Pharm 3

Front 1

What population is pain more commonly in?

Back 1

Elderly population

Front 2

Pain in general, is a very UNDERTREATED condition, why is this?

Back 2

~Miconceptions from both pt and provider
~Inadequate clinical knowledge
~Misunerstanding about misuse and addiction

Front 3

What are the FOUR main types of pain?

Back 3

~Nociceptive- pain detected by specialized sensory nerves (normal pain--pinch yourself)
~Inflammatory- from an injury
~Neuropathic- spontaneous pain w/ damage in CNS
~Functional- abnormal nervous system

Front 4

What are the THREE classifications of pain?

Back 4

~Acute (adaptive)
~Chronic (maladaptive)
~Cancer Pain

Front 5

What are the different types of Nociceptive receptors?

Back 5

~Thermal
~Chemical
~Mechanical

Front 6

Describe the process of how we perceive Nociceptive pain?

Back 6

1. Stimulation/Sensation
2. Transmission
3. Perception
4. Modulation

Front 7

If we were to try Distraction or Mediation in a pt w/ pain, what are we hoping wil happen?

Back 7

Transmission of pain will decrease

Front 8

What will depression and anxiety cause in regard to pain?

Back 8

Might cause pain to increase in severity

Front 9

What are the type of nerve fibers that transmit very fast and are Myelinated?

Back 9

Alpha and Delta Fibers

Front 10

What are the type of nerve fibers that transmit slow and are UNmyelinated?

Back 10

C Fibers

Front 11

Nociception Modulation causes what?

Back 11

Inhibition of pain impulse transmission

Front 12

What are the different ways to Modulate Nociceptive pain?

Back 12

~Gate Control:
-only so musch info can be processed at once
-using TENS or Ben Gay helps crowd the system and
decreases pain
~Endogenous Opiate System (enkephalins, dynorphins, and endorphins)
~Descending pathway

Front 13

Of the Endogenous Opiate System, what are the three Opioid receptors that inhibit pain impulses and alter perception? What one is MOST important?

Back 13

~Mu (<-- Most important)
~Delta
~Kappa

Front 14

Of the Endogenous Opiate System, what Opioid receptor decreases Mu receptor response by decreasing release of Glutamate (major excitatory NT)?

Back 14

NMDA Receptor

Front 15

What does the Mu receptor do?

Back 15

Serves as an analgesic (pain relief) Receptor!!

Front 16

Nerve damage and/or repeated stimulation leads to neuronal plasticity, which is the ability of neural circuits to undergo changes in function or organization. This is an example of what types of pain?

Back 16

Neuropathic and Functional

Front 17

Changes in the balance between excitatory and inhibitory neurotransmission results in sensitization and "Wind Up". What does this mean?

Back 17

This means, Increased stimulation will cause exaggerated responses to pain (Allodynia and Hyperalgesia)

Front 18

What is the difference between Allodynia and Hyperalgesia?

Back 18

~Allodynia- pain from stimuli which are not normally painful or pain which occurs other than in the area stimulated (ie. pain from the touch of clothing)
~Hyperalgesia- increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves (ie. small pinprick results in intense, sharp, stabbing pain)

Front 19

In a pt w/ Neuropathic/Functional pain, NMDA receptor involvement and neuron recruitment will cause Increased or Decreased intensity of nerve fiber conduction?

Back 19

It will cause INCREASED intensity of nerve fiber conduction

Front 20

What causes the increase in NMDA receptor involvement and neuron recruitment?

Back 20

Increased amount of Glutamate!

Front 21

In regard to pain classification, what class of pain is a result of an injury, usually nociceptive, and is self limiting?

Back 21

Acute Pain

Front 22

In regard to pain classification, what class of pain can be nociceptive, neuropathic/functional or both, and persists beyond healing time for acute injury?

Back 22

Chronic Pain

Front 23

In regard to pain classification, what class of pain is associated w/ life threatening conditions?

Back 23

Chronic Malignant/Cancer Pain

Front 24

What is by far the best way to Dx pain?

Back 24

ASK THE PATIENT!!!!

