Neuro exam 1 Flashcards

1
Q

Physiological mechanism of migraine

A

trigger event -> cortical spreading depression:
trigeminal nerve -> vasodilation and pain OR
inferior subcortex -> no aura OR
surface cortex -> aura

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

Blood vessel abnormalities are a component of vascular headaches such as ________ and ________ headaches

A

migraine
cluster

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

______ play a critical role in vascular headaches involving nerves

A

5-HT

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

What does a low 5-HT level cause

A

migraine, it reduces urinary and platelet 5-HT w/ elevations in 5-hydroxyindole acetic acid during mirgraine

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

Where are the 5-HT1B receptors located

A

endothelium of the micro vessels and mediate vasodilatory and contractile effects

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

How does 5-HT receptors act in the meninges

A

block the release of inflammatory chemical

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

How does 5-HT receptors act in the brainstem

A

block the pain impulses and central brain perception via trigeminal nerve

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

Sumatriptan (5-HT1B receptor agonist) MOA

A

inhibits the release of calcitonin gene-related peptide (CGRP) which acts in the superior sagittal sinus following stimulation of trigeminal ganglion

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

What are the 5-HT1B/1D agonists

A

Triptans
sumatriptan, zolmitriptan, naratriptan, rizatriptan
produce vasoconstriction
not for prophylatic treatment

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

5-HT2 receptor antagonists

A

methysergide
used for prophylatic measure

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

ADE of triptans

A

cardiac effects (vasospasm, myocardial ischemia, arrhythmias in pt with coronary artery disease)
pain at inj site
paresthesia, asthenia, fatigue, flushing, pressure in chest, neck, jaw, drowsiness, dizziness

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

Triptans contrindications

A

pt with coronary artery disease, ischemia, or cerebrovascular disease
pt taking MAO-I

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

How does ergotamine and caffeine help migraines

A

ergotamine: block NE reuptake and stimulates adrenergic receptors, activates serotonin pathways, reduces intracranial blood flow
caffeine: adenosine receptor antagonist

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

Reyvow (lasmiditan) use in migraines

A

acute tx w/ or w/out aura not preventative

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

Reyvow (lasmiditan) MOA

A

bind to 5-HT1F receptors, mediated by agonist effects at the receptor

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

Reyvow (lasmiditan) ADE

A

dizziness, fatigue, burning or prickling sensation in the skin, sedation
serotonin syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Increased comorbidity with migraine

A

stroke, epilepsy, depression, sleep apnea, obesity, anxiety, pain disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Pathophysiology of migraine headaches

A

vasodilation of intracranial extracerebral blood vessels -> activation of perivascular trigeminal nerves that release vasoactive neuropeptides
CGRP, neurokinin A, substance P

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Vasoactive neuropeptides promote ________ _________ around vascular structures in the brain -> pain

A

neurogenic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Associated symptoms of central pain transmission that activate other brainstem nuclei

A

nausea, vomiting, photophobia, phonophobia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Medications that can precipitate a migraine headache

A

antibiotics (tetracyclines, SMZ,TMP)
NSAIDs
bronchodilators (theophylline, pse)
GI (cimetidine, omeprazole)
CV (vasodilators, nitrates, dipyridamole)
Reproductive (estrogen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Clinical Presentation of migraine headache

A

common, recurrent, severe headache that interferes w/ normal functioning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is aura

A

complex of positive and negative focal neurologic symptoms that proceed or accompany an attack
evolves over 5 min and lasts less than 60 minutes
headache occurs w/in 60 min of the end of the aura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Positive visual auras

A

scintillations (flash of light)
photopsia (perceived flashes of light)
teichopsia (transient sensation of bright shimmering colors)
fortification spectrum (zigzag banding of light)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Negative visual auras

A

scotoma (partial loss of vision or blind spot)
hemianopsia (blindness over half the field)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Sensory and motor auras

A

paresthesias or numbness in the arms and face
dysphasia or aphasia
weakness
hemiparesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Symptoms of migraine headaches

A

recurring episodes of throbbing head pain. frequently unilateral, lasting 4-72 hours is left untreated
associated w/ n/v, sensitivity to light, sounds, movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Diagnostic alarms for migraine headaches

