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Block 8 Week 1 > Drug Actions in the CNS- Craviso > Flashcards

Drug Actions in the CNS- Craviso Flashcards

1
Q

What is an important factor in CNS pharm?

A

the blood brain barrier (BBB)

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2
Q

What does the BBB do?

A

maintains brain homeostasis and transport of endogenous and exogenous compounds by controlling their selective and specific uptake, efflux, and metabolism in the brain

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3
Q

What will the BBB allow to go through channels from the blood to the brain?

A

Small ions and water

K+, Cl-, Na+, H20

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4
Q

What will the BBB allow to go through membrane transport (passive diffusion) from the blood to the brain?

A

small lipophilic molecules (o2, co2, anesthetics, barbiturates, ethanol, nicotine, caffeine)

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5
Q

What will the BBB allow to go through carrier-mediated transport (solute carriers)?

A

Energy transport systems (glucose, monocarboxylates, lactate, pyruvates (MCT1) creatine)
Amino acid transport systems

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6
Q

What will the BBB allow to go through receptor-mediated transport?

A

insulin, transferrin, leptin, IgG, TNFalpha

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7
Q

What will the BBB allow to go through the adsorption-mediated transcytosis systems?

A

histone, albumin

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8
Q

What will the BBB allow to go through the active efflux transporters?

A

P-glycoprotein****
BRCP
MRP

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9
Q

What is P-glycoprotein?

A

it is an active efflux transporter that pumps many foreign substances out of cells (i.e it can kick out drugs, toxins and stuff out of the brain)

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10
Q

What is this:

belongs to a family of membrane transporters that modulate drug distribution

A

P-glycoprotein (P-gp)

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11
Q

Capillary endothelial cells of the BBB express high levels of (blank) as compared to other tissues

A

P-gp

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12
Q

What are some substrates that the active efflux transporter P-gp will transport?

A
  • chemotherapeutic agents (vinka alkaloids, doxorubicin)
  • antibiotics such as rifampicin
  • anti-epileptic drugs
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13
Q

What is the clinical significance of P-gp?

A

a drug that is a substrate for active efflux transporters result in VERY LOW levels of the drug in the brain

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14
Q

It has been proposed that (blank) of P-gp plays a role in drug refractory epilepsy and multidrug resistance in general

A

overexpression

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15
Q

Membrne transport of drugs by passive diffusion depends on the (Blank) of the drug

A

lipid solubility

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16
Q

The greater the lipid solubility, the (slower/faster) a drug enters the CNS

A

faster

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17
Q

In general, the oil-water partition coeffcient indicates the relationship between lipid solubility and brain uptake. However there are exceptions, what are they and why?

A

glucose and L-dopa are not lipidphilic however they have transporters in the brain so get taken up in the brain quickly
Phenobarbital and phenytoin are highly lipidphiic but get metabolized quickly and bind to plasma binding proteins so do not get taken up by the brain

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18
Q

What are the regions where the BBB is more permeable?

A
  • area postrema
  • median eminence
  • pituitary gland
  • pineal gland
  • choroid plexus capillaries
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19
Q

(blank) and (blank) cause an increase in BBB permeability

A

Bacterial and viral infections

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20
Q

What is the most promising route for global drug delivery to the brain? WhY?

A

vascular route

Because each neuron has its own capillary (for oxygen, ridding of waste, and nutrients)

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21
Q

Can you directly and locally deliver a drug to a particular part in the brain?

A

yes

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22
Q

Psych drugs act by doing what (generally speaking)?

A

enhancing or inhibiting neural excitability usually by targeting a specific transmitter system

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23
Q

What are drugs targeting pre-synaptically?

A

-effects on synthesis, storage, release, reuptake and/or degradation of neurotransmitters; agonist or antagonist activity at nerve terminal autoreceptors

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24
Q

What are drugs targeting post-synaptically?

A

receptor agonist, antagonist, or modulatory activity, degredation of neurotransmitters

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25
Q

How else can drugs influence behavior and neural excitability?

A
  1. effects on voltage-gated ion channels

2. non-selective effects on membranes

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26
Q

What do you target in antiemetic therapy?

A

blocking chemoreceptor trigger zone, at afferent inputs to the emetic center and in emetic center

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27
Q

Where do you find the chemoreceptor trigger zone?

A

area postrema

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28
Q

What directly affects the chemoreceptor trigger zone?

A

blood borne emetics (cytotoxic drugs etc)

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29
Q

What indirectly affects the chemoreceptor trigger zone?

A

local irritants
blood borne emetics
vagal and sympathetic afferents

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30
Q

What directly affects the emetic center (found in medulla)?

A

chemoreceptor trigger zone, solitary tract nucleus, cereblellum (inner ear motion), higher centers (memory, fear, anticipation)

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31
Q

How do you prevent nausea and vomiting?

A

suppress emetic center

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32
Q

What are the major neurotransmiters involved with nausea and vomiting?

A

NK (neurokinin), Dopamine, 5-HT3

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33
Q

What do you use antiemetics drugs for?

A
  • preventon and tx of chemotherapy induced (CTI) nausea and vomiting
  • treating radiation induced (RI) and post-operative (PO) emesis
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34
Q

How do 5HT3 receptor antagonists work?

A

block 5ht3 receptors and thus inhibit sodium influx, and block intestinal vagal affarents

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35
Q

What are the 2 important 5-HT3 receptor antagonists?

A

Ondansetron (zofran)

Granisetron (kytril)

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36
Q

How do you give Ondansetron (zofran)?

A

oral, oral soluble film, IV

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37
Q

How do you give Granisetron (Kytril)?

A

oral, IV, transdermal pathc (Sancuso)

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38
Q

What is the important NK1 (Substance P/neurokinin) receptor antagonist?

A

Aprepitant (Emend)

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39
Q

How do you give Aprepitant (emend)?

A

oral and IV (fosaprepitant)

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40
Q

What antiemetic do you give someone before you knock them out in surgery so that when they wake up they wont vomit from the anesthesia?

A

ondansetron (zofran)

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41
Q

What is the best way to give medication to someone who needs antiemetics?

A

Combine 5HT3 antagonist with a NK1 antagonist

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42
Q

Wht besides 5ht3 antagnoists and NK1 antagonists can you use to treat nausea and vomiting (antiemetic)?

A
  • corticosteroids

- D2 receptor antagnoists

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43
Q

What is the important corticosteroid used as an antiemetic?

A

Dexamethasone

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44
Q

How can you give dexamethasone?

A

oral, IV

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45
Q

How do D2 receptor antagonists work as antiemetics?

A

-act peripherally to enhance GI motility

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46
Q

When do you use D2 receptor antagonists?

A

for treating CTI nausea and vomiting and for treating unproductive nausea and vomiting

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47
Q

What is the important D2 receptor antagonist?

A

Metoclopramide (reglan)

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48
Q

How do you give metoclopramide (reglan)?

A

Oral, IM, IV

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49
Q

What are the SEs of D2 receptor antagonists?

A

Dystonias
Tardive dyskinesia
restlessness, fatigue, headache, insomnia, confusion

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50
Q

How do oral cannabinoids work as antiemetics?

A

work at high cortical centers

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51
Q

When do you use oral cannabinoids as antiemetics?

A

with other antiemetics for treatment of breakthrough or refractory emesis

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52
Q

What is the important oral cannabinoid?

A

Dronabinol (marinol)-synthetic form of THC

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53
Q

What are the SEs of oral cannabinoids?

A

euphoria, dysphoria, hallucinations; abuse potential

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54
Q

What else do you use marijuana for?

A

to decrease pain, inflammation, and spasticity

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55
Q

What is breakthrough, refractory emesis?

A

when you vomit as soon as the antiemesis is removed

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56
Q

What are the drugs typically used to control non-productive nausea and vomiting?

A

D2 receptor antagonists (phenothiazines) and H1 receptor antagonist

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57
Q

What is the D2 receptor antagonists (phenothiazines) used to control non-productive nausea and vomiting?

A

promethazine (phenergan)

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58
Q

How do you give promethazine (phenergan)?

A

oral, suppositories, IM, IV

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59
Q

What else can you use promethazine (phenergan) for?

A

as an antihistamine (blocks histamine H1 receptors)

60
Q

D2 receptor ntagonists also block (blank) receptors

A

mACh

61
Q

H1 receptor antagonists also block (blank) receptors.

A

mACh

62
Q

What is the most impoortant H1 receptor antagonist?

A

Doxylamine plus pyridoxine (Diclegis)

63
Q

What is doxylamine plus pyridoxine (Diclegis) used for?

A

delayed-release combination for nausea and vomiting of pregnancy

64
Q

What are the side effects of doxylamine plus pyridoxine (Diclegis)?

A

sedation and antimuscarinic effects

65
Q

What H1 receptor antagonists are used for motion sickness?

A
  • Dimenhydrinate (dramamine)

- Meclizine (antivert)

66
Q

How do you administer Dimenhydrinate (dramamine)?

A

oral, IM, IV

67
Q

How do you adminster Meclizine (antivert)? What else can you use Meclizine for?

A

Orally

vertigo

68
Q

What are the muscarinic (mACh) receptor antagonists that are used for long-term, sustained control of motion sickness?

A

Scopolamine (transderm scop)

69
Q

What are the 2 types of drugs used for motion sickness?

A
  • H1 receptor antagonist

- Muscarinic (mACh) receptor antagonist

70
Q

What are these:
skin patch placed behind the ear that produces less side effects than via the oral route; however, some are highly sensitive to the drowsiness and effects on concentration

A

Scopolamine (transderm scop)

71
Q

What is the main goal of antiseizure therapy?

A

involves multiple strategies to prevent excessive synchronized neuronal discharges w/out impeding normal neuronal function

72
Q

One way antiseizure therapy works, is by enhancing (blank) neurotransmission.

A

GABAergic

73
Q

What are the four ways to enhance GABAergic neurotransmission?

A
  1. enhance synthesis
  2. block degredation
  3. block reuptake
  4. enhance postsynaptic GABA-A receptor activity
74
Q

How does Tigabine work?

A

blocks GABA reuptake

75
Q

How does Benzodiazepines and Phenobarbital work?

A

Enhances postsynaptic GABA-A receptor activity

76
Q

How does Vigbatrin work?

A

it blocks GABA degredation

77
Q

What can you attentuate to work as an antiseizure therapy?

A

glutaminergic neurotransmission

78
Q

How does gabapentin and pregabalin work ?

A

blocks L-type calcium channels resulting in decreased Glutamate release ALSO upreguates GABA acting as an agonist
i.e attenuates gluatminergic neurotransmission.

79
Q

How does Levetiracetam work?

A

Modulates release of glutamate—-attenuates glutaminergic neurotransmission

80
Q

How does Felbamate work?

A

blocks the NMDA receptor thus reduces glutaminergic neurotransmission

81
Q

How does topiramate work?

A

blocks AMPA and Kainate receptors and thus attenuates glutaminergic neurotransmission

82
Q

What drugs modify ion conductance through channels presynaptically and are used as antiseizure therapies?

A

Phenytoin, carbamazepine, lamotrigine, retigabine

83
Q

What drugs modify ion channels postsynaptically and are used as antiseizure therapies?

A

ethosuximide, valproate

84
Q

What neurotransmitter is deficient in Alzheimers?

A

Acetylcholine (ACh)

85
Q

In Alzheimers disease, what do you lose that causes the loss in acetylcholine (ACh)?

A

loss of hippocampal pyramidal neurons and basal forebrain cholinergic neurons

86
Q

What will the loss of hippocampal neurons cause deficits in?

A

memory and cognition

87
Q

How do you treat alzheimers?

A

increasing ACh levels using cholinesterase inhibitors
AND
open channel blocker of NMDA receptors

88
Q

What are the cholinesterase inhibitors you use to treat alzheimers?

A

Donepezil (aricept)

Ravistigmine (excelon)

89
Q

What low affinity open channel blocker of NMDA receptors do you use to treat alzheimers?

A

Memantine (namenda)

90
Q

In alzheimers, the NMDA receptor opens pathoglocially this is why Memantine works. T OR F

A

T

91
Q

What neurotransmitter is deficient in parkinson’s disease?

A

dopamine

92
Q

How does parkinsons’s happen?

A

you get a progressive loss of dopaminergic (DM) neurons in the substantia nigra, leading to a shortage of DM in the extrapyramidal movement circuit

93
Q

What is the primary treatment for parkinson’s disease?

A

L-dopa and DM agonists

94
Q

Do the drugs that treat Alzheimer’s disease and Parkinson’s disease stop the progression of the disease?

A

no they just slow the process

95
Q

What can be a side effect of memenatine?

A

can cause exocitoxicity

96
Q

What is an inherited disorder due to a mutation in the protein hutingtin (htt)?

A

huntington’s disease (HD)

97
Q

What is chorea and what disease is characterized by this?

A

irregular, unpredictabe involuntary muscle jerks at different parts of the body that impair voluntary activity that is the result of a loss of neurons from structures of the basal ganglia, imbalances both in GABA functions (diminished) and dopamine functions (enhanced)

98
Q

How do you treat huntingotns disease (HD)?

A
  • Tetrabenazine (xenazine)

- D2 receptor antagonists

99
Q

Wht does tetrabenazine (xenazine) do?

A

a selective and reversible centrally-acting dopamine depleting drug (inhibits VMAT2)

100
Q

What does the D2 receptor antagonist do for huntingtons?

A

to control abnormal movements and relieve the psychosis that accompanies the disease

101
Q

What are some other classes of drugs that you give to people with huntingtons disease?

A

Antidepressants for depression

anxiolytics for anxiety

102
Q

What does VMAT2 do?

A

causes uptake and storage of dopamine

103
Q

In huntingtons you have too much of the neurotransmitter (blank)

A

dopamine

104
Q

In Parkinson’s disease you have too little of the neurotransmitter (blank)

A

dopamine

105
Q

What is amyotrophic lateral sclerosis (ALS)?

A

degeneration of spinal, bulbar and cortical motor neurons

106
Q

What are the clinical manifestations of ALS?

A

muscle weakness, muscle atrophy, fasciculations, spasticity, dysarthria, dysphagia, and respiratory compromise

107
Q

How do you treat ALS?

A

You inhibit glutamate release by blocking NMDA and kainate glutamate receptors, and inhibiting voltage dependent Na+ channels

108
Q

What drug can block NMDA and kainate glutamate receptors and inhibit Na+ voltage gated ion channels and thus inhibit glutamate release? WHat do you use this drug in?

A

Riluzole (rilutek)

ALS

109
Q

What drugs are used to treat the spasticity associated with ALS?

A

Baclofen (Lioresal)

Tizanidine (Zanflex)

110
Q

How does Baclofen (Lioresal) work?

A

A GABA-B receptor agonist (oral or via intrathecal admin)

111
Q

How does Tizanidine (Zanflex) work?

A

an alpha 2 arenergic receptor agonist

112
Q

What is this:

reduced drug effect with repeated use and higher doses required to produce the same effect

A

Tolerance

113
Q

What are some ways you can get tolerance?

A
  • pharmacokinetic i.e altered metabolism (induction)

- physiologic (long term alterations), more or less receptors, messed up synapses

114
Q

What is this:
tolerance to a drug in one class (e.g sedative-hypnotics) will lead to tolerance to others in the SAME class (sedative-hypnotics)

A

Cross-tolerance

115
Q

What is this:
Repeated, compulsive use of a drug that deviates from the social norms of a given culture; disregard of harmful interpersonal or social consequences (e.g ethanol, opiate analgesics, cocaine and other recreational drugs)

A

Dependence

116
Q

What is the psychologic reason behind substance use disorder (SUD)? What is the physiologic?

A
  • drug use primarily to receive rewarding effects; craving (e.g cocaine)
  • drug use to avoid withdrawal
117
Q

What is this:
drugs within a pharmacological class (e.g. opiate analgesics) support individuals physically dependent on other drugs in the same class- useful property for detox

A

Cross-dependence

118
Q

How are drugs ranked?

A

according to abuse potential

119
Q

What is a controlled (scheduled) drug?

A

one whose use and distribution is tightly controlled because of its abuse potential or risk.

120
Q

The drugs with the highest abuse potential are placed in schedule (Blank) and those with the lowest abuse potential are in the schedule (blank)

A

I

V

121
Q

What defines a schedule I drug?

A

-all non-research use illegal under federal law (highest abuse potential)

122
Q

What defines a schedule II drug?

A

-no telephone prescriptions, no refills

123
Q

What defines a schedule III drug?

A

prescription must be rewritten after 6 months or 5 refills

124
Q

What defines a schedule IV drug?

A

prescription must be rewritten after 6 months or 5 refills; differs from schedule III in penalties for illegal possession

125
Q

What defines a schedule V drug?

A

no need for prescription

126
Q

What are the categories of schedule I drugs?

A
  • Stimulants
  • Depressants
  • Hallucinogens
  • Narcotics
  • Marijuana
127
Q

What are some schedule I stimulants?

A

MDMA (ecstacy) and related drugs (MDA,MMDA), mephedrone (bath salts)

128
Q

What are some schedule I depressants?

A

GHB (but approved to treat narcolepsy)

129
Q

What are some schedule I hallucinogens?

A

LSD, STP, DMT, DET, mescaline, peyote, psilocybin, phencyclidine (PCP- angel dust)

130
Q

What are some schedule I narcotics?

A

Heroin and many non-marketed synthetic narcotics (e.g. fentanyl congeners-“china white”)

131
Q

What are the categories of schedule II drugs?

A

Opoids

Stimulants

132
Q

What are the opoids that are schedule II drugs?

A 
morphine
hydromorphone
oxymorphone
oxycodone (dihydroxycodeinone, a component of percodan, percocet)
codeine

designated synthetic drugs: meperidine, methaone, levorphanol, fentanyl

133
Q

What are the schedule II stimulants?

A 
Cocaine
Amphetamine
Amphetamine complex
Amphetamine salts
Dextroamphetamine
Methylphenidate
134
Q

Some drugs can have CNS effects and cause psychiatric symptoms…. what can ACE inhibitors cause?

A

Mania, anxiety, hallucinations, depression, psychosis

135
Q

Some drugs can have CNS effects and cause psychiatric symptoms ….What can acetazolamide cause?

A

depression, delirium, confusion, stupor (elderly very prone)

136
Q

Some drugs can have CNS effects and cause psychiatric symptoms…what can clarithromycin cause?

A

mania

137
Q

Some drugs can have CNS effects and cause psychiatric symptoms…what can digoxin cause?

A

delirium, depression, psychosis, mania, visual hallucinations (elderly at high risk)

138
Q

Some drugs can have CNS effects and cause pyschiatric symptoms….what can mefloquine cause?

A

vivid dreams or nightmares

139
Q

Some drugs can have CNS effects and cause pyschiatric symptoms….what can metronidazole cause?

A

depression, agitation, confusion

140
Q

What are some pharamcokinetic considerations when prescribing CNS drugs?

A
  • Lipophilicity
  • High degree of plasma protein binding
  • Metabolism via the liver
141
Q

What will a high degree of plasma protein binding potential cause with your drugs?

A

displacement of drug

142
Q

What will displacement lead to?

A

increased side effects cuz you have basically increased the effective concentrations of that drug.

143
Q

Whats up with carbomezopene?

A

it metabolizes itself so you have to up the dosage to compensate

144
Q

What are some concerns for prescribing CNS drugs for the elderly?

A
  • dimished hepatic and renal function
  • paradoxical reactions
  • polypharmacy
  • greater susceptibility to SEs (some may be life-threatening)
145
Q

Antipsychotics in elderly patients have a high risk of (blank)

A

death

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