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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
What is the mechanism of action for an NSAID
They inhibit cyclooxygenase enzymes that allow for prostaglandin synthesis
26
What enzyme is prostaglandin generally synthesized from
Arachidonic acid
27
What does blocking cyclooxygenase cause
Decreased prostaglandin levels
28
What are the cyclooxygenase enzymes that are involved with prostaglandin synthesis
COX-1 and COX-2
29
Why do we avoid using drugs that are ONLY COX-2 inhibitors
They can cause cardiovascular issues
30
What does the production of prostaglandins do for the body?
Regulates homeostasis
31
what causes an increase in COX-2 in the body
oxidative stress injury ischemia *Upregulates during inflammation
32
What is the structural difference between COX-1 and COX-2
COX-2 has a larger and more flexible substrate channel as well as a larger target space for inhibitors to bind
33
What is the abbreviation for asprin
ASA
34
What is aspirin
Acetylsalicylic acid
35
What is unique about aspirin as an NSAID
Aspirin irreversibly inhibits the enzymes
36
How long do you hold Aspirin for before surgery and why
7 days because of anticoagulation effects
37
What does low dose aspirin inhibit
COX-1
38
What do high doses of aspirin inhibit
COX-1 and COX-2
39
How is Aspirin metabolized
Rapidly hydrolyzed in the liver to salicylic acid and excreted by the Kidney
40
How long does it take an uncoated aspirin to be metabolized by the liver
about two hours
41
What happens with metabolism if aspirin is enteric coated
It takes longer to metabolize
42
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
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
What happens with metabolism at really high doses of aspirin
Turns into zero order kinetics which in turn can cause toxic side effects
44
What effect does aspirin have on platelets
They block prostaglandin synthesis which intern inhibits TXA2 production = low platelet aggregation
45
What are the side effects of aspirin
anti-inflammatory analgesia (not for severe visceral pain) Antipyretic
46
What are the adverse effects of aspirin at therapeutic dosage
GI upset gastric/duodenal ulcers
47
What are the adverse effects of high dose aspirin
Salicylism (vomiting, tinnitus, decreased hearing, vertigo)
48
What are the adverse effects of very large doses of aspirin
Hyperpnea (Increased depth and rate of respiration) Respiratory alkalosis Elevated body temperature
49
Why does hyperpnea occur with very large doses of aspirin
ASA will have a direct effect on the respiratory centers in the medulla
50
why can very large doses of ASA cause an elevated body temp
It causes uncoupling of the oxidative phosphorylation which could potentially result in sever hyperthermia
51
What will happen with oxidative phosphorylation is inhibited
There will be a release of lactic acid from cells
52
What adverse effect is generally seen first with ASA
Respiratory alkalosis
53
What are the adverse effects of non ASA NSAIDs
Increased risk of cardiac thrombotic event Increased risk of fatal GI upset -> bleeding ulcer, stomach/ intestinal perf
54
Which cardiac patients can not be given non ASA NSAIDs
CABG patients
55
What is recommended when giving NSAIDs
- give at lowest effective dose
56
Who should not be given NSAIDs
Pregnant patients children hypertensive patients hypercholesterolemia patients
57
What can happen in children who are given ASA during viral illness
Reye's syndrome
58
What is an example of a COX-2 inhibitor
Celecoxib (Celebrex)
59
What is the benefit of a COX-2 inhibitor
Minimal to no GI effects
60
When do you never use COX-2 inhibtors
Patients with heart disease
61
Why is celecoxib one of the few COX-2 inhibitors still on the market
Has less thrombotic potential
62
Where are COX-2 inhibitors metabolized
Liver by CYP enzyme
63
What is the half life of COX-2 inhibitors
Roughly 11 hours
64
Who should not take COX-2 inhibitors
patients with severe hepatic and renal disease
65
What happens when COX-2 inhibits CYP enzyme
it may increase levels of celecoxib, fluconazole, fluvastatin
66
What else can happen when Celecoxib blocks CYP enzymes
Can lead to the elevation of beta-blockers, anti-depressants, and anti-psychotics
67
What does acetaminophen do
inhibits prostaglandin synthesis in the CNS
68
What is acetaminophen taken for
antipyretic and analgesic properties
69
What does acetaminophen have no effect on
platelets
70
Where is acetaminophen metabolized
the GI tract after first-pass metabolism and then secreted in urine
71
What is acetaminophen metabolized to
Gets hydrolyzed into NAPQI
72
What is NAPQI
potentially dangerous metabolite ( can cause quick liver failure)
73
At normal doses was happens with NAPQI
reacts with glutathione to form a nontoxic metabolite
74
How do corticosteroids work
bind to a glucocorticoid receptor and passes into the nucleus to regulate DNA translation = decreased expression of inflammatory genes
75
Which processes are inhibited by corticosteroids to manage inflammation
decrease COX-2 up regulation Inhibits inflammatory cytokines
76
What are some adverse side effects of corticosteroids
adrenal suppression increased blood glucose psychiatric disturbances
77
Which patients do you avoid using corticosteroids on
people at risk for osteoporosis Patients with renal impairment

Pharm exam module 2 (2 decks)

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