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Path: Hemodynamics > Ch. 4 part. 2 > Flashcards

Ch. 4 part. 2 Flashcards

1
Q

Coagulation cascade

A

amplifying enzyme conversions culminating in thrombin formation

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2
Q

Thrombin

A

most important coagulation factor. converts fibrinogen to fibrin (fibrin gel). Proinflammatory.

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3
Q

2 standard coagulation pathway assays

A

Prothrombin time (PT) and Partial Thromboplastin time (PTT)

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4
Q

Prothrombin time (PT) assay

A

Extrinsic pathway protein function. Factors 2, 5, 7, 10, and fibrinogen.

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5
Q

PT assay accomplished how?

A

adding tissue factor and phospholipids to citrated plasma (want to prevent spontaneous clotting). adding exogenous calcium.

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6
Q

Partial Thromboplastin time (PTT) assay

A

Intrinsic pathway protein function. Factors 2, 5, 8-12, and fibrinogen.

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7
Q

How is PTT assay initiated?

A

By addition of negatively charged particles (activate factor 12, hagemans)

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8
Q

Protease Activated Receptors (PARs)

A

mechanism of thrombin effects.

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9
Q

3 categories of endogenous anticoagulants

A

antithrombins (antithrombin III), Protein C and S, TFPI

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10
Q

Antithrombin (antithrombin III)

A

inhibit thrombin and factors 9-12a. Activated by binding heparin-like molecules.

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11
Q

Protein C and S

A

Vitamin K-dependent. inhibit factors 5a and 8a.

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12
Q

TFPI

A

produced by endothelium. inhibits tissue factor 7a.

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13
Q

3 primary abnormalities that lead to thrombosis (Virchow’s triangle)

A

Endothelial injury, turbulence/stasis, hypercoagulability

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14
Q

Endothelial cell injury

A

Cardiac chambers (after MI), ulcerated plaques, vasculitis

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15
Q

Insults of endothelial injury

A

Hypertension, turbulence, bacterial endotoxin, radiation, metabolic abnormalities, toxicity smoke

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16
Q

Turbulence

A

countercurrents or pockets of stasis.

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17
Q

stasis and turbulence promote

A

pro-coagulation by bringing platelets in contact to epithelium.

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18
Q

Hypercoagulability

A

thrombophilia. any alteration of coagulation that predisposes thrombosis.

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19
Q

Primary hypercoagulability (genetic) gene locations

A

Point mutations at Factor 5 and prothrombin genes.

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20
Q

primary hypercoag cause

A

elevated levels of homocysteine. (thioester linkages- thrombic), deficiency of antithrombin III, protein C or S.

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21
Q

Clinical presentation of primary hypercoag

A

venous thrombosis, recurrent thromboembolism

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22
Q

Heparin-induced thrombocytopenia (HIT) syndrome occurs when?

A

following the administration of unfractionated herparin, which induces Ab production to recognize complexes of heparin and platelet factor 4 (and like molecules)

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23
Q

Effects of HIT syndrome

A

causes platelet activation, aggregation, and consumption leading to thrombocytopenia (hence the name)

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24
Q

Antiphospholipid antibody syndrome (or lupus anticoagulant syndrome) clinical manifestations

A

recurrent thrombosis, miscarriages, cardiac valve vegetations, thrombocytopenia, pulmonary hypertension, pulmonary embolism, etc.. has primary and secondary forms.

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25
Q

Antiphospholipid antibody syndrome (lupus anticoagulant syndrome) effect.

A

antibodies induce a hypercoagulable state. endothelial injury results, activation of platelets and complements

26
Q

Secondary antiphospholipid antibody syndrome

A

individuals who have a well defined autoimmune disease (SLE) and exhibit hypercoagulability

27
Q

Primary antiphospholipid antibody syndrome

A

exhibit only the manifestations of the hypercoagulable state. do not have autoimmune disease

28
Q

Arteriole thrombi

A

usually due to turbulence or endothelial injury. Grow retrograde.

29
Q

Venous thrombi

A

usually due to stasis. grow with blood flow.

30
Q

Lines of Zahn (antemortem clot)

A

pale platelet and fibrin deposits alternating with darker red cell-rich layers. distinguishes between antemortem and postmortem

31
Q

Postmortem clot

A

RBC settle to bottom and have plate platelets and fibrin on top layer. (chicken fat top)

32
Q

Mural thrombi

A

thrombi occurring in the heart chambers or aortic lumen

33
Q

promotions of mural thrombi

A

abnormal myocardial contraction (arrhythmias, MI), endomyocardial injury (myocarditis, catheter)

34
Q

Aortic thrombi

A

in the aorta, usually due to aneurysm.

35
Q

Arterial thrombi

A

frequently occlusive. common sites: coronary, cerebral and femoral arteries

36
Q

Venous thrombi (phlebothrombosis)

A

long cast of the lumen, formed by stasis. usually in LE

37
Q

vegetations

A

thrombi on heart valves. caused by blood-borne bacteria or fungi. (infective endocarditis)

38
Q

sterile vegetations

A

nonbacterial thrombotic endocarditis.

39
Q

Libman-Sacks endocarditis

A

sterile verrucous endocarditis. (SLE)

40
Q

DVT

A

Larger leg veins. may cause pulmonary infarcts. collateral channels offset.

41
Q

Disseminated intravascular coagulation (DIC)

A

sudden or insidious systemic thrombi. cause organ dysfunction in brain, heart, lungs, kidneys.

42
Q

DIC complication

A

uses all platelets and coagulation factors and causes bleeding catastrophe

43
Q

what is an embolus

A

detached intravascular solid, liquid, or gaseous mass

44
Q

Pulmonary embolism (large emboli)

A

95% originate from LE. large emboli - sudden death (right heart failure- cor pulmonale). saddle emboli.

45
Q

Pulmonary embolism (small)

A

minimal Sx, except inadequate bronchial circulation. causes: immobile, HF, hypercoagulable

46
Q

Pulmonary embolism clinical course

A

cardiopulm resus. ECG has rhythm but do not palpate pulse. survival mimics MI

47
Q

Pulmonary embolism Dx

A

spiral CT. may indicate with Hampton Hump, lower right lung

48
Q

Pulmonary embolism gross exam

A

75% lower lung, wedge shaped, hemorrhagic, fibrinous exudate,

49
Q

Pulmonary embolism microscopic exam

A

ischemic (coagulative) necrosis, infected embolus (neutrophil inflamm, septic infarct)

50
Q

Fat and marrow embolism

A

fat globules, hematopoietic marrow. Fractured long bones, soft tissue trauma and burns.

51
Q

Air embolism

A

gas bubbles in circulation. need more than 100cc air.

52
Q

Air embolism effect

A

obstruct vascular flow (distal ischemic injury)

53
Q

Air embolism cause

A

decompression sickness. (decrease in atm pressure)

54
Q

The bends

A

gas bubbles in skeletal muscle and joints

55
Q

the chokes

A

gas bubbles in vasculature. causes: edema, hemorrhage, focal atelectasis or emphysema. (pulm distress)

56
Q

Caisson disease

A

chronic decompression sickness. (femoral heads, tibia, humeri)

57
Q

Amniotic fluid embolism

A

complication of labor. dyspnea, cyanosis, shock, neurologic impairment

58
Q

Cause of amniotic fluid embolism

A

infusion of amniotic fluid or fetal tissue into maternal circulation via tear in placenta.

59
Q

Shock causes

A

hemorrhage, trauma or burns, MI, pulmonary embolisms, microbial sepsis

60
Q

consequences and 3 categories of shock

A

impaired tissue perfusion and hypoxia. cardiogenic, hypovolemic, septic shock.

61
Q

hypovolemic and cardiogenic shock

A

hypotension, weak rapid pulse, cyanosis

62
Q

septic shock

A

flushing due to peripheral vasodilation

Path: Hemodynamics (2 decks)

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