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8/29/2017

Hematology:
Essentials of Hematology The study of blood and blood
forming tissues (bone marrow, blood, spleen
and lymph system)
Clinical Relevance
Essential blood components are
Gail L. Lupica PhD, RN, CNE necessary for clot formation (pharm to
Nursing 211 reverse that process).
oxygenation
immune function
transport

WHOLE BLOOD
Plasma- 55% -proteins 6%-
albumins
>>>
globulins
fibrinogin

Water- 92% of plasma


other solutes 2%

Formed elements- PLTS


45% LEUKOCYTES (WBCs)
ERYTROCYTES

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Three Types of Formed Elements


Three types of blood cells:
Erythrocytes (RBCs)
Leukocytes (WBCs)
Thrombocytes (PLTs)

bone marrow suppression


Affects
1. RBC
production(erythrocyte)
2. WBC production
3. PLT production

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LETS TALK ABOUT ERYTHROCYTES


(RBCs)_
Disc shape
Flexible
Live 120 days
Produce Hgb
Heme component needs Fe to carry 4
O2 molecules

Erythrocytes:
Hemoglobin is the oxygen carrying
component (protein) of the erythrocyte.
It makes up 90% of the cells weight.
A single erythrocyte can carry 300
hemoglobin molecules, which pick up O2
from the lungs, carry it to the tissues and
exchange it for the by-product of cellular
metabolism = WHATS THAT???
Hgb gives blood its red color.

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Clinical Relevance-
Administering packed red blood cells
(PRBCs) is giving the patient only the
erythrocyte portion of the blood for its O2
carrying capacity.
Each heme site, is produced and bound
with Ferrous Iron.(Fe +2) An Fe deficient
diet disenables these cells to bind to Fe and
the pt is ANEMIC!! WHAT KIND OF
ANEMIA IS THIS?????

Clinical Relevance-
Clinical Relevance-
CO (carbon monoxide) competes with The hormone, erythropoietin,
the O2 on the on the Heme molecule. prompts the bone marrow to form a
The affinity of CO is 200x greater Red blood cell according to demands
than O2. THIS WOULD RESULT of the body, from an immature cell.
IN???? In fact, WBCs and platelets also develop
from that same immature stem cell
WHICH PATIENTS HAVE BEEN according to demands.
EXPOSED TO CO???

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Lets Talk about Leukocytes =


Clinical Relevance
White Blood Cells (WBCs)
Erythropoietin is Theyre white.
secreted by the kidney. Theres five different kinds
Patients in end stage with very variable life spans.
renal disease are terribly (Well talk about that more in
anemic!! the immune unit.)

Contd Types of WBCs contd


Five types of WBC: 4. Lymphocytes: 20-40% of all
1. Neutrophil: most common, accounts WBCs, t-lymphocytes (cell
for 50-70% of all WBCs. They are a key mediated) and B-lymphocytes
player in the immune response (humoral immunity) form the
responsible for phagocytosis in an basis of the immune response.
acute inflammatory response. EVER
5. Monocytes: 4-8% of all WBCs. They are
HEARD OF NEUTROPENIC phagocytes.
PRECAUTIONS???
2. Eosinophils:2-4% of WBCs with some ability for
phagocytosis
3. Basophils: < 2% of WBCs

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Thrombocytes = Platelets
Platelets that initiate the clotting process.
Platelet plugs are initiated at the site of
any break of capillary integrity.
1. WHAT HAPPENS IF THEYRE TOO MANY???
2. WHAT HAPPENS IF THEYRE TOO FEW??
WHATS THE NORMAL PLT RANGE???

The Spleen
Lets look at some more Removes old RBCs from the circulation
Helps to Makes RBCs (Returns the iron
structures and functions of component of hemoglobin to the bone
the hematologic system: marrow for reuse)
Filters circulating bacteria with its rich
supply of lympocytes, monocytes and
explain their
and immunoglobins
Stores RBCs and PLTS
importance -WHAT WOULD HAPPEN IF YOUR SPLEEN
ENLARGED??? = SPLENOMEGALY

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The Livers Role PLT aggregation


Platelets clump and are attracted to
manufactures prothrombin (and other clotting factors).
manufactures albumin
each other when activated.
manufactures bile which is critical to the absorption of Platelet plugs begin the blood
fat soluble vitamins like vitamin K (A,E,D).
Vitamin K in turn. produces blood clotting factors Vll,
clotting cascade.
lX, X) Substances that activate PLT
The liver converts bilirubin to bile and stores large
quantities of blood and extra iron.
activation include ADP, Ca+,
thromboxane A2 (TXA2), and
collagen.
These substances may come from the
PLT or from the endothelial lining.

THE DRUGS YOU NEED TO


KNOW!!!!!!
1. ASPIRIN- inhibits an enzyme needed
by PLTS to synthesize TXA2.

1. PLAVIX- blocks binding of ADP to the


PLT ADP receptor site.
2. TICLID- blocks binding of fibrinogen to the GP 11b/11a
receptor on the PLT surface. (Called GP 11b/11a
receptor antagonists)
3. PERSANTINE- same

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So, They dont let PLTS


aggregate!! Anti-platelet drugs

Helps prevent platelet


plugs (which is the
foundation for a fibrin
clot) the arteries.

