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Pharm > Anti-platelets & fibrinolytics > Flashcards

Anti-platelets & fibrinolytics Flashcards

1
Q

Platelet aggregation is physiologically facilitated by

A
  • thromboxane (TXA2)
  • ADP receptor stimulation
  • GP IIb/IIIa receptor stimultation
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2
Q

platelet aggregation is pharmacologically inhibited by

A
  • TXA2 synthesis inhibitor aspirin
  • ADP receptor antagonists Ticlopidine and Clopidogrel
  • dipyridamole
  • GP IIb/IIIa receptor antagonists Abciximab
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3
Q

Use of aspirin & MOA

A

low dose aspirin (81-325)
Use: antiplatelet

MOA: irreversibly inhibit platelet COX enzyme by acetylating the enzyme and also inhibits thromboxane synthetase

  • as platelets cannot synthesize new COX (no nucleus)
  • no thromboxane TXA2 synthesis
  • antithrombotic effect lasts for 3 days

High dose aspirin = COX 1 and 2

Use: low dose daily prevents ischemic attack and MI

> 1000mg/day has NO anti platelet effect

  • high dose is anti-inflammatory dose
  • high dose inhibits prostacyclin (PGI) synthesis
  • PGI normally prevents platelet aggregation
  • therefore prophylactic benefit of aspirin as an anti platelet drug is always in low doses

MC use of aspirin = coronary artery disease

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4
Q

COX 1

A

COX1 = housekeeping; important with PG in mucous production

aspirin-induced ulcers result from inhibition of this –> not seen much with low-dose aspirin

Remember: aspirin acetylates serine residue on COX –> inhibits TXA2 synthetase

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5
Q

Ticlopidine: MOA, use, A/E

A

ADP receptor antagonist

MOA: blocks platelet ADP receptor and prevents platelet aggregation

Uses:

  • for prevention of TIA, post MI, unstable angina and as an alternative to aspirin
  • adjunct therapy with aspirin following coronary stent implantation to decrease incidence of stent thrombosis

A/E:
- severe neutropenia, thrombocytopenic purpura

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6
Q

GP IIb/IIIa receptor antagonists

A
  • Abciximab
  • Eptifibatide
  • Tirofiban
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7
Q

Fibrinolytics / Thrombolytics

A
  • streptokinase
  • urokinase
  • tissue plasminogen activator (tPA)

fibrinolytic therapy should be used ASAP to reestablish blood flow following AMI; >60% decrease in mortality post-MI if used within 3 hours!

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8
Q

Antifibrinolytics

A

aminocaproic acid

tranexamic acid

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9
Q

Clopidogrel: MOA, use, A/E

A

ADP receptor antagonist

MOA: blocks platelet ADP receptor and prevents platelet aggregation

Uses:

  • for prevention of TIA, post MI, unstable angina and as an alternative to aspirin
  • adjunct therapy with aspirin following coronary stent implantation to decrease incidence of stent thrombosis

A/E:
- less incidence of neutropenia or thrombocytopenia

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10
Q

Eptifibatide: MOA and use

A

GP IIb/IIIa receptor antagonist

MOA: Inhibit binding of fibrinogen to the GPIIb/IIIa receptor –> thereby inhibiting the final, common pathway of platelet aggregation

Use: given along with aspirin and heparin during coronary angioplasty (PTCA)
- markedly reduce the incidence of restenosis

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11
Q

Streptokinase

A

thrombolytic/fibrinolytic

  • obtained from streptococci

MOA: binds to circulating plasminogen–> converts to plasmin

A/E: bleeding, allergic reactions, hypotension, fever

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12
Q

alteplase

A

tPA

MOA: binds to & activates fibrin bound plasminogen (more local action on the thrombus)

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13
Q

Dipyridamole MOA

A

Inhibits phosphodiesterase –> increased cAMP –> prevents aggregation

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14
Q

Abciximab:

