Studied by 37 people
What is the Z-line?
sharp transition at the gastroesophageal junction from squamous to simple columnar epithelium of the stomach
In a normal esophagus pressure is ___ in the body of the esophagus and __ at the UES and LES to prevent aspiration and gastric reflex.
low; high
What is a major cause of esophageal reflux?
disordered lower esophageal tone
What is dyspepsia?
sensation of pain or discomfort in the upper abdomen
What are the primary S&S of dyspepsia?
upper abd pain, belching, nausea, vomiting, early satiety
What is heartburn?
painful burning felling in the chest or throat typically after eating and worsens when lying down/bending over
What is reflux esophagitis?
inflammation of the esophageal mucosa resulting from persistent or repeated acid exposure
What does reflux esophagitis do to the Z-line?
it can destroy it over time
What are the predominant S&S of reflux esophagitis?
heartburn that worsens a night and lying supine
What is the etiology of reflux esophagitis?
drugs that dec LES tone (morphine, dopamine, CCB), foods that dec LES pressure (chocolate, caffeine, spice, alc), smoking
What else can contribute to the development of reflux esophagitis?
pregnancy, alkaline injury, gastric outlet obstruction, hiatal hernia, reflux of pepsin or bile
What complications can reflux esophagitis cause?
strictures in the distal esophagus, dysphagia, hemorrhage, perforation, hoarseness, coughing, wheezing, aspiration pneumo
What is the pathophysiology behind reflux esophagitis?
loss of LES tone → inc transient relaxations, inc stomach V inc production of stomach acid → epithelial damage, inflammation, & erosion → sphincter function compromised
What is Barrett’s esophagus?
continued reflux of gastric contents results in a change of esophageal epithelium from normal squamous to columnar/intestinal metaplasia
What can Barrett’s esophagus develop into? What increases this risk?
adenocarcinoma of the esophagus; smoking and alc abuse
What does Barrett’s do to the Z-line?
distorts it and slowly erodes it
What is a hiatal hernia?
portion of the proximal stomach slides into the chest cavity through the opening in the diaphragm
What is the most common type of hiatal hernia?
sliding hiatus hernia
What does a hiatal hernia do to the LES?
causes upward displacement → competency is lost
What type of hiatal hernia is characterized but constant displacement of the stomach?
paraesophageal hiatus hernia
What protects the stomach from auto-digestion?
Gastric mucus and the Epithelial barrier
What is the rate of gastric emptying dependent on?
the chemical & physical composition of the chyme entering the duodenum
What hormones are stimulates in the intestinal feedback loop?
Acetylcholine
What hormones are inhibitory in the intestinal feedback loop?
VIP & nitric oxide
What type of pts does dumping syndrome occur in?
pts S/P surgical procedures (partial gastrectomy, gastric bypass, nonselective vagotomy)
What S&S are associated w/ dumping syndrome?
N/V, bloating, flushing, diaphoresis, explosive diarrhea; typically w/in 15-30 minutes after eating
What is the etiology of gastroparesis?
idiopathic, complication of DM, vagus nerve disruption via surgery
What is gastroparesis?
delayed gastric emptying due to improper functioning of stomach muscles
What S&S are associated w/ gastroparesis?
N/V, bloating, heartburn, early satiety, wt loss, lack of appetite, malnutrition, can affect blood sugar levels
What types of medications can cause gastroparesis?
antidepressants, narcotic pain medications
What is a bezoar?
solid, hardened mass of undigested food
What complications can arise from gastroparesis?
bacterial overgrowth from fermentation of food, bezoar, alteration in blood sugar → worsening DM
How does alterations in blood sugar affect gastroparesis?
make it worse
What is melena? What causes it?
black tarry stools; from bleeding in the upper GI tract
What is hematochezia? What causes it?
bright red blood in the stool; from lesions in the colon or rectum
What is hematemesis? What causes it?
blood in vomitus; bleeding in the esophagus or stomach
What is the integrity of the upper GI tract dependent on?
balance between “hostile” factors and “protective” factors affecting GI mucosa
What are “hostile” factors?
gastric acid, H. pylori, NSAIDs, pepsin
What are “protective” factors?
prostaglandins, mucus, bicarb, blood flow to mucosa
What factors contribute to the pathogenesis of PUD?
excessive gastric acid secretion and decreased mucosal defense
How does chronic gastritis contribute to pernicious anemia?
lack of B12 absorption secondary to decreased intrinsic factor
How does gastritis contribute to gastric ulcer formation?
reducing the quantity of prostaglandins that may otherwise diminish acid secretion
weakens the epithelial cell barrier or the mucous & bicarb secreted
How does the mucosa present on pts w/ chronic atrophic gastritis?
dry due to the lack of mucosa & barrier destruction
What is chronic atrophic gastritis associated w/?
H. pylori infection, development of pernicious anemia, gastric adenocarcinoma, GI endocrine hyperplasia
What is the pathophysiology behind chronic gastritis?
auto-Ab to parietal cells, intrinsic factor & gastrin
inflammatory cell infiltration → mucosal atrophy and loss of glands
reduced capacity to secrete gastric acids
inc serum levels of gastrin → inc acid secretion
What are the S&S of a gastric ulcer?
chronic, mild, gnawing or burning abd or chest pain
superficial or deep erosion of GI mucosa
Pain intensifies w/ food ingestions
avoids food → wt loss
often in the antrum (distal)
What are the S&S of a duodenal ulcer?
gnawing or burning epigastric pain 1-3 hrs after eating
can awaken them at night
antacids or food intake provides relief → wt gain
can be Asx
What causes GI ulcers?
H. pylori infection, NSAIDs, alc abuse, shock, uremia, severely burned pts (stress ulcers), hypersecretion of gastric acid (gastrinoma)
What are the characteristics of gastric ulcers?
superficial or deep erosion of GI mucosa, most occur on the lesser curvature of the stomach
What can contribute to the development of a gastric ulcer?
motility defects, reflux of acids, mucosal ischemia from acid erosion or prostaglandin deficiency
What are the characteristics of duodenal ulcers?
more common, heritable component, penetrate mucosa, sequela of H. pylori infection, less association w/ development of gastric adenocarcinoma
What are duodenal ulcers caused by?
altered mucosal response, excessive acid secretion, psychologic stress
What complications can arise from ulcers in peptic acid disease?
acute/chronic GI bleeding → dec Hct, hematemesis, hematochezia, melena, gastric outlet obstruction, life threatening perforation & obstruction
What is H. pylori highly associated w/?
development of gastric carcinoma
What would an endoscopy of a H. pylori infection show?
gastritis, duodenitis, or Asx
What is the H. pylori pathophysiology?
moves in corkscrew fashion through mucous layer and attaches to gastric epithelial cells (in duodenum, only areas that are a result of excess acid damage)
produces urease: converts urea to ammonia to help it survive by forming alkaline cloud around the bacteria
What proteins is the cytotoxicity caused by H. pylori linked to?
cagA & vacA
What are the risk factors for developing an ulcer from NSAIDs?
advanced age, hx of ulcer disease, higher doses, serious systemic disorders, concomitant us of corticosteroids or anticoagulants
How do NSAIDs contribute to the development of ulcers?
diminish the hydrophobicity of gastric mucus
decrease synthesis of mucosal prostaglandins via arachidonic acid and its catalyst
adverse effects are due to the constitutively expressed cyclo-oxygenase-1
Which type of ulcer are NSAIDs more likely to cause?
gastric
What is cholelithiasis?
gall stones
What S&S are associated w/ cholelithiasis?
vary: mild nausea → severe RUQ pain (can be midepigastric), ± jaundice, mild sx w/ eating
What is biliary colic?
GB attack
Who is a “typical” cholelithiasis pt?
“Female Fat Fertile Forty”; F>M, obese, pregnant, inc age
How can pregnancy cause cholelithiasis?
estrogen causes excess cholesterol to be released into the bile → inc stone formation
What is the relationship between cholesterol in the blood and cholesterol gallstones?
none
Is the diet responsible for the development of cholesterol gallstones?
no
What contributes to the formation of cholelithiasis?
supersaturation, loss of GB muscular wall motility, chronic bacterial colonization/infection, estrogens & prostaglandins inc mucous & glycoprotein production → inc in bile cholesterol
What is the most common type of gallstone?
cholesterol
What are the different types of gallstones?
cholesterol, bilirubin, sludge
What is cholecystitis?
inflammation of the gallbladder
What is the triad of acute cholecystitis?
fever, RUQ pain, leukocytosis
What is cholecystitis associated w/?
cholelithiasis
What causes acute cholecystitis?
irritation of the GB mucosa caused by bacteria or lysolethicin
What is the pathophysiology of cholecystitis?
damage to the GB wall → release of phospholipase A → phospholipase A converts lethicin to lysolethicin → widespread irritation of GB wall
What is the duration of acute diarrhea? What typically causes it?
< 2 wks; usually infectious
What is the duration of chronic diarrhea? What usually causes it?
> 4 wks; usually medication side effects
What causes secretory diarrhea?
abn secretion of fluid by intestinal cells caused by bacteria (cholera)
What causes osmotic diarrhea?
drawing in more fluid/retaining water in the gut lumen due to excessive amount of solutes in the intestinal lumen
What causes inflammatory diarrhea?
inflammatory fluid present/ irritation
What causes motility diarrhea?
moving too fast through the GI system
What causes malabsorption?
altered motility, digestion, absorption
Does osmotic diarrhea stop when the pt fasts?
Yes!
Osmotic diarrhea typically results from what?
ingestion of poorly absorbed substrate = pulls water into gut
Malabsorption of certain carbs: lactose intolerance
Does secretory diarrhea stop when the pt fasts?
No!
What kind of diarrhea does Cholera cause?
vomiting & watery diarrhea, “rice water” (secretory)
What causes the sx of infectious diarrhea?
toxins that alter small bowel secretions & absorption OR direct mucosal invasion
What are complications that diarrhea can cause?
dehydration, malnutrition, wt loss, vit deficiency, intestinal perforation (rare)
How can IBD be distinguished from infectious states?
recurrent episodes of mucopurulent bloody diarrhea, negative cultures, failure to respond to Abx
What is IBD characterized by?
exacerbations & remissions; mostly a disease of exclusion
What are the 2 forms of IBD?
Chron’s & ulcerative colitis (UC)
What is the etiology of IBD?
unknown; genetic & environmental factors play a role (bacteria, dietary psychosocial, defective immune response)
What is the pathogenesis of Crohn’s?
inflammation may be due to cytokines (interleukins & TNF)
What is the pathogenesis of UC?
inflammation due cytokines, infection, allergies to specific foods, psychosocial, immune responses to bacteria & self-antigens
What S&S are associated w/ Crohn’s?
colicky abd pain, intermittent bloody diarrhea, flatulence, fevers, erythema nodosum, arthritis, stomatitis
What S&S are associated w/ UC?
abd pain, tenesmus, diarrhea, rectal bleeding, uveitis, stomatitis, pyoderma gangrenosum
What are the complications of UC?
toxic megacolon (inc risk of perforation), hemorrhage, high risk of colon cancer
When do you need to start screening for colon cancer in pts w/ UC?
7 yrs after dx
Where is Crohn’s most frequently located?
distal (terminal) ileum; can be anywhere in the GI tract
What are the skip lesions seen in Crohn’s?
areas of inflammation & ulceration are interspersed w/in areas of unaffected tissue (discontinuous)
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