Pain Control Flashcards

1
Q

Gate-Control Theory of Pain

A
  • Sensory/emotional experience
  • Impulse transmission can be adjusted
  • Interneurons can act as “gates”
  • Factors: learned experiences, cultural expectations, individual tolerance, and the placebo effect, can activate the descending inhibitory nerves from the upper central nervous system.
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2
Q

Drugs Used to Relieve Pain

A

*Non-Opioid medications= Acetaminophen, NSAID, ASA.

Narcotics: Opium derivatives used to treat many types of pain

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3
Q

Gate-Control Theory of Pain

A
  • Sensory and emotional experience
  • impulse transmission can be adjusted
  • Interneurons can act as “gates”
  • Several factors, including learned experiences, cultural expectations, individual tolerance, and the placebo effect, can activate the descending inhibitory nerves from the upper central nervous system.
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4
Q

Opioid Receptors

A

receptor sites found in the CNS, on nerves in the periphery, and on cells in the gastrointestinal (GI) tract.

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5
Q

More on Gate Control Theory of Pain

A

*impulses travel from the spine to the cortex via tracts that can be modulated along the way at specific gates. These gates can be closed to block the transmission of pain impulses by the upper CNS, which relate to emotion, culture, placebo effect, and stress, and by large-diameter sensory A fibers, which are associated with touch.

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6
Q

1st generation NSAID & ASA Use Mechanisms

A

inhibition of cyclooxgenase pathways 1 & 2 (nonselective) . These pathways promote inflammation and cause pain, promote platelet aggregation for blood clotting after an injury

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7
Q

1st generation NSAID & ASA Uses/Indications

A

reduce inflammation, fever, pain and low level anti-clotting drug (1 ASA daily for stroke and heart attack risk prevention)

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8
Q

1st generation NSAID & ASA Major Adverse Effects:

A

GI symptoms including increased risk for bleeding; salicylism (ASA), Reyes syndrome (ASA) –can lead to kidney dysfunction

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9
Q

2nd generation NSAID (–coxib)

A

Selective for COX2 pathway only
Controvery over increased risk for stroke and heart attack (one drug withdrawn by FDA)
Celecoxib (Celebrex) still on the market

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10
Q

2nd generation NSAID (–coxib)

A

Uses/Indication: reduce inflammation, fever, pain in chronic pain states esp. osteoarthritis
Major Adverse Effects: GI symptoms including increased risk for bleeding; monitor for stroke and heart attack symptoms and increased risk

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11
Q

Acetaminophen

A

Acts on thermoregulatory cells of the hypothalamus
unknown mechanism of analgesic effects
Used to treat pain and fever
Tx Prophylaxis of children receiving diphtheria–pertussis–tetanus (DPT) immunizations
Relief of musculoskeletal pain associated with arthritis

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12
Q

Acetaminophen Teaching Pts.

A

Educate patients on accidental overdose—>leads to liver failure
Max dose 4 grams for young healthy adults
Max dose 2.5 grams 55+
Avoid use in persons with high levels of alcohol intake ↑ risk for hepatic toxicity

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13
Q

ASA & NSAIDS Teaching Pts.

A

Take with food to avoid GI upset

DC use 7 days prior to surgery

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14
Q

Narcotic Agonists

A

drugs that react with the opioid receptors throughout the body to cause analgesia, sedation, or euphoria (Figure 26.2). Anticipated effects other than analgesia are mediated by the types of opioid receptors affected by each drug.

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15
Q

Narcotic Agonists Prototype med-Morphine,

A

*add fentanyl and other stronger narcotics
Actions
Act at specific opioid receptor sites in the CNS
Produce analgesia, sedation, and a sense of well-being
Indications
Relief of severe acute or chronic pain
Analgesia during anesthesia
Cross placenta

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16
Q

Narcotic Agonists Pharmacokinetics

A

IV most reliable way to achieve therapeutic response
IM and sub-q rate of absorption varies
Hepatic metabolism and generally excreted in the urine and bile

17
Q

Narcotic Agonists Contraindications/Cautions

A
Known allergy
Diarrhea caused by poisons
Cautions:
Respiratory dysfunction
GI or GU surgery
Acute abdomen or ulcerative colitis
18
Q

Narcotic Agonists Adverse Reactions

A
Respiratory depression with apnea
Cardiac arrest Shock
Orthostatic hypotension
Nausea, vomiting, constipation
Biliary spasm
Dizziness, psychoses, anxiety, fear, hallucinations
19
Q

location of Opioid Receptors

A

Cells in the gastrointestinal (GI) tract
Nerves in the periphery
CNS and Brain

20
Q

What happens when Opioid receptors are stimulated?

A

In the hypothalamus- may interrelate the endocrine and neural responses to pain.
In the limbic system, the receptors incorporate emotional aspects of pain and response to pain. At peripheral nerve sites, they may block the release of NT’s that are related to pain and inflammation.

21
Q

Narcotic Agonists Prototype Morphine

A

*may also add fentanyl and other stronger narcotics.

22
Q

Narcotic Agonists

A

drugs that react with the opioid receptors throughout the body to cause analgesia, sedation, or euphoria