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PaedsY5 Renal > A-N > Flashcards

A-N Flashcards

1
Q

What is Cryptorchidism?

A

Failure of normal descent of the testes into position

Undescended testes UDT: testes can be found anywhere along normal path with pateint processus vaginalis.

Ectopic: descended through the inguinal canal but ended up somewhere abnormal i.e. femoral, perineum, suprapubic.

Acquired: failure of growth of the spermatic cord in proportion to scrotal growth.

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2
Q

What is the aetiology and epidemiology of Cryptorchidism?

A

3% male infants, 30% premature.

Normal testicular descent:

  1. Stage 1 transabdominal: Fetal gubernaculum enlarges under the influence of INSL3/AMH/MIS and fetal testosterone. This anchors the testicle near the inguinal region.
  2. Stage 2 inguinoscrotal: Occurs from week 28. Migration of the gubernaculum to the scrotum via the PV with the testes in it. Under androgen control.

Common in prematurity, low BW, hypospadias, PPV, hypopitiutarism if bilateral.

DDX: retractile testes with positive cremasteric response, congenital absence, atrophic testis due to neonatal torsion.

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3
Q

What would you find in the history and exam of Cryptorchidism?

A

Usually asymptomatic, picked dup during child health screen. May present with associated inguinal hernia in ectopic.

Examin a child relaxed in warm room. Most common locaion for the testes is in the inguinal canal, followed by prescrotal, and abdominal.

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4
Q

What would you find in the investigations of Cryptorchidism?

A

Dx is clinical, USS ay help if location not determined. Bilateral impalpable testes require BHCG stimulation test, and potentially laproscopic exploration and chromosomal mapping.

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5
Q

What is the management of Cryptorchidism?

A

Orchidoplexy with PPV ligation preformed at 6m-1y.

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6
Q

What are the complications of Cryptorchidism?

A

Abnormal testes location can lead to infertility, difficulty in spermatogenesis and increased risk of malignancy by 60%. Good prognosis with intervention.

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7
Q

What is Faecal soiling (encopresis) move to GI?

A

Voluntary or involuntary passing of faeces after the age where continence control is normal (3-4y).

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8
Q

What is the aetiology and epidemiology of Faecal soiling (encopresis)?

A

3/100, decreases with age.

Retentive encopresis: most common. Functional retention of faeces -> stretching of rectum and anal sphincter -> loss or tolerance to stretch response and decreased drive to pass stool due to loss of defecation sensation.

Non retentive: occurs without constipation

Emotional: In distressed child. Conflict abuse and behavioural issues.

May be associated with surgical intervention for Hirschprungs, ARMs, neuropathy and behavioural problems.

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9
Q

What would you find in the history and exam of Faecal soiling (encopresis)?

A

Detailed history from carer on stool habits/sensations/constipation. Detailed social hx.

Abdominal: fecal loaing may be felt.

DRE: may feel rectum filled with soft stool. Examine for anal fissures or tear. May have reduced anal wink and tone. Anal sphincter lax due to chronic distension.

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10
Q

What would you find in the investigations of Faecal soiling (encopresis)?

A

Anorectal manomerty

Radionuclear transit scintiography: due visualize passage of stool and exclude Hirschprungs etc.

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11
Q

What is the management of Faecal soiling (encopresis)?

A

Medical: constipation management and diet control. Colonic evacuation / laxatives / enemas.

Behavioral strategies, parent and child education, biofeedback training. Surgical intervention with an anterograde continence enema (ACE) may be required.

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12
Q

What are the complications of Faecal soiling (encopresis)?

A

Psychosocial, stress for individual and family.

Good with treatment, most resolve in a few years.

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13
Q

What is Hypospadias?

A

Abnormality of urethral/penile development resulting in ectopic urethral opening.

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14
Q

What is the aetiology and epidemiology of Hypospadias?

A

1/200 live births.

Can be anywhere from glans to perineum. Distal more common than proximal. Genetic, environmental and endocrine factors. Polygenic inheritance, mainly 5a-reductase or androgen synthesis mutations. Higher in IVF babies due to progesterone administration.

Associated with cryptorchidism, PPV, abnormal shaft curvature.

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15
Q

What would you find in the history and exam of Hypospadias?

A

Most detected postnatally with associated hooded prepuce. Glandular may present later. Position may be glandular, coronal, subcoronal, distal shaft, mid shaft, proximal shaft, perineal. May be associated with bifid scrotum.

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16
Q

What would you find in the investigations of Hypospadias?

A

RUSS. More investigations if there is a severe or proximal hypospasdias and associated cryptorchidism. (exclude ambiguous genitalia).

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17
Q

What is the management of Hypospadias?

A

Initially do not circumcise because foreskin may be used in reconstruction. Parental counselling.

Surgery 9-12m, to reconstruct urethra and produce a glandular opening in normal place. Mild glandular hypospadias may be managed conservatively. May have to preform staged procedure in proximal hypospadias. Tubularised incised plate (TIP) is the most commonly used procedure.

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18
Q

What are the complications of Hypospadias?

A

Surgical: stenosis, infection, urethrocele, fistula formation.

Generally very good, complications depend on technique.

19
Q

What is Nephrotic syndrome?

A

NePHOtic: proteinuria, hypoalbumin, odema.

20
Q

What is the aetiology and epidemiology of Nephrotic syndrome?

A

Developed countries: MCD is the main cause in 90% of children.

Non developed countries: most infectious, malaria highest cause, HepB and GBS.

Glomerulonephritis -> nephrotic syndrome.

· Primary: minimal change disease MCD, focal segmental glomerulosclerosis FSGS, and membranous nephropathy MN.

· Secondary: post infection (malaria, GBS, HepB, VZV, syphillis, HIV, Tb, EBV), Collagen vascular disease, HSP, Congenital (Alports syndrome) Siclke cell disease.

21
Q

What would you find in the history and exam of Nephrotic syndrome?

A

General: anorexia, oliguria, lethargy, hypertension

GI: diahrrea, nausea, poor feeding, pain

Odema: swelling of etelids, face, ascites, legs and scrotum.

Complications: infections, renal vein thrombosis, loin pain, haematuria.

22
Q

What would you find in the investigations of Nephrotic syndrome?

A

Bloods: Ues, albumin, FBC, CRPESR high, lipid profile.

Post infectious: ASOT, Thick and thin films, HBV/EBV/HIV serology.

Urine dipstick: high protein, high blood.

MSU: MCS. 24h urine collection for creatinine clearance.

Renal USS and biopst: other renal disease causing proteinuria (polycyst) biopsy for older children with persistent hematuria.

Doppler USS if renal vein thrombosis suspected.

23
Q

What is the management of Nephrotic syndrome?

A

Symptom treatment – low Na and water diet.

Monitor BP, Ues, Ca, weight, fluid balance.

6 month daily prednisolone on first presentation, then on relapse Prednisolone daily until remission. Alternating prednisolone with steroid sparing agent (cyclophosph) in steroid resistant patients.

Treat HTN with ACEi. Penicillin prophylaxis to prevent peritonitisand avoid septicaemia if thrombosis.

24
Q

What are the complications of Nephrotic syndrome?

A

Renal failure from hypovolaemia or thrombosis.

Infeciton susceptibiity, peritonitis and pneumococcal sepsis.

Hypercoaguability: renal vein thrombosis and DVTs due to hypovolaemia, urinary loss of proteins (antithrombin, protein C/S.

Hyperlipidaemia: high synthesis of TG and cholesterol in liver (combined with albumin increased synthesis due to wasting.

Before steroids, 60% children used to die. Steroids revolutionised and now pgx affectd by cmx and S/E of tx.

25
Q

What is enuresis?

A

normal micturition occurring at an inappropriate or socially unacceptable time or
place, occurring after a developmental age when bladder control should be established (~5
years)

26
Q

What are the types of enuresis?

A

o Primary nocturnal enuresis: nocturnal enuresis in which the child has never had a
period of dryness longer than 6 months
o Secondary nocturnal enuresis: nocturnal enuresis recurring after a period of more
than 6 months of the child being dry at night
o Daytime enuresis

27
Q

What is daytime enuresis?

A

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

28
Q

What are the causes of daytime enuresis?

A

o Lack of attention to bladder sensation (manifestation of developmental or
psychogenic problem)
o Detrusor instability (sudden, urgent urge to void induced by sudden bladder
contractions)
o Bladder neck weakness
o Neuropathic bladder (bladder is enlarged and fails to empty properly, irregularly thick
wall, associated with spina bifida and other neurological conditions)
o UTI
o Constipation
o Ectopic ureter (causes constant dribbling)

29
Q

What investigations do you do for enuresis?

