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Pharmacology > Anatomy and Physiology of Pain > Flashcards

Anatomy and Physiology of Pain Flashcards

1
Q

What is pain?

A

An unpleasant sensory and emotional experience

  • there is NO WAY to be objective about quantifying it
  • may not be proportional to tissue damage
  • is PURELY an emotionally preceptive thing
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2
Q

What does it stimulate and retard?

A
  • amplifies the stress response (sympathetic NS) to traumatic injury
  • stimulates endocrine and metabolic systems
  • retards patient’s recovery from trauma, surgery and disease
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3
Q

What is the difference between acute and chronic pain?

A

Acute pain: lasts longer than 6 months (subsides once the healing process has occurred)
Chronic Pain: involves complex processes and pathology. Involves altered anatomy and neural pathways. Lasts longer than 6 mo (causes re-wiring of the spinal nerves)

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4
Q

Why do we want to be quick about treating pain?

A

Tissue damage has the potential to elicit mechanisms that can create disabling situations that may outlast the period of healing

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5
Q

Cousin’s Theory of Pathophysiology of Acute Pain

A

-that sever, unrelieved pain can result in abnormally enhances physiological responses that lead to progressively increased pathophysiology

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6
Q

What are the harmful organ effects of pain?

A
  • there is increased adrenergic stimulation (SNS)
  • increase the heart rate
  • increase cardiac output
  • increase myocardial oxygen consumption
  • decreases pulmonary vital capacity
  • decreases alveolar ventilation
  • decreases functional residual capacity
  • atrial hypoxemia
  • suppression of immune functions, predisposing trauma patients to wound infections and sepsis
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7
Q

What is chronic pain syndrome?

A
  • pain is the focus of life

- sometimes the result of acute, unrelieved pain, sometimes from a near-muscular disorder like fibromyalgia or MS

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8
Q

Why is it so important that pain is not left without tx for a few weeks?

A
  • a person with severe pain that does not treat their pain symptoms will re-wire their pain signals and will experience pain in the absence of any major stimulation for the rest of their lives
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9
Q

What are the receptors of pain?

A

free nerve endings

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10
Q

What are the different ways that nerves can be stimulated to elicit a pain response?

A
  • through mechanical damage, extreme temperature, or chemical irritation
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11
Q

What are the 2 types of neurons involved in pain?

A
  • A delta: first pain, sharp (protective pain)

- C: second pain, dull (learning and behavioural pain)

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12
Q

What are the 4 processes involved in pain stimulation?

Define each

A
  • transduction: local biochemical changes in nerves endings that generate a signal
  • transmission: movement of that signal from the site of pain in the spinal cord and the brain
  • modulation: endogenous systems in place that can inhibit pain at any point along the pathway
  • perception: synthesis and analysis in the brain
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13
Q

What are nociceptors?

A
  • free nerve endings with the capacity to distinguish between noxious and innocuous stimuli
  • when exposed to mechanical, thermal or chemical stimuli, tissue damage occurs
  • substances are released by the damaged tissue which facilitate the movement if pain impulse to the spinal cord
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14
Q

What are some of the substances released from traumatized tissues that cause pain? What do they do?

A
  • bradykinin
  • serotonin
  • substance P
  • histamine-> inflammation and exacerbation
  • prostaglandin -> target of NSAIDs
  • – these cause cell depolarization by sodium flux
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15
Q

How do NSAIDs reduce pain?

Corticosteroids?

A

because they minimize production of prostaglandin

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16
Q

What is the transmission pathway of pain in the body?

A

initial damage -> nerve-> spinal cord -> thalamus -> central structures of the brain where pain is processed

  • transmission of pain requires NT (opioids inhibit the release of NT)
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17
Q

Describe A delta fibers

Fast pain

A

large diameter fibers (2-5 uM) and allow the pain signal to be transferred very fast
- causes the body to withdraw immediately from a painful stimulus-protective

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18
Q

Describe slow pain

A
  • pain stars more slowly
  • transmitted by small diameter (0.2-1 uM)
  • signal travels at a speed of less than 2/s
  • body response: immobilization (guarding, spasm or rigidity) Healing and behaviour modification learning
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19
Q

Explain what is necessary for the perception of pain?

A
  • cortical structures (higher functioning)
  • there is no pain without relatively large cortical structures and the ability to generate emotional responses
  • vertebrates
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20
Q

What does modulation do in the pain response?

A
  • this list he portion of the pain system that reduces the pain sensation
  • mediated by endorphins (endogenous opioids). Both descending fibres in the spinal tract and higher cordial enters release endorphins to modulate both transmission and perception
  • in addition, central NT such as serotonin modulate perception. This explains why antidepressants can decrease pain
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21
Q

How do endorphins work as natural endorphins?

A
  • released from their storage areas in the brain
  • when a pain impulse reaches the brain - they bind to receptors in the pain pathway to block transmission and perception of pain
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22
Q

What can activate the descending pain modulation system?

