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Pharmacology > Anticoagulants & Antiplatelets > Flashcards

Anticoagulants & Antiplatelets Flashcards

1
Q

What are the 4 main types of anti platelets

A

Aspirin (COX inhibitor)

Clopidogrel, Ticagrelor, Prasugrel, Ticlopidine (ADP receptor antagonist)

Abciximab, Tirofiban, Eptifibatide (Glycoprotein 2b/3a inhibitor)

Dipyridamole, Cilostazol (PDE & Adenosine uptake inhibitor)

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2
Q

Aspirin MOA

A

Irreversibly inhibits COX1 and COX2.

COX1 is responsible for converting arachidonic acid to prostaglandin H2 Which is converted to TXA2

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3
Q

Aspirin SIDE EFFECTS

A 
Gastrointestinal toxicity,
nephrotoxicity, 
hyperventilation, 
hypothermia, 
coma in over dose
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4
Q

Aspirin C/Is

A 
Hypertension, 
kidney dysfunction, 
Stomach ulcers, 
Asthma.
known hypersensitivity to NSAIDs 
Rhinitis
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5
Q

Aspirin USE

A

Antiplatet effect
Analgesic
Antiinflammatory

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6
Q

Aspirin SIDE EFFECTS

A

Fatal hepatotoxicity with overdose

treat w/active charcoal

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7
Q

Glycoprotein 2b/3a Inhibitor EXAMPLES

A

Abciximab
Tirofiban
Eptifibatide

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8
Q

GLYCOPROTEIN IIb/IIIa INHIBITOR: MOA

A

Abciximab Tirofiban Eptifibatide

● These agents prevent platelet aggregation by binding to the glycoprotein 2b/3a and hence prevent cross link between platelet Glycoprotein 2b/3a and fibrinogen
● Hence prevents platelet aggregation
● They are reversible Inhibitors of fibrin
● They are administered only intravenously.
● Clinical application: Acute coronary syndrome
● Prevents restenosis after coronary angioplasty

GP 2a/3b Inhibition means no fibrin links which means no clots

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9
Q

ADP RECEPTOR ANTAGONIST

EXAMPLES

A

Clopidogrel
Ticagrelor
Prasugrel
Ticlopidine

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10
Q

Clopidogrel
Ticagrelor
Prasugrel
Ticlopidine

MOA

A

They block the ADP receptor (specifically P2Y12)
● Activated platelet release another chemical mediator called ADP
● ADP binds to P2Y12 and that leads to the activation of Glycoprotein IIb/IIIa which are
required for fibrin mediated crosslink.
● Thus by blocking P2Y12 ADP receptors, these drugs effectively block the formation of
platelet aggregation
● Clinical application: Acute coronary syndrome, prevention and treatment for arterial
thrombosis
● Prevents transient ischemic attacks and strokes, Clopidogrel is used to prevent
thrombosis in patients who have received coronary artery Stent, and in patients who can’t tolerate aspirin.

In summary P2Y12 receptor inhibitor means ADP can’t bind which means no clot

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11
Q

Clopidogrel
Ticagrelor
Prasugrel
Ticlopidine

ADVERSE EFFECT

A

bleeding,

gastrointestinal disturbances

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12
Q

Clopidogrel
Ticagrelor
Prasugrel
Ticlopidine

CONTRAINDICATIONS

A

Anaplastic anemia

TTP ( Thrombotic thrombocytopenic purpura )

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13
Q

PDE AND ADENOSINE UPTAKE INHIBITOR/PHOSPHODIESTERASE INHIBITOR:

EXAMPLES

A

Dipyridamole

Cilostazol

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14
Q

PDE AND ADENOSINE UPTAKE INHIBITOR/PHOSPHODIESTERASE INHIBITOR:

MOA

A

Inhibit enzyme called phosphodiesterase
● Phosphodiesterase is responsible for breaking down of cAMP to AMP
● By blocking phosphodiesterase, there is
, which

inturn leads to
● This automatically leads to inhibition of platelet activation.
● These agents also inhibit phosphodiesterase in the vascular wall as well as uptake of
adenosine which promotes vasodilation
● Cilostazol and Dipyridamole gives headache (adverse effect)
● Clinical application: prevention of thromboembolic complications of cardiac valve
replacement

