Paediatrics- GI + Liver

Question 1

What are the differences between ‘Posseting’, ‘Regurgitation’, and ‘Vomiting’?

Answer 1

Posseting is the small amounts of milk that accompany the return of swallowed air (wind)- happens in nearly all babies

Regurgitation describes larger, more frequent losses and may indicate GORD

Vomiting is forceful ejection of gastric contents

Question 2

What are the causes of vomiting in children?

Answer 2

1) Gastro-oesophageal reflux
2) Feeding problems
3) Infection (GE, urinary tract, meningitis, pertussis, resp tract etc.)
4) Food allergy/intolerance
5) Intestinal obstruction (pyloric stenosis etc.)
6) Inborn errors of metabolism
7) Congenital adrenal hyperplasia
8) Renal failure

Question 3

What are the causes of vomiting in preschool children?

Answer 3

1) GE
2) Infection (meningitis, pertussis, resp tract, urinary tract etc.)
3) Appendicitis
4) Intestinal obstruction
5) Raised ICP
6) Coeliac
7) Renal failure
8) Inborn errors of metabolism
9) Testicular torsion

Question 4

What are the causes of vomiting in school age and adolescent children?

Answer 4

1) GE + Infection (pyelonephritis, septicaemia)
2) Peptic ulcer + H. Pylori infection
3) Appendicitis
4) Migraine
5) Raised ICP
6) Coeliac disease
7) Renal failure
8) Diabetic ketoacidosis
9) Alcohol/drug ingestion or meds
10) Cyclical vomiting syndrome
11) Bulimia/anorexia nervosa
12) Pregnancy
13) Testicular torsion

Question 5

What are the red flags in the vomiting child?

Answer 5

1) Bile-stained vomit (obstruction)
2) Haematemesis (ulcer)
3) Projectile vomiting (pyloric stenosis)
4) Vomiting at end of cough (whooping cough)
5) Abdominal tenderness/pain on movement
6) Hepatosplenomegaly (chronic liver disease, metabolism problems)
7) Blood in stool (infection, obstruction)
8) Severe dehydration/shock (severe GE, systemic infection, ketoacidosis)
9) Bulging fontanelle/seizures (raised ICP)
10) Faltering growth (GORD, coeliac)

Question 6

Gastro-oesophageal reflux is more common in what type of children?

Answer 6

1) Cerebral palsy or other neurodevelopmental disorders
2) Preterm infants (esp. bronchopulmonary dysplasia)
3) Following surgery for oesophageal atresia or diaphragmatic hernia

Question 7

What are the complications of gastro-oesophageal reflux?

Answer 7

1) Faltering growth
2) Oesophagitis
3) Recurrent pulmonary aspiration
4) Dystonic neck posturing (Sandifer syndrome)
5) Apparent life-threatening events

Question 8

How is gastro-oesophageal reflux investigated?

Answer 8

Usually clinically diagnosed- investigations indicated if atypical history, complications, or failure to respond to treatment

1) 24 hour oesophageal monitoring
2) 24 hour impedance monitoring
3) Endoscopy with oesophageal biopsies

Question 9

How is gastro-oesophageal reflux managed?

Answer 9

Uncomplicated: good prognosis, managed by parental reassurance, thickening agents to feeds, making feeds smaller + more frequent

Significant reflux: ranitidine or omeprazole

Complicated + doesn’t respond to treatment/oesophageal stricture: Nissen fundoplication

Question 10

What is pyloric stenosis?

Answer 10

Hypertrophy of the pyloric muscle causing gastric outlet obstruction. It presents at 2-8 weeks of age. More common in boys.

Question 11

What is the presentation of pyloric stenosis?

Answer 11

Vomiting- increases in frequency/forcefulness until projectile

Hunger after vomiting until dehydration leads to loss of interest in feeding

Weight loss (if delayed presentation)

Hypochloraemic metabolic alkalosis w/ a low plasma sodium + potassium

Question 12

How is pyloric stenosis diagnosed?

Answer 12

1) Test feed: give milk feed, gastric peristalsis is seen moving from left to right across abdomen. Pyloric mass feels like an olive and is usually palpable in the RUQ
2) USS to confirm diagnosis if in doubt

Question 13

How is pyloric stenosis managed?

Answer 13

1) Correct fluid + electrolyte imbalance with IV fluids

2) Pyloromyotomy (division of hypertrophied pyloric muscle down to the mucosa)

Question 14

Name some extra-abdominal causes of acute abdominal pain:

Answer 14

1) URTI
2) Lower lobe pneumonia
3) Testicular torsion
4) Hip and spine

Question 15

Name some intra-abdominal (medical) causes of acute abdominal pain:

Answer 15

1) GE
2) Urinary tract (UTI etc.)
3) Henoch-Schonlein purpura
4) Diabetic ketoacidosis
5) Sickle cell disease
6) Hepatitis
7) IBD
8) Constipation
9) Recurrent abdominal pain of childhood
10) Gynaecological
11) other (psychological, lead poisoning, acute porphyria)
12) Non-specific abdominal pain

Question 16

Name some intra-abdominal (surgical) causes of acute abdominal pain:

Answer 16

1) Acute appendicitis
2) Intestinal obstruction
3) Inguinal hernia
4) Peritonitis
5) Inflamed Meckel diverticulum
6) Pancreatitis)
7) Trauma

Question 17

What are the symptoms of acute appendicitis?

Answer 17

1) Anorexia
2) Vomiting
3) Abdominal pain (initially central + colicky –> localises to the RIF

Question 18

What are the signs of acute appendicitis?

Answer 18

1) Flushed face with oral fetor
2) Low grade fever
3) Abdominal pain aggravated by movement)
4) Persistent tenderness with guarding in the RIF (McBurney’s point)
5) If retrocaecal there may be no guarding. If pelvic there may be few abdominal signs

Question 19

How is acute appendicitis investigated?

Answer 19

1) Diagnosis made by repeat observation and clinical review. Avoid delay and unnecessary laparotomy.
2) USS- may support clinical diagnosis and demonstrate complications (perforation, abscess etc.).

Question 20

How is acute appendicitis managed?

Answer 20

Uncomplicated: appendicectomy

Perforation: fluid resus + IV antibiotics given prior to laparotomy

Palpable mass w/ no signs of generalised peritonitis: IV antibiotics with surgery a few weeks later. If symptoms progress, do laparotomy

Question 21

What is non-specific abdominal pain and mesenteric adenitis?

Answer 21

NSAP: abdominal pain which resolves in 24-48 hours.

Mesenteric adenitis: diagnosed in children who have large mesenteric nodes on laproscopy and whose appendix is normal.

Question 22

How do you distinguish between non-specific abdominal pain and appendicitis?

Answer 22

The pain is less severe than appendicitis

Tenderness in the RIF is variable

Often accompanied with an URTI with cervical lymphadenopathy

Question 23

What is intussusception and where does it normally happen?

Answer 23

Invagination of proximal bowel into a distal segment

Most commonly involves ileum passing into the caecum through the ileocaecal valve

Question 24

When does intussusception tend to present?

Answer 24

Peak presentation is between 3 months and 2 years of age

Question 25

What are the complications of intussusception?

Answer 25

Stretching and constriction of the mesentery --> results in venous obstruction --> causes engorgement and bleeding from the bowel mucosa, fluid loss, and subsequently bowel perforation, peritonitis, and gut necrosis

Question 26

How does intussusception present?

Answer 26

1) Redcurrant jelly stool comprising blood stained mucus (CHARACTERISTIC) 2) Paroxysmal, severe colicky pain with pallor (becoming increasingly lethargic) 3) Sausage-shaped mass (often palpable in abdomen) 4) Abdominal distension and shock

Question 27

How is intussusception investigated?

Answer 27

1) X-ray of abdomen: distended small bowel and absence of gas in distal colon or rectum 2) Abdominal USS: useful to confirm diagnosis and check response to treatment

Question 28

How is intussuception managed?

Answer 28

1) Immediate IV fluid resus 2) If no signs of peritonitis: reduction of the intussusception by rectal air insufflation 3) If this fails, surgery is required

Question 29

What is Meckel Diverticulum?

Answer 29

An ileal remnant of the vitello-intestinal duct which contains ectopic gastric mucosa or pancreatic tissue

Question 30

What is the presentation of Meckel Diverticulum?

Answer 30

1) Most are asymptomatic 2) May present with severe rectal bleeding (neither bright red nor true melaena) 3) Other forms of presentation include intussusception, volvulus, or diverticulitis

Question 31

How is Meckel Diverticulum investigated?

Answer 31

1) Usually an acute reduction in haemoglobin | 2) A technetium scan will demonstrate increased uptake by ectopic gastric mucosa (in 70% of cases)

Question 32

How is Meckel Diverticulum managed?

Answer 32

Surgical resection

Question 33

What is the pathology of malrotation?

Answer 33

During rotation of the small bowel in foetal life, if the mesentery is not fixed at the duodenojejunal flexure or in the ileocaecal region its base is shorter than normal and is predisposed to volvulus Ladd bands are peritoneal bands which may cross the duodenum, often anteriorly. They obstruct the duodenum or volvulus

Question 34

What are the two ways in which malrotation presents?

Answer 34

Obstruction Obstruction with a compromised blood supply: emergency

Question 35

What are the presenting features of malrotation?

Answer 35

Bilious vomiting (often first few days of life) Abdominal pain and tenderness (from peritonitis or ischaemic bowel)

Question 36

How is malrotation investigated?

Answer 36

Urgent upper GI contrast study to assess intestinal rotation (always do when bilious vomiting) If compromised blood supply: urgent laparotomy

Question 37

How is malrotation treated?

Answer 37

Urgent surgical correction Appendix is generally removed to avoid diagnostic confusion

Question 38

What is the definition of recurrent abdominal pain?

Answer 38

Pain sufficient to interrupt normal activities that lasts over 3 months

Question 39

How does recurrent abdominal pain present?

Answer 39

Characteristic peri-umbilical pain Children are otherwise entirely well

Question 40

What are the causes of recurrent abdominal pain?

Answer 40

IBS, Constipation, dyspepsia, abdominal migraine, gastric/peptic ulceration, eosinophilic oesophagitis, IBD, malrotation Gynaecological Psychological Hepatobiliary (hepatitis, gallstones, pancreatitis) Urinary tract (UTI, PUJ obstruction)

Question 41

How is recurrent abdominal pain managed/investigated?

Answer 41

1) Full history + thorough examination (check growth) 2) Urine microscopy and culture 3) USS to exclude gallstones and PUJ obstruction 4) Coeliac antibodies and TFTs

Question 42

What is the prognosis of recurrent abdominal pain?

Answer 42

50%: rapidly become free of symptoms 25%: symptoms take months to resolve 25%: symptoms continue or return in adulthood as migraine, IBS, or functional dyspepsia

Question 43

Abdominal Migraine: Definition

Answer 43

Often associated with abdominal pain in addition to headaches, and in some children the abdominal pain predominates

Question 44

Abdominal Migraine: Epidemiology

Answer 44

Usually a personal or FH of migraine

Question 45

Abdominal Migraine: Presentation

Answer 45

Characteristic history with long periods of no symptoms and then a shorter period (12-48 hours) of non-specific abdominal pain and pallor, with or without vomiting The attacks of pain are midline, associated with abdominal pain and facial pallor

Question 46

Abdominal Migraine: Management

Answer 46

Treatment with anti-migraine medication may be beneficial if the problem causes school absence

Question 47

IBS: Pathology

Answer 47

Associated with altered GI motility and an abnormal sensation of intra-abdominal events Symptoms may be precipitated by a GI infection Often a positive FH

Question 48

IBS: Presentation

Answer 48

Non-specific abdominal pain, may be worse before or relieved by defecation Explosive, loose, or mucus stools Bloating Feeling of incomplete defecation Constipation (often alternating with normal or loose stools)

Question 49

Peptic ulceration/Gastritis/Functional Dyspepsia: Causes

Answer 49

H. Pylori infection is a strong predisposing factor

Question 50

Peptic ulceration/Gastritis/Functional Dyspepsia: Presentation

Answer 50

Ulcers: epigastric pain that wakes them up at night, and radiates to the back Gastritis: abdominal pain + nausea Functional Dyspepsia: peptic ulcer symptoms + early satiety, bloating, post-prandial vomiting, delayed gastric emptying

Question 51

Peptic ulceration/Gastritis/Functional Dyspepsia: Investigations

Answer 51

1) Gastric antral biopsies (H. Pylori produces urease) 2) 13C breath test 3) Stool antigen may be positive for H.Pylori

Question 52

Peptic ulceration/Gastritis/Functional Dyspepsia: Management

Answer 52

Peptic ulceration: PPI (omeprazole) + clarithromycin/metronidazole + amoxicillin. If they fail to respond do upper GI endscopy If normal, then functional dyspepsia is diagnosed (some children respond to a hypoallergenic diet)

Question 53

Eosinophilic Oesophagitis: Definition

Answer 53

Inflammatory condition affecting the oesophagus caused by activation of eosinophils in the mucosa and submucosa

Question 54

Eosinophilic Oesophagitis: Presentation

Answer 54

1) Vomiting 2) Discomfort on swallowing 3) Bolus dysphagia (food 'sticks' in the upper chest)

Question 55

Eosinophilic Oesophagitis: Investigations

Answer 55

Endoscopy

Question 56

Eosinophilic Oesophagitis: Management

Answer 56

Oral corticosteroids (fluticasone or viscous budesonide)

Question 57

Gastroenteritis: Causes

Answer 57

Virus: rotavirus (also adenovirus, norovirus, coronavirus) Bacterial (less common- blood in stool): campylobacter jejuni, shigella, salmonella, cholera, enterotoxigenic E.Coli) Protozoan parasite (giardia, cryptosporidium

Question 58

How is degree of dehydration assessed and what are the degrees?

Answer 58

Body weight 1) No clinically detectable dehydration (<5% loss of body weight) 2) Clinical dehydration (5-10% loss of body weight) 3) Shock (>10% loss of body weight)

Question 59

What is post-gastroenteritis syndrome?

Answer 59

Following an episode of GE, the introduction of a normal diet causes a return of watery diarrhoea --> Return to the use of ORT

Question 60

In what 3 ways do disorders affecting digestion or absorption of nutrients present?

Answer 60

1) Abnormal stools 2) Poor weight gain/faltering growth 3) Specific nutrient deficiencies (single or combination)

Question 61

Coeliac Disease: Pathology

Answer 61

1) An enteropathy in which the gliadin fraction of gluten provokes a damaging immunological response in the proximal small intestinal mucosa 2) As a result, enterocytes start moving up the villi at a higher rate but it isn't enough to compensate for increased cell loss from villous tips 3) Villi become progressively shortened and then absent, leaving a flat villi

Question 62

Coeliac Disease: Presentation

Answer 62

1) Faltering growth 2) Abdominal distension 3) Buttock wasting 4) Abnormal stools 5) General irritability Other (anaemia, short stature, mild + non-specific GI symptoms)

Question 63

Coeliac Disease: Investigations

Answer 63

1) Serology (IgA tissue transglutaminase and endomysial antibodies) 2) Endoscopy w/ biopsy: confirmation depends on mucosal changes (increased intraepithelial lymphocytes, villous atrophy and crypt hypertrophy, with catch-up growth on gluten withdrawal)

Question 64

Coeliac Disease: Management

Answer 64

Gluten-free diet

Question 65

Other than coeliac disease, name 6 other (uncommon) causes of nutrient malabsorption:

Answer 65

1) Short bowel syndrome 2) Exocrine pancreatic dysfunction (CF) 3) Small-intestinal mucosal disease 4) Lymphatic leakage or obstruction 5) Loss of terminal ileal function (Crohn's) 6) Cholestatic liver disease or biliary atresia

Question 66

What is the most common cause of persistent loose stools in preschool children?

Answer 66

Chronic Non-specific Diarrhoea (previously known as Toddler diarrhoea)

Question 67

Crohn's Disease: How does it present in children and adolescents?

Answer 67

1) General ill health (fever, lethargy, weight loss) 2) Growth failure 3) Delayed puberty 4) Classic presentation: abdominal pain, diarrhoea, weight loss 5) Extra-intestinal manifestation: oral lesions (or perianal skin tags), uveitis, arthralgia, erythema nodusum

Question 68

Crohn's Disease: How is it investigated?

Answer 68

Endoscopy with biopsy (non-caseating epithelioid granulomata) May also have raised ESR, CRP, platelet count May have iron deficiency anaemia and low serum albumin

Question 69

Crohn's Disease: How is it managed?

Answer 69

1) Remission is induced with nutritional therapy or steroids 2) Relapse: immunosuppressants (azathioprine, mercaptopurine, or methotrexate). Anti-TNF (infliximab or adalimumab) 3) Surgery for complications

Question 70

Ulcerative colitis: presentation

Answer 70

1) Rectal bleeding, diarrhoea, and colicky pain 2) Weight loss and growth failure (less common than Crohn's) 3) Extraintestinal (erythema nodusum, arthritis)

Question 71

Ulcerative colitis: diagnosis

Answer 71

1) endoscopy w/ biopsy (mucusal inflammation, crypt damage 2) exclude infection 3) small bowel imaging to check that extra-colonic inflammation suggestive of Crohn's is not present

Question 72

Ulcerative colitis: management

Answer 72

Mild disease: aminosalicylates (balsalazide and mesalazine) More aggressive disease: systemic steroids for exacerbations and immunomodulatory therapy (azathioprine) to maintain remission Surgery for severe disease

Question 73

Name 7 causes of constipation

Answer 73

1) Idiopathic 2) Hirschsprung disease 3) Lower spinal cord problems 4) Anorectal abnormalities 5) Hypothyroidism 6) Coeliac disease 7) Hypercalcaemia

Question 74

What is the presentation of constipation in children?

Answer 74

1) Abdominal pain, which changes with passage of stool or overflow soiling 2) Constipation may be precipitated by dehydration or anal fissure 3) Older children: problems with toilet training, anxieties about opening bowels in unfamiliar toilets 4) Soft faecal mass in lower abdomen on examination

Question 75

What are the red flags of constipation in children?

Answer 75

1) Failure to pass meconium in first 24 hours (Hirschsprung) 2) Faltering growth/growth failure (hypothyroid/coeliac) 3) Abdominal distension 4) Abnormal lower limb neurology or deformity 5) Sacral dimple over natal cleft (spina bifida occulta) 6) Abnormal appearance/position/patency of anus (anormal anorectal anatomy) 7) Signs of sexual abuse 8) Perianal fistulae, abscesses, or fissures

Question 76

How is constipation investigated?

Answer 76

History and clinical findings (do not do DRE)

Question 77

What can occur in longstanding constipation and how should this be explained to the child and parents?

Answer 77

The rectum becomes distended, with a loss of the need to defecate. Involuntary soiling may occur as contractions of the full rectum inhibit the internal sphincter, leading to overflow. Explain that the soiling is involuntary and that recovery of normal rectum size and sensation can be achieved but may take a long time

Question 78

What is the general aim of constipation management?

Answer 78

Evacuate the overloaded rectum completely. This is done using a disimpaction regime of stool softeners, followed by maintenance treatment to unsure ongoing regular pain-free defecation.

Question 79

What is Hirschsprung Disease?

Answer 79

The absence of ganglion cells from the large bowel, resulting in a narrow contracted segment. The abnormal bowel extends from the rectum proximally, ending in a normally innervated, dilated colon

Question 80

Hirschsprung Disease: Presentation

Answer 80

1) Usually presents in neonatal period 2) Intestinal obstruction with failure to pass meconium in first 24 hours 3) Followed by abdominal distension and bile-stained vomiting 4) Rectal exam: narrow segment, withdrawal of finger releases gush of liquid stool and flatus 5) In later childhood: profound chronic constipation, abdominal distension, growth failure

Question 81

Hirschsprung Disease: Diagnosis

Answer 81

Suction rectal biopsy is diagnostic (demonstrates absence of ganglion cells and presence of large, acetylcholinesterase-positive nerve trunks

Question 82

Hirschsprung Disease: Management

Answer 82

Surgical: initial colostomy followed by anastomosing normally innervated bowel to the anus

Question 83

What is the most common presentation of liver disease in the neonatal period?

Answer 83

Prolonged (persistent) neonatal jaundice

Question 84

At what point is physiological jaundice in newborns considered prolonged?

Answer 84

If the jaundice doesn't subside after 2 weeks (3 if premature)

Question 85

Why must prolonged neonatal jaundice be investigated promptly?

Answer 85

To distinguish between unconjugated hyperbilirubinaemia (resolves spontaneously) and conjugated (sign of liver disease)

Question 86

What are the causes of prolonged neonatal jaundice?

Answer 86

Unconjugated: breastmilk jaundice, infection (UTI), haemolytic anaemia, hypothyroidism, Crigler-Najjar syndrome Conjugated: bile duct obstruction (biliary atresia, choledochal cyst), neonatal hepatitis syndrome, intrahepatic biliary hypoplasia

Question 87

What is the characteristic appearance of prolonged neonatal jaundice?

Answer 87

Raised conjugated bilirubin (>20) accompanied by: 1) Pale stools 2) Dark urine 3) Bleeding tendency 4) Failure to thrive

Question 88

What is biliary atresia?

Answer 88

Progressive fibrosis and obliteration of the extrahepatic and intrahepatic biliary tree Leads to chronic liver failure and death within 2 years unless treated

Question 89

What is the presentation of biliary atresia?

Answer 89

1) Mild jaundice 2) Pale stools (increasingly pale as disease progresses) 3) Normal birthweight followed by faltering growth 4) Hepatomegaly initially, then splenomegaly due to portal hypertension

Question 90

How is biliary atresia investigated?

Answer 90

1) ERCP is diagnostic 2) Raised conjugated bilirubin 3) Fasting abdominal USS: may show contracted or absent gallbladder 4) Liver biopsy: extrahepatic biliary obstruction 5) LFTs abnormal but of little value to diagnosis

Question 91

How is biliary atresia managed?

Answer 91

1) Kasai hepatoportoenterostomy 2) If surgery fails: liver transplant (nutrition and fat-soluble vitamin supplementation is essential)

Question 92

Choledochal cysts: pathology

Answer 92

cystic dilatations of the extrahepatic biliary system

Question 93

Choledochal cysts: presentation

Answer 93

Abdominal pain, palpable mass, jaundice, or cholangitis

Question 94

Choledochal cysts: investigations and management

Answer 94

Investigate: USS or MRCP Manage: surgical removal of cyst

Question 95

Neonatal hepatitis syndrome: pathology

Answer 95

Prolonged neonatal jaundice and hepatic inflammation

Question 96

Neonatal hepatitis: presentation

Answer 96

1) Low birthweight + faltering growth | 2) Jaundice may be severe

Question 97

A1AT Deficiency: pathology

Answer 97

Inherited autosomal recessive disorder --> accumulation of protein in hepatocytes --> lack of circulating A1AT results in emphysema in adults

Question 98

A1AT Deficiency: presentation

Answer 98

1) Prolonged neonatal jaundice 2) Bleeding (vit K deficiency) 3) Hepatosplenomegaly

Question 99

A1AT Deficiency: Investigation and management

Answer 99

Investigation: estimating the level of A1AT in plasma and identify protein phenotype Management: 50% good prognosis, rest develop liver disease and may require transplant

Question 100

What are the clinical features of acute viral hepatitis?

Answer 100

1) Nausea and vomiting 2) Abdominal pain 3) Lethargy 4) Jaundice 5) Large, tender liver