GI MTM Patho for PUD, GERD, and Pancreatitis

• 1.  Temporary Food Storage
• 2. Control the rate at which food enters the duodenum
• 3. Acid secretion and antibacterial action
• 4. Fluidisation of stomach contents
• 5. Prelim digestion with pepsin, lipases, ect.

Collects digestive gases and produces pepsinogen

acid

gastrin, acid

mucin/mucus

Transition from the esophagus to the gastric mucosa

• 1. Dysphagia (difficulty swallowing)
• 2.heartburn/chestpain
• 3. pain after meals, when lying down or bending over

• age >40
• overweight
• pregnant
• those who use tobacco or drink alcohol

• 1. LES pressure: spontaneous relaxation
• 2. delayed gastric emptying and/or increased gastric volume
• 3.decreased esophageal clearance:  (acid stays in esophagus)---decreased mucous with age increases this issue
• 4. Mucosal resistance: acid damage over time
• 5. refluate composition: concentration of the acid, pepsin, or bile

• 1. common
•     a. Gastric: H. pylori, nsaids, older patients
•     b. duodenal: h. pylori, younger patients, type O blood

• 1. prostaglandins
• 2. mucosal blood flow
• 3. bicarb secretions
• 4. mucous secretion

• Epigastric pain, iron def. anemia (due to bleeding)
• Gastric ulcer: increased pain with meals
• Duodenal: decreased pain with meals

• 1. 80-90% asymptomatic
• 2. Mild: epigastric pain, N&V
• 3. Severe: mucosal erosion, ulceration, hemorrhage, blood loss
• 4. Stomach and duodenal ulcers

• 1. increased incidence with age
• 2. poverty
• 3. household crowding
• 4. minority population
• 5.rural areas

H. pylori (helix shaped gram negative bacteria that move away from acid).  They burrow into the mucosal layer to get away from the acid

• 1. Occurs mostly in children
• 2. Occurs in individuals with increased acid levels
• 3.Infection causes G cells to secrete gastrin which causes the parietal cells to secrete more acid  (this causes the bac to burrow deeper) over time the # of periatal cells increases which causes an increase in acid secretion (leads to damage)

• 1. Occurs mostly in elderly who have decreased acid levels
• 2. Body of the stomach colonization
• 3. This causes damage and loss of protection and atrophy of the stomach
• 4. Ulcer forms as you lose cells

• 1. H. pylori secretes urease whose biproduct is ammonia
• 2. ammonia and acid produce ammonium which would normally neutralize acid however it is also damaging to the epithelium itself
• 3. More urease in produced in stomach ulcers

• Mild: shallow erosions w/ superficial epithelial damage
• Moderate-Severe: erosions that penetrate hte depth of the mucosa
• USUALLY MULTIPLE ULCERS THROUGHOUT THE DUODENUM AND THE STOMACH

NSAID users w/in 6 months of use, age > 65, previous PUD, high dose NSAID, h. pylori infection, alcohol

Block prostaglandins which would normally inhibit acid secretion, stimulate mucus, stimulate bicarb, and increase mucosal blood flow

• 1. Crohn Disease: transmural inflammation of the GI tract (mouth-anus)
• 2. Ulcerative colitis: mucosal inflammation of the GI tract (colon-rectum)

• 1. Nothern latitudes
• 2. teens-20s or 60-80 yo
• 3. women> men
• 4. Caucasion
• 5. Hygeine hypothesis

• SMALL BUT DEEP
• 1. Discontinous skip lesions throught intestines
• defects in intestinal tight junctions and treansepithelial transport of paneth cells

• Intermittent attacks of mild diarrhead
• lower right quadrant pain, bloody diarrhea, fever
• Fibrous strictures can form

• BIG BUT SHALLOW
• 1. Superfical continous colonic inflammation

intermittent attacks of urge to defacate, chronic bloody diarrhea with mucoid material (HALLMARK), lower abdominal pain, and cramps

• 1. Chronic, relapsing abdominal pain, bloating, changes in bowel habits
• 2. 3days/month for 3 months, improvement in pain with defecation
• 3. Change in stool frequency or form

• 20-40 yo
• F>M

Triggers: stress, diet, abnormal GI motility, enteric sensory function

• 1. severe abdominal pain that can be referred to upper back and left shoulder
• 2. anorexia, N&V
• 3. Elevated amylase and lipase
• 4. Shock
• 5. Infection from necrosis

Fairly common, 80% associated with billary tract disease F>M, and alcoholism, 30-60% related to gallstones

• 1. Pancreatic duct obstruction: intestinal backup which causes local inflammation, edema, and lack of blood flow
• 2.  Direct acinar cell injury by alcohol, drugs, trauma, ischemia, and viruses
• 3. Inappropriate delivery of proenzymes within acinar cells leading to activation of digestive enzymes w/in acinar cells

• 1. Asymptomatic until diabetes mellitus or pancreatic insufficiency develops
• 2. epigastric pain, jaundice, and indigestion, mild fever, increase in serum lipase/amylase
• 3. malabsorption and chronic pain

most commonly middle aged alcoholic men

If 20-25yo 50% mortality

Mild inflammation-> tissue destruction -> inflammation resolves -> damaged pancreatic tissue is replaced by scar tissue -> progressive destuction of pancrease