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Renal Flashcards

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1
Q

Causes of pre-renal AKI

A

hypovolaemia - D&V
Renal artery stenosis

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2
Q

Causes of intrinsic AKI

A

Glomerulonephritis
Acute tubular necrosis
Rhabdomyolysis
Tumour lysis syndrome

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3
Q

Causes of post-renal AKI

A

Kidney stone
BPH
External ureter compression

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4
Q

Diagnosis of AKI

A

rise in creatinine >= 26 in 48hrs
rise in creatinine >=50% in 7 days
fall in urine OP <= 0.5mls/kg/hr
US KUB if ?cause

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5
Q

Common causes CKD

A

diabetic nephropathy
chronic glomerulonephritis
chronic pyelonephritis
HTN
APCKD

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6
Q

GFR equating to CKD

A

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

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7
Q

Use of ACR

A

detects proteinuria
first pass morning sample
>3 = clinically signifcant

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8
Q

management of proteinuria in CKD

A

ACE inhibs (increase Cr 30% and decrease GFR 25% acceptable)
ARBs
SGLT2s

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9
Q

Causes of anaemia in CKD

A

low erythropoietin
low iron
Anorexia/nausea due to uraemia

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10
Q

Management of anaemia in CKD

A

erythropoiesis stimulating agents
PO iron (IV if not improved in 3 months)

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11
Q

What causes bone disease in CKD

A

Low vit D and high phosphate cause low Ca
Above causes secondary hyperparathyroidism

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12
Q

Clinical manifestations of bone disease in CKD

A

Osteitis fibrosa cystica
osteomalacia
osteoporosis

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13
Q

Management of bone disease in CKD

A

reduce dietary phosphate
Phosphate binders (Sevelamer)
Vit D
parathyroidectomy

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14
Q

Complications of AV fistulas

A

Infection
Thrombosis
Stenosis
Steal syndrome

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15
Q

Time for AV fistula to develop

A

6-8 weeks

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16
Q

Symptoms of BPH

A

Voiding: weak flow, straining, hesitancy, terminal dribbling, incomplete emptying

Storage: urgency, frequency, nocturia

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16
Q

Scoring for BPH

A

International Prostate Symptom Score
<7 : mild
8-10: mod
>20: severe

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17
Q

Management of BPH

A

alpha 1 antagonists e.g. tamsulosin, alfuzosin

5 Alpha reductase inhibitors e.g finasteride

TURP

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17
Q

MOA alpha 1 antagonists

A

tamsulosin, alfuzosin
decrease smooth muscle tone in prostate and bladder

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18
Q

SE alpha 1 antagonists

A

dizziness, postural hypotension, dry mouth

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19
Q

MOA 5 alpha reductase inhibs

A

finasteride
block conversion of testosterone to DHT which induces BPH
reduces size of prostate, can take 6 months to see effects

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20
Q

SE 5 alpha reductase inhibs

A

erectile dysfunction, decreased libido, ejaculation issues, gynaecomastia

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21
Q

Pathophysiology of PKD

A

cysts form, reduce function + compress other nephrons
initial compensation but when disease progresses GFR drops

