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STEPH (NFR) Nephrology Fellowship Reviewer > Tables > Flashcards

Tables Flashcards

1
Q

Na transport in the tubules

A

PCT - 60%
LOH - 30%
DCT - 7%
CD - 2-3%

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2
Q

Proximal tubule Na transporters

A

A: Cl/IOH, NHE3
B: NaKATPase, KCC3/4

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3
Q

LOH Na transporters

A

A: NKCC2, ROMK, Claudin
B: NaKATPase, KCC4, ClC-NKB

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4
Q

DCT Na transporters

A

Apical/lumen: NCC, NHE2, ROMK, HCO0/Cl; ENac, ROMK
Baseolateral: NaKATPase, ClCK-2, Kir, KCC4

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5
Q

K transport in tubules

A

DCT 65%

TAL 25%

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6
Q

Ca transport in tubules (?reabsorption)

A

PCT 70%
TAL 20%
DT 8%

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7
Q

Ca transport proximal tubule

A

paracellular, TRPV5, V6

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8
Q

Ca transport TAL

A

Clauding 16, 19

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9
Q

Mg transport tubules (% reabsorption)

A

PT 20%
TAL 70%
DT 5%

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10
Q

Mg transport TAL

A

paracellular 16, 19

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11
Q

Mg transport DCT

A

TRPM6/7

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12
Q

Phos transport proximal tubule

A

NaPiIIa/IIc

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13
Q

% Bicab reabsorption tubules

A

PT 80%
TAL 15%
CD 5%

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14
Q

Proximal tubule HCO3

A

A: NHE3, AQP1
B: NBce1, NaKATPase

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15
Q

DCT Type A intercalated cell Hco3 reabsorption

A

A: HKATPase, HATPase
B: kAE1, KCC4, Clc-2-K-Barttin

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16
Q

DCT Type B Intercalated cell Hco3 reabsorption

A

A: Cl/HCO3, NDCBe, HKATPase
B: HATPase, Clc-K2, AE4

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17
Q

IgA: predictive of ESKD or 50% decline in GFR

A

Mesangial hypercellularity, tubular atrophy./interstitial fibrosis

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18
Q

IgA: not predictive

A

endocapillary hypercellularity

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19
Q

IgA: predictive of rate of decline in kidney function

A

segmental sclerosis

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20
Q

Chronic lesions in SLE

A

GIFT - Glomerular sclerosis, Interstitial fibrosis, fibrous crescents, tubular atrophy

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21
Q

Acute lesions in SLE

A

Fibrinoid necrosis, cellular crescents karyorrhexis, endocapillary hypercellularity, subendothelial deposits, wireloop lesions, rupture of GBM

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22
Q

Treatment of SLE Class II

A

proteinuria >3g, steroids + CNI

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23
Q

Class 3 SLE Treatment

A

Corticosteroids + cyclophosphamide/MMF

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24
Q

Class IV SLE treatment

A

Azathioprine 1.5-2.5 mkd
MMF 1-2 g/day
low dose steroids
or CNI if intolerant to aza and MMF

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25
Q

Class V SLE treatment

A

corticosteroids + cyclophosphamide, CNI, MMF, azathioprine

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26
Q

1st line initial therapy in SLE

A

cyclophosphamide or MMF

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27
Q

Maintenance therapy in SLE

A

AZA or MMF

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28
Q

Class 3 or 4 initial therapy options for cyclophosphamide

A

IV 0.5-1 g/m2 monthly for 6 months, 500 mg q2 weeks for 3 months, 1-1.5 mkd po 2-4 months

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29
Q

Cause of hypercalcemia: High PTH, Uca less than 100 mg/24h, FeCa < 0.01

A

FHH, NSHPT, Lithium

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30
Q

Cause of hypercalcemia: High PTH, UCa>200 mg/24h, FeCa> 0.01

A

primary or tertiary hyperparathyroidism

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31
Q

Cause of hyperCa: low PTH, low PTHRP, high 25(OH), high 25 (OH)2

A

Vitamin D overodse

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32
Q

Cause of hyperCa: low PTH, low PTHrP, low 25 (OH), high 25 (OH)2

A

Granulomatous disorders

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33
Q

Cause of hypercCa: low PTH, low PTHrp, low 25 (OH) and 25 (OH)2

A

LOH, milk alakali syndrome, immobilization, vitamin A, Drugs

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34
Q

Cause of hyperca: Low PTH, high PTHrP

A

HHM

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35
Q

Cause of hypoca, High crea

A

renal failure

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36
Q

Cause of hypoca: Normal Crea, Low PTH

A

hypoparathyroidism, low Mg, genetic

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37
Q

Cause of hypoca: Normal Crea, High PTH, Low Vitamin D

A

Vitamin D deficiency

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38
Q

Cause of hypoca: Normal Crea, high PTH, normal vitamin D, Normal 1, 25 (OH)2D

A

pseudohypoparathyroidism, Vit D dependent rickets

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39
Q

Cause of hypoca: Normal Crea, high PTH, normal vitamin D, High 1, 25 (OH)2D

A

Vit D resistant rickets

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40
Q

Cause of hyperK: TTKG>8

A

advanced kidney failure; dec ECV

41
Q

HyperK: TTKG <5, TTKG <8 after fludrocortisone

42
Q

HyperK: TTKG <5, TTKG > 8 after fludrocortisone, low aldosterone, low renin

A

DM, GN, NSaids, b-blockers

43
Q

HyperK: TTKG <5, TTKG > 8 after fludrocortisone, low aldosterone, high renin

A

AI, ACE, Ketoconazole

44
Q

HypoK: UrineK < 15 mmol/day, 15 mmol/g/Crea, metabolic acidosis

A

GI K losses

45
Q

HypoK: Urine K < 15 mmol/day, 15 mmol/g/Crea, Normal acid base

A

profuse sweating

46
Q

HypoK: Urine K < 15 mmol/day, 15 mmol/g/Crea, Metabolic alkalosis

A

remote diuretic use, vomiting

47
Q

HypoK: Urine K > 15 mmol/day, 15 mmol/g/Crea, TTKG >4, low/normal BP/volume, Metabolic acidosis

48
Q

HypoK: Urnie K > 15 mmol/day, 15 mmol/g/Crea, TTKG >4, low/normal BP/volume, Metabolic alkalosis, UCl>20, UCa/Crea <0.15

49
Q

HypoK: Urnie K > 15 mmol/day, 15 mmol/g/Crea, TTKG >4, low/normal BP/volume, Metabolic alkalosis, UCl>20, UCa/Crea > 0.20

A

Bartter Syndrome

50
Q

HypoK: Urnie K > 15 mmol/day, 15 mmol/g/Crea, TTKG >4, low/normal BP/volume, Metabolic alkalosis, UCl < 10

A

extrarenal losses

51
Q

HypoK: Urnie K > 15 mmol/day, 15 mmol/g/Crea, TTKG >4, high BP/volume, Low aldosterone, normal cortisol

A

Liddle, licorice, AME

52
Q

HypoK: Urnie K > 15 mmol/day, 15 mmol/g/Crea, TTKG >4, high BP/volume, low aldosterone, high cortisol

A

Cushing syndrome

53
Q

HypoK: Urnie K > 15 mmol/day, 15 mmol/g/Crea, TTKG >4, high BP/volume, High aldosterone, Low Renin

54
Q

HypoK: Urnie K > 15 mmol/day, 15 mmol/g/Crea, TTKG >4, high BP/volume, high aldosterone, high renin

A

RAS, Malignant hypertension

55
Q

Metabolic alkalosis, UCl> 20, UK > 30, HTN, low renin

A

primary hyperaldosteronism

56
Q

Normal or micronodularity and B masses in Adrenal CT

A

idiopathic hyperaldosteronim vs GRA

57
Q

Unilateral hypodense nodule > 1 cm in Adrenal CT, > 40 years old, with no lateralization

A

GRA screening

58
Q

Unilateral hypodense nodule > 1 cm in Adrenal CT, > 40 years old, with lateralization

A

adrenal adenoma, primary adrenal hyperplasia

59
Q

Unilateral hypodense nodule > 1 cm in Adrenal CT < 40

A

adrenal adenoma, PAH

60
Q

Hyponat, hypovolemic, UNa < 30

A

Extrarenal losses

61
Q

HypoNat, Hypovol, UNa > 30

A

Diuretic, mineralocorticoid deficiency

62
Q

Hyponat, euvol, UNa>30

A

glucocorticoid deficiency, hypothyroidism, SIADH

63
Q

Hyponat, Hypervol, UNa < 30

A

Acute renal failure

64
Q

Hyponat, Hypervol, UNa > 30

A

Nephrotic syndrome, cirrhosis, heart failure

65
Q

Metabolic alkalosis, UCl < 2o

66
Q

Met alk, UCl>20, UK < 30 meq

67
Q

Met alk, UCl>20, UK > 30 meq, normal BP

A

Barter, Gitelman, Diuretics

68
Q

Met alk, UCl>20, UK > 30 meq, high BP, high renin, high cortisol

A

cushing syndrome

69
Q

Met alk, UCl>20, UK > 30 meq, high BP, high renin, normal cortisol, high renin in renal vein

