NURSING CLIENTS WITH HEMATOLOGIC

○ Humerus
DISORDERS ○ Ribs
○ Tibula/Fibula
○ Iliac crest (pelvis)- the most
INTRODUCTION
common site for bone
● Hematologic Disorder aspiration.
● Hormones need of each blood cells:
○ Hema- means blood.
○ RBC- erythropoietin that can
● Blood includes: be found in the kidney.
○ 45% of blood cells ○ WBC- CSF (Colony Stimulating
3
RBC 4-6 M/𝑚𝑚 Factors)
3 ○ Platelets- thrombopoietin
WBC 4,000-11,000/𝑚𝑚
3
Platelets 250,000-500,000/𝑚𝑚
○ 55% of plasma RED BLOOD CELL (RBC)
Water 90% in our body
● Other name: Erythrocyte
Electrolytes
● 1 RBC= 250 M of Hgb
Substances ● 1 Hgb= 4 oxygen
● 1 RBC= 1 Billion of oxygen
● Hematocrit (Hct)- the amount of RBC ● Lifespan: 120 days
that can take up space in the blood. ● Hemolysis occurs after 120 days or
○ Dehydration= ↑Hct phagocytes will eliminate dead RBC.
● Hemoglobin (Hgb)- a protein in the RBC These phagocytes will deliver dead RBC
that delivers oxygen and iron. “Heme” to the liver or spleen, which will be
converted into urine or other forms of
means Iron. “Globin” means oxygen
end product to be expelled out of the
transport protein. body.
○ Normal Values:
Female: 12-16 g
Male: 14-18 g WHITE BLOOD CELL (WBC)

● Other name: Leukocyte

● DIAPEDESIS- a process in which the
WBC leaps out from the blood vessels
to attact invaders or infection.
● Acts as a DEFENSE
○ Includes phagocytes,
B-lymphocytes (produces
antibodies), and T-lymphocytes
● ↑WBC= leukocytosis
● ↓WBC= leukopenia

HEMATOPOIESIS WBC is composed of:

