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Renal > Distal Renal Tubular disorders > Flashcards

Distal Renal Tubular disorders Flashcards

1
Q

% sodium reabsorbed in PT?

A

65-70%

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2
Q

% sodium reabsorbed in T.A.L.

A

25%

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3
Q

% sodium reabsorbed in DT

A

5%

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4
Q

Na transporter in TAL

A

NK2C co-transporter

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5
Q

Na transporter in DT

A

Thiazide-sensitive co-transporter Na/Cl

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6
Q

% sodium reabsorbed in CD

A

1-2% (by epithelial Na channel)

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7
Q

Acetazolamide target

A

carbonic anhydrase

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8
Q

Furosemide/bumetanide/ethacrynic acid target

A

NK2C cotransporter

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9
Q

Thiazides target

A

Na-Cl cotransporter

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10
Q

What targets epithelial sodium channels

A

amiloride and triamterene

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11
Q

What targets the mineral corticoid receptor

A

spironolactone and eplerenone

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12
Q

Hyperplasia of JG apparatus, elevated plasma renin and aldosterone

A

Bartter Syndrome

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13
Q

Presentation of Bartter Syndrome

1) acid base status
2) potassium
3) aldosterone
4) renin
5) 2 other features

A

1) Hypochloremic met alkalosis,
2) hypokalemia,
3) hyperaldosteronism,
4) hyperreninemia,
5) elevated PGE2, failure to thrive

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14
Q

Bartter treatment

A

potassium supplements, magnesium (also spironolactone)

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15
Q

What presents with prenatal massive polyhydramnios (due to fetal polyuria)

A

Neonatal Bartter (also has massive salt wasting at birth)

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16
Q

In neonatal Bartter, the amniotic fluid has elevated levels of

A

PGE2 (this is a target for treatment with COX inhibitors)

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17
Q

Bartter Mutations (5)

A

NKC2, ROMK, CLCNKA, CLCNKB, Barttin

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18
Q

What is barttin

A

Cl channel A/B inserter in kidney/inner ear

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19
Q

Presentation of Gitelman Syndrome

1) acid base status
2) potassium
3) magnesium
4) calcium (blood/urine)
5) other feature

A

1) hypochloremic met alkalosis,
2) hypokalemia,
3) hypomagnesemia,
4) Hypercalcemia / hypocalciuria
5) (presents later in life with Normal growth)

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20
Q

Gitelman mutation

A

Na-Cl co transporter of the DCT (thiazide sensitive)

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21
Q

Liddle syndrome presentation

1) [main feature]
2) renin
3) aldosterone
4) potassium
5) acid base status

A

1) hypertension,
2) low renin,
3) low aldosterone,
4) hypokalemia,
5) met alkalosis

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22
Q

Liddle syndrome closely resembles

A

Pseudohypoaldosteronism type 1

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23
Q

mutation in Liddle

A

gain of function in the Beta or gamma subunit of the epithelial sodium channel (aldosterone sensitive channel, stuck open)

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24
Q

Liddle treatment

A

salt restriction and diuretics

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25
Q

causes of Hypokalemia

A

diuretics and hyperaldosteronism

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26
Q

causes of hyperkalemia

A

hypoaldosteronism and pseudohypoaldosteronism

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27
Q

TTKG tests what?

A

aldosterone response in the DT

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28
Q

for TTKG, urine sodium must be?

A

greater than 25 mmol/L

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29
Q

TTKG formula

A

[urine potass over plasma potass] divided by [urine osm over plasma osm]

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30
Q

simplified TTKG formula

A

UK x Posm / PK x Uosm

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31
Q

Normal range for TTKG

A

2-8

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32
Q

Less than 2 on TTKG is?

A

hypokalemia

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33
Q

greater than 4 on TTKG is?

A

hyperkalemia

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34
Q

‘Pitfalls’ (what makes test invalid) of TTKG tests

A

1) urine Na less than 20 mEq/L

2) urine osm less than 300 mOsm/kg

35
Q

Primary cause of hyperaldosteronism

A

adrenal tumor

36
Q

secondary causes of hyperaldosteronism

A

dehydration (pyloric stenosis), sodium wasting (Barterr-Gitelman)

37
Q

Genetic disorders that cause hyperaldosteronism

A

GRA, AME

38
Q

GRA mutation

A

recombination of 11BHSD and aldosterone synthase (at promoter)

39
Q

result/presentation of the GRA mutation

A

hypertension during stress

40
Q

GRA causes

A

low renin HTN and hypokalemia

41
Q

GRA treatment

A

glucocorticoids

42
Q

GRA stands for

A

Glucocorticoid Remediable hyperaldosteronism

43
Q

AME stands for

A

Apparent Mineralocorticoid Excess

44
Q

AME mutation

A

11BHSD

45
Q

AME results in

A

increase levels of cortisol (which activates the mineralocorticoid receptor), low renin HTN, hypokalemia

