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Year 3 > Paediatric Gastroenterology > Flashcards

Paediatric Gastroenterology Flashcards

1
Q

indications for enteral nutrition: inadequate oral intake

A 
disorders of suckling and swallowing
prematurity
neurological impairment
congenital abnormalities of oesophagus
oral/head neck tumours
trauma and extensive burns
severe gastroesophageal reflux
mechanical ventilation/cardiorespiratory disease
food aversion
anorexia
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2
Q

indications for enteral nutrition: disorders of digestion and absorption

A 
CF
short bowel syndrome
IBD
malabsorption due to food allergy
protracted diarrhoea of infancy
chronic liver disease
intestinal fistula
disorders of gastrointestinal motility e.g. chronic pseudo-obstruction, gastroparaesis
growth failure or chronic malnutrition
metabolic disease
hypermetabolic status
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3
Q

factors to consider for percutaneous endoscopic gastrostomy

A 
psychosocial factors
ethics and prognosis
quality of life
information and consent
clinical status
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4
Q

complications of enteral tubes

A

infection of stoma site
over granulation of stoma site
buried bumper (Freka PEG)
tube dislodgement

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5
Q

risks of enteral tubes

A

wrong port used
blockage of tube
tube falls out

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6
Q

types of vomiting

A
  • Vomiting with retching
  • Projectile vomiting
  • Bilious vomiting
  • Effortless vomiting
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7
Q

phases of vomiting with retching

A 
• Pre-ejection phase
o Pallor
o Nausea
o Tachycardia
• Ejection Phase
o Retch
o Vomit
• Post-ejection Phase
o Weakness
o Shivering
o Lethargy
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8
Q

stimulation of vomiting centre

A
  • Enteric pathogens
  • Intestinal inflammation
  • Metabolic derangement
  • Infection
  • Head injury
  • Visual stimuli
  • Middle ear stimuli
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9
Q

who gets pyloric stenosis?

A

babies 4-12 weeks

boys>girls

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10
Q

pyloric stenosis features

A

projectile non-bilious vomiting
weight loss
dehydration +/- shock

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11
Q

characteristic electrolyte disturbance in pyloric stenosis

A 
o Metabolic alkalosis (↑pH)
o Hypochloraemia (↓Cl)
o Hypokalaemia (↓K)
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12
Q

gastroesophageal reflux in children

A
  • Movement of gastric contents into the oesophagus
  • Effortless vomiting
  • Very common problem in infants
  • Usually self-limiting and resolves spontaneously
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13
Q

presenting symptoms of malabsorption in children

A 
• Gastrointestinal
o Vomiting
o Haematemesis
• Nutritional
o Feeding problems
o Failure to thrive
• Respiratory
o Apnoea
o Cough
o Wheeze
o Chest infections
• Neurological
o Sandifer’s syndrome
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14
Q

what is Sandifer’s syndrome?

A

Sandifer’s syndrome is the association of gastro-oesophageal reflux disease with spastic torticollis and dystonic body movements. Nodding and rotation of the head, neck extension, gurgling sounds, writhing movements of the limbs, and severe hypotonia have been reported. It is hypothesised that such positionings provide relief from discomfort caused by acid reflux. A causal relation between gastro-oesophageal reflux disease and the neurological manifestations of Sandifer’s syndrome is supported by the resolution of the manifestations on successful treatment of gastro-oesophageal reflux disease. The clinical manifestations almost invariably arouse the suspicion of neurological disease and lead to unnecessary investigative procedures.

