alimentary Flashcards

1
Q

what are the different phases of vomiting

A

pre-ejection phase

ejection phase

post-ejection phase

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2
Q

what are the clinical features of each phase

A

pre ejection: pallor, nausea, tachycardia

ejection: retch, vomit

post ejection: weakness, shivering, lethargy

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3
Q

what causes vomiting?

A

stimulation of vomiting centre in medulla triggered by:

  • enteric pathogens
  • infection
  • visual/olfactory stimuli - fear
  • head injury/raised ICP
  • inner ear stimuli
  • metabolic derangements/chemotherapy
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4
Q

what are the different types of vomiting?

A
  • vomiting with retching
  • projectile vomiting
  • bilious vomiting
  • effortless vomiting
  • haemetemesis
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5
Q

what are the causes of vomiting?

A

infants: GOR, cow’s milk allergy, infection, intestinal obstruction
children: gastroenteritis, infection, appendicitis, intestinal obstruction, raised ICP, coeliac disease

young adults: gastroenteritis, infection (H. Pylori), appendicitis, raised ICP, DKA, cyclical vomiting syndrome, bulimia

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6
Q

describe presentation of pyloric stenosis

A
babies 4 - 12 weeks
boys > girls
projectile non-bilious vomiting
weight loss
dehydration +/- shock
electrolyte disturbance: metabolic alkalosis (↑pH), hypochloraemia (↓Cl), hypokalaemia (↓K)
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7
Q

what are the investigations for pyloric stenosis

A
  • test feed

- blood gases: hypokalemic, hypocholermic metabolic alkalosis after prolonged vomiting

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8
Q

what is the management for pyloric stenosis

A

fluid resuscitation

refer to surgeons if obstruction

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9
Q

describe effortless vomiting

A

due to gastro-oesophageal reflux
self-limting
symptoms:
- vomiting, haematemesis
- nutritional: feeding problems, failure to thrive
- respiratory: apnoea, cough, wheeze, chest infections
- neurological: sandifer’s syndrome

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10
Q

what are the investigations for effortless vomiting

A

history and examination
oesophageal pH study/impedance monitoring
endoscopy
imaging: video fluoroscopy, barium swallow

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11
Q

what is the management for effortless vomiting

A

feeding advice: thickeners, feeding position & volumes
nutritional support: calories supplements, exclusion diet, nasogastric tube, gastrostomy
medical treatment (rare): prokinetic drugs, acid suppressing drugs, H2 receptor blockers, proton pump inhibitors
surgery (rare): nissen fundoplication

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12
Q

what should bilous vomiting always be presumed to be due to?

A

intestinal obstruction until proved otherwise

ALWAYS ring alarm bells

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13
Q

what are the causes of bilious vomiting

A
intestinal atresia (in newborn babies only)
malrotation
intussusception
ileus
crohn’s disease with strictures
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14
Q

what are the investigations for bilious vomiting

A

abdominal x-rays
consider contrast meal
surgical opinion regarding laparotomy

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15
Q

what is the fluid balance of the GI system?

A

9L fluid enters duodenum
1.5L gets to colon
<200ml lost in faeces

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16
Q

how is the surface area of the small intestine increased?

A

mucosal folds

villi

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17
Q

What is there increased risk of in untreated coeliac disease?

A

Small bowel lymphoma

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18
Q

what is the definition of chronic diarrhoea?

A

4 or more stools per day for more than 4 weeks

  • <1 week: acute diarrhoea
  • 2 - 4 weeks: persistent diarrhoea
  • > 4 weeks: chronic diarrhoea
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19
Q

what can cause diarrhoea?

A

motility disturbance: toddler diarrhoea, irritable bowel syndrome

active secretion: acute infective diarrhoea, inflammatory bowel disease

malabsorption of nutrients: food allergy, coeliac disease, cystic fibrosis

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20
Q

what types of diarrhoea are there?

A

osmotic

  • movement of water into bowel to equilibrate osmotic gradient
  • usually a feature of malabsorption (enzymatic defect or transport defect)
  • mechanism of action of lactulose/movicol

secretory

  • classically associated with toxin production from vibrio cholerae and enterotoxigenic Escherichia coli
  • intestinal fluid secretion predominantly driven by active Cl- secretion via CFTR
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21
Q

what drives intestinal fluid secretion in secretory diarrhoea?

