Pain Pharmacology Flashcards

Question 1

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Pain meds pharmacology

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Here’s a detailed overview of the pharmacology for each of the pain medications you mentioned:

Mechanism: Not fully understood but believed to involve inhibition of prostaglandin synthesis in the central nervous system, affecting pain perception.
Uses: Mild to moderate pain, fever reduction.
Side Effects: Liver toxicity (especially with overdose), minimal gastrointestinal effects.
Nursing Considerations: Monitor liver function, avoid exceeding the recommended dose, assess for signs of hepatotoxicity, especially in patients with liver disease.

Examples: Ibuprofen, aspirin, naproxen.
Mechanism: Inhibit cyclooxygenase (COX) enzymes (COX-1 and COX-2), reducing prostaglandin production, thereby decreasing inflammation and pain.
Uses: Mild to moderate pain, inflammation, fever.
Side Effects: Gastrointestinal irritation, ulcers, renal impairment, increased bleeding risk.
Nursing Considerations: Monitor for GI bleeding, renal function, and signs of allergic reactions. Administer with food or milk to minimize gastrointestinal irritation.

Examples: Morphine, oxycodone, fentanyl.
Mechanism: Bind to opioid receptors (mu, kappa, delta) in the central nervous system, altering pain perception and emotional response to pain.
Uses: Moderate to severe pain, often in cancer care, post-surgical pain.
Side Effects: Respiratory depression, constipation, nausea, sedation, potential for addiction.
Nursing Considerations: Monitor respiratory rate and depth, manage constipation with laxatives, assess pain levels, and educate patients on the risks of dependency and proper use.

Mechanism: An opioid that is metabolized into morphine in the body. It binds to opioid receptors to provide pain relief.
Uses: Mild to moderate pain, often combined with acetaminophen or aspirin in combination products.
Side Effects: Similar to other opioids—constipation, nausea, sedation, and potential for addiction. It also has a risk of causing respiratory depression.
Nursing Considerations: Monitor for signs of respiratory depression and constipation, and ensure proper dosing to minimize risk of side effects.

Mechanism: Binds to voltage-gated calcium channels in the central nervous system, which reduces excitatory neurotransmitter release.
Uses: Neuropathic pain, seizure disorders.
Side Effects: Dizziness, drowsiness, peripheral edema, and weight gain.
Nursing Considerations: Monitor for signs of dizziness and drowsiness, assess for effective pain relief, and adjust doses carefully.

Mechanism: Similar to gabapentin, it binds to calcium channels in the central nervous system, reducing the release of excitatory neurotransmitters.
Uses: Neuropathic pain, fibromyalgia, and seizure disorders.
Side Effects: Dizziness, drowsiness, weight gain, and edema.
Nursing Considerations: Monitor for signs of sedation and weight gain, ensure dose adjustments for renal impairment, and assess pain control.

Mechanism: A centrally acting analgesic with a dual mechanism—binds to opioid receptors and inhibits the reuptake of norepinephrine and serotonin.
Uses: Moderate pain.
Side Effects: Nausea, dizziness, constipation, headache, and potential for serotonin syndrome.
Nursing Considerations: Monitor for signs of serotonin syndrome, drowsiness, and constipation. Adjust dose in patients with renal or hepatic impairment.

Examples: Lidocaine, bupivacaine.
Mechanism: Block sodium channels in nerve membranes, preventing the propagation of nerve impulses and thereby providing localized pain relief.
Uses: Localized pain relief during minor surgical procedures, dental work, or regional blocks.
Side Effects: Systemic toxicity (e.g., seizures, cardiovascular effects) if used excessively or improperly, local irritation or allergic reactions.
Nursing Considerations: Monitor for signs of systemic toxicity, ensure proper technique and dosage, and assess the effectiveness of pain relief.

Each medication requires careful consideration of its specific pharmacokinetics, interactions, and patient-specific factors to ensure effective and safe pain management.

Question 2

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Morphine pharamacology

Answer

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Morphine is a potent opioid analgesic used primarily to manage severe pain. Here’s an overview of its pharmacology:

Receptor Interaction: Morphine binds predominantly to the mu-opioid receptors in the central nervous system. These receptors are involved in modulating pain perception and emotional response to pain.
Action: Upon binding, morphine inhibits the release of neurotransmitters involved in pain transmission, thereby reducing the sensation of pain.

Absorption: Morphine can be administered orally, intravenously, intramuscularly, subcutaneously, or via other routes. It has variable bioavailability depending on the route of administration; oral morphine is less bioavailable (about 20-40%) due to first-pass metabolism in the liver.
Distribution: Morphine is widely distributed throughout the body and crosses the blood-brain barrier. It is also distributed into breast milk.
Metabolism: Morphine is metabolized mainly in the liver by conjugation with glucuronic acid to form morphine-3-glucuronide and morphine-6-glucuronide. The latter has analgesic properties.
Excretion: It is primarily excreted by the kidneys. About 90% of morphine is eliminated in the urine, mostly as metabolites.

