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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
What is the treatment for pyloric stenosis?
``` Correct electrolytes Laparoscopic pyloromyotomy (Ramstedt's operation) ```
26
What is mesenteric adenitis?
Similar to appendicitis but no guarding or rebound tenderness Follows viral infection Conservative management
27
What is nectrotising enterocolitis? (NEC)
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
What is the most common GI emergency in neonates?
Necrotising enterocolitis (NEC)
29
What is the clinical presentation of NEC? What would find on examination?
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
What is the diagnostic test for NEC?
Abdominal X-ray - Shows gas in gut wall - Portal vein gas
31
What is the general and medical management for NEC?
NBM + barrier nursing NG tube IV fluids, TPN IV Abx 10-14 days = Cefotaxime or Vancomycin Surgery if perforation/ deterioration
32
What is Hirschprung's disease?
Congenital condition - nerve cells of myenteric plexus are absent in distal bowel and rectum *absence of parasympathetic ganglion cells*
33
What is meant by total colonic aganglionosis?
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
What are the genetic associations with hirschprungs?
FHx Down's syndrome Neurofibromatosis Waardenburg syndrome
35
What is the clinical presentation of Hirschprungs?
``` >24 hour delay in passing meconium Abdo distension Vomiting (billous, green) Possible megacolon Chronic constipation or diarrhoea ```
36
What is the main complication associated with Hirschprungs?
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
How is Hirschprung's diagnosed?
Abdo xray - obstruction / HAEC | **Rectal biopsy = diagnostic**
38
What is the management of Hirschprunugs?
Bowel washout / irrigation straight away Surgical removal of aganglionic bowel
39
What is Meckel's diverticulum?
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
Is neonatal jaundice within the first 24 hours normal?
NO!!! Sepsis is a common cause of this and should be treated promptly! Normal jaundice = days 2-7, resolved by day 10
41
What are some common causes of neonatal jaundice due to increased production of bilirubin?
``` Haemolytic disease of the newborn Haemorrhage Thrombocytopaenia Sepsis DIC G6PD deficiency ```
42
'Reduced clearance' causes of neonatal jaundice?
``` Prematurity Biliary atresia (prolonged, conjugated bilurubin + pale stools) Gilbert syndrome Endocrinological disorders Breastmilk jaundice Neonatal cholestasis ```
43
What investigations are needed in neonatal jaundice?
Bilirubin levels FBC and Blood film Infection screen Coombs test - blood and Rh type in mother and infant
44
What is the treatment for neonatal jaundice?
Urgent treatment if <24 hours (sepsis) Phototherapy Exchange transfusion
45
What is Kernicterus?
Clinical features of acute bilirubin encephalopathy: - Cerebral palsy - Learning difficulties - Deafness
46
How does GORD present in infants/ children? How is it usually diagnosed
``` Regurgitation Chronic cough Distress after feeds Poor weight gain Reluctant to feed ``` - Clinical dx - endoscopy rarely done
47
What is the management for GORD?
``` Avoid overfeeding Keep baby upright Try thickened feed Antacid + sodium/Mg alginate PPI ``` Mostly resolves at 6-9 months
48
What is congenital diaphragmatic hernia?
Herniation of abdo contents into chest --> pumonary hypoplasia and HTN
49
What is gastroschisis?
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
What is exomphalos?
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
Oesophageal atresias and trachea-oesophageal fistulas are a spectrum of abnormalities. What is the most common? What is the general presentation?
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
What is the presentation of biliary atresia? What is the tx?
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
What is the presentation, dx and tx of appendicitis?
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
What is Wilson's disease? What is the genetics?
Genetic condition - excess copper build up Autosomal recessive mutation in ATP7B copper-binding protein on chromosome 13
55
How does Wilson's disease present
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
How is Wilson's disease diagnosed?
1. Raised serum caeruloplasmin (non specific) 2. Liver biopsy = gold standard 3. 24 hour urine copper assay - Serum copper = low - MRI brain
57
What is the management of Wilson's disease?
Copper chelation - Penicillamine or Trientene
58
What is a choledochal cyst?
congenital abnormality of bile duct --> abdo mass, RUQ pain, jaundice, vomiting, fever Mx = laparoscopic surgery
59
What is neonatal hepatitis syndrome?
inflammation of liver 1-2 months after birth can be caused by virus (CMV, hepatitis A/B/C, Rubella) Tx = supportive + vits

Phase 3a (13 decks)

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