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Botany 3% exam weight

Topic 4

Part of the FMGE study roadmap. Botany topic pathol-004 of Botany.

Hemodynamic Disorders

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Hemodynamic Disorders — Key Facts for FMGE Core concept: Edema, congestion, hemorrhage, thrombosis, embolism, and infarction result from disruptions in normal blood flow and fluid balance High-yield point: Virchow’s triad (stasis, endothelial injury, hypercoagulability) explains thrombosis risk ⚡ Exam tip: Know the difference between congested and infarcted organs on pathology examination


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Hemodynamic Disorders — FMGE Study Guide

Edema

Definition

Excess fluid accumulation in interstitial tissue spaces or body cavities

Mechanisms

1. Increased hydrostatic pressure:

  • Systemic venous congestion (right heart failure)
  • Local venous obstruction (DVT → leg edema, portal hypertension → ascites)
  • Arterial vasodilation (heat, inflammation)

2. Decreased plasma oncotic pressure (hypoalbuminemia):

  • Nephrotic syndrome (proteinuria → albumin loss)
  • Liver cirrhosis (decreased synthesis)
  • Malnutrition/protein deficiency
  • Protein-losing enteropathy

3. Increased vascular permeability:

  • Acute inflammation (histamine, kinins)
  • Allergic reactions (angioedema)
  • Burns, toxins
  • Angioedema (C1 esterase inhibitor deficiency)

4. Lymphatic obstruction:

  • Lymphedema: Non-pitting edema, skin thickening
  • Causes: Lymphadenectomy (post-mastectomy), filariasis (Wuchereria bancrofti)
  • Elephantiasis: Severe lymphatic obstruction with skin thickening

Transudate vs Exudate

FeatureTransudateExudate
Protein<3 g/dL>3 g/dL
Specific gravity<1.015>1.015
Cell count<500 WBCs/μL>500 WBCs/μL
LDHLowHigh
CausesCHF, nephrosis, cirrhosisInflammation, infection

Serous effusion: Transudate from systemic causes Purulent effusion: Exudate with脓性 cells (empyema)

Sites of Edema

  • Dependent edema: Feet/ankles (gravitational, CHF)
  • Pulmonary edema: Left heart failure, kidney disease (pink frothy sputum)
  • Cerebral edema: Trauma, tumors, encephalitis (herniation risk)
  • Periorbital edema: Nephrotic syndrome (morning puffiness)
  • Ascites: Portal hypertension (liver cirrhosis)
  • Anasarca: Generalized severe edema (severe hypoalbuminemia)

Congestion

Active (Hyperemic) Congestion

  • Inflow of oxygenated blood exceeds outflow
  • Red, warm tissue (inflammation)
  • Cause: Vasodilation (heat, inflammation, prostaglandins)

Passive (Congestive) Congestion

  • Impaired outflow (venous drainage)
  • Dark, bluish discoloration (cyanosis)
  • Acute: Single organ affected (e.g., hepatic vein occlusion - sudden death)
  • Chronic: Systemic venous congestion (left/right heart failure)

Chronic Congestive Changes

Liver (Nutmeg liver/Central congestion):

  • Enlarged, tender, dark red central zones with pale peripheral zones
  • Histology: Central vein dilation, hepatocyte atrophy, necrosis
  • Eventually leads to cardiac cirrhosis

Lung (Brown induration):

  • Firm, brown lungs due to hemosiderin-laden macrophages (heart failure cells)
  • Alveolar capillary congestion, interstitial fibrosis

Spleen (Splenic congestion):

  • Enlarged, firm, dark (chronic congestive splenomegaly)

Hemorrhage

Types

  • External: Bleeding from body surface
  • Internal: Bleeding into tissue/cavity (hemothorax, hemopericardium, hemoperitoneum, intracranial hemorrhage)

Effects

  • Small bleed: Absorbed without significant effect
  • Large bleed: Hemorrhagic shock, organ dysfunction
  • Localized collection: Hematoma (organized/calcified → ossify)
  • Apoplexy: Sudden massive hemorrhage (brain, adrenal gland)

Petechiae and Purpura

  • Petechiae: 1-2 mm hemorrhages in skin/mucosa (thrombocytopenia)
  • Purpura: 3-10 mm (coagulation disorders, vasculitis)
  • Ecchymosis: >10 mm bruise
  • Vibices: Linear hemorrhages (increased intra-abdominal pressure)

Thrombosis

Definition

Thrombus: Blood clot formed in situ within the cardiovascular system during life

Virchow’s Triad (Predisposing Factors)

1. Endothelial injury:

  • Trauma, surgery, catheterization
  • Atherosclerosis (intimal damage)
  • Hypertension, vasculitis

2. Stasis/turbulent flow:

  • Immobility, prolonged bed rest
  • CHF, atrial fibrillation
  • Varicose veins

3. Hypercoagulability:

  • Primary (rare): Factor V Leiden, Protein C/S deficiency, antithrombin III deficiency, prothrombin mutation
  • Secondary: Malignancy (Trousseau syndrome), pregnancy, oral contraceptives, smoking, hyperhomocysteinemia

Thrombus Characteristics

Arterial thrombus: White (fibrin + platelets) - grey-white, attached to damaged wall Venous thrombus: Red (RBCs + fibrin) - dark red, gelatinous Mixed thrombus: Lines of Zahn (alternating pale platelet/fibrin and dark RBC layers) Mural thrombus: Attached to heart chamber or aortic wall Occlusive thrombus: Blocks entire lumen (common in veins)

Fate of Thrombus

  1. Resolution: Fibrinolysis dissolves thrombus
  2. Organization: Ingrowth of granulation tissue → fibrosis → recanalization
  3. Propagation: Continued growth, can cause complete obstruction
  4. Embolization: Part breaks off → thromboembolism

Embolism

Definition

Embolus: Detached intravascular mass carried by blood to distant sites

Types of Emboli

Thromboembolism (most common):

  • Venous → right heart → pulmonary arteries (pulmonary embolism)
  • Arterial → systemic organs (kidney, spleen, brain)
  • Paradoxical embolism: Venous thrombus crosses to arterial side via patent foramen ovale

Fat embolism:

  • Bone marrow fat enters circulation after long bone fractures
  • Classic triad (Arnold Gurd criteria): Respiratory distress, neurological symptoms, petechial rash
  • Appears within 24-72 hours of injury

Air embolism:

  • 100 mL air rapidly entering venous system

  • Diving accidents (decompression sickness, “the bends”)
  • Surgical procedures, catheter placement

Amniotic fluid embolism:

  • Rare, catastrophic (DIC, sudden death)
  • Squamous cells and fetal tissue in maternal circulation
  • During labor/delivery (tear in uterine veins)

Septic embolism:

  • Infected material (vegetations in infective endocarditis)
  • Pyaemic abscesses (multiple small abscesses)

Cholesterol embolism:

  • Atheromatous plaque disruption → cholesterol crystals
  • “Blue toe syndrome”, renal failure
  • Post-catheterization or anticoagulation

Tumor embolism:

  • Cancer cells entering circulation
  • Precursor to metastasis

Pulmonary Embolism

Risk factors: Virchow’s triad (especially stasis from immobility), hypercoagulable states Causes: DVT (most common), pelvic vein thrombosis Clinical features: Dyspnea, chest pain, hemoptysis, tachycardia Types:

  • Saddle embolism: Large, blocks both pulmonary arteries → sudden death
  • Massive: >50% obstruction → hypotension
  • Small/segmental: May be asymptomatic

Infarction

Definition

Infarct: Area of tissue necrosis resulting from ischemia (inadequate blood supply)

Types

White (Anemic) infarct:

  • Solid organs with end-arterial blood supply
  • Kidneys, spleen, heart (arterial occlusion)
  • Pale, well-demarcated wedge shape
  • Firm consistency

Red (Hemorrhagic) infarct:

  • Loose tissues with dual blood supply or venous occlusion
  • Lungs (bronchial collateral supply), liver, GI tract
  • Also occurs with: arterial occlusion in tissues that can bleed (brain, though = liquefactive)
  • Hyperemic, red-brown appearance

Factors Determining Severity

  • Duration of ischemia (complete vs incomplete occlusion)
  • Collateral blood supply (liver has dual → rarely infarcts)
  • Oxygen content of blood (anemia worsens ischemia)
  • Metabolic demand of tissue (neurons require constant oxygen)

Common Infarcts

OrganTypeCommon Cause
HeartWhite (coagulative)Coronary atherosclerosis, thrombus
BrainLiquefactiveCerebral atherosclerosis, emboli
KidneyWhiteRenal artery thrombosis, emboli
LungRed (hemorrhagic)Pulmonary embolism
IntestineRedMesenteric artery emboli, volvulus
SpleenWhiteSplenic artery emboli

Wound Healing

  • Acute inflammation → neutrophils (24-72 hours)
  • Macrophages (3-7 days)
  • Granulation tissue (1-3 weeks)
  • Fibrosis and scar formation (months)

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