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CNS Pharmacology > Pharmacology of Neurodegenerative Disease > Flashcards

Pharmacology of Neurodegenerative Disease Flashcards

1
Q

Drugs acting on CNS are two types

A

1 Work on presynaptic neurons:

Affect the synthesis of neurotransmitter
Affect the storage of neurotransmitter
Affect the release of neurotransmitter
Affect the termination of action of
neurotransmitter

2 Work on post synaptic receptors:
Activate the receptors
Blocks the receptors

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2
Q

What is the shared basic function of neurons in both the CNS and ANS?
a) Sensory perception
b) Transmission of information
c) Muscle contraction
d) Hormone secretion

A

b) Transmission of information

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3
Q

How do neurons in both the CNS and ANS primarily communicate?
a) Electrical impulses only
b) Chemical signals only
c) Both electrical impulses and chemical signals
d) Hormonal signals

A

c) Both electrical impulses and chemical signals

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4
Q

Differences between CNS and ANS

A

ANS
1) There are two neurotransmitters
2)less complex
3)Much lesser number of synapsis
4)No inhibitory neurons

CNS
1) There are numerous.
neurotransmitters
2) More complex circuits
3) Much greater number of
synapsis
4)There are networks of
inhibitory neurons constantly
active modulating the rate of
neuronal transmission

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5
Q

Types of neurodegenerative Disease

A
  1. Dementia type:
    Alzheimer’s disease
  2. Demyelinating disease:
    Multiple Sclerosis (MS)
  3. Parkinson Type
    Parkinson disease
    Other forms of parkinsonism
  4. Motor neuron disease
    Amyotrophic lateral Sclerosis
    (ALS)
    5.Prion disease لم ندرسه
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6
Q

Neurodegenerative disorders those
respond to drug therapy

A

Parkinson’s disease
Alzhiemer’s Disease
Multiple Sclerosis (MS)
Amyotrophic Lateral Sclerosis (ALS)

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7
Q

Which of the following statements correctly describes the neurotransmitter characteristics of the Central Nervous System (CNS)?
a) The CNS utilizes only two neurotransmitters.
b) The CNS exhibits numerous neurotransmitters.
c) The CNS does not utilize neurotransmitters.
d) The CNS primarily relies on electrical impulses for communication.

A

b) The CNS exhibits numerous neurotransmitters.

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8
Q

In terms of circuit complexity, which nervous system component displays more intricate circuits?
a) Central Nervous System (CNS)
b) Autonomic Nervous System (ANS)
c) Both CNS and ANS exhibit similar circuit complexity.
d) Neither CNS nor ANS exhibits circuit complexity.

A

a) Central Nervous System (CNS)

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9
Q

Which nervous system component is characterized by a significantly higher number of synapses?
a) Central Nervous System (CNS)
b) Autonomic Nervous System (ANS)
c) Both CNS and ANS have a similar number of synapses.
d) Neither CNS nor ANS have synapses.

A

a) Central Nervous System (CNS)

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10
Q

What distinguishes the Central Nervous System (CNS) from the Autonomic Nervous System (ANS) regarding the presence of inhibitory neurons?
a) The CNS has inhibitory neurons, while the ANS does not.
b) The ANS has inhibitory neurons, while the CNS does not.
c) Both CNS and ANS lack inhibitory neurons.
d) Both CNS and ANS have inhibitory neurons, but they function differently.

A

a) The CNS has inhibitory neurons, while the ANS does not.

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11
Q

Excitatory Postsynaptic Potentials (EPSP) are initiated by the release of neurotransmitters such as:
a) Dopamine and serotonin
b) Glutamate and GABA
c) Acetylcholine and dopamine
d) Glutamate and acetylcholine

A

d) Glutamate and acetylcholine

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12
Q

During an EPSP, neurotransmitters bind to:
a) Presynaptic receptors
b) Dendritic spines
c) Axon terminals
d) Postsynaptic receptors

A

d) Postsynaptic receptors

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13
Q

What is the primary effect of an EPSP on the postsynaptic neuron?
a) Hyperpolarization
b) Inhibition of neurotransmitter release
c) Depolarization due to an influx of sodium ions
d) No change in membrane potential

A

c) Depolarization due to an influx of sodium ions

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14
Q

How does an EPSP affect the membrane potential of the postsynaptic neuron?
a) The membrane potential becomes more negative
b) The membrane potential remains unchanged
c) The membrane potential becomes more positive, moving closer to its firing threshold
d) The membrane potential becomes more positive, moving further away from its firing threshold

A

c) The membrane potential becomes more positive, moving closer to its firing threshold

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15
Q

Inhibitory Postsynaptic Potentials (IPSP) are initiated by the release of neurotransmitters, such as:
a) Glutamate and acetylcholine
b) Serotonin and dopamine
c) Gamma-aminobutyric acid (GABA) and glycine
d) Norepinephrine and histamine

A

c) Gamma-aminobutyric acid (GABA) and glycine

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16
Q

During an IPSP, neurotransmitters bind to:
a) Presynaptic receptors
b) Dendritic spines
c) Axon terminals
d) Postsynaptic receptors

A

d) Postsynaptic receptors

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17
Q

What is the primary effect of an IPSP on the postsynaptic neuron?
a) Depolarization due to an influx of sodium ions
b) Hyperpolarization due to an influx of potassium ions
c) Hyperpolarization due to an efflux of potassium ions and influx of chloride ions
d) No change in membrane potential

A

c) Hyperpolarization due to an efflux of potassium ions and influx of chloride ions

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18
Q

How does an IPSP affect the membrane potential of the postsynaptic neuron?
a) The membrane potential becomes more positive, moving closer to its firing threshold
b) The membrane potential remains unchanged
c) The membrane potential becomes more negative, moving further away from its firing threshold
d) The membrane potential becomes more negative, moving closer to its firing threshold

A

c) The membrane potential becomes more negative, moving further away from its firing threshold

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19
Q

What neurotransmitter is primarily released by neurons in the substantia nigra?
a) Serotonin
b) Dopamine
c) Acetylcholine
d) GABA

A

b) Dopamine

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20
Q

Which term best describes the firing pattern of dopaminergic neurons from the substantia nigra?
a) Phasic
b) Sporadic
c) Tonic
d) Oscillatory

A

c) Tonic

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21
Q

What is the primary function of the mutual inhibitory pathway between the substantia nigra and neostriatum?
a) Excitation of both areas
b) Inhibition of both areas
c) Excitation of substantia nigra and inhibition of neostriatum
d) Inhibition of substantia nigra and excitation of neostriatum

A

b) Inhibition of both areas

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22
Q

Which system does the substantia nigra belong to?
a) Limbic system
b) Autonomic nervous system
c) Central nervous system
d) Extrapyramidal system

A

d) Extrapyramidal system

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23
Q

What role does the nigrostriatal pathway play in motor activity?
a) Excitatory
b) Inhibitory
c) Both excitatory and inhibitory
d) No role in motor activity

A

b) Inhibitory

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24
Q

What neurotransmitter is primarily released by neostriatum neurons to the substantia nigra?
a) Dopamine
b) Glutamate
c) GABA
d) Serotonin

A

c) GABA

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25
Q

Dysfunction of the nigrostriatal pathway is associated with which neurological disorder?
a) Alzheimer’s disease
b) Parkinson’s disease
c) Huntington’s disease
d) Multiple sclerosis

A

b) Parkinson’s disease

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26
Q

Which neurotransmitter deficiency is characteristic of Parkinson’s disease?
a) Dopamine
b) Serotonin
c) Acetylcholine
d) Glutamate

A

a) Dopamine

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27
Q

What type of neurons originate from the substantia nigra and terminate in the neostriatum?
a) Glutamatergic
b) GABAergic
c) Dopaminergic
d) Serotonergic

A

c) Dopaminergic

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28
Q

What is the primary cause of Parkinson’s disease?
a) Overproduction of dopamine
b) Destruction of cells in the neostriatum
c) Degeneration of nerve terminals secreting dopamine in the neostriatum
d) Excessive activity of cholinergic neurons in the substantia nigra

A

c) Degeneration of nerve terminals secreting dopamine in the neostriatum

Destruction of cells in the substantia nigra results in the
degeneration of the nerve terminals that secrete dopamine in
the neostriatum.

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29
Q

How does the diminished inhibitory influence of dopamine in the neostriatum contribute to Parkinson’s disease?
a) It leads to overproduction of acetylcholine
b) It increases the production of dopamine
c) It decreases the production of acetylcholine
d) It has no effect on neurotransmitter levels

A

a) It leads to overproduction of acetylcholine

the normal inhibitory influence of dopamine on
cholinergic neurons in the neostriatum is significantly
diminished
That results in overproduction, or a relative overactivity, of
acetylcholine by the stimulatory neurons.

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30
Q

What is the primary pharmacological action of antipsychotic drugs that can lead to secondary parkinsonism?
a) Stimulation of dopamine receptors
b) Inhibition of cholinergic receptors
c) Blockade of dopamine receptors
d) Blockade of acetylcholine receptors

A

c) Blockade of dopamine receptors

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31
Q

What is the term used to describe parkinsonian symptoms induced by antipsychotic drugs such as phenothiazines and haloperidol?
a) Primary parkinsonism
b)c&d
c) Pseudoparkinsonism
d) Drug-induced parkinsonism

A

b)c&d

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32
Q

Parkinson’s disease primarily affects which aspect of neurological function?
a) Sensory perception
b) Memory formation
c) Muscle movement
d) Language comprehension

A

c) Muscle movement

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33
Q

What is the typical age group that Parkinson’s disease mostly affects?
a) Under 30 years
b) Between 30 and 45 years
c) Between 45 and 65 years
d) Over 65 years

A

d) Over 65 years

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34
Q

What is the estimated incidence of Parkinson’s disease in the general population?
a) 1 in 1,000 individuals
b) 1 in 500 individuals
c) 1 in 100 individuals
d) 1 in 50 individuals

A

c) 1 in 100 individuals

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35
Q

Manifestations of Parkinson’s Disease
“ 4 Ds “

A

1) Motor Manifistations
Dyskinesia

2) Non Motor Manifistations
Depression
Dementia
Disturbance of Sleep

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36
Q

Dyskinesia of
Parkinson Disease

6”

A

1 Akinesia
2 Bradykinesia
3 Muscular rigidity
4 Tremors
5 Postural abnormalities
6 Gait abnormalities

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37
Q

What is the primary goal of therapy for Parkinson’s disease?

a) Increasing the number of cholinergic neurons in the neostriatum
b) Inhibiting the release of dopamine in the basal ganglia
c) Antagonizing the excitatory effect of acetylcholine
d) Reducing the number of inhibitory dopaminergic neurons

A

c) Antagonizing the excitatory effect of acetylcholine

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38
Q

Which neurotransmitter is primarily targeted for restoration in the basal ganglia during Parkinson’s disease therapy?
a) Serotonin
b) Glutamate
c) Dopamine
d) GABA

A

c) Dopamine

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39
Q

What is the main aim of antagonizing the excitatory effect of acetylcholine in Parkinson’s disease therapy?
a) To increase cholinergic activity
b) To reduce dopamine levels
c) To restore the balance between dopamine and acetylcholine
d) To enhance inhibitory dopaminergic neurons

A

c) To restore the balance between dopamine and acetylcholine

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40
Q

What neurotransmitter imbalance characterizes Parkinsonism?

A) GABAergic and glutamatergic imbalance
B) Serotonergic and noradrenergic imbalance
C) Cholinergic and dopaminergic imbalance
D) Adrenergic and histaminergic imbalance

A

C) Cholinergic and dopaminergic imbalance

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41
Q

Strategy of Parkinson Disease
Therapy is aimed at:

A

1.Restoring dopamine in the basal ganglia.
2. Antagonizing the Cholinergic excitatory effect.
(reestablishing the correct dopamine/acetylcholine balance)

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42
Q

Antiparkinson’s Disease

A

A) Drugs enhance Dopaminergic
pathway
1) Central Dopamine release enhancers
a) Dopamin Precursors
L.dopa
b)Peripheral decarboxylase inhibitors
Carbidopa
c) COMT inhibitors
Entacapone , Tolcapone
2)Central Dopamine degradation inhibitors
“MAOB inhibitors”
Selegiline , Rasagiline
3) Dopamine Agonist
Bromocriptine

    4) Dopamine facilitators
           **Amantadine , Apomorphine

B) Centrally Acting Anticholinergics
Trihexiphenidyl
Benztropine

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43
Q

Which of the following drugs inhibits the peripheral decarboxylation of levodopa?
A) Selegiline
B) Rasagiline
C) Carbidopa
D) Tolcapone

A

C) Carbidopa

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44
Q

Trihexyphenidyl and benztropine are examples of:
A) Dopamine precursors
B) Peripheral decarboxylase inhibitors
C) MAOB inhibitors
D) Centrally acting anticholinergics

A

D) Centrally acting anticholinergics

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45
Q

Levodopa enhances dopamine synthesis in the CNS by:
A) Crossing the blood-brain barrier as dopamine
B) Inhibiting the decarboxylase enzyme
C) Acting as a direct precursor to dopamine
D) Inducing dopamine release from synaptic vesicles

A

C) Acting as a direct precursor to dopamine

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46
Q

How does levodopa cross the blood-brain barrier?
A) Through passive diffusion
B) Via specific dopamine transporter proteins
C) Using large neutral amino acid transporter (LAT1)
D) By undergoing active transport mediated by COMT

A

C) Using large neutral amino acid transporter (LAT1)

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47
Q

Which enzyme converts levodopa to dopamine in the CNS?
A) Catechol-O-methyl transferase (COMT)
B) Monoamine oxidase B (MAOB)
C) Dopamine beta-hydroxylase
D)L-amino acid decarboxylase

A

D)L-amino acid decarboxylase

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48
Q

The main purpose of administering levodopa in Parkinson’s disease is to:
A) Inhibit the breakdown of dopamine
B) Increase the synthesis of serotonin
C) increase the activity of cholinergic neurons
D) Compensate for the deficiency of dopamine in the brain

A

D) Compensate for the deficiency of dopamine in the brain

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49
Q

Which peripheral enzyme is responsible for the metabolism of levodopa into dopamine?
A) Catechol-O-methyl transferase (COMT)
B) Monoamine oxidase B (MAOB)
C) Dopamine beta-hydroxylase
D) L-amino acid decarboxylase

A

D) L-amino acid decarboxylase

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50
Q

What is the primary function of levodopa in the treatment of Parkinson’s disease?
A) Inhibition of dopamine degradation
B) Enhancement of dopamine synthesis
C) Blockade of dopamine receptors
D) Inhibition of acetylcholine release

A

B) Enhancement of dopamine synthesis

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51
Q

Chat gpt
Why can’t dopamine itself effectively cross the blood-brain barrier?
A) It is too large to pass through
B) It is rapidly metabolized in the bloodstream
C) It is actively transported out of the brain
D) It is degraded by enzymes in the blood

A

A) It is too large to pass through

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52
Q

What is the primary location in the brain where levodopa is converted to dopamine?
A) Substantia nigra
B) Striatum
C) Hippocampus
D) Thalamus

A

A) Substantia nigra

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53
Q

What is the primary reason for the short half-life of levodopa?
A) Rapid metabolism by catechol-O-methyl transferase (COMT)
B) Inhibition of absorption in the gastrointestinal tract (GIT)
C) High protein binding in the bloodstream
D) Limited ability to cross the blood-brain barrier

A

A) Rapid metabolism by catechol-O-methyl transferase (COMT)

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54
Q

How does levodopa primarily cross the blood-brain barrier?
A) Passive diffusion
B) Active transport via dopamine transporter proteins
C) Utilization of specific amino acid transporters (LAT1)
D) Conversion to dopamine prior to crossing the barrier

A

C) Utilization of specific amino acid transporters (LAT1)

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55
Q

Which enzyme metabolizes levodopa into 3-O-Methyldopa in the circulation?
A) Aromatic L-amino acid decarboxylase (AADC)
B) Monoamine oxidase (MAO)
C) Catechol-O-methyl transferase (COMT)
D) Dopamine beta-hydroxylase

A

C) Catechol-O-methyl transferase (COMT)

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56
Q

Why does the amount of levodopa that reaches the CNS remain limited?
A) Rapid degradation by MAO in the bloodstream
B) Competition at LAT1 by 3-O-Methyldopa
C) Inhibition of absorption in the small intestine
D) High affinity for binding to plasma proteins

A

B) Competition at LAT1 by 3-O-Methyldopa

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57
Q

How does the extensive metabolism of levodopa in the gastrointestinal tract (GIT) affect its bioavailability?
A) Increases bioavailability due to enhanced absorption
B) Decreases bioavailability due to decreased absorption
C) Does not affect bioavailability as levodopa is not absorbed in the GIT
D) Converts levodopa into dopamine, increasing its bioavailability

A

B) Decreases bioavailability due to decreased absorption

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58
Q

Which enzyme is primarily responsible for the metabolism of levodopa in the gastrointestinal tract (GIT)?
A) Monoamine oxidase (MAO)
B) Catechol-O-methyl transferase (COMT)
C) decarboxylase
D) Dopamine beta-hydroxylase

A

C) decarboxylase

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59
Q

Why is levodopa preferably administered on an empty stomach?
A) To minimize gastrointestinal side effects
B) To enhance its absorption from the small intestine
C) To reduce the risk of drug interactions
D) To prevent rapid metabolism by COMT

A

B) To enhance its absorption from the small intestine

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60
Q

What is the primary metabolic pathway of levodopa in the circulation?

A) Conversion to dopamine by monoamine oxidase (MAO)
B) Metabolism into 3-O-Methyldopa by catechol-O-methyl transferase (COMT)
C) Breakdown into inactive metabolites by aromatic L-amino acid decarboxylase (AADC)
D) Direct excretion unchanged through the kidneys

A

B) Metabolism into 3-O-Methyldopa by catechol-O-methyl transferase (COMT)

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61
Q

G.R
The amount of levodopa that reaches the CNS is too small?

A

due to peripheral decarboxylation and competition at LAT1
by 3-O-Methyldopa.

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62
Q

Which of the following side effects is primarily caused by the peripheral metabolism of levodopa leading to an increase in dopamine?
A) Muscle rigidity
B) Dyskinesias
C) Nausea and/or vomiting
D) Depression

A

C) Nausea and/or vomiting

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63
Q

Stimulation of dopaminergic receptors by dopamine produced from the decarboxylation of levodopa can lead to:
A) Hypertension
B)Hypoglycemia
C) Cardiac arrhythmias
D) Hyperglycemia

A

C) Cardiac arrhythmias

The peripheral metabolism of levodopa
will cause the increase in dopamine that
will cause the following side effects:

Nausea and/or vomiting
Cardiac arrhythmias
Hypotension

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64
Q

The peripheral metabolism of levodopa can contribute to which of the following cardiovascular side effects?
A) Hypertension
B) Bradycardia
C) Hypotension
D) Peripheral edema

A

C) Hypotension

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65
Q

Which receptor type is primarily involved in mediating the side effects such as nausea, vomiting, and cardiac arrhythmias caused by the peripheral metabolism of levodopa?
A) Alpha-adrenergic receptors
B) Beta-adrenergic receptors
C) Dopaminergic receptors
D) Serotonergic receptors

A

C) Dopaminergic receptors

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66
Q

What is the underlying mechanism of the side effects induced by the peripheral metabolism of levodopa?
A) Stimulation of adrenergic receptors
B) Inhibition of acetylcholine release
C) Stimulation of dopaminergic receptors
D) Blockade of glutamatergic neurotransmission

A

C) Stimulation of dopaminergic receptors

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67
Q

How Can be done to increase the
amount of Levodopa that reaches
the CNS and reduce the side
effects related to overproduction
of Dopamine in peripheral
tissues???

A

That can be done by preventing
decarboxylation of levodopa by adding
decarboxylase enzyme inhibitor.
(Carbidopa)

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68
Q

Which of the following drugs can be co-administered with levodopa to increase the amount of levodopa that reaches the CNS and reduce the side effects related to the overproduction of dopamine in peripheral tissues?

A) Bromocriptine
B) Selegiline
C) Tolcapone
D) Carbidopa

A

D) Carbidopa

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69
Q

G.R
Levodopa should always be giving combined with
carbidopa?

A

The addition of carbidopa lowers the dose of
levodopa needed by four- to five-fold and,
consequently, decreases the severity of adverse
effects arising from peripherally formed dopamine.

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70
Q

Cautions when taking levodopa:

A

1) To be given on empty stomach (at least 30 minutes before food) (because proteins interferes with its absorption).
On - Off phenomenon: (when given with food it cause
fluctuation in the effect&raquo_space; sudden onset tremors, cramps and loss of ability to move).
2) Should not be stopped suddenly.

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71
Q

Which medication should always be combined with levodopa to enhance its efficacy and reduce the severity of adverse effects arising from peripherally formed dopamine?
A) Bromocriptine
B) Selegiline
C) Tolcapone
D) Carbidopa

A

D) Carbidopa

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72
Q

What is the primary reason for combining carbidopa with levodopa?
A) To inhibit the peripheral metabolism of levodopa
B) To enhance the central metabolism of levodopa
C) To potentiate the effects of levodopa on dopamine receptors
D) To reduce the risk of gastrointestinal side effects

A

A) To inhibit the peripheral metabolism of levodopa

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73
Q

What phenomenon may occur when levodopa is taken with food?
A) Tolerance development
B) On-off phenomenon
C) Placebo effect
D) Drug-induced psychosis

A

B) On-off phenomenon

74
Q

GPT
Why is it cautioned against stopping levodopa suddenly?
A) Due to the risk of rebound hypertension
B) To prevent the development of drug resistance
C) To avoid exacerbation of Parkinson’s symptoms
D) Because of the potential for serotonin syndrome

A

C) To avoid exacerbation of Parkinson’s symptoms

75
Q

Adverse Effects of Levodopa

A

1)GIT Side Effects:
Anorexia, nausea, and vomiting
(chemoreceptor trigger zone).
2)Cardiac Side Effects:
-Tachycardia and ventricular extra-systole.
-Hypotension (postural /orthostatic)
3)Mixed Side Effects:
-Blood dyscrasias
-Sweat, saliva and urine may turn brownish
color.
-Visual and auditory hallucinations
4)Motor Side Effects:
-Dyskinesia (repetitive involuntary abnormal
movements affecting the face, trunk, and limbs)
(Akinesia paradoxia is a sudden freezing of movement).= mask face
5)CNS Side efects:
Mood changes
Depression
Psychosis (exacerbation of pre-existing psychotic symptoms)
Dream alterations

76
Q

Anorexia, nausea, and vomiting associated with levodopa primarily result from stimulation of receptors in which area?
A) Substantia nigra
B) Striatum
C) Chemoreceptor trigger zone
D) Hypothalamus

A

C) Chemoreceptor trigger zone

77
Q

Which of the following cardiac side effects is commonly associated with levodopa therapy?
A) Bradycardia
B) Hypertension
C) Tachycardia

A

C) Tachycardia

78
Q

Which of the following is considered a mixed side effect of levodopa?
A) Hyperthermia
B) Respiratory depression
C) Blood dyscrasias
D) Peripheral neuropathy

A

C) Blood dyscrasias

79
Q

The discoloration of sweat, saliva, and urine to a brownish color is a result of the metabolism of levodopa into which compound?
A) Dopamine
B) Serotonin
C) Epinephrine
D) Melanin

A

A) Dopamine

80
Q

Visual and auditory hallucinations are among the adverse effects of levodopa due to its actions on which neurotransmitter system?
A) Dopaminergic
B) Serotonergic
C) GABAergic

A

A) Dopaminergic

81
Q

Levodopa can cause tachycardia and ventricular extrasystoles as part of its:
A) Gastrointestinal side effects
B) Cardiac side effects
C) Mixed side effects
D) Central nervous system effects

A

B) Cardiac side effects

82
Q

Levodopa can cause discoloration of sweat, saliva, and urine, which may turn a:
A) Yellowish color
B) Greenish color
C) Bluish color
D) Brownish color

A

D) Brownish color

83
Q

What sensory disturbances are commonly associated with levodopa use?
A) Gustatory hallucinations
B) Tactile hallucinations
C) Visual and auditory hallucinations
D) Olfactory hallucinations

A

C) Visual and auditory hallucinations

84
Q

Which of the following motor side effects is characterized by repetitive involuntary abnormal movements affecting the face, trunk, and limbs?
A) Akathisia
B) Bradykinesia
C) Dyskinesia
D) Dystonia

A

C) Dyskinesia

85
Q

What is akinesia paradoxia?
A) Sudden onset of rapid movements
B) Inability to initiate voluntary movements despite the intention to move
C) Sudden freezing of movement
D) Repetitive involuntary abnormal movements

A

C) Sudden freezing of movement

86
Q

Which of the following central nervous system side effects is associated with levodopa therapy?
A) Memory loss
B) Euphoria
C) Dysarthria
D) Dream alterations

A

D) Dream alterations

87
Q

Levodopa therapy may lead to exacerbation of pre-existing psychotic symptoms, known as:
A) Dystonia
B) Akathisia
C) Psychosis
D) Dyskinesia

A

C) Psychosis

88
Q

Which vitamin is known to increase the peripheral breakdown of levodopa?
A) Vitamin C (ascorbic acid)
B) Vitamin B6 (pyridoxine)
C) Vitamin B12 (cobalamin)
D) Vitamin D

A

B) Vitamin B6 (pyridoxine)

89
Q

Nonselective monoamine oxidase inhibitors (MAOIs), such as phenelzine, when used together with the levodopa can lead to:
A) Bradycardia
B) Hypertensive crisis
C) Hypotension
D) Hyperthermia

A

B) Hypertensive crisis

90
Q

How do antipsychotic drugs typically affect dopamine receptors?
A) Enhance dopamine release
B) Inhibit dopamine reuptake
C) Potently block dopamine receptors
D) Increase dopamine synthesis

A

C) Potently block dopamine receptors

91
Q

Which class of antipsychotic drugs is commonly used to treat levodopa-induced psychotic symptoms?
A) Typical antipsychotics
B) Benzodiazepines
C) Selective serotonin reuptake inhibitors (SSRIs)
D) Atypical antipsychotics

A

D) Atypical antipsychotics

Antipsychotic drugs potently block dopamine
receptors.
Low doses of atypical antipsychotics, such as
quetiapine or clozapine, are used to treat
levodopa-induced psychotic symptoms.

92
Q

Contraindications of levodopa:

A

1)Psychotic patients&raquo_space; levodopa exacerbates
symptoms.
2)Cardiac patients&raquo_space; possible development
of arrhythmias.
3)Patients with narrow-angle glaucoma.!
4)Patients with peptic ulcer disease.!

93
Q

Which patient population should avoid levodopa due to the possible development of arrhythmias?
A) Patients with Parkinson’s disease
B) Patients with congestive heart failure
C) Patients with rheumatoid arthritis
D) Patients with depression

A

B) Patients with congestive heart failure

94
Q

GPT
Levodopa is contraindicated in patients with narrow-angle glaucoma due to its potential to:
A) Worsen visual acuity
B) Increase intraocular pressure
C) Cause retinal detachment
D) Induce cataract formation

A

B) Increase intraocular pressure

95
Q

GPT
Patients with peptic ulcer disease should avoid levodopa due to the risk of:
A) Gastrointestinal bleeding
B) Gastric perforation
C) Esophageal stricture
D) Intestinal obstruction

A

A) Gastrointestinal bleeding

96
Q

Carbidopa protects levodopa from
peripheral decarboxylation, but, what
can increase levodopa transport
through blood brain barrier??

A

Adding COMT inhibitor will reduce formation of 3 - 0 - Methyldopa that
compete with Ldopa at LAT1&raquo_space; more levodopa can be transported to
the CNS

Tolcapone
Entacapone

97
Q

What is the primary function of carbidopa when administered with levodopa?
A) Inhibiting peripheral decarboxylation
B) Enhancing dopamine synthesis
C) Blocking COMT activity
D) Preventing levodopa metabolism in the liver

A

A) Inhibiting peripheral decarboxylation

98
Q

Which of the following drugs increases levodopa transport through the blood-brain barrier by inhibiting COMT activity?
A) Tolcapone
B) Amantadine
C) Pramipexole
D) Benztropine

A

A) Tolcapone

99
Q

Which statement accurately describes the absorption of entacapone and tolcapone?
A) Tolcapone is better absorbed than entacapone from the gastrointestinal tract (GIT).
B) Entacapone has a longer duration of action compared to tolcapone.
C) Both entacapone and tolcapone are poorly absorbed from the GIT.
D) Both entacapone and tolcapone are well absorbed from the GIT.

A

D) Both entacapone and tolcapone are well absorbed from the GIT.

100
Q

Why is entacapone preferred over tolcapone in clinical practice despite both drugs improving response to levodopa-carbidopa therapy?
A) Entacapone has fewer side effects compared to tolcapone.
B) Entacapone has a shorter duration of action compared to tolcapone.
C) Tolcapone induces fulminant hepatic necrosis, whereas entacapone does not.
D) Tolcapone has a faster onset of action compared to entacapone.

A

C) Tolcapone induces fulminant hepatic necrosis, whereas entacapone does not.

101
Q

Which statement accurately describes the pharmacokinetic properties of tolcapone and entacapone?
A) Tolcapone has a shorter duration of action compared to entacapone.
B) Both tolcapone and entacapone require dose adjustment in liver cirrhosis.
C) Entacapone improves response to levodopa-carbidopa therapy, while tolcapone reduces the wearing-off phenomenon.
D) Tolcapone has a faster onset of action compared to entacapone.

A

B) Both tolcapone and entacapone require dose adjustment in liver cirrhosis.

102
Q

Which statement accurately describes the pharmacokinetic properties of tolcapone and entacapone?
A) Tolcapone has a longer duration of action compared to entacapone.
B) Entacapone improves response to levodopa-carbidopa therapy, while tolcapone reduces the wearing-off phenomenon.
C) Tolcapone has a faster onset of action compared to entacapone.

A

A) Tolcapone has a longer duration of action compared to entacapone.

103
Q

Which statement accurately describes the pharmacokinetic properties of tolcapone and entacapone?
A) Tolcapone has a shorter duration of action compared to entacapone.
B) Both tolcapone and entacapone does not require dose adjustment in liver cirrhosis.
C) Both tolcapone and entacapone improve response to levodopa-carbidopa therapy and reduce the wearing-off phenomenon.
D) Tolcapone has a faster onset of action compared to entacapone.

A

C) Both tolcapone and entacapone improve response to levodopa-carbidopa therapy and reduce the wearing-off phenomenon.

104
Q

Which statement accurately describes the side effects of tolcapone and entacapone?
A) Tolcapone and entacapone have distinct side effect profiles compared to levodopa.
B) Both tolcapone and entacapone have similar side effects to levodopa.
C) Tolcapone has fewer side effects compared to entacapone.
D) Entacapone has a higher incidence of gastrointestinal side effects compared to tolcapone.

A

B) Both tolcapone and entacapone have similar side effects to levodopa.

105
Q

What is the effect of selective MAO-B inhibitors on dopamine levels in the brain?
A) Decrease dopamine levels
B) Have no effect on dopamine levels
C) Increase dopamine levels
D) Convert dopamine into serotonin

A

C) Increase dopamine levels

106
Q

In what capacity are selective MAO-B inhibitors typically used in relation to levodopa-carbidopa therapy?
A) They replace levodopa-carbidopa
B) They enhance the peripheral decarboxylation of levodopa
C) They antagonize the effects of levodopa-carbidopa
D) They are used as adjuvants to levodopa-carbidopa

A

D) They are used as adjuvants to levodopa-carbidopa

107
Q

Which medications should be avoided when taking selective MAO-B inhibitors?
A) Non-steroidal anti-inflammatory drugs (NSAIDs)
B) Selective serotonin re-uptake inhibitors (SSRIs)
C) Beta-blockers
D) Calcium channel blockers

A

B) Selective serotonin re-uptake inhibitors (SSRIs)

These drugs should be avoided in patients taking
selective serotonin re-uptake inhibitors (SSRIs),
tricyclic antidepressants, and meperidine.

108
Q

What is the primary effect of selective monoamine oxidase B (MAO-B) inhibitors on dopamine levels in the brain?
A) Decrease dopamine levels
B) Have no effect on dopamine levels
C) Increase dopamine levels
D) Convert dopamine into serotonin

A

C) Increase dopamine levels

109
Q

GPT
Why are selective monoamine oxidase B (MAO-B) inhibitors well tolerated at recommended doses?
A) Due to their high toxicity profile
B) Because they have minimal effect on dopamine levels
C) Because they selectively inhibit MAO-A
D) Due to their minimal side effects

A

D) Due to their minimal side effects

110
Q

MAOB inhibitors are primarily used in the treatment of:
a) Hypertension
b) Depression
c) Parkinson’s disease
d) Schizophrenia

A

c) Parkinson’s disease

111
Q

MAOB inhibitors prevent the degradation of which neurotransmitter in the brain?
a) Serotonin
b) Dopamine
c) Acetylcholine
d) GABA

A

b) Dopamine

112
Q

Which MAOB inhibitor is known to be metabolized into amphetamine and methamphetamine, potentially causing insomnia if administered later in the day?
a) Selegiline
b) Rasagiline
c) Safinamide
d) Entacapone

A

a) Selegiline

113
Q

Among the listed MAOB inhibitors, which one is irreversible and possesses five times the potency of Selegiline? And it is not
metabolized to an amphetamine-like substance.
a) Selegiline
b) Rasagiline
c) Safinamide
d) Entacapone

A

b) Rasagiline

114
Q

Which MAOB inhibitor is not metabolized into amphetamine-like substances?
a) Selegiline
b) Rasagiline

A

b) Rasagiline

Note
Safinamide:
Is also a selective inhibitor, of MAO-B

115
Q

Dopamine agonists “Bromocriptine” are preferred in Parkinson’s disease patients experiencing fluctuations in response to levodopa due to:
a) Shorter duration of action compared to levodopa
b) Longer duration of action compared to levodopa
c) Greater risk of dyskinesias compared to levodopa
d) Lower efficacy compared to levodopa

A

b) Longer duration of action compared to levodopa

116
Q

Compared to initial therapy with levodopa, initial therapy with dopamine agonists “Bromocriptine” is associated with:
a) Higher risk of dyskinesias
b) Lower risk of dyskinesias and motor fluctuations
c) Faster onset of action
d) Greater efficacy in treatment-naive patients

A

b) Lower risk of dyskinesias and motor fluctuations

117
Q

Dopamine agonists “Bromocriptine” are ineffective in patients who:
a) Have not responded to levodopa
b) Have never been treated with levodopa
c) Are resistant to dopamine
d) Are not experiencing motor fluctuations

A

a) Have not responded to levodopa

118
Q

Bromocriptine’s actions are similar to which other medication?
a) Amantadine
b) Selegiline
c) Levodopa
d) Benztropine

A

c) Levodopa

119
Q

Which of the following best describes the mechanism of action of bromocriptine?
a) Cholinergic agonism
b) Dopaminergic agonism
c) GABAergic antagonism
d) Serotonergic agonism

A

b) Dopaminergic agonism

120
Q

Compared to levodopa, bromocriptine is less likely to cause:
a) Dyskinesia
b) Psychiatric illness
c) Peripheral vascular disease
d) Myocardial infarction

A

a) Dyskinesia

121
Q

Bromocriptine is contraindicated in patients with a history of the following except :
a) Dyskinesia
b) Myocardial infarction
c) Peripheral vascular disease
d) Psychiatric illness

A

a) Dyskinesia

122
Q

Which of the following is a specific adverse effect of bromocriptine due to its ergot derivative nature?
a) Dyskinesia
b) Pulmonary and retroperitoneal fibrosis
c) Peripheral vascular disease
d) Myocardial infarction

A

b) Pulmonary and retroperitoneal fibrosis

123
Q

Bromocriptine, an ergot derivative, shares similar actions to levodopa, with adverse effects that are also similar to levodopa, except for….

A

Dyskinesia

124
Q

Bromocriptine Contraindications:

A

1 psychiatric illness.
2 Patients with a history of myocardial infarction or
peripheral vascular disease due to the risk of vasospasm.

125
Q

Bromocriptine (dopamine agonist)has the potential to
cause pulmonary and retroperitoneal fibrosis?

A

Because it is an ergot derivative .

126
Q

The antiparkinsonian action of amantadine was accidentally discovered while it was primarily used as a(n):
a) Antibiotic
b) Antiviral drug
c) Antifungal agent
d) Anticoagulant

A

b) Antiviral drug

127
Q

Which of the following is NOT an adverse effect associated with amantadine use in Parkinson’s disease?
a) Restlessness
b) Agitation
c) Confusion
d) Bradycardia

A

d) Bradycardia

The drug may cause
restlessness
Agitation
Confusion
Hallucinations

128
Q

Amantadine is believed to exert its antiparkinsonian effects by inhibiting which type of glutamate receptors?
a) NMDA
b) AMPA
c) Kainate
d) Metabotropic glutamate receptors

A

a) NMDA

129
Q

Amantadine Mechanism of Action:

A

Not exactly known but it could be through
1 ) Increases the release of dopamine.
2) Blocking cholinergic receptors
3) Inhibiting NMDA type of glutamate receptors.

130
Q

The main mechanism of action of benztropine and trihexyphenidyl in treatment of Parkinson’s disease involves:
a) Increasing dopamine release
b) Decreasing acetylcholine activity
c) Enhancing serotonin signaling
d) Blocking glutamate receptors

A

b) Decreasing acetylcholine activity

131
Q

Which symptom of Parkinson’s disease do benztropine and trihexyphenidyl have a significant effect on?
a) Bradykinesia
b) Tremors and rigidity
c) Postural reflexes
d) Cognitive decline

A

b) Tremors and rigidity

They have a significant effect on tremors and rigidity but
little effect on bradykinesia and postural reflexes.

132
Q

Which of the following is NOT a side effect commonly associated with benztropine and trihexyphenidyl?
a) Mood change and confusion
b) Xerostomia and constipation
c) Visual problems
d) Insomnia and nightmares

A

d) Insomnia and nightmares

Side effects:
Mood change and confusion (CNS)
Xerostomia and Constipation (GIT)
Visual problems (Eye)

133
Q

Contraindications for the use of benztropine and trihexyphenidyl (centrally acting anticholenergics ) include:
a) Glaucoma
b) Hypertension
c) Renal failure
d) Osteoarthritis

A

a) Glaucoma

Contraindications:
1. Glaucoma
2. Prostatic hyperplasia
3. Pyloric stenosis.

134
Q

Benztropine and trihexyphenidyl, compared to levodopa, are characterized by:
a) Greater efficacy in treating Parkinson’s disease
b) Lower efficacy in treating Parkinson’s disease
c) Comparable efficacy in treating Parkinson’s disease
d) Similar efficacy but different mechanism of action in treating Parkinson’s disease

A

b) Lower efficacy in treating Parkinson’s disease

135
Q

Alzheimer disease has three distinguishing features:

A
  1. Accumulation of senile plaques (beta-amyloid
    accumulations),
  2. Formation of numerous neurofibrillary tangles
    3.
    Loss of cortical neurons, particularly cholinergic neurons.
136
Q

Alzheimer’s therapies aim either to:
“2”

A

1)To Improve cholinergic transmission within the CNS
2)To prevent excitotoxic actions resulting from overstimulation of NMDA-glutamate receptors in selected areas of the brain.

137
Q

What are the three distinguishing features of Alzheimer’s disease?
a) Accumulation of senile plaques, loss of cortical neurons, and formation of numerous neurofibrillary tangles
b) Accumulation of tau proteins, loss of dopaminergic neurons, and formation of senile plaques
c) Accumulation of amyloid-beta, loss of hippocampal neurons, and formation of neurofibrillary tangles
d) Accumulation of neurofibrillary tangles, loss of cholinergic neurons, and formation of senile plaques

A

a) Accumulation of senile plaques, loss of cortical neurons, and formation of numerous neurofibrillary tangles

138
Q

Which of the following is NOT a therapeutic target for Alzheimer’s disease?
a) Improving cholinergic transmission within the CNS
b) Preventing excitotoxic actions resulting from overstimulation of NMDA-glutamate receptors
c) Inhibiting the accumulation of tau proteins
d) Alleviating symptoms through palliative care

A

c) Inhibiting the accumulation of tau proteins

139
Q

True or False: Current pharmacologic interventions for Alzheimer’s disease can alter the underlying neurodegenerative process.
a) True
b) False

A

b) False

140
Q

Which protein accumulations are primarily associated with Alzheimer’s disease?
a) Tau proteins
b) Amylin
c) Beta-amyloid
d) Alpha-synuclein

A

c) Beta-amyloid

141
Q

What is the primary aim of therapies targeting cholinergic transmission in Alzheimer’s disease?
a) Enhancing memory formation
b) Reducing neuroinflammation
c) Improving motor function
d) Alleviating behavioral symptoms

A

a) Enhancing memory formation

142
Q

What is the mechanism of action of therapies aiming to prevent excitotoxic actions in Alzheimer’s disease?
a) Blocking acetylcholine receptors
b) Inhibiting NMDA-glutamate receptors
c) Enhancing serotonin reuptake
d) Promoting dopamine release

A

b) Inhibiting NMDA-glutamate receptors

143
Q

Which of the following is a characteristic feature of Alzheimer’s disease pathology?
a) Increased GABAergic neurotransmission
b) Accumulation of Lewy bodies
c) Loss of dopaminergic neurons in the substantia nigra
d) Accumulation of beta-amyloid plaques and neurofibrillary tangles

A

d) Accumulation of beta-amyloid plaques and neurofibrillary tangles

144
Q

.

A
145
Q

Which of the following is NOT a reversible acetylcholinesterase inhibitor approved for the treatment of Alzheimer’s disease?
a) Donepezil
b) Galantamine
c) Rivastigmine
d) Memantine

A

d) Memantine

146
Q

Which acetylcholinesterase inhibitor is specifically approved for the management of dementia in Parkinson’s disease?
a) Donepezil
b) Galantamine
c) Rivastigmine
d) Memantine

A

c) Rivastigmine

147
Q

What is a common adverse effect associated with the use of acetylcholinesterase inhibitors?
a) Tachycardia
b) Hypertension
c) Nausea
d) Hyperglycemia

A

c) Nausea

148
Q

What is the proposed mechanism of action of acetylcholinesterase inhibitors in Alzheimer’s disease?
a) Increasing the production of acetylcholine
b) Blocking the release of acetylcholine
c) Inhibiting the degradation of acetylcholine
d) Enhancing the reuptake of acetylcholine

A

c) Inhibiting the degradation of acetylcholine

149
Q

Which formulation of rivastigmine is specifically mentioned as being available for the management of dementia in Parkinson’s disease?
a) Oral tablets
b) Intravenous injection
c) Transdermal patch
d) Sublingual spray

A

c) Transdermal patch

150
Q

Which of the following is NOT a common adverse effect associated with acetylcholinesterase inhibitors?
a) Nausea
b) Diarrhea
c) Hypertension
d) Tremors

A

c) Hypertension

151
Q

True or False: Acetylcholinesterase inhibitors can completely halt the progression of Alzheimer’s disease.
a) True
b) False

A

b) False

152
Q

The reversible AChE inhibitors approved for the treatment of Alzheimer’s
disease include

A

Galantamine
Rivastigmine
++dr.f Donepezil

153
Q

Acetylcholinesterase inhibitors that used for ttt of Alzheimer’s disease A/E ?

A

Common adverse effects include
• Nausea, diarrhea, vomiting, anorexia,
• tremors, and muscle Cramps.
• bradycardia.

154
Q

Alzheimer’s disease therapy ?

A

A. Acetylcholinesterase inhibitors
Galantamine
Rivastigmine

B. NMDA receptor antagonist
Memantine
indicated for moderate-to-
severe Alzheimer’s disease.
is often given in combination with an AChE inhibitor.

155
Q

Memantine ( NMDA antagonist) A/E ?

A

• Confusion
• Agitation
• Restlessness

156
Q

What is the role of glutamate NAMDA receptors in memory formation in the CNS?
A. Inhibition of memory consolidation
B. Excitotoxicity on neurons
C. Critical for memory formation
D. Induction of neurodegenerative processes

A

C. Critical for memory formation

157
Q

Which of the following best describes the potential consequence of overstimulation of NMDA receptors?
A. Facilitation of memory retrieval
B. Excitotoxic damage to neurons
C. Enhanced neuronal regeneration
D. Promotion of synaptic plasticity

A

B. Excitotoxic damage to neurons

158
Q

Overstimulation of NMDA receptors in Alzheimer’s disease is implicated in:
A. Enhancing long-term memory
B. Neuroprotective effects
C. Excitotoxicity
D. Decreasing synaptic plasticity

A

C. Excitotoxicity

159
Q

G.R using NMDA receptor antagonist for ttt of Alzheimer’s disease?

A

Stimulation of glutamate receptors in the CNS appears to be
critical for the formation of certain memories.
However, overstimulation of glutamate receptors, particularly
of the NMDA type, may result in excitotoxic effects on
neurons and is suggested as a mechanism for
neurodegenerative or apoptotic processes.

160
Q

Which of the following is NOT a common goal of multiple sclerosis MS treatment?
A. Slowing disease progression
B. Reducing frequency of relapses
C. Restoring lost neurological function
D. Managing symptoms to improve quality of life

A

C. Restoring lost neurological function

161
Q

• Multiple sclerosis (MS) is…

A

an autoimmune inflammatory
demyelinating disease of the CNS.
• Medications are used to modify the disease course, treat
relapses (exacerbations or attacks), and manage
symptoms.

162
Q

Treatment for multiple sclerosis MS may include

A

the following:
1. Treating relapses of MS symptoms (with steroid
medication dexamethasone ad prednisolone)
2. Treating specific MS symptoms
3. Treatment to reduce the number of relapses (disease-
modifying therapies)

163
Q

Treatment for MS may include

A

the following:
1. Treating relapses of MS symptoms (with steroid
medication dexamethasone ad prednisolone)
2. Treating specific MS symptoms
3. Treatment to reduce the number of relapses (disease-
modifying therapies)

164
Q

Which of the following best describes the purpose of disease-modifying therapies for MS?
A. They primarily treat symptoms of MS.
B. They aim to reverse existing damage to the myelin sheath.
C. They target immune processes to reduce relapses and disability progression.
D. They are designed to improve cognitive function in MS patients.

A

C. They target immune processes to reduce relapses and disability progression.

165
Q

What is the primary mechanism of action of disease-modifying therapies in multiple sclerosis MS?
A. Enhancing myelin regeneration
B. Decreasing nerve cell apoptosis
C. Modifying the immune response
D. Stimulating oligodendrocyte function

A

C. Modifying the immune response

Explanation: Disease-modifying therapies work by targeting immune processes, particularly inhibiting white blood cell-mediated inflammatory processes that lead to myelin sheath damage in MS.

166
Q

In which types of MS are disease-modifying agents most useful?
A. Primary progressive MS
B. Relapse remitting MS and secondary progressive MS
C. Progressive relapsing MS
D. Clinically isolated syndrome (CIS)

A

B. Relapse remitting MS and secondary progressive MS

Disease-modifying agents are useful in certain patients with
relapse remitting MS or secondary progressive MS.

167
Q

What is the primary goal of disease-modifying therapies in MS?
A. To cure the disease
B. To manage pain associated with MS
C. To restore lost neurological function
D. To decrease the number and severity of relapses

A

D. To decrease the number and severity of relapses

168
Q

Disease-modifying therapies for MS “multiple sclerosis “ ?

A
  1. Interferon beta 1a and interferon beta1b (injections):
  2. Glatiramer (injections):
  3. Fingolimod (oral):
  4. Teriflunomide (oral):
  5. Dimethyl fumarate (oral):
  6. Monoclonal antibodies (injections):
    • Alemtuzumab
    • Daclizumab
    • Natalizumab
    • Ocrelizumab
169
Q

Which mechanism of action is associated with interferon beta 1a and interferon beta-1b in the treatment of multiple sclerosis MS?
A. Enhancing myelin regeneration
B. Inhibiting axonal degeneration
C. Diminishing inflammatory responses that leading to demyelination
D. Blocking voltage-gated calcium channels

A

C. Diminishing inflammatory responses that leading to demyelination

170
Q

How does glatiramer primarily function in the treatment of MS?
A. By promoting remyelination of damaged axons
B. By acting as an antioxidant to protect neurons
C. By inhibiting B-cell proliferation
D. By acting as a decoy to T-cell attack

A

D. By acting as a decoy to T-cell attack

Explanation: Glatiramer resembles myelin protein and may act as a decoy to divert T-cell attack away from myelin, thus reducing autoimmune damage in MS.

171
Q

What is the primary effect of fingolimod in the treatment of MS “multiple sclerosis” ?
A. Inhibiting microglial activation
B. Reducing astrocyte proliferation
C. Altering lymphocyte migration into the CNS
D. Enhancing oligodendrocyte differentiation

A

C. Altering lymphocyte migration into the CNS

Explanation: Fingolimod alters lymphocyte migration, resulting in fewer lymphocytes entering the central nervous system (CNS), which helps to reduce autoimmune activity in MS.

172
Q

What is the primary mechanism of action of teriflunomide in the treatment of MS?
A. Inhibiting microglial activation
B. Enhancing oligodendrocyte differentiation
C. Blocking voltage-gated calcium channels
D. Synthesis pyrimidine inhibitors leading to lower concentrations of active lymphocytes in the CNS

A

D. Synthesis pyrimidine inhibitors leading to lower concentrations of active lymphocytes in the CNS

Explanation: Teriflunomide inhibits the synthesis of pyrimidines, which leads to a reduction in the number of active lymphocytes in the central nervous system (CNS) in MS.

173
Q

How does dimethyl fumarate primarily affect disease progression in MS?
A. By enhancing myelin repair mechanisms
B. By reducing oxidative stress responses
C. By promoting axonal regeneration
D. By inhibiting T-cell proliferation

A

B. By altering the cellular response to oxidative stress to reduce disease progression

Explanation: Dimethyl fumarate may alter the cellular response to oxidative stress, thereby reducing disease progression in MS.

174
Q

Monoclonal antibodies (injections) used as disease modifying therapy for multiple sclerosis MS? “ 4”

A

• Alemtuzumab
• Daclizumab
• Natalizumab
• Ocrelizumab

175
Q

TTT of multiple sclerosis MS?

A

A.disease modifying therapy:
1. Interferon beta 1a and interferon beta1b (injections):
2. Glatiramer (injections):
3. Fingolimod (oral):
4. Teriflunomide (oral):
5. Dimethyl fumarate (oral):
6. Monoclonal antibodies (injections):
• Alemtuzumab
• Daclizumab
• Natalizumab
• Ocrelizumab

B.symptomatic treatment:
Dalfampridine
• potassium channel blocker, improves walking speeds in
patients with MS. It is the first drug approved for this use.

176
Q

Which symptom of MS does Dalfampridine primarily target?
A. Spasticity
B. Constipation
C. Bladder dysfunction
D. Impaired walking speed

A

D. Impaired walking speed

Explanation: Dalfampridine, a potassium channel blocker, is approved to improve walking speeds in patients with MS,

177
Q

What is the primary mechanism of action of Dalfampridine in MS?
A. Blocking acetylcholine receptors
B. Enhancing neurotransmitter release
C. Inhibiting voltage-gated calcium channels
D. Blocking potassium channels

A

D. Blocking potassium channels

Explanation : Dalfampridine works by blocking potassium channels, which can improve nerve conduction and enhance walking speed in MS patients.

178
Q

Multiple sclerosis symptoms?

A

• Spasticity
• Constipation
• Bladder dysfunction
• Depression

179
Q

Which of the following best describes the primary mechanism of action of Riluzole in the treatment of ALS “ amyotrophic lateral sclerosis?
A. Enhancing acetylcholine release at neuromuscular junctions
B. Inhibiting glutamate release and blocking sodium channels
C. Activating GABA receptors in motor neurons
D. Stimulating dopamine production in the brain

A

B. Inhibiting glutamate release and blocking sodium channels

Explanation: Riluzole acts as an NMDA receptor antagonist, inhibiting glutamate release and blocking sodium channels, which helps to reduce excitotoxicity and slow disease progression in ALS.

180
Q

What is the proposed benefit of Riluzole for patients with ALS?
A. It reverses motor neuron damage
B. It alleviates muscle stiffness and spasticity
C. It improves survival time
D. It enhances muscle strength and coordination

A

C. It improves survival time

Explanation: Riluzole may improve survival time in patients suffering from ALS by slowing down the progression of the disease.

181
Q

How does Edaravone primarily function in the treatment of ALS?
A. By enhancing neuromuscular transmission
B. By inhibiting acetylcholinesterase activity
C. By acting as a free radical scavenger and antioxidant
D. By reducing inflammation in the central nervous system

A

C. By acting as a free radical scavenger and antioxidant

Explanation: Edaravone functions as a free radical scavenger and antioxidant, which may help to slow the progression of ALS by reducing oxidative stress and neuronal damage.

182
Q

Amyotrophic lateral sclerosis (ALS) is characterized by

A

progressive degeneration of motor neurons, resulting in
the inability to initiate or control muscle movement.

CNS Pharmacology (7 decks)

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