Pain/inflammation: Opioid Analgesics - Pharmacology

Front 1

Prototypical opioid?

Back 1

Morphine

Front 2

Uses other than analgesia for opioids?

Back 2

1) Cough suppressant
2) Component of anesthesia
3) Decreases GI motility
4) Adjunct to pulmonary edema
5) Drug abuse

Front 3

3 Major type of opiod receptors?

Back 3

1) Mu
2) Kappa
3) Delta

Front 4

Mu opioid

Back 4

1) Strongest analgesic
2) Most and most severe sideE
3) Resp. depression, constipation, increased risk

Front 5

Side effects of Mu opioids

Back 5

Resp. depression, Constipation, Highest risk of dependence

Front 6

Kappa opiod

Back 6

Analgesia, sedation, psychotropic
Less likely to have as severe SE as Mu

Front 7

Delta opiod

Back 7

Analgesic, SideE are least severe.
No risk for resp. depression, no psychotropic effects

Front 8

Describe a Mixed opioid

Back 8

Opioid is agonist to 1 or more receptor and antagonist to others.

i.e, Agonist = kappa; antagonist = Mu

Front 9

Opiod mechanism?

Back 9

Binds to opioid G-coupled protein receptor

Front 10

Opioids affect on presynpatic transmission of pain?

Back 10

G-proteins inhibit the release of Ca++ and cAMP release this causes less neurotransmitter release

Front 11

Opioid's effect on postsynaptic neuron?

Back 11

The G-proteins create an outflux of K+ which causes hyperpolarization making it more difficult of a synapse to occur.

Front 12

A way that opiods can alter descending pathways?

Back 12

Via disinhibition. The G-protein coupled receptors disinhibit descending pain control pathways.

Front 13

Mild-to-moderate agonist (i.e. codeine)

Back 13

Works for all receptors but has a lower affinity -> lower efficacy

Front 14

Which opioid receptors lead to possible CV problems?

Back 14

All

Front 15

Define tolerance

Back 15

Requires a greater dose for the same functional effect

Front 16

Opioid withdrawal symptoms?

Back 16

Flu-like symptoms, irritability, insomnia, tachycardia, uncontrollable yawning, muscle aches

Front 17

Methadone

Back 17

Strong opioid agonist used to taper for addicts

Front 18

Buprenex

Back 18

Buprenophine. A mixed agonist-antagonist - partial Mu agonist and Kappa antagonist.

Front 19

Prototypical NSAID?

Back 19

Aspirin

Front 20

Uses/Effects of NSAIDS?

Back 20

1) Decreased inflammation
2) Analgesic
3) Decreased fever (antipyretic)
4) Anticoagulant

Front 21

Mechanism of NSAIDS?

Back 21

Anti-inflammatory/analgesic d/t inhibition of eicosanoid synthesis

Front 22

3 Eicosanoids?

Back 22

Porstaglandins, Thrombaxanes, Leuokotrienes

Front 23

Prostaglandin

Back 23

Endogenous lipidlike compound that is pro-inflammatory

Front 24

Thrombaxane

Back 24

Vasoconstriction & Platelet aggregation

Front 25

Leukotrienes

Back 25

Pro-inflammatory (esp. in air way)

Front 26

Function (PGs &TXs)

Back 26

Cause inflammation, pain, fever, menstral problems, clots.

Front 27

Brief description of how PGs and TXs are formed?

Back 27

Arachadonic acids (phospholipase) -> COX (cycloxagenase) -> Variety of PGs and TXs

Front 28

Which pathway formed from arachadonic acid creates leukotrienes?

Back 28

The LOX pathway (lipoxygenase)

Front 29

Which two eicosanoids are inhibited with NSAIDS?

Back 29

PGs and TXs

Front 30

Which COX is normally produced in our bodies?

Back 30

COX-1

Front 31

Why do NSAIDS cause GI disturbances?

Back 31

b/c NSAIDS often inhibit COX-1s and COX-1s help supply the protective lining to our GI tract

Front 32

Two conditions that ASA may cause Renal and/or liver problems?

Back 32

1) Pre-existing disease
2) decreased body water

Front 33

signs/symptoms of ASA OD?

Back 33

HAs, decreased hearing, confusion, GI distress, possible metabolic acidosis & dehydration

Front 34

What can induce Reye syndrome?

Back 34

Adversion to ASA in children. The children can be intolerant (supersensitive) to the drug. Usually onsets after flu or chicken pox.

Front 35

Adverse effects of celebrex?

Back 35

1) MI
2) Stroke

Front 36

Why are COX-2 inhibitors potentially very harmful?

Back 36

Because the cause a shift that favors increased platelet aggregation which increases the pt's risk of clotting.

Front 37

Popular analgesic OTC that is not an NSAIDS?

Back 37

Acetaminophen (Tylenol/Excedrin)

Front 38

Anti-inflammatory effects of acetaminophen?

Back 38

There are none

Front 39

Risk of high doses of acetaminophen?

Back 39

Liver toxicity

Front 40

Mechanism of acetaminophen?

Back 40

Inhibits COX, probably inhibits PGs may preferentially inhibit CNS PGs (COX-3?)

Front 41

What is odd about the pharmacokinetics of ASA?

Back 41

1) Most is bound to plasma proteins
2) Unbound drug is hydrolyzed in the blood and not the liver

Front 42

Which chemical in the breakdown of acetaminophen is responsible for liver toxicity?

Back 42

NAPQI (must be conjugated for detoxification and excretion).