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Interviewing Techniques 2/Neurobiology > Why do we have a test about neurotransmitters in this class? > Flashcards

Why do we have a test about neurotransmitters in this class? Flashcards

1
Q

What does the term cholinergic refer to? Anticholinergic?

A

Cholinergic refers to the release or response of acetylcholine
Anticholinergic blocks the release or response to acetylcholine

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2
Q

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

A

Decreased central acetylcholine can result in confusion, anxiety, agitation, dementia, and hallucinations.

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3
Q

What conditions are treated with therapies that increase central ACh?

A

Primarily to treat dementia, but also used in schizophrenia and autism.

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4
Q
  1. When might you prescribe a medication that decreases central ACh?
A

Vertigo, especially motion sickness.

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5
Q
  1. In the somatic NS, where is ACh used as the neurotransmitter
A

a. Neuromuscular junction of skeletal muscle

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6
Q
  1. In the sympathetic NS, where is ACh used as the neurotransmitter
A

a. At ganglia, adrenal medulla, and sweat glands

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7
Q
  1. In the parasympathetic NS, where is ACh used as the neurotransmitter
A

At ganglia and at parasympathetic end-organs.

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8
Q
  1. What is the effect of increased ACh on skeletal muscle? When might you want to increase ACh in skeletal muscle?
A

a. Increased Ach causes skeletal muscle spasms and/or spastic paralysis.
b. Therapies that increase Ach skeletal muscle activity are used for muscle weakness, as in myasthenia gravis.

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9
Q
  1. What is the effect of decreased Ach on skeletal muscle? When might you want to decrease ACh in skeletal muscle?
A

a. Decreased Ach causes skeletal muscle weakness and/or flaccid paralysis.
b. Therapies that decrease Ach skeletal muscle activity are used for muscle spasm (e.g. Botox).

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10
Q

What are the effects of increased ACh on eyes

A

constricted pupils

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11
Q

What are the effects of increased ACh on heart

A

bradycardia

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12
Q

What are the effects of increased ACh on lungs

A

bronchoconstriction

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13
Q

What are the effects of increased ACh on GI

A

vomiting/diarrhea

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14
Q

What are the effects of increased ACh on sweat glands

A

increased sweating

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15
Q

What are the effects of increased ACh on salivary glands

A

increased salivation

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16
Q

What are the effects of increased ACh on bladder/urination

A

increased urination

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17
Q
  1. What conditions are treated by increasing the parasympathetic effects of ACh?
A

a. Therapies that increase peripheral Ach are used for Sjogren’s syndrome, delayed gastric emptying and glaucoma.

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18
Q

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

A

a. Therapies that decrease peripheral Ach activity are used for bradycardia, hyperhidrosis, incontinence, IBS-D, COPD.

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19
Q
  1. What are the names of some tropane alkaloids? What are the effects of tropane alkaloids on ACh? What plants contain tropane alkaloids?
A

Atropine (from Belladonna), hyoscyamine (from Hyoscyamus), and scopolamine (from Datura) are naturally occurring tropane alkaloids that act as ACh antagonists. Other tropane alkaloids may act as stimulants (cocaine)

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20
Q
  1. What are the precursors for ACh synthesis?
A

Acetyl CoA + choline

Note: Acetyl CoA is made via cellular metabolism, choline is obtained from diet (lecithin)

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21
Q
  1. What enzyme breaks down ACh? How does inhibition of this enzyme affect ACh concentration in the synaptic cleft? What are these inhibitors used for?
A

Acetylcholinesterase (AChe). Inhibition of AChe results in increased and prolonged transmission of cholinergic transmission. AChe’s may be used for Alzheimer’s (Donepezil, Huperzine A, Rivastigmine), as an insecticide, as a nerve gas, for glaucoma/delayed gastric emptying/ antidote to tropane alkaloid poisoning (Physostigmine), or myasthenia gravis (Edrophonium).

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22
Q
  1. What are the two main types of ACh receptors? Where is each found?
A

Nicotinic: neuromuscular junction and autonomic ganglia (both parasympathetic and sympathetic)
Muscarinic: parasympathetic end-organs and sweat glands
both are found throughout the CNS

23
Q
  1. What are examples of monoamine neurotransmitters?
A

Catecholamines: dopamine, norepinephrine, epinephrine
Tryptamines (serotonin, melatonin)
Histamine

24
Q
  1. What neurotransmitter concentrations might increase if L-tyrosine is given?
A

L-tyrosine -> L-Dopa -> Dopamine -> Norepinephrine -> Epinephrine

25
Q
  1. Why is Parkinsons treated with L-dopa rather than with dopamine?
A

Because Dopamine cannot cross the BBB

26
Q
  1. What effect might a lack of SAMe have on epinephrine synthesis?
A

Reduced synthesis of epi since SAMe is a cofactor from NE–>epi

27
Q
  1. What is the mechanism of action of reserpine? Why does this lower blood pressure?
A

Blocks transportation of catecholamines into storage vesicles, leaving the NT unprotected from degradation. Lowers BP because NE is a catecholamine, and low levels in the PNS lowers BP

28
Q
  1. What is the effect of amphetamines on catecholamine release?
A

Amphetamines inhibit the reuptake of catecholamines
Catecholamines are released from vesicles when the nerve cell depolarizes. One of the actions of amphetamines is to cause increased catecholamine release.

29
Q
  1. How is catecholamine neurotransmission terminated?
A

By the reuptake of the NT from the synaptic cleft into the presynaptic neuron

30
Q
  1. What enzymes break down catecholamines?
A

Monoamine Oxidase (MAO) and Catechol-O-methyltransferase (COMT)

31
Q
  1. 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.

32
Q
  1. What is low dopamine associated with?
A

Anxiety, depression, movement disorders, prolactinemia

33
Q
  1. What are dopamine agonists used for?
A

Parkinson’s, prolactinemia, ADHD, anxiety, depression, acromegaly

34
Q
  1. What is excess dopamine associated with?
A

Serious mental illness like schizophrenia, decreased prolactin

35
Q
  1. What conditions are dopamine antagonists used for? What are some side effects of these drugs?
A

a. schizophrenia, bipolar disorder, and stimulant psychosis
b. Dopamine antagonists, especially the typical antipsychotics like haloperidol can cause permanent side effects that include parkinsonism, tardive dyskinesia (involuntary writhing movements), dystonia (prolonged muscle spasms) and akathisia (restlessness)

36
Q

What does “adrenergic” refer to?

A

a. The term adrenergic is used to describe things related to both norepinephrine (NE) and epinephrine (EPI). The two compounds are very similar and act on the same receptors, with somewhat different affinities.

37
Q
  1. In the CNS, what are adrenergic neurons involved with?
A

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

38
Q
  1. In the PNS, where is NE secreted? EPI?
A

Norepinephrine is secreted at postganglionic sympathetic fibers to effector organs and chromaffin cells of adrenal medulla
Epinephrine is secreted mostly from the chromaffin cells of the adrenal medulla

39
Q
  1. What are the effects of NE and EPI on eyes
A

pupil dilation

40
Q

What are the effects of NE and EPI on heart

A

increased rate and contractility

41
Q

What are the effects of NE and EPI on lungs

A

bronchodilation

42
Q

What are the effects of NE and EPI on GI

A

decreased motility

43
Q

What are the effects of NE and EPI on bladder/urination

A

decreased

44
Q

What are the effects of NE and EPI on blood sugar

A

increase

45
Q

What are the effects of NE and EPI on blood lipids

A

increase

46
Q
  1. In what ways do NE and EPI cause blood pressure to rise?
A

Contraction of smooth muscle in blood vessels

47
Q
  1. What conditions might be treated by therapies that increase peripheral adrenergic activity?
A

Bronchoconstriction, hemorrhoids, nasal congestion, priapism

48
Q
  1. What conditions might be treated by therapies that decrease peripheral adrenergic activity?
A

Hypertension, BPH, ED, arrhythmias, complex regional pain syndrome

49
Q
  1. Why should people on MAO inhibitors be advised against eating tyramine-containing foods?
A

a. Tyramine is a monoamine found in high concentration in certain foods such as aged cheese and wine. Tyramine increases the release of norepinephrine from the presynaptic neuron, and because tyramine is metabolized by MAO, MAO inhibitors will prevent the breakdown of both tyramine and NE. Combined with the increased release of NE, this can lead to a hypertensive crisis.

50
Q
  1. What are the effects of stimulating alpha-1 adrenergic receptors? What are alpha-1 agonists used for? Alpha-1 antagonists?
A

a. Stimulates smooth muscle contraction of blood vessels, bladder neck, GI sphincters, prostate, iris (radial muscle). Increases glycogenolysis and gluconeogenesis from adipose tissue and liver
b. Alpha-1 agonists are used for nasal congestion, hypotension, and weight loss. They may cause hypertension, urinary retention, increased blood sugar, and pupil dilation (may cause glaucoma). Ephedra sinica is an agonist at all the adrenergic receptors. Its use as a decongestant is due to its action at alpha-1 receptors.
c. Alpha-1 antagonists are used for hypertension and urinary retention (e.g. BPH).

51
Q
  1. 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

a. Acts pre-synaptically to reduce the release of NE both in the brain and in the periphery as part of a negative feedback loop to prevent excess NE release.
b. Alpha-2 agonists are used for hypertension.
c. Yohimbine is an alpha-2 antagonist used for erectile dysfunction. It can be found in the bark of P. yohimbine and Aspiderma quebracho.

52
Q
  1. What are the effects of stimulating beta-1 adrenergic receptors? What are beta-1 antagonists used to treat?
A

a. Beta-1 agonists Increase heart rate and force of contraction and increase renin release from the kidney.
b. The term “beta blockers” refer to beta adrenergic antagonists. Selective beta-1 antagonists are used for HTN, angina, arrhythmias, and anxiety.

53
Q
  1. What are the effects of stimulating beta-2 adrenergic receptors? What are beta-2 agonists used to treat?
A

a. Causes smooth muscle relaxation of blood vessels, bronchi, GI, uterus, bladder, ciliary m. · Increases renin release, glycogenolysis, lipolysis.
b. Beta-2 agonists are used for asthma and COPD.

54
Q
  1. If a non-selective beta blocker (such as propranolol) is used, what effect might it have on the lungs?
A

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

Interviewing Techniques 2/Neurobiology (1 decks)

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