Nsaids

Front 1

NSAIDS act at the site of tissue ____.

Back 1

damage

Front 2

Local anesthetics act on primary _____ fibers.

Back 2

afferent

Front 3

Opioids act at the _____ level and higher in the CNS.

Back 3

Spinal

Front 4

Painful stimuli cause a CNS-based increased sensitization to previously non-noxious stimuli. Involves enhancement of primary afferent synapse in DORSAL horn of spinal cord using substance P and glutamate as co-transmitters. Activation of NDMA receptor appears to trigger increased synaptic efficacy.

Concept of ______.

Back 4

Spinal wind-up

Front 5

_____ _____ reduce pain post-surgically even when general anesthetics are used for avoiding spinal wind-up.

Back 5

Local anesthetics

Front 6

Tissue damage leads to release of...

Back 6

potassium
serotonin
bradykinin
histamine
prostaglandins
leukotrienes
substance P

Front 7

Pain, edema, and leukocyte infiltration compose the ___ inflammatory response

Back 7

acute

Front 8

Histamine comes from _____ and aids most in vascular permeability.

Back 8

mast cells

Front 9

Serotonin comes from platelets and aids most in ______.

Back 9

vascular permeability

Front 10

Bradykinin comes from ____ and aids most in vasodilation and pain.

Back 10

plasma

Front 11

Prostaglandins come from damaged cells and aid most in _____ and _____.

Back 11

vasodilation and chemotaxis

Front 12

Leukotrienes come from ______ _______ and aid most in vascular permeability and chemotaxis.

Back 12

damaged cells

Front 13

NSAIDS as analgesics...

Back 13

help with integumentary pain/associated with inflammation

poor for visceral/neurogenic pain

Front 14

NSAIDS as antipyretics....

Back 14

blocks IL-1 action during illness

no effect on hyperthermia from exercise/ambient conditions

Front 15

NSAIDS as anti-inflammatories...

Back 15

reduces erythema, edema & hyperalgesia

Front 16

NSAIDS act largely by inhibiting _____ synthesis.

Back 16

prostaglandins

Front 17

Prostaglandins do not directly activate nociceptors but instead sensitize the ____ gray of the spinal cord to nociceptive input.

(hint: dorsal or ventral)

Back 17

dorsal

Front 18

Prostaglandins applied to ____ do not evoke pain.

Back 18

skin

Front 19

NSAIDS may also block ____-sensing ion channels on nociceptors.

Back 19

acid

Front 20

The endogenous pyrogen is _____.

(hint: interleukin)

Back 20

IL-1

Front 21

FYI...

Back 21

Piroxicam>Indomethacin>Mefenamic acid>Phenylbutazone>ASA>Acetaminophen

(PIMP AA?)

Front 22

___is the enzyme inhibited by NSAIDS in pathway leading to prostaglandin synthesis.

Back 22

COX (cyclooxygenase)

Front 23

_____ acid in membrane lipids is the starting material.

Back 23

Arachidonic

Front 24

Arachidonate also leads to ____ synthesis.

Back 24

leukotriene

Front 25

COX-1 is _____. (gene is always on; not very regulated)

Back 25

constitutive

Front 26

COX-1 regulates production of effectors such as ___ (platelet adhesion) and ____ (GI tract, renal).

Back 26

thromboxane
prostacyclin

Front 27

adverse effects of NSAIDS are largely due to inhibiting of ____.

Back 27

COX-1

Front 28

COX-2 is _____.

Back 28

inducible

Front 29

COX-2 is normally made at ____ levels in most tissues.

Back 29

low

Front 30

_____ contributes to renal prostaglandins and endothelial cell prostacyclin.

Back 30

COX-2

Front 31

COX-2 is induced locally at sites of inflammation and is responsible for many problems associated with _____ inflammation.

(hint: acute or chronic?)

Back 31

chronic

Front 32

In general, anti-inflammatory doses of NSAIDS are _____ than antipyretic or analgesic doses.

Back 32

higher

Front 33

Activation of transcription factor ______ by some NSAIDS can antagonize NFKB and reduce inflammatory cytokine synthesis.

Back 33

PPAR-gamma

Front 34

Some NSAIDS modify _____ secretase activity and reduce A-beta amyloid production.

Back 34

gamma

Front 35

GI tract ____ is a major problem of NSAID usage. Due to reduced blood supply caused by vasoconstriction and increased endothelial adhesion.

Back 35

bleeding

Front 36

hypertension due to ___actions is a second common side effect.

Back 36

renal

Front 37

Excess bleeding and inhibition of smooth muscle contraction contraindicate use during _____.

Back 37

labor

Front 38

Hypersensitivity (allergic) reactions can be ____. Common in patients with adult onset asthma and nasal polyps.

Back 38

fatal

Front 39

Prostaglandins largely counteract the effects of _______ in regulating renal function.

Back 39

angiotensin II

Front 40

Inhibiting PG synthesis will have effects similar to ____ Ag II resulting in ______.

Back 40

Excess

hypertension

Front 41

_____ is the most commonly used pharmaceutical agent in the world.

Back 41

Aspirin

Front 42

Salicylic acid derived from _____ bark was used to treat fever in 1700s.

Back 42

willow

Front 43

Aspirin is the only NSAID which _____ inhibits COX. Makes it effective for anti-platelet therapy at low doses.

Back 43

IRREVERSIBLY

*acetylates COX active site and permanently kills it---"suicide inhibitor"

Front 44

Aspirin is the only NSAID that increases bleeding for _____ after use.

Back 44

days

Front 45

Development of ___ is a good indicator that the patient is approaching toxic doses of the drug.

Back 45

tinnitus

Front 46

For severe overdose treat the hyperthermia, dehydration, and provide respiratory support. ____ the urine. No sedatives. Pump stomach if ingestion is within 4 hours.

Back 46

Alkalinize

*brings more acidic ASA into kidney for excretion

Front 47

Prototypical chemopreventative drug

Back 47

aspirin

Front 48

Aspirin reduces risk of CV disease and appears to reduce ___ cancer risk.

Back 48

colon

Front 49

____ is an irreversible COX inhibitor, therefore requires synthesis of new enzyme to relieve inhibition.

Back 49

Aspirin

Front 50

____ is not a true NSAID. Has antipyretic and analgesic properties but lacks anti-inflammatory property.

Back 50

Acetaminophen

Front 51

Inflammation associated ____ limit effectiveness during inflammation

Back 51

peroxides

Front 52

Acetaminophen has delayed hepatotoxicity at high doses particular with combination of ____ consumption. Normal metabolism is non-toxic. Overflow into CYP450 oxidation produces toxic metabolite that is neutralized by glutathione.

Back 52

ethanol

Front 53

Hepatotoxicity treated with oral _____ and ____ (restores glutathione)

Back 53

charcoal, N-acetylcysteine

Front 54

Propionic acids (IBU), have ____ GI toxicity than aspirin.

Back 54

less

Front 55

Propionic acids may interfere with chemopreventive aspirin therapy by transiently occupying the ____ site.

Back 55

active

*take aspirin (ASA) before IBU to avoid problem

Front 56

Once daily propionic acid drug

Back 56

Oxaprozin

Front 57

IBU is a PPAR-gamma ____.

(hint: agonist or antagonist?)

Back 57

agonist

Front 58

Indomethacin is reportedly more efficacious against inflammation than any other NSAID, also ____ GI toxicity.

Back 58

more

Front 59

___ is useful in closing a patent ductus arteriosus in newborns.

Back 59

Indomethacin

Front 60

Indomethacin is a PPAR-gamma ____.

(hint: agonist or antagonist?)

Back 60

agonist

Front 61

Highly post operative analgesic

Back 61

ketorolac

Front 62

Reduced GI tract toxicity due to addition of prostaglandin to replace GI tract prostacyclin.

Back 62

Arthotec (diclofenanc+misoprostol)

Front 63

COX-2 selective drugs (2)
-little inhibition of COX-1

Back 63

celecoxib
valdecoxib

*active in assays of inflammation; no anti-platelet activity

Front 64

____ risk greatly reduced with COX-2 selective drugs.

Back 64

Ulcer

*may still exacerbate existing ulcers

Front 65

COX-1 and COX-2 are both involved in ulcer formation because neither COX-1 or COX-2 ___ drugs alone cause ulcers.

Back 65

selective

Front 66

Increased _____ due to failure to inhibit platelet thromboxane (COX-1) combined with inhibition of endothelial prostacyclin (COX-2)

Back 66

thrombosis

Front 67

____ has the lowest relative risk for a cardiovascular event.

Back 67

Naproxen