MEDICAL SURGICAL FINALS

CARE FOR CLIENTS WITH HEMATOLOGIC DISORDER| BSN - III

Pathophysiology
Physiological Assessment  The body stores of iron decreases as
 Hematologic disorders are a broad do the stores of transferrin which binds
group of conditions that affect the and transports iron. This leads to
blood and its components, including depletion of red blood cells,resulting in
red blood cells, white blood cells, decreased hemoglobin concentration
platelets, and the bone marrow. These and decreased oxygen-carrying
disorders can be inherited or capacity of the blood.
acquired, and they can range from
mild to life-threatening.
ASSESSMENT  A careful health history and
physical assessment
 Ethnicity and family history
 Nutritional history
 Onset of a symptom or
finding
DIAGNOSTIC  CBC
 Peripheral blood smear

SPECIFIC SYMPTOMS OF HEMATOLOGIC

DISEASES: Clinical Manifesation
1 Extreme fatigue  Patients with iron deficiency primarily have
2 Delayed clotting of blood symptoms of anemia. If the deficiency is
3 Easy or deep bruising severe or prolonged, they may also have a
4 Abnormal bleeding - smooth, red tongue
5 Abdominal pain -brittle and ridged nails
- angular cheilosis.
These signs subside after iron replacement
PHYSICAL ASSESSMENT therapy. The health history may be significant for
1 Skin (petechiae, purpura, or ecchymoses) multiple pregnancies, GI bleeding, and pica
2 Oral cavity (ulceration, enlarged gums) Diagnostics
3 Lymph nodes (neck, axillae, and groin)  Complete blood count - The CBC documents
4 Spleen the severity of the anemia. In chronic iron
deficiency anemia, the cellular indices show
microcytic and hypochromic erythropoiesis
Iron Deficiency Anemia that is both the mean corpuscular volume
develops when the body’s stores of iron drop (MCV) and the mean corpuscular hemoglobin
concentration (MCHC) have values below the
too low to support normal red blood cell (RBC)
normal range for the laboratory performing the
production. Iron deficiency anemia is the most test
common type of anemia in all age groups,  Peripheral smear- Examination of the
and it is the most common form of anemia erythrocytes shows microcytic and
worldwide. Iron deficiency anemia results hypochromic red blood cells in chronic iron
when the intake of dietary iron is inadequate deficiency anemia; the microcytosis is
for synthesis of hemoglobin. Iron deficiency apparent in the smear long before the MCV is
anemia may occur when total body iron stores decreased after an event producing iron
deficiency.
are adequate
 Bone marrow aspiration - A bone marrow
Etiolog  Dietary factors (insufficient iron aspirate can be diagnostic of iron deficiency;
y intake) the absence of stainable iron in a bone
 Chronic blood loss from GI marrow aspirate that contains spicules and a
bleeding simultaneous control specimen containing
 Impaired GI absorption of iron stainable iron permit the establishment of a
(prolonged diarrhea, diagnosis of iron deficiency without other
gastrectomy) laboratory tests.
 Stool testing - Testing stool for the presence of
 Increased iron requirements
hemoglobin is useful in establishing
(rapid body growth, gastrointestinal (GI) bleeding as the etiology of
menstruation,pregnancy iron deficiency anemia
 Iron-refractory deficiency Medical Management
anemia  Iron therapy - Oral iron supplementation is

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often the primary mode of treatment for iron

deficiency anemia. Several oral iron
preparations, including ferrous sulfate, ferrous Pernicious Anemia
gluconate, and ferrous fumarate
is defined as a type of vitamin B12 deficiency
 Parenteral Iron Formulations
- Older formulations of parenteral iron had a high
that results from impaired uptake of vitamin
molecular weight and carried a significant risk for B12 due to the lack of substance known as
hypersensitivity reactions, including anaphylaxis. intrinsic factor produced by the stomach lining
Newer formulations have a low molecular weight
and a markedly lower risk for anaphylaxis.
 Ferric gluconate: Each 5 mL contains 62.5 mg Etiolog  Vitamin B12 deficiency
of elemental iron; 125 mg is diluted in 100-mL y  Gastric resection and bypass
normal saline and infused over 1 hour, or 5 mL
 Gastric mucosal atrophy
undiluted is given as a slow IV push injection
over 5 minutes. Although the likelihood of an
 Distal bowel resection or disease
allergic reaction is very low, a test dose is often There 1. Intrinsic factor blocking antibody
given prior to the first infusion. are (type 1), which blocks the binding
 Iron sucrose: Each 5 mL contains 100 mg of two site of vitamin B12 to intrinsic factor.
elemental iron; 100 to 200 g can be given, types This is more specific for pernicious
undiluted, as a slow IV push over 2 to 5 minutes. of IF anemia and is the one that is usually
This procedure can be repeated as often as antibo tested
every 3 days for a cumulative dose of 1000 mg
dies 2. Intrinsic factor binding or
within a 2-week period. Ferumoxytol injection:
The 17 mL vial is diluted in 50 to 200 mL of
that precipitating antibody (type 2),
normal saline or 5% dextrose and water and may which interferes with the uptake of
infused over 15 minutes. Close observation for be the vitamin B12-instrinsic factor
signs and symptoms of hypersensitivity tested complex in the small intestine
reaction, including monitoring blood pressure :
and pulse, is recommended. Pathophysiology
Nursing Management  From its background, lack of healthy
 Taking Oral Iron Supplements
red blood cells caused by vitamin b12
- Take iron on an empty stomach (1 hour before or 2
hours after a meal), preferably with orange juice or deficiency; type of megaloblastic
other source of vitamin C. Iron absorption is reduced anemia which can be considered an
by food, especially dairy products auto immune disease. The risk factors
- Reduce gastrointestinal distress by using the are family history, chronic gastritis,
following schedule when more than one tablet per medications, vegetarian diet, gastric
day is prescribed: Take one tablet per day for the surgery. This includes lack of intrinsic
first few days, then increase to two tablets per day, factor, inability to absorb vitamin b12
then three tablets per day in divided doses. This
from small intestine, insufficient
allows gradual adjustment to the iron. If unable to
tolerate oral supplements due to gastrointestinal creation of healthy red blood cells.
distress despite using this intervention, a reduced Lastly, the signs and symptoms:
amount of iron may be used rather than stopping it paleness of skin & mucous
completely. Reduced doses will require that the membranes, general weakness,
treatment duration is extended to adequately fatigue, nausea, vomiting, glossitis,
replenish iron stores and loss of appetite.
 Increase intake of foods rich in vitamin C to
enhance iron absorption (citrus fruits and
juices, strawberries, tomatoes, broccoli).
 Note that stool will be dark in color and often
appear black.
 Eat foods high in fiber to reduce problems with
constipation. A stool softener may be needed.
 Be aware that liquid iron preparations may
stain the teeth. They may be taken through a
straw or by placing the spoon at the back of
the mouth. Rinse the mouth thoroughly after
each dose

Clinical Manifesation
 severe: weakness, listlessness, fatigue
 pernicious anemia: smooth, sore, red
tongue and mild diarrhea

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Diagnostics balance.
 Complete blood countof the erythrocytes Diagnostics
 Upper endoscopy  Schilling Test - traditional method of
Medical Management determining the cause of vitamin B12
 Folic acid - taking 1 mg of folic acid daily deficiency
as a supplement. Can easily treat folate  CBC - Healthcare providers use this test to
acid deficiency evaluate your red blood cell count and
 can be given intramuscularly function.
 oral supplements with vitamins or fortified  Peripheral blood smear - This test is a
soy milk technique healthcare providers use to
 intranasal spray examine your blood cells.
Nursing Management  Reticulocyte count - measures the
 Assessment of patients who have or are number of immature red blood cells
at risk for megaloblastic anemia includes (reticulocytes) in your bone marrow.
inspection of the skin, tongue, and
mucous membranes.
 Maintain adequate nutrition.
 Assess and monitor activity intolerance.
 Advice client to take foods rich in iron
and vitamins.

