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General Pathology (DENF 2701)General Pathology (DENF 2701)Fall, 2005Fall, 2005
deficiencies Purpuras: 3-5 mm bleeds beneath surfaces
– Same causes as petechiae, but also trauma, vessel inflammation
(vasculitis), increased vascular fragility Ecchymosis: 1-2 cm subcutaneous or submucosal hemorrhages
(bruise)
– Color change: red/blue (hemoglobin) >> blue/green (bilirubin) >>
golden brown (hemosiderin) Hemothorax (chest), hemopericardium (heart), hemoperitoneum
(gut), hemarthrosis (joints) Problems: jaundice; iron deficiency anemia
Hematoma/Ecchymosis/Petechiae/PurpuraHematoma/Ecchymosis/Petechiae/PurpuraSubmucosal Hemorrhage; Extravasation of ErythrocytesSubmucosal Hemorrhage; Extravasation of Erythrocytes
Albumin = the protein most responsible for colloid osmotic pressure Reduced albumin in blood >> Decreased osmotic pressure >> Not as much fluid reabsorbed across endothelium >> More fluid outside vessels (edema) and less inside vessels >> Less plasma volume >> Renal hypoperfusion >> secondary aldosteronism, etc.
Albumin loss from leaky glomerular capillary walls: nephrotic syndrome Reduced albumin synthesis: liver diseases (e.g. cirrhosis); malnutrition Problem: salt and water retention don’t help; salt isn’t large molecule -- It exacerbates the edema
Extra Credit QuestionExtra Credit Question
Ascites refers to severe edema of:
A. Brain
B. Pericardium
C. Peritoneum
D. Lungs
E. Lower extremities
Edema: Clinical ProblemsEdema: Clinical Problems
Subcutaneous edema: mostly a annoyance, but points to underlying cardiac failure (right sided) or renal failure – Dependent edema (pitting edema): gravity draws fluids downward Impaired wound healing or clearance of infection Brain edema: Swollen brain is painful, may be fatal, may force brain substance out through foramina (herniated) -- May compress vascular supply in brain stem -- Trauma, brain abscess, viral infections, etc. Pulmonary edema: fluid fills lungs >> less oxygen diffusion, maybe infection; can be fatal – Especially in left ventricular heart failure – Also: pneumonia, hypersensitivity reactions, adult respiratory distress syndrome (ARDS)
Pulmonary EdemaPulmonary Edema
Excess BloodExcess Blood
Hyperemia: Local increase in blood volume from active process
– E.g.: arterial dilation during exercise, etc. Tissue is more red than normal (excess oxygenated blood;
erythema)
Congestion: Local increase in blood volume from passive process
– E.g.: cardiac failure, venous obstruction Tissue is blue-red (poorly oxygenated blood; cyanosis) Congestion of capillary beds >> edema Chronic passive congestion: long-standing stasis and hypoxia; may
rupture vessel walls (hemorrhage and hemosiderin deposits)
Organ CongestionOrgan Congestion
Lungs: Acute pulmonary congestion: engorged alveolar capillaries and
Photo: Stevens A, Lowe J. Slide atlas of pathology. Mosby, London, 1995.; Kumar, Cotran, Robbins. Robbins Basic pathology, 7th ed., Saunders, Philadelphia, 2003.
Types of ShockTypes of ShockGeneralized Failure of Tissue PerfusionGeneralized Failure of Tissue Perfusion
From profound hypotension (low blood pressure) Cardiogenic shock -- failure of heart to pump Hypovolemic shock -- lack of blood to pump (hemorrhage, fluid loss) Septicemic/Septic/Endotoxic shock -- bacterial infections (dilated veins, no blood return) Obstructive shock -- blockage of major artery Anaphylactic shock -- allergic reaction (dilated veins, no blood return) Neurogenic shock -- dilated veins, no blood return
Persistence of shock: Systemic acidosis >> dilation of previously constricted vessels >> hypotension Blood diverted from gut and kidneys to maintain perfusion of heart & brain Kidney damage; urine output falls Gut stasis, then necrosis
ShockShock
TissueTissue Early ChangeEarly Change Late ChangeLate Change
SkinSkin Pale, coldPale, cold CyanosisCyanosis
KidneysKidneys Low urine outputLow urine output Necrosis of tubular epitheliumNecrosis of tubular epithelium
GutGut Bowel stasisBowel stasis Necrosis of lining epitheliumNecrosis of lining epithelium
LungsLungs TachypnoeaTachypnoea Necrosis of alveolar epitheliumNecrosis of alveolar epithelium
LiverLiver Fatty changeFatty change Necrosis of neuronsNecrosis of neurons
BrainBrain Reduced consciousnessReduced consciousness Necrosis of neurons, comaNecrosis of neurons, coma
Cerebral venous sinusCerebral venous sinusInflammation following infectionInflammation following infection
Hypercoagulability stateHypercoagulability state
Thrombosis RiskThrombosis RiskGenetic and AcquiredGenetic and Acquired
Factor V Leiden mutation Prothrombin mutation Antithrombin III deficiency Protein C deficiency Protein S deficiency Prolonged bed rest; immobilization Myocardial infarction Tissue damage Cancer Prosthetic cardiac valves Disseminated intravascular coagulation (DIC) Lupus anticoagulant (anticardiolipin antibody) Corticosteroid use Congenitally elevated levels of homocysteine Atrial fibrillation/Cardiomyopathy Nephrotic sydnrome Hyperestrogenic states/Oral contraceptive use Sickle cell anemia Smoking
Factor V Leiden mutationThe most common of the hypercoagulation mutations – 2-15% of population – 60% of patients with deep vein thrombosis – 75% of patients with ischemic osteonecrosis
Mutant factor Va: in the 3' untranslated region of prothrombin gene (G20210A mutation)
Mutation cannot be inactivated by protein C >> less antithrombotic activity
Effects of Vascular InjuryEffects of Vascular Injury