Anemia - created from Mind Map

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Deficiency in the = 1. number of erythrocytes (RBCs), 2. volume of packed RBCs (hematocrit), 3. quantity of hemoglobin

CAUSES: -blood loss -impaired production of erythrocytes -increased destruction of erythrocytes

NOT a disease but a manifestation of a pathologic process. It is ID and classified by lab dianosis

MILD ANEMIA: 10-14 g/dl Hb. May not have symptoms -possible symptoms are palpitations, dyspnea, diaphoresis (perspiring profusely)

MODERATE: 6-10 g/dl Hb Increased cardiopulmonary symptoms and experienced at rest or during activity

SEVERE: Hb less than 6 g/dl. causes pallor, jaundice, tachycardia, tachypnea, headache, anorexia, bone pain, sensitivity to cold, lethargy

IRON DEFICIENCY ANEMIA

Results in MICROCYTIC (small RBC), hypochromic cells (small, pale color)

CAUSES: inadeq dietary intake, malabsorption, blood loss, hemolysis, gastrectomy

WHO ARE AT RISK?: premenopausal women, pregnant wmn, low socioeconomic bg, older adults

SOME DIAGNOSTIC TESTS: Hb and Hct levels, RBC count, reticulocyte count, serum iron, serum ferritin, serum transferrin, stool guaiac test (test for blood in stool), endoscopy, colonoscopy

SYMPOMS

MANAGEMENT

NURSING TEACHING

Dyspnea, fatigue/exhaustion, trachycardia

iron replacement

Ferrous sulfate (feosal) Fe SO4 over 2-3 months. CONTRAINDICATED: with normal iron balance (toxicity) and inflammatory bowel diease

DRUG-DRUG Interaction- tetracycline, fluroquinolone antibiotics, levothyroxine

Take on an empty stomach or with fluids containing vit c (enhances absorption). MILK, antacids, coffee, tea all IMPAIR absorption. Take the pill form (preferred) bc liquid form will stain teeth, IM route is painful and must be Z-track, IV route needs test dose and can casue anaphylaxis

GI SIDE EFFECTS:

gastritis, constipation, change in stool color to blackish-green

THALASSEMIA:

Common in ethnic group near the Mediterranean sea and equatorial regions of Asian and Africa. HEMOLYSIS also occurs. There's a probelm w/ globulin protein that causes abnormal hemoglobin synthesis

MICROCYTIC & HYPOCHROMIC

Causes mild jaundice due to hemolysis of RBC -> byproduct of billirubin ->yellowing

Splenomegally- enlarged spleen

an autosomal recessive genetic disorder of inadeq production of normal Hb that causes moderate anemia.

MEGALOBLASTIC

Def: grp of disorders caused by impaired DNA synthesis (stuck in G2 growth phase, so cell gets big) and is characterized by the presence of large RBCs

Macrocytic and normachromic

COBALAMIN DEFICIENCY (Vit b12)

FOLIC ACID Deficiency

Can cause pernicious anemia: which is caused by an absence of IF (intrinsic factor). The gastric mucosa is not secreting IF because of either gastric mucosal atrophy or autoimmune destruction of parietal cells. In the autoimmune process anti- bodies are directed against the gastric parietal cells and/or IF itself. Because parietal cells also secrete hydrochloric acid (HCl), 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.

Intrinsic factor is required for vit b12 absorption in the stomach

Other caused: gastrectomy, chronic alcoholism, dietary deficiency (vegetarians), long term use of H2-histamine receptor blockers, idiopathoc

CLINICAL MANIFESTATIONS:

NEUROMUSCULAR MANFESTATIONS

DIAGNOSTIC STUDIES

MANAGEMENT

For the development and maintenance of RBCs, nerve cells and normal myelination of nerve cells, the production of neurotransmitters, production of DNA/RNA

SYMPTOMS: numbness and tingling and confusion

General Symptoms of anemia - sore tongue and red tongue - anorexia - vomiting - abdominal pain

weakness - paresthesias of the feet and hands - -ataxia (imbalance) - -muscle weakness - impaired though process

RBCs appear large, abnormal shapes, lowered serum folate levels, use schilling test (to determine whether the body absorbs vitamin B12 normally)

IM daily for 1-2 wks then monthly. -Nasal spray (Nacobal) maintenance after injection or preventive -quickly reverses most symptoms. - oral route ineffective (not absorbed in stomach) SIDE EFFECTS: hypokalemia

Folic acid is required for DNA synthesis leading to RBC formation and maturation. But vit b12 is needed to successfully incorprate circulating folate into develeoping RBC

MANAGEMENT

CAUSES

The absence of neurologic problems is an important diagnostic finding and differentiates folic acid deficiency from cobalamin deficiency.

Folic acid deficiency is treated by replacement therapy. The usual dosage is 1 mg/day by mouth. In malabsorption states or with chronic alcoholism, up to 5 mg/day may be required. Encourage the patient to eat foods containing large amounts of folic acid

dietary deficiency, malabsorption syndrome (celiac and Crohn's, drugs interfering w/ absorption (eg methotrexate & antiseizure drugs), alcohol abuse and anorexia and lost during hemodialysis

oral supplement folic acid for 4 months

APLASTIC

patient has peripheral blood pancytopenia (decrease of all blood cell types—RBCs, white blood cells [WBCs], and platelets) and hypocellular bone marrow.

not very common only 4 in 1 million

TYPES

Clinically the patient may have symptoms caused by suppression of any or all bone marrow elements. General manifestations of anemia: fatigue and dyspnea, as well as cardiovascular and cerebral responses

Diagnostic Studies

1. Congenital (Chromosomal Alterations) 2. Acquired

confirmed by laboratory studies. hemoglobin, WBC, and platelet are low. normocytic, normochromic (normal size and color) anemia

HEMOLYTIC

Destruction of RBCs at a rate that exceeds production. Third major cause of anemia

TYPES:

Manifestations

INTRINSIC

EXTRINSIC

usually hereditary, result from defects in the RBCs themselves

RBCs are normal but damage is caused by external factors

Jaundice is likely because the increased destruction of RBCs causes an elevation in bilirubin levels. The spleen and liver may enlarge because of their hyper- activity, which is related to macrophage phagocytosis of the defective erythrocytes.

When RBCs are hemolyzed (intravascular & extravascular), the hemoglobin molecule is released and filtered by the kidneys. The accumulation of hemoglobin molecules can obstruct the renal tubules and lead to acute tubular necrosi

SICKLE CELL ANEMIA

a group of inherited, autosomal recessive disorders characterized by an abnormal form of hemoglobin in the RBC. Sickled RBCs become rigid and take on an elongated, crescent shape. Sickled cells cannot easily pass through capillaries or other small vessels and can cause vascular occlusion, leading to acute or chronic tissue injury.

COMPLICATIONS

DIAGNOSTIC STUDIES

Goal of treatment: alleviate symptoms of disease complications, give O2, pain management, folic acid daily supplements. For acute chest syndrome, give antibiotics, O2 and fluids

gradual involvement of all body systems, usually fatal by middle age from renal and pulmonary failure, prone to infection and pneumonia is the common

peripheral blood, sickling test, electrophoresis of hemoglobin, DNA testing, skeletal xray, MRI

Anemia