Ch. 4 part. 2

Question 1

Coagulation cascade

Answer 1

amplifying enzyme conversions culminating in thrombin formation

Question 2

Thrombin

Answer 2

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

Question 3

2 standard coagulation pathway assays

Answer 3

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

Question 4

Prothrombin time (PT) assay

Answer 4

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

Question 5

PT assay accomplished how?

Answer 5

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

Question 6

Partial Thromboplastin time (PTT) assay

Answer 6

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

Question 7

How is PTT assay initiated?

Answer 7

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

Question 8

Protease Activated Receptors (PARs)

Answer 8

mechanism of thrombin effects.

Question 9

3 categories of endogenous anticoagulants

Answer 9

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

Question 10

Antithrombin (antithrombin III)

Answer 10

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

Question 11

Protein C and S

Answer 11

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

Question 12

TFPI

Answer 12

produced by endothelium. inhibits tissue factor 7a.

Question 13

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

Answer 13

Endothelial injury, turbulence/stasis, hypercoagulability

Question 14

Endothelial cell injury

Answer 14

Cardiac chambers (after MI), ulcerated plaques, vasculitis

Question 15

Insults of endothelial injury

Answer 15

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

Question 16

Turbulence

Answer 16

countercurrents or pockets of stasis.

Question 17

stasis and turbulence promote

Answer 17

pro-coagulation by bringing platelets in contact to epithelium.

Question 18

Hypercoagulability

Answer 18

thrombophilia. any alteration of coagulation that predisposes thrombosis.

Question 19

Primary hypercoagulability (genetic) gene locations

Answer 19

Point mutations at Factor 5 and prothrombin genes.

Question 20

primary hypercoag cause

Answer 20

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

Question 21

Clinical presentation of primary hypercoag

Answer 21

venous thrombosis, recurrent thromboembolism

Question 22

Heparin-induced thrombocytopenia (HIT) syndrome occurs when?

Answer 22

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

Question 23

Effects of HIT syndrome

Answer 23

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

Question 24

Antiphospholipid antibody syndrome (or lupus anticoagulant syndrome) clinical manifestations

Answer 24

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

Question 25

Antiphospholipid antibody syndrome (lupus anticoagulant syndrome) effect.

Answer 25

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

Question 26

Secondary antiphospholipid antibody syndrome

Answer 26

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

Question 27

Primary antiphospholipid antibody syndrome

Answer 27

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

Question 28

Arteriole thrombi

Answer 28

usually due to turbulence or endothelial injury. Grow retrograde.

Question 29

Venous thrombi

Answer 29

usually due to stasis. grow with blood flow.

Question 30

Lines of Zahn (antemortem clot)

Answer 30

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

Question 31

Postmortem clot

Answer 31

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

Question 32

Mural thrombi

Answer 32

thrombi occurring in the heart chambers or aortic lumen

Question 33

promotions of mural thrombi

Answer 33

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

Question 34

Aortic thrombi

Answer 34

in the aorta, usually due to aneurysm.

Question 35

Arterial thrombi

Answer 35

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

Question 36

Venous thrombi (phlebothrombosis)

Answer 36

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

Question 37

vegetations

Answer 37

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

Question 38

sterile vegetations

Answer 38

nonbacterial thrombotic endocarditis.

Question 39

Libman-Sacks endocarditis

Answer 39

sterile verrucous endocarditis. (SLE)

Question 40

DVT

Answer 40

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

Question 41

Disseminated intravascular coagulation (DIC)

Answer 41

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

Question 42

DIC complication

Answer 42

uses all platelets and coagulation factors and causes bleeding catastrophe

Question 43

what is an embolus

Answer 43

detached intravascular solid, liquid, or gaseous mass

Question 44

Pulmonary embolism (large emboli)

Answer 44

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

Question 45

Pulmonary embolism (small)

Answer 45

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

Question 46

Pulmonary embolism clinical course

Answer 46

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

Question 47

Pulmonary embolism Dx

Answer 47

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

Question 48

Pulmonary embolism gross exam

Answer 48

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

Question 49

Pulmonary embolism microscopic exam

Answer 49

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

Question 50

Fat and marrow embolism

Answer 50

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

Question 51

Air embolism

Answer 51

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

Question 52

Air embolism effect

Answer 52

obstruct vascular flow (distal ischemic injury)

Question 53

Air embolism cause

Answer 53

decompression sickness. (decrease in atm pressure)

Question 54

The bends

Answer 54

gas bubbles in skeletal muscle and joints

Question 55

the chokes

Answer 55

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

Question 56

Caisson disease

Answer 56

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

Question 57

Amniotic fluid embolism

Answer 57

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

Question 58

Cause of amniotic fluid embolism

Answer 58

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

Question 59

Shock causes

Answer 59

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

Question 60

consequences and 3 categories of shock

Answer 60

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

Question 61

hypovolemic and cardiogenic shock

Answer 61

hypotension, weak rapid pulse, cyanosis

Question 62

septic shock

Answer 62

flushing due to peripheral vasodilation