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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
The gastric lumen of the stomach is ________
strongly acidic
26
Describe the mechanisms the stomach has to protect against gastric mucosa
1) Mucus coating 2) Bicarbonate secretion 3) Rich vascular supply 4) Mucosa regenerates
27
List the sphincters of the stomach
2 sphincters control opening/closing: -Lower esophageal sphincter -Pyloric sphincter
28
List the functions of the stomach
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
Acute Gastritis/Gastropathy
Mucosal injury of stomach lining due to acid - Acute Gastritis = PMNs present - Gastropathy = no inflammatory cells present
30
What is the pathogenesis of Acute Gastritis/Gastropathy? Oral/Clinical signs?
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
Acute Ulcers
Ulceration of stomach lining *Usually multiple ulcers occur; less than 1cm in diameter; normal adjacent mucosa; heal with re-epithelialization
32
What is the pathogenesis of Acute Ulcers? Oral/Clinical signs?
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
Helicobactor pylori Gastritis
Bacterial induced neutrophilic inflammation/atrophy of antrum **Most common cause of chronic gastritis --> 90%
34
What is the pathogenesis of Helicobactor pylori Gastritis? The oral/clinical signs?
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
Helicobactor pylori Gastritis increases the risk for...
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
Auto-Immune Gastritis
Autoimmune antibodies to parietal cells + intrinsic factor *triggers T-cell type IV hypersensitivity
37
What is the pathogenesis of Auto-Immune Gastritis? Oral/Clinical signs?
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
Auto-Immune Gastritis increases the risk for....
Adenocarcinoma (higher risk than with H. pylori Gastritis)
39
Comparison of H. pylori Gastritis and Autoimmune Gastritis
**know chart on slide 42**
40
Peptic Ulcer Disease
Solitary, well-demarcated 2-3mm ulcer deep into submucosa or muscle of proximal duodenum (90%) or distal stomach (10%)
41
What is the pathogenesis of Peptic Ulcer Disease? The locations it is found? The overall risk?
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
What are the complications of Peptic Ulcer Disease?
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
What is the treatment for Peptic Ulcer Disease?
1) Test for H. pylori 2) Antibiotics (amoxicillin/metronidazole) 3) Proton Pump Inhibitors (pepcid/zantac/tagamet)
44
Gastric Peptic Ulcer
Solitary mucosal ulcer of antrum (10%) - chronic and recurring
45
What is the pathogenesis of Gastric Peptic Ulcer? The oral/clinical signs?
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
Duodenal Peptic Ulcer
Solitary mucosal ulcer of proximal duodenum (90%) *Healing followed by recurrent ulcer formation
47
What is the pathogenesis of Duodenal Peptic Ulcer? The oral/clinical signs?
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
Zollinger-Ellison Syndrome
Multiple peptic ulcers of stomach, duodenum, and jejunum
49
What is the pathogenesis of Zollinger-Ellison Syndrome? The oral/clinical signs?
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
Gastric Adenocarcinoma
Malignancy of surface epithelial cells *Most common malignancy of stomach - 90%
51
What are the 2 types of Gastric Adenocarcinoma?
1) Intestinal type = most common --> diet/chronic gastritis 2) Diffuse type = rare --> blood type A
52
What is the pathogenesis of Gastric Adenocarcinoma? The oral/clinical signs?
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
What is caused by Obstructive/Vascular?
Esophageal Varices
54
What is caused by trauma?
-Mallory-Weiss Syndrome -Esophagitis -GERD -Hiatal Hernia -Barrett Esophagus -Plummer-Vinson Syndrome
55
What is caused by Neoplasia?
-Squamous Cell Carcinoma -Adenocarcinoma -Gastric Adenocarcinoma -Carcinoma of Ampulla -Adenomatous Polyps -Adenocarcinoma - Colorectal Carcinmoa
56
What is caused by Acute Gastritis/Gastropathy?
Acute Ulcers
57
What is caused by Chronic Gastritis?
-H. Pylori Gastritis -Auto-immune Gastritis -Peptic Ulcer Disease *Gastric peptic ulcer *Duodenal peptic ulcer *Zollinger-Ellison Syndrome
58
What in the small intestine is caused by developmental problems?
-Pyloric Stenosis -Meckel Diverticulum
59
What in the small intestine is caused by obstruction?
-Volvulus -Hernia -Adhesions -Intussesception
60
What in the small intestine is caused by Vascular/Obstructive?
-Mesenteric Arterial Occlusion -Mesenteric Venous Occlusion
61
What in the small intestine is caused by Malabsorption?
-Crohn Disease -Celiac Disease
62
What in the large intestine is caused by Obstruction?
-Megacolon (congenital) *Hirschsprung disease -Megacolon (acquired) -Diverticular Disease
63
What in the large intestine is cause by inflammatory
-Inflammatory bowel disease (IBD) *ulcerative colitis *crohn disease -Pseudomembranous Colitis -Appendicitis
64
What in the large intestine is caused by Genetic - Polyposis Syndromes?
-FAP- Familial Adenomatous Polyposis -Gardner Syndrome -Peutz-Jeghers Syndrome

General Pathology (32 decks)

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