Pathophysiology Final NUR 2063 final
exam questions and correct answers
Gastritis and Etiology and patho - ANS 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 - ANS 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 - ANS 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) - ANS 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 - ANS ETIOLOGY: most commonly H. pylori
and NSAID use.
PATHO: develops because of an imbalance between destructive forces and protective
mechanisms
PUD duodenal ulcers - ANS most commonly associated with excessive acid or H.
pylori infections
typically present with epigastric pain relieved in the presence of food
PUD gastric ulcers - ANS less frequent-more deadly
typically associated with malignancy and NSAIDS
pain worsens with eating
,PUD Stress ulcers - ANS 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 - ANS 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 - ANS 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 - ANS 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 - ANS 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
aplastic anemia - ANS 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 - ANS 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 - ANS 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) - ANS 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 - ANS 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
Thrombocytopenia - ANS a condition in which there is an abnormally small number
of platelets circulating in the blood
hemostasis - ANS 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.
exam questions and correct answers
Gastritis and Etiology and patho - ANS 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 - ANS 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 - ANS 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) - ANS 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 - ANS ETIOLOGY: most commonly H. pylori
and NSAID use.
PATHO: develops because of an imbalance between destructive forces and protective
mechanisms
PUD duodenal ulcers - ANS most commonly associated with excessive acid or H.
pylori infections
typically present with epigastric pain relieved in the presence of food
PUD gastric ulcers - ANS less frequent-more deadly
typically associated with malignancy and NSAIDS
pain worsens with eating
,PUD Stress ulcers - ANS 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 - ANS 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 - ANS 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 - ANS 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 - ANS 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
aplastic anemia - ANS 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 - ANS 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 - ANS 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) - ANS 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 - ANS 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
Thrombocytopenia - ANS a condition in which there is an abnormally small number
of platelets circulating in the blood
hemostasis - ANS 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.
