Brainscape's Knowledge GenomeTM

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


See full index

4th Year > Paeds - renal (0-finals + textbook ckd) > Flashcards

Paeds - renal (0-finals + textbook ckd) Flashcards

1
Q

What are the 5 stages of CKD?

A

Stage 1 = eGFR >90ml/min

  • normal renal function, but structural abnormality or persistent haematuria or proteinuria

Stage 2 = 60-89ml/min

  • mildly reduced function

Stage 3 = 30-49 ml/min

  • moderately reduced renal function, renal osteodystrophy

Stage 4 = 15-29ml/min

  • severely reduced renal function, metabolic derangements, anaemia

Stage 5 = <15ml/min

  • end stage renal failure, renal replacement therapy required
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are some symptoms of stage 4-5 CKD in children?

(kidneys have pretty good compensatory mechanisms so mamy pts will be asymptomatic until significant impairment of kidney function)

A
  • anorexia, lethargy
  • polydipsia, polyuria
  • faltering growth/ growth failure
  • bony deformities from renal osteodystrophy (renal rickets)
  • HTN
  • Acute on chronic renal failure (precipitated by infection or dehydration)
  • Incidental finding of proteinuria
  • unexplained normochromic, normocytic anaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How would you manage the symptoms of CKD in children?

A

Anorexia and Vomiting

  • calorie supplements or NG/Gastrostomy feeding
  • ensure protein intake is sufficient to maintain growth and normal albumin

Prevention of renal osteodystrophy

  • Decrease dietary intake of milk products to restrict phosphate
  • calcium carbonate as phosphate binder
  • activated Vit D supplements

Prevention of salt/water loss (common in ckd caused by congenital structural malformations and renal dysplasia)

  • salt supplements
  • access to water
  • Bicarbonate supplements to prevent acidosis

Anaemia

  • Subcutaneous Recombinant human erythropoietin

Growth hormone resistance

  • recombinant human growth hormone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

When would dialysis be a management option in children?

A

Dialysis and Transplantation once stage 5 CKD is reached.

  • child must be >10kg to avoid risk of renal vein thrombosis
  • Immunosuppression with tacrolimus and mycophenolate mofetil and prednisolone
  • minimal steroid regimens to improve growth
  • Peritoneal dialysis can be either continuous cycling peritoneal dialysis (cycling overnight on a machine) OR continuous ambulatory peritoneal dialysis (manual exchanges over 24 hours)
    • can be done by parents at home
    • less disruptive to family life and child’s schooling
  • Haemodialysis = 3-4x a week in hospital
  • Ideally a child is transplanted before dialysis is required, but if not possible, a period of dialysis may be required.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the most common causes of CKD in children?

A

Congenital (structural malformations and hereditary nephropathies)

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

How would CKD typically be picked up early on in children?

A

an abnormal antenatal ultrasound

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

What are some other congenital abnormalities that can be detected on antenatal US screening?

A
  • renal agenesis (absence of both kidneys)
    • severe oligohydramnios as amniotic fluid is derived from fetal urine = Potters syndrome (fatal)
  • Multicystic dysplastic kidney
    • These are non functioning kidneys with large fluid filled cysts, atresia of the ureter, no renal tissue and no connection with bladder
    • Potters syndrome can occur if this is bilateral as no urine is produced.
  • Other causes of large kidneys (however these conditions are always bilateral and maintain some or normal renal function)
    • Autosomal Recessive Polycystic Kidney Disease (diffuse bilateral enlargement of both kidneys)
    • Autosomal Dominant Polycystic Kidney Disease (separate cysts of varying size between normal renal parenchyma)
    • Tuberous sclerosis
  • Abnormal caudal migration can cause a pelvic kidney or a horseshoe kidney
    • predisposition to infection or obstruction of urinary drainage
  • Obstruction to urine flow
    • at bladder neck due to eg. neuropathic bladder
    • at vesicoureteric junction
    • at pelvi-ureteric junction
    • at posterior urethra in males due to eg. posterior urethral valves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is Potter Syndrome?

A

Intrauterine compression of the foetus from oligohydramnios caused by lack of foetal urine (eg. from Bilateral renal agenesis or Bilateral multicystic dysplastic kidneys)

  • Potter facies = low set ears, beaked nose, prominent epicanthic folds, downward slant to eyes
  • Lung hypoplasia causing resp failure
  • Postural and Limb deformities (eg. severe talipes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How would you manage babies who have diagnosed congenital abnormalities postnatally?

