5070: TEA/ACS
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Flashcardswhat is hemostasis? what type of feedback is it?
what 2 things does it consist of?
arrest of bleeding, positive feedback
platelets and clotting factors
what 2 things are circulating in the body constantly, waiting for activation signals?
platelets and clotting factors
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171 Terms
what is hemostasis? what type of feedback is it?
what 2 things does it consist of?
arrest of bleeding, positive feedback
platelets and clotting factors
what 2 things are circulating in the body constantly, waiting for activation signals?
platelets and clotting factors
what do endothelial cells contribute to hemostasis?
line all blood vessels, normal healthy endothelium inhibits clotting
under normal/healthy circumstances, clotting is a local/widespread phenomenon?
local
what 2 anticlotting substances does a healthy endothelium release ?
prostacyclin
nitric oxide
what are the 4 steps of normal hemostasis?
after injury, vasoconstriction occurs
platelets bind w/ GP1B receptors to von Willebrand factor on exposed extracellular matrix, are activated/change shape and release granules
Released ADP and thromboxane A2 (TxA2) induce additional platelet aggregation through binding of platelet GpIIb-IIIa receptors to fibrinogen. This platelet aggregate fills the vascular defect, forming the primary hemostatic plug.
Local activation of the coagulation cascade results in fibrin “cementing” the platelets into secondary hemostatic plug that contains red cells and leukocytes.
what is the normal count of platelets?
what is considered thrombocytopenia?
150,000-400,000 /uL
below 50,000
platelets are a source of what bone marrow cell?
what is the lifespan of a platelet?
megakaryocytes
5-10 days
what is platelet adhesion normally inhibited by? x 2 things
what are they produced by?
prostacyclin and nitric oxide
healthy, intact endothelial cells
how do platelets become activated? x 3 things
exposure to collagen via von Willebrand factor, ADP, thrombin
what do activated platelets release?
granules w/ mediators that promote and amplify platelet aggregation
what do platelets have receptors for?
pro-clotting signals
what does von Willebrand Factor do? x 2 things
connects/links the platelet to subendothelial collagen exposed on damaged endothelium
contributes to fibrin clot formation
how does vWF contribute to fibrin clot formation?
why does VIII need vWF?
it acts as a carrier protein for factor VIII
it has a very short ½ life and low serum [ ] unless it’s bound to vWF
what is gp1b?
what can’t platelets do w/o this?
a platelet surface membrane glycoprotein that acts as a receptor for vWF
adhere to the exposed collagen
what is gpIIb/IIIa? x 2 things
what couldn’t platelets do w/o this?
an integrin complex found on platelets
receptor for fibrinogen
platelet aggregation is inhibited
what is thromboxane A2 and ADP functions?
what does TXA2 also do?
potent promoters of platelet aggregation
stimulates the expression of gpIIb/IIIa receptors
what does fibrinogen do?
what does it play a key role in?
permits connecting/linking of adjoining platelets
formation of a stable clot
how do platelets get serotonin?
what happens when platelets are activated?
take it up from plasma via SERT proteins and store it
serotonin is released
what are the 2 likely roles of serotonin in hemostasis?
contributing to reflex vasoconstriction
enhancing platelets’ ability to aggregate
a person taking a SSRI/SNRI could have what type of disorder because of the behavior of platelets taking up serotonin from environment?
clotting disorder
what feature of platelets enhance aggregation of platelets?
what else do they play an important role in ?
filopodia
later clot contraction
what is the main source of prostacyclin?
what is the main source of thromboxane A2?
healthy endothelium
platelets
what are the names of the 2 ways that clotting can begin?
intrinsic and extrinsic pathway
how is the intrinsic clotting pathway activated? x 1 step
what is it also referred to as ?
factor XII (hageman factor) contacts subendothelial substances exposed by vascular injury
contact pathway
how is the extrinsic pathway activated?
tissue factor (tissue thromboplastin) is released by damaged endothelial and tissue cells
TF forms complex with factor VII in the presence of calcium
factor VII activated to factor VIIa
which pathway of clotting requires direct tissue penetration?
extrinsic pathway
what could be some things that cause injury that causes the intrinsic pathway to begin? x 2 things
smoking, uncontrolled htn
what is factor 2 also known as?
what pathway is factor X part of and what is it’s function?
thrombin
common pathway- thrombin activator
what are 3 proteases of intrinsic pathway?
what is the protease of the extrinsic pathway?