Megaloblastic Anemia
Megaloblastic anaemia is a form of
macrocytic anaemia, a blood disorder that
happens when your bone marrow produces Medical Management
stem cells that make abnormally large red  Vitamin B12 deficiency treatment - can
blood cells. Megaloblastic anaemia is a type be an oral supplement with vitamins or
of vitamin deficiency anaemia that happens fortified soy milk.
when you don’t get enough vitamin B12  Vitamin B12 can be given intramuscular
and/or vitamin B9 (folate). injections and another method such as
Etiolog  Vitamin B12 deficiency nasal spray and gels for those people
y  Folic Acid Deficiency who have a impaired absorption.
 Pernicious Anemia  Vitamin B9 deficiency treatment -
increasing the amount of folic acid in the
diet and taking 1mg of folic acid daily as
a supplement.
Nursing Management
 Assessment inspection of the skin
 Careful Neurologic assessment
 Test position, vibration sense, and
cognitive function.
 Instruct the patient on how to use Physical
and occupational therapy.
 Instruct the patient to avoid excessive
heat and cold.
Clinical Manifesation  Instruct the patient to choose soft bland
 Typical manifestations of anaemia : foods that are less likely to cause further
weakness, listlessness, fatigue (may not discomfort.
appear apparent initially).
 The hematologic of vitamin B12
deficiency are accompanied by effects
on other organ systems, particularly the GI
tract and nervous system.
 Patients with pernicious anaemia develop
smooth, sore, red tongue and mild
diarrhoea, extremely pale, confused,
paresthesias, and difficulty in maintaining

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genes are inherited, one from

the mother and one from the
father.
 Hemoglobin S is an abnormal
Sickle Cell Disease form of hemoglobin that causes
 Is an inherited condition passed from the red cells to become rigid,
parents to children through genes. This and sickle shaped. This is
genetic disorder is caused by mutation in commonly called sickle cell
the beta globin genes that leads to faulty anemia and is usually the most
hemoglobin, called hemoglobin S. This severe form of the disease
abnormal Hemoglobin S. causes the red Pathophysiology
blood cells to change their shape.  Hemoglobin S (HbS) Formation: In
Instead of being round, the red blood cell individuals with sickle cell disease, the
shape looks like a banana or a sickle. genetic mutation leads to the
These sickle cells can block blood flow production of abnormal hemoglobin,
and result in pain and organ damage. HbS.
 As a result of the abnormal shape, the red  Polymerization of HbS: Under certain
blood cells become hard and sticky, conditions, such as low oxygen levels,
causing them to have trouble moving dehydration, or increased acidity, HbS
through small blood vessels. When they molecules have a tendency to
clog up these blood vessels, blood polymerize and form long, rigid
cannot bring oxygen to the tissues. This structures within the red blood cells.
causes pain and eventually damages the This process causes the red blood cells
tissue. to become less flexible and assume a
1. SICKLE CELL TRAIT - People who inherit one characteristic sickle or crescent
sickle cell gene and one normal gene, have shape.
sickle cell trait (SCT). People with SCT usually  Rigid and Deformed Red Blood Cells:
do not have any of the symptoms of sickle cell The sickle-shaped red blood cells are
disease (SCD), but they can pass the trait on
less flexible and more prone to getting
to their children. stuck in small blood vessels. These
2. SICKLE CELL CRISES - sickle cell crisis occurs deformed cells can lead to blockages
when sickle-shaped red blood cells clump in the blood vessels, causing reduced
together and block small blood vessels that blood flow to various organs and
carry blood to certain organs, muscles, and
tissues.
bones. This causes mild to severe pain. The Vaso-Occlusion: The blockage of

pain can last from hours to days. "Painful blood vessels by the rigid, sickle-
event" and " painful crisis " are other terms shaped cells results in vaso-occlusion.
used to describe these episodes Ischemia and Tissue Damage:

THREE TYPES OF SICKLE CELL DISEASED Reduced blood flow to organs and
A. ACUTE VASOMOOCLUSSIVE CRISIS - The tissues leads to ischemia (lack of
most common, this occurs when sickled red oxygen), resulting in damage to these
blood cells block blood flow to the point that areas. Organs commonly affected
tissues become deprived of oxygen. include the spleen, liver, lungs, bones,
B. APLASTIC CRISIS - Is a condition in which the and brain.
bone marrow of someone with sickle cell  Hemolysis: Sickle cells are fragile and
disease suddenly stops producing red blood prone to breaking apart (hemolysis),
cells. This causes sudden and severe anemia. leading to a decreased number of
The crisis is usually caused by an infection with red blood cells and anemia.
parvovirus.  Inflammatory Response: Vaso-
C. SEQUESTRATION CRISIS - When sickled cells occlusion and tissue damage trigger
block the blood vessels leading out of the an inflammatory response, further
spleen, blood stays in the spleen instead of contributing to the overall pathology
flowing through it. This causes the spleen to get of sickle cell disease. Chronic
bigger. inflammation can contribute to
Etiolog  Sickle cell is an inherited disease complications such as pain, organ
y caused by a defect in a gene. damage, and an increased risk of
 A person will be born with sickle
infections
cell disease only if two abnormal Clinical Manifesation

