Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
74 Cards in this Set
- Front
- Back
|
T/F Pain is just nociception
|
False
Pain is more than nociception. It includes emotional and psychological aspects. |
|
|
What is the best way to tx pain
|
Multimodal approach
Surgical Behavioral Medical Physical Invasive Pain management Financial, etc |
|
|
Tx modalities for pain
|
Numerous
Medication Manipulative Therapy Physical Therapy Biofeedback Hypnosis Relaxation Techniques Guided Imagery Neurolysis (cryoprobe, radiofrequency) Injection of neurolytic substances (iced saline, phenol, alcohol, etc.) Spinal cord stimulation Injection of steroids Injection of local anesthetics Maintenance opioids Intrathecal opioids |
|
|
T/F we are currently sufficiently controlling post op pain.
|
False
Studies show that currently post op pain is NOT being controlled. |
|
|
Differentiate Acute Pain and Chronic Pain
|
ACUTE PAIN
* Short Duration * Identifiable Pathology * Serves a clear purpose * Predictable prognosis * Treated with 'conventional' analgesics CHRONIC PAIN * Long duration (mths - yrs) * Pathology may be unclear * Serves no biological purpose * Unpredictable prognosis * Treatment must be multidisciplinary |
|
|
Shat are the three types of pain and what are there subtypes?
|
1) NOCICEPTIVE PAIN: Caused by tissue damage. Usually time limited and responds to drug treatment.
--->Somatic Pain ---> Visceral Pain 2) NEUROPATHIC PAIN - caused by a primary lesion in the CNS ---> Centrally mediated ---> Peripherally mediated 3) IDIOPATHIC PAIN ---> Cannot find a cause. |
|
|
Pain of bones, joints, muscle skin, or connective tissue that is aching and throbbing and well-localized is...
|
Somatic Pain
|
|
|
If visceral pain is due to a tumor of an organ capsule how does it feel?
|
It's localized and aching.
|
|
|
If visceral pain is due to an obstruction of a hollow organ, how does it feel?
|
It is Poorly localized, intermittent and cramping.
|
|
|
What is referred pain?
|
Visceral pain referred to a somatic surface.
|
|
|
Pain from phantom limb and Burning below the level of a spinal cord lesion is what type of pain?
|
Deafferentation pain.
This is a type of Centrallly mediated neuropathic pain. |
|
|
Chronic Regional Pain Syndrome (CRPS) is what type of pain?
|
Sympathetically maintained pain (via a dysregulation of the ANS).
|
|
|
Painful polyneuropathies are what type of pain..
|
Peripherally mediated pain
Caused by demyelination or axonal loss. Can occur across mx nerves in diabetes, alcoholism, Guillian-Barre, chemotherapy |
|
|
Painful mononeuropathies are what type of pain?
|
Peripherally mediated pain neuropathic pain.
Single nerves are compressed, entraped, or trigeminal neuralgia. |
|
|
What are the four steps of nociception?
Describe them. |
1) TRANSDUCTION
---> Tissue damage occurs. There is a release of prostaglandins, bradykinin, histamines, and substance P at the site of injury. These activate an AP via nociceptors at nerve endings (Delta and C fibers). 2) TRANSMISSION ---> AP's travel up afferent nerve into the spinal cord. AP is transferred to a second order neuron. This neuron ascends the SPINOTHALAMIC TRACT to the THALAMUS (relax station) and then the AMYGDALA, and CEREBRAL CORTEX. 3) PERCEPTION ---> AP reaches the thalamus and cortex, etc. There is localization of the injury within the somatosensory cortex. The amydala and limbic system provide an emotional context to the pain. 4) MODULATION ---> The brain responds to the sensory inputs by triggering descending pathways (periaqueductal grey) that can modulate and moderate pain signals by decreasing serotonin and NE release. Descending endogenous pain analgesia tracts are also stimulated they activate enkaphalin- containing interneurons in the DORSAL HORN of the spinal cord. The enkaphalins inhibit the nociceptor fibers that synapse here from secreting Substance P onto the second order neuron, so no pain signal is transmitted. |
|
|
Describe the 2 types of nociceptor fibers.
|
A-delta: Small diameter, myelinated fibers--> FIRST PAIN: sharp, shooting.
