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Pharmacology - Fall > Lecture 7 - Pain, NSAIDs, Migraine > Flashcards

Lecture 7 - Pain, NSAIDs, Migraine Flashcards

1
Q

What is pain?

A

An unpleasant sensory and emotional experience associated w/ actual or potential tissue damage

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2
Q

What does pain cause?

A

Endocrine and metabolic abnormalities

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3
Q

What is acute pain?

A

Lasts less than 6 months and subsides once healing is accomplished

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4
Q

What is chronic pain?

A
  • Constant and prolonged, lasting longer than 6 months

- Usually involves altered anatomy and neural pathways

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5
Q

What is the pain theory?

A
  • Severe, unrelieved acute pain results in abnormally enhanced physiological responses that lead to pronounced and progressively increased pathophysiology
  • Increased pathophysiology causes increased significant organ dysfunction => increased morbidity and mortality
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6
Q

Which systems are most affected by the pathophysiology of pain?

A
  • Cardiovascular and respiratory systems

- Immune system becomes repressed, predisposing trauma patients to wound infections and sepsis

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7
Q

What are the 2 causes of chronic pain syndrome?

A

1) Acute, unrelieved pain

2) Neuro-muscular disorders

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8
Q

Which nerves can send pain signals, and what does this tell us?

A
  • Almost every nerve

- Shows that pain is a perception b/c the signal might not be different, but that’s how the brain perceives it

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9
Q

What are the 2 types of pain nerve fibers and which type of pain do they transmit?

A

1) A-delta – fast, sharp pain

2) C – second pain, dull

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10
Q

What are the 4 processes of pain?

A
  • Transduction
  • Transmission
  • Modulation
  • Perception
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11
Q

What is transduction?

A
  • Local biochemical changes in nerve endings that generate a signal
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12
Q

What are nociceptors?

A

Free nerve endings w/ the capacity to distinguish btwn noxious and innocuous stimuli

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13
Q

What happens when a nociceptor is exposed to mechanical, thermal, or chemical stimuli?

A

Tissue damage occurs and substances are released which facilitates the movement of the pain impulse to the spinal cord

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14
Q

Does every stimulation to a nociceptor cause pain?

A

Yes

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15
Q

What are the primary known substances released from the traumatized tissue that cause pain?

A
  • Bradykinin
  • Serotonin
  • Substance P
  • Histamine
  • Prostaglandin
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16
Q

What type of pain are corticosteroids used for and what do they do?

A
  • Cancer pain

- Interfere w/ production of prostaglandins

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17
Q

What is transmission?

A

Movement of the signal from the site of pain to the spinal cord and brain

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18
Q

Where is pain processed?

A

Central structures of the brain

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19
Q

___ are needed to continue the pain impulse from the spinal cord to the brain

A

Neurotransmitters

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20
Q

Why are opioids effect analgesics?

A

B/c they block the release of NT, which prevents the pain impulse from entering the brain

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21
Q

Which pain nerve fibre is myelinated?

A

A-delta

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22
Q

What is the thickness of A-delta fibres and what does this mean?

A
  • Relatively thick

- Allow pain stimulus to be transferred very fast

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23
Q

What is the purpose of a-delta fibres?

A

To make the body withdraw immediately from the painful and harmful stimulus to avoid further damage

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24
Q

Does pain from a-delta fibres radiate?

A

No

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25
Q

How can pain from a-delta fibres be overcome?

A

Infiltration of the affected area or nerve w/ a local anesthetic

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26
Q

When does slow pain begin?

A

Immediately after fast pain

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27
Q

What is the body’s response to slow pain?

A

Immobilization (guarding, spasm, or rigidity) so healing can occur

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28
Q

Does slow pain radiate?

A

Yes, it poorly localized

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29
Q

What is an effective treatment for slow pain?

A

Opioids

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30
Q

What is perception?

A
  • Synthesis and analysis in the brain

- End result of transmission

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31
Q

Where does perception occur and what does this mean?

A

Cortical structures, so behavioural strategies and therapy can be applied to decrease pain

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32
Q

What do the somatosensory and cingulate cortices control?

A
  • Sensory discrimination

- Emotional response – fear, anxiety, panic, and subjective experience

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33
Q

What does the reticular formation control?

A
  • Increases arousal
  • Emotional response
  • Somatic and autonomic motor reflexes
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34
Q

What is modulation?

A

Changing or inhibiting pain impulses in the descending tract (brain -> spinal cord)

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35
Q

How is modulation accomplished?

A
  • Descending fibres release substances called endogenous opioids or endorphins which can inhibit transmission of noxious stimuli
  • Endorphins also work at the nerve junction to slow pain impulses
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36
Q

What type of antidepressants does cancer pain respond to and why?

A
  • Antidepressants that interfere w/ reuptake of serotonin and NE
  • Increases the availability to inhibit noxious stimuli
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37
Q

_____ pathways modify ____ nociceptive info

A

Efferent; afferent

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38
Q

What does failure of inhibition lead to?

