Cardiovascular and Renal Drugs Flashcards
(121 cards)
digoxin MOA
-inhibits Na+/K+ ATPase -
( “knocked over banana vending machine”)
-leads to increased intracellular Na+
(“offwhite man holding salty peanuts, salty peanuts in floor”)
-increase intracellular Na+ promotes Calcium inlfux through the Na+/Ca+2 exchanger
(“salty peanuts guy opens the door for the Calci-YUM guy”)
-results in increased contractillity
(“blue shirt guy flexes his arm “)

what is Digoxin used for ?
- Anti-arrhythmic effect (“turntable”)
- symptomatic treatment of chronic systolic HF (“deflated balloon”)
-direct stimulation of the Vagal nerve can treat Atrial arrhythmias
(“las VAGas”)

side effects of Digoxin
-hyperkalemia as a result of acute toxicity
(“pile of bananas”)
-induce various Arrhythmias
(“various dancers on heart shaped dancing floor”)
-chronic use of Digoxin may cause scooped concave ST segment on ECG
(scooped ice cream can says :”taSTy”)
-Bradycardia due to parasympathetic activation of SA node
(“Dangling heart watch” , “SA music note”)
- Heart block in case of toxicity (“AV music note”)
- GI symptoms (“nauseated dancer”)
- Xanthopia (“yellow spotlight”)

Digoxin is contraindicated in …
-SA node heart block
(**use with caution in beta blockers**)

what may exacerbate digoxin toxicity ?
Hypokalemia
- loop diuretics may cause hypokalemia , diarrhea , vomiting
Renal insufficiency
can make digoxin toxicity worse and will precipitate digoxin rise, the long flag indicates the long 1⁄2 life of digoxin, and increasing susceptibility to toxicity
- many arrhythmics inhibit renal clearance of digoxin, increasing susceptibility to toxicity

what can reverse digoxin Toxicity ?
immune fab (“FAB uolous las vegas” sign)
which drugs can treat Acute heart failure ?
Milirinone
(donkey sign says “hes One in a million”)
Nesiritide
(elephant sign says “necessary to turn the tide”)

Milirinone MOA
-inhibits phosphodiesterase
(“don’t phoster disinterest”)
-decreases CAMP breakdown
(sign says “join the CAMPaign”)
-increases cardiac contractility
(“red donkey flexing arms”)
-causes arteriolar dilation in HF, but watch for hypotension
(“dilated red donkey ears”)

Nesiritide MOA
-BNP analog that increases cGMP
-Nesiritide causes arteriolar AND venous dilation, reducing afterload and preload→natiuresis
(“elephant has dilated red ears and blue legs”)
(“BuMP the GruMP”)

Name the ACE inhibitors
- *-PRIL**
- *CAPTO/**pril
- *ENALA/**pril
- *RAMI/**pril
- *LISINO/**pril
ACE inhibitors MOA
inhibit ACE ⇒ATI is not converted to ATII
→ counteracts ATII effects
- dilate efferent arteriole → decrease GFR
- decrease Aldosterone Release →decrease Na+ reabsorption (natiuresis)
- decrease pressor effects of ATII
(“floppy red suspenders”)
ACE inhibitors are used to treat …
-1st line treatment for CHF
(“failing heart balloon”)
-used in myocardial infarction
(“mandolina player playin dem Broken heart strings”)
-1st line agents used for HTN
(“High pressure candy pipes”)
-slow the progression of diabetic nephropathy
(“Diasweeties Candy shop”)
- ACEi reduce Mortality
(“Angel above le cross”)

which patients should be started on ACEi therapy ?
-patients with albuminuria and BP > 130/80
(“albums in diasweeties candy shop”)

what side effects might ACEi cause ?
-can cause significant hypotension and syncope in patients with high renin levels (in heart failure)
(“fainting poker player with floppy red suspenders”)
-can cause hyperkalemia due to decreased aldosterone levels
(“raised banana daquiri”)
-dry cough due to an increase of bradykinin
(“coughing dealer”)
-ACE increases the risk of fetal hypotension
(“Tarantula on mama’s back”)

when are ACEi contraindicated and why ?
- ACE inhibitors are contraindicated inhereditary angioedema ( to C1 esterase deficiency) due to increased Bradykynin activity .
- ACE inhibitors are contraindicated in bilateral renal artery stenosis due to further decrease in GFR
- use of ACEi can precipitate acute renal failure charachterized by persistent increase in creatinine levels-azotemia

which drugs should be avoided during ACEi therapy ?
NSAIDs should be avoided since they inhibit the actions of prostaglandins and bradykynin , causing vasoconstriction of afferent arteriole→GFR decrease
- can precipitate acute kidney injury

Possible side effects of ARBs
- Hyperkalemia (“banana daquiri on taken chair”)

Name a drug which can directly inhibit renin
Aliskiren
(“high limit-high risk slots”)

name a possible side effect of Aliskiren ?
Hyperkalemia
(“slot machine showing 3 bananas”)

in case of Hereditary angioedema , which drugs can replace ACEi therapy ? why ?
ARBs can be used as a replacement therapy since they don’t affect bradykynin serum levels
Name the ARBs
-SARTAN (chair says “SoRry TAkeN”)
LO/ sartan
CANDE/ sartan
VAL/ sartan
MOA OF ARBs
Angiotensin II receptor blockers
which drugs act on the Proximal Convoluted Tubule ?
**Acetazolamide
Mannitol**
Acetazolamide MOA
Inhibits Carbonic Anhydrase enzyme
- less H+ into the interstitium
- Na+/H+ exchanger inhibited
-cause bicarbonate (HCO3-) to stay in the tubular lumen leading to urine alkalization
(“Spilled alkaline substance on inside track”)
-prevent sodium reabsorption leading to natiuresis
(“Dropping salty peanuts on the inside of track”)
(“Acid from battery breaks car battery”)


























































































