Antifungals

Antifungals US Medical PG Question 1: You are taking care of a patient with renal failure secondary to anti-fungal therapy. The patient is a 66-year-old male being treated for cryptococcal meningitis. This drug has a variety of known side effects including acute febrile reactions to infusions, anemia, hypokalemia and hypomagnesemia. What is the mechanism of action of this drug?

• A. Inhibition of squalene epoxidase
• B. Binding of the 50S subunit
• C. Pore formation secondary to ergosterol binding (Correct Answer)
• D. Disruption of microtubule formation
• E. Inhibition of 1,3-beta-glucan synthase

Antifungals Explanation: ***Pore formation secondary to ergosterol binding*** - This describes the mechanism of action of **amphotericin B**, the antifungal agent used for cryptococcal meningitis. - Amphotericin B binds to **ergosterol** in the fungal cell membrane, leading to the formation of pores, disruption of membrane integrity, and ultimately cell death. - The side effects described—**nephrotoxicity with renal failure, hypokalemia, and hypomagnesemia**—are classic adverse effects of amphotericin B due to its effect on renal tubular cells and electrolyte wasting. *Inhibition of squalene epoxidase* - This is the mechanism of action for **terbinafine**, an antifungal primarily used for dermatophyte infections (e.g., onychomycosis), not systemic infections like cryptococcal meningitis. - Terbinafine inhibits ergosterol synthesis at an earlier step but does not cause the severe nephrotoxicity and electrolyte disturbances described. *Binding of the 50S subunit* - This mechanism of action is characteristic of **macrolide antibiotics** like azithromycin or clarithromycin, which are antibacterial agents, not antifungals. - These drugs inhibit bacterial protein synthesis and are ineffective against fungal infections. *Disruption of microtubule formation* - This is the mechanism of action for **griseofulvin**, an antifungal drug used for dermatophyte infections of the skin, hair, and nails. - Griseofulvin interferes with fungal cell division and is not used for life-threatening systemic infections like cryptococcal meningitis. *Inhibition of 1,3-beta-glucan synthase* - This mechanism is associated with **echinocandins** (e.g., caspofungin, micafungin), which inhibit fungal cell wall synthesis. - While echinocandins are used for some systemic fungal infections (particularly Candida and Aspergillus), they do not typically cause the severe renal failure and electrolyte disturbances characteristic of amphotericin B.

Antifungals US Medical PG Question 2: A 37-year-old woman with a history of anorectal abscesses complains of pain in the perianal region. Physical examination reveals mild swelling, tenderness, and erythema of the perianal skin. She is prescribed oral ampicillin and asked to return for follow-up. Two days later, the patient presents with a high-grade fever, syncope, and increased swelling. Which of the following would be the most common mechanism of resistance leading to the failure of antibiotic therapy in this patient?

• A. Intrinsic absence of a target site for the drug
• B. Use of an altered metabolic pathway
• C. Production of beta-lactamase enzyme (Correct Answer)
• D. Altered structural target for the drug
• E. Drug efflux pump

Antifungals Explanation: ***Production of beta-lactamase enzyme*** - The patient's symptoms of a rapidly worsening infection despite ampicillin treatment suggest the presence of a **beta-lactamase producing organism**. Ampicillin is a **beta-lactam antibiotic** that is inactivated by these enzymes. - Anorectal abscesses and rapidly progressing soft tissue infections are often caused by **polymicrobial flora**, including staphylococci and enterococci, many of which can produce **beta-lactamase**. *Intrinsic absence of a target site for the drug* - While some bacteria inherently lack the target site for certain drugs (e.g., mycoplasma lacking a cell wall, thus being resistant to beta-lactams), this is less likely to be the **most common mechanism of acquired resistance** leading to treatment failure in a typical perianal infection. - The rapid progression and failed initial treatment point towards an **acquired mechanism of resistance** rather than an intrinsic one. *Use of an altered metabolic pathway* - This mechanism, such as altered **folate synthesis pathways** in resistance to trimethoprim-sulfamethoxazole, is less common as the primary mechanism for ampicillin resistance. - Ampicillin's mechanism of action primarily targets the **bacterial cell wall**, not a metabolic pathway in the same way. *Altered structural target for the drug* - This involves modifications to the **penicillin-binding proteins (PBPs)**, which are the targets of beta-lactam antibiotics like ampicillin. While a valid mechanism (e.g., in MRSA), the **production of beta-lactamase** is generally a more widespread and common cause of ampicillin failure, especially in infections involving mixed flora from the perianal region. - Given the abrupt failure of ampicillin, **beta-lactamase inactivation** is a more immediate and common cause than a rapid mutational change in PBPs. *Drug efflux pump* - **Efflux pumps** actively remove antibiotics from the bacterial cell, contributing to resistance against various drug classes. - While efflux pumps can play a role, the dominant mechanism for resistance to **ampicillin** in many common perianal pathogens is the **enzymatic degradation by beta-lactamases**.

