Pharmacology Flashcards
Heparin MOA
activates anti-thrombin III
Clopi MOA
P2Y12 inhibitor
Abciximab MOA
glycoprotein IIb/IIIa inhibitor
Dabigatran MOA
direct thrombin inhibitor
Rivaroxaban MOA
direct factor X inhibitor
Amiodarone MOA
Blocks K+ channels
furosemide site of action
ascending loop of henle
Furosemide MOA
inhibits the Na-K-Cl cotransporter in the thick ascending limb of the loop of Henle
ACE inhibitor MOA
inhibits conversion of angiotensin I to angiontensin II
Where are ACE inhibitors activated?
Liver
Common SE of ACE Inhibitors?
cough, angioedema, High K+
Can you give ACE inhibitors in pregnancy?
No
Beta Blockers MOA
Bind to beta-adrenoreceptors which prevents adrenaline/noradrenaline binding. This inhibits sympathetic effects
Beta blockers SE
bronchospasms, cold peripheries, fatigue, erectile dysfunction
Beta blockers CI
asthma, sick sinus syndrome, verapamil
Ivabradine SE
visual effects, particular luminous phenomena, are common
headache
bradycardia, heart block
Nicorandil MOA
potassium-channel activator with vasodilation through activation of guanylyl cyclase which results in increase cGMP
Nicorandil SE
headache
flushing
skin, mucosal and eye ulceration
gastrointestinal ulcers including anal ulceration
Renal causes of secondary hypertension
glomerulonephritis, pyelonephritis, PCKD
Endocrine causes of secondary hypertension
primary hyperaldosteronism
Cushings, Liddles
Drug causes of secondary hypertension
Steroids, COCP, NSAIDS
What normally happens to BP during pregnancy?
Decreases until 20-24 weeks then increases back to pre-pregnancy level
What is considered HTN in pregnancy
140/90 or an increase of 30/15
1st line management of HTN
<55/T2DM: ACE inhibitor or ARB
>55 or A/AC: CCB