Platelets

PLATELETS
DR.A.KUMAR
1-YEAR PG STUDENT

BLOOD
DEFINITION:
Blood is a fluid connective tissue
which transports substances from one part of the
body to another.It provides nutrients and
hormones to the tissues and removes their waste
products

COMPOSITION
1.Red blood cells (erythrocytes)
2.White blood cells (leukocytes)
3.Platelets (thrombocytes)
4.Plasma proteins

SIZE COMPARISON
7.5micron 2-4micron 10-14

INDEX-PLATELETS
INTRODUCTION
STRUCTURE & COMPOSITION
1.Cell membrane
2.Microtubule
3.Cytoplasm
FORMATION OF PLATELETS
HEMOSTASIS
11..VVaassccuullaarr CCoonnssttrriiccttiioonn
22..FFoorrmmaattiioonn ooff PPllaatteelleett PPlluugg
3.Blood coagulation
44..FFiibbrriinnoollyyssiiss
Thrombocytosis
Thrombocytopenia
HEMOSTATIC FUNCTION TESTS
DENTAL COSIDERATION

INTRODUCTION
small
granulated
Non-nucleated
round or oval
2 – 4 μ in diameter
1,50,000 – 3,50,000/mm³
life span average 8 days

Resting platelets
Activated platelets

Scanning electron micrographs of different stages of
platelet adhesion
Resting platelet (left, x10,000);
Attached platelet showing shape change and pseudopodia
emission (center, x3,000);
Spread platelet (right, x3,000).
Copyright © 2003-2014 Platelet Research Laboratory

STRUCTURE
• 1.Cell membrane
• 2.Microtubule
• 3.Cytoplasm

1.Cell Membrane
It is 6 nm thick and contain
Carbohydrates(glycocalyx),
Proteins (Glycoproteins)
lipids (phospholipids, cholesterol
and glycolipids)
Out of all glycoprotein and phospholipids
are functionally important

plasma membrane contains
glycoprotein receptors
For Phospholipids
Include
• collagen
• fibrinogen
• vessel von-Willebrand factor
• platelet factor 3

Glycopropteins
• Prevents the adherence of platelets to
normal endothelium.
• Accelerates the adherence of platelets
to collagen and damaged endothelium
in ruptured blood vessels.
• Forms a receptor for ADP and
thrombin.

2.Microtubule
• Made up of tublins (proteins)
• It responsible for the discoid shape of the
platelets

3.Cytoplasm
• Contractile proteins
• Golgi apparatus
• Endoplasmic reticulum
• Mitochondria
• Lyzosomes
• Glycogen granules
• Enzymes
• Chemical substances
• Granules

Contractile proteins
actin thrombosthenin myosin
enable activated platelets to change
their shape

Residuals of
endoplasmic reticulum Golgi apparatus
Synthesis
of enzymes
Calcium
store
Mitochondria and enzyme system for synthesis of
ATP and ADP

Lyzosomes containing hydrolytic enzymes.
Glycogen granules for production of energy
anaerobically.
Enzyme system that synthesize prostaglandins
from phospholipids of the Platelet membrane.

Chemical substances:
• Calcium ions
• Mg- ions.
• Adenosine triphosphate (ATP)
• Adenosine diphosphate (ADP)

Types of granules
A) Dense granules b) Alpha granules
contain non-protein
substances
( ATP, ADP, Ca++
and serotonin)
contain the secreted
proteins
• clotting factors
• fibrin stabilizing
factor XIII
• platelet derived
growth factor

INDEX
INTRODUCTION
1.Cell membrane
2.Microtubule
3.Cytoplasm
HEMOSTASIS
3.Blood coagulation
Thrombocytosis
Thrombocytopenia
DENTAL COSIDERATION

FORMATION
OF PLATELETS
(Thrombopoises
)

FORMATION OF
PLATELETS(Thrombopoises)
• Megakaryoblast :
• Large,oval,kidney shaped nucleus
• 20-30 micron diameter
• Megakaryocyte:
• Multi lobed (4-16) nucleus
• Cell marigin shows pseudopodias
• Platelets formed from pseudopodias of the megakaryocyte
• Each megakaryocyte forms upto 4000 platelets
• Formation of platelets from stem cells takes 10 days

HEMOSTASIS
• DEFINITION
- Heme = blood
- stasis = to halt
It is the process of forming clots in the wall of
damaged blood vessels & preventing blood loss
while maintaining blood in a fluid state with in
the vascular system.

SSttaaggeess ooff HHeemmoossttaassiiss
FFiibbrriinnoollyyssiiss
VVaassccuullaarr CCoonnssttrriiccttiioonn
FFoorrmmaattiioonn ooff PPllaatteelleett PPlluugg
Blood coagulation

VVaassccuullaarr CCoonnssttrriiccttiioonn

It is the first response to injury.
It reduces the amount of blood flow in
damaged areas and limits the amount of blood
loss.
These response is triggered by some chemicals
released by endothelial cells(endothelin) and
platlets (5HT and other vasoconstrictors)

FFoorrmmaattiioonn ooff PPllaatteelleett PPlluugg
• PPllaatteelleett AAddhheessiioonn
• PPllaatteelleett AAccttiivvaattiioonn
• PPllaatteelleett AAggggrreeggaattiioonn

PPllaatteelleett AAddhheessiioonn
Following VVaassccuullaarr CCoonnssttrriiccttiioonn ppllaattlleettss bbeeccoommee
ssttiicckkeeyy aanndd aaddhheerree ttoo tthhee ccoollllaaggeenn mmaattrriixx iinn ssuubb
eennddootthheelliiuumm

PPllaatteelleett AAccttiivvaattiioonn
After platelets adhere to the collagen fibers it
become spiked and much stickier.
Platelets released large quanity of ADP and
thromboxane A2 from its storage granules
These chemicals are attracts the nearby platlets

PPllaatteelleett AAggggrreeggaattiioonn
Large number of activated platlets stick to each other and
forming platelet aggregation or platelet plug.
Platelet plug is fairly loose but it successful in blocking the
blood loss
That’s why its called temporary haemostatic plug

BLOOD COAGULATION
SECONDARY HAEMOSTASIS
DEFINITION:
Blood remains in fluid condition
within the blood vessels through out life.but
when the blood is shed from the blood vessels or
collected in a container,it looses it fluidity within
a few minutes and gets converted into jelly-like
mass,which is called” clot”.This phenomenon is
called coagulation.

CLOTTING FACTORS
Factor I Fibrinogen
Factor II Prothrombin
Factor III Thromboplastin
Factor IV Calcium
Factor V Labile factor, or proaccelerin
Factor VI Non – existent
Factor VII Stable factor or proconvertin
Factor VIII Antihaemophilic factor / globulin A
Factor IX Christmas factor or Antihaemophilic factor B
Factor X Stuart – Prower factor
Factor XI Plasma thromboplastin antecedent or
Antihaemophilic factor C
Factor XII Hageman factor or Contact factor
Factor XIII Fibrin stabilizing factor or Laki – Lorand factor

MNEMONICS
Foolish People Try Climbing Long Slopes
After Christmas Some People Have Fallen

MECHANISM OF COAGULATION
The process of coagulation involves cascade of
reactions
Activation of one factor leads to activation of next
clotting factor
This enzyme cascade reaction is also called
“WATER FALL SEQUECE”

STEPS IN COAGULATION
Three main steps:
 Formation of prothrombin activator
Conversion of prothrombin to thrombin
Conversion of fibrinogen to fibrin

Formation of prothrombin activator
Intrinsic pathway Extrinsic pathway

Conversion of prothrombin to
thrombin
Prothrombin activator
Prothrombin Thrombin
Ca2+
This process is caused by the prothrombin
activator in the precence of ca2+ .
This occurs at the surface of platelets which
form the platelet plug at the site of injury.

Conversion of fibrinogen to fibrin
It involves 3 reactions
Proteolysis
Polymerization
Stabilization of fibrin polymers

Soluble fibrinogen
Proteolysis
Fibrin monomer
Polymerization
Fibrin polymer
(Soluble fibrin clot)
Stabilization of polymer
Insoluble fibrin clot

In this stage formation of covalent crosslinkages
between fibrin threads.
It adds tremendous strength to the fibrin
meshwork.
This insoluble fibrin meshwork traps the
remaining components of plasma and blood cells
to form a solid mass called clot

BLOOD CLOT RETRACTION
Within a few minutes after a clot is
formed it begins to contract
Platelets are essential for clot retraction
The contractile proteins
(actin,myosin,thrombosthenin) present in
the cytoplasm of platelets causing strong
contraction.

Why circulating blood does not
clot?
Endothelial surface factor
-smoothness
-layer of glycocalyx
-Negatively charged
Velocity of circulation
Natural anticoagulants
Activation of Fibrinolytic system
Liver removes activated clotting factors

FIBRINOLYSIS
It is a process that prevents blood clots from
growing and becoming problematic.
In fibrinolysis,a fibrin clot,the product of
coagulation ,is broken down.
Its main enzyme plasmin cuts the fibrin mesh at
various places

me Fibrinolytic mecchhaanniissmm
As soon as clot develops,another series of events take place
locally.
Plasminogen adsorbed on the clot
Plasmin
Breaks down fibrin threads
Fibrin threads are engulfed by reticulo -endothelial
system

Factors aaffffeeccttiinngg ccooaagguullaattiioonn
 Role of vitamin k – required for the synthesis of prothrombin,
VII,IX and X by the liver. Hence these factors are called vitamin
k dependent pro-coagulants.
 Role of liver – liver synthesizes pro-coagulants like
prothrombin, fibrinogen,factors V,VII IX,X XI.
 Role of blood vessels – releases substances like plasminogen
activators, tissue factors, von -willebrand factor.
 Role of von- willebrand factor – acts as a bridge between
denuded vascular endothelium and platelets.
Also acts as a carrier of factor VIII.

IInnhhiibbiittoorrss ooff ccooaagguullaattiioonn

HEMOSTATIC BALANCE
Anticoagulant Coagulant
Eg: Heparin, Antithrombin Eg: Fibrin
Thrombin
Excessive:Hemophilia Excessive:Thrombosis
TEAM GENESIS

Thrombocytosis or thrombocythemia is the
presence of high platelet count in the
blood.
(leads to arteriosclerosis and
atherosclerosis)
· Reactive
oTumors, inflammation, hemolysis,
splenectomy
· Autonomous
oMyeloproliferative disorder (PRV,
CML)
Thrombocytosis

THROMBOCYTOPENIA
• Defined as reduced in the platelet count< 150, 000μL
• It characterized by spontaneous bleeding, a prolonged bleeding time,
and a normal PT and PTT.
• The risk of bleeding depends on the level of the platelet count:
Mild
thrombocytope
nia (platelet
<150 000
cells/μL)
Moderate
thrombocytopen
ia (platelet 20
000 - 50 000
cells/μL)
Severe
thrombocytope
nia (platelet
<20 000
cells/μL)

•Thrombocytopenia
¯ in platelets production
oBM problem
 aplastic anemia, acute leukemia, megaloblastic
anemia
oDisorder in distribution
 Hyperspleenism: more than 1/3 sequestered in
spleen
 destruction
 CLL, SLE
 Autoimmune Thrombocytopenia Purpura (ITP)
 Acute: children with virus (CMV, hepatitis,
rubella)
 Chronic: adult women with SLE
oDisseminated intravascular coagulation (DIC)
oVasculitis
oDrugs: quinine, sulfa drugs,

Sign and symptoms
• bruising, petechiae, purpura and mucosal
bleeding (epistaxis @ gum bleeding)
• major haemorrhage like severe GI bleeding,
intracranial bleeding or haematuria.
• normal platelet count may present in platelet
dysfunction

METHOD OF STUDY
• HEMOSTATIC FUNCTION TESTS
Bleeding time
Clotting time (Thrombin time)
Prothrombin time
Partial thromboplastin time (PTT)
-

What is the clinical significance of
doing BT & CT ?
1. History of frequent, persistent or
spontaneous bleeding
2.Before every minor and major surgery
-(e.g. tooth extraction)
3.Before taking biopsy
-( bone marrow, liver, kidney etc.)
4.Before and during anticoagulant therapy
5.Family history of bleeding disorder
80

BLEEDING TIME (B.T)
Definition ;
- time interval between the skin puncture and spontaneous ,
unassisted stoppage of bleeding.
Method ; “Duke’s method”,
Other methods ; “ivy” Bleeding time
Apparatus Required ;
- sterile finger prick, clean filter paper, stop watch.
Normal bleeding time ; 1 – 5 min.
81

Duke Method
With the Duke method, the patient is pricked with a special
needle or lancet, preferably on the earlobe or fingertip.
The prick is about 3–4 mm deep. The patient then wipes the
blood every 30 seconds with a filter paper.

