Gastroenterology

Question 1

Causes of chronic abdominal pain?

Answer 1

> 90% have no structural cause!

GI causes: constipation, IBS, non-ulcer dyspepsia, abdominal migraine, gastritis, eosinophilic oesophagitis (rare but saw 2pt with it…), IBD, malrotation

Gynae: dysmenorrhoea, ovarian cysts

HPB: hepatitis, gallstones, pancreatitis

UT: UTI, PUJ obstruction

Psychological: bullying, abuse, stress (a manifestation of stress causing physical pain, perpetuated by family distress/requests for Ix)

Question 2

How would you explain IBS + functional dyspepsia to a parent?

Answer 2

The insides of the intestines are very sensitive so child is feeling the food going around the bends. May be painful but is never dangerous

Question 3

Abdominal migraine?

Answer 3

Pain (midline, a/w vomiting + pallor) + headache

Lasts 12-48h, then often weeks of no sx then recurs

If causing school absence etc then anti-migraine meds can help

Question 4

IBS?

Answer 4

altered GI motility + abnormal sensation of intra-abdominal events + forceful contraction

can be precipitated by gastroenteritis or stress/anxiety

cf: peri-umbilical/non specific abdo pain, often relieved on defecation, explosive/loose/mucusy stools, tenesmus, constipation

check for coeliac

Question 5

Stomach issues?

Answer 5

duodenal ulcer: rare in kids but consider if epigastric pain radiating to back/FH. ulcers give PPI

antral gastritis: abdo pain + nausea, caused by H pylori. Check for it with stool antigen/urea breath test - eradicate triple therapy with PPI + amoxicillin + metronidazole/clarithromycin

functional dyspepsia: normal gastroscopy, prob variant of IBS. non-specific sx like early satiety, bloating, postprandial vomiting

Question 6

Eosinophilic oesophagitis?

Answer 6

activation of eosinophils in oesographus (prob related to allergy)

cf: vomting, discomfort on swallowing, bolus dysphagia. endoscopy
m: oral steroids, exclusion diets may help young

Question 7

Infant colic

Answer 7

Symptom complex in first few months, v common, usually resolved by 12m

CF: paroxysmal inconsolable crying, draw up knees, excessive farting

benign but frustrating for parents

m: support, ‘gripe water’ often recommended but unproven

if severe + persistent may be CMPA so trial 2w of hydrolysed milk, then trial GORD treatment

Question 8

Define constipation and its causes

Answer 8

Infrequent passage of hard dry faeces, often w straining/pain/bleeding

On average by 1y then poo 2x a day, breastfed may not pass for a few days but still be healthy, after 1y poo daily

Precipitated by dehydration, pain e.g. fissure, toilet training issues, anxieties about BO at school

Occasionally there’s an underlying cause like lower SC issues, anorectal abnormalities, hypothyroid, coeliac, hypercalcaemia

Question 9

Red flags in constipation

Answer 9

Failure to pass meconium in first 24h-Hirschsprung
Growth faltering-coeliac, hypothyroidism
Gross abdo distension-Hirschsprung, other dysmotility
Abnormal neuro-talipes, spina bifida occult (pit + hair over spine)
Anorectal abnormality
Perianal fistula/abscess/fissure-perianal Crohn’s
Perianal bruising/multiple fissures-sexual abuse

Question 10

Management of constipation

Answer 10

Acute e.g. after a febrile illness: maintenance laxatives + extra fluids

Chronic: rectum over distended so lose sensation so may get involuntary soiling (explain not their fault and it can recover). Need disimpaction with stool softeners (osmotic laxative e.g. polyethylene glycol) + electrolytes (Movicol), escalate dose until works, if not working try stimulant (senna, sodium picosulfate)

Maintenance for regular pain-free poops e.g. polyethylene glycol +/- stimulant; fluid + balanced diet (extra fibre not helpful as makes poos even bigger), encourage regularly sitting on loo after meals (utilises gastrocolic reflex)

