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21 fall: Biochem > Test 2 Lecture 30-31 > Flashcards

Test 2 Lecture 30-31 Flashcards

1
Q

DIC

A

bleeding disorder where all the clotting is used up and then the rest of the body bleeds out of every opening

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2
Q

Platelets adhere to subendothelial ____

A

collagen.

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3
Q

Platelets release ___ and _____, which stimulate platelet aggregation and vasoconstriction of smooth muscle.

A

ADP
thromboxane

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4
Q

blood encounters ___ on cells outside of the blood vessel. This triggers the formation of ___

A 
tissue factor (protein)
fibrin
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5
Q

Fibrin fibers, aggregated platelets and trapped red blood cells form a ___.

A

clot

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6
Q

platelets come from

A

cell fragment of megakaryocyte

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7
Q

platelet like cells in non mammals

A

thrombocytes- nucleated

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8
Q

Common pathway

A

Cofactor 5 (Thrombin)(Factor 10a)(calcium) =Cofactor 5a

Prothrombin (Factor 10a)(Cofactor 5a)(Ca2+)=Thrombin

Fibrinogen(Thrombin)(Ca2+)= Fibrin Monomer

Factor 13(Thrombin)(Calcium)(Fibrin)=Factor 13a

Fibrin Monomer(Factor 13a) =Fibrin Threads

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9
Q

How is thrombin formed

A

Prothrombin is cut at two spots (274,323)

large part of protein is lost, the two smaller pieces are held together by a disulfide bond

these two smaller pieces are Thrombin

Calcium ions are required

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10
Q

Prothrombin is cleaved at two specific sites, ___ and ___, to form ___

A

274

323

thrombin

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11
Q

___ are required for prothrombin to thrombin and many other steps in the common pathway

A

calcium ions

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12
Q

____ helps hold together the A and B chains of thrombin

A

Disulfide bond

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13
Q

explain fibrinogen into fibrin threads

A

fibrinogen (thrombin)= Fibrin monomer

Fibrin monomer (polymerization)= fibrin threads (long chains held together by covalent bonds)

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14
Q

___ has
three subunits: alpha, beta and gamma.

A

Fibrinogen

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15
Q

___ cleaves short peptides off the N-termini of the alpha and beta chains, to form the fibrin monomer.

A

thrombin

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16
Q

This exposes N-terminal structures that can
interact with other fibrin monomers, leading to the formation of ____that are held together by _____ interactions.

A

Fibrin fibers/threads

non- covalent bonds

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17
Q

Covalent cross-linking of the Fibrin Fiber by ___

A

Factor XIIIa

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18
Q

___ is also known as fibrin stabilizing factor.

A

Factor XIIIa

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19
Q

Factor XIIIa crosslinks ___ residues from one fibrin monomer to ____ residues in a different fibrin monomer.

A

glutamine

lysine

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20
Q

Defects in factor XIII lead to

A

delayed bleeding

clots from: stops bleeding: clot is broken down too quickly and bleeding restarts

common in DIC and Liver disease

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21
Q

pathway that is activated when blood comes in contact with tissue factor

A

extrinsic Pathway

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22
Q

pathway activated when blood comes in contact with anionic surfaces

A

intrinsic pathway

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23
Q

Pathway activated by tissue factor, a membrane protein present on most cells outside of the blood, but is not normally present on cells in the blood or the inner layer of the blood vessel

A

extrinsic pathway

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24
Q

pathway activated by exposure of the blood to anionic surfaces. This can occur in vivo when the blood leaves the vessel or in vitro when the blood contacts glass or other surfaces.

A

intrinsic pathway

(blood taken out and put in glass tube will clot on its own)

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25
Q

factors in the coagulation pathway are present as ___

A

zymogens- inactive precursors

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26
Q

Activation of factors in the coagulation pathway involves ___

A

proteolytic cleavage

(breaking proteins)

efficient and rapid

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27
Q

Most activated factors in the coagulation pathway are ___, exceptions are ___, ___ and ___

A

proteases

Cofactor proteins: Tissue factor, VIIIa, Va

Fibrin: structural component of clots

Factor XIIIa: cross links Fibrin monomers

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28
Q

extrinsic pathway of coagulation

A

Trauma: blood will spill out and interact with

Tissue factor binds to 7

these are cleaved by traces of active protease in the blood (Factor 10a, thrombin, factor 7a, Factor 9a) and calcium will form: 7a +Tissue Factor complex

