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Child Health > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Infant feeding guidelines

A

DoH & WHO: breast feed exclusively for the 1st 6m
NICE: first feed ideally given within the 1st hour after birth
Skilled professionals should be available to support breast feeding and give appropriate counselling

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2
Q

Advantages of breastfeeding

A

Ideal nutrition
Life-saving in developing countries
Reduces GI infection and necrotising enterocolitis (preterm)
Enhances relationship
Reduces the risk of insulin dependent diabetes, hypertension and obesity later in life: metabolic disorder
Reduction in breast cancer risk in the mother

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3
Q

Potential complications of breastfeeding

A

An unknown quantity is taken each time
Transmission of some diseases: maternal CMV, hep B, HIV
Breast-milk jaundice
Transmission of drugs (antimetabolites) and environmental contaminants (nicotine, alcohol, caffeine)
Less flexible than formula feeding
Nutrient inadequacies: poor weight gain/Rickets if only breast fed over 6m
Vitamin K deficiency: insufficient to prevent haemorrhagic disease of the newborn –> supplementation required

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4
Q

Breast-feeding advice & support

A

Within the first 24h: information pack given about breast feedings, what to do and where to get help

Skilled support offered from the first feed: healthcare professional, mother-mother or peer support

A woman’s experience of breast feeding discussed at each contact to establish any concerns

Help in hospital from the maternity nurses and midwives, health visitors in the community, community nurses in 1st few days

If weaning takes place <6 months: wheat, eggs and fish should be avoided, as should all food high in salt, sugar or containing honey (risk of botulism)

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5
Q

Formula milk/cow’s milk guidelines

A

Breast feeding/formula feeding: 12m with weaning after 6m
Pasteurised cow’s milk may be given from 1yr: deficient in vits A, C, D and iron –> supplementation needed unless the infant is having a good diet of mixed solids
Alternatively, follow-on formula can be used
Children should receive full fat milk up to the age of 5

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6
Q

Specialised formula milk uses, and components

A

Uses: cow’s milk protein allergy/intolerance, lactose intolerance, CF, neonatal cholestatic liver disease or after intestinal resection

Protein: hydrolysed cow’s milk protein, amino acids or from soya
Carbohydrate: glucose
Fat: a combination of medium & long chain triglycerides (medium can be absorbed without bile or pancreatic enzymes)

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7
Q

Hydrolysed formula contents and indication

A

Cow’s milk but the proteins and lactose have been broken down –> easier to digest

‘partially’ or ‘extensively’ hydrolysed

Partial hydrolysates: larger proportion of long chains and are considered more palatable than extensively hydrolysed formula
prophylactic use to reduce risk of cow’s milk allergy in formula fed babies where there is a FHx of allergy
Not suitable for treatment of cow’s milk allergy/intolerance

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8
Q

First milks contents and indication

A

For newborns
Based on the whey of cow’s milk: more easily digested than other milks contains lactose and long-chain triglycerides

Unless otherwise told, this is the best type of infant formula for newborns

Bottle feeding: 1st milk is the only food needed for 6m, after 6m continue to give 1st milk and introduce solid foods
By 1yr old ordinary cow’s milk can be given

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9
Q

Second milks contents and indication

A

Described as formula for ‘hungrier babies’
No evidence that babies settle better or sleep longer if given these milks
Based on the curd of cow’s milk so take longer to digest than 1st milks
Not recommended for young babies

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10
Q

Follow-on milks indications

A

Described as suitable for babies >6 months: not necessary for all babies
Should never be used for babies <6 months as they are not nutritionally suitable

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11
Q

Goodnight milks contents and indications

A

Advertised as suitable for babies from 6 months – 3 years
They contain follow-on milk and cereal
Should never be given to babies <6 months as they are not nutritionally suitable
They are not necessary for any baby and have no evidence to support the claim that they help babies settle

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12
Q

Soya formula milk contents and indication

A

Soya contains high levels of phytoestrogen: may have negative effects on babies
Should not be used in <6 months due to the phytoestrogens and high aluminium content
Should only be used in exceptional circumstances and only under the recommendation of a doctor

