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555 > Final Exam review > Flashcards

Final Exam review Flashcards

1
Q

Dementia background

A

-AD is most common
-prevalence is expected to increase
-huge cost to healthcare system

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2
Q

Social cognition

A

-recognizing other’s emotions

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3
Q

Learning and memory

A

-long term memory
-cued recall
-unprompted recall

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4
Q

Executive function

A

-planning
-decision making
-IADL functions

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5
Q

Complex Attention

A

-processing speed
-divided attention

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6
Q

Language

A

-object naming
-animal fluency
-receptive language

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7
Q

Early stages of dementia

A

-chronic cognitive decline
-Instrumental activities of Daily Living affected: Managing finances, medication managment, Housekeeping, driving, shopping, meal prep

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8
Q

Middle to later stages of dementia

A

-activities of daily living
-bathing
-toileting
-dressing
-grooming
-walking
-eating meals

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9
Q

Lab tests in demential

A

-used to rule out differential diagnosis
-Vitamin B12: < 400
-TSH
-CBC: anemia and infection
-BMP: hyponatremia
-HIV
-Syphilis

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10
Q

Mini-cog for dementia

A

-3 item repeat
-clock draw
-3 item recall

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11
Q

Medications that contribute to cognitive changes

A

-ANTICHOLINERGICS
-antihypertensives
-benzos
-corticosteroids
-hypoglycemic agents
-muscle relaxants
-opioid
-NSAIDs
-sedative hypnotics

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12
Q

Alzheimer’s risk factors

A

-age
-genetics
-vascular
-head injury
-poor education
-poor hearing
-depression
-social isolation

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13
Q

Alzheimer’s pathophysiology

A

-accumulation of lesions leads to neurodegeneration and cognitive decline
-Aggregated amyloid and tau
-begins 20 years before symptoms develop
-affects language. learning/memory, and executive function

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14
Q

Alzheimer’s lifestyle modifications

A

-Omega 3
-folic acid
-Vitamin B
-Vitamin E
-physical activity
-mental activity
-social engagement
-music therapy

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15
Q

Vascular dementia

A

-caused by stroke/TIA, uncontrolled BP, diabetes, high cholesterol
-affects executive function and complex attention
-Donepezil, galantamine, rivastigmine

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16
Q

Lewy Body Dementia(DLB)

A

-fluctuating cognition, hallucinations, parkinsonism
-affects learning/memory and cognitive function
–Donepezil, galantamine, rivastigmine
-avoid antipsychotics
-levodopa for parkinsonism
-fludrocortisone or midodrine for orthostatic hypotension

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17
Q

Frontotemporal Dementia (FTLD)

A

-affects younger patients
-behavioral disinhibition, apathy, and compulsivity
-NO PLAQUES OR TANGLES
-affects executive function and social cognition
-no FDA approved treatments
-nonpharmacologic interventions focus on safety and health maintenance
-AChE inhibitors may worsen symptoms

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18
Q

Type III diabetes

A

-insulin resistance in the brain leads to increased plaque formation
-impacts neurocognition
-risk is modifiable

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19
Q

Prevention of Dementia

A

-controlling cardio risks
-depression management
-social engagement
-early detection

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20
Q

Acetylcholinesterase Inhibitors: Dementia

A

-Donepezil
-Galantamine
-Rivastigmine

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21
Q

NMDA receptor antagonists: dementia

A

memantine

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22
Q

Monoclonal antibodies: dementia

A

-Docanemab
-Lacanemab
-Aducanumab

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23
Q

mild-moderate Alzheimer’s treatments

A

-donepezil
-galantamine
-rivastigmine

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24
Q

Moderate-severe Alzheimer’s treatments

A

-Donepezil
-memantine
-Rivastigmine PATCH

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25
Q

When should therapy be discontinued for dementia?

A

-no response in 3 months
-institutionalized with severe dementia treated >/= 2 years
-patient/family believe patient has stopped responding
-goal of slowing progression is no longer reasonable

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26
Q

how to taper dementia meds

A

-taper using 50% reductions q4w

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27
Q

Rivastigmine patch therapy interuptions

A

-<3 days: restart at same or lower dose
-> 3 days, retitrate starting at 4.6 mg/hr patch

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28
Q

Rivastigmine patch: switching from oral

A

-apply patch the day following last oral dose
- <6 mg oral=4.6 mg patch
- 6-12 mg oral=9.5 mg patch

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29
Q

Donepezil patch

A

-7 day patch
-refrigerated: allow to reach RT before applying
-lower back, upper butt, or upper outer thigh
-Switch from oral to patch: apply patch at same time as last oral dose

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30
Q

True or False: When initiating a new AChEI after severe side effects with another, a 3 week washout is required.

A

False, 1 week washout
-take in AM with food
-baseline HR needed

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31
Q

side effects of acetylcholinesterase inhibitors

A

-N/V
-diarrhea
-upset stomach
-syncope
-bradycardia
-insomnia/agitation
-increased pulmonary secretion

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32
Q

monitoring for AChEI’s

A

-BP and HR
-drug interactions with Beta Blockers, diltiazem, and verapamil

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33
Q

NMDA receptor antagonists side effects

A

-hypertension
-constipation
-dizziness
-headache
-aggressive behavior

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34
Q

Donanemab

A

-binds to b-amyloid and aids plaque removal through phagocytosis
-Significantly slows clinical progression at 76 weeks in those with low/medium tau or
combined low/medium and high tau

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35
Q

Lecanemab

A

-binds amyloid beta protofibrils
-moderately less decline in measures of cognition and function than placebo

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36
Q

Aducanumab

A

-blocks second phase of aggregation
-approval was controversial

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37
Q

Who are monoclonal antibodies more effective for?

A

-noncarriers
-heterozygotes
-males
-older ages
-white

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38
Q

clinical outcomes of donanemab and locanemab

A

-Significant decrease in the amyloid burden
-Slowed decline in CDR-SB dementia rating scale

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39
Q

Adverse effects of monoclonal antibodies

A

-ARIA-E: cerebral edema
-ARIA-H: cerebral microhemorrhages
-AVOID IN ANTICOAGULATED PATIENTS

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40
Q

Initiation of Lecanumab

A

-IV biweekly for 1 hour
-mandatory monitoring after infusion: 3 hours after 1st infusion, 2 hours after 2nd, 30 min after
-safety should be monitored at 2,3, and 6.5 months
-provider must be enrolled in a patient registry

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41
Q

Vitamin E: Alzheimers

A

-antioxidant
-may combat AD
-only use if prescribed

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42
Q

Fish oil: AD

A

-may reduce beta amyloid and inflammation
-high incidence of ADRs/bleeding

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43
Q

Vitamin B12: AD

A

-lower levels associated with neurocognitive disorders
-target >500

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44
Q

Prevagen and Ginko Biloba: AD

A

-impacts on oxidative stress
-inconsistent and unreliable benefit

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45
Q

Huperzine: AD

A

-natural acetylcholinesterase inhibitor
-mor studies needed

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46
Q

Primary Open Angle Glaucoma

A

-chronic, progressive
-open anterior chamber angle
-atrophy of optic nerve
-loss of ganglion cells and their axons result in optic nerve damage and visual field loss
-both eyes affected

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47
Q

risk factors for POAG

A

-intraocular pressure> 22 mmHg
- >40 years
-family history
-African or latino
-T2DM
-high myopia
-HX of eye trauma
-vascular disease
-smoking

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48
Q

Intraocular pressure (IOP)

A
  • normal: 12-22 mmHg
  • insensitive, nonspecific diagnostic and monitoring tool
    -Patients with a normal IOP may still develop POAG and those with an IOP >22 may not
    develop it
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49
Q

formation of aqueous humor

A

-in cilliary body
-Involves carbonic anhydrase,
alpha and beta adrenergic
receptors, and sodium- and
potassium-activated adenosine
triphosphatases

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50
Q

how does aqueous humor move into the anterior chamber?

A

-pushed between the iris and lens
-then through the pupil due to pressure is posterior chamber

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51
Q

How does aqueous humor leave the eye?

A

-filtration through trabecular meshwork to the Schlemm’s canal and
through the ciliary body and
suprachoroidal space
-(uveoscleral/unconventional
outflow)

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52
Q

True or false: As ganglion nerve cells die and axon loss increases, cup becomes larger than disk in glaucoma.

A

true

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53
Q

prognosis of POAG

A

-slow progression of months to years
-functional loss is NOT REVERSIBLE
-can be treated early on

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54
Q

goal of treating glaucoma

A

preserve visual field

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55
Q

initial target reduction reduction in glaucoma

A

> /= 25% reduction in IOP
-continually reassess

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56
Q

Medications that increase aqueous humor outflow

A

-rho kinase inhibitors
-alpha-adrenergic agonists
-prostaglandin analogues
-cholinergic agents

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57
Q

Medications that decrease aqueous humor production

A

-Rho kinase inhibitors
-alpha-adrenergic agonists
-beta-adrenergic blockers
-carbonic anhydrase inhibitors

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58
Q

Keratitis

A

corneal inflammation

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59
Q

Macular edema

A

swelling in the macula

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60
Q

Uveitis

A

swelling of the uvea, the colored portion of the eye

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61
Q

Conjunctival hyperemia

A

redness of the eye

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62
Q

Blepharitis

A

inflammation of the eyelid

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63
Q

conjuctivitis

A

pink eye

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64
Q

corneal edema

A

swelling of the cornea due to fluid accumulation

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65
Q

Blood dyscrasias

A

a general term for disorders of the blood and its components

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66
Q

True or false: Systemic effects occur when the volume of eye drop exceeds the volume the eye can absorb so extra volume drains through the tear duct to nose.

A

true

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67
Q

how do you prevent nasolacrimal drainage?

A

-Putting pressure on tear duct and
closing eyes

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68
Q

True or false: Nasolacrimal occlusion increases risk and severity of systemic side effects

A

False. reduces risks

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69
Q

Prostaglandin analogues MOA

A

-increase uveoscleral and trabecular outflow of AH

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70
Q

Prostaglandin analogues considerations

A

-darkens hazel eyes
-avoid in pregnancy
-QHS

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71
Q

Prostaglandin analogues side effects

A

-EYELASH CHANGES
-HYPERPIGMENTATION
-HERPES VIRUS ACTIVATION
KERATITIS
-blurry vision
-burning/stinging
-dry eyes
-conjunctival hyperemia
-macular edema
-uveitis

-well tolerated overall

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72
Q

examples of Prostaglandin analogues

A

-LATANOPROST
-Bimatoprost
-tafluprost
-Travoprost
-Latanoprostene bunod(prodrug)

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73
Q

Beta-Adrenergic Blockers MOA

A

-reduce AH production by ciliary body

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74
Q

Beta-Adrenergic Blockers considerations

A

-use with caution and ensure NS technique if asthma, COPD, or CVD (hypotension, bradycardia, heart block, HF)
-given BID

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75
Q

Beta-Adrenergic Blockers side effects

A

-BRADYCARDIA
-BRONCHOSPASM
-DEPRESSION
-fatigue
-hypotension
-syncope
-burning/stinging
-dry eyes
-keratitis
-Uveitis

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76
Q

Selective Beta-Adrenergic Blockers for glaucoma

A

Betaxolol

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77
Q

Non-Selective Beta-Adrenergic Blockers for glaucoma

A

Timolol
-Carteolol
-Levobunolol
-Metipranonolol

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78
Q

Alpha-Adrenergic Agonists MAO

A

Decrease AH production & increase uveoscleral outflow

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79
Q

Alpha-Adrenergic Agonists considerations

A

-BID/TID: NS technique may improve response and allow for longer dosing interval
-SAFEST IN PREGNANCY
-caution with CVD, kidney disease, cerebrovascular disease, diabetes, hypertension, MAOIs, TCAs

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80
Q

Alpha-Adrenergic Agonists side effects

A

-BLEPHARITIS
-ALLERGIC TYPE RXN
-blurry vision
-burning/stinging
-conjunctivitis
-dry mouth
-fatigue
-GI upset
-headache
-hypotension
-somnolence

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81
Q

Selective Alpha-Adrenergic Agonists for glaucoma

A

-BRIMONIDINE
-Apraclonidine

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82
Q

Cholinergic Agent MOA

A

Contraction of ciliary muscle causes scleral spur to unfold
trabecular meshwork, increasing AH outflow

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83
Q

Cholinergic Agent considerations

A

-TID/QID
-caution with ocular conditions(: INFLAMMATION, cataracts, hx of retinal detachment, severe myopia)
-asthma, bladder dysfxn, CVD, COPD, GI disease

84
Q

Cholinergic Agent side effects

A

-CATARACT
-RETINAL DETACHMENT
-BRONCHOSPASM
-ciliary spasms
-conj scar/shrink
-corneal edema
-keratitis
-angle closure
-Diaphoresis
-NVD
-Salivation

85
Q

Cholinergic Agents for glaucoma

A

-pilocarpine

86
Q

Carbonic Anhydrase Inhibitors

A

Inhibit ciliary epithelium carbonic anhydrase to decrease production of AH

87
Q

Carbonic Anhydrase Inhibitors considerations

A

-BID/QID
-SULFONAMIDE ALLERGY

88
Q

Carbonic Anhydrase Inhibitors side effects

A

-ANOREXIA
-ELECTROLYE IMBALANCES
-KIDNEY STONES
-BITTER METALLIC TASTE

89
Q

Ocular Carbonic Anhydrase Inhibitors for glaucoma

A

-brinzolamide
-Dorzolamide

90
Q

Oral Carbonic Anhydrase Inhibitors for glaucoma

A

-acetazolamide
-methazolamide

91
Q

Rho Kinase Inhibitors MOA

A

Increase AH outflow through trabecular meshwork & decrease AH production

92
Q

Rho Kinase Inhibitors considerations

A

> 4 mmHg additional lowering when used as combo therapy
-QHS
-53% occurance of conjuctival hyperemia

93
Q

Rho Kinase Inhibitors side effects

A

-instillation site pain
-conjunctival hyperemia
-hemorrhage
-erythema of eyelid
-keratitis
-corneal deposits

94
Q

Rho Kinase Inhibitors for glaucoma

A

-Netarsudil (prodrug)

95
Q

Initiating medication therapy for glaucoma

A

1st line: PROSTAGLANDIN ANALOGUES, beta blockers
2nd line: all others

96
Q

how to switch glaucoma meds?

A

-initiate wwith single agent first
-if target IOP not reached
—->switch to another in same class
—>add second with different MOA
—->add 3rd with another MOA
-combo product preferred: reduce exposure to preservatives
-check IOP 4-6 weeks

97
Q

consults of ophthalmic products

A

-wait 3-5 min between products
-store in fridge if pt can’t feel drops

98
Q

Cannabinoids for glaucoma

A

-neuroprotective
-lower IOP
-poor clinical utility: short term memory and motor coordination

99
Q

how to manage burning/stinging or pain in eye drops?

A

use artificial tears 5 min before drug

100
Q

how to conjunctival hyperemia in eye drops?

A

use OTC brimonidine tartrate 0.025% drops

101
Q

Causes of erectile dysfunction

A

-Drugs: alcohol, nicotine
-diabetes
-many causes

102
Q

What causes sexual dysfunction?

A

-many hormonal changes with age
-Prevalence of SD is likely increased with advancing age

103
Q

Hormones that decrease with age?

A

-testosterone
-bioactive testosterone
-dehydroepiandrosterone

104
Q

hormones that increase with age

A

-sex hormone binding globulin (SHBG)
-Luteinizing hormone

105
Q

Data for sexual adverse effects

A

-data is not very good

106
Q

Central effects on sexual function

A

-excessive amount of 5-HT has negative effects
-inhibits dopamine, norepi, and testosterone

107
Q

Prolactin-Dopamine Relationship

A

-inverse relationship
-prolactin shuts down sexual desire: inhibitory
-at orgasm, dopamine drops and prolactin rises

108
Q

GABA, opioid peptides: sexual response

A

-decrease activation of nitric oxide synthase
-impairs erection

109
Q

Increased serotonin in lateral hypothalamus…

A

-decrease libido and impaired orgasm and ejaculation
-how?: modulation of CNS dopamine, inhibition of NO synthase

110
Q

Estrogen: sexual response

A

-small effect on sexual desire(men and women)
-important in maintaining arousal in women

111
Q

Androgens: sexual response

A

-maintain arousal in women
-Testosterone and DHT largely modulate male sexual behavior
-Very low levels of testosterone associated with decreased desire and occasionally ED
-VERY HIGH TESTOSTERONE LEVELS DO NOT MODIFY DESIRE OR BEHAVIOR

112
Q

medical conditions associated with sexual dysfunction

A

adrenal disease
-alcoholism
-atherosclerosis
-cardiac disease
-diabetes
-liver disease
-Psychiatric illness

113
Q

sexual dysfunction: antihypertensive agents

A

-beta blockers: -olol
-calcium channel blockers: nifedipine, verapamil, diltiazem

114
Q

sexual dysfunction: antidepressants

A

-SSRI: >30% fluoxetine, paroxetine…
-MAOI: 10-30% citalopram, duloxetine, venlafaxine
-TCAs: <10% bupropion, mirtazapine

115
Q

sexual dysfunction: CNS depressants

A

-barbiturates
-benzos
-alcohol

116
Q

sexual dysfunction: antipsychotics

A

-chlorpromazine
-haloperidol
-olanzapine

117
Q

sexual dysfunction: anticholinergics

A

benztropine

118
Q

sexual dysfunction: antiepileptics

A

-phenobarbital
-phenytoin
-carbamazepine

119
Q

sexual dysfunction: anti-ulcer drugs(H2 receptor blocker)

A

cimetidine

120
Q

sexual dysfunction: multiple sclerosis

A

-may occur early in course of MS
Predictive factors include:
● Increased disease activity,
● Depression and fatigue,
● Long duration of disease,
● Spasticity, bladder and bowel sx

121
Q

sexual dysfunction: Parkinson’s disease in women

A

-Hypoactive sexual desire and dysfunction
● Female orgasmic dysfunction
● Hypersexuality

122
Q

sexual dysfunction: Parkinson’s disease in men

A

-Hypoactive sexual desire and disorder
● Erectile dysfunction
● Premature ejaculation
● Anorgasmia
● Hypersexuality

123
Q

sexual dysfunction: Epilepsy

A

-30-60% of patients
-higher incidence in men

124
Q

glaucoma diagnosis

A

-tonometry: air pulse to measure IOP
-IOP not a single determinant of glaucoma
-Fundus exam
Perimetry: visual field progression

125
Q

sexual dysfunction: depression

A

Reported rates of sexual dysfunction due to SSRIs are likely
underestimate
-erectile dysfunction

126
Q

Psychotic illness

A
127
Q

Non modifiable risk factors for developing MS

A

-genetics
-age: 20-50
-geography
-viral infection

128
Q

modifiable risk factors MS

A

-smoking
-vitamin D deficiency < ng/mL
-excess body weight
-sodium intake > 4.8 g/day

129
Q

Clinically isolated syndrome (CIS)

A

-first acute episode of inflammatory demyelinating event in CNS
-one or more symptoms
-lasts 24 hours or more
-may or may not progress to MS

130
Q

MS Exacerbation/Relapse

A

-Inflammatory demyelinating event in CNS with objective
findings
-lasts 24 hours+
-Separated from prior attack by 30 days or more

131
Q

“Pseudo Relapse”

A

-Worsening or reoccurrence of neurologic symptoms without
objective findings
● Due to medical conditions or environmental factors
● NOT new disease activity

132
Q

Primary MS

A

-central: fatigue, depression, cognitive impairment
-muscular: weakness, cramping, spasm, lack of coordination
-visual: optic neuritis, nystagmussenses:
-senses: pain, tingle, burning

133
Q

Secondary MS

A
  • Respiratory infections
    ● Recurrent urinary tract
    infections
    ● Urinary calculi
    ● Depression
    ● Osteoporosis

*arise as a consequence to MS disease

134
Q

Tertiary MS

A

-Vocational problems
● Financial problems
● Social/Personal issues
● Emotional problems

-occurs after disease has progressed over long time

135
Q

Diagnosis of MS

A

combo of:
● Signs and symptoms
● Radiographic findings
● Laboratory findings

136
Q

Diagnostic tests for MS

A

-MRI: CNS lesions
-CSF studies: oligoclonal bands and IgE index
-Optical Coherence Tomography (OCT)

137
Q

Relapsing-remitting MS

A

Clinical attacks and MRI lesions with objective clinical evidence

138
Q

hallmarks of parkinson’s disease

A

-depigmentation of DA producing neurons
-presencse of lewy bodies

139
Q

drugs that can mimic parkinsons

A

-dopamine antagonist
-antiepileptics
-typical antipsychotics
-calcium channel agents
-antiemetics: PROCHLORPERAZINE AND METOCLOPRAMIDE
-ATYPYCAL ANTIPSYCHOTICS
-antihypertensives
-tetrabenazine

140
Q

PD diagnosis

A

–bradykinesia AND (resting tremor, rigidity, postural instability)
-Unilateral
-olfactory loss

141
Q

Cure of PD

A

none!

142
Q

Exercise in PD

A

-treadmill and tai chi can benefit
-help improve balance, flexibility, strength
-reduce 2nd effects of rigidity and flexed posture

143
Q

Benztropine and Trihexyphenidyl

A

-anticholinergic: don’t use in older adults
-some antiparkinsonian efficacy(tremor)
-cheat

144
Q

Anticholinergic agents: disadvantages

A

-COGNITIVE SIDE EFFECTS: MEMORY, CONFUSION, HALLUCINATIONS
-need to taper
-only helpful for tremor

145
Q

MAO-B inhibitors

A

selegiline
safinamide
rasagiline

146
Q

MAO-B advantages

A

-spares levodopa
-reduced motor fluctuation and increases on time with levodopa

147
Q

MAO-B disadvantages

A

-confusion more common with selegiline
-don’t use Safinamide with: ST Johns wort, antidepressants

148
Q

Are MAO B inhibitors neuroprotective?

A

no

149
Q

Amantadine

A

-levodopa dyskinesia
-younger patients <70
-taken at bedtime

150
Q

Does levodopa prevent mortality compared to placebo?

A

yes

151
Q

Levodopa disadvantages

A

-motor complications
-neuropsychiatric problems
-associated with peak plasma conc

152
Q

Administration of carbidopa levodopa

A

-titrate dose slowly
-ex) start with IR C/L 25/250 and increase every 1-2 days
-maximum of 8 tablets of any strength per day or no more than 200 mg carbidopa/day
-MAX 2000 mg LEVODOPA/DAY

153
Q

how to handel carbidopa/levodopa nausua?

A

-Solo doses of carbidopa 25 mg

154
Q

Levodopa absorption

A

-empty stomach without food
-dietary protein bad for absorption

155
Q

Complications of levodopa treatment

A

-wearing off
-on-off phenomena
-peak dose dyskinesias
-start hesitation(freezing)
-slow onset of response

156
Q

Ropinirole

A

Dopamine agonist

157
Q

Dopamine agonist for PD

A

-work well on motor sysmtems
-no metabolites

158
Q

dopamine agonist side effects

A

-Pleuropulmonary fibrosis
-constipation
-nasal stifness

159
Q

Serious concerns with dopamine agonists

A

-impulse control
-psychosis
-sleep attacks

160
Q

Pramipexole for PD max dose

A

4.5 mg

161
Q

Discontinuation Ropinirole, Pramipexole for PD

A

-SLOWLY
-may cause neuroleptic malignant syndrome or akinetic crisis

162
Q

Management of nausea with dopaminergic agents

A

-food or extra carbidopa

163
Q

Management of orthostasis with dopaminergic agents

A

-taper and dc amantidine, MAO-A, and DA
-lower doses of BP meds
-droxidopa

164
Q

Management of confusion with dopaminergic agents

A

-taper and dc amantidine
–reduce levodopa dose

165
Q

Management of ICD with dopaminergic agents

A

reduce dose of DA or d/c

166
Q

Management of dopamine dysregulation syndrome with dopaminergic agents

A

-limit dose increases of DA
-cutaneous apomorphine infusion
-low dose clozapine or quetiapine

167
Q

COMT inhibitor example

A

Entacapone

168
Q

why do we not use tocapone?

A

-hepatotoxicity

169
Q

When adding Entacapone, what do you need to do to levadopa?

A

reduce dose by 10-30% to reduce risk of dyskinesia

170
Q

Advanced PD strategies

A

-dose more frequently
-add dopamine agonist-add COMT inhibitor
-add selegiline, rasagiline, amantidine

171
Q

Unpredictable on off

A

-entacapone
-rasagiline
-dopamine agonist
-apomorphine
-selegiline
-consider

172
Q

Dyskinesia

A

-decrease levodopa and increase frequency
-add DA agonist
-amantadine
-clozapine
-early morning levodopa

173
Q

Sudden off periods

A

-apomorphine: causes nausea
-hypotension
-pretreat nausea with Trimethobenzamide 3 days before

174
Q

Istradefylline substrate

A

-3A4
-Digoxin(increased digoxin)
-Dofelilide (increased dofetilide)
-St Johns( decrease drug conc)

175
Q

Define mindfulness

A

brain, mind, body and
behavior , and on the powerful ways in which
emotional, mental, social, spiritual and
behavioral factors can directly affect health

176
Q

Identify examples of mindfulness practices.

A

-movement
-breathing
-meditation
-journaling

177
Q

Discuss the mental health benefits of practicing mindfulness

A

-depression
-anxiety
-stress
-sleep

178
Q

what is mindfulness NOT

A

NOT religion

179
Q

Relapsing-Remitting (RRMS)

A

-short duration: days to months
-remain symptoms free for months or years
-NO PROGRESSION OF DISEASE DURING REMISSION
-most common form

180
Q

Secondary-Progressive (SPMS)

A

-Relapses do not fully remit
-slow, steady progression

181
Q

Primary Progressive (PPMS)

A

-DO NOT have periodic relapses and remissions
-steady worsening from the start

182
Q

Poor Prognostic factors for MS

A

-male
-onset>40
-high relapse rate
-early motot/cerebellar symptoms
-early disabillity
-progressive course
-lesion size

183
Q

Vaccine reccomendations in MS

A

-2-6 weeks before starting DMT
-avoid live attenuated if:
-immunosuppressed
-recently dc DMT
-MS relapse
-high dose steriods

184
Q

Inactivated vaccines in MS

A

immune response may be diminished if receiving DMT

185
Q

MS relapse: moderate to severe

A

-oral Prednisone daily for 3-7 days
-IV methylprednisolone 3-5 dys

186
Q

MS relapse: refractory relapses

A

Plasmapheresis

187
Q

Interferons for MS

A

-low efficacy, low risk
-IM and SC forms
-High incidence of flu like symptoms with less injections
-AVOID IN SEVERE DEPRESSION

188
Q

Interferon monitoring

A

-CBC
-LFT
-thyroid function
-electrolytes

189
Q

Copaxone

A

-glatiraramer acetate drug for MS
-20 mg SC every day
-low efficacy, low risk
-flushing, chest pain, anxiety

190
Q

Glatopa

A

-glatiraramer acetate drug for MS
-20 mg SC every day
-low efficacy, low risk
-flushing, chest pain, anxiety

191
Q

Aubagia

A

-Teriflunomide MS drug
-decreases warfarin effect
-baseline pregnancy test

-HAPATOTOXICITY AND TERATOTOXICITY

192
Q

Dimethyl Fumarate

A

-may cause flushing and GI SE
-administer with high fat/protein food or nonenteric coated aspirin 30 min prior

193
Q

Diroximel Fumarate

A

-avoid with alcohol
-take with aspirin to decrease flushing
-Limit fat to < 30g and calories <700 if take with
food

194
Q

Monomethyl Fumarate

A

-store unopened bottle in fridge
-3 months at room temp
-take with aspirin to reduce flushing

195
Q

Sphingosine I Phosphate Modulators (SIP)

A

-mod, mod for MS
-REBOUND SYNDROME WHEN D/C
-contraindicated if experianced a cardiac event in last 6 months or 2nd, 3rd degree heart block.
-NIOSH hazard

196
Q

Sphingosine I Phosphate Modulators (SIP) examples

A

-fingolimod: >10, HR for 6 hours
-ozanimod: not in all hepatic impair
-siponimod: HR for 6 hours specific people
-ponesimod: HR for 6 hours specific

197
Q

Natalizumab (Tysabri)

A

-IV infusion for MS
-REBOUND SYNDROME
-JCV antibody
-high efficacy but high risk

198
Q

Anti-CD20 Monoclonal Antibodies

A

-Ocrelizumab only approved DMT for PPMS
-base line pregnancy test
-high efficacy, high risk

199
Q

Ocrelizumab

A

-IV every 4 months
-pre meds: methylpred, antihistamine, tylenol

200
Q

Ocrelizumab/hyaluronidase

A

-SC every 6 months
-pre meds: dexamethasone, antihistamine, tylenol

201
Q

Ofatumumab

A

-SC weekly for 3 weeks, then monthly
-first dose with health care professional

202
Q

Ubituximab

A

-IV treatment
-pre meds: methylpred, antihistamine, tylenol

203
Q

Cladribine (Mavenclad) monitoring

A

-baseline and prior to each treatment: CBC, pregnancy
-LYMPHOCYTES MUST BE OVER 800 BEFORE 2ND YEAR

204
Q

Cladribine (Mavenclad) contradictions

A

-current malignancy
-pregnant or breastfeeding
-HIV or active chronic infection

205
Q
A

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