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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
Q

where do endorphins come from

A

descending fibers in spinal tract and hihger cortical centers released when pain impulse reaches brain binds to receptors in pain pathway to block transmission

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26
Q

what activates the descending pain modulation system

A 
stress
fear
hunger
thirst
fatigue 
prolonged motor activity 
hypnosis
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27
Q

what drugs block transduction

A 
nsaids 
antihistamines 
membrane stabilizing agents
local anesthetic cream 
opioids
bradykinin and serotonin antagonists
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28
Q

what drugs block modulation

A 
spinal opiods 
alpha2 agonists 
NMDA receptor antagonists 
anticholinesterases
nsaids 
cck antagonist 
NO inhibitos
k channel openers
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29
Q

what drugs block transmission

A

local anesthetics

30
Q

what drugs block perception

A

parenteral opiods
alpha 2 agonists
anesthetics

31
Q

what is nociceptive pain

A

injury
trauma
infection

32
Q

what is neuropathic pain

A

damage or dysfunction of peripheral or CNS

33
Q

what is visceral pain

A

arises from an internal organ

34
Q

wht is hyperalgesia

A

intense pain in response to mildly painful stimulus

35
Q

what is allodynia

A

pain in response to completely innocuous stimulus

36
Q

what are theffect caused by inhibition of prostaglandins by nsaids

A

analgesic
antipyretic
anit inflammatory

37
Q

what does cox-1 do

A

found in many cells constantly maintain stomach lining and many critical functions

38
Q

what does cox-2 do

A

induced in immune cells

cause pain inflammation and fever

39
Q

what are the 3 phases of inflammation

A
  1. acute transient -vasodilate, cap permeability
  2. delayed subacute phase - leukocytes and phagocytes
  3. chronic proliferative phase - tissue degeneration and fibrosis
40
Q

what do prostaglandins do upon cell damage

A

released cause local inflammation and pain

41
Q

how can prostaglandins be used in birth

A

cause uterine cramping to injection to abort and inibitos to delay delivery

42
Q

what other effects do prostaglandins have

A

platelet aggregation formation of clots - ASA

modulate stomach acidity and mucous lining - NSAIDS

43
Q

how does aspirin work

A

irreversibly acetylates COX enzymes so effect lasts as long as it takes to replace the enzyme

44
Q

how is caffiene used as a coanalgesic

A

60-120mg will increase the analgesic effect of all non opiod analgesic drugs

45
Q

what are signs and symptoms of salicylate overdose

A

tinnitus***
increase in metabolic rate burns glucose and oxygen causing increased co2 - initial hyperventilation, metabolic acidosis, sever hypoglycemia

46
Q

what are the immediate dangers of salicylate overdose

A

hyperthermia
deydration
hypoglycemia

47
Q

treatment of salicylate overdose

A

parenteral fluids and glucose

keep cool

48
Q

salycilates

A 
methylsalicylate - oil of wintergreen 
bismuth salicylate (peptobismol) 
aspirin
49
Q

proprionic acids

A

ibuprofen

naproxen

50
Q

diclofenac

A

high potency and GI bleed risk

prescriptions for inflammation pain such as arthritis

51
Q

indomethacin

A

gout pain and swelling

less common for chronic conditions

52
Q

GI side effects

A

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
Q

misoprostol

A

prostaglandin analog that supplies stomach with prostaglandin effect lost with non sleective COX inhibitors - not very effective and more likely to cause diarrhea

54
Q

what is reyes syndrome

A

fetal hepatic encephalopathy (liver induced brain disease) in children with viral infection, associated with SAS

55
Q

nsaids and hypertension

A

increase in circulating volume

56
Q

nsaids and bleeding disorders

A

inhibition of COX decreases ability to make clots

interferes with alcohol and warfarin

57
Q

what were the results of a cox2 selective inhibitor

A

strokes and heart attacks due to the inhibition of prostocyclin

58
Q

how is acetaminophen different

A

centrally acting analgesic
no ceiling effect
not anti-inflammatory

59
Q

what happens in acetaminophen overdose

A

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
Q

signs of tylenol overdose

A

elevated serum transaminase levels
hepatic encephalopathy
jaundice - too late

61
Q

symptoms of migraine

A

throbbing!
nausea
preceded by aura
variable duration and incidence

62
Q

whos more prone to migraines

A

more common in boys than girls adn reverses after puberty

63
Q

triggers of migraines

A 
weather 
missing a meal 
stress
alcohol 
food 
menses
64
Q

phases of a migraine

A

prodrome - feeling
aura - visual
headache and associated features
postdrome - exhausted

65
Q

how do you treat an acute headache

A

nsaids
combo with caffiene and ice water
try avoid triggers

66
Q

ergot alkaloid cautions

A 
serotonin agonists
liver disease
rebound headache
cadriovascular disease - vasoconstrict
poor peripheral circulation
67
Q

what are the triptans

A

agonists at serotonin receptors
side effect similar to ergot alkaloids
relieve nausea and headaches

68
Q

why cant you take triptans with antidepressants

A

serotonin syndrome both increase serotonin

restless, twitches, sweatingm shivering, tremor

69
Q

how can beta blockers be used in migraine prevention

A

propanalol regulates blood flow, reduces blood pressure

may cause tiredness, dizzyness

70
Q

how can you use amitryptiline for migraine prevention

A

lower doses than in depression

may cause dry mouth and eyes, drowsiness

71
Q

drugs for migraine prophylaxis

A 
beta bloackers 
TCAs
gabapentin
candesartan 
some dietary supplements

Pharmacology 2100 (13 decks)

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