A

acute onset of first or worst headache ever
accelerating pattern of headache following subacute onset
onset of headache after age 50
headache w/ systemic illness (fever, N/V, stiff neck, rash)
headache w/ focal neurologic sx or papilledema
new-onset headache in pt w/ cancer or HIV infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Signs of migraine headaches

A

stable pattern, absence of daily headache
positive family history for migraine
normal neurologic examination
food and menstruation mat serve as triggers
improvement in headache w/ sleep
aura can signal migraine headache but not required for diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Diagnosis for migraine without aura

A

at least 5 attacks (POUND)
Pulsating
One day duration
Unilateral location
Nausea, vomiting, photophobia, phonophobia
Disabling intensity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Diagnosis for migraine with aura

A

at least 2 attacks
migraine aura fulfills criteria for typical aura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Diagnosis for typical aura

A

Full reversible visual, sensory, speech symptoms but no motor weakness
Visual symptoms including positive features or negative features, or unilateral sensory symptoms, or any combo
At least two:
1 sx that develops over 5 minutes
Each symptoms lasts for 5-60 min
Headache that meets criteria for migraine w/out aura begins during the aura or follows aura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Episodic vs chronic headache migraine

A

epi: 0-14 months MHD (monthly migraine headache days)
chronic: >15 months MDHs for at least 3 months where at least 8 are migraines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Goals for long-term migraine tx

A

reduce migraine frequency, severity, and disability
improve qol
prevent headache
educate and enable pt to manage their disease
reduce headache-related distress and physiological sx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Goals for acute migraine treatment

A

tx migraine attacks rapidly w/out recurrence
restore the pt ability to function
minimize the use of backup and rescue meds
optimize self-care for overall management
cost-effective in management
cause minimal or no adverse effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is medication overuse headache

A

frequent use of migraine med increase headache frequency
headache returns when med wears off leading to more meds
limit use to <10 d per month

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

When to consider preventative migraine therapies

A

recurring migraines that produce disability
frequent attacks occurring more than 2x per week
sx therapies are ineffective or contraindicated
pt preference to limit number of attacks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Max benefit of migraine meds is __ months while continuing med for ___ to ___ months with a gradual taper

A

6
6 to 12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

nonpharm tx for migraine

A

ice
sleep in dark, quiet environment
exercise, eating habits, smoking cessation, limit caffeine
relaxation therapy
avoid triggers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Abortive tx (acute) start on onset of pain (not aura): NSAIDs/Analgesics

A

first line choice for mild-to-moderate attacks
Metoclopramide: speed absorption of analgesics and decrease migraine related n/v
Fioricet, Codeine: limit use, med overuse headache more common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Abortive tx (acute) start on onset of pain (not aura): Serotonin receptor agonist

A

Triptans
if one fails, pt can be switched to another
sumatriptan: 2 hr, SQ, oral, intranasal
Frovatriptan/Naratriptan: for patients with attacks of slow onset and longer duration
Lasmiditan: no heavy machines for at least 8 hr following dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Triptans contraindications

A

h/o ischemic heart disease
uncontrolled HTN
cerebrovascular disease
pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

When to supervise doses of triptans for patients

A

postmenopausal women
men >40 yo
uncontrolled CV risk factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

When to avoid triptans

A

w/in 24 hr of ergotamine derivatives
w/in 2 wks of MAO-Is
with SSRI or SNRI (serotonin syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Abortive tx (acute) start on onset of pain (not aura): Ergot Alkaloids and Derivatives

A

mod-to-severe attacks
ergotamine tartrate has more potent arterial effects than DHE
intranasal, IM, SQ, IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Ergot Alkaloids and Derivatives contraindications

A

renal or hepatic failure
coronary, cerebral, or peripheral disease
uncontrolled HTN
sepsis
pregnancy (nursing)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Abortive tx (acute) start on onset of pain (not aura): CGRP receptor antagonists

A

when triptan is CI, ineffective, not tolerated
Ubrelvy
Nurtec ODT
Zavzpret nasal spray

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Abortive tx (acute) start on onset of pain (not aura): Antiemetics

