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PHASE 3A > PAEDS - renal/urinary, neuro, psych, endocrine/reproductive > Flashcards

PAEDS - renal/urinary, neuro, psych, endocrine/reproductive Flashcards

1
Q

what is testicular torsion?

A

a twisted spermatic cord, ischaemia of testes

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2
Q

when are the two peaks of incidence of testicular torsion?

A

neonatal and puberty

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3
Q

presentation of testicular torsion (4)

A
  1. SUDDEN ONSET SEVERE PAIN (unilateral)
  2. vomiting/nausea
  3. tender testicle
  4. abdominal pain
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4
Q

what are LATE signs of testicular torsion?

A

redness and swelling

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5
Q

investigations for testicular torsion

A

clinical - only reliably diagnosed with surgical exploration

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6
Q

what is the window of time for surgically treating testicular torsion?

A

6 hours

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7
Q

key differential for testicular torsion and how it presents differently

A
  • torsion of appendix testes (called the hydatid of morgagni)
  • this is a remnant of the Mullarian duct
  • mimics testicular torsion but pain not as severe/acute, prepuburtal, looks like “blue dot”
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8
Q

what constitutes an atypical UTI in children? (5)

A
  1. septicaemia
  2. non e.coli organism
  3. poor urine flow
  4. not responding to tx in 48h
  5. abdominal/bladder mass
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9
Q

what is the most common bacterial cause of UTIs in children? what are two other possible causes and which is more common in boys?

A

E.COLI

others - proteus mirabilis (boys) and staph saprophyticus

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10
Q

what is a big risk factor for paediatric UTIs? give 3 examples

A

structural abnormalities e.g.
- horseshoe kidney
- duplex kidney (two ureters from one kidney)
- vesicoureteric reflux (VUR)

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11
Q

UTI signs/symptoms in infants <3m

A

common
- fever
- vomiting
- lethargy
- irritability
- poor feeding
- failure to thrive

less common
- abdo pain
- jaundice
- haematuria
- offensive urine

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12
Q

signs and symptoms of UTIs in children/infants >3m

A
  • fever
  • frequency/dysuria
  • dysfunctional voiding/changes to continence
  • abdominal pain
  • loin tenderness
  • less common = malaise, vomiting, haematuria, offensive/cloudy urine
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13
Q

signs of acute pyelonephritis in children (2)

A
  1. fever >38 degrees
  2. loin pain/tenderness
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14
Q

what may be the ONLY sign of a UTI in children?

A

FEVER

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15
Q

investigating UTIs in children - what are some urine sampling techniques? what is gold std?

A
  1. cotton wool in nappy
  2. bag urine
  3. clean catch (midstream)
  4. gold std = in/out catheter or suprapubic aspirate
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16
Q

what tests are done on a child’s urine sample when investigating a UTI?

A
  • urine dipstick
  • MSU for culture and sensitivity testing
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17
Q

what indicates a UTI on a urine dipstick?

A

high nitrites
high leukocyte esterase

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18
Q

what are the 3 indications for ultrasound scanning when investigating a paediatric UTI?

A
  1. all children <6 months
  2. children with recurrent UTIs
  3. children with atypical UTIs (e.g. not treating w abx)
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19
Q

what imaging techniques can be used when investigating paeds UTIs? (3)

A
  1. ultrasound
  2. micturating cystourethrogram (MSUG)
  3. DMSA scan
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20
Q

when are IV vs oral abx indicated in the tx of children with UTIs?

A

IV if <3 months
oral if >3m (if otherwise well)

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21
Q

UTI management in:
a) <3m old
b) >3m old with upper UTI
c) >3m old with lower UTI

A

a) immediate referral to paediatrician
b) consider admission to hospital, if not oral abx e.g. cephalosporin/co-amoxiclav for 7-10 days
c) oral abx for 3 days

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22
Q

oral abx options for children with a lower UTI

A
  • trimethoprim (usually)
  • nitrofurantoin
  • cephalosporin
  • amoxicillin
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23
Q

3 indications for follow-up clinics following a UTI in children

A
  1. all children <3m
  2. children of any age who were systemically unwell
  3. children with recurrent UTIs
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24
Q

long-term complications of UTIs in children

A
  • kidney scarring
  • HTN
  • CKD
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25
Q

when should most children have achieved day AND night continence?