XII, XI, IX
VII
what are cofactors definition?
accelerators of protease enzyme activity; aren’t enzymes themselves, but help proteases do their job faster and better
what are 2 cofactors?
V and VIII
proteases and cofactors circulate in inactive/active form?
what letter is added to the end of their roman numeral once activated?
inactive
-a
what is the function of reglulatory proteins?
what are 2 examples of this?
anti-clotting
protein C and Protein S
what does activated protein C do?
splits and inactivates cofactors V and VIII, slowing clotting
what does activated protein S do in the body?
what is the result of this?
works together with Protein C to inactivate cofactors V and VIII
slow clotting
both protein C and S do what in the body?
slow clotting
what is the clot from the clotting cascade made of?
fibrin
what is the function of thrombin? x 5 things
to catalyze the conversion of fibrinogen into fibrin
activates factor XIII → causes fibrin threads to crosslink and form a mesh
activates factor V and VIII
also activates platelets
what is fibrinogen?
what happens to it to make fibrin?
a large soluble protein
thrombin cleaves off peptides
what are fibrils?
what do these do to platelets and what does this form?
adhered and assembled insoluble fibrin molecules made into threads
entangle platelets, build a spongy mass that hardens and contracts to form blood clot
what does factor XIII cause fibrin threads to do and what does it form?
crosslink
form a strong mesh
what does antithrombin III block? x 2 things
thrombin
factor Xa
protein C is able to handle the clotting, but what makes it work more efficiently for anti-clotting?
protein S
what is fibrinolysis?
the plasmin system breaks down clots when they are no longer needed
what is the process of fibrinolysis? x 3 things
factor XII, HMWK (high mw kininogen), kallikrein, thrombin release plasminogen activators
cleve plasminogen to form plasmin
plasmin digests fibrin and fibrinogen (f 1), inactivates factors V and VIII
what does INR stand for?
what does it measure?
what is the normal value of INR?
international normalized ratio
how long it takes your blood to clot
1
what is used to monitor warfarin activity in the body?
PT/INR
what are 5 lab assessments used to check clotting function?
platelet count
prothrombin time (PT)
activated partial thromboplastin time (aPTT)
ANTI-Xa assay (AXA)
D-dimer
what is activated partial thromboplastin time (aPTT) used to measure?
heparin activity
what is anti-Xa assay used for?
what is it an alternative for ?
to monitor enoxaparin/oral anticoagulant medications
alt to aPTT to monitor heparin activity
what is a d-dimer test?
when could this be ordered? x 3 things
a fibrin degradation product, created by breakdown of cross-linked fibrin, often due to plasmin activity
DVT, PE, DIC (disseminated intravascular coagulation)
what pathway does aPTT evaluate?
what about PT?
intrinsic pathway
extrinsic pathway
what does INR do?
normalizes PT so that it be compared, regardless of reagents used
what is hemostasis a delicate balance between? x 2 things
pro-clotting forces
anti-clotting factors
what are 4 pro-clotting forces in the body?
exposed collagen
von Willebrand factor
platelets
clotting cascade proteins
what are 6 anti-clotting forces?
intact endothelium
nitrous oxide
prostacyclin
protein C to inactivate factor V
plasmin to break down clots
other proteins
we want clotting to be limited to the
a. sites of injury
or b. throughout the body?
sites of injury
clotting should be freely _____ and _____ at all times, to prevent ___ ____ during trauma
freely available, efficient
prevent blood loss
what is a hypocoaguable state?
what is a hypercoaguable state?
excessive bleeding
excessive clotting
what are 3 situations of hypocoaguable states?
platelet deficiencies
deficiencies of clotting factors or cofactors
anti-clotting factor excesses
von Willebrand disease is an example of what type of state?
what happens during this disease? x 2 things
hypocoaguable
abnormal platelet adhesion, decreased factor VIII due to deficiency of vWF
what is the most common inherited bleeding disorder?
