Organ Failure Flashcards

1
Q

define lymphatics

A

blind ended capillaries that dump into venous system
low pressure, muscle contractions maintain flow

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2
Q

here for Liz Brain

A
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3
Q

list the main controls of fluid movement

A

hormones - RAAS, ANP (cardiomyocytes)
receptors - osmoreceptors, baroreceptors
osmotic/hydrostatic forces
integrity of vascular system

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4
Q

define shock

A

cardiovascular collapse - systemic hypoperfusion dur to macro/micro-circulatory failures

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5
Q

describe the outcome of shock

A

hypotension > impaired tissue perfusion > cellular hypoxia > anaerobic metabolism > cellular degeneration > cell death

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6
Q

describe the progression of shock to an irreversible state

A

hypovolemic shock > initial compensation > progression, metabolism shift to glycolysis > progressive morphological deterioration of cells

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7
Q

list the types of shock via macrocirculatory failure

A
  1. cardiogenic - failure of heart to properly pump blood
  2. hypovolemic - reduced circulation of blood volume by massive blood/fluid loss
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8
Q

list examples of cardiogenic macrocirculatory failure

A

myocardial infarction
ventricular tachycardia
dilated CM
pericardial tamponade

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9
Q

ID pathology

A

cardiogenic shock - macrocirculatory failure in horse

expanded pericardial sac, cardiac tamponade

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10
Q

define cardiac tamponade

A

compression of heart caused by fluid collecting in sac surrounding the heart
*example of macrocirculatory failure

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11
Q

ID pathology

A

aortic rupture and cardiac tamponade

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12
Q

ID pathology

A

hemangiosarcoma at R auricle and cardiac tamponade

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13
Q

list the types of shock due to microcirculatory failure

A

blood maldistribution
1. anaphylactic shock
2. septic shock
3. neurogenic shock

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14
Q

anaphylactic shock is generalized ___

A

type I (IgE) hypersensitivity

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15
Q

what mainly causes septic shock?

A

endotoxemia

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16
Q

what causes neurogenic shock?

A

trauma, electrocution, fear, emotional stress

17
Q

anaphylactic shock pathogenesis

A

exposure of insect/plant/drug/vaccine > IgE mediated mast cell degranulation > histamine/mediators > systemic vasodilate and increased vascular permeability > blood hypotension > tissue hypoperfusion

18
Q

septic shock (most common) pathogenesis

A

toxin (LPS from gram neg cell wall) > LPS forms complex with blood proteins > LPS binds to TLR-4 > downregulation of anticoags (endothelium) and increased production of IL-1, IL-6, TNF (monocytes and macrophage)

19
Q

list the major antithrombotic systems

A
  1. protein c - protein s thrombomodulin system
  2. antithrombin III
  3. tissue factor pathway inhibitor
20
Q

LPS intoxication is ___ dependant

21
Q

LPS effect on endothelium triggers coag cascade and damages capillaries, which can lead to what two things?

A

DIC aka disseminated intravascular coagulopathy
ARDS aka acute respiratory distress syndrome

22
Q

what can be a result from pathological activation of coagulation due to disseminated intravascular coagulopathy (DIC)?

A
  1. small blood clot form inside blood vessels throughout body
  2. consumption of coag proteins and platelets > disruption of normal coag causing abnormal bleeding
  3. clots plug normal blood flow to organs > ischemic injury
23
Q

list what could trigger disseminated intravascular coagulopathy (DIC)

A

bacterial endotoxins, sepsis
parasites
viruses
carcinoma, hemangiosarcoma, leukemia
heat stroke, antigen-Ab complexes

*diffuse endothelial damage and/or generalized platelet activation initiates

24
Q

define acute respiratory distress syndrome (ARDS)

A

multifactorial source of injury to respiratory capillary endothelium (primary)
epithelium (secondary)

25
list the main causes of acute respiratory distress syndrome (ARDS)
endotoxemia, sepsis, extensive trauma (hit by car), DIC, pancreatitis
26
ID pathology
ARDS blue - inflammatory cells dilated blood vessels
27
*Liz Brain
28
neurogenic shock pathogenesis
trauma, spinal cord injury, fear, electricity > triggers generalized ANS > sympathetic tone lost, parasympathetics dominate > massive peripheral dilation and bradycardia > pooling of blood > hypoperfusion
29
describe what occurs at each stage in the development of shock
compensation - increased HR, vasoconstriction, ADH and AII released, increased BP and blood diversion to vital tissue progression - anaerobic metabolism, acidosis, peripheral vasoconstrict cannot be maintained so dilation occurs irreversible - cell and tissue necrosis
30