12- Paediatric Gastroenterology Flashcards

1
Q

Abdominal pain Background

A

Very common and split into:
- Non-organic causes/ functional
o very common in >5 years
- medical causes
- surgical causes

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2
Q

abdominal pain causes

A

Medical causes

  • Constipation is also very
    common (ALWAYS CONSIDER) -> often coincides with eating
  • Urinary tract infection
  • Coeliac disease
  • Inflammatory bowel disease
  • Irritable bowel syndrome
  • Mesenteric adenitis
  • Abdominal migraine
  • Pyelonephritis
  • Henoch-Schonlein purpura
  • Tonsilitis
  • Diabetic ketoacidosis
  • Infantile colic
    There are addition causes in adolescent girls:
  • Dysmenorrhea (period pain)
  • Mittelschmerz (ovulation pain)
  • Ectopic pregnancy
  • Pelvic inflammatory disease
  • Ovarian torsion
  • Pregnancy
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3
Q

surgical causes of abdominal pain

A
  • Appendicitis causes central abdominal pain spreading to the right iliac fossa
  • Intussusception causes colicky non-specific abdominal pain with redcurrant jelly stools
  • Bowel obstruction causes pain, distention, absolute constipation and vomiting
  • Testicular torsion causes sudden onset, unilateral testicular pain, nausea and vomiting
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4
Q

Red flags for abdominal pain

A
  • Persistent or bilious vomiting
  • Severe chronic diarrhoea
  • Fever
  • Rectal bleeding
  • Weight loss or faltering growth
  • Dysphagia (difficulty swallowing)
  • Nightime pain
  • Abdominal tenderness
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5
Q

investigations for abdominal pain

A
  • Anaemia can indicate inflammatory bowel disease or coeliac disease
  • Raised inflammatory markers (ESR and CRP) can indicate inflammatory bowel disease
  • Raised anti-TTG or anti-EMA antibodies indicates coeliac disease
  • Raised faecal calprotectin indicates inflammatory bowel disease
  • Positive urine dipstick indicates a urinary tract infection
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6
Q

Functional abdominal pain

A

Examples
e.g. Recurrent abdominal pain syndrome
e.g. Abdominal migraine

A child presenting with repeated episodes of abdominal pain without identified underlying cause
- Psychosocial problems- e.g. missed days at school and parental anxiety

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7
Q

functional abdominal causes

A
  • Non-organic o/ functional
  • Often corresponds to stressful life events such as bullying
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8
Q

pathophysiology of functional abdominal pain

A

Leading theory for the cause is increased sensitivity and inappropriate pain signals from the visceral nerves (the nerves in the gut) in response to normal stimuli.

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9
Q

Management of functional constipation

A

Careful explanation and reassurance

  • Distracting the child from the pain with other activities
  • Encourage parents not to ask about or focus on the pain
  • Advice about sleep, regular meals, healthy balanced diet, staying hydrated, exercise and reducing stress
  • Probiotic supplements may help symptoms of irritable bowel syndrome
  • Avoid NSAIDs such as ibuprofen
  • Address psychosocial triggers and exacerbating factors
  • Support from a school counsellor or child psychologist
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10
Q

abdominal migraine background

A

This may occur in young children before they develop traditional migraines as they get older. Abdominal migraine presents with episodes of central abdominal pain lasting more than 1 hour.

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11
Q

presentation of abdominal migraine

A

Examination will be normal.
- Signs
o Nausea and vomiting
o Anorexia
o Pallor
o Headache
o Photophobia
o Aura

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12
Q

management of abdominal migraine

A

Management of abdominal migraine is similar to migraine in adults. Careful explanation and education is important. It involves treating acute attacks and preventative measures. Preventative medications are initiated by a specialist.

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13
Q

abdominal migraine treating an attack

A

o Low stimulus environment (quiet, dark room)
o Paracetamol
o Ibuprofen
o Sumatriptan

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14
Q

preventative medications

A
  • Pizotifen, a serotonin agonist
    Main preventative medication to rmemeber for abdominal migraine
  • Propranolol, a non-selective beta blocker
  • Cyproheptadine, an antihistamine
  • Flunarazine, a calcium channel blocker
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15
Q

Pizotifen

A

MOA: Serotonin agonist

Needs to be withdrawn slowly when stopping due to withdrawal
* Depression
* Anxiety
* Poor sleep
* Tremor

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16
Q

coeliac disease background

A

Autoimmune condition where exposure to gluten causes an immune reaction that creates inflammation in the small intestine
- Usually develops early childhood

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17
Q

pathophysiology of coeliac disease

A
  • Autoantibodies are created response to gluten (gliadin)
    –> IgA Anti-tissue transglutaminase (anti-TTG) and anti-endomysial (anti-EMA)
    –> These antibodies rise and fall with disease activity
  • These antibodies target the epithelial cells of the intestine and lead to inflammation
  • Location: small bowel (jejunum particularly)
    –> Causes atrophy of intestinal villi
    –> Villi important for absorbing nutrient malabsorption and symptoms
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18
Q

RF of coeliac disease

A
  • Female
  • T1DM
  • Hereditary: HLA-DQ2 gene (90%) and HLA-DQ8 gene
  • DS
  • Autoimmune thyroid disease
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19
Q

Coeliac disease presentation

A

is often asymptomatic, so have a low threshold for testing for coeliac disease in patients where it is suspected. Symptoms can include:
* Failure to thrive in young children
* Diarrhoea
* Fatigue
* Weight loss
* Mouth ulcers
* Anaemia secondary to iron, B12 or folate deficiency
* Dermatitis herpetiformis is an itchy blistering skin rash that typically appears on the abdomen

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20
Q

Rarely coeliac disease can present with neurological symptoms:

A

due to vitamin E deficiency
* Peripheral neuropathy
* Cerebellar ataxia
* Epilepsy

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21
Q

coeliac disease investigation

A
  • Patient must remain on gluten diet when investigations are happening (otherwise inflammation and antibodies may be missing)
  • TEST: total immunoglobulin A levels to exclude IgA deficiency before checking for coeliac disease specific antibodies
    o Raised anti-TTG antibodies (first choice)
    o Raised anti-endomysial antibodies
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22
Q

coeliac disease: why check IgA first

A

total immunoglobulin A levels to exclude IgA deficiency before checking for coeliac disease specific antibodies

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23
Q

coeliac disease specific antibodies

A
  • Raised anti-TTG antibodies (first choice)
  • Raised anti-endomysial antibodies
24
Q

Management of coeliac disease

A
  • Lifelong gluten free diet -> curative
  • Relapse will occur if gluten consumed
  • Checking antibodies can be helpful
  • Doesn’t cause any vitamin deficient
25
Q

Gluten examples

A
  • Wheat
  • Barley
  • Rye
26
Q

Complications of coeliac

A
  • Vitamin deficiency
  • Anaemia
  • Osteoporosis
  • Ulcerative jejunitis
  • Enteropathy-associated T-cell lymphoma (EATL) of the intestine
  • Non-Hodgkin lymphoma (NHL)
  • Small bowel adenocarcinoma (rare)
27
Q

constipation background

A

Common

Split into
- Idiopathic
- Functional
- Secondary causes

28
Q

secondary causes of constipation

A
  • Hirschsprung’s disease
  • Cystic fibrosis
  • Hypothyroidism
29
Q

pathophysiology of constipation: life style

A

o Habitually not opening bowels e.g. if painful
o Low fibre
o Poor fluid intake and dehydration
o Sedentary
o Psychosocial problems (think safeguarding)

30
Q

constipation secondary causes (detailed)

A

o Hirschsprungs
o CF (meconium ileum)
o Hypothyroidism
o Spinal cord lesion
o Sexual abuse
o Intestinal obstruction
o Anal stenosis
o Cows milk intolerance

31
Q

presentation of constipation

A

How often someone opens their bowels varies between individuals. This is even more variable in breast-fed babies, which can have as little as one stool a week. Someone opening their bowels daily may be constipated, whereas someone opening their bowels twice a week may not, if that is normal for them.
Typical features in the history and examination that suggest constipation are:
* Less than 3 stools a week
* Hard stools that are difficult to pass
* Rabbit dropping stools
* Straining and painful passages of stools
* Abdominal pain
* Holding an abnormal posture, referred to as retentive posturing
* Rectal bleeding associated with hard stools
* Faecal impaction causing overflow soiling, with incontinence of particularly loose smelly stools
* Hard stools may be palpable in abdomen
* Loss of the sensation of the need to open the bowels

