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My Pharm > Adrenergic > Flashcards

Adrenergic Flashcards

1
Q

What are the four major groups with therapeutic implications in terms of NE-EPI receptor interactions?

A

A1 receptors

A2 receptors

B1, B2, B3

All members of super family of G protein coupled receptors.

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2
Q

a1 physiological function?

A

Gq protein activates PLC –> formation of IP3 (releases intracellular Ca2) and DAG (activates PKC)

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3
Q

a2 receptors mechanism?

A

Variety of effectors

Gi protein –> inhibits AC –> decreases cAMP levels

Go protein can inhibit voltage Ca2+ (L and N type)

Can activate K+ channels (hyperpolarization)

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4
Q

B1 b2 b3 receptor mechanism?

A

Gs protein that stimulates AC

Increases cAMP levels (activates PKA)

B1 –> increase Ca2+ movement through L-type Ca2+ channels.

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5
Q

An action common to activation of BOTH a1-adrenergic and M1-muscarinic cholinergic receptors is:

A.Constriction of vascular smooth muscle

B.Dilatation of vascular smooth muscle

C.Constriction of bladder sphincter

D.Increase in intracellular Ca++ mediated via Gq-proteins

E.Decrease in intracellular cAMP levels mediated via Gi/o-proteins

F.Contraction of radial muscle of pupil (mydriasis)

A

Answer is D - increase intracellular Ca2+ mediated via Gq proteins.

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6
Q

Adrenergic agonists produce the same effect as? What do direct agonists do and what do indirect agonists do?

A

Produce the same effect as NE and Epi at a- and B- adrenergic receptors on sympathetic end organs

Direct agonists activate adrenergic receptors

Indirect agonists increase NE release (eg pseudoephedrine)

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7
Q

Adrenergic antagonist function? What about sympatholytic agents?

A

Adrenergic receptor antagonist block effects of NE and Epi at a- and B-adrenergic receptors on sympathetic end organs

Sympatholytic agents - cause interference with adrenergic function in the pre-synapse neuron via block of synthesis (storage or relase)

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8
Q

Common, expected signs of epinephrine toxicity following administration of an Epi-Pen could include:

A.Miosis

B.Fatigue

C.Sweating

D.Drowsiness and sedation

E.Muscle tremors

F. Urinary incontinence (loss of bladder control

A

E) muscle tremors.

Sweating done by M3

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9
Q

Activation of the sympathetic nervous system in response (flight-or-fight response) to an environmental stressor causes epinephrine release from the adrenal gland, resulting in which of the following actions? (2)

A.Decreased blood glucose levels

B.Bronchodilation

C.Pupil constriction (miosis)

D.Increase in AV node conduction velocity

E.Increased GI motility

F.Loss of bladder sphincter tone

A

B and D

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10
Q

An action common to both indirect-acting adrenergic and indirect-acting cholinergic agonists is:

A.Inhibition of acetylcholinesterase

B.Inhibition of monoamine oxidase

C.Inhibition of choline uptake into the neuron

D.Inhibition of the norepinephrine transporter (NET)

E.Increase neurotransmitter levels in the synapse

A

e) increase neurotransmitter levels in the synapse.

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11
Q

Multiple mechanisms exist in or near the adrenergic nerve terminal that can diminish the action of norepinephrine. The major action that terminates the synaptic activity of norepinephrine is:

A.Metabolism by catechol-O-methyl transferase (COMT)

B.Metabolism by monoamine oxidase (MAO)

C.Reuptake into neuron by norepinephrine transporter [NET] on nerve terminal)

D.Uptake into non-neuronal cells by the Uptake 2 transporter

E.Metabolism by acetylcholinesterase (AChE)

A

c) Reuptake into neuron by norepinephrine transporter (NET) on nerve terminal

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12
Q

Which of the following organ systems is INCORRECTLY matched with the predominant adrenergic receptor subtype present in that tissue?

A.Heart - β1

B.Bronchiolar smooth muscle - β2

C.Bladder sphincter - α1

D.Uterine smooth muscle - α1

E.Urinary bladder sphincter - α1

F.Radial pupillary dilator muscle - β1

A

D) uterine smooth muscle a1 should be B2

F - Radial pupillary dilator muscle - should be a1

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13
Q

What are the direct acting alpha agonists? Nonselective, a1 selective, a2 selective

A

nonselective - EPI-NE

A1 selective - phenylephrine

a2 selective - clonidine (anti-adrenergic)

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14
Q

What are the direct acting B agonists. Nonselective, B1 selective, B2 selective

A

Nonselective - isoproterenol

B1 selective - dobutamine

B2 selective - albuterol

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15
Q

What are the indirect acting adrenergic agonists? Releaser and reuptake inhibitor?

A

Releaser - Pseudoephedrine

Reuptake inhibitors- cocaine.

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16
Q

An A-methyl group has what effect on bioavailability?

A

a-methyl group tells you if it is a MAO substrate or not.

If it has an a-methyl group it is not an MAO substrate and therefore has increased bioavailability.

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17
Q

What does an OH group on a ring tell you about adrenergic agonists?

A

If there are no ring OH groups this leads to increased lipid solubility and increased CNS access.

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18
Q

Stimulating the a1 receptor has what clinical value for blood pressure? What 3 drugs can you use to do so?

A

Stimulating a1 would cause vasoconstriction - lead to a vasopressor action - elevation of BP (a1/B1 actions)

Epinephrine - a1, b1, b2

Norepinephrine, a1, b1

Phenylephrine a1

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19
Q

Relief of nasal congestion (decongestants) stimulate what receptor? What 3 drugs are useful for this?

A

Stimulate a1 receptor - cause vasoconstriction

Pseudoephedrine - indirect (via release of NE at a1 receptors)

Phenylephrine (a, topical/oral)

oxymetazoline (a, topical)

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20
Q

Local vasoconstriction in local anesthetic solution is caused by what drug?

A

Epinephrine (a1/b1/b2 infiltration)

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21
Q

Stimulating B1 receptors is useful for cardiogenic shock, acute heart failure, ACLS protocols, and Bradyarrhthmias. What 4 drugs can be used to do this?

A

Epinephrine (a1, b1, b2, infusion)

Isoproterenol (b1, infusion)

Dobutamine (b1, infusion)

Dopamine (d1 and indirect (via NE release) at a1 and B1, infusion.

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22
Q

B2 receptors are useful for smooth muscle relaxation. What medication would you use for anaphylaxis?

A

Epinephrine - B2 mediated bronchodilation

epi- a1/b1/b2

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23
Q

B2 receptor agonists are useful in smooth muscle relaxation, what agonist would you use for asthma/COPD?

A

Albuterol b2 inhalation

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24
Q

B2 receptor agonists are useful for smooth muscle relaxation - what drug would you use in suppression of premature labor contractions?

A

Terbutaline (b2, subcutaneous, oral)

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25
Q

Which of the following autonomic nervous system drugs would be MOST likely to predispose a patient to cardiac arrhythmias due to an increase in cardiac conduction rate?

A.Albuterol

B.Atenolol

C.Isoproterenol

D.Pilocarpine

E.Propranolol

A

Answer is c - isoproterenol (B1-B2 agonist)

albuterol is b2

atenolol is a b1 ANtagonist

pilocarpine is a M agonist

propranolol - b1 b2 antagonist

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26
Q

Which set of direct action / reflex compensatory response would you see following IV administration of a selective α1-adrenergic receptor agonist?

A.Vasodilation Reflex bradycardia

B.Vasodilation Reflex tachycardia

C.Vasoconstriction Reflex bradycardia

D.Vasoconstriction Reflex tachycardia

A

c) vasoconstriction, reflex bradycardia.

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27
Q

What are adverse effects at a1 receptors? What are adverse effects at b1 receptors?

A

a1 receptors – marked elevations in blood pressure –> cerebral and pulmonary hemorrhage

effects at b1 receptors –> increased cardiac work and myocardial o2 demand, severe angina, myocardial infarction, tachycardia, palpitations, serious ventricular arrhythmias.

28
Q

What are adverse effects of adrenergic agonists in the CNS?

