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Pharm > Coagulation Disorders > Flashcards

Coagulation Disorders Flashcards

Test 4

1
Q

What does hemostasis mean?

A

The ability of the body to stop itself and bleeding out

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2
Q

Coagulation causes ______

A

hemostasis

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3
Q

What causes injury?

A

A break in the epithelial or endothelial layers

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4
Q

What activates the clotting cascade?

A

Exposed collagen & vWF from injury to the endothelial layer

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5
Q

vWF =

A

Von Williebrand Factor

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6
Q

What does a red thrombus consist of vs a white thrombus?

A

Red: lots of RBC trapped in a vein

White: fibrin & platelets in an artery

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7
Q

What is an embolism?

A

When a thrombi breaks off & moves through vessels

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8
Q

What does thrombogenesis mean?

A

Formation of a thrombi

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9
Q

Describe how thrombogensis works

A

A brick & mortar structure that will clog a bleeding area

Bricks = platelets
Mortar (glue) = fibrin

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10
Q

Damage to blood vessels cause ________

A

Vasoconstriction

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11
Q

What does serotonin do in ther peripheral vascular?

A

increases vascular tone

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12
Q

T/F: Thrombocytes are cells

A

F

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13
Q

What are Thrombocytes?

A

Components that are broken off of megakaryocytes

they allow for platelet aggregation by degranulation to activate other platelets in the are

this allows platelts to stick together by fibrin & form a clot

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14
Q

Define coagulation

A

Forming a clot

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15
Q

Define Fibrinolysis

A

dissolving an existing clot (lyse)

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16
Q

Describe the 4 platelet phases

A
  1. exposure of collagen & vWF -> causes platelets to ADHERE to surface
  2. adhesion to the surface causes platelet AGGREGATION
  3. platelets SECRETE substances: serotonin (primary) ADP, TXA2
  4. The secretion encourages CROSS-LINKING OF ADJACENT PLATELETS which allows a clot to form (coagulation)

AASC

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17
Q

A megakaryocyte is a _______ cell

A

bone marrow

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18
Q

What do endothelial cells produce? What does this do?

A

PGI2 - prostacyclin (part of AA cascade)

Inhibits platelet aggregation

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19
Q

What does prostacyclin (PGI2) do?

A

Inhibit platelet aggregation

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20
Q

Describe the platelet aggregation pathway

A
  1. Cell wall damage d/t injury to the epithelial and endothelial cells; This releases collagen & vWF
  2. Collagen binds to GP1a receptor & vWF binds to GP1b receptor which causes a signaling in the platelet & activates the release of Serotonin, ADP, & TXA2 (Thromboxane A2)
  3. Once released, these bind to their respective receptors on other platelets which causes degranulation.
  4. A positive feedback system is activated
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21
Q

T/F: both platelet aggregation and coagulation cascade are required in order to form a staple clot

A

T

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22
Q

What are the 2 clotting cascade pathways called?

A

Intrinsic (Inside): damage to endothelial

extrinsic (outside): exposes tissue factor

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23
Q

What is the common pathway in the clotting cascade? What does this mean?

A

Xa

Both pathways meet here

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24
Q

What does factor Xa do?

A

Converts Prothrombin to Thrombin

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25
Q

What is the active form of Prothrombin?

A

Thrombin

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26
Q

What general effects does Thrombin have?

A

-Converts Fibrinogen to Fibrin
-Activates platelets
-Increases production of more thrombin

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27
Q

What is the active form of fibrinogen?

A

Fibrin

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28
Q

When you get to ________ you are in the common pathway

A

factor Xa

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29
Q

Describe the extrinsic pathway in the clotting cascade

A
  1. Trauma activates factor VII
  2. factor VII -> factor X
  3. factor Xa –> converts prothombin to thrombin
  4. thrombin -> activates platelets & converts fibrinogen to fibrin
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30
Q

What factors are involved in the extrinsic pathway in order?

A

7
10
2
1
13

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31
Q

Describe the intrinsic pathway in the clotting cascade

A
  1. Trauma to the endothelial layer activates factor XII
  2. factor XII -> XI
  3. XI -> IX
  4. IX -> X
  5. factor Xa –> converts prothombin to thrombin
  6. thrombin -> activates platelets & converts fibrinogen to fibrin
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32
Q

What is thrombin’s MAIN effect?

A

convert fibrinongen to fibrin

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33
Q

What factors to thrombin effect? How?

A

-Activates factor XIII (13): allows for cross link
– V (5): assists factor Xa
– IIX (8): assists Xa but isnt needed
– XI (11): intrinsic cascade
– Protein C: C+S INHIBIT factor V & IIX

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34
Q

Active protein C inhibits which factors? What does this cause?

A

Factors V & IIX

Prevents conversion of prothrombin to thrombin

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35
Q

What does antithrombin do?

