NSAIDs Flashcards by Kim Grace

a physiological response to tissue injury and infection

inflammation

How well did you know this?

Not at all

Perfectly

other term for inflammation

inflammatory response

How well did you know this?

Not at all

Perfectly

T or F: inflammation is not a synonym for infection

True

How well did you know this?

Not at all

Perfectly

Mediate response to inflammation

vascular diameter, vascular permeability

How well did you know this?

Not at all

Perfectly

increases blood flow to the area of injury, resulting in the heating and reddening of the tissue

vascular diameter (vasodilation)

How well did you know this?

Not at all

Perfectly

allows leakage of fluid from the blood vessels into the damaged tissue, resulting in swelling (edema)

vascular permeability

How well did you know this?

Not at all

Perfectly

when will NSAIDs be used

when inflammation is CHRONIC

How well did you know this?

Not at all

Perfectly

During chronic inflammation - leukocytes arrive at the site of injury to _________ the invading pathogens and release __________

phagocytize; soluble mediators

How well did you know this?

Not at all

Perfectly

soluble mediators released during chronic inflamm

cytokines, prostaglandins, leukotrienes

How well did you know this?

Not at all

Perfectly

response to tissue injury

Acute inflamm

How well did you know this?

Not at all

Perfectly

leading to progressive tissue destruction, as seen in chronic infections, autoimmunity, and certain cancers

Chronic inflamm

How well did you know this?

Not at all

Perfectly

T or F: chronic inflamm can lead to autoimmunity and cancers

True

How well did you know this?

Not at all

Perfectly

Type of inflamm wherein clotting and kinin systems are activated

Acute

How well did you know this?

Not at all

Perfectly

fibrin strands to form clots, limiting the spread of infection into the blood

Clotting systems

How well did you know this?

Not at all

Perfectly

Clotting systems - ________ strands to form clots, limiting the spread of infection into the blood

fibrin

How well did you know this?

Not at all

Perfectly

Kinin system results in the production of ____________

bradykinin

How well did you know this?

Not at all

Perfectly

a peptide that induces vasodilation and enhanced vascular permeability

bradykinin

How well did you know this?

Not at all

Perfectly

dominate the landscape during acute inflammation

Non-protein–based soluble factors

How well did you know this?

Not at all

Perfectly

represent a diverse family of lipid mediators with fundamental roles in physiology and disease

Eicosanoids

How well did you know this?

Not at all

Perfectly

results from continuous exposure to the
offending element.

Chronic inflammation

How well did you know this?

Not at all

Perfectly

Due to _____________, autoimmune diseases in which self-antigens continuously activate T cells, and cancers.

pathogen persistence

How well did you know this?

Not at all

Perfectly

Hallmark of chronic inflammation

the accumulation and activation of macrophages and lymphocytes and fibroblasts

How well did you know this?

Not at all

Perfectly

primary factors of chronic inflammation

Cytokines, chemokines, growth factors, and secreted/released enzymes, and ROS

How well did you know this?

Not at all

Perfectly

The treatment of patients with inflammation involves two primary goals:

the relief of symptoms (NSAIDS) and the maintenance of function, slowing or arrest of the tissue-damaging processes is desirable, and
disease-modifying drugs (DMARDs) are necessary.

How well did you know this?

Not at all

Perfectly

the most abundant of the eicosanoid precursors

Arachidonic acid (AA) (5,8,11,14-eicosatetraenoic acid)

an essential fatty acid, is converted to linolenic acid, followed by conversion to AA. (omega-6-fatty acid)

Linoleic acid

Major Effects of PG Synthesis Inhibition

1. Analgesia 2. Antipyresis 3. Anti-inflammatory 4. Anti-thrombotic 5. Closure of Ductus Arteriosus

generates prostanoids for “housekeeping” functions such as gastric epithelial cytoprotection

COX-1

is the major source of prostanoids in inflammation and cancer.

COX-2

All NSAIDs inhibit

PG synthesis

Prostaglandin, prostacyclin (PG1) and thromboxane (TXA2) are produced from _____________

Arachidonic acid

The enzyme responsible for NSAIDs is ______________ also known as cyclooxygenase or COX

prostaglandin synthase

COX in 2 forms:

constitutive COX-1 and inducible COX 2

NSAIDs ADR for CNS

Headaches, tinnitus, dizziness, and rarely aseptic meningitis.

NSAIDs ADR for Cardiovascular

Fluid retention, hypertension, edema, and rarely myocardial infarction and congestive heart failure (CHF).

Gastrointestinal ADR of NSAIDs

Abdominal pain, dyspepsia, nausea, vomiting, and rarely ulcers or bleeding

Hematologic ADR of NSAIDs

Rare thrombocytopenia, neutropenia, or even aplastic anemia.

Hepatic ADR of NSAIDs

Abnormal liver function test results and rare liver failure.

Pulmonary ADR of NSAIDs

Asthma

Skin ADR of NSAIDs

Rashes, all types, pruritus

Renal ADR of NSAIDs

Renal insufficiency, renal failure, hyperkalemia, and proteinuria.

Aspirin irreversibly inhibits platelet _________

COX

aspirin’s antiplatelet effect lasts ____________ (the life of the platelet)

8–10 days

T or F: Aspirin is now rarely used as an anti-inflammatory medication

True

decreases the incidence of transient ischemic attacks, unstable angina, coronary artery thrombosis with myocardial infarction, and thrombosis after coronary bypass grafting

Aspirin

Aspirin ADR

gastric upset (intolerance) and gastric and duodenal ulcers. Hepatotoxicity, asthma, rashes, GI bleeding, and renal toxicity rarely if ever occur at antithrombotic doses

Aspirin is contraindicated inpatients with ___________.

hemophilia

Long-term low-dose aspirin usage in patients with type 2 diabetes increases risk for ___________

GI bleeding

NONACETYLATED SALICYLATES

Magnesium choline salicylate, sodium salicylate, and salicyl salicylate

All nonacetylated salicylates are effective anti-inflammatory drugs, and they _______ (inhibit/do not inhibit) platelet aggregation

do not inhibit

non acetylated salicylates is preferable when COX inhibition is undesirable such as in patients with ________-

asthma, bleeding tendencies, renal dysfunction (under close supervision)

were developed in an attempt to inhibit prostaglandin synthesis by the COX-2 isozyme induced at sites of inflammation without affecting the action of the constitutively active “housekeeping” COX-1 isozyme found in the GI tract, kidneys, and platelets

Cox 2 selective inhibitors

COX-2 selective inhibitors, or _______, were developed in an attempt to inhibit ____________ by the COX-2 isozyme induced at sites of inflammation without affecting the action of the constitutively active “housekeeping” COX-1 isozyme found in the GI tract, kidneys, and platelets

coxibs; prostaglandin synthesis

COX-2 selective inhibitors, or coxibs, were developed in an attempt to inhibit prostaglandin synthesis by the COX-2 isozyme induced at sites of inflammation __________ affecting the action of the constitutively active _____________ found in the ______________

without: “housekeeping” COX-1 isozyme; GI tract, kidneys, and platelets

COX-2 inhibitors at usual doses have no impact on ___________ which is mediated by ____________ produced by the ________

platelet aggregation; thromboxane; COX-1 isozyme

have no impact on platelet aggregation, which is mediated by thromboxane produced by the COX-1 isozyme.

COX-2 inhibitors at usual doses

do not offer the cardioprotective effects of traditional nonselective NSAIDs

COX-2 inhibitors

a benzenesulfonamide

Celecoxib

is a selective COX-2 inhibitor, about 10–20 times more selective for COX-2 than COX-1

Celecoxib

is indicated for the treatment of OA, RA, JRA, and AS

Celecoxib

Usual dose of Celecoxib

100–200 mg bid

Celecoxib at _________ has also shown efficacy as an adjunctive therapy for improving __________, most likely due to suspected __________ in the disorder

400 mg/d; schizophrenic symptoms; neuroinflammation

racemic acetic acid derivative whose mechanism of action has been described as relatively COX-2 selective

Etodolac

Etodolac is indicated for the treatment of __________

OA, RA, and JRA

recommended dosage of etodolac

300 mg bid–tid or 500 mg bid initially, then 600 mg/d

an enolcarboxamide related to piroxicam and is a relatively selective COX-2 inhibitor, particularly at 7.5 mg/d

Meloxicam

T/F: even at subtherapeutic doses, meloxicam's blockade of thromboxane A2 does not reach levels that result in decreased in vivo platelet function

True

Indications and Dosage of meloxicam

OA, RA, and JRA patients. Dosage is 7.5–15 mg/d

phenylacetic acid derivative

Diclofenac

difluorophenyl derivative of salicylic acid

Diflunisal

propionic acid derivative

Flurbiprofen

simple phenylpropionic acid derivative

Ibuprofen

a naphthyl-propionic acid derivative

Naproxen

another propionic acid derivative NSAID

Oxaprozin

pyrrole alkanoic acid derivative

Tolmetin

an indole derivative) and a potent nonselective COX inhibitor that may also inhibit phospholipase A and C, reduce neutrophil migration, and decrease T-cell and B-cell proliferation

Indomethacin

Indomethacin may also inhibit

phospholipase A and C, reduce neutrophil migration,

Indomethacin may also decrease

T-cell and B-cell proliferation

T/F: Because of perceived toxicity, indomethacin is used less commonly than other NSAIDs

True

a propionic acid derivative that inhibits both COX (nonselectively) and lipoxygenase.

Ketoprofen

is the only nonacid NSAID in current use and resembles naproxen in structure

Nabumetone

an enolcarboxamide derivative is a nonselective COX inhibitor

Piroxicam

Piroxicam at high concentrations also inhibits _________, decreases _______, and inhibits __________.

polymorphonuclear leukocyte migration; oxygen radical production; lymphocyte function

is a sulfoxide nonselective prodrug whose active metabolite is a nonselective COX inhibitor

Sulindac

Asprin ____________ (reversibly/irreversibly) acetylates and blocks platelet COX

irreversibly

T/F: non-COX-selective NSAIDs are reversible inhibitors

True

The selective COX-2 inhibitors (do not affect/affects) platelet function at their usual doses

do not affect

T/F: The in vivo efficacy of COX-2-selective drugs equals that of the older NSAIDs, while GI safety may not be improved

False; may be improved

selective COX-2 inhibitors increase the incidence of ____________, ____________ and _________

edema, hypertension, and possibly myocardial infarction

T/F: all newer NSAIDs are analgesic, anti-inflammatory, and antipyretic, and all including the COX-2–selective agents and the nonacetylated salicylates inhibit platelet aggregation.

false; except the COX-2–selective agents and the nonacetylated salicylates

T/f: NSAIDs are all gastric irritants and can be associated with GI ulcers and bleeding as well

True

T/F: the newer agents tend to cause less GI irritation than aspirin

True

seems not to be effective for gout, and is less effective than other NSAIDs (eg,indomethacin) for AS Ankylosing spondylitis

tolmetin

T/F: The GI and renal side effects of ketorolac limit its use

True

best for renal insufficiency

nonacetylated salicylates

__________ and _______are associated with more liver function test abnormalities than other NSAIDs

Diclofenac and sulindac

___________ is probably safest for patients at high risk for GI bleeding but may have a higher risk of cardiovascular toxicity

celecoxib

NSAIDs Flashcards

(97 cards)