Disorders of Hemostasis Flashcards
Hemostasis
stopping blood flow, literally taking blood from a liquid state into a solid state
-Either inappropriate clotting or insufficient clotting
Platelets (Thrombocytes)
- Platelets live 8-10 days in circulation
- Many stored in the spleen
- are disc shaped
What is the normal value for platelets
150,000 - 400, 000
What are mediators hemostasis
Chemicals produced by platelets that are released at an injury to start the clotting process
What is the blood vessels role in clotting
The prevent and control the formation of blood clots. Blood vessels are lined with epithelial cells that either promote blood flow by blocking platelet adhesion and lysing blood clots
How is the endothelium activated?
by infectious agents
hemodynamic factors
plasma mediators
and cytokines that are liberated during the inflammatory process
Epithelium cells elaborate and enzyme called
adenosine diphosphatase
Phase 1 of hemostasis
Vessel spasm
vasoconstricton
formation of soft plug
short lived
Phase 2 of hemostasis
Release of Von Willebrand Factor by endothelial cells
ADP helps stick together
Release of factor 3 which constricts the vessel so that the platelet doesn’t get kicked off
platelet plug
Phase 3 of hemostasis
Coagulation phase
Extrinsic pathways, Intrinsic Pathways start 30 seconds to several min after phase 1 and 2
which both end in x factor (common pathway) prothombin to thrombin (without this it cannot occur)
Fibrinogen to fibrin
Extrinsic Pathway (tissue factor)
much faster
begins with trauma to the tissue to release
very rapid, 12-15 seconds (smaller clots)
chemical shortcut
Ends in factor x
factor x
prothombin activator
Without this, you cannot clot
Intrinsic Pathway (Blood Vessel injury)
slow (5-10 min)
collagen in the blood vessel wall activates
Larger amounts of thrombin= larger clots
ends in factor x
Ptt
Intrinsic- heparin, already have a clot
aPt
Extrinsic- coumadin- to avoid a clot
factor v complex
prothombin to thrombin, without this you cannot clot
Prothombin to thrombin ——–>
fibrogenogen to fibrin =clot
Clot retraction IV
pulls tight on top of injury site in order to reduce further hemorrhage
Fibrinolysis V
and enzyme plasmin digests or degrades the clot
T-PA tissue plasminogen activator converts plasminogen into plasmin and eats the clot
then plasmin digests the clot
All but 2 of the hemostasis phases require calcium to clot except for stages
1 and 2
Thrombocytopenia
Platelet count less than 150,000
Less than 50,000 means hemorrhage
Less than 15,000 means spontaneous bleeding
less than 10,000 means severe bleeding
What causes thrombocytopenia
Hyperspleenism,
autoimmune disease
hypothermia
viral or bacterial infections that cause DIC
Too much vitamin K =
clot
Too little vitamain K=
bleed
Where is vitamin k stored
in the liver
Liver disease causes
defects in coagulation
fibrinolysis
platelet number and function
NASH
non alcoholic fatty liver
Hypercoaguability states
Inherited genetically and acquired
Increased platelet function
Inheritated hypercoagulation
usually associated with venous thrombosis
C protein down will create DVT
S protein down will create arterial thrombosis
C breaks down
clots
Factor V leiden AKA activated protein resistance (Inherited hypercoaguability)
resists protein c from breaking down a clot due to genetic mutation
Most common acquired increased clotting
Smoking Disseminated Cancer Obesity sickle cell Most common female aquired oral contriceptives
Hemophilia
most common x linked genetic disease (female carrier)
Hemophilia A or classic, factor 8 most common and is a lack of factor 8
Hemophilia b is a lack of factor 9 and is called christmas disease
DIC
is acquired
is where clotting and bleeding at the same time
Caused by sepsis, cancer, trauma, blood transfusion
causes tissue damage and has 85% mortality rate
What would you expect to see if your patient had widespread thrombosis followed by widespread bleeding?
symmetrical blue fingers and toes
Anticoagulant drugs
Heparin- Binds to ATP
Coumadin- interfere with vit K (oral)
Antiplatelet drugs
Inhibits platelet formation
Asprin plavix
Thrombocytic drugs
tissue plasminagin actorvator tPA plasmin to plasmin
