Drug interactions with antifungals

Drug interactions with antifungals US Medical PG Question 1: A 50-year-old woman presents with acute onset fever and chills for the past hour. She mentions earlier in the day she felt blue, so she took some St. John’s wort because she was told by a friend that it helps with depression. Past medical history is significant for hypertension, diabetes mellitus, and depression managed medically with captopril, metformin, and fluoxetine. She has no history of allergies. Her pulse is 130/min, the respiratory rate is 18/min, the blood pressure is 176/92 mm Hg, and the temperature is 38.5°C (101.3°F). On physical examination, the patient is profusely diaphoretic and extremely irritable when asked questions. Oriented x 3. The abdomen is soft and nontender with no hepatosplenomegaly. Increased bowel sounds are heard in the abdomen. Deep tendon reflexes are 3+ bilaterally and clonus is elicited. The sensation is decreased in the feet bilaterally. Mydriasis is present. Fingerstick glucose is 140 mg/dL. An ECG shows sinus tachycardia but is otherwise normal. Which of the following is the most likely cause of this patient’s condition?

• A. Sepsis
• B. Anaphylactic reaction
• C. Diabetic ketoacidosis
• D. Neuroleptic malignant syndrome
• E. Serotonin syndrome (Correct Answer)

Drug interactions with antifungals Explanation: ***Serotonin syndrome*** - The patient's presentation with **fever, diaphoresis, hypertension, tachycardia, hyperreflexia, clonus, mydriasis**, and **agitation** after combining an **SSRI (fluoxetine)** with **St. John's wort** (a serotonin-enhancing herbal supplement) is highly characteristic of serotonin syndrome. - This condition results from excessive serotonergic activity in the central and peripheral nervous system. *Sepsis* - While **fever, chills, and tachycardia** can be indicators of sepsis, the presence of specific neurological and neuromuscular signs like **hyperreflexia, clonus, and mydriasis** points away from it. - The patient's **irritable state and normal mental orientation** is less typical for severe sepsis, which often involves altered mental status. *Anaphylactic reaction* - **Anaphylaxis** presents with rapid onset of symptoms such as **urticaria, angioedema, bronchospasm, and hypotension**, which are not observed in this patient. - There is no history of allergen exposure, and the prominent neurological symptoms are not typical of anaphylaxis. *Diabetic ketoacidosis* - **DKA** is characterized by **hyperglycemia, metabolic acidosis, and ketonemia**, often presenting with Kussmaul respirations and fruity breath odor. - The patient's **fingerstick glucose (140 mg/dL)** is not significantly elevated, and there is no mention of deep, rapid breathing or other DKA-specific symptoms. *Neuroleptic malignant syndrome* - **NMS** is typically associated with exposure to **dopamine antagonists (antipsychotics)** and is characterized by **severe muscle rigidity, hyperthermia, altered mental status, and autonomic instability.** - While some symptoms overlap, this patient's history of St. John's wort and fluoxetine points to increased serotonin, and the specific neuromuscular findings like clonus are more indicative of serotonin syndrome.

Drug interactions with antifungals US Medical PG Question 2: A 63-year-old man with high blood pressure, dyslipidemia, and diabetes presents to the clinic for routine follow-up. He has no current complaints and has been compliant with his chronic medications. His blood pressure is 132/87 mm Hg and his pulse is 75/min and regular. On physical examination, you notice that he has xanthelasmas on both of his eyelids. He currently uses a statin to lower his LDL but has not reached the LDL goal you have set for him. You would like to add an additional medication for LDL control. Of the following, which statement regarding fibrates is true?

• A. Fibrates inhibit the rate-limiting step in cholesterol synthesis
• B. Fibrates can potentiate the risk of myositis when given with statins (Correct Answer)
• C. Fibrates can cause significant skin flushing and pruritus
• D. Fibrates can increase the risk of cataracts
• E. The primary effect of fibrates is to lower LDL

