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STEP1 > AUTONOMIC DRUGS > Flashcards

AUTONOMIC DRUGS Flashcards

1
Q

Bethanechol

A

Direct Cholinomimetic Agent

Mechanism:
Binds to muscarinic AChR → direct AChR agonism
Activates bowel and bladder smooth muscle
Promote gastric acid secretion by stimulating parietal cell M3 receptors.
No nicotinic agonism
Resistant to AChE

Clinical Use:
Urinary retention
Postoperative ileus
Neurogenic ileus

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2
Q

Carbachol

A

Direct Cholinomimetic Agent

Mechanism:
Bind to muscarinic/nicotinic AChR → direct AChR agonism
Carbon copy of acetylcholine (but resistant to AChE)
Nicotinic and muscarinic agonism
Increase trabecular outflow through M3 agonism

Clinical Use:
Open-angle and closed-angle glaucoma (alleviates intraocular pressure and causes miosis-

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3
Q

Methacholine

A

Direct Cholinomimetic Agent

Mechanism:
Bind to muscarinic/nicotinic AChR → direct AChR agonism
Predominantly muscarinic agonism
Can not cross blood-brain barrier (quaternary amine)

Clinical Use:
Diagnosis of bronchial hypersensitivity (activates muscarinic receptors on airway smooth muscle)

Positive test for airway hyperactivity if FEV1 drops by 20% or more with methacholine
Not specific 
Can give positive a postive test:
Smoking
Respiratory infections
Allergic Rhinitis
GERD
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4
Q

Pilocarpine

A

Direct Cholinomimetic Agent

Mechanism:
Bind to muscarinic/nicotinic AChR → direct AChR agonism
Predominantly muscarinic agonism
Resistant to AChE
Can cross blood-brain barrier (tertiary amine)

Clinical Use:
Open-angle and closed-angle glaucoma (↑ contraction of ciliary muscle of the eye, ↑ contraction of pupillary sphincter, opening meshwork into canal of Schlemm)
Xerostomia (e.g., in Sjogren syndrome) (↑ sweat, tears, and saliva production)
Cystic fibrosis sweat test

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5
Q

Cevimeline

A

Direct Cholinomimetic Agent

Mechanism:
Bind to muscarinic/nicotinic AChR → direct AChR agonism
Predominantly muscarinic agonism

Clinical Use:
Keratoconjunctivitis sicca (Sjogren syndrome) (↑ sweat and saliva production)
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6
Q

Donepezil

A

Indirect Cholinomimetic Agent

Mechanism:
Inhibit AchE → ↓ breakdown of ACh → ↑ ACh levels
Centrallly acting AChE inhibitors

Clinical Use:
Alzheimer disease

Adverse Effects:
Nausea, dizziness, insomnia.
Inhibition of acetylcholinesterase and a consequent reduction in acetylcholine breakdown may improve cognitive function in some patients. However, this mechanism also produces enhanced parasympathetic tone that can lead to adverse effects. Underlying age-related degeneration of the conduction system is common in the elderly, and the effects of acetylcholinesterase inhibition can precipitate bradycardia and atrioventricular block in such patients. These conduction abnormalities lead to reduced cardiac output that may manifest as presyncope (ie, lightheadedness) or syncope.

Contraindications:
Cardiac conditions (e.g., conduction abnormalities)
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7
Q

Rivastigmine

A

Indirect Cholinomimetic Agent

Mechanism:
Inhibit AchE → ↓ breakdown of ACh → ↑ ACh levels
Centrallly acting AChE inhibitors

Clinical Use:
Alzheimer disease

Adverse Effects:
Nausea, dizziness, insomnia.
Inhibition of acetylcholinesterase and a consequent reduction in acetylcholine breakdown may improve cognitive function in some patients. However, this mechanism also produces enhanced parasympathetic tone that can lead to adverse effects. Underlying age-related degeneration of the conduction system is common in the elderly, and the effects of acetylcholinesterase inhibition can precipitate bradycardia and atrioventricular block in such patients. These conduction abnormalities lead to reduced cardiac output that may manifest as presyncope (ie, lightheadedness) or syncope.

Contraindications:
Cardiac conditions (e.g., conduction abnormalities)
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8
Q

Galantamine

A

Indirect Cholinomimetic Agent

Mechanism:
Inhibit AchE → ↓ breakdown of ACh → ↑ ACh levels
Centrallly acting AChE inhibitors

Clinical Use:
Alzheimer disease

Adverse Effects:
Nausea, dizziness, insomnia.
Inhibition of acetylcholinesterase and a consequent reduction in acetylcholine breakdown may improve cognitive function in some patients. However, this mechanism also produces enhanced parasympathetic tone that can lead to adverse effects. Underlying age-related degeneration of the conduction system is common in the elderly, and the effects of acetylcholinesterase inhibition can precipitate bradycardia and atrioventricular block in such patients. These conduction abnormalities lead to reduced cardiac output that may manifest as presyncope (ie, lightheadedness) or syncope.

Contraindications:
Cardiac conditions (e.g., conduction abnormalities)
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9
Q

Edrophonium

A

Indirect Cholinomimetic Agent

Mechanism:
Inhibit AchE → ↓ breakdown of ACh → ↑ ACh levels
Very short duration of action (∼ 10 minutes)

Clinical Use:
Diagnosis of myasthenia gravis (Edrophonium test, Tensilon test)

Exacerbation of myasthenia gravis in a patient treated with long-acting acetylcholinesterase inhibitors (eg, pyridostigmine) occurs due to myasthenic or cholinergic crisis. The edrophonium (Tensilon) test helps to differentiate these 2 conditions. Clinical improvement after edrophonium administration indicates that the patient is undertreated (myasthenic crisis).

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10
Q

Neostigmine

A

Indirect Cholinomimetic Agent

Mechanism:
Inhibit AchE → ↓ breakdown of ACh → ↑ ACh levels
Can not cross the blood-brain barrier (quaternary amine)

Clinical Use:
Myasthenia gravis
Postoperative and neurogenic ileus and urinary retention (indirect parasympathomimetics can be used in cases of ileus but are contraindicated in cases of bowel obstruction)
Postoperative reversal of neuromuscular blockade

Adverse Effects:
Cause bradycardia if muscarinic antagonist such as glycopyrrolate is not given
Increasing the dose can cause desensitization of nicotinic receptors

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11
Q

Physostigmine

A

Indirect Cholinomimetic Agent

Mechanism:
Inhibit AchE → ↓ breakdown of ACh → ↑ ACh levels
Lipophilic
Can cross the blood-brain barrier (tertary amine)

Clinical Use:
Atropine, atropa belladonna or Jimson Weed (Datura) overdose (antidote)
Glaucoma

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12
Q

Pyridostigmine

A

Indirect Cholinomimetic Agent

Mechanism:
Inhibit AchE → ↓ breakdown of ACh → ↑ ACh levels
Can not cross the blood-brain barrier (quaternary amine)
Typically used with glycopyrrolate, hyoscyamine, or propantheline to control side effects

Clinical Use:
Myasthenia gravis (longer action compared to neostigmine) (improves muscle strength)
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13
Q

Echothiphate

A

Indirect Cholinomimetic Agent

Mechanism:
Inhibit AchE → ↓ breakdown of ACh → ↑ ACh levels
Irreversible AChE inhibitor
Long-acting
Increase outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork

Clinical Use:
Glaucoma

Adverse Effects:
Miosis (contraction of pupillary sphincter muscles) and cyclospasm (contraction of ciliary muscle)

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14
Q

Distigmine

A

Indirect Cholinomimetic Agent

Mechanism:
Inhibit AchE → ↓ breakdown of ACh → ↑ ACh levels
Longer duration of action than pyridostigmine and neostigmine

Clinical Use:
Postoperative ileus and urinary retention
Myasthenia gravis

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15
Q

Pralidoxime

A

Mechanism:
Regenerates AChE via dephosphorylation (organophosphates bind to the esteratic site of acetylcholinesterase. Oximes cleave this phosphate ester bond and, thereby, reactivate acetylcholinesterase)
Works at both nicotinic and muscarinic sites
Poor blood-brain barrier penetration

Clinical Use:
Initial management of organophosphate toxicity
Should be administered to any patient with neuromuscular dysfunction (eg, weakness, fasciculations).
It should be given only after atropine because can cause transient acetylcholinesterase inhibition, which can momentarily worsen symptoms

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16
Q

Obidoxime

A

Mechanism:
Regenerates AChE via dephosphorylation (organophosphates bind to the esteratic site of acetylcholinesterase. Oximes cleave this phosphate ester bond and, thereby, reactivate acetylcholinesterase)
Works at both nicotinic and muscarinic sites
Poor blood-brain barrier penetration

Clinical Use:
Initial management of organophosphate toxicity
Should be administered to any patient with neuromuscular dysfunction (eg, weakness, fasciculations).
It should be given only after atropine because can cause transient acetylcholinesterase inhibition, which can momentarily worsen symptoms

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17
Q

Atropine

A

Antimuscarinic
Tertiary amine
Lipophilic (good oral bioavailability and CNS penetration)

Mechanism:
Inhibit the effect of acetylcholine on muscarinic receptors
↑ Heart rate (by inhibiting vagal input)
↓ Secretions of exocrine glands
↓ Tone and motility of smooth muscles (i.e., ↓ urgency in cystitis)
↓ Cholinergic overactivity in CNS
Mydriasis and cycloplegia

Clinical Use:

  • First drug of choice in unstable (symptomatic) sinus bradycardia (IV)
  • Premedication prior to intubation to decrease salivary, respiratory, and gastric secretions
  • Uveitis (to prevent and treat anterior and posterior synechiae)
  • Urinary urgency, urge incontinence, urinary frequency and/or nocturia (symptoms resulting from, e.g., overactive bladder syndrome) (tolterodine has a more selective effect on the smooth muscle of the bladder and is the preferred drug for treating urinary incontinence)
  • Antidote for anticholinesterase poisoning (carbamate insecticides, nerve agents, organophosphate insecticides) (reverses the muscarinic effects of cholinergic poisoning (e.g., bronchoconstriction) but does not reverse the nicotinic effects (e.g., muscle weakness, paralysis)).
  • Scorpion stings (to reduce hypersalivation and bronchoconstriction)

Adverse Effects:
Can cause acute angle-closure glaucoma in elderly (due to mydriasis), urinary retention in men with prostatic hyperplasia, and hyperthermia in infants

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18
Q

Scopolamine (hyoscine)

A

Antimuscarinic
Tertiary amine
Lipophilic (good oral bioavailability and CNS penetration)
↓ Vestibular disturbances (antiemetic)

Mechanism:
Inhibit the effect of acetylcholine on muscarinic receptors

Clinical Use:
Motion sickness

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19
Q

Homatropine

A 
Antimuscarinic
Tertiary amine
Lipophilic (good oral bioavailability and CNS penetration)
Mydriasis
Impaired accommodation

Mechanism:
Inhibit the effect of acetylcholine on muscarinic receptors

Clinical Use:
Therapeutic use in patients with uveitis (to prevent synechiae between the iris and the anterior lens capsule)
Diagnostic use (pupillary dilation to allow ocular fundus examination and cycloplegia to allow refractory testing)

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20
Q

Tropicamide

A 
Antimuscarinic
Tertiary amine
Lipophilic (good oral bioavailability and CNS penetration)
Mydriasis
Impaired accommodation

Mechanism:
Inhibit the effect of acetylcholine on muscarinic receptors

Clinical Use:
Therapeutic use in patients with uveitis (to prevent synechiae between the iris and the anterior lens capsule)
Diagnostic use (pupillary dilation to allow ocular fundus examination and cycloplegia to allow refractory testing)

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21
Q

Benztropine

A

Antimuscarinic
Tertiary amine
Lipophilic (good oral bioavailability and CNS penetration)
↓ Cholinergic overactivity in CNS

Mechanism:
Inhibit the effect of acetylcholine on muscarinic receptors

Clinical Use:
Antiparkisonian effect (improves tremor and rigidity but has little effect on bradykinesia)
↓ Extrapyramidal symptoms (EPS) caused by antipsychotics

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22
Q

Biperiden

A

Antimuscarinic
Tertiary amine
Lipophilic (good oral bioavailability and CNS penetration)
↓ Cholinergic overactivity in CNS

Mechanism:
Inhibit the effect of acetylcholine on muscarinic receptors

Clinical Use:
Antiparkisonian effect (improves tremor and rigidity but has little effect on bradykinesia)
↓ Extrapyramidal symptoms (EPS) caused by antipsychotics

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23
Q

Trihexyphenidyl

A

Antimuscarinic
Tertiary amine
Lipophilic (good oral bioavailability and CNS penetration)
↓ Cholinergic overactivity in CNS

Mechanism:
Inhibit the effect of acetylcholine on muscarinic receptors

Clinical Use:
Antiparkisonian effect (improves tremor and rigidity but has little effect on bradykinesia)
↓ Extrapyramidal symptoms (EPS) caused by antipsychotics

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24
Q

Oxybutynin

A

Antimuscarinic
Tertiary amine
Lipophilic (good oral bioavailability and CNS penetration)
↓ Tone and motility of smooth muscle cells

Mechanism:
Inhibit the effect of acetylcholine on muscarinic receptors

Clinical Use:
↓ Bladder spasms and urgency in overactive bladder incontinence

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25
Q

Tolterodine

A

Antimuscarinic
Tertiary amine
Lipophilic (good oral bioavailability and CNS penetration)
↓ Tone and motility of smooth muscle cells

Mechanism:
Inhibit the effect of acetylcholine on muscarinic receptors

Clinical Use:
↓ Bladder spasms and urgency in overactive bladder incontinence

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26
Q

Solifenacin

A

Antimuscarinic
Tertiary amine
Lipophilic (good oral bioavailability and CNS penetration)
↓ Tone and motility of smooth muscle cells

Mechanism:
Inhibit the effect of acetylcholine on muscarinic receptors

Clinical Use:
↓ Bladder spasms and urgency in overactive bladder incontinence

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27
Q

Butylscopolamine (hyoscine butylbromide)

A

Antimuscarinic
Quarternary amine
Hydrophilic (poor oral bioavailability and CNS penetration)
In contrast to scopolamine, butylscopolamine does not cross the blood-brain barrier and thus has no effect on the CNS.
↓ Tone and motility of the gut (antispasmodic effect)

Mechanism:
Inhibit the effect of acetylcholine on muscarinic receptors

Clinical Use:
Antispasmodics for colicky pain (intestinal, biliary or ureteric colic)

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28
Q

Glycopyrrolate

A

Antimuscarinic
Quarternary amine
Hydrophilic (poor oral bioavailability and CNS penetration)
↓ GI and respiratory secretions

Mechanism:
Inhibit the effect of acetylcholine on muscarinic receptors

Clinical Use:
Preoperative IV use to decrease respiratory secretions
Oral → reduces drooling, peptic ulcer

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29
Q

Ipratropium bromide

A

Antimuscarinic
Quarternary amine
Hydrophilic (poor oral bioavailability and CNS penetration)

Mechanism:
Inhibit the effect of acetylcholine on muscarinic receptors
Bronchodilation (competitive inhibition of muscarinic receptors prevents bronchoconstriction.)
Antimuscarinics cause bronchodilation but actually impair mucociliary clearance and thus cause secretions to remain in the lung; only ipratropium bromide causes bronchodilation without impairing mucociliary clearance.

Clinical Use:
Short duration of action
Treatment of COPD grade I and higher
Acute management of refractory asthma

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30
Q

Tiotropium bromide

A

Antimuscarinic
Quarternary amine
Hydrophilic (poor oral bioavailability and CNS penetration)

Mechanism:
Inhibit the effect of acetylcholine on muscarinic receptors
Bronchodilation (competitive inhibition of muscarinic receptors prevents bronchoconstriction.)
Antimuscarinics cause bronchodilation but actually impair mucociliary clearance and thus cause secretions to remain in the lung; only ipratropium bromide causes bronchodilation without impairing mucociliary clearance.

Clinical Use:
Longer duration of action (LAMA)
Long-term treatment of COPD (grade II and above)

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31
Q

Dicyclomine

A

Antimuscarinic
Tertiary amine
Lipophilic (good oral bioavailability and CNS penetration)
↓ Tone and motility of smooth muscle cells

Mechanism:
Inhibit the effect of acetylcholine on muscarinic receptors

Clinical Use:
Antispasmodics (irritable bowel syndrome)

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32
Q

Hyoscyamine

A

Antimuscarinic
Tertiary amine
Lipophilic (good oral bioavailability and CNS penetration)
↓ Tone and motility of smooth muscle cells

Mechanism:
Inhibit the effect of acetylcholine on muscarinic receptors

Clinical Use:
Antispasmodics (irritable bowel syndrome)

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33
Q

Darifenacin

A

Antimuscarinic
Tertiary amine
Lipophilic (good oral bioavailability and CNS penetration)
↑ Sphincter tone

Mechanism:
Inhibit the effect of acetylcholine on muscarinic receptors

Clinical Use:
Urinary urgency, urge incontinence, urinary frequency, and/or nocturia (symptoms resulting from, e.g., overactive bladder)

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34
Q

Flavoxate

A

Antimuscarinic
Tertiary amine
Lipophilic (good oral bioavailability and CNS penetration)
↓ Tone and motility of smooth muscle cells

Mechanism:
Inhibit the effect of acetylcholine on muscarinic receptors

Clinical Use:
↓ Bladder spasms and urgency in overactive bladder incontinence

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35
Q

Albuterol

A

Short-acting β2 adrenergic agonist
Onset of action → 1-5 minutes
Duration of action → 4-6 hours
A face mask is recommended for children < 4 years on inhalational therapy.

