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Pharmacology 2100 > Pain Physiology > Flashcards

Pain Physiology Flashcards

1
Q

what is pain

A

unpleasant sensory and emotional experience completely subjective and not proportional to the tissue damage

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2
Q

how does pain stimulation of the sympathetic nervous system affect the body

A

stimulates endocrine and metabolic systems and causes abnormalities
retards recovery from trauma, surgery, and disease

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3
Q

define acute pain

A

lasts less than 6 months

subsides once healing process is accomplished

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4
Q

define chronic pain

A

constant and prolonged over 6 months, involves altered anatomy and neural pathways, sometimes for life

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5
Q

why should you treat pain

A

tissue damage can cause disabling, refractory, chronic situations that pain prolongor outlast the period of healing

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6
Q

what is cousins theory of acute pain

A

severe unrelieved acute pain results in abnormally enhanced response that cause pronounced and increasing pathophysiology

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7
Q

what are some harmful effects of pain

A

increased adrenergic stimulation
increase heart rate, cardiac output, and myocardial oxygen consumption
decreased pulmonodayr vital capacity, alveolar ventilation, and functional residual capacity
arterial hypoxemia
suppression of immun functions

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8
Q

what are the pain receptors

A

free nerve endings

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9
Q

what are the two types of pain neurons

A

A delta- first pain, sharp (protective)

C- second pain, dull (learning)

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10
Q

what can stimulate these receptors

A

mechanical damage
extreme temp
chemical irritation

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11
Q

what are the four distinct processes in the pain pathway

A

transduction
transmission
modulation
perception

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12
Q

what is transduction

A

local biochemical changes in nerve endigns that generate a signal

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13
Q

what is tranmission

A

movement of a signal from the site of pain to the spinal cord and brain

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14
Q

what is perceptions

A

synthesis and analysis in the brain

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15
Q

what is modulation

A

endogenous systems in place that can inhibit pain at any point along the pathway

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16
Q

what are nociceptors

A

free nerve endings that can distinguish between noxious and innocuous stimuli

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17
Q

what are some substances released from traumatized tissue that cause pain

A

bradykinin
serotonin
substance P histamine * inflammation
prostaglandin*

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18
Q

what do the substances released from traumatized tissues cause

A

sodium influx and depol

facilitates movement of pain impulse to spinal cord

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19
Q

what are two drugs that inhibit transduction

A

NSAIDS minimize prostaglandin production

corticosteroids inhibit prostaglandins and other inflammatory mediators

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20
Q

how is pain transmitted

A

damage - nerve - spinal cord - brain stem - thalamus - central structures of brain where processed

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21
Q

describe the a delta pain fibers

A

large diameter so can be transferred very fast and immediately can withdraw from painful stimulus to prevent further damage

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22
Q

describe the c pain fibers

A

small diameter slower causes immobilization healing and behavour modification

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23
Q

where is pain perceived

A

cortical structures

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24
Q

how is modulation mediated

A

endorphins reduce pain sensation and neurotransmitters

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25
where do endorphins come from
descending fibers in spinal tract and hihger cortical centers released when pain impulse reaches brain binds to receptors in pain pathway to block transmission
26
what activates the descending pain modulation system
``` stress fear hunger thirst fatigue prolonged motor activity hypnosis ```
27
what drugs block transduction
``` nsaids antihistamines membrane stabilizing agents local anesthetic cream opioids bradykinin and serotonin antagonists ```
28
what drugs block modulation
``` spinal opiods alpha2 agonists NMDA receptor antagonists anticholinesterases nsaids cck antagonist NO inhibitos k channel openers ```
29
what drugs block transmission
local anesthetics
30
what drugs block perception
parenteral opiods alpha 2 agonists anesthetics
31
what is nociceptive pain
injury trauma infection
32
what is neuropathic pain
damage or dysfunction of peripheral or CNS
33
what is visceral pain
arises from an internal organ
34
wht is hyperalgesia
intense pain in response to mildly painful stimulus
35
what is allodynia
pain in response to completely innocuous stimulus
36
what are theffect caused by inhibition of prostaglandins by nsaids
analgesic antipyretic anit inflammatory
37
what does cox-1 do
found in many cells constantly maintain stomach lining and many critical functions
38
what does cox-2 do
induced in immune cells | cause pain inflammation and fever
39
what are the 3 phases of inflammation
1. acute transient -vasodilate, cap permeability 2. delayed subacute phase - leukocytes and phagocytes 3. chronic proliferative phase - tissue degeneration and fibrosis
40
what do prostaglandins do upon cell damage
released cause local inflammation and pain
41
how can prostaglandins be used in birth
cause uterine cramping to injection to abort and inibitos to delay delivery
42
what other effects do prostaglandins have
platelet aggregation formation of clots - ASA | modulate stomach acidity and mucous lining - NSAIDS
43
how does aspirin work
irreversibly acetylates COX enzymes so effect lasts as long as it takes to replace the enzyme
44
how is caffiene used as a coanalgesic
60-120mg will increase the analgesic effect of all non opiod analgesic drugs
45
what are signs and symptoms of salicylate overdose
tinnitus*** increase in metabolic rate burns glucose and oxygen causing increased co2 - initial hyperventilation, metabolic acidosis, sever hypoglycemia
46
what are the immediate dangers of salicylate overdose
hyperthermia deydration hypoglycemia
47
treatment of salicylate overdose
parenteral fluids and glucose | keep cool
48
salycilates
``` methylsalicylate - oil of wintergreen bismuth salicylate (peptobismol) aspirin ```
49
proprionic acids
ibuprofen | naproxen
50
diclofenac
high potency and GI bleed risk | prescriptions for inflammation pain such as arthritis
51
indomethacin
gout pain and swelling | less common for chronic conditions
52
GI side effects
cox- 1 makes PGE2 and PGI1 which suppresses acid production, increases gastric blood flow, and increases secretion of mucin so non selective cox inhibitors increase acid and reduce mucous
53
misoprostol
prostaglandin analog that supplies stomach with prostaglandin effect lost with non sleective COX inhibitors - not very effective and more likely to cause diarrhea
54
what is reyes syndrome
fetal hepatic encephalopathy (liver induced brain disease) in children with viral infection, associated with SAS
55
nsaids and hypertension
increase in circulating volume
56
nsaids and bleeding disorders
inhibition of COX decreases ability to make clots | interferes with alcohol and warfarin
57
what were the results of a cox2 selective inhibitor
strokes and heart attacks due to the inhibition of prostocyclin
58
how is acetaminophen different
centrally acting analgesic no ceiling effect not anti-inflammatory
59
what happens in acetaminophen overdose
metabolized by GSH an antioxidant and at high levels depletes it causing oxidative damage to liver cells and direct damge to liver from the highly reactive intermediate
60
signs of tylenol overdose
elevated serum transaminase levels hepatic encephalopathy jaundice - too late
61
symptoms of migraine
throbbing! nausea preceded by aura variable duration and incidence
62
whos more prone to migraines
more common in boys than girls adn reverses after puberty
63
triggers of migraines
``` weather missing a meal stress alcohol food menses ```
64
phases of a migraine
prodrome - feeling aura - visual headache and associated features postdrome - exhausted
65
how do you treat an acute headache
nsaids combo with caffiene and ice water try avoid triggers
66
ergot alkaloid cautions
``` serotonin agonists liver disease rebound headache cadriovascular disease - vasoconstrict poor peripheral circulation ```
67
what are the triptans
agonists at serotonin receptors side effect similar to ergot alkaloids relieve nausea and headaches
68
why cant you take triptans with antidepressants
serotonin syndrome both increase serotonin | restless, twitches, sweatingm shivering, tremor
69
how can beta blockers be used in migraine prevention
propanalol regulates blood flow, reduces blood pressure | may cause tiredness, dizzyness
70
how can you use amitryptiline for migraine prevention
lower doses than in depression | may cause dry mouth and eyes, drowsiness
71
drugs for migraine prophylaxis
``` beta bloackers TCAs gabapentin candesartan some dietary supplements ```

Pharmacology 2100 (13 decks)

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