Disease and Healing: Inflammatory Process Exam 1 Flashcards
1
Q
Physiologic stress
A
stress on the body outside of normal activities
2
Q
Example of physiologic stress
A
working out when you don’t usually
-muscles become inflamed
-cells are inflamed but don’t die
3
Q
Pathologic stimuli
A
surpass the capacity of the cells —> leads to injury (tears, breaks, etc.)
4
Q
Homeostasis
A
state of balance/normalcy
5
Q
Cells tend to preserve their environment to maintain __________
A
homeostasis
6
Q
During physiologic stress and pathologic stimuli cells undergo __________
A
adaptation (and find a new steady state, preserving viability
7
Q
Adaptations:
A
-atrophy
-hypertrophy
-hyperplasia
-metaplasia
8
Q
Injury develops when adaptive capability is ________
A
exceeded
9
Q
Can injury be reversible?
A
yes, but with persistent or sever stress it is irreversible (cell death)
10
Q
Atrophy
A
a decrease in cell size (usually because they aren’t being used)
11
Q
Hypertrophy
A
an increase in cell size (used often-physiologic stress causes the increase)
12
Q
Hyperplasia
A
an increase in the # of cells (ex: mammary glands when a female is pregnant)
13
Q
Metaplasia
A
the change in cell type (ex: smokers cilia cells change to cuboidal cells)
14
Q
Where does the right ventricle send blood?
A
to the lungs
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
16
Q
Where does the left ventricle send blood?
A
the rest of the body
17
Q
High blood pressure
A
-high resistance
-heart works harder to send blood out
-hypertrophy
18
Q
Heart attack
A
-exceeded what the heart can do
-cell death
-injury
19
Q
What are the two types of cell death?
A
-necrosis
-apoptosis
20
Q
Necrosis
A
loss of blood supply or exposure to toxins: cellular swelling, protein denaturation
21
Q
What does necrosis result in?
A
tissue dysfunction
22
Q
Apoptosis
A
programmed cell death – dead cells are removed with minimal disruption of the surrounding tissue
23
Q
Causes of cell injury:
A
-oxygen deprivation
-chemical agents
-infectious agents
-genetic defects
-immunologic reactions
-nutritional imbalances
-physical agents
-aging
24
Q
Hypoxia
A
-oxygen deprivation
-cause of cell injury
-3 forms:
ischemia
inadequate oxygenation
reduced oxygen carrying capacity
25
Ischemia
loss of blood supply in a tissue due to impeded arterial flow or reduced venous drainage
26
Example of ischemia
tourniquet
27
Examples of inadequate oxygenation
-pneumonia
-emphysema
28
Example of reduced oxygen carrying capacity
anemia -- not enough red blood cells to carry oxygen
29
Chemical agents
any chemical substance can cause cell injury
-water
-salt
-oxygen
-ethanol
30
What damage does ethanol have on the body?
(whiskey, beer, vodka, etc)
it causes liver damage that is reversible initially but chronic abuse will lead to irreversible liver injury
31
Infectious agents
-viruses
-bacteria
-worms
-fungi
-protozoan
32
How do genetic defects cause cell injury?
it may result in pathologic changes
33
An example of genetic defects causing cell injury:
lethal white in horses
34
Everything is toxic, what determines the type of toxicity?
the dose/amount of the toxin
35
Examples of immunologic reactions
-anaphylactic shock
-auto-immune diseases
36
Anaphylactic shock
-allergic reaction where the lungs and throat swells and closes
-an exaggerated immune response
37
Auto-immune disease
loss of self-tolerance
38
Examples of nutritional imbalances than lead to cell injury
-malnourishment
-obesity
39
Examples of physical agents
-trauma (cuts, bruises, concussions)
-burns
-cold (frostbite)
40
Examples of how aging leads to cell injury
-repeated trauma
-imperfect restoration of structure or function
-cellular senescence (old cells don't replicate perfectly anymore)
41
What happens to the immune system during pregnancy?
it decreases
42
What does responses to injurious stimuli depend on?
-type of injury
-duration and severity
-some regeneration can happen depending on where, what, and how long
43
What do the consequences of injury depend on?
the type, adaptability, and genetic makeup of the injured cell
44
Fever
-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
What happens to the brain in high fever temperatures?
it melts
46
How long can striated muscle accommodate complete ischemia?
2-3 hrs without irreversible injury
47
How long can cardiac muscle accommodate complete ischemia?
20-30 min.
48
How long can the brain accommodate complete ischemia?
4-5 min. - even then some damage may already be irreversible
49
Inflammation
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
The immune system cannot be activated without an _________ response first
inflammatory
51
What does inflammation help to do?
-clear infection
-make wound healing possible
52
What are examples of the inflammation process causing harm?
