Weeks 5-8
GASTROINTESTINALPATHOLOGIES:
Pathophysiology of GERD:
Lower esophageal sphincter (LES) dysfunction: reduced pressure or improper relaxation
allows gastric acid to flow back into the esophagus; Loss of muscle tone at LES.
Hiatal hernia: contributes to GERD by disrupting the normal barrier between the
esophagus and stomach
Esophageal motility disorders: impaired esophageal peristalsis and reduces esophageal
clearance can lead to pooling of gastric acid in the esophagus
Acidic acid contents: Gastric acid, bile acids, and pepsin are the major components of the
gastric contents that reflux into the esophagus. These substances can cause direct mucosal
damage and trigger inflammation, leading to the characteristic symptoms of GERD.
Risk Factors of GERD:
Over the age of 50
Dysphagia (difficulty with swallowing food)
Odynophagia (pain on swallowing)
Nausea and vomiting
Weight loss
Melena (digested blood in GI tract)
Early satiety (feeling full after eating very little food).
Pharmacologic Mgmt of GERD:
Antacids – Calcium carbonate (Tums), Magnesium hydroxide, Aluminum hydroxide,
(Maalox, Mylanta)
H2Receptor Antagonists (Block H2 receptors of parietal cells and reduce acid) –
Famotidine, Nizatidine
PPI’s (1st line) – Omeprazole, Pantoprazole, Esomeprazole, Lansoprazole
Prokinetic Agents – Metoclopramide (Reglan)
Risk Factors for Esophageal Stricture:
Long-standing, untreated GERD
Meds that cause pill esophagitis (e.g., doxycycline, bisphosphonates, potassium chloride,
NSAIDs, iron supplements)
Hiatel hernia
,Pathophysiology of Appendicitis:
Obstruction of lumen with stool, tumors or foreign bodies with subsequent bacterial
infection.
Symptoms of Appendicitis:
Epigastric, periumbilical pain that increases over 3-4 hours. Pain subsides and then pain
in RLQ (a tender or nontender mass). Nausea, vomiting, anorexia, low-grade fever.
Leukocytosis. Diarrhea (children). Constipation. Peritontitis, perforation, and abscess are
most serious.
Labs for Appendicitis:
CBC (WBC), increased neutrophils and C-Reactive Protein (CRP)
Risks for Appendectomy in Adults:
Increased risk for colon cancer post-appendectomy for adults aged 50-54. Colonoscopy
recommended.
Peptic Ulcer Disease (PUD) Pathophysiology:
Break or ulceration in the protective mucosal lining, usually located in the stomach or
proximal duodenum; however, they can be found in the esophagus.
Mucosal protective factors are overcome by erosive factors such as fastric acid secretion
or pepsin.
Risk Factors for PUD:
H-Pylori, NSAIDS
Medications: corticosteroids, bisphosphonates, potassium chloride, and fluorouracil
Smoking, alcohol consumption
Zollinger-Ellison syndrome (gastrin-secreting neuroendocrine tumor or multiple tumors),
systemic mastocytosis, cystic fibrosis, hyperparathyroidism, and antral G-cell hyperplasia
,Gastric vs. Duodenal Ulcers:
Causes of Gastric Ulcers:
Chronic gastritis is often associated with the development of gastric ulcers and may
precipitate ulcer formation by limiting the mucosa's ability to secrete a protective layer of
mucus.
Decreased mucosal synthesis of prostaglandins
Damage to the mucosal membrane from duodenal reflux of bile and pancreatic enzymes
, Use of NSAIDs (decreases prostaglandin synthesis)
H. pylori infection
Signs/Symptoms of Duodenal Ulcer:
Chronic, intermittent pain in the epigastric area
The pain begins 2 or 3 hours after eating, when the stomach is empty. It is not unusual for
pain to occur in the middle of the night and disappear by morning.
Pain is relieved rapidly by ingestion of food or antacids, creating a typical pain-food-
relief pattern
Some have no symptoms; the first manifestation may be hemorrhage or perforation,
particularly with a history of NSAID or anticoagulant use.
Pathophysiology of Ulcerative Colitis (UC):
The primary lesion of UC begins with inflammation at the base of the crypt of
Lieberkühn in the large intestine.
The disease begins in the rectum (proctitis) and may extend proximally to the entire colon
(pancolitis). The lesions are limited to mucosal epithelium, are not transmural, and do not
involve skip lesions.
Risk factors for UC and Crohn’s Disease:
Pathophysiology of Crohn’s Disease:
Inflammation begins in the intestinal submucosa and spreads with discontinuous
transmural involvement or “skip lesions”( inflamed areas mixed with uninflamed areas,
noncaseating granulomas, fistulas, and deep penetrating ulcers) that can involve any part
of the GI tract from the mouth to the perianal area.
The distal small intestine and proximal large colon are most involved
A granuloma or a mass of inflammatory tissue with a cobblestone appearance of
inflamed tissue surrounded by ulceration.
Treatment of Crohn’s Disease:
No specific biomarkers or definitive treatments
Smoking cessation
GASTROINTESTINALPATHOLOGIES:
Pathophysiology of GERD:
Lower esophageal sphincter (LES) dysfunction: reduced pressure or improper relaxation
allows gastric acid to flow back into the esophagus; Loss of muscle tone at LES.
Hiatal hernia: contributes to GERD by disrupting the normal barrier between the
esophagus and stomach
Esophageal motility disorders: impaired esophageal peristalsis and reduces esophageal
clearance can lead to pooling of gastric acid in the esophagus
Acidic acid contents: Gastric acid, bile acids, and pepsin are the major components of the
gastric contents that reflux into the esophagus. These substances can cause direct mucosal
damage and trigger inflammation, leading to the characteristic symptoms of GERD.
Risk Factors of GERD:
Over the age of 50
Dysphagia (difficulty with swallowing food)
Odynophagia (pain on swallowing)
Nausea and vomiting
Weight loss
Melena (digested blood in GI tract)
Early satiety (feeling full after eating very little food).
Pharmacologic Mgmt of GERD:
Antacids – Calcium carbonate (Tums), Magnesium hydroxide, Aluminum hydroxide,
(Maalox, Mylanta)
H2Receptor Antagonists (Block H2 receptors of parietal cells and reduce acid) –
Famotidine, Nizatidine
PPI’s (1st line) – Omeprazole, Pantoprazole, Esomeprazole, Lansoprazole
Prokinetic Agents – Metoclopramide (Reglan)
Risk Factors for Esophageal Stricture:
Long-standing, untreated GERD
Meds that cause pill esophagitis (e.g., doxycycline, bisphosphonates, potassium chloride,
NSAIDs, iron supplements)
Hiatel hernia
,Pathophysiology of Appendicitis:
Obstruction of lumen with stool, tumors or foreign bodies with subsequent bacterial
infection.
Symptoms of Appendicitis:
Epigastric, periumbilical pain that increases over 3-4 hours. Pain subsides and then pain
in RLQ (a tender or nontender mass). Nausea, vomiting, anorexia, low-grade fever.
Leukocytosis. Diarrhea (children). Constipation. Peritontitis, perforation, and abscess are
most serious.
Labs for Appendicitis:
CBC (WBC), increased neutrophils and C-Reactive Protein (CRP)
Risks for Appendectomy in Adults:
Increased risk for colon cancer post-appendectomy for adults aged 50-54. Colonoscopy
recommended.
Peptic Ulcer Disease (PUD) Pathophysiology:
Break or ulceration in the protective mucosal lining, usually located in the stomach or
proximal duodenum; however, they can be found in the esophagus.
Mucosal protective factors are overcome by erosive factors such as fastric acid secretion
or pepsin.
Risk Factors for PUD:
H-Pylori, NSAIDS
Medications: corticosteroids, bisphosphonates, potassium chloride, and fluorouracil
Smoking, alcohol consumption
Zollinger-Ellison syndrome (gastrin-secreting neuroendocrine tumor or multiple tumors),
systemic mastocytosis, cystic fibrosis, hyperparathyroidism, and antral G-cell hyperplasia
,Gastric vs. Duodenal Ulcers:
Causes of Gastric Ulcers:
Chronic gastritis is often associated with the development of gastric ulcers and may
precipitate ulcer formation by limiting the mucosa's ability to secrete a protective layer of
mucus.
Decreased mucosal synthesis of prostaglandins
Damage to the mucosal membrane from duodenal reflux of bile and pancreatic enzymes
, Use of NSAIDs (decreases prostaglandin synthesis)
H. pylori infection
Signs/Symptoms of Duodenal Ulcer:
Chronic, intermittent pain in the epigastric area
The pain begins 2 or 3 hours after eating, when the stomach is empty. It is not unusual for
pain to occur in the middle of the night and disappear by morning.
Pain is relieved rapidly by ingestion of food or antacids, creating a typical pain-food-
relief pattern
Some have no symptoms; the first manifestation may be hemorrhage or perforation,
particularly with a history of NSAID or anticoagulant use.
Pathophysiology of Ulcerative Colitis (UC):
The primary lesion of UC begins with inflammation at the base of the crypt of
Lieberkühn in the large intestine.
The disease begins in the rectum (proctitis) and may extend proximally to the entire colon
(pancolitis). The lesions are limited to mucosal epithelium, are not transmural, and do not
involve skip lesions.
Risk factors for UC and Crohn’s Disease:
Pathophysiology of Crohn’s Disease:
Inflammation begins in the intestinal submucosa and spreads with discontinuous
transmural involvement or “skip lesions”( inflamed areas mixed with uninflamed areas,
noncaseating granulomas, fistulas, and deep penetrating ulcers) that can involve any part
of the GI tract from the mouth to the perianal area.
The distal small intestine and proximal large colon are most involved
A granuloma or a mass of inflammatory tissue with a cobblestone appearance of
inflamed tissue surrounded by ulceration.
Treatment of Crohn’s Disease:
No specific biomarkers or definitive treatments
Smoking cessation
