NUR2 Decreased Circulating Oxygen/Anemia Test 2

Anemia

1.) Decrease O2 carrying capacity due to: A deficiency in the -Number of erythrocytes (RBCs) -Quantity of hemoglobin -Or both 2.) Common S&S: 3.) SOB, Fatigue, Tachycardia, HF, Pallor, dyspnea, intolerance to activity, dizzy, dont feel like eating -anemia is a symptom of a problem -decreased ability of delivery of oxygen to a tissue -anemia=hypoxia -causes: not enough iron to make hgb, not making enough RBCs, bleeding internally, chronic kidney disease and kidney failure, kidney makes erythropoietin= hormones that stimulates the bone marrow to make RBCs, you can make RBCs but they can get destroyed= RBCs lifespan 120 days, circular concave- sickle cell anemia when RBC gets destroyed, not eating enough iron. lacking an enzyme for glucose 6 phosphate dehydrogenase (G6PDH

Causes of Anemia

1.) Decreased RBC production -Deficient nutrients: iron, cobalamin (fit b 12) , folic acid= help d and a of RBC to mature and condense, its going to stay bigger= macrocitic anemia -Decreased erythropoietin -Decreased iron availability 2.) Blood loss -chronic hemorrhage: bleeding duodenal ulcer, colorectal cancer, liver disease 2.) Acute trauma, ruptured aortic aneurysm, GI Bleeding 3.) increased RBC destruction -Hemolysis: sickle cell disease, medicaiton (methyldopa: alpha antagonist), Aldomet), incompatible blood. Trauma (cardiopulmonary bypass)

Folic Acid Deficiency Common causes

1.) Dietary deficiency 2.) Malabsorption syndromes 3.) Drugs 4.) Increased requirement 5.) Alcohol abuse and anorexia 6.) Loss during hemodialysis 7.) Serum folate level is low. -Normal is 3 to 25 mg/mL (7 to 57 mol/L). 8.) Serum cobalamin level is normal. 9.) Treated by replacement therapy -Usual dose is 1 mg per day by mouth. 10.) Encourage patient to eat foods with large amounts of folic acid. -The diagnostic findings for folic acid deficiency are presented in Table 31-6. -Also during diagnostic studies, the gastric analysis is positive for hydrochloric acid. -Replacement therapy is the treatment of choice: In malabsorption states or with chronic alcoholism, up to 5 mg per day may be required. Duration of treatment depends on the reason for the deficiency. -See Table 31-5 for foods high in folic acid. -dont need intrinsic factors

Anemia Nursing Diagnoses

1.) Fatigue 2.) Imbalanced nutrition: Less than body requirements 3.) Ineffective self-health management -Assume normal activities of daily living -Maintain adequate nutrition -Develop no complications related to anemia

Cobalamin Deficiency Clinical Manifestations General manifestations of anemia develop slowly due to tissue hypoxia.

1.) Gastrointestinal manifestations: Sore tongue, anorexia, nausea, vomiting, & abdominal pain 2.) Neuromuscular manifestations: Weakness, paresthesias of feet & hands, ↓ vibratory and position senses, ataxia, muscle weakness, and impaired thought processes -Because cobalamin deficiency-related anemia has an insidious onset, it may take several months for these manifestations to develop.

Iron-Deficiency Anemia Clinical Manifestations

1.) General manifestations of anemia 2.) Pallor is the most common finding. 3.) Glossitis is the second most common. -Inflammation of the tongue 4.) Cheilitis -Inflammation of the lips -In the early course of iron-deficiency anemia, the patient may not have any symptoms, but as the disease becomes chronic, any of the general manifestations of anemia may develop. -In addition, 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.

Iron-Deficiency Anemia Collaborative Care

1.) Goal is to treat the underlying disease causing reduced intake or absorption of iron. 2.) Efforts are aimed at replacing iron. -Nutritional therapy -Oral or occasional parenteral iron supplements -Transfusion of packed RBCs -The main goal of collaborative care of iron-deficiency anemia is to treat the underlying disease that is causing reduced intake (e.g., malnutrition, alcoholism) or absorption of iron. -Teach the patient which foods are good sources of iron. -If nutrition is already adequate, iron supplements are used. -foods with folic acid: Leafy green vegetables, such as spinach. Citrus fruits, such as orange juice. Beans. Bread. Cereals. Rice. Pasta. -foods with vitamin b 12: Animal Liver and Kidneys. Organ meats Clams. Sardines. Beef. Fortified Cereal. Tuna. Fortified Nutritional Yeast. Trout. -If the iron deficiency is from acute blood loss, the patient may require a transfusion of packed RBCs.

Megaloblastic Anemias

1.) Group of disorders -Caused by impaired DNA synthesis -Presence of megaloblasts 2.) Majority result from deficiency in -Cobalamin (vitamin B12) -Folic acid -Megaloblastic anemias are a group of disorders caused by impaired deoxyribonucleic acid (DNA) synthesis and characterized by the presence of large RBCs. -When DNA synthesis is impaired, defective RBC maturation results: The RBCs are large (macrocytic) and abnormal and are referred to as megaloblasts. Macrocytic RBCs are easily destroyed because they have fragile cell membranes. -Although the overwhelming majority of megaloblastic anemias result from cobalamin (vitamin B12) and folic acid deficiencies, this type of RBC deformity can also occur from suppression of DNA synthesis by drugs, inborn errors of cobalamin and folic acid metabolism, and erythroleukemia (malignant blood disorder characterized by a proliferation of erythropoietic cells in bone marrow).

Case Study

How should K.L.'s anemia be treated: -Increasing her dietary intake of iron or beginning iron supplementation.

Polycythemia vera: making too many RBCs

A neoplastic disease arising from a chromosomal mutation 1.) Inc. production of -erythrocytes -granulocytes -platelets 2.) Therefore, increases in blood viscosity, blood volume, & congestion of organs/tissues with blood -Develops insidiously, follows a chronic vacillating course, usu >50 yrs age -chronic hypoxia: too many RBCS (COPD, asthma) hgb 19 or 20 -too many rbcs it clogs system and blood becomes very viscous and difficult to move through small objects= HTN, blood clots -drink a lot of water to decrease viscosity of the blood -donate blood

Learning Objectives

•Differentiate between the different types of anemias. •Compare and contrast the physiologic mechanisms, clinical manifestations, medical management, and nursing interventions for each. •Identify therapies for different types of anemias, including the nursing implications for the administration of blood components. •Review steps for blood products transfusions •Discuss the S&S of the common types of blood transfusion reactions and collaborative management

Anemia Classified as

1.) Morphologic -Cellular characteristics -microcitic anemia: cell is smaller and doesn't have enough hgb decreased MCV=deficiency of iron , macrocitic anemia: cell is big increased MCV -folic acid or vit b deficiency gives you macrocitic anemia 2.) Etiologic -Underlying cause

Anemia Clinical Manifestations

1.) Caused by the body's response to tissue hypoxia -Manifestations vary based on rate of development, severity of anemia, presence of co-existing disease. 2.) Hemoglobin (Hgb) levels are used to determine the severity of anemia.

Anemia of Chronic Disease Anemia of Inflammation Caused by

1.) Chronic inflammation 2.) Autoimmune and infectious disorders -HIV, hepatitis, malaria 3.) Heart failure 4.) Malignant diseases Bleeding episodes

Anemia Gerontologic Considerations

1.) Common in older adults -Chronic disease -Nutritional deficiencies 2.) Signs and symptoms may go unrecognized or may be mistaken for normal aging changes. tired, fatigue -cytokines destroy RBCs -iron deficiency and RBCs dont live long enough treated with iron supplements

A 71- year-old patient with a history of rheumatoid arthritis and HTN has been admitted to the hospital for the treatment of a suspected upper GI bleed. When performing an assessment of this patient, which of the following questions most directly addresses a likely cause of thepatient's bleeding disorder?

1."How closely do you tend to monitor your BP when you're at home?" 2."Has your doctor prescribed a water pill for your high BP?" 3.Do you ever take aspirin to treat the pain of your arthritis?" (correct) 4."Did either of your parents or siblings have problems with bleeding?" -aspirin causes bleeding ulcers

The nurse provides patient education related to the management of iron deficiency anemia. Which of the following statements made by the patient signifies understanding of the education provided?

1."I should take my iron pills with a glass of OJ." 2."I should take my iron pills with breakfast to decrease stomach upset." 3."Iron pills often cause constipation, should I should decrease my fluid and fiber intake." 4."I will only need to take these pills for a few days and then my problem will be fixed."

