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Advanced Pharm Exam 2 > Neurology Pt 1 Alzheimers and Parkinson's > Flashcards

Neurology Pt 1 Alzheimers and Parkinson's Flashcards

1
Q

Central Nervous System

  • _____ and _____ cord
  • Integrates _____ information and generates ______ output
  • Billions of _______ and surrounding _____ cells
  • _______ are responsible for the flow of information
  • ___________- chemicals relay, amplify, and modulate signals
    • Excitatory or Inhbitory
A
  • brain, spinal
  • sensory, motor
  • neurons, glial
  • Neurons
  • NeurotransmittersAttach Sounds
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2
Q

Neuron

  • Building block of the CNS
    • Process/transmit information
  • Classified based on f_____, l_____, and n______ released
  • Form dendritic trees - receive from other neurons and transmit to cell body =
  • Cell body =
  • Carries signal from cell body eventually to synapse =
  • Junction of neurons where NT are released to interact with receptors or other neurons
    • ultimately stimulates channels that allow _____ and ______ allowing for necessary communication/processes
A
  • function, location, neurotransmitter
  • Dendrites
  • Soma
  • Axons
  • Synapse
    • ​opening, closing
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3
Q

Voltage vs. Ligand Gated Channels

  • Voltage - ____ mediated
    • Primarily located on the initial segment of the axon as well as axon itsself (___ action potential)
  • Ligand - ______ mediated
    • Ligand (inotropic) receptor - _____ opens
    • Metabotropic receptor - engages _-protein to produce ______ messanger (_____-gated)
      • Calcium-___synaptic-____ channel function
      • Potassium-___synaptic-____ opening of channel
A
  • ion
    • fast
  • neurotransmitter
    • directly
    • G, second, voltage
      • pre, inhibit
      • post, slow

  • Voltage such as Na, Ca, K*
  • Ligand more neurotransmitter based*
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4
Q

Where do CNS drugs primarily work?

  • 1) Supplementing the NT*
  • ex) deficiency in norepi, give norepi*
A
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5
Q

Neurotransmitters and Receptors

  • Serotonin is responsible for a myriad of things*
  • Notice there are so many different receptors*
  • ex) dopamine has like 4 receptors
A
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6
Q

Neurotransmitters and Receptors cont.

  • Gaba-primary inhibitory transmitter*
  • Glutamate-primary excitatory transmitter*
A
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7
Q

Neurotransmitters and Receptors cont.

A
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8
Q

Alzheimer’s Disease

Characterized by?

A

Acetylcholine Deficiency

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9
Q

Acetylcholine (Ach)

  • Neurotransmitter responsible for _____ contraction (n____ receptors) and ________ component of the autonomic nervous system (_______ receptors)
  • Central Nervous System
    • Assists in: l____, m_____, neuro_____, c______
  • Peripheral Nervous System
    • _____ relaxation, skeletal and _____ contraction
A
  • muscle (nicotinic), parasympathetic (muscarinic)
  • learning, memory, neuroplasticity, concentration
  • Cardiac, muscle
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10
Q

What is Alzheimers?

Accounts for __-__% of dementia

A

A progressive degenerative disease ultimately resulting in cerebral atrophy

50-75%

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11
Q

Primary risk factors for Alzheimers

A

Age and Family Hx

  • Cerebral trauma, Vascular disease
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12
Q

Signs and Symptoms of Alzheimers

  • Difficulty performing ____ t____
  • Difficulty r_____ and w______
  • Loss of _______
  • D_____, D______, A_______
A
  • basic tasks
  • reading, writing
  • memory
  • Delusions, Depression, Agitation
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13
Q

Three histopathological hallmarks can impair neurotransmitter function of ________ leading to _____ deficits

    1. 3.
A
  1. Beta-amyloid-rich senile plaques (lots of ongoing research)
  2. Neuritic plaques and neurofibrillary tangles
  3. Neuronal degeneration
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14
Q

Pharmacological Considerations

  • Cholinergic pathways are damaged -> ____ of Ach transmission
  • Overstimulation of _____ receptor by ______ -> neuronal damage
  • Inhibition of ________ receptors -> impairs cognition
A
  • loss
  • NMDA, glutamate

- nicotinic

Perhaps inhibiting glutamate will prevent further progression of disease

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15
Q

Goals of Therapy

  • Improve _ _ _
  • Improve or slow the loss of ____/_____
  • Maintain and maximize independent ______
  • Minimize _ _ of drug therapy
A
  • QOL
  • memory/cognition
  • function
  • AE

NO CURE =(

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16
Q

Medications Used in the Tx of Alzheimer’s

2 classes, 5 agents

A
  • Cholinesterase Inhibitors
    • ​Donepezil (Aricept)
    • Rivastigmine (Exelon)
    • Galantamine (Razadyne)
  • ​NMDA receptor Antagonist
    • ​Memantine (Namenda)​
  • Combination
    • ​Donepezil + Memantine (Namzaric)

  • Not many tx options unfortunately*
  • Aricept and Memantine most common*
  • Onset: takes about 2-4 wks for these drugs to kick in*
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17
Q

Cholinesterase Inhibitors

MOA

A

Selectively inhibits cholinesterase (enzyme that hydrolyzes (inactivates) Ach) in the CNS

  • Increases Ach concentrations in the cerebral cortex
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18
Q

Cholinesterase Inhibitors

Indication

A

For mild to moderate disease

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19
Q

Cholinesterase Inhibitors

Agents

Routes

A

Donepezil (Aricept) - oral, ODT

Rivastigmine (Exelon) - oral, transdermal patch

Galantamine (Razadyne) - oral

Oral disintegrating tablet since alot of older adults have trouble swallowing

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20
Q

Cholinesterase Inhibitors

  • May _____ deterioration of ______ function
    • Preserves m_____, l_____, a______
  • Does not effect:
A
  • slow, cognitive
    • memory, learning, attention
  • underlying degenerative process
21
Q

Cholinesterase Inhibitors Adverse Effects

  • Donezepil:
  • Galantamine:
  • Rivastagmine:
  • ALL (3) - (_____ titrate dose)
  • ____cardia, d_____, s______
  • Urinary ______
  • Hyper______, sw_______
A
22
Q

Cholinesterase Inhibitors

Drug Interactions

A

Anticholinergic drugs (drugs that block cholinergic receptors)

Donepezil is a minor substrate of CYP3A4

  • Anticholinergic = blocks acetylcholine receptors*
  • Know that its a minor substrate, will not question on enzymes*
23
Q

Cholinesterase Inhibitor Adverse Effects

  • D
  • U
  • M
  • B
  • E
  • L
  • S
A
  • Diarrhea
  • Urination
  • Miosis
  • Bronchospasm
  • Emesis
  • Lacrimation
  • Salivation
24
Q

Cholinergic Crisis Signs and Symptoms

What is it?

  • S
  • L
  • U
  • D
  • G
  • E
A

To much Ach from inactivity of AchE enzyme that usually breaks it down

  • Salivation
  • Lacrimation
  • Urination
  • Defecation
  • Gastric upset
  • Emesis
25
Q

Memantine (Namenda)

MOA

A

NMDA (glutamate receptor) antagonist

  • Attenuates (reduces) excitotoxic effects of glutamate (neuroprotective)
  • Glutamate is very excitatory but very neurotoxic as well*
26
Q

Memantine

Drug Interactions

A

No CYP 450 drug interactions

27
Q

Memantine

Indication

A

Moderate to severe Alzheimer’s disease

  • often used in combination with cholinesterase inhibitor
28
Q

Memantine (Namenda)

Adverse Effects

A
  • Constipation
  • HA, confusion, dizziness, hallucinations
  • HTN
29
Q

Memantine (Namenda)

Route

A

Oral

  • Available as combination with donepezil (Namzaric) which is also given PO
30
Q

Parkinson’s Disease

What’s the issue?

A

Lack of Dopamine

Goal: Increase Dopamine

31
Q

Background

  • Degenerative disease of the _____ ______, resulting in gradual decline in _____, ______, and _____ functioning
  • Severe loss (~80%) of dopaminergic neurons of the substantia nigra
    • Presence of _____ _____ (intracellular inclusions)
    • Creates _______ of acetylcholine and dopamine
  • __ treatment = progresses to an ______ state (5-10 yrs)
  • Mortality due to ______ (aspiration pneumonia, clotting disorders, etc)
A
  • basal ganglia, motor, autonomic, cognitive
    • Lewy bodies
    • imbalance
  • No, akinetic
  • imobility
  • Occurs when you have about 80% loss of dopaminergic neurons**​*
  • Due to Lewy Bodies that block transmission of neuro signals*
  • Homeostasis of acetylcholine and dopamine messed up*
  • IMMOBILITY*-**All the effects usually secondary to immobility*
32
Q

Dopamine (DA)

  • Catecholamine, synthesized in dopaminergic neurons from tyrosine
  • DA receptors ( __ total, grouped into D_ and D_)
    • D1 - _____ synthesis of cyclic AMP (_____)
    • D2 - _____ synthesis of cyclic AMP, suppresses CA currents, activate K currents (_____)
  • ​Neostriatum of the basal ganglia regulates flow of information from the _____ cortex to the motor neurons of the _____ cord
A
  • 5, D1, D2
    • stimulate, excitatory
    • inhibit, inhibitory
  • cerebral, spinal

5 diff dopamine receptors - 2 types

33
Q

Pathophysiology

  • ___ receptors impacted
    • _____ _____ -*> protein degradation -> terminal degredation
A
  • D2
  • -* Lewy Bodies
34
Q

Pharmacologic Targets

_____ and _______ function depend on the coordinated ____ of _____ and ______

How to treat?

