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MRCP 2 > Renal > Flashcards

Renal Flashcards

1
Q

pre-renal uraemia vs acute tubular necrosis

A

sodium and water reabsorption
clinical response to fluid resus:
PRU > diuresis
ATN > remain oliguric

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2
Q

rhabdo features

A

raised K, PO4, CK
low Ca

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3
Q

diagnosing AKI

A

rise of creatinine 26 in 48h
rise in creatinine 50% in 7 days
oliguria 0.5ml/kg/h in 6h

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4
Q

alport syndrome

A

x linked, auto rec, auto dom or auto digenic
type IV collagen basement membrane
COL4A3, COL4A4, COL4A5
CKD, sensorineural hearing loss, lenticonus
> ACEi or ARB if proteinuria/HTN

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5
Q

testing for iron def in CKD patients

A

percentage of hypochromic RBCs
if thalassaemia trait, use transferrin sat and serum ferritin

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6
Q

managing anaemia in CKD patients

A

(occurs only when eGFR < 60)

not on dialysis:
PO iron > IV iron if required

on dialysis:
IV iron (or PO if required)

treat iron def before or in parallel with EPO
aim for rate of Hb increase 10-20 per month
maintain 100-120 Hb
monitor Hb every 2-4 weeks during induction then 1-3 months

blood transfusion if failing to respond to EPO

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7
Q

analgesic nephropathy

A

daily use of preparations containing at least 2 analgesics
reduced kidney size
papillary calcifications

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8
Q

CKD stages

A
  1. normal eGFR. urinary or structural abnormalities
  2. eGFR 60-89 and urinary or structural abnormalities
    3a. eGFR 45-59
  3. eGFR 30-44
  4. eGFR 15-29
  5. ESRF
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9
Q

CKD bone mineral disorder

A

increased PO4 > reduced calcium
> increased PTH > bone turnover

decreased vit D > osteomalacia, reduced GI absorption of Ca

monitor Ca, PO4, PTH, ALP in patients eGFR < 30
monitor Ca, PO4, PTH, vit D in patients eGFR > 30

FGF23 normally maintains normal serum PO4 levels by reducing reabsorption and reducing vit D production

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10
Q

causes of nephrogenic diabetes insipidus

A

hypercalcaemia
hypokalaemia
lithium
renal disease
demeclocycline
x linked/dom abnormality in tubular ADH receptor

tx: bendroflumethiazide

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11
Q

diabetic nephropathy

A

chronic hyperglycaemia > glomerulosclerosis
most common cause of ESRF un UK

increased blood viscosity
> reduced flow in small capillaries
> small infarcts to glomerulus
> hypoxia and inflammation from capillary leak

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12
Q

stages of diabetic nephropathy

A
  1. GFR elevated by 20% and increased urinary albumin excretion rate
  2. GFR remains elevated due to hyperfiltration, kidneys are hypertrophied. BP and albumin excretion normal.
    GBM thickening, mesangial expansion
  3. microalbuminuria or urine ACR 3-30, BP starts rising
  4. established nephropathy, increasing macroproteinuria, declining GFR, most will be hypertensive, diffuse glomerular sclerosis, some have kimmelstein wilson nodules
  5. ESRF 7 years from stage 4
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13
Q

eosinophilic granulomatosis with polyangiitis renal involvement

A

necrotising crescenteric GN
eosinophilic interstitial nephritis
mesangial GN
focal segmental glomerulosclerosis

> haematuria, proteinuria, HTN, raised creat
50% pANCA, 90% eosinophilia

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14
Q

focal segmental glomerulosclerosis

A

podocyte injury > detach from BM
> BM exposed
> proliferation of epithelial, endothelial, mesangial cells
> cell proliferation and leak of protein into Bowmans space
> collagen deposition
> nephrotic syndrome (or asymptomatic)

tx: corticosteroids

inherited forms:
finnish congenital nephrotic syndrome
late onset auto dom FSGS
childhood onset steroid resistant FSGS

secondary causes:
HIV, CMV, parvo B19, hepC
reduced renal mass
lithium, IFNa, heroin, pamidronate, sirolimus
obesity
renal ischaemia and VTE

