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Pharmacology > Exam 4: Coagulation > Flashcards

Exam 4: Coagulation Flashcards

1
Q

What are the 5 inherited risk factors for DVT?

A
  1. Antithrombin III deficiency
  2. Protein C deficiency
  3. Protein S deficiency
  4. Sickle cell anemia
  5. Activated protein C resistance
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2
Q

What are the 6 acquired risk factors for DVTs?

A
  1. Bedridden
  2. Surgery/trauma
  3. Obesity
  4. Estrogen use
  5. Malignancies
  6. Chronic venous insufficiency
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3
Q

What is DIC?

A

Disseminated Coagulation
Overstimulation of the blood clotting mechanism

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4
Q

What usually causes DIC?

A

Bacterial sepsis (gram-negative bacteria)

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5
Q

What are the 4 causes of DIC?

A
  1. Massive tissue injury
  2. Malignancy (cancer)
  3. Bacterial sepsis
  4. Abruptio Placentae
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6
Q

What are the 2 ways we regulate coagulation?

A
  1. Fibrin inhibition
  2. Fibrinolysis (breaking down fibrin)
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7
Q

What are protease inhibitors?

A

Enzymes that rapidly inactivate coagulation proteins

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8
Q

What 3 things break down active clotting factors?

A
  1. A1-antiprotease
  2. A2-macroglobulin
  3. A2-antiplasmin
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9
Q

What are the 4 types of coagulation modifier drugs?

A
  1. Anticoagulants
  2. Antiplatelet drugs
  3. Thrombolytic drugs
  4. Antifibrinolytic drugs
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10
Q

What are the 9 contraindications for taking heparin? What question do we normally think of when thinking of contraindications?

A

Will this patient likely bleed out? If so, that is a contraindication
1. Active bleeding
2. Hemophilia
3. Thrombocytopenia (decreased plts)
4. Severe HTN
5. Intracranial hemorrhage
6. Infective endocarditis
7. Active TB
8. GI ulcers
9. Advanced hepatic disease

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11
Q

What 3 things do blood vessels normally do when there is damage?

A
  1. Vasoconstriction
  2. Form platelet plugs
  3. Regulate coagulation and fribinolysis
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12
Q

What are the 4 phases of thrombogenesis?

A
  1. Adhesion
  2. Aggregation
  3. Secretion
  4. Cross-linking of adjacent platelets
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13
Q

What is the difference between the extrinsic and intrinsic pathway?

A

Extrinsic - exposes tissue factor
Intrinsic - damage endothelium

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14
Q

What is Virchow’s triad?

A
  1. Stasis
  2. Hypercoagulability
  3. Endothelial injury
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15
Q

What are the characteristics of white thrombi?

A

Thrombi in high-pressure arteries w/ abnormal endothelium
Only plt and fibrin crosslinking
Cause ischemia downstream
Forms fibrin clot

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16
Q

What are the characteristics of red thrombi?

A

Thrombi in low pressure veins
RBC build up around the white thrombus
There is lots of fibrin and a long tail b/c of the build up
They usually become detached and lead to pulmonary emboli

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17
Q

What are the treatments for DIC?

A
  1. Plasma transfusions (w/ plts or clotting factors)
  2. Treat the underlying cause
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18
Q

What are the 3 indirect thrombin inhibitors?

A
  1. Heparin
  2. LMW Heparin
  3. Fondapurinux
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19
Q

What are the 2 direct thrombin inhibitors?

A
  1. Lepirudin (Hirudin)
  2. Argatroban (Pradaxa)
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20
Q

How do indirect thrombin inhibitors work?

A

They inactivate factor Xa and enhance antithrombin activity

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21
Q

What is heparin’s MOA?

A

Binds and activates antithrombin; enhancing its activity and blocking thrombin

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22
Q

What is the MW of unfractionated/unpurified heparin?

A

5-30,000

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23
Q

Where is Heparin extracted from?

A

Pig intestinal mucosa and cow lung (porcine and bovine)
Family of molecules w/ different molecular weights

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24
Q

What is the difference between LMW heparin and unfractionated?

A

LMW heparin is more specific for factor Xa

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25
Q

How can you recognize LMW heparin drugs?

A

-parin

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26
Q

What are the major toxicities of heparin?

A

BLEEDING
HIT and TTP

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27
Q

What is HIT?

A

Heparin induced thrombocytopenia; heparin is recognized by the immune system and makes antibodies against it causing the body to get rid of platelets

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28
Q

Who is more prone to hemorrhage while taking heparin?

A

Elderly women and patients with renal failure

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29
Q

What two lab tests do we do to monitor bleeding/coagulation time?

A

aPTT and PT

30
Q

What is PT and aPTT?

A

Prothrombin time - assesses the extrinsic system
Activated partial thromboplastin time - monitors the intrinsic pathway

31
Q

Explain PT

A

Looks at the extrinsic system
Tissue factor is added and we record the time it takes to clot
We compare these numbers to normal patients (INR) and see the difference

32
Q

What is a normal INR?

A

0.8-1.2

33
Q

Explain aPTT

A

Looks at the intrinsic system
We add phospholipids to induce the intrinsic pathway

34
Q

What is a normal aPTT?

