GIT #1

Congenital Anomolies
(A) TracheaoEsophageal
Atresia
(B) Lower
Esophageal
Fistula
Most Common
(C) TracheoEsophageal
Fistula
Diaphragmat
ic Hernia
Omphalocele
Gastroschisis
Morgagni

hernia
Meckel

Diverticulum
Pyloric

Stenosis

Small Bowel
Atresia &

Stenosis

Hirschsprung
Disease
Congenital
Aganglionic

Megacolon

failure of abdom wall to form

Memb. Sac w/ Intestines
exposed intestines w/o Sac covering the Intestines
defect is through the front of the diaphragm towards the heart

(Rule of 2s: 2ft from Iliocecal Valve, appears at 2yrs old, 2M>F,)
Current Jelly colored stool
Projectile, Non-Bilious Vomiting
Gastric Peristaltic Wave, Olive Shaped Mass
low Cl & low K
Billious vomiting, 1st wk, no passage of meconium
double-bubble sig on Abd- X ray
Assoc w/ Down Syndrome
Migration of neural crest cells arrested prematurely or undergo death lack of
Meissner and Auerbach plexus in distal intestinal segm (aganglionosis)
functional obstruction dilation proximal to affected segm
Assoc w/ Down Syndrome
Complications: enterocolitis, fluids and electrolytes disturbances, perforation
and peritonitis.
Chagas associated with loss of Ganglia
Esophageal Obstruction

Nutcracker
Esophagus
Stenosis
Achalasia

Esophagea
l Mucosal
Web

Lack of coordination

Congenital or Acquired from: Inflammation Scarring, Irradiation, GER, caustic Inj.

Failure of Lower Esphageal Sphinctor to relax, LES tone
Primary (Idiopathic) Failure of distal esophag inhib neuron.
Secondary (Chagas disease) damages the Ganglions
May have absent myenteric plexi (mega esoph/ureter/colon )
DX: Beaked Tapering Bird Beak w/ Barium Swallow
TX: Botox
Semi circumferential protusions of mucosa
Webs (Upper): When accompanied by Iron-deficiency anemia, glossitis, and
cheilosis (Paterson Brown-Kelly syndrome or Plummer-Vinson syndrome)
Esophageal rings or Schatzki rings (Lower): circumferencial and thicker. (A
and B rings)


Dysphagia Diseases of skeletal muscle such as Myasthenia gravis, Dermatomyositis and
Differential
Polymyositis
Diagnosis Scleroderma causes dysphagia because of extensive fibrosis mostly in the lower
portion of the esophagus
Clinical manifestations: dysphagia, heartburn /GERD. Mask-like, leathery
facies. CREST (calcinosis, Raynaud, esoph dysmotility, sclerodactyly,
telangiectasia)
Diagnosis: Screening test: ANA
anticentromere Ab (CREST), anti-topoisomerase (anti-SCL70) (scleroderma)
Hiatal
Cardia of the stomach slides up into the esophagus, Hour Glass appearance
Hernia
Diverticula
Zenkers False Diverticulum
Diverticulu Outpouching of the Mucosa, the lumen is not usually affected
m
Eosinophili Dysphagia (adults), feeding intolerance or GERD-like symp (children)
c
Associated with atopic dermatitis, allergic rhinitis, asthma, modest peripheral
Esophagiti
eosinophilia
s
Dx: GERD, other esophagitis
Micro: intraepith eos
TX: dietary restriction (cows milk). Steroids
Esophagea Dilated submucosal esophageal veins d/t portal hypertension can result in
l Varices
upper GI hemorrhage (hematemesis) (peptic ulcer, Mallory-Weiss synd)
Assoc w/ Liver Cirrhosis & Portal HTN Alcohol & hepatic schistosomiasis
MC cause of death in cirrhosis: ruptured EV
Often asymptomatic, but can have Hematemesis
May rupture: (inflamm erosion, venous pressure, vomiting). 50% die in 1 st
episode.
TX: balloon tamponade, rubber band ligation, sclerother
Barretts Glandular cell Metaplasia due to GERD causes Adenocarcinoma
Esophagus Occurs in the Lower 1/3 of esophagus
DX: Goblet cell metaplasia & Inc Mucus production
MalloryWeiss
syndrome

Esophagitis
Longitudinal tears usually shallow in the esophago-gastric junction
Predisposing factors: alcoholics due to episodes of excessive vomiting & Bulimia
Hematemesis can occur but not as severe as varices
Esophageal rupture is known as Boerhaaves syndrome