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 ANEMIA Anemia is typically present THALASSEMIA

hemoglobin between 5 and Group of hereditary anemias in which the
11g/dLpernicious body makes an abnormal form or inadequate
 Jaundice amount of hemoglobin. It is characterized by
 Enlargement of bones hypochromia, extreme microcytosis, hemolysis,
 Dysrhthmia and variable degrees of anemia.
Diagnostics
 Blood tests- Are part of the preliminary Two major groups according to which
evaluation for SCD. Common hemoglobin chain is affected:
hematologic abnormalities in patients  Alpha-thalassemia
with SCD  Beta-thalassemia
 Sickle-turbidity tube test: Routine Etiolog  Genetic defect
screening test that determines the y  G-6-PD
presence of hemoglobin S (HbS) but does
not differentiate between sickle cell Risk Factors:
anemia and trait. Being an Asian, Chinese,
 Hemoglobin electrophoresis: Identifies Mediterranean, or African American
any abnormal hemoglobin types and ethnicity
differentiates between sickle cell trait and Family history
sickle cell anemia. Pathophysiology
Medical Management  one of the polypeptide chains of Hgb
 Hematopoietic Stem Cell Transplant - structure is deficient
HSCT may cure sickle cell diseased,  decreased Hgb synthesis and RBC
however this treatment modality is production
available to only a small subset, due to  Accumulation of polypeptide chains
lack of compatible donor, or due to affect the maturation of RBC
severe organ damage  RBC are destroyed that leads to large
 Pharmacologic Therapy - Hydroxyurea is amounts of hemolysis
a chemotherapeutic agent. It is the only  normal polypeptide accumulated
drug currently approved by the FDA for within normal RBC
treatment SCD.  develops as pathological fragment
 Transfusion therapy - Chronic RBC called Heinz Bodies
transfusion therapy may be effective in Clinical Manifesation
preventing or managing complications  Pallor
from sickle cell anemia  Fatigue
 Supportive therapy- Adequate hydration  Weakness
is important during a painful sickling  Protruding abdomen
episode; aspirin is very useful in  Facial bone deformities
diminishing mild to moderate pain; NSAIDs  Abdominal swelling
are useful for moderate pain or in  Jaundice
combination with opioid analgesics.  Dark urine
Nursing Management  Stunted growth
 Check vitals  Hemoglobinuria
 Determine the degree of pain Diagnostics
 Assess hydration status  Complete blood count
 Assess mental status  Peripheral smea
 Determine oxygenation  ECG
 Give pain medications  Iron Study
 IV fluids  Skeletal survey
 Administer antibiotics as prescribed  HLA typing
 Administer blood transfusions Medical Management
 Bed rest  Discontinuation of the offending agent
 Clean wounds  Blood transfusion is needed when severe
 Avoid restrictive clothing hemolysis is present
 Encourage a healthy diet with folate  Folic acid supplements
 Iron chelation therapy
supplements
 Splenectomy
Nursing Management
 Educate the patient that Folic Acid

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supplementation helps the body build normal  Spontaneous hematuria and

RBC. gastrointestinal bleeding can occur.
 Patients with G-6-PD should always seek  Hematomas within the muscle
medical advice before taking any new
Diagnostics
medication or supplement
 Encourage patient to have frequent rest  Laboratory tests include clotting factor
periods to reduce oxygen consumption measurement and CBC count
 Educate the patient regarding the risk of Medical Management
thalassemia major in offspring  Factors VIII and IX concentrates are given
when active bleeding occurs or as a
preventive measure before traumatic
procedures
HEMOPHILIA
 Plasmapheresis or concurrent
 RARE DISEASE GENETIC BLOOD DISEASE immunosuppressive therapy
 DISORDER THAT AFFECTS THE BLOOD'S  Aminocaproic acid may slow the dissolution of
ABILITY TO CLOT PROPERLY. blood clots
Etiolog Hemophilia is caused by a deficiency  Desmopressin is useful for patients with mild
y or absence of specific clotting forms of hemophilia A.
factors in the blood Nursing Management
 Instruct patients to avoid any agents that
 HEMOPHILIA A interfere with platelet aggregation: such as
aspirin, nonsteroidal antiinflammatory drugs
-Clotting factor VIII is missing.
(NSAIDs), herbs, nutritional supplements, and
-Hemophilia A is about three times alcohol.
more common than hemophilia B.  Bleeding Prevention: minimize the risk of
bleeding episodes.
 HEMOPHILIA B  Bleeding Episode Management: Instruct
-Clotting factor IX Is missing patients and their families on how to recognize
Pathophysiology and respond to bleeding episodes promptly.
 Promote good dental hygiene: as a preventive
 In individuals with hemophilia, the measure because dental extractions are
deficient or defective clotting factor hazardous.
leads to prolonged bleeding and  Avoid all injections; minimize invasive
difficulty in forming stable blood clots. procedures: at least after factor replacement.
 This happens because the clotting  Carefully assess bleeding during hemorrhagic
factors are unable to work effectively episodes: warrants close observation
in the clotting cascade, which is a  Assist family and patient in coping with the
condition:
series of chemical reactions that
 Recommend genetic testing and counseling to
occur to form a blood clot. female carrieers: so that they can make
 Without enough functional clotting informed decisions regarding having children
factors, the blood clotting process is and managing pregnancy.
impaired, resulting in prolonged
bleeding episodes, even from minor
injuries.
 Overall, the pathophysiology of
hemophilia involves a deficiency or
defect in clotting factors, leading to
impaired blood clotting and
increased susceptibility to bleeding.
Clinical Manifesation
 Excessive bleeding
 Easy bruising, prolonged bleeding after
injuries or surgeries, and spontaneous joint
bleeding.
 The most dangerous site of hemorrhage is
in the head
 The severity of sympoms varies
depending on the level of clotting factor
deficiency.
 Chronic pain or ankylosis (fixation) of the
joint may occur with recurrent
hemorrhage

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to agglutinate platelets in the presence of

the antibiotic Ristocetin.)
VON WILLEBRAND DISEASE  ·coagulant activity of factor VIII
 Is an inherited bleeding disorder  Type 3 vWD is diagnosed when vWF
characterized by a deficiency in von antigen is undetectable (or the level is
Willebrand factor (vWF), which is less than 5 IU/dL
necessary for factor VIII activation. Medical Management
 Most common inherited bleeding  The goal of treatment is to replace the
disorder. deficient protein (e.g., vWF or factor VIII) at the
 It typically has an autosomal dominant time of spontaneous bleeding or prior to an
invasive procedure to prevent subsequent
inheritance pattern, affecting both
bleeding.
genders equally  Desmopressin (DDAVP) is often used to prevent
 vWD is divided into types 1, 2, and 3. bleeding associated with dental and surgical
TYPES OF VWD procedures or to manage mild bleeding after
1) von Willebrand Disease Type 1 surgery in patients with mild vWD; it is often not
Characterized by a quantitative deficiency of effective in treating those with type 3 vWD
vWF.  Factor replacement concentrates of vWF and
factor VIII are the treatments of choice for
patients with type 3 vWD and most patients
2) von Willebrand Disease Type 2
with type 2.
Caused by dysfunctional vWF.  Other agents are also effective in controlling
bleeding:
Further subdivided on the basis of certain 1. Aminocaproic acid
phenotypic characteristics 2. Topical agents
2A – impaired multimerization 3. Estrogen-progesterone
2B – hyperfunctional platelet binding 4. Platelet transfusions
2N – Decreased Factor VIII binding 5. Cryoprecipitate
2M – Decreased GPlb binding
 Herbs and medications that interfere with
platelet function should be avoided
3) von Willebrand Disease Type 3 Nursing Management
Most severe form, and is caused by the  Patient Education
absence of circulating vWF.  Bleeding Precautions
Etiolog  A fault in the gene involved in  Medication Management
y the production of von  Desmopressin (DDAVP) Administration
Willebrand factor.  Von Willebrand Factor Replacement Therapy
 Management of Bleeding Episodes
Pathophysiology  Regular Follow-Up
 When there is a decrease in plasma
levels or defect in the von Willebrand
factor, the ability of the blood to clot
decreases leading to a heavy and
continuous bleeding after an injury.
Clinical Manifesation
 Bleeding most often involves the mucous
membranes.
 Nosebleeds, heavy menses, easy bruising,
and prolonged bleeding from cuts and
surgical sites are common.
 Soft tissue and joint hemorrhages are not
seen often, unless the patient has type 3
vWD.
 As laboratory values fluctuate, so does
bleeding.
Diagnostics
The diagnosis of vWD is based on
measurements of vWF antigen;
 ·level of vWF–dependent platelet
adhesion - measured with the use of the
vWF–ristocetin cofactor activity assay
(measures the ability of a plasma sample

