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Platelets

Dr. Noualsalhin Alaagib


Platelets
(Thrombocytes)
are small granulated oval discs
2- 4µm in diameter.
Normal platelet count:
150,000- 300,000 /µL of blood.
Formed in the BM from large cells
known as megakaryocytes,
fragment into the minute platelets.
Platelets
60- 70% of platelets are in the blood,
The remainder are found in the
spleen
Splenectomy → ↑ platelets count
(thrombocytosis)..
Its half life in the blood is 8- 12
days.
Then it is eliminated from the
circulation mainly by the tissue
macrophage system.
Platelets do not have nuclei and
cannot reproduce.
In their cytoplasm are:
(1) contractile proteins: actin, myosin &
thrombosthenin,
that can cause the platelets to contract
(2) residuals of the endoplasmic
reticulum & Golgi apparatus,
that synthesize various enzymes and
store large quantities of Ca2+
(3) mitochondria (forming ATP and ADP)
(4) enzyme systems that synthesize
prostaglandins
(5) Fibrin-stabilizing factor
(6) a growth factor:
that causes vascular endothelium, smooth
muscle and fibroblasts to multiply and grow
→ helps repair damaged vessels.
2 types of granules:
Dense granules:
ADP, serotonin.
α granules:
clotting factors (V, VIII, I), VWB,
PDGF.
VWBF:
 present in blood vessel & platelets
has a role in platelets adhesion,
 regulates circulating levels of factor
VIII
Summary

Questions
Hemostasis
means prevention of blood loss
(stop the bleeding).
Mechanism of Hemostasis
(1) vascular constriction
(2) formation of a platelet plug
(3) formation of a blood clot
(4) growth of fibrous tissue into the clot
& fibrinlysis
I. Local vasoconstriction
Occurs immediately after the injury.
The more severely a vessel is
traumatized, the greater the degree of
vasoconstriction.
Vasoconstriction results from:
(1) local myogenic spasm:
initiated by direct damage to the vascular
wall.
2)Humoral:
platelets release vasoconstrictor substances,
thromboxane A2, serotonin, Catecholamines
from the adrenal medulla.
3) Nervous reflexes:
initiated by pain or other sensory impulses.
Formation of the Platelet Plug
(1) Platelets adhesion:
When a blood vessel is injured, platelets
adhere to the exposed collagen
(2) Platelets activation:
their binding to collagen results in:
1. Release of their granules content
e. g. ADP, thrombin, serotonin.
2. Formation & secretion of thromboxane A2
(TXA2 vasoconstrictor & platelets aggregator)
3. Change in shape (metamrophosis):
swell, put on psudopodia, become sticky.
(3) Platelets aggregation:
ADP, thrombin, TXA2 & PAF activate
more platelets to adhere.
(4) Platelet plug formation:
The first activated platelets (by
adherence to collagen) release
substances which activate other
platelets
(+ve feed back).
Platelet plug stops bleeding of small
holes in small blood vessel.
If not fibrin formation is needed.
A person with few platelets
(thrombocytopenia ) develops
small hemorrhagic areas under the
skin.
Formation of blood clot
Platelet plug is converted to clot by fibrin
formation.
Clotting occurs by activating clotting
factors which in turn activate other clotting
factors.
By 2 pathways:
1. Extrinsic pathway.
2. Intrinsic pathway.
Extrinsic pathway
Extrinsic pathway
Intrinsic Pathway
Intrinsic Pathway
Common Pathway
Hemostasis
Fibrinolytic System
Bleeding Time
If a sharp pin pierces the tip of the
finger or lobe of the ear, bleeding lasts
for 1 - 6 minutes.
Prolonged bleeding time →
lack of platelets.
Or abnormal function of platelets
Clotting Time
A test of clotting factors of the
intrinsic pathway.
Normally < 10 minutes.
If one of the clotting factors is
deficient, the coagulation time is
prolonged.
Prothrombin Time
A test of clotting factors of the
extrinsic pathway.
The normal prothrombin time is
about
12 seconds.
Anticoagulants
Inhibits coagulation in the blood.
Natural anticoagulants:
1. Smoothness of the endothelium.
2. Rapid blood Flow.
Synthetic anticoagulents e. g.
(1) Substances which remove Ca2+ from
the blood:
Oxalate
Citrate
EDTA
(2) Heparin: is antithrombin.
(3) Warfarin:
Inhibits synthesis of vitamin K
dependant factors
(II, VII, IX, X).

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