thrombosis

CONTENTS
 Introduction
 Coagulation of blood
 Factors involved in clotting
 Sequence involved in clotting
 Coagulation cascade
 Stages of clotting
 Haemostasis
 Clotting disorders

CONTENTS
 DEFINITION
 PATHOGENESIS
 VIRCHOW’S TRIAD
 ENDOTHELIAL INJURY
 ALTERATION IN BLOOD FLOW
 HYPERCOAGULABILITY
 DEFFERENCE BETWEEN ARTERIAL AND
VENOUS THROMBI
Thrombosis

 POSTMORTEM CLOT AND ANTEMORTEM
CLOT
 FATE OF THROMBUS
 CONCLUSION
 REFERENCES

COAGULATIONOFBLOOD
• Definition: Asthe process in which the blood
looses its fluidity and becomes ajelly likemass
few minutes after it is shed out or collected in
acontainer.
KSembulingamEssentialsOf MedicalPhysiology

STAGES OF BLOOD CLOTTING:
1.Formation of prothrombin
activator
2.Conversion of prothrombin into
thrombin
3. Conversion of fibrinogen intofibrin

SEQUENCEOF CLOTTINGMECHANISM:
Enzymecascadetheory::
• Most of the clotting factors in the form ofenzymes.
• Normally all the factors are present in the form of
inactive proenzyme.
• Thistheory explains how various reactions involved in
the conversation of proenzymes to activeenzymestake
place in form ofcascade.
• Cascaderefers to aprocess that occurs through aseries
of steps, each step initiating the next, until the final
step is reached.

FACTORSINVOLVED IN BLOODCLOTTING:
Christmas factor
Stuart factor
• Factor I: Fibrinogen
• Factor II: Prothrombin
• Factor III: Thromboplastin
• Factor IV: Calcium
• Factor V:Labile factor
• Factor VI: Prescence has not beenproved
• Factor VII: Stable Factor
• Factor VIII:Antihemophilic
• Factor IX:
• FactorX:
• Factor XI: Plasma Thromboplastinantecedent
• Factor XII: Haganfactor
• Factor XIII: Fibrin stabilizingfactor

HEMOSTASIS
Defined asarrest or stoppage of bleeding.
Stages:
Vasoconstriction.
Formation of plateletplug.
Coagulation of blood.

Blood clot
BLOODCLOT
• Defined asthe massof coagulated
blood which contains RBC’sWBC’s
and platelets entrapped in fibrin
meshwork.
• RBC’sand WBC’sare not necessary
for clotting process. However when
clot is formed these cells aretrapped
in it along withplatelets.
• Thetrapped RBC’sare responsible for
the red color of theclot.
• Theexternal blood clot is alsocalled
scab.It adheres to the opening of
damaged blood vesseland prevents
blood loss.

TESTSFORCLOTTING
• Bleeding time
• Clotting time
• Prothrombin time
• Partial prothrombin time
• Thrombin time.

BLEEDINGTIME:
• Time interval from oozing of blood after a cut or injury
till arrest ofbleeding.
• Determined by Duke method using blotting paperor
filter papermethod.
• Its normal duration is 3-6min
• Prolonged in purpura

CLOTTINGTIME:
• Time interval from oozing of blood after cut or injury till
the clot formation.
• Usually determined by capillary tubemethod.
• Normal duration is 3-8 minutes
• Prolonged in Hemophilia.

PROTHROMBINTIME:
• Time taken by blood to clot after adding tissue Thromboplastin to it.
• Normal duration is 12seconds
• Prolonged in prothrombin
Deficiency and other factors like
factorI, V
,VII andX.
• Normal in hemophilia

PARTIALPROTHROMBINTIME:
• Is the time taken for blood to clot after adding
phospholipid and calcium to blood.
• It is also called activated prothrombintime.
• Normal duration is 30-50 sec.
• Prolonged in heparin therapydeficiency of factors II,V
,
VIII, IX,X,XI, XII

THROMBINTIME:
• Time taken for the blood to clot after adding thrombin to
it.
• Done to investigate the presence of heparin in plasmaor
to detect fibrinogenabnormalities.
• Normal duration is 12-20 sec.
• Prolonged in heparintherapy
and during dysfibrinogenimia.

HEMOPHILIA.
• Group of sexlinked inherited disorders featuredby
prolonged clotting time.
• Usually affects males, females being the carriers.
• Damageof skin while falling
or extraction of toothcause
excessbleeding for few
weeks.
• Easybruising and
hemorrhage in musclesand
joints are also
common.
HarshMohan EssentialPathologyfor DentalStudents

CAUSES
• Due to lack of formationof
prothrombin activator.
• Bleeding time andprothrombin
time are normal.
Types of hemophilia:
HemophiliaA orclassic
hemophilia:
• Due to the deficiency offactor
VIII. 85% of peopleare
affected.
Hemophilia B orChristmas
Factor IX:
• Itis due to the deficiency of
factor IX. 15% areaffected.
Hemophilia Cor factorXI
deficiency:
• Due to deficiency of factor XI.It
is a very raredisorder.

