Pharm Quiz 6 Flashcards
1
Q
Ester-type Anesthetics
A
Procaine and Cocaine
Low allergy
Metabolized by plasma esterases
2
Q
Amide-type Anesthetics
A
Lidocaine
Very low allergy
Metabolized by liver
3
Q
MOA Local Anesthetics
A
Block sodium channels in axons
4
Q
Order of feelings that are lost with local anesthetics:
A
Pain, Cold, Warm, Touch, Deep Pressure
5
Q
Why is epi used with local anesthetics?
A
It prolongs length and decreases toxicity.
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.
7
Q
Procaine
A
Must be injected. Low risk for toxicity. Higher risk for allergy.
8
Q
Lidocaine
A
Topical or injection. Stronger than Procaine. Higher risk for toxicity.
9
Q
Cocaine
A
Used for ENT. Causes vasoconstriction by blocking NorEpi, which also effects the SNS.
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.
11
Q
Infiltration Anesthesia
A
Lidocaine and Bupivacaine are used in the general area of procedure.
12
Q
Nerve Block Anesthesia
A
Short Procedures: Lidocaine or Mepivacaine
Long Procedures: Bupivacaine
13
Q
What happens when opioid agonists are combined with agonist-antagonists?
A
Withdrawal reaction
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
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.
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.
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.
18
Q
Strong Opioid Agonists
A
Morphine, Fentanyl, Methadone, Hydromorphone, Oxymorphone, Levorphanol
19
Q
Moderate to Strong Opioid Agonists
A
Codeine
20
Q
Agonist-Antagonist Opioids
A
Buprenorphine, Butorphanol, Nalbuphine, Pentazocine
21
Q
Codeine
A
Schedule II
30mg = 325mg of Tylenol
Antitussive = 10mg (Schedule V)
22
Q
Codeine BB
A
Ultrarapid metabolizers (specifically children) converts to Morphine and can cause death.
23
Q
Oxycodone
A
Schedule II
Analgesic effects = Codeine
24
Q
Hydrocodone
A
Schedule II
ER always combined with NSAID.
25
Tapentadol
Blocks reuptake of NorEpi and causes less constipation.
26
Pentazocine
Mild to moderate pain
Antagonizes u. Agonizes K --> respiratory depression (not dose dependent), analgesia, sedation.
Dependence is possible but withdrawal is minimal.
27
Buprenorphine
Schedule III
Partial agonist at u. Antagonist at K.
No tolerance. No severe respiratory depression.
Naloxone does not readily reverse.
QT prolongation
28
Naloxone
Antagonizes Mu, Kappa, and Sigmoid
29
Mehtylnaltrexone, Naloxegol, Naldemedine
Selectively antagonizes Mu. They only help with constipation.
30
Naltrexone
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.
31
Embeda
When swallowed intact, only Morphine is absorbed. Otherwise Naltrexone will prevent high. Only used when abuse is suspected. ETOH accelerates absorption leading to fatality.
32
Tramadol MOA
Slightly Agonizes Mu. Mostly blocks uptake of Serotonin and NorEpi.
33
Tramadol Use
Schedule IV
Moderate pain
Onset: 1 hr Duration: 6h
34
Tramadol Drug Interactions
MAOI
Serotonin Syndrome with SNRIs, SSRIs, TCAs
35
What drugs does the Risk Evaluation and Mitigation Strategy included?
IR opioids, ER opioids, and long-acting prescription opioids to educate members of the healthcare team.
36
CDC Guidelines for safe opioid prescribing:
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.
37
Avoiding a withdrawal reaction
Dependence can start after 20 days, so taper off over 3-10 days.
38
Characteristics of Migraines
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
39
How does CGRP affect migraines?
CGRP rises during a migraine.
Sumatriptan decreases CGRP.
Stimulation of neurons in the trigeminal vascular system --> CGRP release --> inflammation and dilation
40
How does Serotonin affect migraines?
Serotonin drops during a migraine.
