ANEMIA

GROUP 1
 DEFINITION

A condition of low Hb levels

compared with normal levels,
indicating a lack of circulating red
blood cells.
Anemia is not a disease, but a
reflection of the state of a disease /
due to impaired body functions.
Physiologically anemia occurs when
there is a lack of hemoglobin to
transport oxygen to the tissues
 ETIOLOGY

1. Loss of red blood cells

2. Reduced production of red blood cells
3. Increased destruction of blood cells red
(hemolysis)
1. LOSS OF RED BLOOD CELLS

Occurs due to bleeding caused by major

causes (gastrointestinal, uterus, nose,
wound)
2. REDUCED PRODUCTION OF RED BLOOD CELLS

The low production of human

resources due to factor deficiency plays a
role in erythropoesis (Folic acid, Vit B
12, iron).
Also in bone marrow depression
(tumor, treatment, toxin) or inadequate
stimulation due to lack of erythropoietin
(in patients with renal impairment)
3. INCREASED DESTRUCTION OF BLOOD CELLS RED (HEMOLYSIS)

Overactive endoplasmic reticular /

RES (including hypersplenism) or
due to abnormal HR production
destroyed by RES (eg sickle cell
anemia)
Extrinsic due to trauma, antibodies
& infectious agents / toxins
 CLINICAL SYMPTOMS
• Physical performance decline
• Anorexia
• Weak
• Tired
• Lethargic
• Limp
• Sklera (pale color)
• Lips look pale
• Shortness of breath due to shortness of breath
• Heart rate increases
• Dizzy
• Easy to drowsy
 CLASSIFICATION OF ANEMIA

Iron Deficiency Anemia

• Heme synthesis disorder

• 2/3 of iron in Heme-shaped body in hemoglobin,
1/3 in the form of ferritin and hemosiderin in bone
marrow, spleen, liver
• Etiology: inadequate intake, malabsorption, blood
loss and haemolysis
 MEGALOBLASTIC ANEMIA

• Cobalamin Deficiency (Vit B 12)

Parietal cells in the gastric mucosa do not
produce intrinsic factors so that absorption of
Vit B 12 (extrinsic factor)
• As Folate Deficiency
Folic acid is needed for DNA synthesis in the
manufacture and maturation of red blood cells
 APLASTIC ANEMIA

Diseases where there is a decrease of all types

of blood cells (RBC, WBC, platelets) and
hypocellular bone marrow
Etiology: Congenital (Fanconi syndrome),
Acquired (chemical agent, toxin, drug,
idiopathic, pregnancy, radiation, viral and
bacterial infections)
 SUPPORTING
INVESTIGATION
• Hb and Ht decreased
• Erythrocytes decline
• Reticulocytes increase due to bone marrow response to
blood loss (haemolysis)
• Human color staining detects changes in color & shape
can determine the type of anemia
• The lifespan of HR is useful in distinguishing the
diagnosis of anemia
 MANAGEMENT

Aim :
• Eliminating / controlling factors
• Eliminate clinical manifestations
• Prevent complications
 MEDICAL MANAGEMENT
• Oxygen Therapy
Compensation for reduced oxygen transport and help reduce heart
work
• Blood transfusion
Particularly in acute blood loss (Hb <6gr / dl) or that does not
respond to other treatments.
Long-term administration of high-risk excess iron (cardiomyopathy,
pericarditis, arrhythmia, GJK, thyroid insufficiency, pancreatic and
endocrine malfunctions, hepatic fibrosis, skin discoloration)
• An iron-smashing agent
Defroksamine can prevent excess iron
• Erythropoetin
Subcutaneous injection to treat chronic anemia disease. Bone marrow
should be able to produce human resources and must be available
nutrients
• Diet high in iron
In nutritional deficiency disease or blood loss, nutrition can increase
the production of human resources
 PRINCIPLE OF CARE

1. Improve tissue perfusion

2. Meet fluid and nutritional needs
3. Prevent complications
4. Provides information about the disease
process, prognosis and treatment
 TREATMENT OBJECTIVES

1. ADLs are met independently or assisted

2. Complications can be prevented / mitigated
3. The process of disease, prognosis and
treatment is understood
THANK YOU