Pain Management: Used for moderate to severe pain, including pain from cancer, post-surgical pain, and pain from severe injuries or conditions.
Other Uses: Sometimes used for acute pulmonary edema and as part of palliative care.

Common: Constipation, nausea, vomiting, sedation, and dizziness.
Serious: Respiratory depression, hypotension, bradycardia, urinary retention, and potential for addiction or overdose.

Monitoring: Regularly monitor pain levels, respiratory rate, sedation levels, and bowel function. Be vigilant for signs of opioid toxicity.
Dosing: Start with a lower dose and titrate based on patient response and side effects. Adjust doses for renal or hepatic impairment.
Education: Educate patients about the risk of dependency, proper use of the medication, and possible side effects.

Caution with CNS Depressants: Morphine’s sedative effects can be potentiated by other CNS depressants, such as benzodiazepines or alcohol, increasing the risk of severe respiratory depression.
Other Interactions: May interact with medications that affect liver enzymes involved in its metabolism.

Morphine remains a critical tool in managing severe pain, but it requires careful management due to its potential for significant side effects and the risk of addiction.

Question 3

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Opioid antagonists

Answer

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Opioid antagonists are drugs that block the effects of opioids by binding to opioid receptors without activating them. They are primarily used to reverse opioid overdose and manage opioid-induced side effects. Here’s a detailed look at their pharmacology:

Naloxone (Narcan)
- Mechanism of Action: Naloxone is a competitive antagonist at mu-opioid receptors and, to a lesser extent, kappa and delta receptors. It displaces opioids from these receptors, reversing their effects.
- Pharmacokinetics:
  - Absorption: Rapidly absorbed when administered intranasally or intramuscularly. The oral bioavailability is low due to first-pass metabolism.
  - Distribution: Widely distributed in the body, including the brain.
  - Metabolism: Metabolized in the liver.
  - Excretion: Excreted primarily through the urine.
- Uses: Primarily used to reverse opioid overdose, including respiratory depression, sedation, and hypotension.
- Onset and Duration: Rapid onset (within minutes) when administered intranasally or intramuscularly. Duration of action is shorter than many opioids, often requiring repeated doses.
- Side Effects: May induce withdrawal symptoms in opioid-dependent individuals, nausea, and vomiting.
Naltrexone
- Mechanism of Action: Similar to naloxone, naltrexone is a competitive antagonist at mu-opioid receptors and, to a lesser extent, kappa and delta receptors.
- Pharmacokinetics:
  - Absorption: Well absorbed orally.
  - Distribution: Widely distributed.
  - Metabolism: Metabolized in the liver.
  - Excretion: Excreted primarily via the urine.
- Uses: Used for opioid dependence treatment and to reduce alcohol cravings. Also used in managing opioid overdose in a long-term setting.
- Onset and Duration: Slower onset than naloxone, with a longer duration of action.
- Side Effects: Hepatotoxicity, nausea, headache, and potential withdrawal symptoms in opioid-dependent individuals.
Methylnaltrexone
- Mechanism of Action: Methylnaltrexone is a peripherally acting opioid antagonist, primarily blocking mu-opioid receptors in the gastrointestinal tract.
- Pharmacokinetics:
  - Absorption: Poorly absorbed from the gastrointestinal tract.
  - Distribution: Limited systemic distribution.
  - Metabolism: Metabolized in the liver.
  - Excretion: Excreted primarily through the urine.
- Uses: Used to treat opioid-induced constipation in patients with chronic pain or advanced illness.
- Onset and Duration: Rapid onset of action in the gastrointestinal tract.
- Side Effects: Abdominal pain, flatulence, nausea, and diarrhea.

Emergency Use: Naloxone is critical in emergency situations for reversing opioid overdose and should be administered promptly.
Long-Term Management: Naltrexone is used in a more controlled environment for managing opioid dependence and should be started after the opioid has cleared from the body to avoid withdrawal symptoms.
Monitoring: For opioid antagonists, especially in overdose situations, continuous monitoring of respiratory status and level of consciousness is essential.

Opioid antagonists play a crucial role in the management of opioid effects, especially in emergency settings and long-term treatment of addiction and opioid-related complications.

Question 4

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Lithium pharmacology

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Lithium is a medication commonly used in the treatment of bipolar disorder, primarily for its mood-stabilizing properties. Here’s an overview of its pharmacology:

Neurochemical Effects: Lithium’s exact mechanism of action is not fully understood, but it is believed to involve several neurochemical pathways:
- Modulation of Neurotransmitters: It affects neurotransmitter systems, including serotonin and norepinephrine.
- Inositol Pathway: Lithium inhibits inositol monophosphatase, leading to reduced levels of inositol triphosphate and diacylglycerol, which impacts intracellular signaling.
- Neuroplasticity: It may influence neuronal growth and neuroplasticity, enhancing resilience to mood disturbances.

