Anemia is the reduction in the RBC and/or hemoglobin concentration compared with normal

values of age. There are two types of anemia- erythrocyte or hgb depletion and change in RBC
morphology.
IRON DEFICIENCY ANEMIA is the inadequate supply of iron. It is caused by (1) Inadequate
supply of iron, (2) impaired iron absorption, (3) blood loss and (4) excessive demands for iron
required for growth. The babies with this disorder are termed as “milk babies” because they are
fed with breastmilk alone even after 6 months of age. They can also have edema, retardation in
growth, irritable, tachycardic, fatigue and may have (+) koilonychia. Management for this
disease is to add oral supplemental of iron. If supplemental iron is not sufficient, administration
of iron parenterally will be used via the Z-track technique.
SICKLE CELL ANEMIA is a hereditary disorder wherein a normal adult hemoglobin is replaced
by sickled hemoglobin. It is transmitted when both parents are carrier of the recessive trait of the
hemoglobin trait (chromosome 11), then they have 25% chance of having a child with this kind
of disease. Although inherited, sickling is not apparent until later life of infancy because they
have fetal hemoglobin which is formed during the 32nd week of gestation. This HgbF is
decreases rapidly and sickling of the cell and its symptoms will be apparent to later years of
infancy or early years of toddlerhood. The sickling will cause obstruction in the veins or arteries
and there will be increases RBC destruction. In handling patients with this kind of condition, it is
important to provide adequate bedrest to conserve oxygen use, hydrate the patient vial oral and
IV therapy, give blood transfusion to provide healthy RBC and give medications for pain and
infection.
APLASTIC ANEMIA is the medical term for bone marrow failure. It is also characterized by
pancytopenia or the triad of profound anemia, leukopenia and thrombocytopenia. It can be
congenital or acquired. The best-known congenital disorder of which aplastic anemia is an
outstanding feature is Fanconi syndrome which is characterized by pancytopenia, hypoplasia of
the bone marrow and patchy discoloration of the skin due to the deposition of melanin and that
is associated with multiple congenital anomalies of the musculoskeletal and genitourinary
system. This disease can be acquired via the human parvovirus infection, hepatitis, prolonged
exposure to radiation, chemotheraphy, antibiotics particularly Chloramphenicol, inhalation and
exposure to industrial household chemicals and infiltration and replacement of myeloid elements
(found to leukemia patients). For this disease, it is important to watch for hypoxia, bleeding and
infection. The management for this disease is directed in restoring function of the bone marrow
by blood transfusions and bone marrow replacement.
VON WILLEBRAND DISEASE is the deficiency in von Willebrand factor (vWF) which
contributes to the adherent of platelets to damaged endothelium and carries protein for factor
VIII; because of this, patient are at risk for prolonged bleeding. The most characteristic clinical
feature is an increased tendency toward bleeding from mucous membrane- particularly
epistaxis. The correct management for epistaxis is to have the child sit up and lean forward,
apply continuous pressure to the nose for 10 minutes, apply ice cold cloth to bridge of nose and
keep the child calm and quiet.
IDIOPATHIC THROMBOCYTOPENIC PURPURA is an acquired disorder although the cause in
unknown. It is believed as an autoimmune response to disease-related antigens. It is
characterized by thrombocytopenia, purpura and normal bone marrow with a usual increase in
large, young platelets. Management is focused on supportive managements since the disease
is self-limited. Activity is restricted while the platelet is low, prednisone, IV immunoglobulin and
anti-D body may be given (take note: give acetaminophen first before giving anti-D body).
Splenectomy may be done for chronic severe ITP.
DISSEMINATED INTRAVASCULAR COAGULATION is a secondary disorder of coagulation
that complicates a number of pathologic processes. It occurs when the first stage of the
coagulation process is abnormally stimulated. There is a massive activation of the coagulation
system leading to clot formation leading to necrosis of the affected organ. At the same time,
there is a rapid consumption of clotting factors leading to bleeding. The patient will manifest
petechiae, purpura, hypotension, bleeding from opening in the skin and ischemia/infarction of
organs. It is expected to have a prolonged prothrombin, partial prothrombin and thrombin times,
there will also be low platelet count, fragmented RBC and depleted fibrinogen level.
Management is to administer platelet and fresh frozen plasma and IV heparin to prevent
coagulation.

ANSWER TO NUMBER 6:
The biggest problem that I may encounter with JN’s condition is the repeated episodes of
hemarthrosis since it may result to contractures and joint fixation. As a knowledgeable nurse
with this disease, I do recognize the importance of keeping the optimum integrity of the body in
order for a person to do activities of daily living by their own self; since this enhances self-worth
and confidence of an individual with self-limiting disease. I will promote maximum function of the
joint and unaffected body parts by instructing and assisting him in doing active range of motion
exercises to mobilize blood circulation thus, preventing hemostatsis. I will also listen to his
thoughts regarding his disease to support him emotionally thereby reducing his anxiety and
uncertainties.