Dsa18 Pathology Of Inflammatory Disorders Of The Gi Tract

Front 1

What are Mallory-Weiss tears, and what are they associated with?

Back 1

• Longitudinal mucosal tears near the gastroesophageal junction.

• Most often associated with severe retching or vomiting secondary to acute alcohol intoxication
  

• Comes from rapid change in gastrointestinal pressure

Front 2

Pathogenesis of Mallory-Weiss tears

Back 2

• During prolonged vomiting, the reflex relaxation of the esophagus fails, and the refluxing gastric contents overwhelm the gastric inlet and cause esophageal wall to stretch and tear
• Heals pretty easily

Front 3

What is Boerhaave syndrome?

Back 3

• Transmural, usually distal esophageal rupture with pneumomediastinum due to violent retching
• Also shows subcutaneous emphysema
• Surgical emergency due to shock, chest pain, tachypnea, etc.

Front 4

Difference between dysphagia (1) and odynophagia (2)

Back 4

1) Difficulty swallowing

2) pain with swallowing

Front 5

Presentation, morphology and predisposing factors for oral "thrush" and candidiasis of the esophagus.

Back 5

• AIDS patients and those with hematolymphoid malignancies
  

• Odynophagia, retrosternal pain

• Plaques, pseudomembranes on esophageal mucosa

Front 6

Morphology of graft-versus-host esophagitis

Back 6

• Basal epithelial cell apoptosis
  
• Mucosal atrophy
• Submucosal fibrosis without significant acute inflammatory infiltrates

Front 7

Pathophysiology of Reflux Esophagitis

Back 7

• Normally, submucosal glands in proximal and distal esophagus secrete mucin and bicarbonate to protect stratified squamous of the esophagus from acid

• The tone of the lower esophageal sphincter prevents reflux of acidic gastric contents.

• Transient lower esophageal sphincter relaxation (can be triggered by gastric distention, mild pharyngeal stimulation that doesn't trigger swallowing, or stress)
• After you swallow, cough, or strain and the LES relaxes, gastroesophageal reflux occurs

Front 8

Clinical presentation, and treatment of GERD

Back 8

• Usually in patients older than 40
• Heartburn, dysphagia, regurgitation of sour-tasting stuff

• Rarely, can be punctuated by attacks of severe chest pain that can be mistaken for heart disease
• Treat with PPI's (which have replaced H2 antagonists)

Front 9

Presentation of hiatal hernia

Back 9

• Separation of diaphragmatic crura and protrusion of stomach into thorax through the gap

• Presents like GERD with heartburn and regurgitation of gastric juices.

Front 10

Morphology of reflux esophagitis

Back 10

• Eosinophils into squamous mucosa, followed by neutrophils
• Basal zone hyperplasia >20% of total epithelial thickness
• Elongation of lamina propria papillae such that they extend into upper 1/3 of epithelium

Front 11

What is eosinophilic esophagitis, and treatment?

Back 11

• Food impaction and dysphagia in adults, feeding intolerance in children.

• Large number of intraepithelial eosinophils, particularly superficial.

• Loads of eosinophils + no real acid reflux (PPI's don't help)

• Majority are atopic, have atopic dermatitis, allergic rhinitis, or modest peripheral eosinophilia.
• Treatments include dietary restrictions to avoid allergens, and corticosteroids

Front 12

Barrett esophagus pathophysiology and complication concern

Back 12

• Complication of GERD characterized by intestinal metaplasia within the esophageal squamous mucosa

• Nonkeratinized stratified squamous epithelium of esophagus is replaced by nonciliated columnar epithelium with goblet cells

• Increased risk of esophageal adenocarcinoma

Front 13

Difference between gastritits (1), acute gastritis (2), gastropathy (3)

Back 13

1) Mucousal inflammatory process

2) Neutrophils present

3) Inflammatory cells rare/absent

Front 14

What mechanisms are present to prevent damage to the gastric mucosa from gastric acid?

Back 14

• Mucin from foveolar cells forms a thin layer that protects and keeps large frood from directly touching epithelium

• Bicarbonate is secreted to keep mucin at neutral pH

• Gastric epithelial cells limit back diffusion of acid or leakage of other luminal materials

• In the acid secreting portions, bicarb is put into the vessels at the same time, and this vasculature washes away back diffused acid and delivers the bicarb around.

Front 15

How do NSAID's cause gastropathy/gastritis?

Back 15

• Inhibit COX dependent synthesis of PGE2 and PGI2

• PGE2 and PGI2 stimulate mucus and bicarb and increase mucosal blood flow

• Inhibiting these means more acid production and less blood flow

Front 16

Difference between stress ulcers (1), Curling ulcers (2) and Cushing ulcers (3)

Back 16

1) Most common in shock, sepsis, severe trauma

2) proximal duodenum, severe burns/trauma

3) gastric, duodenal, esophageal in persons with intracranial disease. High incidence of perforation.

Front 17

Pathogenesis and clinical features of stress-related mucousal ulcers

Back 17

• Usually due to local ischemia, either due to systemic hypotension or reduced blood flow from induced splanchnic vasoconstriction.

