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Pathology > Ischemia, Emboli, Infarctions, Shock > Flashcards

Ischemia, Emboli, Infarctions, Shock Flashcards

(50 cards)

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1
Q

Ischemia

A

Loss of blood supply from impeded arterial flow or venous drainage from a tissue
- compromises supply of oxygen, glucose, and metabolic substrates

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2
Q

Are ischemic tissues injured more rapidly than hypoxic tissues?

A

Yes

- hypoxia can still provide glucose and remove by products

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3
Q

What are the 4 causes of ischemia?

A
  • pressure (ex: bed sores)
  • vascular constriction
  • thrombi
  • thromboemboli
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4
Q

Infarction outlined process

A

All emboli lodge into vessels too small to allow further passage = partial or complete vascular occlusion = infarction with coagulative necrosis

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5
Q

Embolism

A

Detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin
- hemic or lymphatic

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6
Q

Most emboli represent some part of a dislodged _____

A

Thrombus (aka: thromboembolus)

- all embolisms should be considered thrombotic in origin

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7
Q

What are other forms of emboli?

A
  • droplets of fat
  • bubbles of air/nitrogen
  • atherosclerotic debris
  • bits of bone marrow
  • foreign bodies
  • tumor fragments (METS)
  • septic emboli
  • miscellaneous
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8
Q

What are common types of thromboembolisms in vet med?

A
  • pulmonary thromboembolism (venous emboli)
  • systemic thromboembolism (arterial emboli)
  • bacterial emboli
  • neoplastic emboli
  • fibrocartilagenous emboli
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9
Q

Arterial embolisms

A

End stage capillaries (in an organ)

- most often organs with high amount of blood flow (kidney, brain)

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10
Q

Venous embolisms

A

End up in lung (pulmonary thromboembolus)

  • embolus carried to right heart from periphery –> pushed into pulmonary tree –> obstructs blood flow to lungs –> acute death
  • dual blood supply = some recovery if small embolus
  • could also end up in portal vein of the liver
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11
Q

Lymphatic embolisms

A

Draining regional lymph node

- can stay local or go into thoracic duct, end up in venous system and go to lung

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12
Q

Bacterial (septic) emboli

A

Clusters of bacteria and platelets that are carried by blood and lodge in very small vessels or capillaries

  • kidney glomeruli are common site
  • arise from vegetative valvular left heart lesion
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13
Q

Parasitic emboli

A

Pieces of intravascular nematodes that break off and lodge at a distant site
- common complications in dogs after therapy for hw disease
= verminous pulmonary thromboembolism

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14
Q

Fibrocartilagenous emboli

A

From ruptured IV discs –> nucleus pulposus herniates directly into venous sinus or enter small arteries
- cause spinal cord infarcts in dogs, cats, horses, cattle

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15
Q

Fat emboli

A

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

  • seldom cause infarction
  • gross lesions not obvious
  • capillaries in lungs contain small masses of fat
  • emboli could lodge in renal glomerulus = lipid glomerulopathy (rare in dogs)
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16
Q

Infarction

A

Ischemic necrosis of tissue caused by occlusion of either the arterial supply or the venous drainage in a particular tissue
- most result from thrombotic or embolic events in arteries

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17
Q

Does venous thrombosis cause infarction?

A

It could, but usually results in venous obstruction and congestion
- infarcts due to venous thrombosis are more common in organs with single venous outflow (testis, ovary)

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18
Q

Infarcts often have a sharp line of _____ between normal and necrotic tissue

A

Demarcation

- surrounded by zone of hyperemia early on

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19
Q

Infarct in tissues with dual circulation

A

Red or dark purple

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20
Q

Infarcts in solid organs

A

Start out red due to back flow of blood and leakage from injured vessels
- rapidly become pale as RBCs and tissue proteins break down

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21
Q

Chronic versus acute infarction

Study These Flashcards
A

Chronic: sunken and firm due to scar tissue
Acute: if not sunken and firm, then it is acute infarction, no matter what color it is

22
Q

Venous infarcts are caused by ____, with necrosis secondary to ______

Study These Flashcards
A

Obstructed veins; hypoxia

- ex: twisted intestine collapses veins but muscular arterioles allow some blood to be pumped into area

23
Q

________ becomes venous infarction when the tissue dies

Study These Flashcards
A

Passive congestion

24
Q

Renal infarction

Study These Flashcards
A

Infarction of arteries has sharp lines of demarcation that delineate the vascular field of that particular artery
- often wedge shaped

