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Anticoagulant Drugs Flashcards

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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
Why is LMWH given s/c? Benefit of LMWH
Due to better bioavailability by this route. 2-4 longer t1/2, hence once daily dosing is required.
26
Types of VitK
K1: from plants- phytonadione K2: from bacteria: menaquinone K3: synthetic: menadione
27
T1/2 of Vit K T1/2 of warfarin MOA of VitK
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
A/e of Vit K
Menadione- hemolysis ; so C/I in G6PD and neonates. Menadione competitively inhibits glucoronidation of bilirubin —> displaces bilirubin—> kernicterus
29
Sequence fall of various factors with warfarin action.
Factor 7: 6 hrs Factor9: 24 hrs Factor 10: 40 hrs Factor 2: 60 hrs
30
Longest and shortest acting warfarin
Longest: dicumarol -bishydoxycaumarin Shortest: ethylbiscoumaacetate
31
Dosage of heparin in iv and sc
Iv: 5000-10000 U bolus —-> continues infusion @750 -1000U/hr S/c: 5000 Unit S/C every 8-12 hrs
32
Uses of VitK (3)
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
Structure of heparin vs warfarin.
Heparin: large, anionic, acidic polymer Warfarin: small lipid soluble molecule
34
IM route is not given for heparin. Why? Site of action of heparin vs warfarin
Hematoma Heparin: blood Warfarin: liver
35
Inhibit coagulation of heparin vs warfarin
Heparin : both in vivo and vitro Warfarin: only in vivo
36
Rx for acute overdose of heparin vs warfarin
Heparin : protamine sulfate Warfarin : bleeding: prothrombin complex /FFP Stable: Vit K
37
Monitoring of heparin vs warfarin
Heparin : APTT Warfarin: PT/INR
38
Chemistry of heparin vs warfarin
Heparin : mucopokysaccharide Warfarin: coumarin
39
Source of heparin vs warfarin
Heparin : hog liver, pig intestine Warfarin : synthetic
40
Heparin causes ……renal problem Long term use of heparin causes …. Calciphylaxis seen with …..
Type 4 RTA Osteoporosis Warfarin
41
Warfarin was initially marketed as … C/I of warfarin (7)
Rat poison C/I 1. Bleeding 2. HIT 3. Severe HTN- increased risk of cerebral hge, threatened abortion, piles,GI ulcer 4. SABE 5. Chronic alcoholics, cirrhosis,renal failure 6. Aspirin and other plt products 7. Pregnancy
42
Interactions of warfarin (5)
1. Enzyme inhibitors - increase action 2. Broad spectrum Ab 3. Aspirin 4. Long acting sulfonamide, indomethacin, phenytoin,, probenecid 5. Liquid paraffin
43
Define Glansmann thrombasthenia Defect is in ……
AR Defect in Gp 2b/3a Defect in platelet aggregation
44
Define Bernard soulier syndrome Defect is in…..
AR Defect in Gp 1b/2a Defect in platelet adhesion
45
Function of Gp 2b3a Eg of gp 2b3a antagonist Use. Which one is given iv?
Causes fibrogen to bind to the receptor —> platelet aggregation Mab- abciximab For percutaneous angioplasty Tirofiban.
46
S/e of gp 2b 3a antagonist
1. Bleeding —> rx: platelet infusion 2. Thrombotic TCP
47
Side effects of gp 2b3a antagonists (3)
Nausea Back pain Hypotension
48
Classification of ADP receptor antagonist
Irreversible inhibitors of P2Y12: Ticlopidine Clopidogrel Prasugrel Reversible inhibitor of P2Y12: Ticagrelor Cangrelor
49
S/e of ticlopidine
BMS- TCP/neutropenia
50
S/e of clopidogrel
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
Prazugrel is also a ….. S/e
Prodrug Increases bleeding —> c/i in stroke
52
Which of the reversible P2Y12 inhibitor is given iv? Action.
Cangrelor Fastest -5-10mins
53
Action of ticagrelor MOA of vorapaxar S/e
2hrs Platelet PAR-1 antagonist Inhibits thrombin mediates aggregation Similar to prasugrel-c/I in stroke
54
What are the ADP receptor antagonist?
ADP + P2Y12–> inhibit adenylate Cyclase—> decrease CAMP—-> change in gp2b 3a to go to the surface and cause aggregation.
55
MOA of PDE inhibitors Eg
Increase CAMP Dipyridamole, cilostazole adenosine reuptake inhibitor
56
S/e of dipyridamole S/e of cilostazole Use.
Coronary steal syndrome Do not give in heart failure - Milrinone like action-increase mortality. Antiplatelet+ vasodilators action - used for intermittent claudication.
57
Use of pentoxiphylline
Improve flexibility of RBC, use for intermittent Claudication- beurger’s ds
58
Thromboxane A2 synthase inhibitor …. Aspirin inhibits ….
Dazoxiban COX , which inhibits PGI2, TXA2.
59
Drug of choice for arterial vs venous thrombus
Arterial: MI/ stroke : Antiplatelet drugs work better as thrombus in artery is rich in platelets. Venous : DVT/P.E Anticoagulant-warfarin
60
What is Reye’s syndrome?
When a child recovering from viral ds is ( influenza / chicken pox) is given aspirin , can cause liver failure and encephalopathy .
61
Egs of fibrinolytics MOA
Streptokinase, urokinase,TPA, reteplase. Directly/indirectly convert plasminogen/plasmin- which cleaves thrombin and fibrin clots.
62
Labs for thrombolytics Which thrombi works better with fibrinolytics ?
Increase PT,APTT no change in platelet count. Venous thrombi lysed better, recent thrombi <3 days.
63
Clinical indications of fibrinolytics (2)
Early MI Early ischemic stroke
64
Adverse effects of thrombolytics?
Bleeding - c/I in active bleeding , recent surgery, IC bleeds, severe HTN.
65
MOA of antifibrinolytics
Inhibit plasminogen activation and dissolution of clot . Inhibit fibrinolysis associated bleeding
66
Most potent antifibrinolytic use . (4)
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.

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