angina Flashcards
stable/atherosclerotis angina aka
angina of effort, classic angina, angina pectoris
Prinzmetal’s angina aka
rest angina, variant angina, vasospastic angina, angina inversa
unstable angina aka
crescendo angina, ACS
MOA: irreversibly inhibits COX1 causing dec PG and thromboxane A2 so platelets dont stick
aspirin
SE aspirin
SE- inc bleeding, tinnitus, reyes syndrome
TxA2?
vasoconstriction and platelet aggregant
1st line antiischemic therapy?
beta blockers
2nd line antiischemic therapy
CCB
_____ is hallmark of any nitrate
HA
Only use if beta blockers or CCB are contraindicated
nitrates
Big 1st pass metabolism
Isosorbide dinitrate (DN)
need nitrate free period
Isosorbide dinitrate (DN)
SE- HA, HoTN/orthostatic HoTN
Isosorbide dinitrate (DN)
diff btwn Isosorbide mono and dinitrate
mono is the active metabolite of di. It has a high bioavailability and longer half life
Ranolazine treats ______
chronic angina
MOA: blocks Na from coming into the cell so Ca overload does not occur and coronary blood flow is improved
Ranolazine
Lipid lowering therapy
Omega 3 fatty acids
Niacin
Fibrates
_________ For pts with CAD and stable ischemic heart disease (SIHD)
lipid lowering therapy
2 essential events must occur in ACS
Disruption of atherosclerotic plaque causes platelet aggregation
Platelet rich clot forms
Unstable angina is _____ for troponin
-
NSTEMI is ____ for troponin
+
acs presentation in females
dyspepsia and indigestion
Earliest response to vasc injury is ______
vasospasm
What triggers platelet activation?
Collagen- exposed by vascular injury
ADP- sec from activated platelets
TXA2- diffuses out of activate platelets (remember ASA blocks this)
Thrombin- formed by coagulation cascade
Clopidogrel
P2Y12 inhibitors
Prasugrel
P2Y12 inhibitors
Ticagrelor
P2Y12 inhibitors
Ticlopidine
P2Y12 inhibitors
Cangrelor
P2Y12 inhibitors
Abciximab
GPIIb/IIIa inhibitors
Cilostazol
PDE inhibitors
Dipyridamole
PDE inhibitors
Eptifibatide
GPIIb/IIIa inhibitors
Tirofiban
GPIIb/IIIa inhibitors
Dipyridamole/ ASA
PDE inhibitors
Progrug activated in the liver by CYP2C19 that irreversibly blocks P2Y12 receptors
Clopidogrel
BBW: effectiveness depends on CYP450
Clopidogrel
Prodrug that irreversible blocks P2Y12 receptors
Prasugrel
Inhibits platelet aggregation faster than clopidogrel
Prasugrel
Not a prodrug
cangrelor and Ticagrelor
Reversibly binds to platelet ADP P2Y12 receptors
Ticagrelor
Acts faster but not as long as clopidogrel or prasugrel
Ticagrelor
Significant drug interactions with CYP3A4 inhibitors and inducers
Ticagrelor
MOA: Selectively and reversibly binds to P2Y12 receptors
Cangrelor