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Questions and Answers
What is the main difference between human and fungi cells?
What is the main difference between human and fungi cells?
How do Azoles act as antifungal agents?
How do Azoles act as antifungal agents?
What are the main side effects of antifungal agents?
What are the main side effects of antifungal agents?
Can Amphoterocin-B be given orally?
Can Amphoterocin-B be given orally?
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What is the main difference between imidazoles and Triazoles?
What is the main difference between imidazoles and Triazoles?
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How do anti-metabolites act as antifungal agents?
How do anti-metabolites act as antifungal agents?
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Which antifungal drug is the first-line treatment for severe and potentially fatal systemic mycoses?
Which antifungal drug is the first-line treatment for severe and potentially fatal systemic mycoses?
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Which drug is used for confirmed dermatophyte infections of the nails or skin?
Which drug is used for confirmed dermatophyte infections of the nails or skin?
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Which antifungal drug has a similar structure to amphotericin and its use is limited to C. albicans infections of the skin and mucous membranes?
Which antifungal drug has a similar structure to amphotericin and its use is limited to C. albicans infections of the skin and mucous membranes?
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Which antifungal drug is converted in fungal cells, but not in human cells, into fluorouracil that inhibits fungal DNA synthesis?
Which antifungal drug is converted in fungal cells, but not in human cells, into fluorouracil that inhibits fungal DNA synthesis?
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Which antifungal drug inhibits squalene epoxide and leads to toxic levels of squalene accumulating in the fungal cells?
Which antifungal drug inhibits squalene epoxide and leads to toxic levels of squalene accumulating in the fungal cells?
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Which antifungal drug binds to tubulin and interferes with microtubule formation (Mitosis +cell wall synthesis)?
Which antifungal drug binds to tubulin and interferes with microtubule formation (Mitosis +cell wall synthesis)?
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What is the mode of action of imidazoles?
What is the mode of action of imidazoles?
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What is the major side effect of amphotericin-B?
What is the major side effect of amphotericin-B?
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Which antifungal drug results in renal impairment when administered with other nephrotoxic drugs?
Which antifungal drug results in renal impairment when administered with other nephrotoxic drugs?
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Which antifungal drug is a polyene antibiotic that binds to ergosterol in the fungal cell membrane and forms channels through which essential fungal cell constituents are lost?
Which antifungal drug is a polyene antibiotic that binds to ergosterol in the fungal cell membrane and forms channels through which essential fungal cell constituents are lost?
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Which antifungal drug has a relatively selective action on fungal cells because the major sterol in human cells is cholesterol rather than ergosterol?
Which antifungal drug has a relatively selective action on fungal cells because the major sterol in human cells is cholesterol rather than ergosterol?
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What is the main change in cell physiology that leads to the formation of the malignant phenotype?
What is the main change in cell physiology that leads to the formation of the malignant phenotype?
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Which type of mutations in growth factor receptors can lead to uncontrolled cell growth?
Which type of mutations in growth factor receptors can lead to uncontrolled cell growth?
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What is the main effect of sustained angiogenesis in cancer cells?
What is the main effect of sustained angiogenesis in cancer cells?
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Which gene, when mutated, causes disruption in the control of cell proliferation?
Which gene, when mutated, causes disruption in the control of cell proliferation?
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What enzyme, when activated, can maintain normal telomere length in tumor cells?
What enzyme, when activated, can maintain normal telomere length in tumor cells?
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Which of the following is a characteristic of tumor suppressor gene TP53?
Which of the following is a characteristic of tumor suppressor gene TP53?
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What is the main consequence of evasion of apoptosis in cancer cells?
What is the main consequence of evasion of apoptosis in cancer cells?
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What is the main function of signal-transducing proteins in cancer cells?
What is the main function of signal-transducing proteins in cancer cells?
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Which factor allows tumor cells to maintain high sensitivity to normal levels of growth factors?
Which factor allows tumor cells to maintain high sensitivity to normal levels of growth factors?
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What is the main purpose of sustained angiogenesis in cancer cells?
What is the main purpose of sustained angiogenesis in cancer cells?
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Which characteristic allows tumor cells to acquire self-sufficiency in growth signals?
Which characteristic allows tumor cells to acquire self-sufficiency in growth signals?
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What is the main consequence of overexpression of growth factor receptors in cancer cells?
What is the main consequence of overexpression of growth factor receptors in cancer cells?
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Which regulatory genes are the main targets of genetic damage in carcinogenesis?
Which regulatory genes are the main targets of genetic damage in carcinogenesis?
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What is the main characteristic of oncoproteins derived from mutations in protooncogenes?
What is the main characteristic of oncoproteins derived from mutations in protooncogenes?
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Which of the following is a main change in cell physiology that leads to the formation of the malignant phenotype?
Which of the following is a main change in cell physiology that leads to the formation of the malignant phenotype?
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What is the role of sustained angiogenesis in cancer cells?
What is the role of sustained angiogenesis in cancer cells?
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What is the main function of signal-transducing proteins in cancer cells?
What is the main function of signal-transducing proteins in cancer cells?
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What enzyme, when activated, can maintain normal telomere length in tumor cells?
What enzyme, when activated, can maintain normal telomere length in tumor cells?
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What is the main consequence of evasion of apoptosis in cancer cells?
What is the main consequence of evasion of apoptosis in cancer cells?
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Which type of mutations in growth factor receptors can lead to uncontrolled cell growth?
Which type of mutations in growth factor receptors can lead to uncontrolled cell growth?
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What is the major side effect of amphotericin-B?
What is the major side effect of amphotericin-B?
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How do Azoles act as antifungal agents?
How do Azoles act as antifungal agents?
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Which antifungal drug binds to tubulin and interferes with microtubule formation (Mitosis +cell wall synthesis)?
Which antifungal drug binds to tubulin and interferes with microtubule formation (Mitosis +cell wall synthesis)?
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Which antifungal drug is converted in fungal cells, but not in human cells, into fluorouracil that inhibits fungal DNA synthesis?
Which antifungal drug is converted in fungal cells, but not in human cells, into fluorouracil that inhibits fungal DNA synthesis?
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Study Notes
Cell Biology
- The main difference between human and fungi cells is the presence of ergosterol in the fungal cell membrane, whereas human cells have cholesterol.
Antifungal Agents
- Azoles act as antifungal agents by inhibiting the production of ergosterol in the fungal cell membrane.
- The main side effects of antifungal agents include renal impairment, especially when administered with other nephrotoxic drugs.
- Amphoterocin-B cannot be given orally.
- Imidazoles and Triazoles differ in their mechanism of action, with imidazoles inhibiting the production of ergosterol and Triazoles inhibiting the lanosterol 14-alpha-demethylase.
Antifungal Drug Mechanisms
- Anti-metabolites act as antifungal agents by inhibiting fungal DNA synthesis.
- Amphotericin-B is the first-line treatment for severe and potentially fatal systemic mycoses.
- Terbinafine is used for confirmed dermatophyte infections of the nails or skin.
- Nystatin has a similar structure to amphotericin and is limited to C. albicans infections of the skin and mucous membranes.
- Flucytosine is converted in fungal cells, but not in human cells, into fluorouracil that inhibits fungal DNA synthesis.
- Terbinafine inhibits squalene epoxide, leading to toxic levels of squalene accumulating in the fungal cells.
- Griseofulvin binds to tubulin and interferes with microtubule formation (Mitosis + cell wall synthesis).
Cancer Cell Biology
- The main change in cell physiology that leads to the formation of the malignant phenotype is the acquisition of self-sufficiency in growth signals.
- Mutations in growth factor receptors can lead to uncontrolled cell growth.
- Sustained angiogenesis in cancer cells leads to the formation of new blood vessels, providing oxygen and nutrients to the tumor.
- The TP53 gene, when mutated, causes disruption in the control of cell proliferation.
- Telomerase, when activated, can maintain normal telomere length in tumor cells.
- Tumor suppressor gene TP53 is characterized by inducing apoptosis in response to DNA damage.
- Evasion of apoptosis in cancer cells leads to uncontrolled cell growth.
- Signal-transducing proteins in cancer cells transmit signals from growth factors, promoting cell growth and proliferation.
- Constitutive activation of signal-transducing proteins allows tumor cells to maintain high sensitivity to normal levels of growth factors.
- Sustained angiogenesis in cancer cells enables the formation of new blood vessels, providing oxygen and nutrients to the tumor.
- Overexpression of growth factor receptors in cancer cells leads to uncontrolled cell growth.
- Regulatory genes are the main targets of genetic damage in carcinogenesis.
- Oncoproteins derived from mutations in protooncogenes promote cell growth and proliferation.
- Sustained angiogenesis in cancer cells enables the formation of new blood vessels, providing oxygen and nutrients to the tumor.
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Description
Test your knowledge of antifungal drugs with this pre-LBL quiz! Questions cover topics such as mycosis, types of medical fungi, the difference between human and fungi cells, the actions of Azoles, side effects of antifungal agents, administration of Amphoterocin-B, and more.
