HEMOSTASIS
- Involves the interaction of vasoconstriction, BLOOD VESSEL TYPES
platelet adhesion and aggregation, and
1. Capillaries - smallest
coagulation enzyme activation to stop
bleeding. 2. Veins- back
3. Arteries- away
- Stopping the flow of blood
- Coagulation process BLOOD VESSEL LAYER
- Maintenance of the normal blood flow
1. Tunica intima/interna
2. Tunica media
3. Tunica adventitia/externa
TYPES OF HEMOSTASIS
a. Primary hemostasis
- Blood vessel & platelet
o produces 1’ primary platelet plug
o temporary/reversible plug
Note: BV is intact & unbroken.
b. Secondary hemostasis
- Coagulation proteins/factors
o Stable fibrin clot
o Permanent/ irreversible
1st : Neurological response
c. Tertiary hemostasis (fibrinolysis) - VASOCONSTRICTION
- tPa (tissue plasminogen activator)
o plasminogen plasmin 2ND: Stimulation of platelet function
- plasmin- lysis/degregation of fibrin clot 1. Adhesion - Glycoprotein Ib/IX/V
- leads to production of fibrin split products 2. Activation - Thromboxane A2
3. Secretion- contains alpha granules and dense
granules
BLOOD VESSEL/ PLATELETS 4. Aggregation – Glycoprotein IIb/IIIa
- Forms primary plt plug
- intact and unbroken BV:
- inside plasma PRIMARY HEMOSTASIS CONCLUDES------
o fibrinogen
o no coagulation
o increase anticoag subs SECONDARY HEMOSTASIS
- (PK) Prekallikrein
ANTI-COAGULATION SUBSTANCE - (HMWK) High molecular weight kininogen
- I-XIII FACTORS
o heparin
- FIII- not impossible
o heparin sulfate
- FXII- not lead to bleeding
o nitrous oxide
o AT III (anti thrombin time
o APCR (activated protein c-receptor)
STABLE FIBRIN CLOT (fibrinogen clot) II. Thrombocytic or Platelet disorders
a. Thrombocytosis (increase plt)
i. Chronic myeloid leukemia
ii. Essential thrombocytemia
iii. Polycythemia vera
iv. Myelofibrosis with myeloid
metaplasia
> 400,00 cell/uL
b. Thrombocytopenia (decrease plt)
i. Decrease megakaryopoiesis
ii. Increase plt destruction
iii. Increase plt loss
iv. Increase plt sensation
<150,00 cells/uL
PPL- plt phospholipids CELL BASED COAGULATION
Ca+- calcium
QUALITATIVE PLATELET DISORDERS
1. Gray platelet syndrome
TERTIARY HEMOSTASIS 2. Glanzmann thrombastenia
3. Bernard-soulier syndrome
Plasminogen plasmin 4. Wiskott-aldrich syndrome
5. Hermansky pudlak syndrome
Fragments: 6. Chediak higachi syndrome
Fibrin Fibrinogen
DED X
E Y SECONDARY COAGULATION
YY E -decrease CF
DD D - VIII HEMOPHILIA A
DXD
Detects deficient
-mixing studies
PATHOLOGIC HEMOSTASIS -substitution studies
DISORDERS OF PRIMARY COAGULATION
I. Vascular Disorders
a. Inherited
i. Marfan syndrome
ii. Ehler’s-banlos syndrome
iii. Kasabach-merlit syndrome
iv. Congenital hemangiomata
b. Acquired
i. Henoch- schonlein purpura
ii. Senile purpura
iii. Scurvy (vit-C def)
iv. Thrombotic thrombocytopenic
purpura
c. Idiopathic
i. Psychogenic purpura
I. TUNICA INTIMA/INTERNA
HEMOSTASIS Innermost
- Maintenance of the body Houses endothelial cells (endothelium)
- Blood inside the intravascular vessels Single layered cell (monolayer)
maintains FLUID STATE
II. TUNICA MEDIA
Yung drawing na parang SEESAW ito kapag Thickest
ahhhhhhh, kayo nanto mag draw Houses smooth muscles, elastin &
collagen
Collagen- very important in secretion
III. TUNICA ADVENTITIA
Versatile/flexible
Houses fibroblast
VASA VASORUM – specialized type of
capillary that transports nutrients to
E.C, S.C, & fibroblast
TISSUE INJURY
HOMEIOSTASIS
- State of BALANCE VASOCONSTRICTION
Immediate response to injury
Neurologic response (autonomic
1. PLATELETS nervous system)
- Adhesion, activation, secretion and Formation – “STENOSIS”
aggregation Narrowing of lumen
- Product: primary plt plug Less blood escape
- Parts of Hemostasis: CLOTTING FACTORS Pathologic
o Kinin system
o Complement system
o Fibrinolytic action- degradation of fibrin PROCOAGULANTS
o Plasmin
I. von Willebrand factor (vWF)
2. BLOOD VESSELS - large glycoproteins
- “unused” / UlvWF
ARTERY (thickest wall) - ultra long von willebrand factor
- Strong foundation (holds too much - largest of clotting factor/procoag
pressure) - stabilizes F VIII (easily dehydrated)
- Arterioles metarterioles capilliaries - primary coag: binding plt to COLLAGEN
vWF secreted by ENDOTHELIAL CELLS
VEINS (largest /widest lumen) inside EC: slowed in WELBEL PALADE
- Lesser smooth muscle BODIES
- Lesser interventions Adhesion- ( gp Ib/IX/V )
- VENULES – major portal of blood Activation- slowed by alpha granules
circulation. and produce by MEGARYOCYTE III
CAPILLARIES (most numerous) MODULATION OF vWF
- (+) SINUSOIDS
- BM, liver & spleen (more prominent) I. ADAMTS – 13
- Other parts ( transport/exchange of o a disintegrin and metaloprotenase
nutrients) with a thrombospontin type 1 motif
member 13)
3 LAYERS OF BV II. TAFI (thrombin activatable fibrinolytic
inhibitor)
- Procoagulant
- inhibits fibrinolysis
ANTICOGAULANT
1. ENDOTHELIAL CELLS
- Rhomboid
- Smooth inner surface of BV
- Facilitate smooth flow of blood
2. NITROUS OXIDE
- Vasodilation
- From intact EC
- Inhibits plt activation
-
3. HEPARIN SULFATE
- Weakly enhances Anti-thrombin III
4. ANTI-THROMBIN III
- Antagonizes the action of FIIa
(thrombin) I, V, VIII, XIII
-
5. THROMBOMODULIN
- HS + FIIa – activated
- Binds to endothelial protein C
(EPCR) Activated protein C (APC)
- Degrades action of Va & VIIIa
6. PROTACYCLIN (PGI2)
- Produced by eicosanoid pathway
Endothelial cell Platelet
anticogaulant procoagulant
PGI2 PGH2TXA2
inhibits plt activation promotes plt activation
7. TFPI (tissue factor pathway inhibitor)
- Antagonizes FIII
- Further; X,VII, CA, PPL
