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Child Health > Nephrology & genito-urinary > Flashcards

Nephrology & genito-urinary Flashcards

1
Q

Acute nephritis causes

A

Post-infectious: incl. streptococcus
Vasculitis: Henoch–Schönlein purpura, SLE (young females with autoantibodies), Wegener granulomatosis (resp tract involement), microscopic polyarteritis, polyarteritis nodosa –> ANCA (anti-neutrophil cytoplasm antibodies) =diagnostic
IgA nephropathy
Mesangiocapillary glomerulonephritis
Familial: Alport syndrome (X-linked recessive)
Anti-glomerular basement membrane disease: Goodpasture syndrome

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2
Q

Acute nephritis clinical features

A

Decreased urine output and volume overload: oliguria
Hypertension: which may cause seizures
Oedema: characteristically peri-orbital oedema
Haematuria & proteinuria

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3
Q

Henoch-Schönlein purpura clinical features

A

3-10y, most boys, winter months, following URTI
Fever
Characteristic palpable rash: buttocks, extensor surfaces of legs & arms and ankles (urticarial –> maculopapular & purpuric)
Arthralgia: knees and ankles
Periarticular oedema: knees and ankles
Abdominal pain: haematemesis, melaena, intussuception
Glomerulonephritis: microscopic/macroscopic haematuria (80%) and nephrotic syndrome (rare)

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4
Q

Possible long-term complications of HSP

A

Ileus
Protein-losing enteropathy
Orchitis
CNS involvement

Severe proteinuria –> nephrotic syndrome may result
Risk factors for progressive renal disease: heavy proteinuria, oedema, hypertension, deteriorating renal function (renal biopsy determines treatment)

Hypertension and declining renal function may develop after an interval of several years

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5
Q

HSP management

A

Joint pain: resolves spontaneously
Abdo pain: corticosteroids. Be wary of intussuseption
Renal involvement: attention to both water and electrolyte balance and the use of diuretics when necessary
Long term follow up for severe renal involvement

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6
Q

Glomerulonephritis investigations

A 
Electrolytes and creatinine: to assess renal function
FBC: infection, anaemia
Urinalysis: infection, protein, blood
Urine culture: infection
Complement levels: strep, SLE
ASO titre: group A strep
Anti-DNAase B
Serum IgA measurement

Hx: consistent with acute post-streptococcal glomerulonephritis, low C3 and +ve ASO
and Anti-DNAase B is enough to provide a provisional diagnosis
If this seems unlikely: renal biopsy
Renal ultrasonography: exclude other causes of hypertension and haematuria

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7
Q

What condition shares the same histopathological features of HSP nephritis?

A

IgA nephropathy
May present with episodes of macroscopic haematuria commonly in association with upper respiratory tract infections
Management for both conditions is the same

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8
Q

Nephrotic syndrome definition

A

Proteinuira >200mg protein/mmol creatinine
Serum albumin >25
Oedema
Hypercholesterolaemia

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9
Q

Nephrotic syndrome clinical signs

A

Periorbital oedema: particularly on waking (earliest sign)
Scrotal or vulval, leg & ankle oedema
Ascites
Breathlessness: pleural effusions + abdominal distension
Cloudy/frothy urine

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10
Q

Features suggesting steroid sensitive nephrotic syndrome

A 
1-10yo
No macroscopic haematuria
Normal blood pressure
Normal complement levels
Normal renal function
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11
Q

Complications of nephrotic syndrome

A

Hypovolaemia: indicators = faintness, abdo pain, urinary Na <20mmol/L + high PCV. Treatmeant = i.v. albumin

Thrombosis: hypercoagulable state due to urinary losses of antithrombin, exacerbated by steroid therapy, increased synthesis of clotting factors and increased blood viscosity from the raised haematocrit

Infection: relapse = risk of infection with capsulated bacteria (pneumococcus), spontaneous peritonitis may occur, pneumococcal and seasonal influenza
vaccination is recommended. Chickenpox/shingles: aciclovir

Hypercholesterolaemia: correlates inversely with the serum albumin

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12
Q

Nephrotic syndrome management

A 
Oral corticosteroids (60 mg/m2 per day of prednisolone) (unless atypical features)
After 4 weeks, the dose is reduced to 40 mg/m2 on alternate days for 4 weeks
The median time for the urine to become free of protein is 11 days
Frequent relapses: other drugs may be used to avoid steroids
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13
Q

Steroid resistant nephrotic syndrome causes

A

Focal segmental glomerulosclerosis
Mesangiocapillary glomerulonephritis
Membranous nephropathy

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14
Q

Steroid resistant nephrotic syndrome management

A

Management of oedema: diuretics, salt restriction, ACEIs, NSAIDs (may reduce proteinuria)

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15
Q

Nephrotic syndrome atypical features

A

No response to 4-8w corticosteroid therapy = renal biopsy
Renal histology in steroid-sensitive nephrotic syndrome is usually normal on light microscop, but fusion of
podocytes is seen on electron microscopy (minimal change disease)

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16
Q

Why is it important to diagnose UTIs in children

A

1/2 of patients have a structural abnormality of their urinary tract
Pyelonephritis may damage the growing kidney by forming a scar –> predisposing to hypertension& chronic renal failure if bilateral

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17
Q

UTI common organisms

A

E. Coli
Klebsiella
Proteus: boys (presence under the prepuce). Predisposes to the formation of phosphate stones by splitting urea to ammonia –> alkalinising the urine
Pseudomonas: may indicate the presence of some structural abnormality in the urinary tract affecting drainage
Strep. Faecalis

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18
Q

Haematuria differentials

A

UTI: bacterial, viral (adenovirus), schistosomiasis, TB
Glomerular: post-infectious glomerulonephriti, HSP, IgA
nephropathy, SLE, thin basement membrane, Alport syndrome
Urinary tract stones: due to hypercalciuria
Trauma
Renal tract pathology: tumour, polycystic kidney disease
Vascular: arteries, renal vein thrombosis
Haematological: coagulopathy, sickle cell
Drugs: cyclophosphamide
Exercise-induced

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19
Q

UTI presentation in an infant

A 
Fever
Vomiting
Lethargy and irritability
Poor feeding/failure to thrive
Jaundice
Septicaemia
Offensive urine
Febrile convulsion (>6 months)
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20
Q

UTI presentation in a child

A 
Dysuria and frequency
Abdominal pain or loin tenderness
Fever with or without rigors
Lethargy and anorexia
Vomiting and diarrhoea
Haematuria
Offensive/cloudy urine
Febrile convulsion
Recurrence of enuresis
21
Q

Urine sample collection methods

A

‘Clean catch’ with nappy removed
Urethral catheter
Suprapubic aspiration: invasive, not commonly used
Older children: mid-stream sample

22
Q

Dipstick nitrites and leucocytes result interpretation

A

Leucocyte +ve nitrite +ve: UTI
Leucocyte -ve nitrite +ve: start abx, diagnosis depends on urine culture
Leucocyte +ve nitrite -ve: start abx if clinical evidence of a UTI
Leucocyte -ve nitrite -ve: UTI unlikely

23
Q

Atypical UTI features

A 
Seriously ill
Poor urine flow
Abdominal or bladder mass
Raised creatinine
Septicaemia
Failure to respond to suitable antibiotics within 48 hours
Infected with non-E.coli organisms
24
Q

Recurrent UTI definitions

A

2 or more UTIs with acute pyelonephritis/upper UTI

1 episode of UTI with acute pyelonephritis/upper UTI + 1 or more episodes of UTI with cystitis/lower urinary tract infection

3 or more episodes of UTI with cystitis/lower urinary tract infection

25
Q

Atypical/recurrent UTI investigations

A

USS during acute infection
DMSA 4-6 months following acute infection
<6m: MCUG

26
Q

Vesicoureteric reflux incidence

A

10x more common in white children than black
Red hair = increased risk
5-6x more common in females
30-70% of infants with febrile UTIs

27
Q

Vesicoureteric reflux investigations

A

Voiding cystourethrogram (VCUG): main diagnostic + grading test. Catheterisation to administer radiocontrast
Renal bladder USS
DMSA: radionucleotide

28
Q

Pyelonephritis treatment >3m

A

Oral abx for 7-10d: cephalosporin, co-amoxiclav

If cannot use oral abx, IV abx: cefotaxime or ceftriaxone for 2-4 days followed by oral antibiotics for a total duration of 10 days

29
Q

Cystitis treatment >3m

A

3d p.o. abx: trimethoprim, nitrofurantoin, cephalosporin, amoxicillin

Advised to bring the child for reassessment if still unwell after 24-48 hours –> if an alternative diagnosis is not made, a urine MCS should be sent

30
Q

Vulvovaginitis aetiology

A 
Infection: bacterial or fungal
Specific irritants: e.g. bubble bath
Poor hygiene
Sexual abuse
Threadworm infestation
31
Q

Pre-renal causes of AKI

A

Hypovolaemia: gastroenteritis, burns, sepsis, haemorrhage, nephrotic syndrome
Circulatory failure

32
Q

Renal causes of AKI

A

Vascular: haemolytic uraemic syndrome, vasculitis, embolus, renal vein thrombosis
Tubular: acute tubular necrosis, ischaemic, toxic, obstructive
Glomerular: glomerulonephritis
Interstitial: interstitial nephritis, pyelonephritis

33
Q

Post-renal causes of AKI

A

Congenital: e.g. posterior urethral valves
Acquired: e.g. blocked urinary catheter, urethral stones

34
Q

Stages of CKD

A

1: normal GFR>90ml/min per 1.73m2 + persistant albuminuria
2: GFR 60-89ml/min per 1.73m2 + persistant albuminuria
3: GFR 30-59ml/min per 1.73m2
4: GFR 15-30ml/min per 1.73m2
5: GFR<15ml/min per 1.73m2 or end stage renal disease

35
Q

CKD clinical features

A 
Symptoms rarely develop before renal function falls to <1/3 of normal
Anorexia or lethargy
Polydipsia and polyuria
Failure to thrive/grow
Bone deformities
Hypertension
Acute-on-chronic renal failure
Proteinuria
Normochromic, normocytic anaemia
36
Q

