Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
52 Cards in this Set
- Front
- Back
|
Aspirin
|
Platelet (COX-1) Inhibitor, irreversible
|
|
|
NSAID
|
Platelet inhibitor, reversible:
inhibits TXA-2 dependent platelet function |
|
|
Dipyridamole (Persantine)
|
PDE-Inhibitor
ATP --> cAMP --[PDE]--> AMP Thus, cAMP accumulates, which is platelet inhibitor Vasodilator & anti-platelet properties |
|
|
Cilostazole
|
PDE-Inhibitor
ATP --> cAMP --[PDE]--> AMP Thus, cAMP accumulates, which is platelet inhibitor Vasodilator & inhibit platelet aggregation Used to treat intermitten claudication |
|
|
The 2 PDE-Inhibitors?
|
Dipyridamole
Cilostazole |
|
|
What's a P2Y12 receptor?
|
ADP binds to it --> it causes platelet aggregation
|
|
|
The 4 P2Y12-Receptor Inhibitors?
|
Clopidogrel (Plavix)
Ticlopidine (Ticlid) Presugrel & Ticagrelor (newer ones) |
|
|
Which P2Y12 receptor inhibitor is dependent on CYP2C19 to get metabolized?
(the other 3 aren't sensitive to CYP2C19) |
CLOPIDOGREL
Many people have mutant 2C19 enzyme! |
|
|
Clopidogrel
|
P2Y12 receptor inhibitor
- Fastest onset of inhibition of platelets (2 hr w/ high dose, 2 days w/ low dose) - Metabolized by CYP2C19 - Absorbed orally |
|
|
Ticlopidine
|
P2Y12 receptor inhibitor
- Slow onset of effect (2 wk), thus NOT good for acute situations like unstable angina - May cause neutropenia and TTP - NOT sensitive to mutations in CYP2C19 |
|
|
Presugrel & Ticagrelor
|
P2Y12 receptor inhibitor (new one)
- REVERSIBLE inhibition!! (distinct from the older classes, Clopidogrel & Ticlopidine) - NOT sensitive to mutations in CYP2C19 - ORAL!! |
|
|
The 3 Glycoprotein IIb/IIIa (aIIbB3) antagonists?
|
Abciximab
Tirofiban Eptifibatide - aIIbB3 receptor (in platelets) binds fibrinogen & promote platelet aggregation! - Given ACUTELY via IV ONLY!! |
|
|
Abciximab
|
Glycoprotein IIb/IIIa (aIIbB3) antagonist (monoclonal antibody)
Goal: reduce number of UNBOUND receptors to <20,000 per platelet! This decreases platelet aggregation enough to prevent thrombus formation VERY SHORT half-life: <10-30 minutes |
|
|
Tirofiban
|
Glycoprotein IIb/IIIa (aIIbB3) antagonist
- Derivative of tyrosine. inhibits aIIbB3 receptor w/ minimal effects on vitronectin receptors - May cause severe but reversible thrombocytopenia! |
|
|
Eptifibatide
|
Glycoprotein IIb/IIIa (aIIbB3) antagonist
Synthetic disulfide-linked cyclic hepatapeptide |
|
|
Bivalrudin
|
Direct Thrombin Inhibitor
- Directly (-) thrombin activation in circulation - Half-life: 30 min!! Proteolytically broken down in circulation --> metabolized by liver, cleared by kidney **ONLY AVAILABLE AS IV** - Used only if Heparin isn't an option (ie. HITT) |
|
|
Gold standard for anti-platelet therapy?
|
Aspirin
|
|
|
Drug of choice for Acute Coronary Syndrome
|
Aspirin
|
|
|
DTI vs LMW-Heparin
|
DTI has lower mortality, and further reaching effects!
|
|
|
Drugs of choice (2) for A-Fib
|
Warfarin or Vitamin K
Prevents cardioembolic strokes |
|
|
Not DOC, but equal efficacy for treating A-Fib
|
Oral DTI - equal efficacy to Warfarin (a DOC)
|
|
|
3 Regiments of choice for Transient Ischemic Attacks
|
HIGH-dose aspirin (but risk of GI effects and intracranial hemorrhage)
LOW-dose aspirin + Dipyridamole LOW-dose aspirin + ADP-Inhibitor (P2Y12-receptor: Clopidogrel, Ticlopidine, Presugrel, Ticagrelor) |
|
|
Treatment for HIT (besides discontinuing Heparin)
**bonus: which 2 are CONTRAINDICATED for HIT treatment? |
DTI (Bivalrudin) - give ASAP!
