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Pathology > Exam 1: Ischemia: Emboli, Infarctions, and Shock > Flashcards

Exam 1: Ischemia: Emboli, Infarctions, and Shock Flashcards

1
Q

What are causes of disseminated intravascular coagulation (DIC)?

A

Massive tissue destruction
Sepsis
Endothelial injury

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2
Q

What is the clinical sign of DIC?

A

Bleeding

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3
Q

How do you treat DIC?

A

Anticoagulants

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4
Q

Look at DIC pathophysiology and understand broad picture

A

Look at DIC pathophysiology and understand broad picture

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5
Q

What is ischemia?

A

Loss of blood supply from impeded arterial flow or venous drainage from a tissue

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6
Q

What does ischemia compromise?

A

The supply of oxygen and metabolic substrates (glucose)

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7
Q

What is a result of shutting down the blood supply with ischemia?

A

Ischemic tissues are injured more rapidly and severely than hypoxic tissues

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8
Q

What are causes of ischemia?

A

Pressure
Vascular constriction
Thrombi
Thromboemboli

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9
Q

What is the outcome of ischemia?

A

Inevitably all emboli lodged in vessels too small to permit further passage— result in partial or complete vascular occlusion
Typically leads to infarction with coagulative necrosis

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10
Q

What is an embolism?

A

A detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin

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11
Q

What do most emboli represent?

A

Some part of a dislodged thrombus (thromboembolus)

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12
Q

What should an embolism be considered as?

A

Thrombotic in origin

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13
Q

What are other forms of emboli?

A 
Droplets of fat
Bubbles of air or nitrogen
Antherosclerotic debris
Bits of bone marrow
Foreign bodies (bullets)
Tumor fragments (METS)
Septic emboli
Miscellaneous (found in lung; hair, skin, liver cells)
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14
Q

What are comon types of thromboembolism and embolism?

A

Pulmonary thromboembolism (venous emboli)
Systemic thromboemblism (arterial emboli)
Bacterial emboli
Neoplastic emboli
Fibrocartilaginous emboli (ruptured intervertebral discs)

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15
Q

Describe air emboli

A

Injected via syringe

can be deadly if injected into veins

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16
Q

Describe fat emboli

A

When a bone fractures, adipose from bone marrow can enter blood stream and cause embolism
Seldom cause infarction

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17
Q

If there is an embolus that starts in the arteries, where does it end up?

A

End stage capillaries (in an organ)

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18
Q

If there is an embolus that starts in the venous system, where does it end up?

A

In the lung

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19
Q

If there is an embolus in the lymphatics, where does it end up?

A

Draining regional lymph node (can stay local or if it goes to the thoracic duct, ends up in the venous system and goes to the lung)

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20
Q

Describe (venous) pulmonary thromboembolus

A

Embolus is carried to the right heart from the periphery
Pushed into the pulmonary tree
Obstructs blood flow to the lungs
Results in acute death

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21
Q

What is a septic embolus?

A

Clusters of bacteria and platelets that are carried by blood and lodge in very small vessels or capillaries
Kidney glomeruli are a common site
Usually arise from vegetative valvular left heart lesion

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22
Q

What is a parasitic embolus?

A

Pieces of intravascular nematodes that break off and lodge at a distant site
This is a common complication in dogs after therapy for heartworm disease
The result would be verminous pulmonary thromboembolism

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23
Q

What is a neoplastic embolus?

A

Tumor cells grow into a vessel and flow through blood to a new site where they can develop into a MET

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24
Q

Describe fibrocartilagenous emboli

A

Emboli frequently from ruptured IV discs
Cause spinal cord infarcts
Seen in dogs, cats, horses, and cattle
Emboli wedges in aa or vv of meninges and spinal cord causing necrosis of tissue

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25
Q

What does a fat emboli arise as?

A

Arise as a complication of bone fracture, prolonged surgery, or osteomyelitis

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26
Q

What is infarction?

A

Ischemic necrosis of tissue caused by occlusion of either the arterial supply or the venous drainage in a particular tissue

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27
Q

What do most infarcts result from?

A

Thrombotic or embolic events in arteries

28
Q

What does an infarction usually result in?

A

Venous obstruction and congestion

29
Q

What is an infarct?

A

A localized area of ischemic necrosis

Sharp line of demarcation between normal and necrotic tissue

30
Q

Early on, what is the line of demarcation of an infarct surrounded by?

A

A zone of hyperemia

31
Q

What do infarcts tend to be like in tissues with dual circulation?

A

Red or dark purple

32
Q

What are infarcts like in solid organs?

A

Frequently start out red due to back flow of blood and leakage of blood from injured vessels, but they rapidly become pale as RBCs and tissue and proteins break down

33
Q

What is a venous infarct caused by?

A

Obstructed veins

34
Q

How do all infarcts heal?

A

By scarring because all tissue is dead and there is nothing left to heal

35
Q

What are consequences of ischemia/necrosis?

A

Earliest change is cell swelling and disintegration of mitochondria
Loss of energy leads to cell membrane damage

36
Q

What happens cell membrane damage?

