large intestine Flashcards

(38 cards)

1
Q

what is inflammatory bowel disease ?

A

Chronic condition resulting from inappropriate mucosal immune activation

Idiopathic etiology

unknown cause

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2
Q

how to distinct between ulcerative colitis and crohn disease ?

A

Regional enteritis because of frequent ileal involvement is based on :

1-Distribution of affected site

2- Morphology

Crohn disease : more general affect the entire GIT column

Ulcerative colitis : ulceration in the colon

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3
Q

what are the common features of IBD?

A

Female > males

whites

Adolescence or in young adults

Developed countries

Colonic inflammation

Similar Rx

Both have increased cancer risk

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4
Q

describe the pathogenesis of IBD ?

A

idiopathic unknown

Combination of aberrant host interaction with intestinal microbiota , intestinal epithelial dysfunction and aberrant mucosal immune responses

Normal GIT :

Unresponsive to normal intestinal microflora
Responds against ingested pathogen

IBD :

Strong immune response against normal flora

Defects in epithelial barrier function

It is thought to result from UNREGULATED AND EXAGGERATED LOCAL IMMUNE RESPONSE to commensal microbes in the gut , GENETICALLY SUSCEPTIBLE INDIVIDUALS

Failure of immune regulation
Genetic susceptibility
Environmental triggers

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5
Q

describe the immune response in IBD?

A

T cell mediated response

Particularly CD4+ T cells

Lesions are likely to be caused BY T CELLS and their products

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6
Q

describe the immune response in crohn disease ?

A

Polarization of helper T cells to TH1 type

Delayed- type hypersensitivity reaction INDUCED by IFN-Y producing T helper 1 cells

Presence of GRANULOMAS is CONSISTENT WITH TH1 RESPONSE

SO :

T helper 1 —> IFNY –> MACROPHAGES —> GRANULOMAS

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7
Q

describe the immune response in ULCERATIVE COLITIS?

A

Significant TH2 mediated component

NO GRANULOMAS

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8
Q

how do we diagnose IBD?

A

CD and UC have characteristics clinical and pathologic findings

Based on clinical history, RADIOGRAPHIC EXAMINATION, Laboratory finding, HISTOPATHOLOGY

in some cases differentiation is not possible

Autoantibodies : pANCA -> perinuclear antineutrophilic cytoplasmic antibody ) is positive in :

75% WITH Ulcerative colitis

11% —-> CROHN DISEASE

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9
Q

What is crohn disease ?

A

Idiopathic chronic regional enteritis that most commonly affects TERMINAL ILEUM

but has the potential to affect any part of GIT

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10
Q

describe the distribution of Crohn disease ?

A

Might involve the whole GIT :

From the mouth to the anus

small bowel alone –> 40% ( most common in small intestine )
colon alone —> 30%
Both sites —> 30%

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11
Q

describe the gross morphology of crohn disease ?

A

Sharply delimited and typically TRANSMURAL ( ALL LAYERS ) of the bowel by an inflammatory process with mucosal damage

Segmental with SKIP AREA lead to alternative name REGIONAL ENTERITIS —> so area with and area without INTERMITTENT

Lumen is narrowed

Mucosa FISSURING WITH COBBELESTONE APPEARANCE

Fistula and sinus : Bowl to bowel , Bowel to skin or anus

Thickening of mesentery

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12
Q

describe crohn disease HISTOPATHOLOGY?

A

Mucosal inflammation , Distortion, Ulceration

Transmural involvement ( ALL LAYERS)

Noncaseating granulomas :

Present in 50% of the cases
When present strongly favor CD
May occur in any part of bowel or adjacent lymph nodes
Absence does not EXCLUDE CD ( if no granuloma that doesnt mean its not CD )

Dysplasia and carcinoma :

Long standing disease
Less frequent compared to ulcerative colitis

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13
Q

describe the clinical presentation of Crohn disease ?

A

Intermittent attacks of relatively mild diarrhea , fever, abdominal pain

Fibrosing strictures , particularly of the terminal ileum

Fistulas to other loops of bowel or anus

EXTRAINTESTINAL MANIFESTATION —> SINCE ITS IMMUNOLOGICAL DISEASE IT WILL AFFECT OTHER SYSTEMS :

Migratory polyarthritis , Sacroiliitis , ANKYLOSING , SPONDYLITIS

Erythema NODOSUM, CLUBBING OF THE FINGERTIPS

Hepatic primary sclerosing cholangitis

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13
Q

describe the epidemiology of Crohn disease ?

