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Therapeutics 4 > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

What is pain?

A

An unpleasant sensory and emotional experience that has actual or potential tissue damage. The emotional response to pain is very important.

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2
Q

Nociceptors

A

Free nerve endings of primary afferent A and C fibers. Detect noxious stimuli.

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3
Q

Nociception

A

The process by which information about tissue damage is conveyed to the CNS. Transient process that should be relieved in the absence of painful stimuli.

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4
Q

5 steps in nociception

A
  1. ) Transduction and inflammation
  2. ) conduction
  3. ) transmission
  4. ) modulation
  5. ) perception
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5
Q

Transduction

A

An injury stimulates the peripheral ends of our nociceptors. This stimulus is translated (transduced) from a physical signal into an electrical action potential.

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6
Q

Inflammation

A

Trauma causes damaged cells to release inflammatory substances. Different cell types release different substances. Substances can directly stimulate an action potential while others increase the sensitivity of nociception.

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7
Q

Which inflammatory substances increase the sensitivity of nociception?

A

Prostaglandins
Leukotrienes
Substance P

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8
Q

Conduction

A

Once pain signals have been transduced, those electrical action potentials are conducted along the nerve fibers.

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9
Q

What are the 2 types of pain fibers?

A

A-delta

C fibers

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10
Q

A-Beta fibers

A

Touch receptor,
synapses in the dorsal horn and onto inhibitory interneurons.
Largest in diameter and the most myelinated.

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11
Q

A-Delta fibers

A

Transmits fast, sharp pain. Prickling, cold, heat. Easily located.
Medium size in diameter, myelinated

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12
Q

C fibers

A

Most common throughout the body. Slowly transmits pressure, aching, burning pain.
Dull pain, temp, itch
Unmyelinated, small diameter

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13
Q

Transmission

A

When one nerve ends and connects (synapses) with the beginning of another nerve.
First order neuron to second order neuron.
The electrical signals transmits across the synaptic cleft via neurotransmitters.

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14
Q

What neurotransmitters help the electrical impulse transmit across the synaptic cleft?

A

Glutamate, substance P, NE, dopamine, serotonin

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15
Q

Where does transmission occur?

A

Transmission occurs in the spinothalamic tract/ ascending pathway.

  1. )First order neuron meets second order neuron at the Dorsal horn of spinal cord.
  2. ) Second order neuron travels up and meets a third order neuron in the thalamus and the top of the brain stem.
  3. ) The third order neuron then finally synapses in the cerebral cortex (somatosensory cortex).
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16
Q

Anterolateral System

A

Made up of 3 main tracts:

  1. ) Spinothalamic tract
  2. ) Spinomesencephalic tract
  3. ) Spinoreticular tract
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17
Q

Modulation

A

Modulation is the reduction of pain intensity using an anti-nociception system in our bodies. Endogenous opioids and other anti-nociceptive neurotransmitters act on nerve junctions to modulate pain transmission.

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18
Q

Where does modulation occur?

A

In various places- periphery, spinal cord, and within supraspinal structures

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19
Q

Spinomesencephalic tract

A

Modulates pain,

Innervates the descending tract from the PAG

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20
Q

Which neurotransmitters modulate pain?

A

Opioids (enkephalins), NE, serotonin, GABA

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21
Q

Perception

A

Pain is processed in the brain as the signals reach the cerebral cortex via the thalamus.
The thalamus acts as a “relay station” within the brain.

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22
Q

T/F: Our pain processing system can become sensitized over time

A

True

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23
Q

Peripheral sensitization

A

Injury in the periphery leads to the release of inflammatory mediators. These lead to vasodilation and local swelling (increases blood flow). Leads to inflammation as a guard against infection and protected the area/promote healing.

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24
Q

Allodynia

A

Normally innocuous stimuli now cause a pain resposne

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25
Q

Hyperalgesia

A

Painful stimuli may illicit a pain response that is more significant than what would normally be felt.

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26
Q

Central sensitization

A

At the synaptic junction in the dorsal horn, glutamate is released to stimulate the second order neuron. In central sensitization, the neuron is constantly stimulated. The consistent stimulation of the AMPA receptor changes the resting membrane potential and displaces magnesium ions. Glutamate then binds the NMDA receptor which leads to a hyperresponsiveness and increases the threshold of opioid receptors.

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27
Q

When does central sensitization occur?

A

Can be due to peripheral sensitization or can result from damage to a c-fiber

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28
Q

What causes allodynia and hyperalgesia?

A

Peripheral or central sensitization

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29
Q

Secondary hyperalgesia

A

Hyperalgesia that occurs in locations other than the area of injury.

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30
Q

When does central sensitization heal?

A

When the injury heals. Goal of process is for human to protect the injury.

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31
Q

T/F: Central sensitization occurs on the post-synaptic neuron in the dorsal horn

A

T

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32
Q

Acute pain

A

Suden onset
Warning to tissue injury, disease, procedure
May see increased HR and BP
Pain subsides when stimulus does

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33
Q

Chronic pain

A

Pain which exists past the normal healing time,
Pain without an identifiable etiology
May be nociceptive, result from nerve damage, or be both

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34
Q

Nociceptive pain

A

Temporary, localized pain resulting from the direct activation of nociceptors by noxious stimuli. Pain is then classified by where the nociceptors are located.

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35
Q

Neuropathic pain

A

Pain is caused by damage to the nervous system rather than tissue damage.

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36
Q

Somatic pain

A

Pain involving skin, bones, joints, or soft tissue.
Pain is well localized, patients can typically point to the sight of pain.
Sharp, aching, throbbing pain

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37
Q

Visceral pain

A

Arises from the stimulation of afferent nerves located on soft tissue or viscera. Commonly cardiac, lung, GI tract pain.
Mostly due to c-fibers
Pain is poorly localized and not well described.

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38
Q

What causes neuropathic pain?

A

Typically caused by injured C-fibers that cause pain signals to continuously or intermittently fire without direct nociception

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39
Q

Opioids receptor locations and effect

A

Dorsal horn- inhibit the transmission of nociceptive input
PAG- activate descending inhibitory pathways limiting pain transmission
Limbic system- modify the emotional repsonse to pain (euphoria), addiction
Brain stem-inhibits the respiratory systems response to CO2 levels in the blood

Receptors in the periphery-activates opioid receptors in the gut, decreasing peristalsis

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40
Q

Tolerance

A

The body will adapt to the presence of exogenous opioids by down regulating opioid receptors at the neuronal junction (synapse). This leads to a decrease in effect over time.

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41
Q

Cross Tolerance

A

Tolerance to one drug may produce tolerance to other drugs within the same class. The development of cross tolerance is incomplete in opioids, meaning if a patient is tolerant to an opioid they will not have the same level of tolerance to another opioid.

