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PATHO > Pain Patho > Flashcards

Pain Patho Flashcards

1
Q

Pain as a subjective experience

A

It is what the patient says it is; phys, cognitive, emotional, spiritual, environmental combo

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2
Q

Afferent pathway

A

Begins in PNS and impulses ascend thru base of spine

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3
Q

Interpretive centers

A

Cortical and subcortical areas of the brain and cortex that interpret sensations as pain

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4
Q

Efferent pathways

A

Send messages from the interpretive centers back to the PNS and elicit a response

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5
Q

3 parts of NS messaging

A

Sensation, perception, response

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6
Q

Nociceptors

A

Pain receptors; free nerve endings in afferent peripheral systems that cause nociceptive pain when stimulated by stimuli of certain intensities or that are close to causing tissue injury

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7
Q

Target for pain meds

A

Nociceptors

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8
Q

Nociceptors location

A

Dental pulp, skin, meninges, internal organs, periosteum, few in brain, alveoli, deep tissue

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9
Q

NTs role in pain

A

Control transmission of pain impulse; excitatory or inhibitory

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10
Q

Endorphins

A

Endogenous opioids that aid in inhibition of pain response; mediate pre-synaptic transmission

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11
Q

What do excitatory NTs do?

A

Enhance, increase pain response in injury or chronic inflammation

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12
Q

What do inhibitory NTs do?

A

Block pain (GABA is the main)

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13
Q

4 stages of pain processing

A

Transduction, transmission, perception, modulation

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14
Q

Transduction

A

Painful stimuli are converted to APs at sensory receptor; occurs along a-delta and C fibers; NTs released from direct injury and inflammation cause APs

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15
Q

Prostaglandin

A

Important mediators that lowers the pain threshold when activated; promote inflammation, pain, fever, blood clotting, protecting the stomach lining from acid, kidney function; dilate BVs that lead to kidneys; what we target with pharmacotherapy

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16
Q

A-delta fibers

A

Small, myelinated fibers that cause stinging, sharp, cut, pinch feeling; LOCALIZED pain

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17
Q

C fibers

A

Unmyelinated, slower, small diameter, dull pain, burn, ache, poorly localized; workout ache

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18
Q

A-alpha and A-beta fibers

A

Larger diameter nerve fibers that don’t transmit pain; activated in the gate control theory

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19
Q

Transmission

A

APs move from peripheral receptors to spinal cord and brain via the dorsal horn located in the spinal cord; end up in thalamus; A-delta and C fibers carry

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20
Q

Pain perception is influenced by…

A

Influenced by fatigue, attention, distraction, fear, anxiety, previous expectations and experiences, age, concept of health, education, gnetics

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21
Q

Pain tolerance

A

Greatest intensity a person can handle; varies with time (ex: women’s is higher at childbirth but they can’t feel that pain all the time—unreasonable)

22
Q

Pain threshold and influencing factors

A

Lowest intensity of pain a person can recognize; influenced by sleep, injury, frustration/emotions; when these are worsened the threshold is decreased

23
Q

Opioid tolerance and pain threshold

A

Opioid tolerance can decreased with time—neuro synapses change with long-term use

24
Q

Perceptual dominance occurs when…

A

Pain in 1 area is worse so it masks pain in another area

25
Q

What increases pain threshold?

A

Alcohol, hypnosis, strong faith, acupuncture, sex, exercise

26
Q

Modulation

A

Synaptic transmission of pain signals can be altered or dampened by pain meds and endorphins

27
Q

Gate control theory

A

Blocking the pain before it gets to the brain by stimulating A-alpha and A-beta fibers which inhibit C and A-delta fibers, lowering pain perception; touch, rub, get active which decreases excitation and pain by inhibiting nerve impulses before they reach the thalamus; works for mild or chronic pain

28
Q

Where does the gate control theory work?

A

Substantial geltianosa

29
Q

What produces s/s or inflammation?

A

Prostaglandins—Chemical mediators in the plasma that are activated by tissue injury (ex: arachidonic metabolites which causes production of prostaglandins)

30
Q

Acute pain

A

Nociceptive, normal and protective; sudden and resolves when chemical mediators leave; transient—seconds to months; lasts under 3 months; stims ANS which causes physical response to pain (HR, BP, diaphoresis, diluted pupils)

31
Q

Chronic pain

A

Lasts beyond expected healing time (over 3-6 months); no purpose and out of proportion to observable tissue damage; ongoing or intermittent; change in PNS or CNS that causes dysregulation of nociception and pain modification; often no ANS and associated with psychosocial problems

32
Q

Nociceptive pain

A

Acute pain that rises from peripheral pain receptors or nociceptors; response to actual tissue damage; ache/gnaw/pound

33
Q

Neuropathic pain

A

Results from direct injury to peripheral nerve; does not respond to usual pain meds, involves nerves or abnormal sensory input, shooting, burning, numb, shock, abnormal sensation (ex: diabetic neuropathy, phantom limb pain); poorly localized; tx with adjuvant analgesics

34
Q

Visceral pain

A

Involves organs, sometimes, inflammation, poorly localized, diffuse, deep; often referred pain; kidney stones, diaphoresis, cramping, splitting, N/V (appendicitis, bladder spasm, constipation, heart attack)

35
Q

Idiopathic pain

A

Chronic pain without a cause; exceeds typical pain levels; associated with conditions—cause apathy, insomnia, anorexia

36
Q

Cutaneous/somatic pain

A

A-delta usually; sharp, localized, constant, achy, well-localized in skin and SQ tissue, muscle, BVs and connective tissue

37
Q

Referred pain

A

Felt at a distance from actual pathology (ex: radiating arm pain from heart attack)

38
Q

Phantom pain

A

Felt from amputation, brain sense something not there, constant, most intense right after amputation, resolves with time

39
Q

Atypical meds

A

Adjuvants

40
Q

Tramadol (Ultram) class and MOA

A

Centrally acting analgesic; binds weakly to mu opioid receptor, inhibits reuptake of NOR and Sr

41
Q

What is tramadol for

A

Moderate-severe pain

42
Q

Tramadol SE and NC

A

SE: none often, drowsy, dizzy, headache, nausea, constipation, resp dep; seizures and CNS dep (rare)
NC: Can be given with Tylenol, not best for people who get seizures; schedule 4

43
Q

Gabapentin (Neurontin) and pregabalin

A

Anticonvulsants that spontaneously suppress neuronal firing

44
Q

gabapentin and pregablin SE and NC

A

SE: drowsy, dizzy, vision problems; Can be partially reversed with Narcan; no ceiling effect; schedule 5

45
Q

Aspirin (ASA) class and MOA

A

NSAIDS; non-selective COX inhibitor; Dec formation of thromboxine which causes less clotting

46
Q

Aspirin SE and NC

A

GI ulcers, GI bleed, rash, edema, kidney failure, increased BP, decreased platelet aggregation, SOB with asthma; salicylate poison/toxicity; Not best for people with asthma; black box for GI issues—don’t give to elderly and people with past hx, must eat first; NEVER GIVE TO KIDS WITH VIRAL INFX—cause Reye’s sx (severe brain and liver damage, high mortality); Is Excedrin when combined with caffeine, don’t give to; sal tox from acute use—edema, N/V, seizure; sal tox from chronic use—N/V, tinnitus, hearing loss

47
Q

What do nociceptors respond to?

A

Hot/cold, sharp, electric

48
Q

Ceiling effect

A

The phenomenon when increasing a dose of medication does not increase its effectiveness

49
Q

When does acute pain end?

A

When chemical mediators leave

50
Q

Tx for nociceptive pain

A

Opioids and analgesics

51
Q

Tx for chronic pain

A

Adjunct analgesics? (Neuropathic)

PATHO (32 decks)

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