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IPCS 3 > Neurology > Flashcards

Neurology Flashcards

1
Q

What is the mechanism of action of Avonex?

A

Suppresses t-cell proliferation, decreases BBB permeability

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2
Q

What are warnings/precautions with Avonex and Betaseron?

A

Depression
Seizures
Albumin allergy

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3
Q

What are common ADRs of Avonex and Betaseron?

A

flu-like symptoms, leukopenia, injection site reactions, depression

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4
Q

What type of MS is Avonex approved for?

A

RRMS

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5
Q

What type of MS is Betaseron approved for?

A

RRMS
SPMS with relapses

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6
Q

What medications may help with flu-like symptoms caused by Avonex and Betaseron?

A

NSAIDs or ASA

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7
Q

What labs should be checked with Avonex and Betaseron?

A

CBC and LFTs

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8
Q

What is the mechanism of action of Copaxone?

A

Suppresses t-cell activation, reduces inflammation, demyelination, and axonal damage at the site of the MS lesion

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9
Q

What type of MS is Copaxone indicated for?

A

RRMS

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10
Q

What is the warning associated with Copaxone?

A

not for IV use

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11
Q

What is the most common ADR associated with Copaxone?

A

flushing

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12
Q

What is the mechanism of action of Cladribine?

A

Impairs DNA synthesis, which results in dose-dependent depletion of both B and T cells

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13
Q

What type of MS is Cladribine approved for?

A

RRMS
active SPMS

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14
Q

What is a BBW for Cladribine?

A

bone marrow suppression, neurotoxicity, renal toxicity, malignancy, risk of teratogenicity

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15
Q

What is unique about Cladribine?

A

It has 2 courses administered 1 year apart max lifetime dose of 2.5mg/kg

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16
Q

What type of MS is Mitoxantrone approved for?

A

SPMS
PRMS
and worsening RRMS

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17
Q

What is unique about Mitoxantrone?

A

IV infusion Q3 months
Lifetime cumulative dose is 140mg/m^2

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18
Q

What limits the use of Mitoxantrone?

A

cardiotoxicity

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19
Q

What is a BBW of Mitoxantrone?

A

bone marrow suppression, cardio toxicity, secondary leukemia

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20
Q

What is the mechanism of action of Fingolimod?

A

Reduces lymphocyte migration to the CNS

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21
Q

What is a serious ADR of fingolimod?

A

bradycardia, macular retinal edema

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22
Q

What type of MS is fingolimod approved for?

A

RRMS

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23
Q

What should be monitored in patients on fingolimod?

A

ophthalmological exam

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24
Q

When is Ozanimod contraindicated?

A

severe untreated sleep apnea
concomitant MAOI use

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25
Q

What is a clinical pearl of ponesimod?

A

Shorter half-life than other S1P agonists, leaves the body in about 1 week if treatment needs to be stopped for any reason

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26
Q

What is a consideration with siponimod?

A

Requires genetic screening prior to initiation
dose dependent on CYP2C9 genotype
CI in CYP2C193/3 genotype

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27
Q

What is a BBW for teriflunomide?

A

hepatotoxicity, embryofetal toxicity

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28
Q

What type of MS is teriflunomide approved for?

A

relapsing forms of MS

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29
Q

What is the mechanism of action of teriflunomide?

A

Reduces activated lymphocytes in the CNS, decrease inflammation and demyelination

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30
Q

What is a consideration with teriflunomide?

A

Avoid pregnancy for 2 years after discontinuation

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31
Q

What are common ADRs with dimethyl fumarate, diroximel fumarate, and mono methyl fumarate?

A

flushing, abdominal pain, infection

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32
Q

What can be used as pretreatment for flushing with dimethyl fumarate?

A

ASA 325 30 minutes prior to dose, take with food

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33
Q

What is the mechanism of action of dimethyl fumarate?

