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D&T Exam 3 > Autonomic Pharmacology > Flashcards

Autonomic Pharmacology Flashcards

1
Q

What is a problem with ANS drugs and what is one common side effect?

A

The problem is ANS receptors are repeated diffusely throughout the body so it is a challenge to minimize ANS drug side effects.

Example 1: tachycardia is common side effect and can lead to coronary events. Prazosin, scopolamine, terbutaline, nitroglycerine can cause it

Example 2: non selective beta blockers can increase hypoglycemia risk for DM patients because beta 2 block can block hepatic gluconeogenesis

Example 3: drugs targeting muscarinic receptors in incontinence or overactive bladder can effect brain M receptors leading to confusion or mental clouding. Developed non lipophilic quaternary amine in attempt to avoid CNS side effects

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2
Q

Where is a common place for drugs to work in neuron signaling?

A

Neurons use both electrical (neuroconduction) and chemical (neurotransmission) to have physiological impact. Most drugs work at neurotransmission at multiple steps.

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3
Q

Where are adrenergic (NE and epi) NT released at?

A

NE is primary NT of most sympathetic postganglionic neuroeffector junctions except sweat glands

Epi is principle catecholamine released from chromaffin cells of adrenal medulla

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4
Q

Where does Ach work and what is special about it?

A

It is always the preganglionic NT used and then works at nicotinic receptors. It works at nicotinoic receptors in one neuron somatic skeletal muscle. But its special in that it is the main PSNS NT but drugs that increase Ach could increase SNS too by working at preganglionic ganglion to increase NE/epi at postganglionic or Ach at postganglionic in sweat glands

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5
Q

In neurotransmission what are the mechanisms of maintaing ion gradient, membrane pot, neuro conduction, NT release, response

A

Maintence of ionic gradient: Na-K atpase
Membrane potential: K leak channels
Neuro conduction: voltage gated Na K channels
NT release: vg Ca channels
Post synaptic response: ligand gated ion channels or GPCR

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6
Q

What drugs did Dr. D mention in her tegrity snippet that can block cholinergic transmission and where do they do this?

A

1) cell needs to take up choline to make Ach via Na dependent carrier- blocked by hemicholinium
2) Ach must be transported into a vessicle- vesamicol blocks entry into vessicle
3) depolarization causes Ca influx which promotes fusion of vessicular membrane to cell membrane and exocytosis of Ach occurs- botulism toxin stops EXOCYTOSIS and keeps vessicle in fusion step

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7
Q

In the adrenergic snippet, what drugs were discussed to effect NE transmission?

A

1) DA is taken up by vessicles by VMAT2 transporter- blocked by reserpine
2) Depolarization release Ca from vg Ca channels to move vessicles to cell membrane for exocytosis- bretylium blocks exocytosis, amphetamines increase exocyotosis of NE
3) Once in synaptic cleft NE can be broken down by MOA and COMT- can inhibit to increase DA and NE
4) Once in cleft NE can be reuptaken back to pre ganglionic cell- cocaine blocks and increases NE for excitation

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8
Q

Compare and contract Ach release to NE release

A

Ach- just choline+ acetyl= Ach, interacts with N or M receptor on post ganglionic effector cell, degraded by AchE to choline and acetate or interacts with N and M receptors on PRE ganglionic cell to negative feedback and stop Ach release

NE- comes in as Tyr, made to dopa by TH then DA by AAADC, converted to NE by DBH, stored with co transmittors NPY and ATP, works at alpha beta receptors, degraded by MOA and COMT, reuptake can be stopped by cocaine

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9
Q

What is difference in agonist and indirect agonists?

A

Agonists in synaptic cleft increase effect at NEJ by directly stimulating receptor mimicking the NT

Indirect agonist increase the release (amphetamines) or block removal (cocaine) of NT from synaptic cleft

Both increase NT in synaptic cleft

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10
Q

What is the role of antagonists?

A

Decrease the effect at NEJ by blocking the receptor

Another way to limit NEJ activity is to interfere with one or more of the presynaptic steps (synthesis, storage, or release) or decrease amount of NT in synapse

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11
Q

How does Epi and NE effect HR?

A

NE is a site directed NT that works via sympathetic neurons to increase HR. Epi is a neurohormone secreted by the adrenal medulla that travels in the blood stream to the heart to supplement NE increase in HR and to other sites in the body

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12
Q

What is the NT of sympathetic neurons to the kidneys? What is the effect and target?

A

DA instead of usual NE

The target is D1 receptors in the kidney to produce dilation of blood vessels and decrease resistance to flow

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13
Q

What is exogenous DA useful in treating? What is target?

A

DA dilates renal blood vessels to increase renal blood flow useful in treating cardiogenic hypovolemic shock (severely reduced BP and CO). By maintaing perfusion during low blood flow DA can prevent renal failure.

Exogenous DA stims the D1 receptors AND alpha1 beta1

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14
Q

What is a DA agonist and what is it used for? Target?

A

Fenoldopam is a selective D1 agonist that can be used in cardiogenic shock, or exogenous DA can be used but stims alpha1 beta1 as well

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15
Q

What NANC NT are part of the SNS and what is their role?

A

In SNS NANC NT include ATP and neuropeptide Y, called cotransmitters bc thought to help with efficient and precise control of target tissues, stored and released in varying amount depending of target tissue and exocrine glands

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16
Q

What are other NANC NT not specifically used in SNS? What is their role?

A

Others include VIP, NO and CO. All involved in relaxing smooth muscle surrounding tubular structures such as airways, intestine, GI tract, and blood vessels.

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17
Q

What is the order of potency in adrenergic receptors?

A

Epi> NE> isoproternol

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18
Q

Describe the process of adrenergic NT production

A

Tyrosine into cell and made to DOPA via TH in cytoplasm
DOPA to DA via AAADC in cytoplasm
DA into vessicle via VMAT
DA to NE via dopamine beta hydroxylase (obviously not in DA neurons)
NE to epi via phenlyethanolamine methyl-transferase in adrenal medullary chromaffin cells

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19
Q

Describe NE and epi ability to stim adrenergic receptors

A

NE and epi both activate alpha1 and beta1 similarly
NE activates alpha2
Epi activates beta2

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20
Q

What is the effect of giving NE IV

A

NE will stimulate alpha 1- to markedly increase BP
And although stims beta1 the baroreceptor reflex will decrease HR

A side note: NE also activates alpha 2 to decrease insulin secretion

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21
Q

What is the effect of giving Epi IV?

A

Epi IV will stim beta 1 to increase HR
Also stim beta2 and decrease smooth muscle contraction, decrease peripheral vascular resistance widening the pulse pressure

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22
Q

What are some ways NE can be inactivated?

A

COMT degrades in cleft, MOA degrades in the neuron
NRT can reuptake the NE to the neuron, coke and tricyclic antidepressants block this
NE can stim alpha 2 receptors on pre synaptic cell membrane to feedback inhibit release

If block these you are using an indirect acting sympathomimetic

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23
Q

What are characteristics of indirect SNS inhibitors

A

They have a long duration of action, they can develop sensitivity with prolonged use via post synaptic receptor up-regulation, releasers worker less after using indirect SNS inhibitors

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24
Q

What are the inhibitors of adrenergic NT storage or release and what is their therapeutic effects?

A

Reserpine, guanethidine, bretylium

CV: lower BP from decreased CO and PVR
ANS: decreased SNS and increased PSNS
CNS: only reserpine works in CNS, others are quaternary amines dont cross BBB

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25
Q

What are the side effects of adrenergic NT inhibitors?

A

PSNS predominance= diarrhea, GI cramps, nasal stuffiness, ulcers
Postural hypotension
Sexual dysfunction in males
CNS actions with reserpine may cause sedation nightmare and depression

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26
Q

Talk about reserpines effects and side effects and action

A

it depletes monoamine transporters into vessicles from PNS and CNS, increases MAO mediated metabolism of NE or DE in neurons or Epi in adrenal chromaffin cells.

Tx: pheochromocytoma
Once used for HTN but not today
Too many side effects including PSNS dominance and CNS problems like sedation depression and nightmares. Led to suicides so stopped
Also hypotension and fluid retention are side effects

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27
Q

How does guanethidine work and what what effects/side effects are seen

A

Guanethidine gets into synaptic vessicle and causes displacement of and slow release of catechomaine NT and eventual depletion of NT from vessicle. Guanethidine is released from vessicle as false NT

No CNS activity= quat amine
Old HTN tx not anymore
Some blockade of postsynaptic receptors and reuptake as minor effect

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28
Q

What is the action, effects, and therapeutic uses of bretylium

A

Bretylium blocks the depolarization induced NE release/exocytosis from vessicles.

Quat amine= no CNS activity
It has pronouced membrane stabilizing (local anesthetic) effects
It used to be used for ventricular fibrillations and dysrythmias but better drugs now

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29
Q

What are the indirect acting sympathomimetics? And their action?

A

Ephedrine/pseudoephedrine- first oral sympathomimetic, mild caridac stimulation, part of action is to NE release, can make meth with it

Amphetamines- indirect agonist, increased NE and DA release, increases NE at NEJ, increases activation of alpha/beta receptors, much of action is due to NE release, ADHD, cardiac stimulation
Side effects: systemic and coronary vasoconstriction, angina, tachycardia, cardiac arrythmias (alpha and beta)

Cocaine- decreased NE reuptake from NRT, increases NE at NEJ and increases alpha/beta activation, used as a local anesthetic, side effects same as amphetamines

MOA inhibitors- decrease MOA and increase NE DA Epi, depression and parkinson, tachy elevated BP mania are side effects

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30
Q

What are the usual (not always) suffixes of the direct acting sympathomimetics

A
  • nidine= alpha2 agonist
  • terol= beta2 agonist
  • osin= alpha 1 antagonist
  • olol= beta antagonist
  • stigmine= AchE inhibitor
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31
Q

What class is isoproteronol, what is its target, tx, and effect

A

Isoproteronol- nonselective beta agonist, used to treat bradycardia but also has profound vasodilation which causes reflex tachycardia

Used as cardiac stimulant for bradycardia and in certain arrythmias

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32
Q

What are the beta 2 selective agonists? What is their effect and what is their treatment?

A

Albuterol, terbutaline, levalbuterol, saltmeterol are beta 2 selective agonist with preferential effect on smooth muscle.

Used in asthma and COPD, stim beta 2 on bronchodilators to relax the smooth muscle and open the airway

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33
Q

What beta 1 specific drug did we talk about? What is the effects and what are treatment?

A

Dobutamine is a beta 1 agonist primarily used for cardiogenic shock IV in ICU to increase CO via increased HR and contractility with less vasoconstrictive effects that other sympathetic agonists

It is actually a non selective beta with some alpha agonist activity, used in acute CHF or MI

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34
Q

What is the effect of beta 2 activation

A

Generally relaxes smooth muscle: asthma, premature labor

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35
Q

What does activation of beta 1 do

A

Produces tachycardia, increased contractility, and increased renin secretion

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36
Q

What are the adverse effects of beta agonists?

A

Severe tachycardia from stim of beta receptors on SA node
Cardiac arrythrimias- stim beta receptors on conducting tissue and cardiomyocytes decreases electrical stability
Angina- over stim of cardiomyocytes increases contraction force and HR and O2 demand leading to angina necrosis or MI in vulnerable patients
Skeletal muscle weakness- stim beta 2 receptors on skeletal muscles promotes movement of K ions from blood into the muscle cells producing hypokalemia, hyperpolarization and weakness

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37
Q

What are the general therapeutic effects of beta blockers?

A

They slow HR down via SA and AV node inhibition and decrease inotropic activity useful for CHF and angina to reduce O2 demand

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38
Q

What are the adverse effects of beta blockers

A

1) bronchoconstriction- due to blockade of beta2 receptors on bronchodilator smooth muscle, probably can be used safely in COPD thought
2) severe bradycardia heart block due to over blockade of cardiac beta1 receptors

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39
Q

What class of drug is propranolol in? What is the targets and what is special about it

A

Propranolol is a B1 and B2 blocker
It has a marked first pass effect resulting in poor bioavailability, decreased liver function produce higher blood levels and increased toxicity

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40
Q

What are the beta 1 blockers

A

Atenolol, bisoprolol, metoprolol

And esmolol is a beta 1 block with short half life in plasma, given IV in ICU setting bc can DC and wears off quickly

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41
Q

What drugs have mixed beta blocking ability. What is their effect

A

Carvedilol and labetalol
Mixed antagonist of beta1 and beta2 and alpha1

Produce less increase in peripheral vascular resistance due to alpha 1 activity

Alpha 1 blockade means they do not directly relax vascular smooth muscle and don’t provide vasodilating effect desirable in HTN or CHF

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42
Q

What is the use for alpha 1 and 2 agonists?

A

They increase vasoconstriction and are used topically or IV

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43
Q

What is the effect of alpha 2 agonists?

A

They decrease sympathetic tone, slow the HR and decrease CO, and vasoconstrict

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44
Q

What are the pure alpha agonists? What is their use and side effects

A

Pure alpha agonist stim alpha 1>alpha2 are methoxamine and phenylephrine

Methoxamine used for acute hypotensive crisis

Produce baroreceptor diving reflex bradycardia indirectly

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45
Q

What is the effect of NE as drug

A

NE stims alpha and beta1 (minimal alpha 2)

Net effect is vasoconstriction and decreased HR from reflex bradycardia and increased contractility

46
Q

What is the actions and uses of phentermine

A

Alpha > beta agonist

Used in weight loss alone or with topiramate

47
Q

What is action of clonodine

A

Selective centrally acting alpha 2 agonist

For anti HTN

48
Q

What is the action and uses of methlydopa

A

A centrally acting prodrug which has net effect of decreased SNS flow, anti HTN, must be converted to methyl NE in CNS

49
Q

What are the adverse effects of alpha agonists?

A

Adverse effects happen when alpha agonists get to systemic circulation resulting in hypertension, coronary ischemia, cerebral ischemia and local necrosis at site of injection

50
Q

What are some uses of alpha agonist epi and pseudoephridrine

A

Nasal congestion- constrict blood vessels in nasal mucosa
Local anestethics- constrict blood vessels to prolong effect
Occular preperations- constrict blood vessels to reduce redness
Anaphylatic shock- epi reverses hypotension (alpha1) and bronchoconstriction (beta 2) and inhibits histamine release (beta2)

51
Q

What are adverse effects of alpha agonists?

A

Hypertension via vasoconstriction of alpha1 on smooth muscle
Myocardial necrosis/infaract- extreme vasoconstriction of coronary arteries
cerebrovascular event from constricting cerebral vasculature

52
Q

What is the effects of epi? What is the target specificity and effects

A

Epi is a cardiac stimulant via Beta1 and vasoconstrictor via alpha 1. It has equal beta 1 beta 2 and alpha 1 potencies

Beta receptors are more sensative and stimmed at low doses. At high doses alpha receptor stimulation overrides beta stimulation.
Will see alpha effect (increased BP) when first injected at high doses. And then beta1 increase in CO as drug reaches heart. Can increase HR conduction velocity and ventricular muscle contraction. At low concentrations BP decreases from less alpha 1 stim

53
Q

What are the functions of epi on peripheral smooth muscle?

A

Generally alpha increases vasoconstriction and increases BP- with beta1 cardiac input would see SBP, DBP and MAP go up

Beta2 can produce vasodilation and decrease BP- would increase mean and diastolic but not systolic with beta 1

54
Q

What are the alpha 1 and 2 antagonists and uses

A

Phentolamine and pheonxybenzamine

Used in acute pheochromcytoma and renauds syndrome

55
Q

What is the suffix for alpha1 selective antagonists

A

Osin

56
Q

What alpha 1 selective antagonist is used to treat BPH

A

Tamsulosin treat prostatic hypertrophy bc more specific for that tissue

57
Q

Describe the process of Ach production. What is the rate limiting step? What is the enzyme used?

A

Choline is first taken up into the nerve terminal by a high affinity choline uptake pump- this is the rate limiting and regulatory step in synthesis of Ach.

Once in neuroterminal choline is acetylated by choline acetlytransferase to form Ach from choline and acetyl coA.

58
Q

How is Ach stored and released?

A

Stored: active pump to get into vessicles, stored with ATP and proteins

Released: depol causes Ca influx through vg Ca channels, this recruits docking proteins particularly synaptobrevin resulting in fusion of vessicles with active zones on presynaptic membranes and release of NT into cleft

59
Q

How is Ach removed from cleft or inactivated?

A

Metabolism is major mechanism of removal of Ach from synaptic cleft. Ach is hydrolyzed to acetate and choline by AchE.

60
Q

What are the two main subtypes of AchE

A

AchE- in all cholinergic clefts, needed for life, does NOT hydrolyze succinylocholine (a depolarizing neuromuscular blocking agent).

Butyrylcholinesterase- BChE, or psuedo plasma serum ChE. Non neuronal (in liver, plasma, glia cells). Not necessary for life, does hydrolyze succinylocholine

61
Q

Describe the Muscarinic receptor functions

A

M receptors either activate more signaling pathways in the cell producing a signal mediated response or change conductance of K channel hyperpolarizing the cell

62
Q

What are M receptor subtypes and what are their action

A

M1-5 throughout the body, all GCPR
M1 in brain for cognition
M2 in smooth muscle of heart and bladder
Causes tachycardia
M3 in bladder GI and salivary glands- effector organs
Cause bladder contraction, GI motility and secretions
M4 brain and M5 eye for accommodation

63
Q

Where are Nicotinic receptors and what is there action

A

N receptors are mainly Na channel receptors. Found at autonomic ganglia, adrenomedullary chromafin cells or innervate skeletal muscle cells

Let Na in so increase release of NT or increase frequency of AP

64
Q

What are the most potent and specific muscarinic receptor blocker? what drugs are in this class

A

Bella donna alkaloids are the most potent and specific muscarinic receptor blocker

Atropine, hyoscyamine, scopolamine are the drugs

65
Q

What is atropine’s effect and uses?

A

Atropine is a muscarinic receptor blocker. it is used for tachycardia in critical where vagal activity is pronounced. Also used for dilating pupils, pre anesthetic to reduce respiratory tract secretions for intubation

in first degree heart block atropine can block M receptors on AV node to antagonize the slowing by the vagus to improve conduction block

drug of choice in AchE overdose

66
Q

What are hyoscyamine effect and uses?

A

Hyoscyamine is a muscarinic receptor blocker and used to manage overactive GI symptoms like IBS and gastric cramping

67
Q

what are scopalamine effects and uses

A

It is a muscarinic blocker and used for anti nausea and sea sickness prevention

68
Q

What are the tertiary amine anti muscarinic drugs. what is the implication of this

A

Benztropine and ipratopium are tertiary muscarinic blockers. they can cross BBB and have CNS effects.

69
Q

What is benztropine effects and uses

A

it is a synthetic tertiary muscarinic blocker, it is used to manage movement disorders like extrapyramidal syndrome from antipyschoitics

70
Q

what is ipratropium effects and uses?

A

ipratropium is an inhaled antimuscarinic for patients with COPD to keep secretions under control without having to take oral anticholinergics

71
Q

What are a biggest challenges of strong anticholinergic drugs? what is done about this

A

they can cause memory impairment, somnolence, and can lead to falls. Developed quaternary polar amines to keep from entering the CNS

72
Q

what are some side effects of muscarinic antagonists?

A

tachycardia, xerostomia, blurred vision from knocking out accommodation, pupil dilation (mydriasis), anhydrosis

cause orthostatic hypotension

73
Q

what is a depolarizing ganglionic blocker of nicotinic receptors

A

Nicotine, it is an agonist so has initial stimulation followed by polarization blockade= a depolarizing ganglionic blocker

74
Q

what is a non depolarizing ganglionic blocker

A

mecamylamine, an antagonist to nicotinic receptor, in past used to treat HTN

at very high doses could block NMJ and cause paralysis

75
Q

what effect does ganglionic blockers have on: systemic arterioles, cardiac ventricles, SA node, salivary glands, sweat glands

A

vasodilates and reduces BP in arterioles, depressed contractility of ventricles, tachycardia in SA node, xerostomia or dry mouth, anhydrosis or lack of sweat

they act like alpha blockers on arterioles, beta blockers on ventricles, and M blockers on SA node and glands

76
Q

What is bethanechol effects and uses?

A

bethanechol is a quat amine muscarinic agonist no CNS, poor oral absorption

used in gastric atony to stimulate tonic movement, used in urinary retention to stim M receptors of smooth muscle of GU tract and contractilie acitivity and urinary excretion

77
Q

What is pilocarpine and its uses?

A

A tertiary muscarinic agonist with CNS activity, muscarinic selective

used to stim salivary glands in xerostomia. In acute narrow angle glaucoma it produces meiosis (pupil contraction) and ciliary body constriction to promote draining of fluid from canal of Schlemm to improve symptoms

78
Q

What are muscarinic agonist from nature

A

muscarine is from mushrooms- no therapeutic use

arecoline is from Betel nut, psychoactive properties

79
Q

What are the effects of muscarinic agonists?

A 
Think PSNS overstimulation:
Marked meiosis
respiratory distress from bronchospasm and increased secretions
hypersalavation
sweating
intestinal hyper activity
hypotension
bradycardia
80
Q

describe nicotine’s effects at low and high doses

A

at low does it is a ganglionic nicotinic agonist enhancing SNS and PSNS transmission.

at high doses or prolonged use nicotine becomes a depolarizing blockade antagonist. this causes respiratory paralysis nausea and vomiting

it is a tertiary amine and enters CNS

81
Q

what are the organ specific effects of nicotine

A

Heart: tachycardia bc increases epi
Blood vessels- vasoconstrictions from SNS and epi, increase BP
tolerance can occur to these

CNS: increased attention, DA release for reward, decreased appetite and increased metabolic activity

at high toxic doses
somatic- muscle twitching progressing to polarizing block of ganglia and in NMJ

82
Q

What is the effect of varenicline and what is it uses

A

it is a partial nicotinic agonist with some antagonist?

the antagonist action blocks reinforcing properties of nicotine while agonist activity helps prevent withdrawls

83
Q

What is the effect of edrophonium and its uses?

A

eddrophonium is a short acting competitive inhibitor of AchE, used for dx and dose adjustment in MGravis

84
Q

What is the effect of donepezil and uses

A

donepezil is a non competitive AchE inhibitor, lipophillic reversible, produces effective AchE inhibition in CNS. Alzheimers treatment

85
Q

What is the effects and uses of rivastigmine

A

non competitive AchE inhibitor, for Alzheimers tx in patch or oral dose

86
Q

what is the effects of physostigmine and uses

A

slow hydrolysis of carbamate enzyme, lipid soluble and safe, from bean, used for century in glaucoma

87
Q

What are the effects of neostigmine and pyridostigmine and uses

A

they are quaternary derivatives of physostigmine so carbamate AchE inhibitor, does not cross BBB, used in tx of MGravis and to reverse paralysis from non depolarizing muscle blockers

88
Q

What are the organophosphate drugs action, what are they, and what are their uses

A

Organophosphates have very slow hydrolysis of phosphorylated enzyme leading to inhibition of AchE. Long acting.

Insectisides- malathion and parathion are thiophosphates that are prodrugs must be metabolized to organophosphates in vivo. in mammals and birds they are converted to inactive metabolites so safe

Nerve gases- sarin and VX, irreversible AchE inhibitors, highly potent and lipid soluble, used in war

89
Q

What is the acronym for AchE inhibitor side effects

A

DUMBELS

Diarrhea, diaphoresis
Urination
Miosis
Bradycardia, Bronchospasm, Brochorrhea
Emesis
Lacrimation
Salivation, sweating
90
Q

What is the treatment for AchE inhibitor toxicity

A

Atropine or Pralidoximine (2PAM)

Pralidoximine restores cholinesterase bc has higher affinity for organophosphate than AchE. rips organophosphate off AChE. will only work for organophaste poisoning.

91
Q

Describe the use of 2PAM (pralidoximine)

A

used in AchE inhibitor poisoining. needs to get there before aging occurs to break bond btn organophosphate and AchE. does not cross BBB. Not effective for respiratory effects so always use with atropine, not effective for carbamate (stigmine) poisoning bc they don’t have the phosphate group for 2PAM to rip off

Not for patients with MGravis bc could make worse. also effects intensified in kidney disease

92
Q

what drugs used to treat MGravis

A

Neostigmine and pyridostigmine bc charged AChE inhibitors which do not enter CNS and have some direct receptor stimulation to increase ACh in MG

93
Q

how does edrophonium work?

A

AchE inhibitor. In normal person it decreases their muscle strength via depolarizing blockade. In MG it increase strength by increasing Ach in cleft

94
Q

How is Somatomotor neurons similar or different from ANS neurons

A

Different in that they are not interrupted by a ganglia

Same in the predominant receptors are nicotinic, different in that they are Nm subtype and not Nn receptors. Both respond to Ach but are affected by different drugs.

Nm activation leads to MEPP

95
Q

what are the non depolarizing Nm blockers?

A

tubocuraine, atracurium, pancuronium

96
Q

what is a depolarizing Nm blocker

A

succinylcholine

97
Q

What drugs can physostigmine overcome and which can it not?

A

physostigmine is an Anti AchE that can overcome blockade from non depolarizing agents like curare drugs but not depolarizing drugs likes sucs

98
Q

What are two main ways that doctors cause muscle paralysis

A

1) nicotinic Ach receptor antagonist- tubcurarine

2) neuromuscular junction nicotinic Ach receptor agonist- sucs

99
Q

What are properties of all NM blockers

A

all are charged, no CNS and quick onset, IV
paralysis of skeletal muscle
hit fast twitch muscles> limb> respiratory
hypotension from histamine release
tachycardia from hypotension

100
Q

What are the side effect of Nm blockers. What patients are at higher risk

A

most serious is respiratory paralysis, can use neostigmine plus atropine to reverse. neostigmine to increase Ach and atropine to block the muscarinic stimulation (just want Nm reversal) and antihistamines to reverse histamine release

MGravis patient bc less functional Nm receptors. and with drugs that stabalize membrane potential and inhibit Ach and patients with hypokalemia (hyper polarization)

101
Q

what is succinylcholine used for and what is its effect

A

Succs is a depolarizing Nm blocker. It is drug of choice in intubation bc rapid onset. Not metabolized by AchE but by BChE so can cause depolarizing blockade. Infused, action is about 5 minutes

102
Q

What is tubocurarine and what is its uses

A

protype non depolarizing Nm blocker, action 90-120minutes is medium

side effect is release of histamine from mast cells cause hypotension

103
Q

what is atracurium and what is its use

A

Short active nondepolaring Nm blocker. useful in patients with hepatic and renal failure bc undergoes hoffman degradation for elimination and not rely on hepatic metabolism

104
Q

What is pancuronium and what is its use

A

long acting non depolarizing Nm blocker. 3times more potent that curare with less side effects

105
Q

What are the adverse effects of Nm muscle blockers? what is the most serious and how to treat?

A

Most serious is malignant hyperthermia from contraction of all muscles, Tx with dantrolene to interfere with Ca release in muscle from depolarizing muscle blockers

Other side effects
hyperkalemia- from depolarizing muscle blocker from depolarization moves K from cells to blood

histamine release- from curare non depolarizing blockers only

Ganglionic block- at high doses can block Nn in addition to Nm

106
Q

When are muscle blockers used the most

A

typically in surgery to relax muscles for respirator, intibutation, fx fix, scopes

107
Q

What is diazepam and what is its effect

A

Diazepam is a benzo muscle relaxer that facilitates GABA action of CNS, reduces spasticity, partially mediated in spinal cord, useful in SCI

108
Q

What is baclofen and its effect

A

it is a partial GABA agonist muscle relaxer. results in hyper polarization by increasing K conductance, decreasing Ca presynaptically and in dendrites

reduces excitatory NT in brain and SC
reduces sensory afferent, spinal interneurons and motor neurons
reduces sub P to reduce pain
not reduce muscle strength as much as dantrolene

109
Q

What is cyclobenzaprine/methocarbamol and uses

A

it is a muscle relaxer. related to trycyclic anti depressants, produces anti muscarinic side effects leading to sedation
block the reuptake of NTto inhibit muscle stretch reflex in SC
Good for injury related muscle spasm
Not good for CP or SCI muscle spasms

110
Q

What is dantrolene and its uses

A

muscle relaxer that inhibits Ca release from SR of skeletal muscle. reduces muscle tension. not affect neurotransmission.

Not useful for acute muscle spasm of local origin
Good in acute attacks of malignant hyperthermia and used to treat hyperthermia and muscle rigiditiy in neurologic malignant syndrome (NMS)- a complication of treatment with anti or succs with anethesia.

D&T Exam 3 (5 decks)

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