11/9/25, 6:48
PM
PATHOPHYSIOLOGY FINAL NUR 2063 FINAL EXAM
QUESTIONS WITH COMPLETE SOLUTIONS VERIFIED
UPDATE 2025/2026
inflammation of stomach's mucolas lining
(can involve entire stomach or region)
Gastritis and Etiology can be acute or chronic.
and patho may be caused by h. pylori infection
(imbeds in mucosal layer activating
toxins and enzymes that cause
inflammation. NSAIDS, chronic alcohol
consumption, stress, trauma, burns, or
infections, autoimmune conditions
indigestion, heartburn, epigastric pain,
abdominal cramping, nausea, vomiting,
manifestations of anorexia, fever, malaise.
gastritis hematemesis and dark, tarry stools
indicate ulceration and bleeding. chronic
gastritis increases risk for peptic ulcers,
gastric cancer, anemia, and hemorrhage.
h&p, GI tract x ray, egd, serum h. pylori
antibodies, h. pylori breath test, stool
analysis (h. pylori and occult blood
1/36
,11/9/25, 6:48
PM
gastritis treatment-acute is self limiting ususally resolves
diagnosis/treatment meds-antacids, acid-reducing
agents, and mucosal barrier
agents other strategies include
those for GERD (diet, small meals,
antacids)
refers to erosive lesions affecting
Peptic ulcer disease the muscularis mucosa of the
(PUD) stomach or duodenum. ulcers vary in
size and severity, ranging from
superficial erosions to complete
penetration through GI tract wall
ETIOLOGY: most commonly H. pylori and NSAID
peptic ulcer disease use.
etiology and patho PATHO: develops because of an
imbalance between destructive forces
and protective mechanisms
PUD duodenal ulcers most commonly associated with
excessive acid or H. pylori
infections typically present with
epigastric pain relieved in the
presence of food
less frequent-more deadly
PUD gastric ulcers typically associated with
malignancy and NSAIDS
pain worsens with
2/36
,11/9/25, 6:48
PM
eating
3/36
, 11/9/25, 6:48
PM
develop because of major
physiological stressor on body due to
PUD Stress ulcers local tissue ischemia, tissue acidosis,
bile salts entering stomach, and
decreased GI motility most frequently
develop in stomach; multiple ulcers can
form within hours of the precipitating
event
often hemorrhage is the first indication
(vomiting blood or blood in stool)
epigastric, abd. pain, abd. cramping,
heartburn, indigestion, chest pain,
PUD nausea/voimiting, melena (dark, tarry
manifestations/treat stools), fatigue, unexplained weight loss
ment Treatment: same as gastritis: antacids,
mucosal barrier agents, acid-reducing
agents possible surgical repair
Not enough iron for
hemoglobin production
Iron-deficiency Anemia erythrocytes pale and
small
Etiology: decreased iron
consumption/absorption, increased
bleeding manifestations in addition to
"anemia": brittle nails, headache/irritability,
4/36
PM
PATHOPHYSIOLOGY FINAL NUR 2063 FINAL EXAM
QUESTIONS WITH COMPLETE SOLUTIONS VERIFIED
UPDATE 2025/2026
inflammation of stomach's mucolas lining
(can involve entire stomach or region)
Gastritis and Etiology can be acute or chronic.
and patho may be caused by h. pylori infection
(imbeds in mucosal layer activating
toxins and enzymes that cause
inflammation. NSAIDS, chronic alcohol
consumption, stress, trauma, burns, or
infections, autoimmune conditions
indigestion, heartburn, epigastric pain,
abdominal cramping, nausea, vomiting,
manifestations of anorexia, fever, malaise.
gastritis hematemesis and dark, tarry stools
indicate ulceration and bleeding. chronic
gastritis increases risk for peptic ulcers,
gastric cancer, anemia, and hemorrhage.
h&p, GI tract x ray, egd, serum h. pylori
antibodies, h. pylori breath test, stool
analysis (h. pylori and occult blood
1/36
,11/9/25, 6:48
PM
gastritis treatment-acute is self limiting ususally resolves
diagnosis/treatment meds-antacids, acid-reducing
agents, and mucosal barrier
agents other strategies include
those for GERD (diet, small meals,
antacids)
refers to erosive lesions affecting
Peptic ulcer disease the muscularis mucosa of the
(PUD) stomach or duodenum. ulcers vary in
size and severity, ranging from
superficial erosions to complete
penetration through GI tract wall
ETIOLOGY: most commonly H. pylori and NSAID
peptic ulcer disease use.
etiology and patho PATHO: develops because of an
imbalance between destructive forces
and protective mechanisms
PUD duodenal ulcers most commonly associated with
excessive acid or H. pylori
infections typically present with
epigastric pain relieved in the
presence of food
less frequent-more deadly
PUD gastric ulcers typically associated with
malignancy and NSAIDS
pain worsens with
2/36
,11/9/25, 6:48
PM
eating
3/36
, 11/9/25, 6:48
PM
develop because of major
physiological stressor on body due to
PUD Stress ulcers local tissue ischemia, tissue acidosis,
bile salts entering stomach, and
decreased GI motility most frequently
develop in stomach; multiple ulcers can
form within hours of the precipitating
event
often hemorrhage is the first indication
(vomiting blood or blood in stool)
epigastric, abd. pain, abd. cramping,
heartburn, indigestion, chest pain,
PUD nausea/voimiting, melena (dark, tarry
manifestations/treat stools), fatigue, unexplained weight loss
ment Treatment: same as gastritis: antacids,
mucosal barrier agents, acid-reducing
agents possible surgical repair
Not enough iron for
hemoglobin production
Iron-deficiency Anemia erythrocytes pale and
small
Etiology: decreased iron
consumption/absorption, increased
bleeding manifestations in addition to
"anemia": brittle nails, headache/irritability,
4/36
