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Interviewing Techniques > Quiz 2 > Flashcards

Quiz 2 Flashcards

1
Q

What does the term cholinergic refer to?

A

Refers to the NT acetylcholine

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2
Q

What does the term anticholinergic refer to?

A

Refers to the blocking of the NT acetylcholine

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3
Q

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

A

confusion, anxiety, agitation, dementia, hallucinations

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4
Q

What conditions are treated with therapies that increase central ACh?

A

dementia, schizophrenia, autism

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5
Q

When might you prescribe a medication that decreases central ACh?

A

vertigo, motion sickness

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6
Q

In the somatic nervous system, where is ACh used as a NT?

A

NMJ of skeletal muscle

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7
Q

In the sympathetic nervous system, where is ACh used as a NT?

A

Ganglia, adrenal medulla, sweat glands

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8
Q

In the parasympathetic nervous system, where is ACh used as a NT?

A

Ganglia, parasympathetic end-organs

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9
Q

What is the effect of increases ACh on skeletal muscle?

A

Muscle spasms and/or spastic paralysis

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10
Q

When might you want to increase ACh in skeletal muscle?

A

myasthenia gravis

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11
Q

What is the effect of decreased Ach on skeletal muscle?

A

muscle weakness and/or flaccid paralysis

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12
Q

When might you want to decrease ACh in skeletal muscle?

A

muscle spasm (botox)

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13
Q

What are the effects of increased ACh on the eyes?

A

pupil constriction

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14
Q

What are the effects of increased ACh on the heart?

A

reduces HR

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15
Q

What are the effects of increased ACh on the lungs?

A

bronchoconstriction

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16
Q

What are the effects of increased ACh on the digestive tract?

A

stimulates GI tract
stimulates pancreas
stimulates gall bladder

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17
Q

What are the effects of increased ACh on the sweat glands?

A

increased perspiration via SNS

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18
Q

What are the effects of increased ACh on the salivary glands?

A

increases saliva production

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19
Q

What are the effects of increased ACh on the bladder/urination?

A

constricts urinary bladder

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20
Q

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

A

Sjogren’s syndrome, delayed gastric emptying, glaucoma

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21
Q

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

A

bradycardia, hyperhidrosis, incontinence, IBS-D, COPD

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22
Q

What are the effects of tropane alkaloids on ACh?

A

Anticholinergics

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23
Q

What plants contain tropane alkaloids?

A

Belladonna, Henbane, Mandrake, Jimson weed

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24
Q

What are the precursors for ACh synthesis?

A

Acetyl CoA + choline

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25
Q

What enzyme breaks down ACh?

A

Acetylcholinesterase

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26
Q

How does inhibition of this enzyme affect ACh concentration in the synaptic cleft?

A

Inhibiting AChE increases concentrations of ACh.

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27
Q

What are acetylcholine esterase inhibitors used for?

A

Myasthenia gravis, glaucoma, Alzheimer’s, Parkinson’s, schizophrenia, autism, antidote to anticholinergic poisoning

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28
Q

What are the two main types of ACh receptors?

A

Nicotinic, muscarinic

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29
Q

Where are the two main types of ACh receptors found?

A

Nicotinic - NMJ, autonomic ganglia (both PNS/SNS)

Muscarinic - PNS end-organs and sweat glands

30
Q

What are examples of monoamine NTs?

A

Catecholamines (Dopa, NE, EPI), Tryptamines (Serotonin, Melatonin), Histamine

31
Q

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

A

Catecholamines

32
Q

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

A

Dopamine does not cross the BBB

33
Q

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

A

Decreased synthesis because it is a cofactor

34
Q

What is the MOA of reserpine?

A

Blocks transport of catecholamines into storage vesicles, causing degradation

35
Q

Why does reserpine lower BP?

A

BC depletion of NE in the PNS decreases BP

36
Q

What is the effect of amphetamines on catecholamine release?

A

Increased release

Inhibits reuptake

37
Q

How is catecholamine neurotransmission terminated?

A

Reuptake of NT from synaptic cleft into presynaptic neuron

38
Q

What enzymes break down catecholamines?

A 
Monoamine oxidase (MAO)
Catechol-O-methyltransferase (COMT)
39
Q

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

A

Reward signals, addiction

40
Q

What is low dopamine associated with?

A

Anxiety, depression, movement disorders (Parkinson’s, RLS), prolactinemia

41
Q

What are dopamine agonists used for?

A

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

42
Q

What is excess dopamine associated with?

A

Mental illness (schizophrenia), N/V, decreased prolactin release

43
Q

What conditions are dopamine antagonists used for?

A

Antipsychotics

44
Q

What are some side effects of dopamine antagonists?

A

Parkinsonism, tardive dyskinesia, dystonia, akathisia

45
Q

What does adrenergic refer to?

A

Related to NE/EPI

46
Q

In the CNS, what are adrenergic neurons involved with?

A

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

47
Q

In the PNS, where is NE secreted?

A

Postganglionic sympathetic fibers at effector organs

Chromaffin cells of the adrenal medulla

48
Q

In the PNS, where is EPI secreted?

A

Chromaffin cells of the adrenal medulla

49
Q

What are the effects of NE/EPI on the eyes?

A

Pupil dilation

50
Q

What are the effects of NE/EPI on the heart?

A

Increased HR, force of contraction

51
Q

What are the effects of NE/EPI on the lungs?

A

bronchodilation

52
Q

What are the effects of NE/EPI on the digestive tract?

A

decreased GI motility and secretions

53
Q

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

A

Decreased urination

54
Q

What are the effects of NE/EPI on blood sugar?

A

Increased blood sugar

55
Q

What are the effects of NE/EPI on blood lipids?

A

Mobilization of fat

56
Q

In what ways do NE and EPI cause BP to rise?

A

Increases vascular tone through alpha-adrenergic receptor activation

57
Q

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

A

bronchoconstriction, nasal congestion, hemorrhoids, priapism

58
Q

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

A

HTN, arrythmias, CHF, BPH, erectile dysfxn, CRPS

59
Q

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

A

MAO inhibitors prevent breakdown of tyramine, leading to potential HTN crisis

60
Q

What are the effects of stimulating alpha-1 adrenergic receptors?

A

SM contraction of blood vessels, bladder neck, GI sphincters, prostate, iris

Inc. glycogenolysis and gluconeogenesis

61
Q

What are alpha-1 agonists used for?

A

nasal congestion, hypotension, weight loss

62
Q

What are alpha-1 antagonists used for?

A

HTN, urinary retention

63
Q

What are the effects of stimulating alpha-2 adrenergic receptors?

A

Decrease release of NE

64
Q

What are alpha-2 agonists used for?

A

HTN

65
Q

What plant constituent is an alpha-2 antagonist?

A

Yohimbine

66
Q

What are the effects of stimulating beta-1 adrenergic receptors?

A

Increase HR/force of contraction

Increase renin release from KD

67
Q

What are beta-1 antagonists used to treat?

A

HTN, angina, arrhythmias, anxiety

68
Q

What are the effects of stimulating beta-2 adrenergic receptors?

A

SM relaxation of blood vessels, bronchi, GI, uterus, bladder, ciliary muscle

Increases renin release, glycogenolysis, lipolysis

69
Q

What are beta-2 agonists used to treat?

A

asthma, COPD

70
Q

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

A

bronchoconstriction

Interviewing Techniques (3 decks)

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