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pharm week 1 > Week 4: Pain, opioid use disorder, cannabis > Flashcards

Week 4: Pain, opioid use disorder, cannabis Flashcards

1
Q

Two examples of painful conditions with episodic flares without baseline pain?

A

migraine attacks

trigeminal neuralgia

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2
Q

Nociceptive pain is:

A

somatic r/t bone or muscle involvement

visceral (r/t underlying solid or hollow viscous)

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3
Q

What is the goal of buprenorphine for OUD?

A

Bring them from a 3/10 (withdrawal state) to a 5 or 6/10. Feels better but not “high”.

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4
Q

What happens if buprenorphine is given to a patient on another opioid? Why?

A

They go from 9/10 (high) to a 5/10 and feel like crap.

That is because buprenorphine is an PARTIAL OPIOID AGONIST. Therefore it has a high affinity to the opioid receptors and kicks other opioids off.

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5
Q

How is buprenorphine administered?

A

Sublingual or IV (NOT PO)
No talking or drinking at the same time (this will decrease the effectiveness)
Don’t smoke prior (will dry-out their mouth and decrease absorption).

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6
Q

If buprenorphine is not working ask this…

A

How are you taking it?

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7
Q

Why naloxone with the buprenorphine?

A

If naloxone is take sublingually with buprenorphine= no effect.
If naloxone is injected = opioid withdrawal.

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8
Q

What is delerium tremens? Sx?

A

Delirium tremens (severe, life-threatening manifestation of alcohol withdrawal).

Sx: agitation, aggression, irritability

Confusion

Severe autonomic hyperactivity (trembling, sweating, tachycardia, N + V

Impaired consciousness

Visual, tactile, auditory hallucinations

Tremors, seizures

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9
Q

Drug interactions with buprenorphine/ naloxone?

A

Alcohol

Benzos

CNS depressants

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10
Q

How many hours to achieve moderate withdrawal from heroin, morphine, hydrocodone?

A

12-16 hours for short acting

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11
Q

How many hours to achieve moderate withdrawal from slow release products?

A

17-24 hours

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12
Q

Why might someone go into withdrawal upon initiation of buprenorphine/naloxone treatment?

A

They already had opioid in their system “I was nervous so I took something”.
Buprenorphine is a partial opioid receptor agonist, therefore it will overtake opioid receptors being used by other opioid and cause withdrawal from the other drug

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13
Q

What is the recommended starting dose for buprenorphine/naloxone therapy?

A

4 mg buprenorphine/1 mg naloxone

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14
Q

When would you use a lower dose of buprenorphine/naloxone (such as 2mg buprenorphine/0.5 mg naloxone)?

A

Pt looking well, at a higher risk for withdrawal from other opioid possibly taken

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15
Q

When would you use a higher dose of buprenorphine/ naloxone therapy (such as 6mg buprenorphine/ 1.5 mg naloxone)?

A

Pt in moderately severe withdrawal (COW score > 24)

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16
Q

COW stands for?

A

Clinical opioid withdrawal scale

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17
Q

What do you do on day 1 of buprenorphine/naloxone therapy if sx are controlled after 1-3 hours?

A

Titration for day one is complete

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18
Q

What do you do on day 1 of buprenorphine/naloxone therapy if sx are NOT controlled after 1-3 hours?

A

If sx are not controlled = more medication

Increase by 2mg/0.5 or 4mg/1mg increments

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19
Q

What is the maximum dose for buprenorphine/naloxone on day one of tx?

A

12mg buprenorphine/ 3 mg naloxone

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20
Q

2 parts of the autonomic nervous system?

A

Sympathetic

Parasympathetic

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21
Q

Max dose day 1: buprenorphine/naloxone therapy induction?

A

12mg buprenorphine/3 mg naloxone

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22
Q

Max day 2 dose buprenorphine/naloxone induction?

A

16mg/ 4mg

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23
Q

Why can’t someone resume methadone after 3 days of not having it?

A

The body looses tolerance to methadone quickly. Can lead to a fatal overdose.

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24
Q

What is asthenia?

A

Body lacks strength/ looses muscle strength (i.e. wasting disease, anemia, cancer, disease of the adrenal gland).

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25
Q

What is the target dose for HOME dosing of buprenorphine/naloxone therapy?

A

12-16mg buprenorphine/ 3-4mg naloxone daily

Max dose: 24mg/6mg

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26
Q

Other name for suboxone?

A

buprenorphine/naloxone

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27
Q

What is plasma?

A

55% of overall blood volume
liquid portion of blood, 90% water
Contains:
- fibrinogen
-albumin
-transports antibodies, proteins, nutrients, hormones
-also collects waste from cells and removes it

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28
Q

Plasma versus Serum?

A

Plasma:
-is a liquid.
-Contains fibrinogen.
-Contains albumin
-Obtained BEFORE the clotting of blood.
-Used to treat blood clotting related problems.
Serum:
-is a fluid (less dense than liquid, contains more matter particles).
- obtained AFTER clotting of blood.
- used for blood typing/ diagnostic tests.

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29
Q

What do primary afferent C nerve fibres convey?

A

Dull, perfuse burning pain.

Unmyelinated.

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30
Q

What kind of pain to A beta fibres convey?

A

Sharp, well localized pain.

