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Paediatrics > Paediatric gastroenterology > Flashcards

Paediatric gastroenterology Flashcards

1
Q

Coeliacs in children : Definition

A

Sensitivity to gluten - repeated exposure leads to villous atrophy which in turn causes malabsorption

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2
Q

Coeliacs in children : Age of presentation

A

Before 3 years old - following introduction of cereals into diet

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3
Q

Coeliacs in children : Clinical features

A
  • Failure to thrive - low BMI, height
  • Abdominal pain and distention
  • Diarrhea
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4
Q

Coeliacs in children : Diagnosis

A
  • Biopsy of the jejunum : subtotal villous atrophy
  • Bloods : Anti-endomysial and anti-gliadin antibodies
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5
Q

Constipation in children : average BO for children

A

< 6 months : average 3 times a day
+3 years : Once a day

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6
Q

Constipation in children : Life style causes

A
  • Habitually not opening the bowels
  • Low fibre diet
  • Poor fluid intake and dehydration
  • Sedentary lifestyle
  • Psychosocial problems such as a difficult home or school environment
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7
Q

Constipation in children : Secondary causes

A

Diet : Low fibre diet and dehydration, Cow’s milk intolerance
Anal stenosis : Anal fissure, IBD
Hirschsprung’s disease
Hypothyroidism

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8
Q

Constipation in children : Most common cause

A

Idiopathic - majority of children, cause is unknown

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9
Q

Constipation : Diagnosis in children

A

2 or more symptoms of the following:

  • Stool pattern
    1. Less than 3 stools a week
  1. Hard large stool which is difficult to pass
  2. ‘Rabbit dropping stool’
  3. Overflow soiling - Faecal impaction causing overflow soiling, with incontinence of particularly loose smelly stools
  • Symptoms associated with defecation
    1. Pain
    1. Straining and painful passages of stools
    1. Abdominal pain and poor appetite which improved with passage of stool
    1. Rectal bleeding associated with hard stool
  • Signs
    1. Holding an abnormal posture, referred to as retentive posturing
    1. Hard stools may be palpable in abdomen
    1. Loss of the sensation of the need to open the bowels
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10
Q

Constipation : Diagnosis of Idiopathic Constipation

A
  • Step 1 : Diagnosis of Constipation
  • Step 2 : Rule of secondary causes of constipation by considering the following symptoms
    • > 48 hours for meconium passage
    • ‘Ribbon’ stool : indicates anal stenosis - may be secondary to anal fissure/ IBD
    • Failure to thrive - low weight, height
    • Neurological weakness/development delay
  • Step 3 : If ruled out - can diagnose idiopathic constipation
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11
Q

Constipation : Faecal incontinence

A

Considered pathological > 4 years
1. Sign of chronic constipation
2. Rectum becomes stretched chronically and looses sensation
3. Hard stool remains and only loose stool are able to bypass the blockage - leaking out without sensation
4. ‘Overflow soiling’

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12
Q

Constipation : Faecal impaction

A
  1. Habit of not opening bowels and ignoring sensation of full rectum
  2. Lose sensation to open bowels - reduced frequency of bowel opening
  3. Retention of faeces .
  4. Faecal impaction : large, hard stool block the rectum

Symptoms are : severe constipation, overflow soiling, faecal mass in abdomen

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13
Q

Constipation : Management of faecal impaction

A

First line : Polyethylene glycol + Movicol } both osmotic laxatives
If no disimpaction in 2 weeks
Second line : Add stimulant laxative (Senna)

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14
Q

Constipation : Maintainance therapy

A
  1. First line : Movicol
    If no response
  2. Second line : Add stimulant laxative (Senna)
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15
Q

Appendicitis : Incidence in children

A
  • Occurs in children > 4 years
  • If < 4 years : Presents with perforation
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16
Q

Hirschsprung’s disease : Definition

A

congenital condition characterised by partial or complete colonic functional obstruction associated with the absence of ganglion cells

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17
Q

Hirschsprung’s disease : Pathophsyiology

A
  1. Development failure results in lack of parasympathetic plexus innervation of a segment of the bowel
  2. Aganglionic segment of the bowel results in uncoordinated peristalsis of the bowel
  3. Functional obstruction
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18
Q

Hirschsprung’s disease : Risk factors

A
  • 3x more common in males
  • Down’s syndrome
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19
Q