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42
Q

Ceiling effect

A

Some drugs will not exert more beneficial effects after achieving a specific blood concentration. Opioids do not have a ceiling effect. No max dose and increased doses will have increasing effects

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43
Q

Dependence and withdrawal

A

The body will begin to rely on the presence of exogenous opioids. The drug becomes required for the individual to function normally. Removal of opioid will cause withdrawal symptoms

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44
Q

Addiction

A

The use of the drug is beginning to impact normal functioning. Repeated use in hazardous situations, use despite negative personal consequences, unsuccessful attempts to curb use.

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45
Q

Opioid induced hyperalgesia

A

With chronic use, opioids may induce hyperalgesia and worsen pain as doses increase. This is complex and rare.

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46
Q

When do we use opioids for pain?

A

Severe pain
Acute- surgery, trauma
Breakthrough pain prn
cancer pain
chronic noncancer pain (usually try to avoid)
Opioids are only effective in nociceptive pain

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47
Q

Why are opioids not effective in neuropathic pain?

A

Due to the near constant signals of damaged c fibers, neuropathic pain opens up the NMDA receptor. Opioids do not act on the NMDA receptor.

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48
Q

How do you classify opioids?

A

Impact on opioid receptors (mu, kappa, delta)
DOA
Where they came from

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49
Q

Full mu agonists- opioids

A 
Morphine sulfate
Oxycodone
Hydrocodone
Hydromorphone
Codeine
Meperidine
Fentanyl
Oxymorphone
Methadone
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50
Q

Partial agonist and/or mixed agonist/antagonist- opioids

A

Buprenorphine, butorphanol, nalbuphine

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51
Q

Dual mechanism opioids

A

Tramadol

Tapentadol

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52
Q

Which opioids are naturally short acting but have long acting oral forms available?

A 
Morphine
Oxycodone
Hydrocodone
Hydromorphone
Buprenorphine
Tramadol
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53
Q

Which opioids are naturally short acting and do not have long acting forms available?

A

Codeine
Meperidine
Fentanyl

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54
Q

Which opioids are naturally long acting

A

Oxymorphone

Methadone

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55
Q

Short acting formations onset and dosing

A

Onset: 10-30 min
Dosing: Q 4-6 H

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56
Q

Long acting forms onset and dosing

A

Onset: 30-60 min

Dosing- QD or BID

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57
Q

Morphine

A 
The gold standard opioid
Available in PO, SL, IV, SQ, Epidural
IR lasts 3-6 H
Long acting lasts 12-24 h
Various long acting forms available 
Causes significant histamine release, leading to rash, itching, and potentially hypotension
Doesnt cross the BBB as quickly as others, slower IV onset
May accumulate in renal or liver failure
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58
Q

Hydromorphone

A

Alternative option to morphine.
Available in variety of routes (PO, iV, SQ, epidural)
IR lasts 4-6 H
LA lasts 24 H
Significantly less bioavailability with PO dosing vs IV dosing.
Around 5 times more potent than morphine.
Better tolerated than morphine with less histamine release.

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59
Q

Oxycodone

A

Well tolerated but may have a higher euphoric effect than other opioids.
PO have IR, LA and combo pills
No IV
Greater potency than morphine (5mg oxy= 7.5mg morphine)

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60
Q

Hydrocodone

A

Similar potency to morphine
Only PO, but has IR and LA forms
IR forms only available as combo med
LA forms can be Q12 or Q24 H

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61
Q

Why might we use ER/LA opioid forms?

A

Low peaks- less euphoria
Higher troughs- more consistent pain control
Less frequent dosing, potentially better adherence

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62
Q

Issues with long acting opioids

A

Indicated for chronic pain. Should not be used for prn use
May lead to more tolerance, dependence, and withdrawal
Only effective if used appropriately. A lot of misuse.

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63
Q

Codeine

A

Has a low affinity for the opioid receptor and considered a “weak” opioid.
Much of its activity comes from its active metabolite (morphine). About 10% of patients cant metabolize.
Most common opioid for cough.

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64
Q

Meperidine

A

Different class of opioid than morphine, alternative if there is an allergy.
Only used for acute pain (PO and IV)
Not commonly used
Can cause CNS toxicity and accumulate in renal failure
Risk of Neuroleptic Malignant Syndrome if given with MAO-Is

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65
Q

Fentanyl

A

Same chemical class as meperidine, good option for allergies.
100 x more potent than IV morphine.
10mg morphine= 0.1mg Fentanyl= 100mcg
Fentanyl is dosed in micrograms
Short IV half life (1-2 hours). No active metabolite.
Commonly used for analgesia/sedation in ICU and during procedures
Not available PO

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66
Q

Transmucosal Immediate Release Fentanyl

A

Lozenges, SL tablet, buccal tablet, nasal spray, buccal soluble film, SL spray
All products dosed differently
Only PRN for breakthrough pain in the chronic setting, typically only for cancer patients.

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67
Q

REMS program

A

All transmucosal IR fentanyl products approved under a shared REMS program.
Requirement for REMS program:
Prescriber must enroll
Pharmacies must be certified
Patient must sign a patient-prescriber agreement

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68
Q

Transdermal fentanyl

A

Absorbs the the skin to form a subq depot. Takes 6-12 hours to reach the blood. Blood levels continue to rise for 24 hours.

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69
Q

How often do you change fentanyl patches?

A

Apply to a new sight every 24 hours. Do not titrate the patch dose for 72 hours.

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70
Q

Can you use fentanyl patches in opioid naive patients?

A

No

Patients must have taken >60 MME’s for >1 week.

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71
Q

Temperature effect on fentanyl patches

A

Increasing temperature will increase absorption

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72
Q

Disposal of fentanyl patches

A

Sticky sides together then flush

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73
Q

Oxymorphone

A

Technically LA but the duration of action is only 6 hours. IR form has a slower onset than other IR medications.
Expensive and rarely used.

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74
Q

Methadone

A

Full mu agonist and NMDA antagonist
LA, accumulates with repeated dosing.
Only use in chronic pain
Takes about 3-5 days to achieve SS

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75
Q

Which opioid is most effective in neuropathic pain?

A

Methadone

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76
Q

Methadone dosing

A

Start with small doses (2.5mg-10mg) Q 8-12h
Do NOT adjust sooner than Q 3 days
Breakthrough pain relief should rely on other opioids
Potency charts are not accurate to methadone, dose conversion must be done carefully based on MMEs

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77
Q

Methadone warning

A

Can cause life threatening QTc prolongation

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78
Q

Buprenorphine MOA

A

Partial mu agonist with high binding affinity.

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79
Q

Buprenorphine uses

A

OUD >2mg

Acute pain 0.2mg

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80
Q

Butorphanol

A

Partial mu antagonist
Full Kappa agonist
Used to reduce post operative shivering

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81
Q

Nalbuphine

A 
Mixed antagonist (mu) and kappa agonist
Commonly used for analgesia during labor and delivery.
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82
Q

Tramadol

A

Weak mu agonist

Inhibits the reuptake of NE and serotonin

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83
Q

Tramadol warnings

A

Can reduce seizure threshold

High doses can cause serotonin syndrome

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84
Q

Tapentadol

A

Weak my opioid receptor agonist. Inhibits reuptake of NE.