A

o Urine should be sent for MC&S
o Ultrasound may reveal abnormalities
o Urodynamic studies may be required
o MRI may be used to exclude a spinal defect

30
Q

What is secondary enuresis?

A

The loss of previously achieved urinary continence may be due to:
o Emotional upset (MOST COMMON)
o UTI
o Polyuria from an osmotic diuresis (e.g. diabetes mellitus, diabetes insipidus, CKD)

31
Q

What investigations do you do for secondary enuresis?

A

o Urine dipstick to check for infection, glycosuria and proteinuria
o Assessment of urine concentrating ability by measuring osmolality of an early
morning urine sample
o Ultrasound of the renal tract

32
Q

What is the management in enuresis >5yrs?

A

▪ If bedwetting is infrequent (< 2 per week) reassure the parents and offer
watch-and-see approach
▪ If long-term treatment is required, offer:
• 1st line: enuresis alarm with positive reward system e.g. star
charts
• 2nd line: desmopressin
o NOTE: fluid should be restricted 1 hour before desmopressin
until 8 hours after
If rapid or short-term control is required (e.g. school trips), offer
desmopressin
▪ If bedwetting recurs following treatment, restart previously successful
treatments and offer combination treatment with desmopressin and an
enuresis alarm
▪ TCAs and antimuscarinics may be considered in special cases
▪ Referral
• If bedwetting has NOT responded to two courses of treatment, refer
to secondary care, enuresis clinic or community paediatrician

33
Q

What is the management of enuresis <5yrs?

A

▪ Reassure the parents that many children aged < 5 yrs wet the bed and this
usually resolves without intervention
▪ Ensure easy access to the toilet at night (e.g. potty near the bed)
▪ Encourage bladder emptying before bed
▪ Consider a positive reward system

34
Q

What might you also consider managing in secondary enuresis?

A

o The following underlying causes can be managed in primary care
▪ UTI
▪ Constipation
o The following underlying causes are likely to need specialist referral
▪ Diabetes
▪ Recurrent UTI
▪ Psychological problems
▪ Family problems
▪ Developmental, attention or learning difficulties
▪ Known or suspected physical or neurological problems

35
Q

Where may you refer a child with enuresis?

A

Secondary care/ enuresis clinic

36
Q

What is acute glomerulonephritis?

A

Acute glomerulonephritis (GN) comprises a specific set of renal diseases in which an immunologic mechanism triggers inflammation and proliferation of glomerular tissue that can result in damage to the basement membrane, mesangium, or capillary endothelium.

37
Q

What investigations would you do for acute glomerulonephritis?

A

Must carry out U&Es, urine dip, creatinine and blood pressure to check
renal function

38
Q

What are the clinical features of acute glomerulonephritis?

A

Characteristically presents with red-brown (coca cola) urine,
proteinuria, oedema, hypertension and acute renal failure (elevated
serum creatinine)

39
Q

What is the management of acute glomerulonephritis?

A

Supportive – treat volume overload e.g. sodium and water restriction, loop diuretics

40
Q

What is a nephroblastoma?

A

The most common form of renal malignancy in childhood.

Originates from embryonal renal tissue.

41
Q

What is the epidemiology of nephroblastoma?

A

Usually occurs in first 2-5 years of life

Rarely seen after 10 years of age

42
Q

What are the clinical features of a nephroblastoma?

A

• Abdominal mass
o Usually found incidentally in otherwise well child

• Haematuria

• Less common
o Abdominal pain
o Anorexia
o Anaemia (haemorrhage into mass)
o Hypertension
43
Q

What investigations would you use for a nephroblastoma?

A

• Ultrasound
• CT/MRI: shows intrinsic renal mass
o Characteristically shows mixed tissue densities (cystic and solid)
o Arises within the kidney and envelops a remnant of normal renal tissue

44
Q

What is the management of nephroblastoma?

A

• Surgery and chemotherapy (may be post-operative or pre-operative)
• Subsequent management is dependent on histological findings
o Advanced disease → radiotherapy
• 5% have bilateral disease
• More than 80% of patients are cured

PaedsY5 Renal (4 decks)

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