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PR3154 > hemostasis/ clotting > Flashcards

hemostasis/ clotting Flashcards

1
Q

hemostasis

A

process aimed at closing a leak in vascular system, prevent loss of blood

3 phases

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2
Q

hemostasis 3 phase and time

rest of process and time

A

1) vasoconstriction (immediate)
2) plt plug (in secs)
3) fibrin clot (in mins)

clot retraction 20min-1h
healing 1-2wks

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3
Q

what is Vasoconstriction

A
  • Vascular spasm, SM contract
  • Initiated by sympathetic nerves
  • Mediated by vascular smooth muscle cells
  • Correlate with damage
  • Lasts for 30min ~ hrs
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4
Q

vasoconstriction function

A

○ Provide time for PLT and coagulation phase
○ Endothelial cells of opp side stick tgt
○ Reduce blood loss, most times not suff
○ Endothelial cells contract, expose basal lamina

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5
Q

PLT phase

A

Damage to endothelial wall exposes collagen

○ Plt stick
○ Plt secrete contents
○ More plt stick
○ Plt plug (+VE feedback cascade)

1. Plt adhere to exposed collagen fibers, activated 
2. Release granules with PLT agonists 
3. Plt aggregates to form plug, release more plt, attract subs
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6
Q

PLT main function

A

○ Closure of leak by formation of temp patch
○ Release chemical mediators, regulate blood clotting
○ Contraction of blood clot

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7
Q

how to prevent unintentional PLT activation/ aggregation

(endo cells)

A

Intact endothelial cells release NO, Prostacyclins
Inhibit unintentional PLT activation/ aggregatiom

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8
Q

how does PLT adhesion occur

A

Von Willebrand’s Factor (vWF)
○ Plasma protein produced by PLT
○ Allow PLT bind to exposed collagen through glycoprotein receptors
- Adhesion leads to Plt activation
□ Morphological change
- Trigger release of granules for aggregation

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9
Q

how does PLT aggregation occur

A

PLT agonists

ADP
□ Attract, activate more plt
Thromboxane A2
□ Promote aggre & further vasoconst

Fibrinogen links plt through glycoprotein receptors
□ Fibrinogen links stabilise by factor XIII

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10
Q

3) Formation of fibrin mesh steps

A
  • Thrombin converts
    ○ Fibrinogen –> fibrin
  • Crosslink to form fibrin mesh
    ○ Pulls PLT tgt, mesh over PLT plug over wound
  • Factor 13 to make plug stronger
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11
Q

Thrombin activities ** key regulator of hemostasis

A

○ Enhance own generation (+ve feedback loop)
○ Factor XIII activation (stabilise fibrin mesh)
○ PLT activation
○ Release PF3 from PLT (activate intrinsic pathway)

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12
Q

coagulation cascade EXTRINSIC

A
  1. Vessal injury
  2. Exposed molecules of vessel wall release TISSUE FACTOR/ THROMBOPLASTIN

1) Allow Factor 7 (VII) activation to VIIa

2) VIIa activates factor X (with Ca2+)
3) Xa activates prothrombin –> thrombin (with Ca2+, Va)

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13
Q

extrinsic requires

A

tissue factor (thromboplastin)
VII
Ca2+

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14
Q

intrinsic pathway (slows - mins, involves many enzymes)

A

Various pathway, chains reaction, activation cascade
Form complex with additional cofactor to activate factor 10

1) exposed to collagen fibers - damage inside blood vessels/ foreign surfaces (glass)
2) plt phospholipids conformational change (activates XII –> XIIa)
3) XIIa activate XI –> XIa
4) XIa activate IX –> IXa (with ca2+)
5) IXa activate X –> Xa (with Ca2+, VIIIa)

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15
Q

intrinsic pathway need

A

plt phospholipid
XII (12)
XI (11)
IX (9)

Ca2+
VIIIa, Va

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16
Q

common pathway

A

x – > Xa (Ca2+, Va or VIIIa)

by Xa: prothrombin –> thrombin +Ca2+ + Va

by thrombin: fibrinogen –> fibrin

fibrin + XIIIa + thrombin

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17
Q

clotting factors
foolish people try climbing fast
I,II,III,IV,XIII

A

I – fibrinogen
II – prothrombin
III – tissue factor
IV – Ca2+
V –
VII –
VIII –
IX – plasma thromboplastin
X –
XI – plasma thromboplastin
XII –
XIII – fibrin stabilising

18
Q

clotting factors feature

A

clotting factors require vit K (II, VII, IX, X)
all produced by liver

19
Q

Clot retraction

A

Stabilise clot by squeeze serum from fibrin clot

Further closure of leak

20
Q

Repair

A
  • PDGF stimulates vascular SM cells to build new vessel wall
  • endothelial cells multiply and restore inner endothelial lining (Stimulated by VEGF)
21
Q

Regulate blood clotting

A

anti-coagulants (prostacyclin, serotonin, blood clots)

(Smooth endothelial surface, antithrombin III, heparin, thrombomodulin, tissue plasminogen activator)

VS

pro coagulants (tissue factor EXT, collagen XIII INT, collagen)

22
Q

Prostacyclin

A

PG produced by intact endothelial cells
- Inhibit plt activation
- Limit spread of blood clotting

23
Q

Serotonin

A

High conc inhibits ADP activity (ADP is plt agonist, that attracts and activates more PLT)

24
Q

Serotonin

A

High conc inhibits ADP activity (ADP is plt agonist, that attracts and activates more PLT)

25
Q

Blood clot

A

Limit spread of thrombin, other procoagulants

26
Q

artificial anticoagulants

A

Chelators (citrate, EDTA)
vit K antagonists (warfarin, coumarin)
DOAC - CLC

27
Q

FIBRINOLYSIS is to __

A
  • Dissolution of clots
  • Constantly at low lvl (balanced with coagulation) by eqm of thrombin + plasmin
28
Q

fibrinolysis steps

A
  1. Plasminogen trapped inside clot
    i. Plasma protein and protease precursor made by liver
  2. Surrounding tissue and vascular endothelial cells release
    i. Tissue plasminogen activator tPA
  3. Cleaves inactive plasminogen –> plasmin
    i. Digest fibrin, dissolve clot
  4. Macrophage remove remains of clot
29
Q

Blood clotting disorders, unable to clot

A

hemophilia (X linked)
liver disease
vit K deficiency
thrombocytopenia

30
Q

blood clotting disorders (too much clot)

A

thrombosis
thromboembolism
strokes & Afib

31
Q

hemophilia (X linked)

A

○ Excessive bleeding after injury
○ Hereditary hemophilias, lack of clotting factors
- Hem A: lack factor VIII
□ Use recomb factor
- Hem B: lack factor IX (ext)
- Hem C: lack factor XI (ext)

32
Q

Liver disease

A

Hepatitis, hepatocell carcinoma, liver cirrhosis = Inability to produce
- to synthesise procoagulant (tissue factors, collagen)
- Most clotting factors produced by liver
- Produce bile, absorb fat and vit K

33
Q

Vit K deficiency

A

○ Essential for synthesis of several clotting factors

○ 1/2 from gut bact (methionine), 1/2 diet
○ LT Abx use results in vit K deficiency (cephalosporins) and bleeding disorders

34
Q

Thrombocytopenia

A

○ Circulating PLT too low (<50 million/mL)
- Normal 200-500mil/mL

○ Spontaneous, widespread hemorrhage, visible by small purple spots on skin

○ Cause by:
-Damage to bone marrow (Malignancy, chemo)
= Tx with fresh whole blood / plt transfusion

35
Q

Thrombosis

A

○ Inapp clotting
- Roughened surface of vessel, endothelial cell injury, disturbed blood flow

Thrombus: clot develops and persists in unbroken blood vessel

Thrombi can block circ, result in tissue death
- Coronary: thrombus in heart = Lead to HA
- Cerebral: thrombus in brain = Lead to stroke

36
Q

Thromboembolism

A

○ DVT. Embolus: thrombus free float in blood stream
-Impair body ability to obtain O2
-Cerebral: stroke
-Cardiac: HA
○ Tx: tPA, heparin + vit K antagonist

○ Risk factors: Smoke, dehydration, oral contraceptives, polycythemia, surg, immobility

Freq: 1 in 1000, mortality 1-5%

37
Q

Strokes and Afib

A

○ Afib: cause blood to collect in heart, clot formation, incr risk of strokes
○ Hemorrhagic stroke: need blood to clot
○ Ischemic stroke: need dissolve the clot

38
Q

blood coagulation tests

A

1) partial thromboplastin time – INT and COMMON

2) prothromnin – citrated plasma + Ca + tissue factor (EXT and COMMON)

3) INR: ratio of PT/ population
norm = 0.9-1.3

39
Q

PTT measures

A

I, II, V

intrinsic: VIII, IX, X, XI, XII

monitor heparin
range: 25-39s

40
Q

PT measures

A

factors: I, II , V

EXT: VII, X

monitor warfarin
range: 12-15s

PR3154 (11 decks)

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