NR 324 EXAM 2 (Final Exam) STUDY GUIDE NOVEMBER 2021
NAME: ___Skiler
Williams_________________________________D#______41116723______________
THIS IS A SUPPLEMENTAL TOOL TO HELP YOU WITH YOUR STUDIES.
1. List the risk factors, assessment findings, diagnostics and/or labs, nursing management
including diet, plan of care, medications, and patient teaching for each of the following.
Iron deficiency anemia.
Risk factors: deficient nutrients, decreased erythropoietin, decreased iron availability,
blood loss, increased RBC destruction, very young, poor diet, women in reproductive
years(pregnancy).
Assessment Findings: Pallor is the most common finding. Glossitis (inflammation of the tongue) is the
second most common. Another finding is cheilitis (inflammation of the lips). The patient may report
headache, paresthesia, and a burning sensation of the tongue, all of which are caused by lack of iron in
the tissues.
Clinical manifestations: sensitivity to cold, weight loss, lethargy, pallor, jaundice, pruritis,
glossitis, smooth tongue, tachycardia, angina, heart failure, MI, tachypnea, orthopnea,
dyspnea at rest, headache, vertigo, irritability. Hemoglobin <6 (severe anemia)
Nursing Management: blood transfusion, drug therapy, RBC replacement, O2 alternate
rest and activity, aid minimize risk for injury, evaluate nutritional
needs, encourage increased intake of foods high in iron.
Diagnostics: Hgb, Hct, MVC, MCH, MCHC, reticulocytes, serum iron, TIBC, bilirubin,
plt’s, stool occult blood test, endoscopy, colonoscopy
Medications/Treatments: Replace iron (diet, oral, parenteral, transfusion of packed
RBCs), teaching, emphasize compliance.
Patient teaching: Take meds as prescribed, eat iron-rich foods, black tarry stools are
okay, constipation can happen; eat fiber-rich food, no contact sports, no straight razors.
Thalassemia
Thalassemia: is a group of diseases involving inadequate production of normal
hemoglobin due to reduced or absent α-globin or β-globin protein decreased
erythrocyte production. Thalassemia has an autosomal receive genetic link common in
persons of ethnic groups near the Mediterranean Sea, regions of Asia, Middle East, and
Africa.
S/S: May have both physical and mental developmental delays, jaundice, pallor,
hepatomegaly and cardiomyopathy may occur from iron deposits, splenomegaly
(Thalassemia major).
Management: blood transfusions in conjunction with iron chelation, folic acid, zinc,
, ascorbic acid and iron should NOT be given, monitor hepatic, cardiac, and pulmonary
organ function.
Megaloblastic Anemias: 2 TYPES
Caused by impaired DNA SYNTHESIS
EARLY detection and treatment are key
Protect from fallings, burns, and trauma (they have a diminished sensation to heat and pain from the
neurologic impairment)
Physical therapy may be needed
Cobalamin Deficiency (vitamin b12)
Without IF (intrinsic factor) a protein that is secreted by partial cell of gastric mucosa there
is no EF (extrinsic factor) which is the cobalamin absorption in the ileum.
Manifestations: GI: N/V, Neuromuscular: weakness, swelling of the hands and feet,
impaired thought process
Patient education: informed on how to replace the vitamin b12. Reduce alcohol intake,
smoking cessation, avoid h2 histamine receptor blockers
Parenteral or intranasal administration is the treatment of choice because there is no
absorption occurring in the GI tract. Without the treatment patient’s lifespan is 1-3
years.
Folic Acid Deficiency
Causes: Chronic alcoholism(malabsorption), sclerosis of the liver, loss of folic acid through
hemodialysis
Normal levels 5-25 ng/ml
Aplastic Anemia
Aplastic anemia is a disease in which the patient has peripheral blood pancytopenia (decrease of all
blood cell types—RBCs, white blood cells [WBCs], and platelets) and hypocellular bone marrow.
Clinical Manifestations
Aplastic anemia can manifest abruptly (over days) or insidiously over weeks to months. It can vary from
mild to very severe. The patient may have symptoms caused by suppression of any or all bone marrow
elements. General manifestations of anemia, such as fatigue and dyspnea, as well as cardiovascular and
cerebral responses, may be seen (Table 30.3). The patient with neutropenia (low neutrophil count) is
susceptible to infection and is at risk for septic shock and death. Thrombocytopenia is manifested by a
predisposition to bleeding (e.g., petechiae, bruising, nosebleeds).
Diagnostic Studies
Laboratory studies confirm the diagnosis. Because aplastic anemia affects all marrow elements,
hemoglobin, WBC, and platelet values are decreased.
