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Neurology-Week 4 & 5 > Drugs-Dementia > Flashcards

Drugs-Dementia Flashcards

1
Q

An autosomal dominant genetic disorder in which mutations in the Huntingtin protein allow it to damage and progressively kill neurons in the brain; characterized by jerking or writhing movements (chorea), muscle problems, dystonia, etc.

A

Huntington Disease

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2
Q

The movement symptoms of HD is due to ____________ pathway that connects substantial nigra to the striatum.

A

nigrostriatal dopaminergic

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3
Q

Early-stage HD is characterized by an increased _______

A

dopamine

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4
Q

Examples of dopamine-depleting drugs

A

Tetrabenazine

Deutetrabenazine

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5
Q

drug that reduce the amount of dopamine that is released by nigrostriatal neurons by inhibiting the vesicular monoamine transporter (vMAT), which transports DA into presynaptic vesicles.

A

DA-depleting drugs (Tetrabenazine, Deutetrabenazine)

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6
Q

Examples of dopamine antagonists

A

Aripiprazole

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7
Q

Drug that directly compete with dopamine (DA) for binding to DA receptors on the post-synaptic cells

A

Dopamine antagonists (Aripiprazole)

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8
Q

Drugs that are also atypical 2nd generation anti-psychotics and may also treat agitation and psychosis associated with HD

A

Aripiprazole

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9
Q

Atypical 2nd generation anti-psychotics can antagonize several other, non-therapeutic receptors and can lead to other toxicities.

Antagonizing Ach receptors (M2/3) can cause

A

Constipation
Xerostomia
Urinary Retention
Blurred vision

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10
Q

Atypical 2nd generation anti-psychotics can antagonize several other, non-therapeutic receptors and can lead to other toxicities.

Antagonizing NE receptor (a1) can cause

A

Orthostatic hypotention

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11
Q

Atypical 2nd generation anti-psychotics can antagonize several other, non-therapeutic receptors and can lead to other toxicities.

Antagonizing histamine (H1) can cause

A

Sedation

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12
Q

Atypical 2nd generation anti-psychotics can antagonize several other, non-therapeutic receptors and can lead to other toxicities.

Antagonizing K+ channels can cause

A

P-QT sudden death

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13
Q

Atypical 2nd generation anti-psychotics can antagonize several other, non-therapeutic receptors and can lead to other toxicities.

Antagonizing Dopamine receptors (D2) beyond therapeutic effects can lead to toxic effects such as

A 
EPS
NMS
Gynecomastia
Amenorrhea
Sexual Dys.
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14
Q

Atypical 2nd generation anti-psychotics can antagonize several other, non-therapeutic receptors and can lead to other toxicities.

Antagonizing serotonin receptors (5-HT) beyond therapeutic effects can lead to toxic effects such as

A

Metabolic syndromes (weight gain, hyperglycemia, hyperlipidemia, type 2 DM)

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15
Q

A dementia disorder caused by a progressive loss of dopaminergic neurons in the nigrostriatal pathway

A

Parkinsons’ Disease

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16
Q

Examples of DA precursor drug

A

Levodopa (L-DOPA)

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17
Q

Drug that is an intermediate in the biosynthesis of DA that can cross the BBB and enter remaining nigrostriatal neurons, where it gets converted into DA by DOPA decarboxylase (DDC)

A

Levodopa (L-DOPA)

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18
Q

What enzyme converts levodopa into dopamine in peripheral tissues?

A

DOPA decarboxylase (DDC)

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19
Q

An inhibitor of DDC; co-administered with levodopa to increase the amount of drug that reaches the brain for conversion into DA; itself doesn’t cross the BBB

A

Carbidopa

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20
Q

COMT inhibitors; typically added only after the therapeutic effects of levodopa + carbidopa begin to fluctuate or wear off following YEARS of use

A

Entacapone

Tolcapone

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21
Q

The phenomenon which results from the fact that there are fewer neurons available in later stages of the disease to convert levodopa to dopamine and store it as a neurotransmitter

A

“Wearing off” phenomenon of levodopa (+carbidopa)

22
Q

Dyskinesia that follows hours of each dose of levodopa during the wearing off phase; it’s a toxicity from a long-term use of levodopa

A

levodopa-induced dyskinesia (LID)

23
Q

Other toxicities of levodopa; can be exacerbated with the addition of COMT inhibitor

A

Nausea/vomiting
Orthostatic hypotension (at the beginning of therapy)
Psychosis

24
Q

Toxicities caused by COMT inhibitors alone

A

Diarrhea

25
Q

Toxicities caused by only tolcapone

A

Hepatotoxicity

26
Q

Combination of levodopa with ______ can increase dopamine synthesis while also inhibiting its breakdown, which could increase levels of DA to a danger point

A

Non-selective MAOIs

27
Q

Examples of DA agonists

A

Bromocriptine
Pramipexole
Ropinirole

28
Q

Drugs that directly substitute for DA and binds to DA receptors in the striatum in both direct and indirect pathways

A

DA agonists (Bromocriptine, Pramipexole, Ropinirole)

29
Q

What drug causes a suppression of prolactin secretion from pituitary gland?

A

Bromocriptine (only this drug)

30
Q

Normally, DA released from ___________ pathway inhibits prolactin secretion

A

Tuberoinfundibular

31
Q

B/c of its prolactin secretion suppression toxicity, Bromocriptine can treat

A

prolactinomas

32
Q

What drug causes a cardiac valve fibrosis making it a less preferred drug to treat PD these days?

A

Bromocriptine

33
Q

Toxicities of Pramipexole and ropinirole

A

Sedation
Somnolence
Sleep Attacks

34
Q

Drugs that block the breakdown of DA in neurons and increase its release

A

Monoamine Oxidase B inhibitors (MAOB inhibitors)

35
Q

Examples of MAOB inhibitors

A

Selegiline

Rasagiline

36
Q

An antiviral drug that was initially used to tx influenze in the past; Currently used to treat EARLY-stage PD

A

Amantadine

37
Q

Hypothesized moa of Amantadine

A
  1. Stimulates the release of DA from nigrostriatal neurons
  2. Act as an anticholinergic
  3. Act as an antagonist of glutamate signaling in direct and indirect pathways
38
Q

Toxicities of Amantadine

A

Dizziness
Insomnia
Somnolence
Hallucinations

39
Q

Competitive Ach antagonists; act at the synapses of striatal cholinergic interneurons to reduce their contributions to the direct and indirect pathways; DO NOT affect the DP levels in treating PD; DO NOT act within the nigrostriatal pathway

A

anti-cholinergics (Benztropine, Trihexiphenidyl)

40
Q

Toxicities of anti-cholinergics

A

Anti-parasympathetic toxicities

  • Dry Mouth
  • Tachycardia
  • Constipation
  • Urinary Retention
41
Q

Drugs to treat mild symptoms of PD

A
  1. MAOIs
  2. Amantadine
  3. Anti-cholinergic (<65)
  • Anti-cholinergic must be AVOIDED in older pts due to their parasympathetic toxicities.
42
Q

Drugs to treat mild to moderate symptoms of PD

A
  1. Levodopa/carbidopa
  2. DA agonist (<65)
  • DA agonist must be AVOIDED in older pts.
43
Q

Drugs to treat moderate to severe symptoms of PD

A

Levodopa/carbidopa + DA agonist

OR

Levodopa/carbidopa + MAOI

44
Q

Drugs to treat cognitive symptoms, especially DLB (dementia with lewy bodies); also used to treat cognitive symptoms of PD and AD (Alzheimer’s disease) as well

A

Cholinesterase inhibitor (Donepezil, Galantamine, Rivastigmine)

GDR
(Get Dementia Right/corrected)

45
Q

(True/False) the same drugs to treat PD can be used to treat parkinson-like movement symptoms in DLB

A

True

46
Q

Drugs that block the normal degradation of Ach at the synapse following its release

A

Cholinesterase inhibitor (Donepezil, Galantamine, Rivastigmine)

47
Q

Toxicities of Cholinesterase inhibitors

A
  1. Parasympathetic CARDIAC effects
    - Arrythmias
    - Bradycardia
    - Syncope
  2. Insomnia
  3. Vivid dreams
48
Q

What drugs must NOT be coadministered with AV-blocking drugs (B-blockers, Ca+2 channel blockers) due to its parasympathetic cardiac toxicity?

A

Cholinesterase inhibitor (Donepezil, Galantamine, Rivastigmine)

49
Q

For AD, what Cholinesterase inhibitor drugs are used for mild-moderate symptoms?

A

Galantamine

Rivastigmine

50
Q

What Cholinesterase inhibitor drugs are used for all stages of AD tx?

A

Donepezil

51
Q

Drug to tx AD; acts as competitive glutamate antagonist; inhibits neuronal death caused by extra-synaptic glutamate receptors in the post-synaptic neurons to slow disease progression

A

Memantine

52
Q

A monoclonal antibody that targets the extracellular AD amyloid beta plaques but has NO effect on tau protein tangles; DOES NOT slow the cognitive decline

A

Aducanumab

Neurology-Week 4 & 5 (14 decks)

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