● Granulocytes- contains several
● A blood cell production that happens in
granules seen under microscope.
the bone marrow.
● Sites of bone marrow:
○ Femur - epiphyseal line
○ Sternum
 1.) IRON DEFICIENCY ANEMIA
These three increases due to acute conditions.
○ Neutrophils- becomes
elevated due to infection.
3
(3,000-7,000/𝑚𝑚 )
○ Eosinophils- elevates due to
allergic reaction. (100-400/
3
𝑚𝑚 )
○ Basophils- elevates due to
3
inflammation. (20-50/𝑚𝑚 )
● Agranulocytes- no granules.
○ Consists of lymphocytes and
monocytes.
○ Lymphocytes- these are the
CLINICAL MANIFESTATIONS
T-cells and B-cells.
○ Monocytes- are the
phagocytes that engulf foreign
bodies, bacteria and dying
cells. This increases due to
chronic conditions.
PLATELETS
● Other name: Thrombocytes
● Helps in clot formation to stop
bleeding.
● Megakaryocytes- source of platelets or
a rupture of 50 pieces or more
fragments leads to sealing of the injury
with the help of fibrin.
● ↓platelets = thrombocytopenia ; leads
to bleeding which has signs of purpura
(4-10 mm), petechiae (4 mm), and
ecchymosis (10 mm or 1 cm) also called
as hematoma.
○ Med: Vitamin K- a coagulant.
● ↑platelets = thrombosis which can lead
to thromboembolism if the pt also has
an embolism.
○ Med: Heparin- a anticoagulant.
● Hemophilia- a problem in the clotting
factor ; lacks clotting factor.
● ↓Hgb = ↓Iron
● CAUSES:
○ Poor dietary intake
○ Bleeding
● Results when the intake of dietary iron
is inadequate for hemoglobin synthesis.
● Occurs when total body iron stores are
adequate but the supply of iron to the
bone marrow is inadequate (Functional
Iron Deficieny)
● Most common anemia
● Poor dietary habits leading to
inadequate intake of iron, vitamin B12
and/or folacin and/or blood loss
● Smooth, red tongue (glossitis)
● Brittle and ridged nails
● Fatigue
● Headache
● Paresthesia (prickling sensation in the
extremities; restless leg syndrome)
● Ankle edema- due to poor circulation
of blood which leads to the retention of
electrolytes thus, does the blood flow
does not reach the peripheral
extremities.
○ Pitting edema- w/ indention.
○ Non-pitting edema- w/o
indention.
● Dry, pale mucous membrane
● Pearly white sclera (pale conjunctiva)
● Decreased hemoglobin and
erythrocytes
● Increased iron-binding capacity
○ Can be checked using TIBC or
Total Iron Binding Capacity
which checks for the iron level
in the body.
● Megaloblastic of blood- increased
production of RBC in bone marrow that
leads to abnormally large immature
RBC.
 ● Angular cheilosis – fissures in the
mouth
○ Cheilitis- sores or ulcers in the
mouth.
PLUMMER-VINSON SYNDROME (P-V-S)
● A chronic Iron Deficiency Anemia
(matagal nang mababa ang Iron)
● Cause: Prolonged poor dietary/ iron
intake.
● Triad symptoms of anemia
○ Dysphagia (difficulty of
swallowing) - due to spasm in
the esophagus specifically in
the cricoid cartilage.
○ Stomatitis (inflammation of
the mouth)
○ Atrophic glossitis (absence of
pappilae)
● Additional symptom
○ Koilonychia- a concave nail bed
● Leukemia- a tumor (cancer) which
leads to increased rapid production of
WBC.
DIAGNOSTIC FINDINGS
● Definitive method- bone marrow
aspiration.
● CBC- checks for hgb level
● Hct and TBC are also slow
MEDICAL MANAGEMENT
● If bleeding determines the cause (GI
bleeding)
● Occult blood - stool is the specimen
used.
● Colonoscopy, endoscopy- uses local
anesthetic spray before inserting
flexible tube through the mouth or
colon without reaching into the small
intestine or stomach.
THERAPEUTIC INTERVENTIONS
● Improve diet: include ascorbic acid,
which stimulates iron uptake
● Appropriate supplements of iron,
vitamin B12 and folic acid
○ Vitamin B12- helps in RBC
formation.
NURSING INTERVENTIONS
● Teach clients food high in iron, folic acid
and vitamin B12
○ Foods such as internal organs,
red meat, green leafy
vegetables, egg yolk
● Teach about the side effects of
medications
● Assists client with ADL as needed
SEVERAL IRON PREPARATIONS
Iron Salts/ Iron Amount of Elemental
Supplements Iron Content
● Ferrous - 12%
gluconate
● Ferrous - 20%
sulfate
● Ferrous - 33%
fumarate
➔ ↑E.I = ↑S.E
➔ Side Effects include:
constipation/diarrhea,
nausea/vomiting, gastric irritation and
black stool due to iron.
➔ Example administration of Iron Salts:
325 mg TID- 20% of 325 mg= 65% E.I
Iron Preparations:
● Take with meals
● Take on empty stomach or 1 hr before
meal or 2 hrs after meal.
 ● Avoid coffee, spices, oily and ANTACIDS
such as milk.
● Best taken with vitamin C or citric
juices.
Iron Tablets:
● Swallow it whole, do not chew.
● They are ENTERIC COATED TABLETS
(shiny, smooth tablets) which help
delay absorption in the stomach by
protecting it from the acidic
environment and be able to dissolve in
the small intestine where the pH
changes into a 5-6 alkalinity
environment.
Liquid Iron:
● Best to use straw to avoid metallic taste
and staining of the teeth.
○ Drops- used by babies.
Parenteral: IM (intramuscular):
● Uses Z track
● WOF: hypotension, headache, and
urticaria.
○ Adverse Effects caused by
DIAGNOSTIC PROCEDURES
overdose:
↓HR, ↓BP, renal failure, liver
failure, lethargy (comatose),
cardiac arrest due to
dysrhythmia, etc.
○ Mgt: Gastric Lavage
○ Antidote: Deferoxamine- a
chelating agent which acts
against heavy metals such as
iron.
2.) PERNICIOUS ANEMIA or ADDISONIAN
ANEMIA
● ↓RBC and ↓Vit. B12 (cobalamin) - The
stomach helps in the formation of B12,
a pt with this type of anemia cannot
absorb Vit. B12 in the Ileum or
stomach, particularly in the
mucosal/parietal cells.
● Vitamin B12- helps in the RBC synthesis
or formation. They are also good for
nerves.
● CAUSES:
○ Dietary
○ Hereditary- common in
Europeans, or due to
autoimmune that would attack
intrinsic factors in the mucosal
cells in the stomach.
○ G.I Surgery
● Lack of intrinsic factor in the stomach
prevents the absorption of vitamin B12
in the lower portion of the ileum;
subsequent reduced number of
erythrocytes formed, leading to anemia
● I.F + B12 travels to the S. Intestine,
particularly in the Ileum into the
bloodstream and into the bone marrow
for RBC synthesis.
● Schilling Test- checks for the intrinsic
factor or the Vitamin B12 absorption.
○ Pt must be NPO and should
given a radioactive cobalamin
(B12) per orem in small doses
and injection, to be collected
for the 24-hour urine
collection.
○ Normal Value of B12:
200-900 pg/mL (pg=picogram)
○ Mgt: Cyanocobalamin- used to
treat Vit.B12 deficiency.
● Romberg Test
Normal Findings:
● Negative Romberg: may sway slightly
but is able to maintain an upright
posture and foot stance.
Deviation from normal:
● Positive Romberg: cannot maintain foot
stance; moves feet apart to maintain
stance.
CLINICAL FINDINGS
● Weakness
● Sore mouth
● Paresthesia (tingling sensation)
● Dyspnea (sob)
● Pallor (pale)
● Beefy red tongue (glossitis)
● Positive Romberg test (loss of balance
when eyes close)
● Gastric analysis: no intrinsic factor
● Schilling test; urine test for B12
absorption (positive result is less than
6-8% of the radioactive cobalamin in a
24 hr urine collection)
THERAPEUTIC INTERVENTION
● Lifelong injection of cyanocobalamin
(B12) via SQ or IM.
NURSING INTERVENTIONS
● Explain the disease process and the
need for continued treatment.
● Teach family members how to give IM
injections or make a referral to a
visiting nurse.
● Teach pt foods rich in Vit.B12 such as
poultry, fish, meat, and milk.
3.) APLASTIC ANEMIA (HYPOPLASTIC ANEMIA
or PANCYTOPENIA)
● Bone marrow is depressed
(suppressed) or destroyed by a
chemical or drugs that are myelotoxic
such as hemotherapeutic drugs,
immunosuppressants, and Ionizing
radiation. (commonly used by pt with
cancer)
● Leukocytopenia, thrombocytopenia
and decreased erythrocytes,
agranulocytosis.
● (PANCYTOPENIA)- all components of
blood cells are decreased: ↓RBC ↓WBC
↓Platelets ↓Neutrophils or ANC
(Absolute Neutrophil Count)
● CAUSES:
○ Chemicals
○ Autoimmune
DIAGNOSTIC TEST
● Bone Marrow Aspiration
● CBC- always comes first before BMA.
CLINICAL FINDINGS
● Headache
● Weakness
● Anorexia
● Dyspnea
● Fever
● Bleeding from mucous membrane
● Decreased leukocytes, erythrocytes and
platelets
THERAPEUTIC INTERVENTIONS
● Identify and eliminate causative agent
● Blood transfusions
● Maintenance of fluid and electrolyte
balance
● Corticosteroids and androgens to
stimulate bone marrow function
● Splenectomy when enlarged organ
destroys normal RBC’s- due to
splenomegaly or enlarged spleen. This
occurs when the function of the spleen
 has been destroyed due to the dead
cells that keep coming.
NURSING INTERVENTIONS
● Prevent infection by protective
isolation.
○ A pt taking
immunosuppressants have
high risk for infection.
○ Mgt: Reverse Isolation- isolates
pt to prevent more infection
coming to the body from
outside.
● Provide blood transfusion therapy as
ordered.
○ WOF reactions within 15 mins.
○ S.E: itchiness (urticaria),
dyspnea, fever, chills
○ Mgt: Check for blood type and
cross-matching. (within 30
mins, blood must be
transferred from the fridge to
thaw and given to the pt.
○ Mgt: Observe VS q15, q30, q1h
● Encourage pt to eat foods:
○ Cooked meat- avoid raw
○ Fruits/vegs- unpeeled is not
allowed
○ Milk/dairy- unpasteurized is
not allowed to prevent
infection due to bacteria,
molds, and microorganisms.
○ Poultry and eggs
MEDICAL TX
● Bone marrow transplant/ Stem cell
transplant
4.) HEMOLYTIC ANEMIA
● RBC’s have a shortened life span; thus,
the number of RBCs in circulation is
reduced.
● ↓RBC- hemolysis occurs due to
shortened lifespan.
5.) SICKLE CELL ANEMIA
● A severe hemolytic anemia that results
from the inheritance of the sickle
hemoglobin (Hbs) gene.
● Occurs due to the increased demand
for oxygen.
● ↑RBC ↓Hbg
● RBC is in a crescent shape which blocks
small blood vessels due to the blood
viscosity or blood thickening that will
cause obstruction.
● CAUSES:
○ Acquired
○ Hereditary- if both parents
have sickle cell anemia.
- Hbs → (+) carrier + (-) =
carrier of SCA.
● Normal Hbg- Hgb A
● Abnormal Hbg- Hbs (hemoglobin sickle)
● Commonly seen in Black Africans.
CLINICAL MANIFESTATIONS
● Anemic, usually with hemoglobin
values of 5 to 11 g/dL
● Jaundice in sclera (icteric sclera)
● Tachycardia, cardiac murmurs, and
often an enlarged heart (cardiomegaly)
● Dysrhythmias and heart failure
● Low hematocrit
TYPES OF SICKLE CELL CRISIS
● Very painful acute vaso-occlusive crisis
○ Blood clumping and stasis will
lead to obstruction and cause
thrombophlebitis or more
serious complication such as
thromboembolism.
 ○ Ischemia (reduced blood flow,
oxygen is restricted due to
clot) occurs and leads to
infarction (tissue
death/necrosis)
● Aplastic crisis due to infection
● Sequestration crisis – splenic infarction
○ A life-threatening situation due
to splenomegaly leading to the
death of spleen or lost of
function of spleen due to dead
cells. This occurs due to the
sickle cells going to the spleen.
○ May lead to hypovolemic
shock.
MEDICAL MANAGEMENT
Pharmacologic Therapy
● Hydroxyurea (Hydrea)
○ A chemotherapy agent,
effective in increasing
hemoglobin levels, thereby
decreasing the permanent
formation of sickled cells.
○ Antibiotic therapy (to fight
bacteria), incentive spirometry,
corticosteroids (to relieve
pain), hydration.
Transfusion Therapy
● RBC transfusion- uses packed RBC
within 4 hrs.
Supportive Therapy
● Pain management
● Adequate hydration (increase fluid
intake to change the blood viscosity of
sickle cell).
● Intravenous hydration with dextrose
5% in water (D5W) or dextrose 5% in
0.25 normal saline solution (3 L for 24
hours)
● O2 administration
● Hematopoietic Stem Cell Transplant-
also called as Bone Marrow Transplant.
● Relaxation techniques, breathing
exercises, and distraction are helpful
for some patients.
Prevent infection
● Antibiotic therapy
● Monitor signs of infection
5.) POLYCYTHEMIA VERA
● Poly= means “many”
● A chronic blood disorder.
● A sustained increase in the number of
erythrocytes, leukocytes, and platelets.
● ↑RBC ↑WBC ↑Platelets ↑Hbg
● Platelet aggregration will lead to
clumping.
● Happens in people living in high
altitude.
● Increased demand for oxygen.
CLINICAL FINDINGS
● Headache
● Weakness
● Itching
● Increased hemoglobin
● Purple-red complexion (blushing)
● Dyspnea
● Bleeding from mucous membrane- due
to ↓iron levels.
ETIOLOGY
● Unknown
● Hepatoma
● Lung tumor
● Adrenal cancer
PATHOGENESIS OF INCREASED PLATELETS

NURSING MANAGEMENT

Relieve pain
● Support and elevate swollen joints until
the swelling diminishes. (Bed rest)
THERAPEUTIC INTERVENTIONS
● Phlebotomy- blood withdrawal which
decreases blood volume. (1 pint = 173
ml)
● Diet low in iron- to avoid increased Hct.
Low purine to lower uric acid, low fat,
low sugar and low oxalate.
● Radioactive phosphorus; busulfan
(Myleran) - low type IV drug
NURSING INTERVENTIONS
● Discuss diet with the client and family.
● Provide supportive care and prevent
hemorrhage.
● Assist with phlebotomy.
● Instruct the client to elevate legs while
sitting.
PLATELET and CLOTTING
THROMBOCYTOPENIC PURPURA
● Appears to result from the production
of an antiplatelet antibody which coats
the surface of platelets, making them
easily destroyed by phagocytic
leukocytes.
● Antibody-bound platelets are ingested
and destroyed by the
reticuloendothelial system (RES).
● ↓Platelets
● Has 2 types: Acute & Chronic
CLINICAL MANIFESTATIONS
● Easy bruising
● Heavy menses
● History of epistaxis
● History of gum bleeding
● Low platelet count less than
30,000/mm3
● Ecchymotic areas
● Hemorrhagic petechiae in the
extremities or trunk
MEDICAL INTERVENTIONS
● Aminocaproic acid – slows dissolution
of clots. It is a hemostatic/
anti-fibrinolytic agent.
● Corticosteroids
● Immunosuppressive agents such as
Tacrolimus.
● IVIG (Intravenous Immunoglobin),
rituximab, Nplate (SQ q 1 week ;
contains thrombopoietin, a hormone
used for platelet production), Promacta
(oral)
● Splenectomy- to remove antibodies.
Since the spleen produces antibodies
and acts as a defense, and filters blood.
● Platelet transfusions- to stop the
bleeding for 1 hr.
NURSING INTERVENTIONS
● Prevent injury and bruises
● Encourage client to adhere to medical
regimen
● Teach the side effects of meds,
particularly proneness to infection
DISSEMINATED INTRAVASCULAR
COAGULATION (DIC)
● Not a disease but a sign of underlying
condition.
● Body’s response to injury or disease in
which microthrombi obstruct the blood
supply of organs; complicated by
hemorrhage at various sited
throughout the body. It is triggered by
sepsis, trauma, cancer, shock,
abruption placenta, toxins, allergic
reactions and etc.
● ↓ platelets
● Stage 1: The platelets are overactive,
which means it will clot any part in the
body.
● Stage 2: Consumption of other clotting
factors.
Clotting Formation:
 1. Platelet clot formation.
2. Release of serotonin from the
platelets. Which would then result in
vasospasms or constrictions in the BV.
3. Injured site/tissue will release
thromboplastins then the blood vessels
will release Ca and will combine
together, leading to the conversion of
prothrombin to thrombin. Second
conversion is from Fibrinogen to Fibrin.
4. Clotting time/duration: 2 to 6 mins.
CLINICAL MANIFESTATIONS
● Bleeding from mucous membrane and
etc.
● Restlessness
● Anxiety
● Low fibrinogen and prolonged
prothrombin and partial
thromboplastin
● Hemorrhage
● Rales
● Acrocyanosis
● Dyspnea
● Oliguria
● Joint pain
ETIOLOGY
● Unknown (but has triggering factors)
● Gram-negative sepsis
● Neoplastic disease
● Massive burns or trauma
● Anaphylaxis
● Chronic disease
THERAPEUTIC INTERVENTIONS
Explanation:
- Cryo is a portion of plasma, it is rich in clotting
factors including fibrinogen, which are proteins
that can reduce blood loss by helping to slow or
stop bleeding. It is done using a whole blood
sample.
The whole blood is then
centrigufe or separates
the RBC from the
plasma. Then the plasma
is also separated from
the platelets. With the
plasma remaining, it will be freeze within 6 to 8
hrs. Then thawed, and be given to the pt within
15-30 mins.
● Transfusion of blood products (fresh
frozen plasma)
NURSING INTERVENTIONS
● Observe for bleeding
● Minimize skin punctures
● Prevent injury
● Provide emotional support
● Semi fowler

● Treat the underlying cause

● Heparin to prevent the formation of
thrombi
● Cryoprecipitate- includes clotting
factors. Should be given to pt within
15-30 mins.