circulation II

Question 1

what are the three causes of thrombosis?

Answer 1

virchow’s triad:

1: injury to the vessel wall
2: increased blood coagulability
3: decreased blood flow (stasis)

Question 2

what is hemostasis?

Answer 2

normal physiological process

blood is maintained clot-free in normal vessels and hemorrhage is stopped by sealing vessels after rupture

Question 3

what is thrombosis?

Answer 3

pathologic process
inappropriate intravascular clotting in a liveing person - clot formation on uninjured endothelium
thrombotic occlusion of vessels after minor injury

Question 4

what is a thrombi?

Answer 4

coagula that form inside blood vessels and heart chambers

Question 5

what are clots?

Answer 5

coagula that form outside of blood vessels or in blood vessels after flow has ceased

Question 6

what is normal coagulation/clotting?

Answer 6

1: injury to vessel wall exposes collagen fibers and causes vasoconstriction
2: factors in blood or tissue activate the clotting cascade to produce thrombin and fibrin
3: thrombrin aggregates and activates platelets
4: platelets attach themselves to the vascular surface to form a primary hemostatic plug
5: clump of fibrin grows on this primary plug with red and white blood cells caught in the interstices => secondary/permanent plug
6: from this point, thrombi are lysed and/or organized (replaced with granulation tissue)

Question 7

what are the causes of endothelial dysfunction?

Answer 7

• haemodynamic stress (in hypertension)
• turbulent flow
• bacterial endotoxins
• homocystinuria, hypercholesterolemia, radiation, cigarette smoke

Question 8

describe normal blood flow

Answer 8

laminar
blood cells flow centrally in the vessel
separated from wall by a thin layer of slower moving plasma

Question 9

describe abnormal blood flow

Answer 9

brings platelets closer to wall
does not dilute the clotting factors and/or bring enough anti-clotting factors
activates endothelial cells => endothelial dysfunction

Question 10

what are the causes of ventricular mural thrombosis?

Answer 10

injury to the endocardium (endothelium lining the heart chambers)
or decreased flow following a MI

Question 11

what can cause thrombosis of the heart valves?

Answer 11

endothelial injury (bacteria, antibodies or immune complexes, trauma of instrumentation)
hypercoagulable states

Question 12

what is the result of thrombosis of the heart valves?

Answer 12

vegetations = brownish material - irregular reddish tan tissues - accumulation of bacteria

caused by endothelial injury or hypercoagulable states

Question 13

what causes phlebothrombosis? where does it occur most often?

Answer 13

stasis of blood in uninfammed veins - hypercoagulability might be an aggravating factor
occurs most often in deep veins in calf, popliteal fossa, tributeries of IVC

Question 14

what is the gross appearance of phlebothrombosis?

Answer 14

firmly anchored head

loosely anchored tail or propagated thrombosis

Question 15

what are the complications of phlebothrombosis?

Answer 15

pulmonary embolism

edema of distal extremities

Question 16

what are the two types of venous thrombosis?

Answer 16

phlebothrombosis

thrombophlebitis

Question 17

what is thrombophlebitis? what are the two types and what are the causes?

Answer 17

thrombosis in inflammed veins
sterile - due to trauma, radiation, or chemicals
septic - due to bacteria

Question 18

what are the outcomes of thrombosis? (4)

Answer 18

1: can be lysed and vessel wall restored entirely
2: thrombi is incorporated into vessel wall and is organized into CT
3: propagation towards the heart
4: embolization to the lungs

Question 19

what are the most frequent types of embolism (list)?

Answer 19

1: pulmonary thromboembolism
2: systemic embolism
3: fat embolism
4: air embolism - decompression sickness
5: amniotic fluid embolism

Question 20

what is an embolism?

Answer 20

intravascular mass (solid, liquid or gaseous)
detached - not adherent to the vascular wall
carried by the blood to a distant site from its point of origin

Question 21

what are some common types of embolism?

Answer 21

1) a part of a dislodged thrombus - thromboembolism (the most frequent)
2) droplets of fat (fat emboli)
3) bubbles of oxygen or nitrogen (e.g. decompression sickness)
4) atherosclerotic debris (cholesterol emboli)
5) tumor fragments
6) bits of bone marrow (e.g. fractures of the long bones)
7) foreign bodies (e.g. bits of bullets)
8) amniotic fluid

Question 22

what are the three types of thromboembolism? where do they each originate? where do the lodge?

Answer 22

1: venous - origin venous circulation - lodge in PC
2: arterial - origin heart and large vessels - lodge in SC
3: paradoxical - venous origin pass through a shunt and lodge in SC

Question 23

what is the most frequent type of emboli? what is their usual path?

Answer 23

pulmonary thromboembolism

95% originate in the deep veins of the legs and pass through the right heart into the pulmonary circulation

Question 24

what is the clinical outcome of small pulmonary emboli?

