Gastroenterology Flashcards

1
Q

red flags for constipation in a child?

A

-symptoms appearing from birth or during 1st few wks of life- may indicate Hirschsprung’s disease (congenital aganglionic megacolon).
-delay in passing meconium for more than 48 hours after birth, in a full-term baby-may indicate Hirschsprung’s disease or CF.
-abdo distension with vomiting-may indicate Hirschsprung’s disease or intestinal obstruction.
-FH of Hirschsprung’s disease.
-ribbon stool pattern-may indicate anal stenosis (more likely to present in a child younger than 1 yr of age).
-leg wkness or motor delay-may indicate a neurological or SC abnormality.
examination may reveal unexplained lower limb deformity or abnormal neuromuscular signs, including abnormal reflexes.
-abnormal anus appearance (including fistulae,bruising,fissures,tight or patulous (widely patent) anus,anteriorly placed anus (anal ectopia),lichen sclerosis, or an absent anal wink (a reflex contraction of the external anal sphincter when the skin around the anus is stroked, may indicate spinal or neurological pathology), bruising or multiple fissures-?sexual abuse.
-abnormalities in LS and gluteal regions (such as asymmetry of the gluteal muscles, evidence of sacral agenesis, scoliosis, discoloured skin, naevi, hairy patch, sinus or central pit)-?spina bifida occulta.

child should be r/f urgently to appropriate specialist.

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2
Q

what are amber flags in presentation of constipation in children?

A

child needs r/f for specialist assessment but can be treated in primary care whilst waiting assessment:

  • evidence of faltering growth, developmental delay, or concerns about wellbeing that may indicate systemic condition-should arrange testing for possible coeliac disease, hypothyroidism, CF and electrolyte disturbance if appropriate.
  • constipation triggered by intro. of cows milk
  • concern of possible child maltreatment-follow local safeguarding procedure.
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3
Q

diagnostic concern if constipation and failure to thrive/growth failure symptoms?

A

hypothyroidism
coeliac disease
CF-usually diarrhoea and failure to thrive in infants
hirschsprung disease

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4
Q

why is knowing whether a baby is breast or bottle fed import with regards to constipation presentation?

A

in determining whether stool pattern normal for child, as breast fed infants may not pass stools for several days and be entirely healthy.

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5
Q

management of patients with overflow soiling due to long standing constipation?

A
  • must explain to child and parents that soiling is involuntary and recovery can be achieved with treatment to recover normal rectal size and sensation that has been disturbed with rectum overdistension.
  • initial aim=evacuate rectum completely-disimpaction regimen with Movicol laxative-stool softener, escalating dose regimen over 1-2wks, or until impaction resolution, stimulant laxative may also be needed if this is unsuccessful. if can’t tolerate movicol may use osmotic laxative.
  • follow with maintenance tment e.g. movicol, which is gradually reduced over mnths.
  • ensure sufficient fluid and fibre in diet, and encourage child to sit on toilet post meals to utilise physiological gastrocolic reflex.
  • explore child’s concerns and motivation to change, provide encouragement e.g. star chart, for regular defecation in the toilet.
  • some cases may require psychiatric r/f.
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6
Q

presentation of Hirschsprung disease?

A

neonate: failure to pass meconium within 1st 24hrs of life-*alternative differential is meconium ileus due to CF, or small bowel obstruction from another cause resulting in subsequent delayed or absent passage of meconium.
later, abdo distension-tympanic on percussion and bile stained vomiting
rarely neonatal meconium plug syndrome or appendicitis
later childhood: chronic constipation-resistant to usual tments and enemas, usually without soiling, assoc. with abdo distension and possible growth failure as disease causes early satiety and abdo discomfort and distention due to constipation causing poor nutrition and weight gain. DRE-empty rectum, but may cause forceful faecal material expulsion on exam. completion.

note constipation presenting after 1mnth of age unlikely hirschsprung’s

infants occasionally may present with severe, life threatening hirschsprung enterocolitis during 1st few wks of life, sometimes due to C.diff infection-abdo pain, fever, foul smelling and poss. bloody diarrhoea with vomiting.