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22
Q

Types of PKD

A

Autosomal dominant
PKD 1: polycystin 1 Ch 16
PKD 2: polycystin 2 Ch 4

Autosomal recessive
PKHD1: fibrocystin Ch 6

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23
Presentation of PKD
HTN haematuria, polyuria abdo/flank pain UTIs renal stones
24
Extra renal manifestations of PKD
liver cysts Berry aneurysm mitral valve prolapse
25
Diagnosis of PKD
US abdo <30 yo 2 cysts 30-59 yo 2 cysts bilaterally >60 yo 4 cysts bilaterally
26
Management of PKD
Vasopressin receptor 2 antagonist (tolvaptan) ACE/ARB statin RRT
27
Pathophysiology amyloidosis
proteins which fold incorrectly then stick together forming Beta sheet which deposits in tissues causing damage
28
Types of amyloidosis
AL - plasma cell disorder, increased light chain production, leak into blood, fold incorrectly AA - chronic inflam causes increased serum amyloid A in blood, fold incorrectly
29
Examples of systemic amyloidosis
Nephrotic syndrome Restrictive Cardiomyopathy
30
Investigations for amyloid
Biopsy Congo red staining: pink Polarised light: apple green
31
What is nephrotic syndrome
- proteinuria >3.5g/day - hypoalbuminaemia <30 - hyperlipidaemia - oedema
32
How does nephrotic syndrome present
- oedema: legs, face, SOB - hyperlipidaemia: xanthelasma - recurrent infections: immunoglobulins lost in urine - frothy urine - hypercoagubility: antithrombin III lost in urine, increased risk of DVT/PE -hypocalcaemia: vit D and binding protein lost in urine
33
Causes of nephrotic syndrome
Minimal change focal segmental glomerulosclerosis membrane nephropathy diabetic nephropath amyloidosis
34
diagnosis of nephrotic syndrome
PCR >300mg/mmol hypoalbuminaema
35
Management of nephrotic syndrome
steroids - pred 10/20% steroid resistant (50% more likely to go to end stage renal failure) immunosuppressants - diuretics statins prophylactic LMWH
36
Bladder cancer type
transitional cell
37
What is Calciphylaxis and how does it present
deposition of calcium within arterioles causing microvascular occlusion and necrosis of the supplied tissue. It most commonly affects the skin and presents with painful necrotic skin lesions.
38
Treatment of Calciphylaxis
reducing calcium and phosphate levels, controlling hyperparathyroidism and avoiding contributing drugs such as warfarin and calcium containing compounds.
39
What causes chronic pyelonephritis
recurrent infections lead to scarring of renal parenchyma and impaired function
40
Predisopising factors of chronic pyelo
obstruction (Stones) vesicourethral reflux in kids
41
exam features of chronic pyelo
blunted calyx corticomedullary scarring with atrophy of tubules eosinophilic casts in tubules
42
What is diabetes insipidus
either decrease in secretion of ADH (cranial) or insensitivity to ADH (nephrogenic)
43
Causes of cranial DI
idiopathic head injury pituitary surgery craniopharyngiomas infiltrative (sarcoid)
44
causes of nephrogenic DI
genetic hypercalcaemia hypokalaemia lithium tubulo-interstitial disease: obstruction, sickle cell, pyelo
45
symtoms of DI
polyuria polydypsia
46
investigations of DI
increased plasma osm and decreased urine osmo (if urine >700 cannot be DI) water deprivation test
47
Management of DI
Cranial: desmopressin Nephrogenic: thiazides, low salt low protein diet
48
Causes of epididymo-orchitis
genital: chlamydia, gonorrhoea bladder: e.coli
49
Features of epididymo-orchitis
unilateral tesicular pain/swelling *in torsion, <20yo, severe acute pain
50
Ix for epididymo-orchitis
STI check MSU
51
Mx epididymo-orchitis
if STI: sexual health check ?organism ceftriaxone 500mg IM once + doxy 100mg BD 10-14/7 if enteric: PO quinolone (ofloxacin) 2/52
52
pathophysiology of minimal change disease
T cells release cytokines that flatten podocytes (effacement) so the negative charge barrier is reduced allowing albumin through Larger proteins cannot get through = selective proteinuria
53
Features of minimal change disease
- nephrotic syndrome - selective proteinuria - renal biopsy: podocyte fusion and effacement of foot processes, normal glomeruli
54
Management of minimal change disease
PO cortiocosteroids -> cyclophosphamides
55
prognosis of minimal change disease
1/3 single episode 1/3 infrequent relapse 1/3 frequent relapse
56
causes of minimal change disease
mostly idiopathic NSAIDS Hodgkins infective mono
57
causes of focal segmental glomerulosclerosis
idiopathic secondary to renal pathology - IgA nephropathy HIV heroin SSD
58
Pathophysiology of FSGS
damaged podocytes -> proteins through trapped proteins/lipids in glomerulous -> hyalinosis -> sclerosis
59
Ix FSGS
renal biopsy -> focal and segmental sclerosis and hyalinosis effacement of foot processes
60
Mx FSGS
steroids +/- immunosuppressants
61
causes of membranous glomerulonephritis
idiopathic hep B, malaria, syphilis malig: prostate, lung, lymphoma, leukaemia SLE, rheumatoid, thyroiditis
62
Membranous glomerulonephritis diagnosis
nephrotic symptoms renal biopsy: spike and dome appearance of basement membrane
63
Management of membranous glomerulonephritis
ACEI/ARB cortiocosteroids= + cyclophosphamide anticoag if high risk
64
Prognosis of membranous glomerulonephritis
1/3 spontaneous recovery 1/3 persistent proteinuria 1/3 ESRF Good prognostic factors: female, young, asymptomatic
65
What type of tumour is Wilms
nephroblastoma
66
management of wilms
nephrectomy chemo radio

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