Paediatric GI Flashcards

1
Q

What is gastroenteritis?

What is the most common cause in children?

Mx?

What complications can arise?

How would you test for post infective lactose intolerance?

A

Sudden onset D+/-V + pain

Rotavirus (part of vaccine schedule)

Mx = Oral rehydration therapy, IV therapy if deterioration

Dehydration, malnutrition
Transient lactose intolerance (confirmed by +ve clinitest)

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2
Q

What is colic?

A

Paroxysmal crying with pulling up of the legs for >3 hours on >3 days/week

Associated with feeding problems
Mx = Movement and let baby finish first breast first as hind milk easier to digest

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3
Q

How may a cow’s milk allergy present?

How would you confirm it?

What is the management and prognosis?

A

Widespread itching, facial swelling, loose stools, FTT, colic symptoms
Severe = stridor, wheeze, blood/mucus in stools, collapse

Dx = cow’s milk challenge - skin prick test + IgE antibodies in blood (RAST test)
Mx = Avoid cow’s milk, antihistamines if allergic reaction, adrenaline if severe
Often resolves by 5 years

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4
Q

What is toddler’s diarrhoea?

What is the management?

A

Chronic, non-specific diarrhoea which varies in consistency (mucus / undigested vegetables).

  • Child is well and thriving
  • 1st stool of day often large

Mx

  • adequate fat and fibre
  • usually stops by 5 years
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5
Q

What is the basic science of coeliac disease?

What are the genetic links?

A

A damaging immunological response to gluten in the mucosa of the proximal small intestine.

HLADQ2 and maybe HLADQ8

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6
Q

What are the risk factors for coeliac?

A

T1DM
Autoimmune thyroid disease
Down’s syndrome
1st degree relatives with coeliac

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7
Q

What are the main GI symptoms of coeliac?

A
\++Malabsorption between 8-24 months after intro of wheat containing foods
Failure to thrive
Anaemia (?low folate, ferritin)
Weight loss
Abdo distension
Abnormal stools
Irritability
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8
Q

What are the main non-GI manifestations of coeliac disease?

A

Dermatitis herpetiformis
- erythematous macules, severe pruritus
Dental enamel defects
Osteoporosis

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9
Q

How is coeliac disease diagnosed?

What is the management?

A

IgA tissue transglutaminase (TTG) and endomysial antibodies = suggestive of disease

Biopsy to confirm:

  • Villous atrophy
  • Intraepithelial lymphocytes
  • Crypt hypertrophy

Mx = gluten free diet will resolve symptoms and antibodies

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10
Q

What is the general presentation of IBD?

A
Growth failure / puberty delay
Weight loss
Nausea/ vomiting
Abdominal pain
Stool = blood/ mucus / diarrhoea
Lethargy
?Fever
Oral lesions
Clubbing
Uveitis
Arthralgia, arthritis
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11
Q

What investigations would you do to diagnose IBD?

A

Exclude infections - stool MCS
Faecal calprotectin
Endoscopy and biopsy

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12
Q

Crohn’s vs UC:

  1. Location
  2. Endoscopic
  3. Histology
  4. X-ray barium swallow
  5. Symptoms
A

CROHN’S

  1. Distal ileum and proximal colon
  2. Small bowel narrowing + fissuring, skip lesions
  3. transmural inflammation + granuloma
  4. String-like appearance of intestines
  5. Less likely to have blood or mucus

ULCERATIVE COLITIS

  1. Extends from rectum
  2. Continuous lesions
  3. Mucosal inflammation + crypt damage
  4. Lead pipe colon sign
  5. Blood or mucus more common
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13
Q

What is the management for IBD?

A

Maintenance = Mesalazine, Sulfasalazine (5-ASAs)

Aggressive/ exacerbations = Corticosteroid + Azaothioprine (immunosuppressant)

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14
Q

What is Kwashiorkor?

A

Low intake of protein
- poor growth, diarhhoea, anorexia, oedema, distended abdomen

  • gradullay increaseprotein and vitamins
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15
Q

What is Marasmus?

A
Lack of calories and discrepancy between height and weight
Associated with HIV
- Distended abdoomen
- Diarrhoea
- infectioin
- Low albumin
  • gradual refeednig
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16
Q

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

A

Intussusception

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17
Q

What is the basic science of intussusception?

Where is the most common location of intussusception in children?

A

One bowel segment goes inside another, the bowel wall distends and obstructs lumen –> lymphatic + venous obstruction causing ischaemia

Most common location = ileocaecal

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18
Q

What are the main non-pathological and pathological lead points in intussusception?