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15
Q

gitelmans

A

loss of NaCl cotransporter in DCT
> mimics thiazide toxicity
> hypomagnesaemia, hypokalaemia, hypocalciuria, alkalosis

tx: high salt diet, Mg and K supplements
can consider potassium sparing diuretic
indomethacin in infants/children

SLC12A3 gene auto rec

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16
Q

Bartters

A

NaKCl in ascending loop
> hypokalaemic alkalosis

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17
Q

commonest causes of GN

A

min change disease in under 15ys
IgA nephropathy (Berger’s) in white adults
FSGS in black adults

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18
Q

primary GN

A

nephrotic:
membranous
min change
FSGS
mesangiocap GN

nephritic:
IgA/Bergers
rapidly progressive

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19
Q

secondary GN

A

nephrotic:
diabetes
amyloid
hep B/B
SLE class 5, 6

nephritic:
post strep
HSP, wegeners
goodpastures
SLE class 1-4

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20
Q

treating GN

A

high dose prednisolone
IV pulsed cyclophosphamide if steroid resistant

ACEi, diuretics, statins
anticoagulants for nephrotic syndrome

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21
Q

goodpasture

A

AKA anti GBM
antibodies against alpha 3 chain of type IV collagen (in glomerular and alveolar BM)
> complement activated. C3, IgG deposits
> crescenteric GN

HLA-DR15, HLA-DRB1
not all pts have pulm involvement

tx: plasma exchange, prednisolone, cyclophosphamide

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22
Q

granulomatosis w/ polyangiitis

A

necrotising granulomatous vasculitis
small to medium vessels
> haematuria, proteinuria
> haemoptysis
> epistaxis, saddle nose, subglottic stenosis
cANCA

tx: steroids, cyclophosphamide, plasma exchange
maintenance: MTX or azathioprine, also steroids
for recurrence: steroids or rituximab or cyclophosphamide or plasma exchange

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23
Q

haemolytic anaemia syndrome

A

microangiopathic haemolytic anaemia
thrombocytopaenia
AKI

most common cause of AKI in children
90% are secondary to Ecoli O157:H7

causes:
E coli
strep pneumonia
shigella type 1
HIV, coxsackie
atypical- tacrolimus, ciclosporin, complement mutations, pregnancy, SLE

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24
Q

HSP triad

A

palpable rash
joint pain
renal and GI involvement

triggered by virus or solid tumour

IgA antibodies deposited in skin, joints, kidneys, GIT
> mild proliferative and crescenteric GN
> micro haematuria, proteinuria

most resolve without treatment

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25
Q

Bosniak system

A

used to classify malignant risk of renal cysts based on CT
I: simple
IV: malignant
II, III: indeterminant

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26
Q

inherited cystic renal diseases

A

PKD
VHL
tuberous sclerosis
Dandy Walker syndrome

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27
Q

PCKD

A

auto dom:
PKD1 chromo 16 in 80%
PKD2 chromo 4 in 15%

auto rec:
PKHD1 chromo 6 (ESRF in childhood)

tx: ACEi, tolvaptan

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28
Q

VHL

A

auto dom
chromo 3

premalignant renal cysts, clear cell renal ca
phaeochromocytomas
spinocerebellar haemangioblastomas
retinal angiomas
pancreatic cysts, islet cell tumours

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29
Q

tuberous sclersosis

A

renal cysts, angiomyolipomas
epilepsy, LDs, ASD
hamartomas, shagreen patches, ash leaf spots, adenoma sebaceum

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30
Q

APKD criteria

A

2 cysts < 30y
2 cysts bilaterally 30-59y
4 cysts bilaterally > 60y

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31
Q

BP targets

A

80 and over: 145/85
below 80: 135/85

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32
Q

drugs causing tubulointerstitial nephritis

A

rifampicin
allopurinol
methicillin, penicillin, cephalosporins
sulfonamides
furosemides, thiazides
cimetidine
amphoteracin
aspirin, NSAIDs

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33
Q

causes of chronic tubulointerstitial nephritis with macroscopically normal kidneys

A

reflux nephropathy
analgesic nephropathy
obstructive and cystic disease

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34
Q

presentation of interstitial nephritis

A

acute:
mild renal impairment
hypersensitivity (fever, arthralgia, rash, eosinophilia, raised IgE)

chronic:
HTN, anaemia, proteinuria
CKD or ESRF
RTA type 1
nephrogenic DI
salt wasting

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35
Q

diagnosing tubulointerstitial nephritis

A

biopsy

acute:
interstitial oedema
plasma cell infiltration w/ lymphocytes and monocytes
granulomatoses if sarcoid

chronic:
chronic inflammatory infiltrate
granulomatous in sarcoid and TB
extensive scarring and tubular loss

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36
Q

how might someone be exposed to lead?

