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MRCP 1 > Renal > Flashcards

Renal Flashcards

1
Q

how do you tell the difference between acute tubular necrosis and prerenal uraemia?

A

in prerenal uraemia the kidneys hold on to sodium to try and preserve volume. Therefore test urinary sodium
Prerenal uraemia responds to fluid challenges (ATN doesn’t)

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2
Q

what is a significant albumin:creatinine ratio?

A

non-diabetics >30 is clinically significant

in diabetics ACR >2.5 in men and 3.5 in women is significant

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3
Q

what is nephrotic syndrome?

A

proteinuria
hypoalbuminaemia
peripheral oedema

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4
Q

pathology of MGN?

causes of membranous glomerulonephritis?

A

immune complex formation in the glomerulus -> inflammation and nephrotic syn

idiopathic
infection - malaria, hep B
malignancy - lung ca, lymphoma, leukaemia
drugs - gold, penacillamine, NSAIDS
SLE
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5
Q

management of membranous glomerulonephritis

A

immunosuppression - corticosteroids + other (eg chlorambucil)
antihypertensives (ACEi for proteinuria)
?anticoagulant

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6
Q

PCKD type 1 inheritance

A

auto dominant chromosome 16

0.1% of caucasians

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7
Q

what’s the pathology in Alport’s syndrome?

what’s the inheritance?

A

defect in gene for type 4 collagen, leading to defective glomerular basement membranes
X-linked dominant

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8
Q

features of Alport’s syndrome

A 
presents in childhood
sensorineural deafness
microscopic haematuria
progressive renal failure and episodic frank haematurea
ocular pathology
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9
Q

features of Goodpasture’s syndrome

A

pulmonary haemorrhage

rapidly progressive glomerulonephritis (IgG)

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10
Q

what is Goodpasture’s syndrome

HLA association

A 
autoimmune antibodies to type 4 collagen in BM (anti GBM antibodies)
(type 2 hypersensitivity)
HLA DR2 (narcolepsy and goodpastures)
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11
Q

Ix and Mx of goodpasture’s syndrome

A

renal biopsy - linear IgG deposits
transfer factor - raised due to pulmonary haemorrhage

plasma exchange, steroids, cyclophosphamide

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12
Q

how do you calculate the anion gap?

what is normal?

A

(Na + K) - (Cl + HCO3) (cations(+) - anions(-))

normal 10-18

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13
Q

causes of a metabolic acidosis with normal anion gap

A

GI bicarb loss: diarrhoea, fistula etc
renal tubular acidosis
Addison’s disease (no aldosterone)
drugs eg acetazolamide

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14
Q

causes of a metabolic acidosis with raised anion gap

A

lactate: shock, hypoxia, metformin
ketones: DKA, alcohol,
urate: renal failure
acid poisoning; salicylate, methanol

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15
Q

variables in eGFR calculation

A 
CAGE
creatinine
age
gender
ethnicity
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16
Q

what are the eGFR boundaries for CKD staging?

A

1: >90
2: 90 - 60
3a: 59 - 45
3b: 44 - 30
4: 29 - 15
5: <15

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17
Q

action of Spironolactone and eplerenone

where does it act?

A 
aldosterone antagonist (eplerenone more selective)
acts on the distal convoluted tubule
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18
Q

What is Henoch-Schonlein Purpura?

features?

A

IgA mediated vasculitis
usually in children post infection
palpable purpuric rash on buttocks and extensor surfaces, IgA nephropathy (haematuria, RF - resolves), abdo pain, poly arthritis

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19
Q

What is the composition of a staghorn calculus?

risk factors?

A

Struvite (triple phosphate)
form in alkaline urine so proteus and ureaplasma urealyticum infections (which produces ammonia) predispose to their formation.

20
Q

Features of haemolytic uraemic syndrome

Mx

A

triad:
acute renal failure
thrombocytopenia
microangiopathic haemolytic anemia

generally seen in young children after E.coli 157:H7
Supportative, plasma exchange if severe with no diarrhoea

21
Q 
Type 1 renal tubular acidosis
pathology?
causes?
features?
Mx
A

unable to make acidic urine in distal CT (pH >5.5)
idiopathic, SLE, Sjogren’s syn
metabolic acidosis, hypokalaemia, renal stones
Mx: correct K then give bicarbonate 1-3mmol/kg/day

22
Q

Type 2 renal tubular acidosis
pathology?
causes?
features?

A

Inability to reabsorb HCO3 in PCT
Fanconi syn, Wilsons, cystinosis, idiopathic
hypokalamia, osteomalacia

23
Q

Type 4 renal tubular acidosis
pathology?
causes?
features?

A

decreased aldosterone -> decreased NH3 excretion
hypoaldosteronism, diabetes
hyperkalaemia

24
Q

Where do renal cell carcinomas originate from?

A

PCT

25
Q

RCC associations/RFs

A

smoking
Von-Hippel-Lindau disease
tuberous sclerosis

26
Q

RCC features

A 
loin pain, haematuria, abdo mass
left varicocele (left testicular vein occlusion)
endo: may secrete PTH, erythropoetin, renin, ACTH
27
Q

Mx of RCC

5 yr survival?

A

nephrectomy even if mets as these may regress
- C/I if bilateral tumours or poor renal function
small molecule kinase inhibitors
interferon alpha and IL-2
no benefit in radio/chemotherapy
5yr survival - 60-70% without mets, 5% with mets

28
Q

features of minimal change glomerulonephritis

pathology

A

T-cell and cytokine BM damage leads to loss in electrostatic charge, increased permeability to albumin
Sx: nephrotic syn, normotensive
renal biopsy - fusion of podocytes

29
Q

Mx of minimal change glomerulonephritis

prognosis

A

oral prednisolone
1/3rd have single episode
1/3rd have infrequent recurrences
1/3rd have frequent relapses, which stop before adulthood

30
Q

features of IgA nephropathy

A

deposits of IgA immune complexes
positive immunoflorescence for IgA and C3
typically in young males, following an URTI
as seen in Henoch Schoelein Purpura

31
Q

most common organism infecting peritoneal dialysis

A

staph epidermis

32
Q

Mx of renal stones

A 
diclofenac/naproxen analgesia
alpha blockers (tamsulosin) to aid stone passage
stones <5mm will pass spontaneously
33
Q

imaging of choice for renal stones

A

non contrast CT (99% reliability)

xray KUB shows 60% of stones

34
Q

Membranous glomerulonephritis:
presentation
prognosis

A

proteinurea/nephrotic syn, CKD

1/3rd resolve, 1/3rd respond to cytotoxics, 1/3rd develop CKD

35
Q

Diffuse proliferative glomerulonephritis
presentation
disease association

A

classical post-strep nephritis in children
presents as nephritic syn (haematuria, proteinurea, HTN, uraemia) or AKI
most common renal disease in SLE

36
Q

Minimal change disease
presentation
causes
Mx

A

child with nephrotic syn (80%)
causes: Hodgkin’s, NSAIDs,
good response to steroids

37
Q

Focal segmental glomerulonephritis
presentation
causes

A

proteinurea / nephrotic syn / CKD

may be idiopathic or 2ndary to HIV, heroin

38
Q

Rapidly progressive glomerulonephritis
presentation
causes

A

rapid onset AKI
causes: Goodpastures, ANCA positive vasculitis
both can be managed by plasma exchange

39
Q

Mesangiocapillary glomerulonephritis

associations

A

type 1: cryoglobinaemia, Hep C

type 2: partial lipodystrophy.

40
Q

most common type of renal stone

A 
calcium oxalate (40%) - radio-opaque
note urate and xanthine stones are radiolucent (can't be seen on xray)
41
Q

causes of nephrogenic diabetes insipidus

A

genetic
hypercalcaemia, hypokalaemia
demeclocycline (reduces response to ADH), lithium
sickle cell disease, obstruction, pyelonephritis

42
Q

Indications for emergency renal replacement therapy

A

hyperkalaemia refractory to medical management
refractory volume overload
severe metabolic acidosis
uraemic pericarditis

43
Q

how do you treat hyperphosphataemia?

A

sevelamer - a phosphate binder

44
Q

Indications for spironolactone

A 
ascites (cirrohsis -> 2ndary hyperaldosteronism therefore high doses 100-200mg needed)
HF (NYHA stage 3-4)
nephrotic syn (proteinurea, hypoalbuminaemia, oedema)
Conns syn. (too much aldosterone)
45
Q

What is the usual precipitating factor for mesangioproliferative (IgA) nephropathy?

A

upper respiratory tract infection 2-3 days prior

46
Q

What are the microscopic findings in chronic glomerulonephritis?

A

glomeruli filled with hyaline (homogenous pink substance) with dilation of the remaining tubules.

47
Q

What age group are affected by renal artery stenosis?

how should it be managed?

A

hypertension in young adults (30s)

AVOID ACEis

MRCP 1 (15 decks)

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