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HSF > HSF 2 - Unit 1 Biochemistry: Coagulation TBL > Flashcards

HSF 2 - Unit 1 Biochemistry: Coagulation TBL Flashcards

1
Q

what must be balanced to prevent death by bleeding or clotting?

A

coagulation and fibrinolysis

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2
Q

what are the different ways people could die due to clotting?

A

stroke, MI, thrombosis

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3
Q

what are the different ways people could die due to bleeding?

A

trauma, major surgery, hemophilia

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4
Q

what is hypercoagulation?

A

results in excess and or inappropriate clotting; can lead to blocking of vasculature, resulting in MI, stroke, or thrombosis; can occur when coagulation is either hyperactivated or not properly inhibited of when fibrinolysis is inhibited or not properly stimulated

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5
Q

what is hypocoagulation?

A

results in an inability to properly form clots, and results in excessive bleeding; fibrinolysis is either hyperactivated or not properly inhibited or coagulation is inhibited or not properly stimulated

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6
Q

what are the inherited disorders in clotting?

A

hemophilia A, B, factor V Leiden, vonWillebrand disease

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7
Q

hemophilia A

A

X-linked deficiency in factor VIII

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8
Q

hemophilia B

A

X-linked deficiency in factor IX

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9
Q

factor V Leiden

A

mutation in factor V such that it cannot be inactivated by active protein C

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10
Q

vonWillebrand disease

A

deficiency in vonWillebrand factor (vWF), most common inherited clotting disorder, vWF is required for primary plug formation, and it stabilizes factor VIII in the serum; can be developed late in life and may not necessarily be due to an inherited defect

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11
Q

what are the acquired disorders in clotting?

A

Vitamin K deficiency, liver disease, antiphospholipid antibody syndrome, vonWillebrand disease

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12
Q

Vitamin K deficiency

A

rare because of intestinal microbes’ production of vitamin K, but can occur in newborns or in combination with medical treatments or conditions that severely alter gut microbiota

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13
Q

liver disease

A

several of the soluble clotting factors, proteins C and S, are produced by the liver, so diseases that may impair the liver’s production of these factors will result in clotting abnormalities; sometimes hypo- and sometimes hypercoagulation

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14
Q

antiphospholipid antibody syndrome

A

an autoimmune disorder in which antibodies attack phospholipids, this can damage cells in the blood or the lining of the blood vessels, subsequent release of phospholipids and other contents to the serum triggers clotting

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15
Q

what does a platelet count consist of?

A

part of a CBC, includes hemoglobin concentration and WBC count; normal levels are 150,000-450,000 platelets per microliter

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16
Q

what does PT measure? how is it performed?

A

PT= prothrombin time; measures rate of clotting by the extrinsic and common pathways, and is determined mainly by the amount of prothrombin in the plasma; oxalated blood is treated with thromboplastin, which contains excess Ca2+, phospholipids, and tissue factor, and clotting times is measured, normal time = 11-14 seconds

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17
Q

what does a sample vial from a PT test contain? why?

A

citrate, oxalate, or EDTA; all of these are able to chelate Ca2+, and thus inhibit coagulation of the sample prior to analysis

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18
Q

what is an INR?

A

international normalized ratio; it is a standardized method of PT so we can compare with other labs; each lab runs own control samples (control PT) and uses that with the ISI value (specific for each lot of thromboplastin) to determine INR; = (patient’s PT/control PT)

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19
Q

what is ISI?

A

international sensitivity index; usually around 0.9

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20
Q

what is a normal INR value?

A

0.8-1.2

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21
Q

what is a PTT? what is a normal result?

A

partial thromboplastin time; measures the rate of clotting by the intrinsic and common pathway; oxalated blood is treated with excess Ca2+, phospholipid, and a nucleating surface such as kaolin and clotting time is measured; normal = 30-42 seconds

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22
Q

what is the activating agent in a PTT?

