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GIR Test 4 > B5-045 Renal Physiology V > Flashcards

B5-045 Renal Physiology V Flashcards

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1
Q

what part of the tubule

  • reabsorption of solutes/fluid
  • secretion of organic anions/cations
A

proximal tubule

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2
Q

what part of the tubule

reabsorption of Na+, Cl-, K+

A

ascending loop of Henle

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3
Q

what part of the tubule

  • reabsorption of Na+, Cl-, and water
  • secretion of K+ and H+

2

A

distal tubule
collecting duct

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4
Q

[…] is required to drive all transporters in the proximal tubule

A

sodium

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5
Q

what part of the tubule

all transport depends on NaKATPase

A

proximal

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6
Q

what part of the tubule

glucose, amino acids, and phosphate are absorbed by apical Na+ cotransporters

A

proximal

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7
Q

what part of the tubule

protons are secreted by Na+ proton exhanger

A

proximal

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8
Q

what part of the tubule

chloride follows the paracellular pathway and base-dependent exchanges

A

proximal

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9
Q

what part of the tubule

organic anions are secreted by Na-dependent and independent OAT transporters

A

proximal

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10
Q

transport defects in the proximal tubule result in a kidney reabsorptive condition called

A

Fanconi syndrome

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11
Q
  • polyuria, polydipsia, and dehydration
  • hypophosphatemic rickets/osteomalacia
  • growth failure
  • metabolic acidosis
A

Fanconi

symptoms vary depending on extent

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12
Q
  • hypokalemia
  • hyperchrolemia
  • hypophosphatemia, phosphaturia
  • glucosuria, aminoaciduria
A

Fanconi

symptoms vary depending on extent

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13
Q

environmental causes of Fanconi syndrome

A
  • heavy metals (lead)
  • tetracyclins, gentamycin
  • toluene (paint/dyes)
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14
Q

what part of tubule

Na+, K+ and Cl- are co-transported in the apical side by NKCC

A

ascending loop of Henle

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15
Q

what part of tubule

K+ and Cl- are absorbed together at the basolateral side or independently through channels

A

ascending loop of Henle

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16
Q

what part of tubule

K+ also leaks to the tubular side via ROMK1, helps with K+ recycling and maintains function of NKCC2

A

ascending loop of Henle

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17
Q

transport defects in the ascending loop of Henle depend on alterations in […], […], and […]

A

ROMK1
NKCC2
Barttin

Bartter’s syndrome

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18
Q
  • polyuria, polydipsia
  • poor muscle tone
  • heart repolarization abnormalities
A

Bartter’s syndrome

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19
Q
  • hyponatremia
  • hypokalemia
  • hypochloremia
  • ECF volume contraction
  • high renin aldosterone
  • metabolic alkalosis
A

Bartter’s syndrome

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20
Q

environmental causes of Bartter’s syndrome

A

furosemide and bumetanide

inhibit NKCC2

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21
Q

malfunction of the countercurrent mechanism in Bartter’s syndrome causes

A

polyuria/polydipsia

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22
Q

malfunction of the NKCC, ROMK1, and Cl channels in Bartter’s syndrome causes

A

solute diuresis
wasting of Na+, K+, Cl-

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23
Q

malfunction of the juxtaglomerular apparatus in Bartter’s results in

A

hyper-reninemia, high aldosterone, alkalosis

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24
Q

activates proton pumps

hormone

A

aldosterone

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25
Q

treatment of Bartter’s

A
  • postassium supplement
  • aldosterone antagonists
  • ACE inhibitors
  • NSAIDs
  • Ca+ and Mg+ supplements
  • growth hormone
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26
Q

what part of tubule

Na+ and Cl- are cotransporterd in the apical side and reabsorped basolaterally

A

distal tubule

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27
Q

what part of tubule

K+ is secreted to the tubular fluid via K+ channels

A

distal

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28
Q

what part of tubule

Ca2+ is reabsorbed via channels and the basolateral Na/Ca exhanger

A

distal

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29
Q

transport defects in the distal tubule are due to mutations in […] or [..]

A
  • TSC (Na/Cl exchanger)
  • TRPM6 (magnesium)
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30
Q
  • hyponatremia
  • hypokalemia, high urine K+
  • hypomagnesemia, high urine Mg+
  • hypocalciuria
  • ECF volume contraction
  • normotensive
A

Gitelman’s syndrome

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31
Q

environmental cause of Gitelman’s

A

thiazide OD

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32
Q

what part of tubule

Na+ is reabsorbed apically by ENAc

A

collecting duct

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33
Q

what part of tubule

K+ is secreted to the tubular fluid via K+ channels

A

collecting duct

34
Q

what part of tubule

water is reabsorbed via aquaporins

A

collecting tubule

35
Q

transport defects in the collecting tubule are due to mutations in […] or […]

A

ENac (Liddle’s)
aquaporins (DI)

36
Q
  • increased ECF volume
  • hypertension
  • decreased renin-aldosterone
  • hypokalemia
  • metabolic alkalosis
A

Liddle’s syndrome

37
Q

in Liddle’s syndrome, ENac is […]

sodium coming in all the time

A

constantly activated

water coming in, hypertension

38
Q
  • polyuria, polydipsia
  • risk of dehydration
  • dilute urine with low osmolarity
  • sometimes hypernatremia
A

nephrogenic diabetes insipidus

39
Q

environmental cause of nephrogenic diabetes insipidus

A

lithium

batteries

40
Q

defects in proton secretion cause renal

A

acidosis

depending on transporter proximal or distal

41
Q

in the proximal tubule, H+ is secreted by

transporter

A

Na/H exchanger

42
Q

in distal and collecting tubules, H+ is secreted by

transporter

A

ATPases

43
Q
  • muscle weakness
  • cardia repolarization problems
  • growth retardation
  • kidney stones
  • hypokalemia
  • hyperchloremia
  • hypercalciuria
  • metabolic acidosis
  • low excretion of H+
A

proximal and distal renal tubular acidosis

44
Q
  • renal failure at early age (40-60)
  • hematuria
  • flank pain
  • hypertension
A

adult polycystic kidney disease

45
Q
  • multiple kidney cysts
  • liver
  • aneurisms
A

adult polycystic kidney disease

46
Q

mutations in PKD1 and PKD2 cause

A

adult polycystic kidney disease

protein: polycystin

47
Q

mutations in PKHD cause

A

child polycystic kidney disease

protein: fibrocystin

48
Q

chracterized by the growth of multiple fluid filled cysts that affect kidney structure and function

A

autosomal dominant polycystic kidney disease

49
Q

responsible for 10% of all cases of ESRD

A

autosomal dominant polycystic kidney disease

50
Q

[…] control normal kidney developent and function via Ca and cAMP

A

polycystins

51
Q

polycystin alterations cause

A

autosomal dominant polycystic kidney disease

52
Q
  • hematuria
  • hypertension
  • ESRD
A

autosomal dominant polycystic kidney disease

53
Q

best imaging modality for autosomal dominant polycystic kidney disease

A

US or MRI

54
Q

treatment of autosomal dominant polycystic kidney disease

A

hypertension, pain mangement
inhibit cAMP and ADH

will cause polyuria though

55
Q

salt wasting due to malfunction of NKCC causes hypokalemia

disease

A

Bartter’s

56
Q

characterized by mutations in ENaC

disease

A

Liddle’s

57
Q

hyperactivity of ENac increases sodium reabsorption causing water retention and high blood pressure

A

Liddle’s

58
Q

mutations of Na/Cl co transport in the distal tubule

A

Gitelman’s

59
Q

characterized by low FENa

A

Liddle’s

60
Q

Furosemide OD will present similar to what syndrome?

A

Bartter’s

61
Q

increase in renin due to malfunction of the NKCC in macula densa

A

Bartter’s

causes secondary hyperaldosteronism

62
Q

how does high aldosterone lead to an increase in blood pH?

A
  • aldosterone stimulates the proton ATPasese in the distal and collecting tubule
  • more H+ release via kidneys –> metabolic alkalosis
63
Q

causes metabolic acidosis due to the inability to secret protons and acidify the urine below 5.5

A

renal distal tubular acidosis
(Type 1)

64
Q

polycystic kidney disease also present with cysts in the

A

liver

65
Q

which diuretic is the most effective treatment of Liddle’s?

A

triamtrene

66
Q

medications that inhibits ENac

A

triamterene

67
Q

what medication targets carbonic anhydrase?

A

acetazolamide

68
Q

what medication inhibits NKCC in the loop of Henle

A

furosemide

69
Q

what medications block Na/Cl transport in the distal tubule?

A

thiazides

70
Q

generalized reabsorption defect in PCT causing increased secretion of amino acids, glucose, bicarb, and phosphate

A

Fanconi

71
Q
  • causes metabolic acidosis (proximal RTA)
  • hypophosphatemia
  • hypokalemia
A

Fanconi

72
Q
  • growth retardation and rickets/osteopenia are common due to hypophosphatemia
  • volume depletion also common
A

Fanconi

73
Q
  • reabsorption defect in the ascending loop of Henle
  • affects NKCC transporter
A

Bartter

74
Q
  • metabolic alkalosis
  • hypokalemia
  • hypercalciuria
A

Bartter

75
Q

present similarly to chronic loop diuretic use

A

Bartters

76
Q

reabsorption defect of NaCl in DCT

A

Gitelman

77
Q
  • metabolic alkalosis
  • hypomagnesemia
  • hypokalemia
  • hypocalciuria
A

Gitelman

78
Q

presents similarly to chronic thiazide diuretic use

A

Gitelman

less severe than Bartter

79
Q

GOF mutation causing decreased Na+ channel degradation leading to increased Na+ reabsorption in collecting tubules

A

Liddle

80
Q
  • metabolic alkalosis
  • hypokalemia
  • hypertension
  • decreased aldosterone
A

Liddle

81
Q

presents similarily to hyperaldosteronism but aldosterone is nearly indectable

A

Liddle

82
Q

treatment for Liddle

A

amiloride or triametere
(ENac inhibitors)

GIR Test 4 (18 decks)

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