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CPR Exam 1 > 27. Hemostasis & Clotting > Flashcards

27. Hemostasis & Clotting Flashcards

1
Q

what are platelets derived from

A

megakaryocytes

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2
Q

what is a normal platelet count

A

150,000 - 400,000 / uL

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3
Q

what is considered a low platelet count

A

<50,000

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4
Q

what is a potentially lethal platelet count

A

<10,000

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5
Q

what makes the cytoskeleton of platelets

A

actin, myosin & thrombosthenin

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6
Q

what organelles do platelets have & what is its purpose

A

Mitochondria- attach and contract

ER, golgi remnant - store Ca

dense-core granules & alpha-granules

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7
Q

what substances are in platelets

A

Cox-1 (makes thromboxane A2)

5-HT -vasoconstict

fibrin stabilizing factor (clot stability)

platelet derived growth factor (repair)

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8
Q

what controls platelet regulation

A

thrombopoietin

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9
Q

what is TPO make by

A

liver & kidneys

*regulation will be affected w/ kindey/liver failure*

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10
Q

how does TPO fxn

A

increase differentiation & maturation rate of hematopoietic stem cells

–> more megakaryocytes & platelets

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11
Q

what receptor does TPO bind to on platelets & megakaryocytes

A

c-MPL (CD-110)

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12
Q

when you have high platelet count, TPO will —

A

be bound to c-MPL –> internalized and degraded in platelets/megakaryocytes –> little free TPO available

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13
Q

if you have low platelet count, then what happens to TPO

A

little TPO bound to c-MPL –> NOT degraded so more free TPO available

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14
Q

what are the 4 basic steps of hemostasis

A
    • Vascular spasm
    • Formation of platelet plug
    • Formation of blood clot
    • Repair of damage
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15
Q

what is the purpose of vasospasm

A

disrupt blood flow by contracting upstream to prevent blood loss

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16
Q

what factors contribute to vasospasm

A
  • Myogenic: response to damage to smooth muscle
  • Serotonin and TXA2
  • Release of molecules from endothelial cells
  • neural reflex initiated by mechanical injury and/or pain
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17
Q

which proteins do platelets adhere to beneath the endothelial lining during vascular injury

A

collagen and laminin

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18
Q

what prevents platelets from adhering to endothelium in normal situations

A

negative charge of glycoproteins

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19
Q

What is the role of von Willebrand factor?

A

produced by endothelial cells and by platelets

—serves as a ligand for platelet receptors

–> activate platelets –> bind fibrinogen –> help form platelet plug

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20
Q

what do dense granules release once platelet receptors are activated

A

release ATP, ADP, 5-HT & Ca

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21
Q

What is the platelet receptor for collagen?

A

Gp Ia/IIa

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22
Q

What platelet receptor does lamnin bind

A

Gp Ic/IIa

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23
Q

what do alpha granules release when platelet receptors are activated

A

release growth factors, vWF, factor V & fibrinogen

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24
Q

what does ADP bind to activate platelet aggregation

& what medication inhibits this

A

P2Y12 receptor

inhibited by plavix (clodpidogrel) - antiplatelet agent

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25
Q

what does aspirin bind to inhibit clotting

A

cyclooxygenase receptor

-by reducing release of thromboxane A2 –> reduce clotting

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26
Q

how does blood clot form

A

thrombin generate fibrin –> stimulate polymerization and contraction of clot

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27
Q

How are vessel walls repaired?

A

platelet-derived growth factor stimulates fibroblasts to grow into the area differentiation for remodeling

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28
Q

What is the role of protein C in clot breakdown?

A

inactivates the t-PA inhibitor

no tPA is active –> so it converts plasminogen to plasmin –> which remove & lyse fibrin

29
Q

what does fibrin inhibit

A

thrombin

limit clotting

30
Q

What is the function of prostacyclin?

A

vasodilation and a potent inhibitor of platelet aggregation

limit clotting

31
Q

When does antithrombin III act as an anticoagulant?

A

when it is bound with thrombin

32
Q

what does heprin do

A

increase anti-thrombin efficacy

(from mast cells)

33
Q

Which factors are utilized by the extrinsic clotting pathway?

& when is it activated

A

Factor III (tissue factor) –> Factor VII/TF complex –> Xa

activated by external trauma &

quick

34
Q

Which factors are utilized by the intrinsic pathway?

& when is it activated

A

Factors XIIa > XIa > IXa + VIII > Xa

-actived by truama inside (vasculature, platelets, exposed endothelium, chemicals or collagen) = slow

35
Q

Which factors are utilized by the common pathway?

