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Year 4 - Paediatrics > Gatroenterology > Flashcards

Gatroenterology Flashcards

1
Q

Medical causes of abdominal pain.

A
  • constipation
  • UTI
  • coeliac disease
  • IBD
  • IBS
  • mesenteric adenitis
  • abdominal migraine
  • pyelonephritis
  • Henoch-Schonlein purpura
  • tonsilitis
  • DKA
  • infantile colic
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2
Q

Medical causes of abdominal pain (F specific).

A
  • dysmenorrhoea
  • Mittelschmerz
  • ectopic pregnancy
  • PID
  • ovarian torsion
  • pregnancy
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3
Q

Surgical causes of abdominal pain.

A
  • appendicitis
  • intussusception
  • bowel obstruction
  • testicular torsion
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4
Q

Red flags for serious abdominal pain.

A
  • persistent vomiting
  • severe chronic diarrhoea
  • fever
  • rectal bleeding
  • weight loss / growth delay
  • dysphagia
  • night time pain
  • abdominal tenderness
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5
Q

What is recurrent abdominal pain?

A

A common diagnosis in children aged 5 years and above, that is made when a child presents with repeated episodes of abdominal pain without an identifiable underlying cause.

The pain is described as non-organic or functional.

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6
Q

Associations of recurrent abdominal pain.

A

Often corresponds to stressful life events, such as loss of a relative or bullying.

These events cause increased sensitivity and inappropriate pain signals from the visceral nerves in response to normal stimuli.

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7
Q

Management of recurrent abdominal pain.

A
  • distracting the child from the pain
  • encourage parents not to ask about or focus on the pain
  • advice about sleep, regular meals, healthy balanced diet, staying hydrated, exercise
  • probiotic supplements
  • avoid NSAIDs (e.g. ibuprofen)
  • address psychosocial triggers
  • support from school counsellor or child psychologist
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8
Q

Pain characteristic of abdominal migraine.

A

Episodes of central abdominal pain lasting more than 1 hour, with normal examination.

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9
Q

Associated symptoms / signs in abdominal migraine.

A
  • nausea and vomiting
  • anorexia
  • pallor
  • headache
  • photophobia
  • aura
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10
Q

Management of abdominal migraines - acute attack.

A
  • low stimulus environment
  • paracetamol
  • ibuprofen
  • sumatriptan
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11
Q

Management of abdominal migraines - prevention.

A

Pizotifen is a serotonin agonist that is used as prevention for abdominal migraine.

It needs to be withdrawn slowly when stopping, as it is associated with withdrawal symptoms such as depression, anxiety, poor sleep and tremor.

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12
Q

Presentation of constipation.

A
  • less than 3 stools per week
  • hard stools that are difficult to pass
  • rabbit dropping stools
  • straining and painful passage of stools
  • abdominal pain
  • retentive posturing
  • rectal bleeding
  • hard stool palpable in abdomen
  • loss of the sensation of the need to open the bowels
  • overflow diarrhoea
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13
Q

Define encopresis.

A

Faecal incontinence

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14
Q

When is encopresis considered to be pathological?

A

After 4 years of age.

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15
Q

Commonest cause of encopresis.

A

Usually a sign of constipation, where the rectum becomes stretched and looses sensation.

Large hard stools remain in the rectum, and only loose stools are able to bypass the blockage and leak out, causing soiling.

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16
Q

Secondary causes of encopresis.

A
  • Spinal bifida
  • Hirschprung’s disease
  • cerebral palsy
  • learning disability
  • psychosocial stress
  • abuse
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17
Q

Lifestyle factors that can result in constipation.

A
  • low fibre diet
  • poor fluid intake and dehydration
  • sedentary lifestyle
  • psychosocial problems (i.e. difficult home / school environment)
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18
Q

What is desensitisation of the rectum in constipation?

A

Patients develop a habit of not opening their bowels and ignoring the sensation of a full rectum.

Over time, this causes faecal impaction and damage to the nerves, causing desensitisation.

The longer this goes on, the more difficult it is to treat the constipation and reverse the problem.

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19
Q

Secondary causes of constipation.

A
  • Hirschsprung’s disease
  • cystic fibrosis
  • hypothyroidism
  • spinal cord lesions
  • sexual abuse
  • intestinal obstruction
  • anal stenosis
  • cows milk intolerance
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20
Q

What could constipation, associated with not passing meconium within 48 hours of birth be associated with in children?

A
  • cystic fibrosis
  • Hirschsprung’s disease
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21
Q

What could constipation, associated with neurological signs or symptoms be associated with in children?

A
  • cerebral palsy
  • spinal cord lesion

Particularly in the lower limbs.

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22
Q

What could constipation, associated with vomiting be associated with in children?

A
  • intestinal obstruction
  • Hirschsprung’s disease
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23
Q

What could constipation, associated with ribbon stool be associated with in children?

A
  • anal stenosis
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24
Q

What could constipation, associated with abnormal anus be associated with in children?

A
  • anal stenosis
  • inflammatory bowel disease
  • sexual abuse
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25
Q

What could constipation, associated with abnormal lower back or buttocks be associated with in children?

A
  • spinal bifida
  • spinal cord lesion
  • sacral agenesis
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26
Q

What could constipation, associated with failure to thrive be associated with in children?

A
  • coeliac disease
  • hypothyroidism
  • safeguarding
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27
Q

What could constipation, associated with acute severe abdominal pain and bloating be associated with in children?

A
  • intestinal obstruction
  • intussusception
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28
Q

Complications of constipation.

A
  • pain
  • desensitisation
  • anal fissures
  • haemorrhoids
  • overflow and soiling
  • psychosocial morbidity
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29
Q

What investigations are required to diagnose idiopathic constipation?

A

Can be made without investigations, provided red flags are considered.

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30
Q

Management of idiopathic constipation.

A
  • high fibre diet
  • good hydration
  • start laxatives (movicol first line)
  • encourage and praise visiting the toilet

Faecal impaction may require a disimpaction regime, with high doses of laxatives at first.

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31
Q

What is gastro-oesophageal reflux (GORD) in children?

A

Incompetence of the lower oesophageal sphincter allows stomach reflux into the oesophagus, throat and mouth.

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32
Q

Why is GORD common in babies?

A

Immaturity of the lower oesophageal sphincter allows stomach contents to easily reflux into the oesophagus.

It is normal for a baby to reflux feeds, provided there is normal growth and the baby is otherwise well.

90% of infants stop having reflux by 1 year.

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33
Q

Signs of problematic reflux.

A
  • chronic cough
  • hoarse cry
  • distress, crying or unsettled after feeding
  • reluctance to feed
  • pneumonia
  • poor weight gain
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34
Q

Causes of vomiting in children.

A
  • overfeeding
  • GORD
  • pyloric stenosis
  • gastritis / gastroenteritis
  • appendicitis
  • UTI
  • tonsillitis
  • meningitis
  • intestinal obstruction
  • bulimia nervosa
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35
Q

Red flag vomiting symptoms in children.

A
  • not keeping down any feed
  • projectile vomiting
  • bile stained vomit
  • haematemesis or malaena
  • abdominal distention
  • reduced consciousness, bulging fontanelle, neurological signs
  • respiratory symptoms
  • blood in the stools
  • signs of infection
  • rash, angioedema and other signs of allergy
  • apnoeas
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36
Q

Home management of GORD in children.

A
  • small, frequent meals
  • burping regularly to help milk settle
  • not over-feeding
  • keep the baby upright after feeding
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37
Q

Medical management of GORD in children.

A
  • Gaviscon mixed with feeds
  • thickened milk or formula
  • PPIs (e.g. omeprazole)
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38
Q

What is Sandifer’s syndrome?

A

A rare complication of GORD causing:

  • torticollis: forceful contraction of the neck muscles causing twisting of the neck
  • dystonia: abnormal muscle contractions causing twisting movements, arching of the back or unusual postures

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

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39
Q

Features of pyloric stenosis.

A

Presents within the first few weeks of life:
- hungry baby
- failure to thrive
- projectile vomiting

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40
Q

Capillary blood gas analysis of pyloric stenosis.

A

Hypochloric metabolic alkalosis.

The baby is vomiting hydrochloric acid from the stomach.

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41
Q

Examination findings of pyloric stenosis.

A

Firm, round mass felt in the upper abdomen.

Peristalsis can often be seen by observing the abdomen.

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42
Q

Diagnosis of pyloric stenosis.

A

Abdominal ultrasound to visualise the thickened pylorus.

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43
Q

Management of pyloric stenosis.

A

Laparoscopic pyloromyotomy.

An incision is made in the smooth muscle of the pylorus to widen the canal.

Prognosis is excellent following the operation.

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44
Q

Differential diagnoses for diarrhoea.

A
  • gatroenteritis
  • IBD
  • lactose intolerance
  • coaliac disease
  • cystic fibrosis
  • Toddler’s diarrhoea
  • IBS
  • medications (e.g. abx)
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45
Q

What are the common viral causes of gastroenteritis in children?

