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SP15 Pathology > Exam 1; Thrombosis/Embolism/Infarction/Shock > Flashcards

Exam 1; Thrombosis/Embolism/Infarction/Shock Flashcards

1
Q

This is an intravascular clot, often impeding blood flow

A

thrombus

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2
Q

This is the formation or presence of a thrombus, which may result in infarction

A

thrombosis

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3
Q

What is the “Virchow’s” triad that leads to thrombosis

A

endothelial injury
alterations in blood flow
hypercoagulability

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4
Q

What two things can cause the endothelial injury leading to thrombosis

A

loss of barrier

increased pro-thrombin activity caused by many things

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5
Q

What three things can cause the alteration in blood flow leading to thrombosis

A

turbulence
stasis; allowing the concentration of clotting factors, activates endothelial cells
aneurysms/atherosclerotic plaques

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6
Q

What type of conditions can cause hypercoaguability

A

inherited

acquired

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7
Q

What are the three inherited conditions that can cause hypercoaguability

A

factor V leiden
AT III deficiency (anticoagulant protein)
prothrombin mutation

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8
Q

What are some acquired conditions that can cause hypercoaguability

A 
prolonged bed rest
extensive tissue injury
pregnancy
cancer
anti-PL antibodies (phospholipid)
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9
Q

This is also known as a white thrombi and it tends to occur at sites of turbulence or endothelial injury and loss; may be occlusal or mural, typically lodging in small arterioles or heart valves

A

arterial thrombi

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10
Q

What kind of lines of Zahn does a white thrombi have

A

distinct

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11
Q

This is also known as a red thrombi and is often found in the deep veins of the legs

A

venous thrombi

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12
Q

What kind of lines of Zahn does a red thrombi have

A

indistinct

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13
Q

This fate of a thrombi is when it can enlarge by additional fibrin/platelet deposition

A

propagation

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14
Q

This fate of a thrombi is when the entire thrombus dislodges or a piece breaks loose

A

embolization

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15
Q

This fate of a thrombi is when it lyses by fibrinolytic activity

A

dissolution

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16
Q

This fate of a thrombi is an ingrowth of fibroblasts and smooth muscle cells, leading to deposition of collagen and recanalization, which may re-establish flow through the thrombus

A

organization

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17
Q

This is the widespread activation of the coagulation cascade and fibrinolytic system leading to depletion of coagulation factors and platelets and accumulation of fibrin split products

A

disseminated intravascular coagulation (DIC)

18
Q

What can DIC be associated with

A

widespread formation of micro thrombi and risk of hemorrhage

conditions associated are infection, obstetric complications, neoplasm, shock, massive injury, etc.

19
Q

What is the treatment for DIC

A

highly variable
dependent upon management of the underlying disorder
potentially life-threatening

20
Q

What is the origin of a pulmonary thromboembolism

A

thromboemboli that lodges in pulmonary arteries usually arising from deep veins in the legs

21
Q

What are the five consequences of a pulmonary thromboemboli

A

no clinical manifestation
pulmonary hemorrhage and hematemesis
pulmonary infarction
sudden death due to large emboli obstructing the large pulmonary artery or straddling the bifurcation as a saddle
gradual obstruction of many small pulmonary arteries resulting in pulmonary hypertension

22
Q

This is an embolism that arises in a systemic vein and crosses a communication from the venous side to the arterial side of circulation; usually through the foramen ovale

A

paradoxical embolus

23
Q

This is an embolism that originates usually from the left atrium, left ventricle or ulcerated atherosclerotic plaque; they can travel to any systemic artery

A

systemic embolism

24
Q

This type of emboli may arise from a fracture of a large long bone, soft tissue injury

A

fat

25
Q

This type of emboli may arise from a chest wall injury or decompression sickness

A

air

26
Q

This type of embolism is a rare complication of pregnancy, associated with DIC

A

amniotic fluid

27
Q

This type of embolism is from debris from the central core of an atherosclerotic plaque

A

atherosclerotic

28
Q

This is an ischemic necrosis involving all cell types in a segment of an organ or the entire organ

A

infarction

29
Q

Infarction is usually due to what

A

arterial obstruction, less often due to vessel twisting, venous obstruction or slow flow from the cause such as shock

30
Q

What are some conditions that lead to hemorrhagic infarcts

A

venous occlusion
loos tissue
dual circulation or extensive arterial supply overlap
previos congestion
infarction followed by a re-flow of blood to the area

31
Q

What are some conditions that lead to white (pale) infarcts

A

arterial occlusion in solid organs (like kidney where there is only one way in)
where tissue density limits blood seepage from adjacent vascular beds

32
Q

Infarcts tend to be which shape

A

wedge shaped with the point of the lede at the site of arterial obstruction

33
Q

Infarction is followed by which kind of response

A

acute inflammatory response that begins within several hours

healing occur by granulation tissue ingrowth followed by scar formation

34
Q

Infarctions of the brain result in what

A

liquefactive necrosis and heal with formation of cystic space

35
Q

What are four factors that influence infarction development

A

nature of the blood supply (dual vs single)
rate of development of occlusion; slow occlusion allows time for opening of collateral vessels
vulnerability to hypoxia; some tissue are more vulnerable
oxygen carrying capacity of the blood

36
Q

This is “systemic hypoperfusion” - low blood perfusion to the tissues

A

shock

37
Q

What are the five different type of shock

A 
cardiogenic
hypovolemic
septic
anaphylactic
neurogenic
38
Q

What are the four associated pathogenicities of septic shock

A

PAMPs (like LPS) bind to TLRs on monocytes and neutrophils mediating the release of IL-1 and TNF
secondary release of cytokines
vasodilation, hypotension, endothelial cell activation, reduced myocardial contractility

39
Q

This stage of shock is when compensatory mechanisms maintain tissue perfusion by tachycardia, renal conversation of water, redistribution of the blood to vital organs.

A

non-progressive

40
Q

This stage of shock is when inadequaate perfusion with metabolic imbalances such as acidosis and increased lactic acid leads to pooling of blood and reduced perfusion. Hypoxic injury to endothelium results in DIC

A

progressive

41
Q

This stage of shock is when tissue injury cannot be reversed by re-perfusion

A

irreversible

42
Q

What are some clinical manifestations of shock

A 
tachycardia/tachypnea (rapid breathing)
hypotension
cold, clammy skin
pallor/cyanosis
confusion
low urine output
acidosis; high lactic acid

SP15 Pathology (17 decks)

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