How do developmental anomalies affect the function of the digestive tract?
Both structural and functional
structural = anatomic development (largely 1st 3 fetal months)
e.g. cleft lip and esphagel atresia
functional = usually related to enzyme deficiency
What is dental caries and how can it be prevented?
1. Begins as bacterial plaque
2. Leads to defect in enamel
3. Deeper defects allow entry of bacteria into pulp cavity
pulpitis = bacterial infection into the root canal
periodontal disease = gingival pockets
periapical granuloma= periapical bone
What are the main complications of dental caries?
Can extend to the root canal and invoke >> periapical ganuloma
Can extend to the jaw >> osteomyelitis
What causes periodontal disease?
Colonization of periodontal pockets with bacteria.
>> plaque formation >> calcification (tartar) >> gingival inflammation >> impedes blood supply to tooth
What is stomatitis, and what are its causes?
May be result of systemic disease, but also viruses, bacteria, fungi.
C. albicans, herpes, canker sores
What is the significance of oral leukoplakia and erythroplakia?
What are the risk factors for oral cancer?
Is a complication of smoking, pipes, chewing tobacco
- also chronic alcoholism
- M > F
How does oral cancer present clinically?
What is sialadenitis, and what are its causes?
Inflammation of the salivary glands
Either infectious or immune
Infectious: most commonly staph/strep
Immune: sjogren's syndrome (infiltrates of lymphocytes and plasma cells)
How does Sjogren's disease affect the salivary glands?
Enlarges gland >> infiltrates of lymphocytes and plasma cells >> glandular insufficiency (fibrosis)
Are salivary gland tumors mostly benign or malignant?
Major glands: Most are benign
Minor glands: 50% malignant
What is the most common salivary gland tumor?
- epithelial and myoepithelial
What are the clinical signs and symptoms of esophageal disease?
- esophageal pain
May be colic (spasmodic substernal pain) or retrosternal burning (heartburn)
- aspiration regurgitation
What is esophagitis, and what are its causes?
- infection: viruses and fungi (esp immunosuppressed)
- reflux of gastric juice: LES function compromised**
- exogenous irritants: swallowing of chemicals, etc
** Pepsin and HCl >> ulceration of squamous epithelium >> gets repaired by glandular (resembles columnar epithelium) >> foci of esophageal mucosa (metaplastic glandular epithelium) = Barret's esophagus
What is a hiatal hernia, and how does it present clinically?
= displacement of the cardiac portion of the stomach from the abdominal cavity into the thoracic cavity through the diaphragmatic hiatus
What is achalasia, and what are its causes?
= spasm of the LES
dilation of the esophagus proximal to spasm >> dysphagia, usually idiopathic
What is the most common cause of esophageal varices?
-cirrhosis of the liver
- portal HTN
* Malory weiss syndrome = occurs with strenuous vomiting (often alcoholic)
What are the risk factors for esophageal cancer and how do they account for the differences in the incidence of this disease in various parts of the world?
- High incidence: China, Iran, South Africa
- 3x more common in AA
- M > F (US), M = F (INTL)
- tobacco and alcohol use
Correlate the pathologic and clinical features of esophageal carcinoma.
Most originate from lower 1/3
- grow as endophytic or exophytic
Upper/middle 1/3 = squamous cell
Lower 1/3 = adenocarcinomas
What are the main forms of gastritis?
Acute and Chronic
- self limited
- shallow mucosal defects limited to upper layers of the epithelium
(erosions = superficial, ulcers = through mucosa)
- atrophic (may have metaplasia, hyperplasia)
- predisposed to gastric cancer
What causes gastritis?
- caused by irritants or ischemia:
Curling's ulcer = assoc with burns >> bleeding
Cushing's ulcer = assoc with brain tumors >> large
- H. pylori or immune
Explain the pathogenesis of peptic ulcer, placing special emphasis on the role of gastric juice, the mucosal barrier, and H pylori?
= mucosal ulceration extending through the entire gastric epithelial layer and into the muscularis
Can occur anywhere in the GI tract, but most often duodenum or stomach.
- gastric juice
- breakdown of mucosal barrier (increased by alcohol, smoking, stress, drugs)
- H. pylori (found in most patients with ulcer)
Describe the gross and microscopic pathology of peptic ulcer and correlate these morphologic findings with the clinical signs and symptoms of the disease.
- sharply punched out
- glandular amorphous material (bottom)
- "clean" d/t Hcl (no necrotic tissue)
- surface necrotic tissue
- zone of acute/chronic inflammation
- vascular granulation tissue
- fibrous scar tissue
What are the main complications of peptic ulcer?
1. Hemorrhage: usually causes melena, large ulcers can erode arteries >> massive bleeding
2. Penetration: can erode into pancreas >> pancreatitis
3. Perforation: intestinal hole >> peritonitis
4. Cicatrization: extensive scarring >> intestinal stenosis
How common is gastric cancer in the United States in comparison with the incidence of this neoplasm in other parts of the world?
Has decreased in the US.
8x lower than Japan/Chile
Likely due to decreased nitrosamines in US food (processing). Bacteria conver nitrate > nitrites > carcinogenic nitrosamines
How does gastric carcinoma present to the naked eye examination?
- diffuse carcinoma
Where do gastric carcinomas metastasize?
To regional lymph nodes to the LIVER
also through supraclavicular nodes (Virchow's)
- abdominal organs
- bilateral ovaries (Krukenberg's tumor)
What are the clinical signs and symptoms of gastric carcinoma?
- weight loss
- loss of appetite
How is gastric lymphoma related to MALT?
The lymphomas can originate in MALT . . . often related to H. pylori infection.
*stomach = most common site
Compare atresia of the small intestine with Hirschbrung's disease.
atresia of the SI = complete obstruction of the lumen (must surgically resect)
hirschsprung's = lack of innervation (ganglion cells) >> permanent spasm. Prevents passage of feces, which accumulate proximal to the obstructed segment >> megacolon.