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Therapeutics 4 > Exam 3- part 2 > Flashcards

Exam 3- part 2 Flashcards

1
Q

Etiology of parkinsons disease

A

Degeneration of dopaminergic neurons in the substantia nigra, presence of Lewy bodies and non-dopaminergic neuron degeneration

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2
Q

Parkinsons disease course

A

Starts with non-motor symptoms (hypotension, anxiety, depression, urinary dysfunction)
Progresses to having motor symptoms (tremor, bradykinesia, rigidity, postural instability)

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3
Q

Parkinsons Disease- general treatment approach

A

All treatments are symptomatic. There are currently no proven neuroprotective therapies.
Levodopa with carbidopa is the gold standard for symptomatic treatment
Need to treat motor and non motor symptoms

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4
Q

Nonpharm treatments for PD

A

Lifestyle modifications- nutrition, exercise, speech
Surgery:
Pallidotomy- helps tremors and drug induced dyskinesia
Thalamotomy- helps tremors
Deep brain stimulation- less traumatic surgery

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5
Q

Medication classes used for PD

A 
Carbidopa/Levodopa
Dopamine agonists
COMT inhibitors
MAO-B inhibitors
Adenosine receptor antagonist
NMDA antagonist/DA release
Anticholinergics
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6
Q

What are the PK differences in the forms of levodopa/carbidopa

A

IR- Great bioavailability, but short T1/2. Needs to be dosed frequently.
CR- Lasts longer, but poor F
Rytary- Better F, preferred formulation

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7
Q

Absorption of carbidopa/levodopa

A

Active transport into the BBB

Diets high in proteins (large neutral AA) may decrease abs and reduce clinical response.

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8
Q

When is Rytary preferred?

A

Ideal for pts who have predictable motor fluctuations, end of dose wearing off, and/or dyskinesia

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9
Q

Levodopa/ Carbidopa and the BBB

A

Levodopa is absorbed in the small intestine and transported into the BBB via active transport. Carbidopa does not cross the BBB.

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10
Q

Why use Levodopa/Carbidopa in PD?

A

It is the most efficacious
Increases QOL
Increases survival

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11
Q

Complications of levodopa

A 
N/V- decreased by carbidopa 
Neurogenic Orthostatic hypotension (nOH)
Constipation
Motor complications/fluctuations- wearing off, unpredictable "on-off"
Dyskinesias 
Mental status changes
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12
Q

What happens to the efficacy of levodopa as PD progresses?

A

The therapeutic window narrow.

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13
Q

Wearing- off of levodopa

A

Regular and predictable decline in response 2-4 hours after LD dose.
The benefits from each dose get shorter over time, symptoms return between doses.

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14
Q

Strategies to address levodopa wearing off

A

Increase LD dose or frequency of doses
Add (not change to) Rytary formulation
Add DA or COMT inhibitor

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15
Q

Carbidopa/Levodopa withdrawal

A

Rapid cessation of Simemet can result in a syndrome like neuroleptic malignant syndrome.
-Rigidity, altered consciousness, fever, tremors

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16
Q

Duodopa

A

Carbidopa/Levodopa enteral suspension

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17
Q

Inbrija

A

Levodopa inhalation powder

Fastest onset of action

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18
Q

Dopamine agonists

A

Bromocriptine, pramipexole, ropinirole, rotigotine, apomorphine

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19
Q

When are DA used?

A

Primarily used in early tx of PD before initiating levodopa and in patients with motor fluctuations in order to prolong response to levodopa

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20
Q

Which DA is renally excreted?

A

Pramipexole

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21
Q

DA adverse effects

A 
Sedating effects
Unintended sleep episodes
Hypotension
Hallucinations
May cause dyskinesias ( less likely than LD)
N/V
Leg edema
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22
Q

Which DA requires pre-med with an anti-emetic before administering?

A

Apomorphine

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23
Q

DA and impulse control disorders

A

There is an association between DA and ICD. Pts most at risk are those with a previous history of impulsive activity.
Typically ICS’s are reversible with DA dose reduction or d/c

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24
Q

Rotigotine

A

DA transdermal patch

Overnight switch to rotigotine is effective if pt is having sleep issues.

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25
Q

How do COMT inhibitors work?

A

Increase levodopa bioavailability in the brain
Reduce levodopa burden
Increase “on” time

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26
Q

COMT inhibitors agents

A

Tolcapone, Entacapone, Opicapone

Stalevo- combo entacapone/ LD/ carbidopa

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27
Q

Monitoring for COMT inhibitors

A

LFT monitoring for tolcapone

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28
Q

AE for COMT inhibitors

A

Brownish orange fluid discoloration

Orthostasis

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29
Q

Tolcapone BBW

A

COMT inhibitor

BBW- hepatotoxicity. Informed consent available

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30
Q

Which COMT inhibitor has no evidence of hepatotoxicity?

A

Entacapone

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31
Q

Which COMT inhibitor is QD?

A

Opicapone

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32
Q

Opicapone absorption

A

Food decreases the abs

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33
Q

MAO-B inhibitor agents

A

Selegiline, Rasagiline, Safinamide

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34
Q

Which MAO-B inhibitor is reversible?

A

Safinamide

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35
Q

When do you use MAO-B inhibitors?

A

In mild symptomatic PD pts who choose to delay dopaminergic meds.
Combining with LD in early tx may delay motor symptoms.
Use to improve wearing off in advanced disease

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36
Q

Selegiline BBW

A

BBW- suicidal thoughts and behaviors (patch)
It is an amphetamine metabolite, so it is neurotoxic

MAO-B inhibitor

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37
Q

Selegiline and food

A

Bioavailability increases 3-4 fold when taken with food

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38
Q

Safinamide metabolism

A

Metabolized by oxidation

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39
Q

MAO-B inhibitor interactions

A 
Theoretical risk of serotonin syndrome
Tyramine reaction (hypertensive crisis)
Avoid Cipro with rasagiline
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40
Q

Istradefylline

A

Adenosine receptor antagonist that is indicated as adjunct tx to LD in pts experiencing “off”episodes

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41
Q

When do you need to dose adjust with Istradefylline?

A

Cigarette smoke
CYP3A4 inducers- avoid
CYP3A4 inhibitors- adjust dose

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42
Q

Istradefylline AE

A

Dyskinesia, insomnia, dizziness, hallucinations, N, constipation

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43
Q

Amantadine

A

Monotherapy option for newly diagnosed patients with mild PD symptoms. Provides mild to moderate benefit for tremor, rigidity, and bradykinesia

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44
Q

Amantadine AE

A

Neuropsychiatric AE limit use in older patients or those with dementia
-confusion, hallucinations, nightmares, insomnia
Other AE- anticholinergic, livedo reticularis

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45
Q

When to use anticholinergics in PD

A

Option for younger patients (<60) whose predominant symptom is resting tremor.
No effect on bradykinesia

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46
Q

Available anticholinergic agents for PD

A

Trihexyphenidyl
Benztropine
Diphenhydramine

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47
Q

AE of anticholinergics

A

Memory impairment, confusion, hallucinations, sedation, dysphoria, antimuscarinic effects, dry mouth, blurred vision

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48
Q

Preferred anti-emetics for parkinsons

A

Domperidone and Trimethobenzamide

Ondansetron, dolasetron, granisetron

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49
Q

Which anti-emetics should you avoid in PD

A

Metoclopramide, promethazine, prochlorperazine

Have dopamine antagonist properties and can worsen PD

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50
Q

Psychosis with PD

A

Common
Hallucinations, delusions, sensory disturbances like illusions
Risk factors- age, illness severity, cognitive impairment, depression, insomnia

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51
Q

Management of psychosis in PD

A

Assess for triggers- infection, electrolyte imbalance, sleep disorfer
Minimize polypharmacy
Reduce PD med doses
Add atypical antipsychotics - quetiapine or clozapine
Add cholinesterase inhibitor

52
Q

Atypical antipsychotics in PD

A

Quetiapine
Clozapine
Pimavanserin

53
Q

Droxidopa

A

NE prodrug
Approved for nOH
BBW for supine HTN

54
Q

Clozapine AE

A

Need blood count monitoring due to risk of fatal agranulocytosis

55
Q

Management of orthostatic hypotension in PD

A

Fludrocortisone
Midodrine
Droxidopa

56
Q

Management of hypersomnia in PD

A

Sleep hygiene
Modafinil
Armodafinil
Methylphenidate

57
Q

Management of dyskinesia in PD

A

Does not always need to be treated
Lower dose of LD if practical
Amantadine
DBS

58
Q

Benztropine brand and dose

A

Cogentin

0.5-3mg BID

59
Q

Pramipexole brand and dose

A

Mirapex

0.125-1.5mg TID

60
Q

Ropinirole brand and dose

A

Requip 1-4mg TID

Requip XL 1-6 QD

61
Q

Levodopa/ Carbidopa brand and dose

A

Sinemet- 10/100-25/100 Q8H

Sinemet CR- 50/250 Q12H

62
Q

Parkinsons disease- should you ever substitute meds or stop levodopa abruptly?

A

No, doing so may cause neuroleptic malignant syndrome (NMS)

63
Q

Which pain medicines to avoid if patient is taking MAO-B inhibitor?

A

Meperidine

64
Q

Which anesthetics to avoid if patient is taking MAO-B inhibitor?