A

STRESS- modulates pain and causes you to not feel it

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23
Q

What drugs alter the perception of pain?

A

parenteral opioids, a2 agonists, general anesthetics

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24
Q

What drugs alter the transmission of pain?

A

local anesthetics - peripheral nerve, plexus, epidural block

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25
Q

What drugs alter the modulation of pain?

A

spinal opioids, a2 agonist, NMDA receptor antagonists, NSAIDS, anticholinesterases, CCK antagonists, NO inhibitors, potassium channel openers

26
Q

What drugs alter the transduction of pain?

A

NSAIDS, antihistamines, membrane stabilizing agents, local anesthetic, opioids, bradykinin and serotonin antagonists

27
Q

What is the gate control theory?

A
  • physiological and psychological interactions
  • suggest spinal gates in the dorsal form at each segment of the spinal cord
  • competition at each gate for heat, touch or pain to be transmitted at each point
28
Q

What are the categories of pain?

A
  • Nociceptic: injury, trauma, and infection
  • Neuropathic: damage or dysfunction of the peripheral or CNS
  • Visceral: arising from an internal organ - myocardial infarction, appendicitis, small bowel obstruction
29
Q

What is hyperalgesia?

A

intense pain in response to a mildly painful stimulus

30
Q

What is allodynia?

A

Pain in response to completely innocuous stimulus (touch)

31
Q

What is neuropathic pain?

A
  • abnormal processing of the impulsed either by the peripheral or central nervous system
  • may be caused by injury, scar tissue from surgery, nerve entrapment, or damaged nerves
  • IT IS NOT TOTALLY UNKNOWN IN ALL CASES
32
Q

What effects do NSAIDs have? (3)

A

analgesic, antipyretic, anti-inflammatory (these effects are all caused by inhibition go prostaglandins)

33
Q

What are the 3 COX enzymes?

A

COX 1- non-inducible, found in many cell types constitutively.
- this isoform has critical functions, such as maintaining the stomach lining
COX 2- the form induced in immune cells
- this isoform is responsible for pain, inflammation and fever
COX 3- highest content in brain and heart

34
Q

What are the 3 phases of inflammation?

A
  1. acute transient phase (local vasodilation, increased capillary permeability)
  2. delayed subacute phase (infiltration of leukocytes and phagocytes)
  3. chronic proliferative phase (tissue degeneration and fibrosis)
35
Q

When are prostaglandins released by a cell?

A

Released following cell damage - cause pus and inflammation

36
Q

What is a fever caused by?

A
  • set point regulated by the hypothalamus - dedicated balance between heat loss and production
  • caused by: infection, tissue damage, inflammation, graft rejection, malignancy
  • release of prostaglandins near hypothalamus under these conditions induces fever
  • NSAIDs reduce fever, but do not reduce increased body temp due to exercise/ambient heat
37
Q

How to prostaglandins induce pain?

A
  • they induce pain by stimulating the local pain fibres
  • inflammation also induces hyperalgesia
    • NSAIDs can actually be superior to opioids for inflammation induced pain
38
Q

What are some other effects of prostaglandins?

A
  • platelet aggregation and formation of clots (accounts for coronary benefits of ASA)
  • PGs are important in modulating stomach acidity and mucous lining (accounts for all the GI side effects of NSAIDs)
  • PGs are important for uterine contraction- may account for some cases of dysmenorrhea
39
Q

What are the two mechanisms of action of ASA?

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. metabolite of ASA, gentisic acid, is a competitive inhibitory of COX enzymes, thus this effect depends upon clearance
40
Q

How does caffeine act as a coanalgesic?

A
  • caffeine increases the analgesic effect of all nonopioid analgesic drug - the cause of the effect is unknown (may be due to cortical vasoconstriction)
  • the required dose is 60-120 mg - most preps have less than this however
  • ingesting foods and beverages with caffeine also contributes to coanalgesic effects
41
Q

What is the most effective way to take acetaminophen or ibuprofen?

A
  • take the max amount with a coffee as well as a glass of ice water
  • ice water causes the stomach contents to dump into the intestine- increases the absorption rate
42
Q

What can contribute to a salicylate overdose?

A
  • 10-30 g dose can cause fatality
  • pepto-bismol can cause salicylate toxicity
  • salicylate is also found in acetaminophen
43
Q

What are the signs and symptoms of salicylate overdose?

A
  • tinnitus
  • marked increase in metabolic waste
    • intital hyerventilation- due to futile cycle burning of O2, overproduction of CO2
  • metabolic acidosis- overproduction of CO2
  • severe hypoglycemia - futile cycle uses up all the glucose
44
Q

What is the treatment of a salicylate overdose?

A
  • treat with parenteral fluids and glucose
  • parenteral sodium bicarbonate solution
  • acetazolimide
  • activated charcoal
45
Q

What are the immediate dangers of salicylate overdose?

A
  • hyperthermia, dehydration and hypoglycemia
46
Q

NSAID classes?

A
  1. salicylates: methylsalicylate- oil of wintergreen. Bismuth salicylate, asa
  2. proprionic acid
    - ibuprofen
    - - generally similar effects to other non similar COX inhibitors
    - - generally less GI side effects (but still major problem)
    - naproxen
    - - naproxen have a half like of 12 -18 hours, effective from 2-12 hours. Naproxen peaks within 1 hour. Can only be dosed 2x daily!
  3. Diclofenac
    - high potency but also have a higher GI bleed risk
    - prescription only! Used for inflammatory pain, such as arthritis, post op swelling, gout. Sometimes endometriosis
    - in gel, used for muscular/joint pain (tennis elbow, muscle, low back pain)
  4. Indomethicin
    - specifically used for gout pain and swelling
    - less common for chronic conditions than diclofenac
47
Q

When do GI symptoms typically arise?

A
  • primary problem with no-selective COX inhibitors
  • PGE2 and PGI2(products of COX-1) are made by the gastric mucosa. These PGs suppress acid production, increase gastric blood flow and increases the secretion of mucin
  • inhibition of COX-1 thus increases acid production and decreases mucous protection, inc addition to local effects of drugs
48
Q

What is misoprostol?

A

prostaglandin analog

  • used to supply the stomach with PG effect lost with non-selective COX inhibitors
  • adverse effects and effectiveness - around 1% risk prevention, 15% induction of diarrhea
49
Q

What are the main adverse effects and drug interactions associated with NSAIDS?

A
  • Reye’s syndrome - fatal hepatic encephalopathy in children with viral infection- associated with SAS - chicken pox and influenza
  • Hypertension and Angina
    increase in circulating blood volume
  • Bleeding disorders- inhibition of cyclooxygenase, alcohol, warfarin and rofecoxib
50
Q

Inhibition of which COX enzyme causes the most side effects?

A

inhibition of COX1

51
Q

What do the analgesic antipyretic and anti-inflammatory effects primarily arise from? (which COX enzyme?)

A

COX2

- looking for COX 2 selective inhibitors now because of this

52
Q

Why is acetaminophen the DOC in children?

A

Because of Reye’s syndrome

53
Q

What is the MOA of acetaminophen overdose?

A
  • a minor clearance pathway for a highly reactive metabolite of acetaminophen at low doses is through glutathione in the liver. GSH is a critical antioxidant. At high doses, this reactive depletes GSH
  • this causes oxidative damage to liver cells from loss of anti-oxidant and direct damage to liver cells from the highly reactive intermediate
54
Q

What are the signs and symptoms associated with acetaminophen overdose?

A
  • severly elevated serum transaminase levels
  • hepatic encephalopathy
  • jaundice- by the time this is reached tx is too late
55
Q

What would you do if you found a child with an empty tylenol bottle on the ground around him?

A
  • pump the stomach and give a glutathione treatment
56
Q

Management of acute migraines

A
  • often NSAIDs will be effective and should be tried first
  • combination of acetaminophen, acetylsalicylic acid and caffeine may be effective
  • occasionally opioid drugs may be used to treat refractory migraine headaches but should always be last resort
57
Q

What else can be used to treat acute headaches?

A
  • ergot alkaloids
  • ergotamine, dihydroergotamine
  • postulated mechanism of action- nonspecific serotonin agonists
  • side effects most often related to arteriolar constriction
  • coanalgesic with caffeine
58
Q

What are the cautions that could be used with ergot alkaloids?

A
  • liver disease
  • rebound headache with frequent use
  • cardiovascular disease- causes arteriolar vasoconstriction
  • poor peripheral circulation
59
Q

What else can be used to treat an acute headache?

A
  • can use the triptans
    (sumatriptan, naratriptan, risatriptan, zolmitriptan)
  • postulated MOA: agonist at the serotonin receptor
  • side effects similar to ergot alkaloids
60
Q

How do the triptans work to treat a migraine headache?

A
  • these are serotonin receptor agonists
  • very effective for migraines but also very expensive
  • usually relieve nausea as well as headaches
61
Q

What is the caution associated with triptans?

A
  • the concurrent MAOI or SSRI antidepressants - when used in conjunction with triptans can cause serotonin syndrome - akathisia like restlessness, muscle twitches, myoclonus, hyperreflexia, sweating, shivering and tremor - can possibly lead to seizures and coma
  • NOT to be used concurrently with ergot alkaloids
62
Q

What can be used for migraine prophylaxis?

A
  • propanolol and other B blockers can be used as a preventative treatment
  • – regulates blood flow, reduces blood pressure
  • – side effects are: tiredness, dizziness, dec libido, dream effects and can exacerbate asthma
  • amitryptiline
  • – much lower doses than is used for depression
  • – side effects: dry mouth and eyes, drowsiness
  • Gabapentin
  • – modulated GABA receptors
  • Candesartan
  • – angiotensin II receptor antagonist, reduces blood pressure

Pharmacology (23 decks)

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