Pharmacology Analgesics Flashcards
What are Analgesics
relieve pain without significantly disturbing consciousness or altering actions of sensory nerves.
What is the word for medications that reduce fever
Antipyretics
What is pain
Central nervous system’s reaction to potentially harmful stimuli characterized by physical discomfort.
Lets say a girl fell and got scratched walk through the physiological process the body undergoes
1) Histamine, prostaglandins, serotonin, and bradykinin are released and initiate action potential along sensory nerve fiber.
2) Nociceptors (pain receptors) are activated and message is sent to brain cortex.
3). Nociceptors are mechanical, chemical, thermal, silent (inflammation) and polymodal.
Explain the MAIN diffrence between nocicireceptor and neuropathic pain.
Nociceptive pain comes from tissue injury and activates pain receptors.
Neuropathic pain stems from nerve damage or malfunction, even without a clear injury.
What is neuropathic pain
caused by dysfunction in the nervous system or damage to the nerve itself.
How is Neuropathic pain described as
as burning, 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.
What is Nociplastic Pain where does it come from
From abnormal pain processing, even without clear injury (e.g., fibromyalgia).
-this type of pain does not respond to most medicines
What are the bodys natural pain killers and how do they work
Endorphins and enkephalins bind with opiate receptors in the CNS and inhibit transmission of pain impulses.
How do pain medication -analgesics work?
-Stop pain signals rom going to the brain
-Alter the brains perception of pain
-Do not treat the cause of pain
-Take 30-60 minutes to start working.
What are the diffrent types of analgesics
Non-opioids: like acetaminophen
Opioids: morphine, Codeine.
What does upper limit/no upper limit mean in pain medication
Non opiods have an upper limit of effectivness meaning dose beyond which taking more does not increase pain relief and may cause harm
Meanwhile opiodis have no upper limit meaning higher doses can provide more pain relief
What are some types of NSAIDs
include Salicylates and antipyretics
What is the mechanism of action for Nonsteroidal Anti-infalmmatory drugs
Belived to act by blocking prosaglandin synthesis.
Explain how prostaglandin is synthesized
1) the process begins with membrane phospholipids, which are broken down by an enzyme (phospholipase A₂) into arachidonic acid.
2) from there, there are 2 pathways… first is Lipo-oxygenase and this makes leukotrienes which affect the lungs
3) the other pathway is cyclo-oxygen pathway which produces Cox 1 and 2
4) Cox 1 makes = is good, found in most tissue and protects the stomach lining
Also cox 1 makes thromboxane which helps with blood clotting and narrow blood vessels.
Cox 2= makes pro-inflammatory prostaglandins, which increase pain, fever, and swelling.
List the 6 types of NSAIDs
-Aspirin
-Ibuprofen aka (advil)
-Naproven(aleve)
-Diclofenac (Voltaren)
-Ketorolac
-Cox-2 inhibitor
List what you know about Aspirin
-Most common salicylate
-Used as antipyretic and analgesic
-One of the safest and most effective against fever
-Low dose used as ANTIcoagulant in cardiovascular disease paitents
What is the mechanism of aspirin
Detailed mechanism is unknown but thought to reduce pain and inflammation by inhibiting the synthesis of prostaglandins.
How does aspirin impede blood clotting
inhibits platlet aggregation
How does aspirin reduce fever
acts on hypothalamic heat regulating centre
What are SERIOUS adverse effects associated with aspirin
Massive Gi hemorrage.
-Reye syndrome in children
note= ALL NSAIDS except aspirin increase the risk of serious adverse cardiovascular events.
Ibuprofen use, mechanism and serious side effects
-Nonsalicylate
-all types of arthritis and dysmenoorhea/fever.
