Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Paediatrics > Kidney and Urinary Tract Disorders > Flashcards

Kidney and Urinary Tract Disorders Flashcards

1
Q

GFR at 28 weeks gestation compared to term infant

A

At 28 weeks the GFR is only 10% of term infant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

GFR at term

A

15-20ml/min per 1.73m2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Changes in GFR post-partum

A

Rapidly rises to 1-2 years of age when adult rate of 80-120ml/min per 1.73m2 is reached

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How are congenital renal abnormalities identified?

A

Before antenatal US they wouldn’t be detected until caused symptoms in infancy/childhood or occasionally adulthood - now detected in utero

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is renal agenesis?

A

Absence of both kidneys congenitally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is Potters syndrome?

A

Oligohydramnios due to decreased urine production due to renal problems (as urine makes up majority of amniotic fluid) leading to fatal condition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Symptoms of Potters syndrome?

A

Specific facies with low-set ears, beaked nose, prominent epicanthic folds
Pulmonary hypoplasia
Deformed limbs
May be stillborn or die soon after birth due to resp. failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Plasma Creatinine concentration in children

A

Main test of renal function

Rises progressively throughout childhood according to height and muscle bulk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

eGFR in children

A

Better measure of renal function than creatinine and useful to monitor renal function serially in children with renal impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Inulin or EDTA GFR in children

A

More accurate as clearance from plasma of substrates freely filtered and not secreted or reabsorbed - but need for repeated blood tests limits use in children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Creatinine clearance in children

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Plasma urea concentration in children

A

Same as adults

Increased in renal failure often before creatinine starts rising, raised levels may be symptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is DMSA scan?

A

Static scan of renal cortex - detects functional defects such as scars but v.sensitive therefore need to wait 2 months after UTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is Micturating cystourethrogram?

A

MCUG - contrast into bladder through urethral catheter - visualise bladder and urethral anatomy - detects reflux and obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is MAG3 renogram?

A

Dynamic isotope scan - measures urinary drainage - best performed with high urine flow
In children >4 (can cooperate) can identify reflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is multicystic dysplastic kidney (MCDK)?

A

Results from failure of union of ureteric bud (ureter/pelvis/calyces/collecting duct) with nephrogenic mesenchyme
Therefore leaves non-functioning structure with multiple large fluid-filled cysts - no renal tissue and no collection to bladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What happens normally to MCDK?

A

Half will have involuted by 2 years of age

Nephrectomy only indicated if remains large or hypertension develops (rare)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is risk with MCDK?

A

Produce no urine therefore if bilateral will get Potters syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Other causes of large cystic kidneys other than MCDK?

A

Autosomal recessive and autosomal dominant polycystic kidney disease and tuberous sclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Difference between other cystic kidney disorders and MCDK?

A

Bilateral BUT some or normal renal function is maintained

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Main symptoms of ADPKD in childhood?

A

Hypertension, haematuria

Renal failure in late adulthood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Extra-renal symptoms with ADPKD? x4

A

Cysts in liver and pancreas, cerebral aneurysms and mitral valve prolapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What can abnormal caudal renal migration lead to x2 and possible consequence x2?

A

Pelvic kidney or horseshoe kidney (lower poles fused in midline) can predispose to infection or obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What does premature division of the ureteric bud lead to?

A

Duplex system - can be bifid pelvis or complete division with two ureters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Consequence of duplex system x3

A

Ureters frequently have abnormal drainage so ureter from lower pole moiety often refluxes, whereas upper pole may drain ectopically into urethra or vagina or may prolapse into bladder - therefore obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is bladder extrophy?

A

Exposed bladder mucosa as a result of failure of fusion of infraumbilical midline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is absent musculature syndrome/prune belly syndrome?

A

Absence or severe deficiency of anterior abdominal wall muscles - frequently associated with a large bladder and dilated ureters and cryptorchidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Where can obstruction occur in boys?

