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Exam 3 Pharm Flashcards

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1
Q

What is the mechanism of action (MOA) of 1st generation antihistamines?

A

Block histamine H1 receptors, preventing histamine from binding and triggering allergic symptoms

They also cross the blood-brain barrier, leading to sedative effects, and possess anticholinergic, antimuscarinic, and anti-serotonin activity.

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2
Q

What are the pharmacokinetics of 1st generation antihistamines regarding absorption?

A

Rapid from the GI tract

Onset is 15-60 minutes and duration is 4-6 hours.

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3
Q

Which major CYP450 isoenzyme is sometimes involved in the metabolism of 1st generation antihistamines?

A

CYP2D6

Specifically relevant to diphenhydramine.

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4
Q

What are common adverse effects of 1st generation antihistamines?

A
  • Sedation
  • Anticholinergic effects
  • Cognitive impairment
  • Paradoxical excitation in children

Anticholinergic effects include dry mouth, urinary retention, constipation, and blurred vision.

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5
Q

What are the therapeutic uses of 1st generation antihistamines?

A
  • Allergic rhinitis
  • Urticaria
  • Anaphylaxis adjunct
  • Nausea and vomiting
  • Motion sickness
  • Insomnia
  • Parkinsonian symptoms

Examples include meclizine and diphenhydramine.

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6
Q

What are some contraindications for 1st generation antihistamines?

A
  • Narrow-angle glaucoma
  • BPH
  • Severe liver disease
  • Infants/neonates

Urinary retention is a concern in BPH.

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7
Q

How do 2nd generation antihistamines differ in mechanism of action compared to 1st generation?

A

Selective H1 receptor antagonists that do not significantly cross the BBB

This results in minimal CNS effects.

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8
Q

What is the pharmacokinetics of loratadine?

A

Metabolized by CYP3A4 and CYP2D6 to active metabolite desloratadine

It is well-absorbed orally with an onset within 1-3 hours.

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9
Q

What are the common adverse effects of 2nd generation antihistamines?

A
  • Headache
  • Dry mouth
  • Fatigue (rare)
  • Minimal sedation

Cetirizine is slightly more sedating than others.

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10
Q

What is a key contraindication for the use of codeine?

A

Children under 12 years old

Due to the risk of life-threatening respiratory depression.

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11
Q

What is the mechanism of action (MOA) of codeine?

A

Binds to opioid receptors in the CNS to suppress the cough reflex and produce analgesia

It is converted to morphine via CYP2D6.

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12
Q

What are common adverse effects of codeine?

A
  • Constipation
  • Nausea/vomiting
  • Dizziness
  • Sedation

Serious effects include respiratory depression and hypotension.

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13
Q

What is the mechanism of action of inhaled corticosteroids (ICS)?

A

Suppress airway inflammation by inhibiting the release of inflammatory mediators and reducing inflammatory cell infiltration

They also increase β2 receptor sensitivity.

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14
Q

What are common adverse effects of inhaled corticosteroids?

A
  • Oropharyngeal candidiasis
  • Dysphonia
  • Adrenal suppression
  • Growth suppression in children

Long-term use can lead to bone loss and cataracts.

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15
Q

What is a significant drug-drug interaction concern with inhaled corticosteroids?

A

Strong CYP3A4 inhibitors can increase systemic corticosteroid levels

This increases the risk of side effects like adrenal suppression.

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16
Q

What is the therapeutic use of albuterol?

A

Rescue therapy for acute bronchospasm in asthma and COPD

It can also prevent exercise-induced bronchospasm.

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17
Q

What are the common adverse effects of albuterol?

A
  • Tremor
  • Tachycardia
  • Palpitations
  • Nervousness

Less common effects include hypokalemia and hyperglycemia.

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18
Q

What is the black box warning for formoterol?

A

Increased risk of asthma-related death when used as monotherapy in asthma

It should only be used in combination with inhaled corticosteroids.

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19
Q

What is the mechanism of action of anticholinergics like ipratropium?

A

Block muscarinic (M3) receptors in the airway smooth muscle to inhibit bronchoconstriction

This leads to bronchodilation.

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20
Q

What distinguishes tiotropium from ipratropium?

A

Tiotropium is long-acting (LAMA) with a duration of ≥24 hours

Ipratropium is short-acting (SAMA) with a duration of 4-6 hours.

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21
Q

What is the onset time for Tiotropium?

A

~30 minutes

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22
Q

What is the duration of action for Tiotropium?

A

≥24 hours

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23
Q

What is the primary route of administration for Tiotropium?

A

Inhalation

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24
Q

What is the bioavailability of Tiotropium?