A

35-45 seconds

35
Q

What is the reversal for heparin?

A

STOP THE DRUG
Give protamine sulfate

36
Q

How does protamine sulfate work?

A

Since it is positively charged, it binds together w/ negatively charged heparin and gets rid of the heparin

37
Q

What are the effects of protamine sulfate on LMW and fondaparinux?

A

Less effect on LMW and no effect on fondaparinux

38
Q

Where does protamine sulfate come from?

A

Salmon sperm

39
Q

Why do we need to taper protamine sulfate?

A

Excess can act as an anticoagulant

40
Q

What is fondaparinux?

A

Pentasaccharide molecule of heparin that is synthetic

41
Q

What is the benefit of fondaparinux?

A

Less bleeding risks

42
Q

What can fondaparinux be used for?

A

HIT

43
Q

What is the difference between Hirudin (Lepirudin) and Argatroban/Dabigatran (Pradaxa)

A

Hirudin binds both to the active and substrate recognition sites of thrombin
Pradaxa binds only to the thrombin active site

44
Q

Where do we get hirudin from?

A

Leeches

45
Q

Where do we get Argatroban and Pradaxa from?

A

Biological sources

46
Q

What are 3 coumarin anticoagulants?

A

Warfarin (coumadin)
Rivaroxaban (Xarelto)
Apixaban (Eliquis)

47
Q

Where was warfarin discovered?

A

University of wisconsin

48
Q

What was warfarin originally used for?

A

Rat poison; cause for cattle hemorrhagic disease

49
Q

How is warfarin administered? What is the bioavailability? What is the half life? What is the delay in onset?

A

Orally; 100%; 36 hours; 8-12 hours

50
Q

What is the MOA of warfarin?

A

Warfarin blocks the gamma carboxylation of several glutamate residues
Warfarin will block vitamin K reductase

51
Q

What 4 clotting factors production are blocked by warfarin?

A

2, 7, 9, 10
1972

52
Q

What are the 3 main toxicities of warfarin?

A
  1. Hemorrhagic disorder in the fetus
  2. Birth defects
  3. Cutaneous necrosis
53
Q

What is warfarin’s therapeutic range determined by? What’s the target ranges for warfarin?

A

INR; 2-3

54
Q

What are the 3 important things to do when reversing warfarin?

A
  1. Stop the drug and give vitamin K
  2. Give FFP that contain clotting factors
  3. Give factor 9 concentrates
55
Q

What are rivaroxaban (xarelto) and apixaban (eliquis) specific for? What is the benefit of them? What is their reversal?

A

Specific for acting on Xa
They cause less problems w/ bleeding out
There is no reversal

56
Q

What do fibrinolytics do?

A

Rapidly lyse thrombi and catalyze the formation of serine protease plasmin

57
Q

What are the 3 fibrinolytics?

A
  1. TPA
  2. Streptokinase
  3. Urokinase
58
Q

Where is TPA produced?

A

Directly in the spot of damage and recombinantly in the lab

59
Q

Where are streptokinase and urokinase synthesized from?

A

Streptococci and the kidney

60
Q

What are 3 antiplatelets?

A
  1. Aspirin
  2. Clopidogrel (plavix)
  3. Abciximab
61
Q

How does ASA work?

A

COX1 selective; prevents activation of arachidonic acid cascade and produces less TXA
This inc. bleeding time and reduces plt aggregation

62
Q

How does clopidogrel (plavix) work?

A

Irreversibly inhibits the ADP receptor on plts and reduces platelet aggregation

63
Q

What does plavix reduce?

A

Ischemic events

64
Q

When is plavix generally used?

A

Angioplasty and stent placements

65
Q

How does abciximab work?

A

Targets GP2b and 3a = which are the glycoproteins that cause plt aggregation to occur
Blocks receptors and blocks aggregation

66
Q

What 3 drugs are used for bleeding disorders?

A
  1. Vitamin K
  2. FFP (plasma fractions)
  3. Desmopressin
67
Q

Is vitamin k water or fat soluble? Where does it come from? What does vitamin K help with? Where does vit. K work on?

A

Fat-soluble
Leafy green veggies and gut bacteria
Helps w/ making residues needed for clotting factors
Works on prothrombin, and factors 7,9 and 10

68
Q

What does desmopressin do? What 2 things does it help with?

A

Inc. factor 8 availability
Mild hemophilia A and Von Willebrand disease

69
Q

What are 2 fibrinolytic inhibitors?

A
  1. Aminocaproid acid
  2. Tranexamic acid (TXA)
70
Q

What are the 4 uses for aminocaproic acid?

A
  1. Adjunctive hemophilia therapy
  2. Bleeding from fibrinolytic therapy
  3. Intracranial aneurysms
  4. Post-surgical bleeding
71
Q

What does TXA do?

A

Decreases the risk of death in major bleeding by inhibiting the conversion of plasminogen to plasmin

72
Q

How does aminocaproic acid work?

A

Competitively inhibits plasminogen activation and stabilizes the clot and prevents it from breaking down

Pharmacology (15 decks)

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