Chapter 13: The GI Tract Flashcards Preview

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Flashcards in Chapter 13: The GI Tract Deck (78)
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Disordered esophageal motility (uncoordinated peristalsis) with inability to relax the lower esophageal sphincter (LES)
S/S: Dysphagia for solids & liquids, putrid breath, High LES pressure on esophageal manometry, "bird-beak" sign on barium swallow study
Results in hypertrophy/dilation of esophagus
What is damaged?
How can the damage occur?
What is there an increased risk of?

1) Loss or damaged ganglion cells in the myenteric plexus
2) idiopathic or secondary to known insult (viral, autoimmune, genetic) In Latin America, complication of Chagas Disease
3) Esophageal Squamous cell carcinoma


Thin protrusion of esophageal mucosa membranes, most often into the lumen of upper esophagus
Presents with dysphagia for poorly chewed food, esophageal substernal pain, and aspiration or regurgitation of foods and liquids
Increased risk for esophageal sqamous cell carcinoma

Esophageal Web
Rings are thicker and contain smooth muscle


Cervical esophageal web (cause dysphagia)
Mucosal lesions of the mouth and pharynx
Iron-deficiency anemia
What is a potential complication?

Plummer-Vinson Syndrome
Carcinoma of oropharynx and upper esophagus
Remember: Plummers DIG (dysphagia, iron def, glossitis)


Autoimmune disease characterized by activation of fibroblasts and deposition of collagen (fibrosis)
Esophageal smooth muscle atrophy, decreased LES pressure, dysmotility, then acid reflux and dysphagia, then stricture > Barrett esophagus, and aspiration
Which antibodies would you look for?
What is CREST Syndrome (throwback thursday)?
Why do we care about this in the GI Unit?

Anti-Scl70 and anti-Centromere antibodies (for CREST)
CREST (systemic sclerosis, limited type): Calcinosis/anti-Centromere antibodies, Raynaud Phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasias of the skin

Disease affects the lower esophageal sphincter primarily, lack of peristalsis, dysphagia


Outpouching of pharyngeal mucosa through an acquired defect in the muscular wall (false diverticulum)
Arises above the upper esophageal sphincter at the junction of the esophagus and pharynx
Cause: disordered fxn of cricopharyngeal musculature
Presents with dysphagia, obstruction, and halitosis
Regurgitation of food eaten previously in absence of dysphagia

Zenker Diverticulum


Herniation of the stomach through an enlarged diaphragmatic opening
S/S: heartburn, regurgitation due to incompetence of LES
2 types:
1) cap of gastric mucosa move upward, above diaphragm due to enlargement of hiatus and laxity of circumferential CT, resolves on its own
2) portion of gastric fundus herniates through a defect in the diaphragmatic CT and lies beside the esophagus, extreme case = stomach herniates into thorax, these hernias need surgery

Hiatal Hernia
1) Sliding hernia
2) Paraesophageal hernia


Name it!
Transmural, usually distal esophageal rupture due to violent retching; surgical emergency
Leads to air in mediastinum, subcutaneous emphysema

Boerhaave syndrome


Name it!
Infiltration of esosinophils in the esophagus in atopic pts.
Food allergens lead to dysphagia, heartburn, strictures.
Sensation of food "sticking" upon swallowing
ID'd after found Unresponsive to GERD therapy

Eosinophilic esophagitis


1) associated with lye ingestion and acid reflux
2) Painless bleeding of dilated submucosal veins in lower 1/3 of esophagus 2ndary to portal HTN & cirrhosis, these veins are prone to rupture and hemorrhage

1) Esophageal strictures
2) Esophageal varices


Associated with reflux, infection in immunocompromised
Dysphagia, severe pain on swallowing
Can have Candida (white pseudomembrane), herpes (punched-out ulcers), CMV (linear ulcers) or be due to chemical ingestion

(Infective) esophagitis


Commonly presents as heartburn and regurgitation upon lying down. May also present with nocturnal cough and dyspnea, adult-onset asthma. Decrease in LES tone.

Gastroesophageal Reflux Disease


Mucosal lacerations at the gastroesophageal junction due to severe vomiting. Leads to painful hematemesis. Usually found in alcoholics and bulimics.

Mallory-Weiss Syndrome


Glandular metaplasia: replacement of nonkeratinized stratified squamous epithelium with intestinal epithelium (nonciliated columnar w/goblet cells) in the distal esophagus.
Due to chronic acid reflux (GERD)
Associated with esophagitis, esophageal ulcers, and increased risk of esophageal adenocarcinoma correlated with length of esophagus involved and the degree of dysplasia

Barrett Esophagus


Patient presentation: progressive dysphagia (first solids, then liquids) and weight loss, poor prognosis
2 Types of cancer? Usual locations for each?
Risk factors? AABCDEFFGH

Esophageal cancer
1) Squamous cell carcinoma = worldwide, upper 2/3 of esophagus, (achalasia, alcohol, cigs, diverticula (Zenker), esophageal web, hot liquids)

2) Adenocarcinoma = US, lower 1/3, (Barrett esophagus, cigs, Fat (obesity), GERD)

