thrombosis, embolism, infarction, shock Flashcards Preview

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Flashcards in thrombosis, embolism, infarction, shock Deck (53):
1

what is a thrombus?

intravascular clot, often impeding blood flow

2

what is a thrombosis?

formation or presence of a thrombus, may result in infarction

3

what is Virchow’s triad?

its the pathogenesis of thrombosis formation

-Endothelial injury

-Alterations in blood flow

-Hypercoagulability

4

_________ induces endothelial dysfunction and activation

Turbulence

5

what effect does blood flow stasis have on thrombosis formation?

endothelial activation

peripheral displacement of platelets

concentration of clotting factors

6

what inheritable conditions cause hypercoagulation?

Factor V Leiden (Va can not be cleaved)

AT III deficiency

Prothrombin mutation

7

list the various ACQUIRED conditions that can cause hypercoagulation

a) prolonged bed rest
b) extensive tissue damage for example in burns and surgery
c) cancer
d) antiphospholipid antibody syndrome (anti-PL), also called lupus anticoagulant
e) pregnancy

8

________ thrombi tend to occur at sites of turbulence or endothelial injury and loss

arterial

9

arterial thrombi have a pale (“white”) appearance with distinct _________

lines of Zahn

10

Sterile (non-infectious) thrombi on heart valves are called what?

nonbacterial thrombotic endocarditis (NBTE)

11

what are the characteristics of venous thrombi?

These have a dark maroon color (“red”) and indistinct lines of Zahn

12

where do venous thrombi often form?

Often form in deep veins of the legs

13

what are the 4 "fates" of formed thrombi?

1) Propagation

2) Embolization

3) Dissolution (resolution)

4) Organization (recanalization)

14

what occurs during the "organization" of a thrombus?

ingrowth of fibroblasts and smooth muscle cells, leads to deposition of collagen (replacing the fibrin) and recanalization, which may re-establish some flow through the thrombus

15

disseminated intravascular coagulation (DIC) is caused by what?

Widespread activation of the coagulation cascade and fibrinolytic systems

16

what are the effects of DIC's widespread activation of the coagulation cascade?

-Depletion of coagulation factors and platelets

-Elevation of fibrin split products

17

disseminated intravascular coagulation is also known as "_______________"

“consumptive coagulopathy”

18

what are the etiologies (causes) of DIC?

-Infection

-Obstetric complications
a) placental abruption
b) retained dead fetus

-Neoplasm

-Shock

-Massive tissue injury

19

infections from __________ bacteria are a common etiology for DIC

gram negative bacteria

20

what is an embolus?

a solid, liquid or gas (bubble) carried from one point to another point in the vascular system

21

the treatment of _____ is dependent upon management of underlying disorder

DIC

(disseminated intravascular coagulation)

22

a vast majority of embolisms are made of what substance?

dislodged thrombus material

23

a __________ is the name of an embolism caused by thrombus material

thromboembolism

24

what is the origin of a pulmonary thromboembolism?

deep leg veins (usually)

25

how can a thromboembolism cause sudden death?

due to large emboli obstructing:
1) a large pulmonary artery
or
2) straddling the bifurcation of the pulmonary arterial trunk

26

gradual obstruction of many small pulmonary arteries by repeated embolization over time can result in _________________

pulmonary hypertension

27

what is a Paradoxical embolus?

embolus that arises in a systemic vein and crosses a communication from the venous side to the arterial side of the circulation

28

where does the communication occur during a paradoxical embolism?

usually in the heart through:
1) a patent foramen ovale

2) atrial septal defect

3) or other anomalous communication

29

where does Systemic embolization usually start?

usually left atrium, left ventricle (including heart valve vegetation) or ulcerated atherosclerotic plaque

30

systemic embolisms can travel to any _______ artery

systemic

31

where do air embolisms usually begin? what conditions are associated with them?

- chest wall injury, decompression sickness

- the “bends” and caisson disease

32

________ are defined as ischemic necrosis involving all cell types in a segment of an organ or the entire organ

infarctions

33

infarctions are usually caused by what?

arterial obstruction

34

what conditions lead to Red (hemorrhagic) Infarctions?

a) venous occlusion
b) loose tissue (lung)
c) dual circulation or extensive overlap of arterial supply (lung, small intestine)

d) previous congestion
e) infarction followed by reflow of blood into the area (reperfusion injury).

35

what are the characteristics of white (pale) infarctions?

1. Occur with arterial occlusions in solid organs

2. Where tissue density limits blood seepage from adjacent vascular beds

36

what factors influence infarct development?

Nature of vascular supply
Rate of occlusion
Vulnerability to hypoxia
Oxygen carrying capacity of cardiovascular system

37

what is "shock"?

systemic hypoperfusion (lack of perfusion) of tissues

38

what are the pathophysiological categories of shock?

1. Cardiogenic – loss of pumping capacity of the heart

2. Hypovolemic – blood loss

3. Septic – bacterial infection

4. Anaphylactic – hypersensitivity reaction mediated by IgE

5. Neurogenic – loss of vascular tone (anesthesia, spinal cord injury)

39

septic shock is the #1 cause of death in _______________

intensive care units

40

during septic shock, PAMPS (microbial products) bind to toll-like receptors (TLRs) on monocytes and neutrophils mediating the release of _________ and _______

IL-1 and TNF

41

what are the clinical effects of septic shock?

Vasodilation
hypotension
endothelial cell activation and injury
reduced myocardial contractility

42

what occurs during nonprogressive shock?

compensatory mechanisms maintain perfusion

43

what "compensatory mechanisms" maintain perfusion during nonprogressive shock?

catecholamines, renin, ADH, sympathetic nervous system stimulation

44

tachycardia, renal conservation of water, redistribution of blood to vital organs are all signs of what STAGE of shock?

nonprogressive

45

the _________ stage is characterized by Inadequate perfusion with metabolic imbalances such as acidosis and increased lactic acid

progressive

46

what are the effects of acidosis (produced by progressive shock)

The acidosis reduces vasomotor response to sympathetic stimulation
- leads to pooling of blood and reduced perfusion

47

Hypoxic injury to endothelium during shock will results in what condition?

DIC

(disseminated intravascular coagulation)

48

during the _______ stage of shock, there is tissue injury that can not be reversed by reperfusion

irreversible

49

during shock, Ischemic necrosis of neurons in the brain effects which regions most severely?

hippocampus and cerebellum

50

during shock, contraction band necrosis occurs in ___________

the heart

51

what are the clinical manifestations of shock?

1. Tachycardia
2. Tachypnea
3. Hypotension
4. Cool clammy skin (may be warm and flushed in septic shock)

5. Decreased urinary output
6. Confusion
7. Low blood pH (acidosis) with elevated lactic acid

52

Centrizonal necrosis occurs in the _______ during shock

liver

53

Infarcts in the brain result in ______________ necrosis and heal with formation of a cystic space.

liquefactive (not coagulative)