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Pharma From Sure Success > Anticoagulant Drugs > Flashcards

Anticoagulant Drugs Flashcards

1
Q

The clot does not extend beyond wound site into general circulation. Why?

A

Fibrin absorbs thrombin into the clot and inactivates it.

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2
Q

Natural Mechanisms to control blood clotting (4)

A
  1. PGI2: inhibit platelet aggregation
  2. ATIII: blocks factors 12,11,9,10,2
  3. Protein C: inactivates factor 5 and 8
  4. Heparan sulfate:
    synthesized by endothelial cells
    Enhance the activity of ATIII
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3
Q

Drugs given to
1. Prevent thrombus
2. Rx thrombus
3. Delay resolution of thrombus

A
  1. Anticoagulants, anti platelets
  2. Fibrinolytics
  3. Anti fibrinolytics.
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4
Q

How does the body maintain hemostasis?

A

After few mins bleeding stops
1. Vasoconstriction
2. Formation of primary plug-platelet adhesion, activation,aggregation
3. Formation of secondary plug
Platelets + fibrin = clot
4. Dissolve plasmin

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5
Q

Natural coagulant and anticoagulants

A

Coagulant: vit K , factor 1-12
Anticoagulants :
AT3
ATP
Protein C
Protein S
Plasminogen

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6
Q

At which step does bleeding stop?
Test for any abnormality

A

Primary plug

Bleeding time: tests for platelet count and quality
Normal: 2-9 mins

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7
Q

Normal BT,APTT,PT,TT values

A

BT: 2-9mins
APTT: 28- 35 secs
PT: 11-13 secs
TT: 15 -20 secs

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8
Q

How is testing for BT,PT,APTT , TT done ?

A

BT: take a filter paper, needle prick , and see the time blood clots.

PT: take blood in test tube , centrifuge it, separates the plasma-> add tissue thromboplastin + ca2+——> clot.

APTT: take blood in test tube, centrifuge it, separates the plasma—> add kaolin + ca2+ ———> clot

TT: fibrinogen——> fibrin
Activated by factor 2.
Used for fibrinogen deficiency

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9
Q

Steps to primary homestasis

A

Injury, exposes VWF and collagen, platelet adhesion, activation of secretary granules (ADP, TXA2) ,platelet aggregation and clot.

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10
Q

Steps to secondary homestasis

A

Tissue factor is exposed to injury , activates intrinsic (factor 12) and extrinsic clotting factors (factor7) and cause clot.

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11
Q

Causes of high INR (3)

A
  1. Anticoagulants-warfarin
  2. Decreased synthesis of clotting factor : CLD,
    vit K def: malnutrition,malabsorption,antibiotic
  3. Increased consumption of clotting factor : sepsis,DIC
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12
Q

Heparin consists of …….units

A

Polymer consisting of 2 sulfated dissarcharide units.
D-glucosamine-L-iduronic acid
D-glucosamine-D-glucoronic acid

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13
Q

Heparin is naturally occuring in …..
Synthetic ones are produced from ….

A

Mast cells
Ox lung and pig intestine mucosa

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14
Q

MOA of unfractionated heparin

A
  1. Provides scaffolding of AT 3 to factor 2,10.
  2. Provides confirmational change to AT 3.
    For Xa inhibition: only the above is needed
    For factor 2a inhibition: both are required.

AT3 + heparin —> inhibit intrinsic factor by binding and inactivating them.

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15
Q

Difference between unfractionated heparin , LMWH, Fondaparinox in terms of:
1. Nature
2. MOA
3. t1/2

A
  1. Heteropolysaccharides: UFH,LMWH
    Pentazaccharide : Fondaparinox
  2. UFH: inhibit both 10a, 2a
    LMWH, Fondaparinox: only 10a,
  3. UFH : 2hrs
    LMWH: 4 hrs
    Fondaparinox: 17hrs
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16
Q

Difference between UFH,LMWH,Fp in terms of:
1. Bioavailability
2. Response
3 . monitoring
4. S/e HIT,TCP

A
  1. UFH: 30%, LMWH: 90%, FP: 100%
  2. UFH: variable
    LMWH, FP: predictable
  3. UFH: APTT
    LMWH, FP: no monitoring
  4. More for UFH
    less for LMWH,Fp
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17
Q

Egs of direct thrombin inhibitors
Parenteral, oral

A

Parenteral:
lepirudin,Bivalirudin , argatroban

Oral:
Dabigatran

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18
Q

Monitoring for parenteral anticoagulants required for ….

