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Yr4: Child Health > Renal & Urology > Flashcards

Renal & Urology Flashcards

1
Q

Children may present similarly to adults when they have a UTI however babies will present with non-specific symptoms; state some of these non-specific symptoms

A
  • Fever
  • Lethargy
  • Irritability
  • Vomiting
  • Poor feeding
  • Urinary frequency
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2
Q

A diagnosis of acute pyelonephritis is made if there is either…(2)?

What needs to be found on urine M,C&S to diagnose UTI?

A
  • Temp >38 degrees
  • Loin pain or tenderness

To diagnose UTI on urine MC&S need to have 105 CFU/mm3 of the causative organism

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3
Q

Which is a better indicator of a UTI: nitrites or leukocytes?

A

Nitrites

  • *If both nitrites & leucocytes present treat as UTI*
  • *If only nitrites present worth treating as a UTI*
  • *If only leukocytes present do not treat as UTI unless clinical evidence of one*
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4
Q

Discuss the management of UTIs in children

A
  • Children <3months: urgent referral to paediatrician for IV abx (e.g. ceftriaxone) & have full septic screen
  • Children >3months with upper UTI/acute pyelonephritis: consider referral to paeds for IV abx if systemically uwell or start PO antibiotic treatment (e.g. co-amoxiclav) for 7-10days if otherwise well
  • Children >3 months with lower UTI: 3 days of abx according to local guidelines (e.g. trimethoprim, nitrofurantoin)
  • *Typical abxs used: trimethoprim, nitrofurantoin, cefalexin, amoxicillin*
  • *See image for Leicester’s choice of abx in lower UTIs (due to cost as nitrofurantoin liquid is expensive)*
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5
Q

UTIs in infants or recurrent UTIs in children require investigation; discuss which children with UTIs should be investigated (including what investigations are done and when)

A

Abdo Ultrasounds

  • All infants <6months should have abdo US within 6 weeks of their 1st UTI or during illness if there are recurrent UTIs or atypical bacteria
  • Children with recurrent UTIs should have abdo US within 6 weeks
  • Children with atypical UTIs should have abdo US during illness

DMSA (dimercaptosuccinic acid) scan

  • If had atypical or recurrent UTIs should have DMSA scan 4-6 months after illness

Micturating cystourethrogram (MCUG)

  • Used if:
    • Infant <6months had atypical or recurrent UTIs
    • FH of reflux
    • Dilation of ureter on US
    • Poor urinary flow

*for image talking about in first 3yrs of life

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6
Q

UTIs in infants or recurrent UTIs in children require investigation; discuss which children with UTIs should be investigated (including what investigations are done and when)

A

Abdo Ultrasounds

  • All infants <6months should have abdo US within 6 weeks of their 1st UTI that responds to treatment
  • Children >6 months with recurrent UTIs should have abdo US within 6 weeks
  • All infants & children with atypical UTIs should have abdo US during illness; atypical UTIs indicated by:
    • Poor urine flow
    • Abdo or bladder mass
    • Raised creatinine
    • Sepsis
    • Failure to respond to abx within 48hrs
    • Infection with non-E.coli organism

DMSA (dimercaptosuccinic acid) scan

  • If child <3yrs with atypical or recurrent UTIs should have DMSA scan 4-6 months after illness
  • If child >3yrs with recurrent UTI should have DMSA scan within 4-6 months after illness
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7
Q

Explain how DMSA scan works

A
  • Inject radioactive DMSA into veins
  • Use gamma camera to assess how well DMSA is taken up by kidneys
  • Areas where it is not taken up indicates scarring that may have been caused by previous infection
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8
Q

What is a micturating cystourethrogram (MCUG) used to diagnose and what does it involve?

A
  • Vesicoureteric reflux
  • Catheterise child, inject contrast into bladder, take series of x-rays to see if contrast refluxing into ureters. Give prophylactic abx for 3/7 around time of MCUG
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9
Q

For vesicoureteric reflux, discuss:

  • What it is
  • What it predisposes children to
  • How diagnosed
  • How managed
A
  • Tendency of urine to flow from bladder back into ureters
  • Predisposed to upper urinary tract infections & subsequent renal scarring
  • MCUG
  • Management:
    • Avoid constipation
    • Avoid excessively full bladder
    • Prophylactic abx
    • Surgical input from paediatric urology
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10
Q

What is the most common cause of haemolytic uraemic syndrome?