**Platelet transfusions are CONTRAINDICATED!!! "Fuel the fire" **Warfarin (used alone, without a DTI) also CONTRAINDICATED --> makes venous gangrene worse! |
|
|
Lepuridin (class & origin)
|
DTI, highly specific
Lepuridin is a recombinant HIRUDIN (from saliva of leeches) |
|
|
Lepuridin metabolism/clearance
|
Renally cleared, thus must ADJUST DOSE in renal failure!
|
|
|
Lepuridin: goals of treatment (3)
|
KEEP LEPURIDIN ADMINISTRATION UNTIL:
1. INR > 2.0 2. No new thromboembolic complications 3. Platelet recovery |
|
|
Lepuridin (Hirudin) half-life is affected by...
|
Half-life is prolonged by Antibodies that may form against Hirudin!
|
|
|
Argatroban (class & short/vs/long half-life)
|
DTI (synthesized from L-Arginine)
SHORT half-life! 45 min |
|
|
Argatroban metabolism
|
LIVER
|
|
|
Major problem with DTI's
|
NO reversal agent (antidote) if bleeding were to occur!
|
|
|
3 Thrombolytic Therapy drugs
|
Streptokinase (not used anymore)
Urokinase t-PA: Alteplase & Reteplase |
|
|
Streptokinase (class; origin)
|
Thrombolytic therapy (complexes w/ plasminogen & cleaves it into plasmin)
Created by beta-hemolytic streptococci |
|
|
Streptokinase: how is it dosed?
|
Loading dose - to overcome Ab to protein
|
|
|
Urokinase (class; origin)
|
Direct plasminogen activator (for thrombolytic therapy)
From human kidney cells |
|
|
Alteplase (class)
|
t-PA (direct plasminogen activator)
Works best when fibrin is present! |
|
|
Reteplase (class)
what's the difference between Reteplase and the other RX in this class? |
t-PA (direct plasminogen activator)
Reteplase has FASTER onset of action & LONGER duration of action than Alteplase! |
|
|
5 Indications for Thrombolytic Therapy (Streptokinase, Urokinase, t-PA: Alteplase & Reteplase)
|
1. MI (within 6 hr of symptoms)
2. Peripheral arterial or graft occlusion (give RX directly to site via catheter!) 3. CVA (within 3 hr of symptoms) 4. Pulmonary embolism (if massive PE w/ shock) 5. DVT |
|
|
8 CONTRA-Indications for Thrombolytic Therapy (Streptokinase, Urokinase, t-PA: Alteplase & Reteplase)
|
1. Surgery within 10 days
2. Trauma within 10 days 3. Serious GI bleeding in the past 3 mo 4. History of HTN (Diastolic >110) 5. Active bleeding or hemorrhagic disorder 6. Previous CVA or active intracranial process 7. Aortic dissection 8. Acute pericarditis |
|
|
ALL thrombolytic drugs require followup treatment with which of 2 agents:
|
1. Antiplatelet AND/OR
2. Anticoagulant |
|
|
POINT 1 FROM ANTICOAGULANT LECTURE:
What is the goal of Heparin administration & monitoring? (achieve what outcome & in what timeframe?) |
GOAL OF HEPARIN THERAPY:
Achieve therapeutic aPTT in the FIRST 24 HOURS OF HEPARIN THERAPY!! -- This prevents recurrent DVT's and PE's |
|
|
POINT 2 FROM ANTICOAGULANT LECTURE:
What drug to reverse the effects of Heparin? MOA? |
PROTAMINE SULFATE
- Is a strong base. Complexes with the strongly acidic Heparin --> forms a stable salt - Reverses Heparin's effect within 5 MINUTES of administration!! **But beware of hypersensitivity reaction in sensitive patients. DO NOT give protamine too fast!!** |
|
|
POINT 3 FROM ANTICOAGULANT LECTURE:
Mechanism of elimination of LMWH? |
LMWH is RENALLY excreted! Thus, must adjust dose in kidney failure!
|
|
|
POINT 4 FROM ANTICOAGULANT LECTURE:
What's the best way to monitor Warfarin therapy? |
BEST WAY TO MONITOR WARFARIN:
INR (prothrombin time) |
|
|
MOA of Heparin (unfractionated vs LMWH)
|
Binds Antithrombin --> Inhibit Factor Xa + IIa (thrombin)
LMWH is small, so it mainly inhibits Factor Xa VERY SHORT half-life (1-1.5 hr) |
|
|
Where is Unfractionated Heparin eliminated?
|
Reticuloendothelial System
(Small fraction renally excreted; not as significantly as LMWH!!) not removed by hemodialysis |
|
|
3 LMWH (names)
|
Enoxaparin
Dalteparin Tinzaparin **-PARIN** |
|
|
Indication for Heparin
|
Acute treatment of DVT, PE
|
|
|
Which drug is given for Secondary Prevention (prevent recurrent DVT/PE in the 3-6 mo of Heparin Therapy)
|
Warfarin (Coumadin) to prevent recurrent DVT/PE during the next 3 to 6 months of therapy
|
|
|
MOA of Warfarin
|
Inhibits Eposide reductase & Vitamin K reductase --> causes the synthesis of dysfunctional coagulation factors II, VII, IX, X, Protein C + S
|
|
|
Fondaparinux (class, MOA)
|
Pentasaccharide of Heparin
Also binds AT --> inhibit Factor Xa |
|
|
Fondaparinux excretion?
|
(Pentasaccharide of Heparin)
RENALLY excreted! |
|
|
Agent to reverse effect of Fondaparinux
|
NO REVERSING AGENT!! Protamine doesn't work for Fondaparinux!
|
