W06 - PAEDS: GI, Infant Feeding, Liver, Growth & Endocrine Flashcards

1
Q

Causes of Vomiting in Children

A

Enteric pathogens
Infection
Stimuli / Fear
Head injury / ICP = morning vomiting w/ retching
Inner ear stimuli
Metabolic derangements

Haemetemesis: peptic ulcers, portal hypertension

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2
Q

GORD in Paediatrics

A

effortless vom.

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3
Q

Location of the vomitting centre

A

Medulla oblongata

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4
Q

Common causes of vom in infants

A

GOReflux
Cow’s Milk allergy
Infection
Intestinal obstruction

+ pyloric stenosis = olive tumour = projectile non billous vom after feed
+ overfeeding

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5
Q

Common causes of vom in childrena nd YA

A
  • gastroenteritis
  • infection
  • raised ICP
  • Obstruction
  • Coeliac

+h pylori
+ DKA
+ cyclical vomiting syndrome
+ bulimia

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6
Q

Common causes of vom in childrena nd YA

A
  • gastroenteritis
  • infection
  • raised ICP
  • Obstruction
  • Coeliac

+h pylori
+ DKA
+ cyclical vomiting syndrome
+ bulimia

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7
Q

Pyloric stenosis

A

olive tumour, non-billous projectile vom., M>F
- wt loss
- dehydration

*HYPOKALEMIC
* HYPOCHLOREMIC METABOLIC ALKALOSIS

> Fluid resus
Pyloromectomy

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8
Q

Effortless Vomiting

A

almost always dt GOReflux, very common, self-limiting, worse at 4-6mos, improves by 1st year

  • laxed lower oesoph. sphincter
  • exacerbated by nature of liquid foods
  • resp symptoms: apnoea, cough, wheeze, chest infections
  • sandifer’s syndrome = dystonic positioning dt reflux

*pH meter = looking at how often pH drops below 4
*pH study = combined w/ meter, to detect significant reflux
* endo. (reflux, eosophagitis), vid fluoroscopy (aspiration pneumon.), barium swallow (hiatus)

> feeding advice: thickener etc.
nutritional support: NG tube
medical: feed thickener, prokinetic drugs, ACID SUPPR. DRUGS
Sx: for resistant, and failure to thrive, aspiration, oesophpagitis

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9
Q

Indication for upper GI endoscopy in children

A

growth faltering
persistent sympoms
unresponsive to anti-reflux rx

*requires GA

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10
Q

Bilious vomiting

A

red flag!!

*intestinal obstr. dt
- atrsia
- malrotation, interssuspection, ileus, crohns + strictures

  • abdo xr
    contrast meal
    sx: exploratory lap.
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11
Q

Definition of chronic diarrhoea

A

4 or more stools per day for more than 4 weeks

  • <1w = acute diarr.
    2-4w = persistent
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12
Q

Significance of nocturnal defecation in chronic diarr.

A

suggestive of organic path.

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13
Q

OSMOTIC vs SECRETORY DIARRHOEA

A

OSMOTIC
- small stool volume, responds to fasting
- low in metabolites and ions

SECRETORY
- large volume, continuous despite fasting
- high in metablites and ions.

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14
Q

Fat malabs and chronic diarrhea in children

A

PANCREATIC
- lack of lipase = steatorrhoea
- CF

HEPATOBILIARY
- chronic liver disease
- cholestasis

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15
Q

Commonest cause of malabs in children

A

Coeliac Disease
* symptomatic children are tip of iceberg
* latent, genetics testing but negative predictive value

  • dermatitis herpatiformis, other auimm conditions: IDDM
  • short stature, failure to thrive

*anti-TTG,
+vantiendomysial, serum igA
DUODENAL BIOPSY
* abdo bloatedness

if symptomatic, positive serology and genetics, can be diagnosed WITHOUT biopsy
* if any serology is not present, requires endoscopy.