• If there's intracranial injury (Cushing ulcer), it can directly stimulate vagal nuclei, increasing gastric acid, causing systemic acidosis commonly.

Front 18

What is a dieulafoy lesion?

Back 18

• Submucosal artery does not branch properly in wall of stomach

• Results in a mucosal artery with a huge diameter

• Usually found in lesser curvature, near GEJ

• Erosion of the overlying epithelium leads to gastric bleeding

Front 19

What is GAVE (gastric antral vascular ectasia)?

Back 19

• Longitudinal stripes of edematous erythematous mucosa alternating with less injured, paler mucosa (watermelon stomach)

• Can be associated with cirrhosis, but most often idiopathic

• May have occult blood or iron deficiency anemia

Front 20

Morphology of Helicobacter pylori and the properties that allow it to reside in acid secreting gastric mucosa.

Back 20

• Spiral shaped or curved bacilli

• Usually antral gastritis with normal or increased acid production, then spreads to rest of stomach

• Flagella to move through mucus

• Urease to generate ammonia and raise local pH to survive

• Adhesins to adhere to foveolar cells

• Toxins (CagA)

Front 21

Diagnostic tests for H. pylori

Back 21

• Noninvasive serologic test for Ab's

• Fecal bacterial detection

• Urea breath test (due to bacterial urease)

Front 22

Compare and contrast H. pylori (1) and autoimmune gastritis (2)

Back 22

• (2) typically spares antrum
• (2) associated with hypergastrinemia
• (2) shows Ab's to parietal cells and IF
• (2) can show B12 deficiency

Front 23

Pathophysiology of autoimmune gastritis

Back 23

• CD4+ T cells against parts of the parietal cell (including H/K ATPase)

Loss of parietal cells
-----increased gastrin = increased G-cells in the antrum, hypergastrinemia

-----Lack of IF = Disabled B12 absorption

Loss of chief cells
----reduced pepsinogen I

Front 24

Morphology of autoimmune gastritis

Back 24

• Diffuse mucosal damage of acid-producing mucosa within body and fundus, damage to antrum and cardia usually absent or mild

• Inflammation is deep and centered on gastric glands

• Hypergastrinemia can stimulate endocrine cell hyperplasia in fundus and body, rarely causing progression to small low-grade carcinoid tumors

Front 25

Most common sites of peptic ulcers

Back 25

1) proximal duodenum

2) antrum lesser curvature at interface with body

3) Stomal ulcers at margins of gastroenterostomy

4) multiple sites in Zollinger Ellison syndrome

5) within or adjacent to Meckel diverticulum.

Front 26

Pathogenesis of Peptic Ulcer Disease

Back 26

• Imbalances between mucosal defense and damaging facotrs that cause chronic gastritis

• Most common causes (90%) are H. pylori, NSAIDs, or cigarette smoking

• If it's in the body or fundus, there's mucosal atrophy and it is accompanied by lesser acid secretion, and therefore generally protected from antral/duodenal ulcers.

Front 27

Morphology of peptic ulcer disease

Back 27

• Solitary in 80% of patients
  
• Sharply-punched-out-defect is classic morphology
• Heaped-up margins = more associated with cancer
• Base of ulcer is smooth and clean, with granulation tissue + leukocytes underneath
  
• Thick vessel walls around, danger for hemorrhage
• Malignant transformation is rare

Front 28

Clinical features of PUD

Back 28

• Epigastric burning or aching pain

• Significant fraction present with iron deficiency anemia, hemorrhage, or perforation

• Pain 1-3 hours after meals, worse at night

Front 29

MC cause of intestinal metaplasia in the stomach and why is it important?

Back 29

• Long standing chronic gastritis leads to loss of parietal cell mass

• Presence of goblet cells, strongly associated with gastric adenocarcinoma

• Greatest risk in autoimmune gastritis

Front 30

What is gastritis cystica?

Back 30

• Reactive epithelial proliferation associated with entrapment of epithelial-lined cysts

• These cysts may be in submucosa (polyposa) or deeper (profunda)

Front 31

What is ménétrier disease?

Back 31

• Excess secretion of TGF-α
• Gastric hyperplasia of mucosa, hypertrophied rugae
• excess mucus production with resultant protein loss and parietal cell atrophy with decreased acid production.
• Precancerous
  

Front 32

What is Zollinger-Ellison Syndrome?

Back 32

• Gastrinoma of pancreas or duodenum.
• Acid hypersecretion causes PUD.
• Presents with abdominal pain (peptic ulcer disease, distal ulcers), diarrhea (malabsorption).
• Positive secretin stimulation test: gastrin levels remain elevated after administration of secretin, which normally inhibits gastrin release.
• May be associated with MEN 1.
  

Front 33

Pathogenesis of acute appendicitis

Back 33

• Initiated by progressive increases in intraluminal pressure, compromising venous outflow
• The stasis of luminal contents favors bacterial proliferation, triggering ischemia and inflammatory responses.