Myelinated. (allows for more precise signal transfer)

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31
Q

Hyperalgesia

A

Pain evoked by a mild noxious stimulus

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32
Q

Allodynia

A

Pain evoked by a non- noxious stimulus

i.e. feather

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33
Q

Opioid

A

an endogenous or synthetic substance that produces morphine-like effects and can be blocked by antagonists like naloxone.

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34
Q

Opiate

A

Morphine/ codeine like compounds that come from the opium poppy.

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35
Q

Narcotic analgesic

A

Old term for opioid. Use to mean “to induce sleep”. Now used to refer to drugs of abuse.

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36
Q

Endorphins

A

endogenous opioid peptides

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37
Q

What receptors are responsible for the analgesic effects of opioids and resp depression, constipation, euphoria, sedation, dependence?

A

U receptors

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38
Q

What analgesics suppress cough in subanalgesic doses ?

A

Codeine

Pholcodine

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39
Q

Opioid antagonists that help with GI side effects? How?

A

methylnaltrexone bromide
Alvimopan
Naloxegol
- don’t cross the blood brain barrier. Therefore, don’t stop all analgesic effects (only the peripheral ones)

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40
Q

What opioids do not release histamine from mast cells?

A

Pethidine

Fentanyl

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41
Q

What are some effects of histamine?

A

urticaria
itching
bronchoconstriction
hypotension

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42
Q

What is the relationship between codeine and morphine?

A

Codeine is slowly converted to morphine via liver metabolism. Usually codeine does not produce euphoria.

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43
Q

What is the First line treatment for neuropathic pain? (2)

A
  1. Anti epileptic medications (gabapentin, pregabalin)

2. Anti depressants (amitriptyline, nortriptyline, duloxetine, venlafaxine).

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44
Q

What is the maximum dose of gabapentin per day?

A

Gabapentin, also known as Neurontin, has a maximum dose of 1800 mg per day. Bio availability decreases as doses increase.

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45
Q

What are the most common adverse events from gabapentin?

A

Somnolence
Dizziness
Peripheral Edema
(ADE get worse as doses increase. Consider this as the bio availability decreases with increased doses).

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46
Q

What is a side effect of gabapentin that can lead to misuse?

A

Anxiolytic and euphoric affects similar to opioid and benzodiazepines

Gabapentin miss use his higher among patients with concurrent opioid use.

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47
Q

What are two conditions that black evidence to support gabapentin usage?

A

Fibromyalgia

Neuropathic pain

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48
Q

What is the other name for pregabalin?

A

Lyrica

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49
Q

What is the other name for gabapentin?

A

Neurontin

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50
Q

Does gabapentin help with lower back pain?

A

No

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51
Q

What are indications for use for preGabalin?

A

Fibromyalgia, spinal cord injury, DPN (Diabetic peripheral neuralgia), PHN (post herpetic neuralgia).

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52
Q

What are 3 side effects of pregabalin?

A

Diplopia, blurred vision
Exacerbation of heart failure (similar to Gabapentin).
Cognitive decline (in elderly)

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53
Q

What is the other name for a duloxetine?

What is it indicated to treat in Canada?

A 
Cymbalta
Txs: 
DPN
Fibromyalgia 
Chronic LBP
OA of the knee
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54
Q

What are contraindications to duloxetine?

A

Hepatic impairment
CrCl < 30ml/min
Uncontrolled glaucoma

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55
Q

What is the starting dose for duloxetine?

Max dose?

A

30 mg/day

Max= 60mg/day

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56
Q

What are the most common adverse effects of duloxetine?

A

Nausea
Dry mouth
Somnolence
Dizziness

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57
Q

Tolerance versus physical dependence?

A

Tolerance: reduced responsiveness to achieve the desired clinical outcome. R/t u receptor desensitization.
Physical dependence: withdrawal from the drug results in adverse physiological effects.

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58
Q

Dyskinesia

A

impairment of voluntary muscle movements = fragmented or jerky movements

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59
Q

Ataxia

A

lack of muscle control or coordination of voluntary movements such as walking or picking up objects

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60
Q

Max useful dose of duloxetine/Cymbalta?

A

60mg /day (delayed release caps)

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61
Q

Why is pregabalin/lyrica not recommended in the elderly?

A

Risk of falls/ other injuries. Benefit doesn’t significantly outweigh the risk.

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62
Q

What does Cymbalta/Duloxetine treat?

A

DPN
fibromyalgia
chronic LBP
OA of the knee

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63
Q

Side effects of Pregabalin (Lyrica)

A

Diplopia
blurred vision
dose related abnormal vision

Exacerbation of heart failure (same for Gabapentin and Pregabalin)

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64
Q

What is the BEERS criteria

A

A website listing medications that are not appropriate in older adults (r/t ADEs)

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65
Q

What to monitor when initiating or changing amitriptyline or nortriptyline doses?

A

Na level
It is a anticholenergic
sedating
orthostatic hypotension

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66
Q

Clonus

A

involuntary muscle contractions, = uncontrollable, rhythmic, shaking movements.

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67
Q

Myoclonus

A

quick, involuntary muscle jerk (i.e. hiccups)

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68
Q

3 triad signs of serotonin syndrome?

A

1- neuromuscular excitation (clonus, hyerreflexia, myoclonus, rigidity)
2- autonomic excitation (hyperthermia, tachycardia)
3- altered mental state (agitation, confusion)

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69
Q

Mild signs of serotonin syndrome

A 
Nervousness
Insomnia
Nausea/diarrha
Tremor
big pupils
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70
Q

Moderate signs of serotonin syndrome

A

Hyperreflexia
sweating
agitation/restlessness
inducible clonus (with dorsiflexion of the foot)
side to side eye movements (ocular clonus)

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71
Q

Severe serotonin syndrome (5)

A 
Fever >38.5
confusion/delirium
sustained clonus/rigidity
rhabdomyolysis (kidney failure from the byproduct of muscle breakdown)
death
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72
Q

How to prevent serotonin syndrome: (6)

A

Use lowest effective dose

Ask about ilicit drugs

Check drug monographs for tapering and wash-out periods

Follow up 1-2 days after upper dose or starting new drug

Reassess need for serotonin drug yearly

Teach pt to recognize SS

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73
Q

3 guiding principles of pain medication?

A
  1. Measure pain individually
  2. expect the drugs to fail (no false expectations)
  3. prepare for the next step when failure occurs
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74
Q

Odds ratio > 1 =?

A

Roughly speaking >1 for odds ratio means ur more likely to have the odds of what they’re studying.
Higher the OR (odds ratio= higher chance of happening)

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75
Q

What are the 5 points of evidence to practice for medications for treating neuropathic pain? (from PAD provincial academic detailing service)

A
  1. Set realistic expectations with clear goals for therapy before trialing medications
  2. Aim to evaluate success of trial med by weeks 2-4
  3. Discuss discontinuing ineffective medications before trialing another.
  4. Consider renal function, med dosage, drug interactions with efficacy and safety.
  5. Revisit if ongoing medication is useful or harmful
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76
Q

Examples of anticholinergics, antimuscarinics? (7)

A
  • antidepressants
  • antihistamines
  • antipsychotics
  • opioids
  • antispasmodics
  • bladder drugs
  • antimuscarinic inhalers
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77
Q

What are LAMAs?

A

Long acting muscarinic antagonists (i.e. long acting bronchodilators)

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78
Q

What do muscarinic antagonists do?

A

Competitively block cholinergic responses from acetylcholine binding muscarinic receptors.

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79
Q

Where do muscarinic antagonists work in the body?

A
  • exocrine glandular cells
  • cardiac muscles
  • smooth muscles
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80
Q

What nerve is stimulated in COPD?

A

Vagus nerve

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81
Q

What does Vagus nerve stimulation in the lungs do?

A

Increases ACh
= bronchoconstriction of smooth muscles
=inflammation
= mucous

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82
Q

What is acetylcholine?

A

Main neurotransmitter of the parasympathetic nervous system

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83
Q

What is the effect of acetylcholine?

A 
From the parasympathetic NS:
- slows HR
-bronchoconstriction
-dilated blood vessels
-contracts smooth muscle
(opposite of what you want for people with COPD- hence the use of MA (muscarinic antagonists)
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84
Q

What does blocking acetylcholine do?

A
  • bronchodilation
  • decreases secretions
  • increases HR
  • constricts blood vessels
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85
Q

What is the key point to this whole course?

A

Use the lowest effective dose for the shortest duration of time.

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86
Q

What meds are supported with evidence to treat neuropathic pain?

A
  • Gabapentinoids

- Tricyclic antidepressants

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87
Q

Summary points for treating neuropathic pain? (5)

A
  • set realistic goals with the patient (only 50% will get relief from medication)
  • Follow up in 2-4 weeks (onset of effect should occur in a few days but this allows for lifestyle modifications as well).
  • Higher dose isn’t NOT better
  • NO combos
  • stop drugs that don’t work
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88
Q

What is nociceptive pain?

A

Pain caused by tissue injury. Usually sharp, aching, throbbing.
-examples: stub your toe, sports injury, dental procedure, burn

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89
Q

What does the somatosensory NS perceive: (7)

A
  • Touch
  • Pressure
  • Pain
  • Vibration
  • Temperature
  • Position
  • Movement
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90
Q

Where are somatosensory nerves located? (4)

A
  • muscles
  • facia
  • skin
  • joints
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91
Q

What is neuropathic pain?

A

Pain caused by lesions or disease to the somatosensory nervous system (includes peripheral nerve fibres and central neurons).

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92
Q

What is radiculopathy? (and 3 kinds of sx)

A

A type of neuropathic pain caused by the pinching of a nerve root in the spinal column (cervical, thoracic, lumbar).
= pain, weakness, tingling

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93
Q

What is Syringomyelia (sih-ring-go-my-E-lee-uh) ?

A

the development of a fluid-filled cyst (syrinx) within your spinal cord. Cause of neuropathic pain,

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94
Q

7 P’s of pain

A 
1-intellectual pain
2-Financial pain
3-emotional pain
4-spiritual pain
5-physcial pain
6-interpersonal pain
7-bureaucratic pain
95
Q

Visceral pain is?

A

pain that arises as a diffuse and poorly defined sensation usually perceived in the midline of the body, at the lower sternum or upper abdomen.

Can radiate from adjacent organ (ie. Left ureter = left lower quadrant, loin).

often associated with marked autonomic phenomena, including: pallor
profuse sweating
nausea
GI disturbances
changes in body temperature, blood pressure and heart rate
-“sharp, cramping, aching”
-“referred pain”

96
Q

2 types of nociceptive pain:

A

Somatic

Visceral

97
Q

Somatic nociceptive pain…?

A 
- can be localized
Effects the:
- bone
-muscles
-soft tissues
-joints
-"throbbing, aching, boring, deep.."
98
Q

What does the OPQRSTUV pain assessment stand for?

A 
O-Onset
P-Provoked
Q-quality
R-region/radiation
S-severity
T-treatment
U-understanding
V-values
99
Q

Max dose of acetaminophen in elderly?

A

2600mg/day

100
Q

Dosing of acetaminophen in children and adults? Chronic use dosage maximum?

A

15mg/kg q4h (children)

Max 4000mg/ day (adults)
Max 3200mg/day for chronic use
Avoid in liver impairment

101
Q

How are NSAIDS anti-inflammatory?

A

Inhibit prostaglandins (PGE)

102
Q

NSAID categories? (6)

A

1- salycilates (ASA)
2- proprionic (ibuprofen, ketoprofen, naproxen)
3- Indole (indomethacin, sulindac)
4- Fenamate (mefanamic acid)
5- Other (piroxicam, meloxicam, ketorolac, diclofenac)
6- Cox 2 inhibitors (Celecoxib)

103
Q

What does COX stand for?

A

Cyclooxygenase

104
Q

What do COX 1 and COX 2 inhibitors block?

A

Prostacyclins: inhibits platelet aggregation, vasodilation
Prostaglandins: hyperalgesia, vasodilation

105
Q

What do COX-1 (only ) inhibitors do?

A

Blocks the effect of arachidonic acid on Thromboxane A2 (which would cause vasoconstriction and stimulate platelet aggregation).

106
Q

What do NSAIDS react with?

A

1- lithium (decreased renal clearance= lithium toxicity)
2- ACE inhibitors/ diuretics = less antihypertensive effects
3- Warfarin= increased risk of bleeding

107
Q

what do non-selective NSAIDs do?

A

-Decrease prostaglandin and thromboxane A2

=decreased platelet aggregation

108
Q

What do COX 2 inhibitors do?

A

Decrease only prostaglandins (potential shift towards thrombosis).

109
Q

Who should avoid NSAIDS and COX 2 inhibitors?

A

Renal patients

110
Q

The WHO step ladder approach to pain is for?

A

Palliative/ cancer pain

111
Q

First steps for treating cancer pain? (3)

A

1- treat underlying disease
(i.e. radiotherapy for bony metastases)
2- psychosocial support
3- consider non-pharmacological thearpy (i.e. massage, relaxation, acupuncture, TENS)

112
Q

Opiate

A

Any natural compound derived from opium

• Morphine (principal alkaloid of opium), codeine, papaverine

113
Q

Opioid

A

All compounds derived from opium (natural or synthetic), and any compound with opioid like actions that are blocked by non-selective opioid antagonists

114
Q

What is the deciphering factor for incident pain?

A

It is predictable (i.e. dressing changes).

115
Q

What is the breakthrough pain dose?

A

5-10% of the total daily opioid dose
q 1h po
q 1/2 hour for parenteral.

116
Q

How to calculate adequate pain med dosages in palliative care?

A

Take the TDD and divide into q 4h *this is your new regular medication plan. (i.e. 45mg / 6 = 7.5mg q4h)

Take 5-10% of the TDD and use that as the BTP dose. (i.e. 45mg TDD= 4 -4.5 mg q 1h po for BTP).

117
Q

What should you consider ALWAYS when doing an opioid conversion dose?

A

Consider cross tolerance reduction: Give 50% of expected dosage. Easier to go up than to revive after overdose.

118
Q

What genetic variability impairs conversion of codeine to morphine in the liver?

A

• Low expression of CYP 2D6

119
Q

What is the “wind up” phenomenon?

A

Glutamine and aspartate = sensitization of the central nervous system
NMDA receptor antagonists
“If pain not controlled it will become chronic”

120
Q

Examples of when to use adjuvant therapy for palliative pain?

A
  • neuropathic pain
  • visceral
  • somatic
  • anxiety related pain
  • managing side effects
121
Q

S and S of opioid intoxication:

A
  • Recent use of an opioid
  • significant problematic behavioural or psychological changes (e.g., initial euphoria followed by apathy, dysphoria, psychomotor agitation or retardation, impaired judgment) that developed during, or shortly after, opioid use
  • Pupillary constriction (or pupillary dilation due to anoxia from severe overdose) AND one (or more) of the following signs or symptoms developing during, or shortly after, opioid use:
  • Drowsiness or coma
  • Slurred speech
  • Impairment in attention or memory
  • not attributable to another medical condition, mental disorder, or intoxication with another substance
122
Q

Opioid withdrawal symptom criteria (2)?

Symptoms of opioid withdrawal? (10)

A

Presence of either:
1. Cessation of (or reduction in) opioid after heavy and prolonged (i.e., several weeks or longer)
2. Administration of an opioid antagonist after a period of opioid use
3. Three (or more) of the following developing within minutes to several days after Criterion A:
Dysphoric mood
Nausea or vomiting
Muscle aches
Lacrimation or rhinorrhea
Pupillary dilation, piloerection or sweating
Diarrhea
Yawning
Fever
Insomnia

123
Q

What does the COWS scale assess? (2)

A

the stage or severity of opiate withdrawal
-the level of physical
dependence on opioids

124
Q

When assessing opioid use disorder test for?

A
  • Laboratory tests and/or imaging to assess comorbidities/complications revealed in history and physical
  • routine (pregnancy test, CBC, renal/liver function, electrolytes, magnesium, phosphorus)
  • as indicated (chest x-ray, CT head, ultrasound).

-Toxicology, including urine testing for drugs of abuse; ethanol and its metabolite, ethyl glucuronide.

125
Q

The most effective treatment for opioid use disorder?

A
  • maintenance therapy with a long-acting agonist like methadone or the partial agonist buprenorphine. *high risk of overdose upon relapse for individuals who have recently undergone detoxification due to loss of tolerance.
  • Detoxification in pregnancy should be avoided due to risk of spontaneous abortion.
126
Q

What is clonidine?

A
  • alpha-2 adrenergic agonist
  • decreases neuronal output of norepinephrine
  • can blunt the noradrenergic sx of withdrawal such as chills, flushing
  • N + V, diarrhea, muscle aches, cravings usually persist.
127
Q

Maintenance therapies for treating moderate to severe opioid use disorder? (1,2nd and 3 line tx)

A

First line tx= buprenorphine/naloxone
2nd line= methadone
3rd (off label)= slow release morphine

128
Q

How buprenorphine works? (receptors?)

A

Buprenorphine is a partial agonist at the mu opioid receptor and an antagonist at other receptors, e.g., kappa

129
Q

Complications of alcohol use disorder?

A
  • Poor nutrition: thiamine def., hypokalemia, low magnesium, low phosphorus
  • Liver disease
  • bleeding diathesis
  • Tremor, ataxia, seizures, Wernicke encephalopathy
  • Autonomic dysfunction (hypertension, dehydration, pyrexia)
  • neuropathy
  • trauma
  • increased risk of mouth, throat, liver, colon, breast ca
  • infections (aspiration pneumonia, cellulitis)
  • concurrent psychiatric disorders (depression, anxiety)
  • psychosis (hallucinations, delusions)
  • insomnia, sleep apnea
130
Q

Alcohol use disorder has 2 + of these:

A

1- alcohol in large amounts/longer period of time than intended
2- persistent desire/ unsuccessful attempts to decrease/ control alcohol use
3- A lot of time spent to obtain, use or recover from alcohol
4- Craving, strong desire, or urge for alcohol
5- = failure to fulfill roles at work, school or home
6- continue with alcohol despite its’ negative effects on social/ interpersonal life.
7- social, occupational, recreational activities given up because of alcohol
8-recurrent use in physically hazardous situations
9-alcohol used even though it caused/ exacerbated physical or psychological problem
10-Tolerance: more needed to obtain effect
11. withdrawal experience, other meds taken to alleviate withdrawal sx.

131
Q

Alcohol withdrawal sx:

A
  1. autonomic hyperactivity: sweating, HR> 100bpm
  2. increased hand tremor
  3. Insomnia
  4. N + V
  5. Transient visual, tactile, auditory hallucinations/ illusions
  6. psychomotor agitation (movements without purpose)
  7. Anxiety
  8. Generalized tonic-cldonic seizures
132
Q

Immunoassay vs. Chromatography urine drug screening

A

Immunoassay: doesn’t differentiate b/w opioids, false positive for poppy seeds, quinolone abx.
Chromatography: no reaction to poppy seeds, differentiates opioids, better at detecting semi and synthetic opioids.

133
Q

Immunoassay detects which drug that chromatography doesn’t in a urine drug screen?

A

Benzodiazepines- 20+ days after regular use.

-intermediate acting benzos such as clonazepam often not detected.

134
Q

What does an opioid agreement do?

A
  • shows you care
  • shows your doing your due-diligence
  • shows you may discontinue the medication
135
Q

What are indications that an opioid is not working and should be discontinued?

A
  • 2 to 3 dose increases

- no benefit after a few weeks

136
Q

Signs of a failed opioid trial?

A
  • no increase in functioning
  • signs of misuse, diversion, harm
  • no meaningful reduction in pain
  • intolerance to opioid
137
Q

What to do if opioid trial fails?

A
  • cautiously trial a different opioid

- consult pain specialist

138
Q

Morphine is…

A
  • Mu agonist
  • Low pharmacokinetic drug interactions (no phase 1 CYP450 metabolism)
  • low potential for MAOI interactions (depends on timing)
  • many formulations and strengths (PO only for CNCP)
  • cheap
  • potential for neurotoxicity due to morphine-3-glucuronide
139
Q

Codeine…

A
  • weak Mu agonist
  • conflicting evidence: belief is it needs to be converted to morphine via CYP2D6 metabolism to have full effect
  • Genetic polymorphism in CYP2D6 can affect safety and efficacy
140
Q

Genetic polymorphism in CYP2D6 can affect safety and efficacy of codeine by: (3)

A
  • poor metabolizer = no effect (doesn’t mean they have an opioid tolerance)
  • Ultra rapid metabolizers= morphine effect FAST
  • risk for morphine toxicity
  • 1-10% of Caucasians
  • risk for breast feeding (can’t predict how much the baby gets via breast milk)
141
Q

What is drug conversion that is a high risk for toxicity?

A

Codeine to Fentanyl (pt. may be a poor metabolizer, could lead to overdose of fentanyl even though codeine didn’t work).

142
Q

Hydromorphone…

A
  • Mu and Delta agonist
  • Glucuronidation via UGT2B7
  • hydromorphone 3-G-glucuronide (active)
  • No significant CYP450 metabolism
  • low DDI’s (drug drug interactions) with CYP450 metabolism
143
Q

Oxycodone… (5)

A
  • Mu, Delta, Kappa agonist
  • Metabolites:
  • CYP2D6 (oxymorphone-active)
  • CYP3A4 (noroxycodone-active)
  • Potential interaction with: CYP2D6, CYP3A4
  • SR non-beneficial
  • Combos with acetaminophen
144
Q

Oxycontin is … (3)

A

“TIN”= long acting
-is now called OxyNeo

-difficult to swallow = jelly when wet

145
Q

Fentanyl…

A
  • steady state after 6 days (2 x 72 hr applications)
  • CYP3A4 DDIs (highly clinically relevant)
  • renal and hepatic precautions
  • only if 60-90 mg morphine x 2 weeks (NOT for opioid naïve patients).
  • Serotonin toxicity
  • accidental exposure risk (disposal, removal precautions)
  • HIGH ALERT MED
  • EDUCATE IN PROPRER ADMINISTRATION AND DISPOSAL.
146
Q

Fentanyl conversion NOT established for these 3 drugs:

A
  • tapentadol
  • buprenorphine
  • tramadol
147
Q

How long after an MAOI is it safe to administer fentanyl?

A

14 days

148
Q

Precaution of fentanyl when used with:

A
  • renal
  • hepatic
  • cachectic patients (wasting syndrome)
  • elderly
149
Q

Naloxone is not effective in
reversing respiratory
depression due to overdose of:

A

Buprenorphine

150
Q

Buprenorphine is a …

A
  • opioid agonist (mu)

- opioid antagonist (Kappa, delta)

151
Q

Tapentadol

A
  • not commonly used
  • exact mechanism unknown (possible DDIs)
  • opioid agonist (MU)
  • norepinephrine reuptake inhibitor
  • weak serotonin reuptake inhibitor
  • not reversible by naloxone
  • linked to seizures, HTN, serotonin toxicity
  • high rates of withdrawal r/t ADE
  • no direct conversion to morphine
152
Q

Drugs that interact with opioids to put a patient at risk for serotonin toxicity? (2 neuro drugs, 5 opioids)

A 
SSRIs
SNRIs
with
-meperidine
-tramadol
-fentanyl
-pentazocine
-tapentadol
153
Q

Symptoms of serotonin syndrome?

A 
muscle jerking
muscle rigidity
tremors
sweating
fever
agitation
154
Q

CAN pneumonic for serotonin toxicity?

A

C- conscious state changes
A-autonomic changes
N-neuromuscular changes

155
Q

Conscious state changes in serotonin toxicity? (8)

A 
agitation
delirium
restlessness
disorientation
anxiety
lethargy
seizures
hallucinations
156
Q

Autonomic changes in serotonin toxicity? (9)

A 
diaphoresis
hypertension
hyperthermia
vomiting
tachycardia
dilated pupils
unreactive pupils
diarrhea
abdominal pain
157
Q

Neuromuscular changes in serotonin toxicity? (5)

A 
myoclonus
tremor
muscle rigidity
hyperreflexia
nystagmus
158
Q

How to compensate for incomplete cross-tolerance when switching to a new opioid? (2 options)

A

≤ 75mg oral morphine (or equivalent) in 24 hours = decrease by 60-70%

> 75mg oral morphine (or equivalent) in 24 hours= decrease by 50%.
OR: Just decrease everyone by 50% . Easier to increase than to reverse! CNCP= non-actue/urgent setting.

159
Q

How to practice good opioid stewardship? 5

A
  1. communicate/collaborate with patient’s community pharmacist
  2. Write clear and specific Rx
  3. Educate pt re: possible adverse events, toxicity, opioid storage and disposal
  4. Set realistic goals and expectations
  5. avoid interacting medications when possible
160
Q

MME?

A

Milligrams Morphine Equivalent

161
Q

What is the max MME increase per day? What is the absolute MAX?

A

Max= 50 MME/day

ABSOLUTE MAX with good justification of patient benefit and safety= 90 MME/day

162
Q

Opioid associated harms: (serious) 3

A 
Serious
• Falls leading to fractures
• Respiratory Depression
– Dosing changes, errors, or
misuse
• Deaths
– Increasing use, inappropriate
intake, rapid dose escalation,
high doses in opioid-naïve
patients, diversion
163
Q

Opioid associated harms: (other) 4

A 
Other Harms
• Opioid induced androgen
deficiency (OPIAD)
• Opioid induced
hyperalgesia
(experimental settings)
• Potential for misuse and
opioid addiction
• Sedation and cognitive
impairment
164
Q

What should you avoid prescribing concurrently?

A

Opioids + Sedatives (benzos)

165
Q

What are the effects of benzodiazepines? (5)

A 
1-anxiolytic
2-hypnotic
3-muscle relaxant
4-anticonvulsant
5-amnesic
166
Q

What are the short term benefits to benzodiazepines?

A
  • efficacy
  • rapid onset
  • low acute toxicity
167
Q

How do benzodiazepines work?

A
  • increases affect of GABA’s inhibitory influence on neurons in the brain.
  • booster GABA receptor sites= more CL released= more inhibitory
168
Q

What are the brain’s excitatory neuro transmitters? (those halted by benzos) 4

A 
excitatory neurotransmitters, include: 
norepinephrine  
serotonin, 
acetylcholine
dopamine,
169
Q

What do excitatory neurotransmitters control?

A 
normal alertness
memory
muscle tone
co-ordination
emotional responses
endocrine gland secretions
heart rate and blood pressure --all of which may be impaired by benzodiazepines.
170
Q

Benzo receptors not linked to GABA are located here:

A

Kidney
Colon
Blood cells
Adrenal cortex

171
Q

4 main types of opioid receptors?

A

µ (mu), δ (delta), κ (kappa), NOP

172
Q

Where are opioid receptors located?

A

Dorsal horn of the spinal cord

173
Q

What does activation of the opioid receptor by an agonist result it?

A
  1. Closing of the Ca channels= decreases release of neurotransmitters: glutamate, substance P and calcitonin-gene-related-peptide (CGRP).
  2. Opening of K channels
    = efflux of K ions
    = hyperpolarization= less sensitive to excitatory inputs
174
Q

Examples of synthetic opioids: (7)

A 
Fentanyl
Methadone
Meperidine
Oxycodone
Oxymorphone
Hydromorphone
Hydrocodone
175
Q

What causes nausea after opioid administration?

A

Direct stimulation of the chemo receptor in the medulla

176
Q

How does Naloxone work?

A

pure opioid antagonist with affinity for all 3 classic opioid receptors µ (mu), δ (delta), κ (kappa)

177
Q

4 main opioid receptors?

A

µ (mu)

δ (delta)

κ (kappa)

NOP

178
Q

Effect of µ (mu) opioid receptor? 6

A
  • most analgesic effects of opioids
  • euphoria
  • respiratory depression
  • constipation
  • sedation
  • dependence
179
Q

Effect of δ (delta) opioid receptor?

A
  • analgesic

- can be proconvulsant

180
Q

Effect of κ (kappa) opioid receptor (4)?

A
  • contribute to analgesia at spinal level
  • sedation
  • dysphoria
  • hallucinations
181
Q

Effect of NOP receptors?

A

-activation results in antiopioid effect (supraspinal), analgesia (spinal), immobility and impairment of learning.

182
Q

Hyperanalgesia:

A

= pain sensitization or allodynia
=reduced analgesic response to opioid
=NOT the same as tolerance (which is reduced responsiveness a u receptors, occurs with euphoria and respiratory depression).
tx= ketamine, Propofol, decrease analgesic, change analgesic

183
Q

What do opioids do to the GI tract?

A 
Increase tone (less easy to move)
Decrease motility
184
Q

Tolerance?

A
  • develops within a few days of rapid administration
  • mechanism involves u receptor de-sensitization
  • Not pharmacological in origin
  • overcome through drug rotation
  • doesn’t decrease constipation or pupillary constriction
185
Q

NSAIDS should be avoided in these pts:

A

with a history of peptic ulcer disease
renal failure
heart failure
ischemic heart disease

186
Q

What to use on children prior to IV/ IM treatment?

A

Liposomal lidocaine is as effective as EMLA in decreasing pain associated with venipuncture or IV cannulation. It has minimal vasoactive properties and requires an application time of 30 minutes.

187
Q

What bacteria are becoming resistant to Cipro?

relating to UTIs

A

e. Coli
Proteus mirabilis
Klebsiella pneumoniae

188
Q

What bacteria is becoming resistant to TMP/SMX (related to UTIs)?

A

E, Coli

189
Q

Common pathogens for Pyelonephritis?

A 
E. Coli 
Enterobacteriaceae (gram negative bacilli):
- Proteus mirabilis
-Klebsiella pneumonia
-Staphylococcus saprophyticus (gram +)
190
Q

Treatment of recurrent female cystitis?

A

< 1 month since tx and different organism= treat same 1st episode (new infection)

< 1 month= Same organism= tx for pyelonephritis

> 1 month = same as tx for 1st episode (this is a new infection)

191
Q

1st line tx for uncomplicated pyelonephritis:

A

Cefixime 400 mg PO daily x 10 days

192
Q

When should nitrofurantoin be avoided?

A

Near term (36-42 weeks)

193
Q

1st order

Kinetics

A

Concentration dependent drug elimination. A constant percentage of drug is eliminated per unit time.
Half life IS constant

194
Q

Zero Order Kinetics

A

Drug saturates elimination routes.
NOT eliminated in a concentration dependent manner.
Half life is NOT constant.

195
Q

Antagonist

A

Reverse the effect of the agonist. Have no biological effect of their own.

196
Q

Agonist

A

Produces a biological response when bound to a receptor

197
Q

Lethal dose (LD50)

A

Dose that is lethal to 50% of those taking it.

198
Q

Toxic Dose

A

Dose that is toxic to 50% of those taking it

199
Q

The higher the therapeutic index =?

A

Safer drug.

Higher index = safer than narrow index.

200
Q

Efficacy

A

Maximum effect a drug can have.

201
Q

Alpha errors?

A

AAAA! I have a condition!!!! (but you actually don’t).
Null hypothesis rejected when it is true!
aka: Say “there is a difference/significant result” when there actually isn’t one!

202
Q

Beta errors?

A

You are told you don’t have the condition but you do (BAD).

Failing to reject the null hypothesis “there is something wrong even though we are saying there isn’t”

203
Q

Norepinephrine is released as part of the ?

A

Sympathetic NS
Alpha 1 & 2
Beta 1,2 & 3

204
Q

Anabolism

A

Anabolism= growth and building of tissues/cells (parasympathetic)

205
Q

Catabolism

A

Digestion of food molecules to produce energy (sympathetic NS)

206
Q

All values within a CI are statistically possible in a ?

A

Superiority Trial

207
Q

Likely pathogens for AECB?

A 
Rhinovirus
H. influenzae
Streptococcus pneumoniae
Moraxella catarrhalis
Pseudomonas aeruginosa
208
Q

Labs for vanco?

A

Serum Creatinine (Scr) baseline, then weekly (more if renal fx changing or on other nephrotoxic drugs)
*collect 30 minutes or less prior to next dose
Scr increases by 50% or > = to 40 umol/L = trough level needed to assess dosing
CBC weekly
Peak (post) levels not needed
Trough only if meets guidelines

209
Q

Vancomycin clearance in enhanced in these patients

A

Morbidly obese

210
Q

GFR levels (3 categories)

A

A GFR of 60 or higher =normal range.
A GFR below 60 = possible kidney disease.
A GFR of 15 or lower= possible kidney failure

211
Q

< 6mths, immunodeficiencies, craniofacial abnormalities, chronic cardiac or pulmonary conditions, Down syndrome, underlying hearing impairment, history of OM with suppurative complications or chronic perforation

A

90mg/kg/day (amox) and 6.4mg/kg/day (clavulanate)

TWO prescriptions
- Amoxicillin 45mg/kg/day (div bid-tid) x 10 days
AND
- Amox-clav (7:1) 45mg/kg/day amox (div BID- TID) x 10 d

212
Q

Bacteriocidal are? (2)

A

Time dependent or
Concentration dependent
MIC = MBC

213
Q

Time dependent Bactericidal Abx?
4 examples
2 things they need?

A

B lactams
Vanco
Macrolides
Clindamycin

Need: frequent dosing, must stay above the MIC

214
Q

Examples of concentration dependent bactericidal abx?

2 aspects of these?

A

Aminoglycosides
Quinolones
1- less frequent dosing
2-dose to achieve higher peaks

215
Q

What does amoxicillin cover that PCN doesn’t? (Hint: It’s gram negative)

A

H. Influenzae

216
Q

Normal Creatinine Clearance? Male and Female

A

Female 22–75 µmol/L

Male 49–93 µmol/L

217
Q

Which drug is used off label to tx Raynauds?

A

Calcium channel blockers

218
Q

Which drug is contraindicated in Raynaud’s ?

A

Beta blocker

Can cause cold extremities

219
Q

Which drug should be used with caution in COPD?

A

Beta blockers

B2= bronchodilator (blocked= bronchi construction)

220
Q

Example of a calcium channel blocker that causes flushing and edema?

A

Dihydropyridine

“2 water filled pyramids”

Aka: Nifedipine

221
Q

Side effect of verapamil

A

Headache
Constipation

risk of cardiac failure and heart block

222
Q

Verapamil works on?

A

The cardiac muscles

Causes: constipation

223
Q

Dihydropyridine works on?

A

Smooth muscle. = edema

224
Q

Diltiazem works on ?

A

Both cardiac and smooth muscle

225
Q

Amlodipine and nifedipine are in this drug grouping?

A

Dihydropyridines

226
Q

CCB that tx HTN are usually?

A

Dihydropyridines such as nifedipine or amlodipine.

227
Q

This CCB treats cerebral vascular vaso spasms after sub arachnoid hemorrhage?

A

Nimodipine

228
Q

These CCB help prevent angina (2)

A

Dihydropyridines

Diltiazem

229
Q

This CCB category causes headache, flushing and ankle edema

A

Dihydropyridines (nifedipine)

230
Q

What is pulse pressure?

A

Difference between systolic and diastolic pressure.

Affected with age r/t aortic stiffness

231
Q

ACE does what to bradykinin?

A

Inactivates it.

Therefore, ACE inhibitors allow an increase in bradykinin (I. E. Ramipril cough).

232
Q

Which pts should not combine ACE and ARBS?

A

Renal impairment

Diabetic

233
Q

Valvular a fib includes:

A

rheumatic mitral stenosis

mechanical/ bioprosthetic heart valve

mitral valve repair

234
Q

What is a pro drug?

A

A drug that needs to be activated before it will work.

pharm week 1 (8 decks)

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