1.
Institute of Health Science
School of Nursing and Midwifery
Department of AHN.
Advanced Adult Health Nursing II
Seminar presentation on Anemia.
By Nasira Jemal
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2.
Out Line
 Definition of anemia
 Classification of anemia
 Clinical Manifestation of anemia
 Causes of anemia
 Assessment and Diagnostic Findings
 Medical Management.
 Application of nursing Process
 Reference
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3.
Objectives
At the end of the presentation students will be able to:-
 Define Anemia
 List classification of anemia
 Describe clinical manifestation of anemia
 Identify cause of anemia
 Explain Assessment and Diagnostic Findings
 Explain Medical Management.
 Apply nursing Process
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4.
Anemia
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5.
Anemia
Anemia:-
 Is a Greek word (‘An’=without,‘emia’= blood).
 Is a condition in which the hemoglobin concentration
is lower than normal
 It reflects the presence of fewer than the normal
number of erythrocytes .
 As a result, the amount of oxygen delivered to body
tissues is also diminished.
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6.
Cont…
 Anemia is not a specific disease state but a sign of an
underlying disorder.
 It is by far the most common hematologic condition.
 WHO criteria for anemia in men and women are
hemoglobin values <13 and <12 g/dl, respectively
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7.
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8.
Classification of Anemia
 Anemia classified in several ways
 A physiologic approach classifies anemia according
to whether the deficiency in erythrocytes is caused by
Hypo-proliferative anemia- defect in their
production
Hemolytic anemia by their destruction , or
By their loss (i.e., bleeding)
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9.
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10.
Classification…
In hypo proliferative anemia :-
 Bone marrow does not produce adequate numbers of
erythrocytes, may result from:-
 Marrow damage due to :-
- Medications e.g. chloramphenicol (Chloromycetin),
- Chemicals e.g. benzene
 lack of factors e.g.( Iron, vitamin B12, folic acid,
erythropoietin; necessary for erythrocyte formation)
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11.
Classification…
In hemolytic anemia:-
 Premature destruction of erythrocytes results in the
liberation of hemoglobin from the erythrocytes into the
plasma,
 The released hemoglobin is converted in large part to
bilirubin and, then bilirubin concentration rises.
 The increased erythrocyte destruction leads to tissue
hypoxia,
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12.
Cont…
 Tissue hypoxia stimulates erythropoietin production(a
glycoprotein hormone, naturally produced by the
peri-tubular cells of the kidney, that stimulates red
blood cell production).
 This increased production is reflected in an increased
reticulocyte (immature red blood cells) count as the
bone marrow responds to the loss of erythrocytes.
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13.
Cont…
Hemolysis can result from
 Abnormality within the erythrocyte itself (eg, sickle
cell anemia, glucose-6-phosphate dehydrogenase [G-
6-PD] deficiency) or
 Within the plasma (eg, immune hemolytic anemias),
 From direct injury to the erythrocyte within the
circulation (eg, hemolysis caused by mechanical heart
valve).
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14.
Cont…
 Pernicious anemia is an inherited disorder caused by
lack of intrinsic factor and inability to absorb vitamin
B 12
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15.
Hypo Proliferative Anemia.
Iron Deficiency Anemia
 The most common type of anemia in all age groups,
and in the world.
 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
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16.
Hypo Proliferative Anemia…
 It is particularly prevalent in developing countries,
where inadequate iron stores can result from
inadequate intake of iron; e.g. vegetarian diets) or
from blood loss (eg, from intestinal hookworm).
 Iron deficiency is also common among adults in the
United States and the most common cause is blood
loss
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17.
Hypo Proliferative Anemia…
Anemias In Renal Disease
 As renal function decreases, erythropoietin, which is
produced by the kidney, also decreases.
 This anemia is caused by both a mild shortening of
erythrocyte lifespan and a deficiency of
erythropoietin (necessary for erythropoiesis).
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18.
Hypo Proliferative Anemia…
 Because erythropoietin is also produced outside the
kidney ( liver), some erythropoiesis continues, even
in patients whose kidneys have been removed.
 Patients undergoing long-term hemodialysis lose
blood into the dialyzer and therefore may become
iron deficient
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19.
Hypo Proliferative Anemia…
Anemia of Inflammation
 Many chronic inflammatory diseases are associated
with a normochromic, normocytic anemia (i.e., the
erythrocytes are normal in color and size),
 The deficiency is due to impaired production of
RBCs.
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20.
Hypo Proliferative Anemia…
Aplastic anemia:-
 Is a rare disease caused by a decrease in or, damage
to the microenvironment within the marrow, and
replacement of the marrow with fat.
 Can be acquired or, rarely, congenital,
 Viral infections and pregnancy can trigger it, or it
may be caused by certain medications, chemicals, or
radiation damage.
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21.
Hypo Proliferative Anemia…
Folic Acid Deficiency
 The folate stores in the body are much smaller than
those of vitamin B12can become depleted within
months when the dietary intake of folate is deficient.
 Folate is found in green vegetables and liver.
 Thus, folate deficiency occurs in people who rarely
eat uncooked vegetables.
