Paeds 3 Flashcards

1
Q

How is nocturnal enuresis defined?

A

involuntary wetting during sleep, without any inherent suggestion of frequency or pathophysiology.
generally considered to be normal in children younger than 5 years of age

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2
Q

Describe the different types of enuresis

A

primary without daytime symptoms - the child has never achieved sustained continence at night and does not have daytime symptoms.

primary with daytime symptoms - the child has never achieved sustained continence at night and has daytime symptoms such as urgency, frequency, daytime wetting, abdominal straining, or poor urinary stream, or pain passing urine.

secondary - bedwetting occurs after the child has been dry at night for more than 6 months

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3
Q

What are the causes of primary enuresis without daytime symptoms

A

Sleep arousal difficulties — inability to wake to noise, the sensation of a full bladder, or bladder contractions.

Polyuria — a larger than normal production of urine at night which is greater than bladder capacity.

Bladder dysfunction — a small bladder capacity or overactive bladder.

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4
Q

What are the causes of primary enuresis with daytime symptoms

A

An overactive bladder.
Structural abnormalities (for example ectopic ureter).
Neurological disorders (for example neurogenic bladder secondary to spinal dysraphism).
Chronic constipation.
Urinary tract infection.

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5
Q

What are the causes of secondary enuresis

A

underlying cause:
diabetes,
urinary tract infection,
constipation,
psychological problems (for example behavioural or emotional problems),
family problems (vulnerable child or family)

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6
Q

What are the risk factors for enuresis

A
FH
male
delay in development
constipation
psych or behavioral problems - ADHD, ASD, anxiety, depression, conduct disorder
sleep apnoea
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7
Q

What questions are important to ask in a history of enuresis

A
primary or secondary
any day time symptoms
medical or physical tigger
social, emotional or enviromental problems
?child maltreatment
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8
Q

What would be red flags for child maltreatment in an enuresis history

A

parents blaming the child - think the child is wetting onpurpose
punishments for bedwetting
bedwetting persists after adequate managment

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9
Q

What investigaitons could be done in enuresis

A

urinalysis if started recently, daytime symptoms, child seems unwell or history suggesting UTI/diabetes

ask parents to keep diary with fluid intake, toilet use and wetting recorded

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10
Q

What is the management for enuresis

A

<7y - usually resolves over time. ensure fluid intake not excessive, encourage to empty bladder before bed

> 7y - first line is enuresis alarm
next desmopressin

if daytime symptoms, need referral

if secondary, exclude cause before referral

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11
Q

Describe the enuresis alarm and its usefulness

A

most effective long term treatment
useful in those >7y

An enuresis alarm has a sensor pad which senses wetness. The sensor is linked to an alarm which wakes the child if it becomes wet. There are two main types of enuresis alarms:
Beside alarms — where a noise box is placed next the child’s bed and a sensor pad is positioned under a draw sheet beneath the child in the bed.
Body-worn alarms — where a tiny sensor is attached to the child’s pants for example between two pairs of tightly fitting underpants and the alarm is worn on the pyjama top.

contunue to use until 14 dry nights in a row

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12
Q

Who might an enuresis alarm not be suitable for?

A

The child or parents and carers do not want to use one.
The child wets the bed (infrequently) less than once or twice a week.
Parents or carers have emotional difficulty coping with the burden of bedwetting.
Parents or carers express anger, negativity, or blame towards the child.
The child is younger than 7 years of age and is not able to use an alarm.

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13
Q

What are the signs of response to enuresis alarm treatment

A

Smaller wet patches.
Waking to the alarm.
The alarm going off later and fewer times per night.
Fewer wet nights.

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14
Q

Describe the mechanism of action of desmopressin and its usefulness in managing enuresis

A

ADH analogue so reduces quantity of urine produced

used in short term management if:
A rapid onset in improvement or a short-term improvement is required (for example for sleepovers or school trips).
The child or parents or carers are unable to use an alarm or do not want to use a alarm as first-line treatment.
The child or parents and carers are currently using an alarm and want to stop.

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15
Q

How should desmopressin be taken?

A

take at bedtime

sips only from one hour before taking until 8 hours after taking - reduces risk of hyponatraemia and fluid overload

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16
Q

When can desmopressin not be prescribed

A

heart failure
HTN
taking diuretics
psychogenic polydipsia

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17
Q

What is necrotising enterocolitis

A

vascular, mucosal, toxic and other insults to the immature gut leads to serious intestinal injury
damage to the mucosa leads to the spread of commensal organisms

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18
Q

What are the features of necrotising enterocolitis

A
occurs in preterm or very low birth weight neonates
in first two weeks of life
bilious vomiting
bloody mucoid stool
feeding difficulties
abdominal distension and erythema
intestinal loops visible
abdominal mass present/ascites
reduced bowel sounds
bradycardia, lethargy, shock, apnoea, resp distress
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19
Q

What investigations should be done in suspected necrotising enterocolitis

A

FBC CRP VBG U+E

AXR

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20
Q

What can be seen on AXR in necrotising enterocolitis

A

wall thickening
gas filled loops of bowel
pneumatosis intestinalis = intramural gas
portal venous gas

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21
Q

What is the management of necrotising enterocolitis

A
NBM - bowel rest
NG tube to decompress bowel with intermittent suction
IV fluids
IV abx - cefotaxime + metronidazole
TPN
intubation or ventilation if apnoea
surgery if perforation/necrotic bowel
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22
Q

What are the potential complications of necrotising enterocolitis

A
Perforation.
Acquired short bowel syndrome (following surgery).
DIC.
Sepsis and shock.
Intestinal strictures (~30%).
Enterocolic fistulae.
Abscess formation.
Iatrogenic complications - eg, central venous catheter-related thrombotic events and nosocomial infections, metabolic complications secondary to prolonged hyperalimentation (a nutrient mixture given to premature babies before giving milk).
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23
Q

How can necrotising enterocolitis be prevented?

A

breast milk
small feeds - increase volume slowly
probiotics

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24
Q

What is coeliac disease?

A

autoimmune condition in which glutens activate an abnormal mucosal response leading to chronic inflammation and damage (mucosal atrophy) to the lining of the small intestine

25
Q

What are the risk factors for coeliac disease

A

FH - first degree relatives
genetic - HLA DQ2 and HLA DQ8
other automimmune - T1DM, automimmune thyroid
down’s, turner’s william’s syndromes

26
Q

What are the symptoms of coeliac disease

A
failure to thrive
prolonged and unexplained diarrhoea, bloating, constipation, indigestion
fatigue
weight loss
mouth ulcers - severe or persistent
27
Q

What skin condition is associated with coeliac disease

A

dermatitis herpetiformis

28
Q

Describe dermatitis herpetiformis

A

symmetrical
on extensor surfaces, scalp and natal cleft
vesciles or papules on erythematous patch of skin
intensely itchy

29
Q

How is dermatitis herpetiformis treated

A

Dapsone PO

30
Q

How is coeliac disease investigated

A

serology testing - IgA and tTGA
FBC, B12, ferritin, LFTs, calcium
jejunal biopsy

31
Q

What is important to ask patients before serology testing for coeliac disease

A

have they been eating gluten??iac d

need to have been eating gluten at least twice a day for past 6 weeks in order for test to give reliable answer

32
Q

What does tTGA stand for?

A

tissue transglutaminase

33
Q

What is seen on jejunal biopsy in coeliac disease?

A

subtotal villous atrophy
crypt hyperplasia
increase in intraepithelial lymphocytes
lamina propria infiltration with lymphocytes

34
Q

What is the management of coeliac disease?

A

gluten free diet

supplements if needed eg. calcium or vit D

35
Q

Give some differentials for coeliac disease?

A
Crohn's disease 
Ulcerative colitis.
Malignancy
Infections such as HIV and tuberculosis infection — presenting with possibly mouth ulcers (in HIV infection and AIDS), prolonged fatigue, and unexpected weight loss. 
Irritable bowel syndrome 
Cow's milk protein allergy 
Aphthous ulcer
36
Q

What are the potential complications of coeliac disease

A

Anaemia, due to deficiency of iron, folate, or vitamin B12 due to malabsorption
Osteoporosis, due to malabsorption of calcium and/or vitamin D.
Increased risk of fragility fractures.
Chronic pancreatitis with pancreatic insufficiency.
Hepatobiliary abnormalities such as autoimmune hepatitis, primary biliary cirrhosis, and primary sclerosing cholangitis.
Splenic dysfunction - hyposplenism
Subfertility.
Lactose intolerance.
Faltering growth.
Delayed puberty.
enteropathy-associated T-cell lymphoma of small intestine

37
Q

What is VUR

A

vesicoureteric reflux
abnormal backflow of urine from bladder to ureter and kidneyu

primary is due to ureters being displaced, entering bladder at a perpendicular angle and having a shorter intramural course.
VUJ does not close as bladder distends
so urine flows up the ureters