A

UFH, direct thrombin inhibitors (parenteral)

LMWH,oral direct thrombin and factor 10a inhibitors don’t need monitoring

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19
Q

Dabigatran is a prodrug.T or F
Antidote for dabigatran associated bleeding

A

True:
Dabigatran etoxilote—-> dabigatran

Idarucizumab

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20
Q

S/e of direct thrombin inhibitor (2)

A

Hemorrhage
Hypotension

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21
Q

Direct factor Xa inhibitors
MOA

A

Rivaroxaban and all xabans
Reversible
Oral
Xa
Inhibitor

Inhibit both free and plasma Factor Xa attached to prothrombin complex

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22
Q

Antidote of direct factor Xa inhibitors

A

Andexanet alfa

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23
Q

MOA of Fondaparinox
C/I

A

Oral indirect factor Xa inhibitor without activity against thrombin.

Renal failure

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24
Q

Advantages of rivaroxaban (3)

A
  1. No lag time, rapid action
  2. No lab monitoring of PT,APTT
  3. Efficacy similar to LMWH+ warfarin
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25
Q

Why is LMWH given s/c?
Benefit of LMWH

A

Due to better bioavailability by this route.
2-4 longer t1/2, hence once daily dosing is required.

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26
Q

Types of VitK

A

K1: from plants- phytonadione
K2: from bacteria: menaquinone
K3: synthetic: menadione

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27
Q

T1/2 of Vit K
T1/2 of warfarin

MOA of VitK

A

72 hours
36 hours

Factor 2,7,9,10 is glutamate chains —> gamma carboxylation —> active factor 2,7,9,10.
Vit K is cofactor.
It gets inactivated in the process by enzyme Vit K Epoxide reductase.

Warfarin-inactivates VitKER

28
Q

A/e of Vit K

A

Menadione- hemolysis ; so C/I in G6PD and neonates.

Menadione competitively inhibits glucoronidation of bilirubin —> displaces bilirubin—> kernicterus

29
Q

Sequence fall of various factors with warfarin action.

A

Factor 7: 6 hrs
Factor9: 24 hrs
Factor 10: 40 hrs
Factor 2: 60 hrs

30
Q

Longest and shortest acting warfarin

A

Longest: dicumarol -bishydoxycaumarin
Shortest: ethylbiscoumaacetate

31
Q

Dosage of heparin in iv and sc

A

Iv:
5000-10000 U bolus —-> continues infusion @750 -1000U/hr

S/c:
5000 Unit S/C every 8-12 hrs

32
Q

Uses of VitK (3)

A
  1. Defiency states :
    CLD
    Obstructive jaundice
    Prolonged Ab
    Malabsorption syndrome
    Dietary deficiency
  2. Hemorrhagic disease of new born
    1mg VitK is given IM at time of delivery
  3. overdose of oral anticoagulants
33
Q

Structure of heparin vs warfarin.

A

Heparin: large, anionic, acidic polymer
Warfarin: small lipid soluble molecule

34
Q

IM route is not given for heparin. Why?

Site of action of heparin vs warfarin

A

Hematoma

Heparin: blood
Warfarin: liver

35
Q

Inhibit coagulation of heparin vs warfarin

A

Heparin : both in vivo and vitro
Warfarin: only in vivo

36
Q

Rx for acute overdose of heparin vs warfarin

A

Heparin : protamine sulfate
Warfarin : bleeding:
prothrombin complex /FFP
Stable: Vit K

37
Q

Monitoring of heparin vs warfarin

A

Heparin : APTT
Warfarin: PT/INR

38
Q

Chemistry of heparin vs warfarin

A

Heparin : mucopokysaccharide
Warfarin: coumarin

39
Q

Source of heparin vs warfarin

A

Heparin : hog liver, pig intestine
Warfarin : synthetic

40
Q

Heparin causes ……renal problem
Long term use of heparin causes ….

Calciphylaxis seen with …..

A

Type 4 RTA

Osteoporosis

Warfarin

41
Q

Warfarin was initially marketed as …

C/I of warfarin (7)

A

Rat poison
C/I
1. Bleeding
2. HIT
3. Severe HTN- increased risk of cerebral hge, threatened abortion, piles,GI ulcer

  1. SABE
  2. Chronic alcoholics, cirrhosis,renal failure
  3. Aspirin and other plt products
  4. Pregnancy
42
Q

Interactions of warfarin (5)

A
  1. Enzyme inhibitors - increase action
  2. Broad spectrum Ab
  3. Aspirin
  4. Long acting sulfonamide, indomethacin,
    phenytoin,, probenecid
  5. Liquid paraffin
43
Q

Define Glansmann thrombasthenia
Defect is in ……

A

AR
Defect in Gp 2b/3a
Defect in platelet aggregation

44
Q

Define Bernard soulier syndrome
Defect is in…..

A

AR
Defect in Gp 1b/2a
Defect in platelet adhesion

45
Q

Function of Gp 2b3a
Eg of gp 2b3a antagonist
Use.
Which one is given iv?

A

Causes fibrogen to bind to the receptor —> platelet aggregation

Mab- abciximab

For percutaneous angioplasty
Tirofiban.

46
Q

S/e of gp 2b 3a antagonist

A
  1. Bleeding —> rx: platelet infusion
  2. Thrombotic TCP
47
Q

Side effects of gp 2b3a antagonists (3)

A

Nausea
Back pain
Hypotension

48
Q

Classification of ADP receptor antagonist

A

Irreversible inhibitors of P2Y12:
Ticlopidine
Clopidogrel
Prasugrel

Reversible inhibitor of P2Y12:
Ticagrelor
Cangrelor

49
Q

S/e of ticlopidine

A

BMS- TCP/neutropenia

50
Q

S/e of clopidogrel

A

Requires CYP2C19 to activate it.
This enzyme is acted upon by PPI,especially omeprazole, lansoprazole —> failure of clopidogrel.

Those that have least action on CYP2C19: pantoprazole
Rabiprazole

51
Q

Prazugrel is also a …..
S/e

A

Prodrug
Increases bleeding —> c/i in stroke

52
Q

Which of the reversible P2Y12 inhibitor is given iv?
Action.

A

Cangrelor
Fastest -5-10mins

53
Q

Action of ticagrelor

MOA of vorapaxar
S/e

A

2hrs

Platelet PAR-1 antagonist
Inhibits thrombin mediates aggregation

Similar to prasugrel-c/I in stroke

54
Q

What are the ADP receptor antagonist?

A

ADP + P2Y12–> inhibit adenylate Cyclase—> decrease CAMP—-> change in gp2b 3a to go to the surface and cause aggregation.

55
Q

MOA of PDE inhibitors
Eg

A

Increase CAMP
Dipyridamole, cilostazole
adenosine reuptake inhibitor

56
Q

S/e of dipyridamole

S/e of cilostazole
Use.

A

Coronary steal syndrome

Do not give in heart failure - Milrinone like action-increase mortality.

Antiplatelet+ vasodilators action - used for intermittent claudication.

57
Q

Use of pentoxiphylline

A

Improve flexibility of RBC, use for intermittent Claudication- beurger’s ds

58
Q

Thromboxane A2 synthase inhibitor ….
Aspirin inhibits ….

A

Dazoxiban

COX , which inhibits PGI2, TXA2.

59
Q

Drug of choice for arterial vs venous thrombus

A

Arterial: MI/ stroke :
Antiplatelet drugs work better as thrombus in artery is rich in platelets.

Venous : DVT/P.E
Anticoagulant-warfarin

60
Q

What is Reye’s syndrome?

A

When a child recovering from viral ds is ( influenza / chicken pox) is given aspirin , can cause liver failure and encephalopathy .

61
Q

Egs of fibrinolytics
MOA

A

Streptokinase, urokinase,TPA, reteplase.

Directly/indirectly convert plasminogen/plasmin- which cleaves thrombin and fibrin clots.

62
Q

Labs for thrombolytics
Which thrombi works better with fibrinolytics ?

A

Increase PT,APTT no change in platelet count.

Venous thrombi lysed better, recent thrombi <3 days.

63
Q

Clinical indications of fibrinolytics (2)

A

Early MI
Early ischemic stroke

64
Q

Adverse effects of thrombolytics?

A

Bleeding - c/I in active bleeding , recent surgery, IC bleeds, severe HTN.

65
Q

MOA of antifibrinolytics

A

Inhibit plasminogen activation and dissolution of clot .
Inhibit fibrinolysis associated bleeding

66
Q

Most potent antifibrinolytic use . (4)

A

Tranexaminic acid
Prevent /control excess bleeding due to:
1. Fibrinolytic drugs
2. Tonsillectomy/tooth extraction in hemophilics
3. Menorrhagia
4. Recurrent epistaxis, hyphema-due to ocular trauma,peptic ulcer etc.

Pharma From Sure Success (10 decks)

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