GI

Question 1

How do developmental anomalies affect the function of the digestive tract?

Answer 1

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

e.g. abetalipoproteinemai

Question 2

What is dental caries and how can it be prevented?

Answer 2

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

Question 3

What are the main complications of dental caries?

Answer 3

Can extend to the root canal and invoke >> periapical ganuloma

Can extend to the jaw >> osteomyelitis

Question 4

What causes periodontal disease?

Answer 4

Colonization of periodontal pockets with bacteria.

>> plaque formation >> calcification (tartar) >> gingival inflammation >> impedes blood supply to tooth

Question 5

What is stomatitis, and what are its causes?

Answer 5

May be result of systemic disease, but also viruses, bacteria, fungi.

C. albicans, herpes, canker sores

Question 6

What is the significance of oral leukoplakia and erythroplakia?

Answer 6

Cancerous

Question 7

What are the risk factors for oral cancer?

Answer 7

• Is a complication of smoking, pipes, chewing tobacco*
• also chronic alcoholism
• M > F

Question 8

How does oral cancer present clinically?

Answer 8

• leukoplakia
• eyrthoplakia
• ulcer
• crater
• nodule/plaque

Question 9

What is sialadenitis, and what are its causes?

Answer 9

Inflammation of the salivary glands

Either infectious or immune

Infectious: most commonly staph/strep

Immune: sjogren’s syndrome (infiltrates of lymphocytes and plasma cells)

Question 10

How does Sjogren’s disease affect the salivary glands?

Answer 10

Enlarges gland >> infiltrates of lymphocytes and plasma cells >> glandular insufficiency (fibrosis)

Question 11

Are salivary gland tumors mostly benign or malignant?

Answer 11

**Major glands: **Most are benign

**Minor glands: **50% malignant

Question 12

What is the most common salivary gland tumor?

Answer 12

• pleomorphic adenoma*
• • *benign
• epithelial and myoepithelial

Question 13

What are the clinical signs and symptoms of esophageal disease?

Answer 13

- dysphagia

- esophageal pain
May be colic (spasmodic substernal pain) or retrosternal burning (heartburn)

- aspiration regurgitation

Question 14

What is esophagitis, and what are its causes?

Answer 14

• 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

Question 15

What is a hiatal hernia, and how does it present clinically?

Answer 15

= displacement of the cardiac portion of the stomach from the abdominal cavity into the thoracic cavity through the diaphragmatic hiatus

causes GERD

Question 16

What is achalasia, and what are its causes?

Answer 16

= spasm of the LES

dilation of the esophagus proximal to spasm >> dysphagia, usually idiopathic

Question 17

What is the most common cause of esophageal varices?

Answer 17

Caused by

• cirrhosis of the liver
• portal HTN

* Malory weiss syndrome = occurs with strenuous vomiting (often alcoholic)

Question 18

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?

Answer 18

• High incidence: China, Iran, South Africa
• 3x more common in AA
• M > F (US), M = F (INTL)
• tobacco and alcohol use

Question 19

Correlate the pathologic and clinical features of esophageal carcinoma.

Answer 19

Most originate from lower 1/3

• grow as endophytic or exophytic

Histology

Upper/middle 1/3 = squamous cell

Lower 1/3 = adenocarcinomas

Question 20

What are the main forms of gastritis?

Answer 20

Acute and Chronic

Acute

• self limited
• shallow mucosal defects limited to upper layers of the epithelium
  (erosions = superficial, ulcers = through mucosa)

Chronic

• atrophic (may have metaplasia, hyperplasia)
• predisposed to gastric cancer

Question 21

What causes gastritis?

Answer 21

Acute

- caused by irritants or ischemia:

Curling’s ulcer = assoc with burns >> bleeding

Cushing’s ulcer = assoc with brain tumors >> large

Chronic

- H. pylori or immune

Question 22

Explain the pathogenesis of peptic ulcer, placing special emphasis on the role of gastric juice, the mucosal barrier, and H pylori?

Answer 22

= 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.

Causes

• gastric juice
• breakdown of mucosal barrier (increased by alcohol, smoking, stress, drugs)
• H. pylori (found in most patients with ulcer)

Question 23

Describe the gross and microscopic pathology of peptic ulcer and correlate these morphologic findings with the clinical signs and symptoms of the disease.

Answer 23

Appear

• sharply punched out
• glandular amorphous material (bottom)
• “clean” d/t Hcl (no necrotic tissue)

Histology

• surface necrotic tissue
• zone of acute/chronic inflammation
• vascular granulation tissue
• fibrous scar tissue

Question 24

What are the main complications of peptic ulcer?

Answer 24

**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

Question 25

How common is gastric cancer in the United States in comparison with the incidence of this neoplasm in other parts of the world?

Answer 25

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*

Question 26

How does gastric carcinoma present to the naked eye examination?

Answer 26

1. superficial 2. polypoid 3. ulcerated 4. diffuse carcinoma

Question 27

Where do gastric carcinomas metastasize?

Answer 27

**To regional lymph nodes to the LIVER** * also through supraclavicular nodes (Virchow's)* * - abdominal organs* * - lungs* * - bilateral ovaries (Krukenberg's tumor)*

Question 28

What are the clinical signs and symptoms of gastric carcinoma?

