Quiz 2: Neurotransmitters Flashcards Preview

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Flashcards in Quiz 2: Neurotransmitters Deck (40)
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1

What does the term cholinergic refer to? Anticholinergic?

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

2

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

Confusion, anxiety, agitation, dementia, and hallucinations.

3

What conditions are treated with therapies that increase central ACh?

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

4

When might you prescribe a medication that decreases central ACh?

Vertigo, esp. motion sickness

5

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. 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).

6

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

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

7

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

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

8

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. 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

9

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

Sjögren's syndrome, delayed gastric emptying, glaucoma.

10

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

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

11

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

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

12

What are the precursors for ACh synthesis?

Acetyl CoA + choline

13

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?

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).

14

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

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

15

What are examples of monoamine neurotransmitters?

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

16

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

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

17

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

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

18

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

Reduced. SAMe is a cofactor for NorEpi --> Epi

19

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

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

20

What is the effect of amphetamines on catecholamine release?

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

21

How is catecholamine neurotransmission terminated?

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

22

What enzymes break down catecholamines?

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

23

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

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

24

What is low dopamine associated with?

Anxiety and depression, movement disorders, prolactinemia.

25

What are dopamine agonists used for?

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

26

What is excess dopamine associated with?

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

27

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

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

28

What does “adrenergic” refer to?

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

29

In the CNS, what are adrenergic neurons involved with?

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

30

In the PNS, where is NE secreted? EPI?

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

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. 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

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

Vasoconstriction.
Probably something else.

33

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

Bronchoconstriction, nasal congestion, hemorrhoids, and priapism.

34

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

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

35

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

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

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

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

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?

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

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

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

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

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

40

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

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