A

Meperidine, tramadol, droperidol, propoxyphene, cyclobenzaprine, halothane

65
Q

Which antidepressant are safe in PD

A

Fluoxetine, sertraline, paroxetine, citalopram, escitalopram, venlafaxine

66
Q

PD S/S

A

Tremor
Rigidity
Akinesia/Bradykinesia
Postural instability

67
Q

A 40 yo pt with no pmh presented to the neurologist with mild
left hand tremor x 6 months & no other symptoms. He is
diagnosed with Parkinson’s Disease. Which of the following
regimens is most appropriate for initial treatment?

A

Amantadine 100mg QD

68
Q

What is MS?

A

Most common disabling neurological disease of young adults.
Characterized by areas of inflammation, demyelination, axonal loss and gliosis in CNS
Unknown cause

69
Q

Potential triggers of MS

A

Infectious agent, genetic predisposition, environmental factors

70
Q

Symptoms of MS

A

Spasticity, bladder symptoms, visual symptoms, bowel symptoms, cognitive symptoms, depression and mood symptoms, sexual dysfunction, pain, incontinence, optic neuritis, diplopia, constipation

71
Q

Clinical course of MS

A

Relapsing Remitting MS- most common
Primary progressive MS
Secondary Progressive MS- common after 10 years
Progressive relapsing MS

72
Q

Why should you treat MS?

A

Disease modifying therapies (DMT) have been shown to reduce long term disability and rate of relapse. Treating early may delay progression to clinically relevant MS.

73
Q

Treatment goals for MS

A

No evidence of disease activity (NEDA)

Rio score

74
Q

MS treatment of acute relapses

A

IV methylprednisolone

PO prednisone

75
Q

Choosing initial DMARD for MS

A

No consensus on initial therapy, but alemtuzumab should not be used

76
Q

Immunomodulators used in MS

A

Interferons, Teriflunomide, Glatiromer, Dimethyl fumarate, Diroximel fumarate

77
Q

Common AE of interferons

A

Injection site reactions, flulike symptoms

78
Q

Monitoring for interferons

A

CBC, LFT, Thyroid

79
Q

Teriflunomide contraindications

A

Contraindicated in patients with severe hepatic impairment and in pregnancy

80
Q

Glatiramer AE

A

Injection site reactions, lipoatrophy, rash, vasodilation, skin necrosis

81
Q

Which is better tolerated, dimethyl fumarate or diroximel fumarate?

A

Diroximel fumarate

82
Q

Cell traffickers for MS

A 
Fingolimod
Siponimod
Ozanimod
Ponesimod
Natalizumab
83
Q

AE of fingolimod, siponimod, ozanimod, and ponesimod

A

Bradycardia first dose, mild BP increase, elevated liver enzyme, HA
Shingles, fungal infections, macular edema, PML
Risk of rebound inflammation

84
Q

Natalizumab AE

A

PML

Must check for JCV-Ab

85
Q

Cell depleting therapies in MS

A

Ocrelizumab
Ofatumumab
Alemtuzumab
Cladripine

86
Q

Cladripine BBW

A

Tumor development

87
Q

Cell depleting therapies AE

A

Infusion site reactions, UTI, URI, neutropenia, hypogammaglobulinemia, reactivation of Heb or TB

88
Q

DMT transition considerations

A

There is no standard protocol and reason for switching must be considered.
After DMT is effective, switch after one or more relapses, two or more lesions, or increased disability.

89
Q

Which MS drug is safest in pregnancy?

A

Copaxone

90
Q

Teriflunomide and vaccines

A

No live vaccines until 6 months after stopping teriflunomide

91
Q

S1Ps and vaccines

A

Immunize for Varicella if not immune, no live vaccines during therapy or until 2 months post therapy

92
Q

Ocrelizumab and vaccines

A

Complete live vaccines at least 4 weeks prior to initiation of drug
Complete non-live vaccines at least 2 weeks prior to initiation of drug

93
Q

Alemtuzumab and vaccines

A

No live vaccines 6 weeks prior to therapy and during therapy

Wait 6 months after infusion to re-initiate vaccine

94
Q

Which of the following are oral modifying therapies for MS?
A.) Interferons, copaxone, alemtuzumab
B.) Copaxone, fingolimod, mitoxantrone
C.) Fingolimod, teriflunomide, dimethyl fumarate
D.) Alemtuzumab, natalizumab, copaxone

A

C- Fingolimod, teriflunomide, dimethyl fumarate

95
Q

Which of the following medications are most similar to dimethyl fumarate (Tecfidera)?

a. Avonex & Betaseron
b. Plegridy & copaxone
c. Vumerity & Bafiertam
d. Fingolimod & teriflunomide

A

C

96
Q

Avonex class

A

Immunomodulator

97
Q

Safest during pregnancy

A

Glatiramer (Copaxone)

98
Q

Oral MS agents

A 
Fingolimod
Teriflunomide
Dimethyl fumarate
Ozanimod
Ponesimod
99
Q

Which MS agent has the highest incidence of GI effects?

