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Pharma > Coagulation > Flashcards

Coagulation Flashcards

1
Q

What are COX inhibitors?

A

Include aspirin

  1. In platelets:
    * acetylates serine residues the COX-1 enzyme
  • irreversible inactivation
  • —> ⬇️ TxA2
  1. In endothelial cells:
    * inhibit COX levels
  • doesn’t affect PGI2 production except in ⬆️ doses —> by ⬆️ it
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2
Q

What does is eff for aspirin?

A

Effective as antiplatelet agent at low dose of 80 mg.

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3
Q

What are the indications of aspirin use?

A
  1. T of acute coronary syndromes, ischemic stroke, and transient ischemic attack
  2. 1ry P of chronic CAD
  3. P of arterial thrombosis in AF patients
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4
Q

What are the AE of aspirin?

A
  1. GI irritation
  2. Bleeding
  3. Airway hyper-reactivity
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5
Q

What are PDE inhibitors ?

A

Include Dipyridamole

  • prevent cAMP breakdown by PDE ( phosphodiesterase ) —> PKA activation and ⬇️ platlets aggregation
  • cAMP levels are regulated by
    1. TxA2 —> ⬇️cAMP
    2. PGI2 —> ⬆️cAMP
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6
Q

What are indications of PDE inhibitors?

A
  1. P of thromboembolism in patients with cardiac valve in comb with aspirin or warfarin bcz they ⬆️ it’s potency
  2. D of CAD —> stress ECG test
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7
Q

What are the AE of dipyridamole?

A
  1. GI distubance
  2. Headache bcz of its vasodilator effects
  3. Induction of angina in CAD
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8
Q

What are ADP antagonists?

A

Include

  1. Clopidogrel
  2. Prasugrel
  3. Ticlopedine
  4. Ticogrelor
  5. Cangrelor
  • irreversible ( like aspirin ) inhibitors of P2Y1 & P2Y12 ( ADP receptors ) —> ⬆️cAMP levels —> 🚫 of platelet aggregation
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9
Q

Why is clopidogrel proffered to ticlopidine ?

A
  1. Rapid onset of action
  2. More potent
  3. superior dosing profile
  4. ⬆️ safety
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10
Q

Why are ticogrelor and prasugrel preferred to ticlopidine and clopidogrel?

A
  1. More rapid onset of action
  2. ⬆️ inhibition
  3. More predictable 🚫 of ADP-induced platelet aggregation
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11
Q

Win acute coronary syndrome, which ADP antagonist have ⬆️ reduction of CV death, MI, and stroke ?

A

Ticogrelor

Prasugrel have similar reduction but at ⬆️ rates of bleeding and death—> contraindicated in TIA or stroke

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12
Q

What are the indications of ADP antagonists?

A

P of
1. Arterial thromboembolism in patients w/:
A. ACS: unstable angina and MI
B. history of ischemic stroke or transient ischemic attack

  1. Coronary stent thrombosis after PCI
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13
Q

What are the AE of ADP Antagonists?

A
  1. GI disturbance
  2. rash
  3. bleeding
  4. neutropenia
    Mainly TICLOPIDINE
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14
Q

What are Gb 2b/3a receptor antagonists?

A

They include:

  1. Eptifibatide
  2. Tirofiban
  3. Abciximab
  • prevent fibrinogen interaction with Gb2b/3a and bridging of platlets to one another
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15
Q

What are the signaling molecules that induce Gb2b/3a expression?

A 
TxA2
ADP
epinephrine
thrombin
collagen
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16
Q

What are the indications of Gb2b/3a receptor antagonists

A

T of unstable angina and MI undergoing medical T or PCI —> favor Abciximab

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17
Q

What are the AE of Gb2b/3a receptor antagonists ?

A

Bleeding
allergic reactions
thrombocytopenia

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18
Q

What are PAR-1 ( protease activated receptor 1 ) antagonist ?

A

Include vorapaxar

  • Inhibit PAR-1, the major thrombin receptor on platelets —> inhibit platelet activation and aggregation
  • orally
  • slowly eliminated t1/2 is 200 hrs
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19
Q

What are the indications of PAR-1 antagonist?

A
  1. 2ry P of MI
  2. P of stroke
  3. Prop of thrombosis in patients with previous MI or PAD
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20
Q

What are the AE of PAR-1?