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15
Q

medical assessment of vomiting and malabsorption

A 
• History & examination often sufficient
• Radiological investigations
o Video fluoroscopy(only if swallowing problems)
o Barium swallow
§ Dysmotility
§ Reflux
§ Gastric emptying
§ Strictures
• pH study
• Oesophageal impedance monitoring
• Endoscopy
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16
Q

treatment of vomiting and malabsorption in children

A

feeding advice
nutritional support
medical treatment
surgery

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17
Q

feeding advice in vomiting and malabsorption in children

A 
o Feed thickeners (Carobel)
o Appropriateness of foods
§ Texture
§ Amount
o Behavioural programme
§ Oral stimulation
§ Removal of aversive stimuli
o Feeding position
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18
Q

nutritional support in vomiting and malabsorption in children

A

o Calorie supplements
o Exclusion diet (milk free)
o Nasogastric tube
o Gastrostomy

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19
Q

medical treatment n vomiting and malabsorption in children

A 
o Feed thickener
§ Gaviscon, Thick and Easy
o Prokinetic drugs
o Acid suppressing drugs
§ H2 receptor blockers
§ PPIs
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20
Q

surgery n vomiting and malabsorption in children

A 
o Indications
§ Failure of medical treatment
§ Persistent
• Failure to thrive
• Aspiration
• Oesophagitis
o Vomiting without complications is not an indication
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21
Q

describe nissen fundoplication

A

Children with cerebral palsy are more likely to have complications of bloat, dumping and retching after surgery. Successful surgery may unmask more generalised GI motility problems in the child. The postoperative course may be more complicated in children with cerebral palsy. Dumping relates to early jejunal filling due to rapid gastric emptying and can lead to unpleasant symptoms such as intermittent sweating and diarrhoea following meals.

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22
Q

causes of bilious vomiting in children

A
  • Intestinal atresia (in newborn babies only)
  • Malrotation +/- volvulus
  • Intussusception
  • Ileus
  • Crohn’s disease with strictures
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23
Q

bilious vomiting in should is always what until proven otherwise

A

intestinal obstructions

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24
Q

investigations of bilious vomiting in children

A
  • AXR
  • Consider contrast meal
  • Surgical opinion re exploratory laparotomy
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25
Q

the small intestine secretory component

A

• Water for fluidity/enzyme transport/absorption
• Ions e.g. duodenal HCO3
-
• Defence mechanism against pathogens/harmful substances/antigens
o Flushes them out

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26
Q

define chronic diarrhoea in children

A

presence of 4 or more stools per day for more than 4 weeks

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27
Q

causes of diarrhoea in children

A 
• Motility disturbance
o Toddler diarrhoea
o Irritable bowel syndrome
• Active secretion (Secretory)
o Acute infective diarrhoea
o Inflammatory bowel disease
• Malabsorption of nutrients (osmotic)
o Food allergy
o Coeliac disease
o Cystic fibrosis
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28
Q

type of carbohydrate malabsorption in children

A 
• Primary lactose malabsorption very rare
• Secondary lactose malabsorption
• Glucose-galactose malabsorption
Figure 8 Small Intestine Mucosa
• Fructose malabsorption
• Disaccharidases deficiency
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29
Q

causes of fat malabsorption in children

A 
• Pancreatic Disease
o Diarrhoea due to lack of lipase and resultant steatorrhoea
o Classically cystic fibrosis
• Hepatobiliary Disease
o Chronic liver disease
o Cholestasis
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30
Q

features of Shwachman-Diamond syndrome?

A

pancreatic insufficiency and bone marry dysfunction

neutropenia

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31
Q

secretory diarrhoea mechanism

A

Secretory diarrhoea is classically associated with toxin production from vibrio cholerae and enterotoxigenic Escherichia coli. In cholera you can lose 24l of fluid per day. Intestinal fluid secretion is predominantly driven by active Cl- secretion via CFTR. This is classically toddler’s diarrhoea. Other causes include IBS, congenital hyperthyroidism, and chronic intestinal pseudo-obstruction.

