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SPP2 CNS > PD > Flashcards

PD Flashcards

1
Q

PD symptoms

A

resting tremor, rigidity, bradykinesia, impaired balance, mask-like appearance, speech difficulties, cognitive deficits*

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2
Q

PD is characterized by…

A
  • PD is characterized by a loss of dopaminergic neurons in the substantia nigra**: Gradual loss of darkly pigmented, dopamine-releasing neurons in the SN pars compacta in the midbrain
  • presence of Lewy bodies in the various regions of the brain: Enriched with fibrillar forms of the protein α-synucelin, Aggregation of α-synuclein: Stage 1: Lower brainstem**, Stage 2: Raphe, Stage 3: SN (-> classic PD symptoms), Stage 4: mesocortex/thalamus, Stage 5: neocortex, Stage 6: entire neocortex
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3
Q

Neurotoxic/ Neuroprotective mechanisms in PD

A
  • Mitochrondria: electron chain dysfunction increase build up of ROS
  • α-synuclein is oxidized and aggregates
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4
Q

Midbrain

A
  • SN pars compacta provides input to the basal ganglia and supplies dopamine
  • Undergoes neurodegeneration in PD
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5
Q

Basal Ganglia

A
  • Striatum (caudate nucleus, putamen*)
  • Globus pallidus (external and internal segments)
  • Dopamine Signaling: Direct Pathway: involving D1 receptors in the striatum; Indirect Pathway: involving D2 receptors in the striatum; Effect of thalamocortical signaling is disrupted in PD**
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6
Q

antimuscarinics

A
  • adjunct therapy
  • Loss of dopamine = increase in cholinergic activity** (sort of compensation)
  • Cholinergic antagonists (antimuscarinic) can partially compensate for over activity
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7
Q

LDOPA

A
  • gold standard for PD therapy
  • Precursor of dopamine, but needs to be converted in SN, not periphery
  • L-DOPA crosses BBB, dopamine does not cross BBB
  • Carbidopa is a peripherally acting DOPA decarboxylase inhibitor** to prevent conversion of L-DOPA -> dopamine in the periphery
  • Carbidopa does not penetrate BBB, so does not inhibit conversion in SN
  • Challenges: In PD there are less nigral dopaminergic neurons to convert L-DOPA to dopamine over time, Dyskinesias : aberrant and exaggerated motor effects, Address these challenges by using dopamine receptor analogs as a possible alternative
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8
Q

DA receptor agonists

A

apomorphine, ergolines, nonergolines

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9
Q

apomorphine

A

(mixed D1/D2 agonist): used in late-stage PD; use is limited due to N/V

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10
Q

ergolines

A

bromocriptine, pergolide

  • Bromocriptine: used as adjunct to L-DOPA to be able to lower dose
  • Pergolide: very potent D2 agonist used to treat PD (no longer in US)
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11
Q

nonergolines

A

ropinirole, pramipexole, rotigotine

  • D2/D3 agonists with fewer side effects than ergolines
  • Generally used as monotherapy for early-stage PD
  • Rotigotine offered in a transdermal patch
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12
Q

MAOB inhibitors

A

selegiline and rasagiline**

  • These drugs inhibit the oxidation of dopamine to DOPAL by MAO-B
  • Both drugs can initially be used to delay first use of L-DOPA or as adjuncts to L-DOPA
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13
Q

dopamine metabolism inhibition

A

COMT inhibitors (entacapone, tolcapone)

  • Inhibition of COMT by entacapone decreases metabolism of L-DOPA in the periphery, allowing more to reach the brain
  • Tolcapone works in CNS to increase CNS levels of dopamine from L-DOPA
  • Entacapone can increase duration of effect
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14
Q

propargylamines

A

R2N-CH2-C—CH

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15
Q

PD motor symptoms

A

tremor, bradykinesia, rigidity, Parkinsonian gait

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16
Q

PD nonmotor symptoms

A

Anxiety, depression, constipation, dementia, insomnia, orthostatic hypotension, psychosis/delirium, sexual dysfunction

