Nephrology Flashcards

1
Q

Renal rejection: minutes to hours

A

Hyperacute rejection

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2
Q

Renal rejection: <6 months

A

Acute graft failure

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3
Q

Renal rejection: >6 months

A

Chronic graft failure

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4
Q

Cause of hyperacute rejection

A

Antibodies against ABO or HLA antigens

Examples of type II hypersensitivity

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5
Q

Cause of acute rejection

A

Mismatched HLA - Cell-mediated (cytotoxic T cells)

CMV infection

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6
Q

Acute rejection: Mx

A

Steroids and immunosuppressants

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7
Q

Chronic graft failure: causes

A

Antibody and cell mediated causing fibrosis to the transplanted kidney

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8
Q

Chronic kidney disease: bone labs

A

Low vitamin D
High phosphate
Low calcium
Secondary hyperparathyroid

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9
Q

IgA nephropathy: features

A

Macroscopic haematuria in young people following upper respiratory tract infection

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10
Q

IgA nephropathy: associations

A

Alcoholic cirrhosis
Coeliac disease / dermatitis herpetiformis
HSP

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11
Q

Mesangial hypercellularity

Positive immunofluorescence for IgA and C3

A

IgA nephropathy: histology

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12
Q

Difference between IgA nephropathy and post-strep GN

A
  • Post strep associated with low complement levels
  • Post strep associated with proteinuria
  • Post strep is weeks following infection
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13
Q

IgA nephropathy: treatment

A

Persistent proteinuria - ACEi

Renal failure - steroids

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14
Q

IgA nephropathy: poor prognostic factors

A

Male, proteinuria >2g, hypertension, hyperlipidaemia, ACE DD

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15
Q

Post-strep GN: features

A

7-14 days post infection

Haematuria, proteinuria, hypertension, oliguria

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16
Q

Post-strep GN: histology

A

Subepithelial humps caused by immune complex deposits

Granular or starry sky appearance on immunofluoresecnce

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17
Q

SLE: class II

A

Mesangial GN

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18
Q

Focal and segmental proliferative GN

A

SLE: class III

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19
Q

Diffuse proliferative GN (most common)

A

SLE: class IV

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20
Q

Diffuse membranous GN

A

SLE: class V

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21
Q

Sclerosing GN

A

SLE: class VI

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22
Q

Glomeruli endothelial and mesangial proliferation, wire loop appearance
Granular appearance

A

SLE Class IV: histology

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23
Q

SLE kidney disease: Mx

A

Steroids +/- mycophenolate or cyclophosphamide

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24
Q

ATN: urine sodium

A

Raised

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25
Q

ATN: urine osmolality

A

Low

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26
Q

ATN: Fractional sodium excretion

A

> 1%

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27
Q

ATN: response to fluid challenge

A

Poor

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28
Q

ATN: serum urea:creatinine ratio

A

normal

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29
Q

DM: stage 1 nephropathy

A

Hyper-filtration

Increase in GFR

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30
Q

DM: stage 2 nephropathy

A

Silent / latent phase

GFR elevated

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31
Q

DM: stage 3 nephropathy

A

Incipient nephropathy

Microalbuminuria

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32
Q

DM: stage 4 nephropathy

A

Overt nephropathy
Persistent proteinuria
HTN

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33
Q

DM: stage 5 nephropathy

A

ESRF

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34
Q

What is Fanconi syndrome?

A

Generalised reabsorptive disorder in the PCT

35
Q

Fanconi syndrome: features

A
Type 2 (proximal) RTA
Polyuria
Aminoaciduria
Glycosuria
Phosphaturia
Osteomalacia
36
Q

Basement membrane is thickened with subepithelial electron dense deposits
Spike and dome appearance

A

Membranous GN: histology

37
Q

Membranous GN: causes

A
Idiopathic (anti-phospholipase A2 antibodies)
Infections: HBV, malaria, spyhilis
Malignancy
Drugs
Autoimmune disease
38
Q

GN: nephritic syndrome

A

Rapidly progressive
IgA nephropathy
Alport

39
Q

GN: nephrotic syndrome

A
Minimal change disease
Membranous GN
Focal segmental glomerulosclerosis
Amyloidosis
Diabetic nephropathy
40
Q

GN: mixed

A

Diffuse proliferative
Membranoproliferative
Post-strep

41
Q

Radio-opaque stones

A

Calcium oxalate
Mixed calcium - phosphate stones
Phosphate stones

42
Q

Radio-lucent stones

A

Urate

Xanthine stones

43
Q

Semi-opaque stones

A

Cystine stones

44
Q

Hypercalcaemia causes what stones?

