Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm II > Dementia Meds > Flashcards

Dementia Meds Flashcards

1
Q

ssxs of dementia?

A

severe impairment in intellectual abilities (memory loss, areas of cognition including attention, language skills and problem solving)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how to dx dementia?

A

ssxs of cognitive dysfxn have to present for at least 6 mos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

is dementia a normal consequence of aging?

A

NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what needs to be addressed when a pt presents w/dementia/delirium?

A

neuro, vascular, endocrine, nutritional, infection, metabolism, trauma, toxicity
careful hx and PE as well as lab tests

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

supplementation w/what vitamin may be beneficial in preventing or diminishing dementia? how? potential risk?

A

Vit E
lowers free radical formation and ROS in the brain which may be neuroprotective
potential risk is that when given over 2000 IU of Vit E there is an increased risk for thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

three OTC meds that were explored as alternatives to prevent dementia?

A

NSAIDS
estrogen
statins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

labs to workup dementia? imaging?

A

labs: CBC, CMP (electrolytes, Ca2+, renal fxn, liver enzymes), thyroid tests, Vit B12, folic acid levels
imaging: CT, MRI, SPECT scan or PET scan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

MC causes of dementia?

A

alzheimer’s dz
parkinson’s dz
dementia w/lewy bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

dementia w/lewy bodies is characterized by what?

A

presence of lewy bodies which are clumps of alpha-synuclein and ubiquitin proteins in neurons
dx is usu only through post-mortem brain biopsies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

DLB is more associated with what dz?

A

Parkinson’s over alzheimer’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what do you lose in DLB, this leads to what? how does this differ from what happens in Alzheimer’s?

A

in DLB you lose cholinergic (Ach producing) neurons which is though to lead to the degradation of cognitive fxn (Alzheimer’s)
where as in Parkinson’s dz you lose dopaminergic neurons and this is thought to be the cause of the loss of motor control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

does DLB appear slowly or quickly?

A

quick in onset usually

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

current approved meds for tx of Alzheimer’s?

A

AChE inhibitors, donepezil, galantamine, rivastigmine for mild to moderate AD
memantine (NMDA receptor partial antagonist) for moderate to severe AD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

selectivity of doneprezil, rivastigmine and galantamine?

A

donepezil has higher selectivity for AChE
rivastigmine inhibits butyrylcholinesterase as well as AChE inhibitors
galantamine also effects nicotinic receptors as well as AChE inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

SE of anticholinergic meds?

A

commonly cause memory impairment and confusion (thus why AChE inhibitors can be used to tx AD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

when treating AD and PD, tx themselves can cause what?

A

when treating the movement portion of PD, hallucinations and psychosis can worsen
while when treating the hallucinations and psychosis of AD it can worsen PD sxs

17
Q

AChE inhibition leads to what?

A

results in increased ACh in synaptic cleft = brain has enhanced cholinergic transmission which can help to reduce the ssxs of Alzheimer’s dementia

18
Q

approved uses of AChE inhibitors?

A

AD
DLB
myasthenia gravis
antidote to anti-cholinergic poisoning as can occur with organophosphate poisoning and nerve gas exposure

19
Q

actions of AChE inhibitors on autonomic NS?

A

potent parasympathetic effects such as bradycardia, hypotension, increased urination, increased lacrimation, bronchoconstriction, GI tract hypermotility, N/V

20
Q

what does SLUDGEM stand for? applicable to what?

A 
Salivation
Lacrimation
Urination
Defecation
GI upset
Emesis
Miosis (pinpoint pupils)
mnemonic to remember what acetylcholine causes
21
Q

action of donepezil/aricept? main therapeutic use? off-label use? useful SEs? solubility? half life?

A

action: centrally acting reversible acetylcholinesterase inhibitor
main therapeutic use: AD (increases cortical ACh)
off-label: cognitive d/os including DLB and vascular dementia
useful SE: has been shown to improve sleep apnea in AD pts; possibly improves and increases vocabulary and expressive language of children with autism
easily crosses BBB, half life of ~70hrs so take once a day

22
Q

SEs of donepezil/aricept?

A

most commonly experience bradycardia, N/D, anorexia, abd pn, vivid dreams

23
Q

MOA of rivastigmine/exelon? approved for tx of what to do what? administration?

A

MOA: centrally acting reversible acetylcholinesterase inhibitor
approved to tx mild to moderate dementia dt AD/PD, has shown to provide meaningful symptomatic effects in these pts
can administer via orally or transdermal patch (scapulae, lower back, deltoids or pecs)

24
Q

rivastigmine/exelon is particularly effective in treating what pt population? proposed MOA of this?

A

those w/a more aggressive course of the disease such as w/younger onset, poor nutritional status or those experiencing sxs such as delusions or hallucinations
proposed that these effects might be dt additional inhibition of butyrylcholinesterase which has been implicated in symptom progression

25
Q

rivastigmine/exelon can potentially be used for what? SEs?

A

could potentially be used in those w/schizophrenia b/c of potential butyrylcholinesterase activity
SEs: N/V, dizziness, diarrhea, H/A, anorexia, abd pn (uncommonly decreased wt, insomnia, anxiety, asthenia, vertigo, fatigue)

26
Q

use of galantamine/razadyne? indications?

A

indicated for AD and mild to moderate vascular dementia
can be used w/other cholinergics and anticholinergics such as Huperzine A; has been used as a “brain enhancer” to improve memory in brain-damaged adults

27
Q

overdose of ACh-ase inhibiting drugs can cause what SEs? antidote?

A

N/V, salivation, sweating, bradycardia, hypotension, convulsions, circulatory collapse
antidote is atropine (acteylcholinesterase)

28
Q

is there definitive proof that donepezil or similar agents alter AD course? what can you add to donepezil to enhance effects?

A

NO
but there is evidence suggesting that these drugs can delay the course of AD ssxs
can add memantine - has been shown to improve cognition, functioning and behavior

29
Q

rivastigmine/exelon can potentially be used for what? SEs?

A

could potentially be used in those w/schizophrenia b/c of potential butyrylcholinesterase activity
SEs: N/V, dizziness, diarrhea, H/A, anorexia, abd pn (uncommonly decreased wt, insomnia, anxiety, asthenia, vertigo, fatigue)

30
Q

MOA of memantine/namenda? other effects?

A

blocks NMDA glutamate receptors; antagonist of glutamatergic NMDA receptor sites
by binding to nMDA receptors it inhibits the prolonged influx of Ca2+ which appears to play an important role in neuronal excitotoxicity
other effects: non-competitive antagonist at 5HT3 receptor with a potency similar to that for the NMDA receptor; non-competitive antagonist at different neuronal nicotinic acetylcholine receptors similar to 5HT3 and NMDA sites; D2 receptor agonist

31
Q

what happens to # of nicotinic receptors in pts w/AD?

A

of nicotinic receptors decreases in AD pts (thus why we can target them)

32
Q

all the site memantine/namenda acts on?

A

non-competitive antagonist at 5H3 receptor
agonist at dopamine D2 receptor site
antagonist at nicotinic acetylcholine receptor sites
blocks NMDA glutamate receptors

33
Q

abn functioning of what neurotransmission is hypothesized to also contribute to AD etiology? how does it work? drug ex?

A

glutamatergic neurotransmission
so targeting glutamatergic system, specifically NMDA receptors is a new approach to treating AD
memantine is the 1st drug which acts to block NMDA glutamate receptors

34
Q

MOA of memantine/namenda? secondary effects?

A

blocks NMDA glutamate receptors; antagonist of glutamatergic NMDA receptor sites
by binding to nMDA receptors it inhibits the prolonged influx of Ca2+ which appears to play an important role in neuronal excitotoxicity
secondary effects: non-competitive antagonist at 5HT3 receptor with a potency similar to that for the NMDA receptor

35
Q

what happens to # of nicotinic receptors in pts w/AD?

A

of nicotinic receptors decreases in AD pts (thus why we can target them)

36
Q

all the site memantine/namenda acts on?

A

non-competitive antagonist at 5H3 receptor
agonist at dopamine D2 receptor site
antagonist at nicotinic acetylcholine receptor sites
blocks NMDA glutamate receptors

37
Q

SEs of memantine/namenda? possible other indications for its use? (+) SEs of memantine/namenda?

A

confusion, dizziness, drowsiness, insomnia, H/A, agitation, hallucinations (less common = vomiting, anxiety, increased libido)
can possibly be used to reverse neurological impairment associated with MS
(+) SEs: positive effect on cognition, mood, behavior, ability to perform ADLs in moderate to severe AD

Pharm II (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions