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Pathology > Adrenergics > Flashcards

Adrenergics Flashcards

1
Q

Sympathetic:
Length and nt of preganglionic axons
Length and nt of postganglionic axons

A

Short + nicotinic Ach

Long + adrenergic NE

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2
Q

Parasympathetic:
Length and nt of preganglionic axons
Length and nt of postganglionic axons

A

Long + nicotinic Ach

Short + muscarinic Ach

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3
Q

Somatic Motor:
Length of axon
Neurotransmitter

A

Ach, premotor neuron stretches from ventral horn to muscle

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4
Q

List the major visceral organs that are innervated by the parasympathetic nervous system (as discussed in lecture) and describe the functional responses of the organs to activation of either system. (5)

A 
Eye: Pupillary Constriction (miosis)
Heart: Negative Chronotropy (bradycardia)
Bronchioles:  Constriction
GI tract:  Increased Motility
Bladder:  Stimulates Emptying
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5
Q

Exceptions to the autonomic neurochemistry rules

A

Sympathetics that innervate sweat glands and vascular blood vessels that perfuse skeletal muscles

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6
Q

List the major visceral organs that are innervated by the sympathetic nervous system (as discussed in lecture) and describe the functional responses of the organs to activation of either system. (6)

A

Eye: Pupillary Dilation (mydriasis)
Heart: Increased Chronotropy (tachycardia), Increased Inotropy
Bronchioles: Smooth muscle relaxation
Blood vessels: Constriction and relaxation
GI: Decreased Motility
Bladder: Inhibits Emptying (sphincter contraction)
Metabolic functions: Increased Blood Sugar

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7
Q

Which tissues have alpha-1 receptors?

A

Most vascular smooth muscle

Pupillary dilator muscle

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8
Q

Where on neurons are alpha-2 receptors located?

A

a2’s are found on adrenergic nerve terminals and inhibit neurotransmission (know mechanism).

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9
Q

Which tissues have beta-1 receptors?

A

Heart and juxtagomerular cells

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10
Q

Which tissues have beta-2 receptors?

A

Respiratory, uterine and vascular smooth muscle

Somatic motor nerve terminals

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11
Q

Which tissues have dopamine-1 receptors?

A

Renal and other splanchnic blood vessels

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12
Q

Effect of alpha-1 and alpha-2 receptors on vascular smooth muscle

A

vasoconstriction and increase of resistance

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13
Q

Effect of alpha-1 receptors on pupillary dilator muscle

A

Contraction (mydriasis)

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14
Q

Effect of beta-1 receptors on the heart

A

Increases heart rate and contractility

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15
Q

Effect of beta-1 receptors on the juxtaglomerular cells

A

Stimulates renin release

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16
Q

Effect of beta-2 receptors on vascular smooth muscle, respiratory, and uterine tissue

A

Relaxation

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17
Q

Effect of beta-2 receptors on somatic motor nerve terminals

A

Tremor (common side effect of adrenergics)

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18
Q

Which second messenger system is coupled to a1r’s?

How does this second messenger mediate the responses of the vascular smooth muscle and the eye?

A

a1R’s are coupled to
Gaq proteins. These activate the PKC pathway.
Increased cystosolic Ca
This results in an activated protein kinase–> muscle contraction
Vasoconstriction and mydriasis

In the bronchial vasculature, vasoconstriction means that there is less of a chance for mucus to leak out–> decreasing bronchial secretions (counteracts histamine-mediated vasodilation, vessels less leaky, fewer secretions)

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19
Q

Which second messenger system is coupled to a2r’s?

How does this second messenger mediate the vascular response?

A

a2R’s are coupled to
Gi proteins. When activated, the protein inhibits adenylyl cyclase.
Less cAMP
Less phosphorylation of Ca channels
Channel still opens, but the effect is attenuated
Presynaptic neurons release less NE

This results in a less drastic vasoconstriction than would occur without a2r’s. Because there are fewer a2r’s than a1r’s, the vessel still constricts. Additionally, if enough NE is taken back into the neuron, the transporter flips, and norepinephrine enters the synapse.
Also, a2r’s mediate vasoconstriction on endotheilial cells distant from sympathetic termini

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20
Q

Which second messenger system is coupled to b1r’s?

How does this second messenger mediate the response of the heart?

A

b1R’s are coupled to
Gas proteins. When activated, the protein stimulates adenylyl cyclase.
More cAMP
More phosphorylation of Ca channels
Probability of calcium channels opening increases, lowering the threshold for depolarization
Influx of funny current makes depolarization faster
Calcium-induced calcium release from endoplasmic reticulum results in increased contractility
Thus B1 agonists increase both chonotropy and inotropy

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21
Q

Which second messenger system is coupled to b2r’s?

How does this second messenger mediate the response of the relevant organs?

A

B2 agonists act on Gas proteins, increasing cAMP.

PKA also phosphorylates myosin light chain kinase, resulting in muscle relaxation

This occurs in the bronchioles, uterus, and vascular smooth muscle

Also results in increased aqueous humor production

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22
Q

How does a2r signaling affect blood vessels in the skeletal muscle?

A

Agonist activates Gi
cAMP is decreased
Myosin light chain kinase is phosphorylated
This results in smooth muscle contraction

Vasoconstriction

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23
Q

List the two adrenergic receptors that are expressed on the pre-synaptic membrane of both
noradrenergic and non-noradrenergic nerve terminals and describe how their activation
influences neurotransmitter release.

A

a2r activation serves as a type of negative feedback for NE
M3 receptor
Transporter normally takes NE back into cell. If enough NE accumulates in the cytoplasm, transporter reverses direction, releases NE from cell.

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24
Q

Arrange epinephrine, norepinephrine and the prototypical beta-adrenergic receptor agonist,
isoproterenol, in order of their affinity for the 4 main adrenergic receptors discussed in
lecture

A

a1-receptors: EPI ≥ NE&raquo_space; Iso
a2-receptors: EPI ≥ NE&raquo_space; Iso
b2-receptors: Iso > Epi&raquo_space; NE
b1-receptors: Iso > Epi = NE

25
Q

Which receptor does epinephrine act on?

A

Low doses- beta receptors

High doses- beta and alpha receptors

26
Q

Which receptor does norepinephrine act on?

A

A1, A2 and B1 receptors

27
Q

Describe how dopamine influences cardiovascular function and what receptors mediate these effects.

A

At lower doses, dopamine acts on D1-receptors and decreases total peripheral resistance

At lower doses, dopamine increases cardiac output via B1-receptors

At higher doses, a1, a2 and b1 receptors would be activated, and both MAP and TPR would increase (cardiac and vascular effects)

28
Q

Describe how norepinephrine influences cardiovascular function and what receptors mediate these effects.

A

Norepinephrine acts on b1 receptors to increase cardiac output

Norepinephrine acts on a1 and a2 to increase TPR

Due to the increased resistance, the baroreflex decreases heart rate

This increases MAP

29
Q

Which receptor does dopamine act on?

A

a1, a2, b1 and d1 receptors

30
Q

Describe how epinephrine influences cardiovascular function and what receptors mediate these effects.

A

Lower doses of epinephrine act on b1 receptors to increase cardiac output.

They also act on b2 receptors to decrease TPR and thus diastolic pressure

Higher doses of epinephrine act on a1, a2, and b1, increasing both TPR and cardiac output

31
Q

Describe how epinephrine influences respiratory function and what receptors mediate these effects.

A

Acts on b2 to relax smooth muscles in the bronchioles (bronchodilation)

Acts on a1 to decrease bronchial secretions

32
Q

Isoproterenol

Relative affinity for the different adrenergic receptors
How does this relate to their ability to influence vascular tone, bronchiole smooth muscle relaxation and cardiac contractility.

A

beta agonist

B2- Decrease TPR, bronchodilation

B1 - increase cardiac output

33
Q

Dobutamine

A

b1 agonist
can bind b2 and then alpha receptors at higher concentrations

b1- Increase cardiac output
Toxicity - hypotension via b2 activation

34
Q

Terbutaline and Albuterol

A

b2 agonist

b2 - bronchodilation and uterine relaxation

35
Q

Isoproterenol

All indications

A

Bradycardia or heart block when TPR is high

36
Q

Clonidine

A

selective a2 agonist
crosses BBB

Binds a2 receptors in the brain to reduce sympathetic input, decreasing blood pressure
???
Reduced a2 results in decreased tonic drive to preganglionic fibers, decreased activation of the motor neuron, and- decreased contraction

37
Q

Phenylephrine

Mechanisms behind side effects

A

Hypertension via increased TPR ???

38
Q

Phenylephrine

All indications

A

Hypotension during anesthesia
SV tachycardia
Mydriatic agent in ophthalmic Rx
Nasal congestion

39
Q

Dobutamine

Mechanisms behind side effects

A

Hypotension - if too much is given, dobutamine starts to stimulate b2 receptors, and this can result in hypotension

40
Q

Dobutamine

All indications

A

Short-term Rx for CHF or cardiogenic shock

41
Q

Terbutaline and Albuterol

Mechanisms behind side effects

A

Tachycardia - B1 receptors, stimulated at high doses
Muscle Tremor - b2 agonists on skeletal muscle can cause tremor when stimulated
Tolerance - b2 receptors internalize after a while

42
Q

Terbutaline and Albuterol

All indications

A

Bronchospasm

Chronic rx of obstructive airway dx

43
Q

Clonidine

Mechanisms behind side effects

A

a2 agonist, reduced sympathetic input can lead to:
Dry mouth - sns allows for salivary secretion
Sedation - alertness requires sns
Bradycardia - increased heart rate requires sns
Hypertensive crisis
(after acute withdrawal) - sudden surge of sns

44
Q

Clonidine

All indications

A

Hypertension due to sympathetic activation

45
Q

Dopamine

All indications

A

/

46
Q

Norepinephrine

All indications

A

/

47
Q

Epinephrine

All indications

A

/

48
Q

List 4 commonly used indirect acting sympathomimetics

A

(NE and DA reuptake transporter inhibitor)
Methamphetamine

Pseudoephedrine + ephedrine

Amphetamine

Methylphenidate
(Tyramine - found in food, acts like NE)

49
Q

Describe the most important toxic side effects of indirect acting sympathomimetic drugs.

A

Can cross the blood-brain barrier and become addictive
Tachycardia (b1)
Don’t take with MAOI’s, as this will further increase NE and DA in the cytoplasm, which can reverse more transporters

50
Q

Describe the most important therapeutic uses indirect acting sympathomimetic drugs.

A

Attention Deficit Disorder
Narcolepsy
Nasal congestion

51
Q

List the 5 conditions that are most commonly treated with b-blockers and the mechanism by which b-blockers produce their beneficial effects in that condition.

A

Hypertension - blockage of b1 receptors decreases heart rate, contractility and renin release. Sympathetic activation is also decreased by an unknown mechanism.

Angina is a sign of myocardial ischemia - b-blockers reduce contractility and thus, o2 consumption

Glaucoma - decreased sns activity reduces aqueous humor production

Congestive Heart Failure - b-blockers reduce contractility and thus, o2 consumption

Arrhythmia- decreased hr may help restore normal rhythm or resolve tachycardia

52
Q

List the 5 conditions that are most commonly treated with b-blockers and the mechanism by which b-blockers produce their beneficial effects in that condition.

A

Hypertension - blockage of b1 receptors decreases heart rate, contractility and renin release. Sympathetic activation is also decreased.

Angina is a sign of myocardial ischemia - b-blockers reduce contractility and thus, o2 consumption

Glaucoma - decreased sns activity reduces aqueous humor production

Congestive Heart Failure - b-blockers reduce contractility and thus, o2 consumption

Arrhythmia- decreased hr may help restore normal rhythm or resolve tachycardia

53
Q 
Identify the 7 b-adrenergic antagonists discussed in class and assign them to one of the 3
commonly recognized categories of b-blockers they belong.
A

Nonselective beta-blockers - propanolol, naldolol, timolol
Cardioselective beta-blockers - atenolol, metoprolol, esmolol
Partial beta-agonist - pindolol

54
Q

Describe how the 7 b-adrenergic antagonists discussed in class differ from one another in their:

a. ) receptor subtype selectivity
b. ) relative duration of action
c. ) ability to cross the blood brain barrier

d.)and describe what advantage these attributes may provide in treating particular patient populations.

A

a.) Propanolol, naldolol and timolol bind b1 and b2.
Atenolol, esmolol and metoprolol bind b1.
Pindolol is a partial b-agoninst that binds b1 and b2.

b. ) Naldolol has a long half life.
c. ) Atenolol and metoprolol can cross the blood-brain barrier and shut down sympathetic activation.

d.) Due to the lack of metabolic effects (no b2 activation), cardioselective b-blockers are better suited for treating diabetics.
Naldolol has a long half-life and is well-suited for noncompliance populations (elderly, dementia pts. etc.).
Timolol can cross the blood-eye barrier and treat glaucoma.
Atenolol and metoprolol cross the blood-brain barrier and can shut down sympathetic activation.

55
Q

Describe how toxic side effects of the drugs differ with their receptor subtype selectivity.

A

Bronchospasm - though mediated via b2 inactivation, it is possible that even cardioselective beta blockers can block b2 at a high enough dose. Because different patients have different sensitivities, beta blockers shouldn’t be given to asthmatics

Both non-selective b-blockers and partial b-agonists decrease b2 activity. Since b2r’s seem to mediate glucose metabolism to some degree, if a diabetic taking one of these were to become hypoglycemic, the resulting increase in plasma epinephrine would not signal the cells to release glucose, and the b2r’s in muscle would not elicit a tremor in response to the plasma epinephrine.

B1 activity is blocked in both non-selective b-blockers and cardioselectives. Bradycardia can then result. as there is less stimulation of the SA node. Partial agonists weakly activate B1’s but do that block them. For this reason, they do not cause bradycardia.

Increased triglycerides - b2 receptors might be involved in lipolysis and the release of fats into the blood. Partial agonists still allow this to happen, and cardioselectives do not block b2 receptors. Only seen with non-selective b-blockers.

Hypotension - seen in cardioselectives and partial agonists. If too much is given, b2r’s can mediate hypotension. This is not allowed in the case of non-selectives, as the b2 receptors are blocked.

56
Q

List the 2 non selective a-adrenergic antagonists discussed in lecture, their receptor subtype
selectivity and the conditions for which they are used.

A

Phentolamine, Phenoxybenzamine: non-specific alpha-antagonists. Phentolamine is reversible and phenobenzamine is irreversible.

Rx for hypertension associated w/ pheochromocytoma (because a-blocking would decrease TPR) and Vasoconstrictor-induced extravasation (if a vasoconstrictive drug seeps out of vasculature, it can cause massive vasoconstriction in the area and ischemia, leading to necrosis. These drugs can reverse that.)

57
Q

List the most serious side effects produced by selective and non-selective a-adrenergic receptor antagonists.

A

Non-Selectives:

Prolonged hypotension - Large drop in bp due to blockage of alpha receptors

Reflex tachycardia - Blocking a2’s stops the negative feedback that reduces NE release. The excess NE then binds to beta receptors, causing a large tachycardic response (B1). b/c of this, non-selective a-blockers are normally paired with b-blockers.

Selectives:

Orthostatic hypotension- Large drop in bp due to blockage of alpha-1 receptors

58
Q

Explain why selective a1-adrenergic receptor antagonists are more preferable for use in
hypertension than non-selective a-adrenergic receptor antagonists.

A

A2r’s have no effect on heart rate because a2r’s are unbound and thus, free to mediate NE negative feedback. Additionally, because more a2 are open, there is less beta-binding and thus, less cardiac side effects. They also do not need to be co-prescribed with beta-blockers.

Pathology (17 decks)

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