Hirschsprung’s disease : Incidence

A

new-born period to 1 year of age

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20
Q

Hirschsprung’s disease : Clinical features

A

Neonatal period
-Delay of > 48 hr or failure to mass meconium

Older children
-Constipation and abdominal distention
-Vomitting
-Failure to thrive

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21
Q

Hirschsprung’s disease : Investigations

A
  1. Rectal biopsy : Gold standard for diagnosis
  2. Abdominal X-ray
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22
Q

Hirschsprung’s disease : Management

A
  1. Initial management
    - Rectal washout/ Bowel irrigation : poor peristalsis means stool/flatus is not completely cleared
  2. Definitive management
    - Surgery to affected segment of the colon
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23
Q

Cow’s milk protein allergy/intolerance : Definition

A
  • Immune-mediated allergic response to proteins in the milk
  • It is one of the most common childhood food allergies
  • Allergy : Immediate IgE mediated
  • Intolerance : Delayed, non IgE mediated
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24
Q

Cow’s milk protein allergy/intolerance : Incidence

A

< 3 month old infants - formula fed infants,
Very rare in breast fed infants

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25
Q

Cow’s milk protein allergy/intolerance : Risk factors

A

Formula fed infants

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26
Q

Cow’s milk protein allergy/intolerance : Clinical features

A
  1. After feeds ;
    * Regurgitation and Vomiting
    * Diarrhoea
    2 . Atopy symptoms `; Urticaria, Ectopic eczema, wheeze
    3 . Colic symptoms : Irritability, crying
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27
Q

Cow’s milk protein allergy/intolerance : Diagnosis

A
  1. Clinical diagnosis : Improvement with cow’s milk protein elimination
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28
Q

Cow’s milk protein allergy/intolerance : Investigations

A
  • Skin prick/patch testing
  • Total IgE and specific IgE (RAST) for cow’s milk protein
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29
Q

Cow’s milk protein allergy/intolerance : Management

A

Formula fed
1. First line
* Mild-moderate sx : Extensive hydrolysed formula milk

  1. Second line
    * Severe sx or no response to eHF : Amino acid-based formula

Breast fed
1. Eliminate cow’s milk from maternal diet

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30
Q

Cow’s milk protein allergy/intolerance : Prognosis

A

Resolves on its own in most children
* IgE mediated - 55% will be milk tolerant by 5 years old
* Non-IgE - Most will be milk tolerant by age 3

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31
Q

Paediatric GORD : definition

A

Pathological regurgitation of oesophageal contents - regurgitation is not physiological and is associated with other symptoms

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32
Q

Paediatric GORD : Incidence

A

< 8 week infants

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33
Q

Paediatric GORD : Clinical features

A
  1. Vomiting / Regurgitation
    -Milky vomits after feeds
    -May occur after being laid flat
  2. Failure to thrive
  3. Distressed behaviour / Feeding aversion - excessing crying especially when feeding, refusing to feed, gagging
34
Q

Paediatric GORD : Diagnosis

A

Clinical diagnosis

35
Q

Paediatric GORD : Management

A
  1. Feeding position : -30 degrees, head up
  2. Avoid overfeeding : Smaller, more frequent feeds
  3. Trail - not at the same time
    * Aligante : Gaviscon
    * Thickening agent
36
Q

Paediatric GORD : Management with PPI

A

Trail PPI only if one of the following symptoms apply with regurgitation;
1. Feeding aversion : refusing feeds, gagging, choking
2. Distressed behaviour
3. Failure to thrive

37
Q

Paediatric GORD : Complication

A
  1. Failure to thrive
  2. Aspiration : Pneumonia
38
Q

Intussusception : Definition

A
  1. Inversion of one portion of the intestine with another
  2. Commonly in ileo-caecal region
  3. Most common cause of bowel obstruction in children
39
Q

Intussusception : Incidence

A
  • 6 months - 1 1/2 year olds
  • Mainly Boys x2 as often
40
Q

Intussusception : Clinical features

A
  1. Abdominal pain ;
    * Intermittent, severe, crampy abdominal pain
    * During episode - Infant will draw knees up and turn pale

2 . Insonsolable crying (due to pain)

3 . Vomitting

4 . Bloodstained stool - ‘Red-currant jelly’

41
Q

Intussusception : Clinical sign

A
  • sausage-shaped mass in the right upper quadrant
42
Q

Intussusception : Investigation

A

US Abdomen : Target-like mass

43
Q

Intussusception : Management

A

First line : Reduction by air insufflation } creates pressure within the intestines and seperate them

44
Q

Pyloric stenosis : Definition

A

Condition where the muscle passage (pylorus) between the stomach and small bowel (duodenum) becomes hypertrophied and narrows.

