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Review: Drug-Receptor Interactions. What is a receptor?Drugs bind to receptor and cause specific activity of cell to be either enhances or inhibited.What is:An AgonistA Partial AgonistAn Antagonist. Pain Management. What is essential to successfully manage pain?What does pain management therapy depend upon? Describe a comprehensive pain assessment.How is pain classified?.
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1. Unit III: The Nervous System Chapter 18
Drugs for Control of Pain
2. Review: Drug-Receptor Interactions What is a receptor?
Drugs bind to receptor and cause specific activity of cell to be either enhances or inhibited.
What is:
An Agonist
A Partial Agonist
An Antagonist Receptor: “cellular macromolecule to which a medication binds to initiate its effect” ; most are proteins; drugs attach in a specific manner (lock and key)
Bound drugs can either directly enhance or inhibit a cell or may initiate a second messenger event which will start a biochemical cascade which will initiate the drug action by stimulating or inhibiting normal cell activity.
Agonist: same response as endogenous substance; stimulates a particular receptor
Partial agonist: produces weaker, or less efficacious response that an agonist
Antagonist: prevents endogenous chemical from acting; blocks receptorsReceptor: “cellular macromolecule to which a medication binds to initiate its effect” ; most are proteins; drugs attach in a specific manner (lock and key)
Bound drugs can either directly enhance or inhibit a cell or may initiate a second messenger event which will start a biochemical cascade which will initiate the drug action by stimulating or inhibiting normal cell activity.
Agonist: same response as endogenous substance; stimulates a particular receptor
Partial agonist: produces weaker, or less efficacious response that an agonist
Antagonist: prevents endogenous chemical from acting; blocks receptors
3. Pain Management What is essential to successfully manage pain?
What does pain management therapy depend upon?
Describe a comprehensive pain assessment.
How is pain classified? To successfully manage pain
Must accurately assess the degree of pain experienced and the potential underlying disorders that may be causing pain
Therapy is dependent upon: nature and character of pain
Comprehensive pain assessment includes:
Onset and duration
Location
Intensity
Quality
Relief measures (facilitating factors)
Contributing symptoms (precipitating factors)
Effects of pain on client
Client expectations
Classifications:
Acute vs. Chronic
Nociceptor vs. neuropathic
Other sources include cancer pain or idiopathic pain To successfully manage pain
Must accurately assess the degree of pain experienced and the potential underlying disorders that may be causing pain
Therapy is dependent upon: nature and character of pain
Comprehensive pain assessment includes:
Onset and duration
Location
Intensity
Quality
Relief measures (facilitating factors)
Contributing symptoms (precipitating factors)
Effects of pain on client
Client expectations
Classifications:
Acute vs. Chronic
Nociceptor vs. neuropathic
Other sources include cancer pain or idiopathic pain
4. Compare and Contrast Nociceptor Pain and Neuropathic Pain Nociceptor
Injury to tissues
Somatic: sharp, localized sensations
Visceral : generalized, dull, throbbing or aching
Responds well to conventional pain relief medications Neuropathic
Injury to nerves
Burning, shooting or numb
Less therapeutic response to conventional pain relief medications
5. Nonpharmacologic Techniques May replace or be an adjunct to pharmacotherapy
How does the concurrent use of nonpharmacologic therapies impact pharmacotherapy? Impact– may allow for lower medication doses and possibly fewer side effects Impact– may allow for lower medication doses and possibly fewer side effects
6. Neural Mechanism of Pain Pain receptor (nociceptor) is stimulated
Nerve impulse signaling pain is sent to spinal cord along Ad (myelinated, signal sharp, well-defined pain)
and C (unmyelinated, conduct dull, poorly localized pain) fibers
Neurotransmitters pass message along to next neuron
Opioids (enkephalins, dynorphins, endorphins)
Serotonic
Norepinephrine
Descending neurotransmitters have an inhibitory effect and modify sensory information at level of spinal cord
