Nephrology Flashcards
Diuretics that work on Proximal Tubule
Carbonic Anhydrase inhibitors, Osmotics
25% of plasma that arrives here passes through the filtration barrier to become filtrate
Glomerulus w/ Bowman’s capsule
Concentrates urine
loop of Henle
Descending Loop
NaCl diffuses in, water reabsorbed
Ascending Loop
NaCl actively reabsorbed, water stays in
Distal Tubule diuretics
Thiazides
Collecting duct diuretics
Potassium sparing and aldosterones
Collecting Duct
Reabsorption:
Water
CKD
Kidney damage for > 3 months
GFR < 60 mL/min for > 3 months
Pre-renal AKD
likely dehydration
Intrinsic AKD
damage along nephron, med induced, toxin induced
Post-renal AKD
outflow obstruction, kidney stones, tumors
Bicarb and sodium are blocked from reabsorption. Effect is short lived due to compensation at loop of Henle.
Carbonic Anhydrase Inhibitors
Acetazolamide (Diamox)
Diamox off-label use
metabolic alkalosis (commonly happens when “over-diuresing” CHF patients)
-Loss of Sodium Bicarb
-Hypokalemic metabolic acidosis
-tolerance develops after 2-3 days
Carbonic Anhydrase Inhibitors
CAIs side effects
acts on CNS
-loss of water
-reduce intracellular volume
-Hypernatremia risk
MANNITOL
Urinary pH is _______ altered by mannitol-induced osmotic diuresis.
NOT
IV Mannitol _______ plasma osmolarity and draws fluid from _______ spaces to ________ spaces.
-increases
-intercellular to extracellular
Acutely expands the intravascular fluid volume
Clinical uses of Mannitol
-Prophylaxis against acute renal failure (ARF)
-Differential diagnosis of acute oliguria
-Treatment of increased intracranial pressure (ICP)
-Decreasing intraocular pressure (IOP)
is there evidence that mannitol is nephroprotective?
NO
If glomerular or renal tubular function is severely compromised then……
mannitol will NOT increase UO
Mannitol for increased ICP
Requires intact BBB ——> cerebral edema
Mannitol side effects
-Precipitate pulmonary edema
-Hypovolemia, electrolyte disturbances, plasma hyperosmolarity d/t water and NaCl secretion
Increased B.U.N. after administration of UREA should _______ be confused with acute renal failure
NOT
Loop Diuretics MOA
Inhibits Na and Cl reabsorption in the Ascending loop and to a lesser extent in the proximal tubule
Loop Diuretics main points
-loss of Na and Water
-HYPOkalemic metabolic ALKOLOSIS
-increased Ca++ loss
Loop diuretics will make you lose which electrolytes
Na+, K+, Cl-, Ca++, Mg++
Most Agressive Diuretics?
LOOP Diuretics
Furosemide-induced increases in RBF are inhibited by _______ and ________.
NSAIDs AND ASA
INCREASE loop diuretic induced kidney failure
LOOPS: clinical uses
Mobilization of edema fluid due to renal, hepatic, or cardiac dysfunction
Treatment of increased ICP
Treatment of hypercalcemia
Differential diagnosis of acute oliguria
ICP decreased by what with loop diuretics.
Systemic diuresis
Decreasing CSF production by interfering with Na transport in glial tissue
Resolving cerebral edema by improving cellular water transport
Compared to Mannitol, Furosemide:
-Not as effective in decreasing ICP
-Immediate or subsequent effects of furosemide on ICP not affected by alterations in BBB
Loop Diuretics fluid and electrolyte abnormalities
Hypokalemia
Hypochloremia
Hyponatremia
Hypomagnesemia
Metabolic alkalosis
If electrolytes not replaced, will lose electrolyte induced water gradient
Acute Tolerance (Braking Phenomenon)
Loop Diuretics: Side Effects
-Deafness
-Cross-sensitivity (SULFAS!!!!)
Higher risk with bolus doses – dose related
Ethacrynic acid does not have sulfa component
Thiazide Diuretics MOA:
MOA: Compete for the Na-Cl cotransporter in the distal tubule to inhibit reabsorption. Inhibit only urinary diluting capacity, not concentrating capacity.
Thiazides Main Points:
-Loss of Na & Water
-HYPOkalemic metabolic ALKOLOSIS
-INCREASED Ca++ Reabsorption
-HYPERCALCEMIA!
Clinical uses for Thiazides
Hypertension
Mobilization of edema
Thiazides: Metabolic and Electrolyte Side Effects
Hypokalemia, hypochloremia, hypercalcemia, metabolic alkalosis with chronic administration
Na and Mg depletion may accompany kaliuresis
Thiazides: Side Effects
-Decreased intravascular volume
-Hyperglycemia
-Hyperuricemia (GOUT)
-Decreased renal or hepatic function
Aldosterone Antagonists (K+ Sparing) Main Points:
-Loss of Na+ and Water
-HYPERkalemia
-Some risk for acidosis
K Sparing Diuretics clinical uses
Less effective diuresis so used in combo
-Teatment of refractory edematous states due to:
CHF Cirrhosis of the liver
K Sparing: Increased risk of hyperkalemia in patients also taking other drugs associated with increased plasma K concentrations
NSAIDs
Ace inhibitors (i.e. lisinopril)
Beta blockers
Side Effects Comparison Chart
Hyperkalemia:
Renal failure, hypoaldosteronism, K supplements, ACEi/ARB, Heparin, NSAIDs, K sparing diuretics, Digoxin
Hypokalemia:
Loop diuretics, thiazide diuretics, osmotic diuretics, hyperaldosteronism, mineralocorticoids, fluid loss (vomit/diarrhea
HYPERkalemia Tx
-IV Calcium
lowers the threshold potential of the myocardium
Insulin and Dextrose 50%
Inhaled Beta2 agonists
Dialysis:
Treatment of last resort
“See” BIG K Drop
C = Calcium (cardiac stabilizer)
B = beta agonists (intracellular shift)
I = Insulin (followed by..)
G = Glucose (given with insulin)
K = Kayexalate (mainly chronic RF)
D = Diuretics (renal elimination)
ROP = Renal unit for dialysis Of Patient
VAPTANS
For euvolemic and hypervolemic hyponatremia
Hypercalcemia:
Hyperparathyroidism, cancer, thiazides
Ca:Normal range: 8.5-10.5 mg/dL
Dependent upon albumin
Hypocalcemia:
Hypoparathyroidism, renal disease, loop diuretics
Check albumin before replacing!
Hypercalcemia Picture
Only use these diuretics for hypercalcemia
LOOP
