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Inflammatory Process Flashcards

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1
Q

Cell atrophy

A

decrease in cell size to use less nutrients

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2
Q

Cell hypertrophy

A

increase in cell size - muscle building

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3
Q

Cell hyperplasia

A

Increase in number of cells (growing, uterus)

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4
Q

Cell metaplasia

A

change in cell type

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5
Q

Necrosis causes and effects

A 
loss of blood supply
exposure to toxins
cellular swelling
protein denaturation
tissue dysfunction
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6
Q

Apoptosis

A

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

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7
Q

Hypoxia

A

oxygen deprivation

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8
Q

ischemia

A

loss of blood supply

due to impeded arterial flow or reduced venous drainage

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9
Q

Causes of hypoxia

A

ischemia
inadequate oxygenation (pneumonia, emphysema)
reduced oxygen carrying capacity (anemia)

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10
Q

Causes of cell injury

A
  1. oxygen deprivation
  2. chemical agents
  3. infectious agents
  4. genetic defects
  5. immunologic reactions
  6. nutritional imbalance
  7. physical agents
  8. aging
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11
Q

Response to injurious stimuli depends on

A

type of injury
duration
severity

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12
Q

Immunologic reactions can cause cell injury by

A

anaphylactic shock - exaggerated response

auto-immune disease

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13
Q

Auto-immune disease is loss of

A

self tolerance

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14
Q

Tolerable time of complete ischemia without irreversible injury: skeletal muscle

A

2-3 hours

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15
Q

Tolerable time of complete ischemia without irreversible injury: cardiac muscle

A

20-30 mins

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16
Q

Tolerable time of complete ischemia without irreversible injury: brain

A

4-5 mins

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17
Q

Why does aging contribute to cell injury?

A

imperfect restoration of structure or function
cellular senescence
reduced immune strength
shorter telomeres

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18
Q

Inflammation definition

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

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19
Q

Benefits of inflammation

A

helps clear infection

makes wound healing possible

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20
Q

Negative to inflammation

A

potential to cause harm (heaves, asthma, anaphylaxis, etc)

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21
Q

Acute inflammation

A

delivers leukocytes to injury site

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22
Q

Leukocytes

A

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

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23
Q

5 classic signs of acute inflammation

A 
heat
redness
swelling
pain
loss of function
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24
Q

2 components of acute inflammation

A

vascular changes

cellular events

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25
vascular change in acute inflammation
vasodilation
26
cellular events in acute inflammation
cellular recruitment and activation
27
Types of leukocytes
Neutrophils Eosinophils Basophils
28
Neutrophil activity and death
forms pus
29
Eosinophils primarily deal with
parasitic infections
30
Basophils release
histamine, causing inflammation
31
Basophils are chiefly responsible for
allergic and antigen response
32
B cells and T cells are
Lymphocytes
33
Monocyte functions (2)
phagocytosis | present pathogen pieces to T cells for memory or so antibody response may be mounted
34
Macrophage function
phagocytosis
35
Macrophages develop from
monocytes
36
Vascular and cellular changes - acute inflammation (6)
1. initial vasoconstriction 2. vasodilation 3. increase vascular permeability 4. Leukocytes arrive 5. Leukocytes release chemical mediators 6. phagocytosis
37
Steps to stop bleeding
platelet aggregation > blood coagulation > clot
38
redness and heat of inflamed area is caused by
histamine
39
Blood becomes
more viscous
40
Why does circulation slow and blood viscosity increase?
So that cells can leave the blood vessel and go to injury site
41
Leukocytes (neutrophils) will transmigrate through ____________ to ____________
intercellular junction | extracellular matrix
42
Describe phagocytosis
Leukocytes engulf the injurious particle and degrade it. This can kill bacteria and clean up dead cells.
43
Outcomes of acute inflammation (3)
1. resolution 2. scarring/fibrosis 3. progression to chronic inflammation
44
Resolution
limited or short lived injury minimal tissue damage tissue replaces any dead cells with perfect new cells
45
Scarring/Fibrosis
substantial tissue damage non-regenerating tissues cases of abscess formation
46
Chronic inflammation
``` persistent viral or bacterial infection prolonged exposure to potentially toxic agents autoimmune disease can lead to regeneration or fibrosis anti-inflammatories necessary ```
47
angiogenesis
new blood vessel formation
48
infarction
death of tissue due to lack of oxygen due to an obstruction in blood supply
49
extracellular matrix (ECM) critically regulates
the growth, movement and differentiation of cells
50
Roles of ECM
1. mechanical support 2. determination of cell orientation 3. control of growth 4. organized regeneration of tissues
51
Components of ECM
collagen elastin glycosaminoglycans hyaluronic acid
52
purpose of collagen in ECM
tensile strength
53
purpose of elastin in ECM
recoil and return to baseline structure
54
what are glycosaminoglycans and hyaluronic acid?
highly hydrated compressible gels conferring resilience and lubrication
55
Fibrosis
in severe or persistent injury, repair occurs by replacement of what should be normally functioning cells with connective tissue.
56
components of granulation tissue
angiogenesis fibroblasts loose ECM
57
What is granulation tissue highly populated with and what do they do?
macrophages | clear debris and allow for fibroblast proliferation and ECM production
58
First intention
clean, uninfected surgical incision cells are regenerated w/ normal function scar is minimal
59
Second Intention
open wound, abscess, ulceration extensive growth of granulation tissue fibrotic scar formation
60
Wound strength compared to unwounded tissue
sutured: 70% suture removed: 10% after 3 wks: 70-80%
61
Acute inflammation is essential to
the normal outcome of wound regeneration/repair
62
Healing by ______ intention is better than by _______ intention
first | second
63
Abscesses leave a scar….
always
64
If inflammation becomes chronic, it contributes to the...
pathogenesis of the disease, excessive fibrosis and scarring

EQM351 (26 decks)

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