Study guide for Exam II NR 324 August 2021
Types of anemia: iron deficiency, folate, and pernicious – nursing care,
etc…
Nursing interventions for anemias: Correcting the cause of the anemia is the goal of
therapy. The many causes of anemia necessitate different nursing interventions specific
to the patient’s needs. Acute interventions may include blood transfusions, drug therapy
(e.g., erythropoietin, vitamin supplements), and O2 therapy to stabilize the patient.
Dietary and lifestyle changes (described in sections on specific types of anemia) can
reverse some anemias. For the patient with fatigue, encourage alternate rest and activity
periods. Help the patient prioritize activities to accommodate energy levels. Arrange
physical activities (e.g., avoid activity right after meals) to reduce competition for O2
supply to vital functions. Aid with regular physical activities (e.g., ambulation, transfers,
personal care) to minimize fatigue and risk for injury from falls. Monitor the patient’s
cardiorespiratory response to activity (e.g., tachycardia, dysrhythmias, dyspnea,
diaphoresis, pallor, respiratory rate). Iron-deficiency anemia is the most
common nutritional disorder in the world. Those most susceptible to iron-deficiency
anemia are the very young, those on poor diets, and women in their reproductive years.
Iron-deficiency anemia may develop because of inadequate dietary intake,
malabsorption, blood loss, or hemolysis. Normal dietary iron intake is usually enough to
meet the needs of men and older women. It may be inadequate for people with higher
iron needs (e.g., menstruating or pregnant women). Iron malabsorption may occur after
certain types of gastrointestinal (GI) surgery and in malabsorption syndromes. (Iron
absorption occurs in the duodenum, so malabsorption may occur after a surgical
procedure that involves removal or bypass of the duodenum). Another cause of iron
deficiency anemia is bleeding (Common causes of GI blood loss are peptic ulcer,
gastritis, esophagitis, diverticula, hemorrhoids, and cancer. GU blood loss occurs
primarily from menstrual bleeding). Clinical manifestations include:
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, paresthesias, and a burning sensation of the tongue, all of which are
caused by lack of iron in the tissues. Nursing interventions: The main goal is to identify
and treat the underlying problem that is causing iron loss or reduced intake (e.g.,
malnutrition, alcoholism) or poor absorption of iron. Teach the patient which foods are
good sources of iron (lean meat, turkey, pork, chicken, fish, legumes, dark leafy
vegetables, beans, whole grains and enriched bread and cereals). If nutrition is already
adequate, increasing iron intake by dietary means may not be enough. The patient may
need oral, or occasionally, parenteral iron supplements. If the iron deficiency is from
acute blood loss, the patient may need a transfusion of packed RBCs.
Folate anemia: Folic acid (folate) deficiency also causes megaloblastic anemia. Folic
acid is needed for DNA synthesis leading to RBC formation and maturation. Some
causes of folate anemia are chronic alcoholism, chronic hemodialysis (folic acid lost
during dialysis), dietary deficiency (deficiency of leafy green vegetables, citrus fruits),
drugs interfering with absorption or use of folic acid (methotrexate, antiseizure drugs-
e.g., phenobarbital, phenytoin), increased requirement (pregnancy), and malabsorption
syndromes (celiac disease, Crohn’s disease, small bowel resection). Clinical
Manifestations: The disease develops insidiously. The patient’s symptoms may be
attributed to other coexisting problems (e.g., cirrhosis, esophageal varices). GI problems
may include stomatitis, cheilosis, dysphagia, flatulence, and diarrhea. Thiamine
deficiency, which is often present with folate deficiency, can cause neurologic symptoms.
,Nursing interventions: We treat folic acid deficiency with replacement therapy. The
usual dosage is 1 mg/day by mouth. The patient with malabsorption or chronic
alcoholism may need up to 5 mg/day. The duration of treatment depends on the reason
for the deficiency. Teach the patient to eat foods high in folic acid (green leafy
vegetables, orange juice, peanuts, avocado, enriched grain products and breakfast
cereals)
Pernicious anemia: is caused by an absence of intrinsic factor (IF). Intrinsic factor is
essential for the absorption of cobalamin (extrinsic factor) in the terminal ileum. Because
cobalamin is essential for the growth and maturation of RBCs, the lack of cobalamin
results in pernicious anemia and neurologic complications.Pernicious anemia is a
disease of insidious onset. It begins in middle age or later (usually after age 40), with 60
years being the most common age at diagnosis. Pernicious anemia occurs most often in
persons of Northern European ancestry (particularly Scandinavians) and blacks. There is
a familial predisposition for pernicious anemia, so evaluate patients who have a positive
family history of pernicious anemia for symptoms. Although the disease cannot be
prevented, early detection and treatment can lead to reversal of symptoms.
Clinical manifestations: General manifestations of anemia related to cobalamin
deficiency develop because of tissue hypoxia. GI manifestations include a sore, red,
beefy, and shiny tongue; anorexia, nausea, and vomiting; and abdominal pain. Typical
neuromuscular manifestations include weakness, paresthesias of the feet and hands,
reduced vibratory and position senses, ataxia, muscle weakness, and impaired thought
processes ranging from confusion to dementia. Because cobalamin deficiency–related
anemia has an insidious onset, it may take several months for manifestations to develop.
Nursing interventions: If intrinsic factor is lacking or if absorption in the ileum is
impaired, the patient will not be able to absorb cobalamin regardless of how much they
ingest. For this reason, increasing dietary cobalamin does not correct this anemia.
Parenteral vitamin B12 (cyanocobalamin, hydroxocobalamin) or intranasal
cyanocobalamin (Nascobal) is needed. Without cobalamin administration, the patient will
die in 1 to 3 years. A typical treatment schedule consists of 1000 mcg/day of cobalamin
,. IM for 2 weeks and then weekly until the hemoglobin is normal and then monthly for
life.High-dose oral cobalamin and sublingual cobalamin are options for those in whom GI
absorption is intact. Also assess for neurological difficulties that are not fully corrected by
replacement therapy. Implement measures to reduce the risk for injury from the
decreased sensitivity to heat and pain related to neurologic impairment. Protect the
patient from falling, burns, and trauma. In some people, the neuromuscular
complications may not be reversible and physical therapy may be needed.
Care of patients with DIC and Sickle Cell Anemia
Sickle cell anemia: Sickle cell disease (SCD) is a group of inherited, autosomal
recessive disorders characterized by an abnormal form of hemoglobin (hemoglobin S,
Hgb S) 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. Clinical
manifestations: chronic health problems and pain because of organ tissue hypoxia and
damage (e.g., involving the kidneys or liver). The typical patient is anemic but
asymptomatic except during sickling episodes. Sickling episodes are most often
triggered by low O2 tension in the blood. Hypoxia or deoxygenation of the RBCs can be
caused by viral or bacterial infection, high altitude, emotional or physical stress, surgery,
,and blood loss. The main symptom associated with sickling is pain. The pain severity
can range from trivial to excruciating. During sickle cell crisis, the pain is severe because
of ischemia of tissue. The episodes can affect any area of the body or several sites
simultaneously. The back, chest, extremities, and abdomen are affected most often. Pain
episodes are often accompanied by other manifestations, such as fever, swelling,
tenderness, tachypnea, hypertension, nausea, and vomiting. Nursing
interventions: Interprofessional care for a patient with SCD is directed toward (1)
preventing sequelae from the disease; (2) alleviating the manifestations from the
complications of the disease; (3) minimizing end-organ damage; and (4) continuously
assessing for and promptly treating serious sequelae, such as acute chest syndrome,
that can lead to immediate death. A patient in sickle cell crisis may need hospitalization.
O2 therapy treats hypoxia and controls sickling. Always administer O2 to patients in a
sickling episode. After O2 is managed, then provide management. Assess for any
changes in respiratory status and encourage incentive spirometry. Rest can reduce
metabolic requirements. DVT prophylaxis (using anticoagulants) should be prescribed.
