Gastroenterology Flashcards

(91 cards)

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

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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
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
26
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 ```
27
Normal bowel motion frequency
Infant: 4x a day 1y: 2x a day By 4y: same as adult
28
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
29
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
30
Encopresis definition
Toilet trained child (>4yrs) soiling their clothes | With/without constipation and overflow
31
Functional encopresis causes
Never being toilet trained, toilet phobia, manipulative soiling, IBS
32
Overflow encopresis
Soft stools may be around the faeces | The colon is completely full, so stools force their way out
33
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
34
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
35
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
36
Hirschprung's disease investigations
AXR: distal intestinal obstruction | Rectal biopsy: no ganglion cells in the submucosa
37
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
38
Hirschprung's disease complications
Enterocolitis: a gastroenteritic illness characterised by abdominal distension, bloody watery diarrhoea, circulatory collapse and septicaemia Mortality is 10%
39
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 ```
40
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
41
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
42
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
43
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
44
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
45
Serious forms of diarrhoea
``` Coeliac disease Gastroenteritis Lactose intolerance Post-operative bowel surgery Malabsorption ```
46
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
47
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
48
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 ```
49
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
50
GORD complications
``` Oesophageal stricture: dysphagia Barratt's oesophagus: premalignant intestinal metaplasia Faltering growth Anaemia: chronic blood loss Lower respiratory disease ```
51
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
52
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
53
Causes of neonatal jaundice <24h
Haemolytic disorders: rhesus/ABO incompatibility, G6PD deficiency, spherocytosis, pyruvate deficiency Congenital infection
54
Causes of neonatal jaundice 24h to 2w
``` Physiological jaundice Breast milk jaundice Infection: UTI Haemolysis: G6PD deficiency, ABO incompatibility Bruising Polycythaemia Crigler-Najjar syndrome ```
55
Causes of neonatal jaundice >2w
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
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
57
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
58
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
59
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
60
Viral hepatitis clinical features
``` Nausea Vomiting Abdominal pain Lethargy Jaundice: 30-50% will not develop Hepatomegaly Splenomegly: 30% Raised LFTs: transaminases ```
61
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
62
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
63
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
64
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
65
EBV effects on liver in children
Usually asymptomatic 40% have hepatitis that may become fulminant <5% are jaundiced
66
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)
67
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
68
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
69
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
70
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
71
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)
72
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
73
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 ```
74
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
75
Other malabsorption precursors
Immunodeficiency syndromes: eg. HIV Drug reaction: eg. cytotoxics, post-radiation Bacterial overgrowth: eg. pseudo-obstruction
76
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 ```
77
Parasitic infection in GI tract presentation
``` Abdominal pain Diarrhoea, dysentery, flatulence Malabsorption & FTT Abdominal distension Intestinal obstruction Biliary obstruction, liver disease Pancreatitis Fever ```
78
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
79
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
80
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
81
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 ```
82
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
83
Functional abdominal pain investigations
If organic cause is suspected: FBC, ESR/CRP, U&E, LFT, urine/faecal MC&S and coeliac antibody screening
84
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 ```
85
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
86
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
87
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 ```
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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
89
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 ```
90
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
91
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