Gastroenterology Flashcards
(159 cards)
1
Q
Non-organic/ functional abdominal pain
A
Very common in over 5
No disease process can be found to explain the pain
2
Q
Medical causes of abdominal pain
A
Constipation is very common UTI Coeliac disease IBD IBS Mesenteric adenitis Abdominal migraine Pyelonephritis Henoch-Schonlein purpura Tonsilitis DKA Infantile colic
3
Q
Causes of abdominal pain in adolescent girls
A
Dysmenorrhea (period pain) Mittelschmerz (ovulation pain) Ectopic pregnancy PID Ovarian torsion Pregnancy
4
Q
Surgical causes of abdominal pain
A
Appendicitis: central abdo pain-> RIF
Intussusception: red jelly stools, colicky non-specific pain
Bowel obstruction: pain, distension, absolute constipation, vomiting
Testicular torsion
5
Q
Red flags for serious abdominal pain
A
Persistent or bilious vomiting Severe chronic diarrhoea Fever Rectal bleeding Weight loss or faltering growth Dysphagia Nighttime pain Abdominal tenderness
6
Q
Abdominal pain investigations
A
Anaemia: IBD, coeliac disease ESR/CRP: indicates IBD Raised anti-TTG or anti-EMA; coeliac disease Raised faecal calprotectin: IBD Positive urine dipstick: UTI
7
Q
Recurrent abdominal pain
A
Repeated episodes of abdominal pain
No identifiable underlying cause
Non-organic/ functional pain
8
Q
Effects of recurrent abdominal pain
A
Psychosocial problems
Missed days at school
Parental anxiety
9
Q
Association of recurrent abdominal pain
A
Abdominal migraine
IBS
Functional abdominal pain
10
Q
Causes of recurrent abdominal pain
A
Stressful life events
Loss of relative or bullying
Inappropriate pain signals from visceral nerve
11
Q
Management of recurrent abdominal pain
A
Distract child
Encourage parents to not ask about the pain
Advice about sleep, regular meals, healthy balanced diet, staying hydrated, exercise and reduced stress
Probiotics with IBS
Avoid NSAIDs
Address triggers, psychosocial
Support from school counsellor and child psychologist
12
Q
Abdominal migraine
A
Occur in young children before traditional migraines
Episodes of central abdominal pain
Lasting >1hr
Normal examination
13
Q
Associated features of abdominal migraine
A
N/V Anorexia Pallor Headache Photophobia Aura
14
Q
Management of acute abdominal migraine
A
Low stimulus environment (quiet, dark room)
Paracetamol
Ibuprofen
Sumatriptan
15
Q
Medications to prevent abdominal migraine
A
Pizotifen, serotonin agonist
Propanolol
Cyproheptadine: antihistamine
Flunarazine: CCB
16
Q
Pizotifen for abdominal migraine
A
Main preventative measure
Needs to be withdrawn slowly
Withdrawal symptoms; depression, anxiety, poor sleep and tremor
17
Q
Secondary causes of constipation
A
Hirschsprung’s disease
CF
Hypothyroidism
18
Q
Features in history and examination
Constipation
A
<3 stools/week Hard stools are difficult to pass Rabbit dropping stools Straining and passage of stools Abdominal pain Retentive posturing Rectal bleeding Overflow soiling from faecal impaction, incontinence of loose smelly stools Hard stools palpable in abdomen Loss of sensation of need to open the bowel
19
Q
Encopresis
A
Faecal incontinence
Not pathological in <4
Chronic constipation-> rectum stretched and lose sensation
Loose stools bypass blockage of hard stools, soiling
20
Q
Causes of encoparesis
A
Chronic constipation Spina bifida Hirschsprung’s disease Cerebral palsy Learning disability Psychosocial stress Abuse
21
Q
Lifestyle factors causing constipation
A
Habitually not opening bowels Low fibre diet Poor fluid intake and dehydration Sedentary lifestyle Psychosocial problems: safeguarding
22
Q
Desensitisation of rectum
A
Develop habit of not opening bowels Ignore sensation of full rectum Over time lose sensation of needing to open bowels Open bowels even less frequently Retain faeces in rectum Faecal impaction Rectum stretches Leads to more desensitisation Need to treat constipation
23
Q
Secondary causes of constipation
A
Hirschsprung’s disease CF (meconium ileus) Hypothyroidism Spinal cord lesions Sexual abuse Intestinal obstruction Anal stenosis Cow’s milk intolerance
24
Q
Constipation red flags
A
Delayed passing of meconium (>48hrs): CF/ Hirschsprung’s
Neurological signs or symptoms: cerbral palsy, spinal cord lesion
Vomiting; intestinal obstruction, Hirschsprung’s disease
Ribbon stool: anal stenosis
Abnormal anus: anal stenosis, IBD, sexual abuse
Abnormal lower back or buttocks: spina bifida, spinal cord lesion, sacral agenesis
Failure to thrive: coeliac disease, hypothyroidism, safeguarding
Acute severe abdominal pain and bloating; obstruction or intussusception
25
Complications of constipation
```
Pain
Reduced sensation
Anal fissures
Haemorrhoids
Overflow and soiling
Psychosocial morbidity
```
26
Management of constipation
Correct any reversible contributing factors
High fibre and good hydration
Movicol
Disimpaction regimen for faecal impaction With high laxative dose
Encourage and praise visiting toiletry
Scheduling visits, bowel diary, start charts
Long-term laxative and slowly weaned off
27
GORD
Contents from stomach reflux through lower oesophageal sphincter into oesophagus, throat and mouth
Babies have an immature LOS, normal to reflux contents
Should be better by 1 year
28
Regurgitation
Reflux of stomach contents beyond the oesophagus
29
Epidemiology of GORD
Regurgitation and GORD usually appear in the first 2 weeks of life
30
Why is tone of LOS too low in infants in GORD
| Anatomical and physiological features
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
31
Risk factors for GORD
Prematurity
Parental history of heartburn or acid regurgitation
Obesity
Hiatus hernia
Hx of congenital diaphragmatic hernia (repaired)
Hx of congenital oesophageal atresia
Neurodisability (cerebral palsy)
32
History of GORD
Distressed behaviour: excessive crying, unusual neck posture, back arching
Unexplained feeding difficulties: refusing feeds, gagging, choking
Hoarseness and/or chronic cough in children
Single episode of pneumonia
Faltering growth
Retrosternal/ epigastric pain
Feeding history
33
Feeding history GORD
Position, attachment, technique, duration, frequency, type of milk
Calculate volume of milk being given: can be over-fed and have gastric over-distension
Frequency and volume of vomits
Relationship of symptoms to feeds
34
Examination of GORD
Hydration status
Signs of malnutrition
Abnormalities indicating DD
Assess growth charts
35
GORD dd
```
Pyloric stenosis
Intestinal obstruction
Any acute surgical abdominal issue
Upper GI bleed: haematemesis
Sepsis
RICP
Bacterial gastroenteritis, cows milk protein allergy
Chronic diarrhoea
UTI
If onset >6 months of age or if symptoms persist beyond 1 year then reflux is unlikely
```
36
Investigations GORD
Not needed to diagnosis
Barium swallow
Ph study
Endoscopy
37
Causes of vomiting
```
Over feeding
GORD
Pyloric stenosis
Gastritis or gastroenteritis
Appendicitis
Infections such as UTI, tonsilitis or meningitis
Intestinal obstruction
Bulimia
```
38
Management of GORD if breast fed with frequent regurgitation causing marked distress
Self-resolve by 1 year of age
1. Use alginate (Gaviscon) mixed with water immediately after feeds for 2 week trial
2. Start PPI or histamine antagonist (e.g. omeprazole or ranitidine)
3. If symptoms persist refer to paediatrics and reconsider differential diagnosis
39
Management of GORD in formula-fed with frequent regurgitation causing marked distress
1. Ensure infant isn’t over-Fed (<150ml/kg/day)
2. Decrease feed volume be increasing frequency (2-3hourly)
3. Use feed-thickened (or pre-thickened formula)
4. Stop thickener and start alginate added to formula
5. Start PPI or histamine antagonist (e.g. omeprazole or ranitidine)
6. If symptoms persist refer to paediatrics and reconsider differential diagnosis
40
Red flags for GOR
Not keeping down any food: pyloric stenosis or intestinal obstruction
Projectile or forceful vomiting: pyloric stenosis or intestinal obstruction
Bile stained vomit: intestinal obstruction
Haematemesis or malaena: peptic ulcer, oesophagitis or varices
Abdominal distension: intestinal obstruction
Reduced consciousness, building fontanelle, neurological sign: meningitis or RICP
Respiratory symptoms: aspiration and infection
Blood in stools: gastroenteritis or Cows milk protein allergy
Signs of infection: pneumonia, UTI, tonsilitis, otitis, meningitis
Rash, angioedema, signs of allergy: cows milk protein allergy
Apnoea
41
Simple cases of GORD mx
Small, frequent meals
Burping regularly to help milk settle
Not over-feeding
Keep baby upright after feeding
42
Complex cases of GORD mx
Gaviscon mixed with feeds
Thickened milk or formula
Ranitidine
Omeprazole with ranitidine is inadequate
Barium meal
Endoscopy
Fundoplication
43
Complications of GORD
90% will resolve in first year: older, more solid diet, more upright
Reflux oesophagitis
Recurrent aspiration pneumonia
Recurrent acute otitis media (>3 episodes in 6 months)
Dental erosion (children with neuro disability)
Apnoea
Apparent life-threatening events: apnoea, colour change, change in muscle tone, choking and gagging
44
Sandifers syndrome
Brief episodes of abnormal movements
Associated with GORD in infants
Infants usually neurologically normal
45
Key features of sandifers syndrome
Torticolis: forceful contraction of neck muscles causes twisting of neck
Dystonia: abnormal muscle movements causing twisting movements, arching of back or unusual postures
Self-resolves
DD: infantile spasms and seizures
46
Epidemiology of gastroenteritis
Common isolates: Rotavirus and Campylobacter
| Adenovirus, respiratory infections
47
Acute gastroenteritis
Inflammation of stomach and intestines
| Main concern is dehydration
48
Viral causes of gastroenteritis
Rotavirus
Norovirus
Adenovirus (less common), more subacute diarrhoea
Highly contagious
49
When to consider Differential diagnosis of gastroenteritis
```
Temperature >38 if <3months
Temperature >39 of >3 months
Breathlessness or tachypnoea
Altered GCS
Blood/ mucous in stool
Bilious vomit
Severe/ localised abdominal pain
Abdominal distension or guarding
```
50
Differential diagnosis of diarrhoea
```
Infection
IBD
Lactose intolerance
Coeliac disease
CF
Toddlers diarrhoea
IBS
Medications
```
51
Rotavirus gastroenteritis
Most common cause
<5 years
Uncommon in adults, vaccine given at 8 and 12 weeks
Faecal oral route or by environmental contamination
Incidence peaks over winter months
52
Norovirus gastroenteritis
Single stranded RNA viruses
Commonest cause of gastroenteritis in all age groups
Faecal oral contamination and environmental contamination
53
Adenovirus gastroenteritis
Infections of respiratory system
| <2 years
54
E.coli for gastroenteritis
Most strains are harmless
VTEC E.coli 0157:H7 can cause haemorrhagic colitis and haemolytic uraemic syndrome
Spread through contaminated food, person-to-person contact, contact with infected animals
E.coli 0157 produces the Shiga toxin
55
Shiga toxin
```
Produced by Ecoli 0157
Abdominal cramps
Bloody diarrhoea
Vomiting
Shiga toxin: destroys blood cells and leads to HUS, ax increases this risk
```
56
Campylobacter jejuni
Travellers diarrhoea
Most common cause of bacterial gastroenteritis in the UK
Gram negative bacteria: curved or spiral shape
57
Campylobacter transmission
Raw or improperly cooked poultry
Untreated water
Unpasteurised milk
58
Campylobacter incubation
2-5 days
| Symptoms resolve after 3-6days
59
Campylobacter symptoms
Abdominal cramps
Diarrhoea, often with blood
Vomiting
Fever
60
Campylobacter management
Severe symptoms
Other risk factors: HIV, heart failure
Azithromycin, ciprofloxacin
61
Clinical features of gastroenteritis
Sudden onset of loose/ watery stool with/without vomiting
Abdominal pain/crams
Mild fever
Recent contact with someone with diarrhoea or vomiting
62
Which diarrhoea children are more at risk of dehydration
Young children <6 months
Children who have passed >5 diarrhoea stools in last 24hrs
Children who have vomited >2x in last 24 hrs
Children who have stopped breast feeding during illness
63
Symptoms of dehydration
```
Appears to be unwell or deteriorating
Altered responsiveness
Decreased urine output
Skin colour unchanged
Warm extremities
```
64
Symptom of shock
```
Decreased level of consciousness
Pale or mottled skin
Cold extremities
Decreased urine output
Appears to be unwell or deteriorating
```
65
Signs of clinical dehydration
```
Altered responsiveness
Skin colour unchanged
Warm extremities
Sunken eyes
Dry mucous membranes
Tachycardia
Tachypnoea
Normal, peripheral pulses
Normal CRT
Reduced skin turgor
Normal blood pressure
```
66
Signs of clinical shock
```
Decreased level of consciousness
Pale or mottled skin
Cold extremities
Sunken eyes
Dry mucous membranes
Tachycardia
Tachypnoea
Weak peripheral pulses
Prolonged CRT
Reduced skin Turgor
Hypotension
```
67
Investigations for gastroenteritis
Stool sample if:
Septicaemia suspected
Blood and/or mucus in stool
Immunocompromised child
Measure Na, K, Cr, Ur and glucose if:
IV fluids are going to be used
Symptoms/signs of hypernatraemia (jittery, increased muscle tone, hyperreflexia, convulsions, drowsiness or coma)
Measure acid-base status
Chloride concentration
Shock
68
Management of gastroenteritis
| Immediate if not clinically dehydrated
Continue breast feeding/ other milk feeds
Encourage fluid intake
Discourage fruit juices and carbonated drinks
Oral rehydration salt solution as supplemental fluid to those at risk of dehydration
69
Management of gastroenteritis
| Immediate if dehydrated
Use IV therapy if shock is suspected, red flags, evidence of dehydration, vomiting persistently
Oral therapy:
ORS solution: 50mL/kg over 4 hours
Plus maintenance fluid
If child is refusing oral fluid, consider NG tube
70
```
Maintenance fluid calculation
Childs weight
0-10kg
10-20kg
>20kg
```
0-10kg: 100ml/kg/day
10-20kg: requirement for first 10kg + 50mL/kg/day
>20kg: requirement for first 20kg (1500ml) + 20ml/kg/day
71
Following rehydration after gastroenteritis
Advise parents to give full strength milk straight away
Slowly re-introduce the child’s solid food
Suggest that fruit juices and carbonated drinks are avoided until the diarrhoea has resolved
Advice on hand washing and avoiding towel sharing
Wait 48hours since last D/V before school
Child shouldn’t swim for 2 weeks after last episode
72
Complications of gastroenteritis
Haemolytic uraemic syndrome
Reactive complications with bacterial gastroenteritis
Toxic mega colon
Acquired/ secondary lactose intolerance
Diarrhoea lasts 5-7 days
Vomiting lasts 1-2 days
73
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
74
Reactive complications of bacterial gastroenteritis
Including arthritis, carditis, urticaria, erythema nodosum and conjunctivitis.
REMEMBER: Reiter’s syndrome (the combination of urethritis, arthritis, and uveitis).
75
Toxic mega colon
Rare but significant complication of rotavirus gastroenteritis
76
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 (5).
Gastroenteritis complication
77
Shigella gastroenteritis
Spread by faces contaminated drinking water, swimming pools and food
Incubation: 1-2days
Symptoms resolve within 1 weeks without treatment
Causes bloody diarrhoea, abdominal cramps and fever
Shiga toxin: HUS
Mx: azithromycin or ciprofloxacin
78
Salmonella gastroenteritis
Transmission: raw eggs, poultry, faeco-oral
Incubation: 12hrs-3days, symptoms resolve at 1week
Watery diarrhoea associated with mucus or blood, abdominal pain and vomiting
Ax: stool culture and sensitivities
79
Bacillus cereus gastroenteritis
```
Gram positive rod
Spread through inadequately cooked food
Fried rice left out at room temperature
Produces toxin:: cereulide
Vomiting within 5 hours, diarrhoea within 8 hours, resolution within 24hours
```
80
Cereulide
Produced by bacillus cereus
Within 5 hours of ingestion: Causes abdominal cramping and vomiting
8 hours after ingestion: Produces toxins in intestine, watery diarrhoea
Usually all symptoms resolve within 24hours
81
Yersinia enterocolitis
Gram negative bacillus
Pigs, raw or uncooked pork can cause infection
Also spread through contamination with urine or faeces of other mammals, such as rats and rabbits
82
Yersinia clinical presentation
Most frequently affects children
Watery or blood diarrhoea, abdominal pain, fever and lymphadenopathy
Incubation 4-7days, illness can last longer that other causes of enteritis
Symptoms lasting 3 week or more
Older children: can present with fever and right sided abdominal pain due to Mesenteric lymphadenitis
Impression of appendicitis
83
Staphylococcus aureus toxin
S.aureus produces enterotoxin when growing on eggs, dairy and meat
Small intestine inflammation
Symptoms: diarrhoea, perfuse vomiting, abdominal cramps and fever
Symptoms start within hours of ingestion
Settle within 12-24hours
Enterotoxin causes enteritis
84
Giardiasis
```
Giardia lambia
Parasite
Small intestines of mammals
Releases cysts, Falcon oral
Diagnosis with stool microscopy
Metronidazole
```
85
Principles of gastroenteritis management
Good hygiene
Isolate patients
Barrier nursing and rigorous infection control
No school for 48hrs after symptoms have resolved
Faecal sample: microscopy, culture and sensitivities
Attempt fluid challenged
Diorylate rehdration fluid
86
Complications post-gastroenteritis
Lactose intolerance
IBS
Reactive arthritis
Guillian-Barre syndrome
87
Coeliac disease
Autoimmune condition
Gluten causes an immune response
And inflammation in small intestine
Usually develops in childhood
88
Pathophysiology of coeliac disease
Immunological response (antibodies) to gliadin in gluten
Antibodies: anti-TTG, anti-EMA
Genetic factors (HLA-DQ2/DQ8)
Antibodies target epithelial cells, damage villi of small intestine
Lead to inflammation and Malabsorption
Epithelial cell destruction and villous atrophy
T-cell mediated immune disorder
Development of inflammatory anti-gluten CD4 T-cell response, anti-gluten ab, autoantibodies against tissue transglutaminase, endomysium, activation of intraepithelial lymhphocytes
89
Risk factors coeliac disease
```
Wheat, barley, rye
Bread, beer, squash, biscuits, cereal, cake, pasta, pies
TY1 diabetes
Down syndrome
Turner syndrome
Thyroid disease, RA, Addison’s disease
HLA-DQ2 gene
```
90
Classic coeliac presentation
```
9-24months presentation
Malabsorption
Failur yo thrive
Diarrhoea
Steatorrhea
Anorexia
Abdominal pain
Abdominal distension
Muscle waste
Crypt hyperplasia and villous atrophy on histology
Mouth ulcers
Anaemia
```
91
Coeliac disease neurological symptoms
Rare
Peripheral neuropathy
Cerebellar ataxia
Epilepsy
92
Extra-intestinal symptoms coeliac
```
Dermatitis herpetiformis
Dental enamel Hypoplasia
Osteoporosis
Short stature
Iron-deficient anaemia- resistant to oral Fe
Liver and biliary tract disease
Arthritis
Peripheral neuropathy, epilepsy, ataxia
```
93
DD coeliac
```
Tropical spruce
CF
IBD
Post-gastroenteritis
Autoimmune encephalopathy
Eosinophilic enteritis
```
94
Genetic associations coeliac
HLA-DQ2
| HLA-DQ8
95
Coeliac autoantibodies
Anti-TTG: tissue transglutaminase antibodies
EMAs: endomysial antibodies
Anti-DGPs: deaminated gliadin peptides antibodies
Also check IgA deficiency
96
Diagnosis coeliac
Need patient having gluten in diet, 6 weeks before testing
IgA TOTAL
IgA TTG
IgA EMA
Avoid HLA DQ2/8 testing
Endoscopic intestinal biopsy if serology positive
Duodenal biopsy
97
Duodenal biopsy coeliac disease
Crypt hypertrophy
| Villous atrophy
98
Management of coeliac
Lifelong diet free of gluten
Iron supplements
Annual follow up: compliance, development, growth and long-term complications
99
Complications coeliac
```
Vitamin deficiency
Anaemia
Osteoporosis
Refractory coeliac, need steroid treatment
Malignancy: Non-Hodkin lymphoma
Ulcerative jejunitis
Fertility problems
Depression/ anxiety
Enteropathic-associated T-cell lymphoma of the intestine
Small bowel adenocarcinoma
```
100
Crohn’s disease
```
Crows NESTS
No blood or mucus
Entire GI tract
Skip lesions on endoscopy
Terminal ileum most affected and transmural inflammaiton
Smoking is a risk factor
```
Also weight loss, strictures, fistula
101
Ulcerative colitis
```
U-C-CLOSEUP
Continuous inflammation
Limited to colon and rectum
Only superficial mucosa affected
Smoking is protective
Excrete blood and mucus
Use aminosalicylates
Primary sclerosing cholangitis
```
102
Presentation of IBD
```
Diarrhoea
Abdominal pain
Bleeding
Weight loss
Anemia
Systemically unwell during flares, fever, malaise, dehydration
```
103
Extra-intestinal manifestations IBD
```
Finger clubbing
Erythema nodosum
Pyoderma gangrenosum
Episcleritis and iritis
Inflammatory arthritis
Primary sclerosing cholangitis (UC)
```
104
IBD testing
Blood tests for: anaemia, infection, thyroid, kidney, liver function
Raised CRP: indicates active inflammation
Faecal calprotectin: released by intestines when inflamed
Endoscopy (OGD and colonoscopy) with biopsy is Gold-standard
Imaging with US, CT, MRI: look for fistula, abscesses, strictures
105
General management IBD
MDT
Monitor growth and pubertal development, especially for exacerbations or when treated with steroids
Inducing remission during flares
Maintaining remission
106
Inducing remission Crohn’s
Steroids: oral prednisolone,v IV hydrocortisone
Enteral nutrition to improve gut microbiome
Azathioprine
Mercaptopurine
Methotrexate
Infliximab
Adalimumab
107
Maintaining remission Crohn’s
First line: azathioprine, mercaptopurine
| Alternatives: methotrexate, infliximab, adalimumab
108
Surgery for Crohn’s
Surgically resect distal ileum
| Surgery to treat strictures and fistula
109
Inducing remission in ulcerative colitis
| Mild/moderate disease
First line: aminosalicylate (e.g. mesalazine oral or rectal)
| Second line: corticosteroids (e.g. prednisolone)
110
Inducing remission in ulcerative colitis
| Severe disease
First line: IV corticosteroids (e.g. hydrocortisone)
| Second line: IV cyclosporin
111
UC maintaining remission
Aminosalicylate (e.g. mesalazine)
Azathioprine
Mercaptopurine
112
Surgery UC
Remove colon and rectum (panproctocolectomy)
Patient left with permanent ileostomy or ileo-anal anastomosis (J-pouch)
J-pouch collects stools prior to patient passing motions
113
Cows milk protein allergy
Immune-mediated allergic response to naturally-occurring milk proteins casein and whey.
114
Pathophysiology of Cow’s milk protein allergy
IgE mediated: TY1 hypersensitivity reactions, histamine and cytokines released from mast cells and basophils
Non-IgE-mediated: involves T cell activation against cows milk protein
115
Risk factors CMPA
Personal history of atopy (eg. asthma, eczema, allergic rhinitis, other food allergies)
Family history of atopy (only allergic predisposition is inherited, not specific allergies)
116
IgE mediated cows milk protein allergy
```
Acute and frequently rapid onset
Pruritis
Erythema
Acute urticaria
Angio-oedema
Oral pruritis
Nausea
Colicky abdominal pain
V/D
LRT symptoms: cough, chest tightness, wheezing, SoB
URT symptoms: nasal itching, sneezing, rhinorrhea, congestion
```
117
Non-IgE mediated CMPA
```
Non-acute and generally delayed onset
Pruritis
Erythema
Atopic eczema
GORD
Loos or frequent stools
Blood/mucus in stools
Abdominal pain
Infantile colic
Food refusal or aversion
Constipation
Perianal redness
Pallor/tiredness
Faltering growth
LRI symptoms: cough, chest tightness, wheezing, SoB
```
118
CMPA history
```
Personal and family history of atopy
Diet and feeding history 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
```
119
CMPA examination
General physical examination of patient with a focused gastrointestinal examination, specifically signs of malnutrition.
Review growth charts
Signs of atopic comorbidities such as asthma, eczema, allergic rhinitis.
120
DD CMPA
Food intolerance (eg. lactose) may present as abdominal pain and diarrhoea following exposure to certain foodstuffs
Allergic reaction to other food or non-food allergens
Anatomical abnormalities such as Meckel’s diverticulum
Chronic gastrointestinal disease (e.g. gastro-oesophageal reflux disease, coeliac disease, inflammatory bowel disease, constipation, gastroenteritis)
Pancreatic insufficiency (eg. as a complication of cystic fibrosis)
Urinary tract infections
121
Investigations CMPA
RAST-radioallegosorbent test: looks for IgE antibodies
Non-IgE CMPA is clinically diagnosis diagnosed
Check for iron deficiency anaemia
122
Mx CMPA
```
Avoidance of Cow’s milk for 6 months until infant is 9-12months
MAP guidance milk ladder
Nutritional counselling
Extensively hydrolysed formula
Amino acid formula
```
123
Complications of CMPA
Malabsorption
| Reduced intake
124
When to suspect spontaneous bacterial peritonitis
Undiagnosed fever
Abdominal pain
Tenderness
Unexplained deterioration in hepatic/renal function
125
How to diagnose bacterial peritonitis
Diagnostic paracentesis
| Send fluid for WCC, differential and culture
126
How to treat bacterial peritonitis
Broad spectrum antibiotics
127
Clinical feature of viral hepatitis
```
Nausea
Vomiting
Abdominal pain
Lethargy
Jaundice
Hepatomegaly
Splenomegaly
ALT/AST elevated
Coagulation normal
```
128
Hepatitis A
RNAvirus
Faeco-oral transmission
Vaccination for travellers to endemic areas
129
Clinical features of HepA
```
May be asymptomatic
Majority have mild illness, 2-4weeks
Prolonged cholestatic hepatitis (self-limiting)
Fulminant hepatitis
No chronic liver disease
```
130
HepA diagnosis
Detect IgM antibody to virus
131
HepA Mx
No treatment
Vaccinate close contacts within 2 weeks of illness onset
At risk (CLD), giving human normal immunoglobulin
132
HepB
DNA virus
| Sub-Saharan Africa and Far East
133
HepB transmission
Sexually
Blood
Perinatal, horizontal spread: infants become chronic carriers
134
Clinical features HepB
Infants who contract perinatally are asymptomatic chronic carriers
Classic features of hepatitis or asymptomatic
Small chance of developing hepatic failure
135
HepB diagnosis
Detect HBV antigens and antibodies
IgM antibodies (anti-HBc) are positive in acute infection
Hepatitis B surface Antigen (HBsAg) denotes ongoing infectivity
136
HepB mx
No treatment for acute HBV infection
137
Chronic HepB
Asymptomatic carrier children-> chronic HBV liver disease
Progress to cirrhosis
Risk of hepatocellular carcinoma
138
Management of chronic HepB
Interferon
Pegylated interferon
>2s: entecacir, tenofovir
139
Prevention of chronic HepB
Immunisation
Screen pregnant women for HBsAg: if +ve give infant additional vaccine doses at birth
HBeAg+ve: give infant HepB Ig after birth
140
Hepatitis C
RNA virus
Post-transfusion hepatitis
IVDU
141
HepC transmission
Vertical transmission
Transmission more common if HIV+ve
Majority becom,e chronic carriers
142
HepC clinical features
Chronic carriers
| Can progress to cirrhosis or hepatocelllar carcinoma
143
HepC Mx
Sofosbuvir
Ledipasvir
Treatment not indicated ~<3years, may resolve spontaneously
144
HepD
RNA virus
Depends on HepB for replication
Superinfection
Cirrhosis occurs in chronic HDV infection
145
HepE virus
RNA virus
| Low-income countries
146
HepE transmission
Enterally, contaminated water
Mild self-limiting illness
Blood transfusion
Infected pork
147
HepE presentation
Fulminant hepatic failure in pregnant wo en
| High mortality rate
148
Acute liver failure (fulminant hepatitis)
Development of massive hepatic necrosis
Loss of liver function
With/without hepatic encephalopathy
High mortality
149
Presentation acute liver failure (fulminant hepatitis)
Preceding infection/ metabolic condition
Hours/weeks later with jaundice, encephalopathy, coagulopathy, hypoglycaemia, electrolyte disturbance
Early signs of encephalopathy: irritability/ confusion with drowsiness
Older children may be aggressive and difficult
150
Complications of acute liver failre
```
Cerebral oedema
Haemorrhage from gastritis
Coagulopathy
Sepsis
Pancreatitis
```
151
Causes of acute liver failure in <2
```
Infection (herpes simplex)
Metabolic disease
Sero negative hepatitis
Drug-induced
Gestational alloimmune liver disease
```
152
Children >2years causes of acute liver failure
```
Sero-negative hepatitis
Paracetamol overdose
Mitochondrial disease
Wilson disease
Autoimmune disease
```
153
Diagnosis of acute liver failure
```
Elevated transaminases
Alkaline phosphatase is increased
Coagulation is very abnormal
Plasma ammonium is elevated
Monitor acid-base balance
Blood glucose
Coagulation times
EEG: acute hepatic encephalopathy
CT: cerebral oedema
```
154
Management of acute liver failure
Refer to national paediatric liver centre
Maintain blood glucose >4mmol/L
Prevent sepsis: Ax, antifungal
Prevent haemorrhage with IV vitK, and PPI, H2 antagonists
Prevent cerebral oedema with fluid restriction and mannitol diuresis if oedema develo[s
155
Features suggestive of poor prognosis in acute liver failure
```
Shrinking liver
Rising bilirubin
Failing transaminases
Worsening coagulopathy
Progression to coma
Liver transplantation needed
```
156
Peptic ulcer diseae
Duodenal ulcers uncommon in children
157
When to consider peptic ulcers
Epigastric pain
Wakes them at night
Pain radiating to back
FH of peptic ulceration
158
Diagnosis of peptic ulcer disease
Gastric biopsy on endoscopy for H.pylori
Carbon 13 breath test, detects urea s produced
Stool antigen tests for H.pylori
159
Management of peptic ulcer disease in children
PPI: omeprazole
| Antibiotics if H.pylori
