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Pharm Exam 1 > Autonomic Pharmacology Part II > Flashcards

Autonomic Pharmacology Part II Flashcards

(48 cards)

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1
Q

What neurotransmitter is released at target organs in the sympathetic nervous system?

A

Norepinephrine - activates alpha and beta receptors

or

circulating epinephrine from adrenal gland

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2
Q

All adrenergic receptors are

A

G protein-coupled receptors that work by activating secondary messengers within the cell

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3
Q

Alpha receptors

A

Alpha 1 = causes calcium release inside the cell

  • Smooth muscle contraction
  • Stimulates “tone” on the postsynaptic side

Alpha 2 = presynaptic; inhibits neurotransmitter release

  • Works via negative feedback
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4
Q

Beta Receptors

A
  • Beta 1 = increases HR
    • Both beta 1 and 2 are found on the heart but Beta 1 is the most important for HR increase
  • Beta 2 = triggers relaxation of smooth muscles along respiratory tract and certain blood vessels
    • found in airways and BV that cause relaxation, particularly BV in skeletal muscles
  • Beta 3 = leads to lipolysis, breakdown of triglycerides in adipocytes (releases energy reserves)
    • This is about getting more fuel, this releases more energy into the blood for more movement and fuel the fight or flight response, glucose and adipose mobilization
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5
Q

Dopamine, norepinephrine and epinephrine are all derived from?

A

Tyrosine

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6
Q

How does the catecholamines differ?

A

by functional group

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7
Q

How do norepinephrine and epinephrine differ?

A

Where they are released

NE - sympathetic neurons

Epi - adrenal gland when SNS is activated

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8
Q

Are Ne and Epi equivalent?

A

Relatively

The exception is that NE has a low potency at beta 2 receptors

Epi activates all alpha and betas; however, NE doesn’t activate beta 2

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9
Q

Draw the diagram showing epinephrine and norepinephrine actions on receptors

A

Epinephrine: agonist at ALL ANDROGENIC RECEPTORS

  • little change in blood pressure due to the fact that it activates a wide range of areas

Norepinephrine: Minimal activity at Beta 2 adrenergic receptors

  • Large increase in Blood pressure because it acts on specifically beta 1 receptors
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10
Q

Blood pressure =

A

cardiac output x vascular resistance (TPR)

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11
Q

Does epinephrine cause a large change in blood pressure?

A

No, but norepinephrine has a large increase (doesn’t activate Beta 2 for vasodilation)

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12
Q

Enhancing/decreasing sympathetic NS is known as

A

Increase = sympathomimetic

Decrease = sympatholytic

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13
Q

What are the drug mechanisms?

A
  1. Block adrenergic receptors - using antagonist
  2. Activate adrenergic receptors - using agonists
  3. Block uptake transporters
  4. Increase release of neurotransmitters - increase NE
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14
Q

What is known as the prototypical adrenergic agonist since it activates all receptors?

A

Epinephrine

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15
Q

What are the main effects of SNS activation?

A

Vasoconstriction in most tissues - alpha 1

Vasodilation in skeletal muscles - Beta 2

Increase HR and contractility - Beta 1

Dilate/relax bronchial smooth muscle - beta 2

Mydriasis - dilate pupil - alpha 1

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16
Q

What system is responsible for attention, arousal, wakefulness, anxiety, memory formation/ retention and vigor?

A

Noradrenergic system in the brainstem

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17
Q

T/F peripheral norepinephrine and epinephrine can cross the blood-brain barrier

A

FALSE but many adrenergic drugs do and can regulate brain adrenergic receptors to produce therapeutic or side effects

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18
Q

Cardiac output =

A

stroke volume x HR

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19
Q

Mean arterial pressure =

A

cardiac output x total peripheral resistance

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20
Q

Alpha 1 adrenergic agonists are used clinically for

Study These Flashcards
A

vasoconstriction - increasing TPR (CO goes down to maintain MAP)

mydriasis for eye exam

21
Q

Alpha 2 adrenergic agonist are used to

Study These Flashcards
A

reduce blood pressure

location is usually presynaptic; inhibits neurotransmitter release (works via negative feedback)

if vasodilation, TPR goes down; then the CO goes up (SNS activates increasing CO, maintaining MAP)

22
Q

Phenylephrine

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A

Alpha 1 selective - activation

used as a decongestant

reflex response - decreases SNS and increases PSNS - vagus nerve activity

Reflex bradycardia = reflex that is happening due to vasoconstriction that is occurring

23
Q

Histamine does what to the body

Blood pressure

Sympathetic nerve activity

Vagus nerve activity

Heart rate

Study These Flashcards
A

Causes vasodilation

Alpha antagonist - or alpha-blocker would give a similar but milder effect

Blood pressure - decreases BP

Sympathetic nerve activity - increased activity

Vagus nerve activity - decreased activity

Heart rate - increase HR

Reflex tachycardia

24
Q

Alpha-adrenergic agonists

Study These Flashcards
A

Major Uses

  • Alpha 1 - selective
    • Vasoconstriction
    • To cause mydriasis for eye exam
  • Alpha 2 - selective: reduce blood pressure

Drugs:

  • Epinephrine
    • used as vasoconstriction in combination with local anesthetics (also levonordefrin)
  • Phenylephrine (PE) - another vasoconstrictor
    • Alpha 1 - selective - sometimes used as a local vasoconstrictor
    • Used as a decongestant - PE is Sudafed
      • Causes vasoconstriction in the nose
  • Oxymetazoline
    • Somewhat alpha 1 - selective, primarily acts on alpha 1 because it is applied directly to tissue
    • Decongestant nasal spray - vasoconstriction
  • Clonidine
    • Alpha 2 selective
    • Decreases sympathetic outflow, reduces blood pressure
    • still in use but not a first line agent
      • Sometimes used for hypertension
        • used when someone is resistant to other hypertension medication
25
Oxymetazoline
**somewhat alpha - 1 selective** primarily acts on alpha 1 because it is applied directly to tissue Decongestant nasal spray - vasoconstriction
26
Clonidine
**Alpha 2 selective** Decreases sympathetic outflow, reduces blood pressure
27
Prazosin
**Alpha 1 selective antagonist** Antihypertensive
28
Tamsulosin
**Alpha 1 selective antagonist** Relaxes prostatic smooth muscle in benign Prostatic hyperplasia (BPH)
29
What could be the consequence of an alpha-blocker that is non-selective
Can cause **tachycardia** by blocking presynaptic alpha 2 receptors leads to **increased NE release** which can then **stimulate beta receptors**
30
Alpha blocker side effects
**Orthostatic hypotension** (decreases in BP due to changes in body position - sit to stand, common for people taking alpha blockers) **Reflex tachycardia** (less prevalent with alpha-1 selective drugs, drop in TPR and therefore body would try and increase CO) **Nasal congestion** (like phenylephrine - opposite of this)
31
What are the major uses of beta-adrenergic agonists?
**Beta 1** - stimulate cardiac output (rarely used) **Beta 2** - relax bronchial smooth muscle (very commonly used) = used *_primarily in asthma_*
32
Which drug works by activating alpha - 1 receptors?
oxymetazoline
33
Albuterol
**Beta 2 selective agonist for acute asthma exacerbations (rescue inhaler)** Short-acting drug, reacts quickly and lasts for a few hours
34
Salmeterol
**Long-acting beta 2 selective agonist used for asthma** lasts for 12-24 hours
35
Major uses of "beta blockers" = beta adrenergic receptor antagonists
* **_Nonselective or beta 1 selective agents_** * ***Decrease cardiac work*** (rate, force of contraction) * Anti-arrhythmic - decrease excitability of the myocytes of the heart * Antihypertensive (cardiac effect plus reduced renin) * Anti-angina - reduces the workload of the heart, decreases the O2 requirement of the heart * Treatment of heart failure * ***Decrease intraocular pressure (glaucoma)*** * **Beta 2 - selective**: none in clinical use, although nonselective drugs do block beta 2 * causes constriction of the airways, opposite of albuterol inhalers for asthma
36
Beta-blocker (beta-adrenergic receptor antagonists) major side effects
**_Related to Beta 1 blockade_**: hypotension, heart failure **_Related to Beta 2 blockade:_** hypoglycemia, bronchoconstriction
37
Propranolol
**Non-selective beta blockers (-****olol****)** * **Decreased cardiac output** by blocking beta 1 receptors in the heart * May produce **bronchoconstriction** by blocking beta 2 receptors in the lungs * contraindicated in asthmatics - inhaler will not work * **May impair glucose mobilization** by blocking Beta 2 receptors in the liver * impairs recovery from hypoglycemia in diabetics on insulin * **Inexpensive** * lots of history of use and therefore predictable, commonly used beta blocker
38
Metoprolol
**_Beta 1 selective (cardioselective) beta blockers_** * **Similar** usage and effects compared to **propranolol** * **Avoids bronchoconstriction and hypoglycemia** * Maybe more **expensive**
39
Acebutolol
Other beta blockers * Has **intrinsic** **sympatheticmimetic** activity (ISA) * Functions as **partial** **agonist** * **Avoids bradycardia** that occurs in some patients * this drug still gives heart SNS but also blocks the full agonist effects of EPI and NE, not as strong as an effect as a full beta blocker * on their own they can act as a weak agonist but can also block the receptor site
40
Labetalol
other beta blockers * **Blocks beta 1 , beta 2 and alpha 1** * Neat thing is that this also blocks alpha 1 * **Useful in hypertension** * affects both CO and peripheral resistance and therefore can treat hypertension - not a common drug
41
Unopposed alpha stimulation
Beta receptors blocked while alpha are being stimulated Leads to large increase in vascular resistance; reflex bradycardia This is why the use of **EPI is contraindicated for people on beta blockers**
42
How does cocaine act on receptors?
**_Indirect or mixed acting Sympathomimetics_** (indirect because they do not directly activate NE) they enhance sympathetic effects - sympathomimetrics **inhibits NET and NE reuptake** NET = NE reuptake terminal **raise NE levels in the synapse**
43
How does amphetamine act on receptors?
Enhances NE release and blocks reuptake
44
How does ephedrine/pseudoephedrine act?
Enhances NE release and has direct agonist activity Agonist on alpha and beta receptors
45
Abuse potential is increased in drugs that
readily enter the CNS block dopamine reuptake
46
Risk is highest with (direct/indirect) sympathomimetic drugs since adrenergic receptors are non-selectively activated
indirect
47
Sympathomimetic toxidrome
**_MATHS_** Mydriasis Agitation, arrhythmia, angia Tachycardia Hypertension, hyperthermia Seizure, sweating
48
Sympathomimetic drugs should be avoided or used only with extreme caution in individuals with pre-existing cardiovascular disease: such as
hypertension angina pectoralis (coronary heart disease) History of myocardial infarction (MI; heart attacks) Cardiac arrhythmias

Pharm Exam 1 (5 decks)

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