A

Posterior urethra due to mucosal folds or a membrane called posterior urethral valves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What can occur in severe obstruction

A

Dysplastic kidney - small, poorly functioning and may contain cysts and aberrant embryonic tissue
Most severe = Potters syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Antenatal treatment for obstruction

A

Intrauterine bladder drainage procedures have been attempted but results have been disappointing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Postnatal management of obstruction

A

Can start prophylactic antibiotics to prevent UTI
If bilateraly hydronephrosis detected in male then ultrasound within 48h to exclude posterior urethral valves
In females or if unilateral hydronephrosis then wait 4-6weeks before US to allow GFR and urine flow to increase because mild outflow obstruction may not be detected with low GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Management of posterior urethral valves

A

Cystoscopic ablation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Why is UTI in childhood important? x2

A

because up to 1/2 have a structural abnormality in urinary tract
and pyelonephritis may damage growing kidney leaving scars which predispose to hypertension and chronic renal failure if bilateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

UTI presentation in infants

A

Non-specific, fever normally always present, otherwise generally unwell, lethargy, vomiting, prolonged jaundice and poor feeding etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

UTI presentation in older children

A

Classical symptoms of loin pain, dysuria, enuresis and frequency become more common with increasing age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Different ways of obtaining a urine sample from a child?

A

Clean-catch sample when nappy is removed (recommended)
Adhesive plastic bag attached to perineum after careful washing
Catheter - if urgent
Suprapubic aspiration if child unwell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Nitrites in children

A

Positive result very likely UTI - but some can have nitrite-negative UTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Leucocyte in children

A

May be present in UTI but may also be negative
May be present in febrile illness in child without UTI
Positive in balanitis and vulvovaginitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Normal origin of bacteria causing UTI in children?

A

Usually from bowel flora unless neonate in which case it is usually haemotogenous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Bacterial cause of UTI in infant?x4

A

Most common is e.coli (80%)

But can also be proteus, pseudomonas, klebsiela and strep.faecalis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What dose proteus UTI predispose to

A

Formation of struvite stones - splits urea to ammonia and thus alkalinising the urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What does pseudomonas UTI indicate

A

Presence of some structural abnormality hindering drainage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is vesicoureteric reflux (VUR)?

A

Developmental abnormality at vesicoureteric junctions - ureters displaced laterally and enter directly rather than at angle therefore with short or absent intramural course

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What can severe cases of VUR be associated with?

A

Renal dysplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Inheritance of VUR

A

familial with 30-50% chance of occurring in 1st degree relative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Variation in severity of VUR?

A

Can be mild reflux into end of undilated ureter during micturition to severest which is reflux during bladder filling and voiding - distended ureter and clubbed calyces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What can severe VUR lead to?

A

Intrarenal reflux (IRR) - very high risk of scarring if UTI occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What usually happens to VUR?

A

It usually resolves with age - especially low grade VUR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is reflux nephropathy?

A

Small, scarred and shrunken poorly-functioning section of kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Management of child with UTI if atypical infection

A

Atypical = seriously ill, poor urine flow, abdominal/bladder mass, raised creatinine, failure to respond to antibiotics within 48hr, non-e.coli - then USS with DMSA and MCUG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Investigation of UTI

A

Ultrasound and MCUG (if abnormal USS findings)

52
Q

Management of infants less than 3 months old with UTI

A

Hospitalised and IV antibiotics until temperature has settled and then oral antibiotics

53
Q

Management of acute pyelonephritis/upper UTI in >3 months old (bacteriuria and fever or loin pain/tenderness even if no fever)

A

Co-amox, cefalexin or cefixime (over 6m)

7-10days

54
Q

Management of lower UTI/cystitis in >3 months old

A

Oral ab’s eg. trimethoprin ,cefalexin or amoxicillin for 3 days

55
Q

Prevention of UTI x7

A

High fluid intake
Regular voiding
Double micturition
Prevention of constipation
Good perineal hygiene
Lactobacillus acidophilus probiotic to reduce other organisms in gut
Antibiotic prophylaxis if under 2 years old with abnormalities of kidneys or urinary tract, upper UTI or severe reflux (trimethoprim)

56
Q

What is daytime enuresis?

A

lack of bladder control during the day in a child old enough to be continent (3-5years)

57
Q

Causes of daytime enuresis?x7

A 
Lack of attention to bladder sensation 
Detrusor instability 
Weakness of bladder neck 
Neuropathic bladder 
UTI 
Constipation 
Ectopic ureter - constant dribbling
58
Q

What is neuropathic bladder?

A

Distended/enlarged bladder - fails to empty properly, irregular thick wall
Associated with spina bifida and other neurological conditions

59
Q

Investigation of daytime enuresis x5

A 
Neurological exam 
US 
Urodynamic studies 
X-ray or MRI may show spinal abnormalities
Microscopy, culture and sensitivity
60
Q

Management of daytime enuresis if no neurological cause

A

Star charts, bladder training and pelvic floor exercises

If this fails then anticholinergic drugs to reduce bladder contractions eg. oxybutynin

61
Q

What is secondary enuresis?

A

Loss of previously achieved urinary continence

62
Q

Causes of secondary enuresis? x3

A

Emotional upset (commonest)
UTI
Polyuria from osmotic diuresis eg. DM or renal concentrating disorder eg. sickle or chronic renal failure

63
Q

Investigation of secondary enuresis x3

A

Urine test for infection, glycosuria and proteinuria
Assessment of urinary concentrating ability by measuring osmolality of an early morning sample
US of renal tract

64
Q

When can transient proteinuria occur in children?

A

During febrile illness or after exercise - does not require investigation

65
Q

Common cause of persistent proteinuria in children? Diagnosis and management

A

Orthostatic proteinuria - only found when child is upright aka during the day
Diagnosed by measuring urine protein/creatinine ratio in series of early morning urine specimens
Prognosis is excellent no further investigation needed

66
Q

Clinical signs of nephrotic syndrome x4

A

Periorbital oedema
Scrotal, vulval, leg and ankle oedema
Ascites
Breathlessness due to pleural effusions and abdominal distention

67
Q

What occurs pathologically in nephrotic syndrome?

A

Heavy proteinuria results in low plasma albumin and oedema

68
Q

What can be used to treat the majority of nephrotic syndromes in children?

A

85-90% of children with nephrotic syndrome - proteinuria resolves with corticosteroid therapy and therefore do not progress to renal failure = Steroid-sensitive nephrotic syndrome

69
Q

Treatment regime in Steroid-sensitive nephrotic syndrome?

A

Oral steroids daily for 4 weeks and then reducing regime on alternate days until stopping

70
Q

Response to steroids in SSNS

A

Usually urine is protein free after 11 days - but now good evidence that extending initial course of steroids can reduce relapse

71
Q

Features suggesting SSNS x5

A 
Age 1-10 years
No macroscopic haematuria
No hypertension 
Normal complement levels 
Normal renal function
72
Q

Serious complications of nephrotic syndrome x4

A

Hypovolaemia (in extravascular space therefore intravascularly depleted - treat with IV albumin)
Thrombosis (loss of antithrombin in urine, thromocytosis increased with steroids, increased viscosity from raised haemotocrit)
Infection (esp. pneumococcus)
Hypercholesterolaemia (don’t know why)

73
Q

Steroid-resistant nephrotic syndrome management?

A

Refer to specialist

Diuretics, salt restriction, ACEi and sometimes NSAIDs - for oedema

74
Q

What is congenital nephrotic syndrome?

