Antiretroviral resistance — MCQs

10 questions

A 32-year-old man comes to the physician for a follow-up examination 1 week after being admitted to the hospital for oral candidiasis and esophagitis. His CD4+ T lymphocyte count is 180 cells/μL. An HIV antibody test is positive. Genotypic resistance assay shows the virus to be susceptible to all antiretroviral therapy regimens and therapy with dolutegravir, tenofovir, and emtricitabine is initiated. Which of the following sets of laboratory findings would be most likely on follow-up evaluation 3 months later? $$$ CD4 +/CD8 ratio %%% HIV RNA %%% HIV antibody test $$$

An HIV-positive 48-year-old man comes to the emergency department because of a 3-month history of recurrent, painful mouth ulcers. This time, the pain is so severe that the patient cannot eat. He has a history of a seizure disorder but currently does not take any medications. He appears very ill. His temperature is 39.0°C (102.2°F). Physical examination shows numerous vesicular ulcerations on the lips and sloughing of the gums, buccal mucosa, and hard palate. Genetic analysis of the pathogen isolated from the lesions shows a mutation in a gene encoding viral phosphotransferases. Which of the following drugs is the most appropriate treatment?

A 49-year-old homeless man comes to the emergency department because of fatigue, cough, and worsening shortness of breath for 2 weeks. He was diagnosed with HIV-infection 25 years ago but has never had any symptoms. He has always refused to take antiretroviral medication. Pulmonary examination shows diffuse crackles over bilateral lower lung fields. An x-ray of the chest shows diffuse, symmetrical interstitial infiltrates. His serum level of beta-d-glucan is elevated. Further testing shows a heterozygous mutation that prevents entry of HIV into macrophages. Which of the following proteins is most likely affected by the mutation in this patient?

A 27-year-old G2P1 woman is diagnosed with an HIV infection after undergoing routine prenatal blood work testing. Her estimated gestational age by first-trimester ultrasound is 12 weeks. Her CD4 count is 150 cells/mm^3 and her viral load is 126,000 copies/mL. She denies experiencing any symptoms of HIV infection. Which of the following is appropriate management of this patient's pregnancy?

A 32-year-old man presents to an outpatient clinic for tuberculosis prophylaxis before leaving for a trip to Asia, where tuberculosis is endemic. The Mantoux test is positive, but the chest X-ray and AFB sputum culture are negative. He was started on isoniazid. What is the most likely mechanism of resistance to isoniazid?

A scientist is studying the mechanisms by which bacteria become resistant to antibiotics. She begins by obtaining a culture of vancomycin-resistant Enterococcus faecalis and conducts replicate plating experiments. In these experiments, colonies are inoculated onto a membrane and smeared on 2 separate plates, 1 containing vancomycin and the other with no antibiotics. She finds that all of the bacterial colonies are vancomycin resistant because they grow on both plates. She then maintains the bacteria in liquid culture without vancomycin while she performs her other studies. Fifteen generations of bacteria later, she conducts replicate plating experiments again and finds that 20% of the colonies are now sensitive to vancomycin. Which of the following mechanisms is the most likely explanation for why these colonies have become vancomycin sensitive?

A student health coordinator plans on leading a campus-wide HIV screening program that will be free for the entire undergraduate student body. The goal is to capture as many correct HIV diagnoses as possible with the fewest false positives. The coordinator consults with the hospital to see which tests are available to use for this program. Test A has a sensitivity of 0.92 and a specificity of 0.99. Test B has a sensitivity of 0.95 and a specificity of 0.96. Test C has a sensitivity of 0.98 and a specificity of 0.93. Which of the following testing schemes should the coordinator pursue?

An investigator studying viral replication isolates the genetic material of an unidentified virus strain. After exposing a cell culture to the isolated, purified viral genetic material, the cells begin to produce viral polymerase and subsequently replicate the viral genome. Infection with the investigated strain is most likely to cause which of the following conditions?

A 26-year-old female medical student presents to occupational health after sustaining a needlestick injury. She reports that she was drawing blood from an HIV-positive patient when she stuck herself percutaneously while capping the needle. She immediately washed the puncture wound with betadine. The medical student has a negative HIV serology from the beginning of medical school two years ago. She is monogamous with one male partner and denies any intravenous drug use. The source patient was recently diagnosed with HIV, and has a CD4 count of 550 cells/µL. His most recent viral load is 1,800,000 copies/mL, and he was started on HAART three days ago. Which of the following is the best next step to manage the female medical student’s exposure?

Q10

A 35-year-old man comes to the physician because of a 6-month history of fatigue and increased sweating at night. He says that he feels “constantly tired” and needs more rest than usual although he sleeps well. In the morning, his sheets are often wet and his skin is clammy. He has not had any sore throat, runny nose, or cough recently. He has not traveled anywhere. Over the past 4 months, he has had a 6.8-kg (15-lb) weight loss, despite having a normal appetite. He does not drink or urinate more than usual. He is 181 cm (5 ft 11 in) tall and weighs 72 kg (159 lb); BMI is 22 kg/m2. His temperature is 37.9°C (100.2°F), pulse is 65/min, and blood pressure is 120/70 mm Hg. Physical examination shows no abnormalities. An HIV screening test and confirmatory test are both positive. The CD4 count is 600 cells/μl and the viral load is 104 copies/mL. Treatment with lamivudine, zidovudine, and indinavir is begun. The patient is at greatest risk for which of the following adverse effects?

Antiretroviral resistance US Medical PG Practice Questions and MCQs

Question 1: A 32-year-old man comes to the physician for a follow-up examination 1 week after being admitted to the hospital for oral candidiasis and esophagitis. His CD4+ T lymphocyte count is 180 cells/μL. An HIV antibody test is positive. Genotypic resistance assay shows the virus to be susceptible to all antiretroviral therapy regimens and therapy with dolutegravir, tenofovir, and emtricitabine is initiated. Which of the following sets of laboratory findings would be most likely on follow-up evaluation 3 months later? $$$ CD4 +/CD8 ratio %%% HIV RNA %%% HIV antibody test $$$

A. ↓ ↓ negative
B. ↑ ↑ negative
C. ↓ ↑ negative
D. ↑ ↓ positive (Correct Answer)
E. ↓ ↑ positive

Explanation: ***↑ ↓ positive*** - With effective **antiretroviral therapy (ART)**, the **CD4+/CD8 ratio** would increase as **CD4+ T cell counts rise** and **CD8+ T cell counts decrease**. - **HIV RNA (viral load)** would significantly decrease (ideally to undetectable levels) due to the suppression of viral replication, but HIV antibodies would remain positive indefinitely. *↓ ↓ negative* - A decrease in the **CD4+/CD8 ratio** and **HIV RNA** (viral load) along with a negative **HIV antibody test** is inconsistent with successful ART. - A negative HIV antibody test would mean the patient was never infected, which contradicts the initial positive result and symptoms. *↑ ↑ negative* - An increase in the **CD4+/CD8 ratio** is expected with ART, but an increase in **HIV RNA** (viral load) indicates treatment failure. - A negative **HIV antibody test** is impossible after a confirmed positive result, regardless of treatment success. *↓ ↑ negative* - A decrease in the **CD4+/CD8 ratio** would suggest worsening immune function, while an increase in **HIV RNA** indicates treatment failure. - A negative **HIV antibody test** is not possible once a patient has developed antibodies to HIV. *↓ ↑ positive* - A decrease in the **CD4+/CD8 ratio** would indicate immune decline, contrary to the expected improvement with effective ART. - An increase in **HIV RNA (viral load)** would signify treatment failure, even if HIV antibodies remain positive.

Question 2: An HIV-positive 48-year-old man comes to the emergency department because of a 3-month history of recurrent, painful mouth ulcers. This time, the pain is so severe that the patient cannot eat. He has a history of a seizure disorder but currently does not take any medications. He appears very ill. His temperature is 39.0°C (102.2°F). Physical examination shows numerous vesicular ulcerations on the lips and sloughing of the gums, buccal mucosa, and hard palate. Genetic analysis of the pathogen isolated from the lesions shows a mutation in a gene encoding viral phosphotransferases. Which of the following drugs is the most appropriate treatment?

A. Acyclovir
B. Famciclovir
C. Cidofovir
D. Ganciclovir
E. Foscarnet (Correct Answer)

Explanation: ***Foscarnet*** - The presence of **recurrent, painful vesicular ulcerations** in an HIV-positive patient, especially with **gingivostomatitis-like symptoms** (sloughing gums, buccal mucosa), points to a severe **herpes simplex virus (HSV) infection**, likely resistant to nucleoside analogues given the **phosphotransferase mutation**. - **Foscarnet** is a pyrophosphate analog that directly inhibits viral DNA polymerase without requiring phosphorylation by viral thymidine kinase, making it effective against **acyclovir-resistant HSV** strains, which often develop resistance via mutations in viral phosphotransferases or thymidine kinase. *Acyclovir* - **Acyclovir** is a nucleoside analog that requires phosphorylation by viral thymidine kinase (a phosphotransferase) to become active. - A **mutation in viral phosphotransferases** would render the virus resistant to acyclovir, making it an ineffective treatment. *Famciclovir* - **Famciclovir** is a prodrug of penciclovir, which is also a nucleoside analog that requires phosphorylation by viral thymidine kinase for activation. - Similar to acyclovir, a **mutation in viral phosphotransferases** would lead to resistance and make famciclovir ineffective. *Cidofovir* - **Cidofovir** is a nucleotide analog that does not require phosphorylation by viral enzymes for its initial activation. - While it can be effective against some resistant strains, **foscarnet is generally preferred** for severe, resistant HSV infections as cidofovir is primarily used for **CMV retinitis** and is associated with significant nephrotoxicity. *Ganciclovir* - **Ganciclovir** is a nucleoside analog primarily used for **CMV infections**, and it also requires phosphorylation by viral kinases for activation. - It is not the first-line treatment for HSV, and the **phosphotransferase mutation** would likely confer resistance to ganciclovir as well.

Question 3: A 49-year-old homeless man comes to the emergency department because of fatigue, cough, and worsening shortness of breath for 2 weeks. He was diagnosed with HIV-infection 25 years ago but has never had any symptoms. He has always refused to take antiretroviral medication. Pulmonary examination shows diffuse crackles over bilateral lower lung fields. An x-ray of the chest shows diffuse, symmetrical interstitial infiltrates. His serum level of beta-d-glucan is elevated. Further testing shows a heterozygous mutation that prevents entry of HIV into macrophages. Which of the following proteins is most likely affected by the mutation in this patient?

A. ICAM-1
B. Gp120
C. CD4
D. P antigen
E. CCR5 (Correct Answer)

Explanation: ***CCR5*** - The mutation preventing HIV entry into **macrophages** points to an issue with a coreceptor, most commonly **CCR5**, which is crucial for macrophage-tropic HIV strains. - A **heterozygous mutation** in CCR5 (CCR5-Δ32) can confer partial resistance to HIV-1 infection, explaining why the patient has been asymptomatic for 25 years despite refusing antiretroviral therapy. - This is a well-documented host genetic factor that slows HIV disease progression. *ICAM-1* - **ICAM-1 (Intercellular Adhesion Molecule 1)** is involved in cell adhesion and immune cell trafficking, but not directly in HIV entry into macrophages. - Mutations in ICAM-1 would not specifically prevent HIV entry, nor would it explain the long-term asymptomatic status in an HIV-positive individual. *Gp120* - **Gp120** is an HIV envelope glycoprotein that binds to the **CD4 receptor** and a coreceptor (CCR5 or CXCR4) on host cells. - While gp120 is essential for HIV entry, it is a **viral protein**; the question asks about a mutation in a **host protein** that prevents viral entry. *CD4* - **CD4** is the primary receptor for HIV on T cells and macrophages, essential for viral entry. - However, a **heterozygous CD4 mutation** would not provide meaningful protection against HIV, as one functional copy would be sufficient for viral entry. - In contrast, heterozygous **CCR5-Δ32** mutation provides documented partial resistance, making CCR5 the better answer given this patient's 25-year asymptomatic course. *P antigen* - **P antigen** typically refers to a red blood cell antigen and is not involved in HIV entry into macrophages. - There is no known direct association between P antigen and HIV susceptibility or disease progression.

Question 4: A 27-year-old G2P1 woman is diagnosed with an HIV infection after undergoing routine prenatal blood work testing. Her estimated gestational age by first-trimester ultrasound is 12 weeks. Her CD4 count is 150 cells/mm^3 and her viral load is 126,000 copies/mL. She denies experiencing any symptoms of HIV infection. Which of the following is appropriate management of this patient's pregnancy?

A. HAART (Correct Answer)
B. Breastfeeding
C. Vaginal delivery
D. HAART after delivery
E. Avoidance of antibiotic prophylaxis

Explanation: ***HAART*** - **Highly active antiretroviral therapy (HAART)** is recommended immediately for pregnant women with HIV, regardless of CD4 count or viral load, to reduce maternofetal transmission. - Starting HAART early in pregnancy significantly lowers the **viral load**, protecting the fetus from HIV infection. *Breastfeeding* - **Breastfeeding** is contraindicated in HIV-positive mothers in developed countries because it carries a risk of HIV transmission to the infant. - Formula feeding is recommended to prevent **postnatal HIV transmission**. *Vaginal delivery* - A **vaginal delivery** may be considered if the viral load is undetectable or very low (<1,000 copies/mL) at the time of delivery. - Given this patient's **high viral load** (126,000 copies/mL), a scheduled cesarean section would be indicated to minimize the risk of perinatal transmission. *HAART after delivery* - Delaying **HAART until after delivery** would increase the risk of maternofetal HIV transmission during pregnancy and delivery. - Prompt initiation of HAART is crucial for both maternal health and **fetal protection**. *Avoidance of antibiotic prophylaxis* - **Antibiotic prophylaxis** is commonly used in combination with antiretroviral agents to prevent opportunistic infections, especially when the **CD4 count is low** (<200 cells/mm³). - Given a CD4 count of 150 cells/mm³, prophylaxis against opportunistic infections like **Pneumocystis jirovecii pneumonia** might be indicated, making avoidance inappropriate.

Question 5: A 32-year-old man presents to an outpatient clinic for tuberculosis prophylaxis before leaving for a trip to Asia, where tuberculosis is endemic. The Mantoux test is positive, but the chest X-ray and AFB sputum culture are negative. He was started on isoniazid. What is the most likely mechanism of resistance to isoniazid?

A. Methylation of the RNA binding site
B. Plasmid-mediated resistance
C. Reduction of drug binding to RNA polymerase
D. Increased efflux from the cell
E. Mutations in katG (Correct Answer)

Explanation: ***Mutations in katG*** - The **katG gene** encodes **catalase-peroxidase**, an enzyme essential for activating isoniazid into its active form within *Mycobacterium tuberculosis*. - Mutations in *katG* prevent the activation of isoniazid, thereby conferring **resistance**. *Methylation of the RNA binding site* - This mechanism is primarily associated with **aminoglycoside resistance**, where methylation of ribosomal RNA prevents antibiotic binding. - It is not a known mechanism for resistance to **isoniazid**. *Plasmid-mediated resistance* - While common in many bacteria for antibiotic resistance, **plasmid-mediated resistance** is rare for **first-line anti-tuberculosis drugs** like isoniazid in *Mycobacterium tuberculosis*. - Most *M. tuberculosis* resistance mechanisms involve **chromosomal mutations**. *Reduction of drug binding to RNA polymerase* - This mechanism is typically associated with resistance to **rifamycins** (e.g., rifampin), which target the **bacterial RNA polymerase**. - Isoniazid's mechanism of action involves **mycolic acid synthesis inhibition**, not RNA polymerase binding. *Increased efflux from the cell* - While efflux pumps contribute to antibiotic resistance in many bacteria, they are less commonly the primary mechanism for high-level **isoniazid resistance** in *M. tuberculosis*. - Resistance is predominantly linked to target modification or enzyme deficits, like those involving **katG**.

Question 6: A scientist is studying the mechanisms by which bacteria become resistant to antibiotics. She begins by obtaining a culture of vancomycin-resistant Enterococcus faecalis and conducts replicate plating experiments. In these experiments, colonies are inoculated onto a membrane and smeared on 2 separate plates, 1 containing vancomycin and the other with no antibiotics. She finds that all of the bacterial colonies are vancomycin resistant because they grow on both plates. She then maintains the bacteria in liquid culture without vancomycin while she performs her other studies. Fifteen generations of bacteria later, she conducts replicate plating experiments again and finds that 20% of the colonies are now sensitive to vancomycin. Which of the following mechanisms is the most likely explanation for why these colonies have become vancomycin sensitive?

A. Point mutation
B. Gain of function mutation
C. Viral infection
D. Plasmid loss (Correct Answer)
E. Loss of function mutation

Explanation: ***Plasmid loss*** - The initial **vancomycin resistance** in *Enterococcus faecalis* is often mediated by genes located on **plasmids**, which are extrachromosomal DNA. - In the absence of selective pressure (vancomycin), bacteria that lose the plasmid (and thus the resistance genes) have a **growth advantage** over those that retain the energetically costly plasmid, leading to an increase in sensitive colonies over generations. *Point mutation* - A **point mutation** typically involves a change in a single nucleotide and could lead to loss of resistance if it occurred in a gene conferring resistance. - However, since there was no selective pressure for loss of resistance, it is less likely that 20% of the population would acquire such a specific point mutation to revert resistance. *Gain of function mutation* - A **gain of function mutation** would imply that the bacteria acquired a *new* advantageous trait, not the *loss* of resistance. - This type of mutation would not explain why some colonies became sensitive to vancomycin after the drug was removed. *Viral infection* - **Viral infection** (bacteriophages) can transfer genes through transduction or cause bacterial lysis, but it's not the primary mechanism for a widespread reversion of resistance in the absence of antibiotic pressure. - It would not explain the observed increase in vancomycin-sensitive colonies due to evolutionary pressure. *Loss of function mutation* - While a **loss of function mutation** in a gene conferring resistance could lead to sensitivity, it's generally less likely to explain a 20% shift without selective pressure than **plasmid loss**. - Plasmids are often unstable and are easily lost in the absence of selection, whereas a specific gene mutation causing loss of function would need to arise and become prevalent in the population.

Question 7: A student health coordinator plans on leading a campus-wide HIV screening program that will be free for the entire undergraduate student body. The goal is to capture as many correct HIV diagnoses as possible with the fewest false positives. The coordinator consults with the hospital to see which tests are available to use for this program. Test A has a sensitivity of 0.92 and a specificity of 0.99. Test B has a sensitivity of 0.95 and a specificity of 0.96. Test C has a sensitivity of 0.98 and a specificity of 0.93. Which of the following testing schemes should the coordinator pursue?

A. Test A on the entire student body followed by Test B on those who are positive
B. Test A on the entire student body followed by Test C on those who are positive
C. Test C on the entire student body followed by Test B on those who are positive
D. Test C on the entire student body followed by Test A on those who are positive (Correct Answer)
E. Test B on the entire student body followed by Test A on those who are positive

Explanation: ***Test C on the entire student body followed by Test A on those who are positive*** - To "capture as many correct HIV diagnoses as possible" (maximize true positives), the initial screening test should have the **highest sensitivity**. Test C has the highest sensitivity (0.98). - To "capture as few false positives as possible" (maximize true negatives and confirm diagnoses), the confirmatory test should have the **highest specificity**. Test A has the highest specificity (0.99). *Test A on the entire student body followed by Test B on those who are positive* - Starting with Test A (sensitivity 0.92) would miss more true positive cases than starting with Test C (sensitivity 0.98), failing the goal of **capturing as many cases as possible**. - Following with Test B (specificity 0.96) would result in more false positives than following with Test A (specificity 0.99). *Test A on the entire student body followed by Test C on those who are positive* - This scheme would miss many true positive cases initially due to Test A's lower sensitivity compared to Test C. - Following with Test C would introduce more false positives than necessary, as it has a lower specificity (0.93) than Test A (0.99). *Test C on the entire student body followed by Test B on those who are positive* - While Test C is a good initial screen for its high sensitivity, following it with Test B (specificity 0.96) is less optimal than Test A (specificity 0.99) for minimizing false positives in the confirmation step. - This combination would therefore yield more false positives in the confirmatory stage than using Test A. *Test B on the entire student body followed by Test A on those who are positive* - Test B has a sensitivity of 0.95, which is lower than Test C's sensitivity of 0.98, meaning it would miss more true positive cases at the initial screening stage. - While Test A provides excellent specificity for confirmation, the initial screening step is suboptimal for the goal of capturing as many diagnoses as possible.

Question 8: An investigator studying viral replication isolates the genetic material of an unidentified virus strain. After exposing a cell culture to the isolated, purified viral genetic material, the cells begin to produce viral polymerase and subsequently replicate the viral genome. Infection with the investigated strain is most likely to cause which of the following conditions?

A. Rotavirus infection
B. Poliomyelitis (Correct Answer)
C. Hepatitis B
D. Rabies
E. Influenza

Explanation: ***Poliomyelitis*** - The isolation of **purified viral genetic material** directly leading to viral protein production (polymerase) and genome replication indicates the virus has an **RNA genome that can directly serve as mRNA**. - **Poliovirus** is a **positive-sense single-stranded RNA (+ssRNA) virus**, meaning its genome can immediately be translated by host ribosomes upon entry, acting like mRNA. *Rotavirus infection* - Rotavirus is a **double-stranded RNA (dsRNA) virus** and requires its own **RNA-dependent RNA polymerase** to synthesize mRNA before protein production and genome replication can occur. - Its purified genetic material alone would not directly lead to viral protein synthesis in the absence of viral enzymes. *Hepatitis B* - Hepatitis B virus (HBV) is a **DNA virus** and replicates through an **RNA intermediate** via **reverse transcriptase**. - Its genetic material cannot directly initiate the production of viral polymerase or genome replication without complex cellular machinery and viral enzymes. *Rabies* - Rabies virus is a **negative-sense single-stranded RNA (-ssRNA) virus**, which means its genome cannot be directly translated into protein. - It requires its own **RNA-dependent RNA polymerase** to first synthesize complementary positive-sense mRNA strands. *Influenza* - Influenza virus is also a **negative-sense single-stranded RNA (-ssRNA) virus**. - Like rabies, it carries its own **RNA-dependent RNA polymerase** to transcribe its genome into mRNA before protein synthesis can begin.

Question 9: A 26-year-old female medical student presents to occupational health after sustaining a needlestick injury. She reports that she was drawing blood from an HIV-positive patient when she stuck herself percutaneously while capping the needle. She immediately washed the puncture wound with betadine. The medical student has a negative HIV serology from the beginning of medical school two years ago. She is monogamous with one male partner and denies any intravenous drug use. The source patient was recently diagnosed with HIV, and has a CD4 count of 550 cells/µL. His most recent viral load is 1,800,000 copies/mL, and he was started on HAART three days ago. Which of the following is the best next step to manage the female medical student’s exposure?

A. Draw her repeat HIV serology and initiate three-drug antiretroviral therapy if positive
B. Perform genotype testing on source patient and initiate antiretroviral therapy tailored to results
C. Immediately initiate three-drug antiretroviral therapy
D. Draw her repeat HIV serology and immediately initiate three-drug antiretroviral therapy (Correct Answer)
E. Draw her repeat HIV serology and initiate three-drug antiretroviral therapy if negative

Explanation: ***Draw her repeat HIV serology and immediately initiate three-drug antiretroviral therapy*** - This approach ensures that baseline **HIV status** is established while simultaneously providing **post-exposure prophylaxis (PEP)** as quickly as possible. Time is critical for PEP efficacy. - The patient has a high-risk exposure (percutaneous injury, high viral load source) warranting immediate initiation of a **three-drug antiretroviral regimen** to prevent seroconversion. *Draw her repeat HIV serology and initiate three-drug antiretroviral therapy if positive* - Waiting for serology results before initiating therapy would delay PEP, significantly reducing its effectiveness in potentially preventing **HIV transmission**. - If the student is already HIV-positive from a prior undisclosed exposure, PEP for a new exposure is not the primary concern; rather, she would need full **HIV treatment**. However, the immediate concern after an exposure is always prevention. *Immediately initiate three-drug antiretroviral therapy* - While immediate initiation of PEP is correct, it is still crucial to obtain a **baseline HIV serology** for the exposed individual. - This baseline allows for clear documentation of the pre-exposure HIV status, which is vital for any future testing and counseling following the exposure. *Draw her repeat HIV serology and initiate three-drug antiretroviral therapy if negative* - Waiting for serology results to return before starting PEP is incorrect as this would significantly delay the initiation of therapy. - The critical window for effective PEP is within hours of exposure, ideally within 72 hours. *Perform genotype testing on source patient and initiate antiretroviral therapy tailored to results* - While **genotype testing** on the source patient provides valuable information about drug resistance, it should not delay the immediate initiation of **empiric PEP** for the exposed individual. - PEP must be started as soon as possible, and the regimen can be adjusted later if the genotype results indicate resistance to the initial drugs.

Question 10: A 35-year-old man comes to the physician because of a 6-month history of fatigue and increased sweating at night. He says that he feels “constantly tired” and needs more rest than usual although he sleeps well. In the morning, his sheets are often wet and his skin is clammy. He has not had any sore throat, runny nose, or cough recently. He has not traveled anywhere. Over the past 4 months, he has had a 6.8-kg (15-lb) weight loss, despite having a normal appetite. He does not drink or urinate more than usual. He is 181 cm (5 ft 11 in) tall and weighs 72 kg (159 lb); BMI is 22 kg/m2. His temperature is 37.9°C (100.2°F), pulse is 65/min, and blood pressure is 120/70 mm Hg. Physical examination shows no abnormalities. An HIV screening test and confirmatory test are both positive. The CD4 count is 600 cells/μl and the viral load is 104 copies/mL. Treatment with lamivudine, zidovudine, and indinavir is begun. The patient is at greatest risk for which of the following adverse effects?

A. Urolithiasis (Correct Answer)
B. Stevens-Johnson syndrome
C. Hypersensitivity reaction
D. Chronic kidney disease
E. Pancreatitis

Explanation: ***Urolithiasis*** - The patient is receiving **indinavir**, a protease inhibitor known to cause **nephrolithiasis** (kidney stones) due to the drug's poor solubility. - Patients on indinavir should be well-hydrated to reduce the risk of stone formation. *Stevens-Johnson syndrome* - This severe skin reaction is more commonly associated with non-nucleoside reverse transcriptase inhibitors (NNRTIs) like **nevirapine** and **efavirenz**, or with sulfonamide antibiotics, rather than indinavir. - While possible with many drugs, it is not the *greatest risk* among the options for this specific regimen. *Hypersensitivity reaction* - While hypersensitivity can occur with many drugs, particularly abacavir (an NRTI not included in this regimen), it is not the most prominent or specific adverse effect for the given combination, especially indinavir. - Symptoms usually include fever, rash, and multi-organ involvement, which can be acute. *Chronic kidney disease* - While some antiretrovirals, particularly **tenofovir disoproxil fumarate (TDF)**, can cause renal tubular dysfunction and lead to chronic kidney disease, TDF is not part of this patient's regimen. - Indinavir's primary renal complication is acute stone formation, not typically chronic kidney disease in the absence of pre-existing conditions or other nephrotoxic drugs. *Pancreatitis* - Pancreatitis is a known adverse effect of some NRTIs, particularly **didanosine** and **stavudine**, neither of which are in this patient's treatment plan. - Lamivudine and zidovudine have a lower risk of pancreatitis compared to other NRTIs.

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