A

deteriorating paint surfaces
battery manufacturing
radiator repairing
bullet firing ranges
contaminated water
toys
foetal exposure

lead is stored in bone so can provide long term storm after exposure has ended

37
Q

features of lead toxicity

A

renal- fanconi
CVS- HTN, CAD, PAD
neurodevelopmental

38
Q

lead chelation therapy

A

dimercaprol
succimer
sodium calcium edetate

39
Q

liddle syndrome

A

auto dom, SCNN1B, SCNN1G
dysfunctional gain of Na channels in collecting ducts
> severe HTN, hypokalaemic metab alkalosis, reduced renin and aldosterone

HTN is not responsive to typical antihypertensives
tx: Na restriction, K supplements, amiloride or triamterene (K sparing diuretics)

40
Q

causes of membranous nephropathy

A

HLADR3 risk factor
idiopathic
AI
hep B, C, syphilis
malignancy
gold, lithium, NSAIDs, penicillamine
post transplant, sarcoid

circulating antibodies to M type phospholipase A2 receptor PLA2R

41
Q

membranous nephropathy diagnosis

A

nephrotic syndrome
biopsy: thick GBM, spike formation
immunofluorescence: IgG and C3 deposits in GBM

42
Q

treating membranous nephropathy

A

can resolve spontaneously, persist or progress to renal failure
ACEi if HTN
statin if hyperlipid
furosemide/hydrochlorthiazide if oedema
steroids if medium/high risk to ESRF

43
Q

causes of minimal change disease

A

usually idiopathic
leukaemia, hodgkins
hep B, hep C
NSAIDs
allergic reactions
immunisations

44
Q

minimal change disease diagnosis

A

biopsy only if not responding or frequently relapsing
light microscopy: no changes
electron microscopy: podocyte effacement

45
Q

managing minimal change disease

A

85% of children respond well to steroids
about 4-12 weeks

add ciclosporin or tacrolimus or high dose IV steroids if not responding to PO steroids in 4 weeks or if frequently relapsing

relapse: proteinuria for 3 days
treat similarly to initial episode and wean steroids once no proteinuria for 3 days, then maintenance steroids for several weeks

46
Q

complications of minimal change disease

A

loss of antithrombin > thrombosis
loss of IgG and immunosuppressive treatment > infection and spontaneous peritonitis
relapse (75%)
renal failure (rare)
HTN

47
Q

symptoms of polyarteritis nodosa

A

haematuria, proteinuria, AKI/CKD
subcut nodules, livedo reticularis
necrotic ulcers
HTN
ischaemic abdo pain
mononeuritis multiplex

48
Q

diagnosing polyarteritis nodosa

A

ANCA negative
necrotising inflammation on biopsy of arteries/muscle/skin
rosary beads microaneurysms on angiography

49
Q

diagnosing post strep GN

A

nephritic picture
low C3
recent strep infection (pharyngitis or impetigo)
biopsy: diffuse proliferative GN, global increase in cellularity, infiltration of polymorphonuclear cells

50
Q

treating post strep GN

A

loop diuretics for oedema and HTN
ACEi or CCB second line for HTN
usually resolves spontaneously

51
Q

adverse effects of immunosuppressants

A

ciclosporin- hirsuitism, gum hyperplasia, liver dysfunction, HTN, chronic renal allograft nephropathy
azathioprine- bone marrow suppression, esp w/ allopurinol
MMF- diarrhoea, bone marrow suppression
sirolimus- hyperlipidaemia