A

Presents in first 3 months of life - recessively inherited (consangueous families)
High mortality due to complications of hypoalbumnaemia rather than renal failure

75
Q

Management of congenital nephrotic syndrome

A

May need nephrectomy - followed by dialysis until can have renal transplant

76
Q

Signs of glomerular haematuria

A

Brown urine, presence of deformed red cells (as pass through BM), often with proteinuria

77
Q

Signs of lower UT haematuria

A

Red colour, at beginning or at end
No proteinuria
Unusual in children

78
Q

Most common cause of haematuria

A

UTI (usually not only symptom though)

79
Q

Pathology of acute nephritis

A

Increased glomerular cellularity restricts blood flow and therefore decreased filtration

80
Q

Symptoms of acute nephritis x4

A

Decreased urine output and volume overload
Hypertension (seizures)
Oedema esp. around eyes
Haematuria and proteinuria

81
Q

What is post-streptococcal nephritis

A

Follows streptococcal sore throat or skin infection - common in developing countries but uncommon in developed - prognosis is good

82
Q

What is Henoch-Schonlein purpura?

A

Combination of skin rash, arthralgia, oedematous joints (knees and ankles), abdominal pain and glomerulonephritis

83
Q

When does Henoch-Schonlein purpura occur and in who? x4

A

Ages 3-10, peak in winter
More common in boys (x2)
Often preceeded by URTI

84
Q

Presenting feature in Henoch-Schonlein purpura

A

Rash and fever

85
Q

Where is rash found in HSP? and what sort

A 
Buttocks
Extensor surfaces of arms and legs 
Ankles
Not on torso 
Maculopapular and purpuric
86
Q

Joint pain in HSP x3 details

A

Occurs in 2/3rds - especially ankles and knees where there is periarticular oedema - no longterm damage to joints

87
Q

Abdominal symptoms in HSP

A

Colicky abdominal pain - treated with steroids
GI petechiae can cause haematemesis and melaena
Intussusception can occur

88
Q

Renal in HSP

A

Over 80% have microscopic or macroscopic haematuria or mild proteinuria
Not usually 1st symptom
Make complete recovery normally

89
Q

If severe proteinuria in HSP

A

Nephrotic syndrome may result

90
Q

Presentation of IgA nephropathy

A

Episodes of macroscopic haematuria

Associated with URTI

91
Q

What is Alport syndrome? x4

A

Most common familial nephritis
X-linked recessive
Progresses to end-stage renal failure by early adult life in males
Associated with nerve deafness and ocular defects

92
Q

Other vasculitis causing haematuria and other symptoms

A

Wegener disease - prominent involvement of respiratory tract
Also get fever, malaise, weight loss, skin rash and arthropathy
ANCA positive

93
Q

Treatment of vasculitis causing haematuria eg. Wegeners x3

A

Steroids, plasma exchange and IV cyclophosphamide

94
Q

Presentation of HTN in children x6

A

Vomiting, headache, facial palsy, convulsions, hypertensive retinopathy or proteinuria

95
Q

Most common features of HTN in infants x2

A

Failure to thrive and cardiac failure

96
Q

Causes of unilateral palpable kidneys x5

A 
MCKD 
compensatory hypertrophy
Obstructed hydronephrosis
Renal tumour (Wilms)
Renal vein thrombosis
97
Q

Causes of bilateral palpable kidneys x4

A

ADPKD (adults) and ARPKD (children)
Tuberous sclerosis
Renal vein thrombosis

98
Q

Which polycystic kidney disease presents with enlarged kidneys early in life

A

Recessive - associated with hypertension, hepatic fibrosis and progresses to chronic renal failure
Dominant is benign in childhood and renal failure onset is in adulthood

99
Q

Commonest type of renal stones in children and cause?

A

Struvite stones caused by proteus

100
Q

Stones which occur with most common metabolic abnormality in children?

A

Calcium stones occurring in idiopathic hypercalciuria - increased urinary urate and oxalate excretion

101
Q

Presentation of renal stones in children x4

A

Haematuria, loin/abdominal pain, UTI or passage of stone

102
Q

What is Fanconi syndrome?

A

Generalised proximal tubular dysfunction leading to inadequate reabsorption

103
Q

What does Fanconi syndrome cause pathologically?

