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BPT Written > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Aldosterone stimulates which part of the renal tubule to reabsorb Na?

A

Cortical collecting duct

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2
Q

ANP affects which part of the renal tubule to inhibit Na reabsorption?

A

Medullary collecting duct

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3
Q

Which part of the tubule is the site for excretion of trimethoprim?

A

Proximal tubule

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4
Q

Dapagliflozin exerts its effect on which part of the renal tubule?

A

Proximal tubule

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5
Q

Why is Gaddolinium avoided in CKD?

A

Nephrogenic systemic fibrosis from gad chelators

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6
Q

Renal Tx, detection of graft rejection risk modalities and when risk is greatest

A

CDC +ve> Flow cytometry > virtual cross matching

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7
Q

Renal transplant x2 induction agents

A

Basilixumab (anti-CD25) and ATG (superior in high risk)

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8
Q

Renal Tx Immunosuppression maintenance

A

Pred + Tac + MMF

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9
Q

CNI pathway affected:

A

Signal 1: TCR/CD3 -> calcineurin -> NFAT -> IL-2,IL2R

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10
Q

mTORi pathway

A

Signal 3: IL2 -> CD25/JAK3 -> mTOR -> cell cycling

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11
Q

What is belatacept?

A

soluble CTLA4-Fc

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12
Q

Tacrolimus side effects

A

Twitchy and shorn, more diabetes, seizures

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13
Q

Cyclosporin side effects

A

Cheesy (gums) and neanderthal (hirsuitism)

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14
Q

MMF MOA

A

Inhibits IMPDH

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15
Q

MMF side effects

A

myelosuppressive, diarrhoea

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16
Q

Everolimus vs. Sirolimus side effects

A

Everolimus less cancer and less infection

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17
Q

Most important HLA group re. rejection

A

HLA-DQ

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18
Q

T cell mediated rejection rx

A

Methylpred and increase maintenance

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19
Q

Ab mediated rejection Rx

A

PLEX or IVIg or Rituximab

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20
Q

CMV prophy duration

A

6/12 if mismatch, 3/12 if R+ irrespective of donor; give if needing ATG

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21
Q

CMV rx

A

double dose valgan or gan

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22
Q

Rx for resistant CMV

A

foscarnet, cidofovir, CMV Ig, reduce anti-metabolite immunosuppression

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23
Q

Change of immunosuppression because of skin cancer

A

cease Aza and use mTORi

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24
Q

pattern of transplant glomerulopathy

A

MPGN

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25
Q

BK nephropathy specific stain

A

Simian virus 40 stain

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26
Q

Areas of kidney most susceptible to AKI

A

outer medulla and proximal tubules

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27
Q

biggest risks for contrast induced nephropathy

A

CKD and diabetes

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28
Q

Mgmt of Contrast induced nephropathy

A

isotonic IVH, iso/low osmolar contrast low volume

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29
Q

MOA of rhabdo

A

Causes vasoconstriction, direct tubular damage and cast nephropathy

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30
Q

Top 3 causes of isolated glomerular haematuria

A

IgA, Alport’s, Thin BMD

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31
Q

Nephrotic diseases

A

Kids- MCD; middle age= FSGS; old- membranous

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32
Q

Nephritic diseases

A

Kids- Post-infectious; young- IgA, SLE; old- AAN

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33
Q

What GN often recurs early post Tx?

A

FSGS

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34
Q

Secondary MCD is due to

A

NSAIDs, infection, allergy, cancer

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35
Q

2nd most common Ab in primary membranous

A

THSD7A (thrombospondin)

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36
Q

Secondary causes of membranous GN

A

cancer or SLE

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37
Q

main cell damaged in membranous GN

A

podocyte

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38
Q

Rx for primary membranous GN

A

Rituximab

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39
Q

Primary FSGS MOA

A

Elevated suPAR (soluble urokinase-type Plasminogen Activator Receptor) gets trapped in BM -> protease results in foot process effacement

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40
Q

Causes of secondary FSGS

A

HIV (collapsing), obesity, heroin, cancer, hyperfiltration

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41
Q

What is TINU?

A

Tubulointerstitial nephritis with uveitis. Occurs in young women, HLA assoc, Rx AIN w. steroids

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42
Q

Where go Ig complexes deposit in IgA GN?

A

mesangium

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43
Q

Biggest predictor of ESRF in IgA?

A

proteinuria >1g/day

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44
Q

When to biopsy in SLE?

A

Any renal involvement unless bland urine with <0.5g/day or creatinine too high to salvage

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45
Q

Mgmt of lupus nephritis

A

steroids + cyclophosphamide -> MMF maintenance

46
Q

classic cause of secondary MPGN

A

chronic infection, Hep C +/- cryo

47
Q

IN relapsing AAV mgmt

A

Rituximab better than cyclophosphamide. Argument for Ritux upfront if PR3

48
Q

To what are antibodies directed in Anti-GBM disease?

A

against noncollagenous domain of alpha 3 chain of type 4 collagen

49
Q

HLA/other links w. Anti-GBM

A

HLA-DR2; lung damage from smoking, hydrocarbons, influenza A, Alemtuzumab

50
Q

Immunuotactoid GN details

A

Monoclonal IgG GN. usually IgG1. proliferative. nephritic. forms microtubular structure with HOLLOW tubes on EM. usually assoc. w. lymphoproliferative malignancy

51
Q

Fibrillary GN details

A

Monoclonal IgG GN. MPGN. IgG in all. Bad nephritic/ RPGN. <20% have MGUS. Assoc. w. Hep C/Ca/AID. Tubules are thick

52
Q

Type 1 cryo =

A

Monoclonal PTN due to haem usu. CLL/Waldenstroms. Often hyperviscous. TMA presentation

53
Q

Type 2 cryo =

A

mixed, usually IgM-k mono + polyclonal IgG. Often assoc. infection Hep B/C. present as arthralgia, weakness, rash, neuropathy

54
Q

Type 3 cryo =

A

mixed. polyclonal from infection/ AID. complement mediated MPGN.

55
Q

PCKD % 1 vs. 2

A

78% 1 vs. 15% 2

56
Q

PCKD inheritance

A

AD, complete penetrance

57
Q

PCKD mutation type

A

point mutations causing either truncating (66%) or non-truncating in rest (milder).

58
Q

Risk factors for progression in PCKD

A

PKD1 truncating > non-truncating > PKD2. Male, early onset sx, FHx. ESRF, proteinuria, HTN, size on MRI

59
Q

Extra-renal manifestations ADPKD

A

MCA berry aneurysms/ hepatic cysts/ pancreatic and seminal vesical cysts/ valvular (MVP, AR)/ aorta (Dissection, aneurysm), GI (diverticulae, hernias)

60
Q

PCKD diagnosis

A

No Fhx: >10 cysts bilateral with renal enlargement. FHx: 15-40yrs 3 cysts total. 40-60 2 cysts each. >60 4 cysts each

61
Q

Tolvaptan MOA

A

Vasopressin-2 receptor antagonist

62
Q

uOsmol aim of Tolvaptan

A

<280

63
Q

Causes of death in PCKD

A

CVD > ICH

64
Q

Dialysis Kt/V aim

A

HD 1.2, PD 1.7

65
Q

Dialysis adequacy urea reduction ratio

A

Urea pre-urea post/ urea pre

66
Q

single factor w. biggest impact on longevity of PD

A

PD peritonitis

67
Q

Biggest factor to improve dialysis adequacy

A

time on dialysis

68
Q

Best access method of dialysys

A

AVF

69
Q

Dialysis disequilibrium mechanism

A

osmotic gradient -> cerebral oedema

70
Q

Ways to improve Peritoneal dialysis

A

higher dextrose, more bags, higher volume

71
Q

Where are aldosterone receptors located?

A

cortical collecting duct

72
Q

Where does ANP work?

