Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Health Assessment > Exam 3 Pharm > Flashcards

Exam 3 Pharm Flashcards

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

CYP2D6

Specifically relevant to diphenhydramine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are common adverse effects of codeine?

A
  • Constipation
  • Nausea/vomiting
  • Dizziness
  • Sedation

Serious effects include respiratory depression and hypotension.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the common adverse effects of albuterol?

A
  • Tremor
  • Tachycardia
  • Palpitations
  • Nervousness

Less common effects include hypokalemia and hyperglycemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the onset time for Tiotropium?

A

~30 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the duration of action for Tiotropium?

A

≥24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the primary route of administration for Tiotropium?

A

Inhalation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the bioavailability of Tiotropium?

A

~19%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How is Tiotropium metabolized?

A

Partial hepatic via CYP2D6 and CYP3A4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What percentage of Tiotropium is excreted via urine?

A

~74%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

True or False: Tiotropium has significant interactions with CYP2D6 and CYP3A4.

A

False

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are common adverse effects of Ipratropium?

A
  • Dry mouth
  • Cough
  • Headache
  • Dizziness
  • Bitter taste
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are serious adverse effects of Tiotropium?

A
  • Glaucoma exacerbation
  • Paradoxical bronchospasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the approved use of Ipratropium?

A
  • Acute asthma exacerbation (off-label)
  • COPD maintenance
  • Allergic rhinitis (nasal spray)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is a contraindication for Tiotropium?

A

Hypersensitivity to drug or components

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What should be monitored for patients using Tiotropium?

A
  • Symptom improvement
  • Spirometry (FEV1)
  • Adherence and inhaler technique
  • Anticholinergic side effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the mechanism of action for Montelukast?

A

Selectively blocks leukotriene D4 receptors (CysLT1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the common adverse effects of Montelukast?

A
  • Headache
  • GI disturbances (nausea, diarrhea)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is a rare but serious adverse effect of Montelukast?

A

Neuropsychiatric symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the main therapeutic use of Montelukast?

A

Maintenance treatment of asthma (≥1 year old)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

True or False: Montelukast is used for acute asthma attacks.

A

False

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the three main types of inhalers used in asthma and COPD?

A
  • Metered-Dose Inhalers (MDIs)
  • Dry Powder Inhalers (DPIs)
  • Nebulizers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is a key advantage of using spacers with MDIs?

A

Enhance lung delivery and reduce oropharyngeal deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the primary goal of asthma therapy?

A

Prevent chronic symptoms (e.g., coughing, breathlessness)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the primary goal of COPD therapy?

A

Reduce symptoms (dyspnea, cough)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the primary mechanism by which leukotrienes contribute to asthma?

A

Bronchoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Fill in the blank: Theophylline is used as a last-line treatment for _______.

A

COPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the half-life of Montelukast?

A

2.7–5.5 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What type of drug interactions does Montelukast have?

A

Minimal clinically significant DDIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the effects of Tiotropium on COPD?

A
  • Improves FEV1
  • Reduces COPD exacerbations and hospitalizations
  • Improves exercise tolerance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What should be monitored for behavioral changes when using Montelukast?

A

Monitor for behavioral and mood changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is the effect of phenytoin on Montelukast levels?

A

May decrease montelukast levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the typical delivery method for nebulizers?

A

Converts liquid medication into a mist for inhalation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is a key characteristic of Dry Powder Inhalers (DPIs)?

A

Breath-activated devices delivering dry, micronized medication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the duration of use for LABAs in asthma?

A

Used with ICS for long-term control (not monotherapy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is a common medication used in nebulizers?

A
  • Albuterol
  • Ipratropium
  • Budesonide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the primary nonpharmacologic step for COPD management?

A

Promote smoking cessation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is the potency of Fentanyl compared to morphine?

A

80–100× more potent than morphine

Used for rapid-onset severe pain, surgical settings, and cancer breakthrough pain. Avoid in opioid-naïve patients.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the preferred opioid for patients requiring strong pain relief with lower volume?

A

Hydromorphone

~5–7× more potent than morphine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is the potency of Oxycodone compared to morphine?

A

~2× potency of morphine

Used for moderate to severe pain, often combined with non-opioids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is Codeine’s role in pain management?

A

Weaker analgesic used for mild to moderate pain

Often combined with acetaminophen; not preferred in CYP2D6 ultrarapid metabolizers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

How is Codeine metabolized?

A

Metabolized by CYP2D6 to morphine

Risk of toxic morphine levels in ultrarapid metabolizers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are the risks associated with Oxycodone metabolism?

A

Drug interactions via CYP450 pathway

Metabolized by CYP2D6 to oxymorphone (active) and CYP3A4 to inactive.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What should be avoided in patients with renal impairment?

A

Morphine

Active metabolites accumulate; prefer hydromorphone or fentanyl.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is a safer option for patients with hepatic impairment?

A

Morphine (cautiously) or hydromorphone

Avoid fentanyl and oxycodone due to CYP metabolism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is the preferred opioid for an opioid-naïve elderly patient with renal impairment?

A

Hydromorphone

Potent, safer metabolism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are early symptoms of opioid withdrawal?

A

Anxiety, restlessness, sweating, runny nose, yawning, lacrimation, piloerection, myalgia

Occurs 6–12 hours after last dose of short-acting opioids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are late symptoms of opioid withdrawal?

A

Abdominal cramping, nausea, vomiting, diarrhea, dilated pupils, tachycardia, hypertension, insomnia, chills, fever, intense cravings

Occurs 24–72 hours after last dose.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is Buprenorphine used for in opioid withdrawal management?

A

Opioid partial agonist that reduces withdrawal symptoms and cravings

Has a ceiling effect on respiratory depression.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is Methadone’s role in opioid withdrawal management?

A

Long-acting opioid agonist that tapers withdrawal symptoms

Must be administered in certified settings.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What supportive measures are important in opioid withdrawal management?

A

Hydration & electrolyte balance, comfort measures, psychological support, referral to long-term treatment

Essential for effective management.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the indications for opioids?

A

Moderate to severe pain, particularly when other therapies are ineffective

Includes acute pain, chronic pain, and special indications like antitussive use.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What are common risks associated with opioids?

A
  • Respiratory depression
  • Constipation
  • Sedation, nausea, vomiting
  • Dependence, tolerance, and addiction
  • Opioid-induced hyperalgesia
  • Withdrawal symptoms on abrupt discontinuation

Significant risks, particularly with long-term use.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the mechanism of action of Morphine?

A

μ-opioid receptor agonist that inhibits ascending pain pathways

Alters perception of pain and produces analgesia, euphoria, and sedation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What is the absorption characteristic of Morphine?

A

Variable oral bioavailability due to first-pass hepatic metabolism

Higher oral doses are needed compared to IV dosing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is a key reason for switching between opioids?

A

Pain is inadequately controlled or side effects are intolerable

Also considered when there are concerns for drug interactions or tolerance develops.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is the MME conversion factor for Hydromorphone?

A

4

7.5 mg of hydromorphone is equivalent to 30 mg of morphine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What should be done when switching to a new opioid?

A

Always reduce the calculated dose by 25–50%

To account for incomplete cross-tolerance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What are the symptoms of CNS toxicity from local anesthetics?

A

Dizziness, tinnitus, altered mental status, seizures

Caused by local anesthetic systemic toxicity (LAST).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What are the cardiovascular symptoms of local anesthetic toxicity?

A

Hypotension, bradycardia, arrhythmias, cardiac arrest

More common with bupivacaine and etidocaine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What are the risks of using epinephrine with local anesthetics?

A
  • Ischemia & tissue necrosis
  • Systemic effects: hypertension, tachycardia, palpitations, arrhythmias
  • Delayed wound healing

Avoid in areas with end-arterial blood supply.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What factors influence the effectiveness of local anesthetics?

A
  • pKa (Ionization)
  • Lipid solubility
  • Fiber type

Lower pKa leads to faster onset; higher lipid solubility increases potency and duration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is the metabolism difference between amides and esters in local anesthetics?

A

Amides are metabolized in the liver; esters are metabolized by plasma cholinesterases

Important for understanding drug selection in patients with liver issues.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is the primary method of metabolism for amide anesthetics?

A

Metabolized in the liver

Amide anesthetics include lidocaine and bupivacaine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

How are esters like chloroprocaine and tetracaine metabolized?

A

Metabolized by plasma cholinesterases

Esters are more prone to allergic reactions due to PABA byproduct.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

True or False: Allergic reactions are more common with esters than amides.

A

True

Use amide anesthetics in patients with ester allergies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What impact does low pKa have on anesthetic effectiveness?

A

Faster onset

Low pKa indicates a higher proportion of the drug is in its uncharged form.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is the effect of high lipid solubility on anesthetics?

A

Greater potency & longer duration

Lipid solubility enhances the drug’s ability to cross nerve membranes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

How does infection (low pH) affect anesthesia?

A

Slower/ineffective anesthesia

Infected tissues have lower pH, which reduces the effectiveness of local anesthetics.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Which nerve fibers are blocked more easily by anesthetics?

A

Smaller nerve fibers

Smaller fibers, like C fibers, are responsible for pain transmission.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is the risk associated with repeated doses or systemic absorption of anesthetics?

A

Risk for LAST (Local Anesthetic Systemic Toxicity)

LAST can lead to serious cardiovascular and central nervous system complications.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

List three contraindications for the use of NSAIDs.

A
  • Anticoagulation therapy
  • Cardiovascular disease
  • Chronic kidney disease (CKD)

These conditions increase the risk of significant side effects when using NSAIDs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What is the contraindication of NSAIDs in patients on anticoagulation therapy?

A

Increased risk of bleeding

Especially with aspirin and nonselective NSAIDs due to platelet inhibition.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

True or False: Aspirin is contraindicated in patients with bleeding disorders.

A

True

Aspirin can prolong bleeding time due to its antiplatelet effects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What cardiovascular risk is associated with nonaspirin NSAIDs?

A

Increased risk of MI, stroke, and heart failure

COX-2 selective NSAIDs like celecoxib carry higher cardiovascular risks.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What is the recommendation for taking aspirin and NSAIDs together?

A

Take aspirin 30 minutes before NSAIDs if co-administered

This timing helps preserve aspirin’s cardioprotective effect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What does the inhibition of prostaglandins by NSAIDs lead to in CKD patients?

A

Sodium and water retention, edema, risk of acute kidney injury (AKI)

Prostaglandins are essential for maintaining renal blood flow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What are the common indications for NSAIDs?

A
  • Musculoskeletal conditions
  • Inflammatory disorders
  • Pain relief
  • Fever reduction
  • Cardiovascular prophylaxis (aspirin only)

NSAIDs are effective for various conditions due to their analgesic and anti-inflammatory properties.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What is a significant gastrointestinal risk associated with NSAIDs?

A

Risk of ulcers, bleeding, dyspepsia

This is due to COX-1 inhibition decreasing protective gastric prostaglandins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What is the primary mechanism by which opioids exert their effects?

A

Binding to opioid receptors in the CNS and peripheral nervous system

These receptors include mu (μ), kappa (κ), and delta (δ).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What is the black box warning associated with codeine?

A

Respiratory depression and death in children

This risk is particularly high in ultrarapid CYP2D6 metabolizers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What risk arises from combining opioids with benzodiazepines?

A

Additive CNS depression leading to respiratory depression

This combination increases the risk of sedation and falls, especially in the elderly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What is a potential consequence of NSAIDs combined with corticosteroids?

A

Synergistic GI toxicity, increased risk for peptic ulcers or GI bleeding

Corticosteroids further thin the GI mucosa, compounding NSAID risks.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Fill in the blank: COX-1 selective NSAIDs have a ________ risk compared to COX-2 selective NSAIDs.

A

Higher GI risk

COX-2 selective NSAIDs are preferred for patients with a history of GI ulcers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What effect do NSAIDs have on platelet function?

A

Aspirin irreversibly inhibits COX-1, increasing bleeding risk

Other NSAIDs can also prolong bleeding time but do not have long-term cardioprotective effects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What adverse effect is associated with the use of NSAIDs during pregnancy?

A

Premature closure of the ductus arteriosus

NSAIDs should be avoided in the third trimester.

103
Q

What is the primary mechanism of action (MOA) of opioids?

A

Opioids primarily work by binding to opioid receptors in the CNS and peripheral nervous system.

104
Q

What are the three main types of opioid receptors?

A
  • μ (mu)
  • κ (kappa)
  • δ (delta)
105
Q

What is the MOA of Morphine?

A

Full μ-opioid receptor agonist

106
Q

What is Codeine’s MOA?

A

Prodrug → converted to morphine → weak μ-opioid agonist

107
Q

How does Oxycodone function?

A

Full μ-opioid agonist

108
Q

What is the MOA of Hydromorphone?

A

Full μ-opioid agonist; more potent than morphine

109
Q

What is Fentanyl’s classification?

A

Full μ-opioid agonist; synthetic, highly lipophilic

110
Q

What is the MOA of Buprenorphine?

A

Partial μ-opioid agonist + κ-antagonist

111
Q

What distinguishes Tramadol’s MOA?

A

Weak μ-opioid agonist + inhibits norepinephrine & serotonin reuptake

112
Q

What is Naloxone’s function?

A

Opioid receptor antagonist – displaces opioids from receptors to reverse effects

113
Q

What is the half-life of Morphine?

A

~2–4 hrs

114
Q

How does Codeine’s half-life compare?

115
Q

What is Oxycodone’s half-life?

A

~3–4.5 hrs

116
Q

What is the half-life of Hydromorphone?

A

~2–3 hrs

117
Q

What is the half-life of Fentanyl (IV)?

A

~2–4 hrs (very short acting)

118
Q

What is the half-life of Fentanyl (patch)?

A

~17 hrs (after removal)

119
Q

What is Buprenorphine’s half-life?

A

~24–60 hrs

120
Q

What is Tramadol’s half-life?

121
Q

What is Naloxone’s half-life?

A

~30–90 min

122
Q

What is the risk of respiratory depression with short-acting opioids?

123
Q

True or False: Buprenorphine has a ceiling effect on respiratory depression.

124
Q

What are common risks/adverse effects of Oral (PO) opioid administration?

A
  • First-pass metabolism
  • GI side effects: constipation, nausea, vomiting
  • Sedation, respiratory depression
125
Q

What advantages does IV opioid administration provide?

A
  • Rapid onset
  • Precise dose titration
126
Q

What is a risk associated with IV opioid administration?

A

Respiratory depression (especially with rapid administration)

127
Q

What is a major disadvantage of Transdermal opioid patches?

A

Delayed onset/offset—takes 12–24 hours to work

128
Q

What is a key risk of Transmucosal opioid administration?

A

Risk of overdose in opioid-naïve patients

129
Q

What are the risks associated with Epidural/Intrathecal opioid administration?

A
  • Respiratory depression (delayed)
  • Pruritus, urinary retention, hypotension
130
Q

What is the definition of half-life (t½)?

A

The time it takes for the plasma concentration of a drug to decrease by 50%.

131
Q

What is a clinical implication of prolonged half-life in opioid overdose?

A

Prolonged toxicity

132
Q

What is the risk associated with short-acting opioids in overdose?

A

May resolve quickly, but high potency can still cause life-threatening respiratory depression.

133
Q

What should be monitored after naloxone administration?

A

Extended monitoring is critical after reversal, especially with long-acting opioids.

134
Q

What enzyme is responsible for converting Codeine to morphine?

135
Q

What are the concerns for ultrarapid metabolizers of Codeine?

A

Produce excess morphine, leading to increased risk of toxicity.

136
Q

What is the recommendation for aspirin use in children with viral illnesses?

A

Avoid aspirin due to the risk of Reye’s syndrome.

137
Q

What is the recommendation for low-dose aspirin in adults?

A

Used for cardiovascular prevention.

138
Q

What is the pregnancy consideration for aspirin use?

A

Avoid routine use, especially in the third trimester.

139
Q

What is the MOA of Aspirin (ASA)?

A

Irreversibly inhibits COX-1 and COX-2 enzymes.

140
Q

What is the half-life of low-dose Aspirin?

A

~3.5 hours

141
Q

What is a clinical implication of high-dose Aspirin?

A

Half-life can extend to ≥12 hours.

142
Q

What are the indications for initiating Buprenorphine?

A
  • Chronic pain
  • Opioid use disorder (OUD)
143
Q

What should be monitored in patients taking high doses of Buprenorphine?

A

QT prolongation

144
Q

What is a key advantage of Buprenorphine in overdose situations?

A

Ceiling effect for respiratory depression.

145
Q

What is a risk associated with CYP3A4 inhibitors when using Buprenorphine?

A

Increases buprenorphine levels → risk of toxicity.

146
Q

What is the typical onset of action for SSRIs?

A

2–6 weeks for full antidepressant effects; some improvement may occur within 1–2 weeks.

147
Q

What is the onset of action for SSRIs in anxiety disorders?

A

Delayed 4–6 weeks; initial jitteriness or worsening anxiety may occur.

148
Q

What is the approximate half-life of Fluoxetine?

A

2–4 days (active metabolite: 7–15 days).

