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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 Papyrus
 22yrd 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 cocaine
 Aid 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 seallike 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.
2.
3.
Lab/Animal Studies (up to 3 yrs)
Company files for investigational new drug
Clinical Study:
1. Phase I: Human volunteers (1 yr)
2. Phase II: Human Patients (2 yrs)
3. Phase III: Human Patients (3 yrs)
4.
5.
FDA Review (2-3 yrs)
FDA Approval of New Drug (~12 yrs after
initiation)
Name of Drugs
 Chemical
name
 N-acetyl-para-
aminophenol
 Generic
 Brand
name
name
 Acetaminophen
 Tylenol®
Brand vs Generic
 Brand-name
drugs usually have a patent,
granted by FDA, for 17 years
 After 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
Pharmacodynamics:
how drugs
affect the body
Pharmacokinetics:
does to the drugs
what the body
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
Definitions
– 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
 Agonist
Definitions
– 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
 Affinity
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:
 Sublingual
 Oral
 Intravenous
 Transdermal (topical)
 Inhalation
Distribution
Mouth
GI Tract
Bloodstream
Liver
Bloodstream (to entire body)
Intravenous
Administration
Target site
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 site
 Exp: Lidocaine, if given orally, will be completely
broken down by the liver
Excretion

Primary organ of excretion = Kidney

Water-soluble drugs easily excreted
 Too much vitamin C…flushed down the toilet

Lipid-soluble drugs are reabsorbed
 Vitamins D,E,A,K: Fat-soluble, stored in
liver, toxic in large quantities
Factors that affect drug response
 Infants/Children
 Enzymes do not fully develop until12 y/o
 Older Adults
 Elderly have decreased kidney function
 Timing
of Food
 Before, during, after meal
 Person’s
weight (fat distribution)
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 phase
 Repair-regeneration phase
 Maturation 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:
 Histamine
 Serotonin
 Leukotrienes
 Prostaglandins
 Thromboxanes (causes vasoconstriction and
promotes clotting)
Cell Membrane Disrupted/Damaged
Phospholipids Released
Block 2:
NSAID’s block
production of
prostaglandins
Arachidonic Acid
Cyclooxygenase
Lipooxygenase
Prostaglandins/
Thromboxane
Leukotrienes
Inflammation
Swelling
Pain
Inflammation
(Respiratory)
Block 1:
Corticosteroids
block production
of arachidonic
acid
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 only
 Zyflo, 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 contraction
 Contractions during birth
 Released 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 person
 If one drug doesn’t work within 1-2 wks, try another
Cell Membrane Disrupted/Damaged
Phospholipids Released
Block 2:
Arachidonic Acid
Aspirin/NSAID
Cyclooxygenase
Prostaglandins/
Thromboxane
Inflammation
Swelling
Pain
Lipooxygenase
Leukotrienes
Inflammation
(Respiratory)
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, ulcers
 Prevention: take w/ food or use coated aspirin
(buffering action)

Prolonged bleeding times
 Inhibits thromboxane (promotes clotting)
 Irreversible bond w/ Cyclooxygenase
 Decreased 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 & effect

 Linked 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 (1015% DC)
 T1/2 = 2 hours
 Onset = 15-30 minutes
 Dose:







200-400mg every 4-6 hours
600mg every 6 hours
800mg every 8 hours
Anti-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 after
 Linked 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 antihypertensive 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 analgesic
 Not an anti-inflam because it cannot inhibit
cyclooxygenase
No GI issues or prolonged bleeding time
 Abreviation: APAP

 Sometimes combined w/ other meds
 Percocet = oxycodone + APAP

Mechanism of Action: acts directly onto the
CNS
Acetaminophen

Dose: 325-650mg every 4 hrs
 Regular strength: 325 mg
 Extra strength: 500mg
 Maximum strength: 650mg

Toxicity: 5,000mg/day
 5,000-8,000mg/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 pathways
 Used 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 site

 Linked 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 contusions

 Atrophy and decrease force generation
 Due 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

Chapter 4
Muscle Spasm vs Spasticity

Spasm:
 Loss of range of motion, increased pain, &
involuntary tension
 Athlete is unable to completely relax
muscle
 Typically 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 CNS
 Mechanism: 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
Chapter 5
Type II Oral Agents
Stimulate
insulin release or help the body
with glucose uptake
Taken
Most
once a day or just a.c.
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 precise
 College & 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 meals
Short acting: 30-60min a meals
Intermediate: b.i.d
Long acting: once daily
Chapter 7
Asthma Medications
 “Rescue
inhalers” – broncodilators
 Rescue or control
 Corticosteroids
– controls inflammation
 Controlling 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,
 Most commonly used
only lasts ~4 hrs
 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 Use
1)
2)
3)
4)
5)
6)
Shake the albuterol inhaler
Breath out deeply
Place mouth piece to your mouth
Press the canister down at the same time
you breath in
Hold breath for about 10 sec, or as long
as you can
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 ® – fluticasone
 Asmanex ® – mometasone
 Pulmicort ® – budesonide

Corticosteroid w/ Beta-2 Agonist:
 Advair ® – fluticasone + salmeterol
Other Types
 Prednisone:
 Tablets or liquid
 Short tx course to reduce inflam p an attack
○ ~ 5 days
 Singulair:
 Disrupt the ability of leukocytes to increase
inflammation
 Oral tablets
Treatment for Asthma Attack
Stay calm
2) Have them in a sitting position
3) Let them use their inhaler: 3-4 puffs
4) Talk to them, encourage them to control their
breathing
5) If no improvement in ~ 30 min, call 911
1)
1) Only call 911 if sy’s don’t respond to medicine
6)
7)
Keep using the albuterol inhaler every 20 min
for up to 1 hr
If they pass out, use mouth to mouth
Antihistamine - Allergies

1st Generation: Benadryl (Night time)
 4-6 hrs sx relief
 Cause drowsiness
 Dry mouth

2nd Generation: Claritin, Zyrtec, Allegra (Day
time)
 Up to 12 hrs sx relief
 Less drowsiness
 Nasal 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: Guaifenesin
 Exp: Mucinex, Robitussin Chest Congestion

Antitussive: Suppress action of coughing
 Dry cough: Dextomethorphan (DM)
○ DM is most common ingredient in cough syrup
OTC’s
 Exp: Robitussin, Tylenol Cold products, & NyQuil
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, Streptococcus
 Red/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
 Strep throat
 Pneumonia
 Skin infections
 Ear infections
tx:
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 antibiotics
 Methicillin, 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 penicillin
 Also susceptible to beta-lactamase producing
bacteria
 Many 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 disease
 Acne
 Tooth infections
 Pneumonia, respiratory infections
 Chlamydia, gonorrhea, syphilis
Macrolides

Similar coverage as penicillins:
 Pneumonia, strep, skin infections, chlamydia,
syphilis
 Can be used in patients w/ penicillin allergy

Exp:
 Erythromycin
 Clarithromycin
 Azithromycin (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:








Polio
Small pox, chicken pox, shingles
Rabies
Measles, Mumps, Rubella (MMR)
Hepatitis A, B, D
HPV
Flu (yearly)
No Vaccine available:
 Common cold, HIV, Mono, Herpes simplex,
Hepatitis C, E, F, G
Chapter 10
Pain Management
Severity of Pain
Drug Use
to moderate
NSAID’s or acetaminophen
Moderate to Severe Low dose Opioid
Severe
High dose Opioid plus
nonopioid
Mild
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 patients
 Surgery
 Severe 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:
 Oxycontin
 Percocet
 Percodan
 Oxycodone
Time to Onset: 15-30min
 Duration: 4-6hrs

Percocet: Oxycodon + Acet
Doses:
 5/325 mg (5 mg oxycodone + 325mg APAP)
 7.5/325
 10/650
Take
1 tablet every 4-6 hours as needed for
pain
 Can 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 use
 Sometimes 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 min
 Duration: 30-60 min
Lidocaine:
 Onset: <10 min
 Duration: 1-3 hrs
Cocaine:
 Still used (rarely) during nasal surgeries
Warning
Using
pain relievers or local
anesthetics during sports
participation may cause further
injury!