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Yr 5 - Paeds > Revision - GI > Flashcards

Revision - GI Flashcards

1
Q

What is the 1st line preventative medication to remember for abdominal migraine?

A

Pizotifen (serotonin agonist) –> needs to be withdrawn slowly due to risk of withdrawal symptoms

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2
Q

At what age is encopresis considered pathological?

A

≥4y

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3
Q

What 2 conditions may not passing meconium within 48 hours of birth indicate?

A

CF or Hirschsprung’s

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4
Q

Prior to starting treatment for constipation, what does the child need to be assessed for?

A

Faecal impaction

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5
Q

What are some factors that suggest faecal impaction?

A
  • symptoms of severe constipation
  • overflow soiling
  • faecal mass palpable in the abdomen (digital rectal examination should only be carried out by a specialist)
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6
Q

1st line management if faecal impaction is present?

A

Disimpaction regime with high doses of laxatives –> Polyethylene glycol 3350 + electrolytes (Movicol Paediatric Plain), using an escalating dose regimen.

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7
Q

What type of laxative is Polyethylene glycol 3350 (Movicol Paediatric Plain)?

A

Osmotic

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8
Q

2nd line management of faecal impaction if Movicol Paediatric Plain does not lead to disimpaction after 2 weeks?

A

Add stimulant laxative

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9
Q

What is the 1st line laxative for the management of constipation in children?

A

Movicol (osmotic)

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10
Q

What are some risk factors for GORD in infants?

A

1) prematurity

2) hiatus hernia

3) history of congenital diaphragmatic hernia or oesophageal atresia

4) neurodisability e.g. cerebral palsy

5) parental history of heartburn or acid regurgitation

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11
Q

GOR vs GORD?

A

Gastro-oesophageal reflux (GOR) is the passage of gastric contents into the oesophagus and is normal in infants if it is asymptomatic.

Gastro-oesophageal reflux disease (GORD) is the term used to describe this process in the presence of symptoms or complications from the reflux.

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12
Q

If the infant is breastfed with frequent regurgitation causing marked distress, what is the management step?

A

Use alginate (e.g. Gavisocon) mixed with water immediately after feeds.

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13
Q

If the infant is formula-fed with frequent regurgitation causing marked distress, what is the management?

A

Stepwise approach:

1) Ensure infant is not over-fed (no more than 150ml/kg/day total milk)

2) Decrease feed volume by increasing frequency (eg. 2-3 hourly)

3) Use feed-thickener (or pre-thickened formula)

4) Stop thickener and start alginate added to formula

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14
Q

For both bottle and breastfed infants with marked GORD, if there is no response to alginate therapy after a 2 week trial, what can be given?

A

PPI or histamine antagonist (e.g ranitidine).

If symptoms persist refer to paediatrics and reconsider differential diagnosis

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15
Q

What is Sandifer’s syndrome?

A

A rare condition causing brief episodes of abnormal movements associated with gastro-oesophageal reflux in infants. The infants are usually neurologically normal.

The condition tends to resolve as the reflux is treated or improves.

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16
Q

What are the 2 key features of Sandifer’s syndrome?

A

1) torticollis

2) dystonia

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17
Q

Is CMPA seen more frequently in breast or bottle-fed infants?

A

Bottle fed

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18
Q

Management of CMPA?

A

Breast feeding mothers should avoid dairy products

Replace formula with special hydrolysed formulas designed for cow’s milk allergy

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19
Q

What age should children grow out of CMPA?

A

Approx 3y

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20
Q

Cow’s milk intolerance vs CMPA?

A

Cow’s milk intolerance presents with the same gastrointestinal symptoms as cow’s milk allergy (bloating, wind, diarrhoea and vomiting), however it does NOT give the allergic features (rash, angio-oedema, sneezing and coughing).

Infants with cow’s milk allergy will not be able to tolerate cow’s milk at all, as it causes an allergic reaction, whereas infants with cow’s milk intolerance will be able to tolerate and continue to grow and develop, but will suffer with gastrointestinal symptoms whilst having cow’s milk.

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21
Q

Is vomiting in pyloric stenosis bilious or non-bilious?

A

Non-bilious

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22
Q

When does pyloric stenosis typically present?

A

First few weeks or life

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23
Q

What metabolic changes can vomiting in pyloric stenosis result in?

A

Hypokalaemic hypochloraemic metabolic alkalosis

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24
Q

What is a +ve US result in pyloric stenosis?

A

Pyloric thickness >3mm and pyloric length >15-17mm

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25
Q

What sign is often described on US in pyloric stenosis?

A

‘Target sign’ –> due to hypertrophied hypoechoic muscle surrounding echogenic mucosa

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26
Q

What is the definitive mx of pyloric stenosis?