A

Activator of the nuclear factor erythroid-derived-2-like-2 (Nrf2) pathway
involved in cellular response to oxidative stress

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34
Q

What type of MS is dimethyl fumarate approved for?

A

RRMS

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35
Q

What is a BBW for natalizumab?

A

progressive multifocal leukoencephalopathy
rare brain infection

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36
Q

What are risk factors for PML in patients taking natalizumab?

A

> 24 months of treatment
prior use of immunosuppressives
history of JCV

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37
Q

What is a consideration with natalizumab?

A

REMS program
reserved for patients who have not responded to or cannot tolerate ABC therapy

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38
Q

What are serious ADRs of daclizumab?

A

hepatic injury including autoimmune hepatitis
REMS program

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39
Q

What is a BBW of alemtuzumab?

A

autoimmune effects, infusion reactions, malignancy, stroke

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40
Q

What is the mechanism of action of alemtuzumab?

A

Anti-CD-52, depletes circulating T and B cells

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41
Q

What are clinical pearls related to alemtuzumab?

A

high risk of infusion related reactions and malignancies
REMS program

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42
Q

What is the mechanism of action of ocrelizumab?

A

Anti-CD-20, humanized version of the rituximab monoclonal antibody

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43
Q

What type of MS is alemtuzumab approved for?

A

RRMS

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44
Q

What type of MS is ocrelizumab approved for?

A

RRMS
PPMS

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45
Q

What are clinical pearls related to ocrelizumab?

A

hep B screening required prior to initiation
increased risk of infections
case reports of PML

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46
Q

What is a BBW with Arzerra?

A

Hepatitis B virus infection, progressive multifocal leukoencephalopathy

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47
Q

What is the mechanism of action of ofatumumab?

A

Anti-CD-20, selectively depletes B cells

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48
Q

What type of MS is ofatumumab approved for?

A

RRMS
active SPMS

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49
Q

What are clinical pearls related to ofatumumab?

A

hep b screening required prior to initiation
increased risk of infections, including PML

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50
Q

What is multiple sclerosis?

A

an inflammatory disease of the CNS

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51
Q

Multiple sclerosis is more common in male/female

A

females

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52
Q

What are risk factors for multiple sclerosis?

A

female
greater distance from the equator
living in a high risk area prior to age 15
genetics
caucasian

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53
Q

What are the etiology theories of multiple sclerosis?

A

environmental
genetic
autoimmune
viral/microbial

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54
Q

What is the pathophysiology of multiple sclerosis?

A

demyelination and inflammatory response

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55
Q

Are demyleination and the inflammatory process happening at the same time?

A

yes

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56
Q

How are symptoms categorized in multiple sclerosis?

A

primary
secondary
tertiary

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57
Q

What are the most common primary symptoms of multiple sclerosis?

A

visual complaints/optic neuritis
gait problems
falls
paresthesias

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58
Q

What are two scales used to help in weighing the severity of multiple sclerosis?

A

EDSS
MSFC

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59
Q

What test is used to diagnose multiple sclerosis? What is seen?

A

MRI
Axonal damage is seen as a lesion

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60
Q

What are factors reported to aggravate symptoms or lead to an acute attack of MS?

A

infections
malnutrition
anemia
child birth
fever
organ dysfunction
sleep deprivation
exertion
stress

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61
Q

How is MS diagnosed?

A

MRI lesions
diagnosis of exclusion
cerebrospinal fluid evaluation

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62
Q

What is considered an attack/exacerbation of MS?

A

new symptoms lasting at least 24 hours and separated from other symptoms by at least 30 days

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63
Q

What is RRMS?

A

relapsing-remitting
clearly defined disease relapses
full recovery or residual effect
no disease progression between relapses

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64
Q

What is SPMS?

A

secondary progressive
Develops after an initial RRMS course

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65
Q

What is PPMS?

A

primary progressive
disease progression from onset, with almost continuous worsening
occasional plateau in clinical state
temporary minor improvements

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66
Q

What is PRMS?

A

progressive relapsing
progressive disease from onset
continuities progression between relapses

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67
Q

What are favorable indicators of prognosis in MS?

A

<40 years
female
optic neuritis or sensory symptoms develop first
Low attack frequency in early disease
relapsing/remitting

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68
Q

Treatment of acute MS depends on __

A

severity of the attack

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69
Q

How should mild acute MS be treated?

A

may not require treatment, some may use PO steroids

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70
Q

What is considered a mild MS attack?

A

does not produce functional decline

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71
Q

What is considered a moderate MS attack?

A

functional ability is affected

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72
Q

How should a moderate acute MS exacerbation be treated?

A

high dose corticosteroids

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73
Q

What is considered a severe MS attack?

A

manifested by hemiplegia, paraplegia, or quadriplegia

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74
Q

How should a severe MS attack be treated?

A

plasma exchange every other day for 7 treatments

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75
Q

What corticosteroid is used in the treatment of acute MS attacks?

A

methylprednisolone IV 3-10 days

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76
Q

What is first line therapy in PPMS?

A

ocrelizumab

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77
Q

What is first line therapy in RRMS?

A

ABC therapy

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78
Q

What is first line therapy in SPMS?

A

ocrelizumab

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79
Q

What medications are used to manage gait difficulties and spasticity in MS?

A

baclofen and tizanidine and gabapentin

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80
Q

What are considerations with baclofen?

A

ADRs: somnolence and confusion
Should not be discontinued rapidly to avoid the possibility of seizures

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81
Q

What is the diagnosis of a patient complaint of urgency, frequency, and eventually incontinence of the bladder?

A

hyperreflexic bladder

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82
Q

What can be used to treat hyperreflexive bladder?

A

anticholinergic agents: oxybutynin, tolterodine
Antimuscarinic agents: trospium, solifenacin, darifenacin

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83
Q

What is the diagnosis for patients complaining of hesitancy, retention, and overflow incontinence of the bladder?

A

sphincter detrusor dyssynergia

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84
Q

What can be used to treat sphincter detrusor dyssynergia?

A

alpha adrenergic blockers -prazosin

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85
Q

What can be used in patients with high risk for developing UTIs?

A

vitamin C, antiseptics

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86
Q

What can be used for patients complaining of constipation?

A

increase dietary fiber and hydration, laxatives and enemas may be necessary

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87
Q

What can be used to manage trigeminal neuralgia in patients with MS?

A

carbamazepine

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88
Q

What can be used to manage neuropathic pain in patients with MS?

A

TCAs, pregabalin, gabapentin, duloxetine

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89
Q

What is the most common complaint of patients with MS?

A

fatigue

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90
Q

What can be used to manage fatigue in patients with MS?

A

amantadine
methylphenidate
modafinil or armodafinil
switch antidepressant to fluoxetine

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91
Q

What can be used to manage tremor in patients with MS?

A

propranolol, primidone, and isoniazid

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92
Q

What is required with S1P agonists at baseline?

A

ECG -risk of first-dose bradycardia
Eye exam - macular edema

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93
Q

What is the mechanism of action of acetaminophen, aspirin, naproxen, diclofenac, ketorolac, and ibuprofen?

A

centrally inhibits COX enzyme pathway, reducing pain and inflammatory signaling in the CNS

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94
Q

What is the mechanism of action of dihydroergotamine and ergotamine tartrate?

A

non-selective 5-HT antagonist, resulting in constriction of blood vessels in the brain and decreased neurogenic inflammation

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95
Q

What is a major problem with dihydroergotamine?

A

poor oral bioavailability
slow onset of action
ergotamine-induced headache and rebound headache associated with frequent use

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96
Q

Ergotamine tartrate is structurally similar to __ and structurally/biochemically related to __

A

neurotransmitters
ergoline

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97
Q

What is the mechanism of action of triptans?