A

GP IIb/IIIa receptor antagonist

MOA: monoclonal antibodies directed against GP IIb/IIIa receptor complex

Use: given along with aspirin and heparin during coronary angioplasty (PTCA)
- markedly reduce the incidence of restenosis

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15
Q

urokinase

A

fibrinolytic/thrombolytic

- derived from human tissue

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16
Q

reteplase

A

tPA

MOA: binds to & activates fibrin bound plasminogen (more local action on the thrombus)

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17
Q

aminocaproic acid: MOA, Uses

A

antifibrinolytic

MOA: Inhibits the plasminogen activation

Uses: to treat excessive bleeding due to overdose of fibrinolytic agents

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18
Q

Tissue plasminogen activator (tPA)

A

fibrinolytic/thrombolytic
- Alteplase, reteplase (recombinant DNA technology)

MOA: binds to & activates fibrin bound plasminogen (more local action on the thrombus)

used to help re-canalize bv after AMI

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19
Q

Tirofiban: MOA and use

A

GP IIb/IIIa receptor antagonist

MOA: monoclonal antibodies directed against GP IIb/IIIa receptor complex

Use: given along with aspirin and heparin during coronary angioplasty (PTCA)
- markedly reduce the incidence of restenosis

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20
Q

tranexamic acid: MOA, Uses

A

antifibrinolytic

MOA: Inhibits the plasminogen activation

Uses: to treat excessive bleeding due to overdose of fibrinolytic agents

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21
Q

Anticoagulants

A
  • Heparin
  • warfarin (Oral anticoagulant)
  • dicumarol (Oral anticoagulant)
  • hirudin (direct thrombin inhibitor)
  • bivalirudin (direct thrombin inhibitor)
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22
Q

heparin: MOA, Pharmacokinetics,

A

Anticoagulant: indirect thrombin inhibitor

  • unfractionated Heparin (UFH)
  • low molecular weight heparins (LMWH)–longer DOA
  • monitor via aPTT

MOA: activates ATIII –> inactivates clotting factors in intrinsic pathway
- thrombin IIa, IXa, Xa

Pharmacokinetics:

  • hepatin is a strong acid and can be neutralized by basic compounds like protamine***
  • highly ionized –> not absorbed orally
  • -> does not cross placenta; safe in pregnancy*
  • given via IV/ S.C.
  • dose monitored by aPTT (activated partial thromboplastin time) –> normally 25-39 sec
  • with heparin: 45-75 sec; beyond this–>bleeding!
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23
Q

warfarin

A

Oral Anticoagulant

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24
Q

intrinsic coagulation system

A

Intrinsic pathway: factors XII, XI, IX, and VIII

  • begins with activation of factor XII (Hageman factor)
  • exposed sub-endothelial collagen and HMWK activate factor XII to form factor XIIa
  • factor XIIa is also known as activated Hageman factor
  • factor XIIa activates factor XI to form factor XIa
  • factor XIIa activates 3 substances:
  • –> factor XI to form factor XIa
  • –> plasminogen to form plasmin
  • –> kininogen system to produce chalkier and bradykinin
  • XIa activates factor IX to form IXa
  • IXa complexes with factor VIII, CA2+, and PF3 to form a four component complex: factor IXa, factor VIII, PF3 and Ca2+
  • in the final common pathway this complex activates factor X
    _____________________________________________
    XII –> XIIa
    XI –> XIa
    IX –> IXa
    VIII + IXa + PF3 + Ca2+ —>common pathway
Common pathway: 
X --> Xa
V + Xa + PF3 + Ca2+
prothrombin --> thrombin
fibrinogen --> fibrin monomer
fibrin monomer aggregate--> soluble fibrin --> cross-linked insoluble fibrin
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25
Q

extrinsic coagulation pathway

A 
Extrinsic pathway: factor VII
- begins with activation of factor VII
- Tissue Thromboplastin released from injured tissue activates factor VII resulting in formation of factor VIIa
- in the final common pathway factor VIIa  activates factor X
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
VII --> VIIa
----> common pathway: 
X --> Xa
V + Xa + PF3 + Ca2+
prothrombin --> thrombin
fibrinogen --> fibrin monomer
fibrin monomer aggregate--> soluble fibrin --> cross-linked insoluble fibrin
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26
Q

