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Pharmacology- Test 3 > Anticoagulants > Flashcards

Anticoagulants Flashcards

1
Q

Blood coagulation consists of how many factors? Pathways?

A

13 clotting factors (factor XIII crosslinks fibrin to make a more stable clot), 2 pathways (Intrinsic system and Extrinsic system)

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2
Q

What is factor IV?

A

Calcium

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3
Q

What is factor VI?

A

Factor V activated

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4
Q

What is factor V?

A

Part of the Xa complex

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5
Q

What is the Extrinsic Pathway?

A

Tissue Factor Pathway

(1) Operates during tissue injury
(2) Bypasses several steps
(3) Occurs in seconds

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6
Q

<p>
What test will you use to evaluate the extrinsic system? What factor is dependent upon this process? What drug is it used to monitor?</p>

A

<p>

| PT test; normal value ~13 seconds; Depends on factor VII levels; used to monitor Coumadin levels</p>

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7
Q

What is the Intrinsic Pathway?

A

Contact activation pathway

(1) requires almost all the factors
(2) is relatively slow

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8
Q

<p>

| What test will you use to evaluate the intrinsic system? What drug is it used to monitor?</p>

A

<p>
PTT test, normal value is ~30 seconds; used to monitor Heparin levels (hemophilia) (Heparin is also monitored by &quot;heparin levels&quot; now)</p>

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9
Q

What is the Common Pathway? What is important about this pathway?

A

The pathway in which both Extrinsic and Intrinsic meet; Thrombin, the last enzyme, converts soluble fibrinogen to insoluble fibrin mesh in which blood cells are trapped, forming a clot.

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10
Q

What factors are vitamin K dependent?

A

IX, VII, X, II (Prothrombin)

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11
Q

T/F vitamin K dependent factors are only within the intrinsic and common pathways.

A

FALSE, all the pathways!

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12
Q

Heparin: Mechanism of Action

A

(1) Activates antithrombin III in the plasma

(2) Antithrombin inhibits thrombin (IIa), IXa, Xa

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13
Q

How is Heparin given?

A
  • Given S.C. or I.V. (not effective orally)

- Has rapid onset of action when given parenterally

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14
Q

Heparin: Uses

A

(1) immediate anticoagulation (i.e. in M.I.)
(2) Venous thrombosis
(3) Pulmonary embolism
(4) Thrombosis prophylaxis

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15
Q

What is the general usage of Heparin in the hospital?

A

Used for the first 7-10 days followed by warfarin with a 3-5 day overlap (have to overlap warfarin and heparin until the warfarin takes therapeutic effect)

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16
Q

T/F Heparin is used both in vivo and in vitro

A

TRUE

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17
Q

Heparin: Overdose/Adverse Effects

A
  • Causes increased bleeding (internally or externally)
  • Is of animal origin, may produce allergic reactions in some patients
  • Causes transient thrombocytopenia in ~25% of cases (10% drop in platelet count)
  • Can cause Heparin Induced Thrombocytopenia (HIT) in ~1-4% of patients (immune response against heparin and factor IV;7-10 days after- 50% drop in platelet count)
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18
Q

What is the antidote for HIT?

A

Protamine (a basic protein) neutralizes acidic heparin

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19
Q

What is the difference between unfractioned and low molecular weight heparins?

A
  • Low molecular weight heparins are smaller forms of heparin with better bioavailability and longer half lives
  • Unfractioned heparin has antithrombin activity by a long arm wrapped around ATIII and thrombin
  • LMWH doesn’t have the long arm so has more anti Xa activity (how it is measured in the lab)
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20
Q

How is LMWH given?

A

SQ injection

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21
Q

LMWH: Contraindications

A

Renal disease

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22
Q

How can you follow levels of LMWH?

A

By following levels of anti-Xa activity

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23
Q

What are names of LMWH?

