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

A

dose

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
Q

list the main causes of acute respiratory distress syndrome (ARDS)

A

endotoxemia, sepsis, extensive trauma (hit by car), DIC, pancreatitis

26
Q

ID pathology

A

ARDS

blue - inflammatory cells
dilated blood vessels

27
Q

*Liz Brain

A
28
Q

neurogenic shock pathogenesis

A

trauma, spinal cord injury, fear, electricity > triggers generalized ANS > sympathetic tone lost, parasympathetics dominate > massive peripheral dilation and bradycardia > pooling of blood > hypoperfusion

29
Q

describe what occurs at each stage in the development of shock

A

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
Q
A