The serum iron and total iron-binding capacity (TIBC) may be high as initial signs of erythropoiesis
suppression. Bone marrow biopsy, aspiration, and pathologic examination may be done. The marrow in
aplastic anemia is hypocellular with increased yellow marrow (fat content).
, Interprofessional and Nursing Management
Management of aplastic anemia is based on identifying and removing the causative agent (when
possible) and providing supportive care until the pancytopenia reverses.
Hemolytic Anemia (Destruction of RBC at a rate that is greater than the production)
Caused by problems intrinsic and extrinsic to the RBC such as physical destruction (exertion or
traumatic events), antibody reactions, infectious agents/ toxins
Assessment Findings: jaundice, enlargement of spleen and liver.
Diagnostics/Labs: Factor assays, bleeding time, PTT, PT, platelet count, CBC.
Collaborative Care: A hematologist, a RN specializing in bleeding disorders,
orthopedists, physical therapists, social worker, or psychologist.
Medications/Drug Therapy: aggressive hydration and electrolyte replacement; STOP TRANSFUSION
and use NEW tubing to hydrate patient.
Patient teaching: Educate patient which activities to avoid and which are ok, to see a
dentist regularly, check with their Dr. about any procedures/surgeries prior to, Take all
prescription medications as directed, attend all doctor visits regularly, and enroll in a
hemophilia treatment center. Teach them about the S/S of recognizing possible bleeding,
how to treat minor scrapes/cuts, when to call their physician or go to the ER
Sickle Cell Disease
Risk factors: Sickle cell disease (SCD) is a group of inherited, autosomal recessive disorders characterized by
an abnormal form of hemoglobin in the RBC. Because this is a genetic disorder, SCD is usually found during
routine neonatal screening. Although median survival can now exceed 45 years old, the disease often results in
irreversible damage of the lungs, kidneys, brain, retina, or bones that significantly affects patients’ quality of
life.
Genetics, more common in AA, Indian American, Asian- American
Assessment Findings: asymptomatic until they have a crisis/episode; may include pain
from tissue hypoxia and damage, pallor of mucous membranes, jaundice from hemolysis,
prone to gallstones. Severe pain = Hypertension, tachypnea, joint swelling/tenderness,
N/V. Triggers: low oxygen levels, infection, dehydration.
NAME: ___Skiler
Williams_________________________________D#______41116723______________
THIS IS A SUPPLEMENTAL TOOL TO HELP YOU WITH YOUR STUDIES.
1. List the risk factors, assessment findings, diagnostics and/or labs, nursing management
including diet, plan of care, medications, and patient teaching for each of the following.
Iron deficiency anemia.
Risk factors: deficient nutrients, decreased erythropoietin, decreased iron availability,
blood loss, increased RBC destruction, very young, poor diet, women in reproductive
years(pregnancy).
Assessment Findings: Pallor is the most common finding. Glossitis (inflammation of the tongue) is the
second most common. Another finding is cheilitis (inflammation of the lips). The patient may report
headache, paresthesia, and a burning sensation of the tongue, all of which are caused by lack of iron in
the tissues.
Clinical manifestations: sensitivity to cold, weight loss, lethargy, pallor, jaundice, pruritis,
glossitis, smooth tongue, tachycardia, angina, heart failure, MI, tachypnea, orthopnea,
dyspnea at rest, headache, vertigo, irritability. Hemoglobin <6 (severe anemia)
Nursing Management: blood transfusion, drug therapy, RBC replacement, O2 alternate
rest and activity, aid minimize risk for injury, evaluate nutritional
needs, encourage increased intake of foods high in iron.
Diagnostics: Hgb, Hct, MVC, MCH, MCHC, reticulocytes, serum iron, TIBC, bilirubin,
plt’s, stool occult blood test, endoscopy, colonoscopy
Medications/Treatments: Replace iron (diet, oral, parenteral, transfusion of packed
RBCs), teaching, emphasize compliance.
Patient teaching: Take meds as prescribed, eat iron-rich foods, black tarry stools are
okay, constipation can happen; eat fiber-rich food, no contact sports, no straight razors.
Thalassemia
Thalassemia: is a group of diseases involving inadequate production of normal
hemoglobin due to reduced or absent α-globin or β-globin protein decreased
erythrocyte production. Thalassemia has an autosomal receive genetic link common in
persons of ethnic groups near the Mediterranean Sea, regions of Asia, Middle East, and
Africa.
S/S: May have both physical and mental developmental delays, jaundice, pallor,
hepatomegaly and cardiomyopathy may occur from iron deposits, splenomegaly
(Thalassemia major).
Management: blood transfusions in conjunction with iron chelation, folic acid, zinc,
, ascorbic acid and iron should NOT be given, monitor hepatic, cardiac, and pulmonary
organ function.
Megaloblastic Anemias: 2 TYPES
Caused by impaired DNA SYNTHESIS
EARLY detection and treatment are key
Protect from fallings, burns, and trauma (they have a diminished sensation to heat and pain from the
neurologic impairment)
Physical therapy may be needed
Cobalamin Deficiency (vitamin b12)
Without IF (intrinsic factor) a protein that is secreted by partial cell of gastric mucosa there
is no EF (extrinsic factor) which is the cobalamin absorption in the ileum.
Manifestations: GI: N/V, Neuromuscular: weakness, swelling of the hands and feet,
impaired thought process
Patient education: informed on how to replace the vitamin b12. Reduce alcohol intake,
smoking cessation, avoid h2 histamine receptor blockers
Parenteral or intranasal administration is the treatment of choice because there is no
absorption occurring in the GI tract. Without the treatment patient’s lifespan is 1-3
years.
Folic Acid Deficiency
Causes: Chronic alcoholism(malabsorption), sclerosis of the liver, loss of folic acid through
hemodialysis
Normal levels 5-25 ng/ml
Aplastic Anemia
Aplastic anemia is a disease in which the patient has peripheral blood pancytopenia (decrease of all
blood cell types—RBCs, white blood cells [WBCs], and platelets) and hypocellular bone marrow.
Clinical Manifestations
Aplastic anemia can manifest abruptly (over days) or insidiously over weeks to months. It can vary from
mild to very severe. The patient may have symptoms caused by suppression of any or all bone marrow
elements. General manifestations of anemia, such as fatigue and dyspnea, as well as cardiovascular and
cerebral responses, may be seen (Table 30.3). The patient with neutropenia (low neutrophil count) is
susceptible to infection and is at risk for septic shock and death. Thrombocytopenia is manifested by a
predisposition to bleeding (e.g., petechiae, bruising, nosebleeds).
Diagnostic Studies
Laboratory studies confirm the diagnosis. Because aplastic anemia affects all marrow elements,
hemoglobin, WBC, and platelet values are decreased.
The serum iron and total iron-binding capacity (TIBC) may be high as initial signs of erythropoiesis
suppression. Bone marrow biopsy, aspiration, and pathologic examination may be done. The marrow in
aplastic anemia is hypocellular with increased yellow marrow (fat content).
, Interprofessional and Nursing Management
Management of aplastic anemia is based on identifying and removing the causative agent (when
possible) and providing supportive care until the pancytopenia reverses.
Hemolytic Anemia (Destruction of RBC at a rate that is greater than the production)
Caused by problems intrinsic and extrinsic to the RBC such as physical destruction (exertion or
traumatic events), antibody reactions, infectious agents/ toxins
Assessment Findings: jaundice, enlargement of spleen and liver.
Diagnostics/Labs: Factor assays, bleeding time, PTT, PT, platelet count, CBC.
Collaborative Care: A hematologist, a RN specializing in bleeding disorders,
orthopedists, physical therapists, social worker, or psychologist.
Medications/Drug Therapy: aggressive hydration and electrolyte replacement; STOP TRANSFUSION
and use NEW tubing to hydrate patient.
Patient teaching: Educate patient which activities to avoid and which are ok, to see a
dentist regularly, check with their Dr. about any procedures/surgeries prior to, Take all
prescription medications as directed, attend all doctor visits regularly, and enroll in a
hemophilia treatment center. Teach them about the S/S of recognizing possible bleeding,
how to treat minor scrapes/cuts, when to call their physician or go to the ER
Sickle Cell Disease
Risk factors: Sickle cell disease (SCD) is a group of inherited, autosomal recessive disorders characterized by
an abnormal form of hemoglobin in the RBC. Because this is a genetic disorder, SCD is usually found during
routine neonatal screening. Although median survival can now exceed 45 years old, the disease often results in
irreversible damage of the lungs, kidneys, brain, retina, or bones that significantly affects patients’ quality of
life.
Genetics, more common in AA, Indian American, Asian- American
Assessment Findings: asymptomatic until they have a crisis/episode; may include pain
from tissue hypoxia and damage, pallor of mucous membranes, jaundice from hemolysis,
prone to gallstones. Severe pain = Hypertension, tachypnea, joint swelling/tenderness,
N/V. Triggers: low oxygen levels, infection, dehydration.