A

Neuropathic pain

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39
Q

When are endorphins released?

A

When a pain impulse reaches the brain

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40
Q

Which type of cells do endorphins excite and which type do they inhibit?

A
  • Excite cells in midbrain (PAG, periaqueductal gray matter) and medulla
  • Inhibit cells in spinal cord
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41
Q

What activates the descending pain modulation system (the system that decreases pain)?

A
  • Stress
  • Fear
  • Hunger, thirst
  • Fatigue
  • Prolonged motor activity
  • Hypnosis
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42
Q

What are the 3 categories of pain?

A

1) Nociceptive
2) Neuropathic
3) Visceral

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43
Q

What is nociceptive pain?

A

Injury, trauma, infection

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44
Q

What is neuropathic pain?

A

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

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45
Q

What is visceral pain?

A

Arising from an internal organ (ex: MI, appendicitis, small bowel obstruction)

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46
Q

What are common feelings of neuropathic pain?

A

Fire or electricity

47
Q

Where does neuropathic pain normally occur?

A
  • Feet, legs, and hands

- Trigeminal neuropathy occurs in face

48
Q

What is hyperalgesia?

A

Intense pain in response to mildly painful stimulus (pinprick)

49
Q

What is allodynia?

A

Pain in response to completely innocuous stimulus (touch)

50
Q

What can cause neuropathic pain?

A
  • Injury (amputation w/ subsequent phantom limb pain)
  • Scar tissue from surgery
  • Nerve entrapment (carpal tunnel)
  • Damaged nerves (diabetic neuropathy)
51
Q

In neuropathic ____ and _____ are spontaneous and repetitive

A

Depolarization and transmission

52
Q

Can a treatment for nociceptive pain also be used for neuropathic pain?

A

No

53
Q

What are common causes of headaches?

A
  • Neck and jaw tension
  • Nasal pressure
  • Caffeine withdrawal
  • Lack of sleep
  • Eye strain
54
Q

What are characteristics of NSAIDs?

A
  • Analgesic (anti-pain)
  • Antipyretic
  • Anti-inflammatory (except acetaminophen!!)
55
Q

What is the common mechanism of NSAIDs that elicits its effects?

A

Inhibition of COX enzymes, which convert arachidonic acid into prostaglandins; so therefore inhibits prostaglandins

56
Q

What is the function of COX-1 enzyme?

A

Maintenance of stomach lining, so don’t want to inhibit it

57
Q

Where is COX-2 enzyme found and what is its function?

A
  • Immune cells

- Responsible for pain, inflammation, and fever

58
Q

Where is COX-3 enzyme found?

A

Brain and heart

59
Q

What causes inflammation?

A
  • Infectious agents
  • Ischemia
  • Antigen/antibody reaction
  • Thermal and other damage
60
Q

What are the 3 phases of inflammation?

A

1) Acute transient - local vasodilation and increased capillary permeability
2) Delayed subacute - infiltration of leukocytes and phagocytes
3) Chronic proliferative - tissue degeneration and fibrosis

61
Q

Which phases of inflammation do NSAIDs control?

A

1st phase

62
Q

What would injection of prostaglandins cause?

A
  • Local inflammation, increased blood flow, and severe pain

- Cause uterine cramping, so injection used to cause abortion

63
Q

What effect would morphine have on uterine cramping?

A

At low doses, morphine increases smooth muscle contraction, so would make uterine cramping worse

64
Q

What are some other effects of prostaglandins?

A
  • Critical to platelet aggregation and formation of clots

- Important in modulating stomach acidity and mucous lining

65
Q

What are the 2 mechanisms of action for aspirin?

A

1) Irreversibly acetylates COX enzymes, so its effect lasts as long as it takes to replace the enzyme
2) A minor metabolite of ASA, gentisic acid, is a competitive inhibitor of COX enzymes, thus its effect depends upon clearance

66
Q

Which NSAID destroys COX enzymes?

A

ASA

67
Q

What effect does caffeine have on all non-opioid analgesic drugs?

A

Will increase analgesic effect

68
Q

What is the required dose of caffeine for a coanalgesic effect?

A

60-120 mg

69
Q

Why should drugs be taken w/ ice water?

A

Ice water causes the stomach open its sphincter into the intestine, where the drug is absorbed

70
Q

____ overdose is a very common overdose in children

A

Salicylate

71
Q

What are signs and symptoms of salicylate toxicity?

A
  • Tinnitus (ringing in the ears) – first sign of aspirin overdose
  • Marked increase in metabolic rate – initial hyperventilation and metabolic acidosis (overproduction of CO2), then severe hypoglycemia
72
Q

What is the immediate danger of salicylate toxicity?

A

Hyperthermia, dehydration, and hypoglycemia

73
Q

What is the treatment for salicylate toxicity?

