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
Q

name 4 NSAIDS that are a little more selective for COX2 than for COX1**

A

Diclofenac
Etodolac
Sulindac
Meloxicam

26
Q

name an NSAID in which there is a limit on the max daily dose because it can become nephrotoxic

A

ketorolac

27
Q

true or false

both ibuprofen and naproxen are nonselective NSAIDS

A

true

28
Q

name 3 things that NSAIDS (nonselective) reduce the synthesis of

A

TXA2
PGI2 (prostacyclin)
prostaglandins (the whole point)

29
Q

TRUE OR FALSE***

NSAIDS are not very highly bound to albumin

A

FALSE

they are HIGHLY bound

30
Q

as mentioned, NSAIDS are highly bound to albumin. this limits their ___________

A

distribution

31
Q

NSAIDS being highly bound to albumin makes them subject to….

A

drug-drug interaction

32
Q

true or false

NSAIDS can be used to treat OA/RA

A

true

33
Q

what can occur with high dose and chronic use of NSAIDS**
why?

A

analgesic induced nephropathy(kidney disease)
because of decreased glomerular filtration

34
Q

NSAIDS can cause asymptomatic ______

A

hepatitis

35
Q

state a respiratory side effect of NSAIDS

A

at high doses (overdose) they can stimulate respiration and result in alkalosis and later acidosis

36
Q

name some GI effects of NSAIDS

A

NVD
gastric ulceration and bleeding

37
Q

explain the mechanism in which NSAIDS can cause gastric ulcers

A

NSAIDS inhibit the production of prostaglandins (eicosanoids) — even the protective ones in the stomach. more prone to ulceration

38
Q

name some blood changes that can occur as a result of NSAIDS

A

decrease in hemoglobin/hematocrit
thrombocytopenia (low platelet count)

39
Q

what is a concern of pts with HTN taking NSAIDS

A

NSAIDS can cause fluid retention, increasing BP

40
Q

what is AIN and what can cause it

A

analgesic induced nephropathy

can be caused by chronic use of high dose NSAIDS

41
Q

***Acetaminophen MOA

A

inhibition of COX3 (central prostaglandin synthase)

42
Q

another name for acetaminophen/tylenol

A

paracetamol

43
Q

when COX2 inhibitors and ____ inhibitors are taken together, caution must be exercised because COX2 levels can be increased

A

CYP2D6 inhibitors

44
Q

COX2 inhibitors may increase the risk of renal failure when taken with…

A

ACE inhibitors and diuretics

45
Q

____ work in the brain AND body while ____ only in the brain

A

NSAIDS in both brain and body and tylenol only brain

46
Q

what is the BLACK BOX WARNING for tylenol****

A

hepatotoxicity

47
Q

true or false

acetaminophen has NO anti inflammatory effect

A

TRUE

48
Q

which has a longer duration of action - tylenol or ibuprofen

A

ibupofen

49
Q

another name for COX3

A

central prostaglandin synthase

50
Q

briefly name 2 ways in which tylenol works in the brain (not just inhibit COX3)

A

inhibits reuptake of endocannabinoid

activates central serotonergic pain modulation

51
Q

the biggest concern with tylenol is ________ toxicity

A

HEPATO (liver)

52
Q

acetaminophen is a _____ and ______

A

analgesic and antipyretic

53
Q

what is the antidote for acetaminophen overdose and why is it effective***

A

N-acetyl cysteine

substitute for endogenous GSH pathway of detoxification when the body runs out

54
Q

besides n acetyl cysteine, name 2 other things that are hepato protective in the case of an acetaminophen overdose

A

silymarin and silibilin

55
Q

what is the max daily dose of acetaminophen

A

generally 3000mg a day, but can go up to 4000mg

56
Q

true or false

acetaminophen is relatively safe and effective

A

true

57
Q

what is the most COMMON adverse effect associated with acetaminophen use**

A

GI bleeding in an alcoholic patient

58
Q

hypo_____ is an adverse effect of acetaminophen

A

hypophosphatemia (low phosphate in blood)

59
Q

name 3 types of drugs used in arthritis

A

NSAIDS
steroids
immunosuppressants (in case of RA)

60
Q

what is gouty arthritis

A

excessive uric acid deposits in the joints

61
Q

aside from inhibiting COX3, name another mechanism of acetaminophen

A

suppresses serotenergic and NE pain transmission

62
Q
A