This process of the pain signal beginning at nociceptors within the peripheral tissues and proceeding to the CNS allows several opportunities (targets) for pharmacologic intervention Pain receptor (nociceptor) is stimulated
Nerve impulse signaling pain is sent to spinal cord along Ad (myelinated, signal sharp, well-defined pain)
and C (unmyelinated, conduct dull, poorly localized pain) fibers
Neurotransmitters pass message along to next neuron
Opioids (enkephalins, dynorphins, endorphins)
Serotonic
Norepinephrine
Descending neurotransmitters have an inhibitory effect and modify sensory information at level of spinal cord
This process of the pain signal beginning at nociceptors within the peripheral tissues and proceeding to the CNS allows several opportunities (targets) for pharmacologic intervention
7. Analgesics Classes of Pain Medications
NSAIDs
Opioids
Action results from interaction with receptors
Mu-1 and Mu-2
Kappa
Sigma
Delta
Epsilon Non-steroidal anti-inflammatory drugs: Aspirin and Ibuprophen
Opioids- natural (opiates) or synthetic morphine-like substances; aka: narcotics
The mu and kappa receptors are most important to pain management Non-steroidal anti-inflammatory drugs: Aspirin and Ibuprophen
Opioids- natural (opiates) or synthetic morphine-like substances; aka: narcotics
The mu and kappa receptors are most important to pain management
8. Compare and Contrast Responses Mu
Analgesia
Decreased GI motility
Euphoria
Physical dependence
Respiratory depression
Sedation Kappa
Analgesia
Decreased GI motility
Miosis
Sedation Miosis: constriction of the pupil secondary to contraction of the iris
What is similar? Both cause analgesia, decreased gi motility, and sedation
What is different? Kappa causes miosis and doesn’t cause euphoria, physical dependence, or respiratory depression
Mu does not cause miosisMiosis: constriction of the pupil secondary to contraction of the iris
What is similar? Both cause analgesia, decreased gi motility, and sedation
What is different? Kappa causes miosis and doesn’t cause euphoria, physical dependence, or respiratory depression
Mu does not cause miosis
9. Prototype Opioid: Morphine See box on page 228
Produces analgesia, cough suppression and decreased GI motility
CNS depressant
Adverse effects
Respiratory depression
Sedation
Nausea and vomiting CNS effect:
Sedation
Euphoria
Intense relaxation
Euphoria and relaxation are key reasons the drug is abusedCNS effect:
Sedation
Euphoria
Intense relaxation
Euphoria and relaxation are key reasons the drug is abused
10. Risk of Dependence All narcotic (opioid) analgesics have the potential to cause physical and psychological dependence.
What factors increase the likelihood of developing dependence Factors
Larger doses over extended period of timeFactors
Larger doses over extended period of time
11. Case Study Mr. J, a 56-year-old, had an inguinal hernia repair through ambulatory surgery. His discharge medications included Vicodin (hydrocodone 5 mg and acetaminophen 500 mg) one or two tablets every 4 hours prn.
What is the drug classification for this medication? Analgesic: opioid and non-opioidAnalgesic: opioid and non-opioid
12. Combination Drugs Opioid + non-opioid (non-narcotic) analgesics
What is the reason to combine these medications?
What are the benefits of combined analgesics? Reasons: Together they have a synergistic effect (one substance augments or adds to the activity of the other)
Benefits: Can use a lower dose of the narcotic and avoid dependence and avoid or decrease opioid related side effects Reasons: Together they have a synergistic effect (one substance augments or adds to the activity of the other)
Benefits: Can use a lower dose of the narcotic and avoid dependence and avoid or decrease opioid related side effects
13. Nursing Considerations: Opioids Carefully monitor client’s condition
Provide education as it relates to the prescribed drug treatment
Assess current and past history
Diagnostics
Baseline and continuing VS
Comprehensive pain assessment before administration Assess for presence or history of:
Severe respiratory disorders
Increased ICP
Seizures
Liver or renal disease
Allergies
Current meds (especially alcohol and CNS depressants)
Diagnostics:
CBC
LFT– ALT, AST, Amylase, bilirubin
RFT
VS: monitoring for respiratory depression cause by mu receptor activation; monitor for decreased LOC
Assess for presence or history of:
Severe respiratory disorders