A

for n/v with migraines: single dose 15-30 min before oral abortive migraine med (metoclopramide, prochlorperazine)
migraines: alternative to narcotic analgesics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Abortive tx (acute) start on onset of pain (not aura): Opiate Analgesics

A

combo w/ codeine or tramadol w/ APAP are more effective
increase risk of medication overuse headaches
only for: mod-to-severe infrequent headaches when other therapies are CI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Abortive tx (acute) start on onset of pain (not aura): corticosteroids

A

rescue therapy (dexamethasone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Abortive tx (acute) start on onset of pain (not aura): Valproate

A

mod-to-sever intensity (valproate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Abortive tx (acute) start on onset of pain (not aura): magnesium sulfate

A

in migraine with aura (mag sul)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

PPX pharm tx for migraine headaches: anti epileptic drugs

A

useful w/ cormorbid epilepsy, anxiety, bipolar illness
valproate/divalproex: get baseline LFT
topiramate: best use for pts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

valproate/divalproex contraindications

A

pancreatitis and chronic liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

topiramate avoid/caution in what pt

A

kidney stone
cognitive impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

PPX pharm tx for migraine headaches: antidepressants

A

amitriptyline: limit use in BPH and glaucoma, give in evening, orthostatic hypotension
venlafaxine: n/v, drowsiness, risk of 5-HT w/ triptan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

PPX pharm tx for migraine headaches: antihypertensives

A

beta blockers: metoprolol, propranolol, timolol, good for HTN or angina
CCB: not in guidelines yet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Beta blockers caution for migraine headaches

A

AV conduction disturbances, asthma, diabetes

59
Q

PPX pharm tx for migraine headaches: NSAIDs

A

naproxen has the best data
decrease frequency, severity, duration
GI/renal w/ prolonged use
prevent predictable headaches (menstrual)
give 1 wk prior to onset
cont for no more than 10 days

60
Q

PPX pharm tx for migraine headaches: triptans

A

menstrual headaches
Frovatriptan for efficacy
give 1-2 d before expected onset

61
Q

PPX pharm tx for migraine headaches: CGRP inhibitors

A

for episodic and chronic migraines
monoclonal antibodies: given IV or SQ
receptor antagonists: gepants given ODT
Nurtec for preventative or acute care
Atogepant only for prevention

62
Q

PPX pharm tx for migraine headaches: Onabotulinumtoxin A (botox)

A

for pt >15 headache days per month w/ inadequate response to at least two:
topiramate
divaloprex, valproate
beta-blocker
TCA
SNRI
given 155 units over 30 sites every 12 wks

63
Q

Consider ppx tx when what

A

recurring migraines produce significant disability
frequent attacks occuring more than 2x/wk
sx therapies are ineffective or CI
pt preference to limit number of attacks

64
Q

Tension-type headache epidemiology

A

infrequent: <1 episode/month
frequent: 1-14 days per month
risk factors: coexisting migraine, depression, anxiety, poor stress management

65
Q

Tension-type headache pathophysiology

A

pain from myofascial and peripheral sensitization of nociceptors

66
Q

Tension-type headache clinical presentation

A

mild-mod pain
dull, non-pulsatile tightness or pressure
bilateral
mild photophobia or phonophobia

67
Q

Tension-type headache nonpharm tx

A

stress management, relaxation, biofeedback

68
Q

Tension-type headache pharm tx

A

analgesics +/- cffine and NSAID
combo analgesics: no more than 10 d/month
NSAID: no more than 15 d/month
TCA may be prescribed
maybe: topiramate, gabapentin, tizanidine

69
Q

Cluster headache epidemiology

A

4:1 male to female, in 20-30 yo
h/o smoking
unilateral pain that occur in series lasting for weeks-months (clusters) remission periods last months-years

70
Q

Cluster headache pathophysiology

A

neuroimaging of hypothalamus

71
Q

Cluster headache clinical presentation

A

hallmark: circadian rhythm of painful attacks
daily x 1wk to several months
average remission is 2 years
common at night in spring/fall
pain lasts 15-180 minutes
excruciating, penetrating, boring, lacrimation, nasal stuffiness, rhinorrhea, miosis

