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Renal > Firecracker > Flashcards

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
Q

What competes with K for reabsorption by NKCC?

A

NH4

26
Q

fxn of intercalated cells in collecting tubule

A

secrete H & reabsorbs K

27
Q

How do the intercalated cells secrete H into the collecting tubule lumen?

A

primary active H-ATPase

primary active H-K-ATPase

28
Q

How do the intercalated cells reabsorb K from and secrete H into the collecting tubule lumen?

A

Primary H-K-ATPase

29
Q

Aldosterone effect on intercalated cells, aldosterone further increases H secretion by

A

intercalated cells

30
Q

Under conditions of K depletion, K reabsorption by Type A intercalated cells predominates over what to → net K reabsorption.

A

K secretion by principal cells in the distal nephron

31
Q

When K intake is normal or high, K secretion by principal cells far outweighs what to→ net K secretion.

A

K reabsorption by Type A intercalated cells in the distal nephron

32
Q

In PCT, what pump maintains a gradient that favors passive Na reabsorption from the lumen into the renal tubular cells?

A

Na/K ATPase in the basolateral membrane extrudes Na from renal tubular cells into the interstitium

33
Q

Spironolactone and eplerenone are

A

competitive aldosterone receptor antagonists which act on the cortical collecting tubule.

34
Q

Where does spironolactone work?

A

cortical collecting tubules

35
Q

What drugs directly block epithelial sodium channels to inhibit sodium reabsorption in the collecting ducts without depleting potassium.

A

Amiloride and triamterene

36
Q

necessity of aldosterone for spironolactone?

A

imperative

37
Q

necessity of aldosterone for amiloride?

A

not necessary

38
Q

[Na+] – ([HCO3-] + [Cl-])

A

serum anion gap

39
Q

normal serum anione gap

A

8-16

40
Q

How is Na reabsorbed in the distal convoluted tubule?

A

Na-Cl cotransporter

41
Q

What artery supplies the bladder?

A

internal iliac artery.

42
Q

Is the urine osmolarity increased or decreased as it advances into the distal convoluted tubule?

A

decreased

43
Q

sympathetic relaxes or contracts bladder tone?

A

relaxes

44
Q

parasympathetic relaxes or contracts bladder tone

A

contracts (–>empties)

45
Q

In PCT, reabsorption of phosphate is directly linked to

A

NPT2, a sodium-phosphate cotransporter which serves as the primary functional regulator of phosphate reabsorption.

46
Q

PTH (parathyroid hormone) induces NPT2 endocytosis →

A

↓ reabsorption of phosphate and ↓ reabsorption of HCO3-

47
Q

sympathetic innervation of bladder

A

Preganglionic cell bodies located in the intermediolateral cell column –> inferior hypogastric plexus –> postganglionic cells project to the vesical plexus.

48
Q

histo DCT

A

simple cuboidal cells with NO brush border

49
Q

Mannitol works by osmotic diuresis in which part of the nephron?

A

PCT

50
Q

MOA loop diuretics

A

block the NKCC symporter in the TAL) of Henle’s loop

51
Q

loop diuretic examples

A

furosemide, bumetanide, ethacrynic acid

52
Q

site of action for K sparing diuretics

A

principal cells

53
Q

examples of K sparing diuretics

A

amiloride, triamterene, spirinolaction, eplerenone

54
Q

splay can be explained by

A

1) Nephron heterogeneity

2) Relatively low affinity of Na-glucose cotransporters

55
Q

afferent arterioles contract in response to stretch caused by increased arterial pressure

A

Myogenic mechanisms of RBF autoregulation

56
Q

type 4 renal tubular necrosis (aldosterone deficiency or resistance):

A

hyperkalemia, urine pH<5.5.

57
Q

Principal cell function

A

secrete K+; reabsorb Na+ and H2O

58
Q

Principal cell function

A

secrete K+; reabsorb Na+ and H2O

Renal (22 decks)

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