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Blood and Lymph_pharm_misc > Tx of Hemostasis Disorders > Flashcards

Tx of Hemostasis Disorders Flashcards

1
Q

Aspirin inhibits the synthesis of thromboxane A2 by IRREVERSIBLE acetylation of COX-1 in platelets. How long until anti-thrombic effects are seen?

A

1-2 days after administration and lasts for the duration of the platelet lifespan (7-10 days)

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2
Q 
Ticlopidine
Route
MOA
AE
Tx
A

Route: oral
MOA: ADP antagonist , prevents activation of GPIIb-IIIa, promotes platelet aggregation
-prevents platelet adhesion and platelet-platelet interaction
AE:
-severe bone marrow toxicity (rare cases)
-increases liver functional enzymes
-drug-drug interactions w/:
-warfarin
-heparin
-other antiplatelet drugs
-NSAIDS
Tx: limited to patients who are intolerant or unresponsive to aspirin
*Clopidogrel is usually preferred

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3
Q 
Clopidogrel
Route
MOA
AE
Tx
A

Route: oral
MOA: ADP antagonist , prevents activation of GPIIb-IIIa, promotes platelet aggregation
-prevents platelet adhesion and platelet-platelet interaction
AE: less adverse cutaneous, GI, or HEMATOLOGIC rxns than ticlopidine
Tx: reduce atherosclerosis in pts w/ Hx of recent stroke, MI peripheral vascular disease, use in pts w/ stents

*It inhibits the activity of CYP2C9 and therefore may increase the plasma concentrations of drugs such as:
fluvastatin
many NSAIDs
phenytoin
tamoxifen
tolbutamide
Warfarin
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4
Q 
Abciximab
Route
MOA
AE
Tx
A

Route: IV, monoclonal-Ab
MOA: Inhibits platelet aggregation by preventing binding of fibrinogen to glycoprotein receptor IIb/IIIa on activated platelets.
AE: bleeding
Tx: high-risk patients undergoing coronary angioplasty and patients undergoing angioplasty, atherectomy and stent placement often with clopidogrel

*expensive

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5
Q

Name 2 platelet-receptor glycoprotein inhibitors which are NOT monoclonal antibodies

A
  1. Tirofiban (non-peptide)
  2. Eptifibatide (cyclic peptide)

*These are intravenous platelet glycoprotein IIb/IIIa inhibitors similar to abciximab, but they are not monoclonal antibodies

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6
Q

Because decreased protein kinase A (PKA) activity leads to platelet activation via decreased cAMP levels, what drug class can be given to increase the levels of cAMP and therefore lead to inhibition of platelet activation?

A

Phosphodiesterase Inhibitors

  • Dipyridamole
  • Cilostazol
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7
Q

Dipyridamole
MOA
AE
Tx

A

MOA: phosphodiesterase inhibitor; increases cAMP and therin inhibits platelet activation
-A coronary vasodilator that also inhibits platelet aggregation
Tx:
In combination with aspirin, reduces thrombosis in patients with thrombotic disease

In combination with warfarin, inhibits embolism from prosthetic heart valves (main use)

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8
Q

Cilostazol
MOA
AE
Tx

A

MOA: Inhibits phosphodiesterase type III, and thereby, increases cAMP levels; antithrombic, antiplatelet, vasodilator
AE
Tx: Used for intermittent claudication and peripheral vascular disease

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9
Q

Anagrelide
MOA
Tx

A

MOA: Inhibits megakaryocyte development in the late postmitotic stage
Tx: Approved for the treatment of thrombocytocytosis secondary to myeloproliferative disorders, such as, polycythemia vera and chronic myelogenous leukemia to reduce the risk of stroke and myocardial infarction

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10
Q

What drug class inhibits blood coagulation ‘in vitro’ and can be used as coagulants for blood draws etc.?

A

Calcium chelators

  1. oxalic acid
  2. sodium citrate
  3. disodium edetate (EDTA)
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11
Q

Class of drugs which directly inhibit thrombin

A

Rudins

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12
Q

derivatives which interfere w/ hepatic synthesis of functional vit K-dependent clotting factors. What are the vit-K dependent factors?

A

Coumarin derivatives

Factors: II, VII, IX, X
also Protein C and S

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13
Q

What drug is a sulfated mucopolysaccharide (acidic molecule), has an immediate onset of action (due to continuous infusion pump or intermittent SubQ admin), has DOSE-DEPENDENT clearance and demonstrates extensive binding to endothelial cells/proteins?

A

Standard Heparin (UFH)

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14
Q

Warfarin and Heparin are both monitored using the PT/PTT tests, which test is used for each drug?

A

Heparin–PTT

Warfarin–PT

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15
Q 
Standard Heparin (UFH)
MOA
A

MOA: The protease inhibitor, antithrombin III, forms a 1:1 complex with clotting factor proteases

This interaction is slow, but is stimulated 1000-fold by heparin, which binds to antithrombin III

The heparin-antithrombin III complex inactivates factor IIa (thrombin); main mechanism

The heparin-antithrombin III complex also inactivates factor Xa, which occurs earlier in the cascade
AE:

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16
Q 
Standard Heparin (UFH)
Contraindications
A

contraindicated pts w/:

  • Bleeding disorders and disorders that predispose to bleeding (e.g., hemophilia, thrombocytopenia), hemorrhage and several other diseases
  • Patients with advanced liver or kidney disease, severe hypertension and certain infections (active tuberculosis, infective endocarditis)

*Preferable to other anticoagulants during pregnancy due to lack of placental transfer (contrast to warfarin)

17
Q 
Standard Heparin (UFH)
AE:
A
  • Bleeding/hemorrhage
    * Bleeding is minimized with careful monitoring of PTT and platelet counts
  • Allergic reaction (heparin is an animal product)
  • Osteoporosis (long-term therapy)
  • Transient and occasionally severe heparin-induced thrombocytopenia (HIT)
18
Q

Describe the 2 types of Heparin-induced thrombocytopenia (HIT)

A

-Type I = Transient and rapidly reversible.
Antibodies are generated against platelets.
Results in a decrease in platelet count.

-Type II = Severe
Antibodies decrease platelet count.
The antibodies also activate platelets.
This may produce a thromboembolism, which may be life-threatening.

19
Q

Standard Heparin undergoes DOSE-RELATED clearance once binding sites are saturated. What is the antidote for this phenomena? CAREFUL!!! because excessive antidote is itself an anticoagulant

A

Protamine sulfate
-basic peptide that binds heparin (anion/cation interaction)

  • Protamine is much less capable of reversing the effects of LMWH (disadvantage of LMWH)
  • LMWH–low molecular weight heparin
20
Q

Identify 3 low molecular weight heparin (LMWH)

A

Enoxaparin = low MW (2,000 – 6,000)

Dalteparin = low MW (2,000 – 9,000)

Tinzaparin = low MW (3,000 – 8,000)

21
Q

Low molecular weight heparin (LMWH)

  • indication
  • kinetics
  • what test is used to monitor it?
A

Indication: LMWH’s were first approved for primary prevention of deep vein thrombosis after hip replacement therapy

LMWH’s are being evaluated and used for the treatment of other thromboembolic diseases

Kinetics: dose-independent (1st order)
-Monitored by anti-Xa activity assay

22
Q

Compare/Contrast unfractionated/standard heparin w/ its low molecular weight counterpart:

  1. inhibits platelet function
  2. increases vascular permeability
  3. endothelial cell/protein binding
  4. dose-dependent clearance
  5. T 1/2
A 
1.  inhibits platelet function
UFH- +++++
LMWH- ++
2. increases vascular permeability
UFH- YES
LMWH- NO
3. endothelial cell/protein binding
UFH- extensive
LMWH- minimal
4. dose-dependent clearance
UFH- YES
LMWH- NO
5. T 1/2
UFH- 50-90min
LMWH- 3-6hr
23
Q

Fondaparinux
Route
MOA
Tx

A

Route: SubQ–half-life is 18 hrs
MOA: synthetic pentasaccharide anticoagulant; It exerts antithrombotic activity as a result of ATIII-mediated selective inhibition of factor Xa
*should not cause HIT b/c it does not bind platelet factor 4
Tx:
–Venous thromboembolism prophylaxis following orthopedic surgery
–pulmonary embolism (PE)
–deep venous thrombosis (DVT)
–coronary artery thromboembolism; promising but still under study

24
Q
  • 65 amino acid peptide

- This is a specific thrombin inhibitor obtained from leeches

A

Hirudin

25
Q

Which drug is a recombinant yeast-derived form of hirudin?

It is approved for anticoagulation in patients with heparin-induced thrombocytopenia (HIT)

A

Lepirudin

26
Q

new recombinant hirudin analogs that may be used instead of heparins in the future
[2]

A
  1. Desirudin

2. Bivalirudin

27
Q

Which drug is the 2nd agent (1st is lepirudin) to be approved for HIT?
–unlike lepirudin, it is cleared by liver and can be used in patients with end-stage renal disease

A

Argatroban

28
Q 
Warfarin
T 1/2
CYP?
MOA
AE
Tx
test used to monitor
A

T 1/2: 36hr (extensive plasma protein binding–very low volume of distribution)
CYP2C9
MOA: Vitamin K epoxide reductase
AE: bleeding in brain, pericardium, stomach, intestine
–contraindicated in pregnancy (category X)
*fetal warfarin syndrome
*tetratogen in 1st trimester
*fetal hemorrhage during pregnancy
–contraindicated in pts w/ liver disease (impaired drug metabolism)
Tx:
–venous/arterial thrombi
–prevent blood clots in pts w/ a-fib
*test used to monitor is PT (INR)

29
Q

Warfarin Drug-Drug interactions (diminished response)

  • -inhibitor of warfarin absorption
  • -drug class which induces hepatic microsomal enzymes
  • -hormone which stimulates clotting factor synthesis
A
  • -inhibitor of warfarin absorption
  • cholestyramine (also affects vit K absorption)
  • -drug class which induces hepatic microsomal enzymes
  • anticonvulsants
  • -hormone which stimulates clotting factor synthesis
  • estrogen
  • also vit K from diet and bacteria
30
Q

Warfarin Drug-Drug interactions (enhanced response)

  • displacement from plasma albumin
  • inhibition of anticoagulant metabolism [8]
  • reduction in availability of vit K
A
  • displacement from plasma albumin
  • sulfonamides
  • inhibition of anticoagulant metabolism [8]
  • Amiodarone
  • Allopurinol
  • Cimetidine
  • Ciprofloxacin
  • Erythromycin
  • Co-trimoxazole
  • Metronidazole*
  • Fluconazole*
  • reduction in availability of vit K
  • broad-spectrum antibiotics
31
Q

Novel orally bioavailable anticoagulants [3]

A
  1. Dabigatran etexilate–first oral direct thrombin inhibitor, approved for a-fib pts
  2. Rivaroxaban–direct FXa inhibitor, approved for post-surgical VTE (improved efficacy over LMWH)
  3. Apixaban
32
Q

Streptokinase
MOA
AE

A

MOA: Facilitates thrombolysis through formation of activator complex with plasminogen results in formation of plasmin

Plasmin degrades fibrin, fibrinogen, and procoagulant factors V and VIII

AE: hypersensitivities

33
Q

Urokinase
Route
AE
Tx

A

Route parenteral thrombolytic agent (from cultured human kidney cells)
AE: hypersensitivity occur less frequently
Tx: Indicated for lysis of pulmonary emboli, lysis of coronary artery thrombi associated with evolving transmural myocardial infarction

34
Q

Recombinant Thrombolytic Agents [3]

A
  1. Alteplase–recombinant form of t-PA, expensive, no hypersensitivity rxns
  2. Reteplase–recombinant plasminogen activator, longer half-life than alteplase
  3. Tenecteplase, TNK-t-PA–modified human t-PA, prolonged half-life, increased specificity for fibrin and increased resistance to plasminogen activator inhibitor-1
35
Q

Aminocaproic acid

Tx

A

MOA: fibrinolytic inhibitors
Tx:
–Systemic or urinary hyperfibrinolysis ( e.g., aplastic anemia, abruptio placentae, hepatic cirrhosis)
–Bleeding associated with neoplastic diseases (carcinoma of the prostate, lung, stomach, or cervix)
–Bleeding following cardiac surgery

Blood and Lymph_pharm_misc (4 decks)

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