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Interviewing Techniques 2 > Quiz 2: Neurotransmitters > Flashcards

Quiz 2: Neurotransmitters Flashcards

1
Q

What does the term cholinergic refer to? Anticholinergic?

A

Cholinergic: term referring to things having to do with acetylcholine.
Anticholinergic: agent that blocks the acetylcholine in the central and the peripheral nervous system

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2
Q

What are the effects of decreased central acetylcholine (ACh)?

A

Confusion, anxiety, agitation, dementia, and hallucinations.

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3
Q

What conditions are treated with therapies that increase central ACh?

A

Primarily dementia. May also be used in schizophrenia and autism.

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4
Q

When might you prescribe a medication that decreases central ACh?

A

Vertigo, esp. motion sickness

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5
Q

In the PNS, where is ACh used as the neurotransmitter

a. In the somatic nervous system?
b. In the sympathetic nervous system?
c. In the parasympathetic nervous system?

A

a. Somatic: at the neuromuscular junction of skeletal muscle.
b. Sympathetic: ganglia, adrenal medulla, and sweat glands.
c. Parasympathetic: ganglia and at parasympathetic end-organs (such as eyes, heart, lungs, GI, bladder, etc).

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6
Q

What is the effect of increased ACh on skeletal muscle? When might you want to increase ACh in skeletal muscle?

A

Increased ACh causes skeletal muscle spasms and/or spastic paralysis.
Can be used for muscle weakness, as in myasthenia gravis.

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7
Q

What is the effect of decreased Ach on skeletal muscle? When might you want to decrease ACh in skeletal muscle?

A

Decreased Ach causes skeletal muscle weakness and/or flaccid paralysis.
Might want to use for muscle spasm. Botox does this.

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8
Q

What are the effects of increased ACh on:

a. Eyes
b. Heart
c. Lungs
d. Digestive tract
e. Sweat glands
f. Salivary glands
g. Bladder/urination

A

a. Eyes: constricts pupils
b. Heart: reduces heart rate
c. Lungs: constricts bronchia
d. Digestive tract: increased activity
e. Sweat glands: hypersecretion
f. Salivary glands: hypersecretion
g. Bladder/urination: increased

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9
Q

What conditions are treated by increasing the parasympathetic effects of ACh?

A

Sjögren’s syndrome, delayed gastric emptying, glaucoma.

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10
Q

What conditions are treated by decreasing the parasympathetic effects of ACh?

A

Bradycardia, hyperhidrosis, incontinence, IBS-D, COPD.

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11
Q

What are the names of some tropane alkaloids? What are the effects of tropane alkaloids on ACh? What plants contain tropane alkaloids?

A

Atropine (Belladonna), scopolamine (Datura), hyoscyamine (Hyoscamus, Mandrake).
Act as Ach antagonists (anticholinergics).

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12
Q

What are the precursors for ACh synthesis?

A

Acetyl CoA + choline

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13
Q

What enzyme breaks down ACh and how does inhibition of this enzyme affect ACh concentration in the synaptic cleft?
What are these inhibitors used for?

A

Acetylcholinesterase (AChE) breaks down ACh.
Inhibition increases and prolongs cholinergic transmission.

Used for drugs (physostigmine, rivastigmine), nerve gases (sarin), pesticides, and herbs (huperzine A from Huperzia serrata).

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14
Q

What are the two main types of ACh receptors? Where is each found?

A

Nicotinic: neuromuscular junction and at autonomic ganglia (both parasympathetic and sympathetic).
Muscarinic: parasympathetic end-organs and sweat glands.

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15
Q

What are examples of monoamine neurotransmitters?

A

Catecholamines (dopamine, norepinephrine, epinephrine), tryptamines (serotonin, melatonin), and histamine.

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16
Q

What neurotransmitter concentrations might increase if L-tyrosine is given?

A

Dopamine. (L-tyrosine –> L-dopa –> dopamine)

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17
Q

Why is Parkinson’s treated with L-dopa rather than with dopamine?

A

Dopamine does not cross the blood-brain barrier, so L-dopa is given for diseases related to low dopamine.

18
Q

What effect might a lack of SAMe have on epinephrine synthesis?

A

Reduced. SAMe is a cofactor for NorEpi –> Epi

19
Q

What is the mechanism of action of reserpine? Why does this lower blood pressure?

A

Blocks the transport of catecholamines (dopamine, norepi, epi) into storage vesicles, which leaves them to be degraded. Reduced norepi causes decreased blood pressure.

20
Q

What is the effect of amphetamines on catecholamine release?

A

Causes increased catecholamine (dopamine, norepi, epi) release.

21
Q

How is catecholamine neurotransmission terminated?

A

By the reuptake of neurotransmitter from the synaptic cleft into the presynaptic neuron.

22
Q

What enzymes break down catecholamines?

A

Monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT).

23
Q

What are some of the main functions of dopaminergic pathways in the brain?

A

Motivation, arousal, reward, learning, executive function, sexual function, lactation, and motor control.

24
Q

What is low dopamine associated with?

A

Anxiety and depression, movement disorders, prolactinemia.

25
Q

What are dopamine agonists used for?

A

ADHD, depression, anxiety, movement disorders (Parkinson’s, RLS), prolactinoma, acromegaly.

26
Q

What is excess dopamine associated with?

A

Serious mental illness (e.g. schizophrenia), nausea and vomiting (DA antagonists are used as antiemetics), decreased prolactin.

27
Q

What conditions are dopamine antagonists used for? What are some side effects of these drugs?

A

Antipsychotics (haloperidol).

Side effects can include parkinsonism, tardive dyskinesia, dystonia, and akathisia (restlessness)

28
Q

What does “adrenergic” refer to?

A

Things related to both norepinephrine (NE) and epinephrine (EPI).

29
Q

In the CNS, what are adrenergic neurons involved with?

A

Regulating arousal, attention, cognition, and consolidation of emotional memories.

30
Q

In the PNS, where is NE secreted? EPI?

A

NE is secreted from postganglionic sympathetic fibers at effector organs.
EPI is released from the chromaffin cells of the adrenal medulla (NE is too, but EPI is the principle hormone).

31
Q

What are the effects of NE and EPI on:

a. Eyes
b. Heart
c. Lungs
d. Digestive tract
e. Bladder/urination
f. Blood sugar
g. Blood lipids

A

a. Eyes: pupil dilation
b. Heart: increased heart rate
c. Lungs: bronchodilation
d. Digestive tract: decreased motilitiy
e. Bladder/urination: decreased
f. Blood sugar: increased
g. Blood lipids: increased

32
Q

In what ways do NE and EPI cause blood pressure to rise?

A

Vasoconstriction.

Probably something else.

33
Q

What conditions might be treated by therapies that increase peripheral adrenergic activity?

A

Bronchoconstriction, nasal congestion, hemorrhoids, and priapism.

34
Q

What conditions might be treated by therapies that decrease peripheral adrenergic activity?

A

Hypertension, arrhythmias, CHF, BPH, erectile dysfunction, CRPS.

35
Q

Why should people on MAO inhibitors be advised against eating tyramine-containing foods?

A

Tyramine is metabolized by MAO, therefore MAO inhibitors prevent the breakdown of tyramine. Tyramine increases the release of NE, thus excess tyramine can lead to a hypertensive crisis.

36
Q

What are the effects of stimulating alpha-1 adrenergic receptors? What are alpha-1 agonists used for? Alpha-1 antagonists?

A

Stimulates smooth muscle contraction of blood vessels, bladder neck, GI sphincters, prostate, iris.
Alpha-1 agonists are used for nasal congestion, hypotension, and weight loss.
Antagonists are used for hypertension and urinary retention

37
Q

What are the effects of stimulating alpha-2 adrenergic receptors? What are alpha-2 agonists used for? What plant constituent is an alpha-2 antagonist?

A

Reduces the release of NE both in the brain and in the periphery.
Agonists are used for hypertension.
Yohimbine is a plant constituent alpha-2 antagonist.

38
Q

What are the effects of stimulating beta-1 adrenergic receptors? What are beta-1 antagonists used to treat?

A

Increases heart rate and force of contraction, and increases renin release from the kidney.
Beta-1 antagonist = beta-blocker; used for HTN, angina, arrhythmias, and anxiety.

39
Q

What are the effects of stimulating beta-2 adrenergic receptors? What are beta-2 agonists used to treat?

A

Causes smooth muscle relaxation of blood vessels, bronchi, GI, uterus, bladder, ciliary muscle.
Used for asthma and COPD.

40
Q

If a non-selective beta blocker (such as propranolol) is used, what effect might it have on the lungs?

A

Non-selective beta blockers act on both beta-1 and beta-2; cause bronchoconstriction via beta-2 blockade.

Interviewing Techniques 2 (1 decks)

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