Production of Platelet Counts

Platelet
 Also known as Thrombocytes

 They are unique
❑ Non-nucleated cell, Biconvex or Discoid, ave.
diameter (2.5 um)
❑ FUNCTIONS:
❖ Promote blood clotting
❖ Help repair minor tears or leaks in the walls
of blood vessels
❖ Prevents loss of blood from the vasculature
❑ Lifespan: 10 Days
❑ 1/3 of platelets are found in the circulation / blood
❑ 2/3 of platelets are sequestered in the Spleen
❑ Normal Platelet Count: 150,000 – 400,000/ul
Less than 150, 000 platelet = there is greater tendency that the
patient will suffer from bleeding /blood loss
Greater than 400, 000 or increase platelet count=
thrombocytosis and can form clotting
Splenectomy – surgical removal of spleen
If the patient undergo splenectomy, the Platelet will remain in our blood and then the result would be, increase
of platelet count.
Splenomegaly – enlargement of spleen
If the patient spleen enlarge, the platelet will more likely go to our spleen causing now decrease platelet count in
our blood.
PRODUCTION OF PLATELET COUNTS

Megakaryocytopoiesis
❑ AKA Thrombopoiesis
❑ Common Myeloid Progenitor → CFU-Meg → Precursor
cells (Megakaryoblast → Promegakaryocyte →
Megakaryocyte → Platelets
❑ Thrombopoietin:
❖ Mitogen/ CSF(colony - stimulating factor) for megakaryocyte
maturation and differentiation
❖ Produced from the Kidney and Liver
Precursor/ Megakaryocyte will now mature to platelet but it will only

shed-off the platelet. Platelet is comes from the structure of
platelet.
While RBC/WBC mature in Precursor
Stages of Maturation
Features MK-1 MK-II MK-III Metamegakar
yocyte
Megakaryo Promegakary Megakary
blast ocyte ocyte
% of pre- 20% 25 55
cursors
Nucleus Round Indented Multilobed
Chromati Homogeno Moderately Deeply
n us Condensed and
variably
condense
d
No. of 1 Double 2 or more 4 or more
Nucleus
Nucleolu 2-6 variable Not visible
s
N:C ratio 3:1 1:2 1:4
Endomit Present Present but absent
osis ends here
Cytoplas basophilic Basophilic Azurophili
m and granular c and
granular
Cytoplas few numerous aggregated
mic absent
granule
Cytoplas present present absent absent
mic tags
Alpha present present Present
and
dense
Demarca Present(st present present
tion art)
system
Platelets No no yes yes
Visible
Megakaryocyte – largest cell in bone marrow

Monocyte – largest cell in peripheral
MK-1 to MK-III can be seen in bone marrow and when they shed-
off that’s the only time platelets is produced
❑ Endomitosis:
❖ DNA Replication without cytoplasmic
division
There is nuclear division without cytoplasmic division
❑ Demarcation Membrane System
❖ Invagination of the plasma membrane
that becomes the future site of platelet
fragmentation
❑ Thrombocytopoiesis
❖ Platelet shedding from megakaryocyte
proplatelet
❑ 1 Megakaryocyte= 2,000 – 4,000 platelets
Platelets composed of :
❖ Chromomere (located centrally)
❖ Hyalomere (surrounds the chromomere)
❑ Alpha Granules:
❖ Plt factor 4; B-Thromboglobulin, PDGF(Platelet derived growth
factor),
❖ Thrombospondin, VWF (Von Willbrand Factor), Fibrinogen,
❖ Fibronectin, Factor V
❑ Dense Granules: Mnemonics : CAPAS

❖ Ca, ATP, Pyrophosphate, ADP, Serotonin
❑ Lysosomal Granules:
❖ Acid Phosphatase, Hydrolytic enzymes
RBC and Platelet- non-nucleated
WBC- nucleated
Function of Platelet:
Hemostasis- to prevent blood loss
Primary Hemostasis
 Role of blood vessel and platelets in response to vascular
injury/ process of preventing blood loss
 Responsible are platelet and blood vessel
 Product: produce platelet plug
Responses:
1. Vasoconstriction: Injury- smooth muscle contract, the vascular
lumen closes/narrow- decrease blood flow
-thromboxane A2, Serotonin, Epinephrine induce
vasoconstriction
For example, may sugat sa blood vessel, our body will do
vasoconstriction, the lumen of our body will become smaller to
decrease the blood flow
2. Platelet adhesion
 Platelets bind to non-platelet surfaces such as
subendothelium(collagen, Fibronectin)
 Von Willerbrand Factor: Synthesize in megakaryocyte and
endothelial cell (Weibel-Palade Bodies)
-VWF links platelet through (GP IB/IX/V receptor) to
endothelial bindingsite/collagen
Diseases:
-Von Willbrand Disease: lacks/abnormal VWF – impaired
Plt adhesion
-Bernard Soulier Syndrome: platelets lack GP IB/IX/V
receptor – impaired Plt adhesion(Giant Plt Syndrome)
Platelet will didikit sa ating sub endothelial tissue sa wound natin. GP
Ib/IX/V will bind to collagen through Von Willerbrand Factor. The
platelet will only adhere in our sugar
3. Platelet activation
 Morphologic and functional change in platelets
4. Platelet Secretion
 Platelet changes to disk shape to spherical shape to
granules to open canalicular system secretion
 Masesecrete yung mga granules
Alpha Granules(most numerous)
 Platelet factor 4 / B-thromboglobulin / Platelet-derived
growth factor(PDGF)
 Thrombospondin/ VWF / Fibrinogen / Fibronectin / Factor V
Dense Granules
 Calcium / ATP / Pyrophosphate / ADP / Serotonin
Promote Promote Vasoconstri Vascular Inhibits

Coagulati Aggregation ction Repair heparin
on  ADP,  Seroto  PDGF  B-
 HM Calcium, nin  B- thrombo
WK, PF 4,  Throm thrombo globulin
Fibri Thromb boxan globulin  Plt
noge ospondi e A2 Factor 4
n, n
Fact
or V,
VIII:
VwF
5. Platelet aggregation: platelets bind to one another

 Finrinogen binds to GP IIb/IIIa receptor on adjacent
platelets and joins them together plus ionized calcium
 In vitro: Platelet agonists which induce aggregation:
(Thrombin , Collagen, ADP, Epinephrine, Ristocetin)
 Glanzmann’s Throbasthemia: lacks GP IIb/IIIa to impaired
plt aggregation
 Afibrogenemia: No fibrinogen that’s why you have impaired
plt aggregation
 Platelet binds to one another to have platelet plug and to
stop the bleeding. It happens by fibrinogen binding GP
IIb/IIIa receptor on adjacent platelets and joins them
together plus ionized calcium
 For example, GP IIb/IIIa receptor is our platelet 1. So the
GP IIb/IIIa receptor will bind now to our fibrinogen of platelet
II.
6. Platelet Plug Formation: Final Product of primary hemostasis
Secondary Hemostasis – coagulation factors

Product: produce fibrin clot(it will make the platelet clot stronger)
Fibrinolysis – because of plasmin
Removal of fibrin clot
For example, you have scar/sugat, so our body will stop the bleeding
by doing primary and secondary hemostasis. It will form clot then if
the clot is okay, natatangal siya because of fibrinolysis.
Platelet plug formation will enhance by secondary hemostasis and
these secondary hemostasis will form stable clit which is the fibrin
clot.It will enhance to stop the bleeding. Next, fibrinolysis will
removed the clot once it the blood vessel is healed.
Skeletal Muscle Cardiac Muscle Smooth Muscle
Action Voluntary Involuntary Involuntary
Fibers Single Aligned cells in Single small,
Multinucleated branching closely packed
cells arrangement fusiform cells
Cell/Fiber Cylindrical, 10- Cylindrical, 10- Fusiform,
shape and size 100 um 20 um diameter 0.2-10
diameter, many diameter, 50- um
cm long 100 um long
Striations Present Present Absent
Location of Peripheral, Central Central, at
nuclei adjacent to widest part of
sarcolemma cell
T tubules Center of triads In diads at z Absent:
at A-1 junctions discs Caveole may
be functionally
similar
Sarcoplasmic Well-developed Less well- Irregular
reticulum(SR) , with two developed, one smooth ER
terminal small terminal without
cisterns per cistern per distinctive
sarcomere in sarcomere in organization
triads with T diad with T
tubule tubule
Special Very well- Intercalated Gap junctions,
structural organized discs joining caveolae,
features sarcomeres cell, with many dense bodies
SR, and adherent and
transverse gap junctions
tubule system

Production of Platelet Counts

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Production of Platelet Counts

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Platelet

 Also known as Thrombocytes

Splenectomy – surgical removal of spleen

Splenomegaly – enlargement of spleen

PRODUCTION OF PLATELET COUNTS

Precursor/ Megakaryocyte will now mature to platelet but it will only

Megakaryocyte – largest cell in bone marrow

❑ Dense Granules: Mnemonics : CAPAS

Promote Promote Vasoconstri Vascular Inhibits

5. Platelet aggregation: platelets bind to one another

Secondary Hemostasis – coagulation factors

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