> GF diet

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16
Q

Significance of toddler’s diarrhea

A

well
undigested veg in stool
= chronic non-specific toddlers diarrhea

will improve with age

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17
Q

Constipation vicious cycle (organic cause)

A

constipation => large hard stool => pain/anal fissure => withholding of stool

+ social causes too: diet, xs milk
+ physical: intercurrent illness, medication
+ 2º to psychological

18
Q

Management approaches to constipation

A

> Dietary - social

> Ensure toilet a pleasant experience
* reward good behaviour

> osmotic lax (lactulose)
stimulant lax (senna etc)
isotonic laxatives (movicol)

  • provide adequate tx until no longer required
    ?compliance, sfx monitoring

!megarectum
> stimulatory suppositories

19
Q

Significance of crohns in scottish children

A

incidence has been increasing in the last 20 years, panenteric disease most common thus more widespread.

!WT LOSS
!GROWTH FAILURE = growth and sexual development disruption
!ABDO PAIN

extramanifs:
-erythema nodosum
- oral changes: rolled edge ulcer
- perianal tags and fissures

anemia, thrombocytosis, raised ESR
* stool calprotectin

* raised CRP, low albumin

Vs UC
diarrhoea
rectal bleeding
abdo pain

20
Q

Colitis red flags

A
  • nocturnal diarrhoea
  • bloody diarrhoea
21
Q

UC in Children

A

not as common in children
diarrhoea (nocturnal)
rectal bleeding
abdo pain

*pancolitis more common - more widespreadextensive phenotype

22
Q

Investigations & mgmt in paed UC or Crohns

A
  • radiology (crohns)
  • MRI altnernatively USS for younger
  • barium meal (younger but rarely)
  • endoscopy
  • colonoscopy & upper GI: ALWAYS ILEAL COLONOSCOPY
  • mucosal biopsy
  • capsule enteroscopy
    -enteroscopy

UC: crypt abscess, disordered crypts histology
CD: serpingous ulcer: slimy snail-like, granulomatous histology

> remission
correct nutritional deficiencies
maintain normal growth and development - steroid risk

> > (1) nutritional rx for crohns, space food, liquid therapy etc. - aim for abs. in upper GI. + pred
(2) steorid sparing: azathioprine, mtx.
(3) biologics)
anti-inflamm, imm suppr., biologics = used to get remission for relapsing flare-up
immune modulation
sx: stricture

23
Q

Investigations & mgmt in paed UC or Crohns

A
  • radiology (crohns)
  • MRI altnernatively USS for younger
  • barium meal (younger but rarely)
  • endoscopy
  • colonoscopy & upper GI: ALWAYS ILEAL COLONOSCOPY
  • mucosal biopsy
  • capsule enteroscopy
    -enteroscopy

UC: crypt abscess, disordered crypts histology
CD: serpingous ulcer: slimy snail-like, granulomatous histology

> remission
correct nutritional deficiencies
maintain normal growth and development - steroid risk

> > (1) nutritional rx for crohns, space food, liquid therapy etc. - aim for abs. in upper GI. + pred
(2) steorid sparing: azathioprine, mtx.
(3) biologics)
anti-inflamm, imm suppr., biologics = used to get remission for relapsing flare-up
immune modulation
sx: stricture

24
Q

To compare breast and formula feeding

A

a

25
Q

To explain the management of cow’s milk protein allergy

A

> NUTRAMIGEN
APTAMIL

(2)
> sma: AMINO ACID BASED FEEDS
* SEVERE COLITIS/ENTEROPATHY

+APTAMIL PEPTI SYNEO: COWLS MILK PROTEIN WITH ADDED PROBIOTIC
+ NEOCATE SYNEO “”
+ neocate junior: amino acid for children 1yr+ with allergy

*SOYA INFANT FORMULA: dental caries risk, phytoestrogens risk, cross-react with cows milk

+ENSURE CALCIUM REQUIREMENTS ARE MET.

26
Q

Avg term infant

A

3.3kg

27
Q

Infant Nutrition

A

high risk for malnutrition

*human milk fortifiers: dietary supplement

28
Q

Avg weight gain in infants

A

0-3months 200g per week
3-6 months 150g per week
6-9 months 100g per week
9-12 months 75-50g per week

x2 weight by 6mos and x3 by 1 year

*after 1ur, 2kg, and 5cm/year until puberty

29
Q

Know the clinical manifestations of paediatric liver disease

A

JAUNDICE >40-50umol/l
- prehepatic jaundice = unconjugated
- intrahepatic = mixed
- posthepatic jaundice = conjugated (cholestasis)

Incidental finding of abdn bloos

Chronic liver disease symptoms/signs
- growth failure
- ascites, splenomegaly w/ portal HT
- spider naevi
- fat malabs, deficienvy of fat-soluble vitamins
- rickets (vit d def.)