A

Blocks thrombin & has effects on factor X

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36
Q

What factors are your thrombin activators?

A

5, 8, 11, 13, & Protein C

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37
Q

What factors are your thrombin inhibitors?

A

Protein C with 5 & 8
Antithrombin with 10

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38
Q

What factors are involved in the intrinsic pathway in order?

A

12
11
9
10

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39
Q

What factor is prothrombin/thrombin?

A

II
2

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40
Q

What is hemophilia?

A

Factor 8 deficiency

41
Q

Where do DVTs form?

A

Large veins of lower limbs

42
Q

DVT =

A

Deep vein thrombosis

43
Q

Why are DVTs an emergency?

A

They are in the veins. They are break off go into the heart and into the pulm artery and cause a PE.

44
Q

What type of thrombi is associated with DVTs?

A

Red Thrombi

45
Q

What is Virchow’s Triad? How is that related to DVTs?

A
  1. Stasis: decreased skeletal muscle movement = decreased blood flow
  2. Hypercoagulability: dt genetics or leaky veins esp varicose veins
  3. Endothelial injury: exposes collagen

SHE

Increases the likelihood of developing DVTs

46
Q

Describe a white thrombus

A

-platelets & fibrin crosslinked

occurs in high pressure arteries
-will get stuck in capillary beds downstream

Caused by damage to endothelium; plaque

47
Q

Describe a red thrombus

A

-RBC around a white thrombus (platelets & fibrin)

occurs in veins
–has a long tail d/t being built up for awhile d/t low pressure area

High Risk for PE

48
Q

What are DVT risk factors?

A

Genetics:
Antithrombin III deficiency, Protien C deficiency, Protein S deficiency, Sickle cell anemia, Activated protein C resistance

Lifestyle:
Bedridden, surgery, trauma, obesity, estrogen, use, malignancies, chronic venous, insufficiency

49
Q

How does sickle cell anemia contribute to DVT risks?

A

RBC become trap and damage endothelium cells

50
Q

How often should you stretch her legs when flying for a long time?

A

Every 2-3 hours

51
Q

Why is it important to keep coagulation localized?

A

unregulated coagulation can cause DIC (microclots everywhere)

52
Q

Describe DIC

A

Disseminated coagulation
Microclots everywhere

Uses up all platelets & clotting factors
Increases risks of bleeding out
medical emergency High mortality

Causes: Trauma; gram neg. bacterial infection/sepsis, cancer, abruptio placentae

53
Q

What is the Tx for DIC?

A

Plasma/Platelet transfusion
Tx underlying cause

54
Q

What are 2 ways to prevent over coagulation?

A

Fibrin inhibition
Fibrinolysis

55
Q

What are the 3 proteins that break down active clotting factors?

A

A1-antiprotease
A2-macroglobulin
A2-antiplasmin

56
Q

What 4 things rapidly inactivate coagulation proteins?

A

A1-antiprotease
A2-macroglobulin
A2-antiplasmin
antithrombin

57
Q

What does plasminogen convert to? what does it do?

A

plasmin

-Regulation of coagulation by breaking down & limiting fibrin/fibrinogen into split products
- remodels & limits extension of thrombus

58
Q

Describe endogenous tPA

A

Tissue plasminogen activator

Released from injured cells

Converts plasminogen to plasmin

59
Q

What 3 things permit conversion of plasminogen to plasmin?

A

tPA
Urokinase
Streptokinase

60
Q

What 2 things protect clots from lysis and stop conversion of prothombin to thrombin?

A

Aminocaproic acid
TXA

61
Q

What are the 4 classes of coagulation modifiers?

A
  1. Anticoahulants: prevent clot formation
  2. Antiplatelets: inhibit platelet aggregation
  3. Thrombolytics/Fibrinolytic: breakdown existing clots
  4. Hemostatics/Antifibrinolytics: promote blood coagulation
62
Q

Where are coagulation factors produced?

A

Liver

63
Q

What is the antiplatelet prototype?

A

ASA

64
Q

What is the anticoagulant oral prototype?

A

Warfarin

65
Q

What is the anticoagulant IV prototype?

A

Heparin

66
Q

What is the thrombolytic prototype?

A

Streptokinase

67
Q

Drugs: Heparin
Please list and compare all 3

A

Class: Indirect Thrombin inhibitor

MOA: Binds & activates antithrombin (conformational change) enhance AT activity 1000x -> inactivates factor Xa -> inhibits thrombin

  1. Unfractioned Heparin
    -MW 5,000-30,000
    -unpurified
    -made from pig intestine/cow lung
  2. LMW Heparin
    -More specific for factor Xa -> less effect on thrombin -> less effect on coagulation
    --parin
  3. Fondaparinux
    -Pentasaccharide
    -synthetic
    -Selective for factor X –> least effective –> least bleedind risk
    -no interaction with thrombin
68
Q

What lab is used for heparin?

