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54 Cards in this Set
- Front
- Back
Primary hemostasis-- step 1
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1. Transient vasoconstriction of damaged vessel
2. Mediated by reflex neural stimulation and endothelin release from endothelial cells |
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Primary hemostasis-- step 2
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1. Platelet adhesion to the surface of disrupted vessel
2. vWF binds exposed subendothelial collagen 3. Platelets bind vWF using GPIb |
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Primary hemostasis-- step 3
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1. Platelet degranulation
2. Adhesion induces shape change in platelets and degranulation with release of multiple mediators 3. ADP is released from platelet dense granules |
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ADP promotes
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a. Exposure of GPIIb/IIIa receptor on platelets
b. TXA2 is synthesized by platelet cyclooxygenase and released→ promotes platelet aggregation |
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Primary hemostasis-- step 4
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1. Platelets aggregate at site of injury via GPIIb/IIIa using fibrinogen as a linking molecule→ platelet plug
2. Platelet plug is weak→ stabilized by coagulation cascade |
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Secondary homeostasis
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i. Coagulation cascade stabilizes weak platelet plug
1. Cascade generates thrombin |
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Thrombin
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a. Converts fibrinogen in platelet plug to fibrin
b. Fibrin cross-linked yielding a stable platelet-fibrin thrombus |
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Factors of coagulation cascade
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1. Produced in liver in an inactive state
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Activation of cascade requires...
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1. Exposure to an activating substance
2. Tissue thromboplastin activates factor VII (extrinsic) 3. Subendothelial collagen activates factor XII (intrinsic pathway) 4. Phospholipid surface of platelets 5. Calcium (derived from dense granules) |
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Thrombosis
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a. Pathologic formation of an intravascular blood clot
b. Can occur in artery or vein c. Most common location is deep veins of the leg below the knee |
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Thrombosis characterized by--
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i. Attachment to vessel wall
ii. Lines of Zahn iii. Both help distinguish thrombus from postmortem clot |
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Lines of Zahn
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1. Alternating layers of platelets/fibrin and RBCs
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Disruption in normal blood flow
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i. Stasis and turbulence of blood flow increases risk for thrombosis
ii. Blood flow is normally continuous and laminar iii. Keeps platelets and factors dispersed and inactivated |
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Increased risk for DVT
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a. Immobilization
b. Cardiac well dysfunction c. Aneurysm |
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Endothelial cell damage
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i. Endothelial damage disrupts the protective function of endothelial cells increasing risk for thrombosis
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Prevention of thrombosis by sub endothelial cells
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(one way)
1. Block exposure to subendothelial collagen and underlying tissue factor |
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Produces prostacyclin (PGI2) and NO
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a. Vasodilation and inhibition of platelet aggregation
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Secrete heparin-like molecules
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a. Augment antithrombin III
b. Inactivates thrombin and coagulation factor |
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Secrete tissue plasminogen activator
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a. tPA
b. Converts plasminogen to plasmin which→ c. Cleaves fibrin and serum fibrinogen d. Destroys coagulation factors e. Blocks platelet aggregation |
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Secretes thrombomodulin
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a. Redirects thrombin to activate protein C
b. Inactivates factors V and VIII |
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Embolism
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a. Intravascular mass that travels and occludes downstream vessels
b. Symptoms depend on the vessel involved |
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Thromboembolus
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i. Due to a thrombus that dislodges
ii. Most common type of embolus |
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Atherosclerotic embolus
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i. Due to an atherosclerotic plaque that dislodges
ii. Characterized by the presence of cholesterol clefts in the embolus |
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Fat embolus
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i. Associated with bone fractures
ii. Particularly long bones and soft tissue trauma iii. Develops while fracture is still present or shortly after repair iv. Characterized by dyspnea and petechiae on skin overlying chest |
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Gas embolus
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i. Classically seen in decompression sickness
ii. N2 gas precipitates out of blood due to rapid ascent iii. Present with joint and muscle pain and respiratory symptoms iv. May also occur during laparoscopic surgery |
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Amniotic fluid embolus
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i. Enters maternal circulation during labor or delivery
ii. Presents with shortness of breath, neurologic symptoms, and DIC iii. Characterized by squamous cells and keratin debris from fetal skin in embolus |
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Systemic embolism
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i. Due to thromboembolus
ii. Most commonly arise in the left heart iii. Travel down systemic circulation to occlude flow to organs, most commonly the lower extremities |
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Pulmonary emboli
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i. Usually due to thromboembolus
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Pulmonary emboli most often clinically silent because....