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32
Q

inflammatory diarrhoea mechanism

A

Inflammatory diarrhoea is a mixed bad. Malabsorption due to intestinal damage and secretory effect of cytokines. There is accelerated transit time in response to inflammation. Protein exudate across the inflamed epithelium

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33
Q

clinical approach to diarrheoa in children

A 
• History
o Age at onset
o Abrupt/gradual onset
o Family history
o Nocturnal defecation suggests organic pathology
• Consider growth and weight gain of child
• Faeces analysis
o Appearance
o Stool culture
o Determination of secretory vs osmotic
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34
Q

symptoms of coeliac

A
  • Abdominal bloatedness
  • Diarrhoea
  • Failure to thrive
  • Short stature
  • Constipation
  • Tiredness
  • Dermatitis herpatiformis
35
Q

susceptible asymptomatic group to coeliac

A
  • Type 1 diabetes
  • Autoimmune thyroid disease
  • Down’s syndrome
  • First degree relatives with coeliac
36
Q

screening tests for coeliac

A 
• Serological Screens
o Anti-tissue transglutaminase
o Anti-endomysial
o Concurrent IgA deficiency in 2% may result in false negatives
• Gold standard duodenal biopsy
• Genetic testing
o HLA DQ2, DQ8
37
Q

ESPGHAN/BSPGHAN guidelines for diagnosis of coedliac in children

A
  • Symptomatic children
  • Anti TTG >10 times upper limit of normal
  • Positive anti endomysial antibodies
  • Normal serum IgA
  • HLA DQ2, DQ8 positive
  • Diagnose without biopsy
38
Q

treatment of coeliac in children

A

• Strict Gluten-free diet for life
o (avoid wheat, rye, barley)
• Gluten must not be removed prior to diagnosis as serological and histological features will
resolve
• In very young <2yrs, re-challenge and re-biopsy may be warranted
• Increased risk of rare small bowel lymphoma in untreated

39
Q

clinical manifestations of paediatric liver disease

A
  • Jaundice
  • Incidental finding of abnormal blood test
  • Symptoms/signs of chronic liver disease
  • Growth failure
40
Q

describe bilirubin metabolism and jaudice

A

see notes

41
Q

causes of early jaundice (<24 hrs old)

A

always pathological
haemolysis
sepsis

42
Q

causes of intermediate jaundice (24hrs - 2 weeks)

A

physiological
breast milk
sepsis
haemolysis

43
Q

causes of prolonged jaundice (> 2 weeks)

A

extrahepatic obstruction
neonatal hepatitis
hypothyroidism
breast milk

44
Q

physiological jaundice

A

Relative polycythaemia and immaturity of liver function. It is unconjugated jaundice and develops after the first day of life.

45
Q

life span of RBCs in children

A

80-90 days

46
Q

breast milk jaundice

A

The exact reason for prolongation of jaundice in breastfed infants is unclear. It may be due to
inhibition of UDP by progesterone metabolite or increased enterohepatic circulation. It is
unconjugated jaundice that can persist up to 12 weeks.

47
Q

causes of early/intermediate unconjugated infant jaundice and their diagnosis

A

• Sepsis – urine and blood cultures, TORCH screen
• Haemolysis
o ABO incompatibility – blood group, DCT
o Rhesus disease – blood group, DCT
o Bruising/cephalohematoma – clinical examination
o Red cell membrane defects e.g. spherocytosis – blood film
o Red cell enzyme defects e.g. G6PD – G6PD assay
• Abnormal conjugation
o Gilbert’s disease – genotype/phenotype
o Crigler-Najjar syndrome – genotype/phenotype

48
Q

name and describe a complication of jaundice in children

A

Kernicterus
Unconjugated bilirubin is fat soluble (water insoluble) so can cross the blood brain barrier. Bilirubin is neurotoxic and deposits in the brain. Early signs include encephalopathy resulting in poor feeding, lethargy and seizures. Late consequences include: severe choreoathetoid cerebral palsy, learning difficulties and sensorineural deafness.

