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BMS 2 > Coagulation and Fibrinolysis > Flashcards

Coagulation and Fibrinolysis Flashcards

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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

Study These Flashcards
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
DONT FUCKING FORGET
THAT THIS IS HAPPENING ALL THE TIME IN CELLS
26
Extrinxic pathway
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
TF
tissue factor-normally not exposed or exist in blood stream exist in sub epithelium
28
ebola
tells body to make tissue facgtor-consupmotion of clotting factors-have herorages becuase none left
29
factor 7
always a little active-but low concentration so cant initate coagulation witout tssue factor
30
common pathway
9a activating 10, 10a activating 2 (prothrombin) to make 2a -apparently small amount of thrombin formed 2a cleaving firbrinogen to make fibrin
31
thombin activiates
cleaves fibinogen to fibrin activates more factor 9 and 8
32
factor 8
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
VWF functions 2
VWF links platelets of subendothelial BM Binds to and stabilizes factor 8
34
factpr 8 and 9
form complex activate factor 10 ALOT FASTER -alot more thrombin and fibrin
35
factor 8 or9 defecenincy
8-hemophilia a-factor 8 defecineny-sponteous bleeding defecinecy in 9-hemo b-not as severe both are x linked recessive
36
factors 10 and 5
accelerates prothrombin activation complex together-converrts at 300000x faster
37
factor 5
soluble co-factor catalyst activated by thrombin accelerates factor 10a conversion of protrombin (2) to thrombin
38
three complexes essential for coagulation
tissue factor, factor 7a,9=10 initiation factor 9a, 8a=10 amplifciation 1 10, 5a=2 (prothrombin) amplification 2 idk about this one....
39
which factors are depend
2, 7, 9, 10 (serine proteases) proteins C, S, z-ANTICOAGULATNATS
40
what does vit k do
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
warfari
blocks oxidation of vit k
42
vitamin k deficiency
cased by giving antibiotics to newborns-kill thier vit k synthesizing colonic flora
43
intrinsic pathway activation
contact activaton with negative glass tube tf independent
44
Intrinsic pathway proteins
factor 7 high molecular weight kiniogen factor-11-ONLY ONE THAT RESULTS IN EXCESS bLEEDING IF DONT HAVE Prekallikrien
45
how is factor 12 activatd
contact with negatively charged surface (usualy phosphate residues) ]normall just circulating in blood stream
46
HMKG use
required for facttor 11 to attach to negatively charged surface and become factor 11a
47
factor 11a
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
11 and 5 and 8 and 9 and 11 (but mostly 11 and 5 i htink)
both activated by thrombin to amplify (check)
49
fibrinogen vs fibrin
only a small cleave
50
fibrin when cleaved
can self assemble into multimers and into fibers - spontaoues - essentally the glue that holds platlets totgher alliowing for clotting
51
factor 13
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
how to get coagulation to shut off
coagulation/cofactrs adhere to membranes-confined process locally to area of injury -thrombomodulin
53
thrombomoldulun
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
Protein c
turns of factors 5 and 8 *(cleave but not sure) thrombin+ thrombomodulin complex activate protein c
55
protein c and s
inhibiors of pro-coagulant system -anticoaulants vitamin k depedent activated by thrombin+thrombomodulin complex
56
factor 5 leiden mutation
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
fibrinolysis
as clotting becomes activated, fibrinolysis becomes actiacated - creates force that keep clot from gettin into ECM - also keeps clot from spreading
58
plasminogen
activated by thrombin or TPA becomes plasmin (when activated) degreads fibrin and keeps clot from spreading
59
TPA
tssue plasmonogen activator | used to chew up and spit out clots in MI or stroke

BMS 2 (41 decks)

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