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Pharmacology > Lecture 7 - Anatomy & Physiology of Pain > Flashcards

Lecture 7 - Anatomy & Physiology of Pain Flashcards

1
Q

Define pain

A
  • unpleasant sensory and emotional experience
  • pain is whatever the experiencing person says it is
  • pain is a perception
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2
Q

Is there a way to quantify pain?

A

No - no way to quantify pain objectively or biochemically

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3
Q

Is pain proportional to tissue damage?

A

may or may not be

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4
Q

_______ is usually the issue because of subjective nature of pain

A

Undertreatment

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5
Q

Pain amplifies the body’s stress response (_____) to traumatic injury

A

sympathetic nervous system

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6
Q

Pain ____ patient’s recovery from trauma, surgery, and disease.

A

stops

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7
Q

Pain overactivates the SNS:

what are symptoms of this?

A
  • keeps intestines from working properly

- increase HR

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8
Q

acute pain

A
  • lasts less than 6 months

- subsides once the healing process is accomplished

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9
Q

chronic pain

A
  • involves complex processes and pathology
  • usually involves altered anatomy and neural pathways
  • constant and prolonged
  • lasts longer than 6 months and sometimes, for life
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10
Q

_____ and ______ systems are significantly affected by the pathophysiology of pain

A

cardiovascular

respiratory

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11
Q

Give examples of how cardiovascular and respiratory systems are significantly affected by the pathophysiology of pain

A
  • adrenergic stimulation (SNS)
  • increased HR
  • increased cardiac output
  • increased myocardial oxygen consumption
  • decreased pulmonary vital capacity
  • decreased alveolar ventilation
  • decreased functional residual activity (so decreased O2 delivery during healing, decreased cardiac O2 during increased demand)
  • arterial hypoxemia
  • suppression of immune functions, predisposing trauma patients to wound infections and sepsis
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12
Q

What can chronic pain result from?

A

acute, unrelieved pain - such as trauma, phantom limb, repeated back surgeries, etc.

can also stem fro neuromuscular disorders such as fibromyalgia, RA, MS, etc

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13
Q

Why is it important to treat pain?

A

so it doesn’t become chronic pain and worsen the condition

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14
Q

T or F: neuropathic pain is always from a known cause

A

False - it can be from a known or unknown cause

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15
Q

Two types of neurons involved in pain pathway: Describe them

A

1) A-delta: first pain, sharp

2) C: second pain, dull

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16
Q

Pain pathway:

specialized receptors = ?

A

free nerve endings

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17
Q

Types of stimulation of pain pathway? (3)

A
  • mechanical damage
  • extreme temperature
  • chemical irritation
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18
Q

Pain pathway:

4 distinct processes

A

transduction
transmission
modulation
perception

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19
Q

Transduction

A

local biochemical changes in nerve endings that generate a signal

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20
Q

Transmission

A

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

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21
Q

Perception

A

Synthesis and analysis in the brain

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22
Q

Modulation

A

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

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23
Q

Nociceptors are involved in transduction: Describe them

A
  • free nerve endings with the capacity to distinguish between noxious and innocuous stimuli
  • when exposed to mechanical (incision or tumor growth), thermal (burn), or chemical (toxic substance) stimuli, tissue damage occurs
  • substances are released by the damaged tissue which facilitates the movement of pain impulse to the spinal cord
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24
Q

Substances released from traumatized tissue during transduction that cause pain?

A 
bradykinin
serotonin
substance P
histamine - inflammation and exacerbation
prostaglandin - target of NSAIDS
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25
Q

Substances released from traumatized tissue during transduction that cause ??

A

cell depolarization by sodium flux

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26
Q

How do NSAIDs (aspirin, ibuprofen, and diclofenac) help with pain during transduction?

A

reduce pain because they minimize the production of prostaglandins

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27
Q

How do corticosteroids (cortisone and dexamethasone)

A

also inhibit prostaglandins as well as other inflammatory mediators

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28
Q

Describe transmission

A
  • initial damage/ stimulation
  • nerve
  • spinal cord
  • brain stem
  • thalamus
  • central structures of brain (where pain is processed)
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29
Q

Transmission requires ___________

A

neurotransmitters

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30
Q

_____ inhibit release of neurotransmitters

A

Opioids

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31
Q

Two types of nerve fibres:

A-delta = ?

