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Anesthesia Pharmacology > Lecture 7 (Exam 2) - Pain Pathways > Flashcards

Lecture 7 (Exam 2) - Pain Pathways Flashcards

1
Q

The increased responsiveness of peripheral neurons responsible for pain transmission to heat, cold, mechanical or chemical stimulation is called ____?

A

Sensitization

(Slide 18, pg. 370 Stoeltings)

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2
Q

The release of _________ mediators and adaptation of signaling pathways in primary sensory neurons induced by noxious stimuli causes sensitization.

This process usually resolves as tissues heal and the peripheral sensitization diminishes. ________ pain occurs when this does NOT happen.

A

inflammatory; Chronic

(Slide 18, pg 370 Stoeltings)

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3
Q

Increased pain sensations to normally painful stimuli is called ______?

Perception to pain sensations in response to normally non-painful stimuli is called _______?

A

Hyperalgesia

Allodynia

(Slide 18, pg 370 Stoeltings)

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4
Q

This type of hyperalgesia results from the presence of enhanced pain from heat AND mechanical injury.

This type is characterized by the uninjured skin surrounding the injury and sensitization of central neuronal circuits? (mechanical only)

A

Primary hyperalgesia. (Heat & Mechanical)

Secondary hyperalgesia. (only mechanical)

*remember this is describing pain at the PERIPHERAL level

(Slide 19, pg. 371-372)

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5
Q

When pain enters the spinal cord and travels to the brain, it changes from peripheral pain to _______ _____!

A

Central pain!

(Slide 20)

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6
Q

What is the relay center in the spinal cord for nociceptive & other sensory activity?

A

The Spinal Dorsal Horn

Slide 20

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7
Q

Pain signals use ________ pathways to reach the brainstem and forebrain (SI and SII).

What does SI and SII stand for and what does this structure do?

A

afferent

Somatosensory cortex, it accounts for the perception of pain location and intensity (the discrimination of pain stimuli)

(Slide 20, pg. 372 Stoeltings)

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8
Q

Is the dorsal root ganglia peripheral or central?

Which fibers are myelinated?
Unmyelinated?

A

DRG = peripheral (the dorsal root is central)

Mylelinated = A beta, A delta
Unmyelinated = C fibers

(Slide 21, pg 373 Stoeltings)

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9
Q

Lamina I (marginal layer) and lamina II (substantia gelatinosa) are innervated by _____ fibers.

A

C fibers

(slide 21)

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10
Q

What are the laminae and area that become desensitized/affected with spinal/subarachnoid or epidural agents (Ketamine, opioids, or local anesthetics)?

A

Laminae I, II, III, IV, VII and NKI receptor

(Slide 21)

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11
Q

Which lamina do opioids work on specifically?

A

Lamina II (substantia gelatinosa)
*says it’s on boards

(Slide 21)

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12
Q

The ventral horn and laminae ___, ___, ___ are innervated by _____ fibers that innervate the muscles and viscera, so this means they are also affected by our anesthetic agents.

Both the dorsal and anterior section will be affected.

A

I, IV, Vll

Myelinated fibers

(Slide 21)

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13
Q

Laminae III and IV, where the NKI with substance P can be affected by spinals and epidurals, too.
T/F?

A

True!

(Slide 21)

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14
Q

What are the 5 excitatory Neuromodulators in the CNS?

A
  • Glutamate
  • Calcitonin
  • Neuropeptide Y
  • Aspartate
  • Substance P

(slide 28)

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15
Q

What are the 5 inhibitory Neuromodulators in the CNS?

A
  • GABA
  • Glycine
  • Enkephalins
  • Norepinephrine
  • Dopamine

(slide 28)

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16
Q

What specific inhibitory Neuromodulator in the CNS is most specific to Midazolam?

A

GABAa

(slide 28)

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17
Q

In the CNS, what are the 4 Ascending pathways of nociceptive information?

A
  • Spinothalamic
  • Spinomedullary
  • Spinobulbar
  • Spinohypothalamic

(slide 29)

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18
Q

What type of impulses and laminae are associated with the Spinothalamic tract? (STT)

A

Pain, temperature, and itch (Laminae I, VII, & VIII: All afferent fibers)
(direct projections to the thalamus)

(slide 29)

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19
Q

What type of impulses and laminae are associated with the Spinomedullary tract?

