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gen path- exam 1 > thrombosis, embolism, infarction, shock > Flashcards

thrombosis, embolism, infarction, shock Flashcards

1
Q

what is a thrombus?

A

intravascular clot, often impeding blood flow

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2
Q

what is a thrombosis?

A

formation or presence of a thrombus, may result in infarction

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3
Q

what is Virchow’s triad ?

A

its the pathogenesis of thrombosis formation

  • Endothelial injury
  • Alterations in blood flow
  • Hypercoagulability
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4
Q

_________ induces endothelial dysfunction and activation

A

Turbulence

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5
Q

what effect does blood flow stasis have on thrombosis formation?

A

endothelial activation

peripheral displacement of platelets

concentration of clotting factors

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6
Q

what inheritable conditions cause hypercoagulation?

A

Factor V Leiden (Va can not be cleaved)

AT III deficiency

Prothrombin mutation

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7
Q

list the various ACQUIRED conditions that can cause hypercoagulation

A

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

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8
Q

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

A

arterial

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9
Q

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

A

lines of Zahn

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10
Q

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

A

nonbacterial thrombotic endocarditis (NBTE)

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11
Q

what are the characteristics of venous thrombi?

A

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

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12
Q

where do venous thrombi often form?

A

Often form in deep veins of the legs

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13
Q

what are the 4 “fates” of formed thrombi?

A

1) Propagation
2) Embolization
3) Dissolution (resolution)
4) Organization (recanalization)

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14
Q

what occurs during the “organization” of a thrombus?

A

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

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15
Q

disseminated intravascular coagulation (DIC) is caused by what?

A

Widespread activation of the coagulation cascade and fibrinolytic systems

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16
Q

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

A

-Depletion of coagulation factors and platelets

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17
Q

disseminated intravascular coagulation is also known as “_______________”

A

“consumptive coagulopathy”

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18
Q

what are the etiologies (causes) of DIC?

A

-Infection

  • Obstetric complications
    a) placental abruption
    b) retained dead fetus
  • Neoplasm
  • Shock
  • Massive tissue injury
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19
Q

infections from __________ bacteria are a common etiology for DIC

A

gram negative bacteria

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20
Q

what is an embolus?

A

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

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21
Q

the treatment of _____ is dependent upon management of underlying disorder

A

DIC

disseminated intravascular coagulation

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22
Q

a vast majority of embolisms are made of what substance?

A

dislodged thrombus material

23
Q

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

A

thromboembolism

24
Q

what is the origin of a pulmonary thromboembolism?

A

deep leg veins (usually)

25
Q

how can a thromboembolism cause sudden death?

A

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

26
Q

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

A

pulmonary hypertension

27
Q

what is a Paradoxical embolus?

A

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

28
Q

where does the communication occur during a paradoxical embolism?

A

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

2) atrial septal defect
3) or other anomalous communication

29
Q

where does Systemic embolization usually start?

A

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

30
Q

systemic embolisms can travel to any _______ artery

A

systemic

31
Q

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

A
  • chest wall injury, decompression sickness

- the “bends” and caisson disease

32
Q

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

A

infarctions

33
Q

infarctions are usually caused by what?

A

arterial obstruction

34
Q

what conditions lead to Red (hemorrhagic) Infarctions?

A

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
Q

what are the characteristics of white (pale) infarctions?

A
  1. Occur with arterial occlusions in solid organs

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

36
Q

what factors influence infarct development?

A

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

37
Q

what is “shock”?

A

systemic hypoperfusion (lack of perfusion) of tissues

38
Q

what are the pathophysiological categories of shock?

A
  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
Q

septic shock is the #1 cause of death in _______________

A

intensive care units

40
Q

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

A

IL-1 and TNF

41
Q

what are the clinical effects of septic shock?

A

Vasodilation
hypotension
endothelial cell activation and injury
reduced myocardial contractility

42
Q

what occurs during nonprogressive shock?

A

compensatory mechanisms maintain perfusion

43
Q

what “compensatory mechanisms” maintain perfusion during nonprogressive shock?

A

catecholamines, renin, ADH, sympathetic nervous system stimulation

44
Q

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

A

nonprogressive

45
Q

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

A

progressive

46
Q

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

A

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

47
Q

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

A

DIC

disseminated intravascular coagulation

48
Q

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

A

irreversible

49
Q

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

A

hippocampus and cerebellum

50
Q

during shock, contraction band necrosis occurs in ___________

A

the heart

51
Q

what are the clinical manifestations of shock?

A
  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
Q

Centrizonal necrosis occurs in the _______ during shock

A

liver

53
Q

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

A

liquefactive (not coagulative)

gen path- exam 1 (10 decks)

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