Advanced Pharmacology

Front 1

Where do Pain medications work related to the Gate Control Theory?

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Front 2

Which opiods are Natural, Semi-synthetic, and Full Synthetic?

Back 2

Natural- Morphine & Codeine

Semi-synthetic-Oxycodone & Hydrocodone

Synthetic-Meperidine & Fentanyl

Front 3

What type of drug is codeine, what metabolizes it, and what is its metabolite?

Back 3

A pro-drug (needs to be metabolized to be active)

Metabolized by CP450-2D6

Morphine

Front 4

What are other opioid pro-drugs that are metabolized by CP450-2D6 and what are their active metabolites?

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Front 5

How does Lipophilicity affect the spread of spinal epidural opioid medications?

Back 5

Greater spread of medication (risk of high block) with lower lipophilicity.

Front 6

Which part of the pain pathway do local, regional, and systemic opioids work on?

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Front 7

How do enkephalins modulate pain?

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Front 8

How do opioids reduce pain?

Back 8

Mimic endorphins by binding to opioid receptors activating pain modulation system thought to block the release of Substance P.

Work Centrally and do not have a ceiling effect.

There is an antagonist.

Front 9

What type of receptor is an Opioid receptor and what is the cellular response?

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Front 10

What are the three type of receptors and what effect do they have on the body?

Back 10

Mu: Responsible for supraspinalanalgesia, euphoria, respiratorydepression, bradycardia and physicaldependence.

Delta: Modulate mu receptor activity.

Kappa: Analgesia with little or norespiratory depression.

Front 11

What is the affinity of medications and the receptors they affect?

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Front 12

What are examples of partial agonists & Agonist/antagonists, what type of pain are they effective for, and advantages/disadvantages?

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Front 13

What are examples of a weak agonists, what type of pain are they effective for, and advantages/disadvantages?

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Front 14

Describe Tramadol.

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Ultram® 50mg & Ultracet® 37.5/325mg Actions: Binds weekly to mu opioid receptors and inhibits re-uptake of serotonin and norepinephrine.

Disadvantages: Expensive and appears to be no more effective than APAP with codeine. Seizures have been reported.

Front 15

Codeine/Hydrocodone/Oxycodone

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Profile:Mild to moderate to severe pain. Advantages: Good first line agent if nonsteroidalineffective and good agents forbreakthrough pain.

Disadvantages: Opioid side effects, CodeinePO is very nauseating, Watchacetaminophen.

Front 16

Morphine Sulfate

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Actions: Onset 5-10min, peak 30min, andduration 3-4 hr. when given IV.

Advantages: Good analgesic, positive effects on preload for post-MI

Disadvantages: Long onset, opioid side effectsand morphine-6 glucronide metaboliteaccumulation, histamine release

Front 17

Methadone

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Use

Advantages: Good analgesic, long half life beneficial in chronic pain, d-isomer has NMDA antagonist effects lowers tolerance

Disadvantages: Accumulates and opioid side effects.

Causes 1/3 of Narcotic Overdose-Difficult Pharmacodynamics

Front 18

Meperdine

Back 18

Actions

Advantages: May be given to morphine allergic patients, may have less effect on biliary spasm, and very efficacious for chills.

Disadvantages: Long onset, Nor-meperdine metabolite may accumulate, and opioid side effects.

MAOIs can cause Seratonin Syndrome

Front 19

Fentanyl

Back 19

Actions

Advantages: Rapid onset, may be used for morphine allergies, and very effective analgesic

Disadvantages: Opioid side effects, and chest wall rigidity following rapid IV administration.

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Front 21

Narcan (Naloxone)

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Pharmacology: Competitiveinhibitor of opioids at the mu, kappa, and deltareceptors.

Actions: Onset 1-2 min, & duration 30-90 min

Dose: Naloxone - 0.05-0.1 mg IV repeated every2-3 min. titrate dose up depending on clinicalresponse.

Cautions: Maycause severe hypertension, ventriculardysrythmias and acute, sometimes fatalpulmonary edema.

Front 22

How do you dose a medication if there is a cross sensitivity?

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Incomplete Cross tolerance- Need to reduce dose (~1/3) & titrate up

Front 23

How do NSAIDs work?

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Inhibit the enzyme cyclooxygenase,resulting in a decreased synthesis & release of prostaglandin

Work primarily peripherallyrather than centrally

Have a “ceiling effect”.

Front 24

What is sensitization of pain receptors?

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Front 26

NSAIDs

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Examples: Ibuprofen, Naproxen, ASA,indomethacin

Profile: Treatment of mild pain

Advantages: Help to reduce inflammation,low CNS side effects, no physicaldependence

Disadvantages: Hematological, renal andhepatic adverse effects.

Front 27

What are possible renal effects of NSAIDs?

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Long-term administration of NSAIDs has resulted inrenal papillary necrosis and other renal injury.

Renal toxicity has been seen in patients that rely onrenal prostaglandins for maintenance of renalperfusion.

Both Cox 2 selective inhibitors and nonselectiveinhibitors may cause this effect.

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Front 29

What are risk factors that increase the risk of renal effects of NSAIDs?

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Impaired renal function

Heart failure

Liver dysfunction

Taking diuretics and ACE inhibitors

Elderly

Front 30

How to calculate Creatinine Clearance.

Back 30

CrCl=(140-age)*Wt/(Cr*72)

For women multiply by 85%

Front 31

What is the difference between Cox-1 & Cox-2?

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Cox-1 is found throughout the body, it is found in the GI tract, where it producesprostaglandins that are considered cytoprotective, is also found in the kidneys and inplatelets.

Cox-2 derived prostaglandins were considereddeleterious because they are found mainly at thesites of inflammation.

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Front 33

What is the Cardiovascular ToxicityHypothesis for why Cox-2 inhibitors cause more clotting issues?

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Front 34

What medications have the risk of life-threatening skin reactions potentially these include:Steven-Johnson SyndromeToxic epidermal necrolysis?

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NSAIDS, Abx (sulfonamides), Allopurinol, Anticonvulsants

Front 35

Acetaminophen

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Mechanism: Similar to nonsteroidal, however: Effect more via central mechanism. No clinical effect on inflammation. Essentially no clinical effect on platelets.

Disadvantages: Potentially fatal hepatic necrosis.

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Front 37

Tylenol Metabolism

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CYP metabolism to a reactive metabolite which depletesglutathione and covalently binds to proteins

Mitochondrial permeability transition occurring with additionaloxidative stress, loss of mitochondrial membrane potential,and loss of the ability of the mitochondria to synthesize ATP

Front 38

When is IV Tylenol most appropriate?

Back 38

For first dose to get it in faster, subsequent dose should be give by a different route to save money and is as effective.

Front 39

What is the summary of NSAIDs

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Front 40

What is the difference between an ester and an amide local anesthetic?

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Front 41

What are the effects of Cocaine?

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Blocks reuptake of Norepinepherine.

Front 42

What are examples of Ester Local Anesthetics?

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Cocaine

Procaine

Tetracaine

Benzocaine

Front 43

What are examples of Amide Local Anesthetics?

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Lidocaine

Mepivacaine

Bupivacaine

Etidocaine

Prilocaine

Ropivacaine

Front 44

How do Local Anesthetics block pain transmission?

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Front 45

Where do Local Anesthetics work on the cell membrane?

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Has to be an activated channel to get the action of the local, inactivated gate blocks local from reaching receptor

Front 46

What does frequency dependence mean related to Locals?

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Frequency dependant block-nerve that fires faster is easier to block than one that fires slowly

Front 47

What are Important Factors affecting Anesthetic Action in general?

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Type of fiber

Small nerve fibers are more susceptible than large

Degree of myelination

Fiber length

Fiber placement

Frequency dependency

Front 48

What are the different Nerve fibers and susceptibility to Local Anesthetics?

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Front 49

For mylenated nerves how many nodes need to be blocked?

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Need 2-3 nodes to block

Front 50

What is the order that sensation is blocked?

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1. pain

2. cold

3. warmth

4. touch

5. deep pressure

6. motor

Front 51

Procaine (Novacaine)

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Type Ester (prototype)

Profile Slow onset, Short duration, Low toxicity

Use Local infiltration, Spinal

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Chloroprocaine

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Type Ester

Profile Very Fast onset, Short duration, Very Low toxicity

Use Local infiltration, Nerve Blocks, Epidural

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Tetracaine

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Type Ester

Profile Slow onset, Long duration, Moderate toxicity

Use Spinal

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Lidocaine

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Type Amide (prototype)

Profile Fast onset, Moderate duration, Moderate toxicity

Use Most frequently used local anesthetic for all types of regional anesthesia

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Bupivacaine

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Type Amide

Profile Slow onset, V long duration, High toxicity

Use Most local and regional anesthesia where long duration is desired. Bupivacaine Liposome is a different formulation and is restricted use.

Front 56

Etidocaine

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Type Amide

Profile Fast onset, Very long duration, Moderate toxicity

Use Nerve blocks, Epidural

Front 57

Ropivacaine

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Type Amide

Profile Slow onset, Very long duration, Moderate toxicity

Use Similar to bupivacaine, less cardiac toxicity

Front 58

What are factors that affect distribution of Local Anesthetics?

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Front 59

How many mg of lidocaine per CC is 1%?

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1% LIDOCAINE SOLUTION CONTAINS 10 MG OF LIDOCAINE PER ML.

Front 60

How many mcg of Epinephrine per CC in 1:100,000 1:200,000 or 1:400,000?

Back 60

A 1:100,000 solution contains 10 micrograms per ml.

A 1:200,000 solution contains 5 micrograms per ml.

A 1:400,000 solution contains 2.5 micrograms per ml.

Front 61

What are precautions for using Epinephrine with Local Anesthetics?

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Front 62

Where are ester and amide LA metabolized?

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Esters in the plasma

Amides in the liver

Front 63

What are signs of Lidocaine Toxicity?

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Front 64

Which class of medication is likely to have an true allergic reaction?

Back 64