Renal osteodystrophy pathophysiology and management

A

Decreased activation of vitD/calcitriol production –> phosphate retention + hypocalcaemia –> secondary
hyperparathyroidism –> osteitis fibrosis + osteomalacia

Management: phosphate restriction…
Decreasing dietary intake of milk products
Calcium carbonate as a phosphate binder
Activated vitamin D supplements

37
Q

CKD management

A

Diet: adequate protein intake to maintain growth + albumin production, but prevent accumulation of toxic byproducts
Renal osteodystrophy: phosphate restriction, calcium carbonate, calcitriol supplements
Salt & water balance + acidosis: salt supplements, bicarbonate supplements to prevent acidosis
Anaemia: recombinant human EPO
Hormonal abnormalities: recombinant human growth hormone

38
Q

Dialysis & kidney transplantation in children

A

10kg weight must be reached before transplantation to avoid renal vein thrombosis
Kidneys from living doners (HLA type matched) have a higher success rate
Immunosuppression: prednisolone, tacrolimus, azathioprine, mycophenolate mofetil
Ideally transplant occurs before dialysis is required

39
Q

Haemolytic uraemic syndrome triad

A

Acute renal failure
Microangiopathic haemolytic anaemia
Thrombocytopenia

40
Q

HUS aetiology and pathophysiology

A

Secondary to gastrointestinal infection with verocytotoxin-producing E. coli
Acquired through contact with farm animals, eating uncooked beef, Shigella

Prodrome: bloody diarrhoea –> verocytotoxin enters the gastrointestinal mucosa & preferentially localises to the endothelial cells of the kidney –> intravascular thrombogenesis
Coagulation cascade is activated –> platelets are consumed
Microangiopathic haemolytic anaemia: damage to red blood cells as they circulate through occluded microcirculation
Brain, pancreas and heart may also be involved.

41
Q

Difference between diarrhoea associated and non-diarrhoea associated HUS

A

Diarrhoea-associated HUS: good prognosis with early supportive therapy + dialysis
Follow-up: check for persistent proteinuria, hypertension, declining renal function

Atypical HUS (no diarrhoeal prodrome): may be familial and frequently relapses
High risk of hypertension, chronic renal failure, high mortality
Intracerebral involvement/atypical HUS: may be treated with plasma exchange or plasma infusions
42
Q

Causes of hypertension in children

A

Renal: renal parenchymal disease, renovascular (eg. renal artery stenosis), polycystic kidney disease (ARPKD and ADPKD), renal tumours
Coarctation of the aorta
Catecholamine excess: phaechromocytoma, neuroblastoma
Endocrine: congenital adrenal hyperplasia, cushing syndrome, corticosteroid therapy, hyperthyroidism
Essential hypertension: diagnosis of exclusion

43
Q

Hypertension presentation

A 
FTT
Cardiac failure
Vomiting
Headahces
Facial palsy
Hypertensive: over 95th percentile for height, age, sex
Retinopathy
Convulsions
Proteinuria
Paroxysmal palpitations and sweating: phaechromocytoma
44
Q

Renal anomalies detectable on antenatal USS screening

A

Absence of both kidneys (renal agenesis): severe oligohydramnios –> Potter syndrome
Multicystic dysplastic kidney: a non-functioning structure with large fluid filled cysts and no renal tissue or connection to the bladder
Autosomal dominant or recessive polycystic kidney disease: some renal function is maintained but both kidneys are always affected
Pelvic/horseshoe shaped kidneys: predisposed to infection or obstructs drainage
Duplex system: varies from a bifid pelvis to complete division and two ureters –> reflux and obstruction
Posterior urethral valves: obstruction and reflux
Hydronephrosis

45
Q

Antenatal urinary tract abnormalities investigations

A

USS: provides anatomical assessment but not function
DMSA scan: detects functional defects
MCUG/VCUG: visualise bladder and urethral anatomy,
detect reflux + obstruction
MAG3 isotope scan: isotopes excreted from the blood into the urine can be measured
Plain abdominal X-ray: spinal abnormalities, renal stones

46
Q

Antenatal urinary tract abnormalities management

A

Postnatally
Prophylactic abx
USS delayed for several weeks, unless bilateral hydronephrosis in a male infant (to exclude posterior urethral valves)

47
Q

Hypospadias presentation

A

Ventral urethral meatus: normally on the glans penis but can be on the corona, shaft or perineum.
Hood dorsal foreskin: that has failed to fuse ventrally and a chordae-ventral curvature (of the penis
head) (severe hypospadias)

48
Q

Neuropathic bladder symptoms

A

Urinary incontinence: increased frequency + urgency, dribbling urine, loss of sensation of bladder fullness
Urinary tract infection: urine retention
Kidney injury: high pressure caused by urine back log
Kidney stones: difficult to detect if the child cannot feel pain due to spinal injury
Pain, haematuria and fever/chills
Erectile dysfunction may present in later life

Child Health (15 decks)

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