Drug interactions with antifungals Explanation: ***Fibrates can potentiate the risk of myositis when given with statins*** - **Fibrates** and **statins** can both independently cause muscle toxicity (myopathy, rhabdomyolysis). - When used concomitantly, especially **gemfibrozil** with statins, there is an **increased risk of muscle adverse events** due to pharmacokinetic interactions that raise statin levels. - This combination requires careful monitoring and is often avoided; **fenofibrate** is preferred over gemfibrozil when combination therapy is needed. *Fibrates inhibit the rate-limiting step in cholesterol synthesis* - This statement describes the mechanism of action of **statins**, which inhibit **HMG-CoA reductase**, the rate-limiting enzyme in cholesterol synthesis. - Fibrates, on the other hand, act primarily by activating **PPAR-alpha receptors**, leading to altered lipid metabolism (increased lipoprotein lipase activity, decreased VLDL synthesis). *Fibrates can cause significant skin flushing and pruritus* - **Niacin (nicotinic acid)** is the lipid-modifying agent most commonly associated with significant **skin flushing and pruritus**, mediated by prostaglandin release. - Fibrates do not cause significant flushing; their side effects include GI disturbances, gallstones, and potential muscle toxicity. *Fibrates can increase the risk of cataracts* - This is **not an established adverse effect** of the fibrate class. - While **clofibrate** (an older, largely discontinued fibrate) showed some association with cataracts in older studies, this is not a recognized risk with modern fibrates like **fenofibrate** and **gemfibrozil**. - Current fibrate therapy does not require routine ophthalmologic monitoring for cataracts. *The primary effect of fibrates is to lower LDL* - The primary effect of **fibrates** is to significantly **lower triglycerides** (by 30-50%) and **increase HDL cholesterol** levels (by 10-20%). - While they can cause a modest decrease in LDL cholesterol (10-15%), this is not their primary or most pronounced lipid-modifying effect. - Fibrates are primarily indicated for **hypertriglyceridemia** and mixed dyslipidemia.

Drug interactions with antifungals US Medical PG Question 3: A 45-year-old man presents to the emergency department with difficulties swallowing food. He states that he experiences pain when he attempts to swallow his medications or when he drinks water. He reveals that he was diagnosed with HIV infection five years ago. He asserts that he has been taking his antiretroviral regimen, including emtricitabine, rilpivirine, and tenofovir. His temperature is 98°F (37°C), blood pressure is 100/60 mmHg, pulse is 90/min, respirations are 22/min, and oxygen saturation is 99% on room air. His physical exam is notable for a clear oropharynx, no lymphadenopathy, and a normal cardiac and pulmonary exam. No rashes are noted throughout his body. His laboratory results are displayed below: Hemoglobin: 12 g/dL Hematocrit: 37 % Leukocyte count: 8,000/mm^3 with normal differential Platelet count: 160,000/mm^3 Serum: Na+: 138 mEq/L Cl-: 108 mEq/L K+: 3.5 mEq/L HCO3-: 26 mEq/L BUN: 35 mg/dL Glucose: 108 mg/dL Creatinine: 1.1 mg/dL CD4+ count: 90/mm^3 HIV viral load: 59,000 copies/mL What is the best next step in management?

• A. Fluconazole (Correct Answer)
• B. Nystatin
• C. Oral swab and microscopy
• D. Methylprednisolone
• E. Esophageal endoscopy and biopsy

Drug interactions with antifungals Explanation: ***Fluconazole*** - The patient's **odynophagia**, low **CD4+ count**, and high **HIV viral load** are highly suggestive of **esophageal candidiasis**. - **Fluconazole** is the initial empiric treatment of choice for suspected esophageal candidiasis in HIV-positive patients, given its high efficacy and good tolerability. *Nystatin* - **Nystatin** is typically used for **oral candidiasis (thrush)**, which presents with white plaques in the mouth. - The patient has a **clear oropharynx** and **odynophagia**, indicating esophageal involvement, for which nystatin is less effective. *Oral swab and microscopy* - While an **oral swab** can confirm oral candidiasis, it is not sufficient for diagnosing **esophageal candidiasis**. - Given the patient's symptoms of odynophagia and high clinical suspicion in an immunocompromised patient, empiric treatment is preferred over initial diagnostic testing for uncomplicated esophageal candidiasis. *Methylprednisolone* - **Methylprednisolone** is a corticosteroid used to reduce inflammation and is not indicated for the treatment of **candidal infections**. - Using corticosteroids in an immunocompromised patient with an active opportunistic infection could worsen his condition. *Esophageal endoscopy and biopsy* - **Esophageal endoscopy and biopsy** are typically reserved for patients who **fail empiric antifungal therapy** or present with **atypical symptoms** not consistent with candidiasis. - Given the clear clinical picture, initial empiric treatment with fluconazole is the standard first step.

Drug interactions with antifungals US Medical PG Question 4: A 35-year-old African American male is admitted to the hospital following a recent diagnosis of systemic histoplasmosis and subsequently treated with an intravenous anti-fungal agent. During the course of his hospital stay, he complains of headaches. Work-up reveals hypotension, anemia, and elevated BUN and creatinine. His medication is known to cause these side-effects through its binding of cell membrane ergosterol. With which anti-fungal is he most likely being treated?

• A. Griseofulvin
• B. Amphotericin B (Correct Answer)
• C. Flucytosine
• D. Fluconazole
• E. Terbinafine

Drug interactions with antifungals Explanation: ***Amphotericin B*** - **Amphotericin B** is known for its significant side effects, including **nephrotoxicity** (leading to elevated BUN and creatinine, and potentially anemia due to reduced erythropoietin production) and **infusion-related reactions** like headache and hypotension. - It works by binding to **ergosterol** in fungal cell membranes, forming pores that lead to cell death, but it can also bind to cholesterol in mammalian cell membranes contributing to its toxicity. *Griseofulvin* - **Griseofulvin** primarily acts by binding to **keratin** and interfering with fungal **mitosis**; it does not bind to ergosterol. - Its main side effects include **GI upset**, headache, and photosensitivity, but not prominent nephrotoxicity or hypotension in the manner described. *Flucytosine* - **Flucytosine** is an antimetabolite that is converted to **5-fluorouracil** within fungal cells, interfering with RNA and DNA synthesis. It does not bind to ergosterol. - Its major adverse effects include **bone marrow suppression** (leukopenia, thrombocytopenia) and liver enzyme elevation, not the constellation of symptoms (hypotension, renal failure) described. *Fluconazole* - **Fluconazole** is an azole antifungal that inhibits **ergosterol synthesis** by blocking fungal cytochrome P450 enzymes. It does not directly bind to ergosterol. - While it can cause some GI upset and liver enzyme elevation, it is generally well-tolerated and less associated with acute nephrotoxicity or hypotension compared to Amphotericin B. *Terbinafine* - **Terbinafine** inhibits **squalene epoxidase**, an enzyme involved in ergosterol synthesis, rather than binding directly to ergosterol itself. - Its main side effects include **GI disturbances**, headache, and liver enzyme abnormalities, but typically not the severe nephrotoxicity and hypotension associated with Amphotericin B.

Drug interactions with antifungals US Medical PG Question 5: A 28-year-old woman with HIV comes to the physician because of an 8-day history of severe pain while swallowing. She has been hospitalized several times with opportunistic infections and has poor adherence to her antiretroviral drug regimen. Endoscopy shows extensive, white, plaque-like lesions in the proximal esophagus. Culture of a biopsy specimen grows Candida albicans. Treatment with intravenous anidulafungin is initiated. Which of the following is the primary mechanism of action of this drug?

• A. Binding to tubulin
• B. Inhibition of squalene epoxidase
• C. Decreased DNA synthesis
• D. Binding to ergosterol
• E. Decreased glucan synthesis (Correct Answer)

Drug interactions with antifungals Explanation: ***Decreased glucan synthesis*** - **Anidulafungin** is an **echinocandin** antifungal drug that inhibits the synthesis of **β-(1,3)-D-glucan**, a crucial component of the fungal cell wall. - By disrupting the fungal cell wall, **anidulafungin** causes **osmotic instability** and ultimately leads to cell lysis and death, making it effective against *Candida* infections. *Binding to tubulin* - This is the mechanism of action of **griseofulvin**, an antifungal agent primarily used for dermatophyte infections. - **Griseofulvin** interferes with **microtubule formation**, thus inhibiting fungal mitosis. *Inhibition of squalene epoxidase* - This is the mechanism of action of **terbinafine**, an antifungal drug commonly used for dermatophyte infections like onychomycosis. - **Terbinafine** blocks the synthesis of **ergosterol**, an essential component of the fungal cell membrane, by inhibiting **squalene epoxidase**. *Decreased DNA synthesis* - This mechanism is associated with **flucytosine**, an antifungal agent that is converted to 5-fluorouracil inside fungal cells. - **Flucytosine** then inhibits fungal **DNA and RNA synthesis** and is often used in combination with amphotericin B for severe systemic candidiasis or cryptococcosis. *Binding to ergosterol* - This is the mechanism of action of **polyene antifungals** like **amphotericin B** and **nystatin**. - These drugs bind to **ergosterol** in the fungal cell membrane, forming pores that lead to leakage of intracellular contents and cell death.