Depletion of serotonin can precipitate a migraine.
Administration of Serotonin can abort an attack.
41
Drug selection for Migraines:
NSAID
Migraine-specific drug (triptan or ergot alkaloid)
Opioid agonist
42
How often can abortive medications be used?
1-2x/weeks at most or a medication overdose headache can occur.
43
What antiemetic is used for migranies?
Metoclopramide and Prochlorperazine
44
What medication combination works as well as Sumatriptan?
ASA and metoclopramide
45
Excedrin
Tylenol (should not be used alone), ASA, and caffeine
46
What opioid medication is used for migraines?
Butorphanol nasal spray
47
Triptans
Abortive
40% of patients will have another migraine in 24h
Serotonin receptor agonists constrict intracranial blood vessels and decrease secretion of inflammatory neuropeptides
48
Triptan AE
Bad taste
Chest pressure
Coronary vasospasm
Teratogenesis
49
Ergotamine MOA
Decreases CGRP
Enhances Serotonin
Decreases vasodilation
50
Ergotamine therapeutic use
Second-line after triptans due to dependence
51
Ergotism
Ischemia in peripheral arteries
52
Dihydroergotamine
Given IM, IV, or SQ.
Less effective than triptan but better at reducing recurrence.
53
Ergotamines BB
CYP3AV inhibitors can raise levels to dangerous amounts.
54
When should preventative migraine agents be given?
If patients have >3 attacks/month, they are more severe than usual, do not respond to abortive agents.
55
Prophylactic medications for migraines:
Propanolol
Depakote
TCA
Estrogen
56
Depakote (Divalproex) BB
Pancreatitis and Hepatitis
57
Medications for menstrualy associated migraine:
Estrogen 2 days within the onset of menses.
Triptans for 6 days starting 2 days before menses.
Naproxen sodium given 6 days before menses
58
Erenumab
Monoclonal antibody that decreases CGRP.
59
Botulinum Toxin
For patients with >15 migraines per month. Only decreases amount by 2.
60
Cluster HA Characteristics
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.
61
Prophylaxis medications for cluster HA
Verapamil
Suboccipital steroid injections
Glucocorticoids
Lithium
62
Cluster HA Abortive Meds:
Sumatriptan SQ
Oxygen 7-10L for 10-15 min
63
When should antidepressants be discontinued?
For 4-9 months after alleviation of symptoms. Slowly taper down.
64
What are SSRIs indicated for?
Bipolar
Premenstrual Dysphoric Disorder
Bulimia
65
Fluoxetine SA
Sexual Dysfunction, Weight Gain, Serotonin Syndrome, teratogenesis.
66
Fluoxetine Withdrawal
Withdrawal symptom starts within 1-3 days and lasts up to 3 weeks. It causes dizziness, headaches, dysphoria, and anxiety.
67
SSRIs
Escitalopram
Citalopram
Fluvoxamine
Paroxetine
Sertraline
68
SNRIs
Venlafaxine
Duloxetine
Desvenlafaxine
Levomilnacipran
69
Venlafaxine Therapeutic Uses
Depression
Anxiety
Panic Disorder
Social Anxiety Disorder
70
TCA AE
Sedation, OH, Anticholinergic, Diaphoresis, Cardiac dysfunction, Seizures
71
TCA MOA
Block reuptake of MOA and Serotonin
72
TCA Therapeutic Uses
Anxiety
Fibromyalgia
Neuropathic pain
ADHD
73
TCA Drug Interactions
Epi and Dopamine
Amphetamine
Ephedrine
74
MAOI MOA
Increase amount of NE and Serotonin available for release.
75
MAOI Therapeutic Use
Atypical Depression
76
MAOI AE
CNS stimulation
Hypertensive crisis with tyramine.
OH
77
Selegiline
Transdermal MAOI
Much lower chance of a hypertensive crisis
78
Bupropion Therapeutic Use
Depression
Neuropathic pain
Smoking Cessation
ADHD
79
Mirtazapine
Increase release of Serotonin and NE.
