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PHARMACOLOGY (undergrad) > CHAPTER 8: NEURODEGENERATIVE DISEASES > Flashcards

CHAPTER 8: NEURODEGENERATIVE DISEASES Flashcards

(41 cards)

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1
Q

What does CNS consist of?

A

brain and spinal cord, meninges, BBB, blood supply to the brain

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2
Q

what are the CNS functions?

A

sensory, motor, intellect/emotion

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3
Q

common neurotransmitters?

A

ACh, NE, glutamate, glycine, dopamine, serotonin, Gamma-aminobutyric acid (GABA)

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4
Q

excitatory vs. inhibitory neurotransmission/pathway

A
  • both bind to post synaptic receptor, transiently open ion channels, and alter the post synpatic POTENTIAL

excitatory DEpolarizes, inhibitory HYPERpolarizes post synaptic membrane

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5
Q

why are some pathways meant to be inhibitory?

A

because certain pathways must remain inhibitory to be kept NORMAL

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6
Q

Excitatory post synaptic potentials (EPSP) are generated by:

A
  • release of neurotransmitters, inc permeability on Na+ ions
  • influx Na+, weak depol, and move post syn potential TOWARDS firing threshold
  • inc stimulation of excitatory neurons, depol PASSES threshold, and generates “all or none” AP
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7
Q

Inhibitory post synaptic potentials (IPSP) are generated by:

A
  • stimulating inhibitory neurons, releasing neurotransmitters like GABA or GLYCINE—> transient inc permeability for SPECIFIC IONS

GABA induces hyperpol

  • influx Cl-, efflux, K+—> weak hyperpolarization, move post syn potential AWAY from firing threshold (less firing)
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8
Q

which specific ions are moving in excitatory vs inhibitory

A

excitatory: Na+ influx
inhibitory: Cl- influx, K+ efflux

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9
Q

Neurodegenerative Diseases: list and explain what it is

A

Parkinson’s (PD), Alzheimer’s (AD), Multiple Sclerosis (MS), Amyotrophic Lateral Sclerosis (ALS)

  • PROGRESSIVE loss of selective neurons in discrete brain areas
  • cause characteristic disorders of movement and cognition
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10
Q

PARKINSON’S DISEASE: what is it? age range? cure?

A
  • progressive chronic neurological disorder
  • develop in ANY age– most in middl age/past 60
  • NO CURE
    therapy aims to manage the symptoms/signs not necessarily slow down progression (not possible)
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11
Q

PARKINSON’S: signs and symptoms

A
  • lack of coordination
  • rhythmic tremors
  • rigidity/weakness
  • trouble maintaining position/posture
  • bradykinesia—> slow movement
  • difficutly walking
  • drooling/affect speech
  • mask-like expressions
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12
Q

PARKINSON’S: mechanism

A
  • destruction of dopaminergic neurons in SUBSTANTIA NIGRA—> reduces dopamine actions in CORPUS STRIATUM

cells in substantia nigra are destroyed, results in degeneration of nerve terminals that secerete dopamine
dopamine depletion—-> blocks the autoinhibition of ACh and releases MORE in corpus—-> triggers chain of abnormal signaling resulting in motor impairment

SIMPLE: dopamine neurons destroyed, not able to inhibit ACh firing, starts firing like crazy and results in motor impairment

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13
Q

secondary parkinsonism

A

drugs blocking dopamine receptors in brain may produce Parkinsonism SYMPTOMS
- drugs should be used cautiously in PD patients

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14
Q

Substantia Nigra and Corpus Stratum importance

A
  • these are parts of basal ganglia system that are involved in motor control
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15
Q

Drugs used in PARKINSON’S, categories?