A

3-4 years old

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26
Q

what is primary vs secondary nocturnal eneuresis?

A

primary - child has never achieved continence

secondary - child has been dry for at least 6m before

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27
Q

causes of secondary nocturnal enuresis

A
  1. diabetes
  2. constipation
  3. UTI (if v recent)
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28
Q

why is nocturnal enuresis common in young children? (2)

A
  1. smaller bladder = less capacity
  2. sensation of full bladder doesnt wake up child when they’re young
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29
Q

management of nocturnal enuresis if child <5

A

reassurance - will most likely self resolve

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30
Q

management of nocturnal enuresis if child >5
a) general advice
b) 1st line
c) 2nd line

A

a) fluid intake, toileting patterns e.g. regular emptying, lifting and waking, reward systems

b) enuresis alarm

c) desmopressin (for short-term e.g. sleepover or if enuresis ineffective/unacceptable)

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31
Q

criteria for diagnosing paediatric AKI
- creatinine
- urine output
- eGFR
(4)

A

either:
- rise in creatinine of 26umol/L in 48 hours

  • > 50% rise in creatinine over 7 days
  • fall in urine output to <0.5ml/kg/hr for more than 8 hours
  • > 25% fall in eGFR in 7 days
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32
Q

AKI stage 1 (3)

A
  1. increase in creatinine to 1.5-1.9 times baseline

OR

  1. increase in creatinine by >26.5umol/L

OR

  1. reduction in urine output to <0.5ml/kg/hr for >8 hours
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33
Q

AKI stage 2 (2)

A
  1. increase in creatinine to 2.0-2.9 x baseline

OR

  1. reduction in urine output to <0.5ml/kg/hour for >12 hours
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34
Q

AKI stage 3 (4)

A
  1. increase in creatinine to 3.0 x baseline

OR

  1. increase in creatinine to >353.6umol/l

OR

  1. reduction in urine to <0.3ml/kg/hr in >24 hours

OR

  1. decrease in eGFR to <35
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35
Q

causes of paediatric AKI (4)

A
  1. obstruction/blockage e.g. PUV, PUJ obstruction
  2. haemolytic uraemic syndrome
  3. glomerulonephritis
  4. decreased blood to kidneys e.g. blood loss, surgery, shock
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36
Q

causes of paediatric CKD (5)

A
  1. prolonged urinary tract obstruction
  2. alport syndrome (inherited)
  3. nephrotic syndrome
  4. PKD
  5. cystinosis
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37
Q

signs and symptoms of AKI

A
  • fever
  • rash
  • haemorrhage
  • bloody diarrhoea
  • vomiting
  • abdo pain
  • pale skin
  • no urine or high urine output
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38
Q

signs and symptoms of CKD

A
  • poor appetite
  • vomiting
  • bone pain
  • headache
  • no urine
  • urinary incontinence
  • recurrent UTIs
  • pale skin
  • malaise
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39
Q

investigations for paediatric AKI/CKD (4)

A
  1. bloods - high creatinine
  2. urinary tests - may have haematuria
  3. renal USS - mass, stones, cyst, obstruction
  4. renal biopsy
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40
Q

management of paediatric AKI

A

depends on cause!!!

  • IV fluids
  • diuretic therapy
  • monitor electrolytes
  • antihypertensives
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41
Q

management of paediatric CKD

A
  • meds for growth, prevent bone density loss, tx anaemia
  • diuretic therapy (increase UO, lower BP)
  • dialysis
  • kidney transplant (definitive)
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42
Q

what is nephrotic syndrome?

A

inflammation of podocytes, causing kidneys to leak PROTEIN

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43
Q

peak incidence of nephrotic syndrome in children

A

2-5 years

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44
Q

what is the most common nephrotic syndrome in children?