 Vasoconstrictive measures, transfusions and balloon tamponade may be required

Gross- shows multiple esophageal tears which has extended from the stomach
Most often associated with severe retching and vomiting d/t acute alcohol
intoxication
Dx: endoscopy
Chemical & Alcohol
Infectious Corrosive (acids / alkalis)
Esophagitis Hot fluids
Heavy smoking
Pill-induced esophagitis
Iatrogenic (chemo, radioth)
GVHD
HSV, CMV, candida, aspergillosis
Bullous pemphigoid, epidermolysis bullosa, Crohn disease
Viral
CMV - infected endothelial cells with nuclear and cytoplasmic inclusions
Esophagitis HSV - nuclear inclusions in Multinucleate squamous cells (Multinucleated
Giant Cells, Margination, Molding, Ground-Glass appearance)
GERD
MCC of Esophagitis
Reflux of gastric juices, and bile from duodenum
LES tone, or abdominal pressure. Also (caffeine, etoh, tobacco, obesity,
pregnancy, CNS depressantshiatal hernia, delayed gastric emptying)
DX: 24-hour esophageal pH monitoring
TX: head of bed, avoid (coffee, etoh, tobacco, chocolate, spicy and fatty foods,
anticholinergic med). Antacid, H blockers, PPI, and Surgery (Nissen
fundoplication)
Squamous
cell CA
w/ Keratin
Pearls

Neoplasms of Esophagus
4M : F
Risk factors: etoh, tobacco, poverty, caustic injury, achalasia, tylosis, PlummerVinson synd, freq consump of hot beverages, and previous radiation
Other Risk Factors:
- Western hemisphere Smoking & Alcohol
- Asia Dietary role
- Fungal contamination
- Lack of Vitamin & Trace elements
- Nitrites & Nitosamines
Pathogenesis: incompletely defined but loss of p53 and p16 are involved
Location 50% Middle third

30% lower third

20% upper third

Presents as: - Polypoid exophytic growth

- Diffuse infiltrative encircling growth

- Excavated (Ulcerative growth)

Clinical features:
Progressive dysphagia
Weight loss and anorexia
Blood loss
Hoarseness and cough
Aspiration of food due to TE fistula
9% five-year survival rate (overall)

Adenocarcino
ma

Inc in Mucin

Dysphagia first to solids and then with liquids

Risk Factor: dysplasia, tobacco, obesity, radiation therapy
Often involves the Gastric Cardia.
High incidence in U.S. UK, Canada, Australia, Brazil
Low incidence Korea, Thailand, Japan, Ecuador
Pathogenesis: chromosomal abnormalities and genetic mutations have been
involved (p53, c-ERB-B2, cyclin D1, cyclin E, and p16)
Morphology: distal third. Flat, raised, infiltrative, ulcerated
Micro: well to poorly differentiated. Infiltra signet-ring cell
Clinical features: discovered in evaluation of GERD or BE. Dysphagia, chest
pain, weight loss, hematemesis, vomiting
Stomach

Mucosal Protection:
Mucus secretion, Bicarbonate secretion, Epithelial barrier, and Rich mucosal blood flow

Mechanisms of gastric injury and protection. This diagram illustrates the progression from
more mild forms of injury to ulceration that may occur with acute or chronic gastritis. Ulcers
include layers of necrosis (N), inflammation (I), and granulation tissue (G), but a fibrotic scar (S),
which takes time to develop, is only present in chronic lesions.
Acute
Definition: acute mucosal inflammatory process, usually transient and selfGastritis
limited, in which there is focal necrosis of the mucosa, in an otherwise normal
stomach
Cause: Loss of gastric defenses allowing back diffusion of H+ ions
Associated conditions:
Use of non-steroidal drugs and corticosteroids
Alcohol abuse
Cigarette smoking
Shock
Uremia
Morphology: Mild (only edema of lamina propria) active inflammation
erosion acute erosive hemorrhagic gastritis
Clinical: may be asymptomatic painless bleeding, occasionally massive & fatal,
- Variable epigastric pain, nausea & vomiting
- One of the major causes of hematemesis (AEG)

Acute Gastric
Ulcer

Pyloric
Stenosis

Focal, acutely developing mucosal defects

Well known complication of NSAIDs
Stress ulcers (shock, sepsis, severe trauma).
Curling ulcers (proximal duodenum): assoc with burns or trauma
Cushing ulcers (gastric, duoden, esopha): intracranial disease
Morphology: rounded, , 1-cm, brown/black, anywhere, more often multiple,
not indurated margins or base
Prophylaxis: with H2 histamine blockers, PPI. Correct the underlying condition
Projectile Vomiting, Delayed onset (6wks)

GIT #2
Chronic Gastritis
Chronic Inflammation of the stomach mucosa
Causes: H. Pylori (MCC), NSAIDs, Autoimmunity, Allergic response
also Smoking, Alcohol, Psychological stress
Dx: usually asymptomatic but may manifest as epigastric pain or, rarely, with nausea, vomiting,
anorexia, or significant weight loss. Symptoms may occur with the development of
complications (peptic ulcers, gastric adenocarcinoma, and MALT lymphoma)
- serologic tests for Ab to HP, fecal bact detection, urea breath test.
- Gastric Bx for micro, stain, rapid urease test, culture, PCR
H.Pylori
Effects the Antrum of the Stomach
Gastritis
Features linked to H. Pylori virulence:
- Non-sporing, curvilinear gram-negative rod
- Flagella,
- Urease + ammonia from urea
- Adhesins (blood group O),
- Cytotoxin-associated gene A (CagA) (assoc risk Ca)
- Vacuolating toxin A (VacA) are more likely to develop peptic ulcers
Tx: Antibiotics & PPI
Complications: if untreated Peptic Ulcer, Gastric Cancer, and MALT
Lymphoma
Autoimmune Typically spares the antrum and includes hypergastrinemia
Gastritis
Characterized by:
- Ab to parietal cells and Intrinsec factor
- serum pepsinogen concentration
- G-cell hyperplasia
- Vit B12 deficiency
- Achlorhydria
Parietal cell destruction dec Intrinsic Factor dec Vit-B12 Pernicious
Anemia
Parietal cell destruction dec Gastric Acid inc Gastrin G-cell
Hyperplasia
Pathogenesis:
It was initially thought that the autoantibodies to parietal cell components,
most prominently the H+,K+-ATPase, were involved in the pathogenesis of
autoimmune gastritis. However, this is unlikely because passive transfer of
these antibodies does not produce gastritis in experimental animals.

Reactive

Gastropathy

Eosinophilic
Gastritis

Lymphocytic
Gastritis

(Varioliform)
Granulomat
ous Gastritis
Peptic Ulcer

It is more likely that CD4+ T cells directed against parietal cell components,
including the H+,K+-ATPase, are the principal agents of injury.
This is supported by the observation that transfer of H+,K+-ATPase-reactive
CD4+ T cells into naive mice results in gastritis and production of H+,K+ATPase autoantibodies.
Clinical features: median age of diagnosis at 60. Symptoms of anemia. Vit B12
def atrophic glossitis, malabsorptive diarrhea, peripheral neuropathy
Foveolar hyperplasia, glandular regenerative changes, and mucosal ededma.
Causes: NSAIDs, chemical injury, bile reflux, and mucosal trauma d/t prolapse.
After gastric surgery.
Gastric antral vascular ectasia (GAVE) associated with antral trauma.
Reactive GP with dilated capillaries containing fibrin thrombi
Reactive gastropathy. Gastric mucosa, showing hyperplasia of foveolar surface
epithelial cells, glandular regenerative changes, and smooth muscle fibers
extending into lamina propria.
Gastric antral vascular ectasia (GAVE): uncommon cause of chronic GI
Bleeding or iron deficiency anemia. The condition is associated with dilated
small blood vessels in the antrum. Called watermelon stomach because
streaky long red areas that are present in the stomach may resemble the
markings on watermelon
Dense infiltrate of eos in mucosa and muscularis
Antral and pyloric regions involved
Also in other areas of GI. Peripheral eosinophilia. IgE
Causes: allergic reactions (cows milk, soy protein), drugs, systemic
collagen vasc diseases, parasitic infections, H pylori
Idiopathic. 40% assoc with celiac disease
Entire stomach is involved
Marked increase in intraepithelial lymphocytes mostly CD8+
Crohn disease, and sarcoidosis. Mycobacteria, fungi, CMV, H pylori

A chronic ulcer with a breach in mucosa extending to submucosa or deeper

MC associated to HP chronic gastritis
HP present in 85% to 100% with DU, and 65% with GU
Common sites: In order of decreasing frequency
Duodenum: 1st portion (4x more common in Prox Duodenum > Stomach)
Stomach usually Antrum (due to H.Pylori)
Gastro-esophageal junction (with GERD)
Within the margins of gastro-jejunostomy
Multiple site in patients with Zollinger-Ellison syndrome
Within the ectopic gastric mucosa of Meckel diverticulum
Pathogenesis: Imbalances of mucosal defenses & damaging forces are
responsible for PUD
H. pylori and NSAIDs primary underlying causes
Cigarrette, alcohol, psychologic stress, COPD

Gastric
Location: Lesser curvature, antrum
Peptic Ulcer Up to 50% of those with gastric peptic ulcer have concurrent duodenal ulcer
Causes: H.Pylori, NSAIDs, and GERD
Gross Appearance:
Less than 4 cms in diameter
Round to oval in shape

Punched-out area with clean base

Margins are usually level with surrounding mucosa or slightly elevated due to
edema (heaped up margins should arouse the suspicion of Ca)
Rugosal folds radiate from ulcer in a spoke like fashion

Hypertrophi Giant cerebriform enlargement of the rugal folds d/t epithelial hyperplasia
c
without significant inflammation
Gastropathi Menetrier disease (Giant fold disease): diffuse hyperplasia of foveolar
es
epithelium (body/fundus) with overexpression of TGF-alpha with protein loss,
malabsorption & risk for adeno ca in adults.
- In children is self limited and second to CMV, HSV, giardia, H pylory.
Clinical manifestations: upper abd pain, n/v, diarrhea, and weight loss
Dx: endoscopy, Bx

Zollinger-Ellison syndrome Gastric gland hyperplasia secondary to

excessive gastrin secretion by gastrinoma (small intestine and pancreas).
parietal, mucous, and endocrine cells. Risk for peptic ulcers (often
multiple and resistant to treat).
60% to 90% are malignant.
75% sporadic. 25% MEN I (parathyrroid H/A, pancreatic endocrine tumor G/I,
pituitary adenoma)
Clinical manifestations: related to peptic ulcers or chronic diarrhea
Dx: high gastrin level. Endoscopic U/S, Bx, somatostatin receptor scintigraphy.

Fundic
Gland
Polyps

Gastric
Adenoma

Gastric
AdenoCA

Gastric Tumors
Sporadic and in Familial adenomatous polyposis (FAP)
5F : M
Well circumscribed. Single or multiple
Micros: cystically dilate, irregular glands lined by parietal and chief cells
No association with adenoCa
10% of all gastric polyps
50 to 60 y/o. 3M : F
High incidence in FAP
In a background of atrophy, and IM
Risk for adenoCa related to size (>2-cm)
Usually solitary. In antrum. < 2-cm
Intestinal type columnar epithelium, and dysplasia
The MC malignancy of stomach (90%)
High incidence in Japan, Chile, China, Portugal, Russia (up to 20 fold higher than
USA)
M:F = 2:1
Age: >50 yrs
It still exceeds lung cancer as the leading cause of cancer death worldwide
Overall incidence is , but gastric cardia is
20% 5 year survival
Risk Factors: H.Pylori, Nitrates, Smoked food, Pickled veggies, Excessive Salt
intake, Menetrier disease, Adenomatous polyps, Chronic atrophic gastritis,
Pernicious anemia
Location - Pylorus & Antrum

 Signet-ring cells can be recognized by their large cytoplasmic mucin vacuoles

and peripherally displaced, crescent-shaped nuclei.
Krukenberg Tumour Metastasis to Ovaries bilaterally
Sister Mary Joseph Nodules metastasis to skin around umbilicus
producing nodules
Mesenchym GIST (Gastro-Intestinal Stromal Tumor)
al
Presentation: Incidental. Bleeding
Neoplasms Pathology:
GIST
Sheets of spindle cells
Previously mistaken for leiomyoma
Origin cell interstitial cell of Cajal
C-kit + and CD34+
Small Intestine
Intestinal
Adhesion of Small Intestine is MCC
Adhesions: after
Obstruction MCCs:
surgical procedures,
peritoneal infections,
Adhesions (Adults
endometriosis
Intussusception or invagination (3mo-6yrs)
Volvulus: complete
Incarcerated inguinal hernia & Meckel div
twisting of an intestinal
(child)
loop. Affects sigmoid,
Clinical: Abd pain, Vomiting, constipation, and
cecum, SB, stomach
failure to pass flatus
Intussusception:
segment of intestine,
constricted by a wave of
peristalsis, telescopes
into the immediate
distal segment. Location
Illieocecal Junction
Causes: anatomic defect
or Rotavirus , Lymphoid
Hyperplasia (child), or
Tumors (adults)
Ischemic
Nonocclusive (Low flow states)- more common than occlusive
Bowel
Vasoconstriction, due to decreased cardiac output
Disease
Hypovolemia
Dehydration
Hypotension
Transmural Infarction
Angiodyspla Dilations of peri-crypt vascular plexuses, with dilation of submucosal veins
sia Vascular Most commonly, >55 y/o, cecum / R sided colon
Ectasia
20% of major episodes of lower intestinal bleeding
Pathogenesis: mechanical / congenital?
Diagnosis: difficult, usually requires selective angiography or colonoscopy
Rx: resection is curative
Malabsorption Syndromes
Celiac Sprue Gluten-sensitive Enteropathy, Non-Tropical Sprue
Pathogenesis: Antibodies against Gliadin
Gliadin is presented by APCs via MHC II cells), T-helper cells mediate the
tissue damage
Exposure to gliadin, a component of gluten causes mucosal injury in loss of

Tropical

Sprue

Disaccharida
se (Lactase)
def.

Abetalipopr
ote-inemia

Cholera

villi and absorptive surface area

Duodenum* is the most affected area
Can be Immune Mediated or Genetic (HLA-DQ2 or DQ8)
Also Assoc w/: DM 1, Hashimotos Thyroiditis, Sjogren synd
Types:
Silent CD: pos serology and villous atrophy w/o symptoms
Latent CD: pos serology w/o villous atrophy
Chronic diarrhea, anemia, bloating, weight loss
Children: typical start 6 to 24 months
Dermatitis Herpetiformis (itchy, blistering) due to IgA deposition on Dermal
Papillae
Lymphocytic gastritis or colitis
Enteropathy-associated T-cell lymphoma, SB adenoCa
Dx / Clinical manifestations:
IgA anti-tissue transglutamionase or IgA/IgG anti-Gliadin in blood
IgA against-Endomysial (more specific, less sensitive)
HLA-DQ2 or HLA-DQ8 (high neg predictive value)
Flattening of Villi & Hyperplasia of Crypts
Bx Duodenal/jejunal)
Prognosis: most do well with gluten free diet. If not, consider non compliance,
refractory celiac or cancer
Dermatitis herpetiformis (itchy, blistering) in 10%
Lymphocytic gastritis or colitis
Enteropathy-associated T-cell lymphoma, SB adenoCa
Same symps as ^ but due to Parasite
Jejunium & Ileum* are most affected areas
Congenital (hereditary) lack of enzymes in infants in the Brush Border cells
Aquired Lactase deficiency occurs commonly in Native Americans and African
Americans
Symps: Osmotic diarrhea
Bacterial fermentation of unabsorbed sugar leads to increased hydrogen
production--- measured by gas chromatography of exhaled air (hydrogen
breath test)
Inborn error of metabolism AR, inability to synthesize Apolipoprotein-B
TGL gets stored in the cells causing lipid vacuolation. There is complete
absence of chylomicrons, VLDL, LDL in the plasma.
Clinical: infancy present w/ failure to thrive, diarrhea and steatorrhea
Dx: Peripheral blood smear- Burr cells ***(Acantholytic erythrocytes)

GIT #3
Infectious Enterocolitis
Vibrio cholera , G(-) comma-shaped (India, Gulf of Mexico). V
parahemoliticus (the MCC of sea-food assoc gastroenteritis in US)
Cause: Eating raw sea-food***
Clinical features:
Most are asymptomatic or mild diarrhea.
In severe cases: watery diarrhea (rice water, fishy odor) /vomiting after IP of
1-5 days. Dehydration, hypotension, shock
Dx: stool cultures. Rapid test kits
Tx: Oral or IV fluids. Doxixyclin

Campylobater
Enterocolitis

Campylobacte
r jejuni
Shigellosis

Salmonellosis

Typhoid Fever

Yersinia

Enterocolitica &
Pseudotuberculo
sis

The MC bacterial enteric pathogen in developed countries, and

important cause of traveler diarrhea
Symp: Bloody Diarrhea***
Dysentery with crypt abscesses and ulcer resembling Ulcerative colitis
Incubation period: up to 8 days
Assoc w/ Reactive Arthritis (HLA-B27)***, erythema nodosum, GuillainBarre synd
15% to 50% of pts with G-B synd have stool culture (+) for Campylobacter J.
Only 0.1% of Camp J + in stool G-B syn
Dx: watery diarrhea, flu-like prodrome, dysent(15%). Stool for culture
infection produces acute, self-limited colitis. Neutrophils can be seen within
surface and crypt epithelium and a crypt abscess is present at the lower
right.
Humans the only known reservoir
The MCC of bloody diarrhea.
Daycares, travelers to developing countries, nursing homes
Micro similar to Campylobacter. If aphtous ulcers present, may mimic Crohn
dis
IP of 4d. Self-limited about 6d with diarrhea, fever, abd pain
Dx: stool culture
Complications: Reiter synd (arthritis, urethr, conjuntivitis), Hemolytic
uremic synd (S. dysenteriae with shiga toxin)
Cant See, Cant Pee, Cant climb a Tree describes the Symps
Treat: antibiotics. NO antidiarrheal
Infections caused by salmonella spp. Typhi, (Typhoid fever) Paratyphi (TP),
and non-typhoid (S. enteritidis: food poisoning)
Clinical features: mild to profuse watery diarrhea to dysentery. Fever
resolves within 2d, but diarrhea can persists for 1wk (stool cult +)
Antibiotic therapy NOTa recommended in most cases (can prolong carrier
state or relapse). Most are self limited but complications can occur mainly in
pts with malign, alcoholic, sickle cell, and hemolyitic anemia
Caused by S. typhi (endemic) and paratyphi (travelers to India, Mexico, El
Salvador, Pakistan, Haiti, Philippines)
- Wk 1: invades Peyers patches and bacterem (blood cult best for Dx. >
90% + during febrile phase)
- Wk 2: diarrhea (pos stool cult); classic triad of bradycardia, neutropenia,
splenomegaly. Chronic carrier state d/t gallbladder colonization
Clinical features: anorexia, abd pain, N/V, bloody diarrhea short
asymptomatic phase , bacteremia, fever with flu-like symp
-Rose spots: small erythematous maculopapular lesion in chest and abd.
May mimic appendicitis
Treat: antibiotics
Complications: encephalopathy, meningitis, seizures, endocarditis,
myocarditis, pneumonia,
Pts with sickle cell are particula/ susceptible to Salmonella osteomyelitis
Enterocolitica more common than pseudotuberculosis.
Source: Seafood, Fish
Preferencially ileum, appendix, R colon
Lymph node and Peyers patch hyperplasia
When aphtous ulcers are present can be confused with Crohn dis
When regional lymph node involvement, can mimic appendicitis

Escherichia
Coli

Whipples
disease

Extraintestinal manifest: arthralgias, pharyngitis, and erythema nodosum

Complications: arthritis, Reiter synd, myocarditis, glomerulonephritis
G neg bacilli that colonize the healthy GI tract
Most are nonpathogenic
Subgroups with clinical relevance:
Enterotoxigenic E. coli (ETEC): ppal cause of travelers diarrhea.
Produces Heat-labile (LT) and Heat stable toxin (ST). Secretory
noninflammatory diarrhea, dehydration, and shock in severe cases
Enterohemorrhagic E. coli (EHEC): O:157:H7 (developed countries. Fast
foods. undercooked beef). Non-O157:H7 serotypes. Both produce shigalike toxin. Morphology and clinical like shigella (dysentery and hemolyticuremic synd)
Enteroinvasive E. coli (EIEC): no toxins. Acute self-limited colitis, most
common in children in developing countries.
Enteroaggregative E. coli (EAEC): non bloody prolonged diarrhea in
AIDS pts
Multisystemic infectious disease due to Gram-positive bacilli called
Tropheryma whippelii, which belongs to actinomycetes
- Macrophages, packed w/ PAS (+) bacilli are seen in the small intestine,
mesenteric lymph nodes, synovial membranes, heart, and other organs.
- Affects whites in their 30s. Diarrhea, weight loss, malabsorption,
polyarthalgia, generalized lymphadenopathy
- M:F = 10:1
Differential includes Mycobacterium avium intracellulare infections
Electron micrograph of one lamina propria macrophage shows these
bacilli within the cell (top) and at higher magnification (inset).

Pseudomemb. AKA antibiotic associated colitis or antibiotic associated diarrhea

Colitis
caused by the toxin from Clostridium difficile. Also Salmonella, C perfringes,
Staph aureus (food poisoning, the latter 2))
Cause: treatment with broad-spectrum antibiotics, 3 rd generation
cephalosporins, clindamycin , and ampicilin
Microscopic features
Pseudomembrane is composed of fibrin, mucin, inflammatory cells, and
cellular debris
Symps: Fever, toxicity, and diarrhea
Laboratory: C. difficile toxin assay
Tx: Metronidazole (Flagyl)
Viral Gastroenteritis
Norovirus
(previously known as Norwalk-like V). Causes half of all gastroenteritis
worldwide and is a common cause of sporadic gastroent in developed
countries. Self-limited disease
Rotavirus
MCC of severe childhood diarrhea, and diarrhea mortality worlwide.
> 6m < 2y/o. Vaccine now available
Adenovirus
2nd MCC of pediatric diarrhea. Symptoms resolve in 10d
Parasitic Enterocolitis
Ascaris
infects over a billion individuals worldwide d/t oral-fecal contamination
lumbricoides Ingested eggs hatch in the intestine and larvae penetrate intest mucosa
splanchnic circul syst circulac liver abscess or peumonitis larvae
migrate trachea swallowed and mature in intest into adult. Worm masses
induce eosinophilic response intest or biliary obstruc
Dx: detection of eggs in stool

 In industrialized and developing countries.

Adult worms migrate to the anal orifice at night. Female deposits eggs.
Perianal pruritus. Finger contamination. Human to human transmission
Dx: applying cellophane tape to the perianal skin and looking for eggs
under a microscope.
Schistosomiasi granulomatous reaction in intest, with bleeding and obstruction. Assoc with
s
Bladder Sq cell Ca in Middle East and Africa (S. hematobium)
Intestinal Cestodos
Diphyllobthriu fish tapeworm. Abd symptoms and vit B12 deficiency
m latum
Taenia solium pork tapeworm. Encysted larvae. Enlarges by formation of eggs-filled
segement (proglottids). Adult worms can grow several meters
Seizures with ring-enhancing brain lesions on CT or MRI
(cysticercosis)
Hymenolepsis one of the most common cestodes of humans in the world, only cestode that
nana
does not require intermediate host to develop into its infective stage
Protozoal causes for diarrhea
Giardia
Initially described by van Leeuwenhoeck, inventor of microscope, who
lamblia
discovered it in his own stool
- A cause of Travelers diarrhea. Also in campers, after hiking or drinking
from a stream
- Resistant to chlorine.
malabsorption syndrome; diarrhea, abdominal pain
Dx: cysts and trophozoites in feces
Amoebiasis
Flask-shaped ulcer in cecum or ascending colon
Biopsy- Erythrophagocytosis by trophs is diagnostic
Dx: cysts or trophozoites in stool
Cryptosporidiu Acute self-limited diarrhea in immunologically normal pts.
m
Chronic diarrhea in AIDS Pts***
Worldwide except Antartica
Dx: by finding the oocysts in the stool
organisms are seen as small blue spheres that appear to lay on top of the
brush border but are actually enveloped by a thin layer of host cell
cytoplasm. Most concentrated in terminal ileum and proximal colon
Enterovius
vermicularis
(pinworm)

IBS

Irritable Bowel
Synd

IBD

Irritable Bowel Dis

Common cause of GI complains

More common in female
Undefined pathogenesis
Clinical features: classic pt is anxious/neurotic, symptoms aggravated by
stress, alternating D/C, bloating, abd pain relieved by defecation, and or
mucous in the stool. Clinical criteria: abd pain or discomfort 3d/m over 3m,
improvement with defecation, and change in stool frequency or form. Also
fibromyalgia, depression,
Dx: of exclusion
Treat: avoid triggering subst( caffeine, lactose), med, and reassurance
Chronic inflammatory disorders of the gut.
Crohn's disease and ulcerative colitis are the best known forms of IBD
both fall into the category of "idiopathic
Primary Symptom: Bloody diarrhea of > 6 months often relapsing and
remitting

Crohn's

Disease

Ulcerative
colitis (UC)

Microscopic
Colitis

Diverticulosis

Lab Testing: pANCA 75% of UC, and 11% in CD

pANCA (perinuclear antineutrophil cytoplasmic antibody)
There is a bimodal incidence (teens& twenties, 50s & 60s)
increased incidence in women and persons of Caucasian race.
Morphology: any part of the GI tract, but most frequently involves the
terminal ileum, ileocecal valve, and cecum. (Terminal Ileitis & Regional
ileitis)
4 Important Features;
The transmural inflammation of the bowel
Presence of non-caseating granulomas
Inflammation leading to the development of fissures & fistulas between
loops of bowel and other structures.
Inflammation is typically segmental with uninvolved bowel separating
areas of involved bowel. Skip Lesions***, Cobblestone appearance
Diseased bowel - The serosa is granular and dull gray with mesentric fat
wrapping the bowel Creeping fat
Intestinal wall is rubbery and thick due to edema, inflammation and fibrosis.
Lumen is narrowed and X-ray shows string sign
Early disease focal mucosal ulcers Apthous ulcers
Later form longitudinal ulcers
Lab Testing: anti-Saccharomyces cerevisiae antibody (ASCA) are often
present in CD
Clinical Presentations:
Cramping abdominal pain
Watery Diarrhea (SI involvement), Bloody (Large intestine involvement)
Fever
Weight loss
Perinicious Anemia (B12 deficiency b/c illium involvement)
Generalized malabsorbtion
Enterocutaneous Fistula - Perirectal disease (fistula, fissure, abscess)
Extraintestinal manifestations of arthritis, uveitis, erythema nodosum,
and ankylosing spondylitis. PSC and pericholangitis
Increased risk for intestinal cancer (5-6 fold increase)
UC is more common in persons of Caucasian race, in women, and in young
persons (peak incidence at ages 20 - 25 years).
Morphology: involves the colon as a diffuse mucosal disease with distal
predominance.
Rectum is virtually always involved. Pancolitis. Backwash ileitis
Mucosa surface: Broad-base ulcers, pseudopolyps, and mucosal bridges
Microscopic Feature:
Crypt Abscesses***
Muscularis propria and serosa are unaffected***
Overall thickness of the bowel wall is within normal limits
Increased risk of: Colon Cancer, Sclerosing cholangitis, & bile duct
carcinoma
Chronic , nonbloody, watery diarrhea without weight loss
B-Collagenous colitis: in middle age women. Dense subepith collagen layer,
intraepith lymph, mixed infl infilt LP
C-Lymphocytic colitis: strong assoc with celiac dis and autoimmune dis
(lymphocytic gastritis)
Colonic diverticuli are protrusions of mucosa and submucosa through

a defect in the musculature of the colon.

Pathogenesis
High incidence in W countries: environmental, not genetic
Low fiber diet results in small stools which require high intraluminal
pressures for propulsion. Highest pressure occurs in the sigmoid colon. This
disordered motility results in herniations of mucosa through muscularis
propria
90% Left colon (Sigmoid, )
Crampy pain, usually LLQ , have a sense of incomplete defecation
Dx: CT scan with Barium contrast (best test to confirm)

Melanosis Coli melanotic pigment is felt to be a breakdown product of laxatives and is a

strong indicator of laxative abuse.
Dx: use Prusian Blue to stain the Iron
Hyperplastic
Polyps

Hamartomatou
s - Juvenile

Polyp

Peutz-Jeghers
Polyps/syndro
me

Inflammatory
Polyps

Polyps
These are the most common colonic polyps occuring predominantly in
rectum.
Age: After 60s & 70s
They are small (1 to 5mm.) ,typically dome shaped (Dew drop size)
Their histology is that of well formed glands with prominent infoldings giving a
serrate or saw tooth appearance
(juvenile, retention) polyps: They are hamartomatous (Haphazard Growth)
These occur more often in children below 5 yrs
SMAD4 and BMPR1A gene mutations
< 3-cm in . Peduncul. Cystic on section
Micro: cystic gland with mucin and inflamm debris
risk thyroid, breast, lung, panc adenoca
Autosomal Dominant
STK11/LKB1 gene mutation
Multiple hamartamatous polyps through out GIT (Small bowel, most) and
melanotic mucosal & cutaneous pigmentation Mouth, genitalia, palm
Large and pedunculated
Micro: Disorganized growth pattern with branching network of connective
tissue and smooth muscle lined by normal intestinal epithelium
risk for extra-intestinal carcinoma (colon, panc, thyroid, breast, lung,
gonadal, bladder
Assoc Clinical Symps: Mucocutaneous Hyperpigmentations (Lip
Pigmentation
Result from chronic cycles of injury and healing
The classical example: IP that form as part of the solitary rectal ulcer synd
Pts often present with rectal bleeding, mucus discharge, and inflammatory
lesion of the anterior rectal wall
Micro: Granulation tissue-like capillary proliferation within the lamina propria
caused by repeated erosion and re-epithelialization.

GIT #4
Colon Cancer
Neoplastic Polyps malignant risk is correlated with size, histologic architecture, and severity
(Adenomatous
of dysplasia
polyps)
Tubular adenomas pedunculated or sessile (Low Ca risk. Ca is rare in

TA < 1-cm))
Tubulo-villous adenomas (Intermediate Ca risk)
Villous adenomas often sessile (High Ca risk. 40% in SVA > 4-cm)

Familial
chromosome 5q21, APC (Adenomatous Polyposis Coli) tumor
Adenomatous
suppressor gene
Polyposis (FAP) / Precancerous: virtually 100% will develop cancer within 10 to 15 years
Familial Polyposis
Variants:
Coli (FPC)
o Gardners Syndrome
AD. High risk for colon cancer
In addition to intest polyps, osteomas of mandible/skull/long
bones, desmoid tumors, epidermal cysts, thyroid Ca.
o Turcot Syndrome AR. Familial adenomatous Polyposis with CNS
neoplasms, 2/3 medulloblastoma, 1/3 glioblastoma
o Attenuated FAP: delayed polyp development, less than 100
adenomas,and delayed appearance of colon cancer

Hereditary Non- AD.

Polyposis
Missmatch repair defect. MSH2 / MLH1 gene mutations
Colorectal Cancer Colorectal cancer with fewer polyps than FAP
(HNPCC) Lynch
In younger pts than sporadics
Syndrome
Often located in R colon
AdenoCA of Colon
Colorectal
Most Common Malignancy of GIT
Adenocarcinoma Peak age of incidence: 60 79 years (in younger person, its due to FAP or
UC)
Pathogenesis:
APC/-catenin pathway (classic adenoma-carcinoma sequence), and
the microsatellite instability pathway
CpG methylation w/o instability also exists. May have KRAS
mutations
Risks:
Low intake of unabsorbable vegetable fiber
High content of refined carbohydrates
Decrease intake of protective micronutrients (particularly vitamin A, C &
E)
Aspirin or other NSAIDs have protective effects
Clinical Features:
Right Colonic cancers brought to attention (early) because these
bulky tumors bleed; they also produce fatigue, weakness & iron def.
Anemia
Left Colonic cancers - usually detected (Late) even though they
produce prominent changes in bowel habits (diarrhea, constipation,
melena). They also cause crampy abdominal pain & occult bleeding.
Obstruction
Important tumour marker CEA
Liver the MC site of met. Also reg LN, lungs, bones

Astler-Coller Staging

Duke Staging:
Duke's A - spread into submucosa but not through muscle
Duke's B - spread through muscle but nodes negative
Duke's C - lymph node metastases present
Advantages of the Dukes classification are that it
Is simple and reproducible
Accurately reflects prognosis
Accepted nationally and internationally
Five year survival - 90%, 70% and 30% for Stages A, B and C respectively
The two most important prognostic factors are depth of invasion and the presence or
absence of lymph node metastases
Appendicial
Carcinoid
Carcinoid
Syndrome

Carcinoid Tumor
Metastasizes to Liver
Inc Serotonin:
Urinary excretion of 5-HIAA*** The most useful initial diagnostic
test for the carcinoid syndrome is to measure 24-hour urinary
excretion of 5-hydroxyindoleacetic acid (HIAA), which is the end
product of serotonin metabolism
Skin Flushing, Telengectasia, and cyanosis
GIT Diarrhea, cramps, vomiting
Asthmatic attacks With wheezing & dyspnea
Hepatomegaly
Systemic fibrosis
Heart-Valvular thickening, Endocardial fibrosis (Rt Ventricle)
Rertoperitoneal fibrosis
Collagenous pleural & intimal plaques

G.I. Lymphomas
Sporadic lymphoma Arise from B-cells of gut MALT, assoc w/ t(11;18)
(western type)
Maltomas
Sprue associated Usually lymphoma of T-cell type
lymphoma
Prognosis is poor
Age 30-40 yrs
Tend to arise from jejunum and forms ulcerative plaques and mass
Mediterranean

lymphoma
Gastric Lymphoma: The MC site of extranodal lymphomas
The MC extra-nodal marginal zone B-cell lymphoma ( MALTomas).
Low grade B-cell lymphoma
B-cell Markers: CD19(+), CD20(+), CD5(-), CD10(-)
The MC pro-lymphomatous inflammation in stomach: chronic H. pylori
infection
Acute Appendicitis
Differential Dx:
Mesenteric lymphadenitis
PID
Ectopic pregnancy
Meckels diverticulitis

Mucocoele of
Appendix
Pseudomyxoma
Peritonei

may occur simply by blockage of the lumen of the appendix with

inspissated mucus.
Other causes - mucin secreting cystadenoma or carcinoma