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Pharm exam 2 > Autonomic pharm > Flashcards

Autonomic pharm Flashcards

1
Q

Neurotransmitter

A

Small amounts released from the nerve terminals into the synaptic cleft

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2
Q

Action of neurotransmitter

A

Activates or inhibits the postsynaptic cell by binding to a receptor molecule

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3
Q

The cholinergic junction

A
  • small vesicles contain Ach
  • Ach synthesized within neuron
  • Released is dependent on extracellular calcium
  • metabolized by acetylcholinesterase.
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4
Q

structure of parasympathetic system

A
  • very long, pre synaptic fibers, shorter post synaptic neuron in tissue
  • normally not seen with ganglia.
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5
Q

structure of sympathetic system

A

-short pre synaptic fibers, to ganglia, and long post synaptic fibers that go to organs.

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6
Q

Sympathetic neurotransmitter

A

Norepinephrine

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7
Q

Parasympathetic neurotrnasmitter

A

Acetylcholine.

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8
Q

describe the somatic nervous system

A
  • voluntary

- long fibers run from spinal cord to muscle tissue.

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9
Q

What are the 2 networks that make up plexus

A
  • Myenteric plexus and submucosal plexus;.
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10
Q

How many cholinorecptors are there, and what are the types?

A

7 receptor types, 5 are muscarinic and 2 are nicotinic.

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11
Q

What determines agonist selectivity?

A

Is determined by the subtypes of muscarinic and nicotinic receptors present in a given cell.

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12
Q

What are catecholamines?

A

Neurotransmitters or drugs that affect the sympathetic nervous system

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13
Q

What is tyrosine?

A

A neurotransmitter where all catecholamines are synthesized.

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14
Q

Biosynthesis of catecholamines

A
  • Tyrosine turns into dopa, which turns into dopamine and gets stored.
  • When it is activated, it joins cell membrane and releases dopamine into synapse.
  • End result is NE or epinephrine
  • go to receptors on post synaptic membrane.
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15
Q

The Noradrenergic junction

A
  • Release process similar to that of cholinergic terminals.

- NE is released with ATP, dopamine, peptide cotransmitters

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16
Q

Termination of noradrenergic transmission results from:

A
  • Diffusion away from the receptor site with eventual metabolism in the plasma or liver
  • Ruptake into the nerve terminal by NET (norepinephrine transporter)
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17
Q

Conversion of tyrosine to dopa can be inhibited by the ______

A

-tyrosine analog metyrosine

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18
Q

VMAT can be inhibited by ________

A

-reserpine, resulting in depletion of transmitter stores

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19
Q

NET can be inhibited by _________

A

-cocaine and tricyclic antidepressant drugs, resulting in an increase of transmitter activity in the synaptic cleft.

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20
Q

Release of NE blocked

A

guanethidine & bretylium.

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21
Q

What does a drug blocking a neurotransmitter do?

A

Decrease sympathetic function

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22
Q

How do antidepressants work?

A

Block reuptake, drug sits in synapse longer, and serotonin (etc) sits in the synapse longer, providing lasting effect.

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23
Q

Indirectly acting & mixed sympathomimetics can cause release of stored_____

A

NE

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24
Q

How many adrenoceptors are there?

A

Five. 2 alpha, and 3 beta

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25
Q

What are nonadrenergic, noncholinergic neurons?

A

Autonomic effector tissues contain nerve fibers that do not show no characteristics of cholinergic or adrenergic fibers.

  • Both motor and sensory NANC fibers are present
  • peptides are the most common transmitter substances found in these nerve endings
  • they are poorly understood
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26
Q

Autonomic function is _____ and _____ at many levels, from the CNS to the effector cells.

A

Integrated, regulated

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27
Q

Important cooperative interactions occur between the parasympathetic and sympathetic systems at the level of the

A

Brain stem, medulla, and spinal cord.

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28
Q

Most regulation uses____

A

negative feedback. Negative feedback is particularly important in the responses of the ANS to the administration of autonomic drugs.

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29
Q

The sympathetic nervous system directly influences 4 major variables:

A
  • Peripehral vascular resistance
  • Heart Rate
  • Force
  • Venous tone
  • Also directly modulates renin production.
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30
Q

The parasympathetic nervous system directly influences:

A
  • Heart rate.

- stimulating aldosterone secretion

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31
Q

Choline esters

A
  • hydrophillic
  • poorly absorbed
  • poorly distributed into CNS
  • hydrolyzed in GI tract
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32
Q

Tertiary Cholinomimetic Alkaloids

A

Well absorbed from most sites of administration

-Nicotine is sufficiently lipid-solute to be absorbed across the skin.

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33
Q

Activation of the parasympathetic nervous system modifies organ function by 2 major mechanisms:

A
  • Ach muscarinic receptors on effector cells to alter organ function directly.
  • Ach interacts with muscarinic receptors on nerve terminals to inhibit the release of neurotransmitter (auto inhibition)
34
Q

In what 2 ways do muscarinic receptors work?

A

By increasing second messengers or open ion channels.

35
Q

Muscarinic signaling

A
  • Ach is released from post-ganglionic cholinergic axon, act interacts with M2 receptor on a SA node cell, and opens K+ channels.
  • Ach acts on an axonal muscarinic receptor to cause inhibition of Ach release.
36
Q

Nicotinic agonists

A
  • Nicotinic receptor binding opens ion channels that allow sodium and potassium ions to diffuse rapidly down their concentration gradients
  • Cause depolarization of the nerve cell or neuromuscular end plate membrane
  • paralytic drugs- paralyzing skeletal muscle.
37
Q

Nicotinic signaling

A
  • Ach released from the motor nerve terminal
  • Ach interacts with subunits of the nicotinic receptor to open it, allowing Na+ influx to produce an excitatory postsynaptic potential.
  • The EPSP depolarizes the muscle membrane, generating an action potential, and triggering contraction.
38
Q

Nicotinic agonists

A
  • Prolonged agonist receptor occupancy abolishes the effector response
  • prevents electrical recovery of the post junctional membrane cause “depolarizing blockade”
39
Q

CNS effects of cholinergic agonists

A
  • CNS contains both muscarinic and nicotinic receptors
  • M1 receptors richly expressed in brain areas involved in cognition.
  • nicotine stimulates the Ach receptors on dopamine-containing neurons: causes release of dopamine in the mesolimbic system
40
Q

Indirect-acting cholinomimetics: Mechanism of action

A
  • Ach actions are terminated by acetylcholinesterase
  • indirect acting cholinomimetics exert their primary effect at the active site of this enzyme, although some also have direct actions at nicotinic receptors.
41
Q

Hydrolytic enzyme presents in cholinergic synapses, 2 step process:

A
  • Ach binds to the enzymes active site and is hydrolyzed, yielding free choline and the acetylated enzyme.
  • The covalent acetyl-enzyme bond is split, with the addition of the water (hydration), producing choline and acetic acid.
42
Q

How to irreversible agents work?

A

-By taking enzyme out of activity.

43
Q

What is myasthenia gravis

A

An autoimmune disease affecting skeletal muscle neuromuscular junctions.

  • Autoantibodies produced against the alpha 1 subunits of the nicotinic receptor.
  • Severe disease may affect all the muscles, including respiratory.
  • very sensitive to some drugs, such as curariform drugs.
44
Q

MG clinical findings:

A

Ptosis(upper eyelid drooping), diplopia(double vision), difficulty speaking/swallowing, extremity weakness

45
Q

Which are preferred in myasthenia graves therapy, cholinesterase inhibitors or direct acting acetylcholine receptor agonists?

A

Cholinesterase inhibitors

46
Q

Diagnosis of myasthenia gravis

A
  • Edrophonium.

- If patient has MG, an improvement in muscle strength that lasts about 5 minutes can usually be observed.

47
Q

How does edrophonium work?

A
  • Inhibits acetylcholinase
  • when given, symptoms should improve because each competes with antibodies for receptor, by increased Ach, likelihood of binding act to receptor should increase and symptoms should improve
48
Q

Why receptors are effected by myasthenia graves

A

nicotinic

49
Q

Treatment of myasthenia graves

A
  • long term therapy usually accomplished with pyridostigmine, neostigmine is an alternative.
  • relatively short acting
  • muscarinic side effects can be controlled with antimuscarinic drugs
50
Q

How to determined difference between severe MG vs. Excessive drug therapy

A

-Give edrophonium, if nothing happens…drug problem

51
Q

Alzheimer’s disease

A

A progressive, fatal neurodegenerative disorder manifested by: cognitive and memory decline, progressive impairment of activities of daily living, neuropsychiatric and behavioral symptoms.

52
Q

Hallmarks of AD

A
  • Deposition of neurofibrillary tangles

- Beta- amyloid plaques

53
Q

Cholinergic hypothesis

A
  • Proposes that AD is caused by reduced synthesis of acetylcholine
  • Cholinergic neurons play a key role in memory and attentional function
  • blockade of muscarinic cholinergic receptors result in cognitive dysfunction
  • Widespread, progressive decline
  • Decreased ACh synthesis
54
Q

AD treatment options

A

-Acetylcholinesterase inhibitors (donepezil, galantamine, rivastigmine), NMDA receptor antagonists (memantine).

55
Q

What kind of receptor are muscarinic receptors?

A

G protein- coupled receptors.

56
Q

What do muscarinic antagonists do?

A

Block the effects of parasympathetic autonomic discharge.

57
Q

What type of selectivity are antimuscarinic agents?

A

Non-selective, some newer agents are modernly more selective.

58
Q

tertiary amines

A
  • Lipophillic
  • Most are well absorbed from GI tract and conjunctival membranes
  • Widely distributed in the body
59
Q

Quaternary amines

A
  • Hydrophilic

- Distributed poorly into the CNS: limited ability to cross the blood brain barrier.

60
Q

Anticholinergic side effects:

A

Decreased secretions (dry mouth), slow GI motility (constipation) urinary retention, dry eyes, visual distance.

61
Q

Overactive bladder

A

Urgency (with or without urge incontinence)
Urgency= defined as a sudden and complaing desire to pass urine that is difficult to defer.
Nocturia= defined as walking one or more times per night to void urine.

62
Q

Frequency definition

A

-Urination >8 times per

63
Q

How many receptors have been identified in the bladder?

A

All 5

64
Q

OAB SNS factor

A

-As bladder begins to fill & tension in bladder wall increases, activates spinal reflex pathways in the brainstem.

65
Q

OAB PNS -

A

Responsible for bladder contraction and bladder outlet relaxation, mostly quiescent throughout the process of bladder filling.

66
Q

Antimuscarinic agents in OAB

A
  • Emerging evidence suggests competitive antagonism at urothelial muscarinic receptors during bladder filling (storage phase), decreasing urge and increasing bladder capacity
  • Focus on M3 receptors
67
Q

Darifenan is specific to ____

A

M3

68
Q

Pathophysiology of Nonneurogenic OAB

A
  • Excessive Ach release from urothelium during bladder filling
  • Increased sensitivity of detrusor receptors to Ach
69
Q

Pharmacotherapy of OAB

A
  • Antimuscarinic agents
  • Drugs that block Ach in the bladder
  • Competitive antagonism at urothelial muscarinic receptors during bladder filling, decreasing urge and increasing bladder capacity.
70
Q

Oxybutynin

A
  • First drug used for OAB

- First pass metabolism

71
Q

Oxybutynin characteristics (size etc).

A

Small size, highly lipophilic, neutral charge

-More likely to cross BBB than other antimuscarinic OAB agents.

72
Q

Oxybutynin formulation

A

-Immediate release, extended release, transdermal patches and gel formulation.

73
Q

Toletrodine

A
  • Tertiary-amine, nonselective antimuscarinc agent
  • First pass metabolism
  • Low lipophillicity
  • comparable to oxybutynin, but reduced side effects
  • limited ability to distribute across BBB and cause CNS affects
74
Q

Trospium

A
  • Quaternary- amine, nonselective muscarinic agent
  • first pass metabolism
  • 60% excreted unchanged in urine
  • May be concerned with renal patients
75
Q

Fesoterodine

A
  • Tertiary-amine, nonselective antimuscarinic agent
  • First pass metabolism
  • 70% really excreted as active and inactive metabolites
  • low lipophillicity
  • limited ability to distribute across BBB and cause CNS effects
76
Q

Darifenacin

A
  • Tertiary-amine, M3 selective receptor antagonist
  • First pass metabolism
  • 60% really excreted, 3% unchanged.
77
Q

Solifenacin

A
  • Quaternary-amine, nonselective muscarinic agent
  • First pass metabolism
  • low lipophillicity
78
Q

Generally, _________ are associated with fewer side effects and adverse events.

A

Controlled-release medications.

79
Q

For patients who have pre-existing constipation, which drugs are preferred?

A

-Non-selective antimuscarinics are preferable to M3 selective blockers.

80
Q

Which drugs are best for patients with hepatic impairment?

A
  • Trospium or fesoterodine

- Avoid darifenacin

81
Q

Specific guidance for OAB treatment

A
  • Begin with either tolterodine or oxybutynin

- If pt has cognitive issues, use darifenacin (ex. with constipation), tolterodine, or solifenacin.

Pharm exam 2 (6 decks)

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