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Analgesics Flashcards

0
Q

Where do A delta fibers synapse vs. C fibers?

A

A delta: lamina I, II, III, V

C: lamina I and II (substantia gelatinosa is lamina II/III, it is richly populated with opioid receptors)

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1
Q

Hyperalgesia vs. allodynia vs. spontaneous pain

A

Hyperalgesia: pain out of proportion to noxious stimuli
Allodynia: pain evoked by a non-noxious stimuli
Spontaneous pain: pain with no apparent stimuli

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2
Q

The dorsal horn neurons (from lamina I and V) send fibers via the pathway of neospinothalamic tract vs. paleospinothalamic tract.. what is the difference?

A

Neospinothalamic: fast pain pathway, to the thalamus then to the somatosensory cortex
Paleospinothalamic tract: slow pain pathway, to the brain stem (and thalamus) then to the thalamus, hypothalamus and elsewhere

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3
Q

When modulating pain signals, descending inhibitory pathways originate in the _____ and project to the ______ which sends neurons down the spinal cord to synapse in the ________

A

Descending inhibitory pathways originate in the **midbrain/brain stem and project to the **nucleus raphe magnus which sends neurons down the spinal cord to synapse in the **substantia gelatinosa

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4
Q

What are the three major sites of action of opioids?

A

Brain (supraspinal): opioids work pre and post synaptically to activate descending inhibitory pathways
Spinal cord (spinal): directly on the dorsal horn of the spinal cord
Periphery: nociceptive neurons

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5
Q

Why are opioids used in anesthesia?

A

Lessen SNS response to noxious stimuli
Adjunct to inhaled agents
Sole anesthetic
Peri-op and post-op control of pain

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6
Q

Opioid characteristics: do they have a ceiling effect?

A

There is no max dose (no ceiling effect)

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7
Q

Which of these are naturally occurring vs. semisynthetic?

Morphine, heroin, codeine, dihydromorphone

A

Naturally occurring: morphine and codeine

Semisynthetic: heroin and dihydromorphone

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8
Q

Opioid mechanism of action? G-protein response?

A

Synthetic opioids mimic the action of endogenous opioids by binding to opioid receptors
G-protein response: presynaptic- inhibits release of excitatory neurotransmitters (Ach, dopamine, norepi, substance P)
postsynaptic- decreases neurotransmission by increased K conductance (hyperpolarization), Ca channel inactivation, modulates phospoinositide, inhibits adenylate cyclase (decreased cAMP)

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9
Q

Mu-1 receptor effects

A

SUPRASPINAL, spinal, and peripheral analgesia, euphoria, miosis, bradycardia, urinary retention, and hypothermia
*All endogenous and synthetic opioid agonists act on these receptors

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10
Q

Mu-2 receptor effects

A

Hypoventilation, physical dependence, SPINAL analgesia (some supraspinal), constipation
**All endogenous and exogenous agonists act on these receptors

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11
Q

Kappa receptor effects

A

SUPRASPINAL, SPINAL and peripheral analgesia, dysphoria, sedation, miosis, diuresis
**Dynorphins act on these receptors
Opioid agonist-antagonists often have principle actions at the kappa receptors

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12
Q

Delta receptor effects

A

PERIPHERAL, supraspinal, and spinal analgesia
Hypoventilation, constipation, urinary retention
**Enkephalins work on these receptors

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13
Q

Why do people respond differently to the same opioid?

A

Receptor binding can be affected by SNP or other mutations that don’t allow the binding, ex: chromosome 6q24-q25, nucleotide 118 and 17 affect nucleotide binding
Also metabolism can be affected by genetics, ex: CYP2D6 has common mutations

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14
Q

Opioid CV side effects, which drug is the big exception?

