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Block 2 > Block 2 pharma > Flashcards

Block 2 pharma Flashcards

1
Q

Isoproterenol

Classification and main clinical applications

A

Classification:
• Sympathomimetic
• Nonselective beta agonist

Main clinical applications:
• Bronchodilator

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2
Q

Epinephrine

Classification and main clinical applications

A

Classification:
• Sympathomimetic
• Alpha1,2 / beta1,2 adrenergic agonist

Main clinical applications:
• Cardiac stimulant
• Bronchodilator
• Vasoconstrictor

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3
Q

Isoproterenol

Pharmacodynamics and adverse effects

A

Pharmacodynamics: Mechanisms/sites of action:
• B1 stimulation leads to positive inotropic and chronotropic effects
• B2 stimulation causes relaxation of bronchial smooth muscle and vasodilation in skeletal muscle
• As an inotrope, isoproterenol has largely been replaced by dobutamine, a B1 selective agonist

Adverse effects:
• Dizziness, flushing, headache; mild tremors

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4
Q

Epinephrine

Pharmacodynamics and adverse effects

A

Pharmacodynamics: Mechanisms/sites of action:
• Stimulation of alpha receptors leads to arteriolar vasoconstriction; increases gluconeogenesis and inhibits insulin release
• Stimulation of beta receptors induces positive chronotropic and inotropic responses
• Stimulation of beta2 receptors: increases glycogenolysis in liver and skeletal muscle

Adverse effects:
• Rapid heart beat, headache, tremors

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5
Q

Norepinephrine

Classification and main clinical applications

A

Classification:
• Sympathomimetic
• Alpha1,2/beta1 adrenergic agonist

Main clinical applications:
• Potent vasoconstrictor and positive inotropic agent

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6
Q

Norepinephrine

Pharmacodynamics and adverse effects

A

Pharmacodynamics: Mechanisms/sites of action
• Acts on alpha adrenergic receptors to induce vasoconstriction, resulting in increases in peripheral vascular resistance
• Acts on beta1 receptors, resulting in cardiac stimulation

Adverse effects
• Hypertension, local vasoconstriction

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7
Q

Dobutamine

Classification and main clinical applications

A

Classification:
• Sympathomimetic
• Selective B1 adrenergic agonist with weak B2 agonist activity

Main clinical applications:
• Increases myocardial contractility and stroke volume
• Short-term management of patients with cardiac decompensation

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8
Q

Dobutamine

Pharmacodynamics and adverse effects

A

Pharmacodynamics: Mechanisms/sites of action:
• Increases myocardial contractility in a dose-dependent manner acting on beta1 receptors
• Half-life is approx. 2 min (note: unlike dopamine, dobutamine does not affect dopaminergic receptors)
• Mild increase in vasodilation

Adverse effects:
• Increased BP, increased ventricular ectopic activity, sinus tachycardia

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9
Q

Phenylephrine

Classification and main clinical applications

A

Classification:
• Sympathomimetic
• Selective alpha1 adrenergic agonist

Main clinical applications:
• Vasoconstrictor used to treat nasal congestion
• Can be used topically to induce mydriasis

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10
Q

Phenylephrine

Pharmacodynamics and adverse effects

A

Pharmacodynamics: mechanisms/sites of action
• Agonist actions at alpha1 receptors

Adverse effects:
• Peripheral and visceral vasoconstriction, reflex bradycardia

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11
Q

Terbutaline

Classification and main clinical applications

A

Classification:
• Sympathomimetic
• Selective B2 adrenergic agonist

Main clinical applications:
• Bronchodilator used for the treatment of bronchospasm / asthma

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12
Q

Terbutaline

Pharmacodynamics and adverse effects

A

Pharmacodynamics: mechanisms/sites of action:
• Selective agonist actions at B2 receptors

Adverse effects:
• Central nervous system: nervousness
• Neuromuscular/skeletal: tremor

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13
Q

Alpha adrenergic partial agonists (oxymetazoline, tetrahydrozoline, naphazoline)

