Renal + Urinary Flashcards

1
Q

Pyelonephritis can lead to ______ in the kidney tissue and therefore a ______ in kidney function

A

scarring

reduction

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2
Q

Always consider ____ in a child with temperature, unless there is a clear alternative source of infection

A

UTI

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3
Q

Which symptoms do babies with UTI present with?

A
Fever
Lethargy
Irritability
Vomiting
Poor feeding
Urinary frequency
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4
Q

Signs and symptoms in older infants and children of UTI

A
Fever
Abdo pain (suprapubic pain)
Vomiting
Dysuria (painful urination)
Urinary frequency
Incontinence
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5
Q

What is the fine, thin hair that grows on babies in utero called?

A

Ianugo

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6
Q

Diagnosis of acute pyelonephritis is made when:

Temp __________

____ pain/tenderness

A

38c

Loin

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7
Q

Main investigation for UTI

A

Clean catch sample for urine dipstick

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8
Q

What would show on a urine dipstick for a UTI?

A

Nitrites
Leukocytes
Blood

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9
Q

Children under 3 months old with fever should be given what drug immediately?

A

IV ceftriaxone

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10
Q

Children under 3 months old with fever should have which investigations?

A
Septic screen (blood cultures, bloods and lactate)
LP
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11
Q

List antibiotic choices that can be used in children with UTI

A

Trimethoprim
Nitrofurantoin
Cefalexin
Amoxicillin

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12
Q

What 3 investigations can be used to investigate recurrent UTIs?

A

USS abdo
DMSA
MCUG

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13
Q

When is USS used in children under 6 months with UTI?

A

Within 6 weeks

Or during illness if recurrent UTIs or atypical bacteria

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14
Q

How does DMSA scan work?

A

Uptake of DMSA material by kidneys.

Patches with no uptake = scarred tissue due to previous infection

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15
Q

List the gold standard investigation for VUR

A

MCUG

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16
Q

How can VUR be treated?

A

Avoid constipation
Avoid excessively full bladder
Prophylactic antibiotics
Surgical input from paeds urology

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17
Q

How does MCUG investigation work?

A

Catherise child, inject contrast into bladder.

Series of X-rays taken and see whether contrast is refluxing into ureters

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18
Q

List the most common microorganism of UTI. List 2 other bugs?

A

E.coli
Klebsiella
Proteus

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19
Q

Define nocturnal enuresis

A

Bed wetting at night

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20
Q

Define diurnal enuresis

A

Wetting self during day

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21
Q

What is the most common cause of primary nocturnal enuresis?

A

Normal variation on normal development

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22
Q

What is primary vs secondary nocturnal enuresis?

A

Primary - never managed to control wetting self yet

Secondary - previously managed to control wetting for 6 months but now not

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23
Q

Other causes of primary nocturnal enuresis apart from normal development

A

Overactive bladder
Fluid intake
Failure to wake up
Psych distress

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24
Q

How do you establish the cause of primary nocturnal enuresis?

A

Toileting 2 week diary

History and examination to exclude psych or physical causes

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25
Q

Give management options for primary nocturnal enuresis

A
Conservative
Reassurance to parents
Reduced fluid in evenings
Pass urine before bed
Easy toilet access
Encouragement
Treat underlying causes
Enuresis alarm

Medical
Pharmacological treatment

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26
Q

Causes of secondary nocturnal enuresis

A
UTI
Constipation
T1DM
New psych problems
Maltreatment (safeguarding)
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27
Q

2 main types of incontinence and what they mean

A

Urge - overactive bladder that gives little warning before emptying

Stress - leaking urine during exertion (coughing/laughing etc)

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28
Q

What drugs can be given to stop enuresis?

A

Desmopressin (ADH analogue)

Oxybutinin (anticholenergic - reduces bladder contractility)

Imipramine - (TCA - relax bladder and lightens sleep)

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29
Q

Causes of prerenal failure

A
- Hypovolaemia due to:
Gastroenteritis
Burns
Sepsis
Haemorrhage
Nephrotic syndrome
  • Circulatory failure
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30
Q

Causes of renal failure

A
Vascular:
HUS
Vasculitis
Embolus
Renal vein thrombosis
Tubular:
Acute tubular necrosis
Ischaemic
Toxic
Obstructive

Glomerular:
Glomerulonephirtis

Interstitial:
Interstitial nephritis
Pyelonephritis

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31
Q

Cause of post-renal failure

A

Obstruction:

  • congenital (valve abnormality)
  • acquired (blocked urinary catheter)
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32
Q

What is the last line of AKI management?

A

Dialysis

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33
Q

Management topics for CKD

A
  1. Diet
  2. Prevent renal osteodystrophy
  3. Salt/water balance/acidosis
  4. Anaemia
  5. Hormonal abnormalities
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34
Q

What is the last line of CKD management?

A

Dialysis or kidney transplant

35
Q

Presentation of CKD

A
Anorexia
Lethargy
Polydipsia/polyuria
Faltering growth/growth failure
Renal rickets 
HTN
Proteinuria
Anaemia
36
Q

How is HUS managed?

A
Supportive management
Urgent referral if dialysis needed
Anti-HTN if needed
Fluid balance
Blood tranfusion if needed
37
Q

What is hypospadias?

A

Urethral meatus displaced posteriorly on penis

38
Q

When is hypospadias diagnosed?

A

Newborn examination

39
Q

When is surgery on hypospadias performed?

A

Surgery done 3-4 months of age

Mild cases DON’T need treatment

40
Q

Complications of hypospadias?

A

Difficulty directing urination
Cosmetic and psych concerns
Sexual dysfunction

41
Q

What is phimosis?

A

Non-retractile foreskin when trying to pull down foreskin to expose glans.

Glans is “muzzled”

42
Q

What is chordee?

A

Head of penis is extremely curved

43
Q

Most common condition giving rise to “true” phimosis?

A

BXO

Balanitis Xerotica Obliterans

44
Q

List clinical features of Wilm’s Tumour

A

Mass in abdomen

Abdo pain
Haematuria
Lethargy
Fever
HTN
Weight loss
45
Q

Where does Wilm’s tumour occur? and at what age?

A

Kidneys

Children under 5 years old

46
Q

Investigation to explore Wilm’s Tumour

A

USS abdomen

CT/MRI to stage tumour

Renal biopsy for definitive diagnosis

47
Q

Management of Wilm’s Tumour

A

Surgical excision of tumour and nephrectomy (of affected kidney)

Adjuvant treatment after surgery:
chemo or radiotherapy

48
Q

What is renal agenesis?

A

Congenital absence of both kidneys

49
Q

Amniotic fluid is mainly derived from which fluid?

A

Fetal urine

50
Q

What is Potter’s syndrome?

A

Both kidneys absent so oligohydramnios occurs.

Less cushioning of the baby due to less aminotic fluid.

Baby compressed and does not develop properly -> Potter’s syndrome (fatal)

Most have end-stage renal failure by adulthood

51
Q

How is multicystic dysplastic kidney different from PKD?

A

One kidney is made up of many cysts, other is normal.

52
Q

How is multicystic dysplastic kidney diagnosed?

A

Antenatal USS

53
Q

What are complications of having a single kidney?

A

UTI
HTN
CKD

54
Q

Give the two types of PKD. Which presents more commonly in children?

A

ARPKD
ADPKD

ARPKD is more common in children

55
Q

Which gene/chromosome results in ARPKD?

A

PKHD1 gene on chromosome 6

Codes for FPC complex

56
Q

Give pathological features of PKD on the developing fetus

A
Cystic enlargement of renal collecting ducts
Oligohydramnios
Pulmonary hypoplasia
Potter syndrome
Congenital liver fibrosis
57
Q

List complications of PKD

A
Liver fibrosis --> failure
Portal HTN --> oesophageal varices
Progressive renal failure
HTN 
Chronic lung disease
58
Q

Briefly, what is the pathology in nephrotic syndrome?

A

Basement membrane in the glomerulus becomes highly permeable to protein.

Protein leaks from blood into urine.

59
Q

Which ages is nephrotic syndrome most common in?

A

2-5 years old

60
Q

Frothy urine
Generalised oedema
Pallor

All features in what?

A

Nephrotic syndrome

61
Q

What is the classic triad of nephrotic syndrome?

A

Hypoalbuminaemia
Proteinuria (3+ protein on dipstick)
Oedema

62
Q

Give 3 other features (apart from classic HPO triad) in nephrotic syndrome

A

Hyperlipidaemia, cholesterol
HTN
Hyper-coagulability

63
Q

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

A

Minimal change disease

64
Q

Causes of nephrotic syndrome?

A

Primary: no underlying cause

Secondary to:
Intrinsic kidney disease (focal segmental glomeruloscelorosis) or membranopoliferative glomerulonephritis

Secondary to:
Systemic illness:
HSP
Diabetes
Infection (HIV/hepatitis/malaria)
65
Q

Give the standard investigations for minimal change disease. What will they show?

A

Renal biopsy with microsocopy (shows no abnormality)

Urinalysis (shows small molecular weight proteins and hyaline casts)

66
Q

How is minimal change disease treated?

A

Corticosteroids - prednisolone

67
Q

How is nephrotic syndrome managed conservatively?

A

Low salt diet

68
Q

How is nephrotic syndrome managed pharmacologically?

A
High dose steroids (prednisolone)
Diurietics (for oedema)
Albumin infusions (severe hypoalbuminaemia)
Antibiotic prophylaxis (severe cases)
69
Q

How can steroid resistant nephrotic syndrome be treated?

A

ACE inhibitors

Immunosuppresants (cyclosporin, tacrolimus, rituximab)

70
Q

How is fluid shifted in nephrotic syndrome and why?

A

Hypovolaemia (low fluid intravasc), oedema (high fluid extravasc) and low BP

All due to loss of oncotic pressure in blood vessels as proteins leak into urine!

71
Q

Give some complications of nephrotic syndrome

A
Oedema
Low BP
Thrombosis
Infection (immunoglobulins leak into urine)
Acute or chronic renal failure
Relapse
72
Q

Give the classic triad for nephritis

A

Reduction in kidney function
Haematuria
Proteinuria

73
Q

2 most common nephritis causes in children?

A

Post-streptococcal glomerulonephritis (Group B strep)

IgA nephropathy (Berger’s disease)

74
Q

Tonsillitis —> nephritis

What is the causative pathogen

A

Strep pyogenes (Group B strep)

75
Q

How does Group B strep cause nephritis? Give the pathophysiology

A

Immune complexes made of strep antigens, antibodies and complement get stuck in glomeruli and cause inflammation

Leads to acute loss of kidney function –> AKI

76
Q

How is post-strep glomerulonephritis diagnosed?

A

Recent tonsillitis

Positive throat swab

Anti-streptolysis antiobody titres (ASO) on blood test

77
Q

How is post-strep glomerulonephritis treated?

How about if kidney function worsens?

A

Supportive treatment

If kidney function worsens:
Anti-HTN meds
Diuretics (if HTN/oedema)

78
Q

What is IgA nephropathy also known as?

A

Berger’s disease

79
Q

What other condition is IgA nephropathy related to?

A

HSP (this is an IgA vasculitis)

80
Q

Which antibody can cause inflammation in kidneys by leaving deposits and “glomerular mesangial proliferation”?

A

IgA (in IgA nephropathy - a type of nephritis)

81
Q

What ages does IgA nephropathy usually present in?

A

Teenagers/young adults

82
Q

How to treat a child with IgA nephropathy?

A

Supportive treatment of renal failure

Immunosuppressants (steroids/cyclophosphamide) to slow disease progression

83
Q

How is IgA nephropathy diagnosis confirmed?

A

Renal biopsy with histology.

Shows IgA deposits and glomerular mesangial proliferation.