A

(1) Enoxaparin
(2) Deltaparin
(3) Fondaparinux

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24
Q

Warfarin: Mechanism of Action

A
  • Inhibits the proper synthesis of vitamin K- dependent factors (II, VII, IX, X)
    ~Vit K is needed for gamma carboxylation of glutamic acid residues in these factors
  • Has a delayed onset of action: time required to decrease the plasma levels of preformed clotting factors
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25
Q

T/F Warfarin acts as an anticoagulant directly

A

FALSE; indirectly

26
Q

How long does it take to produce the effect of Warfarin? Why?

A

~72 hours; delay is related to half lives of these clotting factors (II-60hr, VII-6hr, IX-24hr, X-40hr)

27
Q

How is Warfarin used?

A
  • Orally; effective in vivo only because of its indirect effect
  • Long-term therapy (6 weeks to 6 months or longer)
28
Q

T/F Warfarin is highly bound to albumin (plasma proteins).

A

TRUE

29
Q

What are the high drug interactions with warfarin?

A

because of the displacement of warfarin from plasma albumin by other drugs (too much warfarin in the blood)

30
Q

Warfarin- Uses

A

(1) Venous thrombosis
(2) Pulmonary Embolism
(3) Atrial fibrillation
(4) Mechanical heart valves
(5) MI after starting heparin

31
Q

Warfarin- contraindications

A

Pregnancy because it can cross placenta (safe with breast feeding)

32
Q

How do you monitor Warfarin?

A

PT; want International normalized ratio of 2-3 (start with 5 mg and slowly go up because everyone responds to it different)

33
Q

Warfarin: Overdose/Antidotes

A
  • Causes increased bleeding
  • Antidotes:
    ~ Vitamin K1 (phytonadione): recovery is slow, requires synthesis of new clotting factors (12-24 hrs)
    ~ Transfusion of fresh frozen plasma (to get someone else’s coagulation factors)
    ~ Prothrombin complex concentrates (rapid) (PCCs contain either activated or non-activated coagulation factors)
34
Q

What are the types of drug interactions with warfarin?

A

(1) Pharmacokinetic: change in plasma levels of warfarin due to enzyme induction, enzyme inhibition, and reduced plasma protein binding
(2) Pharmacodynamic: synergism due to reduced clotting factor synthesis (in liver disease of vit K deficiency) or interference with hemostasis

35
Q

Which are more serious interactions: increasing anticoagulant effect or decreasing anticoagulant effect?

A

Increasing anticoagulant effect

36
Q

Examples of drugs that increase its anticoagulant effect (pharmacokinetic type)

A

(1) Drugs such as phenylbutazone decrease warfarin binding to plasma proteins and increase free (effective) concentration
(2) Trimethoprim-sulfamethoxazole, metronidazole, fluconazole, amiodarone, cimetidine, and disulfiram increase warfain concentration due to inhibition of its metabolism

37
Q

Examples of drugs that increase its anticoagulant effect (pharmacodynamic type)

A

(1) Aspirin and other NSAIDs increase its anticoagulant action due to the inhibition of platelet function
(2) Third generation cephalosporins increase its anticoagulant action due to elimination of gut bacteria that produce vitamin K

38
Q

Examples of drugs that decrease its anticoagulant effect (pharmacokinetic type)

A

(1) Barbiturates and rifampin decreased anticoagulant action of warfarin due to an increase in its metabolism because of induction of hepatic metabolic enzymes
(2) Cholestyramine binds warfarin in the gut and reduces its bioavailability

39
Q

Examples of drugs that decrease its anticoagulant effect (pharmacodynamic type)

A

(1) Diuretics may increase concentration of clotting factors and thus decrease the effect of warfarin
(2) Hypothyroidism may decrease the turnover of clotting factors and may decrease the effect of warfarin

40
Q

What is the fibrinolytic system?

