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Therapeutics 3 - Spring 2018 > Exam 3 - Rochet/Campbell (Parkinsons/Alzheimer's) > Flashcards

Exam 3 - Rochet/Campbell (Parkinsons/Alzheimer's) Flashcards

1
Q

Parkinson’s Disease (PD):

it is progressive (reversible or irreversible) disease resulting in neurological deficit in the ________ system

A

Irreversible;

deficit in extrapyramidal

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2
Q

Parkinson’s Disease Symptoms?

A 
Resting tremor
Rigidty
Bradykinesia
Impaired balance/coordination
Mask-like appearance
speech difficulties, cognitive deficits
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3
Q

Parkinson’s Disease (PD) is characterized by a loss of _________ in the _______

A

dopamine neurons; in substantia nigra

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4
Q

what is a lewy body?

A

there are dense spherical protein deposits in the brain

surviving neurons in the brains of PD pt have them

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5
Q

where are lewy bodyies found in PD pt?

A

in the substantia nigra and other parts like cortex

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6
Q

Lewy bodies are enriched with what things?

A

fibrillar forms of protein alpha-synuclein

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7
Q

what are the Braak stages?

A

way to stage Parkinsons;

based on “alpha-synuclein neuropathology”

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8
Q

how many braak stages are there

A

6

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9
Q

Stage 1 of Braak – means neuropathology starts in ______

A

lower brainstem

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10
Q

List Stages 1 - 6 of Braak Stages

A 
1 - lower brainstem (starts here and ascends!)
2 - Raphe
3 - Substania Nigra
4 - Mesocortex/Thalamus
5 - Neocortex/Prefrontal Cortex
6 - Entire Neocortex
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11
Q

Environmental poisons that are linked to increased PD risk happen because they do what?

A

they inhibit mitochondrial function and/or trigger oxidative stress

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12
Q

what are examples of environmental poisons that are linked to Parkinson’s Disease (PD)

A
  • Pesticides
  • Herbicides
  • Metals (manganese)
  • MPTP (a heroin contaminant, complex I inhibitor)
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13
Q

Basal ganglia is made up of the ________ and ______

A

striatum and globus pallidus

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14
Q

The striatum is made of ______ and _____

A

caudate nucleus; putamen

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15
Q

the globus pallidus is broken into what?

A

GPi and GPe

Globus pallidus internal and globus pallidus external

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16
Q

Dopamine Neurons and Pathways:

Indirect pathway involves D1 or D2 receptors?

A

D2

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17
Q

Dopamine Neurons and Pathways:

Direct pathway involves D1 or D2 receptors?

A

D1

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18
Q

Dopamine Neurons and Pathways:

D1 receptor works through direct or indirect pathway?

A

direct

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19
Q

Dopamine Neurons and Pathways:

D2 receptor works through direct or indirect pathway?

A

indirect

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20
Q

what is an antimuscarinic that be used as adjunct therapy in PD

A

benzotropine

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21
Q

why are antimuscarinics used as adjunct therapy in parkinsons?

A

when dopamine decreases — the cholinergic pathway ramps up (aka chill out that pathway by using anticholinergics)

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22
Q

what is the “gold standard” for PD therapy

A

L-DOPA

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23
Q

why cant we give dopamine directly?

A

dopamine has a + charge and cant enter CNS;

L-DOPA = no charge = CAN enter CNS!

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24
Q

what can be added to L-DOPA as a regimen to decrease the dose of L-DOPA needed

A

add carbidopa

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25
Q

why does giving carpidopa lead to a lesser dose of L-DOPA being needed

A

Carbidopa inhibits DCC (aka L-DOPA does not turn to Dopamine)

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26
Q

L-DOPA —(what enzyme?)–> Dopamine

A

DCC (DOPA decarboxylase)

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27
Q

T or F: Carbidopa can cross the blood brain barrier

A

FALSE!

it can NOT cross BBB – aka cannot inhibit DCC in the SN

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28
Q

what is definition of dyskinesias

A

exaggerated/aberrant motor effects

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29
Q

L-DOPA Therapy:

__________ are seen immediately after dosage of L-DOPA

A

Dyskinesias

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30
Q

to prevent dyskinesias and the on/off effect it is best ot give L-DOPA in a ______ manner

A

continuous manner!!

pulsatile is crap

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31
Q

L-DOPA Therapy:
a key limitation is associated with _________; this becomes a bigger issue when the patients get older/the disease progresses

A

prodrug conversion

as disease progresses — pts become less responsive to L-DOPA because they cant convert it to dopamine as easily

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32
Q

Dopamine Agonist or Inhibitor of Dopamine Metabolism?