SYMPTOMS:
• Spontaneous bleeding.
• Prolonged bleeding due to cuts, tooth extractionand
surgery.
• Hemorrhage in gastrointestinal and urinary tract.
• Bleeding in joints followedby
swelling and pain.
• Appearance of blood andurine.
TREATMENT:
• Replacing the missing
clotting factor.

PURPURA:
• Characterized by prolonged bleeding time.
• Characteristic feature is spontaneous bleeding under
skin from ruptured capillaries.
• Causessmall tiny hemorrhagic spots in many areasof
the body.
• Thesespots under the skin are called purpuricspots.
• Blood also sometimes collects in large areasbeneath the
skin which are called Ecchymoses.
• But clotting time isnormal

• Typesand causes:
• Depending upon causesclassified as
i. Thrombocytopenic purpura:
• Dueto deficiency of platelets.
• In bone marrow diseaseplatelet production isaffected
leading to deficiency ofplatelets.
ii. Idiopathic thrombocytopenicpurpura:
• Dueto some unknown causecalled idiopathic
thrombocytopenic purpura.
• Platelet is count is decreased due to developmentof
antibodies against platelets

• iii. It is due to structural or functional
abnormality of platelets.
• Platelet count isnormal.
• Normal clotting time, normal or prolongedbleeding
time but defective clotretraction.

VONWILLEBRAND
DISEASE:
• Characterized by excessbleeding
even with amildinjury.
• Dueto inherited deficiency ofvon
willebrand factor.
• Responsible for adherence of
platelets to endothelium of blood
vesselsduring hemostasis after an
injury.
• Thisresults in excessbleedingthat
occurs during plateletdysfunction.

• TypeI. Most common characterized by mild to
moderate decrease in plasmavWF
.
• TypeII. Much lesscommon and is characterized by
normal or near normal levels of vWFwhich is
functionally defective.
• TypeIII. Extremely rare and most severe form of disease.
Bleeding episodes are treatedby
Cryoprecipitates.

ORALHEALTHCONSIDERATIONS
• Platelet deficiency and vascular wall disorders result in
extravasations of blood into connective tissues of the skin and
mucosa creating pinpoint hemmorages called petechiae and
larger patches called Ecchymoses.
• Hemarthrosis is acommon complications in hemophiliac’s.
• An acute TMJarthrosis associated with FIXdeficiency was
resolved with factorreplacement.
Burket’s OralMedicine

DENTALMANAGEMENT:
• Dental modifications required for patients with bleeding disorders
depend on both the type and invasiveness of dental procedure and
the type and severity ofthe bleeding disorder.
• Lessmodification is needed for patients with mild-coagulopathies
in dentalprocedures.
• When significant bleeding is expected, the goal ofmanagement is
to preoperatively restore the hemostaticsystem.
• For reversible coagulopathies the best toremove the causative
agents or primarily treat theillness.
• For irreversible coagulopathies the treatment is missing or
defective element may be replaced from exogenous sourceto
allow control ofbleeding.

• PLATELETDISORDERS:
• When medical management is unable to
restore the platelet level of 50,000/mm3
required for surgical hemostasis,platelet
transfusions must be required prior to
dental extractions or other oral surgical
procedures.
• Sixunits of platelets arecommanly
expected to infuse at atime.
• Local hemostatic methods arealso
important .
• Thethromosthenic patients needing
dental extractions maybe succesfully
treated with microfibrillar collagenand
antifibrinolytic drugs.
• If using of aspirin, avoidance of aspirin is
recommended, when possible for 1week
prior to extensive oralprocedures
• Adjunctive local hemostatic agents are
useful in preventing post operativeoozing
when aspirin therapy is in useat the time
of minor surgicalprocedures.

• Adjunctive local hemostatic agents are useful in preventingpost
operative oozing when aspirin therapy is in useat the time of
minor surgicalprocedures.
• When extensive surgery is emergently indicated DDAVP can be
used to decrease the aspirin induced prolongation of the BTor
to treataspirin related postoperative oozing.

• Restorative and
prosthodontictherpy:
• Rubber dam isolation is advised ti
minimize the risk of laceration soft
tissue in operative field and toavoid
creating ecchymoses and
hematomes.
• Careis taken to select tooth clamp.
Matrices, wedges and hemostatic
gingival retraction cord are used
with caution toprotect soft tissues.
• Endodnotic therapy:
• Isoften the treatment of choicefor
patient with severebleeding.
• Generally no contraindications for
root canal treatment, provided that
instrument does not extendbeyond
the apex.
• Application of epinephrine
intrapulpally to apical area is
succesfulin providinghemostasis.

PEDIATRICDENTALTHERAPY:
• Administration of factor concentrate and extraction of decidious
teeth with curretage may be neccesary for patient comfort and
hemorrhage control.
• Hemorrhage control is obtained by guagepressure andseepage
generally stops by 12hours.
• Pulpotomies can be performed without excessivepulpal bleeding.
• Topical fluoride applications and pit and fissure sealantsdecrease
the need for extensivetherapy.
Orthodontic therapy:
• Avoid mucosallacerations,
• Minor cuts usually respondto
local pressure.

• Fibrin sealants or fibrin glue hasbeen used effectively asan
adjunct with adhesive andhemostatic effects to controlbleeding
at wound or surgicalsites.
Preventive and periodontaltherapies:
• Periodontal probing and suprgingival scaling can beroutinely
done.
• Subgingival scaling rarely warrents replacementtherapy.
• Severly inflammed and swollen tissues are best treated initiallyby
chlorhexidine oral rinses or by grossdebridement with hand
instruments to allow gingivalshrinkage.
• Deep subgingival and root plannning performed by quadrentto
reduce potential bleeding
• Locally applied pressure and antifibrinolytic mouth rinsesare
usually succesful
• Periodontal packing material aids hemostasis and protectsthe
surgical site.

THROMBOSIS
 ‘The process of formation of a solid mass in
circulatory system from constituents of blood’
 Aggregation of blood factors primarily platelets
& fibrin with entrapment of cellular elements,
frequently causing vascular obstruction at the
point of its formation
Thrombus

 Embolus:
 Detached intravascular solid, liquid or
gaseous mass that is carried by the blood
to a site distant from its point of origin

ENDOTHELIAL INJURY
 Endothelial injury is an important cause of
thrombosis,
 Particularly in the heart and the arteries,
where high flow rates might otherwise
impede clotting by preventing platelet
adhesion or diluting coagulation factors

THROMBOSIS DUE TO ENDOTHELIAL INJURY
 Thrombi in the cardiac chambers after
myocardial infarction,
 Over ulcerated plaques in atherosclerotic
arteries,
 Sites of traumatic or inflammatory vascular
injury,vasculitis

Endothelium need not be denuded or physically
disrupted to contribute to the development of
thrombosis; any perturbation in the dynamic
balance of the prothrombotic and antithrombotic
effects of endothelium can lead toTHOMBOTIC
EFFECT

ENDOTHELIAL DYSFUNCTION
 Hypertension
 Turbulent blood flow
 Bacterial products
 Radiation injury
 Homocystinuria
 Hypercholesterolemia,
 Toxins absorbed from cigarette smoke.

ALTERATIONS IN NORMAL BLOOD
FLOW ( TURBULENCE & STASIS)
Turbulence - arterial and
cardiac thrombosis
Stasis - venous
Thrombosis

 Stasis and turbuleny cause
 • Both promote endothelial cell activation and
enhanced procoagulant activity,
 • Stasis allows platelets and leukocytes to
come into contact with the endothelium when
the flow is sluggish.
 • Stasis also slows the washout of activated
clotting factors and impedes the inflow of
clotting factor inhibitors

 myocardium – stasis: Mural Thrombi
 Abnormal aortic and arterial dilations
(Aneurysms) – Favored sites of Thrombosis

 Hypercoagulability
 Infrequently to arterial or intracardiac
thrombosis but is an important underlying
risk factor for venous thrombosis.
► Causes :
 ► Primary (Genetic)
 ►Secondary (Acquired)

:
 Hypercoagulability seen with advancing
age
 Due to Increased susceptibility to platelet
aggregation
 Smoking and obesity promote
hypercoagulability by unknown mechanisms.

Composed
of:
Tangled mesh of
platelets, fibrin,
erythrocytes &
degenerating
leucocytes
More enmeshed
erythrocytes
Common Coronory Arteries Veins
sites Cerebral arteries Lower extremities
(In descending
order)
Femoral arteries upper extremities
Less common:
Periprostatic plexus
Ovarian and Peri uterine
veins
3/20/2021
Thrombosis

Post Mortem Clots Red Thrombi
Gelatinous; red cells
settled by gravity
More enmeshed
erythrocytes, under
transection reveal vague
strands of pale gray fibrin
Not attached to the
underlying wall
Firmer, almost always
have a point of
attachment

Propagation. The thrombus enlarges
through the accretion of additional
platelets and fibrin, increasing the odds
of vascular occlusion or embolization.
• Embolization. Part or all of the
thrombus is dislodged and transported
elsewhere in the vasculature.

Dissolution.
Recanalization
and organization

REFERENCES
 ROBBIN’S BASIC PATHOLOGY 9TH
EDITION
 TEXTBOOK OF PATHOLOGY BY
HARSHMOHAN
 K SEMBULINGAM MEDICAL PHYSIOLOGY

thrombosis

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