A

intestinal fluid secretion predominantly driven by active Cl- secretion via CFTR

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22
Q

what is the clinical approach to chronic diarrhoea?

A

history: age, abrupt/gradual onset, family/travel history

growth and weight gain of child

faeces analysis: appearance, stool culture, determination of secretory vs osmotic

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23
Q

what types of disease does fat malabsorption occur in?

A

pancreatic disease
- lack of lipase and resultuant steatorrhoea; clasically cystic fibrosis

hepatobiliary disease
- cholestasis; clasically chronic liver disease

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24
Q

how does coeliac disease present in children?

A
  • abdominal bloatedness
  • diarrhoea
  • failure to thrive
  • short stature
  • constipation
  • tiredness
  • dermatitis herpatiformis
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25
Q

what screening tests are there for coeliac disease?

A

serological screens

  • anti-tissue transglutaminase
  • anti-endomysial
  • anti-gliadin
  • IgA screen

duodenal biopsy (gold standard)

genetic testing
-HLA DQ2, DQ8

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26
Q

what histological characteristics are associated with coeliac disease?

A

lymphocytic infiltration of surface epithelium
partial /total villous atrophy
crypt hyperplasia

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27
Q

what guidelines determine whether a biopsy is required to diagnose coeliac disease?

A

ESPHGHAN/BSPGHAN

  • symptomatic children
  • anti TTG >10 times upper limit of normal
  • positive anti endomysial antibodies
  • HLA DQ2, DQ8 positive

if all present -> diagnosis
if not all present -> endoscopy -> diagnosis

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28
Q

what is the treatment for coeliac disease?

A

gluten-free diet for life

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

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29
Q

what are the essential secretory components

A

water for fluidity, enzyme transport, absorption
ions
defense mechanism against pathogens/harmful substances/antigens

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30
Q

how has the incidence of Crohn’s disease changed in Scottish children?

A

dramatically increased and continues to

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31
Q

what are the presenting features of Crohn’s in children?

A
  • weight loss
  • growth failure
  • abdominal pain
  • diarrhoea
  • rectal bleeding
  • arthritis
  • mass
  • fever
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32
Q

what are the presenting features of UC in children?

A
  • diarrhoea
  • rectal bleeding
  • abdominal pain
  • arthritis
  • fever
  • weight loss
  • growth failure
  • no mass
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33
Q

what history and examination is required when diagnosing IBD?

A
intestinal symptoms
extra-intestinal manifestations: erythema nodosum
exclude infection
family history
growth and sexual development
nutritional status
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34
Q

what laboratory investigations should be carried out?

A

full blood count & ESR: anaemia, thrombocytosis, raised ESR

biochemistry: stool calprotectin, raised CRP, low Albumin
microbiology: no stool pathogens

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35
Q

how does Crohn’s usually present in children?

A
  • lack of specific symptoms (present with weight loss and growth failure)
  • abnormal blood tests and high calprotectin
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36
Q

how does UC usually present in children?

A
  • symptomatic with bloody diarrhoea
  • do not necessarily have abnormal growth or blood tests
  • high calprotectin
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37
Q

what are the definitive radiological investigations for IBD?

A
  • MRI (usually >5 years due to the need to keep still without a GA)
  • barium meal and follow through (younger kids)
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38
Q

what types of endoscopy are used in the definitive diagnosis of IBD?

A
  • colonoscopy
  • upper GI endoscopy
  • mucosal biopsy
  • capsule endoscopy
  • enteroscopy
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39
Q

what are the aims of treatment in IBD?

A
  • induce and maintain remission
  • correct nutritional deficiencies
  • maintain normal growth and development
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40
Q

What are the treatment for IBD in children?

A

Medical

  • Anti-inflammatory
  • Immuno-suppressive
  • Biologicals ( Infliximab)

Nutritional

  • Immune modulation
  • Nutritional supplementation
  • Milkshake diet

Surgical

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41
Q

what is constipation?

A

infrequent passage of stool

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42
Q

what do you want to know about the child presenting with constipation?

A
  • frequency
  • hardness
  • painful
  • has there been a change?
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43
Q

what is normal stool frequency?

A

4 per day to 1 per week

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44
Q

what does stool frequency depend on?

A
  • age

- diet

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45
Q

what are the components of the Bristol stool chart?

