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PHRM-1058 > Drugs Affecting the Nervous System > Flashcards

Drugs Affecting the Nervous System Flashcards

1
Q

What is the cortex the location of? (7)

A

thought, memory, self-awareness, personality, speech, perception of sensation, control of body movement

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2
Q

What is the function of the midbrain?

A

relax station for cortex, integrates/modulates autonomic functions

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3
Q

What is the function of the brainstem (medulla)?

A

control area for breathing and cardiovascular control, alertness

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4
Q

What is the function of the cerebellum?

A

fine motor control, coordinates movement

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5
Q

Each neuron usually releases how many neurotransmitters?

A

one

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6
Q

T or F: most neurotransmitters are returned to the pre-synaptic nerve terminal and are recycled?

A

T

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7
Q

How do CNS drugs act?

A

increase or decrease individual neuronal activity and exert effects by interaction with neurotransmission

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8
Q

What do CNS drugs affect?

A

NT release, metabolism, and re-uptake

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9
Q

What do the clinical effects of CNS drugs depend on?

A

localization of neurotransmitters in specific brain areas

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10
Q

List some factors that will impact effect of CNS drugs. (6)

A

amount released, availability of transport proteins, previous release of NT, degradation of NT in synaptic space, efficiency of re-uptake process, activities of modulating interneurons

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11
Q

What are the 3 major neurotransmitters involved in antidepressant medication?

A

serotonin, dopamine, norepinephrine

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12
Q

How do antidepressants act?

A

inhibitors slow the process by which neurotransmitters are reused, resulting in an increased amount of neurotransmitter that are available to stimulate neurons

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13
Q

What are first-line treatment antidepressants? Second? Third?

A

SSRIs or SRIs: e.g. Celexa, Prozac
SNRIs: e.g. Effexor, Cymbalta
Dopamine re-uptake inhibitors: e.g.Wellbutrin, Zyban

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14
Q

Describe and provide an example for TCAs.

A

effect on norepinephrine and serotonin, added effect of influencing histamine and acetylcholine
e.g. Remeron

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15
Q

Describe and provide an example(s) for MAOIs.

A

removes norepinephrine, serotonin and dopamine from the brain
e.g. Nardil, Parnate

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16
Q

Lithium:

function? action? side effects?

A

mood stabilizer
monovalent cation that can replace Na in some biological cells
tremors, cognitive slowing, hypothyroid, renal insufficiency, leukocytosis, polyuria, polydipsia, coma
*narrow therapeutic window

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17
Q

Anticonvulsants:

function? +/- sedation? ex.?

A

mood stabilizer
may cause sedation
Valproic acid, Carbamazepine

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18
Q

What do antipsychotics target? AKA? What is the therapeutic goal? ex.?

A

limbic system and “calming effect”
major tranquillizers
increase dopamine levels in the brain
Olanzapine, Risperidon

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19
Q

What type of drug is used for Alzheimer Dementia? How do these act? Side effects? ex.?

A

cholinesterase inhibitors
increased acetylcholine levels in the brain in an attempt to increase cognitive function
GI side effects
Donenzepil, Galantamine, Thorazine, Haldol

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20
Q

How do anxiolytics function?

A

inhibition of the neuron through hyperpolarization: GABA increased chloride conductance, more chloride is able to move into the cell and create a state of hyperpolarization

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21
Q

Benzodiazepines:

function? uses? action? effects? antagonist?

A 
anxiolytic
anesthesia induction
hyperpolarize neurons
amnestic, promote sleep, terminate seizures, augment respiratory depression
flumazenil
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22
Q

Barbiturates:

function? uses? risks?

A

anxiolytic
anesthesia induction (thiopental), hypnotics (pentobarbital), and seizures (phenobarbital)
rapid tolerance, toxic potential, high risk of addiction/abuse

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23
Q

What type of CNS drug is ethyl alcohol? What is the dose that results in respiratory arrest?

A

nonprescription sedative-hypnotic

400-600 mg/dL

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24
Q

Describe delirium tremens (DTs).

A

withdrawal effect of CNS hyperactivity (hyperthermia, increased BP, hallucinations, seizures, etc.)

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25
Q

What do analeptic drugs do? What can this be used to treat? ex.?

A

increase activity of the brain
narcolepsy, ADHD, obesity, depression, AOP
caffeine, aminophylline, doxapram

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26
Q

T or F: analeptic drugs have a clinical role in treating respiratory failure or drug induced respiratory depression?

A

F

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27
Q

NSAIDS:

function? action? ex.?

A

analgesic
affect hypothalamus and inhibit production of inflammatory mediators at the pain site
salicylates (aspirin) - antipyretic, analgesic, antiplatelet, increased incidence of Reye’s in children

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28
Q

Acetaminophen (Tylenol) is an example of what? Effects?

A

nonnarcotic analgesic

effective on mild/moderate pain, may cause lethal hepatic necrosis, OD can be treated with N-acetylcysteine

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29
Q

List and describe 2 naturally occurring opioids.

A

enkephalins - morphine like neurotransmitter found in the brain and adrenal glands
endorphins - morphine like neurotransmitter found in the brain and pituitary gland

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30
Q

Describe exogenous opioids.

A

euphoric effect, high doses may cause LOC and respiratory arrest, strong ones are called narcotics

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31
Q

List some examples of exogenous opioid analgesics.

A

morphine, codeine, fentanyl, heroin, hydrocodone, hydromorphone, oxycodone, tramadol

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32
Q

List some side effects of opioid analgesics.

A

respiratory depression, constipation, nausea, vomiting, antitussive

33
Q

T or F: opioid analgesics activate only 1 opioid receptor?

A

F

34
Q

What are the 3 opioid receptors?

A

mu, kappa, delta

35
Q

Opioid analgesics bind selectively to receptor sites found where?

A

CNS and GI tract

36
Q

What types of effects do opioid analgesics produce?

A

inhibitory

37
Q

Describe opioid analgesic drugs.

A

lipid soluble, weak bases, highly protein bound

38
Q

What is the antagonist to opioid analgesics? Action?

A

Narcan

occupies opioid receptors and prevent agonist binding

39
Q

List and describe the different routes of opioid administration.

A

injection
PCA pumps - keeps control
inhalation - decreases dyspnea, alternative when IV unavailable

40
Q

Describe combination of analgesic classes.

A

widely available, separate dosing may prove better with various side effects, toxicities, and half-lives

41
Q

List some side effects that accompany central sensitization in chronic pain syndromes.

A

hyperesthesia, hyperpathia, allodynia

42
Q

What may reduce likelihood of neuropathic problems in chronic pain syndromes?

A

treatment during acute phase

43
Q

List some characteristics of neuropathic pain.

A

evidence of primary injury, pain involving body area with sensory loss, pain characterized as burning, electric, or shooting, dysesthesias in the area, sympathetic hyperactivity, hyperalgesia, hyperpathia, allodynia

44
Q

PNS:

how many synapses? afferent vs efferent? branches from autonomic neurons?

A

1
afferent - from skin/muscles/organs to CNS
efferent - from CNS to muscles
sympathetic and parasympathetic

45
Q

T or F: autonomic system is generally considered an efferent system?

A

T there are afferent fibres running back to CNS providing feedback about body functions

46
Q

Where are highly regulated complex function controlled? Where are unrefined, quick reflexes controlled?

A

brain

spinal cord

47
Q

How is neural singling both electrical and chemical?

A

electrical AP signal carried along nerve fibres
at axon terminal, electrical signal causes release of vesicles containing neurotransmitter
chemical signal at synapse

48
Q

What are the 2 key neurotransmitters involved in neural signalling?

A

AcH and NE

49
Q

Define neuroeffector site.

A

location where nerve interacts with effector organ, gland, or muscle

50
Q

What is the neurotransmitter associated with the pre and postganglionic fibres in efferent parasympathetic pathways?

A

ACh

51
Q

What are the neurotransmitters associated with the pre an postganglionic fibres and adrenal medulla in efferent sympathetic pathways?

A

pre - ACh
post - NE, ACh
medulla - epi

52
Q

Where do parasympathetic fibres arise from? Which fibre is short vs long? How do these fibres lie in relation to effector organs?

A

cranial nerves and sacral portions of spinal cord
pre is long, post is short
lie near or on effector organ

53
Q

Where do sympathetic fibres arise from? Which. fibre is long vs short? How do these fibres lie in relation to the vertebral column?

A

thoracic/lumbar regions of spinal cord
pre is short, post is long
lie adjacent to vertebral column

54
Q

How do ANS drugs work?

A

mimic or block effect of NT at effector site

55
Q

What type of effect do parasympathetic neurons provide vs. sympathetic neurons?

A

para - discrete

sympathetic - broad

56
Q

Describe cholinergic.

A

refers to a drug or endogenous molecule (NT) that stimulates ACh receptors

57
Q

Describe adrenergic.

A

refers to a drug or endogenous molecule (NT) that stimulates NE receptors

58
Q

Describe the suffix mimetic vs. lytic

A

mimetic (‘mimic’) - up regulation

lytic (‘destruction of’) - down regulation

59
Q 
Parasympathomimetic = ?
Parasympatholytic = ?
Sympathomimetic = ?
Sympatholytic = ?
A 
parasympathomimetic = cholinergic
parasympatholytic = anti-cholinergic
sympathomimetic = adrenergic
sympatholytic = anti-adrenergic
60
Q

Describe parasympathetic effects.

A

decreased HR/BP/RR, bronchoconstriction, increased secretions, mitosis, increased salivation, increased motility, relaxation of sphincters, increased insulin secretion/energy storage

61
Q

Where are nicotinic receptors found? What are they?

A

between pre/post ganglia in both para/sympathetic nervous systems and NMJ
ligand-gated ion channels

62
Q

What is ACh inactivated by?

A

cholinesterase

63
Q

What types of receptors do parasympathetic NT act on?

A

cholinergic (pre/post), nicotinic, muscarinic (2,3 )

64
Q

Describe the 3 subtypes of muscarinic receptors that are innervated by the parasympathetic NS. Where else can M receptors be found?

A

M1 - nasal mucosa
M2 - heart
M3 - a/w smooth muscle

blood vessels

65
Q

Describe the different acting cholinergic agents.

A

direct - mimic ACh, methacholine (diagnostic for asthma)

indirect - inhibit cholinesterase enzyme, neostigmine (reversal of non depolarizing muscle relaxants)

cholinesterase reactivate - pralidoxime (tx of organophosphate toxicity)

66
Q

What is the action of anticholinergic agents? Provide and describe an example.

A

block ACh receptors

atropine - parasympatholytic agent, competitive antagonist

67
Q

Describe parasympatholytic (antimuscarinic) effects of atropine.

A

bronchodilator, prep drying of secretions, antidiarrheal agent, prevention of bed-wetting in children, tx of peptic ulcers/organophosphate poisoning/mushroom ingestions/bradycardia

68
Q

Describe sympathetic effects.

A

increased HR/force of contraction/BP/RR, bronchodilation, mydriasis, vasodilation, decreased motility, increased lipolysis and decreased insulin production

69
Q

What is the adrenergic NT function in SNS? Describe the terminating action of NE.

A

sympathetic effects at neuroeffector site and systemic effects through action of epi

reuptake process: COMT, MAO (inactivate catecholamines)

70
Q

Describe the receptors types that are acted upon by the SNS.

A

a1 (peripheral blood vessels), a2 (auto receptors, CNS), B1 (increased HR/force), B2 (bronchial smooth muscle, cardiac muscle), dopaminergic (similar to epi)

71
Q

Describe sympathomimetic agents. Provide examples.

A

stimulate the sympathetic system and produce adrenergic effects
e.g. epi, dextroamphetamine, dopamine, salbutamol

72
Q

Describe and provide an example for sympatholytic agents.

A

block adrenergic effects

e.g. propanolol

73
Q

List all the things involved in neural control of lung function.

A

a/w smooth muscle/tone, submucosal and surface secretory cells, bronchial epithelium, pulmonary and bronchial blood vessels

74
Q

Describe direct vs indirect effects in relation to sympathetic innervation.

A

direct - innervation of nerve fibres

indirect - catecholamine release

75
Q

List and describe the receptors involved in sympathetic innervation of the a/w smooth muscle.

A

b2 - mediate relaxation

a - less abundant, minor effect (possible bronchoconstriction)

76
Q

Describe nonadrenergic, noncholinergic excitatory nerves (NANC).

A

neither parasympathetic nor sympathetic, causes contraction of smooth a/w muscle

77
Q

Describe nonadrenergic, noncholinergic inhibitory nerves (NANC).

A

neither parasympathetic nor sympathetic, causes relaxation of a/w smooth muscle

78
Q

Which fibre system has been considered as a possible cause of a/w hyperactivity observed in asthmatics?

A

NANC excitatory C-fibre

PHRM-1058 (7 decks)

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