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Y3 paediatrics > vomiting and malabsorption > Flashcards

vomiting and malabsorption Flashcards

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
Q

why is pH studies combined w/ impendance monitoring

A

impendance monitoring detects acid, non-acid and air monitoring

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26
Q

when would an upper GI endoscopy be carried out in children

A

persistent symptoms, faltering growth, non-response to anti-reflux therapy

done under GA

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27
Q

what is looked for on upper GI endoscopy

A

reflux oesophagitis

oesophagitis due to other causes

28
Q

treatment for GOR

A

feeding advice

nutritional support

medical treatment

surgery

29
Q

treatment for GOR - feeding advice

A

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
Q

treatment for GOR - nutritional support

A

calorie supplements

exclusion diet - cow milk protein free trial for 4wks

NG tube

gastrostomy

  • NG tube/gastrostomy for severe reflux or unsafe swallow
30
Q

treatment for GOR - nutritional support

A

calorie supplements

exclusion diet - cow milk protein free trial for 4wks

NG tube

gastrostomy

  • NG tube/gastrostomy for severe reflux or unsafe swallow
31
Q

treatment for GOR - medical treatment

A

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
Q

treatment for GOR - indications for surgery

A

failure of medical treatment

persistent: FTT, aspiration, oesophagitis

vomiting w/o complications may not be an indication

33
Q

treatment for GOR - surgical treatment

A

Nissen fundoplication

  • fundus is wrapped round oesophageal sphincter
  • usually required in children w/ cerebral palsy or neurodisabilities
34
Q

complications of Nissen fundoplication

A

children w/ cerebral palsy are more likely to have complications - bloat, dumping, retching

successful surgery may unmask more generalised GI motility problems

35
Q

what does billous vomiting indicate

A

intestinal obstruction until proven otherwise

should always be investigated

36
Q

causes of billous vomiting

A

intestinal atresia - neonates

malrotation +/- volvulus

intussusception

ileus

Crohn’s disease w/ strictures

37
Q

investigations for billous vomiting

A

abdo XR

consider contrast meal

surgical opinion - exploratory laparotomy

38
Q

fluid passage in intestines

A

9L enters duodenum

1.5L gets to colon

<200ml lost

39
Q

SA of small intestine

A

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
Q

secretory component of S intestine

A

water for fluidity/enzyme transport/absorption

ions e.g. duodenal bicarbonate

defense mechanisms against pathogens/toxins/antigens

41
Q

small intestine histology

A
  • stem cells arise from crypts of Leiberkuhn
  • extruded into lumen at tip of villi
42
Q

what is chronic diarrhoea

A

≥4 stools/day for >4wks

<1wk - acute

2-4wks - persistent

>4wks - chronic and requires investigation for cause

43
Q

causes of diarrhoes

A
  • motility disturbance: toddler diarrhoea, IBS
  • active secretion (secretory): acute infective, IBD
  • malabsorption (osmotic): food allergy, coeliac, CF
44
Q

what is osmotic diarrhoea

A

movement of water into the bowel to equilibrate osmotic gradient

45
Q

what is osmotic diarrhoea usually a feature of

A

malabsorption

  • enzymatic defect e.g. 2y lactase deficiency
  • transport deficit e.g. glucose galactose transporter deficit
46
Q

how can ostomic diarrhoea be utilised

A

mechanism of action of lactulose/movicol

47
Q

clinical remission of osmotic diarrhoea

A

seen w/ removal of causative agent

48
Q

what is secretory diarrhoea classically associated with

A

toxin production from vibrio cholerae and enterotoxigenic escherichia coli

causes XS secretion of water and ions

  • can lose 24L/day in cholera
49
Q

what is intestinal fluid secretion driven by in secretory diarrhoea

A

predominantly driven by active chloride secretion via CFTR

50
Q

clinical approach to chronic diarrhoea

A

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
Q

faeces analysis

A

undigested food

greasy/frothy/foul smelling - malabsorption

52
Q

differentiation of osmotic and secretory diarrhoea

A
53
Q

when is fat malabrosption seen

A

pancreatic disease - diarrhoea due to lack of lipase and resultant steatorrhoea

classically CF

hepatobiliary disease - chronic liver disease, cholestasis

54
Q

what is the commonest cause for malabsorption in children

A

coeliac disease

55
Q

what is coeliac disease

A

AI

gluten sensitive enteropathy - wheat, rye, barley

56
Q

how common is coeliac disease

A

1% of western population affected

57
Q

genetic susceptibility to coeliac

A

DQ2/DQ8

  • not everyone w/ susceptibility will develop disease
  • if you don’t have genetics - unlikely to develop coeliac - high -ve predictive value
58
Q

symptoms of coeliac disease

A

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
Q

screening tests for coeliac disease

A

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
Q

endoscopic findings in coeliac

A

oedema

erythematous mucosa

blunting of villi

scalloping and dipping

61
Q

histology in coeliac disease

A

lymphocytic infiltration of surface epithelium

partial/total villous atrophy

crypt hyperplasia

62
Q

diagnosing coeliac - ESPGHAN/BSPGHAN guidelines

A

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
Q

treatment of coeliac disease

A
  • 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
Q

what is the risk in untreated coeliac disease

A

rare small bowel lymphoma

Y3 paediatrics (45 decks)

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