A

Allows entry of water, electrolytes, and plasma proteins into cells
Increases intracellular Ca lead to irreversible cytopathic changes and necrosis
Cellular enzymes are released into interstitial fluid as the cell dies

37
Q

What is shock?

A

Failure of the circulatory system to adequately perfuse vital organ

38
Q

What is shock characterized by?

A

Low systemic blood flow due to reduction in cardiac output and reduction in circulating blood volume

39
Q

What are the end results of shock?

A

Hypotension followed by impaired tissue perfusion and cellular hypoxia

40
Q

Describe the initial phase of shock

A

Reflex compensatory activities occur and perfusion to vital organs is maintained
Increased HR, peripheral vasoconstriction, renal conservation of fluid

41
Q

Describe the progressive phase of shock

A

Tissue are under perfused (hypoxia)
Anaerobic glycolysis leads to lactic acid production (acidosis)
Arteriole dilation with blood pooling in the microcirculation

42
Q

Describe the irreversible phase of shock

A

Peripheral vasodilation persists
Heart muscle loses contractility
Multiple organ failure

43
Q

What is the primary goal of therapy for shock?

A

Rapid restoration of systemic blood flow by replacement of intravascular fluid and use of drugs that increase vascular tone and support cardiac function

44
Q

What are the types of shock?

A

Cardiogenic
Hypovolemic
Septic
Anaphylactic

45
Q

What is cardiogenic shock caused by?

A

Insults that reduce cardiac output (decrease heart’s ability to pump blood)

46
Q

Describe cardiac tamponade

A

Occurs when fluid accumulates rapidly in the pericardial space
Impedes the ability of the ventricles to dilate and fill with blood
Will cause acute heart failure and result in cardiogenic shock

47
Q

What is hypovolemic shock cause by?

A

Sudden and severe loss of blood volume

48
Q

What are examples of sudden and severe loss of blood volume?

A

Acute hemorrhage involving greater than 1/4 to 1/3 total blood volume
Loss of intravascular and extravascular fluid
Increased vascular permeability

49
Q

What does septic shock result from?

A

A bacterial infection where large quantities of endotoxin are released into the circulation

50
Q

What are endotoxins?

A

Complex components of bacterial cell walls of gram negative bacteria or breakdown products of cell wall degradation

51
Q

What is the toxic molecule of endotoxins?

A

Lipopolysaccharide

52
Q

What happens in low doses of endotoxins?

A

LPS causes acute inflammation to help eliminate the bacteria

53
Q

What happens in high doses of endotoxins?

A

LPS causes widespread endothelial damage, initiation of the coagulation cascade, decreased myocardial contractility, peripheral vasodilation, can lead to irreversible shock and DIC

54
Q

What is the septic shock course of events?

A

Gram negative bacteria in localized infection
Bacterial eall endotoxin released in local inflammation
Endotoxin enters bloodstream
Activates circulating monocytes/macrophages
Monocytes/macrophages produce tumor necrosis factor
Release of cytokines
Systemic vasodilation and systemic inflammatory response
Altered myocardial contractility
Widespread endothelial damage, platelet activation, coagulation cascade
Multiorgan failure
DIC

55
Q

What is anaphylactic shock?

A

Systemic manifestation of acute hypersensitivity response

Idiosyncratic reaction that occurs in certain predisposed individuals upon exposure to certain allergins

56
Q

What happens upon exposure to antigens to cause anaphylactic shock?

A

Histamine and other mediators are released causing vasodilation and increased vascular permeability with loss of intravascular fluid

57
Q

What does anaphylactic shock result in?

A

Eventual cardiovascular collapse

58
Q

What are the gross and histologic lesions of shock?

A

Lesions associated with the presenting complaint
Systemic vasodilation leads to pooling of blood in various organs and maybe hemorrhage
Liver, GI tract, lungs, kidneys, and adrenal glands
Degeneration/necrosis of cells due to hypoxia/anoxia

59
Q

What is the biggest clinical consequence of shock?

A

Oxygen does not get to cells causing multiple organs to eventually fail

60
Q

What makes endothelial injury a consequence of shock?

A

Increased vascular permeability and loss of intravascular fluid further aggravate hypovolemia and anoxia

61
Q

What results in metabolic acidosis in shock?

A

Descreased kidney function and muscle perfusion

62
Q

What happens to the heart in shock?

A

Decreased perfusion of heart muscle causes anoxic injury to myocytes

63
Q

What are the cardiovascular and systemic responses to shock?

A

The body responds to attempting to increase cardiac output by shunting blood to vital organs
If these adjustments fail and inciting cause is not corrected, uncompensated shock results
Microvasculature is unresponsively dilated (end stage vasodilatory shock)
Death is the outcome

64
Q

What is the cardiac support to shock?

A

Epinephrine and norepinephrine from adrenal medulla to increase heart rate
Aldosterone from adrenal cortex to retain sodium and water, thereby increasing blood volume

65
Q

What is the vascular support to shock?

A

Epinephrine and norepinephrine stimulate vasoconstriction

Renin-angiotensin system produce angiotensin II which stimulates vasoconstriction

Pathology (16 decks)

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