52
Q

immunosuppression for renal transplant

A

tacrolimus + antimetabolite e.g. MMF + prednisolone

53
Q

peritoneal dialysis

A

continuous amubulatory:
1.5-3L per day
effective for 3-6y

automated:
overnight

54
Q

haemodialysis access

A

AV fistula takes 4-6 weeks to mature

temporary tunnelled vascular access catheter can be used for those who present late or with fistula complications

55
Q

absolute contraindications to renal donation

A

pre-existing renal disease
disease of unknown aetiology (e.g. MS or sarcoid)
recent malignancy
overt IHD

56
Q

renal transplant exclusion criteria

A

current or recent malignancy
severe comorbidity (COPD, uncontrolled IHD, extensive PVD, CVA, dementia)
active infection
AIDs with opportunistic infection
active substance misuse
uncontrolled psychiatric disease

57
Q

complications of peritoneal dialysis

A

bacterial peritonitis- coag neg staph, gram neg bacteria, staph aureus

ultrafiltration failure- APD and polymer based solutions may help

encapsulating peritoneal sclerosis- peritoneum thickens and encases bowel

hernias, fluid leak (pleural effusion), malnutrition

58
Q

CVS complications of dialysis

A

arrhythmia, congestive cardiomyopathy
vascular calcification
valve calcification, esp aortic

59
Q

dialysis related amyloid

A

beta2 microglobulin increased and deposited as amyloid within carpal tunnel, joints, bones

60
Q

acute vs chronic renal transplant dysfunction

A

acute:
first 2 weeks
fluid retention, rising BP, rapidly rising creat
> IV steroids

chronic:
after 1y
gradual rise in creat, proteinuria, resistant HTN
vascular changes, fibrosis, tubular atrophy
not responsive to increasing immunosuppression

61
Q

post renal transplant non renal complications

A

non hodgkins, skin cancer
all other malignancies
IHD
infections esp PJP, CMV
osteoporosis
gout
new onset diabetes
vasculitis recurrence

> cotrimox is given for 1st 6 months as PJP prophylaxis
previous TB or Asian patients are given isoniazid for 1y as TB prophylaxis

62
Q

indications for haemodialysis over peritoneal

A

abdo surgery or irremediable hernia
recurrent/persistent peritonitis
peritoneal membrane failure
age, general frailty
severe malnutrition
hypercatabolic states
chronic severe chest disease

63
Q

indications for nephrectomy before transplant

A

pyonephrosis or any suppuration within urinary tract
massive polycystic kidneys
uncontrollable HTN
renal/urothelial malignancy

64
Q

transplant rejection

A

hyperacute:
recipient abs against donor kidney
within minutes

acute:
acute deterioration in function assoc w/ pathological changes in graft
acute cell mediated- mononuclear infiltration
acute antibody mediated- C4d

chronic:
from 3 months
HTN, proteinuria, transplant vasculopathy

65
Q

immunosuppression for transplant surgery

A

methylprednisolone
anti CD25 mono ab e.g. basiliximab

66
Q

types of RTA1

A

1 (distal):
alpha cells in DCT fail to excrete H+ and absorb K+
hypokalaemic hyperchloraemic acidosis
> calculi
diabetes insipidus, salt wasting

2 (proximal):
PCT fails to reabsorb bicarb
less severe acidosis
hypokalaemic hypercholaemic acidosis
osteomalacia, rickets

3:
rare
impaired PCT bicarb resorption and DCT acid excretion
biochemical abnormalities dependent on whether PCT or DCT is predominant

4:
low or resistant to aldosterone
hyperkalaemic hyperchloraemic acidosis
CKD

67
Q

causes of RTA

A

1:
primary
SLE, sjogren, hepatitis
tubulointerstitial disease
nephrocalcinosis
lithium, amphoteracin, toluene

2:
idiopathic
Fanconi- wilsons, fructose intolerance, sjogrens
tubulointersitial disease
tetracyclines, lead, mercury, sulfonamides, acetazolamide

4:
low renin and aldo- diabetes, NSAIDs, ciclosporin
high renin low aldo- adrenal destruction, ACEi, ARB

68
Q

RTA and urinary calculi

A

urinary calcium excretion is increased in severe acidosis
calcium salts are more insoluble in alkaline urine
develops in distal RTA (type 1)

69
Q

managing RTA

A

potassium citrate to alkalinise urine
PO K and HCO3 for type 1 and 2
fludrocortisone for type 4 if acidotic or hyperkalaemic