A
  • type 1 = separate hard lumps
  • type 4 = smooth sausage like
  • type 7 = entirely liquid
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46
Q

what are other signs and symptoms of constipation?

A
  • poor appetite
  • irritable
  • lack of energy
  • abdominal pain or distension
  • withholding or straining
  • diarrhoea
  • urinary issues
  • pale with bags under their eye
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47
Q

Why do children become constipated?

A

social: poor diet (lack of fluid, excess milk), potty training/toilets issue
physical: intercurrent illness, medications (opiates and gaviscon)

psychological

organic

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48
Q

what is the vicious cycle of constipation?

A
  • large hard stool
  • leads to pain and fissuring
  • child withholds stool
  • becomes constipated
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49
Q

how does overflow diarrhoea develop?

A
  • child enters the vicious cycle of constipation
  • rectum tells them they need to go but the child clenches the external sphincter
  • poo continues to be dehydrated by bowel becoming harder
  • back passage begins to stretch and creates a mega rectum
  • soiling occurs when the mega rectum holds the internal sphincter open and the child is unable to clench the external sphincter
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50
Q

what is the treatment of constipation

A

social

  • explain treatment to parents
  • dietary: increase fibre, fruit, vegetables, fluids, decrease milk

psychological

  • reduce the aversive factors by making going to the toilet a pleasant
  • reward good behaviour

soften stool and stimulate defecation

  • osmotic laxatives (lactulose)
  • stimulant laxatives (senna, picosulphate)
  • isotonic laxatives (movicol, laxido)

give enough to make them go and make sure stool is always soft and never painful; until no longer is required

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51
Q

how is impaction treated?

A
  • empty impacted rectum
  • empty colon
  • maintain regular stool passage
  • slow weaning off treatment
  • ensure compliance
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52
Q

what are the functions of the liver?

A
  • waste handling
  • water handling
  • salt balance
  • acid base control
  • endocrine: produces albumin, clotting factors
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53
Q

what is included in LFTs?

A
  • bilirubin (total and split)
  • ALT/AST (alanine aminotransferase/aspartate aminotransferase)
  • alkaline phosphatase
  • gamma glutamyl transferase (GGT)
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54
Q

when is ALT/AST elevated?

A

in hepatocellular damage (hepatitis)

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55
Q

when are alkaline phosphatase and GGT elevated?

A

biliary disease

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56
Q

what tests are used to assess the function of the liver?

A
  • coagulation (prothrombin time (PT)/INR, APTT)
  • albumin
  • bilirubin
  • blood glucose
  • ammonia
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57
Q

how can paediatric liver disease manifest?

A
  • jaundice
  • incidental finding of abnormal blood test
  • symptoms/signs of chronic liver disease
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58
Q

what are the signs of chronic liver disease in children?

A
59
Q

what is jaundice?

A

yellow discolouration of skin and tissues due to accumulation of bilirubin
usually most obvious in sclera; visible when total bilirubin >40-50 umol/l

60
Q

what is diagnosis of infant jaundice dependent on?

A
  • bilirubin metabolism

- age

61
Q

how is bilirubin metabolised?

A
  • post mature RBC broken down in the reticuloendothelial system to bilverdin
  • converted to unconjugated bilirubin
  • bound to albumin and conjugated in the liver
  • mixes with bile in gallbladder and enters small intestine
  • converted to urobilinogen and excreted by the kidneys as urine or in faeces
62
Q

what is the solubility of bilirubin?

A

conjugated: water soluble/ fat insoluble
unconjugated: water insoluble/ fat soluble

63
Q

describe the conjugation of bilirubin and jaundice

A

pre hepatic: unconjugated bilirubin (excess)
intra hepatic: mixed bilirubin (liver issues)
post hepatic: conjugated bilirubin (obstruction: cholestasis)

64
Q

describe neonatal jaundice?

A

early (<24 hours old): haemolysis, sepsis (always pathological)

intermediate (24 hours - 2 weeks): physiological, breast milk, haemolysis

prolonged (>2 weeks): extrahepatic obstruction, neonatal hepatitis, hypothyroidsim, breast milk

65
Q

why does physiological jaundice occur?

A
  • develops after the 1st day of life as it takes time for RBC to break down
  • shorter RBC life span in infants (80-90 days)
  • relative polycythaemia
  • relative immaturity of liver function
66
Q

what type of jaundice is physiological jaundice?

