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PHARMACOLOGY > 20-Drugs for Coagulation Disorders > Flashcards

20-Drugs for Coagulation Disorders Flashcards

1
Q

what is the purpose of a vessel spasm?

A

constricts vessels and limits blood flow to site on injury

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2
Q

What do activated platelets release? and what do these stimulate?

A

ADP, thromboxane A2

stimulate activation of new platelets, platelet agg, and vasoconstriction

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3
Q

role of thrombin

A

converts fibrinogen into fibrin

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4
Q

what does fibrin act as

A

scaffolding to form a clot

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5
Q

explain the process small vessels undergo after injury (acute)

A

injury
spasm
platelets adhere to injury site and agg to form plug
formation of insoluble fibrin strands and coagulaiton

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6
Q

the common pathway:

A

begins when the intrinsic and extrinsic pathways of coagulation converge at the time of factor Xa synthesis

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7
Q

when is fibrinolysis initiates and what enzyme is responsible for this process? (how it is produced?)

A

initiated 24-48h our clot formation
plasmin digests fibrin and destroys the clot
cells adjacent to the clot release t-PA (tissue plasminogen factor) that converts plasminogen into plasmin

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8
Q

antifibrinolytics:

A

inhibit clot breakdown

inhibit conversion of plasminogen into plasmin

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9
Q

Thrombolytics Action

A

dissolve blood clots

increase activation of plasminogen activator to increase conversion of plasminogen into plasmin

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10
Q

thromboembolic disorders lead to

A
  • formation of non-therapeutic clots
  • occlusion of arterial vessels leading to MI and/or CVA
  • embolus
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11
Q

thrombocytopenia and hemophilia and examples of

A
  • bleeding disorders

thrombocytopenia - low platelet count due to bone marrow suppression

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12
Q

anticoagulant: type of modification, mechanism (general)

A
  • prevention of clot formation

- inhibition of specific clotting factors

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13
Q

anticoagulant/antiplatelet: type of modification, mechanism

A
  • prevention of clot formation
  • inhibition of platelet actions
  • increase time needed to form a clot
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14
Q

thrombolytic: type of modification, mechanism

A

removal of existing clot

dissolving clot

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15
Q

antifibrinolytic: type of modification, mechanism

A

promotion of clot formation

inhibition of destruction of fibrin

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16
Q

what are the most commonly prescribed coagulation modifiers? why?

A

anticoagulants. work predominantly w venous system

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17
Q

5 “sub-classes” of anticoagulant drugs

A 
heparin
warfarin
low molecular weight heparins
direct thrombin inhibitors
direct acting factor Xa inhibitors
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18
Q 
antidotes:
heparin:
warfarin:
low molecular weight heparins:
direct thrombin inhibitors:
direct acting factor Xa inhibitors:
A

heparin: protamine sulphate
warfarin: vit K
low molecular weight heparins: protamine sulphate
direct thrombin inhibitors: idracizumab (praxibind)
direct acting factor Xa inhibitors: andexanet alfa (Andexxa)

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19
Q

Heparin: mechanism of action, uses, monitoring

A
  • very potent anticoagulant
  • catalyzes inactivation of thrombin (enhances antithrombin effects and thrombin no longer converts fibrinogen into fibrin, inhibiting factor Xa and intrinsic pathway)
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20
Q

LMWH (low molecular weight heparin): mechanism of action, uses, monitoring

A
  • anticoagulant that inhibits factor Xa (thrombin is active, more stable response)
  • reduced risk of thrombocytopenia
  • reduced dose frequency, longer duration of action
  • drug class of choice for DVT
  • less monitoring, SC by weight
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21
Q

Warfarin: mechanism of action, uses, monitoring

A
  • anticoagulant; blocks synthesis of clotting factors thrombin, VIIa, IXa, Xa (inhibits epoxide reductase which recycles vit k)
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22
Q

Direct acting thrombin inhibitors: mechanism of action, uses, antagonist

A
  • anticoagulant; directly binds and inhibits thrombin (prevents fibrinogen into fibrin)
  • reduces risk of stroke, systemic embolism in pt.s w AF, DVT, and pulmonary embolism
  • expensive - used in cases of heparin-induced thrombocytopenia
  • antagonist: Praxbind (IV)
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23
Q

praxbind (IV): uses

A
  • antagonist for directly acting thrombin inhibitors (anticoagulant), promotes clotting
  • used for life-threatening bleeding or uncontrolled bleeding and in emergency surgery or procedures
  • dabigatran? binds to praxbind w higher affinity than thrombin
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24
Q

Direct Acting Factor Xa Inhibitors: mechanism of action, uses, antagonist

A
  • highly selective inhibition of factor Xa
    (inhibit intrisic and extrinsic pathways and reduce thrombin formation w not direct effects on thrombin or platelets)
  • used to prevent and treat DVT (pulmonary embolus in pt.s w knee surgery)
  • replacing warfarin and some LMWHs
  • antagonist: Andnexaet (Andexxa, IV)
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25
Q

Why are Direct acting thrombin and Factor Xa inhibitors beginning to replace warfarin and some LMWHs?

A
  • PO, predictable effects, less monitoring, few (known) drug drug interactions
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26
Q

Andnexaet (Andexxa, IV)

A
  • antagonist for direct acting factor Xa inhibitors
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27
Q

anticoagulant drugs: general cautions, common adverse effects

A

caution w hemorrhagic disorders, recent trauma, spinal puncture, GI ulcers, recent surgery
- adverse effects: bleeding, INR (internal normalized ration - prothrombin lvls), prothrombin time

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28
Q

Antiplatelet Drugs: 3 types w ex.

A
  1. irreversible COX inhibitors: aspirin
  2. ADP receptor antagonists: Clopidogrel, Ticagrelor
  3. Glycoprotein IIb/IIIa receptor antagonists (IV only): Abciximab, Tirofiban, Eptifibatide
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29
Q

Antiplatelet Drugs: Cautions and common adverse effects

A
  • presence of known bleeding disorder, recent surgery, closed head injuries
  • adverse effect: bleeding, increased bruising, bleeding while brushing teeth
  • gastritis, ulcerations
30
Q

Aspirin: type, mechanism of action, who does it benefit?

A

antiplatelet: irreversible binding to COX 1 and 2
- inhibits PG synthesis and thromboxane A2
- sig. benefit for pt.s w CVD, controversial for pt.s without CVD (increased bleeding risk)

31
Q

Why is it beneficial that aspirin can have anticoagulant factors at a lower dose (81mg)?

A

no association w gastric ulcers

32
Q

ADP receptor antagonists:

A
  • antiplatelet, irreversibly changes molecular conformation of ADP receptors on platelets
  • PO alt. to ASA
  • reduction in relative risk of ischemic stroke, MI, or vascular death compared to aspirin
  • Ticagrelor - faster onset, greater efficacy
33
Q

role of ADP and glycoproteins IIb/IIIa in coagulation

A

recruit platelets to aggregate

34
Q

Glycoprotein IIb/IIIa inhibitors: class, use

A
  • antiplatelet
  • expensive!
  • reserved for pt/s w recent MI or stroke undergoing angioplasty (IV)
35
Q

Thrombolytic Drugs:

A
  • lysis clots, not preventative
  • increase the conversion of plasminogen to plasmin to breakup clots
  • used for MI, pulmonary embolism, DVT, CVA, and ischemnic stroke
36
Q

Do platelets bind with high or low affinity to the damaged vessel?

A

High

37
Q

What do activated platelets release? And what does that stimualte?

A

ADP and thromboxane A2

- stimulated new platelets, platelet aggregation and vasoconstriction

38
Q

What is the function of thrombin?

A

Converts fibrinogen to fibrin

39
Q

T/F: Fibrin forms the clot and provides clot robust

A

true

40
Q

Extrinsic pathway

A
  • outside vessel
  • damaged tissue produce thromboplastin released from damaged cells
  • factor Xa produced
41
Q

Intrinsic Pathway

A
  • inside bv
  • collagen is exposed at injury site
  • produce Xa
42
Q

What is produced in both intrinsic and extrinsic pathways and what is its purpose?

A

Factor Xa; important in converting prothrombin to thrombin so fibrin is made

43
Q

What is the function of plasminogen activator?

A

Converts plasminogen to plasmin which dissolves fibrin so clot is broken down

44
Q

When would you give a drug that enhances plasmin?

A
  • MI

- Stroke

45
Q

What are the most prescribed coagulation modifiers?

A

anticoagulants

46
Q

Which route would you administer an anticoagulant in an emergency? ex of drug

A

IV or SC; heparin

47
Q

Which route would you administer in an emergency when stabilized? ex of drug

A

PO or SC; warfarin

48
Q

Types of anticoagulants

A
  • heparin
  • warfarin
  • Low molecular weight heparins
  • direct thrombin inhibitors
  • direct acting factor Xa inhibitors
49
Q

How is heparin administered? What is the antidote?

A

IV, SC; protamine sulphate

50
Q

How is warfarin administered? and what is the antidote?

A

PO; Vitamin k

51
Q

How is low molecular weight heparins administered? and antidote?

A

SC; protamine sulphate

52
Q

How are direct thrombin inhibitors administered?antidote?

A

PO, praxbind

53
Q

How are direct acting factor Xa inhibitors administered? Antidote?

A

Po; Andexxa

54
Q

What drug is known as the natural coagulant and where is it found?

A
  • heparin; is found in liver and lining of bv
55
Q

What is heparin used to prevent?

A
  • used to prevent DVT, pulmonary embolism, DIC, treat Mi and stroke
  • monitor for bleeding (risk of thrombocytopenia)
56
Q

What should be monitored while using heparin?

A

Bleeding

57
Q

What is the drug class of choice to prevent DVT?

A

Low molecular weight heparins

58
Q

If one was to be switching meds from heparin to warfarin how long would the drugs be coadministered?

A

3 days due to increased risk of bleeding and anticoagulants effects lasting 4-5 days

59
Q

How much of warfarin is bound to plasma proteins?

A

95-99%

60
Q

T/F: patients on warfarin should avoid foods high in Vit K

A

true

61
Q

T/F: patients should avoid things that could potentially cause injury resulting in blood lose while on warfarin?

A

true

62
Q

Direct acting thrombin inhibitors results in

A
  • thrombin not being able to convert fibrinogen into fibrin

- no clot formation

63
Q

When is praxbind used and what does it do?

A
  • uncontrolled bleeding/life threatening
  • case of emergencies
  • binds with higher affinity than thrombin and doesnt allow for anticoagulation effects
64
Q

T/F: Warfarin is contraindicated in pregnancy and during lactation

A

true

65
Q

T/F: Heparin is contraindicated in lactation and pregnancy

A

false; does not cross placental barrier

66
Q

When should caution be used with anti-platelet drugs?

A
  • presence of any known bleeding disorder
  • recent surgery
  • closed head injuries
67
Q

Adverse effects of anti-platelet drugs

A
  • bleeding, bruising

- risk of excessive bleeding with combination of drugs affecting blood clotting

68
Q

Issues with ASA

A
  • gastritis

- ulcerations

69
Q

T/F: Thrombolytics dissolve all clots (therapeutic and non therapeutic)

A

true

70
Q

Thrombolytic drugs are contraindicated with

A
  • any recent surgerys
  • internal bleeding
  • monitor for cerebral hemorrhage
71
Q

Which drug can only be administered once? (thromboylitic) and why?

A
  • streptokinase

- body forms antibodies against this drug

PHARMACOLOGY (27 decks)

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