Same warnings as tramadol

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85
Q

Opioid AE

A 
Itching
Respiratory distress
Constipation
Sedation 
Nausea
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86
Q

Pruritis with opioids

A

All opioids induce histamine release which leads to itching. Most common with morphine.
Least common with methadone and fentanyl.

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87
Q

Constipation with opioids

A

Tolerance does not develop.
Need a stimulant laxative- senna
Can use local opioid antagonists- naloxegol and methylnaltrexone but use is limited due to cost.

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88
Q

Nausea with opioids

A

Primarily mediated via dopaminergic pathways (some serotonin involvement as well)
Also caused by reduced gastric motilty.
Treat with prochlorperazine and metoclopramide.
Tolerance develops quickly.

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89
Q

Sedation with opioids

A

Occurs most commonly as initiation and after dose increases.
Use the Ramsay Sedation Scale to assess (1-6)
A score of 5 or 6 suggests we should reduce or hold the dose.

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90
Q

Respiratory depression with opioids

A

Tolerance develops over time
Greatest risk when starting therapy, raising dose, or changing agents
Sedation almost always proceeds respiratory distress. Administer an opioid antagonist (naloxone) if sedated and respiratory rate <8

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91
Q

Naloxone

A

Opioid antagonist
Used for acute reversal of opioid toxicity
Short duration of action. Need continuous drip in hospital

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92
Q

Naltrexone

A

Opioid antagonist
Slower onset of action
Not for acute OD

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93
Q

Suboxone

A

Buprenorphine/naloxone
Naloxone has extremely poor oral bioavailability and is not effective when suboxone is used appropriately.
It is in the drug to prevent tampering.

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94
Q

Acetaminophen MOA

A

Not fully known, thought to inhibit central cox enzymes.

Lacks anti-inflammatory activity

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95
Q

Acetaminophen max dose

A

4g

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96
Q

Acetaminophen caution

A

Hepatotoxicity. make sure to account for all products containing tylenol

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97
Q

COX-2 selective NSAIDs

A

Celecoxib

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98
Q

Semi-selective NSAIDs

A 
Diclofenac
Etodolac
Indomethacin
Meloxicam
Nabumetone
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99
Q

Nonselective NSAIDs

A

Ibuprofen
Naproxen
Ketorolac
Aspirin

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100
Q

NSAIDs MOA

A

Inhibits COX1 and 2

Decreases prostaglandin production

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101
Q

NSAID AE

A

Gastrointestinal
Renal
CV

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102
Q

Which NSAID is safest for GI issues?

A

Celexocib followed by Ibu

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103
Q

Which NSAID has the highest rate if GI ulceration and bleeding?

A

Ketorolac

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104
Q

Renal Effects of NSAIDs

A

Can cause AKI and worsen CKD
No recommendations for one NSAID vs another
Avoid NSAIDS in CrCl <30
NSAIDs constrict blood from into the glomerulus via the afferent arteriole

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105
Q

NSAID CV effects

A

Increase BP, fluid retention, edema

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106
Q

Which NSAID has the highest chance of causing CV events?

A

Systemic diclofenac and celexocib

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107
Q

Which NSAID has the best CV safety profile?

A

Naproxen

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108
Q

Dosing of aspirin and other NSAIDs?

A

Give the non-aspirin NSAID 30 minutes before or 8 hours after aspirin

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109
Q

NSAIDs in pediatrics

A

Ibuprofen if >6 months, naproxen >12 years
Acetaminophen DOC if <6 months
Do not use aspirin

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110
Q

Topical NSAIDs

A

Little systemic abs and therefore a favorable safety profile.
Very effective for localized pain (osteoarthritis of hand)
Can be considered in patients who otherwise wouldnt be an NSAID candidate.
Diclofenac

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111
Q

Topical anesthetics- Lidocaine

A

MOA- blocks Na channels within nerves to prevent depolarization. Preventing both the initiation and conduction of nerve impulses.
Used for neuropathic pain

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112
Q

Capsaicin

A

Induces burning via the release of substance P. After repeated use (2-4 weeks) substance P is depleted and blocked from reaccumulating.
Used for neuropathic pain primarily.

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113
Q

Counter irritants

A

Methyl-salicylate and menthol
These products irritate the skin (typically via hot or cold) and induce a non-nociceptive signal that will override the nociceptive signal at the spinal cord.

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114
Q

Spasticity

A

An increase in contraction/muscle stiffness and tone (hypertonicity) due to underlying damage to the brain or spinal cord.
This increase in tone/contraction mat lead to involuntary muscle movements (spasms)

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115
Q

Antispastics

A

Improve (reduce) muscle hypertonicity and reduce involuntary spasms.
Baclofen, dantrolene

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116
Q

Spasm

A

A sudden stiffening of a muscle which may cause a limb to kick out or jerk towards your body.

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117
Q

Antispasmotics

A

Decrease muscle spasms by altering CNS conduction and transmission.
Benzodiazepines- inhibit transmission on the postsynaptic GABA neurons
Non-benzos- act at the brain stem and spinal cord.

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118
Q

Antispasmotic agents

A 
Carisoprodol
Cyclobenzaprine
Metaxalone
Methocarbamol
Orphenadrine
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119
Q

Antispastic agents

A

Baclofen

Dantrolene

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120
Q

Combo antispasmodic/ antispastic agents

A

Diazepam

Tizanidine

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121
Q

Antispasmodic key points

A

Recommended as adjunct to rest and PT for short term use (<2-3weeks)
All cause sedation
Caution in elderly

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122
Q

What is the preferred antispasmodic?

A

Cyclobenzaprine

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123
Q

Cyclobenzaprine

A

Related to TCAs
Antispasmodic
Anticholinergic AE

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124
Q

Carisoprodol

A

Antispasmodic

High abuse potential

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125
Q

Orphenadrine

A

Antispasmodic

Anticholinergic AE

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126
Q

Tizanidine

A

Alpha 2 adrenergic agonist
-Antispasmodic and antispastic
Can cause orthostatic HTN and rebound HTN

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127
Q

Components of a pain assessment

A

Build rapport
Subjective assessment of pain
Objective assessment of pain

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128
Q

Unidimensional assessment of pain

A

Subjective

Pain scales

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129
Q

Multidimensional assessment of pain

A

Subjective
Evaluates pain in several domains
PQRSTU method

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130
Q

PQRSTU method

A

P (palliative/provocative)- what makes it better/worse?
Q (quality)- what does the pain feel like?
R (region/radiating)- Where do you feel the pain? Does it move?
S (severity)- How would you rate your pain 1-10? Give directionality.
T (timing/treatment)- when did the pain first start? Is it constant or intermittent? How long does it last? Have you tried anything/ did it work?
U (you)- how is th epain impacting you physically, mentally, spiritually?

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131
Q

Common PQRSTU findings with somatic pain

A

P- may be provoked by movement
Q- The pain is sharp or dull, achy. The pain is familiar.
R- well localized, doesnt move
S- varies
T- may have a specific start time (injury), may have been present for years and recently worsened.