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22.
Hypo Proliferative Anemia…
 Folic acid requirements are also increased in patients
who used alcohol with liver disease, chronic
hemolytic anemia and in women who are pregnant,
because the need for erythrocyte production is
increased in these conditions.
 Some patients with mal absorptive diseases of the
small bowel, such as celiac disease, may not absorb
folic acid normally(Green, 2
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23.
Hypo Proliferative Anemia…
Vitamin B12 Deficiency
 can occur in several ways.
 Inadequate dietary intake is rare but can develop in
strict vegans who consume no meat or dairy products.
 Faulty absorption from the GI tract is more common,
particularly in the older adult also occurs in
conditions such as Crohn’s disease or after ileal
resection, bariatric surgery, or gastrectomy
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24.
Hemolytic Anemia
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.
 The sickle hemoglobin (HbS) acquires a crystal-like
formation when exposed to low oxygen tension.
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25.
Hemolytic Anemia…
 The erythrocyte containing HbS loses its round,
pliable, biconcave disc shape and becomes
dehydrated, rigid, and sickle shaped
 These long, rigid erythrocytes can adhere to the
endothelium of small vessels;
 when they adhere to each other, blood flow to a
region or an organ may be reduced ischemia or
infarction results, the patient may have pain, swelling,
and fever
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26.
Hemolytic Anemia…
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A normal red blood cell (upper left) and a sickled red blood cell.

27.
Hemolytic Anemia…
 If the erythrocyte is again exposed to adequate
amounts of oxygen before the membrane becomes
too rigid (e.g., when it travels through the pulmonary
circulation), it can revert to a normal shape
 For this reason the “sickling crises” are intermittent.
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28.
Hemolytic Anemia…
 Sickled cells are rapidly hemolyzed and thus have a
very short life span.
 Anemia is always present; usually, hemoglobin values
range between 5 and 11 g/dL (Natrajan & Kutlar,
2016).
 Jaundice is characteristic and is usually obvious in the
sclerae.
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29.
Hemolytic Anemia…
 Complications of sickle cell disease include :-
Infection,
Stroke,
kidney injury,
Impotence,
Heart failure, and
Pulmonary hypertension
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30.
Hemolytic Anemia…
 The bone marrow expands in childhood in a
compensatory effort to offset the anemia,
 Sometimes leading to enlargement of the bones of the
face and skull.
 Unusually susceptible to infection, particularly
pneumonia and osteomyelitis.
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31.
Hemolytic Anemia…
Sickle Cell Crisis
 There are three types of sickle cell crisis in the adult
population.
 acute vaso-occlusive crisis The most common & is
the very painful, which results from entrapment of
erythrocytes and leukocytes in the microcirculation,
causing tissue hypoxia, inflammation, and necrosis
due to inadequate blood flow to a specific region of
tissue or organ
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32.
Hemolytic Anemia…
 Aplastic crisis
 Results from infection with the human parvovirus.
 The hemoglobin level falls rapidly and the marrow
cannot compensate, as
 Evidenced by an absence of reticulocytes (Natrajan &
Kutlar, 2016).
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33.
Hemolytic Anemia…
 Sequestration crisis results
 when other organs pool the sickled cells.
 Although the spleen is the most common organ
responsible for sequestration in children, most
children with SCD have had a splenic infarction by
10 years of age, and the spleen is then no longer
functional (auto-splenectomy) (Natrajan & Kutlar,
2016).

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34.
Hemolytic Anemia…
Thalassemia :-are a group of hereditary anemia
characterized by:-
 Hypochromia -abnormal hemoglobin content of
erythrocytes),
 Extreme microcytosis (smaller-than-normal
erythrocytes),
 Hemolysis, and variable degrees of anemia.
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35.
Hemolytic Anemia…
 Thalassemia are associated with defective synthesis of
hemoglobin; the production of one or more globulin
chains within the hemoglobin molecule is reduced.
• This increases the rigidity of the erythrocytes and thus
the premature destruction of these cells.
 Thalassemia are classified into two major groups
according to which hemoglobin chain is diminished:
alpha or beta.
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36.
Hemolytic Anemia…
 When thalassemia is called “alpha” or “beta,” this
refers to the part of hemoglobin that isn't being made.
 If either the alpha or beta part is not made, there
aren't enough building blocks to make normal
amounts of hemoglobin.
 Low alpha is called alpha thalassemia.
 Low beta is called beta thalassemia.
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37.
Hemolytic Anemia…
 The alpha thalassemia are milder than the beta forms
and often occur without symptoms
 If left untreated, severe beta-thalassemia can be fatal
within the first few years of life
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38.
Hemolytic Anemia…
Glucose-6-Phosphate Dehydrogenase Deficiency
 G6PD deficiency is inherited, Children who have it
are born with it because it was passed down in genes
from one or both of the parents.
 The gene responsible for this condition is on the X
chromosome .
 This gene produces an enzyme within the erythrocyte
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39.
Hemolytic Anemia…
Immune Hemolytic Anemia
 Hemolytic anemia can result from exposure of the
erythrocyte to antibodies.
