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1643 Cards in this Set

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cardiac glads (non gastric)
MUCUS secretion
LP of esophagus
-gastroesophageal border
esophageal glands
MUCUS secretion
-lube the lining of the esophagus and lack capacity to buffer acid
esophageal submucosa
cardiac glands
MUCUS
-gastric pits 1/4 to 1/2 into mucosa
-highly coiled
-uniform H&E
where esophaus meets the stomach
gastric glands
SEROUS
-gastric pits 1/4 into mucosa
-straight
-hetero H&E
fundus and body of stomach
pyloric glands
MUCUS
-gastric pits >1/2 mucosa
-coiled
-uniform H&E
pylorus (distal stomach)
SMCs
MUCUS and BICARB
-columnar
-single basal nucleus
-abundance of mucin granules in apical cytoplasm
-gastric mucosal defense
entire stomach lining (gastric mucosa)
mucous neck cells
MUCUS
-simple columnar
more acidic than SMCs
below gastric pits (gastric mucosa)
undifferentiated cells
-progenitor cells that migrate up and down to replace senescent or injured cells
below gastric pits (gastric mucosa)
parietal cells
HYDROCHLORIC ACID and INTRINSIC FACTOR
-large spherical to ovoid
-uni/binucleate
-LOTS of mitochondria
-intensely eosinophilic H&E
high up in gastric gland below base of gastric pit (gastric mucosa)
APUD
no H&E staining
endocrine
gastric mucosa
Brunner's glands
MUCUS (ALKALINE)
-coiled
-neutralize acidic chyme
small intestine submucosa
Auerbach's plexus
well developed parasympathetic ganglia
-regulate peristalsis
between inner circular and outer longitudinal muscularis externa of small intestine
enterocyte
-columnar with microvili coated with glycocalyx
-single nucleus at base
-supranuclear golgi
-abundant R and SER
-interdigitations
-tight junctions and desmosomes
-terminal digestion of carbs and protein
small intestine mucosa
goblet cell
-hour glass shape
MUCIN (by exocytosis to lube GI tract)
-basal nucleus and large pale staining supranuclear region
increases as progresses distally in small intestine and large intestine
undifferentiated cells (SI)
-stem cells
-columnar
-replace senescent or injured cells thru migration and observed differentiation
small intestine at base of crypts
paneth cells
-intense H&E
-large cells
-single nucleus
-well devo RER
-large secretory granules in apical cytoplasm containing lysozyme to degrade walls of certain bacteria
very base of crypts of small intestine
peyer's patches
-large aggregates of confluent lymphatic nodules (lymph, plasma, Macs)
-M cells on luminal surface
ileal mucosa (and sometimes into submucosa)
M cells
-transport luminal Ag to underlying lymphocytes
-no H&E
overlying peyer's patches at luminal surface
colonic epithelium
-lacks vili
-no well devo crypts
-simple columnar
-absorptive
large intestine mucosa
lymphatic nodules (numerous)
isolated and confluent
-chronic state of inflammation
mucosa and submucosa of appendix (extending from cecum)
circumanal glands
specialized apocrine sweat glands
anal canal LP
chief cells
PEPSINOGEN (housed in secretory granules) cleaved to pepsin (active form)
-polygonal to round
-basophilic H&E due to abundance of RER in basal component of cell
base of gastric glands (gastric mucosa)
role of bicarb in stomach protection
works with mucus to keep secreted hydrogen ions from reentering the mucosa in a phenomenon referred to as hydrogen ion back diffusion
role of epithelial renewal in stomach protection
SMCs (3-5 days)
parietal cells (3 weeks)
-ensures healthy cells on demand
role of blood flow in stomach protection
-serve metabolic needs of organ
-buffer hydrogen ions that may get past the mucus/bicarb barrier
-acid can be picked up in blood stream and effectively buffered and eliminated
role of motility in stomach protection
substances don't stay in contact with its lining for any great length of time normally

mixed and dispensed in alliquots that the duodenum can handle
role of H. pylori in stomach at risk
-attaches physically to surface mucous cells and injects them with cytotoxic factors
-negates mucous and bicard secretion protection (no cells, no mucus, no bicarb)
effect of ethanol in putting stomach at risk
-tonic effect
-great dessicant and great fixative
effect of smoking in putting stomach at risk
predispose to ulcers
-nicotine is powerful vasoconstrictor and this negates the effects of robust blood flow
effect of zollinger ellison syndrome in putting stomach at risk
-raging ulcer disease produced from extremely high concentrations of gastrin
-small tumors (gastrinomas) are found in liver, small I, mainly in pancreas
-gastrin causes the parietal cells to become hyperstimulated to produce overwhelming amounts of acid
-no cells, no mucus, no bicarb)
effect of NSAIDS in putting stomach at risk
-second leading cause of ulcers
-ability to inhibit endogenous PG synthesis in the body
-PGs linked to inflammation and pain
-PGs also mediate protective responses of stomach
-NSAIDS will inhibit the good PG effects on the gut (#1-5)
protective features of stomach
1) mucus
2) bicarb
3) epithelial renewal
4) blood flow
5) motility
aggressive features on stomach
1) h. pylori
2) NSAIDs
3) EtOH
4) smoking
5) Zollinger Ellison syndrome
major salivary glands
1) parotid
2) sublingual
3) submandibular
minor salivary glands
1) Labial
2) Buccal
3) Molar
4) Lingual
5) Palatine
serous acini secrete:
zymogen (amylase and lipase)
mucous acini secrete:
mucus
seromucous acini secrete
zymogen and mucus
cell shape of serous glands
pyramidal cells arranged in circular groups around central lumen
cell shape of mucous glands
pyramidal cells arranged in circular groups around central lumen
nuclei of serous glands
single
basal
nuclei of mucous glands
flattened
basal
organelles:
serous vs. mucous
both have RER, Mi, golgi

serous just has more
glands containing myoepthelial cells
serous and mucous

semi: seromucous
hallmark of seromucous glands
demilunes: few serous secreting cells "cap" an acinus (which is mostly composed of mucus)
H&E: serous glands
DARK (all serous acini)
H&E: mucous glands
LIGHT (mucus is extracted)
H&E: seromucous glands
hetero
parotid gland is made up of what type of acini
serous
submandibular gland is made up of what type of acini
serous > mucinous
mucous gland is made up of what type of acini
mucous > serous
salivary gland ducts
-intercalated
-striated
-interlobular
-stenson's
-wharton's
lining of intercalated duct
low cuboidal to squamous
lining of striated duct
columnar
lining of interlobular duct
pseudostratified columnal -> stratified columnar -> stratified squamous
what is stenson's duct
main excretory duct of parotid gland
what is wharton's duct
main excretoy duct of submandibular gland
pancreatic ducts
-intercalated
-intralobular
-interlobular
-excretory
lining of intercalated pancreatic ducts
squamous to low cuboidal
lining of intralobular pancreatic ducts
cuboidal or low columnar
excretory pancreatic ducts
santorini
wirsung
pancreatic acini cell shape
pyramidal; circular pattern
pancreatic acini nucleus
euchromatic at base
H&E for pancreatic acini
basal: basophilic
apical: eosinophilic
pancreatic secretory granule contents
digestive enzymes: lipase, amylase
portal triad
hepatic artery, portal vein, bile duct
characteristics of sinusoid
-thin, discontinuous highly fenestrated endothelium (squamous cells)
-resting on incomplete basal lamina
what is the space of disse
-interposed between endothelial lining and underlying hepatocytes
-hepatocytes gain access to soluble components of blood
arrangment of hepatocytes
in plates, one cell layer thick (adults) or 2 layers (children) separated by sinusoids
formation of bile canaliculi
fusion of plasma membranes sealed by tight junctions
location of hepatocytes
parenchyma in between sinusoids
location of kupffer cells
-w/in liver sinusoids
-spanning the lumen
or
-attached to endothelium
location of hepatic stellate cells
within space of disse
locaton of fibroblasts
stroma
(and sometimes within space of disse)
function of kupfer cells
-phagocytic and help eliminate particular matter
-plays a role in breakdown of RBCs
function of hepatic stellate cells
-store vit A in droplets
-source of collagen and extracellular matrix components deposited in excess during development of cirrhosis
location of gall bladder
posterior aspect of Right lobe of liver
lining of gall bladder
simple columnar epithelium
organelles of gall bladder epithelium
microvilli, Mi, golgi, RER, pinocytic vesicles, tight junctions
layers of gall bladder
-simple columnar epi
-lamina propria
-single layer of smooth m
-serosa
function of gall bladder
-stores and concentrates bile
-contracts with meals
GI is all smooth muscle except:
1) pharnx
2) proximal 1/3 esophagus
3) external anal sphincter
phasic contractions
efficient mixing and transit of chyme
tonic contractions
limit flow or provide a reservoir function (e.g. sphincters)
what are caveolae
micropits on surface of smooth muscle
-allow for increased surface area
-role in transmembrane calcium flux during muscle cell stimulation
gap junctions in smooth muscle
areas of close apposition for intercellular communication through ion channels
what is a syncytium
large number of individual cells become activated and contract as though one unit
smooth muscle is lacking what compared to skeletal muscle
-sarcomeres (A and M are arranged in myofilaments)
-troponin
plasticity
ability to stretch to a greater length and compress to a shorter length than skeletal m
phasic contraction (smooth m)
-short duration of contraction followed by relaxation
-segmentation and peristalsis
segmentation contraction
-small and large intestine
-segment contracts with muscles on either side relaxing
-chyme moves along intestine
peristalsis
-circular and longitudinal muscle layers
-in presence of bolus distension
-contraction proximal to bolus, relaxation below
tonic contraction( smooth m,)
-sphincters
-divide GI into functional segments
-maintain tone at baseline and relax to allow contents to pass
caveolae
microits on the surface of smooth m cells
gap junction (smooth m cells)
-areas of close apposiion for intercellular communication thru ion channels
-functionally couple cells to each other - stim or one results in activation of a number of cells
syncytium
large number of individual cells become activated and contract as though one unit
myofilaments
-thin and thick filaments run thorugh roughly parallel to the long axis of the smooth m with greater thin than thick filaments

-shortening the muscle along its long axis
plasticity
ability to stretch to a greater length and compress to a shorter length than skeletal m
gut electromechanical channels
-slow-leaking Ca
-ligand-gated
-voltage-gated Na
phasic contraction (smooth m)
-short duration of contraction followed by relaxation
-segmentation and peristalsis
segmentation contraction
-small and large intestine
-segment contracts with muscles on either side relaxing
-chyme moves along intestine
peristalsis
-circular and longitudinal muscle layers
-in presence of bolus distension
-contraction proximal to bolus, relaxation below
tonic contraction( smooth m,)
-sphincters
-divide GI into functional segments
-maintain tone at baseline and relax to allow contents to pass
caveolae
microits on the surface of smooth m cells
gap junction (smooth m cells)
-areas of close apposiion for intercellular communication thru ion channels
-functionally couple cells to each other - stim or one results in activation of a number of cells
syncytium
large number of individual cells become activated and contract as though one unit
myofilaments
-thin and thick filaments run thorugh roughly parallel to the long axis of the smooth m with greater thin than thick filaments

-shortening the muscle along its long axis
plasticity
ability to stretch to a greater length and compress to a shorter length than skeletal m
gut electromechanical channels
-slow-leaking Ca
-ligand-gated
-voltage-gated Na
slow waves affect on smooth m contraction
determine the maximum FREQUENCY of contraction but are not sufficient to cause contraction
regulatory step of smooth m contraction
binding of Ca to calmodulin
ICCs location
between 2 layers of muscularis externa and muscular plexus

between nerve terminals and smooth m cells
ICCs function
-establish rhythmicity of contraction in the gut by acting as pacemakers for the electrical slow waves

-relays for transmission from enteric motor neurons to GI musculature
effect of ACh on slow waves
-inc slow wave amplitude and duration
-inc AP frequency
-inc contraction strength
effect of NE on slow waves
-dec slow wave amplitude and duration
-dec AP frequency
-dec contraction strength
3 pharmoco-mechanical mechanisms in Ca+ movement
-neurocrine (released from nerves)
-paracrine (non-neural cells in close proximity to the muscle)
-endocrine (hormones delivered to the muscle by blood)
sequnece of smooth m contraction
extracellular Ca enters the cell -> calmodulin binds Ca and activates MLCK -> MLCK phosphorylates myosin turning it on -> m interacts with a -> contraction
Why do some depolarizations cause
smooth muscle cells to contract and
others do not?
motorneurons (innervate smooth m. -> When motor neurons produce action
potentials, Ach is liberated)
layers of enteric nervous system
mucosa
submucosal plexus
circular muscle
longitudinal muscle (w/ myenteric plexus ganglia and intragang fiber tract)
predominant functions of ENS
-peristalsis
-secretion and maintenance of interdigestive migrating motor complex
sensory function of ENS
-wall tension
-pH
-osmolality
2 ganglionated plexuses of ENS
1) myenteric (Auerbachs)
2) submucosal (Meissners)
location of myenteric plexus
between circular and longitudinal muscle layers
location of submucosal plexus
in submucosal region between circular m layer and mucosa
role of glial cells in ENS
modulating inflammatory responses in intestine
inhibitory NTs in ENS
VIP, NO synthase
excitatory NTs in ENS
ACh, tachykinins, substance P, substance K
inhibitory role of sphincters
inhibitors are nL off
-activated in relaxation of anal sphincter during defacation
inhibitory role of non-sphincters
inhibitorys control extent of progression of myogenic excitation
intrinsic neurons of ENS
sensory of myenteric and submucosal plexuses
interneurons of ENS
multisynaptic pathway and control distances along intestine for which parastaltic waves are propogated
motor neurons of ENS
excitatory: locally, orally, ACh, Substance P

inhibitory: caudally, NO, VIP
parasymp nerves of ENS
vagal n.
sacral n (2,3,4)
sympathetic nerves of ENS
interomediolateral column of spinal cord between the levels of the 5th thoracic and 3rd lumbar segments
cell bodies of parasympathetics ENS
ganglion cells within enteric nervous system
cell bodies of sympathetics ENS
cell bodies located in perverterbral ganglia (outside the GI tract)
function of vagal n

-P or S
P

motor and secretomotor of upper GI: esophagus, stomach, prox small intestine, prox colon
area of control of sacral n

P or S
P

distal colon and rectum
area of control of extrinsic 2,3,4 and pelvic n

P or S
P

anorectum and left hemicolon
area of control of 2,3,4 and pudendal n

P or S
P

external anal sphincter
thoracolumbar

P or S

alpha function
S

contraction of sphincter
thoracolumbar

P or S

beta function
S

relaxation of sphincter
thoracolumbar

P or S

alpha 2 function
S

inhibition of non-sphincter
function of vagal and splanchnic
primary afferent

mechanical distension of the gut, lumincal concentration of glucose, AA, or LCFAs
function of vagal n. in ENS
Controls upper gut
tonic and phasic
contractions

-Fundic relaxation
-Antral contraction
peristaltic reflex: trigger
distension: caused by bolus of food, gas, or foreign body
peristaltic reflex: response
above/proximal contraction due to ACh/SP/SK

below/distal relaxation due to VIP/NO
locations for:
Water and electrolyte secretion
- Stomach, pancreas, liver and gut
locations for: Enzyme secretion
- Stomach and pancreas
locations for: Trophic effect
- Gastric mucosa, pancreas, gut mucosa
responsible for:
Endocrine secretion
- GI hormones, insulin, glucagon,
calcitonin
locations for: motility
- Hollow gut, sphincters and gallbladder
locations for: Intestinal absorption
- Water, electrolytes, nutrients
peptide families






-Gastrin/CCK
-Secretin/Glucagon/VIP/GIP
-Pancreatic Polypeptide/PYY/NPY
-Tachykinins (substance P,K)/Bombesin
-Opioid Met- and Leu-enkephalin,dynorphin
gastrin: what's required for bio activity
c term
where is gastrin released from
G cell antral mucosa and some duodenal
functions of gastrin
-released in response to products of protein digestion, gastric distension
-stimulates acid release
-trophic mucosal effect
-inhibited by antral acidification (pH <3)
CCK: what's required for bio activity
c term
(-sulfation)
functions of CCK
-gall bladder contraction
-pancreatic enzyme secretion
-sphincter of Oddi relaxation
-trophic effect on pancreas
-release stimulated by digested protein, fatty acids, not carbs
secretin relased from
released from S cells in the duodenum and proximal jejunum
CCK released from
I cells of duodenum and proximal jejunum
functions of secretin
-stimulates pancreatic, water, bicarb secretion
-inhibits acid secretion
-stimulates growth of exocrine pancreas
-release stimulated by acid
GIP function
-stimulation of insulin release
motilin functions
-potent stimulator of upper gut motility
somatostatin functions
-potent inhibitor of gut hormone release, secretion, and motility
somatostatin is released from
D cells in pancreatic islets
VIP functions
-mediates gut relaxation (especially sphincter)
watery diarrhea syndrome is seen bc of what hormone
VIP
VIP is what type of hormone
neurocrine
function of enkephalins
-activate opiate receptors, sphinteric muscle contraction, inhibit secretion
location of enteroglucagon
distal gut
enteroglucagon function
ileal break
glucagon like peptide - 1 function
may stimulate insulin release
pancreatic polypeptide function
islet cell peptide released in response to vagal stimulation
peptide YY function and location
distal gut - ileal break
nitric oxide function
smooth m relaxation
somatostatinoma characteristics
-gall stones, low acid secretion, steatorrhea, and glucose intolerance
tx of somatostatinoma
the analogoue: treat functional islet cell tumors, some diarrheal state
what can augment CCK induced enzyme secretion
secretin
what stimulates GIP
glucose, fat, AA
what stimulates somatostatin
luminal fat and Protein
location of neurotensin
distal small bowel
what hormone is involved in zollinger-ellison syndrome
gastrin (producing tumor)
peptide YY function and location
distal gut - ileal break
nitric oxide function
smooth m relaxation
somatostatinoma characteristics
-gall stones, low acid secretion, steatorrhea, and glucose intolerance
tx of somatostatinoma
the analogoue: treat functional islet cell tumors, some diarrheal state
what can augment CCK induced enzyme secretion
secretin
what stimulates GIP
glucose, fat, AA
what stimulates somatostatin
luminal fat and Protein
location of neurotensin
distal small bowel
what hormone is involved in zollinger-ellison syndrome
gastrin (producing tumor)
2 products of pancreas (function of each)
bicarb (neutralize gastric acid)

enzymes (digestion of protein/fat/starch, digestion required for absorption)
incomplete pancreas divisum
significant accessory duct connecting main pancreatic duct and duodenum
pancreas divisum
accessory duct drains via the minor papilla without connection to main duct (all ducts are connected together - draining from 2 orifaces)
ducts of pancreas
-accessory duct (santorini)
-main duct (wirsons)
-minor and major papilla
acinar cells produce:
digestive enzymes
ductal cells produce
bicarb
basal pancreatic secretion level
0.2-0.3 mL/min
stimulated pancreatic secretion
4-4.5 mL/min
definition of protease
break down large proteins into smaller oligos and even into a few individual amino acids
3 pancreatic proteases
-trypsin
-chymotrypsin
-carboxypeptidases
2 types of starches
-amylose
-amylopectin
bonds seen in amylose
amylose:
linear string of simple sugars held together by alpha 1-4

600 glucose residues
bonds seen in amylopectin
branched string of simple sugars held together by alpha 1-4 linkages but punctuated by alpha 1-6 linkages

6000 glucose residues
end products of amylase:
-amylose
-amylopectin
amylose: maltose, maltotriose

amylopectin: maltose, maltotriose, alpha-limit dextrins
brush border enzymes that further break down oligos produced by amylose (oligos)
-isomaltose (alpha -limit dextrin)
-glucoamylase
-sucrase (sucrose)
-lactase (lactose)
2 enzymes needed for fat digestion and absorption
lipase
colipase
lipase characteristics
-secreted in active form (alkaline environment)
-dysfunctional in presence of bile
-inactivated in pH < 4
colipase characteristics
-secreted in inactive form (procolipase)
-procolipase is converted to active form with trypsin
-allows lipase to work in presense of bile
-does not protect lipase from low pH
steps of bicarb secretion
-CO2 enters the cell by diffusion or generated by cell metabolism
-carbonic anhydrase catalyzes the hydration of CO2 into carbonic acid
-carbonic acid dissociates to produce bicarb
-luminal Cl- is required which is released by the cAMP regulated CFTR
4 categories of pancreatic simulation
1) basal
2) cephalic
3) gastric
4) intestinal
basal pancreatic secretion
minimal secretion
cephalic secretion
CNS integration to GI tract
-efferent vagal impulses
-stimulates enzyme and bicarb secretion
-20% with most meals, up to 50% if intense
gastric secretion
initiated by gastric distension
-vagally mediated
-release of enzyme > bicarb
-no more than 10% of meal-induced pancreatic stimulation
intestinal secretion
most powerful
-cholinergic reflexes
-2 hormones: cholecystokinin and secretin
secretin:
-produced/released by?
-in response to..
-responsible for?
neuroendocrine S cells
-acidic pH
-production of bicarb, slows gastric emptying, gastric acid production
cholecystokinin:
-produced/released by?
-in response to..
-responsible for?
-I cells
-fatty acid, amino acids, peptides
-production of pancreatic enzymes
CCK releasing peptide:
-produced by?
-in response to?
-action
-degraded by?
-duodenal cells
-chyme
-acts on I cells causing them to secrete more CCK
-proteolytic enzymes from pancrease which act on CCK-rp
sites where atresia can occue
-esophagus
-small intestine
-large intestin
-anus
-biliary tree
clinical characteristics of atresia
-polyhydramnios
-obstruction
-ab distension
-biliary vomitting
-failure to pass meconium
tx of atresia
-relieve obstruction
-anastomose ends
cause of esophageal atresia
-failure of division of foregut into respiratory and digestive portions at wk 4-5
most common TEF
-blind-ended proximal esophagus and fistula b/w trachea and distal esophagus
unique clinical presentation of TEF
resp distress
pts seen with duodenal atresia
-premature babies
-down syndrome
tx of duodenal atresia
duodeno-duodenostomy
or
duodeno-jejunostomy
unique clinical presentation of duodenal atresia
-double bubble on Xray (stomach, prox duodenum)
-mucosal web distal to ampulla
associated anamolies with TEF
-VATER syndrome
-Down syndrome
unique clinical presentation of jejunal atresia
-bilious vomitting without distension
unique clinical presentation of ileal atresia
-distended loops of bowel (with calcification)
-small unused colon
calcification in ileal atresia
-dystrophic calcification with fibrosis, scarring, and granulation tissue which all replaces the lumen
sasuage/beads on a string looking bowel
ileal atresia
2 theories about etilogy of small intestinal atresia
1) failure of recanalization of lumen (esp in duod)
2) in utero mesenteric vascular accident (jej and il -> ischemia, necrosis -> disintegration of bowel and mesentary supplied by vasculature -> wedge-shaped defect
types of small intestine atresa
I: lumen interrupted, intact mes
II: blind ends, mes intact, fibrous cord
III: blind ends, unattached mes
clinical findings of colonic atresia
-rarest form
-obstruction
-blind ended distal colon
tx of colonic atresia
-colostomy
-reanastomosis
clinical charac of anal atresia
-most common
-males > females
cause of anal atresia
abnL devo of urorectal septum

or

imperforate anal membrane
location of intestinal duplication cysts
-esophagus, small I, large I

rare: colon and stomach
what are intestinal duplication cysts
saccular or cystic duplication of gut
cause of intestinal duplication cysts
abnL recanalization into 2 parts - one part is nL gut, one part is the cyst
clinical presentation of IDCs
-abdominal pain, mass, vomitting

-cyst on mesenteric side

-does not communicate with nL bowel
what is meckle's diverticulum?
-persistance of omphalomesenteric (vitelline) duct
-connection between midgut and umbilicus
clinical features of meckle's
-most common congenital abnL of gut
-male > female
-may perforate, ulcerate, bleed, inteusscept
meckle's main features
-solitary
-always ileum
-2 ectopias: gastric, pancreatic
-antimesenteric
rule of twos
(what dz?)
meckle's diverticulum
-2% of population
-2 ectopias
-2 cm long
-2 feet from ileocecal valve
clinical characterisitics of pyloric stenosis
-projectile vomitting at 2-3 weeks old
-M > F (first born males)
-familial, multifactorial
-hypertrophied pylorus
-firm oval mass "olive"
tx of pyloric stenosis
pyloromyotomy
hirschsprungs dz aka?
-aganglionosis
-congenital megacolon
what is hirschsprungs?
-distal obstruction due to absence of myenteric, submucosal enteric ganglia
-aganglionic segment always distal - rectum and extends prox
cause of hirschsprungs
-failure of neuroblast migration, division, survival, and differentiation
nL migration location:
week 8
transverse colon
nL migration location:
week 9
descending colon
nL migration location:
week 10
sigmoid colon
nL migration location:
week 12
anus
genetics of hirschsprungs
RET gene which codes for receptor for devo regulator involved in neuronal migration

hetero, LOF mutation
hallmark of hirschsprungs
transition zone
clinical features of hirschsprungs
-m > f
-newborn with obstruction or older child with long hx of constipation
assoc syndromes with hirschsprungs
downs, FH, GU tract, anorectal anomalies
dx of hirschsprungs
-transition zone
-delaed empyting of barium enema
tx of hirschsprungs
relieving obstruction, connecting ganglionated bowel to anus
without tx hirschsprungs has risk of...
necrotizing enterocolitis
transition zone is seen with
pseudomembrane of inflamm cells and necrotic debris due to obstruction -> distension -> dec perfusion -> ischemia -> necrosis
what is extrahepatic biliary atresia
partial or complete absence of bile ducts between porta hepatis and duodenum
clinical features of extrahepatic biliary atresia
-persistent neonatal cholestasis
-acholic stools
assoc anamolies with extrahepatic biliary atresia
polysplenia
situs inversus
pathology of extrahepatic biliary atresia
extra bile ducts: fibrous cords
intra bile ducts: proliferation to compensate

-can devo into cirrhosis if not tx
tx of extrahepatic biliary atresia
surgery!
kasai portoenterostomy: prox jejunum up into porta hepatis

or

transplantation
2 types of body wall defects
omphalocele
gastroschisis
etiology of omphalocele
-gut fails to return to abdomen
pathology of omphalocele
-sac covers intestine, liver
(may rupture)
-small perioneal cavity
tx of omphalocele
-get guts into abdomen
-primary closure or staged closure (silo)
associated anamolies with omphalocele
-malrotation
-diaphragmatic hernia
-cardiac, renal abnL
-trisomay 13, 18, 21
-beckwith-wiedemann syndrome (chrom 11)
gastroschisis cause

aka?
due to antenatal evisceration

-hernation of bowel on one side of cord

belly cleft
pathology of gastroschisis
-full thickness ab wall defect
-usually R of umbilicus
-no SAC, guts are external but not liver
-peritonitis! exposure of serosa to amniotic fluid
assoc anaomlies with gastroschisis
-malrotation
-atresia
-premature
-SGA
-lower mortality than omphalocele
necrotizing enterocolitis presentation
-premature
-shock, sepsis
-ab distension
-pneumatosis
necrotizing enterocolitis pathology
-distended loops of bowel
-ischemic necrosis
-pneumatosis
-iliocolic region most affected
location of necrotizing enterocolitis
iliocolic region
hallmark of necrotizing enterocolitis
pneumotosis

-air bubbles in walls of bowel
tx of necrotizing enterocolitis
Abx, fluids, surgery
downs assoc with what conditions
-hirschsprungs
-omphalocele
-duodenal atresia
wedge shaped mesenteric defect seen in what locations
jej and ile
types of esophageal diverticulum
-zenker's diverticulum
-traction diverticulum
-epiphrenic diverticulum
location of zenkers
-posterior to cricopharyngeous muscle
location of traction div
midpoint of esophagus
location of epiphrenic div
above LES
features of zenkers
-mass lesion
-regurg
-oropharyngeal dysphagia
-halitosis
-respiratory complications
feature of tractiion div
granulomatous inflammation
-histo/TB in adjacent lymph nodes
feature of epiphrenic div
assoc motility disorder
schiatski's ring
-mucousal ring at GE junction
-marks squamocolumnar junction
-intermetent solid food dysphagia
-treat with dilation
location of esophageal webs
cervical/mid esophagus
-anterior projections
clinical features of esophageal webs
older women, skin blistering dz, chronic GVHD, GERD, solid food dysphagia
epithelium of esophageal webs
thin stratified squamous
epithelium of esophageal rings
squamocolumnar junction
clinical features of eosinophilic esophagitis
-young men
-history of atopy (allergies, asthma, hayfever)
-sx: dysphagia, food impaction, heartburn
tests for eosinophilic esophagitis
lab: elevated IgE, peripheral eosinophilia

barium swallow: small caliber, focal or long tapered strictures, concentric rings

EGD-ringed esophagus, linear furrows, eosinophilic abscesses

must exclude GERD

biopsies: >15 eos/HPF
tx for eosinophilic esophagitis
-trial of PPI
-corticosteroids
-dietary changes
-allergy referral
-cautious dilation
other causes of dysphagia
-extrinsic compression
-NM disorders (motility, infiltrative)
***characteristics of plummer vinson syndrome
-dysphagia
-cervical web
-iron deficiency**
-inc risk of squamous cell carcinomas of pharynx/esophagus
symptoms of medication induced esophagitis
-chest pain, pain with swallowing, acute heartburn
-underlying risk factor
-presence of offending medication
location of medication induced esophagitis
-mid esophagus/aortic arch
-transition zone between skeletal/smooth muscle
tx of medication induced esophagitis
-avoid offending agent
-symptom control
-acid reflux prevention
-behavioral changes
causes of infectious esophagitis
-candida
-HSV
-CMV
-HIV
candida - infectious esophagitis
-use of inhaled corticosteroid
-immunocompentent or immunocompromised
-odynophagia or dysphagia
-KOS/PAH stain
-oral thrush in 2/3
-fluconazole
-systemic therapy
HSV : infectious esophagitis
-immunocomp
-odynophagia, dysphagia, chest pain, fever
-vesicles, small ulcers, "volcano like"
-biospy from edge of ulcer
-multinucleated giant cells, ground glass nuclei, eosinophilic inclusions
-acyclovir, famcyclovir, valcyclovir
cells seen in HSV infectious esophagitis
-multinucleated giant cells, ground glass nuclei, eosinophilic inclusions
cells seen in CMV infectious esophagitis
intranuclear inclusion bodies
ulcers seen in HSV infectious esophagitis
vesicles, small ulcers, volcano like
ulcers seen in CMV infectious esophagitis
linear and deeper, larger
HIV infectious esophagitis
idiopathic ulcer
-dx of exclusion
-steroids
-CD <100
-thalidomide for refractory cases
two types of esophageal cancer
-adenoCA
-SCCA
symptoms of esophageal CA
-dysphagia
-odynophagia
-weight loss
-GI bleeding
-chest pain
-vomitting
risk factor and type of CA assoc:
black men
SCC
risk factor and type of CA assoc:
white men
adeno
risk factor and type of CA assoc:
GERD/obesity
adeno
risk factor and type of CA assoc:
etoh
SCC
risk factor and type of CA assoc:
tobacco
SCC
risk factor and type of CA assoc:
nitrosamine exposure
SCC
risk factor and type of CA assoc:
corrosive injury
SCC
risk factor and type of CA assoc:
vit def
SCC
risk factor and type of CA assoc:
achalasia
SCC
risk factor and type of CA assoc:
tylosis
SCC
risk factor and type of CA assoc:
HPV
SCC
risk factor and type of CA assoc:
plummer vinson
SCC
tx of esophageal CA
-stage with CT, EUS, PET CT
-surgery
-neoadjuvant chemo
types of gastrides (location)
1) h. pylori (distal antral)
2) environmental (body and antral)
3) autoimmune (body)
h. pylori gastritis characteristics
-asymp
-low socioeconomic, immigrant
-chronic inflammatory cells (lymphocytes)
-high acid production, hypogastrinemia
-duo ulcers common
environmental gastritis characteristics
-mucosal atrophy/intestinal metaplasia (risk for gastric CA)
autoimmune metaplastic atrophic gastritis
-assoc with pernicious anemia, Ab to IF/parietal cell, vit B12 def, elevated gastrin levels
-autoimmune dz
-relation to gastric carcinoids
sx of reactive gastropathies
-hemorrhage, erosions, ulcers without significant inflammation
causes of reactive gastropathies
-NSAIDS, alcohol, cocain, bile reflux, stress
what is a peptic ulcer
defects or breaks in mucousa with depth and have extended through muscularis mucousa
clinical presentation of PUD
-epigastric pain "dull, aching, hunger like, empty
-duodenal ulcer relieved with food
-gastric ulcers: eating makes worse
-alarm symptoms: acute change in pain, overt GI bleeding, anemia, weight loss, vomitting, early satiety
ulcer relived with ingestion of food
duodenal
ulcer made worse with ingestion of food
gastric
alarm symptoms of ulcer dz
-change in pain
-overt GI bleeding
-anemia
-weight loss
-vomitting
-early satiety
pathogenesis of PUD
-multifactorial
-imbalance between gastrin/pepsin > gastric mucousal defenses
-h. pylori
-NSAIDS
-malignancies/disorders/infections
gastric ulcers assoc with?
malignancies
duodenal ulcers assoc with?
ZE syndrome
4 other risk factors assoc with PUD
-smoking (slows healing)
-corticosteroids (suppress PG synthesis and impair healing)
-stress/criticallyill
-hyperCa+ (stimulates gastrin)
stress ulcers: head/SCI trauma
cushing
stress ulcers: severe burn
Curling
etiology of stress ulcers
decreased mucousal protection and mucousal ischemia
how does h. pylori do its damage?
-produces urease which alkalinizes the mucousa and forms ammonia
-ammonia is toxic to cells which causes inflammation which allows pepsin and gastrin to overwhelm protective measures
h. pylori acting as carcinogen can lead to
gastric adeno
MALT
how do NSAIDS do their damage
-inhibit COX1
-dec PG synthesis
-dec mucousal protection
complications of PUD
childhood games: silly PUddy and BOP 'eM

-GI bleeding
-obstruction
-Penetration/perforation
-mortality (10%)
diagnostics of PUD
-EGD > barium because you can biopsy for both h. pylori and malignancy
tx of PUD
-heal, prevent recurrence, h. pylori test, NSAID use, acid suppression
h. pylori tx
-PPI and 2 Abx (amox, clary, metro, tetra)
-7-14 days
what are hypertrophic astropathies
-giant gastric folds
-epithelial hyperplasia
-no inflammation
menetriers dz
protein losing gastropathy with enlarged folds in body of stomach

hypochlorhydria
etiology of menetriers dz
overexpression of TGF
assoc with h. pylori and CMV
symptoms of menetriers dz
-epigastric pain
-vomitting
-GI bleeding
-weight loss
-anorexia
-dyspepsia
-diarrhea
tx of menetriers dz
secretion
suppression
nutrition
what is ZE syndrome
-gastrin secerting endocrine tumor (gastrinoma)
-5 fold incerase in parietal cell mass -> gastrin hypersecretion
clinical ZE
-PUD
-chronic diarrhea
-solitary tumors in SI/pancreas
dx of ZE
-increased gastrin levels, EUS/oct scan
MEN 1 (name?) - features
multiple endocrine neoplasia

-AD
-3 Ps (pancreatic > parathyroid, pituitary)
MEN 1 tx
somatostatin receptors
gastric polyps
-due to hyperplasia of epithelial or stomal cells
-ectopia
-inflammation
-neoplasia
fundic gland polyps
-inc gastrin
-acid suppression
most common location for gastric adenoma
antrum
gastric adenocarcinoma: symptoms
-weight loss, anorexia, epigastric abdominal pain, iron deficiency anemia
most common location for gastric adenocarcinoma:
lesser curvature of antrum
virchow's node
mets to supraclavicular sentinal lymph node
sister mary joseph nodule
mets to periumbilical region to form subQ nodule
linitus plastica appearance:
what is it?
when is it seen?
rugal flattening and thick/rigid wall

diffuse gastric adenoCA
types of gastric adenoCA
-intestinal (metaplasia/atrophy, bulky tumors)
-diffuse (poor prog, younger pts)
gastric lymphoma characteristics
-extranodal lymphoma
-B cell tumor, lymphocytic infiltrate
-chronic inflammation
-h. pylori
gastric lymphoma symptoms
-weight loss, epigastric pain, dysopepsia, GI bleeding

-B: fever, night sweats

-mucuousal erythema, nodularity, ulcer, polyp, infiltrative
gastric carcinoids features
-arise from enterochromaffin like cells - endocrine cells
-sheets of uniform cells
-yellow or tan and firm submucosal masses
-SBO
-40% in small intestine
-synaptophysin and chromogranin A positive stains
classification of carcinoids
foregut
midgut
hindgut
foregut carcinoid tumors
stomach (chronic atrophic gastritis/pernicious anemia)
dudodenum (prox to ligament of treitz)
esophagus (b9, cured with resection
midgut carcinoid tumors
jejunum and ileum
-poorer prognosis
-more likely assoc with carcinoid syndrome
-multiple and aggressive
hindgut carcinoid tumors
appendix and colorectum
-usually b9
carcinoid syndrome symptoms
-sweating
-flushing
-colicky ab pain
-right sided cardica valvular fibrosis
-bronchospasm
carcinoid syndrome etiology
release of vasoactive substances in systemic circulation
GIST arise from
intersitial cells of cajal (pacemaker cells of gut)
GIST features
-men
-mesenchymal cells
-60s (age)
GIST causes
ckit oncogenic GOF
what is acute pancreatitis
-acute inflammatory event that originates in pancreas
pathophys acute pancreatitis
autodigestion of pancreas by enzymes meant for secretion
dynamic process of pancreatitis
insult -> trypsin (with tissue damage activates -> zymo and lyso fuse -> blocks secretion) tissue damage -> inflamm response ->SIRS -> MOF
initiating factor of acute pancreatitis
increase in intracellular Ca+ flux with premature activation of trypsinogen within the pancreas
acute pancreatitis: intracellular injury results in...
generation of proinflammatory cytokines
release of proinflamm cytos into the circulation results in
SIRS -> MOF
dx of acute pancreatitis
-abdominal pain
-amylase and/or lipase > 3X ULN
-CT ab imaging
other dz with elevates amylase and lipase
-intestinal infarction
-perforation
-renal failure
-severe nausea
-vomitting
symptoms of acute pancreatitis
-ab pain, radiates to back
-grey-turner sign
-epigastric tenderness
-nausea
-anorexia
grey-turner seen in
acute pancreatitis
complications of acute pancreatitis
-shock
-pulmonary edema
-bac infection of destroyed tissue
elevated markers of inflammation
WBC, CRP
markers of MOF
elevated creatinine, hypoxemia
elevated AST, ALT, and bili may indicate?
gallstone pancreatitis
classification of acute pancreatitis
intersitial
necrotizing
less common etiologies of acute pancreatitis
-drugs
-outflow obstruction
-hyperlipidemia
-post ERCP
strong evidence of drug etiology of acute pancreatitis
positive Re-challenge with drug
management of acute pancreatitis
-iv hydration
-nutritional support
-abx
-endoscopy
abx needed in acute pancreatitis when
-sepsis
-proven pancreatic or extra-pan infection
-MOF
where does stimulation occur in TPN
proximal
where does inhibition occur in TPN
distal
what is chronic pancreatitis
diffuse fibrosis of the pancreas with loss of pancreatic mass
clinical manifestations of chronic pancreatitis
-abdominal pain
-foul smelling oily stool
-weight loss
-nausea/vom
-diabetes
pathogenesis of chronic pancreatitis
recurrent low grade episodes of injury lead to fibrosis
cause of chronic pancreatitis
alcohol
congenital abnLs that predispose to chronic low grade injury
complications of chronic pancreatitis
-pancreatic insufficiency
-debilitating pain
-adenoCA
dx of chronic pancreatitis
-pancreatic calcifications on xray
-small pancreas on CT
-amylase and lipase not elevated
tx of chronic pancreatitis
-alleviation of pain
-enzyme therapy
-surgical drainage of pancreatic duct into jejunum
how does enzyme tx work to alleviate pain
-negative feedback inhibition
-enzyme supplement -> inactivates CCK-rp by serine proteases -> reduces pancreatic stimulation
genetics of hereditary pancreatitis
-AD
-PRSS1 mutation
-cationic trypsinogen gene
-causes trypsin to be resistant to lysis or causes premature trypsinogen activation
hereditary pancreatitis shows inc risk of what?
pancreatic CA
genetics of familial pancreatitis
-AR
-CFTR or SPINK1
-binds and inactivates intra-pancreatic trypsin activity
what is a pseudocyst
non-neoplastic

cyst without lining, complication of pancreatitis
what is a true cyst
non-neoplastic

lined by epithelium, occur in PCdz and von-hippel lindau
serous cystadenoma: m or b9
b9
mucinous cystic neoplasm: m or b9
risk of m
intraductal papillary mucinous neoplasm: m or b9
risk of m
ductal adenoCA neoplastic
with cystic degen
pancreatic adenoCA location
head>body>tail
symptoms of pancreatic adenoCA
-painless jaundice (+ diltation of gall bladder) (courvoiseir sign)
-abdominal pain
trousseau's syndrome:
-what CA
-signs
pancreatic adenoCA
-hypercoAg state with formation of thrombi all over the body called migration thrombophlebitis
what is gallbladder dyskinesia
delayed empyting of gall bladder in absence of stone or sludge
what is sphincter of oddi dysfunction
-stenosis/fibrosis, inflammation or both

-can cause biliary pain, biliary obstruction, and abnL liver enzymes
what is sphincter of oddi
valve that controls the flow of digestive juices thru ampulla of vater into the second part of the duodenum

-relaxed by CCK via VIP
occurence of gallstones
10-20% of adults
classic gall stone pain
constant aching/pressure RUQ or epigastric pain radiating to the back lasting 1/2-4 hours (esp after fatty meal)

nausea
gallstones
passage of stone fragment or impacion in gallbladder neck, cystic duct, or phincter of Oddi
cholesterol stone
-yellow, yellow tan round, faceted

-when cholesterol concentration exceeds the soluilizing capability of the bile and precipitates out
pigmented stone
-calcium bilirubinate
-multiple small black or brown
-inc unconjugated (insoluble) bilirubin in the bile
dx of gall stone
ab ultrasound
thickened gall bladder wall
tenderness over gall bladder
risk factors of cholesterol stone
female, fat, forty (old age)
risk factors for pigmented stone
chronic hemolysis
what is acute cholecystitis
inflammation of gall bladder due to
-infection
-obstruction
-distension
-action of bile on GB wall
pathogenesis of acute cholecystitis
-gall stones
-acalculous
what is acalculous
ishcemic compromise of cystic artery
symptoms of acute cholecystitis
RUQ pain, hx of biliary colic, jaundice, inc WBC and chills
complications of acute cholecystitis
-gangrene
-2 infection
-perforation
most common dz in gall bladder
chronic cholecystitis
hallmark of chronic cholecystitis

inc risk of...
procelain gall bladder (calcified wall)

cancer
adenomyoma
b9
hyperplasia of muscularis
most common tumor of gall bladder
adenoCA
what is choledocolithiasis
stones in the common bile duct at level of ampulla
symptoms of choledocolithiasis
jaundice
pain
acute pancreatitis
complications of choledocolithiasis
acute pancreatitis
jaundice
cholangitis
dx of choledocolithiasis
AUS
dilated common bile duct
tx of choledocolithiasis
cholecystectomy and removal of stones from common bile duct
charcot's triad in cholangitis
-jaundice
-RUQ pain
-fever/chill
reynolds pentad in cholangitis
-jaundice
-RUQ pain
-fever/chill
-hypotension
-mental confusion
etiology of cholangitis
usually bacterial infection
-biliary stone dz
-malignant stricture (primary sclerosing cholangitis)
tx of cholangitis
-relieve obstruction
-abx
what is cholangitis
infection of common bile duct
klatskin tumor
carcinoma of bifurcation of right and left hepatic bile ducts
cholangiocarcinoma
cancer arising from the bile duct epithelium
major risk factor for cholangiocarcinoma
primary sclerosing cholangitis
mirizzi syndrome:
what is it?
complication of what?
stone in cystic duct compressing neighboring bile duct causing biliary obstruction

-acute cholecystitis
cullen's sign
ecchymosis on periumbilical area

-acute pancreatitis
abdominal CT may show what in acute pancreatitis
-pancreatic swelling
-peripancreatic inflammation
-pancreatic necrosis
-abdominal fluid collections
the bulk of the pancreas drains through
dorsal pancreatic duct and minor papilla
cause of pancreas divisum
failure of dorsal and ventral buds to fuse
cystic fibrosis
-CFTR anion channel allows for chloride and bicarb secretion into the pancreatic ducts and thus allows flushing of liberated enzymes and proenzymes into duodenum

-mutation produce a viscous, conentrated, acidic pancreatic juice leading to ductal obstruction
gallstone pancreatitis
impacted gallstone in distal bile duct leadin to obstruction of pancreatic duct
micro findings in chronic cholecystitis
-fibrosis
-chronic inflamm
-rokitansky-aschoff sinuses may be prominent
pathology of adenoCA
glands in desmoplastic stroma, direct spread to liver via venous drainage to gallbladder ged (quadrate lobe)
periampullary CA
ampulla of vater
-better prog than adeno
-presents early with signs of obstruction
what is primary sclerosing cholangitis?
chronic, progressive, irreversible scarring of bile ducts
results of primary sclerosing cholangitis
strictures and obstruction of intrahepatic ducts and extrahep biliary tract
primary sclerosing cholangitis assoc with
ulcerative colitis
symptoms of primary sclerosing cholangitis (ROBE)
jaundice
pruritis
pain
weight loss
fatigue
complications of primary sclerosing cholangitis
bacterial cholangitis
malnutrition
biliary cirrhosis
cholangiocarcinoma
ERCP findings in primary sclerosing cholangitis
multifocal strictures with dilated segments
what is a diverticula
an outpouching of alimentary tract containing all visceral layers
zenker diverticula
immediately above UES, due to weakness of striated muscle
traction diverticula
middle of esophagus, due to attachment to mediastinal lymph node
mucosal web (common location)
ledge like protrusions of the mucosa into esophageal lumen

(upper esophagus)
mucosal rings
-concentric plates of tissue protruding into lumen of distal esophagus
schatzki ring
mucosal ring at gastro-esophageal junction (GE)
achalasia
failure of relaxation of LES
known causes of achalasia
chagas dz (tryp cruzi in s. america)
micro findings in achalasia
absence of myenteric ganglia
achalasia : at risk for...
SCCA
xray characteristic in achalasia
bird beak
gross findings in ahclasia
esophageal dilation proximal to LES
macro/micro findings in candida esophagitis
gray-white pseudomembranes

yeast and pseudohyphae
pts with candida esophagitis
chemotherapy
transplant
HIV
macro/micro findings in herpes esophagitis
-punches out ulcer
-ulceration
-pink to purple intranuclear inclusions (cowdry type a)
-multinucleated giant cells (cowdry type b)
macro/micro findings in CMV esophagitis
-discrete superficial ulcer
-squamous epithelium with neutros
-prominent intranuclear basophilic inclusions
eosinophilic esophagitis micro
large numbers of eos superficially
mallory-weiss tears
-longitudinal linear tears at the GE junction
symptoms of MW tears
prolonged vomitting, often in alcoholism

hematemesis
boerhaave syndrome
esophageal rupture
GERD
-esophageal irritation and inflammation due to reflux of gastric secretion into esophagus
causes of GERD
dec LES tone or inc ab pressure (alcohol, tobacco, obesity, hiatus hernia)
hiatal hernia
protrusion of portion of stomach above diaphragm
types of hiatal hernia
sliding hernia
paraesophageal
macro findings in GERD
-hyperemia
-bleeding
-ulcerations
-stricture
-barretts esophagus
microfindings in GERD
1) presence of inflammatory cells (eos, neutros, lymphos)
2) basal cell hyperplasia
3) elongation of papillae
barrets esophagus
replacement of squamous mucosa with intestinalized mucosa because of response to prolonged injury
micro findings of barretts
columnar mucosa contain intestinal metaplasia

increase risk of dysplasia and CA
varices
dilated submucosal veins in the lower third of the esophagus
varices are usually secondary to
portal HTN
most common cause of varices
cirrhosis
alcoholic
macro findings in acure gastritis
acute mucosal inflammation, erosion, and hemorrhage due to breakdown of the mucosa barrier and acid-induced injury

petechial hemorrhage, mucosal or submucosal hemorrhage
pathogenesis of acute gastritis
unbalance of defensive factors and damaging forces (increased damage or impaired defenses)
defensive factors of the stomach
-surface mucin
-bicarb secretion
-mucosal blood flow
damaging forces of the stomach
-aspirin
-NSAIDS
-steroids
-smoking
-alcohol
-shock
-CA chemo
micro findings of acute gastritis
-mucosal hemorrhage
-erosion (loss of superfiicial epi and neutro infiltrate within the mucosa)
acute gastric ulceration: macro
small, often multiple and anywhere
acute gastric ulceration: micro
abrupt lesion with unremarkable adjacent mucosa
chronic gastritis
mucosal inflammatory changes leading eventually to mucosal atrophy and intestinal metaplasia
types of gastritis
-h. pylori
-autoimmune
-environmental
micro findings of h pylori chronic gastritis
acute and chronic inflammation with lymphoid follicles, intestinal metaplasia
h pylori chronic gastritis is assoc with
duodenal and gastric ulcer
lymphoma
adenoCA
DAG seen in what?
(diffuse antral)
chronic non-atrophic gastritis
MAG seen in what?
(multifocal atrophic)
chronic atrophic gastritis
autoimmune gastritis
antibodies to parietal cells and intrinsic factor
-loss of parietal
-dec acid decretion
-inc serum gastrin
autoimmune gastritis is assoc with
pernicious anemia due to lack of IF and B12 malabsoprtion
autoimmune gastritis macro findings
loss of rugal folds in body and fundus
autoimmune gastritis micro findings
mucosal atrophy with loss of glands and parietal cells

intestinal metaplasia in body
second most common form of chronic gastritis
reactive gastropathy
reactive gastropathy
NSAID use, bile reflux
reactive gastropathy micro findings
-foveolar hyperplasia
-smooth m hyperplasia
-paucity of inflammation
PUD
ulcers of distal stomach and proximal duodenum caused by gastric secretions and imparied mucosal defenses
features of gastric ulcer
-worse when eating
-antrum lesser curvature
-h. pyolir 70%
features of dudodenal ulcer
-worse at night, relieved with eating
-first portion of duodenum, anterior
-h pylori 90%
micro findings in PUD
superficial necrosis with underlying acute inflammation, granulation tissue, and scar
complications of PUD
obstruction
hemorrhage
perforation
menetrier dz
inc transforming growth factor alpha (TGF-alpha)

protein losing enteropathy
menetrier dz micro
foveolar hyperplasia with glandular atrophy
menetrier dz assoc with
inc gastric CA
zollinger-ellison syndrome
gastric glands hyperplasia due to excessive gastric secretion in gastrinoma

-inc acid secretion

-multiple ulcers
patho of acute pancreatitis
-microvascular leakage causing edema
-fat necrosis by lipase
-acute inflammation
-vascular destruction by lipase and interstitial hemorrhage
micro findings of acute pancreatitis
region of fat necrosis on the right and focal pancreatic parenchymal necrosis

hemorrhagic
macro findings in chronic pancreatitis
-chronic inflammation
-atrophy
-fibrosis

due to repeated bouts of pancreatitis
micro findings in chronic pancreatitis
-calcifications, fibrosis
-dec # and size of acini
-pseudocyst lacks a true epi lining and instead is lined by fibrin and granulation tissue
-dilation of ducts
cholesterol stone risk factors
Forty
Fat
Fertile
Female
pigmented stone risk factors
chronic hemolysis
biliary infection
ileal dz
pathogenesis of cholesterol gallstones
1) bile must be supersaturated with cholesterol
2) hypomotility of the gall bladder promotes nucleation
3) cholesterol nucleartion in the bile is accelerated
4) hypersecretion of mucus in gall bladder traps the nucleated crystals, leading to their aggregation into stones
pathogenesis of pigmented gallstones
-inc unconjugated bili in bile precipitate as Ca+ bilirubinate around nudus of mucinous glycoPr
-intravasc hemolysis causes inc biliary excretion o conjugated bili
-bac enzyme hydrolyze conjugated bili to unconj
most common cause of pigmented gallstones
e. coli
macro findings in acute cholecystitis
congestion
edema
fibrinous exudate with stone obstruction
patho of acute pancreatitis
-microvascular leakage causing edema
-fat necrosis by lipase
-acute inflammation
-vascular destruction by lipase and interstitial hemorrhage
micro findings of acute pancreatitis
region of fat necrosis on the right and focal pancreatic parenchymal necrosis

hemorrhagic
macro findings in chronic pancreatitis
-chronic inflammation
-atrophy
-fibrosis

due to repeated bouts of pancreatitis
micro findings in chronic pancreatitis
-calcifications, fibrosis
-dec # and size of acini
-pseudocyst lacks a true epi lining and instead is lined by fibrin and granulation tissue
-dilation of ducts
cholesterol stone risk factors
Forty
Fat
Fertile
Female
pigmented stone risk factors
chronic hemolysis
biliary infection
ileal dz
pathogenesis of cholesterol gallstones
1) bile must be supersaturated with cholesterol
2) hypomotility of the gall bladder promotes nucleation
3) cholesterol nucleartion in the bile is accelerated
4) hypersecretion of mucus in gall bladder traps the nucleated crystals, leading to their aggregation into stones
pathogenesis of pigmented gallstones
-inc unconjugated bili in bile precipitate as Ca+ bilirubinate around nudus of mucinous glycoPr
-intravasc hemolysis causes inc biliary excretion o conjugated bili
-bac enzyme hydrolyze conjugated bili to unconj
most common cause of pigmented gallstones
e. coli
macro findings in acute cholecystitis
congestion
edema
fibrinous exudate with stone obstruction
micro findings in acute cholecystitis
hemorrhage
inflammation
gangrenous cholecystitis
macro findings in chronic cholecystitis
thickened wall
porcelain gall bladder (extensive calcification)
hydrops of gall bladder
hydrops of gall bladder
atrophic pale gall bladder with clear secretion due to obstruction of cystic duct
micro findings in chronic cholecystitis
outpouching of the mucosa though the wall forms rokitansky-aschoff sinuses

chronic inflamm
intestinal obstruction location
small bowel > colon
intestinal obstruction etiology
SBO
strictures
CA
diverticuli
compression
intestinal obstruction mechanisms
herniation
adhesions
volvulus
intussusception
intestinal obstruction: pathophys
-inc fluid secretion and motility
-accum of fluid in lumen
-systemic hypovolemia
-local ischemia
-transloaction of intestinal bacteria, sepsis
clinical manifestations of intestinal obstruction
ab pain, nausea, vom, obstipation
physical exam for intestinal obstruction
acutely ill, hypovolemia, ab distension, high pitched bowel sounds actively alternating with quiet exam, minimal tenderness
CT scan findings in intestinal obstruction
distension, air/fluid levels, transition zone
SBO findings
distended SB, decompressed colon
intestinal pseudoobstruction
failure of nL motility
intestinal pseudo-obstruction : acute
ileus, small bowel +/- colon
intestinal pseudo-obstruction : chronic
proper
causes of intestinal pseudo-obstruction
-surgery, electrolyte abnL, drugs, infection, inflammation, neuropathies, myopathies, mech vent
ogilvie's syndrome
acute colon intestinal pseudo-obstruction
presentation of intestinal pseudo-obstruction :
distension, some pain, nausea, dec bowel sounds, obstipation
cause of appendicitis
-obstruction of the lumen leading to inflammation, infection, ulceration or perforation

-infection leading to ulceration and perforation
clinical manigestations of appendicitis
-vague ab pain
-poorly localized (periumb or epigastric or R ab)
-nausea, anorex, vom, fever, chills
-12-24 hours: pain shifts to RLQ
-rebound tenderness
true vs false diverticular dz
true: all layers of the wall
false: mucosal herniation through a hiatus in the wall
most common location of diverticular dz
colonic
meckel's diverticulum
persistence of the communication between the small int and vitelline duct
rule of twos:
what dz?
rules
meckles diverticulum
-2% symptomatic
-2 ft from IC valve
-2 yo onset
-2 types of ectopia (gastric and pancreatic)
pathogenesis of colonic diverticuli
-in sites of penetration of vasa recta
-L > R
-thickened wall
-segmentation
complications of colonic diverticuli
-difficult to dx and differentiate between IBS

-diverticulitis and bleeding
diverticulitis
inflammation and infection
CT scan findings of diverticulitis
peritonitis
inflammation
macro-abscess
diverticular bleeding is due to
thinning of the vasa recta at the done of the diverticulum
clinical presentation of diverticular bleeding
-acute, sudden hemorrhage with/without hypovolemia symptoms

-red, maroon stools

-not a cause of chronic GI blood loss (iron def)
two types of intestinal ischemia
-mesenteric (superior mesenteric) or colonic (ischemic colitis)
presentation of acute mesenteric ischemia
-severe, unexplained ab pain, CV risk factors,

later: peritoneal signs, bleeding
presentation of ischemic colitis
-LLQ pain, bloody diarrhea, low grade fever, anorexia, nausea, leukocytosis (diverticulitis with bleeding)
most common vascular lesion of gI tract
angioectasia
pathology of angioectasia
-ectatic, dilated, distorted and thin walled venules, capillaries, and arterioles
location of angioectasia
-anywhere
-R colon is most common
GI adenoCA locations
esophagus and stomach
intestine
pancreas
biliary tract
GI SCCA locations
esophagus
anus
other GI cancers
lymphoma
neuroendocrine tumoe
T =
extension of tumor
N =
lymph node mets
M =
distant mets
hyperplastic polyp location
L colon
hallmark of hyperplastic polyp (due to) bp or m
serrated surface achitecture

delayed shedding of colonocytes

b9
sessile serrated adenoma/polyp vs hyperplasti polyp
bigger
m potential
R colon
serrate throuhout the full thickness, lateral growth and crypt dilation
inflammatory polyp

b9 or m
b9
elevated nodules of inflamed, regen epihelium
inflammatory polyp
assoc with?
IBS
ulcerative colitis
chrons
adenoma: gross
peducnulated or sessile
adenoma: micro
presence of epithelial dysplasia
hallmark of dysplasia in adenoma
-nuclear hyperchromasia
-elongation
-stratification
adenomatous polyp names
tubular
tubulovillous
villous

m
harmartomatous polp

b9 or m
tumorlike growths composed of mature tissue nL present

b9
assoc syndromes with harmartomatous polyp
-juvenile polyps
-peutz-jeghers
-cowden
-cronkhit-canada
-tuberous sclerosis
juvenile polyposis
dilated glands filled with inflammation and mucin

assoc with adenoCA

sporadic or syndromic
peutz=jeghers
multiple GI harmartomas and mucocutaneous hyperpigmentation
peutz=jeghers: location
small > colon > stomach
peutz=jeghers: micro
branching bands of smooth m surrounded by glandular tissue (christmas tree)
FAP genetics/location
AD with APC gene mutations
> 100 polpys
anywhere
teenager
special variants of FAP
gardner
turcot
MUTYH
gardner syndrome
FAP gene mutation
fibromatosis (retroperitoneum)
osteomas of mandible, skull, and long bonds

desmoid tumor in mesentary
hereditary non-polyposis colorectal cancer - aka
lynch syndrome
lynch syndrome genetics
mismatch repair deficiency and microsatellite instabiliy
lynch location
R
lynch histology
sessile serrated adenoma, mucinous adenoCA
3 pathways in colon cancer
1) classic adenoma-CA sequence
2) DNA mismatch repair deficiency (HNPCC)
3) inc CpG island methylation in absence of mismatch repair deficiency
classic adenoma-CA sequence
germline mutation of APC -> second hit -> protooncogene mutations -> p53 mutation -> adenomas -> additional hit -> CA
DNA mismatch repair def
germline mutation of mismatch repair gene -> accumulated -> sessile serrated -> CA
staging:
T1 =
mucosa and submucosal invasion
staging:
T2=
muscularis propria invasion
staging:
T3=
subserosal invasion
staging:
T4 =
penetrate serosa
staging:
N0 =
no lymph node mets
staging:
N1 =
1-3 lymph nodes mets
staging:
N2 =
more than 3 lymph nodes
staging:
M0 =
no distant mets
staging:
M1 =
distant mets
well diff adenoCA
95% gland formation
poorly diff adenoCA
<50% gland formation (poor prognosis)
subtype of adenos (3)
-mucinous (mismatch repair gene)
-signet ring cell
-undifferentiated
cloacogenic CA
arose in transitional epithelum, mixed with adenoCA and squamous CA

anal canal
b9 esophageal CAs
leiomyoma (smooth m)
lipoma (adipose)
risk factors for esophageal CAs
Alcohol
Barretts esophagus
Cigs
Diet
Esoph dz
Familial
esophageal dz assoc with esoph CA
-plummer vinson
-achalasia
-esophagitis
barretts assoc with what type of esophageal CAs
adeno
dysplasia in SCCA
starts in basal cell layer
gastric polyp 2 types
hyperplastic polyp
fundic glands polyp
hyperplastic polyp
nonneoplastic
-cystically dilated mucous glands with inflamed LP
fundic glands polyp
nonneoplastic
-cystially dilated fundic type glands
-may related with use of PPI
gastric: ectopic pancreatic tissue
b9
-asymp
-damage and inflamm
adenomatous polpy in stomach
neoplastic
-proliferative dysplastic epithelium
diff shapes of advanced stomach CA
-polypoid
-ulcerating
-infiltrating
stoamch CA: intestinal type: micro
malignant glands resembling colon CA

ulcers
stoamch CA: diffuse type: micro
diffuse infiltration by poorly deff cells

linitus plastica - rigid ticened leather bottle like
krukenberg tumor
mets to one or both ovary
GI tract lymphoma (2)
B cell
Tcell
B cell GI lymphoma
MALToma
-h. pylori
T cell GI lymphoma assoc with
celiac sprue
GI stromal tumor
originate in cell of cajal which control peristalsis
-spindle lesion
-tyrosine kinase constantly stimulated
-b9 or malignant
GI stromal tumor: genetics
tyrosine kinase inhibitor which inhibits ckit and PDGFR is effective
carcinoid tumor
well deff neuroendocrine tumor
which carcinoid tumor is the worst
midgut (jej and il)