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MRCP 2 > Renal > Flashcards

Renal Flashcards

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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
Bosniak system
used to classify malignant risk of renal cysts based on CT I: simple IV: malignant II, III: indeterminant
26
inherited cystic renal diseases
PKD VHL tuberous sclerosis Dandy Walker syndrome
27
PCKD
auto dom: PKD1 chromo 16 in 80% PKD2 chromo 4 in 15% auto rec: PKHD1 chromo 6 (ESRF in childhood) tx: ACEi, tolvaptan
28
VHL
auto dom chromo 3 premalignant renal cysts, clear cell renal ca phaeochromocytomas spinocerebellar haemangioblastomas retinal angiomas pancreatic cysts, islet cell tumours
29
tuberous sclersosis
renal cysts, angiomyolipomas epilepsy, LDs, ASD hamartomas, shagreen patches, ash leaf spots, adenoma sebaceum
30
APKD criteria
2 cysts < 30y 2 cysts bilaterally 30-59y 4 cysts bilaterally > 60y
31
BP targets
80 and over: 145/85 below 80: 135/85
32
drugs causing tubulointerstitial nephritis
rifampicin allopurinol methicillin, penicillin, cephalosporins sulfonamides furosemides, thiazides cimetidine amphoteracin aspirin, NSAIDs
33
causes of chronic tubulointerstitial nephritis with macroscopically normal kidneys
reflux nephropathy analgesic nephropathy obstructive and cystic disease
34
presentation of interstitial nephritis
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
35
diagnosing tubulointerstitial nephritis
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
36
how might someone be exposed to lead?
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
features of lead toxicity
renal- fanconi CVS- HTN, CAD, PAD neurodevelopmental
38
lead chelation therapy
dimercaprol succimer sodium calcium edetate
39
liddle syndrome
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
causes of membranous nephropathy
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
membranous nephropathy diagnosis
nephrotic syndrome biopsy: thick GBM, spike formation immunofluorescence: IgG and C3 deposits in GBM
42
treating membranous nephropathy
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
causes of minimal change disease
usually idiopathic leukaemia, hodgkins hep B, hep C NSAIDs allergic reactions immunisations
44
minimal change disease diagnosis
biopsy only if not responding or frequently relapsing light microscopy: no changes electron microscopy: podocyte effacement
45
managing minimal change disease
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
complications of minimal change disease
loss of antithrombin > thrombosis loss of IgG and immunosuppressive treatment > infection and spontaneous peritonitis relapse (75%) renal failure (rare) HTN
47
symptoms of polyarteritis nodosa
haematuria, proteinuria, AKI/CKD subcut nodules, livedo reticularis necrotic ulcers HTN ischaemic abdo pain mononeuritis multiplex
48
diagnosing polyarteritis nodosa
ANCA negative necrotising inflammation on biopsy of arteries/muscle/skin rosary beads microaneurysms on angiography
49
diagnosing post strep GN
nephritic picture low C3 recent strep infection (pharyngitis or impetigo) biopsy: diffuse proliferative GN, global increase in cellularity, infiltration of polymorphonuclear cells
50
treating post strep GN
loop diuretics for oedema and HTN ACEi or CCB second line for HTN usually resolves spontaneously
51
adverse effects of immunosuppressants
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
immunosuppression for renal transplant
tacrolimus + antimetabolite e.g. MMF + prednisolone
53
peritoneal dialysis
continuous amubulatory: 1.5-3L per day effective for 3-6y automated: overnight
54
haemodialysis access
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
absolute contraindications to renal donation
pre-existing renal disease disease of unknown aetiology (e.g. MS or sarcoid) recent malignancy overt IHD
56
renal transplant exclusion criteria
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
complications of peritoneal dialysis
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
CVS complications of dialysis
arrhythmia, congestive cardiomyopathy vascular calcification valve calcification, esp aortic
59
dialysis related amyloid
beta2 microglobulin increased and deposited as amyloid within carpal tunnel, joints, bones
60
acute vs chronic renal transplant dysfunction
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
post renal transplant non renal complications
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
indications for haemodialysis over peritoneal
abdo surgery or irremediable hernia recurrent/persistent peritonitis peritoneal membrane failure age, general frailty severe malnutrition hypercatabolic states chronic severe chest disease
63
indications for nephrectomy before transplant
pyonephrosis or any suppuration within urinary tract massive polycystic kidneys uncontrollable HTN renal/urothelial malignancy
64
transplant rejection
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
immunosuppression for transplant surgery
methylprednisolone anti CD25 mono ab e.g. basiliximab
66
types of RTA1
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
causes of RTA
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
RTA and urinary calculi
urinary calcium excretion is increased in severe acidosis calcium salts are more insoluble in alkaline urine develops in distal RTA (type 1)
69
managing RTA
potassium citrate to alkalinise urine PO K and HCO3 for type 1 and 2 fludrocortisone for type 4 if acidotic or hyperkalaemic
70
diagnosing rhabdo
CK 5x upper limit
71
non traumatic causes of rhabdo
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
DIC from rhabdo
thromboplastin released during muscle injury > DIC
73
rhabdo biochemistry
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
renal involvement of sarcoid
hypercalcaemia granulomatous intersitial nephritis
75
renal involvement of systemic sclerosis
scleroderma renal crisis: malignant HTN rapid renal impairment onion skin intrarenal vasculature tx> ACEi steroids increase risk of renal crisis
76
urinary tract TB
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
investigating urinary tract TB
urine culture, TB testing, CXR IV pyelogram- beaded appearance of ureters CT most useful MCU- irregular wall and decreased capacity plain KUB
78
metabolic factors predisposing to stones
hypercalciuria, hyperoxaluria hyperuricuria cystinuria hypocitraturia
79
most common sites of stone
VUJ renal pelvis is most common site of kidney stone
80
causes of stones
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
when is a stone likely to pass?
ureteric: < 4mm and in lower ureter renal: < 5mm
82
preventing recurrence of stones
potassium citrate if mostly calcium oxalate stone thiazide diuretics if mostly calcium oxalate stones
83
surgery for stones
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
diagnosing UTI according to bacterial growth
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
treating UTI in pregnant pt
nitro 7/7 (avoid if at term) amox 7/7 cefalexin 7/7
86
VHL
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
types of VHL
1: low risk of phaeochromocytoma 2: phaeochromocytoma 2A low risk renal ca 2B high risk renal ca 2C only phaeochromocytoma
88
stages of lupus nephritis
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

MRCP 2 (12 decks)

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