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3A > Paediatric Gastro > Flashcards

Paediatric Gastro Flashcards

1
Q

What is pyloric stenosis

A

Hypertrophy of the pyloric muscle causing gastric outlet obstruction

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2
Q

When does pyloric stenosis present?

A

At 2-8 weeks.
More common in boys, particularly the first born

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3
Q

How does pyloric stenosis present?

A

Projectile non-bilious vomiting - typically 30 mins after feed, becomes increasingly projectile over time
Constipation
Dehydration- tachycardia, decreased wet nappies, dry mucous membranes, flat or depressed fontanelles
Palpable upper abdominal mass- olive sign
Hunger after vomiting (until severe dehydration sets in)

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4
Q

What blood gas abnormality occurs in pyloric stenosis and why?

A

Hypochloraemic, hypokalaemic metabolic alkalosis
-Occurs as prolonged vomiting leads to hypovolaemia
-This causes increase in aldosterone and renal absorption of sodium and water
-This causes subsequent loss of hydrogen ions
-This increases bicarbonate
-Chloride is loss in vomit
-Potassium is used in H+ K+ pump in kidney (kidney tries to keep as much H+ as it can)

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5
Q

How is pyloric stenosis diagnosed?

A

Gold- abdominal USS ( muscle thickness >4mm and muscle length >14mm)
May also do a test feed and capillary blood glucose (hypochloraemic hypokalaemic metabolic alkalosis)

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6
Q

How is pyloric stenosis treated?

A

Correct fluid and electrolyte abnormalities - IV fluids (1.5 maintenance with 10% dextrose and 0.9% saline)
Ramstedt pyloromyotomy - division of the hypertrophied muscle

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7
Q

What is Hirschsprung’s disease?

A

The absence of ganglion cells from the myenteric and submucosal plexus of part of the large bowel which leads to a narrow contracted segment

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8
Q

How common is Hirschsprung’s disease?

A

Occurs in 1 in 5000 births
More common in males
Increased in Down’s syndrome

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9
Q

Pathophysiology of Hirschsprung’s disease?

A

There is an absence of parasympathetic ganglion cells in the myenteric plexus.
These cells start higher up in the GI tract in development and move down towards the colon and rectum
In Hirschsprung’s the migration doesn’t happen so the distal end of colon has no ganglion cells
The aganglionic section of bowel does not relax causing it to become constricted (causing faecal obstruction)
The more proximal area becomes dilated.

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10
Q

Presentation of Hirschsprung’s disease?

A

Failure to pass Meconium in the first 24 hours
Chronic constipation since birth
Abdominal distention
Bile stained vomiting
Hirschsprung- associated enterocolitis

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11
Q

Diagnosis of Hirschsprung’s disease

A

Abdominal x ray
Contrast enema
Gold- rectal biopsy (shows absence of ganglion cells and large acetylcholinesterase- positive nerve trunks

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12
Q

Management of Hirschsprung’s disease

A

Initial - rectal washouts and bowel irrigation
Gold- surgery to remove the effected part of bowel (usually in first week of life)

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13
Q

What is intussusception

A

Invagination of one part of the bowel into the lumen of the adjacent bowel

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14
Q

Where does intussusception usually occur?

A

The ileo-caecal region

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15
Q

Epidemiology of intussusception

A

Infants aged 6-18 months
More common in boys

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16
Q

Presentation of intussusception

A

Severe colicky abdominal pain - infant will bring knees up and turn pale
Isolable crying
Vomiting
Red-current jelly stool
Sausage shaped mass in right upper quadrant

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17
Q

How is intussusception diagnosed?

A

USS- shows donut sign

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18
Q

How is intussception managed

A

Most can be treated with an air enema
10% need surgery

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19
Q

Illnesses associated with intussusception

A

Concurrent viral illness, henoch- schonlein purpura, cystic fibrosis, intestinal polyps, Meckel diverticulum

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20
Q

Complications of intussusception

A

Obstruction, gangrenous bowl, perforation, death

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21
Q

What is meckel’s diverticulum?

