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Pathology > Ischemia, Emboli, Infarctions, Shock > Flashcards

Ischemia, Emboli, Infarctions, Shock Flashcards

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

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 ______

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

A

Passive congestion

24
Q

Renal infarction

A

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

25
Q

Coagulative necrosis

A

Loss of cellular detail

26
Q

All infarcts heal by ________

A

Scarring

27
Q

Consequences of ischemia/necrosis

A
  • 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
Q

Shock

A

Failure of circulatory system to adequately perfuse vital organs

29
Q

Shock is also called:

A
  • cardiovascular collapse

- vascular embarrassment

30
Q

Shock is characterized by low _______

A

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
Q

Initial phase of shock

A

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
Q

Progressive phase of shock

A

Tissue under perfused (hypoxia)

  • anaerobic glycolysis leads to lactic acid production (acidosis)
  • arteriole dilation with blood pooling in microcirculation
33
Q

Irreversible phase of shock

A
  • peripheral vasodilation persists
  • heart muscle loses contractility
  • multiple organ failure
34
Q

What is the primary goal for therapy of 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

35
Q

Types of shock

A
  • cardiogenic
  • hypovolemic
  • septic
  • anaphylactic
  • neurogenic
    Classified on basis of primary general cause
36
Q

Cardiogenic shock

A

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
Q

Cardiac tamponade

A

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
Q

Cardiac tamponade can occur from _____ or _______

A

Neoplasia (hemangiosarcoma of right artrium) or hit by car

39
Q

Hypovolemic shock

A

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
Q

Septic shock

A

Results from bacterial infection (localized, systemic) where large quantities of endotoxin are released into circulation

41
Q

Endotoxins

A

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
Q

LPS effects

A

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
Q

Septic shock - course of events

A

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
Q

Anaphylactic shock

A

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
Q

Gross and histologic lesions of shock

A

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
Q

Clinical consequences of shock

A

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
Q

Endothelial injury

A

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
Q

Cardiovascular and systemic responses to shock

A

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
Q

Cardiac support

A

Epinephrine and norepinephrine from adrenal medulla increase HR
Aldosterone from adrenal cortex retains sodium and water = increase blood volume

50
Q

Vascular support

A

Epinephrine and norepinephrine stimulate vasoconstriction

Renin-angiotensin system produce angiotensin 2 to stimulate vasoconstriction

Pathology (19 decks)

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