A

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

104
Q

Presentation of Fanconi syndrome x5

A 
Polydipsia and polyuria
Salt depletion and dehydration 
Hyperchloraemic metabolic acidosis 
Rickets 
Failure to thrive/poor growth
105
Q

Commonest type of acute kidney injury in children?

A

Prerenal

106
Q

What occurs in renal acute kidney injury

A

Salt and water retention, blood/protein/casts often in urine
May be symptoms specific to the cause

107
Q

Management of prerenal causes of AKI

A

Prerenal AKI is suggested by hypovolaemia therefore correct this - fluid replacement and circulatory support

108
Q

Management of renal failure AKI

A

If circulatory overload then fluid restrict and diuretics to increase urinary output
Manage electrolyte imbalances
Treat cause - may need biopsy to identify it

109
Q

Two commonest causes of renal failure AKI in children in UK

A

Haemolytic Uraemic Syndrome

Acute Tubular necrosis

110
Q

Management of post-renal AKI

A

Relieve obstruction by nephrostomy or bladder catheterisation
Correct obstruction with surgery once fluid and electrolytes have been corrected

111
Q

What is Haemolytic Uraemic syndrome (HUS)?

A

Triad of acute renal failure, microangiopathic haemolytic anaemia and thrombocytopenia

112
Q

What is HUS typically caused by

A

Secondary to GIT infection with verocytotoxin producing E.coli
Acquired through farm animals or eating uncooked beef

113
Q

Prodrome for HUS

A

Bloody diarrhoea

114
Q

Pathology of HUS

A

Toxin localises to kidney - causes intravascular thrombogenesis
Coagulation cascade activated, normal clotting (unlike DIC) - platelets consumed - microangiopathic haemolytic anaemia occurs due to damage to RBC as pass through microcirculation which is occluded

115
Q

What organs other than kidneys can be affected by HUS x3

A

Pancreas, brain and heart

116
Q

Management of HUS

A

Early support and dialysis when prodrome of bloody diarrhoea can give good prognosis
Follow up needed
If no prodrome, may be familial and frequently relapses - high risk of HTN and chronic renal failure

117
Q

Chronic kidney disease in children

A

Very rare

10 per million each year

118
Q

Causes of chronic kidney disease in children

A

Congenital and familial are more common in childhood than acquired diseases

119
Q

Clinical features of CKD in children x8

A

Anorexia and lethargy
Polydipsia and polyuria
Failure to thrive/grow
Bony deformities from renal osteodystrophy
HTN
Acute on chronic renal failure precipitated by infection/dehydration
Proteinuria
Unexplained normochromic, normocytic anaemia

120
Q

Aims of management of CKD in children

A

Prevent symptoms and metabolic abnormalities of CKD to allow normal growth

121
Q

Management of CKD against anorexia and vomiting

A

Calorie supplements, may need NGtube or gastrostomy

Protein intake should be sufficient

122
Q

Pathology of renal osteodystrophy in CKD

A

Phosphate retention and hypocalcaemia due to decreased activation of vit D leads to secondary hyperparathyroidism - leading to osteitis fibrosa and osteomalacia

123
Q

Management of renal osteodystrophy in CKD x3

A

Phosphate restriction (decrease intake of milk products) calcium carbonate as phosphate binder and vit d supplementation

124
Q

Management of salt and water in CKD

A

Increased salt and water loss
Therefore salt supplements and water
Bicarbonate supplements to prevent acidosis

125
Q

Cause and management of anaemia in CKD

A

Reduced production of erythropoeitin and circulation of toxic metabolites to bone marrow - therefore recombinant human erythropoietin given

126
Q

Management of hormonal abnormalities in CKD

A

Recombinant human growth hormone given

127
Q

Optimal management of CKD

A

Renal transplant preferably from living related kidneys (higher success rate) and before dialysis is required. But dialysis in the meantime can be given - need to have a minimum weight before transplant can occur to avoid renal vein thrombosis

Paediatrics (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions