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YEAR 4 PAEDS > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Nephrotic syndrome triad?

A

Low serum albumin
High urine protein content ( > 3 + protein on dipstick)
Odema

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2
Q

Other features (not the triad) seen in nephrotic syndrome?

A

Deranged lipid profile with levels of cholesterol, triglycerides and low density lipoproteins

High blood pressure

Hyper-coagulability, with an increased tendency to form blood clots

Immunocompromised due to loss of immunoglobulins (and treatment is steroids which lead to immunosupression too)

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3
Q

Most common cause of nephrotic syndrome in children?

A

Minimal change disease

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4
Q

Investigations in Minimal change disease?

A

FBC: usually high
U&Es
Albumin- low
Urine dip: protein 3+
Urinalysis: small molecular weight proteins and hyaline casts
Renal biopsy: not a lot of abnormality
Chickenpox status: due to immunosuppression of drugs

N.B. Would not routinely do urinalysis or renal biopsy

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5
Q

Managment of Minimal change disease?

A

Steroids: oral Prednisolone
Dose: 60mg for 4 weeks, followed by 40mg on alternate days for 4 weeks and wean off until 2 months after

Oral abx (Pen V) for prophylaxis against pneumococcal

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6
Q

What do you do if minimal change does not respond to oral steroids?

A

IV steroids

If THAT doesn’t work, then renal biopsy and genetic testing

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7
Q

What is remission in nephrotic syndrome/ MCD?

A

Urine protein negative or trace for 3 consecutive days

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8
Q

What is relapse in Nephrotic syndrome/ MCD?

A

Urine protein 3+ or more for 3 consecutive days

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9
Q

What is a frequent relapser in Nephrotic syndrome/ MCD?

A

2 or more relapses in 6 months or 4 or more in 12 months

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10
Q

What is steroid dependence in Nephrotic syndrome?

A

If a child relapses whilst on steroid or within 2 weeks of stopping them

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11
Q

Prognosis of MCD?

A

90% will respond to steroids

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12
Q

Who gets MCD?

A

Peak incidence between 2-5 years

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13
Q

Complications of MCD/ being in a nephrotic state?

A

They need to be treat ASAP as:
Increased triglycerides: Increased risk of thrombi/stroke/VTE

Increased risk of AKI if dehydrated: CANNOT give saline or bolus- give them albumin instead

Increased risk of infection: give pneumococcal vaccine and penicillin vaccine (worried about peritonitis)

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14
Q

Apart from MCD what are causes of nephrotic syndrome in children?

A

Secondary to underlying kidney disease:
Focal segmental glomerulosclerosis
Membranoproliferative glomerulonephritis

Secondary to systemic illness:
Henoch schonlein purpura
Diabetes
Infection e.g. HIV, Hepatitis and malaria

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15
Q

What is vesicoureteric reflux?

A

Abnormal backflow of urine from the bladder into the ureter and kidney

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16
Q

Pathophysiology of Vesicoureteric reflux?

A

Ureters are displaced laterally, entering the bladder in a more perpendicular fashion than at an angle

Therefore shortened intramural course of the ureter

Vesicoureteric junction cannot, therefore, function adequately

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17
Q

How may VUR present?

A

Antenatally: Hydronephrosis on USS

50% present postnatally:

Recurrent childhood urinary tract infections

Reflux nephropathy: this is the term used to describe chronic pyelonephritis secondary to VUR, its the commonest cause of chronic pyelonephritis–> can lead to scarring

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18
Q

Why is renal scarring so bad?

A

Produce increase renin

Lead to hypertension

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19
Q

Investigations of VUR?

A

Normally diagnosed after Micturating Cystourethrogram: you inject dye using a catheter, then take the catheter out and watch them pee (can see if there is reflux)

DMSA scan may also be performed to look for renal scarring

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20
Q

Outline the grading for VUR?

A

1: reflux into the ureter only, no dilatation
2: Reflux into the renal pelvis on micturition, no dilatation
3: Mild/moderate dilatation of the ureter, renal pelvis and calyces
IV: dilation of the renal pelvis and calyces with moderate ureteral tortuosity
V: Gross dilatation of the ureter, pelvis and calyces with ureteral tortuosity

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21
Q

Management of VUR?

A

Most will get better–> prophylactic abx until potty trained, if does not work, change abx.

If STILL getting UTIs- deflux procedure by urologists is done

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22
Q

Causative organisms for UTIs in children?

A

Escherichia coli (around 80% of cases)
Proteus
Pseudomonas

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23
Q

Possible causes of UTIs in children?

A

UTI in childhood should prompt investigation for underlying causes and damage to the kidneys.

Incomplete bladder emptying:
Infrequent voiding
Hurried micturition
Obstruction by full rectum due to constipation
Neuropathic bladder

Vesicoureteric reflux

Poor hygiene e.g. wiping back to front in girls

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24
Q

Do boys or girls get more UTIs?

A

Boys up until 3 months due to more congenital abnormalities and then girls have a higher incidence

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25
Q

Presentation of UTIs in children?

