Loop (amboss ir UW) Flashcards
Agents?
Sulfonamides: furosemide, torsemide, bumetanide
Other: ethacrynic acid
Sulfonamides?
Sulfonamides: furosemide, torsemide, bumetanide
Other agents?
Other: ethacrynic acid
Indications of loops?
Hypertension, edema, renal failure (acute and chronic), hypercalcemia, forsed diuresis, sequential nephron blocade
For what kind of edema are used loops?
Edema:
Cardiac (acute and congestive heart failure, peripheral edema, lung edema)
Renal (nephrotic syndrome)
Hepatic (liver cirrhosis)
Forced diuresis definition?
Massive diuresis for forced renal elimination of (toxic) substances
Forced diuresis implementation?
IV administration of large amounts of fluids in combination with loop diuretics
Forced diuresis indications?
Hypercalcemic crisis, severe hyperkalemia, rhabdomyolysis, intoxication (e.g., lithium)
What is sequential nephron blockade?
A combination of low-dose diuretics with different sites of renal action.
Sequential nephron blockade results in ……
progressive increases in sodium depletion.
why used sequential nephron blockade?
Used to overcome resistance to diuretic treatment.
Inefficient diuresis despite high doses of loop diuretics is caused by either renal failure (reduced number of functioning nephrons) or increased resorption of sodium in the DCT to compensate for the loss of Na+. !!!!This second effect is seen primarily in cases of monotherapy with loop diuretics.
Method sequential nephron blockade?
Method: combination of loop diuretics and thiazides → restoration of diuretic effects
Why to loops added thiazides?
Thiazides affect the distal convoluted tubule and are able to counteract the increased reabsorption of sodium caused by loop diuretics.
Method: combination of loop diuretics and thiazides → restoration of diuretic effects
How its called?
Sequential nephron blockade
If diuresis is still ineffective after sequential nephron blockade?
If diuresis continues to be insufficient, exogenous depletion of volume (typically via hemofiltration) should be considered.
What precautions show be considered in FORCED DIURESIS?
Because of the increased risk of hypokalemia and hypovolemia during forced diuresis, rigorous monitoring is necessary.
Hypokalemia and/or hypomagnesemia can lead to ……………
Hypokalemia and/or hypomagnesemia can lead to life-threatening arrhythmias
Side effects of loops? 4
Metabolic imbalances
Ototoxicity
Dehydration/hypovolemia
Sulfonamide hypersensitivity
Mechanism of action of loops? location and cotransporter?
Blockage of Na+-K+-2Cl-cotransporter in the thick ascending loop of Henle
what does cotransporter that is blocked by loops?
Cotransporters normally reabsorb Na+, K+, and Cl-.
between what structures diminish concentration gradient when loops used?
Diminishing concentration gradient between the (usually hypertonic) renal medulla and the cortex → concentration of urine is no longer possible → increased diuresis
Apart Na, K and Cl, what other electrolites also are excreted?
Decreased reabsorption of Ca2+ and Mg2+
Loop leads to what increase of what substance?
Increased PGE release (can be inhibited by NSAIDs
effect of increased release of PGE due to loops?
Dilation of renal afferent arterioles → diuresis
General venodilation (rapid venous pooling) → ↓ cardiac preload
Metabolic imbalances due to loops?
Hypokalemia, hyponatremia (moderate), hypochloremia
hypomagnesemia, hypocalcemia
Metabolic alkalosis
Hyperuricemia/gout
Hyperglycemia
why occurs hyperuricemia/gout due to loops?
Increased retention of uric acid and dehydration lead to a higher risk of gout attacks.
Why occurs hyperglycemia when used loops?
Loop diuretics decrease glucose tolerance, which increases the blood sugar level.
Why loops have effect on ears?
Na+-K+-2Cl-cotransporters are also found in the stria vascularis of the inner ear.
The risk of hearing damage is particularly high with high doses of loop diuretics, in renal failure (drug accumulation), or if patients take additional ototoxic drugs (e.g., aminoglycoside antibiotics). Ethacrynic acid has particularly high ototoxicity.
Which medication has highest risk to cause ototoxicity?
Ethacrynic acid
How long lasts ototoxicity?
Ototoxicity (potentially permanent hearing damage)
What should we consider when dehydration is present?
Consider thrombosis prophylaxis.
Which medication does not cause sulfa alergy?
ethacrynic acid
Manifestation of sulfa alergy?
rash, interstitial nephritis
is patient has sulfa alergy, what medication from loops prescribe?
ethacrynic acid
GO PANDA meaning?
To recall the side effects of loop diuretics, think of “GO PANDA”: Gout, Ototoxicity, low Potassium, Allergy, Nephritis, Dehydration, Alkalosis.
Loops contraindications. Anuria?
all are contraindicated
Loops contraindications. sulfa hypersensitivity?
contraindicated furosemide, torsemide and bumetanide
Indicated: ethacrynic acid
Loops contraindications. Hepatic coma or severe electrolyte depletion?
None of them are contraindicated. Can use all, but with caution
Loops contraindications. History of severe watery diarrhea (caused by the drug)?
Ethacrynic acid is strictly contraindicated.
Other loop - indicated.
what metabolic disorder occurs due to loop?
metabolic alkalosis
general clinical indications for loop?
volume-overload states (eg congestive HF)
What is the most potent diuretics?
loops
What is the most important electrolyte decrease in loop?
Na (most prominently decrease)
therefore water excretion is high
why occur metabolic alkalosis due to loops?
- Na and water losses induced by loops CAUSE INCREASED ALDOSTERONE-MEDIATED RENAL EXCRETION OF H+ AND K+.
- Loops cause relatively greater loss of Cl- than Na+, resulting in decreased total body electronegativity. In response, the kidneys retain more HCO3, the second most abundant anion in the body, to maintain electrochemical balance.
How changes body electronegativity when loops are used?
decreased total body electrogenicity (due to loss of Cl)
Loop. How changes K in total body?
Decr. (2 arrows down)
Loop. How changes HCO3 in total body?
Incr. (2 arrows up)
Loop. How changes Ca2 in total body?
Decr. (1 arrow down)
Loop. How changes uric acid in total body?
incr. (1 arrow up)
How changes of natriuresis when loops are prescribed?
Initially results in natriuresis. Eventually occurs significant volume depletion that counteracts diuretic effect –> decreased glomerular filtration pressure –> reduced pressure natriuresis results in decreased distal tubule Na delivery –> it sensed by macula densa –> activation of RAAS –> aldosterone on collecting tubule –> enhanced Na reab and promote K and H loss.
Result: hypokalemia, metabolis alkalosis [secondary to volume contraction].
Absorption in thick ascending henle loop is needed to maintain corticomedullary concentration gradient. When inhibited by loops - inability to concentrate urine thus substantial loss of both salt and water. –>
In contrast, thiazides have normal corticomedullary concentration gradient and are better able to retain free water in response to increased vasopressin levels. (vasopressin works on collecting tubule)
Patients with THIAZIDES tend to have what disturbances?
Retain water and develop hyponatremia (dilution?).
Loops on Ca?
decrease reabsorption –> hypocalcemia
THIAZIDES!!!!! (cia tiesiog loops tema, tai nesusimaisyti) on Ca?
increased proximal and distal tubule Ca2 reabsorption –> secondary HYPERCALCEMIA
In what cells are Na,K,Cl cotransporters?
in apical membranes of cells in the thick ascending limb of Henle’s loop.
In decompensated HF what is first line diuretic treatment?
loop diuretics