Others: familial


Hypertrophy of the pylorus causes obstruction.
Palpable "olive" mass in epigastric region
Nonbilious projectile vomiting in first month of life
Could lead to hypochloremic alkalosis (loss of HCl)
Most common indication for abdominal surgery in the 1st 6 months of life (treat: surgical incision)
More often in firstborn males

Congenital pyloric stenosis


Mucosal barrier breakdown/necrosis, may extend to deeper tissues forming ulcer = inflammation b/c permit acid-induced injury (hypersecretion of gastric acid usually)
Widespread petechial hemorrhages
Could be benign abdominal discomfort or full on hemorrhage
NSAIDs (decreased PGE2 leads to decreased gastric mucosa protection)
burns (decreased plasma volume leads to sloughing of gastric mucosa) SPECIAL NAME?
brain injury (Increased vagal tone => increased ACh => increased H+ production) SPECIAL NAME?

Acute gastritis (erosive)

BURNED by the CURLING iron.
Always CUSHion the BRAIN.


Chronic, diffuse inflammatory disease of the body and fundus of stomach
Autoimmune disorder characterized by:
destruction of parietal cells, Autoantibodies to parietal cells & intrinsic factor, pernicious Anemia, and Achlorhydria
Associated with other autoimmune disorders: grave's, addison, vitiligio, T1DM etc.
What's pernicious anemia? No, really I don't remember Unit 1. GAHHHHH.
Increased risk for what?

Autoimmune atrophic gastritis (chronic gastritis) Remember: type A (Autoimmune), type B (H. pylori Bacteria)
Pernicious anemia = megaloblastic anemia caused by malabsorption of Vit B12 owing to a deficiency of intrinsic factor.
Increased risk for gastric adenocarcinoma (intestinal type)


Break time. I dare you to stand up and dance to this for 30 seconds.


Chronic inflammatory disease of antrum of stomach
PMNs, plasma cells
What is the most common cause of this disease?
What is there an increased risk for ?

Chronic gastritis
H. pylori found on epithelial surface of stomach (no invasion)
Increased risk of ulcercation, MALT lymphoma, and gastric adenocarcinoma


Gastric hypertrophy with protein loss (albumin), parietal cell atrophy, and increase mucous cells.
Hyperplastic hypersecretory gastropathy
Precancerous, need regular endoscopy
Rugae of stomach are so hypertrophied they look like brain gyri. ENLARGED RUGAE = enlarged stomach.
S/S: postprandial pain, relieved by antacids, weight loss, peripheral edema, maybe ascites

Menetrier disease


Normal flat mucosal surface of stomach replaced by villiform projections with fibromuscular proliferation in the lamina propria
Inflammation is minimal unlike H. pylori gastritis

Reactive (Chemical) gastropathy
Chronic NSAID use


Focal destruction of gastric mucosa
Pain can be greater with meals = weight loss
H. pylori in 70%
Mechanism is decreased mucosal protection (due to H. pylori chronic gastritis causing epithelial injury) against gastric acid
These pts secrete waay less acid than normal ppl (gastric hyposecretion)
Other causes are NSAIDS
Increased risk of carcinoma
Often occurs in older patients

Peptic Ulcer Disease
Specifically Gastric Ulcer


Focal destruction of duodenal mucosa
Pain decreases with meals = weight gain
H. pylori infection in 100% (=> cytokines => increased gastrin release/decreased somatostatin => increased gastric acid secretion)
Mechanism is decreased mucosal protection or increased gastric acid secretion
Other causes are Zollinger-Ellison syndrome
Generally benign
Hypertrophy of Brunner glands
Seen in ppl with cirrhosis 10x than normal ppl

Peptic Ulcer Disease
Duodenal Ulcers


Tend to be nonagressive tumors in the stomach
Aggressive in small & large intestines
Overexpression of c-kit (gain of function mutation)
Derived from pacemaker cells of Cajal
Usually submucosal, covered by intact mucosa, spindle shaped cells in whorls and interlacing bundles w/cytoplasmic vacuoles embedded in a collagenous stroma

Gastrointestinal Stromal Tumors (GISTs)


What is the most important causative agent for stomach cancer and is implicated in about 2/3rds of cases?

H. pylori


H. pylori
A diet high in starch, smoked, or cured fish and meat, pickled vegetables

Possible factors in carcinoma of stomach


Stomach cancer is almost always adenocarcinoma.
Early aggressive local spread and node/liver metastasis. Often presents with acanthosis nigricans.
Two types?
1) associated with H. pylori, dietary nitrosamines (smoked foods), tobacco smoking, achlorhydria, chronic gastritis. Commonly located on lesser curvature; looks like ulcer with raised margins, originate from areas of intestinal metaplasia
2) not associated with H. pylori, signet ring cells, stomach wall grossly thickened and leathery (linitis plastica)

1) Intestinal
2) Diffuse *linitis plastica = entire stomach involved


Difference in appearance of a benign peptic ulcer and an ulcerating adenocarcinoma?

Benign ulcer = punchout margins and a smooth base
Cancer = firm, raised and nodular, lateral margins are irregular and its base is ragged


Involvement of left supraclavicular node by metastasis from stomach

Virchow node


Bilateral metastases to ovaries, abundant mucus, signet ring cells

Krukenberg Tumor