Treats Diabetic Nephropathy Causes Dry Cough Causes Angioedema

(Kidney shaped jelly beans) (cough) (duck face= swelling of lips/mouth)

 Side effect of ACE  Rapid-onset swelling of the eyes, tongue,
lips, and larynx that may compromise the
inhibitors and may airway.
shows patient  Thought to result from accumulation of
intolerance to drug. bradykinin.
 ACEIs are contraindicated in patients at
risk of angioedema (e.g. C1 esterase
inhibitor deficiency).

Treats Heart Failure

(heart beating out of chest)
 Provides a mortality benefit, by slowing pathologic
cardiac tissue growth and remodelling. It also reduces
systemic BP and hence after load.
May cause Hyperkalemia
(raised Banana=High potassium)

Increase Bradykinin Levels

(braids = bradykinin) Reduces Angiotensin II
End in –pril  ACE normally inactivates
(angel 2 wings)
(pearls) bradykinin.
 Causes an accumulation of
Drug names for ACE
bradykinin, causing cough
inhibitors all end in –pril. and angioedema.

 Captopril
 Lisinopril
 Enalapril
 Ramipril
 Benazepril Treats Hypertension
(Deflating Pool ring)
Reduction in angiotensin II inhibits
vasoconstriction and reduction in
down stream aldosterone signaling
ACE Inhibitors reduces blood volume to cause a
(aces) decrease in blood pressure.
ACE inhibitors function by blocking angiotensin converting
enzyme (ACE). Blocking conversion of angiotensin I to II.
 Summary of ACE inhibitors:
 ACE inhibitors (ACEIs) are a class of drugs that work by inhibiting angiotensin-converting enzyme
(ACE). ACE inhibitors as a drug class have names ending in the suffix -pril, including lisinopril,
enalapril, ramipril, captopril, and benazepril. The clinical effects of ACE inhibitors can be primarily
broken into two main effects: first, they prevent conversion of angiotensin I into angiotensin II by
ACE. Second, ACE is also used for bradykinin breakdown, so ACE inhibitors can increase bradykinin
levels.
 Reducing levels of angiotensin II decreases blood pressure by way of reducing vasoconstriction and
reducing aldosterone release. This can be helpful in the treatment of hypertension, although high
doses of ACE inhibitors can go too far the other way and induce hypotension. By reducing systemic
blood pressure, ACE inhibitors reduce the work of the heart and are therefore useful in the
treatment of heart failure. In heart failure patients, ACE inhibitors are first-line because they confer a
mortality benefit. ACE inhibitors also have a renoprotective effect, which means that they can
protect the kidneys in patients with hypertension or diabetes.

 Besides the hypotension that we already talked about, other side effects of ACE inhibitors include
angioedema and the development of a dry cough, both which are related to increased bradykinin
levels in the body. ACE inhibitors can also cause hyperkalemia by reducing aldosterone release.
Lastly, ACE inhibitors are teratogenic and should be particularly avoided in pregnant women to
reduce the risk of kidney malformations in the fetus.
 Can cause Gynecomastia Spironolactone (drug)
(bra on male mannequin) (spire)
Antiandrogenic effects of aldosterone receptors
blockers like spirolactone can lead to male breast
development, also know as gynecomastia.

Aldosterone Receptor Blockers = Mechanism

(duster = alDUSTERone, Falling = blocking)
 Include drugs spironolactone and
Treats Heart Failure
eplerenone
(heart-shaped chocolates)
• Androgen receptor blockers
have a proven mortality benefit
in treatment of systolic heart
Decrease H+ Secretion failure, by preventing
(caught lemon from falling) pathological cardiac tissue
This can lead to non-anion gao metabolic acidosis growth and remolding.
in high doses.
Eplerenone (drug)
(Pear = ep-PEAR-enone)

Decreased K+ Secretion Treats Hirsutism

(caught banana from falling)
(hairy arm)
This can lead to hyperkalemia in high
Antiandrogenic effects of
doses.
spirolactone can be used to
treat hirsutism (excess hair
growth , esp. in women)
Antiandrogenic Effect
(broken android device)
 Antagonist at the androgen receptor
(AR)Androgen receptors are normally bound by
testosterone and dihydrotestosterone (DHT).
 Summary Of Aldosterone receptor
antagonists:
 Aldosterone receptor antagonists are a class of diuretics that include Spironolactone and Eplerenone.
As their name suggests, these drugs inhibit aldosterone receptors located in the principal cells of the
distal tubules and collecting ducts of the kidneys. By blocking aldosterone signaling, these drugs
increase the excretion of sodium and water, causing diuresis. These drugs also reduce the excretion
of potassium and hydrogen ions, which is why they are sometimes called “potassium-sparing” drugs.

