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Pharmacology- Test 1 Material > 05- Adrenergics > Flashcards

05- Adrenergics Flashcards

1
Q

atenolol (Tenormin)

A

adrenergic antagonist that is B1 SELECTIVE (post-junctional inhibition)

  • will decrease HR, force of contraction and result in dec. CO
  • major clinical use: anti-hypertensive
  • cardiac selective and does not block B2 receptors which is beneficial for those with asthma or COPD
  • Half-Life: 6-9 hrs
  • produces few CNS effects because does not cross BBB easily
  • can induce cardiac failure in those with cardiac insufficiency
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2
Q

betaxolol (Betoptic, Kerlone)

A

adrenergic antagonist that is B1 SELECTIVE (post-junctional inhibition)

  • will decrease HR, force of contraction and result in dec. CO
  • major clinical use: treatment of glaucoma (given topically)
  • cardiac selective and does not block B2 receptors which is beneficial for those with asthma or COPD
  • Half-Life: 14-22 hrs
  • can induce cardiac failure in those with cardiac insufficiency
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3
Q

metoprolol (Lopressor)

A

adrenergic antagonist that is B1 SELECTIVE (post-junctional inhibition)

  • will decrease HR, force of contraction and result in dec. CO
  • major clinical use: anti-hypertensive and angina pectoris
  • effective prophylactic agent to prevent recurrence of myocardial infarction
  • long-term use following MI prolongs survival (may suppress arrhythmias)
  • cardiac selective and does not block B2 receptors which is beneficial for those with asthma or COPD
  • Half-Life: 3-4 hrs
  • ataxia and dizziness are common, esp. with initial therapy
  • can induce cardiac failure in those with cardiac insufficiency
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4
Q

propranolol (Inderal)

A

adrenergic antagonist that is NON-SELECTIVE BETA BLOCKER (post-junctional inhibition)

  • Major clinical use: anti-hypertensive, anti-arrhythmic, angina pectoris, and migraine headaches
  • will cause B2 blockade my inhibit dilation of bronchioles, which may be significant for patients with asthma
  • effective prophylactic agent to prevent recurrence of myocardial infarction
  • Half-life: 3-6 hrs
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5
Q

pindolol (Visken)

A

adrenergic antagonist that is NON-SELECTIVE BETA BLOCKER (post-junctional inhibition)

  • Major clinical use: anti-hypertensive
  • will cause B2 blockade my inhibit dilation of bronchioles, which may be significant for patients with asthma
  • Half-life: 3-4 hrs
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6
Q

nadolol (Corgard)

A

adrenergic antagonist that is NON-SELECTIVE BETA BLOCKER (post-junctional inhibition)

  • Major clinical use: anti-hypertensive
  • will cause B2 blockade my inhibit dilation of bronchioles, which may be significant for patients with asthma
  • minimal CNS effect b/c cannot cross BBB
  • Half-life: 14-24 hrs
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7
Q

timolol (Timoptic)

A

adrenergic antagonist that is NON-SELECTIVE BETA BLOCKER (post-junctional inhibition)

  • Major clinical use: anti-hypertensive, angina pectoris, and decrease intraocular pressure
  • will cause B2 blockade my inhibit dilation of bronchioles, which may be significant for patients with asthma
  • effective prophylactic agent to prevent recurrence of myocardial infarction
  • Half-life: 4-5 hrs
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8
Q

a-methldopa (Aldomet)

A

acts BOTH as an adrenergic agonist that is A2 SELECTIVE and as a MISC. PRE-JUNCTIONAL

  • major use: anti-hypertensive
  • stimulate pre-synaptic a2 receptors as well as post-synaptic a2 receptors on nerve terminals in CNS
  • inhibits NE release by nerve terminal (feedback inhibition)
  • able to enter both PNS and CNS adrenergic neurons
  • partially replaces DOPA in synthetic pathway leading to NE synthesis
  • synthesized and stored in vesicles (instead of NE)
  • known as a false transmitter because after exocytosis from vesicles, its efficacy is greatly reduced as compared to NE as agonist
  • hypotensive activity results from potent stimulation within the brainstem affecting vasomotor center
  • decreases TPR, HR, CO; does not affect baroreceptor reflexes and rarely elicits orthostatic hypotension
  • Adverse Effects: sedation , postural hypotension, dizziness, sleep disturbances, impotence, dry mouth, nasal congestion
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9
Q

guanethidine (Ismelin)

A

misc. PRE-JUNCTIONAL inhibition of NE release through synaptic vesicle depletion, and membrane stabilization
- orally effective anti-hypertensive usually reserved for therapy of most severely elevated arterial pressures
- transported into adrenergic neurons via NE transporter
- hypotensive activity elicited by reducing NE release
- agents that inhibit transport (cocaine, tricyclic antidepressants) will antagonize desired hypotensive activity
- stabilizes membranes, interfering with exocytosis
- chronic administration accompanied by depleting NE within synaptic vesicles
- minimal effects observed w/ other biologic amines (Epi, DA)
- minimal adverse effects in CNS since does not cross BBB

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10
Q

reserpine

A

misc. PRE-JUNCTIONAL inhibition of NE release through synaptic vesicle depletion (reduce concentrations of NE stored within synaptic vesicles, thus decreasing the overall amount of NE released into synapse)
- depletes stores of biogenic amines (Epi, NE, DA, serotonin) in both PNS and CNS by blocking transport into storage vesicles
- very potent, orally effective, long duration of action
- adverse effects are primarily in CNS (sedation, depression, Parkinsonian symptoms); inc. GI motility leads to ulcers

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11
Q

cocaine

A

AMINE I TRANSPORTER (NET) inhibitor

  • prevents reuptake of NE from the synapse thus synaptic levels of NE rise allowing further sympathetic stimulation of target site (vasoconstriction, tachycardia, mydriasis)
  • inhibitors of NET is important within PNS when considering drug interactions and potential toxicological problems
  • can be used to achieve decreased blood flow such as hemostasis during surgery
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12
Q

DMI (desmethylimipramine)

A

AMINE I TRANSPORTER (NET) inhibitor

  • a tricyclic anti-depressant
  • prevents reuptake of NE from the synapse thus synaptic levels of NE rise allowing further sympathetic stimulation of target site (vasoconstriction, tachycardia, mydriasis)
  • inhibitors of NET is important within PNS when considering drug interactions and potential toxicological problems
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13
Q

tyramine

A

RELEASING AGENT

  • pre-junctional sympathetic stimulation
  • enter nerve terminal via NET
  • NE gets displaced from storage vesicles and released into synapse
  • found in certain food products (cheddar, Guyere cheese, salami, yeast)
  • may elicit side effects for individuals on MAO inhibitors through combination of dec. synaptic NE metabolism (MAO inhibitor) and inc. NE release (tyramine) elevates Art. pressure
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14
Q

pseudoephedrine (Sudafed)

A

RELEASING AGENT

  • pre-junctional sympathetic stimulation
  • enter nerve terminal via NET
  • NE gets displaced from storage vesicles and released into synapse
  • used to reduce congestion of mucous membranes
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15
Q

doxazosin (Cardura)

A

Competitive adrenergic antagonist.

  • selective α1 antagonist/blocker
  • -Use: HTN, urinary obstruction (BPH)
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16
Q

prazosin (Minipress)

A

Competitive adrenergic antagonist.

  • selective α1 antagonist/blocker
  • tachycardia is mild to none because there is no significant effect on α2 receptors.
  • long DOA (12’).
  • -Use: HTN, urinary obstruction (BPH)
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17
Q

tamsulosin (Flomax)

A

Competitive adrenergic antagonist.

  • selective α1 antagonist/blocker
  • Use: HTN, urinary obstruction (BPH)
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18
Q

terazosin (Hytrin)

A

Competitive adrenergic antagonist.

  • selective α1 antagonist/blocker
  • -Use: HTN, urinary obstruction (BPH)
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19
Q

phenoxybenzamine (Dibenzyline)

A

Non-competitive adrenergic antagonist.

  • slightly more selective for α-1 vs α-2.
  • alkylates α1 and α2 receptors.
  • inhibits NET.
  • no β1 inhibition, so may produce orthostatic HOTN and tachycardia.
  • Use: pheochromocytoma
20
Q

phentolamine (Vasomax)

A

Competitive adrenergic antagonist.

  • equal selectivity for α1 and α2
  • α1 blockade produces vasodilation
  • α2 blockade inhibits NE negative feedback leading to increased release of NE. This can produce tachycardia (no blockade of β1).
  • Considered “dirty” drug because it acts at multiple sites (i.e. α, muscarinic, histamine).
  • Use: pheochromocytoma
21
Q

labetelol (Trandate)

A

Mixed α and β antagonist.

  • non-selective β blocker.
  • displays antagonism of β1 and β2.
  • β1 blockade reduces heart rate and contractility/CO. Caution in patients with severe LV dysfunction.
  • β2 blockade can precipitate bronchoconstriction in asthmatic patients
22
Q

dopamine

A
  • dopamine receptor agonist released by renal and splanchnic vascular smooth muscle
  • D1 binds Gs: vasodilation (renal, msenteric)
  • D2 binds Gi: negative feedback to decrease NT release from terminals
  • High doses have alpha 1 and beta 1 agonist effects
23
Q

dobutamine

A
  • Beta 1 selective agonist. B1>B2»»alpha

- drug of choice along with dopamine with cardiogenic shock following myocardial infarction

24
Q

isoproterenol

A
  • non selective beta agonist. B1=B2»»alpha
  • potent vasodilator, decreased MAP due to B2 activity
  • increased cardiac output due to B1 activity
25
Q

albuterol

A
  • B2 selective agonist. B2»B1»»alpha
  • smooth muscle relaxation/dilation (e.g. myometrium, bronchial ree, GI tract)
  • first line treatment for bronchial asthma attack
26
Q

metaproterenol

A
  • B2 selective agonist. B2»B1»»alpha

- smooth muscle relaxation/dilation (e.g. myometrium, bronchial ree, GI tract)

27
Q

terbutaline

A
  • B2 selective agonist. B2»B1»»alpha
  • smooth muscle relaxation/dilation (e.g. myometrium, bronchial ree, GI tract)
  • relax pregnant uterus
28
Q

bromocriptine

A
  • Dopamine D2 receptor agonist
  • primarily used as an anti-parkinson agent w/ CNS activities
  • peripheral side effects: postural hypotension during initial therapy and development of cardiac arrhythmia
  • D2 receptors on post-synaptic effector sites in the CNS are not involved in feedback inhibition
29
Q

fenoldopam

A
  • dopamine receptor agonist. D1»D2
  • D1 binds Gs: vasodilation (renal, msenteric)
  • D2 binds Gi: negative feedback to decrease NT release from terminals
  • High doses have alpha 1 and beta 1 agonist effects
30
Q

metaraminol

A

Alpha-1 agonist

  • substitution to benzene ring (decreases COMT metabolism)
  • substitution to alpha carbon (block oxidation by MAO & displaces NE from vesicles)
31
Q

methoxamine

A

Alpha-1 agonist

32
Q

phenylephrine

A

Alpha-1 agonist

  • substitution to benzene ring (decreases COMT metabolism)
  • nasal decongestant
  • mydriasis
  • vasoconstricts (protects cerebral and coronary blood flow)
  • reduces diffusion of local anesthetics from injection site
33
Q

clonidine

A 
Alpha-2 agonist
presynaptic nerve terminal
negative feedback to decrease NE release
-decrease blood pressure
-sedation is a side effect
34
Q

guanabenz

A 
Alpha-2 agonist
presynaptic nerve terminal
negative feedback to decrease NE release
-decrease blood pressure
-sedation is a side effect
35
Q

amphetamine

A
  • mixed Alpha-1 Beta-1 agonist
  • releasing agent
  • taken in via NET, block NE re-uptake and reverse transport to release intraneuronal NE
  • CNS effects: alertness and mood
  • depresses appetite
36
Q

ephedrine

A
  • mixed Alpha-Beat agonist
  • releasing agent
  • substitution to benzene ring (decreases COMT metabolism)
  • substitution to alpha carbon (blocks oxidation by MAO, displaces NE from vesicles)
  • elevates cardiac output & arterial pressure
  • CNS stimulant
  • Beta-2 activity to dilate bronchial smooth muscle
  • nasal decongestant
37
Q

epinephrine

A

Alpha-1 and Beta-1 agonist

  • released from adrenal medulla
  • low dose stimulates Beta only
  • potent vasoconstrictor and cardiac stimulant
  • vasodilation of vessels to skeletal muscles d/t B2 activity, may decrease TPR
  • with bolus, sharp rise in MAP elicits baroreceptor response & vagal reflex to decrease MAP
  • hemostasis during surgery
  • reducing diffusion of local anesthetics from injection site
  • cardiac arrest and heart block
  • anaphylaxis
38
Q

norepinephrine

A

Alpha and Beta-1 agonist

  • primary NT of adrenergic nerves
  • increase blood pressure
  • reduces diffusion of local anesthetics from injection site
39
Q

Alpha-1 receptor activation

A
  • arterial and venous constriction
  • vagal response leads to bradycardia
  • pupillary dilator muscle contraction (mydriasis)
  • myometrium muscle contraction
  • urinary bladder sphincter contraction
  • relaxation of intestinal smooth muscle
  • increased glycogenolysis
  • contraction of vas deferens
  • increased secretions: salivary & sweat glands
40
Q

Alpha-2 receptor activation

A

presynaptic nerve terminals

negative feedback to decrease NE release

41
Q

Beta-1 receptor activation

A
  • increase HR and contractile force
  • directly activates SA node
  • increase renin secretion
  • increase lipolysis in fat cells
42
Q

Beta-2 receptor activation

A
  • vascular smooth muscle dilation
  • bronchial tree relaxation
  • GI tract and myometrium relaxation
  • decreased intraocular pressure
43
Q

Beta-3 receptor activation

A
  • increased lipolysis in fat cells

- decreased micturition

44
Q

Dopamine-1 receptor activation

A
  • vasodilation (renal/splanchnic)

- increase blood flow

45
Q

Dopamine-2 receptor activation

A

PNS: presynpatic nerve terminals, modulatory role to derease NT release from terminals

CNS: postsynaptic, NT

46
Q

COMT

A

found in liver

transfers OH group with methyl group for catecholamine metabolism

47
Q

MAO

A

found in adrenergic nerve terminals, liver, and brain
removes NH2 group
deamination

Pharmacology- Test 1 Material (8 decks)

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