Hemodynamic Disorders 2 Flashcards
What 3 different categories lead to thrombosis?
Endothelial injury
Abnormal blood flow
Hypercoagulability
Define thrombosis.
Clotting blood
Describe the procoagulant and antifibrinlytic effects of the endothelium.
Procoagulant changes:
Downregulates expression of thrombomodulin Downregulates Protein C and tissue factor inhibitor
Antifibrinolytic effects:
Secrete plasminogen activator inhibitors (PAIs)
What is thrombomodulin?
Thrombin receptor present on endothelial cell membrane, plays an important role as a natural anticoagulant. It acts as a cofactor of thrombin-catalyzed activation of protein C, and inhibits the procoagulant functions of thrombin.
What are some causes of endothelial injury?
Hypertension, bacterial products, radiation injury, hypercholesterolemia (high cholesterol), toxin from cigarette smoke, inflammation
Describe the effects of turbulence and stasis (abnormal blood flow)?
Endothelial activation
• Procoagulant changes
• Increased leukocyte adhesion
Disrupt laminar flow-platelets in contact with endothelium
Prevent washout and dilution of activated clotting factors
by fresh flowing blood and the inflow of clotting factor inhibitors
What are some causes of stasis and turbulence (abnormal blood flow)?
Aneurysms (stasis), atherosclerotic plaque
(turbulence), myocardial infarctions (stasis), rheumatic
mitral valve stenosis (stasis), sickle cell anemia (stasis)
What is hypercoagulability (thrombophilia)?
Disorder of blood that predisposes to thrombosis
Primary or secondary
Describe primary hypercoagulability (thrombophilia).
Genetic
Causes:
Factor V mutation (most common)
Prothrombin mutation
Increased levels of Factors VIII, IX, XI, or fibrinogen
Describe secondary hypercoagulability (thrombophilia).
Acquired
Bed rest, atrial fibrillation, malignancy, development of anti-phospholipid antibodies
Describe Factor V Leiden that causes hypercoagulability of the blood.
Single nucleotide mutation (Arg to Glu substitution)
Factor V resistant to cleavage and inactivation by protein C
(Always active can’t be inactivated by C)
Describe Antiphospholipid Antibody Syndrome (lupus anticoagulant syndrome) that causes hypercoagulability of the blood.
What does it cause?
Binding of the antibodies to epitopes (part of antigen) on proteins that are induced or “unveiled” by phospholipids
Recurrent thromboses, repeated miscarriages, cardiac valve vegetations, and thrombocytopenia
Immune system attacks normal proteins in blood
What happens when thrombus forms?
Propagate (larger)
Resolve (TPA)
Become organized (incorporate into BV wall, difficult to get rid of)
Embolize (travel)
Is thrombosis a local or distal process?
causes tissue injury by local vascular occlusion or by distal embolization.
Describe venous thrombosis. Where are they mainly located? What is the difference between superior and deep thrombosis?
Mostly in veins of the leg
Superficial veins-local congestion, swelling, pain, and
tenderness, but rarely embolize
Deep veins- Can embolize to lung (DVT)
Describe arterial or cardiac thrombosis. Do they embolize?
Atherosclerosis-major cause of arterial thrombosis (plaque deposition)
Myocardial infarction-causes cardiac mural thrombi
Cardiac and aortic mural thrombi (heart walls/lining) are prone to
embolization (stroke)
What is a embolism? Examples?
Intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin (travels)
Ex.dislodged thrombus, fat droplets, bubbles of air or nitrogen, atherosclerotic debris (cholesterol emboli), tumor fragments, bits of bone marrow, amniotic fluid
What is a pulmonary thromboembolism? What extremity does it derive from?
derive primarily from lower-extremity deep vein thrombi
effects depend mainly on the size of the embolus and the location in which it lodges
Why are pulmonary thromboembolisms not as much of a concern?
Dual blood supply in lungs
What are some consequences of pulmonary thromboembolism?
right-sided heart failure, pulmonary hemorrhage, pulmonary infarction, or sudden death
What is a systemic thromboembolism? From where is it derived?
derive mainly from cardiac mural or valvular thrombi, aortic aneurysms, or atherosclerotic plaques
ischemic necrosis (infarction) of downstream tissues depends on site of embolization and the presence or absence of collateral circulation.
What is Hollenhorst plaque?
Cholesterol emboli
Seen where bv branch in ON
What is a calcific embolus?
Calcium from heart or necrotic tissue in ON
What is a a fibrin platelet embolus?
Embolus in ON elongated along retinal vessels
What is an infarction?
an area of ischemic necrosis caused by occlusion of the vascular supply to the affected tissue
(Death of tissue from lack of oxygen)
What causes infarctions?
Arterial thrombosis or arterial embolism underlies the vast majority of infarctions, venous outflow obstruction is a less frequent cause.
What accounts for the red vs white infarcts?
Infarcts caused by venous occlusion or occurring in spongy tissues (or dual blood supply) typically are hemorrhagic (red)
Arterial occlusion in compact tissues typically are pale (white/yellow (single blood supply)).
What 4 factors influence infarct development?
- Anatomy of vascular supply (dual blood supply)
- Rate of occlusion (long period of time allows tissue or organ to for own blood supply)
- Tissue vulnerability to ischemia (neurons and cardiac more sever than fibroblasts or collagen)
- Blood oxygenation (if blood oxygen is already low effects will be worse)
Describe the difference between a branch and central retinal artery occlusion.
Branch- effects only certain part of the retina
Central- effects the entire retina (ICA)
What is the result of retinal vein occlusion? Describe the difference between branch and central.
Causes hemorrhaging in retina
Central- hemorrhaging all over the retina
Branch- hemorrhaging only in certain part
What is shock? What causes it? What are the general outcomes of shock?
Systemic hypoperfusion (ischemia/low blood flow) of tissues
Can be caused by diminished cardiac output or by reduced effective circulating blood volume (heart is not pumping enough, trauma induced blood loss, lack of oxygen)
Inadequate tissue perfusion, Global cellular hypoxia, If not corrected: fatal
What are the 3 classifications of shock?
Cardiogenic- reduced output, damage, obstruction
Hypovolemic- inadequate blood or plasma volume
Associated with systemic inflammation- activation of cytokine cascades, peripheral vasodilation, Endo injury, leukocyte induced damage, intravascular coagulation
What is septic shock?
Results from arterial vasodilation and venous blood pooling that stems from the systemic immune response to microbial infection (bacteria or virus)
Kills 20% of its victims, multi organ failure
What are the triggers for septic shock?
Gram + (most common)
Gram -
Fungi
What are the stages of septic shock?
Nonprogressive
– Compensatory mechanisms activated (temporary)
– Vital organ perfusion is maintained (sympathetic activation to send blood to vital organs)
Progressive
– Hypoperfusion
– Circulatory and metabolic derangement
Irreversible (death phase, nothing can be done)
– Severe cellular and tissue injury
– Hemodynamic corrections are of no use
What is the clinical progression of symptoms for septic shock (cardiogenic and hypovolemic)?
Hypotension (BV dilating) →
Tachycardia (heart pumping faster →
Tachypnea (more breathing) →
Cool skin→ Cyanosis (vasoconstriction to compensate Renal insufficiency (kidneys and other organs shut down)→ Altered consciousness→
Death