 Because aldosterone receptor antagonists are not very specific for aldosterone receptors, they can
also bind to and block androgen receptors, leading to anti-androgenic effects blocking the actions of
testosterone. As such, aldosterone receptor antagonists are known as antiandrogen drugs.

 Clinically, aldosterone receptor antagonists are used for the treatment of systolic heart failure. Being
diuretics, they are also used to treat ascites and other fluid overload states. Finally, because of their
antiandrogenic effects, they can be used to treat hirsutism, such as that caused by polycystic ovarian
syndrome.

 Potential side effects to know for these drugs include gynecomastia, reduced libido and impotence,
which are all related to antiandrogenic effects. Since these drugs increase the retention of potassium
and hydrogen ions, they can potentially lead to hyperkalemia and metabolic acidosis.
 Loop Diuretic
Ototoxicity
(loops) (covering ears)
Ethacrynic acid is one of the most Ethacrynic acid is more ototoxic than
potent loop diuretic primarily used in other loop diuretics (eg, Furosemide)
patients with sulfa allergies.

Causes Hyperuricemia / Gout Used with Sulfa Allergiees

(swollen big toe = podagra) (rotten sulfur eggs)
Loop diuretics can reduce excretion of uric acid in  Ethacrynic acid is not a sulfa
the urine, leading to hyperuricemia and gout. drug and can be used as a
Gout is known as large deposit in interphalangeal loop diuretic in these patients.
joint of the great toe, formally called as podagra.

Ethacrynic Acid
(‘Etha Allen”)
 Summary Of Ethacrynic acid:
 Ethacrynic acid is a type of loop diuretic. Like all loop diuretics, it works
by inhibiting the sodium-potassium-chloride cotransporter in the
ascending loop of henle to induce diuresis. The net effect of ethacrynic
acid is increased excretion of water, sodium, and potassium. It also
causes an increase in calcium and magnesium excretion.
 Ethacynic acid has nearly identical clinical uses to other loop diuretics.
However, because they do not contain the sulfonamide groups
generally found in other diuretics, ethacrynic acid is particularly good
for treatment of patients with sulfa allergies.

 However, there are a few adverse effects of ethacrynic acid. Firstly,

because ethacrynic acid can interfere with ion balance within the ear, it
is ototoxic and can cause hearing loss or tinnitus. Secondly, ethacrynic
acid can cause hyperuricemia, leading to gout.
 Loop Diuretics targets Loop of Henle Induces Diuresis / Treats Edema
(race track loop) (dumping water)
High does can lead to hypervolemia and hypotension = (empty water bucket)

Causes Ototoxicity
(covering ears)

Furosemide (drug)
(furious driver)

Torsemide (drug)
(taurus)

Bumetanide (drug)
(boombox)
Sulfa Drugs / Causes Allergy
(sulfurous rotten eggs)
Loop diuretics are sulfa drugs should be
avoided in patients with sulfa drugs
allergy.

Blocks Na+/K+/2Cl- triple Transporter

(ruined salty peanuts = Na+,) (banana =K+), (chlorine pool =Cl-)
 These drugs work by inhibiting the sodium-potassium-chloride triple
transporter in the ascending limb of the loop of henle. This decreases the
medullary concentration gradient, preventing water reabsorption.
 Summary Of Loop Diuretics:
 Loop diuretics are powerful diuretics that include furosemide, bumetanide,
and torsemide. These drugs work by inhibiting the sodium-potassium-
chloride triple transporter in the ascending limb of the loop of henle.
 This decreases the medullary concentration gradient, preventing water
reabsorption. The net effect of loop diuretics is increased excretion of
water, sodium, and potassium. Because of their potent diuretic effects,
loop diuretics are often used in the treatment of volume overload states as
well as in the treatment of hypertension.
 Important side effects to note include ototoxicity, sulfa allergy, as well as
severe hypotension and hypovolemia, which may result in contraction
alkalosis and even acute kidney injury! Because these drugs increase
potassium excretion, loop diuretics are notorious for causing hypokalemia.
Lastly, like most other diuretics, loop diuretics can increase uric acid levels
to increase the risk of gout.
 Osmotic Diuretic Treats Elevated ICP
(pooling sweat) (steam coming out of ears = elevated intracranial pressure)
 By increasing serum osmolality, mannitol pulls water from
the brain into the blood, reducing brain water content,
bulk, and therefore ICP.
 Mannitol is an intravenous osmotic diuretic used primarily
to lower intracranial pressure and treat acute
glaucoma.

May cause Early Pulmonary

Edema Causes Late Hypernatremia
( water sprying fan = wet lungs) (salted peanuts= high sodium)
Mannitol is not used to treat heart
failure as it can cause an initial rise  As mannitol works, it first increases
in extracellular fluid volume due to Hypertonic Fluid the intravascular free water content
hyper tonicity. (Gatorade rich in electrolytes) which can worsen electrolyte
abnormalities including
Mannitol is a hypertonic fluid hyponatremia.
which is excreted by the kidney  In the second phase of action,
and not reabsorbed. Therefore mannitol gets excreted in the urine
it first pulls fluid out of tissue with excess free water, which can
into blood, and afterwards cause hypernatremia due to the
Mannitol induced diuresis.
pulls fluid from the blood into
(tall man)
urine for excretion.
These are osmotic
diuretic.
 Summary Of Mannitol:
Mannitol is an osmotic diuretic that works in two phases. Firstly, mannitol in the
bloodstream creates a hypertonic solution that draws water out of the surrounding
tissues and into the bloodstream. Next, mannitol is excreted by the kidneys, where it
acts as a diuretic to osmotically draw water out of the blood and into the filtrate to
increase urine production.

The net effect of mannitol is to draw water out of cells into blood, and then eventually
into the urine. Mannitol is therefore useful in treating elevated intracranial pressure.

However, there are a couple adverse effects of mannitol. Firstly, because mannitol
creates a temporary increase in intravenous fluid volume before it is excreted, it may
lead to pulmonary edema in individuals with congestive heart failure. Secondly,
mannitol use over time can cause hypernatremia through increased loss or diuresis of
water in urine! The risk of hypernatremia is even more common in patients who are
anuric, since mannitol pooling in the kidney will cause greater and greater amounts of
water to be pulled out of the blood.
 Treats Idiopathic Intracranial Hypertension
(steam coming out of ears = increased ICP)
Decreased Excretion of H+ / causes Acidosis
(Lemons = acid, stuck in hopper = decreased excretion)
Acetazoloamide causes increase in blood acid levels.

It causes Urinary alkalization which is help full in

treating Salicylate overdose, Cystinuria

Treats Glaucoma
(Foggy safety goggles)
Via reduction of aqueous humor production.

Acts on Proximal Convoluted Tubules

(twisted tube of food processor)
Carbonic Anhydrase Inhibitor
(coal = carbonic, Dehydrator = Anhydrase, broken =
Inhibitor)

Sulfa Drugs (causes Allergy) = Side Effect

(smelly eggs)
Acetazolamide is a sulfa drug, containing a
sulfonamide group that can lead to allergic
reactions in patients allergic to other sulfa
drugs.
So it is contraindicated in sulfur drug allergy
Acetazolamide
(cedar soles)
 Summary Of Acetazolamide:
 Acetazolamide is a carbonic anhydrase inhibitor. It works primarily by
blocking the actions of carbonic anhydrase in the proximal convoluted
tubule, leading to reduced excretion of acidic protons into the urine.
 As a result, acetazolamide increases blood acidity levels, causing a
metabolic acidosis. Clinically, the alkalinization of urine can be useful for
treating diseases like salicylate overdoses and cystinuria, while the
retention of acidic protons in blood can be useful for treating alkalosis
from causes like altitude sickness.
 Since acetazolamide can decrease production of both CSF production in
the brain and aqueous humour in the eye, it can also be used to treat
idiopathic intracranial hypertension and glaucoma. However,
acetazolamide is also a sulfa drug, so it is important to remember that
acetazolamide is contraindicated in patients with sulfa allergies.
 Decreased Excretion of Acid (H+) Treats Nephrogenic DI (by lithium)
(catching lemon from falling) (prevents water loss)

 Defective ADH receptors in the kidney and

an inability to concentrate urine.
 Particularly in patients with lithium-induced
DI [UTD]

Epithelial Sodium Channel (ENaC)

Treats Liddle Syndrome
(pot LID = LIDdle)
Idle syndrome is an autosomal dominant renal disease
caused by a gain of function mutation in the ENaC
channel, leading to unregulated Na+ reabsorption. By
blocking ENaC channels, Amiloride can reduce the rate of
reabsorption and restore a normal Na+ balance.
Amiloride (drug)
(millipede)
Blockers
(breaking salt crust)
Decreased Excreation Of potassium /
Potassium Sparng
(catching banana from falling)
By inhibiting the reabsorption of Na+, ENaC blockers cause
the tubular fluid to have a more positive luminal potential.
This creates an unfavourable charge environment for the
secretion of K+ and H+ (positive charges repel positive
charges).

Increased Excretion/Loss of sodium)

Triamterene (drug) (falling salt)
ENaC channels in the principal cells of the
(trampoline)
collecting tubules are used to reabsorb sodium in
tubular fluid, blocking them prevents reabsorption
and leads to urinary loss of sodium.
 Summary Of ENaC blockers:
 ENaC blockers are a class of drugs that include Triamterene and Amiloride. As their
name suggests, ENaC blockers inhibit the epithelial sodium channels located in the
distal tubules and principal cells of collecting ducts in the kidneys. By inhibiting
sodium reabsorption, ENaC blockers increase sodium excretion into the urine. They
also reduce potassium and hydrogen ion secretion, which is why these drugs are
sometimes called “potassium-sparing” drugs.

 These drugs are often used for the treatment of nephrogenic diabetes insipidus,
including that caused by lithium. These drugs can also be used to treat Liddle
disease, a syndrome of overactive ENaC channels. The adverse effects of the ENac
blocks are related to their mechanism. In particular, retention of potassium and
hydrogen ions can lead to hyperkalemia and metabolic acidosis.
 Increased Absorption Of Calcium / Ca2+
(increased cow-cium ice cream)
May lead to hypercalcemia at high doses.

Increased Excretion of Sodium/ Na+

(fallen salt shaker)

Causes Hyperuricemia/ Gout

(swollen big toe = podagra)

Blocked Na+/ Cl- co-transporters

(ruined salt shaker = sodium, chlorine pool=
chloride)
Thiazide diuretics function by blocking Na+/Cl-
cotransporter at distal tubule (distant pool tubes) of
the kidney.
Induce Diuresis
(water around pool)

Increased Excretion Of
Potassium K+
(fallen banana)

Thiazide Diuretics Treats Hypertension

(thigh-high boots) (deflating pool Float)
Following are the drugs included in this class. 1st line treatment for essential
 Hydrochlorothiazide (HCTZ) hypertension in OPD.
 Chlorthalidone
 Indapamide
 Metolazone
Increased Lithium Toxicity
(lithium Batteries)
 Summary Of Thiazide diuretics:
Thiazide diuretics are a class of drugs that include HCTZ, chlorthalidone, indapamide, and
metolazone. Thiazides work by inhibiting the sodium-chloride cotransporter in the distal tubules
of the kidneys, increasing the excretion of sodium and water and inducing diuresis. Thiazide
diuretics lead to decreased sodium and potassium reabsorption, and increased calcium
reabsorption from the urine.

Clinically, thiazide diuretics are used for inducing diuresis to treat fluid overload states, like heart
failure and pulmonary edema. The reduction of blood volume is also useful in the treatment of
hypertension. Thiazides can treat nephrogenic diabetes insipidus by stimulating sodium and
water reabsorption in the proximal tubule. Finally, because thiazides stimulate calcium
reabsorption from urine, they can reduce the risk of osteoporosis and treat calcium oxalate
kidney stones.

However, thiazide diuretics do have some adverse effects. For example, these drugs can increase
lithium levels to increase the risk of toxicity. Secondly, thiazides can cause hyperuricemia,
precipitating an acute gout attack.
 Angiotensin II receptor blockers = Mechansim Treats Hypertension
(blocked angel = angiotensin blockers) (deflating balls)
Blocks the angiotensin II type 1 (AT1) receptor. May
cause a compensatory increase in plasma renin
activity (PRA)

Teratogenic
(trantula)
 ARBs are teratogens that
cause fetal kidney
malformations.
 Should be avoided in
pregnant women.

-sartan Endings
(Satan)
Treats Diabetic Nephropathy
 Losartan (kidney-shaped jellybeans)
 Candesartan ARBs decreased rate of glomerular basement
 Valsartan membranes thickening, prevents progression
to chronic kidney disease.

Treats Heart Failure

(ripped heart)
ARBs have been shown to provide a mortality
benefits in patients with heart failure by
preventing pathological cardiac growth and
remodeling. May cause Hyperkalemia
(spilling bananas)
Decreased downstream aldosterone signaling causes increased
potassium retention in kidneys, causing hyperkalemia.
For this reason ARBs may also be used to treat hypokalemia.
Summary Of Angiotensin receptor blockers:
Angiotensin receptor blockers, or ARBs for short, are a class of drugs that have a common “-sartan” ending.
These drug names include losartan, candesartan, and valsartan. As their name suggests, these drugs work by
blocking angiotensin II receptors. This reduces angiotensin-mediated vasoconstriction and suppresses
aldosterone release - both factors that contribute to lowering of blood pressure.

ARBs have very similar clinical uses to ACE inhibitors. Clinically, ARBs are used in the treatment of high blood
pressure, although they are a second-choice drug, used in patients who cannot tolerate ACE inhibitors. By
reducing blood pressure and afterload, ARBs are also helpful in the treatment of heart failure. Finally, ARBs can
help protect the kidneys from damage in patients with diabetes or hypertension. In general, ARBs are
prescribed to patients who are intolerant to ACE inhibitors, providing similar vascular benefits without the
same side effect profile.

However, ARBs do have some of their own side effects. For example, high doses of these drugs can lead to
hypotension. They can also induce hyperkalemia by decreasing aldosterone release. ARBs are also teratogenic
and should be avoided in pregnant women. Lastly, ARBs are contraindicated in people with bilateral renal artery
stenosis, as their use can lead to rapid kidney failure.