CV agents C7 Flashcards
(24 cards)
what are some examples of antiplatelet drugs
aspirin, clopidogrel, prasugrel, warfarin, ticagrelor
clopidogrel MOA
ADP receptor antagonist
prevents activation of P2Y12 receptor by ADP on platelets
preventing platelet aggregation
glycoprotein IIb/IIIa inhibitors (abcixmab, eptifibatide) mechanism of action
prevent platelet aggregation by blocking the binding of fibrinogen to receptors on platelets
types of antiplatelet drugs
ADP/P2Y12 receptor antagonists
glycoprotein IIb/IIIa inhibitors
ADP: adenosine diphosphate
aspirin MOA
irreversible COX-1 inhibitor
prevents formation of TXA2 and therefore platelet synthesis and aggregation
what is reyes syndrome
swelling in liver and brain
can be caused by taking aspirin in under 16’s - contraindicated
aspirin adverse effects
asthma
GI irritation
haemorrhage
increased bleeding
rhinitis
skin reactions
examples of ADP/P2Y12 receptor antagonists
clopidogrel
cangrelor
pasugrel
ticagrelor
antiplatelet drugs general adverse effects
GI bleeding
hypersensitivity
increased risk of bleeding - can present as unexplained bruising, excessive bleeding
what is GTN and MOA
Glyceryl trinitrate
used to treat acute angina/acute coronary syndrome
converted to nitric oxide in body - vasodilator. ACTIVATES and therefore modulates guanylate cyclase (enzyme) - signalling pathway leading to relaxation of vascular smooth muscle
vasodilation improves blood flow to heart, reducing oxygen demand and preload and afterload
how do nitrates work
coronary vasodilation
decrease preload and reduction in cardiac work
why is a nitrate free period needed when using long acting nitrates such as isosorbide mononitrate
prolonged exposure can mean build up of tolerance and therefore reduce effectiveness
aim for nitrate free period
achieved through assymmetric dosing - 1st dose in moring, 2nd early afternoon
nitrates adverse effects
hypotension
headache
burning/stinging/tingling of mouth
difference between GTN and Isosorbide mononitrate
same MOA
- conversion into NO
GTN: rapid onset, shorter duration, sublingual administration = bypass 1st pass metabolism, short half life - metabolised in the liver
ISMN: slower onset, longer duration, oral administration - slower absorption, long half life
MOA statins (atorvastatin, simvastatin, pravastatin)
The enzyme HMG-CoA reductase is involved in the synthesis of cholesterol
Statins inhibit this enzyme to therefore, stop the synthesis of cholesterol and, therefore, reduce plasma cholesterol levels
The reduction of plasma cholesterol leads to the upregulation of LDL (bad cholesterol) receptors in the liver, leading to the uptake of cholesterol from the plasma into the liver, therefore also lowering plasma cholesterol levels
when are statins used
acute coronary syndrome as secondary prevention
hypercholesterolaemia
what are the lipids that should be monitored when using statins (hint: 4)
total cholesterol
HDL-cholesterol
non-HDL cholesterol
LDL cholesterol
why should creatinine kinase conc be measured in patients taking a statin before and of they have muscle pain
rhabdomylosis
what hepatic test should take place prior to statin treatment
liver transaminases
statins are metabolised via the liver so where there is liver impairment due to disease or infection, lower doses should be used to prevent accumulation and toxicity
MOA and use of fondaparinux
Fondaparinux sodium is a synthetic pentasaccharide that inhibits activated factor X.
treatment of NSTEMI
why is fondaparinux used instead on enoxaparin in the management of the acute coronary syndrome NSTEMI
lower associated bleed risk
MOA ace inhibitors - Ramipril, perindopril, lisinopril
block the conversion of angiotensin 1 to angiotensin 2 by inviting the angiotensin converting enzyme (ACE)
angiotensin 2 is related to vasoconstriction, raising blood pressure.
The blockage of its formation leads to marinating vasodilation and keeping blood pressure low.
MOA beta blockers - bisoprolol, atenolol, labetalol
block the adrenoceptors in the heart and peripheral vasculature (Beta 1)
also have some effect at bronchi, pancreas and liver
results in lower cardiac output
block activity of epinephrine
= lowers BP and HR
monitor for low heart rate (symptoms: dizziness, lightheadedness)
MOA ARBs - candesartan, losartan, irbesartan
angiotensin receptor blockers
These are angiotensin receptor blockers that prevent the binding of angiotensin 2 to the angiotensin receptor.
The angiotensin receptor when active, stimulates vasoconstriction, increasing blood pressure.
