circulation II Flashcards

1
Q

causes of thrombosis

A

virchow’s triad:
1 - injury to vessel wall
2 - increased coagulability
3 - decreased flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

hemostasis

A
  • normal
  • blood maintained clot free
  • hemorrhage stopped by sealing vessels after rupture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

thrombosis

A
  • pathological
  • inappropriate clotting in living person
  • clot formation on uninjured endothelium or occlusion of vessels after minor injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

thrombus

A

coagula that forms inside blood vessels or heart chambers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

clot

A

coagula outside of blood vessels or in vessels after death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

pathogenesis of thrombosis - endothelial injury

A
1 - injury/loss to endothelial cells
2 - inflammation
3 - anatomic alterations - plaques
4 - trauma/surgery
5 - endothelial dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

pathogenesis of thrombosis - abnormal blood flow

A
  • non-laminar - brings platelets closer to wall, does not dilute clotting factors or bring enough anti-clotting factor
  • decreased blood flow - patients confined to bed, dilated atria or vessels, venous thrombosis
  • turbulence - endothelial injury and dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

pathogenesis of thrombosis - hypercoagulability

A

1 - primary (genetic)
common: factor V (G1691A), prothrombin (G20210A), (C677T) mutations, or increased factors VIII, IX, XI, or fibrinogen
rare: protein C or S, or antithrombin III deficiency
2 - secondary (acquired) - cardiac failure, tissue damage, oral contraceptives, hyperestrogenic state, disseminated cancer, increased platelets, lifestyle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

heparin-induced thrombocytopenia (HIT)

A

unfractionated heparin induces formation of antibodies against heparin-platelet factor 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

anti phospholipid antibody syndrome

A
  • antibodies bind ot plasma proteins causing endothelial damage, hypercoagulant state
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

ventricular mural thrombosis

A
  • caused by injury to endocardium or decreased flow following MI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

vegetations

A
  • thrombosis of heart valves

- endothelial injury from bacteria, antibodies, trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

venous thrombosis - phlebothrombosis

A
  • stasis of blood in uninflamed veins
  • deep veins in calf, popliteal fossa
  • firmly anchored head, loosely anchored tail
  • can lead to embolism, edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

venous thrombosis - thrombophlebitis

A
  • thrombosis in inflamed veins

- can be sterile due to trauma or septic due to bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

thrombosis of microcirculation - DIC

A
  • disseminated intravascular coagulation

- fibrin thrombi consume platelets and coagulation proteins which leads to bleeding disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

outcomes of thrombosis (4)

A

1 - lysis (dissolution)
2 - organization in connective tissue
3 - propagation towards heart
4 - embolization

17
Q

five most frequent types of embolisms

A
1 - pulmonary thromboembolism
2 - systemic embolism
3 - fat embolism
4 - air embolism
5 - amniotic fluid embolism
18
Q

embolus

A
  • intravascular mass that is detached and carried

- can be part of thrombus, fat, cholesterol, gas, part of a tumor, bone marrow, foreign body, amniotic fluid

19
Q

pulmonary thromboembolism

A
  • most common embolism (95%)
20
Q

systemic thromboembolism

A
  • origin 80% in left side heart, large part mural thrombi
  • rest from aortic aneurisms, plaques, vegetations
  • lodge - 75% lower extremities, 10% brain
21
Q

fat embolism

A
  • origin - fractures of long bones, trauma of fat tissue, burns
  • usually silent
  • fat embolism syndrome in severe cases with pulmonary insufficiency, neurologic symptoms, anemia, thrombocytopenia, petechiae
22
Q

air embolism

A
  • obstetric procedures, chest trauma, decompression sickness
  • bends - gas bubbles out of solution to form gas emboli
  • treatment - high pressure with slow decompression
23
Q

caisson disease

A
  • chronic decompression syndrome

- focal necrosis (femur, humerus, tibia)

24
Q

amniotic fluid embolism

A
  • infusion of amniotic fluid into maternal circulation via tear in the placenta or rupture of uterine veins during labor or immediately postpartum
25
Q

shock

A

decreased systemic perfusion of tissues

26
Q

5 types of shock

A
1 - cardiogenic - low cardiac output
2 - hypovolemic - low circulating volume
3 - septic
4 - anaphylactic
5 - neurogenic
27
Q

three stages of shock

A

1 - nonprogressive or compensated
2 - progressive but reversible
3 - irreversible