Front 25

The fifth vital sign, PQRST-U, what does the U stand for?

Back 25

YOU! How are "YOU" doing?

Front 26

What are the different types of pain assessment tools?

Back 26

~Initial Pain Assessment Tool
~Brief Pain Inventory
~McGIll Pain Questionaire
~Neuropathic Pain Scale
~Oswestry Disability index

Front 27

All these tools give you a Number score (1-10), define Mild, Mod, and Severe Pain in regard to the scoring system?

Back 27

~Mild Pain = 1-3
~Mod Pain = 4-6
~Severe Pain = >6

Front 28

What can you tell me about the WHO Pain Relief Ladder? How does it work?

Back 28

If your pt has pain, what is the pain severity --> Mild pain is Tx'ed w/ Non-Opioids (NSAID or APAP), +/- adjuvant --> Mod Pain is Tx'ed w/ Combo Opioid and Non-Opioid, +/- adjuvant --> Severe pain is Tx'ed w/ Opioids mainly, +/- Non-Opioid, +/- Adjuvant --> reassess pt pain level

Front 29

Regarding pain management, what are the THREE ways you want to Tx your Pt?

Back 29

~By the Ladder
~By the Clock (ie. pain relief only lasts 6hrs -- Tx longer)
~By Mouth (PO)

Front 30

What are the Different Classes of Non-Opioids?

Back 30

~NSAIDS
~Salicylates
~Acetaminophen (N-Acetyl-p-Aminophenol; APAP)

Front 31

What are the Different Classes of Opioids?

Back 31

~Phenanthrenes (Morphine-Like)
~Phenylpiperidines (Meperidine-Like)
~Diphenylheptanes (Methadone-Like)

Front 32

What other two drug classes are used in the Tx of Pain?

Back 32

~Mixed Agonist-Antagonists
~Central Analgesics

Front 33

What are the effects of NSAIDs?

Back 33

~Analgesia for Mild (1-3) to Mod (4-6) pain
~Anti-Inflammatory
~Antipyretic
~Antiplatelet

Front 34

What is the MOA of NSAIDs?

Back 34

Reversible inhibition of COX 1 and 2 Enzymes resulting in decreased prostaglandin formation

Front 35

What are the functions of Prostaglandins?

Back 35

~Regulate gastric and renal blodd flow
~Mediate INFLAMMATION

Front 36

What enzymes are required for the synthesis of Prostaglandins?

Back 36

Cyclooxygenase 1 and 2 (COX 1 & 2)

Front 37

Give a brief description of COX 1 and COX 2?

Back 37

~COX 1- is ubiquitous (everywhere) and helps maintain homeostasis
~COX 2- is manufactured in activated macrophages in response to injury

Front 38

What population is pain more commonly in?

Back 38

Elderly population

Front 39

Pain in general, is a very UNDERTREATED condition, why is this?

Back 39

~Miconceptions from both pt and provider
~Inadequate clinical knowledge
~Misunerstanding about misuse and addiction

Front 40

What are the FOUR main types of pain?

Back 40

~Nociceptive- pain detected by specialized sensory nerves (normal pain--pinch yourself)
~Inflammatory- from an injury
~Neuropathic- spontaneous pain w/ damage in CNS
~Functional- abnormal nervous system

Front 41

What are the THREE classifications of pain?

Back 41

~Acute (adaptive)
~Chronic (maladaptive)
~Cancer Pain

Front 42

What are the different types of Nociceptive receptors?

Back 42

~Thermal
~Chemical
~Mechanical

Front 43

Describe the process of how we perceive Nociceptive pain?

Back 43

1. Stimulation/Sensation
2. Transmission
3. Perception
4. Modulation

Front 44

If we were to try Distraction or Mediation in a pt w/ pain, what are we hoping wil happen?

Back 44

Transmission of pain will decrease

Front 45

What will depression and anxiety cause in regard to pain?

Back 45

Might cause pain to increase in severity

Front 46

What are the type of nerve fibers that transmit very fast and are Myelinated?

Back 46

Alpha and Delta Fibers

Front 47

What are the type of nerve fibers that transmit slow and are UNmyelinated?

Back 47

C Fibers

Front 48

Nociception Modulation causes what?

Back 48

Inhibition of pain impulse transmission

Front 49

What are the different ways to Modulate Nociceptive pain?

Back 49

~Gate Control:
-only so musch info can be processed at once
-using TENS or Ben Gay helps crowd the system and
decreases pain
~Endogenous Opiate System (enkephalins, dynorphins, and endorphins)
~Descending pathway

Front 50

Of the Endogenous Opiate System, what are the three Opioid receptors that inhibit pain impulses and alter perception? What one is MOST important?

Back 50

~Mu (<-- Most important)
~Delta
~Kappa

Front 51

Of the Endogenous Opiate System, what Opioid receptor decreases Mu receptor response by decreasing release of Glutamate (major excitatory NT)?

Back 51

NMDA Receptor

Front 52

What does the Mu receptor do?

Back 52

Serves as an analgesic (pain relief) Receptor!!

Front 53

Nerve damage and/or repeated stimulation leads to neuronal plasticity, which is the ability of neural circuits to undergo changes in function or organization. This is an example of what types of pain?

Back 53

Neuropathic and Functional

Front 54

Changes in the balance between excitatory and inhibitory neurotransmission results in sensitization and "Wind Up". What does this mean?

Back 54

This means, Increased stimulation will cause exaggerated responses to pain (Allodynia and Hyperalgesia)

Front 55

What is the difference between Allodynia and Hyperalgesia?

Back 55

~Allodynia- pain from stimuli which are not normally painful or pain which occurs other than in the area stimulated (ie. pain from the touch of clothing)
~Hyperalgesia- increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves (ie. small pinprick results in intense, sharp, stabbing pain)

Front 56

In a pt w/ Neuropathic/Functional pain, NMDA receptor involvement and neuron recruitment will cause Increased or Decreased intensity of nerve fiber conduction?

Back 56

It will cause INCREASED intensity of nerve fiber conduction

Front 57

What causes the increase in NMDA receptor involvement and neuron recruitment?

Back 57

Increased amount of Glutamate!

Front 58

In regard to pain classification, what class of pain is a result of an injury, usually nociceptive, and is self limiting?

Back 58

Acute Pain

Front 59

In regard to pain classification, what class of pain can be nociceptive, neuropathic/functional or both, and persists beyond healing time for acute injury?

Back 59

Chronic Pain

Front 60

In regard to pain classification, what class of pain is associated w/ life threatening conditions?

Back 60

Chronic Malignant/Cancer Pain

Front 61

What is by far the best way to Dx pain?

Back 61

ASK THE PATIENT!!!!

Front 62

The fifth vital sign, PQRST-U, what does the U stand for?

Back 62

YOU! How are "YOU" doing?

Front 63

What are the different types of pain assessment tools?

Back 63

~Initial Pain Assessment Tool
~Brief Pain Inventory
~McGIll Pain Questionaire
~Neuropathic Pain Scale
~Oswestry Disability index

Front 64

All these tools give you a Number score (1-10), define Mild, Mod, and Severe Pain in regard to the scoring system?

Back 64

~Mild Pain = 1-3
~Mod Pain = 4-6
~Severe Pain = >6

Front 65

What can you tell me about the WHO Pain Relief Ladder? How does it work?

Back 65

If your pt has pain, what is the pain severity --> Mild pain is Tx'ed w/ Non-Opioids (NSAID or APAP), +/- adjuvant --> Mod Pain is Tx'ed w/ Combo Opioid and Non-Opioid, +/- adjuvant --> Severe pain is Tx'ed w/ Opioids mainly, +/- Non-Opioid, +/- Adjuvant --> reassess pt pain level

Front 66

Regarding pain management, what are the THREE ways you want to Tx your Pt?

Back 66

~By the Ladder
~By the Clock (ie. pain relief only lasts 6hrs -- Tx longer)
~By Mouth (PO)

Front 67

What are the Different Classes of Non-Opioids?

Back 67

~NSAIDS
~Salicylates
~Acetaminophen (N-Acetyl-p-Aminophenol; APAP)

Front 68

What are the Different Classes of Opioids?

Back 68

~Phenanthrenes (Morphine-Like)
~Phenylpiperidines (Meperidine-Like)
~Diphenylheptanes (Methadone-Like)

Front 69

What other two drug classes are used in the Tx of Pain?

Back 69

~Mixed Agonist-Antagonists
~Central Analgesics

Front 70

What are the effects of NSAIDs?

Back 70

~Analgesia for Mild (1-3) to Mod (4-6) pain
~Anti-Inflammatory
~Antipyretic
~Antiplatelet

Front 71

What is the MOA of NSAIDs?

Back 71

Reversible inhibition of COX 1 and 2 Enzymes resulting in decreased prostaglandin formation

Front 72

What are the functions of Prostaglandins?

Back 72

~Regulate gastric and renal blodd flow
~Mediate INFLAMMATION

Front 73

What enzymes are required for the synthesis of Prostaglandins?

Back 73

Cyclooxygenase 1 and 2 (COX 1 & 2)

Front 74

Give a brief description of COX 1 and COX 2?

Back 74

~COX 1- is ubiquitous (everywhere) and helps maintain homeostasis
~COX 2- is manufactured in activated macrophages in response to injury

Front 75

What population is pain more commonly in?

Back 75

Elderly population

Front 76

Pain in general, is a very UNDERTREATED condition, why is this?

Back 76

~Miconceptions from both pt and provider
~Inadequate clinical knowledge
~Misunerstanding about misuse and addiction

Front 77

What are the FOUR main types of pain?

Back 77

~Nociceptive- pain detected by specialized sensory nerves (normal pain--pinch yourself)
~Inflammatory- from an injury
~Neuropathic- spontaneous pain w/ damage in CNS
~Functional- abnormal nervous system

Front 78

What are the THREE classifications of pain?

Back 78

~Acute (adaptive)
~Chronic (maladaptive)
~Cancer Pain

Front 79

What are the different types of Nociceptive receptors?

Back 79

~Thermal
~Chemical
~Mechanical

Front 80

Describe the process of how we perceive Nociceptive pain?

Back 80

1. Stimulation/Sensation
2. Transmission
3. Perception
4. Modulation

Front 81

If we were to try Distraction or Mediation in a pt w/ pain, what are we hoping wil happen?

Back 81

Transmission of pain will decrease

Front 82

What will depression and anxiety cause in regard to pain?

Back 82

Might cause pain to increase in severity

Front 83

What are the type of nerve fibers that transmit very fast and are Myelinated?

Back 83

Alpha and Delta Fibers

Front 84

What are the type of nerve fibers that transmit slow and are UNmyelinated?

Back 84

C Fibers

Front 85

Nociception Modulation causes what?

Back 85

Inhibition of pain impulse transmission

Front 86

What are the different ways to Modulate Nociceptive pain?

Back 86

~Gate Control:
-only so musch info can be processed at once
-using TENS or Ben Gay helps crowd the system and
decreases pain
~Endogenous Opiate System (enkephalins, dynorphins, and endorphins)
~Descending pathway

Front 87

Of the Endogenous Opiate System, what are the three Opioid receptors that inhibit pain impulses and alter perception? What one is MOST important?

Back 87

~Mu (<-- Most important)
~Delta
~Kappa

Front 88

Of the Endogenous Opiate System, what Opioid receptor decreases Mu receptor response by decreasing release of Glutamate (major excitatory NT)?

Back 88

NMDA Receptor

Front 89

What does the Mu receptor do?

Back 89

Serves as an analgesic (pain relief) Receptor!!

Front 90

Nerve damage and/or repeated stimulation leads to neuronal plasticity, which is the ability of neural circuits to undergo changes in function or organization. This is an example of what types of pain?

Back 90

Neuropathic and Functional

Front 91

Changes in the balance between excitatory and inhibitory neurotransmission results in sensitization and "Wind Up". What does this mean?

Back 91

This means, Increased stimulation will cause exaggerated responses to pain (Allodynia and Hyperalgesia)

Front 92

What is the difference between Allodynia and Hyperalgesia?

Back 92

~Allodynia- pain from stimuli which are not normally painful or pain which occurs other than in the area stimulated (ie. pain from the touch of clothing)
~Hyperalgesia- increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves (ie. small pinprick results in intense, sharp, stabbing pain)

Front 93

In a pt w/ Neuropathic/Functional pain, NMDA receptor involvement and neuron recruitment will cause Increased or Decreased intensity of nerve fiber conduction?

Back 93

It will cause INCREASED intensity of nerve fiber conduction

Front 94

What causes the increase in NMDA receptor involvement and neuron recruitment?

Back 94

Increased amount of Glutamate!

Front 95

In regard to pain classification, what class of pain is a result of an injury, usually nociceptive, and is self limiting?

Back 95

Acute Pain

Front 96

In regard to pain classification, what class of pain can be nociceptive, neuropathic/functional or both, and persists beyond healing time for acute injury?

Back 96

Chronic Pain

Front 97

In regard to pain classification, what class of pain is associated w/ life threatening conditions?

Back 97

Chronic Malignant/Cancer Pain

Front 98

What is by far the best way to Dx pain?

Back 98

ASK THE PATIENT!!!!

Front 99

The fifth vital sign, PQRST-U, what does the U stand for?

Back 99

YOU! How are "YOU" doing?

Front 100

What are the different types of pain assessment tools?

Back 100

~Initial Pain Assessment Tool
~Brief Pain Inventory
~McGIll Pain Questionaire
~Neuropathic Pain Scale
~Oswestry Disability index

Front 101

All these tools give you a Number score (1-10), define Mild, Mod, and Severe Pain in regard to the scoring system?

Back 101

~Mild Pain = 1-3
~Mod Pain = 4-6
~Severe Pain = >6

Front 102

What can you tell me about the WHO Pain Relief Ladder? How does it work?

Back 102

If your pt has pain, what is the pain severity --> Mild pain is Tx'ed w/ Non-Opioids (NSAID or APAP), +/- adjuvant --> Mod Pain is Tx'ed w/ Combo Opioid and Non-Opioid, +/- adjuvant --> Severe pain is Tx'ed w/ Opioids mainly, +/- Non-Opioid, +/- Adjuvant --> reassess pt pain level

Front 103

Regarding pain management, what are the THREE ways you want to Tx your Pt?

Back 103

~By the Ladder
~By the Clock (ie. pain relief only lasts 6hrs -- Tx longer)
~By Mouth (PO)

Front 104

What are the Different Classes of Non-Opioids?

Back 104

~NSAIDS
~Salicylates
~Acetaminophen (N-Acetyl-p-Aminophenol; APAP)

Front 105

What are the Different Classes of Opioids?

Back 105

~Phenanthrenes (Morphine-Like)
~Phenylpiperidines (Meperidine-Like)
~Diphenylheptanes (Methadone-Like)

Front 106

What other two drug classes are used in the Tx of Pain?

Back 106

~Mixed Agonist-Antagonists
~Central Analgesics

Front 107

What are the effects of NSAIDs?

Back 107

~Analgesia for Mild (1-3) to Mod (4-6) pain
~Anti-Inflammatory
~Antipyretic
~Antiplatelet

Front 108

What is the MOA of NSAIDs?

Back 108

Reversible inhibition of COX 1 and 2 Enzymes resulting in decreased prostaglandin formation

Front 109

What are the functions of Prostaglandins?

Back 109

~Regulate gastric and renal blodd flow
~Mediate INFLAMMATION

Front 110

What enzymes are required for the synthesis of Prostaglandins?

Back 110

Cyclooxygenase 1 and 2 (COX 1 & 2)

Front 111

Give a brief description of COX 1 and COX 2?

Back 111

~COX 1- is ubiquitous (everywhere) and helps maintain homeostasis
~COX 2- is manufactured in activated macrophages in response to injury