1) _____ Dopamine
2) _____ Acetylcholine

A

Motor, Cognitive, interaction, Dopamine, Acetylcholine

1) Increase
2) Decrease

35
Q

Presentation

  • ________ Symptoms
    • ________ (slow/lack of movements)
    • Muscular _______ (e.g. cogwheel)
    • ______ tremor (e.g pill rolling)
    • ______ instability
    • ____ (e.g shoulder shrugs)
  • Dys______
  • Loss of _____
  • A_______
A
  • Extrapyramidal
    • Bradykinesia
    • Muscular Rigidity
    • Resting tremor
    • Postural instability
    • Tics
  • Dystonia voice changes
  • Loss of Smell
  • Anxiety
36
Q

Risk Factors

(3)

A
  1. Age
  • Natural loss of DA neurons of the corpus striatum (70-80% loss)
    • ​Terminal of DA neuron degenerates
    • Lewy bodies form in the soma of DA neuron which results in protein degradation amongst others
  1. Environmental exposures (amphetamine and cocaine use)
  2. Hereditary
  • Chromosomal mutations
37
Q

Goals of Therapy

  • Improve ____ and _ _ _
  • Prevent long term ______, minimize _____ disability
  • Slow disease _______
  • Maximize ___ therapy and minimize _ _
A
  • symptoms, QOL
  • complications, functional
  • progression
  • drug, AE
38
Q

Medications Used in the Treatment of Parkinson’s Disease

(7)

A
  1. Dopaminergic agents (think replacement)
  2. Decarboxylase Inhibitor
  3. Caetchol O methyl transferase (COMT) inhibitors
  4. MAO-B Inhibitors
  5. Dopamine receptor agonists (NOT ON EXAM)
  6. Acetylcoline receptor agonists
  7. Adenosine A2A receptor antagonist (NOT ON EXAM)
39
Q

1) Dopaminergic agents

(2)

A
  • Levodopa (L-DOPA)
  • Amantadine (Symmetrel)
40
Q

2) Decarboxylase Inhibitors

(1)

A

Carbidopa

  • always used with levodopa (Sinemet)
  • NOT ACTIVE ALONE
41
Q

3) COMT Inhibitors

(3)

A

Entacapone (Comtan)

Tolcapone (Tasmar

Opicapone (Ongentys)

42
Q

4) MAO-B Inhibitors

(3)

A

Safinamide (Xadago)

Selegline (Eldepryl)

Rasagline (Azilect)

43
Q

6) Acetylcholine Receptor Antagonists

(2)

A

Benztropine (Cogentin)

Trihexyphenidyl (Artane)

44
Q
  • Dopamine in the periphery =
  • Goal is to get levodopa to the?
  • 2 enzymes that break down down in the periphery (2)
A
  • Does nothing and wreaks havoc
  • Brain
  • COMT, Decarboxylase
45
Q

Levodopa

  • What is it?
  • Metabolized by what in the peripheral tissue?
  • If given as a monotherapy, what happens?
  • Always give it with?
A
  • Biosynthetic precursor of dopamine
    • Increases concentration of dopamine in the brain
  • Decarboxylase and Catechol-O-methyl transferase (COMT)
  • Less than 1% reaches the brain (always need decarboxylase inhibitor and often also needs COMT-inhibitor)
  • ALWAYS give in combo with carbidopa

  • What dopamine itself causes - GI upset*
  • Too much dopamine = depression, delirium, paranoia, hallucinations -> makes sense bc in schizophrenia they have too much dopamine*
46
Q

Levodopa

AE (4)

A
  • N/V (Antacid 30-60min before may help)
  • Orthostatic hypotension, Sedation
  • Depression, Delirium, Paranoia, Delusions, Hallucinations (CNS effects associated with long-term use)
  • Motor fluctuations (end of dose wearing off: peak-pose dyskinesa)

Breakthrough dyskinesia

47
Q

Levodopa

  • Always combined with _____
    • Examples of combined formulations
A
  • Carbidopa
    • Sinemet, Sinemet CR, Parcopa ODT
    • Rytary (new formulation that has advanced control release to reduce motor fluctuations, less frequently dosed, can be opened and sprinkled unlike sinemet (not interchangeable with), expensive/should not be first line)
48
Q

Carbidopa

MOA

A

Decarboxylase Inhibitor

  • Inhibits conversion of levodopa to dopamine in peripheral tissues (thereby decreasing GI and CV effects)
  • Increases amount of levodopa in the brain
49
Q

Carbidopa

  • Always give in combination with ______ (_____)
  • Titrate dose ____ up to __ mg of carbidopa daily
    • Reduce incidence of peripheral conversion = reduced _ _
  • Wearing off Phenomenon, what is it?
A
  • Levodopa (Sinemet)
  • Slowly, 75
  • Loss of efficacy over time (proven effective for 2-5 yrs) OR Fluctuation in response to meds occurs over time and may need higher doses

Story time: Carbidopa is that friend you bring to the grocery when you are super hungry to stop you from grabbing too much food and not getting to your destination> always have carbidopa by your side bc it inhibits dopamine breakdown in periphery

Advanced Pharm Exam 2 (2 decks)

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