Decreased hemoglobin synthesis Defective DNA synthesis in RBCs Diminished availability of erythrocyte precursors

Anemia caused by decreased Erythrocyte Production Iron-deficiency Thalassemia Sideroblastic anemia anemia Megaloblastic anemias Aplastic anemia Anemia of chronic disease

Iron-Deficiency Anemia Etiology 1. 2. 3. 4. Inadequate dietary intake. Malabsorption. Blood loss. Hemolysis Malabsorption: GI surgery: procedures that involve removal or bypass of the duodenum Malabsorption syndromes: disease of duodenum in which the absorption surface is altered or destroyed Blood loss: Major sources: GI & GU systems GI: peptic ulcer, gastritis, esophagitis, diverticuli, hemorrhoids, neoplasia. GU: primarily from menstrual bleeding Other: postmenopausal bleeding in older woman, chronic renal failure & dialysis treatment Specific clinical symptoms: 1. Pallor 2. Glossitis (inflammation of the tongue) 3. Cheilitis (inflammation of the lips) 4. Headache, paresthesisas, & burning sensation of the tongue

Clinical Manifestations

Early Course: may be free of symptoms Chronic: general manifestations of anemia

Laboratory abnormalities

Diagnostic Studies Collaborative Therapy

Hb/Hct: MCV: Reticulocytes: N or slight or Serum Iron: TIBC: Transferrin: N or Ferritin: Bilirubin: N or 1. Stool Guaiac test 2. Endoscopy & colonoscopy to detect GI bleeding 3. A bone marrow biopsy 1. Main goal: treat underlying disease that is causing reduced intake or absorption of iron (malnutrition, alcoholism). 2. Efforts toward replacing iron. 3. Teach the pt. which foods are good sources of iron (liver & muscle meats, eggs, dried fruits, legumes, whole-grain & enriched bread & cereals, potatoes). 4. If iron deficiency is from acute blood loss- the pt. may require a transfusion of packed RBCs. 5. Iron dextran, sodium ferrous gluconate, iron sucrose IM or IV (parenteral iron)

History & physical examination Hct & Hb levels, RBC count, including morphology Reticulocyte count, serum iron, ferritin, transferrin, TIBC Stool examination for occult blood Drug therapy: Five factors should be considered: 1. Iron is absorbed best from the duodenum & proximal jejunum. (Enteric-coated or sustained release capsules, release iron farther down in GI tract are counterproductive/expensive) 2. The daily dosage should provide 150 to 200 mg of elemental iron. Ingested in 3 to 4 daily doses, each tablet or capsule containing btwn 50 to 100mg of iron. 3. Iron is best absorbed as ferrous sulfate (Fe2+) in an acidic environment. Iron should be taken about an hour before meals, when the duodenal mucosa is most acidic. (Taking iron with Vitamin C (ascorbic acid) or OJ enhances iron absorption). 4. Undiluted liquid iron may stain the patients teeth; dilute it & ingest through a straw. 5. GI side effects of iron administration may occur; such as heartburn, constipation, & diarrhea. Ferrous gluconate may be used as substitute. All pts. should know stools will become black because the GI tract excretes excess iron. Constipation is common- start patient on stool softener or laxative.

Etiology

Clinical Manifestations

Lab Abnormalities

Collaborative Care

Thalassemia 1. Heterozygous has one thalassemic gene & one Group of diseases that have an autosomal normal gene- thalassemia minor recessive genetic basis involving 2. Homozygous person has two thalassemic genesinadequate production of normal thalassemia major hemoglobin Due to absent or reduced globulin protein Abnormal Hb synthesis Thalassemia major: Both physical & mental growth retarded Pale & other general symptoms that devlop in childhood by 2 years of age Pronounced splenomegaly & hepatomegaly Jaundice from RBC hemolysis Chronic bone marrow hyperplasia & expansion of marrow space Thickening of cranium & maxillary cavity Hb/Hct: MCV: N or Reticulocytes: Serum Iron: TIBC: Transferrn: Ferritin: Bilirubin: Thalassemia minor: requires no treatment Thalassemia major: because the body adapts to the reduction of Symptoms are managed with blood transfusions or normal hemoglobin exchange transfusions in conjunction with oral deferasirox (Exjade) or IV or subcutaneous Hep C may result in cirrhosis & hepatocellular deferoxamine (Desferal) carcinoma Folic acid is given if there is sign of hemolysis Zinc may be needed (reduced with chelating Cardiac complications from iron overload, therapy) as well as ascorbic acid during chelation pulmonary disease, & hypertension early therapy (increases the excretion of iron) death Iron supplements should not be given Splenectomy Hepatic, cardiac, & pulmonary organ function Hep C is present in most patients older than 25 should be monitored years- because of receiving blood transfusions before they were screen for hep C Endocrinopathies (hypogonadotrophic hypogonadism) & thrombosis complications Hematopoietic stem cell transplantation remains the only cure- risk outweigh the benefits

Megaloblastic Anemias: Caused by impaired DNA synthesis Presence of large RBCs Result from cobalamin (vitamin B12) & folic acid deficiencies Other: drug-induced suppression of DNA synthesis, inborn errors, & erythroleukemia Cobalamin (Vitamin B12) Deficiency GI surgery: Long-term users of Most common cause H2-histamine is pernicious Gastrectomy, gastric receptor blockers anemia: a disease in bypass which the gastric Patients who have had a & proton pump inhibitors, & mucosa is not small bowel resection vegetarians secreting IF because involving the ileum of antibodies being Crohns disease, ileitis, directed against the celiac disease, gastric parietal cells diverticuli of the small and/or IF itself intestine, chronic atrophic gastritis Deficiency is the result from loss of IF-secreting gastric mucosal cells or impaired absorption of cobalamin in the distal ileum.

Etiology

Pernicious anemia: caused by the absence of IF- from either gastric mucosal atrophy or autoimmune destruction of parietal cells

Clinical Manifestations:

Diagnostic Studies:

Collaborative Care:

GI: Sore, red, beefy, & shiny tongue Anorexia, nausea, & vomiting Abdominal pain Neuromuscular: Weakness, paresthesias of feet & hands Reduced vibratory & position senses Ataxia Muscle weakness Impaired thought processes ranging from confusion to dementia Hb/Hct: If serum cobalamin levels are low & folate levels are normal cobalamin MCV: deficiency. Reticulocytes: N or A serum test for anti-IF antibodies may be done = specific for pernicious Serum Iron: anemia. TIBC: N Schilling test- radioactive cobalamin is administered to patient- absorption of Transferrn: cobalamin when IF is added is diagnostic of pernicious anemia Ferritin: MMA- elevated in cobalamin Bilirubin: Pt should be instructed High-dose oral cobalamin & sublingual cobalamin are available for those in on adequate dietary whom GI absorption is intact intake to maintain good nutrition Parenteral or intranasal administration of cobalamin is the treatment of choice

Etiology

Clinical Manifestations:

Collaborative Care

Folic Acid Deficiency Dietary deficiency Malabsorption syndromes Drugs interfering with absorption/use of folic acid- Methotrexate & Antiseizure drugs Alcohol abuse Anorexia Hemodialysis patients Disease develops insidiously Symptoms may be attributed to other coexisting problems such as cirrhosis or esophageal varices GI: Dyspepsia Smooth, beefy red tongue The absence of neurologic problems Treated with replacement therapy Ensure that injuries are not sustained because of the Usual dose is 1 mg per day by mouth diminished sensations to heat & pain resulting from the Patient should be encourage to eat neurologic impairment foods containing large amounts of folic Protect the patient from falling, burns, & trauma acid

