Gastroenterology Flashcards
Infant feeding guidelines
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
Advantages of breastfeeding
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
Potential complications of breastfeeding
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
Breast-feeding advice & support
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)
Formula milk/cow’s milk guidelines
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
Specialised formula milk uses, and components
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)
Hydrolysed formula contents and indication
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
First milks contents and indication
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
Second milks contents and indication
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
Follow-on milks indications
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
Goodnight milks contents and indications
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
Soya formula milk contents and indication
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
Goats milk-based infant formula indication
Still unsuitable for babies with an allergy to cow’s milk as the proteins are very similar
Ordinary cows milk contents and indication
Should not be given to any babies <1 years old
Not nutritionally suitable until then: too much protein, electrolytes and inadequate iron & vitamins
Failure to thrive definition and types
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
Causes of failure to thrive
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
Consequences of poor nutrition
Reduced immunity, increased susceptibility to disease, impaired physical and mental development and reduced productivity
Severe/prolonged ‘failure to thrive’ = malnutrition
5 Paediatric York Malnutrition Score (PYMS) steps
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
Marasmus cause and presentation
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
Kwashiorkor cause and presentation
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
Acute management of kwashiorkor/marasmus
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
Recommended intake for infants 0-6m
Breastfeeding: recommended exclusively for the first
6 months
Energy requirement: 115kcal/kg per 24h
Recommended intake for infants 6-12m
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
Foods to be avoided during weaning
Salt, sugar, honey, shark, marlin, swordfish, raw eggs, whole nuts
Signs and symptoms of overfeeding
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
Causes of overeating
Sleep deprivation Misinterpreting baby’s desire to suck as hunger An active sucking reflex Feeding too quickly Feeding sleep association Overlooking/ignoring satiety cues
Normal bowel motion frequency
Infant: 4x a day
1y: 2x a day
By 4y: same as adult
Red-flag constipation symptoms
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
Management of simple consipation
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
Encopresis definition
Toilet trained child (>4yrs) soiling their clothes
With/without constipation and overflow
Functional encopresis causes
Never being toilet trained, toilet phobia, manipulative soiling, IBS
Overflow encopresis
Soft stools may be around the faeces
The colon is completely full, so stools force their way out
Sources of support for children and families with soiling/encopresis
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
Hirschprung’s disease pathophysiology
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
Hirschprung’s disease presentation
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
Hirschprung’s disease investigations
AXR: distal intestinal obstruction
Rectal biopsy: no ganglion cells in the submucosa
Hirschprung’s disease management
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
Hirschprung’s disease complications
Enterocolitis: a gastroenteritic illness characterised by abdominal distension, bloody watery diarrhoea, circulatory collapse and septicaemia
Mortality is 10%
Gastroenteritis presentation
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
Gastroenteritis investigations
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
Gastroenteritis management
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
Cow’s milk protein allergy presentation
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
Cow’s milk protein allergy treatment
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
Toddler diarrhoea clinical features
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
Serious forms of diarrhoea
Coeliac disease Gastroenteritis Lactose intolerance Post-operative bowel surgery Malabsorption
GORD causes
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
GORD symptoms
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
GORD medical management
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 & alginate: gaviscon Domperidone: prokinetic Mucosal protectors: Sucralfate, Corticosteroids
GORD surgical management
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
GORD complications
Oesophageal stricture: dysphagia Barratt's oesophagus: premalignant intestinal metaplasia Faltering growth Anaemia: chronic blood loss Lower respiratory disease
Kernicterus pathophysiology
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
Kernicterus presentation
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
Causes of neonatal jaundice <24h
Haemolytic disorders: rhesus/ABO incompatibility, G6PD deficiency, spherocytosis, pyruvate deficiency
Congenital infection
Causes of neonatal jaundice 24h to 2w
Physiological jaundice Breast milk jaundice Infection: UTI Haemolysis: G6PD deficiency, ABO incompatibility Bruising Polycythaemia Crigler-Najjar syndrome
Causes of neonatal jaundice >2w
Unconjugated: physiological or breastmilk
jaundice, infection (UTI), hypothyroidism, haemolytic anaemia (G6PD deficiency), high gastrointestinal
obstruction (pyloric stenosis)
Conjugated (>25mol/L): bile duct obstruction (choledochal cysts), neonatal hepatitis (toxoplasmosis, rubella, CMV, Hep B&C)
Neonatal jaundice treatment
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
Stool colour relation to jaundice
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
Biliary atresia presentation
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
Biliary atresia investigations
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
Viral hepatitis clinical features
Nausea Vomiting Abdominal pain Lethargy Jaundice: 30-50% will not develop Hepatomegaly Splenomegly: 30% Raised LFTs: transaminases
Hep A method of transmission and resulting disease + treatment
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
Hep B method of transmission and resulting disease + treatment
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
Hep C method of transmission and resulting disease + treatment
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
Hep D, Hep E, non A-G hep methods of transmission
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
EBV effects on liver in children
Usually asymptomatic
40% have hepatitis that may become fulminant
<5% are jaundiced
Presentations that are indications for coeliac serological testing
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)
Coeliac investigations for diagnosis
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
Coeliac disease management
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
Primary vs secondary food allergies vs non-IgE allergy
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
Food allergy risk factors
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
Type 1 sensitivity reaction pathophysiology, symptoms, and management
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)
Type 2 sensitivity reaction pathophysiology, symptoms, and management
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
Intraluminal digestive defects leading to malabsorption
Carbohydrate intolerance: eg. lactose intolerance Protein-energy malnutrition Cystic fibrosis Shwachman-Diamond syndrome Chronic pancreatitis Cholestasis Pernicious anaemia Specific digestive enzyme deficiency: eg. lipase
Mucosal abnormality leading to malabsorption
Coeliac disease
Short bowel syndrome
Dietary protein intolerance: eg. milk protein allergy
Intestinal infection or parasites: eg. giardiasis
IBD
Abetalipoproteinaemia: disorder of lipid metabolism
Other malabsorption precursors
Immunodeficiency syndromes: eg. HIV
Drug reaction: eg. cytotoxics, post-radiation
Bacterial overgrowth: eg. pseudo-obstruction
Malabsorption investigations
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 & biopsy: enteropathy Ileocolonscopy if features suggest colitis: ensure clotting is normal prior Sweat test: CF Immune function tests Faecal fat measurement & elastase Faecal alpha-1 anti-trypsin Exocrine pancreatic function tests
Parasitic infection in GI tract presentation
Abdominal pain Diarrhoea, dysentery, flatulence Malabsorption & FTT Abdominal distension Intestinal obstruction Biliary obstruction, liver disease Pancreatitis Fever
Protozoal GI infection
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
Colic prevalence and treatment
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
Functional/recurrent abdominal pain definition
> 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
Organic causes of functional/recurrent abdominal pain
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
Functional/recurrent abdominal pain presentation
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
Functional abdominal pain investigations
If organic cause is suspected: FBC, ESR/CRP, U&E, LFT, urine/faecal MC&S and coeliac antibody screening
Presenting features of crohns/UC
Anorexia, weight loss & lethargy Abdominal cramps Diarrhoea ± blood/mucus, urgency & 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
Crohns disease features
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
UC features
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
UC/Crohns complications
Toxic mega colon: UC>CD GI perforation or strictures Pseudopolyps Massive GI haemorrhage Colon carcinoma: UC 50% risk after 10-20yrs Fistula Abscesses: CD
UC/Crohns management
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
Causes of gastritis
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
Gastritis presentation
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
Mesenteric adenitis presentation
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
