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Neuro > Peripheral Neuro-Pharmacology > Flashcards

Peripheral Neuro-Pharmacology Flashcards

1
Q

What is the effect of anticholinesterases on synaptic action?

A

It potentiates nerve stimulation by inhibiting cholinesterases, impairing the hydrolysis of ACh and thus increases the twitch to both nerve stimulation and exogenous ACh

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2
Q

What is the relationship between Calcium and end plate potential?

A

The end plate potential size depends on calcium concentration (and subsequently the amount of ACh released)

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3
Q

What is the effect of curare on end plate potential?

A

The end plate potential is decreased (due to decreased ACh release)

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4
Q

What are MEPPs?

A

Miniature end plate potentials that occur due to spontanous release of ACh

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5
Q

What is the effect of anti-cholinesterases on MEPPs? What about curare?

A

Anticholinesterase - increases amplitude

Curare - decreases amplitude

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6
Q

What are the three SNARE proteins involved in neurotransmitter release?

A

Syntaxin, synaptobrevin/VAMP, and SNAP-25

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7
Q

Which SNARE protein is cleaved by type A botulinum toxin?

A

SNAP-25

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8
Q

What is the structure of the SNARE apparatus for neurotransmitter release?

A

Syntaxin is associated with the nerve terminal membrane

Synaptobrevin is associated with the vesicle

SNAP-25 is associated with the nerve terminal membrane (loosely)

Synaptotagmin is intertwined with the SNAREs as a calcium sensor that triggers vesicle fusion

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9
Q

What is the process of triggering secretion of ACh from the nerve terminal?

A

ACh synthesized and stored in synaptic vesicles of nerve terminal –> Nerve action potential invades the nerve terminal –> Specific Ca2+ channels (linked to SNAREs) are opened and Ca2+ enters cell down electrochemical gradient –> Ca2+ binds to synaptotagmin and triggers vesicle/SNARE fusion –> ACh is secreted

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10
Q

What is the immediate response of a stimulated muscle cell in response to ACh release in the synaptic cleft?

A

ACh reacts with nicotinic receptor, which opens ion channels that allow flow of positively charged ions –> Na+ flows through because they are the furthest from equilibrium at rest

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11
Q

What terminates the action of ACh at the post-junctional membrane?

A

It is terminated by acetylcholinesterase

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12
Q

What is the function of hemicholinium-3?

A

It competitively inhibits the uptake of choline via the choline transporter –> number of molecules of ACh per vesicle is smaller

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13
Q

What causes small sized MEPPs in myasthenia gravis?

A

A postsynaptic deficit that reduces the number of ACh receptors, reducing sensitivity to ACh

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14
Q

What is the function of tetrodotoxin?

A

It blocks the electrophysiological input to the nerve ending (via blocking Na+ conductance) and the electrophysiological output on the other side of the synapse.

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15
Q

What is the effect of Mg2+ on the neuromuscular junction?

A

It reduces neurally-evoked ACh release by competing with Ca2+ at the channels

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16
Q

What is the cause of Lambert-Eaton Myasthenic Syndrome (LEMS)?

A

It is caused by a reduced number of P/Q type Ca2+ channels in the nerve ending, reflected as a reduced number of ACh vesicles released into the synapse

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17
Q

What is the mechanism of black widow spider venom?

A

The active ingredient causes a huge amount of ACh vesicular release due to a rise in cytoplasmic calcium concentration from a rise in the venom

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18
Q

What are possible clinical uses of botulinum toxin type A?

A

Blepharospasm/ocular disorders, hemifacial spasms, laryngeal problems, peripheral spaticity

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19
Q

What changes in EPP and MEPP amplitudes are associated with a postjunctional deficit?

A

Both are decreased (reduced responsiveness to ACh)

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20
Q

What changes in EPP and MEPP amplitudes are associated with a prejunctional deficit?

A

The EPP amplitudes are decreased without a change in MEPP amplitudes (the ratio of average EPP amplitude to MEPP amplitude decreases) –> decrease in evoked ACh release

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21
Q

Which SNARE is associated with the neurotransmitter vesicle?

A

Synaptobrevin

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22
Q

What SNARE is cleaved by botulinum toxin type B?

A

Synaptobrevin

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23
Q

What is the treatment for botulism?

A

Heptavalent anti-toxin (to treat the seven different serotypes)

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24
Q

What is the upstroke of muscle action potential?

A

Opening of voltage-gated sodium channels after the EPP

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25
Q

What is the cause of the falling phase of the muscle action potential?

A

Sodium channel inactivation at first, followed by a delayed rise in potassium conductance (through a K+ channel)

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26
Q

What are the two requirements for depolarization and membrane excitation?

A

Driving force (voltage difference) and conductance increase (channel opening) for a specific ion

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27
Q

Which types of blocking drugs have effects that are surmountable by increasing the ACh concentration?

A

Non-depolarizing blocking drugs (competitive inhibitors)

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28
Q

What class of drug is succinylcholine?

A

Depolarizing blocking drugs

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29
Q

What occurs during phase I of the response to depolarizing blocking drugs?

A

The depolarizing drug prevents ACh released synaptically from interaction with post-junctional receptors –> ALSO there is no driving force for current flow because the drug pushes receptors towards equilibrium potential

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30
Q

What occurs during phase II of the response to depolarizing blocking drugs?

A

Nicotinic receptors are desensitized and cannot be activated by any agonist –> muscle cell repolarizes to normal resting level but the nicotinic receptors are not conducting sodium ions

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31
Q

What is the effect of direct muscle stimulation during phase I of the response to a depolarizing blocking drug? Phase II?

A

Phase I –> even direct stimulation cannot activate the muscle

Phase II –> direct stimulation can activate the muscle (muscle is repolarized, so volt-gated sodium channels can be stimulated again)

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32
Q

What suffix is associated with clinically-used non-depolarizing neuromuscular blockers?

A

…curonium

pancuronium, vecuronium, and rocuronium

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33
Q

What suffix is associated with cholinesterase inhibitors? What are they used for?

A

…stigmines

Used to treat MG, diagnose MG, and reverse non-depolarizing block at the end of surgery

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34
Q

What is the function of sugammadex?

A

A drug that encapsulates the …curoniums and rapidly terminates non-depolarizing block

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35
Q

What is synergy between two drugs?

A

An effect that occurs when two drugs that are both capable of producing the same effect BUT they both act at different sites

two drugs that act at the same site can not be synergists

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36
Q

What is the effect of tubocurarine on ACh function?

A

It is a competitior of ACh (surmountable inhibition)

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37
Q

What is the pattern of potential changes after treatment with a depolarizing blocking drug?

A

It initially causes rapid firing action potentials and then settles down to the level of an MEPP throughout phase I. Eventually the potential repolarizes and drops to baseline (phase II).

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38
Q

What is the mechanism of phase I (depolarization block)?

A

Persistent depolarization leads to inactivation of electrically activated sodium channels. It ALSO 1) blocks access of ACh on receptors and 2) eliminates the driving force necessary for current flow of ACh

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39
Q

What is the mechanism of phase II block (desensitization block)?

A

Continued presence of the drug leads to desensitization of the nicotinic receptor, which leads to repolarization to normal levels. The desensitized receptors are still incapable of responding to ACh release.

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40
Q

What isthe duration of Pancuronium? What are the advantages of pancuronium over tubocurarine? Side effects?

A

Long duration (1 hr)

More potent, does not release histamine, does not cause ganglionic blockade

Blocks vagal tone causing tachycardia

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41
Q

What is the duration of vecuronium? What are the advantages of it?

A

Intermediate duration

No tachycardia or histamine release, no cardiovascular effects, eliminated by the liver (good for people with kindey failure)

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42
Q

What is the duration/onset of rocuronium? What is it usually used for?

A

Rapid onset, intermediate duration

Used for intubation and surgical procedures

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43
Q

What are the main therapeutic uses of succinylcholine?

A

Used during intubation for rapid and temporary neuromuscular block

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44
Q

What are the side effects of succinylcholine?

A

Bradycardia, malignant hyperthermia

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45
Q

What is malignant hyperthermia?

A

An inherited myopathy where certain drugs can cause huge amounts of calcium release from the SR, which causes massive muscle contraction and body temperature elevation

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46
Q

Which blocking drugs have the most rapid onset?

A

Succinylcholine and rocuronium

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47
Q

Which blocking drugs are often used during the duration of surgery?

A

Rocuronium or vecuronium

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48
Q

What drugs are used to reverse non-depolarizing block?

A

Anticholinesterases or sugammadex

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49
Q

What is neuromuscular depression? What is the origin/casue of it (generally)?

A

Neuromuscular depression is a decrease in end-plate potential amplitude with repetitive motor nerve activation.

Origin: pre-synaptic

Cause: decreased release of acetylcholine

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50
Q

What is the chemical cause of endogenous neuromuscular depression? What is the mechanism?

A

Endogenous adenosine (derived from ATP and released from NMJ with ACh) –> reduces calcium currents in nerve terminal

Also depletion of vesiular stores of ACh contributes to depression at high nerve frequency stimulation

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51
Q

What is the clinical presentation of neuromuscular depression/depression of EPPs?

A

Not observed clinically - multiple back up mechanisms prevent it from manifesting as a decline in muscle twitch tension

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52
Q

What is the effect of a non-depolarizing blocking drug on muscle twitch and neuromuscular depression?

A

It causes neuromuscular depression to be observed clinically due to the reduction in the “safety factor” that normally acts as a back up

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53
Q

What would the twitch tests results look like for a patient treated with a non-depolarizing blocker (ex. rocuronium)?

A

Initial depression in the first train of four twitches, depression during the extended stimulation, and depression in the second train of four twitches after

increased response in second twitches is due to acumulation and increased availability of residual nerve terminal calcium ions fter high frequency stimulation (post-tetanic potentiation)

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54
Q

What is the effect of a phase I depolarization block on neuromuscular depression?

A

The twitch response to repetitive motor nerve stimulation is well maintained, but at a reduced level

aka the twitch is smaller, but there is no depression with repeated stimulation

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55
Q

What would the twitch tests results look like for a patient treated with a depolarizing blocker (ex. succinylcholine)?

A

There would be a consistent low-level twitch with repeated stimulation with no neuromuscular depression

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56
Q

What is the effect of a phase II desensitiation block on the twitch response?

A

It depresses the twitch response and appears similar to a non-depolarizing blocker

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57
Q

What is the pattern of twitch seen on exam in patients with myasthenia gravis?

A

They will have a depression in twitch tesnsion in the absence of a neuromuscular blocker

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58
Q

What type of treatment “rescues” the normal twitch response in patients with myasthenia gravis?

A

Treatment with a cholinesterase inhibitor (ex. neostigmine)

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59
Q

What is the pattern of twitch seen on exam in patients with LEMS?

A

The twitch response to the initial stimulus is smaller but becomes enormous after higher frequency stimulation due to accumulation of calcium and absence of depression

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60
Q

What twitch pattern is observed during surgery for treatment with succinylcholine for intubation followed by vecuronium during surgery?

A

Succinylcholine - wait until twitches go away and the patient is relaxed to intubate

Vecuronium - train of four stimulations –> two positive twitches, two negative twitches with four successive stimulations

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61
Q

What is the pattern of twitches seen post-operatively with neostigmine treatment after surgery with succinylcholine and vecuronium?

A

Four stimulations resulting in four twitches

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62
Q

What twitch pattern is observed with treatment of rocuronium before surgery for intubation and during surgery?

A

Four stimulations resulting in one positive twitch and three negative twitches

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63
Q

What twitch pattern is observed when sugammadex is given post-operatively after a surgery where rocuronium was used?

A

Four successive twitches with stimulation

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64
Q

How many twitches (out of four) need to be present to determine full reversal of NM block?

A

Four - any less is not full reversal

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65
Q

What is the definition of the sympathetic and parasympathetic ANS?

A

Grouped based on anatomical locus, not function.

Parasympathetic - craniosacral localization

Sympathetic - thoracolumbar localization

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66
Q

What types of synapses are the synapses for preganglionic axons of both divisions of the ANS?

A

Nicotinic cholinergic synapses

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67
Q

Where are the cell bodies for preganglionic axons of both divisions of the ANS?

A

Within the CNS - emerges as myelinated nerve fibers

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68
Q

What is the difference between sympathetic and parasympathetic ganglia?

A

Sympathetic ganglia are located near the spinal cord, parasympathetic ganglia are located in or near target tissues

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69
Q

What type of receptor acts at the neuro-effector junction of parasympathetic nerves?

A

Almost always Muscarinic receptors that respond to ACh

the exception is nitric oxide for parasympathetic arousal

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70
Q

What type of receptor acts at the neuro-effector junction for mostsympathetic nerves?

A

Catecholamine receptors that respond to norepinephrine (and epinephrine)

The exceptions are sympathetic cholinergics (signaled by ACh) of eccrine sweat glands

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71
Q

What is the signaling pathway for eccrine sweat glands?

A

Sympathetic cholinergic: neuro-effector junction has a muscarinic receptor unlike most sympathetic junctions

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72
Q

What mechanisms control pupil size?

A

Parasympathetics: synapse in ciliary ganglion –> contraction of muscle leads to miosis (constricted pupil)

Sympathetics: synapse in paraspinal ganglion –> contraction of muscle leads to mydriasis (dilated pupil)

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73
Q

What is the effect of sympathetic stimulation on the pupil? Parasympathetic?

A

Sympathetic: dilation (mydriasis)

Parasympathetic: constriction (miosis)

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74
Q

What is the effect of sympathetic stimulation on the bronchioles? Parasympathetic?

A

Sympathetic: Dilation

Parasympathetic: Constriction

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75
Q

What is the effect of sympathetic stimulation on the GI muscle wall? Parasympathetic?

A

Sympathetic: Relaxation

Parasympathetic: Contraction

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76
Q

What is the effect of sympathetic stimulation on the GI Sphnicter? Parasympathetic?

A

S: Contraction

P: Relaxation

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77
Q

What is the effect of sympathetic stimulation on the urinary bladder muscle wall? Parasympathetic?

A

S: Relaxation

P: Contraction

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78
Q

What is the effect of sympathetic stimulation on the urinary bladder sphincter? Parasympathetic?

A

S: Contraction

P: Relaxation

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79
Q

What is the effect of sympathetic stimulation on the sinus heart rate? Parasympathetic?

A

S: Acceleration

P: Slowing

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80
Q

What is the effect of sympathetic stimulation on the ventricular contractile force of the heart? Parasympathetic?

A

S: Increased

P: no effect

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81
Q

What is the effect of sympathetic stimulation on the liver? Parasympathetic?

A

S: glycogenolysis, gluconeogenesis

P: glycogen synthesis

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82
Q

What is the effect of sympathetic stimulation on fat deposits? Parasympathetic?

A

S: fatty acids released

P: no effect

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83
Q

What is the effect of sympathetic stimulation on most blood vessels (but not skeletal muscle or liver)? Parasympathetic?

A

S: Constriction (via alpha receptors)

P: no effect

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84
Q

What is the effect of sympathetic stimulation on skeletal muscle and liver blood vessels? Parasympathetic?

A

S: Dilation due to sympathetic, cholinergic, and EPI from medulla on beta2 receptors

P: No effect

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85
Q

What is the effect of sympathetic stimulation on the sexual organs? Parasympathetic?

A

S: Semen discharge, vasoconstriction

P: Vasodilation (erection)

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86
Q

What is the effect of sympathetic stimulation on piloerectors? Parasympathetic?

A

S: contraction

P: no effect

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87
Q

What is the effect of sympathetic stimulation on the spleen? Parasympathetic?

A

S: contraction

P: no effect

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88
Q

What is the effect of sympathetic stimulation on the salivary glands? Parasympathetic?

A

S: secretion

P: secretion

only parallel effects

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89
Q

What is the effect of sympathetic stimulation on the eccrine sweat glands? Parasympathetic?

A

S: secretion (via cholinergics!)

P: no effect

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90
Q

What is the effect of sympathetic stimulation on respiratory and digestive glands? Parasympathetic?

A

S: no effect

P: secretion

  • exception –> insulin*
  • S: inhibits insulin secretion*
  • P: stimulates secretion*
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91
Q

What is the primary regulator of total peripheral resistance?

A

Sympathetic outflow to blood vessels

  • increased sympathetic tone = constricts BVs*
  • decreased sympathetic tone = dilated BVs*
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92
Q

What is the pathway of the barostatic response to increases in blood pressure?

A

Increased BP sensed by stretch receptors in aortic arch (CN X) and carotid sinus (CN IX) –> fires to CN IX and X –> IX and X synapse in medullary NTS –> stimulates the vagal nucleus (also called nucleus ambiguous) –> signals the vagus nerve (X) to slow heart rate

NON VAGAL COMPONENT: nerve from NTS signals to rostral ventral medulla and induces a reduction in sympathetic tone

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93
Q

What is the pathway of the barostatic response to decreases in blood pressure?

A

Drop in BP sensed by receptors in aortic arch (CN X) and carotid sinus (CN IX) –> decreased firing of baroreceptor afferents –> increases release of NE –> increases vasomotor tone AND increases heart rate

decreased heart rate ALSO due to decreased stimulation of vagal nucleus

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94
Q

What is orthostatic hypotension?

A

Failure to maintain arterial pressure in upright posture due to low vasomotor tone

can be induced by drugs that block sympathetic signaling to periphery via alpha1 receptors

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95
Q

What isthe micturition reflex?

A

A pure parasympathetic reflex in newborns

Distension of bladder –> increased intravescal tension –> activates sensory neurons in bladder wall –> sends afferent nerve stimulation to spinal cord –> efferent nerves return to bladder from spinal cord to activate the detrusor muscle and inhibit the sphincter trigone (causing urination)

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96
Q

What plexi are part of the enteric nervous system?

A

Submucous (Meissner’s) and myenteric (Auerbach’s) plexi

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97
Q

What system of neurons controls the peristaltic reflex?

A

Enteric nervous system

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98
Q

What is the path of sympathetic cholinergic nerves through the sympathetic ganglion?

A

Preganglionic fiber enters via white ramus –> synapses in ganglion –> exits through grey ramus

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99
Q

What is the difference between salivary secretions from sympathetic and parasympathetic stimulation?

A

S: small volume of potassium and water

P: serous, watery

100
Q

What division of the ANS normally dominates?

A

Parasympathetic tone

exception: sympathetic tone controls BV diameter/TPR

101
Q

What effect does the signaling pathway from the NTS to the RVM have on the heart in response to high or low BP?

A

High BP: pathway is inhibited, leading to decreased BV constriction and decreased TPR

Low BP: pathway is disinhibited, leading to increased BV constriction and increased TPR

102
Q

What is the relationship between arterial size and BP?

A

It is the major determinant of BP because there is a reciprocal fourth power relationship (aka a small increase/decrease in arterial size leads to a large decrease/increase respectively in BP)

103
Q

What is the major difference between nicotinic and muscarinic receptor structure?

A

Nicotinic: ACh gated ion channels

Muscarinic: GPCRs signaled by ACh

they also bind to different sides of the ACh molecule

104
Q

What are the parts of an action potential at the SA node?

A

If channels open (triggered by hyperpolarization) and Na+ moves to depolarize the membrane

L-type Ca2+ channels open (upstroke)

Potassium current (delayed rectifier channel) repolarizes membrane

105
Q

What are the three mechansism of control of ACh on the SA node?

A

1) Increased potassium conductance (hyperpolarizes membrane) –> viacomponent of muscarinic GPCR
2) Inhibits If channels
3) Inhibits L-type calcium channels
* 2 and 3 inhibit the entire upstroke of SA node*
* leads to decreased conduction –> parasympathetic stimulation reduces heart rate at SA node*

106
Q

What is the effect of ACh on the AV node?

A

It decreases AV conduction via an increase in potassium conductance

107
Q

What is the effect of ACh on blood vessels?

A

It causes a decrease in blood pressure via dilation of blood vessels

This signaling is due to muscarinic receptors in the endothelium that triggers a cascade of NO synthesis and release, which leads to smooth muscle vasodilation (aka no direct parasympathetic innervation on blood vessels)

108
Q

What is the pathway of ACh stimulation on blood vessels?

A

Ach –> stimulates muscarinic receptor –> stimulates phospholipase C –> causes Ca2+ release from ER –> binds calmodulin –> activates NO synthesis –> NO migrates to smooth muscle cells and binds guanylyl cyclase –> activates a protein kinase (PKG) –> smoothmuscle relaxes

109
Q

What is the overall effect of ACh alone on the cardiovascular system?

A

Vasodilation (decrease in BP)

Reflex tachycardia (in response to decreased BP)

110
Q

What is the effect of ACh + neostigmine on the cardiovascular system?

A

Produces a much larger fall in blood pressure (vasodilation) and a decrease in heart rate when injected IV

Neostigmine inhibits acetylcholinesterases, which leads to increased ACh stimulation of muscarinic receptors on the heart that can overcome the reflex tachycardia. Without this, the reflex tachycardia dominates.

111
Q

What is the difference between methacholine and acetylcholine?

A

It has a methyl group on the beta carbon, making it specific for muscarinic receptors and slightly more resistant to hydrolysis by ChE

112
Q

What is the therapeutic use of methacholine?

A

It is used as a test for bronchial asthma (methacholine challenge)

113
Q

What does the drug bethanechol do?

A

It is a drug with an altered ACh-like structure that is specific for muscarinic receptors and very resistant to hydrolysis by cholinesterases

114
Q

What are the therapeutic uses of bethanechol?

A

GI tract: treats disorders of low bowel tone

Urinary bladder: treats urinary retention

bethanechol is a muscarinic agonist

115
Q

What are the contraindications of bethanechol?

A

Can produce shock when given IV (must give sub Q or oral)

Bad for asthmatics

Hyperthyroid patients (due to susceptability to arrhythmia)

Peptic ulcers

Intestinal/bladder obstruction

bethanechol = muscarinic agonist

116
Q

What type of drug is pilocarpine?

A

It is a muscarinic agonist that is not hydrolized by cholinesterases

117
Q

What are the therapeutic uses of pilocarpine?

A

Glaucoma therapy (especially narrow angle glaucoma)

Treats dry mouth/exocrine gland symptoms of Sjogren’s syndrome

  • Pilocarpine = muscarinic agonist*
  • Functions by contracting the irisand uncrowding the filtration angle to improve outflow of aqueous humor*
118
Q

What type of drug is cevimeline? What is the therapeutic use of it?

A

It is a newer form of pilocarpine (a muscarinic agonist that is not hydrolyzed by AChEs) that treats Sjogren’s syndrome symptoms

119
Q

What are the general signs and symptoms of poisoning with anticholinesterase agents?

A

SLUD

Salivation

Lacrimation

Urination

Defecation

120
Q

Why are high doses of anticholinesterase agents toxic?

A

They allow so much ACh to accumulate, leading to both postsynaptic effects and presynaptic nicotinic effects –> causes an avalanche of cholinergic activity –> leads to a block (due to excess signaling) at nicotinic sites in skeletal NMJs and in the CNS, but not in the peripheral muscarinic sites (due to the coupling of second messengers rather than direct depolarization) –> leads to POWERFUL mimicry of parasympathetics and sympathetic cholinergics

121
Q

What type of drug is physostigmine? What is it used to treat?

A

A reversible cholinesterase inhibitor

Uses: glaucoma therapy

122
Q

What type of drug is neostigmine? What are its therapeutic uses?

A

Reversible cholinesterase inhibitor

Skeletal NMJ uses: treat myasthenia gravis, reverse non-depolarizing block post-op

Autonomic uses: glaucoma therapy, urinary retention, treat GI stasis

123
Q

What type of drug is pyridostigmine? What are its therapeutic uses?

A

Reversible cholinesterase inhibitor

Therapeutic uses: treats myasthenia gravis

124
Q

What type of drug is edrophonium? What are its therapeutic uses?

A

Reversible cholinesterase inhibitor

Therapeutic uses: test for MG (short acting)

125
Q

How do cholinesterases hydrolyze ACh?

A

ACh anchors at the anionic site, but part of it hangs over onto the esteratic site (enzyme activity here) where hydrolysis is facilitated by a serine residue

The enzyme becomes acetylated and must react with water before regnerating (occurs rapidly)

126
Q

What is the mechanism of reversible cholinesterase inhibition?

A

Forms a bond at the esteratic site that is hydrolyzed more slowly than the normal acetylated enzyme (keeps ChEs inactivated for longer, but not permanent)

127
Q

What is the mechanism of ChE inhibition via organophosphorus inhibitors (ex. DFP)?

A

They react with the serine residue of the esteratic site and form a permanent phosphorylation that cannot be hydrolyzed

restored ChE function only occurs after re-synthesis of the enzyme which takes 3-6 weeks

128
Q

What is DFP?

A

A nerve gas and insecticide that functions as a non-reversible cholinesterase inhibitor

129
Q

What is parathion?

A

An insecticide that acts as a non-reversible cholinesterase inhibitor

130
Q

What is malathion?

A

An insecticide that causes non-reversible cholinesterase inhibition in lower animals (not humans) and is used to treat head lice

131
Q

What is chlorpyrifos?

A

An insecticide that is a non-reversible cholinesterase inhibitor

132
Q

What is sarin?

A

A nerve gas that functions as a non-reversible cholinesterase inhibitor

133
Q

What is VX?

A

A deadly nerve gas that functions as a non-reversible cholinesterase inhibitor

134
Q

What are treatments for cholinesterase inhibitor toxicity?

A

1) decontaminate skin (if that was the form of contact)
2) block excess muscarnic activity (high doses of atropine)
3) treat skeletal muscle effects (artificial respiration, reactivate enzyme at skeletal NMJ with pralidoxime)
* 4) pyriostimgine pretreatment –> doesn’t work*
* 5) anticonvulsants if sever*

135
Q

What are the general effects of muscarinic antagonists?

A

Opposite of parasympathetic stimulation

pupil dilation, bronchiolar dilation, constipation, urinary retention, decreased secretions, decreased sweating, increased heart rate

136
Q

What type of drug is atropine? What does it do?

A

It is a competitive inhibitor of ACh at muscarinic receptors, leads to effects opposite of parasympathetic stimulation

137
Q

What is accommodation (in context of eyes)?

A

Changing of lens shape in response to viewing a close object –> occurs due to parasympathetic firing that contracts ciliary fibers and slacks ligaments to the lens, which allows it to relax into a natural round shape

138
Q

What is cyclospasm?

A

Spasm of the ciliary muscle that results in blurred vision

139
Q

What is cycloplegia?

A

Paralysis of accommodation that fixes lens for distant vision

140
Q

What drugs are used frequently to dialate the pupil and induce cycloplegia?

A

Cyclopentolate, tropicamide

both muscarinic blockers

141
Q

What drug is used for ciliary spasm due to injury?

A

Homatropine

muscarinic blocker

142
Q

What type of durg is Ipratropium/Tiotropium? What are their clinical uses? What is the difference between them?

A

Type of drug: muscarinic blocker

Clinical use: bronchodilators for patients with asthma or COPD

Difference: ipratropium is a short acting muscarinic antagonist (SAMA), tiotropium is a long acting muscarinic antagonist (LAMA)

143
Q

What are the drugs of choice for GI spasms?

A

Muscarinic blockers: atropine (most common), lomotil, glycopyrrolate

144
Q

What type of drug is often used for bladder spasms? How effective are these drugs?

A

Muscarinic blockers, not very effective and have lots of side effects (related to blocking of parasympathetic function elsewhere –> dry mouth, constipation, blurry vision)

145
Q

What is the utility of muscarinic antagonists in the blockade of secretions?

A

They can be used to block respiratory secretions (atropine used to be used), acid secretions (atropine used to be used), and to block secretions during surgery

Only really used now for blocking of secretions during surgery

146
Q

What is the effect of atropine on the heart rate? When is it used clinically?

A

It increases the heart rate (muscarinic agonist)

It is used to oppose decreased heart rate during anaesthesia

147
Q

What is the role of muscarinic antagonists in treatment of parkinsons disease?

A

They can alleviate symptoms by blocking ACh effects or increasing the effects of dopamine

148
Q

What drug is used to prevent excessive muscarinic effects of neostigmine when reversing non-depolarizing block post-op?

A

Glycopyrrolate

149
Q

What are the effects of scopolamine treatment?

A

It is anti-emetic but can also cause sedation, amnesia, and increased risk of dimentia because it has CNS depressant effects

150
Q

What are the symptoms of toxicity of antimuscarinic agents?

A

Dry as a bone (no sweating, dry mouth, dry eyes)

Red as a beet (flushed face)

Mad as a hatter (CNS effects/delirium)

Hot as a stove (increased body temperature)

Blind as a bat (dilated pupils)

151
Q

What is the treatment for toxicity of muscarinic agonists (ex. atropine, scopolamine)?

A

1) gastric lavage
2) activated charcoal
3) physostigmine reversible cholinesterase inhibitor

(this one can cross BBB, neostigmine can’t)

152
Q

What is the structure of a postganglionic adrenergic neuron?

A

They have long postganglionic axons with varicosities (looks like beads) on the nerve terminals that contain NE vesicles

153
Q

What are the main similarities and differences between cholinergic and adrenergic transmission?

A

Similar: NE and ACh are both synthesized and stored in vesicle pools that are released when an action potential invades the nerve ending an dpromotes Ca2+ ion entry –> leads to vesicle fusion and NT release into the synapse

Different: NE action is terminated by UPTAKE, ACh action is terminated by DESTRUCTION

154
Q

What is the mechanism of termination of NE signaling?

A

It is terminated by uptake via Uptake 1 (NET or SLC6A2 alternate names) on the nerve terminal

OR

It is terminated by uptake via Uptake 2 (ENT or OCT3 alternate names) on the effector cell

155
Q

How is NE synthesized?

A

Tyrosine in cytoplasm –> DOPA and DOPAMINE in cytoplasm –> DOPAMINE uptake into vesicles –> oxidized to NE in a complex with ATP

156
Q

What happens to NE after uptake from the synapse?

A

It is either degraded by monoamine oxidase (MAO) or COMT or it is taken back up into the vesicle pool

157
Q

What type of reaction does monoamine oxidase (MAO) facilitate?

A

Phase I non-CYP oxidation reaction

158
Q

What type of reaction does catechol-O-methyltransferase (COMT) facilitate?

A

Phase II methylation reaction

159
Q

What is the difference in capacity/affinity between Uptake 1 and Uptake 2?

A

Uptake 1 has high affinity but low capacity (and is major route of NE inactivation)

Uptake 2 has low affinity but high capacity (works with all catecholamines)

160
Q

If the main termination mechanism for NE is via uptake, why are there metabolic pathways (MAO, COMT)?

A

They are needed anyways to degrade exogenous amines (ex. tyrosine from foods)

161
Q

What urinary markers are used to test for pheochromocytoma?

A

Metanephrines, catecholamines

excess production of catecholamines leads to excessive production of metabolites (metanephrines)

162
Q

What is the effect of MAO inhibition or COMT inhibition on the effects of NE?

A

No effect - not the main mechanism of elimination

163
Q

What is the effect of MAO inhibition in a patient treated with tyramine, amphetamines, or ephedrine?

A

Profound sympathomimetic effects (excessive NE signaling)

Tyramine/amphetamines/ephedrine normally are metabolized by MAO, so when MAO is inhibited they are left in the nerve ending and displace NE from nerve endings leading to increased NE signaling

164
Q

What is the effect of Uptake I blockers on NE signaling?

A

They enhance the effects of exogenous or synaptically released NE

165
Q

Describe the phenomenon of EPI reversal.

A

Normally, high doses of epinephrine leads to increased blood pressure (via alpha 1 receptors). When an ergotoxin (blocks alpha 1 receptors) is also administered with epinephrine, the result is decreased blood pressure (via beta 2 receptors).

166
Q

What is the selectivity of alpha receptors for EPI, NE, and ISO?

A

EPI > NE >>> Isoproterenol

true for both alpha 1 and alpha 2

167
Q

What is the selectivity of beta1 receptors for EPI, NE, and ISO?

A

ISO >> EPI = NE

168
Q

What is the selectivity fo beta2 receptors for EPI, NE, and ISO?

A

ISO > EPI > NE

NE has virtually no effect

169
Q

What is the general effect of alpha 1 receptors?

A

Smooth muscle contractions

170
Q

What is the general effect of alpha 2 receptors?

A

Inhibitory receptors –> inhibits nerve signaling in a number of different pathways

171
Q

What is the general effect of beta1 receptors?

A

Heart muscle contraction

172
Q

What is the general effect of beta2 receptors?

A

Bronchiolar and other muscle relaxation

173
Q

What is the general effect of beta3 receptors?

A

Mediates lipolysis and bladder relaxation

174
Q

List some inhibitors of Uptake 1 and Uptake 2

A

Uptake 1: Tricyclic antidepressants, cocaine, ritalin

Uptake 2: Steroids

175
Q

What is the effect of alpha receptors on the iris? Beta?

A

Alpha1: contraction (mydriasis)

Beta: none

176
Q

What is the effect of alpha receptors on the bronchioles? Beta?

A

Alpha: none

Beta2: relaxation

177
Q

What is the effect of alpha receptors on uterine smooth muscle? Beta?

A

Alpha1: contraction

Beta2: relaxation

178
Q

What is the effect of alpha receptors on male sexual organs? Beta?

A

Alpha1: Contraction

Beta: none

179
Q

What is the effect of alpha receptors on pilomotor muscles? Beta?

A

Alpha1: contraction

Beta: none

180
Q

What is the effect of alpha receptors on the gastrointestinal tract? Beta?

A

Alpha1: contraction (sphincters)

Alpha2: relaxation of muscle via inhibition of cholinergic nerves (presynaptic inhibition of ACh release)

Beta2: relaxation (muscle)

181
Q

What is the effect of alpha receptors on the urinary bladder? Beta?

A

Alpha1: Contraction (sphincters)

Beta2/3: Relaxation (muscle)

182
Q

What is the effect of alpha receptors on the splenic capsule? Beta?

A

Alpha1: Contraction

Beta2: Relaxation

183
Q

What is the effect of alpha receptors on vascular smooth muscle? Beta?

A

Alpha1: Contraction

Beta2: Relaxation

184
Q

What is the effect of alpha receptors on the cardiac sinus rate? Beta?

A

Alpha2: Decreased rate via presynaptic inhibition of NE release

Beta1: Increased rate

185
Q

What is the effect of alpha receptors on the cardiac contractile force? Beta?

A

Alpha1: Increase

Beta1: increase

186
Q

What is the effect of alpha receptors on cardiac conduction? Beta?

A

Alpha: no effect

Beta1: Increase in conduction velocity

187
Q

What is the effect of alpha receptors on the kidney? Beta?

A

Alpha: none

Beta1: increased renin release

188
Q

What is the effect of alpha receptors on fat? Beta?

A

Alpha2: Accumulation of fat (via inhibition of lipolysis)

Beta1/2/3: lipolysis

189
Q

What is the effect of alpha receptors on pancreatic insulin secretion? Beta?

A

Alpha2: Decreases

Beta2: Increases (minor)

190
Q

What is the effect of alpha receptors on salivary glands? Beta?

A

Alpha1: K+ and water secretion

Beta: amylase secretion (minor)

191
Q

What is the effect of alpha receptors on the liver? Beta?

A

Alpha1: Glycogenolysis

Beta2: Glycogenolysis

192
Q

What is the effect of alpha receptors on skeletal muscle? Beta?

A

Alpha1: None

Beta2: Tremors, K+ uptake

193
Q

What is the effect of alpha receptors on aqueous humor secretion? Beta?

A

Alpha2: Decreased

Beta1: Increased

194
Q

What is the general mechanism of alpha 1 receptors causing smooth muscle contraction?

A

Alpha 1 agonist stimulates Alpha 1 GPCR –> subunit of GPCR activates phospholipase C –> PLC produces IP3 –> triggersCa2+ release from ER –> triggers more calcium entry through CRAC channels of membrane –> smooth muscle contracts

195
Q

What is the general signaling pathway for beta receptor activation?

A

Beta agonist stimulates a beta receptor (GPCR) –> a GPCR subunit stimulates adenylyl cyclase –> produces cAMP –> activates protein kinase A –> PKA substrates proteins, leading to a number of downstream effects (glycogenolysis, lipolysis, cardiac muscle contraction, smooth muscle relaxation, secretion)

196
Q

What are the three mechanisms alpha2 receptors use to inhibit excitable cell function?

A

1) Increases K+ currents (via beta/gamma GPCR subunit)
2) Inhibits Ca2+ channels (via beta/gamma GPCR subunit)
3) Inhibition of adenylyl cyclase (via Gi GPCR subunit)
* different mechanism depending on location/type of receptor to be inhibited*

197
Q

What is the mechanism of Beta1 receptors on the SA node?

A

They stimulate increased contration rate of diastolic depolarization through stimulation of If and L-type calcium currents

198
Q

What is the mechanism of Beta1 receptors on contraction force?

A

They increase calcium entry from outside of the cell and load the SR to increase calcium-induced calcium release

199
Q

What is the effect of epinephrine on vascular beds in the skin/mucosa?

A

It increases TPR (constricts vessels) because there are only alpha receptors in these beds

200
Q

What is the effect of epinephrine on vascular beds in the liver/skeletal muscle?

A

Low doses of epinephrine decrease peripheral resistance (dilate vessels) and high doses of epinephrine initially increase peripheral resistance followed by a decrease

these beds have both alpha and beta2 receptors, but beta2 is more sensitive to epinephrine so the alpha effect (increased resistance) only occurs when there is a lot of epinephrine

201
Q

What is the effect of norepinephrine, epinephrine, and isoproterenol on blood vessels?

A

NE: vasoconstriction through alpha receptors

EPI: variable

ISO: vasodilation through beta2 receptors

202
Q

What is the change in pulse rate, blood pressure, peripheral resistance, and cardiac output associated with norepinephrine?

A

Slightly decreased pulse rate (reflex bradycardia)

Increase in mean blood pressure (both systolic and diastolic increase)

Large increase in peripheral resistance

Cardiac output unchanged or decreased

203
Q

What is the change in pulse rate, blood pressure, peripheral resistance, and cardiac output associated with Isoproterenol?

A

The pulse rate increases (reflex tachycardia and direct beta effect)

The mean blood pressure decreases

The peripheral resistance decreases

The cardiac output increases

204
Q

What is the change in pulse rate, blood pressure, peripheral resistance, and cardiac output associated with low doses of epinephrine?

A

Increased pulse rate (direct effect)

Unchanged/slightly increased blood pressure

Decreased peripheral resistance

Increased cardiac output

205
Q

What is the effect of high dose epinephrine on blood pressure?

A

Large dose of epinephrine leads to increased cardiac rate and force (increases systolic BP) and vasoconstriction (increased diastolic BP)

reflex bradycardia restores a normal heart rate to combat the increased rate from the epinephrine

206
Q

What are the therapeutic uses of epinephrine?

A

cardiac arrest, vasoconstrictor (to keep local anaesthetics local), rescue inhalers, treatments for anaphylaxis

207
Q

What is the therapeutic use of norepinephrine?

A

Treats severe hypotension in the ICU

208
Q

What are the main uses of isoproterenol?

A

It is rarely used but can be used for cardiac stimulation (beta 1) or asthma (beta 2)

209
Q

What type of drug is phenylephrine? What are its therapeutic uses?

A

It is a selective alpha1 agonist

It is used as a nasal decongestant, for pupilary dilation, and to increase BP during surgery

210
Q

What type of drugs are imidazoline derivatives? What is their effect?

A

They are selective agonists of postsynaptic alpha1 receptors and are not substrates for MAO or COMT (makes them long acting)

They also act as agonists for alpha2b receptors on blood vessels in the nasal mucosa (constricts the blood vessels)

Functions as a nasal decongestant (vasoconstriction of nasal mucosa)

211
Q

What are some side effects of phenylephrine and imidazoline derivatives?

A

Rebound congestion with prolonged use (reactive hyperemia)

212
Q

What type of drug is midodrine? What is it used for?

A

A selective alpha1 receptor agonist

It is used to increase BP for severe liver or kidney disease, but mostly used to treat orthostatic hypotension (esp in patients with autonomic failure or diabetic autonomic neuropathy)

213
Q

What is the mechanism of clonidine? What is it used for?

A

It is an alpha2 agonist that inhibits sympathetic outflow from the CNS to the periphery (leads to reduced sympathetic tone, reduced HR, and dilation of BVs)

Used as an antihypertensive and to treat opiate withdrawal

can also cause an initial vasoconstriction at high doses due to alpha2b stimulation

214
Q

What type of drug is guanfacine?

A

selective alpha 2 agonist

215
Q

What type of drug is alpha-methyl dopa? What is it used for?

A

selective alpha 2 agonist, sometimes used to treat htn in pregnancy

216
Q

What types of drugs are apraclonidine and brimonidine? What are they used for?

A

selective alpha2 receptor agonists, used to treat glaucoma (inhibits aqueous humor secretion)

217
Q

What type of drug is dobutamine? What is it used for?

A

selective beta1 receptor agonist, used to treat acute heart failure by increasing the force of cardiac contraction without increasing rate

218
Q

What type of drug is albuterol? What is it used for?

A

selective beta2 receptor agonist, used as a rescue inhaler (SABA)

219
Q

What types of drugs are salmeterol and formoterol? What are they used for?

A

Both are selective beta2 receptor agonists, both are long acting drugs for asthma (LABAs)

must be given with inhaled corticosteroids for asthma (ok alone for COPD)

220
Q

What type of drug is terbutaline? What is it used for?

A

selective beta2 receptor agonist, used for uterine relaxation during premature labor

221
Q

Where are beta3 receptors located?

A

Brown/white fat cells and in urinary bladder

222
Q

What type of drug is mirabegron? What is it used for?

A

selective beta3 receptor agonist, used to treat overactive bladder

223
Q

How do indirect-acting sympathomimetic amines function?

A

They enter the nerve ending and displace NE from storage sites. Displaced NE then activates adrenoreceptors (hence sympathomimetic).

examples: tyramine and amphetamines

224
Q

What type of drugs are ephedrine derivatives? What are they used for?

A

Mixed-acting sympathomimetic agents (work by stimulating alpha dn beta and ALSO indirectly leads to NE release from nerve endings)

They are used as nasal decongestants (and anti-asthma OTCs)

also abused to make recreational drugs

225
Q

What is the effect of alpha 2 activation on the heart?

A

It decreases heart rate via NE signaling that provides negative feedback on the beta1 signaling (which increases HR)

226
Q

What is the effect of alpha 1 activation on the GI tract?

A

It decreases GI motility by pre-synaptically regulating ACh signaling in GI parasympathetics

227
Q

What is the effect of alpha 2 activation on the corpus cavernosum?

A

It decreases erection by pre-synaptically inhibiting the parasympathetic nerve pathway that leads to erection

228
Q

What is the effect of alpha2 stimulation on the CNS?

A

It has a depressant effect (including decreased BP) via postsynaptic inhibition of the nerves from the vasomotor center

229
Q

What type of drug is phenoxybenzamine? What is it used for?

A

Non-selective alpha blocker (with slight selectivity for alpha 1) that provides irreversible blockade.

Used to treat pheochromocytoma

230
Q

What type of drug is phentolamine? What is it used for?

A

It is a non-selective alpha blocker (equal selectivity a1 and a2) that is a short-acting and competitive blocker

It is used to treat a hypertensive crisis caused by tyramine in patients on an MAO inhibitor and to treat hypertensive paroxysms in pheochromocytoma

231
Q

What type of drug is prazosin? What is it used for?

A

Alpha 1 receptor blocker. Used to decrease blood pressure (late add on therapy) and to treat resistance to urine outflow

232
Q

What types of drugs block alpha1a vs alpha1b? What is their utility?

A

-osins (-azosins block both), have selectivity for the prostate and bladder and are used to treat BPH

233
Q

What is the effect of selective alpha2 receptor blockers?

A

Disinhibits neurotransmitter release (aka acts like nerve stimulation)

Can lead to tachycardia and increased GI motility

234
Q

What type of drug is propranolol? What is it used for? Contraindications?

A

First generation non-selective beta blocker

Used for hypertension (blocks renin release), anti-arrhythmic, anti-anginal, etc.

Asthma (because of non-selectivity), diabetes (masks hypoglycemia symptoms are contraindications

235
Q

What are second generation beta blockers? What do they do?

A

Selective beta1 blockade at low doses (spares bronchioles)

Examples: metoprolol, atenolol, etc.

236
Q

What are third generation beta blockers? What do they do?

A

They are beta blockers with an extra vasodilatory component

Examples: labetalol (beta1 + alpha1 block), carvedilol (beta + alpha1 + calcium channel block)

237
Q

Which of the following agents could be A:

Bethanechol

Homatropine

Succinylcholine

Vecuronium

Midodrine

Prazosin

Tamsulosin

Pilocarpine

Epinephrine

Propranolol

Metoprolol

Neostigmine

Methacholine

Isoproterenol

Norepinephrine

A

Methacholine

muscarinic vasodilation via NO

238
Q

Which of the following agents could be B:

Bethanechol

Homatropine

Succinylcholine

Vecuronium

Midodrine

Prazosin

Tamsulosin

Pilocarpine

Epinephrine

Propranolol

Metoprolol

Neostigmine

Methacholine

Isoproterenol

Norepinephrine

A

Isoproterenol

ISO leads to decreased BP and reflex tachycardia, it is a non-selective beta agonist

239
Q

Which of the following agents could be C:

Bethanechol

Homatropine

Succinylcholine

Vecuronium

Midodrine

Prazosin

Tamsulosin

Pilocarpine

Epinephrine

Propranolol

Metoprolol

Neostigmine

Methacholine

Isoproterenol

Norepinephrine

A

Epinephrine

  • increases BP and decreases HR*
  • note: EPI reversal demonstrated at second C –> unmasked by alpha1 blockade*
240
Q

Which of the following agents could be D:

Bethanechol

Homatropine

Succinylcholine

Vecuronium

Midodrine

Prazosin

Tamsulosin

Pilocarpine

Epinephrine

Propranolol

Metoprolol

Neostigmine

Methacholine

Isoproterenol

Norepinephrine

A

Prazosin

alpha1 blocker that leads to epi reversal

241
Q

Which of the following agents could be E:

Bethanechol

Homatropine

Succinylcholine

Vecuronium

Midodrine

Prazosin

Tamsulosin

Pilocarpine

Epinephrine

Propranolol

Metoprolol

Neostigmine

Methacholine

Isoproterenol

Norepinephrine

A

Propranolol

Blocks effects of A and C (both beta receptor agonists)

242
Q

Which of the following agents could be F:

Bethanechol

Homatropine

Succinylcholine

Vecuronium

Midodrine

Prazosin

Tamsulosin

Pilocarpine

Epinephrine

Propranolol

Metoprolol

Neostigmine

Methacholine

Isoproterenol

Norepinephrine

A

Neostigmine

enhances cholinergic action (aka effect of A)

243
Q

Which of the following agents could be G:

Bethanechol

Homatropine

Succinylcholine

Vecuronium

Midodrine

Prazosin

Tamsulosin

Pilocarpine

Epinephrine

Propranolol

Metoprolol

Neostigmine

Methacholine

Isoproterenol

Norepinephrine

A

Homatropine

muscarinic antagonist that blocks effects of A

244
Q

What is a drug or drug category that produces similar effects to the answer to this question?

A

Answer: C) myasthenia gravis

Drug/drug category: non-depolarizing blockers

since all three are proportionally down, the issue must be at the nicotinic receptor

245
Q
A

E) Botulism

Similar effects: LEMS

no change in sensitivity to acetylcholine = presynaptic effect

Neuro (12 decks)

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