A

(direct projections to homeostatic control regions in the medulla and brainstem)
- pg. 376

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20
Q

What type of impulses and laminae are associated with the Spinobulbar (the hindbrain) tract?

A

Behavior component toward pain (Laminae I, V, & VII)

(direct projections to homeostatic control regions in the medulla and brainstem)

(slide 29)

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21
Q

What type of impulses and laminae are associated with the Spinohypothalamic tract? (SHT)

A

Autonomic, neuroendocrine, and emotional aspects of pain (Laminae I, V, VII, & X)

(direct projections to the hypothalamus and ventral forebrain)

(slide 29)

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22
Q

What are the 6 most commonly activated supra-spinal Modulations of the nociception?
(the regions involved in nociceptive perception.
in the CNS)

A
  • Forebrain S I & S II (somatosensory)
  • Anterior cingulate cortex (ACC)
  • Insular cortex (IC)
  • Prefrontal cortex
  • Thalamus
  • Cerebellum

“These brain regions form a cortical and subcortical network, which are critically involved in the formation of emotional aspects of pain and the central modulation of pain perception.” - pg. 377

(slide 30)

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23
Q

The Supra-spinal modulator: Forebrain S I & S II receives input from where?
And is responsible for the perception of what?

A

Input from the Thalamus

For the location and intensity of pain
- pg. 377

(slide 30)

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24
Q

The Supra-spinal modulator: Anterior cingulate cortex (ACC)
receives input from where?
And is responsible for the perception of what?

A

Input from the medial thalamic nuclei, the ventrocaudal part of nucleus medialis dorsalis, and the lateral thalamic regions. (So the Thalamus)

Responsible for the emotional and motivational aspects of pain.
- pg. 377

(slide 30)

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25
Q

The Supra-spinal modulator: Insular cortex (IC),
receives input from where?
And is responsible for the perception of what?

A

Input from the Thalamus

Responsible for emotional and motivational aspects of pain. (goes through the amygdala)
-pg. 377

(slide 30)

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26
Q

The Supra-spinal modulator: Prefrontal cortex
receives input from where?

A

“Receives input from Anterior cingulate cortex (ACC), but there is no evidence that it receives direct thalamocortical nociceptive input.” - pg. 377

(slide 30)

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27
Q

The Supra-spinal modulator: Thalamus
receives input from where?

A

Input from the dorsal horn
- pg. 377

(slide 30)

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28
Q

The Supra-spinal modulator: Cerebellum
receives input from where?
And is responsible for the perception of what?

A

Has reciprocal spinal connectivity.

“Anesthetized humans, without conscious awareness of pain, still exhibit significant pain-evoked cerebellar activation, suggesting that pain-evoked cerebellar activity may be more important in regulation of afferent nociceptive activity than in the perception of pain.” (so regulation over the perception of pain)
-pg. 377

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29
Q

Once pain had been interpreted, it also must be acted upon. Which tract is responsible for this action?

A

Descending Inhibitory Tract

(slide 31)

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30
Q

What are the 3 supra-spinal modulation Descending Inhibitory Tracts/pathways that promote and suppress nociceptive transmission through the dorsal horn of the CNS?

A
  • Originate Periaqueductal gray (PAG)
  • Neurotransmitters
  • Hyperpolarize A-delta and C fibers

(slide 31)

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31
Q

How does the Originate Periaqueductal gray (PAG) of the supra-spinal modulation Descending Inhibitory Tract, inhibit activity of nocireceptors?

A
  • Through rostral ventromedial medulla (RVM)
  • Dorsolateral funiculus
  • Synapse in dorsal horn

-pg. 378

(slide 31)

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32
Q

Which 3 Neurotransmitters of the supra-spinal modulation Descending Inhibitory Tract, inhibit activity of nocireceptors?

A

Endorphins
enkephalins
serotonin

(slide 31)

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33
Q

How does Hyperpolarized A-delta and C fibers of the supra-spinal modulation Descending Inhibitory Tract, inhibit activity of nocireceptors?

A
  • Decrease release of substance P
  • Opening of K+ channels/inhibition of Ca++ channels

pg. 392 (slide 31)

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34
Q

The Descending Pathways of pain modulation in the CNS can either be Inhibitory (DI) or Faciliatory (FD) based on what factors?

A
  • Other somatic stimuli
  • Psychological factors (arousal, attention, and expectation)

(slide 32)

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35
Q

The PAG-RVM system contains what 3 opioid receptors and contributes to what 2 physiological pain sensations?

A
  • µ, κ, δ opioid receptors
  • hyperalgesia & Allodynia

(slide 32)

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36
Q

Where does the pain impulse originate if it is pertaining to the descending inhibitory tract?

A

PAG-RVM

(slide 34)

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37
Q

What two components does the pain include?

A

Sensory- discriminative
Motivational- effective
(pain can be affected by physical, emotional, spiritual, or psychological)
Slide 3

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38
Q

IS sensory-discriminative ascending or descending?

A

Its ascending pathway
Slide 3

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39
Q

Describe the pathway of sensory-discriminative.

A

Nerve impulse at the site (Skin, muscles, or organs) –>spinothalamic and trigemino-thalamic tracts –> cerebral cortex(somatosensory cortex) –> perception of pain
Slide 3

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40
Q

What does motivational-affective response to painful stimuli include?

A

Attention and arousal
somatic and autonomic reflexes
Endocrine responses (make sure endocrine and stress response system is adequate when we are experiencing pain)
Emotional changes
Slide 3

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41
Q

Why is attention and arousal important in the context of pain management?

A

Lack of sleep makes us more irritable and susceptible to pain.
Slide 3
(Use a holistic approach of pain management like how your patient is sleeping, eating, or exercising. All of this affects the management of pain. )
Slide 3

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42
Q

Does pain and tissue always go hand in hand?

A

No
from the video.
Slide 4

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43
Q

What is Nociception?

A

It is part of the nervous system that protects from the response of harmful or potentially harmful stimuli.
Slide 4

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44
Q

What Kind of stimuli do specialized nerve endings like nociceptors detect?

A

mechanical
Chemical
Thermal
Slide 4

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45
Q

Pain helps body from further ____ or ____.

A

Injury or damage
Slide 4

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46
Q

Besides nociception what other factor can influence the pain?

A

Biological factors
( It amplifies nociception signal to the brain–> nerve fibers are activated repeatedly –> brain decides that the body needs more stress sensors –>body becomes so sensitive to pain that with light touch body feels intense pain)
(slide 4)

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47
Q

Patient who has _____pain are more susceptible to pain related to ________.

A

Chronic pain
Biologic factors
(slide 4)

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48
Q

What defines chronic pain?

A

Pain lasting more than 3 months.
(Chronic pain outlasts the physical pain and is difficult to reverse if this continues to go.)
slide 4

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49
Q

What influences the pain in the video?

A

Emotional state
Memory about pain
Expectations about treatment
Slide 4

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50
Q

According to the experiment, who experienced more pain? Children who believe that they had no control over pain or children who had some control?

A

Children who believed that they had no control over pain.
(psychological factor)
Slide 4

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51
Q

What are the location of Nociceptors we talked about in class?

A

Skin, muscles, joints, viscera, & vasculature.
(Slide 13)

52
Q

If you get stabbed🔪 in the leg, what would be the pathway the pain impulse would travel?
Hint: You start off with stimulus

A

Stimulus -> Nociceptor: Resting Threshold -> Transmission -> Modulation (where you rate your pain) -> Interpretation
(Slide 13)

53
Q

In an experiment, volunteers with the cold rod (with the same temperature) placed on the back of their hands experienced ___ pain when they were shown red light than volunteers who were shown blue light.

A

More pain
(Features of the environmental factor on pain)
Slide 4

54
Q

What would be an example of modulation when discussing pain?

A
  1. You get stabbed in the leg before Schmidt’s test and decide it is not that bad because you really have to take that test!
  2. You get stabbed in the leg and decide that you have to go to the hospital because your in-laws are visiting.

(Castillo)

55
Q

______ factor like availability of family and support matters in the perception of pain.

A

Social factor
Slide 4

56
Q

Define pain

A

(According to international Association for the study of pain) Pain - as a physical, emotional, and psychological condition.
Slide 5

57
Q

Does the degree of tissue damage tantamount to the amount of pain the patient feels?

A

According to the video from slide 4. No
(The degree of damage caused by injury is not actually related to the degree of pain.)
Slide 5

58
Q

What are the two types of afferent fibers that deal with pain?

A

C fibers and A fibers
(Slide 14)

59
Q

Define nociception.

