Anemia

Norfidah Binti Mohamad

 Definition
□ Abnormally low number of circulating RBCs,
hemoglobin concentration or both

□ Usual cause of low number

1.Blood loss
2.Inadequate production
3.Increased RBC destruction

□ Depending on severity, anemia affects all

major organ systems
 Pathophysiology
□ Altered hemoglobin synthesis such as
iron deficiency

□ Altered DNA synthesis such as Vitamin

B12 or folic acid deficiency

□ Bone marrow failure such as aplastic

anemia (stem cell dysfunction)
□ Increased RBC loss or destruction
1. Acute or chronic blood loss

2. Increased hemolysis such as sickle cell

anemia, infection
 Manifestations
a. Pallor of skin, mucous membranes,
conjunctiva, nail beds

b. Increased heart and respiratory rates as

body compensates

c. Angina, fatigue, dyspnea on exertion,

night cramps

d. Increased erythropoetin activity may

cause bone pain
e. Cerebral hypoxia: headache, dizziness,
dim vision

f. Heart failure with severe anemia

g. Signs of circulatory shock with rapid blood

loss

h. Systolic heart murmur with chronic blood

loss due to decreased viscosity of blood
 Categories of Anemia
a. Blood Loss Anemia
□ Acute blood loss
□Circulating blood volume decreases
and fluid shifts from interstitial space
into vascular bed

□Circulating RBCs are of normal size

and shape; hemoglobin and
hematocrit are reduced
□ Chronic blood loss

□ Depletion of iron stores as RBC production

attempts to maintain supply

□ RBCs are microcytic (small) and

hypochromic (pale)
b. Nutritional anemias

□Affect RBC formation or hemoglobin

synthesis

□Causes include inadequate diet,

malabsorption, increased nutrition
need
 Common types

a. Iron deficiency anemia

b. Vitamin B12 anemia

c. Folic acid deficiency anemia

 Iron deficiency anemia
1.Most common type of anemia

2.With inadequate supply of iron; body

cannot synthesize hemoglobin

3.Due to inadequate dietary iron intake,

malabsorption, increased iron needs
as with pregnancy and lactation
4.Due to chronic bleeding
□ Menstrual blood loss

□ Chronic occult (hidden) blood loss in

older adults: slowly bleeding ulcers, GI
inflammation, hemorrhoids, cancer
 Additional manifestations
a. Brittle, spoon-
shaped nails
b. Cheilosis (cracks
at corners of
mouth)
c. Pica (craving for
unusual
substances such
as clay, starch)
 Vitamin B12 deficiency anemia
1. Vitamin B12 necessary for DNA synthesis

2. Food sources of Vitamin B12 occur in foods

derived from animals

3. RBCs
□ Macrocytic (large) misshapened (oval) with
thin membranes
□ Fragile, have shortened life span
□ Do not carry adequate oxygen
4. Pernicious anemia
□ Failure to absorb dietary Vitamin B12 due to lack
of intrinsic factor which is secreted by gastric
mucosa

□ Intrinsic factor binds with Vitamin B12 and is

absorbed in ileum

□ Occurs in clients who have stomach or ileal

resections, loss of pancreatic secretions, chronic
gastritis

□ Strict vegetarians
 Manifestations
gradual onset

a. Pallor, slight jaundice

b. Sore beefy red tongue and diarrhea

c. Impaired neurologic functioning

□ Paresthesias (numbness and tingling) in extremities

□ Difficulty with balance

 Treatment
□ Increase intake of
meats, eggs, dairy
products;
supplements for
vegetarians

□ Parenteral Vitamin
B12 replacement for
malabsorption
disorders or lack of
intrinsic factor
 Folic acid deficiency anemia
□ Folic acid is required for DNA synthesis and
normal maturation of RBCs

□ Characterized by fragile megaloblastic cells

□ Causes
□ Inadequate intake (Chronically malnourished
Older adults, Alcoholics)

□ Increased need (Pregnant women at greatest

risk)
 Manifestations (develop
gradually)
□ Pallor, progressive weakness and
fatigue, shortness of breath,
palpitations

□ Glossitis, cheilosis, diarrhea

□ No neurological symptoms, but may

co-exist with Vitamin B12 deficiency
 Treatment
□ Diet high in green leafy vegetables,
fruits, cereals, meats