A

medullary collecting duct

73
Q

Where are V1 receptors?

A

On vasculature

74
Q

Where are V2 receptors?

A

On TAL/DCT/CD

75
Q

V2 receptor activation ->

A

aquaporin channels and free water re-absorption

76
Q

What does CA-inhibition cause e.g. acetazolamide

A

metabolic acidosis from excess bicarbonate loss from proximal tubule (form of T2 RTA)

77
Q

Where is Na reabsorbed in kidney

A

67% PCT, 25% TAL Na-K-Cl. 5% DCT

78
Q

Where do thiazides work?

A

DCT Na-Cl channel

79
Q

Channel on which loop diuretics work

A

Na-K-Cl

80
Q

electrolyte changes of Bartters

A

HypoK, HypoCa,HypoMg, volume depletion, alkalosis; secondary hyperaldosteronism

81
Q

Rx of Bartter’s

A

NSAIDs, Electrolyte replacement

82
Q

Gitelman’s inheritance

A

AR

83
Q

What are prostaglandins in Bartter’s

A

elevated +++ due to poor perfusion

84
Q

Gitelman’s sx

A

polyuria, cramps

85
Q

Liddle’s defect

A

ENaC in collecting tubule permanently turned on -> excessive Na reabsorption -> HTN (like apparent mineralocorticoid excess)

86
Q

Liddle rx

A

Amiloride

87
Q

Gordon’s defect

A

defect in thiazide sensitive Na-Cl co-transporter, gain of function; excessive Na reabsorption (opposite of Gitelman)

88
Q

Findings in Gordon’s

A

HTN, Acidosis, Hyperkalaemia

89
Q

Rx of Gordon’s

A

Thiazide

90
Q

RTA Type 1 features

A

NAGMA, hypokalaemia, alkaline urine, nephrolithiasis

91
Q

T1 RTA causes

A

AID- SS, RA

92
Q

T2 RTA features

A

NAGMA, hypokalaemia, urine pH low

93
Q

T2 RTA causes

A

Monoclonal IgG disease, drugs- Tenofovir, Fanconi’s

94
Q

T4 RTA features

A

hypoaldosteronism, low BP, NAGMA, hyperkalaemia

95
Q

T4 RTA causes

A

adrenal insufficiency, CNIs, NSAIDs, interstitial nephritis, DM nephropathy, acute GN

96
Q

T4 RTA mgmt

A

fludrocortisone

97
Q

Gentamicin type of nephrotoxicity

A

ATN

98
Q

Top 4 medications in order of benefit for BP/proteinuria

A

ACE-i/ARB, diuretics/ CCB/ spiro

99
Q

FIrst biochemical change in CKD-MBD

A

lose klotho; FGF23 rises

100
Q

why is 1,25-vitD reduced in CKD-MBD?

A

FGF-23 inhibition of 1-OH and destruction of 25-OH-vitD

101
Q

FGF23 normally suppresses

A

PO4 and PTH

102
Q

Most common form of CKD-MBD in dialysis patients

A

adynamic bone disease

103
Q

PTH target in dialysis patients

A

2-9x ULN

104
Q

Iron target in ESRF

A

Ferritin >100-200 and TfSat >20%

105
Q

side effects of EPO

A

pure red cell aplasia with Abs to EPO; stroke

106
Q

Target Hb of ESRF

A

100-110

107
Q

Diabetic nephropathy biopsy finding

A

Kimmelstiel-wilson nodules = nodular glomerulosclerosis

108
Q

Lithium action on tubules

A

Nephrogenic DI- from impaired responsiveness of distal nephron to ADH/ decreased expression AQP2
Hypercalcaemia- impairs CaSR so doesn’t inhibit Ca reabsorption in the tubule

109
Q

Response to desmopressin in nephrogenic DI

A

no/minimal rise in urine osmolality

110
Q

mgmt lithium DI

A

thiazides and amiloride when urine vol >4L/day

BPT Written (21 decks)

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