Question 11

Types of dehydration

Answer 11

Dehydration=total body deficit of sodium + water

Hyponatraemic: sodium lower than water (drink lots of water) so shift of water to ICF - may result in greater brain volume (seizures) + ECF depletion more shock. More common in poorly-nourished

Isonatraemic: sodium normal range

Hypernatraemic: infrequent but more water lost than sodium e.g. high fever, or profuse low-sodium diarrhoea. ECF becomes hypertonic so water moves to ECF (signs of dehydration less obvious so harder to recognise), water drawn out of brain + cerebral shrinkage can cause hypertonia/hyperreflexia/altered consciousness/multiple haemorrhages

Question 12

Chronic non-specific diarrhoea

Answer 12

Used to be toddler diarrhoea

Varied consistency, often undigested food, child otherwise well. Usually due to gut dysmotility (fast transit) which improves with age; uncommonly can be from undiagnosed coeliac/excessive apple juice/temporary CMPA after gastroenteritis

Question 13

Causes of faltering growth

Answer 13

Poor intake (environmental): food not available (poverty, breast milk supply issues, conflict over feeding), psychosocial deprivation, neglect inc FII

Poor intake (disease): impaired swallow/suck, chronic illness anorexia

Increased loss: vomiting, GORD

Malabsorption: coeliac, CF, CMPA, short gut syndrome, post-NEC

Failure to utilise nutrients: chromosomal syndromes, IUGR, congenital infection, storage disorders, congenital hypothyroidism

Increased requirements: hyperthyroidism, CF, cancer, CHD, CKD

Question 14

Management of faltering growth

Answer 14

Mealtime observations, food diaries, may need paediatric dietician, SALT for feeding disorders. Rise in weight centiles 4-8w after intervention. if <6m may need hospital

Question 15

Vitamin deficiency manifestations

Answer 15

A-night blindness
B1-polyneuropathy, Wernicke-Korsakoff syndrome
B3-pellagra
B6-anaemia, irritability, seizures
B7-dermatitis, seborrhoea
B9 (folic acid)-megaloblastic anaemia, NTD
B12-megaloblastic anaemia, peripheral neuropathy
C-scurvy
D-rickets
E-mild haemolytic anaemia in newborns, ataxia, peripheral neuropathy
K-haemorrhagic disease of the newborn, bleeding problems

Question 16

Causes + CF of gastroenteritis + differentials

Answer 16

Causes: rotavirus (now in immunisation), adenovirus/norovirus/coronavirus etc; bacterial less common but may suspect if blood in stool like Campylobacter jejune (severe abdo pain), Shigella/Salmonellae (dysenteric infection + pus, pain, tenesmus), cholera/E coli (profuse rapidly dehydrating diarrhoea); protozoal e.g. Giardia

CF: sudden change to loose/watery stools, often vomiting, may have h/o contact/travel, shock is most serious complication

Ddx: systemic infection, local infections like URTI/UTI/AOM, surgical like PS/intussusception/appendicitis, DKA, haemolytic uraemic syndrome, coeliac, CMPA, lactose intolerance

Question 17

Management of gastroenteritis

Answer 17

No clinical dehydration: continue bf/milk, encourage fluids to compensate for higher GI losses (discourage fruit juice/carbonated), oral rehydration solution (salts + sugars so draws fluid in).

• Fluid deficit by weight%dehydration10
• Can also estimate if have recent weights e.g. 0.5kg lost ~ 500ml deficit
• Remember ongoing losses

ORS: Usually 50ml/kg + maintenance over 4h ((e.g. a child of 10kg needs 500ml ORS plus their maintenance fluids over 4h). Oral fluid challenge of small amount every 5m

Clinical dehydration: regular ORS in small amounts, continue bf, consider ORS via NG tube if vomiting too much; if persisting may need IV rehydration.
-Assume dehydration is 10% if there is clinical dehydration

Shock:

• Bolus of normal saline (20ml/kg bolus, can repeat 1/2; if in DKA/heart issue 10ml/kg)
• Correct deficit over 48h with normal saline + 5% dextrose. Deficit assumed to be 10% of weight if clinically dehydrated
• Monitor U+E + glucose regularly. If hypernatraemic call for senior as need slower replacement

Maintenance (if not tolerating enteral) over 24h with NaCl + dextrose: 100ml/kg for first 10kg, 50ml/kg for second 10kg, 20ml/kg for every subsequent kg

After rehydration: reintroduce usual solids, avoid fruit juice/carbonated, adv on strict hand washing, don’t return to nursery/school till 48h after last episode

Question 18

Gastro oesophageal reflux

Answer 18

Functional immaturity means LOS to relaxed + infants have short intra-abdominal oesophagus, and made worse in infants as they mostly drink milk + lie down

Majority resolve by 12m as they start walking + weaning. Can be frustrating/gross with the recurrent regurg/vomiting.

Is GORD when becomes a significant problem (faltering growth, oesophagitis [haematemesis, discomfort, iron def anaemia], recurrent pulmonary aspiration, dystonic neck posturing)

RF for GORD are cerebral palsy, preterms, oesophageal atresia, CDH

Ix: may do 24h pH monitoring to quantify, endoscopy + biopsy for oesophagitis etc, contrast studies may help exclude anatomical abnormalities

M: uncomplicated give reassurance/thickening agents for feeds/smaller more frequent feeds/gaviscon for symptom relief; medical acid suppress with H2RA/PPI (reduces volume + treats oesophagitis from the acid), consider CMPA if not responding, surgery for unresponsive/oesophageal stricture (Nissen fundoplication: wrap the fundus of the stomach around the intra-abdominal oesophagus)

Question 19

Jaundice (not neonatal)

Answer 19

Unconjugated: haemolytic anaemias, inherited like Gilbert’s syndrome (AR, common, mildly high bili triggered by infection/exercise/stress)

Conjugated: infections causing intrahepatic cholestasis (hepatitis, EBV, CMV, HSV, gram neg sepsis), metabolic (Wilson’s disease, alpha 1 antitrypsin def, CF), biliary obstruction (cholelithiasis, cholecystitis, sclerosing cholangitis [a/w IBD]), autoimmune, hepatoxins (paracetamol main cause of liver failure in older children), vascular e.g. Budd Chiari syndrome (obstructed hepatic veins-abdo pain, ascites, hepatomegaly)

Question 20

Vomiting

Answer 20

Forceful ejection of gastric contents (cf posseting/regurgitation which is non-forceful)

Causes:

• Infants: GOR, feeding problems, any infection, food intolerance/allergy, eosinophilic oesophagitis, any cause of intestinal obstruction, IEM, CAH, renal failure
• Preschool age: gastroenteritis, other infection, appendicitis, obstruction of intestines, RICP, coeliac, renal failure, IEM, testicular torsion
• School age: gastroenteritis, other infection, peptic ulcer, appendicitis, migraine, RICP, coeliac, renal failure’s, DKA, alcohol/drugs, cyclical vomiting syndrome, bulimia/anorexia nervosa, pregnancy, testicular torsion

Question 21

Red flags in a vomiting child

Answer 21

Bile: intestinal obstruction (distal to AoV) like intussusception/malrotation/strangulated inguinal hernia
Haematemesis: oesophagitis, peptic ulcer, oral/nasal bleeding, varices
Projectile vomiting in first 2-8w: pyloric stenosis
Vomiting after paroxysmal coughing: whooping cough
Abdo tenderness: surgical
Hepatosplenomegaly: liver disease, IEM
Abdo distension: intestinal obstruction
Blood in stool: intussusception, bacterial gastroenteritis
Severe dehydration/shock: severe gastroenteritis, systemic infection, DKA
Bulging fontanelle, seizures: RICP
Faltering growth