A

E.coli 0157 which produces shiga toxin (shigella also produces this toxin)

*NOTE: use of abx & loperamide to treat gastroenteritis caused by the toxins increases risk of HUS

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11
Q

State the classic triad of HUS

A
  • Haemolytic anaemmia
  • AKI
  • Thrombocytopenia
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12
Q

Explain pathophysiology of HUS

A
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13
Q

Describe presentation of HUS

A
  • History of gastroenteritis (~5 days ago)
  • Reduced urine output
  • Haematuria or dark brown urine
  • Abdo pain
  • Lethargy
  • Confusion
  • Oedema
  • Hypertension
  • Bruising

*Think of triad to help you remember symptoms

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14
Q

Discuss the management of HUS

A

Medical emergency (mortality of 10%) so needs specialist management. Management is mostly supportive:

  • Urgent referral paediatric renal team
  • Fluids & careful monitoring of fluid balance
  • Antihypertensive if required
  • Blood transfusion if required
  • Dialysis if required
  • Plasma exchange or eculizumab in severe HUS

70-80% make full recovery

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15
Q

State two most common causes of nephritis in children

A
  • Post-streptococcal glomerulonephritis (occurs 7-14 days after infection)
  • IgA nephropathy (Berger’s disease)
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16
Q

For post-streptococcal glomerulonephritis, discuss:

  • Cause
  • Pathophysiology
  • Investigation findings
  • Management
A
  • Beta-haemolytic streptococcus infection (e.g. tonsillitis caused by S.pyogenes)
  • Immune complexes (made of streptococcal antigens, antibodies, complement proteins) get stuck in glomeruli and cause inflammation leading to AKI
  • Investigation findings: raised ASO titre, low C3
  • Management is supportive and 80% make full recoery:
    • Fluids
    • Antihypertensive
    • Diuretics
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17
Q

For IgA nephropathy (Berger’s disease), discuss:

  • Cause
  • How it usually presents
  • Renal biopsy findings
  • Management
  • Prognosis
A
  • IgA deposits in nephrons causing inflammation
  • Presents as macroscopic haematuria in teens & young adults 1-2 days after URTI
  • Associated conditions: HSP, coeliac disease
  • IgA deposits & glomerular mesangial proliferation
  • Management is supportive:
    • Fluids
    • Antihypertensive if required
    • May require immunosuppression with corticosteroids
  • Prognosis:
    • 25% develop ESRD
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18
Q

Compare IgA nephropathy & post-streptococcal glomerulonephritis

A
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19
Q

What aged children is nephrotic syndrome most common in and how does it present?

A
  • 2-5yrs
  • Presents with frothy urine, oedema & pallor
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20
Q

What is most common cause of nephrotic syndrome in children?

A

Minimal change disease (>90%)

However can be secondary to:

  • Intrinsic kidney disease: focal segmental glomerulosclerosis, membranoproliferative glomerulonephritis
  • Underlying systemic illness: HSP, diabetes, infection (HIV, malaria, hepatitis)
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21
Q

For minimal change disease, discuss:

  • Cause
  • What you would find on renal biopsy
  • What you would find on urinalysis
  • Management
A
  • Cause not clear
  • Renal biopsy is normal
  • Urinalysis shows small molecular weight proteins & hyaline casts
  • Management: corticosteroids
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22
Q

What is the triad of nephrotic syndrome?

What other features may occur?

A

Triad:

  • Hypalbuminaemia
  • Massive proteinuria (>3+ on dipstick or >3.5g/24hr)
  • Oedema

Other features:

  • Hypercholesterolaemia
  • Hypertension
  • Hypercoagulabilty
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23
Q

Discuss the management of nephrotic syndrome

A
  • High dose steroids (e.g. prednisolone. Given for 4/52 then gradually weaned over next 8/52)
  • Low salt diet
  • Diuretics for oedema
  • Albumin infusions if severe hypoalbuminaemia
  • Abx prophylaxis if severe
  • If steroid resistant, ACE inhibitors & immunosuppressants may be used
24
Q

State some potential complications of nephrotic syndrome

A
  • Hypovolaemia: fluid leaks into interstitial space depleting intravascular volume
  • Thrombosis: proteins that normally prevent clotting are lost in kidneys and liver responds to low albumin by producing pro-thrombotic proteins
  • Infections: kidneys leak immunoglobulins (risk increased by use of immunosuppressant medications)
  • Acute or chronic renal failure
  • Relapse
25
Q

There are two types of polycystic kidney disease; which one presents in neonates & is usually detected on antenatal scans?

A

Autosomal recessive polycystic kidney disease (ARPKD)

ADPKD presents later in life- usually adults.

26
Q

What mutation is found in autosomal recessive polycystic kidney disease?

A
  • Mutation in polycystic kidney & hepatic disease 1 gene (PKHD1 gene) on chromosome 6
  • Gene codes for fibrocystin/polyductin protein complex (FPC) which is responsible for creation of tubules and maintenance of healthy epithelial tissue in kidneys, liver & pancreas
27
Q

The mutation in ARPKD causes various problems in the neonate; state these

A
  • Cystic enlargement of renal collecting ducts
  • Oligohydramnios, pulmonary hypoplasia and Potter syndrome
  • Congenital liver fibrosis

*Lack of amniotic fluid leads to underdeveloped lungs resulting in respiratory failure shortly after birth. Large cystic kidneys also make it difficult for neonate to breath adequately. Lack of amniotic fluid also causes Potter syndrome (which has dysmorphic features e.g. underdeveloped ear cartilage, low set ears, flat nasal bridge, abnormalities of skeleton)

28
Q

How is ARPKD usually detected?

A

During antenatal scans: oligohydramnios & polycystic kidneys

29
Q

ARPKD can cause problems both in the neonatal period and life-long; state some of the ongoing problems these pts experience

A
  • Liver failure (due to fibrosis)
  • Portal hypertension (leading to oesophageal varices)
  • Progressive renal failure (most have ESRD before adulthood)
  • Hypertension (due to renal failure)
  • Chronic lung disease
30
Q

Discuss the prognosis of ARPKD

A
  • Poor
  • Around ⅓ die in neonatal period
  • Around ⅓ survive to adulthood
31
Q

For multicystic dysplastic kidney, discuss:

  • What it is
  • How it is detected
  • Compatible with life
  • Treatment
A
  • One of baby’s kidneys has many cysts (other is normal) *Different condition to ARPKD
  • Antenatal ultrasound scans
  • Single healthy kidney is sufficient; cystic kidney often atrophies and disappears by 5yrs of age. However, single kidney increases risk of UTIs, hypertension & CKD later in life
  • No treatment usually needed. May have follow up renal US to monitor abnormal kidney and prophylactic abx to protect healthy kidney

**NOTE: can rarely be bilateral in which case it causes death in infancy

32
Q

What is Wilms tumour?

A

Specific type of tumour affecting kidneys in children (usually <5ys)

32
Q

What is Wilms tumour?

A

Specific type of tumour affecting kidneys in children (usually <5ys)

33
Q

Discuss the presentation of Wilms tumours

A
  • Mass in abdomen
  • Abdo pain
  • Haematuria
  • Lethargy
  • Fever
  • Hypertension
  • Weight loss
34
Q

How is Wilms tumour diagnosed?

A
  • Initial investigation= ultrasound of abdomen
  • Biopsy for definitive diagnosis
  • CT or MRI to stage
35
Q

Discuss the management of Wilms tumour

A
  • Surgical excision of tumour & affected kidney
  • Adjuvant therapy:
    • Chemotherapy
    • Radiotherapy
36
Q

Discuss the prognosis of Wilms tumour

A
  • Early stage has good chance of cure (90%)
  • Metastatic disease= poorer prognosis (metastasis found in 20%- most commonly lung)
37
Q

Wilms tumour has a few associations; about ⅓ are associated with…?

A

Loss of function mutation in WT1 gene on chromosome 11

38
Q

What is the average children develop:

  • Day time control urination
  • Night time control urination
A
  • Day time control urination: 2yrs
  • Night time control urination: 3-4yrs
39
Q

State some causes of primary nocturnal enuresis- highlighting most common

A
  • Variation of normal development
  • Overactive bladder
  • Fluid intake prior to bedtime (fizzy drinks, juice, caffeine)
  • Psychological distress (high stress/pressure)
  • Failure to wake due to deep sleep or underdeveloped bladder signals
  • Secondary causes (e.g. chronic constipation, UTIs, learning disability, cerebral palsy)
40
Q

Discuss the management of primary nocturnal enuresis

A

Initial management is to establish underlying cause (may be helpful to keep diary of toileting, fluid intake & bed wetting. Good history- explore psychological stressors. Physical examination e.g. constipation.)

Once know the cause management may involve:

  • Reassurance that is likely to resolve without treatment
  • Lifestyle changes (reduce fluid intake in evenings, go for a wee before bed)
  • Encouragement & positive reinforcement (avoid shame & punishment)
  • Waterproof mattresses & duvet covers
  • Treat any underlying causes/exacerbating factors (e.g. constipation)
  • Enuresis alarms (first line for children under 7rys. If older can consider alarm or pharmacological treatment)
  • Pharmacological treatment e.g. desmopressin (particularly if rapid treatment required e.g. school trip)
41
Q

What is secondary nocturnal enuresis?

A

Child begins wetting bed at night when they have been dry at night for at least 6 months. More indicative of underlying illness than primary enuresis

42
Q

State some potential causes of secondary nocturnal enuresis

A
  • UTI
  • Constipation
  • T1DM
  • New psychological problem
  • Maltreatment *always think about abuse & safeguarding
43
Q

Discuss the management of secondary nocturnal enuresis

A
  • Treat underlying cause (most commonly UTI, constipation)
  • Referral to secondary care if underlying cause cannot be managed by GP
44
Q

What is diurnal enuresis?

A

Daytime incontinence (dry at night but still incontinent in day); more common in girls.

45
Q

State some potential causes of diurnal enuresis

A
  • Urge incontinence
  • Stress incontinence
  • Recurrent UTIs
  • Psychosocial problems
  • Constipation
46
Q

Explain how enuresis alarms work

A
  • Devices that make noise when sensor starts to get wet and idea is it wakes child up to stop they urinating and go to toilet
  • Needs to be used consistently for prolonged period (e.g. 3/12)
47
Q

Pharmacological treatments for nocturnal enuresis is started by specialists; state 3 options

A
  • Desmopressin: ADH analogue; reduces volume of urine produced. Take at bedtime.
  • Oxybutinin: anticholinergic that reduces contractility of bladder (helpful in overactive bladder)
  • Imipramine: TCA (unclear how works but may relax bladder and lighten sleep)
48
Q

What is a posterior urethral valve?

A

When there is tissue at proximal end of urethra that causes obstruction; this creates backpressure into bladder, ureters & kidneys leading to hydronephrosis. Impaired emptying of bladder increases risk of UTIs.

49
Q

Describe presentation of posterior urethral valve

A

Varies in severity hence can be asymptomatic or present with:

  • Difficulty urinating
  • Weak urinary stream
  • Chronic urinary retention
  • Palpable bladder
  • Recurrent UTIs
  • Impaired kidney function

Severe cases an obstruct urine flow in fetus causing bilateral hydronephrosis and oligohydramnios (which has complications such as pulmonary hypoplasia, Potters sydnrome)

50
Q

What investigations would you consider for posterior urethral valve?

A
  • Abdo ultrasound: enlarged, thickened bladder & bilateral hydronephrosis
  • Micturating cystourethrogram: show extra urethral tissue and reflux of urine into bladder
  • Cystoscopy: visualise extra tissue (can also be used to remove extra tissue)
51
Q

Discuss the management of posterior urethral valve

A
  • Mild cases= observe & monitor
  • Temporary catheter to bypass valve whilst waiting for definitive management
  • Definitive management= ablation or removal of tissue during cystoscopy
52
Q

What is vulvovaginitis?

A

Inflammation & irritation of vulva & vagina; commonly affects girls aged 3-10yrs.

53
Q

State some exacerbating factors for vulvovaginitis

A
  • Wet nappies
  • Use of chemicals/soap
  • Tight clothing that traps moisture or sweat
  • Poor toilet hygiene
  • Constipation
  • Threadworms
  • Pressure on area
  • Heavily chlorinated pools
54
Q

Why is vulvovaginitis much less common after puberty?

A

Oestrogen helps keep skin and vaginal mucosa healthy & resistant to infection

55
Q

Describe presentation of vulvovaginitis

A
  • Soreness
  • Itching
  • Erythema around labia
  • Dysuria
  • Vaginal discharge
  • Constipation

**Urine dipstick may show leucocytes but no nitrites

56
Q

Often, children with vulvovaginitis will have already been treated for UTIs and thrush with little improvement. Discuss the management of vulvovaginitis

A
  • Avoid washing with soaps & chemicals
  • Avoid perfumed or antiseptic products
  • Good toilet hygiene (front to back wiping)
  • Keep area dry
  • Emollients e.g. sudacrem to soothe
  • Loose cotton cothing
  • Treat exacerbating factors e.g. constipation, worms
  • Avoid activities which exacerbate problem

In severe cases may recommend oestrogen cream.

*NOTE: thrush before puberty is uncommon.

Yr4: Child Health (21 decks)

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