Mechanism:
β2 > β1
Stimulate β2 adrenergic receptors.
Relaxes bronchial smooth muscle

Clinical Use:
Bronchial asthma (used to achieve spasmolysis of the bronchi)
Acute exacerbation (use short-acting selective β2-agonists (e.g., albuterol))
COPD (used to achieve spasmolysis of the bronchi) (Short-acting beta agonist inhalers are often combined with ipratropium bromide)
Hyperkalemia (drive K+ intracellularly)

Adverse Effects:

  • Ventricular arrhythmias, vasoconstriction, angina pectoris, tachycardia, and palpitations; may aggravate cardiomyopathy in patients with cardiovascular disease (these effects are due to several processes: 1. β1-mediated cardiac stimulation (no absolute β2 selectivity); 2. reflex tachycardia after β2-mediated vasodilation; and 3. the results of potential hypokalemia)
  • Tremor (β2-mediated skeletal muscle stimulation with potential initiation of a tremor)
  • Headache, anxiety, and sleep disturbances
  • Hyperglycemia (β2-mediated stimulation in the liver → elevated cAMP levels → increased glycogenolysis)
  • Hypokalemia (risk of life-threatening arrhythmias) (β2-mediated stimulation of Na+/K+-ATPase → intracellular K+ shift (hyperglycemia also contributes) (increased insulin secretion → activates Na+/K+-ATPase)
  • Development of tolerance
  • Paradoxical bronchospasm may occur

Use with caution in patients with the following conditions:
Hyperthyroidism
Glaucoma
Diabetes
Hypokalemia
Seizures
Cardiovascular disease (e.g., heart failure, hypertension, arrhythmias, coronary artery disease)

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36
Q

Terbutaline

A

Short-acting β2 adrenergic agonist
Onset of action → 1-5 minutes
Duration of action → 4-6 hours
A face mask is recommended for children < 4 years on inhalational therapy.

Mechanism:
β2 > β1
Stimulate β2 adrenergic receptors.
Relaxes bronchial smooth muscle

Clinical Use:
Bronchial asthma (used to achieve spasmolysis of the bronchi)
Acute exacerbation (use short-acting)
COPD (used to achieve spasmolysis of the bronchi) (Short-acting beta agonist inhalers are often combined with ipratropium bromide)
Hyperkalemia (drive K+ intracellularly)
Tocolysis (often used to suppress contractions in pregnant women undergoing preterm labor, with pyelonephritis (which can induce preterm labor), or umbilical cord prolapse)

Adverse Effects:

  • Ventricular arrhythmias, vasoconstriction, angina pectoris, tachycardia, and palpitations; may aggravate cardiomyopathy in patients with cardiovascular disease (these effects are due to several processes: 1. β1-mediated cardiac stimulation (no absolute β2 selectivity); 2. reflex tachycardia after β2-mediated vasodilation; and 3. the results of potential hypokalemia)
  • Tremor (β2-mediated skeletal muscle stimulation with potential initiation of a tremor)
  • Headache, anxiety, and sleep disturbances
  • Hyperglycemia (β2-mediated stimulation in the liver → elevated cAMP levels → increased glycogenolysis)
  • Hypokalemia (risk of life-threatening arrhythmias) (β2-mediated stimulation of Na+/K+-ATPase → intracellular K+ shift (hyperglycemia also contributes) (increased insulin secretion → activates Na+/K+-ATPase)
  • Development of tolerance
  • Paradoxical bronchospasm may occur

Use with caution in patients with the following conditions:
Hyperthyroidism
Glaucoma
Diabetes
Hypokalemia
Seizures
Cardiovascular disease (e.g., heart failure, hypertension, arrhythmias, coronary artery disease)

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37
Q

Pirbuterol

A

Short-acting β2 adrenergic agonist
Onset of action → 1-5 minutes
Duration of action → 4-6 hours
A face mask is recommended for children < 4 years on inhalational therapy.

Mechanism:
β2 > β1
Stimulate β2 adrenergic receptors.
Relaxes bronchial smooth muscle

Clinical Use:
Bronchial asthma (used to achieve spasmolysis of the bronchi)
Acute exacerbation (use short-acting)
COPD (used to achieve spasmolysis of the bronchi) (short-acting beta agonist inhalers are often combined with ipratropium bromide)
Hyperkalemia (drive K+ intracellularly)

Adverse Effects:

  • Ventricular arrhythmias, vasoconstriction, angina pectoris, tachycardia, and palpitations; may aggravate cardiomyopathy in patients with cardiovascular disease (these effects are due to several processes: 1. β1-mediated cardiac stimulation (no absolute β2 selectivity); 2. reflex tachycardia after β2-mediated vasodilation; and 3. the results of potential hypokalemia)
  • Tremor (β2-mediated skeletal muscle stimulation with potential initiation of a tremor)
  • Headache, anxiety, and sleep disturbances
  • Hyperglycemia (β2-mediated stimulation in the liver → elevated cAMP levels → increased glycogenolysis)
  • Hypokalemia (risk of life-threatening arrhythmias) (β2-mediated stimulation of Na+/K+-ATPase → intracellular K+ shift (hyperglycemia also contributes) (increased insulin secretion → activates Na+/K+-ATPase)
  • Development of tolerance
  • Paradoxical bronchospasm may occur

Use with caution in patients with the following conditions:
Hyperthyroidism
Glaucoma
Diabetes
Hypokalemia
Seizures
Cardiovascular disease (e.g., heart failure, hypertension, arrhythmias, coronary artery disease)

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38
Q

Levalbuterol

A

Short-acting β2 adrenergic agonist
Onset of action → 1-5 minutes
Duration of action → 4-8 hours
A face mask is recommended for children < 4 years on inhalational therapy.

Mechanism:
β2 > β1
Stimulate β2 adrenergic receptors.
Relaxes bronchial smooth muscle

Clinical Use:
Bronchial asthma (used to achieve spasmolysis of the bronchi)
Acute exacerbation (use short-acting)
COPD (used to achieve spasmolysis of the bronchi) (short-acting beta agonist inhalers are often combined with ipratropium bromide)
Hyperkalemia (drive K+ intracellularly)

Adverse Effects:

  • Ventricular arrhythmias, vasoconstriction, angina pectoris, tachycardia, and palpitations; may aggravate cardiomyopathy in patients with cardiovascular disease (these effects are due to several processes: 1. β1-mediated cardiac stimulation (no absolute β2 selectivity); 2. reflex tachycardia after β2-mediated vasodilation; and 3. the results of potential hypokalemia)
  • Tremor (β2-mediated skeletal muscle stimulation with potential initiation of a tremor)
  • Headache, anxiety, and sleep disturbances
  • Hyperglycemia (β2-mediated stimulation in the liver → elevated cAMP levels → increased glycogenolysis)
  • Hypokalemia (risk of life-threatening arrhythmias) (β2-mediated stimulation of Na+/K+-ATPase → intracellular K+ shift (hyperglycemia also contributes) (increased insulin secretion → activates Na+/K+-ATPase)
  • Development of tolerance
  • Paradoxical bronchospasm may occur

Use with caution in patients with the following conditions:
Hyperthyroidism
Glaucoma
Diabetes
Hypokalemia
Seizures
Cardiovascular disease (e.g., heart failure, hypertension, arrhythmias, coronary artery disease)

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39
Q

Formoterol

A

Long-acting β2 adrenergic agonist
Onset of action → 1-5 minutes
Duration of action → > 12 hours
A face mask is recommended for children < 4 years on inhalational therapy.

Mechanism:
β2 > β1
Stimulate β2 adrenergic receptors.
Relaxes bronchial smooth muscle

Clinical Use:
Bronchial asthma (used to achieve spasmolysis of the bronchi)
Prophylaxis (in chronic disease) use long-acting selective β2-agonists (e.g., salmeterol)
COPD (used to achieve spasmolysis of the bronchi) (short-acting beta agonist inhalers are often combined with ipratropium bromide)
Hyperkalemia (drive K+ intracellularly)

Adverse Effects:

  • Ventricular arrhythmias, vasoconstriction, angina pectoris, tachycardia, and palpitations; may aggravate cardiomyopathy in patients with cardiovascular disease (these effects are due to several processes: 1. β1-mediated cardiac stimulation (no absolute β2 selectivity); 2. reflex tachycardia after β2-mediated vasodilation; and 3. the results of potential hypokalemia)
  • Tremor (β2-mediated skeletal muscle stimulation with potential initiation of a tremor)
  • Headache, anxiety, and sleep disturbances
  • Hyperglycemia (β2-mediated stimulation in the liver → elevated cAMP levels → increased glycogenolysis)
  • Hypokalemia (risk of life-threatening arrhythmias) (β2-mediated stimulation of Na+/K+-ATPase → intracellular K+ shift (hyperglycemia also contributes) (increased insulin secretion → activates Na+/K+-ATPase)
  • Development of tolerance
  • Paradoxical bronchospasm may occur

Use with caution in patients with the following conditions:
Hyperthyroidism
Glaucoma
Diabetes
Hypokalemia
Seizures
Cardiovascular disease (e.g., heart failure, hypertension, arrhythmias, coronary artery disease)

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40
Q

Salmeterol

A

Long-acting β2 adrenergic agonist
Onset of action → 30-45 minutes
Duration of action → >12 hours
A face mask is recommended for children < 4 years on inhalational therapy.

