Hemodynamic Disorders 2

Question 1

What 3 different categories lead to thrombosis?

Answer 1

Endothelial injury
Abnormal blood flow
Hypercoagulability

Question 2

Define thrombosis.

Answer 2

Clotting blood

Question 3

Describe the procoagulant and antifibrinlytic effects of the endothelium.

Answer 3

Procoagulant changes:
Downregulates expression of thrombomodulin Downregulates Protein C and tissue factor inhibitor

Antifibrinolytic effects:
Secrete plasminogen activator inhibitors (PAIs)

Question 4

What is thrombomodulin?

Answer 4

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.

Question 5

What are some causes of endothelial injury?

Answer 5

Hypertension, bacterial products, radiation injury, hypercholesterolemia (high cholesterol), toxin from cigarette smoke, inflammation

Question 6

Describe the effects of turbulence and stasis (abnormal blood flow)?

Answer 6

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

Question 7

What are some causes of stasis and turbulence (abnormal blood flow)?

Answer 7

Aneurysms (stasis), atherosclerotic plaque
(turbulence), myocardial infarctions (stasis), rheumatic
mitral valve stenosis (stasis), sickle cell anemia (stasis)

Question 8

What is hypercoagulability (thrombophilia)?

Answer 8

Disorder of blood that predisposes to thrombosis

Primary or secondary

Question 9

Describe primary hypercoagulability (thrombophilia).

Answer 9

Genetic

Causes:
Factor V mutation (most common)
Prothrombin mutation
Increased levels of Factors VIII, IX, XI, or fibrinogen

Question 10

Describe secondary hypercoagulability (thrombophilia).

Answer 10

Acquired

Bed rest, atrial fibrillation, malignancy, development of anti-phospholipid antibodies

Question 11

Describe Factor V Leiden that causes hypercoagulability of the blood.

Answer 11

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)

Question 12

Describe Antiphospholipid Antibody Syndrome (lupus anticoagulant syndrome) that causes hypercoagulability of the blood.
What does it cause?

Answer 12

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

Question 13

What happens when thrombus forms?

Answer 13

Propagate (larger)
Resolve (TPA)
Become organized (incorporate into BV wall, difficult to get rid of)
Embolize (travel)

Question 14

Is thrombosis a local or distal process?

Answer 14

causes tissue injury by local vascular occlusion or by distal embolization.

Question 15

Describe venous thrombosis. Where are they mainly located? What is the difference between superior and deep thrombosis?

Answer 15

Mostly in veins of the leg

Superficial veins-local congestion, swelling, pain, and
tenderness, but rarely embolize

Deep veins- Can embolize to lung (DVT)

Question 16

Describe arterial or cardiac thrombosis. Do they embolize?

Answer 16

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)

Question 17

What is a embolism? Examples?

Answer 17

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

Question 18

What is a pulmonary thromboembolism? What extremity does it derive from?

Answer 18

derive primarily from lower-extremity deep vein thrombi

effects depend mainly on the size of the embolus and the location in which it lodges

Question 19

Why are pulmonary thromboembolisms not as much of a concern?

Answer 19

Dual blood supply in lungs

Question 20

What are some consequences of pulmonary thromboembolism?

Answer 20

right-sided heart failure, pulmonary hemorrhage, pulmonary infarction, or sudden death

Question 21

What is a systemic thromboembolism? From where is it derived?

Answer 21

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.

Question 22

What is Hollenhorst plaque?

Answer 22

Cholesterol emboli
Seen where bv branch in ON

Question 23

What is a calcific embolus?

Answer 23

Calcium from heart or necrotic tissue in ON

Question 24

What is a a fibrin platelet embolus?

Answer 24

Embolus in ON elongated along retinal vessels

Question 25

What is an infarction?

Answer 25

an area of ischemic necrosis caused by occlusion of the vascular supply to the affected tissue

(Death of tissue from lack of oxygen)

Question 26

What causes infarctions?

Answer 26

Arterial thrombosis or arterial embolism underlies the vast majority of infarctions, venous outflow obstruction is a less frequent cause.

Question 27

What accounts for the red vs white infarcts?

Answer 27

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)).

Question 28

What 4 factors influence infarct development?

Answer 28

1. Anatomy of vascular supply (dual blood supply)
2. Rate of occlusion (long period of time allows tissue or organ to for own blood supply)
3. Tissue vulnerability to ischemia (neurons and cardiac more sever than fibroblasts or collagen)
4. Blood oxygenation (if blood oxygen is already low effects will be worse)

Question 29

Describe the difference between a branch and central retinal artery occlusion.

Answer 29

Branch- effects only certain part of the retina

Central- effects the entire retina (ICA)

Question 30

What is the result of retinal vein occlusion? Describe the difference between branch and central.

Answer 30

Causes hemorrhaging in retina

Central- hemorrhaging all over the retina
Branch- hemorrhaging only in certain part

Question 31

What is shock? What causes it? What are the general outcomes of shock?

Answer 31

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

Question 32

What are the 3 classifications of shock?

Answer 32

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

Question 33

What is septic shock?

Answer 33

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

Question 34

What are the triggers for septic shock?

Answer 34

Gram + (most common)
Gram -
Fungi

Question 35

What are the stages of septic shock?

Answer 35

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

Question 36

What is the clinical progression of symptoms for septic shock (cardiogenic and hypovolemic)?

Answer 36

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