pharmacology part 1 Flashcards

1
Q

what is COX1 stimulated by vs CX2

A

COX1 is stimulated by hormones/growth factors while COX2 is induced in response to inflammation

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2
Q

the expression of COX___is suppressed by corticosteroids

A

COX2

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3
Q

***explain what low dose aspirin inhibits and how it inhibits it

A

pseudoirreverisibly inhibits COX1 and thus also TXA2 because COX1 produces TXA2

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4
Q

TXA2 is involved with…

A

platelet aggregation and thrombus formation

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5
Q

______ is central prostaglandin synthase

A

COX3

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6
Q

______ inhibits PLA2

A

sterouds

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7
Q

what does PLA2 do

A

cleaves arachidonic acid from cell membrane

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8
Q

what do coxibs inhibit

A

COX2

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9
Q

true or false

NSAIDS inhibit both COX1 and COX2

A

true

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10
Q

_____ is a vasodilator that inhibits platelet aggregation

what produces it?

A

PG12

produced by COX2

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11
Q

differentiate between the locations of TXA2 and PGI2

A

TXA2 = platelet

PGI2 = endothelial cells

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12
Q

what is ASA

A

acetyl salicylic acid (aspirin)

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13
Q

true or false

low dose aspirin pseudoirreversibly inhibits COX2

A

false

COX1

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14
Q

What is the typical mg strength of low dose aspirin

A

75mg-81mg

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15
Q

taking _______ regularly abolishes the preventative effects of low dose aspirin

A

NSAIDS

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16
Q

explain the mechanism of how low dose aspirin as an antithrombotic effect
(3 components)

A

-inhibit PGH2 synthesis – reducing TXA2 formation

-promotes fibrinolysis (breakdown of clots)

-downregulates release of dense granules in platelets (they would promote platelet aggregation)

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17
Q

aspirin uncouples _________ and suppresses signaling through ______

A

uncouples MITOCHONDRIAL OXIDATIVE PHOSPHORYLATION and suppresses SIGNALING THROUGH NFKB (like an on switch for inflammation)

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18
Q

as mentioned, aspirin uncouples mitochondrial oxidative phosphorylation

what is the result of this

A

platelets less active

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19
Q

what specific amino acid on COX1 is acetylated by aspirin

A

serine 529

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20
Q

what is the antiplatelet dose of aspirin

A

75-81 mg

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21
Q

what does of aspirin is used for STROKE prophylaxis

A

325mg

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22
Q

name some side effects/adverse drug reactions of aspirin

A

NVD
GI upset
GI bleeds
tinnitus
hoarseness
heartburn
wheezing
asthma
tachycardia

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23
Q

as mentioned, aspirin can cause GI bleeds

how can you tell if the bleed is upper or lower

A

upper - vomit will look like coffee grounds

lower - dark or black tarry (sticky) stool

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24
Q

true or false***

NSAIDS inhibit both COX1 and COX2

A

true

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25
name 4 NSAIDS that are a little more selective for COX2 than for COX1****
Diclofenac Etodolac Sulindac Meloxicam
26
name an NSAID in which there is a limit on the max daily dose because it can become nephrotoxic
ketorolac
27
true or false both ibuprofen and naproxen are nonselective NSAIDS
true
28
name 3 things that NSAIDS (nonselective) reduce the synthesis of
TXA2 PGI2 (prostacyclin) prostaglandins (the whole point)
29
TRUE OR FALSE*********** NSAIDS are not very highly bound to albumin
FALSE they are HIGHLY bound
30
as mentioned, NSAIDS are highly bound to albumin. this limits their ___________
distribution
31
NSAIDS being highly bound to albumin makes them subject to....
drug-drug interaction
32
true or false NSAIDS can be used to treat OA/RA
true
33
what can occur with high dose and chronic use of NSAIDS**** why?
analgesic induced nephropathy(kidney disease) because of decreased glomerular filtration
34
NSAIDS can cause asymptomatic ______
hepatitis
35
state a respiratory side effect of NSAIDS
at high doses (overdose) they can stimulate respiration and result in alkalosis and later acidosis
36
name some GI effects of NSAIDS
NVD gastric ulceration and bleeding
37
explain the mechanism in which NSAIDS can cause gastric ulcers
NSAIDS inhibit the production of prostaglandins (eicosanoids) --- even the protective ones in the stomach. more prone to ulceration
38
name some blood changes that can occur as a result of NSAIDS
decrease in hemoglobin/hematocrit thrombocytopenia (low platelet count)
39
what is a concern of pts with HTN taking NSAIDS
NSAIDS can cause fluid retention, increasing BP
40
what is AIN and what can cause it
analgesic induced nephropathy can be caused by chronic use of high dose NSAIDS
41
*******Acetaminophen MOA
inhibition of COX3 (central prostaglandin synthase)
42
another name for acetaminophen/tylenol
paracetamol
43
when COX2 inhibitors and ____ inhibitors are taken together, caution must be exercised because COX2 levels can be increased
CYP2D6 inhibitors
44
COX2 inhibitors may increase the risk of renal failure when taken with...
ACE inhibitors and diuretics
45
____ work in the brain AND body while ____ only in the brain
NSAIDS in both brain and body and tylenol only brain
46
what is the BLACK BOX WARNING for tylenol******
hepatotoxicity
47
true or false acetaminophen has NO anti inflammatory effect
TRUE
48
which has a longer duration of action - tylenol or ibuprofen
ibupofen
49
another name for COX3
central prostaglandin synthase
50
briefly name 2 ways in which tylenol works in the brain (not just inhibit COX3)
inhibits reuptake of endocannabinoid activates central serotonergic pain modulation
51
the biggest concern with tylenol is ________ toxicity
HEPATO (liver)
52
acetaminophen is a _____ and ______
analgesic and antipyretic
53
what is the antidote for acetaminophen overdose and why is it effective*******
N-acetyl cysteine substitute for endogenous GSH pathway of detoxification when the body runs out
54
besides n acetyl cysteine, name 2 other things that are hepato protective in the case of an acetaminophen overdose
silymarin and silibilin
55
what is the max daily dose of acetaminophen
generally 3000mg a day, but can go up to 4000mg
56
true or false acetaminophen is relatively safe and effective
true
57
what is the most COMMON adverse effect associated with acetaminophen use**
GI bleeding in an alcoholic patient
58
hypo_____ is an adverse effect of acetaminophen
hypophosphatemia (low phosphate in blood)
59
name 3 types of drugs used in arthritis
NSAIDS steroids immunosuppressants (in case of RA)
60
what is gouty arthritis
excessive uric acid deposits in the joints
61
aside from inhibiting COX3, name another mechanism of acetaminophen
suppresses serotenergic and NE pain transmission
62