A

Anxiety, restlessness, insomnia (non-catechols). (rare with CAs-phenylephrine b/c of decreased CNS penetration, some effects due to sensory input form periphery)

Paranoid state –> high doses of lipid soluble phenyllisopropanoloamines (eg. amphetamine

Use with caution in: elderly, hypertensive patients, hyperthyroid patients, diabetics, patients with congestive heart failure

29
Q

Which therapeutic action listed below results from stimulation of β2-adrenergic receptors?

A.Vasoconstriction in anaphylactic reactions

B.Decrease in aqueous humor production in glaucoma

C.Increase in cardiac output during acute congestive heart failure

D.Mydriasis for ophthalmic examinations

E.Attenuation of premature labor contractions

F.Suppression of catecholamine-induced tachyarrhythmias

G.Relief of acute bronchospastic episodes in asthma

A

E) attenuation of premature labor contractions (B2 agonist terbutaline)

G. relief of acute bronchospastic episodes in asthma - B2 albuterol

30
Q

What 2 medications are both alpha blockers and beta blockers?

A

Labetalol

Carvedilol

31
Q

What are the nonselective b-blockers, beta1 selective blockers - and the alpha 2 agonists?

A

Nonselective bb - propranolol

beta1 selective - metoprolol-atenolol

Alpha 2 agonists - clonidine

Labetalol and carvedilol are both alpha and beta blockers.

32
Q

What are the alpha 1 selective blockers? Out of the nonselective, which is reversible and what is not reversible?

A

Doxazosin - alpha 1 selective

phenoxybenzamine - irreversible alpha blocker (nonselective

phentolamine - reversible alpha blocker (nonselective)

Both labetalol and carvedilol are alpha blockers and beta blockers.

33
Q

How do adrenergic sympatholytic agents work?

A

Interference with adrenergic function in presynaptic neuron - lack of specificity of action - limits clinical utiltiy

Inhibitors of catecholamine storage -

  • Resperine

Inhibitors of catecholamine synthesis -

  • tyrosine hydxoyalse (rate limiting): metyrosine
  • DOPA decarboxylase: a-methyldopa, carbidopa
  • Dopamine B hydroylase - Disulfiram

Inhibitors of catecholamine release

  • bretylium
34
Q

what are the anti-adrenergic agents - that are selective a1 blockers? Nonselective?

A
  • Selective
    • Doxazosin
    • But also prazosin, terazosin
  • Nonselective
    • phentolamine (reversible)
    • phenoxybenzamine (irreversible)
35
Q

what is the use of blockade of a1 receptors on blood vessels?

A

Vasodilation

Hypertesnion/vasospastic conditions (raynauds disese) - Doxazosin/prazosin

Local vasoconstrictor excess- inadvertenet NE infiltration - Phentolamine (a1-a2)

Preoperative management of pheochromocytoma - phenoxybenzamine (irreversible a1-a1) oral

36
Q

what is the use for a1 blockers on sphincters?

A

Causes sphincter relaxation - can be used for urinary obstruction (urinary symptoms of BPH)

Doxazosin or tamsulosin a1a selective - blocking action at sphincter>blood vessels

37
Q

Which of the following drugs causes vasoconstriction that can be blocked by doxazosin?

A.Atropine

B.Epinephrine

C.Isoproterenol

D.Labetalol

E.Phenylephrine

A

Answer is B and E

A.Atropine (M antagonist)

B.Epinephrine (α1 - β1 - β2 agonist)

C.Isoproterenol (β1 - β2 agonist)

D.Labetalol (α1 - β1 - β2 antagonist)

E.Phenylephrine (α1 agonist)

38
Q

A concern when examining patients is the possibility that they may be taking medications that interfere with the function of the baroreceptor reflex and can increase the potential for orthostatic hypotension. This would be most likely to occur with which class of autonomic nervous system drugs?

