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IPT: Neuro > Block 1 > Flashcards

Block 1 Flashcards

1
Q

What does a neurologic exam show?

A

Symmetrical vs asymmetrical function; may identify local lesions within NS

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2
Q

Imaging Tools

PET
SPECT
MRI
CT

A

CT; images of brain in slices in 1-10mm thickness

MRI; more detailed image vs CT, uses magnet of H+ and protons

PET; excellent resolution, rates of biological process w/ C14-deoxyglucose

SPECT; poorer resolution than PET, radiotracer where tissue uptake gives image

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3
Q

Delirium DSM5

A

Environmental + Medications

Occurs most in older individuals at ICU, nursing homes, or hospice

Can be caused by substance intoxication

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4
Q

Epidemiology of migraines?

A

17.1% women and 5.6% men in US have ≥1migraine/yr

After age 12, females are 2-3x more likely to suffer

Highest prevalence in both women and men are aged 30-49

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5
Q

Migraine pathophysiology?

A

Activity of trigeminovascular system

Vasodilation and activation of perivascular trigeminal nerve which releases vasoactive peptides

Activates hypothalamus and brainstem

Releases CGRP + PACAP

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6
Q

What are the genetic mechanisms behind migraine triggers?

A

Calcium and sodium channels and PP abnormalities that regulate cortical excitability via SEROTONIN release

Increased levels of excitatory AA such as glutamate

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7
Q

IHS diagnostic classification of Migraine w/o Aura?

A

≥5 attacks

Lasts 4-72hrs

Lots of sx such as pulsing quality, N/V, photophobia, etc

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8
Q

IHS diagnostic classification of Migraine w/ Aura?

A

≥2 attacks

Fulfills criteria for atypical pain or aura

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9
Q

What is an aura?

A

Affects 25% of migraineurs

Lasts for 1 hr

Has both “positive” and negative visual effects

Sensory and motor symptoms occur as well

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10
Q

Epidemiology of tension headache?

A

1yr prevalence is 31-86%

Peaks in 4th decade and decreases incidence w/ age

Women>Men

Functional impairment occurs in 60% of tension type headache sufferers

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11
Q

Pathophysiology of tension headache?

A

May originate from myofascial factors, peripheral sensitization of nociceptors, and heightened sensitivity of pain pathways in CNS

Stimuli such as mental stress, etc

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12
Q

How does tension headache present?

A

Bilateral pain in a hatband pattern

No aura

Minor disabilities vs other headaches

Physical activity doesnt affect severity

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13
Q

Epidemiology of cluster headaches?

A

Lifetime prevalence is 0.12%

Male:Female ratio is 3:1

Men typically get it in 3rd decade, women at younger age

Predisposition in certain families

65% of pt w/ this headache are current/former tobacco users however cessation doesnt improve the headache :(

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14
Q

Pathophysiology of cluster headaches?

A

Modulator = hypothalamus

Secondary activation of trigeminal autonomic reflexes

Alterations in circadian rhythm

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15
Q

Clinical presentation of cluster headaches?

A

Daily attacks for 2wks to several months followed by long pain-free intervals

Occurs commonly at night and in spring/fall

Lasts 15 to 180min

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16
Q

Migraines are typically (bilateral/unilateral)

A

Unilateral

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17
Q

What are the CGRP receptor antagonists used for migraine prophylaxis?

A

Erenumab
Fremanezumab
Galcanezumab

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18
Q

What is MIG-99?

A

Used prophylactically for migraines that is extracted of feverfew daisies

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19
Q

What are the 1st and 2nd Gen serotonin 5-HT1 agonists? Major differences?

A

Sumatriptan is the only one that is first gen

Everything else is second (rizatriptan, etc)

2nd gen = higher oral bioavailability

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20
Q

What functional group is vital for 5-HT1 agonists?

A

Indole group

2 benzene rings with one having an N-H

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21
Q

What specific receptors do 5-HT1 agonists target and their MOA?