A

Levodopa w carbidopa
selegiline, rasagiline, safinamide
entacapone and tolcapone
amantadine

MAO-B selective Inhibitors, COMT Inhibitors, Dopamine Agonists, Antimuscarinic Agents

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16
Q

Therapeutic Strategies of treating PARKINSON’S

A

need to try and reestablish correct dopamine/ACh balance by:
- restoring dopamine in basal ganglia
- antagonizing excitatory effect of cholinergic neurons

restore balance in this CIRCUIT

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17
Q

GOALS of treating PARKINSON’S

Study These Flashcards
A

drug therapy is aimed at achieving a balance between stimulating cholinergic effects and inhibitory effects of dopamine in basal ganglia

18
Q

type 1 drugs vs. type 2 drugs

Study These Flashcards
A

type 1: for inhibition
- inc dopamine conc
- inc dopamine release
- stimulate dopamine receptors

type 2: stimulation
- anticholinergic drugs block stimulant (of cholinergic neurons)

19
Q

LEVODOPA and CARBIDOPA: MOA

(combination therapy)

Study These Flashcards
A

levodopa: restore dopaminergic neurotransmission in the neostriatum, ENHANCE synth of dopamine in surviving neurons of susbstantia nigra

carbidopa: diminish metabolism of levodopa in periphery, inc levodopa availability to CNS (gets in through transporter AADC)

20
Q

neurotransmission L-dopa and carbidopa

Study These Flashcards
A

PERIPHERY: Carbidopa stops DDC (dopa decarboxylase) inhibits levodopa metabolism, L-dopa turns into DOPA, and crosses BBB into neuron to be turned into dopamine

CNS: tyrosine converted by TH (tyrosine hydroxylase) into L-dopa, AADC (amino acid decarboxylase) makes that into Dopamine

21
Q

administered levodopa vs. levodopa plus carbidopa

Study These Flashcards
A

administered levodopa will undergo metabolism in peripheral tissues and GI tract, cause undesirable side effects and result in LOST LEVODOPA (less drug to go to CNS)

levo+carbidopa decreases metabolism in periphery/GI, less side effects, and MORE levodopa to go into CNS (cross BBB)

22
Q

what does carbidopa do for levodopa?

Study These Flashcards
A

it blocks the DECARBOXYLASE ENZYME that is trying to metabolize levodopa

LEts CARry the drug to the brain!

23
Q

LEVODOPA and CARBIDOPA: indications and therapeutic effects, withdrawal?

Study These Flashcards
A
  • treat PD
    effects:
  • dec rigidity, tremor, and other symptoms

