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General Pathology > GI Path: Esophagus & Stomach > Flashcards

GI Path: Esophagus & Stomach Flashcards

1
Q

Esophagus Location

A

-Extends from the epiglottis to gastroesophageal junction
-Inferior to larynx –> posterior to trachea and anterior to aorta –> penetrates diaphragm at esophageal hiatus –> meets stomach at cardiac orifice = lower esophageal sphincter

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2
Q

Describe the rich lymphatics of the esophagus

A

-Upper esophagus drains to cervical nodes
-Mid esophagus drains to paratracheal nodes
-Lower esophagus drains to gastric nodes

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3
Q

Esophagus function

A

-Transports food, liquids, and saliva from pharynx to stomach via peristalsis
- 2 sphincters control opening/closing:
*upper esophageal sphincter
*lower esophageal sphincter

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4
Q

Esophageal Varices

A

Distended esophageal veins that protrude into lumen

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5
Q

What is the pathogenesis of Esophageal Varices? The oral/clinical signs?

A

Pathogenesis:
-Portal hypertension –> reverse flow of portal blood from gastric coronary vein into esophageal veins

Oral/Clinical:
-Asymptomatic
-Rupture = massive hematemesis
- 50% of ruptures lead to death

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6
Q

Mallory-Weiss Syndrome

A

Esophageal linear lacerations - oriented longitudinally

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7
Q

What is the pathogenesis of Mallory-Weiss Syndrome? What is is associated with? The oral/clinical signs?

A

Pathogenesis:
-Prolonged vomiting prevents relaxation of gastroesophageal musculature and sphincter –> esophageal walls stretch and tear

Associated with:
1) repetitive vomiting - alcoholism/bulimia
2) hiatal hernia

Oral/Clinical:
-Abdominal pain
-Hematemesis - “coffee grinds” in vomitus
-Melana - “black tar” stool

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8
Q

Esophagitis

A

Inflammation of esophagus

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9
Q

What is the pathogenesis of Esophagitis? Oral/clinical signs?

A

Pathogenesis:
1) GERD - #1 cause in US men
2) Irritants - alcohol/smoking
3) Allergy
4) Drugs (doxycycline)
5) Chemo/radiation therapy
6) Infections (CMV/HSV)

Oral/Clinical:
-Dysphagia
-Odynophagia
-Chest pain; heart burn; acid reflux

**Can lead to scarring and constriction if untreated

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10
Q

GERD (Gastroesophageal Reflux Disease)

A

Reflux/backflow of gastric contents into the esophagus

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11
Q

What is the pathogenesis of GERD? Clinical/oral signs? Tx?

A

Pathogenesis:
1) Incompetent sphincter
2) Hiatal hernia
3) Slowed gastric emptying

**Can lead to Barrett esophagus

Oral/Clinical:
-Erosion of teeth - lingually
-Heartburn
-Adult-onset asthma
-Hoarseness

TX:
-Diet changes
-Lose weight; incline bed
-Meds = antacids; H2 inhibitors; proton pump inhibitors

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12
Q

Hiatal Hernia

A

Widened opening in the diaphragm where esophagus penetrates allowing part of the stomach to enter the thorax

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13
Q

What is the pathogenesis of Hiatal Hernia? Oral/Clinical signs?

A

Pathogenesis:
-Muscle weakness of diaphragm

Oral/Clinical:
-Difficulty swallowing
-Heartburn
-Belching
- 50+ yrs

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14
Q

Barrett Esophagus

A

Intestinal metaplasia within distal esophagus mucosa
**squamous epithelium to non-ciliated columnar epithelium

**most Esophageal Adenocarcinomas are associated with Barrett Esophagus but most Barrett esophagus cases do NOT develop into adenocarcinomas

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15
Q

What is the pathogenesis of Barrett Esophagus? Oral/Clinical signs?

