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What are the two parts to pain:
sensory and reactionary
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What is the sensory part of pain and where does it originate from
- The actual painful stimulus
- comes from the PNS.
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What is the reactionary part of pain and where does it originate from
- The emotional response to pain
- originates from the CNS
-
Acute pain has a
short time course. Usually simple to evaluate and treat
-
Chronic pain has a
undetermined time course, more complex evaluation, treatment not as successful
-
Orofacial pain is classified into:
- Nociceptive pain
- Neuropathic pain
-
Nociceptive pain is
pain arising from a stimulus such as injury to tissue, bone, joint muscle or connective tissue outside of the CNS. A scaler/currette
-
Neuropathic pain
also called neuralgia. Originates in a damaged or compromised nerve
-
Nociceptive pain can be ______ or _______
somatic or visceral
-
Somatic pain is
sharp, well-localized sensations
-
Visceral (deep) pain is ________ associated with a phenomenon called _______
- a generalized dull, throbbing or aching, poorly localized pain.
- referred pain, which detects the painful stimulus in areas removed from the site where the pain originated
-
Nociceptive pain is pain that occurs when _______ (located on the ends of nerves transmitting stimuli) are stimulated by _______
- nociceptors
- noxious stimuli
-
What are some examples of Neuropathic Orofacial Pain
trigeminal neuralgia, postherapeutic neuralgia, burning mouth, burning tongue syndrome
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Drug therapy for Neuropathic Orofacial Pain includes what class of drugs and what specific drugs
- tricyclic antidepressants, analgesics, and anticonvulsants
- gabapentin (Neurontin) (antiepileptic drug that enhances neuronal stability, which results in pain relief)
- 5% lidocaine patch
- Tricyclic antidepressants
-
Narcotics are NOT FDA approved for
chronic neuropathic pain
-
Drug Therapy for Nociceptive Pain include
- Nonnarcotic (nonopioid) analgesics–Nonsteroidal anti-inflammatory drugs (NSAIDs)
- Narcotic (opioid) analgesics–Ex. codeine, hydrocodone
-
Non narcotics analgesics include:
- salicylates (Aspirin)
- acetaminophen (Tylenol)
- Nonsteroidal anti-inflammatory drugs (NSAIDs)including selective COX2 inhibitors
-
Trauma to a nerve fiber following tissue trauma/damage stimulates ______, which causes _______ to break off from _________
- phospholipase A
- arachidonic acid
- phospholipids on cell membrane
-
Arachidonic acid follows two paths: Interactions with _____ or ______
- lipoxygenase
- Cyclooxygenase (COX) I and II enzymes
-
Interaction of arachidonic acid with lipoxygenase creates ________ which leads to _______
- Leukotrienes
- bronchoconstriction (in asthma) and other localized allergic reactions
-
Interaction of arachidonic acid with cyclooxygenase creates _______, ______, and _______
Prostaglandins, Prostacyclin and Thromboxane A2
-
Prostaglandins are _______ that are made in _______ and serves what purposes
- Fatty acids found in all tissues
- cell during inflammation
- Promote pain, inflammation, and fever
- Protect lining of stomach from damaging acid
- Cause uterine contractions during labor
- Maintain renal (kidney) blood flow
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________ is a potent mediator of inflammation. High levels are found in ________
- Prostaglandin E2 PGE2
- inflammatory periodontitis
-
Thromboxane A2 is synthesized and found in _______ and functions to ______
- platelets
- Prevents bleeding; potent vasoconstrictor which induces platelet aggregation for clotting
-
Prostacyclin (PGI2) is found in _______ and functions to _______
- blood vessel cell walls
- Prolongs bleeding; vasodilator (opposite function of thromboxane A2), prevents platelet aggregation
-
Cox 1 is a _________ found inside ________ such as the ______ and functions to _______
- "Housekeeping enzyme”
- most cells in the body
- GI tract, kidney, platelets
- Protect the lining of the stomach from stomach (gastric) acids, maintain normal platelet function, and regulate renal blood flow
-
COX-2 is produced only
during inflammation
-
Aspirin is also known as
acetylsalicylic acid
-
Aspirin inhibits _______ and _______ but predominately _________ thus causes many problems such as ________
- COX-1 and COX-2
- COX-1
- GI problems –Bleeding, ulcer
-
What are the therapeutic effects of aspirin
- Analgesia
- Anti-inflammatory
- Antipyretic
- Antiplatelet effects
-
Aspirin has analgesic effects due to
Due to inhibition of prostaglandins and bradykinin (bradykinin, an inflammatory mediator, sensitizes nociceptor peripheral terminals) reducing pain threshold
-
What is the ceiling effect
Increasing dose beyond a point does not increase analgesia
-
Aspirin has anti-inflammatory effects due to
–blocking formation of PGE2
-
Aspirin has antiplatelet effects due to
inhibiting thromboxane A2
-
Low dose aspirin ___mg is used for ______ and primarily inhibits _______
- 81
- prophylactic treatment for heart attacks and stroke
- thromboxane A2
-
Normal strength aspirin is ____ mg
325
-
Primary prevention is using low dose aspirin to _______ while secondary prevention is using low dose aspirin to ________
- prevent a first cardiovascular event for most patients who are at moderate risk
- prevent cardiovascular or cerebrovascular events in patients with a history of heart conditions
-
Reye’s syndrome is
primarily a children’s disease. Children are at increased risk to develop Reye’s Syndrome if they take aspirin to treat viral illnesses including chicken pox or flu
-
Patients taking aspirin with nasal polyps and allergic rhinitis are at risk of
developing bronchoconstriction and anaphylaxis
-
What are some adverse effects of aspirin
- Gastrointestinal upset–Reduces some with enteric-coated tablets
- Bleeding
- Salicylism (toxicity)
- Nausea/vomiting
- Renal dysfunction
- Excessive doses stimulate the depth and rate of respiration (hyperventilation)
-
What drugs have an interaction with aspirin and what is that reaction
- Oral antidiabetic: increases Hypoglycemic response of oral antidiabetic drugs
- Angiotensin-converting enzyme (ACE) inhibitors: decreases effectiveness of the hypertensive drug
- Other aspirin-containing OTC drugs: increases Aspirin effects
- Thiazide or loop diuretics: decreases Actions of diuretic
- Anticoagulants (e.g., warfarin): increases Bleeding
- Alcohol: increases GI irritation and bleeding
- Herbs (dong quai, chamomile, ginseng, ginger, and red clover): Increased bleeding
-
In a child toxicity is seen with _____ , and a lethal dose is _____g
-
Diflunisal (______)
- Dolobid
- –Derivative of salicylic acid but is not converted to salicylic acid
- –It is a more potent anti-inflammatory than aspirin, and it is an inhibitor of cyclooxygenase.
- It does not have antipyretic activity because it penetrates poorly into the CNS
- –Anti-inflammatory for arthritis and for dental pain
- –Less intense gastrointestinal and antiplatelet effects than aspirin
- Good for dental pain
- Use loading dose of 500-1000mg followed by 250-500mg q8-12h
-
Prototype for NSAID's is __________(________)
-
What is the action of NSAID's
- Block the COX enzymes and reduce prostaglandins throughout the body
- Ongoing inflammation, pain, and fever are reduced
- –Reduces protection of gastric mucosa Ulcers
- NSAIDs differ in how strongly they inhibit COX-1 and thus their tendency to cause ulcers and bleeding is less than aspirin
-
What are the indications of NSAIDs
- Analgesia –Dental pain – very effective.
- Anti-inflammatory
- Antipyretic
-
What is the mechanism of action of NSAIDs
- Inhibition of COX-1 also inhibits the production of thromboxane A2, which prevents platelet aggregation
- NSAIDs do not covalently bind to the cyclooxygenase enzymes and do not irreversibly inhibit platelet function as does aspirin
-
What are some adverse effects of NSAIDs
- –Due to COX-1 inhibition, which decreases GI mucosal defense mechanisms and increases gastric acid secretion, which leads to ulceration
- Take with food or milk
- Kidney function –Depressed due to inhibition of prostaglandin synthesis, which plays a protective role in kidney function
- All NSAIDs can lead to the onset of new hypertension or worsening of preexisting disease
-
Patients with a Hypersensitivity to NSAIDs include patient with
asthma and nasal polyps
-
What are the drug interactions of NSAIDs
- Counteracts the antihypertensive effects of angiotensin converting enzyme inhibitors (ACE inhibitors) and beta-blockers
- increases Lithium levels by decreasing renal excretion of lithium (can cause lithium toxicity)
- increases bleeding with anticoagulants
- increases Hypoglycemic effects with oral antidiabetic drugs
-
_________ is the only COX-2 inhibitor currently available and has a black box warning of the potential for ________
- Celecoxib (Celebrex)
- increased risk of cardiovascular events as well as serious and potentially life-threatening gastrointestinal bleeding
-
What is the mechanism of action of celebrex
- Only inhibits cyclooxygenase-2Inhibits prostaglandin synthesis
- Analgesic
- Antipyretic
- Anti-inflammatory
- Antiplatelet–Not used for prevention of strokes/heart attacks because it reversibly binds to the platelets
-
The major advantage of acetaminophen (__________) compared to other NSAIDs is
- Tylenol
- its lack of effect on platelet function and less or no gastric irritation
-
After ingestion Acetaminophen reaches peak blood levels in ______ minutes
30 to 60
-
What are the adverse effects of acetaminophen and what is an overdose treated with
- Hepatotoxicity (liver necrosis)
- acetylcysteine
-
Maximum dose of acetaminophen is
3 to 4 g
-
What are the drug interactions of acetaminophen
- Alcohol–Increase liver damage (hepatotoxicity)
- Carbamazepine (Tegretol), phenytoin (Dilantin), and rifampin (Rifadin)–Increase liver damage (hepatotoxicity)
-
Acetaminophen has a __ pregnancy category
B
-
OPIOID ANALGESICS act on _______ of pain and act as agonists and affect specific binding sites called _______ in the _____
- central components
- opiate receptors
- CNS
-
What is the mechanism of action of opioids
- Enkephalins and endorphins are released from neurons in the brain and activate opioid receptors, thereby blocking the transmission of pain impulses
- These substances are the body’s natural opiates that inhibit painful stimuli
-
What are the three main opioid receptors
-
Morphine has an affinity for _____ and ______receptors.
mu and kappa
-
Mu receptors are involved in the _______ effects
analgesic, respiratory, depressant, and euphoric effects
-
Kappa receptors are involved with
respiratory depression, miosis (pupil constriction), and sedation
-
What are the Opioid Adverse effects
- CNS
- –Respiratory depression
- –Cough suppression
- –Nausea/vomiting
- GI
- –Constipation
- Tolerance can develop
-
What are the Drug Interactions with Opioids
- Antihistamines, sedative/hypnotics, alcohol, and psychotropics
- –Increased CNS effects (e.g., sedation)
-
Opioids are readily absorbed from the
GI tract, nasal mucosa, and lungs (smoke)
-
What are the three classifications of opioids
- Full agonists: Strong or moderate in producing an analgesic (relief of pain) effect
- Mixed opioid agonist/antagonists: Analgesic effect with some antagonist activity
- Pure antagonists: No analgesic effects; used in opioid overdose
-
What drug is the prototype for Opioid Agonists
Morphine
-
What are the Central Actions of Morphine
- Analgesia
- Drowsiness and sleep
- Cough suppression
- Vomiting (due to stimulation of chemoreceptor trigger zone in the brain)Hypotension
- Miosis (papillary constriction)
- Respiratory depression (high doses) –Major toxic effect and cause of death because no tolerance is developed to respiratory depression
- Euphoria (ecstasy; develop tolerance rapidly to euphoric actions)
- Increased release of ADH (antidiuretic hormone), which causes urinary retention
-
What are the Peripheral Actions of Morphine
- Constipation (due to stimulation of cholinergic activity in the GI tract)
- Body warmth/flushing/itching (due to histamine release)
-
Methadone
- Long-acting synthetic morphine derivative used orally in the treatment of opioid (usually heroin) addiction
- “Wean” patients off narcotics because it does not produce euphoria (ecstasy).
-
Meperidine (Demerol)
is a less effective analgesic than morphine with half the duration of action (75 mg meperidine IM [intramuscular injection] = 10 mg morphine IM)
-
What are some adverse effects of Oxycodone and Hydrocodone
Respiratory depression, antitussive, constipation, and dependence
-
Hydrocodone is a Schedule ____ drug
III
-
hydrocodone + APAP (acetaminophen) =
Vicodin
-
hydrocodone + aspirin =
Lortab
-
hydrocodone + ibuprofen =
Vicoprofen
-
Oxy + APAP (acetaminophen) =
Percocet / Tylox
-
-
Oxy + ibuprofen =
Combunox
-
OxyContin is the brand name for
pure oxycodone HCl extended release for long term pain control
-
Codeine is a naturally occurring narcotic agonist obtained from the ______ but in lesser amounts than _______
-
What drug is more orally active than other opioids
codeine
-
What are the effects of Codeine and what is it usually combined with
- Less respiratory depressant and constipation and has less dependence potential
- other nonnarcotic drugs such as acetaminophen (Tylenol) for the relief of acute nociceptive mild to moderate dental pain
- Antitussive–Cough syrups (Schedule V)
-
What are some Guidelines for Patients Taking Codeine
- Monitor patient for dry mouth; fluoride rinses if indicated.
- Monitor vital signs because of potential effects on the heart and respiratory system.
- Causes drowsiness/sedation
-
Dextromethorphan
- –Opioid without any analgesic activity
- –High antitussive effects
- Cough medicines: Some trade names are Benylin, Delsym, and Vicks
-
Loperamide (________)
- Imodium
- –Opioid without analgesic effects
- –Increases smooth muscle tone in the gastrointestinal tract and is used as an antidiarrheal
-
Diphenoxylate
- –Antidiarrheal
- –Combined with atropine in a product called Lomotil
- It can cause severe respiratory depression, coma, and death after overdose in children
-
Tramadol (_______)
- Ultram
- –Unique analgesic having both opiate and central acting adrenergic qualities
- Not a controlled substance
- FDA approved for moderate to moderately severe pain
- Can cause serious neurotoxicity and is not the first-line drug of choice
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