Gastro Flashcards

1
Q

Define coeliac disease

A

Primarily digestive disorder
Most common genetically related food intolerance
Life-long gluten-sensitive autoimmune disease of small intestine

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2
Q

Epidemiology of coeliac disease

A

Approx 1%

Often seen more in diabetes, autoimmune disorders and relative of Coeliac disease individuals

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3
Q

Pathophysiology of coeliac disease

A

Combination of immunological responses to an environmental factor (gliadin) and genetic factors (HLA-DQ2/DQ8)
Body’s immune system overreacts to in food
- damages villi of small intestine
T-cell mediated immune disorder
- anti-gluten CD4 T cell response
- anti-gluten antibodies
- autoantibodies against tissue transglutaminase
Epithelial cell destruction and villous atrophy

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4
Q

Which types of cereal is gluten found in?

A

Wheat
Barley
Rye

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5
Q

Presentation of coeliac disease

A

Classical form
- 9-24 months
- malabsorption, failure to thrive, weight loss, loose stool, steatorrhea, anorexia, abdo pain, abdo distention, muscle water
- histology reveals crypt hyperplasia and villous atrophy
Atypical form
- no intestinal symptoms a/w extra-intestinal symptoms
- osteoporosis, peripheral neuropathy, anaemia and infertility
- positive coeliac serology, limited abnormalities of small intestine
Latent form
- presence of predisposing gene
- normal intestinal mucosa and possible positive serology
Silent form
- damaged small intestinal mucosa
- positive serology but no clinical symptoms
Potential
- normal mucosal morphology, positive autoimmune serology and asymptomatic
- genetically predisposed to develop at some point

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6
Q

Extra-intestinal symptoms of coeliac disease

A
Dermatitis herpetiformis
Dental enamel hypoplasia
Osteoporosis
Delayed puberty
Short stature
Iron-deficient anemia - resistant to oral Fe
Liver and biliary tract disease
Arthritis
Peripheral neuropathy, epilepsy, ataxia
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7
Q

Differential diagnosis of coeliac disease

A
Tropical sprue
Cystic fibrosis
IBD
Post-gastroenteritis
Autoimmune enteropathy
Eosinophilic enteritis
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8
Q

Investigations for coeliac disease

A

Serology
- test total immunoglobulin A (IgA) and IgA tissue transglutaminase (tTG)
- if IgA tTG weakly positive then use IgA endomysial antibodies
- must have gluten in diet at period of testing and for at least 6 weeks before
Biopsy
- duodenal biopsy gold standard to diagnose
- ensure findings improved on gluten free diet or diagnose different GI disorder

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9
Q

Who should be offered serological testing for coeliac disease

A

Children with
- persistent unexplained abdo or GI symptoms
- faltering growth
- prolonged fatigue
unexpected weight loss
- severe or persistent mouth ulcers
- unexplained iron, vit B12 or folate deficiency
- type 1 diabetes
- autoimmune thyroid disease
- IBS
First degree relatives of people with coeliac disease

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10
Q

Marsh classification of coeliac disease biopsy

A

Stage 0 = normal
Stage 1 = increased intraepithelial lymphocytes
Stage 2 = increased inflammatory cells and crypt hyperplasia
Stage 3 = all of the above plus mild to complete villous atrophy

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11
Q

Management of coeliac disease

A

Lifelong diet free of gluten
Supplementation if obvious malabsorption
Annual follow up to check symptoms, diet compliance, development, growth and long term complications

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12
Q

Complications of coeliac disease

A

Anaemia
Osteopenia/osteoporosis
Refractory coeliac disease - symptoms persist despite diet
Malignancy
Fertility problems / adverse events during pregnancy
Depression/anxiety

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13
Q

Define cow’s milk protein allergy

A

Immune-mediated allergic response to naturally-occuring milk proteins casein and whey

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14
Q

Epidemiology of cow’s milk protein allergy

A

Most common childhood food allergies

7% of formula/mixed-fed infants

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15
Q

Pathophysiology of cow’s milk protein allergy

A

IgE-mediated
- Type-1 hypersensitivity reaction
- CD4+ TH2 stimulate B cells to produce IgE antibodies against cow’s mild protein
- trigger release of histamine and other cytokines from mast cells and basophils
Non-IgE-mediated
- involves T cell activation against cow’s milk protein

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16
Q

Risk factors for cow’s milk protein allergy

A

Personal hx of atopy
Family hx of atopy
Exclusive breastfeeding is possible protective factros

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17
Q

Clinical features of IgE-mediated cow’s milk protein allergy

A
Acute and rapid onset (2 hours post ingestion)
Skin reactions
- pruritus
- erythema
- acute urticaria
- acute angioedema
GI symptoms
- angioedema
- oral pruritus
- N+V
- colicky abdo pain
- diarrhoea
Resp symptoms
- lower - cough, chest tightness, wheezing or SOB
- upper - nasal itching, sneezing, rhinorrhoea or congestion
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18
Q

Clinical features of Non-IgE-mediated cow’s milk protein allergy

A
Non-acute and generally delayed
Skin reactions
- pruritus
- erythema
- atopic eczema
GI symptoms
- GORD
- loose or frequent stools
- blood / mucus in stool
- abdo pain
- infantile colic
- food refusal or aversion
- constipation
- perianal redness
- pallor and tiredness
- faltering growth
Lower resp tract symptoms
- cough
- chest tightness
- wheezing
- SOB
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19
Q

Features of an allergy focused history

A
Personal or family history of atopy
Diet and feeding hx of infant
Mother's diet if breastfed
Any previous management used for symptoms
Which milk/foods
Age of onset
Speed of onset following exposure
Duration
Severity and frequency of occurrence
Setting of reaction
Reproducibility of symptoms
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20
Q

Differential diagnosis of cow’s milk protein allergy

A
Food intolerance
Allergic reaction to other food/non-food allergens
Anatomical abnormalities such as Meckel's diverticulum
Chronic GI disease
- GORD
- coeliac disease
- IBD
- constipation
- gastroenteritis
Pancreatic insufficiency
UTI
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21
Q

Investigations for cow’s milk protein allergy

A

Usually clinically diagnosed
Blood test looking for specific IgE antibodies - RAST
- low specificity resulting in false positives
Skin prick test

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22
Q

Refer for IgE antibody test for cow’s milk protein allergy

A

Faltering growth with symptoms
One or more acute systemic or severe delayed reactions
Confirmed IgE mediated food allergy with asthma
Persistent parental suspicion of a food allergy despite lack of clear hx
Clinical suspicion of multiple food allergies

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23
Q

Management of cow’s milk protein allergy

A

Avoidance of cow’s milk
- including from mother’s diet if breastfeeding
- elimination diet required for at least 6 months or until infant 9-12 months
- extensively hydrolysed formula - cheaper
- made from cow’s milk but casein and whey broken down into smaller peptides
- 90% of children ok
- amino acid formula - more expensive
- soy-based formulas not recommended in infants <6 months due to weak oestrogenic effects
Nutritional counselling and regular monitoring of growth

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24
Q

Complications of cow’s milk protein allergy

A
Malabsorption
Reduced intake
Chronic iron-deficiency anaemia
Faltering growth
Anaphylaxis - rare
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25
Q

Define GORD

A

Gastro-oesophageal reflux (GOR)
- passage of gastric contents into oesophagus
- normal in infants if asymptomatic
Gastro-oesophageal reflux disease (GORD)
- presence of symptoms or complications from reflux
Regurgitation (posseting)
- reflux of stomach contents beyond the oesophagus

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26
Q

Epidemiology of GORD

A

Regurgitation extremely common - occurs in approx 40% of infants
Usually appears in first 2 weeks of life

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27
Q

Pathophysiology of GORD

A

LOS muscle tone too low

-> uncontrolled reflux of stomach content

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28
Q

Features of infants that can contribute to GORD

A

Short, narrow oesophagus
Delayed gastric emptying
Shorter, lower oesophageal sphincter that is slightly above the diaphragm
Liquid diet and high calorie requirement, distending the stomach and increasing pressure gradient between stomach and oesophagus
Larger ratio of gastric volume to oesophageal volume
Spending significant periods recumbent