□ Supplementation with folic acid

 c. Hemolytic anemias
1. Characterized by premature lysis of RBCs within
circulation

2. Increased hematopoetic activity of bone marrow

causing increased number of circulating
reticulocytes

3. Characterized by normocytic and normochromic

RBCs

4. Causes
□ Intrinsic (within RBC)
□ Extrinsic (outside RBC): including drugs, bacteria
infections and toxins , trauma
a. Sickle cell anemia
□ Hereditary, chronic hemolytic anemia

□ Characterized by episodes of sickling in

which RBC become abnormally crescent
shaped

□ Autosomal recessive genetic defect

causing abnormal form of hemoglobin
(HbS) within RBC
 Pathophysiology
□ HbS becomes deoxygenated under hypoxemia
and RBC deform into crescent or sickle shape

□ Sickled cells clump together and obstruct capillary

blood flow leading to ischemia and possible
infarction of surrounding tissue

□ Under normal oxygen tension, sickled RBCs regain

normal shape and unsickle

□ Repeated episodes weakens RBC and they are

hemolyzed; RBCs have shortened life span
 Manifestations
Occur with episodic sickling episodes known
as sickle cell crises, triggered by
1. Hypoxia
2. Low environmental or body temperature
3. Excessive exercise
4. Anesthesia
5. Dehydration
6. Infection
□ General manifestations: pallor, fatigue, jaundice,
irritability

□ With vaso-occlusive crises (4 – 6 days): Painful

swelling hands and feet, large joints, priapism
(persistent, painful erection), abdominal pain, stroke

□ Aplastic anemia: due to shortened life span or RBC

and compromised erythropoesis

□ Sequestration crises: pooling of large amounts of

blood in liver and spleen occurring more in children
 Treatment

□ Largely supportive: rest, oxygen, pain

management, adequate hydration
□ Treat precipitating factors
□ Folic acid supplementation
□ Blood transfusions
□ Genetic counseling
b. Thalassemia

□ Inherited disorders characterized by

abnormal production of hemoglobin. They
result in low hemoglobin production, and
excessive destruction of red blood cells.

□ hemoglobin synthesis in which alpha or beta

chains of hemoglobin are missing or
defective
 Thalassemia
□ Defects in the genes producing
hemoglobin- Two major forms:

□ Thalassemia minor is mild and those

suffering from this condition go on to live a
full life. Treatment is often unnecessary.

□ Thalassemia major can be serious, but it is

very rare. Also called Cooley's anemia.
Causes
□ An imbalance in the alpha or beta globin
necessary for the production of hemoglobin is
caused by the inheritance of abnormal genes.

□ Abnormal genes must be inherited from both

parents to develop the disease. If one gene is
inherited, the person will be a carrier of the disease,
but will not have symptoms.
 Risk Factors
□ Geographic location of ancestors, including
□ Alpha thalassemias - Southeast Asia, Malaysia,
and Southern China
□ Beta thalassemias - areas surrounding the
Mediterranean Sea, Africa, and Southeast
China

□ A family history of the disorder

□ Symptoms
□ Anemia, jaundice,
enlarged spleen, fatigue,
reduced appetite, fragile
bones, growth problems,
increased susceptibility to
infection, palor, heart
failure, SOB, liver problems
□ Treatment
□ Blood Transfusions
□ Bone Marrow Transplant

□ Prevention
□ Blood tests and family genetic studies can show
whether an individual has thalassemia or is a
carrier.
□ A genetic counselor can detail the family
background, discuss risks, and available testing.
c. Glucose -6-Phosphate Dehydrogenase
(G6PD) Anemia
□ Red blood cells carry oxygen in the body and
G6PD protects these cells from natural oxygen
chemicals (oxidative substances) that may
build up.

□ G-6-PD deficiency is a hereditary, sex-linked

enzyme defect that results in the breakdown
of red blood cells when the person is exposed
to the stress of infection or certain drugs,
fever.
□ Risk factors- being black, male (defective
gene is located on X chromosome, a family
history of G6PD deficiency.

Drugs that can bring on this reaction include:

□ antimalarial agents
□ antibiotic
□ aspirin
□ nonsteroidal anti-inflammatory drugs
(NSAIDs)
□ Body responds in 7 – 12 days and
manifestations occur several days post
stressor exposure: pallor, jaundice,
hemoglobinuria, elevated reticulocyte
count
 d. Aplastic anemia
Bone marrow failure
□ Resulting in pancytopenia (low levels of RBC, WBC,
platelets)
□ Marrow replaced with fat

Causes are idiopathic

a. Viral infections
b. Stem cell damage from radiation
c. Exposure to chemicals
d. Certain antibiotics (chloramphenicol)
e. Chemotherapeutic drugs
 Manifestations
vary with onset and severity of
pancytopenia

□ Pallor, fatigue, headache, exertional

dyspnea, tachycardia, heart failure

□ Bleeding due to low platelet levels

□ Fever, increased infection risk due to low

WBC
 Treatment

□ Removal of causative agent

□ Blood transfusions

□ Bone marrow transplant

 Diagnostic Tests
□ CBC:
□ blood cell count, hemoglobin,
hematocrit, RBC indices

□ Iron levels and total iron-binding

capacity (TIBC):
□ deficits occur with iron deficiency anemia
□ Serum ferritin
□ Low with depletion of total iron reserves
□ Ferritin is iron-storage protein produced by liver,
spleen, bone marrow

□ Sickle cell test:

□ screening test to evaluate hemolytic anemia,
detect HbS

□ Hemoglobin electrophoresis:
□ separation of normal from abnormal forms of
hemoglobin
□ Schilling Test
□ Measures vitamin B12 absorption before
and after intrinsic factor administration

□ Includes 24-hour urine collection

□ Used to differentiate between pernicious

anemia and intestinal malabsorption
□ Bone marrow examination:
□ diagnosis of aplastic anemia

□ Quantitative assay of G6PD:

□ diagnosis of G6PD deficiency
 Collaborative Care
□ Ensure adequate tissue oxygenation

□ Treatment determined by underlying

cause
Treatment
 Pharmacology
Iron deficiency anemia

□ is treated with iron (ferrous sulphate) supplements

(t.d.s.).

□ If nausea, stomach cramps, diarrhea or

constipation occur- medication may be taken with
a little bit of food.

□ Continue- 3 to 6 months in order for the body to

fully replenish its iron supply.

□ Will be corrected within a few weeks.

vitamin B-12 deficiency
□ is treated by a life-long course of intramuscular
injections of B-12.

Folic acid deficiency anemia

□ corrected by taking folic acid supplements once a
day.
Thalassamia
□ eliminating any existing infections and avoiding
medications that suppress the body's immune
system. These medications may attack red blood
cells. may require regular blood transfusions.

Sickle cell anemia

□ given oxygen, oral and intravenous fluids and
pain-killing drugs to reduce pain and prevent
complications, antibiotics, blood transfusions-
anemia becomes severe, bone marrow transplant.
□ aplastic anemias
□ Steroids,
□ removal of the spleen (failure to respond to
steroids) which can become enlarged with
defective red blood cells.
□ blood transfusions
□ medications to fight infections.

□ If bone marrow has failed because of leukemia-

intensive chemotherapy may be required.
□ Bone marrow transplantation may be
contemplated if a suitable donor exists.
 Dietary
□ Red meats
□ Organ meats
□ Milk
□ Eggs
□ Green leafy vegetables
 Nursing diagnoses
□ Activity intolerance related to weakness,
fatigue and general malaise

□ Altered nutrition, less than body

requirements, related to inadequate intake
of essential nutrients

□ Altered tissue perfusion related to

inadequate blood volume or hematocrit

□ Noncompliance with prescribed therapy

Nursing interventions
Managing fatigue
□ Assisting in activities- according to energy level
□ Establish balance between activity and rest

Maintaining adequate nutrition

□ Encourage balanced diet
□ Avoid alcohol
□ Dietary teaching- cultural aspect
□ Supplements
Maintaining adequate perfusion
□ O2 supply
□ Blood transfusion, IV fluids
□ Vital signs, pulse oxymetry
□ Assess for pallor, cynosis

Complying with prescribed therapy

□ Understand the purpose of medication
□ “6 R”
Managing potential complication
□ Limits activity- cause dyspnea, palpitation,
dizziness, or tachycardia
□ Vital signs
□ Oriented to time, place and situations
□ Ambulates safely
□ Remains free from injury
□ Serial CBC
Thank you