A

has a high negative charge density, and mimics the effects of exposed subendothelial collage, thus stimulating the intrinsic pathway, can be varying things

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23
Q

what are the deficiencies that PT/INR and PTT are sensitive to?

A

deficiencies in the common pathway: factors X, V, II, and I

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24
Q

how are serum fibrinogen and clotting factor concentrations be determined?

A

typically a follow-up to PT/INR and aPTT in order to determine the exact deficiency/excess that is causing the problem; D-dimers are soluble in the serum and are elevated in the serum following intravascular coagulation

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25
Q

an injured blood vessel will initially ______, which … then …

A

contract; restricts the blood flow; platelets begin to aggregate at the site and form a hemostatic plug

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26
Q

what do platelets signal after gathering at the site of injury? what happens?

A

initiate the clotting cascade, in which a fibrin network is formed and this is the secondary hemostatic plug

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27
Q

when does the fibrin network begin to develop? what does it require?

A

during primary hemostatic plug formation, and requires the activation of prothrombin to form thrombin, which then activates fibrinogen to form fibrin

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28
Q

when does primary hemostatic plug formation begin?

A

when circulating platelets adhere to exposed subendothelium

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29
Q

what do platelets contain?

A

granules that are released upon platelet activation; hold calcium, ADP, serotonin, heparin antagonist, fibrinogen, some clotting factors, platelet derived growth factor, vWF

30
Q

what will COX do?

A

produce thromboxane A2 (TrxA2) after platelet activation

31
Q

what does PAR1/PAR2 do?

A

binds activated thrombin

32
Q

what does GPIa do?

A

binds collagen

33
Q

what does GPIb do?

A

binds vWF

34
Q

what do GPIIb/GPIIIa do?

A

binds fibrinogen and vWF

35
Q

what does the binding of plateletis to subendothelium result in?

A

platelet activation and aggregation

36
Q

thrombin binds to _____ and activates…

A

PAR1/PAR and activates a Galphaq signaling pathway; the resulting increase in intracellular calcium activates phospholipase A2 as well as granule release

37
Q

binding of ______ to collagen causes…

A

GPIa/IIA to collagen causes platelets to swell and produce pseudopods

38
Q

binding of _____ to vWF causes…

A

GPIb to vWF increases GPIIb-IIIa exposure on plasma membrane surface

39
Q

ADP binds…

A

P2Y12, stimulating production of more GPIIb/IIIa

40
Q

platelet activation and aggregation is ______, facilitates …, and is the target of …

A

autocatalytic, wound closure, anti-platelet drugs

41
Q

what do ADP and TxA2 have in common?

A

both have autocatalytic functions; they stimulate further activation and aggregation of platelets

42
Q

what are TxA2 and serotonin?

A

vasoconstricters, released from granules

43
Q

what facilitates formation of the secondary hemostatic plug?

A

calcium, clotting factors, fibrinogen, and heparin agonist that are released from granules; platelet derived growth factor will stimulate repair of the endothelium

44
Q

what do anti-platelet drugs do?

A

inhibit platelet activation/aggregation; aspirin inhibits COX, preventing TxA2 and plavix is an antagonist of the P2Y12 (ADP) receptor

45
Q

how is fibrin produced?

A

upon proteolytic cleavage of fibrinogen by thrombin and subsequent covalent cross-linking by factor XIIIa

46
Q

fibrinogen is a _____ of ______, linked by…

A

dimer; heterotrimers; disulfide bonds

47
Q

what does cleavage by thrombin release?

A

fibrinopeptides A and B

48
Q

most clotting factors are…

A

zymogens that are activated by proteolytic cleavage

49
Q

what do the zymogen forms of clotting factors contain?

A

binding domains that attract them to the area of endothelial damage, and/or growth factors that will facilitate endothelial repair

50
Q

glu-rich regions in clotting factors

A

get modified by vitamin K-dependent carboxylase: carboxylation at the gamma carbon of glutamate forms gamma-carboxuglutamyl (Gla) residues

51
Q

what is Gla?

