Lecture 6 Flashcards
Hemostasis
all processes that minimize blood loss when a blood vessel is opened
includes 4 related events –> vasoconstriction, platelet plug, fibrin web, clot retraction/dissolution
Vasoactive amines
Serotonin
Histamine
Enzymes derived from plasma
blood coagulatoin cascade
Fibrinogen
soluble plasma protein that can be acted upon by clotting factors to ultimately form insoluble fibrin
a part of the plasma
Platelets
release serotonin
a part of formed elements
increased amount can cause venous thromboembolism
decreased amount can be infection, leukemia
Initial steps of hemostasis
Platelets and fibrinogen circulate in the blood
when a blood vessel is injured or ruptures, platelets release serotonin and aggregate to form platelet plug
Coagulation
processes by which liquid blood changes to a solid clot (thrombus)
uses platlets, RBC, fibrin
The platelet plug is not ___ ______ to curtail ____ _____
strong enough/blood loss
must be reinforced by solid strands of fribrin
Clotting factors
enzymes made by the liver
12 –> little a means that clotting factor is activated
Intrinsic Pathway
activation of complement proteins occurs within system
Extrinsic pathway
outside factor helps to activate the system
What protein do the intrinsic and extrinsic pathway come together?
10
Many complement proteins are _____ ______ dependent
vitamin K
can be found in diet or normal flora
Coagulation disorders
Too much BLEEDING
Too much CLOTTING
Coagulation disorders that result in deficient clotting
hemophilia A and B
von Willebrand disease
Hemophilia A
genetic deficiency in clotting factor 8
Hemophilia B
Christmas disease
genetic deficiency in clotting factor 9
Hemophilia A/B
most often these are x-linked recessive traits
treatment for both–> infusion of respective deficient clotting factors
von Willebrand disease
genetic deficiency or defective von willebrand factor
VWF = plasma protein that binds factor 8 and platelets
Functions of VWF
assists in formation of plug
helps initiate initial adhesion of platelets at sites of bleeding injury
binds and stabilizes clotting factor 8
treatment depends on severity
Fibrinogen is
SOLUBLE
Fibrin is
INSOLUBLE
Factor V Leiden thrombophilia
common inherited form of thrombophilia
clotting process remains active longer than normal, increases changes of blood clots and emboli
What factors increase the risk of clotting?
dehydration
increasing age (decreased mobility)
obesity
injury
srugery
pregnancy
co-morbidities
medications
Medications that can increase clotting
birth control
hormone replacement therapy
fertility related drugs
NSAIDs
anabolic steroids
chemotherapy
marijuana
Anticoagulants
warfarin
heparin
lovenox
Antiplatelet drugs
asprin
clopidogrel (plavix)
Thrombolytics
tPA–> tissue plasminogen activator
Anticlotting drugs
Anticoagulants
Thrombolytics
Antiplatelet drugs
Anticoagulants definition
used primarily to prevent clot fomration in venous system
work by preventing or disrupting the synthesis and/or function of clotting factors
these drugs do NOT dissolve the thrombus/clot
Heparin
not orally active, typically given subcutaneous or intravenous
Low molecular weight heparins
not orally active
given SQ
lovenox/enoxaparin
Warfarin
orally active
(Coumadin)
Direct oral anticoagulants
orally active, direct thrombin inhibitor and direct factor Xa inhibitors
Anticoagulant therapy
generally starts with heparin and is then followed by warfarin or lovenox
these drugs are used in the treatment of DVT
anticoagulants do NOT dissolve the clot
ANticoagulants help to
prevent enlargement of thrombus
allow for further attachment of the thrombus to the vessel wall, which reduces the likelihood of an embolus
Antiplatelet drugs
used primarily to prevent clot formation in the arterial system
work by inhibiting platelet function
aspirin and clopidogrel
Aspirin
antithrombotic effect at very low doses
Clopidogrel
plavix
inhibits platelet aggregation/clumping
Clinical uses of Antiplatelet drugs
prevention and treatment of arterial thrombosis
prevention of clot in people with high risks of clots
ADRs of Antiplatelet drugs
ADRs: increases risk of bleeding, increased risk of hemorrhagic CVA, long term effect on kidneys, liver, GI
Thrombolytics
clot bisters
used in emergent circumstatnces to re-establish blood flow through vessels that have been occluded
work by facilitating destruction of blood clots
only used within short well-defined window of known vessel occulusion
tissue plasminogen activator is common drug
DVT
common postoperative complication
exacerbated by prolonged immobility and decreased activity
Strategies to decrease DVTs
anti-coagulants
hydration
mobilization
sequential compression device
What can be caused by a DVT?
stroke
pulmonary embolism
heart attack
Risk factors for DVT
DAMAGE TO VEINS
previous DVT, surgery, trauma, LE fracture, varicose veins, sepsis, childbirth
STASIS
prolonged bedrest, heart failure, heart attack, neurologic disorders, chronic venous insufficiency, immobilization, prolonged air travel
HYPERCOAGUABILITY STATES
cancer, autoimmune disorder, oral contraceptives, late pregnancy
OTHERS
age >60, obesity
Symptoms of DVT
pain
dull ache
tightness
Signs of DVT
Erythema
Edema
Positive Homan’s Sign
Warmth
Modified Wells Clinical Prediction Rule for DVT
if pt exhibits any S/S of DVT
has excellent sensitivity and specificity for DVT
Scoring of Modified Wells
0 = not present
1 = predictor is present
-2 = alternative diagnosis likely
d-dimer test
blood test for teh presence of a small fragment of fibrin from a blood clot
negative rules out DVT
positive = additional testing, doppler ultrasound
Treatment of a DVT
anticaogulation therapy will be started
PT may be delayed so that clot can stabilize
Lovenox and mobilizing
You can mobilize in about 5 hours
Heparin and mobilizing
2 days before mobilizing
Higher INR =
increased bleeding
Warfarin/Coumadin
pt should have plasma INR checked regularly
Therex range is 2-3
higher than this indicates bleeding and could cause hemarthrosis
