Inflammation: Causes and Characteristics

Complex biological response of vascular tissues triggered by stimuli like pathogens, damaged cells, or irritants.
Purpose: removal of harmful stimuli and initiation of healing
Non-specific response serving a protective function.
Classified by the type of exudates produced
- Acute: Typically lasts less than 2 weeks
- Subacute Inflammation: Gradual onset, potential progression to chronic or severe reaction
- Chronic: Lasting for months or years

Vascular Changes:
- Vasodilation: Occurs from arteriole level, progresses to capillaries leading to increased blood flow, resulting in redness and heat
- Increased permeability: Caused by movement of plasma into tissues resulting in stasis (slowed blood flow) and swelling
Release of bradykinin: Vasoactive protein inducing vasodilation, increased vascular permeability, and pain.

Initial tissue injury: Releases chemicals like bradykinins, serotonin, lymphokines, prostaglandins, and histamine, acting as chemical messengers
Increased blood flow to the injured area
Increased capillary permeability
Leukocyte migration: Caused by chemotaxis (chemical messengers), leading to migration of white blood cells (leukocytes) to the damaged area.
- Two primary types of leukocytes involved:
  - Neutrophils: First responders to neutralize bacteria
  - Macrophages: Involved in the healing process by engulfing bacteria
Tissue regeneration: Destroyed cells are replaced by identical or similar structural and functioning cells and/or fibrous tissues.

Gastrointestinal Disorders

Group of chronic disorders:
- Crohn's disease (regional enteritis)
- Ulcerative colitis
Inflammation and/or ulceration of the bowel
Unknown cause but potential factors include:
- Environmental triggers (air pollutants)
- Food, tobacco
- Viral illness
- Genetic hereditary

Subacute and chronic inflammation of the GI tract wall affecting all layers
Commonly occurs in the distal ileum and ascending colon
Characterized by periods of remission and exacerbation
Regional enteritis/Skip lesions: Diseased bowel segments are sharply demarcated by adjoining areas of normal bowel tissue

Crypt inflammation and abscesses develop into small, focal ulcers.
Ulcers deepen into longitudinal and transverse ulcers separated by edematous patches, giving a cobblestone appearance.
Inflammation extends into the peritoneum, leading to the formation of fistulas, fissures, and abscesses.
Interference with intestinal peristalsis due to constricted lumen leads to crampy abdominal pain, tenderness, and spasm.
In advanced disease, the bowel wall thickens and becomes fibrotic (tissue dysfunction) leading to a narrowed intestinal lumen.
Diseased bowel loops may adhere to surrounding loops

Right lower quadrant pain and diarrhea not relieved by defecation
Crampy abdominal pain after meals
Anorexia, weight loss, and malnutrition due to limited food intake to prevent further abdominal pain
Nutritional deficiencies (e.g., anemia)
Chronic diarrhea
Fever and leukocytosis: Possible if inflamed intestine perforates, leading to intra-abdominal and anal abscesses
Steatorrhea (excess fat in feces)

Barium Study of the Upper GI Tract: String sign of the terminal ileum (traditional diagnostic test) .
Improved diagnostic exams: CT scan and MRI, highlight bowel wall thickening, mesenteric edema, and identify obstructions, abscesses, and fistulae.
CT scan has greater diagnostic sensitivity for Crohn's disease.