GI Flashcards
1
Q
Define GORD
What is the cause?
Which age is most affected?
A
- Involuntary passage of gastric contents into the oesophagus
- caused by relaxation of the lower oesophageal sphincter due to functional immaturity
- affects 0-12 month olds
2
Q
Which group of children is GORD most common in?
A
- cerebral palsy or other neurodevelopmental disorder
- preterm esp. with bronchopulmonary dysplasia
- Following surgery for oesophageal atresia or diaphragmatic hernia
3
Q
What are potential complications of GORD?
A
- Faltering growth
- Oesophagitis –> hematemesis, discomfort on feeding or heartburn, iron deficinecy anaemia
- recurrent pulmonary aspiration - recurrent pneumonia, cough, wheeze, apnoea
- dystonic posturing (sandifer syndrome)
- life threatening events
4
Q
How is GORD diagnosed and which investigations can be done?
A
- usually diagnosed clinically
- 24 hr oesophageal pH monitoring to quantify degree of reflux
- 24 hr impedance monitoring
- endoscopy with oesophageal biopsies
5
Q
What is the management of GORD?
uncomplicated
significant
and failure to respond?
A
- uncomplicated - reassure parents, add thickening agent to feed, smaller more frequent feeds
- significant - H2 receptor antagonist (ranitidine) or PPI (omeprazole)
- fails to respond - consider other diagnosis e.g cows milk protein allergy
unresponsive to medical - Nissen fundoplication
6
Q
What is the cause of pyloric stenosis in children?
A
hypertrophy of pyloric muscle causing gastric outlet obstruction
7
Q
Who does pyloric stenosis mostly
affect?
A
- babies 2-8 weeks
more common in:
- boys
- first borns
- could be familial history
8
Q
What are the features of pyloric stenosis?
A
- Vomiting, can be projectile
- peristaltic wave and palpable mass after feeding
- hunger and dehydration
- weight loss
- Hypocholaraemic metabolic alkalosis
- low plasma Na+, Low K+
9
Q
How do you diagnose Pyloric stenosis?
A
- Test feed - palpable mass RUQ, Gastric peristalsis
- if stomach over-distended with gas, empty with NG tube
- US - helpful to confirm diagnosis pre surgery
10
Q
How do you manage pyloric stenosis?
A
- IV fluids to correct electrolyte imbalance
2. Ramsted Pyloromyotomy - division of hypertrophied muscle down to mucosa
11
Q
What are the symptoms of acute appendicitis?
A
- anorexia
- vomiting
- Abdo pain - inititally central and colicky –> localizing to RIF (from localised peritoneal inflammation)
12
Q
What are the signs of acute appendicitis?
A
- Fever
- Abdo pain (worse on movement)
- persistent tenderness and guarding of RIF (McBurneys point)
13
Q
What is intussusception?
Where is the commonest site?
Which age does it affect the most?
A
- invagination of proximal bowel into a distal segment.
- most common is ileum into caecum at the illeocaecal valve
- 3 months - 2 years
14
Q
What are some complications of intussusception?
A
- stretching and constriction of mesentry
leading to venous obstruction leading to engorgement and bleeding from bowel mucosa - fluid loss
- bowel perforation
- peritonitis
- gut necrosis
15
Q
What are the symptoms of intussusception?
A
- paroxysmal, severe colicky pain with pallor- during pain episode child is pale, draws up legs
- Lethargy between episodes
- refuse feeds
- vomiting- bile stained depending on site of intussusception
16
Q
What are the signs of intussusception?
A
- Sausage-shaped mass- palpable
- Characteristic passage of redcurrant jelly stool comprising blood-stained mucus- may be seen on rectal exam or late sign
- Abdominal distention or shock
17
Q
What are the investigations of intussusception and what do you see in each?
A
- X-ray abdomen- distended small bowel and absence of gas in the distal colon or rectum
- Abdominal USS- confirms diagnosis (target/doughnut sign)
18
Q
What is the management for intussusception?
A
- IV fluid resuscitation immediately, as there is often pooling of fluid leading to hypovolaemic shock
- Reduction of intussusception by recta air insufflation – risk of bowel perforation
- Remaining 25% that are unsuccessful or where peritonitis present then –> operative reduction
19
Q
What is Meckels Diverticulum?
