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MRCP Part 1 > Nephrology > Flashcards

Nephrology Flashcards

1
Q

PSGN - when does it present?

A

Weeks post URTI

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2
Q

IgA nephropathy - when does it present?

A

Days post URTI

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3
Q

How does PSGN present?

A

Proteinuria

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4
Q

How does IgA nephropathy present?

A

Haematuria

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5
Q

Who does PSGN affect?

A

Young children

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6
Q

Who does IgA nephropathy affect?

A

Young men

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7
Q

Bloods in PSGN

A

High ASO titre, low C3

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8
Q

Histology in PSGN

A

EM: subepithelial humps
Histology: diffuse proliferative glomerulonephritis
Immuno: starry sky

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9
Q

Histology in IgA nephropathy

A

Histology: mesangial hypercellularity
Immunofluorescence: IgA and C3 light up

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10
Q

Pathophysiology of PSGN

A

IgG, IgM and C3 complexes deposit in the glomeruli

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11
Q

Pathophysiology of IgA nephropathy

A

IgA complexes deposit in the mesangium

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12
Q

Management of IgA nephropathy

A

Haematuria + preserved GFR = watch and wait

Proteinuria + preserved GFR = ACEi

Proteinuria + reduced GFR = prednisolone

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13
Q

How do NSAIDs cause AKI?

A

They block vasodilation of afferent arteriole

Results in reduced renal perfusion

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14
Q

Indications for Dialysis

A 
A - acidosis 
E - electrolyte disturbance (hyperkalaemia)
I - intoxications
O - overload 
U - uraemia encephalopathy
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15
Q

Drugs which can be removed by dialysis

A

SLIME:

  • Salicylates
  • Lithium
  • Isopropanol
  • Methanol
  • Ethylene glycol
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16
Q

Definition of AKI

A
  • Cr rise by 26mmol in 48h, or
  • Cr rise by 50% in 7 days, or
  • Oliguria for 6h in adults
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17
Q

Investigations in in renal artery stenosis secondary to fibromuscular dysplasia

A
  • Urine dip: normal
  • US: asymmetrical kidneys
  • Renal artery visualisation e.g. Doppler
  • MR angiography: string of beads
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18
Q

Management of renal artery stenosis

A

1st line: ACEi + statin + aspirn

2nd line: Revascularisation + medical + DAPT

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19
Q

What treatment is contraindicated in bilateral renal artery stenosis, and why?

A

ACE inhibitors are contindicated in bilateral renal artery stenosis.

  • Angiotensin II preferentially vasoconstricts the efferent arterioles, maintains eGFR despite reduced perfusion arterioles.
  • Therefore ACE inhibitors would cause vasodilation of efferent arterioles and overall reduced eGFR
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20
Q

Features of hyperacute renal transplant rejection

A

Minutes - hours

  • Type 2 hypersensitivity reaction
  • Host antibodies against graft antigens
  • Thrombosis and necrosis
  • Mx: graft removal
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21
Q

Features of acute renal transplant rejection

A

< 6 months

  • T-cell mediated/CMV infection
  • Due to HLA mismatch (usually HLA-DR)

Generally asymptomatic with rising Cr, proteinuria

Mx: steroids

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22
Q

Chronic renal transplant failure

A

> 6 months

HLA-A or B

Recurrence of original renal disease
- MCGN > IgA > FSGS

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23
Q

Calcium phosphate renal stones are associated with what condition?

A

Renal tubular acidosis

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24
Q

Prevention of uric acid stones

A
  • urinary alkalisation e.g. sodium bicarbona

- allopurinol if raised serum urate

25
Q

Prevention of oxalate stones

A

Pyridoxine

Colestyramine

26
Q

Prevention of renal calculi (general)

A

Increased fluid intake
Reduce salt
Thiazide diuretics

27
Q

Rhabdomyolysis triad

A

AKI
Hyperkalaemia
Metabolic acidosis

28
Q

Drugs which can cause rhabdomyolysis

A

Statins (esp if with clarithromycin)

Ecstasy

29
Q

Diagnostic criteria for rhabdomyolysis

A

5x increased CK in absence of cardiovascular or CNS injury

30
Q

Electrolytes in rhabdomyolysis

A

Raised K, PO4

Low Ca

31
Q

Presentation of PKD

A

Flank pain
Recurrent UTIs
HTN

32
Q

What heart condition is PKD associated with?

A

mitral prolapse

33
Q

Drugs which can cause acute interstitial nephritis

A

5 Ps:

  • Penicillin
  • Pee (diuretics)
  • Pain (NSAIDs)
  • alloPurinol
  • rifamPicin
34
Q

Acute interstitial nephritis - presentation

A

Fever
Arthralgia
Rash

35
Q

Acute interstitial nephritis investigations

A

Urine dip: sterile pyuria

Bloods: eosinophilia

Biopsy: interstitial oedema in the connective tissue

36
Q

Conditions which show podocyte foot process effacement on EM

A

Focal segmental glomerulosclerosis

Minimal change disease

Membranous glomerulonephritis

37
Q

How does focal segmental glomerulosclerosis present?

A

NEPHROTIC SYNDROME

38
Q

Findings on microscopy in FSGS

A

LM: focal and segmental hyalinosis and sclerosis

EM: effacement of podocyte foot processes

39
Q

Antibody in idiopathic membranous glomerulonephritis

A

Anti-phospholipase A2 antibodies

40
Q

Histology in membranous glomerulonephritis

A

EM: Subepithelial electron-dense deposits which resemble a “spike and dome” appearance

Effacement of podocyte foot processes

41
Q

Management of membranous glomerulonephritis

A
  • All patients: ACEi or ARB

- Severe or progressive disease: steroids + cyclophosphamide
Steroid monotherapy is not effective

42
Q

How does membranous nephropathy present?

A

Nephrotic syndrome

most common glomerulonephritis in adults

43
Q

How does FSGS present?

A

Nephrotic syndrome

44
Q

How does minimal change disease present?

A

Nephrotic syndrome

45
Q

How does Alport syndrome present?

A

Nephritic syndrome
Eyes: Lenticonus, retinosa pigmentosum
Ears: bilateral sensorineural deafness

46
Q

Which HLA is Goodpastures disease associated with?

A

HLA-DR2

47
Q

How does Goodpastures disease present?

A

Nephritic syndrome + pulmonary haemorrhage

48
Q

Biopsy findings in Goodpasture’s

A
  • Epithelial crescents in glomeruli

- Immuno: Linear IgG deposits along GBM

49
Q

Features of acute tubular necrosis

A

Raised urine sodium >40
Urine Osm <350
Normal Ur:Cr ratio

Poor response to fluid challenge

Muddy brown casts

50
Q

Features of pre-renal uraemia

A

Raised serum Ur:Cr ratio
Good response to fluid challenge

Urine Na < 20
Urine Osm > 500

Normal sediment

51
Q

Effects of sevelamer

A

Reduce intestinal phosphate absorption
Reduce serum lipids
Reduce serum uric acid levels

52
Q

Drugs which cause “haematuria”

A

Rifampicin

Doxorubicin

53
Q

Who should be referred for haematuria 2WW?

A

Under 45 with visible haematuria in absence of UTI OR after successful treatment of UTI

Over 60 with non-visible haematuria with raised WCC and dysuria

54
Q

Where does renal cell cancer most commonly arise?

A

proximal tubular epithelium

55
Q

Risk factors for renal cancer

A

Smoking
von Hippel Lindau
Tuberous sclerosis

56
Q

What is Stauffer syndrome?

A

Seen in renal cell cancer

Hepatomegaly + cholestasis

57
Q

Tumour markers in testicular cancer

A

Seminoma: hCG

Non-seminoma: AFP (or bHCG)

58
Q

Glomerulonephritis with low complement

A
  • Post-streptococcal glomerulonephritis
  • Subacute bacterial endocarditis
  • Systemic lupus erythematosus
  • Mesangiocapillary glomerulonephritis

MRCP Part 1 (8 decks)

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