49
Q

treatment of jaundice in children

A

Phototherapy can be used to treat unconjugated jaundice. Visible light (450nm), not UV, converts
bilirubin into water soluble isomer (photoisomerization). The threshold for phototherapy in infants is
guided by charts.

50
Q

what is prolonged jaundice?

A

beyond 2 weeks of life or 3 weeks for preterm babies

51
Q

causes of prolonged infant jaundice

A 
• Conjugated
o Anatomical – biliary obstruction
o Neonatal hepatitis
• Unconjugated
o Hypothyroidism
o Breast milk jaundice
52
Q

biliary obstruction in infants

A

• Biliary atresia
• Choledochal cyst
o Conjugated jaundice, pale stool
o Split bilirubin, stool colour, ultrasound
• Alagille syndrome
o Intrahepatic cholestasis, dysmorphism, congenital cardiac disease
o Dysmorphism, genotype

53
Q

biliary atresia in children

A

o Conjugated jaundice, pale stools
o Split bilirubin, stool colour, ultrasound, liver biopsy
Biliary atresia is a congenital fibro-inflammatory disease of bile ducts leading to destruction of extra hepatic bile ducts. It presents with prolonged, conjugated jaundice, pale stools and dark urine. Progression to liver failure if not identified and treated. Timely diagnosis is critical as time to treatment determines prognosis. The most common indication for liver transplantation in children. Treatment is with Kasai portoenterostomy. The success rate for this diminishes rapidly with age. Best results if performed before 60 days (<9 weeks).

54
Q

causes of neonatal hepatitis

A
  • Alpha-1-antitrypsin deficiency (phenotype/level)
  • Galactosaemia (GAL-1-PUT)
  • Tyrosinaemia (amino acid profile)
  • Urea cycle defects (ammonia)
  • Haemochromatosis (iron studies, liver biopsy)
  • Glycogen storage disorders (biopsy)
  • Hypothyroidism (TFTs)
  • Viral hepatitis (serology, PCR)
  • Parenteral nutrition (history)
55
Q

why is nutrition important in children

A

Nutrition is a fundamental aspect of life. Growth is not just increasing size but change in body structure, composition and function. Globally, malnutrition contributes to 54% of the deaths in under 5s. breast feeding is important in disease prevention. The primary treatments are metabolic disease and exclusion of allergens.

56
Q

why do we need nutrition?

A

• Energy is needed for:
o Physical activity
o Thermogenesis
o Tissue maintenance
o Growth
• Energy requirement = energy expended + energy deposited in new tissue
• Growth demands - about 35% of energy intake in infants but falls for rest of childhood

57
Q

risks of infant nutrition

A

• Characteristic feature is the need to fuel both rapid growth and maintenance
o Infants can rapidly become malnourished.
o Dependent on carer
o High demands for growth and maintenance
§ Infants 100kcal and 2g protein/kg/day
§ Adults 35kcal and 1g protein/kg/day
o Low stores (Fat and protein)
o Frequent illness

58
Q

average weight gain of infants

A
  • 0-3months – 200g
  • 3-6 months – 150g
  • 6-9 months – 100g
  • 9-12 months - 75-50g
  • Double weight by 6 months and triple by 1 year
  • After 1 year approx. 2kg and 5cm/year until puberty
  • 4kg baby with 4 weeks of static weight ,20% underweight, like an adult losing 20kg.
  • Growth charts, plot and interpret
59
Q

why is breast best?

A 
Nutritionally best for full term babies
o Well tolerated
o Less allergenic
o Low renal solute load
o Ca:PO4, Iron, LCP FAs
• Improves cognitive development
• Reduces infection
o Macrophages and lymphocytes
o Interferon, lactoferrin, lysozyme
o Bifidus factor
60
Q

breast milk vs formula

A

Suckling/bonding ?”near-perfect” nutrition for up to a year
(?preterms)
“Perfect” nutrition for 6 months for most infants Non anti-infection properties
Tailor-made passive immunity Risk of contamination
Increased development of infant’s active
immunity
No transition of BBVs/drugs
Increased development of infant’s gut mucosa High antigen load
Reduced infection Expensive
Antigen load minimal Doesn’t need mum
?decreased breast cancer Accurate feed volume
Provides vit K
Less jaundice

61
Q

UNICEF baby friendly - 10 steps

A
  1. Have a written breast-feeding policy routinely communicated to all staff
  2. Train all health care staff in skills necessary to implement this policy.
  3. Inform all pregnant women about the benefits/management of breastfeeding.
  4. Help mothers initiate breastfeeding within a half-hour of birth.
  5. Show mothers how to breastfeed, and how to maintain lactation even if they should be separated from their infants.
  6. Give newborn infants no food and drink other than breast milk, unless medically indicated.
  7. Practise rooming-in - allow mothers+ infants to remain together - 24h/day
  8. Encourage breast-feeding on demand.
  9. Give no artificial teats, pacifiers (dummies) to breastfeeding infants.
  10. Foster the establishment of breast-feeding support groups and refer mothers to them on discharge from the hospital or clinic.
62
Q

options if breast feeding is not possible

A 
• Formula feeding is common
• All are cow’s milk based
• Various brands available
o No significant difference
o Use” first milks” for 0-6 months
• Powder or ready to feed
• Various compositions based on age
63
Q

types of milk for children

A

• Milk is the exclusive feed for 4-6 months
• Breast is Best- WHO recommendation
o 36% Aberdeen babies exclusively at 6 weeks
• Standard formula (Cow’s milk based)
• Specialised
o for cow’s milk protein allergy
o nutrient dense
o disease specific
• Cow’s milk not as main drink until 1 year
o Contains no iron
• Pre-term formulae
o Example SMA Gold Prem 1
o Typically, 2g (vs 1.5) protein and 80kcal (vs 68)/100ml
o Post discharge prescribable eg Nutriprem 2
• Nutrient dense formulae
o Infatrini 100kcal/100ml ,prescribable to 18 months

64
Q

cows milk protein allergy in kids alternatives

A 
• First line feed choice
o Extensively hydrolysed protein feeds
o 90% should respond (10% react)
o Palatability a problem in older babies
§ Nutramigen LGG Lipil 1 and 2
§ Aptamil Pepti 1 and 2
• Second line feeds
o Amino acid based feeds
o Babies with severe colitis/enteropathy/ symptoms on breast milk
o Are over prescribed (and expensive!)
65
Q

lactose free milks in children

A

• Lactose intolerance
o Not allergy.
o Reduced levels of the enzyme (lactase)
o Seen to minor degree in some breast fed babies
o Post gastro enteritis (Transient and self-resolving)
o Also, in certain ethnic groups post weaning
• For secondary lactose intolerance
o Short lived condition eg post gastro-enteritis
o Confused with cow’s milk protein intolerance
o Lactose free/ “Comfort” milks are not CMP free

66
Q

soya milks for children

A

phytoestrogens
cross reactivity with cows milk
Soya indications
o Milk allergy when hydrolysed formulae refused
o Vegan families, if not breast fed
o Consider for children>1 year still on milk free diet

67
Q

weaning from breast milk

A

• Transition from milk to a mixed diet
o nutritional and developmental changes
• Starts at about 5-6 months
o Smooth purees cereal, fruit, veg, meat
o Lumps/finger foods from 6-7 months
o Cup from 7 months
Can be associated with: Higher risk of Fe deficiency and coeliac disease. Concern over higher incidence
of food allergies. Increased weaning issues around bitter tastes and lumpy food. Pragmatic answer:
All babies are different, “not before 17 weeks and not after 6 months”.

68
Q

nutritional supplements recommended

A

• All pregnant and breastfeeding women (10 μg/day)
• Infants aged 1-6 months who are exclusively breastfed and where the mother has a low
vitamin D status (7.5 μg/day)
• All infants and children aged from 6 months to 5 years, unless they are drinking 500 ml (a pint)
or more of infant formula a day (only recommended for children up to the age of 1 year) (7.5
μg/day)
• People who are not exposed to much sun, e.g. housebound and those who cover their skin
for cultural reasons (10 μg/day)
• All people aged 65 years and over, in particular those living in institutions or who are not
regularly exposed to sunlight (10 μg/day)

69
Q

nutrition beyond infancy: toddler and preschool

A

o Learning to feed self and find food
o Picky eaters/excess milk
o Dependent on carer
o Frequent illness

70
Q

nutrition beyond infancy: school age

A

o Learning to be independent
o Chronic disease
o Obesity
§ 12 % of Aberdeen primary 1’s are overweight and 10% obese

71
Q

nutrition beyond infancy: adolescent

A

o Independent, puberty, eating disorders

72
Q

signs and symptoms of chronic constipation

A
  • Poor appetite
  • Irritable
  • Lack of energy
  • Abdominal pain or distension
  • Withholding or straining
  • Diarrhoea
73
Q

why do children become constipated?

A 
• Social
o Poor diet
§ Insufficient fluids
§ Excessive milk
o Potty training / school toilet
• Physical
o Intercurrent illness
o Medication
• Family history
• Psychological (secondary)
• Organic
74
Q

treatment of chronic constipation: social

A 
• Explain treatment to parents
• Dietary
o i fibre
oi  fruit
o i vegetables
o i fluids
o d milk
75
Q

treatment of chronic constipation: psychological

A 
• Reduce aversive factors
o Make going to the toilet a pleasant experience
§ Correct height
§ Not cold
§ School toilets
§ Soften stool and remove pain
o Avoid punitive behaviour from parents
• Reward ‘good’ behaviour
o General praise
o Star charts
76
Q

treatment of chronic constipation: medications

A 
• Soften stool and stimulate defecation
o Osmotic laxatives (lactulose)
o Stimulant laxatives (senna, picolax)
o Isotonic laxatives (movicol)
• Advantages
o Non invasive
o Given by parents
• Disadvantages
o Non-compliance
o Side effects
77
Q

treatment of impaction in kids

A
  • Empty impacted rectum
  • Empty colon
  • Maintain regular stool passage
  • Slow weaning off treatment
78
Q

diagnosis of IBD, Crohn’s UC: hx and exam kids

A 
o Intestinal symptoms
o Extra-intestinal manifestations
o Exclude infection
o Family History
o Growth and sexual development
o Nutritional status
79
Q

diagnosis of IBD, Crohn’s UC: lab investigations kids

A 
o Full blood count &amp; ESR
§ Anaemia
§ Thrombocytosis
§ Raised ESR
o Biochemistry
§ Stool calprotectin
§ Raised CRP
§ Low Albumin
o Microbiology
§ No stool pathogens
80
Q

diagnosis of IBD, Crohn’s UC: definitive investigations kids

A 
o Radiology (especially Crohn’s disease)
§ MRI
§ Barium meal and follow-through (younger kids)
o Endoscopy
§ Colonoscopy
§ Upper GI endoscopy
§ Mucosal biopsy
§ Capsule endoscopy
§ Enteroscopy
81
Q

treatment of IBD, Crohn’s UC in kids

A 
• Medical
o Anti-inflammatory
o Immuno-suppressive
o Biologicals ( Infliximab)
• Nutritional
o Immune modulation
o Nutritional supplementation
• Surgical
82
Q

type of jaundice in choledochal cyst

A

o Conjugated jaundice, pale stool

83
Q

investigations for choledochal cyst

A

o Split bilirubin, stool colour, ultrasound

84
Q

features of alagille syndrome

A

o Intrahepatic cholestasis, dysmorphism, congenital cardiac disease
o Dysmorphism, genotype

Year 3 (164 decks)

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