A
  • Breaking up clots
  • Plasminogen activators (serine proteases) convert plasminogen to plasmin
  • Plasmin can digest fibrin (in the clot) and fibrinogen in the plasma, also degrades factor V and VIII
  • Fibrinolytic drugs with a higher activity against fibrin-bound plasminogen than plasma plaminogen are called clot-selective (i.e. TPA)
41
Q

What is the test you use to monitor breaking down of clot levels?

A

D-dimer

42
Q

What is Altepase?

A

(1) a tissue-type plasminogen activator (t-PA) which preferentially activates plasminogen that is bound to fibrin (i.e. is clot selective); it is manufactured by means of recombinant DNA technology
(2) can directly convert plasminogen to plasmin

43
Q

Altepase- Uses

A

(1) MI
(2) Acute ischemic stroke
(3) Massive pulmonary embolism

44
Q

How is Altepase given?

A

Bolus over 1-2 minutes, then I.V. infusion over 2 hours (SHORT HALF LIFE)

45
Q

T/F Altepase is not antigenic.

A

TRUE; it can be used in patients likely to have antibodies to Steptokinase (hard to reduce/control if they bleed afterwards)

46
Q

What does Aminocaproic acid do? What is it used for?

A

inhibits plasminogen activators and has some antiplasmin activities; it is used systemically or with pills or local control in the mouth (Amicar swish and spit or amicar soaked gauze can be used after extractions of surgery where there is local bleeding)

47
Q

Who will use these Amicar swishes?

A

Hemophiliacs, where there is excess fibrinolysis

48
Q

How does platelet aggregation work?

A
  • When endothelium is damaged, the platelets adhere to the exposed collagen via GP receptors and vWF
  • This reaction leads to the release of TxA2, ADP, 5-HT, etc from platelets
  • These chemicals increase the expression of GP receptors and promote platelet aggregation
49
Q

Aspirin- Mechanism of Action

A
  • Prevents platelet aggregation by irreversible acetylation of COX 1, resulting in inhibition of synthesis of TxA2 in the platelets
  • Platelets, being anuclear, do not synthesize new COX and the action of aspirin on platelets lasts for the life of the platelets (7-10 days)
50
Q

Aspirin- Doses

A
  • Inactivation of COX 1 in platelets occurs with LOW doses of aspirin
  • High doses also inhibit synthesis of PGI2 in endothelial cells, a vasodilator agent (don’t want this)
51
Q

Clopidogrel/Ticlopidine- Mechanism of Action

A

(1) Reduce platelet aggregation by inhibiting ADP pathway of platelets
(2) They irreversibly block ADP receptors on the platelets
(3) They inhibit ADP-induced expression of platelet GP receptors
(4) They irreversibly inhibit the platelet function for the life of the platelets

52
Q

Clopidogrel/Ticlopidine- Uses

A

Commonly used in patients who have undergone placement of a coronary stent

53
Q

Which drugs have no effect on prostaglandin formation, and may be given with aspirin?

A

Clopidogrel/Ticlopidine

54
Q

IV direct Thrombin inhibitors- Uses

A

Used in patients with heparin induced thrombocytopenia (~1-4% of patients)

55
Q

Which is the oral direct thrombin inhibitor? What are its uses?

A

Dabigatran; used in stroke prevention in patients with atrial fibrillation
- does not need to be monitored!-

56
Q

T/F There is not an antidote for Dabigatran.

A

TRUE

57
Q

Dabigatran- Adverse effects

A

GI upset

58
Q

What are the IV Direct Thrombin Inihibtors

A

(1) Lepirudin (renally metabolized)

2) Argatorban (hepatically metabolized

59
Q

What is the Oral Anti- Xa Inhibitor? What are its uses?

A

Rivaroxaban; DVT prophylaxis in patients undergoing hip/knee surgery; stroke prevention; acute treatment of DVT, PE
- works within 4 hours after taking dose and lasts 12-24 hours

60
Q

T/F There is an antidote for Rivaroxaban.

A

FALSE

Pharmacology- Test 3 (7 decks)

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