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Path Quiz 1 > circulation II > Flashcards

circulation II Flashcards

1
Q

what are the three causes of thrombosis?

A

virchow’s triad:

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

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2
Q

what is hemostasis?

A

normal physiological process

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

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3
Q

what is thrombosis?

A

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

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4
Q

what is a thrombi?

A

coagula that form inside blood vessels and heart chambers

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5
Q

what are clots?

A

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

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6
Q

what is normal coagulation/clotting?

A

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)

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7
Q

what are the causes of endothelial dysfunction?

A
  • haemodynamic stress (in hypertension)
  • turbulent flow
  • bacterial endotoxins
  • homocystinuria, hypercholesterolemia, radiation, cigarette smoke
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8
Q

describe normal blood flow

A

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

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9
Q

describe abnormal blood flow

A

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

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10
Q

what are the causes of ventricular mural thrombosis?

A

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

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11
Q

what can cause thrombosis of the heart valves?

A 
endothelial injury (bacteria, antibodies or immune complexes, trauma of instrumentation)
hypercoagulable states
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12
Q

what is the result of thrombosis of the heart valves?

A

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

caused by endothelial injury or hypercoagulable states

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13
Q

what causes phlebothrombosis? where does it occur most often?

A

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

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14
Q

what is the gross appearance of phlebothrombosis?

A

firmly anchored head

loosely anchored tail or propagated thrombosis

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15
Q

what are the complications of phlebothrombosis?

A

pulmonary embolism

edema of distal extremities

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16
Q

what are the two types of venous thrombosis?

A

phlebothrombosis

thrombophlebitis

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17
Q

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

A

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

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18
Q

what are the outcomes of thrombosis? (4)

A

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

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19
Q

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

A

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

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20
Q

what is an embolism?

A 
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
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21
Q

what are some common types of embolism?

A

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

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22
Q

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

A

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

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23
Q

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

A

pulmonary thromboembolism

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

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24
Q

what is the clinical outcome of small pulmonary emboli?

A

silent unless they are septic => pneumonia

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25
Q

what are the causes of endothelial injury? (list)

A

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

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26
Q

what are the causes of endothelial function?

A

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

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27
Q

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

A

patients confined to bed
dilated atria or dilated vessels
venous thrombosis

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28
Q

where does turbulent blood flow often occur?

A

arterial and cardiac thrombosis
aneurism
arterial bifurcations

results in endothelial injury and dysfunction

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29
Q

what is hypercoagulability?

A

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

30
Q

what are the primary (genetic) causes of hypercoagulability?

A 
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

31
Q

what are the secondary (acquired) causes of hypercoagulability?

A

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)

32
Q

what is heparin-induced thrombocytoneuria?

A

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

33
Q

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

A

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

34
Q

what is thrombosis in microcirculation called?

A

disseminated intravascular coagulation (DIC)

35
Q

what is the cause of DIC?

A

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

36
Q

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

A

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

37
Q

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?

A

sudden death
right heart failure
cardiogenic shock

38
Q

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

A

may lead to hemorrhage (due to bronchial circulation)

a wedge-shaped infarct in the setting of left heart failure

39
Q

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

A

infarction

hemorrhage

40
Q

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

A

pulmonary hypertension with right heart failure

41
Q

what is a systemic thromboembolism?

A

thromboemboli that travel in the systemic circulation

42
Q

where do systemic thromboemboli originate?

A

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

43
Q

where do systemic thromboemboli lodge?

A

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

44
Q

what is the consequence of systemic thromboemboli?

A

usually infarction of tissue downstream from occluded artery

depends on collateral supply and tissue resistance to ischemia

45
Q

what is a fat embolism?

A

multiple microscopic fat globules enter the circulation and obliterate an artery

46
Q

what is the origin of fat emboli?

A

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

47
Q

what are the consequences of a fat embolism?

A

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

48
Q

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

A

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

49
Q

what is an air embolism?

A

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

50
Q

when do air embolisms occur?

A

obstetric procedures
large chest trauma
decompression sickness

51
Q

what is acute decompression sickness?

A

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

52
Q

what are the bends?

A

consequence of acute decompression sickness/air embolism

pain due to rapid formation of air bubbles in the muscles and supporting tissue of the joints

53
Q

what are the chokes?

A

consequence of acute decompression sickness/air embolism

lung edema, hemorrhages

54
Q

how is acute decompression sickness treated?

A

high pressure with slow decompression

55
Q

what is chronic decompression sickness (caisson disease)?

A

cause of air embolism

56
Q

what caused caisson disease?

A

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

57
Q

what is the mechanism and consequence of caisson disease?

A

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

58
Q

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

A

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

59
Q

when does amniotic fluid embolism occur? how often?

A

during labor
immediately postpartum

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

60
Q

how would you pathologically identify an amniotic fluid embolism?

A

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

61
Q

what is shock? what are the causes?

A

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

62
Q

what are the consequences of shock?

A

hypotension => impaired tissue perfusion => cell hypoxia

63
Q

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

A

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

64
Q

what can cause decreased cardiac output, leading to shock?

A

myocardial pump fails

65
Q

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

A

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

66
Q

what are the stages of shock? (list)

A

progressive disorder

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

67
Q

describe the first stage of shock.

A

nonprogressive or compensated

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

68
Q

describe the second stage of shock

A

progressive but still reversible

generalized tissue hypoperfusion and worsening of circulatory and metabolic imbalances

69
Q

describe the third stage of shock

A

irreversible

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

70
Q

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

A

hypoxic injury to tissue

widespread thrombi, multiple foci of ischemic necrosis, hemorrhage

71
Q

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

A

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

Path Quiz 1 (12 decks)

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