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D2 - FALL - Par 2 > Pharmacology - Autonomic Drugs > Flashcards

Pharmacology - Autonomic Drugs Flashcards

1
Q

which part of the nervous system makes no synaptic junction in (ganglia) betw the spinal cord and effector organ?

A

somatic (voluntary) nervous system

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2
Q

are the nerves of the somatic nervous system myelinated?

A

yes

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3
Q

if you section the somatic nn, what happens?

A

muscle paralysis, resulting in muscular atrophy

*somatic nn regenerate very slowly

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4
Q

which part of the nervous system makes synaptic junction in (ganglia) betw the spinal cord and effector organ?

A

autonomic nervous system

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5
Q

are autonomic nn myelinated?

A

preganglionic fibers are myelinated; postganglionic fibers are not.

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6
Q

In the parasympathetic nervous system, where does the cranial outflow originate?

A

CN’s III, VII, IX, & X

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7
Q

In the parasympathetic nervous system, where does the sacral outflow originate?

A

sacral nn = 2, 3, 4

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8
Q

Which part of the autonomic nervous system has more preganglionic nn? which one has more postganglionic nn?

A

more preganglionic to postganglionic nn = parasympathetic sys

more postganglionic to preganglionic = sympathetic sys

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9
Q

Where do the SNS’s preganglionic nerve fibers originate?

A

lateral horns of spinal cord (T2 to L2 or L3)

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10
Q

What type of innervation does the bronchi have? What about bronchial smooth muscles?

A

bronchi = sympathetic; bronchial SM = parasympathetic

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11
Q

What would happen if you sectioned autonomic nns?

A

does not completely abolish function of organ bc most of the organs have intrinsic functions

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12
Q

What NT does the somatic nerv sys use? And what is the effector organ?

A

AcH; skeletal muscle (motor)

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13
Q

What are the NTs for sympathetic inn to the smooth muscles, cardiac cells, and gland cells? Include pre-/postganglionic.

A 
preganglionic = Ach
postganglionic = NE
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14
Q

What are the NTs for sympathetic inn to the sweat glands? Include pre-/postganglionic.

A 
preganglionic = Ach
postganglionic = Ach
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15
Q

What are the NTs for sympathetic inn to the adrenal gland’s medulla ganglion? Include pre-/postganglionic.

A 
preganglionic = Ach
postganglionic = cells of the medulla which secrete epi/NE
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16
Q

How do the postganglionic cells of the adrenal medulla secrete epi/NE?

A

directly into the blood stream rather than into a synapse

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17
Q

What role does NE have in the brain?

A

for arousal

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18
Q

What role does dopamine have in the brain?

A

motor coordination, pleasure

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19
Q

What role does serotonin have in the brain?

A

appetite, depression

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20
Q

What role does glycine have in the CNS?

A

inhibitory NT in the spinal cord

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21
Q

What role does GABA have in the CNS?

A

suppresses activity of neurons in CNS

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22
Q

What is anandamide?

A

endogenous cpd similar to marijuana that has anti-anxiety effects and related to bliss or delight

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23
Q

what are enkaphalins?

A

endogenous opioids for suppressing pain

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24
Q

All of the inner linings of blood vessels in the periphery (endothelial cells) produce what continuously? And what type of nerves supply this?

A

NO; adrenergic

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25
Q

What does NO do?

A

opposes the excitatory actions of blood vessels (vasodilation, inc blood flow); in smooth muscle it will cause hypotension

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26
Q

What are the events occurring during an erection involving NO and NE?

A

NE is released in blood vessels all the time, but when NO is released during erection, its effect overpower the vasoconstriction caused by NE until ejaculation. Then the NE overpowers the NO lowering the blood flow.

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27
Q

What molecule does NO activate during an erection?

A

activates soluble guanylate cyclase

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28
Q

what does guanylate cyclase do?

A

synthesizes cGMP from GTP

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29
Q

_____ is believed to be the main vasoactive nonadrenergic, noncholinergic neurotransmitter and chemical mediator of penile erection

A

Nitric oxide (NO)

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30
Q

Acting as a second messenger molecule, ____ regulates the activity of calcium channels as well as intracellular contractile proteins that affect the relaxation of corpus cavernosum smooth muscle

A

cGMP

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31
Q

What are some excitatory NTs?

A

dopamine, NE, epi, glutamate, acetylcholine

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32
Q

What are some inhibitory NTs?

A

serotonin, GABA, anandamide (this last one could also have excitatory effects–not sure yet)

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33
Q

____ has an important role in cognition and memory. (Think Alzheimer’s.) Also in motor movements. (Think Parkinson’s.)

A

Ach

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34
Q

What is released from terminals of specific sensory neurons and associated w/ inflamm and pain?

A

Substance P!

  • it coexists w/ excitatory NT glutamate in primary afferents that respond to painful stimul.
  • may be involved in neurogenic inflamm
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35
Q

what types of fibers/nerves are cholinergic?

A
  1. pregang fibers of both sympathetic & parasympathetic nerv sys
  2. postgang PS fibers
  3. post gang sympathetic n for sweat gland
  4. pregang sympathetic fibers to adrenal gland
  5. somatic nn
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36
Q

what types of fibers/nerves are adrenergic?

A

postgang fibers of sympathetic sys (except for those innervating sweat glands–cholinergic nn)
*also adrenal medulla are modified sympathetic neurons that release epi/NE

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37
Q

what types of fibers/nerves are nitrergic?

A

postgang fibers innervating sex organs, some postgang fibers in intestine & lower esophageal sphincter

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38
Q

What effect does NE have on the heart? On the brain? On the eyes? In the intestine?

A

heart - inc HR, force, BP
brain - inc signals (inc alertness)
eyes - dilates pupil
intestine - inc sphincter tone (contracts) & relaxes mm–can cause constipation

*recall that NE is released during postgang sympathetics (w/ the exception of sweat glands & adrenal medulla)

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39
Q

what is Ach’s effect on the sphincter?

A

Ach relaxes sphincter.

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40
Q

how much NE is taken back up in the synaptic cleft?

A

80-90%; the majority!

*process called neuronal uptake

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41
Q

Small fraction of NE in the cytosol is metabolized by what?

A

MAO–monoamine oxidase

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42
Q

Some of the NE is taken up by extraneuronal cells and metabolized by?

A

COMT

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43
Q

Epi & NE are synthesized from what AA?

A

tyrosine

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44
Q

How is tyrosine converted to DOPA? And then how is DOPA converted to dopamine?

A
  • Tyrosine to DOPA via tyrosine hydroxylase

- DOPA to dopamine via L-DOPA decarboxylase (aka L-aromatic AA decarboxylase aka LAAD)

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45
Q

How is NE made from dopamine?

A

chromogranins (aka Dopamine-B-hydroxylase)

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46
Q

What ion influx triggers exocytosis of NE into the synaptic cleft?

A

Calcium

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47
Q

What enzyme converts NE to epi?

A

PNMT = phenylethanolamine N-methyltransferase

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48
Q

What are differences between NE & epi?

A
  • NE = NT; acts locally—is released from the nn.

- Epi = hormone; can act at a distance (circulates, acts on many tissues)

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49
Q

What is a neuromodulator and an example of a neuromodulator?

A
  • substance that can enhance/reduce release of NTs; ex. angiotensin 2
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50
Q

Metyrosine is used to treat what disease?

A

pheochromocytoma (tumor of adrenal gland)–secrete high amts of catecholamines

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51
Q

what is the rate limiting step of NE synthesis?

A

tyrosine hydroxylase step; used in tx for pheochromacytoma (drug: Metyrosine)

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52
Q

Issues w/ DOPA decarboxylase results in…? What is the tx for this?

A

degeneration of neurons in brain that release DOPA; L-DOPA or carbidopa

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53
Q

What is carbidopa used for?

A

Tx for Parkinson’s; used in adjunct w/ L-DOPA

  • carbidopa does NOT cross the blood-brain barrier, so it works in the periphery (reduces metabolism of L-DOPA in periphery)
  • L-DOPA is in the periphery, but is not blocked completely in the brain–so it is more available there, if we reduced its metabolism in the periphery.
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54
Q

What is the main goal of the tx for parkinson’s?

A

inc production of dopamine!

  • this is done by increasing levels of DOPA by using L-DOPA & carbidopa.
  • reduce DOPA metabolism in the periphery (you want more of it in the brain!)
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55
Q

Disulfiram is used to treat what?

A

alcoholism; inhibits actylaldehyde dehydrogenase; disulfiram chelates w/ Cu in dopamine-B-hydroxylase (enzyme that converts dopamine to NE), inhibiting it!
- you will accumulate acetylaldehyde if you use this drug… so if you drink and take this drug, you may get hypertension!!

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56
Q

What effect does excess acetylaldehyde cause?

A

flushing, headache, nausea, vomiting, perfuse sweating

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57
Q

vesicular monoamine transport system (VMAT)?

A

transport NE and dopamine into synaptic vesicles; H out and NE in

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58
Q

What is reserpine? Tx for?

A
  • an inhibitor of DA & NE uptake into synaptic vesicles (blocks VMAT)
  • inhibits NE production bc blocked entry of dopamine into the vesicle
  • also no storage of NE (depletes NE from nn)
  • tx for hypertension & psychosis; to reduce agitation in horses
  • does NOT interfere w/ uptake from nerve memb–only the vesicles!!
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59
Q

What is reserpine’s effect in the brain?

A

depletes dopamine, NE, serotonin

*when they began to use reserpine to treat hypertension & psychosis, pts began to show suicidal tendencies.

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60
Q

What does the PSNS do to the GI system?

A

promotes peristalsis and gut motility

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61
Q

What nerv system causes GI cramps & diarrhea?

A

dec in NE (dec in SNS); inc in PSNS

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62
Q

what converts a-methyldopa to a-methyldopamine?

A

dopadecarboxylase

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63
Q

what converts a-methyldopamine to a-methylNE?

A

dopamine-B-hydroxylase

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64
Q

What is a-methyldopa (aldornet) used for?

A

pregnancy induced hypertension (preecalampsia)

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65
Q

a-methylNE is taken up by the nerves and…?

A

displaces NE (“false NT” bc it is not an endogenous substance but stored and acts like NE); activates alpha-2-receptors and reduces the flow of impulses from the brain

  • it dec sympathetic activity > leads to dec in flow of impulses > dec NE release

MAIN PT: a-MNE lowers BP

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66
Q

Pre-junctional/Pre-synaptic actions of a drug acts on the _______.

A

nerve terminal

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67
Q

What is Bretylium Tosylate?

A

an IV or IM injection that inhibits NE release and is used in intensive care or coronary care units for life threatening ventricular arrhythmias.

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68
Q

How does Bretylium Tosylate work?

A
  • It increases ventricular fibrillation threshold.
  • produces initial transient inc followed by inhibition of NE release
  • increases action potential duration & effective refractory period
  • it basically dec the output of the SNS in the periphery
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69
Q

What happens when you take cocaine in the body?

A
  • cocaine blocks the reuptake of NE at varicosity memb
  • NE will accumulate = more energetic, higher BP/HR/etc
  • in the brain - also inhibits uptake of dopamine & serotonin
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70
Q

which agent will not be able to alter blood pressure after taking cocaine?

A

amphetamine

*must know that this occurs when you take cocaine before MAO or amphetamine due to the transport pump being blocked.

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71
Q

how can cocaine cause a cardiac arrest?

A

blocks Na conduction in the heart due to its local anesthetic effect

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72
Q

The amine pump on the varicosity memb can take up what substances?

A

NE, epi, DA, & indirect sympathetic amines (amphetamine, tyramine)

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73
Q

What is the diff betw the 2 indirect sympathetic amines?

A

Tyramine is metabolized by MAO in the GI tract, but
amphetamine is not.

*if you take an inhibitor of MAO, you will inc tyramine and thus inc NE release from nerves.

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74
Q

What is the main action of amphetamine and tyramine?

A

They get into the nerve and pumps NE out of the nn. Indirectly, cause inc in HR, BP, etc.

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75
Q

What metabolizes extraneuronal uptake of catecholamines? What inhibits this?

A

metabolized by MAO & COMT; inhibited by corticosterone

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76
Q

What drugs block neuronal uptake of NE into nn?

A

cocaine, tricyclic antidepressants (desipramine)

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77
Q

What is desipramine used for?

A

tx of depression & migraine headache

78
Q

Only therapeutic use of cocaine is?

A
  • Diagnosis of Horners Syndrome, where a pt has uneven size of pupils and drooping eyes due to dmg to pre/postgang sympathetic neurons.
  • need a release of NE to get an effect from cocaine, so you give these pts cocaine… if there is dilation, means cocaine worked. if there is no dilation, Horner’s syndrome–lack of NE.
79
Q

if you give amphetamine to a pt w/ horner’s syndrome and it does not work, this means there is…?

A

postganglionic dmg (recall that amphetamine is taken up by amine pump and releases NE)

80
Q

What are the major urinary metabolites of EPI & NE?

A

VMA, MHPG, MOPEG, normetanephrine (from NE), and metanephrine (from epi)

81
Q

MAO-B is found especially in ______.

MAO-A is present in _____ and also in the ______.

A

MAO-B is found especially in brain and platelets.

MAO-A is present in brain and also in the GIT and liver.

82
Q

What are the major urinary metabolites of dopamine?

A

Homovanillic acid (HVA) and dihydroxyphenylacetic aicd (DOPAC)

*Ex. which of the following is not a metabolite of NE? answer could be HVA

83
Q

Important MAO-A and B inhibitor? What are they used for?

A

phenelzine (Nardil); used for tx of depression and panic disorders

84
Q

Important MAO-B inhibitor? What are they used for?

A

Selegiline; used to treat depression, dementia, early stages of parkinson’s (with or without L-DOPA)

85
Q

What is entacapone, and what is it used for?

A

a COMT inhibitor; in adjunct w/ DOPA for Parkinson’s

  • it does not cross the blood brain barrier!!
  • it blocks the enzyme that metabolizes L-DOPA (DOPA decarboxylase, COMT) from the brain
86
Q

What 3 drugs in adjunct w/ L-DOPA can be used to treat parkinson’s?

A

Selegiline, entacapone, carbidopa

87
Q

What does atropine do?

A

selectively blocks the activity of ACH

88
Q

What type of adrenergic receptors are in the blood vessels? Activation of them causes what?

A

a1 & a2 - vasoconstriction

B2 - dilation or relaxation

89
Q

What adrenergic receptors does NE activate?

A

only a1, a2, B1

*NE doesn’t stimulate B2 anywhere.

90
Q

In the heart, there is primarily what type of adrenergic receptor? Stimulating it causes what?

A

B1; increases HR–coronotrophic effect, and increases contractility or ionotrophic effect.

91
Q

What adrenergic receptors does epi activate?

A

all of the diff types: a1/a2/B1/B2/B3

92
Q

Direct-acting a1 adrenergic agents? (Include agonists, distribution & responses, and adrenergic receptors.)

A

Epi (a1, a2, B1, B2)

NE (a1, a2, B1) [Levarterenol]

Phenylephrine (a1) [Neo-synephrine]

vasoconstriction in blood vessels, contraction of radial muscle in the eyes, decrease tone & motility (GIT), contraction of sphincter m. (GIT & bladder)

93
Q

Direct-acting a2 adrenergic agents? (Include agonists, distribution & responses, and adrenergic receptors.)

A

Epi (a1, a2, B1, B2)

NE (a1, a2, B1) [Levarterenol]

Clonidine [Catapress]

vasoconstriction in blood vessels, platelet aggregation, decrease tone & motility (GIT), hypotension (RVLM)

*dec sympathetic outflow to the heart and BVs

94
Q

What does Ach do to sphincters?

A

relaxes sphincter

95
Q

What does Ne do to sphincters?

A

reduces activity of musc; cause contraction of sphincter

96
Q

What does clonidine do?

A
  • initially it will inc the BP via vasoconstriction, but once it reaches the brain, it reduces the BF (vasodilation).

NET effect: lower BP

97
Q

What effect does clonidine have in the brain?

A
  • causes inhibitory effects/reduces the flow of impulses in the RVLM.
98
Q

So when asked what alpha-2 adrenergic agonist lowers blood pressure…?

A

Clonidine

99
Q

What adrenergic receptors are associated with the heart?

A

B1

100
Q

Direct-acting B1 adrenergic agents? (Include agonists, distribution & responses, and adrenergic receptors.)

A

Epi (a1, a2, B1, B2)

NE (a1, a2, B1) [Levarterenol]

Isoproterenol (B1, B2)

Dobutamine (higher doses: a1, B1, B2) [Dobutrex]

cardiac stimulation (heart), FA mobilization (adipose tissue), dec tone and motility (GIT), inc in renin release (kidney)

101
Q

What type of adrenergic receptors are in fatty tissue?

A

B1

102
Q

How is renin production stimulated?

A

NE binds onto receptors on JG (Juxtaglomerular cells)

103
Q

Direct-acting B2 adrenergic agents? (Include agonists, distribution & responses, and adrenergic receptors.)

A

Short Duration:

  • Epi (a1, a2, B1, B2)
  • Isoproterenol (B1, B2)
  • Terbutaline [Brethin]
  • Albuterol [Proventil]

Long Duration:

  • Salmeterol [Serevent]
  • Formoterol [Foradil]
  • Indacaterol [Arcapta Neohaler] (24 hour)

Dilation of aa & vv, relaxation of GIT smooth muscle, relaxation of bronchial smooth muscle, inc insulin secretion, relaxation (pregnant) (uterus)

104
Q

What type of tissue has the highest density of B2 receptors?

A

Bronchial Smooth Muscle!

105
Q

What will happen if you block B2 receptors?

A

inc airway resistance and vascular resisitance

106
Q

What will happen if you block B1 receptors?

A

dec in HR, force, and renin production

107
Q

In the heart, activation of B1 receptors lead to ….?

A

increases in contractile force & HR

108
Q

Activation of the beta2 receptor leads to …?

A

vascular and nonvascular smooth muscle relaxation

109
Q

Alpha2 receptors also exist presynaptically associated with nerve terminals. Activation of these receptors cause… ?

A

inhibition of the release of NE.

*NE acts at presynaptic alpha2 receptors to inhibit its own release

110
Q

Associated with vascular smooth muscle are a large number of alpha1 receptors relative to beta2 receptors. Activation of these receptors by sympathetic nervous system transmission or drugs will result in …?

A

vasoconstriction and an increase in peripheral resistance and systemic arterial blood pressure.

111
Q

What would happen if we blocked alpha receptors?

A

vasodilation; used for tx of hypertension

112
Q

What are the effects when stimulating postjunctional dopaminergic receptors (D1 receptors)?

A
  1. vascular relaxation (renal & mesenteric blood vessels)
  2. natriuresis & diuresis (kidney)
  3. stimulation of PTH release (parathyroid gland)

*these drugs are used for shock

113
Q

What is the selective DA agonist, Fenoldopam, used for?

A

renal failure

114
Q

What do indirectly acting sympathomimetic drugs do?

A

they mimic the sympathetic nervous system and stimulate NE release (indirect bc the NE causes the effects/does the actions)

115
Q

What 2 drugs have mixed actions?

A

Mixed actions means they act both directly and indirectly. Examples: Ephedrine (direct a1/B2) & Metaraminol (direct a1).
- They both facilitate the release of NE and can stimulate the adrenergic receptors.

116
Q

Positive chronotropic effect means?

A

increase in heart rate-direct action on B1 adrenergic receptors most prominent w/ isoproterenol & less w/ epi. NE decreases heart rate by a reflex-effect due to constriction of BVs and marked increase in blood pressure resulting in activation of baroreflex.

TL;DR = inc in HR

117
Q

Positive inotropic effect means…

A

contraction via the direct action on B1 receptors

118
Q

Positive dromotropic effect means?

A

increase conduction through the conducting tissue via direct action on B1 receptors. (inc in conduction velocity)

119
Q

If blood pressure is high, what occurs in the brain?

A
  • vagal activity & AcH would increase and NE release dec if your BP increases
  • Ach slows the heart, thus HR dec
120
Q

If blood pressure is low, what occurs in the brain?

A
  • dec vagal activity, inc sympathetic activity, dec Ach release, & inc NE release.
121
Q

Blood vessels have what type of inn?

A

ONLY sympathetic–NE.

  • Recall that NE inc BP & stim B1 receptors in the heart (dec in HR = net effect bc it isn’t potent enough)
  • Ach reduces HR–more potent than NE.
122
Q

If epi is more potent than NE and Ach, what is its net effect?

A

inc HR or canceling out reducing effects of Ach

123
Q

What would an increase in BP do to HR?

A

inc BP > causes reflex > dec sympathetic action on heart > vasodilation > dec HR

  • inc Ach & vagal activity; dec NE in heart
  • Ach slows the heart and thus HR dec–Ach is more potent than NE
124
Q

What would a decrease in BP do to HR?

A

dec BP > brain inc sympathetic action > inc HR

  • dec Ach & vagal activity; inc NE in heart
125
Q

What would happen if you gave atropine and Ach together?

A
  • give NE = inc BP, but dec HR due to action of Ach predominating
    **if you block the action of Ach on heart w/ drug (ex. atropine) and then give NE, what will happen to the heart? INCREASE.
    + recall that atropine blocks muscarinic cholinergic receptors (its a competitive antagonist of cholinergic receptors)
126
Q

What would happen to HR if you give epi?

A
  • Epi is more potent than NE in stimulating B1 receptors.

- Ach & Epi compete, so the net effect is small inc, small dec, or cancels out.

127
Q

Inc in vagal activity will do what to HR?

A

dec HR

128
Q

What substance has a really high affinity to B2 receptors?

A

epi!

  • recall that B2 receptors cause vasodilation, so epi would cause inc BP = dec HR normally when stimulating B2, but epi has more potent effects on stimulating heart than NE
  • epi buffers reflexive effect, so may see no change in HR instead
129
Q

What receptor does isoproterenol stimulate?

A

B1 & B2 receptors; acts on B1 receptors in the heart to inc BP; acts on B2 receptors in the BV’s to cause vasodilation.
*isoproterenol is more potent than NE/epi in stim heart

130
Q

What substance causes the contraction of the circular fiber? Does the pupil get smaller or larger with this contraction?

A

Ach causes the contraction of the circular fiber, making the pupil smaller–miosis.
*circular fibers are inn by PSNS

131
Q

a1 receptor activation causes contraction of what fibers of the eye? What substance causes this activation? And what is the effect on the pupils?

A

a1 receptor activation causes contraction of the radial fibers, dilating the pupil. NE causes a1 activation.

  • radial fibers are SNS
  • **All sympathomimetics (drugs that stimulate the sympathetic nervous system) cause pupil dilation.
  • These include norepinephrine and epinephrine (aka adrenaline).
132
Q

How else can we increase the size of the pupil without activating the a1 receptors?

A

You can block the effect of Ach w/ atropine.

133
Q

If you have blocked the a1 receptor, causing a pupil constriction, what drug would you give to counteract this?

A

a1 agonist

134
Q

What drug would you give if you needed to produce vasoconstriction w/ local anesthetics to prolong their duration of action?

A

epinephrine (reduces BF due to vasoconstriction)

135
Q

What drug would you give if you have bronchial asthma? What are their receptor selectivity?

A
  1. epi (a1, a2, B1, B2)
  2. ephedrine - indirect (a, B1), direct (a, B2)
  3. Albuterol, terbutaline (short acting)
    * **4. salmeterol & formoterol (long acting-used w/ only glucocorticoids–B2)

You give B2 agonist for bronchial asthma.
Asthma is an inflamm. disease, so give glucocorticoid to reduce inflamm and inhalers to dilate vessels.

136
Q

What would you give if you needed a nasal decongestant?

A

phenylphrine (a1) - constricts BVs

137
Q

What 2 types of drugs will increase the effects of epi?

A

cocaine (prevent epi uptake) and amphetamine (releases epi)—with epi, these drugs will inc the BP a lot

138
Q

What can you give to reduce a pt having a seizure from numbing due to excess epi?

A

phentolamine

139
Q

What would you give for short term tx. of cardiac decompensation after cardiac surgery or in CHF? Mention what receptors are involved.

A

Dobutamine (a1, B1, B2)

- used for cardiac stimulation

140
Q

What drug would you give if you need to elevate the BP, treat hypotension produced by drugs, spinal anesthesia or pheochromocytoma, and orthostatic hypotension?

A

metaraminol (indirect/direct a1)

- recall that this is a mixed drug that facilitates the release of NE

141
Q

to reduce the BP, what drug would you give?

A

clonidine (a2), a-methyldopa via formation of a-methylNE (a2)
- recall that clonidine reduces release of NE from sympathetic nn.

142
Q

What drug would produce sedation & decrease anxiety & pain, used as preanesthetic medication, and tx for heroin or nicotine withdrawal?

A

clonidine (a2 agonist)

143
Q

What drug would you give for mydriasis, conjunctival decongestion & to control hemorrhage, or diagnose horners syndrome?

A

phelylephrine, epi, ephedrine, hydroxyamphetamine

144
Q

For glaucoma, give what drug?

A

Epi or brimonidine (a2 agonist)

145
Q

for narcolepsy, give?

A

modafinil (Provigil, a1 agonist)

– low lvls of NE, so you can give them amphetamine or ephedrine as well.

146
Q

What is the normal outflow of aqueous humor?

A

Predominantly via the trabecular meshwork and to a lesser extent via the uveosclera route. Drain occurs by the eye’s venous circulation.

147
Q

where is aq. humor made and its pathway?

A

Aq. humor is formed by ciliary processes & enters the anterior chamber. Then it goes through the trabecular meshwork and then Schlemm’s canal mostly.

148
Q

What occurs in glaucoma? What drug can we give to resolve this?

A

There is a blockage in the drainage of aq. humor. The drainage can be stimulated by epi.

149
Q

What is an open-angle glaucoma?

A

Most common form of glaucoma. Inc in trochlear pressure (inc in fluid in ant. chamber). Gradual, painless, but inevitable vision loss due to optic nerve damage!

150
Q

What is the tx for an open-angle glaucoma?

A

Treatment with epinephrine (Propine) and beta-adrenergic blocker (Timolol)

151
Q

What is acute closed-angle glaucoma?

A
  • iris muscle is angulated and blocks route of Aq humor to flow to ant. chamber.
  • its a common cause of dilation of pupil to be set off by an emotional crisis, which results in sympathetic discharge of NE & inc circulating epi.
  • onset is rapid and accompanied by pain
152
Q

What is tx for acute closed-angle glaucoma?

A

miotic agent (pilocarpine) essential to preserve vision; iris m has closed the route not allowing Aq. humor to flow thru–corrected surgically

153
Q

What are side effects and toxicity of sympathomimetics?

A
  1. Throbbing headache
  2. Precordial pain
  3. Cerebral hemorrhage
  4. Palpitations
  5. Cardia arrhythmias
  6. Restlessness
  7. Anxiety!
154
Q

What are contraindications to sympathomimetics?

A
  1. Hyperthyroidism
  2. Heart disease
  3. Severe hypertension
  4. Inhalation anesthesia (arrhythmias)!
155
Q

what are adrenergic receptor antagonists?

A

These agents inhibit the activity of sympathetic nervous system and the actions of administered adrenergic receptor agonists by occupying the adrenergic receptors at the postsynaptic sites of α and β adrenergic receptors.

156
Q

Which a-adrenergic receptor antagonists are selective for a1 adrenergic receptors?

A

prazosin, terazosin, trimazosin, doxazosin, tamsulosin

*notice they all end in -sin.

157
Q

Which a-adrenergic receptor antagonists are selective for a2 adrenergic receptors?

A

rauwolscine

158
Q

Which a-adrenergic receptor antagonists are nonselective having more or less similar affinity for a1 & a2 receptors?

A

phenoxybenzamine, phentolamine

**KNOW: these 2 reverse the effects of NE, EPI, & anesthetics.

159
Q

Reflex tachycardia results during blockage of….?

A

alpha adrenergic receptors.

  • basically alpha blockers cause tachycardia bc sympathetic activity is directed twds B receptors since a-receptors are blocked.
  • tachycardia = HR goes up
  • if you want to block the reflex tachycardia effect, add in a B-blocker
160
Q

α-adrenergic receptor blockers by antagonizing the effect of cate- cholamines in various vascular beds…? (effects/actions)

A

reduce sympathetic tone and produce vasodilation, decrease peripheral vascular resistance and a fall in blood pressure.

161
Q

What is the sequence of alpha blockers causing reflex tachycardia?

A
  • alpha receptors are present in all BVs; if given alpha blocker, blocking action of NE, so vasodilation will occur.
    + fall in BP; baroreflex gets activated; dec vagal activity/inc sympathetic activity. —> “Reflex tachycardia” w/ B receptors in heart
162
Q

What is phentolamine used for?

A

diagnosis of pheochromocytoma, erectile dysfunction, to reverse the anesthesia of soft tissues in dentistry***
- phentolamine = vasodilator (“no doggy sex” lol! you can’t possibly forget this… get dizzy bc blood goes south when you stand up)

163
Q

What is the lipid solubility and specificity of Timolol?

A

Timolol = B-adrenergic receptor antagonist

- low-moderate solubility; B1/B2 (nonselective)

164
Q

What is the lipid solubility and specificity of Propranolol?

A

Propranolol = B-adrenergic receptor antagonist

- high solubility; B1

165
Q

What is the lipid solubility and specificity of Atenolol?

A

Atenolol = B-adrenergic receptor antagonist

- low solubility; B1

166
Q

What is the lipid solubility and specificity of Metaprolol?

A

Metaprolol = B-adrenergic receptor antagonist

- moderate-high solubility; B1

167
Q

What is the lipid solubility and specificity of Nebivolol (NO release)?

A

Nebivolol (NO release) = B-adrenergic receptor antagonist

- moderate-high solubility; B1

168
Q

For asthma, what blocker would you select?

A

B1 blocker bc selective B1 will block action of NE in heart, but not effect the lungs (which
are only B2)
*recall that NE does not act on B2 receptors, which are in bronchial tissues and veins.

169
Q

What are B-blockers effects on the heart and vasculature? (very long answer… 14 points…fml not sure how important it is…)

A
  1. Dec in HR, myocardial contractile force, CO, conduction velocity, & myocardial O2 consumption by blocking B1 receptors in heart
  2. Produce direct myocardial depressant effect (local anesthetic, memb stabilziing, or quinidine-like action); direct effect on Na conduction
  3. Antiarrhythmic actions
  4. Reduction in peripheral vascular resistance. Fall in BP esp in pts w/ high renin & CO. (affect brain by reducing sympathetic impulse flow–lowers BP)
  5. Acute dissecting aortic aneurysm (Marfan’s syndrome)
  6. Fallot’s Tetrology
  7. Congestive Heart Failure
  8. Reflex tachycardia during antihypertensive agents
  9. stress or fear induced tachycardia (B2 receptors sometimes in skeletal m.–tremors)
  10. hypertension (B blockers block release of renin)
  11. hyperthyroidism
  12. pheochromocytoma (**combine a & B blockers!!!)
  13. glaucoma (Timolol)
  14. migrane headache (propranolol, timolol)
170
Q

What are B-blockers effects on the resp system?

A

bronchoconstriction & block the bronchial relaxation caused by sympathomimetic agents action on B2 receptors

171
Q

What are B-blockers effects on the GI smooth mm?

A

slight inc in motility and tone

172
Q

What are B-blockers effects on the metabolic actions?

A

Glycogenolysis in heart and skeletal muscle is inhibited. These agents also inhibit insulin secretion elicited by catecholamines. Free fatty acid release is blocked.

173
Q

What are B-blockers effects on the CNS?

A

Fall in blood pressure produced by these drugs has been attributed partly to their actions in CNS.

174
Q

What are the therapeutic uses for B-blockers?

A
  1. Cardiac arrhythmias. Overdosage of catecholamines, during anesthesia and digitalis toxicity
  2. Hypertrophic obstructive cardiomyopathies
  3. Myocardial infarctions
  4. Angina pectoris
  • recall that high lvls of NE/epi in arrhythmias.
  • can reduce workload for heart by increasing B-blockers, which reduce HR, heart’s workload, and output
  • *B-blockers reduce function of NE/epi
175
Q

What is angina? What would you prescribe for it?

A
  • angina = chest pain or discomfort that occurs if an area of your heart muscle doesn’t get enough oxygen-rich blood.
  • tx: to inc BF and reduce demand of O2 by the heart–B-BLOCKERS to reduce NE/Epi!
176
Q

What is an inotropic effect?

A
  • effect influence myocardial contractility.
  • POSITIVE INOTROPIC: effect strengthen or increase the force of myocardial contraction
  • NEGATIVE INOTROPIC: effect weaken or decrease the force of myocardial contraction.
177
Q

What is an chronotopic effect?

A
  • action affect heart rate.
  • POSITIVE CHRONOTROPIC: effect is produced if the drug accelerate the heart rate by increasing the rate of impulse formation in the SA Node.
  • NEGATIVE CHRONOTROPIC: drug has the opposite effect and slows the heart rate by decreasing impulse formation.
178
Q

What is an dromotopic effect?

A
  • effect refers to drugs that affect conduction velocity through specilized conducting tissues.
  • POSITIVE DROMOTROPIC: actions speeds conduction
  • NEGATIVE DROMOTROPIC: action delays conduction
179
Q

Phenylephrine (PHE) can be given to increase BP. What happens to HR?

A

HR will decrease as a reflex in the body.

180
Q

What occurs when you go into a supine position while on alpha blockers?

A

Orthostatic hypotension

  • blockage of a-receptors causes no BV constriction, which causes blood to go to the periphery.
  • side effects: dizziness
181
Q

What are the results/consequences of taking alpha blockers?

A

reflex tachycardia & orthostatic hypotension

182
Q

What drug would you give to dilate renal and mesenteric vessels? And what receptors does it act on?

A

Dopamine, B1 receptors

183
Q

What is Raynaud’s and Buergers’ syndrome characterized by?

A

constriction of BVs (higher BP) in fingers causing them to turn blue; use a-blockers for this

184
Q

What is the initial tx for shock? If the vasoconstriction still persists?

A

fluid replacement & dopamine (vasodilation); give alpha blockers if vasoconstriction persists

185
Q

If a person has prostatic hypertrophy, what would you give them?

A

alpha blocker bc they are having difficulty urinating.

  • this could be due to NE release via a1 receptors, which causes contraction of sphincter muscles in the bladder.
  • alpha blockers would block this and make it easier for them to go “paypay”
186
Q

What does phentolamine do/block?

A

blocks actions of EPI on a1 receptors, causing vasodilation

187
Q

What is a common trait of all B-adrenergic receptor antagonists?

A

all B-blockers have a direct effect on Na channel–membrane stabilizing effect, and of course, they all block the actions of NE.

188
Q

How would B blockers help in tx of Marfan’s syndrome?

A

in Marfan’s syndrome (CT disease), the tissue walls of valves are thin, so beta blockers reduce the heart workload and thus the pressure created against the valves.

189
Q

What is associated w/ blue baby syndrome?

A

Fallot’s tetrology (4 congenital heart defects–mixing out venous & aortic blood)

190
Q

What are the 3 drugs used for pheochromocytoma?

A

metyrosine (blocks tyrosine hydrolase, so not tyrosine into DOPA); alpha blocker & beta blocker together

191
Q

Why do some beta blockers cause nightmares?

A

due to high lipid solubility, they go easily to the brain.

192
Q

What happens if a diabetic pt takes too much insulin? Would you take B blockers to treat this?

A

excess insulin in diabetics results in hypoglycemia, which can cause tachycardia. Tachycardia = contraindication for taking B blockers bc if you take

D2 - FALL - Par 2 (7 decks)

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