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Pharm 2 > Nephrology > Flashcards

Nephrology Flashcards

(55 cards)

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1
Q

Diuretics that work on Proximal Tubule

A

Carbonic Anhydrase inhibitors, Osmotics

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2
Q

25% of plasma that arrives here passes through the filtration barrier to become filtrate

A

Glomerulus w/ Bowman’s capsule

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3
Q

Concentrates urine

A

loop of Henle

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4
Q

Descending Loop

A

NaCl diffuses in, water reabsorbed

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5
Q

Ascending Loop

A

NaCl actively reabsorbed, water stays in

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6
Q

Distal Tubule diuretics

A

Thiazides

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7
Q

Collecting duct diuretics

A

Potassium sparing and aldosterones

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8
Q

Collecting Duct
Reabsorption:

A

Water

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9
Q

CKD

A

Kidney damage for > 3 months

GFR < 60 mL/min for > 3 months

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10
Q

Pre-renal AKD

A

likely dehydration

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11
Q

Intrinsic AKD

A

damage along nephron, med induced, toxin induced

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12
Q

Post-renal AKD

A

outflow obstruction, kidney stones, tumors

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13
Q

Bicarb and sodium are blocked from reabsorption. Effect is short lived due to compensation at loop of Henle.

A

Carbonic Anhydrase Inhibitors

Acetazolamide (Diamox)

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14
Q

Diamox off-label use

A

metabolic alkalosis (commonly happens when “over-diuresing” CHF patients)

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15
Q

-Loss of Sodium Bicarb
-Hypokalemic metabolic acidosis
-tolerance develops after 2-3 days

A

Carbonic Anhydrase Inhibitors

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16
Q

CAIs side effects

A

acts on CNS

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17
Q

-loss of water
-reduce intracellular volume
-Hypernatremia risk

A

MANNITOL

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18
Q

Urinary pH is _______ altered by mannitol-induced osmotic diuresis.

A

NOT

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19
Q

IV Mannitol _______ plasma osmolarity and draws fluid from _______ spaces to ________ spaces.

A

-increases
-intercellular to extracellular

Acutely expands the intravascular fluid volume

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20
Q

Clinical uses of Mannitol

A

-Prophylaxis against acute renal failure (ARF)
-Differential diagnosis of acute oliguria
-Treatment of increased intracranial pressure (ICP)
-Decreasing intraocular pressure (IOP)

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21
Q

is there evidence that mannitol is nephroprotective?

A

NO

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22
Q

If glomerular or renal tubular function is severely compromised then……

A

mannitol will NOT increase UO

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23
Q

Mannitol for increased ICP

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A

Requires intact BBB ——> cerebral edema

24
Q

Mannitol side effects

Study These Flashcards
A

-Precipitate pulmonary edema

-Hypovolemia, electrolyte disturbances, plasma hyperosmolarity d/t water and NaCl secretion

25
Increased B.U.N. after administration of UREA should _______ be confused with acute renal failure
NOT
26
Loop Diuretics MOA
Inhibits Na and Cl reabsorption in the Ascending loop and to a lesser extent in the proximal tubule
27
Loop Diuretics main points
-loss of Na and Water -HYPOkalemic metabolic ALKOLOSIS -increased Ca++ loss
28
Loop diuretics will make you lose which electrolytes
Na+, K+, Cl-, Ca++, Mg++
29
Most Agressive Diuretics?
LOOP Diuretics
30
Furosemide-induced increases in RBF are inhibited by _______ and ________.
NSAIDs AND ASA INCREASE loop diuretic induced kidney failure
31
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
32
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
33
Compared to Mannitol, Furosemide:
-Not as effective in decreasing ICP -Immediate or subsequent effects of furosemide on ICP not affected by alterations in BBB
34
Loop Diuretics fluid and electrolyte abnormalities
Hypokalemia Hypochloremia Hyponatremia Hypomagnesemia Metabolic alkalosis
35
If electrolytes not replaced, will lose electrolyte induced water gradient
Acute Tolerance (Braking Phenomenon)
36
Loop Diuretics: Side Effects
-Deafness -Cross-sensitivity (SULFAS!!!!) Higher risk with bolus doses – dose related Ethacrynic acid does not have sulfa component
37
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.
38
Thiazides Main Points:
-Loss of Na & Water -HYPOkalemic metabolic ALKOLOSIS -INCREASED Ca++ Reabsorption -HYPERCALCEMIA!
39
Clinical uses for Thiazides
Hypertension Mobilization of edema
40
Thiazides: Metabolic and Electrolyte Side Effects
Hypokalemia, hypochloremia, hypercalcemia, metabolic alkalosis with chronic administration Na and Mg depletion may accompany kaliuresis
41
Thiazides: Side Effects
-Decreased intravascular volume -Hyperglycemia -Hyperuricemia (GOUT) -Decreased renal or hepatic function
42
Aldosterone Antagonists (K+ Sparing) Main Points:
-Loss of Na+ and Water -HYPERkalemia -Some risk for acidosis
43
K Sparing Diuretics clinical uses
Less effective diuresis so used in combo -Teatment of refractory edematous states due to: CHF Cirrhosis of the liver
44
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
45
Side Effects Comparison Chart
46
Hyperkalemia:
Renal failure, hypoaldosteronism, K supplements, ACEi/ARB, Heparin, NSAIDs, K sparing diuretics, Digoxin
47
Hypokalemia:
Loop diuretics, thiazide diuretics, osmotic diuretics, hyperaldosteronism, mineralocorticoids, fluid loss (vomit/diarrhea
48
HYPERkalemia Tx
-IV Calcium lowers the threshold potential of the myocardium Insulin and Dextrose 50% Inhaled Beta2 agonists Dialysis: Treatment of last resort
49
“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
50
VAPTANS
For euvolemic and hypervolemic hyponatremia
51
Hypercalcemia:
Hyperparathyroidism, cancer, thiazides Ca:Normal range: 8.5-10.5 mg/dL Dependent upon albumin
52
Hypocalcemia:
Hypoparathyroidism, renal disease, loop diuretics Check albumin before replacing!
53
Hypercalcemia Picture
54
Only use these diuretics for hypercalcemia
LOOP
55

Pharm 2 (5 decks)

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