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7
Q

how is hirschsprung disease diagnosed?

A

suction rectal BIOPSY or transanal wedge resection biopsy-absence of ganglion cells, along with presence of large acetylcholinesterase-+ve nerve trunks.
suction biopsy 2-2.5cm above dentate line on poster. wall to reduce perforation risk.

unreliable for diagnosis but anorectal manometry-failure of internal sphincter relaxation in response to balloon inflation or barium studies can be useful for giving idea to surgeon of length of aganglionic segment.
double contrast barium enema-proximal dilated colonic segment with transition zone and narrowed distal colonic segment.

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8
Q

mangement of hirschsprung disease?

A
  • acute problems-intestinal obstruction-IV rehydration, bowel decompression-NGT and DRE or normal saline enemas OD/BD.
  • broad spec Abx-metronidazole and aggressive fluid rehydration if enterocolitis. bowel irrigation to evacuate rectosigmoid contents, overcoming distal obstruction.

-surgical definitive management: usually initial colostomy followed by anastamosing normally innervated bowel to anus.
?transanal approach or Swenson’s procedure-full thickness excision of rectum and remaining aganglionic bowel. normal ganglionic bowel is then pulled through.
surgical complications: specific immediate, early-anastamosis leakage, persisting constipation, soiling and incontinence, and late-intestinal obstruction poss. due to adhesions, resected segment stricture.

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9
Q

what is hirschsprung disease?

A

aganglionic large bowel with absence of parasympathetic ganglion cells from myenteric and submucosal plexuses extending proximally from rectum, producing a narrow, contracted segment as unable to relax.
5X more common in boys

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10
Q

diseases associated with hirschsprung disease?

A

Down’s syndrome-prognosis less favourable, permanent colostomy may be recommended
MEN-MEN2A and MEN2B
gastric diverticulum
intestinal atresia
Waardenburg’s syndrome-congenital deafness, partial albinism

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11
Q

what accounts for most mortality assoc. with hirschsprung disease?

A

enterocolitis-can progress to sepsis, transmural intestinal necrosis and perforation if not treated early.

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12
Q

what is failure to thrive?

A

failure of weight gain in particular, but espec. if long standing, may also include lack of linear growth.
if head circumference significantly affected then this suggests and intrauterine onset

must demonstrate inadequate weight gain on centile chart-mild failure to thrive if weight falls across 2 centile lines, 3=severe.
most have weight below 2nd centile. below 0.4 should always trigger evaluation.

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13
Q

how does pattern of height, weight and head circumference curves on percentile charts relative to each other help with determining cause of failure to thrive?

A

if all percentiles equally affected, might be intrauterine TORCH infections-toxoplasma, other-syphilis, rubella, CMV, HSV and VSV, or chromosomal abnormalities.

height most affected-?endocrinopathies and skeletal dysplasias

weight most affected-?malnutrition-height less so, and head circumference relatively normal.

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14
Q

what should skin be examined for in failure to thrive patient?

A

dermatitis herpetiformis-symmetrical distribution of VERY itchy papules (prurigo) and vesicles on normal or erythematous skin, so often presents as erosions and crusting due to immediate scratching, found on elbows, knees, scalp, shoulders and buttocks. ? underlying coeliac disease.
erythema nodosum-IBD
pyoderma gangrenosum-IBD
ichthyosis-sign of malnutrition, shwachman-diamond syndrome-AR congenital disorder with exocrine pancreatic insufficiency.

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15
Q

features to look out for on hand examination of failure to thrive pt?

A

nails: clubbing-CF, chronic liver disease, cyanotic congenital heart disease, IBD. leukonychia.
hand structure-dysmorphic syndromes
radial and femoral pulses-coarctation of aorta, CHD.
moving to brachial area-BP for aorta coarctation and renal disease, hypotension-Na+ low, dehydration.

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16
Q

features of TORCH congenital infection o/e of baby with failure to thrive?

A

low weight, height and head circumference on percentile charts
eyes-cataract, chorioretinitis
abdomen-hepatosplenomegaly

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17
Q

head and neck features to look out for in o/e of infant with failure to thrive?

A

nutrition related signs e.g. conjunctival pallor-anemia
dysmorphic features, macrocephaly, scars, shunts
eyes-cataract, chorioretinitis, retinitis pigmentosa (abetalipoproteinaemia, shwachman’s syndrome), papilloedema (hydrocephalus, IC tumour), EO movements (neurol. disease)
mouth-thrush (cell-mediated immunity defects), cleft palate (?DiGeorge syndrome-deletion on chromosome 22), observe method of feeding.

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18
Q

examples of chest deformities that may be seen in failure to thrive infant?

A

harrison’s sulcus-horizontal groove along lower border of thorax corresponding to costal insertion of diaphragm, ?chronic lung disease e.g. CF.
sternal deformity-pectus excavatum and carinatum-syndromes

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19
Q

what cause of failure to thrive may be indicated by buttock excoriations o/e of pt?

A

carbohydrate intolerance

look also for reducing substances in urine

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20
Q

how would you consider investigating a child with failure to thrive?**

A

admit child to hospital if undernutrition seems possible and see if child can gain weight with adequate calories.
if they don’t, investigate for malabsorption or any chronic disease*
investigations to consider: FBC-anaemia-may be Fe deficiency, neutropenia, lymphopenia-immune deficiency
CRP
serum ferritin-Fe deficiency
Igs
anti-TTG and anti-EMA-coeliac
serum creatinine, Us and Es, acid base, Ca2+, PO43-metabolic disorders, renal failure, renal tubular acidosis, william syndrome
LFTs-liver disease, malabsorption, metabolic disorder
TFTs
urine microscopy, culture and dip-UTI, renal disease
stool microscopy, culture and faecal elastase-intestinal infection, parasites, pancreatic insufficiency e.g. CF
karyotype in girls-Turner
CXR and sweat test-CF

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21
Q

organic causes of failure to thrive due to inadequate intake?

A

impaired suck/swallow: oro-motor dysfunction, neurological disorder e.g. cerebral palsy
chronic disease leading to anorexia: Crohns, chronic renal failure, CF, liver disease.

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22
Q

effects of CF on the liver?

A

liver cirrhosis and portal HTN-due to plugging of liver bile ducts with dehydrated bile
cholelithiasis

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23
Q

inorganic causes of failure to thrive due to inadequate intake?

A

inadequate food availability:
feeding problems-insufficient breast milk or poor technique, incorrect preparation of formula
insufficient or unsuitable food offered
lack of regular feeding times
infant difficult to feed-resists feeding or disinterested
intolerance over normal feeding behaviour e.g. throwing food around, leading to early meal cessation
problems with budgeting, shopping, cooking food
low SE status

PS deprivation: poor maternal-infant interaction
maternal depression
poor maternal education

neglect or child abuse:
includes factitious illness-deliberate underfeeding to generate failure to thrive

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24
Q

causes of failure to thrive other than inadequate food intake?

A

inadequate retention-severe GOR, vomiting
malabsorption-coeliac, CF, cow’s milk protein intolerance, cholestatic liver disease, short gut syndrome, post-necrotising enterocolitis (NEC)
failure to utilise nutrients-syndromes, chromosomal disorders e.g. downs, IUG, extreme prematurity, congenital infection, metabolic disorders e.g. congenital hypothyroidism, storage disorders, amino and organic acid disorders
increased requirements-thyrotoxicosis, CF, malignancy, chronic infection e.g. immune deficiency, congenital heart disease, chronic renal failure.

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25
Q

key components to hx of pt with failure to thrive?

A

detailed dietary hx, food diary over several days
feeding, what happens at mealtimes?
other symptoms-are they well with lots of energy or is there diarrhoea, vomiting, cough, lethargy
birth hx: premature or IUGR?, significant med problems?
growth of other family members and illnesses in family
?development
PS problems at home?

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26
Q

management of failure to thrive pt?

A

most non-organic causes manged in primary care with MDT approach: health visitor assess eating behaviour and provide support, paed dietician-assess food intake, SALT-feeding disorders, clinical psychologist and social services, nursery placement-relieve stress at home and assist with feeding.

admit children under 6mnths with severe failure to thrive requiring active refeeding.

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27
Q

most common cause of gastroenteritis in young children?

A

viral infection-rotavirus main cause of winter epidemics

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28
Q

commonest bacterial causes of gastroenteritis in children?

A

E coli
shigella
salmonella
campylobacter

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29
Q

features of bacterial gastroenteritis caused by shigella?

A

children 1-5yrs
febrile fits
watery, blood, mucus, pus-diarrhoea

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30
Q

differentials for vomiting after feeds?

A

normal positing-small amount of vomit in mouth-effortless, non forceful low volume, frequent spills from mouth, may be related to overfeeding-espec. bottle fed, try and reduce occurrence with winding baby during and post feeds, gentle handling, prevent upset and baby from air swallowing before feeds, propping baby after feed. common under 6 mnths, usually resolve by 1yr. can add food thickeners to milk if very troublesome and baby bottle fed
GOR-normal in baby, can be severe-GORD-requiring med., e.g. if failure to thrive, haematemesis, frequent chest infections
cows milk allergy

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31
Q

common causes of vomiting in infancy?

A
overfeeding
GOR
gastroenteritis
anatomic obstruction: pyloric stenosis, intussusception, atresia-dudoenal, malrotation, volvulus, strangulated inguinal hernia, hirschsprung disease
systemic infection-meningitis, pyelonephritis, UTI, URT/otitis media, whooping cough-?vomiting after paroxysmal coughing
dietary protein intolerances-allergy*
inborn errors of metabolism
CAH
renal failure
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32
Q

common causes of vomiting in childhood?

A
gastroenteritis
systemic infection-meningitis, UTI, URT
toxic ingestion or medications
whooping cough
appendicitis
bowe obstruction-adhesions, FB-bezoar
raised ICP
coeliac disease
renal failure
inborn errors of metabolism
testicular torsion
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33
Q

common causes of vomiting in adolescence?

A
gastroenteritis
systemic infection-pyelonephritis, septicaemia, meningitis
peptic ulceration and H pylori infection
appendicitis
rasied ICP
coeliac disease
migraine
pregnancy
bulimia
DKA
alcohol
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34
Q

red flag features of vomiting in a child?

A

bile in vomitus (green/yellow)-suggests intestinal obstruction-need paed surgical r/f, upper GI contrast study to be done
blood in vomitus-*inflammation in upper GIT, need specialist r/f, unless due to swallowed blood e.g. from epistaxis
frequent forceful (projectile) vomiting-hypertrophic pyloric stenosis in infants up to 2mnths old, needs paed surgical r/f
blood in stool-‘redcurrant jelly’ stools-intussusception
abdo distension, tenderness or palpable mass-obstruction, need paed surg r/f
chronic diarrhoea-cow’s milk protein allergy
drowsiness
refusal to feed
malnutrition
dehydration
lethargy or irritability-meningitis
late onset-after 6mnths or persisting after 1 yr, late onset maybe UTI?

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35
Q

what do we want to know in hx of vomiting?

A

what is the vomiting like?-amount, ?projectile, blood stained, bile stained, coughing
assoc. symptoms?-diarrhoea-gastroenteritis, constipation-intestinal obstruction, irritability or pain-infection, pain before or after vomiting-before ?appendicitis GOR, aspiration and apnoea-GOR
how well is child?-fever-infection, appetite, weight
baby bottle or breast fed-if bottle, how much are they taking, in excess of 200ml/kg/24hr with no weight loss likely regurgitation due to overfeeding
headache, visual aura, facial wkness, paraesthesia-?migraine in adolescents, abdo pain-gynaecological? periods-?pregnancy

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36
Q

features of gastroenteritis on exam.?

A

look for signs of dehydration-loss of skin turgor, sunken eyes, dry mucous membranes, oliguria, tachycardic, low BP-severe, CRT slow, lethargic, sunken fontanelle in baby
abdo exam-tenderness, increased bowel sounds

37
Q

what is diagnostic of pyloric stenosis on examination of abdomen?

A

palpation of an ‘olive’

if suspected, USS definitive if pyloric tumour seen

38
Q

what should be excluded on exam. of a child with vomiting?

A

HTN

39
Q

what is it important to consider in infective causes of acute diarrhoea in a child?

A

infection can be outside GIT e.g. URTI e.g. otitis media, pneumonia, UTI
pneumonia, UTI and otitis media require correct antibiotic to be given

40
Q

features suggestive of bacterial cause of diarrhoea?

A

fever
abdo pain
blood and mucus in stools-need to do stool microscopy and culture

41
Q

why do we want to know about well being of other family memebers in pres of acute diarrhoea?

A

?food contamination, viral gastroenteritis?

42
Q

how can rotavirus be detected in stool?

A

stool immunoassay

43
Q

management of acute diarrhoea?

A

mild or absent signs of dehydration-manage at home, cows milk usually stopped, clear fluids for 1st day if child on bottle, toddler and older child-dilute apple juice, babies-oral rehydration fluids, gradual introd. solids-BRAT-bananas, rice, apple sauce and toast

44
Q

common causes of chronic diarrhoea?

A

watery:
overflow diarrhoea in constipation-?diet, adequate fluid and fibre, exercise, soiling, palpable stools abdo or PR
nonspecific-may follow acute gastroenteritis episode
toddler diarrhoea-undigested food in stool, may have large fluid intake, thriving child
lactose intolerance-reducing substances in stool, low pH, follows acute gastroenteritis, baby and toddlers
cow’s milk protein allergy-can be bloody, may have urticaria, bronchospasm, stridor
parasites-giardia lamblia-weight loss and abdo pain variable
fatty:
coeliac disease-muscle wasting, abdo distension
CF
blood:
IBD

45
Q

when should formed stools like adult be achieved in a child?

A

after 1 yr
up till then, 0.4mnths and breast fed-2-4/day, range 1-7, yellow to golden porridgy consistency, also may be infrequent
bottle fed-2-3/day, pale yellow to light brown, firm
4mnths-1yr-1-3/day, darker yellow, firmer

46
Q

what is likely seen under microscope of stools in pt with CF?

A

fat globules due to pancreatic exocrine insufficiency

47
Q

causes of chronic diarrhoea with occult blood found in stools?

A

IBD

non-IgE mediated cow’s milk protein allergy

48
Q

what causes GOR in children?

A

chronically lax GO sphincter, or frequent spontaneous decreases in sphincter tone
contributing factors: predom fluid diet, horizontal posture, short intra-abdominal length

49
Q

clinical features of GOR in child?

A

positing after feeds, vomiting-may cause failure to thrive, blood in vomitus
aspiration-may be episodes of choking, recurrent chest infections-pneumonia
apnoea
irritability and appetite loss-oesophagitis
opisthotonus-baby arching back after feeds to try and reduce pain of reflux
heartburn
common in children with down’s syndrome and severe cerebral palsy-in neurodevelopmental problems, often difficult to differentiate between vomiting from GOR and that assoc. with gut dysmotility
note more common in child with asthma
more common if premature, obese, FH

nearly all symptomatic GOR resolves spontaneously by 12mnths

50
Q

in suspected GOR, what are the indications for specialist hosp assessment with upper GI endoscopy and biopsies?

A

haematemesis not caused by swallowed blood (assessment to
take place on the same day if clinically indicated
melaena-assessment to take place on the same day if clinically indicated
dysphagia (assessment to take place on the same day if clinically indicated)
no improvement in regurgitation after 1 year old
persistent, faltering growth associated with overt regurgitation
unexplained distress in children and young people with communication difficulties
retrosternal, epigastric or upper abdominal pain that needs ongoing medical therapy or
is refractory to medical therapy
feeding aversion and a history of regurgitation
unexplained Fe deficiency anaemia
a suspected diagnosis of Sandifer’s syndrome-episodic torticollis with neck extension and rotation.

51
Q

management of formula fed infants with frequent regurgitation due to GOR assoc. with marked distress-GORD?

A

stepped care approach:
r/v feeding hx, then reduce feeding volumes if excessive for infant’s weight then offer trial of smaller more frequent feeds then offer trial of thickened formula. can add thickeing agents to feeds e.g. nestargel.
if unsuccessful, stop and trial alginate therapy 1-2 wks e.g. gaviscon, continue if successful but trying stopping at regular periods

ensure child propped up after feeding in 30 degree head up prone position, small regular feeds, but allow to sleep on back
if breast fed, need breast feeding assessment

52
Q

complications of GOR in infants, children and young people?

A

failure to thrive from severe vomiting
reflux oesophagitis-can cause irritability and anorexia, haematemesis, Fe deficiency anaemia and discomfort/heartburn on feeding
recurrent pulm aspiration-pneumonia, cough or wheeze, apnoea in preterm infants
frequent otitis media e.g. more than 3 episodes in 6 mnths
dental erosion, espec. in cerebral palsy
acute life threatening events

53
Q

indications for oesophageal pH study (24hr study to quantify degree of reflux) in child with GOR?

A

suspected recurrent aspiration pneumonia
unexplained apnoeas
unexplained non-epileptic seizure-like events
unexplained upper airway inflammation
dental erosion associated with a neurodisability
frequent otitis media
a possible need for fundoplication
a suspected diagnosis of Sandifer’s syndrome

54
Q

management of infant or young child with overt GOR who can’t tell you about their symptoms and have 1 or more of unexplained feeding difficulty, distressed behaviour or faltering growth?

A

4 wk trial of PPI or H2RA

55
Q

when is enteral tube feeding used in GORD?

A

to promote weight gain in infants and
children with overt regurgitation and faltering growth if:
other explanations for poor weight gain have been explored and/or
recommended feeding and medical management of overt regurgitation is unsuccessful

consider Nissen fundoplication in infants, children and young people with severe,
intractable GORD if:
appropriate medical treatment has been unsuccessful or
feeding regimens to manage GORD prove impractical, for example, in the case of
long-term, continuous, thickened enteral tube feeding.

56
Q

what is colic?

A

describes a common symptom of paroxysmal inconsolable crying occurring in babies principally under 3mnths, and presumed to be intestinal in origin
may be assoc with hunger and swallowed air, or discomfort and distension due to overfeeding

For more than 3 hrs for more than 3 days of the week

57
Q

clinical features of colic?

A

sudden attack with crying or screaming, often continuous for several hrs, may end when infant completely exhausted but often relief on passing flatus or faeces
face may be flushed, abdo distended and tense, legs drawn up, hands clenched
usually late afternoon or evening attacks

58
Q

what disorders must be ruled out via careful exam. in presentation of colic?

A

intussusception
strangulated hernia

other differentials-reflux oesophagitis, otitis media
*note also that a baby who is always crying may have had NAI, or be at risk of it
colic babies may also precipitate NAI

59
Q

management of colic?

A

reassurance and support, usually resolves by 3 mnths old
holding baby or carrying them in a sling close to parent can soothe, and secure swaddling occasionally helps
?sucrose and changes of infant formula

if severe and persistent, may be due to cow’s milk protein allergy or GOR, and empirical 2 wk trial of whey hydrolysate formula followed by trial of anti-reflux tment may be considered.

60
Q

serological testing requested in investigating coeliac disease in children?

A

total IgA and IgA tTG as 1st choice
consider IgG EMA, IgG DGP or IgG tTG if IgA deficient
consider HLA DQ2/8 testing only in specialist setting e.g. children who are not having a biopsy or those who already have limited gluten ingestion and choose not to have a gluten challenge
positive result=IgA tTG more than 10 times upper limit of normal, OR weakly positive and positive IgA EMA.
do not test in infants before gluten has been introduced into the diet.

61
Q

possible presenting complaints of malabsorption?

A
failure to thrive
loose and frequent bowel motions
abdo distension
short stature
anemia-Fe-microcytic hypochromic, folate or Vit B12 deficiency-macrocytic
chest infection-CF
62
Q

common causes in developed world for malabsorption in children?

A
CF
coeliac disease
post-gastroenteritis syndrome
giardiasis
bacterial overgrowth-usually assoc. with congenital gut anomalies or prior GI surgery
63
Q

classification of mechanism of malabsorption?

A

digestive factors:
insufficient pancreatic enzymes e.g. CF, SDS-shwachman-diamond syndrome
lack of functioning bile salts-insufficent supply-CLD, ileal resection, coeliac, and deconjugation-bacterial overgrowth
inadequate brush border enzymes e.g. lactose intolerance

absorptive factors:

64
Q

HLA subtypes assoc. with coeliac disease?

A

HLA-DQ2-in 95% and DQ8

65
Q

D2 biopsy findings in coeliac disease?

A

villous atrophy-severe, also seen in congenital microvillus inclusion disease-present with intractable diarrhoea as neonate
crypt hyperplasia, less severe with allergic enteropathies
lymphocyte infiltration

66
Q

what is mesenteric adenitis?

A

acute enlargement of intra-abdominal LNs, due to infection in URT, LRT or abdomen.
so usually recent hx of infection, and may still be signs present in throat or chest.

67
Q

characteristic presentation of toddler diarrhoea?

A

loose stools with undigested food
thriving child, may have large fluid intake
likely to be result of a rapid gastro-colic reflex

68
Q

management of toddler diarrhoea?

A

reduction in fluid intake may be helpful
usually all that is needed is reassurance if child is thriving
loperamide may sometimes be used to slow bowel transit time in some cases of frequent stooling and severe parental anxiety
symptoms resolve as child matures

69
Q

causes of neonatal small bowel obstruction?

A

meconium ileus-thick inspissated meconium, impacted in lower ileum, most assoc. with CF. may be dislodged using gastrografin contrast medium.
meconium plug-plug of meconium causes lower intestinal obstruction, usually passes spontaneously
duodenal atresia or stenosis-1/3 have Down’s, also assoc. with other congenital malformations
jejunum or ileum atresia or stenosis
malrotation with volvulus-whole migut may infarct

70
Q

AXR appearance of duodenal atresia?

A

‘double bubble’= due to distension of stomach and duodenal cap, absence of air distally.

71
Q

recognised associations of echogenic bowel on 2nd trimester antenatal US imaging? (increased bowel brightness)

A
trisomy 21
CF
IUGR
intrauterine CMV infection
intra-amniotic haemorrhage
intrauterine fetal demise
72
Q

causes of large bowel obstruction in neonate?

A

hirschprung disease-note 15% present as acute enterocolitis
rectal atresia-anus is absent at normal site, requires surgical tment. high lesions-bowel ends above levator ani, there is fistula to bladder or urethra in boys, or adjacent to vagina or to the bladder in girls.

73
Q

what does bile-stained vomiting in neonates indicate?

A

intestinal obstruction until proved otherwise, distal to ampulla of vater.

74
Q

what is constipation in pre-school period often associated with?

A

pain, anal fissure, stressful toilet training, fear and avoidence of defecation with assoc. intra-family stress.

75
Q

general advice for constipation prevention in children?

A

increase fluid intake to 7 drinks per day
increase fibre intake-5 pieces per day
avoid excessive milk drinking in later infancy
discourage too early or too coercive potty training in 2-3yr old.

76
Q

1st step in constipation management?

A

softening retained faeces:
increase fluid intake
increase fibre intake in over 5s
give lactulose (osmotic laxative) or docusate to soften
if faecal mass not too big, can give senna or picosulfate in addition to oppose withholding of faeces
if large faecal mass or BNO for several days, give senna only after 1 or 2wks of softener
movicol (stool softener) 1st line if large faecal mass at presentation.

77
Q

next step in constipation management if stools not being evacuated after softening?

A

-stimulant: senna-single daily dose, increase dose until stool passed
sodium picosulfate elixir can be used as alternative
-movicol osmotically acting laxative-stat dose, rpt daily until result
-if above unsuccessful, picolax sachets-stat dose and rpt in 6hrs if no result, need nurse observ at 1st dose + drink lots of fluid
-suppository e.g. glycerine in babies under 1 year.
-enema – olive oil – 2ml/kg using catheter to insert -phosphate, if olive oil unsuccessful. (consider sedation).
-manual evacuation under GA if stool is so large it cannot be flushed from a megarectum. (examine carefully for ectopia and stenosis.) Consider anal dilatation
and rectal biopsy. Refer to paediatric surgeon.

78
Q

after stool evacuation achieved, how is constipation continually managed?

A

increase dietary fibre and fluids, consider r/f to dietician for advice
regular softening laxative e.g. lactulose
regular stimulant laxative e.g. senna
if these don’t work, consider daily movicol
picolax sachets at weekends if above doesn’t help
explain need to persist with med over several mnths
encourage regular sitting on toilet after meals and before bed in correct position with hips flexed and feet resting on stool, in quiet encouraging environment.

need frequent and regular OP contact, consider psychology r/f.

79
Q

organism causes of blood in stool in gastroenteritis?

A

shigella
salmonella?
campylobacter

80
Q

when is sever GOR more common?

A

children with cerebral palsy or other neurodevelopmental disorders
preterm infants, espec. if coexistent bronchopulmonary dysplasia
following surgery for oesophageal atresia e.g. in downs, or diaphragmatic hernia

81
Q

how much weight should a baby gain?

A

200grams per week

82
Q

specific aspects of examination which are useful in a baby who had previous good weight gain, but now has slow weight gain?

A

abdomen-distension?-malabsoprtion, organomegaly
chest-chronic resp disease e.g. CF-chest deformity, harrison’s sulcus, recurrent chest infections-coarse crackles
general-wasting, pallor, activity
height and OFC-to compare to weight

83
Q

a 4wk old baby presents with projectile non-bilious vomiting, which has increased in forcefulness and frequency, what is the likely diagnosis and what will be the results of blood gas analysis?

A

pyloric stenosis

blood gas: metabolic alkalosis-high HCO3-, very positive base excess.

84
Q

causes of encopresis and soiling as a result of faecal retention?

A

constipation, possibly following dehydration during an illness
defecation inhibition due to pain from an anal fissure
inhibition because of fear of punishment for incontinence
anxieties about using the toilet

85
Q

when might soiling happen in children who do not have faecal retention?

A

neuropathic bowel secondary to occult spinal abnormality, usually assoc. with urinary incontinence
general learning disability so child unaware of expectations of social bowel control
child may intentionally defecate as a hostile act and require psychiatric r/f.

86
Q

causes of acute liver failure?

A

infection-Hep A, B, C, non-A to G
drugs-paracetamol, isoniazid, halothane, amanita phalloides (poisonous mushroom)
metabolic-wilson disease, tyrosinaemia
AI hepatitis
Reye syndrome-acute non-inflammatory encephalopathy with microvesicular fatty infiltration of liver, close assoc. with aspirin therapy.

87
Q

causes of chronic liver disease?

A
chronic hepatitis-post viral Hep B, C (most common), AI hepatitis, drugs, IBD, PSC
Wilson disease (over 3 years)
alpha 1 antitrypsin deficiency
CF
neonatal liver disease
bile duct lesions
88
Q

how is definitive diagnosis of abdominal TB made?

A

laparoscopic biopsy of intrabdominal lymph nodes or omental/peritoneal TB nodules, with demonstration of culture +ve for TB, presence of acid-fast bacilli and caseating granulomas