A

fast pain (protective pain)

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32
Q

Two types of nerve fibres:

C-fibres = ?

A

slow pain (learning and behavioural modification)

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33
Q

A-delta fibres:

describe the size of fibres and speed of signal transmission

A

large diameter fibres (2-5 microM)

-allow the pain signal to be transferred very fast (5-30 meters/second)

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34
Q

What do A-delta fibres cause the body to do?

A

withdraw immediately from the painful stimulus in order to avoid further damage - therefore “protective”

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35
Q

C-fibres:

describe the size of fibres and speed of signal transmitted

A 
small diameter (0.2-1.0 microM)
-signal travels at a speed of less than 2 m/s
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36
Q

What does the C-fibres cause the body to do?

A
  • immobilization (guarding spasm or rigidity)

- healing and behaviour modification learning

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37
Q

When does slow pain (transmitted by C-fibres) start?

A

starts more slowly after the fast pain

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38
Q

Where does pain perception happen?

A

cortical structures (higher functioning)

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39
Q

There is no pain without ?

A

relatively large cortical structures and the ability to generate emotional responses

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40
Q

Who can experience pain?

A

vertebrates (at least the level of fish)

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41
Q

see slide 20

A

kay man

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42
Q

Modulation - portion of pain system which ____ pain sensation

A

reduces

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43
Q

Modulation is mediated by _______

A

endorphins (endogenous opioids)

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44
Q

What releases endorphins?

A
  • descending fibres in spinal tract

- higher cortical enters

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45
Q

Endorphins modulate both pain ____ and ______

A

transmission

perception

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46
Q

Additional neurotransmitters such as _____ modulate perception

A

serotonin

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47
Q

Can antidepressants decrease pain?

A

yes - because they interfere with the reuptake of serotonin and norepinephrine and can decrease pain

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48
Q

Natural opioids (endorphins) are released from their storage areas in the ____ when pain impulse reaches the brain.

A

brain

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49
Q

What do natural opioids (endorphins) bind to ?

A

receptors in the pain pathway to block transmission and perception of pain

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50
Q

What activates descending pain modulation system?

A 
stress
fear
hunger
thirst
fatigue
prolonged motor activity
hypnosis
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51
Q

more opioids = ____ pain

A

less

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52
Q

understand diagram on 24

A

ya ya ya

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53
Q

Describe the Gate Control Theory

A
  • physiological and psychological interactions
  • suggested spinal gates in the dorsal horn at each segment of the spinal cord
  • competition at each gate for heat, touch or pain to transmitted at each point
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54
Q

List the 3 categories of pain

A
  • Nociceptic
  • Neuropathic
  • Visceral
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55
Q

Describe nociceptic pain

A

injury, trauma, infection

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56
Q

Describe neuropathic pain

A

damage or dysfunction of the peripheral or central nervous system

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57
Q

Describe visceral pain

A

arising from an internal organ - myocardial infarction, appendicitis, small bowel obstruction

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58
Q

Postoperative pain and mechanical low back pain are examples of _____ pain

A

nociceptive

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59
Q

Trigeminal neuralgia and polyneuropathy (diabetic, HIV) are examples of _____ pain

A

neuropathic

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60
Q

Postherpetic neuralgia, neuropathic low back pain, arthritis, sports/exercise injuries are all examples of ________ pain

A

mixed type (nociceptive and neuropathic pain mixed together)

61
Q

Define neuropathic pain

A

initiated or caused by a primary lesion or dysfunction in the nervous system

62
Q

hyperalgesia

A

intense pain in response to mildly painful stimulus (pinprick)

63
Q

allodynia

A

pain in response to completely innocuous stimulus (touch)

64
Q

neuropathic pain

A

-abnormal processing of the impulses either by the peripheral or central nervous system

65
Q

neuropathic pain can be caused by ?

