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TPX Neuro, Psych, & Sub abuse > Week 4: Parkinsons, Dementia > Flashcards

Week 4: Parkinsons, Dementia Flashcards

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1
Q

parkinsonism

A

any disordewr presenting with classic signs and symptoms; usually secondary to some other factor

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2
Q

parkinson disease

A

idiopathic form of parkinsonism

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3
Q

PAtho of parkinsons disease

A

dopamine deficiency

causes imbalance btw. inhibitory dopamine and excitatory acetylchaline

2 primary patho features:
*loss of dopamine producicing cells in substantia niagara
*formation of lewy bodies in remianing substantia niagara

requires 80% of nigral cell death before disease manifests clinically

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4
Q

dx of parkinsons disease

A

bradykinesia: slowness and difficulty initiating voluntary movement …
and atleats 2 of the following

rigidity: usually begins unilateraly and then progresses
resting tremor
pustural instability: stooped forward

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5
Q

other causes of parkinsonism

A

drug induced: such as APS.

other neurodegenerative conditions

toxins: CO poisening, manganeses, hydrogen sulfide

neoplasms, stroke

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6
Q

bradykinesia

A

early signs may be isolated to distal muscles.

might start out with having trouble writing etc.

facial masking

motor acts become increasingly difficult

freezing can occur

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7
Q

clinical presentations of parkinsons disease besides primary

A

autonimic:
bladder and anal sphincter
constipation
diaphoresis

mental changes:
confusion
dementia
psychosis

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8
Q

main aproaches to parkinsons disease treatment

A

increase endogenous dopamine

decrease cholinergic activity

activate dopamine receptors using synthetic agonists

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9
Q

Anticholinergics used in Parkinsons disease

examples
indication
MOA
AE

A

examples: Benztropine (cogentin), Trihexylphenidyl (artane)

indication: used to decrease tremors in Parkinsons disease

MOA: antimuscuranic

AE: ANTIcholinergic SE
blind as a bat (mydriasis)
dry as a bone: (dry skin)
hot as a hare (fever)
mad as a hatter (depressed/altered mental status)
red as a beet (flushed skin)

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10
Q

MEdications that increase endogenous dopamine

A

Levodopa

Carbidopa

COMT inhibitors

MAOB-I

Amantadine

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11
Q

LEvodopa

examples
dosing
indication
MOA
pk/pd
CI
AE
ddi

A

examples

dosing: start 200-300mg/day in divided doses, 100 BID or TID
indication:

MOA:precursor to dopamine, crosses BBB

pk/pd: extensively broken down in periphery, carbidopa prevents breakdown

CI: breast feeding, closed angle glaucoma, melanoma??

AE:
*dyskenisia: choreiform and dystonic reactions, esp. at high doses or prolonged use
*“on-off phenomena, decreased effectiveness overtime
*GI effects(due to activation of dopamine receptors in the gut)
*orthostatic hypotension
*saliva, sweat, or urine discoloration
*Neuroleptic malignant syndrome (NMS) w. abrucpt d/c

DDI: dopamine antag (metoclopramide, APS)
non selective MAOI’s
high protein intake decrease absorption
iron salts
pyridoxine

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12
Q

Levedopa considerations for parkinsons

A

Gold standard for parkinsons treatment

precursor to dopamine

AE: dyskenesia, decreased efficacy over time, ortho HTN, saliva, sweat, urine discoloration

DDI: dop. antag such as metaclopramide, non selective MAO’s decreased absorp. w. high protein intake, iron salts, pyroxidine

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13
Q

CArbidopa

examples
dosing
indication
MOA
pk/pd
CI
AE
ddi

A

examples: CArbidopa/Levadopa (Sinemet, Sinement CR)

dosing: maintain carbidope dose 70-100mg/day
*available ratios: 1:10 or 1:4

indication

MOA: noncompetative dopa decarboxylase inhibitor: inhibits peripheral l-dopa metabolism

pk/pd: does not cross BB

CI: pregnancy, lactation

AE
ddi

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14
Q

Sinemet CR considerations

A

decrease “off time” and decreased dosing frequency

decreased bioavailability

delayed onset of affect, esp. when taken in morning: time to peak 2hrs vs 30 min for IR: can dose IR and CR in the morning , or set alarm 30-60 min
or can haelp w. morning rigidity if taken at bedtime

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15
Q

Inbrija Considerations

A

levadopa powder for inhalation

indication: used for treatment of off episodes in pts. being treated with sinemet

NOT a replacement

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16
Q

COMT inhibitor considerations

A

moa: prevents breakdown of levadopa

no acitivty in absense of levadopa

Entacapone(Comtan)
*no CI
*same SE as levadopa: dyskenesia, decreased efficacy over time, ortho HTN, saliva, sweat, urine discoloration
*may produce brown/orange urine
stalevo is carbi/levo/enta drug: 1:4:200mg

Tolcapone (Tasmar)
*CI in hepatic disease
*no diff in effectiveness btw. entacapone and it.

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17
Q

MAO-B inhibitors

examples
dosing
indication
MOA
pk/pd
CI
AE
ddi

A

examples: Selegline, Reseligine

dosing
indication: ADJUNCTIVE TO L-dopa for wearing off symptoms
MOA: noncompetitive selective antagonists of monoamine oxidase type b. decreases break down of dopamine. (MAO-A activation causes serious tyramine reactions such as hypertensive crisis, so nonselective maos are not preffered)

pk/pd
CI
AE
ddi

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18
Q

MAO-B considerations

A

selective MAO-B inhibitors
Rasagiline has potential disease-modifying
when used in combo w. L.dopa, pts can reduce ldopa dose

Selegeline:
*active amphetamine metabolites: insomnia, jitteriness, anorexia
CNS, GI
*htn crisis(at higher doses due to loss of selectivity)

Rasageline
*possible disease modifying
*does not have amphetamine metabolites
*CNS and GI symptoms
*orthostasis

New drug: Safinamide (Xadago)
*same SE and CI

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19
Q

Amantadine considerations

A

*Symmetrel, Gocovri, Osmolex)

*poorly understood MOA

*DECREASES L-DOPA INDUCED DYSKENESIA as an add on

*renal adjustment

*precautions: exac. CHF, orthostatic hypotension, peripheral edema

AE:ortho htn,dizziness, falls
hallucinations
anticholinergic AE
NMS w. abrupt
*livedo reticularis-mottling of skin w. LE edema

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20
Q

Drugs that act as dopamine agonists

A
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21
Q

dopamine agonists use considerations

A

can be used as monotherapy esp. in younger, healthier pts.

START LOW AND GO SLOW

reduced risk of developing motor complications liek bradykinesia

can also be used as adjunctive agents in case ofdeteriationin response to l-dopa

*most common N/V, vivid dreams, daytime sedation, orthostatic hypotension, impulsive behaviors and psychosis

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22
Q

List of dopamine agonists

A

pramipexole (Mirapex)
Ropinirole (Requip)
Bromocriptine (Parlodel)
Pergolide (Permax) WITHDRAWN
Cabergoline
Rotigotine
Apomorphine (apokyn)

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23
Q

pramipexole considerations

A

most commmon dopamine agonist
renal adjustment Crcl<60
DI w. cimetidine
START LOW AND GO SLOW with dosing

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24
Q

Ropinirole considerations

A

*cyp1a2 substrate
*IR&ER formulation

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25
Q

Bromocriptine (Parlodel) considerations

A

*also used for hyprprolactinemia more so
CI: in breast feeding, eclampsia, ergot alkaloid sensitivity, uncontrolled HTN
DI: *antihypertensive agents (decrease effectiveness)

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26
Q

Ritogotine considerations

A

*transdermal patch
*should not be worn in an MRI machine, can cause skin burns
*same AE: as other dopamine agonists, also aplication site reaction

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27
Q

Apomorphine (Apokyn)

A

used in advanced parkinson disease prn for off episodes

needs a 2 mg test dose under medical supervision
monitor BP predose, and 20,40,min and 60 min

*pretreat with antiemetic 3 days before and continue for 2 months. NOT 5HT3 ANTAGONISTS OR ANTIDOPAMINERGIC. CONTRAINDICATEDDDD

*can cause qt prolongation: added

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28
Q

nonpharm treatments of parkinsons disease

A

phsyical therapy and exercise (boxing and tai chi)

surgery:deep brain stimulation

adequate fluids and fiber can prveent constipation
omega-3 fatty acids

accupational therapy and fall precautions

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29
Q

evaluation a patiens response to levadopa

A

stage I: patient not aware of variation in the effect of an individual dose

stage II: midafternnoon loff of benefit requirs additional dose

stage 3: good response to levadopa, sleep benefit is lost eaely morning akinesia appears

stage 4: regular “wearing off” q4hrs or more hours then levodopa response gradually worsens

stage 5: wearing off from each dose of levodopa as well as abrupt “off periods’ pts require dosing at intervals of 2 hrs or less

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30
Q

long term complications of levodopa

A

fluctuations in motor performance

wearing off phenomenom, end of dose deteriation

peak effect dyskinesia

dyskinesia or abnormal involuntary movement

31
Q

when to start L-dopa?

A

controversy

l.dopa therapy associated w. motor complications,

not a clear reference on whether or not to delay ldopa initaition as much as possible until its absolutely needed , or use it early on due to great benefits and relatively inexpensive

32
Q

motor complications of Parkinson disease and PD treatment

A

wearing off response

peak effect dyskinesia

delayed onset

off,no on

off period dystonia

diphsaic dystonia

unpredicatble off

bebginning of dose deterioration

freezing

33
Q

nonmotor complocations of PARkinson disease and PD treatment

A

psychosis

anxiety and depression

dementia

sleep disturbances

somnolenceorthostatic hypotensino

sweating episodes

sexual dysfunction

constipating

urinary incontinance

34
Q

mangement of motor complications

“on-Off”

A

On-Off: Increase frequency dosing before choosing to increase dose

switch to CR

add adjunctive agents such as DA ag/ MAOI/COMT/amantadine

35
Q

mangement of motor complications

off- no on

A

look to see possibledelayed absoprtion

take med on empty stomach

increase dose, frequence,

use ODT

a pt w. advance disease

sub q apomorphine

36
Q

mangement of motor complications

delayed onset

A

empty stomach, water, avoid protein

if on CR, can consider switching off CR or adding IR

37
Q

mangement of motor complications

peak efectc dyskenesia

A

dec dose

inc frequency

add amantadine

use CR sinemet, or switch to DA agonsit(have less risk of bradylinesia)

38
Q

mangement of motor complications

dsytonia (painful cramping)

A

often occurs at early morning

give sinement at bedtime

39
Q

mangement of motor complications

freezing

A

increase dose
add DA agonist
gait modification/ physical therapy

40
Q

management of non motor symptoms

depression

A

pramipexole (clinically useful)

SSRI’s (possibly useful)

venlafaxine (clinically useful)

41
Q

management of non motor symptoms

dementia and cognitive impairment

A

ACH: esterase inhibitors such as Rivastigmine

42
Q

management of non motor symptoms

insomnia

A

eszopiclone

melatonin

43
Q

management of non motor symptoms
excessive daytime somnelence

A

modafnil

44
Q

management of non motor symptoms
orthostatic hypotension

A

fluticortisone

midodrine

droxidopa

45
Q

management of non motor symptoms
sexual dysfunction

A

sildenifil

46
Q

management of non motor symptoms
urinary frequency

A

solifenacin

47
Q

management of non motor symptoms
drooling

A

glycopyrrolate

botox

48
Q

apprach to psychosis in PD

A
  1. evaluate hypoxemia, infection, electrolyte disturbance
  2. simplify regimen
    *d/c meds w. highest risk such ass…
    a. anticholinergics (benztropine, oxybutinin)
    b.taper and d/c amantadine (abrupt withdrawal can cause delerium
    c)selegiline (from amphetamine like metabolites)
    d. taper and d/c agonists
    consider d/c l.dopa

3.consider atypical APS such as
*quetiapine
clozapine
pimavanserin tartrate (nuplazid): specifically indicated for parkinsons related psychosis. inverse agonist of 5HT2A/2C
BBW: increased death in elderly in pts. with dementia

49
Q

demntia

A

syndrome characterized by progrressive decline of intellectual ability from a previous attained level

involves varibale deteriation from speech, memory, judgement, and mood

50
Q

what is alzheimers disease

A

progressive neurodegenerative disease affecting cognition, behavior

most common form of dementia

51
Q

AD patho

A

brain atrophy with ventricular enlargement

degeration of cholinergic and other neurons

absent or minimal vascular disease

signs of AD are first noticed in the entorhinal cortex, then proceed to the hippocampus

memoryloss is the first sign of AD

anyloid plaques and neurofibrillary tangles form as well

52
Q

mild signs of AD

A

memory loss, confusion, trouble handling money, poor judgement, mood changes, and increased anxiety

53
Q

moderate signs of AD

A

increased memory loss and confusion , problems recognizing ppl, difficulty w. language and thoughts, restlessness, agitation, wandering, and repetitive statements

54
Q

severe AD

A

extreme shrinkage of the brain

wieghtloss, seizures, skin infections, groaning moaning, grunting, increased sleeping, loss of bladder and bowel control

55
Q

differential dx of dementia

A

alzheimers disease: 70%

multi-infarct dementia-10-20%:

brain tumors: 5%

unkown causes: 10-15%

56
Q

10 warning signs of alzhemiers disease

A

problems w. words in speaking or writing

misplacing things and losing ability to retrace steps

decreased poor judgement

withdrawal from work or social acitivites

changes in mood or personality

memory loss that disrupts daily life

challenges in plNNING or solving problems

difficulty completing familiar tasks

confusion with time or place

problems w. visual images and spatial relationships

57
Q

evaluation for AD

A
  1. history
  2. physical and neurologic examinations
  3. screening lab studies (CBC, chem panel, TSH, syphillis, UA, b12 and folate levels, chest xray, EKG, CT scan
  4. neuroimaging (MRI OR CT)- MRI superior. used to rule out other sources of cholinergic hypothesis
58
Q

anticholinergic effects in alzheimers disease

A

concentrations of acetylcholine are markedly decreased in AD

59
Q

anticholinergic effect

A

blind as a bat (mydriasis)

dry as a bone (dry skin and mouth)

hot as a hare (fever)

mad as a hatter (depressed/agitated mental status)

red as a beet (flushed skin)

60
Q

other anticholinergic meds

A

Sleep medications (diphenhydramine)
* Antihistamines (diphenhydramine)
* Certain bladder medications (oxybutynin)
* Certain pain medications (codeine)
* Antiemetics/antivertigo (meclizine, scopolamine, promethazine,
prochlorperazine)
* Medications for Parkinson’s disease (benztropine, trihexphenidyl)
* Gastrointestinal (GI) antispasmotics (belladonna, clindinium,
hyoscyamine, scopolamine)
* Tricyclic antidepressants (TCAs) (cyclobenzaprine, amitriptyline)
* Typical antipsychotics (chlorpromazine, thioridazine)
* Atypical antipsychotics (clozapine)

61
Q

non pharm treatment for AD

A

comprehensive techniques (memory books)

environmental adaptations

case manegement

exercise programs, occupatinoal therapy

psych education/ psychotherapeutic approaches, cognitive rehabilitation

caregiver support groups, counseling

alzheimers association

the 36 hr day

respite/day care

advanced directives, power of attorney, living will, DNR orders, healthcare proxy

62
Q

pharm treatment of AD symptoms

acetylcholinesterase inhibitors
moa:
AE

A

moa: block acetylcholinesterase, block metabolism of Ach

AE:
cholinergic SE:
SLUDGE
siallorhea
LAcrimation
urination
defacation
GI(emesis, diarrhea)
Emesis

cns: headahce, insomnia, vivid dreams
cardiac: bradycardia, syncope, heartblock, hypotension
CI: in pts with bradycardia/ known conduction system disease

63
Q

pharm treatment of AD symptoms

Donepezil considerations

A

*cns selective noncompetative, reversible AchE-i
for mild-severe

indicated for all 3 stages of AD (mild mod. severe)

1 tab @bedtime w. or w.o food

met. by 2d6 and 3a4

lmost likely to be titrated to max dose and least likely to be d/c due to cost

less likely to cause GI effects and more likely to cause sleep sleep disturbances

64
Q

pharm treatment of AD symptoms

Rivastigmine (Exelon) considerations

A

*cns selective, non competitve reversible ACHEi

*available in capsules and patches

poor tolerabi;oity

capsule:must start low and titrated slowly to prevent gi disturbances
start at 1.5 mg bid, increase 3 mg q2w

patch dosed 4.6 mg/24 hrs initially and hsould be increased to 9.5 mg/24hrs

can cause site reactions, rotate patch. can be used chest, upper and lower back and upper arms

higher rates of d/c

65
Q

how to switch from rivastigmine capsule to patch

A

<6mg of oral R.= exelon patch 4.6 mg/24hrs

6-12 of ral R: exelon 9.5 mg/24hrs

66
Q

pharm treatment of AD symptoms

Galantamine considerations

A

cns selective competitive reversible ache-i; modulates nicotinic ach receptor to increase ach from surviging presynaptic nerve

available in tablet, ER capsule, solution

metabolized by cyp2d6 and 3a4

67
Q

AChE-I

A

Donezepil

Rivastigmine (Exelon)

Galamantine (Razadyne)

68
Q

ACHE-I considerations

A

d/c other anticholinergic drugs

slection based on ease of use, individual tolerability, cost and pt preference

not disease modifying, just for symptomatic improvement

69
Q

NMDA receptor antagonists

A
70
Q

Memantine considerations

A

NMDA receptor antagonists: nmda sustained low level activation in AD cause neuronal damage and loss, and cholinergic deficit

approved for mod-severe stages

NOT disease modifying

use in caution w. pts with seizure disorders or CV disorders

IR dose :
initial 5 mg: 5mg/wek titration
target dose 20 mg

ER:
start 7 mg
target dose: 28 mg: tmg/day titration’

if renal impairment (5-29mL/min): IR: MDD 5 mg bid
ER: target dose 14 mg qd

AE: cv effects
constipation

71
Q

Namzeric considerations

A

Memantine ER+donezepil

taken in evening w. or w.o food

do not divide/crush/chew

pts must be on donezepil 10 mg to be eligible for this combo

72
Q

management of confusion, agitation and behaviors

A

non pharm:
*provide structure and routine
*follow regular predicatable routines
*encourage pleasant activities
participate in activities they used to enjoy
keep things simple

pharm treatment

behaviors
*non drug approaches
*antidepressants, anxiolytics, APS, AED

sleep changes
*TCA’s, benzos, sedative/hypnotics, APS

avoid anticholinergic, benzos, sedative hypnotics

73
Q

emerging therapies for AD

A

Riluzole: small gutamatergic agent.

antisense technology: IONIS-MAPTRX reduce tau protein production, to decrease

antiinflammatory agents

TPX Neuro, Psych, & Sub abuse (7 decks)

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