WITHDRAWAL MUST BE GRADUAL

24
Q

LEVODOPA and CARBIDOPA: absorption/metabolism

Study These Flashcards
A
  • SHORT half-life (1-2 hrs), fluctuates in plasma conc.
  • motor fluctuations–> PT may suddenly lose normal mobility, experience tremors, cramps, immobility
25
when is it best to take levodopa and carbidopa?
on an empty stomach, if you take it after eating there are amino acids present trying to break down/metabolize your food and the DRUG! this will let less drug go to the brain! eating=harder for L-dopa to get to brain
26
LEVODOPA and CARBIDOPA: peripheral and CNS effects
PERIPHERAL - anorexia - nausea, vomiting - tachycardia, ventricular extrasystole (DA action on heart) - possible develop of hypotension - mydriasis--> adrenergic action CNS - visual/auditory hallucinations - dyskinesia--> abnormal involun movements (overactivity of dopamine in basal ganglia) - mood changes, depression, psychosis (activation dopamine receptors), anxiety
27
why don't we just use dopamine to treat PD?
it does NOT cross the BBB, so we use L-dopa and transporters. dopamine interferes with ADRENERGIC RECEPTORS as well
28
LEVODOPA and CARBIDOPA: interactions
- vitamin B6--> inc peripheral breakdown levodopa - co-administration L-dopa and nonselective MAOIs---> hypertensive crisis (enhanced catecholamine production) - psychotic PT---> worsens symptoms (build up central catecholamines) - cardiac PT: monitor for arrhythmia CONTRAINDICATE: antipsychotic drugs (potently block DA receptors/augment PD symptoms)
29
MAO INHIBITORS: what are the differences between MAO-A and MAO-B? (not the inhibition)
MAO type A--> metabolism of NE and 5-HT MAO type B--> metabolism of DA
30
MAOB Selective Inhibitors: SELEGILINE
LOW DOSE: REVERSIBLE selective inhibitor MAOB HIGH DOSE: lose selectivity - inc dopamine in brain - metabolize to methamphetamine and amphetamine--> may produce insomnia
31
MAOB Selective Inhibitors: RASAGILINE
- IRREVERSIBLE, selective MAOB inhibitor - MORE POTENT THAT SELEGILINE - inc dopamine in brain NOT metabolized to amph and meth
32
MAOB Selective Inhibitors: SAFINAMIDE
REVERSIBLE, selective MAO B inhibitor - inc dopamine in brain NOT metabolized to amph and meth
33
COMT Inhibitors: entacapone and tolcapone - MOA
- selectively and reversibly inhibit COMT
34
Entacapone and Tolcapone: therapeutic effects
- inhibit COMT--> dec plasma conc of 3-O-methyldopa---> INC uptake L-dopa---> inc conc brain dopamine -reduce wearing off symptoms in levi-carbi pts ## Footnote REMEMBER L-dopa and 3OMD compete for entry into BBB, so we want to dec 3OMD and allow more L-dopa in
35
explain how COMT inhibitors work step by step
when carbidopa inhibits peripheral DDC (the thing that metabolizes) L dopa, 3-O-methyldopa is created which competes L-dopa for active transport into CNS inhibiting COMT, decreases conc 3-O-methyldopa and allows inc central uptake L-dopa into brain and therefore inc dopamine in brain!
36
Entacapone and Tolcapone: adverse effects
- diarrhea - nausea - anorexia - postural/orthostatic hypotension - dyskinsesias - hallucinations - sleep disorders - suddenly developed hepatic necrosis w TOLCAPONE entacapone doesn't exhibit this toxicity, largely replaced tolcapone
37
Dopamine Agonists: bromocriptine, ropinirole, pramipexole, rotigotine, apomorphine - routes of administration
bromocriptine (oral), ropinirole (oral), pramipexole (oral), rotigotine (transdermal), apomorphine (injectable for severe/advanced stages)
38
Dopamine Agonists: MOA
type 1: STIMULATE dopamine receptors - - longer duration of action than L-dopa - effective in PT exhibiting fluctuations in response to L-dopa - initial therapy associated w/less risk dyskinesias/motor fluctuations compared to L-dopa fluctuations in L-dopa, wear off effect, its difficult to maintain a constant level of dopamine so the effect fluctuate throughout the day
39
Dopamine Agonists: adverse effects
- sedation - nausea - confusion - hallucinations - hypotension
40
Antiviral: Amantadine - therapeutic effects and adverse effects
-accidentally discovered to help PD treatment therapeutic: - inc dopamine release - block cholinergic receptors - inhibit NMDA (type of glutamate receptor) ADVERSE: - restlessness, agitation, confusion, hallucinations HIGH DOSES: acute toxic psychosis, orthostat hypotension, urinary retention, peripheral edema, dry mouth
41
Antimuscarinic Agents : benztropine, trihexyphenidyl, biperiden, procyclidine - main purpose - therapeutic effects - adverse effects - contraindications
INHIBIT PSNS muss less efficacious than L-dopa, only play ADJUVANT ROLE therapeutic: - block cholinergic transmission, correct imbalance of DA/ACh activity adverse: - mood change, confusion, xerostomia, constipation, visual problems, GI peristalsis interference contraindications: - PT w/ glaucoma, prostatic hyperplasia, pyloric stenosis

PHARMACOLOGY (undergrad) (29 decks)

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