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116 Cards in this Set

  • Front
  • Back
___ pain is in response to a noxious stimuli.
___ pain occurrs when tissue damage occurs. Pain hypersensitivity occurs to prevent contact or movement of the injured part
___ is spontaneous pain and hypersensitivity associated with changes in PNS
___ pain is due to an abnormal processing or funciton of CNS response to normal stimuli
Describe the physiology of nocioceptive pain.
1. stimulation: injury causes release of bradykinins, prostaglandins, histaines, etc... sensitize and activate nocioceptors
2. Transmission: impulse transmitted along myelinated A-S fibers (sharp, local pain), and unmyelinated C fibers (visercal diffuse pain) to dorsal horn and releases neurotransmitters
3. Perception: transmission continues along spinal cord to thalamus where pain is perceived
4. modulation: complex process, with an endogenous opiate system.
Inflammation with pain is associated by interactions such as:
- histamines
- kinins
- neuropeptides
- cytokines
- arachidonic acid pathway
Changes in local blood vessels due to pain are primarily resutling from___ and include:
-trauma or antigens
- dilation, increased permeability, increased receptivenes for leukocytes (leukotriene chemotaxic response)
Leukotriene chemotaxic response involves accumulation of what inflammatory cells?
- neutrophils
- leukocytes
- macrophages
- lymphoctes, basophils, eosinophils (depending on type of inflammation)
Disturbance of the cell membrane activates ___ and the ___ pathway
phospholipase A2 and the arachodonic pathway
Cyclooxygenase 1 includes the ___ and ___. What functions does it have ?
1, prostaglandins and thrombonxanes
2. Gastroprotection, platelet aggregation, renal functionc
Cyclooxygenase 2 includes ___ and is responsiblefor ____
Pain, fever, renal function, tissue repair
___ persists beyond expected normal time for healing and serves no physiologic purpose.
Chronic pain
Mild/moderate acute pain should first be treated with ____ and then ___ as needed.
NSAIDs or APAP, then opiods as needed
Severe acute pain should be treated first with ___ then ___ in addition.
First opiods, then APAP or NSAID as needed
Describe how the following chronic pain shold be treated:
1. visceral
2. Inflammatory
3. neuropathic (central)
4. Neuropathic (peripheral)
5. Functional
1. Opioids if severe, add TCA or similar as needed.
2. APAP or NSAID, possibly long-acting opioid if needed
3. Clonidine or baclofen
4. TCA, Lidocaine, SSRI, Long acting opiod
5. TCA or Tramadol, SSRI or SNRI
Describe the MOA for NSAIDs
Inhibit cyclooxygenase and result in inhibited synthesis of prostaglandin.
- results in: analgesia, anti-inflammatory, and antipyretic
Irreversible inhibition of COX is done by _____ . Competetive inhibition is by something like ____
1. ASA - acetylation of active site
2. Ibuprofen - acts as competitive substrate
How do NSAIDs provide alalgesia?
- inhibition of prostaglandin synthesis prevents sensitization of nerves to bradykinin, histamines, etc
- reducing prostaglanding synthesis in CNS (small degree)
How do NSAIDs provide for anti-inflammatory action?
Blocking prostaglandin synthesis wihch preventts increased asodilation, vascular permeability, and edema.
How do NSAIDs have an antipyretic action?
- Prevents release of leukocytes by thromboxane.
List the indications for use of an NSAID
- musculoskeleatal and joint pain
- mild to moderate pain relieve of HA, dysmenorrhea, sunburn.
- Symptomatic relief of fever
How do NSAIDs effect the kidney?
- vasodilation of the renal vasculature, constriction of renal tubules
- glomerular flow suffers, result in renal failure
- retention of NA and H20, edema, hyperkalemia
Describe Adverse effects of NSAIDs
- GI bleeding
- Tinnitus
- edema/ hyperkalemia
- harmful in CHF, cirrhosis, RF
NSAIDs are contraindicated in
- pts with GI bleeds or ulcers
- Hypersensitivity to NSAIDS
- Caution in asthmatics, renal impairment, pts with thrombocytopenia
- avoid 1 week prior to surgery
How does ASA inhiibit COX?
- hydrolyzed to salicylic acid.
- salicylic acid is repsonsible for ihibtion of COX
Why is ASA a more potent anti-platelet aggregation than other NSAIDs?
it works at COX and at thromboxane A2 production - leads to ineffective platelets for clotting
Describe 4 therapeutic uses for ASA.
1. CV - prophylactic to reduce risk for TIA, MI, angina (81-162mg)
2. Antipyretic & analgesic (325-650mg qid)
3. Colon cancer prevention
4. Anti-inflammatory (high dose 4-8g/day)
Describe adverse effects of ASA
- salicylate poisoning due to high level of salicylic acid (n/v, confusion, tinnitus, coma, convulsion, hallucination, etc)
- Respiratory (hyperventilation leads to resp alkalosis)
- Reye's syndrome (hepatitis and cerebral edema, often fatal, esp in children with viruses)
- Hypersensitivities
What medications should you be aware of for interactions with ASA?
1. heparin or oral anticoagulants (increased hemorrhage)
2. Decreased uric acid excretion with probenecid or sulfinpyrazone
3. Antacids decrease absorption
4. ibuprofen inhibits antiplatelet effect of low-dose ASA (competitive inhibition)
___ is a derivative of salicylic acid that is more potent than ASA but doesn't cause salicylate intoxication or antipyretic effects.
Ibuprofen, fenoprofen oxaprozin, ketoprofen, naproxen, and flurbiprofen are all ____
proprionic acids
Indoleactetic acids include:
Oximcoms class of NSAIDs includes:
Piroxicam, Meloxicam
Salicylates include:
ASA, Diflunisal, Salsalate
____ possess anti-inflammatory, analgesic, and antipyretic activity with GI effects less than ASA.
Proprionic acids
Side effects of proprionic acid derivatives include:
1. dyspepsia (GI Bleeding)
2. CNS: HA, tinnitus, dizziness
Which proprionic acid derivative has the longest half-life?
What is imporatant to remember about prescribing indomethacin?
Side effects limit use: dizziness, severe GI complaints, HA, dizziness, mental confusion, hepatic and pancreatic effects
Indomethacin is used therapeutically for ___ or ___
gouty arthritis, osteoarthritis of the hip
Etolodac use may be limited due to ____
1. fluid retention, renal and liver function abnormalities
2. interactions with digoxin, lithium, and cyclosporine enhances nephrotoxicity
Diclofenac is approved for therapeutic use in __
RA, OA, and ankylosing spondylitis
One problematic caution when prescribing diclofenac is ___
it can elevate hepatic enzymes
___ is an indoleacetic acid prodrug that is as potent as ASA for RA or OA, but with fewer side effects
Which NSAID is Cox-2 selective and low-mod doses>
Oxicam derivatives have what adverse effects?
- high instance of GI problems
- interaction with renal excretion of lithium
A Cox-2 selective medication woudl be ____ and would be prescribed for:
1. meloxicam at mod-low dose, celecoxib, rolecoxib, or valdecoxib (Only 1st two on market wtih black boxes)
2. antiinflammatory, analgesia with fewer side effects? also lack anti-coagulant effects
Fenamates include ___ and ___ and would be prescribed when?
1. mfenamic acid, meclofenamate
2. never - no advantages and cause severe diarrhea, inflammation of bowel, and hemolytic anemia
Phenylbutazone is a _____, but use is limted due to:
- powerful anti-inflammatory
- side effects of agranulocytosis and aplastic anemia, insomnia, euphoria, nervousness.
- also interacts with warfarin, oral hypoglycemics, and sulfonamides
The only injectable NSAID is ____. What is important about this medication?
- Ketorolac
- high rate of GI bleed, only give 5 days at a time.
- decrease dose in elderly
___ inhibits prostaglandins int he CNS but little effects on COX in the periphery.
Describe the therapeutic properties of APAP
- analgesic
- antipyretic
- weak anti-inflammatory
- no anti-platelet effects
Decribe the pharmacokinetics of APAP
1. absorbed rapidly from GI
2. undergoes 1st pass metabolism and conjugated into inactive metabolites and sulfated metabolites
3. hydroxylated to N-BQI (reacts with sulfhydrl groups of glutahtione to form a non-toxic substance)
4. excreted in the urine
What occurs in an APAP OD?
- glutathione is depleted
- NBQI binds to sulfhydrl groups of hepatic proteins causing hepatic necrosis and renal tubular necrosis
What is used to counteract APAP OD? How much is too much APAP?
1. NAC (Mucomyst) - creats sulfhydryl groups for metabolite to bind
2. 3g/24h
What is the difference between physical dependence and addiction?
- physical dependence - effect of the drug is defined by occurrence of an abstinence syndrome after administrationof an antagonist, dose reduction, or discontinuation

Addiction - a behavioral pattern characterized by loss of control over drug use, compulsive use, and continued drug use despite harm
What is tolerance?
Diminution of a drug effect over time as consequesnce of exposure to the drug
What is pseudoaddiction?
Iatrogenic syndrome resulting from inadequate pain management. Patients engage in relief-seeking behaviors as though they are drug-seeking, but resolve upon appropriate analgesic therapy
Describe drug schedules
V- can sign for some at the pharmacy (uncommon), may or may not need RX (cough meds with codeine)
IV- low risk of abuse, can refill for 6 months
III - modreate risk, refill x 6 mos (Hydrocodone)
II - high risk for abuse, need Rx every month (MS, Oxy, methadone)
I - illegal agents, very high risk of abuse (cocaine, heroin)
Opiate drugs mimic actions of what 3 endogenous peptides-neurotransmitters?
1. endorphins
2. enkephalins
3. dynorphins
What are the four types of opiate receptors?
Mu, Kappa, Delta, Sigma
What are the effects at the Mu receptor?
Respiratory depression,
physical depression,
primary analgesia response
What are the effects at the kappa opiate receptor?
spinal-level analgesia and sedation
no respiratory depression
What are the effects at the sigma opiate receptor?
vasomotor stimulation
psychotomimetic effects
binds non-opioid agesnts
What are the effects at the delta opiate receptor?
enkephalons are more selective, esp at periphery
Opiates primarily work at what receptor?
Where are opiate receptors in teh body?
- brainstem
- thalamus
- spinal cord
- hypothalamus
-limbic system
- periphery
- immune cells
What are the three-classes of pure-agonist opiods?
1. phenanthrenes
2. phenylpiperidine
3. diphenylheptante
Why should you be careful about prescribing a partial agonist to a patient on a pure-agonist?
competetive inhibition can induce withdrawal and block effects
Partial opiate agonists are useful in which patients?
- opioid naiive pts - reduced side effects at mu receptor, but psychotomimetics due to efect at kappa
Phenanthrenes include which opiates?
morphine, hydropmorphone
An example of a phenylheptylamine is ___
Phenylpiperidines include:
meperidine, fentanyl
What is the MOA for morphine?
- interacts with specific opiate receptors in the CNS and GI (high affinity for Mu, low for sigma)
- inhibition of neurotransmitter release
- inhibit action of neurons conveying pain to higher brain centers
Describe the actions of morphine>
1. analgesia (reduce threshold, altered perception of pain)
2. euphoria (contentment, well-being)
3. Respiratory (depression due to reduced sensitivtiy of CO2 receptors)
4. depression of cough reflex (antitussive by other receptors)
5. miosis (mu and kappa)
Describe the effects of MS at:
1. GI
2. CV
3. Histamines
4. Hormones
1. stimulates vomiting receptor, relieves diarrhea, decreases GI motility (need stool softener)
2. bradycardia, hypotension, can increase CSF pressure
3. Urticaria, sweating, and vasodilation can ensue
4. Inhibits reproductive hormones, increases ADH
What are the therapeutic uses for moprhine?
- analgesia
- diarrhea (rare)
- cough (rare - usually codeine or dextromethorphan)
Morphine undergoes 1st pass effect, what is its active metabolite?
morphine-6-glucoronide = active, potent, and will buidl in pts iwth renal failure
What adverse reactions should you consider with morphine?
- respiratory and circulatory depression
- constipation
- worse in pts with RF
- sedation, dizziness, HOTN, N/v, sweating
- euphoria, dysphoria, dry mouth, syncope, urniary retention.
