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.
Describe diverticula of the large intestine and their complications.
outpouching of intestinal wall
(solitary/multiple, congenital acquired)
In the colon = protrusion of the mucosa/submucosa
complications >> perforation >> pericolonic abscess, fistulas, fibrosis, bleeding
Compare hemorrhoids and intestinal angiodysplasia.
Hemorrhoids = varicosities of anal/perianal region
External = below anorectal line
Internal = above anorectal line
Angiodysplasia = localized vascular lesion (colon)
dilated thin-walled BV that anastamose between arteries/veins in mucosa/submucosa
Compare occlusive and nonocclusive ischemic bowel disease.
occlusive = caused by thrombi/emboli
thrombus often found in superior mesenteric artery. Can lead transmural infarction of intestine >> high mortality
nonocclusive = atherosclerotic narrowing of arteries
scattered multiple infarcts >> hemorrhagic patches (ulcerate and become fibrotic)
How common is inflammatory bowel disease?
Ulcerative colitis 3x more common than Crohn's
- more common in whites, Jews
- peaks 20-30 yrs/o
- family predisposition
Compare Crohn's and ulcerative colitis.
Crohn's = chronic inflammation of the terminal ileum/colon
- begins with "apthous ulcers" over peyer's patches
- shallow mucosal defects >> transmural inflammation *often assoc. with granulomas
- fibrosis of muscularis and serosa = cobblestone appearance
>> strictures, adhesions >> fistulas
What is pseudomembranous colitis?
When balance between host and intestinal flora has been lost.
e.g. c difficile after broad-spectrum antibiotics
- predominantly involves colon
- exotoxin of c diff acts on epithelial cells of the intestine >> ulcers (superficial) and focal necrosis
- ulcers covered wth layer of exudative fibrin, inflammatory cells, mucin = pseudomembranes
Compare diarrhea caused by small intestinal disease with diarrhea caused by large intestinal disease.
SI: large, watery, rarely have blood
LI: small, mucoid, commonly have blood, may have leukocytes
What are the clinical and pathologic features of acute appendicitis?
= usually caused by enterogenic bacteria that become pathogenic after obstruction of the lumen of the appendix
Bacteria become trapped >> multiply become noxious and cause ulceration
Sudden fever, leukocytosis, abdominal pain
Compare infectious and sterile peritonitis.
= bacterial invasion of abdominal cavity
- rupture of stomach, abscess
- preexisting ascites
- infection from fallopian tubes
= chemical irritation
- rupture of gallbladder
Describe the pathogenesis and pathology of acute peritonitis.
serosal surface (intestines) and parietal peritoneum are congested and edematous
** exudate contains PMNs and fibrin >> fibrous adhesions
Symptoms: sharp abd pain, rebound tenderness, guarding. Intestines become paralzyed (high mortality)
List the most common causes of intestinal obstruction.
What are the most common types of hernia?
Inguinal = most common
Inguinal: protrudes through inguinal canal or into scrotum
Femoral: occurs through femoral canal (groin)
Periumbilical: around umbilicus, ant abd wall
Diaphragmatic: through hiatus and exctends into thoracic cavity
Compare intussusception and volvulus.
intussusception = invagination of one segment of the intestine into another
compromised blood flow >> necrosis
volvulus = rotation around its mesenteric attachment site
twisting of arteries/veins >> infarction
Classify malabsorption syndromes according to their pathogenesis.
Inadequate intraluminal digestion
Primary mucosal absorptive defects
Impeded transport of nutrients
1. those that have characteristic findings
2. those that have non-specific findings
3. Those that have no pathologic findings
Compare celiac sprue and tropical sprue.
Celiac = hypersensitivity to gliadin in dietary grains
- SI shows mucosal atrophy with flattening of villi
- may develop T cell lymphoma
- affects proximal > distal intestine
Tropical = caused by bacteria
SI looks the same as Celiacs
- affects distal > proximal
- no allergy to gliadin
- responds to ABs
What are the clinical features of malabsorption syndrome?
Most prominent deficiencies = protein and lipids
protein (+ iron malabs) >> anemia
hypoalbuminemia >> edema
amenorrhea, impotence, muscle weakness
steatorrhea >> decreased vit ADKE
>> bleeding disorders
How common are intestinal neoplasms and where are they most often located?
Classify intestinal neoplasms.
What are the risk factors for intestinal neoplasms?
Genetics: polyposis syndroms (FAB or Gardners, autosomal dominant), non-polyposis colorectal cancer
Diet: red meat, fat, refined carbs, lo vegetables
Oncogenes/TSG: TP53, KRAS; dysregulation of epithelial mucosal cells
What are polyps, and how are these intestinal lesions classified?
Polyps occur as the result of accumulation of irregular cells. They protrude into the lumen of the intestine
villous or tubular
Compare neoplastic and non-neoplastic polyps.
Hyperplastic: most common, rectosigmoid area
Hamartoma: children < 5, retention polyps, peutz-jeghers (autosomal dominant)
Inflammatory: IBD, pseudopolyps
Tubular: pedunculated polyps, cuboidal epithelium
Tubulovillous: predominantly tubular that appear villous 25%
Villous: sessile, fingerlike villi, lined with single nonclassifiable cell type
What are the clinical features of large intestinal cancer?
adenocarcinomas 50x more common in the LI
Early = no symptoms
Late = chronic blood loss, constpation, pencil-like feces, hematochezia, bleeding
Compare adenocarcinomas of the right and left colon.
right = intraluminal fungating or ulcerating masses
left = napkin ring stenotic lesions
What is CEA, and what is the clinical value of this tumor marker?
CEA is normally produced by embryonic intestine. In adult not found, except for special circumstances like regenerating epithelium of ulcerative colitis.
CEA can be measured in serum . . . but is NOT useful for early detection or screening. Useful for recurrence.
How do carcinoids differ from adenocarcinoma of the large intestine?
Carcinoids = neuroendocrine tumors of low malignancy
- located in submucosa where they form small modules elevating the overlying mucosa)
- mostly small < 2cm
What is carcinoid syndrome?
When carcinoids metastasize to the liver, they release their secretory product into venous blood >>
symptoms: serotonin, bradykinin, histamine, bronchial wheezing, flushing, colic, diarrhea
Ulcerative colitis = intestinal inflammation (colon)
- starts with initial rectal lesions, spreads proximally
- mucosa with "sandpaper" appearance, prone to bleeding and infection
- atrophy of crypts + aggregate of leukocytes = crypt abcesses
- confluent ulcerations = serpiginous
- formation of pseudopolyps (residual, heavily inflamed mucosa)