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Pharm Summer 2020 > Sympathetic System > Flashcards

Sympathetic System Flashcards

1
Q

Sympathomimetics

A

effects of sympathetic stimulation are mediated by NE.

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2
Q

NE and epi

A

NE is released from nerve terminals.

Epi is released into blood from adrenal medulla (adrenaline)

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3
Q

Receptor types of sympathomimetic drugs

A

Adrenergic:
Alpha 1 and Alpha 2
Beta 1 and Beta 2
*All are GPCR. Slow on/slow off. Desensitization can occur.
Main diff of all of these are location
*many agonists have selectivity for one of the major subtypes of receptors, but not specificity!

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4
Q

Selectivity vs specificity

A

Selectivity: Has diff affinities for many receptor types. Will be non- selective at high concentration. More selective at lower doses.

Specificity: No matter the concentration, will always bind 1 type of receptor.

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5
Q

Alpha 1 adrenoceptor

A 
Vasoconstriction 
Increased peripheral resistance 
Increased blood pressure 
Mydriasis 
Increased closure of internal sphincter of bladder (hold in urine)
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6
Q

Alpha 2 adrenoceptor

A

Inhibition of NE, Ach, and insulin release

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7
Q

Beta 1 adrenoceptor

A

Increased HR- Tachycardia
Increased lipolysis
Increased myocardial contractility
Increased release of renin

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8
Q

Beta 2 adrenoceptor

A

Vasodilation
Decreased peripheral resistance
Decreased blood pressure
Bronchodilation
Increased muscle and liver glycogenolysis (more glucose)
Increased release of glucagon
Relaxed uterine smooth muscles (have to pee)

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9
Q

Drugs that cause vasoconstriction. What is the reflex??

A

Reflex decreased HR

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10
Q

Drugs that cause vasodilation. What is the reflex?

A

Reflex increased HR

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11
Q

The net effect of any sympathomimetic will be a combo of

A

Its direct effect on a receptor and a counteraction by compensatory mechanisms. The bodys goal is to maintain homeostasis.

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12
Q

Cardiovascular system and Alpha 1 activation

A

Arterial and venous vasoconstriction–> leads to increased peripheral tolerance, which increases BP.
As reflex, will get a decrease in HR.

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13
Q

Cardiovascular system and Alpha 2 activation

A

Decrease transmission of NE (sympathetic info) resulting in a decrease in BP. Prob due to vasodilation (from parasympathetic becoming more dominant)

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14
Q

Cardiovascular system and Beta 1 activation

A

Increased HR (tachycardia) and increased contractility. Leads to an increase in CO and blood pressure.

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15
Q

Cardiovascular system and Beta 2 activation

A

Vasodilation –> Decreased peripheral tolerance –> decrease in blood pressure –> reflex of increased HR.

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16
Q

A non selective beta agonist will have a net effect of?

A

Decreasing blood pressure through B2 activation.

B1 increases BP and B2 decreased BP but B2 wins.

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17
Q

Respiratory system activation of Beta 2

A

Bronchodilation.

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18
Q

Eye and alpha 1 activation

A

Mydriasis (contraction of pupillary dilator muscle)

Good dilation drop

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19
Q

Eye and alpha 2 activation

A

Acts on iris and ciliary body to decrease IOP.
Decrease aqueous production
Increase uveoscleral outflow.

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20
Q

Eye and beta 2 activation

A

Relaxation of ciliary muscle- dilation but not significantly. Would not be a good drop.
Production of aqueous- increases IOP.

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21
Q

Urinary system and activation of Alpha 1

A

Constriction of bladder and prostate. Urinary retention.

22
Q

Beta 1 and beta 2 on metabolism

A

Beta 1: Increased lipolysis (breakdown of fat)

Beta 2: glycogenolysis (breakdown of glycogen into glucose) and Increased glucagon release from the liver from breaking down glycogen. This increases blood sugar.

23
Q

Epinephrine

A

Sympathomimetics.
Non-selective
Potent vasoconstrictor and cardiac stimulant (dose dependent- low dose, beta predominates)
Increases blood flow.

24
Q

Norepinephrine given as drug

A

Non selective Sympathomimetics. (little effect on Beta 2 bc B2 vasodilates)
Intense increase in peripheral resistance and blood pressure.

25
Q

Dopamine

A

Sympathomimetics. Precursor to NE. Has similar effects to NE.

26
Q

Phenylephrine

A

Direct acting Sympathomimetics
Alpha 1 selective
Mydriatic and decongestant (vasoconstriction)

27
Q

Midodrine

A

Direct acting Sympathomimetics
Alpha 1 selective
Treatment of orthostatic hypotension (decrease in BP that happens due to change in BP) Helps bc it constricts blood vessels and keeps blood at brain and not in extremities.