Blocks reuptake of Serotonin.
80
Medication for peripartum depression
SSRIs
TCA
Another drug mom has had before.
81
First-line Tx for Anxiety
Benzos
SSRIs
SNRIs
Buspirone
82
Buspirone
Labeled only for short-term use
Little to no risk for suicide
83
Benzos usually used for anxiety
Lorazepam and Alprazolam
84
Tx for Panic Attacks
All antidepressants but especially
Benzos
SSRIs
Venlafaxine
85
Tx for OCD
Preferably start with SSRIs but SNRIs, MAOIs, and TCAs work as well.
86
Tx for SAD
SSRIs
Propranolol, 1-3mg/day Clonazepam, or 1-4 mg/day Alprazolam for performance anxiety
87
PTSD components for diagnosis
Re-experiencing the event
Avoiding reminders
Constant state of hyperarousal
88
Therapy for PTSD
Trauma-focused therapy and stress inoculation therapy
89
Tx for PTSD
Paroxetine and Sertraline
90
Axonal Conduction
Not very selective. Local anesthetics are an example.
91
What is a neuronally regulated drug dependent on?
Its ability to directly or indirectly affect receptors on target cells.
92
Steps of Synaptic Transmission
1. Transmitter synthesis
2. Transmitter storage
3. Transmitter release
4. Transmitter binding
5. Termination of release
93
What division of the autonomic nervous system provides basal control for most organs?
PSNS except for vessels which are controlled by the SNS.
94
Where do most PSNS drugs work?
The junction between preganglionic and postganglionic neurons or the synapse between postganglionic neurons and their effector organs.
95
What neurotransmitters does the PSNS use?
Acetylcholine
Epinephrine
Norepinephrine
Dopamine (possibly)
96
Where is Acetylcholine released?
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
Where is NorEpi released?
SNS postganglionic neurons (except sweat glands)
98
NicotinicN
Stimulation of PSNS and release of Epi from adrenal medulla
99
NicotinicM
Contraction of skeletal muscle
100
Muscarinic
Miosis
Focus for near vision
Bronchial constriction
Vasodilation
Sweat
101
A1
Mydriasis
Ejaculation
Constriction:
Skin
Arterioles
Veins
Bladder
102
A2
Inhibits transmitter release in presynaptic nerve terminals
103
B1
Heart
Release renin
104
B2
Gluconeogenesis Liver
Skeletal muscle contraction
Dilation:
Skin
Arterioles
Veins
105
Dopamine
Dilation of kidney vasculature
106
What receptors does Epi activate?
A1, A2, B1, B2
107
What receptors does NorEpi activate?
A1, A2, B1
108
What receptors does Dopamine activate?
A1, B1
109
What are important considerations when treating SUDs?
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
Schedule II
Cannot be refilled.
Oral only in emergency and must be written in 72 hours.
111
Schedule III and IV
May be refilled up to 5x in 6 months.
May be written, oral, or electronic.
112
Schedule V
Can be dispensed without a prescription if recorded by a pharmacist and the amount is limited.
113
What label must be included on Schedule II-V drugs?
Federal law prohibits transfer of this drug to any other person than who it is prescribed.
114
How does ETOH affect receptors in the brain?
Binding to GABA and Glutamate depresses the CNS and 5HT rewards the brain.
115
Wernicke Encephalopathy
S&S: Confusion, Nystagmus
Tx: Reversible with Thiamine
116
Korsakoff Psychosis
S&S: Polyneuropathy, confabulation, memory loss
Unreversible
117
What negative effects does ETOH have on the body?
Dose dependent HTN, damage to myocardium
Erosive gastritis
Acute pancreatitis
Cancer
118
What positive effects does ETOH have on the body?
Decreases dementia
Raises HDLs
Decreases clotting factors
Prevents DM2
Increases bone mineral density
119
What drugs does ETOH develop a cross tolerance to?
General anesthetics
Barbituates
General CNS depressants
not opioids
120
What ETOH amount is deemed more than safe?
Males >4/day or 14/week
Females >3/day or 7/week
121
What drugs are used to facilitate ETOH withdrawal?
Benzos (stabilize VS and prevent seizures)
Adjuncts:
BB and Clonidine (stabilize autonomic withdrawal)
Carbamazepine (decreases seizures)
122
Acamprosate
Decreases negative effects of abstinence
123
What does Disulfiram cause?
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
Low dose effect of Nicotine on body:
Promotes release of Epi and NorEpi from adrenals.
CNS stimulant
Promotes release of Dopamine
Increases alertness and facilitates memory
125
Nicotine withdrawal syndrome:
Nervousness
Increased hostility
Increased appetite
126
Nicotine Toxicity
Low doses are extremely toxic.
Cold sweats, irregular pulses, respiratory depression
Nicotine undergoes rapid metabolism, so symptoms can resolve in hours.
127
Best drugs for Nicotine addiction:
Varenicline alone
Nicotine patch combined with nicotine spray or gum
Combined with counseling
128
Nicotine Gum and Lozenge
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
Nicotine Patch
Apply q24h to a different location.
Start with a large patch and slowly reduce.
129
Nicotine Inhaler
Replaces hand-to-mouth behavior.
Menthol replaces feeling in back of mouth.
Blood levels are less than half of cigarettes.
130
Nicotine Nasal Spray
Blood levels rise rapidly, which means it is still hard to give it up. However, risks are reduced as compared to cigarettes.
131
Buproprion for Smoking
Reduces appetite and urge to smoke while also reducing withdrawal effects such as irritability.
Best if combined with patch.
132
Bupropion BB
Can cause serious psychological changes including suicidality.
133
Varenicicline
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
How should Methadone be prescribed?
Progressively higher doses are given until the patient is tolerant to Methadone and street opioids.
135
Methadone BB
QT prolongation and respiratory depression
136
Suboxone/Buprenorphine
Partial agonist at Mu and antagonist at Kappa
Alleviates craving
Ceiling for respiratory distress making it safer than Methadone
137
Bunavail
Buprenorphine combined with Naloxone in the cheek to prevent IV drug use.
138
Kratom
Interacts with opioid receptors but may be safer and less chance for abuse than opioids.
139
Barbiturates
Schedule II
Tolerance develops to high but not respiratory depression.
Cross-dependence develops to other CNS depressants but not opioids.
140
Barbiturate Withdrawal Tx
Abstinence can be life threatening. Phenobarbital is a barbiturate with a long half-life.
141
Benzodiazepine
Schedule IV
Oral alone is rarely lethal.
When taken correctly, tolerance and dependence is moderate.
Withdrawal should be done very slowly over months.
142
Benzo Antagonist
Flumazenil
143
Tx for Cocaine Toxicity
Diazepam for seizures, HTN, and cardiac dysrhythmias.
IV Nitroprusside for HTN
ASA for thrombin
144
Cocaine Abuse Tx
Psychosocial therapy works the best.
Disulfiram may also decrease use.
145
Methamphetamine
Increases release of Epi and Dopamine.
Users feel little or no need for food and sleep.
Can cause hallucinations and paranoia.
146
Methamphetamine Tx
Matrix Model combines group counseling, individual counseling, family education, and drug monitoring.
Bupropion and Modafinil (nonamphetamine stimulant) may be used.
147
THC Receptors Location
Mainly in appetite, pleasure, memory, concentration, sensory perception, time perception, and coordination of movement.
148
What does marijuana cause?
Sedation, euphoria, and hallucinations
149
Chronic effects of Marijuana use:
Amotivational syndrome
Cyclical N/V relieved by hot showers
150
Physical effects of Marijuana
Tachycardia
Decreases fertility
Reduces hippocampus and amygdala size.
151
Indications for Cannabinoids:
Anti-emetic
Appetite stimulation
Neuropathic pain
Tx of seizures
Glaucoma
MS
152
Salvia
Hallucinogenic herb native to Mexico
153
Ketamine and Phencyclidine (PCP)
Dissociative drugs that distort perception of sight and sound causing euphoria and CNS depression or excitation.
154
MDMA
Elevates mood and sensory awareness
Loss of serotonergic neurons --> insomnia
Hyperpyrexia and rhabdomyolysis
155
Inhibition of COX1 Effects:
Gastric ulceration
Bleeding
Kidney impairment
156
Inhibition of COX2 Beneficial Effects:
Suppression of inflammation
Alleviation of pain
Reduction in fever
Protection against colorectal cancer
157
Inhibition of COX2 Negative Effects:
Renal impairment
Promotion of MI and stroke secondary to reduction in inflammation
158
First-Gen COX1+2 Inhibitors
ASA
Ibuprofen
159
Second-Gen COX2 Inhibitors
Celexicob
160
How does ASA decrease pain?
Decrease prostanoids to decrease pain sensitivity.
Decreases pain in the CNS.
Most effective against joint, muscle, and headache. Not against severe visceral pain.
161
ASA for stroke:
Inhibits COX essential for TXA.
Used for stroke, MI, chronic stable angina, and angioplasty.
162
AE ASA
Salicylism: Tinnitus, acid-base disturbances (from increased breathing), HA, sweating, and dizziness.
Reye's Syndrome: Encephalopathy and fatty liver degeneration
163
NSAID interaction with ASA:
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
Nonaspirin NSAIDs
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
First-Gen NSAID BB
Increased GI bleeding risk
Increased CVD events
166
Celexicob
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
Acetaminophen MOA
Selectively inhibit CNS COX
168
Acetaminophen Liver Damage
N/V, abdominal discomfort at first and then 48-72 hours later more overt symptoms will occur.
169
Tx for Acetaminophen Liver Damage
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
What is the max amount of Tylenol that can be given?
4g/day
171
4 Step Approach to COX inhibitors per the AHA:
1. Nonpharmacologic measures
2. Tylenol or ASA w/ least CVD risk
3. Nonselective NSAIDs
4. Celexicob b/c has most CVD risk
172
What do endogenous glucocorticoids do?
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
Control of glucocorticoid synthesis and creation:
Hypothalamus (CRH)
Pituitary (Adrenocorticotropic Hormone)
Adrenal cortex (cortisol)
174
Therapeutic uses for glucocorticoids in nonendocrine disorders:
Exacerbations of rheumatic arthritis
Exacerbations of systemic lupus erythematous
IBD
Asthma
Preventing RDS in premies
175
Adverse Effects of Glucocorticoids
Osteoporosis
Decreased immune system
Impaired wound healing
Hyperglycemia
Myopathy
Growth delay
Cataracts
PUD
176
Cushing Syndrome
Electrolyte disturbances
Hyperglycemia
Osteoporosis
Striations
Central obesity and rounded face
177
Adrenal Suppression from Glucorticoids
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
Contraindications for Glucocorticoids
Systemic fungal infections and live vaccines
179
What determines glucocorticoid half-life?
How quickly they are removed from tissues.
180
Titrating Glucocorticoids
Start with the lowest dose possible dose unless life-threatening emergency.
181
Alternate Day Therapy
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
Glucocorticoid Withdrawal symptoms
Hypotension
Hypoglycemia
Myalgia
Fatigue
183
How to withdraw glucocorticoids:
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
Patient Education for Glucocorticoids
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
Monitoring for Glucocorticoids:
CBC, lipids, electrolytes, and glucose every 6-12 months.
186
Preventing Osteoporosis with Glucocorticoids:
Local is best.
BMD of initial lumbar spine.
Ca and Vit D supplements.
187
Preventing infection with Glucorticoids:
If significant infection develops, only continue glucocorticoids if absolutely necessary.
Consider prevention for pnemocystis jirovecci.
188
Glucocorticoid Considerations:
Limit Na intake.
Depression (long-term)
Mania (short-term)