Drug interactions with antifungals US Medical PG Question 6: A 12-year-old girl is brought to the physician for a follow-up examination. Two months ago, she was diagnosed with asthma and treatment was begun with an albuterol inhaler as needed. Since then, she has had episodic chest tightness and cough 2–3 times per week. The cough is intermittent and nonproductive; it is worse at night. She has been otherwise healthy and takes no other medications. Her vital signs are within normal limits. Pulmonary examination shows mild expiratory wheezing of all lung fields. Spirometry shows an FEV1:FVC ratio of 81% and an FEV1 of 80% of predicted; FEV1 rises to 93% of predicted after administration of a short-acting bronchodilator. Treatment with low-dose inhaled beclomethasone is begun. The patient is at greatest risk for which of the following adverse effects?

• A. Hypoglycemia
• B. Easy bruisability
• C. Oropharyngeal candidiasis (Correct Answer)
• D. Bradycardia
• E. High-pitched voice

Drug interactions with antifungals Explanation: ***Oropharyngeal candidiasis*** - **Inhaled corticosteroids** like beclomethasone can suppress the local immune response in the oral cavity and pharynx, leading to opportunistic fungal infections. - This condition, commonly known as **thrush**, presents as white patches on the tongue and oral mucosa, which can be mitigated by rinsing the mouth after inhaler use. *Hypoglycemia* - **Inhaled corticosteroids** typically have minimal systemic absorption at low doses and are not associated with hypoglycemia. - **Hypoglycemia** is more commonly associated with diabetes treatment or conditions affecting glucose regulation. *Easy bruisability* - While **systemic corticosteroids** can cause skin thinning and easy bruising with long-term use, **inhaled corticosteroids** at low doses have very limited systemic effects. - The risk of easy bruisability is extremely low with the prescribed treatment in this patient. *Bradycardia* - **Beta-agonists** (like albuterol) can cause tachycardia, but inhaled corticosteroids themselves do not significantly affect heart rate. - **Bradycardia** is not a characteristic adverse effect of beclomethasone; it is typically associated with certain cardiac conditions or medications like beta-blockers. *High-pitched voice* - **Inhaled corticosteroids** can sometimes lead to hoarseness or dysphonia due to local irritation or candidiasis of the vocal cords, but not specifically to a high-pitched voice. - A high-pitched voice is not a recognized adverse effect; rather, a change in voice quality such as hoarseness is more typical.

Drug interactions with antifungals US Medical PG Question 7: A 45-year-old man comes to the physician because of a 3-day history of pain in his mouth and throat and difficulty swallowing. He has a history of COPD, for which he takes theophylline and inhaled budesonide-formoterol. Physical examination shows white patches on the tongue and buccal mucosa that can be scraped off easily. Appropriate pharmacotherapy is initiated. One week later, he returns because of nausea, palpitations, and anxiety. His pulse is 110/min and regular. Physical examination shows a tremor in both hands. Which of the following drugs was most likely prescribed?

• A. Amphotericin B
• B. Griseofulvin
• C. Terbinafine
• D. Fluconazole (Correct Answer)
• E. Nystatin

Drug interactions with antifungals Explanation: ***Fluconazole*** - Fluconazole is a potent **CYP450 inhibitor**, specifically **CYP2C9 and CYP3A4**, which can significantly increase the levels of drugs metabolized by these enzymes, such as **theophylline**. - The patient's symptoms of nausea, palpitations, anxiety, tremor, and tachycardia are consistent with **theophylline toxicity**, which would be exacerbated by co-administration with fluconazole. *Amphotericin B* - Amphotericin B is a powerful antifungal, but its primary side effects include **nephrotoxicity**, **infusion-related reactions** (fever, chills, rigors), and **electrolyte disturbances**, not theophylline toxicity. - It is typically reserved for **severe systemic fungal infections** and is not a first-line treatment for uncomplicated **oral candidiasis**. *Griseofulvin* - Griseofulvin is used to treat **dermatophyte infections** (tinea infections) and is not active against *Candida*. - Its main side effects include **gastrointestinal upset**, **headache**, and **photosensitivity**, and it does not significantly interact with theophylline. *Terbinafine* - Terbinafine is an allylamine antifungal primarily used for **dermatophyte infections**, particularly **onychomycosis**, and is not effective for candidiasis. - While it can cause liver enzyme elevation, it does not typically lead to theophylline toxicity or the constellation of symptoms described. *Nystatin* - Nystatin is a **topical or oral non-absorbable antifungal** used for superficial candidal infections, including oral thrush. - It is not absorbed systemically, so it has **virtually no drug interactions** or systemic side effects, and therefore would not cause theophylline toxicity.

Drug interactions with antifungals US Medical PG Question 8: A 74-year-old man is admitted to the medical ward after he developed a fungal infection. He has aplastic anemia. The most recent absolute neutrophil count was 450/µL. An anti-fungal agent is administered that inhibits the fungal enzyme, (1→3)-β-D-glucan synthase, and thereby disrupts the integrity of the fungal cell wall. He responds well to the treatment. Although amphotericin B is more efficacious for his condition, it was not used because of the side effect profile. What was the most likely infection?

• A. Invasive aspergillosis
• B. Mucormycosis
• C. Histoplasmosis
• D. Paracoccidioidomycosis
• E. Candidemia (Correct Answer)

Drug interactions with antifungals Explanation: ***Candidemia*** - The patient's **neutropenia** (absolute neutrophil count of 450/µL) due to aplastic anemia is a major risk factor for invasive candidiasis, including candidemia. - The antifungal agent's mechanism of action, targeting **(1→3)-β-D-glucan synthase**, is characteristic of **echinocandins**, which are first-line agents for candidemia, especially in critically ill or neutropenic patients, and often preferred over amphotericin B due to a better side effect profile. *Invasive aspergillosis* - While neutropenia is a significant risk factor for invasive aspergillosis, the primary antifungal drugs for this condition are typically **voriconazole** or **isavuconazole**, although echinocandins may be used as salvage therapy or in combination. - The description of the drug's mechanism specifically targeting **(1→3)-β-D-glucan synthase** does not make aspergillosis the *most likely* infection, as some Aspergillus species may have less β-D-glucan in their cell walls compared to *Candida*. *Mucormycosis* - This aggressive fungal infection is often seen in immunocompromised patients, particularly those with **diabetes** or profound neutropenia, but the primary treatment is usually **amphotericin B**. - Mucorales fungi typically **lack ergosterol** and their cell walls do not contain **(1→3)-β-D-glucan**, making echinocandins ineffective. *Histoplasmosis* - This is a dimorphic fungal infection endemic to certain geographic regions, primarily affecting the lungs and disseminating in immunocompromised individuals. - The drug of choice for severe or disseminated histoplasmosis is **amphotericin B**, followed by azoles; echinocandins are generally not active against *Histoplasma*. *Paracoccidioidomycosis* - This is a chronic systemic mycosis found in Latin America, primarily affecting the lungs, skin, and lymph nodes. - Treatment for severe forms typically involves **amphotericin B**, followed by sulfonamides or azoles for maintenance; echinocandins are not effective against *Paracoccidioides*.

Drug interactions with antifungals US Medical PG Question 9: A 57-year-old woman with non-small cell lung cancer comes to the physician 4 weeks after her tumor was resected. She takes no medications. The physician starts her on a treatment regimen that includes vinblastine. This treatment puts the patient at highest risk for which of the following?

• A. Pulmonary embolism
• B. Invasive fungal infection (Correct Answer)
• C. Progressive multifocal leukoencephalopathy
• D. Pulmonary fibrosis
• E. Heart failure

Drug interactions with antifungals Explanation: ***Invasive fungal infection*** - Vinblastine is an **antimitotic chemotherapy agent** that, like other chemotherapeutic agents, can cause **myelosuppression**. - **Myelosuppression** (particularly **neutropenia**) severely compromises the immune system, making patients highly susceptible to **opportunistic infections**, including invasive fungal infections. *Pulmonary embolism* - While cancer itself is a risk factor for **venous thromboembolism**, including pulmonary embolism, vinblastine itself **does not directly increase the risk** more than other chemotherapy agents. - The highest risk with vinblastine specifically relates to its impact on bone marrow. *Progressive multifocal leukoencephalopathy* - This is a rare, severe opportunistic infection of the brain caused by the **JC virus**, primarily seen in patients with **severe immunosuppression**, such as those with HIV/AIDS or on chronic immunosuppressive therapy (e.g., natalizumab). - While chemotherapy can cause immunosuppression, PML is not the most common or highest specific risk directly associated with vinblastine or its immediate, acute side effects compared to myelosuppression and opportunistic infections. *Pulmonary fibrosis* - **Pulmonary fibrosis** is a known side effect of certain chemotherapeutic agents like **bleomycin** and **busulfan**, but it is **not a primary or common adverse effect of vinblastine**. - The side effect profile of vinblastine primarily involves myelosuppression, neurotoxicity, and gastrointestinal effects. *Heart failure* - **Cardiotoxicity leading to heart failure** is a significant concern with certain chemotherapy drugs, particularly **anthracyclines** (e.g., doxorubicin) and some tyrosine kinase inhibitors. - **Vinblastine is not typically associated with cardiotoxicity or heart failure** as a primary or high-risk adverse effect.