A

selective agonist of 5-HT1B and 1D receptors, which inhibit vasoactive peptide release and decrease neurogenic inflammation via vasoconstriction

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98
Q

What are serious ADRs of triptans?

A

cardiovascular effects

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99
Q

What are limitations to sumatriptan?

A

low lipophilicity
low oral bioavailability

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100
Q

What are improvements seen with zolmitriptan?

A

highly lipophilic - crosses BBB
longer half-life

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101
Q

What are significant med chem points with naratriptan?

A

it is a sulfonamide
piperidine ring is incorporated
binds selectively and with high affinity

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102
Q

What are improvements seen with naratriptan?

A

low side effects
highest oral bioavailability
longer half life

103
Q

What are significant med chem considerations with frovatriptan?

A

functional group at position 5 of indole structure is replaced by more metabolically stable functional groups
highest affinity

104
Q

What are improvements seen with frovatriptan?

A

moderate affinity for 5-HT7
slow onset of action, but long half-life

105
Q

What is the mechanism of action of lasmiditan?

A

high-affinity, highly-selective 5-HT1F receptor agonist, resulting in deactivation of the trigeminal system without vasoconstriction

106
Q

What are the most serious ADRs with lasmiditan?

A

serotonin syndrome, CNS depression

107
Q

What is the most serious ADR with CGRP antagonists?

A

hypersensitivity

108
Q

What is the mechanism of action of CGRP antagonists (gepants and monoclonal antibodies)?

A

inhibits the CGRP, when CGRP is released in excess, it causes intense inflammation and causes migraine headaches

109
Q

Which of the Gepants are abortive medications?

A

ubrogepant
rimegepant
zavegepant

110
Q

Which of the gepants are preventative medications?

A

rimegepant
atogepant

111
Q

What are the CGRP receptor antagonist monoclonal antibodies?

A

eptinezumab
erenumab
fremanezumab
galcanezumab

112
Q

What is the mechanism of action of metoclopramide and prochlorperazine?

A

dopamine receptor antagonist, which suppresses signaling leading to nausea

113
Q

What are serious ADRs related to metoclopramide and prochlorperazine?

A

extrapyramidal side effects
risk of QT prolongation
tarsades de pointes

114
Q

What is a BBW with ketorolac?

A

should not be used longer than 5 days due to increased risk of GI bleeding, CV events, and renal impairment

115
Q

What is the proposed mechanism of action of verapamil on cluster headaches?

A

exerts a vasodilatory effect on cerebral arterioles resulting in cluster headache relief

116
Q

What are serious ADRs associated with verapamil?

A

heart block, increased risk for acute decompensated heart failure

117
Q

What are serious ADRs of lithium?

A

hypotension, nephrotoxicity, seizures, hypercalcemia, hyperparathyroidism

118
Q

What is the role of the 5-HT1B receptor in migraines?

A

induces constriction of cranial vessels/cerebral blood vessels

119
Q

What is the role of the 5-HT1D receptor in migraines:

A

inhibits trigeminal vascular activity, inflammatory neuropeptide release, and nociception

120
Q

What is included in the chemical structure of classic triptans?

A

side chain on the indole ring and a basic nitrogen in a similar distance from the indole structure

121
Q

Which triptan is a secondary amine?

A

frovatriptan

122
Q

Which triptans do not have active metabolites?

A

sumatriptan
almotriptan
naratriptan

123
Q

Abnormal sensory modulation involving __ is critical in the induction of migraine

124
Q

5-HT acts through receptors in the meninges to __

A

block the release of inflammatory chemical

125
Q

5-HT acts through receptors in the brainstem to __

A

block the pain impulses and central brain perception via trigeminal nerve

126
Q

What vasoactive neuropeptides are related with migraines?

A

CGRP
neurokinin A
substance P

127
Q

What are medications that can precipitate a migraine headache?

A

tetracyclines, bactrim
theophylline, pseudoephedrine
NSAIDs
cimetidine, omeprazole
vasodilators, nitrates, dipyridamole
estrogen

128
Q

What is the definition of an aura?

