Nursing Care of Clients with Hematologic Problems Part 2 of 2 : Thrombocytes (Platelets)

P R E P A R E D B Y :

M A R I A C A R M E L A L . D O M O C M A T , R N , M S N

Platelets

Platelets (Thrombocytes)

o Platelets are not complete cells, but fragments of

large cells called megakaryocytes.o very small, colorless cell fragments (2-4 microns in

diameter)

o enclosed in a membrane but have no nucleus and

cannot reproduce

o have mitochondria and enzyme system (enzyme –

needed for synthesis of prostaglandin)

o contains 2 types of granules � alpha ( ά)granules

• express P-selection on their surface:

contains fibrinogen, fibronectin, factors V

and VIII, platelet factor 4 (heparin - binding and VIII, platelet factor 4 (heparin - binding

chemokine), platelet-derived growth factor

(PDGF), transforming growth factor-alpha

(TGF- ά)

� gamma ( δ)granules or dense granules• contain ADP and ATP, ionized calcium,

histamine, epinephrine

o must be adequate in number and

function in order to participate

optimally in hemostasis

o normally circulate as individual o normally circulate as individual

cell -like structure, not attached

to each other, suspended in plasma,

and do not clump together until

activated

Functions

o help to prevent or stop bleeding, a

process called hemostasis

o Initiate contraction of damaged blood

vessels to minimize blood loss

o Form hemostatic plugs in injured blood

vessels to help stop bleeding

o Along with plasma, they provide

materials that accelerate blood clot

formulation, or coagulation

Hematopoiesis: Blood Cell Formation

Formation

� bud off from megakaryocytes � giant multinucleate bone marrow cells derived from the

myeloid stem cell line

� stem cell

� Hemotocytoblast� Hemotocytoblast

� Megakaryoblast

� Promegakaryocyte

� Megakaryocyte � megakaryocyte: large multilobed nucleus

� platelets � platelets: anucleated parts of megakaryocyte cytoplasm

o develop by endomitosis o Formation of platelets involves repeated mitoses

of megakaryocytes without cytokinesis.

� Megakaryocytes undergo mitosis but not

cytokinesis thus cell does not divide cytokinesis thus cell does not divide

into 2 daughter cells • Without cytokinesis – cell does not divide into

2 daughter cells but expands to accommodate the

doubling of its DNA (nuclear) content and

breaks up into fragments known as platelets

�

� Coagulate, form plug, prevent blood loss

� Formed by fragmentation from megakaryoctyes

Blood Components: Platelets

Figure 16-10c: Megakaryocytes and platelets

o newly formed platelets that are

released from bone marrow spend up

to 8 hours in the spleen before

being released into the blood being released into the blood

o Life Span: 10 days

Regulators Of Platelet Production

� includes:• GM-CSF (granulocyte-macrophage colony-

stimulating factor)• Thrombopoietin

o source: kidney, liver, smooth muscle, bone marrow marrow

� production and release is regulated by the number of platelets in circulation

� stimulate committed cells and further stages of differentiation

Destruction (Hemolysis)

o Senescent platelets – phagocytosed

by neutrophils and monocytes if

circulating freely� If part of thrombus or clot - phagocytosed If part of thrombus or clot - phagocytosed

by neutrophils and macrophage

� Can be removed also by tissue macrophages of

the MPS (mononuclear phagocyte system) in

the liver or spleen

�

Hemostasis

Hemostasis

� Refers to the stoppage of bloodflow

• Designed to maintain integrity of

vascular compartment

• Normal• when it seals a blood vessel to prevent blood

loss and hemorrhage

• Abnormal• when it causes inappropriate blood clotting

or when clotting is insufficient to stop the

flow of blood from the vascular compartment

Control of hemostasis

o Endothelium – major site of hemostasis o Despite the continual presence of

clotting factors and platelets in circulation, blood normally remains fluid fluid

o 2 properties of normal vascular endothelium prevent clotting� Smooth texture of endothelial lining� Negative charge of protein in endothelial cells

– which repel some negatively charged platelets if clotting factors

Three hemostatic compartments

Damage to small blood vessels and capillaries

frequently occurs. When these vessels are damaged,

there are 5 basic mechanisms that promote there are 5 basic mechanisms that promote

hemostasis or the stoppage of bleeding

5 stages of Hemostasis

1. Vessel or vascular spasm -

(vasoconstriction at injured site)

2. Formation of the platelet plug

(plugging the hole)

3. Blood coagulation or development of an

insoluble fibrin clot (blood clotting

- complex mechanism)

4. Clot retraction

5. Clot dissolution

5 stages of Hemostasis

1. Vessel or vascular

spasm(vasoconstriction at injured

site)

� (1) Blood Vessel Spasm

• triggered by pain receptors, platelet release, or serotonin

• smooth muscle in vessel contracts

5 stages of Hemostasis

1. Vessel or vascular spasm

2. Formation of the platelet plug

(plugging the hole)

� (2) Platelet Plug Formation

• triggered by exposure of platelets to collagen

• platelets adhere to rough surface to form a plug

Platelet Plug Formation

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Vasoconstriction & Plug Formation

Figure 16-12: Platelet plug formation

5 stages of Hemostasis

1. vascular spasm

2. platelet plug

3. Blood coagulation or development of an

insoluble fibrin clot (blood clotting

- complex mechanism)

� (3) Blood Coagulation

• triggered by cellular damage and blood contact with foreign surfaces

• blood clot forms• blood clot forms

Clot Formation Formation

& Vessel Repair

� Prothrombin

� Ca++

Fibrinogen

Clot Stabilization

� Fibrinogen

� Fibrin

� Polymerization

Blood Coagulation

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Blood Coagulation

Extrinsic Clotting Mechanism• chemical outside of blood triggers blood coagulation• triggered by thromboplastin (not found in blood)• triggered when blood contacts damaged tissue

Intrinsic Clotting Mechanism• chemical inside blood triggers blood coagulation• triggered by Hageman factor (found inside blood)• triggered when blood contacts a foreign surface

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Blood Clots

• After forming, blood clot retracts and pulls the edges of a broken vessel together

• Platelet-derived growth factor stimulates smooth muscle cells and fibroblasts to repair damaged blood vessels

• Plasmin digests blood clots

• thrombus – abnormal blood clot• embolus – blood clot moving through blood

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5 stages of Hemostasis

1. vascular spasm

2. platelet plug

3. Blood coagulation

4. Clot retraction

5. Clot dissolution

5 stages of Hemostasis

1. vascular spasm

2. platelet plug

3. Blood coagulation

4. Clot retraction

5. Clot dissolution

� Bleeding stopped

� Vessel repair

Plasmin

Dissolving the Clot and Anticoagulants

� Plasmin

� Fibrinolysis

� Clot dissolved

Dissolving the Clot and Anticoagulants

Figure 16-14: Coagulation and fibrinolysis

Prevention of Coagulation

• The smooth lining of blood vessels discourages the accumulation of platelets

• As a clot forms, fibrin absorbs thrombin and prevents the reaction from • As a clot forms, fibrin absorbs thrombin and prevents the reaction from spreading

• Antithrombin interferes with the action of excess thrombin

• Some cells secrete heparin

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� Hemophilia

� Cardiovascular Diseases

� Key problem – clots block undamaged blood vessels

� Anticoagulants prevent coagulation

Coagulation and Disease

� Keep platelets from adhering

� Prevent fibrin coagulation

� "Clot Busters": Prevent further clotting

� Speed fibrinolysis

� Limit tissue damage (heart, brain…)

Factor Function Coagulation disorders in children Incidence

I: Fibrinogen Afibrinogenemia, hypofibrinogenemia

0.1 x 106

II: Prothrombin Hypoprothrombinemia 0.1 x 106

III: Tissue thromboplastin

IV: Calcium divalent cation; a cofactor for most of the enzyme-activated processes required in blood coagulation; enhances platelet aggregation and makes RBCs clump together

V: Proaccelerin Parahemophilia, Factor V deficiency

0.1 x 106

VI: discovered to be an artifact

No factor VI is involved in coagulation -

VII: Proconvertin Factor VII deficiency 0.1 x 106

VIII: Anithemophilic combined with von Willebrands factor help platelets adhere to capillary walls in areas of tissue injury

Hemophilia A, von Willebrand disease

30-40 x 106

IX: Plasma thromboplastin component (Christmas factor

essential in common pathway between intrinsic and extrinsic clotting cascades

Hemophilia B 3-4 x 106

X: Stuart-Power factor Factor X deficiency 0.1 x 106

XI: Plasma thromboplastin antecedent (PTA)

Hemophilia C, PTA deficiency 0.1 x 106

XII Hageman factor critically important in intrinsic pathway Hageman trait 0.1 x 106

XIII Fibrin-stabilizing factor

assist in forming links among fibrin threads to form a strong fibrin clot

Factor XIII deficiency 0.1 x 106

Laboratory tests

Peripheral blood smear

� platelet count

� bleeding time

� PT (extrinsic pathway)

� activated thromboplastin time (intrinsic pathway),� activated thromboplastin time (intrinsic pathway),

� thrombin time

Disorders of Hemostasis

Two main categories of disorders of hemostasis

1. Inappropriate formation of clots

within the vascular system (i.e.,

thrombosis)

2. Failure of blood to clot in 2. Failure of blood to clot in

response to an inappropriate

stimulus (i.e., bleeding)

Impaired hemostasis

� Vitamin K deficiency

� Liver disease

Thromboembolic Disorders

� undesirable clottinga. thrombus

b. embolus

Clotting Disorders

�Coagulation disorders result from

defects in the clotting cascade or

fibrinolytic process. These

disorders may be inherited or disorders may be inherited or

acquireda. Hemophilias

b. Von Willebrand disease

c. Disseminated intravascular coagulation

(DIC)

Quantitative platelet disorders

a. Thrombocythemia

b. Thrombocytopenia

Petechiae and purpura

Large ecchymosis

Thrombus / embolus

Embolus /embolism

Hemarthrosis

MelenaMelenaHematuriaHematuria

Subdural Subdural SubungualSubungual

Hematoma