C-fibers: Small diameter, unmyelinated fibers (slower)-->SECOND PAIN: dull, throbbing, happens several minutes after you injure yourself. |
|
|
What are the 3 ways that descending endogenous pathways block pain and what does this mean for medication for pain?
|
Via the release of
1) Enkephalins - bind to mu receptors...opiods mimic them 2) Serotonin - therefore, SSRI's could actually treat pain. 3) a2 Adrenergic - therefore Alpha 2 Agonists could actually block pain. |
|
|
Tell me all the places where local anesthetics can have action...
|
Dorsal Horn of the spinal cord (epidural or spinal)
Periperal Nerves At the site of Tissue Damage (injected locally) (They work on the nerve itself...block Na channels). |
|
|
Where is the site of action of NSAIDS?
|
At the site of tissue injury...inhibit prostaglandin release.
|
|
|
Where is the site of action of Alpha2 Agonists for medication of pain?
|
Dorsal Ganglia of the spinal cord.
Inhibits NE release, so it decreases transmission of the pain signal. |
|
|
Opiods work at what areas of the body to medicate pain?
|
In the brain.
Dorsal root ganglia of the spinal cord. (Peripheral Opiods injected at the site of injury). |
|
|
What all meds work at the site of tissue injury to medicate pain?
|
NSAIDS
Antihistamines Capsaicin Peripherally Restricted Opiods |
|
|
What all meds work at the Dorsal Root GAnglion of the spinal cord to medicate pain?
|
Opiods
LA's a2 Agonists Conotoxins Acupunture Surgery Stimulators Peripherally restricted Opiods |
|
|
What meds work in the brain to reduce pain?
|
Opiods
Antidepressants (SSRI's) Anticonvulsants Acupunture Surgery Electrical Stimulators |
|
|
List some full Mu agonists Opiods
|
Codeine
Fentanyl Hydrocodone Hydromorphone Meperidine Methadone Morphine Oxycodone |
|
|
Mixed Mu agonist-antagonists Opiods
|
Butorphanol
Nalbuphine Pentazocine Buprenorphine |
|
|
What are adjuvent analgesics?
|
Adjuvant analgesics refer to a diverse group of drugs that have a primary indication other than pain but are also analgesic in some painful conditions.
Example: AMITRYPTALINE, which has a primary indication for depression but has also proven analgesic effects for many types of pain, such as the continuous neuropathic pain with burning and aching qualities that patients with diabetic neuropathy experience. Adjuvants are used for: 1-Multipurpose for chronic pain --->Antidepressants: amitriptyline, desipremine, nortriptyline ---> Corticosteroids: Dexamethasone ---> Psychostimulants: Dextroamphetamine, methylphenidate 2- Multipurpose for acute pain ---> Local Anesthetics (Lidocaine IV) ---> Intravenous anesthetics (Ketamine) 3- Continuous neuropathic pain ---> Antidepressants: Amitriptyline ---> Oral Local Anesthetics: Mexiletine 4 -Lancinating neuropathic pain ---> Anticonvulsants: Gabapentin, Carbamazepine, Phenytoin, clonazepam ---> Muscle relaxants: Baclofen 5- Malignant bone pain ---> Dexamethasone ---> Bone hormones: calcitonin |
|
|
Tx of chronic pain is ___________.
|
Tx of chronic pain is multidisciplinary.
SSRI's Lidocaine Patch Gabapentin (anticonvulsant) Tramadol Psychotherapy |
|
|
T/F Pain never killed anyone.
|
FALSE
Pain can be lethal: Postoperative pain can cause life-threatening complications and delay healing Chronic pain suppresses the immune system Chronic, unrelieved pain can lead to suicide |
|
|
Chronic pain is most often ignored in what population?
|
Pediatrics
|
|
|
Pathophysiology of neuropathic pain?
|
Chemical excitation of non-nociceptors
Recruitment of nerves outside of the site of injury. Excitotoxicity Sodium Channels Ectopic Discharge Deafferentation Central Sensitization (maintained by peripheral input). Sympathetic involvement Antidromic neurogenic inflammation |
|
|
The most accurate pain scale is the...
|
visual analog scale.
ask them to make a mark an measure. |
|
|
What is an opiod that is okay for long term tx of pain?
|
Tramadol
combines the effects of antidepressant drugs and opiod interactions. |
|
|
Opium
|
Extracted from poppy seeds
Produces: Euphoria Analgesia Sedation Stops diarrhea Cough suppression |
|
|
What is laudanum?
|
Opium combined with alcohol.
|
|
|
What do you call the juice/ exudate from the poppy plant?
|
Opium
|
|
|
What do you call a drug extracted from the juice/exudate of a poppy plant?
|
Opiate
|
|
|
What do you all a natural or synthetic drug that binds to mu receptors producing agonist effects?
|
Opiod
|
|
|
Natural Opiods occur from what two places
|
1) Opium exudate (morphine and codeine)
2) Endogenous opiod peptides (endorphins) |
|
|
How are synthetic opiods prepared?
|
Prepared from morphine (heroin) or from precursor compounds (synthetic opiods such as meperidine and fentanyl).
|
|
|
Explain all the effects of Mu receptors
|
Supraspinal and spinal analgesia
Sedation Inhibition of respiration Slowed GI transit Modulation of hormone and NT release |
|
|
Explain all the effects of Delta Receptors
|
Supraspinal and Spinal Analgesia
Modulation of Hormone and NT Release |
|
|
Explain all the effects of Kappa receptors
|
Supraspinal Analgesia (small amt)
MAINLY Spinal Analgesia Psycotomimetric Effects Slowed GI Transit Also has a hyperalgesia pathway that accentuates pain ?????????? |
|
|
What is the significance of Mu1 receptors?
|
They ONLY treat analgesia...no other side effects.
If we could find a Mu1 agonist only, then we could have the perfect pain med. |
|
|
What is the significance of kappa receptors?
|
They only effect analgesia, w/ no bad side effects except for dysphoria (psychomimetric) and GI effects.
If we could find a kappa selective drug we could avoid resp depression. |
|
|
What is the mechanism of action of Opiod Receptors?
|
Opiods are coupled to Gi/Go, which decrease cAMP in the cell.
This leads to hyperpolarization by increasing outward K+ currents, which inhibits AP's. They also work presynaptically to block Ca effects at Ca channes and consequently decrease NT release. This is seen in the dorsal horn when Substance P release is inhibited. Opioids have been shown to inhibit the release of substance P, acetylcholine, norepinephrine, glutamate, and serotonin |
|
|
Name the diff opiod receptors
|
1) Mu1 and Mu2
2) Kappa1 and Kappa3 3) Delta1 and Delta 2 (there are also non-opiod sigma receptors) |
|
|
Name the endogenous opiods:
|
Pro-opiomelanocortin peptides: (primarily mu)
--->Beta-endorphin Pro-enkephalin peptides: (primarily delta) met-enkephalin and leu-enkephalin Prodynorphin peptides: (primarily kappa) Dyn-A, Dyn-B and alpha-neo-endorphin Endomorphins: (primarily mu) Endomorphin-1 and Endomorphin-2 |
|
|
What two opiod meds can be given orally?
|
Oxycodone and codeine d/t reduced 1st pass metabolism.
|
|
|
How are opiods metabolized?
|
Opioids are converted in large part to polar metabolites (mostly glucuronides), which are more water soluble and then readily excreted by the kidneys. They can accumulate in patients with renal damage.
Hepatic oxidative metabolism is the primary route of degradation of the phenylpiperidine opioids (meperidine, fentanyl, alfentanil, sufentanil) |
|
|
T/F
Demerol causes just as much respiratory depression as fentanyl |
False
Equi-analgesic doses of all opioids produce equivalent amounts of respiratory depression. (Therefore partial agonists which only cause partial analgesia only cause partial resp depression, and are less threatening.) |
|
|
CNS effects of Opiods
|
Cough suppression (antitussive)
Miosis (pupil constriciton) (stimulates Edinger-Westphal nucleus) Truncal rigidity (supraspinal - Fentanyl) Seizures (especially with Meperidine) N & V (Direct stimulation of the CTZ in the midbrain) |
|
|
CV effects of opoids
|
CV effects of opiods are easily managed and therefore opiods are good to use with cardiac surgery.
Decrease in central SNS tone causes vasodilation and orthostatic hypotension Effects on both capacitance and resistance of vessels Bradycardia by stimulating central vagal nuclei Little or no myocardial depression |
|
|
GI effects of opiods
|
Constipation
Delayed gastric emptying – directly effects smooth muscle in GI tract Spasm of smooth muscle all along the GI tract |
|
|
Miscellaneous effects of Opiods
|
Can precipitate biliary colic
Can cause urinary retention Morphine, codeine, meperidine cause non-immunologic histamine release from mast cells (but facial itching probably a dysesthesia if it occurs after a spinal) Stimulate release of ADH, prolactin, somatotropin Inhibit the release of luteinizing hormone |
|
|
Effects of opiods on pregnancy and the neonate
|
All cross the placenta: Don’t use epidural fentanyl…lipid soluble…with cross all membranes and get to fetus…if you have to use an intrathecal or eipdural opiod…give a water soluble one (morphine).