dicumarol

A

Oral anticoagulant

27
Q

Common Pathway

A

Factors X, V, II (prothrombin) and I (fibrinogen)
- begins with activation of factor X by:
–> factor VIIa (extrinsic pathway)
–> four component complex [(factor IXa, factor VIII, PF3, Ca2+) intrinsic pathway]
-activated factor Xa complexes with factor V, PF3, and Ca2+ to form a complex = the Prothrombin complex
—-> prothrombin complex cleaves prothrombin to the enzyme thrombin
_____________________________________
X –> Xa
V + Xa + PF3 + Ca2+
prothrombin –> thrombin
fibrinogen –> fibrin monomer
fibrin monomer aggregate–> soluble fibrin –> cross-linked insoluble fibrin

28
Q

LMW heparins: names, MOA, Advantages, A/E

A

enozaparin
dalteparin
tinzaparin

  • selectively inhibit Xa, less effect on thrombin
  • given subcutaneously

advantages:

  • less hemorrhagic complication, less thrombocytopenia
  • equally efficacious
  • increased bioavailability
  • less frequent dosing, bc longer half life
  • less effect on aPTT

A/E: BLEEDING!

  • close monitoring of activated partial thromboplastin time (aPTT)
  • PROTAMINE is used to stop bleeding due to heparin
  • Moderate & transient thrombocytopenia –> immune mediated
  • Osteoporosis on prolonged use
29
Q

Hemopoietic agents used in treatment of anemias and hemopoietic growth factors

A
  • iron
  • vitamin B12
  • folic acid
  • erythropoietin
  • myeloid growth factors
  • platelet growth factor
30
Q

hirudin

A

direct thrombin inhibitor

31
Q

bivalirudin

A

direct thrombin inhibitor

32
Q

Used to stop bleeding due to heparin

A

PROTAMINE

33
Q

Enoxaparin: MOA, Advantages, A/E

A

LMWH

  • selectively inhibit Xa, less effect on thrombin
  • given subcutaneously

advantages:

  • less hemorrhagic complication, less thrombocytopenia
  • equally efficacious
  • increased bioavailability
  • less frequent dosing, bc longer half life
  • less effect on aPTT

A/E: BLEEDING!

  • close monitoring of activated partial thromboplastin time (aPTT)
  • PROTAMINE is used to stop bleeding due to heparin
  • Moderate & transient thrombocytopenia –> immune mediated
  • Osteoporosis on prolonged use
34
Q

Direct Thrombin Inhibitors: names & MOA

A

Lepuridin
bivalirudin
argatroban

  • directly bind to thrombin and inhibits the downstream effects
  • obtained from proteins made by medicinal leech
35
Q

Warfarin MOA

A
  • decrease hepatic synthesis of Vit K dependent clotting factors: Prothrombin, VII, IX, X
  • by preventing the gamma carboxylation of glutamine residues of clotting factors
  • this is done by inhibiting Vitamin K Epoxide Reductase–> which prevents the regeneration of hydroquinone form of Vit K
36
Q

Dalteparin: MOA, Advantages, A/E

A

LMWH

  • selectively inhibit Xa, less effect on thrombin
  • given subcutaneously

advantages:

  • less hemorrhagic complication, less thrombocytopenia
  • equally efficacious
  • increased bioavailability
  • less frequent dosing, bc longer half life
  • less effect on aPTT

A/E: BLEEDING!

  • close monitoring of activated partial thromboplastin time (aPTT)
  • PROTAMINE is used to stop bleeding due to heparin
  • Moderate & transient thrombocytopenia –> immune mediated
  • Osteoporosis on prolonged use
37
Q

Lepuridin

A

Direct Thrombin Inhibitor

  • directly bind to thrombin and inhibits the downstream effects
  • obtained from proteins made by medicinal leech

Uses: alternative to heparin in heparin-induced thrombocytopenia

38
Q

Warfarin A/E

A
  1. Bleeding: ecchymosis, epistaxis, hematuria
    - monitor, prothrombin time
    - treatment: stop the drug, Vitamin K1, fresh frozen plasma
  2. Skin Necrosis: rare complication seen during first week of therapy with warfarin
    - due to reduced protein c synthesis
    - manifests as dermal necrosis of extremities or breast
39
Q

Tinzaparin: MOA, Advantages, A/E

A

LMWH

  • selectively inhibit Xa, less effect on thrombin
  • given subcutaneously

advantages:

  • less hemorrhagic complication, less thrombocytopenia
  • equally efficacious
  • increased bioavailability
  • less frequent dosing, bc longer half life
  • less effect on aPTT

A/E: BLEEDING!

  • close monitoring of activated partial thromboplastin time (aPTT)
  • PROTAMINE is used to stop bleeding due to heparin
  • Moderate & transient thrombocytopenia –> immune mediated
  • Osteoporosis on prolonged use
40
Q

Uses of Heparin

A

used when anticoagulation is required immediately (rapid anticoagulation)

  • DVT
  • PE
  • AMI
  • coronary angioplasty along with fibrinolytic
  • anticoagulant of choice during pregnancy*
  • Atrial fibrillation
  • cerebrovascular disease
  • vascular surgery
  • prosthetic heart valves
41
Q

alternatives to heparin in heparin-induced thrombocytopenia

A
  • Lepuridin

- argatroban

42
Q

Bivalirudin

A

Direct Thrombin Inhibitor

  • directly bind to thrombin and inhibits the downstream effects
  • obtained from proteins made by medicinal leech

Uses: used in combination with aspirin during angioplasty

43
Q

Phytonadione

A

Preparation of Vitamin K1

  • given orally
  • Vitamin K is a Cofactor for synthesis of clotting factors Prothrombin, factor VII, IX and X
44
Q

Factors increasing Iron absorption

A
  • acid
  • ascorbic acid
  • aminoacids
  • meat
45
Q

Argatroban

A

Direct Thrombin Inhibitor

  • directly bind to thrombin and inhibits the downstream effects
  • obtained from proteins made by medicinal leech

Uses: alternative to heparin in heparin-induced thrombocytopenia

46
Q

Warfarin Pharmacokinetics

A

Inhibits synthesis of clotting factors by liver but doesn’t affect clotting factors that’s already made!

  • given orally –> onset of action delayed
  • highly bound to plasma proteins (99%)
  • crosses placenta –> can cause hemorrhagic disorder, bone defects in fetus
  • monitored by INR (international normalized ratio)
  • recommended INR = 2-3

INR = test prothrombin time / control prothrombin time

47
Q

Warfarin Uses

A

same as heparin

  • used for long-term anticoagulation; FOR MAINTENANCE!
  • DVT, PE
  • AMI
  • Coronary angioplasty along with fibrinolytics
  • NOT anticoagulant of choice during pregnancy!!!!!
  • Atrial fibrillation
  • Cardiovascular disease
  • vascular surgery
  • prosthetic heart valves
48
Q

filgrastim

A

granulocyte colony stimulating factor (G-CSF)

49
Q

Vitamin K

A

Cofactor for synthesis of clotting factors Prothrombin, factor VII, IX and X

  • preparation: phytonadione (Vit K1)
  • given orally

Uses:

  • obstructive juandice, liver disease
  • malabsorption syndromes
  • newborns (premature Vit K1 mg IM)
  • overdose of oral anticoagulants
50
Q

Which form of iron is absorbed?

A

Fe2+ (ferrous)
- max absorption in duodenum

Fe3+ = ferric iron

51
Q

Oral iron preparations: types & A/E

A
  • ferrous sulfate
  • ferrous gluconate
  • ferrous fumerate

A/E:

  • Epigastric pain
  • constipation
  • metallic taste
  • nausea, vomiting
  • staining of teeth
52
Q

Factors decreasing Iron absorption

A
  • antacids
  • phosphates
  • phytates
  • tetracyclines
  • presence of food
53
Q
  • Vomiting, hematemesis, bloody diarrhea followed by shock,

- severe metabolic acidosis, coma and death

A

acute iron poisoning

  • common in infants and children

Treatment: Deferrioxamine: iron chelating agent

54
Q

parenteral iron: names, indications for use, and uses

A
  • iron dextran (IV/IM)
  • sodium ferric gluconate complex (only IV)
  • iron sucrose (only IV)

indications for use:

  • oral iron not tolerated
  • severe deficiency
  • malabsorption
  • non-compliance

Uses:

  1. iron deficiency anemia
    - nutritional deficiency (premature infants, growing children)
    - anemia of pregnancy
    - blood loss (GI bleeding)
    - malabsorption
  2. pregnant and lactating women – prophylaxis
55
Q

Cyanocobalamine

A

Vitamin B12 Preparation

Absorption: intrinsic factor (gastric parietal cell) + Vit B12 –> absorbed in distal ileum

Uses: megaloblastic anemia and pernicious anemia

56
Q

sargramostim

A

granulocyte/macrophage colony stimulating factor (CM-CSF)

57
Q

Folic Acid

A

Folic acid –Folic reductase (enzyme)–> dihydrofolic acid –dihydrofolate reductase (enzyme)–> tetrahydrofolic acid

dihydrofolate reductase (enzyme) is inhibited by methotrexate

Uses: megaloblastic anemia caused by

a) nutritional deficiency, alcoholics, liver diseases
b) pregnancy, malabsorption
d) pregnancy–maternal FA deficiency, associated with neural tube defects (i.e. spinabifida)
c) drugs:
- phenytoin: antiepileptic
- sulfonamides: treat malaria, antibacterial (in high [ ] –> anemia)
- methotrexate: anti-cancer drug
- INH: tx malaria
- OCP

Methotrexate toxicity:

  • leucovorin (aka folinic acid = active form of folic acid)/citrovorum factor/folinic acid
  • Mtx-DHFR inhibitor (FA is not effective)

Leucovorin rescue: giving leucovorin when used to give high dose of methotrexate because rescuing bone marrow cells

58
Q

Hydroxyocobalamine

A

Vitamin B12 Preparation

Absorption: intrinsic factor (gastric parietal cell) + Vit B12 –> absorbed in distal ileum

Uses: megaloblastic anemia and pernicious anemia

59
Q

Acute Iron Poisoning

A
  • common in infants and children

Symptoms:

  • Vomiting, hematemesis
  • bloody diarrhea followed by shock
  • severe metabolic acidosis, coma and death

Treatment: Deferrioxamine: iron chelating agent

60
Q

Hemopoietic growth factors

A

recombinant human erythropoietin:

  • erythropoitin
  • darbopoietin
  • colony stimulating factors: G-CSF and GM-CSF

Uses:

  • anaemic of chronic renal failure (because doesn’t form enough EPO –> anemia)
  • cancer chemo induced anemia
  • anemia in AIDS patients–Zidovudine–> causes BM suppression
61
Q

Myeloid Growth Factors

A

promote WBC

  • granulocyte colony stimulating factor (G-CSF) –>filgrastim
  • granulocyte/macrophage colony stimulating factor (CM-CSF)–>sargramostim

Use: to treat neutropenia with anticancer drugs & zidovudine

62
Q

Megakaryocytic Growth Factors

A 
Interleukin 11 (oprelvekin)
- stimulate the formation of megakaryocytic and increase their number in peripheral blood

Use: thrombocytopenia after a cycle of cancer chemotherapy

63
Q

Deferrioxamine

A

iron chelating agent

- used to treat acute iron poisoning

64
Q

Which anticoagulant has a delayed onset?

A

Warfarin

Heparin has an immediate onset

Pharm (32 decks)

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