NUR / NUR: Essentials of Pathophysiology Final Exam Test
UPDATED ACTUAL Exam Questions and CORRECT Answers
Question 1.
manifestations of gastritis
Correct Answer: indigestion, heartburn, epigastric pain, abdominal cramping,
nausea, vomiting, anorexia, fever, malaise. hematemesis and dark, tarry
stools indicate ulceration and bleeding. chronic gastritis increases risk for
peptic ulcers, gastric cancer, anemia, and hemorrhage.
Question 2.
gastritis diagnosis/treatment
Correct Answer: h&p, GI tract x ray, egd, serum h. pylori antibodies, h. pylori
breath test, stool analysis (h. pylori and occult blood treatment-acute is self
limiting ususally resolves meds-antacids, acid-reducing agents, and mucosal
barrier agents other strategies include those for GERD (diet, small meals,
antacids)
Question 3.
Peptic ulcer disease (PUD)
Correct Answer: refers to erosive lesions affecting the muscularis mucosa of
the stomach or duodenum. ulcers vary in size and severity, ranging from
superficial erosions to complete penetration through GI tract wall
Question 4.
peptic ulcer disease etiology and patho
Correct Answer: ETIOLOGY: most commonly H. pylori and NSAID use. PATHO:
develops because of an imbalance between destructive forces and protective
mechanisms
Question 5.
PUD duodenal ulcers
Correct Answer: most commonly associated with excessive acid or H. pylori
infections typically present with epigastric pain relieved in the presence of
food
Question 6.
PUD gastric ulcers
,Correct Answer: less frequent-more deadly typically associated with
malignancy and NSAIDS pain worsens with eating
Question 7.
PUD Stress ulcers
Correct Answer: develop because of major physiological stressor on body due
to 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)
• PUD manifestations/treatment -✓✓epigastric, abd. pain, abd. cramping,
heartburn, indigestion, chest pain, nausea/voimiting, melena (dark, tarry
stools), fatigue, unexplained weight loss Treatment: same as gastritis:
antacids, mucosal barrier agents, acid-reducing agents possible surgical
repair
Question 8.
Iron-deficiency Anemia
Correct Answer: Not enough iron for hemoglobin production erythrocytes pale
and small Etiology: decreased iron consumption/absorption, increased
bleeding manifestations in addition to "anemia": brittle nails,
headache/irritability, pica, cyanosis of sclera of eyes, delayed healing
Question 9.
Anemia
Correct Answer: common acquired or inherited disorder of erythrocytes that
impairs the bloods oxygen-carrying capacity. ETIOLOGY: decrease in # of
circulating erythrocytes, reduction in hemoglobin content, presence of
abnormal hemoglobin MANIFESTATIONS: weakness, fatigue, pallor, syncope,
dyspnea, tachycardia
Question 10.
Pernicious anemia
Correct Answer: B12 deficiency or megaloblastic anemia large, immature
erythrocytes. usually lack of intrinsic factor (protein necessary for b12
absorption in stomach) b12 is needed for cell division and maturity. too little
b12 gradually causes neuro problems because of the breakdown in myelin,
neuro effects may be seen before anemia is diagnosed. Additional
manifestations: bleeding gums, diarrhea, impaired smell, DTR loss, anorexia,
personality/memory changes, + babinski sign, stomatitis, paresthesia of
hands and feet, unsteady gait
,Question 11.
aplastic anemia
Correct Answer: bone marrow fails to make enough blood cells leading to
pancytopenia MANIFESTATIONS: general anemia, leukcytopenia, and
recurrent infections can be caused by cancers, cancer treatment, pesticides
Question 12.
Sickle cell anemia
Correct Answer: genetic, hemoglobin-s trait vs. gene crescent shape during
times of hypoxia, can clump together and clog vessels. MANIFESTATIONS:
swelling in hands and feet, sickle cell crisis, abd. pain, bone pain, jaundice,
skin ulcers, stroke, chest pain tissue ischemia and necrosis. electrophoresis
and stem cell transplant may cure
Question 13.
thalassemia
Correct Answer: genetic, not RBC problem, hemoglobin problem. lack one or 2
proteins that make up hemoglobin MANIFESTATIONS: heart failure,
splenomegaly, hepatomegaly, bone deformities, jaundice, fatigue, dyspnea
• Idiopathic thrombocytopenia purpura (ITP) -✓✓hypocoagulopathy due to
immune system destroying its own platelets (autoantibodies) Circulating IgG
reacts with the platelets which are then destroyed in the spleen and liver. can
be acute or chronic ETIOLOGY: idiopathic, autoimmune disease, live vaccines,
immunodeficiency disorders, viral infections Manifestations: abnormal
bleeding (petechiae, epistaxis [nose bleed], hematuria) ACUTE TREATMENT:
glucocorticoid steroids, immunoglobulins, plasmapheresis and platelet
pheresis CHRONIC TREATMENT: splenectomy, blood transfusions,
immunosuppressants
Question 14.
Thrombotic thrombocytopenia purpura
Correct Answer: coagulation disorter d/t deficiency of enzyme responsible for
cleaving von Willebrand factor increased clotting which decreases available
platelets --> bleeding under skin and purple colored spots called "purpura"
manifestations: thrombi>thrombocytopenia>bleeding purpura, LOC changes,
confusion, fatigue, fever
Question 15.
Thrombocytopenia
Correct Answer: a condition in which there is an abnormally small number of
platelets circulating in the blood
, Question 16.
hemostasis
Correct Answer: stoppage of bleeding
1. vasospasm (vasoconstriction)-brief reflex blood vessel narrows to decrease
blood flow to injury and increase bp
2. platelet plug formation-involves activation, aggregation, and adherence of
platelets into a plug that serves as a barrier against blood flowing out of
vessel. 3 coagulation-or clotting changes blood into gel through cascade of
events. fibrin mesh is cleaved from fibrinogen. fibrin acts like glue during clot
formation holding the platelet plug together. Once blood flow is stopped
tissue repair can begin
Question 17.
parathyroid hormone (PTH)
Correct Answer: Works in opposite way to calcitonin to regulate serum calcium
levels. PTH secreted with Ca levels drop. PTH increases osteoclast activity
which releases Ca from bone. Also increases absorption of Ca in GI tract and
kidneys. PTH also regulates phosphate levels by reducing renal reabsorption
of phosphate in proximal tubule and increasing the uptake from the intestines
and bones into blood
Question 18.
hyperparathyroidism and etiology
Correct Answer: condition of excessive PTH production by parathyroid glands
causes: tumors, hyperplasia, chronic hypocalcemia (renal failure)
Question 19.
hyperparathyroidism manifestations/treatment
Correct Answer: osteoporosis, renal calculi, polyuria, abd. pain, constipation,
fatigue, weakness, flaccid muscles, dysrhythmias, hypertension, depression,
forgetfulness,
• Cushing's syndrome -✓✓excessive cortisol that results from the increased
ACTH levels
Question 20.
Cushing's syndrome etiology
Correct Answer: iatrogenic from ingestion of glucocorticoid meds, adrenal
tumors that secrete glucocorticoids, pituitary tumors that secrete ACTH and
cortisol, and paraneoplastic syndrome (rare disorders triggered by abnormal
immune response to a cancerous tumor called neoplasm)
UPDATED ACTUAL Exam Questions and CORRECT Answers
Question 1.
manifestations of gastritis
Correct Answer: indigestion, heartburn, epigastric pain, abdominal cramping,
nausea, vomiting, anorexia, fever, malaise. hematemesis and dark, tarry
stools indicate ulceration and bleeding. chronic gastritis increases risk for
peptic ulcers, gastric cancer, anemia, and hemorrhage.
Question 2.
gastritis diagnosis/treatment
Correct Answer: h&p, GI tract x ray, egd, serum h. pylori antibodies, h. pylori
breath test, stool analysis (h. pylori and occult blood treatment-acute is self
limiting ususally resolves meds-antacids, acid-reducing agents, and mucosal
barrier agents other strategies include those for GERD (diet, small meals,
antacids)
Question 3.
Peptic ulcer disease (PUD)
Correct Answer: refers to erosive lesions affecting the muscularis mucosa of
the stomach or duodenum. ulcers vary in size and severity, ranging from
superficial erosions to complete penetration through GI tract wall
Question 4.
peptic ulcer disease etiology and patho
Correct Answer: ETIOLOGY: most commonly H. pylori and NSAID use. PATHO:
develops because of an imbalance between destructive forces and protective
mechanisms
Question 5.
PUD duodenal ulcers
Correct Answer: most commonly associated with excessive acid or H. pylori
infections typically present with epigastric pain relieved in the presence of
food
Question 6.
PUD gastric ulcers
,Correct Answer: less frequent-more deadly typically associated with
malignancy and NSAIDS pain worsens with eating
Question 7.
PUD Stress ulcers
Correct Answer: develop because of major physiological stressor on body due
to 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)
• PUD manifestations/treatment -✓✓epigastric, abd. pain, abd. cramping,
heartburn, indigestion, chest pain, nausea/voimiting, melena (dark, tarry
stools), fatigue, unexplained weight loss Treatment: same as gastritis:
antacids, mucosal barrier agents, acid-reducing agents possible surgical
repair
Question 8.
Iron-deficiency Anemia
Correct Answer: Not enough iron for hemoglobin production erythrocytes pale
and small Etiology: decreased iron consumption/absorption, increased
bleeding manifestations in addition to "anemia": brittle nails,
headache/irritability, pica, cyanosis of sclera of eyes, delayed healing
Question 9.
Anemia
Correct Answer: common acquired or inherited disorder of erythrocytes that
impairs the bloods oxygen-carrying capacity. ETIOLOGY: decrease in # of
circulating erythrocytes, reduction in hemoglobin content, presence of
abnormal hemoglobin MANIFESTATIONS: weakness, fatigue, pallor, syncope,
dyspnea, tachycardia
Question 10.
Pernicious anemia
Correct Answer: B12 deficiency or megaloblastic anemia large, immature
erythrocytes. usually lack of intrinsic factor (protein necessary for b12
absorption in stomach) b12 is needed for cell division and maturity. too little
b12 gradually causes neuro problems because of the breakdown in myelin,
neuro effects may be seen before anemia is diagnosed. Additional
manifestations: bleeding gums, diarrhea, impaired smell, DTR loss, anorexia,
personality/memory changes, + babinski sign, stomatitis, paresthesia of
hands and feet, unsteady gait
,Question 11.
aplastic anemia
Correct Answer: bone marrow fails to make enough blood cells leading to
pancytopenia MANIFESTATIONS: general anemia, leukcytopenia, and
recurrent infections can be caused by cancers, cancer treatment, pesticides
Question 12.
Sickle cell anemia
Correct Answer: genetic, hemoglobin-s trait vs. gene crescent shape during
times of hypoxia, can clump together and clog vessels. MANIFESTATIONS:
swelling in hands and feet, sickle cell crisis, abd. pain, bone pain, jaundice,
skin ulcers, stroke, chest pain tissue ischemia and necrosis. electrophoresis
and stem cell transplant may cure
Question 13.
thalassemia
Correct Answer: genetic, not RBC problem, hemoglobin problem. lack one or 2
proteins that make up hemoglobin MANIFESTATIONS: heart failure,
splenomegaly, hepatomegaly, bone deformities, jaundice, fatigue, dyspnea
• Idiopathic thrombocytopenia purpura (ITP) -✓✓hypocoagulopathy due to
immune system destroying its own platelets (autoantibodies) Circulating IgG
reacts with the platelets which are then destroyed in the spleen and liver. can
be acute or chronic ETIOLOGY: idiopathic, autoimmune disease, live vaccines,
immunodeficiency disorders, viral infections Manifestations: abnormal
bleeding (petechiae, epistaxis [nose bleed], hematuria) ACUTE TREATMENT:
glucocorticoid steroids, immunoglobulins, plasmapheresis and platelet
pheresis CHRONIC TREATMENT: splenectomy, blood transfusions,
immunosuppressants
Question 14.
Thrombotic thrombocytopenia purpura
Correct Answer: coagulation disorter d/t deficiency of enzyme responsible for
cleaving von Willebrand factor increased clotting which decreases available
platelets --> bleeding under skin and purple colored spots called "purpura"
manifestations: thrombi>thrombocytopenia>bleeding purpura, LOC changes,
confusion, fatigue, fever
Question 15.
Thrombocytopenia
Correct Answer: a condition in which there is an abnormally small number of
platelets circulating in the blood
, Question 16.
hemostasis
Correct Answer: stoppage of bleeding
1. vasospasm (vasoconstriction)-brief reflex blood vessel narrows to decrease
blood flow to injury and increase bp
2. platelet plug formation-involves activation, aggregation, and adherence of
platelets into a plug that serves as a barrier against blood flowing out of
vessel. 3 coagulation-or clotting changes blood into gel through cascade of
events. fibrin mesh is cleaved from fibrinogen. fibrin acts like glue during clot
formation holding the platelet plug together. Once blood flow is stopped
tissue repair can begin
Question 17.
parathyroid hormone (PTH)
Correct Answer: Works in opposite way to calcitonin to regulate serum calcium
levels. PTH secreted with Ca levels drop. PTH increases osteoclast activity
which releases Ca from bone. Also increases absorption of Ca in GI tract and
kidneys. PTH also regulates phosphate levels by reducing renal reabsorption
of phosphate in proximal tubule and increasing the uptake from the intestines
and bones into blood
Question 18.
hyperparathyroidism and etiology
Correct Answer: condition of excessive PTH production by parathyroid glands
causes: tumors, hyperplasia, chronic hypocalcemia (renal failure)
Question 19.
hyperparathyroidism manifestations/treatment
Correct Answer: osteoporosis, renal calculi, polyuria, abd. pain, constipation,
fatigue, weakness, flaccid muscles, dysrhythmias, hypertension, depression,
forgetfulness,
• Cushing's syndrome -✓✓excessive cortisol that results from the increased
ACTH levels
Question 20.
Cushing's syndrome etiology
Correct Answer: iatrogenic from ingestion of glucocorticoid meds, adrenal
tumors that secrete glucocorticoids, pituitary tumors that secrete ACTH and
cortisol, and paraneoplastic syndrome (rare disorders triggered by abnormal
immune response to a cancerous tumor called neoplasm)