Anemia caused by decreased Erythrocyte ProductionDecreased hemoglobin synthesis
Iron-deficiency anemia
Thalassemia Sideroblastic anemia
Defective DNA synthesis in RBCs
Megaloblastic anemias
Diminished availability of erythrocyte precursors
Aplastic anemia Anemia of chronic disease
Iron-Deficiency AnemiaEtiology 1. Inadequate dietary intake.
2. Malabsorption.3. Blood loss.4. 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 destroyedBlood loss: Major sources: GI & GU systemsGI: peptic ulcer, gastritis, esophagitis, diverticuli, hemorrhoids, neoplasia.GU: primarily from menstrual bleedingOther: postmenopausal bleeding in older woman, chronic renal failure & dialysis treatment
Clinical Manifestations
Early Course: may be free of symptomsChronic: general manifestations of anemia
Specific clinical symptoms:1. Pallor2. Glossitis (inflammation of the tongue)3. Cheilitis (inflammation of the lips)4. Headache, paresthesisas, & burning sensation of the tongue
Laboratory abnormalities
Hb/Hct: ↓MCV: ↓Reticulocytes: N or slight ↑or ↓Serum Iron: ↓TIBC: ↑Transferrin: N or ↓Ferritin: ↓Bilirubin: N or ↓
Diagnostic Studies
1. Stool Guaiac test2. Endoscopy & colonoscopy to
detect GI bleeding3. A bone marrow biopsy
History & physical examinationHct & Hb levels, RBC count, including morphologyReticulocyte count, serum iron, ferritin, transferrin, TIBCStool examination for occult blood
Collaborative Therapy
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)
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.
ThalassemiaEtiology Group of diseases that have an autosomal
recessive genetic basis involving inadequate production of normal hemoglobin
Due to absent or reduced globulin protein Abnormal Hb synthesis
1. Heterozygous has one thalassemic gene & one normal gene- thalassemia minor
2. Homozygous person has two thalassemic genes- thalassemia major
Clinical Manifestations
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
Lab Abnormalities
Hb/Hct: ↓MCV: N or ↓Reticulocytes: ↑Serum Iron: ↑TIBC: ↓Transferrn: ↓Ferritin: N∨↑Bilirubin: ↑
Collaborative Care
Thalassemia minor: requires no treatment because the body adapts to the reduction of normal hemoglobin
Hep C may result in cirrhosis & hepatocellular carcinoma
Cardiac complications from iron overload, pulmonary disease, & hypertension – early death
Hepatic, cardiac, & pulmonary organ function should be monitored
Endocrinopathies (hypogonadotrophic hypogonadism) & thrombosis –complications
Hematopoietic stem cell transplantation remains the only cure- risk outweigh the benefits
Thalassemia major: Symptoms are managed with blood transfusions or
exchange transfusions in conjunction with oral deferasirox (Exjade) or IV or subcutaneous deferoxamine (Desferal)
Folic acid is given if there is sign of hemolysis Zinc may be needed (reduced with chelating
therapy) as well as ascorbic acid during chelation therapy (increases the excretion of iron)
Iron supplements should not be given Splenectomy Hep C is present in most patients older than 25
years- because of receiving blood transfusions before they were screen for hep C
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) DeficiencyEtiology Most common cause
is pernicious anemia: a disease in which the gastric mucosa is not secreting IF because of antibodies being directed against the gastric parietal cells and/or IF itself
GI surgery: Gastrectomy, gastric
bypass Patients who have had a
small bowel resection involving the ileum
Crohns disease, ileitis, celiac disease, diverticuli of the small 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.
Long-term users of H2-histamine receptor blockers & proton pump inhibitors, & vegetarians
Pernicious anemia: caused by the absence of IF- from either gastric mucosal atrophy or autoimmune destruction of parietal cells
Clinical Manifestations:
GI: Sore, red, beefy, & shiny tongue Anorexia, nausea, & vomiting Abdominal painNeuromuscular: Weakness, paresthesias of feet & hands Reduced vibratory & position senses Ataxia Muscle weakness Impaired thought processes ranging from confusion to dementia
Diagnostic Studies:
Hb/Hct: ↓MCV: ↑Reticulocytes: N or ↓Serum Iron: N∨↑TIBC: NTransferrn: Slight ↑Ferritin: ↑Bilirubin: N∨slight ↑
If serum cobalamin levels are low & folate levels are normal cobalamin deficiency.A serum test for anti-IF antibodies may be done = specific for pernicious anemia.Schilling test- radioactive cobalamin is administered to patient- absorption of cobalamin when IF is added is diagnostic of pernicious anemiaMMA- elevated in cobalamin
Collaborative Care:
Pt should be instructed on adequate dietary intake to maintain good nutritionParenteral or intranasal administration of cobalamin is the treatment of choice
High-dose oral cobalamin & sublingual cobalamin are available for those in whom GI absorption is intact
Folic Acid DeficiencyEtiology Dietary deficiency
Malabsorption syndromes Drugs interfering with absorption/use of folic acid- Methotrexate & Antiseizure drugs Alcohol abuse Anorexia
Hemodialysis patientsClinical Manifestations:
Disease develops insidiously Symptoms may be attributed to other coexisting problems such as cirrhosis or esophageal
varicesGI:
Dyspepsia Smooth, beefy red tongue
The absence of neurologic problemsCollaborative Care
Treated with replacement therapyUsual dose is 1 mg per day by mouthPatient should be encourage to eat foods containing large amounts of folic acid
Ensure that injuries are not sustained because of the diminished sensations to heat & pain resulting from the neurologic impairmentProtect the patient from falling, burns, & trauma
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 Addison’s disease
Differentiated from anemia’s 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
Aplastic AnemiaEtiology: Pt. has peripheral
blood pancytopenia (↓ of all blood cell types- RBCs, WBCs, platelet) & hypocellular bone marrow
Two major groups:1. Congenital2. Acquired
(70% are idiopathic & thought to be autoimmune)
Congenital (Chromosomal alterations): Fanconi syndrome Congenital
dyskeratosis Amegakaryocytic
thrombocytopenia Schwachman-
Diamond syndrome
Acquired: Idiopathic/autoimmune Chemical agents & toxins (benzene,
insecticides, arsenic, alcohol) Drugs (alkylating agents,
antiseizure drugs, antimetabolites, antimicrobials, gold)
Radiation Viral & bacterial infections
(hepatitis, parvovirus)
Clinical Manifestations:
Abruptly (over days) or insidiously over wks to months
Can vary in mild to severe
Manifestation: fatigue & dyspnea
Cardiovascular & cerebral responses
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:
Hemoglobin, WBC, & platelet values are decreased Marrow is hypocellular with increased yellow marrow (fat content)
Collaborative Care:
Identifying the causative agent & providing supportive care until the pancytopenia reverses
Prevent complications from infection & hemorrhage
HSCT and ATG Cyclosporine or high-dose cyclophosphamide (Cytoxan) ATG- horse serum that contains polyclonal antibodies against human T cells
Acute Blood Loss: AnemiaEtiology: Result of sudden
hemorrhage Causes: trauma,
complications in surgery, & conditions or diseases that disrupt vascular integrity
1. Sudden reduction in the total blood volume that can lead to hypovolemic shock
2. If the acute blood loss is more gradual the body maintains its blood volume by slowly increasing the plasma volume
Clinical Manifestations:
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
Collaborative Care:
1. Replacing blood volume to prevent shock
2. Identifying the source of the hemorrhage & stopping the blood loss. (IV fluids used in emergencies include 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
For postoperative patient: Monitor the blood loss from various
drainage tubes & dressings & implement appropriate actions
Administration of blood products
Chronic Blood Loss: AnemiaEtiology: (similar to those of iron-deficiency anemia)
Sources: Bleeding ulcers Hemorrhoids Menstrual &
postmenopausal blood loss
Effects: Depletion of iron
stores & considered as iron-deficiency anemia
Management: identifying the source & stopping the bleeding