Antifungals US Medical PG Question 3: An 18-year old college freshman presents to his university clinic because he has not been feeling well for the past two weeks. He has had a persistent headache, occasional cough, and chills without rigors. The patient’s vital signs are normal and physical exam is unremarkable. His radiograph shows patchy interstitial lung infiltrates and he is diagnosed with atypical pneumonia. The patient is prescribed azithromycin and takes his medication as instructed. Despite adherence to his drug regimen, he returns to the clinic one week later because his symptoms have not improved. The organism responsible for this infection is likely resistant to azithromycin through which mechanism?

• A. Mutation in topoisomerase II
• B. Methylation of ribosomal binding site
• C. Presence of a beta-lactamase
• D. Decreased binding to RNA polymerase
• E. Insertion of drug efflux pumps (Correct Answer)

Antifungals Explanation: ***Insertion of drug efflux pumps*** - **Azithromycin** is a macrolide antibiotic that inhibits bacterial protein synthesis by binding to the **50S ribosomal subunit**. - In **Mycoplasma pneumoniae** (the most common cause of atypical pneumonia in young adults), the **most common** mechanism of macrolide resistance is through **efflux pumps**, particularly the **mef genes**. - These efflux pumps actively transport macrolides out of the bacterial cell, reducing intracellular drug concentration and conferring resistance. - This mechanism is responsible for the majority of macrolide-resistant *M. pneumoniae* isolates worldwide. *Methylation of ribosomal binding site* - **Methylation** of the ribosomal binding site (specifically the **23S rRNA** via erm genes) does prevent azithromycin from binding effectively. - While this is a valid macrolide resistance mechanism seen in organisms like *Streptococcus pneumoniae* and *Streptococcus pyogenes*, it is **less common** in *Mycoplasma pneumoniae*. - Efflux pumps (mef) are the predominant mechanism in *M. pneumoniae* resistant strains. *Mutation in topoisomerase II* - **Topoisomerase II** (DNA gyrase) is the target of **fluoroquinolone antibiotics**, not macrolides. - Mutations in this enzyme lead to resistance against fluoroquinolones, such as **ciprofloxacin**. *Presence of a beta-lactamase* - **Beta-lactamase enzymes** inactivate **beta-lactam antibiotics** (e.g., penicillin, cephalosporins) by hydrolyzing their beta-lactam ring. - Additionally, *Mycoplasma pneumoniae* **lacks a cell wall**, making it inherently resistant to all beta-lactam antibiotics regardless of beta-lactamase production. *Decreased binding to RNA polymerase* - **RNA polymerase** is the target for antibiotics like **rifampin**, which inhibits bacterial transcription. - Decreased binding to RNA polymerase would lead to rifampin resistance, not azithromycin resistance.

Antifungals US Medical PG Question 4: A 57-year-old florist presents to his family physician with nodular lesions on his right hand and forearm. He explains that he got pricked by a rose thorn on his right "pointer finger" where the first lesions appeared, and the other lesions then began to appear in an ascending manner. The physician prescribed a medication and warned him of gynecomastia as a side effect if taken for long periods of time. Which of the following is the mechanism of action of the medication?

