Anemia definition, etiology, types, medical management, nursing management

1. ANEMIA
Presented by: Ms. Avelin D

2. Anemia, per se, is not a specific disease state
but a sign of an underlying disorder. It is by
far the most common hematologic
condition.
Anemia, a condition in which the
hemoglobin concentration is lower than
normal, reflects the presence of fewer than
normal RBCs within the circulation.
As a result, the amount of oxygen delivered
to body tissues is also diminished
Introduction

3. A pathological deficiency in the oxygen-
carrying component of the blood, measured
in unit volume concentrations of
hemoglobin, red blood cell volume, or red
blood cell number.
Definition

4. Globally, anemia affects 1.62 billion people,
which corresponds to 24.8% of the population.
The highest prevalence is in preschool-age
children, and the lowest prevalence is in men.
However, the population group with the
greatest number of individuals affected is
non-pregnant women 468.4 million. - WHO
Incidence

5. Blood is a constantly
circulating fluid providing
the body with nutrition,
oxygen, and waste removal.
Blood is mostly liquid, with
numerous cells and proteins
suspended in it, making
blood "thicker" than pure
water. The average person
has about 5 liters (more than
a gallon) of blood.
Anatomy and physiology Of Blood

6. A liquid called plasma makes up
about half of the content of blood.
Plasma contains proteins that help
blood to clot, transport substances
through the blood, and perform
other functions. Blood plasma also
contains glucose and other
dissolved nutrients.
About half of blood volume is
composed of blood cells:
• Red blood cells, which carry
oxygen to the tissues
• White blood cells, which fight
infections
• Platelets, smaller cells that help
blood to clot

10. There may be three kinds of anemia
 Loss of RBCs—occurs with bleeding, potentially from any
major source, such as the gastrointestinal tract, the uterus,
the nose, or a wound
 Decreased production of RBCs (hypoproliferative)—can be
caused by a deficiency in cofactors (including folic acid,
vitamin B12, and iron) required for erythropoiesis; RBC
production may also be reduced if the bone marrow is
suppressed (e.g., by tumor, medications, toxins) or is
inadequately stimulated because of a lack of erythropoietin
(as occurs in chronic renal disease).
 Increased destruction of RBCs (hemolytic)—may occur
because of an overactive RES reticuloendothelial system
(including hypersplenism) or because the bone marrow
produces abnormal RBCs that are then destroyed by the RES
(e.g., sickle cell anemia).

11. Classification based on morphology

12. It is characterized by the presence in the
circulating blood of red cells that are smaller
than normal and poorly filled with
hemoglobin, fall into two main categories. The
first is a result of a deficiency of iron, and the
second is a result of impaired production of
hemoglobin; in either case there is an
inadequate amount of the final product in the
red cell.
Hypochromic microcytic anemias

14. In this the average size of circulating red
cells is larger than normal, results from
impaired production of red cells. A
macrocytic class of anemia is an anemia
(defined as blood with an insufficient
concentration of hemoglobin) in which the
red blood cells (erythrocytes) are larger than
their normal volume.—e.g., when vitamin
B12 or folic acid is lacking.
Macrocytic anemia

16. In this the red blood cells (erythrocytes) are paler
than normal. (Hypo- refers to less, and chromic
means color.) A normal red blood cell will have
an area of pallor in the center of it; it is biconcave
disk shaped. In hypochromic cells, this area of
central pallor is increased. This decrease in
redness is due to a disproportionate reduction of
red cell hemoglobin (the pigment that imparts
the red color) in proportion to the volume of the
cell.
Hypochromic anemia

19. Basically, only three causes of anemia exist: blood
loss, increased destruction of RBCs (hemolysis),
and decreased production of RBCs. Each of these
causes includes a number of disorders that require
specific and appropriate therapy.
Etiology

20. Iron deficiency anemia typically results when the intake of dietary
iron is inadequate for hemoglobin synthesis. The body can store
about one fourth to one third of its iron, and it is not until those
stores are depleted that iron deficiency anemia actually begins to
develop. More than 500 million people are affected, more
commonly in underdeveloped countries, where inadequate iron
stores can result from inadequate intake of iron (seen with
vegetarian diets) or from blood loss (e.g., from intestinal
hookworm)
Hypoprofliferative anemia

21.  The most common cause of iron deficiency in men and
postmenopausal women is bleeding (from ulcers, gastritis,
inflammatory bowel disease, or gastrointestinal tumors).
 The most common cause of iron deficiency anemia in
premenopausal women is menorrhagia (excessive menstrual
bleeding) and pregnancy with inadequate iron supplementation.
 Patients with chronic alcoholism often have chronic blood loss
from the gastrointestinal tract, which causes iron loss and
eventual anemia.
 Other causes include iron malabsorption, as is seen after
gastrectomy or with celiac disease.
Etiology

