1. Pharmacology Application in Athletic Training

2. 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
BC Greeks: developed pharmacopeias
Defined preparation, action of drug,etc
Middle Ages: Pharmacy recognized as a separate profession from medicine

3. 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

4. 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

5. 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

6. 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
Sulfa-nil-a-mide

7. 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
Even w/ the Food and Drug Act of 1938, drugs were still often mislabeled and there was no distinction between prescription and OTC meds. Individuals often took prescription drugs w/o supervision.

8. Durham-Humphrey Amendment: 1952
Distinction between prescription and OTC drugs
Warning Label for Prescription Drugs:
“Caution: Federal law prohibits dispensing without a prescription”

9. 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
FDA refused to give approval for US sale due to lack of adequate safety information. Took over 10 years to realize the connection between the sleeping pill and the birth defect.

10. 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
As a result, many were withdrawn from market
Ke-fauv-er

11. 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

12. 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
Schedule I: not accept for medical use in the US
Schedule II: High affinity for abuse, but acceptable for medicinal use
Schedule III: lower abuse potential

13. 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

14. 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
Fast-track: unknown risks are balanced by urgent need for the drug

15. FDA Approval Process Lab/Animal Studies (up to 3 yrs)
Company files for investigational new drug
Clinical Study:
Phase I: Human volunteers (1 yr)
Phase II: Human Patients (2 yrs)
Phase III: Human Patients (3 yrs)
FDA Review (2-3 yrs)
FDA Approval of New Drug (~12 yrs after initiation)
Phase I: evaluate drug metabolism and side effects
Phase II: Therapeutic effects, dosing
Phase III: Safety and efficacy

16. Name of Drugs Chemical name Generic name Brand name
N-acetyl-para-aminophenol
Acetaminophen
Tylenol®

17. 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
After 17 years, other companies can use the same chemical ingredients to produce a generic equivalent.

18. PHARMACOKINETICS AND PHARMACODYNAMICS18

19. Pharmacodynamics: how drugs affect the body
Pharmacokinetics: what the body does to the drugs 19

20. 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

21. 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 21

22. 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 22

23. 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 23

24. 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 24

25. Pharmacokinetics What does the body do to the drug? Absorption
Distribution
Metabolism
Excretion 25

26. 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 26

27. Distribution GI Tract Bloodstream Liver Bloodstream (to entire body)
Mouth
GI Tract
Bloodstream
Liver
Bloodstream (to entire body)
Target site
Takes smaller does of intravenous or intramuscular injection than oral administration because it doesn’t have to go through the liver
Intravenous Administration

28. 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 28

29. 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

30. 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)
Food can decrease potency of drug, no food can cause irritation 30

31. Anti-Inflammatory Medications

32. 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

33. 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
Maturation: is the final phase and occurs once the wound has closed. This phase involves remodelling of collagen from type III to type I. Cellular activity reduces and the number of blood vessels in the wounded area regress and decrease.
Collagen is “glue that keeps the body together”, in all fibrous tissue, an amino acid/protein, accounts for 30% of protein in our bodies

34. 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

35. Injury Cycle
Cellular injury signals the release of chemical mediators, which (mostly) cause vasodilation:
Histamine
Serotonin
Leukotrienes
Prostaglandins
Thromboxanes (causes vasoconstriction and promotes clotting)

36. Cell Membrane Disrupted/Damaged
Phospholipids Released
Block 1: Corticosteroids block production of arachidonic acid
Block 2: NSAID’s block production of prostaglandins
Arachidonic Acid
Block 3: Lipoox inhibitors block metab of arach acid to reduce inflam
Cyclooxygenase
Lipooxygenase
Cy-clo-oxy-gen-ase
Leukotrienes
Prostaglandins/
Thromboxane
Inflammation
Swelling
Pain
Inflammation
(Respiratory)

37. Leukotrienes Bronchoconstriction, attracts inflammatory cells
Have no role with systemic anti-inflam medications
Leukotriene Inhibitors:
Currently used to treat asthma only
Zyflo, Accolate, Singulair

38. 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)

39. Thromboxane Promotes platelet aggregation (clot formation)
Potent vasocontrictor

40. 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

41. 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

42. Cell Membrane Disrupted/Damaged
Phospholipids Released
Block 2:
Aspirin/NSAID
Arachidonic Acid
Cyclooxygenase
Lipooxygenase
Leukotrienes
Prostaglandins/
Thromboxane
Inflammation
Swelling
Pain
Inflammation
(Respiratory)

43. 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
Acetyl-sal-a-cyl-ic

44. 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

45. 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

46. NSAID’s Motrin ®, Advil ® = ibuprofen Aleve®, Naprosyn® = naproxen
Relafen® = nabumetone
Indocin® = indomethacin
Mechanism of action: reversibly bind to COX (cyclooxgenase)
Na-bume-a-tone
in·do·meth·a·cin

47. Ibuprofen Most frequently used NSAID Introduced OTC in 1985
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

48. Ibuprofen Analgesic, antipyretic, anti-inflammatory
Most popular NSAID/Lowest risk of GI sy (10-15% DC)
T1/2 = 2 hours
Onset = minutes
Dose:
mg every 4-6 hours
600mg every 6 hours
800mg every 8 hours
Anti-inflam: mg t.i.d (2,400-3,200/day)
Should not exceed 3,200mg/day

49. 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: mg b.i.d
Maximum daily dose = 1,000mg

50. 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: min
Dose: mg
Side-effects limit its’ use (< 5 days)
Renal failure, gastric lining damage, GI bleeding

51. 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

52. 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!!!

53. 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

54. 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)

55. 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

56. Acetaminophen Dose: 325-650mg every 4 hrs Toxicity: 5,000mg/day
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

57. 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)

58. 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)

59. 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 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

60. 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

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

62. Skeletal Muscle Relaxants
Chapter 4

63. Muscle Spasm vs Spasticity
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

64. 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: min
Duration: Most 4-6 hrs, some hrs
Does not cure muscle injury, just relieves symptoms!

65. 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

66. Chapter 5
Diabetes 66

67. 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
a.c.: before meals
Gluco-fage 67

68. Insulin Subcutaneous injection Insulin pump
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 68

69. Chapter 7
Respiratory Drugs

70. 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

72. 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

73. Proper Inhaler Use 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

74. 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

75. Corticosteroid Medications
Flovent ® – fluticasone
Asmanex ® – mometasone
Pulmicort ® – budesonide
Corticosteroid w/ Beta-2 Agonist:
Advair ® – fluticasone + salmeterol

76. Other Types Prednisone: Singulair:
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

77. Treatment for Asthma Attack
Stay calm
Have them in a sitting position
Let them use their inhaler: 3-4 puffs
Talk to them, encourage them to control their breathing
If no improvement in ~ 30 min, call 911
Only call 911 if sy’s don’t respond to medicine
Keep using the albuterol inhaler every 20 min for up to 1 hr
If they pass out, use mouth to mouth
As long as their sy’s get better, no need to call 911.

78. 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

79. 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
Epa-stak-sis

80. 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
Gweye-FEN-eh-sin

81. Drugs for Infections
Chapter 9

82. 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

83. 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

84. Antibacterial Drugs Mechanisms of action: Inhibit cell wall synthesis
Inhibit protein synthesis
Inhibit DNA synthesis
Inhibit folic acid synthesis

85. 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

86. 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

87. 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

88. Penicillin Drugs Penicillin VK Amoxicillin Methicillin
Used primarily to tx:
Strep throat
Pneumonia
Skin infections
Ear infections

89. Penicillin Allergy
One of the most commonly reported drug allergy is penicillin
Mild reactions:
Rash, itching, hives, swelling
Severe reactions:
Bronchospasm, laryngeal edema

90. MRSA Methicillin Resistant Staphylococcus Aureus
“Superbug”
Resistant to beta-lactam antibiotics
Methicillin, Penicillin, and Amoxicillin
Staph-elo-kok-es o-ri-es

91. 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

92. Inhibit Protein Synthesis
Binds to bacterial ribosomes & block production of amino acids
Suppress bacteria growth
Classes:
Tetracyclines
Macrolides
Clindamycin
Aminoglycosides

93. Tetracyclines Broad spectrum antibiotic
Effective against wide variety of conditions:
Lyme disease
Acne
Tooth infections
Pneumonia, respiratory infections
Chlamydia, gonorrhea, syphilis

94. 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)

95. Clindamycin Only agent in its class
Used to treat wide variety of infections:
Pneumonia, respiratory track infections, skin infections, acne

96. 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

97. Minor Skin Infections: OTC Topical Anitbiotics
Bacitracin:
Bacitracin zinc: inhibits DNA synthesis
Triple Antibiotic & Neosporin:
Polymyxin B sulfate: inhibits cell wall
Neomycin sulfate: inhibits protein synthesis

98. 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

99. Analgesics & Local Anesthetics
Chapter 10
Analgesics & Local Anesthetics 99

100. Pain Management Mild to moderate Moderate to Severe Severe
Severity of Pain
Mild to moderate
Moderate to Severe
Severe
Drug Use
NSAID’s or acetaminophen
Low dose Opioid
High dose Opioid plus nonopioid
100

101. 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
101

102. 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®
102

103. Hydrocodone Hydrocodone c acetaminophen Vicodin & Lortab
Most commonly prescribed pain medicine in 2000
Vicodin & Lortab
Time to Onset: 10-30min
Duration: 4-6hrs

104. Oxycodone Typical Brand Names: Time to Onset: 15-30min
Oxycontin
Percocet
Percodan
Oxycodone
Time to Onset: 15-30min
Duration: 4-6hrs

105. 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
105

106. Codeine Exp: Uses: Time to Onset: 10-30min Duration: 4-6hrs
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
106

107. 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
107

108. Side Effects Combined c alcohol can be lethal! Addiction Sedation
Nausea/Vomiting
Constipation
CNS/Respiratory Depression
Combined c alcohol can be lethal!
108

109. 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
109

110. Commonly Used Local Anesthetics
Novocaine:
Onset: min
Duration: min
Lidocaine:
Onset: <10 min
Duration: 1-3 hrs
Cocaine:
Still used (rarely) during nasal surgeries
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111. Warning
Using pain relievers or local anesthetics during sports participation may cause further injury!
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