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Pharm III > Lecture 5 (neuro)-Exam 3 > Flashcards

Lecture 5 (neuro)-Exam 3 Flashcards

1
Q
A
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2
Q

Tension HA:
* Common or rare?
* What is the etiology? (2)
* More common in who? (gender)
* How to dx it?

A
  • Most common type of headache
  • Etiology - stress / dehydration
  • F>M
  • Dx: clinical
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3
Q

Tension Headaches
* What is the criteria? (6)

A
  • Bilateral
  • Pressing / tightness (band-like)
  • Mild to moderate pain
  • Not aggravated by usual physical activity (walking / climbing stairs)
  • NO nausea / vomiting (can r/o if they have this)
  • NO more than one of photophobia or phonophobia (one of these, not both)
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4
Q

Tension headache – Acute Therapy
* What is the first line therapy? (3)

A
  • NSAIDs (ibuprofen / naproxen)
  • Aspirin
  • Acetaminophen
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5
Q

Tension headache – Acute Therapy
* What are the goals? (4)

A
  • Pain free / functioning after treatment
  • Consistent efficacy
  • Limited disability
  • Minimal medication side effects
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6
Q

Tension headache – Acute Therapy
* What is the adjuvtive therapy? (3)

A
  • Caffeine 100 to 200mg PO with first-line therapy (if not effective alone)
  • Biofeedback
  • Massage
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7
Q

Tension headache – Acute Therapy
* What is not recommended? (2)

A
  • Triptans
  • Muscle relaxants
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8
Q

Tension headaches – Prophylactic therapy
* What is acute?
* What is chronic?
* What are the goals? (3)

A

Acute: 1 to 14 HA days/month
Chronic: ≥ 15 HA days/month (I think this is when you start prophylactic therapy)

Goals:
* Decrease the frequency, severity and duration of HA
* Increase response to acute treatments
* Increase function / decrease disability

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9
Q

Tension headaches – Prophylactic therapy
* What is the first line? (4)

A

First-line – tricyclic antidepressants
* Amitriptyline (MC)
* Nortriptyline
* Imipramine
* Doxepin

DANI

Second-line
* Mirtazapine
* Venlafaxine
* Acupuncture
* Trigger point injections

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10
Q

NSAID mechanism of action
* What is the pathway of thromboxane, and prostaglandins

A

Phospholipase A2 released in response to inflammation

Converts phospholipids into arachidonic acid

Arachidonic acid is a substrate for two enzymes
* 5-lipoxygenase (5-LOX)
* Cyclooxygenase (COX-1 and COX-2)

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11
Q

NSAID Mechanism of action
* What is always circulating and active?
* What does thromboxane promote?
* What does Prostaglandins and prostacyclin cause?

A
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12
Q

NSAID Mechanism of action
* When is COX 2 activated? What does it mediate?

A

COX-2 activated at sites of inflammation
* Mediates inflammation, pain, and fever

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13
Q

NSAID Mechanism of action
* What does NSAIDS block and cause?

A

NSAIDs block COX-1 and COX-2
* Reduce prostaglandin, thromboxane, prostacyclin synthesis
* Reduce inflammation, pain, and fever

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14
Q

NSAID classification
* What is the example of irreversible COX inhibitors?
* What does non-selective and selective reversible cox inhibitors do?

A

Irreversible COX inhibitors
* Aspirin

Reversible COX inhibitors
* Non-selective: Inhibit COX-1 and COX-2
* Selective: Inhibit COX-2

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15
Q
A
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16
Q

NSAID adverse effects
* Whatis the MC SE?
* Why does this happen?

A
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17
Q

NSAID adverse effects
* What are the other GI SE? (besides gastric ulcer)

A

Other gastrointestinal adverse effects
* Dyspepsia
* Abdominal pain
* Nausea / vomiting

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18
Q

Nsaid adverse effects
* Why is there an increased bleeding risk?
* Strongest effect with What?

A

Increased bleeding risk
* Inhibition of thromboxane -> decrease in platelet aggregation

Strongest effect with:
* Aspirin – irreversible inhibition
* Increased COX-1 selectivity

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19
Q

Nsaid adverse effects
* Why is there an increased clotting risk and CV events?
* MC with increased what?

A
  • MC with increased COX-2 selectivity
  • Less COX-1 inhibition = less inhibition of thromboxane A2
  • More COX-2 inhibition = more vasoconstriction
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20
Q

NSAIDs - Adverse Effects
* What are the kidney effects?

A

NSAIDs inhibit prostaglandins -> VASOCONSTRICTION

Decrease renal blood flow
* Kidneys think blood pressure is low and retain fluid ->
increase blood pressure / peripheral edema

Increase risk of renal injury
* Effect more pronounced with underlying decrease in renal perfusion

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21
Q

NSAIDs - Adverse Effects
* What can happen to the skin?

A

Rash – hypersensitivity reactions rare / cross sensitivity

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22
Q

NSAIDs: Black box warnings
* What are the serious Cardiovscular events? When is it contraindicated?

A

Serious cardiovascular events
* Increased risk of embolic events including myocardial infarction and stroke
* Contraindicated in the setting of coronary artery bypass surgery

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23
Q

NSAIDS: black box warning
* What are the Increased risk of serious gastrointestinal adverse events?

A
  • Bleeding, ulceration, perforation
  • Elderly at greatest risk
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24
Q

NSAIDS: black box warning
* When it is contraindated? (4)

A
  • Aspirin allergy – watch for patients with Samter’s triad
  • Peptic ulcer. GI bleed or perforation
  • Advanced renal impairment
  • Cerebrovascular bleeding
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25
Q

NSAIDs: Black box warning
* What are the pregnancy considerations?

A

Avoid if possible; especially in first and third trimesters

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26
Q

Most important: Know the dose for ibuprofen

A
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27
Q

What is unique about meloxicam and celecoxib?

A
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28
Q

ketorolac
* More _
* What is the indication for keterolac IV/IM?
* Do not recommend use of what?

A
  • More potent
  • Short-term management of moderate to severe acute pain requiring opioid-level analgesia
  • Do not recommend use of oral product for home use (causes a lot of issues like renal disorders)
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29
Q

ketorolac
* Do not use more than how many days?
* What are the contraindications? (4)

A

Warning
* Do not exceed 5 days combined (inj + tabs) therapy

Contraindications
* Hypovolemia
* Incomplete hemostasis
* Bleeding disorders or high risk of bleeding
* Concomitant epidural or intrathecal injections

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30
Q

Acetaminophen mechanism of action
* What is the MOA? What are the effects? (3)

A

Inhibits COX-1 and COX-2 in the central nervous system
* Decreases pain and fever
* No anti-inflammatory effects because it does not inhibit peripheral COX receptors
* No effects on platelets

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31
Q

Acetaminophen mechanism of action
* Preferred for patients with what? (5)

A
  • Bleeding disorders
  • Peptic ulcer disease
  • Cardiovascular disease
  • NSAID allergy
  • Children < 6 months of age
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32
Q

Acetaminophen
* What is the adult dosages?
* What are the children dosage?

A

Adult Dosage:
* 650mg to 1000 mg every 4 to 6 hrs

Children Dosage:
* 12.5 to 15 mg/kg/dose every 4 to 6 hours
* (Max 5 doses daily – 75 mg/kg/day)

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33
Q

Acetaminophen
* What are the daily doses (short term, elderly, chronic use and alcohol?

A
  • Short term (≤10 days): 4 grams/day
  • Elderly or debilitated: 3 grams/day
  • Chronic use: 3 grams/day
  • Alcohol intake ≥ 2 ounces daily: 2.5 grams/day
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34
Q

Acetaminophen
* What are the dosage forms?

A
  • Tablets / capsules
  • Oral suspension
  • Suppositories
  • Intravenous
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35
Q

Acetaminophen
* What is the MC side effect? Who is high risk of this SE? (5)

A

Hepatotoxicity MC
* Preexisting liver disease
* Concurrent hepatotoxic medications
* Poor nutrition
* Regular alcohol consumption
* Chronic overuse

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36
Q

Acetaminophen
* What is the metabolism? What is toxic?

A

NAC = N-aceylcysteine

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37
Q

What are the symptoms of migraines?

A
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38
Q

Migraine pathophysiology
* Begins with activation of what?
* Patients can be predisposed how?
* Imbalance between what?
* What is the result?

A

A migraine headache begins with activation of the trigeminal nerve
* Patients with migraines genetically predisposed to hyperresponsiveness to environmental circumstances or triggers
* Imbalance between excitatory and inhibitory signals
* Result = TN activation leads to irritation of nociceptors in the meninges

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39
Q

Migraine pathophysiology
* What does nociceptor irritation cause? (3)
* NP release causes what?

A

Nociceptor irritation causes release of specific neuropeptides (NP):
* Vasoactive inhibitory peptide (VIP)
* Substance P
* Calcitonin gene regulated peptide (CGRP)

NP release causes neurogenic inflammation of meningeal vasculature

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40
Q

Migraine pathophysiology
* Inflamationn results in what? (3)

A

Vasodilation of meningeal capillaries

Increased meningeal capillary membrane permeability

Mast cells degranulation
* Release histamine – vasodilation, increased capillary permeability
* Release prostaglandin - proinflammatory

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41
Q

Migraine pathophysiology
* What are the end results? (2)

A
  • Activation of meningeal nociceptors
  • PAIN
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42
Q

Migraine treatment
* What are the general principals? (4)
* What is not be recommended?

A
  • Avoid triggers
  • Regular sleep pattern
  • Treat early – first symptoms
  • Treat aggressive
  • Opioids and barbiturates not recommended
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43
Q

Migraine
* What are the common triggers?

A
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44
Q

Migraines – acute / abortive treatment
* What is first line?
* What is second line?

A

First-line
* NSAIDS / acetaminophen
* May be adequate for mild to moderate migraines

Second-line
* Triptans if NSAIDS / acetaminophen not effective and for Moderate to severe migraines (super bad and need both)

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45
Q

Low yield

Migraines – acute / abortive treatment
* What is third line?

A
  • Ergots
  • Ditans
  • Grepans
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46
Q

Triptan-MOA
* What type of agonist?
* Binds to what?
* What does it inhibit and decrease (5)?
* Reduce activation of what?

A

Serotonin agonists

Bind to pre-synaptic 5-HT1 B and D receptors

Inhibit the release of neuropeptides (decrease down cascade)
* Decrease mast cell degranulation
* Decrease prostaglandin release
* Decrease vasodilation
* Decrease cell permeability

Reduce activation of nociceptors

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47
Q

Triptans – general principals
* What are pros (5)?
* Patients who do not respond to triptans may what?
* Recommend trial of how long?
* Best results seen when?

A
  • Common MOA; different does, pharmacokinetics, costs, routes
  • Patients who do not respond to one triptan may respond to others
  • Recommend trial of single agent x 3 attempts before switching agents (gettings better with each dose)
  • Best results seen when started with initiation of pain (not aura aka visual changes)
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48
Q

Triptans – general principals
* Variable evidence regarding what?
* Few what?
* What is the oldest and most studied?
* Specific agent chosen often depends on what?

A
  • Variable evidence regarding benefits from concomitant NSAIDS
  • Few head-to-head comparisons exist
  • Sumatriptan oldest and most studied; NNT SQ for complete pain relief at two hours = 2
  • Specific agent chosen often depends on insurance / cost
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49
Q

Know routes because you need to be careful if pt is vomiting

A
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50
Q

Triptans
* What are the SE? (6)

A
  • Fatigue
  • Dizziness
  • Nausea
  • Somnolence
  • Chest discomfort
  • Paresthesias, flushing, tingling, neck pain, chest tightness (triptan sensation)

Last two because of vasospasm

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51
Q

Triptans
* What are rare SEs? (3)

A
  • Myocardial infarction
  • Arrythmias
  • Stroke
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52
Q

What are the contraindications of triptans? (9)

A
  • History of MI
  • Coronary artery disease
  • Angina
  • History of stroke
  • Uncontrolled hypertension
  • Peripheral vascular disease
  • Hemiplegic migraines
  • Severe renal or hepatic dysfunction
  • Age > 65 years

Because of the side effects

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53
Q

Triptans
* Use in pregnancy?
* Administration with what? Iimited info with what?

A
  • All triptans except sumatriptan are CI during pregnancy
  • Administration with ergot alkaloids or MAOIs; limited information with SSRI coadministration
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54
Q

Ergots
* Ergotamine / dihydroergotamine: What type of the agonist? (2)

A
  • 5HT agonists – not specific to 5-HT1 (more adverse effects-> why it is not first line)
  • Alpha 1 agonist – peripheral vasoconstriction
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55
Q

Ergots
* What are the SE? (5)

A
  • Nausea and vomiting – 5HT-3 agonism
  • Vasoconstriction
  • Leg weakness
  • Extremity muscle pain
  • Uterine contractions
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56
Q

Ergots
* What is the BBW?
* Administration during or within what?

A
  • BBW: administration with strong CYP3A4 inhibitors has been associated with life-threatening peripheral ischemia (protease inhibitors, macrolide antibiotics)
  • Administration during or within 14 days of an MAOI or triptan; limited evidence for coadministration with SSRIs
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57
Q

Ergots
* What are the contraindications? (8)

A
  • History of MI
  • Coronary artery disease
  • Angina
  • History of stroke
  • Uncontrolled hypertension
  • Peripheral vascular disease
  • Severe renal or hepatic dysfunction
  • Pregnancy
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58
Q

Ergots

A

No oral
* The time you would use this is because status migrainosus or resistance to triptian

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59
Q

Status migrainosus
* Severe migraine lasting how long?
* Refractory to what?
* R/o other?
* No standard what?

A
  • Severe migraine lasting > 72 hours
  • Refractory to standard treatment
  • Rule out other diagnoses (usually need to get scan of head)
  • No standard treatment approach
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60
Q

Status migrainosus
* What is the first line therapies? (7)

A

Make a cocktail

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61
Q

Migraine – acute medication over use
* _ of patients with migraines
* Frequent use of what?
* Leads to what?
* Progression to what?

A

15% of patients with migraines
* Frequent use of acute migraine treatments
* Leads to increased attack frequency
* Progression to chronic migraines

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62
Q

Migraine – acute medication over use
* How do you dx it?

A

≥ 3 months of the following:
* ≥ 10 days per month triptans or ≥ 15 days per month NSAIDS or acetaminophen

Need a good medical hx

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63
Q

Migraine – acute medication over use
* What is the tx?

A

Wean medications

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64
Q

Prophylactic therapy
* Migraine attacks that interfere with what?
* What is the criteria for prophylactic therapy? (4)

A

Migraine attacks that interfere with function, are frequent, or debilitating
* ≥ 6 headache days per month
* ≥ 4 headache days per month with some impairments
* ≥ 3 headache days per month with severe impairment
* Lack of efficacy with acute treatments

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65
Q

Migraine Prophylactic Therapy Goals
* 50% reduction in what?
* Significant decrease in what?
* Improved response to what?
* Improved what?

A
  • 50% reduction in days of migraine frequency
  • Significant decrease in duration or severity of migraines
  • Improved response to acute therapy
  • Improved QOL
66
Q

Migraine Prophylactic Therapy Goals
* Dimished what?
* Specific therapy dependent on what?
* Equivalent what?

A
  • Diminished migraine disability
  • Specific therapy dependent on patient comorbidities and adverse effects
  • Equivalent efficacy – 1 to 3 fewer migraine days on average
67
Q

Migraine prophylaxis
* What are the non-pharm treatment? (8)

A
  • Avoid triggers
  • Adequate hydration (2 liters in adults)
  • Biofeedback
  • CBT-stress reduction
  • Neuromodulation devices
  • Relaxation / imagery techniques
  • Acupuncture
  • Massage

Usually with pharm therapy

68
Q
A

Be careful about propranolol because it can cause depression therefore if you have a depressed patient on it then need to look at hx.

70
Q

Cluster headaches
* Cluster when?
* HA begins when? (2)

A

Clustered” at same time of day, and often during a season
* HA begins 2-3 hours after going to bed and lasts 30-90 min
* Mornings in spring

71
Q

Cluster HA:
* Attacks are without what?
* Escalate how?
* Individual attacks last how long?
* Occurs how often?
* Typically precipitated by what?

A
  • Attacks are without prodrome (or aura)
  • Escalate rapidly within 15 minutes,
  • Individual attacks last 15-180 minutes if untreated
  • Occur from once every other day to 8x/day
  • Typically precipitated by ETOH

Male > Female: (2-3:1)

73
Q

Cluster Headache - pathophysiology
* What are the triggers? (3)

A
  • Smoking
  • Red wine
  • Stress
74
Q

Cluster Headache - pathophysiology
* What becomes activated and what does that stimulate?

A
  • Dysfunctional hypothalamus becomes activated
  • Stimulates parasympathetic nervous system
75
Q

Cluster Headache - pathophysiology
* Since PNS is activated what happens? (3)

A

Lacrimal glands – tearing

Nasal glands – congestion/rhinorrhea

Vessels – vasodilation
* Neuroinflammation – activation of nociceptors of trigeminal nerve – PAIN (periorbital)
* Conjunctival hyperemia

76
Q

Cluster Headache - pathophysiology
* What happens to cavernous sinus?
* No what?

A
  • Inflammation cavernous sinus – miosis, ptosis (sympathetic inflammation)
  • No anhidrosis (Not full Horner’s syndrome)
77
Q

Cluster Headache
* What is first line acute treatment?

A

Oxygen: 100% @ 6-12 L/min x 15min, via nonrebreather mask
* High efficacy – 75% patients with pain relief
* Lack of adverse effects
* Initial acquisition may be difficult

78
Q

Cluster Headache
* What can be used after if oxygen does not work?

A

Sumatriptan 6mg SC

79
Q

Cluster HA: Sumatriptan
* Efficacy?
* What is possible?
* Greater than what?
* What has some benefit?
* No role for what?

A
  • High efficacy – 75% patients with pain relief within 15 minutes
  • Adverse effects possible
  • Greater than recommended doses possible
  • Intranasal with some benefit – longer time to pain relief
  • No role for oral therapy
80
Q

Cluster Prophylaxis
* When do you start it?

A

Start immediately with acute treatments to prevent reoccurrence

81
Q

Cluster Prophylaxis
* What are all the options?

A
  • Verapamil (1st line)
  • Lithium
  • Topiramate
82
Q

Cluster prophylaxis

6

83
Q

Cluster prophylaxis

5/3

84
Q

Cluster headache – transitional treatment
* Started concurrently with what?
* Onset of effects more what?
* Prevents what?

A
  • Started concurrently with prophylactic medication titration (a brigde between acute and prophylactic txt)
  • Onset of effects more rapid
  • Prevent recurrent cluster headaches while prophylactic therapy is titrated
85
Q

Cluster headache – transitional treatment
* Benefits are limited how?
* What are the options?

A

Benefits are uaully limited-weeks to months
* Prednisone
* Greater occipital nerve injection->Lidocaine and / or bupivacaine

86
Q

Bacterial Meningitis
* Most likely organism varies by what?
* What is key to decrease long-term sequelae?
* What should be done before antibiotic txt? Do not delay initiation for what?

A

Most likely organism varies by age

Rapid diagnosis and treatment is key to decrease long-term sequelae

Ideally blood cultures and lumbar puncture should be completed before antibiotic treatment
* Do not delay initiation of therapy for LP / neuroimaging

87
Q

Bacterial Meningitis
* Neuroimaging (CT) indicated for patients with what?

A

Neuroimaging (CT) indicated for patients with focal neurologic deficits, seizures, immunocompromised, papilledema, altered consciousness to rule out mass or increased ICP

88
Q

Bacterial Meningitis
* Empiric therapy should be based on what?
* Empiric therapy should continue when?

A
  • Empiric therapy should be based on most likely organism and antibiotic ability to penetrate the CNS
  • Empiric therapy should continue for 48 to 72 hours; until bacterial meningitis is ruled out – culture or PCR
89
Q

Bacterial Meningitis
* Tailor therapy when?
* Treatment duration varies with what?

A
  • Tailor therapy once pathogen is identified
  • Treatment duration varies with pathogen but generally 7 to 21 days of intravenous antibiotics
90
Q

BBB penetration
* What are the factors that increase antibiotic pentration into CNS? (5)
* Maximize antibiotic dose for what?

A

Inflammation of the meninges – causes gaps in tight junctions and decreases activity of efflux pump

Antibiotics with:
* Low molecular weight
* Non-ionized state at physiologic pH
* Low protein binding
* High lipid solubility

Maximize antibiotic doses to optimized CNS penetration

92
Q

Meningitis: empiric therapy for newborn to 1m
* What are the most likely organisms (4)
* What is the empiric therapy?
* What is the typical regimen?

93
Q

Meningitis: empiric therapy for 1m to 50 years
* What are the most likely organisms (4)
* What is the empiric therapy?
* What is the typical regimen?

94
Q

Meningitis: empiric therapy for 50 years or co-morbidities
* What are the most likely organisms (4)
* What is the empiric therapy?
* What is the typical regimen?

95
Q

Neonatal HSV Encephalitis
* What is the etiology?
* What is the presentation?

A
  • Etiology: perinatal transmission of HSV (1 or 2); often no history of maternal herpes infection; maternal disease may be asymptomatic
  • Presentation: fever, lethargy, poor feeding, seizures, increased liver enzymes, herpes lesions uncommon; most commonly seen within first month of life
96
Q

Neonatal HSV Encephalitis
* How do you dx it?
* What is the txt?

A

Diagnosis: HSV PCR of CSF; high sensitivity PCR required

Treatment:
* Acyclovir 20mg/kg/dose IV Q8H until HSV ruled-out or 21 days minimum
* Test for cure via CSF PCR at 21 days; if positive treat 7 more days
* Suppressive therapy with acyclovir continued for 6 months

97
Q

Viral Meningitis (Aseptic)
* Acute meningeal inflammation with no what?
* More common than what?
* Peaks when? (what time of year)
* Occurs how?
* Cannot be distingusihed clinically from what?

A
  • Acute meningeal inflammation with no identifiable bacteria in the CSF
  • More common than bacterial meningitis in pediatric population, RARE in elderly
  • Peaks in late summer – early fall
  • Occurs in outbreak and sporadic forms
  • Cannot be distinguished clinically from bacterial
98
Q

Viral Meningitis (Aseptic)
* >90% are caused by what? What are the other causes?

A

> 90% are caused by enterovirus (Coxsackie virus A or B, echoviruses) family. Others are herpes Simplex 2 and arthropod-borne viruses

100
Q

What is the biofire meningitis/encephalitis panel? What happens if HSV is negitive on it?

A

If it is negative, would do a high sen. HSV test

101
Q

Meningitis-Bacterial
* What are the classic signs? (2)
* What do you need to remember about with elderly and infants?

A

Classic:
* + Brudzinski sign
* + Kernig sign

Remember:
* Elderly: subtle findings, often include confusion
* Infants: irritability, lethargy, poor feeding

102
Q

Reyes syndrome
* Encephalopathy associated with what?
* MC in who?
* Associated with what?

A

Encephalopathy associated with liver damage and liver failure
* MC in children 4 to 12 years of age
* Associated with viral infections (influenza, chicken pox) and aspirin / salicylate ingestion

103
Q

Reyes syndrome
* What is damaged on a cellular level?
* What does it mostly effect?
* Increased what? (2)
* What happens with sugar?

A

Mitochondrial damage – cells can’t make energy and die
* Mostly effects liver cells
* Increased ammonia – encephalitis (swelling and increased ICP)
* Increased AST, ALT, PT/INR
* Hyper or hypoglycemia

104
Q

Reyes syndrome
* What is the txt? (2)

A
  • Supportive – mostly aimed at decreasing intracranial pressure
  • Hyperventilation / mannitol
106
Q

Essential tremors
* What is the txt?
* What is the goal?
* Sxs still generally worsen when?
* Avoid what?

A
  • Treatment is symptomatic
  • Goal is to reduce symptoms
  • Symptoms still generally worsen over time and may require additional treatments
  • Avoid substances that worsen it
107
Q

Essential tremors
* What can help?
* Treatment should be considered for who?

A
  • Modest amounts of alcohol may help (60 to 70%)
  • Treat should be considered for patients with daily symptoms or with intermittent symptoms that cause patient distress
108
Q

What are the substances that may exacerbate essential tremor?

109
Q

Essential tremor – treatment
* What are two options?

A
  • Propranolol (MC in most pts)
  • Primidone
110
Q
A

induces hepatic enzymes

(*)Lower doses in elderly patients
(#)induces hepatic enzymes

112
Q

Parkinson Disease (PD)
* Occurs in who? Starts when?
* Dengeneration of what?
* Essential features of what? (4)
* What type of impairment?

A
  • Occurs in all ethnicities; 45-65 years start
  • Degeneration of dopamine-producing neurons in the substantia nigra causing deficiency of dopamine
  • Essential features resting tremors, bradykinesia, rigidity, and unstable posture
  • Depression and cognitive impairment
113
Q

Parkinson’s pathophysiology
* Complex interplay between what?

A

Complex interplay between excitatory and inhibitory neurons in the basal ganglia that regulate desired and undesired motor movements

114
Q

Parkinson’s pathophysiology
* What is the direct pathway?

A

Direct pathway – movement stimulation
* Glutamate neurons stimulate GABA neurons striatum
* Stimulation of GABA neuron -> inhibition of GABA in GPI
* Inhibition of GABA second motor neuron in GPI -> less inhibition on thalamus
* Thalamus receives and sends signal for movement to the cerebral cortex
* DA from the SN binds to D1 receptors -> enhances activity of pathway

115
Q

Parkinson’s pathophysiology
* What is the indirect pathway?

A

Indirect pathway – movement suppression
* Glutamate neurons stimulate GABA neurons in striatum
* Stimulation of GABA in striatum -> inhibition of second GABA neuron in GPE
* Inhibition of GABA in GPE -> less GABA released in subthalamic nucleus
* Less GABA released in subthalamic nucleus ->less inhibition of glutamate
* Glutamate stimulates GABA in GPI
* GABA stimulation in GPI ->inhibitory signals sent to thalamus
* Inhibitory signals sent to cortex to decrease muscle movement
* DA from the SN binds to D2 receptors in striatum ->opposes the activity of pathway -> less inhibitory effects

116
Q

Parkinson’s pathophysiology
* Loss of what?
* What does that cause with the direct pathway?

A

Parkinson’s = loss of DA in SN

Decreased DA in direct pathway
* Less DA binding to D1 receptor -> less excitation of the GABA motor neuron in the striatum
* Less GABA release from striatum -> less inhibition on GABA motor neuron in GPI
* Increase GABA release from GPI ->inhibitory effect on motor neuron

117
Q

Parkinson’s pathophysiology
* Overall excess inhibitory stimulation to thalamus causes what?

A

bradykinesia / akinesia / mask face / postural instability

  • T = tremor
  • R = rigidity
  • A = akinesis / bradykinesia
  • P = postural instability
118
Q

Parkinson’s pathophysiology
* What happens in the indirect pathway due to loss of DA

A

Decreased DA in indirect pathway
* Less DA binding to D2 receptor -> less inhibition of GABA motor neuron in striatum
* GABA neuron overactive -> releases more GABA
* Inhibits second GABA motor neuron -> cannot release GABA and inhibit glutamate release
* Glutamate released and stimulates GABA neurons in GPI -> inhibitory effect on motor movement

119
Q

Parkinson’s pathophysiology
* What does cholinergic neurons oppose?
* What happens with direct and indirect pathway?

A

Cholinergic neurons oppose the activity of D1 and D2 receptors

Direct pathway
* D1 receptors – excitatory / cholinergic activity inhibitory

Indirect pathway
* D2 receptors – inhibitory / cholinergic activity excitatory

120
Q

Parkinson’s pathophysiology
* What is the overall effect of cholinergic motor neurons?

A

Overall effect = unopposed cholinergic activity
* Tremors and rigidity

121
Q

PD treatment
* What is the goal?
* What are the examples of medications? (5)

A

Decrease symptoms by increasing dopamine or restoring balance between dopamine and acetylcholine
* Levodopa
* Dopamine agonists
* MAO type B inhibitors
* Amantadine
* Anticholinergics

122
Q

Dopamine synthesis
* What are the steps?

A
  • Tyrosine is absorbed from the GI tract
  • Readily crosses the BBB and into the CNS
  • Synthesized into dopamine which is packaged into vesicles
  • Released by stimulus into synaptic cleft
123
Q

Dopamine synthesis
* What happens after DA is release?

A
  • Pumped back into the presynaptic cleft and repackaged into vesicles or
  • Sent to glia cells and is metabolized by monoamine oxygenase type B (MAO-B) and catechol-O-methyltransferase (COM-T
124
Q

PD treatment: MAO-B inhibitors
* Decreases what?
* Often used alone for who? What are the examples (3)

A

Decrease DA metabolism in the CNS

Often used alone for early treatment of mild symptoms
* Selegiline
* Rasagiline
* Safinamide

125
Q

PD treatments: MAO-B inhibitors
* May help with what?
* Interactions with what is rare?

A

May help with wearing “OFF” symptoms with patients also taking levodopa in late disease

Interactions with SSRIs and SNRIs and MAOB inhibitors is rare
* Can use together with caution

126
Q

PD treatments: MAO-B inhibitors
* What are the SE? (7)

A
  • Nausea and headache (MC)
  • Confusion
  • Hallucinations
  • Excitement
  • Anxiety
  • Insomnia
  • Dyskinesia
127
Q

PD treatments: Amantadine
* What is the mechanism?
* What does it increase (2) and decrease (1)?
* Minimal what?

A

Antiviral, unknown mechanism
* Increase DA synthesis
* Increase DA release
* Decrease DA reuptake

Minimal effects

128
Q

PD treatments: Amantadine
* Used for what?

A

Used for initial treatment with mild symptoms or with levodopa to decrease motor complications

129
Q

PD treatments: amantadine
* Best for who?
* What are the SEs? (4)

A

Best for patients < 70 years
* Effects last 1 to 2 years

Adverse Effects
* Lethargy
* GI effects
* Strange dreams
* All mild and rare

130
Q

PD treatments:
* What is the DA / acetylcholine balance issue?

A
  • Decreased DA causes unopposed acetylcholine (Ach) effects
  • Ach stimulates muscarinic receptors responsible for smooth motor control
  • Excess Ach causes tremors and rigidity
131
Q

PD treatments: Antimuscarinic agents
* Blocks what?
* What does it decrease?
* What are the examples (2)

A

Block muscarinic receptors and restore the balance between DA and Ach

Reduce tremors / rigidity
* Benztropine
* Trihexyphenidyl

132
Q

PD treatments: Antimuscarinic agents
* What are the SE?
* Best for who?

A
  • Anticholinergic
  • Best for patients ≤ 65 years
133
Q

PD treatments: DA agonist
* WHat is the MOA?
* What are the examples? (4)

A

Binds to DA receptors and stimulates them
* Pramipexole
* Ropinirole
* Rotigotine (transdermal)
* Bromocriptine

134
Q

PD treatments: DA agonist
* What are the se? (7)

A
  • Nausea / vomiting
  • Somnolence
  • Orthostatic hypotension
  • Peripheral edema
  • Hallucinations
  • Confusion
  • Impulse control disorders
135
Q

PD treatments: DA agonist
* What do you need to caution with? What crisis?
* CI in who?

A

Caution: do not discontinue abruptly
* Hyperkinetic crisis – mimics neuroleptic malignant syndrome

CI: breast feeding mothers – decrease prolactin – decrease milk production

136
Q

PD treatments
* What can and cannot cross the BBB?

A

Dopamine
* Cannot cross the blood brain barrier (BBB)

Levodopa
* Crosses BBB readily and gets converted to DA via DOPA decarboxylase (DDC)

137
Q

PD treatments: levodopa
* What is the challenge? What are the SE?(5)

A

Peripheral DOPA decarboxylase can convert levodopa to DA before it can cross BBB

Peripheral DA accumulates causing unwanted adverse effects:
* Nausea / vomiting
* Anorexia
* Orthostatic hypotension
* Tachycardia
* Arrythmias

138
Q

PD treatments: levodopa
* What is the solution to the challenge one aka increased peripheral DA ?

A

Carbidopa
* PERIPHERAL DDC inhibitor
* Inhibits levodopa conversion to DA outside the CNS

139
Q

Levodopa/carbidopa (Sinemet)
* How do you dose it?
* What are the SEs? (4)

A

Dosing
* Start low and titrate to effect
* Use immediate release products to titrate

Adverse effects
* Nausea
* Dyskinesias
* Hallucinations
* Confusion

140
Q

Levodopa/carbidopa (Sinemet)
* CI in who?
* Caution?

A
  • CI: patients with psychosis; during or within 14 days of MAOIs
  • Caution: do not stop abruptly
141
Q

General dosing recommendation: levodopa/carbidopa
* What is the initial dose? Titrate how?
* What is the usual dose? Consider conversion when?

A

Initial dose:
* 25mg carbidopa/100mg levodopa PO TID with meals (dec. nausea)
* Titrate as tolerated to lowest levodopa dose the produces clinical response

Usual dose:
* 300 to 600mg of levodopa/day
* Consider conversion to controlled release products once stable
* Absorption 30% less that IR tablets

143
Q

PD progression
* What will happen over time? What will happen with treatment?

A

PD is progressive with a continuous decline in DA over time
* Effects of levodopa will begin to decrease
* 30 to 40% of patients see effects of levodopa decrease 3 to 4 hours after the dose after 5 years; 60% by 10 years
* “ON” – levodopa response
* “OFF”- PD symptoms return

144
Q

PD progression
* What is wearing off?
* What is on/off phenomenon?
* What is dyskinesia?

A

Wearing off
* Happens first, MC; decreasing effect of LD at the end of the dosing interval

On/off phenomenon
* Medication works one second and not the next (random-not based on doses)

Dyskinesia
* Less DA available the higher levodopa doses are needed; over excitation can result in dyskinesia

145
Q

PD treatments
* What is the second challenge with levodopa?
* What is the solution?

A

Challenge #2
* Peripheral levodopa and central DA metabolized by catechol-o-methyltransferase (COM-T)

COM-T inhibitors
* Inhibit the break down of peripheral levodopa and / or central DA

146
Q

PD treatments
* What is entacapone? What happens with levodopa?
* What is tolcapone? What does that cause?

A

Entacapone: peripheral COM-T inhibition only (prevents levodopa breakdown)
* More levodopa enters the brain

Tolcapone: central and peripheral COM-T inhibition (prevents both levodopa and DA breakdown)
* More levodopa enters the brain
* More constant, stable DA levels
* Less DA break down in CNS

147
Q

PD treatments-COM-T inhibitors
* Used with what?
* What does it cause? (3)

A

Used with levodopa
* Stabilizes levodopa concentrations in the blood
* Can improve motor complications
* Reduce wearing off phenomenon

148
Q

PD treatments-COM-T inhibitors
* What are the SE of Entacapone / tolcapone (4)

A
  • Nausea
  • Orthostatic hypotension
  • Hallucinations
  • Confusion
149
Q

PD treatments-COM-T inhibitors
* What is the BBW of tolcapone? Closely monitor what? Reserved for what?

A
  • BBW: Liver toxicity / failure
  • Closely monitor AST/ALT
  • Reserved for last-line therapy
150
Q

PD treatment General overview

151
Q

PD treatment General overview

152
Q

PD treatment General overview

153
Q

Huntington Disease (HD)
* What atrophy? What enlarges?
* What is the genetics?
* When is the onset?nFatal when?

A
  • Caudate nucleus atrophy and ventricle enlargement
  • Inherited autosomal dominant (short arm of chromosome 4), progressive, neurodegenerative
  • Insidious after age 30 years; fatal within 15 to 20 years
154
Q

Huntington Disease (HD)
* What is the mvt, mood/cognitive changes?

A
  • Movement disorders – chorea, dystonia, akathisia, athetosis
  • Mood /cognitive changes – depression, personality, dementia
155
Q

HD treatment (symptomatic)
* Regions of the brain impacted by HD have what? (3)

A

Decrease of GABA

Decrease of Ach

Increase of DA
* Medications decrease or antagonize DA

156
Q

HD treatment (symptomatic)
* For moderately severe chorea, there is an increased risk of what?

A

Increased risk of falls, poor sleep, difficulty with speech / swallowing

157
Q

HD treatment (symptomatic)
* What is first line?
* What is second line?

A

First-line
* VMAT-2 inhibitors – DA depletors
* Tetrabenazine, deutetrabenazine

Second-line
* Patients with depression / suicidality (this will be moved to first line with patients of depression)
* Atypical antipsychotics

158
Q

HD treatment (symptomatic): VMAT-2 inhibitors
* What do they deplete and improve?
* What happens presynaptic and postsynaptic?

A

First-line - VMAT-2 inhibitors
* Deplete DA by two primary mechanisms
* Improve symptoms of chorea

Presynaptic
* Inhibit vesicular monoamine transporters (VMAT)
* Vesicles cannot release DA

Postsynaptic
* Weak DA receptor antagonists

159
Q

HD treatment (symptomatic): VMAT-2 inhibitors
* What are the SE? (3)

A
  • Sedation
  • Pseudoparkinsonism
  • Increased depression and suicide risk
160
Q

HD treatment (symptomatic)
* What is second line and when is it used?

A

Patients with depression / suicidality

Atypical antipsychotics
* Olanzapine, risperidone

161
Q

Tourette Syndrome (TS)
* What is it?
* What is txt for mild, nondebilitating tics?

A
  • Tourette syndrome (TS) is a neurological disorder manifested by motor and phonic tics with onset during childhood
  • Mild, nondebilitating tics – no therapy, watch and wait
162
Q

Tourette Syndrome (TS)
* What is first and second line?

A

First-line:
* Habit reversal training where available

Second-line
* VMAT-2 inhibitors (tetrabenazine)
* Atypical antipsychotics (aripiprazole)
* Other: alpha agonists (clonidine, guanfacine) with ADHD-> will go to first line with ADHD patients

Pharm III (14 decks)

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