Fluids are given to reduce blood viscosity and maintain renal function. Priapism (a
prolonged erection of the penis, usually without sexual arousal) is managed with pain
medication, fluids, and nifedipine (Procardia). If it does not resolve within a few hours, a
urologist may be called. Transfusion therapy is indicated when an aplastic crisis occurs.
Aggressive RBC exchange transfusion programs may be implemented for patients who
have frequent crises or serious complications, such as acute chest syndrome. These
patients, like those with thalassemia major, may need iron chelation therapy to reduce
transfusion- produced iron overload.
DIC: a serious bleeding and thrombotic disorder that results from abnormally initiated
and accelerated clotting. With DIC, there is profuse bleeding that results from the
aggregation of platelets and clotting factors.
DIC is always caused by an underlying disease or condition. That underlying problem
must be treated for the DIC to resolve.
Nursing interventions: It is important to diagnose DIC quickly, stabilize the patient
(e.g., oxygenation, volume replacement), treat the underlying causative disease or
problem, and control the ongoing thrombosis and bleeding. Remember that because
DIC is caused by an underlying disease, that problem must be managed while providing
supportive care for the manifestations of DIC (e.g., chemotherapy when DIC is caused
by cancer). Appropriate nursing interventions are essential to the survival of a patient
with acute DIC. Astute ongoing assessment, active attention to manifestations of DIC,
and prompt administration of prescribed therapies are crucial. Early detection of bleeding
and clotting, both occult and overt, must be a primary goal. Assess for signs of external
bleeding (e.g., petechiae, oozing at IV or injection sites), signs of internal bleeding (e.g.,
increased heart rate, changes in mental status, increasing abdominal girth, pain), and
any signs that microthrombi may be causing clinically significant organ damage (e.g.,
decreased renal output). Minimize tissue damage and protect the patient from sources of
bleeding. Give blood products and medications correctly. Blood products are given
cautiously based on specific component deficiencies to patients who have serious
bleeding, are at high risk for bleeding (e.g., surgery), or require invasive procedures.
, Heparin is used in the treatment of DIC only when the benefit (reduce clotting) outweighs
the risk (further bleeding). Chronic DIC does not respond to oral anticoagulants. It is
controlled with long-term use of heparin. WATCH FOR SIGNS OF HEMORRHAGES!!!!
Differences in clinical presentation and management of care for acute
blood loss & chronic blood loss
Anemia can be caused by acute or chronic blood loss. Acute blood loss occurs
because of sudden hemorrhage. Causes of acute blood loss include trauma,
complications of surgery, and conditions or diseases that disrupt vascular integrity. There
are 2 clinical concerns for acute blood loss. First, a sudden reduction in the total blood
volume can lead to hypovolemic shock. Second, if the acute loss is more gradual, the
body maintains its blood volume by slowly increasing the plasma volume which causes
the number of RBCs available to carry O2 to significantly decrease. Nursing
interventions: Assess the patient’s expression of pain. Internal hemorrhage may cause
pain because of tissue distention, organ displacement, and nerve compression.
Interprofessional care is initially concerned with (1) replacing blood volume to prevent
shock and (2) finding the source of the hemorrhage and stopping the blood loss. IV fluids
used in emergencies include dextran, hetastarch, albumin, and crystalloid electrolyte
solutions, such as lactated Ringer’s solution. Blood transfusions (packed RBCs) can be
used depending on the volume lost. If a large volume of blood is lost, platelets, plasma,
and cryoprecipitate may be needed. Some patients may need iron supplements. For the
postoperative patient, carefully monitor the blood loss from various drainage tubes and
dressings and implement appropriate actions. The anemia from acute blood loss
should begin to correct itself once the source of hemorrhage is found, blood loss is
controlled, and fluid and blood volumes are replaced.
Chronic blood loss can result from a bleeding ulcer, hemorrhoids, menstrual and
postmenopausal blood loss (similar to iron deficiency anemia). The effects of chronic
blood loss are usually related to the depletion of iron stores and considered an iron-
deficiency anemia. Management of chronic blood loss anemia involves identifying the
source and stopping the bleeding. Supplemental iron may be needed.
Types of anemia: iron deficiency, folate, and pernicious – nursing care,
etc…
Nursing interventions for anemias: Correcting the cause of the anemia is the goal of
therapy. The many causes of anemia necessitate different nursing interventions specific
to the patient’s needs. Acute interventions may include blood transfusions, drug therapy
(e.g., erythropoietin, vitamin supplements), and O2 therapy to stabilize the patient.
Dietary and lifestyle changes (described in sections on specific types of anemia) can
reverse some anemias. For the patient with fatigue, encourage alternate rest and activity
periods. Help the patient prioritize activities to accommodate energy levels. Arrange
physical activities (e.g., avoid activity right after meals) to reduce competition for O2
supply to vital functions. Aid with regular physical activities (e.g., ambulation, transfers,
personal care) to minimize fatigue and risk for injury from falls. Monitor the patient’s
cardiorespiratory response to activity (e.g., tachycardia, dysrhythmias, dyspnea,
diaphoresis, pallor, respiratory rate). Iron-deficiency anemia is the most
common nutritional disorder in the world. Those most susceptible to iron-deficiency
anemia are the very young, those on poor diets, and women in their reproductive years.
Iron-deficiency anemia may develop because of inadequate dietary intake,
malabsorption, blood loss, or hemolysis. Normal dietary iron intake is usually enough to
meet the needs of men and older women. It may be inadequate for people with higher
iron needs (e.g., menstruating or pregnant women). Iron malabsorption may occur after
certain types of gastrointestinal (GI) surgery and in malabsorption syndromes. (Iron
absorption occurs in the duodenum, so malabsorption may occur after a surgical
procedure that involves removal or bypass of the duodenum). Another cause of iron
deficiency anemia is bleeding (Common causes of GI blood loss are peptic ulcer,
gastritis, esophagitis, diverticula, hemorrhoids, and cancer. GU blood loss occurs
primarily from menstrual bleeding). Clinical manifestations include:
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, paresthesias, and a burning sensation of the tongue, all of which are
caused by lack of iron in the tissues. Nursing interventions: The main goal is to identify
and treat the underlying problem that is causing iron loss or reduced intake (e.g.,
malnutrition, alcoholism) or poor absorption of iron. Teach the patient which foods are
good sources of iron (lean meat, turkey, pork, chicken, fish, legumes, dark leafy
vegetables, beans, whole grains and enriched bread and cereals). If nutrition is already
adequate, increasing iron intake by dietary means may not be enough. The patient may
need oral, or occasionally, parenteral iron supplements. If the iron deficiency is from
acute blood loss, the patient may need a transfusion of packed RBCs.
Folate anemia: Folic acid (folate) deficiency also causes megaloblastic anemia. Folic
acid is needed for DNA synthesis leading to RBC formation and maturation. Some
causes of folate anemia are chronic alcoholism, chronic hemodialysis (folic acid lost
during dialysis), dietary deficiency (deficiency of leafy green vegetables, citrus fruits),
drugs interfering with absorption or use of folic acid (methotrexate, antiseizure drugs-
e.g., phenobarbital, phenytoin), increased requirement (pregnancy), and malabsorption
syndromes (celiac disease, Crohn’s disease, small bowel resection). Clinical
Manifestations: The disease develops insidiously. The patient’s symptoms may be
attributed to other coexisting problems (e.g., cirrhosis, esophageal varices). GI problems
may include stomatitis, cheilosis, dysphagia, flatulence, and diarrhea. Thiamine
deficiency, which is often present with folate deficiency, can cause neurologic symptoms.
,Nursing interventions: We treat folic acid deficiency with replacement therapy. The
usual dosage is 1 mg/day by mouth. The patient with malabsorption or chronic
alcoholism may need up to 5 mg/day. The duration of treatment depends on the reason
for the deficiency. Teach the patient to eat foods high in folic acid (green leafy
vegetables, orange juice, peanuts, avocado, enriched grain products and breakfast
cereals)
Pernicious anemia: is caused by an absence of intrinsic factor (IF). Intrinsic factor is
essential for the absorption of cobalamin (extrinsic factor) in the terminal ileum. Because
cobalamin is essential for the growth and maturation of RBCs, the lack of cobalamin
results in pernicious anemia and neurologic complications.Pernicious anemia is a
disease of insidious onset. It begins in middle age or later (usually after age 40), with 60
years being the most common age at diagnosis. Pernicious anemia occurs most often in
persons of Northern European ancestry (particularly Scandinavians) and blacks. There is
a familial predisposition for pernicious anemia, so evaluate patients who have a positive
family history of pernicious anemia for symptoms. Although the disease cannot be
prevented, early detection and treatment can lead to reversal of symptoms.
Clinical manifestations: General manifestations of anemia related to cobalamin
deficiency develop because of tissue hypoxia. GI manifestations include a sore, red,
beefy, and shiny tongue; anorexia, nausea, and vomiting; and abdominal pain. Typical
neuromuscular manifestations include weakness, paresthesias of the feet and hands,
reduced vibratory and position senses, ataxia, muscle weakness, and impaired thought
processes ranging from confusion to dementia. Because cobalamin deficiency–related
anemia has an insidious onset, it may take several months for manifestations to develop.
Nursing interventions: If intrinsic factor is lacking or if absorption in the ileum is
impaired, the patient will not be able to absorb cobalamin regardless of how much they
ingest. For this reason, increasing dietary cobalamin does not correct this anemia.
Parenteral vitamin B12 (cyanocobalamin, hydroxocobalamin) or intranasal
cyanocobalamin (Nascobal) is needed. Without cobalamin administration, the patient will
die in 1 to 3 years. A typical treatment schedule consists of 1000 mcg/day of cobalamin
,. IM for 2 weeks and then weekly until the hemoglobin is normal and then monthly for
life.High-dose oral cobalamin and sublingual cobalamin are options for those in whom GI
absorption is intact. Also assess for neurological difficulties that are not fully corrected by
replacement therapy. Implement measures to reduce the risk for injury from the
decreased sensitivity to heat and pain related to neurologic impairment. Protect the
patient from falling, burns, and trauma. In some people, the neuromuscular
complications may not be reversible and physical therapy may be needed.
Care of patients with DIC and Sickle Cell Anemia
Sickle cell anemia: Sickle cell disease (SCD) is a group of inherited, autosomal
recessive disorders characterized by an abnormal form of hemoglobin (hemoglobin S,
Hgb S) 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. Clinical
manifestations: chronic health problems and pain because of organ tissue hypoxia and
damage (e.g., involving the kidneys or liver). The typical patient is anemic but
asymptomatic except during sickling episodes. Sickling episodes are most often
triggered by low O2 tension in the blood. Hypoxia or deoxygenation of the RBCs can be
caused by viral or bacterial infection, high altitude, emotional or physical stress, surgery,
,and blood loss. The main symptom associated with sickling is pain. The pain severity
can range from trivial to excruciating. During sickle cell crisis, the pain is severe because
of ischemia of tissue. The episodes can affect any area of the body or several sites
simultaneously. The back, chest, extremities, and abdomen are affected most often. Pain
episodes are often accompanied by other manifestations, such as fever, swelling,
tenderness, tachypnea, hypertension, nausea, and vomiting. Nursing
interventions: Interprofessional care for a patient with SCD is directed toward (1)
preventing sequelae from the disease; (2) alleviating the manifestations from the
complications of the disease; (3) minimizing end-organ damage; and (4) continuously
assessing for and promptly treating serious sequelae, such as acute chest syndrome,
that can lead to immediate death. A patient in sickle cell crisis may need hospitalization.
O2 therapy treats hypoxia and controls sickling. Always administer O2 to patients in a
sickling episode. After O2 is managed, then provide management. Assess for any
changes in respiratory status and encourage incentive spirometry. Rest can reduce
metabolic requirements. DVT prophylaxis (using anticoagulants) should be prescribed.
Fluids are given to reduce blood viscosity and maintain renal function. Priapism (a
prolonged erection of the penis, usually without sexual arousal) is managed with pain
medication, fluids, and nifedipine (Procardia). If it does not resolve within a few hours, a
urologist may be called. Transfusion therapy is indicated when an aplastic crisis occurs.
Aggressive RBC exchange transfusion programs may be implemented for patients who
have frequent crises or serious complications, such as acute chest syndrome. These
patients, like those with thalassemia major, may need iron chelation therapy to reduce
transfusion- produced iron overload.
DIC: a serious bleeding and thrombotic disorder that results from abnormally initiated
and accelerated clotting. With DIC, there is profuse bleeding that results from the
aggregation of platelets and clotting factors.
DIC is always caused by an underlying disease or condition. That underlying problem
must be treated for the DIC to resolve.
Nursing interventions: It is important to diagnose DIC quickly, stabilize the patient
(e.g., oxygenation, volume replacement), treat the underlying causative disease or
problem, and control the ongoing thrombosis and bleeding. Remember that because
DIC is caused by an underlying disease, that problem must be managed while providing
supportive care for the manifestations of DIC (e.g., chemotherapy when DIC is caused
by cancer). Appropriate nursing interventions are essential to the survival of a patient
with acute DIC. Astute ongoing assessment, active attention to manifestations of DIC,
and prompt administration of prescribed therapies are crucial. Early detection of bleeding
and clotting, both occult and overt, must be a primary goal. Assess for signs of external
bleeding (e.g., petechiae, oozing at IV or injection sites), signs of internal bleeding (e.g.,
increased heart rate, changes in mental status, increasing abdominal girth, pain), and
any signs that microthrombi may be causing clinically significant organ damage (e.g.,
decreased renal output). Minimize tissue damage and protect the patient from sources of
bleeding. Give blood products and medications correctly. Blood products are given
cautiously based on specific component deficiencies to patients who have serious
bleeding, are at high risk for bleeding (e.g., surgery), or require invasive procedures.
, Heparin is used in the treatment of DIC only when the benefit (reduce clotting) outweighs
the risk (further bleeding). Chronic DIC does not respond to oral anticoagulants. It is
controlled with long-term use of heparin. WATCH FOR SIGNS OF HEMORRHAGES!!!!
Differences in clinical presentation and management of care for acute
blood loss & chronic blood loss
Anemia can be caused by acute or chronic blood loss. Acute blood loss occurs
because of sudden hemorrhage. Causes of acute blood loss include trauma,
complications of surgery, and conditions or diseases that disrupt vascular integrity. There
are 2 clinical concerns for acute blood loss. First, a sudden reduction in the total blood
volume can lead to hypovolemic shock. Second, if the acute loss is more gradual, the
body maintains its blood volume by slowly increasing the plasma volume which causes
the number of RBCs available to carry O2 to significantly decrease. Nursing
interventions: Assess the patient’s expression of pain. Internal hemorrhage may cause
pain because of tissue distention, organ displacement, and nerve compression.
Interprofessional care is initially concerned with (1) replacing blood volume to prevent
shock and (2) finding the source of the hemorrhage and stopping the blood loss. IV fluids
used in emergencies include dextran, hetastarch, albumin, and crystalloid electrolyte
solutions, such as lactated Ringer’s solution. Blood transfusions (packed RBCs) can be
used depending on the volume lost. If a large volume of blood is lost, platelets, plasma,
and cryoprecipitate may be needed. Some patients may need iron supplements. For the
postoperative patient, carefully monitor the blood loss from various drainage tubes and
dressings and implement appropriate actions. The anemia from acute blood loss
should begin to correct itself once the source of hemorrhage is found, blood loss is
controlled, and fluid and blood volumes are replaced.
Chronic blood loss can result from a bleeding ulcer, hemorrhoids, menstrual and
postmenopausal blood loss (similar to iron deficiency anemia). The effects of chronic
blood loss are usually related to the depletion of iron stores and considered an iron-
deficiency anemia. Management of chronic blood loss anemia involves identifying the
source and stopping the bleeding. Supplemental iron may be needed.