IN SUMMARY inhibits cAMP–>AMP conversion by enzyme phosphodiesterase meaning increased cAMP—> Leading to increased Calcium intracellularly so less is to be used in plt activation

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15
Q

Dipyridamole
Cilostazol

ADVERSE EFFECTS

A

Headache,

Palpitation

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16
Q

PDE AND ADENOSINE UPTAKE INHIBITOR/PHOSPHODIESTERASE INHIBITOR:

Contraindications

A

heart failure

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17
Q

ADVERSE EFFECTS OF ANTIPLATELET DRUGS:

A

● Bleeding

● Headache (Cilostazol and Dipyridamole)

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18
Q

Heparin USE

A

Acute treatment of DVTs,
pulmonary embolism,
Acute myocardial infarction

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19
Q

Heparin MOA

A

Binds to antithrombin 3 which is responsible for degrading several activated clotting factors like thrombin and factor 10a.

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20
Q

HEPARIN S/E

A

Bleeding
HIT
Allergic reactions Can treat excessive bleeding caused by heparin with protamine sulfate!

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21
Q

HEPARIN CONTRAINDICATIONS

A

Hypersensitivity
History of HIT
Active bleeding

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22
Q

NOACS:

Direct inhibitor thrombin:

A

DABIGATRAN

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23
Q

NOACS

Direct inhibitor of X

A

RIVAROXABAN

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24
Q

NOACS USE

A

Acute and chronic anticoagulation needs

Used instead of Warfarin in certain patients.

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25
Q

Heparin EXAMPLES

A

Enoxaparin
Dalteparin
Fondaparinux

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26
Q

DIRECT FACTOR X INHIBITORS

EXAMPLES

A

Apixaban-
Rivaroxaban-
Edoxaban-

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27
Q

Direct thrombin inhibitors: EXAMPLES

A

Bivalirudin
Argatroban
dabigatran

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28
Q

Heparin MOA

A

● Binds to natural anticoagulant called antithrombin III.
● Primary function of antithrombin is to inactivate factor Xa and thrombin.
● Drugs bind to antithrombin and accelerate its activity
● Heparin binds to factor Xa and thrombin and rapidly inactivated them
● Low molecular weight heparin finds it hard to inactivate thrombin hence it radipdly
inactivates factor Xa
● Fondaparinux also finds it hard to inactivate thrombin hence it radipdly inactivates factor
Xa
Side effect is bleeding, HIT(heparin induced thrombocytopenia), osteoporesis
● Bleeding is stopped by Protamine Sulfate (only for heparin) (binds with heparin and
forms stable inactive complex) (no antidote for fondaparinux)
● Clinical application: venous thrombosis, myocardial infarction

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29
Q

Direct Factor X Inhibitors MOA

Apixaban
Rivaroxaban
Edoxaban

A

Apixaban
● NOAC
Rivaroxaban
● NOAC
Edoxaban
● Binds to active site of factor Xa and prevents conversion of prothrombin to thrombin
● Available orally
● Clinical application: venous thrombosis, pulmonary embolism
● Adverse effect - bleeding (no antidote)

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30
Q

DIRECT THROMBIN INHIBITORS:

MOA

A

Directly inhibit thrombin, thereby interfering w/ intrinsic and extrinsic factors.

Humanized antibody fragment (Fab) designed as a specific reversal agent for the anticoagulant effect of dabigatran.
● Idarucizumab binds free and thrombin-bound dabigatran and neutralizes its activity.

