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Paediatrics > Renal and Urogenital > Flashcards

Renal and Urogenital Flashcards

1
Q

GFR in infants

A

15-20ml/min per 1.73m2

rapidly rises within 1-2 years of adult rate of 80-120ml

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2
Q

Abnormalities detectable on antenatal us screening

A

Renal agenesis -absence of both kidneys

Multicystic dysplastic kidney - failure of union of the ureteric bud and kidney replaced by cysts

ARPKD - autosomal recessive polycystic kidney disease and diffuse bilateral enlargement of both kidneys

ADPKD - autosomal dominant polycystic kidney - separate cysts of varying size between normal renal parenchyma - kidneys enlarged.

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3
Q

Signs of potter syndrome

A

low set ears
beaked nose
prominent epicanthic folds and downward slant to eyes

pulmonary hypoplasia causing resp failure

limb deformities

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4
Q

What is potter syndrome

A

intrauterine compression of the foetus from oligohydramnios caused by lack of foetal urine

infant may be stillborn or die soon after brith from resp failure

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5
Q

Plasma creatinine conc

A

main test of renal function - rises progressively throughout childhood according to height and muscle bulk.
may not be abnormal until renal function has fallen to less than half of normal

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6
Q

eGFR

A

eGFR = k x height (cm) / creatinine

better measure of renal function and useful to monitor.

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7
Q

Insulin or EDTA GFR

A

more accurate as clearance form the plasma of substances freely filtered at the glomerulus and is not secreted or reabsorbed by the tubules. need for repeated blood sampling over several hours limits use in children.

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8
Q

Creatinine clearance

A

required timed urine collection and blood tests. Rarely done in children as inconvenient and often inaccurate

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9
Q

Plasma urea conc

A

increased in renal failure and often before creatinine starts rising. Raised levels may be symptomatic
Urea levels also increased by high protein diet in catabolic states or due to GI bleeding.

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10
Q

Radio investigations of kidney and urinary tract

A

USS -

DMSA - detects functional defects

MCUG - bladder and urethral anatomy

MAG3 renogram - Dynamic scan

Plain abdo xray - spinal abnormalities.

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11
Q

Causes Unilateral hydronephrosis

A
  • pelviureteric junction obstruction
  • vesicoureteric junction obstruction
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12
Q

Causes Bilateral hydronephrosis

A

bladder neck obstruction
posterior urethral valves

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13
Q

Why is UTI in childhood important

A

Up to half of pt have a structural abnormality of their urinary tract

pylonephritis may damage the growing kidney by forming a scar - predisposing to hypertension and progressive kidney disease if the scarring is bilateral.

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14
Q

Presentation UTI in infants

A

Fever
vomiting
lethargy or irritability
poor feeding / faultering growth
jaundice
septicaemia
offensive urine
febrile seizure >6months.

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15
Q

UTI symptoms children

A

Dysuria, frequency, urgency
Abdo pain or loin tenderness
Fever with or without riggers
Lethargy and anorexia
Vomiting and diarrhoea
Haematuria
Offensive or cloudy urine
Febrile seizure
Recurrence of enuresis

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16
Q

Dysuria alone causes

A

Cystitis, vulvitis or balanitis in uncircumcised boys.

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17
Q

Dipstick Methods of testing UTI

A

Nitrate stick - positive

Leucocyte esterase stick - may be present - positive in balanitis and vulvovaginitis

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18
Q

Interpretation of results UTI

A

Leucocyte esterase and nitrate positive = UTI

Leucocyte + and nitrate - = start Abx treatment if clinical evidence

Leucocyte - and nitrate + = start Abx if clinical evidence

Leucocyte - and nitrate - = UTI unlikely

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19
Q

How to collect samples from a child in nappies

A

Clean catch - waiting clean pot when nappy removed

Adhesive plastic bag applied to perineum after careful washing - may be contamination with skin

Urethral catheter - if there is urgency in obtaining and sample and no urine has been passed

Suprapubic aspiration - fine needed inserted directly into bladder using US guidance.

