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Nursing Care of Clients with Hematologic Problems Part 2 of 2 : Thrombocytes (Platelets)
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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
14-28
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
14-29
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
14-30
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
14-31
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
14-32
� 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