A

Dimethyl fumarate

100
Q

What class is Ocrelizumab?

A

Cell depleting therapy

101
Q

What class is Betaseron

A

Immunomodulator

102
Q

What class is natalizumab

A

Anti-cell trafficking agent

103
Q

What med is indicated for primary progressive MS

A

Ocrelizumab

104
Q

Glasgow Coma Scale

A

Motor component is most predictive of outcome.
Used to assess injury severity.
13-15= mild
3-8= severe

105
Q

What can decrease outcomes in a TBI?

A

Hypotension and hypoxia

106
Q

Monroe-Kellie Doctrine

A

Brain herniation occurs when something inside the skull produces pressure that moves brain tissues. This results from brain swelling or bleeding from a head injury, stroke, or brain tumor.

107
Q

Elevated Intracranial Pressure (ICP)

A

Normal ICP is <15 in adults and lower in children
S/S- bradycardia, resp depression, HTN, irregular pupil response to light, HA, confusion, loss of consciousness, seizures, diplopia

108
Q

Cerebral Edema therapy

A 
High ICP
Resuscitation- 
Oxygen
BP control (AVOID hypotension)
Fluid management (AVOID free water/ D5W)
Can use fentanyl and/or propofol for pain and sedation
109
Q

How does hypertonic saline and mannitol work cerebral edema?

A

Draws water across BBB, decreasing brain volume

110
Q

Hypertonic saline bolus or “bullet” or high osmolar hypertonic saline

A 
NaCl 23.4%
IV doses prn
Target serum Na 145-155 mEq/L
Watch out for rebound cerebral edema
Administer via central line
111
Q

Hypertonic saline intermittent or infusion

A

NaCl 2 or 3%
Target sodium concentrations per protocol
2% can be given by peripheral line
3% may need central line in some patients

112
Q

Mannitol

A

20% 500ml bags or 25% 50 ml vials
Must use filter due to crystallization
Serum osmolality <320 mmol/L, renal function, electrolytes
Monitor for AKI and dehydration

113
Q

When do post-traumatic seizures (PTS) occur?

A

Immediate
Early (<7 days after injury)
Late (>7 days after injury)

114
Q

Early seizure prophylaxis for TBI

A

Levetiracetam for 7 days preferred

Phenytoin and carbamazepine 2nd line

115
Q

Post-traumatic agitation in TBI

A

Subtype of delirium

Characterized by aggression, inhibition, emotional lability, motor disturbances

116
Q

Treatment of post traumatic agitation

A 
Aggression- serotonin agents
Memory- acetylcholine agents
Arousal/attention- catecholamine agents
Motor disturbances- dopamine agents
Disinhibition- combo
117
Q

TBI possibly harmful agents

A 
Benzodiazepines
Metoclopramide
Neuromuscular blockade
Amitriptyline
Cimetidine
Clonidine, prazosin
Phenytoin, phenobarbital
118
Q

TBI electrolytes

A

Hyponatremia- SIADH, CSW
Potassium
Magnesium
Glucose

119
Q

TBI dysautonomias

A

Suggests poor prognosis

Increase in HR, respiratory rate, temp, BP, tone, posturing, sweating

120
Q

General care for TBI

A

DVT prophylaxis
Enteral feeding
Early rehabilitation

121
Q

Neurostimulants for TBI

A

SSRIs, valproic acid for depression

Behavior/cognitive- SSRI, valproic acid, amantadine, methylphenidate

122
Q

Spasticity agents for TBI

A

Baclofen is most common

Also dantrolene, tizanidine, benzodiazepines

123
Q

Pharmacologic management of elevated ICP includes

A

sedation and hyperosmolar therapies

124
Q 
What is a common adult dose of IVP 23.4% Nacl (aka “bullet” or HOT salt) for lowering intracranial 
pressure (ICP) ?
a. 10 ml given over 60 mins
b. 100 ml given over 2 mins
c. 30 ml given over 15 mins
d. 1000 ml given over 30 mins
A

c. 30 ml given over 15 mins

125
Q

A patient with a severe TBI 7 days ago is ordered baclofen 30 mg pNG tube four times daily (120 mg/day) for spasticity. You call the prescriber to decrease the initial baclofen dose. Which of the following is true about baclofen ?
A. Baclofen is utilized for the therapy of spasticity after sTBI
B. Baclofen can cause significant sedation
C. Sudden cessation of baclofen can lead to
withdrawal symptoms & seizures
D. All of the above are true

A

All of the above

Therapeutics 4 (8 decks)

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