A

5-HT1B + D

Vasoconstriction of intracranial arteries

Inhibits vasoactive peptides released from perivascular trigeminal neurons

Inhibits transmission thru 2nd order neurons ascending to thalamus

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22
Q

Which sumatriptan formulation has significant 1st pass effect? When severe GI symptoms present?

A

1st pass = oral tablet

GI issues = suppositories

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23
Q

Triptans vs ergot alkaloids, which have better anti-migraine efficacies?

A

Triptans

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24
Q

Which triptans have the longest half life?

A

Naratriptan and Frovatriptan

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25
Q

5-HT1 agonist AE?

A

Paresthesia, dizziness, neck pain

Coronary vasospasms

CI in pt w/ CAD and angina, hemiplegic or basilar migraine

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26
Q

What class of drugs are ergotamine and dihydroergotamine (DHE) similar to?

A

5-HT1 agonists

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27
Q

Caffeine can be added to ergotamine to do what?

A

Improve rate and extent of oral absorption

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28
Q

Ergotamine and DHE AE and CI?

A

N/V

CI in renal/hepatic failure, CAD, uncontrolled HTN, pregnancy or nursing mothers

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29
Q

Which receptors do ergotamine and DHE target?

A

5-HT, alpha, and dopamine 2,3,4

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30
Q

CGRP receptor antagonist general info?

A

Erenumab is the only human antibody, the other two are humanized

PREVENTS migraines

Metabolized by non-sepcific proteolysis (not by CYP)

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31
Q

Acupuncture and episodic migraine?

A

They reported less AE vs those w/ Rx and were less likely to drop out

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32
Q

General algorithm for headaches?

A

If mild/moderate symptoms, use NSAIDs,APAP. If that doesnt work, use fiorcet. If that doesnt work then use Triptans, ergotamine/DHE, CGRPs

If severe symptoms, go straight to Triptans, ergotamine/DHE, CGRPs

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33
Q

Non-pharm Headache Tx?

A

Ice on head

Rest in a dark, quiet area

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34
Q

What dose and response rate is used as reference for triptans?

A

Sumatriptan 100 mg dose and 2 hour response rate

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35
Q

What should you NOT take w/ triptans?

A

MAOIs within 2 wks

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36
Q

Lasmiditan (Reyvow®) info

A

Serotonin 5-HT1F r agonist

Dose: Once daily

Possible serotonin syndrome, Inhibits OCT1 w/ no interaction to sumatriptan

Primary endpoint: no pain for 2 hrs (20-40%)

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37
Q

Ubrogepant (Ubrevly®) info

A

First PO CGRP antagonist for acute Tx. PRN

Taken twice a day, max 200mg/24hrs

Second dose is taken 2hrs after the first dose

Metabolized by CYP3A4, avoid with -azoles

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38
Q

Rimegepant (Nurtec ODT®) info

A

Acute Tx. with/without aura and currently NOT approved for prevention

CGRP antagonist given PO or SL

Mostly metabolized by CYP3A4, avoid with -azoles within 48hrs

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39
Q

Pt consideration when using NSAIDs for acute headaches?

A

Use suppositories for those with N/V

Don’t overuse NSAIDs cause it will medication-overuse headaches

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40
Q

NSAIDs alone vs Combo products (fioricet)

Which one has a higher chance of medication-overuse headaches?

A

Combo

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41
Q

Safety tips when using ergotamine?

A

Dont use within 24hrs of triptans

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42
Q

Prophylactic regimen therapy for headaches?

A

Recurrence is predictable? (pregnancy, migraine)
*Use triptan or CGRPs

Healthy or heart issues?
*Beta blockers or verapamil if they are contraindicated not effective

Depression or insomnia?
TCAs

Seizure or bipolar?
Anticonvulsants

None of the above work? Combo products/seek specialist

***go down this list, if anticonvulsants dont work, you may use beta blocker or verapamil then go to last step

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43
Q

NSAID therapy info?

A

Naproxen has the strongest evidence

Use 1-2 days prior to headache and continue using it

Monitor for GI and renal toxicity when using longterm

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44
Q

BB therapy info?

A

Timolol, propranolol, metoprolol

Might raise migraine threshold

BB w/ intrinsic sympathomimetic activity are ineffective

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45
Q

Triptan therapy info?

A

Frovatriptan has established efficacy over naratriptan and zolmitriptan (those only have probable efficacy)

Useful in preventing MENSTRUAL migraine, Use 1-2 days prior to headache and continue using it

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46
Q

Antidepressant therapy info?

A

Amitriptyline, venlafaxine

Downregulates 5-HT2 receptors, increases lvls of norepi, enhanced opioid receptor actions

Limited use due to anticholinergic effects

Caution in BPH and glaucoma and those taking triptans due to serotonin syndrome

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47
Q

Anticonvulsant therapy info?

A

Valproate, divalproex, topiramate

Inhibits GABA, modulates excitatory glutamate, inhibits sodium and calcium channels

Must titrate to avoid AE

Valproate is CI in pregnancy, pancreatitis, and liver disease

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48
Q

CGRP and Eptinuzmab (Vyepti™) info?

A

Galcanuzumab (Emgality™) used for migraine and cluster HA

Preventive drugs

Eptinuzmab is given IV q3months. No interactions w/ sumatriptan

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49
Q

What are used in tension HA?

A

Simple analgesics and NSAIDs

Limit use of NSAIDs for 15 days

Combo 9 days

Butalbital 3 days

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50
Q

Abortive therapy for cluster headaches?

A

Verapamil is first line; takes about a week

Oxygen 100% 12L/hr for 15-30min; caution in those w/ COPD or smoke

SQ or intranasal triptan; 6mg SQ sumatriptan is more effective, but intranasal is better tolerated

IV dihydroergotamine, sublingual or rectal ergotamine can be used as well

Lithium and corticosteroids can be used

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51
Q

Pathophysiology of seizures?

A

Inhibits GABA-A

GABA-B are activated, decreases calcium influx and inhibits neurotransmitter release

Glutamate is the excitatory NT that produces seizures

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52
Q

What are the highest RF for SUDEP?

A

Generalized seizures

Seizures >3/year

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53
Q

Which antiepileptic Rx display non-linear PK?

A

Phenytoin and ethotoin

Valproate when doses >2.5g/day, ethosuximide when doses >1.5g, gaba and pregabalin, and carbamazepine

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54
Q

Antiepileptic therapy + special population?

A

Women = increased drug clearance, secretion of rx in breast milk, fetal malformations

Men = possibility of reduced fertility

Peds = altered PK and need to adjust dose

Geriatric = decrease your dose and many rx interactions

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55
Q

Important Rx interaction with valproate?

A

Lamotrigine

Phenobarbital (increased conc of it)

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56
Q

Which antiepileptic drugs dont have any interactions and why?

A

Gabapentin, pregabalin, Vigabatrin, and Keppra due to renal excretion

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57
Q

General AED AE?

A

Idiosyncratic rxns, blood dyscrasias, SJS/rash, aplastic anemia, pancreatic issues

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58
Q

Carbamazepine AE?

A

Hyponatremia, leukopenia (d/c if WBC<2500), decreased bone density

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59
Q

Ethosuximide AE?

A

N/V, titrate the dose slowly

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60
Q

Cenobamate info?

A

Used for partial onset seizures in adults

DRESS AE

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61
Q

Clobazam info?

A

BZD derivative

Abrupt d/c may cause withdrawal symtpoms

Controlled

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62
Q

Eslicarbazepine info?

A

Pro drug, also better oral absorption vs carbamazepine

Up to 1200mg/day

Hyponatremia

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63
Q

Ezogabine AE?

A

Urinary retention (careful w/ anyone that has BPH or on anticholinergics) and QT prolongation, blue skin discoloration and retina pigment change

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64
Q

Felbamate info?

A

AE = weight loss and anorexia

Limited use and only for those who dont respond to other agents

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65
Q

Gabapentin/Pregabalin info?

A

L-amino acid GI absorption

Pregabalin is a controlled agent and more potent

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66
Q

Lamotrigine info?

A

Pt w/ hx of rash are more likely to have a rash with this Rx

Warning of HLH

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67
Q

Oxcarbazepine info?

A

Prodrug, better oral absorption vs carbamazepine

Can cause hyponatremia

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68
Q

Perampanel info?

A

AMPA receptor antagonist

Causes dizziness and somnolence

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69
Q

Phenobarbital info?

A

Causes delayed development in kids and cognitive impairment in adults, and toxic epidermal necrolysis

Parental product contains propylene glycol and alcohol

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70
Q

Phenytoin info?

A

Do NOT give IM

Uses Michaelis-Menten kinetics

100 mg phenytoin = 92mg phenytoin sodium

Causes gingival hyperplasia and skin issues, ataxia nystagmus

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71
Q

Topiramate AE

A

Can cause kidney stones and metabolic acidosis. Cleft palate in newborns too

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72
Q

Valproic acid info?

A

UGT and beta oxidation

Causes hyperammonemia and platelet issues

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73
Q

Vigabatrin info?

A

S enantiomer is active

Can cause seizures

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74
Q

Zonisamide info?

A

Related to sulfonamide

Can cause decreased sweat, weight loss, and kidney stones

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75
Q

What is Dravet Syndrome?

A

Epilepsy at 1-18 months, variant of SCN1A

Can present in kids or adults

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76
Q

How do you treat Dravet Syndrome?

A

1st line: Valproic acid or Clobazam

2nd line: stiripentol (w/ valproic acid or clobazam) or topiramate or ketogenic diet

3rd line: AED addition or vagus nerve stimulator

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77
Q

Lipophilicity and onset of action/duration?

A

More lipophilic = more rapid onset = shorter duration = high logP

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78
Q

What does primidone form?

A

Phenobarbital + PEMA

PEMA is the weaker anticonvulsant, but is the major metabolite. Is has more toxicity issues

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79
Q

Phenobarbital and primidone induce what?

A

CYP2C

CYP3A

UGT

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80
Q

Barbiturate MOA and application?

A

Increases GABA activity

Partial/generalized tonic-clonic seizures

81
Q

Hydantoins MOA and application?

A

Inactivates Na channels

Partial/generalized tonic-clonic seizures

82
Q

Succinimides MOA and application?

A

Blocks T-type Calcium channels

Absence seizures

83
Q

Phenytoin interaction and induction?

A

90% protein bound which can displace other highly protein bound rx such as Tiagabine

Induces CYP2C, CYP3A, and UGT

84
Q

Phenytoin solubility issues?

A

It has poor solubility at neutral pH

Absorbs CO2 which causes crystallization, IM injections can be painful

85
Q

Fosphenytoin solubility?

A

Highly water soluble prodrug

Given as IM or IV and is consistent and predictable

86
Q

Which epileptic drug is not an enzyme inducer?

A

Ethosuximide even though it is structurally similar

CYP3A4 inducers however can decrease exposure of ethosuximide

87
Q

Which antiepileptic drug is chemically and metabolically reactive at the C10-C11 double bond?

A

Carbamazepine

88
Q

Carbamazepine metabolism pathways?

A

Forms an active and reactive metabolite

Active = more toxic than carbamazepine

Reactive = are electrophilic and readily react with thiols

Induces CYP2C, CYP3A, UGT + CYP1A2

89
Q

Carbamazepine AE?

A

Causes ACHS indicated by fever, rash and hepatotoxicity, blood dyscrasias

90
Q

Whats different about oxcarbazepine vs carbamazepine in terms of metabolism?

A

2nd Gen analog btw

Doesnt undergo CYP3A4 oxidative metabolism

Also no reactive metabolites, just active only

91
Q

Whats different about eslicarbazepine acetate vs carbamazepine and oxcarbazepine in terms of metabolism?

A

Prodrug, converts to (S)-licarbazepine (eslicarbazepine)

Produces greater plasma exposure of active metabolite vs oxcarbazepine

92
Q

Gabapentin info?

A

Not metabolized in human and does NOT bind to proteins

Eliminated renally as unchanged rx

Substrate of L-AA and uses active transport

Transporter protein is saturable and bioavailability is dose-dependent and variable amongst ppl

93
Q

Differences of pregabalin vs gabapentin?

A

Pregabalin is pretty much the same, but is 3-10x more potent as an anti-seizure rx

94
Q

Differences of gabapentin enacarbil (Horizant) vs gabapentin?

A

Gabapentin enacarbil (Horizant) is a prodrug which overcomes absorption issues

95
Q

Vigabatrin MOA and AE?

A

Irreversible (suicide) inhibitor of GABA-transaminase, therefore increases GABA in CNS

Progressive and permanent bilateral vision loss, must be in SHARE program and periodic vision testing

96
Q

Tiagabine metabolism?

A

Highly protein bound ≥95%

Oxidation via CYP3A4, inducers will reduce the drug

97
Q

BZD metabolism?

A

Protein bound correlates w/ lipid solubility

EX: diazepam (98% bound with logP=3) vs lorazepam (85% bound with logP=2.4)

Therefore diazepam reaches CNS concentration faster and redistributes into fat faster

98
Q

Valproic Acid metabolism and AE?

A

Inhibits CYP2C9, UGT, and epoxide hydrolase

Teratogenic! Hepatotoxicity

99
Q

Valproic acid metabolism pathways

A

Forms active and toxic metabolites!

Can deplete glutathione which leads to toxicity too!

100
Q

Which Rx has BBW given by FDA for aplastic anemia and hepatic failure?

A

Felbamate; linked to reactive metabolites via glutathione depletion

101
Q

Lamotrigine MOA?

A

Metabolized by N-glucuronidation, DDI with Rx that induce/inhibit UGT

102
Q

Topiramate metabolism?

A

Absorbed rapidly via oral route, 70-80% of drug is excreted unchanged in urine

Dose goes down in renal insufficiency

Inhibits CYP2C9

103
Q

Keppra and Brivaracetam metabolism?

A

Rapid absorption, minimal protein biding, and NOT metabolized by CYP450, UGT, or epoxide hydrolase

Brivaracetam has affinity towards SV2A + Sodium channel blocking activity

104
Q

Zonisamide metabolism?

A

Half of excreted drug is a a glucuronide conjuagte known as SMAP

Co-adminstration with another CYP3A4 inducing anti-seizure med (phenytoin, carba, etc) will reduce half life and plasma concentration

105
Q

Lacosamide metabolism?

A

Converts to inactive O-desmethyl metabolic via CYP2C19, excreted 40% unchanged rx

No effect on P450s

106
Q

Rufinamide metabolism?

A

Major metabolite (78%) is due to carboxylesterase-mediated hydrolysis which can lead to inactive metabolites

Low protein binding, but can be induced by other anti-seizure meds

Valproic acid DDI, increases rufinamide concentration

107
Q

Ezogabine metabolism?

A

Not metabolized by P450

Pathway includes N-gluc by UGT

108
Q

Perampanel metabolism?

A

Highly protein bound and metabolized by CYP3A

Discovery led to drug design popularity for AMPA receptors..?

109
Q

Cannabidiol info?

A

Component of Cannabis sativa plant, NOT psychoactive like THC

Metabolized by 2C19, 3A4, and UGT

Inhibits 2C19

110
Q

Which drug interacts with cannabidiol?