Mechanism:
β2 > β1
Stimulate β2 adrenergic receptors.
Relaxes bronchial smooth muscle

Clinical Use:
Bronchial asthma (used to achieve spasmolysis of the bronchi)
Prophylaxis (in chronic disease) use long-acting selective β2-agonists (e.g., salmeterol)
COPD (used to achieve spasmolysis of the bronchi) (short-acting beta agonist inhalers are often combined with ipratropium bromide)
Hyperkalemia (drive K+ intracellularly)

Adverse Effects:

  • Ventricular arrhythmias, vasoconstriction, angina pectoris, tachycardia, and palpitations; may aggravate cardiomyopathy in patients with cardiovascular disease (these effects are due to several processes: 1. β1-mediated cardiac stimulation (no absolute β2 selectivity); 2. reflex tachycardia after β2-mediated vasodilation; and 3. the results of potential hypokalemia)
  • Tremor (β2-mediated skeletal muscle stimulation with potential initiation of a tremor)
  • Headache, anxiety, and sleep disturbances
  • Hyperglycemia (β2-mediated stimulation in the liver → elevated cAMP levels → increased glycogenolysis)
  • Hypokalemia (risk of life-threatening arrhythmias) (β2-mediated stimulation of Na+/K+-ATPase → intracellular K+ shift (hyperglycemia also contributes) (increased insulin secretion → activates Na+/K+-ATPase)
  • Development of tolerance
  • Paradoxical bronchospasm may occur

Use with caution in patients with the following conditions:
Hyperthyroidism
Glaucoma
Diabetes
Hypokalemia
Seizures
Cardiovascular disease (e.g., heart failure, hypertension, arrhythmias, coronary artery disease)

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41
Q

Clonidine

A

Sympatholytic drug

Mechanism:
α2 agonist
Stimulates α2-receptors in the brainstem, decreasing peripheral vascular resistance and lowering blood pressure (BP)

Clinical Use:
ADHD
Tourette syndrome
Hypertensive urgency (limited situations)
Symptom control in opioid withdrawal
Adverse Effects:
Orthostatic hypotension
Sedation and CNS depression
Rebound hypertension caused by abrupt discontinuation of medication 
Respiratory depression
Miosis
Dry mouth
Rash
Bradycardia
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42
Q

Guanfacine

A

Sympatholytic drug

Mechanism:
α2 agonist
Stimulates α2-receptors in the brainstem, decreasing peripheral vascular resistance and lowering blood pressure (BP)

Clinical Use:
ADHD
Tourette syndrome
Drug withdrawal
Hypertensive urgency (limited situations)
Symptom control in opioid withdrawal
Adverse Effects:
Orthostatic hypotension
Sedation and CNS depression
Rebound hypertension caused by abrupt discontinuation of medication 
Respiratory depression
Miosis
Dry mouth
Rash
Bradycardia
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43
Q

Dobutamine

A

Direct sympathomimetic drug

Mechanism:
β1 > β2, α
Inotropic effects > chronotropic effects
No change or mild decrease in BP
Raises HR, cardiac output (CO)

Clinical Use:
Heart failure (At high doses, acts as a β-agonist. Therefore, in patients with heart failure, high-dose dobutamine is useful because it increases CO (due to an increase in heart rate as well as contractility by β1 agonism) and decreases cardiac afterload (due to peripheral vasodilation by β2 agonism))
Cardiogenic shock
Cardiac stress testing

Adverse Effects:
Tachycardia and arrhythmias
Can precipitate angina or myocardial infarction in patients with coronary artery disease

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44
Q

Dopamine

A

Direct sympathomimetic drug

Mechanism:
D1 = D2 > β > α
Chronotropic effects at lower doses (β effect)
Vasoconstriction at high doses (α effect)
Raises BP (at high doses), HR, CO

Clinical Use:
Heart failure
Cardiogenic shock
Unstable bradycardia

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45
Q

Epinephrine

A

Direct sympathomimetic drug

Mechanism:
β > α (at high doses the α effect is predominant)
Stronger β2-receptor effect than norepinephrine
Raises BP (at high doses), HR, CO
Clinical Use:
Anaphylaxis
Cardiac arrest (IV epinephrine is used if the patient is hemodynamically unstable and requires cardiopulmonary resuscitation)
Septic shock
Postbypass hypotension
Asthma
Open-angle glaucoma
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46
Q

Fenoldopam

A

Direct sympathomimetic drug

Mechanism:
D1
Vasodilates coronary and peripheral vessels
Promotes natriuresis
Raises CO, HR
Lowers BP (through vasodilatation)

Clinical Use:
Hypertensive crisis
Postoperative hypertension

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47
Q

Isoproterenol

A

Direct sympathomimetic drug

Mechanism:
β1 = β2
Marginal α effect
Raises CO, HR
Lowers BP (through vasodilatation)

Clinical Use:
Bradycardia or heart block
It may worsen ischemia.
Cardiac arrest from heart block when pacemaker therapy is unavailable
Electrophysiologic evaluation of tachyarrhythmias.

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48
Q

Methyldopa

A

Direct sympathomimetic drug

Mechanism:
α2
Lowers BP

Clinical Use:
HTN, especially in pregnancy

Adverse Effects:
Direct Coombs ⊕ hemolysis, drug-induced lupus, hyperprolactinemia, peripheral edema

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49
Q

Midodrine

A

Direct sympathomimetic drug

Mechanism:
α1
Raises BP (through vasoconstriction)
Lowers HR
No change or decrease in CO

Clinical Use:
Autonomic insufficiency and symptomatic orthostatic hypotension

Adverse Effects:
May exacerbate supine hypertension.
Hypertension (due to peripheral vasoconstriction) and reflex bradycardia
Urinary retention
Ischemia and necrosis, especially of the fingers or toes
Piloerection

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50
Q

Mirabegron

A

Direct sympathomimetic drug

Mechanism:
β3
Raises BP

Clinical Use:
Urinary urge incontinence or overactive bladder

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51
Q

Norepinephrine

A

Direct sympathomimetic drug

Mechanism:
α1 > α2 > β1
Raises BP (through vasoconstriction)
Lowers HR (reflex bradycardia) as a response to the increased mean arterial pressure (MAP), which counteracts chronotropic effects
No change or increase in CO

Clinical Use:
Septic shock (used in attempts to increase peripheral vascular resistance. Dobutamine and vasopressin can also be administered in cases of reduced cardiac contractility and septic shock. Norepinephrine has a weaker β2 effect than epinephrine)
Neurogenic shock (preferred agent because α agonism increases peripheral vascular resistance (to counteract hypotension from loss of sympathetic tone) and β agonism increases heart rate (to counteract bradycardia from unopposed parasympathetic vagal tone))
Hypotension

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52
Q

Oxymetazoline

A

Direct sympathomimetic drug

Mechanism:
α1 > α2
May raise BP

Clinical Use:
Epistaxis
Rhinitis, sinusitis (topical decongestant)
Rosacea

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53
Q

Phenylephrine

A

Direct sympathomimetic drug

Mechanism:
α1 > α2
Raises BP (through vasoconstriction)
Lowers HR
No change or decrease in CO

Clinical Use:
Hypotension
Rhinitis, obstructed Eustachian tubes
Phenylephrine acts as a nasal decongestant by reducing hyperemia and mucosal edema
Allergic conjunctivitis
Open-angle glaucoma (has a mydriatic effect without causing cycloplegia)
Ischemic priapism (high-dose intracavernosal phenylephrine injection)

54
Q

Cocaine

A

Indirect sympathomimetic drug

Mechanism:
Increase the synaptic activity of endogenous catecholamines by inhibiting reuptake

Clinical Use:
Local anesthesia
Vasoconstriction
Causes mydriasis in eyes with intact sympathetic innervation –> fŽused to confirm Horner syndrome.

55
Q

Amphetamine

A

Indirect sympathomimetic drug

Mechanism:
Increase the synaptic activity of endogenous catecholamines by increasing presynaptic release and inhibiting reuptake

Clinical Use:
ADHD
Narcolepsy
Obesity

56
Q

Ephedrine

A

Indirect sympathomimetic drug

Mechanism:
Increase the synaptic activity of endogenous catecholamines by increasing presynaptic release

Clinical Use:
Anesthesia-induced hypotension
Urinary incontinence (to improve urinary continuity through activation of α-receptors within the bladder)
Nasal congestion (pseudoephedrine) (reduces hyperemia and edema and opens nasal meatus and Eustachian tubes)

Adverse Effects:
Hypertension
Reflex bradycardia (due to hypertension) or tachycardia
Dizziness
Nausea, vomiting
57
Q

Tizanidine

A

Sympatholytic drug

Mechanism:
α2 agonist

Clinical Use:
Muscle spasticity
ALS
Multiple sclerosis
Cerebral palsy

Adverse Effects:
Hypotension
Weakness
Xerostomia

58
Q

Phenoxybenzamine

A

Sympatholytic drugs

Mechanism:
Nonselective α receptor antagonists
Irreversible blockade can only be overcome by synthesis of new alpha adrenergic receptors, which can take up to 3 days or even longer.

Clinical Use:
Pheochromocytoma

Adverse Effects:
Reflex tachycardia (Caused by antagonism of cardiac α-2 receptors. Normally, these receptors trigger a negative feedback loop after activation of the sympathetic nervous system)
Orthostatic hypotension
59
Q

Phentolamine

A

Sympatholytic drugs

Mechanism:
Competitive and reversible α receptor antagonists

Clinical Use:
Hypertensive emergencies
Tyramine ingestion in patients on MAO inhibitors
Cocaine-induced hypertension (second-line) (should only be given to patients who do not fully respond to benzodiazepines, nitroglycerin, or calcium channel blockers)
Pheochromocytoma
Vasopressor extravasation

Adverse Effects:
Reflex tachycardia (Caused by antagonism of cardiac α-2 receptors. Normally, these receptors trigger a negative feedback loop after activation of the sympathetic nervous system)
Orthostatic hypotension
60
Q

Prazosin

A

Sympatholytic drugs

Mechanism:
α1-antagonist

Clinical Use:
Urinary symptoms of BPH (produce symptomatic improvement in patients with BPH by their action on smooth muscles present in prostate and bladder base. Patients with smooth muscle predominance best respond to treatment with alpha-1 blockers)
Hypertension
PTSD-related nightmares

Adverse Effects:
Orthostatic hypotension (contraction of veins and arterioles helps maintain blood pressure when standing up and is prevented by α-1 antagonism)
Retrograde ejaculation (muscles of the bladder neck are relaxed and cannot prevent retrograde ejaculation)
Dizziness, headache
Peripheral edema
Nausea, constipation
Intraoperative floppy iris syndrome (IFIS) (omplication of cataract surgery characterized by iris prolapse through the surgical incision and intraoperative pupillary constriction. May lead to retinal detachment and endophthalmitis)
Urinary frequency

61
Q

Terazosin

A

Sympatholytic drugs

Mechanism:
α1-antagonist

Clinical Use:
Benign prostatic hyperplasia
Arterial hypertension

Adverse Effects:
Orthostatic hypotension (contraction of veins and arterioles helps maintain blood pressure when standing up and is prevented by α-1 antagonism)
Retrograde ejaculation (muscles of the bladder neck are relaxed and cannot prevent retrograde ejaculation)
Dizziness, headache
Peripheral edema
Nausea, constipation
Intraoperative floppy iris syndrome (IFIS) (omplication of cataract surgery characterized by iris prolapse through the surgical incision and intraoperative pupillary constriction. May lead to retinal detachment and endophthalmitis)
Urinary frequency

62
Q

Doxazosin

A

Sympatholytic drugs

Mechanism:
α1-antagonist

Clinical Use:
Benign prostatic hyperplasia
Arterial hypertension

Adverse Effects:
Orthostatic hypotension (contraction of veins and arterioles helps maintain blood pressure when standing up and is prevented by α-1 antagonism)
Retrograde ejaculation (muscles of the bladder neck are relaxed and cannot prevent retrograde ejaculation)
Dizziness, headache
Peripheral edema
Nausea, constipation
Intraoperative floppy iris syndrome (IFIS) (omplication of cataract surgery characterized by iris prolapse through the surgical incision and intraoperative pupillary constriction. May lead to retinal detachment and endophthalmitis)
Urinary frequency

63
Q

Tamsulosin

A

Sympatholytic drugs

Mechanism:
α1-antagonist
Blocks alpha-1A/D (found on prostate) > alpha-1B receptors

Clinical Use:
Benign prostatic hyperplasia

Adverse Effects:
Orthostatic hypotension (contraction of veins and arterioles helps maintain blood pressure when standing up and is prevented by α-1 antagonism)
Retrograde ejaculation (muscles of the bladder neck are relaxed and cannot prevent retrograde ejaculation)
Dizziness, headache
Peripheral edema
Nausea, constipation
Intraoperative floppy iris syndrome (IFIS) (omplication of cataract surgery characterized by iris prolapse through the surgical incision and intraoperative pupillary constriction. May lead to retinal detachment and endophthalmitis)
Urinary frequency

64
Q

Acebutolol

A

Direct sympathomimetic drug with intrinsic sympathomimetic activity (ISA)

Mechanism:
Partial β-agonists
Selectively bind to and block β1 receptors, which are primarily found in the heart
Decrease the heart rate, contractility, and AVN conductivity

Clinical Use:
Coronary heart disease
Compensated heart failure
Cardiac arrhythmias (e.g., atrial fibrillation, atrial flutter, PSVT)

Adverse Effects:
Bradycardia
Bradyarrhythmia
Cardioselectivity is dose-dependent: β2 receptor blocking activity increases with higher doses (in high doses, cardioselective beta blockers lose their selectivity and can block β2 receptors as well, resulting in β2 receptor blockade-mediated adverse effect)
Generally do not cause bronchoconstriction or vasoconstriction
Generally do not interfere with glycogenolysis; safe in diabetic patients

65
Q

Atenolol

A

Cardioselective beta blockers (β1 selective) without intrinsic sympathomimetic activity (ISA)
Has low potential to penetrate the blood-brain barrier

Mechanism:
Selectively bind to and block β1 receptors, which are primarily found in the heart
Decrease the heart rate, contractility, and AVN conductivity

Clinical Use:
Coronary heart disease
Compensated heart failure
Cardiac arrhythmias (e.g., atrial fibrillation, atrial flutter, PSVT)

Adverse Effects:
Bradycardia
Bradyarrhythmia
Cardioselectivity is dose-dependent: β2 receptor blocking activity increases with higher doses (in high doses, cardioselective beta blockers lose their selectivity and can block β2 receptors as well, resulting in β2 receptor blockade-mediated adverse effect)
Generally do not cause bronchoconstriction or vasoconstriction
Generally do not interfere with glycogenolysis; safe in diabetic patients

66
Q

Bisoprolol

A

Cardioselective beta blockers (β1 selective) without intrinsic sympathomimetic activity (ISA)

Mechanism:
Selectively bind to and block β1 receptors, which are primarily found in the heart
Decrease the heart rate, contractility, and AVN conductivity

Clinical Use:
Coronary heart disease
Compensated heart failure
Cardiac arrhythmias (e.g., atrial fibrillation, atrial flutter, PSVT)

Adverse Effects:
Bradycardia
Bradyarrhythmia
Cardioselectivity is dose-dependent: β2 receptor blocking activity increases with higher doses (in high doses, cardioselective beta blockers lose their selectivity and can block β2 receptors as well, resulting in β2 receptor blockade-mediated adverse effect)
Generally do not cause bronchoconstriction or vasoconstriction
Generally do not interfere with glycogenolysis; safe in diabetic patients

67
Q

Carvedilol

A

Nonselective beta blockers (β1, β2, and β3 receptors) with additional α-blocking action
In addition to its α- and β-blocking action, also has antioxidant properties, which helps in the treatment of heart failure by decreasing disease progression and aiding ventricular remodeling.

Mechanism:
Potent vasodilators because of their α-blocking action (vasodilation → ↓ peripheral vascular resistance, ↓ preload, ↓ afterload, and ↑ renal blood flow; reduce portal hypertension and pressure gradient in hepatic venous)
Improve endothelial function and vascular remodeling (this may make them useful in the management of ischemic stroke.

Clinical Use:
Esophageal variceal bleeding (prophylactic use)

Adverse Effects:
Bronchoconstriction (may exacerbate asthma/COPD)
Vasoconstriction (avoid in patients with peripheral vascular disease)
Hypoglycemia and hyperglycemia
Bradycardia and syncope
Orthostatic hypotension

68
Q

Esmolol

A

Cardioselective beta blockers (β1 selective) without intrinsic sympathomimetic activity (ISA)
Rapidly acting, short-duration

Mechanism:
Selectively bind to and block β1 receptors, which are primarily found in the heart
Decrease the heart rate, contractility, and AVN conductivity

Clinical Use:
Coronary heart disease
Compensated heart failure
Cardiac arrhythmias (e.g., atrial fibrillation, atrial flutter, PSVT)
Aortic dissection

Adverse Effects:
Bradycardia
Bradyarrhythmia
Cardioselectivity is dose-dependent: β2 receptor blocking activity increases with higher doses (in high doses, cardioselective beta blockers lose their selectivity and can block β2 receptors as well, resulting in β2 receptor blockade-mediated adverse effect)
Generally do not cause bronchoconstriction or vasoconstriction
Generally do not interfere with glycogenolysis; safe in diabetic patients

69
Q

Labetalol

A

Nonselective beta blockers (β1, β2, and β3 receptors) with additional α-blocking action

Mechanism:
Potent vasodilators because of their α-blocking action (vasodilation → ↓ peripheral vascular resistance, ↓ preload, ↓ afterload, and ↑ renal blood flow; reduce portal hypertension and pressure gradient in hepatic venous)
Improve endothelial function and vascular remodeling (this may make them useful in the management of ischemic stroke.

Clinical Use:
Pregnancy-induced hypertension (e.g, labetalol)
Esophageal variceal bleeding (prophylactic use)

Adverse Effects:
Bronchoconstriction (may exacerbate asthma/COPD)
Vasoconstriction (avoid in patients with peripheral vascular disease)
Hypoglycemia and hyperglycemia
Bradycardia and syncope
Orthostatic hypotension

70
Q

Metoprolol

A

Cardioselective beta blockers (β1 selective) without intrinsic sympathomimetic activity (ISA)

Mechanism:
Selectively bind to and block β1 receptors, which are primarily found in the heart
Decrease the heart rate, contractility, and AVN conductivity

Clinical Use:
Coronary heart disease
Compensated heart failure
Cardiac arrhythmias (e.g., atrial fibrillation, atrial flutter, PSVT)

Adverse Effects:
Bradycardia
Bradyarrhythmia
Dyslipidemia
Cardioselectivity is dose-dependent: β2 receptor blocking activity increases with higher doses (in high doses, cardioselective beta blockers lose their selectivity and can block β2 receptors as well, resulting in β2 receptor blockade-mediated adverse effect)
Generally do not cause bronchoconstriction or vasoconstriction
Generally do not interfere with glycogenolysis; safe in diabetic patients

71
Q

Nadolol

A

Nonselective beta blockers (β1, β2, and β3 receptors) without intrinsic sympathomimetic activity (ISA)

Mechanism:
Block β1, β2, and β3 receptors

Clinical Use:
Alternative to cardioselective beta blockers
Nonbleeding esophageal varices.

Adverse Effects:
Bronchoconstriction (may exacerbate asthma/COPD)
Vasoconstriction (avoid in patients with peripheral vascular disease)
Hypoglycemia and hyperglycemia
Bradycardia and syncope

72
Q

Nebivolol

A

Cardioselective beta blockers (β1 selective) without intrinsic sympathomimetic activity (ISA)

Mechanism:
Selectively bind to and block β1 receptors, which are primarily found in the heart
Decrease the heart rate, contractility, and AVN conductivity
The only beta blocker that causes NO-mediated vasodilation: it decreases vascular resistance by stimulating β3 receptors and activating NO synthase in the vasculature. The drug has the advantages of a beta blocker with additional alpha-blocking properties. It is a long-acting drug requiring once-daily dosing.

Clinical Use:
Coronary heart disease
Compensated heart failure
Cardiac arrhythmias (e.g., atrial fibrillation, atrial flutter, PSVT)

Adverse Effects:
Bradycardia
Bradyarrhythmia
Cardioselectivity is dose-dependent: β2 receptor blocking activity increases with higher doses (in high doses, cardioselective beta blockers lose their selectivity and can block β2 receptors as well, resulting in β2 receptor blockade-mediated adverse effect)
Generally do not cause bronchoconstriction or vasoconstriction
Generally do not interfere with glycogenolysis; safe in diabetic patients

73
Q

Pindolol

A

Nonselective beta blockers (β1, β2, and β3 receptors) with intrinsic sympathomimetic activity (ISA)

Mechanism:
Partial β-agonists
Block β1, β2, and β3 receptors

Clinical Use:
Alternative to cardioselective beta blockers

Adverse Effects:
Bronchoconstriction (may exacerbate asthma/COPD)
Vasoconstriction (avoid in patients with peripheral vascular disease)
Hypoglycemia and hyperglycemia
Bradycardia and syncope

74
Q

Propranolol

A

Nonselective beta blockers (β1, β2, and β3 receptors) without intrinsic sympathomimetic activity (ISA)

Mechanism:
Block β1, β2, and β3 receptors
Does not significantly lower blood pressure

Clinical Use:
Alternative to cardioselective beta blockers
Essential tremor 
Migraine prophylaxis
Portal hypertension 
Hyperthyroidism and thyroid storm 
Infantile hemangioma
Akathisia

Adverse Effects:
Bronchoconstriction (may exacerbate asthma/COPD)
Vasoconstriction (avoid in patients with peripheral vascular disease)
Hypoglycemia and hyperglycemia
Bradycardia and syncope

75
Q

Timolol

A

Nonselective beta blockers (β1, β2, and β3 receptors) without intrinsic sympathomimetic activity (ISA)

Mechanism:
Block β1, β2, and β3 receptors

Clinical Use:
Alternative to cardioselective beta blockers
Glaucoma
Migraine prophylaxis

Adverse Effects:
Bronchoconstriction (may exacerbate asthma/COPD)
Vasoconstriction (avoid in patients with peripheral vascular disease)
Hypoglycemia and hyperglycemia
Bradycardia and syncope

76
Q

Apraclonidine

A

Direct sympathomimetic drug

Mechanism:
α2-agonist
Decrease aqueous humor synthesis

Clinical Use:
Glaucoma

Adverse Effects:
Blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritus

77
Q

Brimonidine

A

Direct sympathomimetic drug

Mechanism:
α2 adrenergic agonist.
Decreases the production of aqueous humor
Induce vasoconstriction (topical)

Clinical Use:
Open-angle glaucoma and ocular hypertension.
Rosacea-associated erythema.

Adverse Effects:
Do not use in closed-angle glaucoma
Blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritus

78
Q

Pseudoephedrine

A

Direct sympathomimetic drug

Mechanism:
α1 >α2
Constricts blood vessels in the nose and thereby reduces edema, hyperemia, and congestion. Also some stimulation of β2-adrenergic receptors causing smooth muscle tissue in respiratory bronchioles to dilate.

Clinical Use:
Nasal congestion (pseudoephedrine) (reduces hyperemia and edema and opens nasal meatus and Eustachian tubes)

Adverse Effects:
Hypertension
Reflex bradycardia (due to hypertension) or tachycardia
Dizziness
Nausea, vomiting
Rebound congestion (when used > 4–6 days)
Anxiety and/or ↑ CNS stimulation (e.g., alertness, nervousness, insomnia)
Tachyphylaxis

79
Q

Dexmedetomidine

A

Sympatholytic drug

Mechanism:
α2 agonist

Clinical Use:
Sedation

Adverse Effects:
Agitation
Orthostatic hypotension
Bradycardia
Hypertension 
Constipation
Nausea
Sedation
80
Q

Alfuzosin

A

Sympatholytic drugs

Mechanism:
α1-antagonist

Clinical Use:
Benign prostatic hyperplasia

Adverse Effects:
Orthostatic hypotension (contraction of veins and arterioles helps maintain blood pressure when standing up and is prevented by α-1 antagonism)
Retrograde ejaculation (muscles of the bladder neck are relaxed and cannot prevent retrograde ejaculation)
Dizziness, headache
Peripheral edema
Nausea, constipation
Intraoperative floppy iris syndrome (IFIS) (omplication of cataract surgery characterized by iris prolapse through the surgical incision and intraoperative pupillary constriction. May lead to retinal detachment and endophthalmitis)
Urinary frequency

81
Q

Silodosin

A

Sympatholytic drugs

Mechanism:
α1-antagonist

Clinical Use:
Benign prostatic hyperplasia

Adverse Effects:
Orthostatic hypotension (contraction of veins and arterioles helps maintain blood pressure when standing up and is prevented by α-1 antagonism)
Retrograde ejaculation (muscles of the bladder neck are relaxed and cannot prevent retrograde ejaculation)
Dizziness, headache
Peripheral edema
Nausea, constipation
Intraoperative floppy iris syndrome (IFIS) (omplication of cataract surgery characterized by iris prolapse through the surgical incision and intraoperative pupillary constriction. May lead to retinal detachment and endophthalmitis)
Urinary frequency

82
Q

Mirtazapine

A

Sympatholytic drugs

Mechanism:
α2-antagonist
Also inhibits 5-HT2, 5-HT3 receptors, and H1-receptors.

Clinical Use:
Depression

Adverse Effects:
↑ Sedation
↑ Appetite and weight
Hypercholesterolemia

83
Q

Tetrabenazine

A

Monoamine-depleting agent

Mechanism:
Reversible inhibition of vesicular monoamine transporter-2 (VMAT-2) → impaired packaging of monoamines (dopamine, serotonin, and norepinephrine) into presynaptic vesicles → ↓ dopamine release

Clinical Use:
Hyperkinetic disorders (chorea associated with Huntington disease, Tourette syndrome, Tardive dyskinesia, Hemiballismus)
Adverse Effects:
Parkinson-like syndrome
Depression
Suicidal ideation
Sedation
Akathisia
Fatigue
84
Q

Reserpine

A

Monoamine-depleting agent

Mechanism:
Reversible inhibition of vesicular monoamine transporter-2 (VMAT-2) → impaired packaging of monoamines (dopamine, serotonin, and norepinephrine) into presynaptic vesicles → ↓ dopamine release

Clinical Use:
Tardive dyskinesia
Psychiatric disorders
Hypertension

Adverse Effects:
Parkinson-like syndrome
Depression
Angina
Bradycardia
Peripheral edema
Nasal obstruction
Diarrhea
85
Q

Celiprolol

A

Selective β1 blocker with intrinsic sympathomimetic activity (ISA)

Mechanism:
Selectively bind to and block β1 receptors, which are primarily found in the heart
Decrease the heart rate, contractility, and AVN conductivity

Clinical Use:
Coronary heart disease
Compensated heart failure
Cardiac arrhythmias (e.g., atrial fibrillation, atrial flutter, PSVT)

Adverse Effects:
Bradycardia
Bradyarrhythmia
Cardioselectivity is dose-dependent (β2 receptor blocking activity increases with higher doses)
Generally do not cause bronchoconstriction or vasoconstriction
Generally do not interfere with glycogenolysis; safe in diabetic patients

86
Q

Bucindolol

A

Nonselective beta blockers (β1, β2, and β3 receptors) with additional α-blocking action

Mechanism:
Potent vasodilators because of their α-blocking action (vasodilation → ↓ peripheral vascular resistance, ↓ preload, ↓ afterload, and ↑ renal blood flow; reduce portal hypertension and pressure gradient in hepatic venous)
Improve endothelial function and vascular remodeling (this may make them useful in the management of ischemic stroke.

