NSAID 1 Flashcards

1
Q

what are the 2 forms ox cyclo-oxygenase enzymes

A

COX1 and COX2

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2
Q

what is COX1

A

the constitutive form

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3
Q

what is COX2

A

the inducible form

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4
Q

which COX is the constitutive form

A

COX1

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5
Q

which COX is the inducible form

A

COX2

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6
Q

what are eicosanoids derived from

A

arachidonic acid

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7
Q

what are eicosanoids

A

large group of lipid compounds with diverse biological properties

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8
Q

what is the structure of arachidonic acid

A

C20 fatty acid with 4 unsaturated C-C bonds

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9
Q

where is arachidonic acid found

A

in most cell membranes

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10
Q

what happens during inflammation (what is released and how)

A

arachidonic acid liberation by phospholipase A2 and phospholipase C

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11
Q

what does phospholipase A2 do to arachidonic acid

A

snips it off from the phospholipid

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12
Q

what does phospholipase C do to arachidonic acid

A

snips it off from the phospholipid along with an IP/IP2/IP3 pathway (Gq)

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13
Q

what is the main pathway to get arachidonic acid

A

through phospholipid A2

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14
Q

what pathway to get arachidonic acid do muscarinic agonists use

A

the phospholipase C and IP3 pathway

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15
Q

what are the 4 oxidation pathways that stem from arachidonic acid

A

COX
lipoxygenase
P450 enzymes
isoprostane

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16
Q

what are the products made from the COX pathway

A

prostaglandins
thromboxane
prostacyclin

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17
Q

what are the products made from the lipooxygenase pathway

A

leukotrienes

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18
Q

what are prostaglandins involved in (3 things)

A

inflammation, prevention of peptic ulcers, uterine contraction

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19
Q

are prostaglandins vasoconstrictors or vasodilators

A

either or

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20
Q

what kind of blood flow are prostaglandins important for

A

regulation of renal blood flow

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21
Q

what do prostaglandins to do CNS temperature

A

cause fever

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22
Q

which COX product produces fever

A

prostaglandins

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23
Q

how do prostaglandins do its effects

A

via G protein coupled receptors

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24
Q

whats the starting point in the COX pathway

A

arachidonic acid

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25
whats the starting point in the lipooxygenase pathway
arachidonic acid
26
do prostaglandins have a white or black cowboy hat
both
27
does prostacyclin have a white or black cowboy hat
white
28
does thromboxane have a white or black cowboy hat
black
29
what does prostacyclin do (3)
vasodilator inhibits platelet aggregation relaxes bronchiole smooth muscle
30
what is the short-form of writing prostacyclin
PGI2
31
where is prostacyclin synthesized
in the endothelium
32
what does thromboxane do (3)
vasoconstriction platelet aggregation constrict bronchiole smooth muscle
33
what is the short-form of writing thromboxane
TXA2
34
which COX product inhibits platelet aggregation
prostacyclin
35
which COX product causes platelet aggregation
thromboxane
36
which 2 COX products seem to have opposite effects
prostacyclin and thromboxane
37
which COX product always causes vasodilation
prostacyclin
38
which COX product always causes vasoconstriction
thromboxane
39
which COX product always causes relaxation of bronchiole smooth muscle
prostacyclin
40
which COX product always causes constriction of bronchiole smooth muscle
thromboxane
41
what is the main product in the lipoxygenase pathway
leukotrienes
42
where are leukotrienes produced
in inflammatory cells (basophils, mast cells, eosinophils, macrophages)
43
what is the leukotriene pathway of interest (2 disease states)
asthma and anaphylactic shock
44
what are the 2 substances of anaphylactic shock and what are they called
LTC4 and LTD4, the "slow reacting substance" of anaphylactic shock
45
what is the mechanism of action of montelukast
leukotriene antagonist for asthma
46
what concentrations does the platelet activating factor have effect
very low, <10^-10 M
47
what is platelet activating factor involved in (1 word)
inflammation (various aspects)
48
what does platelet activating factor do to lungs
causes constriction of bronchiole smooth muscle
49
where is platelet activating factor from and how
released from activated inflammatory cells by phospholipase A2
50
what is the mechanism of action of glucocorticoids (2 things)
inhibit phospholipase A2 by upregulating expression of lipocortin
51
how are glucocorticoids connected to platelet activating factor
lots of their anti-inflammatory effects may be mediated via inhibition of synthesis of platelet activating factor
52
how is platelet activating factor involved in asthma
constricts bronchiole smooth muscle
53
why is platelet activating factor an example of "lipid remodeling"
because in the structure of platelet activating factor, arachidonic acid is replaced by an acetyl group
54
what are the 4 steps in platelet activating factor synthesis
phosphatidyl choline --> phospholipase A2 --> arachidonic acid --> PAF
55
what are the cardinal signs of the inflammatory response
- redness (rubor) - swelling (tumor) - heat (calor) - pain (dolor) - loss of function
56
what is the inflammatory response (broad, why does it happen)
powerful response to protect from invading pathogens
57
what are the 3 phases of the inflammatory response
- acute inflammation - immune response - chronic inflammation
58
what is released in acute inflammation (1 word for the general class)
autocoids
59
what are 5 things being released in acute inflammation
``` (all autocoids) histamine serotonin bradykinin prostaglandins leukotrienes ```
60
what are 4 things that happen in acute inflammation
- vasodilation - vascular permeability - chemotaxis - pain
61
what is chemotaxis
white blood cells leaving vessel to site of injury
62
what is the innate immune response
activation of immunologically competent cells
63
what does the innate immune response help activate
the adaptive immune response (more specific, antibodies)
64
why can the innate immune response be beneficial
if invading organisms can be phagocytosed or neutralized
65
how can the innate immune response become harmful
if it leads to chronic inflammation
66
what does acute inflammation lead to
innate immune response
67
what are the 2 main mediators of chronic inflammation
interleukins and tumor necrosis factor alpha
68
what can interleukins and tumor necrosis factor alpha initiate
chronic conditions such as rheumatoid arthritis
69
what happens to cells with chronic inflammation
cell damage
70
what do leukocytes do in chronic inflammation
release lysosomal enzymes
71
what do lysosomal enzymes do
cause the release of arachidonic acid
72
what causes the release of lysosomal enzymes in chronic inflammation
leukotrienes
73
what facilitates the release of lysosomal enzymes in chronic inflammation
mediators like bradykinin that stimulate phospholipase A2
74
what does bradykinin stimulate the release of in chronic inflammation
phospholipase A2
75
what are 3 cells that are normally present in tissue that cause the inflammatory response
``` vascular endothelial cells mast cells (histamine) tissue macrophages ```
76
what are 2 cells that gain access from blood that cause the inflammatory response
platelets (thrombocytes) | leucocytes (WBC)
77
where do corticosteroids affect the inflammatory response compared to NSAIDS +where do they effect
much higher (block phospholipids--> arachidonic acid)
78
which COX is the constitutive prostaglandin synthesis
COX1
79
which COX is the inducible prostaglandin synthesis
COX2
80
which COX does mucous gut secretion
COX1
81
which COX does platelet aggregation
COX1
82
what does COX1 do to platelets
aggregation
83
which COX does inflammation
COX2
84
which COX does pain
COX2
85
which COX has a white hat
COX1
86
which COX has a black hat
COX2