25
Coagulative necrosis
Loss of cellular detail
26
All infarcts heal by ________
Scarring
27
Consequences of ischemia/necrosis
- earliest change is cell swelling and disintegration of mitochondria - loss of energy leads to cell membrane damage, allowing entry of water, electrolytes, plasma protein into cells = increase intracellular Ca and irreversible cytopathic changes and necrosis --> cell enzymes are released into interstitial fluid as cell dies
28
Shock
Failure of circulatory system to adequately perfuse vital organs
29
Shock is also called:
- cardiovascular collapse | - vascular embarrassment
30
Shock is characterized by low _______
Systemic blood flow (hypoperfusion) due to - reduction in cardiac output - reduction in circulating blood volume (does not necessarily mean loss of blood) = hypotension followed by impaired tissue perfusion and cellular hypoxia
31
Initial phase of shock
Reflex compensatory activities occur and perfusion to vital organs is maintained - increased HR, peripheral vasoconstriction, renal conservation of fluid - pasty appearance due to vasoconstriction
32
Progressive phase of shock
Tissue under perfused (hypoxia) - anaerobic glycolysis leads to lactic acid production (acidosis) - arteriole dilation with blood pooling in microcirculation
33
Irreversible phase of shock
- peripheral vasodilation persists - heart muscle loses contractility - multiple organ failure
34
What is the primary goal for therapy of shock?
Rapid restoration of systemic blood flow by replacement of intravascular fluid and use of drugs that increase vascular tone and support cardiac function
35
Types of shock
- cardiogenic - hypovolemic - septic - anaphylactic - neurogenic Classified on basis of primary general cause
36
Cardiogenic shock
Caused by insults that reduce cardiac output, decreasing heart's ability to pump blood - anything that can affect HR, stroke volume, myocardial contractility - ex: myocarditis, myocardial degeneration, extrinsic compression, ventricular arrhythmias, outflow obstructions
37
Cardiac tamponade
Occurs when fluid accumulates rapidly in the pericardial space (hemopericardium) - impedes ability of ventricles to dilate and fill with blood - causes acute heart failure and results in cardiogenic shock
38
Cardiac tamponade can occur from _____ or _______
Neoplasia (hemangiosarcoma of right artrium) or hit by car
39
Hypovolemic shock
Caused by sudden and severe loss of blood volume - acute hemorrhage greater than 1/4 to 1/3 total blood volume (lost to exterior or into body cavity) - loss of intravascular and extravascular fluid secondary to water deprivation, vomiting, diarrhea - increased vascular permeability, leading to loss of intravascular fluid, proteins, blood cells (secondary to infection, toxin, immune reactions)
40
Septic shock
Results from bacterial infection (localized, systemic) where large quantities of endotoxin are released into circulation
41
Endotoxins
Components of bacterial cell walls of gram neg bacteria or breakdown products of cell wall degradation - LPS, consisting of toxic FA and polysaccharide coat - analagous components in gram pos and fungi have similar effects
42
LPS effects
Low doses: acute inflammation to help eliminate bacteria High doses: widespread endothelial damage - initiation of coagulation cascade - decreased myocardial contractility - peripheral vasodilation - lead to irreversible shock and DIC
43
Septic shock - course of events
Gram neg bacteria in localized infection --. bacterial wall endotoxin released in local inflammation --> endotoxin enters bloodstream --> activates circulating mono/macrophages --> produce TNF --> release of cytokines --> systemic vasodilation and systemic inflammatory response --> altered myocardial contractility --> widespread endothelial damage, platelet activation, coagulation cascade --> multiorgan failure = DIC
44
Anaphylactic shock
Systemic manifestation of acute hypersensitivity response - idiosyncratic rxn that occurs in certain predisposed individuals upon exposure to certain allergins - histamine and other mediators are released = vasodilation, increased vascular permeability with loss of intravascular fluid = eventual cardiovascular collapse
45
Gross and histologic lesions of shock
Lesions associated with presenting complaint - systemic vasodilation leads to pooling of blood in various organs (congestion) and hemorrhage - degeneration/necrosis of cells due to hypoxia/anoxia
46
Clinical consequences of shock
Anoxia leading to multiple organ failure with myocardial and kidney damage - endothelial injury - decreased kidney function and muscle perfusion = metabolic acidosis - decreased perfusion of heart muscle = anoxic injury to myocytes
47
Endothelial injury
Increased vascular permeability and loss of intravascular fluid - aggravate hypovolemia and anoxia - activate platelets and coagulation cascade (thrombosis) - depletion of clotting factors - hemorrhage with thrombosis (DIC)
48
Cardiovascular and systemic responses to shock
Body attempts to increase cardiac output by shunting blood to vital organs (body is acidotic at this point) - if adjustments fail, and primary cause is not corrected then uncompensated shock occurs - microvasculature is unresponsively dilated = end stage vasodilatory shock = death
49
Cardiac support
Epinephrine and norepinephrine from adrenal medulla increase HR Aldosterone from adrenal cortex retains sodium and water = increase blood volume
50
Vascular support
Epinephrine and norepinephrine stimulate vasoconstriction | Renin-angiotensin system produce angiotensin 2 to stimulate vasoconstriction

Pathology (19 decks)

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