Classification and main clinical applications

A

Classification:
• Alpha adrenergic partial agonist

Main clinical applications:
• Nasal congestion associated with acute or chronic rhinitis, sinusitis, common cold, allergies
• Ocular decongestant to relieve eye redness

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14
Q

Alpha adrenergic partial agonists (oxymetazoline, tetrahydrozoline, naphazoline)

Pharmacodynamics and adverse effects

A

Pharmacodnamics: Mechanisms/sites of action:
• Intranasal and ophthalmic topical vasoconstrictor
• Stimulate alpha-adrenergic receptors; topical application to mucous membranes causes intense vasoconstriction resulting in shrinkage of mucous membranes; ophthalmic administration causes vasoconstriction of conjunctival blood vessels

Adverse effects:
• Transient burning, stinging, dryness of the nasal mucosa
• Upon discontinuation following prolonged use, rebound congestion can occur

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15
Q

Midodrine

Clissification and main clinical applications

A

Classification:
• Selective alpha1 adrenergic agonist

Main clinical applications:
• Symptomatic orthostatic hypotension

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16
Q

Midodrine

Pharmacodynamcis and adverse effects

A

Pharmacodynamics: Mechanism and sites of action:
• Vasoconstriction
• A prodrug that is metabolized to an active metabolite, desglymidodrine, that produces an increase in vascular tone and elevates BP

Adverse effects:
• Usually well tolerated
• Supine hypertension can occur

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17
Q

Clonidine

Classification and main clinical applications

A

Classification:
• Selective a2 adrenergic partial agonist

Main clinical applications:
• Antihypertensive agent (centrally acting)
• Analgesic

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18
Q

Clonidine

Pharmacodynamics

A

Partial agonist actions at presynaptic alpha2 receptors in the medulla brain region result in inhibition of sympathetic outflow and tone. Suppression of efferent sympathetic pathways decreases vascular tone in the heart, kidneys and peripheral vasculature; lowers peripheral resistance and reduces BP. Reflex tachycardia usually does not occur; reciprocal increase in vagal tone, causing an increase in baroreceptor activity and bradycardia.

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19
Q

Clonidine

Adverse effects

A
  • Orthostatic hypotension, palpitations, and sinus bradycardia
  • Drowsiness, fatigue
20
Q

Propanolol

Classification and main clinical applications

A

Classification:
• Sympatholytic
• Nonselective beta receptor antagonist

Main clinical applications:
• Management of hypertension; angina pectoris, arrhythmia
• Migraine headache prophylaxis
• Off label: essential tremor, ethanol withdrawal, performance anxiety

21
Q

Propanolol

Pharmacodynamics and adverse effects

A

Pharmacodynamics: Mechanisms/sites of action:
• Competitively blocks response to beta1 and beta2 adrenergic stimulation; cardiovascular changes: decrease in heart rate, myocardial contractility, blood pressure and myocardial oxygen demand

Adverse effects:
• Generally mild and temporary, bradycardia CNS: dizziness, nausea

22
Q

Metoprolol

Classification and main clinical applications

A

Classification:
• Sympatholytic
• Selective B1 antagonist

Main clinical applications:
• Treatment of angina pectoris, hypertension or hemodynamically stable acute myocardial infarction

23
Q

Metoprolol

Pharmacodynamics and adverse effects

A

Pharmacodynamics: Mechanisms/sites of action
• Negative chronotropic effect that decreases heart rate at rest and after exercise, a negative inotropic effect that decreases cardiac output. There is also reduction of sympathetic outflow from the CNS; suppression of renin release from kidneys

Adverse effects:
• Bradycardia, shortness of breath

24
Q

Carvedilol

Classification and main clinical applications

A

Classification:
• Sympatholytic
• Nonselective beta antagonist; alpha antagonist (beta >> alpha)

Main clinical applications:
• Treatment of mild and moderate CHF; for treatment of hypertension in patients with angina, prior myocardial infarction or heart failure

25
Q

Carvedilol

Pharmacodynamics and adverse effects

A

Pharmacodynamics: Mechanisms/sites of action
• As a racemic mixture, carvedilol has nonselective beta-adrenoreceptor and alpha-adrenergic blocking activity; reduction of cardiac output, exercise- or beta-agonist induced tachycardia, reduction of reflex orthostatic tachycardia, vasodilation, decreased peripheral vascular resistance, decreased renal vascular resistance, reduced plasma renin activity, and increased levels of atrial natiuretic peptied
Adverse effects:
• Bradycardia, postural hypotension

26
Q

Phenoxybenzamine

Classification and main clinical applications

A

Classification:
• Sympatholytic
• Nonselective, irreversible alpha-antagonist

Main clinical applications:
• Symptomatic management of pheochromocytoma; treatment of hypertensive crisis caused by sypathomimetic amines

27
Q

Phenoxybenzamine

Pharmacodynamics and adverse effects

A

Pharmacodynamics: Mechanisms/sites of action
• Irreversible antagonist at both alpha1 and alpha2 receptors

Adverse effects:
• CNS: fatigue, headache

28
Q

Phentolamine

Classification and main clinical applications

A

Classification:
• Sympatholytic
• Non-selective, competitive alpha-antagonist

Main clinical applications:
• Pheochromocytoma and treatment of hypertension in pheochromocytoma

29
Q

Phentolamine

Pharmacodynamics and adverse effects

A

Pharmacodynamics: mechanisms/sites of action
• Competitive antagonist at peripheral alpha1 and alpha2 adrenergic receptors

Adverse effects:
• Cardiovascular: tachycardia, arrhythmia

30
Q

Prazosin (same class: terazosin, doxazosin)

Classification and main clinical applications

A

Classification:
• Sympatholytic
• Competitive alpha1 receptor antagonist

Main clinical applications:
• Treatment of hypertension
• Off-label: benign prostate hypertrophy (BPH)

31
Q

Prazosin (same class: terazosin, doxazosin)

Pharmacodynamics

A

Pharmacodynamics: mechanisms/sites of action
• Causes peripheral vasodilation by selective, competitive inhibition of vascular postsynaptic alpha1 adrenergic receptors, thus reducing peripheral vascular resistance and blood pressure
• BPH: relaxes the bladder neck and the prostate by blocking the alpha1 adrenergic receptors located in their smooth muscle. This causes less pressure on the urethra and increases urine flow

32
Q

Prazosin (same class: terazosin, doxazosin)

Adverse effects

A

Adverse effects:
• CNS: dizziness, headache
• Cardiovascular: orthostatic hypotension

33
Q

Cocaine

Classification and main clinical applications

A

Classification:
• Indirectly acting sympathomimetic
• Ester-type local anesthetic

Main clinical applications:
• Topical anesthetic

34
Q

Cocaine

Pharmacodynamics

A

Pharmacodynamics: mechanisms/sites of action
• Increases extracellular concentrations of catecholamines by blocking their reuptake from the synapse both centrally and peripherally, thus stimulating all adrenergic receptor types; this can lead to vasoconstriction in vasculature
• Na channel blocker; this action stabilizes the nerve membrane, increases the threshold of electrical excitability and inhibits depolarization; results in failure to propagate an action potential, and to initiate or conduct nerve impulses

35
Q

Cocaine

Adverse effects

A

Adverse effects:
• Adrenergic stimulation can lead to tachycardia, hypertension and vasoconstriction, which increases risk of myocardial infarction
• abuse can lead to physical dependence

36
Q

d-Methamphetamine

A

Classification:
• Indirectly acting sympathomimetic
Main clinical applications:
• None
Pharmacodynamics: mechanisms/sites of action
• Increases extracellular concentrations of catecholamines and serotonin by blocking their reuptake from the synapse and also inducing their release; occurs both centrally and peripherally, stimulating all adrenergic and 5-HT receptor types
Adverse effects:
• Tachycardia, hypertension, vasoconstriction leading to MI
• Abuse/dependence

37
Q

Ephedrine

Classification and main clinical applications

A

Classification:
• Indirectly acting sympathomimetic

Main clinical applications:
• Treatment of bronchial asthma, nasal congestion, acute bronchospasm

38
Q

Ephedrine

Pharmacodynamics and adverse effects

A

Pharmacodynamics: mechanisms/sites of action
• Essentially, a less potent analog of amphetamine; increases extracellular concentrations of catecholamines by blocking their reuptake from the synapse and inducing their release, both centrally and peripherally; also direct agonist effects on post synaptic adrenergic receptors
• longer-acting but less potent than epinephrine

Adverse effects:
• Excessive adrenergic stimulation can lead to tachycardia, hypertension and vasoconstriction which increases risk of myocardial infarction

39
Q

Pseudoephedrine

Classification and main clinical applications

A

Classification:
• Indirectly acting sympathomimetic

Main clinical applications:
• Nasal decongestant

40
Q

Pseudoephedrine

Pharmacodynamics and adverse effects

A

Pharmacodynamics: Mechanisms/sites of action
• Has alpha and beta adrenergic agonist activity; also blocks reuptake of norepinephrine and has amphetamine-like properties at the noradrenergic terminal but is less potent than ephedrine
Adverse effects
• Excessive adrenergic stimulation can lead to tachycardia, hypertension and vasoconstriction, which increase risk of MI
• Rebound nasal congestion following discontinuation of pseudoephedrine use

41
Q

Tyramine

Classification and main clinical applications

A

Classification
• Indirectly acting sympathomimetic (acute actions)

Main clinical applications:
• None
• This xenobiotic is found in different foods (e.g. fish, chocolate, fermented foods and some beverages)

42
Q

Tyramine

Pharmacodynamics and adverse effects

A

Pharmacodynamics: mechanisms/sites of action
• Bioactive amine that upon ingestion is metabolized by MAO (mostly MAOA) in periphery; if MAOA inhibitor has been taken, tyramine is not metabolized and is taken up into the presynaptic terminal by norepinephrine transporters; tyramine then displaces norepinephrine from storage vesicles and is released
Adverse effects
• Acute; severe hypertension if a person is on nonselective MAOi’s (MAOA and MAOB both inhibited) when tyramine-containing foods are consumed

43
Q

Reserpine

Classification and main clinical applications

A

Classification
• Sympatholytic
• historical: antihypertensive agent (mostly obsolete because of its main effect of depression)
• historical: treatment of agitated psychotic states (schizophrenia)
Main clinical applications
• Antihypertensive actions due to decrease in peripheral vascular resistance and a lowering of blood pressure

44
Q

Reserpine

Pharmacodynamics and adverse effects

A

Pharmacodynamics:
• Depletes norepinephrine, serotonin and dopamine neuronal content by irreversibly binding to storage vesicles and disrupting their storage function
Adverse effects:
• CNS effects include fatigue, lethargy, etc; mental depression that can last for several months following discontinuance of the drug
• periphery: consequences of norepinephrine depletion that include miosis, hypotension, nausea/vomiting, sexual dysfunction
• effects can last several weeks after drug discontinuation because new vesicles must be synthesized

45
Q

Alpha-methyldopa

Classification and main clinical applications

A

Classification:
• Antihypertensive drug
• Sympatholytic
Main clinical applications:
• Use for hypertension has declined due to the development of other antihypertensive agents with more favorable adverse side effect profile; still used for treatment of hypertension in pregnant women

46
Q

Alpha-methyldopa

Pharmacodynamics and adverse effects

A

Pharmacodynamics:
• After crossing the blood-brain barrier, methyldopa is decarboxylated to produce alpha-methylnorepinephrine. This metabolite stimulates central inhibitory alpha2-adrenergic receptors, thereby reducing NE release in the CNS; this results in a decrease in peripheral resistance and blood pressure.
Adverse effects:
• Drowsiness, sedation
• Orthostatic hypotension

Block 2 (1 decks)

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