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Phar300 > lect 11 Non-steroidal anti-inflammatory drugs > Flashcards

lect 11 Non-steroidal anti-inflammatory drugs Flashcards

1
Q

most common NSAIDS

A

aspirin

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2
Q

two categories of NSAIDS

A

salicylates (aspirin) and non salicylates (ex ibuprofen, acetaminophen)

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3
Q

History: compound extracted from plants and its derivative

A

salicylic acid and acetylsalicylic acid

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4
Q

what does aspirin inhibit

A

synthesis of prostaglandins

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5
Q

what cleaves section of plasma membrane fatty acids and what is being released

A

Phospholipase A2 and release of arachidonic acid

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6
Q

structure of arachidonic acid and what it does

A

20 carbon, polyunsaturated fatty acid and acted on by enzymes to produce biologically active compounds

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7
Q

enzymes that produce prostaglandins and thromboxanes

A

cyclooxygenases

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8
Q

what two cyclo. produce prostaglandins

A

COX-1 AND COX-2

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9
Q

change in structure from arachidonic acid to prostaglandins

A

formation of a ring and adding two carbons

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10
Q

structure, place, role of cyclooxygenases

A

dimers so 2 equal active site, in the ER, converts arachidonic acid to prostaglandins

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11
Q

true or false? prostaglandins have autocrine and paracrine functions

A

True

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12
Q

inactivation of prostaglandins is fast or slow?

A

rapid fast inactivation

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13
Q

other functions of prostaglandins

A

protect stomach from hydrochloric acid and thromboxanes involved in platelet aggregation and blood clotting

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14
Q

true or false? Blocking prostaglandins can prevent intravascular coagulation and heart attacks

A

True

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15
Q

prostaglandins have effects on what? (7)

A

Renal homeostasis, sleep cycle, reproductive system, vasodilation and vasoconstriction, platelet aggregation, blood flow to organs, pain and inflammation

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16
Q

COX 1 activity and use

A

constitutively active and essential for physiological purposes like stomach protection platelet aggregation

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17
Q

COX-2 activity and use

A

inducible, essential for pathological purposes like pain and inflammation

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18
Q

prostaglandins act on what receptors

A

many different prostanoid receptor that have different subunits

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19
Q

NSAIDS block prostaglandins that are implicated in what three things

A

fever (antipyretic), pain (analgesic), inflammation (anti anflammatory)

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20
Q

Pain stimulus pathway

A

painful sensation going to spinal cord, relying in the thalamus, then the cortex, and then instantaneous reflex to withdraw from pain stimulus

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21
Q

periphery in sensation of pain (2)

A

thermoreceptors, nociception

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22
Q

injured cells release what

A

Mediators, including prostaglandins

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23
Q

release on mediators have effect of what

A

nerve endings so impulses sent to spinal cord and up the brain

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24
Q

involved in signaling from a variety of noxious stimuli (mediators released form injured cells and platelets)

A

nociceptive nerve endings

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25
Q

NSAIDS act predominantly where

A

out in the periphery at the origin of pain stimuli and inflammation (nociceptors

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26
Q

How does Nsaids work on periphery in relation to prostaglandins

A

blocks synthesis of PGs to decrease their intensity of the painful signal coming from periphery

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27
Q

First stage usage when pain

A

NSAIDS

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28
Q

Second stage usage when pain

A

OPIOiD and NSAIDS

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29
Q

third stage usage when pain

A

OPIOIDS

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30
Q

therapeutic usage of NSAIDS (5)

A

mild moderate pain like headache, inflammatory disorders, reduce fevers, prophylaxis of myocardial infarction and stroke, reduce risks of certain cancers

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31
Q

chemical mediators inflammation pathway

A

released from injured tissue to local capillary bed which induces vasodilation and fluid and cells are drawn into injured area

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32
Q

inflammatory mediators contribute to sensation of which nociceptors

A

sensitizing PGE2 or activating BK

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33
Q

acute inflammation

A

cuts, allergic reactions

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34
Q

chronic

A

cancer, arthritis, CV and neurological diseases

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35
Q

what is osteoarthritis

A

injury induced joint damage

36
Q

what is Rheumatic arthritis

A

joints inflammed independent on the environment

37
Q

racehorses NSAID

A

equioxx

38
Q

arthritis common in excessive inbreeding

A

canine arthritis

39
Q

ASA or acetominophen should never be given to what animal

A

cat

40
Q

fever is induced by what

A

endogenous pyrogens that raise thermostatic set point in hypothalamus

41
Q

which PG major player for increasing setpoint in hypothalamus for fever

A

PG E2

42
Q

body response to pyrogens

A

temperature regulatying cenetr sends out impulses via ANS leading to increased heat production and decreased heat loss

