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Pathology I > Lecture 6: Organ Failure > Flashcards

Lecture 6: Organ Failure Flashcards

1
Q

___are blind ended capillaries that dump into the venous system

A

Lymphatics

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2
Q

Lymphatics are ___ pressured, valves, and dependent on forces like ___ contraction to maintain flow

A

Low pressure, muscle contraction

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3
Q

Do lymphatic vessels have small or large gaps

A

Large

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4
Q

What percent of the body weight is fluid

A

60%

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5
Q

What percent of fluid body weight is intracellular, extracellular (plasma and interstitial)

A

Intracellular: 40%
Extracellular: 20%- 4% plasma and 16% interstititum

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6
Q

What is the extracellular matrix composed of

A

Structural (collagen type 1, elastin), adhesive (fibronectin, laminin), and absorptive (glycsaminoglycans, proteoglycans)

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7
Q

What 4 things control fluid movement

A
  1. Hormones
  2. Receptors
  3. Osmotic and hydrostatic forces
  4. Integrity of vascular system
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8
Q

What hormones control fluid movement

A

RAAS: vasoconstriction and water retention
Atrial natriuretic peptide: promote renal sodium and water extraction and vasodilation

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9
Q

What receptors control fluid movements

A
  1. Osmoreceptors in hypothalamus
  2. Baroreceptors in blood vessels
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10
Q

What is shock: circulatory failure

A

Systemic hypoperfusion due to macro and/or micro-circulatory failures

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11
Q

What is the outcome of shock: circulatory failure

A

Hypotension—> impaired tissue perfusion—> cellular hypoxia—> anaerobic metabolism—> cellular degeneration—> cell death

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12
Q

Describe the steps that occur when the body tries to compensate during hypovolemia shock

A
  1. Hypovolemia shock
  2. Initial compensation: increase HR, perfuse vital organs
  3. Metabolism shifts to glycolysis
  4. Progressive morphological deterioration of cells—> swelling, necrosis
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13
Q

What are the two forms of macro circulatory failure

A
  1. Cardiogenic
  2. Hypovolemia
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14
Q

What is cardiogenic macro circulatory failure and some examples

A

Failure of heart to adequately pump blood due to MI, ventricular tachycardia, fibrillation, arrhythmias, HCM, DCM, cardiac output obstruction (pulmonary embolism, aortic stenosis), and pericardial tamponade

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15
Q

What is hypovolemic macro circulatory failure and some examples

A

Reduced circulation of blood volume by massive blood loss or fluid (vomiting, diarrhea, burns_, leading to decreased vascular perfusion and tissue hypoperfusion

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16
Q

What happened here

A

Pericardial sac markedly expanded—> cardiogenic shock-macro circulatory failure

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17
Q

What cardiac abnormality can result from compression of the heart cause by fluid collecting in sac surrounding the heart

A

Cardiac tamponade

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18
Q

What happened

A

Cardiogenic shock-macro circulatory failure—> aortic rupture and cardiac tamponade

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19
Q

What this and what happened?

A

Hemangiosarcoma at right auricle, resulting in pericardial sac expanded—> increase pressure on right auricle—> rupture—> cardiac tamponade

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20
Q

What are the types of shock due to microcirculatory failure

A
  1. Blood maldistribution: decreased peripheral vascular resistance and polling of blood in peripheral tissue
21
Q

What are some examples of blood maldistribution

A

Anaphylactic shock- type I, IgE hypersensitivity
Septic shock- endotoxemia
Neurogenic shock-

22
Q

What is the most common type of septic shock

A

Endotoxemia

23
Q

Describe the pathogenesis of anaphylactic shock

A
  1. Exposure of insect, plant, drug or vaccine
  2. IgE mediated mast cells granulation
  3. Histamine and other mediators
  4. Systemic vasodilation and increased vascular permeability
  5. Blood hypotension
  6. Tissue hypoperfusion
24
Q

What is the major cause of septic shock endotoxemia

A

Gram negative bacilli but can be gram positive

25
Q

What is the pathogenesis of septic shock

A
  1. Toxin (ex: LPS)
  2. LPS forms a complex with blood proteins
  3. LPS binds to TLR-4
  4. Endothelium: downregulation of anticoagulations- tissue factor pathway inhibitor and thrombomodulin
  5. Monocytes/macrophages: increasing production of IL-1, IL-6, and TNF
26
Q

