Renal and Urinary System Flashcards

1
Q

By what age are most children dry by day and dry by night?

A

Dry by day at 2 years

Dry by night at 3 years

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2
Q

What are the two types of enuresis (involuntary urination)? More common in M or F?

A

Nocturnal - twice as common in males

Daytime (much rarer) - more common in females

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3
Q

What is primary enuresis?

A

Continence never established

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4
Q

What is secondary enuresis?

A

Loss of continence after a continuous period of at least 6 months dryness (most likely to have organic cause)

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5
Q

What are some biological causes of nocturnal enuresis?

A

1) UTI = 5% secondary enuresis
2) Urinary tract abnormalities
- Low bladder capacity
- Incomplete bladder voiding
- Detrusor instability secondary to constipation
3) Lack of ADH during sleep
4) Genetic predisposition
- 70% have FH
5) Diabetes causing polyuria

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6
Q

What are some psychosocial causes of nocturnal enuresis?

A

1) Inability to wake to full bladder sensation
2) Psychosocial trauma eg distress, bullying, abuse
3) Accidental behavioural conditioning eg child comes to parents bed when wet
4) Developmental delay

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7
Q

What is a major cause of daytime enuresis?

A

Bacteriuria

Cycle - bacteriuria causes detrusor instability causes urge incontinence causes damp pants and perineal irritation causes bacteriuria

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8
Q

What investigations can be done for enuresis? (4)

A

1) DM testing - random and fasting blood glucose
2) Urinalysis if symptomatic
- Bacteriuria is common in girls with daytime enuresis
3) Early morning urine sample - assess urine osmolarity to test ability of kidneys to concentrate urine
4) USS to look for GU tract abnormality
5) Consider psychological screening

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9
Q

What is the management of enuresis?

At what age would you start intervening in enuresis?

A

Intervene from 7 years old

Reassurance and counselling for parents - explain it is beyond child’s conscious control and parents should stop punitive procedures as these are counterproductive

Avoid caffeine and fruit juice

Star charts

Enuresis alarm

Medication

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10
Q

What medications can be given for enuresis?

A

Desmopressin

  • Antidiuretic can be taken as tablets, sublingual or nasal spray at bed time
  • Reduces urine output - provides short-term relief from bedwetting for holidays/sleepovers
  • Avoid excessive fluid intake for 8hrs after dose

Anticholinergics = if daytime symptoms / unresponsive to desmopressin

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11
Q

Why is a UTI significant in young children?

A

It may be a marker for urinary tract abnormalities

Half of child UTI pt have renal tract abnormality

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12
Q

When clinically should an upper UTI be assumed?

A

Fever of 38 or higher + bacteriuria

Fever lower than 38 but with loin pain/tenderness + bacteriuria

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13
Q

When are UTIs considered recurrent?

A

1) 2 x upper UTI
2) 3 x lower UTI
3) 1 x upper + 2 x lower UTI

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14
Q

What features make a UTI atypical?

A

1) Seriously ill / septicaemia
2) Poor urine flow - sign of obstruction
3) Presence of abdo / bladder mass
4) Lack of response within 48hrs to treatment with suitable abxs
5) Not caused by E Coli
6) Raised creatinine

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15
Q

Are UTIs more common in boys or girls?

A

More common in boys up to 6 months

More common in girls after

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16
Q

What are some risk factors for UTI?

A
  • Age < 1 year
    • Urinary tract abnormality
    • Voiding dysfunction
    • Vesicoureteral reflux
    • Spinal abnormalities
    • Constipation
    • Immunosuppression
    • Sexual abuse - more likely to cause urinary symptoms than infection
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17
Q

How may a UTI present in infants <3 months?

A

Presents differently than in older children

Fever
Vomiting
Lethargy
Irritability
\+/- poor feeding
\+/- FTT
Less commonly:
Abdo pain
Jaundice 
Haematuria
Offensive urine

More likely to develop urosepsis

Less likely to be due to E coli

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18
Q

What is the most common presentation of a UTI in a preverbal child?

A

Fever with no apparent cause

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19
Q

How may a UTI present in a child >3yrs?

A

Urinary symptoms eg freq, dysuria, suprapubic / abdo / lumbar pain

Dysfunctional voiding

Fever, malaise, vomiting, haematuria, offensive / cloudy urine

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20
Q

Ddx for UTI (6)

A
Vulvovaginitis
Urethritis
Irritation e.g. soaps
Threadworm infestation
Balanitis
Sexual abuse
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21
Q

What should be included on examination of a child with a UTI?

A

Temperature

Cervical lymph nodes

Abdomen - constipation, masses, tender / palpable kidney

Back - signs of spina bifida

Genitalia - phimosis, labial adhesions, vulvitis, epididymo-orchitis

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22
Q

How may urine be collected in a child with a UTI?

A

Clean catch - most ideal
Collection bag attached to clean genitalia - avoid due to contamination
Urine collection pads - avoid due to contamination
Supra-pubic aspirate - gold-standard but only consider if child is very unwell

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23
Q

What may urinalysis show in a UTI?

A

Nitrites +
Leucocytes +
Haematuria +
Albumin +

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24
Q

Why are nitrites not very sensitive dipstick test in infants?

A

Not all urinary pathogens reduce nitrate to nitrite

Urine not often held in bladder long enough for conversion to occur

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25
Q

What imaging scans should be done in infants/children with atypical/recurrent UTIs?

< 6 months

6 months-3 years

> 3 years

A

< 6 months

  • USS
  • Micturating cystography (MCUG)
  • DMSA scintigraphy

6 months-3 years

  • USS
  • DMSA scan

> 3 years
- USS

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26
Q

What are USS effective and ineffective at visualising when investigating a UTI?

A

Accurately assess renal size and outline and identify most congenital abnormalities, renal calculi and hydronephrosis or hydroureter (indicating the presence of obstruction or severe reflux)

Less effective in detecting mild or moderate vesico-ureteric reflux

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27
Q

How is micturating cystography (MCUG) carried out? What is it looking for?

A

Catheterise bladder, fill with radio-opaque dye, watch on X-ray whilst child micturates

Will see urethral abnormalities or vesico-ureteric reflux

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28
Q

What is the gold standard investigation for VUR?

A

Micturating cystography

Only imaging technique that provides information about the urethra

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29
Q

What DMSA scintigraphy effective at imaging? How does it work?

A

Gold standard for renal parenchymal defects

  • Inject IV radiolabelled isotope and visualise on scintigraphy
  • The working renal tissue picks up the isotope so a renal image is seen, then the scars are shown as blank areas
  • Rate of excretion is seen as the kidney clears the isotope
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30
Q

When are DMSA used?

A

4-6 months post infection - show scarring

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31
Q

Which children presenting with a UTI should be immediately referred to specialist care?

A

Serious illness
3 months or younger

Do not delay treatment if sample cannot be obtained and the child is at serious risk of illness

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32
Q

What is the pharmacological management of a child with a UTI? Lower and upper

A

< 3 months - refer immediately to hospital for IV abx (cefotaxime)

> 3 months with upper UTI
- Usually PO co-amoxiclav for 7-10 days
or
- IV cefotaxime for 2-4 days followed by PO abx for 7-10 days

If lower UTI, trimethoprim PO for 3 days

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33
Q

What is dysfunctional voiding syndrome?

A

Abnormality of emptying, due to either a small-capacity, unstable bladder or a large-capacity, poorly emptying bladder

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34
Q

What are potential complications of a UTI in children? (3)

A

1) Renal scarring - more likely in children with vesico-ureteric reflux
2) Hypertension - associated with renal scarring

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35
Q

What is the diagnosis of infants or children that have:

1) Bacteriuria and a fever of 38 or more
2) Fever <38 associated with loin pain/tenderness and bacteriuria
3) Bacteriuria but no systemic symptoms or signs?

A

1) Pyelonephritis/upper UTI
2) Pyelonephritis/upper UTI
3) Cystitis/lower UTI

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36
Q

What measures can be adopted to prevent UTI?

A

Good fluid intake to increase urine output
Practice regular voiding and ensuring bladder completely emptying
Prevention of constipation
Good perineal hygiene

For girls:

  • Wipe from front to back
  • Avoid perineal irritation from bubble baths or soaps
  • Thorough drying of perineum
  • Wear loose fitting clothes
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37
Q

What causes primary and secondary vesicoureteric reflux?

A

Primary = Incomplete closure of the vesicoureteric valve

Secondary = obstruction in bladder or urethra causing urine to flow back into kidneys e.g. posterior urethral valves in boys

38
Q

List some glomerular and non-glomerular causes of haematuria in children

A

Glomerular
• Acute glomerulonephritis - proteinuria present
○ Post-infectious
○ Vasculitis e.g. Henoch-Schonlein purpura
○ SLE
○ Goodpasture syndrome - anti-glomerular basement membrane disease
• Chronic glomerulonephritis - proteinuria present
• IgA nephropathy
• Familial nephritis e.g. Alport syndrome
• Thin basement membrane disease

Non-glomerular 
• Infections - bacterial, viral, TB, schistosomiasis 
• Trauma - accidents, catheters
• Renal calculi 
• Sickle cell disease
• Coagulopathies 
• Renal vein thrombosis 
• Hypercalciuria
39
Q

What can the colour of the urine tell you in haematuria?

A

Originating from kidney = brown / cola-coloured

Originating from bladder / urethra = red / pink colour and may contain clots

NB not all red urine is blood eg could be from beetroots or blackberries

40
Q

What is important to include on examination of someone presenting with haematuria?

A

BP:
- HTN suggests renal malfunction and child should be admitted to hospital

Oedema:

  • Periorbitally and ankles
  • Can be a feature of glomerulonephritis

Renal mass:
- Palpate abdo for tenderness and renal masses

41
Q

What are the most likely diagnoses if a renal mass is found upon abdo examination of a child presenting with haematuria?

A

Hydronephrosis
Polycystic kidneys
Tumour

42
Q

What investigations are done for all paeds patients presenting with haematuria?

A

1) Urine MC&S
2) KUB USS
3) FBC, U&Es, clotting

43
Q

What further investigations should be done in haematuria if there are signs suggestive of glomerular haematuria?

A
  • ESR, complement levels and anti-DNA antibodies
  • Throat swab
  • Hep B and hep C screen
  • Renal biopsy if recurrent, persistent haematuria and renal function is abnormal
  • Test mother’s urine if Alport syndrome suspected
44
Q

What the relevance of an ASO titre and throat culture when investigating haematuria?

A

Recent strep infection often precedes acute glomerulonephritis

45
Q

What the relevance of serum C3 level when investigating haematuria?

A

Low C3 is specific for certain types of glomerulonephritis

46
Q

What the relevance of ANF / autoantibodies when investigating haematuria?

A

Positive in SLE

47
Q

When is a renal biopsy required when investigating haematuria?

A

If haematuria is persistent with proteinuria, HTN or impaired renal function

48
Q

What does smoky, coca-cola coloured, granular and red cell casts haematuria with malaise, oliguria, HTN and oedema suggest?

A

Glomerulonephritis

49
Q

What does haematuria with renal colic suggest?

A

Renal stone

50
Q

What does haematuria with a renal mass and abdo pain suggest?

A

Tumour

51
Q

What does haematuria with a painless renal mass suggest?

A

Congenital abnormality

52
Q

What is the classical triad of haemolytic uraemic syndrome?

A

Triad of:

1) Microangiopathic haemolytic anaemia - Coombs’ test negative
2) Thrombocytopenia
3) AKI

53
Q

What causes HUS?

A

90% follow infection

Infection with E coli 0157 (15% of cases will develop HUS)

Produces Shiga toxin or verotoxin

HUS can occur up to 2 weeks after infection

54
Q

What is the pathophysiology of HUS?

A
  1. Infection with E. Coli 0157 (or another causative organism)
  2. Mucosal inflammation facilitates bacterial toxins entering the systemic circulation
  3. Toxins cause endothelial cell damage, especially in the glomerulus
  4. Damaged endothelial cells secrete cytokines that promote vasoconstriction and platelet microthrombus formation at the site of damage
  5. The glomerular filtration rate (GFR) decreases and RBCs are mechanically destroyed as they pass through the platelet microthrombi occluding small blood vessels - this results in haemolysis and end-organ damage, especially in the kidneys
55
Q

Other than E coli 0157, what pathogens may induce HUS?

A

Bacteria - strep pneumoniae and shigella dysenteriae type 1

Viruses - HIV and Coxsackievirus

56
Q

What is the incubation period of E coli 0157?

A

1-6 days

HUS usually arises within 14 days, even when appear to be recovering form initial illness

57
Q

When are children with E coli 0157 gastroenteritis able to go back to school?

A

After two negative stool cultures

Post-symptomatic shedding can occur but highest transmissibility thought to occur during acute diarrhoea phase

58
Q

How may HUS present?

A

Bloody diarrhoea for 5-10 days preceding onset of HUS symptoms (due to E Coli infection)

  1. Thrombocytopenia
    a. Petechiae, purpura
    b. Mucosal bleeding
    c. Prolonged bleeding after minor cuts
  2. Microangiopathic haemolytic anaemia
    a. Fatigue, dyspnoea, pallor
    b. Jaundice
  3. AKI
    a. Haematuria, proteinuria
    b. Oliguria, anuria
59
Q

What investigations are performed for HUS?

A
  • FBC - low platelets, raised WCC, low Hb
  • Coagulation screen - slightly raised prothrombin time (PT) and APTT
  • Negative Coombs’ test
  • U&Es - raised LDH (evidence of haemolysis), raised indirect bilirubin (haemolytic anaemia), raised creatinine

• Urinalysis - haematuria, proteinuria
Stool culture for E coli

60
Q

What is the main differential for HUS?

A

Thrombotic thrombocytopenic purpura

  • Less high creatinine
  • Neurological symptoms
  • Less associated with dysentery
61
Q

What is HELLP syndrome?

A

Haemolysis
Elevated Liver enzymes
Low Platelet count

= complication in pregnancy usually presents in women who have pre-eclampsia or eclampsia

62
Q

What gene is affected in autosomal dominant form of HUS?

A

Abnormality of the ADAMTS13 gene which encodes vWF

Tends to present in childhood

63
Q

What is thrombotic thrombocytopenia purpura?

A

Rare form of thrombotic microangiopathy

Characterised by:

1) Microangiopathic haemolysis
2) Thrombocytopenia
3) Neurological abnormalities
4) Renal dysfunction
5) Fever

TTP = medical emergency, without treatment mortality = 90%

64
Q

What is the management of HUS?

A

Infectious diarrhoea, HUS or VTEC (verocytotoxin-producing E coli) = report to public health

Supportive treatment

New treatments include:

  • Early plasma exchange to remove mutant complement proteins
  • Specific targeted treatments eg factor H comcentrate
  • Liver or liver and kidney transplants
65
Q

What are some complications of HUS?

A

GI:

  • Intestinal strictures and perforations
  • Intussusception and rectal prolapse
  • Pancreatitis
  • Severe colitis

Neuro:

  • Altered mental state
  • CVA
  • Seizures

Renal:

  • AKI
  • CKD
  • Haematuria
  • HTN
  • Proteinuria
66
Q

What is nephrotic syndrome?

A

aka nephrosis

1) Proteinuria
2) Low albumin
3) Oedema
4) High triglycerides

67
Q

What is the pathophysiology of nephrotic syndrome?

A

Increased permeability of serum protein through damaged basement membrane in renal glomerulus

Oedema results due to hypoalbuminaemia

68
Q

What values define nephrotic syndrome?

A

Protienuria = to / more than 3.5g/day

Hypoalbuminaemia = serum albumin = to / less than <30g/L

69
Q

What is the most common cause of nephrotic syndrome in children?

A

Minimal change = 85%

Changes on renal biopsy are very mild

70
Q

How does minimal change nephrotic syndrome initially present?

A

PC usually oedema
- Most noticeable in mornings around eyelids and pitting oedema in legs

May be hx of recent viral URTI

71
Q

What is the second most common cause of nephrotic syndrome in children?

A

Focal segmental glomerulosclerosis

72
Q

Following initial presentation of oedema, what symptoms / sign follow?

A

Weight gain
Ascites
Pleural effusion

  • Due to hypoalbuminaemia
Rarely HTN
Anorexia
Abdo pain
Diarrhoea
Oliguria
73
Q

Why is there an increased risk of infections in nephrotic syndrome?

A

Leakage of immunoglobulins

74
Q

What investigations are carried out for nephrotic syndrome?

A

Urinalysis
- 3+ or 4+ protein or microscopic haematuria

Serum albumin
- Low

Serum cholesterol and triglyceride
- High

C3 levels
- High

Renal biopsy only if clinical picture does not appear typical of minimal change nephrotic syndrome or if child does not respond to treatment within a month

75
Q

What is the management of nephrotic syndrome?

A

Hospital admission

Fluid restriction
Low salt diet
Corticosteroids = prednisolone
Prophylactic penicillin until proteinuria cleared

76
Q

How long should prednisolone be continued when treating nephrotic syndrome?

A

Until remission of proteinuria (usually 2 weeks), then continued at a weaning dose over 2-3 months

Advise parents to avoid live vaccines and chickenpox during this time

77
Q

What should be performed in children who are steroid resistant and how may they be treated?

A

Renal biopsy to confirm pathology

May need cyclophosphamide

78
Q

What has the best + worst prognosis of nephrotic syndrome? What % relapse?

A

Caused by minimal change = good prognosis

Other causes worse eg HSP

75% relapse

79
Q

What is acute glomerulonephritis?

A

Results from immunological damage to the glomerulus

Commonest form in childhood results from immune complexes following infection by nephritogenic form of streptococcus

Other forms of glomerulonephritis are rare and only considered if atypical course

80
Q

When does haematuria occur in acute glomerulonephritis?

A

1-2 weeks after throat or skin infection

81
Q

How does acute glomerulonephritis present?

A

Smokey / cola-coloured urine

Otherwise asymptomatic, can have:

  • Malaise
  • Headache
  • Vague loin discomfort
  • Oedema around eyes, necks of hands and geed

Usually mild oliguria, but can have:

  • Renal failure
  • HTN
  • Seizures
  • HF
82
Q

What may be found when investigating acute glomerulonephritis?

A

Urine microscopy shows gross haematuria with granular and red cell casts

Proteinuria

83
Q

How is acute glomerulonephritis confirmed to be post-strep form?

A

Throat swab
ASO titre
Low complement (C3) levels

84
Q

What is the management of acute glomerulonephritis?

A

No specific therapy, managed similarly acute renal failure

Monitor creatinine clearance and fluid balance

Restrict fluid intake if oliguria develops

Diuretics and hypotensive drugs if HTN

Rarely peritoneal dialysis required

Treat strep infection with penicillin but no evidence this affects course of disease

85
Q

What is the prognosis of acute glomerulonephritis?

A

Post-strep has excellent prognosis

Usually resolves in 10-14 days

Other causes have poorer prognosis

86
Q

What is hypospadias?

A

External urinary meatus is abnormally sited

Can be anywhere from ventral aspect of glans penis (most common) to penoscrotal junction or even perineum

87
Q

What is the treatment of hypospadias?

A

May be mild = needing no treatment

Severe = surgical repair (before 2 yrs)

  • Allows boys to void standing
  • Allow future sexual function
  • Psychological impacts

Parents advised not to have the child circumcised so that the foreskin tissue can be used in reconstructive surgery

88
Q

List some RF for vulvovaginitis

A
Close anatomical proximity of rectum
Lack of labial fat pads and pubic hair
Small labia minora
Thin and delicate vulvar skin
Thin, atrophic vaginal mucosa
Poor hygiene
89
Q

How may vulvovaginitis present?

A

Most common gynae problem in prepubertal girls (ages 3-10yrs)

Itching
Redness
Soreness
Green/yellow discharge

90
Q

What are some causes of vulvovaginitis?

A

Infection eg candida, bv
- Prepubertal can be caused by GABS

Dermatological eg allergic dermatitis

91
Q

How is vulvovaginitis managed?

A

Lifestyle advice eg avoid irritants / tight underwear

Treat cause