Cardiovascular and Renal Drugs Flashcards
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”)
Acetazolamide can be used to treat …
-managment of **glaucoma
-**
managment of idiopathic intracranial hypertension
-treats **mountain sickness
-**
prevents formation of uric acid kidney stones due to increase in pH
Acetazolamide side effects
- normal anion gap **metabolic acidosis-type II RTA
- hypokalemia
-**
promote formation of **calcium phosphate stones
-**
Sulfa drug
Mannitol is used to treat …
-increased intracranial pressure
(“High pressure head balloon”)
-increased intraocular pressure
(“Spilled eyeball cups”)
Mannitol Side Effects
- can cause pulmonary edema
- exacerbate heart failure
- hypo/hyper natremia
Mannitol Moa
Osmotic Diuretic
Name the Loop Diuretics
THE MOST EFFICIENT DIURETICS EVA !
Furosemide (SULFA)
Ethacrynic acid (NON-SULFA)
Loop Diuretics MOA
Site of action : TAL
- impermeable to water -diluting segment
(“secured water in car”) - Blocks NKCC transporter and cancels positive luminal charge
- K+ no longer effluxes from cells thus promote excretion of Mg+2 and Ca+2
- induce expression of COX-2 which synthesizes prostaglandins
- prostaglandins dilate afferent arteriole, increase RBF and enhance diuretic action
Loops diuretics are used for …
- 1st line for the symptomatic treatment of acute decompensated heart failure
- 1st line treat symptoms of pulmonary edema in an acute heart failure exacerbation
- loop diuretics treat ascites in liver failure
- can be useful in the treatment of HTN
which group of drugs may interfere with the actions of Loop Diuretics and why ?
NSAIDs - decrease prostaglandins synthesis ,thus interfere with the actions of loop diuretics
Side Effects of Loop Diuretics
- loop diuretics may cause hypokalemia
- prolonged use of loop diuretics can cause hypomagenesmia
- Loop diuretics can cause hypocalcemia (rare)
- can cause dose related hearing loss
- Interstitial nephritis can be caused by loop diuretics
- loop diuretics can cause hyperuricemia, may lead to gouty arthritis
- can cause contraction alkalosis
which group of drugs may interfere with the actions of Loop Diuretics and why ?
NSAIDs - decrease prostaglandins synthesis ,thus interfere with the actions of loop diuretics
Loop Diuretics MOA
Site of action : TAL
- impermeable to water -diluting segment
(“secured water in car”) - Blocks NKCC transporter and cancels positive luminal charge
- K+ no longer effluxes from cells thus promote excretion of Mg+2 and Ca+2
- induce expression of COX-2 which synthesizes prostaglandins
- prostaglandins dilate afferent arteriole, increase RBF and enhance diuretic action
Name the Loop Diuretics
THE MOST EFFICIENT DIURETICS EVA !
Furosemide (SULFA)
Ethacrynic acid (NON-SULFA)
can loop diuretics prolong the the life of the heart ?
No.
Names of the Thiazide Diuretics
-Hydrochloroathiazide (“Chloro-thighs” )
-Chlorothalidone (“thiodore roosevelt”)
Thiazides MOA
-block NaCl Transporter
- intracellular levels of Na+ drops → Ca+2/Na+ exchanger on basolateral membrane is enhanced
- more Ca+2 is reabsorbed
Thiazides are used to treat …
-one of the 1st line treatments for mild-moderate hypertension
(“high pressure pipes”)
-useful in treatment of symptomatic heart failure
(“balloon guy holding lithium and floppy heart balloon”)
- ***Loop Diuretics are 1st Line***
-thiazides may treat nephrogenic diabetes insipidus
and reduce polyuria and polydypsia
-thiazides can prevent Calcium stones
(“worker removing stones from tube slide”)
-patients with osteoporosis may benefit from thiazide treatment
(“life guard holding new calcium chalk”)
what are the side effects seen with Thiazide diuretics treatment ?
HYPER
Glycemia (“elevated candy jar”)
Lipidemia (“elevated butter stick”)
Calcemia (“elevated Calci-YUM ice cream”)
Uricemia - may precipitate gout (“yellow knitting needles”)
HYPO
Kalemia (“Banana peel on floor”)
Natremia (“salty peanuts on floor”)
——————————————————————————–
-can cause contraction/metabolic alkalosis
- may decrease the amount of Lithium cleared from the kidney , thus increase serum Lithium
- Sulfa drugs
Site of Action of Thiazide Diuretics
Distal Convoluted Tubules
what is the difference between Ca+2 Reabsoprtion in PCT and DCT ?
PCT- passive , paracellular
DCT- active , controlled by PTH
what is the site of action of K+ sparing Diuretics ?
Collecting Duct
what are the two types of cells found in the collecting ducts ?
Principal cells
the main Na+ reabsorbing cells and the site of action of aldosterone, K+-sparing diuretics, and spironolactone.
they secrete K+ through an apical membrane potasium channel.
α-intercalated cells
cells which contain apical H+ ATPase, explaining its ability to secrete protons.
Name the K+ sparing Diuretics
Amiloride
(“Almonds”)
Triamterene
(“Tangerines”)
Eplerenone
(“apple with the teacher”)
Spironolactone
(“inspector with spiral bound notebook”)
Aldosterone MOA
- upregulates ENaCs on the apical membrane
- upregulates Na+/K+ ATPse on the basolateral membrane
- upregulates K+ channels on the apical membrane
- upregulates H+ ATPase apical membrane