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183 terms

GI I: esophagus, stomach, sm and large intestine/colon, GI bleeds

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site of terminal digestion and absorption of food stuff
small bowel villi
Where are Brnner's glands located? Function?
Duodenum (jejunum and ileum don't have it)

Brunner's glands secrete bicarb when pyloric sphincter opens and highly acidic gastric slush enters the intestine with a very low ph
Brunners glands Bicarb nuetralizes this and protects the GI tract
In what parts of the GI tract is it normal to see goblet cells?
small and large intestine (NOT esophagus or stomach)
What are paneth cells?
Paneth cells are found throughout the small intestine and the appendix at the base of the intestinal glands.
have antimicrobial DEFENSINS that fight infections

Location just below the intestinal stem cells in the intestinal glands, contain large eosinophilic refractile granules that occupy most of their cytoplasm.

When exposed to bacteria or bacterial antigens, Paneth cells secrete some of these compounds into the lumen of the intestinal gland, thereby contributing to maintenance of the gastrointestinal barrier.
Which parts of the intestine have villi?
Small intestine has villi, colon DOES NOT
Where are lymphatics of the colon located?
LYMPHATICS are in the submucosa (unlike stomach, esophagus, small bowel)
Where is Meissner's plexus located? Auberachs?
Myenteric/Auerbach: between longitudinal and circular muscle layer

Submucsal plexus/Meissner's: between circular muscle and submucosa
"tonsil of small intestine"
Peyers patches in terminal ileum, contain M cells
3 major congenital anomalies of the small and large intestine
Atresia and Stenosis
Meckel's Diverticulum
Hirschsprung's Disease
Meckel's Diverticulum - What is it? Why is it "disease of 2's"?
Persistence of omphalomesenteric duct (vitelline duct which connects the lumen of the developing gut to the yolk sac), usually found in the terminal ileum

Disease of 2's
-2% of population (mostly asymptomatic)
-2:1 M:F
-2" in length
-within 2 ft of ileocecal valve (may confuse pain from inflammation with that of appendicitis)
-2 types of ectopic tissue in 1/2 of cases (gastric and pancreatic)
-2 major complications (pain with inflammation; hemorrhage with ulcer)
Hirschsprung Disease
Pathogenesis: Congenital Aganglionic Megacolon: Absence of ganglion cells (Premature arrest or death of the neural crest cell migrating from the cecum to the rectum)
-Absence of ganglion cells, Rectum ALWAYS involved!!
-Varies from short segment disease to involvement of the entire colon
-"Functional" obstruction with dilation proximal to the effected area

Clinical:
-Presents in NEONATAL period: failure to pass meconium, abdominal distention
-Alternating constipation and diarrhea

Associated with:
-Down syndrome (10%)
-(5%) serious neurologic abnormalities

Risk of perforation, sepsis, enterocolitis, fluid disturbances

Epi: 4x more males than females, 1/5000 live births

Treatment: remove aganglionic section of bowel
Necrotizing Enterocolitis "NEC"
Acute, necrotizing inflammation of small and/or large intestines

Multifactorial

Involves terminal ileum or ascending colon.

Edema to necrosis to gangrenous bowel

Most common acquired GI emergency in premature or low birth weight neonate!
Most common acquired GI emergency in premature or low birth weight neonate
Necrotizing Enterocolitis (NEC)
Malabsorption
Symptoms: Chronic diarrhea, steatorrhea, weight loss, abdominal pain, flatus

Malabsorption leads to deficiencies of
Pyridoxine, folate, Vit B12: anemia
Vit K: bleeding
Ca, Mg and Vit D: osteopenia and tetany
Vit A and Vit D: peripheral neuropathy

Diagnosed with abnormal fecal fat study to detect for steatorrhea

Major diseases of malabsorption in US:
-Celiac disease
-Pancreatic insufficiency: Chronic pancreatitis, Cystic Fibrosis
-Crohn's disease
Steattorhea
72 hour fecal fat (normal <7 grams / 24 hours
Voluminous, malodorous, Bulky
Abates when fasting

USMLE board question (above symptoms and abnormal fecal fat study = malabsoption)
Celiac disease
Gluten sensitive enteropathy
Gluten: protein associated with wheat, barley and rye (cereals, breads)

CLINICAL:
Usually Caucasians of European ancestry
Infants: diarrhea, failure to thrive, abdominal distention, anorexia, weight loss, irritability
--Older children: (non classic symptoms), abdominal pain, nausea, vomiting, bloating or constipation
--Adults: diarrhea, flatulence, weight loss, and fatigue, ANEMIA!!!!! (not absorbing Fe in duodenum)
--DERMATITIS HERPATIFORMIS (skin blistering disease)

PATHOGENESIS: Immune disorder with an environmental precipitant, results due to destruction of intestinal epithelia from immune system's reaction to Gluten metabolite, Gliadin
1) Endoscopically: small intestine mucosa is flat
2) Pathologically: Loss of villi with crypt hyperplasia & Increased numbers of intraepithelial CD8+ T lymphocytes
NOTE: histologically, can mimic colonic mucosa due to flattening of intestinal epithelium!

DIAGNOSIS: via biopsy + TTG most commonly
--Biopsy
--Serologic studies:
1) IgA or IgG antibodies to tissue transglutaminase (TTG)
2) IgA or IgG antibodies to deaminated gliadin
3) IgA endomysial antibodies (specific, but less sensitive)
NOTE: In IgA deficient patients (many with celiac disease are), IgG test are necessary!
**Absence of HLA-DQ2 or HLA-DQ8 has a high negative predictive value
5 types of Enterocolitis
Infectious: cholera, campylobacter, shigella, salmonella, typhoid fever, Yersina, E. Coli
Necrotizing
Pseudomembranous
Collagenous/Lymphocytic
Miscellaneous
Bacterial infectious enterocolitis
Cholera: Minimal alteration on biopsy (non invasive)

Campylobacter: Acute self limited colitis, Associated with Guillain-Barre syndrome (USMLE)
-Crypt abscesses, neutrophils going into crypts (cryptitis) but NO gland distortion

Shigella: Mucosal hemorrhage, ulceration and pseudomembranes, acute self limited colitis

Salmonella: Acute self limited colitis

Typhoid Fever (Salmonella typhi): Oval shaped ulcers with neutrophils in the lamina propria, hyperplasia of Peyers patches

Yersina: Hyperplasia of Peyers patches and apthous ulcers with neutrophils and +/- granulomas

Escherichia coli:
Entertoxigenic (ETEC)
Enterohemorrhagic (EHEC) E. coli O157:H7 Enteroinvasive (EIEC)
Enteroaggregative (EAEC)
Shigella bacterial infectious enterocolitis
Mucosal hemorrhage, ulceration and pseudomembranes, acute self limited colitis
Salmonella enterocolitis
Acute self limited colitis
Campylobacter infectious entocolitis
Acute self limited colitis, Associated with Guillain-Barre syndrome (USMLE)
Which bacterial infectious enterocolitis is associated with Guillain-Barre?
Campylobacter - acute, self limited colitis
What distinguishes campylobacter jejuni from Crohn's and ulcerative colitis?
No gland distortion is what distinguishes it from Crohn's and ulcerative colitis
Typhoid fever bacterial infectious enterocolitis
Typhoid Fever (Salmonella typhi): Oval shaped ulcers with neutrophils in the lamina propria, hyperplasia of Peyers patches
Yersinia bacterial infectious enterocolitis
Hyperplasia of Peyers patches and apthous ulcers with neutrophils and +/- granulomas
Types of E. Coli that cause infectious enterocolitis
Entertoxigenic (ETEC)
Enterohemorrhagic (EHEC) E. coli O157:H7 Enteroinvasive (EIEC)
Enteroaggregative (EAEC)
Which bacterial infectious colitis cause ulcers
Tyhpoid fever, Yersinia
What is unique about the clinical picture of E. Coli O157:h7
it has more of an ischemic picture than the others, which resemble an acute self limited colitis
Rotavirus
Usually affects children
25-65% of cases of severe diarrhea in infants and children
Selectively infects and destroys mature enterocytes in the sm. intestines
Called rotavirus because viral particles in stools look like wheels in stool culture EM
Diagnose with stool antigen

Pathology:
-Modest shortening of the villi
-Vacuolization and loss of the microvillus brush border
-Crypt hypertrophy
-Viral particles in the surface epithelial cells
-May produce a flat mucosa in infants
Norovirus
½ outbreaks gastroenteritis worldwide
Common cause of sporadic gastroenteritis in developed countries
Schools, hospitals, nursing homes and cruise ships
If the patient finds worms in the toilet or in their underwear - what is the likely cause?
Nematode: Ascaris
What flatworms commonly invade the intestine? What symptoms do they cause?
Tapeworm: Taenia and Diphyllobothrium
These worms usually fight for nutrients like vitamin B12
What protozoa commonly invades the GI tract?
Giardia
-Seen in campers who drink fresh water
-Float in small intestine
-Dx: duodenal aspirates, stool studies looking for cyst form, rapid diarrhea commonly with troph form
-may see flattening of villi
Entameoba histolytica
IMPORTANT!
Parasite that can cause bleeding (occult + or some blood stools) because it causes ULCERS.

It has a Erlenmeyer flask-like shaped ulcer where these trophs destroy the tissue and undermine it. Ulcers can lead to blood loss.
Giardia
-Seen in campers who drink fresh water
-Float in small intestine
-Dx: duodenal aspirates, stool studies looking for cyst form, rapid diarrhea commonly with troph form
-may see flattening of villi
Pseudomembranous colitis
Pathogenesis:
-Most often follows a course of broad spectrum antibiotics (clindamycin)
-Toxin forming strains of C. difficile flourish following alteration of the normal intestinal flora.
-Yellow green false membrane (mixture of mucous and neutrophils)

Clinical picture
Intractable diarrhea, cramps, dehydration, shock, death
Whipple Disease
-Agent/pathogen?
Rare, More common in men
--Gram positive rod shaped actinomycete: Tropheryma whippleli (NOT CULTURABLE!)
--Engulfed by MACROPHAGES (PAS positive diastase resistant) --> Malabsorption, lymphadenopathy and arthritis
--Histologically: Foamy macrophages in the lamina propria, Macrophages stain positive for PAS (cell wall of tropheryma)
The actinomycete "Tropheryma whippleli" is the cause of what?
Whipple Disease
Collagenous colitis
-Chronic watery diarrhea: 3-20 nonbloodly stools per day
-Middle age and older women
-Radiographic studies are unremarkable and Endoscopic findings are NORMAL!

Pathology
Chronic inflammation with a thick band of collagen just beneath the surface epithelium --> affects absorption --> more water in the lumen --> diarrhea
INCREASED INTRAEPITHELIAL LYMPHOCYTES and mixed inflammatory infiltrate in the lamina propria
Lymphocytic colitis
-Chronic watery diarrhea: 3-20 nonbloodly stools per day
-Affects males and females equally
-Radiographic studies are unremarkable ad Endoscopic findings are NORMAL
-Strong association with autoimmune diseases!!!

Pathogenesis:
Chronic inflammation with increased numbers of surface lymphocytes and NO SUBEPITHELIAL COLLAGEN (vs. collagenous colitis)
Inflammatory Bowel Disease
Chronic condition, idiopathic disorder that is increasing in incidence

Pathogenesis/etiology
--"hygiene hypothesis": our food is too clean
--Genetics- family members of IBD pt at increased risk
--Mucosal immune response: intestines have lost "discernment"
--Epithelial defects: loosening of tight junctions
Changes in Microbiota

Combination of:
--Defects in host interactions with intestinal microbiota
--Intestinal epithelial dysfunction
--Aberrant mucosal immune responses

--CROHNS DISEASE: may affect any portion of the GI tract from esophagus to anus and typically has transmural inflammation with granulomas
--ULCERATIVE COLITIS: is severe ulcerating inflammatory disease involving the mucosa and submucosa and limited to the colon and rectum
Crohn's disease vs. Ulcerative Colitis
Forms of IBD

-Granulomas: Crohn's has them, UC doesn't
-GI tract portion: Crohn's - any, UC - colon/rectum
-Layers affected: Crohn's -transmural, UC - mucosa/submucosa
Crohn's disease
Form of IBD that may affect any portion of the GI tract from esophagus to anus and typically has transmural inflammation with granulomas

Has tons of names:
--Terminal ileitis: at one time thought to be limited to the terminal ileum ( a common site)
--Regional enteritis: sharply delineated regions with "skip" areas
--Granulomatous colitis: granulomas are seen

Epidemiology:
-Tends to occur in young adults
-Two peaks: teen/twenties and fifties/sixties
-Caucasians> non Caucasian
-Jewish> non Jewish (in US)

Clinical:
--Usually begins with intermittent attacks of mild diarrhea, low grade fever, RLQ abdominal pain
--Can present abruptly with RLQ pain
--Asymptomatic periods and Recurrent attacks or flare ups of diarrhea

Complications:
-fibrosing strictures, fistulas, Extraintestinal manifestations
-Increased incidence of cancer of SI and colon
-Obstruction, occult blood loss, Fe++ def anemia, Malabsorption, malnutrition, weight loss

Pathogenesis:
--May occur at any point along the GI tract
--Usually affects terminal ileum, ileocecal valve, cecum
--Segmental involvement sparing others areas
--Mucosa shows linear ulceration and fistula formation (BEAR CLAW ULCERATIONS)
--Serosal creeping fat

Histology:
Transmural inflammation
Cryptitis, crypt abscesses
Ulceration, penetrating
Non-caseating granulomas
Bear claw linear ulcerations
Crohn's disease
Ulcerative Colitis
ULCERATIVE COLITIS: is severe ulcerating inflammatory disease (form of IBD) involving the mucosa (primarily) and submucosa and limited to the colon and rectum

Clinical: BLOODY, MUCOID DIARRHEA
Relapsing attacks of bloody mucoid diarrhea with pain
Recurs after asymptomatic interval
May have an explosive initial attack with serious bleeding to constitute a medical emergency

Complications: Primary sclerosing cholangitis, inc risk of colon cancer, Toxic megacolon (rare)

Pathogenesis:
1. Inflammation primarily involving the mucosa of the colon
2. Diffuse, continuous inflammation that begins in the rectum and progresses proximally

Histology:
Early phase: neutrophils and crypt abscesses
Later phase: mucosa ulcerates and pseudo-polyps form
Late phase: atrophy and possible dysplasia
Increased risk of colon carcinoma
No granulomas
Pseudopolyps
Ulceratie colitis
UC or Crohns?
Transmural inflammation
Pseudopolyp
Granuloma
Diffuse
Skip lesions
Toxic megacolon
Creeping fat
Primary Sclerosing Cholangitis
Fissures and fistulas
Cancer
At any point in GI tract
Rectum
UC: pseudopolyp, diffuse, toxic megacolon, rectum
Crohn's: transmural inflamm, granuloma, skip lesions, creeping fat, fissures and fistulas, at any poit in GI tract
Both: primary sclerosing cholangitis (more in UC), cancer (more in UC)
Diverticular Disease
Acquired herniation of mucosa and submucosa "pseudo-diverticular outpouching"

Most common in left colon; particularly sigmoid colon

Acute or chronic inflammation may occur
Complicatinos: Perforation, peritonitis, fistula

Rare under 30 but EXTREMELY common over 60 (prevalence 50%)

Clinically
--intermittent cramping, lower abdominal discomfort, constipation, distention, sensation of never being able to completely empty the rectum
--minimal chronic, intermittent blood loss or rarely massive hemorrhage
Most common site of diverticular disease? IS it common?
Left colon (mostly sigmoid)

Rare under 30 but EXTREMELY common over 60 (prevalence 50%)
Hernias
-Serosal lined out-pouching of peritoneum, most common in inguinal and umbilical areas
-Loop of intestines becomes trapped (incarcerated) within the hernia sac
-Bowel compressed, twisted at the mouth of hernia, compromising blood supply - infarction (strangulation)
Adhesions
Fibrous bridges or band-like portions of scar tissue that form during healing after surgery or peritonitis

-May result in obstruction (kinking, compression)
Intussusception
Caused by an in-folding or telescoping of one segment of bowel into the adjacent distal segment

Infants and children: spontaneous and reversible, cam be from aggregate of lymphoid tissue

Adults: usually tumor is a lead point
Volvulus
Obstruction due to rotation or twisting of a loop of bowel around its mesenteric base of attachment
Luminal and vascular compromise
Sigmoid - most common site (cecum next)
Most common site of volvulus
Sigmoid most common, then cecum
Ischemic Bowel Disease
1. Pathology: ranges from mucosal hemorrhage to transmural necrosis of bowel wall

2. Etiology
a. Hypoperfusion
b. Acute vascular obstruction
--Acute arterial occlusion: Atherosclerosis, Aortic aneurysm, Hypercoagulable states, Oral contraceptive use, Embolization of cardiac vegetations or aortic artheromas
--Other cause of intestinal hypoperfusion: Cardiac failure, Shock, dehydration, Vasconstrictive drugs
--Rare: Systemic vasculitis, Mesenteric venous thrombosis

Pathogenesis:
--Hypoxic injury or Reperfusion injury --> hemorraghe + necrosis (of mucosa first)
--Variables for degree of injury: Severity of vascular compromise, Length of time of injury, Vessels effected
--"Watershed" zones: Splenic flexure (gets both the end of the superior and inferior mesenteric artery supply)

Clinical: Sudden severe abdominal pain, Tenderness, Bloody diarrhea, melanotic stools
More severe injury: shock, sepsis, death
Hemerrhoids/anal varices
-5% of the population
-Pathology: Dilated veins of hemorrhoidal plexus
-Internval vs. external: External are PAINFUL due to somatic innervation
-Rectal bleeding, pain, worse with defecation
3 types of nonneoplastic polyps of the colon
Inflammatory: reactive (Ex. solitary rectal ulcer/rectal prolapse syndrome)
Hamartomatous: overgrowth of normal material (ex. juvenile polyps)
Hyperplastic
Inflammatory polyps
Solitary Rectal Ulcer syndrome: Rectal prolapse syndrome
-Anterior wall of the rectum
-Impaired relaxation of the anorectal sphincter
-Chronic injury and healing of the mucosa

Reactive, hyperplastic process
Juvenile polyps
-Rare; hamartomatous polyps
-virtually no malignant potential (exception: Juvenile polyposis syndrome)
-commonly found in children younger than age 5 in the rectum
Peutz Jegher syndrome
Multiple polyps + cutaneous and mucosal pigmentation with increased risk for some forms of cancer

Rare autosomal dominant syndrome

Large polyp with arborizing (tree-like) projections with smooth muscle present at the mucosal surface

Multiple polyps; melantotic mucosal and cutaneous pigmentation

Polyps with no malignant potential, but patients with the syndrome are at risk for other malignancies: pancreas, breast, lung, ovary, uterus, testicles and colon

Germline heterozygous loss of function mutations in LKB1/STK11 gene
Hyperplastic polyps
Benign non-neoplastic polyps
-very common (prevalence: up to 30% of people > 50, commonly found in adults > 60 years old)
-Benign but endoscopically similar to adenomas (may need to biopsy)
-asymptomatic
-proliferation of mature goblet cells; size <0.5 cm

Pathogenesis: unkonwn!
--Decreased epithelial cell turnover
--Slower rate of surface cell exfoliation
Neoplastic polyp adenomas
Benign polyps that are precursors to the majority of colorectal adenocarcinomas
--Range in size from 0.3 to 10 cm
--Types:
1) Tubular (>75% tubular glands) - usually PEDUNCULATED
2) Villous (50% villous) - usually SESSILE
3) tubulovillous (25-50% villous). Villous adenomas that are invading may require taking out a portion of the colon
--Sessile Serrated Adenoma is a special subset

ADENOMATOUS EPITHELIUM: Neoplastic dysplastic epithelium which lines the glands as tall hyperchromatic somewhat disordered cells with or without mucin production. Lies tubular and tubulovillous polyps.

Epi: 50% of people older than 50 in the Western world

Dx:
Screening colonoscopy by age of 50
Positive family history of colon cancer: Screened earlier

Clinical: Most clinically silent, but Larger polyps can result in bleeding and anemia
--Risk of cancer depends on 1) Size 2) Presence of high grade dysplasia
Tubular adenoma
Small, pedunculated neoplastic polyp

Composed of tubular shaped glands lined by adenomatous epithelium + elongated/dark nuclei

Cancer is rare in TAs less than 1.0 cm
Villous adenoma
Neoplastic polyp
-usually sessile, broad base rather than pedunculated

-Architecture of finger-like projections of adenomatous epithelium
TUBULOVILLOUS ADENOMA
Neoplastic polyp
-features of both adenomas
-25-50% (30%) villous
Sessile serated adenomas
like polyps but don't have neoplastic epithelium
However, they DO have chromsomal problems with microsattelite instability
Come in tubular, villous or tubulvillous forms
Look hyperplastic, widened at the base
Familial Adenomatous Polyposis (FAP)
Autosomal dominant; genetic defect is in the APC gene on Ch 5q21

Patients with 100-thousands polyps (min 100 polyps)

100% develop colorectal adenocarcinoma!

Prophylactic colectomy is the standard therapy for ones with APC mutations

Colectomy prevents cancer of colon, but patients may develop adenoma at other sites (ampulla of vater, stomach)

Histologically, the polyps look like adenomas
What percentage of people with FAP develop cancer? Standard therapy?
100% develop colorectal adenocarcinoma!

Prophylactic colectomy is the standard therapy for ones with APC mutations.
Colectomy prevents cancer of colon, but patients may develop adenoma at other sites (ampulla of vater, stomach)
Gardner syndrome
--also autosomal dominant
--polyps similar to FAP but with osteomas of the mandible, skull & long bones, epidermal cysts, desmoid tumors, thyroid tumors and dental abnormalities
Turcots Syndrome
Intestinal adenomas and tumors of the CNS
Variants of polyps similar to FAP
1) Gardner syndrome
2) Turcot's syndrome
Hereditary nonpolyposis colorectal cancer (HNPCC)
Autosomal dominant form of colorectal cancer

Lower number of polyps but still multiple polyps and occur at younger ages than sporadic colon cancer

increase risk of cancers of endometrium, stomach, ureter, renal pelvis, bladder, panceas and biliary tract

caused by mutation in DNA mismatch repair genes
HNPCC is caused by what type of mutations? FAP?
HNPCC by mutation in DNA mismatch repair genes
FAP by mutations in APC
APC/WNT pathway are associated with what forms of neoplasms?
APC/WNT pathway
Familial Adenomatous polyposis 70%
Sporadic colon cancer 80%
DNA mismatch repair mutations are associated with what forms of colon cancer?
Hereditary nonpolyposis colorectal cancer
Sessile Serrated adenomas
10-15% of sporadic colon cancer
<10% of FAP
the majority of sporadic colon cancers are associated with what mutation?
80% with APC/WNT pathway mutations, 15% with DNA mismatch repair mutations
Why do APC genes lead to cancer?
APC normally regulates Beta-catenin from stimulating transcription in the nucleus
Colon cancer/adenocarcinoma

Lifestyle factors that increase risk of Colon cancer?
Risk factors:
-Low content of unabsorbable vegetable fiber
-High content of refined carbohydrates
-Decreased intake of protective micronutrients

Adenocarcinoma
--Accounts for 10% of all cancer related deaths
--peak incidence: 60-79 years (<20%: before 50)

Invasive adenocarcinoma
--The tumor has invaded through the mucosa, into submucosa (in this case it is seen to the level of the muscularis propria)
--The submucosa contains large lymphatics which are conduits for metastases

R vs. L sided cancer
Right versus Left sided colon cancer
RIGHT:
Usually asymptomatic for a long period of time
Signs and symptoms of iron deficiency anemia due to surface ulceration and resulting blood loss

LEFT: stool is harder at this point
Generally annular
narrow the lumen
change in bowel habits or obstruction
blood in stool (maybe obvious/bright red or occult)
originating from ruptured vessels at the edge of the ulceration

Thus
Anemia/blood loss --> think Right
Obstruction --> think Left
TNM Cancer staging
T is intraepithelial or lamina propria

T 1 submucosa

T 2 muscularis propria

T 3 subserosal tissues

T4 invades to visceral peritoneum, other organs or perforates
Appendicitis
Acute
1) Clinical: Nausea/ vomiting with periumbilical pain that localizes to the RLQ
2) Pathogenesis: Obstruction that leads to impaired blood flow and bacterial contamination --> leads to Transmural and luminal acute inflammation
Neoplasms of the appendix
Mucocele - benign dilatation of the lumen by mucinous secretions

Mucinous cystadenoma-proliferation of benign neoplastic cells-dilatation by mucinous material -may rupture

Mucinous cystadenocarcinoma -invasion of neoplastic cells

Can result in Pseudomyxoma peritonei
Mucocele
neoplasm of the appendix: benign dilatation of the lumen by mucinous secretions
Mucinous cystadenoma
neoplasm of appendix: proliferation of benign neoplastic cells-dilatation by mucinous material -may rupture
Mucinous cystadenocarcinoma
neoplasm of appendix: invasion of neoplastic cells
Pseudomyxoma peritonei
Term describing distention of the peritoneal cavity by the presence of semisolid mucin and epithelial mucin producing implants and/or malignant cells
Peritonitis
Inflammation of the peritoneum due to:
1. Sterile peritonitis due to bile or pancreatic juices
2. Surgical procedures
3. Endometriosis
4. Rupture of GI tract (Ruptured appendicitis, acute salpingitis, or diverticulitis)
Neoplasms of the peritoneum
1. Primary mesothelioma -rare
2. Secondary malignancies -extension, seeding, or implantation (more common)
Which is more common - upper or lower GI bleeding? What is the overal mortality of GI bleeds? What is the range of severity?
UGI bleeding>LGI bleeding


8%-10% overall mortality (pts. do not bleed to death.........usually)

Severity : acute massive, chronic, intermittent, occult as manifest by FOBT+, or IDA
Until proven otherwise, iron deficiency anemia in an adult suggests what?
Iron deficiency anemia in an adult = GI blood loss until proven otherwise!!!!

Even iron deficiency anemia in women with heavy menorraghia now need to be sent to GI to R/O GI bleed

IMPORTANT
Definition of Upper vs. Lower GI bleeding
Location:
UGI bleeding - above the Ligament of Treitz
Esophagus, stomach, *duodenal bulb, 2nd/ 3rd portion of duodenum

LGI bleeding - below the Ligament of Treitz
Small bowel, *colon
What separates upper from lower GI?
Ligament of Treitz - anchors the third portion of the duodenum to the peritoneum
Where do most GI bleeding dx come form?
Most all of the diagnoses of LGI bleeds come from colon and rectum

Also common to come from esophagus, stomach and duodenal bulb

Rare from small bowel - Small bowel counts for only 3% of GI diagnoses, even smaller % is bleeding
What are the 4 types of GI bleed presentations?
Hematemesis
Melena
Hematochezia
Occult (FOBT +, or IDA with or without FOBT+)
What type of bleed is hematemesis?
UPPER GI bleed
What type of GI bleed is melena?
UPPER GI usually - in 5-10% of pts with very slow bleeding is from sm intestine or right colon with slow motility in the gut.
What type of GI bleed is hematochezia?
LOWER GI, usually colon, most commonly anorectal (perianal/anal canal)
What type of GI bleed is occult + stool or iron deficiency anemia?
Can be upper OR lower, this is why we teach that IDA is GI blood loss until proven otherwise
How do you determine the urgency of a GI bleed?
Is the patient in shock?
40% decrease in circulating blood volume
Agitation, pallor, hypotension, tachycardia

Is the patient orthostatic?
20%-25% decrease in circulating blood volume
Orthostatic B/P on PE (postural hypotension)

Never rely on initial H/H readings (hemoconcentration)
How do you know if a patient with a GI bleed is in shock?
40% decrease in circulating blood volume
Agitation, pallor, hypotension, tachycardia
How can you tell if a patient with a GI bleed has orthostasis?
20%-25% decrease in circulating blood volume
Orthostatic B/P on PE (postural hypotension)
Initial management of GI bleeders? Diagnosis of GI bleeders?
Initial management
1) History/Physical examination: help smostly if pt has CIRRHOSIS and you can appreciate SPLENOMEGALY = PORTAL HYPERTENSION
2) Replace intravascular volume
3) Nasogastric intubation
4) Supplemental oxygen (nasal cannula)
5) Laboratory evaluation to include: CBC, platelet count, INR (PT), PTT, BUN, Creatinine
6) Severe bleeders need ICU admission

Diagnosis/therapeutic modalities
1) Endoscopy - upper/lower
2) Radionuclide scanning
3) Angiography
4) Capsule endoscopy - NOT in acute bleed
Never use barium in acute GI bleeding!!
Why is nasogastric aspirate useful in the management of GI bleeders?
PRIMARILY helpful in determines the status of UPPER GI bleeders but also gives indirect info on LGI bleeders as well.

Bright red blood/clots - active bleed
Coffee ground - slow bleeding, oozing, stopped
Clear - indeterminate (gastric juice)
Bilious: Best situation the the UGI bleeder
Bright red blood/clots on NG aspiration
active bleed
Coffee ground NG aspirate
slow bleeding, oozing, stopped
Clear NG aspirate
indeterminate
Bilious NG aspirate
best situation in the UGI bleeder
What is the best prognosis for a UGI bleeder in terms of NG aspirate?
bilious- because if the ulcer had been bleeding the bile refluxing back into the pyloris would be blood stained, so if the NG aspirate is JUST bilious and not bloody it means there's probably not a GI bleed
What are some prognostic indicators for GI bleeds?
Severity of initial bleed
Age of patient
Co-morbid disease
Onset of bleeding in hospital
Giant ulcer on endoscopy
Need for emergent surgery
Endoscopic stigmata of recent bleeding
When should barium be used in acute GI bleed?
Never use barium in acute GI bleeding!!
Differential diagnosis for UGI bleed?
MOST COMMONLY - Peptic ulcer disease: DU > Gatric erosions/gatritis > GU
Varices (Ex. portal hypertension)
M-W tears
Esophagitis
Duodenitis
Neoplasm
Esophageal ulcer

Uncommon causes:
Dieulafoy's Lesion
GAVE (Gastric antral vascular ectasia)
Portal Hypertensive Gastropathogy (PHG)
Aorto-enteric fistula
Hemoamtobilia
UGI tumors
What are the best predictors of rebleed and mortality of GI bleed? Which factors have more positive or less serious prgnostic value?
Greatest predictors of rebleed: visible vessel**, active bleeding, adherent clot

Greatest predictors of mortality: active bleeding and visible vessel, or adherent clot

Less serious/good prognostic factors for rebleed and mortality: clean ulcer base or flat pigment spot
UGI bleeding due to PUD
-most impt factor?
-therapy?
GU, DU erosions, "itis", stomal ulcers account for 65%-70% UGI bleeding (all studies)

RISK FACTORS:
1) Heliocobacter pylori is the most important factor
--> Attempt erdication in ALL pts with PUD! (except peptic esophagitis) to reduce recurrence rates!
2) NSAID's/ASA are important factors
-Local effects
-Prostaglandin inhibition
-Elderly at higher risk
-Important factor in non-healing ulcers (OTC)
3) Stress Related Mucosal Disease (SRMD)
Important cause of UGI bleeding in hospitalized patients with non-bleeding illnesses, commonly in ICU patients. Other RF: respiratory failure and coagulopathy
4) Gastric acid: + pepsin is essential cofactor in pathogenesis. Once mucosal integrity is impaired (NSAID's, ischemia, infection), H+ can back diffuse causing intramucosal acidosis and cell death

Medical therapy (antacids/H-2 RA's/PPI)
Endoscopic therapy (heat, argon gas, injection)

Overall goal is to prevent rebleeding!
Why is it so important to treat H. Pylori?
1) it's responsible for RECURRENT ulcers
2) gastric adenocarcinoma will likely be equated with chronic H. pylori infection in our lifetime
How does the effect of food on PUD differ for DU vs. GU?
Food is the trigger for gastric ulcers, but food actually makes duodenal ulcer BETTER

Pts with DU can actually gain weight bc they feel better when they eat, food buffers acid
In what pts should H. pylori not always be attempted?
peptic esophagitis
NSAIDS are an important factor in what type of PUD ulcers?
non-healing ulcers
A patient that is achlorohidric with an ulcer has what?
Cancer until proven otherwise -- this is the one exception to needing to buffer gastric acidity
UGI bleeding due to esophago-gastric varices
-therapy?
High mortality on first bleed, 70% rebleeding in one year if not treated

Therapy
Medical (VP, NTG, octreotide, B-blockers)
Endoscopic (injection, ligation, glues)
Radiologic (TIPS, embolizaytion)
Surgical (shunts, transection, splenectomy)
UGI due to Mallory-Weis tear
-when does it occur?
A result of retching/vomiting
Usually after ETOH intake
Self-limited in most cases
PHT pts. At risk risk of massive bleeding
Prompt UGI endoscopy indicated
Various threrapies available
UGI due to esophagitis/esophageal ulceration
-etiologies?
Massive bleeding is a rare event

Etiologies:
Peptic reflux
Radiation
Infection
Pill-induced
If you see what 3 things while looking for an ucer during endoscopy do you have to do something about it?
1) blood clot
2) central vessel
3) pseudoaneurysm
Red streaks over varicoces "red whales" mean what?
They have bled
hemobilia is seen in what pts?
blood coming out of ampulla of vater - seen in pts with cancer in bile duct that has eroded a large vessel
Capsule endoscopy is used for what? In what patient should it be avoided?
A camera the size of a vitamin that takes 100,000 frames of the GI tract over the course of 8 hours and makes a movie
-- Used to visualize SMALL intestine only
--should NOT be used in an actively bleeding patient
LGI bleeding presentations? Differential diagnosis of LGI bleeds?
Presentation:usually an older patient
Hematochezia
BRBPR
Maroon stool
Occult + stool

Diagnoses:
Diverticulosis (most common!)
Angiodysplasia (2nd most common)
Neoplasia
Colitis
Perianal disease
LGI due to Angiodysplasia
-definition
-clinical presentation?
Degenerative/acquired vascular lesion of the GI tract (AV malformation) that develops in older pts due to cardiopulmonary disease, usually on the R but occurs anywhere in luminal GI tract

2nd most common cause of LGI bleeds

Clinical: Acute, major hemorrhage/slow intermittent bleeding/occult positive stool/iron deficiency anemia

Colonoscopy/capsule endoscopy (SB)/angiography
LGI bleeds due to diverticulitis
-clinical presentation
-most common site?
Occurs in 3% pts with diverticulosis

Clinical: Acute, painless, bleeding presenting with bright red to maroon stools

Right colon 'tics' usual site of bleeding

20% bleeding is recurrent/persistent

Colonoscopy after bowel prep*/angiography/RBC tagged scans

This is a diagnosis of exclusion -- because bleeding from diverticulosis is rapid turn on and then turn off, it is difficult to visualize.
LGI bleeds due to neoplasms
Benign or malignant

Major hemorrhage is rare - usually do NOT rapidly bleed!

Iron deficiency anemia is common presentation +/- occult blood in stool

Diagnosis usually easily established with colonoscopy/capsule endoscopy/angiography
LGI bleeds due to perianal disease
-Causes
-presentation
-how is dx made?
Common causes: hemorrhoids/anal fissures

Minor, intermittent bleeding

Perianal disease always a diagnosis of exclusion after more serious lesions have been ruled out (cancer/polyps/colitis)
If someone has iron deficiency anemia, do you just tell them to take oral iron supplements for 6 months?
NO! It's a GI bleed until proven otherwise!
Where in the esophagus is
1) striated muscle
2) smooth muscle
Striated muscle: upper 2/3rds, Smooth muscle: lower 2/3rds, Middle third contains both striated and smooth muscle
What autoimmune disease can affect motility of the esophagus?
scleroderma
Scleroderma
Autoimmune disease affecting motility, Connective tissue disorder involving damage to small blood vessels and progressive fibrosis in skin and possibly other organs

• GI involvement in 90% of cases (most commonly esophagus)
• Difficulty swallowing, reflux symptoms
• Atrophy of the smooth muscle in the lower 2/3 of the esophagus
• LES injury (reflux, Barrett's esophagus
Achalasia
"Failure to relax": Aperistalsis, Increased resting tone of LES, Partial or incomplete relaxation of the LES with swallowing

Primary vs. Secondary
1) Primary disorder of uncertain etiology
• Progressive dilation of the esophagus above the LES
• Wall can be either thin from dilation OR thick from hypertrophy
•myenteric ganglia are reduced in number from the body of the esophagus

Symptoms: Usually begins in young adulthood
• progressive dysphagia
• nocturnal regurgitation
• aspiration of undigested food

Associated with increased risk of squamous cell carcinoma
Note bird's beak deformity seen on barium imaging study due to LES contraction

2) Can also be Secondary to...
• Chagas
• Diabetic autonomic neuropathy
• disorders of dorsal root ganglia (polio, surgical ablation)
• Infiltrative diseases, malignancy, amyloidosis, sarcoidosis
Mallory-Weiss tear
LES is not opening up with vomiting
• Associated with alcoholics and hiatal hernias with severe retching
• Causes longitudinal lacerations leading to hematemesis
• Surgery is usually not required
Boerhaave Syndrome
esophageal rupture associated with extreme retching, catastrophic event as esophageal contents enter the mediastinum
Esophageal varices
Portal hypertension (MCC is cirrhosis) forces blood back through gastric veins → induced the formation of collateral bypass channels wherever portal and caval systems communicate → Portal blood flow is diverted through the coronary veins of the stomach (gastric veins) into the plexus of the lower esophageal veins → Blood pools in torturous dilated veins in the submucosa of the distal esophagus

Pathology: Tortuous dilated veins lying within the submucosa of the distal esophagus/proximal stomach
• Venous channels directly beneath the esophageal epithelium may become massively dilated → Protrusion into the lumen → Variceal rupture with massive hemorrhage
• Usually asymptomatic until hemorrhage → when rupture cause massive hematemesis

50% fatality from first ruptured esophageal varices, 50% of deaths from advanced cirrhosis are from ruptured varices!
Barrett's esophagus
Complication of GERD - 10% of symptomatic pt's have Barret's, considered a PREMALIGNANT CONDITION

Single most important risk factor for adenocarcinoma (precancerous lesion)

Criteria (BOTH required):
• Gross: Endoscopic appearance of "salmon" or red velvet colored mucosa (columnar epithelial lining) between the smooth pink-white esophageal squamous mucosa and the lusher light brown gastric mucosa
• Histologic: Evidence of intestinal metaplasia (squamous mucosa replace dby columnar cells with goblet cells) + Presence of GOBLET CELLS

Long segment > 3.0 cm, short segment </= 3.0 cm

Pathogenesis: unclear, thought to be an alteration in the differentiation program of stem cells
• Barrett's (metaplasia) --> Dysplasia --> adenocarcinoma
• Classified as low grade dysplasia (LGD) and high grade dysplasia (HGD)
• Approximately 50% with HGD may already have adjacent adenocarcinoma

Epi: Affects males more than females, 40-60 years old, with reflux symptoms

Secondary complications: ulceration, bleeding, stricture, malignancy
--> 30-40x rate of adenocarcinoma with long segment Barrett's esophagus!!
Know the two most common viruses and single fungal agent responsible for infectious esophagitis
Candida, CMV and HSV
Candida infectious esophagitis
fungal, usually in immune compromised patients, see Pseudomembranes from with fungal sttuctures and neutrophils on surface of esophagus
CMV infectious esophagitis
Cytomegalovirus (CMV): produces ulcers, see large cells with intranuclear inclusions
HSV infectious esophagitis
Herpes Simplex Virus (HSV): produces punched out ulcers secondary to vesicles (vesicles destroyed by food), see multinucleated cells with intranuclear inclusions
2 most common types of malignancies associated with the esophagus
o Squamous cell carcinoma
o Adenocarcinoma:
Squamous cell carcinoma of the esophagus
Risk Factors
• Males > Females
• More common in rural and underdeveloped areas
• Linked with alcohol and tobacco, as well as some esophageal disorders
• More common in African Americans than Caucasians

Genetics: Stepwise acquisition and accumulation of genetic alterations
• p53 point mutations associated with tobacco
• p161INK4 mutation

Histology: Infiltrating malignant squamous cells, some with keratinization (keratin pearls)

Clinical
• Insidious onset, pt presents with dysphagia and weight loss, pt switches to liquid diet
• Can affect any segment of esophagus
• Poor prognosis: 9% 5-year survival

Spread
• If primary tumor is in esophagus (20%) it will spread via cervical lymph nodes
• If in middle esophagus (50% - MOST COMMON), it will spread via mediastinal, apratracheal and tracheobronchial lymph nodes
• If in lower (30%), it will spread via gastric and celiac nods
Adenocarcinoma of the stomach
malignant epithelial tumor with glandular differentiation

Risk Factors: used to be rare, but now consists of >1/2 of esophageal cancers in the US
• Follows Barrett's and dysplasia
• Linked with tobacco and obesity, NOT alcohol

Genetics & pathology:
• Stepwise accumulation of mutations leads to development of cancer
• Multistep process with a long latency period associated with many genetic changes
• Development of dysplasia appears to be an important step

Gross appearance is variable
Histology
• Mucin producing glandular tumor with intestinal-type features
• Can be poorly differentiated with signet ring cells
• Usually distal esophagus

Clinical
• > 40 years old M>F
• Caucasian > African-American
• Difficulty swallowing, progressive weight loss, bleeding, chest pain, vomiting, chest pain with normal EKG
• Prognosis
• <25% overall 5 year survival
• ~80% 5 year survival if early and limited to mucosa and submucosa
Benign tumors of the stomach
-which is most common?
leiomyomas (MOST COMMON), fibromas, lipomas, hemangiomas, neurofibromas, lymphangiomas Squamous papilloma, condyloma, Inflammatory polyp
Atresia and fistula
Atresia is a a thin cord-like noncanalized segment of the esophagus associated with a proximal blind pouch and lower pouch leading to the stomach. Usually associated with a fistula connecting with a bronchus or the trachea

o Symptoms: Regurgitation shortly after birth + Aspiration, paroxysmal suffocation, pneumonia, fluid and electrolyte disturbances

o Associated with other anomalies: Congenital heart disease, neurologic and GU diseases, GI malformations and single umbilical artery
Esophagitis
Inflammation of the esophageal mucosa caused by a variety of physical, chemical or biologic agents

1) GERD
2) Infectious/chemical
3) Pill esophagitis
4) Esoinophilic esophagitis
Most frequent cause of esophgitis?
GERD
Most common outpt GI dx in US?
GERD
GERD
Most frequent cause of esophagitis & Most common outpatient GI diagnosis in US

Etiology: Reflux of gastric contents into the lower esophagus is the most important cause of esophagitis. In severe cases, bile from duodenum may contribute to the mucosal injury

Causative factors:
• Decreased LES tone
• Sliding hiatal hernia
• Slowed esophageal clearance of refgluxed material
• Delayed gastric emptying and gastric dilation
• Reduction in repair process

Clinical: Seen in Infants to adults
• Symptoms: Dysphagia, heartburn, regurgitation of sour brash, hematemesis, Severe chest pain mimicking a heart attack
• Complications: bleeding, ulceration, stricture, Barrett's esophagus

Pathology: Inflammatory cells; eosinophils, neutrophils, lymphocytes in squamous epithelium
• Basal zone hyperplasia >20%
• Lamina papillae >2/3 of mucosa
Infectious/chemical esophagitis
• Mucosal irritants; alcohol, Corrosive acids/alkalis (suicide attempts), excessive hot fluids and heavy smoking, Pills
• Cytotoxic anticancer therapy
• Infections, Uremia, other
Eosinophiic esophagitis
increasing in incidence
• Dyspagia, food impaction in adults
• Food intolerance and GERD symptoms in children
• Rapid increase in incidence for unknown reason
• Treatment includes dietary restrictions and topical steroids
Hiatial hernia
=Part of stomach slides through diaphragm, leading to heartburn,
o Widening of space between muscular crura and esophageal wall, Congenital vs. Acquired
o Can be sliding (hiatial hernia - more common) vs. rolling (hiatial paraesophageal hernia - part of stomach encapsulated, may require surgery)
o Symptoms & complications: heartburn, regurg of gastric juices, similar to GERD, ulcers
Congenital diaphragmatic hernia
Defective closure of diaphragm
• weakness or partial to total absence of diaphragm (usually on left)
• Abdominal contents in thorax impinges on development of the lungs, causing lethality through respiratory distress
• In-utero: herniation of abdominal contents into the thorax due to incomplete closure of the diaphragm → may cause respiratory distress syndrome in the newborn (potentially lethal event)
Congenital hypertrophic pyloric stenosis
• 3-4:1 infant boys : infant girls, Presents 2-3 weeks after birth
• Persistent projectile nonbilious vomiting and a palpable mass
• Herpertrophy of muscularis propria of pylorus leading to thickening of wall
• visible peristalsis
• firm ovoid mass may be palpable
• Surgical splitting is curative, occurs in 1 out of every 200-300 live births
H. PYlori
H. Pylori: flagellated gram negative rod transmitted via oral-oral, oral-fecal, environment

Two patterns of H. Pylori gastritis: 1) Antral type most common due to lower acidity 2) Rare pangastritis type

Causes nearly all cases of duodenal ulcer, gastic ulcerations, and chronic gastritis

Pathogenesis: Increased acid production + disruption of normal gastric and duodenal protective mechanisms

Pathology
• Everything looks more blue due to lymphocyte infiltration microscopically
• Chronic inflammatory infiltrate (lymphocytes and plasma cells) in mucosa
• Germinal Centers
• Neutrophil infiltrates
• Regeneration of epithelium
• Peptic ulcer disease
Definitions:
1) gastritis
2) erosion
3) ulcer
• Gastritis = inflammation of gastric mucosa
• Erosion = sloughing of mucosa that does not penetrate the muscularis mucosa
• Ulcer = breach in the mucosa which extends through the muscularis into the submucosa or deeper
NSAID Gastritis
Acute gastritis with erosions, reactive gastropathy
o Pathology: Erosion (grossly) + necrosis (microscopically
o Complications: Acute gastric ulceration
Diff in survival for early vs. advanced gastric adenocarcinoma
early: > 90% 6 year survival, LIMITED TO MUCOSA AND SUBMUCOSA
late: < 20% 5 year survival, INVASION INTO MUSCULARIS PROPRIA
Gastric carcinoma
Adenocarcinoma is the most common malignant gastric neoplasm (90%)

Incidence varies world wide - ie) Higher in Japan and lower in the U.S. but it is Leading cause of cancer death worldwide

Clinical: generally asymptomatic until late in course → weight loss, abdominal pain, anorexia, vomiting

Characteristic lesions
• Exophytic vs. Flat vs. Excavated
• "heaped up" borders and "shaggy" base
• Linitis plastica: extensive infiltration of gastric wall
• thickened leather bottle-like stomach

Factors associated with increased incidence
• diet (nitrits, smoked, salted food)
• low socioeconomic status
• H. pylori infection
• multifocal mucosal atrophy and intestinal metaplasia
• gastric adenomas
• partial gastrectomy
• Germ line mutation in CDH1 which encodes E-cadherin (diffuse type)
• Familial Adenomatous Polyposis (FAP)
Gastric adenocarcinoma
Histology of subtypes
• Intestinal variant: neoplastic glands, decreasing in incidence, related to H pylori
• Diffuse variant: individual signet ring cells, not decreasing in incidence ("linitus plastica"), NOT related to H pylori. Signet ring cells infiltrate stomach wall


Invasion - penetrate wall to involve serosa "early gastric cancer" confined to mucosa and submucosa
• Virchow node: Gastric adenocarcinoma metastatic to supraclavicular node
• Krukenberg tumor: Gastric adenocarcinoma - signet ring cells metastatic to both ovaries
• Sister Mary Joseph's node: Spread to theperiumbilical nodes are associated with poor prognosis
Virchow's node
Gastric adenocarcinoma metastatic to supraclavicular node
Krukenberg tumor
Gastric adenocarcinoma - signet ring cells metastatic to both ovaries
Sister Mary Joseph's node
Gastric adenocarcinoma spread to theperiumbilical nodes are associated with poor prognosis
Describe the important histologic features and molecular findings associated with gastrointestinal stromal tumors (GISTs)
o Tumors with Spindle or epithelioid appearance
o Most important factor is mitotic activity for grading tumor!!

Diagnosis and treatment depends on histological results:
• Stained for CD117 (C-kit mutation positive), 75-80% have C-kit mutations, leading to activation
• Another 8% have PDGF receptor alpha mutations

Imatinib (tyrosine kinase inhibitor) can be used to treat
Most important factor for grading GIST tumors
mitotic activity
Acute gastritis vs. chronic gastritis
inflammation of the gastric mucosa

ACUTE:
Pathology
• Neutrophils in the mucosa ("active inflammation")
• Erosions vs. Punctate hemorrhages vs. Actue erosive gastritis (concurrent erosion and hemorrhage)

Clinical: May be asymptomatic or epigastric pain, N/V, hemorraghe, hematemesis, melena

CHRONIC
Etiology
• H. Pylori (most important)
• autoimmune
• radiation injury
• chronic bile reflux
• mechanical injury
• systemic diseases: Crohn's disease, amyloidosis, GVHD (graft vs. host disease)

Clinical: may be asymptomatic or N/V, upper abd discomfort
Acute ulcers
o Usually multiple!!****

Two special types
• Curling ulcers: duodenum and associated with severe burns and trauma (THINK: burn yourself on a curling iron)
• Cushing ulcers: upper GI and associated with intracranial disease (THINK: might also see Cushing sign with intracranial disease)
Autoimmune gastritis
o Usually involves fundus and body, rather than antrum (H. pylori)
o Less than 10% of gastritis
o Autoantibodies formed to parietal cells and intrinsic factor →loss of IF leads to a secondary deficiency of B12
o Likely cause is CD4 T cells against parietal cell components
• GAVE (watermelon stomach)
o Streaky long red areas resemble the exterior of a watermelon
o associated with dilated blood vessels that can lead to intestinal bleeding
o Stomach prolapse through the pyloric sphincter
PUD (chronic ulcers)
Caused by exposure of tissue to stomach acids and peptic enzymes

Can be found in:
• Gastric antrum and first portion of duodenum (duodenum is most common site)
• Esophagus (GERD or ectropic gastric mucosa)
• Meckel's diverticulum

Unlike acute, usually solitary lesions
Can be associated with Zollinger-Ellison syndrome

Pathologic appearance:
• Spectrum of active necrosis to chronic inflammation (granulation tissue) to scarring
• Sharply goes down to ulcerated base containing inflammatory tissue

Clinical: Risk is that it can look like cancer, needs biopsy. If it heals it is benign (Duodenal ulcers NEVER malignant, only small percentage of gastric ulcers malignant)
Are duodenal ulcers malignant? gastric?
DU NEVER malignant, only small % of gastric ulcers are
Chronic vs. Acute ulcers: # of ulcers
chronic are usually solitary whereas acute are usually multiple
Hypertrophic gastropathies
Group of conditions characterized by enlargement of the gastric rugal folds
1) Menetrier disease
2) Zollinger Ellison syndroem
Menetrier disease (hypertrophic gastropathy)
Form of hypertrophic gastropathy (enlargement of gastric rugal folds)

Giant rugal folds due to hyperplasia of mucus-secreting cells "foveolar cells" causes hypoproteinemia (protein-losing enteropathy)

Atrophy of parietal cells (Achlorhydria): Increased risk of adenocarcinoma
Zollinger Ellison syndrome
Form of hypertrophic gastropathy
• Gastrin secreting tumor
• Hyperplasia of parietal >mucous and endocrine
• Increased acid production
• 25% have MEN type 1 (multiple endocrine neoplasia, type 1: 3Ps...parathyroid, pancreas, and pituitary)
Gastric polyps
Hyperplastic polyp: Majority (~75%) of gastric polyps
Composition:
• Hyperplastic surface epithelium
• Cystically dilated glands
• Increased inflammatory cells and smooth muscle in lamina propria
• No malignant potential!!!

Adenomatous polyp: 10% of stomach polyps
• Increased in FAP (Familial adenomatous polyposis)
• Composition: Proliferative dysplastic epithelium
• Malignant potential ~30% of gastric adenomas contain a focus of cancer (particularly larger ones)

Peutz-Jeghers polyp
Juvenile polyp
Inflammatory polyp
Which gastric polyps have malignant potential?
Adenomatous have 30% malignant potential, hyperplastic have NO malignant potential!!!! Peutz-Jegher's, Juvenile and inflammatory polyps usually not malignant either
Carcinoid tumors
Tumors arising from endocrine cells: Well differentiated neuroendocrine carcinomas
--Majority are found in the GI tract: 40% in the small intestine
--Next most common site is tracheobronchial tree and lungs

Prognosis: Tumor location is the most important prognostic factor
• Foregut (GI tract proximal to the ligament of Trietz): cured by resection, Sporadically arising are much more aggressive
• Midgut (Jejunum and ileum): multiple and aggressive
• Hindgut
--appendix - generally good outcome
--rectal - symptomatic, metastasis uncommon
--proximal colon - large and can metastasize
Gastric lymphoma
o Majority are associated with H. pylori (80%)
o most common site for extra-nodal lymphomas, nearly all are B cell lymphomas
Mesenchymal neoplasms of stomach
Usually of smooth muscle origin
-- Leiomyoma = benign (most common benign tumor in the stomach)
-- leiomyosarcoma = malignant
-- Gastrointestinal stromal tumors (GIST)