Hemodynamic Disorders (Thrombosis/Emboli/Shock) 3 Flashcards

1
Q

thrombosis vs embolic?

A
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2
Q

Thrombosis

what are the risk factors?

what is this called?

A
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3
Q

Triad part 1: endothelial activation

if damaged switches from what to what?

A
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4
Q

endothelial activation

prothrombotic: how?

A
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5
Q

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

bad?

how does this cause increased risk?

A
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6
Q

abnormal blood flow potentiates the triad how?

A
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7
Q

Triad part 2 alterations in blood flow

when/where would this occur? (5)

for the normal one what happens?

A
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8
Q

triad part 2: alterations in blood flow

dilated vessels. examples?

how do they affect?

A
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9
Q

alteration in blood flow

internal obstruction. example?

external interference/compression?

inadequate heart chamber function?

A
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10
Q

triad part 3: hypercoagulability

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

A
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11
Q

hypercoagulability

secondary causes?

A
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12
Q

DVT

what is it? typical location?

risk factors? think about it

signs and symptoms? (3)

how would you check for one?

A
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13
Q

if a thrombus dislodges what do we get?

where will this go?

A
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14
Q

pulmonary embolus

what is it? usually comes from?

lodges where?

A
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15
Q

clinical outcomes of pulmonary embolism

depends on what factors?

3 types?

location of getting lodged?

symptoms?

A
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16
Q

Hypercoagulability

genetic? (3)

acquired? 7 for sure know what 2?

A
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17
Q

most common heritable hypercoagulopathy?

mechanism of action?

tested for how?

A
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18
Q

how to suspect primary hypercoagulable states

events? that happen under what conditions?

tests?

A
19
Q

heparin-induced thrombocytopenia

genetic or acquired?

caused by?

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

steps that lead to this? (4)

A
20
Q

Antiphospholipid antibody syndrome

also called?

antibodies against what?

present with what complications? (where/with who)

another disease it can be present with?

A
21
Q

fate of thrombi? (3)

how does the last step happen?

this can treat stroke under what conditions?

A
22
Q

another fate of thrombi?

A
23
Q
A
24
Q

pathologic features of thromboembolic disease?

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

what does this tell us?

A
25
Q

postmortem clots

what do they look like?

do they contribute to death?

what is it?

A
26
Q

Types of emboli

(5)

the common theme is that all of them do what?

A
27
Q

Fat emboli

what is it made up of?

4 causes? 1 other cause?

A
28
Q

air embolism

usually caused from? (broad)

one potential cause? (specific)

A

iatrogenic means caused by care provider

29
Q

Air embolism

can also be seen in?

caused by?

A
30
Q

Amniotic fluid embolism

special about this?

symptoms?

findings in vessels?

A
31
Q

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?

A
32
Q

infarcts

2 types as examples?

why giving tPA in a certain time period for stroke is important?

A
33
Q

infarction

types of infarcts? (5)

factors influencing infarcts?

A
34
Q

red versus white thrombus?

locations?

rich in?

occur under what stress?

locations?

example of one?

which is more likely for an infarct?

A
35
Q

arterial thromboembolic disease leads to?

why?

A
36
Q

white vs red infarcts.

what determines if which one occurs?

A
37
Q

rate of occlusion (in regards to infarct)

if slow? if fast?

A
38
Q

Shock

is caused by?

3 things that lead to this?

2 more from next slide?

A

neurogenic

anaphylactic

39
Q
A
40
Q

septic shock: how do we get from pathogens to decreased tissue oxygenation?

first step?

what is released?

activation of?

A
41
Q

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

A
42
Q

septic shock: how do we get from pathogens to decreased tissue oxygenation?

after endothelial damage?

(final result)

A
43
Q

manifestations of hypoxic tissue injury

as shock progresses?

(5)

A