Pathophysiology Exam 3 – Lecture
Pathophysiology
Summary andExam
Practice
3 –Questions
Lecture
Pathophysiology
Summary
with Answers.pdf
and
Exam
Practice
3 –Questions
Lecture Summary
with Answers.pdf
and Practice Questions with Answers.pdf
Pathophysiology
Exam 3 – Lecture
Summary and
Practice Questions
with Answers
Pathophysiology Exam 3 – Lecture
Pathophysiology
Summary andExam
Practice
3 –Questions
Lecture
Pathophysiology
Summary
with Answers.pdf
and
Exam
Practice
3 –Questions
Lecture Summary
with Answers.pdf
and Practice Questions with Answers.pdf
,Pathophysiology exam 3.pdf Pathophysiology exam 3.pdf Pathophysiology exam 3.pdf
Terms in this set (83)
dysphagia difficulty swallowing, classified according to location (oropharyngeal,
esophageal) and mechanism (mechanical, functional)
oropharyngeal dysphagia difficulty with the voluntary (CNS) phase of swallowing, involved tongue,
posterior oropharynx, and epiglottis
esophageal dysphagia difficulty with the transfer of food down the esophagus, due to structural issue
with esophagus or external compression/obstruction, motility issues (achalasia)
achalasia functional esophageal dysphagia, autoimmune destruction of inhibitory neurons
in esophageal smooth muscle in lower esophagus
gastric endocrine cells G cells secrete gastrin -> stimulate gastric muscle activity, stimulates histamine
production by ECL cells
ECL cells secrete histamine -> acts on chief cells to stimulate acid production
gastroesophageal reflux disease (GERD) reflux of stomach contents (acid and pepsin) into esophagus, resulting in damage
to the endothelial cells of the esophagus, caused by lower esophageal sphincter
distention or relaxation and delayed gastric emptying
Pathophysiology exam 3.pdf Pathophysiology exam 3.pdf Pathophysiology exam 3.pdf
, Pathophysiology exam 3.pdf Pathophysiology exam 3.pdf Pathophysiology exam 3.pdf
LES relaxation and distention contents reflux into esophagus, caused by medications (nicotine, caffeine,
anticholinergics, nitrates), increased abdominal pressure (obesity, pregnancy), and
hiatal hernia
delayed gastric emptying Slowed movement of food from stomach to intestines, caused by gastroparesis
gastritis inflammation of gastric endothelium, occurs due to disruption of mucosal barrier,
overproduction of acid, infection, ischemia
peptic ulcer breakdown of gastric/duodenal tissue, concerns for bleeding and perforation,
occurs due to disruption of mucosal barrier, overproduction of acid, infection,
ischemia
mucosal barrier disruption less mucus production -> more susceptible to damage from acid and pepsin
caused by chronic NSAID use
H. pylori bacteria that adheres to gastric epithelium and resists destruction by HCl,
replicated and causes inflammation and increased gastric acid production ->
gastritis and PUD
Pathophysiology exam 3.pdf Pathophysiology exam 3.pdf Pathophysiology exam 3.pdf
Pathophysiology
Summary andExam
Practice
3 –Questions
Lecture
Pathophysiology
Summary
with Answers.pdf
and
Exam
Practice
3 –Questions
Lecture Summary
with Answers.pdf
and Practice Questions with Answers.pdf
Pathophysiology
Exam 3 – Lecture
Summary and
Practice Questions
with Answers
Pathophysiology Exam 3 – Lecture
Pathophysiology
Summary andExam
Practice
3 –Questions
Lecture
Pathophysiology
Summary
with Answers.pdf
and
Exam
Practice
3 –Questions
Lecture Summary
with Answers.pdf
and Practice Questions with Answers.pdf
,Pathophysiology exam 3.pdf Pathophysiology exam 3.pdf Pathophysiology exam 3.pdf
Terms in this set (83)
dysphagia difficulty swallowing, classified according to location (oropharyngeal,
esophageal) and mechanism (mechanical, functional)
oropharyngeal dysphagia difficulty with the voluntary (CNS) phase of swallowing, involved tongue,
posterior oropharynx, and epiglottis
esophageal dysphagia difficulty with the transfer of food down the esophagus, due to structural issue
with esophagus or external compression/obstruction, motility issues (achalasia)
achalasia functional esophageal dysphagia, autoimmune destruction of inhibitory neurons
in esophageal smooth muscle in lower esophagus
gastric endocrine cells G cells secrete gastrin -> stimulate gastric muscle activity, stimulates histamine
production by ECL cells
ECL cells secrete histamine -> acts on chief cells to stimulate acid production
gastroesophageal reflux disease (GERD) reflux of stomach contents (acid and pepsin) into esophagus, resulting in damage
to the endothelial cells of the esophagus, caused by lower esophageal sphincter
distention or relaxation and delayed gastric emptying
Pathophysiology exam 3.pdf Pathophysiology exam 3.pdf Pathophysiology exam 3.pdf
, Pathophysiology exam 3.pdf Pathophysiology exam 3.pdf Pathophysiology exam 3.pdf
LES relaxation and distention contents reflux into esophagus, caused by medications (nicotine, caffeine,
anticholinergics, nitrates), increased abdominal pressure (obesity, pregnancy), and
hiatal hernia
delayed gastric emptying Slowed movement of food from stomach to intestines, caused by gastroparesis
gastritis inflammation of gastric endothelium, occurs due to disruption of mucosal barrier,
overproduction of acid, infection, ischemia
peptic ulcer breakdown of gastric/duodenal tissue, concerns for bleeding and perforation,
occurs due to disruption of mucosal barrier, overproduction of acid, infection,
ischemia
mucosal barrier disruption less mucus production -> more susceptible to damage from acid and pepsin
caused by chronic NSAID use
H. pylori bacteria that adheres to gastric epithelium and resists destruction by HCl,
replicated and causes inflammation and increased gastric acid production ->
gastritis and PUD
Pathophysiology exam 3.pdf Pathophysiology exam 3.pdf Pathophysiology exam 3.pdf