A

~19%

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25
How is Tiotropium metabolized?
Partial hepatic via CYP2D6 and CYP3A4
26
What percentage of Tiotropium is excreted via urine?
~74%
27
True or False: Tiotropium has significant interactions with CYP2D6 and CYP3A4.
False
28
What are common adverse effects of Ipratropium?
* Dry mouth * Cough * Headache * Dizziness * Bitter taste
29
What are serious adverse effects of Tiotropium?
* Glaucoma exacerbation * Paradoxical bronchospasm
30
What is the approved use of Ipratropium?
* Acute asthma exacerbation (off-label) * COPD maintenance * Allergic rhinitis (nasal spray)
31
What is a contraindication for Tiotropium?
Hypersensitivity to drug or components
32
What should be monitored for patients using Tiotropium?
* Symptom improvement * Spirometry (FEV1) * Adherence and inhaler technique * Anticholinergic side effects
33
What is the mechanism of action for Montelukast?
Selectively blocks leukotriene D4 receptors (CysLT1)
34
What are the common adverse effects of Montelukast?
* Headache * GI disturbances (nausea, diarrhea)
35
What is a rare but serious adverse effect of Montelukast?
Neuropsychiatric symptoms
36
What is the main therapeutic use of Montelukast?
Maintenance treatment of asthma (≥1 year old)
37
True or False: Montelukast is used for acute asthma attacks.
False
38
What are the three main types of inhalers used in asthma and COPD?
* Metered-Dose Inhalers (MDIs) * Dry Powder Inhalers (DPIs) * Nebulizers
39
What is a key advantage of using spacers with MDIs?
Enhance lung delivery and reduce oropharyngeal deposition
40
What is the primary goal of asthma therapy?
Prevent chronic symptoms (e.g., coughing, breathlessness)
41
What is the primary goal of COPD therapy?
Reduce symptoms (dyspnea, cough)
42
What is the primary mechanism by which leukotrienes contribute to asthma?
Bronchoconstriction
43
Fill in the blank: Theophylline is used as a last-line treatment for _______.
COPD
44
What is the half-life of Montelukast?
2.7–5.5 hours
45
What type of drug interactions does Montelukast have?
Minimal clinically significant DDIs
46
What are the effects of Tiotropium on COPD?
* Improves FEV1 * Reduces COPD exacerbations and hospitalizations * Improves exercise tolerance
47
What should be monitored for behavioral changes when using Montelukast?
Monitor for behavioral and mood changes
48
What is the effect of phenytoin on Montelukast levels?
May decrease montelukast levels
49
What is the typical delivery method for nebulizers?
Converts liquid medication into a mist for inhalation
50
What is a key characteristic of Dry Powder Inhalers (DPIs)?
Breath-activated devices delivering dry, micronized medication
51
What is the duration of use for LABAs in asthma?
Used with ICS for long-term control (not monotherapy)
52
What is a common medication used in nebulizers?
* Albuterol * Ipratropium * Budesonide
53
What is the primary nonpharmacologic step for COPD management?
Promote smoking cessation
54
What is the potency of Fentanyl compared to morphine?
80–100× more potent than morphine ## Footnote Used for rapid-onset severe pain, surgical settings, and cancer breakthrough pain. Avoid in opioid-naïve patients.
55
What is the preferred opioid for patients requiring strong pain relief with lower volume?
Hydromorphone ## Footnote ~5–7× more potent than morphine.
56
What is the potency of Oxycodone compared to morphine?
~2× potency of morphine ## Footnote Used for moderate to severe pain, often combined with non-opioids.
57
What is Codeine's role in pain management?
Weaker analgesic used for mild to moderate pain ## Footnote Often combined with acetaminophen; not preferred in CYP2D6 ultrarapid metabolizers.
58
How is Codeine metabolized?
Metabolized by CYP2D6 to morphine ## Footnote Risk of toxic morphine levels in ultrarapid metabolizers.
59
What are the risks associated with Oxycodone metabolism?
Drug interactions via CYP450 pathway ## Footnote Metabolized by CYP2D6 to oxymorphone (active) and CYP3A4 to inactive.
60
What should be avoided in patients with renal impairment?
Morphine ## Footnote Active metabolites accumulate; prefer hydromorphone or fentanyl.
61
What is a safer option for patients with hepatic impairment?
Morphine (cautiously) or hydromorphone ## Footnote Avoid fentanyl and oxycodone due to CYP metabolism.
62
What is the preferred opioid for an opioid-naïve elderly patient with renal impairment?
Hydromorphone ## Footnote Potent, safer metabolism.
63
What are early symptoms of opioid withdrawal?
Anxiety, restlessness, sweating, runny nose, yawning, lacrimation, piloerection, myalgia ## Footnote Occurs 6–12 hours after last dose of short-acting opioids.
64
What are late symptoms of opioid withdrawal?
