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Pharma > PRELIMS: Opioid > Flashcards

PRELIMS: Opioid Flashcards

1
Q

What are the two main categories of analgesic drugs?

A

Opioid Analgesics
Non-opioid Analgesics

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2
Q

Which opioid receptor is most associated with the analgesic effects of many opioids?

A

Mu receptors

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2
Q

Name a prototypical opioid analgesic.

A

Morphine

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3
Q

What are the three primary classes of opioid receptors?

A

Mu
Kappa
Delta

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3
Q

List two examples of strong opioid agonists.

A

Fentanyl
Morphine

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4
Q

Name a concern associated with the stimulation of mu receptors.

A

Respiratory depression and constipation

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4
Q

What are mixed agonist-antagonists and provide an example?

A

Definition: Drugs that exhibit both agonist and antagonist activity at different opioid receptors.
Example: Buprenorphine

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4
Q

What are endogenous opioid peptides?

A

Endorphins
Enkephalins
Dynorphins

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4
Q

What is the function of opioid antagonists like Naloxone and Naltrexone?

A

Naloxone: Rapidly reverses opioid-induced respiratory depression.
Naltrexone: Used to maintain an opioid-free state and treat alcohol dependence.

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4
Q

How do transdermal patches benefit opioid administration?

A

Provide steady, prolonged administration.
Avoid GI tract, reducing problems like constipation.

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4
Q

What is the primary site of opioid metabolism?

A

Liver

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5
Q

What are the primary routes of administration for opioids?

A

Oral
Suppository
Parenteral (Subcutaneous, Intramuscular, IV)
Transdermal
Iontophoresis
Transmucosal and Intranasal

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5
Q

What are the benefits of opioid analgesics in rehabilitation?

A

Reduce pain
Help patients be more active and engaged in exercise and rehabilitation

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5
Q

Describe the spinal effects of opioids.

A

Location: Dorsal horn of the spinal cord
Action: Inhibit synapses transmitting nociceptive input
Presynaptic Effects: Decrease release of pain-mediating transmitters
Postsynaptic Effects: Hyperpolarize the postsynaptic neuron

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5
Q

List some issues associated with opioid use.

A

Sedative properties
Mood changes
Cardiovascular effects (orthostatic hypotension)
Gastrointestinal distress (nausea, vomiting, constipation)

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5
Q

What are the effects of opioids on peripheral sensory nerve endings?

A

Decrease excitability
Mechanism: Likely involves inhibition of adenyl cyclase activity and control of ion channels

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5
Q

Name two common side effects of opioids.

A

Respiratory Depression
Constipation

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5
Q

Where do opioids act in the brain, and what is their effect?

A

Location: Brain regions associated with pain transmission (e.g., Periaqueductal gray matter)
Effect: Activate descending pain pathways, leading to inhibition of pain transmission at the spinal cord

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5
Q

What is tolerance, and what are its physiological mechanisms?

A

Definition: Need to increase drug dosage to maintain therapeutic effects over time.
Mechanisms:
Receptor Downregulation and Desensitization
Receptor Recycling
G Protein Disruption
Increased Pain Pathways

5
Q

Describe the onset and duration of tolerance.

A

Onset: Begins after the first dose
Noticeable: After 2-3 weeks
Duration: Lasts 1-2 weeks after drug removal

5
Q

What is physical dependence, and how does it differ from addiction?

A

Definition: Onset of withdrawal symptoms when the drug is abruptly stopped.
Symptoms: Peak 2-3 days after last dose, lasting around 5 days.
Distinction: Different from addiction which involves cravings and drug-seeking behavior.

5
Q

How does Patient-Controlled Analgesia (PCA) benefit patients?

A

Allows patients to control their own analgesic delivery
Commonly used post-surgery, for chronic pain, and cancer-related pain

5
Q

What are the effects of opioids on gastrointestinal motility?

A

Decrease GI motility
Used to control severe diarrhea
Can cause severe constipation

5
Q

Define addiction in the context of substance use.

A

Repeatedly ingesting substances for mood-altering and pleasurable effects, such as seeking an opioid “high.”

5
Q

How can opioids positively and negatively affect rehabilitation patients?

A

Positive Effects: Pain relief, facilitating more vigorous rehabilitation, scheduling therapy sessions when opioids are most effective.
Negative Effects: Sedation, GI discomfort, respiratory depression, constipation.

6
Q

Define psychological dependence.

A

Motivation to use drugs to reproduce pleasurable sensations, leading to continued drug-seeking behavior.

6
Q

List some key drugs classified as NSAIDs.

A

Aspirin
Acetaminophen
Other NSAIDs (understanding their mechanisms and effects is crucial for patient management)

6
Q

Describe the key pharmacological properties of NSAIDs.

A

Anti-inflammatory: Decreases inflammation
Analgesic: Relieves mild-to-moderate pain
Antipyretic: Reduces fever
Anticoagulant: Inhibits platelet aggregation

6
Q

What is the historical context of aspirin in relation to NSAIDs?

A

Aspirin is considered the prototype NSAID and is often used as a benchmark for comparing the efficacy and safety of newer NSAIDs.

6
Q

What are opioid-induced hyperalgesia and its potential causes?

A

Definition: Increased pain sensitivity or lack of response to opioids.
Causes: Genetic predispositions, increased glutamate activity, increased sensitivity of NMDA receptors.

6
Q

What are common pharmacological treatments for opioid addiction?

A

Methadone: Substitutes for abused opioids; reduces withdrawal symptoms.
Buprenorphine: Mixed agonist-antagonist; reduces abuse potential when combined with Naloxone.

6
Q

Describe the mechanism of action for aspirin and other NSAIDs.

A

Aspirin and other NSAIDs interfere with the biosynthesis of prostaglandins, which are involved in pain, inflammation, fever, and blood clotting.

6
Q

What was discovered in the early 1970s regarding NSAIDs?

A

Researchers discovered that the therapeutic effects of aspirin and NSAIDs are linked to their impact on prostaglandin biosynthesis.

6
Q

What role do leukotrienes play, and which drugs target them?

A

Leukotrienes are pro-inflammatory and important in airway inflammation (e.g., asthma, allergic rhinitis).

Drugs:
LOX Inhibitors: Zileuton
Leukotriene Receptor Blockers: Montelukast, Zafirlukast

6
Q

How are eicosanoids, including prostaglandins, thromboxanes, and leukotrienes, biosynthesized?

A

: Eicosanoids are derived from arachidonic acid, which is cleaved from cell membranes by phospholipase A2.

COX Enzymes: Produce prostaglandins and thromboxanes.
LOX Enzymes: Produce leukotrienes

6
Q

What are prostaglandins, and where are they produced?

A

Prostaglandins are lipid-like compounds with diverse physiological activities, produced by almost all cells except red blood cells.

6
Q

What is the significance of NSAIDs in physical rehabilitation?

A

Frequently used to manage pain and inflammation, with therapy tailored to each patient’s needs.

6
Q

How do prostaglandins and thromboxanes influence various physiological systems?

A

Vasodilation vs. Vasoconstriction: Some prostaglandins cause vasodilation; others and thromboxanes cause vasoconstriction.
Effects on Systems: Influence cardiovascular, respiratory, renal, gastrointestinal, nervous, and reproductive systems.

6
Q

How does acetaminophen differ from NSAIDs like aspirin?

A

Acetaminophen decreases pain and fever but lacks anti-inflammatory and anticoagulant properties, so it is not classified as an NSAID.

6
Q

How does the inhibition of thromboxane synthesis affect clotting?

A

Inhibition of thromboxane synthesis helps prevent excessive clotting by reducing platelet aggregation and clot formation.

7
Q

What are some pathological conditions associated with prostaglandins and thromboxanes?

A

Inflammation: Prostaglandins mediate erythema, edema, and increase blood flow and capillary permeability.
Pain: Prostaglandins increase the sensitivity of pain receptors.
Fever: Prostaglandins alter the thermoregulatory set-point in the hypothalamus.
Dysmenorrhea: Increased prostaglandin production in the endometrium causes menstrual cramps.
Thrombus Formation: Thromboxanes cause platelet aggregation and clot formation.

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Pharma (9 decks)

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