70
Q

diagnosing rhabdo

A

CK 5x upper limit

71
Q

non traumatic causes of rhabdo

A

thyroid storm
phaeochromocytoma
DKA
seizures
influenza A, clostridium spp
polymyositis, dermatomyositis
cocaine, amphetamines, narcotics, barbiturates, sedatives, diuretics, statins, antipsychotics, antidepressants
cyanide, mercury, copper, CO, bee stings, snake bites

72
Q

DIC from rhabdo

A

thromboplastin released during muscle injury
> DIC

73
Q

rhabdo biochemistry

A

5x elevated CK
raised myoglobin
raised K, Mg, PO4, urea, creat
low Ca
if DIC:
low platelets, fibrinogen, Hb
raised D dimer, PT, APTT

74
Q

renal involvement of sarcoid

A

hypercalcaemia
granulomatous intersitial nephritis

75
Q

renal involvement of systemic sclerosis

A

scleroderma renal crisis:
malignant HTN
rapid renal impairment
onion skin intrarenal vasculature
tx> ACEi

steroids increase risk of renal crisis

76
Q

urinary tract TB

A

pulm infection or reactivation of miliary disease
> haematogenous spread
> seeding
long latency between primary infection and presentation
quiescent granulomas reactivate and shed bacteria in urinary tract
bladder and ureteric TB is usually secondary to renal

presentation:
repeated UTIs unresponsive to abx
nephritic syndrome if renal
bladder irritation symptoms if bladder
incontinence and incomplete urination if ureteric

77
Q

investigating urinary tract TB

A

urine culture, TB testing, CXR
IV pyelogram- beaded appearance of ureters
CT most useful
MCU- irregular wall and decreased capacity
plain KUB

78
Q

metabolic factors predisposing to stones

A

hypercalciuria, hyperoxaluria
hyperuricuria
cystinuria
hypocitraturia

79
Q

most common sites of stone

A

VUJ
renal pelvis is most common site of kidney stone

80
Q

causes of stones

A

hypercalciuria:
loop diuretics, hyperparathyroid

hyperoxaluria:
primary (rare genetic), small bowel malabsorption, increased tea or vit C intake

hyperuricuria:
excess meat (purine), ileostomy, chronic diarrhoea, myeloproliferative disease, gout

cystinuria:
auto rec condition

infection:
MAP staghorn from proteus, pseudomonas, klebsiella

81
Q

when is a stone likely to pass?

A

ureteric: < 4mm and in lower ureter
renal: < 5mm

82
Q

preventing recurrence of stones

A

potassium citrate if mostly calcium oxalate stone
thiazide diuretics if mostly calcium oxalate stones

83
Q

surgery for stones

A

ureteric:
lithotripsy if < 2cm
ureteroscopy

renal:
lithotripsy if < 2cm
percutaneous nephrolithotomy
flexible ureterorenoscopy and lithotripsy for small stones in renal collecting system unsuitable for lithotripsy due to anatomy
open nephrolithotomy
nephrectomy

84
Q

diagnosing UTI according to bacterial growth

A

at least 10^3 Ecoli or staph saprophyticus
at least 10^4 of a single organism
at least 10^5 mixed growth with one predominant organism

85
Q

treating UTI in pregnant pt

A

nitro 7/7 (avoid if at term)
amox 7/7
cefalexin 7/7

86
Q

VHL

A

auto dom (20% de novo mutation)
chromo 3
VHL mutation or deletion
> increased HIF, PDGF, VEGF
haemangioblastomas, phaeochromocytomas, renal cell ca, pancreatic cysts
mortality mostly due to renal cell ca and CNS tumours

87
Q

types of VHL

A

1: low risk of phaeochromocytoma
2: phaeochromocytoma
2A low risk renal ca
2B high risk renal ca
2C only phaeochromocytoma

88
Q

stages of lupus nephritis

A

1: immune deposits
2: mesangial proliferation
3: focal disease
4: diffuse disease
(3 and 4 require steroids + MMF +/- cyclophosphamide)
5: membranous
6: advanced sclerosis
(5 and 6 ACEi)

89
Q
A

MRCP 2 (12 decks)

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