pharmacology application in athletic training. history of drugs and pharmacy around 2100 bc:...
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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!