Parkinson's Disease Medications

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Questions and Answers

Why is carbidopa administered in conjunction with L-Dopa in the treatment of Parkinson's disease?

To enhance the conversion of L-Dopa into norepinephrine, providing an alternative pathway for neurotransmitter synthesis.
To directly stimulate dopamine receptors in the brain, bypassing the need for L-Dopa conversion.
To inhibit the peripheral conversion of L-Dopa to dopamine, increasing the amount of L-Dopa that reaches the brain. (correct)
To reduce the risk of L-Dopa-induced dyskinesias by promoting a more controlled release of dopamine in the brain.

What is the primary mechanism by which entacapone enhances the effectiveness of L-Dopa in managing Parkinson's disease symptoms?

By promoting the release of dopamine from presynaptic terminals, amplifying the effect of dopamine already present in the synapse.
By directly stimulating dopamine receptors in the substantia nigra, compensating for reduced dopamine production.
By reducing the metabolism of dopamine in the synaptic cleft, prolonging the duration of dopamine's action on postsynaptic receptors.
By inhibiting the enzyme COMT, preventing the breakdown of L-Dopa in the periphery and increasing its bioavailability to the brain. (correct)

How does selegiline's mechanism of action contribute to its therapeutic effect in Parkinson's disease?

It inhibits the breakdown of dopamine in the central nervous system, prolonging the action of dopamine. (correct)
It inhibits the reuptake of dopamine from the synaptic cleft, prolonging the duration of dopamine's action.
It stimulates the release of stored dopamine from synaptic vesicles, increasing dopamine availability in the synapse.
It acts as a dopamine receptor agonist, directly stimulating dopamine receptors and bypassing the need for endogenous dopamine.

What is the rationale behind using D2R/D3R dopamine agonists like ropinirole and pramipexole as first-line treatments for Parkinson's disease?

They directly stimulate dopamine receptors, bypassing the need for dopamine production and reducing the risk of motor complications. (A) Signup and view all the answers

How does L-Dopa alleviate the motor symptoms associated with Parkinson's disease?

By being converted into dopamine in the brain, replenishing depleted dopamine levels. (D) Signup and view all the answers

Although aripiprazole is a weak partial D2R agonist, it is typically used as an antipsychotic. Why?

It has dopamine receptor agonist and antagonist properties that help stabilize dopamine levels. (A) Signup and view all the answers

What distinguishes the mechanism of action of ropinirole from that of L-Dopa in treating Parkinson's disease?

Ropinirole directly stimulates dopamine receptors, while L-Dopa is converted into dopamine in the brain. (D) Signup and view all the answers

If a patient on L-Dopa also has hypertension, which medication would require careful monitoring due to potential interactions?

Non-selective MAO inhibitors (B) Signup and view all the answers

What is the most significant advantage of using selective MAO-B inhibitors over non-selective MAO inhibitors in the treatment of Parkinson's disease?

Lower incidence of the 'cheese effect' (B) Signup and view all the answers

How does carbidopa contribute to reducing the side effects associated with L-Dopa therapy?

By preventing the peripheral conversion of L-Dopa to dopamine, reducing the incidence of nausea and orthostatic hypotension. (B) Signup and view all the answers

How does the interaction of quetiapine, aripiprazole, and risperidone with 5-HT2A receptors contribute to their therapeutic effect?

It modulates serotonin activity, which contributes to antipsychotic and mood-stabilizing effects. (C) Signup and view all the answers

If tyrosine hydroxylase is inhibited, what is the most immediate consequence on dopamine synthesis?

A decrease in DOPA production, directly limiting dopamine synthesis. (D) Signup and view all the answers

How does the activation of D1R and D5R influence neuronal function in the direct pathway of the basal ganglia?

Increased cAMP and PIP2 levels leading to neuronal excitation and promotion of movement. (A) Signup and view all the answers

What is the functional consequence of D2R, D3R, and D4R activation on neurons in the indirect pathway of the basal ganglia?

Reduced cAMP levels, increased potassium conductance, and decreased calcium influx, resulting in neuronal inhibition. (C) Signup and view all the answers

Why is the concentration of dopamine-producing cells in the substantia nigra and ventral tegmental area (VTA) critical for motor control and reward processing?

These areas provide the primary source of dopamine for the basal ganglia and limbic system, respectively, influencing movement and motivation. (A) Signup and view all the answers

How do D2R/D3R agonists like ropinirole and pramipexole bypass the typical dopamine synthesis and release mechanisms to alleviate Parkinsonian symptoms?

By directly stimulating dopamine receptors, mimicking the effects of dopamine without increasing dopamine levels. (A) Signup and view all the answers

What is the significance of atypical antipsychotics like quetiapine, aripiprazole, and risperidone acting as antagonists at both D2 receptors and 5-HT2A receptors?

The combined antagonism allows for effective treatment of positive symptoms of psychosis while minimizing extrapyramidal side effects. (A) Signup and view all the answers

How does the rate-limiting nature of tyrosine hydroxylase in dopamine synthesis impact the therapeutic strategies for Parkinson's disease?

It implies that L-DOPA, a downstream precursor, can bypass this regulation to increase dopamine levels. (A) Signup and view all the answers

In what way does the balance between D1R/D5R-mediated excitation and D2R/D3R/D4R-mediated inhibition within the basal ganglia contribute to motor control?

It fine-tunes the selection and execution of movements by modulating the activity of the direct and indirect pathways. (A) Signup and view all the answers

What is the therapeutic rationale for using D2R/D3R agonists like ropinirole and pramipexole in early-stage Parkinson's disease, considering their mechanism of action?

They directly stimulate dopamine receptors, compensating for reduced dopamine levels without relying on neuronal synthesis. (D) Signup and view all the answers

How does the mechanism of action of amphetamine on vesicular monoamine transporter 2 (VMAT2) contribute to its overall effect on dopamine neurotransmission?

It utilizes VMAT2 to displace dopamine from vesicles into the cytoplasm, leading to dopamine release via reverse transport. (A) Signup and view all the answers

What is the functional consequence of methylphenidate's selective blockade of dopamine transporters (DAT) on dopamine neurotransmission?

Decreased dopamine reuptake, prolonging dopamine's presence and action in the synaptic cleft. (A) Signup and view all the answers

How does amphetamine's inhibition of monoamine oxidase (MAO) augment its impact on dopamine levels within presynaptic neurons?

By preventing dopamine breakdown, leading to increased cytoplasmic and vesicular dopamine concentrations. (A) Signup and view all the answers

Given their mechanisms of action, how would the combined use of amphetamine and methylphenidate affect dopamine neurotransmission compared to using either drug alone?

The effects would be synergistic, leading to a significantly amplified concentration of dopamine in the synaptic cleft. (B) Signup and view all the answers

How does the interaction of second-generation antipsychotics with both monoamine receptors and D2 receptors contribute to a reduced risk of extrapyramidal side effects (EPS) compared to first-generation antipsychotics?

By modulating serotonin and other monoamine neurotransmission in addition to dopamine, offering a more balanced receptor profile. (A) Signup and view all the answers

In a neuron treated with amphetamine, what is the sequential pathway of dopamine movement after amphetamine enters the presynaptic neuron?

DAT entry -> VMAT2 entry -> displacement into cytoplasm -> reverse DAT transport. (D) Signup and view all the answers

Consider a scenario where a patient is on methylphenidate for ADHD. Why might administering a drug that inhibits VMAT2 counteract the therapeutic effects of methylphenidate?

Inhibiting VMAT2 would decrease dopamine packaging into vesicles, reducing the amount of dopamine available for release and counteracting methylphenidate's effect. (C) Signup and view all the answers

If a researcher aims to study the specific effect of increased synaptic dopamine caused by DAT blockade, which drug would be most suitable and why?

Methylphenidate, because it selectively blocks DAT without directly affecting dopamine release. (D) Signup and view all the answers

How do second-generation antipsychotics balance dopamine and serotonin receptor antagonism to mitigate the risk of motor-related side effects, such as tardive dyskinesia (TD)?

Simultaneously antagonizing D2 and serotonin receptors, promoting a balance that reduces the likelihood of dopamine-related motor complications. (C) Signup and view all the answers

What distinguishes the mechanism of action of amphetamine from that of methylphenidate in elevating synaptic dopamine levels?

Amphetamine reverses the action of DAT, while methylphenidate inhibits DAT. (A) Signup and view all the answers

Flashcards

What is L-Dopa?

A drug converted to dopamine (DA) in the CNS, used to treat Parkinson's.

What does Carbidopa do?

Prevents peripheral conversion of L-Dopa to dopamine, increasing L-Dopa availability in the CNS.