Hemodynamic Disorders (Thrombosis/Emboli/Shock) 3

Question 1

thrombosis vs embolic?

Answer 1

Question 2

Thrombosis

what are the risk factors?

what is this called?

Answer 2

Question 3

Triad part 1: endothelial activation

if damaged switches from what to what?

Answer 3

Question 4

endothelial activation

prothrombotic: how?

Answer 4

Question 5

Triad part 2: Alterations in blood flow
good type of flow?

bad?

how does this cause increased risk?

Answer 5

Question 6

abnormal blood flow potentiates the triad how?

Answer 6

Question 7

Triad part 2 alterations in blood flow

when/where would this occur? (5)

for the normal one what happens?

Answer 7

Question 8

triad part 2: alterations in blood flow

dilated vessels. examples?

how do they affect?

Answer 8

Question 9

alteration in blood flow

internal obstruction. example?

external interference/compression?

inadequate heart chamber function?

Answer 9

Question 10

triad part 3: hypercoagulability

what 5 primary causes (deficiency or increases) lead to this?

Answer 10

Question 11

hypercoagulability

secondary causes?

Answer 11

Question 12

DVT

what is it? typical location?

risk factors? think about it

signs and symptoms? (3)

how would you check for one?

Answer 12

Question 13

if a thrombus dislodges what do we get?

where will this go?

Answer 13

Question 14

pulmonary embolus

what is it? usually comes from?

lodges where?

Answer 14

Question 15

clinical outcomes of pulmonary embolism

depends on what factors?

3 types?

location of getting lodged?

symptoms?

Answer 15

Question 16

Hypercoagulability

genetic? (3)

acquired? 7 for sure know what 2?

Answer 16

Question 17

most common heritable hypercoagulopathy?

mechanism of action?

tested for how?

Answer 17

Question 18

how to suspect primary hypercoagulable states

events? that happen under what conditions?

tests?

Answer 18

Question 19

heparin-induced thrombocytopenia

genetic or acquired?

caused by?

in what state? caused by formation of? in reaction to?

steps that lead to this? (4)

Answer 19

Question 20

Antiphospholipid antibody syndrome

also called?

antibodies against what?

present with what complications? (where/with who)

another disease it can be present with?

Answer 20

Question 21

fate of thrombi? (3)

how does the last step happen?

this can treat stroke under what conditions?

Answer 21

Question 22

another fate of thrombi?

Answer 22

Question 23

Question 24

pathologic features of thromboembolic disease?

what is present? what does it look like? what does each represent?

what does this tell us?

Answer 24

Question 25

postmortem clots what do they look like? do they contribute to death? what is it?

Answer 25

Question 26

Types of emboli (5) the common theme is that all of them do what?

Answer 26

Question 27

Fat emboli what is it made up of? 4 causes? 1 other cause?

Answer 27

Question 28

air embolism usually caused from? (broad) one potential cause? (specific)

Answer 28

iatrogenic means caused by care provider

Question 29

Air embolism can also be seen in? caused by?

Answer 29

Question 30

Amniotic fluid embolism special about this? symptoms? findings in vessels?

Answer 30

Question 31

Septic emboli (know this one cold) what is it? may occur in what disease? how? gross symptoms you can see? (3) what increases risk of this?

Answer 31

Question 32

infarcts 2 types as examples? why giving tPA in a certain time period for stroke is important?

Answer 32

Question 33

infarction types of infarcts? (5) factors influencing infarcts?

Answer 33

Question 34

red versus white thrombus? locations? rich in? occur under what stress? locations? example of one? which is more likely for an infarct?

Answer 34

Question 35

arterial thromboembolic disease leads to? why?

Answer 35

Question 36

white vs red infarcts. what determines if which one occurs?

Answer 36

Question 37

rate of occlusion (in regards to infarct) if slow? if fast?

Answer 37

Question 38

Shock is caused by? 3 things that lead to this? 2 more from next slide?

Answer 38

neurogenic anaphylactic

Question 39

Answer 39

Question 40

septic shock: how do we get from pathogens to decreased tissue oxygenation? first step? what is released? activation of?

Answer 40

Question 41

septic shock: how do we get from pathogens to decreased tissue oxygenation? after inflammatory response? 3 things in 2 categories know also why its happening

Answer 41

Question 42

septic shock: how do we get from pathogens to decreased tissue oxygenation? after endothelial damage? (final result)

Answer 42

Question 43

manifestations of hypoxic tissue injury as shock progresses? (5)

Answer 43