17
Q

non-pharmacological treatment

A

exercise/physical therapy, nutritional counseling, occupational therapy, psychotherapy, speech therapy, support groups

18
Q

pharmacological treatment

A
  • 1st Line: Dopamine agonist, Dopamine precursor (L-DOPA)

- 2nd Line: MAO-B Inhibitor

19
Q

LDOPA

A
  • Effective monotherapy for motor symptoms (gold standard); adjunctive treatment with DA agonists
  • Side Effects: N/V, orthostatic hypotension, dyskinesias/motor fluctuations, hallucinations
  • Clinical Pearls: on empty stomach if does not cause nausea; titrate up to balance efficacy and side effects
20
Q

dopamine agonists

A
  • Non-Ergots (Pramipexole, Ropinirole, Rotigotine(patch)) are first line for initial therapy
  • Effective monotherapy for motor symptoms**; adjunct with L-DOPA
  • Side Effects: N/V, orthostatic hypotension, sudden onset sleep, hallucination, impulse control disorder (must switch to a different class)**
  • Clinical Pearls: uptitrate dose to minimize side effects; potentially better for younger patients
21
Q

MAOB inhibitors

A
  • Second line for initial PD therapy
  • Managed L-DOPA motor fluctuations*
  • Side Effects: H/V, HA, insomnia, hypotension/hypertension
  • Clinical Pearls: delay need for CD/LD; Risk of serotonin syndrome with serotonin drugs (contraindicated with dextromethorphan, meperidine, methadone, tramadol)
22
Q

COMT inhibitors

A

entacapone

  • Management of CD/LD induced motor fluctuations (i.e. will only be using if on L-DOPA)
  • Side Effects: N/V, brown/orange urine discoloration, hepatotoxicity* (tolcapone limiting side effect*)
  • **Early PD: no benefit of COMT inhibitors with CD/LD versus CD/LD monotherapy
  • **Reserved for management of freezing seen with CD/LD
23
Q

amantadine

A
  • Management of CD/LD induced motor fluctuations; effective for controlling motor symptoms (tremors)
  • Side Effects: insomnia, confusion/hallucinations
  • Clinical Pearls: utility limited due to cognitive side effects; usually reserved for tremors (monotherapy/CD-LD induced)
24
Q

anticholinergics

A
  • Management of tremor***-predominant PD inpatients under 65 years old
  • Side Effects: confusion, urinary retention, constipation, blurry vision, dry mouth
  • Clinical Pearls: used in younger PD patients with tremor as primary symptom; avoid if >65 years old (would use Amantadine if >65 years old)
25
Q

management of motor fluctuations

A
  • Wearing Off: Increase CD/LD dose; add DA agonist or MAO-B inhibitor; CR L-DOPA
  • Peak-dose dyskinesias: Decrease CD/LD dose; adjunct amantadine
  • Delayed onset: Take CD/LD on empty stomach; avoid CR CD/LD; ODT dosage form
  • Freezing: increase CD/LD dose frequency; add MAO-B inhibitor or COMT inhibitor
26
Q

treatment of nonmotor symptoms

A
  • Constipation: increase fluids; stool softeners
  • Insomnia: non-pharmacological counseling; melatonin, non-benzo (e.g. zolpidem), AVOID benzos (Lorazepam, diazepam, oxazepam)
  • Orthostatic Hypotension: non-pharmacological counseling; medical equipment to stabilize patients
  • Anxiety/Depression: MAO-B inhibitor, SSRI, SNRI
  • Dementia: AVOID anti-cholinergics, benzos, antihistamines, sedatives; could try cholinesterase inhibitors (donepezil, rivastigmine)
  • Psychosis/Delirium: Reduce PD doses, Preferred anti-psychotics: quetiapine, clozapine,AVOID: haloperidol, olanzapine, paliperidone, risperidone

SPP2 CNS (4 decks)

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