A

Non-pathological >90%

  • Viral (50%)
  • Amoebomata, shigella
  • Peyer’s patch hypertrophy

Pathological <10%

  • Cystic fibrosis
  • HSP
  • Meckel’s diverticulum
  • Lymphoma + tumours
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19
Q

What is the presentation of intussusception?

A

Sudden onset colicky abdo pain (every 10-20 mins) = drawing up legs, episodic inconsolable crying but child may appear well in between
Early vomiting
Lethargy, hypotonia
Late = mucoid/ bloody stools “redcurrant jelly”, pyrexia

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20
Q

What may be felt on examination in an intussusception?

A

Sausage shaped mass in RUQ

Empty RLL and mass in RUQ = Dance’s sign

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21
Q

What diagnostic tests would indicate insussusception?

A
Abdo XR = dilated gas filled proximal bowel
**USS = doughnut / target sign**
Bowel enema = crescent sign
CT / MRI in older children
FBC - neutrophils+
U+E - dehydration
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22
Q

What is the treatment for intussusception?

A

Reduction with air enema (if no signs of peritonitis, perforation or shock)
Laparotomy if these signs are present
Resuscitation (NG, IV fluids)

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23
Q

What is pyloric stenosis?

When does it typically present?

A

Projectile / profuse vomiting after feeds. No bile just milk.
Child is alert and hungry but may have dehydration + constipation

Presents at 3-8 weeks.

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24
Q

How is pyloric stenosis diagnosed?

A
Metabolic alkalosis
- Hyponatraemia
- Hypochloraemia
- Hypokalaemia
Visible LUQ peristalsis when feeding
Abdominal USS
25
Q

What is the treatment for pyloric stenosis?

A
Correct electrolytes
Laparoscopic pyloromyotomy (Ramstedt's operation)
26
Q

What is mesenteric adenitis?

A

Similar to appendicitis but no guarding or rebound tenderness
Follows viral infection
Conservative management

27
Q

What is nectrotising enterocolitis? (NEC)

A

Inflammatory bowel necrosis (vascular, mucoosal, toxic), mainly affecting premature infants

More infants of very low birth weight are surviving –> increased population risk of NEC

28
Q

What is the most common GI emergency in neonates?

A

Necrotising enterocolitis (NEC)

29
Q

What is the clinical presentation of NEC?

What would find on examination?

A

Often presents in first 2 weeks
Feeding difficulties, vomiting, abdo distension/ tenderness
Bloody, mucoid stool and billious vomiting
Bradycardia, lethary, shck, resp distress, DIC

OE:
Decreased bowel sounds
Erythema of abdomen
Visible boowel looops
Palpable mass
30
Q

What is the diagnostic test for NEC?

A

Abdominal X-ray

  • Shows gas in gut wall
  • Portal vein gas
31
Q

What is the general and medical management for NEC?

A

NBM + barrier nursing
NG tube
IV fluids, TPN

IV Abx 10-14 days = Cefotaxime or Vancomycin
Surgery if perforation/ deterioration

32
Q

What is Hirschprung’s disease?

A

Congenital condition - nerve cells of myenteric plexus are absent in distal bowel and rectum

absence of parasympathetic ganglion cells

33
Q

What is meant by total colonic aganglionosis?

A

When the whole colon is without ganglionic innervation in Hirschprungs disease. This causes this area of the colon to become constricted, causing proximal distension.

34
Q

What are the genetic associations with hirschprungs?

A

FHx
Down’s syndrome
Neurofibromatosis
Waardenburg syndrome

35
Q

What is the clinical presentation of Hirschprungs?

A
>24 hour delay in passing meconium
Abdo distension
Vomiting (billous, green)
Possible megacolon
Chronic constipation or diarrhoea
36
Q

What is the main complication associated with Hirschprungs?

A

Hirschprung-Associated Enterocolitis (HAEC)
- presents 2-4 weeks after birth with fever, abo distension, bloody diarrhoea and features of sepsis

LIFE THREATENING

  • can lead to toxic megacolon + perforation
  • needs IV abx, fluids and bowel decompression
37
Q

How is Hirschprung’s diagnosed?

A

Abdo xray - obstruction / HAEC

Rectal biopsy = diagnostic

38
Q

What is the management of Hirschprunugs?

A

Bowel washout / irrigation straight away

Surgical removal of aganglionic bowel

39
Q

What is Meckel’s diverticulum?

A

Congenital bulging of vowel 2cm from ileocaecal bowel
Reminant of umbilical cord

Asymptomatic but may present with complications such as haemorrhage, intestinal obstruction, diverticulitis, perforation
Tx = depends on complication

40
Q

Is neonatal jaundice within the first 24 hours normal?