46
Q

AME treatment

A

glucocorticoids

47
Q

Hyperkalemic disorders

A

congenital adrenal hyperplasia/hypoplasia, autoimmune, PHA type 1 and 2, Tubular injury (obstructive uropathy)

48
Q

PHA Type 1 lab findings

1) potassium
2) sodium
3) prone to what
4) mirror image of what

A

1) hyperkalemia,
2) hyponatremia,
3) prone to severe volume depletion (hypotension),
4) mirror image of liddle syndrom

49
Q

Causes of PHA type 1

A

mutations in mineralocorticoid receptor and LOF mutation in the ENac (stuck shut)

50
Q

which PHA type 1 cause is recessive

A

LOF in ENac

51
Q

which PHA type 1 cause is auto dominant

A

mutations in M-C receptor

52
Q

Liddle syndrome mode of inheritance

A

auto dominant

53
Q

PHA type 1 treatment

A

sodium supplements, high fluid intake, K binding resin (kayexalate)

54
Q

PHA Type 2 presentation/lab findings

1) potassium
2) acid base status
3) blood volume
4) renin/aldo
5) mirror image of what

A

1) hyperK,
2) hypercloremic met acidosis,
3) HTN,
4) low renin/aldosterone,
5) mirror image of Gitelman

55
Q

PHA Type 2 also known as

A

Gordon syndrome or chloride shunt syndrome

56
Q

treatment for PHA type 2

A

thiazide diuretics

57
Q

PHA type 2 mutations

A

WNK1 and WNK4

58
Q

function of WNK’s

A

serine-threonine kinases that regulate NCCT, the thiazide sensitive Na-Cl contransporter

59
Q

Plasma Anion Gap formula

A

Na- (Cl + HCO3)

60
Q

Normal range of plasma anion gap

A

8-20 at Le Bonheur, adults 10-12

61
Q

Causes of Elevated anion gap acidosis

A

ketoacidosis, lactic acidosis, inborn errors of metab (methylmalonic acidemia, propionic acidemia) and poisons (methanol/ethylene glycol)

62
Q

Causes of normal anion gap acidosis (hyperchlor met acid.) [according to Dr. Ault there are only 3]

A

1) G.I. losses of bicarbonate,
2) exogenous chloride (arginine HCl challenge, vol. expan. with NaCl),
3) renal tubular acidoses

63
Q

RTA anion gap?

A

normal

64
Q

which RTA is associated with Fanconi syndrome

A

type 2 (proximal)

65
Q

which RTA is very rare and presents with hypoK, hypocalciuria, nephrolithiasis, and Failure 2 Thrive

A

Type 1 (classic distal)

66
Q

which RTA is a syndrome of aldost. deficiency or unresponsiveness

A

Type 4

67
Q

how often does RTA present with diarrhea

A

almost never

68
Q

Tests for RTA

A

fractional excretion of bicarb, urine pH, urine anion gap, U-B pC02

69
Q

Fract. Excr. >10-15% in which RTA

A

proximal RTA aka type 2

70
Q

Fract. Excr.

A

classic distal RTA aka type 1

71
Q

fract. excr.

A

hyperkalemic RTA aka type 4

72
Q

Urine pH in classical distal RTA

A

greater than 5.5

73
Q

Urine pH in proximal RTA (if HCO3 is below threshold)

A

less than 5.5

74
Q

Urine anion gap

A

(UNa + Uk) - UCl

75
Q

if UAG is negative….

A

NH4 is present and the CD can secrete H … also neg UAG during diarrhea

76
Q

UAG in proximal, type 1, and hyperkalemic RTA

A

positive

77
Q

can’t use UAG in what conditions

A

DKA, ketoacidosis

78
Q

U-B pCO2 normal level

A

> 10-15 mmHg

79
Q

U-B pCO2 is low in what type(s)

A

type 1 and 4

80
Q

high plasma K, positive UAG, low U-B pCO2

A

type 4

81
Q

low plasma K, pH >5.5, low U-B pCO2

A

type 1

82
Q

low plasma K, pH

A

type 2

83
Q

Type 4 RTA causes

A

primary M-C def., secondary M-C def. (diabetes, HIV), RT dysfunction (obstructive uropathy, Lupus nephritis), M-C resistance (pseudohypoaldosteronism)

84
Q

Hey dipshit, what’s the anion gap in RTA?

A

it’s fucking normal, shit dude just remember it damn it to hell (easy killer, its too early for this shit)

Renal (5 decks)

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