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Pathology > GI > Flashcards

GI Flashcards

1
Q

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

A

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

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2
Q

What is dental caries and how can it be prevented?

A
  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

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3
Q

What are the main complications of dental caries?

A

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

Can extend to the jaw >> osteomyelitis

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4
Q

What causes periodontal disease?

A

Colonization of periodontal pockets with bacteria.

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

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5
Q

What is stomatitis, and what are its causes?

A

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

C. albicans, herpes, canker sores

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6
Q

What is the significance of oral leukoplakia and erythroplakia?

A

Cancerous

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7
Q

What are the risk factors for oral cancer?

A
  • Is a complication of smoking, pipes, chewing tobacco*
  • also chronic alcoholism
  • M > F
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8
Q

How does oral cancer present clinically?

A
  • leukoplakia
  • eyrthoplakia
  • ulcer
  • crater
  • nodule/plaque
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9
Q

What is sialadenitis, and what are its causes?

A

Inflammation of the salivary glands

Either infectious or immune

Infectious: most commonly staph/strep

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

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10
Q

How does Sjogren’s disease affect the salivary glands?

A

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

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11
Q

Are salivary gland tumors mostly benign or malignant?

A

**Major glands: **Most are benign

**Minor glands: **50% malignant

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12
Q

What is the most common salivary gland tumor?

A
  • pleomorphic adenoma*
    • *benign
  • epithelial and myoepithelial
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13
Q

What are the clinical signs and symptoms of esophageal disease?

A

- dysphagia

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

- aspiration regurgitation

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14
Q

What is esophagitis, and what are its causes?

A
  • 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

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15
Q

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

A

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

causes GERD

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16
Q

What is achalasia, and what are its causes?

A

= spasm of the LES

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

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17
Q

What is the most common cause of esophageal varices?

A

Caused by

  • cirrhosis of the liver
  • portal HTN

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

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18
Q

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?

A
  • High incidence: China, Iran, South Africa
  • 3x more common in AA
  • M > F (US), M = F (INTL)
  • tobacco and alcohol use
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19
Q

Correlate the pathologic and clinical features of esophageal carcinoma.

A

Most originate from lower 1/3

  • grow as endophytic or exophytic

Histology

Upper/middle 1/3 = squamous cell

Lower 1/3 = adenocarcinomas

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20
Q

What are the main forms of gastritis?

A

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
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21
Q

What causes gastritis?

A

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

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22
Q

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

A

= 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)
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23
Q

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

A

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
24
Q

What are the main complications of peptic ulcer?

A

**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

25
Q

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

A

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

26
Q

How does gastric carcinoma present to the naked eye examination?

A
  1. superficial
  2. polypoid
  3. ulcerated
  4. diffuse carcinoma
27
Q

Where do gastric carcinomas metastasize?

A

To regional lymph nodes to the LIVER

  • also through supraclavicular nodes (Virchow’s)*
    • abdominal organs*
    • lungs*
    • bilateral ovaries (Krukenberg’s tumor)*
28
Q

What are the clinical signs and symptoms of gastric carcinoma?

A

Nonspecific signs:

  • weight loss
  • anemia
  • weakness
  • *Local signs:**
  • gastritis
  • vomiting
  • loss of appetite
  • dysphagia
  • bleeding
29
Q

How is gastric lymphoma related to MALT?

A

The lymphomas can originate in MALT . . . often related to H. pylori infection.

*stomach = most common site

30
Q

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

A

**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.

31
Q

Describe diverticula of the large intestine and their complications.

A

outpouching of intestinal wall

(solitary/multiple, congenital acquired)

In the colon = protrusion of the mucosa/submucosa

complications >> perforation >> pericolonic abscess, fistulas, fibrosis, bleeding

32
Q

Compare hemorrhoids and intestinal angiodysplasia.

A

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

33
Q

Compare occlusive and nonocclusive ischemic bowel disease.

A

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)

34
Q

How common is inflammatory bowel disease?

A

Ulcerative colitis 3x more common than Crohn’s

  • more common in whites, Jews
  • peaks 20-30 yrs/o
  • family predisposition
35
Q

Compare Crohn’s and ulcerative colitis.

A

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

36
Q

What is pseudomembranous colitis?

A

*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
37
Q

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

A

SI: large, watery, rarely have blood

LI: small, mucoid, commonly have blood, may have leukocytes

38
Q

What are the clinical and pathologic features of acute appendicitis?

A

= 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

39
Q

Compare infectious and sterile peritonitis.

A

INFECTIOUS

= bacterial invasion of abdominal cavity

  • rupture of stomach, abscess
  • preexisting ascites
  • infection from fallopian tubes

STERILE

= chemical irritation

  • pancreatitis
  • rupture of gallbladder
  • postsurgical
40
Q

Describe the pathogenesis and pathology of acute peritonitis.

A

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)

41
Q

List the most common causes of intestinal obstruction.

A

Paralytic ileus

or

Mechanical obstruction

  • atresia
  • stenosis
  • strictures
  • intussusception
  • volvulus
  • hernia
  • adhesions
  • neoplasms
42
Q

What are the most common types of hernia?

A

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

43
Q

Compare intussusception and volvulus.

A

**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

44
Q

Classify malabsorption syndromes according to their pathogenesis.

A

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
45
Q

Compare celiac sprue and tropical sprue.

A

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
46
Q

What are the clinical features of malabsorption syndrome?

A

Most prominent deficiencies = protein and lipids

protein (+ iron malabs) >> anemia

hypoalbuminemia >> edema

amenorrhea, impotence, muscle weakness

steatorrhea >> decreased vit ADKE

>> bleeding disorders

>> osteomalacia

47
Q

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

A
48
Q

Classify intestinal neoplasms.

A

Non-neoplastic polyps

Neoplastic polyps

Malignant neoplasms

49
Q

What are the risk factors for intestinal neoplasms?

A

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

50
Q

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

A

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

51
Q

Compare neoplastic and non-neoplastic polyps.

A

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

52
Q

What are the clinical features of large intestinal cancer?

A

adenocarcinomas 50x more common in the LI

Early = no symptoms

Late = chronic blood loss, constpation, pencil-like feces, hematochezia, bleeding

53
Q

Compare adenocarcinomas of the right and left colon.

A

right = intraluminal fungating or ulcerating masses

left = napkin ring stenotic lesions

54
Q

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

A

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.

55
Q

How do carcinoids differ from adenocarcinoma of the large intestine?

A

Carcinoids = neuroendocrine tumors of low malignancy

  • located in submucosa where they form small modules elevating the overlying mucosa)
  • mostly small < 2cm
56
Q

What is carcinoid syndrome?

A

When carcinoids metastasize to the liver, they release their secretory product into venous blood >>

symptoms: serotonin, bradykinin, histamine, bronchial wheezing, flushing, colic, diarrhea

57
Q

Ulcerative colitis

A

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)

Pathology (16 decks)

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