A

The experience of pain with a series of complex neurophysiologic processes.
Slide 5

60
Q

What fiber is unmyelinated and deal with burning pain from heat and pressure from sustained pressure.

A

C-fibers
(Slide 14)

61
Q

What two myelinated fibers did we talk about in class?

A

Type I fibers ( Aβ & Aδ fibers): Deal with heat, mechanical, chemical pain!
Type II fibers (Aδ fibers): Only specific to heat!

(Slide 14)

62
Q

What are the targets of medication on action of pain?

A

Transduction, transmission, interpretation, and modulation in both PNS and CNS.
Slide 5

63
Q

C-fibers travel ____ than 2m/sec
A-fibers travel ____ than 2m/sec

A

Less, More
(Castillo)

64
Q

About ____ of the adult population experiences chronic pain.

A

40%
Slide 6

65
Q

________ deal with acute pain!
________ deal with chronic pain!

A

A fiber, C fiber
(Castillo)

66
Q

All sensory fibers are ________.

A

Afferent
(Slide 14)

67
Q

______ from 45- 60 yrs old experience lower back pain.

A

8% to 37%
Slide 6

68
Q

About _____ suffers from musculoskeletal pain conditions in US.

A

40 million
Slide 6

69
Q

Annual cost due to pain not including surgery and lost workdays is _____.

A

$40 billion
Slide 6

70
Q

What are 7 chemical mediators of pain?

A
  1. Peptides (Substance P, Calcitonin, Bradykinin, CGRP)
  2. Eicosanoids
  3. Lipids (Prostaglandins, Thromboxanes, Leukotrienes, Endocannabinoids)
  4. Neutrophins
  5. Cytokines
  6. Chemokines
  7. Extracellular proteases and protons
    (Slide 15)
71
Q

What chemical mediators do we target when we are giving spinal anesthetics or epidural anesthetics?

A

Peptides (Substance P, Calcitonin, Bradykinin, CGRP)
(Castillo, slide 15)

72
Q

What chemical mediators are first released when it comes to pain?

A

Peptides such as Substance P, Calcitonin, & Bradykinin
(Slide 15)

73
Q

What is the treatment for the following lipid chemical mediators?
Prostaglandins:
Thromboxanes:
Endocannabinoids:

A

Prostaglandins: NSAIDS
Thromboxanes: NSAIDS
Endocannabinoids: Cannabis 🍃💨. When cannabis binds to the endocannabinoid receptor there is no experience of pain.
(Slide 15)

74
Q

What are the receptors and Ion Channels (Dorsal Root Ganglion & Peripheral Terminals) presented in class via power point?

Hint: he really did not talk much about them……

A

Purinergic
Metabotropic
Glutamatergic
Tachykinin
TRPV I
Neurotrophic
Ion channels (Nav 1.8)

(Slide 16)

75
Q

Label the green blocks in the picture provided.

A

(Slide 17)

76
Q

Label the Purple blocks in the picture provided.

A

(Slide 17)

77
Q

Pain that is limited to the short-term, lasts days to weeks after injury

A

Acute pain
Slide 36

78
Q

Pain that lasts for more than 3-6 months; persists beyond tissue healing

A

Chronic Pain
Slide 36

79
Q

Per lecture, what are some unpleasant emotional experiences that follow the same pathways as those for painful sensory transmission?

A

Anxiety, depression, cognitive deficits, emotional distress
Slide 36

80
Q

Pain that persists after tissue injury
Characterized by reduced sensory and nociceptive thresholds (Allodynia and Hyperalgesia)

A

Neuropathic Pain
Slide 37

81
Q

What type of patients are more susceptible to neuropathic pain?

A

Cancer patients due to chemo and radiation therapy
Slide 37

82
Q

Treatments for patients with neuropathic pain usually treat symptoms and include…

A

Opioids, gabapentin, amitryptiline, cannabis
Slide 37

83
Q

Pain that is diffuse and poorly localized - Referred to somatic sites like muscle and skin

A

Visceral Pain
Slide 37

84
Q

Ischemia, stretching of ligamentous attachments, spasms, and distention are all causes of what type of pain?