A

Intracranial bleeding

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21
Q

What are the INDIRECT thrombin inhibitors?

A

Include heparin and fondaparinux

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22
Q

What is heparin?

A

sulfated mucopolysaccharide

Have 2 categories:
1. UnF-heparin ( 5-30 kDa )
2.LMWT heparin (1-5 kDa )ex: dalteparin / enoxaparin / tinzaparin / ardeparin
—> have ⬆️⬆️ therapeutic index

  • Act as a catalyst for the binding of antithrombin III (AT-III) to thrombin or factors IXa, Xa, XIa, and XIIa ( 9,10,11,12 )
  • LMWH heparins catalyze the inactivation of factor Xa by AT-III, but are less efficient in catalyzing the inactivation of thrombin ( are thought to bind only to antithrombin III (ATIII) and not to thrombin )
  • Unfractionated heparins can catalyze the inactivation of factor Xa and thrombin by AT-III.
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23
Q

How can we administer UnF+heparin and LMWT heparin?

A

Subcutaneously or intravenously and in small doses

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24
Q

What are the indications of heparin use?

A
  1. Prop & T of DVT & PE
  2. Unstable angina
  3. MI
  4. prop of CA thrombosis in PCI
25
Q

What are the AE of heparin?

A
  1. Bleeding

2. Heparin-induced thrombocytopenia

26
Q

How can we treat heparin toxcity ?

A

By protamine sulfate

27
Q

How can we Monitor heparin ?

A

Using activated partial thromboplastin time ( aPTT ) if exceeded this means that you are giving too much heparin

28
Q

What is foundaparinux?

A

pentasaccharides that is a replica of the AT III binding area of the heparin compound

* Binds AT III allowing increased affinity to bind factor Xa and 🚫 its
function —> ⬇️ thrombin generation.

*Does not affect platelet function & or react with heparin platelet factor 4
antibodies, thus potentially eliminating the risk of HIT.

29
Q

What are the indication s for fondaparinux use?

A

Prop of DVT & PE

30
Q

What are the AE of Fonda?

A

Bleeding

31
Q

How to monitor Fonda?

A

Prothrombin time assay

32
Q

What are the DIRECT factor Xa inhibitors?

A

Include :

Rivaroxaban
apixaban
edoxaban

ORAAAAAAL anti-C

  • selectively and potently inhibit coagulation factor Xa (both free and bound forms)
  • rapid ion set of action and shorter t1/2 than WARFARIN
33
Q

What are the indication for direct factor Xa inhibitor?

A
  1. Prop & T of DVT & PE

2. PROP of stroke

34
Q

How do we monitor direct factor 10 inhibitor ?

A

Doesn’t require monitoring

35
Q

What is the AE of factor 10 🚫?

A

Bleeding

36
Q

How to overcome toxicity of factor 10 inhibitor ?

A

effects are not easily reversed for all drugs.

However, recombinant coagulation factor Xa (Andexxa) is approved as an antidote for patients treated with rivaroxaban or apixaban to control life-threatening or uncontrolled bleeding

To remember - factor Xa so andexxa ( all xxxx 💀 )

37
Q

Who are the patients that can’t take factor 10 inhibitors

A

Pregnant women

CrCl < 30 ml/min

Hepatic impairment

38
Q

What are the oral anti-C available?

A
  1. Direct factor 10 inhibitors including: rivaroxaban, apixaban, and endoxaban
  2. Warfarin
39
Q

What is the MoA of warfarin?

A

Competitive antagonist for the reductase enzyme which converts the oxidized form of Vitamin K to its reduced form —> imp for factors 2, 7, 9, & 10

For immediate anti-C effect —> heparin given 1st few days —> then warfarin started

40
Q

What is the indication for warfarin?

A
  1. Prop & T of DVT & PE

2. P of sys thrombosis if intolerant to aspirin

41
Q

What does the reduced form of vit K do?

A
  1. Transform glutamate in the clotting factors to Gama-carbonyl glutamate
  2. Interaction with Ca+2
  3. Active clotting factors in the coagulation cascade
42
Q

How is warfarin absorbed?

A. After oral dose

B. During lactation

C. Existing Gazma-carboxylated factors

A

A. Complete and rapid abs

B. Crosses the placenta and appears in milk

C. Slow onset of action ( after 48 hrs ) bcz its the degradation time of the Gazma-carboxylated factors: factor 7 ( T1/2 —> 6 ) hrs & factor 10 ( T1/2 —> 60 hrs )

43
Q

How can we monitor warfarin ?

A

Prothrombin time assay as INR —> dose adjusted to keep INR 2-4

44
Q

How to reverse warfarin action ?

A
  1. Cessation of the drug
  2. Administration of oral or parenteral vit K
  3. Fresh plasma
45
Q

What are the AE Oof warfarin?

A

Hemorrhage that lead to:

  1. Hematoma
  2. Anemia
46
Q

How is awarfarin metabolized?

A

Hepatic CYP450

47
Q

What ⬆️ & ⬇️ warfarin effect?

A

⬆️:
1. Disease status that ⬆️ degradation of clotting factors
A. Thyrotoxicosis
B. liver disease

  1. Inhibitors of CYP450: amiodarone
  2. Drugs that affect platelet function: NSAID’s or aspirin

⬇️:
1. Conditions:
A. Pregnancy
B. Hypothyroidism

  1. vit K:
    A. Multivitamins
    B. TPN IV
  2. Inducers of CYP450
  3. Drugs affecting warfarin abs : cholestyramine
48
Q

What are the direct thrombin inhibitors?

A

Include

  1. Bivalirudin
  2. Dezirudin
  3. Argatroban
  4. Debigatran
  • Binds to active site of thrombin (independent of AT-III), preventing thrombin-
    mediated activation of fibrinogen & factor XIII.
  • Irreversibly inhibits both free and fibrin-bound thrombin.
49
Q

What are the indications for direct thrombin inhibitors?

A
  1. Prop & T of
    A. DVT & PE in patients with HIT
    B. CAthrombosis in patients with HIT
  2. Unstable angina during PCI
  3. Prop of stroke & sys embolism
50
Q

What are the AE of direct thrombin inhibitors?

A
  1. Bleeding
  2. Back pain
  3. Hypotension
51
Q

Who can’t take direct th inhibitor?

A

Renal failure especially bivalirudin

52
Q

What is the antidote for direct th inhibitors?

A

No antidote for bivalirudin & dabigatran

53
Q

How to monitor direct th inhibitors?

A

aPTT like heparin 😊

Except dabigatran

54
Q

What are the thrombocytes agents ?

A
  1. Alteplase —> Tissue plasminogen activator
  2. Reteplase
  3. Tenecteplase
  4. Anistreplase —> APSAC
  5. Urokinase
  6. Streptokinase
  • eff against pre-existing clots and restore pat envy of the obstructed vessel
55
Q

What is the MoA of thrombolytic agents?

A
  • Activate plasminogen proteolysis to plasmin, a protease which digest fibrin to degradation products.
  • Dissolve pathologic and physiologic thrombi.l
56
Q

What are the indication for thrombolytic agents use?

A
  1. T of Acute MI ( ST- elevation type only )
  2. CAthrombosis in PCI
  3. acute PE, DVT, and acute ischemic stroke (alteplase only)
57
Q

What are the drugs used for bleeding disorders?

A
  1. Vit K
    A. T of ⬇️ prothrombin activity due to warfarin
    B. T of vit K deficiency
  2. Plasma factors
  3. Fibrinolytic inhibitors Ex:
    A. aminocaproic acid
    B. Tranexamic acid
  4. Serine protease inhibitor Ex: Aprotinin
58
Q

What is the MoA , indications and AE of fibrinolytic inhibitors?

A
  • MoA: competitively inhibit plasminogen activation
  • Indications: Adjunctive therapy in hemophilia or bleeding from fibrinloytic drugs.
  • Adverse effects: Intravascular thrombosis, hypotension, and myopathy
59
Q

What is the MoA , indications , And AE of serine protease inhibitors?

A

•*Mode of action: Inhibits fibrinolysis by free plasmin. It also inhibits the plasmin-streptokinase complex in patients receiving streptokinase.

  • Indication: Prophylaxis of bleeding in coronary artery bypass graft
  • Adverse effects: Anaphylaxis ( حساسية مفرطة من النوتة أكيد 🙂)

Pharma (5 decks)

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