A

Calcium stones

45
Q

Risk reduction of calcium stones

A

High fluid intake
Low protein and salt diet
Thiazide diuretics

46
Q

Risk reduction oxalate stones

A

Cholestyramine

Pyridoxine

47
Q

Risk reduction uric acid stones

A

Allopurinol

Bicarbonate

48
Q

Alport inheiritance

A

X-linked dominant

49
Q

Alport defect

A

type IV collagen

50
Q

Alport features

A
Microscopic haematuria
Progressive renal failure
Bilateral sensorineural deafness
Lenticonus
Retinitis pigmentosa
51
Q

Alport: renal histology

A

Splitting of lamina densa

52
Q

Causes of retorperitoneal fibrosis

A
Riedel's thyroiditis
Radiotherapy 
Sarcoid
Inflammaty AAA
Methysergide
53
Q

Anion gap

A

(Na + K) - (Cl - HCO3)

Range: 8-16

54
Q

HSP: features

A

Palpable purpuric rash over buttocks and extensors
Abdo pain
Polyarthritis
IgA nephropathy

55
Q

Management in ADPKD

A

Tolbapatan (vasopressin receptor 2 antagonist)

56
Q

ADPKD features

A
HTN
Recurrent UTI
Abdo pain 
Renal stones
Haematuria
CKD
Liver cysts
Berry aneurysms
MV prolapse
57
Q

Papillary necrosis causes

A
POSTCARDS
Pyelonephritis
Obstruction
Sickle cell 
TB
Cirrhosis of liver
Analegsia/alcohol overuse
Renal vein thrombus
DM
Systemic vasculitis
58
Q

Indications for plasma exchange

A
GBS
Myasthenia gravis
Goodpasture's
ANCA positive vasculitis
TTP/HUS
Cryoglobulinaemia
Hyperviscosity
59
Q

HIV nephropathy: features

A
Proteinuria (nephrotic syndrome)
Normal or large kidneys
Focal segmental glomerulosclerosis
Elevated urea and creatinine
Normotension
60
Q

Minimal change disease: features

A

Nephrotic syndrome

Normotension

61
Q

Normal glomeruli

Electron microscopy shows fusion of podocytes

A

Minimal change disease: biopsy

62
Q

Rapidly progressive glomerulonephritis: features

A

nephritic syndrome

63
Q

Rapidly progressive glomerulonephritis: causes

A

Goodpasture’s
Wegener’s
SLE

64
Q

FSGS: causes

A
Idiopathic
IgA nephropathy
HIV
Heroin
Alport's syndrome
Sickle cell
65
Q

Focal and segemental sclerosis and hyalinosis on light microscopy
Effacement of foot processes

A

FSGS: Biopsy

66
Q

Nephritic syndrome: causes

A

Rapidly progressive GN
IgA nephropathy
Alport syndrome

67
Q

Mixed nephrotic and nephritic syndrome: causes

A

Diffuse proliferative GN
Membranoproliferative GN
Post-strep

68
Q

Nephrotic syndrome: causes

A
Minimal change disease
Membranous GN
FSGS
Amyloidosis
Diabetic nephropathy
69
Q

Metabolic acidosis: normal anion gap

A
GI losses: diarrhoea, ureterosigmoidostomy, fistula
RTA
Acetazolamide
Ammonium chloride injection
Addison's
70
Q

Metabolic acidosis: raised anion gap

A

Lactate: shock, sepsis, hypoxia
Ketones: DKA, alcohol
Urate: renal failure
Acid poisoning: salicyclates, methanol

71
Q

Renal transplant: initial regime

A

Ciclosporin/tacrolimus with monoclonal antibody

72
Q

Renal transplant: maintenance

A

ciclosporin/tacrolimus with MMF or sirolimus

73
Q

Wilm’s tumour: features

A

Abdominal mass, painless haematuria, flank pain, anorexia

74
Q

Wilm’s tumour: Mx

A

Nephrectomy, chemotherapy, radiotherapy

75
Q

AL amyloidosis

A
  • Most common
  • Light chain fragment
  • Myeloma, Waldenstrom’s, MGUS
76
Q

AL amyloidosis: features

A

Nephrotic syndrome, cardiac and nephrotic involvement, macroglossia, periorbital eccymoses

77
Q

AA amyloidosis

A

Acute phase reactant

Chronic inflammation / infection

78
Q

Eythropoitein: SE

A

HTN, bone aches, flu like symptoms, skin rashes, urticaria, red cell aplasia, Raised PCV, IDA

79
Q

Plasma exchange: complications

A

Hypocalcaemia, metabolic acidosis, removal of systemic medication, coagulation factor depletion, immunoglobulin depletion

80
Q

Gosereline

A

Synthetic GnRH agonist

81
Q

Bicalumtmaide

A

Non-steroidal anti-androgen

82
Q

Abiraterone

A

Androgen synthesis inhibitor

83
Q

HLA importance

A

DR > B > A