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Pharm II > test 3 > Flashcards

test 3 Flashcards

1
Q

Arterial thrombus

A
  • Consists mainly of platelets

* Occur in thrombogenic vessels due to atherosclerosis

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2
Q

Venous thrombus

A
  • Consists mainly of fibrin and fewer platelets

* Triggered by blood stasis or inappropriate activation of coagulation cascade

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3
Q

Thrombotic Disorders

A
  • Myocardial infarction (MI)
  • Deep vein thrombosis (DVT)
  • Pulmonary embolism (PE)
  • Acute ischemic stroke
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4
Q

Platelet Response to Vascular Injury

A

• Resting endothelial cells release nitric
oxide and prostacyclin
• Platelet inhibitors
• Binds to receptor that is coupled with
the synthesis of cAMP
• increase in cAMP is associate with:
• decrease in Ca2+ levels
• Inhibits platelet activation
• Inhibits of GP IIb/IIIa receptors
• Inhibits release of granules
• Platelets bind to exposed
collagen
• Promote platelet aggregation
• Release of granules
• ADP
• Serotonin
• Thromboxane A2
• Thrombin
• PAF
• Bind to nearby resting platelets
• Promote platelet activation and aggregation
• Mediated by high levels of Ca2+ and low levels of cAMP
- ending in fibrinolysis

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5
Q

Platelet Inhibitors

A
  • Decrease clot formation
  • Decrease the action of chemical modifiers that promote platelet aggregation
  • Treatment used for:
    * Occlusive cardiovascular disease
    * Maintain patency of arterial vascular grafts
    * Additive therapy to thrombin inhibitors
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6
Q

Aspirin and/or Acetylsalicylic Acid

A
  • Irreversibly binds (inactivates) cyclooxygenase-1 (COX-1)
  • Inhibition lasts the entire life span of the platelet (7-10 days)
  • Inactivates COX-1 by adding an acetyl group serine site of COX-1
  • Inhibition of thromboxane A2 synthesis
    * Inhibits platelet aggregation
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7
Q

Aspirin: Therapeutic Actions

A
  • Anti-inflammatory action
  • Analgesic action (pain killer)
  • Antipyretic action
    * Decrease in prostaglandin synthesis
  • External applications (salicylic acid)
    * Topically to treat acne, corns, calluses, and warts
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8
Q

Aspirin: Therapeutic Uses

A

• Low dose aspirin (81mg) – prophylactically
1. Reduce recurrent cardiovascular events and/or death
2. Reduce risk of transient ischemic attacks (TIAs) or stroke
3. Reduce cardiovascular events in patients with unstable angina
4. Reduce risk of death in patients undergoing certain revascularization procedures
• Chronic low dose allows for continued inhibition as
new platelets are generated

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9
Q

Aspirin: Adverse Effects

A
  • Gastrointestinal (GI) bleeding and ulcers
    * Prostaglandins promote gastric acid secretion and mucus production
  • Increase risk of bleeding
    * Stop 1 week prior to surgery
  • Hemorrhagic stroke
  • Kidney damage
    * Prostaglandins are responsible for maintaining renal blood flow
    * Blocking prostaglandin synthesis can result in retention of sodium and water
  • Should be avoided in patients less than 20 years old with viral infections
    * Prevent Reye syndrome
    * Hepatitis with cerebral edema often resulting in death
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10
Q

Aspirin: Pharmacokinetics

A
  • Rapidly deacetylated by esterases to produce salicylate
    * After oral administration
  • Salicylates can cross the BBB and placenta
  • Salicylates can be absorbed through skin
  • Salicylates are cleared by the kidneys
  • Low dose
    * t1/2 = 3.5hrs
    * First-order elimination
  • High dose
    * t1/2 = 15 hours or longer
    * Zero-order elimination
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11
Q

Thienopyridines

A
  • ADP Receptor Blockers
    • Irreversibly inhibit ADP receptors
    • Subtype P2Y12
    • Inhibit activation GP IIb/IIIa receptors
    • GP IIb/IIIa receptor activation is required for platelets to bind fibrinogen and to each other
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12
Q

