Post on 26-Nov-2015
description
GASTROINTESTINAL
TRACT PATHOLOGY
by
Mary Yvonnette C. Nerves, RMT, MD, FPSP
GIT PathologyCONGENITAL ABNORMALITIES
ESOPHAGUS
STOMACH
SMALL/LARGE BOWEL
APPENDIX
GIT PathologyCONGENITAL ABNORMALITIES
ESOPHAGUS
STOMACH
SMALL/LARGE BOWEL
APPENDIX
CONGENITAL ABNORMALITIES
Atresia/Fistulae
Diaphragmatic Hernia/
Omphalocele/Gastroschisis
Meckel’s Diverticulum
Pyloric Stenosis
Hirschsprung Disease
ATRESIA / FISTULAEAtresia is a condition in which a body orifice or
passage in the body is abnormally closed or absent
Fistula is an abnormal connection or passageway
between two epithelium-lined organs or vessels that
normally do not connect.
OMPHALOCELE (Exomphalos)
defect of the anterior abdominal wall at the
insertion of the umbilical cord
occurs in 1 in 5000 to 1 in 20,000 live births
associated with chromosomal defects,
(trisomies 13, 18, and 21), and with other
disorders such as Beckwith-Wiedemann
syndrome
OMPHALOCELE (Exomphalos)
• Closure of abdominal musculature is incomplete abdominal viscera herniate into a ventral
membranous sac
GASTROSCHISIS (Laparoschisis)
a small (generally < 5 cm) defect of the
abdominal wall just to the right of the umbilical
cord insertion, allowing evisceration of bowel
loops, stomach, and sometimes the gonads
Prevalence: 1 in 10,000 livebirths
GASTROSCHISIS (Laparoschisis)
ventral wall defect involving all layers of theabdominal wall
MECKEL DIVERTICULUM
most common type of true diverticulumoccurs in the ileumoccurs as a result of failed involution ofthe omphalomesenteric (vitelline) duct
RULE of 2s: - 2% of the pop’n- present within 2 feet of the ICV- approx. 2 inches long- 2x as common in males- symptomatic by age 2
MECKEL DIVERTICULUM
TRUE DIVERTICULUM: blind outpouching lined by mucosa that communicates with the lumen and includesall 3 layers of the bowel wall
MECKEL DIVERTICULUM
PYLORIC STENOSIS
due to progressive thickening of the circular muscle of the pylorus gastric
outlet narrowing3-4x more common in MALESgenerally presents in the 2nd or 3rd week of
life new-onset regurgitation and persistent, projectile, nonbilious vomiting
P.E. – hyperperistalsis; ovoidabdominal mass
Tx: Fredet-Ramstedt pyloromyotomy
HIRCHSPRUNG DISEASE
A.k.a. Congenital aganglionic megacolonwhen normal migration of neural crestcells from the cecum to rectum is arrested prematurely or when the ganglion cellsundergo premature deathdistal intestinal segment lacks both Meissner submucosal and the Auerbach myenteric plexus
HIRCHSPRUNG DISEASE
Clinical Features: earliest and mostcommon presentation is delayed (> 48 hrs) passage of meconium inthe newborn
- Infants and older children: chronic
constipation, abdominal distention
and vomiting
Pathologic Feature: distal narrow
aperistaltic hypertonic segment
(aganglionic) and a dilated proximal
segment caused by obstruction
Aganglionic region may have a grossly normal or contracted appearance while the normally innervated proximal colon may undergo progressive dilation
IMPERFORATE ANUS
most common formof congenital intestinal atresia
due to failure of the
cloacal diaphragm
to involute
GIT PathologyCONGENITAL ABNORMALITIES
ESOPHAGUS
STOMACH
SMALL/LARGE BOWEL
APPENDIX
ESOPHAGUS
Esophageal Obstruction
- Achalasia
Esophagitis
Barrett’s Esophagus
Esophageal Varices
Esophageal Tumors
DIVERTICULUM
an outpouching of the alimentary tract that contains one or more layers of the wallZENKER’S DIVERTICULUM (Cricopharyngeal / Pharyngoesophageal): locatedabove the UES
- results from increased intrapharyngeal
pressure in areas of weakness along the
esophageal wall
DIVERTICULUM
ZENKER’S DIVERTICULUM
Diverticulectomy with myotomy
DIVERTICULUM
TRACTION DIVERTICULUM: locatedimmediately above the UES
- located in the lower 3rd of the esophagusand in the region of the hilum of the lung
- attributed to fibrosing mediastinalprocesses or abnormal motility.
EPIPHRENIC DIVERTICULUM: immediately above the LES
- located just above the diaphragm- Cause: unclear
ESOPHAGEAL MUCOSAL WEBS
ledge-like protrusions of mucosaPathogenesis: unknownPATERSON-BROWN-KELLY or PLUMMER-VINSON SYNDROME: webs+ IDA + glossitis + cheilosis
most common in upper esophagus
ESOPHAGEAL RINGS
A.k.a. Schatzki’s / Lower esophagealEsophagogastric rings
similar to webs but are circumferentialand thicker
rings include mucosa, submucosa and, in some cases, hypertrophic muscularis propria
A rings: present in distal esophagus, above the GEJ
B rings: located at the squamocolumnarjunction of the lower esophagus
ESOPHAGEAL RINGS
ACHALASIA
A.k.a. Cardiospasm or megaesophagus
failure of the cardiac mechanism to open
when peristaltic waves conveying food
through the esophagus reach it
nearly complete loss of myenteric
ganglion cells is present in the lower 3rd
of the esophagus
TRIAD:
– Aperistalsis
– Incomplete relaxation of the LES
– Increased LES tone
• Barium swallow: dilated, aperistaltic esophagus
with a beak-like tapering at distal end
• Progressive dysphagia starting in teens
• Pathogenesis: unknown
ACHALASIA
Technique for pneumatic dilation of
achalasia.
Technique for intrasphincteric injection of
botulinum toxin for achalasia.
REFLUX ESOPHAGITISA.k.a. Gastroesophageal Reflux Disease
(GERD)
reflux of gastric contents into the lower
esophagus (most frequent cause of
esophagitis)
Most common clinical symptoms:
dysphagia, heartburn, regurgitation of
sour-tasting gastric contents
Pathogenesis: reflux of gastric juices is
central to the devt of mucosal injury
REFLUX ESOPHAGITIS
Pathogenesis:
- Conditions that decrease LES tone or
increase abdominal pressure:
a) alcohol and tobacco use, obesity
b) central nervous system depressants
c) pregnancy
d) hiatal hernia
e) delayed gastric emptying
f) increased gastric volume
REFLUX ESOPHAGITIS
Gross: marked
hyperemia with
focal hemorrhage
REFLUX ESOPHAGITIS
REFLUX ESOPHAGITISMorphology: intraepithelial eosinophils
and basal zone hyperplasia
HIATAL HERNIACharacterized by separation of the
diaphragmatic crura and protrusion of
the stomach into the thorax through the
resulting gap
VARICESTHREE common areas of portal/caval
anastomoses
Esophageal
Umbilical
Hemorrhoidal100% related to portal hypertension
Found in 90% of cirrhotics
MASSIVE, SUDDEN, FATAL hemorrhage
is the most feared consequence
VARICES
VARICES
VARICESFACTORS that lead to RUPTURE:
- inflammatory erosion of thinned
overlying mucosa
- increased tension in progressively
dilated veins
- increased vascular hydrostatic
pressure associated w/ vomiting
VARICES
VARICES
BARRETT’S ESOPHAGUSCan be defined as intestinal metaplasia of a
normally SQUAMOUS esophageal mucosa.
The presence of GOBLET CELLS in the
esophageal mucosa is DIAGNOSTIC.
SINGLE most common RISK FACTOR for
esophageal adenocarcinoma
10% of GERD patients get it
Most common in white males; between 40-
60 years of age
BARRETT’S ESOPHAGUS
GROSS: patches of red, velvety mucosaextending upward from the GEJ
INTESTINALIZED (GASTRICIZED)
mucosa is AT RISK for glandular
dysplasia.
Searching for dysplasia when
BARRETT’s is present is of utmost
importance
MOST/ALL adenocarcinomas arising in
the esophagus arise from previously
existing BARRETT’s
BARRETT’S ESOPHAGUS
BARRETT’S ESOPHAGUS
BARRETT’S ESOPHAGUS
TUMORS
BENIGN
MALIGNANT
–Squamous cell carcinoma
–Adenocarcinoma
BENIGN TUMORSLEIOMYOMAS
FIBROVASCULAR POLYPS
CONDYLOMAS (HPV)
LIPOMAS
“GRANULATION” TISSUE (PSEUDOTUMOR)
ADENOCARCINOMAArises in a background of Barrett esophagus & long-standing GERD
RISK FACTORS: documented dysplasia
tobacco use
obesity
prior radiation therapy
FACTORS that DECREASE RISK:
- diet rich in fresh fruits and vegetables
- H. pylori serotypes
Most frequent in CAUCASIANS; M > F
Usually occur in the distal 3rd of the esophagus
ADENOCARCINOMA
ADENOCARCINOMA
ADENOCARCINOMA
ADENOCARCINOMA
ADENOCARCINOMA
SQUAMOUS CELL CARCINOMA
Adults over age 45, affects MALES 4x
more than females
RISK FACTORS:
a) alcohol and tobacco use
b) caustic esophageal injury
c) achalasia
RISK FACTORS: d) Plummer-Vinson syndromee) frequent consumption of very hot
beveragessixfold more common in African-American
SQUAMOUS CELL CARCINOMA
Half of SCCs occur in the middle 3rd
of the esophagus
Begins as an in-situ lesion
(SQUAMOUS DYSPLASIA)
SQUAMOUS CELL CARCINOMA
SQUAMOUS CELL CARCINOMA
• DYSPLASIAIN-SITUINFILTRATION
SQUAMOUS CELL CARCINOMA
Adenocarcinoma
• Commonest type in US
• Risk factor: Barrett esophagus
• Distal 1/3 of esophagus
• Symptoms: insidious onset; late obstruction
Squamous cell Carcinoma
• Commonest type worldwide
• Risk factors: esophagitis, smoking, alcohol, genetics
• Middle 1/3 of esophagus
• Symptoms: insidious onset; late obstruction
FACTORS that influence survival:1. Sex – F > M2. Stage – In situ, mucosal CA, superficial CA > deeper tumors3. LN mets – 2 or more involved nodes:
worse prognosis4. Other microscopic findings: vascular/lymphatic
invasion & marked tumor necrosis5. Involvement of circumferential surgical margins high probability of recurrence6. Overexpression of EGFR/p53 – worse prognosis
ESOPHAGEAL CARCINOMA
GIT PathologyCONGENITAL ABNORMALITIES
ESOPHAGUS
STOMACH
SMALL/LARGE BOWEL
APPENDIX
STOMACH
CHRONIC GASTRITIS
PEPTIC ULCER
GASTRIC POLYPS
HYPERTROPHIC GASTROPATHY
TUMORS
CHRONIC GASTRITISH. pylori gastritis: most common
cause of chronic gastritis
Autoimmune gastritis: most common
cause of atrophic gastritis and most
common cause of chronic gastritis in
patients w/o H. pylori infection
CHRONIC GASTRITISH. pylori gastritis:
- H. pylori: spiral shaped or curved
bacilli
- present in almost ALL duodenal
ulcers & majority of individuals with
gastric ulcers or chronic gastritis
- present in 90% of individuals w/
chronic gastritis affecting the
ANTRUM
CHRONIC GASTRITISH. pylori gastritis:
- increased acid secretion may result in
PUD
- H. pylori infection confers increased
risk of gastric Ca
- H. pylori transmission: oral-oral; fecal-
oral; and environmental spread
CHRONIC GASTRITISH. pylori gastritis:
- 4 Features linked to H. pylori virulence:
a) Flagella – allow motility in viscous
mucus
b) Urease – generates NH3 from
endogenous urea & elevates local
gastric pH
c) Adhesins – enhance bacterial adherence
to surface foveolar cells
d) Toxins – cytotoxin-assoc gene A (cagA) –
involved in ulcer & cancer devt
CHRONIC GASTRITISAutoimmune gastritis: spares the
antrum and includes hypergastrinemia
- char by:
a) Abs to parietal cells & IF
b) Reduced serum pepsinogen I conc
c) Antral endocrine cell hyperplasia
d) Vit. B12 def.
e) defective gastric acid secretion
(achlorhydria)
CHRONIC GASTRITISAutoimmune gastritis:
- Pathogenesis: loss of parietal cells
(responsible for secretion of gastric
acid and IF)
loss of gastric acid stimulates
gastrin release hypergastrinemia &
hyperplasia of antral gastrin-
producing G cells
Lack of IF disables ileal vit. B12
abs. B12 def. megaloblastic
anemia
CHRONIC GASTRITISAutoimmune gastritis:
- Morphology:
Diffuse atrophy
Intestinal metaplasia
Antral endocrine hyperplasia
GASTRITISH. PYLORI-ASSOCIATED AUTOIMMUNE
LOCATION antrum body
INFLAM INFILTRATE PMNs, subepith plasma cells Lymphocytes, macrophages
ACID PRODUCTION Increased to sl. decreased Decreased
GASTRIN Normal to decreased Increased
OTHER LESIONS Hyperplastic/inflam polyps Neuroendocrinehyperplasia
SEROLOGY Abs to H. pylori Abs to parietal cells
SEQUELAE Peptic ulcer, adenoCA Atrophy, PA, AdenoCA, carcinoid tumor
ASSOCIATIONS Low socioeconomic status, poverty, residence in rural areas
Autoimmune disease; thyroiditis, DM, Graves dse
COMPLICATIONS of CHRONIC GASTRITIS
Peptic Ulcer Disease
Mucosal atrophy and intestinal
metaplasia
Dysplasia
PEPTIC ULCER DISEASE• Most often associated with H. pylori-
hyperchlorhydric chronic gastritis
• Present in 85-100% persons with duodenal ulcers and 65% with gastric ulcers
PEPTIC ULCER DISEASEPathogenesis: imbalances of mucosal
defenses and damaging forces that
cause chronic gastritis
H. pylori & NSAID use: primary
underlying cause of PUD
Gastric hyperacidity:
- H. pylori infection, parietal cell hyperplasia,
excessive secretory responses or impaired
inhibition of stimulatory mechanisms such as
gastrin release
PEPTIC ULCER DISEASECommon co-factors in peptic
ulcerogenesis:
- chronic NSAID use: direct chemical
irritation & suppress PG release necessary
for mucosal protection
- Cigarette smoking: impairs mucosal blood
flow & healing
- high-dose corticosteroids: suppress PG
synthesis & impair healing
Solitary in > 80% of patients
< 0.3 cm. – shallow ulcers
> 0.6 cm. - deeper ulcers
Round or oval, sharply
punched-out defect –mucosal surface
overhang the base
(heaped up margins
cancer)
PEPTIC ULCER DISEASE
Gnawing, burning, aching pain, epigastric
Fe deficiency anemia
Acute hemorrhage
Penetration, perforation:
Pain in BACK
Pain in CHEST
Pain in LUQ
MALIGNANT TRANSFORMATION – very
rare
PEPTIC ULCER DISEASE
COMPLICATIONS of Gastric Ulcers
Bleeding–Occurs in 15% to 20% of patients
–Most frequent complication
–May be life-threatening
–Accounts for 25% of ulcer deaths
–May be the first indication of an ulcer
Perforation–Occurs in about 5% of patients
–Accounts for two thirds of ulcer deaths
–Rarely, is the first indication of an ulcer
COMPLICATIONS of Gastric Ulcers
Obstruction from edema or scarring–Occurs in about 2% of patients
–Most often due to pyloric channel ulcers
–May also occur with duodenal ulcers
–Causes incapacitating, crampy abdominal pain
–Rarely, may lead to total obstruction with intractable vomiting
COMPLICATIONS of Gastric Ulcers
MUCOSAL ATROPHY and INTESTINAL METAPLASIA
• Strongly associated with increased risk of gastric adenoCA
• The risk of adenoCA is greatest in autoimmune gastritis
Chronic gastritis exposes epith to
inflam-related free radical damage &
proliferative stimuli genetic
alterations
Morphologic HALLMARKS:
a) Variations in epithelial size, shape and
orientation
b) coarse chromatin texture
c) hyperchromasia and nuclear enlargement
DYSPLASIA
HYPERTROPHIC GASTROPATHY
Rugal prominence (cerebriform)
No inflammation
Hyperplasia of mucosa
HYPERTROPHIC GASTROPATHY
Ménétrier disease: resulting from profound hyperplasia of the surface mucous cells with accompanying glandular atrophy, ass. w/ CMV, H. Pylori, ↑TGF-α
Hypertrophic-hypersecretory gastropathy: associated with hyperplasia of the parietal and chief cells within gastric glands
(normal gastrin)
MENETRIER DISEASE
HYPERTROPHIC GASTROPATHY
Gastric gland hyperplasia secondary to
excessive gastrin secretion, in the setting
of a gastrinoma (Zollinger-Ellison syndrome)
ZOLLINGER-ELLISON SYNDROME
GASTRIC POLYPSPolyps: nodules or masses that project
above the level of the surrounding
mucosa
Inflammatory and Hyperplastic Polyps:
approx. 75% of all gastric polyps
usually develop in assoc with chronic
gastritis
Gross: majority are smaller than 1 cm. &
frequently multiple; ovoid w/ smooth
surface
HYPERPLASTIC
POLYP
Micro: irregular,
cysticaly dilated
and elongated
foveolar glands
GASTRIC POLYPSFundic Gland Polyps:
occur sporadically and in individuals w/
familial adenomatous polyposis
5x more common in females (ave. 50 y/o)
occur in the gastric fundus
Gross: well-circumscribed & smooth
Micro: cystically dilated, irregular glands
lined by flattened parietal or chief cells
GASTRIC POLYPSGastric adenoma:
almost always occur on a background of
chronic gastritis with atrophy and
intestinal metaplasia
3x more common in males (50-60 y/o)
increased incidense in pts w/ FAP
Risk of adenoCA is related to the size of
the lesion (> 2 cm.)
CA may be present in up to 30% of gastric
adenomas
GASTRIC POLYPSGastric adenoma:
most commonly located in antrum
Gross: solitary, < 2 cm.
Micro: ALL GI adenomas have epithelial
dysplasia
CARCINOMAPathogenesis: closely related to environmental factors
Arise from the generative or basal cells of the foveolae, on a background of chronic atrophic gastritis w/ intestinal metaplasia and preceded by various stages of dysplasia, CIS, and superficial CA
Accompanied by hypochlorhydria in 85-90% of cases
CARCINOMA(2) Major categories of gastric adenocarcinoma:
a. INTESTINAL-TYPE
- arise from metaplasticepithelium
B. DIFFUSE-TYPE
- best represented by linnitisplastica or signet ring(adeno)carcinoma
ADENOCARCINOMAGROWTH PATTERNS
LINITIS PLASTICA
LINITIS PLASTICA
ADENOCARCINOMADepth of invasion & extent of nodal and distant metastasis at time of diagnosis: MOST powerful prognostic indicators for gastric cancers
Advanced CA: first detected as mets to the supraclavicular sentinel LN (Virchow’s node)
Sister Mary Joseph nodule: marker of metastatic CA
- subcutaneous nodule in periumbilicalregion
GASTRIC CARCINOMAFACTORS related to prognosis:
1. Patient’s age – CA in the young: worse
2. Tumor stage – the deeper the penetration, the greater the chance of mets; polypoid, large intraluminal tumors have lower mets < tumorsgrowing within the wall
3. Location within the stomach: 80% of 5-yr survivors, the lesion is in the distal half of the stomach
4. Tumor margins: pushing/expanding border vs. Diffuse infiltration
GASTRIC CARCINOMAFACTORS related to prognosis:
5. Microscopic type and grading – intestinal
type > diffuse type
6. Inflammatory reaction: cellular infiltrate at
the interface bet tumor & normal tissue: GOOD
px sign
7. Perineural invasion: poor px
8. Regional LN involvement: if NEG, >50% may
survive for 5 years
GASTRIC CARCINOMAFACTORS related to prognosis:
9. Type of surgery – radical subtotal
gastrectomy: best survival
10. Overexpression of c-erbB2 protein, p53 –
poor prognosis
11. Detection of cathepsins and cyclin-
dependent kinase inhibitor (p27Kip1)
expression by IHC: reduced survival
LYMPHOMA5% of gastric malignancies
Most common are extra-nodal marginal zone
B-cell lymphomas (lymphoma of mucosa-
associated lymphoid tissue or MALToma)
Pathogenesis: Usually arise at sites of chronic
inflammation
- pro-lymphomatous inflam: H. Pylori infection
- translocations: t(11;18)(q21;q21) most
common activation of NF-kB, a transcription
factor that promotes B cell growth & survival
LYMPHOMAMicro: dense lymphocytic infiltrate in the
lamina propria lymphoepithelial lesions
- express B cell markers CD19 and CD20
Clinical Features: most common presenting
symptoms dyspepsia & epigastric pain
CARCINOID TUMORArise from the diffuse components of the
endocrine system
Gross: intramural or submucosal masses that
create small polypoid lesions
CARCINOID TUMORMicro: islands, trabeculae, strands, glands, or
sheets of uniform cells with scant, pink
granular cytoplasm and a round to oval,
stipples nucleus
CARCINOID TUMORImmuno: (+) for endocrine granule markers
(synaptophysin and chromogranin A)
The MOST important prognostic factor for GI
carcinoid tumors is LOCATION
Foregut carcinoid tumors RARELY
METASTASIZE
G.I.S.T. Can behave and/or look benign or
malignant
Usually look like smooth muscle, i.e.,
“stroma”, “spindly”
tumor cells are derived from the
interstitial cells of Cajal, a “neural”
type of cell, similar to the neural plexi
found in the intestines (pacemaker
cells for gut peristalsis)
G.I.S.T. Pathogenesis: 75-80% of all GISTS
have oncogenic, gain-of-function
mutations of the gene encoding the
tyrosine kinase c-KIT (receptor for
stem cell factor)
Gross: solitary, well-circumscribed,
fleshy mass
G.I.S.T.
G.I.S.T.
Spindle cell type
Epithelioid type
G.I.S.T.
CD 117
G.I.S.T. Can behave and/or look benign or
malignant
Usually look like smooth muscle, i.e.,
“stroma”, “spindly”
Are usually POSITIVE for c-KIT
(CD117)
tumor cells are derived from the
interstitial cells of Cajal, a “neural”
type of cell, similar to the neural plexi
found in the intestines.
G.I.S.T.
G.I.S.T.
G.I.S.T.
CD 117
GIT PathologyCONGENITAL ABNORMALITIES
ESOPHAGUS
STOMACH
SMALL/LARGE BOWEL
APPENDIX
SMALL/LARGE INTESTINE
INFLAMMATORY BOWEL DISEASE
Crohn’s Disease
Ulcerative Colitis
OBSTRUCTION
TUMORS
IBD
CROHN’S DISEASE (granulomatous
colitis)
ULCERATIVE COLITIS
IBD DIFFERENCES
Crohn’s disease Ulcerative colitis
CHROHN’S DISEASE
CHROHN’S DISEASE
CHROHN’S DISEASE
ULCERATIVE COLITIS
ULCERATIVE COLITIS
ULCERATIVE COLITIS
OBSTRUCTION
Small Intestine – most often involved
Clinical manifestations:
- abdominal pain & distention, vomiting and constipation
OBSTRUCTIONANATOMY– ADHESIONS (post-surgical)
– IMPACTION
– HERNIAS
– VOLVULUS
– INTUSSUSCEPTION
– TUMORS
– INFLAMMATION, such as IBD (Crohn) or diverticulitis
– STRICTURES/ATRESIAS
– STONES, FECALITHS, FOREIGN BODIES
– CONGENITAL BANDS, MECOMIUM, INPERF. ANUS
OBSTRUCTION
HERNIAS
Any weakness in the wall of the peritoneal cavity that permits protrusion of a serosa-lined pouch of peritoneum (hernial sac)
Acquired hernias: most commonly occur anteriorly via the femoral and inguinal canal or umbilicus or sites of surgical scars visceral protrusion
(external herniation)
HERNIAS
ADHESIONS
Surgical procedures, infection or other causes of peritoneal inflam (eg. Endometriosis) adhesions between bowel segments, abdominal wall & operative sites fibrous bridges create closed loops internal herniation
INTUSSUSCEPTIONA length of intestine (intussuscipiens)
literally swallows part of the bowel just
proximal to it (intussusceptum)
most cases are seen during the first 5
yrs of life
Infants & children: rotavirus infection
Older children and adults: intraluminal
mass or tumor serves as point of traction
PHYSIOLOGY– ILEUS, esp. postsurgical
– INFARCTION
– MOTILITY DISEASES, esp., HIRSCHSPRUNG DISEASE
OBSTRUCTION
TUMORS
NON-NEOPLASTIC (POLYPS)
BENIGN
MALIGNANT
POLYPS
Inflammatory Polyps
- forms as a result of chronic cycles of
injury and healing
POLYPS
Hamartomatous Polyps
- occur sporadically
- hamartoma: tumor-like growths of
mature tissues that are normally
present at the site in which they
develop
- assoc w/ genetically determined or
acquired syndromes
POLYPS
Juvenile Polyp
- focal malformations of the mucosal
epith & lamina propria
- majority occur in children <5 y/o
- majority are located in rectum
rectal bleeding
Juvenile (retention) polyp.
Note the ulcerated, highly
hyperemic surface.
POLYPS
Hyperplastic Polyp
- epithelial proliferations discovered in
the 6th and 7th decades of life
- Pathogenesis: decreased epith
turnover & delayed shedding of surface
epith cells piling up of goblet &
absorptive cells
- NO malignant potential
Gross appearance of multiple
hyperplastic polyps. The lesions are
characteristically small, sessile, and
pale.
Microscopic appearance of hyperplastic
polyp. The individual glands show a
typical serration of their mid portion.
POLYPS
Neoplastic Polyp (Adenomas)
- precursors to the majority of
colorectal adenocarcinomas
- char by the presence of epithelial
dysplasias
POLYPS
Sessile polyp Pedunculated polyp
POLYPSNeoplastic Polyp (Adenomas)
- Micro: HALLMARK of epithelial
dysplasia nuclear hyperchromasia,
elongation and stratification
- classified as TUBULAR,
TUBULOVILLOUS OR VILLOUS
Adenomatous polyp showing marked contrast between the dysplastic glands
of the polyp and adjacent normal glands.
Microscopic appearance of
villoglandular polyp. There is an
admixture of villous and
glandular structures.
ADENOCARCINOMA
Most common malignancy of the GIT
Dietary factors assoc w/ increased risk:
low intake of unabsorbable vegetable
fiber & high intake of refined CHOs &
fat
Pathogenesis: APC/Beta-catenin
pathway and microsatellite instability
pathway
GROWTH PATTERNSPOLYPOID: proximal colon
ANNULAR, CONSTRICTING: distal colon
DIFFUSE
Polypoid pattern of growth in a rectal lesion.Cake-like configuration with
central ulceration.
Deeply penetrating and ulcerated
tumor.
Moderately differentiated colonic
adenocarcinoma.
Polypoid pattern of growth in a rectal lesion.Cake-like configuration with
central ulceration.
Gross appearance of signet ring carcinoma. This tumor type is highly malignant,
narrows the lumen, and has a pebbly mucosal surface and thickened muscular
wall.
Stage A tumors invade through the muscularis
mucosae into the submucosa but do not reach the muscularis propria
Stage B1 tumors invade into the muscularis propria
Stage B2tumors completely penetrate the smooth
muscle layer into the serosa
Stage Ctumors encompass any degree of
invasion but are defined by regional lymph node involvement
Stage C1 tumors invade the muscularis propria with fewer than four positive nodes
Stage C2tumors completely penetrate the smooth muscle layer into the serosa with four or
more involved nodes
Stage D lesions with distant metastases
Carcinoma in situ
(may be referred to as high grade dysplasia) – intramucosal carcinoma that does not penetrate the muscularis
mucosae
Dukes’ Classification (Astler-Coller modification)
Tumor Stage Histologic Features of the Neoplasm
Tis Carcinoma in situ (high-grade dysplasia) or intramucosal carcinoma (lamina propria invasion)
T1 Tumor breaches the musc. Muc. invades into submucosa
T2 Extending into the muscularis propria but not penetrating through it
T3 Penetrating through the muscularis propria into subserosa
T4 Tumor directly invades other organs or structures
Nx Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Metastasis in 1 to 3 lymph nodes
N2 Metastasis in 4 or more lymph nodes
Mx Distant metastasis cannot be assessed
M0 No distant metastasis
M1 Distant metastasis
TNM Staging
COLORECTAL CARCINOMAClinical:
- Right-sided: fatigue & weakness due to
IDA
- Left-sided: occult bleeding, changes in
bowel habits or cramping LLQ
discomfort
- Most important prognostic factors:
depth of invasion & +/- LN mets
COLORECTAL CARCINOMAFACTORS related to prognosis:
1. Patient’s age – very young and very old: poor px
2. Sex – better px: F > M
3. CEA serum levels > 5.0 ng/ml
4. Tumor location: favorable px - lesions located in the left colon > lesions in sigmoid colon and rectum
5. Local extent – focal microscopic CA in a polyp/tumor restricted to mucosa & submucosa: good px
COLORECTAL CARCINOMAFACTORS related to prognosis:
6. Obstruction – poor px
7. Perforation – poor px
8. Tumor margins & inflammatory reaction –better px
9. Vascular/perineural invasion: poor px
10. Microscopic tumor type – Mucinous CA, signet ring CA and anaplastic CA: worse px
11. LN involvement - > 6 LNs: <10% survive >5 yrs.
HEMORRHOIDS
Develop secondary to persistently elevated
venous pressure w/in the hemorrhoidal
plexus
Most common predisposing influences:
straining at stool fr constipation & venous
stasis of pregnancy
Pathogenesis: variceal dilatations of anal &
perianal venous plexus that forms collaterals
that connect portal & caval venous systems
to relieve venous HPN
HEMORRHOIDS
External hemorrhoids: collateral vessels w/in
the inferior hemorrhoidal plexus located
below the anorectal line
Internal hemorrhoids: dilatation of the
superior hemorrhoidal plexus within the
distal rectum
HEMORRHOIDS
Micro: thin-walled, dilated, submucosal vessels that
protrude beneath the anal or rectal mucosa
HEMORRHOIDS
ANAL CARCINOMAS
MORE LIKELY TO BE SQUAMOUS, or “basaloid”
F > M (3:1)
Worse in prognosis
HPV – related (HPV16)
ANAL CARCINOMAFACTORS related to prognosis:
1. Tumor stage– depth of invasion & regional
LN involvement; inguinal LN involvement
(grave px sign)
2. Tumor size – inversely related to px
3. Tumor recurrence - tumor recurrence in the
pelvic or perineal regions following APR:
ominous px
GIT PathologyCONGENITAL ABNORMALITIES
ESOPHAGUS
STOMACH
SMALL/LARGE BOWEL
APPENDIX
ACUTE APPENDICITISA normal TRUE DIVERTICULUM of the cecum
GENERALLY, a disease of YOUNGER people
Pathogenesis: OBSTRUCTION by FECALITH
the classic cause but fecaliths present only
about half the time
- Other causes: gallstones, tumor, mass of
worms eg. O. vermicularis
- Ischemic injury & stasis of luminal contents
bacterial proliferation trigger inflam
response eg. tissue edema, PMN infiltration
ACUTE APPENDICITISDDx:
- mesenteric lymphadenitis (sec. to
unrecognized Yersinia infection or viral
enterocolitis)
- acute salpingitis
- ectopic pregnancy
- mittelschmerz (pain fr minor pelvic bleeding
during ovulation)
- Meckel diverticulitis
ACUTE APPENDICITIS
ACUTE APPENDICITISEARLY APPENDICITIS:
NEUTROPHILSMucosa, submucosa
NEED NEUTROPHILS in the MUSCULARIS to
confirm the DIAGNOSIS
Classic clinical finding: MCBURNEY’S SIGN
Perforationperitonitis the rule, if no surgery
Perforationperitonitis the rule, if no surgery
Complications: perforation, pyelophlebitis,
portal venous thrombosis, liver abscess and
bacteremia
ACUTE APPENDICITIS
TUMOR
Carcinoid: most common
- incidental finding
- most frequent location: DISTAL TIP
- distant spread: rare
Mucocele (common): obstructed
appendix w/ inspissated mucin
Mucinous Cystadenoma (rather rare)
Mucinous Cystadenocarcinoma (rare)
- invasion of wall peritoneal implants
MUCOCELECOMMON CYST on APPENDIX filled with MUCIN
Can RUPTURE to become:
PSEUDOMYXOMA PERITONEI
(mucinous ascites and mucinous tumordisseminated on peritoneal surfaces)
MUCOCELE
MUCOCELE
MUCINOUS CYSTADENO(CARCINO)MA
MUCINOUS CYSTADENO(CARCINO)MA
Have a nice day!