A

aPTT
PT

69
Q

Which heparin is useful for HIT?

A

Fondaparinux

70
Q

What is the suffix for LMW heparin?

A

-parin

71
Q

Describe HIT

A

Heparin Induced Thrombocytopenia
- heparin recognized by immune system, and making antibodies against it
- antibodies target are thrombocytes which deplete our platelets
- occurs 7-10 days after given heparin

72
Q

Differentiate between PT, PTT and INR

A

PT/PTT
– Heparin
– Time to clot

INR
– Warfarin
–Time to clot compared to control

73
Q

What labs use for warfarin?

A

INR

74
Q

What are normal INR ranges?

A

Normal: 0.8 - 1.2

While taking warfarin: 2 - 3

75
Q

What is the normal values for aPTT? what have to be added to this lab?

A

35-45

phospholipids

76
Q

Drugs: Protamine Sulfate

A

Heparin Antidote

MOA: (+) charged drug; Heparin is (-) -> they bind and inactivate each other

Only want to give enough to counter heparin
EXCESS CAUSES ANTICOAGULANT

Most effect on unfractioned
No effect on fondaparinux

77
Q

What are heparins contraindications related to?

A

Bleeding

Advanced hepatic disease related to clotting factors

78
Q

Drugs: Lepirudin (Hirudin)

A

Class: Direct Thrombin inhibitors

Comes from leech saliva
Some surgeons still use leeches

MOA: Bind to both active & substrate recognition sites of thrombin

79
Q

Drugs: Argatroban; Dabigatran (Pradaxa)

A

Class: Direct Thrombin Inhibitors

MOA: Bind only to thrombin active sites

80
Q

Drugs: Warfarin

A

Class: Coumarin Anticoagulant
PO

MOA: Blocks gamma-carboxylation of glutamate residues on cloting factors 2, 7, 9, & 10.
- Prevents recyclin of vitamin K by inhibiting Vitamin K reductase

Discovered by University of Wisconsin
Originally was a rat poision

100% PO bioavailability
99% protein binding
36 hours half life

81
Q

When is warfarin taking?

A

When weaning off heparin

82
Q

What clotting factors does heparin effect?

A

2
7
9
10

83
Q

T/F: You can take warfarin while pregnant

A

F

84
Q

Warfarin reduces prothrombin activity to ____ of normal

A

25%

85
Q

T/F: warfarin is metabolize differently in different people, so everyone will need a different does

A

T

86
Q

Drug: Vitamin K

A

Warfarin ANTIDOTE

Confers activity on: Factors VII, IX, X, and prothrombin

Good sources come from green leafy vegetables & gut bateria

87
Q

How do you reverse warfarin?

A

Stop drug
Vit K
FFP
Factor IX concentrates

88
Q

Drugs: Rivaroxaban; Apixaban

A

Class: Indirect Thrombin inhibitors

MOA: Factor Xa inhibitors -> less specific for thrombin -> clotting cascade more closely controlled

No reversal

89
Q

Drugs: tPA, Streptokinase, Urokinase

A

Class: Fibrinolytics

MOA: Lyse thrombi; catalyze formation of plasmin

90
Q

Drugs: Aspirin

A

Class: Antiplatelets

MOA: Blocks COX1 which also inhibits Thromboxane A2 synthesis -> increases bleeding time

91
Q

When should you stop taking aspirin before Sx?

A

A week beforehand

92
Q

How many half life’s before a drug is out of your system?

A

4

93
Q

Drugs: Clopidogrel (Plavix)

A

Class: Antiplatelet

MOA: Irreversibly inhibit ADP receptor on platelets

-8.7% reduction in ischemic events in comparison to aspirin

94
Q

Drugs: Abiciximab

A

Class: Monoclonal antibody/antiplatelet

MOA: Block IIb & IIIa receptors on platelets preventing degranulation and aggregation

95
Q

What are plasma fractions?

A

Isolations in plasma blood where we can get specific factors that we need

Ex) we can isolate and give a patient plasma with factor 8 in hemophilia

96
Q

Drugs: FFP

A

Plasma is what our clotting factors are in girl!!!!!!!!!!!

97
Q

Drugs: Desmopressin

A

Class: ??

MOA: Increases Factor VIII activity

Tx: Mild hemophilia A; Von WIlliebrand disease

98
Q

Drugs: Aminocaproic acid; Tranexamic acid

A

Class: Fibrinolytic inhibitor

MOA: competitively inhibits plasminogen conversion to plasmin
-stabilizes clot & prevents breakdown

Aminocaproic acid Uses: Post surgical, bleeding, intracranial, aneurysm, bleeding from tPA, hemophilia therapy

Tranexamic acid uses: decrease risk of death in major bleeding in: trauma, postpartum, epistaxis, heavy menstrual bleeding

Pharm (30 decks)

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