Neuroscience Week 5: Adrenergic Phys 2 Flashcards

1
Q

Adrenergic Receptors second messenger, targets and effects

A
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2
Q

α1 agonist example

A

Phenylephrine

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3
Q

α2 agonist example

A

Clonidine

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4
Q

Adrenergic receptor type and organ system effects

A
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5
Q

α2 agonist mechanism

A

agonist at α2 receptor decrease excitation-secretion coupling causes even less release of Norepinephrine

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6
Q

Question 1

A

Phenylephrine Nasal Spray

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7
Q

Clonidine historical use

A

Systemic hypertension

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8
Q

α antagonist examples

A
  • Phentolamine
  • Prazosin
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9
Q

Phentolamine Receptor target

A

non-selective α1/α2

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10
Q

Phentolamine uses

A

Some use in control of hypertension

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11
Q

Prazosin Receptor target

A

α1 antagonist

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12
Q

Prazosin Uses

A
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13
Q

Benign Prostatic Hyperplasia description

A
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14
Q

Question 2

A

D.

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15
Q

BPH AKA

A

Benign Prostatic Hyperplasia

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16
Q

Treatment of BPH

A

Prazosin

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17
Q

β Receptor Drug Agonists examples

A

‘enol’

‘erol’

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18
Q

β Receptor Drug Antagonists examples

A

‘olol’

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19
Q

β Agonists to know

A
  • Isoproterenol
  • Albuterol
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20
Q

Isoproterenol receptor target

A

non-selective β1/β2

21
Q

Albuterol Receptor target

A

some β2 selectivity

22
Q

non-selective β agonists effects

A

↑HR

↓relax smooth muscle

23
Q

Question 3

A

E.

24
Q

β receptor agonist side effects in asthma therapy

3 listed

A
  • CV effects
  • Tremor
  • Hypokalemia
25
Q

β receptor agonist actions in asthma therapy

A
26
Q

β receptor antagonist examples

A

Propranolol

Atenolol

27
Q

Propranolol Receptor target

A

non-selective β1/β2

28
Q

Atenolol Receptor target

A

selective β1

29
Q

β1 receptor antagonist effects

A

Opposite of this so decreases excitation

prevents this pathway from getting turned on

30
Q

β receptor antagonists effects in hypertension

A
31
Q

Resting tone

A
32
Q

β receptor antagonist in hypertension Adverse effects

A
33
Q

Indirect acting sympathomimetics examples

4 listed

A
34
Q

Amphetamine MOA Effects

A
35
Q

Amphetamine MOA

A

more NE not packaged in vesicles and so more norepinephrine is being released

36
Q

Amphetamine Therapeutic Uses

3 listed

A
37
Q

Cocaine MOA

A

disrupts sympathetic transmission

binds to transporter and prevents reuptake of NE

38
Q

Cocaine MOA

A

cocaine doesn’t modify nerve activity, cocaine doesn’t cause release but enhances systems already in use by preventing NE reuptake

39
Q

Cocaine Therapeutic Uses

A
  • ENT surgery
  • limits bleeding and local anesthetic effect
40
Q

Cocaine Deleterious effects

A
  • Seizures
  • Hypertensive crisis-cerebral hemorrhage
  • Cardiac arrhythmias
  • Myocardial ischemia (in situ thrombosis or coronary spasm)
41
Q

Tyramine MOA

A

causes release of catecholamines from vesicles, increasing synaptic concentrations

works like amphetamine

42
Q

Tyramine found where

A

tyrosine metabolism - pickled foods or sausage or smelly cheese

43
Q

Tyramine contraindicated in

A

people taking MAOI’s

44
Q

Tyramine Therapeutic Relevance

3 listed

A
45
Q

Ephedrine MOA

A

causes release of catecholamines from vesicles and directly activates adrenergic receptors

46
Q

Ephedrine was used antiquity for?

A

Treatment of asthma

47
Q

Ephedrine therapeutic relevance

A
48
Q

Ephedrine Abuse potential

A
49
Q

Adrenergic Pharmacology Summary

A