Ua Pharmacology Test #2

Front 1

How do opioids work?

Back 1

relief of moderate-severe pain by inhibiting porduction of substance P and prostaglandins.
they induce the endogenous analgesia system.

Front 2

administering opioids:

Back 2

IM, PO, or Sub-Q
*Are sig. 1st. pass metabolism drugs...oral needs much higher doses*

Front 3

What two opioids form active mtabolites?

Back 3

morphine and meperidine(Demerol)
--drug accumulates in liver/kidney disease--

Front 4

What are the major endogenous analgesia receptors?

Back 4

MU (most oppioid effects)
KAPPA (analgesia, sedation, <GI motility)
DELTA (unknown if oppioids bind to these)

Front 5

Acute pain

Back 5

sharp, lancing or cutting
A-delta fibers using glutamate.
usually responds to treatment within a few days.

Front 6

Chronic pain

Back 6

lasts >3 mos
"slow pain"--begins after 1 sec., increases over time.
type C fibers using Substance P

Front 7

Cancer pain

Back 7

can be acute and chronic, constant or intermittent.
usually chronic = tumor spread;acute = due to procedures

Front 8

Somatic pain

Back 8

stimulation of nociceptors in structural tissues.
"sharp, burnig, aching, gnawing, throbbing, or cramping"
can be acute (sprains) or chronic (arthritis)

Front 9

Visceral pain

Back 9

simultaneous stimulation of many nociceptors in abdo/thoracic tissues.
"deep, dull, aching, cramping"
not well-localized: type C fibers

Front 10

Neuropathic pain

Back 10

injury to nervous structures
common cause of chronic pain: "severe, shooting, burning, stabbing"
due to cancer, herpes zoster, DM.
Diff. to treat

Front 11

Contraindications to opioids:

Back 11

Resp. depression, chronic lung disease, liver/kidney disease, BPH, >ICP, or hypersensitivity to opioids/related drugs

Front 12

What are three methods of neurotransmitter removal?

Back 12

reuptake, diffusion, enzymatic destruction

Front 13

Morphine metabolism:

Back 13

Sig. 1st pass, excreted as an active metabolite.
30% bound to plasma proteins.

Front 14

Opioid Analgesic dosing

Back 14

IV, epidural, and intrathecal = acute pain.
Oral = most common in chronic pain. (oral is preferred when effective)

Front 15

Opioid Analgesic frequency

Back 15

Acute pain= PRN
chronic pain= around the clock
no prolonged dosage except for malignancy..stop orders usually = 48-72 hrs.

Front 16

Treatment of opiate withdrawal:

Back 16

1) give tapering doses of opiate.
2) give a long-acting opiate (Methadone) and taper off.
3) give Clonidine (anit-HTN)--=<norepinephrine release, and less sx.

Front 17

What are opioid agonists/antagonists?

Back 17

Have potent analgesic effects w/out high abuse potential due to antagonistic activity.
*may= withdrawal in dependent ppl.*

Front 18

use of opioid antagonists?

Back 18

relieve CNS and Resp. depression from opioids ONLY--not other drugs.

Front 19

Why is morphine often 1st drug used for pain?

Back 19

it is a non-cceiling drug...no up. limit with tolerance.

Front 20

Important teaching points on opioids:

Back 20

*opioids are often combo-ed with acetaminophen drugs--watch for acet. OD.
*Stay in bed 30 min after op. injection.
Take w/6-8 oz H2O, avoid alcohol/depressant drugs, do not crush SR pills.

Front 21

Opioids in clients w/renal disease:

Back 21

Give in min. doses for shortest amt/ time.
Morphine = active metab. that can accumulate.
Meperidine= becomes CNS stimulant Normeperidine--seizures, psychosis--naloxone won't help.

Front 22

Opioid therapeutic effects:

Back 22

pain releif, sleeping, >ADLs, <episodes of non-productive cough, <BP, HR, RR, dyspnea; <diarrhea

Front 23

Opioid adverse effects:

Back 23

Resp. depression; Hypotension; excessive sedation; N/V, constipation

Front 24

Drugs that increase opioid effects:

Back 24

CNS depressants
Anticholinergics (>constipation)
Anti-HTNs; MAO inhibs. (<detox, >CNS depress.)
Protease inhibs, Cimetidine

Front 25

Drugs that decrease opioid effects:

Back 25

opioid antagonists
Butorphanol, nalbuphine (analgesics that weakly interact w/opioids)

Front 26

Functions of COX-1 enzymes:

Back 26

Makes prostaglandins that up GI mucus, lower gastric acid, regulate renal blood flow and function, control vascular tone, and platelet function.

Front 27

Where is COX-1 found?

Back 27

made continuously; found in all tissue types, esp. platelets, endothelial cells, GI, kidneys.

Front 28

Where is COX-2 found?

Back 28

Brain, bone, kidneys, GI, female repro. sys.
Thought to be made only in small amounts or only in response to inflammation/pain.

Front 29

Contra's to aspirin:

Back 29

GI disorders, renal disease, children,pregnant women, HX of hypersensitivity, chronic ETOH abuse.
Lower doses for low serum albumin.

Front 30

Contr's to celecoxib (Celebrex):

Back 30

hx/ peptic ulcers (celecoxib = selective COX-2 inhibitor)
allergies to sulfonamides.

Front 31

metabolism of acetaminophen:

Back 31

4% becomes a toxic metabolite. This must be conjugated w/glutathione and excreted in urine.
Alcohol abuse causes enzyme induction--drug is metabolized quicker than glutathione is made;=toxicity)

Front 32

What are the two categories of migraine meds?

Back 32

Those that prevent migraines and those that treat the pain.

Front 33

What common drug increases most NSAIDs actions?

Back 33

caffeine

Front 34

How do the migraine meds triptans work?

Back 34

Selective Serotonin 5-HT1 receptor agonists--increase serotonin in brain, causing vasoconstriction.

Front 35

What are maximum single and daily doses of APAP?

Back 35

single dose= 1000 mg
daily max= 4000mg
alcoholic daily max= 2000mg

Front 36

AEs of analgesic/anti-pyretic/anti-inflam./antigout meds:

Back 36

GI probs, bleeding probs, bone marrow depression(colchicine), CNS effects, rashes, dermatitis, hypersens. reactions, tinnitus(classic sgn of aspirin OD),blurred vision, nephrotoxicity, CV effects, hepatotoxicity.

Front 37

Drugs that increase aspirin/NSAIDs:

Back 37

acidifying agents (>excretion); ETOH; anticoagulants; opioids; corticosteroids (>GI upset)

Front 38

Drugs that decrease effects of aspirin/NSAIDs:

Back 38

alkanizing agents (<excretion); Misoprostol (Cytotec)--a prostaglandin used to prevent gastric ulcers from these meds

Front 39

Drugs that decrease the effect of antigout meds:

Back 39

alkanizing agents (good--prevent stone formation as acid is excreted)
colchine, diuretics, salicylates

Front 40

What drugs should never be taken w/triptans?

Back 40

MAOIs-->serum triptan levels
Ergots--severe HTN/stroke can occur