A

a complex of positive and negative focal neurologic symptoms that proceed or accompany an attack
evolves over 5 minutes or longer, lasts less than 60 minutes

129
Q

What are examples of positive visual auras?

A

scintillations
photopsia
teichopsia
fortification

130
Q

What are examples of negative visual auras?

A

scotoma
hemianopsia

131
Q

What are examples of sensory and motor auras?

A

parasthesias
dysphasia
weakness
hemiparesis

132
Q

What are symptoms of migraines?

A

recurring episodes of throbbing head pain, frequently unilateral, lasting from 4-72 hours if left untreated

133
Q

What are diagnostic alarms of migraine headaches?

A

acute onset of first or worst headache ever
accelerating pattern of headache following subacute onset
onset of headache after age of 50
Headache associated with systemic illness
Headache with focal neurologic symptoms or papulledema
New onset headache in a patient with cancer or HIV

134
Q

What are signs of a migraine headache?

A

stable patter, absence of daily headache
positive Fx
normal neurologic exam
food and menstruation may serve as triggers
improvement with sleep
aura can signal the migraine

135
Q

What are diagnostic tests done for migraine headaches?

A

general medical and neurologic physical exam
palpitation and auscultation of the head and neck
consider neuroimaging if necessary

136
Q

When can a migraine without aura be diagnosed?

A

at least 5 attacks
pulsating quality
one day duration
unilateral location
nausea, vomiting, photophobia, photophobia
disabiling intensity

137
Q

When can migraine with aura be diagnosed?

A

At least 2 attacks
fulfill aura criteria
pulsating quality
one day duration
unilateral location
nausea, vomiting, photophobia, photophobia
disabiling intensity

138
Q

How should medication overuse headache be managed/prevented?

A

limit use to <10 days per month

139
Q

When should preventative migraine therapies be considered?

A

recurring migraines that produce significant disability
frequent attacks occurring more than BIW
symptomatic therapies are ineffective
pt preference to limit number of attacks

140
Q

What are nonpharm therapies for migraines?

A

application of ice to the head
periods of rest in the dark
wellness program
relaxation therapy
identify/avoid triggers

141
Q

What is the first-line choice for mild-moderate migraine headaches?

A

analgesics
NSAIDs/acetaminophen
combination products

142
Q

When should metoclopramide be avoided?

A

renal disease

143
Q

T/F: if one triptan fails, patient can be switched to another

144
Q

What are the contraindications for triptans?

A

hx of ischemic heart disease
uncontrolled hypertension
cerebrovascular disease
pregnancy

145
Q

In which populations should the first dose of triptans be taken under medical supervision?

A

postmenopausal women, men>40, uncontrolled CV risk factors

146
Q

What are considerations with triptans?

A

avoid within 24 hours of ergotamine derivatives
avoid within 2 weeks of MAOIs
monitor for serotonin syndrome with SSRI/SNRI use

147
Q

What are contraindications of ergot alkaloids and derivatives?

A

renal or hepatic failure
coronary, cerebral, or peripheral vascular disease
uncontrolled hypertension
sepsis
pregnancy/nursing

148
Q

When can CGRP receptor antagonists be used?

A

when triptan is contraindicated, ineffective, or not tolerated

149
Q

When should antiemetics be given for N/V with migraines?

A

single dose 15-20 minutes before oral abortive migraine medication

150
Q

When are corticosteroids used for migraine headaches?

A

status migrainosus
dexamethasone IV

151
Q

When is valproate contraindicated?

A

pancreatitis, chronic liver disease

152
Q

What anti epileptic drugs can be helpful in migraine prevention?

A

valproate
topiramate

153
Q

What antidepressant can be helpful in migraine prevention?

A

amitriptyline
venlafaxine

154
Q

What antihypertensives can be helpful in prevention of migraines?

