Daptomycin and lipopeptides US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Daptomycin and lipopeptides. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Daptomycin and lipopeptides US Medical PG Question 1: A 60-year-old man with a history of coronary artery disease and hyperlipidemia presents to his internist for a follow-up visit 3 weeks after visiting an urgent care center for symptoms of cough, fever, and difficulty breathing. He had been prescribed erythromycin in addition to his usual regimen of rosuvastatin and aspirin. With which potential side effect or interaction should the internist be most concerned?
- A. Myalgia due to decreased rosuvastatin metabolism in the presence of erythromycin (Correct Answer)
- B. Gastric bleeding due to decreased aspirin metabolism in the presence of erythromycin
- C. Unstable angina due to decreased rosuvastatin metabolism in the presence of erythromycin
- D. Tinnitus due to decreased aspirin metabolism in the presence of erythromycin
- E. Metabolic acidosis due to decreased aspirin metabolism in the presence of erythromycin
Daptomycin and lipopeptides Explanation: ***Myalgia due to decreased rosuvastatin metabolism in the presence of erythromycin***
- **Rosuvastatin** is metabolized by **CYP3A4** to a lesser extent, but it's also a substrate for **organic anion transporting polypeptide (OATP) 1B1**. **Erythromycin** is a potent **CYP3A4 inhibitor** and can also inhibit **OATP1B1**.
- Inhibition of rosuvastatin metabolism/transport by erythromycin can lead to increased serum concentrations of rosuvastatin, increasing the risk of **statin-induced myopathy** and **rhabdomyolysis**, a severe adverse effect characterized by **myalgia**.
*Gastric bleeding due to decreased aspirin metabolism in the presence of erythromycin*
- **Aspirin's metabolism** is primarily through hydrolysis to salicylic acid; erythromycin does not significantly affect this pathway.
- Gastric bleeding with aspirin is related to its **antiplatelet effects** and direct gastrointestinal irritation, not typically altered metabolism by erythromycin.
*Unstable angina due to decreased rosuvastatin metabolism in the presence of erythromycin*
- While **rosuvastatin levels** might increase, leading to myalgia, this interaction does not directly cause **unstable angina**.
- Unstable angina is a cardiac event related to **coronary artery disease progression** or plaque rupture, not typically a direct drug-drug interaction with erythromycin and rosuvastatin.
*Tinnitus due to decreased aspirin metabolism in the presence of erythromycin*
- **Tinnitus** is a known side effect of **aspirin toxicity**, particularly at high doses (salicylism).
- Erythromycin does not significantly alter aspirin metabolism in a way that would lead to increased aspirin levels and associated tinnitus.
*Metabolic acidosis due to decreased aspirin metabolism in the presence of erythromycin*
- **Metabolic acidosis** can occur with **high-dose aspirin poisoning** (salicylate poisoning).
- There is no known direct interaction between erythromycin and aspirin metabolism that would lead to clinically significant changes in aspirin levels sufficient to cause metabolic acidosis.
Daptomycin and lipopeptides US Medical PG Question 2: An investigator is studying the chemical structure of antibiotics and its effect on bacterial growth. He has synthesized a simple beta-lactam antibiotic and has added a bulky side chain to the molecule that inhibits the access of bacterial enzymes to the beta-lactam ring. The synthesized drug will most likely be appropriate for the treatment of which of the following conditions?
- A. Folliculitis (Correct Answer)
- B. Nocardiosis
- C. Atypical pneumonia
- D. Erythema migrans
- E. Otitis media
Daptomycin and lipopeptides Explanation: ***Folliculitis***
- The bulky side chain provides **steric hindrance** that prevents **staphylococcal beta-lactamases** from accessing and degrading the **beta-lactam ring**.
- This modification creates an **anti-staphylococcal penicillin** (similar to methicillin, nafcillin, or oxacillin), which is effective against **methicillin-sensitive *Staphylococcus aureus* (MSSA)**.
- **Folliculitis** is most commonly caused by *S. aureus*, making this modified beta-lactam an appropriate treatment choice for MSSA-related folliculitis.
- The bulky side chain specifically protects against the **penicillinase** (beta-lactamase) produced by staphylococci.
*Otitis media*
- Otitis media is commonly caused by beta-lactamase-producing organisms like *Haemophilus influenzae* and *Moraxella catarrhalis*.
- However, the beta-lactamases produced by these gram-negative organisms are **not inhibited by bulky side chains** alone.
- Treatment of beta-lactamase-producing *H. influenzae* and *M. catarrhalis* requires **beta-lactamase inhibitors** (such as clavulanic acid combined with amoxicillin), not steric hindrance.
- The mechanism of protection differs: beta-lactamase inhibitors **suicide inhibitors** that bind to the enzyme, whereas bulky side chains provide **physical blocking**.
*Nocardiosis*
- Nocardiosis is caused by *Nocardia* species, which are **aerobic actinomycetes**.
- These bacteria are typically treated with **sulfonamides** (trimethoprim-sulfamethoxazole) for prolonged periods.
- Beta-lactam antibiotics are generally not first-line treatment, as *Nocardia* species often show intrinsic resistance or require specific antibiotic combinations.
*Atypical pneumonia*
- Atypical pneumonia is caused by organisms like *Mycoplasma pneumoniae*, *Chlamydophila pneumoniae*, and *Legionella pneumophila*.
- These organisms lack a **peptidoglycan cell wall**, which is the target of all **beta-lactam antibiotics**.
- Beta-lactams (regardless of modifications) are completely ineffective against atypical pneumonia pathogens.
- Treatment requires **macrolides** (azithromycin), **tetracyclines** (doxycycline), or **fluoroquinolones**.
*Erythema migrans*
- Erythema migrans is the characteristic rash of early **Lyme disease**, caused by *Borrelia burgdorferi*.
- While *Borrelia* is sensitive to certain beta-lactam antibiotics (amoxicillin, ceftriaxone), it does **not produce beta-lactamases**.
- The bulky side chain modification is unnecessary for treating *Borreria* infections, as there is no beta-lactamase to protect against.
- Standard treatment uses doxycycline, amoxicillin, or ceftriaxone—not anti-staphylococcal penicillins.
Daptomycin and lipopeptides US Medical PG Question 3: A 20-year-old woman is brought to the emergency department because of severe muscle soreness, nausea, and darkened urine for 2 days. The patient is on the college track team and has been training intensively for an upcoming event. One month ago, she had a urinary tract infection and was treated with nitrofurantoin. She appears healthy. Her temperature is 37°C (98.6°F), pulse is 64/min, and blood pressure is 110/70 mm Hg. Cardiopulmonary examination shows no abnormalities. The abdomen is soft and non-tender. There is diffuse muscle tenderness over the arms, legs, and back. Laboratory studies show:
Hemoglobin 12.8 g/dL
Leukocyte count 7,000/mm3
Platelet count 265,000/mm3
Serum
Creatine kinase 22,000 U/L
Lactate dehydrogenase 380 U/L
Urine
Blood 3+
Protein 1+
RBC negative
WBC 1–2/hpf
This patient is at increased risk for which of the following complications?
- A. Myocarditis
- B. Metabolic alkalosis
- C. Compartment syndrome
- D. Acute kidney injury (Correct Answer)
- E. Hemolytic anemia
Daptomycin and lipopeptides Explanation: ***Acute kidney injury***
- The patient's elevated **creatine kinase (CK)** of 22,000 U/L, muscle soreness, and dark urine (positive for blood but negative for red blood cells) are all indicative of **rhabdomyolysis**.
- **Rhabdomyolysis** releases large amounts of myoglobin, which is nephrotoxic and can precipitate in the renal tubules, leading to **acute tubular necrosis** and subsequent acute kidney injury.
*Myocarditis*
- While CK elevations can be seen in myocarditis, this patient's presentation is dominated by **skeletal muscle symptoms** and a history of intense exercise.
- There are no specific cardiac symptoms or signs (e.g., chest pain, arrhythmias) to suggest myocardial involvement.
*Metabolic alkalosis*
- Rhabdomyolysis typically causes **metabolic acidosis** due to the release of cellular contents, including phosphate and sulfate.
- There is no clinical or lab evidence (e.g., vomiting, diuretic use) to suggest metabolic alkalosis.
*Compartment syndrome*
- **Compartment syndrome** involves increased pressure within a muscle compartment, leading to pain, pallor, paresthesia, pulselessness, and paralysis.
- While rhabdomyolysis can occasionally lead to severe swelling that causes compartment syndrome, the diffuse muscle tenderness and absence of focal limb findings make it less likely as the primary direct complication.
