مواضيع المحاضرة: IBD
قراءة
عرض

Prof. Dr. Faeza Aftan

Dept of Pathology
Col of Med
Aliraqia University
Oct. 21st 2015
Small & Large Intestine IBD
Pathology of GIT- Intestine

SMALL/LARGE INTESTINE

NORMAL: Anat., Vasc., Mucosa, Endocr., Immune, Neuromuscular.
PATHOLOGY:
CONGENITAL
ENTEROCOLITIS: DIARRHEA, INFECTIOUS, OTHER
MALABSORPTION: INTRALUMINAL, CELL SURFACE, INTRACELL.
(I)IBD: CROHN DISEASE and ULCERATIVE COLITIS
VASCULAR: ISCHEMIC, ANGIODYSPLASIA, HEMORRHAGIC
DIVERTICULOSIS/-IT IS
OBSTRUCTION: MECHANICAL, PARALYTIC (ILEUS) (PSEUDO)
TUMORS: BENIGN, MALIGNANT, EPITHELIAL, STROMAL


Clinical Features
Adults, celiac disease 30 and 60 Year
silent celiac disease,
anemia (due to iron deficiency, less, B12 and folate deficiency), diarrhea, bloating, and fatigue.
Pediatric celiac disease, 6 and 24 months
dermatitis herpetiformis
Pathology of GIT- Intestine


Pathology of GIT- Intestine




Pathology of GIT- Intestine


Pathology of GIT- Intestine


Pathology of GIT- Intestine

Dermatitis Herpitiformis (DH)

T cell lymphoma,
S Int Ca.
Sq cell ca. esophagus


Causes of subtotal villous atrophy
Coeliac Dis
Giardiasis
Lymphoma
DH
Tropical sprue (Enviromental enteropathy)
AIDS
Others


Pathology of GIT- Intestine


Pathology of GIT- Intestine

Cystic Fibrosis

Lungs of a cystic fibrosis. Extensive mucous plugging the tracheobronchial tree.
The parenchyma is consolidated by both secretions &pneumonia; the greenish discoloration is the Pseudomonas infections.
Cystic fibrosis in the pancreas.
The ducts are dilated and plugged with eosinophilic mucin, and the parenchymal
glands are atrophic and replaced by fibrosis __ Pancreatic insufficiency, ___ Malabsorption


Malabsorptive Diarrhea
Irritable bowel syndrome (IBS); chronic, relapsing abdominal pain, bloating, and changes in bowel habits.
- Stress, Diet, GIT motility
- No gross or Mic abnormalities.
- Colitis, celiac disease, giardiasis, cancer, & IBD should be excluded.
The Microscopic colitis,
collagenous colitis &
lymphocytic colitis,
both cause chronic watery diarrhea.
The intestines are grossly normal, and the diseases
are identified by their histologic features.
- Ass with Celiac & Autoimmune dis.

Infectious Enterocolitis

Vibrio cholerae secretes toxin that causes massive chloride secretion, H2O follows & diarrhea.
Campylobacter jejuni .
Salmonella and Shigella spp. are invasive , dysentery.
Nontyphoid Salmonella cause ood poisoning.
S. typhi cause systemic disease (typhoid fever).
Pseudomembranous colitis ; AB allows C. difficile to grow & releases toxins, The inflammatory response volcanolike eruptions of PMN from colonic crypts that form mucopurulent pseudomembranes.
Rotavirus is the most common cause of childhood diarrhea
Parasitic and protozoal infections affect over half of the world’s population on a chronic or recurrent basis


ENTAMOEBA HISTOLYTICA
Pathology of GIT- Intestine

“please do not drink the water”.

GIARDIA LAMBLIA
Pathology of GIT- Intestine


Pathology of GIT- Intestine


Pathology of GIT- Intestine


Pathology of GIT- Intestine

“please do not drink the water”.

“Environmental (Tropical) Enteropathy
Tropical enteropathy or tropical sprue
Repeated bouts of diarrhea within the first 2 or 3 years of life
Epidemic forms in developing countries
NOT related to gluten
No single infectious agent.
RECOVERY with antibiotics


CLOSTRIDIUM DIFFICILE (ANTIBIOTIC ASSOCIATED) COLITIS
NOSOCOMIAL
CYTOTOXIN (lab test readily available)
PSEUDOMEMBRANOUS (ANTIBIOTIC ASSOCIATED) COLITIS
Pathology of GIT- Intestine




Pathology of GIT- Intestine


Clostridium difficile colitis. A, The colon is coated by tan pseudomembranes composed of neutrophils, dead epithelial cells, and inflammatory debris (endoscopic view). B, Pseudomembranes . C, Typical pattern of neutrophils emanating from a crypt is reminiscent of a volcanic eruption

BACTERIAL OVERGROWTH SYNDROME

One of the main reasons why “normal” gut flora is NOT usually pathogenic, they are constantly cleared by a NORMAL transit time
BLIND LOOPS
DIVERTICULA
OBSTRUCTION
Bowel PARALYSIS

(I) IBD

Idiopathic
females , young adults.
Western industrialized nations
- Genetic factors .
- The hygiene hypothesis;
Early in life Limit mucosal IR & loss of intestinal
epithelial barrier function
- later in life, exposure of susceptible individuals to
harmless microbes triggers inappropriate IR



Pathology of GIT- Intestine

The distinction between UC & CD is based, on

Distribution of the lesion
Morphology of disease

(I) IBD

Ulcerative Colitis
disease begins in rectum & extends proximally (no skip lesions)
does not involve small intestines
superficial mucosal involvement (not transmural)
crypt abscesses (microabscesses) and crypt distortion
Pseudopolyp
increased risk of colon cancer and toxic megacolon
Crohn Disease
transmural involvement → fissures, fistulas, and obstruction
segmental involvement (skip lesions)
may involve small intestines (regional enteritis or ileitis)
Granulomas


Ulcerative Colitis
Ulcerative proctitis or ulcerative proctosigmoiditis
Pancolitis.
Backwash ileitis.
Pseudopolyps
Toxic megacolon
Increased cancer risk
Pathology of GIT- Intestine

Active disease superf. Ulcer & hemorrhage

Pathology of GIT- Intestine

Pseudopolyps

UC
infectious enteritis
psychologic stress,
smoking cessation in some patients, and smoking may partially relieve symptoms.


Pathology of GIT- Intestine



Pathology of GIT- Intestine

Ulcerative Colitis

PSEUDOPOLYPS

Crypt Abscess

Pathology of GIT- Intestine



Pathology of GIT- Intestine


Pathology of GIT- Intestine

Ulcerative Colitis

Crohn disease
Terminal ileum, ileocecal valve, and cecum.
S. Int alone in 40% of cases;
S Int & colon are both involved in 30%
skip lesions
Cobblestone
Fissures
Fistula tracts
Strictures are common


Crohn’s Disease
Transmural inflammation
• Cobblestones
• Skip areas
Scarring and stricture formation
Fistulae
Pathology of GIT- Intestine


Pathology of GIT- Intestine


Pathology of GIT- Intestine




Pathology of GIT- Intestine


Pathology of GIT- Intestine

• Crohn’s Dis.

Pathology of GIT- Intestine



• Cobble stones
• Skip areas


Pathology of GIT- Intestine

Crohn’s Dis.Scarring and stricture formation

Pathology of GIT- Intestine

Transmural Crohn disease with submucosal and serosal granulomas (arrows).

Pathology of GIT- Intestine

Crohn’s Dis.

Pathology of GIT- Intestine


Pathology of GIT- Intestine



Pathology of GIT- Intestine

Cobblestones

Extraintestinal manifestations ;
erythema nodosum , arthritis, uveitis, pericholangitis and ankylosing spondylitis.

Indeterminate Colitis

Pathologic and clinical overlap between UC & CD.
10% of IBD patients
Colonic disease in a continuous pattern (typical UC).
However, patchy pattern, fissures, a family history of Crohn disease, perianal lesions, onset after cigarettes, or other features that are not typical of UC.
Perinuclear anti-neutrophil cytoplasmic Abs are positive in 75% of UC, but only 11% with CD.

Colitis-Associated Neoplasia

The risk of dysplasia is related to :
The frequency & severity of active disease
Duration, risk increases 8 - 10 years after disease initiation.
Pancolitis are at greater risk than those with only left-sided disease
Primary sclerosing cholangitis,


anti-TNF Ab Rx can suppress the development of colitis-associated cancers in experimental animals.




رفعت المحاضرة من قبل: Dr Faeza Aftan Zghair Alrawi
المشاهدات: لقد قام 8 أعضاء و 265 زائراً بقراءة هذه المحاضرة








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