thrombosis

Question 1

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

Answer 1

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

Question 2

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

Answer 2

turbulence; arterial; cardiac

Question 3

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

Answer 3

stasis; platelets; clotting factors

Question 4

stasis is a major factor in ____ and some ____

Answer 4

venous thrombi; intra-cardiac thrombi

Question 5

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

Answer 5

aneurysms; atherosclerotic plaques

Question 6

inherited conditions associated with hypercoagulability

Answer 6

• 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)

Question 7

acquired conditions for hypercoagulability

Answer 7

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

Question 8

arterial thrombi tend to occur at sites of ____ or _____

Answer 8

turbulence; endothelial injury and loss

Question 9

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

Answer 9

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

Question 10

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

Answer 10

nonbacterial thrombotic endocarditis (NBTE)

Question 11

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

Answer 11

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

Question 12

4 fates of thrombi

Answer 12

1. propagation
2. embolization
3. dissolution
4. organization

Question 13

in propagation, thrombi ___ by additional ____ deposition

Answer 13

enlarge; fibrin/platelet

Question 14

dissolution involves ____ by _____ activity

Answer 14

lysis; fibrinolytic

Question 15

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

Answer 15

fibroblasts; smooth m. cells

collagen; recanalization

Question 16

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

Answer 16

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

Question 17

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

Answer 17

microthrombi; hemorrhage

Question 18

etiologies of DIC

Answer 18

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

Question 19

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

Answer 19

• 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)

Question 20

origin of systemic embolization

Answer 20

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

Question 21

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

Answer 21

paradoxical embolus

Question 22

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

Answer 22

heart; patent foramen ovale; atrial septal defect

Question 23

types of emboli

Answer 23

thrombus
fat
air
amniotic fluid
atherosclerotic plaque material

Question 24

conditions leading to red (hemorrhagic) infarcts

Answer 24

• 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)

Question 25

causes of white (pale) infarcts

Answer 25

1. occur with arterial occlusions in solid organs | 2. where tissue density limits blood seepage from adjacent vascular beds

Question 26

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

Answer 26

wedge-shaped; wedge; arterial obstruction

Question 27

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 _____

Answer 27

acute inflammatory response; 2 to 3 days | granulation tissue ingrowth; scar formation

Question 28

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

Answer 28

liquefactive (not coagulative) necrosis; cystic space

Question 29

factors that influence infarct development

Answer 29

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

Question 30

categories of shock

Answer 30

1. cardiogenic 2. hypovolemic 3. septic 4. anaphylactic 5. neurogenic

Question 31

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

Answer 31

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

Question 32

____ occurs in half of septic shock patients

Answer 32

DIC

Question 33

factors assoc with pathogenesis of septic shock

Answer 33

- vasodilation - hypotension - endothelial cell activation and injury - reduced myocardial contractility

Question 34

stages of shock

Answer 34

nonprogressive, progressive, and irreversible

Question 35

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

Answer 35

- tachycardia - renal conservation of water - redist of blood away from vital organs and away from skin through peripheral vasoconstriction

Question 36

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

Answer 36

acidosis; increased lactic acid

Question 37

acidosis reduces vasomotor response to ____ leading to ____ and ____

Answer 37

sympathetic stimulation; pooling of blood; reduced perfusion

Question 38

____ to endothelium leads to ____ in the progressive stage

Answer 38

hypoxic injury; DIC

Question 39

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

Answer 39

reperfusion

Question 40

pathologic changes in shock in the | -brain, heart, kidney, lungs, intestinal tract, and liver

Answer 40

- 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