72
Q

Cluster headache abortive tx

A

oxygen: facial mask
triptans: SQ, intranasal

72
Q

Cluster headache abortive tx if first line does not work

A

ergotamine derivatives: DHE bolus over d to wk, tartrate sublingually
intranasal lidocaine: no systemic side effects

73
Q

Cluster headache ppx tx

A

verapamil (2-3 wk before benefit, first line)
lithium (caution renal, CV, dehydration, pregnancy)
galcanezumab (for pt with headache >1 month who failed primary agents)
corticosteroids (5 d prednisone high dose then taper)

74
Q

Alzheimer is a gradual progressive dementiathat affects what

A

cognition, behavior, and functional status

75
Q

Alzheimer etiology

A

65 and older highest risk
can be 30 and still have it
survival is 4-8 years after diagnosis can live 20 years with
most common death is pneumonia due to swallowing difficulties and immobility in terminal stage of disease

76
Q

Alzheimer etiology of early onset <60 yo

A

error in protein binding
mutation in presenilin 1 on chromosome 14, APP on chromosome 21, presenilin 2 on chromosome 1
increases amyloid beta in brain causing oxidative stress, neuronal destruction, and clinical syndrome

77
Q

Alzheimer etiology of late onset

A

APOE gene on chromosome 19
carriers of >2 APOE4 alleles have higher risk and earleir onset

78
Q

Other factors of Alzheimers with increased risk

A

increase ages
women
decreased reserve capacity in the brain
head injury
down syndrome
depression
mild cognitive impairment
vascular disease

79
Q

Alzheimer pathophysiology

A

tangles
plaques
Ach
glutamine
cholesterol
estrogen (not really)

80
Q

General presentation of Alzheimer

A

vague memory “forgetful”
cognitive decline is gradual
behavioral disturbances present in moderate stages
loss of daily fx

81
Q

Sx of Alzheimer

A

cognitive:
memory loss, aphasia, apraxia, agnosia, disorientation
neuro:
depression, aggression, wandering
functional: inability to care for self

82
Q

Rule out what before Alzheimer

A

Vit B12 deficiency, hypo/hyperthyroidism, anemia, electrolyte imbalance, renal/hepatic dysfunction, syphilis, HIV

83
Q

Diagnostic test for Alzheimer

84
Q

What is the primary clinical diagnosis for Alzheimer

A

cognitive decline, loss of social or occupational fx
PET: flortaucipir F18 (estimate tau protein tangles)

85
Q

MMSE classifications

A

Mild: 26-21 (withdrawal from tasks)
Moderate: 20-10 (suspicious or tearful)
Severe: 9-0 (no speak or walk)

86
Q

What meds to disc for pt w/ Alzheimer

A

benzos, sedative hypnotics, anticholingerics, antipsychotics
H2RA, corticosteroids, opioids

87
Q

Nonpharm tx for Alzheimer

A

avoid environmental triggers
redirect pt environment
calm place, exercise, light therapy, music, relax, massage

88
Q

What is considered successful tx of Alzheimer

A

decline of <2 points per year on MMSE

89
Q

Pharm tx for Alzheimer: cholinesterase inhibitors MOA

A

goal to enhance cholinergic activity
donepezil: reversibly inhibit AChE (ODT, patch, tablet)
rivastigmine: pseudo-irreversible inhibit butyryl and AChE (cap, patch)
galantamine: selective reversible AChE inhibitor, enhance nicotinic receptors (tab, ER cap, soln)

90
Q

Dosing considerations for rivastigmine and

A

if interrupted for several days pt should restart on lowest dose, take with food

91
Q

When switching from one cholinesterase inhibitor to another how long do you have to wait

A

donepezil to another: 7-14 d
from rivastigmine or galantamine: 1-2 d
do not combo drugs together

92
Q

When to use Namenda for Alzheimer

A

mod to severe AD
block glutamatergic neurotransmission by antagonizing NMDA receptors
(soln, tab, ER cap)

93
Q

Role of combo therapy for Alzheimer

A

mod-to-severe AD
memantine + donepezil (namzaric)

94
Q

Use of Monoclonal Antibodies for Alzheimer

A

directed against aggregatted forms of amyloid beta
assist in reducing formation and appearance of plaques

95
Q

What are the

A

aducanumab
lecanemab
donanemab

96
Q

Monoclonal Antibodies for Alzheimer ADE

A

fever, chills, urticaria
ARIA (cerebral edema, hemorrhages)
should do regular MRI

97
Q

Take home points for Monoclonal Antibodies for Alzheimer

A

not for severe stages of AD
further trials are needed to investigate whether reducing plaques correlates w/ clinical meaningful changes in cognition

98
Q

Dietary supplements for Alzheimer

A

Ginko Biloba: 240 mg/d, avoid in anticoagulant, anti platelet therapy, caution with NSAID
Prevagen: is not good

99
Q

What is the pathophysiology of parkinson’s disease

A

degeneration of the pars compacta of the substantia nigra, leading to overactivity in the direct pathway

100
Q

What are the primary treatment compounds of parkinsons disease

A

increase dopamine synthesis
decrease dopamine catabolism
stimulate dopamine receptors (agonists)

101
Q

What are the secondary treatment compounds of parkinsons disease

A

antagonize muscarinic cholinergic receptors
enhance dopamine release
NMDA glutamine receptors

102
Q

Levodopa/Carbidopa (sinemet) MOA

A

levodopa is the immediate metabolic precursor of dopamine which crosses the BBB (decarboxylation to dopamine)
carbidopa is a peripheral dopa-decarboxylase inhibitor

103
Q

The absorption of levodopa in the intestine and at the BBB is mediated by a saturable _____ ______ transporter

A

amino acid

104
Q

Levodopa/Carbidopa (sinemet) DDI

A

pyridoxine (vit B6) enhances the extracerebral metabolism of levodopa

105
Q

Entacapone (comtan) and tolcapone (tasmar) MOA

A

entacapone is a peripherally acting inhibitor of catechol-O-methyltransferase (COMT)
tolcapone is a central and peripheral inhibitor of COMT
(they prolong the action of levodopa by diminishing metabolism)

106
Q

Metabolism of L-dopa

A

peipheral and central metabolism depicting the sites of action of enzyme inhibitors. AAAD, AD, COMT, MAO

107
Q

Selegiline MOA

A

selective inhibitor of MAO-B and at higher doses it does MAO-A
enhances and prolongs the antiparkinson effect of levodopa

108
Q

Rasagiline MOA

A

selective inhibitor of MAO-B (more potent than selegiline)
used as a neuroprotective agent and for early symptomatic tx

109
Q

Can you combine MAO-B and MAO-A with levodopa

A

NO, this may lead to a hypertensive crises dir to peripheral NE

110
Q

Bromocriptone and Pergolide (ergot) MOA

A

Bromocriptone partial D2 agonist
Pergolide parial agonist for D1 and D2 receptors
can be combined with levodopa

111
Q

Pramipexole and Ropinirole (non-ergot) MOA

A

first line in initial tx of PD
Pramipexole: affinity for D3 (may neuroprotect)
Ropinirole: D2 receptor agonist

112
Q

Benztropine and Trihexyphenidyl MOA

A

anticholinergic drugs decrease the excitatory actions of cholinergic neurons in the striatum
may improve tremor and rigidity

113
Q

Amantadine (symmetrel) MOA

A

may potentiate dopaminergic function by increasing the synthesis of release of dopamine or inhibition of dopamine reuptake
may improve bradykinesia, rigidity, tremor

114
Q

Apomorphine (apokyn) MOA

A

non-narcotic derivative (activate D1 and D2 receptors)
temp relief of off-periods of akinesia

115
Q

What are the 4 hallmark features of parkinsons disease

A

Tremor at rest
Rigidity
Akinesia/bradykinesia
Postural instability

116
Q

What is the hallmark sign of parkinsons on a cellular level

A

degeneration of dopaminergic neurons projecting from the substantia nigra pars compacta to the striatum

117
Q

Environmental factors which elevate and lower risk of parkinsons

A

elevate: chronic exposure to pesticides
lower: caffeine and cigs

118
Q

Diagnosis of parkinsons disease

A

presence of bradykinesia + tremor, rigidity, or postural instability
exclude other types of tremor disorders
presence of 3 supporting criteria

119
Q

What are the supporting criteria for parkinsons disease

A

asymmetry of motor signs
unilateral onset
progressive disorder
resting tremor
response to carbidopa/l-dopa
L-dopa response for >5 yr
presence of L-dopa dyskinesia

120
Q

Goals of parkinsons therapy

A

improve motor and nonmotor symptoms
maintain QOL
preserve daily activities, improve mobility, no ADEs

121
Q

nonpharm therapy for parkinsons

A

surgery:
diagnosis of L-dopa-responsive PD
absence of cognitive impairment
Deep brain stimulation (DBS) which targets thalamus

122
Q

When to use anticholinergic meds (benztropine and trihexyphenidyl) in parkinsons

A

increase striatal cholinergic activity
good for tremor
avoid: advanced age, pre cognitive deficits, dysphagia

123
Q

When to use amantadine-1 in parkinsons

A

inhibit NMDA receptors
manages L-dopa-induced dyskinesia
manages tremor, rigidity, bradykinesia
DO NOT rapid w/drawal

124
Q

ADE of amantadine-1

A

livedo reticularis
-mottling of the skin
-upper and lower extremities
-w/ lower edema

125
Q

When to use carbidopa/levodopa in parkinsons

A

symptomatic PD
25/100 TID initial
DO NOT rapid w/drawal

126
Q

What are the formulations for carbidopa/levodopa

A

ODT
capsule (can sprinkle on food)
comes in IR and ER

127
Q

What are the 4 motor functions of L-dopa

A

end-of-dose wearing off
delayed on or no on response
freezing
dyskinesia

128
Q

How to treat end of dose wearing off L-dopa effect

A

increase frequency of dose
add istradefylline, COMT, MAO-B, or dopamine agonist
rapid: apomorphine SC or L-dopa powder for inhalation
overnight: HS admin of dopamine agonist or formulations that provide

129
Q

How to treat delayed on effect L-dopa effect

A

give carbidopa-L-dopa on empty stomach
use ODT carbidopa-L-dopa
avoid SR
use apomorphine SC or L-dopa inhalation

130
Q

How to treat freezing L-dopa effect

A

increase carbidopa-L-dopa dose + dopamine agonist or MAO-B inhibitor
physical therapy or walking assist devices

131
Q

How to treat dyskinesia L-dopa effect

A

provide smaller doses of carbidopa-L-dopa
reduce dose of adjunctive dopamine agonist
add amantadine

132
Q

When to add MAO-B inhibitors in parkinsons

A

cause prolonged dopaminergic activity
DDI: SSRI, meperidine, other opioid analgesics

133
Q

Selegiline (MAO-B) for parkinsons

A

early PD: improve motor functions
advanced PD: adjunctive for “wearing off”
may worsen dyskinesias

134
Q

Rasagiline (MAO-B) for parkinsons

A

early PD: effective as monotherapy
advanced PD: add-on therapy for motor fluctuations

135
Q

Safinamide (MAO-B) for parkinsons

A

advanced PD: adjunctive to carbidopa/L-dopa for wearing off

136
Q

When to add COMT inhibitors for parkinsons (entacapone, tolcapone, opicapone)

A

extend effects of L-dopa
manages wearing off
entacapone: need to give w/ every L-dopa
tolcapone: fatal hepatotoxicity check ALT/AST
opicapone: qd dose

137
Q

When to use dopamine agonist for parkinsons

A

stimulate D1, D2, D3
monotherapy for mild-mod PD
adjunct to L-dopa to reduce off time

138
Q

When to use dopamine agonist for parkinsons: younger pt, older pt, cognitive problems or dementia

A

younger pt: dopamine agonist over L-dopa
older pt: use conservatively
cognitive problems or dementia : AVOID

139
Q

less common but serious ADE of dopamine agonist

A

impulsive and compulsive behaviors
hallucinations and delusions

140
Q

When to use apomorphine in parkinsons

A

SC inj
can cause hypotension
advanced PD w/ intermittent off episodes

141
Q

When to use adenosine receptor antagonist in parkinsons

A

Istradefylline
for off episodes

142
Q

Monitoring for PD

A

med admin times
inquire specifically about dose-by-dose effects of med