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

See More

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