A

unconjugated

67
Q

why does jaundice occur with breast fed babies?

A

exact reason for prolongation of jaundice in breastfed infants unclear

68
Q

what type of jaundice is breast milk jaundice?

A

unconjugated

69
Q

how long can breast milk jaundice persist?

A

up to 12 weeks from birth

70
Q

apart from breast milk and physiological what other causes of unconjugated infant jaundice are there?

A
  • sepsis
  • haemolysis (excessive)
  • abnormal conjugation
71
Q

why might there be excessive haemolysis in a baby leading to jaundice?

A
  • ABO incompatibility
  • rhesus disease
  • bruising/cephalhaematoma
  • red cell membrane defects (e.g. spherocytosis)
  • red cell enzyme defects (e.g. G6PD)
72
Q

what causes of abnormal conjugation are there?

A
  • gilbert’s disease (common, mild)

- crigler-aajjar syndrome (very rare but sever)

73
Q

what are the investigations for jaundice?

A
  • urine culture
  • blood culture
  • TORCH screen
  • blood group
  • DCT
  • clinical examination
  • blood film
  • G6PD assay
  • genotype/phenotype
74
Q

what is a possible complication of unconjugated jaundice?

A

kernicterus
unconjugated (fat-soluble) bilirubin crosses blood-brain barrier and deposits in brain (particularly the basal ganglia); it is neurotoxic

75
Q

what are the signs of kernicterus?

A

early: encephalopathy, poor feeding, lethargy, seizures
late: choreoathetoid cerebral palsy, learning difficulties, sensorineural deafness

76
Q

how is unconjugated jaundice treated?

A

phototherapy: visible light (450nm wavelength) converts bilirubin to water soluble isomer (photoisomerisation)

77
Q

what is prolonged infant jaundice?

A

jaundice persisting beyond 2 weeks of life or 3 weeks of life in preterms

78
Q

what are the causes of prolonged infant jaundice?

A

conjugated: anatomical (biliary obstruction), neonatal hepatitis
unconjugated: hypothyroidism, breast-milk jaundice

79
Q

what causes of biliary obstruction can lead to prolonged jaundice?

A

biliary atresia: pale stools
choledochal cyst: pale stools
alagille syndrome: intrahepatic cholestasis, dysmorphism, congenital cardiac disease

80
Q

what is biliary atresia?

A

congenital fibro-inflammatory disease of the bile ducts leading to destruction of extra-hepatic bile ducts

pale stools, dark urine, liver failure

investigation: split bilirubin, stool colour, ultrasound, liver biopsy
treatment: kasai portoenterostomy

81
Q

what is the most common indication for liver transplant in children?

A

biliary atresia

82
Q

what investigations are done for choledochal cyst?

A
  • split bilirubin
  • stool colour
  • ultrasound
83
Q

what investigations are done for Alagille syndrome?

A
  • dysmorphism

- genotype

84
Q

what causes of neonatal hepatitis are there?

A
  • alpha-1-antitrypsin deficiency
  • galactosaemia
  • tyrosinaemia
  • urea cycle defects
  • haemochromatosis
  • glycogen storage disorders
  • hypothyroidism
  • viral hepatitis
  • parenteral nutrition
85
Q

what should you always ask about with prolonged infant jaundice?

A

stool colour

86
Q

what is the most important test for prolonged infant jaundice?

A

split bilirubin to determine if it is conjugated or unconjugated in nature

87
Q

what is the main diagnosis to exclude with conjugate prolonged jaundice?

A

biliary atresia

88
Q

what jaundice requires further investigation

A

conjugated jaundice is always abnormal and requires further investigation

most important test = split bilirubin

89
Q

what are the recognised phases of childhood?

A
  • neonate (<4w)
  • infant (<12m/1y)
  • toddler (~1-2y)
  • pre-school (~2-5y)
  • school age
  • teenager/adolescent
90
Q

what drives infant growth?

A

nutrition

91
Q

what drives child growth?

A

growth hormone

92
Q

what drives pubertal growth?

A

sex steroids

93
Q

why is nutrition important?

A
  • required for changes in brain and body structure, composition and function
  • prevention of malnutrition and disease
94
Q

What is birth size and weight dependent on?

A
  • Maternal size
  • Placental function
  • Gestation
95
Q

What is the average weigth of a term infant?

A

3.3kg

96
Q

What is energy needed for?

A
  • Physical activity
  • Thermogenesis
  • Tissue maintenance
  • Growth
97
Q

What is the growth demands of infants?

A

About 35% of energy intakee

98
Q

Why can infants rapidly become malnourished?

A
  • high demands for growth and maintenance
  • low stores (protein and fat)
  • frequent illness
99
Q

What is the average weekly weight gain of infants?

A
  • 0-3months 200g
  • 3-6 months 150g
  • 6-9 months 100g
  • 9-12 months 75-50g
100
Q

What are the benefits of breast feeding?

A
  • nutritionally complete for full term babies
  • improves cognitive development
  • reduces risk of infection
  • tailor made passive immunity
  • increase in development of gut mucosa/active immunity
  • decreased risk of breast cancer
101
Q

Why does breast milk reduce infection?

A

Contains

  • Macrophages and lymphocytes
  • Interferon, lactoferrin ad lysozyme
  • Bifidus factor
102
Q

what are the advantages of formula feeding?

A
  • no transfer of BBVs or drugs
  • accurate feed volumes
  • provides vitamin K
  • less jaundice
103
Q

what are the disadvantages of formula feeding?

A
  • no anti-infection properties
  • risk of contamination
  • high antigen load
  • expensive
104
Q

What are UNICEF’s baby friendly 10 steps?

A
  • Written breast feeding policy
  • Train all staff to implement policy
  • Inform all pregnant women about benefits of breast feeding
  • Help mothers initiate breast-feeding (within 30mins of birth)
  • Show mothers how to breastfeed
  • Give new-borns only breast milk
  • Practise rooming
  • Encourage on demand feeding
  • No teats or dummies
  • Advocate breast feeding support groups
105
Q

What happens if breast-feeding is not possible?

A
  • Formula feeding is common
  • All are cows milk based
  • Based on age
106
Q

Why is cows milk not suitable as the main drink for <1 years?

A

Contains almost no iron

107
Q

When is milk the exclusive feed?

A

For the first 4-6 months

108
Q

What type of specialised formulas are there?

A
  • Cows milk protein allergy
  • Nutrient dense
  • Disease specific
109
Q

What formula is available for pre-term infants?

A
  • SMA Gold Prem
  • Typically 2g (vs 1.5) protein and 80kcal (vs 68)/100ml
  • Post discharge prescribable eg Nutriprem 2
110
Q

What nutrient dense formula is available?

A
  • Infatrini/SMA High Energy

- 100kcal/100ml ,prescribable to 18 months

111
Q

What type of reaction is CMPA?

A

Majority are delayed, non IgE reactions

112
Q

How can CMPA present?

A
  • Vomiting
  • Diarrhoea
  • Abdominal discomfort
  • Abdominal distension
  • Eczema
113
Q

What is the test for CMPA?

A

Exclusion of CMPA

114
Q

What is the CMPA pathway?

A
  • 4 week trial of milk avoidance
  • Special formula or milk free diet for breast feeding mums
  • Reintroduction at 4 weeks unless clear benefit
  • Re challenge after 6 months of improvement
  • Milk ladder approach
115
Q

What is the milk ladder approach?

A

Not all forms of milk are equally allergenic

  • Cookie/biscuit
  • Muffin
  • Pancake
  • Cheese
  • Yoghurt
  • Pasteurised milk/infant formula
116
Q

What is the first line feed choice in CMPA?

A
  • Extensively hydrolysed protein feeds
  • 90% should respond (10% react)
  • Palatability a problem in older babies
  • Nutramigen LGG Lipil 1 and 2
  • Aptamil Pepti 1 and 2
117
Q

What is the second line feed choice in CMPA?

A
  • Amino acid based feeds
  • Babies with severe colitis/enteropathy/ symptoms on breast milk
  • Overprescribed and expensive
118
Q

What is lactose intolerance?

A
  • NOT AN ALLERGY

- Reduced levels of lactase enzyme

119
Q

Who can lactose intolerance be seen in?

A
  • Seen to minor degree in some breast fed babies
  • Post gastro enteritis (Transient and self resolving)
  • Also in certain ethnic groups post weaning
120
Q

What is secondary lactose intolerance?