A

NO!!!
Sepsis is a common cause of this and should be treated promptly!

Normal jaundice = days 2-7, resolved by day 10

41
Q

What are some common causes of neonatal jaundice due to increased production of bilirubin?

A
Haemolytic disease of the newborn
Haemorrhage
Thrombocytopaenia
Sepsis
DIC
G6PD deficiency
42
Q

‘Reduced clearance’ causes of neonatal jaundice?

A
Prematurity
Biliary atresia (prolonged, conjugated bilurubin + pale stools)
Gilbert syndrome
Endocrinological disorders
Breastmilk jaundice
Neonatal cholestasis
43
Q

What investigations are needed in neonatal jaundice?

A

Bilirubin levels
FBC and Blood film
Infection screen
Coombs test - blood and Rh type in mother and infant

44
Q

What is the treatment for neonatal jaundice?

A

Urgent treatment if <24 hours (sepsis)
Phototherapy
Exchange transfusion

45
Q

What is Kernicterus?

A

Clinical features of acute bilirubin encephalopathy:

  • Cerebral palsy
  • Learning difficulties
  • Deafness
46
Q

How does GORD present in infants/ children?

How is it usually diagnosed

A
Regurgitation
Chronic cough
Distress after feeds
Poor weight gain
Reluctant to feed
  • Clinical dx
  • endoscopy rarely done
47
Q

What is the management for GORD?

A
Avoid overfeeding
Keep baby upright
Try thickened feed
Antacid + sodium/Mg alginate
PPI

Mostly resolves at 6-9 months

48
Q

What is congenital diaphragmatic hernia?

A

Herniation of abdo contents into chest –> pumonary hypoplasia and HTN

49
Q

What is gastroschisis?

A

Congenital defect where baby’s intestines are outside body through an opening <5cm big - more common in young mothers.

Tx - cover bowel in clingfilm at birth then corrective surgery (good outcome)

50
Q

What is exomphalos?

A

Herniation of abdo contents but they remain covered in peritoneum
Small = contain Meckels
Large = stomach, liver, bladder

Mx

  • protect organs, prevent hypothermia and sepsis
  • staged surgical closure
51
Q

Oesophageal atresias and trachea-oesophageal fistulas are a spectrum of abnormalities. What is the most common?

What is the general presentation?

A

OA with distal TOF

Prenatal:

  • polyhydromnias
  • small stomach

Postnatal:

  • cough, airway obstruction
  • Cyanosis
  • Increased secretions
  • Blowing bubbles
  • distended abdo
Dx = CXR, avoid contrast
tx = surgery
52
Q

What is the presentation of biliary atresia?

What is the tx?

A

Jaundice, yellow urine, pale stools - high CONJUGATED bilirubin
Palpable spleen around 3rd/4th week
Hepatomegaly

tx = Kasai portoenterostomy if caught early, liver transplant within 1 year if caught late

53
Q

What is the presentation, dx and tx of appendicitis?

A

Presentation = central abdo pain that moves to RIF

  • Tenderness on Mcburney’s point
  • anorexia, nausea, vomiting
  • rebound tenderness = peritonitis
Dx = clinical + inflammatory markers
Tx = appidendicectomy
54
Q

What is Wilson’s disease?

What is the genetics?

A

Genetic condition - excess copper build up

Autosomal recessive mutation in ATP7B copper-binding protein on chromosome 13

55
Q

How does Wilson’s disease present

A

Hepatic:
- chronic hepatitis (-> cirrhosis)

Neuro:

  • concentration/ coordinationo difficulties
  • Dysarthria
  • dystonia
  • BASAL GANGLIA -> SYMMETRICAL parkinsonism

Psychiatric:

  • mild depression
  • psychosis
Other:
KAYSER-FLEISCHER RINGS
haemolytic anaemia
osteopenia
renal issues
56
Q

How is Wilson’s disease diagnosed?

A
  1. Raised serum caeruloplasmin (non specific)
  2. Liver biopsy = gold standard
  3. 24 hour urine copper assay
  • Serum copper = low
  • MRI brain
57
Q

What is the management of Wilson’s disease?

A

Copper chelation - Penicillamine or Trientene

58
Q

What is a choledochal cyst?

A

congenital abnormality of bile duct –> abdo mass, RUQ pain, jaundice, vomiting, fever
Mx = laparoscopic surgery

59
Q

What is neonatal hepatitis syndrome?

A

inflammation of liver 1-2 months after birth
can be caused by virus (CMV, hepatitis A/B/C, Rubella)

Tx = supportive + vits