Firecracker Flashcards

1
Q

What is acetazolamide?

A

Carbonic anhydrase inhibitors act in the PCT by inhibiting the reabsorption of filtered HCO3-.

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2
Q

Uses of acetazolamide?

A
  • weak diuretic
  • To alkalinize the urine
  • To treat glaucoma
  • To treat metabolic alkalosis
  • To treat altitude sickness
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3
Q

how does acetazolamide treat glaucoma?

A

(↓ secretion of aqueous humor → ↓ intraocular pressure)

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4
Q

acetazolamide toxicity

A
  • Hyperchloremic metabolic acidosis
  • Hypokalemia
  • NH3 toxicity
  • Neuropathy
  • Sulfa allergy
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5
Q

Effect of ↓FF on protein concentration in peritubular capillary blood?

A

↓ and decreased reabsorption in the proximal tubule

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6
Q

How are Mg and Ca absorbed in the thick ascending loop of Henle?

A

K leak channels in the luminal membrane allow electrochemical potential gradient to drive further reabsorption of cations: K, Mg+ and Ca+

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7
Q

OPgc decreases by decreases in capillary protein concentration, such as in cirrhosis or nephrotic syndrome –> increased GFR.

A

increased GFR.

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8
Q

What effect does the thick ascending loop of Henle have on the tonicity of urine?

A

dilutes

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9
Q

Effect of ↑FF on protein concentration in peritubular capillary blood?

A

↑ –> increased reabsorption in the proximal tubule

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10
Q

If C(x) < GFR, then there is a net tubular

A

reabsorption of X (example: Na, glucose, amino acids, HCO3-, Cl-)

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11
Q

In the PCT (proximal convoluted tubule), name 3 buffer systems which serve to buffer urinary H+.

A

HCO3-
HPO32-
NH3

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12
Q

What is the most important urinary buffer system in the PCT?

A

HCO3-

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13
Q

Describe how ACE-Inhibitors can ↓GFR?

A

Angiotensin II preferentially constricts the efferent aterioles. ACE inhibitors thus dilate efferent arterioles –> ↓ GFR.

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14
Q

MOA thiazide diureteics

A

inhibit Na/Cl cotransporter in DCT

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15
Q

Thiazides are used to treat 4 things:

A
  1. HTN
  2. CHF
  3. Idiopathic hypercalciuria
  4. Nephrogenic DI
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16
Q

Why use thiazides for nephrogenic DI?

A

Thiazides increase renal Na excretion → ECF volume contraction → ↓ GFR → ↑ proximal tubular reabsorption of water and Na
∴ less water and Na are lost as urine

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17
Q

thiazide toxicity –> ↓ serum levels of 3 things:

A

sodium, potassium, H+
K (hypokalemia)
Na (hyponatremia)
H+ (metabolic alkalosis, ↑ HCO3-)

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18
Q

thiazide toxicity –> ↑ serum levels of (mnemonic “GLUC”)

A

Glucose, lipids, uric acid, Ca2+

  • Glucose (hyperglycemia)
  • Lipids (hyperlipidemia)
  • Uric acid (hyperuricemia) → may precipitate gout
  • Ca2+ (hypercalcemia)
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19
Q

Both thiazide diuretics and loop diuretics can cause

A

hypokalemia

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20
Q

thiazide vs. loop effect on calcium

A
  • thiazides increase Ca reabsorption
    ∴ thiazide toxicity may cause hypercalcemia
  • loops increase Ca excretion
    ∴ loop diuretic toxicity may cause hypocalcemia.
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21
Q

What regulates glucose in the PCT?

A

limited number of Na-glucose carriers

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22
Q

How does aldosterone affect electrolyte balance in the kidney’s principal cells?

A

↑ Na reabsorption and ↑ K secretion

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23
Q

cotrasnporter in the TAL of henle

A

NKCC symporter

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24
Q

NKCC actively reabsobds

A

Active reabsorption of Na, K (or NH4+), and Cl-

25
What competes with K for reabsorption by NKCC?
NH4
26
fxn of intercalated cells in collecting tubule
secrete H & reabsorbs K
27
How do the intercalated cells secrete H into the collecting tubule lumen?
primary active H-ATPase | primary active H-K-ATPase
28
How do the intercalated cells reabsorb K from and secrete H into the collecting tubule lumen?
Primary H-K-ATPase
29
Aldosterone effect on intercalated cells, aldosterone further increases H secretion by
intercalated cells
30
Under conditions of K depletion, K reabsorption by Type A intercalated cells predominates over what to → net K reabsorption.
K secretion by principal cells in the distal nephron
31
When K intake is normal or high, K secretion by principal cells far outweighs what to→ net K secretion.
K reabsorption by Type A intercalated cells in the distal nephron
32
In PCT, what pump maintains a gradient that favors passive Na reabsorption from the lumen into the renal tubular cells?
Na/K ATPase in the basolateral membrane extrudes Na from renal tubular cells into the interstitium
33
Spironolactone and eplerenone are
competitive aldosterone receptor antagonists which act on the cortical collecting tubule.
34
Where does spironolactone work?
cortical collecting tubules
35
What drugs directly block epithelial sodium channels to inhibit sodium reabsorption in the collecting ducts without depleting potassium.
Amiloride and triamterene
36
necessity of aldosterone for spironolactone?
imperative
37
necessity of aldosterone for amiloride?
not necessary
38
[Na+] – ([HCO3-] + [Cl-])
serum anion gap
39
normal serum anione gap
8-16
40
How is Na reabsorbed in the distal convoluted tubule?
Na-Cl cotransporter
41
What artery supplies the bladder?
internal iliac artery.
42
Is the urine osmolarity increased or decreased as it advances into the distal convoluted tubule?
decreased
43
sympathetic relaxes or contracts bladder tone?
relaxes
44
parasympathetic relaxes or contracts bladder tone
contracts (-->empties)
45
In PCT, reabsorption of phosphate is directly linked to
NPT2, a sodium-phosphate cotransporter which serves as the primary functional regulator of phosphate reabsorption.
46
PTH (parathyroid hormone) induces NPT2 endocytosis →
↓ reabsorption of phosphate and ↓ reabsorption of HCO3-
47
sympathetic innervation of bladder
Preganglionic cell bodies located in the intermediolateral cell column --> inferior hypogastric plexus --> postganglionic cells project to the vesical plexus.
48
histo DCT
simple cuboidal cells with NO brush border
49
Mannitol works by osmotic diuresis in which part of the nephron?
PCT
50
MOA loop diuretics
block the NKCC symporter in the TAL) of Henle’s loop
51
loop diuretic examples
furosemide, bumetanide, ethacrynic acid
52
site of action for K sparing diuretics
principal cells
53
examples of K sparing diuretics
amiloride, triamterene, spirinolaction, eplerenone
54
splay can be explained by
1) Nephron heterogeneity | 2) Relatively low affinity of Na-glucose cotransporters
55
afferent arterioles contract in response to stretch caused by increased arterial pressure
Myogenic mechanisms of RBF autoregulation
56
type 4 renal tubular necrosis (aldosterone deficiency or resistance):
hyperkalemia, urine pH<5.5.
57
Principal cell function
secrete K+; reabsorb Na+ and H2O
58
Principal cell function
secrete K+; reabsorb Na+ and H2O