A
  • Short lived condition eg post gastro-enteritis
  • Confused with cow’s milk protein intolerance
  • Lactose free/ “Comfort” milks are not CMP free
121
Q

What are the indications for soya milk?

A
  • Milk allergy when hydrolysed formulae refused
  • Vegan families, if not breast fed
  • Consider for children>1 year still on milk free diet
122
Q

Why should soya milks be avoided in infants?

A
  • They contain phytoestrogens

- Cross reactivity with cows milk

123
Q

What non formula milks can be introduced into children’s diets?

A
  • Rice Milk (Not advised for children under 5 years)
  • Goats’ and Sheep’s milk (Not suitable for under 1’s, Many children will react)
  • Oat and nut milks
  • Organic versions are not calcium fortified
124
Q

What is the nutritional value of full fat cows milk?

A
  • 65kcal/100ml and 120 mg calcium/100ml
  • Organic/ unsweetened milk substitutes low in calories
  • Organic milks are no calcium supplemented
125
Q

How much milk is required to meet daily requirements?

A
  • Need 400-500ml of a calcium fortified “milk” to meet calcium requirements
  • Supplement if <500ml calcium fortified substitute
126
Q

What types of calcium supplements are available?

A
  • Alliance calcium liquid or (if >3y) Calcium softies

- For breast feeding mums Accrete or Cacit D3

127
Q

What is weaning?

A

Transition from milk to a mixed diet

128
Q

When does weaning occur?

A

Starts around 6 months

129
Q

Why do we wean children?

A
  • Milk alone is inadequate
  • Source of vitamins and trace elements
  • Man is an omnivore
  • Encourage tongue and jaw movements in preparation for speech and social interaction
130
Q

Who in particular requires vitamin D?

A
  • Dark skinned children, who breast feed from mum not on supplements
  • Scots (unable to synthesis from September to April)
131
Q

Who should receive supplements?

A
  • All breast fed babies from 1 month
  • Bottle fed babies taking <500ml formula
  • All children from 1-4 years
132
Q

What nutrition issues are there beyond infancy?

A
  • Picky eaters
  • Frequent illness
  • Dependence on carer
  • Learning to be independent
  • Chronic disease
  • Obesity
  • Puberty
  • Eating disorders
133
Q

what is constipation?

A

infrequent passage of stool

134
Q

what do you want to know about the child presenting with constipation?

A
  • frequency
  • hardness
  • painful
  • has there been a change?
135
Q

what is normal stool frequency?

A

4 per day to 1 per week

136
Q

what does stool frequency depend on?

A
  • age

- diet

137
Q

what are the components of the Bristol stool chart?

A
  • type 1 = separate hard lumps
  • type 4 = smooth sausage like
  • type 7 = entirely liquid
138
Q

what are other signs and symptoms of constipation?

A
  • poor appetite
  • irritable
  • lack of energy
  • abdominal pain or distension
  • withholding or straining
  • diarrhoea
  • urinary issues
  • pale with bags under their eye
139
Q

Why do children become constipated?

A

social: poor diet (lack of fluid, excess milk), potty training/toilets issue
physical: intercurrent illness, medications (opiates and gaviscon)

psychological

organic

140
Q

what is the vicious cycle of constipation?

A
  • large hard stool
  • leads to pain and fissuring
  • child withholds stool
  • becomes constipated
141
Q

how does overflow diarrhoea develop?

A
  • child enters the vicious cycle of constipation
  • rectum tells them they need to go but the child clenches the external sphincter
  • poo continues to be dehydrated by bowel becoming harder
  • back passage begins to stretch and creates a mega rectum
  • soiling occurs when the mega rectum holds the internal sphincter open and the child is unable to clench the external sphincter
142
Q

what is the treatment of constipation

A

social

  • explain treatment to parents
  • dietary: increase fibre, fruit, vegetables, fluids, decrease milk

psychological

  • reduce the aversive factors by making going to the toilet a pleasant
  • reward good behaviour

soften stool and stimulate defecation

  • osmotic laxatives (lactulose)
  • stimulant laxatives (senna, picosulphate)
  • isotonic laxatives (movicol, laxido)

give enough to make them go and make sure stool is always soft and never painful; until no longer is required

143
Q

how is impaction treated?

A
  • empty impacted rectum
  • empty colon
  • maintain regular stool passage
  • slow weaning off treatment
  • ensure compliance