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Pharmacology > Sympathetic (Adrenergic) Pharmacology > Flashcards

Sympathetic (Adrenergic) Pharmacology Flashcards

1
Q

How does the PNS affect the GI glands, salivary glands, lacrimal glands, nasal glands?

A

The effect is from M3 muscarinic stimulation and produces watery secretory product

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2
Q

How does the SNS affect the GI glands, salivary glands, lacrimal glands, nasal glands?

A

The effect is from beta adrenergic stimulation and produces secretion of protein: enzyme and mucous
The effect alpha adrenergic stimulation and causes vasoconstriction, which decreases water and decreases and concentrates the secretion

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3
Q

How does the SNS affect vascular smooth muscle?

A

Causes contraction in the skin, splanchnic vessels via alpha1 receptors
Causes relaxation of the vessels in the skeletal muscle via muscarinic receptors

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4
Q

How does the PNS affect vascular smooth muscle?

A

It causes the release of EDRF form the endothelial cells via M3, which causes vessel relaxation

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5
Q

Norepinephrine mainly stimulates what receptors?

A

Alpha1 receptors in the vessels, which markedly increases blood pressure

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6
Q

Epinephrine mainly stimulates what receptors?

A

Epinephrine has a higher affinity for beta receptors (in cardiac muscles), which increases heart rate and contractility and has less effect on mean arterial pressure

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7
Q

How does the SNS affect GI smooth muscle?

A

The SNS relaxes the GI smooth muscle via beta2 receptors and causes contraction of the GI sphincter via alpha1 receptors

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8
Q

How does the PNS affect GI smooth muscle?

A

The PNS relaxes the GI sphincter and causes contraction of the GI smooth muscle via M3 receptors

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9
Q

What is denervation supersensitivity?

A

Destruction of sympathetic or parasympathetic nerves causes a decrease in function and there is a chemical adaptation of the organ, hence, an increase in intrinsic tone. There is also an increase in response to external neurotransmitter of organs that have been denervated due to an upregulation of cholinergic and adrenergic receptors in the end organs

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10
Q

What are adrenergic receptors?

A

There are at least 4 types: alpha1, alpha2, beta1 and beta2

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11
Q

Where do the adrenergic receptors work?

A

Effector organs: cardiac muscle, smooth muscle and glands. They all respond to norepinephrine and epinephrine (NE more to alpha and E more to beta)

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12
Q

What does the alpha1 receptor do? And what is the importance, medically?

A 
Vasoconstriction (medical: nasal decongestant, increase BP in trauma/shock)
Pupil dilation (medical: eye exams)
Inhibits uterine contraction in pregnancy (medical: delay birth, side effect)
Ejaculation (medical: none yet; drugs are in development)
Contraction of bladder neck and prostate neck (medical: usually just a negative side effect)
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13
Q

What does alpha2 receptor do?

A

It is located in the presynaptic junction

It inhibits neurotransmitter release, thus inhibiting sympathetic (adrenergic) activation

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14
Q

What are the alpha2 responses?

A

Though it inhibits adrenergic activation, its not complete nor perfectly opposite of alpha1. For example, it causes cardiac (and other) vasoconstriction, decrease norepinephrine release in the brain and inhibits lipolysis and insulin release

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15
Q

What is the primary medical importance of alpha2?

A

It is in the CNS (neuronal) and in hypertension

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16
Q

What are the functions of beta1?

A

In the kidneys it causes the release of renin, which causes vasoconstriction
In the heart it increases heart rate, force of contraction and velocity of conduction in AV nodes

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17
Q

What are the functions of beta2?

A 
Bronchial dilation
Relaxation of uterine muscle
Vasodilation
Glycogenolysis
Glucagon release
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18
Q

What does dopamine do?

A

Dilates renal blood vessels

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19
Q

What are the second messengers of adrenergic receptors?

A

Alpha1: IP3 and DAG
Alpha2: decrease cAMP
Beta1: increase cAMP
Beta2: increase cAMP

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20
Q

What is the distribution of adrenergic receptors?

A

Alpha1: blood vessels and GI spincters
Alpha2: presynaptic terminal
Beta1: heart
Beta2: airway, GI, urogenital

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21
Q

What are agonists of adrenergic receptors?

A

Alpha1: pseudoephedrine
Alpha2: clonidine
Beta1: isoproterenol and dobutamine
Beta2: Isoproterenol and terbutaline

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22
Q

What are antagonists of adrenergic receptors?

A

Alpha1: prazosin

Beta1 and beta2: propanolol

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23
Q

What are adrenergic agonists?

