Neuro 1 Flashcards

1
Q

What are neurotransmitter connector sites called?

A

Neurotransmitters respond through the stimulation of connector sites called synapses

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2
Q

What is the effect of the chloride coming in and potassium coming out in regards to the neurotransmitter?

A

The resulting flow of ions (chloride in; potassium out) increases the membrane potential to the point that it counteracts any excitatory signals that arrive at that neuron

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3
Q

Where is ACh released?

A

Released at the terminals of all motor neurons

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4
Q

What is ACh responsible for?

A

stimulation of muscles (GI tract and movement)
rapid eye movement (REM) sleep
thought, learning, and memory

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5
Q

The use of drugs that enhance/ inhibit the destruction of ACh are helpful in the tx of which diseases?

A

Alzheimer’s disease because acetylcholine levels are low in the brains of these patients

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6
Q

How does the black spider venom work w/ ACh?

A

release of acetylcholine - leads to severe muscle contractions, spasms, paralysis, and even death

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7
Q

How do nerve agents work w/ ACh?

A

Nerve agents, such as sarin gas, are potent acetylcholinesterase inhibitors
Death by asphyxiation due to a loss of control of the respiratory muscles

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8
Q

Blocking/ antagonizing ACh does what to muscles?

A

Causes them to relax

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9
Q

Botulinum toxin (Botox) causes what to ACh?

A

prevents the release of acetylcholine - causing muscle relaxation

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10
Q

What is Dopamine derived from?

A

Manufactured inside dopamine neurons from an amino acid precursor, L-tyrosine

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11
Q

What does the release of dopamine do to the body?

A

Feelings of pleasure, and also addiction
Movement and motivation

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12
Q

How is Parkinson’s tx?

A

Treatment of Parkinson’s disease provides the patient with levodopa (L-dopa)

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13
Q

Midbrain dopamine and its receptors are involved in which actions?

A

Behavior, attention, and arousal (also Parkinson’s disease)

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14
Q

What inactivates endorphins?

A

They are rapidly inactivated by enzymes called peptidases

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15
Q

When are endorphins released?

A

Released during exercise, excitement and sex

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16
Q

Endorphins do what to the body?

A

Act as analgesics by diminishing the perception of pain (also slow HR, respiration, and metabolism)

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17
Q

Is GABA excitatory or inhibitory and why?

A

inhibitory neurotransmitter - responsible for slowing or stopping the excitatory neurotransmitters that give rise to anxiety

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18
Q

What does GABA do in terms of overexcitation?

A

helps induce relaxation and sleep by inhibiting overexcitation

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19
Q

What are gamma-aminobutyric acid enhancers?

A

Drugs that increase GABA levels in the brain

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20
Q

What drugs influence GABA?

A

benzodiazepines*, alcohol, sedatives, narcotics, and barbiturates

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21
Q

What is the MC neurotransmitter in the CNS?

A

Glutamate

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22
Q

Is glutamate excitatory or inhibitory?

A

Excitatory

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23
Q

Where are Noroepi and Epi released for in reflex to stress?

A

Adrenal glands

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24
Q

What do Noroepi and Epi do to the body?

A

Causes increase in heart rate and BP
Causes physical boost and heightened awareness

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25
Q

Is serotonin excitatory or inhibitory?

A

Inhibitory neurotransmitter

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26
Q

Low serotonin leads to what?

A

depression, problems with anger control, obsessive-compulsive disorder, suicidal ideation, increased appetite for carbohydrates, trouble sleeping, irritable bowel syndrome, and fibromyalgia

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27
Q

Appetite suppression drugs

A

benzenediamine
diethylpropion
phentermine* - available PO

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28
Q

Appetite suppression drugs MOA

A

These drugs are sympathomimetic amines - stimulate the hypothalamus mimicking satiety

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29
Q

Drugs for Appetite Suppression use

A

Obesity or overweight in the presence of at least one weight-related comorbidity

30
Q

Drugs for Appetite Suppression SE

A

Hypertension, tachycardia, Dry mouth, Changes in libido, Depression, insomnia

31
Q

Drugs for Appetite Suppression + MAOIs can cause what?

A

Coadministration of monoamine oxidase inhibitors (MAOIs) may cause a life-threatening hypertensive crisis.

32
Q

Drugs for Appetite Suppression + EtOH causes what?

A

Depression

33
Q

Why are Drugs for Appetite Suppression contraindicated in pts w/ substance abuse?

A

Substance abuse (cocaine/methamphetamine) because of the potential for excessive adrenergic stimulation.

33
Q

Why are Drugs for Appetite Suppression contraindicated in pts w/ substance abuse?

A

Substance abuse (cocaine/methamphetamine) because of the potential for excessive adrenergic stimulation.

34
Q

Drugs for Appetite Suppression contraindications

A

Substance abuse (cocaine/methamphetamine) because of the potential for excessive adrenergic stimulation.
Advanced arteriosclerosis
Concomitant use, or use within 14 days, of a MAO inhibitor
Hyperthyroidism
Moderate to severe hypertension
Pregnancy

35
Q

How long should a pt be off of MAOI to be able to use an appetite suppressant?

A

At least 14 days

36
Q

In which pt population can appetite suppressants be used and how should they be used?

A

severely obese patients only as short-term adjuncts to other weight-loss measures

37
Q

What can occur w/ stopping an appetite suppressant?

A

Effective in the short term, but weight gain occurs almost universally upon stopping them.

38
Q

Which schedules are Diethylpropion and phentermine and Benzphetamine and phendimetrazine?

A

Benzphetamine and phendimetrazine are schedule III
Diethylpropion and phentermine are schedule IV

39
Q

What time of day should appetite suppressants NOT be taken in and why?

A

Avoid an evening dose because of resultant insomnia or sleeplessness.

40
Q

Drugs to Aid Sleep schedule rating

A

Schedule IV drugs because they are benzodiazepine-like

41
Q

Drugs to Aid Sleep should not be used for > 7-10 days, why?

A

Can be habit forming because they act on benxo receptors

42
Q

Drugs to Aid Sleep examples (nonbenzos)

A

zolpidem
eszopiclone
zalepon

43
Q

nonbenzodiazepine GABAergics MOA

A

selective for the GABA-1 receptor complex, where they enhance chloride conductance on the neuronal membrane

44
Q

How do nonbenzodiazepine GABAergics compare to regular benzos?

A

Strong hypnotic properties and weak anxiolytic, muscle relaxant, and anticonvulsant properties compared to benzodiazepines

45
Q

Drugs to Aid Sleep use

A

To provide sedation during episodes of insomnia

46
Q

Drugs to Aid Sleep SE

A

xerostomia, Headache, balance disorder, abnormal dreams, sleepwalking, hallucinations, memory impairment, lethargy

47
Q

Drugs to Aid Sleep SE

A

xerostomia, Headache, balance disorder, abnormal dreams, sleepwalking, hallucinations, memory impairment, lethargy

48
Q

Drugs to Aid Sleep contraindications

A

Hypersensitivities
Pregnancy

49
Q

Drugs to Aid Sleep black box warning

A

Rare but serious injures due to abnormal sleep behaviors

50
Q

Drugs to Aid Sleep combined w/ ketoconazole, erythromycin, clarithromycin, and protease inhibitors can cause what?

A

Increased blood levels of sleep aids

51
Q

Sleep aid time limitations

A

It is best if these agents are used no >2 weeks (acutely) or 3 months (chronically) without careful evaluation of the treatment

52
Q

Use of sleep aids for greater than 2 wks then cessation can cause what?

A

withdrawal symptoms (fatigue, nausea, flushing, uncontrolled crying, nausea, vomiting, GI upset, panic attacks, nervousness)

53
Q

What happens to hormones during a migraine HA?

A

During an attack, serotonin levels drop, resulting in expansion of the brain’s blood vessels and throbbing pain

53
Q

What happens to hormones during a migraine HA?

A

During an attack, serotonin levels drop, resulting in expansion of the brain’s blood vessels and throbbing pain

54
Q

What is the goal to migraine HA tx?

A

to minimize the impact these headaches have on the patient’s quality of life and the patient’s ability to work

55
Q

Serotonin Receptor Agonists (Triptans) examples

A

sumatriptan (SC, PO, nasal spray)
zolmitriptan
rizatriptan

56
Q

Serotonin Receptor Agonists (Triptans) MOA

A

Acts selectively on serotonin receptors in cranial arteries, causing vasoconstriction

57
Q

Triptan use

A

Relief of migraine, either to abort an attack or to be used prophylactically

58
Q

Triptan SE

A

Tingling, warm sensation, flushing, paresthesia, dizziness

59
Q

Biggest drug interaction w/ Triptans

A

All triptans can interact with the SSRIs, possibly causing serotonin syndrome

60
Q

Triptan contraindications

A

ischemic heart disease, peripheral vascular disease, cerebral vascular syndromes, or uncontrolled HTN - d/t vasoconstriction

61
Q

When/ how should triptans be used?

A

Should be administered at any sign of an impending migraine attack or during an attack, a second dose may be given if there has been at least 2 hours between doses.

62
Q

Ergotamines examples

A

ergotamine
dihydroergotamine
ergotamine + caffeine

63
Q

Ergotamines MOA

A

Acts selectively on serotonin receptors in cranial arteries, causing vasoconstriction

64
Q

Ergotamines use

A

To abort or prevent vascular-based headaches, such as migraine

65
Q

Ergotamines SE

A

Vasospasm, ischemia, hypertension, Nausea, Hot flashes, paresthesia

66
Q

Ergotamines contraindications

A

pregnancy, Uncontrolled HTN, peripheral vascular disease, and ischemic heart disease.

67
Q

Ergotamines blood levels can increase when used with which drugs?

A

Do not use with strong/potent CYP3A inhibitors, such as azole antifungals, protease inhibitors and macrolides. OR grapefruit juice

68
Q

Ergotamines black box warning

A

Increase in blood levels leading to stroke or MI when combined w/ CYP3A4 inhibitors

69
Q

What can lead to ergotamine noncompliance?

A

Nausea will often limit the dose or lead to nonadherence

70
Q

Ergotamines fail to relieve HA, what should be done?

A

If an initial dose has failed, repeating the dose rarely mitigates the migraine.