A

minimal change glomerulonephritis

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45
Q

primary causes of paediatric nephrotic syndrome (3)

A
  1. minimal change disease
  2. focal segmental glomerulosclerosis (FSGS)
  3. membranous nephropathy (more in adults)
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46
Q

secondary causes of paediatric nephrotic syndrome (4)

A
  1. henoch-schonlein purpura
  2. SLE
  3. infection e.g. malaria
  4. allergens e.g. bee sting
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47
Q

pathophysiology of minimal change disease

A

in general - lose albumin and proteins in clotting cascade

  1. t cells damage, flatten foot processes
  2. podocytes more permeable (defacement)
  3. albumin slips through > lost in urine (hypoalbuminemia)
  4. selective proteinuria e.g. immunoglobulins
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48
Q

why do you get oedema in nephrotic syndrome?

A
  • albumin’s function is osmotic regulation
  • albumin pulls water out of interstitial space into vascular stream
  • so if hypoalbumin > water stays in interstitial space > oedema
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49
Q

nephrotic syndrome triad

A
  1. proteinuria (>3.5g/24hrs)
  2. hypoalbuminaemia (<25g/l)
  3. oedema
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50
Q

signs of nephrotic syndrome

A
  1. oedema - face, scrotum, ankles
  2. frothy urine
  3. pallor

can get hypercoagulability (proteins that prevent clotting are lost in urine)

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51
Q

investigations & results for nephrotic syndrome (5)

what is diagnostic?

A
  1. urinalysis
    - proteinuria
    - ACR
    - microscopy, sensitivity and culture
    - NO HAEMATURIA
  2. bloods - ESR and CRP, LFTs (low protein), U&Es, low serum albumin
  3. BP - high
  4. USS kidneys
  5. diagnostic = renal biopsy
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52
Q

how will minimal change disease present on renal biopsy/microscopy?

A

no abnormalities will be detected

53
Q

management of nephrotic syndrome
a) non pharm
b) pharm

A

a) low salt diet, monitor urine protein and BP

b) - HIGH DOSE oral corticosteroids - prednisolone
- diuretics (reduce oedema)
- albumin infusions if severe hypoalbumin

54
Q

steroid regime in paediatric nephrotic syndrome

A

high dose given for 4 weeks
then gradually weaned over 8 weeks

55
Q

management of nephrotic syndrome in steroid-resistance children (2)

A
  1. ACEis
  2. immunosuppressants e.g. cyclosporine, tacrolimus, rituximab
56
Q

complications of nephrotic syndrome (6)

A
  1. hypovolemia
  2. thrombosis (leak of antithrombin in urine)
  3. infection (leak of immunoglobulins)
  4. renal failure
  5. frequent relapse
  6. hypercholesteremia
57
Q

medical migraine prophylaxis in children
a) 1st line
b) if contraindications

A

a) propranolol

b) contraindications e.g. asthma - use topiramate

58
Q

what is congenital adrenal hyperplasia? (CAH) what is it characterised by?

A

autosomal recessive disorders where adrenal gland is too large > impaired adrenal steroid biosynthesis (lack of cortisol and aldosterone hormone)

59
Q

which enzyme is deficient in congenital adrenal hyperplasia (CAH)? what does this cause?

A

21-hydroxylase

this is needed for the conversion of 17-hydroxyprogesterone to 11-deoxycortisol so > lack of cortisol

60
Q

pathophysiology of CAH - what hormonal dysfunction is caused?

A
  1. deficiency in cortisol production (impaired conversion of 17-hydroxyprogesterone to 11-deoxycortisol)
  2. compensatory overproduction of ACTH by the anterior pituitary
  3. elevated ACTH increases production of adrenal androgens (male sex hormones)
  4. causes virilisation (biological prod of adult male characteristics) in females
61
Q

presentation of CAH in females

A
  1. virilisation - ambiguous genitalia, clitoromegaly
  2. precocious puberty
  3. tall for age, facial hair, deep voice
  4. primary amenorrhoea
  5. infertility
62
Q

presentation of CAH in males

A
  1. appear normal at birth
  2. precocious puberty
  3. tall for age, deep voice
  4. large penis, small testicles
  5. infertility
63
Q

what ‘crisis’ can occur in CAH? why? how does it present?

A

a) salt-wasting crisis

b) dysfunctional adrenal gland doesn’t produce enough aldosterone > this is needed for regulating serum sodium > sodium is lost in urine

c) dehydration, vomiting, diarrhoea, hypotension, electrolyte imbalance

64
Q

what electrolyte abnormalities are typically seen in CAH? (4)

A

hyponatremia and hyperkalemia

hypoglycemia

met. acidosis

65
Q

diagnostic investigation and result in CAH

A

ACTH stimulation testing

  • evaluates adrenal gland’s response to ACTH
  • abnormal increase in 17-hydroxyprogesterone (normally is converted to cortisol)
66
Q

ddx for CAH (3)

A
  • precocious puberty
  • Addison’s
  • PCOS
67
Q

management of CAH (3)

A

specialist paediatric endocrinologists > FU for growth and development

  1. glucocorticoid replacement (hydrocortisone)
  2. if mineralocorticoid deficient > fludrocortisone
  3. females may need corrective surgery
68
Q

complications of CAH (2)

A
  1. infertility
  2. salt-wasting crisis
69
Q

what is Kallman’s syndrome? what is it characterised by? what is its inheritance?

A

a) a genetic disorder causing DELAYED puberty

b) hypogonadotropic hypogonadism

c) x-linked recessive

70
Q

pathophys of Kallman’s syndrome

A
  1. failure of GnRH-secreting neurons to migrate to the hypothalamus
  2. no GnRH to stimulate LH and FSH release
  3. low LH and FSH > no stimulation of sertoli/leydig cells/ ovaries to produce testosterone + inhibin/progesterone + oestrogen
  4. SO low gonadotropins AND low sex hormones&raquo_space; hypogonadotropic hypogonadism
71
Q

RFs for Kallman’s syndrome

A

family hx

72
Q

signs and symptoms of Kallman’s in boys - what is a key question stem?

A

key = boy with lack of smell (anosmia) and delayed puberty

  1. delayed puberty
  2. micropenis, cryptorchidism (dont descend)
  3. anosmia
  4. normal/above avg height
73
Q

signs and symptoms of Kallman’s syndrome in females

A
  1. PRIMARY AMENORRHOEA
  2. anosmia
  3. delayed puberty
74
Q

what birth defects are associated with Kallman’s syndrome?

A

cleft lip/palate and visual/hearing defects

75
Q

investigations and results for Kallman’s syndrome

A

hormone testing
- LH/FSH low
- sex hormones e.g. testosterone low

76
Q

management for Kallman’s syndrome
a) males
b) females

A

a)
1. testosterone supplements
2. gonadotropin supplements (for later in life when fertility desired > sperm production)

b) progesterone and oestrogen

77
Q

complication of Kallman’s

A

infertility, psychosocial probs

78
Q

which gender does androgen insensitivity syndrome occur in?

A

males (XY)

79
Q

what is androgen insensitivity syndrome? what is it characterised by?

A

a genetic condition of end-organ resistance to testosterone, characterised by genotypically male children (XY) to have an external female phenotype

80
Q

how is androgen insensitivity syndrome inherited?

A

x-linked recessive

81
Q

describe how each organ presents in androgen insensitivity syndrome:
a) uterus
b) testes
c) vagina

A

a) absent uterus
b) undescended testes
c) short vagina

82
Q

what causes androgen insensitivity syndrome?

A

mutation in the androgen receptor gene on the X chromosome

83
Q

pathophysiology of androgen insensitivity syndrome

A
  1. mutation in androgen receptor gene
  2. cells unable to respond to androgen hormones (testosterone) due to lack of receptors
  3. extra testosterone turns into oestrogen
  4. typical male sexual characteristics don’t develop
  5. external female genitalia and breast tissue develop
  6. testes in abdomen/inguinal canal produce anti-mullerian hormone > prevent internal female organs from developing
84
Q

signs and symptoms of androgen insensitivity syndrome in infancy

A

inguinal hernias containing testes (on surgical repair of hernia surgeon will find testicles in a baby with external female genitalia)

85
Q

signs and symptoms of androgen insensitivity syndrome at puberty

A

THINK lack of normal ‘female’ pubertal changes and a sprinkle of ‘male’ pubertal changes…

  1. primary amenorrhoea
  2. little/no axillary or pubic hair
  3. facial hair
  4. male type muscle development
86
Q

what will be seen on vaginal examination in androgen insensitivity syndrome?

A

short vagina

87
Q

investigations and results for androgen insensitivity syndrome (2)

A
  1. HORMONE BLOODS
    - raised LH
    - normal/raised FSH
    - normal/raised testosterone (for a male)
    - raised oestrogen (for a male)
  2. buccal smear/chromosomal analysis
    - will show 46XY genotype
88
Q

why is LH raised and FSH normal/raised in androgen insensitivity syndrome?

A

LH - lack of testosterone giving negative feedback to anterior pituitary to stop producing LH

FSH - is regulated by the hormone inhibin so is not as affected by the lack of testosterone -ve feedback

89
Q

what genotype result would you get in androgen insensitivity syndrome?

A

46XY

90
Q

management of androgen insensitivity syndrome (4)

A
  1. counselling - often raised as girl
  2. oestrogen replacement
  3. bilateral orchiectomy
  4. vaginal dilation/surgery - create adequate length
91
Q

complications of androgen insensitivity syndrome

A

risk of testicular cancer (undescended testes)

92
Q

most common location for urethral opening in hypospadias

A

ventral distal surface of penis

93
Q

what is glomerulonephritis (nephritic syndrome)?

A

INFLAMMATION of the glomerular blood vessels

thinning of glomerular basement membrane, porous podocytes

94
Q

when does nephritic syndrome occur in children?
what is the most common cause worldwide?

A
  • 2-15 years old
  • IgA nephropathy
95
Q

causes of nephritic syndrome (3)

A
  1. IgA nephropathy
  2. post-streptococcal glomerulonephritis
  3. Henoch-Schonlein purpura (HSP)
96
Q

what age does IgA nephropathy usually present?

A

teens/young adults

97
Q

RF for post-strep glomerulonephritis/IgA nephropathy

A

recent upper resp infection

98
Q

pathophys of IgA nephropathy

A
  1. abnormal IgA form
  2. deposits of IgA immune complexes in mesangium of kidneys
  3. then attacked by autoantibodies
  4. inflammation and damage
99
Q

pathophys of henoch-schonlein pupura

A
  1. IgA mediated vasculitis
  2. inflammation of small vessels in kidneys
100
Q

GENERAL key features of nephritic syndrome/glomerulonephritis (4)

A
  1. HAEMATURIA (macro or micro)
  2. oedema (less than nephrotic)
  3. HTN
  4. oligouria (<300mls/day)
101
Q

features of nephritic syndrome suggestive of IgA nephropathy cause

A
  1. developing 1-2 DAYS following URTI
  2. young males
  3. macroscopic haematuria
  4. renal failure unusual
102
Q

features of nephritic syndrome suggestive of post-streptococcal glomerulonephritis cause

A
  1. developing 1-2 WEEKS after URTI
  2. low complement
103
Q

features of nephritic syndrome suggestive of Henoch-Schnolein purpura cause

A

nephritic sx PLUS
1. palpable purpura on buttocks/arms/legs
2. abdominal pain
3. polyarthritis
4. haematuria, renal damage

104
Q

gold std investigation for nephritic syndrome and results

A
  1. urinalysis
    - haematuria
    - red cell casts
    - no/little protein
105
Q

management of henloch-schonlein purpura

A
  • usually self-limiting (if no renal involvement)
  • analgesia for arthralgia
  • monitor BP and urinalysis
106
Q

management of post-strep glomerulonephritis

A
  • supportive
  • consider antihypertensives/diuretics if complications
107
Q

management of IgA nephropathy

A
  • supportive tx of renal failure
  • prednisolone and cyclophosphamide (immunosuppressants)
108
Q

complications of nephritic syndrome (4)

A
  1. AKI
  2. uncontrolled HTN
  3. hyperkalaemia
  4. hypovolemic crisis
109
Q

which type of PKD is presents in neonates?