A.Muscarinic antagonists

B.Muscarinic agonists

C.Cholinesterase inhibitors

D.a1 antagonists

E.b2 antagonists

A

answer is d - a1 antagonists

39
Q

What are adverse effects of the blockade of a1 receptors? Selective and nonselective

A

Selective - better tolerated - may cause syncope at onset of treatment or postural hypotension (minimal reflex tachycardia)

a1-a2 (non-selective) receptor blockier and sympatholytics -

  • postural hypertesnion and significant reflex tachycardia
  • nasal stuffiness (via vasodilation)
  • inhibition of ejaculation
  • gastrointestinal upset if given orally
  • sedation, weakness and a sense of fatigue
40
Q

Blockade of α1-adrenergic receptors would result in the therapeutic action of:

A.Relief of nasal congestion

B.Lowering of BP in hypertensive individuals

C.Prolongation of LA action

D.Relief of PSVT

E.Relief of overactive or unstable bladder

F.Restoration of BP in hypotensive states

A

B) lowering of BP in hypertensive individuals

41
Q

What do all b-receptor blockers share? What about differences?

A

Common feature of reversible inhibition of catecholamine binding at B-adrenergic receptors

Differences between agents - include relative affinities for B1 (heart) vs B2 (lungs/blood vessels) vs a1(blood vessels)

Nonselective -propranolol

B1 selective - cardioselective - metorprolol, atenolol - dose dependent

a1, b1 , b2 - vasodilating - labetalol, carvedilol

42
Q

In terms of elimination of B-blockers what is a rule you could follow?

A

More nonselective like propranolol carvedilol, and labetalol are eliminated by the liver - exception is metoprolol (b1 selective eliminated by liver)

Or you could think of it as atenolol is the only one that is eliminated by the kidneys instead of the liver.

43
Q

Beta blockers are useful in hypertension - which ones do we use for this?

A

Atenolol/metoprolol (b1 selective, oral)

Labetolol - a1, b1, b2 - oral

44
Q

Beta blockers are useful in preventing angina. Which one do we use for this?

A

Metoprolol - decreases myocardial 02 demand in stable angina.

B1 selective - oral

45
Q

Beta blockers are useful in treating hyperthyroidism, which ones do we use for this? (2)

A

Block symptoms of thyroid storm due to excessive CAs –> tremors, palpitations, arrhthmias [DEMS]

Metoprolol (b1 selective, oral/parenteral)

Propranolol (b1-b2 oral/ parenteral)

46
Q

Beta blockers are useful in treating arrhythmias such as SVT and afib. - which ones do we use for this?

A

These slow AV conduction rate

Metoprolol (b1 selective)

Esmolol b1 selective

47
Q

Beta blockers are useful in treating heart failure via decreasing cardiac remodeling. Which ones do we use for this?

A

Metoprolol (B1

Carvedilol a1-b1-b2

48
Q

What would be an adverse effect of blocking B-receptors? B1 blockade? B2 Blockade?

A

B1 receptor block - depression of myocardial contractility - can precipiate acute heart failure

B2 receptor block - may worsen pre-existing asthma and can precipitate bronchospasm, undesirable changes in blood lipid profile, may compromise peripheral circulation.

49
Q

What would be an adverse effect of a combined b1-b2 blockade?

A

Hypoglycemic episodes –> masks signs of insulin retraction mediated by epinephrine release

CNS effects: sedation, sleep disturbances, depression

50
Q

What would be adverse response of a2 receptor ACTIVATION?

A

dry mouth - up to 30-40% of patients on clonidine

Drowsiness, sedation, fatigue.

51
Q

What would be a drug interaction with epinephrine and someone taking a-blockers?

A

Mechanism: stimulation of B2 receptors (by EPI) causes vasodilatoin while opposing a1 vasoconstriction being blocked by another drug.

Leads to fall in TPR and decrease in blood pressure, rather than the increase expected with epinephrine.

52
Q

What would be a drug interaction betwween epinephrine and b blockers?

A

B2 non selective blockers would prevent vasodilation effect from epinephrine, but would get an unopposed EPI a1 vasoconstriction - greater elevation of BP

53
Q

If someone was on an a-blocker what would happen if you gave them epi vs phenylephrine?

A

Epi - would unmask B2 receptors - a1 receptors would be blocked - get unopposed vasodilation

Phenylephrine - selective a1 agonist, would suppress the a1 blocker effect but not reverse it. Doesn’t stimulate the b2 receptors.

54
Q

Epinephrine “reversal” (a paradoxical decrease in blood pressure when systemic epinephrine is given) occurs if epinephrine is given with a drug that blocks which receptor type:

A.a1-adrenergic

B.b1-adrenergic

C.b2-adrenergic

D.Muscarinic cholinergic

E.Nicotinic ganglionic-type cholinergic

F.Nicotinic muscle-type cholinergic

A

a) a1- adrenergic blocker

55
Q

The direct actions of epinephrine to increase total peripheral resistance and systolic blood pressure would be further increased if the patient was also given a drug that blocks which receptor:

A.a1-adrenergic

B.b1-adrenergic

C.b2-adrenergic

D.Muscarinic cholinergic

E.Nicotinic ganglionic-type cholinergic

F.Nicotinic muscle-type cholinergic

A

c) B2-adrenergic

Would get unopposed a1-vasoconstriction

B2 - carvedilol, pranolol, labetolol

56
Q

What do a2 agonists do? In the SNS? In the CNS?

A

Reduces symapthetic nervous system activation via

SNS: Stimulation of presyanptic a2 receptors –> decrease NE release from sympathetic neruons

CNS: stimulation of postsynaptic a2 adrenergic receptors in the brain stem vasomotor center –> decrease SNS activity.

57
Q

What are clinical uses for a2 receptors?

A

These decrease SNS outflow

Used in hypertension - Clonidine (a2 oral/transdermal/parenteral)

Used in opiod-alcohol withdrawal symptoms (neuro) - clonidine a2 oral.

58
Q

What are adverse effects of a2 receptor activation?

A

Dry mouth - up to 30-40% of patients on clonidine

Drowsiness, sedation, fatigue.

59
Q

Which action(s) of clonidine explains why it causes xerostomia in 35% of patients?

A.It blocks alpha-2 receptors on cholinergic neurons in the GI tract

B.It activates alpha-2 receptors on adrenergic neurons in the GI tract

C.It activates alpha-2 receptors on cholinergic neurons in the GI tract

D.It blocks M3 receptors on salivary glands in the GI tract

E.It activates alpha-2 receptors on salivary glands in the GI tract

F.It decreases release of ACh from cholinergic neurons innervating salivary glands

A

C and F

60
Q

. Select the optimal receptor action to increase in cardiac output following cardiogenic shock

A.Alpha-1 adrenergic agonist

B.Alpha-1 adrenergic antagonist

C.Beta-1 adrenergic agonist

D.Beta-1 adrenergic antagonist

E.Beta-2 adrenergic agonist

F.Muscarinic agonist

G.Muscarinic antagonist

A

C - beta 1 adrenergic agonist

61
Q

Select the optimal drug action for relief of nasal congestion:

A.Alpha-1 adrenergic agonist

B.Alpha-1 adrenergic antagonist

C.Beta-2 adrenergic agonist

D.Muscarinic agonist

E.Muscarinic antagonist

A

A

62
Q

Select the optimal receptor action to increase salivary flow for treatment of radiation-induced xerostomia

A.Alpha-1 adrenergic agonist

B.Alpha-1 adrenergic antagonist

C.Beta-1 adrenergic agonist

D.Beta-1 adrenergic antagonist

E.Beta-2 adrenergic agonist

F.Muscarinic agonist

G.Muscarinic antagonist

A

F

63
Q

Select the optimal receptor action to decrease GI motility in patients with diarrhea

A.Alpha-2 adrenergic agonist

B.Alpha-1 adrenergic antagonist

C.Beta-1 adrenergic agonist

D.Beta-1 adrenergic antagonist

E.Beta-2 adrenergic agonist

F.Muscarinic agonist

G.Muscarinic antagonist

A

G

64
Q

Select the optimal drug action for relief of overactive bladder:

A.Alpha-1 adrenergic agonist

B.Alpha-1 adrenergic antagonist

C.Beta-3 adrenergic agonist [Mirabegron (Myrbetriq®)]

D.Muscarinic agonist

E.Muscarinic antagonist

A

E

65
Q
A

My Pharm (6 decks)

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