Question 22

Coeliac disease

Answer 22

Enteropathy where gluten in wheat/barley/rye cause damaging immunological response in SI mucosa. Villi become progressively shorter then absent

CF:

• 8-24m classical with abnormal stool, faltering growth, abdo distension, muscle wasting (when foods introduced)
• Subtle: short stature, anaemia (iron or folate def), abdo pain, screening in T1DM, non-specific GI sx

Dx: positive serology of anti-TTG, then exclude gluten to see if sx go, if not clear may need biopsy to demonstrate mucosal changes

M: gluten withdrawal (so no products with wheat barley or rye), dietician needed otherwise risk micronutrient def

Comps: osteopenia, bowel malignancy (esp SB lymphoma)

Question 23

Encopresis + soiling

Answer 23

Usually due to overflow from constipation

Question 24

Crohn’s disease

Answer 24

More common than UC in kids
Transmural, focal, mostly distal ileum/proximal colon (but can affect any GIT).

CF include general ill health (fever, WL, lethargy: may just have these!), delayed puberty, only a quarter have the abdo pain+diarrhoea+WL. Extra-intestinal features (oral lesions, perianal skin tags, uveitis, arthralgia, erythema nodosum). may develop strictures or fistulae

Ix: raised plts, raised ESR/CRP, iron def anaemia, low albumin. Endoscopy for definitive (under GA, upper + lower)-non-caseating granuloma hallmark (only seen in 1/3)

M: induce remission with nutritional therapy (have whole protein molecular feeds instead of food for 6-8w) effective in 3/4 for bowel rest (but some children won’t do it), then systemic steroids if not working. For maintenance use azathioprine (check TPMT first-if deficient more risk of s/es inc BM suppression); or biologics. Surgery for complications like fistulae/abscesses

Question 25

Malabsorption

Answer 25

CF: abnormal stools (not flushing), poor weight gain/growth, specific nutrient deficiencies

Causes include food allergy, coeliac disease, cholestatic liver disease, lymphatic leakage/obstruction, short bowel syndrome, loss of terminal ideal function e.g. resection/CD (absent bile acid + B12 absorption), exocrine pancreas dysfunction (e.g. CF. defective TAG/protein/starch digestion so pan-nutrient malabsorption), SI mucosal disease (lose absorptive SA like in coeliac, specific transport deficits)

Question 26

Mesenteric adenitis

Answer 26

Often diagnosed in children when see mesenteric enlarged LN @ laparoscopy with a normal appendix, presents like appendicitis

unsure if is actually a thing

Question 27

Viral hepatitis

Answer 27

CF: N+V, abdo pain, lethargy, jaundice (up to 50%), large tender liver (common), splenomegaly (30%), liver transaminases v high, coagulation usually normal

Causes:

• Hep A: FO transmission, mostly a mild illness lasting ~4w, travel vaccine
• Hep B: vertical/blood or needle stick transmission. If perinatally contracted asymptomatic but a carrier, older children may get classic hepatitis sx. Some become chronic carriers, some become acute failure. In chronic hep B there is a risk of cirrhosis + HCC, no treatment that really works
• Hep C: vertical transmission usually, no acute infection but majority chronic carriers with 25% risk of future cirrhosis/HCC. M: interferon + ribavirin
• Hep D: depends on hep B for replication
• Hep E: usually water transmitted, mostly mild self-limiting illness
• Seronegative hepatitis (non A-E): similar to hep A

Question 28

Other liver disease in children

Answer 28

Neonatal cholestasis-prolonged conjugated neonatal jaundice. E.g. biliary atresia (fibrosis + obliteration of biliary tree, if not treated die within 2y, Kasai surgery then liver transplant eventually needed), choledochal cysts, neonatal hepatitis syndrome

Neonatal metabolic liver disease: alpha 1 antitrypsin def (AR), usually neonatal jaundice or bleeding from vitamin K def), galactosemia (poor feeding, vomiting, jaundice, hepatomegaly, cataracts, gram neg sepsis; M-galactose free diet)

Acute liver failure: massive hepatic necrosis, loss of liver function, hepatic encephalopathy. Uncommon but high mortality

Post-viral hep B/C

Autoimmune hepatitis (M-azathioprine + prednisolone) + sclerosing cholangitis (M-ursodeoxycholic acid)

Cystic fibrosis: usually fatty liver leading to protein-energy malnutrition/micronutrient deficiencies, or severe biliary fibrosis + portal HTN

Wilson disease

Fibropolycystic liver disease: inherited conditions affecting biliary tree

Non-alcoholic fatty liver disease: steatosis-steatohepatitis-fibrosis-cirrhosis-end stage failure, usually asymptomatic, may have vague RUQ pain/lethargy

Question 29

Complications of chronic liver disease

Answer 29

Malnutrition, pruritus, encephalopathy, cirrhosis, portal HTN, oesophageal varies, ascites, spontaneous bacterial peritonitis, renal failure (renal tubular acidosis or hepatorenal syndrome)

Question 30

What drugs are used in gastroenteritis?

Answer 30

Basically they’re not used lol

Antidiarrhoeals+antiemetics ineffective and may prolong the residence of the causative organism

Antibiotics not usually used even if bacterial cause, only used in sepsis/salmoneall if <6m old/malnourished/immunocompromised, and obv in certain ones like C diff/cholera/giardiasis

Question 31

Ulcerative colitis

Answer 31

Recurrent inflammatory ulcerating disease of colonic mucosa

CF: PR bleeding, diarrhoea, colicky pain; WL/growth faltering less common than in CD

Dx: endoscopy, 90% have pancolitis (whereas in adults is more localised normally), mucosal inflammation, crypt damage

Mild management: aminosalicylates e.g. mesalazine, or topical steroids if just in rectum (rare in kids)

Acute exacerbations: systemic steroids

Severe UC: immunomodulators like azathioprine +/- steroids, biologicals like infliximab, dont delay surgery - need colectomy with ileostomy/ileorectal pouch
-Severe fulminating disease needs IV fluids, steroids, ciclosporin

Question 32

Immunological features of hepatitis B

Answer 32

Surface antigen (HBsAg) is the first marker to appear and causes the production of anti-HBs. 
HBsAg normally implies acute disease (present for 1-6 months), if there for > 6 months then this implies chronic disease (i.e. Infective)

Anti-HBs implies immunity (either exposure or immunisation). It is negative in chronic disease [antibody to the surface antigen]

Question 33

Causes, CF + management of acute liver failure

Answer 33

Causes:

• <2y: infection like HSV, metabolic, seronegative hepatitis, drug-induced, neonatal haemochromatosis
• > 2y: seronegative hepatitis, paracetamol OD, mitochondrial disease, Wilson disease, autoimmune hepatitis

CF: jaundice, encephalopathy, coagulopathy, hypoglycaemia, electrolyte disturbance

Comps: cerebral oedema, haemorrhage from gastritis/coagulopathy, sepsis, pancreatitis

M: maintain BG with IV dextrose, prevent sepsis with Abx + antifungals, prevent haemorrhage with IV It K + PPI, prevent cerebral oedema by fluid restriction, mannitol if develop oedema. Transplant

Question 34

Wilson’s disease

Answer 34

AR - reduced synthesis of caeruloplasmin (it binds copper) + defective excretion of copper in bile. Copper deposited in liver, brain, kidney + cornea. Usually presents in >3y with liver disease, if >10y often p/w neuropsychiatric sx e.g. mood or behaviour change, tremor, dysarthria, other CF include vit D-resistance rocket,s haemolytic anaemia, Kayser-Fleisher rings (copper in cornea)

Ix: low caeruloplasmin + copper in serum, urinary copper excretion increased. Definitive with liver biopsy/genetic

M: penicillamine (chelating agent) or trientine - both promote excretion. Zinc to reduce absorption, pyridoxine to prevent peripheral neuropathy