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20
Q

Why are urinary white cells not able to be used in UTI

A

may lyse during storage and may be present in febrile children without UTI - or in vulvovaginitis and balanitis

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21
Q

Most common organism of UTI

A

e.coli, followed by klebsiella proteus, pseudomonas, and strep.faecalis

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22
Q

which bacteria is more commonly diagnosed in boys

A

Proteus - presence under the prepuce - predisposes the formation of phosphate stones by splitting urea to ammonia and thus alkalinising the urine.

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23
Q

What can pseudomonas indicate

A

presence of some structural abnormality in urinary tract affecting drainage and it is also more common in children with plastic catheters

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24
Q

Factors in incomplete bladder emptying

A
  • infrequent voiding - resulting in bladder enlargement
  • Vulvitis
  • Incomplete micturition with residual postmicruition bladder volumes
  • Obstruction by loaded rectum from constipations
  • neuropathic bladder
  • vesicoureteric reflux
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25
Q

Vesicoureteric reflux

A

Developmental anomaly of the vesicoureteric junctions. Ureters are displaced laterally and enter directly into the bladder rather than at an angle, with shortened or absent intramural course.

Severe cases associated with renal dysplasia

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26
Q

Different severity VUS

A

reflux into the lower end of an undulated ureter during micturition to the severest form with reflux during bladder filling and voiding with a distended ureter, renal pelvis and clubbed calyces.

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27
Q

Intrarenal reflux

A

back flow of urine from renal pelvis into papillary collecting ducts and is associate with a high risk of renal scarring if UTI occur.m

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28
Q

Why is VUR associated ureteric dilation important

A
  • urine returning to bladder from ureters after voiding results in incomplete bladder emptying which encourages infection
  • the kidneys may become infected - pyelonephritis - especially if infrarenal reflux
  • bladder voiding pressure is transmitted to the renal papillae which may contribute to renal damage if voiding pressures are high.
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29
Q

reflux nephropathy

A

infection destroy renal tissue leaving a scar and resulting in shrunken poorly functioning segment of kidney.

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30
Q

Atypical UTI

A

seriously ill or septicaemia
poor urine flow
abdominal or bladder mass
raised creatinine
failure to respond to suitable abx in 48 hours
infection with non e-coli

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31
Q

USS VUS

A

serious structural abnormalities and urinary obstruction
renal defects

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32
Q

When to use MCUG

A

urethral obstruction suspected

otherwise deferred 3 months after UTI

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33
Q

Management UTI <3 months

A

Hospital
IV ABx - co-amoxiclav for 5-7 days and then oral prophylaxis

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34
Q

Infants over 3 moths and acute pyelonephritis or upper UTI

A

oral abx - trimethoprim - 7 days or else IV for 2-4 days followed by oral for 7-10 days.

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35
Q

Infants over 3 months with lower UTI or cystitis

A

Abx orally for 3 days - trimethoprim or nitrofurantoin

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36
Q

Prevention of UTI

A

High fluid intake
Regular voiding
Ensure complete bladder emptying by encouraging child to try a second time to empty bladder.
Treatment and or prevention constipation
Good perineal hygiene
Lactobacillus acidophilus - probiotic
Abx prophylaxis - with congenital abnormality of kidney .

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37
Q

Causes of enuresis

A

lack of attention to bladder sensation
Detrusor instability
Bladder neck weakness
Neuropathic bladder - enlarged and fails to empty properly
UTI
Ectopic ureter - causing constant dribbling and child is always damp
Constipation

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38
Q

Causes of eneuresis

A

neuropathic bladder
Sensory loss in S2, S3 and S4 dermatomes
Spinal lesion
Ectopic ureter

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39
Q

Ix eneuresis

A

urine sample
USS
Xray spine
MRI - spinal defect

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40
Q

Management of children with enuresis and and no neurological cause

A

Star chart
Bladder training
Pelvic floor exercises.
Constipation treatment
Small portable alarm which detects when pad in pants which is activated by urine can be used when lack of attention to bladder sensation.

Anticholinergic drugs - oxybutynin to damped bladder contraction if all other methods fail

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41
Q

Secondary enuresis causes

A

Emotional upset
UTI
Polyuria from osmotic diuresis in DM or renal conc disorder

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42
Q

Ix of secondary enuresis

A

testing a urine sample
Assessment of urinary concentrating ability by measuring osmolality of early morning urine sample
USS of renal tract

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43
Q

Orthostatic Proteinuria

A

Only proteinuria when child is upright during the day - diagnosed by measuring the urine protein-creatinine ratio in a series of early morning samples.

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44
Q

Nephrotic syndrome

A

heavy proteinuria in a low plasma albumin and oedema.

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45
Q

Conditions associated with nephrotic syndrome

A

HSP
SLE
Infections - e.g. malaria
Allergens

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46
Q

Clinical signs of nephrotic syndrome

A

Periorbital oedema - particularly on waking

Scrotal or vulval, leg, and ankle oedema

Ascites

Breathlessness due to pleural effusions and abdominal distention

Infections - peritonitis, septic arthritis or sepsis due to loss of protective immunoglobulins in the urine.

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47
Q

Causes of proteinuria

A
  • orthostatic proteinuria
  • Glomerular abnormalities - minimal change disease, glomerulonephritis, abnormal glomerular basement membrane
  • Increased glomerular filtration pressure
  • Reduced renal mass in CKD
  • Hypertension
  • Tubular proteinuria
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48
Q

Steroid-sensitive nephrotic syndrome

A

Proteinuria resolves with corticosteroid therapy
Do not progress to chronic kidney disease
more common in boys than girls and more common in asian.

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49
Q

Features suggesting steroid nephrotic syndrome

A

age 1-10
no macroscopic haematuria
normal blood pressure
normal complement levels
normal renal function

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50
Q

Management of nephrotic syndrome

A

oral corticosteroids unless there are atypical features.

Starts at 60mg/m2 then after 4 weeks reduced to 40mg/m2 prednisolone on alternate days for 4 weeks then stopped.

51
Q

Minimal change on renal histology

A

usually normal on light microscopy but fusion of the specialised epithelial cells that invest the glomerular capillaries (podocytes) is seen on electron microscopy.

52
Q

Complications of nephrotic syndrome

A

Hypovolaemia
Thrombosis
Infection
Hypercholesterolaemia.

53
Q

Types of steroid resistant nephrotic syndrome

A
  • focal segmental glomerulosclerosis
  • Mesangiocapillary glomerulonephritis
  • Membranous nephropathy
54
Q

Management of steroid resistant nephrotic syndrome

A

diuretic therapy for oedema, salt restriction, ACE inhibitor and sometimes NSAIDS.

55
Q

Congenital nephrotic syndrome

A

first 3 months of life
high mortality - due to complications of hypoalbuminaemia rather than progressive CKD.

Unilateral nephrectomy is option and may be necessary and followed by dialysis for stage 5 CKD.

56
Q

Signs of glomerular haematuria

A

brown urine
presence of deformed red cells and casts
proteinuria.

57
Q

Causes of nonglomerular haematuria

A

infection
trauma to genitalia, urinary tract, or kidneys
Stones
Tumours
Sickle cell
Bleeding disorders
renal vein thrombosis
Hypercalciuria

58
Q

Causes of glomerular haematuria

A

acute or chronic glomerulonephritis
IgA nephropathy
Familial nephritis
Thin basement membrane disease - good pastures

59
Q

Ix haematuria

A

Urine microscopy
Protein and calcium excretion
Kidney and urinary tract US
plasma urea, electrolytes, creatinine, calcium phosphate and albumin

FBC

60
Q

Ix for glomerular haematuria

A

ESR
Throat swab and antistreptolysin O/anti-DNAse B titres
Hep B and C screen
Renal biopsy if indicated
test mothers urine for blood
Hearing test

61
Q

When is renal biopsy indicated

A

there is significant persistent proteinuria
There is recurrent macroscopic haematuria
Renal function is abnormal
The complement levels are persistently abnormal.

62
Q

Acute nephritis

A

increased glomerular cellularity restricts glomerular blood flow and therefore glomerular filtration is decreased.

63
Q

Symptoms of acute nephritis

A

Decreased urine output and volume overload
Hypertension
Oedema - especially around eyes.
Haematuria and proteinuria.

64
Q

Post streptococcal nephritis

A

follows strep sore throat or skin infection and is diagnosed by evidence of a recent infection
Culture of organism - raised ASO/ anti-DNAse B titres and low complement C3 levels that return to normal after 3-4 weeks.

65
Q

HSP symptoms

A

Characteristic skin rash on extensor surfaces
arthralgia
periarticular oedema
colicky abdominal pain
glomerulonephritis
Renal involvement

66
Q

Epidemiology and Pathophysiology HSP

A

Age 3-10 years - 2x as common in boys.
Peaks during winter months and is preceded by upper resp infection
Cause unknown.

Genetic predisposition and antigen exposure increase circulating IgA levels and IgG synthesis.
IgA and IgG interact to produce complexes that activate complement and are deposited in affected organs, precipitating an inflammation response with vasculitis.

67
Q

IgA nephropathy

A

episodes of macroscopic haematuria - commonly associated with upper resp infections.

68
Q

Familial nephritis

A

Alport syndrome

X-linked recessive disorder that progresses to progressive end stage CKD by early adult life in males and is associated with nerve deafness and ocular defects.

Mother may have haematuria

DDX - basement membrane disease

69
Q

Symptoms of vasculitis

A

Fever
malaise
weight loss
skin rash
arthropathy
Prominent involvement of resp tract in granulomatosis with polyangiitis.

70
Q

Vasculitis Ix

A

ANCA - antineutrophil cytoplasm antibodies are present.
Renal arteriography - presence of aneurysms will diagnose polyarteritis nodosa

71
Q

Management vasculitis

A

corticosteroids, plasma exchange and IV cyclophosphamide which may need to be continued for many months.

72
Q

SLE

A

Adolescent girls and young women.
Common in Asia and black
Presence of multiple autoantibodies, including antibodies to double stranded DNA.
C3 and C4 may be low, particularly during active phases.

haematuria and proteinuria are indications for renal biopsies, and immunosuppression is necessary.

73
Q

Hypertension causes

A

renal, cardiac or endocrine causes.

Renal parenchyma disease
Renovascular
Polycystic kidney disease
Renal tumours

Coarctation of aorta

Catecholamine excess - pheochromocytoma
Neuroblastoma

Endocrine - Congenital adrenal hyperplasia

Essential hypertension

74
Q

Presentation of hypertension

A

Vomiting
headaches
facial palsy
hypertensive retinopathy
convulsions or proteinuria
Faltering growth
Cardiac failure.

75
Q

Causes of unilateral palpable kidneys

A

Multicystic kidneys
Compensatory hypertrophy
Obstructed hydronephrosis
Renal tumour
Renal vein thrombosis

76
Q

Causes of bilateral palpable kidneys

A

ARPKD
ADPKD
Renal vein thrombosis

77
Q

Most common causes of renal stones

A

UTI
Structural abnormalities
Metabolic abnormalities - calcium containing stones

Most common are phosphate stones associated with infection - especially with proteus.

78
Q

Causes of nephrocalcinosis

A

Deposition of calcium in parenchyma
Hypercalciuria
Hyperoxaluria
Distal renal tubular acidosis.

Complication of furosemide therapy

79
Q

Generalised proximal tubular dysfunction - fanconi syndrome

A

Damage to proximal tubule cells vulnerable to cellular damage.

79
Q

Cardinal features of fanconi syndrome

A

Excessive urinary loss of amino acids, glucose, phosphate, bicarbonate, sodium, calcium potassium and magnesium.

80
Q

Symptoms of fanconi syndrome

A

Polydipsia,
polyuria
salt depletion and dehydration
Hypercholaraemic metabolic acidosis
rickets
faltering or poor growth.

81
Q

Causes of fanconi syndrome

A

Heavy metals, drugs and toxins, vit d deficiency

Cystinosis
Glycogen storage disorders
Galactosaemia
Fructose intolerance
Wilson disease

82
Q

Prerenal Causes of AKI

A

Hypovolaemia -
Gastroenteritis
Burns
Sepsis
Haemorrhage
Nephrotic syndrome

Circulatory failure

83
Q

Renal causes of AKI

A

Vascular - haemolytic uraemia syndrome, Vaculitis, Embolus, renal vein thrombosis

Tubular - acute tubular necrosis, ischaemia, toxic, obstructive

Glomerular - glomerulonephritis

Interstitial - interstitial nephritis
Pylonephritis

84
Q

Post renal causes AKI

A

Obstruction
congenital or acquired.

85
Q

Management AKI

A

Monitoring.
Surgery - once fluid volume and electrolyte abnormalities been corrected

86
Q

When is dialysis indicated

A

Failure of conservative management
Hyperkalaemia
Severe hyponatraemia or hyper
Pulmonary oedema or severe hypertension due to volume overload
Severe metabolic acidosis
Multisystem failure.

87
Q

Treatment of metabolic acidosis

A

Sodium bicarbonate

88
Q

Treatment hyperphosphataemia

A

Calcium carbonate and dietary restriction

89
Q

Treatment hyperkalaemia

A

Calcium glutinate if ECG changes
Salbutamol
Calcium exchange resin
Glucose and insulin
Dietary restriction
Dialysis

90
Q

What is haemolytic uraemic syndrome

A

Triad of acute renal failure, microangiopathic haemolytic anaemia and thrombocytopenia following a prodrome of bloody diarrhoea most often.

91
Q

Causes of typical HUS

A

secondary to GI infection with verocytotoxin-producing E-coli. Acquired through contact with farm animals, eating uncooked beef, or less often shigella.

92
Q

Pathophysiology HUS

A

Toxin enters GI mucosa and localises to endothelial cells of kidney where causes intravascular thrombogenesis.

Coagulation cascade activated and clotting is normal. Platelets are consumed in this process and microangiopathic haemolytic anaemia results from damage to red blood cells as they circulate;ate through microcirculation which is occluded.

93
Q

Atypical HUS features

A

No diarrhoea prodrome
May be familial and frequently relapses

High risk of hypertension and progressive chronic kidney disease with a high mortality.

94
Q

Treatment HUS

A

Typical - dialysis and supportive treatment

Atypical - monoclonal anti-terminal complement antibody eculizumab. - Plasma exchange more commonly used due to cost.

95
Q

Clinical features of CKD

A

Anorexia and lethargy
Polydipsia and polyuria
Faltering growth
Bony deformities
Hypertension
Acute-on chronic renal failure
Incidental finding of proteinuria
Unexplained normochromic, normocytic anaemia.

96
Q

Stage 1 CKD

A

> 90ml / min per 1.73m2
Normal renal function but structural abnormality or persistent haematuria or proteinuria.

97
Q

Stage 2 CKD

A

60-89ml/min per 1.73m2
Mildly reduced function, asymptomatic.

98
Q

Stage 3 CKD

A

30-59ml
Moderately reduced renalfunction with renal osteodystrophy

99
Q

Stage 4 CKD

A

15-29ml
Severely reduced renal function with metabolic derangement and anaemia

100
Q

Stage 5 CKD

A

<15ml
End stage renal failure - renal replacement therapy

101
Q

When do CKD symptoms develop in children

A

Stage 4 or when renal function falls to less than 1/3 normal

102
Q

Management CKD

A

prevent symptoms and metabolic abnormalities of CKD to allow normal growth and developments.

103
Q

Diet in CKD

A

anorexia and vomiting common.

Improving nutrition using calorie supplements and nasogastric or gastrostomy feeding often necessary.

104
Q

Causes CKD

A

Renal dysplasia
Obstructive uropathy
Glomerular disease
Congential nephrotic syndrome

105
Q

Renal osteodystophy

A

Phosphate retention and hypocalcemia due to decreased activation of Vit D

leads to secondary hyperparathyroidism, which results in osteitis fibrous and osteomalacia of the bones.

106
Q

Prevention of renal osteodystrophy

A

Phosphate restriction by decreasing dietary intake of milk
Calcium carbonate as a phosphate binder
Activated vit d supplements

107
Q

What causes anaemia in CKD

A

reduced production of erythropoetin and circulation of metabolites that are toxic to the bone marrow.

Recombinant human erythropoetin which is administered SC.

108
Q

Types of dialysis

A

Continuous cycling peritoneal dialysis - overnight

Continuous ambulatory peritoneal dialysis - manual exchanges over 24h

Haemodialysis - hospital 3-4 x weekly

109
Q

Management CKD

A

Diet
VIt D
Phosphate restriction

Salt supplements and free access to water

Bicarbonate supplements - prevent acidosis

Erythropeitin to prevent aneamioa

Growth hormone

Dialysis and transplantation

110
Q

Difference in nephrotic vs nephritic syndrome

A

Nephrotic Syndrome is defined by severe proteinuria, pronounced oedema, and usually normal blood pressure.