30
Q

Be aware of the biochemical markers used in the assessment of liver disease in chiildren

A

Total bilirubin
Split: Direct + Indirect Bilirubin

ALT/AST: hepatitis

Alkaline phosphatase: biliary disease

GGT: biliary disease

31
Q

Describe the causes of unconjugated and conjugated hyperbilirubinaemia and prolonged neonatal jaundice (including biliary atresia)

A

<24hr old early neonate jaundice
= haemolysis, sepsis

24hr-2w intermediate neonate
= physiological, breast milk, sepsis, haemolysis

2w+ prolonged
= extrahepatic obstruction, neonatal hepatitis (A,B,C), hypothyroidism, breast milk

compl: KERNICTERUS: deposits of uncon. bili in brain = ENCEPHALOPATHY, late choreoathetoid cerebral palsy = developmental disruption

> PHOTOTHERAPY promotes conjugation to water-soluble

32
Q

Physiological jaundice in neonates

A
  • relative polycythemia
  • relative immaturity of liver funct.

= unconjugated jaundice

33
Q

Breast milk jaundice

A

unclear but ?UDP inhibition via progesterone metbaolite or ?increased enterohepatic circulation

= unconjugated jaundice

34
Q

Common abn conjugation of bilirubin in infant jaundice

A

GILBERT’S DISEASE

35
Q

Prolonged infant jaundice

A

persisting beyond 2w of life
*SPLIT BILIRUBIN TEST
* ASSESS STOOL = PALE = CONJUGATED jaundice

  • Biliary atresia = conj. jaundice; pale stools + dark piss
    > kasai poroenterostomy
    > liver transplant
  • identify and dx early to ensure prompt tx and plan
  • USS, lier biopsy
  • Choledochal cyst = cong. jaundice; pale
  • USS
  • Intrahepatic cholestasis, dysmorphism, congenital cardiac disease
36
Q

Bone Age Assessment in Paeds

A

Tanner-Whitehouse (TW) method involves the scoring of each carpal bone, the radius and ulna leading to a total score, from which age can be estimated.

37
Q

Common Causes of short stature

A

-familial

-constitutional

  • SGA / UGR

+IGR deficiency = isolated GH def.
* MRI
> GH replacement

38
Q

Tanner Staging

A

*Stage I = prepubertal
* Stage II = start of puberty

*breast budding = B2
Testicular enlargement = G2-T 4ml

39
Q

Ages of Puberty

A

Females begin with breast budding at ~10yo
Menarche later development.

Whereas males begin with testicular growth onset at 11/12yo. Male growth spurt later.

40
Q

Abn Growth: Short Stature - pathological

A

Chronic illness

Iatrogenic steroid use

Psychosocial disturbance

SIMPLE OBESITY

  • Thyroid def.
  • Turner Syndrome: female short stature, ovarian dysgenesis
  • karyotyping
  • Prader-willi syndrome: short stature, hypogonadism, obesity in childhood, infantile hypotonia/feeding problem
  • Noonan syndrome: congenital heart disease
  • Achondroplasia - short limb dwarfism
  • long bones dont grow properly
41
Q

Early sexual development

A

*abn steroid prod. = congenital adrenal hyperplasia

  • CENTRAL PRECOCIOUS PUBERTY
  • breast / testicular development
  • growth spurt
  • advanced bone age
  • MRI = ?pit. lesion
  • PRECOCIOUS PSEUDOPUBERTY
  • secondary charac. development
  • independent of LH/FSH
  • exclude congenital adrenal hyperplasia
42
Q

DM in Children

A

PRESENTS T1DM.
* ensure early dx and mgmt. prevent DKA. prevent LT complications and disability.

t4
thirsty
tired
thinner
toilet+++

*bedwetting REDFLAG

+candidiasis
+ skin infections
+ heavier nappies
+ blurred vision

DKA = ap blood glc
11MMOL+ = DM

=> referral