*Hemolytic anemia*
- Though the urine is positive for blood and negative for RBCs, this is characteristic of **myoglobinuria**, not hemoglobinuria, which would indicate hemolytic anemia.
- The patient's **hemoglobin** is normal (12.8 g/dL), and there are no other signs of hemolysis (e.g., jaundice, reticulocytosis).
Daptomycin and lipopeptides US Medical PG Question 4: Six days after undergoing an elective hip replacement surgery, a 79-year-old man develops dysuria, flank pain, and fever. His temperature is 38.5°C (101.3°F). Examination shows marked tenderness in the right costovertebral area. Treatment with an antibiotic is begun, but his symptoms do not improve. Further evaluation shows that the causal organism produces an enzyme that inactivates the antibiotic via phosphorylation. An agent from which of the following classes of antibiotics was most likely administered?
- A. Macrolides
- B. Tetracyclines
- C. Aminoglycosides (Correct Answer)
- D. Glycopeptides
- E. Fluoroquinolones
Daptomycin and lipopeptides Explanation: ***Aminoglycosides***
- **Aminoglycosides** are commonly inactivated by bacterial enzymes through **phosphorylation**, acetylation, or adenylation, leading to resistance.
- The patient's lack of improvement despite antibiotic treatment and the mechanism of inactivation point towards this class of antibiotics.
*Macrolides*
- **Macrolide resistance** typically involves mechanisms such as modification of the ribosomal binding site (e.g., methylation), drug efflux pumps, or enzymatic inactivation by esterases, not phosphorylation.
- While macrolides can treat various infections, their inactivation mechanism is different from what is described.
*Tetracyclines*
- **Tetracycline resistance** is primarily mediated by bacterial efflux pumps that actively transport the antibiotic out of the cell, or by ribosomal protection proteins that interfere with drug binding.
- **Enzymatic inactivation via phosphorylation** is not a characteristic resistance mechanism for tetracyclines.
*Glycopeptides*
- **Glycopeptide resistance**, particularly to vancomycin, is mainly associated with alterations in the cell wall precursor target (e.g., D-Ala-D-Lac modification), which prevents the antibiotic from binding.
- This mechanism is distinct from enzymatic phosphorylation of the antibiotic molecule itself.
*Fluoroquinolones*
- **Fluoroquinolone resistance** primarily arises from mutations in the genes encoding bacterial DNA gyrase and topoisomerase IV, or via efflux pumps.
- There is no significant mechanism of resistance involving direct enzymatic phosphorylation of fluoroquinolone drugs.
Daptomycin and lipopeptides US Medical PG Question 5: A 31-year-old female with a bacterial infection is prescribed a drug that binds the dipeptide D-Ala-D-Ala. Which of the following drugs was this patient prescribed?
- A. Polymyxin B
- B. Nalidixic acid
- C. Chloramphenicol
- D. Vancomycin (Correct Answer)
- E. Penicillin
Daptomycin and lipopeptides Explanation: ***Vancomycin***
- **Vancomycin** is a glycopeptide antibiotic that directly binds to the **D-Ala-D-Ala** terminus of peptidoglycan precursors.
- This binding prevents the **transpeptidation** and **transglycosylation** steps required for bacterial cell wall synthesis, leading to cell lysis.
*Polymyxin B*
- **Polymyxins** are **cationic detergents** that disrupt the integrity of the bacterial **outer membrane** in Gram-negative bacteria.
- They bind to **lipopolysaccharide (LPS)**, causing increased permeability and leakage of intracellular components, but do not target D-Ala-D-Ala.
*Nalidixic acid*
- **Nalidixic acid** is a **quinolone antibiotic** that inhibits bacterial **DNA gyrase (topoisomerase II)** and **topoisomerase IV**.
- Its mechanism of action involves preventing DNA replication and transcription, not cell wall synthesis or D-Ala-D-Ala binding.
*Chloramphenicol*
- **Chloramphenicol** is an antibiotic that inhibits bacterial **protein synthesis** by binding to the **50S ribosomal subunit**.
- It prevents the formation of **peptide bonds** by inhibiting peptidyl transferase, an entirely different target from D-Ala-D-Ala in the cell wall.
*Penicillin*
- **Penicillin** is a beta-lactam antibiotic that inhibits bacterial cell wall synthesis by binding to and inactivating **penicillin-binding proteins (PBPs)**.
- PBPs are **transpeptidases** involved in cross-linking peptidoglycan, but penicillin does not directly bind to the D-Ala-D-Ala substrate itself; instead, it prevents the enzymes from using it.
Daptomycin and lipopeptides US Medical PG Question 6: A drug that inhibits mRNA synthesis has the well-documented side effect of red-orange body fluids. For which of the following is this drug used as monotherapy?
- A. Brucellosis
- B. Tuberculosis
- C. Methicillin-resistant staphylococcus aureus infection
- D. Mycobacterium avium intracellulare infection
- E. Neisseria meningitidis prophylaxis (Correct Answer)
Daptomycin and lipopeptides Explanation: ***Neisseria meningitidis prophylaxis***
- The drug described is **rifampin**, which inhibits bacterial **DNA-dependent RNA polymerase**, thereby blocking **mRNA synthesis** and causes characteristic **red-orange discoloration of body fluids** (tears, urine, sweat).
- Rifampin is used as **monotherapy** for **prophylaxis** against **Neisseria meningitidis** infection in close contacts of infected patients.
- This is the **only indication** where rifampin monotherapy is appropriate, as prophylaxis requires short-term use where resistance development is not a concern.
*Tuberculosis*
- Rifampin is a **first-line agent** for tuberculosis treatment and a cornerstone of all TB regimens.
- However, it is **never used as monotherapy** for TB due to rapid development of resistance.
- Standard TB treatment requires **multidrug therapy** with rifampin, isoniazid, pyrazinamide, and ethambutol (RIPE) for initial phase.
*Methicillin-resistant Staphylococcus aureus infection*
- Rifampin is sometimes used in **combination** with other antibiotics (e.g., vancomycin, daptomycin) to treat **MRSA infections**, especially those involving **prosthetic devices** or **biofilms**.
- It is **not used as monotherapy** for active MRSA infections due to extremely high rates of spontaneous resistance.
*Mycobacterium avium intracellulare infection*
- **Mycobacterium avium complex (MAC)** infections require a multidrug regimen, typically including **macrolides (azithromycin or clarithromycin)**, **ethambutol**, and sometimes **rifabutin** (a rifamycin derivative preferred over rifampin).
- **Monotherapy is never appropriate** for MAC infections due to resistance concerns and treatment failure.
*Brucellosis*
- **Brucellosis** treatment requires **combination therapy**, typically **doxycycline plus rifampin** for 6 weeks or longer.
- **Rifampin monotherapy** is inadequate for eradicating Brucella infection and leads to treatment failure and resistance development.
Daptomycin and lipopeptides US Medical PG Question 7: A 63-year-old African American man presents to the physician for a follow-up examination. He has a history of chronic hypertension and type 2 diabetes mellitus. He has no history of coronary artery disease. His medications include aspirin, hydrochlorothiazide, losartan, and metformin. He exercises every day and follows a healthy diet. He does not smoke. He consumes alcohol moderately. There is no history of chronic disease in the family. His blood pressure is 125/75 mm Hg, which is confirmed on a repeat measurement. His BMI is 23 kg/m2. The physical examination shows no abnormal findings. The laboratory test results show:
Serum
HbA1C 6.9%
Total cholesterol 176 mg/dL
Low-density lipoprotein (LDL-C) 105 mg/dL
High-density lipoprotein (HDL-C) 35 mg/dL
Triglycerides 175 mg/dL
The patient's 10-year risk of cardiovascular disease (CVD) is 18.7%. Lifestyle modifications including diet and exercise have been instituted. Which of the following is the most appropriate next step in pharmacotherapy?
- A. Fenofibrate
- B. Atorvastatin (Correct Answer)
- C. Metoprolol
- D. Liraglutide
- E. Lisinopril
Daptomycin and lipopeptides Explanation: ***Atorvastatin***
- This patient has **diabetes mellitus**, an **LDL-C of 105 mg/dL**, and an estimated **10-year CVD risk of 18.7%**. Current guidelines recommend **high-intensity statin therapy** for individuals with diabetes aged 40-75 with an LDL-C >= 70 mg/dL and a 10-year ASCVD risk of 7.5% or higher.
- Atorvastatin is a **high-intensity statin** that can significantly lower LDL-C and reduce cardiovascular event risk.
*Fenofibrate*
- **Fenofibrate** is primarily used to reduce **elevated triglyceride levels** and can increase HDL-C, but it is **not the first-line therapy** for primary prevention of cardiovascular disease in a patient with diabetes and elevated LDL-C like this one.