-serious side effects include: Aplastic anemia, hematuria, hyperkalemia
Naproxen use, mechanism, adverse effects
Same as ibuprofin
-considered a strong NSAID
-Works by blocking Cox 1 and 2
-used to treat diffrent types of artheritis
Explain Diclofenac mechanism,
-Inhibits both cox 1 and 2 enzymes
-available in cream
-also used to treat symptoms if artharitis but also gout, migranes and dysmenorrgea
Contraindications: during third trimester, nursing women, known hypersensitivity, history of asthma, GI, liver or renal disease
Explain ketorolac
-used in short term managment up to 5 days of acute pain
-most effective NSAID used for moderate to severe pain.
-available in injections, tablets, opthalamic solutions
-should not be used for more than 5 days
-adverse effects: rash, tinnitus, dizziness, abdominal pain, nausea, diarrhea, constipation, dyspepsia, fluid retention. May cause serious injury to the GI tract
What does Cox 2 do
convert arachidonic acid (a fatty acid) into prostaglandins, which cause inflammation, pain, and fever.
COX-2 is mainly produced in macrophages (a type of immune cell) when there is tissue damage, meaning it plays a key role in the body’s inflammatory response.
List 2 types of Cox-2 inhibitor drugs
-celebrex
-movera
What do cox 2 inhibitors used for
treatment of osteoarthritis and rheumatoid arthritis.
What are the serious adverse effects of cox-2 inhibitors
myocardial infarction and stroke
whats the downside of cox-2inhibitors
COX-2 inhibitors were designed to reduce pain and inflammation without harming the stomach, but by disrupting the COX-1/COX-2 balance, they increase the risk of heart attacks and strokes. This is why doctors carefully consider cardiovascular risks before prescribing COX-2 selective NSAIDs.COX-1 helps produce thromboxane, which promotes blood clotting and narrows arteries.
COX-2 helps make prostacyclin, which prevents excessive clotting and keeps blood vessels open (vasodilation).
Normally, these two balance each other out—COX-1 tightens arteries and forms clots, while COX-2 relaxes arteries and prevents too much clotting.
What Happens When Only COX-2 Is Blocked?
Less prostacyclin → The protective, blood vessel-relaxing effect is lost.
COX-1 remains active → Blood clotting and artery tightening continue unchecked.
Higher risk of heart attacks & strokes due to increased clot formation and narrowed arteries.
What is 20-HETE
a vasoconstrictor.
and Blocking COX-2 increases 20-HETE levels, which further narrows arteries and raises blood pressure, adding to the risk of cardiovascular problems.
What drugs do cox-2 inhibitors interact with
ACE inhibitors, fluconazole, and lithium.
How does acetaminophen differ from NSAIDs in terms of its mechanism of action?
Acetaminophen works primarily in the brain by raising the pain threshold, whereas NSAIDs block COX enzymes at the site of pain to reduce inflammation.
Why doesn’t acetaminophen help with inflammation like NSAIDs?
Acetaminophen does not significantly block COX enzymes in peripheral tissues, so it does not reduce inflammation like NSAIDs.
What does it mean when we say acetaminophen “raises the pain threshold”?
It means the brain requires a stronger pain signal before recognizing pain, making discomfort feel less intense.
What is the use of Acetaminophen
What are the risks of long-term acetaminophen use?
Skin eruptions, urticaria (hives), hypotension, and hepatotoxicity (liver damage).
Why is acetaminophen overdose dangerous, and what is the antidote?
Overdose causes hepatotoxicity, coma, and internal bleeding due to the buildup of a toxic byproduct (NAPQI). The antidote is N-acetylcysteine (NAC), which replenishes glutathione to detoxify the liver.
How does N-acetylcysteine (NAC) prevent liver damage in acetaminophen overdose?
NAC restores glutathione, which neutralizes the toxic byproduct NAPQI before it damages liver cells.
How do migranes happen
happens due to waves of activity by groups of excitable brain cells. These trigger chemicals, such as serotonin, to narrow blood vessels.
What is a migraine aura?
An aura is a neurological disturbance that can cause:
Visual symptoms (flashing lights, blind spots).
Sensory changes (tingling, numbness).
Motor symptoms (difficulty speaking, muscle weakness).
What Happens in the Brain During a Migraine
Brain cells become overactive → This triggers the release of chemicals like serotonin, which can make blood vessels narrow or widen unpredictably, leading to migraine pain
What nerve carries pain in head and face
Trigeminal nerve
What is the role of the Trigeminal Nerve in Migraine Pain
Its nerve fibers release chemicals like Substance P and CGRP during a migraine.
CGRP (Calcitonin Gene-Related Peptide) → Causes inflammation and pain by dilating blood vessels.
Substance P → Increases pain sensitivity.
If you have a migrane what should you take
1) Acetaminophen blocks the production of prostaglandins
2)NSAIDs: Block the COX enzymes which produce inflammatory substance
3) Triptan Best for acute migraine relief, act on serotonin receptors and constrict blood vessels.
4)Gepants: Block the CGRP receptors
5) Ergot derivatives:act on seratonin, Similar to triptans but stronger, used when other treatments fail.
What blocks CGRP receptor antagonist and how does it work
Ubrelvy is a CGRP receptor antagonist, meaning it blocks CGRP from binding to its receptors on neurons and blood vessels.
how does Ubrelvy work
It prevents artery dilation without directly constricting blood vessels, reducing pain and inflammation without increasing the risk of heart issues (unlike triptans).
diffrence between Triptans and Gepants
Gepants (like Ubrelvy) only block CGRP receptors, reducing migraine pain without affecting blood pressure. Triptans also block CGRP but constrict blood vessels, which may not be safe for people with heart disease.
Name 2 drugs slide show arrows) used to treat migranes
-Sumatriptan
-caffeine
What are opiates give example
Drugs directly derived from opium poppies (e.g., morphine, codeine).
What are Opioids
Broader term that includes natural, semi-synthetic, and synthetic drugs that act like morphine (e.g., fentanyl, oxycodone, tramadol).
How do Opioids work
They bind to opioid receptors in the brain and body to reduce pain.
What are the diffrent types of opioid receptors
Mu (μ) receptors → Responsible for pain relief, euphoria, but also respiratory depression.
Kappa (κ) receptors → Provide some pain relief, but also cause sedation and dysphoria.
Delta (δ) receptors → Less involved in pain relief but may affect mood.
What are the risks of opioid
No upper limit for effectiveness → Higher doses provide stronger pain relief, but also increase risks.
Danger at high doses → Can cause loss of consciousness and slow or stop breathing, leading to overdose.
Risk of dependency → The brain adapts to opioids, leading to tolerance (needing higher doses) and withdrawal symptoms if stopped.
How Opioids Work at the Cellular Level
When opioids bind to these receptors, they activate G-protein coupled receptors (GPCRs), leading to a series of effects inside the cell.
Binding causes hyperpolarization → This means the inside of the neuron becomes more negatively charged, making it harder for the neuron to fire an action potential (send pain signals).
This reduces pain perception because the nerve cells carrying pain signals become less active
Effects of Opioids on the Brain
Decreased pain signaling → Fewer action potentials mean less pain is felt.
Increased dopamine release → Opioids indirectly increase dopamine, leading to euphoria and addiction potential.
Depressed breathing → Opioids slow down neurons controlling respiration, which is why high doses can cause respiratory failure.
What are two natural Opioids
Codeine
Morphine
What are the primary uses of codeine?
Used to induce sleep in presence of mild pain
Used as analgesic, sedative, hypnotic, antiperistaltic, and antitussive
How does codeine work in the body?
Codeine is a selective agonist of the mu opioid receptor, but it has a weaker affinity for this receptor compared to morphine.
What are serious side effects of Codeine
Cortical and respiratory depression, tolerance, dependence, and addiction.
Common side effect of codeine
miosis (pupil constriction and Postural hypotension
Morphine use, side effects and mechanism
-Management of all types of moderate to severe pain
Derivatives are used for cough inhibition, treatment of GI pain, relieving pain of myocardial infarction.
