lecture 8

Question 1

Analgesics

Answer 1

relieve pain without significantly disturbing consciousness or altering actions of sensory nerves. (pain killing)

Some of these types of drugs also have anti-inflammatory properties.

Question 2

Antipyretics

Answer 2

reduce fever (anti fever)

Some of these types of drugs also have anti-inflammatory properties.

Question 3

What is Pain?

Answer 3

Central nervous system’s reaction to potentially harmful stimuli characterized by physical discomfort.

Question 4

acute pain

Answer 4

severe pain with sudden onset; serves as early warning to seek medical help to prevent damage to body.

Question 5

chronic pain

Answer 5

lasting a long time or marked by frequent recurrence (ex. arthritis)

Question 6

Pain Stimuli

Answer 6

May result from an inflammatory process that causes tissue injury.

Histamine, prostaglandins, serotonin, and bradykinin are RELEASED and initiate action potential along sensory nerve fiber.

NOCICEPTORS (pain receptors in the tissues) are activated and a message is sent to the brain cortex.
Nociceptors are mechanical (ex. putting pressure on receptors), chemical, thermal, silent (inflammation) and polymodal.

Question 7

Types of pain

Answer 7

NOCICEPTIVE PAIN

NEUROPATHIC PAIN

Question 8

NOCICEPTIVE PAIN

Answer 8

sprains, bone fractures, burns, bumps, bruises, inflammation, obstructions, and myofascial pain. (typical trauma-type pain, a lot of painkillers work for this kind of pain)

special nerve ending called nociceptors send pain signals to the CNS (around the nerve)

Nociceptors are the nerves which sense and respond to parts of the body which suffer from damage. They signal tissue irritation, impending injury, or actual injury. When activated, they transmit pain signals (via the peripheral nerves as well as the spinal cord) to the brain. The pain is typically well localized, constant, and often with an aching or throbbing quality. Visceral pain is the subtype of nociceptive pain that involves the internal organs. It tends to be episodic and poorly localized.

Question 9

NEUROPATHIC PAIN

Answer 9

post herpetic (or post-shingles) neuralgia, sciatica, reflex sympathetic dystrophy / causalgia (nerve trauma), components of cancer pain, phantom limb pain (missing part of limb), entrapment neuropathy (e.g., carpal tunnel syndrome), and peripheral neuropathy (widespread nerve damage)

caused by dysfunction in the nervous system or damage to the nerve itself (issue in the nerve)

Among the many causes of peripheral neuropathy, diabetes is the most common, but the condition can also be caused by chronic alcohol use, exposure to other toxins (including many chemotherapies), vitamin deficiencies, and a large variety of other medical conditions. Neuropathic pain is the result of an injury or malfunction in the peripheral or central nervous system.

Question 10

Neuropathic pain is often described as…

Answer 10

burning, shooting, stabbing, prickling, electric shock- like pain, with hypersensitivity to touch, movement, hot and cold and pressure. When you have neuropathic pain, even a very light touch or gentle movement can be very painful.

Question 11

Nociplastic pain

Answer 11

fibromyalgia, chronic pelvic pain, tension-type headaches or chronic low back pain

‘Pain that arises from ALTERED NOCICEPTION despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain’.

This type of pain may reflect changes in the way the nervous and immune systems function. The net effect is that pain can be amplified, may be widespread, involve various tissues and be greater than would be expected given the amount of identifiable tissue or nerve damage. This type of pain does not respond to most medicines and usually requires a tailored program of care that involves addressing factors that can contribute to ongoing pain (lifestyle, mood, activity, work, social factors).

Question 12

Endorphins

Answer 12

Endorphins and enkephalins are neurotransmitters that can bind with OPIATE RECEPTORS in the CNS and INHIBIT transmission of pain impulses.

Body’s natural pain killers

Most pain medications are more effective against nociceptive pain.

(see image)

Question 13

Pain Medication-analgesics

Answer 13

Stop pain signals from going to the brain

Alter the brain’s interpretation of the pain signals

Analgesics do not rely on anesthesia or loss of consciousness (don’t cause it)

Do no treat the cause of the pain

Take 30 - 60 minutes to start working in tablet form

Question 14

Pain Medication-analgesics
Non-opioids

Answer 14

(upper limit of effectiveness)

Acetaminophen (not an NSAID because no anti-inflammatory component)

NSAIDS (Naproxen, salicylates, Ibuprofen, COX-2 inhibitors, etc…)

Upper limit: If you take more after reaching therapeutic dose, it won’t get better

Question 15

Pain Medication-analgesics
Opioids

Answer 15

(no upper limit)

Morphine, codeine, etc

No upper limit: More taken = more pain killing

*there are OTHER pain medication-analgesics as well

Question 16

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

Answer 16

Group of drugs that include salicylates (ex. aspirin) and antipyretics

Used to relieve PAIN and INFLAMMATION, swelling, stiffness, and joint pain of arthritis; treat menstrual cramps, gout attacks, bursitis, tendonitis, sprains, and muscle strains, (and fever)

Mechanism of action: BELIEVED TO ACT BY BLOCKING PROSTAGLANDIN SYNTHESIS

Adverse effects are mostly GI issues.

Question 17

Prostaglandin synthesis

Answer 17

(MUST SEE THE IMAGE AND FULLY UNDERSTAND IT!)

Goes towards cyclo-ocygenase pathway
Increases platelet aggregation
Protects stomach by helping with mucous
So taking NSAIDS regularly can result in stomach aches
COX 1 does good things (you want these prostaglandins)
COX 2 is more inducible
Most NSAIDs inhibit both which is good for COX 2 stuff but not good for COX 1 stuff

Question 18

NSAIDs (6)

Answer 18

Aspirin (Anacin®, Bayer®)
Ibuprofen (Advil®, Motrin®)
Naproxen (Aleve®) –work slower but longer lasting effects
Diclofenac (Volteren®)
Ketorolac (Toradol®)
Cox-2 inhibitors (Celebrex®)

*NSAIDS work for mild - moderate pain (severe is for opioids)
*NSAIDS retain fluid (reducing or increasing hypertension)

Question 19

Aspirin (Bayer, others): Uses

Answer 19

Most common salicylate

Used as an ANTIPYRETIC (fever) and ANALGESIC (pain) to relieve pain of headache, fever, muscular aches and pains

One of safest and most effective drugs to relieve FEVER

Low dose (81 mg) used as ANTICOAGULANT in CVD patients.
Chew 2 aspirins for heart attack (anticoagulant)

Question 20

Aspirin - ADME

Answer 20

(WATCH VIDEO: GOOD VIDEO FOR REVIEW)

Question 21

Aspirin: Mechanism

Answer 21

Detailed mechanism is unknown.

Thought to reduce PAIN and INFLAMMATION by inhibiting the synthesis of prostaglandins.

Thought to reduce FEVER by acting on the hypothalamic heat-regulating centre.

At low doses it IMPEDES BLOOD CLOTTING by INHIBITING PLATELET AGGREGATION

(SEE IMAGE, VERY IMPORTANT)
At low doses it does COX 1!
At higher doses it does COX 1 and COX 2!

Question 22

Aspirin: Adverse Effects

Answer 22

Uncommon: dyspepsia, nausea, vomiting, occult bleeding

Serious: Massive GI hemorrhage at high doses and in elderly patients

May be associated with Reye syndrome in children.

ALL NSAIDS EXCEPT ASPIRIN INCREASE THE RISK OF SERIOUS ADVERSE CARDIOVASCULAR EVENTS .

Question 23

Ibuprofen (Motrin, Advil): Uses and adverse effects

Answer 23

Nonsalicylate used for ANALGESIC, ANTI-INFLAMMATORY, and ANTIPYRETIC activities

Rheumatoid arthritis, osteoarthritis, and arthritis

Mild to moderate pain, dysmenorrhea, and fever.

WORKS BY BLOCKING COX 1 AND COX 2 ENZYMES

Common adverse effects: nausea, occult blood loss, peptic ulceration, diarrhea, constipation, abdominal pain, dyspepsia, flatulence, heartburn, decreased appetite

Serious: azotemia, cystitis, hematuria, aplastic anemia, hypoglycemia, hyperkalemia.

Question 24

Naproxen: uses and adverse effects

Answer 24

Used in the management of mild to moderate PAIN, FEVER and INFLAMMATION.

