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BMS 2 > Coagulation and Fibrinolysis > Flashcards

Coagulation and Fibrinolysis Flashcards

1
Q

proteases

A

2,7,9,10

11,12,13

exist as zymogens

serine proteases

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2
Q

cofactors

A

5, 8
VWF
Tissue factor-bound to cell

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3
Q

clottingorer

A

2, 10, 5,7 9, 8 ,12 ? cjecl

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4
Q

steps of hemostasts

A

aterliolary vasoconstriction

priary hemo

secondary hemo

regulation of thrombous fomration
-antithrombotic activity

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5
Q

local vasoconstriction

A

occurs becuase of endothelin (vasoconstictor)

natural mechanism to restrict blood flow

decrease sheer force-allow paltelets to get in there

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6
Q

primary hemostasis

A

all about paltelets

platelet adhesion, shape chage, granule release, recruitment, aggregaton

vWF

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7
Q

how to platelets form

A

fro megakaryocytse

not much nucelos-may contain RNA/proteins important for thier functn

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8
Q

platelets size

A

size correlates with reactivity

larger platelets are prothrombotic

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9
Q

monolayer normal vs injured

A

nomral-platelets just fly around in blood

injured-basement membrane exposed-strucutreal and ecm proteins are recognied-collagen and VWF

  • platelts attach here-become activitated-silent receptors that undrego conformational change and can bind
  • degranulate-vwf and other trucutra/activating factors pop out
  • degranulate weh nattach to basement membrane
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10
Q

4 steps for formation of platelet plug

A

adherence, activaion, granule release, change shape, aggregation

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11
Q

vwf disease

A

defeinceny of vwf

can happen b/c less or mutated vwf

or problems in receptr for vwf

result in bleeding

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12
Q

vwf fucntin

A

large circulating protein

made in endo cells and platelets

primary and secondary hmostatis

at site of injury-vwf binds to exposed collagen

  • facilitates platelet tethering
  • platelets without vwf- attach but not as stong as with vwf

chaperone for factor 8

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13
Q

what happens after endo exposed and vwf binds

A

sheer causes multimer to expose (VWF)

-platelets can now stick down and ttch to colagen at basement membrane

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14
Q

what releases vasocontrsictors/platele activators

A

collagen and platelets

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15
Q

whats inside platelets

A

have graunlaes that store adhesive proteins, prothrombotic factors, cytrokines, growth factor

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16
Q

how to treat angina

A

(reduced blood flow to heart)

target platlet activation/stickiess
-decrease platelet adhesion and allow more blood flow

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17
Q

petehciae

A

spontaneous small bruising, small amounts of blood leak out of blood vessels

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18
Q

petechaie vs purpura vs eccymoses

A

smaler tolarger bruise caused from not enough platelet

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19
Q

Platlet trophic factors + whjat happens when platelet count low

A

maintain cell-cell contacts

when platelets counts is low-rbc ca go through hole thatnormally platelet would be in the way of

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20
Q

secondary hemostasis

A

first hemostasis is not very strong-need stong sealet in form of cross-linked fibrin

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21
Q

how is fibrin create

A

clotting cascade results in formation of fibrin from fibrinogen

  • small part of fibrinogen cut off
  • rest of ibrinogen multimerizes to make fibrin
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22
Q

what does factor 13 do

A

cross links fibrin

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23
Q

why are serine proteases zymogenic

A

need to be ready to be recruited at moments notice

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24
Q

intrinsic vs extrinsic pathway

A

intrinsic-beginss with accumulation of factor 7 and tissue factor
-factor 12 activated with negative charge-nothing else needed

extrinsic-need ttissue factor to make blood clot

25
Q

DONT FUCKING FORGET

A

THAT THIS IS HAPPENING ALL THE TIME IN CELLS

26
Q

Extrinxic pathway

A

vessel wall injury exposes TISSUE FACTOR and increases TF expression by endothelial cells/monocytes

circulating factor 7 binds to TF, becomes 7a

7 activates 9

9 activates 10

10 activates 2

thrombin is 2a (only moderate amount)
-not as much as when 8 comes into play

2a cleaves fibrinogen to fibrin

27
Q

TF

A

tissue factor-normally not exposed or exist in blood stream

exist in sub epithelium

28
Q

ebola

A

tells body to make tissue facgtor-consupmotion of clotting factors-have herorages becuase none left

29
Q

factor 7

A

always a little active-but low concentration so cant initate coagulation witout tssue factor

30
Q

common pathway

A

9a activating 10,

10a activating 2 (prothrombin) to make 2a
-apparently small amount of thrombin formed