A

A congenital diverticulum in the small intestine which is a remanent of the vitelline duct which has failed to obliterate.

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22
Q

Explain the rule of 2’s for MEckel’s diverticulum

A

It occurs in 2% of the population, it is 2 feet from the ileocaecal valve, it is 2 inches long

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23
Q

How does Meckel’s diverticulum present

A

Can be asymptomatic
Can have pain which mimics appendicitis
Rectal bleeding
Intestinal obstruction - either due to omphalomesenteric band, volvulus or intussusception

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24
Q

How is Meckel;s diverticulum diagnosed

A

If child is stable- Meckel’s scan (99m technetium pertechnetate scan )
If acute then CT imaging or intra-operative diagnostic laparoscopy may be used.
Can also do a mesenteric angiography

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25
Q

How is Meckel’s diverticulum treated?

A

Surgery - removal of the narrow neck

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26
Q

Why does Meckel’s diverticulum cause symptoms?

A

The diverticulum can have ectopic gastric mucosa which secretes acid and can cause ulceration and irritation- this is what causes bleeding.
IT can also act as a lead point for intussusception

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27
Q

What is the vitellointestinal duct and when does it normally disappear

A

It usually connects the yolk sac with the gut but disappears at about 6 weeks gestation

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28
Q

What is biliary atresia?

A

A congenital condition where a section of the bile duct is either narrowed or absent.

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29
Q

Pathophysiology of biliary atresia

A

The narrowed/absent bile duct leads to cholestasis and conjugated bilirubin cannot be excreted
Instead it enters the blood stream and causes obstructive jaundice

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30
Q

Presentation of biliary atresia

A

Significant prolonged jaundice (more than 14 days in term babies and 21 in premature)
Dark stools and pale urine
Failure to thrive, hepatosplenomegaly, ascites etc

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31
Q

Differentials of biliary atresia

A

Extra-hepatic biliary obstruction, hepatic viral infections, alpha-1-anti trypsin deficiency, cystic fibrosis

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32
Q

Diagnosis of biliary atresia

A

Total and direct or conjugated bilirubin levels - conjugated will be abnormally high
LFTs
USS
Percutaneous liver biopsy

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33
Q

Treatment of biliary atresia

A

Surgical intervention - hepatoportoenterostomy
If fails- liver transplant
Consisted ursodeoxycholic acid for jaundice

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34
Q

Complication of biliary atresia

A

Progressive liver disease
Cirrhosis and eventual HCC

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35
Q

What is true regarding jaundice within the first 24 hours of birth

A

It is always pathological - consider rhesus haemolytic disease

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36
Q

How does breast milk jaundice present?

A

Presents 48 hours to 14 days

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37
Q

When does malformation usually occur

A

Neonates in the first 30 days of life

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38
Q

what is the name of threadworms

A

enterobius vermicularis

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39
Q

how do threadworms presetn

A

perianal itching, particularly a tnight
may have vulval symptoms in girls

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40
Q

What is the treatment of malrotation

A

Ladd’s procedure

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41
Q

what is the initial management of hirschprung’s disease

A

rectal washouts and bowel irrigation

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42
Q

passage of meconium after what time is red flag?

A

48 hours

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43
Q

How does the treatment of gastroschisis and exommphalos differ?

A

gastroschisis needs immediate fixation
exommphalos needs gradual repair to prevent respiratoy complications

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44
Q

What is the first line laxative in children

A

osmotic laxative- movicol

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45
Q

what is necrotising enterocolitis?

A

a neonatal condition where the bowel becomes necrotic and is at risk of perforation

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46
Q

Who is affected by necrotising enterocolitis

A

mainly premature infants- usually seen in the first few weeks of life

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47
Q

RF for necrotising enterocolitis

A

maternal factors- illicit drug use, infection, HIV
Fetal factors- prematurity and low birth weight, congenital abnormality
Birth factors- low flow and low perfusion events
neonatal care- respiratory support, assisted ventilation
Sepsis

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48
Q

How does necrotising enterocolitis present?

A

feed intolerance
vomiting- may be bile stained
distended abdomen - may have visible bowel loops
bloody stool
absent bowel sounds
shock

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49
Q

Gold standard investigation for necrotising enterocolitis

A

X ray -
loops of distended bowel
bowel wall oedema
intramural gas- pneumatosis intestinalis
gas in the portal venous tract
air under the diaphragm if the bowel has perforated- pneumoperitoneum

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50
Q

What is the football sign for NEC

A

air outlining the falciform ligament

51
Q

What is the Rigler sign

A

air both inside and outside the bowel wall

52
Q

How is NEC treated?

A

stop oral feeding and give TPN and IV fluids
Give broad spectrum antibiotics (triple therapy for 10-14 days)
NG tube - used to drain fluid and gas from the stomach
Urgent surgery to remove dead bowel and insert a stoma

53
Q

Complications of necrotising enterocolitis

A

perforation
sepsis
death
strictures
abscess formation
recurrence
long term stoma
short bowel syndrome post surgery

54
Q

what is respiratory distress syndrome?

A

a condition commonly affecting neonates caused by inadequate surfactant production in the lungs

55
Q

RF of respiratory distress syndrome

A

premature infants
male
infants delivered by caesarean
hypothermia
perinatal asphyxia
maternal diabetes
family history of RDS

56
Q

what is a hernia?

A

a protrusion of an organ or fascia of an organ through the wall of the cavity that it normally occupies

57
Q

What two types of hernias are common in childen

A

inguinal and umbilical hernias

58
Q

What two types of inguinal hernias are there?

A

indirect and direct

59
Q

Explain an indirect inguinal hernia

A

the bowel herniates through the inguinal canal
Occurs due to the processus vaginalis not obliterating - this is normally a pouch of peritoneum allowing the testes to descend into the scrotum and should be obliterated after descent

60
Q

explain a direct inguinal hernia

A

occurs due to a weakness in the abdominal wall at Hesselbach’s triangle
Allows the hernia to protrude directly through the abdominal wall

61
Q

How can you differentiate an indirect and direct hernia

A

when an indirect hernia is reduced and pressure is applied to the deep inguinal ring the hernia remains reduced

62
Q

What 3 complications can occur to a hernia

A

incarceration, obstruction and strangulation

63
Q

what is incarceration of a hernia

A

occurs when a hernia becomes irreducible- the bowel is trapped in the herniated position

64
Q

what is strangulation of a hernia

A

a hernia is non-reducible and the base of the hernia becomes so tight that it cuts of the blood supply and causes ischaemia

65
Q

what is a congential diaphragmatic hernia

A

herniation of the abdominal viscera into the chest cavity due to incomplete formation of the diaphragm

results in pulmonary hypoplasia and hypertension

66
Q

How does a congenital diaphragmatic hernia present?

A

respiratory distress
displaced apex beat
bowel sounds in chest auscultation

67
Q

When should hernias be repaired in children

A

if presenting in the first few months of life they should have immediate surgery as high risk of strangulation
if over 1 then surgery can be elective

68
Q

RF for cows milk protein allergy

A

personal history of atopy
family history of atopy
existing food allergy
family history of food allergy
male

69
Q

what two types of cows milk protein allergy are there

A

IgE mediated and non-IgE mediated

70
Q

pathophysiology of IgE mediated CMPA

A

type I hypersensitivity reaction - T helper cells stimulate B cells to produce IgE to the cows milk proteins

71
Q

pathophysiology of non IgE mediated CMPA

A

T cell activation against the proteins

72
Q

How does IgE mediated CMPA and non-IgE mediated

A

manifests within 2 hours whereas non IgE is typically 2-72 hours
Non-IgE tends to have faster resolution

IgE usually resolves by 5 years, non-IgE does by 3

73
Q

How does cows milk protein allergy present?

A

GI symptoms:
- diarrhoea
- colicky abdo pain
- vomiting, regurgitation
- oral pruritis
non IgE may have blood or mucous in the stool, constipation, faltering growth

skin reactions:
- pruritis
- erythema
- acute urticaria
- acute angio-oedema

74
Q

How is cows milk protein diagnosed?

A

skin prick testing/ patch testing
total IgE and specific IgE for cows milk protein

75
Q

first line treatment of formula fed infants with CMPA

A

extensively hydrolysed formula

76
Q

second line treatment for formula fed infants with CMPA

A

amino acid based formula

77
Q

first line treatment of breast fed infants with CMPA

A

continue breast feeding
mother to eliminate CMP from diet
MAy give mother calcium supplements

78
Q

what is kwashiorkor

A

oedematous malnutrition

79
Q

definitive investigation for biliary atresia

A

cholangiography

80
Q

What is another name for toddler’s diarrhoea

A

chronic non-specific diarrhoea

81
Q

How does toddlers diarrhoea present?

A

three or more loose stools per day
stools are often pale, smelly and have undigested vegetables in them
mild stomach pain

82
Q

what can contribute to toddlers diarrhoea

A

underlying coeliacs or CMPA
excessive ingestion fruit juice

83
Q

How can toddlers diarrhoea be managed

A

may increase fat content of meals- drinking full fat milk
cut out fruit juice

84
Q

What criteria is used to define infantile colic

A

the rome IV criteria

85
Q

What makes up the rome VI criteria

A
  • the infant is less than 5 when the symptoms start and stop
  • there are prolonged and recurrent episodes of infant crying, fussing, irritability without an obvious cause that cannot be resolved or prevented by the care giver
  • there is not evidence of faltering growth, illness or fever
86
Q

What are some theorised underlying mechanisms of colic

A
  • abnormal gastric motility and pain signals from sensitized pathways in the gut viscera
  • excess gas production
  • possible gut inflammation mediated by the microbiome-gut-brain axis
87
Q

what psychosocial factors may contribute to colic

A

family tension
parental anxiety or depression
overstimulation of the infants
cigarette exposure

88
Q

How does colic present?

A

uncontrollable crying in an otherwise healthy infant
drawing knees up to the chest or arching back when crying
clenching fists

89
Q

management of infantile colic

A

advise on soothing methods- holding baby, reducing environmental noise, gentle motion, white noise, bathing

encourage parental wellbeing

Do not recommend simeticone drops, lactase drops, maternal diet modification, probiotic supplements or herbal supplements

90
Q

what is gastroenteritis

A

inflammation of the stomach to the intestines

91
Q

What is the most common cause of gastroenteritis in children

A

rotavirus

92
Q

what is the most common cause of gastroenteritis in adults

A

norovirus

93
Q

what are some bacterial causes of gastroenteritis

A

E.coli
Campylobacter jejuni
shigella
salmonella
bacillus cereus
yersinia enterocolitica
staph aureus

94
Q

how does e.coli gastroenteritis present

A

cramps, bloody diarrhoea, vomiting
can cause haemolytic uraemic syndrome (particularly if antibiotics are given)

95
Q

What is the pathophysiology of e.coli causing gastroenteritis

A

e.coli produces shiga toxin which causes the symptoms of gastroenteritis

96
Q

how does campylobacter jejuni present

A

flu like prodrome, abdo cramps, blood, vomiting

97
Q

what causes bacillus cereus gastroenteritis

A

food that has been inadequately cooked- typically cooked rice that is left out

98
Q

how does bacillus cereus present?

A

2 illnesses - firstly a vomiting illness within 5 hours which is caused by a toxin called cereulide)
then a few hours later another toxin causes watery diarrhoea

99
Q

what is the presentation of gastroenteritis caused by yersinia enetrocolitica

A

watery bloody diarrhoea, abdominal pain, lymphadenopathy
may get right sided abdo pain due to mesenteric lymphadenitis - presents like appendicitis

100
Q

how can you determine if children with gastroenteritis can be treated at home or in hospital

A

fluid challenge- give small amounts of fluid every 5-10 mins to see if they can hold fluid down.
If they cannot IV fluids may be needed

101
Q

Treatment of gastroenteritis in children

A

oral hydration solution (50ml/kg low osmolarity rehydration solution)
IV fluids if oral not tolerated
Antibiotics in certain organisms- campylobacter jejuni
stay of school until 48 hours after last symptom

102
Q

pathophysiology of appendicitis

A

obstruction of the appendix by lymphoid hyperplasia or faecoliths causes the appendix to become inflammed
it can progress to gangrene and rupture
if ruptured it can lead to peritonitis and inflammation of the peritoneal contents

103
Q

How does appendicitis present?

A

central abdominal pain that moves to settle in the right iliac fossa
tender mc-burnery’s point
nausea and vomiting
anorexia
guarding and rebound tenderness
percussion tenderness

104
Q

what are two key signs of appendicitis on examination

A

Rovsing’s sign= pain when quickly releasing pressure on the right iliac foss
Tender Mc Burney’s point

105
Q

What signs on examination suggest an appendicitis has ruputured

A

rebound tenderness, and percussion tenderness

106
Q

why might some children present atypically with appendicitis ?

A

young children might have a retrocaecal/pelvic appendix

107
Q

differentials for appendicitis

A

ectopic pregnancy
ovarian cyst

108
Q

what is shown on bloods in appendicitis

A

a neutrophil predominant leucocytosis

109
Q

what investigations may be done in the investigations of appendicitis

A

inflammatory markers raised
urine analysis- shows mild leukocytosis but no nitrates
CT may be done
USS - check for ovarian pathology in women

110
Q

what test must be done in females with suspected appendicitis

A

urine pregnancy test

111
Q

how is appendicitis managed?

A

appendicectomy- laparoscopic is first line
prophylactic IV antibiotics

112
Q

What is malrotation?

A

a congenital abnormality where the midgut undergoes abnormal rotation and fixation during embryogenesis.

Makes the bowel susceptible to volvulus (twisting of the bowel around the superior mesenteric artery) and duodenal compression (where the duodenum is compressed by peritoneal bands called Ladd bands)

113
Q

How does malrotation present?

A

can be asymptomatic if no volvulus
- bilious vomiting, often within the first few days of life
- feed intolerance
- abdo pain and distention
- bloody stools
- signs of shock

114
Q

How is malrotation diagnosed?

A

upper GI contrast studies (e.g. CT abdo with contrast)
USS may be used

115
Q

What is gastro-oesophageal reflux (GOR)?

A

the passage of gastric contents into the oesophagus.

It is a normal physiological event that can happen at any age and is often asymptomatic.

116
Q

What is gastro-oesophageal reflux disease?

A

GOR that causes symptoms severe enough to merit medical attention or cause associated symptoms

117
Q

Rf for GORD

A

cerebral palsy and other developmental disorders
preterm infants
bronchopulmonary dysplasia
surgery for oesophageal atresia or diaphragmatic hernia

118
Q

why is GORD increased in infants

A

they have a predominate liquid diet
they mainly lie horizontal
they have a short intra-abdominal length of the oesophagus
the oesophageal sphincter is immature so has inappropriate relaxation

119
Q

How does GORD present in infants?

A

regurgitation of feeds
excessive crying when feeding

120
Q

Complications of GORD in infants

A

-faltering growth
-oesophagitis - haematemesis, discomfort on feeding, heart burn, iron deficiency anaemia
-recurrent pulmonary aspiration
-dystonic neck posturing (sandifer syndrome)
-apparent life threatening events
-dental abnormalities
- recurrent otitis media

121
Q

How is GORD diagnosed

A

usually clinical diagnosis

may do further investigations:
- 24 hour pH impedance monitoring
- gastroscopy
- contrast studies to rule out anatomical abnormalities

122
Q

Management of uncomplicated GORD

A

smaller frequent feeds
head positioning at 30 degrees during feeding
thickening agests- carobel

123
Q

management of more severe, complicated GORD

A

acid suppression with hydrogen receptor antagonist (ranitidine) or PPI (omeprazole)

124
Q
A

3A (32 decks)

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