A
  • rotavirus
  • norovirus

Highly contagious and common.

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46
Q

How is E. coli spread?

A
  • faeco-oral route
  • unwashed salads
  • contaminated water
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47
Q

Why are antibiotics contraindicated in E. coli gastroenteritis?

A

E. coli 0157 produces the Shiga toxin, leading to haemolytic uraemic sydrome (HUS):
- haemolytic anaemia
- thrombocytopenia
- AKI

The use of antibiotics increases the risk of HUS.

48
Q

Presentation of E. coli gastroenteritis.

A
  • abdominal cramps
  • bloody diarrhoea
  • cramping
49
Q

Most common cause of travellers diarrhoea.

A

Campylobacter jejuni.

50
Q

How is Campylobacter spread?

A
  • raw or improperly cooked poultry
  • untreated water
  • unpasteurised milk
51
Q

Symptoms of Campylobacter gastroenteritis.

A
  • abdominal cramps
  • bloody diarrhoea
  • vomiting
  • fever
52
Q

Management of Campylobacter gastroenteritis.

A

If patient has severe symptoms or other risk factors (e.g. HIV, heart failure), antibiotics are indicated.

Azithromycin or ciprofloxacin are popular choices.

53
Q

How is Shigella spread?

A

Faecal-oral route:
- contaminated drinking water
- contaminated foods
- contaminated swimming pools
- anal sex

54
Q

Presentation of Shigella gastroenteritis.

A
  • bloody diarrhoea
  • abdominal cramps
  • fever
55
Q

How does Shigella lead to HUS?

A

Shigella can produce the Shiga toxin, leading to HUS:
- haemolytic anaemia
- thrombocytopenia
- AKI

56
Q

Management of severe Shigella gastroenteritis.

A

Azithromycin or ciprofloxacin.

57
Q

How is Salmonella spread?

A

Eating raw eggs or poultry.

Food contaminated with the infected faeces of small animals.

58
Q

Presentation of Salmonella gastroenteritis.

A
  • watery diarrhoea
  • mucus / blood in diarrhoea
  • abdominal pain
  • vomiting
59
Q

Management of Salmonella gastroenteritis.

A

Antibiotics given in severe cases, guided by stool culture and sensitivities.

60
Q

Course of Bacillus cereus gastroenteritis.

A
  1. Patient eats fried rice left out at room temperature.
  2. Vomiting within 5 hours.
  3. Diarrhoea within 8 hours.
  4. Resolution within 24 hours.
61
Q

Transmission of Giardiasis.

A

Parasitic infection that lives in the small intestines of mammals, releasing cysts in the stools of infected animals.

The cysts contaminate food or water and are eaten.

62
Q

Giardiasis presentation.

A
  • asymptomatic
  • chronic diarrhoea
63
Q

Giardiasis treatment.

A

Metronidazole

64
Q

Gastroenteritis general management.

A
  • infection control
  • stool culture for abx sensitivities
  • fluid challenge
  • rehydration solutions
  • antidiarrhoeal medications (loperamide)
65
Q

What is a fluid challenge?

A

Record a small volume of fluid given orally every 5-10 minutes to ensure they can tolerate it.

If they are able to tolerate oral fluid and are adequately hydrated they can be managed at home.

66
Q

Post gastroenteritis complications.

A
  • lactose intolerance
  • irritable bowel syndrome
  • reactive arthritis
  • Gullain-Barré syndrome
67
Q

Pathophysiology of coeliac disease.

A

Autoantibodies are created in response to exposure to gluten, targeting the epithelial cells of the intestine and leading to inflammation.

Inflammation affects the jejunum mostly, causing atrophy of intestinal villi. This causes malabsorption of nutrients.

68
Q

Presentation of coeliac disease.

A
  • failure to thrive
  • diarrhoea
  • fatigue
  • weight loss
  • mouth ulcers
  • anaemia secondary to iron, B12 or folate deficiency
  • dermatitis herpetiformis
69
Q

Neurological symptoms of coeliac disease.

A

Rare:
- peripheral neuropathy
- cerebellar ataxia
- epilepsy

70
Q

Genetic associations for coeliac disease.

A

HLA-DQ2 gene (90%)
HLA-DQ8 gene

71
Q

Blood tests for coeliac disease diagnosis.

A
  • raised anti-TTG antibodies
  • raised anti-EMA antibodies

Check total IgA levels to exclude IgA deficiency; if total IgA is low the coeliac test will be negative even when they have the condition.

