Exam 3-2 Flashcards
(386 cards)
1
Q
What is the primary mechanism of action of benzodiazepines in seizure management?
A
Enhancing the effect of gamma-aminobutyric acid (GABA) at the GABA-A receptor
2
Q
How do benzodiazepines affect chloride channels?
A
They increase the frequency of chloride channel opening events
3
Q
What is a key point about how benzodiazepines function at the GABA-A receptor?
A
They are GABA-A receptor positive allosteric modulators
4
Q
List the indications for benzodiazepines in seizure management
A
- Acute Seizure Termination / Status Epilepticus
- Breakthrough Seizures / Rescue Therapy
- Adjunctive Long-Term Therapy
- Febrile Seizure Management
5
Q
What is the preferred benzodiazepine for intravenous use in status epilepticus?
A
Lorazepam
6
Q
What are the common routes of administration for diazepam?
A
- IV
- Rectal
7
Q
What is a limitation of long-term benzodiazepine use?
A
Tolerance develops with long-term use
8
Q
True or False: Benzodiazepines directly open chloride channels.
A
False
9
Q
What is the role of midazolam in seizure management?
A
Useful IM or intranasally in prehospital/emergency settings
10
Q
Fill in the blank: Clonazepam is sometimes used for _______ seizures.
A
[myoclonic]
11
Q
What are the major concerns associated with benzodiazepine use?
A
- Sedation
- Respiratory depression
- Dependence/withdrawal risk
12
Q
What is the mechanism of action of phenytoin?
A
Block voltage-gated sodium channels, stabilizing neuronal membranes
13
Q
List the indications for phenytoin.
A
- Focal (partial) seizures
- Generalized tonic-clonic seizures
- Status epilepticus
14
Q
What are some common side effects of phenytoin?
A
- Dizziness
- Ataxia
- Sedation
- Cognitive impairment
15
Q
What is a major risk associated with the intravenous use of phenytoin?
A
Cardiac arrhythmias and hypotension
16
Q
What is the advantage of using fosphenytoin over phenytoin?
A
Better IV tolerability and can be infused faster
17
Q
What is the mechanism of action of levetiracetam?
A
Binds to synaptic vesicle protein 2A (SV2A) and modulates neurotransmitter release
18
Q
What are the key advantages of levetiracetam?
A
- Well tolerated
- Minimal sedation
- No significant drug interactions
19
Q
Fill in the blank: Phenytoin is a strong _______ inducer.
A
[CYP450]
20
Q
What is a known interaction of phenytoin with oral contraceptives?
A
Decreased effectiveness of estrogen/progestin contraceptives
21
Q
What are the common side effects of levetiracetam?
A
- Irritability
- Agitation
- Mood swings
22
Q
What is the pregnancy category of levetiracetam?
A
B/C (risk-benefit based)
23
Q
List the routes of administration for lorazepam.
A
- IV
24
Q
What is the primary pharmacokinetic characteristic of phenytoin?
A
Nonlinear kinetics
25
What is a common adverse effect of long-term use of phenytoin?
Gingival hyperplasia
26
What should be monitored during phenytoin therapy?
Serum drug levels, CBC, LFTs
27
What is the pregnancy category for Linear as a prodrug?
D
28
What are the notable side effects of Linear?
* Gingival hyperplasia
* Rash
* Ataxia
29
Does Linear affect contraceptives?
Yes
30
What are the common drugs classified as Acetylcholinesterase Inhibitors (AChE-Is)?
* Donepezil (Aricept)
* Rivastigmine (Exelon)
* Galantamine (Razadyne)
31
What is the role of Acetylcholinesterase Inhibitors in Alzheimer's Disease treatment?
First-line agents for mild to moderate AD, enhancing cholinergic neurotransmission
32
What should be monitored when using AChE-Is?
* Heart rate
* GI effects
* Cognition and functional status
33
True or False: NMDA receptor antagonists are used in moderate to severe Alzheimer's Disease.
True
34
What are the common adverse effects of AChE-Is?
* Nausea
* Vomiting
* Diarrhea
* Bradycardia
* Dizziness
* Syncope
35
What precautions should be taken when administering AChE-Is to patients with cardiac issues?
Avoid in patients with pre-existing conduction abnormalities
36
What nonpharmacologic approaches are recommended for Alzheimer's Disease management?
* Cognitive stimulation therapy (CST)
* Physical activity
* Structured routine and environmental modifications
* Caregiver support and education
* Behavioral interventions
37
What are the black box warnings associated with Valproate?
* Hepatic failure
* Pancreatitis
* Teratogenicity
38
What is the starting dose for Topiramate in migraine prevention?
25 mg/day
39
Fill in the blank: Memantine is an _______ receptor antagonist.
NMDA
40
What are the common adverse effects of Valproate?
* Nausea
* Fatigue
* Weight gain
* Tremor
* Reversible hair loss
41
What is the mechanism of action for Topiramate?
* Blocks voltage-dependent sodium channels
* Enhances GABAergic inhibitory transmission
* Antagonizes AMPA/kainate glutamate receptors
42
What should be monitored when using Valproate?
* Liver function tests (LFTs)
* Complete blood count (CBC)
* Amylase/lipase
43
What is the preferred class of antidepressants for patients with Alzheimer's Disease?
SSRIs
44
What are the risks of using atypical antipsychotics in dementia patients?
* Increased risk of stroke
* Death in elderly patients with dementia-related psychosis
45
What is an important consideration when prescribing Topiramate?
Avoid in recent alcohol use or concomitant metformin with metabolic acidosis
46
What is the recommended titration strategy for Valproate?
Initiate at 10–15 mg/kg/day; increase slowly
47
True or False: Cognitive enhancers and supplements are standard treatments for Alzheimer's Disease.
False
48
What are the common adverse effects of Amitriptyline?
* Weight gain
* Sedation
* Mental fog
49
What is the impact of AChE-Is and memantine on cognition?
Provide modest improvements or stabilization in memory, attention, function, and behavior
50
What should be monitored in patients taking NMDA antagonists?
* Cognition
* Renal function
* Behavior changes
51
What is the typical starting dose for medications in migraine prevention?
250 mg BID
Doses are often titrated based on effect and tolerability.
52
What is a common adverse effect of medications used in migraine prevention?
Nausea, tremor, weight gain, fatigue, reversible hair loss, bone loss
Serious effects include hepatotoxicity, pancreatitis, teratogenicity, and polycystic ovary syndrome.
53
What are the black box warnings associated with migraine prevention medications?
Hepatic failure, pancreatitis, teratogenicity
These warnings highlight the serious risks involved with these medications.
54
What is the mechanism of action of Tricyclic Antidepressants (TCAs) like Amitriptyline?
Inhibits serotonin and norepinephrine reuptake
This increases their availability, which may help in migraine prevention.
55
How long does it typically take to see results from Amitriptyline for migraine prevention?
2–3 weeks for initial results; 6–8 weeks for full effect
Dosing usually starts low and is titrated based on tolerance.
56
What are some common adverse effects of Amitriptyline?
Anticholinergic effects, orthostatic hypotension, weight gain, sedation
Cardiotoxicity can occur in overdose.
57
Which medication class is commonly used for migraine prevention that includes drugs like Divalproex?
Antiseizure (Antiepileptic) Drugs
These drugs are used off-label for migraine prophylaxis.
58
What is the mechanism of action of Divalproex Sodium?
Enhances GABAergic inhibition; blocks sodium and calcium channels
This reduces neuronal firing and helps in migraine prevention.
59
What are the side effects of Topiramate?
Paresthesia, fatigue, cognitive dysfunction, weight loss, metabolic acidosis
Cognitive side effects are particularly common.
60
What is the recommended dose of folic acid for women of childbearing potential on teratogenic antiseizure medications?
4 mg daily
This should start at least 1 month before conception and continue through the first trimester.
61
What is the role of folic acid in epilepsy management?
Prevention of AED-induced deficiency and teratogenicity
Folic acid supplementation is crucial for women taking certain antiseizure medications.
62
What are the contraindications for Carbidopa-Levodopa therapy?
Cardiac arrhythmias, severe cardiovascular disease, uncontrolled psychosis
Caution is advised due to potential exacerbation of symptoms.
63
What dietary consideration is important when taking Levodopa?
Avoid high-protein meals
Protein can interfere with the absorption of Levodopa.
64
What is the 'On-Off' phenomenon in Parkinson's Disease treatment?
Sudden fluctuations between mobility ('on') and immobility ('off') states
This phenomenon is more common with long-term use of levodopa.
65
What is the mechanism of action of Carbidopa in Carbidopa-Levodopa therapy?
Inhibits peripheral DOPA decarboxylase
This prevents premature conversion of levodopa to dopamine outside the CNS.
66
What are the psychiatric adverse effects associated with Carbidopa-Levodopa?
Hallucinations, delusions, paranoia, vivid dreams
These effects are more prevalent in elderly patients or those with preexisting cognitive dysfunction.
67
What is the importance of timing when administering Levodopa?
Take on an empty stomach 30–60 minutes before meals
This enhances absorption and minimizes protein competition.
68
What is the primary use of carbidopa-levodopa?
Cornerstone therapy for Parkinson’s Disease (PD)
69
What are the components of carbidopa-levodopa?
Dopamine precursor (levodopa) and peripheral decarboxylase inhibitor (carbidopa)
70
What is the mechanism of action of levodopa?
Precursor to dopamine, crosses the blood-brain barrier (BBB)
71
How does carbidopa enhance the effectiveness of levodopa?
Prevents peripheral conversion of levodopa to dopamine, increasing CNS availability
72
What are early side effects of carbidopa-levodopa?
Nausea, vomiting, orthostatic hypotension, somnolence, dizziness
73
What are some late or chronic side effects of carbidopa-levodopa?
Motor fluctuations, dyskinesias, neuropsychiatric symptoms
74
What are contraindications for the use of carbidopa-levodopa?
Narrow-angle glaucoma, history of melanoma, severe cardiovascular disease, psychiatric illness
75
What should be monitored when withdrawing carbidopa-levodopa?
Risk of neuroleptic malignant-like syndrome
76
What are some drug interactions with carbidopa-levodopa?
MAOIs, antipsychotics, high-protein meals
77
What is the recommended timing of administration for carbidopa-levodopa?
On an empty stomach or low-protein meal, divided doses throughout the day
78
What is the clinical impact of carbidopa-levodopa in PD?
Most effective symptomatic treatment for PD motor symptoms
79
What is the mechanism of action of triptans?
Serotonin 5-HT1B/1D receptor agonism
80
What are the clinical indications for triptans?
First-line agents for moderate to severe migraine attacks
81
When is the best time to take triptans?
At the onset of migraine symptoms
82
What are contraindications for triptans?
Coronary artery disease, history of myocardial infarction, uncontrolled hypertension, pregnancy
83
What are common adverse effects of triptans?
Chest symptoms, vasospasm, dizziness, flushing
84
What are key drug interactions with triptans?
SSRIs, SNRIs, MAO inhibitors, ergot derivatives
85
Fill in the blank: Triptans primarily target the ______ receptors to abort migraine attacks.
5-HT₁B/1D
86
What is the effect of activating 5-HT₁B receptors?
Vasoconstriction of dilated intracranial vessels
87
What role does CGRP play in migraines?
Promotes inflammation and pain during migraine attacks
88
What should be avoided when using acetylcholinesterase inhibitors?
Anticholinergic drugs
89
What is the effect of beta-blockers in combination with acetylcholinesterase inhibitors?
Additive effects on bradycardia and AV block
90
What is a significant risk when combining NSAIDs with acetylcholinesterase inhibitors?
Increased risk of GI bleeding
91
Fill in the blank: Donepezil is metabolized by CYP2D6 and ______.
CYP3A4
92
What is the outcome of using CYP450 inducers with donepezil?
Decreased donepezil levels, resulting in reduced efficacy
93
What is the typical onset of action for SSRIs?
2–6 weeks for full antidepressant effects; some improvement may occur in 1–2 weeks.
Initial improvements may include increased energy, appetite, or sleep.
94
How long may the onset of SSRIs be delayed for anxiety disorders?
4–6 weeks
Patients may experience initial jitteriness or worsening anxiety.
95
What is the half-life of Fluoxetine?
2–4 days (active metabolite: 7–15 days)
Long half-life reduces risk of withdrawal symptoms.
96
What are the prescribing implications of Sertraline's half-life?
~26 hours; moderate half-life with fewer drug-drug interactions.
Balances safety and effectiveness.
97
What is the maximum recommended dose of Citalopram for older adults?
20 mg/day
Risk of QT prolongation at higher doses.
98
What is the half-life of Paroxetine?
~21 hours
High risk of discontinuation syndrome; tapering required.
99
What are the risks associated with Fluvoxamine?
~15–22 hours; many drug interactions.
Often used for OCD.
100
What is the recommended approach to initiating SSRIs?
Start low, go slow
Especially for patients with anxiety or prior sensitivity.
101
What is discontinuation syndrome?
Group of symptoms that emerge when stopping or reducing antidepressants abruptly.
Symptoms include dizziness, insomnia, anxiety, and flu-like symptoms.
102
What are common symptoms of discontinuation syndrome?
* Dizziness or 'brain zaps'
* Insomnia
* Irritability
* Anxiety
* Nausea
* Headache
* Flu-like symptoms
* Sensory disturbances
Symptoms typically appear within 1–3 days of stopping.
103
What is the recommended tapering approach for SSRIs?
Gradual tapering
Especially for short half-life SSRIs like paroxetine.
104
What is the washout period required before starting an MAOI after stopping an SSRI?
At least 14 days
At least 5 weeks after fluoxetine due to its long half-life.
105
What are the FDA-approved indications for TCAs?
Major Depressive Disorder (MDD)
Often second- or third-line options due to side effect risks.
106
What is a common off-label use for amitriptyline?
Neuropathic Pain
Also used for migraine prophylaxis and fibromyalgia.
107
What neurotransmitters do TCAs affect?
Serotonin (5-HT) and norepinephrine (NE)
They block reuptake, increasing availability.
108
What are some adverse effects of SSRIs?
* GI upset
* Sexual dysfunction
* Weight gain/loss
* Anxiety/jitteriness
* Hyponatremia
* Increased bleeding risk
* QT prolongation
Monitoring is essential, especially in older adults.
109
What is a key management strategy for SSRIs?
Start low, go slow
To minimize initial side effects.
110
What are common drugs classified as SNRIs?
* Venlafaxine
* Desvenlafaxine
* Duloxetine
Similar side effects to SSRIs.
111
What are the adverse effects of bupropion?
* Activating effects
* Dry mouth
* Tremor
* Weight loss
* Seizures
Avoid in patients with seizure disorders.
112
What are common side effects of TCAs?
* Anticholinergic effects
* Orthostatic hypotension
* Sedation
* Weight gain
* Cardiotoxicity
Risk factors include a narrow therapeutic index.
113
What is the mechanism of action of methylphenidate?
Blocks reuptake of dopamine and norepinephrine
Increases availability, enhancing attention.
114
What is the typical onset for immediate-release methylphenidate?
20 to 60 minutes after oral administration
Peak plasma concentration in 1 to 2 hours.
115
What are the risks associated with benzodiazepine use?
* Drowsiness
* Cognitive impairment
* Dependence and withdrawal
* Anterograde amnesia
Withdrawal symptoms can include anxiety and seizures.
116
What is the recommended management for benzodiazepine overdose?
Flumazenil
GABA-A receptor antagonist; may precipitate seizures.
117
What are common drugs classified as Tricyclic Antidepressants (TCAs)?
Amitriptyline, Nortriptyline, Clomipramine
TCAs are known for their effectiveness but also come with significant risks.
118
What are common adverse effects of Tricyclic Antidepressants (TCAs)?
* Anticholinergic effects (dry mouth, urinary retention, constipation, blurred vision)
* Orthostatic hypotension
* Sedation
* Weight gain
* Sexual dysfunction
* Cardiotoxicity
* Seizures
* Narrow therapeutic index
These adverse effects warrant careful monitoring, especially in elderly patients.
119
What management strategies should be considered when prescribing TCAs?
* Avoid in elderly
* EKG monitoring
* Limit quantities prescribed
* Monitor for anticholinergic burden
These strategies help mitigate risks associated with TCAs.
120
What are the examples of Selective Serotonin Reuptake Inhibitors (SSRIs)?
Fluoxetine, Sertraline, Paroxetine, Escitalopram, Citalopram
SSRIs are commonly used for depression and anxiety disorders.
121
What are contraindications for SSRIs?
* Concomitant use with MAOIs
* Hypersensitivity to the specific drug
* QT prolongation in Citalopram and Escitalopram
These contraindications help prevent serious side effects, such as serotonin syndrome.
122
What precautions should be observed when prescribing SSRIs?
* Suicidality risk
* Bleeding risk with NSAIDs
* Hyponatremia/SIADH risk
* Hepatic impairment
* Discontinuation syndrome
* Sexual dysfunction
These precautions are essential to ensure patient safety.
123
What are examples of Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs)?
Venlafaxine, Duloxetine, Desvenlafaxine
SNRIs are used to treat major depressive disorder and anxiety.
124
What are contraindications for SNRIs?
* Concurrent MAOI use
* Uncontrolled narrow-angle glaucoma
* Severe hepatic impairment
These contraindications prevent serious adverse effects.
125
What are common precautions when prescribing SNRIs?
* Hypertension risk
* Suicidality risk
* Renal impairment
* Discontinuation syndrome
* Bleeding risk
Patients should be monitored closely for these issues.
126
What are the examples of Atypical Antidepressants?
Bupropion, Mirtazapine, Trazodone
Atypical antidepressants are often used for treatment-resistant depression.
127
What are contraindications for Bupropion?
* Seizure disorder
* Eating disorders
* Abrupt discontinuation of alcohol or sedatives
These contraindications are critical due to increased seizure risk.
128
What are precautions associated with Mirtazapine?
* Causes sedation and weight gain
* May increase cholesterol
Patients should be advised about these potential side effects.
129
What distinguishes First-Generation Antipsychotics (FGAs) from Second-Generation Antipsychotics (SGAs)?
* FGAs primarily block dopamine D2 receptors
* SGAs block both D2 and serotonin 5-HT2A receptors
This difference affects their efficacy and side effect profiles.
130
What are common adverse effects associated with FGAs?
* Extrapyramidal symptoms (EPS)
* Neuroleptic malignant syndrome (NMS)
* Anticholinergic effects
* Sedation
* QT prolongation
* Hyperprolactinemia
FGAs carry a higher risk of EPS compared to SGAs.
131
What are common side effects of SGAs?
* Metabolic syndrome
* Lower risk of EPS
* Agranulocytosis (Clozapine)
* QT prolongation
* Sedation
SGAs are often preferred due to their more favorable side effect profile.
132
What is the significance of CYP450 isoenzymes in antidepressant metabolism?
CYP450 enzymes metabolize many antidepressants, affecting drug levels and efficacy
Genetic variability can lead to increased toxicity or subtherapeutic responses.
133
What is a major risk of combining multiple psychotropic drug classes?
* Increased risk of pharmacodynamic interactions
* Cumulative adverse effects
* Altered metabolism of drugs
Careful monitoring is essential when using multiple medications.
134
What are the implications of CYP2D6 polymorphism?
Variability affects metabolism of many antidepressants, influencing drug levels and side effects
Testing for CYP2D6 can guide personalized treatment plans.
135
What is the role of CYP450 in drug metabolism?
CYP450 enzymes may alter the metabolism of drugs, leading to increased serum levels or decreased efficacy.
This can affect various classes of medications.
136
Which psychotropics are known as CYP450 inhibitors?
Fluoxetine, paroxetine, fluvoxamine
These can affect the levels of TCAs, antipsychotics, and benzodiazepines.
137
What effect does carbamazepine have on CYP3A4?
Carbamazepine is a strong CYP3A4 inducer, reducing the effectiveness of other drugs.
This includes oral contraceptives and antipsychotics.
138
What are cumulative adverse effects in drug combinations?
Combining drugs can compound individual side effects.
Examples include weight gain with SGAs and mirtazapine, and sedation in older adults.
139
What special populations are at increased risk with certain medications?
Older adults, pregnant women, patients with hepatic/renal impairment
These groups require careful monitoring or avoidance of certain drugs.
140
What is a risk associated with combining SSRIs and MAOIs?
Risk of serotonin syndrome
This can be a life-threatening condition.
141
What is the mechanism of action of benzodiazepines?
Benzodiazepines enhance the effect of GABA at the GABA-A receptor, increasing neuronal hyperpolarization.
They do not directly activate the receptor.
142
List primary indications for benzodiazepines.
* Generalized Anxiety Disorder (GAD)
* Panic Disorder
* Social Anxiety Disorder (SAD)
* Insomnia
* Acute agitation or psychosis
* Alcohol withdrawal
* Muscle spasms
* Seizures
* Catatonia
Benzodiazepines are not recommended for long-term use due to dependence risks.
143
What are some side effects of benzodiazepines?
Physical and psychological dependence, withdrawal symptoms, cognitive impairment, respiratory depression
Particularly in older adults and when combined with opioids.
144
What are first-line agents for depression?
1. Selective Serotonin Reuptake Inhibitors (SSRIs)
2. Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs)
3. Atypical Antidepressants
SSRIs and SNRIs are considered first-line due to efficacy, safety, and tolerability.
145
What are examples of SSRIs?
Fluoxetine, sertraline, escitalopram, citalopram, paroxetine
These are used to inhibit serotonin reuptake.
146
What are common side effects of SSRIs?
* Sexual dysfunction
* GI upset
* Insomnia/sedation
* Possible increased suicidality in youth
Some may cause QT prolongation or have strong CYP450 interactions.
147
What are second-line agents for depression?
1. Tricyclic Antidepressants (TCAs)
2. Monoamine Oxidase Inhibitors (MAOIs)
These are used when first-line options fail.
148
What is a significant risk of TCAs?
High side effect burden, risk of lethal overdose
Includes anticholinergic effects and arrhythmias.
149
What dietary restrictions are associated with MAOIs?
Avoid tyramine-rich foods to prevent hypertensive crisis
MAOIs require careful management due to dietary interactions.
150
What is the mechanism of action of bupropion?
Norepinephrine-dopamine reuptake inhibitor (NDRI)
It inhibits the reuptake of dopamine and norepinephrine.
151
What are common uses of mirtazapine?
MDD, insomnia, appetite stimulation
It is particularly useful in patients with poor appetite.
152
What is a potential side effect of trazodone?
Sedation and priapism
Priapism is a rare but serious condition.
153
What should be monitored when using lithium?
Serum levels
This is crucial to avoid toxicity.
154
What is the onset time for SSRIs to take effect?
Approximately 2–6 weeks
This is important to consider when starting treatment.
155
What is the risk associated with combining lithium and diuretics?
Lithium toxicity due to altered renal clearance
This requires careful monitoring.
156
What is a key consideration when prescribing antidepressants to older adults?
Increased sensitivity to anticholinergic load and sedation
This can lead to a higher risk of falls.
157
What is the risk of using SSRIs in pregnancy?
Teratogenic risks associated with mood stabilizers
Drugs like valproate and lithium should be avoided.
158
What are SSRIs considered first-line pharmacologic treatments for?
Major depressive disorder (MDD), Generalized anxiety disorder (GAD), Panic disorder, Obsessive-compulsive disorder (OCD), Social anxiety disorder (SAD), Post-traumatic stress disorder (PTSD), Premenstrual dysphoric disorder (PMDD)
SSRIs are also used off-label for conditions like bulimia, body dysmorphic disorder, binge eating, fibromyalgia, and vasomotor symptoms in menopause.
159
What is the typical onset time for SSRIs to exhibit full therapeutic effects?
2–6 weeks
This delay supports the theory of neuroplasticity changes in addition to receptor modulation.
160
What is the half-life of Fluoxetine?
4–6 days
Fluoxetine has the longest half-life among SSRIs, with its active metabolite (norfluoxetine) having a half-life of ~16 days.
161
Which SSRI has the shortest half-life?
Paroxetine
Paroxetine has a half-life of ~21 hours.
162
What are common adverse effects associated with SSRIs?
* GI: Nausea, diarrhea
* Sexual dysfunction: Decreased libido, anorgasmia, delayed ejaculation
* Weight changes: Long-term weight gain
* QT prolongation: Most associated with citalopram and escitalopram
* Others: Headache, insomnia, anxiety, tremor
Individual agents may vary in their side effect profiles.
163
True or False: Fluoxetine is least likely to cause withdrawal symptoms due to its long half-life.
True
164
What symptoms are associated with withdrawal from SSRIs?
* Flu-like symptoms
* Insomnia
* Imbalance
* Sensory disturbances ("brain zaps")
* Irritability
Higher risk with short half-life drugs like paroxetine.
165
What is the recommended washout period when switching to or from an MAOI?
2 weeks for most SSRIs; 5 weeks for fluoxetine
This is necessary to prevent serotonin syndrome.
166
What is the mechanism of action of SNRIs?
Inhibit the reuptake of both serotonin (5-HT) and norepinephrine (NE)
This increases their availability in the central nervous system.
167
What are common agents used as SNRIs?
* Venlafaxine
* Duloxetine
* Desvenlafaxine
168
What are common adverse effects of SNRIs?
* Gastrointestinal: Nausea, constipation
* Neurologic: Dizziness, headache, insomnia
* Cardiovascular: Increased blood pressure
* Sexual dysfunction
* Diaphoresis (sweating)
* Weight loss or fatigue
More common with duloxetine.
169
What is the tapering strategy for discontinuing SNRIs?
Gradual dose reduction over several weeks
This is especially important for venlafaxine to avoid withdrawal symptoms.
170
What are the common uses for Tricyclic Antidepressants (TCAs)?
* Major depressive disorder (MDD)
* Neuropathic pain
* Migraine prophylaxis
* Insomnia
Off-label uses include chronic fatigue syndrome and fibromyalgia.
171
What are the common adverse effects of TCAs?
* Anticholinergic effects: Dry mouth, constipation
* Cardiovascular toxicity: QT prolongation, orthostatic hypotension
* CNS effects: Sedation, confusion
* Weight gain
* Sexual dysfunction
172
What is the mechanism of action of MAOIs?
Inhibit monoamine oxidase, increasing the availability of serotonin, norepinephrine, and dopamine
They can be irreversible or reversible.
173
What dietary restrictions are necessary for patients on MAOIs?
Avoid aged cheeses, cured meats, fermented products, and alcoholic beverages
These foods contain tyramine, which can lead to hypertensive crisis.
174
What is the antagonist used for benzodiazepine overdose?
Flumazenil
It is a competitive GABA-A receptor antagonist.
175
What are the risks associated with long-term use of benzodiazepines?
* Dependence and tolerance
* Withdrawal symptoms
* CNS depression
* Paradoxical reactions
Overdose risk increases when combined with other CNS depressants.
176
What are the classes of hypnotics?
* Benzodiazepines (BZDs)
* Non-benzodiazepines (non-BZDs)
* Melatonin agonists
* Antihistamines
177
What are the primary uses of hypnotics?
Short-term management of insomnia and other sleep disturbances
The goal is to promote sleep onset and/or maintenance.
178
Name the major classes of hypnotics.
* Benzodiazepines (BZDs)
* Non-benzodiazepines (non-BZDs or 'Z-drugs')
* Melatonin receptor agonists
* Sedating antihistamines
Examples include temazepam for BZDs and zolpidem for non-BZDs.
179
What is the onset and duration of action for temazepam?
Fast onset; moderate-long duration
Useful for sleep maintenance with a risk of next-day sedation.
180
How long does zolpidem (IR) take to act, and what is its duration?
~30 mins onset; ~5 hrs duration
Best for sleep onset with a lower risk of hangover.
181
What are the common side effects of benzodiazepines (BZDs) and Z-drugs?
* CNS depression: drowsiness, dizziness
* Complex sleep behaviors
* Anterograde amnesia
* Dependence & tolerance
* Withdrawal symptoms
Particularly concerning with higher doses or alcohol co-use.
182
True or False: Melatonin receptor agonists have a high potential for abuse.
False
They are generally well tolerated and have no abuse potential.
183
What CYP enzyme primarily metabolizes zolpidem and zaleplon?
CYP3A4
This can lead to increased sedation with CYP3A4 inhibitors.
184
What is the recommended duration for short-term use of hypnotics?
≤4 weeks
To avoid tolerance, dependence, and rebound insomnia.
185
What is the mechanism of action for methylphenidate?
Dopamine and norepinephrine reuptake inhibition
Enhances attention and focus while reducing impulsivity and hyperactivity.
186
What are the common adverse effects of methylphenidate?
* Decreased appetite
* Insomnia
* Abdominal pain
* Weight loss
* Anxiety
* Headache
Serious effects may include hypertension and exacerbation of tics.
187
Fill in the blank: Methylphenidate has a high ______ potential due to its dopaminergic effects.
abuse
It is classified as a Schedule II drug.
188
What is a key side effect of first-generation antipsychotics (FGAs)?
Extrapyramidal Symptoms (EPS)
Includes acute dystonia, akathisia, pseudoparkinsonism, and tardive dyskinesia.
189
What is the mechanism of action for second-generation antipsychotics (SGAs)?
D2 and 5-HT2A receptor blockade
Reduces psychotic symptoms and improves negative symptoms.
190
Name a common agent used for schizophrenia and its FDA-approved uses.
* Aripiprazole
* Olanzapine
* Risperidone
* Quetiapine
These agents are also used for bipolar disorder, irritability in autism, and more.
191
What should be monitored to assess the risk of metabolic syndrome in patients taking SGAs?
* Weight and BMI
* Waist circumference
* Blood pressure
* Fasting glucose and lipid profile
Monitoring is recommended at baseline and periodically thereafter.
192
What are the risks associated with combining SSRIs and MAOIs?
High risk of serotonin syndrome
Requires 2-week washout, or 5 weeks for fluoxetine due to its long half-life.
193
What are the symptoms of serotonin syndrome?
* Cognitive: agitation, confusion
* Autonomic: hyperthermia, tachycardia
* Neuromuscular: clonus, rigidity
Symptoms can arise from combining serotonergic agents.
194
What are the symptoms of serotonin syndrome?
Cognitive: Agitation, confusion, hallucinations
Autonomic: Hyperthermia, diaphoresis, tachycardia, hypertension
Neuromuscular: Clonus, hyperreflexia, tremor, muscle rigidity
Serotonin syndrome can occur when MAOIs are used without appropriate washout periods.
195
What is the absolute contraindication for using SSRIs with MAOIs?
High risk of serotonin syndrome
Requires a washout period of 2 weeks, or 5 weeks for fluoxetine due to its long half-life.
196
What is the Black Box Warning associated with BZDs + Opioids?
Risk of profound sedation, respiratory depression, coma, and death
It is advised to use the lowest effective dose and avoid this combination unless no alternative is available.
197
What are the risks of combining BZDs with alcohol or other CNS depressants?
Increased sedation, confusion, falls, especially in the elderly
This combination can be particularly dangerous for older adults.
198
What is the Beers Criteria recommendation regarding BZDs and Z-drugs?
Discouraged for use in the elderly
The Beers Criteria highlights increased sensitivity to CNS effects and risk of falls in older populations.
199
What are the teratogenic risks associated with Valproate during pregnancy?
Neural tube defects
It is recommended to avoid Valproate if possible during pregnancy.
200
Which medication is associated with cardiac malformations during pregnancy?
Paroxetine
Caution is advised when prescribing Paroxetine to pregnant patients.
201
What is the risk associated with BZDs during pregnancy?
Fetal sedation, floppy infant syndrome
This risk necessitates careful consideration when prescribing BZDs to pregnant individuals.
202
What adjustments should be made for drugs requiring hepatic metabolism in patients with hepatic impairment?
Avoid or use lower doses
This includes BZDs (except LOT: lorazepam, oxazepam, temazepam) and SSRIs with long half-lives or strong CYP interactions.
203
What is a significant consideration for prescribing Lithium in patients with renal impairment?
Narrow therapeutic index, renal excretion
Dosing adjustments are critical due to its renal elimination.
204
What dosage adjustments are required for Gabapentin based on renal impairment?
Dose adjustments required based on creatinine clearance
Renal function must be monitored to avoid toxicity.
205
What caution is advised for SNRIs like desvenlafaxine in patients with renal impairment?
Renally excreted
Adjust doses or consider avoiding use in these patients.
206
What is the potency of fentanyl compared to morphine?
80–100× more potent than morphine
Fentanyl is used for rapid-onset severe pain, surgical settings, and cancer breakthrough pain, but should be avoided in opioid-naïve patients.
207
What is the potency of hydromorphone compared to morphine?
~5–7× more potent than morphine
Hydromorphone is preferred for patients requiring strong pain relief with lower volume.
208
What is the potency of oxycodone compared to morphine?
~2× potency of morphine
Oxycodone is used for moderate to severe pain, often combined with non-opioids.
209
What is the primary use of codeine?
Mild to moderate pain; often combined with acetaminophen
Codeine is not preferred in CYP2D6 ultrarapid metabolizers due to toxicity risk.
210
How is codeine metabolized?
Metabolized by CYP2D6 to morphine
Ultrarapid metabolizers may have toxic morphine levels.
211
What is the metabolism pathway for oxycodone?
CYP2D6 to oxymorphone (active), CYP3A4 to inactive
Risk of drug interactions via the CYP450 pathway.
212
What is the metabolism pathway for fentanyl?
CYP3A4 metabolism
Caution is needed due to potentiation with CYP3A4 inhibitors like ketoconazole.
213
What should be avoided in patients with renal impairment?
Morphine
Active metabolites accumulate; prefer hydromorphone or fentanyl.
214
What is a preferred opioid for an opioid-naïve elderly patient with renal impairment?
Hydromorphone
It is potent and has safer metabolism.
215
What are early symptoms of opioid withdrawal?
Anxiety, restlessness, sweating, runny nose, yawning, lacrimation, piloerection, myalgia
These symptoms occur 6–12 hours after the last dose of short-acting opioids.
216
What are late symptoms of opioid withdrawal?
Abdominal cramping, nausea, vomiting, diarrhea, dilated pupils, tachycardia, hypertension, insomnia, chills, fever, intense cravings
These symptoms occur 24–72 hours after the last dose.
217
What is buprenorphine used for in opioid withdrawal management?
Opioid partial agonist
It reduces withdrawal symptoms and cravings and has a ceiling effect on respiratory depression.
218
What is methadone's role in opioid withdrawal management?
Long-acting opioid agonist
It tapers withdrawal symptoms and must be administered in certified settings.
219
What is clonidine used for in opioid withdrawal management?
Reduces autonomic symptoms (sweating, tachycardia, anxiety)
It does not relieve cravings.
220
What is a common risk of opioids?
Respiratory depression
This risk is dose-dependent and highest in opioid-naïve patients or those using sedatives.
221
What is the mechanism of action of morphine?
μ-opioid receptor agonist
It inhibits ascending pain pathways and alters pain perception.
222
What is the absorption characteristic of morphine?
Variable oral bioavailability due to first-pass hepatic metabolism
Higher oral doses are needed compared to IV dosing.
223
What is the distribution characteristic of morphine?
Moderate lipid solubility
Allows it to cross the blood-brain barrier, although not as rapidly as more lipophilic opioids.
224
What is opioid rotation?
Switching between opioids
Considered when pain is inadequately controlled or side effects are intolerable.
225
What are the MME conversion factors for hydromorphone?
4
7.5 mg of hydromorphone is equivalent to 30 mg of morphine.
226
What is the MME conversion factor for oxycodone?
1.5
20 mg of oxycodone is equivalent to 30 mg of morphine.
227
What is the risk associated with using epinephrine with local anesthetics?
Ischemia & Tissue Necrosis
Due to vasoconstriction; avoid in areas with end-arterial blood supply.
228
What are common CNS toxicity symptoms from local anesthetics?
Dizziness, tinnitus, altered mental status, seizures
Caused by local anesthetic systemic toxicity (LAST).
229
What should be done to prevent CNS toxicity from local anesthetics?
Always aspirate before injection
This prevents inadvertent intravascular injection.
230
What is the impact of lower pKa on local anesthetics?
Faster onset
More drug exists in unionized form, allowing rapid nerve membrane penetration.
231
What is a key consideration for children and elderly when using local anesthetics?
More susceptible to toxicity
Physiological changes may alter local anesthetic pharmacokinetics.
232
What are the risks of allergic reactions with local anesthetics?
More common with ester-type anesthetics
Usually due to para-aminobenzoic acid (PABA) metabolites.
233
What is the significance of lipid solubility in local anesthetics?
Greater potency and longer duration
Lipophilic agents penetrate nerve membranes more efficiently.
234
How are esters like chloroprocaine and tetracaine metabolized?
Metabolized by plasma cholinesterases
Esters are broken down in the bloodstream by specific enzymes.
235
What is more common with esters compared to amide anesthetics?
Allergic reactions
This is due to the PABA byproduct formed during the metabolism of esters.
236
What factors impact the effectiveness of anesthetics?
Factors include:
* Low pKa
* High lipid solubility
* Infection (low pH)
* Smaller nerve fibers
* Repeated doses/systemic absorption
* Route & technique
Each factor influences onset, duration, and toxicity of anesthetics.
237
What is a contraindication for using NSAIDs in patients receiving anticoagulation therapy?
Increased risk of bleeding
This includes risks from platelet inhibition and gastrointestinal mucosal damage.
238
What is the cardiovascular risk associated with non-aspirin NSAIDs?
Increased risk of MI, stroke, and heart failure
COX-2 selective NSAIDs like celecoxib carry higher cardiovascular risks.
239
What effect do NSAIDs have in patients with chronic kidney disease (CKD)?
Inhibit prostaglandins that help maintain renal blood flow
This can lead to sodium and water retention, edema, and risk of acute kidney injury.
240
What are the common indications for NSAIDs?
Indications include:
* Musculoskeletal conditions
* Inflammatory disorders
* Pain relief
* Fever reduction
* Cardiovascular prophylaxis (aspirin only)
NSAIDs work by inhibiting COX enzymes to block prostaglandin synthesis.
241
What are the gastrointestinal adverse effects of NSAIDs?
Examples include:
* Dyspepsia
* Gastritis
* Ulcers
* GI bleeding
These effects are due to COX-1 inhibition reducing protective gastric prostaglandins.
242
What is the black box warning for codeine?
Respiratory depression and death in children
Especially in ultrarapid CYP2D6 metabolizers and after tonsillectomy/adenoidectomy.
243
What are the risks associated with combining opioids and benzodiazepines?
Increased risk of additive CNS depression
This can lead to respiratory depression, sedation, and increased fall risk, especially in the elderly.
244
What is the mechanism of action of opioids?
Bind to opioid receptors in the CNS and peripheral nervous system
Receptors include μ (mu), κ (kappa), and δ (delta) for various effects.
245
What are the renal effects of NSAIDs?
Examples include:
* Sodium and water retention
* Edema
* Hypertension
* Acute kidney injury (AKI)
Prostaglandins maintain renal blood flow; NSAIDs inhibit this function.
246
What is the impact of NSAIDs on platelet function?
Aspirin irreversibly inhibits COX-1, reducing TXA2 and inhibiting platelet aggregation
Other NSAIDs can also prolong bleeding time.
247
What is the difference between non-selective NSAIDs and COX-2 selective NSAIDs in terms of GI risk?
Non-selective NSAIDs have a higher GI risk
COX-2 selective NSAIDs have a lower GI risk but higher cardiovascular risk.
248
What should be done to avoid NSAID interference with aspirin's effect?
Take aspirin 30 minutes before NSAID
This timing preserves aspirin's cardioprotective effects.
249
What are some potential adverse effects of opioids?
Potential adverse effects include:
* Respiratory depression
* Sedation
* Constipation
* Nausea
These effects can vary based on the specific opioid and patient condition.
250
What should be considered when using NSAIDs in patients with cardiovascular disease?
Avoid COX-2 inhibitors; consider naproxen if NSAID is necessary
COX-2 inhibitors increase cardiovascular risk.
251
What is the risk of hepatotoxicity associated with NSAIDs?
Potential hepatotoxicity, especially in patients with existing liver dysfunction
This can be idiosyncratic or dose-related.
252
What are the effects of NSAIDs on pregnancy?
Contraindicated in 3rd trimester due to risk of premature closure of ductus arteriosus
Acetaminophen is preferred during pregnancy.
253
What is the primary mechanism of action (MOA) of opioids?
Binding to opioid receptors in the CNS and peripheral nervous system
254
Which opioid receptor is most significant for analgesia?
μ (mu) receptor
255
What is the MOA of Morphine?
Full μ-opioid receptor agonist
256
How is Codeine activated?
Prodrug → converted to morphine → weak μ-opioid agonist
257
What is the half-life of Morphine?
~2–4 hrs
258
What is the half-life of Codeine?
~3 hrs
259
What is the primary risk associated with the use of oral opioids?
First-pass metabolism and GI side effects
260
What is the advantage of intravenous (IV) opioid administration?
Rapid onset and precise dose titration
261
What is a significant risk of using transdermal opioid patches?
Not for opioid-naïve patients due to risk of fatal respiratory depression
262
What is the half-life of Naloxone?
~30–90 min
263
True or False: Long-acting opioids may require continuous naloxone infusions due to their prolonged effects.
True
264
What is the clinical implication of buprenorphine's long half-life?
Less frequent dosing and ceiling effect for respiratory depression
265
What is the primary concern for ultrarapid metabolizers of Codeine?
Increased risk of toxicity due to excess morphine production
266
Fill in the blank: The half-life of Fentanyl (IV) is approximately _______.
2–4 hrs
267
What should be monitored when initiating buprenorphine?
QT prolongation and signs of withdrawal
268
What is the typical starting dose of buprenorphine for opioid use disorder?
2–4 mg sublingually
269
What is the effect of aspirin on COX-1 and COX-2 enzymes?
Irreversibly inhibits COX-1 and COX-2 enzymes
270
What is the risk associated with aspirin use in pregnant women during the third trimester?
Premature closure of the ductus arteriosus
271
For which conditions is low-dose aspirin (81 mg) commonly used in adults?
Cardiovascular prevention
272
What is the half-life of low-dose aspirin?
~3.5 hours
273
True or False: Aspirin should be avoided in children with viral illnesses due to the risk of Reye’s syndrome.
True
274
What is the primary pathway for Codeine metabolism?
CYP2D6 enzyme in the cytochrome P450 system
275
What is a key consideration when initiating buprenorphine in opioid-tolerant patients?
Must wait for withdrawal symptoms before initiating
276
What clinical implication arises from Codeine's dependence on CYP2D6 activity?
Safety and effectiveness vary greatly among individuals
277
What are the advantages of buprenorphine in treating opioid use disorder?
Ceiling effect for respiratory depression and lower risk of misuse
278
What is the mechanism of action of buprenorphine?
Partial mu-opioid receptor agonist + kappa antagonist
Buprenorphine activates the mu-opioid receptor partially and blocks kappa receptors, contributing to its analgesic effect with lower abuse potential.
279
What effect does buprenorphine have on respiratory depression?
Ceiling effect limits respiratory depression
After a certain dose, increased amounts of buprenorphine do not increase respiratory depression, making it safer in overdose situations.
280
What enzyme primarily metabolizes buprenorphine?
CYP3A4
This metabolism pathway presents a risk for drug interactions.
281
What can occur if buprenorphine is given to patients on full opioid agonists?
Precipitated withdrawal
Buprenorphine can cause withdrawal symptoms in patients who are dependent on full agonists.
282
What is the mechanism of action of morphine?
μ-opioid receptor agonist
Morphine binds to and activates μ-opioid receptors in the CNS, reducing pain signal transmission.
283
How is morphine primarily metabolized?
Via glucuronidation in the liver
Unlike many other opioids, morphine is not metabolized via CYP450 enzymes.
284
What are common adverse effects of morphine?
* Sedation
* Respiratory depression
* Constipation
* Nausea
* Vomiting
* Miosis
* Itching
* Physical dependence
* Tolerance
* Risk of misuse/addiction
These effects can vary based on dosage and individual patient factors.
285
What are the contraindications for morphine use?
* Respiratory depression
* Severe asthma in unmonitored settings
* Paralytic ileus
* Use with MAO inhibitors
* Hypersensitivity to morphine
Caution is also advised in patients with head injuries, renal impairment, or hepatic impairment.
286
How does oxycodone compare to morphine in terms of potency?
Approximately 2 times more potent than morphine
This increased potency requires careful dosing to avoid overdose.
287
What CYP enzymes are involved in the metabolism of oxycodone?
* CYP2D6
* CYP3A4
CYP2D6 converts oxycodone to the active metabolite oxymorphone, while CYP3A4 forms other metabolites.
288
What are the differences between immediate-release and extended-release formulations of oxycodone?
* Immediate-Release (IR): Used for acute pain, can be combined with other analgesics
* Extended-Release (ER): Designed for chronic pain management, higher risk for abuse
The choice of formulation depends on the patient's pain management needs.
289
What is the potency of fentanyl compared to morphine?
80–100 times more potent than morphine
This high potency makes fentanyl effective for acute pain but increases overdose risk.
290
What are route-specific considerations for fentanyl administration?
* IV: Fast onset for surgical and acute pain
* Transdermal Patch: For chronic pain, not for opioid-naïve patients
* Transmucosal & Nasal: For cancer-related breakthrough pain
Each route has unique pharmacokinetic profiles and risks.
291
What are the major safety concerns associated with fentanyl?
* Respiratory depression
* Chest wall rigidity
* Drug interactions with CYP3A4
Monitoring is essential, especially in opioid-naïve patients.
292
What is the mechanism of action of naloxone?
Competitive opioid receptor antagonist
Naloxone reverses the effects of opioids, particularly respiratory depression.
293
What is naltrexone's clinical use?
* Opioid Use Disorder (OUD)
* Alcohol Use Disorder (AUD)
Naltrexone helps prevent relapse by blocking opioid effects and reducing cravings.
294
What is the mechanism of action of NSAIDs?
Inhibit cyclooxygenase (COX) enzymes
This inhibition reduces the production of prostaglandins, mediators of pain and inflammation.
295
What are common NSAIDs?
* Ibuprofen
* Naproxen
* Ketorolac
* Aspirin
Each NSAID has unique properties and uses based on its COX inhibition profile.
296
What are the adverse effects associated with NSAIDs?
* GI ulcers
* Renal impairment
* Prolonged bleeding time
* Increased cardiovascular risk
These risks vary based on the specific NSAID and patient factors.
297
What is the unique mechanism of aspirin?
Irreversible inhibition of COX-1
This leads to long-lasting effects on platelet aggregation and cardiovascular protection.
298
What is the mechanism of action of acetaminophen?
Inhibits prostaglandin synthesis in the CNS
Acetaminophen primarily affects central COX-1 and possibly COX-2, resulting in analgesic but minimal anti-inflammatory effects.
299
What is the antidote for acetaminophen overdose?
N-acetylcysteine (NAC)
NAC replenishes glutathione stores and neutralizes toxic metabolites if administered within 8–10 hours of overdose.
300
What is the mechanism of action of local anesthetics such as lidocaine and bupivacaine?
Sodium channel blockade
This action prevents the propagation of action potentials, inhibiting pain transmission.
301
What are the symptoms of Local Anesthetic Systemic Toxicity (LAST)?
* CNS: Agitation, confusion, seizures
* Cardiac: Hypotension, arrhythmias
Management includes stopping the anesthetic, supporting vital functions, and considering lipid emulsion therapy.
302
What are the two categories of local anesthetic duration?
Short to intermediate (~1–2 hrs) and Long-acting (~4–12 hrs)
Duration refers to how long the anesthetic effect lasts after administration.
303
What is the cause of Local Anesthetic Systemic Toxicity (LAST)?
Accidental IV injection or excessive dosing leading to high blood levels
LAST can result in serious complications if not managed promptly.
304
List three CNS symptoms of Local Anesthetic Systemic Toxicity (LAST).
* Agitation
* Confusion
* Tinnitus
* Seizures
* Coma
305
What are two cardiac symptoms of Local Anesthetic Systemic Toxicity (LAST)?
* Hypotension
* Arrhythmias
* Cardiac arrest (especially with bupivacaine)
306
What is the immediate management step for Local Anesthetic Systemic Toxicity (LAST)?
Stop anesthetic administration immediately
This is crucial to prevent further complications.
307
What is the mainstay treatment for Local Anesthetic Systemic Toxicity (LAST)?
Lipid emulsion therapy (e.g., 20% intralipid)
This helps to bind the anesthetic and facilitate its elimination.
308
What should you always do before injecting local anesthetics?
Always aspirate before injecting to avoid IV placement
This helps to prevent systemic toxicity from inadvertent IV injection.
309
What are the maximum dose limits for Lidocaine without epinephrine?
~4.5 mg/kg
This limit helps to prevent toxicity.
310
What are the maximum dose limits for Bupivacaine without epinephrine?
~2.5 mg/kg
This is important for safe administration.
311
What is the focus of patient-centered pain management approaches?
Tailor interventions to patient-specific factors
This includes age, comorbidities, drug metabolism, and psychosocial needs.
312
What is the difference between acute and chronic pain treatment strategies?
Acute pain lasts days to weeks; chronic pain lasts more than 3–6 months
Understanding the duration helps guide treatment options.
313
What is the first-line treatment for acute pain?
Non-opioid analgesics (NSAIDs, acetaminophen)
These medications are effective for short-term pain relief.
314
What is the first-line treatment for chronic pain?
Nonpharmacologic + non-opioids (SNRIs, TCAs, gabapentinoids)
Chronic pain management often requires a multi-faceted approach.
315
What is multimodal analgesia?
Combining agents from different drug classes/mechanisms to enhance analgesia while minimizing opioid use
This approach helps reduce reliance on opioids.
316
Give two examples of modalities used in multimodal analgesia.
* NSAIDs + Acetaminophen
* Gabapentinoids + Antidepressants
317
What is a key prescribing consideration for opioid selection?
Use morphine equivalents (MME) for dosing comparisons
This helps ensure safe and effective opioid prescribing.
318
What should be monitored when prescribing NSAIDs?
* GI risks
* CV risks
* Renal function
319
True or False: Opioids are Schedule II controlled substances due to their high potential for abuse.
True
This classification requires strict regulations for prescribing.
320
What is the purpose of Prescription Drug Monitoring Programs (PDMPs)?
To track prescribing and dispensing of controlled substances
These programs help identify patterns of misuse.
321
What is the importance of informed consent in opioid therapy?
Clarifies risks, benefits, and expectations for opioid therapy
This is crucial for patient understanding and compliance.
322
What is the recommended duration for opioid prescriptions for acute pain?
Limit prescription duration to 3 days
More than 7 days is rarely needed.
323
What is a critical ethical consideration for advanced practice nurses in pain management?
Balancing adequate pain control with risk management to prevent harm
This is essential for ethical practice.
324
What is the mechanism of action (MOA) of 1st generation antihistamines?
Block histamine H1 receptors, preventing histamine from binding and triggering allergic symptoms. Cross the blood-brain barrier (BBB), leading to sedative effects. Also have anticholinergic, antimuscarinic, and anti-serotonin activity.
325
What are the pharmacokinetics of 1st generation antihistamines?
* Absorption: Rapid from the GI tract.
* Onset: 15-60 minutes.
* Duration: 4-6 hours (shorter half-life).
* Metabolism: Primarily hepatic, often through CYP450 isoenzymes.
* Distribution: Cross the BBB easily.
* Elimination: Renal excretion.
326
Which major CYP450 isoenzyme is sometimes involved in the metabolism of 1st generation antihistamines?
CYP2D6.
327
What are common drug-to-drug interactions with 1st generation antihistamines?
* Potentiate CNS depressants (alcohol, sedatives, benzodiazepines, opioids).
* Anticholinergic drugs (TCAs, antipsychotics) increase risk for anticholinergic side effects.
328
What are the adverse effects of 1st generation antihistamines?
* Sedation.
* Anticholinergic effects: dry mouth, urinary retention, constipation, blurred vision.
* Cognitive impairment, confusion (especially in the elderly).
* Paradoxical excitation (in children).
329
What are the therapeutic uses of 1st generation antihistamines?
* Allergic rhinitis, urticaria, anaphylaxis adjunct.
* Nausea and vomiting, motion sickness (meclizine, diphenhydramine).
* Insomnia (diphenhydramine).
* Parkinsonian symptoms (benztropine-like anticholinergic effect).
330
What are contraindications for using 1st generation antihistamines?
* Narrow-angle glaucoma.
* BPH (due to urinary retention).
* Severe liver disease (caution due to hepatic metabolism).
* Infants/neonates (risk of severe CNS depression).
331
What should be monitored when using 1st generation antihistamines?
* Sedation level (especially in elderly).
* Anticholinergic side effects.
* Mental status, especially with prolonged use.
332
What are the clinical effects of 1st generation antihistamines?
Rapid symptom relief for allergic conditions. Sedation limits daytime use.
333
What is a notable black box warning for diphenhydramine?
Serious risk of misuse/overdose, particularly for sleep aid purposes or in children, leading to severe CNS depression or excitation.
334
What is the mechanism of action (MOA) of 2nd generation antihistamines?
Selective H1 receptor antagonists. Do not cross the BBB significantly → minimal CNS/sedative effects. Minimal anticholinergic activity compared to first-generation.
335
What are the pharmacokinetics of 2nd generation antihistamines?
* Absorption: Well-absorbed orally.
* Onset: Within 1-3 hours.
* Duration: Longer half-life allows once-daily dosing.
336
Which CYP450 isoenzymes are involved in the metabolism of loratadine?
CYP3A4 and CYP2D6.
337
What are common adverse effects of 2nd generation antihistamines?
* Headache.
* Dry mouth.
* Fatigue (rare).
* Minimal sedation (cetirizine slightly more sedating).
338
What are the therapeutic uses of 2nd generation antihistamines?
* Allergic rhinitis (seasonal and perennial).
* Chronic idiopathic urticaria.
339
What are contraindications for 2nd generation antihistamines?
* Hypersensitivity to the drug or excipients.
* Caution in renal or hepatic impairment, dose adjustments may be required.
340
What should be monitored when using 2nd generation antihistamines?
* Renal function (especially for cetirizine and fexofenadine).
* Watch for drowsiness, especially with cetirizine at higher doses.
341
What is the mechanism of action (MOA) of codeine?
Codeine is a prodrug that binds to opioid receptors in the CNS to suppress the cough reflex at low doses and produce analgesia at higher doses. It is converted to morphine via CYP2D6.
342
What are the pharmacokinetics of codeine?
* Absorption: Well absorbed orally.
* Metabolism: Primarily in the liver by CYP2D6 to morphine.
* Excretion: Renally excreted.
343
What are common adverse effects of codeine?
* Constipation.
* Nausea/vomiting.
* Dizziness.
* Sedation.
344
What are serious adverse effects of codeine?
* Respiratory depression.
* Hypotension.
* Dependence/addiction potential.
345
What are contraindications for codeine use?
* Children under 12 years old.
* Post-operative pain management in children after tonsillectomy/adenoidectomy.
* Known hypersensitivity to codeine or other opioids.
346
What should be monitored when using codeine?
* Respiratory status.
* Mental status.
* Pain control and cough suppression effectiveness.
347
What is the mechanism of action (MOA) of inhaled corticosteroids (ICS)?
ICS suppress airway inflammation by inhibiting the release of inflammatory mediators, reducing inflammatory cell infiltration, decreasing vascular permeability, and increasing β2 receptor sensitivity.
348
What are the pharmacokinetics of inhaled corticosteroids?
* Administration: Primarily inhaled.
* Absorption: Limited systemic absorption when inhaled correctly.
* Metabolism: Most ICS are metabolized in the liver, primarily via CYP3A4.
349
What are the adverse effects of inhaled corticosteroids?
* Oropharyngeal candidiasis (thrush).
* Dysphonia (hoarseness).
* Adrenal suppression (long-term use).
* Growth suppression in children.
350
What are the therapeutic uses of inhaled corticosteroids?
* First-line therapy for persistent asthma.
* Used in combination with LABAs in moderate to severe asthma or COPD.
351
What should be monitored when using inhaled corticosteroids?
* Inhaler technique.
* Symptom control.
* Peak expiratory flow (PEF) trends in asthma.
352
What is the mechanism of action (MOA) of albuterol?
Selectively stimulates beta-2 adrenergic receptors in bronchial smooth muscle, causing bronchodilation by relaxing smooth muscle.
353
What are the pharmacokinetics of albuterol?
* Onset: Within minutes (peak in 30 minutes).
* Duration: ~4–6 hours.
* Route: Inhaled.
354
What are common adverse effects of albuterol?
* Tremor.
* Tachycardia.
* Palpitations.
* Throat irritation.
355
What is a notable black box warning for formoterol?
Increased risk of asthma-related death when used as monotherapy in asthma.
356
What is the mechanism of action (MOA) of tiotropium?
Blocks muscarinic (M3) receptors in the airway smooth muscle, inhibiting acetylcholine-mediated bronchoconstriction, leading to bronchodilation.
357
What are the pharmacokinetics of tiotropium?
* Onset: ~30 minutes.
* Duration: ≥24 hours.
* Route: Inhalation.
358
What are the drug-drug interactions for tiotropium?
Both drugs have low systemic absorption, so interactions are minimal.
359
What is the duration of action for inhaled medications?
≥24 hours
360
What is the bioavailability of inhaled medications?
~19%
361
How are inhaled medications primarily excreted?
~74% via urine
362
Which CYP450 isoenzymes are involved in the metabolism of inhaled medications?
CYP2D6 and CYP3A4
363
True or False: Tiotropium is significantly metabolized by CYP2D6 and CYP3A4.
False
364
What are common adverse effects of Ipratropium?
* Dry mouth
* Cough
* Headache
* Dizziness
* Bitter taste
365
What serious adverse effect is associated with Tiotropium?
Glaucoma exacerbation (if powder contacts eyes)
366
What is the primary therapeutic use of Ipratropium?
COPD maintenance
367
What condition should be monitored in patients using Tiotropium?
Glaucoma symptoms if accidental ocular exposure
368
What is the mechanism of action for Montelukast?
Selectively blocks leukotriene D4 receptors
369
What is the peak plasma time for Montelukast?
3–4 hours
370
Fill in the blank: Montelukast is extensively metabolized in the liver by _______.
CYP450 enzymes
371
What are common adverse effects of Montelukast?
* Headache
* GI disturbances (nausea, diarrhea)
372
What is the black box warning associated with Montelukast?
Serious neuropsychiatric events
373
What are the three main types of inhalers used in asthma and COPD?
* Metered-Dose Inhalers (MDIs)
* Dry Powder Inhalers (DPIs)
* Nebulizers
374
True or False: Nebulizers require hand-breath coordination.
False
375
What is the main advantage of using spacers with MDIs?
Enhance lung delivery and reduce oropharyngeal deposition
376
What is the primary difference in the use of SABAs in asthma vs COPD?
Rescue medication for asthma; used PRN for COPD symptom relief
377
What is the main goal of asthma therapy?
Prevent chronic symptoms and exacerbations
378
What is the most important nonpharmacologic step in COPD management?
Promote smoking cessation
379
What is the clinical effect of Tiotropium in patients with COPD?
Reduces COPD exacerbations and hospitalizations
380
What is the recommended use of Montelukast in asthma management?
Maintenance treatment of asthma (≥1 year old)
381
Fill in the blank: Theophylline is rarely used in asthma due to its _______.
narrow therapeutic range
382
What should be monitored in patients taking Montelukast?
Behavioral and mood changes
383
What is the bioavailability of Montelukast?
~64%
384
What are the less common adverse effects of Ipratropium?
* Palpitations
* Urinary retention
385
What is a significant drug interaction concern with Montelukast?
Phenytoin may decrease montelukast levels
386
What is the mechanism by which leukotrienes affect the respiratory system?
Cause bronchoconstriction, mucus production, and eosinophilic inflammation