How does it present?
What is the investigation and what does it show?
What is the treatment?
A
- congenital defect, ileal region, left over from umbilical cord
- usually asymptomatic, can present with
- acute Hb decrease,
- bleeding which can be life threatening - characteristically neither bright or malaena,
- intussuception, volvulus
- technetium scan - shows uptake by gastric mucosa
- Tx = surgical resection
20
Q
What are the two types of malrotation?
When does it usually present?
What can happen in volvulus?
A
- obstruction or obstruction with compromised blood supply
- tends to present first 1-3 days of life but can present at any time
- mesentery not fixed - rotation can cause superior mesenteric arterial blood supply to small intestine and proximal large intestine to be compromised –> infarction
21
Q
What is the presentation of volvulus?
What is the investigation?
What is the treatment?
A
- billous dark green vomit, abdo pain, tenderness from peritonitis or ischaemic bowel
- urgent gastro contrast study (indicated if billious vomiting)
- treatment - urgent surgical correction
22
Q
When does cows milk allergy typicall occur and in children being fed what?
Which immune reactions are at play?
Which type of cows milk allergy is each immune reaction associated with?
A
- first three months of life, usually in formula fed infants
- Immediate (IgE mediated) and delayed (non-IgE mediated)
- Immediate - Cows milk protein allergy, delayed - cows milk protein intolerance
23
Q
What symptoms do children with cows milk allergy present with?
How is the diagnosis made?
How do you manage cows milk protein allergy?
when do kids improve?
A
- regurgitation and vomiting
- diarrhoea
- urticaria, atopic ecxma
- colic symptoms: instability, crying
- wheeze, chronic cough
- rarely: angioedema, anaphylaxis
Diagnosis:
- often clinical - challenge test/imrpovement on removal of cows milk
- skin prick/patch test
- total IgE and specific IgE (RAST) for cows milk protein
Management:
- forumala fed - give extensive hydrolysed formula milk if not working, try amino acid based milk
- breastfed - cut out cows milk from maternal diet, give calcium supplements. not working, given extensive hydrolysed formula milk
- CMPA - 50% recover by age 5
- CMPI - usually by age 3
24
Q
What are the causes of gastroenteritis and how do they present?
A
- Bacterial causes
- presence of blood in stools, campylobacter jejuni most common
- shigella and salmonella: dysenteric infection, blood and pus in stool, pain and tenasmus, high temps
- cholera and enterotoxigenic E.coli : profuse rapidly dehydrating diarrhoea
Protozoan: Giardia and cryptosporidium
Giardiasis: protzoan have cystic form in stoolm motile trophozites in small intesntine, villous atrophy with IgA deficiency, diagnosis by cysts in stool. Treat - 3/6 high dose metroniadazole
25
How does gastroenteritis typically present, what can it follow, and what can it lead to in severe cases?
In gastroenteritis: sudden change to loose or watery stool with vomiting
- can be following contact with diarrhoea, recent travel
- dehydration can lead to shock
26
Who is at increased risk of dehydration in gastroenteritis?
- infants >6 months due to greater surface area to weight ratio, those with low birthweight
- >6 diarrhoeal stools in past 24 hrs
- >3/4 vomits in last 24 hrs
- unable to tolerate extra fluids
- malnutritioned
27
How do you assess dehydration in gastroenteritis?
most accurate = degree of water loss
• No clinically detectable dehydration (usually <5% loss of body weight)
• Clinical dehydration (5-10% loss of body weight)
• Shock (>10% loss of body weight)
28
Define isonatraemic and hyponatraemic dehydration and what is the risk in the latter?
1. Isonatraemic: loss of water and sodium is proportionall
2. Hyponatraemic: when children with diarrhoea drink lots of water, greater net loss of sodium. leads to shift of water from extracellular to intracellular compartments.
- risk of increased brain volume leading to seizures
29
What is hypernatraemic dehydration and what are the
- causes
- presentation
- risk
- what else occurs?
- where water loss exceeds relative sodium loss and concentration increases
- caused by insensible water losses - high fever, hot dry environments or from profuse low sodium diarrhoea
- fluid shifts from intracellular space
- presentation: depression of fontanelle, sunken eyes, reduced skin elasticity
- risk of water beinf drawn out of brain leading to
- cerebral shrinkage,
- jittery movements
- increased muscle tone, hyperreflxia
- altered consciousness
- seizures
- multiple cerebral haemorrhages
- transient hyperglycaemia, self correcting.
30
Investigations for Gastroenteritis
Management
- normal
- other meds?
- abx?
Stool culture if septic/blood mucus in stool/immunocompromised
Plasma electrolyes, urea, creatinine and glucose
Management
- oral rehydration therapy if clincially dehydrates
- IV only if shock or deterioration or persistent vomiting
- avoid fruit juices/carbonated drinks
- in hypernatraemic dehydration: slow, ideally oral but IV at least over 48hr due to risk of rapid drop of plasma osmolality leading to cerebral odeama - seizures
- no medications for vomiting and diarrhoea
- abx only if septic, spread of infection, salmonella under 6 months, immunocompromised/malnutritioned
- increase nutritional intake
31
What is IBS?
| the presentation of IBS?
- Altered GI motility and abnormal sensation of intra-abdominal events
Presentation
- non specific abdo pain - often periumbilical, may be improved on defecation
- bloating
- explosive loose or mucousy stool
- feeling of incomplete defecation
- constipation (often alternating with normal/loose stool)
32
What is Coeliac disease? where does ut occur, cause? what does it lead to>
What is the genetic association?
What does it lead to?
- gluten sensitivity enteropathy where gliadin component and other prolamines leads to immune response
- occurs in proximal small intestine mucosa
- leads to cell loss from villous top leading to flat mucosa
- Genetics: Class 2 Human leukocyte antigen (HLA) molecules DQ2* and DQ8
33
What are the risk factors of coeliac disease?
What is the presentation?
1. T1DM
2. Thyroid disease
3. Downs syndrome
4. Family Hx
5. Short stature
6. IgA deficiency
Presentation
- at 8-24 months on intro of wheat containing foods
- faltering growth
- abdo distension
- buttock wasting
- anaemia (iron and folate)
- abnormal stools
- general irritability
- dermatitis herpetiformis
- dental enamel defects
34
What investigations for coeliac disease? what do they show
What is the criteria?
What is the management?
what are the risks if non adherent
* Positive serology- anti-tTG, EMA (endomysial antibodies)
* Mucosal changes (increased intraepithelial lymphocytes, villous atrophy, crypt hypertrophy) on small intestinal biopsy. Resolution of symptoms and catch-up growth upon gluten withdrawal
criteria-
o Characteristic histology (Marsh type III a - c)
o Positive serology
o Symptomatic response to gluten exclusion
o Resolution of antibodies
Management
• All products containing wheat, rye, barley removed from diet
• Dietician supervision
• Gluten challenge later on to show continuing susceptibility
• Risk of osteopenia, osteoporosis, bowel malignancy (small bowel lymphoma) if non-adherent to diet
35
What is chronic non specific diarrhoea/toddlers diarrhoea?
when does it present? when does it resolve?
what are possible causes?
How does it present?
- persistent loose stool in preschool children
- onset 6-20 months, usually resolves by age 3
- can be due to excessive fruit juice
- can be temporary cows milk allergy after gastroenteritis
```
Presentation
• *Normal growth*
• 3-4 stools per day
• 1st stool of day is large, others small
• *Stools contain mucus + undigested food*
• Diarrhoea recurrent or persistent
• No relation to diet
• F.H of functional bowel symptoms
```
36
Which parts of the GI tract can Crohns affect?
is it more or less common than ulcerative colitis?
anywhere from mouth to anus
more common than UC
37
How does Crohns present?
- growth failure
- abdominal pain, diarrhoea, weight loss
- fever, lethargy
- extraintestinal - oral lesions or perianal skin tags, uveitis, arthralgia, erythema nodosum
38
How do you diagnose Crohns disease?
| What is the hallmark?
- Bloods - raised ESR/CRP, iron deficiency anaemia, low serum albumin
- Endoscopic and histological findings on biopsy
- hallmark : non-caseating epitheliod cell granulomata
- stricture and fistula of the bowel may develop
39
How do you manage Crohns disease?
1. induce remission with nutritional therapy (replace diet with whole protein modular feeds - polymeric diet) for 6-8 weeks. If uneffective, use systemic steroids
2. Maintain remission - immunosuppressant medication e.g Azathioprine, methotrexate
3. If conventional treatment fails - TNF agents e.g infliximab, adalimumab
4. Long term supplemental enteral nutrition - NG, gastrostomy
5. surgery for complications - obstruction, ffistula, abscess formation, localised diseases unresponsive to medical treatment
40
Which part of the GI tract does UC affect?
How does it present?
Mucosa of the colon alone
Presentation
1. diarrhoea,
2. rectal bleeding
3. colicky abdominal pain
4. weight loss, growth faltering
5. extraintestinal - erythema nodosum, arthritis
41
How do you diagnose UC? What are the findings?
- endoscopy with biopsy
- --> histological findings: mucosal inflammation, crypt damage (loss, abscesses, distortion) and ulceration
- confluent colitis extending from rectum proximally
- 90% have pancolitis
42
How do you manage Ulcerative Colitis?
mild
disease confined to rectum and sigmoid colon
more extensive/aggressive
Mild Disease
- aminosalicylates e.g Mesalazine: for induction and maintenance
Disease confined to rectum and sigmoid colon: topical steroids
More extensive or aggressive: systemic steroids for acute exacerbations + Azathioprine to maintain remission or in combination with low dose corticosteroids
resistant disease - biological : infliximab or ciclosporins
Severe fulminating disease complicated by toxic megacolon: colectomy with ileostomy or ileorectal pouch
43
What does UC increase risk of as an adult and what has to be done routinely?
- increases risk of adenocarcinoma of colon
| - reiagnosisgular colonscopic screening is performed after 10 years from d
44
What is normal bowel motions for a newborn? for a 1 year old? for a breastfed baby?
- 4 bm per day for newborn
- reduces to 2 per day by 1 year
- breasted infants may have none for several days
45
What is the definition of constipation?
- infrequent passage of dry, hardened faeces often accompanied by straining or pain and bleeding associated with hardened stool
- may be abdo pain
46
What are the possible precipitating factors of constipation and causes in older children?
constipation could be precipitated by
- dehydration/reduced fluid intake
- anal fissure causing pain
older children
- problems in toilet training
- refusal/anxiety about opening bowels at school or in unfamiliar toilets
47
What do each of the following red flag signs suggest could be the cause of contipation?
1. failure to pass meconium within 24hrs of life
2. Faltering growth
3. Gross abdominal distention
4. Abnormal lower limb neurology or deformity e.g talips (clubfoot) or secondary urinary incontinence
5. sacral dimple above natal cleft, over the spine - naevus, hairy patch, central pit
6. Perinal fistula, abscesses, fissures
1. Hirschsprung disease
2. hypothyroidism, coeliac disease,
3. Hirschsprung disease or other gastrointetstinal dysmotility
4. Lumbosacral pathology
5. Spina Bifida Occulta
6. Crohns disease
48
What may happen in long standing constipation?
- the rectum may become over distended leading loss of feeling of urge to defecate,
- involuntary soiling may occur as contractions of the full rectum inhibit the internal sphincter leading to overflow
49
Management of overflow diarrhoea ?
1. initital aim is disimpaction - regimen of stool softeners (macrogel laxative e.g polyethylene glycol + electrolytes).
- escalating dose regiment over 1-2 weeks
- if unsuccesful - stimulant laxatives can be used
2. maintenance using macrogel laxative
50
What is the cause of Hirschsprungs disease?
| where is the majority confined to?
- absence of ganglionic cells in myenteric and submucosal plexus in part of the large bowel resulting in narrow contracted segment
- 75% confined to rectosigmoid
51
What is the presentation of Hirschsprungs disease?
1. neonatal obstruction leading to failure to pass meconium in first 24 hours of life
2. abdominal distension
3. bile stained vomit
4. rectal exam- narrow segment and removal = gush of liquid and flatus
5. later in life constipation, abdo distension with no soiling
6. growth failure may be present
52
How is Hirschsprungs disease diagnosed?
- suction rectal biopsy (absence of ganglion cells)
53
What is the management of Hirschprungs disease?
surgical - initial colostomy followed by anastomising normally innervated bowel to the anus