7a +Tissue factor complex (Ca)cleaves 10 to 10a

Common Pathway

Xa + Cofactor Va will cleave Prothrombin to Thrombin

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29
Q

intrinsic pathway

A

12 (Kiniogen)(Kallikrein)=12a

11 (12a)=11a

9(11a)(calcium)=9a

10 (9a (cofactor 8a)(calcium))=10a

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30
Q

contact phase of coagulation pathway

A

12 (kiniogen)(kallikrein) = 12a

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31
Q

Deficiency of cofactor 8

A

hemophilia A

last step in intrinisc pathway

10((9a)(cofactor 8a))= 10 a

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32
Q

deficiency in factor 9

A

hemophilia B

3rd step of instrinsic pathway

9(11a)=9a

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33
Q

Thrombin can activate

A

Intrinsic pathway:

Factor 11 → Factor 11a

Cofactor 8 → (thrombin)(calcium)(Factor 10a)→Cofactor 8a

common pathway:

Cofactor 5 → (thrombin)(factor 10a)(Calcium)→ Cofactor 5a

Factor 13 →(thrombin)(calcium)(Fibrin)→ Factor 13a

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34
Q

Extrinsic Pathway can turn on Intrinsic pathway by

A

Factor 9 (Factor 7a +Tissue Factor complex)(Calcium)→ Factor 9a

Factor 9a then binds with Cofactor 8a

10 (9a +Cofactor 8a complex) → 10a

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35
Q

Thrombin can turn on intrinsic pathway by

A

Factor 11 (Thrombin)→ Factor 11a

Cofactor 8 (Thrombin)(Factor 10a)(Ca) → Cofactor 8a

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36
Q

thrombin can activate common pathway by

A

Cofactor 5 (thrombin)(Factor 10a)(Calcium)→ Factor 5a

Factor 13 (thrombin)(Fibrin)(Calcium)→ Factor 13a

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37
Q

Why are hemophilia A and B more common than most other genetic clotting disorders?

A

found on X chromosome

if males (XY) only get 1 bad copy and will express the trait

Females (XX) one bad copy → carries

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38
Q

Deficiencies in factors 8, 9 and factor 11 cause bleeding problems showing that intrinsic pathway is important. However, deficiencies in factor 12, kininogen and kallikrein do not. How can this be explained

A

Factor 12, kininogen and kallikrein =contact phase

not needed because other steps of intrinsic pathway can be turned on by thrombin

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39
Q

Initiation occurs by exposure to ____, which is present on the surface of most cells, but is normally absent from cells in the ___and _____

A

tissue factor

blood

endothelial cells

40
Q

Intrinsic pathway is activated by _______, which activates XI to XIa and VIII
to VIIIa. In addition, the VIIa/tissue factor complex activates IX to IXa.

A

thrombin

41
Q

Thrombin also activates factors _____ and _____ of the common pathway.

A

Factor 5

Factor 13

42
Q

Intrinsic pathway required for ______ . Contact phase is not required for
initiation or amplification.

A

amplification

43
Q

The concentration of early coagulation factors is___, and late factors are ___

A

low

high

(more of the things at the end then the things at the beginning)

44
Q

Factor _____ has a short half-life in dogs and humans.

A

7

45
Q

Most factors are made by the ________. Liver disease can lead to excessive or insufficient coagulation, because liver also makes ________ proteins and removes activated coagulation factors from the blood.

A

Liver

anticoagulant

46
Q

What 4 factors are vitamin K dependent

A

Prothrombin(Factor 2), Factor 7, 9 and 10

47
Q

Hemophilia A is a ___ deficiency

A

Factor 8

X linked recessive

intrinsic pathway

Cofactor 8 (thrombin)(Calcium)(10a)→ Cofactor 8a

Factor 10 (Cofactor 8a)(9a)(Calcium)→ Factor 10a

48
Q

Von Willebrand disease

A

found in dogs

autosomal recessive, more commonly incomplete dominance

von Willebrand factor is produced by endothelial cells and circulates in the blood in a complex with factor 8. It is also released by platelets.

It promotes platelet adherence, and its deficiency can cause excess bleeding

Therapies: plasma, cryoprecipitate, DDAVP

49
Q

Hemophilia B is ___

A

deficiency in Factor 9

X linked

intrinsic pathway

9(11a)(calcium)→ 9a

10 (9a + cofactor 8a complex+Calcium)→ 10a

50
Q

Hageman Factor

A

Deficiency in Factor 12

contact phase- 12 (kinionogen)(kallikrein)→ 12a

11 (12a)→ 11a

autocomal recessive

absent in marine mammals, fowl and most reptiles

51
Q

The most common hereditary coagulation deficiencies are

A

Hemophilia A ( Factor 8)and Hemophilia B (Factor 9) because they are X linked

52
Q

Factor ________ deficiency is relatively common in the cat, but does not cause coagulation deficiency.

A

Factor 12

Hageman Deficiency in Factor 12

contact phase- 12 (kinionogen)(kallikrein)→ 12a

11 (12a)→ 11a

autocomal recessive

absent in marine mammals, fowl and most reptiles

53
Q

___ is produced by endothelial cells and circulates in the blood in a complex with factor 8. It is also released by platelets.

A

Von Willebrand Factor

54
Q

___ promotes platelet adherence, and its deficiency can cause excess bleeding.

A

Von willebrand factor

55
Q

what types of dogs are common to get von willebrand

A

Dobermans

56
Q

How to treat von Willebrand Factor

A

give von Willebrand Factor

plasma

Cryoprecipitate – material that comes out of solutions when frozen plasma is thawed. It is enriched in von Willebrand factor and some other coagulation factors.

DDAVP – derivative of arginine vasopressin that stimulates release of stored von Willebrand factor

57
Q

Thromboxane does what ___

A

helps bind platelets to collagen

causes smooth muscle to constrict

58
Q

The activity of four factors: ___ is dependent on ___

A

Factor 2(Prothrombin)

Factor 7,9,10

Vitamin K

59
Q

Vitamin K is cofactor for:

A

protein carboxylase

(add carboxyl group to proteins)

add COOH (HO-C=O)

60
Q

Specific glutamate residues are carboxylated to form a modified glutamate residue called ___

A

gamma carboxyglutamate

61
Q

carboxylation of glutamate to gamma carboxyglutamate happens __

A

in the liver, before it is secreted into the blood (post translation modification)

62
Q

gamma-carboxyglutamate residues bind

A

calcium ions (Ca2+)

2+ binds to the 2- of the gamma-carboxyglutamate

63
Q

explain calcium sandwich

A

Vitamin K dependent coagulation factor has gamma carboxyglutamate (-2 charge) attached

this -2 charge attracts the +2 charge of calcium ions

the +2 charge of calcium ions also attracts the - charged phospholipids of the lipid bilayer of an activated platelet

64
Q

The calcium sandwich allows the coagulation factors to bind to negatively charged ___

A

phospholipids on the lipid bilayer of activated platelets

65
Q

Activated cofactor proteins ___ and ___also associate with platelet membranes this is not a vitamin ___ dependent association.

A

5a and 8a

Vitamin K

prothrombin (Cofactor 5a+10a complex)(Ca)→ Thrombin

Factor 10 (Factor 9a+Cofactor 8a complex)(Calcium))→ Factor 10a

66
Q

The association of vitamin K dependent factors and activated cofactors with activated platelet membranes greatly _______ the coagulation cascade.

A

accelerates

clots occur in seconds

67
Q

how does Vitamin K get recycled

A

vitamin K will give COOH to glutamate to make gamma- carboxyglutamate,

leaving Vitamin K inactive and oxidized with a hypoxide group (3 member ring with O)

this needs to be reduced back into active form of vitamin K

this can be inhibited by warfarin and dicourmarol

68
Q

recycling of vitamin K is inhibited by ___

A

warfarin and discoumarol

69
Q

Vitamin K is oxidized to an ______ by the carboxylation reaction.

A

inactive hypoxide form

(3 member ring with O)

70
Q

Active vitamin K is regenerated by enzymatic ___, this process happens in the ____

A

reduction,

liver

71
Q

Warfarin is used as an ____ in human medicine.

A

anticoagulant

72
Q

It is also used as a ____ poison that causes death by bleeding. Warfarin resistant rats have emerged, leading to the development of different vitamin K recycling antagonists, such as ___. Unintended poisoning of pets and wildlife occurs.

A

rodent

brodifacoum

73
Q

Treatment to inhibition of vitamin K recycling is ___

A

give plasma- short term source of vitamin K Factors

Give vitamin K

74
Q

Dicoumarol is found in moldy ___. Can cause excess bleeding in cattle that eat it.

A

sweet clover.

75
Q

treatment for dicoumarol

A

transfusion, plasma

give vitamin K

76
Q

what is produced by endothelial cells to prevent clotting

A

PGI2 Prostacyclin

77
Q

How does Prostacyclin work

A

inhibits thromboxane

which inhibits vasoconstriction and platelet aggregation

78
Q

What is produced by the liver to stop clotting?

A

antithrombin III

79
Q

Explain Antithrombin III

A

produced by the liver

inhibits Thrombin, Factor 9a, 10a, 11a

needs to be activated by Heparin

common in kidney disease: ATIII is lost in urine and low levels of ATIII leads to excessive clotting

80
Q

Low levels of Antithrombin III leads to

A

thrombosis, excessive clotting

81
Q

Heparin activates ____. Heparin is a negatively charged _______, and related molecules are present on the surface of endothelial cells.

A

antithrombin III

polysaccaride

82
Q

how does thrombin act as anticoagulation

A

Thrombin activates protein C which inactivated Cofactor 5a and 8a

Thrombin activates the release of PGI2 by intact endothelial cells

83
Q

Activated protein C – Inactivates cofactors ___ and ___ by proteolytic cleavage. Protein C is activated by _____. Protein C is a vitamin K dependent blood protein synthesized by the liver.

A

5a and 8a

thrombin

prothrombin (Cofactor 5a+10a complex)(Ca)→ Thrombin

Factor 10 (Factor 9a+Cofactor 8a complex)(Calcium))→ Factor 10a

84
Q

Coagulation

Free thrombin activates platelets, clots fibrinogen, and converts inactive forms of coagulation factors ____ to their active (a) forms.

A

5, 8 and 11

(13 to 13a)

85
Q

When thrombin bound to the cell-surface transmembrane protein, ____, thrombin’s procoagulant properties are neutralized and its ability to activate protein C is tremendously enhanced.

A

thrombomodulin

86
Q

Activated protein C (aPC) is a potent anticoagulant that inactivates factors ___and ___ with assistance from the cofactor, protein S, yielding inactive factor ___ and ____

A

5a and 8a

5i and 8i

87
Q

Thrombin when acting as coagulant helps activate ____, ___ and ____

A

factors 5, 8, 11 and 13

Fibrinogen to Fibrin

Platelet activation

88
Q

___ is present on the surface of endothelial cells. Low levels of thrombin in circulation will have an anticoagulant effect when in contact with normal endothelium.

A

Thrombomodulin

89
Q

____ of thrombin in circulation will have an anticoagulant effect when in contact with normal endothelium, ___ of thrombin in circulation will have an procoagulant effect

A

low levels

high levels

90
Q

Plasminogen ___ is released from damaged tissue and endothelial cells.

A

activator

91
Q

Plasminogen activator cleaves plasminogen to form ______, which is a protease that degrades fibrin.

A

plasmin

92
Q

Plasminogen activator and plasminogen both bind to _______, leading to the selective formation of plasmin in the clot.

A

fibrin clots

93
Q

how to break down clot

A
94
Q

TPA

A

Tissue-type plasminogen activator leads to the dissolution of blood clots.

used to break up clots (stroke treatment)

not very effective in cats: feline aortic thromboembolism (FATE), because of side effects

95
Q

how is heparin work as anticoagulant

A

activates antithrombin III

96
Q

How does coumarin work as anticoagulant

A

inhibits the recycling of Vitamin K

no Vitamin K then glutamate cant change to gamma carboxyglutamate, cant bind to Calcium, wont bind to plasma membrane and trigger cofactors

97
Q

Are these anticoagulants or thrombotic agents: Oxalate, citrate and EDTA

A

anticoagulants

Binds or percipitate Calcium ions

removes Calcium from the blood

no Calcium then factors and plasma membrane of platelets wont interact

21 fall: Biochem (44 decks)

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