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31
Q

DIRECT THROMBIN INHIBITORS:

Side effects:

A 
● Low blood potassium (hypokalemia)
● Delirium.
● Constipation.
● Fever.
● Pneumonia.
● Headache
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32
Q

Subclasses of direct thrombin inhibitors

A

a) univalent direct thrombin inhibitors

b) bivalent direct thrombin inhibitors

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33
Q

Univalent Direct Thrombin Inhibitors:

A

Binds only to the active site
● Drugs:argatroban,dabigatran(NOAC)
(Treatment for overdose of dabigatran - Idarucizumab)

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34
Q

Bivalent Direct Thrombin Inhibitors:

A

Binds to active site and exosite of thrombin
● Drugs:bivalirudin
● Advantage: Does Not join with factor IV and hence good for treatment of HIT(heparin induced thrombocytopenia)
Clinical application: HIT patients Adverse effect = bleeding

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35
Q

Warfarin is a

A

Vitamin K antagonist

36
Q

Warafrin is used in

A

Chronic anticoagulation in patients at risk for thromboembolic events

37
Q

Warfarin MOA

A

Vitamin K is needed for the synthesis of f
● Factors II (thrombin), VII, IX, X are inactive and by vitamin
K(reduced form of vitamin K)
● Vitamin K reduced is converted to Vitamin K epoxide in presence of oxygen and carbon
dioxide
● Hence fully active clotting factors
Vitamin K is needed for the synthesis of f
● Factors II (thrombin), VII, IX, X are inactive and by vitamin
K(reduced form of vitamin K)
● Vitamin K reduced is converted to Vitamin K epoxide in presence of oxygen and carbon
dioxide
● Hence fully active clotting factors

IN SUMMARY, Inhibits the synthesis of Vit. K dependent factors: 2, 7, 9, and 10 thus increasing bleeding

38
Q

Warfarin SE

A

Bleeding
Skin changes
Teratogen

39
Q

Warfarin Contraindication

A

Open wounds
Uncontrolled HTN
Active ulcer disease

40
Q

Clopidogrel
Ticagrelor
Prasugrel
Ticlopidine

USE

A

Treat acute coronary syndrome w/aspirin.

Prevent thrombosis Patients who can’t tolerate aspirin

41
Q

ABCIXIMAB (IV)
EPTIFIBATIDE
TIBROFIBIAN

USE

A

Acute coronary syndromes

42
Q

ABCIXIMAB (IV)
EPTIFIBATIDE
TIBROFIBIAN

MOA

A

Binds to glycoprotein 2b3a located on the surface of platelets, prevents fibrinogen from binding and crosslinking, thus hindering platelet aggregation

43
Q

ABCIXIMAB (IV)
EPTIFIBATIDE
TIBROFIBIAN

SE

A

Bleeding
Thrombocytopenia
Diffuse alveolar hemorrhage

44
Q

ABCIXIMAB (IV) EPTIFIBATIDE TIBROFIBIAN

Contraindications

A

Hypersensitivity Internal bleeding past 6 weeks

45
Q

Phosphodiesterase:

EXAMPLES

A

DIPYRIDAMOLE

CILOSTAZOL

46
Q

DIPYRIDAMOLE
CILOSTAZOL

USE

A

Treat claudication symptoms in patients with peripheral arterial disease.

47
Q

DIPYRIDAMOLE
CILOSTAZOL

MOA

A

Inhibits the enzyme cyclic AMP phosphodiesterase 3, an enzyme involved in breakdown of cAMP, so ↑cAMP → inhibits TxA2 synthesis and ↑prostacyclin production. Platelet aggregation is thus inhibited.

48
Q

DIPYRIDAMOLE
CILOSTAZOL

SEs

A

Headache
Palpitations
Gi upset

49
Q

DIPYRIDAMOLE
CILOSTAZOL

SE

A

Headache
Palpitations
Gi upset

50
Q

DIPYRIDAMOLE
CILOSTAZOL

contraindications

A

Congestive HF

51
Q

LMWH heparin:

EXAMPLES

A

ENOXAPARIN

DALTEPARIN

52
Q

ENOXAPARIN
DALTEPARIN

use

A

Acute treatment of DVTs
Pulmonary embolism
MI

53
Q

ENOXAPARIN
DALTEPARIN

MOA

A

Inactivates both 10 and 2a. They bind to natural anticoagulants circulating in blood - Antithrombin 3.
By binding they accelerate its activity.