A

renovascular htn. JGA tumor

70
Q

Met alk, UCl>20, UK > 30 meq, high BP, high renin, normal cortisol, normal renin in renal vein

A

malignant hypertension

71
Q

Met alk, UCl>20, UK > 30 meq, high BP, low renin

A

primary aldosteronism, licorice

72
Q

Chains involved in alport syndrome

73
Q

chains involved in tbmd

74
Q

a chains in anti-gbm

75
Q

Tx of MCD

A 
corticosteroids (pred 1 mld or 3 mkd for 4-6 weeks)
cycophosphamide 2-2.5 mkd for 8 weeks
cylosporine 3-5 mld 
tacrolimus 0.05 - 1 mld for 1-2 years
MMF 500-1000 mg BID 1-2 years
76
Q

Tx FSGS

A

prednisone > 4-16 weeks
CNI 4-6 months
MMF + dexamethasone

77
Q

Tx MN

A

IV/oral steroids + cyclophosphamimde

cyclosporine/tacrolimus

78
Q

MPGN Type 1

A

oral cyclophosphamide/MMF

low dose alternate day or daily corticosteroids < 6 months

79
Q

Tx IGA nephropathy

A

RAS blcokers; IV/oral steroids

80
Q

AntiGBM tx

A

steroids + cyclophosphamide + plasmapharesis

81
Q

Pauci Immune Tx

A

MPP 7 mkd then pred 1 mkd for 1st month then alternate day 4-5 months; oral pred 2 mkd; cyclophosphamide
rituximab + corticosteroids + plasmapharesis

maintainance: azathioprine 1-2 mkd, MMF 1 g BID, methotrexate 0.3 mk/week

82
Q

Predictors of Likely failure of fluid restriction in Hyponatremia

A

UOsm > 500, UNa + UK > Serum Na, 24H Urine vol < 1500 ml/day, Inc in serum Na <2 in 24 hours on fluid restriction < 1 L/day

83
Q

Acute rejection Banff

A

Glomerular inflammation, Interstitial inflammation, Vascular inflammation, Tubulitis

84
Q

Chronic rejection Banff

A

Interstitial fibrosis, Tubular atrophy, allograft glomerulopathy (GBM duplication), Mesangial matrix increase, Arterial fibrointimal thickening, Arterial hyalinosis, peritubular capillary

85
Q

HSP Class Subtypes

A 
Class I: Minimal alteration
Class II: Pure mesangial proliferation
Class IIIa: Focal <50% crescents
Class IIIb: Diffuse < 50% crescents
Class IVa: Focal 50-75% Crescents
Class IVb: Diffuse 50-75% crescents
Class Va: Focal > 75% crescents
Class Vb: Diffuse > 75% crescents
Class VI Membranoproliferative
86
Q

RPGN Types

A 
Type I: Anti-GBM
Type II: Immune complex 
Type III: Pauci-immune 
Type IV: Type I + III
Type V: Anca negative, pauci immune renal vasculitis
87
Q

DM Classification

A 
Class I: GBM thickening 
Class II: Mesangial expansion 
Class IIa: mild
Class IIb: severe 
CLass III: Nodular sclerosis 
Class IV: Advanced DM sclerosis
88
Q

Factors increasing risk of osmotic demyelination

A 
Serum Na < 105 
Hypokalemia 
Alcoholism 
Malnutrition 
Advanced Liver Disease
89
Q

simple benign cyst

A

Bosniak Cat I

90
Q

benign with thin septa. fine rim like calcification or uniform high density less than 3 cm

A

Bosniak Cat II

91
Q

multiple septa
thick area or nodular calcification
high density ctsts > 3 cm
follow up at 6-12 mos

A

Bosniak Cat IIF

92
Q

thickened irregular walls with enhancement, dense irregular calcficiation

A

Bosniak Cat III

93
Q

clearly malignant

nephrectomy <5-6 cm

A

Bosniak Cat IV

94
Q

absolute contraindications to renal biopsy

A 
uncontrolled htn 
bleeding diathesus 
cystic disease
hydronephrosus
uncooperative patient
95
Q

Bartter Syndrome Type 1

96
Q

Bartter Syndrome Type 2

97
Q

Bartter Syndrome Type 3

98
Q

Bartter Syndrome Type IV

A

Bartin (B subunit of Clc-Ka and Clc-Kb

99
Q

Bartter Syndrome Type V

A

Clc-Ka and Clc-Kb

STEPH (NFR) Nephrology Fellowship Reviewer (29 decks)

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