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Phase 3a Paediatrics > Renal/Urinary > Flashcards

Renal/Urinary Flashcards

1
Q

What is another term for bed wetting?

A

Nocturnal enuresis

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2
Q

What is primary nocturnal enuresis?

A

Where the child has never managed to be consistently dry at night

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3
Q

What is the main cause of primary nocturnal enuresis?

A

Development
Particularly if the child is younger than 5 years

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4
Q

Apart from development, what are the reasons for primary nocturnal enuresis?

A
  • ** Overactive bladder** Frequent small volume urination prevents the development of bladder capacity.
  • Fluid intake prior to bedtimevparticularly fizzy drinks, juice and caffeine → diuretic effect
  • Failure to wake due to particularly deep sleep and underdeveloped bladder signals
  • Psychological distress
  • Secondary causes (chronic constipation, urinary tract infection, learning disability or cerebral palsy)
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5
Q

A there is a family history of nocturnal enuresis, what should you do?

A

Reassurance
No need to jump to further investigations or management

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6
Q

What main investigation would you request when seeing a 4 year old child with primary nocturnal enuresis?

A

2 week diary
* Toileting
* Fluid intake
* Bedwetting

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7
Q

Name 2 management options for primary nocturnal enuresis

A
  • Under 5 → reassurance
  • Lifestyle changes (reduced fluid intake, pass urine before bed, easy access to toilet)
  • Positive reinforcement
  • Treat underlying/exacerbating factors e.g. constipation
  • Enuresis alarms
  • Pharmacological treament
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8
Q

What is secondary nocturnal enuresis?

A

Child begins wetting the bed when theu have previously been dry for at least 6 months

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9
Q

What is the difference between primary and secondary nocturnal enuresis?

A

Primary → never been dry
Secondary → been dry for at least 6 months then starts wetting again

Secondary nocturnal enuresis = more indicative of underlying illness

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10
Q

Name two causes of secondary nocturnal enuresis?

A
  • Urinary tract infection
  • Constipation
  • Type 1 diabetes
  • New psychosocial problems (e.g. stress in family or school life)
  • Maltreatment
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11
Q

What should you always think about when a child presents with bed wetting?

A

Abuse + safeguarding
Particularly with:
* Deliberate bedwetting
* Punishment for bedwetting (despite parental education)
* Unexplained secondary nocturnal enuresis

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12
Q

What is the mangement for secondary nocturnal enuresis?

A

Treating the underlying cause
(most commonly UTIs or constipation)

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13
Q

Name a pharmocalogical treatment for nocturnal enuresis
(initiated by a specialist)

A
  • Desmopressin (vasopressin AKA ADH) taken at night → reduces urine volume
  • Oxybutinin → reduces the contractility of the bladder (especially for overactive bladder)
  • Imipramine
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14
Q

What is hypospadias?

A

Congenital condition where….
Urethral meatus (opening of urethra) = abnormally displaced to the ventral side of the penis (towards the scrotum)
Urethral meatus = located towards bottom of glans (90% of cases), halfway down shaft, or at base at shaft

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15
Q

What is epispadias?

A

The urethral meatus is displaced to the dorsal side (top side) of the penis

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16
Q

What is the difference between hypospadias and epispadias?

A

The urethreal meatus is abnormally located on the:
* Hypospadias → ventral (bottom side)
* Epispadias → dorsal (top side)

Usually, the foreskin is abnormally formed to match the position of the meatus

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17
Q

What is the associated condition with hypospadias?

A

Chordee
Head of the penis bends down

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18
Q

When is hypospadias and epispadias usually diagnosed?

A

Examination of the newborn

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19
Q

What is the management for hypospadias?

A

Don’t circumcise the infant until urologist indicates its okay
* Mild cases → may not require treatement
* Surgery (correct position of meatus + straighten the penis) → performed after 3-4 months of age

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20
Q

Name a complication of hypospadias

A
  • Difficulty directing urination
  • Cosmetic + psychological concerns
  • Sexual dysfunction
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21
Q

What is vesico-ureteric reflux (VUR)?

A

Urine has a tendency to flow from the bladder → ureters

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22
Q

What does vesico-ureteric reflux predispose patients to?

A

Upper urinary tract infections → + renal scarring

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23
Q

How is vesico-ureteric reflux diagnosed?

A

Micturating cystourethrogram (MCUG)

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24
Q

What is the management for vesico-ureteric reflux?

A

Depends on the severity:
* Avoid constipation
* Avoid an excessively full bladder
* Prophylactic antibiotics
* Surgical input from paediatric urology

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25
Q

What is haemolytic uraemic syndrome (HUS)?

A

HUS = thrombosis in throughout the body
(Usually triggered by Shiga toxins from E. coli 0157 or Shigella)

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26
Q

When does haemolytic uraemic syndrome usually occur in children?

A

After an episode of gastroenteritis
* The antibiotics + anti-motility meds (e.g. loperamide) used to treat gastroenteritis caused by E. coli 0157 or Shigella = increase the HUS risk

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27
Q

What are the two bactria that secrete the toxins that cause haemolytic uraemic syndrome?

A

E. Coli 0157
Shigella

28
Q

A child presents with the classic triad of:
* Microangiopathic haemolytic anaemia
* Acute kidney injury
* Thrombocytopenia (low platelets)
He experiences this after an episode of gastroenteritis. Possible diagnosis?

A

Haemolytic uraemia syndrome (HUS)

29
Q

Why do you get thrombocytopenia and an AKI with haemolytic uraemic syndrome?

A
  • Formation of blood clots = consumes platelets → thrombocytopenia
  • Thrombi + damaged RBCs → affected blood flow into kidney → AKI
30
Q

Explain how microangiopathic haemolytic anaemia occurs in haemolyitic uraemic syndrome

A

Microangiopathic haemolytic anaemia = the destruction of RBCs (haemolysis) due to pathology in the small vessels (microangiopathy)

Thrombi = partially obstruct the small blood vessels → churn the RBCs as they pass through → they rupture

31
Q

What is the initial presentation of haemolytic uraemic syndrome

A

Diarrhoea (caused by E. Coli + Shigella):
* 3 days →**diarrhoea turns bloody **
* 7 days → HUS features develop

32
Q

What are the clinical features of haemolytic uraemic syndrome?

A
  • Confusion (uraemia)
  • Pallor (anaemia)
  • Bruising (low platelets)
  • Jaundice (due to haemolysis)
  • Lethargy
  • Abdominal pain

Renal component (damage to the glomeruli)
* Hypertension (renal failure)
* Oliguria (reduced urine output)

33
Q

Main investigation for haemolytic uraemic syndrome?

A

Stool culture
(To establish the causative organism)

34
Q

What is the management for haemolytic uraemic syndrome?

A

Medical emergency (self-limiting but require supportive treatment)
Treatment of:
* Hypovolaemia (e.g., IV fluids)
* Hypertension
* Severe anaemia (e.g., blood transfusions)
* Severe renal failure (e.g., haemodialysis)

35
Q

When is multicystic dysplastic kidney (MCDK) diagnosed?

A

Antenatal ultrasound scans

36
Q

What is multicystic dysplastic kidney?

A

Where one of the baby’s kidneys is made up of many cysts while the other kidney is normal. In rare cases it can be bilateral, which inevitably leads to death in infancy.

37
Q

What 3 things can having a single kidney at risk of?

A
  • UTIs
  • Hypertension
  • Chronic kidney disease
38
Q

Define nephritis

A

Inflammation within the nephrons of the kidney

39
Q

What are the features of nephritis?

A
  • Reduction of kidney function
  • Haematuria: visible or invisible
  • Proteinuria: less than nephrotic syndrome
40
Q

What are the most common causes of nephritis in children?

A
  • Post-streptococcal glomerulonephritis
  • IgA nephropathy (Berger’s disease)
41
Q

What are the added features to LUTS that indicates pyelonephritis?

A
  • A temperature greater than 38C
  • Loin pain or tenderness
42
Q

How will a baby present with a UTI?

A
  • Fever
  • Lethargy
  • Irritability
  • Vomiting
  • Poor feeding
  • Urinary frequency
43
Q

What are the signs and symptoms in older infants + children presenting with a UTI?

A
  • Fever
  • Abdominal pain, particularly suprapubic pain
  • Vomiting
  • Dysuria (painful urination)
  • Urinary frequency
  • Incontinence
44
Q

After what illness does post-streptococcal glmerulonephritis develop?

A

1-3 weeks after a β-haemolytic streptococcus infection e.g. tonsilitis → caused by streptococcus pyogenes

45
Q

Why does post-streptococcal glomulerulonephritis cause damage to the kidneys?

A

The immune complexes (streptococcal antigens + antibodies + complement proteins) = get stuck in the glomeruli of the kidney → cause inflammation → actute detoriation in renal function → acute kidney injury (AKI)

46
Q

What investigations would you request for a patient woth suspected post-streptococcal glomerulonephritis?

A
  • Throat swab (streptococcus positive)
  • Anti-streptolysin antibody titres (blood test)
47
Q

A child presents with haematuria. After initial Ix, you discover reduced renal function and proteinuria. On Hx taking you you note that he had tonsilitis around a week ago. Possible diagnosis?

A

Post-streptococcal glomerulonephritis

48
Q

What is the management for post-streptococcal glomerulonephritis?

A

Supportive (80% patients make a full recovery - some develop worsening renal function). Treat complications:
* Antihypertensives → hypertension
* Diuretics → oedema

49
Q

What is IgA nephropathy also called?

A

Berger’s disease

50
Q

What condition is IgA nephropathy also related to?

A

Henoch-Schonlein Purpura (HSP)
(= a IgA vasculitis)

51
Q

If a patient has IgA nephropathy and a biopsy is taken, what will it show

A

IgA deposits + glomerular mesangial proliferation

52
Q

How does IgA nephropathy cause damage to the kidney?

A

IgA deposits in the nephrons → causes inflammation (nephritis)

53
Q

Who does IgA nephropathy ususally present in?

A

Teenagers + young adults

54
Q

What is the management for IgA nephropathy?

A
  • Supportrive treatment for renal failure
  • Immunosuppressants → steroids + cyclophosphamide (to slow progression)
55
Q

Why does nephrotic syndrome occur?

A

Nephrotic syndrome = occurs when the basement membrane in the glomerulus becomes highly permeable to protein → allowing proteins to leak from blood into urine (proteins: blood → urine)

56
Q

Between what ages is nephrotic syndrome most common in children?

A

2-5 years

57
Q

What are the 3 typical clinical features of nephrotic syndrome?

A
  • Frothy urine
  • Generalised oedema
  • Pallor
58
Q

What is the classic triad of nephrotic sydrome?

A
  • High urine protein content (> 3+ protein on urine dipstick)
  • Low serum albumin
  • Oedema
59
Q

Apart from the classic 3 features of nephrotic syndrome, what are the other 3 features?

A

Classic triad:
* High urine protein content (> 3+ protein on urine dipstick)
* Low serum albumin
* Oedema

3 other features:
* High cholesterol + triglycerides + LDL
* High blood pressure
* Hyper-coagulability (w/ increased tendency to form blood clots)

60
Q

Causes of nephrotic syndrome

A

Primary:
* Minimal change disease (90% cases in children)

Secondary to intrinsic kidney disease:
* Focal segmental glomerulosclerosis
* Membranoproliferative glomerulonephritis

Secondary to underlying systemic illness:
* Henoch schonlein purpura (HSP)
* Diabetes
* Infection (e.g. HIV, hepatitis, malaria)

61
Q

Why does minimal change disease occur?

A

No clear cause

Minimal change disease is the most common cause of nephrotic syndrome in children. It can occur in otherwise healthy children, without any clear risk factors or reason for developing the condition. It is not clear why it occurs in most cases.

62
Q

Is minimal change disease detectable on standard microscopy (from renal biopsy)?

A

No

63
Q

Investigations for minimal change disease

A
  • Renal biosy: Not usually detectable on standard miscroscopy
  • Urinalysis: shows small molecular weight proteins + hyaline casts
64
Q

Management of minimal change disease

A

Corticosteroids (prednisolone)

The prognosis is good and most children make a full recovery, however it may reoccur.

65
Q

A 2-5 year child presents with oedema, proteinuria, low albumin. Most likely underlying cause?

A

Nephrotic syndrome
(90% cases minimal change disease)

66
Q

Management of nephrotic syndrome

A
  • High dose steroids (i.e. prednisolone)
  • Low salt diet
  • Diuretics may be used to treat oedema
  • Albumin infusions may be required in severe hypoalbuminaemia
  • Antibiotic prophylaxis may be given in severe cases

In steroid resistant children: ACE inhibitors +immunosupressants (cyclosporine, rituximab)

67
Q

Complications of nephrotic syndrome

A
  • Hypovolaemia (as fluid leaks from the intravascular space → into interstitial space → causing oedema + low blood pressure)
  • Thrombosis (can occur because proteins that normally prevent blood clotting are lost in the kidneys, and because the liver responds to the low albumin by producing pro-thrombotic proteins.)
  • Infection (occurs as the kidneys leak immunoglobulins → weakening the immune system. This is exacerbated by treatment with medications that suppress the immune system, such as steroids)
  • Acute or chronic renal failure
  • Relapse

Phase 3a Paediatrics (13 decks)

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