A

Annual incidence in the united states around 3 per 100k

Peak ages of detection are the second and third decades

Whites appear to develop the disease 2-5 more often compared to non whites

In uas, CD occurs three to five times more often among JEWS than among non jews

Smoking IS A STRONG EXOGENOUS RISK FACTOR

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14
Q

what is ulcerative colitis ? UC

A

Ulcero inflammatory disease limited to the COLON ONLY

only affect the mucosa and submucosa ( not transmural )

Except in most severe cases

Continuous fashion and not intermittent like Crohn

Proximally from the rectum

NOOOOOOOOOO GRANULOMAS

it is systemic disorder like crohn :

migratory polyarthritis, sacroliitis , ankylosing spondylitis, Uveitis,

HEPATIC INVOLVEMENT –> pericholangitis and pirmary sclerosing cholangitis

PaNCA –> 75% of cases
Crohn was 11% cases

TH2 cells

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15
Q

describe ulcerative colitis Gross morphology ?

A

Red and granular mucosal lesions

Ulceration –> maybe confluent with regenerating mucosa forming PSEUDOPOLYPS

No mural thickening, serosal surface is usually COMPLETELY NORMAL

TOXIN MEGACOLON –> bowel wall THINS and the mucosa is SEVERE ULCERATED , MAY LEAD TO PERFORATION AND DEATH

Backwash ileitis —> INVOLVEMENT OF DISTAL ILEUM WITH EXTENSIVE DISEASE , OF LITTLE CLINICAL SIGNIFICANCE

16
Q

describe the histopathology of ulcerative colitis ?

A

Acute inflammation of crypts :

PMN infiltration of mucosa
Crypt abscess formation ( not specific for UC )

Chronic changes:

Crypt architecture distortion –> crypts may be branched or shortened

Some patients have BASAL PLASMA CELLS AND MULTIPLE BASAL LYMPHOID AGGREGATES

THIS FINDING INDICATES CHRONICITY AND HELP DISTINGUISH UC FROM INFECTION OR SELF LIMITED COLITIS

Dysplasia :

Maybe present in the long standing disease

Surveillance colonoscopy with biopsies recommended

17
Q

describe UC epidemiology ?

A

4 to 12 per 100k population

Slightly greater than CD

whites > blacks

females > males

nonsmoking is associated with UC

peak onset between ages 20 and 25

18
Q

what is the clinical presentation of UC?

A

Relapsing disorders marked by ATTACKS OF BLOODY MUCOID DIARRHEA WITH TENESUM

must be distinguished from infectious colitis

97% of patient have at least one RELAPSE during a 10 year period

30% of patients require colectomy within the FIRST 3 years of onset due to UNCONTROLLABLE DISEASE

19
Q

Describe polyps and their type?

A

most common in the colon

Sessile —> without stalks

Pedunculated : with stalks

Intestinal polys are 2 types :

Neoplastic : most common in adenoma

Non neoplastic : Inflammatory, hamartomatous , hyperplastic

if we have neoplastic then we should be afraid if its :

Very large = higher rate of malig transformation

VIllous appearance = bad

20
Q

describe non neoplastic polyps?

A

Hyperplastic polyps or INFLAMMATORY

small less than 5 mm in diameter

Usually positioned on the tops of mucosal folds

Serrated glands with increased GOBLET CELLS and NO DYSPLASIA

21
Q

describe Hamartomatous polyps ?

A

Benign tumor composed of OVERGROWTH of mature cells and tissues THAT NORMALLY OCCUR in the affected apart BUT DISORGANIZATION

22
Q

Describe juvenile polyps?

A

Most common 80%

less than 5 years of age ( IN CHILDREN )

Located in the rectum

Bleeding per rectum of prolapsed polyp

Pedunculated ( with stalk ) larger than 3 cm

Characteristics CYSTIC SPACES on cut section

Microscopic examination show the spaces to be DILATED GLANDS FILLED WITH MUCIN AND INFLAMMATORY DEBRIS

23
Q

describe PEUTZ JEGHER SYNDROME?

A

Rare, autosomal dominant condition

Multiple hamartomatous polyps scattered through out the entire GIT

Melanotic mucosal and cutaneous pigmentation : Lips , oral mucosa, face , genitalia and palmar surface of the hands

While these HAMARTOMATOUS POLYPS dont have malignant potential

patients with the syndrome have an INCREASED RISK OF DEVELOPING CARCINOMAS of PANCREAS BREAST , lung , ovary and uterus

24
what is adenoma ?
Most common and clinically important are COLONIC ADENOMAS Benign Polyps give rise to a majority of COLORECTAL ADENOCARCINOMAS Most adenomas however dont progress to adenocarcinomas 50% of adults in western world at age 50 HAVE POLYPS
25
describe adenomas?
Glandular architecture : Tubular adenomas : tubular glands Villous adenomas : villous projections --> most dangerous Tubulovillous adenoma : Mixture of the above Cancer risk : Cancer is rare in TUBULAR ADENOMAS less than 1 cm diameter The risk of cancer is HIGH --> approaching 40% in sessile villous adenomas , more than 4 cm in diameter Severe dysplasia , when present is often found in villous areas
26
what is familial adenomatous polyposis ? FAP
Autosomal dominant disorder characterized by the appearance of NUMEROUS COLORECTAL ADENOMAS BY TEENAGE YEARS 100 polyps is necessary for diagnosis of classic FAP Colorectal adenocarcinoma develops 100% of patients with UNTREATED FAP often before AGE 30 Role of total colectomy
27
what causes FAP?
Mutation of ADENOMATOUS POLYPOSIS coli gene APC ( TUMORS SUPRESSOR GENE ) chromosome 5q21
28
what lynch syndrome ?
Hereditary nonpolyposis colorectal cancer ( HNPCC) Autosomal dominant genetic condition that is associated with a high risk of colon cancer as well as other cancers Increased risk of colorectal cancer and EXTRAINTESTINAL CANCER, particularly of the endometrium Adenomas develop but cancer usually not associated with pre existing adenomas NO POLYPS cuz problem is dna repair mechanism = high of developing cancer BUT NO LARGE NUMBER OF POLYPS
29
what happens in lynch syndrome?
Mutation in DNA mismatch REPAIR GENES leading to microsatellite instability ( inactivation of DNA mismatch repair genes )
30
what is colon cancer epidemiology ?
Second only to lung cancer as cause of cancer death in US usually above 50 years less than 50 years consider polyposis syndromes or HNCC should be considered 1% to 3% of colorectal carcinomas occur in patients with familial syndromes Dietary factors : Ca incidence directly associated with calories, meat protien , dietary fat and oil Use of aspirin and other NSAIDS may be protective
31
what are 2 major types of mutations in adeno carcinoma sequence?
Activation of protoooncogen inactivation of tumor supression gene
32
describe the gross morphology of colon cancer?
Distribution : Cecum/ascending colon = 22% Transverse colon = 11% Descending colon= 6% rectum/sigmoid colon = 55% = most common Right colon : Polypoid, exophytic masses obstruction is uncommon cuz its larger Left colon : Tend to be annular , encircling lesions that produce NAPKING RING CONSTRICTION of the bowel Constipation and intestinal obstruction Diffusely infiltrating : IBD tend to be aggressive
33
describe the clinical presentation of right colon cancer?
Bulky lesions bleed readily they need to be bulky cuz the right colon is large so need to be bulky to produce symptoms may present with anemia rather than obstruction
34
describe the clinical presentation of LEFT colon cancer?
occult bleeding or obstructive symptoms more invasive at DX
35
what is the single most important prognostic indicator of colorectal carcinoma ?
Extent of the tumor at the time of diagnosis
36
whats screening test for colon cancer ?
Occult blood testing Colonoscopy --> significance of polyps Computed tomography --> virtual colonoscopy
37
describe colon cancer histopathology ?
98% are adenocarcinomas In situ cancer Intra- mucosal cancer : Tumor doesnt breach muscularis mucosa Not capable of metatasis Invasive cancer : Tumor beneath muscularis mucosa Capable of metastasis Current stagging with the TNM scheme Prognosis strongly related to the stage TNM T1,T2- --> stage 1 T3- Stage 2 N1, N2 = stage 3 M = stage 4 --> distant metastases