A
  • Parenteral fluids and glucose
  • Parenteral sodium bicarbonate solution
  • Acetazolamide to make urine pH > 7
  • Activated charcoal (only effective w/in 2 hours)
  • Hemodialysis for severe overdoses
74
Q

What are the 3 types of salicylates?

A
  • Methylsalicylate
  • Bismuth salicylate
  • Aspirin
75
Q

What are the classes of NSAIDs?

A
  • Salicylates
  • Propionic acid
  • Diclofenac
  • Indomethacin
76
Q

What are the types of propionic acid?

A

Ibuprofen and naproxen

77
Q

Ibuprofen has similar effects to ____

A

Other non-selective COX inhibitors

78
Q

How often can naproxen be dosed?

A

Only twice a day

79
Q

What is an advantage and disadvantage to diclofenac?

A
  • High potency

- High GI bleeding risk

80
Q

What is diclofenac mostly used for?

A

Inflammatory pain, or gel is used for muscular/joint pain

81
Q

What is indomethacin used for?

A

Gout pain and swelling

82
Q

What is the primary problem w/ non-selective COX inhibitors?

A

GI side effects

83
Q

What does inhibition of COX-1 cause?

A
  • PGE2 and PGI2 (products of COX-1) suppresses acid production, increase gastric blood flow, and increase mucin secretion
  • Therefore, COX-1 inhibition causes increased acid production, decreased mucous protection, as well as local effects of drugs
84
Q

What is misoprostol?

A

A prostaglandin analog, similar structure and function

85
Q

What is misoprostol used for?

A

To supply the stomach w/ prostaglandin effect that is lost w/ non-selective COX inhibitors

86
Q

What is the most common side effect of misoprostol?

A

Diarrhea

87
Q

What is Reye’s syndrome?

A
  • Fatal hepatic encephalopathy in children w/ viral infections (flu or chicken pox)
  • Associated w/ ASA
88
Q

What are some adverse effects of NSAIDs?

A
  • Reye’s syndrome

- Hypertension, angina

89
Q

What causes most of the side effects of non-selective COX inhibitors?

A

Inhibition of COX-1

90
Q

What effects are caused by inhibition of COX-2?

A

Analgesic, anti-pyretic, and anti-inflammatory

91
Q

What are characteristics of acetaminophen?

A
  • Analgesic
  • Anti-pyretic
  • **NOT ANTI-INFLAMMATORY
92
Q

What is the drug of choice in children w/ pain or fever?

A

Acetaminophen

93
Q

Does acetaminophen stack w/ NSAIDs?

A

No

94
Q

What are signs and symptoms of acetaminophen overdose?

A
  • Severely increased serum transaminase levels
  • Hepatic encephalopathy
  • Jaundice (by this time, treatment is likely too late)
  • No signs and symptoms recognizable to the average person
95
Q

Which gender is more likely to get migraines?

A
  • Boys > girls

- Women > men

96
Q

What are symptoms of migraines?

A
  • Unilateral or bilateral, throbbing, nausea
  • Often preceded w/ aura
  • Variable duration, hours to days
  • Variable incidence
97
Q

What are common migraine triggers?

A
  • Weather
  • Missing a meal
  • Stress
  • Alcohol
  • Various types of foods
  • Menses
98
Q

What is the first line therapy for acute headaches?

A

Non-opioid analgesics (NSAIDs)

99
Q

What are ergot alkaloids?

A

Non-specific serotonin agonists

100
Q

What is normally the cause of side effects of ergot alkaloids?

A

Arteriolar constriction

101
Q

What should be watched w/ ergot alkaloids?

A
  • Liver disease
  • Rebound headache w/ frequent use
  • CV disease from arteriolar constriction
  • Poor peripheral circulation
102
Q

What is a common side effect of ergot alkaloids?

A

Raynaud’s (discolouration of fingers)

103
Q

What are triptans?

A

Agonist of 5-HT1 receptor

104
Q

What are the side effects of triptans?

A

Similar to ergot alkaloids, but safer

105
Q

What are triptans used for?

A

Migraines, also help relieve nausea

106
Q

What should be watched w/ triptans?

A
  • Concurrent MAOI or SSRi antidepressants, causes serotonin syndrome
  • Not concurrently w/ ergot alkaloids (24 hr washout)
107
Q

What is the most commonly used preventive for migraines and why?

A
  • Propranolol and other beta-blockers

- Regulates blood flow and decreases blood pressure

108
Q

What are side effects of propranolol?

A

Tiredness, dizziness, exacerbate asthma

109
Q

What are side effects to amitryptiline?

A

Dry mouth and eyes; drowsiness

110
Q

Does amitryptiline work directly on migraines?

A

May not, but will decrease stress and symp. NS stimulation

111
Q

What is gabapentin?

A

Anticonvulsant

112
Q

What is candesartan?

A

Angiotensin 2 receptor antagonist

113
Q

Why is it believed that dietary supplements help w/ migraines?

A

Don’t have a positive or negative effect, while many other foods have a negative effect

Pharmacology - Fall (15 decks)

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