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1. Lung has a dual blood supply
2. Embolus is usually small and resolves |
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Pulmonary infarction
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1. Occurs if large- or medium-sized artery is obstructed in patients with pre-existing cardiopulmonary compromise
2. Only 10% of PEs cause infarction |
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Pulmonary infarction presentation
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a. Shortness of breath, hemoptysis, pleuritic chest pain, pleural effusion
b. Spiral CT shows a vascular filling defect in lung c. D-dimer elevated d. Gross examination reveals a hemorrhagic, wedge-shaped infarct |
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Death from pulmonary infarction
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a. Occurs with a large saddle embolus that blocks both left and right pulmonary arteries with significant occlusion of a large pulmonary artery
b. Death is due to electromehcanical dissociation |
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Edema
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a. Abnormal increase in interstitial fluid within tissues
b. Due to increased capillary pressure or diminished colloid osmotic pressure c. Typically a protein-poor transudate |
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Typically seen in patients suffering from....
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i. Heart failure
ii. Renal failure iii. Hepatic failure iv. Malnutrition |
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Inflammatory edema
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i. Fluid will be a protein-rich exudate
ii. Result of increased vascular permeability |
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Reduced plasma osmotic pressure
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i. Occurs when albumin is not synthesized in adequate amounts or is lost from circulation
ii. Levels maintained by kidneys iii. Leads to net movement of fluid into interstitial tissues iv. Low renal perfusion v. Increased renin-angiotensin-aldosterone secretion |
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Low albumin may indicate...
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1. Nephrotic syndrome
2. Liver disease 3. Protein malnutrition |
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Lymphatic obstruction
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i. Lymphedema→ typically localized
ii. Can be due to surgery, neoplasms, inflammation, or occur postirradiation |
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Another name for hydroperioneum
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i. Anasarca
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Hyperemia
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a. Active process
i. Arteriolar dilation leads to increased blood flow and engorgement of vessels with oxygenated blood. |
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Congestion
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a. Passive process
b. Resulting from reduced outflow of blood from a tissue c. Systemic→ cardiac failure d. Local→ venous obstruction |
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Congested tissue characteristics
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i. Cyanosis
ii. Red cell stasis iii. Deoxygenated hemoglobin |
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Acute pulmonary congestion
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i. Engorged alveolar capillaries
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Chronic pulmonary congestion
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i. Septa are thickened and fibrotic
ii. Alveoli contain numerous hemosiderin-laden macrophages (heart failure cells) |
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Acute hepatic congestion
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i. Central vein and sinusoids are distended
ii. Centrilobular hepatocytes are ischemic iii. Periportal hepatocytes develop fatty change |
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Chronic passive hepatic congestion
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i. Centrilobular regions are grossly red-brown and slightly depressed
ii. Accentuated against surrounding zones of uncongested liver iii. “Nutmeg liver” |
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Hemorrhage
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a. Extravasation of blood into the extravascular space
b. Can occur under chronic congestion |
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Hematoma
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i. Any accumulation of blood with a tissue
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Petechiae
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i. 1-2mm hemorrhages on skin, mucous membranes, or serosal surfaces
ii. Associated with increased intravascular pressure |
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Purpura
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3mm
ii. Can be secondary to trauma, vasculitis, or increased vascular fragility |
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Ecchymoses
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i. >1-2 cm
ii. Red cells in lesions phagocytized iii. Hemoglobin is enzymatically converted to bilirubin leading to hemosiderin→accounting for characteristic color changes in a bruise |
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Shock
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a. Characterized by systemic hypotension
b. Due either to reduced cardiac output or to reduced effective circulating blood volume c. Leads to impaired tissue perfusion and cellular hypoxia |
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Cardiogenic shock
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i. Low cardiac output
ii. Due to myocardial pump failure |
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Septic shock
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i. Results from vasodilation and peripheral pooling of blood
ii. Systemic reaction to bacterial or fungal infection |