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PHAR121 > 1.C > Flashcards

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?

A

1st gen

25
Q

True or false: prostaglandins and leukotrienes are newly generated mediators

A

true

26
Q

What is the pre-cursor for prostaglandins and leukotrienes?

A

arachidonic acid

27
Q

Which pathway converts arachidonic acid to prostaglandins? Leukotrienes?

A

prostaglandins=cyclooxygenase
leukotrienes=lipoxygenase

28
Q

True or false: the cyclooxygenase and lipoxygenase pathways occur at different times when arachidonic acid is released

A

false, they occur at the same time

29
Q

What are a few functions of prostaglandins?

A

various functions:
constrict/dilate vascular tissue
aggregation/disaggregation of platelets
induce labour
produce a fever
menstruation
GI mucosal production

30
Q

What is the enzyme that converts arachidonic acid into a prostaglandin?

A

cyclooxygenase

31
Q

Compare and contrast COX-1 and COX-2.

A

COX-1: in all tissues, involved in platelet aggregation
COX-2: specific for inflamed tissue

32
Q

What are the 5 types of drugs that affect inflammation?

A

biologics
anti-histamines
NSAIDs
LTRAs
corticosteroids

33
Q

Which enzyme do NSAIDS target? What effect does this have?

A

inhibits cyclooxygenase
reduces prostaglandin synthesis=less inflammation

34
Q

True or false: NSAIDS can affect prostaglandins that have been synthesized

A

false

35
Q

What are some other uses of NSAIDS?

A

analgesic
antipyretic

36
Q

What do classic NSAIDS target? COX-2 inhibtors? Provide examples for both.

A

classic NSAIDS: inhibit COX-1 and COX-2 (ibuprofen, naproxen, ketorolac, diclofenac, meloxicam)
COX-2 inhibitors: specific inflamed tissue (celecoxib)

37
Q

What are a few adverse effects of NSAIDS?

A

nausea
dyspepsia
hypertension (long term NSAID use)
anti-platelet

38
Q

Where are leukotrienes particularly active?

A

smooth muscle lining the bronchioles

39
Q

Which pathophysiological condition do leukotrienes contribute to?

A

asthma

40
Q

How do leukotriene receptor antagonists (LTRAs) work? Drug example?

A

reduce inflammation by blocking leukotriene receptors
montelukast

41
Q

True or false: LTRAs are a rescue drug

A

false

42
Q

What is cortisol?

A

a hormone released in response to stress
job is to bring the body back to homeostasis

43
Q

What kind of effects does cortisol have?

A

anti-inflammatory
immunosuppressive

44
Q

Where are cortisol receptors?

A

all over the body

45
Q

How are corticosteroids designed?

A

to mimic our endogenous cortisol
they are not very specific

46
Q

How are corticosteroids categorized?

A

pharmacokinetics
potencies

47
Q

When using corticosteroids, why do we attempt to administer locally?

A

to try and prevent adverse effects

48
Q

Describe the anti-inflammatory and immunosuppressant MOA of cortisol.

A

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

PHAR121 (17 decks)

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