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ANEMIA Prepared by: Sangita shrestha Manisha dhungana

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ANEMIA

Prepared by: Sangita shrestha Manisha dhungana

Anemia is usually defined as a decrease in the amount of red blood cells (RBCs) or the amount of hemoglobin in the blood. It can also be defined as a lowered ability of the blood to carry oxygen.

Iron deficiency anemia, pernicious anemia, folic acid deficiency anemia and aplastic anemia are the anemias most commonly seen in adults.

Introduction

There are more than 400 types of anemia, which are divided into three groups:

Anemia caused by blood loss Anemia caused by decreased or faulty red blood

cell production Anemia caused by destruction of red blood cells Anemia caused by fluid overload

What Causes Anemia?

Anemia symptoms vary depending on the cause of your anemia but may include:

Fatigue Weakness Pale skin A fast or irregular heartbeat Shortness of breath Chest pain Dizziness Cognitive problems Cold hands and feet Headache

Sign and symptoms

These factors place you at increased risk of anemia:

A diet lacking in certain vitamins. Choosing a diet that is consistently low in iron, vitamin B-12 and folate increases your risk of anemia.

Intestinal disorders. Having an intestinal disorder that affects the absorption of nutrients in your small intestine — such as Crohn's disease and celiac disease — puts you at risk of anemia. Surgical removal of or surgery to the parts of your small intestine where nutrients are absorbed can lead to nutrient deficiencies and anemia.

Risk factors

Menstruation. In general, women who haven't experienced menopause have a greater risk of iron deficiency anemia than do men and postmenopausal women. That's because menstruation causes the loss of red blood cells.

Pregnancy. If you're pregnant, you're at an increased risk of iron deficiency anemia because your iron stores have to serve your increased blood volume as well as be a source of hemoglobin for your growing baby.

Chronic conditions. For example, if you have cancer, kidney or liver failure, or another chronic condition, you may be at risk of anemia of chronic disease. These conditions can lead to a shortage of red blood cells.

Slow, chronic blood loss from an ulcer or other source within your body can deplete your body's store of iron, leading to iron deficiency anemia.

Family history. If your family has a history of an inherited anemia, such as sickle cell anemia, you also may be at increased risk of the condition.

Other factors. A history of certain infections, blood diseases and autoimmune disorders, alcoholism, exposure to toxic chemicals, and the use of some medications can affect red blood cell production and lead to anemia.

Common types of anemia Common types of anemia and their causes

include: Iron deficiency anemia: It is a condition in which

the total body iron content is decreased below the normal level, affecting hemoglobin synthesis.

This type of anemia is often caused by blood loss, such as from heavy menstrual bleeding, an ulcer, cancer, a polyp somewhere in your digestive system, and prolonged use of aspirin or drugs known as nonsteroidal anti-inflammatory drugs (NSAIDs), pregnancy, a lack of iron supply in diet, inability to absorb iron.

Iron deficiency anemia is caused by a shortage of the element iron in your body. our bone marrow needs iron to make hemoglobin. Without adequate iron, our body can't produce enough hemoglobin for red blood cells. Decreased hemoglobin may result in insufficient oxygen delivery to the tissue. And cause anemia.

Pathophysiology

Headache, dizziness, fatigue, tinnitus. Palpitations, dyspnea on exertion, pallor of

skin and mucous membrane In developing countries: smooth, sore

tongue, cheilosis, koilonchia( spoon shaped nails) and pica

Clinical manifestations

CBC and iron profile: decreased hemoglobin, hematocrit, serum iron, and ferritin; eleveted red cells in distribution width and normal or elevated total iron binding capacity.

Determination of source of chronic blood loss may include sigmoidoscopy, colonoscopy, upper and lower GI studies, stools and urine for occult blood examination.

Diagnostic evaluation

Early diagnosis and correction of chronic blood loss

Oral and parenteral iron therapy

Management

Nursing Assessment Obtain history of symptoms, dietary intake, past

history of anemia, possible sources of blood loss. Examine for tachycardia, pallor, dyspnea, and signs

of GI or other bleeding.Nursing Diagnoses Imbalanced Nutrition: Less Than Body Requirements

related to inadequate intake of iron Activity Intolerance related to decreased oxygen-

carrying capacity of the blood Ineffective Tissue Perfusion related to decreased

oxygen-carrying capacity of the blood

Nursing Interventions Promoting Iron Intake Assess diet for inclusion of foods rich in iron.

Arrange nutritionist referral as appropriate. Administer iron replacement as ordered.

Technique of parenteral iron administration:◦ Allow small amount of air in syringe and use new 2-inch

needle for injection to avoid tracking medication through subcutaneous tissue and resulting painful induration.

◦ Retract skin over muscle of upper outer quadrant of buttock laterally before inserting needle (Z-track technique) to prevent leakage along track and staining of skin.

This very rare life-threatening anemia is caused by bone marrow hypopalsia or aplasia resulting in pancytopania( insufficient numbers of RBCs, WBCs and platelets). . A variety of diseases, such as leukemia, myelodysplasia or myelofibrosis, can cause anemia by affecting blood production in your bone marrow. The effects of these types of cancer and cancer-like disorders vary from a mild alteration in blood production to a complete life-threatening shutdown of the blood-making process.

Other cancers of the blood or bone marrow — such as multiple myeloma, myeloproliferative disorders and lymphoma — also can cause anemia.

Causes of aplastic anemia include infections, drugs , chemical toxins and autoimmune diseases.

Aplastic anemia.

Many diseases, conditions, and factors can cause aplastic anemia, including:

Toxins, such as pesticides, arsenic, and benzene. Radiation and chemotherapy (treatments for cancer). Medicines, such as chloramphenicol (an antibiotic

rarely used in the United States). Infectious diseases, such as hepatitis, Epstein-Barr

virus, cytomegalovirus, parvovirus B19, and HIV. Autoimmune disorders, such as lupus and

rheumatoid arthritis. Pregnancy. (Aplastic anemia that occurs during

pregnancy often goes away after delivery.)

Causes

Anemia with malaise, pallor and associated symptoms such as palpitations

Thrombocytopenia (low platelet counts), leading to increased risk of hemorrhage, bruising and petechiae

Leukopenia (low white blood cell count), leading to increased risk of infection

Reticulocytopenia (low counts of reticulocytes, that is, immature red blood cells)

Clinical manifestations

CBC and peripheral blood smear show decreased RBC, WBC, platelets (pancytopenia)

Bone marrow aspiration and biopsy: bone marrow is hypocellular or empty with greatly reduced or absent hematopoiesis.

Diagnostic evaluation

1.Remove of causative agent or toxin.2.Allogenic bone marrow transplantation (BMT) –

treatment of choice for patient with severe aplastic anemia. This treatment option provides long-term survival for 75% to 90% of patients, depending on the age of the patient, history of prior blood transfusions, and source of marrow.

3.Immunosuppressive treatment with cyclophosphamide and antirhymocyte globulin or cyclophospamide. This treatment option provides long-term survival for 60% to 70% of patients.

Management

4. Androgens (oxymetholone or testosterone enanthate) may stimulate bone marrow regeneration; significant toxicity encountered. They may be used when other treatments have failed.

5. Supportive treatment includes platelet and RBC transfusions, antibiotics, and antifungals.

Untreated severe aplastic anemia is almost always fatal, generally because of overwhelming infection. Even with treatment, morbidity and mortality caused by infections and bleeding are high.

Late complications, even after successful treatment, include clonal hematologic diseases such as paroxysmal nocturnal hemoglobinuria, myelodysplasia, and acute myelogenous leukemia

Complications

Nursing Assessment Obtain thorough history that includes

medications, past medical history, occupation, hobbies.

Monitor for signs of bleeding and infection.Nursing Diagnoses Risk for Infection related to

granulocytopenia secondary to bone marrow aplasia

Risk for Injury related to bleeding

Nursing Interventions Minimizing Risk of Infection Care for patient in protective environment while

hospitalized in private room with strict hand washing and avoidance of any contaminants (see Patient Education Guidelines, page 944).

Encourage good personal hygiene, including daily shower or bath with mild soap, mouth care, and perirectal care after using the toilet.

Monitor vital signs, including temperature, frequently; notify health care provider of oral temperature of 101° F (38.3° C) or higher.

Minimize invasive procedures or possible trauma to skin or mucous membranes.

Obtain cultures of suspected infected sites or body fluids.

Minimizing Risk of Bleeding Use only soft toothbrush or toothette for mouth care

and electric razor for shaving; keep nails short by filing.

Avoid I.M. injections and other invasive procedures. Prevent constipation with stool softeners as

prescribed. Restrict activity based on platelet count and active

bleeding. Monitor pad count for menstruating patient; avoid use

of vaginal tampons. Control bleeding by applying pressure to site, using

ice packs and prescribed topical hemostatic agents. Administer blood product replacement as ordered;

monitor for allergic reaction, anaphylaxis, and volume overload.

A megaloblast is a large, nucleated erythrocyte with delayed and abnormal nuclear maturation. Pernicious anemia is a type of megaloblastic anemia associated with vitamin B12 deficiency because of lack of intrinsic factor in gastric secretion.

MEGALOBLASTIC ANEMIA: PERNICIOUS

Vitamin B12 is necessary for normal deoxyribonucleic acid synthesis in maturing RBCs.

Pernicious anemia demonstrates familial incidence related to autoimmune gastric mucosal atrophy.

Normal gastric mucosa secretes a substance called intrinsic factor, necessary for absorption of vitamin B12 in ileum. If a defect exists in gastric mucosa, or after gastrectomy or small bowel disease, intrinsic factor may not be secreted and orally ingested B12 not absorbed.

Some drugs interfere with B12 absorption, notably ascorbic acid, cholestyramine, colchicine, neomycin, cimetidine, and hormonal contraceptives.

Primarily a disorder of older people.

Pathophysiology and Etiology

pernicious anemia, disease in which the production of red blood cells (erythrocytes) is impaired as the result of the body’s inability to absorb vitamin B12, which is necessary for red blood cells to mature properly in the bone marrow. Pernicious anemia is one of many types of anemia, a disease marked by a reduction in red blood cells or in the oxygen-carrying substance hemoglobin found in those cells.

Pathophysiology

Clinical Manifestations Of anemia:”pallor, fatigue, dyspnea on exertion,

palpitations. May be angina pectoris and heart failure in the elderly or those predisposed to heart disease.

Of underlying GI dysfunction:”sore mouth, glossitis, anorexia, nausea, vomiting, loss of weight, indigestion, epigastric discomfort, recurring diarrhea or constipation.

Of neuropathy (occurs in high percentage of untreated patients): paresthesia that involves hands and feet, gait disturbance, bladder and bowel dysfunction, psychiatric symptoms caused by cerebral dysfunction.

A diagnosis of PA requires several different tests. It requires a:

complete blood count (CBC) test vitamin B-12 deficiency test IF deficiency test proof of stomach destruction CBC measures the amount of: - hemoglobin - protein bound to oxygen to

carry it throughout the blood - hematocrit - used to measure how much

space red blood cells use within the blood

Diagnostic evaluation

Management Parenteral replacement with

hydroxocobalamin or cyanocobalamin (B12) is necessary by I.M. injection from health care provider, generally every month.

Complications Neurologic: paresthesia, gait disturbances,

bowel and bladder dysfunction, and cerebral dysfunction may be persistent.

Nursing Assessment Assess for pallor, tachycardia, dyspnea on

exertion, exercise intolerance to determine patient's response to anemia.

Assess for paresthesia, gait disturbances, changes in bladder or bowel function, altered thought processes indicating neurologic involvement.

Obtain history of gastric surgery or GI disease.

Nursing Diagnoses Disturbed Thought Processes related to

neurologic dysfunction in absence of vitamin B12

Impaired Sensory Perception (kinesthetic) related to neurologic dysfunction in absence of vitamin B12

Nursing Interventions Improving Thought Processes Administer parenteral vitamin B12 as

prescribed. Provide patient with quiet, supportive

environment; reorient to time, place, and person if needed; give instructions and information in short, simple sentences and reinforce frequently.

.

Minimizing the Effects of Paresthesia Assess extent and severity of paresthesia,

imbalance, or other sensory alterations. Refer patient for physical therapy and

occupational therapy as appropriate. Provide safe, uncluttered environment;

make sure personal belongings are within reach; provide assistance with activities as needed

Patient Education and Health Maintenance

Advise patient that monthly vitamin B12 administration should be continued for life.

Instruct patient to see health care provider approximately every 6 months for hematologic studies and GI evaluation; may develop hematologic or neurologic relapse if therapy inadequate.

Chronic megaloblastic anemia caused by folic acid (folate, B9) deficiency.

Pathophysiology and Etiology Dietary deficiency, malnutrition, marginal diets, excessive

cooking of foods; commonly associated with alcoholism. Impaired absorption of iron in jejunum (eg, with small

bowel disease). Increased requirements (eg, with chronic hemolytic

anemia, exfoliative dermatitis, pregnancy). Impaired utilization from folic acid antagonists

(methotrexate) and other drugs (phenytoin, broad spectrum antibiotics, sulfamethoxazole, alcohol, hormonal contraceptives).

MEGALOBLASTIC ANEMIA: FOLIC ACID DEFICIENCY

Clinical Manifestations Of anemia: fatigue, weakness, pallor,

dizziness, headache, tachycardia. Of folic acid deficiency: sore tongue,

cracked lips.Diagnostic Evaluation Vitamin B12 and folic acid level: folic acid will

be decreased. CBC will show decreased RBC, hemoglobin,

and hematocrit with increased mean corpuscular volume and mean corpuscular hemoglobin concentration.

Management Oral folic acid replacement on daily basis.Complications Folic acid deficiency has been implicated in

the etiology of congenitally acquired neural tube defects.

Nursing Assessment Obtain nutritional history. Monitor level of dyspnea, tachycardia, and

development of chest pain or shortness of breath for worsening of condition.

Nursing Diagnosis Imbalanced Nutrition: Less Than Body

Requirements related to inadequate intake of folic acid

Nursing Interventions Improving Folic Acid Intake Assess diet for inclusion of foods rich in folic

acid: beef liver, peanut butter, red beans, oatmeal, broccoli, asparagus.

Arrange nutritionist referral as appropriate. Assist alcoholic patient to obtain counseling

and additional medical care as needed.

Community and Home Care Considerations Encourage pregnant patient to maintain

prenatal care and to take folic acid supplement. Provide alcoholic patient with information about

treatment programs and Alcoholics Anonymous meetings in the community.

Patient Education and Health Maintenance Teach patient to select balanced diet that

includes green vegetables (asparagus, broccoli, spinach), yeast, liver and other organ meats, some fresh fruits; avoid overcooking vegetables.

Encourage patient to follow up periodically to monitor CBC.

Sickle cell anemia

Introduction Sickle cell anemia is an inherited form of anemia —

a condition in which there aren't enough healthy red blood cells to carry adequate oxygen throughout your body.

Normally, your red blood cells are flexible and round, moving easily through your blood vessels. In sickle cell anemia, the red blood cells become rigid and sticky and are shaped like sickles or crescent moons. These irregularly shaped cells can get stuck in small blood vessels, which can slow or block blood flow and oxygen to parts of the body.

Sickle cell anemia

There's no cure for most people with sickle cell anemia. However, treatments can relieve pain and help prevent further problems associated with sickle cell anemia.

Sickle cell anemia is caused by a mutation in the gene that tells your body to make hemoglobin — the red, iron-rich compound that gives blood its red color. Hemoglobin allows red blood cells to carry oxygen from your lungs to all parts of your body. In sickle cell anemia, the abnormal hemoglobin causes red blood cells to become rigid, sticky and misshapen.

The sickle cell gene is passed from generation to generation in a pattern of inheritance called autosomal recessive inheritance. This means that both the mother and the father must pass on the defective form of the gene for a child to be affected.

If only one parent passes the sickle cell gene to the child, that child will have the sickle cell trait. With one normal hemoglobin gene and one defective form of the gene, people with the sickle cell trait make both normal hemoglobin and sickle cell hemoglobin. Their blood may contain some sickle cells, but they generally don't experience symptoms. However, they are carriers of the disease, which means they can pass the defective gene on to their children.

Causes

The loss of red blood cell elasticity is central to the pathophysiology of sickle-cell disease. Normal red blood cells are quite elastic, which allows the cells to deform to pass through capillaries. In sickle-cell disease, low-oxygen tension promotes red blood cell sickling and repeated episodes of sickling damage the cell membrane and decrease the cell's elasticity. These cells fail to return to normal shape when normal oxygen tension is restored. As a consequence, these rigid blood cells are unable to deform as they pass through narrow capillaries, leading to vessel occlusion and ischaemia.

The actual anaemia of the illness is caused by haemolysis, the destruction of the red cells, because of their shape. Although the bone marrow attempts to compensate by creating new red cells, it does not match the rate of destruction. Healthy red blood cells typically function for 90–120 days, but sickled cells only last 10–20 days.

Pathophysiology

Severe pain Anemia Chest pain and difficulty breathing Strokes Joint pain and arthritis and bone infarctions  Blockage of blood flow in the spleen or liver Severe infections Vision problems Delayed growth

Sign and symptom

The patient with sickle trait usually has a normal hemoglobin level, normal hematocrit, and a normal blood smear. In contrast the patient with the sickle cell anemia has a low hematocrit and sickled cells on the smear. The diagnosis is confirmed by hemoglobin electrophoresis.

Diagnostic evaluation

Treatment for sickle cell anemia is the focus of continued research. However, aside from the equally important aggressive management of symptoms and complications, there are currently few primary treatment modalities for sickle cell disease.

Peripheral blood stem cell transplant Pharmacologic therapy Transfusion therapy Supportive therapy

Medical management

Peripheral blood stem cell transplant It may cure sickle cell anemia. However, this

treatment modality is available to only a small subset of affected patients, because of either the lack of a compatible donor or because severe organ damage( eg, renal, liver, lung) that may be already present in the patient is a contraindication for PBSCT.

Pharmacologic therapy Hydroxyurea(Hydrea) a chemotherapy agent has

been shown to be effective in increasing fetal hemoglobin levels in patients with sickle cell anemia, thereby decreasing the formation of sickle cells.

Transfusion therapy RBC transfusion therapy has been shown to be

highly effective in several situations: in acute exacerbation of anemia, in the prevention of severe complications from anesthesia and surgery, in improving the response to infection.

Supportive therapy supportive care is equally important.

Pain management is a significant issue. The use of medication to relieve is important. Aspirin is very useful in diminishing mild to moderate pain; it also diminishes inflammation and potential thrombosis. NSAIDs are useful for moderate pain or combination with opiod analgesics.

Acute pain related to tissue hypoxia due to agglutination of sickled cell with in blood vessels

Risk for infection

Nursing diagnosis

Managing pain - Guide the rate of pain using pain scale. - Provide analgesic agent. - Apply relaxation techniques, breathing exercise

and distraction to the patient Prevention and managing infection - Monitor patient for sign and symptom of

infection - Provide the prescribed antibiotics - Assess for the sign of dehydration

Nursing interventions:

Promoting coping skills - Establish therapeutic relationship to the patient - Encourage patient on their strength rather than

defecit. - Allow the patient to make dicisions about daily

care and explain the rationale. Minimizing Deficient knowledge - Explain all the potential side effects of the used

drugs - Give the sufficient knowledge about the disease

process to the patient

Promoting home and community based care - Provide knowledge on self care and hygiene - Provide follow up care. - Encourage for communication - Guidelines should be given regarding when to

seek the urgent care.