A

Stimulators (sympathomimetics) mimic the action of norepinephrine, dopamine and epinephrine
They can be selective or non-selective (of site, receptor subtype, tissue location)
Almost all are at least partially non-selective (majority of side effects)

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24
Q

How can adrenergic receptors be used?

A

Hemodynamic compromise (shock, depressed cardiac rhythm)
Bronchospasms (asthma)
Nasal and sinus congestion
Often used in emergency situations

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25
Q

What is pseudoephedrine?

A 
Nasal decongestant (non-specific: increases heart rate)
Good for asthmatics
26
Q

What does isoproterenol/dobutamine do?

A

Increases heart activity

27
Q

What does propanolol do?

A

It decreases heart rate, but also contracts lungs

28
Q

What does isproterenol do?

A

Opens lungs, but also increases heart rate

29
Q

How is epinephrine work?

A

It stimulates both alpha and beta receptors (non-selective)
It’s used in emergencies for severe acute asthma, cardiac arrest and anaphylaxis (type 1 hypersensitivity) and an adjunct to anesthetic (keeps it from getting into the system too quickly and keeps it there longer)
It’s given parenterally because the GI tract enzymes destroy it
It doesn’t stay around very long and it has lots of side effects

30
Q

What are the side effects of epinephrine?

A 
Stimulant effects on brain (anxiety, paranoia, headache, tremor)
Hypertension-induced haemorrhage
Cardiac arrythmia
Hyperglycemia in diabetics
Other non-selective effects
31
Q

How do we use epinephrine medically?

A

Primarily used to treat shock (increases blood pressure)

32
Q

What do brain-targeted non-selective adrenergic agonists do?

A

Critical role of norepinephrine and dopamine in mood and motor control
Depression, anxiety and Parkinson’s disease
It has to cross the blood brain barrier to effect the brain
Many side effects come from undesired peripheral SNS activation

33
Q

What are some brain-targeted non-selective sympathomimetics?

A 
Cocaine
Ampetamines
Ritalin
MDMA
Anti-Parkinson's Disease
Anti-depressants
34
Q

What does cocaine do?

A

It inhibits the reuptake of serotonin, norepinephrine and dopamine
Non-selective for receptor subtype and organ
Peripheral activation causes side effects (increased heart rate, sweating, hypertension, etc.)

35
Q

What happens when you have too much cocaine?

A

Causes anhedonia (inability to feel pleasure)

36
Q

What do amphetamines do?

A

They in inhibit uptake and increases neurotransmitter release (including serotonin and norepinephrine)
They have very potent effects in the CNS and periphery
Ritalin and MDMA

37
Q

What are MAOi? What are they used for? What are some examples? What are their side effects?

A

Monoamine oxidase inhibitor
They are anti-parkinson’s disease drugs (also can be used as antidepressants)
Selegiline (used with levadopa)
Side effects: dry mouth, constipation, tachycardia

38
Q

What is an example of an MAOi used as anti-depressants? What are side effects?

A

Phenelzine

Dry mouth, constipation, urinary retention, mydriasis, hyperthermia, sweating, hypertension

39
Q

What is an example of an tricyclic antidepressants? How do they work? What are contraindications?

A

Amytriptyline
They inhibit metabolism of the neurotransmitter, making stay around longer
Contraindications: urinary retention, pregnancy, myocardial infarction, congestive heart failure

40
Q

What receptors do selective sympathomimetics act on?

A

Alpha1, beta1, beta2

Recall that alpha2 receptors inhibit sympathetic response, so activating alpha2 is not sympathomimetic

41
Q

What do peripheral sympathomimetics alpha1 agonist?

A

The primary function of alpha1 is vasoconstriction, so drugs will be usually geared to this:
Nasal decongestant (reduces blood flow, thus fluid release
Increases peripheral resistance, thus increasing blood pressure (trauma, bleeding, shock)
Example: phenylephrine

42
Q

What are the side effects of alpha1 activation?

A

Stimulant effects! Cocaine, nicotine, caffeine, meth all stimulate adrenergic
Sweats, manic behaviour, anxiety, paranoia
Increased thinking speed and reflexes
Weight loss, hyperglycaemia, impotence, hypertension, GI effects, exacerbation of prostatic urinary inhibition, tachycardia (hypertensive response)

43
Q

What does beta1 activation cause?

A

Increases: heart rate, force of contraction, velocity of conduction in AV node
Dobutamine: increases cardiac output; it’s used in congestive heart failure

44
Q

What does beta2 activation cause?

A

Bronchial dilation, relaxation of uterine muscle, vasodilation, glycogenolysis
Almost exclusively found as inhalers
Other uses: IV inhibition of preterm labor

45
Q

What causes short acting bronchial dilation?

A

Albuterol (salbutamol, ventolin) - asthma, COPD

46
Q

What causes long acting bronchial dilation?

A

Salmeterol: works 12 hours vs 2 hours for salbutamol

47
Q

What do anti-adrenergic drugs do?

A

Inhibit or block the effects of sympathetic nerve stimulation (same effect as pro parasympathetic drugs)
Not naturally occurring (synthetic drugs)
Most block (antagonist action) alpha1, beta1 and beta2 receptors
Alpha2 agonists are adrenergic antagonists

48
Q

What do alpha2-adrenergic agonists do?

A

Alpha2 agonists treat hypertension
Despite being an agonist, they produce a blocking of release of sympathetic neurotransmitter
They inhibit the release of norepinephrine in the CNS
They lower blood pressure
Example: clonidine

49
Q

What do alpha1 antagonists do?

A

Remember alpha1 causes vasoconstriction and constriction of the prostate neck. Inhibition of this with drugs such as prazosin and doxasin (competitive alpha1 blockers) would cause a decrease in blood pressure

50
Q

What does tamsulosin do?

A

Treats prostatic hypertrophy and vasospastic (urinary) problems (more selective for alpha1A receptors on prostate)

51
Q

What do alpha1 antagonists do in congestive heart failure?

A

They cause a decrease in preload and afterload by decreasing peripheral resistance (vasodilation)
This means the heart has less resistance to contract against, leading to increased cardiac output, decreased pulmonary congestion (prazosin). So we can use one drug to activate a SNS receptor subtype found on the heart (beta1) to increase cardiac output and a different drug to inhibit a SNS receptor subtype found on peripheral vessels (alpha1) to decrease peripheral resistance to treat the same condition

52
Q

What are the side effects of blocking alpha1 receptors?

A

Early on, it can cause massive orthostatic hypotension (fainting when standing), so start with low doses
Vertigo
Sexual dysfunction
Reflex tachycardia
Vasovagal syncope (standing up and fainting)
Floppy iris syndrome

53
Q

What are beta blockers?

A

They are used to treat rapid pulse arrhythmias, hypertension, myocardial infarction, and other heart problems
They decrease contractility, cardiac output, heart rate and blood pressure
They reduce oxygen demand on the heart
They slow the conduction through the AV node and slow the ventricular response

54
Q

What are the differences between the different generations of beta blockers?

A

First generation: non-selective (beta1 and beta2)
Second generation: cardio-selective (beta1)
Third generation: partially selective (with alpha1 inhibition)

55
Q

What do non-selective beta blockers do?

A

Block both beta1 (heart) and beta2 (lung) receptors (propanolol)
Can cause bronchospasms (not for use with asthma)

56
Q

What does propanolol do?

A

Decreases cardiac output
Reflex peripheral vasoconstriction (slow decrease in hypertension)
Bronchoconstriction (danger to asthmatics and COPD)
Decreased glycogenolysis and glucagon secretion - this amplifies the effect of insulin on hypoglycemia

57
Q

What is propanolol used for?

A

Reduced hypertension through decreased cardiac output, decreased renin and decreased peripheral resistance (long term)
Angina and myocardial infarction form reduced oxygen demands
Blocks the effect of hyperthyroidism on adrenergic system

58
Q

What is timolol?

A

Other non-specific beta blocker - used for glaucoma by decreasing production of aqueous humor and intraocular pressure

59
Q

What do second generation beta blockers do?

A

These are developed to specifically avoid the bronchoconstriction of beta2 receptors
They are used to treat hypertension - they have reduced pulmonary, vascular, and blood glucose effects
They are especially good for diabetic hypertensive patients (very common co-morbidity)
Example: atenalol

60
Q

What do third generation beta blockers do?

A

Block alpha 1 receptors, which leads to reduced peripheral resistance, less load on the heart
Carvedilol: higher affinity for beta1 and beta2 so reduces heart rate significantly and may exacerbate asthma
Labetalol: higher affinity for alpha1, so reduce blood pressure without large effect on resting heart rate. Used for pre-eclampsia (rise in blood pressure in pregnant women) and emergency

61
Q

What do beta2 receptors do and when would you need them?

A

They would cause bronchoconstriction

May be necessary to counteract some toxin

Pharmacology (15 decks)

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