Answer 24

silent unless they are septic => pneumonia

Question 25

what are the causes of endothelial injury? (list)

Answer 25

1: loss of endothelial cells 2: inflammation 3: anatomic alterations 4: trauma or surgery 5: endothelial dysfunction

Question 26

what are the causes of endothelial function?

Answer 26

1: haemodynamic stress (in hypertension) 2: turbulent flow - scarred valves, atheroma 3: bacterial endotoxins 4: homocystinuria, hypercholesterolemia, radiation, cigarette smoke

Question 27

what are the possible reasons for decreased blood flow (stasis)?

Answer 27

patients confined to bed dilated atria or dilated vessels venous thrombosis

Question 28

where does turbulent blood flow often occur?

Answer 28

arterial and cardiac thrombosis aneurism arterial bifurcations results in endothelial injury and dysfunction

Question 29

what is hypercoagulability?

Answer 29

alterations in the coagulation that upset teh balance between pro and anti-coagulant factors

Question 30

what are the primary (genetic) causes of hypercoagulability?

Answer 30

``` common: factor V mutation prothrombin mutation 5,10 methylenetetrahydrofolate reductase increased levels of factors VIII, IX, XI or fibrinogen ``` rare: antithromin III deficiency protein C deficiency protein S deficiency very rare: fibrinolysis defects homozygous homocystinuria

Question 31

what are the secondary (acquired) causes of hypercoagulability?

Answer 31

cardiac failure or tissue damage oral contraceptives, hyperestrogenic state in pregnancy disseminated cancer increased platelets numbers, stickier platelets labile clotting cascades life style (smoking) heparin-induced thrombocytoneuria anti phospholipid antibody syndrome (lupus anticoagulant syndrome)

Question 32

what is heparin-induced thrombocytoneuria?

Answer 32

unfractionated heparin induces the fomration of anti heparin-platelet factor 4 antibodies => activation and aggregation of platelets and endothelial damage => procoagulant state newer heparin preparations induce less antibodies - induce platelet aggregation if the antibodies are formed already secondary cause of hypercoagulability

Question 33

what is anti phospholipid antibody syndrome (lupus anticoagulant syndrome)?

Answer 33

protean clinical manifestations misnomer - the effects are mediated by teh binding of antibodies to plasma proteins => endothelial damage and platelet and complement activation => hypercoagulant state secondary cause of hypercoagulability

Question 34

what is thrombosis in microcirculation called?

Answer 34

disseminated intravascular coagulation (DIC)

Question 35

what is the cause of DIC?

Answer 35

1: widespread fibrin thrombi in the microcirculation cause diffuse circulatory insufficiency (only visible by microscope) 2: massive formation of thrombi consumes platelets and coagulation factors and activates fibrinolytic mechanisms => serious bleeding disorder

Question 36

what are the clinical outcomes of pulmonary thromboembolisms? (summary card)

Answer 36

1: small pulmonary emboli (silent unless septic => pneumonia) 2: large arteries or pulmonary circulation with multiple small emboli => sudden death, right heart failure, cardiogenic shock 3: medium arteries => hemorrhage, wedge-shaped infarct in the setting of left heart failure 4: small end-arteriolar pulmonary branches => infarction or hemorrhage 5: multiple emboli over time => pulmonary hypertension with right heart failure

Question 37

what are the clinical outcomes of a pulmonary thromboembolism that lodges in the large arteries or 60% of the pulmonary circulation with multiple small emboli?

Answer 37

sudden death right heart failure cardiogenic shock

Question 38

what is the clinical outcome if a pulmonary thromboembolism lodges in the medium arteries?

Answer 38

may lead to hemorrhage (due to bronchial circulation) | a wedge-shaped infarct in the setting of left heart failure

Question 39

what are the clinical outcomes if a pulmonary thromboembolism lodges in the small end-arteriolar pulmonary branches?

Answer 39

infarction | hemorrhage

Question 40

what is the clinical outcome if a pulmonary thromboembolism if there are multiple emboli over time?

Answer 40

pulmonary hypertension with right heart failure

Question 41

what is a systemic thromboembolism?

Answer 41

thromboemboli that travel in the systemic circulation

Question 42

where do systemic thromboemboli originate?

Answer 42

80% in left side of heart - 66% mural thrombi associated with MI - 25% dilated fibrillating atria rest from aortic aneurisms, atherosclerotic plaques, valvular vegetations, paradoxical and unknown origin

Question 43

where do systemic thromboemboli lodge?

Answer 43

in any vascular bed - 75% in lower extremities - 10% in brain less commonly in upper extremities, kidneys, spleen, intestine

Question 44

what is the consequence of systemic thromboemboli?

Answer 44

usually infarction of tissue downstream from occluded artery | depends on collateral supply and tissue resistance to ischemia

Question 45

what is a fat embolism?

Answer 45

multiple microscopic fat globules enter the circulation and obliterate an artery

Question 46

what is the origin of fat emboli?

Answer 46

fractures of long bones with fatty bone marrow trauma of fat tissue burns

Question 47

what are the consequences of a fat embolism?

Answer 47

usually silent, but can get fat embolism syndrome in severe cases mechanical obstruction of vasculature local biochemical injury of endothelium => release of free FA from flat globules, platelet aggregation and granulocyte activation

Question 48

what is fat embolism syndrome? what are the clinical symptoms?

Answer 48

when a fat embolism causes severe symptoms can be pulmonary insufficiency: trachypnea, dyspnea, tachycardia (ARDS) neurological: irritability, restlessness, delirium, coma anemia and thrombocytopenia, widespread petechiae due to local RBC and platelet aggregation

Question 49

what is an air embolism?

Answer 49

gas bubbles within the circulation cause physical obstruction by themselves or coalesce forming "frothy masses" that cna occlude large arteries or atria

Question 50

when do air embolisms occur?

Answer 50

obstetric procedures large chest trauma decompression sickness

Question 51

what is acute decompression sickness?

Answer 51

due to sudden transition from high to low pressure cause of air embolism breathed gas bubbles out of solution in the blood => gas emboli => the bends, focal ischemia in the brain and heart, the chokes, focal atelectasis or emphysema

Question 52

what are the bends?

Answer 52

consequence of acute decompression sickness/air embolism pain due to rapid formation of air bubbles in the muscles and supporting tissue of the joints

Question 53

what are the chokes?

Answer 53

consequence of acute decompression sickness/air embolism lung edema, hemorrhages

Question 54

how is acute decompression sickness treated?

Answer 54

high pressure with slow decompression

Question 55

what is chronic decompression sickness (caisson disease)?

Answer 55

cause of air embolism

Question 56

what caused caisson disease?

Answer 56

workers building bridges used to work in compressed chambers (high pressure) - doesn't happen anymore

Question 57

what is the mechanism and consequence of caisson disease?

Answer 57

persistence of gas emboli in the skeletal system => focal necrosis (in femur, humerus, tibia)

Question 58

what is an amniotic fluid embolism? how does it occur?

Answer 58

infusion of amniotic fluid or fetal masses in the maternal circulation via a tear in the placenta or rupture of uterine veins

Question 59

when does amniotic fluid embolism occur? how often?

Answer 59

during labor immediately postpartum very rare (1:50,000) but 20-40% mortality rate

Question 60

how would you pathologically identify an amniotic fluid embolism?

Answer 60

the presence of fetal squamous skin cells, lanugo hair, vernix caseosa fat and mucin from fetal intestine in maternal pulmonary circulation

Question 61

what is shock? what are the causes?

Answer 61

decreased systemic perfusion of tissues due to decrease in effective circulating blood volume or decreased cardiac output

Question 62

what are the consequences of shock?

Answer 62

hypotension => impaired tissue perfusion => cell hypoxia

Question 63

what are the five types of shock? what are causes of each?

Answer 63

1: cardiogenic - MI, myocarditis, cardiac tamponade, pulmonary embolus 2: hypovolemic: hemorrhage, diarrhea, dehydration, burns 3: septic: severe infection 4: anaphylactic: type I hypersensitivity reaction 5: neurogenic: brain damage, spinal cord injury

Question 64

what can cause decreased cardiac output, leading to shock?

Answer 64

myocardial pump fails

Question 65

what can lead to decreased effective circulating blood volume, leading to shock?

Answer 65

decreased blood volume due to hemorrhage or increased vascular permeability increased system volume (vasodilation)

Question 66

what are the stages of shock? (list)

Answer 66

progressive disorder 1: nonprogressive or compensated 2: progressive but still reversible 3: irreversible

Question 67

describe the first stage of shock.

Answer 67

nonprogressive or compensated compensatory mechanisms maintain CO and BP => enables perfusion of vital organs such as heart and brain

Question 68

describe the second stage of shock

Answer 68

progressive but still reversible generalized tissue hypoperfusion and worsening of circulatory and metabolic imbalances

Question 69

describe the third stage of shock

Answer 69

irreversible severe tissue and cellular injury that results in multiple organ failure and death even in the conditions of hemodynamic defects

Question 70

what are the cellular and tissue changes due to shock? (ie what would you see pathologically)

Answer 70

hypoxic injury to tissue | widespread thrombi, multiple foci of ischemic necrosis, hemorrhage

Question 71

what determines O2 supply to tissue? during what types of shock are the altered?

Answer 71

cardiac output (decreased by cardiogenic shock) amount of circulating hemoglobin (decreased in hypovolemic shock) arterial O2 saturation (decreased in both cardiogenic and hypovolemic shock)