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D2 - FALL - Par 2 > PHARM SHIT YOU NEED TO KNOW > Flashcards

PHARM SHIT YOU NEED TO KNOW Flashcards

1
Q

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

A

AcH; skeletal muscle (motor)

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2
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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3
Q

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

A 
preganglionic = Ach
postganglionic = Ach
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4
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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5
Q

What are examples of neurohormones?

A

vasopressin (ADH) & oxytocin

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6
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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7
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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8
Q

What are some excitatory NTs?

A

dopamine, NE, epi, glutamate, acetylcholine

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9
Q

What are some inhibitory NTs?

A

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

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10
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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11
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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12
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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13
Q

What molecule does NO activate during an erection?

A

activates soluble guanylate cyclase

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14
Q

what does guanylate cyclase do?

A

synthesizes cGMP from GTP

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15
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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16
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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17
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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18
Q

calcitonin gene related peptides function?

A

potent vasodilator and can function in the transmission of pain. When CGRP is derived from DRG when synthesized in the dorsal horn of the spinal cord, it may be linked to transmission of pain.

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19
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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20
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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21
Q

What enzyme converts NE to epi?

A

PNMT = phenylethanolamine N-methyltransferase

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22
Q

Metyrosine is used to treat what disease?

A

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

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23
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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24
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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25
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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26
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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27
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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28
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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29
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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30
Q

What does the PSNS do to the GI system?

A

promotes peristalsis and gut motility

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31
Q

What nerv system causes GI cramps & diarrhea?

A

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

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32
Q

what converts a-methyldopa to a-methyldopamine?

A

dopadecarboxylase

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33
Q

what converts a-methyldopamine to a-methylnorepinephrine?

A

dopamine-B-hydroxylase

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34
Q

What is a-methyldopa (aldornet) used for?

A

pregnancy induced hypertension (preecalampsia)

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35
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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36
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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37
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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38
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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39
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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40
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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41
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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42
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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43
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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44
Q

What metabolizes extraneuronal uptake of catecholamines? What inhibits this?

A

metabolized by MAO & COMT; inhibited by corticosterone

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45
Q

What drugs block neuronal uptake of NE into nn?

A

cocaine, tricyclic antidepressants (desipramine)

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46
Q

What is desipramine used for?

A

tx of depression & migraine headache

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47
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.
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48
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)

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49
Q

What are the major urinary metabolites of EPI & NE?

A

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

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50
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

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51
Q

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

A

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

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52
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)

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53
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
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54
Q

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

A

Selegiline, entacapone, carbidopa

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55
Q

What does atropine do?

A

selectively blocks the activity of ACH (blocks nicotinic receptors)

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56
Q

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

A

a1 & a2 - vasoconstriction

B2 - dilation or relaxation

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57
Q

What adrenergic receptors does NE activate?

A

only a1, a2, B1

*NE doesn’t stimulate B2 anywhere.

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58
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.

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59
Q

What adrenergic receptors does epi activate?

A

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

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60
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)

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61
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

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62
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).
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63
Q

What effect does clonidine have in the brain?

A
  • causes inhibitory effects/reduces the flow of impulses in the RVLM.
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64
Q

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

A

Clonidine

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65
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)

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66
Q

What type of adrenergic receptors are in fatty tissue?

A

B1

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67
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)

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68
Q

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

A

Bronchial Smooth Muscle!

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69
Q

What will happen if you block B2 receptors?

A

inc airway resistance and vascular resisitance

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70
Q

What will happen if you block B1 receptors?

A

dec in HR, force, and renin production

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71
Q

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

A

increases in contractile force & HR

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72
Q

Activation of the beta2 receptor leads to …?

A

vascular and nonvascular smooth muscle relaxation

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73
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

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74
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.

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75
Q

What would happen if we blocked alpha receptors?

A

vasodilation; used for tx of hypertension

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76
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

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77
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)

78
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.

79
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
80
Q

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

A
  • dec vagal activity, inc sympathetic activity, dec Ach release, & inc NE release.
81
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.
82
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

83
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
84
Q

What would a decrease in BP do to HR?

A

dec BP > brain inc sympathetic action > inc HR

85
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)
86
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

87
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

88
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).
89
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.

90
Q

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

A

a1 agonist

91
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)

92
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.

93
Q

What would you give if you needed a nasal decongestant?

A

phenylphrine (a1) - constricts BVs

94
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

95
Q

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

A

phentolamine

96
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

97
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

98
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.

99
Q

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

A

clonidine (a2 agonist)

100
Q

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

A

phelylephrine, epi, ephedrine, hydroxyamphetamine

101
Q

For glaucoma, give what drug?

A

Epi

102
Q

for narcolepsy, give?

A

modafinil (Provigil, a1 agonist)

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

103
Q

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

A

prazosin, terazosin, trimazosin, doxazosin, tamsulosin

*notice they all end in -sin.

104
Q

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

A

rauwolscine

105
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.

106
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
107
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
108
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)`

109
Q

What is the lipid solubility and specificity of Timolol?

A

Timolol = B-adrenergic receptor antagonist

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

110
Q

What is the lipid solubility and specificity of Propranolol?

A

Propranolol = B-adrenergic receptor antagonist

- high solubility; B1

111
Q

What is the lipid solubility and specificity of Atenolol?

A

Atenolol = B-adrenergic receptor antagonist

- low solubility; B1

112
Q

What is the lipid solubility and specificity of Metaprolol?

A

Metaprolol = B-adrenergic receptor antagonist

- moderate-high solubility; B1

113
Q

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

A

Nebivolol (NO release) = B-adrenergic receptor antagonist

- moderate-high solubility; B1

114
Q

Anytime you see “-lol”, immediately think…?

A

Beta blocker!

115
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

  • tachycardia lets diabetic know to stop taking insulin
  • beta-blockers will cause loss of sensitivity to tachycardia–pt won’t know when they took too much insulin
116
Q

Bronchial asthma is a contraindication for B-blockers, but if you had to resort to B-blockers. Which one would you use?

A

B1 blockers

117
Q

Where are N2 receptors located at, and what blocks them?

A

N2 receptors are nicotinic receptors located at effector cells’ of skeletal mm–innervated by somatic nn
- curare blocks this receptor

118
Q

Where are N1 receptors located at, and what blocks them?

A

N1 receptors are at autonomic ganglion cells of sympathetic, parasynpathetic, & adrenal medullary cells and adrenergic nerve terminals.

  • hexamethonium blocks this receptor
119
Q

What drug blocks a-adrenergic receptors? Stimulates?

A

phentolamine; E > NE

120
Q

What drug blocks b-adrenergic receptors? Stimulates?

A

propranalol; ISO > E > NE (B1)

121
Q

nicotinic receptors are blocked by _______ except for the ones in muscles which are blocked by ______.

A

hexathonium (blocks N1); curare (blocks N2)

122
Q

What are the inhibitors of the release of Ach?

A

Botulinus toxin, local anesthetics, Mg2+ ions (*he really emphasized botulinus toxin)

123
Q

What does Botulinum Toxin degrade?

A

proteolytically degrades SNAP-25 prot (if this is degraded, there is no release of Ach)

124
Q

what do parasympathomimetics do?

A

aka muscarinic agonists; these drugs produce effects similar to those observed during the stimulation of postganglionic parasympathetic and sympathetic cholinergic nerves.

125
Q

What is an example of a selective muscarinic agonist? What receptor does it activate?

A

Bethanechol; ONLY muscarinic receptors

126
Q

drug to treat Sjogren’s syndrome?

A

Cevimeline

127
Q

What does pilocarpine cause?

A

dry mouth/xerostomia; inc in aq. humor outflow

128
Q

Acetylcholinesterases hydrolyze what?

A

acetylcholine & methacholine

129
Q

What all does stimulation of muscarinic receptors cause?

A
  1. miosis–smaller pupils
  2. contraction of ciliary m. (accomodation for near vision)
  3. more secretion in lacrimal & salivary glands
  4. dec heart SA node activity (brachycardia)
  5. dec atrial m. contractility
  6. dec AV node conduction velocity
  7. contraction of bronchial SM
  8. inc secretion of glands
  9. inc tone, motility, secretions in GI
  10. inc tone & contraction in detrusor m. in bladder
  11. dec tone- relaxation of trigone & sphinctor m.
  12. NO effect on BV’s–most vascular beds lack parasympathetic inn.
130
Q

What are the actions of muscarinic agonists in the heart?

A

dec HR (dec SAN activity), atrial contractility & conduction velocity through AV node

131
Q

What are the actions of muscarinic agonists in the blood vessels?

A

vasodilation of cerebral, cutaneous, splanchnic & other vessels

132
Q

What are the actions of muscarinic agonists in the extravascular SM?

A
  • increased tone & amplitude of SM in: GI tract, bladder, genital tract, bronchi, ciliary mm, sphincter m. of eye
  • relax: sphincters of GI, bladder
133
Q

What are the actions of muscarinic agonists in the exocrine glands?

A

inc secretion of bronchioles, salivary, lacrimal, sweat, & gastric glands

134
Q

What are the actions of muscarinic agonists in the eye?

A

2 effects:

  1. circular fibers have muscarinic receptors–CONSTRICTION/smaller pupils
  2. ciliary m. have no adrenergic nn, only cholinergic–ADJUST/ACCOMMODATION for near vision
    * **atropine blocks Ach, so you would get pupil dilation & accommodation for far vision
135
Q

Best way to administer Ach is intravenously. T/F?

A

FALSE!!! NEVER do this bc it will drop BP way too fast.

136
Q

What type of nicotinic receptors are on all the ganglia?

A

N1

137
Q

What is used to reverse curare?

A

Neostrigmine–reversible antagonist (competitive) to curare

138
Q

What does nicotine do to nerves?

A

Nicotine acts DIRECTLY on nerve terminals–their terminals will DEPOLARIZE –mimicking AP’s, causing Ca influx and release of NT’s

139
Q

What is haloperidol?

A

an antipsychotic medication used in the tx of Tourette’s–functions as an inverse agonist of dopamine
*tourette’s = high dopamine release

140
Q

What is the current tx for nicotine addiction?

A

haliperidol & mecamylamine*

141
Q

what are the 2 types of cholinesterase?

A
  1. true actylcholinesterase

2. pseudocholinesterase

142
Q

what are examples of major neuromuscular blocking agents?

A

d-Tubocurarine, Atracurium, Pancuronium, Succinylcholine

*these drugs block actions of Ach in skeletal m. & cause paralysis or relaxation

143
Q

What does Physostigmine do?

A

it causes buildup of Ach (that can compete w/ atropine) by inhibiting acetylcholinesterase

  • able to cross BBB
  • **produces muscarinic & nicotinic actions–indirectly!
  • **stimulates skeletal muscle & nicotinic actions–indirectly!
  • treats glaucoma & Alzheimer’s disease
144
Q

What does edrophonium do?

A

inhibits cholinesterase & DIRECTLY stimulates skeletal m.

- used in diagnosis of myasthenia gravis

145
Q

What does Neostigmine do?

A

inhibits actylcholinesterase; both muscarinic & nicotinic indirectly; for tx of mysathenia gravis & curare overdose

146
Q

What do insecticides inhibit?

A

acteylcholinesterases; it is an irreversible inhibitor

147
Q

Nerve gases will have what effect on us?

A
  • increase Ach EVERYWHERE
  • in brain, willl cause depolarization & release of glutamate–causing seizures & inc Ca2+
  • death from asphyxia!–contraction of bronchial SM followed by paralysis
148
Q

How do you treat nerve gas problems?

A

atropine or pralidoxime–reactivation of alkylphosphorylated acetylcholinesterase

149
Q

What are the cardinal symptoms of parkinson’s disease?

A
  1. resting tremor
  2. akinesia/bradykinesia
  3. muscle rigidity
  4. postural imbalance
150
Q

loss of dopamine affects what part of the brain (in Parkinson’s)?

A

basal ganglia motor control circuit

151
Q

what does dopamine do in the brain?

A

DA reg the neuronal activity of the basal ganglia motor neuron circuitry feeding-back to motor cortex

152
Q

D2-MSNs need to be constantly inhibited by ____ activation to facilitate movement

A

D2-R

153
Q

____ need to be constantly excited by D1-R activation to facilitate movement

A

D1-MSNs

154
Q

What are 2 classes of receptors that maintain normal regulation of dopamine?

A

D1-like, D2-like receptors

155
Q

What are usu targets of some of the antiparkinson drugs?

A

D1-like, D2-like receptors

156
Q

What are the current pharmocological therapies for parkinson’s?

A
  1. dopamine replacement therapy
    - potent effect
  2. inhibition of dopamine degradation
    - MAO inhibitors: selegiline
    - COMT* inhibitors
    - modest effect
  3. stimulation of dopamine receptors
    - D2-like agonists
    - mild effect
  4. anti-muscarinic drugs
    - modest effect
157
Q

What other substances can contribute to formation of dopamine?

A

serotonin

158
Q

L-DOPA is commonly administered how? And how is it absorbed?

A

orally; absorbed in SI via transporters for aromatic amino acids

159
Q

What is NOT compatible with L-DOPA?

A

iron; it decreases L-DOPA absorption

160
Q

How much of the administered L-DOPA makes it to the brain tissue?

A

~1%

161
Q

What enzyme converts L-DOPA to dopamine?

A

DDC (dopa decarboxylase)

162
Q

what is dyskinesias?

A

involuntary movements

163
Q

L-DOPA advantages?

A
  1. most efficacious antiparkisonian drug
  2. virtually all PD patients respond
  3. improves disability & prolongs capacity to maintain employment & independent
  4. reduces mortality rate
164
Q

L-DOPA disadvantages?

A

motor complications (dyskinesias, motor fluctuations), neuropsychiatric problems (confusion, psychosis), sedation

165
Q

Pramipexole & Ropinirole are what type of agonists?

A

D2-like

  • they are increasingly used as initial tx
  • less efficacious than L-DOPA, but L-DOPA needed eventually
166
Q

What are side effects of Dopamine D2-like receptor agonists?

A

orthostatic hypotension; sleep disorder (rare)

167
Q

What do MAO inhibitors inhibit inside the cell?

A

dopamine oxidation

168
Q

What do muscarinic acetylcholine antagonists?

A
  • These block mAChRs, reduce cholinergic activity, & restore balance DA & ACh systems.
169
Q

What are the advantages of anticholinergic agents?

A
  1. some antiparkinsonian efficacy (esp w/ tremor)

2. peripherally acting agents may be useful in treating sialorrhea

170
Q

What are disadvantages of anticholinergic agents?

A
  1. relatively ineffective for the more disabling features of PD
  2. Cognitive side effects
  3. Troublesome central & peripheral cholinergic side effects
171
Q

Ex of catechol O-methyl transferase (COMT) inhibitors?

A

entacopone, tolcapone

172
Q

Ex of Monoamine oxidase (MAO) inhibitors?

A

selegiline, rasagiline

173
Q

Ex of the anticholinergic agents?

A

biperiden, benztropine, procylidine, trihexyphenidyl

174
Q

Ex of anti-NMDR-R agent?

A

amantadine

175
Q

What does amantadine do?

A

it is a glutamate NMDA receptor antagonist; block dopamine uptake or stimulate release; may reduce L-dopa-induced dyskinesia

176
Q

what are key parkinson’s disease?

A

bradykinesia, muscle rigidity, resting, tremor, & postural imbalance

177
Q

Current pharmacotherapy for parkinson’s targets what..?

A

targets key DA synthesis & metabolism steps to 1. inc DA prod 2. inhibit DA degradation 3. direct DA receptor stimulation

178
Q

Initial tx of parkinson’s? Last resort tx?

A

dopamine agonists = initial; L-DOPA = last

179
Q

Ethanol has its own receptor. T/F?

A

FALSE. It has no receptor.

180
Q

Where is the most rapid absorption of alcohol and its mechanism of absorption?

A

Small intestine; passive diffusion

181
Q

Where is alcohol rapidly distributed?

A

brain, lungs, liver (tissues w/ greatest blood supply affected most)

182
Q

What is the conc of alcohol in alveolar air?

A

0.05% (gives blood alcohol conc–BAC)

183
Q

What level of BAC means you’re legally drunk?

A

0.08%

184
Q

What level of BAC is lethal?

A

0.4 - 0.5%; death from HYPOTENSION–shock, acute renal failure, &/or central respiratory depression

185
Q

Metabolism of ethanol percentages?

A
  • 90-95% alcohol oxidized to ACETIC ACID

- 5% eliminated in breath, urine, sweat

186
Q

Enzyme for ethanol to acetylaldehyde? order of kinetics? It’s effect on FA’s?

A

alcohol dehydrogenase; zero order–rate-limiting step-constant rate; inc FA formation

187
Q

Enzyme for acetalaldehyde to acetic acid? Drug that blocks it?

A

acetylaldehyde dehydrogenase; disulfiram

188
Q

Activates what system in the brain? What receptors do they inhibit? The one it enhances? What drug blocks the activation?

A
  • Dopamine Reward System in the brain–ADDICTIVE INFLUENCE
  • Inhibits glutamate-activated excitatory NMDA receptors (CNS depressant)
  • Enhances inhibitory GABA receptor
  • drug: NALTREXONE
189
Q

Alcohol does direct dmg to what? Indirect dmg?

A

Direct: cell memb lipids, DNA, proteins
Indirect: nutritional, vitamin deficiency

190
Q

What is the acute ethanol effect on the CV system?

A

inc CO & HR (tachycardia) due to catecholamine release by acetylaldehyde

191
Q

What is the long term effect of ethanol on CV system? And its effect on the liver??

A
  • long term = dec myocardial contractility

- increases HDL (good thing!)–carries cholesterol to liver for elim & reduces accum on arterial roll.

D2 - FALL - Par 2 (7 decks)

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