A
  • injury (amputation and subsequent phantom limb pain)
  • scar tissue from surgery (back surgery high risk)
  • nerve entrapment (carpal tunnel)
  • damaged nerves (diabetic neuropathy)
66
Q

analgesic = ?

A

anti-pain

67
Q

What is the difference between acetaminophen and NSAIDs?

A

acetaminophen is not anti-inflammatory

68
Q

antipyretic = ?

A

anti-fever

69
Q

NSAIDs have what 3 properties?

A

analgesic (anti-pain)
antipyretic (anti-fever)
anti-inflammatory

*these effects are all caused by inhibition of prostaglandins

70
Q

NSAIDS stop ____ enzymes which stops the product of ________

A

COX

prostaglandins

71
Q

Describe COX 1

A

Noninducible-found in many cell types constitutively

This isoform has critical functions, such as maintaining stomach lining

*helps reduce acid - COX 1 on all the time

72
Q

Describe COX 2

A

This form induced in immune cells

This isoform is responsible for pain, inflammation, and fever

COX 2 - inducible under disease states and damage

73
Q

Describe COX 3

A

Highest content in brain and heart (a splice variant of COX 1)

*don’t really know what it does

74
Q

COX 1 is NOT ______

A

inducable

75
Q

COX 2 is _____

A

inducible

76
Q

What is inflammation caused by?

A

infectious agents, schema, antigen/antibody reaction, thermal and other damage

77
Q

List the 3 phases of inflammation

A

1 - acute transient phase
2 - delayed subacute phase
3 - chronic proliferative phase

78
Q

Describe phase 1 of inflammation:

Acute transient phase

A

local vasodilation

increased capillary permeability

79
Q

Describe phase 2 of inflammation:

Delayed subacute phase

A

infiltration of leukocytes and phagocytes

80
Q

Describe phase 3 of inflammation:

Chronic proliferative phase

A

tissue degeneration and fibrosis

81
Q

When are prostaglandins released?

A

following cell damage

82
Q

Prostaglandins are found in ?

A

inflammatory exudants

83
Q

What does injection of PGs cause?

A

local inflammation
increased blood flow
severe pain

84
Q

Decrease PG = _____ uterine cramping

A

decrease

*inhibit prostaglandins - you can delay delivery

85
Q

What can a fever be caused by?

A 
infection
tissue damage
inflammation
graft rejection
malignancy
86
Q

What induces a fever?

A

release of prostaglandins near hypothalamus under these conditions

*it changes the set point regulated by hypothalamus

87
Q

How do prostaglandins induce pain?

A

by stimulating local pain fibres

88
Q

inflammation induces _____

A

hyperalgesia (increased pain sensitivity)

89
Q

What are PGs critical for/important for?

A

-critical to platelet aggregation-formation of clots
(accounts for the coronary benefits of ASA)

  • PGs are important in modulating stomach acidity and mucous lining (accounts for the GI side effects of NSAIDs)
  • PGs are important of uterine contraction - may account for some cases of dysmenorrhea
90
Q

Asprin (ASA) has 2 mechanisms of action: explain them

A

1 - ASA irreversibly acetylates COX enzymes, thus this effect lasts as long as it takes to replace the enzyme (not dependent upon aspirin elimination)

2 - a minor metabolite of ASA, gentisic acid, is a competitive inhibitor of COX enzymes, thus this effect depends upon clearance

91
Q

Caffeine will _____ the analgesic effect of all nonopiod analgesic drugs

A

increase

*cause of the effect is unknown (may be due to cortical vasoconstriction)

92
Q

What is the required dose for a coanalgesic effect ?

A

60-120 mg

*although most preparations have far less than this (Excedrin is exception)

93
Q

A typical cup of coffee contains how much caffeine?

A

60-120 mg

94
Q

Caffeine withdrawal is a major contributor to ??

A

sudden onset of headache

95
Q

What is the best treatment for a headache ?

A

ice water
caffeine
NSAIDs
acetaminophen

96
Q

What drug is most common to produce salicylate overdose in children ?

A

ASA ?

97
Q

What does of salicylate can cause fatality?

A

10-30 gram dose can cause fatality

98
Q

Methylsalicylate (oil of wintergreen) can be fatal with as little as __ ml

A

4

99
Q

salicylate overdose alarm = ?

A

fucking tinnitus

100
Q

other signs and symptoms of salicylate overdose?

A

marked increase in metabolic rate (SA overdose interfere with oxidative metabolism)

  • initial hyperventilation - due to “futile cycle” burning of oxygen, overproduction of CO2
  • metabolic acidosis - overproduction of CO2
  • severe hypoglycaemia - futile cycle uses up the available glucose
  • metabolic overdrive
  • mitochondria increases waste cycle
  • body temp increases
  • blood glucose drops
  • CO2 levels go up
  • burning oxygen and making CO2
101
Q

Immediate danger for salicylate overdose is?

A

hyperthermia
dehydration
hypoglycemia

102
Q

Treatment of salicylate overdose is? (6)

A

1-parenteral fluids and glucose (always and immediately)
2-parenteral Na+ bicarbonate solution (caution: K+ depletion)
3-acetazolamide (if parental bicarbonate does not alkalinize the urine) (goal urine pH > 7)
4-activated charcoal (only effective within 2 hr of overdose)
5-polyelectrolyte lavage solution (for modified release salicylate)
-hemodialysis (for severe overdoses)

103
Q

2 classes of NSAIDs?

A

1 - salicylates

2 - proprionic acid

104
Q

Examples of salicylate NSAIDs?

A
  • methylsalicylate (oil of wintergreen - used as topical ointment)
  • bismuth salicylate (peptol bismol)
  • asprin
105
Q

Examples of propionic acid NSAIDs?

A
  • ibuprofen

- naproxen

106
Q

Describe ibuprofen

A
  • COX inhibitor

- generally less GI side effects

107
Q

Describe naproxen

A
  • has a half life of 12-18 hours, effective from 2-12
  • naproxen sodium peaks within one hour
  • can be dosed only twice a day
108
Q

Two other types of NSAIDs

A
  • diclofenac

- indomethacin

109
Q

Describe diclofenac

A

-high potency but also higher GI bleed risk

110
Q

Diclofenac used for ?

A

-Rx only: used primarily for inflammatory pain, such as arthritis, post operative swelling, court, etc.

Sometimes endometriosis

In gel, used for muscular/joint pain (tennis elbow, muscle strains, low back pain)

111
Q

Describe indomethacin

A
  • specifically used for gout, pain, and swelling

- less common for chronic conditions than diclofenac

112
Q

GI side effects are primarily a problem with ________ COX inhibitors

A

non-selective

113
Q

How does inhibition of COX 1 cause GI effects?

A

inhibition of COX 1 increases acid, and decreases mucous production, in addiction to local effects of drugs

114
Q

Misoprostol is a ?

A

PG analog (similar structure and function)

115
Q

What is misoprostol used for?

A

used to supply the stomach with PG effect lost with non-selective COX inhibitors

116
Q

side effects of misoprostol?

A

15% induction of diarrhea

117
Q

Describe some adverse effects/drug interactions of NSAIDs?

A

1-Reye’s syndrome - fatal hepatic encephalopathy in children with viral infection-associated with SAS
-chicken pox, influenza

2-hypertension, angina
-increase in circulating volume

3-bleeding disorders
-inhibition of cyclooxyrgenase, alcohol, warfarin, and rofecoxib

118
Q

Most side effects arise from the inhibition of ??

A

COX 1

119
Q

The analgesic, antipyretic and anti-inflammatory effects arise primarily from inhibition of ??

A

COX 2

120
Q

Acetaminophen is ? (2)

A
  • analgesic
  • anti-pyretic
  • NOT anti-inflammatory
121
Q

What is the drug of choice for children?

A

acetaminophen - because it has no cause for Reye’s syndrome

122
Q

Describe the acetaminophen overdose-mechanism of action

A

a minor clearance pathway for a highly reactive metabolite of acetaminophen t low doses is through glutathione (GSH) in the liver

GSH is a critical anti-oxidant

at high doses, this reactive metabolite depletes GSH

This causes:

1) - oxidative damage to liver cells from loss of the anti-oxidant
2) - direct damage to liver cells from the highly reactive intermediate

123
Q

Signs and symptoms of acetaminophen overdose?

A

1 - severely elevated serum transaminase levels > 1000 U/L

2 - hepatic encephalopathy - 90% probability with serum acetaminophen > 300 mg/L

3 - jaundice - by this time treatment is likely too late

124
Q

slide 57 - important

A

OK

125
Q

migraine headache - prevalence in women?

A

18%

126
Q

migraine headache - prevalence in men?

A

6%

127
Q

migraine headache - prevalence ?

A

more common in boys than girls - then reverses after puberty

128
Q

symptoms of migraine headache ?

A
  • unilateral or bilateral, throbbing, nausea
  • often preceded by an aura - usually visual
  • variable duration - from hours to days
  • variable incidence - from a few per year to a few per month
129
Q

Triggers of migraines?

A
  • weather (50%)
  • missing a meal (40%)
  • stress (50%)
  • alcohol (50%)
  • various types of food (45%)
  • menses (50%)
  • crying (50%)
130
Q

Describe the prodrome part of the migraine attack

A

feeling of about to get a migraine

131
Q

Describe the aura part of the migraine attack

A

-not seen in everyone
-see things or feel things
(hallucinations)

132
Q

Describe the postdrome part of the migraine attack

A

headache’s gone, feeling exhausted after

133
Q

List the 4 parts of the migraine attack

A

Prodrome
Aura
Headache
Postdrome

134
Q

Management of Acute Headache

A
  • often nonopiod analgesics (NSAIDs) will be effective for this purpose and should be tried first
  • combination of acetaminophen, ASA, and caffeine may be effective
  • occasionally opioid drugs may be used to treat refractory migraine
135
Q

Postulated mechanism of action of migraine headache-acute?

A

nonspecific serotonin agonists

136
Q

Side effects of migraine headache-acute most often related to?

A

arteriolar constriction

137
Q

Caution with ergot alkaloids for ??

A
  • liver disease
  • rebound headache with frequent use
  • cardiovascular disease - arteriolar vasoconstriction
  • poor peripheral circulation

*zombie death of st. anthony’s fire ??

138
Q

management of acute headache includes?

A

-the Triptans

sumatriptan, naratriptan, risatriptan, zolmitriptan

139
Q

postulated mechanism of action of the triptans?

A

agonist at serotonin receptor

140
Q

side effects of triptans?

A
  • similar to ergot alkaloids

- #1 side effect is peripheral vasoconstriction

141
Q

What are the triptans available as?

A

a pill, nasal spray, and sublingual preparation

142
Q

Describe the Triptans

A
  • very effective for migraine
  • very expensive
  • relieve nausea as well a headache
143
Q

What can be used for migraine prophylaxis?

A
  • Propanolol (other B-blockers)
  • Amitryptiline (and other TCAs)
  • Gabapentin
  • Candesarta
  • Dietary supplements
144
Q

Describe Propranolol (and other B blockers)

A
  • most commonly used preventative
  • starts at 20-30 mg
  • up to 240 mg
  • regulates blood flow, reduces blood pressure
  • side effects: tiredness, dizziness, decreased libido, dream effects, exacerbate asthma
145
Q

Describe Amitryptiline (and other TCAs)

A
  • much lower doses than used for depression
  • doses from 10 mg-100mg daily
  • side effects: dry mouth and eyes, drowsiness
146
Q

Describe gabapentin

A

anticonvulsant - possibly modulates GABA receptors

147
Q

Describe candesartan

A

angiotensin 2 receptor antagonist - reduces blood pressure

148
Q

Describe dietary supplements

A

riboflavin
coenzyme Q10
magnesium
citrate

Pharmacology (21 decks)

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