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13
Q

Goats milk-based infant formula indication

A

Still unsuitable for babies with an allergy to cow’s milk as the proteins are very similar

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14
Q

Ordinary cows milk contents and indication

A

Should not be given to any babies <1 years old

Not nutritionally suitable until then: too much protein, electrolytes and inadequate iron & vitamins

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15
Q

Failure to thrive definition and types

A

Sub-optimal weight gain in infants and toddlers
Mild failure to thrive: a fall across two centile lines Severe failure to thrive: fall across three centile lines
Organic: associated with illness or anatomy
Non-organic: associated with a broad spectrum of psychosocial and environmental deprivation

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16
Q

Causes of failure to thrive

A

Inadequate intake…
Non-organic/environmental: inadequate availability of food, psychosocial deprivation, neglect or child abuse
Organic: impaired suck/swallow, chronic illness leading to anorexia

Inadequate retention: vomiting, severe GOR
Malabsorption: coeliac disease, CF, cow’s milk protein intolerance, short gut syndrome
Failure to utilize nutrients: syndromes (e.g. Down), congenital infection, metabolic disorders
Increased requirements: thyrotoxicosis, CF, malignancy, chronic infection (HIV), congenital heart disease

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17
Q

Consequences of poor nutrition

A

Reduced immunity, increased susceptibility to disease, impaired physical and mental development and reduced productivity
Severe/prolonged ‘failure to thrive’ = malnutrition

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18
Q

5 Paediatric York Malnutrition Score (PYMS) steps

A

1: measure height and weight to get a BMI score
2: note % unplanned weight loss and score using tables provided
3: assess recent change in diet/nutritional support including reduced intake
4: note risk of being undernourished during hospital admission due to decreased intake, increased gut loss or increased energy requirement
5: use management guidelines and/or local policy to develop care plan

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19
Q

Marasmus cause and presentation

A

Severe protein-energy malnutrition in children
Weight for height more than -3 SD below the median, <70% weight for height, a wasted wizened appearance
Oedema is not present
Skinfold thickness and mid-arm circumference are markedly reduced
Withdrawn and apathetic

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20
Q

Kwashiorkor cause and presentation

A

Severe protein malnutrition –> generalised oedema, severe wasting
Due to the oedema the weight may not be severely reduced
Often develops after an acute intercurrent infection: measles or gastroenteritis

‘flaky-paint’ skin rash with hyperkeratosis (thickened skin) and desquamation
Distended abdomen and hepatomegaly: fatty infiltration Angular stomatitis
Sparse depigmented hair
Diarrhoea, hypothermia, bradycardia and hypotension Low plasma albumin, potassium, glucose and magnesium

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21
Q

Acute management of kwashiorkor/marasmus

A

Hypoglycaemia: common and can lead to coma Hypothermia wrap: especially at night
Dehydration: avoid being overzealous with IV fluids as may lead to heart failure
Electrolytes: especially potassium
Infection: antibiotics (fever and other signs may be absent)
Micronutrients: vitamin A & other vitamins
Initiate feeding: small volumes frequently, including through the night

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22
Q

Recommended intake for infants 0-6m

A

Breastfeeding: recommended exclusively for the first
6 months
Energy requirement: 115kcal/kg per 24h

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23
Q

Recommended intake for infants 6-12m

A

Energy requirement: 95kcal/kg per 24h
Breast/formula milk alone = no longer be sufficient to meet nutritional needs
Infants receiving breast milk as their main drink: supplementation of vitamins A, C & D

Fruit, vegetables and non-wheat cereals are suitable first weaning food
the amount/variety of food should gradually be increased to include other types of cereal, dairy, meat, fish, eggs and pulse

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24
Q

Foods to be avoided during weaning

A

Salt, sugar, honey, shark, marlin, swordfish, raw eggs, whole nuts

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25
Q

Signs and symptoms of overfeeding

A

Baby gains average/greater than average weight
>7 heavily wet nappies per day
Frequent sloppy, foul-smelling bowel motions
Extreme flatulence
Large belching
Milk regurgitation
Irritability
Sleep disturbances
Baby still displays healthy growth: unlike colic/reflux/milk protein intolerance/lactose intolerance

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26
Q

Causes of overeating

A 
Sleep deprivation
Misinterpreting baby’s desire to suck as hunger
An active sucking reflex
Feeding too quickly
Feeding sleep association
Overlooking/ignoring satiety cues
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27
Q

Normal bowel motion frequency

A

Infant: 4x a day
1y: 2x a day
By 4y: same as adult

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28
Q

Red-flag constipation symptoms

A

Failure to pass meconium with 24hrs: Hirschprung’s disease
Failure to thrive/growth failure: hypothyroidism, coeliac disease, other causes
Gross abdominal distension: Hirschprung’s disease or other GI dysmolitiy
Abnormal lower limb neurology or deformity: lumbosacral pathology
Sacral dimple above natal cleft over spine: spina bifida occulta
Abnormal appearance/position/patency of anus: abnormal anorectal anatomy
Perianal bruising/multiple fissures: sexual abuse
Perianal fistulae, abscesses or fissures: perianal Crohn’s disease

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29
Q

Management of simple consipation

A

Encouragement/close supervision/psychological support
Faeces not palpable per abdo: balanced diet & sufficient fluids + maintenance laxatives
Faeces palpable:
1) macrogol laxative + elecrolytes (2w)
If not spontaneously passing stool: 2) stimulant laxactive +/- osmotic laxative
If no success: 3) consider enema +/- sedation or manual evacuation under general anaesthetic

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30
Q

Encopresis definition

A

Toilet trained child (>4yrs) soiling their clothes

With/without constipation and overflow

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31
Q

Functional encopresis causes

A

Never being toilet trained, toilet phobia, manipulative soiling, IBS

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32
Q

Overflow encopresis

A

Soft stools may be around the faeces

The colon is completely full, so stools force their way out

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33
Q

Sources of support for children and families with soiling/encopresis

A

GP usually by the first line
Most see a paediatric gastroenterologist
Psychological and parental help in training the child and parent to reward good behaviours
Wide variety of online information and even encopresis support groups for parents

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34
Q

Hirschprung’s disease pathophysiology

A

The absence of ganglion cells from the myenteric and submucosal plexuses in the large bowel
–> narrow and contracted segments the abnormal bowel extends from the rectum for a variable distance Proximally and ends in a normally innervated, dilated colon

Causes by a failure of ganglion cells to migrate into the hindgut
Leads to an absence of coordinated bowel peristalsis and functional bowel obstruction at the junction between normal bowel and distal aganglionic bowel

75% of cases only affect the rectosigmoid but 10% affect the entire colon

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35
Q

Hirschprung’s disease presentation

A

Neonatal period: intestinal obstruction, failure to pass meconium abdominal distention and bile-stained vomiting develops later

PR: a narrowed segment and withdrawal of examining finger may release a gush of liquid stool and flatus

Severe, life-threatening Hirschsprung enterocolitis: 1st few weeks of life due to C.difficile infection

In later childhood: chronic constipation, associated with abdominal distension, usually without soiling, growth failure may also be present

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36
Q

Hirschprung’s disease investigations

A

AXR: distal intestinal obstruction

Rectal biopsy: no ganglion cells in the submucosa

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37
Q

Hirschprung’s disease management

A

Surgical management: single stage pull-through in the neonatal period managing initial intestinal obstruction with rectal washouts

3 stage procedure is still used:
Defunctioning colostomy & multiple biopsies to confirm the site of the transition zone
Pull-through procedure to bring ganglionic bowel down to the anus
Closure of colostomy

38
Q

Hirschprung’s disease complications

A

Enterocolitis: a gastroenteritic illness characterised by abdominal distension, bloody watery diarrhoea, circulatory collapse and septicaemia
Mortality is 10%

39
Q

Gastroenteritis presentation

A 
Temperature: >38 (<3 months), >39 (>3 months)
SOB, tachypnoea
Altered state of consciousness
Neck stiffness
Bulging fontanelle
Non-blanching rash
Blood and/or mucus in stool
Bilious vomit
Severe abdominal pain
Abdominal distension/rebound tenderness
40
Q

Gastroenteritis investigations

A

60% caused by rotavirus in the developed world
Stool sample: septicaemia suspected, blood/mucus in stool, child is immunosuppressed
MCS: recent travel abroad, not improved in 7 days, uncertain diagnosis

41
Q

Gastroenteritis management

A

Rehydration therapy: replacement and maintenance
Continue breastfeeding if possible
Oral rehydration solution
I.V. fluids: 0.9% sodium chloride
Monitor plasma electrolytes, urea, creatinine, glucose: consider i.v. potassium supplement
Look for dehydration symptoms: altered responsiveness, urine output, tachycardia, tachypnoea, reduced skin turgor

42
Q

Cow’s milk protein allergy presentation

A

Depends where the allergic inflammation is
Upper GI: vomiting, feeding adversion, pain
Small intestine: diarrhoea, abdominal pain, protein-losing enteropathy, failure to thrive
Large intestine: diarrhoea, acute colitis with blood and mucus in stools and rarely chronic constipation

May occur in breastfed infants: reaction is to cow’s milk protein secreted in breast milk following maternal
ingestion –> presents as allergic colitis

43
Q

Cow’s milk protein allergy treatment

A

Limit cow’s milk & soy protein intake: hydrolysed formula & maternal exclusion
Elemental formula may be required
Avoid goat/sheep’s milk as substitute: 25% develop an allergy to these due to crossreactivity
Similar cross-reactivity occurs with soy milk and is not recommended <6 months anyway

After weaning introduce a cow’s milk protein free diet Supplement oral calcium if required
Consider cow’s milk protein challenge after 6-12 months

44
Q

Toddler diarrhoea clinical features

A

Chronic non-specific diarrhoea: commonest cause of persistant loose stools in preschool children
Stools vary in consistency: presence of undigested veg common, pale, foul-smelling
Thriving child, no precipitating dietary factors
Loose stools likely due to intestinal dysmotility, no malabsorption
Most grow out of symptoms by 5yo: achieving faecal continence may be significantly delayed

45
Q

Serious forms of diarrhoea

A 
Coeliac disease
Gastroenteritis
Lactose intolerance
Post-operative bowel surgery
Malabsorption
46
Q

GORD causes

A

Infancy (common): slow gastric emptying, liquid diet, horizontal posture, lower oesophageal sphincter pressure
LOS dysfunction: hiatus hernia
Increased gastric pressure: delayed gastric emptying
External gastric pressure
Gastric hypersecretion: acid
Food allergy
CNS disorders: cerebral palsy

47
Q

GORD symptoms

A

GI: regurg, non-specific irritability, rumination, oesophagitis, faltering growth
Resp: apnoeas, hoarseness, cough, stridor, aspiration, pneumonia, asthma, bronchopulmonary dysplasia
Neuro: Sandifer’s syndrome –> extension and lateral head turning, dystonic postures

48
Q

GORD medical management

A

Positioning: nurse infants on head-up slope of 30 ± prone
Dietary: feed thickener/small frequent meals, avoid food before sleep, fatty foods, citrus juices, caffeine, carbonated drinks, alcohol, smoking

Ranitidine (H2 receptor antagonist)
Omeprazole (PPI)
Antacids &amp; alginate: gaviscon
Domperidone: prokinetic
Mucosal protectors: Sucralfate, Corticosteroids
49
Q

GORD surgical management

A

Nissen’s fundoplication when medical treatment has failed
Indications: oesophageal stricture, barrett’s oesophagus, severe oesophagitis, recurrent apnoea, LRTI, FTT

Complications: ‘gas bloating’ syndrome, dysphagia, profuse retching and ‘dumping’ syndrome

50
Q

GORD complications

A 
Oesophageal stricture: dysphagia
Barratt's oesophagus: premalignant intestinal metaplasia
Faltering growth
Anaemia: chronic blood loss
Lower respiratory disease
51
Q

Kernicterus pathophysiology

A

Neonates more prone to jaundice due to:
Physiological release of haemoglobin from the breakdown of RBC
RBC life span of newborn infants is 70 days (compared to 120)
Inefficient hepatic bilirubin metabolism

Encephalopathy resulting from deposition of unconjugated bilirubin in the basal ganglia
and brainstem nuclei
Occurs when unconjugated bilirubin levels exceed albumin-binding capacity
Neurotoxic effects vary in severity from transient
disturbance to severe damage and death

52
Q

Kernicterus presentation

A

Lethargy and poor feeding
Severe = irritability, increased muscle tone, seizures and coma

infants who survive may develop choreoathetoid cerebral palsy , learning difficulties and sensorineural deafness

53
Q

Causes of neonatal jaundice <24h

A

Haemolytic disorders: rhesus/ABO incompatibility, G6PD deficiency, spherocytosis, pyruvate deficiency
Congenital infection

54
Q

Causes of neonatal jaundice 24h to 2w

A 
Physiological jaundice
Breast milk jaundice
Infection: UTI
Haemolysis: G6PD deficiency, ABO incompatibility
Bruising
Polycythaemia
Crigler-Najjar syndrome
55
Q

Causes of neonatal jaundice >2w

A

Unconjugated: physiological or breastmilk
jaundice, infection (UTI), hypothyroidism, haemolytic anaemia (G6PD deficiency), high gastrointestinal
obstruction (pyloric stenosis)

Conjugated (>25􀁐mol/L): bile duct obstruction (choledochal cysts), neonatal hepatitis (toxoplasmosis, rubella, CMV, Hep B&C)

56
Q

Neonatal jaundice treatment

A

Phototherapy: light (wavelength 450nm) from the blue-green band of the visible spectrum converts unconjugated bilirubin into a harmless water-soluble pigment excreted predominantly in the urine
Side-effects: temperature instability, macular rash
and bronze discolouration of the skin if bilirubin is conjugated
Multiple treatments can be given

Exchange transfusion: blood is removed in small aliquots (arterial line or umbilical vein) and replaced with donor blood (peripheral or umbilical vein), twice the infants blood volume is exchanged (2x80ml/kg)
Procedure does carry some risk of morbidity or mortality

57
Q

Stool colour relation to jaundice

A

Stool colour = conjugated bilirubin
Pale stool indicative of a reduced conjugated bilirubin content
This is most likely due to a biliary tree or post-hepatic obstruction and hence can help locate the problem

58
Q

Biliary atresia presentation

A

Progressive disease due to destruction or absence of
the extrahepatic biliary tree and intrahepatic biliary ducts
Normal birthweight, but have FTT as the disease progresses, mildly jaundice with pale stool and dark urine, hepatomegaly and splenomegaly are often present

59
Q

Biliary atresia investigations

A

LFTs: little value
Fasting USS: demonstrate a contracted or absent gallbladder (may be normal)
Radioisotope scan with TIBIDA: shows good uptake in the liver, but no excretion into the bowel
Liver biopsy: demonstrates features of extrahepatic biliary obstruction (may overlap with those of neonatal hepatitis)
Laparotomy: operative cholangiography fails to outline normal biliary tree

60
Q

Viral hepatitis clinical features

A 
Nausea
Vomiting
Abdominal pain
Lethargy
Jaundice: 30-50% will not develop
Hepatomegaly
Splenomegly: 30%
Raised LFTs: transaminases
61
Q

Hep A method of transmission and resulting disease + treatment

A

RNA virus: faecal-occult transmission
May be asymptomatic
Majority: mild illness, recover within 2-4 weeks
May develop prolonged cholestatic hepatitis (self-limiting) or fulminant hepatitis, but not chronic
liver disease
No treatment
Close contacts given prophylaxis by vaccine

62
Q

Hep B method of transmission and resulting disease + treatment

A

DNA virus :parental transmission (blood, etc)
Infants can contract HBV perinatally: asymptomatic, 90% become chronic carriers
Older children: asymptomatic/classical features of acute hepatitis
Majority resolve spontaneously
1-2% develop fulminant hepatic failure
5-10% become chronic carriers
Perinatal transmission: prevented by maternal screening + giving the infant a course of hep B vaccine if indicated
Infection may result in chronic HBV liver disease –> may progress to cirrhosis and hepatocellular carcinoma

63
Q

Hep C method of transmission and resulting disease + treatment

A

RNA virus: spread parentally (blood)
High prevalence amongst IVDU
Haemoglobinopathies/haemophilia = risk factor
Vertical transmission: 6%, 2x as common if HIV co-infection
Majority become chronic carriers: 20-50% lifetime risk of
progression to cirrhosis or HCC
Treatment: combination of IFN and ribavirin, not undertaken <4yrs old as may resolve spontaneously

64
Q

Hep D, Hep E, non A-G hep methods of transmission

A

Hep D: defective RNA virus, depends on Hep B for replication –> cirrhosis develops in 50-70% of cases
Hep E: RNA virus spread enterally via contaminated water, epidemics occur in some developing countries
Non-A to G hep: clinical presentation is similar to Hep A

65
Q

EBV effects on liver in children

A

Usually asymptomatic
40% have hepatitis that may become fulminant
<5% are jaundiced

66
Q

Presentations that are indications for coeliac serological testing

A

Persistent unexplained abdominal or gastrointestinal symptoms
Faltering growth
Prolonged fatigue
Unexpected weight loss
Severe or persistent mouth ulcers
Unexplained iron, vitamin B12 or folate deficiency
Type 1 diabetes: at diagnosis
Autoimmune thyroid disease: at diagnosis
Irritable bowel syndrome (only in adults)

67
Q

Coeliac investigations for diagnosis

A

Serology: test for total IgA and IgA tTG, as the first choice –> consider using IgG EMA, IgG DGP or IgG tTG if IgA is deficient

+ve serological test = referral to paediatric gastroenterologist for further investigation

Diagnosis = positive serological result + mucosal changes on jejunal biopsy (increased intraepithelial lymphocytes & a variable degree of villous atrophy and crypt hypertrophy)
Followed by resolution of symptoms and catch-up growth upon gluten withdrawal

68
Q

Coeliac disease management

A

Dietary information: avoiding gluten (wheat, rye, barley), food labelling, home cross-contamination,
How to manage social situations: eating out, travelling, coeliac support groups

Annual review: height, weight, review symptoms, diet assessment, dietetic advice
May experience anxiety & depression

A gluten challenge may be required later in childhood if initial biopsy or response to gluten withdrawal is
doubtful, or when the disease presents before the age of 2yrs

69
Q

Primary vs secondary food allergies vs non-IgE allergy

A

Primary: children have failed to ever develop immune tolerance to the relevant food

Secondary: usually due to cross-reactivity between proteins present in fresh fruits/vegetables/nuts and those present in pollens –> very common, but leads to mild allergic reaction, such as itchy mouth, but no systemic symptoms

Non-IgE: typically occurs hours after ingestion and usually involves the GI tract

70
Q

Food allergy risk factors

A

FH: food or atopy
Past food allergies
Other allergies: food or atopy
Age: more common in infants & toddlers
Asthma: if occur together, both likely to be severe

71
Q

Type 1 sensitivity reaction pathophysiology, symptoms, and management

A

IgE binds to a high affinity receptor on mast cell –> exposure to the allergen cross-links the bound IgE on sensitized cells and activates –> anaphylactic degranulation = rapid inflammatory response

Symptoms: urticaria & itchy skin, facial swelling, wheeze, stridor, abdominal pain & D/V, shock/collapse

Management: mild reactions (no cardio/resp symptoms) = anti-histamines, severe reactions = adrenaline IV (Epipen)

72
Q

Type 2 sensitivity reaction pathophysiology, symptoms, and management

A

Neutrophils bind to innocuous substances –> lytic enzymes released causing tissue damage

Symptoms: diarrhoea, abdominal pain, vomiting, colic, failure to thrive

Management: avoidance of the relevant food

73
Q

Intraluminal digestive defects leading to malabsorption

A 
Carbohydrate intolerance: eg. lactose intolerance
Protein-energy malnutrition
Cystic fibrosis
Shwachman-Diamond syndrome
Chronic pancreatitis
Cholestasis
Pernicious anaemia
Specific digestive enzyme deficiency: eg. lipase
74
Q

Mucosal abnormality leading to malabsorption

A

Coeliac disease
Short bowel syndrome
Dietary protein intolerance: eg. milk protein allergy
Intestinal infection or parasites: eg. giardiasis
IBD
Abetalipoproteinaemia: disorder of lipid metabolism

75
Q

Other malabsorption precursors

A

Immunodeficiency syndromes: eg. HIV
Drug reaction: eg. cytotoxics, post-radiation
Bacterial overgrowth: eg. pseudo-obstruction

76
Q

Malabsorption investigations

A

Initial screening: FBC, U&E, creatinine, albumin, total protein, Ca2+, phosphate, LFT, iron status, coeliac antibody screen, coagulation screen, stool MC&S

If diagnosis is still unclear consider: 
Upper GI endoscopy &amp; biopsy: enteropathy
Ileocolonscopy if features suggest colitis: ensure clotting is normal prior
Sweat test: CF
Immune function tests
Faecal fat measurement &amp; elastase
Faecal alpha-1 anti-trypsin
Exocrine pancreatic function tests
77
Q

Parasitic infection in GI tract presentation

A 
Abdominal pain
Diarrhoea, dysentery, flatulence
Malabsorption &amp; FTT
Abdominal distension
Intestinal obstruction
Biliary obstruction, liver disease
Pancreatitis
Fever
78
Q

Protozoal GI infection

A

Giardia lamblia: swallowed cysts develop into trophozoites that attach to the small intestinal villi causing mucosal damage
Entamoeba histolytica
Cryptosporidium: organism causes a mild self-limiting illness except in immunocompromised patients

79
Q

Colic prevalence and treatment

A

40% incidence, in first 4 months of life
Support and reassurance the condition is benign
Gripe water has no proven benefit
Severe/persistent: may be cows milk protein allergy/GORD –> an empirical 2 week trial of a whey hydrolysate formula may be considered
Cry-sis helpline for support

80
Q

Functional/recurrent abdominal pain definition

A

> 2 discrete episodes in 3m interfering with school and/or usual activities
Incidence is 10-15% of school age children
No organic cause found in 90% of cases

81
Q

Organic causes of functional/recurrent abdominal pain

A 
Constipation
Dietary indiscretion
Food intolerance: lactose/fructose
Irritable Bowel Syndrome
Psychogenic pain
Peptic ulcer
Coeliac disease
Abdominal migraine: cyclic vomiting syndrome
Gallbladder disease
Renal colic
Dysmenorrhoea
UTI
Mittleschmerz
Abuse: physical or sexual
82
Q

Functional/recurrent abdominal pain presentation

A

Non-organic disease: thriving, generally well child, short episodes of peri-umbilical pain, good appetite, no other GI symptoms, no FHx of migraine or coeliac disease, normal examination, co-existent symptoms such as headache and fatigue are common

Organic disease: likely if presentation is different to above or child <2yrs
‘red flag’ symptoms: weight loss, diarrhoea, blood per rectum, joint symptoms, skin rashes, FHx of IBD or coeliac disease

83
Q

Functional abdominal pain investigations

A

If organic cause is suspected: FBC, ESR/CRP, U&E, LFT, urine/faecal MC&S and coeliac antibody screening

84
Q

Presenting features of crohns/UC

A 
Anorexia, weight loss &amp; lethargy
Abdominal cramps
Diarrhoea ± blood/mucus, urgency &amp; tenesmus 
Fever
Finger clubbing
Anaemia
Erythema nodosum, pyoderma gangrenosum
Arthritis, ankylosing, spondylitis
Eyes: iritis, conjunctivitis, episcleritis
Poor growth
Delayed puberty
Sclerosing cholangitis
Renal stones
Nutritional deficiencies: vitamin B12
GI signs
Aphthous oral ulcers
Abdominal tenderness
Abdominal distension (UC>CD)
RIF mass (CD)
Peri-anal disease (CD): abscess, sinus, fistula, skin tags, fissure, stricture
85
Q

Crohns disease features

A

Affects whole GI tract: terminal ileum and proximal colon most commonly
Non-continuous: ‘skip’ lesions
Transmural, focal, subacute or chronic inflammatory disease: initial areas of acutely inflamed, thickened bowel –> strictures and fistulae may develop
May be mistaken for psychological problems or anorexia nervosa
Diagnosis: based on endoscopic and histological findings on biopsy, presence of non-caseating epithelioid cell granulomata (30% of cases); small bowel imaging may show narrowing, fissuring, mucosal irregularities and bowel wall thickening
Remission is induced when normal diet is replaced with whole protein modular feeds (polymeric) for
6-8 weeks: effective in 75% of cases, systemic steroids if not effective
Relapse is common and immunosuppressant medication may be required to maintain remission

86
Q

UC features

A

Recurrent, inflammatory and ulcerating disease involving the mucosa of the colon
Rectal is most common or may extend continuously up to involve the entire colon (pancolitis)
Terminal ileum may be affected by ‘backwash ileitis’
Presentation: rectal bleeding, diarrhoea and colicky pain, weight loss and growth failure, erythema nodosum, arthritis
Diagnosis: endoscopy and histological features after exclusion of infective causes of colitis
Histology: mucosal inflammation, crypt damage and ulceration
Management: aminosalicylates (ASA) for maintenance and induction, immunomodulatory therapy may be used in more aggressive/extensive cases
Severe fulminating disease is a medical emergency: requires IV fluid and steroids

87
Q

UC/Crohns complications

A 
Toxic mega colon: UC>CD
GI perforation or strictures
Pseudopolyps
Massive GI haemorrhage
Colon carcinoma: UC 50% risk after 10-20yrs
Fistula
Abscesses: CD
88
Q

UC/Crohns management

A

Supportive: bowel rest, IV hydration and PN
Drug treatment: mesalazine (ASA), corticosteroid enemas, oral prednisolone or IV methylprednisolone
Abx: ciprofloxacin, metronidazole

Maintenance treatment: immunomodifiers (Azathrioprine, Ciclosporin, Tacrolimus or Methotrexate) or Infliximab (anti-TNF)

Dietary treatment: polymeric/elemental diets are useful to induce remission (CD>UC), high relapse rate, dietary supplementation is often required

Surgical treatment:
UC: total colectomy & ileostomy, later pouch creation and anal anastomosis
CD: local surgical resection for severe localised disease

89
Q

Causes of gastritis

A 
H.pylori infection
Stress ulcer: post-trauma, Hypoxic-ischaemic encephalopathy
Drug related: NSAIDs
Increased acid secretion: Zollinger-Ellison syndrome, multiple endocrine neoplasia type I, hyperparathyroidism
Crohn’s disease
Eosinophilic gastroenteritis
Hypertrophic gastritis
Autoimmune gastritis
90
Q

Gastritis presentation

A 
Often asymptomatic
Chronic abdominal and epigastric pain
Nausea ± vomiting
GI haemorrhage
FFT ± anorexia
Iron deficiency anaemia
Peforation (rare)
Indigestion, bloating, hiccups and loss of appetite

Peptic ulcer: burning in the abdomen, below the ribs and above umbilicus, pain reduced by eating, drinking milk, antacids
Bleeding ulcers: haematemesis or melena

91
Q

Mesenteric adenitis presentation

A

Mimics acute appendicitis
Fever, malaise
Non-specific central abdominal pain which resolves in 24-48hrs, pain is less severe than appendicitis, and tenderness if RIF is variable, accompanied by URTI with cervical lymphadenopathy

Child Health (15 decks)

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