149
Q

What are the prescribing implications of Fluoxetine’s long half-life?

A

Reduces risk of withdrawal symptoms; requires 5-week washout before starting MAOIs.

150
Q

What is the approximate half-life of Sertraline?

A

~26 hours.

151
Q

What are the prescribing implications of Sertraline’s half-life?

A

Moderate half-life; fewer drug-drug interactions; good balance between safety and effectiveness.

152
Q

What is the risk associated with higher doses of Citalopram?

A

Risk of QT prolongation, especially in older adults (>60 yrs).

153
Q

What is the approximate half-life of Escitalopram?

A

~27–32 hours.

154
Q

What is the prescribing implication of Paroxetine’s short half-life?

A

High risk of discontinuation syndrome; taper required.

155
Q

What is the approximate half-life of Fluvoxamine?

A

~15–22 hours.

156
Q

What are the adverse effects of hypnotics?

A
  • Drowsiness * Dizziness * Cognitive impairment * Anterograde amnesia * Behavioral disinhibition * Parasomnias.
157
Q

What are common withdrawal symptoms from hypnotics?

A
  • Anxiety * Agitation * Insomnia * Seizures.
158
Q

What is the recommended management strategy for starting SSRIs?

A

Start low, go slow to avoid early side effects.

159
Q

What is the FDA boxed warning related to hypnotics?

A

Risk of behavioral disinhibition leading to injury or death.

160
Q

What is the onset of action for immediate-release Methylphenidate?

A

Typically within 20 to 60 minutes after oral administration.

161
Q

What is the mechanism of action for Methylphenidate?

A

Blocks reuptake of dopamine and norepinephrine.

162
Q

What is discontinuation syndrome?

A

A group of symptoms that emerge when stopping or reducing the dose of certain antidepressants.

163
Q

What are common symptoms of discontinuation syndrome?

A
  • Dizziness * Insomnia * Irritability * Anxiety * Nausea * Headache * Flu-like symptoms.
164
Q

What is the recommended tapering strategy for antidepressants?

A

Gradual tapering over weeks to months.

165
Q

What is the washout period required when switching to MAOIs?

A

At least 14 days between stopping an SSRI/SNRI/TCA and starting an MAOI.

166
Q

What are the FDA-approved indications for TCAs?

A
  • Major Depressive Disorder (MDD) * Neuropathic Pain * Migraine Prophylaxis * Fibromyalgia * Insomnia.
167
Q

What is one reason TCAs are not first-line treatments?

A

Adverse effects including anticholinergic effects and cardiotoxicity.

168
Q

What are common adverse effects of SSRIs?

A
  • GI upset * Sexual dysfunction * Weight changes * Anxiety/jitteriness * Hyponatremia.
169
Q

What are common adverse effects of SNRIs?

A
  • GI upset * Headache * Sexual dysfunction * Hypertension.
170
Q

What are common adverse effects of Atypical Antidepressants?

A
  • Bupropion: Activating effects, dry mouth, seizures. * Mirtazapine: Sedation, weight gain. * Trazodone: Sedation, priapism.
171
Q

What is the risk of overdose with benzodiazepines?

A

Flumazenil may precipitate seizures in dependent patients.

172
Q

What is the recommended tapering strategy for benzodiazepines?

A

Taper by 0.5 mg every 3 days or slower.

173
Q

What are common Tricyclic Antidepressants (TCAs)?

A

Amitriptyline, Nortriptyline, Clomipramine

These medications are primarily used to treat depression and other mood disorders.

174
Q

What are the adverse effects of Tricyclic Antidepressants (TCAs)?

A
  • Anticholinergic effects: dry mouth, urinary retention, constipation, blurred vision
  • Orthostatic hypotension
  • Sedation
  • Weight gain
  • Sexual dysfunction
  • Cardiotoxicity
  • Seizures
  • Narrow therapeutic index

Overdose can be fatal due to the narrow therapeutic index.

175
Q

What management strategies should be used for TCAs?

A
  • Avoid in elderly
  • EKG monitoring
  • Limit quantities prescribed
  • Monitor for anticholinergic burden

These strategies help mitigate risks associated with TCA use.

176
Q

What are the contraindications for SSRIs?

A
  • Concomitant use with MAOIs
  • Hypersensitivity to the specific drug
  • Citalopram and Escitalopram: Avoid in patients with QT prolongation

The risk of serotonin syndrome is significant when SSRIs are combined with MAOIs.