A

Ramstedt’s pyloromyotomy

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27
Q

What is the role of NG tube insertion in pyloric stenosis?

A

This decompresses the stomach and allows accurate recording & replacement of gastric losses.

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28
Q

When is the rotavirus vaccination given?

A

At 2m & 3m

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29
Q

What is the most commonly reported bacterial cause of gastroenteritis in the UK?

A

Campylobacter

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30
Q

What increases the risk of haemolytic uraemic syndrome?

A

Antibiotics

Antibiotics should be avoided if E. coli gastroenteritis is considered.

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31
Q

What is the most common bacterial cause of gastroenteritis worldwide?

A

campylobacter

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32
Q

When should a stool sample should be sent in suspected infantile gastroenteritis?

A

1) septicaemia is suspected

2) blood or mucus present in stool

3) child is immunocompromised

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33
Q

What is the fluid requirement for 24 hours in children weighing:

a) 0-10kg
b) 10-20kg
c) >20kg

A

a) 100 ml/kg/day

b) 50 ml/kg/day

c) 20 ml/kg/day

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34
Q

What is a rare but significant complication of rotavirus gastroenteritis?

A

Toxic megacolon

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35
Q

Which part of the small intestine is most affected in Coeliac disease?

A

jejunum

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36
Q

What are the 2 key autoantibodies to remember in Coeliac disease?

A

1) anti-TTG

2) anti-EMA

These antibodies correlate with disease activity and will rise with more active disease and may disappear with effective treatment.

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37
Q

All patients with a new diagnosis of what are also tested for coeliac disease?

A

T1DM

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38
Q

What is dermatitis herpetiformis?

A

An itchy blistering skin rash that typically appears on the abdomen.

Associated with coeliac disease.

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39
Q

What are some conditions related with coeliac disease?

A

1) T1D

2) Down syndrome

3) Turner syndrome

4) Other autoimmune diseases e.g. thyroid disease, rheumatoid arthritis & Addison’s disease.

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40
Q

What does histology show in Coeliac?

A

Crypt hyperplasia & villous atrophy

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41
Q

What is the ‘atypical’ presentation of coeliac?

A

Usually no intestinal symptoms but associated extra-intestinal symptoms e.g. osteoporosis, peripheral neuropathy, anaemia and infertility.

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42
Q

What are 5 extra-intestinal symptoms of coeliac?

A

1) osteoporosis

2) anaemia

3) dermatitis herpetiformis

4) peripheral neuropathy

5) infertility

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43
Q

What gene is most associated with coeliac?

A

HLA-DQ2

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44
Q

What is it important to also test for when testing for autoantibodies in coeliac?

A

Total IgA

If total IgA is low (in IgA deficiency) the coeliac test will be negative even when they have the condition.

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45
Q

1st line investigation in coeliac?

A

Serology –> test for total immunoglobulin A (IgA) and IgA tissue transglutaminase (tTG)

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46
Q

How long before testing for coeliac must patients be eating gluten for?

A

6 weeks

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47
Q

The diagnosis of which conditions indicates the need to test for coeliac disease?

A

T1DM & autoimmune thyroid disease

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48
Q

When testing for coeliac, if the patient is IgA deficient, what should you use?

A

Consider using IgG EMA, IgG deamidated gliadin peptide (DGP) or IgG tTG.

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49
Q

What investigation is considered the gold standard to diagnose if a child has coeliac disease?

A

Duodenal biopsy

50
Q

When is vomiting bilious?

A

If obstruction is AFTER the junction of the duodenum (with the bile ducts at the ampulla of vater).

51
Q

Give some causes of bilious vomiting in infants (6)

A

1) intestinal malrotation w/ volvulus

2) NEC

3) intussusception (initially non-bilious then progresses to bilious)

4) Hirschsprung’s disease

5) meconium ileus

6) intestinal atresia

52
Q

What happens in intestinal malrotation with volvulus?

A

Twisting of the mesentery around the SMA.

Leads to obstruction, infarction & necrosis

53
Q

Features of intestinal malrotation w/ volvulus?

A

1) acute bilious vomiting

2) abdo distension

3) bloody diarrhoea

4) infarction

5) can damage bowel wall –> sepsis

54
Q

Are air fluid levels seen on AXR in malrotation w/ volvulus?

A

Yes

55
Q

What does upper GI contast studies show in malrotation w/ volvulus?

A

Corkscrew/spiral shaped duodenum in the RLQ instead of LUQ (i.e. more medially placed).

56
Q

Mx of malrotation w/ volvulus?

A

1) Discontinue feedings

2) Fluid resus with saline

3) NG tube decompression

4) Broad spectrum Abx

5) ?emergency surgery

57
Q

Features of atresia?

A

1) polyhydramnios (fetus not able to swallow amniotic fluid)

2) bilious vomiting soon after birth

3) abdo distension

4) absent bowel movements

58
Q

What will an AXR show in duodenal atresia?

A

‘Double bubble’ with gas filled distended stomach and duodenum with an absence of distal gas.

59
Q

Mx of intestinal atresia or stenosis?

A

1) Discontinue feeding

2) IV fluids

3) NG tube decompression

4) Surgery (removal and repair of affected segment)

60
Q

What is the surgery called in duodenal atresia?

A

Duodeno-duodenostomy –> attaching duodenum to duodenum.

61
Q

Mx of Hirschsprung’s?

A

Resection of aganglionic part and healthy end is connected to anus.

62
Q

What can be felt on physical exam in pyloric stenosis?

A

1) Olive shaped mass in RUQ (felt during or at end of feeding)

2) Visible peristalsis of stomach

63
Q

What is annular pancreas?

A

When a ring of pancreatic tissue surrounds and compresses the 2nd part of duodenum (like duodenal atresia).

64
Q

What condition is annular pancreas associated with?

A

Down’s

65
Q

How may annular pancreas present in prenatal US?

A

Polyhydramnios

66
Q

Is vomiting bilious or non-bilious in annular pancreas?

A

Non-bilious

67
Q

What is the definitive investigation in annular pancreas?

A

CT

68
Q

What is the Abx for Shigella or Campylobacter?

A

Oral azithromycin

69
Q

Does biliary atresia prevnet the excretion of conjugated or unconjugated bilirubin?

A

Conjugated bilirubin (as this is excreted in the bile)

70
Q

What classification system is used for classifying biliary atresia?

A

Ohi system

71
Q

What are the 3 types of biliary atresia according to the Ohi system?

A

Type I (~10%): patent proximal ducts but atresia of the common bile duct

Type II (~2%): atresia of the common bile duct and hepatic duct

Type III (~88%): atresia of almost all extrahepatic ducts, including the porta hepatis

72
Q

Biliary atresia can occur on its own (‘isolated’) or with other congenital anomalies.

What is the most common congenital anomaly?

A

Biliary atresia splenic malformation syndrome –> associated with polysplenia, situs inversus, cardiac malformations & vascular anomalies

73
Q

What will LFTs shown in biliary atresia?

A

Will be abnormal with conjugated hyperbilirubinaemia and raised gamma-glutamyltransferase (GGT).

74
Q

When should all children with neonatal jaundice have their bilirubin levels tested?

A

Within 6 hours (if <24h after birth then within 2h)

75
Q

What are the key US features of biliary atresia?

A

1) The triangular cord sign: an echogenic sign representing the fibrous remnant of the extrahepatic bile duct

2) Hepatic artery changes, which will be mainly larger

3) Gallbladder ghost triad: small/atretic gallbladder with a length less than 19 mm, irregular or lobular contour, lack of smooth echogenic mucosal lining with an indistinct wall

76
Q

Gold standard investigation for biliary atresia?

A

Operative cholangiography –> BUT it is only used if there is diagnostic uncertainty before treatment.

77
Q

Ideally, when should surgery be performed in biliary atresia?

A

<45 days of life –> provides the best success rate and helps avoid liver transplantation.

78
Q

What is the surgical intervention of choice in biliary atresia?

A

Kasai portoenterostomy

79
Q

What does a Kasai portoenterostomy involve?

A

Removing the damaged bile ducts and replacing them with a loop of intestine to allow bile to flow from the liver to intestine.

80
Q

If a Kasai portoenterostomy fails in biliary atresia, what is next step?

A

Liver transplant

(sometimes a liver transplant may be required even after a successful Kasai procedure due to the progression of liver damage).

81
Q

What are the indications for liver transplant in biliary atresia?

(4)

A

1) Failure of Kasai portoenterostomy & reappearance of symptoms

2) Development of portal HTN & its complications e.g. variceal bleeding, ascites

3) Growth retardation that is non-responsive to intensive nutritional support

4) Progressive liver dysfunction –> pruritus & coagulopathy

82
Q

What will all patients with biliary atresia require for the first year of life post-surgery?

A

Abx prophylaxis to prevent cholangitis

83
Q

What infection are patients at risk of after surgical intervention in biliary atresia?

A

Ascending cholangitis

84
Q

What are the most common complications of biliary atresia?

A

1) ascending cholangitis

2) cirrhosis

3) portal HTN

85
Q

What are the most common complications of biliary atresia?

A

1) Meconium ileus

2) Hirschsprung’s disease

3) Malrotation w/ volvulus

4) Intussusception

5) Oesophageal atresia

6) Duodenal atresia

7) Imperforate anus

8) Strangulated hernia

86
Q

What is Waardenburg syndrome?

A

Genetic condition causing pale blue eyes, hearing loss & patches of white skin and hair.

Can be associated with Hirschsprung’s.

87
Q

What is Hirschsprung-associated enterocolitis (HAEC)?

A

Inflammation & obstruction of intestine that occurs in around 20% of neonates with Hirschsprung’s disease.

88
Q

What are some complications of HAEC?

A

Life-threatening and can lead to a toxic megacolon and perforation

89
Q

What is the most common site of intussusception?

A

Ileocaecal valve

90
Q

What is the most common cause of intestinal obstruction in infants and young children?

A

Intussusception

91
Q

Which age group is intussusception most common in?

A

6m to 2y

92
Q

Are males or females more commonly affected by intussusception?

A

Males

93
Q

What can intussuscpetion often be preceded by?

A

Viral infection

94
Q

Around 10% of cases of intussusception occur due to the presence of a pathological lead point.

What is this?

A

This is an abnormal area in the bowel which is caught and pulled by peristalsis –> leading to intussusception.

95
Q

Intussusception due to a pathological lead point is more likely to present in which patients?

A

1) Patients presenting outside the typical age range

or

2) Where intussusception occurs away from the ileocaecal valve

96
Q

what are some examples of pathological lead points and other secondary causes of intussusception?

A

1) viral infection

2) enlarged Peyer’s patch (acting as lead point)

3) Meckel’s diverticula

4) intestinal polyps

5) lymphomas & leukaemias

6) HSP

97
Q

What is a Peyer’s patch?

A

Peyer’s patches are groupings of lymphoid follicles in the mucus membrane that lines your small intestine.

Lymphoid follicles are small organs in your lymphatic system that are similar to lymph nodes.

98
Q

What is Henoch-Schonlein Purpura (HSP) often preceded by?

A

Viral URTI

99
Q

What typical triad of symptoms is seen in intussusception?

A

1) intermittent, severe abdo pain

2) vomiting: becomes bilious in later stages when bowel obstruction occurs

3) redcurrant jelly stool (late sign)

100
Q

What can be felt on abdo palpation in intussusception?

A

RUQ mass - ‘sausage shaped’

101
Q

What is the initial investigation of choice in intussusception?

A

US

102
Q

What will an US show in intussusception?

A

‘target sign’ or ‘doughnut ring’ - representing the telescoping bowel segments.

103
Q

What 2 investigations can be diagnostic in intussusception?

A

1) US

2) contrast enema

104
Q

Who should contrast enemas NOT be performed in in intussusception?

A

Unstable patients with an signs of perforation or pertionitis.

105
Q

What is the management of intussusception if enemas do not work?

A

Surgical reduction

106
Q

What are the causes of bilious vomiting in neonates?

A

1) duodenal atresia
2) malrotation w/ volvulus
3) NEC
4) jejunal/ileal atresia
5) meconium ileus

107
Q

What does malrotation refer to?

A

During embryogenesis, the midgut undergoes abnormal rotation and fixation.

This misplacement of the gut makes it susceptible to volvulus and duodenal compression by peritoneal bands (Ladd bands)

108
Q

What is the most common presentation of malrotation?

A

Bilious vomiting in first day of life

109
Q

What is the gold standard investigation for diagnosing malrotation?

A

Upper GI contrast study

Will reveal the obstructon point as no contrast can pass distally from thislocation.

The proximal bowel may demonstrate a corkscrew appearance.

110
Q

Define volvulus

A

Torsion of the colon around its mesenteric plexus, resulting in compromised blood flow and closed loop obstruction.

111
Q

Why are most people not at risk of caecal volvulus?

A

In most people (around 80%) the caecum is a retroperitoneal structure so not at risk of twisting.

In the remaining minority there is however developmental failure of peritoneal fixation of the proximal bowel putting these patients at risk of caecal volvulus.

112
Q

What are some associations with sigmoid volvulus?

A

1) older age
2) Chagas disease
3) chronic constipation
4) neuro: duchenne muscular dystrophy, parkinson’s
5) psych: schizophrenia

113
Q

What are some associations with caecal volvulus?

A

1) all ages
2) adhesions
3) pregnancy

114
Q

Which type of volvulus is associated with Chagas disease?

A

Sigmoid

115
Q

Which type of volvulus is associated with Parkinson’s?

A

Sigmoid

116
Q

Which type of volvulus is associated with pregnancy?

A

Caecal

117
Q

Which type of volvulus is associated with Parkinson’s?

A

Sigmoid

118
Q

Which type of volvulus is associated with adhesions?

A

Caecal

119
Q

Which type of volvulus is associated with schizophrenia?

A

Sigmoid

120
Q
A

Yr 5 - Paeds (10 decks)

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