-Binds to mu-opioid receptor which is responsible for most of its analgesic and euphoric effects
Serious side effects: respitroy depression,
Who should avoid Morphine
Avoid in patients with asthma, emphysema, head injury, increased intracranial pressure, severe liver or kidney dysfunction, acute ulcerative colitis, or convulsive disorders.
Use cautiously in patients with prostatic hypertrophy.
Interacts with alcohol, monoamine oxidase inhibitors, meperidine.
List the semi-synthetic opioids
Hydromorphone, Hydrocodone
Oxycodone
Oxymorphone
When is Hydromorphone used
Used for moderate to severe pain (5-10 times more potent than morphine)
What advatnage does hydromorphone have over morphone
It has much higher bioavailability of 50% compared to morphine
What receptor does hydromorphine work on
works on the mu (μ) opioid receptor.
It has much weaker effects on the delta (δ) and kappa (κ) receptors.
What is Hydrocodone mechanism of action
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
Who can use hydrocodone
Can be used in children younger than 1 year and in pregnant women.
Oxycodone use and serious effects
Postoperative and postpartum pain
Serious: jaundice, hepatotoxicity, respiratory depression
Oxycodone mechanism of action
Binds to Kappa and mu receptors 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.
List the synthetic Opioid Analgesics
Buprenorphine
Fentanyl
Meperidine
Pentazocine
Tramadol
Buprenorphine use
postoperative pain
Administered for pain associated with cancer, accidental trauma, urethral calculi, myocardial infarction
Buprenorphine mechanism of action
It partially activates mu-opioid receptors (for pain relief and reducing cravings).
It blocks kappa-opioid receptors (reducing withdrawal symptoms).
It lasts a long time, so it helps people stop using stronger opioids (like heroin or fentanyl).
It has a ceiling effect, meaning it won’t cause extreme sedation or breathing problems like full opioids.
Fentanyl mechanism of action
-50-100 times more potenet than morphine
-full agonist at the mu-opioid receptor
-Important after surgery Can cause muscle rigidity and abnormal muscle movements after surgery.
Q: Why is meperidine (Demerol) rarely used today?
Meperidine has been largely replaced by safer opioids due to the risk of normeperidine-induced toxicity and serotonin syndrome.
How does meperidine (Demerol) work in the body?
Meperidine is a mu-opioid receptor agonist with mild effects on kappa-opioid receptors, providing pain relief and sedation.
Why is pentazocine (talwin) considered a less addictive alternative to full opioids?
It acts as a partial agonist at kappa receptors (for pain relief) and a weak antagonist or partial agonist at mu receptors, reducing euphoria and addiction risk.
What makes tramadol different from other opioids?
Tramadol weakly binds to mu-opioid receptors and also inhibits serotonin and norepinephrine reuptake, making it useful for neuropathic pain but increasing the risk of serotonin syndrome.
Narcan (naloxone)
-prescribed for narcotic overdose, reversal of narcotic respiratory depression.
-Naloxone works bykicking opioids off the receptors in your brain and binding to those receptors instead.
-Naltrexone is NOT for withdrawal. It is used after detox to help prevent opioid or alcohol relapse by blocking the effects of opioids and reducing alcohol cravings.
Seratonin syndrom
life threatening condition by excessive accumulation of serotonin in the CNS.
What are the three main systems affected by serotonin syndrome?
Neurological → Agitation, confusion, seizures.
Autonomic → Fast heart rate, high blood pressure, sweating.
Muscular → Tremors, rigidity, exaggerated reflexes.
What are some common drug types that can trigger serotonin syndrome?
Antidepressants (SSRIs, SNRIs, MAOIs, TCAs).
Opioids with serotonergic activity (Tramadol, Fentanyl).
Migraine medications (Triptans like Sumatriptan).
Illicit drugs (MDMA/Ecstasy, Cocaine).
Herbal supplements (St. John’s Wort, 5-HTP).
Excess serotonin precursors/stimulants (L-Tryptophan, Amphetamines).