• A. Inhibits squalene epoxidase
• B. Binds to ergosterol, forming destructive pores in cell membrane
• C. Disrupts microtubule function
• D. Inhibits ergosterol synthesis (Correct Answer)
• E. Inhibits formation of beta glucan

Antifungals Explanation: ***Inhibits ergosterol synthesis*** - The clinical presentation of **nodular lesions** on the hand and forearm in an **ascending manner** after a rose thorn prick is characteristic of **sporotrichosis**, caused by *Sporothrix schenckii*. - **Itraconazole** is the treatment of choice for sporotrichosis, and it works by **inhibiting ergosterol synthesis** via the inhibition of **lanosterol 14-alpha-demethylase**. Gynecomastia is a known side effect of long-term itraconazole use. *Inhibits squalene epoxidase* - This is the mechanism of action of **terbinafine**, another antifungal agent. - While terbinafine is used for some fungal infections, it is **not the first-line treatment for sporotrichosis** and is not typically associated with gynecomastia as a common side effect. *Binds to ergosterol, forming destructive pores in cell membrane* - This describes the mechanism of action of **amphotericin B** and **nystatin**. - Amphotericin B is used for severe systemic fungal infections, but sporotrichosis typically responds well to oral itraconazole, and amphotericin B is reserved for severe or disseminated cases. *Disrupts microtubule function* - This is the mechanism of action of **griseofulvin**, an antifungal agent primarily used for dermatophyte infections of the skin, hair, and nails. - It is **not effective against *Sporothrix schenckii*** and is not associated with the clinical scenario described. *Inhibits formation of beta glucan* - This is the mechanism of action of **echinocandins** (e.g., caspofungin, micafungin, anidulafungin). - Echinocandins are effective against *Candida* and *Aspergillus* species but have **limited activity against dimorphic fungi** like *Sporothrix schenckii*.

Antifungals US Medical PG Question 5: 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)

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*.

Antifungals US Medical PG Question 6: A 32-year-old woman presents with three-days of vaginal burning, itching, and pain with intercourse. She is in a monogamous relationship with her husband and has an intrauterine device for contraception. Her past medical history is unremarkable, except for recently being treated with antibiotics for sinusitis. Pelvic exam is remarkable for vulvar excoriations, vaginal wall edema, and thick, white discharge in the vault. Wet mount with KOH staining reveals budding filaments with pseudohyphae and hyphae. Which of the following is the most appropriate treatment?

• A. Voriconazole
• B. Posaconazole
• C. Metronidazole
• D. Itraconazole
• E. Fluconazole (Correct Answer)

Antifungals Explanation: ***Fluconazole*** - The patient's symptoms (vaginal burning, itching, pain with intercourse, thick, white discharge) and **wet mount findings (budding filaments with pseudohyphae and hyphae)** are classic for **vulvovaginal candidiasis (VVC)**, often precipitated by recent antibiotic use. - **Fluconazole** is a highly effective and commonly prescribed oral antifungal for uncomplicated VVC due to its convenience and excellent therapeutic profile. *Voriconazole* - **Voriconazole** is a broad-spectrum triazole antifungal primarily used for invasive fungal infections, such as **invasive aspergillosis** and candidemia, and is not a first-line treatment for uncomplicated VVC. - Its use is typically reserved for more severe or refractory systemic fungal infections, and it has a more significant side effect profile than fluconazole. *Posaconazole* - **Posaconazole** is another extended-spectrum triazole antifungal primarily used for the prophylaxis and treatment of **invasive fungal infections** in immunocompromised patients, particularly those unresponsive to other antifungals. - It is not indicated for the treatment of uncomplicated vulvovaginal candidiasis. *Metronidazole* - **Metronidazole** is an antibiotic and antiprotozoal agent used to treat bacterial vaginosis and trichomoniasis, both of which are common causes of vaginitis. - It is **ineffective against fungal infections**, and the patient's symptoms and wet mount findings rule out bacterial vaginosis and trichomoniasis. *Itraconazole* - **Itraconazole** is an antifungal drug effective against superficial and systemic fungal infections, but it is typically used for more severe or recurrent VVC, or in cases of non-albicans Candida species. - While effective, **fluconazole** is generally preferred as the first-line oral treatment for uncomplicated VVC due to its single-dose efficacy and established safety profile for this indication.

Antifungals US Medical PG Question 7: A 31-year-old female undergoing treatment for leukemia is found to have a frontal lobe abscess accompanied by paranasal swelling. She additionally complains of headache, facial pain, and nasal discharge. Biopsy of the infected tissue would most likely reveal which of the following?

• A. Yeast with pseudohyphae
• B. Septate hyphae
• C. Irregular non-septate hyphae (Correct Answer)
• D. Spherules containing endospores
• E. Budding yeast with a narrow base

Antifungals Explanation: ***Irregular non-septate hyphae*** - The clinical presentation of a **leukemic patient** with a **frontal lobe abscess** and **paranasal swelling**, along with headache, facial pain, and nasal discharge, strongly suggests **mucormycosis**. - Mucormycosis is characterized by **broad, ribbon-like, irregular non-septate hyphae** with **right-angle branching** on tissue biopsy, making this the most likely finding. *Yeast with pseudohyphae* - This morphology is characteristic of **Candida species**, which can cause opportunistic infections but typically manifest as candidemia, esophagitis, or vulvovaginitis in immunocompromised patients, not usually a frontal lobe abscess with paranasal involvement. - While Candida can cause severe systemic infections, the specific combination of a frontal lobe abscess and paranasal swelling points away from Candida as the primary cause in this context. *Septate hyphae* - **Septate hyphae** are typical of **Aspergillus species**, which can cause invasive aspergillosis, including sinopulmonary infections and CNS involvement in immunocompromised hosts. - However, Aspergillus hyphae are typically **narrow (3-6 µm)** with **acute-angle (45-degree) branching**, differentiating them from the broad, irregular hyphae seen in mucormycosis. *Spherules containing endospores* - This morphology is characteristic of **Coccidioides immitis**, the causative agent of coccidioidomycosis. - Coccidioidomycosis is geographically restricted to endemic areas (e.g., southwestern US) and typically presents with pulmonary symptoms, disseminated disease, or meningitis, which does not fit the described paranasal and frontal lobe presentation. *Budding yeast with a narrow base* - This morphology is characteristic of **Cryptococcus neoformans**, an encapsulated yeast that commonly causes **meningitis** and **pneumonia** in immunocompromised individuals. - While Cryptococcus can cause CNS infections, the presence of paranasal swelling and the specific description of a frontal lobe abscess make mucormycosis a more fitting diagnosis.

Antifungals US Medical PG Question 8: A 28-year-old male presents to his primary care physician with complaints of intermittent abdominal pain and alternating bouts of constipation and diarrhea. His medical chart is not significant for any past medical problems or prior surgeries. He is not prescribed any current medications. Which of the following questions would be the most useful next question in eliciting further history from this patient?

• A. "Does the diarrhea typically precede the constipation, or vice-versa?"
• B. "Is the diarrhea foul-smelling?"
• C. "Please rate your abdominal pain on a scale of 1-10, with 10 being the worst pain of your life"
• D. "Are the symptoms worse in the morning or at night?"
• E. "Can you tell me more about the symptoms you have been experiencing?" (Correct Answer)

Antifungals Explanation: ***Can you tell me more about the symptoms you have been experiencing?*** - This **open-ended question** encourages the patient to provide a **comprehensive narrative** of their symptoms, including details about onset, frequency, duration, alleviating/aggravating factors, and associated symptoms, which is crucial for diagnosis. - In a patient presenting with vague, intermittent symptoms like alternating constipation and diarrhea, allowing them to elaborate freely can reveal important clues that might not be captured by more targeted questions. *Does the diarrhea typically precede the constipation, or vice-versa?* - While knowing the sequence of symptoms can be helpful in understanding the **pattern of bowel dysfunction**, it is a very specific question that might overlook other important aspects of the patient's experience. - It prematurely narrows the focus without first obtaining a broad understanding of the patient's overall symptomatic picture. *Is the diarrhea foul-smelling?* - Foul-smelling diarrhea can indicate **malabsorption** or **bacterial overgrowth**, which are important to consider in some gastrointestinal conditions. - However, this is a **specific symptom inquiry** that should follow a more general exploration of the patient's symptoms, as it may not be relevant if other crucial details are missed. *Please rate your abdominal pain on a scale of 1-10, with 10 being the worst pain of your life* - Quantifying pain intensity is useful for assessing the **severity of discomfort** and monitoring changes over time. - However, for a patient with intermittent rather than acute, severe pain, understanding the **character, location, and triggers** of the pain is often more diagnostically valuable than just a numerical rating initially. *Are the symptoms worse in the morning or at night?* - Diurnal variation can be relevant in certain conditions, such as inflammatory bowel diseases where nocturnal symptoms might be more concerning, or functional disorders whose symptoms might be stress-related. - This is another **specific question** that should come after gathering a more complete initial picture of the patient's symptoms to ensure no key information is overlooked.

Antifungals US Medical PG Question 9: A 55-year-old woman presents to the physician because of a fever 4 days after discharge from the hospital following induction chemotherapy for acute myeloid leukemia (AML). She has no other complaints and feels well otherwise. Other than the recent diagnosis of AML, she has no history of a serious illness. The temperature is 38.8°C (101.8°F), the blood pressure is 110/65 mm Hg, the pulse is 82/min, and the respirations are 14/min. Examination of the catheter site, skin, head and neck, heart, lungs, abdomen, and perirectal area shows no abnormalities. The results of the laboratory studies show: Hemoglobin 9 g/dL Leukocyte count 800/mm3 Percent segmented neutrophils 40% Platelet count 85,000/mm3 Which of the following is the most appropriate pharmacotherapy at this time?

• A. Valacyclovir
• B. Vancomycin
• C. Imipenem (Correct Answer)
• D. Caspofungin
• E. Ciprofloxacin

Antifungals Explanation: ***Imipenem*** - This patient presents with **febrile neutropenia** (fever >38.3°C and absolute neutrophil count <500/mm³ or expected to fall below 500/mm³). This is a **medical emergency** requiring prompt empiric **broad-spectrum antibiotic** therapy covering **Gram-positive** and **Gram-negative** organisms. - **Imipenem** is a carbapenem antibiotic with broad-spectrum activity, making it an appropriate choice for empiric treatment of febrile neutropenia, especially in high-risk patients like those undergoing induction chemotherapy for AML. *Valacyclovir* - **Valacyclovir** is an antiviral medication used primarily for **herpes simplex** and **varicella-zoster virus** infections. - While immunocompromised patients are susceptible to viral infections, there is no clinical evidence at this time to suggest a viral etiology, and **febrile neutropenia** takes precedence for immediate broad-spectrum antibacterial coverage. *Vancomycin* - **Vancomycin** is an antibiotic that specifically targets **Gram-positive bacteria**, particularly **methicillin-resistant Staphylococcus aureus (MRSA)**. - Empiric vancomycin is not typically recommended as initial sole therapy for febrile neutropenia unless there is strong suspicion of a Gram-positive infection (e.g., catheter-related infection, mucositis, skin and soft tissue infection, or known colonization with MRSA), which is not present here. *Caspofungin* - **Caspofungin** is an **antifungal** medication used to treat invasive fungal infections, including candidiasis and aspergillosis. - Initial management of febrile neutropenia focuses on bacterial infections; empiric antifungal therapy is usually initiated if fever persists despite broad-spectrum antibiotics for several days. *Ciprofloxacin* - **Ciprofloxacin** is a fluoroquinolone antibiotic with good activity against many **Gram-negative bacteria** but limited activity against **Gram-positive organisms** and anaerobes. - While it can be used for prophylaxis or as part of a combination regimen, it is not considered sufficient as a single agent for empiric treatment of **high-risk febrile neutropenia** due to its limited spectrum and increasing resistance patterns.