A

Factor Xa + V > Thrombin (IIa) > Fibrin (Ia)

include factors I, II, V, & X

36
Q

What is the primary difference between primary and secondary hemostasis?

A

primary makes a weak platelet plug

secondly makes it strong by generating a fibrin mesh on it

37
Q

What does thrombin activate?

A

Factors V, VIII, XIII

protein C

prothrombin

fibrinogen

38
Q

Which clotting cascade is activated first?

A

extrinsic pathway

39
Q

How does activation of the extrinsic pathway cause activation of the intrinsic pathway?

A

activation of the common pathway, and specifically thrombin, has a positive feedback on factors upstream

40
Q

What is the function of antithrombin?

A

inhibits further cleavage of prothrombin and inhibits the production of factor Xa from X

41
Q

What are the two types of short acting oral anticoagulants?

What is their MOA?

A

Hydroxycoumarins (warfarin/coumadin) and indanediones

–> inhibit the action of vitamin K

42
Q

In which form is vitamin K active?

A

quinol form

( converted in liver via quinone reductase )

–> form blood clots

43
Q

Which enzyme does warfarin decrease the activity of?

A

Vit K-dependent epoxide reductase

–> which is responsible for converting vitamin K to the quinone form

44
Q

What is vitamin K a cofactor in synthesizing?

A

Active Factors II, VII, IX, and X,

protein S and C (these are anticoagulant proteins)

45
Q

What is the product of the carboxyglutamination reaction?

A
  1. glutamate (gamma-carboxyglutamate) –> more negatively charged –> recruits activated clotting factors
  2. -Vit K oxidized back to VIt K 2,3 epoxide
  3. activate 2,7,9,10, protein C & S
46
Q

What can be used for a warfarin overdose?

A

vitamin K

47
Q

What is added to the gamma-glutamate residue on Factors II, VII, IX, and X?

A

carboxyl group

48
Q

Which enantiomer of warfarin is more potent?

A

S-enantiomer is 2-5X more potent than R-enantiomer

in produding anticoagulant response

49
Q

Which CYP enzyme metabolizes S-warfarin?

A

CYP2C9

50
Q

If a patient is on a drug or eating a lot of food that is metabolized by CYP2C9, what would be the effects?

A

Increase the blood concentration of active S-warfarin-

-> increasing the potency (metabolism of drug is inhibited)

51
Q

What is the half life of Factor II?

A

60 hours

52
Q

What is the half life of Factor VII?

A

4-6 hours

53
Q

What is the half life of Factor IX?

A

24 hours

54
Q

What is the half life of Factor X?

A

40-60 hours

55
Q

Which factors do protein C and S inactivate?

A

proteolytically inactivate Va and VIIIa

–> degrades clot

56
Q

What is the risk of a protein C deficiency?

A

significantly increased risk of venous thrombosis

57
Q

What is hemophilia A?

A

factor VIII deficiency

Genetic disorder, but 1/3 are caused by a spontaneous mutation

58
Q

What is hemophilia B?

A

factor IX deficiency also called Christmas disease

59
Q

What is hemophilia C?

A

Factor XI deficiency

60
Q

What is INR?

A

International Normalized Ratio measures blood clotting time and compares it to normal values.

61
Q

What is prothrombin time (PT) measuring?

A

Factors I, II, V, VII, and X ( extrinsic coagulation pathway )

62
Q

What is partial thormboplastin time (PTT) measuring?

A

Factors XII, XI, IX, VIII, X, V, II, and I && prekallikrein (PK) and HK

Measures integrity of intrinsic and common clotting pathways

63
Q

how would liver diease affect PT & PTT

A

PT- prolonged

PTT- normal

64
Q

what is the fxn of tPA

A

conversion of plasminogen to plasmin –> cleave thromib & fibrin clots –> actively lyse clots

65
Q

what is used for the activation of antithrombin III

A

anticoagulant (heparin)

-rapid, prevent clot

66
Q

what impairs the synthesis of vit K dependent clotting factor

A

anticoagulant - warfarin

-slow- prevent clot

67
Q

what irreversibly inhibits cyclooxygenase & what is the consequence

A

aspirin

-inhibit platelet aggegration & prevents glot formation (slow)

68
Q

what can cause PT to be prolonged & PTT to stay normal

A

liver disease

decreased vit K,

decreased/defective factor VII,

anticoagulation drug (warfarin) therapy)

chronic low-grade dissminated intravascular coagulation,

CPR Exam 1 (27 decks)

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