Apomorphine

A

DA receptor agonist

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33
Q

Dopamine Agonist or Inhibitor of Dopamine Metabolism?

Ergoline drug class

A

Dopamine receptor agonist

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34
Q

Dopamine Agonist or Inhibitor of Dopamine Metabolism?

Bromocriptine

A

DA receptor agonist (it is an ergoline)

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35
Q

Dopamine Agonist or Inhibitor of Dopamine Metabolism?

Pergolide

A

DA receptor Agonist (it is an ergoline)

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36
Q

What drugs are ergolines

A

Bromocriptine
Pergolide
Cabergoline

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37
Q

Dopamine Agonist or Inhibitor of Dopamine Metabolism?

Non-Ergoline Drug Class

A

DA receptor agonist

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38
Q

Dopamine Agonist or Inhibitor of Dopamine Metabolism?

Ropinirole

A

DA receptor agonist - it is an NON-ergoline

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39
Q

Dopamine Agonist or Inhibitor of Dopamine Metabolism?

Rotigotine

A

DA receptor agonist - it is an NON-ergoline

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40
Q

Dopamine Agonist or Inhibitor of Dopamine Metabolism?

Pramipexole

A

DA receptor agonist - it is an NON-ergoline

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41
Q

Dopamine Agonist or Inhibitor of Dopamine Metabolism?

MAO-B inhibitors

A

inhibit metabolism

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42
Q

Dopamine Agonist or Inhibitor of Dopamine Metabolism?

Selegiline

A

inhibit metabolism (MAO-B inhibitors)

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43
Q

Dopamine Agonist or Inhibitor of Dopamine Metabolism?

Rasagiline

A

inhibit metabolism (MAO-B inhibitor)

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44
Q

Dopamine Agonist or Inhibitor of Dopamine Metabolism?

Safinamide

A

inhibit metabolism (MAO-B inhibitor)

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45
Q

what drugs are MAO-B inhibitors

A

Selegiline
Rasagiline
Safinamide

46
Q

Dopamine Agonist or Inhibitor of Dopamine Metabolism?

Entacapone

A

inhibit metabolism (COMT inhibitors)

47
Q

Dopamine Agonist or Inhibitor of Dopamine Metabolism?

Tolcapone

A

inhibit metabolism (COMT inhibitors)

48
Q

what drugs are COMT Inhibitors?

A

Entacapone

Tolcapone

49
Q

Dopamine Agonist or Inhibitor of Dopamine Metabolism?

COPT inhibitors

A

inhibit metabolism

50
Q

Which dopamine agonist(s) is a mixed D1/D2 agonist

A

Apomorphine

51
Q

“extra” effect of Apomorphine

A

has potent emetic effect (makes people vomit)

52
Q

which dopamine agonist(s) are D2 agonists

A

(Ergolines!!)
bromocriptine
and
pergolide

53
Q

which dopamine agonist is no longer used due to heart valve damage

A

pergolide

54
Q

T or F: Bromocriptine is not very effective on its own and is used as only adjunct

A

truuuuuuue

55
Q

which drug agonist(s) are D2/D3 agonists

A

(the Non-ergonlines)
Ropinirole
Pramipexole
Rotigotine

56
Q

Ergolines are ________ agonists
Non-Ergolines are ______ agonists
(D 1,2,3??)

A

Ergoline: D2

Non-Ergoline: D2/D3

57
Q

what drugs are propargylamines

A

Selegiline
and
Rasagiline

58
Q

what is MAO-B’s normal mechanism of action?

A

turns DA –> DOPAL

59
Q

T or F: Entacapone will increase potency of L-DOPA

A

FALSE!! it increases duration of action NOT potency!!

60
Q

Entacapone and Tolcapone are both COMT inhibitors:

which one decreases L-DOPA in periphery and which one decreases L-DOPA metabolism in the CNS?