 Alloantibodies -antibodies against the host/ “self”)
 From the immunization of a person with foreign antigens
(e.g., the immunization of an Rh-negative person with
Rh-positive blood).
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40.
Hemolytic Anemia…
 Alloantibodies tend to be of the immunoglobulin G
(IgG) type and cause immediate destruction of the
sensitized erythrocytes, either within the blood vessel
(intravascular hemolysis) or within the liver.
 E.g. hemolytic transfusion reaction
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41.
Bleeding(from RBC loss)
 Bleeding from GI tract
 Epistaxis
 Trauma
 Bleeding from genito-urinary tract ( e.g.
menorrhagia)
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42.
Clinical Manifestations
Symptoms of anemia will vary based on the:-
 Severity of the anemia;
 Rapidity of onset;
 Duration of the anemia (ie, its chronicity);
 Metabolic requirements of the patient;
 Cardiac, pulmonary, or other underlying disease; and
 Complications caused by the underlying disorder.
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43.
General symptoms
 Dyspnea, chest pain,
 Muscle pain or cramping,
 Tachycardia, weakness,
 Fatigue, general malaise,
 Pallor of the skin,& mucous membranes,
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44.
Cont…
 Megaloblastic or hemolytic anemia:- Jaundice
 Iron deficiency:
 Brittle, Ridged, concave nails,
 Pica (unusual craving for starch, dirt, ice);
Blood in stool, smooth, red tongue
 Megaloblastic anemia: Beefy, red, sore tongue
Angular cheilosis (ulceration of the corner of the
mouth)
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45.
Complications
 Complications of severe anemia include:-
Heart failure,
Aesthesia, and
Delirium.
 Patients with underlying heart disease are far more
likely to have angina or symptoms of heart failure
than those without heart disease.
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46.
Diagnostic Methods
 Complete hematologic studies :-
hemoglobin,
hematocrit,
reticulocyte count, and
red blood cell (RBC) indices (measure the size,
shape, and quality of RBC,
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47.
Cont…
 Particularly the mean corpuscular volume [MCV] is
the average volume of red cells in a specimen and
 RBC distribution width [RDW] (measures the
differences in the volume and size of RBC).
 Iron studies -serum iron level, total iron-binding
capacity [TIBC], percent saturation, and ferritin (how
much iron your body stores)
 Serum vitamin B 12 and folate levels; haptoglobin
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48.
Treatment
Objectives
 Improve the functional status of anemia
 Prevent development of complications such as Heart
Failure
 Treatment of the underlying cause
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49.
Non pharmacologic
 Packed RBC or whole blood transfusion when thereis
Heart Failure ,
severe hypoxic symptoms,
acute ongoing bleeding)
 Nutritional support
 Non pharmacologic treatment pertinent to the underlying
cause
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50.
Cont…
N.B:-Hematinic (Iron, folate and vitamin B12) should
not be routinely administered to patients with anemia
without a definitive diagnosis of the cause.
 There is no universal pharmacologic treatment for all
causes of anemia
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51.
Medical management
 For Iron deficiency anemia-Oral iron replacement
 N.B. The cause of the iron deficiency state should be
identified and treated.
First line
 Ferrous sulphate , 325mg (65mg elemental iron),
OR 60mg elemental iron, TID between meals for at
least 3 months following correction of the anemia.
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52.
Cont…
 N.B. For patients who do not tolerate ferrous sulfate
tablets, they may be advised to take it with meals, or
to take a smaller dose, or to change the brand to
ferrous gluconate or fumarate tablets or elixir forms.
OR
 Ferrous gluconate, 325mg P.O. (39mg elemental
iron), 1-2tabs, TID
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53.
Cont…
OR
 Ferrous fumarate, 325mg P.O., (107 elemental iron),
one tab, daily to twice per day.
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54.
Cont…
 For (Vitamin B12) deficiency
 Cobalamin, 1000micrograms (1mg), IM, every day
for one week, every week for four weeks and then,
 If the underlying disorder persists, 1mg every month
for the remainder of the patient's life.
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55.
Cont…
For Folate deficiency
 Folic acid, 1 to 5mg P.O., daily for 1-4 months,
 or until complete hematologic recovery.
N.B Folic acid can partially reverse the hematologic
abnormalities of Cobalamin (B12) deficiency BUT
neurologic manifestations will progress.
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56.
Cont…
 Thus, it is important to rule out cobalamin deficiency
before treating a patient with megalo-blastic anemia
with folic acid alone
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57.
Nursing Management
 Preventive education is important
 Nutritional advise
 Administration of prescribed medication
 Managing Fatigue
 Preventing And Managing Infection
 Promoting Coping Skills
 Monitoring And Managing Potential Complications
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58.
Reference
 Handbook_for_Focus_on_Adult_Health_Medical_Surgic
al_Nursing_
 LindaThe Hematological Complications of Alcoholism
HAROLD S. BALLARD, M.D.
 Standard Treatment guide line 2021.
 2018.14edi.Brunner_&_Suddarth’s_Textbook_of medical
surgical nursing
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59.
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