Inflammation Flashcards

1
Q

what is inflammation

A

a local response of vascular tissue to cell injury/death

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2
Q

3 aims of inflammation

A
  • prevent spread (localize injurious agent)
  • removes agent, damaged cells, debris
  • assist with healing
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3
Q

whenever inflammation occurs there is always

A

tissue damage

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4
Q

the suffix for inflammation is

A

-itis

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5
Q

clinical/cardinal signs of inflammation

A
  • erythema
  • swelling
  • warmth
  • pain
  • loss of fx
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6
Q

what are the 2 responses of acute inflammation

A
  • vascular

- cellular

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7
Q

what are the 3 main stages of the vascular response of acute inflammation

A
  • vasoconstriction
  • vasodilation
  • increased permeability
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8
Q

during acute inflammation, vasoconstriction is what kind of response

A

a neuro response

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9
Q

during acute inflammation, what is the purpose of vasoconstriction

A
  • minimize blood loss and reduce flow in order for a clot to form
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10
Q

during acute inflammation, why is the vasoconstriction phase so short

A

because resources and nutrients for healing must reach the site

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11
Q

during acute inflammation, injury activates what

A

plasma and inflammation cell mediators

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12
Q

what are 2 examples of inflammation cell mediators

A

histamines and prostaglandin

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13
Q

during acute inflammation, inflammation cell mediators trigger what

A

vasodilation and increased permeability of blood vessels

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14
Q

during acute inflammation, what does vasodilation cause

A

increased blood flow to the area (hyperemia)

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15
Q

during acute inflammation, why does exudate form in the tissue

A

due to increased permeability of the blood vessels

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16
Q

during acute inflammation, what is the fluid shift

A

when fluid (exudate) moves out of the blood vessels and into the tissue

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17
Q

during acute inflammation, what does the fluid shift cause

A

swelling, and therefore pain and loss of function

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18
Q

during acute inflammation, histamine causes what 2 processes

A
  • vasodilation

- permeability

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19
Q

during acute inflammation, prostaglandin causes what 3 processes

A
  • vasodilation
  • permeability
  • pain
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20
Q

during vasodilation what do erythrocytes do

A

they stack in the rouleau formation

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21
Q

what are 2 manifestations of hyperemia

A
  • erythema

- warmth

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22
Q

what is diapedesis

A

when cells move out of the blood vessels with fluid from the blood (exudate)

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23
Q

what are the 3 stages of the cellular response of acute inflammation

A
  • chemotaxis
  • margination
  • diapedesis
24
Q

what is chemotaxis (inflammation)

A

mediators attract neutrophils and other leukocytes to the site of injury

25
explain what happens during margination (inflammation)
selectins (adhesion molecules) help neutrophils to attach to the endothelium
26
explain what happens during the diapedesis (transmigration) phase of inflammation
cells enter the interstitial space which allows for phagocytosis of microbes and debris
27
what 3 processes occur during chronic inflammation
- angiogenesis - fibrosis - necrosis
28
what are the 5 types of exudate
- serous - purulent (suppurative) - hemorrhagic - membranous - fibrinous
29
what are the main components of serous exudate? what does it indicate?
``` mostly fluid (serum), few proteins and cells. indicates mild injury ```
30
what are the main components of purulent (suppurative) exudate? what does it look like? what does it indicate?
pus = necrotic debris, WBC, proteins cloudy, thick, foul smell more severe injury, likely bacterial infection
31
what does hemorrhagic exudate contain? what does it indicate?
RBC's due to severed vessels | indicates severe injury
32
what does membranous exudate contain? what does it look like?
necrotic cells in fibropurulent exudate | appears membranous due to fibers
33
what does fibrinous exudate contain? what does it look like?
fibrogen | appears like sticky, mesh
34
what 3 things do all exudates contain in varying amounts
- fluid - cells - protein
35
what are some symptoms of systemic manifestations
malaise, headache, fatigue, fever
36
is fever a deliberate process
no
37
what is the temperature set point of the body
hypothalamus
38
what are 3 things fever does
- increases rate of cellular repair - decreases growth/reproduction of pathogens - enhances phagocytosis and immune response
39
what are pyrogens
fever causing chemicals
40
exogenous pyrogens are released by
bacteria
41
endogenous pyrogens are released by
defense cells
42
explain the process of triggering a fever
- bacteria release exogenous pyrogens - exo. pyrogens trigger endogenous pyrogens - endo. pyrogens cause synthesis of PGE2 - PGE2 binds to the hypothalamic receptor - this binding triggers the temperature set point to adjust via cAMP
43
what is PGE2
prostaglandin type E2
44
what are serum markers
markers that are present in the serum and are specific for certain diseases
45
what is CRP and what does it indicate
C- reactive protein - a serum marker | inflammation
46
what does CRP help with
aids complement with defense
47
is CRP a specific or non specific marker of inflammation
non specific
48
should we treat inflammation?
only if it is causing pain | inflammation is beneficial for healing
49
what is the process for treating inflammation
- apply cold - elevate - apply pressure - later apply heat
50
what does applying cold to inflammation do
decreases vasodilation which decreases swelling
51
why does elevation help treat inflammation
blood must work against gravity | therefore decreases hyperemia and blood flow - decreases swelling
52
what does applying pressure to inflammation do?
opposes the formation of exudate (in interstitial fluid) | decreases blood flow
53
what does applying heat to inflammation do
increases phagocytosis and the immune response
54
what do NSAIDS act on
decrease prostaglandin synthesis which decreases pain
55
why are steroidal anti-inflammatory drug useful
they are very efficient
56
steroidal anti-inflammatory drugs cause what
very pressing side effects
57
what do steoidal anti-inflammatory drugs act on
- decrease permeability (decrease exudate formation) - decrease mediator release (inflm relies of mediators) - inhibit leukocyte and mast cell activity at the site