A

metoprolol
propranolol
timolol
CCbs, ACEI, ARBs limited efficacy

155
Q

What triptan can be used as prevention for menstrual migraines?

A

frovatriptan

156
Q

When is botox an option for migraine prevention?

A

patients with at least 15 headache days per month with an inadequate response to at least two of the following:
topiramate, valproate, beta-blocker, TCA, SNRI

157
Q

Botox should be avoided in which patients?

A

pregnancy and breastfeeding

158
Q

What are risk factors for poor outcome with tension-type headaches?

A

coexisting migraine, depression, anxiety, poor stress management

159
Q

What is the pathophysiology of tension-type headaches?

A

Originates from myofascial and peripheral sensitization of nociceptors
activation of supra spinal pain perception structures

160
Q

What is the clinical presentation of tension-type headaches?

A

mild-moderate intensity, dull, non-pulsatile tightness or pressure, bilateral, hatband pattern, mild photophobia or phonophobia

161
Q

What are nonpharm treatments for tension-type headaches?

A

stress management, relaxation training, biofeedback

162
Q

What is abortive therapy for tension-type headaches?

A

simple analgesics +/- caffeine

163
Q

What can be used for prevention of tension-type headaches?

164
Q

What are cluster headaches categorized as?

A

attacks of excruciating, unilateral head pain that occurs in series lasting for weeks-months, remission periods last months to years

165
Q

What is the pathophysiology of cluster headaches?

A

hypothalamus activates trigeminal-automonic reflexes, ipsilateral pain and cranial autonomic features

166
Q

What is the hallmark clinical presentation of cluster headaches?

A

circadian rhythm of painful attacks
occur daily x1 week to several months, followed by long pain-free periods
average period of remission is 2 years

167
Q

What are autonomic symptoms associated with cluster headaches?

A

lacrimation, nasal stuffiness, rhinorrhea, miosis

168
Q

What is first line abortive therapy for cluster headaches?

169
Q

What triptan is most effective for cluster headaches?

A

SubQ sumatriptan

170
Q

If patient is not responding to triptan and has cluster headache, what else can be used?

A

ergotamine derivative
intranasal lidocaine

171
Q

What is first-line prophylactic therapy for cluster headaches?

172
Q

What are other options for prophylactic therapy in cluster headaches?

A

lithium
galcanezumab
corticosteroids

173
Q

When should lithium be used cautiously?

A

significant renal or CV disease, dehydration, pregnancy, concomitant diuretic or NSAID use

174
Q

What drugs are anticholinergics used for Parkinson’s?

A

benztropine
trihexyphenidyl

175
Q

What are serious ADRs associated with anticholinergics?

A

anhidrosis, drug-induced psychosis, heat stroke, increased body temperature, tachycardia, visual hallucinations

176
Q

What are dopamine agonists used in Parkinson’s disease?

A

apomorphine
bromocriptine
pramipexole
ropinirole
rotigotine

177
Q

What are serious ADRs associated with apomorphine?

A

QTc prolongation, hallucinations, psychosis, hemolytic anemia

178
Q

What conformation is preferred for apomorphine?

179
Q

Which receptors does apomorphine activate?

180
Q

What are serious ADRs of bromocriptine and pramipexole?

A

blackouts, heart failure, impulsive behavior, melanoma, pulmonary fibrosis

181
Q

What receptors is bromocriptine an agonist of?

A

partial D1
full D2

182
Q

What receptors is pramipexole an agonist of?

A

full selective agonist at D2 and D3

183
Q

What are serious ADRs of ropinirole?

A

sinus node dysfunction, neuroleptic malignancy syndrome, impulse control/impulsive behaviors

184
Q

What receptors is ropinirole an agonist of?

A

full agonist for D2 and D3

185
Q

What are serious ADRs of rotigotine?

A

blackouts, heart failure, impulsive behavior, melanoma

186
Q

What receptors is rotigotine an agonist of?

A

full agonist for D2 and D3

187
Q

Which medications are COMT inhibitors?

A

entacapone
tolcapone

188
Q

What are serious ADRs of entacapone?

A

neuropsychiatric symptoms

189
Q

Of the COMT inhibitors which inhibits peripheral and which inhibits peripheral and central?

A

entacapone: peripheral
tolcapone: peripheral and central

190
Q

Entacapone is a member of the class of __

A

nitrocatechols

191
Q

What are serious ADRs of tolcapone?

A

neuropsychiatric symptoms, liver toxicity

192
Q

What medications are MAO-B inhibitors?

A

selegiline
rasagiline
safinamide

193
Q

What are serious ADRs associated with selegiline and rasagiline?

A

serotonin syndrome, neuropsychiatric symptoms

194
Q

T/F: selegiline and rasagiline are selective reversible MAO-B inhibitors

A

false
irreversible

195
Q

What is a serious ADR associated with safinamide?

A

serotonin syndrome

196
Q

What is the mechanism of action of amantadine?

A

enhances dopamine release from presynaptic terminals and inhibits NMDA receptors

197
Q

What are serious ADRs associated with amantadine?

A

withdrawal syndrome, impulse control disorders, lived reticularis

198
Q

Amantadine also has __ effects

199
Q

What is the mechanism of action of levodopa?

A

direct precursor to dopamine in its metabolic pathway

200
Q

What is the mechanism of action of carbidopa?

A

helps to prevent its peripheral metabolism in order to increase dopamine concentrations in the brain

201
Q

What are serious ADRs associated with carbidopa/levodopa?

A

orthostatic hypotension, neuroleptic malignant syndrome, hallucinations, sleep attacks, compulsive behaviors

202
Q

What is the mechanism of action of istradefuline?

A

increases movement via inhibition of the adenosine A2A receptor

203
Q

What are serious ADRs associated with astradefuline?

A

hallucinations, behavioral disturbances

204
Q

T/F: there is a correlation between reduced dopamine levels and PD severity

205
Q

The neuropathology of Parkinson’s is related to what two things?

A

deficiency of dopamine in striatum in the forebrain
appearance of lewy bodies

206
Q

What are possible causes of Parkinson’s?

A

neurotoxins, mitochondrial dysfunction, oxidative metabolism, genetics, drugs

207
Q

The side chain of dopamine is __ and has __ rotation about phenyl-beta-carbon single bond

A

flexible
unrestricted

208
Q

Which dopamine agonists are ergot derivatives?

A

bromocriptine and pergolide

209
Q

Which dopamine agonists are non-ergot derivatives?

A

pramipexole and ropinirole

210
Q

What are hallmark motor features of Parkinson’s?

A

Tremor at rest
Rigidity
Akinesia
Postural instability

211
Q

Parkinsons is a disorder of the __ system

A

extrapyramidal

212
Q

Parkinson’s is more common in male/female

213
Q

What is the hallmark sign of Parkinson’s?

A

degeneration of dopaminergic neurons projecting from the substantial nigra pars compact (Sac) to the striatum

214
Q

What environmental factors increases risk of Parkinson’s disease?

A

chronic exposure to pesticides

215
Q

The basal ganglia regulates voluntary movement and includes:

A

Substantia nigra
striatum

216
Q

What are other symptoms of Parkinson’s?

A

motor symptoms
autonomic and sensory symptoms
mental status changes
sleep disturbances

217
Q

What is the diagnosis process of Parkinson’s?

A

1: bradykinesia plus one other hallmark symptom
2: elude other disorders
3: presence of three supportive criteria

218
Q

What is a digital health tool used for Parkinson’s?

A

MyoExo
wearable system that detects movements in muscle

219
Q

What surgery is used for Parkinson’s?

A

Deep brain stimulation

220
Q

What criteria must be met for patients to undergo deep brain stimulation surgery?

A

diagnosis of L-DOPA responsive Parkinson’s disease
absence of cognitive impairment

221
Q

Anticholinergics should be avoided in which populations?

A

advanced age
pre-existing cognitive deficits
dysphagia

222
Q

What are motor complications of L-DOPA?

A

end of dose wearing off
delayed on or no on response
freezing
dyskinesias

223
Q

How can end of dose wearing off be treated?

A

Increase carbidopa/levodopa
Add istradefylline, COMT inhibitor, MAO-B inhibitor, or dopamine agonist

224
Q

How can delayed or no one response be treated?

A

Give carbidopa/levodopa on an empty stomach
use ODT
avoid sustained release

225
Q

How can freezing be treated?

A

increased carbidopa/levodopa dose
Add dopamine agonist or MAO-B inhibitor

226
Q

How can dyskinesias be treated?

A

lower carbidopa/levodopa dose
Use amantadine

227
Q

What are drug-drug interactions with MAO-B inhibitors?

A

SSRIs, meperidine, and other opioid analgesics

228
Q

What is a concern with selegiline?

A

may worsen preexisting dyskinesias or delusions

229
Q

Dopamine agonists should be avoided with which patients?

A

cognitive problems or dementia

230
Q

A patient <65 presents with bradykinesia and rigidity, what is the treatment?

A

dopamine agonist

231
Q

A patient <65 presents primarily with tremor, what is the treatment?

A

anticholinergic

232
Q

Alzheimer’s is described as what?

A

a gradually progressive dementia that affects cognition, behavior, and functional status

233
Q

What are factors associated with increased risk of Alzheimer’s disease?

A

increasing age
female
decreased reserve capacity in the brain
head injury
down syndrome
depression
mild cognitive impairment
risk factors for vascular disease

234
Q

What three gene mutations are associated with early onset Alzheimer’s disease?

A

APP on chromosome 21
Presenilin 1 on chromosome 14
Presenilin 2 on chromosome 1

235
Q

What is a genetic risk factor for late onset Alzheimer’s disease?

A

APOE on chromosome 19

236
Q

What consists of phosphorylated tau protein which is involved in micro tubular assembly?

237
Q

What are extracellular protein deposits of fibrils and amorphous aggregates of beta-amyloid protein?

238
Q

What is responsible for transmitting messages between certain nerve cells in the brain?

A

acetycholine

239
Q

What is an excitatory neurotransmitter involved in memory and learning?

240
Q

What has properties that protect against memory loss associated with normal aging?

241
Q

What are symptoms of Alzheimer’s?

A

memory loss, aphasia, apraxia, agnosia, disorientation, depression, psychotic symptoms, behavioral disturbances, inability to care for self

242
Q

An MMSE score of 26-21 is considered?

A

mild Alzheimer’s

243
Q

An MMSE score of 20-10 is considered?

A

moderate Alzheimer’s

244
Q

An MMSE score of 9-0 is considered?

A

severe Alzheimer’s

245
Q

What is a digital health tool used for Alzheimer’s?

A

Tranquil GPS Watch
has 2-way SOS calling, safe home alerts

246
Q

Successful treatment is considered what in Alzheimer’s?

A

decline of <2 points/year on the MMSE

247
Q

What are cholinesterase inhibitors used in Alzheimer’s?

A

donepezil
rivastigmine
galantamine

248
Q

What is the washout period from donepezil to other agents?

249
Q

What is the washout period from rivastigmine or galantamine to other agents?

250
Q

What test should be done prior to initiating monoclonal antibodies in Alzheimer’s disease?

251
Q

What is the recommendation for treatment of Alzheimer’s?

A

Mild-Moderate: cholinesterase inhibitor
Moderate-Severe: add memantine

252
Q

What is the recommended antidepressant to use in patients with Alzheimer’s disease?

A

citalopram

253
Q

What are recommended antipsychotics to use in patients with Alzheimer’s?

A

olanzapine, risperidone, arirpripazole, brexpiprazole

IPCS 3 (4 decks)

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