Antifungals US Medical PG Question 10: A 72-year-old man is brought to the emergency room by his daughter with complaints of a productive cough, rust-colored sputum, and fever for 1 week. He denies any breathlessness or chest pain. The past medical history is unremarkable. The vital signs include a pulse rate of 103/min, respiratory rate of 34/min, and blood pressure of 136/94 mm Hg, with an axillary temperature of 38.9°C (102.0°F). The SaO2 is 86% on room air. The chest examination revealed a dull percussion note and coarse crepitations over the left mid-chest. The patient was admitted to the medical unit and intravenous antibiotics were started. He responded well, but after 2 days an elevated temperature was noted. The patient deteriorated and he was transferred to the intensive care unit. A few days later, his temperature was 39.0°C (103.2°F), the respiratory rate was 23/min, the blood pressure was 78/56 mm Hg, and the SaO2 was 78%. He also had a delayed capillary refill time with a pulse of 141/min. Blood was drawn for the white cell count, which revealed a total count of 17,000/µL. The attending physician decides to begin therapy for the low blood pressure. After administration of the medication, hemodynamic monitoring reveals an increase in mean arterial pressure, increased venous return (reflected by increased central venous pressure), and increased cardiac output. Which of the following medications was most likely administered to the patient?

• A. Captopril
• B. Norepinephrine (Correct Answer)
• C. Low-dose dopamine
• D. Phenoxybenzamine
• E. Isoproterenol

Antifungals Explanation: ***Norepinephrine*** - The graph shows an increase in both **mean arterial pressure (MAP)** and **venous return** (indicated by an increase in central venous pressure and right atrial pressure proxy), as well as an increase in **cardiac output**. This pattern is consistent with the effects of **norepinephrine**, a potent vasoconstrictor and inotropic agent used in **septic shock**. - **Norepinephrine** primarily acts on **alpha-1 adrenergic receptors** to cause widespread **vasoconstriction**, increasing systemic vascular resistance (SVR) and thus MAP. It also has **beta-1 adrenergic effects**, increasing myocardial contractility and heart rate, which contributes to increased cardiac output. *Captopril* - **Captopril** is an **ACE inhibitor** that causes **vasodilation** by preventing the conversion of angiotensin I to angiotensin II, leading to a decrease in blood pressure. - Administering captopril in a patient with **hypotension** and **septic shock** would worsen the condition by further lowering blood pressure, which is contradictory to the graph showing an increase. *Low-dose dopamine* - **Low-dose dopamine** (renal-dose) primarily acts on **dopamine D1 receptors** in the renal, mesenteric, and coronary beds, causing **vasodilation** and increasing blood flow to these organs. - While it might increase renal perfusion, it is not effective in significantly increasing **mean arterial pressure** or venous return in septic shock, and in higher doses, it can increase heart rate excessively. *Phenoxybenzamine* - **Phenoxybenzamine** is an **irreversible alpha-adrenergic blocker**. It causes **vasodilation** by inhibiting the vasoconstrictive effects of catecholamines on alpha-receptors. - Administering phenoxybenzamine in a hypotensive patient would further **decrease blood pressure** and overall vascular resistance, which is the opposite of the desired effect shown in the graph. *Isoproterenol* - **Isoproterenol** is a **pure beta-adrenergic agonist** that stimulates both **beta-1 and beta-2 receptors**. It causes increased heart rate and contractility (beta-1) but also significant **vasodilation** (beta-2). - While it would increase cardiac output, its strong **vasodilatory effects** would likely lead to a decrease in mean arterial pressure, making it unsuitable for treating hypotension in septic shock, which contradicts the graph.

Antifungals Flashcard 1 of 10

Question: Which antifungal inhibits fungal DNA and RNA synthesis?_____

Answer: Flucytosine

Antifungals Flashcard 2 of 10

Question: Which class of antifungals inhibit cell wall synthesis?_____

Answer: Echincandins

Antifungals Flashcard 3 of 10

Question: Echinocandins are antifungal agents that act at the cell _____

Answer: wall

Antifungals Flashcard 4 of 10

Question: The antifungal class echinocandins can be recognized via the suffix _____

Answer: -fungin (ie: caspofungin)

Antifungals Flashcard 5 of 10

Question: Which class of antifungals inhibit synthesis of -glucan?_____

Answer: Echinocandins

Antifungals Flashcard 6 of 10

Question: ketoconazole

Answer: antiandrogen

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

Antifungals Flashcard 7 of 10

Question: Griseofulvin inhibits the action of fungal cell _____

Answer: microtubules

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

Antifungals Flashcard 8 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 

Antifungals Flashcard 9 of 10

Question: Which antifungal agent inhibits fungal protein synthesis? _____

Answer: Flucytosine

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

Antifungals Flashcard 10 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