Pharmacology Application in Athletic Training

History of Drugs and Pharmacy

Around 2100 BC: Recorded references to drug therapy~250 vegetables, 120 mineral drugs

1500 BC Egyptians: Ebers Papyrus22yrd document: 700+ drugs listed

600-330 BC Greeks: developed pharmacopeias Defined preparation, action of drug,etc

Middle Ages: Pharmacy recognized as a separate profession from medicine

Early 20th Century - History of Drugs

Virtually no laws to govern the sale of drugs

Coca Cola: A tonic that contained cocaineAid respiration and digestion

Paregoric acid:Contained opium Given to teething babies

U.S. History of Pharmacology 1646: 1st American Pharmacy

1821: Philadelphia College of Pharmacy

1852: American Pharmaceutical Association Begins

1870: American Pharmaceutical Assoc developed regulations

U.S. Legal Foundations 1906: Food and Drug Act 1938: FDA and Food, Drug, and Cosmetic Act 1952: Durham-Humphrey Amendment 1962: Kefauver-Harris Amendment 1970: Poison Prevention Packaging Act 1970: Comprehensive Drug Abuse Prevention

and Control Act 1984: Anti-Tampering Act 1992: “Fast-track” drug approval process

Pure Food and Drug Act: 1906

Prohibits contamination & misbranding Ineffective:

1937: Sulfanilamide Elixir (oral anti-biotic) – liquid version contained diethlyene glycol (antifreeze)

>100 people died

FDA & Food, Drug, and Cosmetic Act: 1938 FDA = Food and Drug Administration

Created in 1938 to enforce the Food, Drug and Cosmetic Act of 1938

○ All drugs must be safe before marketed○ Labels w/ warnings, strength/purity, & directions

Ensure the safety of drug production, consumption, and distribution

Drug companies must get approval by the FDA prior to marketing their drug products

FDA regulates adverse drug reactions

Durham-Humphrey Amendment: 1952

Distinction between prescription and OTC drugs

Warning Label for Prescription Drugs:“Caution: Federal law prohibits

dispensing without a prescription”

Thalidomide Popular sleeping pill

taken by pregnant women in Europe (1950’s)

FDA refused to approve sale in US

Thousands of children were born with seal-like deformity

Took 10 yrs to find connection

www.thalidomide.ca

Kefauver-Harris Amendment: 1962

In response to the

Thalidomide tragedy Requires manufactures to test

products for safety and efficacy Also required testing of drugs

manufactured between 1938-1962 As a result, many were withdrawn from

market

Poison Prevention Packaging Act: 1970 Prevent the accidental poisoning of

children Prescription drugs must be dispensed in

child-resistant containers 80% of children under 5 must not be able

to open the container 90% of the adults must be able to open the

container

Controlled Substance Act - 1970

Regulates distribution of drugs w/ potential for addiction/abuse

Schedule: I – V Schedule I – most

abuse potential Schedule V – least

abuse potential

Schedule I: Heroin, LSD Schedule II: Morphine,

Dexedrine, Adderall, OxyContin, Demerol, Percocet, Ritalin

Schedule III: Tylenol w/ Codeine, Vicodin

Schedule IV: Darvocet, Valium, Ativan, Xanax, Ambien

Schedule V: Robitussin A-C

Anti-Tampering Act:1984 A number of people died in the 80’s after

taking Tylenol laced with cyanide

All OTC products must be sold with tamper-resistant packaging Plastic seal over cap or aluminum seal over

opening

FDA Drug Approval Process

~1/5000 drugs tested get to the market Around 12 yrs, costs millions of dollars

Other countries may last 1yr and have lower standards

1992: FDA created “fast track” to decrease approval time for important therapeutic drugs Allows marketing before the last phase of clinical

trials (safety and efficacy portion) Follow-up studies must be performed Unknown risks are balanced by urgent need for

