Final Exam review Flashcards
Dementia background
-AD is most common
-prevalence is expected to increase
-huge cost to healthcare system
Social cognition
-recognizing other’s emotions
Learning and memory
-long term memory
-cued recall
-unprompted recall
Executive function
-planning
-decision making
-IADL functions
Complex Attention
-processing speed
-divided attention
Language
-object naming
-animal fluency
-receptive language
Early stages of dementia
-chronic cognitive decline
-Instrumental activities of Daily Living affected: Managing finances, medication managment, Housekeeping, driving, shopping, meal prep
Middle to later stages of dementia
-activities of daily living
-bathing
-toileting
-dressing
-grooming
-walking
-eating meals
Lab tests in demential
-used to rule out differential diagnosis
-Vitamin B12: < 400
-TSH
-CBC: anemia and infection
-BMP: hyponatremia
-HIV
-Syphilis
Mini-cog for dementia
-3 item repeat
-clock draw
-3 item recall
Medications that contribute to cognitive changes
-ANTICHOLINERGICS
-antihypertensives
-benzos
-corticosteroids
-hypoglycemic agents
-muscle relaxants
-opioid
-NSAIDs
-sedative hypnotics
Alzheimer’s risk factors
-age
-genetics
-vascular
-head injury
-poor education
-poor hearing
-depression
-social isolation
Alzheimer’s pathophysiology
-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
Alzheimer’s lifestyle modifications
-Omega 3
-folic acid
-Vitamin B
-Vitamin E
-physical activity
-mental activity
-social engagement
-music therapy
Vascular dementia
-caused by stroke/TIA, uncontrolled BP, diabetes, high cholesterol
-affects executive function and complex attention
-Donepezil, galantamine, rivastigmine
Lewy Body Dementia(DLB)
-fluctuating cognition, hallucinations, parkinsonism
-affects learning/memory and cognitive function
–Donepezil, galantamine, rivastigmine
-avoid antipsychotics
-levodopa for parkinsonism
-fludrocortisone or midodrine for orthostatic hypotension
Frontotemporal Dementia (FTLD)
-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
Type III diabetes
-insulin resistance in the brain leads to increased plaque formation
-impacts neurocognition
-risk is modifiable
Prevention of Dementia
-controlling cardio risks
-depression management
-social engagement
-early detection
Acetylcholinesterase Inhibitors: Dementia
-Donepezil
-Galantamine
-Rivastigmine
NMDA receptor antagonists: dementia
memantine
Monoclonal antibodies: dementia
-Docanemab
-Lacanemab
-Aducanumab
mild-moderate Alzheimer’s treatments
-donepezil
-galantamine
-rivastigmine
Moderate-severe Alzheimer’s treatments
-Donepezil
-memantine
-Rivastigmine PATCH
When should therapy be discontinued for dementia?
-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
how to taper dementia meds
-taper using 50% reductions q4w
Rivastigmine patch therapy interuptions
-<3 days: restart at same or lower dose
-> 3 days, retitrate starting at 4.6 mg/hr patch
Rivastigmine patch: switching from oral
-apply patch the day following last oral dose
- <6 mg oral=4.6 mg patch
- 6-12 mg oral=9.5 mg patch
Donepezil patch
-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
True or False: When initiating a new AChEI after severe side effects with another, a 3 week washout is required.
False, 1 week washout
-take in AM with food
-baseline HR needed
side effects of acetylcholinesterase inhibitors
-N/V
-diarrhea
-upset stomach
-syncope
-bradycardia
-insomnia/agitation
-increased pulmonary secretion
monitoring for AChEI’s
-BP and HR
-drug interactions with Beta Blockers, diltiazem, and verapamil
NMDA receptor antagonists side effects
-hypertension
-constipation
-dizziness
-headache
-aggressive behavior
Donanemab
-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
Lecanemab
-binds amyloid beta protofibrils
-moderately less decline in measures of cognition and function than placebo
Aducanumab
-blocks second phase of aggregation
-approval was controversial
Who are monoclonal antibodies more effective for?
-noncarriers
-heterozygotes
-males
-older ages
-white
clinical outcomes of donanemab and locanemab
-Significant decrease in the amyloid burden
-Slowed decline in CDR-SB dementia rating scale
Adverse effects of monoclonal antibodies
-ARIA-E: cerebral edema
-ARIA-H: cerebral microhemorrhages
-AVOID IN ANTICOAGULATED PATIENTS
Initiation of Lecanumab
-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
Vitamin E: Alzheimers
-antioxidant
-may combat AD
-only use if prescribed
Fish oil: AD
-may reduce beta amyloid and inflammation
-high incidence of ADRs/bleeding
Vitamin B12: AD
-lower levels associated with neurocognitive disorders
-target >500
Prevagen and Ginko Biloba: AD
-impacts on oxidative stress
-inconsistent and unreliable benefit
Huperzine: AD
-natural acetylcholinesterase inhibitor
-mor studies needed
Primary Open Angle Glaucoma
-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
risk factors for POAG
-intraocular pressure> 22 mmHg
- >40 years
-family history
-African or latino
-T2DM
-high myopia
-HX of eye trauma
-vascular disease
-smoking
Intraocular pressure (IOP)
- 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
formation of aqueous humor
-in cilliary body
-Involves carbonic anhydrase,
alpha and beta adrenergic
receptors, and sodium- and
potassium-activated adenosine
triphosphatases
how does aqueous humor move into the anterior chamber?
-pushed between the iris and lens
-then through the pupil due to pressure is posterior chamber
How does aqueous humor leave the eye?
-filtration through trabecular meshwork to the Schlemm’s canal and
through the ciliary body and
suprachoroidal space
-(uveoscleral/unconventional
outflow)
True or false: As ganglion nerve cells die and axon loss increases, cup becomes larger than disk in glaucoma.
true
prognosis of POAG
-slow progression of months to years
-functional loss is NOT REVERSIBLE
-can be treated early on
goal of treating glaucoma
preserve visual field
initial target reduction reduction in glaucoma
> /= 25% reduction in IOP
-continually reassess
Medications that increase aqueous humor outflow
-rho kinase inhibitors
-alpha-adrenergic agonists
-prostaglandin analogues
-cholinergic agents
Medications that decrease aqueous humor production
-Rho kinase inhibitors
-alpha-adrenergic agonists
-beta-adrenergic blockers
-carbonic anhydrase inhibitors
Keratitis
corneal inflammation
Macular edema
swelling in the macula
Uveitis
swelling of the uvea, the colored portion of the eye
Conjunctival hyperemia
redness of the eye
Blepharitis
inflammation of the eyelid
conjuctivitis
pink eye
corneal edema
swelling of the cornea due to fluid accumulation
Blood dyscrasias
a general term for disorders of the blood and its components
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.
true
how do you prevent nasolacrimal drainage?
-Putting pressure on tear duct and
closing eyes
True or false: Nasolacrimal occlusion increases risk and severity of systemic side effects
False. reduces risks
Prostaglandin analogues MOA
-increase uveoscleral and trabecular outflow of AH
Prostaglandin analogues considerations
-darkens hazel eyes
-avoid in pregnancy
-QHS
Prostaglandin analogues side effects
-EYELASH CHANGES
-HYPERPIGMENTATION
-HERPES VIRUS ACTIVATION
KERATITIS
-blurry vision
-burning/stinging
-dry eyes
-conjunctival hyperemia
-macular edema
-uveitis
-well tolerated overall
examples of Prostaglandin analogues
-LATANOPROST
-Bimatoprost
-tafluprost
-Travoprost
-Latanoprostene bunod(prodrug)
Beta-Adrenergic Blockers MOA
-reduce AH production by ciliary body
Beta-Adrenergic Blockers considerations
-use with caution and ensure NS technique if asthma, COPD, or CVD (hypotension, bradycardia, heart block, HF)
-given BID
Beta-Adrenergic Blockers side effects
-BRADYCARDIA
-BRONCHOSPASM
-DEPRESSION
-fatigue
-hypotension
-syncope
-burning/stinging
-dry eyes
-keratitis
-Uveitis
Selective Beta-Adrenergic Blockers for glaucoma
Betaxolol
Non-Selective Beta-Adrenergic Blockers for glaucoma
Timolol
-Carteolol
-Levobunolol
-Metipranonolol
Alpha-Adrenergic Agonists MAO
Decrease AH production & increase uveoscleral outflow
Alpha-Adrenergic Agonists considerations
-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
Alpha-Adrenergic Agonists side effects
-BLEPHARITIS
-ALLERGIC TYPE RXN
-blurry vision
-burning/stinging
-conjunctivitis
-dry mouth
-fatigue
-GI upset
-headache
-hypotension
-somnolence
Selective Alpha-Adrenergic Agonists for glaucoma
-BRIMONIDINE
-Apraclonidine
Cholinergic Agent MOA
Contraction of ciliary muscle causes scleral spur to unfold
trabecular meshwork, increasing AH outflow
Cholinergic Agent considerations
-TID/QID
-caution with ocular conditions(: INFLAMMATION, cataracts, hx of retinal detachment, severe myopia)
-asthma, bladder dysfxn, CVD, COPD, GI disease
Cholinergic Agent side effects
-CATARACT
-RETINAL DETACHMENT
-BRONCHOSPASM
-ciliary spasms
-conj scar/shrink
-corneal edema
-keratitis
-angle closure
-Diaphoresis
-NVD
-Salivation
Cholinergic Agents for glaucoma
-pilocarpine
Carbonic Anhydrase Inhibitors
Inhibit ciliary epithelium carbonic anhydrase to decrease production of AH
Carbonic Anhydrase Inhibitors considerations
-BID/QID
-SULFONAMIDE ALLERGY
Carbonic Anhydrase Inhibitors side effects
-ANOREXIA
-ELECTROLYE IMBALANCES
-KIDNEY STONES
-BITTER METALLIC TASTE
Ocular Carbonic Anhydrase Inhibitors for glaucoma
-brinzolamide
-Dorzolamide
Oral Carbonic Anhydrase Inhibitors for glaucoma
-acetazolamide
-methazolamide
Rho Kinase Inhibitors MOA
Increase AH outflow through trabecular meshwork & decrease AH production
Rho Kinase Inhibitors considerations
> 4 mmHg additional lowering when used as combo therapy
-QHS
-53% occurance of conjuctival hyperemia
Rho Kinase Inhibitors side effects
-instillation site pain
-conjunctival hyperemia
-hemorrhage
-erythema of eyelid
-keratitis
-corneal deposits
Rho Kinase Inhibitors for glaucoma
-Netarsudil (prodrug)
Initiating medication therapy for glaucoma
1st line: PROSTAGLANDIN ANALOGUES, beta blockers
2nd line: all others
how to switch glaucoma meds?
-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
consults of ophthalmic products
-wait 3-5 min between products
-store in fridge if pt can’t feel drops
Cannabinoids for glaucoma
-neuroprotective
-lower IOP
-poor clinical utility: short term memory and motor coordination
how to manage burning/stinging or pain in eye drops?
use artificial tears 5 min before drug
how to conjunctival hyperemia in eye drops?
use OTC brimonidine tartrate 0.025% drops
Causes of erectile dysfunction
-Drugs: alcohol, nicotine
-diabetes
-many causes
What causes sexual dysfunction?
-many hormonal changes with age
-Prevalence of SD is likely increased with advancing age
Hormones that decrease with age?
-testosterone
-bioactive testosterone
-dehydroepiandrosterone
hormones that increase with age
-sex hormone binding globulin (SHBG)
-Luteinizing hormone
Data for sexual adverse effects
-data is not very good
Central effects on sexual function
-excessive amount of 5-HT has negative effects
-inhibits dopamine, norepi, and testosterone
Prolactin-Dopamine Relationship
-inverse relationship
-prolactin shuts down sexual desire: inhibitory
-at orgasm, dopamine drops and prolactin rises
GABA, opioid peptides: sexual response
-decrease activation of nitric oxide synthase
-impairs erection
Increased serotonin in lateral hypothalamus…
-decrease libido and impaired orgasm and ejaculation
-how?: modulation of CNS dopamine, inhibition of NO synthase
Estrogen: sexual response
-small effect on sexual desire(men and women)
-important in maintaining arousal in women
Androgens: sexual response
-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
medical conditions associated with sexual dysfunction
adrenal disease
-alcoholism
-atherosclerosis
-cardiac disease
-diabetes
-liver disease
-Psychiatric illness
sexual dysfunction: antihypertensive agents
-beta blockers: -olol
-calcium channel blockers: nifedipine, verapamil, diltiazem
sexual dysfunction: antidepressants
-SSRI: >30% fluoxetine, paroxetine…
-MAOI: 10-30% citalopram, duloxetine, venlafaxine
-TCAs: <10% bupropion, mirtazapine
sexual dysfunction: CNS depressants
-barbiturates
-benzos
-alcohol
sexual dysfunction: antipsychotics
-chlorpromazine
-haloperidol
-olanzapine
sexual dysfunction: anticholinergics
benztropine
sexual dysfunction: antiepileptics
-phenobarbital
-phenytoin
-carbamazepine
sexual dysfunction: anti-ulcer drugs(H2 receptor blocker)
cimetidine
sexual dysfunction: multiple sclerosis
-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
sexual dysfunction: Parkinson’s disease in women
-Hypoactive sexual desire and dysfunction
● Female orgasmic dysfunction
● Hypersexuality
sexual dysfunction: Parkinson’s disease in men
-Hypoactive sexual desire and disorder
● Erectile dysfunction
● Premature ejaculation
● Anorgasmia
● Hypersexuality
sexual dysfunction: Epilepsy
-30-60% of patients
-higher incidence in men
glaucoma diagnosis
-tonometry: air pulse to measure IOP
-IOP not a single determinant of glaucoma
-Fundus exam
Perimetry: visual field progression
sexual dysfunction: depression
Reported rates of sexual dysfunction due to SSRIs are likely
underestimate
-erectile dysfunction
Psychotic illness
Non modifiable risk factors for developing MS
-genetics
-age: 20-50
-geography
-viral infection
modifiable risk factors MS
-smoking
-vitamin D deficiency < ng/mL
-excess body weight
-sodium intake > 4.8 g/day
Clinically isolated syndrome (CIS)
-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
MS Exacerbation/Relapse
-Inflammatory demyelinating event in CNS with objective
findings
-lasts 24 hours+
-Separated from prior attack by 30 days or more
“Pseudo Relapse”
-Worsening or reoccurrence of neurologic symptoms without
objective findings
● Due to medical conditions or environmental factors
● NOT new disease activity
Primary MS
-central: fatigue, depression, cognitive impairment
-muscular: weakness, cramping, spasm, lack of coordination
-visual: optic neuritis, nystagmussenses:
-senses: pain, tingle, burning
Secondary MS
- Respiratory infections
● Recurrent urinary tract
infections
● Urinary calculi
● Depression
● Osteoporosis
*arise as a consequence to MS disease
Tertiary MS
-Vocational problems
● Financial problems
● Social/Personal issues
● Emotional problems
-occurs after disease has progressed over long time
Diagnosis of MS
combo of:
● Signs and symptoms
● Radiographic findings
● Laboratory findings
Diagnostic tests for MS
-MRI: CNS lesions
-CSF studies: oligoclonal bands and IgE index
-Optical Coherence Tomography (OCT)
Relapsing-remitting MS
Clinical attacks and MRI lesions with objective clinical evidence
hallmarks of parkinson’s disease
-depigmentation of DA producing neurons
-presencse of lewy bodies
drugs that can mimic parkinsons
-dopamine antagonist
-antiepileptics
-typical antipsychotics
-calcium channel agents
-antiemetics: PROCHLORPERAZINE AND METOCLOPRAMIDE
-ATYPYCAL ANTIPSYCHOTICS
-antihypertensives
-tetrabenazine
PD diagnosis
–bradykinesia AND (resting tremor, rigidity, postural instability)
-Unilateral
-olfactory loss
Cure of PD
none!
Exercise in PD
-treadmill and tai chi can benefit
-help improve balance, flexibility, strength
-reduce 2nd effects of rigidity and flexed posture
Benztropine and Trihexyphenidyl
-anticholinergic: don’t use in older adults
-some antiparkinsonian efficacy(tremor)
-cheat
Anticholinergic agents: disadvantages
-COGNITIVE SIDE EFFECTS: MEMORY, CONFUSION, HALLUCINATIONS
-need to taper
-only helpful for tremor
MAO-B inhibitors
selegiline
safinamide
rasagiline
MAO-B advantages
-spares levodopa
-reduced motor fluctuation and increases on time with levodopa
MAO-B disadvantages
-confusion more common with selegiline
-don’t use Safinamide with: ST Johns wort, antidepressants
Are MAO B inhibitors neuroprotective?
no
Amantadine
-levodopa dyskinesia
-younger patients <70
-taken at bedtime
Does levodopa prevent mortality compared to placebo?
yes
Levodopa disadvantages
-motor complications
-neuropsychiatric problems
-associated with peak plasma conc
Administration of carbidopa levodopa
-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
how to handel carbidopa/levodopa nausua?
-Solo doses of carbidopa 25 mg
Levodopa absorption
-empty stomach without food
-dietary protein bad for absorption
Complications of levodopa treatment
-wearing off
-on-off phenomena
-peak dose dyskinesias
-start hesitation(freezing)
-slow onset of response
Ropinirole
Dopamine agonist
Dopamine agonist for PD
-work well on motor sysmtems
-no metabolites
dopamine agonist side effects
-Pleuropulmonary fibrosis
-constipation
-nasal stifness
Serious concerns with dopamine agonists
-impulse control
-psychosis
-sleep attacks
Pramipexole for PD max dose
4.5 mg
Discontinuation Ropinirole, Pramipexole for PD
-SLOWLY
-may cause neuroleptic malignant syndrome or akinetic crisis
Management of nausea with dopaminergic agents
-food or extra carbidopa
Management of orthostasis with dopaminergic agents
-taper and dc amantidine, MAO-A, and DA
-lower doses of BP meds
-droxidopa
Management of confusion with dopaminergic agents
-taper and dc amantidine
–reduce levodopa dose
Management of ICD with dopaminergic agents
reduce dose of DA or d/c
Management of dopamine dysregulation syndrome with dopaminergic agents
-limit dose increases of DA
-cutaneous apomorphine infusion
-low dose clozapine or quetiapine
COMT inhibitor example
Entacapone
why do we not use tocapone?
-hepatotoxicity
When adding Entacapone, what do you need to do to levadopa?
reduce dose by 10-30% to reduce risk of dyskinesia
Advanced PD strategies
-dose more frequently
-add dopamine agonist-add COMT inhibitor
-add selegiline, rasagiline, amantidine
Unpredictable on off
-entacapone
-rasagiline
-dopamine agonist
-apomorphine
-selegiline
-consider
Dyskinesia
-decrease levodopa and increase frequency
-add DA agonist
-amantadine
-clozapine
-early morning levodopa
Sudden off periods
-apomorphine: causes nausea
-hypotension
-pretreat nausea with Trimethobenzamide 3 days before
Istradefylline substrate
-3A4
-Digoxin(increased digoxin)
-Dofelilide (increased dofetilide)
-St Johns( decrease drug conc)
Define mindfulness
brain, mind, body and
behavior , and on the powerful ways in which
emotional, mental, social, spiritual and
behavioral factors can directly affect health
Identify examples of mindfulness practices.
-movement
-breathing
-meditation
-journaling
Discuss the mental health benefits of practicing mindfulness
-depression
-anxiety
-stress
-sleep
what is mindfulness NOT
NOT religion
Relapsing-Remitting (RRMS)
-short duration: days to months
-remain symptoms free for months or years
-NO PROGRESSION OF DISEASE DURING REMISSION
-most common form
Secondary-Progressive (SPMS)
-Relapses do not fully remit
-slow, steady progression
Primary Progressive (PPMS)
-DO NOT have periodic relapses and remissions
-steady worsening from the start
Poor Prognostic factors for MS
-male
-onset>40
-high relapse rate
-early motot/cerebellar symptoms
-early disabillity
-progressive course
-lesion size
Vaccine reccomendations in MS
-2-6 weeks before starting DMT
-avoid live attenuated if:
-immunosuppressed
-recently dc DMT
-MS relapse
-high dose steriods
Inactivated vaccines in MS
immune response may be diminished if receiving DMT
MS relapse: moderate to severe
-oral Prednisone daily for 3-7 days
-IV methylprednisolone 3-5 dys
MS relapse: refractory relapses
Plasmapheresis
Interferons for MS
-low efficacy, low risk
-IM and SC forms
-High incidence of flu like symptoms with less injections
-AVOID IN SEVERE DEPRESSION
Interferon monitoring
-CBC
-LFT
-thyroid function
-electrolytes
Copaxone
-glatiraramer acetate drug for MS
-20 mg SC every day
-low efficacy, low risk
-flushing, chest pain, anxiety
Glatopa
-glatiraramer acetate drug for MS
-20 mg SC every day
-low efficacy, low risk
-flushing, chest pain, anxiety
Aubagia
-Teriflunomide MS drug
-decreases warfarin effect
-baseline pregnancy test
-HAPATOTOXICITY AND TERATOTOXICITY
Dimethyl Fumarate
-may cause flushing and GI SE
-administer with high fat/protein food or nonenteric coated aspirin 30 min prior
Diroximel Fumarate
-avoid with alcohol
-take with aspirin to decrease flushing
-Limit fat to < 30g and calories <700 if take with
food
Monomethyl Fumarate
-store unopened bottle in fridge
-3 months at room temp
-take with aspirin to reduce flushing
Sphingosine I Phosphate Modulators (SIP)
-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
Sphingosine I Phosphate Modulators (SIP) examples
-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
Natalizumab (Tysabri)
-IV infusion for MS
-REBOUND SYNDROME
-JCV antibody
-high efficacy but high risk
Anti-CD20 Monoclonal Antibodies
-Ocrelizumab only approved DMT for PPMS
-base line pregnancy test
-high efficacy, high risk
Ocrelizumab
-IV every 4 months
-pre meds: methylpred, antihistamine, tylenol
Ocrelizumab/hyaluronidase
-SC every 6 months
-pre meds: dexamethasone, antihistamine, tylenol
Ofatumumab
-SC weekly for 3 weeks, then monthly
-first dose with health care professional
Ubituximab
-IV treatment
-pre meds: methylpred, antihistamine, tylenol
Cladribine (Mavenclad) monitoring
-baseline and prior to each treatment: CBC, pregnancy
-LYMPHOCYTES MUST BE OVER 800 BEFORE 2ND YEAR
Cladribine (Mavenclad) contradictions
-current malignancy
-pregnant or breastfeeding
-HIV or active chronic infection