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used in treatment for AML

 conditioning therapy - to destroy the
ACUTE MYELOID LEUKEMIA hemopoietic functioning in the bone marrow
 Acute myelogenous leukemia (AML) is a and to kill any residual leukemic cells
 human leukocyte antigen (HLA-matched) -
cancer of the blood and bone marrow —
donor stem cells
the spongy tissue inside bones where  enasidenib, a cytarabine-based regimen,
blood cells are made.  along with other agents (e.g., cladribine,
 it affects a group of white blood cells fludarabine, mitoxantrone, etoposide);
called the myeloid cells, which normally palliative care;
develop into the various types of mature  or use of a hypomethylating agent (e.g.,
blood cells, such as red blood cells, white azacitidine or decitabine).
blood cells and platelets.  supportive care
Etiolog  Radiation Exposure Nursing Management
 If the patient is hospitalized, assessments should
y  Benzene and Smoking
be performed daily, or more frequently as
 Previous Cancer Treatment warranted.
 Blood Disorders  The nurse also must closely monitor the results
 Genetic Disorders of laboratory studies, including tracking the
Pathophysiology leukocyte count, ANC, hematocrit, platelet,
 develops as the consequence of a creatinine, electrolyte levels, coagulation and
hepatic function tests.
series of genetic changes in a
 Medication Management
hematopoietic precursor cell. These  Desmopressin (DDAVP) Administration
changes alter normal hematopoietic  Von Willebrand Factor Replacement Therapy
growth and differentiation, resulting in  Management of Bleeding Episodes
an accumulation of large numbers of  Regular Follow-Up
abnormal, immature myeloid cells in
the bone marrow and peripheral
blood. POLYCYTHEMIA VERA
Clinical Manifesation  bone marrow is hypercellular, and the
 Inadequate production of normal blood erythrocyte, leukocyte, and platelet
cells counts in the peripheral blood are often
 Symptoms due to neutropenia include elevated. Erythrocyte elevation
fever and infection predominates; the hematocrit can
 Symptoms related to anemia include exceed 60% in some cases. The median
pallor, fatigue, weakness, dyspnea on age at the onset is 60 years; median
exertion and dizziness survival is typically 14 to 20 years
 Symptoms reflective of Etiolog  Radiation Exposure
thrombocytopenia include eechymosis, y  Benzene and Smoking
petechiae, epistaxis and gingival  Previous Cancer Treatment
bleeding.  Blood Disorders
Diagnostics  Genetic Disorders
 ·CBC Clinical Manifesation
 Bone marrow biopsy  Neurologic symptoms - headache,
 AML Can be further classified into eight dizziness, vision changes, and transient
different subgroups ischemic attacks
Medical Management  Abdominal symptoms - early satiety,
Chemotherapy abdominal discomfort/pain (that can also
 Induction - is the first phase of treatment before be associated with splenomegaly);
higher dose chemotherapy is given Diagnostics
1. cytarabine
 Mutation of the JAK2 gene
2. daunorubicin
 Assessment include palpation of the
3. idarubicin
4. mitoxantrone spleen, and finding if the patient has a
5. etoposid history of thrombotic events or has ever
 Consolidation - patients receive high dosage received a blood transfusion or
aggressive chemotherapy medications associated with causing
 Lower Intensity Therapy erythrocytosis
 ANC (absolute neutrophil count) - identifies  Assessment of cardiovascular risk factors
how many neutrophils are in a sample of your
 elevated RBC mass (a nuclear medicine
blood.
 hematopoietic stem cell trans plant (HSCT) -
procedure)

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 a normal oxygen saturation level HODGKIN LYMPHOMA

 an enlarged spleen.  NEOPLASMS OF CELLS OF LYMPHOID
 elevated WBC and platelet counts. ORIGIN
 erythropoietin level is not as low as would  ABNORMAL GROWTH OF CELLS CALLED
be expected with an elevated REED-STERNBERG CELLS WITHIN LYMPH
hematocrit NODES.
 - it is normal or only slightly low. Causes  TUMORS THAT USUALLY START IN LYMPH
of secondary erythrocytosis should not be NODES BUT CAN INVOLVE LYMPHOID
present TISSUE IN:
Complications  THE SPLEEN
 Increased risk for thromboses - resulting in  GI TRACT
a CVA (brain attack, stroke) or heart  LIVER, OR
attack (MI). Most frequent cause of death  BONE MARROW
 Bleeding - possibly due to the fact that HALLMARK: Reed-Sternberg cells
the platelets (often very large) are  relatively rare malignancy that has a high
somewhat dysfunctional. Can occur in cure rate
the form of;  seen more commonly in patients
- nosebleeds receiving long-term immunosuppressive
- ulcers therapy
- frank gastrointestinal bleeding.  more common in males than in females
Medical Management and has two peaks of incidence:
 Phlebotomy is an important part of therapy to ~ 15 to 35 years old
keep the hematocrit within normal range.
~ after 60 years of age
 Cytoreductive therapy patients who are
symptomatic due splenomegaly, leukocytosis, FIVE SUBTYPES: HODGKIN LYMPHOMA
thrombocytosis, or have poor tolerance to
phlebotomy, or whose disease has progressed
to myelofibrosis or AML, High risk patients first
line of treatment
Nursing Management
 The nurse’s role is primarily that of educator.
 Risk factors for thrombotic complications
should be assessed, and patients should be
instructed regarding the signs and symptoms of
thrombosis.
 Patients with a history of bleeding are usually
advised to avoid aspirin and aspirin-containing
medications
 Minimizing alcohol intake should also be
emphasized
 In pruritus, the nurse may recommend bathing
in tepid or cool water, along with applications
of cocoa butter–based lotions and bath
products. PATHOPHYSIOLOGY
 Abnormal proliferation of B lymphocytes.
 Formation of Reed-Sternberg cells, large
abnormal cells.
 Cells acquire unique features like multiple
nuclei and an owl-like appearance.
 Disease begins in a single lymph node.
 Spreads contiguously through the
lymphatic system.
 Reed-Sternberg cells serve as a crucial
diagnostic marker.
Etiolog  Uknown
y
RISK FACTORS
 Age
 Viral infections: Epstein-bar virus,
human immunodeficiency virus
[HIV], or human herpesvirus 8

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[HHV8]) ACUTE LYMPHOCYTIC LEUKEMIA