A

Infants:
Fever
Lethargy
Irritability
Vomiting
Poor feeding
Urinary frequency

Younger children:
Abdo pain: suprapubic
Fever
Dysuria
Frequency

Older children:
Dysuria
Frequency
Haematuria

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26
Q

What might suggest an upper UTI?

A

Temp > 38 C

Loin pain/tenderness

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27
Q

When should you check urine sample in children?

A

if there are any symptoms or signs suggestive or a UTI

with unexplained fever of 38°C or higher (test urine after 24 hours at the latest)

with an alternative site of infection but who remain unwell (consider urine test after 24 hours at the latest)

28
Q

Outline how to collect urine for a child?

A

Need a clean catch sample- this is hard in babies/ infants esp girls. Parent sits with baby/infant without a nappy on and a sample pot, to catch incase it occurs

If not possible; urine collection pads should b used.

Invasive methods such as suprapubic aspiration ONLY used if non-invasive are not possible

29
Q

Management of UTIs?

A
  • Infants less than 3 months referred immediately to paediatrician: need IV abx and have a full septic screen
  • Children > 3 months with lower UTI: oral abx for 3 days as per guidelines, usually trimethoprim, nitro, cephalosporin or amoxicillin. Advised to come back if child remaining unwell after 24-48 hours
  • Children > 3 months with upper UTI consider admission, if not oral abx e.g. cephalosporin or co-amox for 7-10 days
30
Q

When do you investigate recurrent UTIs?

A
  • All children under 6 months with their first UTI should have an abdominal ultrasound within 6 weeks, or during the illness if there are recurrent UTIs or atypical bacteria
  • Children with recurrent UTIs should have an abdominal ultrasound within 6 weeks
  • Children with atypical UTIs should have an abdominal ultrasound during the illness
31
Q

What is a DSMA scan?

A

DMSA scans should be used 4 – 6 months after the illness to assess for damage from recurrent or atypical UTIs.

Checks for renal scarring

32
Q

How does Nephritic Syndrome present?

A

AKI (low urine output and/or high creatinine)
Haematuria
Hypertension
Mild proteinuria (<3.5g in 24 hours)
Mild/moderate oedema

33
Q

Initial Investigations for Nephritic Syndrome?

A

Urine dip: Blood and protein (mild)
U&Es: creatinine high
Albumin: low (not too low)
FBC: low
Renal USS: to rule out any tumour

34
Q

What is Post- Streptococcal Glomerulonephritis?

A

Occurs weeks after a A and B haemolytic streptococcus infection
* 1-2 weeks post tonsillitis/ pharyngitis
* 3-4 weeks after impetigo/cellulitis

Immune complexes made of streptococcal antigens, antibodies and complement proteins get stuck in glomeruli of kidneys–> inflammation–> AKI

35
Q

Specific investigations for Post-strep glomerulonephritis?

A

Complement: Low C3
Anti-steptolysin O: elevated

36
Q

What would you find on renal biopsy in Post-strep glomerulonephritis?

A
  • Not always indicated
  • Immune complex deposition: IgG, IgM, C3
37
Q

Management of Post-Strep Glomerulonephritis?

A

Usually self-limiting
Supportive therapy: Furosemide for AKI+ fluid imbalance and HTN
Low sodium diet

38
Q

What is IgA Nephropathy

AKA: Berger’s Disease

A
  • Type of vasculitis
  • Episodic gross haemturia during or after URT, GI infections, or strenuous exercise
39
Q

Investigation findings for IgA Nephropathy?

A
  • Increase serum IgA
  • Normal C3, C4
40
Q

Renal biopsy findings in IgA Nephropathy?

A
  • Mesangial immune complex deposits in glomeruli
41
Q

Management of IgA Nephropathy?

A
  • Supportive
  • ACEi/ARB for proteinuria and HTN
42
Q

What is Alport syndrome?

A
  • Nephritic syndrome
  • usually inherited in an X-linked dominant pattern
  • It is due to a defect in the gene which codes for type IV collagen resulting in an abnormal glomerular-basement membrane (GBM).
  • The disease is more severe in males with females rarely developing renal failure.
  • Often leads to Renal failure in men
  • Associated with hearing loss and abnormalities of the eye
43
Q

Symptoms of Alport Syndrome?

A
  • microscopic haematuria
  • progressive renal failure
  • bilateral sensorineural deafness
  • lenticonus: protrusion of the lens surface into the anterior chamber
  • retinitis pigmentosa
  • renal biopsy: splitting of lamina densa seen on electron microscopy
44
Q

Management of Alport syndrome?

A

Supportive
RRT
Renal transplant can lead to development of Anti-GBM

45
Q

Prognosis of IgA Nephropathy?

A

20-35% of patients will progress to end-stage renal failure within 20-25 years

46
Q

What is Wilm’s tumour?

A
  • One of the most common childhood malignancies
  • Typicall presents under 5 years old
47
Q

Associations of Wilms tumour?

