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Mandies Pharm III > anticoagulants > Flashcards

anticoagulants Flashcards

1
Q

prostacyclin (PGI2)

A

factor limiting PLT aggregation

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2
Q

3 factors released that further PLT aggregation

A

ADP, TXA2, 5HT

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3
Q

What activates intrinsic vs extrinsic clotting cascade

A 
intrinsic = IX
extrinsic = VIIa (tissue factor, outside vasculature)
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4
Q

activators of plasminogen to plasmin

A

SK (streptokinase)
UK (urokinase)
tPA (tissue plasminogen activator)

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5
Q

PT measures :

PTT measures

A

PT prothrombin time; extrinsic clotting factor

PTT partial thomboplastin time (intrinsic)

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6
Q

INR

  • what is it?
  • normal/elevated values
A

since PT tests vary widely due to method and activity of tissue factor, INR standardizes measurements of PT
ISI (international sensitivity index) issues to manufactured tissue factors
normal: 0.9-1.3
high 4-5
low 0.5
therapeutic: 2-3

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7
Q

aspirin
action
SE/toxicity
indications

A

-inhibits synthesis of thromboxane A2 by irreversible acetylation of cylooxygenase (TXA2 is a factor that causes PLT aggregation)
-mostly commonly used anti PLT agen
CV indications: reduction of TIA, prevention of stroke, primary and secondary prevention of MI, prevention of coronary restenosis following MI/fibrinolytic therapy or bypass grafting
SE: excessive bleeding

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8
Q

clopidogrel
MOA
indication

A

thienopyridine derivatives that reduce PLT aggregation by irreversibly blocking the P2Y12 receptor (chemoreceptor for ADP) on PLT, no effect on prostaglandin metabolism

  • standard practice in pt undergoing placement of a coronary stent, useful in those that cannot tolerate aspirin
  • fewer side effects and less dosing than ticlopidine, preferred
  • clopidigrel activated by CYP2C19 (2-14% of us pop has genetic variability of this CYP, tests can determine susceptibility)
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9
Q

ticlopidine
MOA
indication
SE

A

thienopyridine derivatives that reduce PLT aggregation by irreversibly blocking the P2Y12 receptor (chemoreceptor for ADP) on PLT, no effect on prostaglandin metabolism
-standard practice in pt undergoing placement of a coronary stent, useful in those that cannot tolerate aspirin
SE: nausea, dyspepsi, diarrhea, hemorrhage, leukopenia

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10
Q

prasugrel

A

thienopyridine derivatives that reduce PLT aggregation by irreversibly blocking the P2Y12 receptor (chemoreceptor for ADP) on PLT, no effect on prostaglandin metabolism

  • decreases PLT aggregation more rapidly and consistently than clopidogrel and is effective in most individuals
  • activated via hydrolysis
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11
Q

heparin (UFH)
MOA
Source

A

catalyzing antithrombin activity, linear polysaccharid must be delivered parenterally.

  • binds to antithrombin, cuasing a conformational change that results in its activation through an increase in the flexibility of its reactive site loop
  • inhibits IIa, Xa, IXa
  • source: extracted from porcine or bovine sources, mixture of smaller molecular wgt fragments is isolated (5000-30000 daltons).
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12
Q

heparin SE

A

bleeding, allergy, thrombosis and osteoporosis. HIT is a systemic hypercoagulable state that occurs in pt rx w UFH for a minimum of 7 days

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13
Q

difference between UFH and LMW heparin

A

UFH binds to PLT, can lead to autoimmune destruction

LMW binds to ATIII, not PLT

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14
Q

reversal of heparin action

A

protamine sulfate

-highly cationic peptide that binds heparin to form a stable ion pair, inhibits anticoag activity

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15
Q

heparin removal

A

saturable (clearance by reticuloendothelial system) and non-saturable (renal excretion)
-contribution of clearance mechanism is determined by dose delivered and MW of heparin prep

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16
Q

dalteparin

A
  • enhances antithrombin action on factor X
  • MW 4K-6K daltons
  • available for prophylaxis and rx
  • no lab monitoring bc specificity, known activity
  • protamine reversal is incomplete
17
Q

enoxaparin

A
  • enhances antithrombin action on factor X
  • MW 4K-6K daltons
  • available for prophylaxis and rx
  • no lab monitoring bc specificity, known activity
  • protamine reversal is incomplete
18
Q

tinzaparin

A
  • enhances antithrombin action on factor X
  • MW 4K-6K daltons
  • available for prophylaxis and rx
  • no lab monitoring bc specificity, known activity
  • protamine reversal is incomplete
19
Q

fondaparinux

A

-factor Xa inhibitor
-MW 4K-6K daltons
-available for prophylaxis and rx
-no lab monitoring bc specificity, known activity
-protamine is not a reversal for fondaparinux; no good reversal agent
fondaparinux is just the pentassacharide w added methyl groups
-parenteral admin
renal clearance

20
Q

metabolism of LMWH, fondaparinux

A

enoxaparin, fondaparinux, tinzaparin, dalteparin

-diff metabolism than UFH. kidney is importance for clearnace of LMWH

21
Q

lepirudin

A
  • renally cleared
  • 65 AA PRO
  • direct thrombin inhibitor
22
Q

bivalirudin

A
  • 20 AA peptide
  • direct thrombin inhibitor
  • hepatic and 20% renal clearance
23
Q

argatroban

A
  • hepatically cleared
  • small molecule, IV only bc short half-life
  • direct thrombin inhibitor
24
Q

dabigatran
MOA
SE

A 
oral
-direct thrombin inhibitor
-no monitoring needed
-short half life
no good reversal agent
SE: GI bleeding
max anticoag effect within 2-3 h
80% renal clearnace
25
Q

choice of direct thrombin inhibitor is dictated by

A

condition of clearing organ

26
Q

warfarin MOA

A

inhibits vitamin K metabolism which disrupts gamma-carboxylation of several glutamate residues in factors II, VII, IX, X & Proteins C/S
-partially inhibits synthesis, but not degredation, thus effect on coagulation is dependent on factor half life
-effects both factors that inhibit and stimulate clotting
-inhibits inactive forms
PRO C/S are inhibited before inhibition of other factors, why need anticoag bridge
-cleared by liver and kidney

27
Q

warfarin SE

A

bleeding, skin necrosis, teratogenesis, thrombosis

-interacts with numerous drugs, diets, disease states

28
Q

reversal of warfarin

A

-stop drug
-admin K
FFP
recombinant factor VIIa

29
Q

rivaroxaban

MOA

A 
oral admin
factor Xa inhibitor
-no monitoring
-short half life
no good reversal agen
max inhibition of factor Xa occurs 4 hr after a dose
once daily
liver, renal, fecal/biliary clearance
30
Q

streptokinase

A 
source: streptococcus
allergic reactions
long half life
plasminogen to plasmin
-agents induce a lytic state that prod a bleeding tendency
-1% risk of ICH
31
Q

urokinase

A 
human source
non allergenic
shorter half life
plasminogen to plasmin
-agents induce a lytic state that prod a bleeding tendency
-1% risk of ICH
32
Q

t-PA

A 
human source
non allergenic
shortest half life
plasminogen to plasmin
-agents induce a lytic state that prod a bleeding tendency
-1% risk of ICH

Mandies Pharm III (10 decks)

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