Increased ICP
Seizures
Liver or renal disease
Allergies
Current meds (especially alcohol and CNS depressants)
Diagnostics:
CBC
LFT– ALT, AST, Amylase, bilirubin
RFT
VS: monitoring for respiratory depression cause by mu receptor activation; monitor for decreased LOC
14. Nursing Considerations: Opioids Have narcotic antagonist and resuscitative equipment available
Ensure safety
Monitor for urinary retention
Can cause constipation and Nausea/Vomiting
Do not administer in infectious diarrheal illnesses Narcotic antagonist: naloxone hydrochloride (Narcan)
Safety: bed in low position, side rails up
Closely monitor I&O and check for bladder distention
Will need to institute measures to prevent or treat constipation
Antiemetics can be used to treat n/v
GI pathogens produce toxins which are shed in the stool, constipation or decreased gi motility would cause the toxins to build up Narcotic antagonist: naloxone hydrochloride (Narcan)
Safety: bed in low position, side rails up
Closely monitor I&O and check for bladder distention
Will need to institute measures to prevent or treat constipation
Antiemetics can be used to treat n/v
GI pathogens produce toxins which are shed in the stool, constipation or decreased gi motility would cause the toxins to build up
15. Contraindications: Opioids Hypersensitivity
Do not administer if:
Acute asthma or upper respiratory obstruction
Respiratory rate < 12
16. Case Study Miss N, 86-years-old, weighs 96 lbs. They physician has ordered 10 mg of morphine sulfate IM for acute abdominal pain. Your are familiar with the drug and know that the ED50 is 10 mg. Miss N’s VS are: 98.6°- 80 – 22, 120/80. Thirty minutes after administering the medication you return to evaluate its effectiveness. You note that Miss N had a decrease in LOC and VS are 98.6° - 68 – 8, 112/60.
17. Case Study Questions What will you do first?
What other things must be done?
Was a medication error made?
What factors may have contributed to Miss N’s response? First:
Stimulate breathing
Prepare to administer naloxone (Narcan)– opioid antagonist to block opioid activity and reverse symptoms of opioid toxicity or overdose
Other things:
Closely monitor respiratory status
Be prepared to initiate resuscitation
Error?
The order was for 10 mg which is the standard dose
Contributing factors:
Age and weight of the patient
Renal and hepatic function may have been impaired
She was outside the 50% who respond to the standard (ED50) dose First:
Stimulate breathing
Prepare to administer naloxone (Narcan)– opioid antagonist to block opioid activity and reverse symptoms of opioid toxicity or overdose
Other things:
Closely monitor respiratory status
Be prepared to initiate resuscitation
Error?
The order was for 10 mg which is the standard dose
Contributing factors:
Age and weight of the patient
Renal and hepatic function may have been impaired
She was outside the 50% who respond to the standard (ED50) dose
18. Nursing Role: Opioid Antagonist Therapy Carefully monitor patient condition
Provide education as it relates to prescribed drug treatment
Administer if RR < 10
Have resuscitative equipment immediately accessible
Gather good medical history
Underlying cardiovascular disease
19. Nursing Role: Opioid Antagonist Therapy Use cautiously in patients physically dependent upon opioids
Comprehensive pain assessment before administration and during treatment
VS every 3-5 minutes
ABGs, ECG
Monitor for drowsiness, tremors, hyperventilation, VT and loss of analgesia Opioid dependent patients will experience more severe opioid withdrawal symptoms after receiving an opioid antagonist
Monitor for s/s of opioid withdrawal: cramping, vomiting, HTN, anxietyOpioid dependent patients will experience more severe opioid withdrawal symptoms after receiving an opioid antagonist
Monitor for s/s of opioid withdrawal: cramping, vomiting, HTN, anxiety
20. Opioid Antagonist Drugs Prototype: naloxone hydrochloride (Narcan)
See box p. 231
Naltrexone
Used for treatment of addiction
Monitor for side effects during RX
VS q 3 – 5 min
Continuous assessment of respiratory and cardiac function Side effects: (opioid withdrawal s/s)- increased thirst, chills, fever, joint/muscle pain, CNS stimulation, drowsiness, dizziness, confusion, seizures, headache, n/v, diarrrhea, rash, tachycardia, tachypnea, pulmonary edema, wheezing)Side effects: (opioid withdrawal s/s)- increased thirst, chills, fever, joint/muscle pain, CNS stimulation, drowsiness, dizziness, confusion, seizures, headache, n/v, diarrrhea, rash, tachycardia, tachypnea, pulmonary edema, wheezing)