Nephritic Syndrome showcases hematuria, hypertension, and moderate glomerular damage.

Nephrotic syndrome occurs when glomeruli do not properly filter the protein albumin. Elevated levels of albumin in the urine is referred to as proteinuria.

Nephritic syndrome occurs when inflamed glomeruli do not properly filter red blood cells.

111
Q

What is phimosis

A

a tight foreskin that cannot be retracted behind the coronal sulcus to expose the glans. In children, this may be due to adhesions between the foreskin and the glans. These adhesions typically breakdown by 5-7 years old, and 99% are retractile by 17 years old.

112
Q

Management of phimosis

A

Phimosis warrants manual retraction of the foreskin. First, attempt to gently introduce an instillagel nozzle to find the urethral meatus. Then, insert a catheter by feel to identify the meatus.

If this is unsuccessful, the following actions may be taken:

Insertion of a suprapubic catheter to drain the bladder, with delayed management of phimosis until it is safe to do so

Emergency dorsal slit procedure to expose the meatus

Elective circumcision

113
Q

Indications for elective circumcision in children

A

Recurrent balanitis

Balanitis xerotica obliterans (BXO) / lichen sclerosis

Urinary tract infection (UTI) with structural abnormality (e.g. posterior urethral valves, neuropathic bladder, vesicoureteric reflux)

Recurrent UTIs

114
Q

Complications Phimosis

A

Paraphimosis: if the foreskin is retracted and unable to return to the anatomical position

Recurrent balanitis, balanoposthitis

There is a higher risk of penile squamous cell carcinoma in uncircumcised males due to a higher incidence of inflammatory episodes to the glans/prepuce

115
Q

Hypospadias

A

occurs due to failure of the urethral folds to fuse, resulting in an abnormal opening of the urethra on the inferior/ventral surface of the penis.

116
Q

Epispadias

A

the condition associated with an opening of the urethra on the superior/dorsal surface of the penis, and it is linked with bladder exstrophy

117
Q

Types of hypospadias

A

Subcoronal: The opening of the urethra is located somewhere near the head of the penis.

Midshaft: The opening of the urethra is located along the shaft of the penis.

Penoscrotal: The opening of the urethra is located where the penis and scrotum meet.

118
Q

Nocturnal enuresis

A

Known as ‘bed wetting’, this is a common problems of middle childhood

  • There is a genetically determined delay in acquiring sphincter competence and
    emotional stress can cause secondary enuresis however underlying disorders should always be considered:
    1. UTI
    2. Faecal retention which is severe enough to reduce bladder volume and cause
    bladder dysfunction
    3. Polyuria from osmotic diuresis

Management
- Explanation to the child and the parent that this is common and beyond conscious
control
- Star charts
- Enuresis Alarm which sounds when it becomes wet to awaken the child
- Desmopressin can be used to provide short term relief from bedwetting

119
Q

Medical management Nephrotic syndrome

A
  1. Corticosteroid therapy:
    - Prednisolone 60 mg/m2 /day in a single morning dose (maximum 80mg/day) for 28
    days.
    - Then reduce dosage to 40mg/m2 /alternate day (maximum 50mg/alternate day) given
    once daily, for 28 days and then stop without tapering.
  2. Diuretics may be needed to control oedema whilst the steroids are taking effect:
    furosemide 1-2mg/kg/day
  3. Diet with reduced salty food diet
  4. Pneumococcal immunisations - 23 valent pneumococcal polysaccharide vaccine
120
Q

Nephritic syndrome

A

Inflammation within the nephrons on the kidneys causing
- Reduction in kidney function - Haematuria
- Proteinuria

121
Q

Causes nephritic syndrome

A

Post strep B

IgA nephropathy

122
Q

Treatment nephritic syndrome

A
  • Supportive therapy of the renal failure
  • Diuretics and antihypertensive medications can be used for complications like HTN
    and oedema
  • Immunosuppressant medications such as steroids
123
Q
A

Paediatrics (17 decks)

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