Clinical Use:
Esophageal variceal bleeding (prophylactic use)

Adverse Effects:
Bronchoconstriction (may exacerbate asthma/COPD)
Vasoconstriction (avoid in patients with peripheral vascular disease)
Hypoglycemia and hyperglycemia
Bradycardia and syncope
Orthostatic hypotension

87
Q

α1-agonists Adverse Effects

A
  • Hypertension (due to peripheral vasoconstriction) and reflex bradycardia
  • Urinary retention (α1 agonists are responsible for the contraction of the bladder neck)
  • Ischemia and necrosis, especially of the fingers or toes (caused by the vasoconstrictive effects of α1 agonists. Patients with hypovolemia are at the highest risk of this side effect)
  • Rebound congestion (with nasal decongestants used > 4–6 days)
  • Piloerection
88
Q

α2-agonists Adverse Effects

A

Mainly due to their sympatholytic effects

  • CNS depression (e.g., sedation)
  • Respiratory depression
  • Bradycardia and hypotension
  • Miosis
  • Rebound hypertension after sudden interruption (can occur up to 20 hours after cessation of the α2-agonist)
  • Dry mouth (typically seen with clonidine; the mechanism by which clonidine causes this side effect is not completely understood)
89
Q

β1-agonists Adverse Effects

A

Tachycardia and arrhythmias

Can precipitate angina or myocardial infarction in patients with coronary artery disease

90
Q

β2-agonists Adverse Effects

A

Tremor (most common side effect), agitation, insomnia, diaphoresis
Hypotension (due to peripheral vasodilation) and reflex tachycardia
Metabolic disturbances (hyperglycemia, hypokalemia)

91
Q

β Blockers Absolute Contraindications

A
  • Symptomatic bradycardia (<50 bpm)
  • Cardiogenic shock and hypotension (systolic blood pressure below 90 mm Hg)
  • Pheochromocytoma (administration of beta blockers before alpha blockers → unopposed α-adrenoceptor mediated vasoconstriction → hypertensive crisis (except nonselective beta blockers with α-antagonism, such as carvedilol and labetalol))
  • Decompensated heart failure
  • Combination with calcium channel blockers (diltiazem or verapamil) because can precipitate AV block (both groups of drugs have a negative dromotropic effect (delayed AV transmission))
  • Sick sinus syndrome (without a pacemaker); heart block greater than first-degree
92
Q

Nonspecific phosphodiesterase inhibitors

inhibitors of PDE3, 4, and 5

A

Theophylline (methylxanthines)

Mechanism:
Nonspecific PDE inhibition → ↓ hydrolysis of cAMP → ↑ cAMP levels
Adenosine receptor blockade
Inhibition of proinflammatory mediators
Deceleration of fibrotic changes in the lung
Relaxation of the bronchial musculature → bronchodilation

Clinical Use:
COPD (severe and refractory cases)
Asthma

Adverse Effects:
Usage is limited because of narrow therapeutic index (cardiotoxicity, neurotoxicity)
Metabolized by cytochrome P-450.
Nausea, vomiting, arrhythmias and seizures
Seizures are the major cause of morbidity and mortality in theophylline intoxication.

93
Q

Theophylline (methylxanthines)

A

Nonspecific phosphodiesterase inhibitors
(inhibitors of PDE3, 4, and 5)

Mechanism:
Nonspecific PDE inhibition → ↓ hydrolysis of cAMP → ↑ cAMP levels
Adenosine receptor blockade
Inhibition of proinflammatory mediators
Deceleration of fibrotic changes in the lung
Relaxation of the bronchial musculature → bronchodilation

Clinical Use:
COPD (severe and refractory cases)
Asthma

Adverse Effects:
Usage is limited because of narrow therapeutic index (cardiotoxicity, neurotoxicity) (adenosine receptor block seems to be mainly responsible for severe cardiac and neurological side effects)
Metabolized by cytochrome P-450.
Nausea, vomiting, arrhythmias and seizures
Seizures are the major cause of morbidity and mortality in theophylline intoxication.

94
Q

Sildenafil

A

Phosphodiesterase type 5 inhibitor (PDE5 inhibitor)

Mechanism:
PDE5 inhibition → ↓ breakdown of cGMP → ↑ cGMP → ↑ smooth muscle relaxation in reaction to nitrous oxide activation → pulmonary vasodilation, penile smooth muscle relaxation, and increased blood flow
Decrease in pulmonary vascular resistance
↑ Blood flow in the corpus cavernosum → increase in penis size during an erection
Inhibition of proinflammatory mediators
Deceleration of fibrotic changes in the lung
Relaxation of the bronchial musculature

Clinical Use:
Erectile dysfunction
Pulmonary hypertension

Adverse Effects:
Headaches, cutaneous flushing (due to vasodilation)
Lightheadedness
Runny nose, nasal congestion
Exanthema
Dyspepsia
Hypotension in patients taking nitrates and alpha blockers
Cyanopia (blue- tinted vision) via inhibition of PDE-6 in retina (only sildenafil)
Rarely → myocardial infarction, stroke, hearing loss, optic neuropathy

95
Q

Tadalafil

A

Phosphodiesterase type 5 inhibitor (PDE5 inhibitor)

Mechanism:
PDE5 inhibition → ↓ breakdown of cGMP → ↑ cGMP → ↑ smooth muscle relaxation in reaction to nitrous oxide activation → pulmonary vasodilation, penile smooth muscle relaxation, and increased blood flow

Clinical Use:
Erectile dysfunction
Pulmonary hypertension
BPH (only tadalafil)

Adverse Effects:
Headaches, cutaneous flushing (due to vasodilation)
Lightheadedness
Runny nose, nasal congestion
Exanthema
Dyspepsia
Hypotension in patients taking nitrates and alpha blockers
Rarely → myocardial infarction, stroke, hearing loss, optic neuropathy

96
Q

Roflumilast

A

Phosphodiesterase type 4 inhibitor (PDE4 inhibitor)

Mechanism:
PDE4 inhibition → ↑ cAMP in bronchial epithelium, granulocytes, and neutrophils
Inhibition of proinflammatory mediators
Deceleration of fibrotic changes in the lung
Relaxation of the bronchial musculature

Clinical Use:
Severe COPD

Adverse Effects:
GI upset (nausea, abdominal pain)
Weight loss
Mental disorders (sleep disturbances, anxiety, depression)

97
Q

Milrinone

A

Phosphodiesterase type 3 inhibitor (PDE3 inhibitor)

Mechanism:
PDE3 inhibition → ↑ cAMP
-In the myocardium → ↑ cAMP → activation of calcium channels → cardiostimulatory effects → ↑ inotropy and ↑ chronotropy
-In peripheral vessels → ↑ cAMP → inhibition of myosin light chain kinase → smooth muscle relaxation → vasodilation with reduced cardiovascular preload and afterload
-In platelets → ↑ cAMP → inhibited platelet aggregation
-Increase cardiac contractility acutely in cardiac failure
-Vasodilation and antiplatelet action in intermittent claudication
-Inhibition of platelet aggregation for angina prophylaxis, TIA/stroke prevention, and deceleration of restenosis in coronary stents

Clinical Use:
Acute treatment of decompensated cardiac failure with cardiogenic shock (usually in combination with other drugs (e.g., ACE inhibitors, diuretics))

Adverse Effects:
Tachycardia, ventricular arrhythmias (most common and severe side effect, so not recommended for chronic use) (the severity of this side effect is the reason why PDE3 inhibitors are not recommended for patients with acute heart failure)
Headaches, nausea
Hypotension
Gastrointestinal upset
Facial flushing

Contraindications:
Severe obstructive cardiomyopathy or ventricular aneurysm
Hypovolemia
Tachycardia

98
Q

Amrinone

A

Phosphodiesterase type 3 inhibitor (PDE3 inhibitor)

Mechanism:
PDE3 inhibition → ↑ cAMP
-In the myocardium → ↑ cAMP → activation of calcium channels → cardiostimulatory effects → ↑ inotropy and ↑ chronotropy
-In peripheral vessels → ↑ cAMP → inhibition of myosin light chain kinase → smooth muscle relaxation → vasodilation with reduced cardiovascular preload and afterload
-In platelets → ↑ cAMP → inhibited platelet aggregation
-Increase cardiac contractility acutely in cardiac failure
-Vasodilation and antiplatelet action in intermittent claudication
-Inhibition of platelet aggregation for angina prophylaxis, TIA/stroke prevention, and deceleration of restenosis in coronary stents

Clinical Use:
Acute treatment of decompensated cardiac failure with cardiogenic shock (usually in combination with other drugs (e.g., ACE inhibitors, diuretics))

Adverse Effects:
Tachycardia, ventricular arrhythmias (most common and severe side effect, so not recommended for chronic use) (the severity of this side effect is the reason why PDE3 inhibitors are not recommended for patients with acute heart failure)
Headaches, nausea
Hypotension
Gastrointestinal upset
Facial flushing

Contraindications:
Severe obstructive cardiomyopathy or ventricular aneurysm
Hypovolemia
Tachycardia

99
Q

Enoximone

A

Phosphodiesterase type 3 inhibitor (PDE3 inhibitor)

Mechanism:
PDE3 inhibition → ↑ cAMP
-In the myocardium → ↑ cAMP → activation of calcium channels → cardiostimulatory effects → ↑ inotropy and ↑ chronotropy
-In peripheral vessels → ↑ cAMP → inhibition of myosin light chain kinase → smooth muscle relaxation → vasodilation with reduced cardiovascular preload and afterload
-In platelets → ↑ cAMP → inhibited platelet aggregation
-Increase cardiac contractility acutely in cardiac failure
-Vasodilation and antiplatelet action in intermittent claudication
-Inhibition of platelet aggregation for angina prophylaxis, TIA/stroke prevention, and deceleration of restenosis in coronary stents