 Family history, RESULTS FROM AN UNCONTROLLED
 Being exposed to cytotoxic PROLIFERATION OF IMMATURE CELLS
agents (LYMPHOBLASTS) DERIVED FROM THE
LYMPHOID STEM CELL.
Clinical Manifesation can occur at any age, but 75% to 80% of all
 INITIAL PRESENTATION - painless, firm cases are found in children, with the median
lymph node enlargement, commonly in age at diagnosis being 15 years (Boys are
the cervical nodes. affected more often than girls) risk factors for
 Symptoms Indicating Advanced Disease: ALL include older age (especially over 70
B symptoms: fever, weight loss, and night years), prior exposure to chemotherapy or
sweats that are seen in about 40% of radiation therapy, having certain genetic
patients, aiding in staging and prognosis conditions (e.g., especially Down syndrome;
determination. also neurofibromatosis, Klinefelter syndrome,
 Additional Symptoms: Pruritus, fatigue, and Fanconi anemia)
decreased appetite, splenomegaly, rare Etiolog  UNKNOWN, HOWEVER, CERTAIN
alcohol-induced pain in affected lymph y ENVIRONMENTAL FACTORS HAVE
nodes, impaired immunity, and increased BEEN IMPLICATED IN THE
susceptibility to infection ETIOLOGY OF ACUTE
Diagnostics LYMPHOCYTIC LEUKEMIA, SUCH
 Excisional Lymph Node Biopsy AS EXPOSURE TO BENZENE,
 Health History: B symptoms IONIZING RADIATION, OR
 Crucial Imaging: Chest X-Ray, CT Scan of PREVIOUS EXPOSURE TO
chest, abdomen, and pelvis CHEMOTHERAPY OR
 PET SCAN RADIOTHERAPY.
 Laboratory Tests Pathophysiology
 MUGA scan and/or ECG  In The Last Several Decades,
Medical Management
Advances In Understanding The
Pathophysiology And Molecular
Genetics, As Well As The Incorporation
Of Targeted Therapy And Hsct, Have
Resulted In Improved Cure Rates And
Overall Longer Survival In Patients With
All.
Clinical Manifesation
 The disease is commonly found
incidentally with routine laboratory studies
or physical exam for another condition
 Manifestations of leukemic cell infiltration
Nursing Management into other organs are more common with
 Discuss the potential for second malignancies ALL than with other forms of leukemia and
at the outset of treatment, emphasizing the include pain from an enlarged liver or
high curability of Hodgkin lymphoma. spleen as well as bone pain.
 Encourage patients to mitigate risks by  The central nervous system (CNS) is
avoiding tobacco/alcohol, limiting exposure to
frequently a site for leukemic cells; thus,
environmental carcinogens, and practicing
patients may exhibit cranial nerve palsies
sun protection.
 Vital to regularly screen for late effects, or headache and vomiting because of
particularly related to chemotherapy meningeal involvement. Other extranodal
 Provide comprehensive education on self-care sites include the testes and breasts.
strategies and disease management to Diagnostics
empower patients in their health journey.  Allogeneic HSCT may be considered
during initial remission if disease features
and testing suggest the risk of relapse is
high
 The development of chimeric 2624
antigen receptor (CAR) T cells has
significantly improved treatment
outcomes and overall survival in patients

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with ALL PET scan; MUGA or ECG; and bone

Medical Management marrow biopsy and aspirate.
 IV treatment with immunoglobulin (IVIG) may Medical Management
be given to select patients with recurrent  Radiation therapy
infection.  Combinatio n chemotherapy
 receive both pneumonia and flu vaccinations  Cranial radiation or intrathecal chemotherapy
as indicated  Chemotherapeutic agents
Nursing Management
MEDICATIONS:  Assess and manage pain; teach relaxation
1. Lymphoid blast cells are typically very techniques
sensitive to corticosteroids and to vinca  Monitor respiratory status and probide
alkaloids; therefore, these medications are supplemental oxygen as necessary.
an integral part of the initial induction  Monitor daily weight and caloric intake;
therapy encourage to eat small frequant meals and
2. The corticosteroid dexamethasone is increase protein intake.
preferred to prednisone, as it is more toxic  Provide supportive comfort measures following
to lymphoid cells and has better CNS radiation and chemotherapy treatments.
penetration. Typically, an anthracycline is
included, sometimes with asparaginase.
3. For patients with relapsed or refractory B-
cell precursor ALL, agents such as
blinatumomab or inotuzumab ozogamicin
have been found to be effective
Nursing Management
 Preventing Or Managing Infection And
Bleeding
 Managing Mucositis
 Improving Nutritional Intake
 Easing Pain And Discomfort
 Decreasing Fatigue And Activity Intolerance

NON-HODGKIN LYMPHOMA
 NHLs area a heterogeneous group of cancers
that
originate from the neoplastic growth of lymphoid
tissue.
 NHL is increased in patients who have immune
deficiencies or autoimmune disorders; had prior
treatment for cancer; been an organ transplant
recipient; had a history of viral infections, and
been exposed to herbicides, pesticides, solvents,
dyes, and defoliating agents

NHLS CAN BE CATEGORIZED AS:

1. Indolent slow-growing cancer that often
remains localized or causes few symptoms
2. Aggressive fast-growing cancer that spreads
rapidly and causes significant morbidity
Clinical Manifesation
 NHL may start as a painless swelling in one
or more lymph nodes in the neck, axillary
region,or groin.
 Enlarged lymph node site and size, which
can compress organs, compromising
function.
Diagnostics
 Incisional or excisional lymph node biopsy
 Flow cytometry
 Fluorescence in situ hybridization (FISH)
 polymerase chain reaction (PCR); CT
scans of the chest, abdomen, and pelvis;

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