Gastro Flashcards
type of CMPA
- IgE mediated - type 1 hypersensitivvity reaction, atopy related
- non IgE mediated - activates T cells (osmotic diarrhoea due to damage to absorptive area)
presentation of CMPA
GI symptoms within 2 hours of cows milk in first 4 weeks of life
wheeze/ rhinitis
atopic eczema/ rash
crying, irritable, milk refusal
failure to thrive
blood in stool - non IgE mediated
presentation of GORD
excessive regurg or vomiting
irritability e.g. back archin
faltering growth
excessive hiccups
apnoeas/ breath holding/ cyanotic episodes
what is sandifers syndrome
abnormal posturing + deviation of head and neck + discomfort with feeds
needs upper GI endoscopy
GORD diagnosed
clinical diagnosis but can do ph study or barium swallow
ph < 4 for 15 secs
management of GORD
- lifestyle - feed upright, reduce feed volume
- add feed thickener for 1-2 weeks e.g. carobel, gaviscon
- add PPI for 4 week trial if flatering growth
- add domperidone
- fundoplication
type of bacteria h.pylori
gram negative flagellated bacteria
(lipopolysaccharide layer, O antigen and lipid A)
releases urease to neutralise stomach acid and releases toxins to mucosal damage
presentation of h.pylori
dysspepsia
epigastric pain and tenderness
nausea
intolerance of fatty food
diagnosis of h.pylori
- urea breath test *- detects CO2 (h.pylori produces urease to convert urea to ammonia + CO2)
- stool antigen test
- endoscopy - affects lesser curvature of stoamch
management of h.pylori
omeprazole + amoxicillin + metro/ clarithromycin for 1-2 weeks (4 weeks if haematemesis)
what is zollinger ellison syndrome
ectopic gastrin secrteion from a gastrinoma
multiple peptic ulcers >2cm diameter
lining og stomach
columnar epithelium
function of parietal cells
produce HCl + intrinsic factor
function of G cells
produce gastrin
function of enterochromaffin like cells
produce histamine (binds to parietal cells to activate)
function of D cells
produce somatostatin which inhibits gastrin secretion
function of mucus neck cells
produce bicarbonate and mucus
function of chief cells
produce pepsinogens
epidemiology of coeliac
1% population
risk factors for coeliac
- HLA-DQ2 or DQ8
- 1st degree family
- autoimmune disease e.g. vitiligo (lack of melanocytes in epidermis)
-Ig A deficiency - Downs syndrome
- Turner syndrome
presentation of coeliac
GASTRO - abdo pain and distension, diarrhoea, vomiting, buttock wasting, constipation, faltering growth
SKIN - dermatitis herpetiformis, aphthous stomatitis, vitiligo
OTHER - vit b12 deficiency, dental enamel defects, iron deficiency, dilated cardiomyopathy
diagnosis coeliac disease
IgA tissue transglutaminase positive*** +/- anti endomysial antibodies
if IgA deficiency -> test IgG ttG
if <10 x maximum, upper Gi endoscopy and duodenal biopsy
findings on duodenal biopsy of coeliac disease
intra epithelial lymphocytosis ***
subtotal villous atrophy
crypt hypertrophy
lamina propria cell infiltrate
enteropathy
complications of coeliac
amenorrhoea
delayed puberty
osteopenia and osteoporosis
hyposplenism
T cell lymphoma
risk factors of pyloric stenosis
male ** -first born
first degree relative (female pass on higher risk)
prematurity
maternal smoking
IUGR
macrolide abx use
presentation of pyloric stenosis
present 4-6 weeks of life with…
projectile vomiting
hungry baby
weight loss
dehydration
palpable olive shaped mass in RUQ
investigations pyloric stenosis
- gas - metabolic alkalosis - hypokalaemia, hypochloraemia
- USS abdomen - wall thickness 4mm, length 17mm, diameter 15mm
management of pyloric stenosis
- rehydration with IVF prior to surgery
- surgical correction with Ramstedt pylomyotomy
viral causes of gastroenteritis
- rotavirus - childcare settings, cause dehydration, doubel stranded rNA virus
- noravirus - healthcare
- adenovrirus
bacterial causes of gastroenteritis
- salmonella - poulty (typhi - travel abroad + salmon pink rash)
- campylobacter *
- e.coli - undercooked meat
- shigella
- staph aureus -ingestion of inadequately reheated food
- cholera - vibrio cholerae, large volume, rice water stools
risk of e.coli enterotoxi 0157
haemolytic uraemic syndrome - reduced renal function + pale + anaemia + bloody stool
type of diarrhoea
- osmotic diarrhoea = damage to intestinal microvilli causing malabsorption, if stop eating, diarrhoea stops
- secretory = enterocyte binding toxin causing release of Cl into intestinal lumen, even if continue eating, diarrhoea continues
type of fluid loss
- hypotonic - highly concentrated urine, high sodium, causes water depletion
- isotonic - water and Na loss causing increased haematocrit
most common sites of crohns
proximal colon and terminal ileum
presentation of crohns
- GI - diarrhoea, abdo pain, weight loss , growth failure, mouth ulcers
- skin - erythema nodosum, pyoderma gangrenosum , psoriasis
- blood - iron deficiency
- eye - episcleritis
- bone - ank spondylitis, sacroilitis, osteoporosis
diagnosis of crohns
upper and lowe endoscopy + biopsy *
non caseating granulomas, multiple lymphoid aggregates, transmural inflammation with skip lesions, fissures, strictures, aphous / linear ulcers
inducing remission in crohns disease
- 1st presentation = glucocorticoids e.g. prednisolone , methylpred, IV if severe
- 6 week enteral nutrition (protein based formula,polymeric 1st line)
- 5-ASA
- azathioprine
maintenance therapy in crohns
1st line = AZATHIORPINE
side effects:
myelosuppression
pancreatitis
hepatitis
indications for surgery in crohns
- ileocaecal disease
- strictures
- fissures
- failure of medical treatment
pathophysiology of UC
diffuse continuous inflammation of intestinal mucosa (usually rectal and colon) and exaggerayed T cell response
associated with HLA-DRB in extensive disease
90% pancolitis !!!!
presentation of UC
- bloody diarrhoea
- night stools
- abdo pain
- weight loss
- erythema nodoum
- iritis, uveitis
-sclerosing cholangitis - autoimmune hepatitis
- arthritis
diagnosis of UC
endoscopy and biospy (sigmoid colon **)
friable mucosa, submucosal and mucosal inflammation, crypts abscesses, goblet cell depletion, ulceration
affects the mucosa layer
complications of UC
toxic megacolon - fever, tachycardia, dilated transverse colon
colon cancer
oxalate renal stones
osteoporosis
management of UC
induction: mesalazine (5-ASA)
maintenance: mesalazine or sulfasazlaline
15% require surgery 5 years from diagnosis
pathophysiology of duodenal atresia
abnormal developement of intestine - failure of canalization of duodenum at 7 weeks gestation
usually occurs at ampulla of vater
associations with duodenal atresia
trisomy 21
prader willi
congenital heart disease
CF
diaphragmatic hernia
presentation of duodenal atresia
present in 1st few days of life with bilious vomiting (non bilious in 20% if above ampulla of vater)
abdo distension
antenatal signs of duodenal atresia
polyhydramnios
double bubble sign of USS
management of duodenal atresia
- NG tube - decompress stomach, NBM
- duodenoduodenostomy by open laparotomy
pathophysiology of necrotising enterocolitis
acute inflammatory injury of small intestine and invasion of enteric organisms and causing ischaemic necrosis of intestinal mucosa
commonly affects terminal ileium, caecum and sigmoid colon
factors contributing to necrotising enterocolitis
- premature gut motility
- reduced igA and reduced barrier function -> initiate mucosal injury _> invasion of gas producing bacteria
- gut hypoxia
- metabolic substarte in gut lumen
risk factors for necrotising enterocolitis
- prematurity (<32 weeks)
- low birth weight , iUGR
- hypothermia
- PROM
- artificial feeds or rapid increase in enteral feeds
- placenta insufficicency, abruption
presentation of necrotising enterocolitis
feed intolerance with gastric residuals
bilious vomiting, diarrhoea
rectal bleeding
abdo distension, abdo tenderness
leading to perforation and shock, mortality 10%
investigations for necrotising enterocolitis
- abdo x ray - pneumoperitoneum, portal venous gas, bowel wall oedema, intramural gas of nitrogen and hydrogen (= pneumatosis intestinalis)
- blood cultures
- gas - metabolic acidosis, high lactate
management of necrotising enterocolitis
- NBM
- NG suctioning
- parental nutrition and IVF
- IV antibiotics 14 days
- +/- surgery if perforation or failure of medical treatment
what is hirschsprungs disease
absence of ganglion cells in the distal part of colon and rectum due to failure of neural crest cells (derived from neuroectoderm) to migrate and populate distal colon
associations with hirschsprungs disease
- downs syndrome
- waardenburg syndrome
- bardet biedl
- males
- mutations in RET and EDNRB
pathophysiology of hirschsprungs disease
lack of ganglion cells in submucosa and myenteric plexus (auerbach ) muscular layer causes….
1. functional obstruction as no contraction of muscles
2. enterocolitis - stool accumulates and causes extension of proximal bowel and bacetria
presentation of hirschsprungs disease
failure to pass meconium in 1st 48 hours of life
abdo distension
poor feeding
enterocolitis - fever, explosive diarrhoea
investigations for hirschsprungs disease
rectal suction biopsy * - lack of ganglion cells
AXR with contrast enema - reveals transition zone
management of hirschsprungs disease
- antibiotics for enterocolitis
- surgical rectal washout and resection of anganglionic segment
pathophysiology of malrotation
intestine in abnormal position in peritoneal cavity - intestine completed by 8-11 weeks and rotates around superior mesenteric artery.
presentation of malrotation
VOLVULUS !! - bilious vomiting, abdo distension, peritonitis, fresh blood in rectum
30% present by 1 month age, 58% present by 1st year of life
investigation of malrotation
AXR - proximal intestine obstruction
upper gI contrast study ** - corkscrew sign, dilated proximal duodenum with failure to pass contrast into 2nd part
management of malrotation
- NG tube on free drainage
- NBM
- iVF
- surgery - laparotoy, resect necrotic bowel +/- stoma
what is exomphalos
herniation of abdominal contents (stomach, intestine, liver or spleen) through umbilical defect and contained in membranous sac from amniotic membrane.
exomphalos associations
trisomy 21, 13, 18
cardiac abnormalities
beckwith wiedeman syndrome
what is gastroschisis
defect in rectus muscle leading to herniation of intestine to right of abdomen
risk factors for gastoschisis
low maternal age
maternal drugs and smoking
low socio-economic class
management of anorectal malformation
- defunctioning colostomy
- MCUG
- staged prolonged surgery 3-6 months old
Tracheo-oesophageal atresia associations
- VACTERL syndrome
- duodenal atresia
- CHARGE syndrome
- trisomy 13,18,21
- diaphragmatic hernia
- cardiac abnormalities
types of oesophageal atresia
type a - oesophageal atresia
B - proximal fistula and distal atresia
C - proximal oesophageal atresia with distal oesophageal fistula *****
D - atresia with fistula between trachea
E - isolated fistula
oesophageal atresia presentation
in 1st few hours of life:
resp distress
excessive salivation + lots of secretions + frothing at mouth
abdo distension
choking on feeds
inability to pass NG
presentation of oesophageal atresia antenatally
polydydramnios
absence of fetal bubble
management of oesophageal atresia
x ray - nG coiled up in proximal oesophagus
echo prior to surgery
replogle tube - suction and aspirate
surgery
causes of pancreatitis
- Idiopathic **
- trauma
- gallstones - cholesterol (obesity), calcium bilirubin
- viral infections - mumps,, enterovirus
- metabolic - hypercalcaemia
6.medications - valproate, steroids, azathioprine
pathophysiology of pancreatitis
inflammation of pancrease due to injury from overactivation of trypsinogen and pancreatic enzymes
Amylase made in acinar cells
causes release of histamine, braydkinin and trypsin
causing vasodilation and fluid loss
presentation of pancreatitis
epigastric abdominal pain
vomiting
jaundice
shock
hypovolaemia
fever
diagnosis of pancreatitis
- raised amylase ( 3 x normal, take 48 hours to reach peak)
- USS - identify gallstones
- CT abodmen - oedema, retroperitoneal fat stranding
- MRI and ERCP
management of pancreatitis
- IV fluids
- analgesia
- bowel rest and TPN
- surgery if complications
cause of wilsons disease
autosomal recessive - mutation in ATB7B on chromosome 13
copper not able to transferred intracellularly so copper accumulates and deposits leading to liver damage
presentation of wilsons disease
- liver disease, cirrhosis, chronic hepatitis
- kayser fleischer rings
- asymmetrical tremor (early sign), ataxida, clumsy
- mood disorder and personality change (1st presentation)
diagnosis of wilsons disease
liver biopsy *** - copper deposits
low caeruloplasmin
basal 24 hr urinary excretion of copper elevated
management of wilsons disease
- penicillamine
- reduced copper containing food - liver, chocolate, nuts, mushrooms
- liver transplant
presentation of biliary atresia
cholestatic jaundice ** - most common causes in first 3 months life
clay coloured stools
dark urine
hepatomegaly
investigations biliary atresia
- high conjugated bilirubin
- HIDA - no excretion of bile ***
- USS - absent gallbladder/ irregular outline
- high GGT and high ALP
management of biliary atresia
- ursodeoxycholic acid (promotes flow of bile)
- fat soluble vitamins
- nutrition
- kasai surgical procedure *** - performed 60 days post birth
what is intussusception
proximal bowel telescopes into distal bowel = most commonly ileocaecal junction
present 4 month - 1 y/o, usually boys
presentation of intussusception
abdominal pain - drawing knees up
red currant jelly stool
palpable abdo pain
vomiting
diagnosis of intussusception
USS abdomen ** - target lesion
management of intussusception
- NG tube on free drainage
- NBM
- IVF
- triple antibiotics
- surgery = rectal air enema **
complication = perfroation and pneumoperitoneum -> immediate needle compression
presentation of appendicitis
abdo pain : peri umbilical _. RIF
rosvings sign : pain in RIF on palpation of LLQ
psoas sign : pain on extension of right hip whilst laid on left
fever
vomiting
anorexia
causes of constipation
poor fluid intake
low fibre diet
child behaviour
ADHD
medications
medical conditions e.g. coeliac, hypothyroidm, CMPA, spina bifida
management of constipation
- conservative - increase fluid intake, reward system, increase fibre
- if impacted stool (faecal mass/ overflow) -> movicol disimpaction regime
- can add stimulatnt e.g. senna, bisacodyl. picosulfate
- surgical - appendicostomy for anterior continence enemas
transmission of hepatitis
hep A - faecal oral route
hep B - vertical or blood
hep c - blood and bodily fluids
presentation of hepatitis
hep A - self resolve, dont progress to chronic disease
Hep B - most self resolve, jaundice, abdo pain, N&v
Hep c - 80% progress to chronic infection and 50% develop chronic liver disease
vaccination of heb B serology
hep B surface antibodies +ve
acute infection Heb B serology
core antibody IgM +ve
surface antigen +ve
high ALT in immune clearance phase
Hep B e antigen = high level of virus
chronic infection Heb B serology
core antibody IgG +ve
surface antigen +ve
inheritance of gilbert syndrome
autosomal recessive
mutation in UGT1A1 gene on chromosome 2q27 which is responsible for conjugation of bilirubin
gilbert syndrome presentation
incidental finding on LFT
mild jaundice at time of stress/ cold/ illness/ alcohol/ dehydration
investigations gilbert syndrome
bilirubin (80-90
FBC normal
causes of jaundice <24 hours old
- sepsis **
- ABO incompatability *
- rhesus haemolytic disorders
- G6PD deficiency, spherocytosis
- congenital infections - conjugated
causes of jaundice 2 days - 2 weeks of age
- infection - sepsis, toxoplasmosis, UTI
- breast milk jaundice ***
- physiological - low glucoronyl transferance levels, low UDPT, low ligandin
- dehydration
- crigler najjar syndrome - absence of glucornyl transferase
causes of prolonged jaundice (> 2 weeks)
UNCONJUGATED **
1. haemolytic anaemia e.g. sickle cell, thalasaaemia
2. hypothyroid
3. infection
4. CF
5. breast milk
CONJUAGTED
1. viral hepatitis
2. biliary atresia
3. neonatal hepatitis
4. alagille syndrome - bile duct malformation, dysmorphic, pulomonary stenosis, butterfly vertebra
5. alpha 1 anti trypsin deficiency
presentation of kernicterus
build up of unconjugated bilirubin can cross blood brain barrier
athetoid cerebral palsya
hearing loss
paralysis
upward gaze
dental dysplasia
learning disability
signs of conjugated jaundice
pale stools (lack of stercobilin)
dark urine
tests for jaundice
- split bilirubin levels
- FBC
- urine MC&s
- TFTs
- viral screen
- blood group and DCT
side effects with exchange transfusion
hyperkalaemia
catheter related complications - emboli, acidosis, hypocalcaemia
hypo/ hyper glucose
haemodynamic instabolity
short gut syndrome complications
- osmotic or secretory diarrhoea
- abdo distesnion
- foul smelling stool
- flatulences
- fat soluble vitamin and vit B12 deficiency
ileum function
- majority of water absorbed here
- bile acids absorbed - help fat absorotion inc fat soluble vitamins
- B12 absorption (terminal ileum)
vit A deficiency signs
night blindness
dry eyes, corneal ulceration
hyperkeratosis
immune dysfunction
growth failure
vit D deficiency signs
ricket - muscle weakness, growth retardation, skeletal deformities (genu varum)
vit E deficiency signs
neuroaxonal degeneration -> ataxia
progressive neuropathy
retinopathy
vit K deficiency
deranged coagulation - Fcator VII, IX,X), bleeding
laxative abuse finding on colonoscopy
dark brown pigmentation of colonic mucosa = melanosis coli and pigment laden macrophages
breakdown of haemoglobin produces..
haem + globin
haem broken down to carbon monoxide and bilverdin which turned into bilirubin
treatment for giardia infection
metronidazole
steattorhoea, watery diarrhoea, nutrient deficiency
tests for lactose intolerance
hydrogen detected in breath
stool sample within 1-2 hours of ingestion
diagnosis of CMPA IGE mediated
skin prick
blood specific IgE testing
management of CMPA
- if breast feeding, strict maternal cows milk free diet
- exclusively hydrolysed formula 2-6 weeks
- amino acid based formula
marker to measure protein losing enteropathy
ALPHA 1 ANTI TRYPSIN
resistant to degradation of proteases
measurement indicates leakage of plasma proteins in the gut
presentation of autoimmune hepatitis
7-10 y/o
acute hepatitis - jaundice, abdo pain, easy bruising
arthritis
skin rash
presence of auto antibdodies
presentation of lymphageictasia
= protein losing enteropathy
oedema + diarrhoea
bloods of refeeding syndrome
hypokalaemia
hypophosphateaemia
hypomagnesium
normal Na and Ca
Mechanism of action fo PPI
inhibit gastric acid secretion by inhibiting H+/K+ ATP pump in gastric parietal cell
mechanism of phototherapy in eczema
targets inflammatory cells, alters cytokine production and antimicrobial
calories in breast milk
70 Kcl/100 mls
high in vit A
BMI diagnosis of obesity
BMI >98TH CENTILE = OBESE
BMI >91ST CENTILE = OVERWEIGHT
Management of umbilical hernia
usually resolves by 1 y/o
surgery at 3-4 y/o
role of GGT
enzyme involved in glutathione metabolsim and acts as transporter molecule and assists in lievr metabolism
role of prebiotics
non digestable food products that stimulate growth + activity of bacteria in digestive system
signs of vitamin C deficiency
curly hair
petechiae and bruising
lethargy
gingivitis
impaired wound healing
signs of zinc deficiency
poor wound healing
eczmea, nappy rashes, dry scaling skin
increased risk of infections
oral ulcers and stomatitis
tremor, nystagmus
delayed puberty
chronic diarrhoea
where is zinc found
red meat, oysters, poultry, beans and nuts
stored in skeletal muscle and bone
causes of B12 deficiency
- vegan diet (found in meat, fish, eggs)
- intrinsic factor deficiency (absorbed in distal ileum) - pernicious anaemia (autoimmune)
- toddlers diarrhoea
- malabsorption e.g. coeliac, IBD
signs of B12 deficiency
failure to thrive, lethargy
peripheral neuropathy
developmental d=regression
glossitis (beefy red tongue)
depression
subacute combined degeneration of the cord
where is iron absorbed
jejunum
- give with vit C to help absorption
- excessive zinc can reduce absorption
signs of B1 deficiency (thiamine)
peripheral neuritis
reduced tendon reflexes
loss of vibration sense
muscular cramps
restless
soundless cry
what should be monitored when starting tPN
- glucose in first 1- 2 hours of starting TPN
- potassium, chloride, ph and calcium measured daily when starting TPN
- LFT weekly
presentation of kwashiokor
protein energy malnutrition (calorie intake adequate)
oedematous
muscular atrophy
hepatomegaly
hormone changes in anorexia
- elevated circulating cortsiol
- reduced T3, NORMAL TSH
- reduced FSH/LH
- increased resting GH
- reduced GnRH
- reduced oestrogen
histology of cows milk enteropathy
patchy enteropathy with mild disturnace of crypt villous architecture, mucosal lymphocytes and increased eosinophils
histology of lymphangiectasia
dilated ectatic villous lacteals with distortion of villi (normal length) and no inflammatory markers
histiological findings of biliary atresia
bile duct proliferation
fibrosis
portal duct oedema
fibrosis
inflammation
bile duct bile plugs
