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Boards: Coag Transfusion > Hemostasis Physiology > Flashcards

Hemostasis Physiology Flashcards

1
Q

What are the platelet precursors and how do they develop into platelets?

A

megakaryocytes

fragment into a lot smaller platelets

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2
Q

Can platelets produce ATP?

A

Yes, have mitochondria

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3
Q

What is the purpose of platelets’ growth factor?

A

induces fibroblast activity after clot formation to cause connective tissue formation and closing of the vessel defect

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4
Q

What are the contractile proteins of platelets?

A

myosin
actin
thrombosthenin

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5
Q

How do platelets prevent binding to healthy endothelial cells?

A

surface is coated by glycoproteins - repulse adherence to normal endothelium - causes only adherence to injured endothelial cells

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6
Q

What is the half life of platelets and how are they eliminated?

A

about 10 days

dogs: 5-7 days

destroyed by macrophages

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7
Q

Describe the formation of a platelet plug

A

tissue injury - exposed collagen and vWF - platelets bind to this and become activated
* form pseudopods
* swell and become sticky
* release granules –> attract more platelets
* release TXA2, ADP, PAF –> attract more platelets

enough to stop bleeding of tiny inuries - otherwise fibrin required

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8
Q

What platelet receptors bind vWF?

A

Gp1b

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9
Q

What are the 2 possible fates of a blood clot?

A
  • dissolution
  • connective tissue integration via fibroblasts
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10
Q

What are the 2 stages of fibrin monomer binding?

A
  1. early stages - fibrin monomers held together by weak noncovalent hydrogen bonding - no cross-linking - weak clot and can be broken apart easily
  2. within next few minutes - fibrin stabilizing factor (XIII, activated by thrombin) - forms covalent bonds ebtween fibrin monomers - strong meshwork
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11
Q

Explain the steps of clot retraction

A

within few min of clot formation - contraction, expression of serum withn 20-60 min
platelets activate thrombosthenin, actin, myosin - cause strong contractions

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12
Q

Describe the steps of the extrinsic pathway

A

TF exposure - activates and binds to circulating FVII –> activates FX —> binds with FV to form prothrombin activator complex with Ca2+ and phospholipids

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13
Q

How is FV activated?

A

Initially inactive as part of the prothrombin activator complex

once small amounts of thrombin activated –> will activate FVa which accelerates the prothrombin activation

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14
Q

Describe the Intrinsic pathway

A

exposure to collagen or blood trauma => FXII activation and phospholipid release from platelets
=> FXIIa activated FXI, this step requires kallikrein and is accelerated by prekallikrein
=> FXIa activates FIX
=> FXIa + VIIIa + phospholipids + platelet factor 3 => activate FX
=> FXa + FV => prothrombin activator

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15
Q

What factor do platelet phospholipids contain?

A

Platelet factor 3

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16
Q

How do the speeds of the extrinsic versus intrinsic pathway compare?

A

Extrinsic pathway is very fast, can happen within seconds
Intrinsic pathways takes minutes to cause clotting

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17
Q

What are characteristics of the endothelium that help keep clotting at bay

A
  • smooth surface - prevents contact activation
  • glycocalyx - repels clotting factors and platelets
  • thrombomodulin on the endothelial surface - binds thrombin and also activates APC
  • endothelial cells produce NO and PGI2 –> vasodilation and platelet inhibition
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18
Q

What are the 2 ways thrombin is removed from the blood to prevent excessive clotting?

A
  • 85-90% of activated thrombin is absorbed by the fibrin fibers of the clot
  • bindings with antithrombin III
19
Q

what factors does the heparin-antithrombin complex bind and inhibit?

A

II
IX
XII

20
Q

What cells produce heparin and in what organs are they most abundent?

A

basophils
mast cells

within the tissues surrounding capillaries of the lungs and liver

21
Q

Describe the role of vitamin K for clotting factors

A

within the liver => cofactor of carboxylase =>

  • gamma-carboxylation of glutamic acid of clotting facotrs => adds carboxyl group to glutamic acid residues on II, VII, IX, X, PC, PS => facilitates addition of extra negative charge on glutamic acid
  • allows these factors to bind Ca++ which enables them to bind Phosphatidylserine of the phospholipid layer

in the process Vitamin K becomes oxidized - inactive
recycled by Vitamin K epoxide reductase complex 1 (VKORC1)

22
Q

How is vitamin K produced and what is needed for its absorption?

A

intestinal bacteria produce Vitamin K

fat absorption - e.g., lack of bile can prevent fat absorption and therefore reduce vitamin K absorption

23
Q

Describe how Prothrombin testing works

A

blood drawn - citrated or oxalated (i.e., binds Ca+)
for test - large amount Ca+ added + TF (usually grown from placentas)
=> activates extrinsic pathway => time to clotting measured

24
Q

What can be used to standardize PT measurements between laboratories and machines?

A

International normalized ratio (INR)

tissue factor batches come with an international sensitivity index (ISI) - i.e., indicates activity of the TF produced

INR = (PT patient/PT control) ^ISI

25
Q

What is the desired INR for warfarin treatment?

A

2-3

26
Q

Name the PLT receptors for these ligands

A
27
Q

Describe the open canalicular system of platelets

A

membrane-lined invaginations that let the PLT secrete products from the cytoplasm and take up products from plasma

28
Q

What is another name for the PLT receptor GPIIbIIIa?

A

integrin alpha-II-b-beta-3

29
Q

List the contents of alpha granules

A

proteins

  • fibrinogen
  • fibronectin
  • vWF
  • FXIII, FIX, VIII, V, Protein S
  • P selectin
  • Albumin
  • Immunoglobulins
30
Q

List contents of dense granules

A
  • Calcium
  • ATP/ADP
  • Serotonin
  • Histamine
31
Q

Where is vWF stored?

A
  • Weibel Palade bodies in the endothelial cells
  • alpha granules PLT
32
Q

What receptor does vWF bind to on PLTs?

A

GP1balpha - subunit of GP1bIXV

33
Q

Describe the three-stage mode lof platelet activation

A

I. Initiation

  • tissue injury - PLT and endothelial cells release vWF
  • shear stress causes conformational change of GPIbalpha
  • => thethering and rolling of PLTs
  • => binding of PLTs to vWF and collagen
  • => PLT monolayer formation

II. Extension
* PLTs release TXA2 and ADP => recruit more platlets
* activation of integrin alpha-IIb-beta-III (GPIIb3a) => fibrinogen binding => platelet aggregation

III. Stabilization
* PLT contraction => strengthens connection + prevents diffusion of activators away from the PLT
* clot retraction

34
Q

Describe how the cells’ phospholipid layer is changed to allow clotting factor binding

A
  • need to bind to phosatidylserine (PS)
  • location of this is mediated by flippase, floppase, scramblase
  • normal homeostasis => PS kept inside by flippase
  • apoptotic cells or activated platelets => scramblase moves PS to the cell surface to bind with clotting factors
35
Q

Where is tissue factor synthesized?

A

in adventitial fibroblasts
Tissue injury - exposure of TF-bound fibroblasts -> FVIIa binding

36
Q

Describe the initiation phase of the cell based model

A

Tissue damage => TF exposed => binds with circulating VIIIa => TF-FVIIa-complex
=> activates small amounts of IX and X
=> FXa activates FV and binds
=> forms prothrombinase complex (FXa-FVa)
=> activates prothrombin to thrombin

37
Q

Describe the amplification phase of the cell based model

A

Platelet activation => exacerbated by thrombin binding to PLTs
* procoagulant membrane surface
* release FV -> supplies large amounts for prothrombinase formation
* VIII dissociates from the PLT bound vWF

38
Q

Describe the Propagation phase of the cell based model of coagulation

A
  • initially formed thrombin activates FXI
  • TF-FVIIa also activated small amounts of FIX
  • FXIa ==> FIX activation
  • FIXa activates and binds with FVIIIa
  • FIXa-FVIIIa - tenase complex - activate FX
  • FXa combined with FVa => thrombin burst
39
Q

List the natural anticoagulants

A
  • endothelial cell secreted Tissue factor pathway inhibitor (TFPI) => inhibits TF-FVIIa
  • Antihrombin => complexes with and inhibits IIa, FIXa, FXa, FXIa, FXIIa
  • Thrombomodulin => bins with thrombin => activates APC => binds with cofactor Protein S => inhibits FVIII and FV
40
Q

Describe how tPA versus uPA activate plasminogen

A

tPA
* activates plasminogen only in the presence of fibrin - tertiary complex
* fibrin binds to the lysine binding site of plasminogen

uPA
* activates plasminogen without needing fibrin present
* binds to cell-bound uPA receptors -> enhances activation of cell-bound plasminogen

41
Q

What triggers tPA release?

A
  • thrombin FXa
  • beta-adrenergic agents
  • histamine
  • bradykinin
42
Q
A
43
Q

What are the 3 most important fibrinolysis inhibitors and how do they work?

A
  • PAI-1 (plasminogen activator inhibitor) - binds to uPA and tPA
  • alpha-2 antiplasmin - binds noncovalently to plasminogen or crosslinks fibrin - prevents their binding
  • TAFI - activated by thrombin/TM complex => removes the lysin on fibrin => can’t bind to plasminogen anymore
44
Q

Describe how NETs partake in clot formation

A

cfDNA - induces XIII activation and initiates contact pathway of coagulation (XII)
histones - activates platelets
histones - increase thrombin generation
histones - inhibit fibrinolysis

Boards: Coag Transfusion (13 decks)

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