GI Flashcards
GA 3.5 wks GI embryology
foregut and hindgut present
liver bud
GA4wk GI
esophagus and stomach separate
intestines is a single tube
hepatobiliary derived from foregut
pancreas derived from midgut
GA 5-9 GI
Wk 7: mouth, esophagus and stomach in normal position
intestinal tube elongates and herniates into umbilical cord
the tube undergoes a series of rotations
villi form in jejunum (week 9)
GA10 GI
tube reenters abdominal cavity after rotated 270deg
formation of microvilli
crypts of lieberkuhn appear
GA 12 GI
parietal cells in stomach
mature taste buds
formation of islet cells and bile secretions
GA13 GI
muscularis and muscle layers of intestine appear
disaccharides present
GA16 GI
swallowing and sucking ability (not coordinated)
lipase can be detected but remains deficient
trypsin present
GA14 GI
villi present throughout intestines
meconium present
GA18
ganglion cells
GA19
crypts well developed
GA20-24 GI
mouth amylase
ciliated columnar cells
maltase
sucrase
amylase liver 22 weeks
GA28 GI
adult level disaccharidases
lactase increases
GA32
normal gastric emptying
HCl detected instomach
34-36
coordinated suck and swallow
rapid peristalsis
lactase adult level
intraepithelial lymphocytes timing and features
GA 8
immune cell - defense
intestinal absorptive epithelium timing and features
GA 9
absorption
goblet cells timing and features
GA8-10
mucin, protection
enteroendocrine cells timing and features
GA9-11
hormone producting
paneth cells timing and features
GA11-12
antimicrobial peptides
stem cells timing and features
GA?? early
give rise to epithelial cells
Microfold (M) cells timing and features
GA 17
uptake antigen for presentation
Dendritic cells timing and features
GA 19
APC
tight junctions timing and features
GA 10
barrier defences
crypt villus architection GA
12
Peyers patches timing and features
GA19
patches of lymphoid tissue for immune response
salivary and pancreatic amylase timing
present at 22 weeks
adult levels 3 months postnatal age
glucoamylase (a-dextrinase) timing and function
normal at birth
removes glucose from end of starch
intestinal disaccharidases
adult levels at 28 weeks except lactase which is adult level at 36 weeks
intestinal transporters of glucose
into enterocyte SGLT1 active
out of enterocyte into circulation GLUT1
intestinal transporters of fructose
into enterocyte GLUT5 passive
out of enterocyte into circulation GLUT2
where are chymotrypsin and trypsin
duodenal fluid
decreased in preterm and FT infants
peptidases timing
well developed early
GI pH in neonates vs adults
increased due to decreased HCl secretion compared to adults
components of fat digestion
- triglyceride hydrolysis by lipases (lingual, GI, pancreatic)
- bile acid emusification
- micelle formations
components of fat absorption
- FFA and monoglycerides transfer easily
- triglycerides reform in enterocytes
- chylomicron formation
- chylomicron enters portal blood or lymphatics
preterm infant fat malabsorption attributed to
reduced bile acid secretion
decreased pancreatic lipase (adult levels at 6 months; lingual and gastric are okay)
function of secretin
stimulates pancrease to release bicarbonate slowing gastric emptying
gastrin inhibitory peptide function
stimulated by protein and fat
slows gastric empyting
decreases gastrin
maltose broken down to
glucose x 2
sucrose broken down to
Fructose + glucose
lactose broken down to
galactose + glucose
posterior pharyngeal perforation on XR
tracks towards right of spine rather than normal left into gastric bubble
eophageal duplication location and diagnosis
posterior mediastinal mass
ultrasound
rate of TEF
1/4500
VACTERL
verterbral
anal
cardiac
TE
radial/renal
limb
pathophysiology of TEF
abnormal formation in GA4
GER vs GERD
GERD has complications ie. growth failure, pain, mucosal damage, aspiration
GERD occurrence
6-7% term
3-10% preterm < 1500g
etiology of duodenal atresia
failure of recanalization GA8-10 after obliteration of lumen by epithelial proliferation during GA6-7
location of duodenal atresia
second part of duodenum
occurrence of duodena atresia and jejunal/ileal atresia
1/20000-40000
1/1500-5000
proportion of atresia in locations of the jejunal/ileal
proximal jejunum 31%
distal jejunum 20%
proximal ileum 13%
distal ileum 36%
etiology of jejunal/ileal atresia
after intestinal development
likely ischemic injury/malrotation/volvulus/ perforation
occurrence of polyhydramnios in jejunal and ileal atresia
1/3 in jejunum
less in ileal
etiology of colonic atresia
vascular compromise
risk of colonic atresia
1/1500-1/20000
risk of hirshprung
1/5000
80% male
recurrence 3-5%
hirshprungs associations
trisomy 21
heterochromia
waardenburg
congenital deafness
13q del
pheochromocytoma
NF
neuroblastoma
etiology of hirshprung
failure of complete cranial to caudal migration of neural crest cells at 8-10 weeks
aganglionic
abnormal parastalsis
Hirschprung:
percent with only rectosigmoid involvement
percent with complete colon involvement
75-80%
5-10%
small left colon syndrome location
splenic flexure transition zone
risk of imperforate anus
1/5000
types of fistulas in anorectal malformations of males and females
males - rectum to GU (rectovesical, rectoprostatic, rectobulbar) or perineal
females - perineal, vestibular, cloacal complex
What is Wangosteen Rice invertogram
used to be used to delineate level of ARM
abnormal fusion of lateral and cephalic folds of abdominal wall
pentalogy of cantrell
1. cleft sternum
2. anterior midline diaphragmatic abnormality
3. pericardial defect
4. ectopic cordis - heart without breastbone - just skin
5. upper abdominal omphalocoele
abnormal fusion of both lateral folds of abdominal wall
omphalocoele
abnormal fusion of the caudal and lateral folds of abdominal wall
cloacal or bladder exstrophy
hypogastric omphalocoele
OEIS complex
omphalocoele
extrophy of bladder
imperforate anus
spinal deformity
etiology of omphalocoele
intestinal loops fail to return to the abdominal cavity at 11 weeks or somatic folds fail to complete formation of the abdominal wall by 18 weeks GA
colorless meconium
cholestasis
intrahepatic duct diseases
neonatal idiopathic hepatitis
alagille paucity of intrahepatic with extrahepatic ducts
nonsyndromic paucity
extrahepatic duct obstruction
biliary atresia
sclerosing cholangitis
bile duct stenosis
choledochal cyst
bile plug
what are the MCC cholestasis
biliary atresia and idiopathic neonatal hepatitis account for 60-70%
what factors improve prognosis in short gut?
intact ileum - bile acid absorption
intact ileocecal valve - delays transit time allowing improved digestion and absoption and prevents overgrowth of colonic bacteria into the small intestines
without ileocecal valve how much intestines do you need
30-45 cm of intestines
air pattern progression on XR after birth
3 hours to small intestines
6-8 hours to large intestines
24 hours to rectum
malrotation with volvulus appearance on barium swallow
complete obstruction: birds beak
partial obstruction: spiral/corkscrew
when are stomach, small intestines and large intestines visible on fetal us
stomach: 13-15 weeks
small intestines - not well until third trimester in center of abdomen
large intestines - 22 weeks
echogenic bowel
most normal
chromosomal abnormalities ie tri 21
congenital infections ie CMV
mec ileus/peritonitis
atresia/volvulus
swallowed blood
proximal bowel obstruction
what is barium study good for?
opacifying stomach and intestines
malrotation or hirschprung
what is gastrograffin study good for>
meconium plug - increased osmolality draws water into lumen and releases plug
monitor electrolytes
what is iohexol or iopamidol study good for?
perforation
a defensins
peptides that interact with phospholipids in microbial cell membranes leading to pores/cell lysis
intestinal fatty acid binding protein
- released from mature enterocytes when cell membrane integrity is compromised
- detected in urine
- may reflect NEC
organs affected in GALD
liver, pancreas, thyroid, heart and adrenal
spared organs in GALD
spleen, LN, BM
glucagon like peptide 2
- antisecretory hormone regulating intestinal transport
- secreted by L cells in terminal ileum and colon
- increases intestinal blood flow
phases of intestinal motor activity during fasting
phase 1: quiescence
phase 2: irregular activity
phase 3: regular phasic propagating + clusters low amplitude non-propagating
MC genetic abnormality in omphalocoele
aneuploidy (tri 13, 18, 21)
method of diagnosing GALD
salivary gland biopsy
primary substrate for enterocytes that increases intestinal cell proliferation via mitogen activate protein kinases
glutamine
serum marker of enterocyte maturation
citrulline