45
Q

Pyloric stenosis : Clinical features

A
  1. Projectile vomiting - 30 minutes after feed
    High frequency of vomiting leads to;
  2. Hypochloraemia, Hypokalaemia Alkalaosis
  3. Dehydration —> Constipation
46
Q

Pyloric stenosis : Clinical signs

A

Palpation : ‘Olive’ Mass in the upper abdomen

47
Q

Pyloric stenosis : Incidence

A

< 4 week old infants

48
Q

Pyloric stenosis : Investigation for diagnosis

A

Abdominal US

49
Q

Pyloric stenosis : Management

A

Ramstedt Pyloromyotomy

50
Q

Biliary atresia : definition

A

Congential abnormality of obstruction of the bile ducts leading from the liver secondary to narrowing.

51
Q

Biliary atresia : Pathophysiology

A
  1. Congential abnormality characterised by the narrowing of the bile ducts this leads to
  2. Obstruction of the biliary ducts which transport bile from the Liver to the Gall bladder and small intestine.
  3. Bile and its components (conjugated bilirubin) back up in tot liver and are released in the blood
52
Q

Biliary atresia : Clinical presentation

A
  1. Jaundice peresistent > 14 days after birth
  2. High levels of conjugated bilirubin } indicates obstructive disease
53
Q

Biliary atresia : Management

A

Surgery - “Kasai portoenterostomy”
-Attach small section of small intestine to opening of the liver

54
Q

Meckel’s diverticulum - definition

A

A congenital out-pouching - diverticulum present in the small intestine at birth

55
Q

Meckel’s diverticulum - Pathophysiology of development

A
  1. < week 8 of development : The omphalmomesenteric duct delivers nutrients from the yolk sac to the midgut/small intestine for developmen
  2. Normally : narrows and disappears before week 8
  3. Pathology : Proximal part of the vitelline duct fails to regress and remains a part of the small intestine
56
Q

Meckel’s diverticulum - Anatomy

A

Meckel’s diverticulum contains;
1. Pluripotent embryonic cells from other tissue times : ectopic illeal, gastric or pancreatic mucosa

  1. Has its own blood supply : Omphalomesenteric artery } prone to obstruction
57
Q

Meckel’s diverticulum : Rule of 2s

A
  1. 2% (of the population)
  2. 2 feet (proximal to the ileocecal valve
  3. 2 inches (in length)
  4. 2 types of common ectopic tissue (gastric and pancreatic)
  5. 2 years is the most common age at clinical presentation
  6. 2:1 male:female ratio
58
Q

Meckel’s diverticulum : Clinical features

A

Usually asymptomatic
1.Abdominal pain - similar to appendicitis
2. Rectal bleeding : most common cause of severe painless GI bleeding in children
3. Vomitting / Constipation

59
Q

Meckel’s diverticulum : Complications

A
  1. Diverticulitis
  2. Ulcers : from HCL secretion of gastric mucosa
  3. Intestinal obstruction : intussusception, volvulus
  4. Perforation
60
Q

Meckel’s diverticulum : Investigation

A
  1. Haemodynamically stable : 99M Technetium scan which has an affinity for gastric mucosa (ectopic)
  2. Unstable : Mesenteric arteriography
61
Q

Meckel’s diverticulum : Management

A

1) Surgery
-Wedge excision or formal small bowel resection and anastomosis

62
Q

Neonatal jaundice : Definition

A

Jaundice describes the condition of abnormally high levels of bilirubin in the blood

63
Q

Neonatal jaundice : Physiology

A

1 . Red blood cells contain unconjugated bilirubin.