Drug interactions with antifungals Flashcard 1 of 10

Question: ketoconazole

Answer: antiandrogen

Extra Information: hirsutism of PCOSgeneral inhibition of steroid synthesisgynecomastian, amenorrhea

Drug interactions with antifungals Flashcard 2 of 10

Question: Griseofulvin inhibits the action of fungal cell _____

Answer: microtubules

Extra Information:    https://onlinemeded.org/spa/microbiology/fungi/acquire?ref=anki 

Drug interactions with antifungals Flashcard 3 of 10

Question: For more severe Tinea infections or persistent Onychomycosis (manifestations of dermatophytes), oral _____ is used

Answer: Griseofulvin

Extra Information:   Watch Epidermophyton spp., Trichophyton spp., Microsporum spp. (dermatophytes) [https://dashboard.sketchy.com/study/medical/courses/medical-microbiology/units/medical-microbiology-fungi/videos/medical-microbiology-fungi-cutaneous-mycoses-epidermophyton-spp-trichophyton-spp-microsporum-spp-dermatophytes?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical] https://onlinemeded.org/spa/dermatology/superficial-skin-infections/acquire?ref=anki 

Drug interactions with antifungals Flashcard 4 of 10

Question: Which antifungal agent inhibits fungal protein synthesis? _____

Answer: Flucytosine

Extra Information:    https://onlinemeded.org/spa/microbiology/fungi/acquire?ref=anki 

Drug interactions with antifungals Flashcard 5 of 10

Question: Which azole is used to treat invasive aspergillosis? _____

Answer: Voriconazole

Extra Information:   Watch Azoles [https://dashboard.sketchy.com/study/medical/courses/medical-pharmacology/units/medical-pharmacology-antimicrobials/videos/medical-pharmacology-antimicrobials-antifungals-azoles?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical] https://onlinemeded.org/spa/microbiology/fungi/acquire?ref=anki  

Drug interactions with antifungals Flashcard 6 of 10

Question: Which azole antifungal is especially prone to inhibition of human CYP450? _____

Answer: Voriconazole

Extra Information:   Watch Azoles [https://dashboard.sketchy.com/study/medical/courses/medical-pharmacology/units/medical-pharmacology-antimicrobials/videos/medical-pharmacology-antimicrobials-antifungals-azoles?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical] https://onlinemeded.org/spa/microbiology/fungi/acquire?ref=anki 

Drug interactions with antifungals Flashcard 7 of 10

Question: Flucytosine is primarily used for _____ meningitis

Answer: cryptococcal

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Drug interactions with antifungals Flashcard 8 of 10

Question: Which antifungal is metabolized to 5-fluorouracil in fungal cells? _____

Answer: Flucytosine

Extra Information:  https://onlinemeded.org/spa/microbiology/fungi/acquire?ref=anki 

Drug interactions with antifungals Flashcard 9 of 10

Question: How is Amphotericin B associated nephrotoxicity prevented? _____

Answer: Hydration w/ IV saline

Extra Information:   Watch Amphotericin, flucytosine [https://dashboard.sketchy.com/study/medical/courses/medical-pharmacology/units/medical-pharmacology-antimicrobials/videos/medical-pharmacology-antimicrobials-antifungals-amphotericin-flucytosine?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical] https://onlinemeded.org/spa/microbiology/fungi/acquire?ref=anki 

Drug interactions with antifungals Flashcard 10 of 10

Question: Azoles are a class of antifungals that can cause _____-toxicity

Answer: hepato

Extra Information:   Watch Azoles [https://dashboard.sketchy.com/study/medical/courses/medical-pharmacology/units/medical-pharmacology-antimicrobials/videos/medical-pharmacology-antimicrobials-antifungals-azoles?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical] https://onlinemeded.org/spa/microbiology/fungi/acquire?ref=anki