28
Q

Clonidine

A

Direct acting Sympathomimetics
Alpha 2 selective
Decrease in BP quickly (turns off sympathetic. Para dominates)

29
Q

Isoproterenol

A

Direct acting Sympathomimetics
Non-selective Beta agonist
Potent vasodilator at B2. Increases CO (more room in vessels for blood) and decreases BP.

30
Q

Dobutamine

A

Direct acting Sympathomimetics
Complex
Considered beta 1 but some have alpha 1 effects

31
Q

Albuterol *

A

Direct acting Sympathomimetics
Beta 2 selective
Causes bronchodilation- typically given as inhaler.

32
Q

Sympathomimetics inducing local vasoconstriction

A

Epinephrine
Phenylephrine
Brimonidine= lumify
Tetrahydrozoline- visine

33
Q

What receptors help treat glaucoma

A

Alpha 2 selective.

Apraclonidine and brimonidine. Causes slight meiosis.

34
Q

Horner syndrome symptoms

A

Unilateral. Ptosis, meiosis, anhydrosis. Can be caused by pre or post ganglionic neuron in the sympathetic system.

35
Q

How to test for Horner’s with 10% ophthalmic cocaine

A

Produces dilation of normal pupil. Prevents reuptake of NE. NE remains in synapse = dilation from sympathetic.

36
Q

How to test for Horner’s with 1% apraclonidine

A

Produces dilation of abnormal pupil. Mild alpha 1 antagonist activity.

37
Q

How to locate the lesion causing sympathetic denervation in Horner’s?

A

Once you already know which eye is abnormal, you can use hydroxyamphetamine drops to locate the lesion.

Dilation= preganglionic lesion
No dilation= postganglionic lesion

38
Q

Which are more common? alpha antagonists or beta antagonists?

A

Beta blockers more common.

Alpha blockers have limited clinical use.

39
Q

Alpha antagonist MOA

A

Bind to alpha receptors and prevent binding of agonist.
There are reversible- can be overcome with more agonists or
irreversible- bond cannot be broken. Effects are long lasting and require production of new receptors.

40
Q

Alpha antagonist effects on cardiovascular

A

Decrease arteriolar and venous tone. Lower peripheral and vascular resistance and blood pressure bc vasodilation. Can result in orthostatic hypotension and reflex tachycardia (bodys way of dealing with sudden vasodilation)

Other effects:
Miosis, Nasal stuffiness, increased urine flow.

41
Q

Phenoxybenzamine

A

Alpha antagonist
Irreversible
Alpha 1 > alpha 2
Also blocks histamine, Ach, and serotonin receptors.

Most SIGNIFCANT effect is stopping sympathetic vasoconstriction. Leads to vasodilation, reflex tachycardia, and orthostatic hypotension.

42
Q

Phentolamine

A

Non selective alpha antagonist (binds A1 and A2)
Reduces peripheral vascular resistance and causes cardiac stimulation. (opposite of A1)

Not available in US. Can cause severe tachycardia, arrhythmias and myocardial ischemia.

43
Q

Two drugs highly selective for A1a and A1d subtypes that are high on prostate smooth muscle.

A

Tamsulosin (Flomax) and alfuzosin. Not used for systemic high BP, only used for prostate.

Caution with Flomax if pt is undergoing cataract surgery

44
Q

IFIS

A

Intraoperative floppy iris syndrome.
Common in cataract surgery if patients are taking Tamsulosin (Flomax).

Causes billowing, flaccid iris. It can prolapse and get in the way. hard for it to dilate. May increase risk of complications.

45
Q

Yohimbine

A

Alpha 2 selective
Promotes NE release, as well as NO. NO increases smooth muscle relaxation and peripheral vasodilation.

Used to treat male erectile dysfunction.
Removed from US market due to financial reasons.
Used as supplement.

46
Q

Pheochromocytoma

A

Can help control hypertension. May be used for preoperative treatment for tumor of adrenal medulla (results in excessive secretion of NE and epi)

47
Q

Role of beta antagonists

A

Occupy beta receptors and prevent binding by agonists. -Competitive antagonism.
-Some are also partial agonists. Inhibit activation in presence of high agonist concentration, but modernly activate receptor in absence of endogenous agonist.

Can be specific for beta-1 receptor based on dose.

48
Q

why should you make sure a patient doesn’t have asthma if you are prescribing a beta blocker?

A

Will cause increase in airway resistance.

49
Q

Cardiovascular effects by beta blockers

A

Decrease in blood pressure in patients with hypertension (prob due to increase in renin release from B1)

Decrease in HR and cardiac output (due to B1)

50
Q

Respiratory tract effects by beta blockers

A

Increased airway resistance

51
Q

Eye effects from beta blockers

A

Decrease aqueous humor production (decrease IOP)

52
Q

Metabolic effects from beta blockers

A

Impair recovery from hypoglycemia.

Increase VLDL and decrease HDL cholesterol.

Pharm Summer 2020 (18 decks)

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