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54 Cards in this Set

  • Front
  • Back
Primary hemostasis-- step 1
1. Transient vasoconstriction of damaged vessel
2. Mediated by reflex neural stimulation and endothelin release from endothelial cells
Primary hemostasis-- step 2
1. Platelet adhesion to the surface of disrupted vessel
2. vWF binds exposed subendothelial collagen
3. Platelets bind vWF using GPIb
Primary hemostasis-- step 3
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
ADP promotes
a. Exposure of GPIIb/IIIa receptor on platelets
b. TXA2 is synthesized by platelet cyclooxygenase and released→ promotes platelet aggregation
Primary hemostasis-- step 4
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
Secondary homeostasis
i. Coagulation cascade stabilizes weak platelet plug
1. Cascade generates thrombin
Thrombin
a. Converts fibrinogen in platelet plug to fibrin
b. Fibrin cross-linked yielding a stable platelet-fibrin thrombus
Factors of coagulation cascade
1. Produced in liver in an inactive state
Activation of cascade requires...
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)
Thrombosis
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
Thrombosis characterized by--
i. Attachment to vessel wall
ii. Lines of Zahn
iii. Both help distinguish thrombus from postmortem clot
Lines of Zahn
1. Alternating layers of platelets/fibrin and RBCs
Disruption in normal blood flow
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
Increased risk for DVT
a. Immobilization
b. Cardiac well dysfunction
c. Aneurysm
Endothelial cell damage
i. Endothelial damage disrupts the protective function of endothelial cells increasing risk for thrombosis
Prevention of thrombosis by sub endothelial cells
(one way)
1. Block exposure to subendothelial collagen and underlying tissue factor
Produces prostacyclin (PGI2) and NO
a. Vasodilation and inhibition of platelet aggregation
Secrete heparin-like molecules
a. Augment antithrombin III
b. Inactivates thrombin and coagulation factor
Secrete tissue plasminogen activator
a. tPA
b. Converts plasminogen to plasmin which→
c. Cleaves fibrin and serum fibrinogen
d. Destroys coagulation factors
e. Blocks platelet aggregation
Secretes thrombomodulin
a. Redirects thrombin to activate protein C
b. Inactivates factors V and VIII
Embolism
a. Intravascular mass that travels and occludes downstream vessels
b. Symptoms depend on the vessel involved
Thromboembolus
i. Due to a thrombus that dislodges
ii. Most common type of embolus
Atherosclerotic embolus
i. Due to an atherosclerotic plaque that dislodges
ii. Characterized by the presence of cholesterol clefts in the embolus
Fat embolus
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
Gas embolus
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
Amniotic fluid embolus
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
Systemic embolism
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
Pulmonary emboli
i. Usually due to thromboembolus
Pulmonary emboli most often clinically silent because....
1. Lung has a dual blood supply
2. Embolus is usually small and resolves
Pulmonary infarction
1. Occurs if large- or medium-sized artery is obstructed in patients with pre-existing cardiopulmonary compromise
2. Only 10% of PEs cause infarction
Pulmonary infarction presentation
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
Death from pulmonary infarction
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
Edema
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
Typically seen in patients suffering from....
i. Heart failure
ii. Renal failure
iii. Hepatic failure
iv. Malnutrition
Inflammatory edema
i. Fluid will be a protein-rich exudate
ii. Result of increased vascular permeability
Reduced plasma osmotic pressure
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
Low albumin may indicate...
1. Nephrotic syndrome
2. Liver disease
3. Protein malnutrition
Lymphatic obstruction
i. Lymphedema→ typically localized
ii. Can be due to surgery, neoplasms, inflammation, or occur postirradiation
Another name for hydroperioneum
i. Anasarca
Hyperemia
a. Active process
i. Arteriolar dilation leads to increased blood flow and engorgement of vessels with oxygenated blood.
Congestion
a. Passive process
b. Resulting from reduced outflow of blood from a tissue
c. Systemic→ cardiac failure
d. Local→ venous obstruction
Congested tissue characteristics
i. Cyanosis
ii. Red cell stasis
iii. Deoxygenated hemoglobin
Acute pulmonary congestion
i. Engorged alveolar capillaries
Chronic pulmonary congestion
i. Septa are thickened and fibrotic
ii. Alveoli contain numerous hemosiderin-laden macrophages (heart failure cells)
Acute hepatic congestion
i. Central vein and sinusoids are distended
ii. Centrilobular hepatocytes are ischemic
iii. Periportal hepatocytes develop fatty change
Chronic passive hepatic congestion
i. Centrilobular regions are grossly red-brown and slightly depressed
ii. Accentuated against surrounding zones of uncongested liver
iii. “Nutmeg liver”
Hemorrhage
a. Extravasation of blood into the extravascular space
b. Can occur under chronic congestion
Hematoma
i. Any accumulation of blood with a tissue
Petechiae
i. 1-2mm hemorrhages on skin, mucous membranes, or serosal surfaces
ii. Associated with increased intravascular pressure
Purpura
3mm
ii. Can be secondary to trauma, vasculitis, or increased vascular fragility
Ecchymoses
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
Shock
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
Cardiogenic shock
i. Low cardiac output
ii. Due to myocardial pump failure
Septic shock
i. Results from vasodilation and peripheral pooling of blood
ii. Systemic reaction to bacterial or fungal infection