22.  Patients with iron deficiency primarily have the
symptoms of anemia.
 Smooth, sore tongue,
 Brittle and ridged nails, and
 Angular cheilosis (an ulceration of the corner of
the mouth).
 These signs subside after iron-replacement
therapy.
Clinical manifestations

23.  Bone marrow biopsy
 Hemogram: After the iron stores are depleted (as
reflected by low serum ferritin levels), the
hemoglobin level falls. The diminished iron stores
cause small RBCs. Therefore, as the anemia
progresses, the MCV, which measures the size of the
RBC, also decreases. Hematocrit and RBC levels are
also low in relation to the hemoglobin level.
 Serum iron level
Diagnostic tests

24. Anemia may be a sign of a curable gastrointestinal cancer or of
uterine fibroid tumors. Stool specimens should be tested for occult
blood.
People 50 years of age or older should have a colonoscopy,
endoscopy, or other examination of the gastrointestinal tract to
detect ulcerations, gastritis, polyps, or cancer.
Several oral iron preparations—ferrous sulfate, ferrous gluconate,
and ferrous fumarate—are available for treating iron deficiency
anemia.
In some cases, oral iron is poorly absorbed or poorly tolerated, or
iron supplementation is needed in large amounts. In these
situations, intravenous or intramuscular administration of iron
dextran may be needed.
Several doses are required to replenish the patient’s iron stores.
Medical Management

25. The degree of anemia in patients
with end-stage renal disease varies
greatly, but in general patients do
not become significantly anemic
until the serum creatinine level
exceeds 3 mg/100 mL.
This anemia is caused by both a
mild shortening of RBC life span
and a deficiency of erythropoietin
(necessary for erythropoiesis). As
renal function decreases,
erythropoietin, which is produced
by the kidney, also decreases.
Anemias in renal disease

26. Patients undergoing long-term
hemodialysis lose blood into the
dialyzer and therefore may
become iron deficient.
Folic acid deficiency develops
because this vitamin passes into
the dialysate.
Erythropoietin, in combination
with oral iron supplements, can
raise and maintain hematocrit
levels to between 33% and 38%.
This treatment has been
successful with dialysis patients.

27. Aplastic anemia is a rather rare
disease caused by a decrease in or
damage to marrow stem cells,
damage to the microenvironment
within the marrow, and replacement
of the marrow with fat. It results in
bone marrow aplasia (markedly
reduced hematopoiesis).
Therefore, in addition to severe
anemia, significant neutropenia and
thrombocytopenia (a deficiency of
platelets) are also seen.
Aplastic anemia

28. Aplastic anemia can be congenital or acquired, but most cases are
idiopathic (i.E., Without apparent cause).
 Infections and pregnancy
 Certain medications, chemicals, or radiation damage.
 Benzene and benzene derivatives (e.G., Airplane glue).
 Certain toxic materials, such as inorganic arsenic and several
pesticides (including ddt, have also been implicated as potential
causes.
 Various medications
Etiology

29.  Bone marrow transplantation
 Peripheral stem cell transplantation
 Immunosuppressive therapy
 Corticosteroids
Medical management

30. Caused by deficiencies of vitamin B12 or folic acid, identical
bone marrow and peripheral blood changes occur, because both
vitamins are essential for normal DNA synthesis.
The RBCs that are produced are abnormally large and are called
megaloblastic RBCs. Other cells derived from the myeloid stem
cell (nonlymphoid WBCs, platelets) are also abnormal.
Megaloblastic anemias

31. Folic acid, a vitamin that is necessary
for normal RBC production, is stored
as compounds referred to as folates.
The folate stores in the body are
much smaller than those of vitamin
B12, and they are quickly depleted
when the dietary intake of folate is
deficient (within 4 months).
Folic acid deficiency

32.  Folate is found in green vegetables and liver.
 Folate deficiency occurs in people who rarely eat uncooked
vegetables.
 Alcohol increases folic acid requirements, and, at the same
time, patients with alcoholism usually have a diet that is
deficient in the vitamin.
 Folic acid requirements are also increased in patients with
chronic hemolytic anemias and in women who are pregnant,
because the need for RBC production is increased in these
conditions.
 Some patients with malabsorptive diseases of the small bowel,
such as sprue, may not absorb folic acid normally
Etiology

33.  Inadequate dietary intake is rare but can develop in strict
vegetarians who consume no meat or dairy products.
 Faulty absorption from the gastrointestinal tract is more
common. This occurs in conditions such as Crohn’s
disease, or after gastrectomy.
 Another cause is the absence of intrinsic factor, as in
pernicious anemia. Intrinsic factor is normally secreted
by cells within the gastric mucosa; normally it binds with
the dietary vitamin B12 and travels with it to the ileum,
where the vitamin is absorbed. Without intrinsic factor,
orally consumed vitamin B12 cannot be absorbed, and
RBC production is eventually diminished.
Vitamin B12
deficiency

34.  Weakness
 Listlessness
 Fatigue
 The hematologic effects of deficiency are accompanied
by effects on other organ systems, particularly the
gastrointestinal tract and nervous system.
Clinical manifestations of megaloblastic anemia

35.  Smooth, sore, red tongue and mild
diarrhea.
 Confusion
 Paresthesia in the extremities
(particularly numbness and tingling in
the feet and lower legs).
 Difficulty maintaining their balance
because of damage to the spinal cord,
and they also lose position sense

36.  Increasing the amount of folic acid in the diet and
administering 1 mg of folic acid daily Vitamin B12
deficiency is treated by vitamin B 12 replacement.
 Vegetarians can prevent or treat deficiency with oral
supplements through vitamins or fortified soy milk.
 Monthly intramuscular injections of vitamin B 12, usually
at a dose of 1000 μg
Medical mangement

37. In hemolytic anemias, the RBCs have a shortened life span; thus,
the number of RBCs in circulation is reduced. Fewer RBCs result
in decrease in available oxygen and causes hypoxia, which in turn
stimulates an increase in erythropoietin release from the kidney.
The erythropoietin stimulates the bone marrow to compensate by
producing new RBCs and releasing some of them into the
circulation somewhat prematurely as reticulocytes.
If the RBC destruction persists, the hemoglobin is broken down
excessively; about 80% of the heme is converted to bilirubin,
conjugated in the liver, and excreted in the bile.
Hemolytic anemias

38.  Sickle cell anemia
 Thalassemia
 Hereditary spherocytosis
 Immune hemolytic anemia
Types

39. Sickle cell anemia is a
severe hemolytic anemia
that results from
inheritance of the sickle
hemoglobin gene. This
gene causes the
hemoglobin molecule to be
defective.
Sickle cell anemia

41. The sickle hemoglobin (HbS) acquires a crystal-like formation
when exposed to low oxygen tension.
The oxygen level in venous blood can be low enough to cause this
change; consequently, the RBC containing (HbS) loses its round,
very pliable, biconcave disk shape and becomes deformed, rigid,
and sickle-shaped.
These long, rigid RBCs can adhere to the endothelium of small
vessels; when they pile up against each other, blood flow to a
region or an organ may be reduced.
If ischemia or infarction results, the patient may have pain,
swelling, and fever. The sickling process takes time; if the RBC is
again exposed to adequate amounts of oxygen (eg, when it travels
through the pulmonary circulation) before the membrane becomes
too rigid, it can revert to a normal shape.
Etiology and pathophysiology

42.  Anemia: Sickle cells are fragile. They break apart easily and die,
leaving you without a good supply of red blood cells. Red blood
cells usually live for about 120 days before they die and need to be
replaced. But sickle cells die after an average of less than 20 days.
 Episodes of pain: Periodic episodes of pain, called crises, are a
major symptom of sickle cell anemia. Pain develops when sickle-
shaped red blood cells block blood flow through tiny blood vessels
to the chest, abdomen and joints. Pain can also occur in the bones.
The pain may vary in intensity and can last for a few hours to a
few weeks.
Clinical manifestations

43. Hand-foot syndrome. Swollen hands and feet may be
the first signs of sickle cell anemia in babies. The
swelling is caused by sickle-shaped red blood cells
blocking blood flow out of their hands and feet.
Frequent infections. Sickle cells can damage the spleen,
an organ that fights infection. This makes a person
more vulnerable to infections.

44. Vision problems. Some people with sickle
cell anemia experience vision problems.
Tiny blood vessels that supply the eyes may
become plugged with sickle cells. This can
damage the retina — the portion of the eye
that processes visual images.
Delayed growth. Red blood cells provide
the body with the oxygen and nutrients
needed for growth. A shortage of healthy
red blood cells can slow growth in infants
and children and delay puberty in
teenagers.

46.  Bone marrow transplant
 Antibiotics
 Analgesics
 Hydroxyurea: hydroxyurea reduces the frequency of
painful crises and may reduce the need for blood
transfusions. Hydroxyurea seems to work by stimulating
production of fetal hemoglobin — a type of hemoglobin
found in newborns that helps prevent the formation of
sickle cells.
Medical Management

47. Thalassemia is an inherited blood disorder
characterized by less hemoglobin and fewer red
blood cells in the body than normal.
Thalassemia

51. Four genes are involved in making the alpha hemoglobin chain. If
a person inherits:
 One mutated gene: no signs or symptoms of thalassemia. But,
will be a carrier of the disease and can pass it on
 Two mutated genes: thalassemia signs and symptoms will be
mild. This condition may be called alpha-thalassemia minor.
 Three mutated genes: signs and symptoms will be moderate to
severe. This condition is also called hemoglobin H disease.
 Four mutated genes: the condition is called alpha-thalassemia
major or hydrops fetalis. It usually causes a fetus to die before
delivery or a newborn to die shortly after birth.

52. Two genes are involved in making the beta hemoglobin chain.
 One mutated gene: there will be mild signs and symptoms. This
condition is called beta-thalassemia minor or referred to as a beta-
thalassemia trait.
 Two mutated genes: signs and symptoms will be moderate to
severe. This condition is called beta-thalassemia major, which is
also known as Cooley's anemia. Babies born with two defective
beta hemoglobin genes usually are healthy at birth, but develop
signs and symptoms within the first two years of life. A milder
form, called beta-thalassemia intermedia, also may occur with two
mutated genes

56. Hereditary spherocytosis is a relatively common (1 in 5,000
people) hemolytic anemia characterized by an abnormal
permeability of the RBC membrane; this permits the cells to
change into a spherical shape. These RBCs are destroyed
prematurely in the spleen.
The severity of this hemolytic anemia varies; jaundice can be
intermittent, and splenomegaly (enlarged spleen) also can occur.
Surgical removal of the spleen is the principal treatment for this
disorder.
Hereditary spherocytosis

66.  Assessment
 History taking
 Physical examination
 Medication history
 Nutritional assessment is important
 Cardiac status should be carefully assessed
 Assessment of the gastrointestinal system
 Neurologic examination is also important

67. Based on the assessment data, major nursing diagnoses for the
anemic patient may include:
• Activity intolerance related to weakness, fatigue, and general
malaise
• Imbalanced nutrition, less than body requirements, related to
inadequate intake of essential nutrients
• Ineffective tissue perfusion related to inadequate blood
volume or hematocrit
• Noncompliance with prescribed therapy
• Acute pain related to tissue hypoxia due to agglutination of
sickled cells within blood vessels
• Risk for infection
• Risk for powerlessness related to illness-induced helplessness
• Deficient knowledge regarding sickle crisis prevention
Nursing diagnoses

68. Activity intolerance related to weakness, fatigue, and general malaise
Interventions
 Assess for: signs and symptoms of fatigue (
 client's perception of the severity of fatigue using a fatigue rating scale
 Inform client that a feeling of persistent fatigue is not unusual and is a
result of the disease itself and to plan activities so that times of greatest
fatigue are avoided.
 Implement measures to reduce fatigue: perform actions to promote rest and/or
conserve energy:
 schedule several short rest periods during the day
 minimize environmental activity and noise
 limit the number of visitors and their length of stay
 assist client with self-care activities as needed
 keep supplies and personal articles within easy reach
 implement measures to reduce fear and anxiety (see Diagnosis 1, action b)
 implement measures to promote sleep (e.g. encourage relaxing diversional
activities in the evening, allow client to continue usual sleep practices
unless contraindicated, reduce environmental stimuli, administer
prescribed sedative-hypnotics)

69.  Determine daily calorie needs are realistic and adequate.
Consultation on nutrition expert.
 Weigh the body weight every day, monitor the results of laboratory
examination.
 Explain the importance of adequate nutrition.
 Teach individuals to use flavorings to help improve the taste and
smell of food (lemon, mint, clove, cinnamon, rosemary)
 Give encouragement of individuals to eat with others (food served
in the family room or group)
 Plan maintenance procedures have an unpleasant or painful not
done before eating.
 Offer to eat small portions but frequently to reduce feelings of
tension in the stomach (six times per day with little food)
Imbalanced nutrition, less than body requirements, related to
inadequate intake of essential nutrients
Interventions :

70.  Monitor vital signs, assess capillary refill, skin color /
mucous membranes, nails.
 Elevate the head of bed as tolerated.
 Monitor respiratory effort: auscultation of breath sounds
adventisius notice.
 Investigate complaints of chest pain / palpitations.
Monitor results of laboratory examination. Give a
complete red blood cells / blood product packed as
indicated.
 Provide supplemental oxygen as indicated.
Ineffective tissue perfusion related to inadequate blood
volume or hematocrit
Interventions: