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Blood : Oral Anticoagulants Flashcards

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1
Q

What type of anticoagulants are coumarin anticoagulants?

A

Vitamin K antagonists

Coumarin anticoagulants, such as warfarin, inhibit the action of vitamin K.

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2
Q

What is the bioavailability of coumarin anticoagulants?

A

100% bioavailability

This means that the entire dose reaches systemic circulation when administered orally.

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3
Q

How are coumarin anticoagulants metabolized?

A

Metabolized by the liver

They are converted into inactive metabolites that are excreted in urine and stool.

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4
Q

Do coumarin anticoagulants cross the placental barrier?

A

Yes, they pass the placental barrier but are not secreted in breast milk

This has implications for use during pregnancy and lactation.

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5
Q

What is the onset of action for coumarin anticoagulants?

A

Delayed onset of 1-2 days

This delay is due to the time required for the clearance of previously synthesized clotting factors.

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6
Q

What is the duration of action for coumarin anticoagulants?

A

About 4-7 days with a half-life of 40 hours

This indicates how long the drug remains active in the body.

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7
Q

What is the initial dose of warfarin?

A

5-10 mg for 1 week until reaching the target INR

This initial dosing is crucial for achieving therapeutic anticoagulation.

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8
Q

What is the maintenance dose of warfarin?

A

5-7 mg/day, adjusted to maintain the target INR

Regular monitoring is essential to ensure safety and efficacy.

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9
Q

What is the prothrombin time (PT) target when using coumarin anticoagulants?

A

PT prolonged to 2-2.5 times the normal which is 12-15 seconds

This indicates the level of anticoagulation achieved.

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10
Q

What is the active form of vitamin K and its role?

A

Active vitamin K is essential for activation of coagulation factors II, VII, IX, and X, and anticoagulant proteins C and S

A decrease in vitamin K leads to failure to activate these coagulation factors.

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11
Q

What should be done at the start of treatment with warfarin?

A

Heparin + oral anticoagulant should be started at the same time

Heparin is typically stopped after 4-5 days when INR levels are appropriate.

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12
Q

What is the action of warfarin in vivo?

A

Anticoagulant only

Warfarin does not have anticoagulant effects outside of the body.

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13
Q

What does warfarin prevent in terms of vitamin K metabolism?

A

Warfarin prevents reductive metabolism of inactive vitamin K epoxide back to active vitamin K

This inhibition is key to its anticoagulant effect.

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14
Q

What does INR stand for?

A

International Normalized Ratio

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15
Q

What is the formula for calculating INR?

A

PT of patient / PT of control

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16
Q

What is the normal range for INR?

A

1

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17
Q

What is the target INR range for most patients?

A

2-3

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18
Q

What should be done in case of overdose or high INR?

A

Stop the drug

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19
Q

What is the recommended dose of Vitamin K1 for treating high INR?

A

50 mg IV

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20
Q

What are some treatments for high INR?

A
  • Fresh frozen plasma
  • Prothrombin complex concentrates
  • Factor II, VII, IX, and X concentrate
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21
Q

What are the uses of anticoagulants like Warfarin?

A
  • Treatment of deep vein thrombosis
  • Treatment of myocardial infarction
  • Prophylaxis of postoperative deep venous thrombosis
  • Prophylaxis of pulmonary embolism
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22
Q

What are common side effects of Warfarin?

A
  • Hemorrhage
  • Hypersensitivity
  • Skin rash
  • Skin necrosis (rare)
  • Gut upset: anorexia, nausea, vomiting
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23
Q

What is a significant teratogenic effect of Warfarin?

A

FDA category X

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24
Q

What does FDA category X imply for Warfarin?

A

Fetal abnormalities and/or positive evidence of human fetal risk

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25
What type of food decreases the effect of Warfarin?
Foods rich in vitamin K
26
Give examples of foods rich in vitamin K.
* Lettuce * Spinach * Broccoli
27
True or False: Warfarin is effective in preventing arterial thrombosis.
False
28
What algorithms are available for managing high INR?
Algorithms define the order of use of treatments according to INR value and bleeding severity
29
What is one of the side effects associated with Warfarin related to the skin?
Skin necrosis (rare)
30
Fill in the blank: The primary treatment for deep vein thrombosis is _______.
[anticoagulants]
31
What factors increase the effect of warfarin, leading to bleeding?
* Reduction of vitamin K production by broad-spectrum antimicrobials * Reduction of vitamin K absorption by liquid paraffin * Displacement from plasma protein binding sites by indomethacin, sulphonamides * Decrease in plasma protein available for binding oral anticoagulant due to liver diseases * Hereditary disease altering activation of vitamin K * NSAIDs like phenylbutazone augment hypoprothrombinemia and decrease platelet aggregation * Enzyme inhibitors such as cimetidine, chloramphenicol, allopurinol inhibit metabolism of warfarin * Aspirin in large doses synergizes anticoagulants by affecting platelet function * Third-generation cephalosporins have an anti-vitamin K effect * Hyperthyroidism due to increased turnover of clotting factors ## Footnote Vitamin K is produced by intestinal bacteria, and antibiotics can disrupt this production.
32
What factors decrease the effects of warfarin?
* Cholestyramine binds to warfarin in the gut, reducing absorption * Enzyme induction by barbiturates, rifampicin, griseofulvin * Increased clotting factors by estrogen * Diuretics decrease effects of warfarin by increasing clotting factor concentration * Hypothyroidism due to decreased turnover of clotting factors ## Footnote These interactions can significantly impact the therapeutic effectiveness of warfarin.
33
What are the contraindications for warfarin?
* Hypersensitivity to the drug * Bleeding disorders (hemophilia, intracranial hemorrhage, threatened abortion) * Liver and kidney disease * Surgery of the brain, eye, or spinal cord * Diseases with increased bleeding liability (subacute bacterial endocarditis, active TB, gut ulcerations, hypertension) * Pregnancy ## Footnote These contraindications are critical for ensuring patient safety when prescribing warfarin.
34
What are Direct Oral Anticoagulants (DOACs)?
Oral Direct thrombin inhibitors and Oral Direct Factor Xa inhibitors ## Footnote DOACs are a newer class of anticoagulants with specific mechanisms of action.
35
What are the advantages of DOACs?
* Predictable pharmacokinetics and bioavailability * Routine coagulation monitoring unnecessary * Less frequent follow-up required * Fixed dosing * Faster onset and offset of action * Fewer drug and food interactions ## Footnote These advantages make DOACs a preferred choice in many clinical settings.
36
Dabigatran - thrombin inhibitor
Oral capsule Dabigatran etexiate, mesylateis (prodru) governed to dabigatran
37
Stroke and systemic embolism in non valvular AF
Dabigatran
38
Venous thromboembolism after hip or knee replacement surgeries
Dabigatran
39
Potentiate dabigatran
Ketoconazole Amiodarone Quinidine Clopidogrel
40
Dabigatran may require dose adjustment with renal impairment Prolongs aPTT and thrombin like others
As its clearance is prolonged
41
Antidote of dabigatran
Idarucuzimab Specific Life threatening or uncontrolled bleeding Rapid reversal needed for urgent and emergent procedure
42
Oral factor 10 inhibitors
Rivar and Ed oxaban Api and betri xaban
43
Inhibit the final common pathway of clotting
Oral factor 10 ihibitors
44
Embolic stroke with patients with AF
Oral 10 inhibitors
45
Oral 10 inhibitors
Affects by renal and hepatic dysfunction
46
10 inhibitor antidote
Andexanetalfa (2018) Modified recombinant factor 10 derivative As a decoy receptor so f10i binds to it rather than the actual f10a as it has higher affinity
47
Coagulants
In hemorrhagic states Fresh whole blood is the best - immediate
48
Astringents act as local hemostatics by
Precipitating blood proteins at the site of bleeding Tannic acid and alum
49
Local hemostatics are either
Active or passive
50
Local hemostatic
VCs - local adrenaline
51
Passive hemostatics
Lattice like matrix Adheres to bleeding site Activates extrinsic clotting pathway Basic platform for platelets to aggregate and form a clot
52
Topical passive hemostatics
Collagen Cellulose Gelatins Polysaccharide spheres
53
Active hemostatics - thrombin
Biological activity Directly participate jn coagulation cascade Induce clot formation
54
Newer hemostatics
Chitosan based products Polysaccharide based hemostats Poly N acetyl glucosamine based Inorganic QuikClot
55
Systemic hemostatics
Vit K Fresh blood Fresh frozen plasma Dried plasma Vit C Protamine sulphate as an antidote to heparin overdose Antihemophilic globulin 4 Human fibrinogen concentrate
56
Special systemics
Cryoprecipitate - get from whole blood for patients with 8 and vWf deficiency plus abnormalities of fibrinogen Desmopressin acetate (IV SC INasal or oral) - get from ADH and releases 8 and vWf from endothelium
57
Sclerosing agents
VaricoSe veins for permanent obliteration -Sodium morrhuate - Sodium Tetracycline sulfate -Polidocanol
58
Vit K on food
K1 - phylloquinone
59
Human tissue intestine
Vit. K2 - Menaquinone
60
Vit Ks
Require bile salts for absorption in intestine
61
Synthetic vit K3
Manaquinone - needs to be converted to menaquinone 4 to be active
62
Co factor for carboxylation of glutamic acid residues in vit. K dependent proteins
Vit K Bone coagulation and metabolism Prevention of vessel mineralisation Regulation of various cellular functions
63
Give vit K to babies
To prevent hemorrhagic diseases as they don't have developed intestinal flora
64
Vit k uses- in vit k deficiency
Inadequate intake or absorption- bike acid sequestration (hide bike acids so not available for vit k absorption) Warfarin Antimicrobials like cephalosporins Hypoprothrombinemia

Pharmacology (27 decks)

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