GI Path Flashcards

crohn
granuloma
how many people will die today of infectious gastroenteritis?
2000
4 causes of mchanical intestinal obstruction
- herniation
- adhesion (fibrosis)
- intussusception (tumor pull things in)
- vovulus - twist on mesentary

Mallory-Weiss
cause of esophageal perforation
intramural perforation
longitudinal mucosal tear
due to severe retching (alcoholism or bulemia)
esophageal rings
lower esophagus: Schatzki’s ring
stenosis, scaring
will have squamous AND columnar epithelium
guillain barre syndrome
assciated with campylobacter jejuni - antibodies and mimicry to gangliocytes - immune mediated attack
inflammatory bowel disease
defective recogntiion, tolerance, or elimination of microbiota in a person who is genetically susceptible

pulsion diverticulum
bulge from inside pressure
usually epiphrenic
why do some people with HLA alleles not have celiac?
if get it - mutation in non coding region - 1 NT
RNA binds 2 molecules in that spot turn off inflammatory respont
if polymorphism - doesn’t work well, inflammation is ON
single nucleotide genetic polymorphism in a long non coding RNA leads to on inflammatory meidators

infective esophagitis causes
fungal (candida)
viral (herpes, cmv)
parasitic (chagas)
chronic colitis histo
distorted crypts

h. pylori gastritis
rob, superficial chronic active gastritis
antrum!
chronic active gastritis with superficial inflammation
lymphoid aggregate
organisms swim in superficial mucin
h pylori and cancer
6x risk of adenocarcinoma
triggers inflammation that leads to atrophy and metaplasia
don’t know why

ulcerative colitis
diffuse predominatly mononuclear mucosal infiltrate
neutrophils in epithelium and in crypt
crypt abcesses
Boerhaave syndrome
cause of esophageal perforation
transmural perforation
rupture of the distal esophagus
retching bulemia endoscopy
pneumomediasgtinum
crohn histo
non caseating granulomas


eosinophilc esophagitis

mallory weiss esophageal tear
genetic mutation in high grade dysplasia and adenocarcinoma of esophagus
beta-catenin
cERB

acute bacterial campylobacter colitis
cryptitis/abcesses, mixed inflammation in lamina propria, no crypt distortion
Eosinophilic Esophagitis
can present by itself or be part of eosinophilic gastroenteeritis
idiopathic EoE is common, seen frequently in children w atopic symptoms
This buildup, which is a reaction to foods, allergens or acid reflux, can inflame or injure the esophageal tissue. Damaged esophageal tissue can lead to difficulty swallowing or cause food to get caught when you swallow.
Eosinophilic esophagitis is a chronic immune system disease. It has been identified only in the past two decades, but is now considered a major cause of digestive system (gastrointestinal) illness.
genetic mutation in barrett’s and low grade dysplasia
p53
shift in cancer prevalence
use to be SCC
now adeno
hypoperfusion watershed
i.e. CHF
can lead to mucosal or mural infarction
- splenic flexure - termination of SMA and IMA
rectosigmoidal - end of IMA, pudendal, iliac

achalasia
dilated lumen
chronic ganglionitis (t cells!) with myenteric plexus destruction in the DILATED part of the esophagus
progressive loss of myenteric plexus due to chronic inflammation of the ganglion cells
risk fo squamous carcinoma
abnormal motility
barrett’s esophagus
replacement of the squamous mucosa normally present in the distal esophagus with metaplastic columnar epithelium containing goblet cells
long standing GERD
bands of salmon pink mucosa

achalasia
non neoplastic gastric polyps
no dysplasia!
hyperplastic
fundic gland polyp
hypertrophic gastropathy
hyperplastic mucous glands replace oxyntic glands
lot of mucus secretions - diarrhea - malabsorption, lose proteins

caustic esophagitis
chemicals
acids
alkali
physical agents
injury
meds sitting in esophagus
epithelium sloughing off

ischemic bowel disease
initial hypoxic injury
secondary reperfusion injury (greatest damage)
usually colon!
arterial throbosis, empolism, non occlusive (cardiac failure, shock)
Hairpin turn of capillary
sharp turn at mucosa - no great blood supply
stem cells are saved so regen
ischemic injury starts at the surface

esophageal hernia
protrusion of a portion of stomach above the diaphragm
granular cell carcinoma

pathogenesis of celiac
gluten - gliadin - tTG - daminated gliadin - presented on HLA DQ2 or DQ8 on APC to T cell - make abs and attack ucosa

Reflux Esophagitis
Reflux of gastric content into lower esophagus
acid-peptic action of gastric juices leds to esophageal mucosal injury
refluxed bile from duodenum may contribute to mucosal diruption
neuroendocrine tumor
carcinoid
can be benighn
antral gastritis
environmental! HP
antral inflammation –> more acid –> increased risk of duodenal ulcer –> decreased risk of gastric cancer!

intestinal type gastric adenocarcinoma
more common in males and elderly
high prevalence areas - likely environmental component
internal hemorrhoids
covered by columnar rectal mucosa

CMV esophagitis
not seen in normal individuals
ulcers are mostly in distal esophagus
infects endothelial and stromal cells

Chagas Disease and te esophagus
can affect peristalsis
secodary cause is esophageal motility disorder
histology bacterial enterocolitis
general pattern:
acute - surface epithelial injury, decreased epithelial mautration, edema neutrophils
pseudomembranous colitis!! volcano lesions (neutrophils, fibrin, inflammation)


Crohn
submucosa
string of pearls
viral gastroenteritis
i.e. norvirus
most are food, some person to person - supportive care no vaccine
gastrointestinal stromal tumors
mesenchymal
stomach or smal bowel
GI bleeding
RTKI
good prognosis, slow growing
gastric MALT lymphoma
assoc w h pylori
may respond to abx! use chemo if spread or resistant
Atresia and tracheoesophageal fistula (TEF)
result from the failure of the foregut to completely divide into the esophagus and the trachea
M
babies (food regurgitation)
VACTERL association!
Type III is most common

celiac alleles
HLADQ2, HLADQ8
necessary but not sufficient! need it to have celiac but don’t automatically have celiac if you have it

false esophageal diverticulum
acquired
only mucosa and submucosa
GIST
mutations in c-kit and PDGFR
Gleevac - TKI -
zollinger ellison syndrome
hypertrophic gastropathy

UC vs Crohn
crohn - transmural, patchy, colon and SB
UC - continuous beginning in rectum, superficial ulceration

Crohn’s
mucosal inflammation AND transmural inflammation
can see granulomas
external hemorrhoids
covered by squamous mucosa


achalasia
ganglion cells destroyed by lymphocytes (ganglionitis)
diff between esophageal AC and SQCC
AC - distal, S - middle
AC - glandular, SQCC - squamous, keratinization
AC - BE, S - toxins
Zenker’s Diverticulum
pharyngeoesophageal (pulsion) diverticulum
carcinoma has been seen
sac

reactive gastripathy
chemical iritational gastrophathy
common reactive change in gastric mucosa in response to chemical or mechanical injury (NSAIDs), bile reflux, mucosal trauma/ulcer

herpes esophagitis
3 Ms
Multinucleated giant cells
Molding
Margination
healthy oung people
ulcers

what gene is involved in some cases of hirschsprung?
ret
imperforate anus
no anus
need surgery
cloaca is divided by urorectal septum - abnormal development (vasc accidnets, maternal diabetes, med)
many have fistula to bladder, vagina, urethra

granulomatous gastritis
epithelioid cell granulma (crohn, sarcoid)
traction diverticulum
bulge ffrom outside pressure
usually thoracic (TB)
glycogenic acanthosis
normal! suprabasal squamous cells with focal excess of glycogen in esiphagus
non axial (rolling) esophageal hernia
para esophageal
portion of somach (greater curvature) pushes into thorax
GE junction remains at level of diaphragm

true esophageal diverticulum
congenital
all layers protrude
acute (hemorrhagic) gastritis
acute, often transient mucosal inflammation
major cause of upper GI hemorrhage
can be erosive in severe
NSAID, alcohol, bile reflux, iron

risk factors for gastric adenocarcinoma
diets high in N compounds
high salt
smoking and EtOH
pernicious anemia
atrophic gastritis
male
gastric surgery

chronic - crypt distortion
gastric adenocarcinoma
second leading cause of global cancer mortality
highest incidence in asia
h pylori, autoimmune, intestinal metaplasia, mcosal atrophy
most are in pyloris/antrum
p53
e cad herin
her-2 nu
angiodysplasia
mucosal and submucosal vascular dilation and malformation
usually cecum and right colon
common cause of chronic GI bleeding - rarely acute and massive
diagnose on EGD
mechanical factors cause! muscula propria contracts - vein becomes tortuous and dilated - AV malformation


reflux esophagitis
big papillae
herediatry diffuse gastric cancer
e cadherin germline mutation
inherited - 70% rosk of diffuse gastric cancer
prophylactic total gastrectomy

h pylori gastritis - follicle and inflammation
treatment for gastric cancer
- surgery! total vs subtotal
(subtotal for proximal lesions, total for distal lesions)
large mid gastric or infiltrative lesions usually require total gastretomy
large (or diffuse) - require total
- much worse survival if nodes
- adjuvent chemo helps

effects in infarcted bowel
congested mucosa
blood in lumen
wall edematous and rubbery
perforation?

hirschsprung
congential aganglionic megacolon * Ret oncogene (enteric neuron formation)
most common caues of intestinal obstruction (boys)
usually rectum or sigmoid
normal migration of neural crest cells from cecum to rectum is arrested prematurely or ganglion cells undergo premature death –> NO meissner submucosal or aurebach myenteric ganglion cells –> no peristalsis –> dilation proximal to affected segment

esophageal mucosal webs
Assoc w Plummer Vinson Syndrome (anemia, glossitis, upper esophageal web)
squamous epithelium + inflammation
strictures/stenosis/scarring
dysphagia
Where do diverticula form?
where blood vessels and nerves penetrate walls
between teniae where wall is thinner
multifocal atrophic gastritis
environmental gastritis - HP
antral inflammation w patchy inflammation and atrophy in body and fundus
decreased acid, intestinal metaplasia, increased risk of gastric cancer

How to tell diff betwen Leiomyoma and GIST?
GIST - marked w C-kit?


esophageal varices
treatment of gastrointestinal stromal tumors
surgical! complete resection
good response to TKI
acute occlusive thrombosis
elderly
sudden abdonomal pain, nausea, vomiting, melena, shock
no bowel sounds/abdnomial rigidity
axial (sliding) esophageal hermia
most!
bell shaped protrusion of proximal stomach into thoracic cavity
through diaphargmatic esophageal hiatus

Histo findings of Reflux esophagitis
basal zone hyperplasia (6-8 cells)
papilla > 2/3 of the epithelium

boerhaave
esophageal tear
squamous cell carcinoma of the esophagus
high dietary and environmental - tobacco, alchool
usually in the middle third p53 is most common mutation
insidious onset with progressive dysphagia, obstruction, weakness
progressive obstruction to solids then liquids - extreme weight loss and debilitation

treatment of esophageal adenoCA
surgical intervention (not many are resectable)
can do endoscopic resections
chemo neoadjuvent - benefit
trials! 5 year survival = 15-20%
diffuse type adenocarcinoma
seen equally in genders
younger
worse
lack of e cadherin
diffuse - through wall - rigid doesn’t fill up

IBD complications
toxic megacolin in UC 0 toxic injury leads to shut down, dilatation, gangrene perforation
dysplasia in both UC and Crohn
low and high grade
flat or polypoid
architectural changes preduct risk of carcinoma
hat is the most common type if intestinal atresia
imperforate anus
hermorrhoids
vericeal dilations of anal and perianal venous plexuses due to chronic elevation of venous pressure
straining stasis
pain rectal bleeding, bright red
2 complications of campylobacter
guillan barre and arthritis
gastric adenocarcinoma world prevalence and moving
child has lower risk
genetic and environmental and dietary
asia!
treatment of esophageal SCC
usually chemo
surgery may help but unclear
Hirschsprung children lack what where?
ganglion cells - meissner and auerbach plexus
bacterial enterocolitis
adhere to epithelial cells and repilcate
make toxins
invade epithelial cells
autoimmune gastritis
nonHP
body and fundus (spares antrum)
autoantibodies to parietal cells –> parietal cell loss and mucosal hypertrophy –> decreased acid, no IF (pernicious anemia), metalasia - high risk of gastric cancer
loss of parietal cells - decreased gastric acid - antral G cell hyperplasia - increased gastrin - ECL cell hyperplasia - endocrine neoplasia

fungal esophagitis
most common is candida albicans
white areas/plaques/ulcers on endoscopy


barrett’s esophagus
esophageal varices
dilated submucosal left gastric veins
uphill = alcoholic cirrhosis
downhill = SVC obstruction due to carcinoma
celiac histo
diffuse villous atrophy and lyphocytosis on initial biopsy
normal histo on gluten free diet
diffuse villous atrophy and lymphocytosis on challenge

Melanoma
dark cells

campylobacter jejuni
most common bacterial pathogen
improperly cooked chicken
in can move in adheres in can invade it makes a toxin
bloody diarrhea = dysentery
guillain barre and reactive arthritis****
giardia lamblia
contaminated water
non invasive
diarrhea/constipaiton/malabsorption
can see parasite!
biopsy can look nrormal or like sprue