Abdominal cramping, nausea, vomiting, diarrhea, dilated pupils, tachycardia, hypertension, insomnia, chills, fever, intense cravings ## Footnote Occurs 24–72 hours after last dose.
65
What is Buprenorphine used for in opioid withdrawal management?
Opioid partial agonist that reduces withdrawal symptoms and cravings ## Footnote Has a ceiling effect on respiratory depression.
66
What is Methadone's role in opioid withdrawal management?
Long-acting opioid agonist that tapers withdrawal symptoms ## Footnote Must be administered in certified settings.
67
What supportive measures are important in opioid withdrawal management?
Hydration & electrolyte balance, comfort measures, psychological support, referral to long-term treatment ## Footnote Essential for effective management.
68
What are the indications for opioids?
Moderate to severe pain, particularly when other therapies are ineffective ## Footnote Includes acute pain, chronic pain, and special indications like antitussive use.
69
What are common risks associated with opioids?
* Respiratory depression * Constipation * Sedation, nausea, vomiting * Dependence, tolerance, and addiction * Opioid-induced hyperalgesia * Withdrawal symptoms on abrupt discontinuation ## Footnote Significant risks, particularly with long-term use.
70
What is the mechanism of action of Morphine?
μ-opioid receptor agonist that inhibits ascending pain pathways ## Footnote Alters perception of pain and produces analgesia, euphoria, and sedation.
71
What is the absorption characteristic of Morphine?
Variable oral bioavailability due to first-pass hepatic metabolism ## Footnote Higher oral doses are needed compared to IV dosing.
72
What is a key reason for switching between opioids?
Pain is inadequately controlled or side effects are intolerable ## Footnote Also considered when there are concerns for drug interactions or tolerance develops.
73
What is the MME conversion factor for Hydromorphone?
4 ## Footnote 7.5 mg of hydromorphone is equivalent to 30 mg of morphine.
74
What should be done when switching to a new opioid?
Always reduce the calculated dose by 25–50% ## Footnote To account for incomplete cross-tolerance.
75
What are the symptoms of CNS toxicity from local anesthetics?
Dizziness, tinnitus, altered mental status, seizures ## Footnote Caused by local anesthetic systemic toxicity (LAST).
76
What are the cardiovascular symptoms of local anesthetic toxicity?
Hypotension, bradycardia, arrhythmias, cardiac arrest ## Footnote More common with bupivacaine and etidocaine.
77
What are the risks of using epinephrine with local anesthetics?
* Ischemia & tissue necrosis * Systemic effects: hypertension, tachycardia, palpitations, arrhythmias * Delayed wound healing ## Footnote Avoid in areas with end-arterial blood supply.
78
What factors influence the effectiveness of local anesthetics?
* pKa (Ionization) * Lipid solubility * Fiber type ## Footnote Lower pKa leads to faster onset; higher lipid solubility increases potency and duration.
79
What is the metabolism difference between amides and esters in local anesthetics?
Amides are metabolized in the liver; esters are metabolized by plasma cholinesterases ## Footnote Important for understanding drug selection in patients with liver issues.
80
What is the primary method of metabolism for amide anesthetics?
Metabolized in the liver ## Footnote Amide anesthetics include lidocaine and bupivacaine.
81
How are esters like chloroprocaine and tetracaine metabolized?
Metabolized by plasma cholinesterases ## Footnote Esters are more prone to allergic reactions due to PABA byproduct.
82
True or False: Allergic reactions are more common with esters than amides.
True ## Footnote Use amide anesthetics in patients with ester allergies.
83
What impact does low pKa have on anesthetic effectiveness?
Faster onset ## Footnote Low pKa indicates a higher proportion of the drug is in its uncharged form.
84
What is the effect of high lipid solubility on anesthetics?
Greater potency & longer duration ## Footnote Lipid solubility enhances the drug's ability to cross nerve membranes.
85
How does infection (low pH) affect anesthesia?
Slower/ineffective anesthesia ## Footnote Infected tissues have lower pH, which reduces the effectiveness of local anesthetics.
86
Which nerve fibers are blocked more easily by anesthetics?
Smaller nerve fibers ## Footnote Smaller fibers, like C fibers, are responsible for pain transmission.
87
What is the risk associated with repeated doses or systemic absorption of anesthetics?
Risk for LAST (Local Anesthetic Systemic Toxicity) ## Footnote LAST can lead to serious cardiovascular and central nervous system complications.
88
List three contraindications for the use of NSAIDs.
* Anticoagulation therapy * Cardiovascular disease * Chronic kidney disease (CKD) ## Footnote These conditions increase the risk of significant side effects when using NSAIDs.
89
What is the contraindication of NSAIDs in patients on anticoagulation therapy?
Increased risk of bleeding ## Footnote Especially with aspirin and nonselective NSAIDs due to platelet inhibition.
90
True or False: Aspirin is contraindicated in patients with bleeding disorders.
True ## Footnote Aspirin can prolong bleeding time due to its antiplatelet effects.
91
What cardiovascular risk is associated with nonaspirin NSAIDs?
Increased risk of MI, stroke, and heart failure ## Footnote COX-2 selective NSAIDs like celecoxib carry higher cardiovascular risks.
92
What is the recommendation for taking aspirin and NSAIDs together?
Take aspirin 30 minutes before NSAIDs if co-administered ## Footnote This timing helps preserve aspirin's cardioprotective effect.
93
What does the inhibition of prostaglandins by NSAIDs lead to in CKD patients?
Sodium and water retention, edema, risk of acute kidney injury (AKI) ## Footnote Prostaglandins are essential for maintaining renal blood flow.
94
What are the common indications for NSAIDs?
* Musculoskeletal conditions * Inflammatory disorders * Pain relief * Fever reduction * Cardiovascular prophylaxis (aspirin only) ## Footnote NSAIDs are effective for various conditions due to their analgesic and anti-inflammatory properties.
95
What is a significant gastrointestinal risk associated with NSAIDs?
Risk of ulcers, bleeding, dyspepsia ## Footnote This is due to COX-1 inhibition decreasing protective gastric prostaglandins.
96
What is the primary mechanism by which opioids exert their effects?
Binding to opioid receptors in the CNS and peripheral nervous system ## Footnote These receptors include mu (μ), kappa (κ), and delta (δ).
97
What is the black box warning associated with codeine?
Respiratory depression and death in children ## Footnote This risk is particularly high in ultrarapid CYP2D6 metabolizers.
98
What risk arises from combining opioids with benzodiazepines?
Additive CNS depression leading to respiratory depression ## Footnote This combination increases the risk of sedation and falls, especially in the elderly.
99
What is a potential consequence of NSAIDs combined with corticosteroids?
Synergistic GI toxicity, increased risk for peptic ulcers or GI bleeding ## Footnote Corticosteroids further thin the GI mucosa, compounding NSAID risks.
100
Fill in the blank: COX-1 selective NSAIDs have a ________ risk compared to COX-2 selective NSAIDs.
Higher GI risk ## Footnote COX-2 selective NSAIDs are preferred for patients with a history of GI ulcers.
101
What effect do NSAIDs have on platelet function?
Aspirin irreversibly inhibits COX-1, increasing bleeding risk ## Footnote Other NSAIDs can also prolong bleeding time but do not have long-term cardioprotective effects.
102
What adverse effect is associated with the use of NSAIDs during pregnancy?
Premature closure of the ductus arteriosus ## Footnote NSAIDs should be avoided in the third trimester.
103
What is the primary mechanism of action (MOA) of opioids?
Opioids primarily work by binding to opioid receptors in the CNS and peripheral nervous system.
104
What are the three main types of opioid receptors?
* μ (mu) * κ (kappa) * δ (delta)
105
What is the MOA of Morphine?
Full μ-opioid receptor agonist
106
What is Codeine's MOA?
Prodrug → converted to morphine → weak μ-opioid agonist
107
How does Oxycodone function?
Full μ-opioid agonist
108
What is the MOA of Hydromorphone?
Full μ-opioid agonist; more potent than morphine
109
What is Fentanyl's classification?
Full μ-opioid agonist; synthetic, highly lipophilic
110
What is the MOA of Buprenorphine?
Partial μ-opioid agonist + κ-antagonist
111
What distinguishes Tramadol's MOA?
Weak μ-opioid agonist + inhibits norepinephrine & serotonin reuptake
112
What is Naloxone's function?
Opioid receptor antagonist – displaces opioids from receptors to reverse effects
113
What is the half-life of Morphine?
~2–4 hrs
114
How does Codeine's half-life compare?
~3 hrs
115
What is Oxycodone's half-life?
~3–4.5 hrs
116
What is the half-life of Hydromorphone?
~2–3 hrs
117
What is the half-life of Fentanyl (IV)?
~2–4 hrs (very short acting)
118
What is the half-life of Fentanyl (patch)?
~17 hrs (after removal)
119
What is Buprenorphine's half-life?
~24–60 hrs
120
What is Tramadol's half-life?
~6 hrs
121
What is Naloxone's half-life?
~30–90 min
122
What is the risk of respiratory depression with short-acting opioids?
Higher
123
True or False: Buprenorphine has a ceiling effect on respiratory depression.
True
124
What are common risks/adverse effects of Oral (PO) opioid administration?
* First-pass metabolism * GI side effects: constipation, nausea, vomiting * Sedation, respiratory depression
125
What advantages does IV opioid administration provide?
* Rapid onset * Precise dose titration
126
What is a risk associated with IV opioid administration?
Respiratory depression (especially with rapid administration)
127
What is a major disadvantage of Transdermal opioid patches?
Delayed onset/offset—takes 12–24 hours to work
128
What is a key risk of Transmucosal opioid administration?
Risk of overdose in opioid-naïve patients
129
What are the risks associated with Epidural/Intrathecal opioid administration?
* Respiratory depression (delayed) * Pruritus, urinary retention, hypotension
130
What is the definition of half-life (t½)?
The time it takes for the plasma concentration of a drug to decrease by 50%.
131
What is a clinical implication of prolonged half-life in opioid overdose?
Prolonged toxicity
132
What is the risk associated with short-acting opioids in overdose?
May resolve quickly, but high potency can still cause life-threatening respiratory depression.
133
What should be monitored after naloxone administration?
Extended monitoring is critical after reversal, especially with long-acting opioids.
134
What enzyme is responsible for converting Codeine to morphine?
CYP2D6
135
What are the concerns for ultrarapid metabolizers of Codeine?
Produce excess morphine, leading to increased risk of toxicity.
136
What is the recommendation for aspirin use in children with viral illnesses?
Avoid aspirin due to the risk of Reye’s syndrome.
137
What is the recommendation for low-dose aspirin in adults?
Used for cardiovascular prevention.
138
What is the pregnancy consideration for aspirin use?
Avoid routine use, especially in the third trimester.
139
What is the MOA of Aspirin (ASA)?
Irreversibly inhibits COX-1 and COX-2 enzymes.
140
What is the half-life of low-dose Aspirin?
~3.5 hours
141
What is a clinical implication of high-dose Aspirin?
Half-life can extend to ≥12 hours.
142
What are the indications for initiating Buprenorphine?
* Chronic pain * Opioid use disorder (OUD)
143
What should be monitored in patients taking high doses of Buprenorphine?
QT prolongation
144
What is a key advantage of Buprenorphine in overdose situations?
Ceiling effect for respiratory depression.
145
What is a risk associated with CYP3A4 inhibitors when using Buprenorphine?
Increases buprenorphine levels → risk of toxicity.
146
What is the typical onset of action for SSRIs?
2–6 weeks for full antidepressant effects; some improvement may occur within 1–2 weeks.
147
What is the onset of action for SSRIs in anxiety disorders?
Delayed 4–6 weeks; initial jitteriness or worsening anxiety may occur.
148
What is the approximate half-life of Fluoxetine?
2–4 days (active metabolite: 7–15 days).
149
What are the prescribing implications of Fluoxetine's long half-life?
Reduces risk of withdrawal symptoms; requires 5-week washout before starting MAOIs.
150
What is the approximate half-life of Sertraline?
~26 hours.
151
What are the prescribing implications of Sertraline's half-life?
Moderate half-life; fewer drug-drug interactions; good balance between safety and effectiveness.
152
What is the risk associated with higher doses of Citalopram?
Risk of QT prolongation, especially in older adults (>60 yrs).
153
What is the approximate half-life of Escitalopram?
~27–32 hours.
154
What is the prescribing implication of Paroxetine's short half-life?
High risk of discontinuation syndrome; taper required.
155
What is the approximate half-life of Fluvoxamine?
~15–22 hours.
156
What are the adverse effects of hypnotics?
* Drowsiness * Dizziness * Cognitive impairment * Anterograde amnesia * Behavioral disinhibition * Parasomnias.
157
What are common withdrawal symptoms from hypnotics?
* Anxiety * Agitation * Insomnia * Seizures.
158
What is the recommended management strategy for starting SSRIs?
Start low, go slow to avoid early side effects.
159
What is the FDA boxed warning related to hypnotics?
Risk of behavioral disinhibition leading to injury or death.
160
What is the onset of action for immediate-release Methylphenidate?
Typically within 20 to 60 minutes after oral administration.
161
What is the mechanism of action for Methylphenidate?
Blocks reuptake of dopamine and norepinephrine.
162
What is discontinuation syndrome?
A group of symptoms that emerge when stopping or reducing the dose of certain antidepressants.
163
What are common symptoms of discontinuation syndrome?
* Dizziness * Insomnia * Irritability * Anxiety * Nausea * Headache * Flu-like symptoms.
164
What is the recommended tapering strategy for antidepressants?
Gradual tapering over weeks to months.
165
What is the washout period required when switching to MAOIs?
At least 14 days between stopping an SSRI/SNRI/TCA and starting an MAOI.
166
What are the FDA-approved indications for TCAs?
* Major Depressive Disorder (MDD) * Neuropathic Pain * Migraine Prophylaxis * Fibromyalgia * Insomnia.
167
What is one reason TCAs are not first-line treatments?
Adverse effects including anticholinergic effects and cardiotoxicity.
168
What are common adverse effects of SSRIs?
* GI upset * Sexual dysfunction * Weight changes * Anxiety/jitteriness * Hyponatremia.
169
What are common adverse effects of SNRIs?
* GI upset * Headache * Sexual dysfunction * Hypertension.
170
What are common adverse effects of Atypical Antidepressants?
* Bupropion: Activating effects, dry mouth, seizures. * Mirtazapine: Sedation, weight gain. * Trazodone: Sedation, priapism.
171
What is the risk of overdose with benzodiazepines?
Flumazenil may precipitate seizures in dependent patients.
172
What is the recommended tapering strategy for benzodiazepines?
Taper by 0.5 mg every 3 days or slower.
173
What are common Tricyclic Antidepressants (TCAs)?
Amitriptyline, Nortriptyline, Clomipramine ## Footnote These medications are primarily used to treat depression and other mood disorders.
174
What are the 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 ## Footnote Overdose can be fatal due to the narrow therapeutic index.
175
What management strategies should be used for TCAs?
* Avoid in elderly * EKG monitoring * Limit quantities prescribed * Monitor for anticholinergic burden ## Footnote These strategies help mitigate risks associated with TCA use.
176
What are the contraindications for SSRIs?
* Concomitant use with MAOIs * Hypersensitivity to the specific drug * Citalopram and Escitalopram: Avoid in patients with QT prolongation ## Footnote The risk of serotonin syndrome is significant when SSRIs are combined with MAOIs.
177
What precautions should be taken when prescribing SSRIs?
* Suicidality risk in youth * Bleeding risk with NSAIDs * Hyponatremia/SIADH * Hepatic impairment * Discontinuation syndrome * Sexual dysfunction ## Footnote These precautions are particularly important in vulnerable populations.
178
What are the examples of SNRIs?
Venlafaxine, Duloxetine, Desvenlafaxine ## Footnote SNRIs are used to treat major depressive disorder and anxiety disorders.
179
What are the contraindications for SNRIs?
* Concurrent MAOI use * Uncontrolled narrow-angle glaucoma * Duloxetine: Avoid in severe hepatic impairment ## Footnote These contraindications help prevent adverse effects and complications.
180
What precautions should be taken when prescribing SNRIs?
* Hypertension risk * Suicidality risk in youth * Renal impairment * Discontinuation syndrome * Bleeding risk ## Footnote Monitoring is essential when prescribing SNRIs.
181
What are examples of atypical antidepressants?
Bupropion, Mirtazapine, Trazodone ## Footnote Atypical antidepressants are used for depression and anxiety disorders.
182
What are the contraindications for Bupropion?
* Seizure disorder * Eating disorders * Abrupt discontinuation of alcohol ## Footnote These contraindications are important due to the increased seizure risk.
183
What precautions should be taken when prescribing Bupropion?
* Dose-related seizure risk * Can worsen anxiety/agitation * Avoid in severe hepatic/renal impairment ## Footnote Close monitoring is needed for patients on Bupropion.
184
What is the primary action of First-Generation Antipsychotics (FGAs)?
Potent dopamine D2 receptor antagonists ## Footnote FGAs are most effective at treating positive symptoms of schizophrenia.
185
What are the indications for Second-Generation Antipsychotics (SGAs)?
* Schizophrenia * Bipolar disorder * MDD (adjunct) * Agitation in dementia ## Footnote SGAs have broader efficacy compared to FGAs.
186
What are the side effects of First-Generation Antipsychotics (FGAs)?
* Extrapyramidal Symptoms (EPS) * Neuroleptic Malignant Syndrome (NMS) * Anticholinergic Effects * Sedation * QT Prolongation * Hyperprolactinemia ## Footnote FGAs have a high risk for EPS and other serious side effects.
187
What are the metabolic side effects associated with Second-Generation Antipsychotics (SGAs)?
* Weight gain * Hyperlipidemia * Insulin resistance * Diabetes ## Footnote Olanzapine and Clozapine have the highest risk of metabolic side effects.
188
What is the significance of CYP450 enzymes in antidepressant metabolism?
* Variability can lead to increased or decreased drug levels * CYP2D6, CYP3A4, CYP2C19, CYP1A2 are key isoenzymes ## Footnote Understanding these enzymes is crucial for predicting drug interactions and responses.
189
What are the risks of combining multiple psychotropic drug classes?
* Pharmacodynamic interactions * Pharmacokinetic interactions * Cumulative adverse effects ## Footnote These risks necessitate careful monitoring and management.
190
Fill in the blank: Combining SSRIs with _______ increases the risk of serotonin syndrome.
MAOIs ## Footnote This combination can lead to severe and potentially fatal side effects.
191
True or False: Second-Generation Antipsychotics have a higher risk of extrapyramidal symptoms compared to First-Generation Antipsychotics.
False ## Footnote SGAs generally have a lower risk of EPS compared to FGAs.
192
What effect do drugs have on the metabolism of others?
Drugs may alter the metabolism of others, leading to increased serum levels or decreased efficacy.
193
Which psychotropics are known to be CYP450 inhibitors?
Fluoxetine, paroxetine, fluvoxamine.
194
What is the effect of carbamazepine on drug metabolism?
Carbamazepine is a strong CYP3A4 inducer, which can reduce effectiveness of other drugs.
195
What are some cumulative adverse effects of combining drugs?
Weight gain, metabolic syndrome, dyslipidemia, sedation, falls, hyponatremia.
196
Which populations are at increased risk for adverse effects from medications?
Older adults, pregnant women, patients with hepatic/renal impairment.
197
What is the risk of combining SSRIs with MAOIs?
Serotonin syndrome.
198
What risk is associated with combining olanzapine and benzodiazepines?
Sedation, hypotension, respiratory depression.
199
What is the main recommendation for starting medication combinations?
Start low, go slow.
200
What are first-line agents for treating depression?
SSRIs, SNRIs, Atypical Antidepressants.
201
What is the mechanism of action of SSRIs?
Inhibit serotonin reuptake → ↑ serotonin levels.
202
What are some examples of SSRIs?
Fluoxetine, sertraline, escitalopram, citalopram, paroxetine.
203
What side effects are associated with SSRIs?
Sexual dysfunction, GI upset, insomnia/sedation, possible increased suicidality in youth.
204
What are SNRIs and their mechanism of action?
Serotonin-Norepinephrine Reuptake Inhibitors; inhibit serotonin & norepinephrine reuptake.
205
What are common examples of SNRIs?
Venlafaxine, desvenlafaxine, duloxetine.
206
What risk is associated with high doses of venlafaxine?
Can increase blood pressure.
207
What are Tricyclic Antidepressants (TCAs) and their mechanism of action?
Inhibit reuptake of serotonin and norepinephrine + anticholinergic, antihistaminic effects.
208
What are examples of TCAs?
Amitriptyline, nortriptyline, clomipramine.
209
What are Monoamine Oxidase Inhibitors (MAOIs) used for?
Inhibit breakdown of serotonin, norepinephrine, dopamine.
210
What is a significant caution when using MAOIs?
Require dietary restrictions (tyramine → hypertensive crisis).
211
What are the indications for benzodiazepines?
Anxiety disorders, insomnia, acute agitation, alcohol withdrawal.
212
What is the mechanism of action of benzodiazepines?
Enhance the effect of GABA at the GABA-A receptor.
213
What risks are associated with benzodiazepine use?
Physical dependence, withdrawal symptoms, cognitive impairment.
214
What is the onset time for benzodiazepines?
Rapid – within minutes to hours.
215
Fill in the blank: SSRIs are first-line for _______.
[depression and anxiety disorders]
216
Fill in the blank: The mechanism of action for TCAs includes inhibition of _______.
[serotonin and norepinephrine reuptake]
217
True or False: Benzodiazepines are recommended for long-term treatment.
False.
218
What is the primary mechanism of action (MOA) of benzodiazepines in seizure management?
Enhancing the effect of gamma-aminobutyric acid (GABA) at the GABA-A receptor.
219
How do benzodiazepines affect neurons?
They hyperpolarize neurons, making them less likely to fire.
220
Do benzodiazepines directly open the chloride channel?
No, they enhance the natural effect of GABA.
221
What are the first-line agents for status epilepticus?
* Lorazepam (Ativan) * Diazepam (Valium) * Midazolam
222
What is the preferred route for administering lorazepam?
IV route due to longer CNS half-life.
223
What are common rescue medications for breakthrough seizures?
* Rectal diazepam * Intranasal midazolam
224
What conditions is clonazepam used for?
* Myoclonic seizures * Atonic seizures * Lennox-Gastaut Syndrome (LGS)
225
What major concerns are associated with long-term use of benzodiazepines?
* Tolerance * Sedation * Respiratory depression * Dependence/withdrawal risk
226
What is the recommended use of rectal diazepam in children?
As a rescue medication for recurrent febrile seizures.
227
What are the indications for phenytoin?
* Focal (partial) seizures * Generalized tonic-clonic seizures * Status epilepticus
228
What is a major risk associated with long-term use of phenytoin?
Gingival hyperplasia.
229
What is the role of fosphenytoin compared to phenytoin?
Preferred IV option due to better safety profile.
230
What side effects are associated with levetiracetam?
* Irritability * Agitation * Mood swings
231
What are the common adjunct treatments for Alzheimer’s Disease?
* Antidepressants * Antipsychotics * Sleep aids * Cognitive enhancers * Nonpharmacologic approaches
232
Which antidepressants are preferred for patients with Alzheimer’s Disease?
SSRIs (e.g., sertraline, citalopram).
233
What are the risks of using atypical antipsychotics in Alzheimer’s patients?
Increased risk of stroke and death.
234
What is a common side effect of topiramate when used for migraine prevention?
Cognitive dysfunction ('brain fog').
235
What are the black box warnings associated with valproic acid?
* Potentially fatal pancreatitis * Hepatitis * Neural tube defects
236
What is the mechanism of action of tricyclic antidepressants in migraine prevention?
Inhibits the reuptake of serotonin and norepinephrine.
237
Fill in the blank: Topiramate is known to cause _______.
paresthesia.
238
True or False: Gabapentin is the first-line treatment for migraine prophylaxis.
False.
239
What is the pharmacological class of amitriptyline?
Tricyclic Antidepressants (TCAs).
240
What should be monitored when using levetiracetam?
Behavioral changes and renal function.
241
What is the risk associated with titration of certain medications?
Risk of serious rash (SJS/TEN); must titrate slowly ## Footnote SJS/TEN stands for Stevens-Johnson syndrome/Toxic epidermal necrolysis, serious skin reactions that can occur with medication use.
242
What is the mechanism of action of Amitriptyline?
Inhibits serotonin and norepinephrine reuptake ## Footnote Amitriptyline is classified as a TCA (tricyclic antidepressant) and is used as a first-line treatment for migraine prevention.
243
What are the common side effects of Topiramate?
Cognitive side effects common ## Footnote Topiramate is an antiseizure medication that can also be used for migraine prevention.
244
List the antiepileptic drugs (AEDs) that can lead to decreased folate levels.
* Phenytoin * Phenobarbital * Carbamazepine ## Footnote These AEDs are enzyme inducers that accelerate the metabolism of folic acid.
245
What is the recommended folic acid supplementation for women of childbearing potential on AEDs?
High-dose folic acid (e.g., 4 mg/day), ideally starting at least 1 month before conception ## Footnote This recommendation is crucial to prevent neural tube defects (NTDs) in fetuses.
246
What are the early side effects of Carbidopa-Levodopa?
* Nausea * Vomiting * Orthostatic hypotension * Somnolence * Dizziness ## Footnote Carbidopa helps reduce nausea and vomiting associated with levodopa treatment.
247
What are the contraindications for Carbidopa-Levodopa?
* Narrow-angle glaucoma * History of melanoma * Severe cardiovascular disease * Psychiatric illness * Cognitive impairment ## Footnote Use caution in patients with these conditions due to potential worsening of symptoms.
248
What is the mechanism of action of triptans in migraine treatment?
* 5-HT₁B receptor activation → Vasoconstriction of dilated intracranial vessels * 5-HT₁D receptor activation → Inhibition of CGRP release and neurogenic inflammation ## Footnote Triptans are effective in aborting migraine attacks by targeting serotonin receptors.
249
True or False: Triptans bind to adrenergic and dopaminergic receptors.
False ## Footnote Triptans selectively bind to serotonin receptors, minimizing unwanted effects.
250
What are the key drug interactions with acetylcholinesterase inhibitors?
* Anticholinergic drugs * Beta-blockers * Drugs that lower heart rate (e.g., Digoxin, CCBs) * NSAIDs * CYP450 inhibitors/inducers ## Footnote Each interaction can lead to decreased efficacy or increased adverse effects of AChEIs.
251
What is the outcome of combining anticholinergic drugs with AChEIs?
Decreased therapeutic effect of AChEIs ## Footnote Anticholinergics oppose the action of AChEIs by blocking acetylcholine receptors.
252
Fill in the blank: Carbidopa does not cross the _______.
BBB ## Footnote BBB stands for blood-brain barrier, which is crucial for the drug's action.
253
What is the clinical impact of Carbidopa-Levodopa in Parkinson's Disease?
Most effective symptomatic treatment for PD motor symptoms ## Footnote It improves quality of life and functional ability but does not halt disease progression.

Health Assessment (10 decks)

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