drug

FDA Approval Process

1. Lab/Animal Studies (up to 3 yrs)

2. Company files for investigational new drug

3. Clinical Study:1. Phase I: Human volunteers (1 yr)

2. Phase II: Human Patients (2 yrs)

3. Phase III: Human Patients (3 yrs)

4. FDA Review (2-3 yrs)

5. FDA Approval of New Drug (~12 yrs after initiation)

Name of Drugs

Chemical name

Generic name

Brand name

N-acetyl-para-aminophenol

Acetaminophen

Tylenol®

Brand vs Generic

Brand-name drugs usually have a patent, granted by FDA, for 17 yearsAfter 17 yrs, other companies can make

generic equivalent Generic drugs must have the same active

ingredient, strength, & dosage as the brand name drug

Generic drugs must be tested for safety & efficacy & produce the same therapeutic effects as the brand name drug

PHARMACOKINETICS AND

PHARMACODYNAMICS

Pharmacodynamics: how drugs affect the body

Pharmacokinetics: what the body does to the drugs

What is a Drug?

A chemical that alters physiological functions by replacing, interrupting, or potentiating (enhancing) existing cellular functions

Exp: Caffeine can produce a stimulating effect on the CNS by attaching to CNS receptors and overriding fatigue messages

Drug Properties

Drugs cannot give cells properties they do not already possess

Drug-receptor interaction: drugs must bind to a receptor on a cell in order to produce an effect

“Lock and key” analogy:Occasionally several drugs

or “keys” can unlock a single

receptor

key

receptor

Definitions Agonist – a drug that binds to a receptor and

produces an effect Antagonist – a drug that binds to a receptor but does

not produce an effect (blocker) Threshold – lowest dose capable of producing an

effect Max effect – greatest response produced regardless

of the dose (efficacy will not increase) Efficacy - the capacity to illicit a response Potency – amount of drug needed to produce an effect

Definitions Affinity – the force that makes two agents bind

together Latency – “onset of action” – time required for a

drug to produce an observable effect Therapeutic Index – range in which desired

effects are produced (narrow therapeutic index drugs have more potential to cause toxicities)

Duration of Action – period of a single dose drug response

Half-life (T ½)

The time required to reduce the amount of drug concentration in the body by 50%

Helps to determine how frequently a drug should be administered

Motrin ~ 4 hours Claritin ~ 15 hours Vicodin ~ 3-4 hrs

Pharmacokinetics

What does the body do to the drug?

Absorption

Distribution

Metabolism

Excretion

Absorption

Most drugs must be absorbed into the blood stream in order to get to the site of action

Methods of administration: SublingualOralIntravenousTransdermal (topical)Inhalation

Distribution Mouth

GI Tract

Bloodstream

Liver Bloodstream (to entire body)

Target site

Intravenous Administration

Metabolism Process of breaking down drugs to be eliminated

from the body First pass metabolism: Oral drugs get absorbed

in the gut, then travel to liver – part of the drug gets broken down

Primary organ of metabolism = Liver Produces enzymes that break down drugs

Not all active drugs will reach their target siteExp: Lidocaine, if given orally, will be completely

broken down by the liver

Excretion

Primary organ of excretion = Kidney

Water-soluble drugs easily excretedToo much vitamin C…flushed down the toilet

Lipid-soluble drugs are reabsorbedVitamins D,E,A,K: Fat-soluble, stored in

liver, toxic in large quantities

Factors that affect drug response

Infants/ChildrenEnzymes do not fully develop until12 y/o

Older Adults Elderly have decreased kidney function

Timing of FoodBefore, during, after meal

Person’s weight (fat distribution)

ANTI-INFLAMMATORY

MEDICATIONS

Anti-Inflammatory Meds

Billion Dollar Industry Approximately 1% of US population uses

NSAID’s daily 14,000 cases each year of GI toxicity based

on 70 million NSAID prescriptions filled (1991) HS FB Study:

75% used NSAID’s in previous 3 mo

Inflammatory Response Inflammation signals the

start of the healing process 3 stages:

Acute inflammation phaseRepair-regeneration phaseMaturation phase

Within 48 hrs of injury, fibroblasts begin process of wound repair & collagen synthesis (‘glue’)

Allows the influx of leukocytes and macrophages to the area Remove damaged tissues or foreign substances

Acute vs Chronic Inflammation

The initial inflammatory response is essential for the resolution of an injury

Excessive edema and vascular damage can disrupt oxygen flow, which can lead to further tissue damage

Injury Cycle Cellular injury signals the release of chemical

mediators, which (mostly) cause vasodilation:HistamineSerotoninLeukotrienesProstaglandinsThromboxanes (causes vasoconstriction and

promotes clotting)

Cell Membrane Disrupted/Damaged

Phospholipids Released

Cyclooxygenase Lipooxygenase

Block 1: Corticosteroids block production of arachidonic acidArachidonic Acid

Prostaglandins/Thromboxane

InflammationSwellingPain

Leukotrienes

Inflammation (Respiratory)

Block 2: NSAID’s block production of prostaglandins

Block 3: Lipoox inhibitors block metab of arach acid to reduce inflam

Leukotrienes

Bronchoconstriction, attracts inflammatory cells

Have no role with systemic anti-inflam medications

Leukotriene Inhibitors: Currently used to treat asthma onlyZyflo, Accolate, Singulair

Prostaglandin Inhibits clotting Inhibits stomach acid secretion Stimulates the mucus lining of the stomach Fever

If hypothalamus senses increase in prost, it will elevate body temp

Uterine muscle contractionContractions during birthReleased at end of menstrual cycle to help shed

uterine lining (causes pain)

Thromboxane

Promotes platelet aggregation (clot formation)

Potent vasocontrictor

History of NSAID’s Bark of Willow trees used for 2000+ yrs Late 19th century: chemists came up w/

aspirin Late 20th century: came up w/ aspirin

derivative (NSAID’s) Same effects w/ less severe side-effects

All NSAID’s inhibit cyclooxgenase activity Effects of each NSAID varies per person

If one drug doesn’t work within 1-2 wks, try another

Effects of NSAID’s

All NSAID’s inhibit cyclooxgenase activity

Effects of each NSAID varies per personIf one drug doesn’t work within 1-2 wks, try another

Cell Membrane Disrupted/Damaged

Phospholipids Released

Cyclooxygenase Lipooxygenase

Arachidonic Acid

Prostaglandins/Thromboxane

InflammationSwellingPain

Leukotrienes

Inflammation (Respiratory)

Block 2:

Aspirin/NSAID

Aspirin Acetylsalicylic acid from bark of Willow tree 1st created by Bayer in 1899

Mechanism of action: blocks the activity of the cyclooxygenase enzyme

Dose: ~3,000-5,000mg/day

Aspirin – Side Effects Side-effects: 2-40% of patients

Gastric bleeding, ulcersPrevention: take w/ food or use coated aspirin

(buffering action)

Prolonged bleeding timesInhibits thromboxane (promotes clotting) Irreversible bond w/ CyclooxygenaseDecreased platelet function last 4-6 days (life span

of platelets) after aspirin intake ○ Since the bond is irreversible

Aspirin – Reye’s Syndrome

Rare condition: impairs mitochondrial function, leads to liver & brain damage

Sx’s & Sy’s: vomiting, lethargy, delirium, hyperventilation, coma, seizures

No definitive cause & effectLinked to aspirin intake in children w/ viral

infections Prudent to DC aspirin in patients <18y/o w/ a

viral infection

NSAID’s

Motrin ®, Advil ® = ibuprofen Aleve®, Naprosyn® = naproxen Relafen® = nabumetone Indocin® = indomethacin

Mechanism of action: reversibly bind to COX (cyclooxgenase)

Ibuprofen Most frequently used NSAID

Includes advil, motrin, and nuprin Introduced OTC in 1985 Among the most beneficial NSAID in relieving

pain assoc w/ dsymennorhea (~400mg every 6hrs)

Still see decreased clotting due to thromboxane inhibition

Ibuprofen Analgesic, antipyretic, anti-inflammatory Most popular NSAID/Lowest risk of GI sy (10-

15% DC) T1/2 = 2 hours Onset = 15-30 minutes Dose:

200-400mg every 4-6 hours600mg every 6 hours 800mg every 8 hoursAnti-inflam: 800-1000mg t.i.d (2,400-3,200/day)Should not exceed 3,200mg/day

Naproxen Chemically similar to ibuprofen Better @ decreasing jt inflam

Naproxen sodium concentrates in joint synovium 20% more potent than aspirin 2x’s more cases of GI bleeding than Ibuprofen Avail Doses: OTC: 220mg/Rx: 250, 375, 500mg T1/2: 12 hours Onset: 2-4 hours Dose: 375-500mg b.i.d

Maximum daily dose = 1,000mg

Ketorolac Only NSAID that can be used for IM, IV or oral

use Has antipyretic & anti-inflam effects, but typically

used as an analgesic 2002: 28/30 NFL teams used IM on game days

for pain relief Pain relief potency similar to opiats w/o

dependency issues Onset: 30-50 min Dose: 15-60 mg Side-effects limit its’ use (< 5 days)

Renal failure, gastric lining damage, GI bleeding

COX-2 Inhibitors 2001: Bextra came onto the market, followed

by Vioxx & Celebrex

2004: FDA recalled Bextra - higher incidence of heart attack & stroke

Vioxx was voluntarily withdrawn soon afterLinked w/ increased risk of myocardial infarction

by 300%

Only Celebrex remains on the market w/ warning

Side-Effects of NSAIDS GI = #1 - nausea, vomiting, stomach

cramping, ulcers, intestinal bleeding Renal toxicity Hepatic failure CNS – headache, confusion, tinnitus Hypersensitivity reactions

Decrease side-effects: Take w/ food and avoid abuse!!!

NSAID Drug Interactions

Taking NSAID’s w/ anti-coagulants, aspirin, corticosteroids, or ALCOHOL: Increase risk of serious GI pathology

NSAID’s will diminish effects of anti-hypertensive meds

Allergy Note Patient’s that have a known allergy to aspirin

should avoid other NSAID’s

They share a common chemical structure

Recommend: Tylenol (acetaminophen)

Acetaminophen Effective fever and pain reducer

Anti-pyretic and analgesicNot an anti-inflam because it cannot inhibit

cyclooxygenase No GI issues or prolonged bleeding time Abreviation: APAP

Sometimes combined w/ other medsPercocet = oxycodone + APAP

Mechanism of Action: acts directly onto the CNS

Acetaminophen Dose: 325-650mg every 4 hrs

Regular strength: 325 mgExtra strength: 500mgMaximum strength: 650mg

Toxicity: 5,000mg/day5,000-8,000mg/day for several days = severe liver

damage/death Onset: < 1hr T ½ = 2 hours Duration: 4-6 hours

Question

A basketball player goes up for a rebound and gets his feet cut out from underneath him and hits his head on the court. He has a mild headache and no other symptoms.

What would you give him for pain? Acetaminophen (Tylenol) or Ibuprofen (Motrin)

Glucocorticosteroids Produced in the adrenal gland Inhibits phospholipase (beginning of cascade)

Blocks both pathwaysUsed to tx asthma, chronic inflammation, and

juvenile rheumatoid arthritis Method of delivery: Oral, IM, US, E-stim

Phonophoresis (US), iontophoresis (e-stim)

Use of Corticosteroids in Sports Medicine No controlled studies to validate practices

surrounding use Use in reducing inflam is controversial, but

widely practiced by physicians Recommended: 2 wks between injections & no

more than 3 injections @ each siteLinked to collagen breakdown

10-14 days of “relative rest” after injection’85 & ’08 articles

Typically it’s 1-3 days of rest before full RTP

Complications GI upset (oral) Immune system suppression Risk of infection Fat necrosis Tendon Rupture: most feared 1999 study found irreversible damage to

muscle when used to tx muscle contusionsAtrophy and decrease force generationDue to inhibition of inflammatory phase of healing