Morphine should be used with major caution in what patients?
- head injuries, ICP
- acute asthmatic attack, COPD
- BPH or urethral stricture
- elderly and neonates
- difficulty maintaining BP
Morpine interacts with which medications?
CNS depressants (ETOH, antipsychotics, benzos)
- cimetidine (increase serum concentrations)
__ is a synthetic opioid that binds to KAPPA receptors.
How does meperidine work?
Antimuscarinic, has excitant properties.
WHat is different about meperidine than other opiods?
- causes MYDRIASIS
- antimuscarinic effects
The active metabolite of meperidine is
When is meperidine usually given?
What adverse reactions should you look for in meperidine?
Seizures (esp in large doses, RF, hx of seizures, cancer pts)
Meperidine is contraindicated for ___
pts taking MAOIs in past 14-21 days
What drugs are interactions with meperidine?
MAOIs, Barbiturates, chlorpromazine (antipsych), phenytoin (decrease meperidine concnentratiosn and increase normeperidine concentrations)
Meperidine (should/should not) be used in pts with crhonic pain.
should NOT
__ is a synthetic opioid with same potentcy as morphine but less euphoria.
Methadone has its greatest action at ___ receptors
What is the therapeutic indicaition for methadone?
- analgesic substituted for morphine or heroin in controlled withdrawal
- long acting pain control
Cautions in the pharmacokinetics of methadone include ___
- variable kinetics and wide range of dose-equivalents
Adverse reactions to methadone and drug interactions include:
- ADR: increased risk for toxicity due to long half life
- inducers decrease methdone levels and effects
- inhibitors increase methadone levels and effects
Opiods are primarily metabolized by ___
Signs of methadone withdrawal include:
insomnia, dilated pupils, restlessness, yawning, diaphoresis, rhinorrhea, lacrimation
What are important elements regarding fentanyl?
- more potent than morphine
- delivered transdermal
- IV with droperidol in anesthesia
WHen would fentanyl be preferred?
When CV stability is an issue - no release of histamines
Fentanyl has interactions with what drugs?
CNS depressants
Inhibitors (increase effects)
Inducers (decrease effects)
___ is a prodrug that metabolizes to morphine.
__ is related to methadone, but has low efficacy and cardiovascular side effects.
____ can be used to manage diarrhea with limited abuse potential.
diphenoxylate, loperamide
What is buprenorphine?
Phenanthrene, partial agonist/antagonist, 20x more potent than morphine, slower effects, antagonizes resp depression caused by MS
What is butorphanol?
A partial agonist/antagonist Morphinan - Kappa agonist, more sedation than partial phenanthrines
What is pentazocine?
partial agonist/antangonist benzomorphan, mild mu and kappa agonist... may have dysphoria
Naloxone and Naltrexone are ____
opiate antagonists (aka antidotes!)
When would naltrexone be used?
as an opiate antagonist in opioid dependent maintenance program (long DOA up to 48 hours)
Why should you use caution using naloxone or naltrexone in those on opiates>
Could induce withdrawals
What is tramadol?
Weak mu agonist opiate,
inhibits norepi/ serotonin reuptake,
- useful in pts with allergies to other analgesic
Combination opiates are usually prescribed to what dose?
- lowest dose opiate/ max dose adjuvant (ibu, apap, )
Name 4 centrally acting skeletal muscle relaxants.
What is the difference between peripheral and central muscle relaxants?
Peripheral = paralysis
Central - relaxation with maintenance of voluntary movement
How do centrally acting muscle relaxants work?
Produce decreased muscle tone either
directly: on contractile mechanism of musculature
indirectly: transmission in spinal cord motor pathway, to elicit varying muscle relaxation
___ are used to relieve muscle spasms and hyperreflexia from inflammation, stress, or neurological disorders
Centrally acting skeletal muscle relaxants
Describe the MOA for peripheral acting muscle relaxants.
- interfere with cholinergic impulses between motor neurons and skeletal fibers at NMJ.
Name 2 peripherally acting muscle relaxants & indication
succinylcholine, cecuronium - primarily as adjuncts to general anestehsia in minor surgery or shock therapy