54
Q

ENOXAPARIN
DALTEPARIN

SEs

A

Bleeding

HIT

55
Q

ENOXAPARIN

DALTEPARIN

A

Active major Gi bleed History of HIT within last 100 days.

56
Q

ACETAMINOPHEN
PARACETAMOL

USE

A

Antipyretic

Analgesic

57
Q

ACETAMINOPHEN
PARACETAMOL

MOA

A

BlocksCOX1&2 permanently, thus blocking TxA2 → bleeding

58
Q

ACETAMINOPHEN/ PARACETAMOL

S/Es

A

Fatal hepatotoxicity with overdose Treat paracetamol overdose with activated charcoal & acetylcysteine.

59
Q

ACETAMINOPHEN/ PARACETAMOL

Contraindication

A

Known hypersensitivity to NSAIDs Asthma

Rhinitis

60
Q

What is the first line treatment of MI in ED?

A

Aspirin

61
Q

How do we control warfarin levels

A

Using INR

62
Q

What is the normal INR range

A

2-3

63
Q

What is the antidote for heparin overdose

A

Protamine Sulfate

64
Q

How do we control heparin dose

A

By checking APTT levels, it should be 1.5-2.5

65
Q

What kind of block does aspirin have to cox 1

A

Ireversible

66
Q

What do medical professionals do in an aspirin overdose ?

A

Platelet infusion because aspirin effect last 7-12 days so we cannot wait

67
Q

What is the recommended aspirin level

A

300mg

68
Q

What is the MOA of heparin

A

Heparin catalyses the formation of antithrombin 3 which blocks factor 10 and 2

69
Q

What are the types of heparin?

A

Unfractioned (Huge Monoamers) - Used in hospitals.

Fractioned/Standard (Smaller)- Used at home ie LMWH

70
Q

What is the indication of use of heparin and warfarin

A

PE,
Pregnancy,
Immobilisation after surgery
Past covid patient (to reduce d-dimer and due to cytokine storm)

71
Q

What is heparin measured in?

A

Units are the safest dose

b/c they are many ways used by companies to process and produce heparin

72
Q

What is the anticoagulant of choice in pregnancy and why?

A

Heparin because it does not cross the placenta

73
Q

Four S/Es of Heparin

A
  1. Bleeding
  2. Thrombocytopenia/HIT
  3. Osteoporosis
  4. Necrosis at site of injection
74
Q

Antidote for heparin overdose

A

Protamine Sulfate

75
Q

List 2 Vitamin K antagonist

A

warfarin & Acenocrumorol

76
Q

List the Vitamin K dependent factors

A

2, 7, 9, 10

77
Q

Disadvantage of vitamin K antagonist

A

Metabolised via Cytochrome 450 therefore there are many interactions with drugs and food, it also stays in the body longer leading to an increased bleeding risk.

78
Q

What do we do in the case of a warfarin overdose

A

Give the patient vitamin k or in emergencies give then 2,7,9,10

79
Q

How long should we wait to se factors after Vit.k Administration

A

Up to 72 hours

80
Q

MOA of vitamin k antagonist

warfarin

A

Blocks enzyme vitamin k epoxide reductase which allows the reduced form of vitamin k to be recycled

81
Q

What class of drug is dabigatran and rivaroxoban

A

New oral anticoagulant

82
Q

MOA of Dabigatran

A

Inhibits thrombin —> No coagulation

83
Q

MOA of Rivaroxaban

A

Inhibits factor X—> No coagulation

84
Q

Should INR be checked?

A

In any case of bleeding

85
Q

Warfarin food and drug interactions

A

Alcohol
Aspirin
Fluoroquinolones
Grapefruit/ Fruit

86
Q

What things may affect the treatment of Vitamin K antagonists

A 
Wrong diet
Hepatocellular disorder
Viral Infection
Chronic alcoholism
Hepatic congestion
Increased catabolism of coagulation/ clotting factors
Hepatitis
87
Q

Describe the effect of cimetidine on Warfarin

A

Pharmacology (22 decks)

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