Test 2: 25 antiinflam Flashcards

1
Q

5 signs of inflammation

A

heat
redness
swelling
pain
loss of function

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2
Q

chronic inflammation results in formation of

A

fibrous tissue

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3
Q

why treat inflammation

A

reduce pain
prevent loss of function
accelerate resolution of inflammation
limit fibrosis and degeneration

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4
Q

what are some mediators of acute inflammation

A

prostaglandins
leukotrienes
bradykinin
serotonin
histamine

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5
Q

what are some mediators of chronic inflammation

A

PDF3- stimulate fibrosis

TNF ⍺, interleukins, interferons
all stimulate acute inflammation factors and cell activation

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6
Q

prostaglandins and leukotrienes are made from

A

arachoidonic acid

(increased Ca, TNF, interleukins and interferons can all increase production)

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7
Q

what is rate limiting step to make leukotrienes and prostandlandins

A

PLA2= phospholipase A2

takes membrane phospholipids and turns it into Arachidonic acid

from there AA can become
* (5-LOX) →Leukotreines
* (COX1 and COX2) → prostanoids

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8
Q

leukoteienes are produced by — cells

A

leukocytes: neutrophils, mast cells, monocytes, macrophages
lungs

mediate inflammation and bronchoconstriction and mucus production in airways →asthma

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9
Q

what do leukotrienes do?

A

mediate inflammation and bronchoconstriction and mucus production in airways →asthma

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10
Q

arachidonic acid (—)→ leukotrenes

A

5-LOX (5-lipoxygenase)

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11
Q

NSAID and aspirin block what part of inflammation cascade

A

COX1 and CO2

prevenets arachidonic acid →prostanoids

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12
Q

Prostaglandins sensitize — to other inflammatory mediators (—)

A

nociceptors
i.e. bradykinin

inflammation associated pain

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13
Q

prostacyclin

A

made by vascular endoethial cells
inhibits platelet aggregation
causes vasodilation/ inhibits smooth muscle contraction

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14
Q

thromboxane is made by — and does —

A

platelets and macrophages

Promotes platelet aggregation (antagonist for PGI2(prostacyclin))

Vasoconstriction- causes smooth muscle contraction

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15
Q

— causes platelet aggregation and vasoconstriction

— inhibits platelet aggregation, and causes vasodilation

A

TXA2 (thromboxane)
* synthesized by platelets + macrophages
* Promotes platelet aggregation (antagonist for PGI2)
* Vasoconstriction- causes smooth muscle contraction

PGI2 (prostacyclin)
* synthesized by vascular endothelial cells
* Inhibits platelet aggregation
* Vasodilation -inhibits smooth muscle contraction

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16
Q

how do eicosanoids work

A

bind to GPCR and induce changed in intracellular calcium levels

eicosanoids = prostaglandins

17
Q

grapiprant/galliprant works by

A

inhibit EP4 receptors

prostaglandin receptor

blocks pain stimuli from inflammation

18
Q

COX1 is found in— cells and does —

A

platelets and other cell

housekeeping enzyme- required for cell-cell signaling, tissue homeostasis and gastric cytoprotection

PGEs stimulate bicarbonate and mucous secretions in gastric mucosa

19
Q

how does COX1 cause gastric cytoprotection

A

PGEs stimulate bicarbonate and mucous secretions in gastric mucosa

this is why you can get gastric ulcers with NSAID cause it blocks COX1

20
Q

COX2 main function

A

is expressed during inflammation and causes inflammatory response

21
Q

— transcription factor is a major regulator of the immune response

A

NK κB

22
Q

how does NFκB work during inflammation

A

will activate and enter nucleus and cause formation of COX2, iNOS and cytokines

does a lot of other stuff

23
Q

how to stop formation of AA from membrane phospholipids

A

corticosteroids

blocks Phopholipase A2 (PLA2)

24
Q

Asprin and NSAID block what part of arachidonic pathway

A

inhibits COX 1 and 2

stops production of prostaglandins

25
Q

— is a Non-selective Cox inhibitors

A

classic NSAIDS: aspirin, ibuprofen

26
Q

— is a Weakly Cox2-selective drug

A

carprofen

27
Q

— Strongly Cox2-selective drugs

A

coxibs

28
Q

— is a EP4 receptor inhibitors

A

Grapiprant/Gallaprant

EP4 is a prostaglandin receptor that leads to pain stimuli from inflammation