what inheritance pattern does this take?
von willebrand disease
autosomal dominant missense mutation
what does von Willebrand disease cause in the body? x 2 things
decreased secretion of vWF from endothelial cells OR
overly-rapid clearance of vWF from circulation
over 20% of girls with heavy menstrual bleeding have what disease but might not know it?
von Willebrand Disease
what are ecchymoses?
blotchy areas of hemorrhage in the skin
what are 2 possible reasons for a hypercoaguable state?
deficient or abnormal anti-clotting factors OR
excessive pro-clotting factors
Factor V Leiden, aka, “activated protein C resistance” can lead to which type of state?
hypercoaguable
what inheritance pattern does Factor V Leiden disease have?
what does this cause in the body?
autosomal dominant inheritance
missense mutation that eliminates the arginine binding site for protein C on Factor V/Va
prothrombin excess, Protein C or S deficiency, and earlier DIC are all examples of which type of state?
hypercoaguable
hemophilia and later DIC are both examples of what coaguable state?
hypocoaguable
what is earlier DIC?
excess tissue factor-like substances promote disseminated clot formation in small vessels throughout the body
what is needed for a DIC to begin?
a triggering event involving activation of systemic inflammation
if a pt has an INR higher than one, this means they can what?
bleed easier
early DIC is all about?
late DIC is all about?
clotting
bleeding
what is Virchow’s triad mean?
three major factors that cause clotting in the absence of injury
what are the 3 things of Virchow’s triad?
blood stasis (absence of normal flow along endothelium)
damaged endothelium
hypercoagulability
what is the definition of blood stasis?
absence of normal flow along endothelium
what is a thrombus?
what is an embolus?
clot that is local
something that breaks off and is moving around
what are venous thrombi associated with generally? x 2 things
what do these things lead to?
blood stasis or acquired hypercoagulability
inappropriate activation of the coagulation cascade
what are arterial thrombi?
what 2 ways do they start?
platelet adhesion to the vessel wall
endothelial dysfunction OR disruption of an atherosclerotic plaque
why is a clot which begins in the cardiac atrium an exception to the atrial thrombi rule?
it begins due to atrial fibrillation, which blood stasis plays a large role in
where is the most common site of venous thromboembolism?
the deep veins of the calf
what is a major risk factor for venous thromboembolism? x 2 things
immobility and/or inflammation
situations that promote decreased bloodflow (stasis)
oral contraceptive or estrogen are risk factors for what ?
especially combined with what habit?
VTE
smoking
in the case of transgender women/AMAB taking estrogen, when is the risk most increased for VTE?
and with what form of estrogen?
during 1st year of treatment
oral estrogen
when is testosterone hormone replacement most at risk for VTE?
during first 6 mo of tx
what are some clinical manifestations of thromboses?
completely asx
leg pain, tenderness, swelling, discolored, cyanotic, venous distension distal
what syndrome could DVT lead to ?
why are DVT’s so dangerous?
post-thrombotic syndrome
if the clot enters systemic circulation, it could cause a PE
are PE difficult to dx?
if these are massive, what might they result in?
yes
rapid death
what fraction of pts with PE are dx at autopsy?
2/3
what are 6 sx of PE?
tachypnea,
dyspnea
pleuritic chest pain
cough
hemoptysis (coughing blood)
leg pain
what is a saddle embolus?
what is this a cause for?
an embolus that bridges across the pulmonary artery from the heart as it divides into R/L pulmonary arteries
sudden death
if there is a thrombus/embolus in the heart what can occur?
what about the brain?
acute coronary syndrome/myocardial infarction
stroke OR transient ischemic attack
what is there is result of a thrombus/embolus in the limb?
kidney?
ischemia, gangrene
acute renal failure
how does atrial fibrillation cause stroke? x 3 steps
the atria fibrillate and allow stasis of blood
causes damage to the endothelium
thrombus can form and dislodge
when does 90% of coronary blood flow through the heart occurs during what cycle?
diastole
if the coronary arteries are 70-90% occluded, there is usually enough blood flow to meet normal demands in what state?
at rest
what is myocardial arterial oxygen extraction % at rest?
75%