Clinical Use:
Acute treatment of decompensated cardiac failure with cardiogenic shock (usually in combination with other drugs (e.g., ACE inhibitors, diuretics))

Adverse Effects:
Tachycardia, ventricular arrhythmias (most common and severe side effect, so not recommended for chronic use) (the severity of this side effect is the reason why PDE3 inhibitors are not recommended for patients with acute heart failure)
Headaches, nausea
Hypotension
Gastrointestinal upset
Facial flushing

Contraindications:
Severe obstructive cardiomyopathy or ventricular aneurysm
Hypovolemia
Tachycardia

100
Q

Cilostazol

A

Nonspecific phosphodiesterase inhibitor

Mechanism:
PDE3 inhibition → ↑ cAMP
-In the myocardium → ↑ cAMP → activation of calcium channels → cardiostimulatory effects → ↑ inotropy and ↑ chronotropy
-In peripheral vessels → ↑ cAMP → inhibition of myosin light chain kinase → smooth muscle relaxation → vasodilation with reduced cardiovascular preload and afterload
-In platelets → ↑ cAMP → inhibited platelet aggregation
-Vasodilation and antiplatelet action in intermittent claudication (especially cilostazol, which has weaker cardiac inotropic effects)
-Inhibition of platelet aggregation for angina prophylaxis, TIA/stroke prevention, and deceleration of restenosis in coronary stents

Clinical Use:
Intermittent vascular claudication
Antiplatelet (antianginal, TIA/stroke prevention) (with aspirin)
Coronary stent restenosis prophylaxis

Adverse Effects:
Nausea, headache, facial flushing, hypotension, abdominal pain

101
Q

Dipyridamole

A

Phosphodiesterase type 3 inhibitor (PDE3 inhibitor)

Mechanism:
PDE3 inhibition → ↑ cAMP
-In the myocardium → ↑ cAMP → activation of calcium channels → cardiostimulatory effects → ↑ inotropy and ↑ chronotropy
-In peripheral vessels → ↑ cAMP → inhibition of myosin light chain kinase → smooth muscle relaxation → vasodilation with reduced cardiovascular preload and afterload
-In platelets → ↑ cAMP → inhibited platelet aggregation; ↓ Adenosine reuptake → ↑ extracellular adenosine concentration → vasodilation (dipyridamole)
-Increase cardiac contractility acutely in cardiac failure (with the exception of cilostazol)
-Vasodilation and antiplatelet action in intermittent claudication (especially cilostazol, which has weaker cardiac inotropic effects)
-Inhibition of platelet aggregation for angina prophylaxis, TIA/stroke prevention, and deceleration of restenosis in coronary stents
-Dipyridamole dilates the coronary arteries and can therefore be used in cardiac stress testing

Clinical Use:
Cardiac stress testing (dipyridamole only, due to coronary vasodilation)
Intermittent vascular claudication
Antiplatelet (antianginal, TIA/stroke prevention) (with aspirin)
Coronary stent restenosis prophylaxis

Adverse Effects:
Nausea, headache, facial flushing, hypotension, abdominal pain

102
Q

Amphetamines Toxicity Antidote/Management

A

Enhance sympathetic effect → serotonin syndrome

Benzodiazepines (sedation and control of seizures)
Ammonium chloride (acidifies urine, which results in increased excretion of basic amphetamines)
103
Q

Antimuscarinic/anticholinergic agents (e.g., atropine, medications with anticholinergic effects, jimson weed, deadly nightshade) Poisoning Antidote/Management

A

Physostigmine (crosses blood brain barrier)

104
Q

Barbiturates Toxicity Antidote/Management

A

Sodium bicarbonate (alkalizes urine, which results in increased excretion of acidic barbiturates)

105
Q

Benzodiazepines Toxicity Antidote/Management

A

Flumazenil

106
Q

Digitalis Toxicity Antidote/Management

A

Inhibits Na+/K+-ATPase → cardiac arrhythmias, xanthopsia

Digoxin-specific antibody

107
Q

Dabigatran Toxicity Antidote/Management

A

Renal elimination → supratherapeutic levels → excessive bleeding, acute renal failure

Idarucizumab

108
Q

Heparin Toxicity Antidote/Management

A

Increases activity of antithrombin → excessive bleeding

Protamine sulfate

109
Q

Opioids Toxicity Antidote/Management

A

Naloxone

110
Q

Salicylates Toxicity Antidote/Management

A

Salicylate metabolites accumulate in liver → hepatic failure and metabolic acidosis

Sodium bicarbonate (alkalinize urine)
Activated charcoal
Dialysis
111
Q

Thrombolytic agents (e.g., recombinant tPA) Toxicity Antidote/Management

A

Catalyze conversion of plasminogen to plasmin → excessive bleeding

Aminocaproic acid

112
Q

Tricyclic antidepressants Toxicity Antidote/Management

A

Muscarinic ACh receptor inhibition → anticholinergic syndrome

Sodium bicarbonate (to stabilize cardiac cell membrane)
Benzodiazepines for control of seizures
Activated charcoal
113
Q

Warfarin Toxicity Antidote/Management

A

Vitamin K antagonism (γ-carboxylation of clotting factors) → excessive bleeding

Fresh frozen plasma (immediate effect) and/or prothrombin complex concentrate (immediate antidote)
Vitamin K (delayed antidote)
114
Q

Carbon dioxide Toxicity Antidote/Management

A

↑ CO2 decreases O2 concentration → headaches, cardiac arrhythmias, respiratory depression, coma

Normal or high concentration oxygen depending on severity

115
Q

Arsenic Toxicity Antidote/Management

A

Dimercaprol

Succimer

116
Q

Carbon monoxide Toxicity Antidote/Management

A

Formation of carboxyhemoglobin → tissue hypoxia → cherry-red skin tone with bullous skin lesions, somnolence, agitation, headache, vomiting, coma

100% high-flow oxygen
Consider HBOT

117
Q

Cyanide Toxicity Antidote/Management

A

Blocks electron transport chain → anion gap metabolic lactic acidosis, bitter almond breath, altered mental status

Hydroxycobalamin
Methemoglobin-forming agents (e.g.,amyl nitrite, sodium nitrite, 4-DMAP)
Sodium thiosulfate

118
Q

Gold Toxicity Antidote/Management

A

Dimercaprol
Succimer
Penicillamine

119
Q

Lead Toxicity Antidote/Management

A

Dimercaprol
Succimer
Penicillamine
EDTA

120
Q

Mercury Toxicity Antidote/Management

A

Dimercaprol

Succimer

121
Q

Copper Toxicity Antidote/Management

A

Penicillamine

Trientine

122
Q

Iron Toxicity Antidote/Management

A

Deferoxamine
Deferasirox
Deferiprone

123
Q

Methanol Toxicity Antidote/Management

A

Formation of toxic metabolites in the liver → anion gap metabolic acidosis, seizures, dyspnea

Fomepizole
Ethanol (less effective than fomepizole)
Dialysis

124
Q

Ethylene glycol (antifreeze) Toxicity Antidote/Management

A

Formation of toxic metabolites in the liver → anion gap metabolic acidosis, seizures, dyspnea

Fomepizole
Ethanol (less effective than fomepizole)
Dialysis

125
Q

Ethylene glycol (antifreeze) Toxicity Antidote/Management

A

Formation of toxic metabolites in the liver → anion gap metabolic acidosis, seizures, dyspnea

Fomepizole
Ethanol (less effective than fomepizole)
Dialysis

126
Q

Methemoglobin Toxicity Antidote/Management

A

Cannot bind oxygen → cyanosis, coma, brown blood (see methemoglobinemia)

Methylene blue
Vitamin C (weak reducing agent)
127
Q

Cytochrome P-450 Inhibitors

A 
Sodium valproate
Isoniazid (weak inhibitor)
Cimetidine
Ketoconazole
Fluconazole
Acute alcohol overuse 
Chloramphenicol 
Erythromycin/clarithromycin Sulfonamides
Ciprofloxacin 
Omeprazole 
Metronidazole 
Amiodarone 
Ritonavir 
Grapefruit juice
Gingko biloba
128
Q

Cytochrome P-450 Substrates

A

Theophylline
OCPs
Anti-epileptics
Statins (except pravastatin)

Lansoprazole
Carbamazepine
Haloperidol
Cyclosporin
Tacrolimus
Benzodiazepine
Ca+2 channel blockers
129
Q

Cytochrome P-450 Inducers

A 
St. John’s wort 
Griseofulvin 
Carbamazepine 
Chronic alcohol overuse 
Rifampin
Modafinil 
Nevirapine 
Phenytoin 
Phenobarbital
Primidone
Glucocorticoids
130
Q

Sulfa Drugs

A 
Sulfonamide antibiotics
Sulfasalazine
Probenecid
Furosemide
Acetazolamide
Celecoxib
Thiazides
Sulfonylureas
131
Q

Platinum agent (eg, cisplatin, carboplatin and oxaliplatin) Toxicity

A

Prevent nephrotoxicity with amifostine (free radical scavenger) and chloride (saline) diuresis.

STEP1 (38 decks)

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