Gastrointestinal Disorders

GERD (heart burn)

 Etiology: weakness of the lower esophageal sphincter: hiatal hernia, gastric contents to
reflux into the esophagus. Impaired esophageal motility: decreased clearance of the
refluxed material. Delayed gastric emptying: results in an increased risk of reflux
(volume/pressure).
 Patho: 30-60 minutes after eating = spontaneous relaxation of LES = regurgitation of
chyme. Chyme with acid, enzymes irritating. inflammatory response. Hyperemia
(increase in blood flow), erosion, fibrosis, strictures (Scar tissue, spasm, edema), ulcers.
 Predisposing factors: women, reduced saliva, impaired swallowing, hiatal hernia,
impaired esophageal motility, delayed gastric emptying. Incompetent LES: chocolate,
caffeine, alcohol, fatty foods, antidepressants. Increased pressure from obesity and
pregnancy (progesterone hormone relaxes LES). smoking.
 Signs and symptoms: *pyrosis (burning), Dyspepsia (noncardiac chest pain), water brash
(throw up in mouth), coughing, hoarseness, sore throat, lump in throat, odynophagia,
dysphagia, regurgitation.
 Common clinical presentation: post-prandial heartburn, following ingestion of food or
drugs that decrease LES pressure, less than 1-2 times per week, immediate relief from
antacid or H2 receptor antagonist, no alarming symptoms, no evidence of mucosal
damage on endoscopy.
 Complications: chronic acid exposure on esophagus, oropharynx, airway and mouth
causes esophagitis, esophageal stricture (dysphagia), asthma, bronchitis, pneumonia,
chronic sinusitis, dental erosions, Barrett’s esophagitis.
o Barrett’s Esophagitis
 Patho: Replacement of normal squamous epithelium cells of esophagus –
intestinal metaplasia. Basically, the lining of the esophagus changes –
becomes bigger. Pre-cancerous.
 Risk Factors: 3-5x higher risk in patients with GERD, middle aged men,
Asymptomatic.
 Diagnosis: endoscopy. Surveillance 3-5 years.
 Diagnosis: history and physical exam, barium swallow, endoscopy, esophageal
manometry = motility study, 24-hour pH study
 Treatment: diet, lifestyle modifications, medications (tums), positioning, surgery.

Achalasia
 Patho: the LES fails to open up during swallowing which leads to a backup of food within
your esophagus. Opposite of GERD. Dilation of esophagus. Food sits there =
inflammatory response.
 Primary Cause: unknown.
 Secondary Cause: due to Chega’s disease, Addison’s disease, neurofibromatosis,
sarcoidosis.
 Esophageal innervation. LES contraction.
  Can Lead to: inflammation, ulceration, aspiration and esophageal cancer.

Gastritis: inflammation of the lining in the stomach. Gastric mucosal barrier: tight cell junctions,
lipid layer, mucus (prostaglandins), result of a breakdown in gastric mucosal barrier, stomach
issue unprotected from autodigestion by HCI acid and pepsin, inflammation: disruption of
capillary walls, tissue edema, bleeding
 Acute Gastritis
o Patho: inflammation of the gastric mucosa. surface epithelium.
o Etiology: drugs or chemicals. Aspirin, NSAIDS, alcohol, steroids, chemo,
radiation, bacterial toxins. GI bug.
o Clinical Manifestations: Sloughing of mucosa and acute gastric
bleeding/hemorrhage. heartburn, asymptomatic, gastric distress, nausea,
vomiting, bleeding, gastric distress, nausea, vomiting
o Treatment: self-limiting, will regenerate and heal in a few days
 Chronic Gastritis
o Patho: thinning and degeneration of gastric mucosa. No grossly visible erosions,
chronic inflammatory changes, atrophy of stomach epithelium (fibrosis,
strictures)
o Etiology: H. Pylori
 Patho: interferes with the protection of gastric mucosa against acid,
continuous inflammatory response, risk for gastric cancer. produces
urease which converts urea to ammonia to buffer the organism from
gastric acid, inflammation of antrum and body of stomach toxins,
interferes with protection of gastric mucosa, peptic ulcer disease,
atrophic gastritis, gastric lymphoma.
 Etiology: bacteria, fecal/oral, oral/oral routes. Gram negative bacteria
colonizes gastric mucosa
 Clinical Manifestations: initially abdominal pain and nausea then
asymptomatic.
 Diagnosis: antibody titer, urea breath test, stool antigen
 Treatment: two different kinds of antibiotics and proton pump inhibitor.

Peptic Ulcer Disease

 Patho: painful lesions or sores in mucosal wall of stomach 15%, duodenum 80% or
esophagus 5%. Causes higher acid-pepsin secretions.
 Risk Factors: smoking, NSAIDS, alcohol, age, hereditary, medications, chronic disease,
steroids.
 Main Etiology: H. Pylori, aspirin, NSAIDS
 Types:
o Curling ulcers: “stress” following major burn, trauma or severe infection (sepsis)
caused by decreased blood flow = ischemia, necrosis, gastric sloughing.
o Cushing ulcers: caused by head trauma, operations tumors. “think head”
 o Zollinger-Ellison syndrome: gastrinoma = tumor that secretes gastrin. small
intestine, pancreas. Results in lesions and diarrhea.
 Clinical Manifestations: burning, gnawing, cramping pain, pain in epigastrium, radiates
to back, episodic pain recurs in weeks or months.
o Gastric ulcers: pain immediately after eating. Directly in stomach.
o Duodenal ulcers: pain between meals (2-3 hours after eating), Pain is relieved by
food. Shuts off pyloric sphincter. More common.
 3 Complications: bleeding/hemorrhage, perforation (peritonitis), obstruction
 Diagnosis: labs, endoscopy, barium swallow
 Management: eradicate H. Pylori, decrease acidity*, lifestyle change.

Appendicitis right lower quadrant

 Patho: inflammation of vermiform appendix projection of cecum. Typically obstructed
with fecalith (inflamed, swollen).
 Risk Factors: 20-30 years of age: obstruction and inflammation, decreased blood flow
and hypoxia, abscesses = gangrene = perforation = leads to peritonitis!
 Clinical Manifestations: continuous periumbilical pain (localizes to the right lower
quadrant), leukocytosis, low grade fever, anorexia, nausea, vomiting, rebound
tenderness, muscle guarding. Increased WBC.
 Treatment: right leg is often positioned flexed for comfort, antibiotics, surgery.

Diverticulosis “losis” = “lower risk”

 Patho: partial herniation in colonic mucosa
 Etiology: low fiber diet, lack of exercise, constipation
 Clinical manifestations: asymptomatic, bloating, vague abdominal discomfort

Diverticulitis it is = inflammation left lower quadrant

 Patho: inflammation of Diverticula: pouches of mucosa that bulge out due to weakness
in colon muscle wall. Full herniation all the way through the colonic mucosa. Increased
intraluminal pressure in haustra causes sigmoid colon to bulge out. intraluminal
pressure = outpouching through haustra. Inflammation of diverticula can cause micro
perforation. Inflammation – bleeding – abscess – peritonitis.
 Clinical Manifestations: LLQ tenderness**, low grade fever, obstruction, constipation,
nausea, vomiting, leukocytosis, fistulas can form
 Diagnosis: CT scan, ultrasound
 Treatment: bulk bowel retraining, bowel rest, IV abx, surgery.

Peritonitis
 Patho: inflammation of the abdominal peritoneum. Indicated leakage, perforation or
infection. Thick sticky exudate, seal off infection and perforation.
 Primary Cause: ascites
 Secondary Cause: appendicitis, trauma
  Clinical Manifestations: severe abdominal pain, distension, rebound tenderness, rigid
board like abdomen, fever, tachycardia, nausea, vomiting, altered bowel habits,
paralytic ileus, fluid shift, Pain that comes back
 Complication: sepsis, shock. Infection
 Treatment: NG tube, IV antibiotics, IV fluids, narcotics, surgery, flex legs

Intestinal Obstruction
bowel obstruction
 Patho: accumulation of fluid and gas proximal to obstruction = distension, altered
absorption, distention moves up. Increases intraluminal pressure = decreased blood
flow, altered bowel wall permeability. fluids shit from bowel into peritoneum =
peritoneal irritation (peritonitis)
 Can lead to: gangrene, perforation of bowel (fluid, electrolyte, acid-base imbalance),
hypovolemia, dehydration, sepsis, shock.
 Etiology: occurs when fluids, solids or gases are unable to pass through the GI tract.
o Mechanical Obstruction:
 Patho: the bowel is physically blocked, and GI contents cannot pass the
area of obstruction
 Etiology: surgical adhesions, hernias, large polyps or tumors (cancer),
volvulus (twisting), intussusception (telescoping), sever diverticular
disease, fecal impaction or obstruction
 Manifestations: intermittent pain, cramping, colicky pain
o Non mechanical Obstruction:
 Patho: bowel isn’t moving things, not blocked just not moving.
 Etiology: paralytic ileus** (paralyzied), post op, medications, peritonitis,
intestinal pseudo-obstruction, mesenteric vascular obstruction
 Manifestations: continuous pain** bowel movement passes feces for a
short period, abdominal distention
 Risk Factors: multiple abdominal surgeries
 Clinical Manifestations:
o Small Bowel: 80%, rapid onset, vomiting is frequent, sometime projectile, fecal.
o Large Bowel: 20%, gradual onset, vomiting is rate, pain is low grade, crampy,
abdominal pain, bowel movement: constipated, abdominal distention is
increased.
 Diagnosis: careful history and physical exam (LACK OF BM’S!!), bowel sounds
(borborygmi heard for mechanical obstruction, absent bowel sounds for non-
mechanical), CBC, BMP, lactate, CRP, U/A, x-rays, CT scan, sigmoidoscopy, colonoscopy
 Treatment: NG tube, surgery, antibiotics, pain meds.
 GI Bleed

 Patho: blood in GI tact

 Clinical Manifestations:
o increased BUN (dehydrated)
o volume depletion
o decreased cardiac output
o hypotension
o tachycardia
o decreased mesenteric flow
o decreased urine output, acute kidney injury, decreased cerebral flow, decreased
coronary flow, angina, MI, heart failure, acidosis, anoxia (mental status changes)
 Diagnosis: Guiac test- occult bleeding*, radionucleotide imaging
 Treatment: Transfusions, IV fluids, treat the cause of bleeding

Upper GI Bleed
 Location: esophagus, stomach, duodenum
 Causes: esophageal varices (liver failure), Mallory-Weiss tear, peptic ulcer (lesion in
stomach)
 Symptoms: frank, bright red hematemesis, coffee grounds emesis, vomiting blood
 Diagnosis: Endoscopy

Lower GI Bleed
 Location: jejunum, rectum
 Causes: polyps, diverticulitis, inflammatory disease, cancer, hemorrhoids
 Symptoms: hematochezia (bright red blood, fresh, rectum), melena (tar colored blood),
blood in poop
 Diagnosis: Colonoscopy

Inflammatory Bowel Disease (IBD)

Inflammatory Bowel Disease

 Patho: chronic, recurrent inflammation of intestinal tract, Periods of remission
interspersed with periods of exacerbation. Tissue damage due to overactive and
sustained inflammatory response.
 Treatment: no cure, surgical therapy
 Clinical manifestations: diarrhea (> 6x daily), colicky abdominal pain, fatigue, weight
loss
 Complications: hemorrhage, strictures and obstruction, perforation
 Extra intestinal complications: fever, anemia, arthritis, joint pain, ankylosing spondylitis
(arthritis of spine), stomatitis, skin lesions, primary sclerosing cholangitis (inflammation,
scarring, obstruction of bile ducts)
  Diagnostic Studies: sigmoidoscopy and colonoscopy, small bowel series, capsule
endoscopy, abdominal CT scan, stool cultures, labs: CBC, ESR, CRP, CMP, B12, Vitamin D
 Goals of IBD Care: rest the bowel, control inflammation, treat infection, correct
malnutrition, alleviate stress, symptomatic relief (pain), reduce inflammation and
infection (anti-inflammatory, steroids, antibiotics, immunosuppressants)
 Etiology: unknown. Inflammation/immune response, epithelial dysfunction, intestinal
bacteria. Genetic and environmental factors also play a role.
o Ulcerative Colitis (rough papillae - tongue) small
 Patho: superficial ulcerations of mucosal and submucosal layer-like
appearance. Rough papillae. Diffuse inflammation beginning in rectum
and spreading up colon to cecum in a continuous pattern. Relapsing. May
be rectal sparing. Does not involve all bowel layers, does not involve
small bowel, major complication = CRC
 Clinical Manifestations: rectal bleeding, tenesmus, diarrhea
 Complications: toxic megacolon, colorectal cancer.
 Treatment: Surgical therapy (25-49% of patients will need)
o Chronis Disease (cobblestones) big
 Patho: inflammation involves all bowel layers, exacerbations and
remissions, can occur anywhere from mouth to anus, skip lesions, deep
ulcerations, fistulas and abscesses anywhere (GI tracts- bladder, vagina,
skin), classic cobblestone appearance of mucosa.
 Complications: scarring = narrowing of the lumen with structure
development = bowel obstruction. Fistulas = microscopic leaks that allow
bowel contents into peritoneal cavity = abscesses and peritonitis.
 Clinical Manifestations: no rectal bleeding, nutritional deficiencies due to
malabsorption (iron, B12, vitamin D), perianal abscess, fistulas or anal
fissure, diarrhea
 Treatment: Surgical therapy (75% of patients will need),

Colorectal Cancer – really bad

 Risk Factors: family, personal history of cancers or adenomatous polyps, FAP or HNPCC
(lynch syndrome), 85% from adenocarcinomas, 15% from hereditary disorders,
increased age, ulcerative colitis, PUD, smoking, alcohol, obesity, diet high in red meat.
 Clinical Manifestations: change in bowel habits (constipation), acute
perforation/obstruction, blood in stool, unexplained iron deficiency anemia,
tenesmus/rectal pain (rectal cancer), weight loss, fatigue,
 Diagnostic Studies: colonoscopy*, staging with CT, ultrasound, MRI
 Treatment: surgery, chemo/radiation
 Prevention: colonoscopy every 10 years starting at age 50, earlier with high risk
patients, if polyps are found then colonoscopy every 5 years
Acute Diarrhea resolves in less than 2 weeks
 Severe Diarrhea: can result in life threatening dehydration, leading cause of death in
developing countries, causes an electrolyte disturbance, hyperactive bowel sounds are
heard.
 Non-Inflammatory: (vibrio cholerae, E. coli, viruses, Giardia) watery, large volume, non-
bloody stools, cramps, nausea, vomiting, bloating, disrupts absorption, secretion in
small intestine, dehydration, acidosis.
 Inflammatory: (salmonella, C. Diff) fever, small volume, bloody, invasion of intestinal
cells and inflammation, leukocytes in feces, lower abdominal pain, urgency.
 C. Diff: antibiotics (1-2 weeks), toxins bind to mucosa, inflammation. Contact plus
precautions.

Chronic Diarrhea lasts for 4 weeks or more, malabsorption and malnutrition.

 Hyperosmotic luminal contents: lactase deficiency, milk of magnesia, decreased transit
time. Increased intestinal secretory process: excess bile acids, bacterial overgrowth in
colon. factitious diarrhea: indiscriminate laxative use
 inflammatory conditions: IBD, frequency, urgency, colicky pain, fecal incontinence,
tenesmus
 Infectious Process: parasitic infection, CMV, giardia
 Diagnostic Studies: colonoscopy with biopsy

Constipation
 Patho: hard stools, infrequent stools, abdominal pain and bloating, straining/incomplete
evacuation, less than 3 stools per week.
 Risk Factors: median prevalence of 16%. Over the age of 60 33%, higher in women (5:1
ratio to males), women are more likely to use laxatives and seek healthcare.
 Etiology: can be a primary disorder or caused by medication or a disease. failure to
respond to urge, inadequate fiber/fluids, weakness of abdominal muscles, pregnancy
(progesterone- relaxes muscles to not work), hemorrhoids.
 Warning Signs: bleeding, sudden change in stool caliber or consistency, new pain, r/o
other pathology, tumors, SCI, hypothyroid, Parkinson’s, MS, celiac, IBD, secondary to
medication. Can lead to bowel obstruction.
 Treatment: high fiber diet, increase fluids, fiber supplementation (preventative only),
laxatives, suppositories, enema, prescription medications, exercises (Kegels), PT,
possible surgical intervention.