- Its role is usually considered in cases of **severe hypertriglyceridemia** (typically >500 mg/dL) to prevent pancreatitis, or as an adjunct to statins if triglycerides remain high, but the primary goal here is LDL reduction.
*Metoprolol*
- **Metoprolol** is a **beta-blocker** primarily used for blood pressure control, heart rate reduction, and in conditions like angina or heart failure.
- The patient's **blood pressure is well-controlled** (125/75 mmHg) with his current regimen, and there is no indication for a beta-blocker in this context for primary CVD prevention.
*Liraglutide*
- **Liraglutide** is a **GLP-1 receptor agonist** used in the management of **type 2 diabetes mellitus** to improve glycemic control and has shown cardiovascular benefits.
- However, the patient's **HbA1c of 6.9%** indicates relatively good glycemic control for a patient with diabetes, and the immediate priority for CVD prevention, given his lipid profile and risk, is LDL-C lowering with a statin.
*Lisinopril*
- **Lisinopril** is an **ACE inhibitor** commonly used for **hypertension**, heart failure, and renal protection in diabetes.
- The patient is already on **losartan**, an angiotensin receptor blocker (ARB), which serves a similar purpose, and his **blood pressure is well-controlled**, so adding lisinopril would be redundant and unnecessary for immediate CVD primary prevention.
Daptomycin and lipopeptides US Medical PG Question 8: A 53-year old man presents for a well physical examination. He reports his diet is suboptimal, but otherwise reports a healthy lifestyle. He has no past medical history and only takes a multivitamin. He has a blood pressure of 116/74 mm Hg and a pulse of 76/min. On physical examination, he is in no acute distress, has no cardiac murmurs, and his lung sounds are clear to auscultation bilaterally. You order a lipid panel that returns as follows: LDL 203, HDL 37, TG 292. Of the following, which medication should be initiated?
- A. Ezetimibe 10 mg daily
- B. Colesevelam 3.75 grams daily
- C. Atorvastatin 40 mg daily (Correct Answer)
- D. Fenofibrate 145 mg daily
- E. Simvastatin 10 mg daily
Daptomycin and lipopeptides Explanation: ***Atorvastatin 40 mg***
- This patient has a **very high LDL level of 203 mg/dL** and is over 40 years old, placing him in a high-risk group that warrants initiation of a **high-intensity statin** for primary prevention of cardiovascular disease.
- **Atorvastatin 40 mg** is a high-intensity statin known to reduce LDL cholesterol by 50% or more, which is appropriate for this patient's elevated risk.
*Ezetimibe 10 mg daily*
- **Ezetimibe** works by inhibiting cholesterol absorption in the small intestine and is typically used as an add-on therapy for patients who do not achieve their LDL goals with statins alone, or for those who are statin-intolerant.
- It is not a first-line monotherapy for a patient with such significantly elevated LDL cholesterol.
*Colesevelam 3.75 grams daily*
- **Colesevelam** is a bile acid sequestrant that lowers LDL by increasing its fecal excretion; however, it has a more modest LDL-lowering effect compared to statins and can sometimes increase triglycerides.
- It is not the most effective or appropriate first-line agent, especially given the patient's existing elevated triglyceride levels.
*Fenofibrate 145 mg daily*
- **Fenofibrate** is primarily used to lower **triglycerides** and can mildly raise HDL, but it has minimal effect on LDL cholesterol.
- While the patient has elevated triglycerides, his primary and most significant lipid abnormality requiring immediate intervention for cardiovascular risk reduction is his severely elevated LDL.
*Simvastatin 10 mg daily*
- **Simvastatin 10 mg** is a **low-intensity statin** dose (typical range: 10-20 mg), which is not sufficient for a patient with an LDL of 203 mg/dL and high cardiovascular risk.
- Guidelines recommend a **high-intensity statin** like atorvastatin 40-80 mg or rosuvastatin 20-40 mg for such elevated LDL levels.
Daptomycin and lipopeptides US Medical PG Question 9: A 62-year-old woman presents to her primary care physician for her annual check-up. She has no current complaints and says that she has been healthy over the last year. Her past medical history is significant for obesity and diabetes that is well controlled on metformin. She does not smoke and drinks socially. Selected lab results are shown below:
High-density lipoprotein: 48 mg/dL
Low-density lipoprotein: 192 mg/dL
Triglycerides: 138 mg/dL
Given these results, the patient is placed on the drug that will be the best therapy for these findings. Which of the following is a potential side effect of this treatment?
- A. Gallstones
- B. Pruritus
- C. Gastrointestinal upset
- D. Malabsorption
- E. Hepatotoxicity (Correct Answer)
Daptomycin and lipopeptides Explanation: ***Hepatotoxicity***
- This patient has significantly elevated **LDL cholesterol**, necessitating treatment with a **statin drug** (HMG-CoA reductase inhibitor).
- A known, though rare, side effect of statin therapy is **hepatotoxicity**, which requires monitoring of **liver enzymes**.
*Gallstones*
- **Fibrates** are a class of lipid-lowering drugs that can increase the risk of **gallstone formation** by increasing cholesterol secretion into bile.
- While fibrates lower triglycerides, they are not the primary treatment for significantly elevated LDL as seen in this patient.
*Pruritus*
- **Niacin** (vitamin B3) is a lipid-lowering agent known for causing significant **cutaneous flushing and pruritus** due to prostaglandin release.
- Niacin is not the first-line treatment for high LDL, especially given the side effect burden.
*Gastrointestinal upset*
- **Bile acid sequestrants** (e.g., cholestyramine, colestipol) often cause gastrointestinal side effects such as **constipation, bloating, and nausea**.
- These drugs are typically used in combination with statins or as an alternative in statin-intolerant patients, but statins are the initial choice for high LDL.
*Malabsorption*
- **Ezetimibe**, a cholesterol absorption inhibitor, can rarely cause gastrointestinal discomfort, but it is not typically associated with widespread **malabsorption of nutrients**.
- Its primary role is to block cholesterol absorption in the small intestine, leading to a modest reduction in LDL, often as an add-on therapy.
Daptomycin and lipopeptides US Medical PG Question 10: Serum studies show a troponin T concentration of 6.73 ng/mL (N < 0.01), and fingerstick blood glucose concentration of 145 mg/dL. The cardiac catheterization team is activated. Treatment with unfractionated heparin, aspirin, ticagrelor, and sublingual nitroglycerin is begun, and the patient's pain subsides. His temperature is 37.3°C (99.1°F), pulse is 65/min, respirations are 23/min, and blood pressure is 91/60 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 96%. Which of the following is the most appropriate additional pharmacotherapy?
- A. Intravenous morphine
- B. Intravenous furosemide
- C. Intravenous insulin
- D. Oral atorvastatin (Correct Answer)
- E. Intravenous nitroglycerin
Daptomycin and lipopeptides Explanation: ***Oral atorvastatin***
- All patients with **acute coronary syndrome (ACS)** should receive high-intensity statin therapy, such as **atorvastatin 80 mg daily**, as early as possible.
- Statins stabilize plaques, reduce inflammation, and improve endothelial function, which are crucial in the acute setting of a myocardial infarction.
*Intravenous morphine*
- Morphine can be used for persistent chest pain refractory to nitroglycerin, but its routine use is now questioned due to potential adverse effects like hypotension and delayed antiplatelet absorption.
- The patient's pain has already subsided with initial treatment, and his blood pressure is already low (91/60 mm Hg), making morphine less appropriate.
*Intravenous furosemide*
- Furosemide is a loop diuretic primarily used for treating **fluid overload** and **pulmonary edema**, which are not indicated by the patient's current presentation (oxygen saturation 96%, no mention of crackles or dyspnea).
- Its use in a patient with **borderline hypotension** could worsen hemodynamic stability.
*Intravenous insulin*
- While the patient has elevated fingerstick glucose (145 mg/dL), this level does not immediately require intravenous insulin unless there is evidence of **diabetic ketoacidosis** or **hyperosmolar hyperglycemic state**, or persistent severe hyperglycemia.
- More moderate hyperglycemia can often be managed with subcutaneous insulin or diet in the acute phase, and focuses remain on cardiac stabilization.
*Intravenous nitroglycerin*
- Intravenous nitroglycerin is indicated for ongoing ischemic chest pain or uncontrolled hypertension in ACS, but the patient's pain has subsided and he is **hypotensive** (91/60 mm Hg).
- Administering more nitroglycerin would likely worsen his hypotension and could compromise coronary perfusion.
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