A
  • Beckwith-Wiedemann syndrome
  • as part of WAGR syndrome with Aniridia, Genitourinary malformations, mental Retardation
  • hemihypertrophy
  • around one-third of cases are associated with a loss-of-function mutation in the WT1 gene on chromosome 11
48
Q

Features of Wilms tumour?

A
  • abdominal mass (most common presenting feature)
  • painless haematuria
  • flank pain
  • other features: anorexia, fever
  • unilateral in 95% of cases
  • metastases are found in 20% of patients (most commonly lung)
49
Q

When do you refer a child for ?Wilms tumour?

A
  • children with an unexplained enlarged abdominal mass in children - possible Wilm’s tumour - arrange paediatric review with 48 hours
50
Q

Investigation for Wilm’s tumour?

A
  • The initial investigation is an ultrasound of the abdomen to visualise the kidneys
  • A CT or MRI scan can be used to stage the tumour
  • Biopsy to identify the histology is required to make a definitive diagnosis.
51
Q

Managment of Wilms Tumour?

A
  • Nephrectomy- remove the tumour and the affected kidney (95% of cases are unilateral presentation)
  • Adjuvant chemo or radiotherapy
52
Q

Prognosis of Wilm’s Tumour

A
  • Good
  • 80% cure rate
53
Q

Differentiate between nocturnal and diurnal enuresis?

A

Nocturnal Enuresis: Bed wetting
Dirurnal Enuresis: Unable to control bladder functiond during the day

54
Q

When to children get control of their bladder function?

A
  • Daytime urination by 2 years
  • Nighttime urination by 3-4 years
55
Q

What is Primary nocturnal enuresis?

A
  • Child has never managed to be consistenly dry at night
56
Q

Causes of primary nocturnal enuresis?

A
  • Most commonly: variation of normal development, esp if child is younger than 5 years old
  • Overactive bladder
  • fluid intake prior to bedtime
  • Filure to wake- due to deep sleep and underdeveloped bladder signs
  • Psychological distress
  • Secondary causes: chronic constipation, UTI, learning disability and cerebral palsy
57
Q

Investigations for primary noctural enuresis?

A
  • Establish underlying cause: hx and exam
  • 2 week diary of toileting, fluid intake and bedwetting episodes
58
Q

What is secondary nocturnal enuresis?

A
  • where child begins wetting the bed when they have previously been dry for at least 6 months
  • More indicative of underlying illness
59
Q

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
60
Q

Treatment of secondary nocturnal enuresis?

A
  • Look for possible underlying causes/triggers:
    constipation
    diabetes mellitus
    UTI if recent onset
  • general advice:
    fluid intake
    toileting patterns: encourage to empty bladder regularly during the day and before sleep
    lifting and waking
  • reward systems (e.g. Star charts)
    NICE recommend these ‘should be given for agreed behaviour rather than dry nights’ e.g. Using the toilet to pass urine before sleep
  • enuresis alarm
    generally first-line for children
    have sensor pads that sense wetness
    high success rate
  • desmopressin
    particularly if short-term control is needed (e.g. for sleepovers) or an enuresis alarm has been ineffective/is not acceptable to the family
61
Q

Causes of dirunal enuresis?

A
  • urge incontinence
  • stress incontinence
  • recurrent urinary tract infections
  • psychosocial problems
  • constipation
62
Q

What is Haemolytic uraemic syndrome?

A
  • Thrombosis within small blood vessels throughout the body
  • Usually triggered by a bacterial toxin called Shiga toxin
63
Q

Classic triad of HUS?

A
  • Haemolytic anaemia
  • AKI
  • Thrombocytopenia
64
Q

What bacteria/ infections cause HUS?

this is essentially secondary- termed ‘typical HUS’

A
  • E.coli 0157
  • Shigella
  • Abx and anti-motility medications e.g. loperamide to treat gastroenteritis caused by these pathogens increases the risk of developing HUS
  • Pneumococcal infection
  • HIV
  • rare: SLE, drugs, cancer
65
Q

How does HUS present?

A
  • symptoms start around 5 days after onset of diarrhoea (if e.coli 0157) is the cause
  • Reduced urine output
  • haematuria or dark brown urine.
  • abdo pain
  • lethargy and irritability
  • confusion
  • oedema
  • hypertension
  • bruising
66
Q

Investigations for HUS?

A
  • FBC: anaemia: microangiopathic haemolytic anaemia characterised by a haemogloblin level than 8g/dL with a negative Coomb’s test
  • Fragmented blood film: schistocytes and helmet cells
  • U&E: acute kidney injury
  • Stool culture: look for evidence of STEC infection, PCR for shiga toxins
67
Q

Management of HUS?

A
  • medical emergency
  • self-limiting and supportive management is the mainstay
  • Fluids, blood transfusion and dialysis if required
  • Plasma exchange is reserved for severe cases of HUS not associated with diarrhoes

YEAR 4 PAEDS (19 decks)

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