A

Visceral pain
Slide 37

85
Q

A variety of painful conditions following injury in a region with impairment of sensory, motor, and autonomic systems

A

Complex Regional Pain Syndromes
Slide 38

86
Q

CRPS (Complex Regional Pain Syndrome) is a neurological disease including:

A

Autonomic, sensory, and motor systems
As well as cortical areas involved in the processing of cognitive and affective information
Slide 38/Book

87
Q

Involves: Spontaneous pain, allodynia, hyperalgesia, edema, autonomic abnormalities, active and passive movement disorders, and trophic changes of skin and SQ tissues

A

Complex Regional Pain Syndromes
Slide 38

88
Q

Pain in the neonate and infant leads to ________ pain threshold and ____________ pain responses

A

Lower
Exaggerated
Slide 38

89
Q

The human fetus develops pain perception by __________ of gestation

A

23 weeks
Slide 38

90
Q

True or False: Toddlers and adolescents exhibit long-lasting hypersensitivity to painful stimuli after painful experiences as neonates

A

True
Slide 38/Book

91
Q

The process by which a noxious stimulus (e.g., heat, cold, mechanical distortion) is converted to an electrical impulse in sensory nerve endings, is known as?

Where does it occur?

A

Transduction

Peripheral nociceptors

(slide 8)

92
Q

____________ is the conduction of (pain-related) nerve/electrical impulses to the ___ with the major connections for these nerves being in the ______ horn of the spinal cord and ________ with projections to the cingulate, insular, and somatosensory cortices.

A

Transmission;
CNS;
Dorsal;
Thalamus

(slide 8)

93
Q

Define Modulation:

Where does it occur in the CNS?

A

Modulation of pain is the process of altering (inhibitory/excitatory) pain transmission mechanisms.

Occurs in the Dorsal Horn of the spinal cord

(slide 9 and 12)

94
Q

At what level on the pain perception pathway do our injectable local anesthetics (LA) become active at?

Will Modulation still occur once LA have been injected properly?

A

between the Transduction and Transmission levels

No: “Hence, there will be NO modulation because there would be no pain transmission to the dorsal horn…”

(slide 8)

95
Q

Name the cardiovascular responses to pain mentioned in lecture.

A

Hypertension
Tachycardia
Myocardial irritability (demand)
Increased SVR
Decreased CO (compromised LV)
Myocardial Ischemia (compromised LV)

Slide 41

96
Q

When is it important to monitor pain in our patients?

A

At all times because it can impact their hemodynamics.

Slide 41

97
Q

Thalamus acts as the _______ _____ _______ for incoming pain signals.

The _____________ ______ serves as the site for discrimination of specific sensory stimuli.

Both of these neurobiological sites determine our __________.

A

central relay station

Somatosensory cortex

Perception

(slide 9)

98
Q

Name the possible pulmonary responses from pain mentioned in lecture.

A

Increased total body oxygen consumption/CO2 production.
Increased minute volume and work of breathing
Decreased movement of chest wall
Atelectasis
Intrapulmonary shunting (VQ mismatch)
Impaired coughing

note the important of splinting when coughing, straining, etc.

Slide 42

99
Q

What is the gate control theory of pain?

A

Made in 1965. “Gates” exist along the pain signaling pathway. Gates along the pathway may open or close to allow the pain signal to continue to the CNS or stop it’s progress. (Slide 22)

100
Q

According to the gate control theory of pain, “gates” can be found where?

A

In the spinal dorsal horn. (Slide 22)

101
Q

According to the gate control theory of pain, if a gate is “open” then the pain signal will reach supraspinal regions of the brain. The supraspinal regions consist of what 4 areas of the brain?

A

Thalamus, medulla oblongata, hindbrain, somatosensory cortex (Slide 22)

102
Q

Name the possible GI responses from pain mentioned in lecture.

A

Enhanced sympathetic tone
Increased sphincter tone
Decreased motility (Ileus)
N/V
Abdominal distention
Hypersecretion of acid (stress ulcer, aspiration risk)

Slide 43

103
Q

How many ml’s of stomach content is considered an increased risk for aspiration?

A

> 25ml’s

Slide 43

104
Q

You bump your elbow and it hurts. You massage the area and now it doesn’t hurt. Using the gate control theory of pain, explain how your elbow stopped hurting.

A

Elbow gets bumped and it hurts. Pain signal travels along “open” gate through A delta + C fibers. A delta = small diameter, myelinated nerve. C = unmyelinated.