What does LPS bind

A

TLR-4

27
Q

T or F: the outcome of bacterial breakdown and LPS is dose dependent

A

True

28
Q

What are the outcomes of low quantity of LPS

A
  1. Monocyte/macrophage/ neutrophil activation
  2. Endothelial cell activation
  3. Complement activation: C3a, C5a

Result: local inflammation

29
Q

What are the effects of moderate quantities of LPS

A
  1. Fever
  2. Acute phase reactants released from liver
  3. Bone releases leukocytes
    Result: systemic effects
30
Q

What are the results of high quantities of LPS exposure

A
  1. Low cardiac output
  2. Low peripheral resistance
  3. Blood vessel injury, thrombosis, DIC
  4. ARDS

Result: septic shock

31
Q

What is the pathogenesis from high LPS exposure

A
  1. Production of TNF, IL-1, IL-6/IL-8, NO, PAF promotes systemic vasodilation and increased vascular permeability
  2. Intravascular plasma protein loss decreases oncotic forces
  3. Additional intravascular fluid loss
  4. Toxins and cytokines induce loss of peripheral vascular tone
  5. Hypotension
  6. Hypoperfusion
  7. Septic shock
32
Q

How can LPS lead to DIC and ARDS

A

LPS effects on endothelium triggers the coagulation cascade and damages capillaries

33
Q

What is DIC

A

Pathological activation of coagulation resulting in:

  1. Small blood clots formation inside blood vessels throughout body
  2. Consumption of coagulation proteins and platelets—> disruption of normal coagulation causing abnormal bleeding
  3. Clots plug normal blood flow to organs (kidneys and distal extremities)—>ischemic injury
34
Q

What are some triggers for DIC

A
  1. Bacterial endotoxins, sepsis
  2. Parasites
  3. Viruses
  4. Carcinomas, hemangiosarcoma, leukemia
  5. Heat stroke, antigen-antibody complexes
35
Q

What bacterial endotoxins can cause DIC

A

Babesia and rickettsia

36
Q

What parasites can cause DIC

A

Dirofilaria and angiostrongylus

37
Q

What viruses can cause DIC

A

FIP, adenovirus, bluetongue

38
Q

Diffuse ___ and/or generalized ___ activation can initiate DIC

A

Endothelial damage and/or platelet activation

39
Q

What is ARDS

A

Multifactorial source of injury to respiratory capillary endothelium (generally primary) and epithelium (diffuse alveolar damage, necrosis)

40
Q

What are some inciting causes of ARDS

A

Endotoxemia, sepsis, disseminated pulmonary infections, extensive trauma (HBC), burns, transfusions, DIC, pancreatitis, aspiration of gastric contents

41
Q

What tissue? Which is normal vs abnormal and what is wrong

A

left: normal lung
Right: ARDS- dilated blood vessels, lots of inflammatory cells (blue dots) and pink-fluid

42
Q

What is wrong here

A

ARDS

43
Q

In ARDS, damaged vessels allowed for leakage of fibrin in fluid leading to formation of ___ and resolution through ___

A

Formation of hyaline membranes (protein, fibrin, surfactant and cell debris), resolution through scarring

44
Q

What makes up hyaline membranes

A

Protein, fibrin, surfactant, and cell debris

45
Q

What is the pathway for neurogenic shocck

A
  1. Trauma, spinal cord injury, fear, electricity
  2. Trigger generalized autonomic NS
  3. SNS tone lost, PNS tone dominants
  4. Massive peripheral vasodilation with bradycardia
  5. Pooling of blood
  6. Hypoperfusion
46
Q

What are the 3 stages in the development of shock

A
  1. Compensation (reversible)
  2. Progression
  3. Irreversible cellular and tissue change
47
Q

What occurs during compensation stage in shock

A
  1. Increase heart rate
  2. Peripheral vasoconstriction
  3. ADH and AII released
    4, increased BP and blood diverted to vital tissue
48
Q

What occurs in the progression stage of shock

A
  1. Anaerobic metabolism
  2. Acidosis
  3. Peripheral vasoconstriction can’t be maintained
  4. Vasodilation
49
Q

What occurs in irreversible cell injury and tissue change during development of shock

A

Cell and tissue necrosis
Hypoxia—> systemic platelet and coagulation activation—> myocardial pump failure—> multiorgan failure—> death

Pathology I (23 decks)

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