2 . RBC breakdown and release of unconjugated bilirubin

3 . Unconjugated bilirubin is conjugated in the liver

4 . Conjugated bilirubin* is excreted in two ways
* via the biliary system into the gastrointestinal tract
* via the urine

64
Q

Neonatal jaundice : Physiological jaundice

A
  1. Foetal cell break down after birth
  2. Increase bilirubin release } rise in bilirubin
  3. Less developed liver function : unable to break down excess bilirubin
  4. Mild yellowing of sclera 2-7 days
  5. Resolves by 10 days
65
Q

Neonatal Jaundice : Due to increase bilirubin break down

A
  1. Increased production of bilirubin: } Excess RBC breakdown
    * Haemolytic disease of new born : Rhesus incompatibility
    * Haemorrhage
    * Polycythaemia
    * Sepsis or DIC
66
Q

Neonatal Jaundice : Due to decrease bilirubin clearance

A

1. Decreased clearance of bilirubin:
* Prematurity : very immature liver
* Breast milk jaundice
-Components of milk inhibit liver breakdown of bilirubin
-Higher risk of dehydration with inadequate feeding - constipation, and more bilirubin absorption

2 . Biliary atresia
3 . Hypothyroidism : lack of T3/T4 inhibits liver enzymes which breakdown bilirubin
4 . Gilbert’s syndrome

67
Q

Neonatal Jaundice : Prolonged jaundice definition

A

Jaundice lasts longer than if physiological
* More than 14 days in full term babies
* More than 21 days in premature babies

68
Q

Neonatal Jaundice : Prolonged jaundice causes

A
  1. G6PD deficiency : Genetic disorder when unable to produce G6PD enzyme which protects RBC from oxidative damage
  2. Hypothyroidism
  3. Biliary atresia
69
Q

Neonatal Jaundice : Investigations for diagnosis

A
  • Full blood count and blood film : polycythaemia or anaemia
  • Conjugated bilirubin: elevated levels indicate a hepatobiliary cause
  • Blood type testing : ABO or rhesus incompatibility
  • Direct Coombs Test (direct antiglobulin test) for haemolysis
  • Thyroid function, particularly for hypothyroid
  • Blood and urine cultures : if infection is suspected. Suspected sepsis needs treatment with antibiotics.
  • Glucose-6-phosphate-dehydrogenase: (G6PD) levels for G6PD deficiency
70
Q

Neonatal Jaundice : Management

A
  1. Treatment threshold chart : age and total bilirubin level monitored - tx commence if threshold reached
  2. Phototherapy with blue light
71
Q

Neonatal Jaundice : Complication

A
  • Kernicterus : Bilirubin deposits in the brain causing CNS damage
    May cause : Cerebral palsy, learning disability and deafness
72
Q

Necrotising enterocolitis : Definition

A

Serious medical condition characterised by inflammation and daage to the tissues of the intestine
* Particularly colon and small intestine
* Commonly affects premature infants with low birth weights

73
Q

Necrotising enterocolitis : Pathophysiology

A
  1. Predominantly affects premature infants (<32 weeks)
  2. Bacterial infection of intestine : immature gut barrier makes it more permeable
  3. Inflammation of intestine 2nd to bacterial colonisation
  4. Intestinal ischaemia —> leads to necrosis of the bowel
    * More vulnerable to damage from inflammation and vessels are more susceptible to ischaemia
74
Q

Necrotising enterocolitis : Incidence

A

Occurs 2nd - 3rd week of life

75
Q

Necrotising enterocolitis : Clinical features

A
  1. Feeding intolerance
  2. Abdominal distention
  3. Blood stools
    May acutely progress to : perforation and peritonitis
76
Q

Necrotising enterocolitis : Investigation

A
  1. Abdominal XR may show
    * Dilated bowel loops
    * Bowel oedema

Abnormal air pockets
* Pnematosis intestinal : gas within the intestinal wall
* Pneumoperitoneal

77
Q

Necrotising enterocolitis : Risk factors

A
  1. Prematurity +++ risk
  2. Formula feed - reduces protective factors for gut health
  3. Enteral feeding
78
Q

Meconium ileus : Definition

A

Aspirated meconium obstructs the small intestine at the level of terminal ileum

79
Q

Meconium ileus : Clinical presentation

A
  1. Intestinal obstruction within hours after birth
  2. Billous vomitting during feeds
80
Q

Meconium ileus : Investigation

A

Abdominal Xray - soap -bubble sign in distal small intestine where meconium mixes with swallowed air

Paediatrics (13 decks)

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