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132
Q

Common examples of somatic pain

A

Joint pain
Bone fractures
skin cuts, scrapes, burns
Muscle pains

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133
Q

Typical analgesic approach of somatic pain

A

Typically APAP and NSAIDs
Duloxetine if it becomes chronic.
Opioids effective but only if severe
Nonpharm (PT, RICE) crucial

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134
Q

Common PQRSTU findings for visceral pain

A 
P- may be provoked by organ functions
Q- Deep, squeezing, crampy, pressure. Often accompanied by N/V/sweating
R- poorly localized, may be referred
S- varies
T- may come about out of nowhere
135
Q

Common examples of visceral pain

A

Cancer pain
Appendicitis
Pancreatitis
Bowel obstruction

136
Q

Typical treatment approach of Visceral pain

A

Treat the underlying cause
Opioids may be required, especially in cancer pain
Non pharm varies greatly between conditions. Cancer- massage, behavioral therapy, etc.

137
Q

Common PQRSTU findings with neuropathic pain

A

P- May be provoked by normally non-painful stimuli and come out of nowhere.
Q- Unfamiliar. Burning, electrical
R- Often radiates
S- varies
T- May have paroxysms of pain (shooting electrical pain)

138
Q

Common examples of neuropathic pain

A

Sciatica, diabetic neuropathy, posttherpetic neuralgia

139
Q

Typical treatment approach for neuropathic pain

A

Antidepressants, anticonvulsants, anesthetics (centrally acting agents)
Limited role of opioids
Non-pharm- crucial
Behavioral therapy, PT, acupuncture, spinal stimulation, nerve block

140
Q

Steps in chronic pain management

A
  1. ) Build rapport
  2. ) Perform a multidimensional pain assessment
  3. ) Establish the goals of tx and ensure pt buy-in
  4. ) Tailor therapy to the pain type present, the location, and the patient characteristics
141
Q

Treatment outcomes and goals of pain therapy

A

Three A’s of pain assessment
Analgesic efficacy- severity of pain
Ability to function- work, sleep, socialize, activities of daily living
AE- GI bleed, liver toxicity, sedation/OD, addiciton

142
Q

Chronic cancer related pain

A

Often visceral
Can be neuropathic or somatic
Mild pain- non-opioid +nonpharm
Mild-moderate pain- Opioid (tramadol) +/- non-opioid + nonpharm
Severe pain- opioid +/- non-opioid + nonpharm

143
Q

Opioid use in cancer pain

A

Start low and titrate up to the desired effect. Titrate with IR, then convert to LA.
Use LA and use IR 10-15% TDD for breakthrough pain
Opioid rotation- switching opioids if one doesnt work

144
Q

Chronic noncancer pain nonpharm

A

PT
Psychological therapy
Integrative health (hypnosis, massage, acupuncture, etc.)

145
Q

Neuropathic pain 1st line treatment

A

Antidepressants- TCA’s or SNRIs
Calcium channel ligands- gabapentin, pregabalin
Topical lidocaine

146
Q

When do you favor use of SNRIs?

A

Depression, anxiety

147
Q

When do you avoid use of SNRIs?

A

Restless leg syndrome, sexual dysfunction

148
Q

When do you favor use of TCAs?

A

Depression, anxiety, insomnia, para/dysthesias

149
Q

When do you avoid use of TCA’s?

A

Cardiac disease, sexual dysfunction, urinary retention, suicidal ideations
elderly, seizure history, glaucoma, orthostasis

150
Q

When do you favor use of calcium channel ligands?

A

Restless leg syndrome
Tremor
Insomnia
Lancinating pain

151
Q

When do you avoid use of calcium channel ligands?

A

Substance use disorder, edema

152
Q

TCA moa

A

Inhibit the reuptake of both NE and serotonin.

153
Q

TCA dosing

A

Analgesia typically achieved at much lower doses than used in depression. Start low and titrate up.
Inexpensive
QD dosing

154
Q

TCA agents

A

Tertiary amines- amitriptyline, imapramine, doxepin

Secondary amines- nortriptyline, desipramine

155
Q

TCA AE

A

Anticholinergic
Tertiary amines have more ae
Nortriptyline has best AE profile. If patient has insomnia use amitriptyline

156
Q

TCA DDI

A

MAOIs, SSRIs, anticholinergic agents, antiarrhythmics, clonidine, lithium, tramadol, agents that prolong QTc

157
Q

SNRIs agents

A

Duloxetine, venlafaxine

158
Q

SNRIs AE

A

Insomnia
Duloxetine- dose related N
Venlafaxine- increased diastolic BP, sexual dysfunction

159
Q

1st line SNRI

A

Duloxetine

160
Q

Calcium channel ligands MOA

A

Modulates the alpha-2-delta protein subunit of the voltage-gated calcium channel blocker. The binding of gabapentin/pregabalin to this presynaptic protein inhibits calcium influx into the neuron and thereby decreases the release of glutamate into the synapse

161
Q

Calcium channel ligands DDI

A

Few, may potentiate opioids, alcohol, benzodiazepines, increase risk of resp depression

162
Q

Calcium channel ligands AE

A

Sedation, edema

Lower doses in elderly and in renal insufficiency

163
Q

Calcium channel ligand agents

A

Gabapentin

Pregabalin

164
Q

Topical lidocaine

A

Patch to be placed at the site of pain unless it is radiating pain, then place patch on the side of the spine at the vertebrae

165
Q

Additional neuropathic agents (2nd line)

A 
Dual mech opioids- tramadol, tapentadol
Capsaicin
Topical clonidine
Other antidepressants and anticonvulsants
Ketamine, dextromethorphan, memantine
166
Q

When should be consider that central sensitization is a factor?

A

When NSAID therapy has failed in nociceptive pain.

167
Q

How do you treat central sensitization?

A

The same way you treat neuropathic pain

168
Q

Opioids in chronic non cancer pain

A

Rarely used

If used, use IR formulations. Do not use ER/LA unless absolutely needed.

169
Q

Clinical features of fibromyalgia

A

Widespread pain, cognitive and memory impairment, tenderness, sleep disturbances, fatigue/stiffness

170
Q

Fibromyalgia ACR diagnostic criteria

A

Widespread pain index (WPI) >7 and symptom severity scale score >5
OR
Symptom severity score >5 or WPI a3-6 and SS >9

Symptoms have been present for at least 3 months with no known cause

171
Q

Non pharm therapy for fibromyalgia

A

Education, aerobic exercise, cognitive-behavioral therapy

172
Q

Fibromyalgia therapy

A

Pregabalin, duloxetine, milnacipron

2nd line- tramadol, cyclobenzaprine, amitriptyline

173
Q

Goals of acute pain therapy

A
  1. ) Patient comfort
  2. ) Promotion of healing/recovery
  3. ) Prevention of chronic pain

If acute pain is inadequately controlled, it can lead to chronic pain

174
Q

Consequences of inadequately controlled pain

A

Patient suffering
Physiological- increased stress hormones, cortisol, glucose, increased risk of diabetes
Psychological- increased risk of anxiety and depression
Functional

175
Q

How do we achieve acute pain goals?

A

Individualized approach to managing pain

Look at severity of pain, etiology of pain, PMH, current treatment settings

176
Q

How do you design therapy for acute pain?

A

Design to take advantage of synergistic effects of multimodal therapy.
Non-pharm + Non-opioid + opioid

177
Q

Opioids for acute pain

A

Opioids should be used prn for acute pain. Only use after non-opioid therapies are maximized and continue non-opioid therapies while taking opioids.
Initiate the lowest effective dose of opioid

178
Q

Opioids for acute pain parenteral agents

A

Morphine, Hydromorphone, fentanyl

179
Q

Opioids for acute pain oral agents

A

Morphine, hydromorphone, oxycodone, hydrocodone, tramadol

180
Q

Opioid administration in acute pain

A

Oral opioids are preferred over IV opioids.

If a pt needs IV opioids, as needed is preferred over continuous infusions. PCA is preferred.

181
Q

Patient controlled analgesia (PCA)

A

Pt can press a button to receive small doses of their IV opioid.
Loading dose- given up front to reach baseline analgesia
Bolus dose- amount of drug the pt self-administers
Lockout interval- minimal time required in between bolus doses

182
Q

What is the purpose of the lockout interval on PCA?

A

Allows the drug time to take effect and the patient time to assess the impact before requesting another dose.
Prevents OD

183
Q

Advantages of PCA

A

Better titration analgesia
Better pain control
Less sedation
Patient has some control and better satisfaction

184
Q

Safety concerns of PCA

A

Operator errors- programming, inappropriate dose, wrong analgesic
Patient errors- triggering by proxy, unable to trigger (physical or mental)
Equipment errors-false triggering, hardware/software failure

185
Q

Therapeutic window of pain control

A

Spot in covering pain and staying within analgesic window.

Less CNS AE with oral opioids

186
Q

Plasma concentrations with PCA?

A

Plasma concentrations stay within the comfort range.

Avoid sedation/ CNS effects and pain

187
Q

PCA patient selection

A

Mentally alert and understands the instructions
Physically capable of operating the device
Pain problem for which PCA represents that most appropriate analgesic treatment
Has active IV access

188
Q

Converting PCA to oral medications

A

Switch as soon as a patient can tolerate.

  1. ) Determine the TDD
  2. ) Covert TDD into total daily oral morphine equivalents. Covert to other opioid if needed.
  3. ) Reduce for cross tolerance if needed
189
Q

Ketamine MOA and uses

A

NMDA receptor antagonist (blocks glutamate)
Used as an anesthetic
Impacts pain, hyperalgesia, central sensitivity
IV only and nasal for refractory depression

190
Q

Ketamine AE

A

Produces a dissociative effect

191
Q

Lidocaine IV

A

Sodium channel blocker. Blocks the transmission of nerve impulses by decreasing the permeability to sodium ions.

192
Q

Sodium channel blockers

A

Block the transmission of nerve impulses by decreasing the permeability to sodium ions. Pain is not the only sense that is impacted- temp, touch, muscle tone
Most common- lidocaine, ropivacaine, bupivacaine

193
Q

Regional anesthesia peripheral nerve blocks

A

Injection near a cluster of nerves.
Commonly used for surgery/trauma on the arms and hands, the legs and feet, groin, or face
Admin-
Single dose with short acting lidocaine, single dose with long acting bupivacaine, continuous infusion

194
Q

Regional anesthesia neuraxial nerve blocks

A

Injection in or around the spine. Commonly used for surgery/trauma in a general region of the body such as the abdomen/hips
Admin- single dose or continual infusion to the epidural space (given outside the dura mater)
Given to intrathecal space (inside the dura mater)

195
Q

Common epidural agents

A

Opioids:
Hydrophilic- morphine, hydromorphone
Lipophilic- fentanyl, sufentanyl

Local anesthetics- bupivacaine, ropivacaine

196
Q

Long acting vs short acting epidural agents

A

Hydrophilic substances have a longer onset of action and duration of action
Lipophilic substances have a short onset of action and DOA

197
Q

Does the location of epidurals matter?

A

Yes
Intrathecal- inside dura mater
Epidural- directly next to dura mater
Doses vary (tiny small doses in intrathecal) and you could easily harm a patient.

198
Q

Non pharm options for acute pain

A

Physical therapy
Distraction (guided imagery)
TENS application (music therapy, massage, hypnosis, biofeedback)
Effective sleep is super important

199
Q

When do you decrease non-opioids in acute pain?

A

Only when patients are already off opioids and returning to baseline

200
Q

Approach to perioperative pain

A
  1. ) Pre-operative
  2. ) Intra-operative
  3. ) Post- operative
201
Q

Goals of perioperative pain

A
  1. ) improve comfort
  2. ) Promote healing
  3. ) Prevent chronic pain
  4. ) minimize AE
202
Q

Pre-operative phase

A

Preemptive analgesia- providing analgesia prior to pain to prevent sensitization to the pain signals.
Reduce peripheral sensitization- 1 dose celecoxib if not contraindicated
Reduce central sensitization- one dose gabapentin, pregabalin 1-2 hours prior if not contraindicated

203
Q

Intra-operative phase

A

Anesthesia. Goal is to prevent painful sensation during the operation and prevent conscious awareness of the procedure
Agents- continuous infusion opioids, NMDA antagonists (ketamine), sodium channel blockers, sevoflurane, isoflurane, desflurane

204
Q

Post-operative phase

A

Goals: improve patient comfort, promote healing, prevent chronic pain, minimize AR
Use multimodal therapy

205
Q

DSM-5 definition of a substance use disorder

A

Control- need more doses, unsuccessful quitting attempts, cravings, large time seeking
Social- work, school, home issues, giving up on other activities
Risky use- use despite harm, use in hazardous situations
Pharmacological- tolerance and withdrawal

206
Q

Intoxication

A

Reversible substance induced- maladaptive behavioral or psychological changes after recent ingestion of substance
NOT due to a medical or psychiatric illness
Does not always co-occur with a SUD

207
Q

DSM-5 classes of drugs

A

Alcohol, caffeine, cannabis, hallucinogens, inhalants, other, tobacco, stimulants, sedative/hypnotics, opioids

208
Q

Health consequences of alcohol use

A

CV- high BP, heart disease, stroke
Malignancies- breast, mouth, throat, liver, colon
Mood and cognition- Depression, anxiety, dementia
Social consequences- unemployment, lost productivity, interpersonal conflict

209
Q

Alcohol effects on glutamate

A

Alcohol inhibits glutamate receptor function.

This causes muscular relaxation, clumsiness, slurred speech, staggering, memory disruption, blackouts

210
Q

Alcohol effects on GABA

A

Alcohol reduces GABA receptor functions

This causes calm, anxiety-reduction, sleep

211
Q

Alcohol effects on dopamine

A

Alcohol raises dopamine levels causing excitement and stimulation

212
Q

Alcohol effects on endorphins

A

Alcohol raises endorphin levels

This kills pain and leads to an endorphin high

213
Q

Binge and excessive drinking in women

A

Binge is 4 or more drinks in 1 sitting.

Heavy drinking is 8 or more drinks in 1 week

214
Q

Binge and excessive drinking in men

A

Binge is 5 or more drinks in 1 sitting.

Heavy drinking is 15 or more drinks in 1 week.

215
Q

CAGE

A 
Substance abuse screening tool
Self administered/interviewed 1 minute assessment. 
Cut down
Annoyed
Guilty 
Eye-opener
216
Q

AUDIT-C

A

Substance abuse screening tool
Self administered 1 min assessment
How often, how much, binge frequency

217
Q

Baseline assessment in patients with AUD

A 
Vitals
EKG
LFTs
Toxicology: Blood alcohol level, co-exposure to other substances 
Infectious disease screening
Pregnancy tests
H/O alcohol withdrawal seizures 
Social history
218
Q

Tx of acute alcohol intoxication

A

Supportive care- IV hydration, education

Banana bag- 100mg thiamine, 1mg folic acid, 1-2 grams magnesium, multivitamin

219
Q

Wernicke-Korsakoff “Wet brain”

A

Due to thiamine deficiency
Wernickes- ataxia, confusion, ophthalmoplegia (oculomotor dysfunction), may progress ot coma/death
Korsacoff syndrome- chronic amnesia, lack of insight, apathy. Consequence of wernickes

220
Q

Alcohol withdrawal symptoms

A

Early: 6-12 h after last drink. Mostly autonomic (increased HR/BP)
Middle: 12-24 hrs after last drink. Tremors and autonomic symptoms, audio/visual hallucinations, anxiety
Late- onset 48-72 hours after last drink. Delirium Tremens (DTs)

221
Q

AUD severe/complicated withdrawal risk factors

A 
H/O alcohol withdrawal delirium or seizures
Multiple prior withdrawal episodes
Traumatic brain injury
Age >65
Long duration of heavy use
Autonomic hyperactivity on presentation
Dependence on CNS depressants
222
Q

CIWA-Ar

A

Withdrawal assessment

Complicated if >19

223
Q

Levels of care for alcohol withdrawal

A

Level 1- mild. Daily monitoring for up to 5 days
Level 2- outpatients who become agitated, oversedated, other conditions worsen, unstable vitals
Inpatient- CIWA >19

224
Q

Inpatient monitoring for alcohol withdrawal

A

Moderate to severe- monitor 1-4 hours for 24 hours or until CIWA-Ar <10 for 24 hours
Mild- every 4-8 hours for up to 36 hours

225
Q

Treatment for alcohol withdrawal- Benzos

A

Benzodiazepines are DOC
Symptom triggered dosing based on CIWA-Ar score is preferred.
Longer acting for pts with rebounding symptoms (diazepam, chlordiazepoxide)
Shorter acting for liver disease, elderly, or overly sedated (lorazepam, oxazepam)

226
Q

Alcohol withdrawal other medications

A

Gabapentin

Carbamazepine

227
Q

Alcohol vs Benzodiazepines

A

Benzos have reversal agent (Flumazenil)

No maintenance treatment for benzos other than recovery programs

228
Q

Benzodiazepine tapers

A

Must taper off of benzos
Withdrawal symptoms can be persistent and unpleasant, lasting weeks-months (“protracted withdrawal”)
When a benzo is used regularly for 8 or more weeks, a taper should be used
10-25% every two to four weeks may be reasonable (can take 6+ months)
Recommend psychotherapy for anxiety/withdrawal

229
Q

Maintenance therapy for AUD

A

Decrease total drinking days and heavy days
Decrease number of drinks/day
Decrease any harm

230
Q

APA guideline recommendations for mod-severe AUD

A

1st line- Naltrexone or acamprosate if the goal is to reduce/abstain

2nd line-Disulfiram only if goal is to abstain, Topiramate or gabapentin

Avoid antidepressants, benzos, etc. for maintenance

231
Q

Acamprosate

A

333mg-666mg TID. Used infrequently because of TID dosing.
AE- diarrhea, suicidality
Avoid use in CrCl <30
Safe in hepatic impairment

232
Q

Disulfiram

A

250-500mg QD
AE- dysgeysia (taste changes), HA, hepatotoxicity, sexual dysfunction
Must be abstinent 12+ hours and 14 days after d/c
Hidden alcohols- mouthwash, hand sanitizer, etc.
Avoid use of metronidazole

233
Q

Naltrexone for AUD

A

Can be orally QD or monthly injection
Causes hepatotoxicity
Do not use in patients that take opioids for pain. Can precipitate opioid withdrawal, only use if opioid free for 7 days.

234
Q

Topiramate

A

Alternative option for AUD
Causes cognitive dulling, kidney stones, appetite suppression
Slow titration improved tolerability
Monitor renal function

235
Q

Gabapentin for AUD

A

Alternative option for AUD
HA, sleep disturbances, suicidality
Dose adjustment required for renal impairment
Risk of misuse

236
Q

S/S of an opioid intoxication

A 
Drowsiness
Slurred speech
Constricted pupils
Impaired attention
Shallow breaths
Bradycardia
OD-death
237
Q

S/S of opioid withdrawal

A 
Nausea
Diarrhea
Coughing
Lacrimation, rhinorrhea
Chills, diaphoresis
Yawning
Piloerection
Drug craving
238
Q

Assessing opioid withdrawal scales

A

COWS
SOWS
WAT-1
Finnegan neonatal abstinence scoring system

239
Q

COWS vs SOWS scales

A

COWS- clinician rated
SOWS- patient rated
Follows opioid withdrawal

240
Q

WAT-1

A

Clinician scale used for iatrogenic withdrawal in pediatrics (ex.- due to receiving opioids for trauma inpatient).
Higher scores= more withdrawal

241
Q

Someone comes in with opioid withdrawal, what do we look at?

A 
Vital signs
EKG
LFTs
Toxicology: Urine drug, consider serum tox
Infectious disease screening
Pregnancy test
Social history
242
Q

Opioid withdrawal timeline

A

Symptoms begin 6-12 hours after short-acting opioid and 30 hours after long-acting opioids
Symptoms peak at 72 hours

243
Q

OUD treatment process

A

Withdrawal
Induction (medication)
Maintenance

244
Q

Which drugs are used to treat OUD detoxification?

A

Clonidine and lofexidine can both be given for symptom support. They do not treat withdrawal.
Buprenorphine and methadone treat detoxidication and withdrawal

245
Q

OUD maintenance treatment

A

Naltrexone- only use if patient is not on opioids
Buprenorphine
Methadone

246
Q

Acute opioid withdrawal treatment approach

A

Medically-assisted opioid withdrawal (detoxification)
Methadone and buprenorphine can be used. Both 1st line.
Buprenorphine is more flexible and safer.
a-2 agonists are considered second line and can reduce symptoms of withdrawal.

247
Q

What is “induction?”

A

Initiating a partial/full opioid agonist, usually during the withdrawal phase.
Need to have confirmation of recent opioid use or forced abstinence.
Initiate therapy when withdrawal symptoms appear (COWS 6-10)
Monitor closely

Agents- Methadone and buprenorphine

248
Q

General evaluation for medications for opioid use disorder (MOUD)

A

Medical conditions- STIs, hepatitis, HIV, trauma, pregnancy
Co-occuring psychiatric illness
Other substance abuse

249
Q

Treatment initiation for OUD

A

Withdrawal management- buprenorphine, methadone for treatment
lofexidine, clonidine for symptoms only (if needed)

MOUD- buprenorphine, methadone, LAI naltrexone

Psychosocial is important

250
Q

Clonidine

A

Hypotension may occur
2nd line for withdrawal management in OUD
a-2 agonist

251
Q

Lofexidine

A

a-2 agonist
2nd line for withdrawal management in OUD

Hypotension, bradycardia, etc.

252
Q

Buprenorphine for OUD

A

Opioid dependence
2-16mg QD daily (max 32mg)
Boxed warnings- REMS program
ADR- CV and resp depression, HA, N/V

253
Q

Methadone for OUD

A

20-120 mg QD
Boxed warnings- death, QTc prolongation
ADRs- resp depression, hypotension.

254
Q

Boxed warning on Naltrexone

A

Hepatocellular injury

REMS- LAI risk of injection site reactions

255
Q

OUD in pregnancy

A

Opioid agonist therapy recommended as early as possible
Should receive methadone or buprenorphine .
Avoid opioid antagonist therapy (naltrexone)

256
Q

Neonatal abstinence syndrome (NAS)

A

Nonpharm- breastfeeding, swaddling, rooming-in, mother education
1st line- morphine, methadone

257
Q

OUD in children

A

Screening for SUD should start at age 11
1st line- psychosocial interventions
Ages 16 and over- buprenorphine, naltrexone
Methadone requires parental consent if <18.

258
Q

OUD in patients with pain

A

Consider non-opioids, behavioral therapies, and physical therapy
With pain and OUD, treat both concurrently. Consider prn buprenorphine if used as MOUD
Consider short acting full agonists if methadone used as MOUD

259
Q

OUD in jails

A

Ensure narcan kits are available in correctional facilities
Care should be patient specific.
Buprenorphine most common

260
Q

Stimulant intoxication S/S

A

Increased attention and wakefulness, decreased appetite, euphoria, increased respiration, rapid HR, hyperthermia

261
Q

Stimulant withdrawal

A 
Hunger/thirst
Difficulty concentrating
Terrible depression/suicidality
Anxiety
Fatigue
Sleep disturbances
262
Q

Tx for stimulant use disorders

A

No medicagtions

behavioral therapy, 12 step programs, support groups

263
Q

Management of acute stimulant intoxication

A

Vital signs
Hydration- decreases risk of rhabdo
Benzos- decreases anxiety, agitation, seizures
Prolonged psychosis- add anti psychotic if it doesnt clear

264
Q

Brain anatomy and addiction

A

3 brain processes involved in addiction
1- Basal ganglia- involved in reward and motivated behaviour. Releases dopamine.
2- Extended amygdala- involved in memory, emotion, stress
3- prefrontal cortex- involved in executive function/decision making

265
Q

3 stages of addiction

A
  1. ) Binge/ intoxication- basal ganglia, euphoria
  2. ) Withdrawal- extended amygdala
  3. ) Preoccupation/Anticipation- prefrontal cortex
266
Q

Binge/intoxication stage in addiction

A

Drugs with high addictive potential release dopamine in the reward pathway (N/ accumbens and dorsal striatum in basal ganglia)
This causes reward, motivated behavior, and habit circuitry
Changes in the dopamine system over time promotes substance taking habits

267
Q

Withdrawal/ negative stage in addiction

A

Diminished activation of reward circuit. Decrease in dopamine receptors and activity in amygdala
Activation of stress systems
Drive to reduce negative affect reinforces drug seeking behavior. Ppl take drugs to feel normal

268
Q

Preoccupation/Anticipation stage in addiction

A

Highlighted by craving
Dysfunction of prefrontal cortex. Hypofrontality.
Increased “GO” system. Enhanced activation of dopamine reward system.
Diminished “STOP” system- increased impulsivity

269
Q

Hypofrontality

A

Addiction begins with the genes and the rewards system
Addiction ends with disorder of choice- loss of insight and impaired decision making.
Ramped up reward system and deficient cortical glutamate system (cognitive system)

270
Q

Pharmacology of alcohol

A 
Activates GABA/Benzo receptor complex. 
Inhibits glutamate receptor function
Releases dopamine 
Releases endogenous opioids
(activates inhibitory system, inhibits excitatory systems)
271
Q

Alcohol effects on glutamate

A

Receptor antagonism and reduces release
Hyper-excitability and up-regulation of receptors.
Behavioral- memory loss, rebound hyper-excitability, brain damage

272
Q

Alcohol effects on GABA

A

Enhances GABA induced Cl influx to hyperpolarize

Behavioral- sedative effects, anxiety, tolerance and signs of hyper-excitability during withdrawal

273
Q

Alcohol effects on dopamine

A

Increases transmission acutely,

Behavioral- reinforcement, withdrawal

274
Q

Alcohol effects on opioids

A

Increases endogenous opioids acutely
Behavioral- reinforcement (euphoria)
dysphoria

275
Q

Metabolism of alcohol

A

2 step process
Alcohol get metabolized into acetaldehyde by alcohol dehydrogenase.
Then gets further metabolized into acidic acid by acetaldehyde dehydrogenase

276
Q

Toxicity of alcohol

A

Brain
Liver
Digestive system: gastritis
Fetal alcohol syndrome

277
Q

Kratom

A

Plant from southeast asia.
Analgesic without much resp. depression
Activates mu opioid receptors, adrenergic mechanism and has serotonergic activity
Withdrawal and high are minimal, but can still OD

278
Q

Sympathomimetic drugs of abuse

A

Mimic stimulation of nervous system
Mephedrone, methamphetamine, methcathinone, MDMA, amphetamine
Release dopamine in reward pathways and NE(increases HR)

279
Q

Bath salts

A

Cathinone analogues

Sympathomimetic stimulant

280
Q

Methamphetamine dependence

A

S/S- decreased appetite, dilated pupils, tooth decay, picking hair or skin, excessive sweating, disregard for physical appearance
No effective pharmacotherapy for meth addiction

281
Q

MOA of cocaine and amphetamine

A

Both increase synaptic dopamine in reward pathway

282
Q

Desired/adverse psychoactive effects in sympathomimetic drugs (ritalin)

A 
Increased concentration
Increased sexual performance
Increased sociability
Increased energy
Euphoria
Mild empathogenic effects
AE: excited delirium
283
Q

Marijuana

A

Cognitive effects: impaired memory, distorted thinking
Psychomotor- performance deficits
Physiological- increased HR and hunger
We have endogenous cannabinoid in body (anandamide)

284
Q

Cannabinoids

A

Marinol and nabilone (synthetic THC)- treatment of AIDS wasting and cancer chemotherapy
Epidiolex (cannabadiol based)- seizure disorders
Sativex (THC and CBD)- approved in Europe for MS

285
Q

Synthetic cannabinoids

A

K2, spice
500x more potent than THC
AE- seizures, agitation, anxiety, confusion, hallucinations, paranoia

286
Q

Psilocybin

A

Tested in end of life anxiety, treatment resistant depression, addiction

287
Q

Psychedelics

A

Indole type (LSD) and phenylethylamine type (mescaline)
Both activate 5-HT2A receptors leading to increased glutamate release in frontal cortex.
5-HT2A is responsible for active coping, cognitive flexibility, creative thinking

288
Q

Psychoplastogens

A

Psychedelics and Ketamine
Neuroplasticity inducing drugs
Both drugs increase glutamate release leading to increased brain growth factors and new synapses.

289
Q

MDMA (ecstasy)

A

Releases serotonin and to a lesser extent dopamine
effects- hug drug, increased awareness of emotions and communication, entactogen (feeling within)
FDA breakthrough status for treatment of PTSD

290
Q

What is inflammation?

A

Complex biological response of bodys tissues to harmful stimuli.
It is an innate, nonspecific response.
It is protective

291
Q

5 stages of inflammation

A 
Rubor (redness)
Calor (heat)
Tumor (swelling)
Dolor (pain)
Functio Laesa (loss of function)
292
Q

Immune systems

A

Innate immune system and adaptive immune system

Both immune systems work together

293
Q

Innate immune system

A

Nonspecific responses involving the activation of Toll- like receptors.
Utilizes neutrophils, macrophages, and NK cells.
Generates a lot of inflammation.
Due to local injury

294
Q

Adaptive immune system

A

Includes antibody- and cell- mediated immunity.

Involves B and T cells

295
Q

B cell activation

A

Activation of B cell receptor (BCR) orchestrates different signaling events.
Acts to change cytoskeletal arrangement and transcription within the cell. Notably within the p38 MAPK and NF-kB signaling.

296
Q

Antibody production

A

Activated B cells turn into plasma cells that make large quantities of antibodies. Expand ER to increase protein synthesis capacity.

297
Q

Inflammatory mediators of the immune system

A

Prostaglandins, Leukotrienes, histamine, bradykinin

298
Q

Cytokines of the immune system

A

Interleukins, Tumor necrosis factor, chemokines

299
Q

Eicosanoids

A

Leukotrienes and prostaglandins.

Have a role in the inflammatory system, CV system, and reproductive system

300
Q

Production of eicosanoids

A

Revolve around arachidonic acid, which is required ot generate a lot of mediators

301
Q

Which COX enzyme is inducible?

A

COX 2

302
Q

What is the main activity of COX enzymes?

A

Primarily vasodilation

303
Q

Arachidonic acid and platelet aggregation

A

Aspirin works by shutting down COX mediated platelet aggregation.

304
Q

Cytokines

A

small protein signaling molecules.
Provide for intercellular communication
IL-1. IL-2, IFN, and TNF-a

305
Q

Interleukin-1 signaling

A

Involved in inflammation, cartilage breakdown, bone reabsorption.
Increases the expression of other cytokines.
Large family

306
Q

Tumor necrosis factor-alpha signaling

A

Secreted by macrophages.
Activates phosphorylation cascades involving p38 MAPK and ultimately alters gene expression.
Bone changes= IL-8
Cartilage degradation- IL-6 signaling downstream of TNF-a

307
Q

Interleukin-6 Signaling

A

Activates JAK/STAT signaling, specifically STAT3

Results in a variety of cellular processes being altered.

308
Q

Which anti-inflammatory meds can be used for RA?

A

Mild- APAP, NSAIDs
Moderate- DMARDs
Severe- steroids, anti-proliferative drugs

309
Q

Anti-histamines

A

Histamine is produced by basophils and mast cells
Local regulation on inflammation
4 isomers of histamine receptors

310
Q

Hydroxychloroquine

A

Can be utilized for inflammatory disorders.
Works through TLR9 blockade.
Rapid abs, slow distribution.
1/2 life of 30-60 days

311
Q

COX-1 expression. tissue localization, role

A

Expression- constitutive
Tissue localization- Ubiquitous
Role- Housekeeping and maintenance roles

312
Q

COX-2 expression, tissue localization, role

A

Expression- inducible by inflammation stimuli
Tissue localization- inflammatory and neoplastic sites
Role- pro-inflammation and mitogenic functions

313
Q

Aspirin MOA

A

Nonselective, irreversible COX inhibitor

314
Q

This cytokine is an orchestrator of inflammatory processes relevant to several disease states

A

IL-1, IL-6, TNF-a

315
Q

Opiates

A

Drugs derived from opium or having morphine like profile.

Morphine and codeine are the only true opiates

316
Q

Endogenous opioid peptides

A

Families of peptides

Endorphins, enkephalins, and dynorphin

317
Q

What is beta-endorphin derived from?

A

Proopiomelancortin (POMC)

318
Q

What is dynorphin derived from?

A

Prodynorphin

319
Q

What is enkephalin derived from?

A

Proenkephalin

320
Q

Which endogenous opioids are analgesic?

A

Endorphin and Enkephalin

321
Q

Which endogenous opioid is hyperalgesic?

A

Dynorphin

322
Q

Opioid receptors

A

Mu- mediates most of morphines effects
Delta- analgesia
Kappa- in spinal cord mediates analgesia

323
Q

Which receptor is morphine selective for?

A

Mu

324
Q

Which receptor(s) are endorphins and enkephalins selective for?

A

Mu and delta

325
Q

Which receptor is dynorphin selective for?

A

Kappa

326
Q

What effects does the mu receptor have?

A

Analgesia, resp. depression, constipation, sedation, euphoria

327
Q

What effects does the delta receptor have?

A

Analgesia

328
Q

What effects does the kappa receptor have?

A

Analgesia, constipation, sedation, psychosis

329
Q

What does activation of DOC and MOR do?

A

activates the inhibitory subunit of the G-protein coupled receptor and alters neuronal excitability through 2 mechanisms.

  1. ) increases K conductance causing membrane hyperpolarization and supressing depolarization (makes neuron less likely to fire)
  2. ) decreases ca activity, decreasing release of neurotransmitters, particularly glutamate.
330
Q

Do opioid receptors alter inflammatory response?

A

no

331
Q

Inhibition of cough by opioids

A

Both the d and L isomers are antitussive.
The L isomer is also analgesic
D isomer does not cause dependence.

332
Q

Which opioid effects have a high tolerance?

A

Analgesia, euphoria/dysphoria, mental clouding, sedation, respiratory depression, antiduresis, N/V, cough suppression

333
Q

Which opioid effects have minimal/none tolerance?

A

Miosis
Constipation
Convulsions

334
Q

Where is functional selectivity (biased signaling) located?

A

GPCR

Therapeutics 4 (8 decks)

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