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thrombosis Flashcards

1
Q

abnormalities that lead to thrombus formation (called Virchow’s triad)

A
  1. endothelial injury
  2. alteration in blood flow
  3. hypercoagulability
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2
Q

____ induces endothelial dysfunction and activation- contributes to ____ and ____ thrombosis

A

turbulence; arterial; cardiac

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3
Q

____ disrupts laminar flow, displacing ____ to periphery of vessel; allows concentration of ____ and activates endothelial cells

A

stasis; platelets; clotting factors

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4
Q

stasis is a major factor in ____ and some ____

A

venous thrombi; intra-cardiac thrombi

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5
Q

____ create local stasis and _____ expose subendothelial ECM and cause turbulence

A

aneurysms; atherosclerotic plaques

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6
Q

inherited conditions associated with hypercoagulability

A
  • factor V Leiden mutation (Va cannot be cleaved; anti-thrombotic mechanism lost)
  • prothrombin mutation (increased prothrombin transcription)
  • deficiencies of anticoagulent proteins (such as AT III)
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7
Q

acquired conditions for hypercoagulability

A
  1. prolonged bed rest
  2. extensive tissue injury
  3. cancer
  4. pregnancy
  5. antiphospholipid antibody syndrome (lupus anticoagulent)
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8
Q

arterial thrombi tend to occur at sites of ____ or _____

A

turbulence; endothelial injury and loss

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9
Q

arterial thrombi have a ____ appearance with distinct ____; may be ___ or ____

A

pale (white); lines of zahn (seen grossly and microscopically); occlusive; mural

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10
Q

sterile (non-infectious) thrombi on heart valves called _____

A

nonbacterial thrombotic endocarditis (NBTE)

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11
Q

venous thrombi have a ____ color and indistinct _____; often form in ____

A

dark maroon (red); lines of zahn; deep veins of the leg

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12
Q

4 fates of thrombi

A
  1. propagation
  2. embolization
  3. dissolution
  4. organization
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13
Q

in propagation, thrombi ___ by additional ____ deposition

A

enlarge; fibrin/platelet

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14
Q

dissolution involves ____ by _____ activity

A

lysis; fibrinolytic

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15
Q

organization involves ingrowth of ____ and ____; leads to deposition of _____ (replacing the fibrin) and _____, which may re-establish some flow through the thrombus

A

fibroblasts; smooth m. cells

collagen; recanalization

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16
Q

disseminated intravascular coagulation (DIC) occurs through widespread act. of the ____ and ____ leading to depletion of ____ and _____ and accumulation of ____

A

coagulation cascade; fibrinolytic system; coagulation factors; platelets; fibrin split products

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17
Q

DIC can be assoc with widespread formation of ____ and risk of _____

A

microthrombi; hemorrhage

18
Q

etiologies of DIC

A
  • infection (gram neg bacteria)
  • obstetric complications (placental abruption, retained dead fetus)
  • neoplasm
  • shock
  • massive tissue injury
19
Q

consequences of pulmonary thromboemboli (mostly from deep veins of the legs)

A
  • no clinical manifestations
  • pulmonary hemorrhage and hematemesis (due to ischemic injury without infarction)
  • pulmonary infarction
  • sudden death (saddle embolus)
  • gradual obstruction of many small pulmonary aas. (can result in pulmonary hypertension)
20
Q

origin of systemic embolization

A

left atrium, left ventricle (including heart valve vegetation), or ulcerated atherosclerotic plaque

21
Q

embolus that arises in a systemic vein and crosses a communication from the venous side to the arterial side of the circulation

A

paradoxical embolus

22
Q

paradoxical embolus communication is usually in the ____ through ____, ____, or other anomalous communication

A

heart; patent foramen ovale; atrial septal defect

23
Q

types of emboli

A 
thrombus
fat
air
amniotic fluid
atherosclerotic plaque material
24
Q

conditions leading to red (hemorrhagic) infarcts

A
  • venous occlusion
  • loose tissue (lung)
  • dual circulation/extensive overlap of arterial supply (lung, small intestine)
  • previous congestion
  • infarction followed by reflow of blood into area (reperfusion injury)
25
Q

causes of white (pale) infarcts

A
  1. occur with arterial occlusions in solid organs

2. where tissue density limits blood seepage from adjacent vascular beds

26
Q

infarcts tend to be ____ with the point of the ____ at the site of _____

A

wedge-shaped; wedge; arterial obstruction

27
Q

infarction is followed by an _____ that begins within several hours and peaks at ____; healing occurs by _____, starting at the edge of the infarct, followed by _____

A

acute inflammatory response; 2 to 3 days

granulation tissue ingrowth; scar formation

28
Q

infarcts in the brain result in _____ and heal with formation of a _____

A

liquefactive (not coagulative) necrosis; cystic space

29
Q

factors that influence infarct development

A
  1. nature of the vascular supply (dual supply vs. single artery)
  2. rate of development of occlusion
  3. vulnerability to hypoxia
  4. oxygen carrying capacity of the blood
30
Q

categories of shock

A
  1. cardiogenic
  2. hypovolemic
  3. septic
  4. anaphylactic
  5. neurogenic
31
Q

in septic shock, ____ bind to ____ on ____ and ____, mediating the release of ___ and ____

A

pathogen-assoc molecular patterns (PAMPS, including LPS); toll-like receptors (TLRs) on monocytes; neutrophils
release of IL-1 and TNF

32
Q

____ occurs in half of septic shock patients

A

DIC

33
Q

factors assoc with pathogenesis of septic shock

A
  • vasodilation
  • hypotension
  • endothelial cell activation and injury
  • reduced myocardial contractility
34
Q

stages of shock

A

nonprogressive, progressive, and irreversible

35
Q

in the nonprogressive stage, compensatory mechanisms maintain tissue perfusion by:

A
  • tachycardia
  • renal conservation of water
  • redist of blood away from vital organs and away from skin through peripheral vasoconstriction
36
Q

in the progressive stage of shock, there is inadequate perfusion with metabolic imbalances such as ____ and _____

A

acidosis; increased lactic acid

37
Q

acidosis reduces vasomotor response to ____ leading to ____ and ____

A

sympathetic stimulation; pooling of blood; reduced perfusion

38
Q

____ to endothelium leads to ____ in the progressive stage

A

hypoxic injury; DIC

39
Q

in the irreversible stage, tissue injury cannot be reversed by _____

A

reperfusion

40
Q

pathologic changes in shock in the

-brain, heart, kidney, lungs, intestinal tract, and liver

A
  • ischemic necrosis of neurons (hippocampus and cerebellum)
  • contraction band necrosis
  • necrosis of tubular epithelial cells (acute tubular necrosis)
  • diffuse alveolar damage due to endothelial injury (adult respiratory distress syndrome/ ARDS)
  • mucosal hemorrhage and necrosis
  • centrizonal necrosis

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