A

MINIMAL when used alone, additive with other anesthetics
Dose dependent bradycardia due to vagal stimulation and direct SA/AV node depression
Vasodilation/decreased SVR (esp in hypovolemic state), impaired SNS response, decreased CO and BP with venous pooling
Morphine and Meperidine (demerol) cause dose dependent histamine release which will cause bronchospasm, drop in SVR/BP
Meperidine is the big exception, for causing tachycardia and more myocardial depression than the other opioids

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15
Q

CNS effects of opioids

A

Analgesia, euphoria
Drowsiness/sleep
Miosis (pupil constriction)
Nausea (chemoreceptor trigger zone)
If hypoventilation prevented, decrease in ICP/CBF
Does NOT produce amnesia (problem with recall)

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16
Q

GI/Liver/Renal side effects of opioids

A

Increased tone and peristaltic activity of ureter and increased detrusor muscle tone = increased URGENCY but less ability to void
Decrease catecholamine release/ stress response
Spasm of sphincter of Oddi with increased biliary pressure
Spasms of GI smooth muscle can cause constipation and prolonged gastric emptying
N/V- chemoreceptor triggers nausea but medullary vomiting center is depressed (so more nausea than vomiting)

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17
Q

Pruritis is a side effect of opioids, where do people commonly itch?

A

“Fentanyl nose itch”

Histamine release can cause this

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18
Q

Opioid skeletal muscle side effects

A

RIGIDITY in chest, abdomen, jaw, extremities, glottic (“wooden chest syndrome”, hard to ventilate) especially in large doses -> high airway pressures decrease venous return

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19
Q

Opioids ventilatory effects

A

Dose dependent respiratory depression (small doses increase TV, decrease RR; large doses decrease RR and TV).. this is why people die of OD
Decreased chest wall compliance
Constriction of pharyngeal and laryngeal muscles
Cough suppression
Decreased response to hypercarbia/hypoxia
Morphine and Meperide cause histamine related bronchoconstriction

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20
Q

What do opioids do to the ventilatory response curve?

A

Shift down and to the right

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21
Q

How does codeine work?

A

It is a pro-drug meaning the body metabolizes 10% of the drug (using CYP2D6) to its active form, morphine. If the patient lacks the enzyme for this then the body won’t convert it and the drug will not have an analgesic effect (some caucasians and asians lack 2D6)
Codeine is better for cough at a lower dose than pain relief, even without conversion to morphine

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22
Q

Uses and routes for morphine vs. codeine

A

Morphine: sharp, acute pain; route PO/IM/IV (PO delayed onset, e1/2t 3-4 hrs, converted to active metabolite- bad for renal pt)
Codeine: mild pain; route PO (e1/2t 3 hrs, combined with acetaminophen, guaifenesin, or promethazine)

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23
Q

Hydrocodone, also known as ______, is used for what?

A

Vicodan
Used for chronic pain (also antitussive)
Always combined with acetaminophen, aspirin, ibuprofen, antihistamine

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24
Oxycodone, also known as ______, is used for what?
Oxycontin, percocet, percodan PO for moderate to severe pain, chronic pain, or post-op pain Used in combination with acetaminophen and aspirin No active metabolites (safer with renal patients)
25
Methadone: route, e1/2t, uses?
PO, IV, subQ Long, variable, unpredictable E1/2t 8-100 hrs (so risk of respiratory depression) Used for chronic pain (bid/tid dose) and for opioid addiction treatment (maintenance, qd dose) No active metabolites- safer in patients with renal dysfunction
26
What is the reversal for opioid agonists?
Naloxone (narcan) | Competitively binds to opioid receptors
27
What are signs of tolerance to opioids? When can this occur?
Tolerance is common after 2-3 weeks of opioid use Pt notices a reduction in adverse effects, shorter duration of analgesia followed by a decrease in effectiveness of each dose This includes tolerance to respiratory and CNS depression, but NOT constipation (they need laxatives/stool softeners)
28
When does physical dependance occur with opioids?
Physical dependence causes symptoms upon sudden d/c. It takes about 25 days to develop fully but some degree of dependence occurs after only 48 hours of continued IV use Note: addiction involves psychological dependence and biologic/social factors
29
How is PO dosage determined for opioids?
No min/max unless it contains acetaminophen or aspirin, the dose is decided by what relieves pain with tolerable side effects For chronic pain, sustained release formula should be used Immediate release doses are for breakthrough pain
30
What are the neuraxial effects of opioids?
Analgesia across dura to mu receptors in substantia gelatinosa then into the vasculature for a systemic effect (NOT true with morphine bc it is not as lipid soluble) Penetration into CSF/vasculature and movement in CSF depends on lipid solubility
31
Dose for epidural is 5-10x _____(lower/higher) than spinal dose
Higher Opioids placed in epidural space may undergo uptake into fat, systemic absorption or diffusion into CSF Spinal is given directly to CSF, requires lower dose
32
A ______(more/less) lipid soluble opioid will remain in CSF for transfer to cephalic location
LESS Ex. Morphine A highly lipid soluble drug, fentanyl, will be limited in migration by uptake into the spinal cord
33
Is there a ceiling effect to non-opioid analgesics? Does tolerance develop?
Ceiling effect of aspirin and acetaminophen between 650-1300 mg (other NSAIDS may be higher) Exceeding the ceiling dose of these drugs will result in increased adverse effects with no added efficacy Tolerance does NOT develop
34
Acetaminophen: uses, MOA
Uses: antipyretic, anti-prostaglandin effect, pain reliever, weak anti-inflammatory, good for peptic ulcer disease, peds, and pt who need well functioning platelets MOA: NOT a true NSAID, pain reduced via blockade of NMDA receptor activation in CNS, blocks substance P in the spinal cord
35
Acetaminophen dose: po and IV
PO: 325-650 mg q4-6h IV: 1 gram over 15 min, q4-6h Don't exceed 4g in 24 hours! If someone is an alcoholic its a good idea to cut this in half.
36
Acetaminophen OD causes what? What is the antidote?
Hepatic injury Liver can only metabolize a limited amount of the toxic metabolite using intrinsic glutathione, when it is outnumbered, hepatic injury occurs Acetylcystein can substitute for glutathione and prevent hepatic injury within 8 hours of OD
37
What carries a higher risk of renal toxicity? Acetaminophen or NSAIDS?
NSAIDS are a higher risk of renal toxicity | **Acetaminophen does carry some risk due to accumulation of metabolites which can cause renal cell necrosis
38
Arachadonic acid released from phospholipids by the enzyme phospholipase A2. It is immediately metabolized by what?
Cyclooxygenase, leading to the formation of prostaglandins, prostacyclin, and thromboxanes Lipoxygenase, leads to the formation of leukotrienes and lipoxins Epoxygenase (not clinically relevant)
39
COX-1 vs. COX-2, what happens when we only block COX-2?
Both COX 1 and 2 lead to prostaglandin production COX-1 is an enzyme widespread through the body, it also does platelet aggregation, GI protection, and renal function COX-2 is an enzyme only active at the site of inflammation When we block ONLY COX-2, risk of platelet aggregation -> stroke/MI Prostaglandins also prevent renal failure, so when blocked, that's an issue. Also when blocking both 1 and 2, we block GI protection, leads to GI bleeds.
40
Salicylates (Aspirin): what are uses and how does it work?
Uses: mild to moderate pain (headache, muscle pain, arthritis), antipyretic, MI/stroke prevention, protection during MI (anti-platelet) Unlike other NSAIDS, it is a IRREVERSIBLE inhibitor of COX (for a lifetime of platelet, 8-10 days), large doses can decrease prothromin When held before surgery, held for 8-10 days bc lifetime of a platelet
41
Is ESRD induced by chronic aspirin use or are other NSAIDs more likely to do this?
Other NSAIDs cause ESRD, NOT aspirin
42
Salicylate side effects?
``` Prolonged bleeding Increased LFTs Asthma ppt Cross-sensitivity with other NSAIDS GI bleed, PUD CNS stimulation ```
43
Salicylate dosing? What is the E1/2t?
Analgesic/antipyretic: 325-650 mg Anti-inflammatory: 1000 mg (3-5 g/day).. rarely used bc GI effects E1/2t 15-20 min for aspirin and 2-3 hr for active metabolite salicylic acid
44
Salicylate overdose symptoms?
Metabolic acidosis, tinnitis
45
Why is Aspirin not used during viral syndromes in children?
Risk of Reye's syndrome
46
Are acetylated or non-acetylated salicylates more favorable by not interfering with platelet aggregation, less GI bleed, and better tolerated by asthmatics?
Non-acetylated
47
NSAID uses and MOA
Uses: analgesic (musculoskeletal pain, headaches, more effective than aspirin/acetaminophen) but ceiling effect with post-op pain, anti-inflammatory, antipyretic MOA: COX inhibition, blocks conversion of arachidonic acid to prostaglandins
48
NSAID is a weak ____ (acid/base), well absorbed, ______ (high/low) protein binding, ______ (small/large) Vd, and what is the half-life?
Weak acid highly protein bound Small Vd Variable half-life, 6-12 hours
49
Side effects of NSAIDs, what are peri-op side effects?
Asthma and anaphylactic reaction in aspirin-sensitive patients Reversible inhibition of platelet aggregation No physical dependence Rare hepatic injury and aseptic meningitis GI effects, renal effects Peri-op inhibition of COX results in renal injury, gastric ulcers, excessive bleeding, and impaired bone healing
50
What pregnancy category are NSAIDs?
Category B until 3rd trimester, category D because usage of NSAIDs can cause the fetus ductus arteriosis could close
51
What GI effects do NSAIDs have? Who is at most risk for these effects?
Dyspepsia, GI bleed, PUD, Increased acid production, decreased mucus production At high risk with high doses, prolonged use, previous GI bleed/ulcer, excessive ETOH intake, elderly, and CORTICOSTEROID use (corticosteroids block higher up on the arachidonic acid chain)
52
What causes the renal effects of NSAIDs? What are the effects? Who is at highest risk?
Due to decreased synthesis of renal vasodilator prostaglandin Decreased renal blood flow Fluid/sodium retention Renal failure, hypertension Interstitial nephritis Risk factors: elderly, CHF, hypertension, DM, renal insufficiency, ascites, volume depletion, diuretic therapy
53
Which specific NSAIDs are at higher risk of renal effects? Which are at lower risk of renal effects?
Higher: ketorolac, indomethacin Lower: sulindac, nabumetone, celecoxib
54
NSAID drug interactions?
Displaces other highly protein-bound agents (increases levels of warfarin, phenytoin, sulfonylureas, digoxin) Reduces effect of diuretics, beta-blockers, ACEIs Increases lithium levels Increased risk of GI bleed with anticoagulants Probencid increases levels of NSAIDs
55
How does Ketorolac compare to other NSAIDs? What is the onset, e1/2t, and doa?
Ketorolac (toradol), is the only IV NSAID Comparable to mild opioid pain relief Adverse effects of NSAIDs are more extreme IV onset in 10 min, E1/2t of 5 hours, DOA 6-8 hours Shouldn't be used for more than 5 days 99% protein bound, conjugated in the liver
56
Ketorolac dose?
30 mg IV once or q6h Daily max 120 mg Decrease dose by 1/2 for elderly
57
Celecoxib (celebrex): What is it and why would you give it? Why would you avoid it
Selective NSAID, selectively inhibits Cox-2 You would give this to someone with NO cardiac or GI issues but arthritis issues (otherwise, use an NSAID) Same risk of renal effects Avoid in patients with a sulfonamide allergy (and cardiac/GI issues)
58
Celecoxib dose?
200 mg/day PO or less (similar effect as naproxen 500 mg bid) Take with food
59
What is the black box warning for selective and non-selective NSAIDs?
CV: increased risk for serious thrombotic events, contraindicated for CABG surgery GI: bleeding, ulcers, perforation
60
Antidepressants and anticonvulsants are good for what type of pain?
Neuropathic pain syndromes TCAs (amitriptyline, nortriptyline) Venlafaxine (effexor), Duloxetine (cymbalta) Anticonvulsants: gabapentin (neurontin), pregabalin (lyrica), carbamazepine (tegretol), phenytoin (dilantin, sodium valproate (depakote), clonazepam (klonopin), topiramate (topamax), lamitrogen (lamictal)
61
Adjunctive analgesics such as hydroxyzine, corticosteroids, and local anesthetics are good for what type of pains?
Hydroxyzine for post op pain, reduces N/V, additive effect to opioids in cancer Corticosteroids for nerve or inflammatory disease Topical analgesics such as 5% lidocaine (lidoderm) for post herpetic neuralgia Topical EMLA for cutaneous anesthesia Capsaicin cream (zostrix) for neuropathic/OA pain Clonidine transdermal patch for pain/hyperalgesia

N550 Pharm (14 decks)

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