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Paediatrics > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

What vitamin supplements should children receive?

A

Vitamins A, C and D and iron

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2
Q

What are WHO guidelines on infant feeding?

A

Breast feeding for 6 months

First feed within 1 hour of birth

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3
Q

What are the pros and cons of breastfeeding?

A

Pros

  • reduces GI infection and NEC
  • enhances relationship
  • reduces risk of insulin dependent diabetes, hypertension and obesity
  • reduces breast cancer risk in mother

Cons

  • unknown quantity fed
  • transmission of diseases and drugs
  • nutrient inadequacies
  • risk of breast-milk jaundice
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4
Q

What foods should be avoided before 6 months?

A 
Wheat
Eggs
Fish
Salt
Sugar
Honey
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5
Q

What is normal formula based on?

A

Formulas are based on cows milk but with more iron and vitamins and less protein and electrolytes

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6
Q

What is specialised formula used for?

A 
Cow's milk protein allergy
Lactose intolerance
CF
Neonatal cholestatic liver disease
Post intestinal resection
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7
Q

What are the components of specialised formula?

A

Protein - hydrolysed cow’s milk protein, amino acids or from soya
Carbohydrate - glucose polymer (normally lactose)
Fat - medium and long chain triglycerides (don’t need bile or pancreatic enzymes)

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8
Q

What is hydrolysed formula?

A

Cow’s milk with milk proteins and lactose broken down to be easier to digest
Partial hydrolysates contain larger proportion of long chains but are only intended for prophylactic use if FH of allergy

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9
Q

What is the normal stool pattern in children?

A

Infant - 4/day
1yo - 2/day
4yo - adult routine

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10
Q

What causes constipation?

A

Hirschsprung’s
Hypothyroidism
Hypercalcaemia
Anorectal abnormalities

Dehydration
Anal fissure

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11
Q

What are red flag symptoms of constipation?

A
  • Failure to pass meconium within 24 hours - Hirschsprung’s
  • Failure to thrive - hypothyroidism, celiac disease
  • Abdominal distension - Hirschsprung’s, GI dysmotility
  • Abnormal lower limb motility - lumbosacral pathology
  • Sacral dimple/naevus, hairy pathc, discoloured skin over spine - spina bifida occulta
  • Perianal bruising/multiple fissures - sexual abuse
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12
Q

How is constipation treated?

A

Mild laxatives - polyethylene glycol (movicol)
Stimulate laxatives - senna or picosulphate
Osmotic laxatives - lactulose
Enema or manual evacuation

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13
Q

How is failure to thrive diagnosed?

A 
Mild = fall across 2 centiles
Severe = fall across 3 centiles

Catch down weight = baby born at normal weight but drops down to genetically determined weight

Non-organic

  • feeding problems
  • lack of food or irregular feeding times
  • maternal depression, abuse or low education

Organic

  • impaired suck/swallow
  • Crohn’s, chronic renal or liver disease, CF

Inadequate retention

  • vomiting
  • severe GOR

Malabsorption

  • coeliac disease
  • CF
  • short gut syndrome
  • NEC
  • cholestatic liver disease

Failure to utilise nutrients

  • Down’s syndrome
  • IUGR
  • prematurity
  • infection

Increased requirements

  • thyrotoxicosis
  • CF
  • malignancy
  • chronic infection
  • congenital heart disease
  • chronic renal failure
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14
Q

What virus commonly causes gastroenteritis?

A

Rotavirus

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15
Q

What children are at risk of dehydration?

A
  • children
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16
Q

What are red flag signs of dehydration?

A
  • altered responsiveness
  • sunken eyes
  • tachycardia
  • tachypnoea
  • reduced skin turgor
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17
Q

How is dehydration treated?

A

Clinical dehydration (5-10%)

  • fluid deficit replacement (50ml/kg) over 4hrs + maintenance fluid
  • ORS often and small amounts
  • ORS via NG tube

Shock (>10%)

  • 0.9% sodium chloride rapid infusion
  • fluid deficit replacement (100ml/kg) over 4hrs + maintenance fluid
  • monitor electrolytes + potassium IV
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18
Q

What medicines are used in gastroenteritis?

A

No anti-diarrhoeal or anti-emetics

Abx if suspect: septicaemia, salmonella,

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19
Q

What is post-gastroenteritis syndrome?

A

Normal diet –> watery diarrhoea
Temporary lactose intolerance can be confirmed by presence of non-absorbed sugar in stools - +ve Clinitest

ORS for 24hrs then normal diet

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20
Q

What is gastro-oesophagealo reflux?

A

Involuntary passage of gastric contents into oesophagus
Common in infancy caused by inappropriate relaxation of the lower oesophageal sphincter as a result of functional immaturity

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21
Q

What is the natural course of GOR?

A

Predominantly fluid diet,
horizontal posture, short intra-abdominal length of oesophagus all
contribute
By 12 months nearly all the symptoms will have spontaneously resolved.
Due to a combination of maturation of the lower oesophageal
sphincter, assumption of an upright posture and more solids in the diet.

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22
Q

How is gastro-oesophageal reflux treated?

A

Uncomplicated - parental reassurance, adding inert thickening agents
to feeds, positioning in a 30 degree head-up position after
feeds

Drugs - ranitidine or omeprazole to reduce volume of gastric contents

Surgery - Nissen fundoplication (fundus wrapped around oesphagus)

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23
Q

What are complications of gastro-oesophageal reflux?

A
  • failure to thrive from severe vomiting
  • oesophagitis - haematemesis, feeding discomfort, heartburn, iron deficiency anaemia
  • pulmonary aspiration
  • SIDS
  • Barret’s oesophagus - cells change from squamous to columnar -> cancer
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24
Q

What causes unconjugated jaundice?

A
  • breast milk jaundice
  • infection
  • haemolytic anaemia
  • hypothyroidism
  • Criger-Najjar syndrome
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25
Q

What causes conjugated jaundice?

A
  • bile duct obstruction - biliary atresia/choledochal cyst
  • neonatal hepatitis syndrome - CF, alpha-1 antitrypsin deficiency, congential infection
  • intrahepatic biliary hypoplasia
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26
Q

What causes jaundice

A

Haemolytic disorders:

  • rhesus haemolytic disease
  • ABO incompatibilty
  • spherocytosis
  • G6PD deficiency

Congenital infection

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27
Q

What causes jaundice 2 days-2 weeks?

A

Physiological jaundice
- change from fetal to neonatal haemoglobin

Breast milk jaundice
- increased enterohepatic circulation (unconjugated)

Dehydration

Infection
- unconjugated hyperbilirubinaemia from poor fluid intake, haemolysis and reduced hepatic function

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28
Q

What causes jaundice >2 weeks?

A

If conjugated - biliary atresia (dark urine and pale stools)

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29
Q

What is biliary atresia and how does it present?

A

Progressive disease with destruction or absence of extrahepatic biliary tree and intrahepatic biliary ducts

–> chronic liver failure + death

Normal birthweight but fail to thrive with hepatomegaly and splenomegaly

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30
Q

How is biliary atresia investigated?

A

Abdo ultrasound - contracted or absent gallbladder
Radioisotope scan - good uptake by liver but no excretion into bowel
Cholangiography - done during laparotomy and fails to outline normal biliary tree

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31
Q

What is coeliac disease?

A

Gluten component provokes a damaging immunological response in proximal small intestinal mucosa

Villi become progressively shorter then absent –> flat mucosa

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32
Q

How does coeliac disease present?

A

8-24 months after introduction of wheat products

Failure to thrive
Abdominal distension
Buttock wasting
Abnormal stools
Irritability
D+V
Fatigue
Iron defiency anaemia
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33
Q

What conditions increase the risk of coeliac disease?

A 
Autoimmune thyroid disease
IBS
Dermatitis herpetiformis
Type 1 DM
FH
Down's syndrome
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34
Q

How is coeliac disease diagnosed?

A

Serological screening of at risk children and children with symptoms
Small intestinal biopsy - mucosal changes (increased lymphocytes and villous atrophy/crypt hypertrophy)

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35
Q

What is colic?

A

Paroxysmal crying
Drawing up of knees
Passage of excessive flatus

Occurs in first few weeks and resolves by 4 months

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36
Q

What is cow’s milk allergy/intolerance?

A

Allergy
Immune response to protein, likely IgE mediated

Intolerance
Not immune mediated

37
Q

How does cow’s milk allergy present?

A

Cutaneous reactions - urticaria, atopic dermatitis, angioedema, contact rashes

GI reactions - N+V, colitis, constipation, diarrhoea

Respiratory reactions - asthma, wheezing, laryngeal oedema, otitis media, anaphylaxis

38
Q

How does Crohn’s disease present?

A
  • lethargy
  • ill health
  • growth failure
  • puberty delay
  • abdo pain
  • diarrhoea
39
Q

Where does Crohn’s affect?

A
  • transmural and focal
  • distal ileum + proximal colon but can affect anywhere
  • inflamed and thickened bowel –> strictures and fistulae
  • oral lesions, perianal skin tags, erythema nodosum
  • histology shows non-caseating epithelioid cell granulomata
40
Q

What are the extra-systemic manifestations of Crohn’s and UC?

A

Crohn’s

  • oral lesions
  • perianal skin tags
  • arthralgia
  • growth failure
  • osteoporosis

UC

  • aphthous ulcers
  • episcleritis
  • arthritis
  • ankylosing spondylitis
  • DVT

Both

  • uveitis
  • erythema nodosum
  • clubbing
41
Q

How is Crohn’s treated?

A
  • nutritional therapy - normal food replaced by whole protein modular feeds for 6-8 weeks
  • systemic steroids
  • immunosuppression (methotrexate, azathioprine) to maintain relapse
  • anti-TNF (infliximab) needed if conventional treatments have failed
  • enteral nutrition - correct growth failure
42
Q

How is UC treated?

A
  • aminosalicylates induce and maintain remission
  • topical steroids for rectum and sigmoid colon
  • systemic steroids for acute exacerbations
  • immunosuppression (methotrexate) to maintain remission
  • screening for adenocarcinomas
43
Q

What is fulminating disease and how is it treated?

A

Occurs with UC

  • IV fluids and steroids
  • ciclosporin
  • colectomy with ileostomy or ileorectal pouch
44
Q

How does UC present?

A
  • rectal bleeding
  • colicky pain
  • diarrhoea
  • weight loss less common
45
Q

Where does UC affect?

A
  • recurrent, inflammatory and ulcerating
  • involves mucosa of colon
  • children more likely to have pan-colitis
  • histology shows mucosal inflammation, crypt damage and ulceration
46
Q

What is encopresis due to constipation and overflow?

A

Child >4 who was previously toilet trained and is passing stools into underwear
constipation –> retention of stools to avoid pain –> water lost in colon so stools become more painful
distension of colon and loss of sensation to defecate –> rectal sphincter distension and stools forced out

47
Q

What is a food allergy?

A
  • pathological immune response against specific food protein
  • usually IgE mediated
  • usually primary where child failed to develop immune tolerance to food
  • can be secondary where they initially tolerate the food and then become allergic (–> itchy mouth but no systemic symptoms)
48
Q

How do food allergies and intolerances present?

A

IgE mediated allergy

  • 10-15 mins after ingestion
  • urticartia –> facial swelling –> anaphylaxis

Non-IgE mediated allergy

  • hours after ingestion
  • D+V, abdo pain, failure to thrive
  • colic or ezcema
  • blood in stools

Intolerance

  • longer after ingestion
  • D+V
49
Q

What are type 1 and 2 allergic reactions?

A

Type 1 - instant
- itching, swelling, hives and breathing difficulties

Type 2 - not immediate
- can be 24-72 hours after ingestion

50
Q

How are food allergies managed?

A
  • avoid triggers with dietician input to minimise nutritional deficits
  • antihistamines if no cardiorespiratory symptoms
  • adrenaline if severe reaction
51
Q

What is the prognosis of food allergies?

A

Cow’s milk and eggs resolve in early childhood

Nuts and seafood persist

52
Q

What is functional/recurrent abdominal pain?

A
  • pain sufficient to interrupt normal activities which lasts for >3 months
  • periumbilical pain
  • commonly IBS, abdomial migraine or functional dyspepsia
53
Q

What investigations are done for recurrent abdominal pain?

A
  • inspect perineum for anal fissures
  • assess growth
  • urine dipstick (UTI)
  • ## abdo ultrasound (gallstones and pelviureteric junction obstruction)
54
Q

What is abdominal migraine?

A
  • abdo pain + headaches

- vomiting and facial pallor

55
Q

What is IBS?

A
  • altered gastrointestinal motility
  • abnormal sensation of intra-abdominal events
  • bloating, feeling of incomplete defecation, constipation
56
Q

What is functional dyspepsia?

A
  • symptoms of peptic ulceration
  • early satiety
  • bloating, vomiting, delayed gastric emptying
57
Q

What is gastritis?

A
  • H. pylori infection can cause peptic ulcers
  • N+V, abdo pain
  • gnawing/burning feeling above navel
  • haematemesis, malaena
  • also caused by pernicious anaemia, infections and bile reflux
58
Q

How is H. pylori tested for and treated?

A

urease breath test

PPIs and amoxicillin + metronidazole or clarithromycin

59
Q

What are lifestyle changes for gastritis?

A
  • eat smaller, more frequent meals
  • avoid acidic, spicy or fried food
  • moderate alcohol
  • avoid NSAIDs
  • reduce smoking
60
Q

What is Hirschsprung disease?

A
  • more common in boys
  • may be associated with Down’s, MEN, malrotation and gastric diverticulum
  • absence of ganglion cells from myenteric and submucosal plexuses of part of colon –> narrow and contracted segment
  • narrow segment extends from rectum for variable distance
  • mostly rectosigmoidal but can affect entire colon
61
Q

How does Hirschsprung’s present?

A
  • intestinal obstruction in neonatal period
  • failure to pass meconium within 24hrs
  • abdo distension
  • bile-stained vomiting
62
Q

How is Hirschsprung’s diagnosed and treated?

A
  • rectal biopsy showing lack of ganglion cells
  • barium study to show length
  • colostomy then anastomoses of normally innervating bowel to anus
63
Q

What are the serious complications of Hirschsprung’s?

A
  • enterocolitis during first few weeks
  • can be due to C. diff
  • abdo pain, fever, foul smelling +/- bloody diarrhoea and vomiting
  • -> sepsis, transmural intestinal necrosis and perforation
  • give broad spectrum Abx and fluids
64
Q

What is malabsorption?

A
  • affects digestion or absorption of nutrients

- presents as abnormal stools, failure to thrive, nutrient deficiencies

65
Q

What are DD in malabsorption?

A
  • coeliac disease
  • cholestatic liver disease/biliary atresia - fat and fat-soluble malabsorption
  • lymphatic leakage/obstruction - chylomicrons (absobed lipids) are unable to reach thoracic duct
  • short bowel syndrome - nutrient, water and electrolyte malabsorption
  • loss of terminal ileal function (resection or Crohn’s) - absent bile acid and B12 absorption
  • exocrine pancreatic dysfunction (CF) - absent lipase, protease and amyase so defetive digestion of triglyceride, protein and starch
  • small-intestinal mucosal disease (coeliac disease) - specific enzyme deficiencies
66
Q

What investigations are done for malabsorption?

A

Stool samples - pH, bile acid so large proteins, parasites
Urinalysis - kidney shares same transporters as gut so substances may be in high concentrations
Endoscopy/biopsy of intestine

67
Q

What is malnutrition and how is it investigated?

A

Nutritional deficiency
Common in chronic disease, eating disorders
Dietary assessment - what the child eats
Weight/height/mid-arm circumference
Impairs immunity, wound healing, worsens outcomes

68
Q

How is malnutrition treated?

A

Enteral nutrition - digestive tract is functioning so feeds given NG, gastrostomy or NJ
Feeds given overnight to allow child to eat normally during day

Parenteral nutrition - can be used exclusively or as adjunct
Feed given IV via peripheral or central catheter
Complications include vascular access, sepsis and liver disease

69
Q

What is the MUST tool?

A

Identifies adults who are malnourished, at risk of or obese. Also includes management guidelines used to develop care plan

Step 1: Calculate BMI
Step 2: Calculate percentage unplanned weight loss and score with table
Step 3: Establish acute disease effect and score
Step 4: Add scores from 1-3 together to obtain risk of malnutrition
Step 5: Create care plan

Paediatric Yorkhill Malnutrition Score used in children

70
Q

What are protein and energy malnutrition?

A

Marasmus - reduced calories (presents in less than 1yo)

Kwashiorkor - reduced proteins (large tummy)

71
Q

What is mesenteric adenitis?

A

Inflamed lymph glands causing abdominal pain

Common cause of abdo pain in

72
Q

What are the main DD for mesenteric adenitis?

A

Ectopic pregnancy
Appendicitis

Ix: blood tests, pregnancy test, PR

73
Q

What is the recommended intake for infants?

A

0-6 months - 115kcal/kg (calories) + 2.2g/kg (protein)

6-12 months - 95kcal/kg + 2.0g/kg

74
Q

What are symptoms of over-feeding?

A

Increased GI reflux
Obesity
Lactose overload - cramps, gas, crying, watery bowel movements

75
Q

What is toddler diarrhoea?

A

Chronic non-specific diarrhoea
Stools of varying consistency - well formed–> explosive and loose
Undigested veg in pale, smelly poo
Child is well and thriving

Thought to be due to underdeveloped intestinal motility –> intestinal hurry
Grow out of symptoms by 5 but faecal continence may be delayed

Tx: diet high in fat and fibre, reduce fresh fruit juice

76
Q

What are more serious causes of diarrhoea?

A 
Coeliac disease
Gastroenteritis
Lactose intolerance
Post bowel surgery
Malabsorption
77
Q

What parasites can affect children?

A

Threadworm - can cause itching around pubic area which is worse at night and disturbs sleep
Tx: mebendazole for entire family

Giardia lamblia - persistent diarrhoea (>10 days) and malabsorption
Faecal-oral through contaminated water

Cryptosporidium - common in AIDS children
Contamination from animals (petting zoo)
Low grade fever, malaise, watery diarrhoea for 2 weeks

78
Q

What are the clinical features of viral hepatitis?

A 
N+V
Abdo pain
Lethargy
Jaundice (only about half)
Hepatomegaly
Splenomegaly
Increased liver transaminases
79
Q

What is Hep A?

A

RNA virus
Faecal-oral transmission
Can be asymptomatic, it recover within 2-4 weeks
–> cholestatic hepatitis or fulminant hepatitis
Close contacts need prophylaxis

80
Q

What is Hep B?

A

DNA virus
Perinatal transmission, blood transfusion, dialysis, horizontal family spread, sexually transmitted
Infants who contract it prenatal are asymptomatic –> chronic carriers
Older children are asymptomatic or have acute hepatitis –> fulminant hepatic failure or chronic carrier

81
Q

What is Hep C?

A

RNA virus
IV drug users, vertical transmission (esp with HIV co-infection)
Most become chronic carriers –> cirrhosis or hepatocellular carcinoma

82
Q

What is Hep D?

A

RNA virus which requires Hep B for replication

Causes acute exacerbation of chronic hepatitis –> cirrhosis

83
Q

What is Hep E?

A

RNA virus

Enterally transmitted

84
Q

What are the nutritional requirements (energy and protein) at different ages?

A

0-6 months - 115 kcal/kg/day + 2.2g/kg/day

6-12 months - 95 kcal/kg/day + 2g/kg/day

Decreases to around 40 in females and 60 in males

85
Q

How is fluid deficit calculated and what fluid is used?

A

% dehydration x weight (kg) x 10

0.9% NaCl with 5% dextrose

10% dextrose if hypoglycaemic

86
Q

How are maintenance fluids calculated?

A

> 10kg - 100ml/kg
10-20kg - 50ml/kg
20kg - 20ml/kg

87
Q

What are types of dehydration?

A

Isonatraemia - normal in unwell people, give 0.9% saline

Hyponatraemia (loss has been replaced with water only) - NaCl headache, N+V, lethargy. seizures
Give 5% dextrose in 0.9% NaCl

Hypernatraemia (loss has been replaced by concentrate)
Give 5% dextrose in 0.9% NaCl slowly over 48hrs

88
Q

What is colostrum?

A

Liquid produced by mother in first few days

Content of protein and immunoglobulin are much higher

Paediatrics (14 decks)

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