Disease and Healing: Inflammatory Process Exam 1 Flashcards

1
Q

Physiologic stress

A

stress on the body outside of normal activities

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2
Q

Example of physiologic stress

A

working out when you don’t usually
-muscles become inflamed
-cells are inflamed but don’t die

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3
Q

Pathologic stimuli

A

surpass the capacity of the cells —> leads to injury (tears, breaks, etc.)

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4
Q

Homeostasis

A

state of balance/normalcy

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5
Q

Cells tend to preserve their environment to maintain __________

A

homeostasis

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6
Q

During physiologic stress and pathologic stimuli cells undergo __________

A

adaptation (and find a new steady state, preserving viability

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7
Q

Adaptations:

A

-atrophy
-hypertrophy
-hyperplasia
-metaplasia

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8
Q

Injury develops when adaptive capability is ________

A

exceeded

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9
Q

Can injury be reversible?

A

yes, but with persistent or sever stress it is irreversible (cell death)

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10
Q

Atrophy

A

a decrease in cell size (usually because they aren’t being used)

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11
Q

Hypertrophy

A

an increase in cell size (used often-physiologic stress causes the increase)

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12
Q

Hyperplasia

A

an increase in the # of cells (ex: mammary glands when a female is pregnant)

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13
Q

Metaplasia

A

the change in cell type (ex: smokers cilia cells change to cuboidal cells)

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14
Q

Where does the right ventricle send blood?

A

to the lungs

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15
Q

Is the right or left ventricle larger/thicker? Why?

A

the left ventricle because it needs more muscle to send blood further out to all the body

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16
Q

Where does the left ventricle send blood?

A

the rest of the body

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17
Q

High blood pressure

A

-high resistance
-heart works harder to send blood out
-hypertrophy

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18
Q

Heart attack

A

-exceeded what the heart can do
-cell death
-injury

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19
Q

What are the two types of cell death?

A

-necrosis
-apoptosis

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20
Q

Necrosis

A

loss of blood supply or exposure to toxins: cellular swelling, protein denaturation

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21
Q

What does necrosis result in?

A

tissue dysfunction

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22
Q

Apoptosis

A

programmed cell death – dead cells are removed with minimal disruption of the surrounding tissue

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23
Q

Causes of cell injury:

A

-oxygen deprivation
-chemical agents
-infectious agents
-genetic defects
-immunologic reactions
-nutritional imbalances
-physical agents
-aging

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24
Q

Hypoxia

A

-oxygen deprivation
-cause of cell injury
-3 forms:
ischemia
inadequate oxygenation
reduced oxygen carrying capacity

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25
Q

Ischemia

A

loss of blood supply in a tissue due to impeded arterial flow or reduced venous drainage

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26
Q

Example of ischemia

A

tourniquet

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27
Q

Examples of inadequate oxygenation

A

-pneumonia
-emphysema

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28
Q

Example of reduced oxygen carrying capacity

A

anemia – not enough red blood cells to carry oxygen

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29
Q

Chemical agents

A

any chemical substance can cause cell injury
-water
-salt
-oxygen
-ethanol

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30
Q

What damage does ethanol have on the body?

A

(whiskey, beer, vodka, etc)
it causes liver damage that is reversible initially but chronic abuse will lead to irreversible liver injury

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31
Q

Infectious agents

A

-viruses
-bacteria
-worms
-fungi
-protozoan

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32
Q

How do genetic defects cause cell injury?

A

it may result in pathologic changes

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33
Q

An example of genetic defects causing cell injury:

A

lethal white in horses

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34
Q

Everything is toxic, what determines the type of toxicity?

A

the dose/amount of the toxin

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35
Q

Examples of immunologic reactions

A

-anaphylactic shock
-auto-immune diseases

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36
Q

Anaphylactic shock

A

-allergic reaction where the lungs and throat swells and closes
-an exaggerated immune response

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37
Q

Auto-immune disease

A

loss of self-tolerance

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38
Q

Examples of nutritional imbalances than lead to cell injury

A

-malnourishment
-obesity

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39
Q

Examples of physical agents

A

-trauma (cuts, bruises, concussions)
-burns
-cold (frostbite)

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40
Q

Examples of how aging leads to cell injury

A

-repeated trauma
-imperfect restoration of structure or function
-cellular senescence (old cells don’t replicate perfectly anymore)

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41
Q

What happens to the immune system during pregnancy?

A

it decreases

42
Q

What does responses to injurious stimuli depend on?

A

-type of injury
-duration and severity
-some regeneration can happen depending on where, what, and how long

43
Q

What do the consequences of injury depend on?

A

the type, adaptability, and genetic makeup of the injured cell

44
Q

Fever

A

-an increase in body temp to fight off infection
-means that your immune system is working but also means it might not be strong

45
Q

What happens to the brain in high fever temperatures?

A

it melts

46
Q

How long can striated muscle accommodate complete ischemia?

A

2-3 hrs without irreversible injury

47
Q

How long can cardiac muscle accommodate complete ischemia?

A

20-30 min.

48
Q

How long can the brain accommodate complete ischemia?

A

4-5 min. - even then some damage may already be irreversible

49
Q

Inflammation

A

a protective response intended to eliminate the initial cause of cell injury as well as the necrotic cells and tissues resulting from the original insult

50
Q

The immune system cannot be activated without an _________ response first

A

inflammatory

51
Q

What does inflammation help to do?

A

-clear infection
-make wound healing possible

52
Q

What are examples of the inflammation process causing harm?

A

-heaves
-asthma
-anaphylaxis

53
Q

How is inflammation interwoven with repair processes?

A

damaged tissue is replaced by regenerated new tissue, residual defect is filled with fibrous scar tissue

54
Q

Acute inflammation

A

-response within 24 hrs of injury
-immediate and early response to injury
-designed to deliver leukocytes to sites of injury

55
Q

What do leukocytes do during acute inflammation?

A

clear any invading microbes and begin the process of cleaning necrotic tissue

56
Q

What are the two components of acute inflammation?

A

-vascular changes
-cellular events

57
Q

Vascular changes during acute inflammation

A

-initially vasoconstriction in case there is bleeding
-than vasodilation (increased blood flow that brings in more leukocytes)

58
Q

Cellular events in acute inflammation

A

cellular recruitment and activation leads to leukocyte migration

59
Q

5 local signs of acute inflammation

A
  1. heat
  2. redness
  3. swelling
  4. pain
  5. loss of function
60
Q

Why does swelling occur?

A

-because vessels become leaky and fluid/plasma comes out of the blood vessels in that area
-the leakiness makes the blood in the area viscous (thicker)
-the slow thick blood gives the cells more time to flow out

61
Q

% of Neutrophils in the body

A

65%

62
Q

% of Eosinophils in the body

A

4%

63
Q

% of Basophils in the body

A

<1%

64
Q

% of Lymphocytes in the body

A

25%

65
Q

% of Monocytes in the body

A

6%

66
Q

% of Macrophages in the body

A

6%

67
Q

Steps of acute inflammation

A
  1. initial vasoconstriction (seconds) to stop bleeding, clot blood
  2. Vasodilation brings in leukocytes
  3. Increase vascular permeability, blood becomes more viscous and slows down, protein rich fluid in extravascular tissue
  4. Leukocytes (neutrophils) will transmigrate through intracellular junction to the extracellular matrix
  5. Leukocytes will release chemical mediators that will recruit more leukocytes to the site of injury
  6. Phagocytosis
68
Q

What purposes does phagocytosis serve?

A

-to kill bacteria or viruses
-to clean up dead cells

69
Q

What chemical mediators do leukocytes release during acute inflammation?

A

-histamine
-cytokines
-leukotrienes
-prostaglandins

70
Q

What symptoms of inflammation does vasodilation cause?

A

the redness and heat of the inflamed area - caused by the histamine release

71
Q

Why would one use antiinflammatories?

A

to slow the inflammation process down

72
Q

Outcomes of acute inflammation:

A
  1. resolution
  2. scarring or fibrosis
  3. progression to chronic inflammation
73
Q

Resolution of acute inflammation

A

when injury is limited or short-lived, minimal tissue damage, tissue is capable of replacing any irreversibly injured cell with new perfect and functional cells
(everything goes back to 100% normal with minimal scarring)

74
Q

Scarring or Fibrosis of acute inflammation

A

after substantial tissue damage, or when injury occurs to tissue that does not regenerate
-some people scar more than other people

75
Q

In cases of abscess formation what is the only outcome?

A

scarring

76
Q

What can lead to progression to chronic inflammation from acute inflammation?

A

persistent viral or bacterial infection which can lead to complete regeneration or fibrosis (ex: tuberculosis)

77
Q

What are some instances in which scars would heal better?

A

-in a younger animal/person
-in areas of the body with more vasculature

78
Q

Chronic inflammation

A

-considered inflammation of prolonged duration
-active inflammation and tissue healing and tissue injury occur simultaneously
-can become acute again

79
Q

What is tissue destruction largely due to in chronic inflammation?

A

the inflammatory process itself

80
Q

What is necessary during chronic inflammation?

A

anti-inflammatories

81
Q

What does chronic inflammation lead to?

A

repair, not regeneration
-new vessel proliferation (angiogenesis) and fibrosis

82
Q

What does chronic inflammation arise from?

A

-persistent microbial infection
-prolonged exposure to potentially toxic agents
-autoimmune diseases

83
Q

Granulomatous inflammation

A

formation of a granuloma, isolating the injurious/insulting site
-tries to keep the inflammation from spreading

84
Q

Granuloma wall

A

fibrous tissue separating the causative agent and areas of necrosis

85
Q

Non-granulomatous inflammation

A

diffuse necrosis and fibrosis occur
-chronic viral infection

86
Q

What does granulomatous inflammation make a challenge?

A

for everything necessary for healing to reach that area to heal

87
Q

Extracellular matrix (ECM)

A

-outside of the cell
-critically regulates the growth, movement, and differentiation of cells

88
Q

Roles of ECM:

A

-mechanical support
-determination of cell orientation
-control of growth
-organized regeneration of tissues (if not scars, fibrosis, and loss of function occur)

89
Q

Components of ECM:

A

-collagen
-elastin
-glycosaminoglycans
-hyaluronic acid

90
Q

Glycosaminoglycans and hyaluronic acid

A

highly hydrated compressible gels conferring resilience and lubrication
-absorbs water and lets it out when compressed

91
Q

An example of glycosaminoglycans and hyaluronic acid

A

joint compression
-compression lets out the liquid to lubricate
-when the joint is not healthy, the fluid starts to corrode the bone

92
Q

An example of why collagen is needed in ECM

A

it helps add stretch when swelling occurs

93
Q

An example of why elastin is needed in ECM

A

it helps return the injury site back to normal after swelling

94
Q

Steps of fibrosis

A
  1. severe or persistent tissue injury
  2. granulation tissue is formed (proud flesh)
  3. granulation tissue becomes fibrotic tissue
95
Q

Granulation tissue

A

-angiogenesis, fibroblasts, loose ECM
-pink, soft, granular-looking tissue
-highly populated with macrophages which clears debris and allows for fibroblast proliferation and ECM production

96
Q

Exuberant granulation tissue formation __________ healing of wounds

A

impedes (horses are very prone to it)

97
Q

Wound healing

A

a very organized event when specialized cells first clean the injured site and progressively build the scaffolding to fill in any resulting defect

98
Q

First intention of wound healing

A

clean, uninfected surgical incision approximated by suture: cells are regenerated, they maintain normal function, scar is minimal

99
Q

Second intention of wound healing

A

open wound, abscesses, ulcerations
-normal architecture is not achieved, extensive ingrowth of granulation tissue, fibrotic scar formation is the result (contacts more)

100
Q

Wound strength

A

-carefully sutured wounds have 70% of normal strength of unwounded tissue
-when suture is removed, wound strength is only about 10%
-by the end of 3 months, the strength is ~70-80%

101
Q

Which is better, healing by first intention of second intention?

A

first intention