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Chapter 33 Anemia
Chapter 33 Anemia
Assessment and Diagnostic Findings smooth, red tongue; brittle and ridged nails; and
angular cheilosis
Hemoglobin
Hematocrit Assessment or Diagnostic findings
reticulocyte count
bone marrow aspiration(definitive method of
mean corpuscular volume (MCV)
establishing the diagnosis)
red cell distribution width
low serum ferritin levels
total iron-binding capacity [TIBC], percent saturation,
low serum iron levels
and ferritin
elevated TIBC
Vitamin B12 and folate
hemoglobin level falls
Complications MCV decreases
Hematocrit and RBC levels low
heart failure Soluble transferring receptor (can be used in
paresthesia differentiating between infection anemia or
Delirium deficiency anemia)
acquired or, rarely, congenital, but mostly deficiencies of vitamin B12 or folic acid, vitamins are
idiopathic essential for normal DNA synthesis
RISK FACTORS: Viral infections, pregnancy erythrocytes that are produced are abnormally large
and called megaloblastic red cell
Chemical or radiation damage
bone marrow analysis reveals hyperplasia
benzene and benzene derivatives
pancytopenia can develop since abnormal erythroid
inorganic arsenic, glycol ethers, plutonium, and and myeloid cells are destroyed within the marrow
radon and mature cells that leave the marrow are actually
fewer in number
Clinical Manifestations
neutrophils are hypersegmented
fatigue erythrocytes are abnormally shaped and vary in
pallor shape (poikilocytosis)
platelets may be abnormally large
dyspnea
skin develops a lemon yellow color resulting from
Typical signs of infection simultaneous pallor and mild jaundice
Purpura Pathophysiology
Folic Acid Deficiency Premature graying of the hair
when the dietary intake of folate is deficient n 2. pay particular attention to ambulation and should
become depleted within month assess the patient’s gait and stability
Folate deficiency occurs in people who rarely eat 3. Physical and occupational therapy referrals may be
uncooked vegetables.
needed
Alcoholism
4. If sensation is altered, the patient needs to be
Folic acid requirements are also increased in
patients with liver disease, chronic hemolytic
instructed to avoid excessive heat and cold
anemias 5. advise the patient to eat small amounts of bland,
women who are pregnant soft foods frequently
malabsorptive diseases HEMOLYTIC ANEMIA
Vitamin B12 Deficiency erythrocytes have a shortened lifespan – which
inadequate dietary intake leads to hypoxia
Faulty absorption from the GI stimulates an increase in erythropoietin
Crohn’s disease
release from the kidney
ileal resection, bariatric surgery, or gastrectomy
histamine blockers, antacids, or proton pump Erythropoietin then stimulates the bone
inhibitors marrow to compensate by producing new
use metformin (Glucophage) in managing diabetes erythrocytes (called reticulocytes)
absence of intrinsic factor (pernicious anemia) Note: laboratory features: the reticulocyte count is
Clinical Manifestations elevated, the fraction of indirect (unconjugated)
folic acid and vitamin B12 deficiencies are similar bilirubin is increased, and the supply of haptoglobin (a
neurologic manifestations is present in vitamin B12 binding protein for free hemoglobin) is depleted as
deficiency more hemoglobin is released
weakness
listlessness
Sickle Cell Disease
Fatigue
results from inheritance of the sickle hemoglobin
Pernicious anemia develop:
(HbS) gene
smooth, sore, red tongue and mild diarrhea,
HbS acquires a crystal-like formation when exposed
extremely pale, may become confused
to low oxygen tension. The oxygen level in venous
confuse
blood can be low enough to cause this change
paresthesia
erythrocyte containing HbS loses its round, pliable,
Assessment and diagnostic findings
biconcave disc shape and becomes dehydrated,
Schilling test
rigid, and sickle shaped
vitamin B12 assay
they adhere to each other, blood flow to a region or
methylmalonic acid and homocysteine levels
an organ may be reduced
intrinsic factor antibody test (positive test Cold can aggravate the sickling process due to
indicates the presence of antibodies, preventing vasoconstriction
its absorption) Less severe forms include sickle cell hemoglobin C
Medical Management (SC) disease, sickle cell hemoglobin D (SD) disease,
Folate deficiency and sickle cell beta-thalassemia
1. diet and administering 1 mg of folic acid daily
2. IM (with malabsorption problems) Clinical manifestations
Vitamin B12 Anemia is always present; usually, hemoglobin
1. oral supplements with vitamins or fortified soy values range between 5 and 11 g/dL
milk Jaundice
2. IM (malabsorption problems or absence of Tachycardia
Cardiac murmurs
intrinsic factor)
Cardiomegaly
Note: To prevent recurrence of pernicious anemia,
Dysrhythmias and heart failure
vitamin B12 therapy must be continued for life
slower circulation, such as the spleen, lungs, and
central nervous system
Nursing Management hypoxic damage or ischemic necrosis
1. Inspection of the skin, mucous membranes, and pneumonia and osteomyelitis
tongue. Complications of sickle cell disease include
infection, stroke, kidney injury, impotence,
Patient with pernicious anemia
heart failure, and pulmonary hypertension
Vitiligo
Sickle Cell Crisis
Mild jaundice
acute vaso-occlusive crisis- which results from white blood cell (WBC) and platelet counts are often
entrapment of erythrocytes and leukocytes in the higher
microcirculation, causing tissue hypoxia, Diagnosis is confirmed by hemoglobin
inflammation, and necrosis electrophoresis.
Aplastic crisis results from infection with the human
parvovirus. Prognosis
Sequestration crisis results when other organs pool Death is most commonly due to heart disease (32%),
the sickled cells. lung disease (28%), kidney disease (16%), infection
Acute chest syndrome (14%), and neurologic system disease (12%); less
commonly, death results from GI tract or liver
fever, respiratory distress (tachypnea, cough, disease (9%) and cancer (<1%)
wheezing)
infiltrates seen on the chest x-ray Medical Management
develop pallor
jaundice
hemoglobinuria (i.e., hemoglobin in the urine
Medical Management
Nursing Management
Polycythemia