A

an excellent chelator of calcium, and allows the negatively charged proteins to interact with negative PL

52
Q

what happens to vitamin K during the carboxylation reaction?

A

gets oxidized; must be reduced by vitamin K epoxide reductase and vitamin K reductase

53
Q

what factors contain Gla regions?

A

X, IX, VII, II, proteins C and S

54
Q

what can prevent carboxylation of proteins and thus act as anticoagulants?

A

vitamin K antagonists, such as warfarin and dicoumarol

55
Q

how does exposure of collagen trigger the intrinsic pathway?

A

exposure to highly negatively charged surfaces, including collagen and glass

56
Q

what is a soft clot?

A

after thrombin cleaves fibrinogen to form fibrin, this aggregates to form this clot

57
Q

how do we strengthen the clot?

A

covalent cross-linking mediated by FXIIIa (activated by thrombin)

58
Q

what is FXIIIa?

A

a transglutamidase

59
Q

what does thrombin activate?

A

factors V, VII, and XI and thereby accelerating the rate of clot formation; also stimulates platelet aggregation, thus further promoting secondary clot formation

60
Q

what is thrombomodulin? where is it expressed?

A

when complexed with thrombin activates protein C, which forms an active complex with protein S to cleave FVa and FVIIIa, thus slowing the clotting cascade; expressed on endothelial cell surfaces, since thrombin’s affinity is high for this it is removed from the plasma

61
Q

what are serpins?

A

serine protease inhibitors; a group of naturally occurring inhibitory proteins

62
Q

how many serpins are there? what do they do?

A

8; inhibit either coagulation or fibrinolysis

63
Q

what is an important example of a serpin?

A

antithrombin III; irreversibly inactivates thrombin, as well as a few other clotting factors; its activity is enhanced x10000 in the presence of heparin, which is normally present in very small amounts in the plasma and is used clinically as an anticoagulant

64
Q

why does blood not clot on intact vascular endothelia?

A
  1. Negatively charged platelets are repelled by the highly glycosylated, negatively charged endothelial surface
  2. Endothelial cells secrete both prostaglandin I2 (PGI2), aka prostacyclin, and nitric oxide, which are vasodilators and powerful inhibitors of platelet aggregation.
    - PGI2 synthesis is stimulated by thrombin – feedback inhibition
  3. Endothelial cells present both thrombomodulin and heparin sulfate (HS) on their luminal surface. (HS is a weak mimic of heparin.)
65
Q

what is a non-thrombogenic surface?

A

The normal endothelial vascular cell lining neither activates coagulation nor supports platelet adhesion

66
Q

how is a clot dissolved?

A

fibrinolysis; plasminogen, a plasma protein, has a high affinity for fibrin and is incorporated into the fibrin clot during coagulation; proteolysis of plasminogen by tissue plasminogen activator (tPA) or urokinase (U-PA) produces plasmin, a protease that cleaves fibrin, as well as several clotting factors

67
Q

what is tPA synthesized by? how are rates of synthesis modified?

A

vascular endothelial cells, and urokinase is produce by most tissues; physical stress, hypoxia, and a number of small molecule regulators increase the synthesis and release of tPA and urokinase

68
Q

what can recombinant tPA and ______ be used to treat?

A

streptokinase; treatment of MI and stroke

69
Q

what is fibrinolysis inhibited by?

A

plasminogen activator inhibitor 1, and by alpha2 - antiplasmin

70
Q

what is PAI-1 and what does it do?

A

plasminogen activator inhibitor 1, inhibits the activation of plasminogen; is inactivated by active protein C (which is activated as clot formation ends)

71
Q

what does alpha1-antiplasmin do?

A

inhibits free, but not clot-bound plasmin; particularly important for inactivation of any plasmin present in the plasma

HSF (23 decks)

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