2a cleaving firbrinogen to make fibrin

31
Q

thombin activiates

A

cleaves fibinogen to fibrin

activates more factor 9 and 8

32
Q

factor 8

A

sex linked recessive disrder

gets activated by thrombin-criculates in complex with VWF

VWF chaperones factor 8
-stabilies and extends half life of factor 8 (60 fold)

soluble cofactor-functions as catalyst

33
Q

VWF functions 2

A

VWF links platelets of subendothelial BM

Binds to and stabilizes factor 8

34
Q

factpr 8 and 9

A

form complex

activate factor 10 ALOT FASTER
-alot more thrombin and fibrin

35
Q

factor 8 or9 defecenincy

A

8-hemophilia a-factor 8 defecineny-sponteous bleeding

defecinecy in 9-hemo b-not as severe

both are x linked recessive

36
Q

factors 10 and 5

A

accelerates prothrombin activation

complex together-converrts at 300000x faster

37
Q

factor 5

A

soluble co-factor

catalyst

activated by thrombin

accelerates factor 10a conversion of protrombin (2) to thrombin

38
Q

three complexes essential for coagulation

A

tissue factor, factor 7a,9=10 initiation

factor 9a, 8a=10 amplifciation 1

10, 5a=2 (prothrombin) amplification 2

idk about this one….

39
Q

which factors are depend

A

2, 7, 9, 10 (serine proteases)

proteins C, S, z-ANTICOAGULATNATS

40
Q

what does vit k do

A

2, 7, 9, 10 all have glutamates at amino terminus-need additional negative charge
-probded by carboxlation (vitamin k dependent)

net negative charge-enables interaction with Ca and membrane interaction

vitamin k is oxized then reduced-then can give carboxylation

41
Q

warfari

A

blocks oxidation of vit k

42
Q

vitamin k deficiency

A

cased by giving antibiotics to newborns-kill thier vit k synthesizing colonic flora

43
Q

intrinsic pathway activation

A

contact activaton with negative glass tube

tf independent

44
Q

Intrinsic pathway proteins

A

factor 7

high molecular weight kiniogen

factor-11-ONLY ONE THAT RESULTS IN EXCESS bLEEDING IF DONT HAVE

Prekallikrien

45
Q

how is factor 12 activatd

A

contact with negatively charged surface (usualy phosphate residues)

]normall just circulating in blood stream

46
Q

HMKG use

A

required for facttor 11 to attach to negatively charged surface and become factor 11a

47
Q

factor 11a

A

binds and activates factor 9, which actviates 10, which cleaves prothrombin to thrombin, to make fibrin

thrombin activates more factor 11

functions in propogation phase of clot-in conjunction iwth 9a
-assocated with hemo c-minor

48
Q

11 and 5 and 8 and 9 and 11 (but mostly 11 and 5 i htink)

A

both activated by thrombin to amplify (check)

49
Q

fibrinogen vs fibrin

A

only a small cleave

50
Q

fibrin when cleaved

A

can self assemble into multimers and into fibers

  • spontaoues
  • essentally the glue that holds platlets totgher alliowing for clotting
51
Q

factor 13

A

transgluaminase

activated bythrombin

  • cross links fibrin chains
  • extensive cross-linking increases fibrin from dimers to trimers to tetramers
  • defects very rare-need this or die

covalent bonds

52
Q

how to get coagulation to shut off

A

coagulation/cofactrs adhere to membranes-confined process locally to area of injury
-thrombomodulin

53
Q

thrombomoldulun

A

high affinity recepotr for thrombin 2

  • meutralizes thrombins procoagulalant activity
  • cofactor for thrombin dependnt activation of protein c

always at surface of cell

thrombin sink-stops thrombin from getting too far away from site of cut

54
Q

Protein c

A

turns of factors 5 and 8 *(cleave but not sure)

thrombin+ thrombomodulin complex activate protein c

55
Q

protein c and s

A

inhibiors of pro-coagulant system
-anticoaulants

vitamin k depedent

activated by thrombin+thrombomodulin complex

56
Q

factor 5 leiden mutation

A

single base pair substituion

icnreased resistance o protein c
-ensures 5 does not get turned off

inherited thrombophilic disorder-cuases clotting to occur

5% higher chance for dvt

57
Q

fibrinolysis

A

as clotting becomes activated, fibrinolysis becomes actiacated

  • creates force that keep clot from gettin into ECM
  • also keeps clot from spreading
58
Q

plasminogen

A

activated by thrombin or TPA

becomes plasmin (when activated)

degreads fibrin and keeps clot from spreading

59
Q

TPA

A

tssue plasmonogen activator

used to chew up and spit out clots in MI or stroke

BMS 2 (41 decks)

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