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Y3 paediatrics > vomiting and malabsorption > Flashcards

vomiting and malabsorption Flashcards

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1
Q

what is vomiting

A

forceful ejection of gastric contents through the mouth

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2
Q

3 phases of vomiting

A

pre-ejction: pallor, nausea, tachycardia

ejection: retch (deep breaths taken against a closed glottis), vomit (contractions of abdo muscles, contraction of upper part of S intestine and stomach)

post ejection: lethargy, pallor, sweathing

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3
Q

why does vomiting occur

A

stimulation of vomiting centre in medulla oblongata

chemoreceptor trigger zone (base of 4th ventricle) is stimulated by certain chemical and toxins

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4
Q

triggers for vomiting

A
  • enteric pathogens
  • infection e.g. meningitis, encephalitis, otitis media, UTI, sepsis
  • visual/olfactory stimuli, fear
  • head injury, raised ICP
  • inner ear stimuli
  • metabolic derangements/chemotherapy
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5
Q

how do GI triggers stimulate vomiting

A

impulses sent to vomiting centre via vagus nerve

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6
Q

types of vomiting

A
  • vomiting w/ retching - associated w/ IC pathology if also in early morning
  • projectile
  • bilious
  • effortless/regurgitation
  • haematemesis
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7
Q

causes of vomiting in children

A

GOR

cow’s milk allergy

infection

intestinal obstruction

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8
Q

causes of vomiting in children

A

gastroenteritis

infection

appendicitis

intestinal obstruction

raised ICP

coealic disease

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9
Q

causes of vomiting in young adults

A

gastroenteritis

infection

H. pylori infection

appendicitis

raised ICP

DKA

cyclical vomiting syndrome

bulimia

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10
Q

what does palpation of an ‘olive’ tumour indicate

A

thickened pylorus - classical of pyloric stenosis

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11
Q

what does hypochloraemic metabolic acidosis indicate

A

large amounts of vomiting

losing HCl from stomach

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12
Q

when does pyloric stenosis typically occur

A

babies 4-12wks

M>F

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13
Q

features of pyloric stenosis

A

projectile non-bilious vomiting

weight loss

dehydration +/- shock

electrolyte disturbance

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14
Q

electrolyte disturbance in pyrloric stenosis

A

metabolic alkalosis

hypochloraemia

hypokalaemia

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15
Q

what is effortless vomiting

prognosis

A

almost always due to GOR

very common in infants

self-limiting and resolves spontaneously in the vast majority

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16
Q

when may effortless vomiting not resolve

A

cerebral palsy

progressive neurological problems

oesophageal atresia +/- TOF operated - associated oesophageal dysmotility, altered use of gastro-oesophageal junction

generalised GI motility issues

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17
Q

pathophysiology of reflex

A

lower oesophageal sphincter and diaphragmatic crura prevent expulsion of gastric contents into oesophagus

in babies LOS is lax and they are generally lying down

feeds are mainly liquid

  • predisposes to GOR

improves w/ age as solids are introduced and more sitting/standing posture

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18
Q

presenting symptoms of effortless vomiting

A
  • vomiting, haematemesis
  • feeding problems, FTT
  • apnoea, cough, wheeze, chest infection - aspiration pneumonia
  • Sandifer’s syndrome
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19
Q

what is sandifer’s syndrome

A

rare pediatric manifestation of gastro-esophageal reflux (GER) disease characterized by abnormal and dystonic movements of the head, neck, eyes and trunk

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20
Q

diagnosis of GOR and further investigations

A

hx and examination often enough

oesophageal pH/impendance monitoring - assess severity

endoscopy

radiological investigations - video fluroscopy (aspiration pneumonia, look for pharyngeal pouch or incoordination of swallowing mechanism) , barium swallow (rule out hiatus hernia or malrotation)

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21
Q

management of GOR

A

often child is thriving well, reassurance

usually starts ~2w/o, worse 4-6m/o, improves 1y/o

investigate for causes if not improving at 1y/o or FTT/growth faltering

  • look for severity and oesophagitis, rule out anatomical problems e.g. hiatus hernia
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22
Q

aims of barium swallow

A

dysmotility

hiatus hernia

reflux

gastric emptying

strictures

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23
Q

problems w/ barium swallow

A

inadequate contrast taken, may require NG tube

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24
Q

what does a pH study detect

A
  • pH sensor place ~5cm above gastro-oesophageal junction or LOS
  • measures number of times pH drops below 4 - suggesting reflux of acid into oesophagus
  • don’t detect weak or non-acid reflux
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25
why is pH studies combined w/ impendance monitoring
impendance monitoring detects acid, non-acid and air monitoring
26
when would an upper GI endoscopy be carried out in children
persistent symptoms, faltering growth, non-response to anti-reflux therapy done under GA
27
what is looked for on upper GI endoscopy
reflux oesophagitis oesophagitis due to other causes
28
treatment for GOR
feeding advice nutritional support medical treatment surgery
29
treatment for GOR - feeding advice
thickeners for liquid appropriateness of food - texture, amount behavioural programme - oral stimulation, removal of aversive stimuli feeding position check feed volumes - neonates: 150ml/kg/day, infants: 100ml/kg/day
30
treatment for GOR - nutritional support
calorie supplements exclusion diet - cow milk protein free trial for 4wks NG tube gastrostomy * NG tube/gastrostomy for severe reflux or unsafe swallow
30
treatment for GOR - nutritional support
calorie supplements exclusion diet - cow milk protein free trial for 4wks NG tube gastrostomy * NG tube/gastrostomy for severe reflux or unsafe swallow
31
treatment for GOR - medical treatment
feed thickener - gaviscon, thick and easy prokinetic drugs e.g. domperidone (usually not recommended due to cardiac side effects) acid suppressing drugs - H2 receptor blocker, PPI
32
treatment for GOR - indications for surgery
failure of medical treatment persistent: FTT, aspiration, oesophagitis vomiting w/o complications may not be an indication
33
treatment for GOR - surgical treatment
Nissen fundoplication * fundus is wrapped round oesophageal sphincter * usually required in children w/ cerebral palsy or neurodisabilities
34
complications of Nissen fundoplication
children w/ cerebral palsy are more likely to have complications - bloat, dumping, retching successful surgery may unmask more generalised GI motility problems
35
what does billous vomiting indicate
intestinal obstruction until proven otherwise should always be investigated
36
causes of billous vomiting
intestinal atresia - neonates malrotation +/- volvulus intussusception ileus Crohn's disease w/ strictures
37
investigations for billous vomiting
abdo XR consider contrast meal surgical opinion - exploratory laparotomy
38
fluid passage in intestines
9L enters duodenum 1.5L gets to colon \<200ml lost
39
SA of small intestine
v. large for absorption functions 600x increase in SA through mucosal folds and villi * S intestine resection or necrotising enterocolitis causes malabsorption - short gut syndrome
40
secretory component of S intestine
water for fluidity/enzyme transport/absorption ions e.g. duodenal bicarbonate defense mechanisms against pathogens/toxins/antigens
41
small intestine histology
* stem cells arise from crypts of Leiberkuhn * extruded into lumen at tip of villi
42
what is chronic diarrhoea
≥4 stools/day for \>4wks \<1wk - acute 2-4wks - persistent \>4wks - chronic and requires investigation for cause
43
causes of diarrhoes
* motility disturbance: toddler diarrhoea, IBS * active secretion (secretory): acute infective, IBD * malabsorption (osmotic): food allergy, coeliac, CF
44
what is osmotic diarrhoea
movement of water into the bowel to equilibrate osmotic gradient
45
what is osmotic diarrhoea usually a feature of
malabsorption * enzymatic defect e.g. 2y lactase deficiency * transport deficit e.g. glucose galactose transporter deficit
46
how can ostomic diarrhoea be utilised
mechanism of action of lactulose/movicol
47
clinical remission of osmotic diarrhoea
seen w/ removal of causative agent
48
what is secretory diarrhoea classically associated with
toxin production from vibrio cholerae and enterotoxigenic escherichia coli causes XS secretion of water and ions * can lose 24L/day in cholera
49
what is intestinal fluid secretion driven by in secretory diarrhoea
predominantly driven by active chloride secretion via CFTR
50
clinical approach to chronic diarrhoea
HX: * age at onset * abrubt/gradual onset * FHx * travel Hx, local outbreaks * noctural defecation - organic pathology consider growth and weight gain of child - growth faltering shouldn't be missed faeces analysis * appearance, stool culture, determination of secretory vs osmotic
51
faeces analysis
undigested food greasy/frothy/foul smelling - malabsorption
52
differentiation of osmotic and secretory diarrhoea
53
when is fat malabrosption seen
pancreatic disease - diarrhoea due to lack of lipase and resultant steatorrhoea classically CF hepatobiliary disease - chronic liver disease, cholestasis
54
what is the commonest cause for malabsorption in children
coeliac disease
55
what is coeliac disease
AI gluten sensitive enteropathy - wheat, rye, barley
56
how common is coeliac disease
1% of western population affected
57
genetic susceptibility to coeliac
DQ2/DQ8 * not everyone w/ susceptibility will develop disease * if you don't have genetics - unlikely to develop coeliac - high -ve predictive value
58
symptoms of coeliac disease
abdo bloating diarrhoea FTT short stature constipation fatigue dermatitis herpatiformis * usually seen between 12-14mths but can be diagnosed later * more common in children w/ other AI conditions and 1st degree relatives
59
screening tests for coeliac disease
serological screens: * anti-tissue transglutaminase - high sensitivity * anti-endomysial - high specificity * serum IgA * concurrent IgA deficiency in 25% may result in false -ve gold standard = duodenal biopsy genetic testing - HLA DQ2/DQ8
60
endoscopic findings in coeliac
oedema erythematous mucosa blunting of villi scalloping and dipping
61
histology in coeliac disease
lymphocytic infiltration of surface epithelium partial/total villous atrophy crypt hyperplasia
62
diagnosing coeliac - ESPGHAN/BSPGHAN guidelines
symptomatic children anti TTG \>10x upper limit of normal +ve anti-endomysial ab HLA DQ2/DQ8 +ve * if all above are present - diagnosis made w/o biopsy * if any of the above aren't present, proceed to endoscopy
63
treatment of coeliac disease
* gluten free diet for life * gluten must not be removed prior to diagnosis as serological and histological features will resolve * \<2y/o - rechallenge and rebiopsy may be warranted
64
what is the risk in untreated coeliac disease
rare small bowel lymphoma

Y3 paediatrics (45 decks)

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