A

autosomal recessive PKD (ARPKD)

110
Q

cause of ARPKD - which gene and which chromosome?

A

mutation in the polycystic kidney and hepatic disease 1 (PKHD1) gene on chromosome 6

111
Q

pathophys of ARPKD

what is the result in the neonate?

A
  1. PKHD1 gene codes for fibrocystin/polyductin protein complex (FPC)
  2. this is responsible for the creation of tubules and maintenance of healthy epithelial cells in the kidney, liver and pancreas
  3. causes
    - cystic enlargement of renal collecting ducts
    - oligohydramnios
    - pulmonary hypoplasia
    - Potter syndrome
    - congenital liver fibrosis
112
Q

how may ARPKD be detected antenatally? what will the results be?

A

picked up on antenatal USS scan - oligohydramnios, polycystic kidneys

113
Q

presentation of ARPKD in newborns

A
  1. potter syndrome - undeveloped ear cartilage, low set ears, flat nasal bridge, skeletal abnormalities
  2. pulmonary hypoplasia (resp failure)
114
Q

presentation of ARPKD in children

A

1/3 pts will not survive past neonatal period, but those that do will have end-stage renal failure in childhood

115
Q

investigations for ARPKD

A
  1. most diagnosed from antental USS scans
  2. in childhood can do renal biopsy - multiple lesions
116
Q

management of ARPKD

A
  • renal dialysis in first few days of life
  • extensive MDT interventions
117
Q

complications of ARPKD

A
  1. 1/3 will die in neonatal period
  2. liver failure (fibrosis)
  3. oesophageal varices
  4. progressive renal failure
  5. HTN
  6. chronic lung disease
118
Q

congenital and acquired causes of GH deficiency

A

CONGENITAL
- genetic mutation
- structural brain malformation

ACQUIRED
- hypothalamic pituitary tumour
- cranial radiotherapy (e.g. for brain tumour)
- TBI
- CNS infection
- TB

119
Q

which gland produces growth hormone?

A

pituitary gland

120
Q

pathophysiology of GH deficiency

A
  1. hypothalamus secretes GHRH (growth hormone releasing hormone)
  2. stimulates release of GH from anterior pituitary gland (this is dysfunctional)
  3. GH is responsible for stimulating cell production, growth of organs/muscles/bones, stimulating release of IGF-1 from liver
121
Q

features of GH deficiency at birth (2)

A
  1. micropenis in males
  2. hypoglycemia and/or severe jaundice
122
Q

features of GH deficiency in older infants/children (4)

A
  1. POOR GROWTH
  2. short stature
  3. slow development of movement and strength
  4. DELAYED PUBERTY
123
Q

main investigation for GH deficiency and its result

A

growth hormone stimulation/provocation test

GH is measured after insulin/glucagon/clonidine/arginine administered

in GH deficiency there will be poor response

124
Q

other investigations for GH deficiency (4)

A
  1. wrist xray - determines bone age and predicts final height
  2. test for other deficiencies e.g. adrenal/thyroid
  3. MRI brain - structural pituitary/hypothalamus probs
  4. genetic testing for Turner’s, Prader-Willi
125
Q

ddx for GH deficiency (4)

A
  1. hypothyroidism
  2. small for gest age
  3. constitutional delay in growth
  4. Turner’s
126
Q

management of GH deficiency

A

managed and FU by paediatric endocrinologist…

  1. daily subcut injections of Somatropin (GH)
  2. tx for other deficiencies
  3. monitor height and development
127
Q

simple vs complex febrile seizure

A

SIMPLE
<15 minutes
generalised
no recurrence within 24h
complete recovery within an hour

COMPLEX
15-30 mins
focal seizure
repeat seizures within 24h
not recovering within an hour

128
Q

how long does a seizure last in febrile status epilepticus

A

> 30 minutes

129
Q

what 2 things should prompt a paediatrics admission/referral in a child with a febrile seizure?

A
  1. first seizure
  2. complex seizure

PHASE 3A (18 decks)

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