NUR 2063 FINAL EXAM 2LATEST VERSIONS 2023 ESSENTIALS OF PATHOPHYSIOLOGY FINAL 200
QUESTIONS AND CORRECT ANSWERS
Gastritis and Etiology and patho - (answer) inflammation of stomach's mucolas lining (can involve
entire stomach or region) can be acute or chronic.
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
manifestations of gastritis - (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.
gastritis diagnosis/treatment - (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)
Peptic ulcer disease (PUD) - (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
peptic ulcer disease etiology and patho - (answer) ETIOLOGY: most commonly H. pylori and NSAID use.
PATHO: develops because of an imbalance between destructive forces and protective mechanisms
PUD duodenal ulcers - (answer) most commonly associated with excessive acid or H. pylori infections
typically present with epigastric pain relieved in the presence of food
PUD gastric ulcers - (answer) less frequent-more deadly
typically associated with malignancy and NSAIDS
pain worsens with eating
,NUR 2063 FINAL EXAM 2LATEST VERSIONS 2023 ESSENTIALS OF PATHOPHYSIOLOGY FINAL 200
QUESTIONS AND CORRECT ANSWERS
PUD Stress ulcers - (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 - (answer) 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
Iron-deficiency Anemia - (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
Anemia - (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
Pernicious anemia - (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
,NUR 2063 FINAL EXAM 2LATEST VERSIONS 2023 ESSENTIALS OF PATHOPHYSIOLOGY FINAL 200
QUESTIONS AND CORRECT ANSWERS
aplastic anemia - (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
Sickle cell anemia - (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
thalassemia - (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) - (answer) 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
Thrombotic thrombocytopenia purpura - (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"
, NUR 2063 FINAL EXAM 2LATEST VERSIONS 2023 ESSENTIALS OF PATHOPHYSIOLOGY FINAL 200
QUESTIONS AND CORRECT ANSWERS
manifestations: thrombi>thrombocytopenia>bleeding
purpura, LOC changes, confusion, fatigue, fever
Thrombocytopenia - (answer) a condition in which there is an abnormally small number of platelets
circulating in the blood
hemostasis - (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
parathyroid hormone (PTH) - (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
hyperparathyroidism and etiology - (answer) condition of excessive PTH production by parathyroid
glands
causes: tumors, hyperplasia, chronic hypocalcemia (renal failure)
hyperparathyroidism manifestations/treatment - (answer) osteoporosis, renal calculi, polyuria, abd.
pain, constipation, fatigue, weakness, flaccid muscles, dysrhythmias, hypertension, depression,
forgetfulness,
Cushing's syndrome - (answer) excessive cortisol that results from the increased ACTH levels
Cushing's syndrome etiology - (answer) iatrogenic from ingestion of glucocorticoid meds, adrenal
tumors that secrete glucocorticoids, pituitary tumors that secrete ACTH and cortisol, and paraneoplastic
QUESTIONS AND CORRECT ANSWERS
Gastritis and Etiology and patho - (answer) inflammation of stomach's mucolas lining (can involve
entire stomach or region) can be acute or chronic.
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
manifestations of gastritis - (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.
gastritis diagnosis/treatment - (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)
Peptic ulcer disease (PUD) - (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
peptic ulcer disease etiology and patho - (answer) ETIOLOGY: most commonly H. pylori and NSAID use.
PATHO: develops because of an imbalance between destructive forces and protective mechanisms
PUD duodenal ulcers - (answer) most commonly associated with excessive acid or H. pylori infections
typically present with epigastric pain relieved in the presence of food
PUD gastric ulcers - (answer) less frequent-more deadly
typically associated with malignancy and NSAIDS
pain worsens with eating
,NUR 2063 FINAL EXAM 2LATEST VERSIONS 2023 ESSENTIALS OF PATHOPHYSIOLOGY FINAL 200
QUESTIONS AND CORRECT ANSWERS
PUD Stress ulcers - (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 - (answer) 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
Iron-deficiency Anemia - (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
Anemia - (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
Pernicious anemia - (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
,NUR 2063 FINAL EXAM 2LATEST VERSIONS 2023 ESSENTIALS OF PATHOPHYSIOLOGY FINAL 200
QUESTIONS AND CORRECT ANSWERS
aplastic anemia - (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
Sickle cell anemia - (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
thalassemia - (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) - (answer) 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
Thrombotic thrombocytopenia purpura - (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"
, NUR 2063 FINAL EXAM 2LATEST VERSIONS 2023 ESSENTIALS OF PATHOPHYSIOLOGY FINAL 200
QUESTIONS AND CORRECT ANSWERS
manifestations: thrombi>thrombocytopenia>bleeding
purpura, LOC changes, confusion, fatigue, fever
Thrombocytopenia - (answer) a condition in which there is an abnormally small number of platelets
circulating in the blood
hemostasis - (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
parathyroid hormone (PTH) - (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
hyperparathyroidism and etiology - (answer) condition of excessive PTH production by parathyroid
glands
causes: tumors, hyperplasia, chronic hypocalcemia (renal failure)
hyperparathyroidism manifestations/treatment - (answer) osteoporosis, renal calculi, polyuria, abd.
pain, constipation, fatigue, weakness, flaccid muscles, dysrhythmias, hypertension, depression,
forgetfulness,
Cushing's syndrome - (answer) excessive cortisol that results from the increased ACTH levels
Cushing's syndrome etiology - (answer) iatrogenic from ingestion of glucocorticoid meds, adrenal
tumors that secrete glucocorticoids, pituitary tumors that secrete ACTH and cortisol, and paraneoplastic