Absorption: Lithium is well absorbed from the gastrointestinal tract, with peak plasma concentrations typically occurring within 1-3 hours after oral administration.
Distribution: It distributes widely in body tissues, similar to sodium, and can cross the blood-brain barrier.
Metabolism: Lithium is not metabolized by the body but is excreted unchanged.
Excretion: Primarily excreted by the kidneys. The rate of excretion is influenced by renal function and sodium levels.

Bipolar Disorder: Effective in managing both manic and depressive episodes. It helps in mood stabilization and prevention of future episodes.
Other Uses: Occasionally used for treatment-resistant depression or certain other psychiatric conditions.

Therapeutic Range: The therapeutic plasma concentration of lithium typically ranges from 0.6 to 1.2 mEq/L. Levels should be monitored regularly to avoid toxicity.
Dosing: The dosage is individualized based on patient response and serum levels. It is usually administered in divided doses.

Common: Tremors, increased thirst and urination, weight gain, and gastrointestinal disturbances.
Serious: Lithium toxicity, which can present as severe tremors, confusion, ataxia, seizures, and renal failure. Chronic use can lead to renal impairment or thyroid dysfunction.

Signs of Toxicity: Include severe gastrointestinal symptoms, persistent tremors, confusion, and renal issues. Severe toxicity may require hospitalization.
Management: In cases of mild toxicity, dose adjustment and monitoring are usually sufficient. Severe toxicity may require discontinuation of lithium, hydration, and supportive care. Hemodialysis may be needed in extreme cases.

Interactions: Lithium levels can be affected by interactions with diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs), and other medications that influence renal function or electrolyte balance.
Precautions: Regular monitoring of renal function, thyroid function, and serum lithium levels is necessary. Patients should maintain adequate hydration and be cautious with salt intake, as changes in sodium levels can affect lithium levels.

Lithium is a cornerstone in the treatment of bipolar disorder, but its use requires careful monitoring due to its narrow therapeutic index and potential for toxicity.

Question 5

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Antipsychotics

Answer

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Antipsychotics are medications used to manage symptoms of psychotic disorders, such as schizophrenia and bipolar disorder. They are categorized into two main classes: typical (first-generation) and atypical (second-generation) antipsychotics. Here’s an overview of their pharmacology:

These drugs primarily act as dopamine D2 receptor antagonists.

Dopamine Receptor Blockade: They mainly block D2 receptors in the mesolimbic and mesocortical pathways of the brain, reducing symptoms of psychosis.
Other Receptors: They may also affect other neurotransmitter systems to a lesser extent, including serotonin, histamine, and adrenergic receptors.

Haloperidol
Chlorpromazine
Fluphenazine

Absorption: Generally well absorbed when administered orally.
Distribution: Distributed widely throughout the body, including the central nervous system.
Metabolism: Metabolized in the liver.
Excretion: Excreted primarily via the urine.

Extrapyramidal Symptoms (EPS): Includes tremors, rigidity, bradykinesia, and tardive dyskinesia due to dopamine blockade in the nigrostriatal pathway.
Neuroleptic Malignant Syndrome (NMS): A rare but serious condition characterized by hyperthermia, muscle rigidity, and autonomic instability.
Other: Sedation, weight gain, anticholinergic effects (e.g., dry mouth, constipation).

These drugs have a broader receptor profile, affecting both dopamine and serotonin systems.

Dopamine Receptor Blockade: They also block D2 receptors, but with a lower affinity compared to typical antipsychotics.
Serotonin Receptor Blockade: They antagonize serotonin 5-HT2A receptors, which may help alleviate both positive and negative symptoms of psychosis.

Risperidone
Olanzapine
Quetiapine
Aripiprazole
Lurasidone

Absorption: Typically well absorbed orally, though the rate can vary.
Distribution: Extensive distribution into body tissues.
Metabolism: Metabolized in the liver, often by cytochrome P450 enzymes.
Excretion: Excreted via urine and feces.

Metabolic Syndrome: Weight gain, diabetes, and dyslipidemia.
EPS: Less common than with typical antipsychotics but can still occur.
Sedation: Common with some atypicals.
Prolonged QT Interval: Certain atypical antipsychotics may increase the risk of cardiac arrhythmias.

Choice of Antipsychotic: The selection of an antipsychotic depends on the specific symptoms, side effect profile, and patient history.
Monitoring: Regular monitoring for side effects such as weight gain, glucose levels, and extrapyramidal symptoms is crucial. Blood tests may be needed for drugs with potential for metabolic side effects.
Adherence: Antipsychotic medications are often used long-term, so strategies to improve patient adherence and manage side effects are important.

Both typical and atypical antipsychotics play vital roles in managing psychotic disorders, but they require careful management to balance efficacy with potential side effects.

Question 6

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