A
  • start prophylactic antibiotics at birth to prevent UTI
  • In bilateral hydronephrosis/ dilated lower urinary tract in males
    • do an US within 48 hours of birth to exclude posterior urethral valves
    • If excluded, stop antibiotics and repeat US in 2-3 months
    • If abnormal US, do a Micturating Cystourethrogram and then surgery if required
  • due to low urine flow and low eGFR in a newborn kidney, mild outflow obstruction may not be immediately evident.
    • Eg. unilateral hydronephrosis in males, any anomaly in females
    • therefore US should be delayed to 4-6 weeks.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a posterior urethral valve?

A

When there is tissue at the proximal end of the urethra (closest to the bladder) that causes obstruction of urine output.

This results in a backpressure into the bladder, ureters, and up to the kidneys = hydronephrosis.

The bladder cannot fully empty so this increases the risk of UTI.

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

How would a posterior urethral valve present?

(antenatal and postnatal)

A

Antenatal

  • bilateral hydronephrosis
  • oligohydramnios = Potter syndrome and pulmonary hypoplasia + resp failure after birth

Postnatal

  • difficulty urinating
  • weak urinary stream
  • chronic urinary retention
  • palpable bladder
  • recurrent UTI
  • impaired kidney function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How would posterior urethral valve be diagnosed?

A

Antenatal scans

Postnatal (eg. investigations in young boys presenting with UTI)

  • Abdo US = enlarged thickened bladder and bilateral hydronephrosis
  • Micturating Cystourethrogram = shows location of extra urethra tissue and reflux of urine back into bladder
  • Cystoscopy = detailed view of extra urethral tissue
    • can also be used to ablate or remove extra tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How would you manage a posterior urethral valve?

A
  • temporary urinary catheter can be inserted to bypass valve while awaiting definitive management
  • Definitive management = ablation or removal of extra tissue during cystoscopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is hypospadias?

A

This is a congenital condition where the opening of the urethra (urethral meatus) is abnormally displaced posteriorly on the penis.

(90% are further towards the bottom of the glans, can also be halfway down the shaft or even at the base of the shaft)

Epispadias = meatus is displaced anteriorly on the top of the penis

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

“Chordee” is an associated condition that can occur, where the head of the penis bends downwards.

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

How would you diagnose and manage hypospadias?

A

It would be diagnosed on the examination of the newborn.

Management

  • refer to paediatric specialist urologist
  • Surgery at 3-4 months of age to correct position of meatus and straighten penis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Autosomal Dominant Polycystic Kidney Disease typically presents later in life.

What is Autosomal Recessive Polycystic Kidney Disease?

A
  • presents in neonates
  • Main features = cystic enlargement of renal collecting ducts, oligohydramnios, pulmonary hypoplasia, Potter syndrome, Congenital Liver Fibrosis
  • picked up on antenatal US scans
    • Oligohydramnios = Potter syndrome and pulmonary hypoplasia (resp failure shortly after birth)
    • Large Polycystic Kidneys that can take up a lot of space in the abdo and make it hard for neonates to breathe adequately
  • Mutation in the polycystic kidney and hepatic disease 1 (PKHD1) gene on Chromosone 6
    • this codes for fibrocystin/ polyductin protein complex which is responsible for tubules and healthy epithelial tissue in kidneys, liver, pancreas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What kinds of problems with people with PKD experience?

A
  • liver failure due to liver fibrosis
  • portal hypertension leading to oesophgeal varices
  • progressive renal failure
  • HTN due to renal failure
  • chronic lung disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are Multicystic dysplastic kidneys?

A

This is a condition where one of the kidneys is made up of many tiny cysts while the other is normal.

Rarely bilateral which will result in infant death.

Diagnosed on antenatal US scans.

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

What is the prognosis and management of MCDK?

A
  • the single healthy kidney can usually sustain a normal life
  • the cystic kidney will atrophy and disappear before 5 years of age
  • however 1 kidney can put person at risk of UTIs, HTN and CKD later in life
  • Follow up with renal US scans to monitor abnormal kidney
  • Prophylactic antibiotics can be used to prevent UTIs in working kidney
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is a hydrocele?

A

a collection of fluid within tunica vaginalis that surrounds the testes.

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

What is the difference between simple and communicating hydrocele?

A

Simple

  • fluid is trapped in the tunica vaginalis
  • Fluid usually gets reabsorbed over time and hydrocele disappears

Communicating

  • when tunica vaginalis is connected with the peritoneal cavity via the processus vaginalis
  • Therefore fluid travels from peritoneal cavity into hydrocele, allowing hydrocele to fluctuate in size
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What would you investigate and examine a hydrocoele?

A
  • smooth, soft, non-tender swelling around one testes
  • swelling is infront of and below testicle
  • simple = remain one size
  • communicating = fluctuate in size
  • Transilluminate with light

Ultrasound is useful for confirming diagnosis

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

How would you manage a hydrocoele?

A

Simple = usually resolve in 2 years. Reassure parents and follow up routinely.

Communicating = surgery to ligate connection between the peritoneal cavity and the hydrocele (processus vaginalis)

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

What is an undescended testes?

A

Normally, testes develop in the abdo and migrate down through the inguinal canal into the scrotum.

However in 5% of boys, the testes do not make it out of the abdo by birth = Undescended Testes (or Cryptorchidism)

  • however you can sometimes palpate partially descended testes in the inguinal canal

Undescended testes after puberty increases the risk of testicular torsion, infertility and testicular cancer

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

What are retractile testicles?

A

In pre-pubertal boys when testes will move out of the scrotum and into the inguinal canal when it is cold or the cremasteric reflex is activated.

Will usually resolve as they go through puberty and testes settle in the scrotum.

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

How would you manage undescended testes?

A
  • watching and wait in newborns
  • Usually they will descend in the first 3-6 months.
  • If they have not descended by 6 months, refer to paediatric urologist
  • Orchidopexy is carried out between 6-12 months old
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is a Wilms’ tumour?

A

specific type of tumour affecting the kidney in children (usually under 5 years old)

28
Q

When would you consider a Wilms tumour?

A
  • under 5 years old presenting with a mass in the abdo
  • abdo pain
  • haematuria
  • lethargy
  • fever
  • HTN
  • weight loss
29
Q

How would you diagnose a Wilms tumour?

A
  • Abdo US to visualise kidneys
  • CT/MRI to stage tumour
  • Biopsy to identify histology
30
Q

How would you manage a Wilms tumour?

A

Surgery

  • surgical excision of the tumour along with the affected kidney (nephrectomy)

Adjuvant treatment (after surgery)

  • adjuvant chemotherapy
  • Adjuvant radiotherapy
31
Q

What is Haemolytic Uraemic Syndrome?

A

A triad of acute kidney injury, microangiopathic haemolytic anaemia, and thrombocytopaenia.

Usually secondary to Gastrointestinal infection due to a toxin produced by E.Coli 0157 (through eating uncooked beef or conatact with farm animals) or less commonly Shigella.

The Toxin enters gastrointestinal mucosa and preferentially localises to the endothelial cells of the kidney where it causes intravascular thrombogenesis.

  • Coagulation cascade is activated and clotting is normal (unlike DIC)
  • platelets are consumed in this process
  • MHAnaemia occurs when RBC try to circulate through the occluded microcirculation and get damaged
32
Q

How would HUS present?

A
  • EColi 0157 causes gastroenteritis and blood diarrhoea
  • HUS syndrome symptoms typically start around 5 days after onset of diarrhoea
    • Reduced urine output
    • haematuria or dark brown urine
    • abdo pain
    • lethargy and irritability
    • confusion
    • oedema
    • HTN
    • bruising
33
Q

How would you manage HUS?

A
  • it is a medical emergency!
  • urgent referral to paediatric renal unit for renal dialysis
  • Antihypertensives if required
  • careful maintenance of fluid balance
  • blood transfusions if required
34
Q

When is acute on chronic renal failure suggested?

A

a child having growth failure, anaemia and disordered bone mineralization (renal osteodystrophy)

35
Q

What are some prerenal, renal and Postrenal causes of AKI?

A

Prerenal (most common cause in children)

  • hypovolaemia (gastroenteritis, burns, sepsis, haemorrhage, nephrotic syndrome)
  • Circulatory failure

Renal

  • vascular (HUS, vasculitis, embolus, renal vein thrombosis)
  • tubular (ATN, ischaemic, toxic, obstructive)
  • glomerular (glomerulonephritis)
  • interstitial (interstitial nephritis, pyelonephritis)

Postrenal

  • congenital obstruction eg. posterior urethral valves
  • acquired obstruction eg. blocked urinary catheter
36
Q

How would nephrotic syndrome present?

A
  • Triad of generalised oedema, heavy proteinuria (>200mg/mmol), hypoalbuminaemia (<25g/L)
    • ​if children present with these 3 features, this is typical nephrotic syndrome. you can just manage them with steroids without the need for a diagnostic renal biopsy.
  • If children present with the following atypical features, you would need to do a diagnostic renal biopsy to confirm
    • age <1 or >12 years old
    • HTN
    • impaired renal function
    • frank haematuria
    • steroid resistant nephrotic syndrome
37
Q

What is the pathophysiology of nephrotic syndrome?

A
  • a damaged glomerulus, resulting in protein leaking out
    • different to nephritis which is inflammation that can involve any part of the nephron or interstitium
  • Podocytes on the GBM are usually fused together to prevent proteins the size of albumin or larger from being filtered
    • in nephrotic syndrome, the podocytes become flattened and allow the leaking of these proteins.
  • Most common cause in children is Minimal Change Disease
    • other causes are congenital nephrotic syndromes, focal segmental glomerulosclerosis, mesangiocapillary glomerulonephritis
38
Q

What else would you consider as a differential when presented with a child with swelling?

A
  • Heart failure (look for heart murmur, breathlessness, cyanosis, hepatomegaly)
  • Allergic reaction especially in facial oedema (hx of potential allergen, sudden onset of symptoms, associated rash, wheeze, stridor)
  • Malnutrition eg. Kwashiorkor
39
Q

What investigations would you do for typical nephrotic syndrome?

A
  • urine dip
  • urine protein:creatinine ratio
  • U&Es
  • FBC
  • Serum albumin
  • Varicella Zoster Serology

Atypical features:

  • Complement levels
  • Hepatitis serology
  • Anti-streptolysin O Titre
  • Autoimmune investigations eg. ANA, ANCA, anti-dsDNA
40
Q

How would you medically manage nephrotic syndrome?

A
  • high dose steroids is 1st line
    • if atypical presentation, make sure to discuss with nephrologist before treatment as steroids can affect results of renal biopsy
  • The majority of kids with minimal change disease will respond to steroids = Steroid Sensitive Nephrotic Syndrome
    • However most will have a relapse (which will respond to further courses of steroids) until they eventually reach remission
    • Some kids have more than one relapse
      • = Frequently Relapsing Nephrotic Syndrome OR Steroid-resistant Nephrotic Syndrome
      • these kids may need low-dose maintenance steroid therapy or immunomodulatory drugs like Levamisole, Cyclophosphamide, Ciclosporin, Tacrolimus
  • Prophylactic antibiotics as kids with nephrotic syndrome can leak immunoglobulins through their kidneys and are at high risk of infection
41
Q

How would you manage nephrotic syndrome lifestyle wise?

A
  • low salt diet to prevent worsening oedema
42
Q

What are some complications of nephrotic syndrome?

A
  • assess childrens hydration status!
    • although they are peripherally oedematous, they may be intravascularly deplete = try albumin but give with care
    • Also assess for fluid overload as they can retain salt and become overloaded = try Diuretics
  • Infection risk due to high dose steroids or immunosuppressants
    • prophylactic antibiotics
    • educate parents to seek urgent medical attention if child develops infectious symptoms or has fever >38C
  • Varicella Zoster risk due to high dose steroids or immunosuppressants
    • may require VZV immunoglobulin or IV acyclovir
  • Thrombosis
    • these children are in a pro-thrombotic state so think PE in chest pain or Mesenteric Ischaemia in abdo pain
43
Q

How would you differentiate between glomerular and LUT haematuria?

A
  • glomerular haematuria is usually brown, there are deformed red cells and casts, and is often accompanied by proteinuria
  • LUT Haematuria is usually red, occurs at the beginning or end of the urinary stream
44
Q

What are some causes of glomerular haematuria?

A
  • acute glomerulonephritis (usually with proteinuria)
  • Chronic glomerulonephritis
  • IgA Nephropathy
  • Familial nephritis eg. Alports Syndrome
  • Thin Basement Membrane Disease
45
Q

What are some causes of non glomerular haematuria?

A
  • Infection eg. TB, Schistosomiasis, etc
  • Trauma to genitalia, urinary tract, kidneys
  • Stones
  • Tumours
  • Sickle cell disease
  • Bleeding disorders
  • Renal vein thrombosis
  • Hypercalciuria
46
Q

How would you investigate haematuria?

A
  • Urine microscopy (with phase contrast) and culture
  • Protein and Calcium excretion
  • Kidney and urinary tract US
  • Plasma urea, electrolytes, creatinine, calcium, phosphate, albumin
  • FBC, platelets, coagulation screen, sickle cell screen

If you suspect glomerular haematuria:

  • ESR, complement levels, anti-dsDNA antibodies
  • Throat swab and antistreptolysin O/ anti-DNAse B titres
  • Hepatitis B and C screen
  • Renal Biopsy if indicated
  • Test Mother’s urine for blood (if Alport Syndrome suspected)
  • Hearing test (if Alport Syndrome suspected)
47
Q

What is nephritis?

Some common causes in children?

A
  • inflammation within the nephrons of the kidneys
  • results in reduced kidney function, haematuria and proteinuria (less than nephrotic syndrome)
  • causes in children are:
    • Post Streptococcal Glomerulonephritis
    • IgA Nephropathy (Berger’s disease)
    • mesangiocapillary glomerulonephritis
    • Vasculitis (Henoch-Schonlein purpura, SLE, Wegener granulomatosis, microscopic polyarteritis, polyarteritis nodosa)
    • Antiglomerular basement membrane disease (Goodpasture syndrome) = very rare
48
Q

What is the pathophysiology of Post-Strep Glomerulonephritis?

A

occurs 1-3 weeks after B-haemolytic streptococcus infection (eg. tonsillitis caused by Streptococcus pyogenes)

Immune complexes made up of streptococcal antigens, antibodies and complement proteins get stuck in the glomeruli of the kidney and cause inflammation + acute deterioration of renal function = AKI

49
Q

When would you consider post-strep glomerulonephritis and how would you prove this?

A

Consider = recent tonsillitis or sore throat caused by strep, recent skin infection

  • +ve throat swab results or cultures
  • raised anti-streptolysin antibody titres on blood test
  • or anti-DNAse B titres
  • low complement C3 levels that return to normal after 3-4 weeks
50
Q

How would you manage post-strep glomerulonephritis?

A
  • mainly supportive
  • antihypertensive medications and diuretics for HTN and oedema
51
Q

How does Henoch-Schonlein purpura (Iga vasculitis) present?

A
  • characteristic skin rash on extensor surfaces
    • symmetrically distributed over buttocks, extensor surfaces of arms/ legs/ ankles, trunk usually spared
    • rash is initially urticarial but becomes maculopapular and purpuric
  • fever
  • joint pain particularly in knees and ankles
  • periarticular oedema
  • colicky abdo pain, can have haematemesis and melaena, intussusception
  • glomerulonephritis
  • microscopic/ macroscopic haematuria
  • typically 3-10 years old (2x more likely in boys)
  • usually preceded by upper resp tract infection
52
Q

What is seen on histology of IgA Nephropathy and what is the pathophysiology?

What is the management?

A
  • IgA deposits in the nephrons of the kidney which causes inflammation (nephritis)
  • renal biopsy shows IgA deposits and Glomerular Mesangial Proliferation
  • Management = supportive treatment of renal failure, immunosuppressant medications eg. steroids and cyclophosphamide to slow disease progression
53
Q

What is the most common cause of haematuria in kids?

How would they present?

A

UTI !!!

  • Fever (can be the only symptom, especially in young children)
  • Babies present very non-specifically:
    • fever, lethargy, irritability, vomiting, poor feeding, urinary freq
  • Older infants and children present more specifically:
    • fever, abdo pain (suprapubic), vomiting, dysuria, urinary freq, incontinence
54
Q

How would acute pyelonephritis present?

A
  • temp >38C
  • Loin pain or tenderness
55
Q

How would you investigate a UTI?

A
  • Urine dipstick
    • ideally a clean catch sample to avoid contamination
    • Nitrites, Leukocytes (if just leukocytes, not enough. nitrites are enough to treat as uti)
    • haematuria
    • Send a Midstream Urine sample to microscopy + culture/sensitivity
56
Q

How would you investigate recurrent UTIs

A
  • Abdo US within 6 weeks, for all children under 6 months old with their first UTI
  • Abdo US within 6 weeks for children with recurrent UTIs
  • Abdo US during the illness for children with atypical UTIs
  • Dimercaptosuccinic Acid (DMSA) Scan 4-6 months after illness to assess for damage/scarring from recurrent UTIs
  • Micturating Cystourethrogram to investigate recurrent/atypical UTI in children under 6 months old
    • use when there is a fhx of Vesico-Ureteric Reflux (urine flows from bladder back into ureters, predisposing pt to upper UTI and renal scarring)
    • use when you see dilation of ureter or poor urinary flow on US
    • kids usually given 3 days of prophylactic antibiotics around this time as it involves catheterisation and injection of contrast into the bladder
57
Q

How would you manage a UTI in children?

A
  • all children under 3 months old with fever
    • start on IV antibiotics eg. ceftriaxone
    • full sepsis screen (blood cultures, lactate, fbc)
    • consider LP
  • children over 3 months old
    • oral antibiotics for 3 days if otherwise well
    • IV antibiotics if sepsis features or pyelonephritis
    • antibiotics eg. trimethoprim, nitrofurantoin, cefalexin, amoxicillin
58
Q

What is enuresis?

(nocturnal, diurnal, primary nocturnal, secondary nocturnal)

A

Involuntary urination.

Bedwetting = nocturnal enuresis

Inability to control bladder function in the day = diurnal enuresis

Primary nocturnal enuresis = child has never managed to be consistently dry at night

Secondary Nocturnal Enuresis = child begins wetting the bed when they have been previously dry for at least 6 months.

59
Q

What are some common causes of primary nocturnal enuresis?

A
  • variation on normal development particularly if kid is <5 years old (typically have a fhx of delayed dry nights)
  • overactive bladder (freq small vol urination prevents development of bladder capacity)
  • fluid intake prior to bedtime (particularly fizzy drinks, juice, caffeine)
  • failure to wake due to particularly deep sleep or underdeveloped bladder signals
  • psychological distress eg. low self esteem, too much pressure or stress at home/school
  • Secondary causes = chronic constipation, UTI, LD, Cerebral Palsy
60
Q

How would you manage primary nocturnal enuresis?

A
  • 2 week diary of toileting, fluid intake, bedwetting episodes
  • Reassure parents of kids under 5 years old that it will likely resolve
  • Lifestyle = reduce fluid intake at night, urinate before bed, ensure easy access to toilet
  • encouragement and positive reinforcement, avoid punishment/blame/shame
  • treat underlying causes eg. constipation
  • enuresis alarms (for at least 3 months. makes a noise at the first sign of bedwetting to wake the child and stop them from urinating)
  • pharmacological treatment
61
Q

What are some pharmacological treatments used for nocturnal enuresis?

A
  • Desmopressin (an analogue of vasopressin) before bedtime
  • Oxybutinin (an anticholinergic that reduces contractility of the bladder) is used for overactive bladder causing urge incontinence
  • Imipramine (tricyclic antidepressant) can relax bladder and lighten sleep
62
Q

What are some causes of secondary nocturnal enuresis?

A
  • UTI
  • Constipation
  • Type 1 Diabetes
  • New psychosocial problems eg. stress in fam or school life
  • Maltreatment (think about abuse and safeguarding!!!)
63
Q

What are the 2 main types of diurnal enuresis and some causes

A
  • Urge incontinence (overactive bladder)
  • Stress incontinence (leakage during physical exertion, coughing, laughing)

Causes:

  • recurrent UTI
  • psychosocial problems
  • constipation
64
Q

What should you be thinking when you get palpable kidneys? (unilateral and bilateral)

A

Unilateral

  • multicystic kidney
  • compensatory hypertrophy
  • obstructed hydronephrosis
  • renal tumour (Wilms tumour)
  • Renal vein thrombosis

Bilateral

  • autosomal recessive polycystic kidneys
  • autosomal dominant polycystic kidneys
  • tuberous sclerosis
  • renal vein thrombosis
65
Q

Renal stones are uncommon in childhood.

However what situation would they typically occur?

A
  • the most common are Phosphate stones associated with infection (eg. Proteus)
  • Calcium containing stones = idiopathic hypercalciuria (most common metabolic abnormality)
  • Nephrocalcinosis may be a complication of furosemide therapy in the neonate
  • Cystine and xanthine stones are rare

4th Year (17 decks)

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