Answer 28

**_Nonspecific signs:_** - weight loss - anemia - weakness * *_Local signs:_** - gastritis - vomiting - loss of appetite - dysphagia - bleeding

Question 29

How is gastric lymphoma related to MALT?

Answer 29

The lymphomas can originate in MALT . . . often related to H. pylori infection. \*stomach = most common site

Question 30

Compare atresia of the small intestine with Hirschbrung's disease.

Answer 30

**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.

Question 31

Describe diverticula of the large intestine and their complications.

Answer 31

**outpouching of intestinal wall** (solitary/multiple, congenital acquired) In the colon = protrusion of the mucosa/submucosa complications \>\> perforation \>\> pericolonic abscess, fistulas, fibrosis, bleeding

Question 32

Compare hemorrhoids and intestinal angiodysplasia.

Answer 32

**_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*

Question 33

Compare occlusive and nonocclusive ischemic bowel disease.

Answer 33

**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)*

Question 34

How common is inflammatory bowel disease?

Answer 34

Ulcerative colitis 3x more common than Crohn's - more common in whites, Jews - peaks 20-30 yrs/o - family predisposition

Question 35

Compare Crohn's and ulcerative colitis.

Answer 35

**_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

Question 36

What is pseudomembranous colitis?

Answer 36

*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

Question 37

Compare diarrhea caused by small intestinal disease with diarrhea caused by large intestinal disease.

Answer 37

SI: large, watery, rarely have blood LI: small, mucoid, commonly have blood, may have leukocytes

Question 38

What are the clinical and pathologic features of acute appendicitis?

Answer 38

= 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_

Question 39

Compare infectious and sterile peritonitis.

Answer 39

INFECTIOUS **= bacterial invasion of abdominal cavity** - rupture of stomach, abscess - preexisting ascites - infection from fallopian tubes STERILE **= chemical irritation** - pancreatitis - rupture of gallbladder - postsurgical

Question 40

Describe the pathogenesis and pathology of acute peritonitis.

Answer 40

serosal surface (intestines) and parietal peritoneum are congested and edematous ## Footnote **\*\* exudate contains PMNs and fibrin \>\> fibrous adhesions** *Symptoms: sharp abd pain, rebound tenderness, guarding. Intestines become paralzyed (high mortality)*

Question 41

List the most common causes of intestinal obstruction.

Answer 41

**_Paralytic ileus_** **_or_** **_Mechanical obstruction_** - atresia - stenosis - strictures - intussusception - volvulus - hernia - adhesions - neoplasms

Question 42

What are the most common types of hernia?

Answer 42

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

Question 43

Compare intussusception and volvulus.

Answer 43

**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*

Question 44

Classify malabsorption syndromes according to their pathogenesis.

Answer 44

Inadequate intraluminal digestion Primary mucosal absorptive defects Impeded transport of nutrients **_Pathologic_** 1. those that have characteristic findings 2. those that have non-specific findings 3. Those that have no pathologic findings

Question 45

Compare celiac sprue and tropical sprue.

Answer 45

**_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

Question 46

What are the clinical features of malabsorption syndrome?

Answer 46

**Most prominent deficiencies = protein and lipids** protein (+ iron malabs) \>\> **anemia** hypoalbuminemia \>\> **edema** *amenorrhea, impotence, muscle weakness* steatorrhea \>\> **decreased vit ADKE** \>\> **bleeding disorders** \>\> **osteomalacia**

Question 47

How common are intestinal neoplasms and where are they most often located?

Question 48

Classify intestinal neoplasms.

Answer 48

Non-neoplastic polyps Neoplastic polyps Malignant neoplasms

Question 49

What are the risk factors for intestinal neoplasms?

Answer 49

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

Question 50

What are polyps, and how are these intestinal lesions classified?

Answer 50

Polyps occur as the result of accumulation of irregular cells. They protrude into the lumen of the intestine **villous or tubular**

Question 51

Compare neoplastic and non-neoplastic polyps.

Answer 51

**_Non-neoplastic_** **Hyperplastic**: most common, rectosigmoid area **Hamartoma**: children \< 5, retention polyps, peutz-jeghers (autosomal dominant) **Inflammatory**: IBD, pseudopolyps **_Neoplastic_** **Tubular: **pedunculated polyps, cuboidal epithelium **Tubulovillous: **predominantly tubular that appear villous 25% **Villous: **sessile, fingerlike villi, lined with single nonclassifiable cell type

Question 52

What are the clinical features of large intestinal cancer?

Answer 52

adenocarcinomas 50x more common in the LI Early = no symptoms Late = chronic blood loss, constpation, pencil-like feces, hematochezia, bleeding

Question 53

Compare adenocarcinomas of the right and left colon.

Answer 53

right = intraluminal fungating or ulcerating masses left = napkin ring stenotic lesions

Question 54

What is CEA, and what is the clinical value of this tumor marker?

Answer 54

**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._

Question 55

How do carcinoids differ from adenocarcinoma of the large intestine?

Answer 55

Carcinoids = neuroendocrine tumors of low malignancy - located in submucosa where they form small modules elevating the overlying mucosa) - mostly small \< 2cm

Question 56

What is carcinoid syndrome?

Answer 56

When carcinoids metastasize to the liver, they release their secretory product into venous blood \>\> symptoms: serotonin, bradykinin, histamine, bronchial wheezing, flushing, colic, diarrhea

Question 57

Ulcerative colitis

Answer 57

**_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)