1.C Flashcards

1
Q

What is inflammation?

A

a physiologic response to tissue injury and infection
chronic or acute

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2
Q

True or false: inflammation is present in almost all diseases or conditions

A

true

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3
Q

What are some symptoms of acute inflammation?

A

swelling
redness
heat
pain

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4
Q

What is the purpose acute inflammatory response?

A

provides protection by:
-restricting damage to the localized site
-recruiting immune cells to eliminate invading pathogens
-initiating wound repair

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5
Q

How do the clotting and kinin systems aid in acute inflammation?

A

clotting: fibrin strands accumulate to stop the spread of infection and bleeding to outside
kinin: produces bradykinin which induces vasodilation and increased permeability

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6
Q

What is the role of mast cells in the acute inflammatory response?

A

degranulate to release histamine and activates prostaglandins and leukotrienes
this allows leakage of fluid from the blood vessels to the damaged tissue

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7
Q

Is acute inflammation a negative or positive feedback loop?

A

positive
more cells are recruited until the problem is resolved

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8
Q

What is the cause of heat, redness, and swelling during acute inflammation?

A

vasodilation (more fluid arrives and moves)

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9
Q

What is the cause of pain during acute inflammation?

A

swelling or the activation of nociceptors

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10
Q

What is diapedesis?

A

the movement of leukocytes out of the blood into the site of infection or tissue damage

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11
Q

What are the 4 steps in diapedesis?

A
  1. chemoattraction: granular substances draw leukocytes to the site of damage
  2. rolling adhesion: leukocyte makes weak bonds to receptors on the endothelial cell wall
  3. tight adhesion: cytokines and integrins bond strongly to the endothelial cell wall
  4. transmigration: leukocytes squeeze into tissue
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12
Q

What do leukocytes do after diapedesis?

A

phagocytize the invading pathogen and release mediators
(cytokines, histamines, PG, LT)

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13
Q

What do mediators do?

A

coordinate and regulate immune cell activities
antiviral, pro-inflammatory, or anti-inflammatory activity
act locally or systemically
they guide cells where to go (chemoattraction)

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14
Q

What does the chronic inflammatory response do?

A

continues after the acute response
cleans up debris
facilitates healing

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15
Q

What is chronic inflammation the result of?

A

continuous exposure to the offender

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16
Q

How do we characterize chronic inflammation?

A

accumulation and activation of macrophages and lymphocytes
fibroblasts that replace the original, damaged, or necrotic tissue

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17
Q

Where are inflammatory mediators found?

A

newly synthesized or preformed in granules

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18
Q

What are cytokines?

A

soluble factors secreted by activated immune cells

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19
Q

What are the major activities of cytokines?

A

promote inflammation and mediate natural immunity (IL-1, IL-8, IL-, TNF, IFN-a)
support allergic inflammation (IL-4, IL-5, IL-13)
immunoregulatory (IL-10, IL-12, TGF-b, IFN-y)
act as hematopoietic growth factors (IL-3, Il-12, GM-CSF)

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20
Q

What are “biologics”?

A

designed to affect cytokines
medications produced using biological processes
large and complex molecules
harvested from living sources

21
Q

How do monoclonal antibodies work?

A

the antibody is the delivery system to target receptors or pathogens
attach a drug to an antibody which then only targets and affects specific cells

22
Q

What kind of drug is Infliximab? How does it work?

A

biologic
Mab designed to target the cytokine TNF to reduce inflammatory bowel disease

23
Q

What is typically used in patients with MS? What does it target?

A

natalizumab (a biologic)
a monoclonal antibody that blocks a4 integrin

24
Q

Which type of antihistamines have a stronger anticholingergic effect?

25
True or false: prostaglandins and leukotrienes are newly generated mediators
true
26
What is the pre-cursor for prostaglandins and leukotrienes?
arachidonic acid
27
Which pathway converts arachidonic acid to prostaglandins? Leukotrienes?
prostaglandins=cyclooxygenase leukotrienes=lipoxygenase
28
True or false: the cyclooxygenase and lipoxygenase pathways occur at different times when arachidonic acid is released
false, they occur at the same time
29
What are a few functions of prostaglandins?
various functions: constrict/dilate vascular tissue aggregation/disaggregation of platelets induce labour produce a fever menstruation GI mucosal production
30
What is the enzyme that converts arachidonic acid into a prostaglandin?
cyclooxygenase
31
Compare and contrast COX-1 and COX-2.
COX-1: in all tissues, involved in platelet aggregation COX-2: specific for inflamed tissue
32
What are the 5 types of drugs that affect inflammation?
biologics anti-histamines NSAIDs LTRAs corticosteroids
33
Which enzyme do NSAIDS target? What effect does this have?
inhibits cyclooxygenase reduces prostaglandin synthesis=less inflammation
34
True or false: NSAIDS can affect prostaglandins that have been synthesized
false
35
What are some other uses of NSAIDS?
analgesic antipyretic
36
What do classic NSAIDS target? COX-2 inhibtors? Provide examples for both.
classic NSAIDS: inhibit COX-1 and COX-2 (ibuprofen, naproxen, ketorolac, diclofenac, meloxicam) COX-2 inhibitors: specific inflamed tissue (celecoxib)
37
What are a few adverse effects of NSAIDS?
nausea dyspepsia hypertension (long term NSAID use) anti-platelet
38
Where are leukotrienes particularly active?
smooth muscle lining the bronchioles
39
Which pathophysiological condition do leukotrienes contribute to?
asthma
40
How do leukotriene receptor antagonists (LTRAs) work? Drug example?
reduce inflammation by blocking leukotriene receptors montelukast
41
True or false: LTRAs are a rescue drug
false
42
What is cortisol?
a hormone released in response to stress job is to bring the body back to homeostasis
43
What kind of effects does cortisol have?
anti-inflammatory immunosuppressive
44
Where are cortisol receptors?
all over the body
45
How are corticosteroids designed?
to mimic our endogenous cortisol they are not very specific
46
How are corticosteroids categorized?
pharmacokinetics potencies
47
When using corticosteroids, why do we attempt to administer locally?
to try and prevent adverse effects
48
Describe the anti-inflammatory and immunosuppressant MOA of cortisol.
anti-inflammatory: decrease production of PG, LT, leukocytes, decrease recruitment of leukocyte to site of injury, stabilize mast cells immunosuppressant: induce T cell apoptosis, decrease T cell recruitment to antigens, no B cell activity, increase T cell redistribution to lymph nodes