Polycythemia Vera S&S

1.) ** Hypervolemia & Hyperviscosity: HTN 2.) Splenomegaly 3.) Thrombophlebitis 4.) Hemmorrhagic phenomena 5.) Ruddy Face 6.) Epigastric pain 7.) Hyperuricemia - gout, pruritus -DX: Hgb > 18.5 (males) >16.5 (females) Increased RBC, platelets, uric acid + JAK2 genetic mutation (skip) Complications--> CVA or MI

Aplastic Anemia Clinical Manifestations

1.) Abrupt or gradual development 2.) Symptoms caused by suppression of any or all bone marrow elements 3.) General manifestations of anemia -Fatigue, dyspnea -Cardiovascular and cerebral responses -Neutropenia -The patient with neutropenia (low neutrophil count) is susceptible to infection and is at risk for septic shock and death. Even a low-grade temperature (>100.4o F) should be considered a medical emergency. -Thrombocytopenia is manifested by a predisposition to bleeding evidenced by petechiae, ecchymosis, and epistaxis.

Megaloblastic Anemia Folic Acid Deficiency

1.) Also a cause of megaloblastic anemia 2.) Folic acid is required for DNA synthesis. -RBC formation and maturation 3.) Clinical manifestations are similar to those of cobalamin deficiency, but absence of neurologic problems differentiates them. -Folic acid deficiency develops insidiously, and the patient's symptoms may be attributed to other coexisting problems (e.g., cirrhosis, esophageal varices). -GI disturbances include dyspepsia and a smooth, beefy red tongue.

Anemia of Chronic Disease

1.) Anemia of chronic disease findings -↑ Serum ferritin -↑ Iron stores -Normal folate and cobalamin levels 2.) Treating underlying cause is best. -Rarely blood transfusions -Conservative use of erythropoietin therapy -procrit -epotin alpha (generic) -Anemia of chronic disease must first be recognized and differentiated from anemia of other etiologies: Elevated serum ferritin and increased iron stores distinguish it from iron-deficiency anemia. Normal folate and cobalamin blood levels distinguish it from those types of anemias. -The best treatment of anemia of chronic disease is correction of the underlying disorder. -If the anemia is severe, blood transfusions may be indicated, but they are not recommended for long-term treatment. -Erythropoietin therapy (Epogen, darbepoetin) is used for anemia related to renal disease and may be used for anemia related to cancer and its therapies.: However, it needs to be used conservatively, as there is an increased risk of thromboembolism and mortality in some patients.

Case Study

1.) Anything that costs money is out of the question. 2.) What can you teach K.L. about effects of anemia if left untreated? -In severe cases, anemia can lead to MI, heart failure (HF), cardiomegaly, pulmonary and systemic congestion, ascites, peripheral edema, jaundice, and pruritus. -Refer her to social services for assistance with affording this important supplement.

Aplastic Anemia Nursing & Collaborative Management

1.) Identify and remove causative agent (when possible). 2.) Provide supportive care until pancytopenia reverses. 3.) Prevent complications from infection. 4.) Prevent hemorrhage. 5.) Prognosis of severe untreated aplastic anemia is poor. -Median survival is 3 to 6 months. -20% survive longer than 1 year. 6.) Treatment options -Immune therapies and bone marrow transplantation can be curative. •Advances in medical management, including hematopoietic stem cell transplant (HSCT) and immunosuppressive therapy with antithymocyte globulin (ATG) and cyclosporine or high-dose cyclophosphamide (Cytoxan), have improved outcomes significantly. •ATG is a horse serum that contains polyclonal antibodies against human T cells. It can cause anaphylaxis and a serum sickness. The rationale for this therapy is that idiopathic aplastic anemia is considered an autoimmune disorder resulting from activated cytotoxic T cells that target and destroy the patient's own hematopoietic stem cells. •The treatment of choice for adults less than 55 years of age who do not respond to the immunosuppressive therapy and who have a human leukocyte antigen (HLA)-matched donor is an HSCT. •The best results occur in younger patients who have not had previous blood transfusions. •Prior transfusions increase the risk of graft rejection. •For older adults without an HLA-matched donor, the treatment of choice is immunosuppression with ATG or cyclosporine or high-dose cyclophosphamide. •High-dose corticosteroids may also be used. However, this therapy may be only partially beneficial. Patients who need ongoing supportive blood transfusion should be on an iron-binding agent to prevent iron overload

Iron-Deficiency Anemia Etiology

1.) Inadequate dietary intake -5% to 10% of ingested iron is absorbed. not well absorbed Vitamin C helps better absorb iron -not absorbed bc surgery, sickness, or dont eat enough of it, 2.) Malabsorption -Iron absorption occurs in the duodenum. -Diseases or surgery that alter, destroy, or remove the absorption surface of this area of the intestine cause anemia. 3.) Blood loss -2 mL whole blood contain 1 mg iron. -Major cause of iron deficiency in adults -Chronic blood loss most commonly through GI and GU systems 4.) Pregnancy contributes to this condition. -Dietary iron is adequate to meet the needs of men and older women, but it may be inadequate for those individuals who have higher iron needs such as menstruating or pregnant women. -As iron absorption occurs in the duodenum, malabsorption syndromes may involve diseases of the duodenum in which the absorption surface is altered or destroyed, or after certain types of GI surgery where the removal or bypass of the duodenum occurs. -50-75 mL of blood loss from the upper GI tract is required for stools to appear black (melena; the black color is from the iron in the RBCs). -Common causes of GI blood loss are peptic ulcer, gastritis, esophagitis, diverticuli, hemorrhoids, and neoplasia. -GU blood loss occurs primarily through menstrual bleeding. -The average monthly menstrual blood loss is about 45 mL and causes the loss of about 22 mg of iron. -Postmenopausal bleeding can contribute to anemia in a susceptible older woman. -In addition to anemia of chronic kidney disease, dialysis treatment may induce iron-deficiency anemia as the result of blood lost in the dialysis equipment and frequent blood sampling. -Pregnancy contributes to iron deficiency because of the diversion of iron to the fetus for erythropoiesis, blood loss at delivery, and lactation.

Case Study

1.) K.L. has lab work done. Her results are back, and her lab values show -↓ Hct, Hgb, MCV, iron, ferritin, and transferrin -↑ TIBC. -transferrin: take iron from liver to cells 2.) What is the likely cause of her anemia?

Case Study

1.) K.L. is a 24-year-old female with complaints of ↑ lethargy, inability to pay attention at work, and headache. 2.) She has a pale, beefy tongue and inflamed lip=glossitis, chelitis 3.) She tells you she is breast-feeding her 4-month old. -What should you do?

Case Study

1.) K.L. tells you she can't afford medicine. 2.) She has 3 children, and her husband is out of work. 3.) Her income is barely keeping the household going -refer her to social worker, community resources.

Polycythemia Vera Teaching Points

1.) Keep well hydrated 2.) Elevate feet when sitting 3.) PROM/AROM, exercise 4.) Electric Shaver 5.) Soft toothbrush 6.) Report chest pain

Iron-Deficiency Anemia Diagnostic Studies

1.) Laboratory findings: Hgb, Hct, MCV, reticulocytes increase, serum iron, TIBC, bilirubin, platelets -Mild --> Hgb 10 - 12: dont treat, maybe supplements - Moderate --> Hgb 6 - 10 - Severe --> Hgb < 6: CHF -no blood transfusion unless less than 7 2.) Stool guaiac test 3.) Endoscopy 4.) Colonoscopy: check for cancer 5.) Bone marrow biopsy: aplastic anemia. RBCs are diseased or not making them at all -diagnostic studies are done to determine the cause of the iron deficiency or to detect GI bleeding. -A bone marrow biopsy may be done if other tests are inconclusive.

Aplastic Anemia Diagnostic Studies: Diagnosis confirmed by laboratory studies

1.) Low Hgb, WBC, and platelet values 2.) Low reticulocyte count 3.) Prolonged bleeding time 4.) Elevated serum iron and TIBC 5.) Hypocellular bone marrow with increased fat content (yellow marrow) -All marrow elements are affected in this disorder. -The condition is classified as a normocytic, normochromic anemia because although Hgb, WBC, and platelet values are decreased, other RBC indices are generally normal. -Aplastic anemia can be further evaluated by assessing various iron studies. The serum iron and total iron-binding capacity (TIBC) may be elevated as initial signs of erythropoiesis suppression. Bone marrow biopsy, aspiration, and pathologic examination may be done for any anemic state. However, the findings are especially important in aplastic anemia because the marrow is hypocellular with increased yellow marrow (fat content).

Aplastic Anemia Etiology

1.) Low incidence -Affecting 2 of every 1 million persons 2.) 2 Major Types -Congenital: Chromosomal alterations 3.) Acquired -Results from exposure to ionizing radiation, chemical agents, viral and bacterial infections -Approximately 75% of the acquired aplastic anemias are idiopathic and are thought to have an autoimmune basis.

Cobalamin Deficiency Diagnostic Studies

1.) Macrocytic RBCs have abnormal shapes and fragile cell membranes. 2.) Serum cobalamin levels are decreased. 3.) Normal serum folate levels and low cobalamin levels suggest megaloblastic anemia is due to cobalamin deficiency. 4.) Upper GI endoscopy with biopsy of gastric mucosa -Laboratory data reflective of cobalamin-deficiency anemia are presented in Table 31-6. -Abnormal RBCs are susceptible to erythrocyte destruction. -A serum test for anti-IF antibodies may be done that is specific for pernicious anemia. -The potential for gastric cancer is increased in patients with pernicious anemia. -Testing of serum methylmalonic acid (MMA) (elevated mainly in cobalamin deficiency) and serum homocysteine (elevated in both cobalamin and folic acid deficiencies) can also be done.

Cobalamin Deficiency Etiology

1.) Most commonly caused by pernicious anemia -Which is caused by an absence of IF -Insidious onset -Begins in middle age or later -Predominant in Scandinavians and African Americans 2.) Can also occur in the following situations: -GI surgery -Chronic diseases of the GI tract -Chronic alcoholics -Long-term users of H2-histamine receptor blockers and proton pump inhibitors: Zantac -Strict vegetarians -Cobalamin deficiency is most commonly caused by pernicious anemia, which results in poor cobalamin absorption through the GI tract. -In pernicious anemia the gastric mucosa is not secreting IF because of either gastric mucosal atrophy or autoimmune destruction of parietal cells: In the autoimmune process antibodies are directed against the gastric parietal cells and/or IF itself. Because parietal cells also secrete hydrochloric (HCl) acid, in pernicious anemia there is a decrease in HCl in the stomach. An acid environment in the stomach is required for the secretion of IF. -Pernicious anemia is a disease of insidious onset that begins in middle age or later (usually after age 40) with 60 years being the most common age at diagnosis. -Pernicious anemia occurs frequently in persons of Northern European ancestry (particularly Scandinavians) and African Americans.: In African Americans, the disease tends to begin early, occurs with higher frequency in women, and is often severe. -Parenteral or intranasal administration of cobalamin is the treatment of choice. -Cobalamin deficiency can also occur in patients who have had GI surgery such as gastrectomy, gastric bypass, small bowel resection involving the ileum, and chronic diseases of GI tract such as Crohn's disease, ileitis, celiac disease, diverticuli of the small intestine, chronic atrophic gastritis. -In these cases, cobalamin deficiency results from the loss of IF-secreting gastric mucosal cells or impaired absorption of cobalamin in the distal ileum. -dont give supplements of vb12 bc they won't absorb it, get an IM injection of vb12 once a month -vitb12 deficiency happens over a period of time, not rapid. it is not reversible. the RBCs suffer and destroys myelin sheath cognitive deficits and neurological damagement. -vit b 12 is water soluble, your body urinates what it does not need

Anemia

1.) Not a specific disease 2.) Manifestation of a pathologic process 3.) Classified by laboratory review of -Complete blood count (CBC) -Reticulocyte count -Peripheral blood smear -look at RBC under a microscope -if you are anemia the bone marrow is hyperactive, but they dont mature because they keep getting destroyed

Iron-Deficiency Anemia Drug Therapy

1.) Oral iron -Inexpensive -Convenient -Factors to consider: a.) Enteric-coated or sustained-release capsules are counterproductive. b.) Daily dose is 150 to 200 mg. c.) Best absorbed as ferrous sulfate in an acidic environment d.) Liquid iron should be diluted and ingested through a straw. iron stains teeth e.) Side effects: Heartburn, constipation, diarrhea stool black -substitute it with glutamate if constipation occurs 2.) Parenteral iron -Indicated for malabsorption, oral iron intolerance, need for iron beyond normal limits, poor patient compliance -Can be given IM or IV -IM may stain skin. -Iron therapy for 2 to 3 months after hemoglobin levels return to normal -can cause severe anaphylactic reaction -Iron is absorbed best from the duodenum and proximal jejunum. Therefore enteric-coated or sustained-release capsules, which release iron farther down the GI tract, are counterproductive and expensive. -The daily dosage should provide 150 to 200 mg of elemental iron. This can be ingested in three or four daily doses, with each tablet or capsule of the iron preparation containing between 50 and 100 mg of iron. -Iron is best absorbed as ferrous sulfate (Fe2+) in an acidic environment. For this reason and to avoid binding the iron with food, iron should be taken about an hour before meals, when the duodenal mucosa is most acidic. Taking iron with vitamin C (ascorbic acid) or orange juice, which contains ascorbic acid enhances iron absorption. -Undiluted liquid iron may stain teeth, thus the reason for ingesting it through a straw. -Side effect example: Many individuals who need supplemental iron cannot tolerate ferrous sulfate because of the effects of the sulfate base. However, ferrous gluconate may be an acceptable substitute. -All patients need to be told that iron will cause their stools to become black because excess iron is excreted in the GI tract. -Because iron causes constipation, patients should be started on stool softeners and laxatives, if needed, when started on iron. -An iron-dextran complex (INFeD) contains 50 mg/mL of elemental iron in 2 mL. Sodium ferrous gluconate and iron sucrose are alternatives and may provide less risk of life-threatening anaphylaxis. -Because IM iron solutions may stain the skin, separate needles should be used for withdrawing the solution and for injecting the medication. A Z-track injection technique should be used.

Anemia Integumentary Manifestations

1.) Pallor -↓ Hemoglobin -↓ Blood flow to the skin 2.) Jaundice -↑ Concentration of serum bilirubin -cells get destroyed quickly. destroy too many of them and they deposit under the skin -jaundice= puritis 3.) Pruritus -↑ Serum and skin bile salt concentrations

Dark Skin Assessments

1.) Pallor of Anemia -Brown skin: yellow-brown -Black skin: ashen gray -Oral mucosa -Nail beds 2.) Jaundice R/T Hemolysis -Oral mucosa & check hard palate -sclera

Aplastic Anemia

1.) Pancytopenia -Decrease in all blood cell types: Red blood cells (RBCs) White blood cells (WBCs) Platelets 2.) Hypocellular bone marrow 3.) Ranges from chronic to critical -Aplastic anemia is a disease in which the patient has peripheral blood pancytopenia. -The spectrum of the anemia can range from a chronic condition managed with erythropoietin or blood transfusions to a critical condition with hemorrhage and sepsis. -chloramphenicol -

Cobalamin Deficiency Collaborative Care

1.) Parenteral or intranasal administration of cobalamin is the treatment of choice. -Patients will die in 1-3 years without treatment. -This anemia can be reversed with ongoing treatment but long-standing neuromuscular complications may not be reversible. -Increasing dietary cobalamin does not correct this anemia if intrinsic factor is lacking or if there is impaired absorption in the ileum. However, good nutrition should still be taught. -The dosage and frequency of cobalamin administration may vary. A typical treatment schedule consists of 1000 mg of cobalamin IM daily for 2 weeks and then weekly until the Hgb is normal, then monthly for life. -High-dose oral cobalamin and sublingual cobalamin are also available for those in whom GI absorption is intact

Management Polycythemia

1.) Phlebotomy: donate blood 2.) Hydration 3.) Myelosuppressive agents: 4.) Allopurinol: anti gout Nursing managament: 1.Assist w/ phlebotomy 2.Strict I's and O's: avoid overload or underhydration which can cause inc viscosity 3.Meds: SE 4.Assess nutritional status, may take in less b/c feel full/dyspepsia 5.PROM/AROM b/c dec mobility 2 risk for thrombosis 6.Will need plebotomy q 2-3 mos, BIGGEST concern: thrombus Mainly in men, affects elderly >60

Anemia Cardiopulmonary Manifestations

1.) Result from additional attempts by heart and lungs to provide adequate O2 to the tissues 2.) Cardiac output maintained by increasing the heart rate and stroke volume

Anemia of Chronic Disease Anemia of Inflammation Associated with

1.) Underproduction of RBCs 2.) Mild shortening of RBC survival -Normocytic, normochromic, and hypoproliferative RBCs -Usually a mild anemia but can become severe if the underlying disorder is untreated -This type of anemia, which usually develops after 1 to 2 months of disease activity, has an immune basis.

Audience Response Question

At an outpatient clinic, K.L.'s 78-year-old grandma is found to have a Hgb of 8.7 g/dL (87 g/L) and a Hct of 35%. Based on the most common cause of these findings in the older adult, the nurse collects information regarding a.a history of jaundice and black tarry stools. b.a 3-day diet recall of the foods the patient has eaten. c.any drugs that have depressed the function of the bone marrow. d.a history of any chronic diseases such as cancer or renal disease. Answer: D Rationale: Anemia in the older adult population is commonly caused by co-morbid conditions such as cancer or renal disease.