Considered a strong NSAID

WORKS BY BLOCKING COX 1 AND COX 2 ENZYMES

Also prescribed for conditions such as rheumatoid arthritis, osteoarthritis and ankylosing spondylitis, dysmenorrhea

Adverse effects: rash, tinnitus, headaches, dizziness, diarrhea, constipation, heartburn, fluid retention and hypertension, shortness of breath, blood clots

Question 25

Diclofenac

Answer 25

Used to treat INFLAMMATION, PAIN and FEVER. Available in tablets, creams or gels INHIBITS BOTH COX 1 AND COX 2 ENZYMES Also used to treat symptoms of rheumatoid arthritis and osteoarthritis, ankylosing spondylitis, gout, migraines and dysmenorrhea. Adverse effects (oral): stomach pain, diarrhea, indigestion, nausea and flatulence. Contraindications: during third trimester, nursing women, known hypersensitivity, history of asthma, GI, liver or renal disease *these are pain killers, you are getting it on your fingers when you use a cream so you should wear gloves *if you use cream, some adverse effects are different??

Question 26

Ketorolac (Toradol)

Answer 26

Used in the short-term management (up to 5 days) of acute INFLAMMATION and PAIN. More effective at managing pain than other NSAIDs, used for MODERATE TO SEVERE PAIN, but is not habit forming. Available in injection, ophthalmic solutions, and tablets Ketorolac should not be used for more than 5 days due to high risk of GI bleeding, ulcers, and kidney damage. INHIBITS BOTH COX 1 AND COX 2 ENZYMES Adverse effects: rash, tinnitus, dizziness, abdominal pain, nausea, diarrhea, constipation, dyspepsia, fluid retention. May cause serious injury to the GI tract Contraindications: do not use during pregnancy, caution in older adults, not recommended for children.

Question 27

commonly used NSAIDS TO KNOW

Answer 27

Aspirin (Anacin®, Bayer®) Ibuprofen (Advil®, Motrin®) Naproxen (Aleve®) –work slower but longer lasting effects Diclofenac (Volteren®) Ketorolac (Toradol®)

Question 28

Prostaglandin Synthesis

Answer 28

(IMPORTANT TO SEE IMAGE AND UNDERSTAND

Question 29

COX-1 ENZYMES

Answer 29

COX-1 enzymes are the only enzyme that makes prostaglandins that help your blood clot and protect the lining of your stomach and intestinal tract from digestive acids. Although COX-1 inhibitors (blockers) block inflammation, they also block the helpful effects — the stomach and intestinal lining protection and blood clotting control.

Question 30

COX-2 ENZYMES

Answer 30

Make prostaglandins that are mainly involved in inflammation. COX-2 inhibitors mostly block inflammation. COX-2 inhibitors don’t block COX-1 enzymes. This means that your stomach and intestinal lining protection and your body’s blood clotting ability are not severely affected.

Question 31

Selective COX-2 Inhibitors: Mechanism of Action

Answer 31

One group of NSAIDs that selectively inhibits CYCLOOXYGENASE-2 (COX-2) (enzymes required to produce prostaglandins from arachidonic acid; appear to be made in macrophages in response to local tissue damage).

Question 32

Selective COX-2 Inhibitors TO KNOW

Answer 32

CELECOXIB MELOXICAM Bextra® and Vioxx® were removed from the market because of cardiovascular effects

Question 33

COX-2 Inhibitors:

Answer 33

Uses CELECOXIB (Celebrex): treatment of osteoarthritis and rheumatoid arthritis. Newer COX-2 inhibitor, MELOXICAM (Mobic) is labeled for treatment of osteoarthritis. Adverse Effects Common: abdominal pain, dyspepsia, diarrhea, hypertension Serious: myocardial infarction and stroke

Question 34

COX-2 Inhibitors-risks

Answer 34

Cox-1 enzymes also help make a chemical that encourages blood clotting and tightens the arteries. Normally, these effects are kept in check by another chemical called prostacyclin. But prostacyclin is made, in part, with the help of Cox-2 enzymes. Blocking only COX-2 upsets the balance of these enzymes. Levels of prostacyclin go down, the influence of COX-1 goes unchecked, and your risk of heart attacks and strokes goes up. Also increases 20-HETE which is a vasoconstrictor. *Usually, COX 1 and COX 2 work in balance in terms of blood clotting?

Question 35

COX-2 Inhibitors: Contraindications

Answer 35

*NSAIDS have an impact on hypertensive medications!!

Question 36

Acetaminophen (Tylenol): Mechanism of Action (NOT an NSAID)

Answer 36

Thought to be inhibition of prostaglandin in peripheral nervous system, making sensory neurons less likely to receive pain signals- raises threshold of pain. Acetaminophen blocks peripheral pain impulses to lesser degree than other NSAIDs; LACKS ANTI-INFLAMMATORY ACTION of salicylates and other NSAIDs. May block COX1 and COX2 indirectly but mechanism is unknown. *SEE IMAGE!! *alternating between acetaminophen and ibuprofen works if headache keeps coming back

Question 37

Acetaminophen: Uses and adverse effects

Answer 37

Treatment of musculoskeletal pain, headache, dysmenorrhea, myalgias, neuralgias, arthritic and rheumatic conditions Reduces fever and discomfort of common cold and viral infections Usually well-tolerated in therapeutic doses Long-term use: skin eruptions and urticaria, hypotension, hepatotoxicity Overdose: hepatotoxicity, coma, internal bleeding (antidote (cure) is N-acetylcysteine (NAC)) Acetaminophen is metabolized by the liver, producing a TOXIC BYPRODUCT (NAPQI) NAC helps replenish glutathione, a substance that detoxifies and prevents liver damage - Glutathione helps neutralize the toxic metabolite

Question 38

Migraines

Answer 38

Has a genetic component- hereditary Chemical compounds and hormones, such as serotonin (both sexes) and estrogen (primarily women), often play a role in pain sensitivity for migraine sufferers. Migraine pain happens due to waves of activity by groups of excitable brain cells. THESE TRIGGER CHEMICALS, SUCH AS SEROTONIN, TO NARROW BLOOD VESSELS Triggers can include: Stress and other emotions, hormonal shifts or exposure to light or smells, fatigue and changes in one's sleep pattern, glaring or flickering lights, weather changes, and certain foods and drinks MIGRAINE AURA is defined as a focal neurological disturbance manifest as visual, sensory or motor symptoms. It is seen in about 30% of patients Trigeminal fibers innervating cerebral vessels arise from neurons in the trigeminal ganglion that contain substance P and CALCITONIN GENE-RELATED PEPTIDE (CGRP), both of which can be released when the trigeminal ganglion is stimulated.

Question 39

Migraine medications

Answer 39

Acetaminophen NSAIDS Tripans Gepants Ergot derivatives

Question 40

Acetaminophen

Answer 40

Block the production of prostaglandins

Question 41

NSAIDS

Answer 41

Block the COX enzymes which produce inflammatory substances

Question 42

Tripans

Answer 42

Act on serotonin receptors and also block the release of CGRP - Treat migraines by constricting blood vessels and reducing inflammation. - Work by binding to 5-hydroxytryptamine (5-HT) receptors in the brain and blood vessels.

Question 43

Gepants

Answer 43

Block the CGRP receptors ( Ex. Ubrelvy)

Question 44

Ergot derivatives

Answer 44

Act on serotonin receptors but differently than the tripans

Question 45

CGRP receptor antagonist

Answer 45

Ubrelvy is a CGRP receptor antagonist prevents CGRP from binding to its receptors on neurons. Blocks the pain signals that cause migraines. Doesn’t affect vasculature in the brain so it doesn’t contribute to migraines?? (SEE IMAGE AND UNDERSTAND THIS CONCEPT!!)

Question 46

Drugs to treat migraines TO KNOW

Answer 46

sumatriptan ergotamine, caffeine

Question 47

Opiates/Opioids

Answer 47

*used when non-opioids don’t work (more for moderate-severe pain) Analgesic effects produced by binding to opioid receptors (mu, kappa, and delta); MOSTLY AFFECT MU RECEPTORS NO UPPER EFFECTIVE LIMIT but can affect consciousness and breathing at higher doses - If you get too much, it affects respiratory system which is bad Risk of dependency *3 receptors (most have the greatest effect on mu receptors but there is also kappa and delta)

Question 48

Opiates

Answer 48

drugs derived from opium poppies: morphine and codeine

Question 49

Opioid

Answer 49

general term referring to natural, synthetic, or ENDOGENOUS morphine-related substances

Question 50

Opioid receptors

Answer 50

!!BINDING CAUSES HYPERPOLARIZATION AND REDUCES LIKELIHOOD OF ACTION POTENTIAL

Question 51

Natural Opioids

Answer 51

Codeine Morphine *we will see semi synthetic and synthetic

Question 52

Codeine: Uses and adverse effects

Answer 52

Used to induce sleep in presence of mild pain Used as ANALGESIC, SEDATIVE, hypnotic, ANTIPERISTALTIC (constipation), and ANTITUSSIVE (cold medication) Commonly given in combination with aspirin, acetaminophen, and other agents. Codeine is a selective agonist for the MU OPIOID RECEPTOR, but with a much WEAKER affinity to this receptor than morphine Common: postural hypotension, nausea and vomiting, constipation, miosis Serious: cortical and respiratory depression Tolerance, dependence, and addiction can occur.

Question 53

Morphine (Astramorph, others): Uses and adverse effects

Answer 53

Management of all types of moderate to severe pain Derivatives are used for cough inhibition, treatment of GI pain, relieving pain of myocardial infarction. Morphine primarily binds to the MU-OPIOID RECEPTOR, which is responsible for most of its analgesic and euphoric effects. Common: nausea and vomiting, constipation, dry mouth, biliary tract spasms, dizziness, sedation, pruritus Serious: respiratory depression Physical and psychological dependence

Question 54

Opioid analgesics TO KNOW

Answer 54

codeine morphine

Question 55

Semi-synthetic opioids

Answer 55

Hydromorphone Hydrocodone Oxycodone Oxymorphone

Question 56

Hydromorphone (Dilaudid)

Answer 56

Used for moderate to severe pain (5-10 TIMES MORE POTENT THAN MORPHINE) May have advantage over morphine for pain control. It has much higher bioavailability of 50% compared to morphine An AGONIST at the MU OPIOID RECEPTOR with much weaker affinity at the DELTA and KAPPA opioid peptide receptors. (mu is bound primarily, binds to the others a little bit) Common side effects include dizziness, sleepiness, nausea, itchiness, and constipation. Serious side effects may include abuse, low blood pressure, seizures, respiratory depression and serotonin syndrome

Question 57

Hydrocodone (Hycodan):Mechanism of Action

Answer 57

Morphine derivative similar to codeine Suppresses cough reflex by direct action on cough center in medulla Acts as CNS depressant to relieve moderate to severe pain *Bind to mu receptor Adverse Effects: Common: dry mouth, nausea and vomiting, constipation, sedation, dizziness, drowsiness Serious: respiratory depression

Question 58

Oxycodone: Uses

Answer 58

Relief of moderate to severe pain (bursitis, dislocations, simple fractures, other injuries) Postoperative and postpartum pain Adverse effects: Common: euphoria, dysphoria, light-headedness, dizziness, sedation, anorexia, nausea and vomiting, constipation Serious: jaundice, hepatotoxicity, respiratory depression

Question 59

Oxycodone (OxyContin): Mechanism of Action

Answer 59

Binds to KAPPA AND MU receptors (maybe kappa a bit more) in various sites of CNS to alter both perception of pain and emotional response to pain. Oxycodone is as potent as MORPHINE and 10–12 TIMES MORE POTENT THAN CODEINE

Question 60

Classification of opioid analgesics

Answer 60

hydrocodone oxycodone

Question 61

Synthetic Opioid Analgesics

Answer 61

They have the properties of morphine as analgesics but have fewer undesirable effects and less addiction potential. Higher risk for serotonin syndrome - Buprenorphine - Fentanyl - Meperidine - Pentazocine - Tramadol

Question 62

Buprenorphine: Uses

Answer 62

Treatment of moderate to severe postoperative pain Administered for pain associated with cancer, accidental trauma, urethral calculi (worse in men due to longer urethra), myocardial infarction

Question 63

Buprenorphine (Buprenex): Mechanism of Action

Answer 63

Synthetic centrally acting narcotic analgesic Opiate AGONIST-ANTAGONIST !!Has high affinity for mu-opioid receptors (partial agonist) !!Acts as antagonist at kappa-opiate receptors in CNS Is a long-acting opioid drug used to replace the shorter-acting opioids to which someone may be addicted. Produces analgesic effects and alleviates opioid cravings but with a ceiling effect that reduces the risk of respiratory depression.

Question 64

Buprenorphine: Adverse Effects

Answer 64

Common: sedation, drowsiness, vertigo, dizziness, headache, amnesia, euphoria, insomnia (SEE IMPORTANT IMAGES X2) *Full agonist binds the best and has the biggest effect **Antagonist inhibits signalling/ effect

Question 65

Fentanyl (Duragesic, Sublimaze)

Answer 65

Analgesic and sedative used during operative and perioperative periods. Produces analgesia, euphoria, sedation, and respiratory depression. Full agonist at the MU-OPIOID RECEPTOR Interacts with alcohol, other CNS depressants, monoamine oxidase inhibitors Instruct postoperative patients to report muscle rigidity or weakness; unusual postoperative muscle movement of the extremities, eyes, or neck; or breathing difficulties. 50–100 TIMES MORE POTENT THAN MORPHINE

Question 66

Meperidine (Demerol)

Answer 66

Synthetic opioid, principally induces analgesia and sedation Used preoperatively, to treat moderate to severe pain, as obstetric analgesia and to support anesthesia May produce less smooth muscle spasm, constipation, and depression of the cough reflex than equivalent doses of morphine. Meperidine acts as a MU-OPIOID RECEPTOR agonist, and mild effects on KAPPA-OPIOID RECEPTORS Meperidine has largely been replaced by safer opioids due to the risk of NORMEPERIDINE-INDUCED TOXICITY and SEROTONIN SYNDROME

Question 67

Pentazocine (Talwin)

Answer 67

Acts as a PARTIAL AGONIST or AGONIST at KAPPA-OPIOID RECEPTORS (binds more to kappa but works on both) Acts as a WEAK ANTAGONIST or PARTIAL AGONIST at MU-OPIOID RECEPTORS For control of moderate to severe pain, preoperative analgesia or sedation, and as supplement to surgical anesthesia. Used for MODERATE TO SEVERE PAIN, particularly when a less addictive alternative to full opioids is needed. Adverse effects, contraindications, and patient information are similar to those of other opioids.

Question 68

Tramadol

Answer 68

A centrally-acting opioid agonist and SNRI used for the management of moderate to severe pain in adults. Tramadol binds weakly to MU-opioid receptors, providing analgesia. Also inhibits norepinephrine (NE) and serotonin (5-HT) reuptake Less effective for severe pain compared to full opioid agonists like morphine or oxycodone. Dependance is lower but may still may be habit-forming, even at regular doses. Useful for neuropathic and mixed types of pain. DO NOT DRINK ALCOHOL. Dangerous side effects or death could occur. SNRI= Serotonin/norepinephrine reuptake-inhibitor

Question 69

Synthetic Opioid Antagonists

Answer 69

NALOXONE (Narcan): prescribed for narcotic overdose, reversal of narcotic respiratory depression. - Naloxone works by KICKING OPIOIDS OFF THE RECEPTORS IN YOUR BRAIN AND BINDING TO THOSE RECEPTORS INSTEAD NALTREXONE (Trexan, ReVia): adjunct for maintaining opioid- free state in detoxified addicts; management of alcohol dependence.

Question 70

Classification of opioid analgesics TO KNOW

Answer 70

SYNTHETIC OPIOID ANTAGONISTS - naloxone SYNTHETIC OPIOID AGONIST/ ANTAGONISTS - buprenorphine - fentanyl - meperidine - pentazocine

Question 71

Serotonin Syndrome

Answer 71

A potentially life-threatening condition caused by an EXCESSIVE ACCUMULATION OF SEROTONIN IN THE CENTRAL NERVOUS SYSTEM Serotonin syndrome is typically triggered by: MEDICATIONS THAT INCREASE SEROTONIN LEVELS, such as: 1. Selective serotonin reuptake inhibitors (SSRIs) (e.g., fluoxetine, sertraline) 2. Serotonin-norepinephrine reuptake inhibitors (SNRIs) (e.g., venlafaxine, duloxetine) 3. Monoamine oxidase inhibitors (MAOIs) (e.g., phenelzine, selegiline) 4. Tricyclic antidepressants (TCAs) (e.g., amitriptyline, clomipramine) 5. Opioids with serotonergic activity (e.g., tramadol, fentanyl) 6. Migraine medications (e.g., triptans like sumatriptan) 7. Illicit drugs (e.g., MDMA/ecstasy, cocaine) 8. Overdose or interaction between serotonergic drugs. 9. Herbal supplements like St. John's Wort or 5-HTP. 10. Excess serotonin precursors or stimulants, such as L-tryptophan or amphetamines Symptoms range from mild to severe and affect three main systems: NEUROLOGICAL (agitation, confusion, seizures), AUTONOMIC (tachycardia, hypertension, sweating), and MUSCULAR (Muscle rigidity, tremors, exaggerated reflexes).

Question 72

Other classes of drugs used to treat pain

Answer 72

More effective against neuropathic pain when used as adjuvant drugs - Anticonvulsants - Antidepressants - Psychostimulants - Cannabinoids - Corticosteroids (reduce inflammation) - Disease modifying antirheumatic drugs *Don’t treat pain directly