Ticlopidine

A
  • Approved for use in prevention of TIAs and thrombotic stroke
  • Approved for use with aspirin to prevent coronary stent thrombosis
  • Onset of action
    * 3 – 4 days
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13
Q

Ticlopidine: Adverse Effects

A
  • Agranulocytosis
    * Low white blood cell count
  • Thrombotic thrombocytopenia purpura (TTP)
  • Hemorrhage
  • Aplastic anemia
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14
Q

Clopidogrel (Plavix)

A
  • Platelet inhibition occurs 3 - 5 days after oral dose

* Duration of antiplatelet effect is 7-10 days

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15
Q

Clopidogrel (Plavix): Uses

A
  • Prevention of atherosclerotic events
    * Patients with recent MI, stroke, or PAD
  • Prevention of thrombotic events in acute coronary syndrome
  • Prevention of thrombotic events associated with percutaneous coronary intervention (PCI)
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16
Q

Clopidogrel (Plavix) Adverse effects:

A
  • bleeding
  • Thrombotic thrombocytopenia (less than ticlopidine)
  • Neutropenia (less than ticlopidine)
17
Q

Prasugrel

A
  • Similar to clopidogrel
  • Onset of action
    * 2 – 4 hr
  • Approved to decrease thrombotic cardiovascular events
    * Patients with acute coronary syndrome
  • Contraindicated in patients with history of TIAs or stroke
  • Black box warning
    * bleeding
18
Q

Ticagrelor

A
  • Reversible inhibition of ADP receptor
  • Onset of action
    * 1 – 3 hr
  • Approved for prevention of arterial thromboembolism
    * Patients with unstable angina
    * Acute MI
    * PCI
19
Q

Ticagrelor Adverse effects

A
  • Bleeding (black box warning)

* GI disturbances

20
Q

Glycoprotein (GP) IIb/IIIa Blockers and adverse effects

A
  • All are given by IV bolus, followed by IV infusion
  • Adverse effect
    * bleeding
21
Q

Abciximab (Reopro)

A
  • Chimeric monoclonal antibody
  • Binds to the GP IIb/IIIa receptor and blocks fibrinogen and von Willebrand factor
    * Blocks aggregation
  • Approved for use in percutaneous coronary intervention
  • Approved for use in acute coronary syndrome
  • Platelet inhibition
    * Within 30 min
    * Lasts 24-48 hrs
22
Q

Eptifibatide

A
  • Cyclic peptide
  • Binds to the GP IIb/IIIa receptor
    * Prevents binding of fibrinogen
23
Q

Tirofiban

A
  • Non-peptide
  • Binds to the GP IIb/IIIa
    * Prevents binding of fibrinogen
24
Q

Dipyridamole

A

• Phosphodiesterase inhibitor
• Increases intracellular levels of cAMP
• Decreases thromboxane A2
synthesis
•Directly stimulates the release of prostacyclin
• Potentiates the antiaggregating action of prostacyclin
• Coronary vasodilator
• Vascular smooth muscle - increase cAMP causes relaxation
• Inhibits myosin light chain kinase

25
Q

Dipyridamole use

A
  • Used for stroke prevention
    * Given with aspirin
  • Adjunct to anticoagulant therapy to prevent thrombus formation
    * Valve replacements
26
Q

Dipyridamole: Adverse Effects

A
  • Headache
  • Postural hypotension
  • Should not be used in patients with unstable angina
    * May worsen ischemia (coronary steal phenomenon)
27
Q

Cilostazol

A

• Phosphodiesterase inhibitor
•Prevents the breakdown of cAMP
•Decreases thromboxane A2
synthesis
• Inhibition of platelet aggregation
• Coronary vasodilator
• Smooth muscle - cAMP causes relaxation
• Inhibits myosin light chain kinase

28
Q

Cilostazol use

A
  • Used to reduce symptoms of intermittent claudication
    * Patients with PVD
  • Decreases triglycerides and increases HDL
  • Adverse effects:
    * Headache
    * GI disturbances
    * Contraindicated in patients with advanced HF

Pharm II (37 decks)

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