Hemodynamic Disorders and Thrombosis

🟢 Lite — Quick Review (1h–1d)

Virchow’s Triad — Risk Factors for Thrombosis:

Endothelial injury, Stasis/Abnormal blood flow, Hypercoagulability

Edema — Mechanisms:

1. ↑ capillary hydrostatic pressure — heart failure, renal failure
2. ↓ plasma oncotic pressure — hypoalbuminemia (liver cirrhosis, nephrotic syndrome, protein-losing enteropathy)
3. ↑ capillary permeability — inflammation, burns, allergies
4. Lymphatic obstruction — filariasis → lymphedema

Transudate vs Exudate:

Feature	Transudate	Exudate
Protein	<3 g/dL	>3 g/dL
LDH	Low	High (serum:pleural LDH ratio >0.6)
Cellular content	Sparse	Rich (WBCs, RBCs)
Specific gravity	<1.015	>1.015
Causes	Hydrostatic/oncotic imbalance	Inflammation, infection, malignancy

Rivalta test — differentiates transudate (negative) from exudate (positive); measures fibrin content

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🟡 Standard — Regular Study (2d–2mo)

Thrombosis — Components of Thrombus (Virchow’s Triad in detail):

1. Endothelial Injury:

   • Most important factor for arterial thrombi
   • Exposes subendothelial collagen → platelet adhesion (via vWF)
   • Risk factors: atherosclerosis, hypertension, smoking, hyperlipidemia, diabetes

2. Abnormal Blood Flow/Stasis:

   • Most important factor for venous thrombi
   • Turbulence → endothelial activation
   • Venous stasis → hypoxia → endothelial injury
   • Rouleaux formation — RBCs stack (↑ fibrinogen, seen in polycythemia)

3. Hypercoagulability:

   • Primary (Inherited):
     • Factor V Leiden — most common inherited thrombophilia; APC resistance; ↑ DVT risk
     • Prothrombin G20210A mutation — ↑ prothrombin levels
     • Antithrombin III deficiency — ↑ thrombosis
     • Protein C/S deficiency — ↑ thrombosis (warfarin-induced skin necrosis if given without heparin)
   • Secondary (Acquired):
     • Malignancy (Trousseau syndrome — migratory thrombophlebitis)
     • Antiphospholipid syndrome (lupus anticoagulant → ↑ aPTT but ↑ thrombosis)
     • Post-surgical state
     • Prolonged immobilization
     • Oral contraceptive pills (↑ factors VII, X, fibrinogen)
     • Smoking
     • Hyperhomocysteinemia

Arterial vs Venous Thrombi:

Feature	Arterial Thrombus	Venous Thrombus
Location	Heart chambers, aorta, arteries	Deep veins (legs most common)
Composition	Platelets + fibrin (pale, “white thrombus”)	RBCs + fibrin (red thrombus)
Primary factor	Endothelial injury	Stasis
Propagation	Proximal	Distal (legs) → proximal
Clinical	MI, stroke, limb ischemia	DVT → PE

Fate of Thrombus:

1. Propagation — extends proximally
2. Embolization — breaks off → lodges elsewhere
3. Dissolution — fibrinolysis (plasmin)
4. Organization — replaced by connective tissue → may recanalize
5. Canalization — new channels form within organized thrombus
6. Calcification — phleboliths (in venous thrombi)

Pulmonary Thromboembolism:

• 95% of PE arises from DVT (deep leg veins — popliteal, femoral, iliac)
• Risk factors: Virchow’s triad (especially stasis)
• Clinical triad: Dyspnea, pleuritic chest pain, hemoptysis
• Massive PE: Saddle embolus at bifurcation → sudden death, hemodynamic collapse
• Mechanism of death: Right heart failure, acute cor pulmonale
• D-dimer: Fibrin degradation product; sensitive but NOT specific for DVT/PE
• Wells Score: Clinical prediction rule for PE probability

Shock — Types:

Type	Mechanism	CVP	CO	Example
Hypovolemic	↓ blood volume	↓	↓	Hemorrhage, dehydration
Cardiogenic	Pump failure	↑	↓	MI, arrhythmias
Distributive (Septic)	Vasodilation + maldistribution	↓	↑ (early) / ↓ (late)	Sepsis, anaphylaxis, neurogenic
Obstructive	Mechanical obstruction	↑	↓	Cardiac tamponade, tension pneumothorax, massive PE

Septic Shock:

• Most common cause of distributive shock
• Gram-negative bacteremia — endotoxin (LPS) → TNF-α, IL-1 → vasodilation, capillary leak
• Warm shock (early): Hyperdynamic; vasodilation predominates
• Cold shock (late): Hypodynamic; myocardial depression

DIC (Disseminated Intravascular Coagulation):

• Widespread microvascular thrombosis + consumption coagulopathy
• Causes: Sepsis (gram-negative), obstetric complications (amniotic fluid embolism, placental abruption), malignancy, severe trauma
• Lab findings: ↓ platelets, ↓ fibrinogen, ↑ PT/PTT, ↑ D-dimer, schistocytes (microangiopathic hemolysis)
• Bleeding + thrombosis simultaneously

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🔴 Extended — Deep Study (3mo+)

Hemodynamics — Key Concepts:

Starling Forces:

Net filtration = Kf × [(Pcapillary - Pinterstitial) - σ(πcapillary - πinterstitial)]

• Pcapillary (hydrostatic) — drives fluid OUT (~35 mmHg arterial end, ~15 mmHg venous end)
• πcapillary (oncotic) — keeps fluid IN (~25 mmHg, due to albumin)
• Net filtration — arterial end: net outward; venous end: net inward
• ~85% of filtered fluid is reabsorbed at venous end; remaining 15% enters lymphatics

Edema — Clinical Correlation:

• Periorbital edema (morning) — nephrotic syndrome, glomerulonephritis
• Dependent edema (ankle) — heart failure, venous insufficiency
• Pitting edema — fluid accumulation; press with thumb → pit forms
• Non-pitting edema — lymphatic obstruction, myxedema
• Ascites — peritoneal fluid accumulation; cirrhosis (↓ albumin), malignancy, heart failure
• Pleural effusion — transudate (heart failure) vs exudate (infection, malignancy)
• Pulmonary edema — left heart failure → ↑ pulmonary capillary pressure → fluid leaks into alveoli

Embolism — Types:

1. Pulmonary thromboembolism (most common, ~95%)
2. Systemic thromboembolism:
   • Arterial: Left heart (mural thrombus post-MI, AFib), aorta (atheroemboli from ulcerated plaques)
   • Paradoxical embolism: DVT → crosses through PFO (patent foramen ovale) → systemic circulation
3. Fat embolism: Long bone fractures, liposuction → fat globules enter venous circulation → ARDS (triad: dyspnea, confusion, petechial rash)
4. Air embolism: Diving, surgical procedures → can cause right heart obstruction
5. Amniotic fluid embolism: Obstetric emergency → DIC + sudden cardiovascular collapse
6. Septic embolism: Infected vegetations (endocarditis) → systemic spread
7. Atheromatous embolization: Cholesterol crystals from atherosclerotic plaques → “blue toe syndrome”

Hyperemia vs Congestion:

Feature	Hyperemia	Congestion
Mechanism	Active arterial inflow ↑	Passive venous outflow ↓
Tissue	Bright red (oxygenated)	Dark red/blue (deoxygenated)
Example	Exercise, inflammation	Left heart failure (lung), right heart failure (liver)

Chronic Venous Congestion (CVC):

• Lung: Brown induration of lung → heart failure cells (hemosiderin-laden macrophages in alveoli)
• Liver: Nutmeg liver (dark mottled appearance on cut surface) → cardiac sclerosis → centrilobular fibrosis
• Spleen: Splenomegaly with fibrosis

Hemorrhage — Types:

Type	Description	Examples
Petechiae	1-2 mm; capillary bleeding	Thrombocytopenia, emboli
Purpura	3-10 mm	Platelet disorders, vasculitis
Ecchymosis	>10 mm; subcutaneous	Trauma
Hematoma	Collection of blood in tissue	Subdural, intramuscular
Hemothorax/Hemopericardium	Blood in body cavities	Trauma

Shock — Progressive Stages:

1. Initial/Compensated: Sympathetic activation → tachycardia, vasoconstriction, ↑ BP; skin cool, clammy
2. Progressive/Meta: Tissue hypoperfusion → lactic acidosis, anaerobic metabolism; oliguria, confusion
3. Irreversible: Multiple organ failure, DIC; cellular death even if perfusion restored
4. Death: Refractory hypotension, bradycardia

Ischemia — Types:

• Global ischemia: Whole organ hypoperfusion (cardiac arrest, shock)
• Focal ischemia: Regional (stroke, MI)
• Partial ischemia: More common; some perfusion maintained
• Reperfusion injury: Worsening after restoration of blood flow → ROS generation

Important Anticoagulant Pathways:

Antithrombin III (AT-III) + Heparin → inhibits Thrombin (IIa), IXa, Xa, XIa

Protein C → activated by Thrombin + thrombomodulin → inhibits Va, VIIIa
            (cofactor: Protein S)

Tissue factor pathway inhibitor (TFPI) → inhibits VIIa-TF complex + Xa

Protein C Pathway — Clinical Pearl:

• Protein C/S deficiency → warfarin-induced skin necrosis (warfarin depletes protein C first, creating hypercoagulable state in first few days)
• Always start warfarin with heparin bridge

Key NEET-PG Clinical Pearls:

• Trousseau syndrome — migratory thrombophlebitis; associated with occult malignancy (especially pancreatic adenocarcinoma)
• Budd-Chiari syndrome — hepatic vein thrombosis → hepatomegaly, ascites, abdominal pain
• Portal vein thrombosis — complication of cirrhosis; causes variceal bleeding
• Superior sagittal sinus thrombosis — causes: dehydration, OCPs, pregnancy, hypercoagulable states; presents with headache, papilledema
• Henoch-Schönlein purpura — IgA vasculitis; palpable purpura on buttocks; associated with nephritis
• Cannonball metastases — multiple round metastases in lung from renal cell carcinoma
• Brown tumor of bone — osteoclast proliferation due to PTHrP in hyperparathyroidism; can mimic bone metastases

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