32
Q

investigations for constipation

A
  • If no red flags -> can diagnose and manage as idiopathic constipation
33
Q

management of constipation

A
  • Improve lifestyle contributing factors
  • Laxatives: Movicol (osmotic laxative) first line
    –> Long term therapy and slowly weaned off as child improves
  • Faecal impact may require disimpaction regimen with high disease of laxative at first
  • Encourage and praise visiting the toilets
    –>Scheduling visits, a bowel diary and star charts
34
Q

encopresis

A

Encopresis is the term for faecal incontinence.

35
Q

when is encopresis considered pathological

A

This is not considered pathological until 4 years of age. It is usually a sign of chronic 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.

36
Q

Other rarer causes of encopresis include:

A
  • Spina bifida
  • Hirschprung’s disease
  • Cerebral palsy
  • Learning disability
  • Psychosocial stress
  • Abuse
37
Q

Desensitisation of the Rectum

A

Often patients develop a habit of not opening their bowels when they need to and ignoring the sensation of a full rectum.

Over time they loose the sensation of needing to open their bowels, and they open their bowels even less frequently. They start to retain faeces in their rectum.

This leads to faecal impaction, which is where a large, hard stool blocks the rectum. Over time the rectum stretches as it fills with more and more faeces. This leads to further desensitisation of the rectum. The longer this goes on, the more difficult it is to treat the constipation and reverse the problem.

38
Q

complications of constipation

A

Complications
* Pain
* Reduced sensation
* Anal fissures
* Haemorrhoids
* Overflow and soiling
* Psychosocial morbidity

39
Q

Red flags of constipation

A
  • Not passing meconium within 48 hours of birth (cystic fibrosis or Hirschsprung’s disease)
  • Neurological signs or symptoms, particularly in the lower limbs (cerebral palsy or spinal cord lesion)
  • Vomiting (intestinal obstruction or Hirschsprung’s disease)
  • Ribbon stool (anal stenosis)
  • Abnormal anus (anal stenosis, inflammatory bowel disease or sexual abuse)
  • Abnormal lower back or buttocks (spina bifida, spinal cord lesion or sacral agenesis)
  • Failure to thrive (coeliac disease, hypothyroidism or safeguarding)
  • Acute severe abdominal pain and bloating (obstruction or intussusception)
40
Q

Hirshsprungs disease background

A

Hirschsprung’s disease is a congenital condition that affects the large intestine (colon) and causes problems with passing stool. The condition is present at birth (congenital) as a result of missing nerve cells in the muscles of the baby’s colon. Without these nerve cells stimulating gut muscles to help move contents through the colon, the contents can back up and cause blockages in the bowel.

Divided into
- Short segment
- Long segment

41
Q

pathophysiology of Hirschsprungs

A
  • Nerve cells of myenteric plexus (Auerbach’s) are absent in the distal bowel and rectum
    o Auerbach’s forms the enteric nervous system – brain of the gut
  • Auerbach’s runs all the way along the bowel in the bowel war and is a complex network of neurones, ganglion cells, receptors, synapses and NT
    o Causes peristalsis of the large bowel
    o Without this stimulation -> bowel loses motility and food cannot pass food along
  • Key pathology: absence of parasympathetic ganglion cells – responsible for peristalsis
  • Foetal development of the parasympathetic ganglion cells
    o During fetal development these start in the upper GI tract and gradually migrate down the distal colon and rectum -> in Hirschsprung’s these cells do not travel all the way down the colon- therefore a section of the colon is left without these parasympathetic ganglion cells
    o Aganglionic sections of the colon cannot relax-> therefore become constricted
    o Proximal bowel will become distended and full
42
Q

Risk factors for Hirschsprungs

A
  • genetic associations
  • Family history
  • Doesn’t usually occur in isolation: Down Syndrome, neurofibromatosis, Waardenburg syndrome, MEN type II
43
Q

Hirschsprungs presentation

A

Presentation
- Delay in passing meconium >24hrs
- Chronic constipation since birth
- Abdominal pain and distention
- Vomiting
- Poor weight gain and failure to thrive

44
Q

investigations for Hirschsprungs

A
  • Abdominal x-ray
    o Intestinal obstruction
  • Rectal biopsy
    o Confirms diagnosis
    o Bowel histology will show absence of
    ganglionic cells
45
Q

Management of Hirschsprungs

A

Unwell child
- Fluid resus and management of obstruction.
- Abx if Hirschsprung’s associated enterocolitis

Definitive management
- Surgical resection of a ganglionic section of bowel
- Most patients live normal life after surgery
- May be left with some degree of incontinence

46
Q

Gastro-oesophageal reflux background

A

Gastro-oesophageal reflux is where contents from the stomach reflux through the lower oesophageal sphincter into the oesophagus, throat and mouth.
- Normal for babies to reflux feeds, provided there is normal growth
- Can be upsetting for patients
- Usually improves as baby grows and 90% infants stop having reflux by 1

47
Q

GORD Pathophysiology

A
  • In babies immaturity of the lower oesophageal sphincter -> stomach contents can easily reflux into the oesophagus
48
Q

presentation of GORD

A

Presentation
Signs of problematic reflux include:
* Chronic cough
* Hoarse cry
* Distress, crying or unsettled after feeding
* Reluctance to feed
* Pneumonia
* Poor weight gain
Children over one year may experience similar symptoms to adults, with heartburn, acid regurgitation, retrosternal or epigastric pain, bloating and nocturnal cough.

49
Q

management of simple GORD

A

reassurance and practical advice
- Small, frequent meals
- Burping regularly
- Not over feeding
- Keeping baby upright after feeding

50
Q

management of problematic GORD

A
  • Gaviscon mixed with feeds
  • Thickened milk or formula (specific anti-reflux formulas)
  • Proton pump inhibitors e.g. neonatal period
51
Q

management of severe GORD

A
  • Barium meal and endoscopy
  • Surgical fundoplication may be considered in very severe cases, however this very rarely required or performed
52
Q

Sandifer’s syndrome

A

a condition characterized by unusual movements of your child’s head, neck and back. The condition can cause temporary muscle spasms as a reaction to acid reflux. Symptoms are most common after your baby eats when the contents of their stomach don’t settle.
- Brief episodes of anormal neck movement associated with GORD -> condition improves as reflux improves

53
Q

presentation of Sandifers syndrome

A

o Torticollis: forceful contraction of neck muscles causing twisting of the next
o Dystonia: abnormal muscle contractions causing twisting movements- arching of back or unusual postures

54
Q

differentials for Sandifers syndrome

A

infantile spasms (west syndrome) and seizures

55
Q

Causes of Vomiting

A

Vomiting is very non-specific and is often not indicative of underlying pathology. Some of the possible causes of vomiting include:
* Overfeeding
* Gastro-oesophageal reflux
* Pyloric stenosis (projective vomiting)
* Gastritis or gastroenteritis
* Appendicitis
* Infections such as UTI, tonsillitis or meningitis
* Intestinal obstruction
* Bulimia

56
Q

red flags for vomiting

A

Certain features in the history should make you think about serious underlying problems:

  • Not keeping down any feed (pyloric stenosis or intestinal obstruction)
  • Projectile or forceful vomiting (pyloric stenosis or intestinal obstruction)
  • Bile stained vomit (intestinal obstruction)
  • Haematemesis or melaena (peptic ulcer, oesophagitis or varices)
  • Abdominal distention (intestinal obstruction)
  • Reduced consciousness, bulging fontanelle or neurological signs (meningitis or raised intracranial pressure)
  • Respiratory symptoms (aspiration and infection)
  • Blood in the stools (gastroenteritis or cows milk protein allergy)
  • Signs of infection (pneumonia, UTI, tonsillitis, otitis or meningitis)
  • Rash, angioedema and other signs of allergy (cows milk protein allergy)
  • Apnoeas are a concerning feature and may indicate serious underlying pathology and need urgent assessment