A

Pathogenesis:
-Chronic GERD –> permanent change in mucosa = resistant to acid –> predisoposed to adenocarcinoma
*10% of chronic GERD cases

Oral/Clinical:
-History of chronic GERD
-Males 4:1
- 40-60yrs
-History of previous radiation exposure

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16
Q

Plummer-Vinson Syndrome

A

Rare disease - classic triad:
1) Dysphasia
2) Esophageal weba
3) Iron-deficiency anemia

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17
Q

What is the pathogenesis of Plummer-Vinson Syndrome? Oral/Clinical signs?

A

Pathogenesis:
-Atrophy of oral mucosa + upper esophageal webs
**Transformation of both into squamous cell carcinoma

Oral/Clinical:
-Dysphasia
-Cheilosis
-Glossitis

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18
Q

Esophageal Squamous Cell Carcinoma (SCCA)

A

Most common malignancy of esophagus

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19
Q

What is the pathogenesis of Esophageal SCCA? Risk factors? Oral/Clinical signs?

A

Pathogenesis:
-Begins as dysplasia in mid-esophagus –> develop into tumors w/in infiltration of esophageal wall = lumen narrows

Risk Factors:
1) Alcohol/tobacco use/very hot drinks
2) HPV
3) Plummer-Vinson Sx

Oral/Clinical:
-Asymptomatic (early)
-Dysphasia; odynophasia; weight loss (late)
-African Americans 6:1
-Males 4:1
- 45yrs+

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20
Q

Esophageal Adenocarcinoma

A

Most common malignancy of esophagus in US

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21
Q

What is the pathogenesis of Esophageal Adenocarcinoma? Risk factors? Oral/Clinical signs?

A

Pathogenesis:
-Begins as dysplasia in distal-esophagus –> develops into large exophytic tumors that ulcerate and deeply infiltrate esophageal wall/gastric wall = lumen narrows

Risk Factors:
1) Barrett esophagus
2) Chronic GERD

Oral/Clinical:
-Asymptomatic (early)
-Dysphasia; odynophasia; weight loss (late)
-Males 7:1
- 45yrs+

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22
Q

Esophageal SCCA and Adenocarcinoma PROGNOSIS

A

-Asymptomatic until advanced
-Dysphasia/Odynophasia
-Weight loss
-Extensive lymphatic spread:
*cervical nodes - upper esophageal tumors
*mediastinal/tracheal nodes - mid/distal esophageal tumors
-Overall 5yr survival rate = 25%
- 5yr survival rate when diagnosed with symptoms = 10%

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23
Q

Stomach Location

A

-Extends from lower esophageal sphincter to pyloric sphincter
-Inferior to the diaphragm

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24
Q

Describe the 4 regions of the stomach and the cells found w/in these regions

A

1) Cardia –> foveolar cells produce mucin
2) Fundus –> parietal cells produces HCl + intrinsic factor & chief cells produce digestive enzymes
3) Body –> parietal cells produce HCl + intrinsic factor & chief cells produce digestive enzymes
4) Antrum –> G-cells produce gastrin –> stimulates parietal cells

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25
Q

The gastric lumen of the stomach is ________

A

strongly acidic

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26
Q

Describe the mechanisms the stomach has to protect against gastric mucosa

A

1) Mucus coating
2) Bicarbonate secretion
3) Rich vascular supply
4) Mucosa regenerates

27
Q

List the sphincters of the stomach

A

2 sphincters control opening/closing:
-Lower esophageal sphincter
-Pyloric sphincter

28
Q

List the functions of the stomach

A

1) Digestive function - proteolytic enzymes; forms/moves chyme
2) Protective function - acidity is hostile to microbes
3) Secretory function - HCl; pepsin; mucus; gastrin; intrinsic factor
4) Temporary storage of food

29
Q

Acute Gastritis/Gastropathy

A

Mucosal injury of stomach lining due to acid
- Acute Gastritis = PMNs present
- Gastropathy = no inflammatory cells present

30
Q

What is the pathogenesis of Acute Gastritis/Gastropathy? Oral/Clinical signs?

A

Pathogenesis:
-Imbalance between mucosal defenses and acidic environment
-NSAIDS
-Alcohol

Oral/Clinical:
- +/- asumptomatic
- Variable epigastric pain
-Nausea; vomiting

*Acute Gastritis can progress to gastric ulceration = Acute Ulcer

31
Q

Acute Ulcers

A

Ulceration of stomach lining

*Usually multiple ulcers occur; less than 1cm in diameter; normal adjacent mucosa; heal with re-epithelialization

32
Q

What is the pathogenesis of Acute Ulcers? Oral/Clinical signs?

A

Pathogenesis:
1) Progression of acute gastritis
2) Stress and shock = local ischemia (75% of critically ill patients develop acute ulcers)

Oral/Clinical:
-Nausea; vomiting
-Coffee-ground hematemesis; melena
- 1-4% require transfusion

33
Q

Helicobactor pylori Gastritis

A

Bacterial induced neutrophilic inflammation/atrophy of antrum
**Most common cause of chronic gastritis –> 90%

34
Q

What is the pathogenesis of Helicobactor pylori Gastritis? The oral/clinical signs?

A

Pathogenesis:
- H. pylori secretes urease –> increased ammonia formed = increased pH around bacteria –> increased gastrin secretion = increased acid from parietal cells of body/fundus = atrophy of mucosa
**Causes imbalance of mucosal defenses resulting in tissue damage

Oral/Clinical:
-Asymptomatic
-Mild epigastric abdominal pain

35
Q

Helicobactor pylori Gastritis increases the risk for…

A

1) Ulceration - peptic ulcer disease
2) Adenocarcinoma
3) Marginal zone lymphoma

**H. pylori can be found in dental plaque –> can cause re-infection; stress good OH

36
Q

Auto-Immune Gastritis

A

Autoimmune antibodies to parietal cells + intrinsic factor
*triggers T-cell type IV hypersensitivity

37
Q

What is the pathogenesis of Auto-Immune Gastritis? Oral/Clinical signs?

A

Pathogenesis:
- T-cell mediated destruction of epithelium of body and fundus including all parietal cells –> metaplasia occurs as gastric mucosa is replaced with intestinal epithelium
*Antrum not affected but G-cells becomes hyperplastic = increases gastrin

Oral/Clinical:
-Pernicious anemia
-Achlorhydria = almost no HCl

38
Q

Auto-Immune Gastritis increases the risk for….

A

Adenocarcinoma (higher risk than with H. pylori Gastritis)

39
Q

Comparison of H. pylori Gastritis and Autoimmune Gastritis

A

know chart on slide 42

40
Q

Peptic Ulcer Disease

A

Solitary, well-demarcated 2-3mm ulcer deep into submucosa or muscle of proximal duodenum (90%) or distal stomach (10%)

41
Q

What is the pathogenesis of Peptic Ulcer Disease? The locations it is found? The overall risk?

A

Pathogenesis:
-Imbalance between mucosal defenses and acidic environment

3 Locations:
1) Gastric
2) Duodenal
3) Jejunal

Overall Risk:
1) Males = 10%
2) Females = 4%

42
Q

What are the complications of Peptic Ulcer Disease?

A

1) Bleeding –> most common (30%)
2) Perforation –> most deadly (65% of deaths)
3) Obstruction –> rare
4) Malignancy –> rare complication of gastric ulcers (*non-existent in duodenal ulcers)

43
Q

What is the treatment for Peptic Ulcer Disease?

A

1) Test for H. pylori
2) Antibiotics (amoxicillin/metronidazole)
3) Proton Pump Inhibitors (pepcid/zantac/tagamet)

44
Q

Gastric Peptic Ulcer

A

Solitary mucosal ulcer of antrum (10%) - chronic and recurring

45
Q

What is the pathogenesis of Gastric Peptic Ulcer? The oral/clinical signs?

A

Pathogenesis:
1) H. pylori - 65%
2) Chronic NSAIDs
3) Chronic high dose steroids
4) Cigarettes
5) Stress
**healing followed by recurrent ulcer formation

Oral/Clinical:
-Epigastric pain 1-3hr after eating
-Nausea, vomiting, bloating
-Risk of hemorrhage or perforation

46
Q

Duodenal Peptic Ulcer

A

Solitary mucosal ulcer of proximal duodenum (90%)
*Healing followed by recurrent ulcer formation

47
Q

What is the pathogenesis of Duodenal Peptic Ulcer? The oral/clinical signs?

A

Pathogenesis:
1) H. pylori (95%) –> bacteria cannot live in duodenum –> H. pylori growth in antrum causes increased acid in duodenum = epithelial metaplasia = H. pylori colonization of duodenum
2) Hypercalcemia –> increased gastrin secretion = parietal cells increase HCl secretion
3) Genetics –> Blood type O

Oral/Clinical:
-Epigastric pain improves after eating
-Risk of hemorrhage or perforation

48
Q

Zollinger-Ellison Syndrome

A

Multiple peptic ulcers of stomach, duodenum, and jejunum

49
Q

What is the pathogenesis of Zollinger-Ellison Syndrome? The oral/clinical signs?

A

Pathogenesis:
-Nuroendrocrine tumor of pancrease –> spreads to liver/intestine –> secretes increased gastrin = stimulation of parietal cells = increased HCl acid secretion not neutralized

Oral/Clinical:
- Adults - 50yrs+
- Abdominal pain
- Nausea/vomiting
- Diarrhea/weight loss

50
Q

Gastric Adenocarcinoma

A

Malignancy of surface epithelial cells
*Most common malignancy of stomach - 90%

51
Q

What are the 2 types of Gastric Adenocarcinoma?

A

1) Intestinal type = most common –> diet/chronic gastritis
2) Diffuse type = rare –> blood type A

52
Q

What is the pathogenesis of Gastric Adenocarcinoma? The oral/clinical signs?

A

Pathogenesis:
1) Diet
2) Autoimmune gastritis
3) H. pylori gastritis
4) EBV
5) Blood type A

Oral/Clinical:
-Asymptomatic (early)
-Weight loss; abdominal pain; anemia (late)
-Males (2:1) - 55yrs

53
Q

What is caused by Obstructive/Vascular?

A

Esophageal Varices

54
Q

What is caused by trauma?

A

-Mallory-Weiss Syndrome
-Esophagitis
-GERD
-Hiatal Hernia
-Barrett Esophagus
-Plummer-Vinson Syndrome

55
Q

What is caused by Neoplasia?

A

-Squamous Cell Carcinoma
-Adenocarcinoma
-Gastric Adenocarcinoma
-Carcinoma of Ampulla
-Adenomatous Polyps
-Adenocarcinoma - Colorectal Carcinmoa

56
Q

What is caused by Acute Gastritis/Gastropathy?

A

Acute Ulcers

57
Q

What is caused by Chronic Gastritis?

A

-H. Pylori Gastritis
-Auto-immune Gastritis
-Peptic Ulcer Disease
*Gastric peptic ulcer
*Duodenal peptic ulcer
*Zollinger-Ellison Syndrome

58
Q

What in the small intestine is caused by developmental problems?

A

-Pyloric Stenosis
-Meckel Diverticulum

59
Q

What in the small intestine is caused by obstruction?

A

-Volvulus
-Hernia
-Adhesions
-Intussesception

60
Q

What in the small intestine is caused by Vascular/Obstructive?

A

-Mesenteric Arterial Occlusion
-Mesenteric Venous Occlusion

61
Q

What in the small intestine is caused by Malabsorption?

A

-Crohn Disease
-Celiac Disease

62
Q

What in the large intestine is caused by Obstruction?

A

-Megacolon (congenital)
*Hirschsprung disease
-Megacolon (acquired)
-Diverticular Disease

63
Q

What in the large intestine is cause by inflammatory

A

-Inflammatory bowel disease (IBD)
*ulcerative colitis
*crohn disease
-Pseudomembranous Colitis
-Appendicitis

64
Q

What in the large intestine is caused by Genetic - Polyposis Syndromes?

A

-FAP- Familial Adenomatous Polyposis
-Gardner Syndrome
-Peutz-Jeghers Syndrome

General Pathology (32 decks)

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