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Pharm > Drugs for CNS Disorders > Flashcards

Drugs for CNS Disorders Flashcards

1
Q

How many different neurotransmitters are in the CNS? How many in the PSNS?

A

21 in CNS
3 in PSNS

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2
Q

CNS functions of acetylcholine

A

memory

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3
Q

CNS functions of dopamine

A

reward circuit
motor control

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4
Q

CNS functions of serotonin

A

digestion
sleep
anxiety
mood
social behavior

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5
Q

CNS functions of histamine

A

wakefulness

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6
Q

CNS functions of glutamate

A

excitation

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7
Q

CNS functions of GABA

A

inhibition (brain primarily)

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8
Q

CNS functions of glycine

A

inhibition (spinal cord primarily)

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9
Q

list examples of adaptive changes

A

cellular atrophy or hypertrophy
metaplasia/dysplasia
alteration in protein synthesis/receptor synthesis

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10
Q

what are adaptive changes

A

changes that cells undergo to cope w/ new environment

occurs in response to prolonged drug exposure

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11
Q

Which two neurotransmitters (NT) does parkinsons involve? Which is decreased in this disease?

A

dopamine (decreased)
acetylcholine (allowed to act unopposed)

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12
Q

What are extrapyramidal side effects (EPS)? What type of drugs elicit these effects?

A

parkinson’s like effects (slowed movement, rigidity, shuffled gait) due to drugs that block dopamine receptors in the CNS

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13
Q

List the drugs that increase dopamine for use in Parkinsons

A

levodopa
MAO-B
amantadine

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14
Q

What is levodopa

A

a precursor to dopamine (is converted to dopamine in the CNS and directly activates dopamine receptors)

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15
Q

List two drugs that augment levodopa

A

decarboxylase inhibitors

COMT inhibitors

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16
Q

How do decarboxylase inhibitors work?

A

*no therapeutic effects of their own!

inhibit levodopa breakdown in peripheral tissues & intestine

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17
Q

How do COMT inhibitors work?

A

*no therapeutic effects of their own

inhibit levodopa breakdown in peripheral tissues & intestine

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18
Q

Besides increasing dopamine, how else is Parkinson’s treated?

A

blocking ACh

restores the ACh/DA balance

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19
Q

Why can we not just give exogenous dopamine?

A

dopamine can’t cross BBB
dopamine has too short of 1/2 life

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20
Q

List a decarboyxlase inhibitor

A

carbidopa

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21
Q

List a COMT inhibitor

A

entacapone

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22
Q

Why should patients on levodopa avoid high protein diets?

A

amino acids compete for transporters to cross the BBB

(thus less levodopa gets to the CNS)

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23
Q

How long does levodopa work for patients?

A

approx 5yrs

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24
Q

adverse effects of levodopa

A
  • N/V
  • dyskinesias
  • postural hypotension
  • psychosis (20%)
  • anxiety/agitation or cognitive changes
  • darkening of sweat/urine
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25
Q

Drug interaction with levodopa

A

MAOI

(severe HTN risk)

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26
Q

List two types of dopamine agonists

A

ergot alkaloids (i.e. bromocriptine, cabergoline)

nonergot alkaloids (i.e. pramipexole, ropinirole, etc.)

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27
Q

Adverse effects of the nonergot alkaloids

A

nausea/vomiting
dizziness
daytime somnolence
constipation
weakness
hallucinations

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28
Q

List three nonergot alkaloid derivatives (dopamine receptor agonists)

A

pramipexole
ropinirole
rotigotine

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29
Q

When is apomorphine used?

A

rescue treatment in episodes of hypomobility with advanced Parkinsons

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30
Q

How do MAO-B inhibitors work?

A

prevent breakdown of dopamine

31
Q

What does MAO-A metabolize?

A

5-HT (serotonin)
NE (norepinephrine)

32
Q

Do MAO-B inhibitors cause hypertension?

A

Not at therapeutic doses - they only inhibit the breakdown of DA.

At higher doses, they lose their selectivity and can cause HTN

33
Q

List two MAO-B inhibitors

A

selegiline
rasagline

34
Q

Adverse effects of MAO-B inhibitors

A

orthostatic hypotension
dizziness
GI symptoms

in high doses = HTN d/t MAO-A inhibition

35
Q

How does amantadine work?

A

Increases DA availability

36
Q

Adverse effects of amantadine

A

CNS = confusion, dizziness, anxiety
peripheral = anticholinergic effects (mild)

long term therapy (>1m) = risk for mottled skin discoloration

37
Q

How do centrally acting anticholinergic drugs work in the treatment of PD?

A

Decreases ACh transmission (restores DA/ACh balance).

38
Q

Adverse effects of centrally acting anticholinergic drugs?

A

CNS = sedation, confusion, hallucinations
peripheral = anticholinergic effects (tachycardia, dry mouth, constipation, etc.)

39
Q

Three drug classes used in Alzheimer’s treatment

A

Acetylcholinesterase inhibitors
NMDA receptor antagonists
2nd generation antipsychotics

40
Q

List acetylcholinesterase inhibitors that are used for Alzheimer’s.

A

donepezil
galantamine
rivastigmine

41
Q

List the NMDA receptor antagonist that is used for Alzheimer’s

42
Q

How do AChE inhibitors work in Alzheimer’s?

A

improve ACh-mediated neurotransmission

can only improve this transmission in nerves that haven’t yet been destroyed.

43
Q

Adverse effects of AChE inhibitors

A

peripheral cholinergic effects (bronchospasm, bradycardia, salivation, diarrhea, etc.)

44
Q

Contraindications for AChE inhibitors

A

COPD/asthma
severe bradycardia or heart block

45
Q

Differentiate between the AChE inhibitors used for Alzheimers

A
  • donepezil = more selective for CNS & highly protein bound
  • rivastigmine = more PNS effects
46
Q

What is the difference between immunomodulators and immunosuppressants?

A

modulators are suppress a more targeted aspect of the immune system versus suppressants suppress the immune system as a whole
- thus suppressants are less safe

47
Q

adverse effects of immunosuppressants

A

bone marrow suppression
heart damage
fetal damage
infections
decrease vaccine response
injection site reactions

48
Q

why do we avoid live vaccines with immunosuppressants?

A

the live vaccine may be a large enough dose to result in systemic infection if the immune system is suppressed

49
Q

adverse effects of immunomodulators

A

hypersensitivity
infections
myelosuppression
liver injury (LFT elevation)
decreased vaccine response
flu-like reactions
depression
injection site reactions

50
Q

What are the differences between traditional and new generation antiseizure drugs?

A

traditional:
- well established
- less well tolerated
- more complex PK
- CYP450 metabolism = drug interactions
- not safe in pregnancy

51
Q

List a few traditional antiseizure drugs

A

phenytoin
fosphenytoin
cabamazepine
valproate
ethosuximide
phenobarbital
primidone

52
Q

List a few new generation antiseizure drugs

A

oxycarbazepine
lamotrigine
gabapentin
pregabalin
levetiracetam
topiramate
tiagabine

53
Q

Worst antiseizure drug to take during pregnancy

54
Q

How does phenytoin work?

A

Na+ channel inhibition in active neurons (i.e. doesn’t depress the ENTIRE CNS, only hyperactive neurons)

55
Q

Why does phenytoin require monitoring of drug levels

A

small increases in doses results in large increases in plasma concentration
(i.e. easy to reach toxic levels with small dose changes)

56
Q

adverse effects of phenytoin

A

CNS = sedation, etc.
gingival hyperplasia
measles-like rash
teratogenic
CV (dysrhythmias & hypotension)
necrosis w/ IV extravasation

57
Q

Three causes of drug interactions with phenytoin

A
  1. phenytoin is a CYP450 inducer (changes concentration of other drugs)
  2. phenytoin is metabolized by CYP450
  3. CNS depression can be amplified w/ other CNS depressants
58
Q

Mechanism of carbamazepine

A

Selective inhibition of Na+ channels

59
Q

Adverse effects of carbamazepine

A

CNS depression
Bone marrow suppression
H2O retention
Rashes + photosensitivity

60
Q

Mechanism of valproic acid

A

GABA enhancement
Selective Na+ inhibition

61
Q

Adverse effects of valproate

A

Pancreatitis
Liver failure
Teratogenesis
Weight gain
Hair loss
Tremor

62
Q

Mechanism of action of ethosuximide

A

Suppression of Ca++ influx

63
Q

Mechanism of action of phenobarbital

A

potentiation of GABA (used more for anesthesia than for antiseizure actions now)

64
Q

Adverse effects of phenobarbital

A

Cns depression
Acute intermittent porphyria
Altered vitamin D metabolism
Physical dependence

65
Q

Other uses for antiseizure medications (besides seizure prevention)

A

Dysrhythmias
Bipolar disorder treatment
Neuralgia
Migraines
Anesthesia
Fibromyalgia pain
Cluster headaches

66
Q

Drugs used to terminate seizures

A

Benzodiazepines
(Lorazepam, diazepam)

67
Q

Mechanism of action of benzodiazepines

A

GABA potentiation

68
Q

Drugs for spasticity

A

Baclofen
Dantrolene
Diazepam
Tizanidine

69
Q

Mechanism of baclofen

A

Mimics GABA at the hyperreflexive motor neurons in spinal cord

70
Q

Mechanism of dantrolene

A

Decreases Ca++ efflux from sarcoplasmic reticulum in muscle cells

(Also used in malignant hyperthermia!)

71
Q

What is a big picture difference between baclofen and dantrolene

A

Baclofen is centrally acting and dantrolene is peripherally acting

(Thus Baclofen doesn’t result in muscle weakness but dantrolene does)

72
Q

Drug used in muscle spasm

A

Cyclobenzaprine

73
Q

Mechanism of cyclobenzaprine

A

Inhibition of neuro transmission in motor neuron pathways in brainstem

74
Q

Drug interactions with cyclobenzaprine

A

ALCOHOL!

MAOIs, TCAs, SSRIs, SNRIs

Pharm (27 decks)

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