177
Q

What precautions should be taken when prescribing SSRIs?

A
  • Suicidality risk in youth
  • Bleeding risk with NSAIDs
  • Hyponatremia/SIADH
  • Hepatic impairment
  • Discontinuation syndrome
  • Sexual dysfunction

These precautions are particularly important in vulnerable populations.

178
Q

What are the examples of SNRIs?

A

Venlafaxine, Duloxetine, Desvenlafaxine

SNRIs are used to treat major depressive disorder and anxiety disorders.

179
Q

What are the contraindications for SNRIs?

A
  • Concurrent MAOI use
  • Uncontrolled narrow-angle glaucoma
  • Duloxetine: Avoid in severe hepatic impairment

These contraindications help prevent adverse effects and complications.

180
Q

What precautions should be taken when prescribing SNRIs?

A
  • Hypertension risk
  • Suicidality risk in youth
  • Renal impairment
  • Discontinuation syndrome
  • Bleeding risk

Monitoring is essential when prescribing SNRIs.

181
Q

What are examples of atypical antidepressants?

A

Bupropion, Mirtazapine, Trazodone

Atypical antidepressants are used for depression and anxiety disorders.

182
Q

What are the contraindications for Bupropion?

A
  • Seizure disorder
  • Eating disorders
  • Abrupt discontinuation of alcohol

These contraindications are important due to the increased seizure risk.

183
Q

What precautions should be taken when prescribing Bupropion?

A
  • Dose-related seizure risk
  • Can worsen anxiety/agitation
  • Avoid in severe hepatic/renal impairment

Close monitoring is needed for patients on Bupropion.

184
Q

What is the primary action of First-Generation Antipsychotics (FGAs)?

A

Potent dopamine D2 receptor antagonists

FGAs are most effective at treating positive symptoms of schizophrenia.

185
Q

What are the indications for Second-Generation Antipsychotics (SGAs)?

A
  • Schizophrenia
  • Bipolar disorder
  • MDD (adjunct)
  • Agitation in dementia

SGAs have broader efficacy compared to FGAs.

186
Q

What are the side effects of First-Generation Antipsychotics (FGAs)?

A
  • Extrapyramidal Symptoms (EPS)
  • Neuroleptic Malignant Syndrome (NMS)
  • Anticholinergic Effects
  • Sedation
  • QT Prolongation
  • Hyperprolactinemia

FGAs have a high risk for EPS and other serious side effects.

187
Q

What are the metabolic side effects associated with Second-Generation Antipsychotics (SGAs)?

A
  • Weight gain
  • Hyperlipidemia
  • Insulin resistance
  • Diabetes

Olanzapine and Clozapine have the highest risk of metabolic side effects.

188
Q

What is the significance of CYP450 enzymes in antidepressant metabolism?

A
  • Variability can lead to increased or decreased drug levels
  • CYP2D6, CYP3A4, CYP2C19, CYP1A2 are key isoenzymes

Understanding these enzymes is crucial for predicting drug interactions and responses.

189
Q

What are the risks of combining multiple psychotropic drug classes?

A
  • Pharmacodynamic interactions
  • Pharmacokinetic interactions
  • Cumulative adverse effects

These risks necessitate careful monitoring and management.

190
Q

Fill in the blank: Combining SSRIs with _______ increases the risk of serotonin syndrome.

A

MAOIs

This combination can lead to severe and potentially fatal side effects.

191
Q

True or False: Second-Generation Antipsychotics have a higher risk of extrapyramidal symptoms compared to First-Generation Antipsychotics.

A

False

SGAs generally have a lower risk of EPS compared to FGAs.

192
Q

What effect do drugs have on the metabolism of others?

A

Drugs may alter the metabolism of others, leading to increased serum levels or decreased efficacy.

193
Q

Which psychotropics are known to be CYP450 inhibitors?

A

Fluoxetine, paroxetine, fluvoxamine.

194
Q

What is the effect of carbamazepine on drug metabolism?

A

Carbamazepine is a strong CYP3A4 inducer, which can reduce effectiveness of other drugs.

195
Q

What are some cumulative adverse effects of combining drugs?

A

Weight gain, metabolic syndrome, dyslipidemia, sedation, falls, hyponatremia.

196
Q

Which populations are at increased risk for adverse effects from medications?

A

Older adults, pregnant women, patients with hepatic/renal impairment.

197
Q

What is the risk of combining SSRIs with MAOIs?

A

Serotonin syndrome.

198
Q

What risk is associated with combining olanzapine and benzodiazepines?

A

Sedation, hypotension, respiratory depression.

199
Q

What is the main recommendation for starting medication combinations?

A

Start low, go slow.

200
Q

What are first-line agents for treating depression?

A

SSRIs, SNRIs, Atypical Antidepressants.

201
Q

What is the mechanism of action of SSRIs?

A

Inhibit serotonin reuptake → ↑ serotonin levels.

202
Q

What are some examples of SSRIs?

A

Fluoxetine, sertraline, escitalopram, citalopram, paroxetine.

203
Q

What side effects are associated with SSRIs?

A

Sexual dysfunction, GI upset, insomnia/sedation, possible increased suicidality in youth.

204
Q

What are SNRIs and their mechanism of action?

A

Serotonin-Norepinephrine Reuptake Inhibitors; inhibit serotonin & norepinephrine reuptake.

205
Q

What are common examples of SNRIs?

A

Venlafaxine, desvenlafaxine, duloxetine.

206
Q

What risk is associated with high doses of venlafaxine?

A

Can increase blood pressure.

207
Q

What are Tricyclic Antidepressants (TCAs) and their mechanism of action?

A

Inhibit reuptake of serotonin and norepinephrine + anticholinergic, antihistaminic effects.

208
Q

What are examples of TCAs?

A

Amitriptyline, nortriptyline, clomipramine.

209
Q

What are Monoamine Oxidase Inhibitors (MAOIs) used for?

A

Inhibit breakdown of serotonin, norepinephrine, dopamine.

210
Q

What is a significant caution when using MAOIs?

A

Require dietary restrictions (tyramine → hypertensive crisis).

211
Q

What are the indications for benzodiazepines?

A

Anxiety disorders, insomnia, acute agitation, alcohol withdrawal.

212
Q

What is the mechanism of action of benzodiazepines?

A

Enhance the effect of GABA at the GABA-A receptor.

213
Q

What risks are associated with benzodiazepine use?

A

Physical dependence, withdrawal symptoms, cognitive impairment.

214
Q

What is the onset time for benzodiazepines?

A

Rapid – within minutes to hours.

215
Q

Fill in the blank: SSRIs are first-line for _______.

A

[depression and anxiety disorders]

216
Q

Fill in the blank: The mechanism of action for TCAs includes inhibition of _______.

A

[serotonin and norepinephrine reuptake]

217
Q

True or False: Benzodiazepines are recommended for long-term treatment.

218
Q

What is the primary mechanism of action (MOA) of benzodiazepines in seizure management?

A

Enhancing the effect of gamma-aminobutyric acid (GABA) at the GABA-A receptor.

219
Q

How do benzodiazepines affect neurons?

A

They hyperpolarize neurons, making them less likely to fire.

220
Q

Do benzodiazepines directly open the chloride channel?

A

No, they enhance the natural effect of GABA.

221
Q

What are the first-line agents for status epilepticus?

A
  • Lorazepam (Ativan)
  • Diazepam (Valium)
  • Midazolam
222
Q

What is the preferred route for administering lorazepam?

A

IV route due to longer CNS half-life.

223
Q

What are common rescue medications for breakthrough seizures?

A
  • Rectal diazepam
  • Intranasal midazolam
224
Q

What conditions is clonazepam used for?

A
  • Myoclonic seizures
  • Atonic seizures
  • Lennox-Gastaut Syndrome (LGS)
225
Q

What major concerns are associated with long-term use of benzodiazepines?

A
  • Tolerance
  • Sedation
  • Respiratory depression
  • Dependence/withdrawal risk
226
Q

What is the recommended use of rectal diazepam in children?

A

As a rescue medication for recurrent febrile seizures.

227
Q

What are the indications for phenytoin?

A
  • Focal (partial) seizures
  • Generalized tonic-clonic seizures
  • Status epilepticus
228
Q

What is a major risk associated with long-term use of phenytoin?

A

Gingival hyperplasia.

229
Q

What is the role of fosphenytoin compared to phenytoin?

A

Preferred IV option due to better safety profile.

230
Q

What side effects are associated with levetiracetam?

A
  • Irritability
  • Agitation
  • Mood swings
231
Q

What are the common adjunct treatments for Alzheimer’s Disease?

A
  • Antidepressants
  • Antipsychotics
  • Sleep aids
  • Cognitive enhancers
  • Nonpharmacologic approaches
232
Q

Which antidepressants are preferred for patients with Alzheimer’s Disease?

A

SSRIs (e.g., sertraline, citalopram).

233
Q

What are the risks of using atypical antipsychotics in Alzheimer’s patients?

A

Increased risk of stroke and death.

234
Q

What is a common side effect of topiramate when used for migraine prevention?

A

Cognitive dysfunction (‘brain fog’).

235
Q

What are the black box warnings associated with valproic acid?

A
  • Potentially fatal pancreatitis
  • Hepatitis
  • Neural tube defects
236
Q

What is the mechanism of action of tricyclic antidepressants in migraine prevention?

A

Inhibits the reuptake of serotonin and norepinephrine.

237
Q

Fill in the blank: Topiramate is known to cause _______.

A

paresthesia.

238
Q

True or False: Gabapentin is the first-line treatment for migraine prophylaxis.

239
Q

What is the pharmacological class of amitriptyline?

A

Tricyclic Antidepressants (TCAs).

240
Q

What should be monitored when using levetiracetam?

A

Behavioral changes and renal function.

241
Q

What is the risk associated with titration of certain medications?

A

Risk of serious rash (SJS/TEN); must titrate slowly

SJS/TEN stands for Stevens-Johnson syndrome/Toxic epidermal necrolysis, serious skin reactions that can occur with medication use.

242
Q

What is the mechanism of action of Amitriptyline?

A

Inhibits serotonin and norepinephrine reuptake

Amitriptyline is classified as a TCA (tricyclic antidepressant) and is used as a first-line treatment for migraine prevention.

243
Q

What are the common side effects of Topiramate?

A

Cognitive side effects common

Topiramate is an antiseizure medication that can also be used for migraine prevention.

244
Q

List the antiepileptic drugs (AEDs) that can lead to decreased folate levels.

A
  • Phenytoin
  • Phenobarbital
  • Carbamazepine

These AEDs are enzyme inducers that accelerate the metabolism of folic acid.

245
Q

What is the recommended folic acid supplementation for women of childbearing potential on AEDs?

A

High-dose folic acid (e.g., 4 mg/day), ideally starting at least 1 month before conception

This recommendation is crucial to prevent neural tube defects (NTDs) in fetuses.

246
Q

What are the early side effects of Carbidopa-Levodopa?

A
  • Nausea
  • Vomiting
  • Orthostatic hypotension
  • Somnolence
  • Dizziness

Carbidopa helps reduce nausea and vomiting associated with levodopa treatment.

247
Q

What are the contraindications for Carbidopa-Levodopa?

A
  • Narrow-angle glaucoma
  • History of melanoma
  • Severe cardiovascular disease
  • Psychiatric illness
  • Cognitive impairment

Use caution in patients with these conditions due to potential worsening of symptoms.

248
Q

What is the mechanism of action of triptans in migraine treatment?

A
  • 5-HT₁B receptor activation → Vasoconstriction of dilated intracranial vessels
  • 5-HT₁D receptor activation → Inhibition of CGRP release and neurogenic inflammation

Triptans are effective in aborting migraine attacks by targeting serotonin receptors.

249
Q

True or False: Triptans bind to adrenergic and dopaminergic receptors.

A

False

Triptans selectively bind to serotonin receptors, minimizing unwanted effects.

250
Q

What are the key drug interactions with acetylcholinesterase inhibitors?

A
  • Anticholinergic drugs
  • Beta-blockers
  • Drugs that lower heart rate (e.g., Digoxin, CCBs)
  • NSAIDs
  • CYP450 inhibitors/inducers

Each interaction can lead to decreased efficacy or increased adverse effects of AChEIs.

251
Q

What is the outcome of combining anticholinergic drugs with AChEIs?

A

Decreased therapeutic effect of AChEIs

Anticholinergics oppose the action of AChEIs by blocking acetylcholine receptors.

252
Q

Fill in the blank: Carbidopa does not cross the _______.

A

BBB

BBB stands for blood-brain barrier, which is crucial for the drug’s action.

253
Q

What is the clinical impact of Carbidopa-Levodopa in Parkinson’s Disease?

A

Most effective symptomatic treatment for PD motor symptoms

It improves quality of life and functional ability but does not halt disease progression.

Health Assessment (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions