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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
Bromocriptine (Parlodel) considerations
*also used for hyprprolactinemia more so CI: in breast feeding, eclampsia, ergot alkaloid sensitivity, uncontrolled HTN DI: *antihypertensive agents (decrease effectiveness)
26
Ritogotine considerations
*transdermal patch *should not be worn in an MRI machine, can cause skin burns *same AE: as other dopamine agonists, also aplication site reaction
27
Apomorphine (Apokyn)
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
28
nonpharm treatments of parkinsons disease
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
29
evaluation a patiens response to levadopa
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
30
long term complications of levodopa
fluctuations in motor performance wearing off phenomenom, end of dose deteriation peak effect dyskinesia dyskinesia or abnormal involuntary movement
31
when to start L-dopa?
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
motor complications of Parkinson disease and PD treatment
wearing off response peak effect dyskinesia delayed onset off,no on off period dystonia diphsaic dystonia unpredicatble off bebginning of dose deterioration freezing
33
nonmotor complocations of PARkinson disease and PD treatment
psychosis anxiety and depression dementia sleep disturbances somnolenceorthostatic hypotensino sweating episodes sexual dysfunction constipating urinary incontinance
34
mangement of motor complications "on-Off"
On-Off: Increase frequency dosing before choosing to increase dose switch to CR add adjunctive agents such as DA ag/ MAOI/COMT/amantadine
35
mangement of motor complications off- no on
look to see possibledelayed absoprtion take med on empty stomach increase dose, frequence, use ODT a pt w. advance disease sub q apomorphine
36
mangement of motor complications delayed onset
empty stomach, water, avoid protein if on CR, can consider switching off CR or adding IR
37
mangement of motor complications peak efectc dyskenesia
dec dose inc frequency add amantadine use CR sinemet, or switch to DA agonsit(have less risk of bradylinesia)
38
mangement of motor complications dsytonia (painful cramping)
often occurs at early morning give sinement at bedtime
39
mangement of motor complications freezing
increase dose add DA agonist gait modification/ physical therapy
40
management of non motor symptoms depression
pramipexole (clinically useful) SSRI's (possibly useful) venlafaxine (clinically useful)
41
management of non motor symptoms dementia and cognitive impairment
ACH: esterase inhibitors such as Rivastigmine
42
management of non motor symptoms insomnia
eszopiclone melatonin
43
management of non motor symptoms excessive daytime somnelence
modafnil
44
management of non motor symptoms orthostatic hypotension
fluticortisone midodrine droxidopa
45
management of non motor symptoms sexual dysfunction
sildenifil
46
management of non motor symptoms urinary frequency
solifenacin
47
management of non motor symptoms drooling
glycopyrrolate botox
48
apprach to psychosis in PD
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
demntia
syndrome characterized by progrressive decline of intellectual ability from a previous attained level involves varibale deteriation from speech, memory, judgement, and mood
50
what is alzheimers disease
progressive neurodegenerative disease affecting cognition, behavior most common form of dementia
51
AD patho
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
mild signs of AD
memory loss, confusion, trouble handling money, poor judgement, mood changes, and increased anxiety
53
moderate signs of AD
increased memory loss and confusion , problems recognizing ppl, difficulty w. language and thoughts, restlessness, agitation, wandering, and repetitive statements
54
severe AD
extreme shrinkage of the brain wieghtloss, seizures, skin infections, groaning moaning, grunting, increased sleeping, loss of bladder and bowel control
55
differential dx of dementia
alzheimers disease: 70% multi-infarct dementia-10-20%: brain tumors: 5% unkown causes: 10-15%
56
10 warning signs of alzhemiers disease
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
evaluation for AD
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
anticholinergic effects in alzheimers disease
concentrations of acetylcholine are markedly decreased in AD
59
anticholinergic effect
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
other anticholinergic meds
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
non pharm treatment for AD
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
pharm treatment of AD symptoms acetylcholinesterase inhibitors moa: AE
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
pharm treatment of AD symptoms Donepezil considerations
*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
pharm treatment of AD symptoms Rivastigmine (Exelon) considerations
*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
how to switch from rivastigmine capsule to patch
<6mg of oral R.= exelon patch 4.6 mg/24hrs 6-12 of ral R: exelon 9.5 mg/24hrs
66
pharm treatment of AD symptoms Galantamine considerations
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
AChE-I
Donezepil Rivastigmine (Exelon) Galamantine (Razadyne)
68
ACHE-I considerations
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
NMDA receptor antagonists
70
Memantine considerations
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
Namzeric considerations
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
management of confusion, agitation and behaviors
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
emerging therapies for AD
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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