McKenna's Pharmacology for Nursing, 2e

777

C H A P T E R 4 9 Drugs used to treat anaemias

not only for the health of the RBCs, but also for the formation and maintenance of the myelin sheath in the central nervous system (CNS). It is found in the diet in meats, seafood, eggs and cheese. Strict vegetarians who eat nothing but vegetables may develop a vitamin B 12 deficiency. Such individuals with a dietary insufficiency of vitamin B 12 typically respond to vitamin B 12 replace- ment therapy to reverse their anaemia. The most common cause of this deficiency, however, is inability of the GI tract to absorb the needed amounts of the vitamin. Gastric mucosal cells produce a sub- stance called intrinsic factor, which is necessary for the absorption of vitamin B 12 by the upper intestine. Pernicious anaemia occurs when the gastric mucosa cannot produce intrinsic factor and vitamin B 12 cannot be absorbed. The person with pernicious anaemia will complain of fatigue and lethargy, and will also have CNS effects because of damage to the myelin sheath. Individuals will also complain of numbness, tingling, and eventually lack of coordination and motor activity. Pernicious anaemia was once a fatal disease, but it is now treated with parenteral or nasal vitamin B 12 to replace the amount that can no longer be absorbed. Sickle cell anaemia Sickle cell anaemia is a chronic haemolytic anaemia that occurs almost exclusively in black people (“haemolytic” means that the anaemia involves a lysing or destruction of RBCs). It is characterised by a genetically inherited haemoglobin S, which gives the RBCs a sickle-shaped appearance. The person with sickle cell anaemia produces fewer than normal RBCs, and the RBCs that are produced are unable to carry oxygen efficiently. The sickle-shaped RBCs can become lodged in tiny blood vessels, where they stack up on one another and occlude the vessel. This occlusion leads to anoxia and infarction of the tissue in that area, which is characterised by severe pain and an acute inflammatory reaction, the person may even have ulcers on the extremities as a result of such occlusions. Severe, acute episodes of sickling with vessel occlusion may be associated with acute infec- tions as well as the body’s reactions to the immune and inflammatory responses. In the past, sickle cell anaemia was treated only with pain medication and support for the person. Now hydroxyurea has been found to be effective in treating this disease in adults.

■■ Anaemia is a state of too few RBCs or ineffective RBCs. Anaemia can be caused by a lack of erythropoietin or a lack of the components needed to produce RBCs. ■■ Anaemia can be categorised as deficiency (iron- deficiency anaemia), megaloblastic (folic acid or vitamin B 12 deficiency) or haemolytic (sickle cell). ERYTHROPOIESIS-STIMULATING AGENTS Individuals who are no longer able to produce enough erythropoietin in the kidneys may benefit from treat- ment with exogenous erythropoietin (EPO), which is available as the drugs epoetin alfa ( Eprex ), epoetin beta ( NeoRecormon ), epoetin lambda ( Novicrit [not availa- ble in New Zealand]), darbepoetin alfa ( Aranesp ) and methoxy polyethylene glycol-epoetin beta ( Mircera ). When agents are used to stimulate the bone marrow to make more RBCs, it is important to ensure that the person has adequate levels of the components required to make RBCs, including adequate iron. See Table 49.1 for additional information about each of these agents. Box 49.1 highlights important considerations for differ- ent age groups when this group of drugs and other drugs used to treat anaemia are administered. Therapeutic actions and indications Epoetin alfa acts like the natural glycoprotein erythro­ poietin to stimulate the production of RBCs in the bone marrow (see Figure 49.2). This drug is indicated in the treatment of anaemia associated with renal failure and for people on dialysis; for anaemia associated with AIDS therapy; and for anaemia associated with cancer chemotherapy when the bone marrow is depressed and the kidneys may be affected by the toxic drugs. It is not approved to treat other anaemias and is not a replace- ment for whole blood in the emergency treatment of anaemia. See Table 49.1 for additional indications.

Safe medication administration

With any of these drugs, there is a risk of decreasing the normal levels of erythropoietin if this drug is given to people who have normal renal functioning and adequate levels of erythropoietin (see Adverse effects for important safety information related to medication administration). Negative feedback occurs with the renal cells and less endogenous erythropoietin is produced if exogenous erythropoietin is given. Administration of this drug to an anaemic person with normal renal function can actually cause a more severe anaemia if the endogenous levels fall and no longer stimulate RBC production.

KEY POINTS

■■ RBCs are produced in the bone marrow in a process called erythropoiesis, which is controlled by the glycoprotein erythropoietin, produced in the kidneys. The bone marrow uses iron, amino acids, carbohydrates, folic acid and vitamin B 12 to produce healthy, efficient RBCs.

Made with