Anemia of Chronic Disease (anemia of inflammation) Underproduction of RBCs Mild shortening of RBC survival RBCs are usually normocytic, normochromic, & hypoproliferative Immune driven Cytokines released by these conditions cause an increased uptake & retention of iron within macrophages Ex: Renal disease: the primary factor causing anemia is decreased erythropoietin (hormone made in the kidneys that stimulates erythropoiesis) Myelosuppression & decreased erythropoiesis caused by disease, medications (chemotherapy), or radiation will contribute to normochromic, normocytic anemia HIV & its treatments, hepatitis, malaria, & bleeding episodes contribute to this anemia Hypopituitary & hypothyroid Adrenal dysfunction caused by either adrenalectomy or Addisons disease Differentiated from anemias of other etiologies: Elevated serum ferritin & increased iron stores distinguish it from iron-deficiency Normal folate & cobalamin blood levels Erythropoietin therapy (Epogen, darbepoetin) is used for anemia related to renal disease

Etiology:

Pt. has peripheral blood pancytopenia ( of all blood cell types- RBCs, WBCs, platelet) & hypocellular bone marrow

Clinical Manifestations:

Abruptly (over days) or insidiously over wks to months Can vary in mild to severe Manifestation: fatigue & dyspnea Cardiovascular & cerebral responses

Aplastic Anemia Two major Congenital Acquired: groups: (Chromosomal Idiopathic/autoimmune 1. Congenital alterations): Chemical agents & toxins (benzene, 2. Acquired Fanconi syndrome insecticides, arsenic, alcohol) (70% are Congenital Drugs (alkylating agents, idiopathic dyskeratosis antiseizure drugs, antimetabolites, & thought antimicrobials, gold) Amegakaryocytic to be thrombocytopenia Radiation autoimmu Schwachman Viral & bacterial infections ne) Diamond (hepatitis, parvovirus) syndrome Pt with neutropenia (low neutrophil count) is susceptible to infection & is at risk for septic shock & death Even a low grade fever (above 100.4F) should be considered an emergency Thrombocytopenia is manifested by a predisposition to bleeding (petechiae, ecchymosis, epistaxis)

Diagnostic Studies: Collaborative Care:

Hemoglobin, WBC, & platelet values are decreased Marrow is hypocellular with increased yellow marrow (fat content) Identifying the HSCT and ATG causative Cyclosporine or high-dose cyclophosphamide (Cytoxan) agent & ATG- horse serum that contains polyclonal antibodies against human T cells providing supportive care until the pancytopenia reverses Prevent complications from infection & hemorrhage

Etiology:

Clinical Manifestations:

Collaborative Care:

Acute Blood Loss: Anemia 1. Sudden reduction in the total blood volume that can Result of sudden lead to hypovolemic shock hemorrhage 2. If the acute blood loss is more gradual the body Causes: trauma, maintains its blood volume by slowly increasing the complications in surgery, plasma volume & conditions or diseases that disrupt vascular integrity Volume Lost (%) 10% - none 20%- no detectable signs or symptoms at rest, tachycardia with exercise & slight postural hypotension 30%- Normal supine blood pressure & pulse at rest, postural hypotension & tachycardia with exercise. 40% - blood pressure, central venous pressure, & cardiac output below normal at rest; rapid, thread pulse & cold, clammy skin 50%- shock & potential death 1. Replacing blood volume to prevent For postoperative patient: shock Monitor the blood loss from various 2. Identifying the source of the drainage tubes & dressings & hemorrhage & stopping the blood loss. implement appropriate actions (IV fluids used in emergencies include Administration of blood products dextran, hetastarch, albumin, and/or crystalloid electrolyte solutions such as lactated Ringers solution. 3. Correcting the RBC loss- body needs 2 to 5 days to manufacture more RBCs in response to increased erythropoietin. 4. Supplemental iron

Etiology: (similar to those of irondeficiency anemia)

Chronic Blood Loss: Anemia Sources: Effects: Bleeding ulcers Depletion of iron stores & considered Hemorrhoids as iron-deficiency Menstrual & anemia postmenopausal blood loss

Management: identifying the source & stopping the bleeding