Indications

Bursitis Rheumatoid Arthritis Severe Osteoarthritis Elbow epiconylitis (tennis elbow) Plantar fasciitis De Quervain’s tenosynovitis Trigger finger

SKELETAL MUSCLE RELAXANTS Chapter 4

Muscle Spasm vs Spasticity

Spasm: Loss of range of motion, increased pain, &

involuntary tensionAthlete is unable to completely relax

muscleTypically result of trauma

Pain-spasm-pain cycle:Increase in pain from muscle sent to CNS

= increase in tension = pain

Central-Acting Drugs

Central-acting – works on the CNSMechanism: Depression of CNS/Reduce CNS

nerve impulses○ Results in overall relaxation

Sedative effect allows athlete to rest & the muscle to repair = decreased muscle spasm

Typically combined w/ an analgesic (aspirin, Tylenol)

Onset: 30-60 min Duration: Most 4-6 hrs, some 12-24 hrs Does not cure muscle injury, just relieves

symptoms!

Side-effects Drowsiness, Confusion, Lack of muscle coordination

Will be unable to practice/compete while taking relaxants!

Encourage athletes to DC as soon as they can function without them

Headache, Dizziness, Blurry vision, Nausea, Vomiting Allergic reactions Addiction

Watch for signs of abuse Most commonly abused drug by health-care professionals

In combination with alcohol = death Increased sedative effect

DIABETESChapter 5

Type II Oral Agents

Stimulate insulin release or help the body with glucose uptake

Taken once a day or just a.c.

Most popular: Glucophage (Metformin)

Beware of hypoglycemia Need to eat regular meals when on medication

Insulin Subcutaneous injection

Upper arm, thigh, abdomen, buttocks Insulin pump

More preciseCollege & HS athletes have played sports w/ pump

○ Precautions must be taken to protect pump for contact sports

Doses are individualized to the person Four types of insulin:

Rapid acting: <15min a mealsShort acting: 30-60min a mealsIntermediate: b.i.dLong acting: once daily

RESPIRATORY DRUGS

Chapter 7

Asthma Medications “Rescue inhalers” – broncodilators

Rescue or control

Corticosteroids – controls inflammationControlling Agent

Athletes should have a controlling agent for inflam & a rescue inhaler for broncoconstriction

Albuterol Inhaler Bronchodilators

Target Beta-2 agonists in bronchial smooth muscle specifically, causing them to relax

Works within minutes, only lasts ~4 hrs Most commonly used

Brand Names:Ventolin HFA®Proventil HFA®Proair HFA®

2 puffs: 30 min a exercise to prevent onset of sx Used as “rescue” inhaler, as needed

Proper Inhaler Use1) Shake the albuterol inhaler

2) Breath out deeply

3) Place mouth piece to your mouth

4) Press the canister down at the same time you breath in

5) Hold breath for about 10 sec, or as long as you can

6) Wait 1 min before repeating

Anti-inflammatory Medications

Corticosteroids: used to prevent inflammation associated w/ chronic asthma

Not used as rescue therapy

Advair®: Combine corticosteroids w/ long acting beta-2 agonist

Must be taken everyday to work properly & prevent asthma attacks

Corticosteroid Medications Corticosteroid:

Flovent ® – fluticasoneAsmanex ® – mometasonePulmicort ® – budesonide

Corticosteroid w/ Beta-2 Agonist:Advair ® – fluticasone + salmeterol

Other Types Prednisone:

Tablets or liquidShort tx course to reduce inflam p an attack

○ ~ 5 days

Singulair:Disrupt the ability of leukocytes to increase

inflammationOral tablets

Treatment for Asthma Attack1) Stay calm2) Have them in a sitting position3) Let them use their inhaler: 3-4 puffs4) Talk to them, encourage them to control their

breathing5) If no improvement in ~ 30 min, call 911

1) Only call 911 if sy’s don’t respond to medicine

6) Keep using the albuterol inhaler every 20 min for up to 1 hr

7) If they pass out, use mouth to mouth

Antihistamine - Allergies

1st Generation: Benadryl (Night time)4-6 hrs sx reliefCause drowsinessDry mouth

2nd Generation: Claritin, Zyrtec, Allegra (Day time)Up to 12 hrs sx reliefLess drowsinessNasal Decongestant (+ psuedoephedrine):

○ Claritin-D & Allegra-D

Steroidal Nasal Sprays (RX only)

Used specifically for allergic rhinitis Not effective for viral conditions (common cold) Effective for decreasing nasal congestion,

sneezing, & rhinorrhea Few side effects due to their direct action

Epistaxis, nasal irritation, dryness

Flonase Nasonex

Expectorants vs Antitussives Ingredients in cough syrups

Expectorant: Promotes removal of mucus from airway Productive cough: GuaifenesinExp: Mucinex, Robitussin Chest Congestion

Antitussive: Suppress action of coughingDry cough: Dextomethorphan (DM)

○ DM is most common ingredient in cough syrup OTC’s

Exp: Robitussin, Tylenol Cold products, & NyQuil

DRUGS FOR INFECTIONS

Chapter 9

Antibiotics Used to treat bacterial infections Choice of antibiotic is based on type of

bacteria

Narrow-spectrum: target specific microorganisms

Broad-sprectrum: active against many categories of bacterial microorganisms

Bacteriocidal: kills bacteria Bacteriostatic: prevents multiplication

Tests for Bacteria Gram stain test: identifies the type of

bacteria Blue: Staphylococcus, StreptococcusRed/Pink: E. Coli, Salmonella

Disk-Diffusion & Broth Dilution: assess drug sensitivity

Antibacterial Drugs

Mechanisms of action:

Inhibit cell wall synthesis

Inhibit protein synthesis

Inhibit DNA synthesis

Inhibit folic acid synthesis

Penicillin

Inhibits cell wall synthesis

1928 – discovered by Alexander Fleming

He noticed mold growing in a petri dish of bacteria

The bacteria were dying as they came in contact with the mold

Thus, penicillin was discovered

Penicillin Passes through small pores in the bacteria’s cell

membrane & binds to penicillin-binding proteins (PBP)

Penicillin inhibits enzymes needed to construct the bacteria’s cell wall

Without the cell wall, the bacteria loses its’ protection & gets broken down

Since human cells do not have a cell wall, the penicillin does not affect our own cells

Penicillin Structure

All penicillin’s have same basic chemical structure: beta lactam ring

The ring is very weak

Some bacteria produce an enzyme: beta lactamase that cleaves the ring structure and inactivates the antibiotic

Penicillin Drugs Penicillin VK Amoxicillin Methicillin

Used primarily to tx:Strep throatPneumoniaSkin infectionsEar infections

Penicillin Allergy

One of the most commonly reported drug allergy is penicillin

Mild reactions: Rash, itching, hives, swelling

Severe reactions:Bronchospasm, laryngeal edema

MRSA Methicillin Resistant Staphylococcus

Aureus“Superbug”

Resistant to beta-lactam antibioticsMethicillin, Penicillin, and Amoxicillin

Cephalosporins – Exp: Keflex (Cephalexin) – 1st Gen.

Four generations: tx different types of bacteria

Inhibits bacteria cellular wall synthesis

Have a beta lactam ring, similar to penicillinAlso susceptible to beta-lactamase producing

bacteriaMany pt’s w/ pen. allergy can take cephalosporins

Used to tx:Skin & soft tissue infections, respiratory tract

infections, & meningitis

Inhibit Protein Synthesis

Binds to bacterial ribosomes & block production of amino acids

Suppress bacteria growth

Classes: 1. Tetracyclines

2. Macrolides

3. Clindamycin

4. Aminoglycosides

Tetracyclines Broad spectrum antibiotic

Effective against wide variety of conditions: Lyme diseaseAcneTooth infectionsPneumonia, respiratory infectionsChlamydia, gonorrhea, syphilis

Macrolides

Similar coverage as penicillins:Pneumonia, strep, skin infections, chlamydia,

syphilis Can be used in patients w/ penicillin allergy

Exp:ErythromycinClarithromycinAzithromycin (Z-Pak)

Clindamycin

Only agent in its class

Used to treat wide variety of infections: Pneumonia, respiratory track infections, skin

infections, acne

Inhibit Folic Acid Synthesis “Sulfa” drugs

Bactrim (sulfamethoxazole)

Suppress bacteria growth

Mostly used for UTI’s

Caution in patients w/ sulfa allergy

Most common side effect is hypersensitivity

Minor Skin Infections: OTC Topical Anitbiotics

1. Bacitracin: Bacitracin zinc: inhibits DNA synthesis

2. Triple Antibiotic & Neosporin: Polymyxin B sulfate: inhibits cell wall Neomycin sulfate: inhibits protein

synthesis Bacitracin zinc: inhibits DNA synthesis

Viral Infections & Vaccines Vaccine available:

PolioSmall pox, chicken pox, shinglesRabiesMeasles, Mumps, Rubella (MMR)Hepatitis A, B, DHPVFlu (yearly)

No Vaccine available:Common cold, HIV, Mono, Herpes simplex,

Hepatitis C, E, F, G

ANALGESICS & LOCAL

ANESTHETICS

Chapter 10

Pain Management

Severity of Pain Mild to moderate Moderate to Severe Severe

Drug Use

NSAID’s or acetaminophen

Low dose Opioid

High dose Opioid plus nonopioid

Analgesics - Opioids

Derived from opium poppy plant Morphine & codeine (most common) Heroin can be extracted w/ further processing

No medically accepted use Can cause severe psychological & physical

dependence Common Uses:

Cancer patientsSurgerySevere trauma

Opioid Mechanism of Action Decreases neurotransmitter activity

Which produces analgesic effect

All opioid drugs are considered controlled substances Class I (Street drug):

Heroin Class II (Highest level of abuse):

Morphine, Oxycodone (Percocet®) Class III (Moderate potential for abuse):

Hydrocodone ○ Vicodin®, Lortab®

Hydrocodone Hydrocodone c acetaminophen

Most commonly prescribed pain medicine in 2000 Vicodin & Lortab

Time to Onset: 10-30min Duration: 4-6hrs

Oxycodone Typical Brand Names:

OxycontinPercocetPercodanOxycodone

Time to Onset: 15-30min Duration: 4-6hrs

Percocet: Oxycodon + Acet Doses:

5/325 mg (5 mg oxycodone + 325mg APAP)7.5/32510/650

Take 1 tablet every 4-6 hours as needed for painCan be taken c or w/o food

Don’t exceed 4g/day (4000mg) limit for acetaminophen

Codeine Exp:

Tylenol #3: 3mg codeine + 300mg APAP

Uses:Mild to moderate pain or dental useSometimes used as an antitussive for individuals

w/ a severe cough

Time to Onset: 10-30min Duration: 4-6hrs

Codeine can be further processed into morphine

Morphine One of the most effective drugs known for pain

relief Used to treat moderate to severe pain

Can also be used to alleviate severe coughing Morphine may be used to ease pain before,

during & after surgery Can cause psychological & physical dependence

With the same addiction potential as heroin

Time to Onset: 15-60min Duration: 3-7hrs

Side Effects

Addiction Sedation Nausea/Vomiting Constipation CNS/Respiratory Depression

Combined c alcohol can be lethal!

Local Anesthetics

To induce a partial or complete loss of sensation

Ice, injection of drug, topical (skin irritants) Action of Drug:

Diminishes ability of the nerve fiber to conduct an action potential

Inhibits number of nerve endings that can transmit impulses to CNS

Commonly Used Local Anesthetics Novocaine:

Onset: 10-30 minDuration: 30-60 min

Lidocaine: Onset: <10 minDuration: 1-3 hrs

Cocaine: Still used (rarely) during nasal surgeries

Warning

Using pain relievers or local anesthetics during sports participation may cause further injury!