A

in periphery: Entacapone
in CNS: Tolcapone*

(Tolcapone does work in periphery too….)

61
Q

Pharmacologic Therapy for Parkinsons:

1st Line?

A

Rule out Drug induced PD
Dopamine Agonist
Dopamine Precursor

62
Q

Pharmacologic Therapy for Parkinsons:

2nd line?

A

MAO-B inhibitor

Amantadine

63
Q

Types of LD Motor Fluctuations

A
  • wearing off
  • freezing
  • delayed onset
  • pear dose dyskinesia
64
Q

definition of peak dose dyskinesia

A

involuntary body movement cause by high DA levels

65
Q

definition of “freezing”

A

inability to move due to fluctuating DA levels

66
Q

side effects of levodopa/carbidopa

A
  • N/V
  • LD motor fluctuations
  • hallucinations
67
Q

what is ICD and examples of it?

A

ICD: impulse control disorder

shopping/gambling/inappropriate sexual behaviors

68
Q

benefits of dopamine agonists (compared to LD/CD)?

A

no motor fluctuations

long acting formulations

69
Q

ADEs of Dopamine Agonists

A
  • N/V
  • Sudden onset sleep
  • hallucinations
  • ICD (impulse control disorder)
  • Edema
70
Q

ADEs of COMT Inhibitors

A

N/V
Brown/Orange Urine Discoloration
Hepatoxicity

71
Q

ADEs of MAO-B inhibitors

A

N/V
HA
Insomnia
Hypotnesion/Hypertension

72
Q

ADEs of Anticholinergics

A

Confusion/Dementia!!

Blurred vision, Urinary Retention, Dry mouth, Constipation

73
Q 
Alzheimers Neuropathology:
Have \_\_\_\_\_\_ plaques
\_\_\_\_\_\_\_\_ tangles
and
\_\_\_\_\_\_\_ loss
A

Amyloid plaques

Neurofibriallary tangles

Synapse loss

74
Q

Alzheimers: AB Peptide

AB peptide is released from _____ by activity of ____ and _____

A

released from APP (amyloid precursor protein)

by activity of beta-secretase and gamma-secretase

75
Q

Alzheimers:
Amlyoid plaques are found ____cellularly
and
Neurofibrillary tangles are found ____cellularly

A

Amyloid: EXTRAcellular

neurofibrillary: INTRAcell

76
Q

Alzheimers:
Amlyoid plaques are made up of ______
and
Neurofibrillary tangles are made up of _______

A

Amyloid: AB peptide (amyloid beta)

Neurofibriallary: Hyperphosphorylated tau

77
Q

There was a debate if AB or tau was the key pathogenic molecule in Alzheimers - which one is it and what evidence is there to support this claim?

A

AB!
Evidence:
- mutations in APP (the AB precursor) is linked to early onset AD
- Downs Syndrome (Trisomy 21) == extra copy of APP gene and they have AD like symptoms around 40 y.o
- Presenlilin Proteins involved are also linked to AD

78
Q

AB peptide is around how many amino acids long

A

40 or 42

79
Q

which AB amino acid length tends to make fibrils more than the other? (AB42 or AB40)

A

AB42 makes fibrils more

80
Q

AB peptide is hydrophobic or hydrophillic

A

phobic!! therefore tend to aggregates easily

81
Q

Alzheimers:

what gene affects the components of the y-secretase complex

A

presenilin-1 or 2

PSEN1 or PSEN2

82
Q

Alzheimers:

Mutations in the PSEN1 or PSEN2 gene leads to what?

A

alters y-secretase complex which causes MORE AB or more AB42

83
Q

Alzheimers:

AB peptide is released from _____ by the activity of _____ and ______

A

released FROM APP (amyloid precursor protein)

by b-secretase and y-secretase

84
Q

Alzheimers:

Cleavage of APP by ________ leads to a non-toxic/non-amyloidogenic fragment being released

A

a-secretase

85
Q

Alzheimers:

how is AB aggregation and neurofibrillary tangles thought to be related?

A

AB peptide oligomers tend to activate kinases - those kinases hyperphosphorylate tau — and lead to neurofibrillary tangles

86
Q

Alzheimers:

Why are neurofibrillary tangles problematic?

A

disruption of cytoskeleton

disruption of axonal trafficking

87
Q

Alzheimers:

when tau is not hyperphosphorylated — what is its normal ufnction

A

stabilize microtubules

88
Q

Alzheimers:

what enzyme can degrade AB

A

Neprilysin

89
Q

Alzheimers:

when AB aggregation occurs - do microglial cells get activated or down regulated

A

activated!

they try to clean up the mess (aka the amyloid clusters)

90
Q

Alzheimers:

when microglia cells are activated — how do they respond

A

they release pro-inflammatory cytokines (causes NEUROINFLAMMATION)
they release reactive oxygen and nitrogen species (causes OXIDATIVE STRESS)

91
Q

Alzheimers:

Risk is increased when LDL levels are _____ and HDL levels are _____

A

if LDL is high and HDL is low

92
Q

what two disease states may increase risk for alzhemiers

A

Vascular disease
and
Diabetes

93
Q

what gene related to cholesterol has an affect AB deposition

A

ApoE

94
Q

Alzheimers:

what are the different isoforms of ApoE

A

ApoE2, ApoE3, ApoE4

95
Q

which ApoE isoform has an increased risk of AD

A

ApoE4

96
Q

Alzheimers:

what drugs are cholinesterase inhibitors

A

Donepezil
Rivastigamine
Galantamine

97
Q

why are cholinesterase inhibitors a beneficial therapy option for Alzheimers?

A

the inhibitor increases the amount of Ach – which is good because AD causes a degeneration of cholinergic nerve terminals

98
Q

Alzheimers:

what drugs are anti-glutamatergic?

A

Memantine (NMDA antagonist)

99
Q

ADEs of Cholinesterase inhibitors

A 
SLUD
(salivation
lacriamation
urination
defication)

You become a leaky mess

100
Q

Key Concepts of Dementia Therapy?

A

Target dose is what is whatever highest dose can be tolerated
Many ADEs- early recognition is better
AVOID Sudden stopping of therapy
Withdrawal of therapy should be considered with progressed symptoms
management of behavioral sxs of dementia poorly responsive to drug (?)

101
Q

Parkinson’s - Managing LD Motor Fluctuations

If medicine is wearing off - what do you do?

A
  • increase CD/LD dose or frequency
  • Add DA agonist, MAOI, COMTI
  • XR CD/LD
102
Q

Parkinson’s - Managing LD Motor Fluctuations

If patient is freezing - what do you do?

A
  • increase CD/LD dose or frequency

- Add DA agonist, MAOI, COMTI

103
Q

Parkinson’s - Managing LD Motor Fluctuations

If delayed onset - what do you do?

A
  • take CD/LD on empty stomach
  • ODT CD/LD
  • Avoid CR/XR or CD/LD
104
Q

Parkinson’s - Managing LD Motor Fluctuations

If peak dose dyskinesias - what do you do?

A
  • Add amantadine

- decrease CD/LD dose

105
Q

Parkinson’s - Treating Non-Motor Symptoms:

If Anxiety or Depression… how to treat?

A

AVOID BZDs
CAUTION: TCAs

CBT (cognitive behavioral therapy), SSRIs, and SNRIs are good options

106
Q

Parkinson’s - Treating Non-Motor Symptoms:

If Dementia… how to treat?

A

Cholinesterase inhibitors!

AVOID: Anticholinergics, BZDs, antihistamine, and sedatives

107
Q

Parkinson’s - Treating Non-Motor Symptoms:

If psychosis… how to treat?

A

Reduce PD medication Doses
Pimvanserin
Clozapine/Quetiapine (are options)
AVOID: haloperidol, olanzapine, paliperidone, risperidone

108
Q

Parkinson’s - Treating Non-Motor Symptoms:

if Constipation… how to treat?

A

increase fluid and fiber intake
stool softeners/laxatives
any meds causing this?

109
Q

Parkinson’s - Treating Non-Motor Symptoms:

If insomnia…how to treat?

A

AVOID: BZDs

Can use melatonin, and non-BZD sedatives (zolpidem, ezopiclone,zaleplon, and zopiclone)

110
Q

Parkinson’s - Treating Non-Motor Symptoms:

if orthostatic hypotension…how to treat?

A

Midodrine
Non-pharm counseling…
medical equipment to stabilize patient

Therapeutics 3 - Spring 2018 (20 decks)

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