21. Compare and Contrast Opioid Tolerance and Opioid Dependence
How is opioid dependence treated? Tolerance:
biologic condition; body adapts to substance after repeated administration
Over time higher doses are required to produce the same initial effect
Common for substances that affect the CNS
Natural consequence, not evidence of addiction
Dependence:
When a person has an overwhelming desire to take a drug and cannot stop
Higher and more frequent doses quickly cause physical dependence
As an individual develops tolerance, dosages will be increased in amount and frequency and physical dependence is more likely
Treatment:
Methadone (Dolophine) maintenance
Does not cure dependence
Must continue drug to avoid withdrawal symptoms
Allows individual to return to productive work and social relationships Tolerance:
biologic condition; body adapts to substance after repeated administration
Over time higher doses are required to produce the same initial effect
Common for substances that affect the CNS
Natural consequence, not evidence of addiction
Dependence:
When a person has an overwhelming desire to take a drug and cannot stop
Higher and more frequent doses quickly cause physical dependence
As an individual develops tolerance, dosages will be increased in amount and frequency and physical dependence is more likely
Treatment:
Methadone (Dolophine) maintenance
Does not cure dependence
Must continue drug to avoid withdrawal symptoms
Allows individual to return to productive work and social relationships
22. Non-opioid Analgesics Acetaminophen
NSAIDs
Ibuprofen and ibuprofen type
Salicylates: ASA
Centrally acting agents
Clonidine (Catapres)
Tramadol (Ultram) Acetaminophen–
analgesic and anti-pyretic, not an anti-inflammatory;
Prototype- see box p 479
Ibuprofen
Analgesic, anti-inflammatory, and anti-pyretic activity
Inhibit cyclooxygenase (enzyme responsible for formation of prostaglandins)
Less effect on COX-1 so produces less gastric bleeding
Drug of choice for mild to moderate pain (esp. pain associated with inflammation)
Inhibit pain mediators at nociceptor level (peripheral)– figure 18.3. p. 234
Long term use can reduce renal function (damages nephrons)
Tissue damage occurs
Chemical mediators are released (histamine, potassium ions, hydrogen ions, bradykinin, and prostaglandins)
Bradykinins are associated with sensory impulse of pain and prostaglandins induce pain through formation of free radicals
Salicylates
ASA is prototype, see box p. 235
Inhibits both COX-1 and COX-2– so is more likely to cause peptic ulcer and GI bleeding and Acute renal failureAcetaminophen–
analgesic and anti-pyretic, not an anti-inflammatory;
Prototype- see box p 479
Ibuprofen
Analgesic, anti-inflammatory, and anti-pyretic activity
Inhibit cyclooxygenase (enzyme responsible for formation of prostaglandins)
Less effect on COX-1 so produces less gastric bleeding
Drug of choice for mild to moderate pain (esp. pain associated with inflammation)
Inhibit pain mediators at nociceptor level (peripheral)– figure 18.3. p. 234
Long term use can reduce renal function (damages nephrons)
Tissue damage occurs
Chemical mediators are released (histamine, potassium ions, hydrogen ions, bradykinin, and prostaglandins)
Bradykinins are associated with sensory impulse of pain and prostaglandins induce pain through formation of free radicals
Salicylates
ASA is prototype, see box p. 235
Inhibits both COX-1 and COX-2– so is more likely to cause peptic ulcer and GI bleeding and Acute renal failure
23. Nursing Role: Non-opioid Analgesics Thorough assessment
Monitoring
Diagnostics
Baseline and continuing comprehensive pain assessment
Give with food and plenty of fluids
Do not crush enteric coated tablets
Use extreme caution with ASA in children and teenagers Assess for presence or history of:
Hypersensitivity
Bleeding disorders
Peptic ulcer disease
Severe renal/hepatic disease
Pregnancy
Monitor for:
Nephrotoxicity
Blood dyscrasias
Hepatitis
Allergic response
n/v; anorexia; dizziness; drowsiness
Diagnostics: (assess before and during pharmacotherapy)
RFTs- BUN, creatinine
LFTs- AST, ALT
Hemoglobin
ASA:
Implicated in development of Reye’s syndrome
Toxicity can develop rapidly in febrile and dehydrated children Assess for presence or history of:
Hypersensitivity
Bleeding disorders
Peptic ulcer disease
Severe renal/hepatic disease
Pregnancy
Monitor for:
Nephrotoxicity
Blood dyscrasias
Hepatitis
Allergic response
n/v; anorexia; dizziness; drowsiness
Diagnostics: (assess before and during pharmacotherapy)
RFTs- BUN, creatinine
LFTs- AST, ALT
Hemoglobin
ASA:
Implicated in development of Reye’s syndrome
Toxicity can develop rapidly in febrile and dehydrated children
24. Headaches Two major types:
Tension
Migraine
Migraine treatment goals:
Stop migraine in progress
Prevent migraine from occuring Tension:
Self-limiting
Treated with OTC analgesics
Migraine:
Painful headache caused by dilation of intracranial vessels
Accompanied by n/v
Sometimes preceded by aura
Often associated with triggers
Tension:
Self-limiting
Treated with OTC analgesics
Migraine:
Painful headache caused by dilation of intracranial vessels
Accompanied by n/v
Sometimes preceded by aura
Often associated with triggers
25. Migraine Treatment Triptans
Ergot alkaloids
Ergot alkaloids are a Category X drug. What does that mean? Triptans and ergot alkaloids are serotonin agonists
To terminate migraine:
Start with OTC acetaminophen or NSAIDs
If unable to abort– triptans (sumatriptan {Imitrex})
If unresponsive to triptans– ergot alkaloids
Category X:
Teratogenic; harmful to fetus, do not use in pregnancy
Triptans and ergot alkaloids are serotonin agonists
To terminate migraine:
Start with OTC acetaminophen or NSAIDs
If unable to abort– triptans (sumatriptan {Imitrex})
If unresponsive to triptans– ergot alkaloids
Category X:
Teratogenic; harmful to fetus, do not use in pregnancy
26. Migraine Prophylaxis Will be used if person has high incidence of migraines and is unresponsive to drugs to abort migraine.
Beta blocker
Propranolol (Inderal)
Tricyclic antidepressant
Amitriptyline hydrochloride (Elavil) Amitriptyline is drug of choice if accompanying mood disorder and insomnia
Table 18.4, p. 238
May also prescribe calcium channel blocker, or depakote (antiseizure medication)Amitriptyline is drug of choice if accompanying mood disorder and insomnia
Table 18.4, p. 238
May also prescribe calcium channel blocker, or depakote (antiseizure medication)
27. Role of Nurse: Migraine Pharmacotherapy Carefully monitor client’s condition
Provide education as it related to prescribed drug treatment
Gather data
Assess
Alter environment
Monitor for possible side effects Gather data:
Frequency and intensity
Presence or history of: MI, angina, HTN, renal or liver disease, diabetes, pregnancy
Assess:
Apical pulse, RR, BP
Stress level and coping
Hypersensitivity
Use of MAOIs, SSRIs (can increase effect of triptans)
Neuro status (LOC, blurred vision, n/v, tingling in extremities
Provide:
Quiet, calm environment with decreased noise and subdued lighting
Limit disruptions
Decrease neural stimulation
Cold packs
Side effects:
Dizziness, drowsiness, vasoconstriction, warming sensation, tingling, light headedness, weakness, neck stiffness Gather data:
Frequency and intensity
Presence or history of: MI, angina, HTN, renal or liver disease, diabetes, pregnancy
Assess:
Apical pulse, RR, BP
Stress level and coping
Hypersensitivity
Use of MAOIs, SSRIs (can increase effect of triptans)
Neuro status (LOC, blurred vision, n/v, tingling in extremities
Provide:
Quiet, calm environment with decreased noise and subdued lighting
Limit disruptions
Decrease neural stimulation
Cold packs
Side effects:
Dizziness, drowsiness, vasoconstriction, warming sensation, tingling, light headedness, weakness, neck stiffness
28. Contraindications to Anti-migraine Therapy Hypertension
Myocardial ischemia
Coronary artery disease
History of MI
Dysrhythmias or heart failure
High-risk CAD profile
Diabetes Ergot alkaloids
Promote vasoconstriction
Side effects include:
n/v, weakness in legs, myalgia, numbness and tingling in fingers and toes, angina-like pain, tachycardia
Toxicity is evidenced by peripheral artery constriction (cold, pale and numb extremity with muscle pain)
Long term use can cause physical dependenceErgot alkaloids
Promote vasoconstriction
Side effects include:
n/v, weakness in legs, myalgia, numbness and tingling in fingers and toes, angina-like pain, tachycardia
Toxicity is evidenced by peripheral artery constriction (cold, pale and numb extremity with muscle pain)
Long term use can cause physical dependence