Pharm Block II - Pain Management Flashcards

1
Q

Gate control theory

A

Substantia gelatinosa (SG) are modulating pain gates between periphery and CNS. Brain interprets pain and sends motor response, pain gates are closed with other sensory nerves. Ex: Rubbing arm to reduce painful stimulus will close pain gates in lower back so no more painful nerve impulses are sent up, rather non-painful impulses sent up instead.

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2
Q

Mu opioid receptors

A

High affinity for enkephalins and beta-endorphin, low affinity for dynorphins

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3
Q

Kappa opioid receptor

A

Binds opioid peptide dynorphin as primary endogenous ligand; natural alkaloids and synthetic ligands bind the receptor

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4
Q

Delta opioid receptors

A

Enkepalins as endogenous ligands. Activation results in some analgesia, less than Mu agonists.

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5
Q

anesthesia

A

partial or complete loss of sensation, w/ or w/out loss of consciousness, as a result of disease, injury, or admin of anesthetic

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6
Q

analgesia

A

absence of normal sense of pain

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7
Q

hyperalgesia

A

an excessive sensitivity to pain ; painful stimuli are perceived as more painful

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8
Q

hyperesthesia

A

an increased sensitivity to sensory stimuli, such as pain or touch

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9
Q

allodynia

A

non painful stimuli are perceived as painful

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10
Q

dysthesia

A

unpleasant sensations (ex: “pins/needles” or “ants crawling on skin”)

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11
Q

hyperpathia

A

all stimuli (noxious & innocuous) are more intense

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12
Q

Point of WHO analgesic ladder

A

Step-wise approach to determine the appropriate anagesic for patient

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13
Q

Mild pain (1-4)

A

Start with step 1 drugs (acetaminophen, NSAIDs, aspirin), max dose should be tried before moving to step 2

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14
Q

Moderate pain (5-6)

A

Start with step 2 drugs (codeine, hydrocodone, oxycodone, propoxyphene), typically prepared with non-opioids, if pain persists or worses move to step 3

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15
Q

Severe pain (7-10)

A

Start with step 3 drugs (morphine - gold standard, hydromorphone, fentanyl, meperidine)

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16
Q

Obtaining pain using ABCDE

A

Ask pt about pain regularly and assess it systematically; Believe pts and families in reports of pain and what relieves it; Choose pain control options approprate for pts, families, settings; Deliver interventions in timely, logical, and coordinated fashion; Empower pts and families and enable them to control their course.

17
Q

neuropathic pain

A

nerve pain, usually burning/tingling, or electric-shock like, a type of chronic pain from nerves in CNS getting damaged

18
Q

nociceptive pain

A

most often derived from stimulation of pain receptors. may arise from tissue inflamm, mechanical deformation, ongoing injury, or destruction. Can be visceral (poorly localized, originating from internal organ/cavity), or somatic (well-localized)

19
Q

idiopathic pain

A

pain that has no apparent underlying cause but is extremely real to the pt

20
Q

psychogenic pain

A

somatoform pain disorder is severe enough to disrupt everyday life. pain is like that of a physical disorder, but no physical cause is found

21
Q

Acute pain

A

Comes on quickly, usually severe, last relatively short period of time, caused by disease or trauma

22
Q

Tx for acute pain

A

Treat insult or remove injury/numb sensation. Block activation of afferent, alter receptor densities, increase endogenous opiates, modulate neurotransmitter activity.

23
Q

Chronic pain

A

Persists beyond normal tissue healing time (3 months)

24
Q

Tx for chronic pain

A

Methods aimed at symptom relief. Address issues beyond physical sensations: emotional, lifestyle, personality, anxiety, sleeplessness, depression.

25
Q

physical dependence

A

a state of adaptation that is manifested by a drug class specific withdrawal syndrome that can be produced by abrupt cessation, rapid dose reduction, decreasing blood level of drug, or administration of an antagonist

26
Q

tolerance

A

a state of adaptation in which exposure to a drug induces changes that result in a diminution of one or more of the drug’s effects over time

27
Q

addiction

A

a primary, chronic disease of brain reward, motivation, memory & related circuitry. Dysfunction in these circuits leads to characteristic biological, psychological, social, &spiritual manifestations

28
Q

Pros and cons of PRN dosing for pain management

A

By time patient feels pain, requests and receives pain med, pain has escalated, analgesic takes time to take effect, not well managed with PRN alone. Scheduled analgesics with PRN for breakthrough pain provide more consistent blood levels of analgesic, preventing peaks in pain - while PRN available for peaks in pain.

29
Q

Nonpharmacologic pain management

A

Cognitivie-Behavioral Therapy: focus on impact that though, behaviors, emotions have on pt’s pain (relaxation imagery). Physical agents: message, heat or cold applications. Trascutaneous Electrical Nerve Stimulation (TENS): noninvasive nerve stimulation to reduce acute/chronic pain.

30
Q

peripheral agents (acetominophen) MOA

A

inhibits prostaglandin synthesis in the CNS which makes it antipyretic and analgesic. No effect on inflamm or platelets

31
Q

NSAIDS MOA

A

propionic acid derivatives. irreversibly inhibit COX-1 and COX-2 & inhibit synthesis of prostaglandin precursors but not leukotrienes. Anti-inflamm, analgesic, anti-pyretic, alter platelet function, and prolong bleeding time)

32
Q

Opiods MOA

A

bind specific opiod receptors in CNS to produce effects that mimic the action of endogenous peptide neurotransmitters such as endorphins, enkephalins, and dynorphins

33
Q

Bisophonates (used for bone pain) MOA

A

analogs of pyrophosphate. decrease osteoclastic bone reabsorption

34
Q

neuropathic agens MOA for pain relief

A

all CNS acting drugs act by altering a step in the neurotransmission process either by affecting a presynaptic neuron from releasing neurotransmitters or by blocking a postsynaptic receptor.

35
Q

antidepressant agents MOA for pain relief

A

increases actions of norepinephrine and/or serotonin in the brain by blocking the neurotransmitter reuptake

36
Q

anticonvulsant agents MOA for pain relief

A

block voltage-gated Na+ or Ca+ channels, enhance inhibitory GABA-ergic impulses, interfere w/ excitatory glutamate transmission.these alter the pain threshold.