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Year II Pharmacology > Anticoagulants Pharmacology > Flashcards

Anticoagulants Pharmacology Flashcards

1
Q

Role of the following

  • PFA100
  • Thromboxane A2
  • ADP receptor
  • GpIIb/IIIa
A
  • PFA100: measure of platelet function
  • Thromboxane A2 (vasoconstrictor)produced by activated platelets using COX1
  • ADP receptor: Platelet aggregation & activation
  • GpIIb/IIIa used to bind to fibrinogen &vWF factor
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2
Q

Three main targets for antiplatlets

A

COX inhibitors
ADP receptor inhibitors
GpIIb/IIIa receptor inhibitor

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3
Q

2 drugs that are COX inhibitors

A
  1. Asprin (irreversible)

2. NSAIDS (reversiable)

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4
Q

Aspirin

Indications

NOT indicated for

Mechanism

Kinetics

SE

A

Indications
• 1 & 2 prevention of peripheral arterial thrombosis
• Placental insufficiency
• Prevention of venous thromboembolism
• CAD/angina/MI
• + warfarin: patients with mechanical heart valves
• Afib in patients who can’t take warfarin

Not indicated for
• Stroke prevention in atrial fibrillation & mechanical heart valves

Mechanism
•	Thromboxane A2 derived from arachidonic acid using COX protein important for platelet aggregation using
•	Aspirin irreversibly acetylates COX 
o	Can’t produce TXA2 
o	Inhibits platelet aggregation

Kinetics
• Short half-life but
• Since irreversible binding you have to wait 7-10 days to replace your platelets
• Stop 10 days before surgery

SE
• GI distress
• Bleeding

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5
Q

NSAIDS

  • Hw long until peak effect?
  • Which has longer half life naproxen or ibuprofen
  • When is platelet function restored
  • SE
A
  • Peak effect 1-2 hours after dose
  • Ibuprofen shorter hl so stopped 1-2 days before surgery
  • Naproxen longer hl so stopped many days before surgery
  • Restore platelet function when drug is cleared
  • Excreted in urine within 24 hours

SE
• GI distress
• Bleeding

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6
Q

2 big categories of ADP receptors

A

THIENOPYRIDINES & TICAGRELOR

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7
Q

2 types of thienopyridines

A

Clopidogrel & prasugrel

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8
Q

3 benefits of prasugrel over clopidogrel

A
  1. Less drug resistance

2. Reach peak effect & steady state sooner

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9
Q

Mechanisms of thienopyridines (clopidergrel & prasugrel)

How is it different from ticagrelor

A
  • Irreversible inhibition of ADP receptor mediated platelet aggregation
  • Prodrug

Ticagrelor - Reversable

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10
Q

Clopidogrel
- Indications

Prassugrel
- Indications

A

Clopidogrel
• 2 prevention arterial thrombosis
• Prevention of coronary stent thrombosis
• Transient cerebral ischemia
• Recurrent arterial Thromboemboli despite treatment with aspirin

Prassugrel (only after acute coronary syndroms)
• Acute coronary syndromes with percutaneous coronary interventions
• Prevent coronary stent thrombosis

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11
Q

Clopidogrel metaobilism inhibited by

A

atovastatin

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12
Q

Side effect unique to clopidergrel

SE unique to prasugrel

SE common to clopidegral & prasgrel

A

SE unique clopidogrel
• Rash & diarrhea
• Drug resistance

SE unique to prasugrel
• Increased risk of stroke so contraindicated in patient with TIA and strike

Common SE
• Bleeding worse with aspirin
• Thrombotic thrombocytopenic purpura (TTP)

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13
Q

Ticagrelor

Indications
Mechanism (how is it different from thienopyridines)

Unique SE

A

Indication
• Acute coronary syndromes

Mechanism
• Reversible inhibition of ADP receptor mediated platelet aggregation
Prodrug and metabolites effective
• Reversible

SE
• Gynecomastia (swelling of breasts)
• Bleeding
• Dyspnea & bradycardia

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14
Q

Role of GpIIb/IIIa

3 example drugs: Abcixmab,

Indications

SE

A

GpIIb/IIIa receptor on platelets used to bind to fibrinogen &vWF factor

Abicixmab- monoclonal antibody
Epitifibatide - cyclic heptapeptide
Tirofiban - Small molucule

SE
Eptifibatide and tirofiban: severe thrombocytopenia

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15
Q

Name 3 big classes of annticoagulants and how the

DIfference in Warfin & Heparin

  • Use
  • Mechanism
  • What is monitored
A

Heprarin, warfin & PARENTERAL DIRECT THROMBIN INHIBITORS

Heparin - acute
Warfin - Longterm chronic use

Heparin: Factor X antagonist
Warfin: Inhibits synthesis of factor 2, 7, 9, 10 & protein C & S

Monitor
HMW: aPTT
LMW: Anti-Xa (aPTT)
Warfarin: INR/PT between 2-3

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16
Q

Benefits of LMW heparin

A
  • Increased bio availability
  • SubQ
  • Fixed dose
  • Limited lab monitoring need
  • Treat patients at home for DVT since SubQ
  • Lower heparin induced thrombocytopenia
  • More predictable response
  • Less HIT
17
Q

Disadvantages of LMW heparin

A
  • Don’t prolong aPTT
  • Test amount with Anti-Xa assay
  • Renal excretion so patients in renal failure will actually bleed because drug concentrated
  • Longer half lives
18
Q

Heparin

  • Indications
  • Mechanisms
  • Kinetics (HMW & LMW)
  • Reversal ( HMW & LMW)
  • Dosing HMW & LMF
  • SE
A

Indications
• “Treatment” after acute arterial venous thromboembolism
• 1 prevention of acute arterial & venous thrombosis

Mechanism
• Inhibits activity of PREFORMED coagulation factors
• Does not breakup existing clot
• Endogenous fibrinolytic system clears the clot
• Prevents thrombus propagation & clot formation

Kinetics HMW
•	Cleared in 2 phases
o	Rapid: Binding to endothelial cells, plasma proteins & macrophages
o	Slow: Renal
•	HL  is dose dependent

Kinetics LWM
Renal excretion

Reversal
HMW: • Protamine sulfate
LMW: Nothing

Dosing
HMW
IV
• Used acutely in bolus
• Individual variability to bioavailability
• Binds to plasma proteins
• Adjust dose based on prolongation of aPTT in common pathway

LMW
SubQ
•	Prophylaxis
•	Poor bioavailability
•	2-3 doses per day
•	Monitor Anti Xa levels but aPTT is not prolonged
SE
Bleeding
HMW: Heparin Induced Thrombocytopenia (HIT)
Osteoporosis
Skin lesions
Hyperaldosteronism
19
Q

Warfarin

  • Indications
  • Mechanism
  • Kinetics
  • Reversal
  • Dosing
  • Contraindications
  • SE
A

Indications
• 1 & 2 prevention of venous thromboembolism
• 1 & 2 prevention of arterial thrombosis
o Stroke prevention after Afib, heart valves, failure of antiplatelet
• Used in conjunction with antiplatelet therapy

Mechanism
•	Inhibits synthesis of vitamin K dependent coagulation factors
o	2, 7, 9, 10, C, S & Z
o	Target epoxide reductase
•	Inhibits gamma carboxylation
•	Superwarfarins get around resistant
Kinetic
•	Not affected by renal dysfunction
•	Crosses placenta so can't use in pregancy
•	33 hour half-life so steady state takes 7-10 days to have an effect so not used for acute treatment
•	Liver metabolism
•	Metabolism decreases with age
•	Food slows absorption
•	Genetic polymorphisms alter metabolism

Reversal
• Plasma
• Vitamin K
• Prothrombin complex concentrates

Dosing
• Dose with aim of getting INR(PT) between 2-3
• Since slow acting, start concurrent therapy with heparin until target INR is reached
• INR/PT used for monitoring because factor 7 1st to show decline (shortest half-life)
• Can induce hypercoagulable state (C and S are vitamin dependent)

Contraindications
•	Medications
•	Food rich in vitamin K
•	Medical conditions
o	Liver
o	CHF
o	Malnutrition
o	Hyper-metabolic states (fever, hyperthyroidism)
•	Warfarin resistance
o	Gastric bypass
o	Pharmacogenomics

Side Effecrs
Bleeding
Skin necrosis (worse in patients with protein C and S because will actually will be pro-coagulation leading to thrombosis)
Teratogenic during fetal development

20
Q

Which anticoagulant safe in pregnancy why?

A

Heparin - does not cross BBB

21
Q

What are pareteral direct thrombin inhibitors

Name 3
What do you monitor?
Method of delivary?

A

Sythetic molecules used in place of heparins

  • Argatroban, bivilirudin & lepirudin
  • Monitor aPTT (targeted 45-90s)
  • Continues IV infusion
22
Q

Name 2 mechanisms of fibrinolytic agents and name drugs in each class

A
  • Mechanism 1: convert plasminogen to plasmin with synthetic plasminogen activators (rTPA, Alteplase)
  • Mechanisms 2: Binds plasminogen to degrade fibrin: Streptokinase
23
Q

Herbs & supplements that are antiplatelet & anticoagulants

A
  • SSRI
  • Gingko
  • Garlic
  • Ginger
  • Fish oil
  • PC-SPES
24
Q

What are the targets in ththe anticoagiulation paththway

DABIGATRAN
RIVAROXABAN
APIXABAN

Longest half life

Benefits of Target specific oral agents

A

DABIGATRAN - IIa (thrombin)
RIVAROXABAN - Xa
APIXABAN - Xa

Longest half life - DABIGATRAN

Benefits
•	Treatment and prevention of arterial and venous thrombosis
•	Direct inhibitors so work quickly
•	Renal excretion
•	No antidote but have a short half life
•	No lab monitoring
•	Uniform dosing across patients
•	Few drug and food interactions

Year II Pharmacology (14 decks)

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