38
Q

What is the function of the ureteric opening being 2cm in to the bladder

A

so that as the bladder distends with urine, the entrance to the ureter closes
acts a valve and prevents backflow of urine into the ureters

39
Q

Describe the stages of VUR

A

I - Reflux into the ureter only, no dilatation

II - reflux into ureters and renal pelvis on micturition, no dilation

III - mild/moderate dilation of ureter, renal pelvis and calyces

IV - dilation of ureter, renal pelvis adn calyces with moderate ureteral tortuosity

V - gross dilation of ureter, renal pelvis and calyces with ureteral tortuosity

40
Q

What complications can VUR lead to

A

recurrent UTI
pyelonephritis
renal scarring
HTN due to renal scarring

41
Q

What investigations need to be done for VUR

A

abdo USS
micturating cystourethrogram
DMSA scanning - looks for renal scarring

42
Q

How can VUR be managed

A

reassurance - in most cases resolves as the ureter and bladder grow over time and valve function improves

can have surgery to repair VUJ valve

43
Q

What is Turner syndrome

A

45X

44
Q

How common is Turner syndrome

A

1 in 2000 live births

45
Q

What are the features of Turner syndrome in a neonate

A

SGA
lymphoedema in hands and feet
excessive skin at nape of neck
cardiac abnormalities

46
Q

What cardiac abnormalities are most common in Turner syndrome

A

bicuspid aortic valve
coarctation of aorta

also
pulmonary stenosis
aortic stenosis

47
Q

What are the features of Turner syndrome in an infant

A

feeding difficultues
poor weight gain
length close to and parallel to the 3rd centile
poor sleep

48
Q

What are the features of Turner syndrome in a preschool age child

A
short statre
high activity
behavioural problems
recurrent middle ear infections
sensorineural hearing loss
49
Q

What are the features of Turner syndrome in a school age child

A
gonadal dysgenesis
obesity
learnign difficulties
social vulnerability
renal anomolies
 foot problems (eg, toenail involution, cellulitis),
50
Q

What renal anomolies are common in Turner syndrome

A
double collecting system
absent kidney
malrotation of kidney
horseshoe kidney
hydronephrosis
51
Q

What are the features of Turner syndrome in an adolescent

A
impaired prepubertal growth spurt
obesity
ovarian failure
HTN
autoimmune disease - autoimmune thyroiditis, coeliac disease, inflammatory bowel disease
specific learning difficulties
52
Q

What are the features of Turner syndrome in an adult

A
infertility
obesity
HTN
aortic dilatation or dissection
autoimmune thyroid disease
osteoporosis
53
Q

What are the dysmorphic features in Turner syndrome.

Eyesm ears, mouth, neck, chest, joints, hands, skin

A

Eyes - epicanthic folds, oblique palpebral fissures, ptosis, squint, nystagmus, cataracts, amblyopia, and hypermetropia.

Ears - low-set, posteriorly rotated ears, prominent upturned lobules.

Mouth - micrognathia, high palate and mandible abnormalities can result in crowding of teeth and malocclusion.

Neck - short, webbed; low hairline.

Chest - broad chest, pectus excavatum, inverted, hypoplastic, widely-spaced nipples.

Joints - cubitus valgus, congenital hip dislocation.

Hands - short 4th/5th metacarpals, short fingers, forearm and carpal developmental abnormalities; nail hypoplasia, hyperconvex nails, nail-fold oedema.

Skin lymphoedema - hands, feet, neck (pterygium coli), pigmented naevi, telangiectasias, vitiligo, keloid, seborrhoeic dermatitis; increased body hair with alopecia. There is a risk of keloid formation with surgery.

54
Q

What investigations can be done in Turner’s

A

ECG, hearing tests
U+E, TFT, HbA1c, FSH, LH, bone profile
chromosome analysis
renal USS, heart echo

55
Q

How can the growth failure in Turner’s be managed

A

GH and oestrogen

56
Q

How is maintenance fluids for children calculated?

A

100ml for 10kg
50ml for next 10kg
20ml for any more kg

given over 24 hours

57
Q

How are fludi replacement amount calculated in children?

A

according to % fluid deficit

weight (kg) x % replacement x 10 given over 48 hours

58
Q

Who is screened for coeliac disease

A

T1DM,
autoimmune thyroid disease,
Trisomy 21,
1st degree relatives with coeliac

59
Q

What is the difference between a simple and complex febrile convulsion

A

Simple: lasts <15mins, not recurring in same illness,
generalised

Complex: >15mins, recur in same illness, focal