Premedication Regimen

No allergy to Penicillin 2g or 2000mg Amoxicillin one hr prior to appt time RX:

Amoxicillin 500mg caps Dispense 4 Take four capsules 1 hour before appointment time. Refills Zero

Premedication Regimen
Allergy to Penicillin 600mg Clindamycin Available in 150 mg or 300mg capsules RX:

Clindamycin 150 mg capsules Take 4 caps 1 h before appointment time. Refills Zero

Nonopioid (Non Narcotic) Analgesics

Chapter 5

Pain

Pain is the means by which the body is made urgently aware of the presence of tissue damage. Suffering or distress of the body and or mind. Protective reflex for self-preservation

Diagnostic symptom of an underlying pathologic condition

Pain

Pain Control is of great importance in the dental office

Pain brings patient to the dental office

Conversely,

pain will keep patient away from the

dental office

Provider needs to recognize and evaluate a patients need for medication

Two components of pain

Perception physical component of pain Involves the message of pain that is carried through the nerves eventually to the cortex. Reaction psychological component of pain, involves the patients emotional response to the pain.

Pain Threshold
Individuals perceive pain but react differently to it. Decrease in pain threshold-greater reaction to pain. Decrease in PT associated with emotional instability, anxiety, youth, fatigue, certain nationalities, women, fear, and apprehension.

Raise Pain Threshold

Getting adequate sleep Sympathy-understanding Activities-hold a pts hand, talk with the patient, stay busy, swim, hot shower, meditation, etc.. Analgesics- Tylenol, Advil, Motrin, Aspirin

Pain Threshold
Analgesic therapy must be selected for the individual A level of discomfort that may not require drug treatment in one person may demand extreme therapy in another

Classification of Analgesic Agents

Divided into 2 groups 1-Nonopiods-aka: nonnarcotic, peripheral, mild, and antipyretic, analgesics.

Site of action-peripheral nerve endings, mediated centrally

2-Opiods-aka: narcotic central, or strong group.

Site of action-act primarily on the central nervous system

More Actions
Action of non-opioid analgesics related to their ability to inhibit prostaglandin synthesis Opioids affect the response to pain by depressing the CNS

Non-Opioids
Non-opioids are divided into: salicylates (aspirin-like) i.e Anacin, Diflunisal

acetylsalicylic acid (ASA) acetic acid and salicylic acid acetic acid imparts the vinegar odor to a bottle of aspirin when it gets old

Non-Opioids
acetaminophen (Tylenol) NSAIDs (nonsteroidal anti-inflammatory drugs/agents) i.e. Advil, ibuprofen, Naproxen, Etodolac, Ketoprofen

Salicylates
From extracts of willow bark and contain salicin that have been used to reduce fever Chemical name: acetylsalicylic acid=ASA=aspirin ASA HA(acetic acid) + SA(salicytic acid) Acetic acid has characteristic of vinegar odor = if your bottle of aspirin STINKS, then it is time for a new one Metabolized via zero order kinetics

Acetylsalicylic Acid Mechanism of Action

Analgesic - pain reliever

Better to give before pain begins, effective against throbbing pain vs. a stabbing pain. Inhibits prostaglandin synthesis

Inhibits

enzyme cyclo-oxygenase (COX or COX II)

What types of procedures or dental problems come to mind when you hear a patient say throbbing pain? Stabbing pain?

Acetylsalicylic Acid Mechanism of Action

What are prostaglandins?

From arachidonic acid Are lipids that are synthesized locally by inflammatory stimuli Sensitize pain receptors to bradykinin

Bradykinin

has two receptors B1 involved with tissue injury, chronic pain and plays a role with inflammation

Acetylsalicylic Acid Mechanism of Action

aspirin blocks the synthesis of prostaglandins

Effective if given before painful stimuli are experienced More effective against throbbing pain

Due

to inflammation

Acetylsalicyclic Acid Mechanism of Action

Antipyretic - fever reducer-induces peripheral vasodilation and sweating

Reduces prostaglandin synthesis in the hypothalamus

The

higher the prostaglandin synthesis the higher the body temp

Anti-inflammatory- inflammation reducer (by inhibiting prostaglandin synthesis)

Prostaglandins strong vasodilators-capillary permeability aspirin decreases erythema and swelling

Acetylsalicyclic Acid Mechanism of Action

Anti-platelet effects blood thinner

Irreversibly binds to platelets and reduces platelet adhesiveness All platelets affected (will not normally clot)

New

platelets will need to form (4-7 days) After 20% of platelets replaced normal clotting returns (about 36 hours)

Taken orally absorbed in small intestine

ASA (cont)

Reaches peak effect on empty stomach in 30 minutes Buffered tablet in 20 minutes- buffer will help the aspirin be dispersed, and dissolved quicker, it has higher blood levels Buffer = slower absorption but that is offset by the faster rate of dissolution

ASA (cont)
Given orally or rectally Never apply directly to tooth or mucosa = painful ulceration Take when MI is suspected GI effects (most frequent effect)-nausea, vomiting, gastric irritation, may exacerbate preexisting ulcers, gastritis, or hernia Antacids reduce absorption with diflunisal Metabolized in the liver Excreted by the kidney

ASA common drug reactions

warfarin (Coumadin)=bleeding Methotrexate (cancer drug) probenecid (gout medicine) Interferes with ACE inhibitors, beta blockers, reducing antihypertensive effects Dosage for aspirin

Fever = 325 to 650mg every 4 hours Arthritis = between 3-6gm a day LD for pediatrics 4 gm, adults 10-30 gm

Enteric-Coated Aspirin-coat dissolves in the intestine rather than the stomach Aspirin with caffeine is more effective

ASA common drug reactions and contraindications

Inhibits prothrombin production resulting in hypoprothrombinemia In children and adolescentsassociated with Reyes Syndrome when taken for chicken pox and influenza. (use Tylenol instead) No use during pregnancy Allergy=usually occurs in asthmatics

Nasal polyps, asthma, and aspirin hypersensitivity Triad usually occurs

ASA common drug reactions and contraindications

True allergy to aspirin is uncommon Toxic levels taken=salicylismtinnitus, headache, dizziness, dimness of vision, electrolyte imbalance, hyperthermia All meds should be in childproof containers

ASA common drug combinations

Can add to a sedative, but preferred to prescribe separately for more control Mix with another opioid can allow a decrease in the amount of opioid in the product and reduce side effects

diflunisal (Dolobid)
Advantages-thought to have no effect on platelets and no cross-hypersensitivity with aspirin Fewer GI side effects (not much proof of) Contain magnesium, contraindicated in renal disease This is a salicylate classified as an NSAID Premed with this to delay post op pain Given 2-3x/day; no useful antipyretic effect

diflunisal (Dolobid)
Classified as an NSAID Peak action 2-3 hrs after ingestion

Not

recommended for acute dental pain

May take before dental pain

NSAIAs or NSAIDs

Generic Brand Names

Nonsteroidal Antiinflammatory Agents

Kissin cousins of aspirin ??Most useful drug group for tx of dental pain Classified by chemical make-up/Name (pg. 57) Common Rx for pain = propionic acid derivitives -naproxen sodium (Anaprox) -naproxen (Naprosyn) -ibuprofen (Advil, Motrin)

NSAIDs
Some other commonly used derivatives: Acetic acid derivatives

indomethacin (Indocin) etodolac (Lodine) diclofenac (Voltaren) Salicylates (but classified as a NSAID)

diflunisal (Dolobid) proxicam (Feldene)

Oxicams

Mechanism of Action
Inhibit prostaglandin synthesis by inhibiting the enzyme COX COX I and II

ibuprofen (Advil) naproxen (Naprosyn, Aleve) meclofenamate (Meclomen)

COX I specific

indomethacin celecoxib (Celebrex)

COX II

Most peak in 1-2 hours

Mechanism of Action

Take with food to reduce the rate of absorption

Antacids have no effect on absorption except diflunisal

Used as an analgesic, anti-inflammatory, antipyretic, especially rec. for menstrual cramps (dysmenorrhea) Metabolized in the liver Excreted via kidneys

Mechanism of Action

Tissue Injury Triggers COXII in periphery tissue

COXII will convert arachidonic acid to prostaglandin E2 (PGE2)

Results in stimulation of the nociceptor in peripheral nerve to send a signal for pain in the CNS

A nociceptor is a sensory receptor that sends signals that cause the perception of pain in response to potentially damaging stimulus

Adverse Reactions
GI irritation, pain, bleeding, increase acid secretion CNS-vertigo, headache, depression, convulsions These are not addicting, no tolerance, no withdrawal

Adverse Reactions

Reversibly inhibit platelet aggregation:

Effect lasts as long as med in blood No need to wait for new platelets to form ibuprofen in the blood 1 day naproxen 4 days oxaprozin 2 weeks

Adverse reactions (cont)

Cause Lithium toxicity, increase effect of digoxin ( used for heart failure), reduces effects for B-blockers, ACE inhibitors and diuretics Hypersensitivity-hives, itching, chills, fever Dry mouth, gingival ulcerations Renal effects Contraindicated for pregnancy prolongs gestation (Category C) Use with caution in pt.s with renal and hepatic conditions, sens. to aspirin

Therapeutic Uses
Osteoarthritis, pain, fever, dysmenorrhea Manage dental pain Take with full glass of water, and food Use caution when driving Do not use with aspirin Do not take OTC analgesics with Rx NSAIAs If pain does not subside call DDS

Specifics on NSAIDs - ibuprofen

Ibuprofen (Advil, Motrin) -onset 30 mins, duration 2-4 hrs. -metabolized in liver, excreted by kidneys -Drug of choice for dental pain -400-800mg every 4-6 hrs. -do not exceed 3200mg in a 24 hour period

- dose = anti-inflam. -200mg capsules, tablet = OTC -400, 600, 800mg = Rx -more effective than ace. with codeine, -double doses of ace.

Cox Inhibitors
Specific Cox II inhibitors block the enzyme that is synthesized when inflammation occurs -Celebra, Celebrex (lowest dose possible)(higher GI upset), refecoxib (Vioxx) and valdecoxib (Bextra) (off the market) (arthritis) Cox I-widely distributed, always present enzyme -responsible for adverse effects of NSAIDs.

Naproxen and Naproxen Sodium

Proprionic acid derivative NSAID Slightly longer half lives Dosed on an 8-12 hour schedule

Longer acting Need loading dose naproxen 500 mg stat; 250 mg q 6-8; max daily = 1500mg (peaks in 2-4h) naproxen sodium 550mg stat;275 mg q6-8h daily max = 1375 (peaks in 1-2h)

Will cause lithium levels to rise

ACETAMINOPHEN

USES
ANALGESIC AND ANTIPYRETIC PT WITH ASPIRIN SENSITIVITY PT WITH GI UPSET FROM ASPIRIN YOUNG CHILDREN Dose 1-2 tabs/caps (325 to 650mg) every 4 -6 hours OR 1000mg -3-4 X/day FDA does not recommend more than 650 mg every 4-6 hours, 3-4X/day

4000mg/day

New recommended single dose Must include a box warning most dangerous type for liver failure

USES
Dose 1-2 tabs/caps (325 to 650mg) every 4 -6 hours OR 1000mg -3-4 X/dayDo not give to children <3 yo or for more than 10 days without seeing physician No more than 4gm in 24 hours

Doses of 1000mg/4X/Day, after 1-2 days can lead to liver toxicity

Large doses=greater propensity for producing hepatic necrosis

Pharmacologic Effects
Rapidly absorbed form GI Peaks in 1-3 hours Large doses produce a metabolite in liver that can be hepatotoxic and nephrotoxic Equally efficacious as aspirin (pain) and just as potent for fever and pain. Alcoholics avoid acetominophen No effect on resp. or CV. No GI bleeding Does not produce or affect platelet adhesiveness, or uric acid excretion

Pharmacologic Effects
Acetaminophen and Alcohol Alcohol stimulates oxidizing enzymes that metabolize acetaminophen to its TOXIC METABOLITE Normal maximum dose for people who DO NOT drink = 325 per pill x2 = 650 mg every 4 - 6 hours For moderate drinkers (< 3 drinks a day), do not exceed 2gm of acetaminophen For people who exceed 3 drinks a day or someone is an alcoholic AVOID ACETAMINOPHEN

DRUGS USED TO TREAT GOUT URICOSURIC EFFECT

GOUT

Inherited disease Primarily in men Involves one joint

Often big toe or knee

Hyperuricemia and urate crystals are found at joints (amount of uric acid) Uric acid must be excreted because it cannot be destroyed within the body Excess acid caused by excessive production or reduced ability to excrete adequate amount of uric acid

GOUT

Colchicine

allopurinol (Zyloprim)

Treatment of an acute case of gout Taken hourly at the onset Interferes with inflammatory response Side effects

Inhibits synthesis of uric acid Prevent excess from forming Used with patients in chemotherapy

Vomiting Diarrhea Nausea

Death of cells release uric acid

Drugs Used to Treat Gout

Gout-inherited disease, mostly men, involves 1 joint (big toe, knee, elbow) probenecid (Benemid) and allopurinol used to prevent gout but have no pain relief Due to an excess or uric acid (produce too much or do not excrete enough) Colchicine - only used to tx attack of gout -taken hourly at the onset of attack -most common side effect = GI

Gout (cont)

allopurinol (Zyloprim)inhibits the synthesis of uric acid

Also used to tx. pts receiving chemo, death of cells cause a release of uric acid

Gout (cont)

probenecid (Benemid)

increase excretion of uric acid GI effects, sore gums, Increases levels of NSAIDs and penicillin

Natural remedy believed by some are natural cherries