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76 Cards in this Set

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  • Back
In the brain, the _______________ is the relay station for incoming sensory stimuli, including pain.
-Brain Stem
-Cerebral Cortex
-Thalamus
-Hypothalamus
-Thalamus

-Brain Stem - Main connection between motor and sensory info btw the body and brain
-Cerebral Cortex - Memory, attention, though, etc. (outside layer of cerebrum)
-Hypothalamus - Links the nervous system w/the endocrine system via the pituitary gland (metabolism and autonomic NS)
What is activated by tissue damage and sends pain signals to the brain?
Nociceptors
What are the 2 causes of pain and how do they work?
Physical - Tissue injury
Chemical - Is released into fluids around nerves and stimulates them.
What are 2 chemicals that stimulate nerves to produce pain?
Prostaglandins - Fast-acting messenger molecules that are produced close to their target cells
Histamine - Inflammatory response
What 6 things do we assess when assessing pain?
1. Location
2. Duration
3. Characteristic
4. Severity
5. Onset
6. Aggravating/Alleviating Factors
What is the difference between Opioid and Nonopioid Analgesics?
Opioid - More powerful and are for moderate to severe pain
Non-opioid - For acute and chronic pain, neuropathic pain, and bone pain
What are characteristics of acute vs. chronic pain?
Acute - Often described as sharp or cutting pain
Chronic - Pain lasting longer than 3 months and is often not accompanied by visible signs of stress (adaptation)
Describe cancer, somatic, and visceral pain.
Cancer - Typically feels like a kind of pressure and can be acute or chronic
Somatic - Well-localized, sharp/burning/ throbbing pain that is associated with bone, skin, muscle, and soft tissue
Visceral - Damage to internal organs (ex. pancreatitis), is diffuse, not well-localized, deep/dull/aching
What characterizes neuropathic disease?
It is a chronic pain usually from damage to nerves. Usually a shooting, burning, or stabbing pain.
What else can be used to try to calm down the nerves reaction to stimulation? What disease might it be used for?
Anticonvulsants
Ex. Diabetic pain is from inappropriate stimulation of pain
What are the general characteristics of Opioid Analgesics?
-Relieve moderate to severe pain by inhibiting pain signal transition from periphery to brain
-Well-absorbed with PO, IM, and SubQ admin
-Metabolized in the Liver, metabolites excreted in the urine
-Exert widespread pharmacologic effects, esp. in the CNS and GI systems
What effects can Analgesics have on the CNS and GI systems?
CNS - Analgesia, CNS depression, respiratory depression, N/V, pupil constriction **Watch for pinpoint pupils!
GI Effects - Slow motility, constipation, bowel and biliary spasm
What are the Black Box Warnings for?
They are warnings for specific drugs, like opioids, that tend to produce a euphoria-like effect in people and are at a high risk for abuse. They also cause respiratory depression that can be fatal.
What are examples of opioids that have the Black Box Warning?
Duragesuc (fentanyl), Dilaudid (hydromorphone), Dolophine (methadone), Contin (morphine), Oxymorphone (oxycodone).
What are the indications, routes, and average doses for Narcan (nalaxone)?
Indication: To treat respiratory depression caused by opioids
Routes: IV, IM, SubQ
Tx: Intentional OD - 0.4mg over 30 seconds
Respiratory Depression - 10mL NS mixed with 0.4mg of Narcan. Give 0.5mL (0.02mg) over 1 minute, every minute.
Unconscious - Give full dose of 10mL bolus
What is the mechanism of action for opioids?
They relieve pain by binding to Mu receptors in the brain, spinal cord, and peripheral tissues to prevent pain impulses from reaching the brain.
What are the indications for opioids?
1. Prevent or relieve acute or chronic pain from trauma such as an acute MI, burns, traumatic injuries, cancer, and L&D
2. Pre- and PostOp - Used for sedation, antianxiety, anesthesia induction
3. To relieve pain from GI disorders, such as cramping and diarrhea (Lomotol)
4. To relieve a severe, unproductive cough (Codeine)
What are contraindications for opioids?
1. Existing respiratory depression
2. Severe chronic lung disease - monitor closely
3. Liver or kidney disease - can reach toxic levels easily
4. Prostatic hypertrophy - can create the inability to initiate a stream
5. Increased ICP - can create a further increase in ICP
6. Known hypersensitivity to opioids - monitor closely with the use of different opioids
After an IV injection of morphine, maximal analgesia and respiratory depression usually occur within:

- 1 minute
- 5 minutes
- 10-20 minutes
- 30 minutes
10-20 minutes
If it is the first time for the pt receiving an opioid, stay with them for the entire time period. If the pt has had opioids previously, make sure and go back to check on them
What drug is the prototype for opioids? What is it used for, how is it administered, and how is it metabolized and excreted?
Morphine!
It is used for moderate to severe pain, most often given IV or PO, and is metabolized in the liver and excreted in the kidneys. It is usually given 1-4mg IV.
Why is morphine toxicity an increased risk for the elderly and how can it manifest?
The elderly tend to have impaired liver and kidney function, which can cause metabolite accumulation and may produce prolonged sedation.
This can manifest in and increased fall risk, a decreased LOC, confusion, toxicity, etc.
For the different routes that morphine is administered, when does the maximum analgesia occur?
10-20 minutes after IV
30 minutes after IM
60 minutes after PO
60-90 minutes after SubQ
What is some general information concerning codeine?
It is weaker than morphine, but is given with Tylenol to suppress a nonproductive cough; given PO; and there are problems with metabolism: some people can't metabolize it for use (10-15%). It is not as widely used now.
What is general information concerning Fentynal?
It is potent and fast acting. It is used for pain, post surgical pain, PCA's, or in a patch for chronic pain (Duragesic). 25mcg is effective for 72h. DO NOT give as a first-time opioid and DO NOT cut patches in half! It can actually increase the dose to the pt.
Give general information about hydrocodone (Vicodin, Lortab).
It is combined with Tylenol (acetaminophen) - do not exceed dosage limits for both!! It is only given PO.
Give general information about hydromorphone (Dilaudid).
Very potent opioid, does not produce active metabolites. It is at least 8X more potent than morphine.
Give general information about meperidine (Demerol).
There are problems with toxic metabolites and CNS stimulation, especially in the elderly. They can build toxic levels faster and it can cause seizures.
Give general information about Methadone.
It has the longest duration of action, is used for severe pain and in treatment of addiction.
Give general information about oxycodone.
It is used alone or in combonation with Tylenol (Percocet). It is also available in short (Percocet, OxylR) or long-acting (OxyContin) formulations.
What are the 5 adverse effects of opioids?
Respiratory Deression
Hypotension
Excessive Sedation
N/V
Constipation
What are the 5 NI's for opioids?
-Assess LOC and RR before and after administration
-Ensure pt safety during and after administration
-Monitor BP before and after administration
-Prevent and treat constipation (Senakot or Pericholase)
-Educate pt about increased fall risks and instruct them to call for help if they need to get up
What are the 5 humane approaches for pain management?
-No person can suffer pain needlessly
-Pain occurs when the pt says it does
-Doses of opioids should be titrated to maximal effectiveness
-Psychological dependence and addiction rarely result from medications taken for physical pain
-Physical dependence can happen with opioids, but it is not an addiction
A nurse will typically have more than one choice in PRN pain medications to administer to a pt. What steps should she go through to decide which one to administer?
-Use a thorough pain assessment
-Use the least potent drug that is effective - with an acute onset of pain, you may want to use IV due to rapid onset of analgesia
-Use the least invasive route of administration possible (don't forget dose depends on route!)
What is Tramadol and what is it typically used for?
It is a low addiction opioid that doesn't cause euphoria-like effects. It is usually used for FM pain.
What is the bioavailability for PO vs IV administration of analgesics?
PO - 30%
IV - 100% availability because there is no Fist Pass
What is the Equanalgesic scale?
It gives related doses for different delivery methods
What are the 6 opioid dosing guidelines?
1. When an order includes a dose range, start with the lowest dose
2. Dosages change when opioids types are changed
3. Reduced dosages should be used for pt's already receiving CNS depressants (antianxiety, antidepressant, antihistamine, antipsychotic meds)
4. For constant, or chronic pain, scheduled dosing should occur - for intermittent pain or breakthrough pain, prn dosing is indicated
5. For severe, acute pain give a parenteral opioid at onset
6. Pre-medicate 1 hour ahead of painful activities, such as therapy
How is opioid dosing changed in opioid-tolerant patients?
A larger than usual dose is required to effectively treat pain - s/s of withdrawal will occur if an adequate dosage is not maintained
What are special considerations when giving opioids to older adults?
Use cautiously because there is an increased risk of respiratory depression, excessive sedation, and confusion
What are special considerations when giving opioids to children?
-Use age-appropriate assessment tools
-Perform more frequent and detailed assessments for adverse effects (dosages in children are less predictable)
-Use non-pharmacological interventions as much as possible
-Dilotid (hydromorphone), oxycodone, and Methadone are NOT indicated for children!
-Be very careful on drug calculations
What is wrong with this case study?
40-yr-old male, surgical repair of small bowel perforation
Hx depression (medicated), chronic back pain, chronic opioid use, chronic renal insufficiency
NG tube to suction, NPO
Med orders - OxyContin, crush and administer via NG tube q 12 h; hydrocodone/acetaminophen (Lortab, Vicodin), crush and administer via NG tube q 4 h prn for mild to moderate pain; meperidine (Demerol) IV q 3 h PRN for severe pain
-You can't crush OxyContin (extended release tablet), it can cause CNS excitation
-There is no dose given on the orders
-PO doesn't work due to probable low motility, which means low absorption
-Antidepressants can increase the chance of CNS depression
-Chronic use of opioids can require an increased dose to prevent DT's and treat pain
What is considered severe pain?
How about moderate pain?
Severe - >8
Moderate - 4-7
Mild - <4
Prostaglandins are chemical mediators found in most body tissues and exert all of the following except:
-Increased platelet aggregation
-Gastroprotection
-Increased body temperature
-Decreased pain sensitivity
**Decreased pain sensitivity
Name 5 antiprostaglandin drugs (NSAID'S):
1. Aspirin
2. Ibuprofen
3. Keterolac (Tordol)
4. Indomethacin
5. Celecoxib
What is the mechanism of action for NSAID's?
They inhibit prostaglandin synthesis in the CNS and PNS by inhibiting COX-1 and COX-2 enzymes, which are required for prostaglandin production
Where do prostaglandins come from and why? What do they do?
They come from mast cells that are responding to stimulation within tissues. Mast cells begin to produce mediators when activated, like prostaglandins. Prostaglandins cause increased vascular permeability, neutrophil chemostaxis, and pain by direct effect on nerves.
What are COX-1 and COX-2 enzymes and why do they need to be inhibited? What inhibits them?
COX-1 enzymes convert chemicals to prostaglandins and decrease platelet aggravation ???????`
COX-2 enzymes are released from inflammatory cells and produce prostaglandins, which result in inflammation and pain. ASA, ibuprofen, and other NSAID's inhibit COX-2.
What are the indications of NSAID's?
They relieve pain by acting centrally and peripherally to block impulse transimission.
They are used to relieve fever by decreasing hypothalamic response and resetting the "thermostat" to lower levels
Non-selective NSAID's have an antiplatelet effect and decrease the inflammatory response
What are 4 specific indications for NSAID's?
-Inflammatory disorders (DJD, OA, RA)
-Mild to moderate pain (HA, minor trauma, minor surgery)
-Fever (ASA is NOT used in children d/t Reye's syndrome which causes encephalopathy)
-Suppress of platelet aggregation (once daily low dose -81mg- is used for MI and stroke prevention and is shown to be just as effective
What are 6 contraindications for NSAID's?
-Peptic ulcer disease
-GI or other bleeding disorders (low platelets)
-Impaired renal function (these are nephrotoxic and increase the workload of the kidneys)
-Hypersensitivity to ASA (an allergic response is usually an adverse effect)
-Do NOT give to children!
-Pregnancy (use with extreme caution, ketoralac (Toradol) is NEVER used!) Results could be increased bleeding for mom and decreased birth weight and death for the fetus
What are 4 adverse effects of NSAID's?
-GI: bleeding, N/V, ulceration
-Tinnitus, especially with large doses of ASA
-Nephrotoxicity
-Rash, itching (most common)
What are 4 NI's concerning NSAID's?
-Assess for allergies
-Assess for adverse effects of bleeding or decreased renal function
-Give with food to avoid GI irritation
-Ensure adequate fluid intake
When looking at renal function and bleeding risks concerning NSAID's, what specific items are we looking at?
Renal function - look at the BUN (will be lowered), creatinine (will be high), and I&O proportions
Bleeding - Refer to the H&H, low systolic BP, increased HR, blood in vomit or tarry stools (do a hemocult)
What are 4 NSAID interactions?
-They decrease the effect of antihypertensives, diuretics, ACE inhibitors, and beta blockers
-They increase the effect of anticoagulants
-They increase the risk of bleeding when taken with herbal remedies such as ginkgo and ginseng
-Ibuprofen may limit the cardioprotective effect of ASA!
What are the adverse effects and actions of COX-1 inhibitors?
-Renal toxicity
-GI toxicity
-Inhibition of platelet aggregation
What are the adverse effects and actions of COX-2 inhibitors?
-We do have selective COX-2 inhibitors (Celebrex -celecoxib), not selective COX-1
-Less renal/GI toxicity or antiplatelet activity
-But, increased risk of CV thrombotic events (MI or stroke)
-Contraindicated with sulfa allergy
What is general information about non-selective and selective COX-2 inhibitors?
-Non-selectives are COX-1 and -2 inhibitors and carry the adverse effects of both
-Selective COX-2 inhibitors don't cause the GI effects, but carry an increased risk for thrombosis and stroke (Vioxx, Celebrex)
What is the good news vs. the bad news concerning acetaminophen?
-Good news: does not cause GI bleeding or N/V, or interfere with blood clotting. Equal to ASA in analgesic and antipyretic effects
-Bad news: no anti-inflammatory properties, small amounts of toxic metabolites remain in the body after being metabolized in the liver, dose limit is 4 Gm/24 hours, which CANNOT be exceeded - there are further dose limits for liver impairment or hx of ETOH abuse
What is an overview of acetaminophen metabolism and possible toxic effects?
-2% of the drug is excreted unchanged
-94% is excreted as non-toxic metabolites
-Toxic metabolites can be produced from microenzymes produced by excessive ETOH and phenobarbitol
-Glutathione normally metabolizes the drug to non-toxic metabolites, but we only have enough to metabolize 4 Gm/24 h - acetaminophen overdose and excessive ETOH use deplete glutathione and more toxic metabolites are produced
Acetaminophen toxicity may occur with:

-A single large dose
-Chronic excessive doses
-Therapeutic doses in those who abuse ETOH
-All of the above
**All of the above
-As little as 6 Gm can cause toxicity problems, usually > 10 Gm, though
-Lower therapeutic doses can end up causing problems, too
State information regarding acetaminophen toxicity:
-May be accidental or intentional
-s/s are nonspecific (prior to liver effects)
-Later manifestations include: jaundice, vomiting, CNS stimulation with excitement and delirium followed by coma and death (hepatic encephalopothy)
What are the treatment options for acetaminophen toxicity?
-Gastric lavage and activated charcoal within 4 hours
-Acetylcysteine (Mucomyst) given orally (tastes horrible) or by IV - Inhaled version of Mucomyst is to thin secretions, not for an OD!
-Tx is most beneficial 8-10 hours after OD, may be helpful within 36 hours
-DOES NOT reverse damage already sustained!
What are some herbal and dietary supplements that can be tried for analgesia?
-Chondroitin and glucosamine - thought to delay breakdown of joint cartilage and stimulate the synthesis of new cartilage, and may help in moderate to sever OA pain
-Capsicum (Cayenne) is thought to reduce pain by depleting Substance P, a mediator in the transmission of pain impulses - it is applied topically and should NOT be applied during pregnancy
Case Study:
76-yr-old female complains of increased pain in right knee
Dx: OA Hx: HTN
Meds: New to this visit - ibuprofen, currently taking a diuretic and ACE inhibitor, Glucosamine/chondroitin, ginkgo, ginseng, and ASA to prevent MI
What are the considerations with this case?
-May need to increase the dose of ibuprofen due to an ACE inhibitor
-ASA, ginkgo, and ginseng interact! Have to decide if she wants pain relief at night, or increased energy during the day
-ASA effects are decreased due to the ibuprofen
-Pt education plan: Monitor BP, stop herbals instead of taking more medication, watch for blood in stools, anemia, decreased RBC's, decreased renal function (drink at least 2 L/day of fluids, when to notify the physician
Define analgesia:
Relief of pain
Define breakthrough pain:
Intense pain that comes on suddenly, lasts for a shorter period of time, and is not controlled by the pt's current pain medication.
Define endogenous analgesia system:
The body's system for relieving pain by suppressing the transmission of pain signals from the PNS to the CNS; may also inhibit pain signals at other points in the pain pathway.
Define endorphins:
Peptides found in the brain that interact with opioid receptors to inhibit perception and transmission of pain signals.
Define neuropathic:
Pain that is caused by lesions or physiologic changes that injure peripheral pain receptors, nerves, or the CNS.
Define nociceptors:
Pain receptors that are abundant in arterial walls, joint surfaces, muscle fascia, periosteum, skin, and soft tissues; they are scarce in most internal organs.
Define non-ceiling opioid:
Opioid with no upper limit to the dosage that can be given to pt's who have developed tolerance to previous dosages.
Define opioid receptors:
Delta, kappa and mu receptors located in the b rain and spinal cord; endogenous opioids as well as opioid meds serve as ligands.
Define ligand:
Neurotransmitters as well as meds and hormones that can bind to receptors in the ANS.
Define pain:
Unpleasant, uncomfortable sensation that usually indicates tissue damage and impels a person to remove the cause of the damage or seek relief from the pain.
Define patient-controlled analgesia:
A pump that allows the pt to self-administer pain meds through the push of a button on an infusion pump; the amount of drug in each dose delivered is preset and limited.
Define tolerance:
Patients who have developed drug tolerance through long-term use of lower doses.