentage.
Q10. Why can a severely anaemic patient not become cyanosed?
A: Total Hb is too low. If Hb = 5 g/dL, even 100% desaturation only gives 5 g/dL of deoxygenated Hb - just reaching the threshold. Practically, a patient with Hb of 3-4 g/dL cannot be cyanosed. This is clinically important: an anaemic hypoxic patient may not look cyanosed.
Q11. How do you distinguish central from peripheral cyanosis at the bedside?
A: Check the tongue - blue tongue = central cyanosis (arterial blood is desaturated). Then warm the finger - peripheral cyanosis resolves with warming (it is due to increased O2 extraction in sluggish peripheral flow), while central cyanosis does not. Also, central cyanosis affects the tongue + lips + fingertips; peripheral only affects the extremities.
Q12. Name five causes of central cyanosis from a cardiac cause.
A: (1) Tetralogy of Fallot - most common cyanotic CHD in children >1yr; (2) Transposition of Great Arteries - most common cyanotic CHD in neonates; (3) Eisenmenger syndrome - reversal of L→R shunt; (4) Total anomalous pulmonary venous connection (TAPVC); (5) Tricuspid atresia.
Q13. What is differential cyanosis?
A: Cyanosis of the lower limbs but NOT the upper limbs (or vice versa). Lower body cyanosis + pink upper body = patent ductus arteriosus (PDA) with Eisenmenger physiology (desaturated blood enters aorta distal to subclavian arteries). Upper body cyanosis + pink lower body is rare but can be seen in TGA with co-arctation.
CLUBBING
Q14. Define clubbing and describe how to test for it.
A: Clubbing is soft tissue hypertrophy of the terminal phalanges with loss of the normal nail fold angle (Lovibond angle normally ~160°, becomes ≥180°). Test using Schamroth's sign: place corresponding fingers back-to-back; normally a diamond-shaped window is visible at the base of the nails - this is obliterated in clubbing.
Q15. What is the most common cause of clubbing?
A: Bronchogenic carcinoma (lung cancer) is the most common acquired cause overall. In children, cystic fibrosis and cyanotic congenital heart disease are common causes.
Q16. Which cardiac conditions cause clubbing?
A: Infective endocarditis (subacute/SBE), cyanotic congenital heart disease (ToF, Eisenmenger, TGA), and atrial myxoma (rare). Acute IE rarely causes clubbing as it develops over weeks-months.
Q17. Which common cardiac/respiratory conditions do NOT cause clubbing?
A: COPD/emphysema (if clubbing present in a COPD patient → suspect lung cancer), asthma, uncomplicated non-cyanotic CHD (VSD, ASD, PDA without Eisenmenger). Pulmonary TB classically does NOT cause clubbing.
Q18. What is hypertrophic pulmonary osteoarthropathy (HPOA)?
A: Grade 5 clubbing where periosteal new bone is laid down along long bones, causing wrist and ankle pain. Most commonly seen with lung cancer. X-ray shows periosteal new bone. Associated with gynaecomastia.
LYMPHADENOPATHY
Q19. What is Virchow's node and what is its clinical significance?
A: Left supraclavicular lymph node enlargement (Troisier's sign). It drains via the thoracic duct and enlarges in GI malignancies (stomach, colon, pancreas, testicular, ovarian cancer). A palpable Virchow's node in a patient with weight loss and dysphagia/dyspepsia strongly suggests upper GI malignancy with metastatic spread.
Q20. How do you differentiate lymphoma from reactive lymphadenopathy on examination?
A: Lymphoma nodes: rubbery, firm, discrete, non-tender, multiple, matted in later stages. Reactive nodes: soft, tender, mobile, associated with local infection site. Metastatic nodes: hard, fixed, irregular, non-tender.
Q21. What are the causes of generalised lymphadenopathy in a young patient?
A: EBV (infectious mononucleosis - most common in young adults, with splenomegaly and atypical lymphocytes), HIV, CMV, toxoplasmosis, ALL/lymphoma, SLE, secondary syphilis.
Q22. What is the significance of bilateral inguinal lymphadenopathy?
A: Can be reactive (minor lower limb/perineal trauma or infection - often normal in adults), or due to STIs (LGV, syphilis, chancroid), pelvic malignancy, lymphoma, or lower limb infection/melanoma.
OEDEMA
Q23. Why does cardiac oedema start at the ankles?
A: Gravity-dependent accumulation - venous hydrostatic pressure is highest at the ankles in ambulant patients. In bed-bound patients, oedema accumulates sacrally. This is why you must examine the sacrum for oedema in bed-bound patients.
Q24. How do you differentiate cardiac oedema from renal (nephrotic) oedema?
A: Cardiac: pitting oedema ankles/legs, raised JVP, hepatomegaly, basal crepitations; worse at night/evening; better in morning. Nephrotic: periorbital oedema (prominent in morning), no raised JVP, generalised anasarca, heavy proteinuria, hypoalbuminaemia.
Q25. What is the difference between pitting and non-pitting oedema?
A: Pitting oedema: free fluid in interstitium displaced by pressure, pit remains for seconds (cardiac, hepatic, renal, nutritional, venous). Non-pitting oedema: fibrosis/protein deposition in interstitium that cannot be displaced - seen in lymphoedema (filariasis, post-surgery/radiotherapy) and myxoedema (hypothyroidism - mucinous deposits).
Q26. Name drugs that cause bilateral pedal oedema.
A: Amlodipine and other dihydropyridine CCBs (most common drug cause), NSAIDs (sodium retention), systemic corticosteroids, thiazolidinediones (rosiglitazone, pioglitazone), minoxidil, oestrogens, gabapentin/pregabalin.
Q27. What is anasarca?
A: Generalised massive oedema involving the entire body including face, ascites, pleural effusions, pericardial effusion. Causes: severe nephrotic syndrome, advanced cardiac failure, severe protein malnutrition (kwashiorkor), severe cirrhosis.
Q28. How does constrictive pericarditis cause oedema disproportionate to the degree of clinical heart failure?
A: Rigid pericardium impairs diastolic filling of both ventricles. This raises systemic venous pressure (↑JVP), activates renin-angiotensin-aldosterone system causing sodium and water retention, and causes hepatic congestion and ascites. The ascites is classically disproportionate to peripheral oedema, mimicking liver disease. JVP rises further on inspiration (Kussmaul's sign) - opposite of normal.
SUMMARY TABLE
| Sign | Where to look | Key Causes | CVS link |
|---|---|---|---|
| Pallor | Conjunctiva, palmar creases | IDA, haemolysis, aplasia, blood loss | Low output, IE haemolysis, valve haemolysis |
| Icterus | Sclerae, frenulum of tongue | Haemolysis, hepatitis, obstruction | RHF hepatic congestion, prosthetic valve haemolysis |
| Cyanosis | Tongue (central), fingertips (peripheral) | Cyanotic CHD, COPD, pulm oedema | ToF, Eisenmenger, decompensated LHF |
| Clubbing | Nail fold angle, Schamroth's | Lung Ca, bronchiectasis, IE, cyanotic CHD | IE, cyanotic CHD |
| Lymphadenopathy | Cervical, axillary, inguinal, supraclavicular | EBV, HIV, lymphoma, TB, metastases | Cardiac sarcoidosis, IE (rare) |
| Oedema | Ankles, sacrum, periorbital | RHF, nephrotic, cirrhosis, drugs | RHF, constrictive pericarditis, TR |
Sources: Harrison's Principles of Internal Medicine 22E (2025), Bailey & Love's Short Practice of Surgery 28E, Textbook of Family Medicine 9E, Braunwald's Heart Disease
This is a shared conversation. Sign in to Orris to start your own chat.