Open gate becomes “closed” when sensory input is received through larger, faster, myelinated A beta fiber. Rubbing at the elbow to relieve pain is sending info to brain about pressure and touch. Because pressure/touch travels along faster nerve, it ends up suppressing the pain signal from the slower nerve, thus “closing” the gate from the original pain signal.
(Slide 22)

105
Q

The stomach is empty. Is the patient at risk of aspiration?

A

Yes. Contents from the small intestine can make their way back into the stomach and be aspirated.

Slide 43

106
Q

Name the GU responses from pain mentioned in lecture.

A

Urinary retention

Slide 43

107
Q

Name the catabolic hormones that are increased as a response to pain.

A

Catecholamines
Cortisol
Glucagon

Slide 44

108
Q

Name the anabolic hormones that are decreased as a response to pain.

A

Insulin
Testosterone

Slide 44

109
Q

In the supraspinal regions, what is the purpose of the PAG - RVM system?

A

The periaqueductal gray - rostral ventromedial medulla system is where a pain signal will first travel through in the supraspinal brain regions.

This usually suppresses a lot of pain signals, but a small portion may travel through this area for further processing in the brain. (Slide 23)

110
Q

Name the endocrine responses from pain mentioned in lecture.

A

Increased catabolic hormones
Decreased anabolic hormones
Negative nitrogen balance
Carbohydrate intolerance
Increases renin, aldosterone, angiotensis system (RAAS)

Slide 44

111
Q

Which are some alpha-2 agonist medication examples mentioned specifically in lecture?

A

dexmedetomidine and clonidine

(Castillo)

112
Q

Name the stress related hematologic responses from pain mentioned in lecture.

A

Platelet adhesiveness
Reduced fibrinolysis
Hypercoagulability

SCD’s. Maybe some prophylactic blood thinning going on

Slide 45

113
Q

Name the emotional responses from pain mentioned in lecture.

A

Anxiety
Sleep disturbance
Depression

Slide 46

114
Q

What is the purpose of the thalamus and somatosensory cortex in the pain pathway?

A

These areas of the supraspinal brain regions are where perception of pain occurs. Here a pain signal is fully processed, and the brain attempts to sort where the pain is coming from, what type of pain it is, and what sort of response should occur. (Slide 23)

115
Q

What is the purpose of the limbic cortex in the pain pathway?

A

This part of the brain is where we deal with the motivational - affective pain components. (Slide 23)

116
Q

Name the immune responses from pain mentioned in lecture.

A

Stress related Leukocytosis
Depressed Reticuloendothelial system (increased chance of infection)

Slide 46

117
Q

Name the meds in their respective sites of action according to the picture

A

Perception: Opioids, alpha-2 agonists, GA

Modulation: LA, opioids, ketamine, alpha-2 agonists

Transmission: LA

Transduction: LA, and NSAIDS

(slide 10)

118
Q

What were to happen if the amygdala was “clipped”?

A

Some pain signals travel through the amygdala before being processed/perceived by the cortex. If the amygdala were “clipped”, then the pain signal would not travel to the cortex. This means you would not feel that you are in pain, even if something painful was happening to you. (Slide 23)

119
Q

What are the 7 neuromodulators that propagate a pain signal?

A

Substance P, Glutamate, CGRP, NMDA, AMPA, BDNF, Cytokines (Slide 24)

120
Q

Which of the 7 neuromodulators that propagate pain can be targeted by ketamine?

A

NMDA receptors (slide 24)

121
Q

Which of the 7 neuromodulators that propagate pain can be targeted by opioids?

A

AMPA, BDNF, Cytokines (slide 24)

122
Q

Nociceptors release ____ and ____ in response to tissue injury.

A

Substance P, Glutamate (slide 25)

123
Q

What 6 mediators are released by damaged cells, mast cells, and platelets to activate nociceptors and start a pain response? What meds can target these mediators to stop them?

A

Bradykinin, histamine, prostaglandins, serotonin, H+, lactic acid. NSAIDs and Opioids can inhibit these. (Slide 25)

124
Q

The choices are GABA, glycine, Glutamate, and Norepinephrine. Which one is an excitatory pain impulse mediator?

A

Glutamate (slide 26 + 27)

125
Q

Is sensory-discriminative ascending or descending path?

A

Its ascending pathway
Slide 3

Anesthesia Pharmacology (20 decks)

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