Drugs used to treat anemia

where does hematopoiesis occur?

• bone marrow (pelvis, sternum, ribs, vertebra in adults)

• stem cells stimulate (blood cell development)

• cytokines or colony stimulating factors are released

  • stimulates production of RBCs, WBCs, platelets

erythrocytes

• erythropoiesis (kidneys)

• Folic acid – for erythropoiesis

• Vitamin B12 – for new erythrocytes to properly synthesize

• Iron – to carry oxygen in the blood

leukocytes

inflammatory processes

• Granulocytes

• Lymphocytes

• Monocytes

thrombocytes

Facilitate the clotting process - hemostasis

erythropoietic growth factor prototype

epoetin alfa

epoetin alfa therapeutic action

works on the bone marrow to increase RBC production

epoetin alfa therapeutic use

Supports production of erythrocytes in

• chronic renal failure

• preoperative anemia

• chemotherapy

• zidovudine therapy for HIV

epoetin alfa adverse drug reactions

• Hypertension

• Seizures

• Cardiovascular and cerebrovascular events (myocardial

infarction, heart failure, cerebrovascular accident, cardiac arrest)

• Malignancy progression

epoetin alfa contraindications

• uncontrolled hypertension

• iron-deficiency anemia

precautions for epoetin alfa

stroke, cardiovascular disease, seizure disorders

nursing considerations for epoetin alfa

• Obtain baseline blood pressure, CBC

• Make sure to control blood pressure for clients with chronic renal

failure prior to starting medication therapy.

• Administer IV or subcutaneously three times a week, or once a

week with some types of chemotherapy.

• Check Hgb twice per week until adequate and then periodically.

• Report Hgb that rises above 12 g/dL or increases more than 1 g/dL

within 2 weeks; for cancer clients, report Hgb that rises to 10 g/dL.

• Monitor iron level and maintain it within the expected range, as

adequate quantities of iron, folic acid, and vitamin B12 are

essential for RBC growth

client instructions for epoetin alfa

• Have frequent blood pressure checks

• Report headaches

• Report sudden chest pain, severe headache, weakness, numbness, paralysis, vision changes, nausea, vomiting, or seizures

microcytic anemia

• caused by Iron Deficiency Anemia (IDA)

• Anemia resulting from an inadequate amount of iron available for erythrocytes to use

macrocytic anemia

• caused by either vitamin B12 malabsorption, or a deficiency of either vitamin B12 , folic acid, or both

• Megaloblastic anemia is sometimes called macrocytic anemia

antianemic prototypes

• ferrous sulfate (feosol) - oral

• iron dextran (INFeD) -IM or IV (parenteral)

ferrous sulfate and iron dextran therapeutic uses

Given to treat secondary to blood loss, or inadequate intake of iron-

containing foods

Iron Deficiency Anemia (IDA)

Prevention of IDA for clients at risk:

• 1. Infants

• 2. Children

• 3. Women who are pregnant

• 4. Clients experiencing acute or ongoing blood loss

• Occult or microscopic bleeding from the GI tract is one reason for ongoing blood loos

ferrous sulfate and iron dextran expected pharmacologic action

• While RBCs are developing, they synthesize hemoglobin into

the cell.

• Hemoglobin is a necessary component for erythrocytes to carry

O2 from the lungs to the entire body

• Hemoglobin made up of 4 heme groups and 1 globin group

• Heme: contains iron

• Globin: protein that binds the heme groups together =

hemoglobin

• Carries oxygen throughout the body

• IDA (Iron Deficiency Anemia) – clients experience weakness,

fatigue, and SOB

• Give iron to replace iron deficiency restore the body’s ability to

carry oxygen

ferrous sulfate and iron dextran adverse drug reactions

• GI effects are most common

• Nausea, epigastric pain (heartburn), diarrhea, constipation

• Metallic taste in mouth (iron dextran)

• Staining of teeth (liquid form)

• Fatal iron toxicity (overdose in children – medication mistaken for “candy” or “gummies’)

ferrous sulfate and iron dextran contraindications

• Anemias not caused by lack of iron =

Hemolytic anemia

• Hemochromatosis

• Severe liver disease,

alcoholism, severe renal

impairment

• Disorders:

• Peptic ulcer disease,

ulcerative colitis, and

regional enteritis

four phases of iron toxicity

1. GI symptoms: stomach pain, N/V (may contain blood),

diarrhea and shock

2. GI symptoms resolve, but damage to organs cause

metabolic acidosis, bleeding disorders and shock.

• Gastric lavage with sodium bicarbonate treats acute

poisoning to remove as much iron still in stomach

• Bowel irrigations may also prevent absorption

3. CV and CNS involvement – coma and

4. Liver dysfunction – patient may die without treatment due

to multiple organ failure

ferrous sulfate and iron dextran safety alert

IV Administration of deferoxamine (Desferal) binds with iron in the blood and promotes its excretion

ferrous sulfate and iron dextran interventions

• best to take on empty stomach, take with food for severe GI symptoms, monitor bowel patterns, staining of teeth, give candy or gum for metallic taste, monitor for toxicity

what do you administer for iron toxicity?

administer a chelating agent, such as deferoxamine (Desferal), parenteral (binds with iron)

iron dextran administration

INJECTABLE

• Give test dose: of 25 mg first to determine if client is sensitive to iron

• Have epinephrine available for hypersensitivity reaction

• Follow prescribed dose 1 hour later (hypersensitivity reaction)

• Administer IM using 2- to 3-inch-long-needle using Z-track technique

• Monitor BP closely

• Check that clients are not taking oral when giving iron dextran (IV)

form due to risk of toxicity

ferrous sulfate administration (liquid form)

• First dilute in another compatible liquid

• Give through a straw (avoids staining teeth)

• Have client rinse mouth with plain water

ferrous sulfate administration (oral but NON-LIQUID)

• Spread doses evenly across waking hours to maximize the production of RBCs

• Give drug on empty stomach for best absorption

• If given with food, may need HCP to increase dosage

• Do not crush or chew sustained-release forms – may stain teeth

for all forms of administration of iron preparations

• Monitor hemoglobin (Hgb), hematocrit (Hct), and reticulocyte (RBC) counts

• Expect to discontinue the drug when anemia resolves (usually within 1 to 2 months)

• Pregnant women: iron therapy for several months

• Recommend foods high in iron (liver, egg yolks, muscle meats, whole grain cereals, leafy green vegetables)

client instructions for iron preparations (ferrous sulfate and iron dextran)

• take on empty stomach

• take iron with food to minimize GI effects (food decreases absorption)

• expect dark green or black stools (harmless)

• increase fluid, exercise, fiber intake, etc.

iron preparation interactions

• vitamin C increases absorption, but also increases risk of GI effects

• antacids reduce absorption

• concurrent use with ACE inhibitors may increase risk of anaphylactic reaction

• calcium and iron compete for absorption

vitamin B12

• necessary to convert folic acid from its inactive to active form

• cells rely on it for DNA

what does vitamin B12 deficiency affect?

all blood cells produced in the bone marrow

• Loss of intrinsic factor within the cells of the stomach

  causes an inability to absorb vitamin B12 , making it

  necessary to administer parenteral or intranasal vitamin B12

  for the rest of the client’s life

• can result in macrocytic anemia and heart dysrhythmias and heart failure

pernicious anemia

disease in which absorption of vitamin B12 is impaired due to a lack of intrinsic factor in the stomach

vitamin B12 deficiency

due to either inadequate absorption of dietary vitamin B12 or to dietary deficiency of vitamin B12

antianemic (vitamin) prototypes

• cyanocobalamin (vitamin B12)

• cyanocobalamin (nascobal)= intranasal form

cyanocobalamin expected pharmacologic action

• Elevated gastric pH (due to H2 receptor blockers: famotidine (PEPCID)

• GI malabsorption syndrome (celiac disease), which

  decreases the absorption of vitamin B12 from the

  intestinal tract

• lack of intrinsic factor (pernicious anemia) –

  parietal cells of the stomach produce intrinsic

  factor, which is necessary for vitamin B12 to be

  absorbed from the ileum. Folic acid uses the

  vitamin B12 for the conversion to its active form

cyanocobalamin adverse drug reactions

Are rare, but can include HTN, erythema, and hypokalemia

hypokalemia

occurs secondary to the resumption of normal erythropoiesis, which can deplete the body’s stores of potassium

cyanocobalamin contraindications

• Sensitivity to cobalt,

vitamin B12, or

other cobalamins

• Hereditary optic nerve

atrophy

• Renal dysfunctions

• Concurrent infections

cyanocobalamin precautions

• CVD

• Pulmonary disease

• Other types of anemia

• Concurrent use of folic acid

cyanocobalamin interventions

• Monitor potassium levels (first few days)–

hypokalemia from restorative hematopoiesis

• Monitor for potassium deficiency

(muscle weakness, cardiac dysrhythmias)

• Recommend potassium supplements for prevention or treatment of

hypokalemia

cyanocobalamin safety alert

• Erythrocyte production requires significant amounts of potassium

• potassium level range: 3.5-5.0 mEq/L

• any small change can result in life-threatening dysrhythmias

• report to HCP any potassium values outside of expected range

cyanocobalamin administration

• Give orally, subcutaneously, IM, or intranasally

• For oral dosing: confirm gastric absorption of B12 via Schilling test

• Schilling test involves oral ingestion of radioactive vitamin B12, first

without intrinsic factor and then with intrinsic factor

• This test determines if oral absorption is possible

• The results of the Schilling test determines the route of vitamin B12

administration

• HCP prescribes vitamin B12 either intranasally or parenterally if a

client cannot absorb it orally

• However, most clients can absorb adequate amounts of vitamin

B12 if taking a large enough oral dose

• Give intranasally or parenterally to clients who have malabsorption syndrome

• Clients receiving vitamin B12 parenterally – receive at least once a month injections

• Gove oral forms with food to enhance adsorption

• Obtain baseline vitamin B12 , Hgb, Hct, RBC, and reticulocyte counts – monitor every 3 to 6 months

• Expect lifelong treatment for clients who have irreversible B12 deficiencies (pernicious anemia)

• Encourage dietary intake of foods high in vitamin B12 – such as dairy products, enriched cereal, egg yolks, and some seafood

client instructions for cyanocobalamin

• Report muscle weakness, nausea, palpitations, or

paresthesia – indication of hypokalemia

Ensure client understands how to take vitamin B12 and the

need to have periodic laboratory values drawn

cyanocobalamin interactions

ascorbic acid (vitamin C) alters the stability of oral forms

folic acid deficiency

• Megaloblastic anemia caused by folic acid deficiency will be treated with this vitamin (folic acid)

• If deficiency is related to diet, improving the diet by

increasing consumption of foods high in folic acid (legumes, citrus fruits, nuts) can often correct the problem

folic acid therapeutic uses

• Folate deficiency:

• secondary to alcoholism or malabsorption syndrome (celiac disease)

• Megaloblastic (macrocytic) anemia

• Depending on the cause, give folic acid alone or with vitamin B12 to

treat megaloblastic anemia, also called macrocytic anemia

• Given as supplement to women of childbearing age, before and during pregnancy, to prevent neural tube defects in developing fetus

antianemic (vitamin) prototype

folic acid (folate/ vitamin B9)

folic acid expected pharmacologic action

Necessary for DNA and RNA synthesis

• Foundation for cell replication in all body tissues

Required for erythropoiesis but first must be changed into tetrahydrofolic acid, following ingestion

folic acid adverse drug reactions

• increased intense yellowing of urine

• masks B12 deficiency in high doses

• increased risk of developing colorectal or prostate cancers (long-term)

folic acid contraindications

• Vitamin B12 deficiency pernicious anemia

(after initial stabilization)

• Other types of anemia

• Neonates

folic acid interventions

• Encourage clients to eat a diet high in folic acid (green vegetables, liver, lentils, certain breakfast cereals fortified with folic acid)

• Clients should be monitored for signs of megaloblastic anemia as well as

plasma folic acid levels

folic acid administration

• Treatment is usually an increase in dietary forms of folic acid

• Give orally (preferable), subcutaneously, IM, or IV

• Check vitamin B12 levels to confirm absence of B12 deficiency

• Risk of permanent neurological damage if a B12 deficiency does exist, and is only treated with folic acid

expect Hct counts to improve within 2 weeks

Obtain baseline serum folate, hemoglobin (Hgb), hematocrit (Hct), red blood cell (RBCs), and reticulocyte counts, and monitor periodically thereafter

client instructions for folic acid

• Report rash as it may indicate hypersensitivity

• Encourage and instruct clients to eat a diet high in folic acid

folic acid safety alert

• Vitamin B12 deficiency primarily affects the production of blood

cells and the maintenance of the myelin sheath of neurons in

the CNS

• While administration of large amount of folic acid contributes

to the re-establishment of hematopoiesis, it will not maintain

the myelin sheaths of neurons, allowing neuronal damage to

occur

• When you give folic acid to correct megaloblastic anemia, you

must determine the presence or absence of a vitamin B12

deficiency in order to prevent neuronal damage from

concurrent administration

folic acid interactions

• Folic acid therapy can mask the symptoms of B12

deficiency

• Oral contraceptives, corticosteroids, methotrexate may cause manifestations of folic acid deficiency, but will not be affected by administering folic acid