-heaves
-asthma
-anaphylaxis
53
How is inflammation interwoven with repair processes?
damaged tissue is replaced by regenerated new tissue, residual defect is filled with fibrous scar tissue
54
Acute inflammation
-response within 24 hrs of injury
-immediate and early response to injury
-designed to deliver leukocytes to sites of injury
55
What do leukocytes do during acute inflammation?
clear any invading microbes and begin the process of cleaning necrotic tissue
56
What are the two components of acute inflammation?
-vascular changes
-cellular events
57
Vascular changes during acute inflammation
-initially vasoconstriction in case there is bleeding
-than vasodilation (increased blood flow that brings in more leukocytes)
58
Cellular events in acute inflammation
cellular recruitment and activation leads to leukocyte migration
59
5 local signs of acute inflammation
1. heat
2. redness
3. swelling
4. pain
5. loss of function
60
Why does swelling occur?
-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
% of Neutrophils in the body
65%
62
% of Eosinophils in the body
4%
63
% of Basophils in the body
<1%
64
% of Lymphocytes in the body
25%
65
% of Monocytes in the body
6%
66
% of Macrophages in the body
6%
67
Steps of acute inflammation
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
What purposes does phagocytosis serve?
-to kill bacteria or viruses
-to clean up dead cells
69
What chemical mediators do leukocytes release during acute inflammation?
-histamine
-cytokines
-leukotrienes
-prostaglandins
70
What symptoms of inflammation does vasodilation cause?
the redness and heat of the inflamed area - caused by the histamine release
71
Why would one use antiinflammatories?
to slow the inflammation process down
72
Outcomes of acute inflammation:
1. resolution
2. scarring or fibrosis
3. progression to chronic inflammation
73
Resolution of acute inflammation
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
Scarring or Fibrosis of acute inflammation
after substantial tissue damage, or when injury occurs to tissue that does not regenerate
-some people scar more than other people
75
In cases of abscess formation what is the only outcome?
scarring
76
What can lead to progression to chronic inflammation from acute inflammation?
persistent viral or bacterial infection which can lead to complete regeneration or fibrosis (ex: tuberculosis)
77
What are some instances in which scars would heal better?
-in a younger animal/person
-in areas of the body with more vasculature
78
Chronic inflammation
-considered inflammation of prolonged duration
-active inflammation and tissue healing and tissue injury occur simultaneously
-can become acute again
79
What is tissue destruction largely due to in chronic inflammation?
the inflammatory process itself
80
What is necessary during chronic inflammation?
anti-inflammatories
81
What does chronic inflammation lead to?
repair, not regeneration
-new vessel proliferation (angiogenesis) and fibrosis
82
What does chronic inflammation arise from?
-persistent microbial infection
-prolonged exposure to potentially toxic agents
-autoimmune diseases
83
Granulomatous inflammation
formation of a granuloma, isolating the injurious/insulting site
-tries to keep the inflammation from spreading
84
Granuloma wall
fibrous tissue separating the causative agent and areas of necrosis
85
Non-granulomatous inflammation
diffuse necrosis and fibrosis occur
-chronic viral infection
86
What does granulomatous inflammation make a challenge?
for everything necessary for healing to reach that area to heal
87
Extracellular matrix (ECM)
-outside of the cell
-critically regulates the growth, movement, and differentiation of cells
88
Roles of ECM:
-mechanical support
-determination of cell orientation
-control of growth
-organized regeneration of tissues (if not scars, fibrosis, and loss of function occur)
89
Components of ECM:
-collagen
-elastin
-glycosaminoglycans
-hyaluronic acid
90
Glycosaminoglycans and hyaluronic acid
highly hydrated compressible gels conferring resilience and lubrication
-absorbs water and lets it out when compressed
91
An example of glycosaminoglycans and hyaluronic acid
joint compression
-compression lets out the liquid to lubricate
-when the joint is not healthy, the fluid starts to corrode the bone
92
An example of why collagen is needed in ECM
it helps add stretch when swelling occurs
93
An example of why elastin is needed in ECM
it helps return the injury site back to normal after swelling
94
Steps of fibrosis
1. severe or persistent tissue injury
2. granulation tissue is formed (proud flesh)
3. granulation tissue becomes fibrotic tissue
95
Granulation tissue
-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
Exuberant granulation tissue formation __________ healing of wounds
impedes (horses are very prone to it)
97
Wound healing
a very organized event when specialized cells first clean the injured site and progressively build the scaffolding to fill in any resulting defect
98
First intention of wound healing
clean, uninfected surgical incision approximated by suture: cells are regenerated, they maintain normal function, scar is minimal
99
Second intention of wound healing
open wound, abscesses, ulcerations
-normal architecture is not achieved, extensive ingrowth of granulation tissue, fibrotic scar formation is the result (contacts more)
100
Wound strength
-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
Which is better, healing by first intention of second intention?
first intention