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29
Q

Risk factors for GORD

A

Prematurity
Parental history of heartburn or acid regurgitation
Obesity
Hiatus hernia
History of (repaired) congenital diaphragmatic hernia
History of (repaired) congenital oesophageal atresia
Neurodisability - cerebral palsy

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30
Q

Clinical features of GORD

A

Distressed behaviour - excessive crying, unusual neck postures, back-arching
Unexplained feeding difficulties - refusing feeds, gagging, choking
Hoarseness and/or chronic cough in children
A single episode of pneumonia
Faltering growth
If child is able to they may report retrosternal or epigastric pain
Take feeding hx - check technique, calculate volume of milk and relationship between symptoms and feeds

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31
Q

Differential diagnosis of GORD

A
Pyloric stenosis 
- frequent forceful vomiting in < 2 months old
Intestinal obstruction
- bile-stained vomit
Acute surgical abdo issue
- abdo distention, tenderness or palpable mass
Upper GI bleed
- haematemesis
Sepsis
- altered responsiveness, severe prolonged vomiting, petechial rash, bulging fontanelle
Raised ICP
- rapid increasing head circumference, persistent headache and vomiting following periods of recumbence
Bacterial gastroenteritis
- blood in stool
Cow's milk protein allergy
- blood in stool
- chronic diarrhoea
UTI
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32
Q

Management of GORD

A

Effortless regurgitation
- reassurance
Breastfed
- alginate (Gaviscon) mixed with water immediately after feeds
Formula-fed
- ensure infant not over-fed - no more than 150ml/kg/day
- decrease feed volume by increasing frequency
- use feed thickener
- stop thickener and start alginate added to formula
If no improvement after 2 weeks trial PPI or histamine antagonist - omeprazole or ranitidine

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33
Q

Complications of GORD

A

90% spontaneously resolve by 1 year
Reflux oesophagitis
Recurrent aspiration pneumonia
Recurrent acute otitis media - >3 episodes in 6 months
Dental erosion - especially in children with neurodisability
Apnoea
Apparent life-threatening events (ALTE): a combination of symptoms including apnoea, colour change, change in muscle tone, choking and gagging

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34
Q

Define gastroenteritis

A

Inflammation of stomach and intestines
Infective gastroenteritis is a temporary disorder due to an enteric infection
- Most commonly caused by viruses, but can also be due to bacterial or parasitic infection
Typically characterised by sudden onset diarrhoea with or without vomiting

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35
Q

Epidemiology of gasteroenteritis

A

Viral causes
- rotavirus
- most common in infants - immunity long lasting
- oral vaccine part of UK vaccination programme at 8-12 weeks
- norovirus
- commonest in all age groups
- spread by faecal oral route or by environmental contamination
- adenovirus
Bacterial
- campylobacter
- bloody diarrhoea
- consumption of undercooked meat and unpasteurised milk
- Escherichia coli
- transmitted through contaminated food, person-to-person and contact with infected animals

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36
Q

Clinical features of gastroenteritis

A

Sudden onset of loose/watery stool with or without vomiting
Abdominal pain/cramps
Mild fever
Recent contact with someone with diarrhoea or vomiting

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37
Q

Groups at high risk for dehydration

A

Young children - under 6months
Children who have passed >5 diarrhoeal stools in the last 24 hours
Children who have vomited >2x in the last 24 hours
Children who have stopped breastfeeding during the illness

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38
Q

Differential diagnosis of gastroenteritis

A
Temperature higher than 38oC if < 3months or higher than 39oC if >3months
Breathlessness or tachypnoea
Altered GCS
Meningism
Blood/mucous in stool
Bilious (green) vomit
Severe/localised abdominal pain
Abdominal distension or guarding
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39
Q

Investigations for gasteroenteritis

A

A stool sample should be sent for microbiological investigations if
- Septicaemia is suspected or
- blood and/or mucus is present in the stool or
- the child is immunocompromised
Do not routinely perform blood tests however measure Na+, K+, Cr, Ur and glucose if
- IV fluids are going to be used
- There are symptoms/signs of hypernatraemia - jittery, increased muscle tone, hyperreflexia, convulsions, drowsiness or coma
Measure acid-base status and chloride concentration is shock is suspected.

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40
Q

Management of gasteroenteritis

A

Immediate
- if not clinically dehydrated
- continue breastfeeding/formula
- encourage fluid intake
- discourage fruit juices and carbonated drinks
- offer oral rehydration salt solution as supplementation
- if dehydrated
- IV therapy - if suspected shock, evidence of red flags, no improvement or vomiting with oral/NG tube fluid
- oral therapy - ORS ml/kg over 4 hours plus maintenance fluid
Following rehydration
- give full strength milk straight away
- slowly introduce child’s solid food
- do not return to nursery/school at least 48hrs have passed since last symptoms

41
Q

Complications of gastroenteritis

A

Haemolytic uraemic syndrome (HUS)
- Rare but serious complication of acute infectious gastroenteritis that occurs mostly in young children and the elderly.
- This can be a life-threatening complication causing
acute renal failure,
haemolytic anaemia
Reactive complications associated with bacterial gastroenteritis
- arthritis, carditis,4 urticaria, erythema nodosum and conjunctivitis.
- Reiter’s syndrome (the combination of urethritis, arthritis, and uveitis).
Toxic megacolon
Acquired /secondary lactose intolerance
- Occurs due to the lining of the intestine being damaged
- Leads to symptoms of bloating, abdominal pain, wind and watery stools after drinking milk
- Improves when infection resolves and gut lining heals

42
Q

Epidemiology of UC

A

Most prevalent among Caucasian population
Bimodal distribution between 15-25 years and 55-65 years
Follows remitting and relapsing course

43
Q

Features of UC

A
Large bowel only
Mucosa only
Microscopic changes
- crypt abscess formation
- reduced goblet cells
- non-granulomatous
Macroscopic changes
- continuous inflammation - proximal from rectum
- pseudopolyps and ulcers from
44
Q

Features of Crohn’s disease

A
Entire GI tract
Transmural
Microscopic changes
- granulomatous - non-caseating
Macroscopic changes
- discontinuous inflammation - skip lesions
- fissures and deep ulcers - cobblestone appearance
- fistula formation
45
Q

Clinical features of UC

A
Insidious onset
Bloody diarrhoea and mucus discharge
Systemic symptoms
- malaise
- anorexia
- low-grade pyrexia
46
Q

Extra-intestinal manifestations of UC

A

Musculoskeletal – enteropathic arthritis (typically affecting sacroiliac and other large joints) or nail clubbing
Skin – Erythema nodosum (tender red/purple subcutaneous nodules, typically found on the patient’s shins)
Eyes – Episcleritis, anterior uveitis, or iritis
Hepatobiliary – Primary sclerosing cholangitis (chronic inflammation and fibrosis of the bile ducts)

47
Q

Ix of UC

A

Routine bloods
Faecal calprotectin - raised in IBD but not IBS
Imaging
- colonoscopy with biopsy
- AXR or CT in acute exacerbations - look for megacolon or bowel perforation

48
Q

Mx of UC

A

Inducing remission
- fluid resuscitation, nutritional support and prophylactic heparin
- corticosteroid therapy and immunosuppressive agents - mesalazine or azathioprine
Maintaining remission
- immunomodulators - mesalazine or sulfasalazine
- colonoscopic surveillance
- IBD nurse specialists
Surgical
- total proctocolectomy is curative

49
Q

Complications of UC

A

Toxic megacolon, present with severe abdominal pain, abdominal distension, pyrexia, and systemic toxicity
Decompression of the bowel is required as soon as possible, due to high risk of perforation, and failure to respond to medical management is an indication for surgery
Colorectal carcinoma
Osteoporosis, requiring regular assessment for fracture risk and treated as necessary
Pouchitis, inflammation of an ileal pouch, with typical symptoms include abdominal pain, bloody diarrhoea, and nausea
Pouchitis should be treated with metronidazole and ciprofloxacin

50
Q

Risk factors for Crohn’s disease

A

Family history
Smoking
- Increases the risk of developing Crohn’s disease and risk of relapse
White European descent (particularly Ashkenazi Jews)
Appendicectomy

51
Q

Clinical features of Crohn’s disease

A
Abdo pain and diarrhoea
Systemic symptoms
- malaise
- anorexia
- low-grade fever
Oral aphthous ulcers
Perianal disease
- skin tags
- perianal abscesses
- fistulae
- bowel stenosis
52
Q

Extra-intestinal features of Crohn’s disease

A

Musculoskeletal
- Enteropathic arthritis or nail clubbing
- Metabolic bone disease (secondary to malabsorption)
Skin
- Erythema nodosum –
- Pyoderma gangrenosum – erythematous papules/pustules that develop into deep ulcers
Eyes
- Episcleritis, anterior uvetitis, or iritis
Hepatobiliary
- Primary sclerosing cholangitis (more associated with UC)
- Cholangiocarcinoma (due to association with primary sclerosing cholangitis)
- Gallstones
Renal
- Renal stones

53
Q

Mx of Crohn’s disease

A
Inducing remission
- fluid resuscitation, nutritional support and prophylactic heparin
- corticosteroid therapy and immunosuppressive agents - mesalazine or azathioprine
Maintaining remission
- azathioprine
- smoking cessation
Surgical
- ileocaecal resection
- surgery for peri-anal disease
- stricturoplasty
- small or large bowel resections
54
Q

Complications of Crohn’s disease

A
GI
- fistula
- stricture formation
- recurrent perianal abscesses/fistulae
- GI malignancy
Extra-intestinal
- malabsorption
- osteoporosis
- increased risk of gallstones
- increased risk of renal stones
55
Q

Define infantile colic

A

Benign condition without any known understanding or surgical cause
Typically begins in the first few weeks of life and resolves spontaneously by 4-5 months

56
Q

Risk factors for infantile colic

A

Age under 5 months
Exposure to cigarette smoke
Formula-fed only

57
Q

Clinical features of infantile colic

A
Paroxysms of crying, often worse in afternoons and evening - high pitched piercing
Difficult to comfort
Grimacing/frowning
Red face
Knees drawn up to chest
Clenched fists
Excessive gas
Flatus - typically relieves symptoms
58
Q

DDx of infantile colic

A
UTI
Cow's milk protein intolerance
GORD
Anal fissure
Intussusception
Pyloric stenosis
Acute otitis media
Non-accidental injury
Meningitis
59
Q

Mx of infantile colic

A

No definitive management
Hold baby through crying episode
Bottle-fed infants may benefit from hydrolysed formula

60
Q

Pathophysiology of constipation

A

95% functional

  • low fibre, low-fluid diet resulting in hardening of school
  • pain on defecation
  • voluntary delay of defecation
  • further hardening of stool
61
Q

Risk factors for functional constipation

A

Low-fibre diet
Poor nutrition
Obesity
Childhood stressors

62
Q

Clinical features of constipation

A

Painful passage of infrequent hard stool
Overflow faecal incontinence - small volume of soft stool
Indentable mass in left LLQ

63
Q

Red flag symptoms for constipation

A
Present from birth
Delayed passage of meconium > 48 hours
Ribbon stools
Neurological symptoms or signs - locomotor delay or falling over/ abnormal gait in older children
Vomiting
Abdominal distension
64
Q

Key features to exclude on examination of constipation

A
Spine
- hairy patches or lipomata - indicative of spina bifida
Gluteal region
- symmetry
Perianal region
- no fissures 
- anatomically normal anus
Lower limbs
- normal power, tone and reflexes
65
Q

DDx of functional constipation

A
Infants
- Hirschsprung disease
- CF
- hypothyroidism
- spinal dysraphism
- anogenital anomalies - imperforate anus
Older children
- neuromuscular disorders - spinal muscular atrophy, cerebral palsy
- hypothyroidism
- anorexia
66
Q

Mx of functional constipation

A
Pharmacological disimpaction
- polyethylene glycol 3350 (Movicol) - osmotic laxative
- lactulose
- if no improvement add stimulant laxative such as senna
Maintenance 
- polyethylene glycol 3350
Dietary advice
- regular scheduled toileting
- increasing dietary fibre and fluids
- increasing exercise
67
Q

Commonly used laxatives in children

A

Macrogols - polyethylene glycol 3350 (Movicol)
- induces effect by retaining water in stool
- softens stool and increases bulk
- increasing frequency
Osmotic - lactulose
- broken down to lactic acid which raises osmotic pressure of bowel
Stimulant - senna
- breakdown products are directly irritant to the bowel wall causing increased fluid secretion and colonic motility

68
Q

Pathophysiology of Hirschsprung disease

A

Absence of ganglion cells in bowel wall myenteric nerve plexus
- in utero cells migrate in craniocaudal fashion - distal bowel most often affected
Lack of peristalsis and muscle spasm
- impaired relaxation of bowel wall and internal anal sphincter
Functional bowel obstruction
Due to stasis of faeces - increased risk of enterocolitis - sepsis

69
Q

Epidemiology of Hirschsprung disease

A

1.6 per 100,000 live births
Male predominance of 2:1
Significant association with Down’s syndrome

70
Q

Clinical features of Hirschsprung disease

A

Delayed passage of meconium - greater than 48 hours
Vomiting - eventually bilious
When stool is passed usually foul (due to bacterial growth) and explosive
If complicated by enterocolitis child will be febrile
Distended abdomen

71
Q

Ix for Hirschsprung disease

A

Bloods if febrile - raised WCC suggests enterocolitis
Abdo XRAY - bowel obstruction
Rectal biopsy - definitive investigation

72
Q

Mx of Hirschsprung disease

A

NBM and commence IV maintenance fluids
Decompress stomach and bowel by NG tube and saline enemas
If enterocolitis present start broad-spec abx IV
Surgical resection of aganglionic segment with coloanal anastomosis

73
Q

Epidemiology of anal fissures

A

Often < 2 years old

Common cause of rectal bleeding in childhood

74
Q

Pathophysiology of anal fissures

A

Hard stool stretches the anal mucosa causing a tear

  • pain during bowel movement
  • spasm of internal anal sphincter causing reduced blood flow and poor healing
  • avoidance of opening bowels - worsening constipation
75
Q

Clinical features of anal fissures

A

Pain during defecation
Small volumes of bright-red blood on paper
Pain leads to toilet avoidance
Fissure seen on examination - break in anal mucosa - often in posterior midline

76
Q

Mx of anal fissure

A

Aim is to soften stool

  • increasing fluid and fibre in the diet is required
  • laxatives - continued for 1 month after symptoms resolve
  • sitting in warm bath 2-3 times per day
77
Q

Epidemiology of threadworm

A

Enterobius vermicularis
Very common infection in childhood
Typically 5-10 years

78
Q

Pathophysiology of threadworm

A

Highly contagious infection with Enterobius vermicularis
Live in bowel but migrate to anus to lay eggs
- highly irritant and cause child to scratch
- eggs on fingers passed to mouth to re-infect or transferred elsewhere to infect others

79
Q

Clinical features of threadworms

A

Intense perianal itching, often worse at night
Disturbs sleep -> behavioural problems
Small, thread-like worms may be seen in perianal region

80
Q

Ix for threadworms

A

If worms seen - not required
Tape-test - parent places piece of sticky tape briefly on child’s anus first thing in the morning which is sent for microscopy

81
Q

Mx of threadworms

A

Antifungal - mebendazole
Measures taken to prevent transmission/prevent re-infection for 2 weeks post treatment as medication only kills like worms
- daily washing of bedding
- fastidious hand hygiene
- bathing every morning with cleansing of perianal region
- storing toothbrushes out of reach

82
Q

IgE-mediated vs non-IgE-mediated cow’s milk allergy

A
IgE-mediated
- within 2 hours onset
- pruritus and erythema
- urticarial rash
- angioedema
- N+V
- colic
- diarrhoea
- lower resp symptoms - wheeze and dyspnoea
- upper resp symptoms - sneezing, rhinorrhoea and nasal itching
Non-IgE-mediated
- between 48 hours and 2 weeks
- pruritis and erythema
- eczematous rash
- angioedema unusual
- colic - may mimic infantile colic
- chronic diarrhoea - may be bloody
- perianal redness
- lower resp symptoms - wheeze and dyspnoea
83
Q

Pathophysiology of lactose intolerance

A

Primary
- autosomal recessive condition leading to reduction in lactase activity
Secondary
- pathology of GI tract damages the villi in small bowel and causes a reduction of activity of lactase
Reduction in lactase activity in small bowel means lactose enters colon
- acts as osmolyte keeping water in bowel
- digested by bacteria to form short-chain fatty acids and gas

84
Q

Risk factors for lactose intolerance

A

Gastroenteritis
FHx
Non-white ethnicity
25% Caucasians and up to 75% other ethnic groups

85
Q

Clinical features of lactose intolerance

A

Watery diarrhoea that follows gastroenteritis

Abdo discomfort, distention and increased flatus

86
Q

Ix for lactose intolerance

A

Stool sample - pH < 6.0 and reducing sugars

Hydrogen breath test or lactose tolerance test - older children

87
Q

DDx for lactose intolerance

A
Cow's milk protein intolerance
IBD
IBS
Gastroenteritis
Coeliac disease
Infantile colic
Giardiasis
Hyperthyroidism
Meckel diverticulum
88
Q

Mx of lactose intolerance

A

Lactose free diet/milk/formula
- varying degrees of lactose may be tolerated
- dietitian referral required
Consider vit D and calcium supplementation
In secondary disease cow’s milk can be reintroduced once symptoms have resolved

89
Q

Define toddler diarrhoea

A

Very common cause of chronic diarrhoea
Children otherwise well
Self-limiting without long term significance

90
Q

Clinical features of toddler diarrhoea

A

Chronic diarrhoea which classically contains particles of undigested food +- mucus
May be exacerbated by high-fibre diets and sugary juices
Examination normal

91
Q

DDx of toddler diarrhoea

A

Malabsorptive disease - IBD, coeliac, pancreatic insufficiency
Food allergy - cow’s milk
Lactose intolerance

92
Q

Mx of toddler diarrhoea

A

Reassurance
- typically resolve by 4-5 years
No medication
Dietary amendments
- limit intake of fruit juice, fizzy drinks, grapes, peas, baked beans, high-fibre cereals
- include full fat milk, lower fibre cereals

93
Q

Pathophysiology of pyloric stenosis

A

Thickening of pyloric musculature leading to narrowing of gastric antrum and subsequent disruption of gastric outflow
Causes forceful vomiting of gastric contents - will not be bilious
Loss of hydrogen and chloride ions orally produces a hypochloraemic metabolic alkalosis
- potassium ions move intracellularly leading to hypokalaemia

94
Q

Risk factors for pyloric stenosis

A

Typically presents between 4th and 6th week of life
Male sex (7:1)
Fhx

95
Q

Clinical features of pyloric stenosis

A

Effortless projectile vomiting during or after feeds
- vomiting never bilious, maybe small amounts of blood
Visible peristaltic waves in upper quadrants of abdomen
Firm mobile olive-sized mass in epigastrium

96
Q

Ix for pyloric stenosis

A

Bloods - blood gases and U+Es show hypochloraemia, hypokalaemia and metabolic alkalosis
Abdo USS

97
Q

DDx for pyloric stenosis

A
GOR
Overfeeding
Duodenal atresia
Gastroenteritis
Food allergy
98
Q

Mx of pyloric stenosis

A

IV access gained - fluid and metabolic derangements corrected
Definitive treatment - Ramstedt’s pyloromyotomy