What diseases do they prevent?

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The Blood Clotting Cascade The Blood Clotting Cascade


The blood clotting cascade is No matter what started the cascade,
triggered by a PLT plug. the end result is the same, A FIBRIN
Its result of either an intrinsic factor CLOT. .IS THIS GOOD OR
(from the blood itselftoxins, debris, BAD?????????
Ag-Ab) or an extrinsic factor (from
trauma to the blood vessel lining)
Different clotting factors are involved
along the way and the two pathways
join a common clotting pathway.

Red blood cells (erythrocytes) trapped in a mesh of fibrin


Intrinsic-Extrinsic> common threads. Fibrin, is an essential component of blood clots.

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Anticoagulant Medications
Inhibit clot formation in the venous
system.
They do not dissolve but inhibit new
clot formation and inhibit growth of
existing clots.
What would dissolve a clot???
Thrombus arising in valve pocket at
upper end of superficial femoral vein

Fibrinolysis. Blue arrows = stimulation,


red arrows = inhibition.

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THE DRUGS YOU NEED TO


KNOW!!!!!! MEMORIZE
Heparin- inhibits the conversion of Hgb 12-16
fibrinogen to fibrin. 14-18g/dl
LMWHLOVENOX Hct 37-47
Have more stable responses at recommended doses so
get less risk of bleeding without needing to check PTT. 42-52%
Coumadin - Prevents the hepatic WBC 5-10,000 /uL
synthesis of Vitamin K dependent PLT 150-400,000
clotting factors.(Vitamin K is a
Prothrombin activator)

ANEMIA- ANEMIAS well look at:


Anemia is the reduction in either Sickle cell anemia
the number of red blood cells, or Iron deficiency anemia
the amount of Hgb, or Hct
B12 deficiency anemia
Anemia is not a specific Aplastic anemia
disease but a Polycythemia vera

manifestation of one of
several abnormal
conditions.

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Sickle cell anemia

Genetic disorder
Abnormal Hgb chains
react to lower oxygen states,
change their shape and pile together.
block blood flow causing even more
hypoxia to the tissues.

Sickle cell anemia

What triggers the sickling???---


dehydration, infections, strenuous exercise,
stress!!
Sequelae??-- Pain, disability, organ
damage, increased risk for infection, and
early death ensues.
Why is this pt in pain???
Why do the organs damage???
Why are they at risk for infection???

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QUESTION
A patient with sickle cell disease is
admitted with a diagnosis of Left arm
fracture. Which nursing intervention
would be the most helpful to prevent
vasocclusive pain?
1. Holding IV fluids until pain subsides
2. Administering pain medication every 3-4
hours as ordered
3. Administer po pain medication every 3-4
hours and IV meds for breakthrough pain
4. Administering IV fluids at an ordered rate of
200 ml/hr

Iron Deficiency Anemia QUESTION


This common type of anemia can 3. The nurse caring for a patient with iron
result from blood loss, or deficiency has performed dietary teaching
inadequate diet. of foods high in iron. The nurse
recognizes that teaching has been
Evaluate adult patients for effective when the patient selects which
abnormal bleeding. meal plan?
Supplemental iron is the treatment. 1. Hamburger, cottage cheese, and tomato
slices and coffee
2. Sliced veal, spinach salad with mandarine
orange slices
3. Vegetable lasagna, Caesar salad, toast
4. Bacon, lettuce, and tomato sandwich, potato
chips, and tea

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Vitamin B12 Deficiency Anemia


(pernicious anemia)
B12 is necessary to
Pernicious anemia
move folic acid into
is caused by failure
the cell where DNA
to absorb vitamin
synthesis occurs and
b12.
RBC production can
take place. Intrinsic factor is
B12 deficiency secreted by the
reduces folic acid gastric mucosa & is
transport, inhibiting needed to absorb
DNA synthesis. B12.

QUESTION
5. Which clinical manifestation, noted in
a patient with pernicious anemia,
would indicate that the patient has
been noncompliant with B12 injections?
1. Weight gain of 10 pounds in one month
2. Weight gain of 5 pounds in one week
B12 deficiency 3. Paresthesia of hands and feet
Glossitis, a smooth tongue as a result of vitamin B12
deficiency anemia
4. Complaints of constipation

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Aplastic Anemia Polycythemia Vera


Deficiency of circulating red blood cells A sustained increase > production
Failure of Bone marrow.
in blood hemoglobin/RBCs
Occurs because of injury to precursor cell-long
term exposure to toxic agents, ionizing Excessive leukocyte production
radiation, or infection ..HTN, thrombosis, K+
Usually occurs with leukopenia and Treat: Phlebotomy
thrombocytopenia
Pancytopenia common
Treat: Increased hydration
Splenectomy may be performed Treat: Anticoagulants/antiplatelet
NURSING DIAGNOSES Nursing Diagnoses

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