Circulation 2

Question 1

hemostasis

Answer 1

the blood is maintained in normal vessels and hemorrhage is stopped by sealing blood vessels after rupture

Question 2

thrombosis

Answer 2

inappropriate clotting in uninjured endothelium or after minor injury

Question 3

thrombi

Answer 3

inside blood vessels and heart tissues

Question 4

clots

Answer 4

outside blood vesses or in blood vessels after flow has ceased

Question 5

causes of thrombosis

Answer 5

virchows triad

endothelial injury- most important factor

abnormal blood flow

hypercoagulability

Question 6

causes of loss of endothelial cells

Answer 6

myocradial infarction

hypertension

inflammation

trauma

anatomic alterations

Question 7

endothelial activation

Answer 7

response to stimuli by adjusting steady-state functions and expressing new properties

show:
adhesion molecules
produce cytokines, vasoactive molecules

Question 8

endothelial dysfunction

Answer 8

shifting of the pattern of gene expression in endotheloium to one that is prothrombotic and proinflammatory

Question 9

causes of endothelial activation

Answer 9

inflammatory cytokines

hemodynamic stress/lipid products (atherosclerosis)

advanced glycation end products (diabetes)

viruses

complement

hypoxia

Question 10

end results of endothelial activation and dysfunction

Answer 10

procoagulant changes and antifibrinolytic effects that cause thrombosis

Question 11

why is aspirin used for CAD?

Answer 11

inhibits platelet activation in the heart, where the circulation is rich in platlets

Question 12

types of abnormal flow

Answer 12

decreased blood flow

turbulence

Question 13

types of hypercoagulability

Answer 13

primary- genetic

secondary- acquired

Question 14

heperain induced thrombocytopenia

Answer 14

unfractionated heparin induces Abs which activate and aggregate platelets causing a procoagulant state

Question 15

anti phospholipid antibody syndrome

Answer 15

effects caused by the binding of Abs to plasma proteins causing damage, and platelet and complement activation

Question 16

ventricular mural thrombosis

Answer 16

caused by injury to endocardium by decreased flow following an MI

Question 17

thrombosis of heart valve

Answer 17

caused by bacteria, immune complexes, or trauma

Question 18

phlebothrombosis

Answer 18

d/t stasis in uninflammed veins

sites: deep veins in calf, popliteal fossa, IVC tributaries

appears w/ anchor and loose tail

can result in pulmonary embolism

Question 19

thrombophlebitis

Answer 19

thrombosis in inflammed veins

sterile: trauma, radiation, chemicals
septic: d/t bacteria

Question 20

thrombosis in microcirculation

Answer 20

disseminated intravasular coagulation

apparent only by microscope

widespread thrombi in microcirulatoin consumes platelets and coagulatoin and manifests itself as bleeding

Question 21

outcomes of thrombosis

Answer 21

lysis = resolution
organization into connective tissue
propogation towards heart
embolization to lungs

Question 22

embolism

Answer 22

intravascular mass that is detached from the vascular wall and carried by the blood to a distant site from its origin

Question 23

pulmonary thromboembolism

Answer 23

most frequent emboli- 95% originate in deep veins of the legs and pass into pulmonary circulation

small artery (60-80%) are silent

large artery- sudden death, right heart failure, shock

medium arteries- hemorrhage d/t infarct/brohial arterys

end artery branches- infarct/hemorrhage

multiple emboli over time- pulmonary hypertensoin w/ right heart failure

Question 24

systemic thromboembolism

Answer 24

origin- 80% in heart

location- can lend in any vascular bed, usually lower extremities

effect- infarction

Question 25

fat embolism

Answer 25

microscopic fat glubles enter circulation and block artery sources: fractures of long bones w/ bone marrow burns trauma usually silent cause blockage and endothelial activation

Question 26

fat embolism syndrome

Answer 26

pulmonary insufficiency, neurologic symptoms, anemia

Question 27

air embolism

Answer 27

gas bubbles within the circulatoin cause physical obstruction by themselves or coalesce forming frothy masses that occlude large arteries occurs: decompression sickness

Question 28

decompression sickness

Answer 28

sudden transition from high to low pressure breathed gas bubbles come out of solution in the blood to form gas emboli "the bends"- pain d/t rapid formation of air

Question 29

amniotic fluid embolism

Answer 29

infusion of amniotic fluid or fetal mass pass into maternal circulation occurs during labor or immediately postpartum very rare, but high mortality site lung

Question 30

shock

Answer 30

decreased systemic perfusion of tissues d/t decreased CO or BV causes- hypotension, impaired perfusion, hypoxia

Question 31

three phases of shock

Answer 31

nonprogressive-compensated - compensatory mechanisms maintain CO and BV enabling brain and heart perfusion progressive-reversible - generalized tissue hypoperfusion and worsening of circulatory and metabolic imbalances irreversible- severe tissue and cellular injury that results in multiple organs that is irreversible even if hemodynamic defects are corrected