43
Q

side effects of nsaids to upper GI tract

A

dyspepsia, erosions, ulcers, GI bleeding

44
Q

side effects of nsaids to renal

A

renal dysfunction, renal failure, blood pressure, heart failure

45
Q

why can NSAIDS cause blood loss

A

because of its anti platelet effect

46
Q

what lines the membrane layer of stomach and is protected by prostaglandins

A

gastric mucosa

47
Q

generic name for acetylsalicylic acid

A

aspirin

48
Q

how does aspirin inactivate COX (antithrombotic)

A

acetyl group of acetylsalicylic acid binds to serine residue in COX

49
Q

what is thromboxane A2

A

made in platelets which causes vasoconstriction and thrombosis (blood clots)

50
Q

does aspirin block thromboxane A2

A

yes

51
Q

true or false? Asprin can lower risks of colon cancer

A

true

52
Q

asprin half life and also at higher doses

A

3 hrs and 15 hrs

53
Q

aspirin (acetylsalicylic acid) is metabolized to what

A

salicylic acid

54
Q

enzymes that break down aspririn in lover

A

P450

55
Q

pharmacokinetics of NSAids in liver

A

P450 enzymes producing metabolites and glucoronyl transferases conjugating the metabolites to make water soluble glucuronide to be excreted by kidney

56
Q

pharmacokinetics of NSAids in liver

A

salicylic acid is an acid so reabsorbed by kidneys if tubules are acidic. for overdose, alkalinize urine so that weak acid wont be in unionized lipid soluble form and not be reabsorbed

57
Q

what do we call aspirin toxicity

A

salicylism

58
Q

sense of ringing in the ear

A

tinnitus

59
Q

neurological syndrom when children take aspirin

A

Reye’s syndrome

60
Q

what can we give children instead of aspirin

A

acetaminophen

61
Q

aspirin binds reversibly or irreversibly

A

irreversiblly

62
Q

ibuprofen binds reversibly or irreversibly

A

reversibly

63
Q

types of ibuprofen

A

motrin, advil

64
Q

ibuprofen blocks what

A

both COX 1 AND 2

65
Q

cox 2 have constituitive effects on what

A

blood flow and kidney

66
Q

cox 2 is important for what

A

platelet inhibition and vasodilation

67
Q

which cox enxyme has a larger channel for arachidonic acid

A

cox 2

68
Q

highly selective and large cox 2 inhibitor drug

A

celecoxib

69
Q

why does cardiovascular problems occur with cox 2 selective inhibitors

A

the balance is shifted towards a prothrombotic state cause does not block cox 1

70
Q

who is prothrombotic

A

cox 1 because they make thromboxane

71
Q

who is antithrombotic

A

cox 2 because make prostacyclin

72
Q

asprin balance on cox enzymes

A

does not affect balance because acts on both cox 1 and cox 2. low doses bllocks cox 1 more and that for people with thrombosis

73
Q

which cox 2 inhibitor was withdrawn

A

rofecoxib

74
Q

cox 1 is highly concentrated where in the body and cox 2 where

A

gi tract and found in many places like brain, kidney…

75
Q

tradename drug most used (acetaminophen)

A

tylenol

76
Q

what is the main difference between acetaminophen and other nsaids

A

it is not anti inflammatory

77
Q

half life of acetaminophen

A

2-3 hours

78
Q

emzymes that break it down to a toxic metabolite

A

CYP450

79
Q

break down in liver of acetaminophen

A

breakon down to a toxic intermediate that is quickly conjugated

80
Q

what congugates acetaminphen

A

glutathione

81
Q

what is cellular necrosis

A

reaction with hepatocytes to kill liver cells if toxic intermediate of acetaminphen is not quickly conjugated

82
Q

overdose of acetaminophen?

A

enzymes that conjugate saturated so more toxic compound

83
Q

who are vulnerable to the toxicity of acetaminophen and why

A

alcoholics because chronic use of ethanol induces P450 enzymes that make the toxic metabolites

84
Q

effects at 0-24 hour stage of acetaminophen poisining

A

anorexia, nausea, vomiting

85
Q

effects at 24-72 hour stage of acetaminophen poisining

A

abdominal pain, elevated serum enzymes

86
Q

effects at 72-96 hour stage of acetaminophen poisining

A

synptoms of liver and renal failure and pancreatitis

87
Q

antidote of acetaminophenoverdose

A

glutathione precursor (N acetylcysteine) so that congugation can happen

Phar300 (18 decks)

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