Diuretics

Front 1

HCTZ
MOA:
uses:
S/E:
what part of nephron?

Back 1

MOA: inhibits Na/Cl cotransporter at the distal convoluted tubule--> Na gets stuck in tubule and becomes super positive--> open voltage sensitive Ca channels on blood side , forcing Ca out of the urine

uses:
-stones caused by high calcium in the blood and thus urine
-HTN
-CHF
-Nephrogenic DI
-osteoporosis
S/E: hyperGLUC, sulfa allergy, gout, hypOk, (high Ca levels us. suppress PTH!!!)

DCT of nephron

Front 2

Name the 4 thiazides
S/E:
what part of nephron?

Back 2

1) HCTZ
2) Metolazone
3) Chlorothalodone
4) Indopamide

S/E: hyperGLUC, sulfur allergy, *hypOk, *hypOmg, hypOna, dehydration

DCT of nephron

Front 3

Mannitol
MOA:
part of tube
uses:
S/E:
CI:

Back 3

MOA: increase tubular osmolarity, producing inc urine flow

part of tube: mostly PCT and loop of Henle

uses: shock, o/d, inc ICP

S/E: pulm edema, dehydration, metabolic acidosis, n/v, headach, hyperNA

CI: anuria, CHF

Front 4

Acetozolamide:
MOA:
uses:
S/E:

Back 4

MOA: carbonic anhydrase inh (will pee out HCO3 and deplete bodies HCO3 stores), will alkalinize the urine

uses: Pseudotumer cerebiri, Glaucoma, Urinary alkalinization (uric acid stones, cysteine stones), Metabolic alkalinization, Altitude sickness

"G. PUMA"

S/E: hyPERchloremic metabolic acidosis, neuropathy, NH3 toxicity (encephalopathy), sulfa allergy

PCT of nephron

Front 5

Name the 2 Carbonic anhydrase inhibitors

Back 5

Acetylzolamide
Dorzolamide

Front 6

Name the 4 loop diuretics

Back 6

1) Furosemide
2) Ethacrynic Acid
3) Butnetamide
4) Toresamide

Front 7

Ethacrynic acid is the exact same as Furosemide, except for 2 things

Back 7

1) is NOT a sulfa drug
2) can be used as a diuretic in patients with hyPERuricemia and gout

Front 8

Furosamide (and all loop diuretics)
MOA:
uses:
surreptitios uses:
toxicity:
what part of nephron?
supplemets:

Back 8

MOA:
1) inhibits cotransport of Na-K-2Cl (by blocking Cl, the leader here) out of the nephron, makes medulla area less hypertonic, causing Ca to be absorbed into nephron
2) stim prostaglandin synt (PGE dilates renal afferent--> inc GFR)... an additive effect to diuresing!

uses: hyPERCa, hyPERMg, HTN, edematous states (cirrhosis, nephrotic synd, pulm edema-bc dilates pulm lymphatics, CHF)

surreptitios uses: wt loss (gymnastics and models are MC offenders); will see a much bigger drop in Cl than in Na and K

S/E: Pancreatitis, Ototoxicity, Dehydration, Allergy (sulfa) so can get Stephen Johnson synd, Nephrotoxic, Gout (hyPERuricemia), Stones, hypOca, hypOk, hypOcl

must supplement with K

"PODANGSH"

Thick ascending loop

Front 9

Name the 4 K-sparing diuretics

Back 9

1) Spironalactone
2) Epelerone
3) Amiloride
4) Triamterone

"SEAT"

Front 10

K-sparing diuretics
MOA
uses:
toxicity:
what part of nephron?

Back 10

MOA: block aldosterone rec (so you pee Na instead of K)
uses: CHF, Conns, hypOk, hirsutism
toxicity: hyPERk --> arrhythmias, gynecomastia, anti-androgen effects, testicular atrophy, metabolic acidosis

proximal/early/cortical collecting tube

Front 11

Which K-sparing diuretic is the DIURECTIC of choice for chirrhosis?

Back 11

Spirinolactone

Front 12

Which K-sparing diuretic is the DOC to treat nephrogenic DI?

Back 12

Amiloride
***causes pts to NOT pee (paradoxical effect)

Front 13

ACE-Inh
MOA:
uses:
S/E:
CI:
Monitor:

Back 13

MOA:
1) inhibit ACE (reduce levels of AT)
2) prevent inh of bradykinin (a potent vasodilator)

uses: CHF, HTN, diabetic renal dz

S/E: Cough
Angioedema/ Acidosis (metabolic)
Proteinuria
Taste changes
hypOtn (esp. unique is "1st dose hypotension")
CI in Pregnancy
Rash
Inc renin & Cr
Low AT- 2 & GFR
CI: preggos (causes fetal renal agenesis), bilateral renal artery stenosis
Monitor:
1) Cr levels (dont want Cr levels to rise >30%)
2) BP: for hypOtn

Front 14

Do ARB's cause cough?
angioedema?

Back 14

cough- no
angioedema- yes

Front 15

90% of dehydration is metabolic ALKALOSIS.....
8 exceptions: (5 drugs, 3 illnesses)

Back 15

causes of dehydration with metabolic ACIDOSIS include
1) ACE-Inh
2) K sparing diuretics
3) Acetozolamide
4) Mannitol
5) B blockers (bc they block
juxtaglomerular cells which
are responsible for making
renin)
6) DKA
7) diarrhea
8) RTA type 2

Front 16

Which is the only loop diuretic who's hearing loss is reversible?

Back 16

Furosemide

Front 17

Which class is the most potent form of diuretic?
Why?

Back 17

Loops
Bc work on the triple transport channel, and don't allow concentration of the interstitium--> interstitium can't pull water out of DCT