Test 2: lecture 31 diuretics part 1 Flashcards
when to use diuretic
CHF
oliguria/anuric renal failure
cavity effusions
peripheral edema
increased intracranial pressure
what drug works here?
- acetazolamide: blocks carbonic anhydrase: ↑ Na and bicarb excretion
- mannitol: osmotic diuretic: ↑ water excretion
- Thiazide diuretics (HCTZ, Naquasone): block sodium chloride transporter: ↑NaCl excretion
loop diuretics (lasix, torsemide): block sodium-potassium chloride cotransporter: increases Na, K and Cl excretion
Aldosterone antagonists (MRA) (spironolactone): antagonises aldosterone receptor: ↑ Na excretion, ↑K retention
Mannitol: osmotic diuretic: ↑water excretion
how does loop diuretic work
blocks Na, K, Cl cotransporter in the thick ascending loop of Henle
leads to ↑Na, K and Cl excretion → water excretion
how does renal blood flow control loop diuretics
loop diuretics bound to proteins in the blood = not filtered by kidney
to get into tubule needs to be absorbed by PCT cells
if there is low renal blood flow then less loop diuretic will be pulled into the tubule
patients with renal disease need higher dose of loop diuretic
clinical characteristics of loop diuretics
potent: can rapidly cause dehydration
electrolyte depletion: cause low Na, Cl and K.
and low calcium and magnesium
can also cause ↑BUN/Creat (azotemia) and metabolic akalosis
rapid onset
ototoxic at high doses
3 causes of loop diuretic resistance
Multiple mechanisms
* Reduced absorption (intestinal edema)
* Reduced GFR (renal failure, dehydration)
* Changes in albumin
Need for increasing dosages or combination therapy
need normal kidney function for PCT to pull loop diuretic into tubule
ceiling effect of loop diuretics
limit to effect of diuretic
can only give a certain amount of drugs cause there is only a certain amount of Na/K/Cl pumps, and there are other places in the tubule that cause Na reabsorption
worsened by CHF
furosemide (lasix)
loop diuretic ( cause excretion of Na, Cl, K and water)
IV: rapid onset
PO: < 60 mins
Duration
IV: 2-3 hours
PO: 6 hours (dog), 12-24 cat
oral bioavailability 40-50% in dogs, better in cats, worse in horses
prone to developing resistance
oral bioavailability for lasix is —
40-50% dogs
Better in cats
Poor in horses
rapid onset (IV 5 mins, PO: 1 hr)
short duration of action (IV: 2-3 hrs, PO: 6 hr dog, 12-24 hr cat)
loop diuretic
furosemide (lasix)
toresmide
torsemide
10 x more potent than furosemide (lasix)
loop diuretic
Duration of action: PO: SID or BID
Oral formulation well absorbed (bioavailable)
less prone to resistance then lasix
what oral loop diuretic can you give to horses
torsemide
— block Na/Cl in the DCT
thiazide diuretics
Hydrochlorothiazide (HCTZ): small animal
Trichlormethiazide and dexamethasone: Naquasone bolus for bovine udder edema,
equine limb edema
Thiazide diuretics cause — increases in urine volume
mild to moderate
Blocks Na-Cl cotransporter in DCT
Hydrochlorothiazide (HCTZ)
◦ Small animals
Trichlormethiazide and dexamethasone
◦ Naquasone bolus for bovine udder edema, equine limb edema
clinical effects of Thiazide diuretics
Blocks Na-Cl cotransporter in DCT
- mild to moderate increases in urine volume
- ↓ potassium and ↑ calcium
- ineffective with low renal blood flow
Hydrochlorothiazide (HCTZ)
◦ Small animals
Trichlormethiazide and dexamethasone
◦ Naquasone bolus for bovine udder edema, equine limb edema
Hydrochlorothiazide (HCTZ)
small animal
Thiazide Diuretics
Blocks Na-Cl cotransporter in DCT
cause ↓ potassium and ↑ calcium
not very potent: only cause mild to moderate increase in urine voume
need working kidney to work
Trichlormethiazide and dexamethasone
Naquasone bolus for bovine udder edema,
equine limb edema
Thiazide Diuretics
Blocks Na-Cl cotransporter in DCT
cause ↓ potassium and ↑ calcium
not very potent: only cause mild to moderate increase in urine voume
need working kidney to work
Spironolactone
Potassium sparing diuretic
Blocks at aldosterone receptor
↑Na excretion
↑K retention
inhibits RAAS
cardioprotective/antifibrotic effects
oral only
mild diuretic effect
used with loop diuretics
peaks diuresis 2-3 days
potassium sparing diuretics work by —
blocking aldosterone receptors
↑Na excretion
↑K retention
inhibits RAAS
cardioprotective/antifibrotic effects
spironolactone
clinical signs of postassium sparing diuretics
Blocks aldosterone receptor
↑Na excretion
↑K retention
inhibits RAAS
cardioprotective/antifibrotic effects
Spironolactone
mild increased urine output
oral only
— is used to treat CHF in addition to loop diuretics
spironolactone
potassium sparing diuretic that blocks aldosterone receptor → ↑Na excretion and ↑ K retention
Potential cardioprotective/antifibrotic effects
mannitol
osmotic diuretic
increases water excretion
used for oliguric renal failure
how to test for oliguria in acute renal failure
give fluids and check for fluid overload
then test with mannitol (osmotic diuretic)
can also test with high dose or CRI furosemide
or furosemdie plus dopamine (FOND)
acetazolamide
carbonic anhydrase inhibitor
can be used to treat
HYPP (gets rid of potassium)
glaucoma (decreases aqeous humor production)
metabolic alkalosis (causes bicarb loss)
— is a carbonic anhydrase inhibitor
acetazolamide
will cause ↑ Na and Bicarb excretion
also causes decreased aqueous humor production in the eye
12 year old broodmare with CHF
how to treat?
IV loop diuretic: furosemide
or oral torsemide
check for pulmonary edema improvement with repeat ultrasound
chronic heart issues and treated at home with lasix but getting worse. How to treat?
ensure pt actually getting meds
increase lasix (loop diuretic) cause ↑ Na, K and Cl excretion. Can lead to azotemia, ↓potassium, ↓ calcium, ↓ magnesium, metabolic alkalosis
add spironolactone ( potassium sparing- blocks aldosterone → ↑Na excretion, ↑K retention, inhibits RAAS, cardioprotective/ antifibrotic effects)