Paediatric Gastro Flashcards

(135 cards)

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
How is Meckel’s diverticulum treated?
Surgery - removal of the narrow neck
26
Why does Meckel’s diverticulum cause symptoms?
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
27
What is the vitellointestinal duct and when does it normally disappear
It usually connects the yolk sac with the gut but disappears at about 6 weeks gestation
28
What is biliary atresia?
A congenital condition where a section of the bile duct is either narrowed or absent.
29
Pathophysiology of biliary atresia
The narrowed/absent bile duct leads to cholestasis and conjugated bilirubin cannot be excreted Instead it enters the blood stream and causes obstructive jaundice
30
Presentation of biliary atresia
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
31
Differentials of biliary atresia
Extra-hepatic biliary obstruction, hepatic viral infections, alpha-1-anti trypsin deficiency, cystic fibrosis
32
Diagnosis of biliary atresia
Total and direct or conjugated bilirubin levels - conjugated will be abnormally high LFTs USS Percutaneous liver biopsy
33
Treatment of biliary atresia
Surgical intervention - hepatoportoenterostomy If fails- liver transplant Consisted ursodeoxycholic acid for jaundice
34
Complication of biliary atresia
Progressive liver disease Cirrhosis and eventual HCC
35
What is true regarding jaundice within the first 24 hours of birth
It is always pathological - consider rhesus haemolytic disease
36
How does breast milk jaundice present?
Presents 48 hours to 14 days
37
When does malformation usually occur
Neonates in the first 30 days of life
38
what is the name of threadworms
enterobius vermicularis
39
how do threadworms presetn
perianal itching, particularly a tnight may have vulval symptoms in girls
40
What is the treatment of malrotation
Ladd's procedure
41
what is the initial management of hirschprung's disease
rectal washouts and bowel irrigation
42
passage of meconium after what time is red flag?
48 hours
43
How does the treatment of gastroschisis and exommphalos differ?
gastroschisis needs immediate fixation exommphalos needs gradual repair to prevent respiratoy complications
44
What is the first line laxative in children
osmotic laxative- movicol
45
what is necrotising enterocolitis?
a neonatal condition where the bowel becomes necrotic and is at risk of perforation
46
Who is affected by necrotising enterocolitis
mainly premature infants- usually seen in the first few weeks of life
47
RF for necrotising enterocolitis
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
48
How does necrotising enterocolitis present?
feed intolerance vomiting- may be bile stained distended abdomen - may have visible bowel loops bloody stool absent bowel sounds shock
49
Gold standard investigation for necrotising enterocolitis
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
50
What is the football sign for NEC
air outlining the falciform ligament
51
What is the Rigler sign
air both inside and outside the bowel wall
52
How is NEC treated?
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
Complications of necrotising enterocolitis
perforation sepsis death strictures abscess formation recurrence long term stoma short bowel syndrome post surgery
54
what is respiratory distress syndrome?
a condition commonly affecting neonates caused by inadequate surfactant production in the lungs
55
RF of respiratory distress syndrome
premature infants male infants delivered by caesarean hypothermia perinatal asphyxia maternal diabetes family history of RDS
56
what is a hernia?
a protrusion of an organ or fascia of an organ through the wall of the cavity that it normally occupies
57
What two types of hernias are common in childen
inguinal and umbilical hernias
58
What two types of inguinal hernias are there?
indirect and direct
59
Explain an indirect inguinal hernia
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
explain a direct inguinal hernia
occurs due to a weakness in the abdominal wall at Hesselbach's triangle Allows the hernia to protrude directly through the abdominal wall
61
How can you differentiate an indirect and direct hernia
when an indirect hernia is reduced and pressure is applied to the deep inguinal ring the hernia remains reduced
62
What 3 complications can occur to a hernia
incarceration, obstruction and strangulation
63
what is incarceration of a hernia
occurs when a hernia becomes irreducible- the bowel is trapped in the herniated position
64
what is strangulation of a hernia
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
what is a congential diaphragmatic hernia
herniation of the abdominal viscera into the chest cavity due to incomplete formation of the diaphragm results in pulmonary hypoplasia and hypertension
66
How does a congenital diaphragmatic hernia present?
respiratory distress displaced apex beat bowel sounds in chest auscultation
67
When should hernias be repaired in children
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
RF for cows milk protein allergy
personal history of atopy family history of atopy existing food allergy family history of food allergy male
69
what two types of cows milk protein allergy are there
IgE mediated and non-IgE mediated
70
pathophysiology of IgE mediated CMPA
type I hypersensitivity reaction - T helper cells stimulate B cells to produce IgE to the cows milk proteins
71
pathophysiology of non IgE mediated CMPA
T cell activation against the proteins
72
How does IgE mediated CMPA and non-IgE mediated
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
How does cows milk protein allergy present?
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
How is cows milk protein diagnosed?
skin prick testing/ patch testing total IgE and specific IgE for cows milk protein
75
first line treatment of formula fed infants with CMPA
extensively hydrolysed formula
76
second line treatment for formula fed infants with CMPA
amino acid based formula
77
first line treatment of breast fed infants with CMPA
continue breast feeding mother to eliminate CMP from diet MAy give mother calcium supplements
78
what is kwashiorkor
oedematous malnutrition
79
definitive investigation for biliary atresia
cholangiography
80
What is another name for toddler's diarrhoea
chronic non-specific diarrhoea
81
How does toddlers diarrhoea present?
three or more loose stools per day stools are often pale, smelly and have undigested vegetables in them mild stomach pain
82
what can contribute to toddlers diarrhoea
underlying coeliacs or CMPA excessive ingestion fruit juice
83
How can toddlers diarrhoea be managed
may increase fat content of meals- drinking full fat milk cut out fruit juice
84
What criteria is used to define infantile colic
the rome IV criteria
85
What makes up the rome VI criteria
- 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
What are some theorised underlying mechanisms of colic
- 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
what psychosocial factors may contribute to colic
family tension parental anxiety or depression overstimulation of the infants cigarette exposure
88
How does colic present?
uncontrollable crying in an otherwise healthy infant drawing knees up to the chest or arching back when crying clenching fists
89
management of infantile colic
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
what is gastroenteritis
inflammation of the stomach to the intestines
91
What is the most common cause of gastroenteritis in children
rotavirus
92
what is the most common cause of gastroenteritis in adults
norovirus
93
what are some bacterial causes of gastroenteritis
E.coli Campylobacter jejuni shigella salmonella bacillus cereus yersinia enterocolitica staph aureus
94
how does e.coli gastroenteritis present
cramps, bloody diarrhoea, vomiting can cause haemolytic uraemic syndrome (particularly if antibiotics are given)
95
What is the pathophysiology of e.coli causing gastroenteritis
e.coli produces shiga toxin which causes the symptoms of gastroenteritis
96
how does campylobacter jejuni present
flu like prodrome, abdo cramps, blood, vomiting
97
what causes bacillus cereus gastroenteritis
food that has been inadequately cooked- typically cooked rice that is left out
98
how does bacillus cereus present?
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
what is the presentation of gastroenteritis caused by yersinia enetrocolitica
watery bloody diarrhoea, abdominal pain, lymphadenopathy may get right sided abdo pain due to mesenteric lymphadenitis - presents like appendicitis
100
how can you determine if children with gastroenteritis can be treated at home or in hospital
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
Treatment of gastroenteritis in children
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
pathophysiology of appendicitis
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
How does appendicitis present?
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
what are two key signs of appendicitis on examination
Rovsing's sign= pain when quickly releasing pressure on the right iliac foss Tender Mc Burney's point
105
What signs on examination suggest an appendicitis has ruputured
rebound tenderness, and percussion tenderness
106
why might some children present atypically with appendicitis ?
young children might have a retrocaecal/pelvic appendix
107
differentials for appendicitis
ectopic pregnancy ovarian cyst
108
what is shown on bloods in appendicitis
a neutrophil predominant leucocytosis
109
what investigations may be done in the investigations of appendicitis
inflammatory markers raised urine analysis- shows mild leukocytosis but no nitrates CT may be done USS - check for ovarian pathology in women
110
what test must be done in females with suspected appendicitis
urine pregnancy test
111
how is appendicitis managed?
appendicectomy- laparoscopic is first line prophylactic IV antibiotics
112
What is malrotation?
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
How does malrotation present?
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
How is malrotation diagnosed?
upper GI contrast studies (e.g. CT abdo with contrast) USS may be used
115
What is gastro-oesophageal reflux (GOR)?
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
What is gastro-oesophageal reflux disease?
GOR that causes symptoms severe enough to merit medical attention or cause associated symptoms
117
Rf for GORD
cerebral palsy and other developmental disorders preterm infants bronchopulmonary dysplasia surgery for oesophageal atresia or diaphragmatic hernia
118
why is GORD increased in infants
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
How does GORD present in infants?
regurgitation of feeds excessive crying when feeding
120
Complications of GORD in infants
-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
How is GORD diagnosed
usually clinical diagnosis may do further investigations: - 24 hour pH impedance monitoring - gastroscopy - contrast studies to rule out anatomical abnormalities
122
Management of uncomplicated GORD
smaller frequent feeds head positioning at 30 degrees during feeding thickening agests- carobel
123
management of more severe, complicated GORD
acid suppression with hydrogen receptor antagonist (ranitidine) or PPI (omeprazole)
124
Describe inflammation in crohn's disease (6)
-mouth to anus -transmural granulomatous inflammation -deep ulcers and skip lesions-> leads to cobbelstone appearance -increased goblet cells -rosethorn ulcers -strictures may give Kantor sign on imaging
125
describe the inflammation of ulcerative collitis
-rectum to ileocaecal valve - continuous superficial inflammation - crypt abscesses and goblet cell depletion - imaging will show loss of haustrations, pseudopolyps (superficial ulcers) and a narrowed colon (drainpipe colon)
126
how is crohn's disease treated?
induce remission= prednisolone maintain remission= azathioprine or mercaptopurine
127
how is ulcerative colitis treated>
induce remission= either rectal or oral aminosalycate (mesalazine) maintain remission: either aminosalycate or azathioprine/mercaptopurine
128
how does the inflammation of coeliac disease present?
villous atrophy, crypt hyperplasia, increases intraepithelial lymphocytes and lymphocyte infiltration into the lamina propria
129
How might cows milk protein allergy present?
Skin reactions- pruritis, erythema, acute urticaria and acute angio-oedma GI symptoms- colicky abdominal pain, diarrhoea, regurgitation and vomiting, oral pruritis may also have wheeze and chronic cough
130
List the 5 categories of the causes of failrue to thrive
- inadequate intake - inadequate retention - malaborbtion - too much used up - abnormal central control of growth and appetite
131
give some causes of inaequate intake
- ineffective sucking of breastfed infant - ineffective bottle feeding - insufficient food or incorrect food - physical disorders : cleft palate, cerebral palsy, - lack of maternal infant interaction - maternal depression - child abuse
132
causes of inadequate food retention
- vomiting (pyloric stenosis) - severe GORD
133
causes of poor absorption in newborns
biliary atresia IBD cystic fibrosis cows milk protein allergy coeliac disease short gut syndrome cholestatic liver disease NEC
134
causes of increased requirement of nutrition in newborns that lead to failure to thrive
congenital infections chronic lung disease of prematurity congenital heart disease thyrotoxicosis asthma malignancy cystic fibrosis
135