In this circumstance you can test for the IgG version of the anti-TTG / anti-EMA antibodies, or do endoscopy with biopsy.

72
Q

Endoscopy and intestinal biopsy findings consistent with coeliac disease.

A
  • crypt hypertrophy
  • villous atrophy
73
Q

Associations of coeliac disease.

A
  • T1DM
  • thyroid disease
  • autoimmune hepatitis
  • primary biliary cirrhosis
  • primary sclerosing cholangitis
  • Down’s syndrome
74
Q

Complications of untreated coeliac disease.

A
  • vitamin deficiency
  • anaemia
  • osteoporosis
  • ulcerative jejunitis
  • Non-Hodgkin lymphoma
  • small bowel adenocarcinoma
75
Q

Treatment of coeliac disease.

A

Lifelong gluten free diet is curative.

76
Q

What are the two types of inflammatory bowel disease?

A
  • ulcerative colitis
  • Crohn’s disease
77
Q

Features of Crohn’s disease.

A

Crow’s NESTS:

No blood or mucus
Entire GI tract affected
Skip lesions on endoscopy
Terminal ileum most affected and Transmural inflammation
Smoking is a risk factor*

*don’t set a nest on fire.

78
Q

Features of Ulcerative Colitis.

A

U - C - CLOSEUP

Continuous inflammation
Limited to colon and rectum
Only superficial mucosa affected
Smoking is protective
Excrete blood and mucus
Use aminosalicylates
Primary sclerosing cholangitis

79
Q

Presentation of inflammatory bowel disease.

A
  • perfuse diarrhoea
  • abdominal pain
  • bleeding
  • weight loss
  • anaemia
  • failure to thrive
80
Q

Extra-intestinal manifestations of inflammatory bowel disease.

A
  • finger clubbing
  • erythema nodosum
  • Pyoderma gangrenosum
  • inflammatory arthritis
  • primary sclerosing cholangitis
81
Q

Diagnostic work-up for inflammatory bowel disease.

A

Bloods:
- FBC (anaemia, infection)
- TFTs
- LFTs
- U&Es
- CRP

Faecal calprotectin used to screen, but not specific.

Endoscopy with biopsy is the gold standard investigation for diagnosing IBD.

82
Q

General management of inflammatory bowel disease.

A

Multi-disciplinary team input:
- monitor growth and pubertal development
- induction of remission during flares
- maintain remission
- dietician input to support growth and development

83
Q

How can remission be induced in acute Crohn’s?

A

Steroids (e.g. oral prednisolone, IV hydrocortisone).

If steroids alone don’t work, add an immunosuppressant medication under specialist guidance (e.g. infliximab).

84
Q

How can remission be maintained in Crohn’s?

A

First line:
- azathioprine
- mercaptopurine

85
Q

Surgical management of Crohn’s.

A

When the disease affects the terminal ileum only, surgical resection of the area is curative.

Surgery can also be used to treat strictures and fistulas secondary to Crohn’s disease.

86
Q

How can remission be induced in acute UC?

A

Mild/Moderate:
First line: aminosalicylate (mesalazine)
Second line: oral corticosteroids (e.g. prednisolone)

Severe:
First line: IV corticosteroids (e.g. hydrocortisone)
Second line: IV ciclosporin

87
Q

How can remission be maintained in UC?

A

Aminosalicylates used first line (e.g. mesalazine).

Azathioprine or mercaptopurine can be used otherwise.

88
Q

Surgical management of UC.

A

Panproctocolectomy will remove the disease as usually limited to the colon and rectum.

The patient is left with either a permanent ileostomy or a J-pouch.

J-pouch is when the ileum is anastamosed to the anus, allowing the person to collect stool prior to defaecation.

89
Q

What is biliary atresia?

A

A congenital condition where a section of the bile duct is narrowed or absent, resulting in cholestasis.

90
Q

Presentation of biliary atresia.

A

Significant jaundice shortly after birth, due to high conjugated bilirubin levels.

91
Q

Investigations for possible biliary atresia.

A

Bloods for conjugated and unconjugated bilirubin levels.

A high proportion of conjugated bilirubin suggests the liver is processing the bilirubin for excretion, but cannot excrete it through the biliary duct.

92
Q

Differentials for jaundice in the neonate.

A
  • breast milk jaundice
  • hepatitis
  • physiological jaundice
  • biliary atresia
93
Q

Management of biliary atreisa.

A

Surgical management to attach a section of the small intestine to the opening of the liver.

This can clear the jaundice and prolong survival. A full liver transplant is the only curative option.

94
Q

Causes of intestinal obstruction in children.

A
  • Meconium ileus
  • Hirschsprung’s disease
  • oesophageal atresia
  • duodenal atresia
  • intussusception
  • imperforate anus
  • volvulus
  • strangulated hernia
95
Q

Presentation of intestinal obstruction.

A
  • persistent vomiting
  • abdominal pain and distention
  • failure to pass stools or wind
  • tinkling / absent bowel sounds
96
Q

Intestinal obstruction diagnostic workup.

A

Abdominal x-ray showing dilated loops of bowel proximal to the obstruction.

Absence of stool in the rectum.

97
Q

Management of intestinal obstruction.

A

Admission to paediatric surgical unit.

Make them nil by mouth.

Insert NG tube to help decompress the stomach and stop vomiting.

IV fluids to correct any dehydration and electrolyte imbalances.

98
Q

Pathophysiology of Hirschsprung’s disease.

A

A congenital conditions where the parasympathetic ganglion cells are absent in the distal bowel and rectum.

This means the aganglionic section of the colon does not relax, causing it to become constricted. This leads to loss of movement of faeces and obstruction in the bowel.

99
Q

Associations of Hirschsprung’s disease.

A
  • family history
  • Downs syndrome
  • Waardenburg syndrome
100
Q

Presentation of Hirschsprung’s disease.

A

Acute intestinal obstruction shortly after birth:
- delay in passing meconium
- chronic constipation since birth
- abdominal pain and distention
- vomiting
- poor weight gain and failure to thrive

101
Q

What is Hirschsprung-Associated enterocolitis (HAEC)?

A

A life threatening complication of Hirschsprung’s disease, caused by inflammation and obstruction of the intestine.

It presents with:
- fever
- abdominal distention
- diarrhoea
- sepsis

It can lead to toxic megacolon and perforation of the bowel.

102
Q

Diagnostic workup of Hirschsprung’s disease.

A

Abdominal xray is useful in diagnosing intestinal obstruction and demonstrating features of HAEC.

Rectal biopsy is used to confirm the diagnosis with presence of aganglionic cells.

103
Q

Management of Hirschsprung’s disease.

A
  • fluid resuscitation
  • NG tube
  • IV abx (HAEC)

Definitive management is by surgical removal of aganglionic bowel.

104
Q

What is intussusception?

A

The bowel folds inwards on itself, thickening the bowel and narrowing the lumen at the folded area.

105
Q

Typical patient for intussusception.

A
  • infants 6 months to 2 years
  • male
106
Q

Conditions associated with intussusception.

A
  • concurrent viral illness
  • Henoch-Schonlein purpura
  • cystic fibrosis
  • intestinal polyps
  • Meckel diverticulum
107
Q

Presentation of intussusception.

A
  • severe, colicky abdominal pain
  • pale, lethargic and unwell child
  • redcurrent jelly stool
  • sausage-shaped right upper quadrant mass
  • vomiting
  • intestinal obstruction
108
Q

Diagnostic workup of intussusception.

A

Ultrasound scan or contrast enema.

109
Q

Management of intussusception.

A

Therapeutic enemas with contrast, water or air can be pumped into the colon to force the folded bowel into the normal position.

Surgical reduction may be necessary if enemas do not work.

110
Q

Complications of intussusception.

A
  • obstruction
  • gangrenous bowel
  • perforation
  • death
111
Q

Management of gangrenous bowel secondary to intussusception.

A

Disruption of blood supply causes the bowel to become gangrenous.

For gangrenous or perforated bowel, surgical resection is required.

112
Q

Presentation of appendicitis.

A
  • central abdominal pain
  • radiates to RIF
  • tenderness in McBurney’s point
  • anorexia
  • nausea and vomiting
  • Rovsing’s sign
  • rebound tenderness in RIF*
  • percussion tenderness*

*suggestive of peritonitis, caused by a ruptured appendix.

113
Q

Diagnostic workup for appendicitis.

A
  • ultrasound scan
  • CT scan
  • diagnostic laparoscopy
114
Q

Appendicitis differentials.

A
  • ectopic pregnancy
  • ovarian cysts
  • Meckel’s diverticulum
  • mesenteric adenitis
  • apendix mass
115
Q

Management of appendicitis.

A

Laparoscopic appendicectomy.

116
Q

Complications of appendicectomy.

A
  • bleeding, infection, pain and scars
  • damage to bowel, bladder or other organs
  • removal of a normal appendix
  • anaesthetic risks
  • VTE

Year 4 - Paediatrics (17 decks)

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