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Pharm exam module 2 > Analgesic, Antipyretic, Anti-inflammatory > Flashcards

Analgesic, Antipyretic, Anti-inflammatory Flashcards

1
Q

What does inflammation start with?

A

Tissue Damage

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2
Q

What happens when histamine, kinins, and prostaglandins are released

A

Activation of innate & Adaptive immune cells

Vasodilation and permeability

Phagocytosis

Elimination of microbes and eventually tissue repair

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3
Q

What else besides injury can cause an inflammation response

A

Inappropriate activation or immune response, often seen in autoimmune diseases

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4
Q

What are the cardinal signals of inflammation?

A

Heat
Redness
Swelling
Pain
Loss of function

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5
Q

What are the main mediator systems of inflammation?

A

Vasoactive amines

Plasma protein systems

Eicosinoids

Platelet activating factor (PAF)

Cytokines

Nitric Oxide

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6
Q

What makes up vasoactive amines?

A

Histamine and serotonin

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7
Q

What makes up the plasma protein system?

A

Complement system

Kinin system

Clotting system

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8
Q

What are Eicosinoids

A

Prostaglandins and Leukotrienes

*Often household/OTC medications

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9
Q

What makes up platelet activating factors?

A

Acetyl Glycerol Ether Phosphocholine (AGEPC)

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10
Q

What do the inflammatory mediators indicate?

A

Tell us what we are targeting with medications to treat the present issue

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11
Q

What is the precursor to prostagladins

A

Cyclooxygenase

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12
Q

What does PGI2 do?

A

Vasodilation which inhibits platelet aggregation

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13
Q

What is TXA2 and what does it do

A

Thromboxane A2

Vasoconstriction which promotes platelet aggregation

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14
Q

What does PGE2 indicate?

A

Inflammation vasopermeability

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15
Q

What are the three main groups of NSAIDS

A

Salicylic acid derivatives

Nonselective COX inhibitors

Selective COX-2 inhibitors

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16
Q

What drug(s) are salicylic acid derivatives?

A

Acetylsalicylic acid (ASA)

Aspirin

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17
Q

What drug(s) are nonselective COX inhibitors?

A

Ibuprofen

Naproxen

Diclofenac

Ketorolac

Indomethacin

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18
Q

What is the brand names of Ibuprofen

A

Motrin or Advil

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19
Q

What is the brand name of Naproxen

A

Aleve

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20
Q

What is the brand name of Ketorolac

A

Toradol

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21
Q

What is indomethacin generally prescribed for?

A

Gout

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22
Q

What drug(s) are COX2 inhibitors?

A

Celecoxib

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23
Q

What’s the brand name of Celecoxib?

A

Celebrex

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24
Q

What Drug(s) are analgesic and antipyretic?

A

Acetaminophen (Tylenol)

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25
Q

What is the mechanism of action for an NSAID

A

They inhibit cyclooxygenase enzymes that allow for prostaglandin synthesis

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26
Q

What enzyme is prostaglandin generally synthesized from

A

Arachidonic acid

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27
Q

What does blocking cyclooxygenase cause

A

Decreased prostaglandin levels

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28
Q

What are the cyclooxygenase enzymes that are involved with prostaglandin synthesis

A

COX-1 and COX-2

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29
Q

Why do we avoid using drugs that are ONLY COX-2 inhibitors

A

They can cause cardiovascular issues

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30
Q

What does the production of prostaglandins do for the body?

A

Regulates homeostasis

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31
Q

what causes an increase in COX-2 in the body

A

oxidative stress
injury
ischemia

*Upregulates during inflammation

32
Q

What is the structural difference between COX-1 and COX-2

A

COX-2 has a larger and more flexible substrate channel as well as a larger target space for inhibitors to bind

33
Q

What is the abbreviation for asprin

A

ASA

34
Q

What is aspirin

A

Acetylsalicylic acid

35
Q

What is unique about aspirin as an NSAID

A

Aspirin irreversibly inhibits the enzymes

36
Q

How long do you hold Aspirin for before surgery and why

A

7 days because of anticoagulation effects

37
Q

What does low dose aspirin inhibit

A

COX-1

38
Q

What do high doses of aspirin inhibit

A

COX-1 and COX-2

39
Q

How is Aspirin metabolized

A

Rapidly hydrolyzed in the liver to salicylic acid and excreted by the Kidney

40
Q

How long does it take an uncoated aspirin to be metabolized by the liver

A

about two hours

41
Q

What happens with metabolism if aspirin is enteric coated

A

It takes longer to metabolize

42
Q

What is the purpose of an enteric coated aspirin and why do you tell someone having an MI to chew it instead of swallow it whole

A

Enteric coating prevents the aspirin from being rapidly absorbed

You tell someone having an MI to chew the aspirin to break that enteric coating and allow for rapid absorption

43
Q

What happens with metabolism at really high doses of aspirin

A

Turns into zero order kinetics which in turn can cause toxic side effects

44
Q

What effect does aspirin have on platelets

A

They block prostaglandin synthesis which intern inhibits TXA2 production = low platelet aggregation

45
Q

What are the side effects of aspirin

A

anti-inflammatory
analgesia (not for severe visceral pain)
Antipyretic

46
Q

What are the adverse effects of aspirin at therapeutic dosage

A

GI upset
gastric/duodenal ulcers

47
Q

What are the adverse effects of high dose aspirin

A

Salicylism (vomiting, tinnitus, decreased hearing, vertigo)

48
Q

What are the adverse effects of very large doses of aspirin

A

Hyperpnea (Increased depth and rate of respiration)

Respiratory alkalosis

Elevated body temperature

49
Q

Why does hyperpnea occur with very large doses of aspirin

A

ASA will have a direct effect on the respiratory centers in the medulla

50
Q

why can very large doses of ASA cause an elevated body temp

A

It causes uncoupling of the oxidative phosphorylation which could potentially result in sever hyperthermia

51
Q

What will happen with oxidative phosphorylation is inhibited

A

There will be a release of lactic acid from cells

52
Q

What adverse effect is generally seen first with ASA

A

Respiratory alkalosis

53
Q

What are the adverse effects of non ASA NSAIDs

A

Increased risk of cardiac thrombotic event

Increased risk of fatal GI upset
-> bleeding ulcer, stomach/ intestinal perf

54
Q

Which cardiac patients can not be given non ASA NSAIDs

A

CABG patients

55
Q

What is recommended when giving NSAIDs

A
  • give at lowest effective dose
56
Q

Who should not be given NSAIDs

A

Pregnant patients
children
hypertensive patients
hypercholesterolemia patients

57
Q

What can happen in children who are given ASA during viral illness

A

Reye’s syndrome

58
Q

What is an example of a COX-2 inhibitor

A

Celecoxib (Celebrex)

59
Q

What is the benefit of a COX-2 inhibitor

A

Minimal to no GI effects

60
Q

When do you never use COX-2 inhibtors

A

Patients with heart disease

61
Q

Why is celecoxib one of the few COX-2 inhibitors still on the market

A

Has less thrombotic potential

62
Q

Where are COX-2 inhibitors metabolized

A

Liver by CYP enzyme

63
Q

What is the half life of COX-2 inhibitors

A

Roughly 11 hours

64
Q

Who should not take COX-2 inhibitors

A

patients with severe hepatic and renal disease

65
Q

What happens when COX-2 inhibits CYP enzyme

A

it may increase levels of celecoxib, fluconazole, fluvastatin

66
Q

What else can happen when Celecoxib blocks CYP enzymes

A

Can lead to the elevation of beta-blockers, anti-depressants, and anti-psychotics

67
Q

What does acetaminophen do

A

inhibits prostaglandin synthesis in the CNS

68
Q

What is acetaminophen taken for

A

antipyretic and analgesic properties

69
Q

What does acetaminophen have no effect on

A

platelets

70
Q

Where is acetaminophen metabolized

A

the GI tract after first-pass metabolism and then secreted in urine

71
Q

What is acetaminophen metabolized to

A

Gets hydrolyzed into NAPQI

72
Q

What is NAPQI

A

potentially dangerous metabolite ( can cause quick liver failure)

73
Q

At normal doses was happens with NAPQI

A

reacts with glutathione to form a nontoxic metabolite

74
Q

How do corticosteroids work

A

bind to a glucocorticoid receptor and passes into the nucleus to regulate DNA translation = decreased expression of inflammatory genes

75
Q

Which processes are inhibited by corticosteroids to manage inflammation

A

decrease COX-2 up regulation

Inhibits inflammatory cytokines

76
Q

What are some adverse side effects of corticosteroids

A

adrenal suppression

increased blood glucose

psychiatric disturbances

77
Q

Which patients do you avoid using corticosteroids on

A

people at risk for osteoporosis

Patients with renal impairment

Pharm exam module 2 (2 decks)

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