Exam 1; Thrombosis/Embolism/Infarction/Shock Flashcards Preview

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

Flashcards in Exam 1; Thrombosis/Embolism/Infarction/Shock Deck (42):
1

This is an intravascular clot, often impeding blood flow

thrombus

2

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

thrombosis

3

What is the "Virchow's" triad that leads to thrombosis

endothelial injury
alterations in blood flow
hypercoagulability

4

What two things can cause the endothelial injury leading to thrombosis

loss of barrier
increased pro-thrombin activity caused by many things

5

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

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

6

What type of conditions can cause hypercoaguability

inherited
acquired

7

What are the three inherited conditions that can cause hypercoaguability

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

8

What are some acquired conditions that can cause hypercoaguability

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

9

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

arterial thrombi

10

What kind of lines of Zahn does a white thrombi have

distinct

11

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

venous thrombi

12

What kind of lines of Zahn does a red thrombi have

indistinct

13

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

propagation

14

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

embolization

15

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

dissolution

16

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

organization

17

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

disseminated intravascular coagulation (DIC)

18

What can DIC be associated with

widespread formation of micro thrombi and risk of hemorrhage
conditions associated are infection, obstetric complications, neoplasm, shock, massive injury, etc.

19

What is the treatment for DIC

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

20

What is the origin of a pulmonary thromboembolism

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

21

What are the five consequences of a pulmonary thromboemboli

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

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

paradoxical embolus

23

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

systemic embolism

24

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

fat

25

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

air

26

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

amniotic fluid

27

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

atherosclerotic

28

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

infarction

29

Infarction is usually due to what

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

30

What are some conditions that lead to hemorrhagic infarcts

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

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

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

Infarcts tend to be which shape

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

33

Infarction is followed by which kind of response

acute inflammatory response that begins within several hours
healing occur by granulation tissue ingrowth followed by scar formation

34

Infarctions of the brain result in what

liquefactive necrosis and heal with formation of cystic space

35

What are four factors that influence infarction development

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

This is "systemic hypoperfusion" - low blood perfusion to the tissues

shock

37

What are the five different type of shock

cardiogenic
hypovolemic
septic
anaphylactic
neurogenic

38

What are the four associated pathogenicities of septic shock

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

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

non-progressive

40

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

progressive

41

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

irreversible

42

What are some clinical manifestations of shock

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