Lecture 14 - Gastrointestinal Pathology I

Question 1

Leukoplakia

Answer 1

• type of oral cavity
• white, fixed patches on oral mucosa (infections found in those w. repressed immunity)
• histological = hyperkeratosis (keratin formation on surface) with or without underlying epithelial changes
• 3-15% undergo malignant transformation
• dentist look for this

Question 2

Sialadenitis

Answer 2

• one of the most common pathologies of salivary gland
• acute inflammation due to bacteria (most often duct obstruction)
• stone can form = sialolithiasis
• can also be caused by autoimmune disorder not associated with stone= sjorgen syndrome -> a chronic process that leads to decreased saliva = dry mouth

Question 3

Barret Esophagus

Answer 3

• replacement of the normal distal stratified squamous mucosa by metaplastic columnar epithelium containing goblet cells
• can be caused by Hiatal Hernia = complication of long standing GERD (gastroesophageal reflux disease)
• similar to intestinal metaplasia
• goblet cell produce mucous that can cause complications = ulcers, stricture
• major problem is the risk of developing adenocarcinoma

Question 4

2 types of Esophageal Carcinoma

Answer 4

1. Squamous cell

2. Adenocarcinoma

Question 5

1. Squamous Cell

Answer 5

• 90% world wide but less common in U.S.
• associated with tobacco/alcohol use and slower moving food through esophagus and toxin
• most common location is in middle third but can occur in more proximal and more distal areas

Question 6

2. Adenocarcinoma

Answer 6

• most common in U.S.

- Barrets Esophagus = precursor lesion, therefore develops in distal one third of esophagus near stomach.

Question 7

Acute vs. Chronic Gastritis

- Acute Gastritis

Answer 7

• usually transient (temporary) = flares up and goes away quickly
• Causes: Heavy use of nonsteriodal; anti-inflammatory drugs, excessive alcohol, heavy smoking, drugs, stress, infections

Question 8

Acute vs. Chronic Gastritis

- Chronic Gastritis

Answer 8

• more common of the two
• leads to metaplasia and mucosal atrophy (not likely to turn into cancer)
• Causes: heliobacter pylori (most important; can thrive in acidic pH of stomach) *Many have organism but are asymptomatic

Question 9

Gastric vs. Peptic Ulcers

- Gastric Ulcer

Answer 9

• ulcers = penetrate mucosa to submucosa
• acute gastric ulcerations = usually stress ulcers
• seen with severe trama/critical illness, chronic exposure to irritants, extensive burns (Curlings ulcers)

Question 10

Gastric vs. Peptic Ulcers

- Peptic Ulcers

Answer 10

• ulcers = penetrate mucosa to submucosa
• more common
• chronic, usually solitary
• found in regions of heavy gastric acid exposure
• 4:1 - first portion of duodenum to stomach
• Causes: H. Pylori and the mucosal exposure to acid

Question 11

Diverticulosis / Diverticulitis

Answer 11

• the state of having many diverticulum = blind pouch that communicates with lumen
• Aquired diverticula - have lack of attenuated muscularis propria
• most common location is in colon where herniations occur around areas of taeniae coli
• Complications = diverticulitis (inflammation of diverticulum); perforations (worst complication, breakage of intestine and fecal gets into peritoneal).

Question 12

Celiac Disease

Answer 12

• most common malabsorption syndrome in U.S.
• “gluten-sensitive enteropathy”
• immunologic sensitivity to gluten causes inflammation that reduces surface area which affects nutrient absorption = lymphocytic infiltrate and blunting of vili

Question 13

Inflammatory Bowel Disease

Answer 13

• chronic relapsing inflammatory disorders
• result from abnormal local immune response against normal flora of the gut and self antigens
• appears to be genetic predisposition
• Two forms: Crohns and Ulcerative Colitis

Question 14

Basic Differences between Crohns and Ulcerative Colitis

- Crohns Disease

Answer 14

• can affect any portion of GI tract (most commonly = terminal ileum)
• skip lesions, transmural involvement, fistual formation
• granulomatus inflammation
• Complications: fistuals, abdominal abscesses, intestinal strictures

Question 15

Basic Differences between Crohns and Ulcerative Colitis

- Ulcerative Colitis

Answer 15

• affects only the colon
• continous involvement (no skip lesions), superficial (mucosal/submucosal)
• no granulomas
• dysplasia sometime present
• Complications: Blood loss, associated with development of colon carcinoma

Question 16

Appendicitis

Answer 16

• affects 10% of Americans
• peak incidence in second and third decades
• Cause: obstruction (fecalith)
• Build up of mucous leads to collapse of veins -> ischemia -> bacterial proliferation
• Clinically: mild periumbilical pain, anorexia, nausea, vomiting, right lower quadrant tenderness, then pain

Question 17

Hyperplastic vs. Adenomatous Polyps

- Hyperplastic Polyps

Answer 17

• non-neoplastic (not associated with colon cancer)
• most common poly
• are sporadic
• most hyperplastic, some congenital (juvenile = hamartoma)

Question 18

Hyperplastic vs. Adenomatous Polyps

- Adenomas Polyp

Answer 18

• neoplastic polyps that result from epithelium proliferation and dysplasia (on their way to malignancy)
• 3 patterns: Tubular (less severe), Villous (more severe), tubularvillous
• malignant risk: Size - rare in less than 1 cm; high in sessile villous; severity of dysplasia (found in villous areas)

Question 19

Colorectal carcinoma

Answer 19

• increased risk if adenomas polyps
• microscopically = adenocarcinoma of varying degrees of differentiation
• two types of lesions: Proximal and Distal

Question 20

Proximal lesions

Answer 20

• tend to be polyploid/exophytic
• obstruction uncommon
• affects cecum/ascending colon
• can be silent for longer

Question 21

Distal lesions

Answer 21

• tend to be annular “napkin ring”
• tend to obstruct
• affects descending/ proximal sigmoid.