No teratogenic effects Withdrawal in infants can be life-threatening Opioids given during labor can cause respiratory depression in baby |
|
|
Signs of an opiod overdose
|
Stuporous or in coma
Respiratory rate extremely low Pinpoint pupils (except meperidine) Low body temperature Flaccid skeletal muscles, jaw relaxed |
|
|
What's the most difficult type of pain to control with opiods? How about the other types?
|
Severe, constant pain is usually relieved
Sharp, intermittent pain is poorly controlled Chronic neuropathic pain is MOST difficult to control. |
|
|
Contraindications for Opiods
|
Opioid dependence on strong agonist (avoid partial agonists and mixed agonist-antagonists like pentazocine or buprenorphine)..will precipitate withdrawal.)
|
|
|
Drug interactions with opiods
|
Sedative-hypnotics/CNS depressants (additive CNS depression, particularly respiratory depression)
|
|
|
What is the mechanism/ type of tolerance that develops with Opiod use?
|
Pharmacodynamic Tolerance
A decrease in receptors on the cell membrane. Mu-receptor mRNA levels are down regulated by activation of NMDA receptors. Therefore: NMDA receptor antagonist ketamine reduces development of tolerance to opioid analgesic effects by preventing NMDA from downregulating the Mu receptor. |
|
|
To what effects of opiods does does tolerance develop the slowest?
|
Constipation and Miosis
Tolerance develops most rapidly to depressant effects like analgesia, respiratory depression, euphoria, but much LESS tolerance to stimulatory effects like constipation or miosis. Thus chronic users have little euphoria from high doses but continue to experience major constipation and miosis. |
|
|
How can taking pain medication cause paradoxical hyperalgesia?
|
You build up a tolerance so you are taking higher doses...this stimulates the kappa receptors to the point to where it stimulates their hyperalgesia tracts (via dynorphins).
|
|
|
T/F tolerance to opiods increases your risk of respiratory depression
|
False.
|
|
|
Signs of Opiod Withdrawal
|
Pain and irritability
Hyperventilation Dysphoria and depression Restlessness and insomnia Fearfulness and hostility Increased blood pressure Diarrhea Pupillary dilation Hyperthermia Lacrimation, runny nose Spontaneous ejaculation Chilliness and “gooseflesh” (VC) |
|
|
Signs of Opiod Intoxication
|
Analgesia
Respiratory Depression Euphoria Relaxation and sleep Tranquilization Decreased blood pressure Constipation Pupillary constriction Hypothermia Drying of secretions Reduced sex drive Flushed and warm skin (VD) |
|
|
Mixed Agonist-Antagonist
|
produces an agonist or partial agonist effect at one opioid receptor subtype and an antagonist effect at another subtype
|
|
|
Partial Agonist
|
has affinity for opioid receptors but low efficacy (e = between 0 – 1.0)
|
|
|
Pure (Competitive) Antagonist
|
has affinity for opioid receptors but no efficacy (e = 0); blocks action of endogenous and exogenous ligands
|
|
|
Full (Strong) Agonist
|
has affinity for opioid receptors plus full efficacy (e = 1.0)
|
|
|
T/F
Dose range of opiods is predictable for dosing of pts. |
FALSE
Analgesic requirements are enormously variable. The usual adult morphine dose (10 mg) is only 70% effective in relieving acute pain. Range of effective concentrations (the “therapeutic window”) is narrow for each patient but varies widely between patients. Implication: “cookbook” analgesia likely to be inadequate or excessive much of the time. |
|
|
Effects of opiods in balanced anesthesia:
|
Analgesia
Additive sedation Reduce stress, elevate mood No amnesia (BDZ needed) High dose opioids are especially useful for cardiac surgeries: Analgesia Attenuation of sympathetic reflex to pain No direct effects on contractility or vascular tone Can provoke histamine release leading to hypotension (reversable with drips, etc). |
|
|
T/F Opiods directly affect heart contractiliy and vascular tone.
|
False
The DO NOT directly affect inotropy or vascular tone. |
|
|
A 36-yr-old male with an open fracture of the left femur was admitted to the hospital for emergency external fixation. On arrival he complained of severe pain with a visual analog scale score (VAS) of 10. Tramadol (50 mg, IV) was given but minimal analgesic effect was achieved (VAS = 8). He refused a regional anesthesia. His medical history included heroin and alcohol ex-addiction and his medication consisted of naltrexone 50 mg orally daily.
How do you manage pain in this man's anesthesia? |
Remi-fentanyl drip - can titrate to effect and it has no metabolite d/t rapid metabolism by esterases and does not build up or cause resp depression either.
|
