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Pharm III > Lecture 6 (neuro) -Exam 3 > Flashcards

Lecture 6 (neuro) -Exam 3 Flashcards

1
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2
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What is the Stroke Management Timeline?

A
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3
Q

Commonly tested on

Stroke
* What is the minimal initial evaluation prior to giving tPA? (2)

A
  • Blood glucose level
  • CT without contrast
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4
Q

Stroke
* What is the txt option and when do you give it? Who is it not recommended for? (3)

A

tPA within 4.5 hours after stroke

Not recommended for
* Nondisabling stroke with NIHSS score 0-5 (not super severe)
* Extensive bleeding risk
* CT evidence of extensive, irreversible injury

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5
Q

Time = brain
* What was the outcome with tPA within 3 hours?

A

32% patients given tPA and 23% of patients given placebo had a good outcome at 3 months (modified Rankin scale score 0 or 1)

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6
Q

Time = brain
* What was the outcome when tPA is given within 3-4.5 hr (2)

A
  • 35% patient given tPA and 30% of patients given placebo had a good outcome at 3 months (modified Rankin scale score 0 to 1)
  • Large intracerebral hemorrhage occurred in 6.8% of patients given tPA and 1.3% of patients given placebo

Over 4.5 hr= decrease outcome

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7
Q

Fill in for the modified rankin scale

A
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8
Q

Wake up trial
* What happened with the patients?
* What was historic recommendation?

A
  • Wake-up stroke-patient goes to sleep normal; wakes up with stroke symptoms
  • Historic recommendation – no tPA (bc did not know duration)
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9
Q

Wake up trial
* What was the populatoin group?
* What was the criteria for the trial? (3)
* What scoring did they use?
* What class recommendation?
* What is still preferred if available?

A

RCT 503 patients with unclear stroke onset (94% woke up with stroke)

Randomized to tPA or placebo within 4.5 hours of stroke discovery
* Abnormal diffuse-weighted MRI, not > 1/3 territory of MCA
* NIHSS score ≤ 25
* No planned thrombectomy

90-day modified Rankin score 0 or 1- 53% treatment group and 42% placebo group

Class IIa recommendation for patients who meet criteria

Thrombectomy still preferred if available

For clinical, not testing-> if over 4.5 hours or unknown, no tPA

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10
Q

What is the TPA criteria? (3)

A
  • Age 18 years or older
  • Clinical dx of ischemic stroke with significant deficit
  • Time of symptom onset established to be < 4.5 hours before treatment
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11
Q

Low yield but know red and the BP

TPA criteria
* Who cannot get tPA?

A
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12
Q

KNOW RED for sure

TPA criteria
* What are the bleeding diathesis? (6)

A
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13
Q

TPA criteria
* What are the additional exclusion criteria between 3-4.5 hrs? (4)

A
  • Age >80 years
  • Severe stroke (NIHSS > 25)
  • History of diabetes and prior stroke
  • Taking an oral anticoagulant regardless of INR
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14
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There was a past question in spring about the MOA

Thrombolytics

A
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15
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Said FYI

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16
Q

tPA monitoring
* Admission to where?
* What do you need to monitor and how often? (3)
* What should the BP be maintained at?

A

Admission to intensive care unit

Close neurologic and cardiovascular including blood pressure
* Every 15 minutes for 2 hours after tPA administration, then
* Every 30 minutes for 6 hours, then
* Every hour for next 16 hours

Blood pressure should be maintained < 180/105 for at least 24 hours

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17
Q

Thrombectomy
* When is it a first line recommended?
* Most studies evaluated what?
* What is the timeframe?

A

First-line recommendation when performed within 6 hours of stroke onset if not a candidate for tPA
* Most studies evaluated internal carotid artery and first segment of MCA
* > 6-to-24-hour thrombectomy

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18
Q

Thrombectomy
* What did the dawn/defuse trials do and show?

A
  • NIHSS ≥ 10 who met specific MRI criteria and stroke onset between 6 and 24 hours earlier
  • Large anterior circulation strokes
  • Modified Rankin scale score of 0 to 2 at 90 days 49% in treatment group; 13% control group
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19
Q

Transient ischemic attack (TIA)
* What is it?
* What can happen after? Who has a higher risk?

A

Transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia without radiographic evidence of infarction

Incidence of subsequent stroke in 48 hours is high (4 to 10%)
* Higher ABCD2 score = higher risk (USE THIS SCORE TO SEE WHO IS HIGHER RISK OF STROKE)

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20
Q

I believe low yield

Transient ischemic attack (TIA)
* What is the risk stratification instrument?

A
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21
Q

Transient ischemic attack (TIA)
* What is the initial txt? (2)

A
  • Evaluation for carotid artery versus cerebral artery
  • Carotid – endarterectomy vs stenting (if candiates for)
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22
Q

Transient ischemic attack (TIA)
* What is the txt for patients without cardioembolic source depending on ABCD2 score?

A
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23
Q

AIS or TIA - Antiplatelet therapy (non cardioembolic)
* When do you start seconday preventation? (2)

A

Therapy at presentation
* Start immediately in patients not candidates for tPA
* Start 24 hours after tPA administration

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24
Q

AIS or TIA - Antiplatelet therapy (non cardioembolic)
* Who is it recommended for? What is the medication/dose?

A

Recommended for patients with
* ABCD2 score < 4 (TIA)
* NIHSS score > 5 (ischemic stroke)

Dose = 162 to 325mg of ASPIRIN daily

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25
Q

AIS or TIA - Antiplatelet therapy (non-cardioembolic)
* Duel antiplatelet therapy is recommended for who? (3)

A
  • NIHSS ≤ 5 who are not candidates for tPA
  • ABCD2 score ≥ 4
  • Intracranial large artery stenosis of > 70 %
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26
Q

AIS or TIA - Antiplatelet therapy (non-cardioembolic)-> Dual Antiplatelet Therapy
* What are the short term benefit?
* What is the long term benfit?
* What is recommended in high risk patients?

A
  • Aspirin + clopidogrel x 21 days lowered 90-day stroke risk
  • Long-term DAPT offered no outcome benefits / increased bleeding risk
  • 90-day therapy recommended in select high-risk patients (see guidelines)
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27
Q

AIS or TIA - Antiplatelet therapy (non-cardioembolic)
* What is the dosage for dual treatment? When do you switch to single treatment?

A
  • Aspirin 325 mg x 1, then 81mg daily plus
  • Clopidogrel 300mg x1, then 75 mg daily
  • Single agent therapy after 21 days
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28
Q

AIS or TIA - Antiplatelet therapy (non-cardioembolic)
* What is the long term single agent therapy? (3)

A
  • Aspirin 81mg PO daily or
  • Clopidogrel 75mg PO daily or
  • Aspirin plus dipyridamole 25mg/200mg PO BID
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29
Q

AIS or TIA – Anticoagulation (cardioembolic)
* TIA: May consider early initation if what?

A

May consider early initiation if clear indication for anticoagulation
* Atrial fibrillation
* Venous thromboembolism
* Mechanical heart valve

Anticoagulation has a limited role for acute therapy

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30
Q

AIS or TIA – Anticoagulation (cardioembolic)
* What is the recommendation for AIS

A

Anticoagulation generally not recommended as acute therapy

Anticoagulation has a limited role for acute therapy-> TPA is antithromblytic

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31
Q

AIS or TIA – Anticoagulation (cardioembolic)
* What is the long term therapy? (2)

A

Oral anticoagulants
* Warfarin if mechanical valve
* DOACs if no mechanical valve

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32
Q

AIS or TIA – Secondary prevention
* What are the risk factor management? (6)

A
  • Weight control
  • Exercise
  • Smoking cessation
  • Limit ETOH
  • Cholesterol control - statin (add on after)
  • Blood pressure control
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33
Q

Blood Pressure Management
* What shows no benefit?
* What is reasonable with BP?

A
  • f BP is < 220/120 mmHg, treatment of HTN within the first 48 to 72 hours after acute ischemic stroke (AIS) is of no benefit
  • If BP is ≥ 220/120 mmHg, the benefit of lowering BP is unknown, but lowering by 15% in the first 48 to 72 hours after AIS is reasonable
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34
Q

Blood Pressure Management
* What is the tPA BP goal ?
* What is the BP goal for mechanical thrombectomy?

A
  • tPA goal: BP should be maintained below 180/105 mmHg and for 24 hours after administration
  • If mechanical thrombectomy: It is reasonable to maintain BP below 180/105 mmHg during and for 24 hours after the procedure
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35
Q

Subarachnoid hemorrhage (SAH)
* What is the MC SXS?
* What is the MCC?

A

Sudden onset of severe headache
* Thunderclap
* “worst headache of my life”

MCC (85%) – ruptured aneurysm

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36
Q

Subarachnoid hemorrhage (SAH)
* Treatment is aimed at what? What are the examples (4)

A

Treatment primarily supportive aimed at decreasing re-rupture
* Surgical coiling (non-invas) or clipping (invas)
* Reverse anticoagulation
* Decrease blood pressure (SBP < 160, MAP < 110mm Hg)
* ± antiepileptics – seizure prophylaxis (all patients-keppra is an example)

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37
Q

Subarachnoid hemorrhage (SAH)
* What is definitive treatment? (2)

A

Definitive coaling or clipping

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38
Q

SAH
* High incidence of what? When?

A

High incidence of vasospasm and delayed cerebral ischemia (DCI) within 2 weeks
* 30% of patients with SAH (4 to 14 days after initial event)

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39
Q

SAH
* What will the patients develop with vasospasms? (6)

A

Patients develop new focal neurologic impairment
* Hemiparesis
* Aphasia
* Apraxia
* Hemianopia
* Decrease of GCS by 2 points for 1 hour
* Not attributed to other causes

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40
Q

SAH - DCI
* What are the treatment goals? (2)
* What is first line+ dose? For who? What does it improve?

A

Treatment goals
* Maintain euvolemia – MC fluid recommendation 0.9% sodium chloride
* Prevent vasospasm

Nimodipine
* All patients with SAH within 48 hours
* 60mg PO/NG Q4H x 21 days
* Improved odds of good outcome, reduced odds of deficit, mortality or both

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41
Q

SAH-DCI
* What is the MOA of CCB?
* What is an unique characteristic of Nimodipine that is good for cerebral BVs?

A
  • Block voltage-gated L-type calcium channels in their inactive conformation
  • Avoid Ca influx; prevents vasoconstriction
  • Lipophilic; preference for cerebral blood vessels
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42
Q

SAH - DCI
* What are the SE of CCB? (5)

A
  • Blood pressure fluctuations
  • Monitor to prevent decrease in cerebral perfusion pressure
  • Headache,
  • Flushing
  • Edema
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43
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A
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44
Q

What do you need to rule out with seizures

A

Need to rule out things that can cause seizures

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45
Q

Generalized (change in consciousness)->MOTOR
* What are the different types (3) Example some of them

A

Tonic (total stiffness) and/or clonic

Myoclonic (think about the girl eating the cereal)
* Small muscle contractions
* MC with stress, sleep deprivation

Atonic – loss of muscle tone
* Drop attacks

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46
Q

Generalized (change in consciousness)->NON- MOTOR-ABSENCE
* MC in who?
* What are the sxs? (4)
* Often midiagnosed as what?

A

MC children / adolescents

Altered consciousness without change in muscle tone
* Starring in space
* Day dreaming
* Inattentive

Often misdiagnosed as ADHD

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47
Q

Focal
* What happens to consciousness?
* What can happen with motor?
* What can happen with sensory?

A
  • ± Change in consciousness (most not)
  • Motor – motor cortex; tonic-clonic of contralateral extremity
  • Sensory – occipital; see flashing lights or smells

Based on my research, they usually have one of the components- motor, sensory, autonomic

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48
Q

Focal
* What are the sxs when autonomic system is involved?
* Can progress to what?

A

Autonomic
* Involve automatisms – chewing, lip smacking, rapid eye movements, weird smells, or feeling of fear (increase anxiety)

Can progress to generalized

Based on my research, they usually have one of the components- motor, sensory, autonomic

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49
Q

It is long lol

Seizure pathophysiology
* What is the pathway during excitation?

A

Voltage-gated Na channels open sending Na into cell – depolarization

Depolarization causes voltage activated Ca channels to open allowing Ca influx (opens them)

Ca influx results in glutamate release from presynaptic vesicles (stimulator NT)

Glutamate binds to
* AMPA – opens to permit Na ion entry
* NMDA –opens to permit Ca ion entry
* Ca influx can also occur through low voltage (T-type) calcium channels
* Depolarization and propagation of action potential

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50
Q

What does overactivation of the excitation pathway lead to?

A

Overactivation – leads to seizure

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51
Q

Seizure pathophysiology
* What does GABA regulate?

A

GABA - Regulates excitatory neurons to help prevent seizures

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52
Q

Seizure pathophysiology
* What is the inhibitory pathway? What helps get rid of GABA (2)

A

GABA is released from inhibitory neurons and binds to GABAA receptors
* GABA binding causes influx of Cl- ions counter acting cell depolarization (decrease excitation)

GABA transporter-1 responsible for GABA reuptake into presynaptic neuron

GABA-aminotransferase (AT) breaks down GABA

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56
Q

Currently available AEDs
* What is the difference between older and newer AEDs?

A

Older AEDs
* Narrow therapeutic index
* Drug interactions
* Serious toxicities

Newer AEDs
* Wide therapeutic index
* Less drug interactions
* More moderate toxicities
* Less side effects

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57
Q

Seizure management
* What are the goals? (4)

A
  • Control seizures
  • Prevent/restore brain development
  • Avoid adverse effects
  • Maximize quality of life
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58
Q

Seizure management: Treatment modalities
* What are the different ways? (4)

A

Medications
* 63% controlled with medications
* Likelihood of response declines with subsequent mediations

Surgery (need focal onset-> ablat via radiofreq or remove connection)

Vagal nerve stimulators (changing excitation and inhibition)

Ketogenic diet

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59
Q

Seizure treatment – General approach
* First Unprovoked Seizure: Individualized based on what? Risk of reoccurence is what?

A
  • Individualized based on risk of seizure reoccurrence vs AED adverse effects
  • Risk of seizure reoccurrence in first 2 years (40 to 50%)
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60
Q

Seizure treatment – General approach
* What are the factors that increase risk? (3)

A
  • Epileptiform activity on electroencephalogram (EEG)
  • Abnormal neuroevaluation
  • First seizure occurs during sleep
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61
Q

Seizure treatment – General approach
* How many people get AED adverse effects ?
* What are the consequences?
* When do you start treatment?

A
  • Risk of AED adverse effects 7 to 31% (mostly mild, reversible)
  • Consequences of recurrent seizure (employment / driving)
  • Second unprovoked seizure – start treatment
62
Q

Seizure treatment – general approach: provoked seizures
* Treatment depends on what? Give examples

A

Treatment dependent on etiology
* Drug withdrawal/intoxication, electrolyte imbalance – immediate treatment, treat underlying cause
* Trauma, tumor – treatment generally recommended [levetiracetam (Keppra)]

63
Q

Seizure treatment – general approach
* Antiepileptic medication selection based on what several factors? (6)

A

Specific seizure type (generalized vs focal vs specific (infantile spasm, Lennox Gastaut)
* Side effect profile
* Dosing frequency
* Concomitant comorbidities and medications
* Age
* Pregnancy status

64
Q

Seizure treatment – general approach
* What is recommended at first?
* All patients should be treated by who?

A
  • Initial monotherapy is recommended
  • ALL patients should be treated by a neurologist
65
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66
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67
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68
Q
A
SJS - PELC CY- Come Lets Try Phenys Beer

(*) Also includes fosphenytoin
(^) warfarin, hormonal contraception, chemotherapy interactions
(#) Drug rash with eosinophilia and systemic symptoms (fever, lymphadenopathy)

69
Q
A
70
Q

Antiepileptic Adverse effects by class
* What are the SE of valproic acid and phenytonin?(4)

A
71
Q

Antiepileptic Adverse effects by class
* What are the SE of topiramate and carbamazepine?

A
72
Q

Antiepileptic Adverse effects by class
* What are the SE of levetiracetam?

A
73
Q

What are the SE of ethosuximide and gabapentin/pregabalin?

A
74
Q

What are the SE of vigabatrin and ketamine?

A
75
Q

barbiturates
* What does it bind to? What does it increase and decrease?

A

Bind GABAA receptor at site different from BDZ and GABA
* Increased duration of GABA channel opening Increasing Cl- influx; hyperpolarizing neuron
* Decreasing ability to create action potential
* Decrease activity of Ach and glutamate

76
Q

barbiturates
* Mimic what at high doses?
* What is its therapeutic index? What are the SE? (3)

A

Mimic GABA at high doses and directly activate GABA receptors

Narrow therapeutic index
* CNS depression
* Hypotension
* Cardiovascular / respiratory depression

77
Q

Infantile spasms (West Syndrome)
* Onset when?
* Generally underlaying what?
* Spasms include what? (aka sxs)
* What is the duration?

A

Onset early infancy (peak 6 months)
* Generally underlying brain abnormality (genetic, metabolic, structural)
* Spasms include stiffening of extremities, neck flexion (single extremity to generalized)
* Duration – 10 to 20 seconds, subtle, occur several times a day

78
Q

Infantile spasms (West Syndrome)
* What are the ways dx it? (3)

A
  • Electroencephalogram (24-video EEG); hypsarrhythmia is classic pattern
  • MRI
  • Blood tests
79
Q

Infantile spasms (West Syndrome)
* What is the prognosis?
* What is the txt? (3)

A

Prognosis generally poor with mild to moderate intellectual delay

Treatment – early intervention key
* Adrenocorticotrophic hormone (ACTH)-> too expensive
* Prednisolone-> first line
* Vigabatrin-> next line if no response to Prednisolone

80
Q

Status epilepticus
* What is the definition?
* What was the old time from?
* What increases likelihood of seizure control?

A
  • Unremitting generalized convulsive seizure lasting > 5 minutes or >1 convulsive seizure without return to baseline level of consciousness
  • Old time frame was > 30 minutes
  • Time to first dose of benzodiazepine increases likelihood of seizure control
81
Q

Status Epilepticus
* What is the supportive care? (4)

A

Supportive care – airway, breathing, circulation
* POC fingerstick glucose (possible hypoglycemia)
* Establish IV / IO
* Initial antiseizure treatment

82
Q

Status Epilepticus
* What is first line?
* What is IV and not IV?
* Repeat how often?

A

First-line = benzodiazepines
* IV – Lorazepam, diazepam
* Not IV - Midazolam (IM, IN, buccal), diazepam (rectal, IN)
* Repeat x 2 if no response

83
Q

status epilepticus
* When do you go to a second line?
* What is the DOC ? (3)

A

Second-line therapy
* Seizures refractory to BDZ
* Seizures responding to BDZ to prevent reoccurrence

DOC depends on patient history
* Levetiracetam
* Phenytoin/Fosphenytoin
* Valproic acid

84
Q

Refractory Status Epilepticus
* What is the definition?

A

Seizure refractory to at least two doses of BDZ and at least two doses of non-BDZ antiepileptic

85
Q

Refractory Status Epilepticus
* Consult who?
* What is necessary?
* What should be monitored?
* What medication can you use? (4)

A

Stat neurology consult

Mechanical ventilation necessary (if not already intubated)

Continuous EEG monitoring
* Midazolam (if you given two doses of benzo, might not be next in line)
* Pentobarbital
* Propofol
* Ketamine

86
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A
87
Q

Dementia
* What is it?
* What happens with cognitive?
* What happens with psychologic?

A
  • Chronic, acquired loss of 2 or more cognitive abilities caused by brain disease or injury
  • Cognitive – memory
  • Psychologic - apathy, depressive symptoms
88
Q

Dementia
* What happens with behavioral?
* What happens with sleep?
* What happens physically?
* What are the MC types?

A
  • Behavioral – withdrawal, disinhibition
  • Sleep – Altered sleep-wake cycle
  • Physical – gait, stability
  • Alzheimer disease and mixed dementia MC
89
Q

Dementia pathophysiology
* What is the cholinergic hypotheses?
* What is the amyloid hypothesis?

A

Cholinergic
* Loss of central cholinergic neurons – ACh deficiency which impairs memory and learning

Amyloid hypothesis
* Accumulation of beta amyloid proteins outside the cell
* Beta amyloid plaques – neuroinflammation, disruption of communication between cells, and weakened blood vessels

90
Q

Dementia pathophysiology
* What is the tau hypotheses?

A

Abnormal aggregation of tau proteins which normally support neuron structure
* Thought to be stimulated by amyloid plaques

Tangles inside nerve cells – decrease biochemical communication within neurons

91
Q

Dementia treatment
* What are the goals? (2)

A
  • Reduce symptoms caused by cognitive decline and accompanying symptoms
  • Delay progressive cognitive decline
92
Q

said fyi

A
93
Q

Dementia pharmacotherapy: Anticholinesterase inhibitor
* Promotes what?

A

Promote relative increases in Ach at the synaptic cleft for cholinergic neurotransmission

94
Q

Dementia pharmacotherapy: Anticholinesterase inhibitor
* What has modest improvement?
* What has minimal improvement?
* All agents in class with what?

A

Modest improvements
* Six-month advantage in cognitive decline
* Prevent 2 months per year of cognitive decline
* NNT = 12 patients

Minimal improvements in activities of daily living

All agents in class with similar efficacy and side effect profiles

95
Q

Dementia Pharmacotherapy
* Amyloid accumulation thought to cause what?

A

Amyloid accumulation thought to cause abnormal rise in extra synaptic glutamate levels (too much NT= decrease cognition)

96
Q

Dementia Pharmacotherapy
* What is the MOA of NMDA receptor antagnoist?

A

Inhibit glutamate from stimulating post-synaptic NMDA receptors

Decrease calcium influx and overstimulation of neuron caused by amyloid
* Calcium influx causes membrane excitability and stimulation
* Excess Ca influx causes cell apoptosis

Block receptor to uptake glutmate and excitation

97
Q

What are the anticholinesterase inhibitors examples? (3) When are they used?

A
98
Q

What are the SE of anticholinesterase inhibitors (donepexil, rivastigmine and galantamine)? What are the advantages?

A
99
Q

What is the NMDA receptor antagonist? When do you use it?

A

Add as disease gets worst

100
Q

What are the NMDA receptor antagonist SE? What is the advantage?

A

SE:
* Headache
* Constipation
* Confusion
* Dizziness

Advantages:
* Can be used with acetylcholinesterase inhibitor or as monotherapy

101
Q

New dementia therapies: Immuniotherapy
* Targets what?
* Appears to work better when?
* What does it clear?

A
  • Targets amyloid plaques -> causes plaque breakdown and slows the progression of disease
  • Appears to work better when used earlier in the disease process
  • Current amyloid plaque clearance rates up to 70%

need clear cut amyloid plaque

102
Q

New dementia therapies: immunotherapy
* Improves what? What are the examples (4)

A

Improves time to decline 20 to 40%
* Donanemab
* Lecanemab
* Remternetug
* Aducanumab

103
Q

Multiple Sclerosis Types
* What is relasping remitting MS
* What is clinically isolated syndrome?

A
  • Relapsing-remitting MS: The most common type, characterized by clearly defined relapses (also known as attacks or exacerbations) with partial or full recovery. Have to exhibit at least 2 or more attacks for diagnosis
  • Clinically isolated syndrome - Patient with a first clinical attack (Optic Neuritis, Transverse Myelitis, etc…)
104
Q

Multiple Sclerosis Types
* What is secondary progressive syndrome?
* What is primary progressive MS?

A
  • Secondary Progressive Syndrome - Gradual worsening of an initially remitting relapsing syndrome
  • Primary progressive MS -Insidious neurological progression of neurological disabilities suggestive of primary progressive MS (no acute relapses)

Relapsing remitting MS can go into secondary progressive syndrom

105
Q

MS – Acute Exacerbations
* What are the sxs? (4)

A

Symptoms variable
* Optic neuritis (unilateral painful vision loss)
* Painless diplopia
* Brainstem or cerebellar syndrome
* Partial transverse myelitis

106
Q

MS – Acute Exacerbations
* What are the treatments? (4)

A

Methylprednisolone (Solu-Medrol): High dose 1000mg IV daily for 5 days
* Oral Prednisone 625-1250 mg daily for 3-7 days with or without short taper
* ACTH Adrenocorticotropic Hormone IM or SQ 80-120 units daily for 1 week
* Plasma exchange daily 3-7 treatments for patients with severe neurological deficit; steroid refractory

107
Q

Treatment of MS
* What are the goals of relapsing remitting MS? (3)

A

Disease modifying therapies
* Relapse reduction
* Reduced accumulation of MRI lesions
* Stabilize, delay, modestly improve disability

108
Q

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Treatment of MS
* Who should start disease modifying therapies?
* What are the 3 examples?

A

Everyone with relapsing remitting MS should begin DMT:
* Infusion Therapies: Natalizumab, Ocrelizumab, Rituximab, Alemtuzumab
* Oral therapies: Dimethyl Fumarate, , Diroximel Fumera5e, Teriflunomide, Fingolimod, Siponimod, Ozanimod.
* Injection therapies: (IM, SQ) Human Interferon beta-1b, human interferon beta-1a, Glatiramer Acetate and Ofatumumab.

109
Q

She skipped this slide

MS – maintenance treatments for highly effective

A
110
Q

She skipped this slide

MS – Maintenance treatments for moderately effective

A
111
Q

She skipped this slide

MS – Maintenance treatments for moderately effective

A
112
Q

She skipped this slide

MS – Maintenance treatments

A
113
Q

Myasthenia Gravis (MG)
* What is it? What is the patho?

A

Myasthenia gravis is an autoimmune disease involving the skeletal muscle
* T-and B-cells produce antibodies which block and destroy acetylcholine (ACh) receptors faster than new ACh receptors can be synthesized

114
Q

Myasthenia Gravis (MG)
* Characterized by what? (2)

A

Characterized by weakness and fatigability

fatigued easily-> rested and feels better (feels better in morning)

115
Q

Myasthenia Gravis (MG)
* What is the early symptom?
* What are the bulbar symptoms?
* What are the generalized myasthenia?

A
  • Ocular Myasthenia – More than 50% of patients present with ocular myasthenia or ptosis, with or without diplopia. Most often only early symptom.
  • Bulbar Symptoms – 15% of patients develop dysarthria, dysphasia and fatigable chewing and swallowing difficulty, while 5% present with proximal muscle weakness.
  • Generalized Myasthenia – Neck and limb muscle weakness, respiratory muscle weakness and facial muscle weakness.
116
Q
  • What are the clinical manifestations of MG?
  • What is a myasthenic crisis?
  • How do you dx it?
A
117
Q

MG

A
118
Q

pyridostigmine (Mestinon)
* What is the MOA?
* What is the usual dose?

A

MOA: Acetylcholinesterase inhibitor; decreased breakdown of acetylcholine (cholinomimetic)

Usual dose:
* Immediate release: 60 to 600mg/day PO divided into 5 to 6 doses
* Sustained release:180 to 540 mg/day PO once or twice daily

119
Q

pyridostigmine (Mestinon)
* Titrate dose to what?
* CI in who?

A
  • Titrate dose to balance symptoms and adverse effects
  • CI: bowel or urinary obstruction
120
Q

pyridostigmine (Mestinon)
* What are the SE? (6)

A
  • GI upset
  • Increased salivation and bronchial secretions
  • Miosis
  • Diaphoresis
  • Muscle cramps
  • Fasciculation and weakness
121
Q
A
122
Q

Encephalopathies with specific treatments

A
123
Q
A
124
Q

Bell’s Palsy
* What are the sxs? (4)

A
  • Facial weakness
  • Decreased lacrimation and salivation
  • Loss of taste (anterior 2/3)
  • Dysacusis
125
Q

Bell’s Palsy
* Rule out what? (2)
* What is the prognosis?

A

Rule out:
* Ramsey hunt
* Lyme’s disease

Prognosis:
* 71% full recovery
* Starts within 3 weeks; takes 6 to 12 months for full recovery

126
Q

Bell’s palsy vs stroke
* What is the patho and sxs difference between bells and stroke?

A

Bell’s Palsy:
* lower motor neuron lesion of cranial nerve VII; upper and lower face affected

Stroke and other upper motor neuron lesions:
* upper face is spared due to input from both sides of the brain

127
Q

Bell Palsy treatment
* What is the House-Brackmann Classification
of facial nerve dysfunction

A
  • Above the line, give only steriods
  • Below the line, give steriods and antivirals

Cannot close eye= need eye protection

128
Q
A
129
Q

Bell Palsy specific treatments
* What do you give to all patients?

A

Glucocorticoids – all patients
* Prednisone 60 mg PO daily x 5 to 7 days (no taper needed)
* Reduced relative risk of incomplete recovery by 37%
* NNT to avoid one incomplete recovery 10

130
Q

Bell Palsy specific treatments
* What is the antiviral therapy?

A
  • Acyclovir 400 mg PO 5 times daily x 10 days
  • Valacyclovir 1000 mg PO TID x 10 days
  • Not effective as monotherapy; minimal improvements overall
131
Q

Carpal tunnel syndrome (CTS)
* Mild to moderate CTS - What are the first and second line nonsurgical options?

A

First-line:
* Nocturnal wrist splinting in neutral position

Second-line
* Local glucocorticoid injection
* Methylprednisolone 40 to 80 mg; symptom improvement up to 1 year (10 weeks MC)

132
Q

Carpal tunnel syndrome (CTS)
* What do you give for patients who fail or decline injection therapy and fail wrist splinting?

A
  • Prednisone 20 mg daily for 10 to 14 days (mean duration of action 8 weeks)
  • Not as effective as local glucocorticoid injections
133
Q

Carpal tunnel syndrome (CTS)
* What is not recommended?
* Surgical decompression should be offered to patients with what?

A
  • NSAIDS not recommended
  • Surgical decompression should be offered to patients with severe CTS with nerve damage
134
Q

Guillain-Barre syndrome (GBS)
* What is it?
* What is the sxs?
* What is the MCC?

A
  • Autoimmune destruction of peripheral nervous system
  • Symmetric ascending paralysis ± dysautonomia
  • MCC – infections

Usually sick a few weeks before

135
Q

Guillain-Barre syndrome (GBS)
* What is the course?

A
  • Worsen over 2 weeks
  • Plateau 2 to 4 weeks
  • Gradual recovery
136
Q
A
137
Q

Guillain-Barré syndrome (GBS)
* What is the supportive care? (2)
* What type of support?

A

Supportive care
* Close respiratory monitoring – hospitalization
* Monitor for bowel and bladder dysfunction

± Ventilatory support

138
Q

Guillain-Barré syndrome (GBS)
* What do you need to monitor? (2)
* What is the pain control?(2)

A

Autonomic dysfunction (20%)
* Monitor BP and HR

Pain control
* Nociceptive and neuropathic pain common
* Agents used for neuropathic pain highest efficacy

139
Q
A
140
Q

GBS treatment
* What is the goal?

A

Disease Modifying Treatments
* Decreases recovery time and ameliorate symptoms

141
Q

GBS treatment
* What do you give? When do you start?

A

Intravenous Immune Globulin (IVIG)
* Best if started within 2 weeks of symptom onset
* 400mg/kg/day x 5 days or 2gm/kg/day x 2 days
* Easier to administer with less complications than plasma exchange

142
Q

GBS treatment
* What can you give besides IVIG? Best when?
* What is not recommended?

A

Plasma exchange
* Removes circulating immune complexes
* Best when initiated within 7 days of symptom onset

Corticosteroids not recommended

143
Q

Intravenous immune globulin
* What is it?
* Important to what?
* What is it made out of?

A

Concentrate of pooled immunoglobulins obtained from healthy volunteers
* Important to humoral immunity
* 90% IgG

144
Q

Intravenous immune globulin
* What are the indications? (3)

A
  • Immunodeficiencies
  • Immunomodulation / anti-inflammatory therapy
  • Hyperimmune therapy against specific infectious agents
145
Q

Intravenous immune globulin
* What is the MOA?
* How is it administered?
* What are the SE? What can help?

A

MOA: Various effects on the inflammatory cascade and mediation of the immune system

Administration: IV or subcutaneously

Adverse effects:
* Infusion reactions
* Slow titration recommend
* Premedication helpful (acetaminophen, diphenhydramine)
* Aseptic meningitis (HA after IVIG-> give dethamethasome)

146
Q

distal symmetric polyneuropathy (DSPN)
* Synonymous with the term what?
* What loss?
* What experience?

A

Synonymous with the term “diabetic neuropathy”
* Sensory loss
* 15 to 20% of patients experience pain

147
Q

distal symmetric polyneuropathy (DSPN)
* What is the prevention/progession control? (3)

A
  • Glycemic control
  • Metabolic syndrome control
  • Foot care – daily inspection
148
Q

Diabetic neuropathy treatments
* What should you control?
* What are the initial therapies? (4)

A
149
Q

Diabetic neuropathy treatments
* Guideline recommneds what?
* Specific agent used determined by what?
* What is second line?

A
  • Guideline recommendations support either gabapentinoids, SNRIs, or TCAs(not first line) as first line
  • Specific agent used determined by comorbidities, costs, drug interactions, side effect profile
  • TCAs generally second-line in most patients due to worse side effect profile
150
Q
A

Pharm III (14 decks)

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