💧 Edema
- Excess fluid in interstitial space — localized or generalized
- Mechanisms
- ↑ hydrostatic pressure: CHF (generalized), portal HTN, renal Na⁺/H₂O retention, DVT (local)
- ↓ colloid osmotic pressure (hypoalbuminemia): liver disease, nephrotic syndrome, protein malnutrition
- Lymphatic obstruction: tumor, post-surgical, filariasis → elephantiasis
- ↑ capillary permeability: inflammation, type I hypersensitivity, drugs (bleomycin, heroin)
- ↑ interstitial Na⁺: high intake, primary hyperaldosteronism, renal failure
- Clinical types
- Anasarca: severe generalized edema
- Effusion: fluid in body cavities (pleural, pericardial, peritoneal)
- Pulmonary edema: fluid in alveoli/interstitium
- Fluid composition
- Transudate: low protein (hydrostatic/oncotic imbalance)
- Exudate: high protein + cells — purulent, fibrinous, eosinophilic, hemorrhagic
- Lymphedema: protein-rich, non-pitting
- Myxedema: glycosaminoglycan-rich (hyaluronic acid, chondroitin sulfate)
- Active vs passive hyperemia
- Active: arteriolar vasodilation (inflammation, exercise)
- Passive (congestion): impaired venous outflow (hepatic congestion, CHF)
- 🔹 Pulmonary edema & anasarca are high‑yield exam presentations
🩸 Hemostasis
- Sequence: vascular spasm → platelet plug → fibrin stabilization
- Vascular phase
- Transient vasoconstriction (endothelin‑1)
- Exposed subendothelial collagen → platelet adhesion via vWF
- ↓ antithrombotic substances (PGI₂, NO, tPA, thrombomodulin)
- Platelet plug formation (3 steps)
- Adhesion: vWF–collagen–GPIb
- Activation: shape change, degranulation (ADP, TXA₂, Ca²⁺), phospholipid exposure
- Aggregation: fibrinogen–GPIIb/IIIa bridges; ADP/TXA₂ amplify
- Coagulation cascade
- Intrinsic: contact (collagen, HMWK, kallikrein) → XII, XI, IX, VIII
- Extrinsic: tissue factor → VII
- Common pathway: X → V → prothrombin → thrombin → fibrinogen → fibrin
- Lab tests
- PT (extrinsic + common): factors VII, X, V, prothrombin, fibrinogen — monitored for warfarin
- PTT (intrinsic + common): factors XII, XI, IX, VIII, X, V, prothrombin, fibrinogen — monitored for heparin
- Thrombin time: fibrinogen levels
- FDP / D‑dimer: fibrinolysis (↑ in DIC)
- ⚠️ Aspirin irreversibly inhibits COX‑1 → ↓ TXA₂ for platelet lifespan
🩹 Bleeding disorders
- Platelet defects
- ITP: IgG anti‑GPIIb/IIIa or GPIb/IX → splenic destruction. Acute (post‑viral, children); chronic (women, SLE)
- TTP: ADAMTS13 deficiency → ultra‑large vWF multimers → microthrombi. Pentad: hemolytic anemia, thrombocytopenia, neuro/renal
- Bernard‑Soulier: GPIb defect → adhesion failure
- Glanzmann: GPIIb/IIIa defect → aggregation failure
- Coagulation factor disorders
- Hemophilia A (VIII, X‑linked): hemarthrosis, prolonged PTT
- Hemophilia B (IX, X‑linked): same as A, treat with rFIX
- vWD (autosomal dominant): vWF defect → mucocutaneous bleeding, ↑ bleeding time, ristocetin abnormal
- Vitamin K deficiency: ↓ II, VII, IX, X, protein C/S
- Liver disease: ↓ all factors (except vWF)
- DIC (consumptive)
- Causes: obstetric complications, sepsis, AML M3, adenocarcinoma (mucin)
- Labs: ↓ platelets, ↑ PT/PTT, ↓ fibrinogen, ↑ D‑dimer
- Treatment: treat underlying disorder
- 🔹 von Willebrand disease is the most common inherited bleeding disorder
🧬 Thrombosis & embolism
- Virchow’s triad
- Endothelial injury: atherosclerosis, vasculitis, HTN
- Stasis/turbulence: immobilization, aneurysms, polycythemia
- Hypercoagulability: factor V Leiden, ATIII deficiency, cancer, OCPs, pregnancy
- Thrombus vs clot
- Thrombus: intravascular, layered (Lines of Zahn), platelet‑rich
- Embolism types
- Thromboemboli (most common), atheromatous, fat, bone marrow, gas (decompression), amniotic fluid, tumor, talc, septic
- Pulmonary embolism
- 95% from DVT; V/Q mismatch, elevated D‑dimer
- Wedge‑shaped hemorrhagic infarct (dual circulation)
- Saddle embolus → sudden death
DVT→
PE→
hemorrhagic infarct→
pulmonary HTN (chronic)
⚡ Infarction
- Ischemic necrosis — most often thrombotic/embolic occlusion
- Gross: wedge‑shaped, apex at occlusion
- Types
- Pale (anemic): solid organs with single supply (heart, kidney, spleen)
- Red (hemorrhagic): dual supply (lung, liver) or venous occlusion (testicular torsion)
- Microscopy
- Coagulative necrosis (most organs) / liquefactive (brain)
- Sequence: ischemia → necrosis → inflammation → granulation → scar
⚠️ Shock
- Types
- Cardiogenic: MI, arrhythmia, PE, tamponade
- Hypovolemic: hemorrhage, burns, dehydration
- Septic: cytokines → vasodilation, ARDS, DIC, MODS (mortality ~20%)
- Neurogenic: anesthesia, spinal cord injury
- Anaphylactic: type I hypersensitivity
- Stages
- Compensated: sympathetic, RAAS activation; vital organs preserved
- Decompensated: lactic acidosis, renal insufficiency, reversible injury
- Irreversible: multi‑organ failure, cell death
- Organ manifestations
- Kidney: fibrin thrombi, ATN → oliguria
- Lung: diffuse alveolar damage (“shock lung”)
- Intestine: mucosal necrosis, hemorrhage, bacteremia