Pharm Quiz 6 Flashcards

1
Q

Ester-type Anesthetics

A

Procaine and Cocaine
Low allergy
Metabolized by plasma esterases

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2
Q

Amide-type Anesthetics

A

Lidocaine
Very low allergy
Metabolized by liver

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3
Q

MOA Local Anesthetics

A

Block sodium channels in axons

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4
Q

Order of feelings that are lost with local anesthetics:

A

Pain, Cold, Warm, Touch, Deep Pressure

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5
Q

Why is epi used with local anesthetics?

A

It prolongs length and decreases toxicity.

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6
Q

Local Anesthetic SA

A

CNS excitation followed by depression.
Bradycardia
Cross-sensitivity has not been observed.
Methemoglobinemia -Hgb cannot release O2. Do not give topical benzocaine to children under 2.

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7
Q

Procaine

A

Must be injected. Low risk for toxicity. Higher risk for allergy.

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8
Q

Lidocaine

A

Topical or injection. Stronger than Procaine. Higher risk for toxicity.

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9
Q

Cocaine

A

Used for ENT. Causes vasoconstriction by blocking NorEpi, which also effects the SNS.

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10
Q

Topical Local Anesthetic Administration

A

Location: skin or mucous membranes
Systemic toxicity can be avoided by avoiding heat, wrapping, and exercise which can increase absorption.

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11
Q

Infiltration Anesthesia

A

Lidocaine and Bupivacaine are used in the general area of procedure.

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12
Q

Nerve Block Anesthesia

A

Short Procedures: Lidocaine or Mepivacaine
Long Procedures: Bupivacaine

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13
Q

What happens when opioid agonists are combined with agonist-antagonists?

A

Withdrawal reaction

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14
Q

Opioid induced Neurotoxicity

A

Cause: Renal impairment, cognitive impairment, long-term use
Prevention: Switching different types of opioids
Tx: Hydration and dose reduction

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15
Q

Fentanyl Patch

A

Takes 24h to kick in and lasts for 48 hours.
Should only be given to tolerant patients or respiratory depression will result.

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16
Q

Transmucosal Fentanyl

A

Only for patients >18 with break through cancer pain who are opioid dependent defined as 30mg Oxy, 25mcg Fent/hr, 8mg Hydromorphone.

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17
Q

Methadone SA

A

Due to QT prolongation consultation with a pain specialist is recommended. Patients should receive and EKG before, 30 days after, and then annually.

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18
Q

Strong Opioid Agonists

A

Morphine, Fentanyl, Methadone, Hydromorphone, Oxymorphone, Levorphanol

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19
Q

Moderate to Strong Opioid Agonists

A

Codeine

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20
Q

Agonist-Antagonist Opioids

A

Buprenorphine, Butorphanol, Nalbuphine, Pentazocine

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21
Q

Codeine

A

Schedule II
30mg = 325mg of Tylenol
Antitussive = 10mg (Schedule V)

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22
Q

Codeine BB

A

Ultrarapid metabolizers (specifically children) converts to Morphine and can cause death.

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23
Q

Oxycodone

A

Schedule II
Analgesic effects = Codeine

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24
Q

Hydrocodone

A

Schedule II
ER always combined with NSAID.

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25
Q

Tapentadol

A

Blocks reuptake of NorEpi and causes less constipation.

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26
Q

Pentazocine

A

Mild to moderate pain
Antagonizes u. Agonizes K –> respiratory depression (not dose dependent), analgesia, sedation.
Dependence is possible but withdrawal is minimal.

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27
Q

Buprenorphine

A

Schedule III
Partial agonist at u. Antagonist at K.
No tolerance. No severe respiratory depression.
Naloxone does not readily reverse.
QT prolongation

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28
Q

Naloxone

A

Antagonizes Mu, Kappa, and Sigmoid

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29
Q

Mehtylnaltrexone, Naloxegol, Naldemedine

A

Selectively antagonizes Mu. They only help with constipation.

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30
Q

Naltrexone

A

Used for ETOH and opioid addiction. Prevents euphoria but not craving.
Complete opioid antagonist which completely blocks euphoria. Should only be given after patient has detoxed.

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31
Q

Embeda

A

When swallowed intact, only Morphine is absorbed. Otherwise Naltrexone will prevent high. Only used when abuse is suspected. ETOH accelerates absorption leading to fatality.

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32
Q

Tramadol MOA

A

Slightly Agonizes Mu. Mostly blocks uptake of Serotonin and NorEpi.

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33
Q

Tramadol Use

A

Schedule IV
Moderate pain
Onset: 1 hr Duration: 6h

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34
Q

Tramadol Drug Interactions

A

MAOI
Serotonin Syndrome with SNRIs, SSRIs, TCAs

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35
Q

What drugs does the Risk Evaluation and Mitigation Strategy included?

A

IR opioids, ER opioids, and long-acting prescription opioids to educate members of the healthcare team.

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36
Q

CDC Guidelines for safe opioid prescribing:

A
  1. Establish realistic goals for pain
  2. Discuss known risks continuously
  3. Start with IR
  4. Evaluate before prescribing >50 Morphine milligram equivalents and avoid adjusting a dose to >90 MMEs
  5. Long-term dependence often starts with acute pain. Pain medication for 3 days is often sufficient.
  6. Prescribe with Naloxone when given with Benzo or >50 MME
  7. Avoid prescribing opioids with Benzos.
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37
Q

Avoiding a withdrawal reaction

A

Dependence can start after 20 days, so taper off over 3-10 days.

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38
Q

Characteristics of Migraines

A

Usually unilateral
Usually with aura
Hyperalgesia -augmented responses to painful stimuli
Allodynia -Painful response to unpainful stimuli
Start in the morning and last 4-72 hours
Family history is normal

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39
Q

How does CGRP affect migraines?

A

CGRP rises during a migraine.
Sumatriptan decreases CGRP.
Stimulation of neurons in the trigeminal vascular system –> CGRP release –> inflammation and dilation

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40
Q

How does Serotonin affect migraines?

A

Serotonin drops during a migraine.
Depletion of serotonin can precipitate a migraine.
Administration of Serotonin can abort an attack.

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41
Q

Drug selection for Migraines:

A

NSAID
Migraine-specific drug (triptan or ergot alkaloid)
Opioid agonist

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42
Q

How often can abortive medications be used?

A

1-2x/weeks at most or a medication overdose headache can occur.

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43
Q

What antiemetic is used for migranies?

A

Metoclopramide and Prochlorperazine

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44
Q

What medication combination works as well as Sumatriptan?

A

ASA and metoclopramide

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45
Q

Excedrin

A

Tylenol (should not be used alone), ASA, and caffeine

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46
Q

What opioid medication is used for migraines?

A

Butorphanol nasal spray

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47
Q

Triptans

A

Abortive
40% of patients will have another migraine in 24h
Serotonin receptor agonists constrict intracranial blood vessels and decrease secretion of inflammatory neuropeptides

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48
Q

Triptan AE

A

Bad taste
Chest pressure
Coronary vasospasm
Teratogenesis

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49
Q

Ergotamine MOA

A

Decreases CGRP
Enhances Serotonin
Decreases vasodilation

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50
Q

Ergotamine therapeutic use

A

Second-line after triptans due to dependence

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51
Q

Ergotism

A

Ischemia in peripheral arteries

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52
Q

Dihydroergotamine

A

Given IM, IV, or SQ.
Less effective than triptan but better at reducing recurrence.

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53
Q

Ergotamines BB

A

CYP3AV inhibitors can raise levels to dangerous amounts.

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54
Q

When should preventative migraine agents be given?

A

If patients have >3 attacks/month, they are more severe than usual, do not respond to abortive agents.

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55
Q

Prophylactic medications for migraines:

A

Propanolol
Depakote
TCA
Estrogen

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56
Q

Depakote (Divalproex) BB

A

Pancreatitis and Hepatitis

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57
Q

Medications for menstrualy associated migraine:

A

Estrogen 2 days within the onset of menses.
Triptans for 6 days starting 2 days before menses.
Naproxen sodium given 6 days before menses

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58
Q

Erenumab

A

Monoclonal antibody that decreases CGRP.

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59
Q

Botulinum Toxin

A

For patients with >15 migraines per month. Only decreases amount by 2.

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60
Q

Cluster HA Characteristics

A

Occur every day for 2-3 months and can be separated by months to years.
Unilateral near the eye.
Causes ptosis, lacrimation, nasal congestion, and miosis.
Occur more in males.

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61
Q

Prophylaxis medications for cluster HA

A

Verapamil
Suboccipital steroid injections
Glucocorticoids
Lithium

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62
Q

Cluster HA Abortive Meds:

A

Sumatriptan SQ
Oxygen 7-10L for 10-15 min

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63
Q

When should antidepressants be discontinued?

A

For 4-9 months after alleviation of symptoms. Slowly taper down.

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64
Q

What are SSRIs indicated for?

A

Bipolar
Premenstrual Dysphoric Disorder
Bulimia

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65
Q

Fluoxetine SA

A

Sexual Dysfunction, Weight Gain, Serotonin Syndrome, teratogenesis.

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66
Q

Fluoxetine Withdrawal

A

Withdrawal symptom starts within 1-3 days and lasts up to 3 weeks. It causes dizziness, headaches, dysphoria, and anxiety.

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67
Q

SSRIs

A

Escitalopram
Citalopram
Fluvoxamine
Paroxetine
Sertraline

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68
Q

SNRIs

A

Venlafaxine
Duloxetine
Desvenlafaxine
Levomilnacipran

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69
Q

Venlafaxine Therapeutic Uses

A

Depression
Anxiety
Panic Disorder
Social Anxiety Disorder

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70
Q

TCA AE

A

Sedation, OH, Anticholinergic, Diaphoresis, Cardiac dysfunction, Seizures

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71
Q

TCA MOA

A

Block reuptake of MOA and Serotonin

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72
Q

TCA Therapeutic Uses

A

Anxiety
Fibromyalgia
Neuropathic pain
ADHD

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73
Q

TCA Drug Interactions

A

Epi and Dopamine
Amphetamine
Ephedrine

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74
Q

MAOI MOA

A

Increase amount of NE and Serotonin available for release.

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75
Q

MAOI Therapeutic Use

A

Atypical Depression

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76
Q

MAOI AE

A

CNS stimulation
Hypertensive crisis with tyramine.
OH

77
Q

Selegiline

A

Transdermal MAOI
Much lower chance of a hypertensive crisis

78
Q

Bupropion Therapeutic Use

A

Depression
Neuropathic pain
Smoking Cessation
ADHD

79
Q

Mirtazapine

A

Increase release of Serotonin and NE.
Blocks reuptake of Serotonin.

80
Q

Medication for peripartum depression

A

SSRIs
TCA
Another drug mom has had before.

81
Q

First-line Tx for Anxiety

A

Benzos
SSRIs
SNRIs
Buspirone

82
Q

Buspirone

A

Labeled only for short-term use
Little to no risk for suicide

83
Q

Benzos usually used for anxiety

A

Lorazepam and Alprazolam

84
Q

Tx for Panic Attacks

A

All antidepressants but especially
Benzos
SSRIs
Venlafaxine

85
Q

Tx for OCD

A

Preferably start with SSRIs but SNRIs, MAOIs, and TCAs work as well.

86
Q

Tx for SAD

A

SSRIs
Propranolol, 1-3mg/day Clonazepam, or 1-4 mg/day Alprazolam for performance anxiety

87
Q

PTSD components for diagnosis

A

Re-experiencing the event
Avoiding reminders
Constant state of hyperarousal

88
Q

Therapy for PTSD

A

Trauma-focused therapy and stress inoculation therapy

89
Q

Tx for PTSD

A

Paroxetine and Sertraline

90
Q

Axonal Conduction

A

Not very selective. Local anesthetics are an example.

91
Q

What is a neuronally regulated drug dependent on?

A

Its ability to directly or indirectly affect receptors on target cells.

92
Q

Steps of Synaptic Transmission

A
  1. Transmitter synthesis
  2. Transmitter storage
  3. Transmitter release
  4. Transmitter binding
  5. Termination of release
93
Q

What division of the autonomic nervous system provides basal control for most organs?

A

PSNS except for vessels which are controlled by the SNS.

94
Q

Where do most PSNS drugs work?

A

The junction between preganglionic and postganglionic neurons or the synapse between postganglionic neurons and their effector organs.

95
Q

What neurotransmitters does the PSNS use?

A

Acetylcholine
Epinephrine
Norepinephrine
Dopamine (possibly)

96
Q

Where is Acetylcholine released?

A

All PSNS preganglionic neurons
All PSNS postganglionic neurons
All SNS preganglionic neurons
Most SNS postganglionic neurons to sweat glands
All motor neurons to skeletal muscles

97
Q

Where is NorEpi released?

A

SNS postganglionic neurons (except sweat glands)

98
Q

NicotinicN

A

Stimulation of PSNS and release of Epi from adrenal medulla

99
Q

NicotinicM

A

Contraction of skeletal muscle

100
Q

Muscarinic

A

Miosis
Focus for near vision
Bronchial constriction
Vasodilation
Sweat

101
Q

A1

A

Mydriasis
Ejaculation
Constriction:
Skin
Arterioles
Veins
Bladder

102
Q

A2

A

Inhibits transmitter release in presynaptic nerve terminals

103
Q

B1

A

Heart
Release renin

104
Q

B2

A

Gluconeogenesis Liver
Skeletal muscle contraction
Dilation:
Skin
Arterioles
Veins

105
Q

Dopamine

A

Dilation of kidney vasculature

106
Q

What receptors does Epi activate?

A

A1, A2, B1, B2

107
Q

What receptors does NorEpi activate?

A

A1, A2, B1

108
Q

What receptors does Dopamine activate?

A

A1, B1

109
Q

What are important considerations when treating SUDs?

A

Uranalysis should be monitored constantly.
Tx should also include HIV, HEP C, etc
Group therapy is effective.
Treat the underlying emotional damage.
Substitute alternative rewards.

110
Q

Schedule II

A

Cannot be refilled.
Oral only in emergency and must be written in 72 hours.

111
Q

Schedule III and IV

A

May be refilled up to 5x in 6 months.
May be written, oral, or electronic.

112
Q

Schedule V

A

Can be dispensed without a prescription if recorded by a pharmacist and the amount is limited.

113
Q

What label must be included on Schedule II-V drugs?

A

Federal law prohibits transfer of this drug to any other person than who it is prescribed.

114
Q

How does ETOH affect receptors in the brain?

A

Binding to GABA and Glutamate depresses the CNS and 5HT rewards the brain.

115
Q

Wernicke Encephalopathy

A

S&S: Confusion, Nystagmus
Tx: Reversible with Thiamine

116
Q

Korsakoff Psychosis

A

S&S: Polyneuropathy, confabulation, memory loss
Unreversible

117
Q

What negative effects does ETOH have on the body?

A

Dose dependent HTN, damage to myocardium
Erosive gastritis
Acute pancreatitis
Cancer

118
Q

What positive effects does ETOH have on the body?

A

Decreases dementia
Raises HDLs
Decreases clotting factors
Prevents DM2
Increases bone mineral density

119
Q

What drugs does ETOH develop a cross tolerance to?

A

General anesthetics
Barbituates
General CNS depressants
not opioids

120
Q

What ETOH amount is deemed more than safe?

A

Males >4/day or 14/week
Females >3/day or 7/week

121
Q

What drugs are used to facilitate ETOH withdrawal?

A

Benzos (stabilize VS and prevent seizures)
Adjuncts:
BB and Clonidine (stabilize autonomic withdrawal)
Carbamazepine (decreases seizures)

122
Q

Acamprosate

A

Decreases negative effects of abstinence

123
Q

What does Disulfiram cause?

A

Acetaldehyde syndrome which in its severe form can cause shock with as little as 7 ml of ETOH. Patients should be monitored and only receive it if they are determined to quit.

124
Q

Low dose effect of Nicotine on body:

A

Promotes release of Epi and NorEpi from adrenals.
CNS stimulant
Promotes release of Dopamine
Increases alertness and facilitates memory

125
Q

Nicotine withdrawal syndrome:

A

Nervousness
Increased hostility
Increased appetite

126
Q

Nicotine Toxicity

A

Low doses are extremely toxic.
Cold sweats, irregular pulses, respiratory depression
Nicotine undergoes rapid metabolism, so symptoms can resolve in hours.

127
Q

Best drugs for Nicotine addiction:

A

Varenicline alone
Nicotine patch combined with nicotine spray or gum
Combined with counseling

128
Q

Nicotine Gum and Lozenge

A

Do not eat for 15 minutes before.
Chew slowly for 30 minutes.
After abstaining from cigarette use for 3 months, slowly decrease use.
Do not use for more than 6 months.

128
Q

Nicotine Patch

A

Apply q24h to a different location.
Start with a large patch and slowly reduce.

129
Q

Nicotine Inhaler

A

Replaces hand-to-mouth behavior.
Menthol replaces feeling in back of mouth.
Blood levels are less than half of cigarettes.

130
Q

Nicotine Nasal Spray

A

Blood levels rise rapidly, which means it is still hard to give it up. However, risks are reduced as compared to cigarettes.

131
Q

Buproprion for Smoking

A

Reduces appetite and urge to smoke while also reducing withdrawal effects such as irritability.
Best if combined with patch.

132
Q

Bupropion BB

A

Can cause serious psychological changes including suicidality.

133
Q

Varenicicline

A

Partial agonist at nicotine receptors and most effective medication.
Associated with small CVD risk.
Should not be used by truck drivers or pilots due to unpredictable physical and psychological effects.

134
Q

How should Methadone be prescribed?

A

Progressively higher doses are given until the patient is tolerant to Methadone and street opioids.

135
Q

Methadone BB

A

QT prolongation and respiratory depression

136
Q

Suboxone/Buprenorphine

A

Partial agonist at Mu and antagonist at Kappa
Alleviates craving
Ceiling for respiratory distress making it safer than Methadone

137
Q

Bunavail

A

Buprenorphine combined with Naloxone in the cheek to prevent IV drug use.

138
Q

Kratom

A

Interacts with opioid receptors but may be safer and less chance for abuse than opioids.

139
Q

Barbiturates

A

Schedule II
Tolerance develops to high but not respiratory depression.
Cross-dependence develops to other CNS depressants but not opioids.

140
Q

Barbiturate Withdrawal Tx

A

Abstinence can be life threatening. Phenobarbital is a barbiturate with a long half-life.

141
Q

Benzodiazepine

A

Schedule IV
Oral alone is rarely lethal.
When taken correctly, tolerance and dependence is moderate.
Withdrawal should be done very slowly over months.

142
Q

Benzo Antagonist

A

Flumazenil

143
Q

Tx for Cocaine Toxicity

A

Diazepam for seizures, HTN, and cardiac dysrhythmias.
IV Nitroprusside for HTN
ASA for thrombin

144
Q

Cocaine Abuse Tx

A

Psychosocial therapy works the best.
Disulfiram may also decrease use.

145
Q

Methamphetamine

A

Increases release of Epi and Dopamine.
Users feel little or no need for food and sleep.
Can cause hallucinations and paranoia.

146
Q

Methamphetamine Tx

A

Matrix Model combines group counseling, individual counseling, family education, and drug monitoring.
Bupropion and Modafinil (nonamphetamine stimulant) may be used.

147
Q

THC Receptors Location

A

Mainly in appetite, pleasure, memory, concentration, sensory perception, time perception, and coordination of movement.

148
Q

What does marijuana cause?

A

Sedation, euphoria, and hallucinations

149
Q

Chronic effects of Marijuana use:

A

Amotivational syndrome
Cyclical N/V relieved by hot showers

150
Q

Physical effects of Marijuana

A

Tachycardia
Decreases fertility
Reduces hippocampus and amygdala size.

151
Q

Indications for Cannabinoids:

A

Anti-emetic
Appetite stimulation
Neuropathic pain
Tx of seizures
Glaucoma
MS

152
Q

Salvia

A

Hallucinogenic herb native to Mexico

153
Q

Ketamine and Phencyclidine (PCP)

A

Dissociative drugs that distort perception of sight and sound causing euphoria and CNS depression or excitation.

154
Q

MDMA

A

Elevates mood and sensory awareness
Loss of serotonergic neurons –> insomnia
Hyperpyrexia and rhabdomyolysis

155
Q

Inhibition of COX1 Effects:

A

Gastric ulceration
Bleeding
Kidney impairment

156
Q

Inhibition of COX2 Beneficial Effects:

A

Suppression of inflammation
Alleviation of pain
Reduction in fever
Protection against colorectal cancer

157
Q

Inhibition of COX2 Negative Effects:

A

Renal impairment
Promotion of MI and stroke secondary to reduction in inflammation

158
Q

First-Gen COX1+2 Inhibitors

A

ASA
Ibuprofen

159
Q

Second-Gen COX2 Inhibitors

A

Celexicob

160
Q

How does ASA decrease pain?

A

Decrease prostanoids to decrease pain sensitivity.
Decreases pain in the CNS.
Most effective against joint, muscle, and headache. Not against severe visceral pain.

161
Q

ASA for stroke:

A

Inhibits COX essential for TXA.
Used for stroke, MI, chronic stable angina, and angioplasty.

162
Q

AE ASA

A

Salicylism: Tinnitus, acid-base disturbances (from increased breathing), HA, sweating, and dizziness.
Reye’s Syndrome: Encephalopathy and fatty liver degeneration

163
Q

NSAID interaction with ASA:

A

NSAIDs can decrease ASA’s antiplatelet effects by binding with receptors. Because ASA produces complete platelet aggregation after 1 hours. Administering NSAIDs 2 hours later will prevent this.

164
Q

Nonaspirin NSAIDs

A

Do not protect against MI and stroke.
Do not use for 14 days before or after a CABG.
Magnesium salicylate contraindicated in renal patients.
Salsalate is broken down in small intestine –> less gastric bleeding.

165
Q

First-Gen NSAID BB

A

Increased GI bleeding risk
Increased CVD events

166
Q

Celexicob

A

Second-Gen COX-2 inhibitor
Due to increased risk for CVD events should not be used for long-term pain management because of vasoconstriction.
Only decreases GI bleeding risk short-term.
Sulfonamide allergy.

167
Q

Acetaminophen MOA

A

Selectively inhibit CNS COX

168
Q

Acetaminophen Liver Damage

A

N/V, abdominal discomfort at first and then 48-72 hours later more overt symptoms will occur.

169
Q

Tx for Acetaminophen Liver Damage

A

Acetylcysteine replaces glutathione and if given within 8 hours of overdose, completely reverses effects. Even if given within 24 hours, it can minimize injury.

170
Q

What is the max amount of Tylenol that can be given?

A

4g/day

171
Q

4 Step Approach to COX inhibitors per the AHA:

A
  1. Nonpharmacologic measures
  2. Tylenol or ASA w/ least CVD risk
  3. Nonselective NSAIDs
  4. Celexicob b/c has most CVD risk
172
Q

What do endogenous glucocorticoids do?

A

Promote synthesis of glucose but depletes protein
Decrease bp
Increase RBC and decrease WBC
Promote retention of Na and H2O but excretion of K

173
Q

Control of glucocorticoid synthesis and creation:

A

Hypothalamus (CRH)
Pituitary (Adrenocorticotropic Hormone)
Adrenal cortex (cortisol)

174
Q

Therapeutic uses for glucocorticoids in nonendocrine disorders:

A

Exacerbations of rheumatic arthritis
Exacerbations of systemic lupus erythematous
IBD
Asthma
Preventing RDS in premies

175
Q

Adverse Effects of Glucocorticoids

A

Osteoporosis
Decreased immune system
Impaired wound healing
Hyperglycemia
Myopathy
Growth delay
Cataracts
PUD

176
Q

Cushing Syndrome

A

Electrolyte disturbances
Hyperglycemia
Osteoporosis
Striations
Central obesity and rounded face

177
Q

Adrenal Suppression from Glucorticoids

A

Pituitary is unable to create ACTH. If patients have been on glucocorticoids for longer than 3 weeks, be alert for this. Patients also need more glucocorticoids during stressful times.

178
Q

Contraindications for Glucocorticoids

A

Systemic fungal infections and live vaccines

179
Q

What determines glucocorticoid half-life?

A

How quickly they are removed from tissues.

180
Q

Titrating Glucocorticoids

A

Start with the lowest dose possible dose unless life-threatening emergency.

181
Q

Alternate Day Therapy

A

Intermediate acting dose of glucocorticoids is given before 9 AM. It allows some ACTH to be created and reduces growth delay, adrenal suppression, and toxicity.

182
Q

Glucocorticoid Withdrawal symptoms

A

Hypotension
Hypoglycemia
Myalgia
Fatigue

183
Q

How to withdraw glucocorticoids:

A

Taper the dose to a physiologic range over 7 days.
Switch from multiple doses to one per day.
Taper the dose to 50% of physiologic doses over a month.
Cease dosing when basal endogenous levels are normal (except for stress).

184
Q

Patient Education for Glucocorticoids

A

Administer with food to decrease GI distress.
Give in morning.
Call the office with any signs of infection.
Call the office for fluid retention or hypokalemia (cramping or irregular pulses).

185
Q

Monitoring for Glucocorticoids:

A

CBC, lipids, electrolytes, and glucose every 6-12 months.

186
Q

Preventing Osteoporosis with Glucocorticoids:

A

Local is best.
BMD of initial lumbar spine.
Ca and Vit D supplements.

187
Q

Preventing infection with Glucorticoids:

A

If significant infection develops, only continue glucocorticoids if absolutely necessary.
Consider prevention for pnemocystis jirovecci.

188
Q

Glucocorticoid Considerations:

A

Limit Na intake.
Depression (long-term)
Mania (short-term)