A

Inhibits 2C19, therefore lacosamide

111
Q

Which anti-seizure meds are NOT metabolized by CYP450?

A

Keppra + Ezogabine + Rufinimide

112
Q

Which anti-seizure meds are metabolized by N-gluc?

A

Ezogabine + Lamotrigine

113
Q

Which anti-seizure med needs to be renally adjusted?

A

Topiramate

114
Q

Which anti-seizure med displaces other Rx?

115
Q

What is the GABA_a receptor?

A

Chloride channel

Activating it hyperpolarizes the potential which inhibits action potential

116
Q

What are the glutamate receptors?

A

Activation increases both sodium and calcium, which causes membrane depolarization, which encourages action potential

117
Q

Do depress neuronal activity, should you open/close what?

Calcium
Chloride
Potassium
Sodium

A

Close both sodium and calcium

Open both potassium and chloride

118
Q

Lamotrigine

Calcium
Chloride
Potassium
Sodium
GABA
Glutamate
A

Sodium inhibition

119
Q

Primadone

Calcium
Chloride
Potassium
Sodium
GABA
Glutamate
A

Sodium inhibition, increase GABA

120
Q

Oxcarbazepine

Calcium
Chloride
Potassium
Sodium
GABA
Glutamate
A

Sodium inhibition

121
Q

Ezogabine

Calcium
Chloride
Potassium
Sodium
GABA
Glutamate
A

Potassium activation

122
Q

Eslicarbazepine

Calcium
Chloride
Potassium
Sodium
GABA
Glutamate
A

Sodium inhibition

123
Q

Lacosamide

Calcium
Chloride
Potassium
Sodium
GABA
Glutamate
A

Sodium inhibition

124
Q

Zonisamide

Calcium
Chloride
Potassium
Sodium
GABA
Glutamate
A

Sodium and T-type calcium inhibition

125
Q

Perampanel

Calcium
Chloride
Potassium
Sodium
GABA
Glutamate
A

AMPA (glutamate) receptor antagonist

126
Q

T-channel calcium blockers are useful for which seizure?

127
Q

Which anti-seizure med undergoes no metabolism and is excreted unchanged by kidney?

A

Gabapentin

Pregabalin

Vigabatrin

Keppra

128
Q

What are the Rx used for absence seizures?

A

Ethosuximide and valproate

129
Q

What are the Rx used for status epilepticus?

A

Phenytoin

Diazepam

Lorazepam

130
Q

Rufinamide AE?

A

Shortens QT interval

131
Q

BZD MOA?

A

Bind to GABA_a receptors by opening chloride channels

132
Q

Which BZD can be given rectally?

133
Q

Which barbiturate has the least sedative effects?

A

Phenobarbital

134
Q

Tiagabine AE?

A

Increases chance of seizures and status epilepticus

135
Q

Which antiepileptic cause blue skin discoloration and retina pigment changes?

136
Q

Felbamate

Calcium
Chloride
Potassium
Sodium
GABA
Glutamate
A

Sodium inhibition, binds to NMDA, calcium inhibition (not T-type)

137
Q

Divalproex

Calcium
Chloride
Potassium
Sodium
GABA
Glutamate
A

Sodium inhibition, reduces T-type calcium

138
Q

Topiramate

Calcium
Chloride
Potassium
Sodium
GABA
Glutamate
A

Sodium inhibition, activates potassium, reduces NMDA

139
Q

Carbamazepine concentration levels?

140
Q

Phenytoin concentration levels?

A

10-20 *also has unbound levels

141
Q

Valproate concentration levels?

A

50-100 (some places go up to 150)

142
Q

Phenobarbital concentration levels?

143
Q

Ethosuximide concentration levels?

144
Q

Lacosamide AE?

A

PR interval increase; Get baseline EKG

145
Q

Which Rx can cause kidney stones?

A

Topiramate and zonisamide

146
Q

Dopamine vs L-dopa

Which one crosses the BBB?

147
Q

What are the excitatory dopamine receptors? Inhibitory?

A

Excitory = D1 + 5

Inhibitory = D2,3,4

148
Q

What kind of neurotransmitter is dopamine?

A

Not excitatory nor inhibitory, but a modulatory of neurotransmission

149
Q

Direct/Indirect dopamine pathway

Which one enables and inhibits movement?

A

Direct = enable

Indirect = inhibit

150
Q

Loss of DA in ____ leads to reduced excitatory input to cortex

151
Q

What happens when you take L-dopa PO?

A

Only 1% reaches brain as DA

Halting conversion of L-dopa to DA in periphery should boost L-dopa taken up into CNS

152
Q

How does carbidopa affect L-dopa?

A

Extends elimination half life from 1hr to 1.5 hrs

153
Q

Does carbidopa penetrate BBB?

154
Q

How do you reduce AE chances of carbidopa?

A

Reduction of peripheral DA concentrations

155
Q

Chronic use of L-dopa leads to what?

A

Prominent dyskinesias

156
Q

How do you want to affect COMT to enhance DA exposure in CNS?

A

Inhibit COMT should extend L-dopa

157
Q

What Rx are COMT inhibitors?

A

Tolcapone and entacapone

158
Q

Main difference between Tolcapone and entacapone?

A

Tolcapone acts in both CNS and periphery w/ liver problems

Entacapone is just peripherally

159
Q

BBW of COMT inhibitors?

A

Just tolcapone, acute liver failure

160
Q

What is the cheese effect?

A

MAOI cant be used w/ L-dopa due to it causing HTN crisis

161
Q

What Rx are MAO-B? Functional group?

A

Selegiline and rasagiline

Terminal alkyne forms covalent bond with protein

162
Q

By products of MAO-B?

A

Selegiline can produce amphetamine metabolites (vasoconstrictors) via CYP-mediated N-dealkylation

163
Q

Carbidopa inhibits what?

164
Q

With Parkinson’s, what is missing?

A

Fewer striatal nerve terminals as decarboxylate L-dopa

165
Q

DA receptor agonists vs L-dopa, which one has a longer duration of action?

A

DA receptor agonists, also less likely to induce on/off effects and dyskinesias

166
Q

Dopamine receptor agonist AE?

A

N/V, sedation, vivid dreams, hallucination

167
Q

Ergot alkaloids AE and MOA?

A

Cardiac issues

Nonselective DA receptor agonists (Serotonin and adrenergic activity)

168
Q

Non-Ergot DA receptor agonist Rx? Which DA receptors do they target?

A

Pramipexole, ropinirole, rotigotine

Pramipexole and ropinirole = D2

Rotigotine = D1,2,3 as a patch

169
Q

What happens if DA is removed completely?

A

Increased cholinergic activity leading to extrapyramidal Sx (tremors)

Use muscarinic ACh antagonists for this

170
Q

Muscarinic ACh antagonists for Parkinson’s example?

A

Trihexyphenidyl

Benztropine

Diphenhydramine

171
Q

Structure of Muscarinic antagonists? AE?

A

Tertiary basic amine + 2x 6 membered rings

AE = sedation and mental confusion

172
Q

What does overactive glutamate transmission in striatum cause? What is used to Tx it? AE?

A

L-dopa induced dyskinesias

Namenda

Confusion and hallucinations

173
Q

What are used to Tx hallucinations/delusions in parkinsons?

A

Pimavanserin (04-29-16)

Inverse agonist of 5-HT2a receptors

AE = QT prolongations and avoid in pt developing cardiac arrhythmias

174
Q

What are used to Tx “off” episodes in Parkinson’s?

A

Istradefylline; caffeine derivative and antagonist of Adenosine A2a receptors

175
Q

What are the hallmark features of PD?

A

Tremors at rest

Rigidity

Bradykinesia

Postural instability

176
Q

What are some environmental and protective factors of PD?

A

Increased risk: rural areas, well water, heavy metal and hydrocarbon exposure

Decreased risk: cigarette smoking, caffeine consumption, NSAID use

177
Q

L-dopa to Dopamine, whats the enzyme?

178
Q

From DA, what other pathways can it go to?

A

DOPAC + H2O2 via MAO-B

HVA via COMT

179
Q

What happens if there is a lot of H2O2 present?

A

Fe 2+ is converted to 3+ which forms OH* radicals

180
Q

General direct and indirect pathway of dopamine + motor function?

A

Both begin at striatum via SNc’s dopamine

Direct = goes straight to GPi, thalamus, then motor cortex

Indirect = stops at GPe first, then subthalamic nuclei, then GPi, thalamus, then motor cortex

181
Q

In PD, what parts of the direct and indirect pathway are affected?

A

SNc cant provide dopamine to striatum

Direct = loses function from striatum to GPi

Indirect = loses function from GPe to subthalamic nuclei

Both pathways lose function from thalamus to motor cortex

182
Q

How is L-dopa in the body made?

A

L-tyrosine is converted to L-dopa via TH

183
Q

What correlation does DA have on ACh?

A

Lowered DA levels will increase ACh which leads to tremors

184
Q

What is the Hoehn and Yahr Severity scale?

A

0 = no signs

I = Unilateral

II = bilateral, no posturing

III = bilateral, mild posturing

IV = bilateral, postural

V = severe, confined to bed or wheelchair

185
Q

What is the first line Tx for PD? What is used for mild tremors?

A

Usually Rasagiline

Amantadine and/or anticholinergics (benztropine, trihexyphenidyl)

186
Q

Tx of PD, pt has tremors

A

≥65yo = carbidopa/levo

<65yo = anticholinergics, then carbidopa/levo

187
Q

Tx of PD, pt has tremors, bradykinesia, rigidity

A

≥65yo = carbidopa/levo

<65yo = dopamine agonist, then carbidopa/levo

188
Q

Tx of PD, pt has tremors, bradykinesia, rigidity, postural instability/gait

A

≥65yo = carbidopa/levo and physical therapy

<65yo = dopamine agonist and physical therapy

anything worse than this with Sx, surgery will be needed

189
Q

Amantadine info?

A

Renal eliminated (decrease dose if CrCl is low)

Causes skin discoloration (molting)

Stimulates DA release, inhibits glutamate

190
Q

How do you Tx end-of-dose- “weaning off”?

A

Increase dose of carbidopa/levo or switch to ER or inhalation

Add either COMTi, MAO-Bi, or dopamine agonist

191
Q

How do you Tx delayed on or “no on” response?

A

Give carb/levo on empty stomach

Use ODT

Avoid SR

Use apomorphine SQ or l-dopa inhalation

192
Q

How do you treat hesitation “freezing”?

A

Increase carb/levo dose

Give MAO-Bi or dopamine agonist

Physical therapy

193
Q

How do you treat peak-dose dyskinesia?

A

Smaller dose of carb/levo

Reduce dose of dopamine agonist

Add amantadine

194
Q

What drug has the “honeymoon period”?

A

Carb/levo for 5-7 yrs

195
Q

COMTi AE?

A

Only Tolcapone has liver issues

Both have delayed onset of diarrhea and cause brownish-orange urine

196
Q

Apomorphine AE?

A

Severe hypotension when given with serotonin blockers (ondansetron)

Pre dose w/ trimethobenzamide to minimize N/V

197
Q

Ropinirole AE?

A

Can cause pt to suddenly fall asleep, pramipexole does this too

198
Q

Pimavanserin info?

A

Used for psychosis in PD

40mg dose, takes a couple weeks to work

Can cause QTc prolongation!!

IPT: Neuro (4 decks)

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