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MDTI > Coagulation > Flashcards

Coagulation Flashcards

1
Q

Hemostasis

A

process which spontaneously arrests the flow of blood from the vessels carrying blood under pressure. Causes bleeding to stop

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2
Q

Thrombosis

A

A pathologic process in which one or more components of the normal hemostatic mechanism is activated wrong place, wrong time

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3
Q

hemostatic thrombus

A

the “plug” that seals off an injured artery or vein. most often referred to as a thrombus

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4
Q

what forms the hemostatic plug?

A

fibrin deposition and platelet plug

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5
Q

what limits and removes the hemostatic plug?

A

anti-coagulant and fibrin lysis

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6
Q

pathology

A

the precise study and diagnosis of disease

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7
Q

virchow’s triad in thrombosis

A

endothelial injury, hyper coagulability, abnormal blood flow. Endothelial integrity is the most important factor.

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8
Q

what causes thrombosis?

A

too much clotting/platelet plug formation or too little anticoagulant/fibrinolytic activity

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9
Q

direction of thrombus movement (typically)?

A

towards the heart. Anterograde in veins and retrograde in arteries

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10
Q

mural thrombi

A

clots occurring in the cardiac chambers and aorta

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11
Q

vegetations

A

thrombi on the heart valves

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12
Q

lines of zahn

A

laminated appearance of thrombi due to the flow of blood over the clot (like rock sedimentation)

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13
Q

white layers in Lines of Zahn

A

platelets & fibrin (pink under microscope)

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14
Q

red layers in Lines of Zahn

A

RBCs

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15
Q

arterial thrombi

A

most common in coronary, cerebral, and femoral arteries. commonly caused by endothelial injury (ruptured atherosclerotic plaque, vasculitis, trauma), white thrombus

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16
Q

venous thrombi

A

most common in lower extremities (90%), upper extremities, pelvic plexi, portal/hepatic veins. caused by stasis, RBC trapping=red thrombus

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17
Q

two main features of thrombi

A

lines of zahn, attachment to endothelial wall

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18
Q

4 fates of thrombi

A

propagation, embolization, dissolution, recanalization

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19
Q

thrombus propagation

A

continued growth

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20
Q

thrombus embolization

A

portion of/entire thrombus dislodges and travels via flow of blood to another site

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21
Q

thrombus dissolution

A

fibrinolysis can result in breakdown

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22
Q

thrombus recanalization

A

become organized via ingrowth of endothelial cells, smoot muscle cells and fibroblasts. new channels form and reestablish blood flow. occurs in older thrombi.

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23
Q

saddle embolus

A

sits between bifurcation of two vessels.

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24
Q

venous thrombi complications

A

pulmonary embolus. thromboemboli are able to pass through large caliber vessels until they reach the smaller arteriolar and capillary bed of the lungs. (arterial thrombi are more likely to affect end organs)

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25
Q

difference between thrombi and postmortem clots?

A

in post mortem clots, the blood separates out into components (current jelly & chicken fat). no adhesion to wall. might fill vessels but don’t over distend them. no lines of zahn.

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26
Q

definition of coagulation

A

forming and getting rid of fibrin clots

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27
Q

what comes in contact with blood when an artery is punctured?

A

collagen and tissue factor

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28
Q

clotting cascade

A

a complex mechanism for producing a limited amount of thrombin quickly at a site of vascular injury

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29
Q

actions of thrombin

A

cleaves fibrinogen, activates platelets, activates 5a/8a/11a (positive feedback of itself), activates protein C (negative regulation of itself)

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30
Q

fibrinogen

A

precursor of fibrin. activated to fibrin via thrombin protease

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31
Q

fibrin

A

forms the mesh plug in clots

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32
Q

goal of clotting cascade

A

convert prothrombin (2) to thrombin (2a)

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33
Q

which of the clotting cascade factors are not proteases?

A

V, VIII (5,8)

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34
Q

Scaffold proteins in clotting cascade

A

5,8. assemble multiprotein complexes that greaty accelerate clotting rxns. substrates for thrombin.

35
Q

clotting cascade number for thrombin

36
Q

extrinsic tissue factor pathway in clotting cascade

A

tissue factor/7a complex activates 10a, which converts prothrombin to thrombin (2a). occurs on surface of cells.

37
Q

mechanism of fibrin creation

A

thrombin (2a) converts fibrinogen to fibrin monomer, which then becomes polymer, which are then cross linked by 13a.

38
Q

Tissue Factor Pathway Inhibitor (TFPI)

A

endogenous inhibitor of extrinsic pathway. shuts down the TF/7a/10a complex. Absence produces a prothrombotic state due to unrestrained thrombin generation.

39
Q

Pathway of clotting cascade that occurs if TFPI is inhibiting the extrinsic tissue factor pathway

A

pathway 2 where Tissue Factor/7a complex activates 9a to activate 10a, using Ten-ase complex with factor 8a scaffold

40
Q

Ten-ase complex

A

Factor 8a, phospholipid, Ca2+ machinery that accelerates conversion to 10a via 9a.

41
Q

Prothrombinase complex

A

Factor 5a, phospholipid, Ca2+ machinery that increases conversion to thrombin from prothrombin via 10a

42
Q

Intrinsic/Contact Pathway of clotting cascade

A

involves kallikrein, HMWK, 12, 11

much slower process that doesn’t require tissue presence

43
Q

Serine proteases

A

12a, 11a, 9a, 10a, 7a, 2a

44
Q

bleeding deficiencies

A

11, 9, 7, 5 8, 10, 5, prothrombin, fibrinogen

45
Q

when does coagulation begin?

A

when tissue factor/7a complex cleaves 10 to 10a

46
Q

Hemophilia A

A

Factor 8 deficiency

47
Q

Hemophilia B

A

Factor 9 deficiency

48
Q

what solution is blood drawn into for clotting tests?

A

citrate solution because it is a negatively charged molecule that binds to Ca ions present in blood. reduces the free ca concentration below the level needed to accelerate coagulation

49
Q

Basic way to prep for clot test

A

blood is treated with citrate, spun to sediment cells. Then Ca, initiator of clotting, and phospholipids are added

50
Q

Prothrombin test (PT)

A

Tests the extrinsic pathway.
initiator of clotting is tissue factor. Start with tissue factor and measure time to fibrin. independent of patients own tissue factor

51
Q

Normal range for prothrombin test

A

10-12 seconds

52
Q

Internationalized Normalized Ratio for the PT

A

compensates for differences between labs and machinery. 1 is normal.

53
Q

activated Partial Thromboplastin Time (aPTT)

A

no tissue factor is added (charged surface activates contact factors instead), so used to test intrinsic pathway. Charged accelerant is added (such as ground glass)

54
Q

Normal range for aPTT

A

28-35 seconds

55
Q

things that increase aPTT

A

inherited factor deficiencies, acquired deficiencies of factor/cofactors, lupus anticoagulant, factor antibodies, drug inhibitors

56
Q

lupus anticoagulant

A

an antibody directed against phospholipid. slows aPTT, but doesn’t signify a bleeding disorder

57
Q

workup if long aPTT is obtained

A

need to know if an inhibitor is present or if there is a factor deficiency. Mix patient plasma 1:1 with normal plasma and repeat aPTT.

58
Q

Normal long aPTT workup

A

signifies a factor deficiency. will always have at least 50% of factor when mixed with normal plasma, which will be enough for normal cascade. will need to conduct factor assays.

59
Q

prolonged long aPTT workup

A

clotting factors are not missing, instead a dominant negative/inhibitor is present. could be lupus inhibitor, factor inhibitor, or other causes like drugs (heparin)

60
Q

tissue factor deficiency

A

embryonic lethal

61
Q

where are most clotting factors synthesized?

A

hepatocytes

62
Q

exceptions to clotting factors synthesized in hepatocytes

A 
Factor 8 (liver, but not hepatocytes)
von Willebrand factor (megakaryocytes)
63
Q

vitamin K

A

cofactor required for protease synthesis in liver for factors 2,7,9,10. necessary for post translational modification of glutamate to gamma carboxylated glutamate (Gla) residues

64
Q

vitamin k dependent clotting factors

A

2,7,9,10, protein C

65
Q

gamma carboxyglutamate

A

converted by vitamin k and carboxylase. sticks better to surface of cells. important in prothrombinase and ten-ase complexes that work on cell surface by attaching to negatively charged phospholipids

66
Q

warfarin role in anticoagulation

A

inhibits the recycling of vitamin k. depletes the liver of it by locking it into epoxide form.

67
Q

another name for warfarin

68
Q

anti-thrombin

A

inhibits thrombin and 10a.

69
Q

protein C

A

inhibits the ten-awe and prothrombinase complexes by inactivating factors 8a&5a

70
Q

heparin

A

binds to anti-thrombin and makes it an even stronger inhibitor

71
Q

factor V Leiden

A

mutation common to northern europeans. point mutation in factor 5 which affects cleavage site for protein C. Increases risk of thrombosis bc ten-awe remains overactive (prothrombotic state)

72
Q

plasmin role

A

degrades clot. a protease that likes many substrates and is therefore present as plasminogen in the plasma

73
Q

marker of clot production

A

Fibrin D Dimer (can only be created if fibrin has been cross linked)

74
Q

epistaxis

A

nose bleed

75
Q

Ecchymosis

76
Q

hemarthrosis

A

joint bleeding

77
Q

where is tissue factor expressed?

A

expressed on the cell surfaces of vascular smooth muscle cells, activated monocytes, diseased endothelial cells. expression is regulated by trauma and TNF

78
Q

platelets

A

serve as binding sites for the assembly of coagulation factor complexes, accelerating the conversion of prothrombin to thrombin and promoting clotting

79
Q

factors tested by PT

A

7, 10, 5, 2, fibrinogen

80
Q

intrinsic pathway scaffold

A

HMWK (high molecular weight kininogen)

81
Q

contact factors

A

12, PK, HMWK

82
Q

accelerants in intrinsic pathway

A

work by increasing the surface area for formation of contact factor complexes

83
Q

factors tested by aPTT

A

12, HMWK, PK, 11, 9, 8, 5, 10, 2, fibrinogen (anything other than 7)

84
Q

what people have the most prolonged aPTT test times?

A

those with 12, HMWK, or PK deficiencies. But they don’t have bleeding disorders! thrombin can produce 11 as well

MDTI (42 decks)

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