Quiz : How Much You Know About Antidepressants
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How much do you know about antidepressants? This quiz can help test your knowledge. Antidepressants work on certain neurotransmitters in the brain. These neurotransmitters mainly include serotonin and norepinephrine, both of which play a role in boosting your mood. Antidepressants can help alleviate the signs of depression, low mood, irritability, and anxiety. If you want to learn more about antidepressants, this quiz can be of service. Take this amazing quiz and prepare to get happy.
- 1.
The two types of unipolar depression are.
- A.
Reactive - biochemical disorder in brain; endogenous - genetic cause
- B.
Reactive - response to death; exogenous - adverse effect of some medication
- C.
Reactive - response to circumstance; endogenous - biochemical disorder
Correct Answer
C. Reactive - response to circumstance; endogenous - biochemical disorderExplanation
The correct answer is reactive - response to circumstance; endogenous - biochemical disorder. This is because reactive depression is a type of depression that is triggered by external events or circumstances, such as the loss of a loved one or a major life change. On the other hand, endogenous depression refers to depression that is caused by internal factors, such as a biochemical imbalance in the brain.Rate this question:
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- 2.
Which of the following statements provides evidence for the monoamine theory of depression?
- A.
Reserpine (inhibits brain storage of noradrenaline and serotonin) causes depression
- B.
Reserpine (inhibits brain storage of adrenaline, histamine and acetylcholine) is a treatment for depression
- C.
Amphetamine (causes release of noradrenaline) has no effect in depressed patients
Correct Answer
A. Reserpine (inhibits brain storage of noradrenaline and serotonin) causes depressionExplanation
Reserpine inhibits the brain storage of noradrenaline and serotonin, which are two monoamine neurotransmitters implicated in depression. This provides evidence for the monoamine theory of depression, which suggests that a deficiency in these neurotransmitters can lead to depressive symptoms.Rate this question:
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- 3.
Which of the following statements provides evidence against the monoamine theory of depression?
- A.
Cocaine (inhibits reuptake of noradrenaline) treats depression
- B.
Urinary excretion of the serotonin metabolite 5-HIAA is unchanged in depressed patients
- C.
Urinary and cerebral spinal fluid concentrations of the noradrenaline metabolite MOPEG are reduced by 25% in depressed patients
Correct Answer
B. Urinary excretion of the serotonin metabolite 5-HIAA is unchanged in depressed patientsExplanation
The fact that the urinary excretion of the serotonin metabolite 5-HIAA is unchanged in depressed patients goes against the monoamine theory of depression. This theory suggests that depression is caused by a deficiency in monoamine neurotransmitters, such as serotonin. If this theory were true, one would expect to see decreased levels of serotonin metabolites in depressed patients. However, since the urinary excretion of 5-HIAA remains unchanged, it suggests that serotonin levels are not significantly affected in depression, contradicting the monoamine theory.Rate this question:
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- 4.
The two sub-types of tricyclic antidepressants are...
- A.
Dibenzazepines; dibenzocycloheptenes
- B.
Hydrazines; propargylamines
- C.
Piperazines; piperidines
Correct Answer
A. Dibenzazepines; dibenzocycloheptenesExplanation
Dibenzazepines and dibenzocycloheptenes are the two sub-types of tricyclic antidepressants. Tricyclic antidepressants are a class of medications commonly used to treat depression. These medications work by increasing the levels of certain chemicals in the brain, such as serotonin and norepinephrine, which help improve mood and relieve symptoms of depression. Dibenzazepines and dibenzocycloheptenes are specific chemical structures that are found in different tricyclic antidepressant drugs.Rate this question:
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- 5.
What is the mechanism of action of TCAs?
- A.
Competitive antagonist for inhibitors of neurotransmitters in synaptic cleft, meaning more re-uptake, so neurotransmitters exert effects for shorter lengths of time
- B.
Non-competitive agonist for re-uptake of neurotransmitters in synaptic cleft, meaning no re-uptake, so neurotransmitters exert effects for longer
- C.
Competitive antagonist for re-uptake of neurotransmitters in synaptic cleft, meaning no re-uptake, so neurotransmitters exert effects for longer
Correct Answer
C. Competitive antagonist for re-uptake of neurotransmitters in synaptic cleft, meaning no re-uptake, so neurotransmitters exert effects for longerExplanation
TCAs (Tricyclic antidepressants) work by competitively inhibiting the re-uptake of neurotransmitters in the synaptic cleft. This means that they block the re-uptake pumps responsible for removing neurotransmitters from the synapse, resulting in increased levels of neurotransmitters in the synaptic cleft. As a result, the neurotransmitters exert their effects for a longer duration, leading to an overall increase in neurotransmitter activity and improved mood.Rate this question:
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- 6.
Which neurotransmitter receptors are potentially affected by TCAs?
- A.
Muscarinic; histaminic; B-adrenoceptors
- B.
Nicotinic; adrenergic (a and b)
- C.
Histaminic; nicotinic; a-adrenoceptors
Correct Answer
A. Muscarinic; histaminic; B-adrenoceptorsExplanation
TCAs, or tricyclic antidepressants, are known to affect muscarinic, histaminic, and B-adrenoceptors. Muscarinic receptors are involved in various functions such as regulating heart rate, smooth muscle contraction, and glandular secretions. Histaminic receptors are involved in allergic responses, gastric acid secretion, and wakefulness. B-adrenoceptors are involved in regulating heart rate, blood pressure, and bronchial smooth muscle relaxation. Therefore, TCAs can potentially affect these neurotransmitter receptors, leading to a variety of effects on the body.Rate this question:
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- 7.
What is the mechanism of action of MAOIs?
- A.
Catalyse breakdown of noradrenaline and serotonin
- B.
Inhibit breakdown of noradrenaline and serotonin
- C.
Inhibit breakdown of adrenaline and serotonin
Correct Answer
B. Inhibit breakdown of noradrenaline and serotoninExplanation
MAOIs (Monoamine oxidase inhibitors) work by inhibiting the breakdown of noradrenaline and serotonin. This allows these neurotransmitters to remain in the synaptic cleft for a longer duration, leading to increased neurotransmission and potentially improving symptoms of depression or other mood disorders.Rate this question:
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- 8.
What is the cheese reaction?
- A.
Decreased absorption of vasoactive amines from diet; too many so pathway becomes saturated, build up; can lead to cerebral hemorrhage and death
- B.
Absorption of vasoactive amines from diet, cannot be broken down, build up; can lead to cerebral hemorrhage and death
- C.
Absorption of vasoactive amines from diet, cannot be broken down, build up; can lead to high intercranial pressure and fitting
Correct Answer
B. Absorption of vasoactive amines from diet, cannot be broken down, build up; can lead to cerebral hemorrhage and deathExplanation
The correct answer explains that the cheese reaction is caused by the absorption of vasoactive amines from the diet, which cannot be broken down and therefore build up in the body. This buildup can lead to cerebral hemorrhage and death. This explanation suggests that consuming cheese or other foods high in vasoactive amines can have severe consequences on the body's ability to regulate blood flow and can result in life-threatening complications.Rate this question:
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- 9.
What are the sub-types of MAOIs?
- A.
Typical, atypical
- B.
Dibenzapines, dibenzocycloheptenes
- C.
Hydrazines, propargylamines, cyclopropylamines, reversible inhibitors
Correct Answer
C. Hydrazines, propargylamines, cyclopropylamines, reversible inhibitorsExplanation
The sub-types of MAOIs are hydrazines, propargylamines, cyclopropylamines, and reversible inhibitors.Rate this question:
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- 10.
What is the mechanism of action of SSRIs?
- A.
Selectively block serotonin reuptake into the pre-synaptic cell
- B.
Non-selectively block serotonin and noradrenaline reuptake into the pre-synaptic cell
- C.
Selectively increase affinity of the post-synaptic receptors for serotonin
Correct Answer
A. Selectively block serotonin reuptake into the pre-synaptic cellExplanation
SSRIs (Selective Serotonin Reuptake Inhibitors) work by selectively blocking the reuptake of serotonin into the pre-synaptic cell. This means that they prevent the serotonin neurotransmitter from being taken back up into the neuron that released it, allowing it to remain in the synaptic cleft for a longer period of time. By doing so, SSRIs increase the concentration of serotonin in the brain, which can help improve mood and alleviate symptoms of depression and anxiety.Rate this question:
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- 11.
Serotonin syndrome is...
- A.
Very common; supraventricular tachycardia; high intercranial pressure and abdominal cramps
- B.
An adverse effect; bradycardia and sweating; fitting and liver failure
- C.
Technically a form of poisoning; tachycardia and shivering; seizures and renal failure
Correct Answer
C. Technically a form of poisoning; tachycardia and shivering; seizures and renal failureExplanation
Serotonin syndrome is a potentially life-threatening condition that occurs when there is an excessive accumulation of serotonin in the body. It is considered a form of poisoning because it results from an overdose or interaction of medications that increase serotonin levels. Symptoms of serotonin syndrome include tachycardia (rapid heart rate), shivering, seizures, and renal failure.Rate this question:
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- 12.
The theory for the 2-3 week delay in effectiveness of SSRIs is...
- A.
They are administered as pro-drugs with exteremely long half-lives
- B.
Autoreceptors quickly become desensitised to newly increased levels of serotonin; 2-3 weeks is the time taken for more to be synthesised
- C.
They are metabolised very slowly by P450 enzymes
Correct Answer
B. Autoreceptors quickly become desensitised to newly increased levels of serotonin; 2-3 weeks is the time taken for more to be synthesisedExplanation
The theory for the 2-3 week delay in effectiveness of SSRIs is that autoreceptors quickly become desensitized to newly increased levels of serotonin. This means that the receptors in the brain become less responsive to the increased serotonin levels, which takes time to readjust. During this time, the body synthesizes more serotonin to compensate for the desensitized receptors. This process typically takes 2-3 weeks, explaining the delayed effectiveness of SSRIs.Rate this question:
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- 13.
Noradrenaline reuptake inhibitors produce...
- A.
Atropine-like side effects
- B.
Alpha-block-like side effects
- C.
Suicidal thoughts
Correct Answer
A. Atropine-like side effectsExplanation
Noradrenaline reuptake inhibitors are a class of medications that work by blocking the reuptake of noradrenaline in the brain, thereby increasing its availability. Atropine is a medication that blocks the action of acetylcholine, a neurotransmitter responsible for various bodily functions. Atropine-like side effects refer to the potential side effects of noradrenaline reuptake inhibitors that are similar to those caused by atropine, such as dry mouth, blurred vision, constipation, and urinary retention. Therefore, the correct answer is Atropine-like side effects.Rate this question:
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- 14.
L-Tryptophan is found in... and contains...
- A.
Evening Primrose Oil; L-Dopa, the precursor to serotonin
- B.
St John's Wort; L-Trytophan, the precursor to serotonin
- C.
St John's Wort; L-Dopa, the precursor to dopamine
Correct Answer
B. St John's Wort; L-TrytopHan, the precursor to serotoninExplanation
L-Tryptophan is an amino acid that is a precursor to serotonin, a neurotransmitter that is involved in regulating mood and sleep. St John's Wort is a herbal supplement that contains L-Tryptophan, making it the correct answer. Evening Primrose Oil does not contain L-Tryptophan, and L-Dopa is a precursor to dopamine, not serotonin.Rate this question:
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- 15.
Lithium is administered as... and is particulraly used in...
- A.
Lithium esters; preventing fluctuations in bipolar depression
- B.
Lithium anhydride; stabilising the depressive phase in bipolar depression
- C.
Lithium carbonate; stabilising the manic phase in bipolar depression
Correct Answer
C. Lithium carbonate; stabilising the manic pHase in bipolar depressionExplanation
Lithium carbonate is administered to stabilize the manic phase in bipolar depression. Bipolar disorder is characterized by alternating episodes of mania (elevated mood, increased energy) and depression. Lithium carbonate helps to reduce the intensity and frequency of manic episodes, preventing extreme mood swings and promoting stability in individuals with bipolar depression.Rate this question:
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Jul 29, 2023Quiz Edited by
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May 19, 2011Quiz Created by
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