CLOTTING TIME ( C.T )
Definition ;
- time interval between entry of blood into
glass capillary tube, and formation of fibrin
threads.
Method ; Wright’s capillary glass tube
Other Methods ; Duke’s Drop method, Lee and
White test-tube method
Normal Clotting Time ; 3 – 6 min.
83

PROTHROMBIN TIME (P.T)
Normal P.T ; 15 – 20 sec.
Clinical Significance ; bleeding tendency occurs
below 20% (Normal plasma prothrombin = 30- 40
mg/dl)
Low prothrombin suggest Vit. K def. and liver and
biliary diseases.
Prolonged suggests deficiency of factor II, V, VII, and
X.
84

Partial thromboplastin time (PTT)
Partial thromboplastin time (PTT) is a blood
test that looks at how long it takes for blood to
clot. It can help tell if you have bleeding or
clotting problems.
The lab specialist will add chemicals to the
blood sample and see how many seconds it
takes for the blood to clot.
Normal value-25-35 sec

DENTAL COSIDERATION
Assessment
Take accurate, comprehensive histories: personal, medical,
dental, and pharmacological. Perform a thorough extra and
intraoral examination to identify lesions indicative of a
bleeding disorder.
History: History of extraction, personal or family history of
blood dyscrasia.
General examination: Look for signs of shock and manage
appropriately if present
Specific examination of the mouth

Types of post extraction
haemorrhage
Immediate haemorrhage at the time of extraction
Reactionary haemorrhage, usually two to three
hours post extraction due to wearing off of the
vasoconstrictor effect of the local anaesthetic
Secondary haemorrhage may occur at any time
within the first week and is always indicative of
infection

Management
Identify where the bleeding is coming from.
From soft tissue: The bleeding stops following digital pressure
using one finger on each side of the bleeding socket and biting
on a rolled up gauze swab moistened with saline or water.
Bleeding from the soft tissues is usually arrested by placing a
horizontal mattress suture across the socket.
From the base of the socket, from bone: The bleeding
continues following digital pressure and biting on a gauze
swab.
Bleeding from the base of the socket, from bone, is usually
arrested using a pack such as 'Surgicel' or in some instances
soaking ribbon gauze in Whitehead's varnish and packing the
socket full.

Bleeding from a vessel; The bleeding is more
profound from within the socket or from a nearby
vessel
Bleeding from a vessel. Within bone this may be
arrested using packs as outlined above. However, if
the vessel is within soft tissues there is a need to
identify the vessel and either cauterise or ligate the
vessel. This may in some instance necessitate a small
flap procedure to identify the site of the vessel

Dental management of patients
with haemophilia

END
INTRODUCTION
1.Cell membrane
2.Microtubule
3.Cytoplasm
HEMOSTASIS
3.Blood coagulation
Thrombocytosis
Thrombocytopenia
DENTAL COSIDERATION

RReeffeerreenncceess--11
BOOKS:
1.Textbook of medical physiology- Guyten & hall
2. Textbook of medical physiology-R.B.
Chaudhary
3.Text book of human physiology for dental
students-Indu khurana

ARTICLES:
1.Rafique S1, Fiske J, Palmer G, Daly B. Special care dentistry:
part 1. Dental management of patients with inherited bleeding
disorders. Dent Update. 2013 Oct;40(8):613-6, 619-22, 625-6
passim.
2.Dental management of medically compromised patient-Little
J,Falace D,Miller C,Rhodes N.
3. Bergmeier W, Chauhan A, Wagner D (2008) Glycoprotein
Ibalpha and von Willebrand factor in primary platelet adhesion and
thrombus formation: lessons from mutant mice. Thromb Haemost
99: 264–270 [PubMed]

WEB-SITES:
1.http://www.britannica.com/EBchecked/topic/720
818/blood-disease
2.http://www.patient.co.uk/doctor/bleeding-disorders
3.http://www.healthline.com/health/blood-cell-disorders#
Types2
4.http://www.platelet-research.
org/1/function_hemo.htm
5.http://www.hopkinsmedicine.org/heart_vascular
_institute/index.html

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