Corticosteroids and mechanisms US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Corticosteroids and mechanisms. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Corticosteroids and mechanisms US Medical PG Question 1: A 52-year-old man presents to his primary care physician for a yearly checkup complaining of recent weight gain. The patient states that he has noticed that, regardless of his diet, his midsection has gotten increasingly larger and his old clothes no longer fit. The patient has a 2-year history of left hip arthritis from a car accident for which he is on prednisone, as well as a history of migraine headaches. The patient has also noticed that in the last 2 months, he has developed acne and his face has become fuller in appearance. On exam, the patient has gained 26 pounds since his previous checkup 1 year prior, and he now has a BMI 28.2 kg/m^2 (up from 24.1 kg/m^2 previously). His temperature is 98.3°F (36.8°C), blood pressure is 134/94 mmHg, pulse is 72/min, and respirations are 12/min. His physical exam is notable for red striae on his shoulders and around his waist. On his labs, the patient’s serum ACTH is found to be decreased. Which of the following changes is most likely expected?
- A. Bilateral adrenal hyperplasia
- B. Lung malignancy
- C. Unilateral adrenal atrophy
- D. Bilateral adrenal atrophy (Correct Answer)
- E. Unilateral adrenal hyperplasia
Corticosteroids and mechanisms Explanation: **Bilateral adrenal atrophy**
- The patient's symptoms (weight gain, central obesity, red striae, acne, moon facies, hypertension) are consistent with **Cushing's syndrome**.
- Given the history of chronic prednisone use for arthritis and decreased ACTH, this points to **exogenous corticosteroid use** causing suppression of the hypothalamic-pituitary-adrenal (HPA) axis, resulting in bilateral adrenal atrophy.
*Bilateral adrenal hyperplasia*
- This would typically be seen in ACTH-dependent Cushing's syndrome, such as from a **pituitary adenoma** (Cushing's disease), where ACTH levels would be elevated or inappropriately normal, not decreased.
- Adrenal hyperplasia implies increased adrenal gland size and activity, which is contrary to the expected effect of chronic exogenous steroid use.
*Unilateral adrenal atrophy*
- Unilateral atrophy would be highly unusual in the context of chronic exogenous steroid use, which affects both adrenal glands equally through ACTH suppression.
- This might be seen if there was a **unilateral adrenal tumor** producing cortisol, leading to decreased ACTH and atrophy of the contralateral gland, but the provided ACTH level and clinical picture don't support this.
*Lung malignancy*
- While **small cell lung cancer** can cause Cushing's syndrome through ectopic ACTH production, this would present with **elevated ACTH** levels, contradicting the patient's decreased ACTH.
- The primary context here is chronic prednisone use, making ectopic ACTH less likely.
*Unilateral adrenal hyperplasia*
- This could occur with a **unilateral adrenal tumor** producing cortisol, leading to Cushing's syndrome and suppressed ACTH, but would cause atrophy of the *contralateral* adrenal gland, not unilateral hyperplasia alone.
- The patient's history of chronic prednisone use is the key factor, leading to bilateral suppression and atrophy.
Corticosteroids and mechanisms US Medical PG Question 2: A 56-year-old woman visits her primary care provider complaining of fatigue, weight gain, increased thirst, hair loss, and headaches. She has been perimenopausal for 3 years. She was diagnosed with rheumatoid arthritis 4 years ago and prescribed oral prednisolone. Currently, she takes prednisolone and omeprazole daily. Her vital signs are as follows: blood pressure 150/90 mm Hg, heart rate 70/min, respiratory rate 13/min, and temperature 36.6°C (97.9°F). Her weight is 95 kg (209.4 lb), height is 165 cm (5 ft 4 in), BMI is 34.9 kg/m2, waist circumference is 109 cm (42.9 in), and hip circumference is 93 cm (36.6 in). At physical exam, the patient has abdominal obesity, round red face, and increased fat deposition on the back and around the neck. Her skin elasticity is diminished. Cardiac auscultation reveals fixed splitting of S2 with an increased aortic component. The rest of the exam is unremarkable. Blood analysis shows the following findings:
Total serum cholesterol 204.9 mg/dL
HDL 50.3 mg/dL
LDL 131.4 mg/dL
Triglycerides 235.9 mg/dL
Fasting serum glucose 192.0 mg/dL
Which of the following options describes the pathogenesis of the patient’s hyperglycemia?
- A. Glucocorticoids bind to surface receptors of the glomerular endothelial cells and inhibit filtration of glucose.
- B. Glucocorticoids activate surface membrane sodium channels in the islet beta-cells, which leads to Na+ influx and inhibition of insulin synthesis.
- C. Binding of glucocorticoids to surface G-protein-coupled corticosteroid receptors leads to activation of the inositol-3-phosphate pathway and consequent transcription of gluconeogenic enzymes.
- D. Upon activation of intracellular corticosteroid receptors in hepatocytes, its DNA-binding domain binds to glucocorticoid response elements and triggers transcription of gluconeogenic enzymes. (Correct Answer)
- E. Extensive gluconeogenic enzyme transcription is activated by glucocorticoids via the cAMP pathway.
Corticosteroids and mechanisms Explanation: ***Upon activation of intracellular corticosteroid receptors in hepatocytes, its DNA-binding domain binds to glucocorticoid response elements and triggers transcription of gluconeogenic enzymes.***
- This option accurately describes the **genomic mechanism** of glucocorticoid action, where activated intracellular receptors translocate to the nucleus and bind to **glucocorticoid response elements (GREs)** on DNA.
- This binding directly upregulates the transcription of genes encoding **gluconeogenic enzymes** in the liver, leading to increased hepatic glucose production and hyperglycemia.
*Glucocorticoids bind to surface receptors of the glomerular endothelial cells and inhibit filtration of glucose.*
- Glucocorticoids do not generally bind to surface receptors of glomerular endothelial cells to inhibit glucose filtration. **Glucose filtration** is primarily determined by glomerular permeability and renal threshold, not by direct glucocorticoid effects on filtration.
- While glucocorticoids can affect kidney function, their primary mechanism for causing hyperglycemia is not through altered glomerular glucose filtration.
*Glucocorticoids activate surface membrane sodium channels in the islet beta-cells, which leads to Na+ influx and inhibition of insulin synthesis.*
- Glucocorticoids primarily **impair insulin sensitivity** in peripheral tissues and increase hepatic glucose output; they do not typically act by activating surface membrane sodium channels in beta-cells.
- The main mechanism of glucocorticoid-induced beta-cell dysfunction is associated with increased oxidative stress and endoplasmic reticulum stress, not direct Na+ channel activation leading to insulin synthesis inhibition.
*Binding of glucocorticoids to surface G-protein-coupled corticosteroid receptors leads to activation of the inositol-3-phosphate pathway and consequent transcription of gluconeogenic enzymes.*
- Glucocorticoid receptors are **intracellular (nuclear) receptors**, not G-protein-coupled receptors on the cell surface. They act genomically by binding to DNA.
- While some rapid, non-genomic effects of glucocorticoids exist, the primary and sustained hyperglycemic effect is mediated through genomic pathways involving intracellular receptors and GREs.
*Extensive gluconeogenic enzyme transcription is activated by glucocorticoids via the cAMP pathway.*
- Glucocorticoids primarily modulate gene expression directly through **intracellular receptors** binding to GREs, not predominantly via the cAMP pathway.
- The **cAMP pathway** is more commonly associated with hormones like glucagon and catecholamines in regulating gluconeogenesis.
Corticosteroids and mechanisms US Medical PG Question 3: An 8-year-old boy is brought to the pediatrician by his parents due to recurrent episodes of wheezing for the last 2 years. He uses a salbutamol inhaler for relief from wheezing, but his symptoms have recently worsened. He often coughs during the night, which awakens him from sleep almost every other day. He is not able to play football because he starts coughing after 10–15 minutes of play. His current physical examination is completely normal and auscultation of his chest does not reveal any abnormal breath sounds. His peak expiratory flow rate (PEFR) is 75% of expected for his age, gender, and height. After a complete diagnostic evaluation, the pediatrician prescribes a low-dose inhaled fluticasone daily for at least 3 months. He also mentions that the boy may require continuing inhaled corticosteroid (ICS) therapy for a few years if symptoms recur after discontinuation of ICS. However, the parents are concerned about the side effects of corticosteroids. Which of the following corticosteroid-related adverse effects is most likely?
- A. Suppression of hypothalamus-pituitary-adrenal (HPA) axis
- B. Short stature
- C. Posterior subcapsular cataract
- D. Steroid psychosis
- E. Hoarseness of voice (Correct Answer)
Corticosteroids and mechanisms Explanation: ***Hoarseness of voice***
- **Hoarseness (dysphonia)** is the **most common local side effect** of inhaled corticosteroids (ICS) due to irritation of the vocal cords or laryngeal deposition.
- Other local effects include **oral candidiasis (thrush)**, though less common in children than adults.
- These adverse effects are localized to the upper airway and are generally **mild and reversible**.
- Can be **minimized** by using a spacer device and rinsing the mouth after each use.
*Suppression of hypothalamus-pituitary-adrenal (HPA) axis*
- While systemic corticosteroids can cause HPA axis suppression, **low-dose inhaled corticosteroids** have minimal systemic absorption (typically <1% bioavailability).
- HPA suppression is unlikely unless used at **very high doses** (>800 mcg/day fluticasone equivalent) or for prolonged periods.
- The pediatrician prescribed a **low-dose ICS**, significantly reducing the risk of this systemic effect.
*Short stature*
- Some studies have shown a small, **transient reduction in growth velocity** (approximately 1 cm in the first year) during ICS therapy in children.
- This effect is typically **minor and does not significantly impact final adult height**.
- The benefits of asthma control **far outweigh** this minimal growth effect.
- Poorly controlled asthma itself can impair growth more than ICS therapy.
*Posterior subcapsular cataract*
- **Systemic corticosteroids**, particularly with prolonged use, are a known risk factor for posterior subcapsular cataracts.
- **Low-dose inhaled corticosteroids** have a **very low risk** of causing cataracts due to minimal systemic exposure.
- Risk increases only with high doses (>1000 mcg/day) used for many years.
*Steroid psychosis*
- **Steroid psychosis** is a rare but serious neuropsychiatric side effect primarily associated with **high-dose systemic corticosteroids**.
- It is **highly unlikely** to occur with **low-dose inhaled corticosteroids** due to their limited systemic bioavailability.
- This effect is not relevant to the clinical scenario presented.
Corticosteroids and mechanisms US Medical PG Question 4: A 56-year-old woman with rheumatoid arthritis comes to the physician for a follow-up examination. She has no other history of serious illness. Menopause occurred 1 year ago. Current medications include antirheumatic drugs and hormone replacement therapy. She exercises regularly. A DEXA scan shows a T-score of -1.80, indicating decreased bone density. Which of the following drugs is most likely involved in the pathogenesis of this finding?
- A. Naproxen
- B. Medroxyprogesterone acetate
- C. Adalimumab
- D. Prednisone (Correct Answer)
- E. Sulfasalazine
Corticosteroids and mechanisms Explanation: ***Prednisone***
- **Glucocorticoids** like prednisone are a major cause of secondary osteoporosis due to their direct inhibitory effects on osteoblast function and promotion of osteoclast activity.
- Long-term use of prednisone, common in managing rheumatoid arthritis, significantly increases the risk of decreased bone density, even with a history of regular exercise and hormone replacement therapy.
*Naproxen*
- **Naproxen** is a **nonsteroidal anti-inflammatory drug (NSAID)** used for pain and inflammation; it does not directly cause bone loss or osteoporosis.
- While it may be used in rheumatoid arthritis, its mechanism of action does not involve bone metabolism.
*Medroxyprogesterone acetate*
- **Medroxyprogesterone acetate (MPA)** is a progestin that can cause **bone mineral density loss** with long-term use, particularly as a contraceptive injection (Depo-Provera).
- However, the patient is on **hormone replacement therapy** (likely estrogen, which is bone-protective) and MPA's effect on bone is generally less significant than that of glucocorticoids in this context, and it's not a typical long-term RA medication.
*Adalimumab*
- **Adalimumab** is a **TNF-alpha inhibitor** used to treat rheumatoid arthritis; it has no known adverse effect on bone density.
- By controlling the inflammatory process in RA, it may indirectly help preserve bone health by reducing inflammation-induced bone erosion.
*Sulfasalazine*
- **Sulfasalazine** is a **disease-modifying antirheumatic drug (DMARD)** used for rheumatoid arthritis and inflammatory bowel disease.
- It does not have any direct adverse effects on bone density or metabolism.
Corticosteroids and mechanisms US Medical PG Question 5: A 19-year-old woman with a history of poorly controlled asthma presents to her pulmonologist for a follow-up visit. She was recently hospitalized for an asthma exacerbation. It is her third hospitalization in the past five years. She currently takes inhaled salmeterol and medium-dose inhaled budesonide. Her past medical history is also notable for psoriasis. She does not smoke and does not drink alcohol. Her temperature is 98.6°F (37°C), blood pressure is 110/65 mmHg, pulse is 75/min, and respirations are 20/min. Physical examination reveals bilateral wheezes that are loudest at the bases. The patient’s physician decides to start the patient on zileuton. Which of the following is the most immediate downstream effect of initiating zileuton?
- A. Decreased signaling via the leukotriene receptor
- B. Decreased signaling via the muscarinic receptor
- C. Decreased mast cell degranulation
- D. Decreased production of leukotrienes (Correct Answer)
- E. Decreased IgE-mediated pro-inflammatory activity
Corticosteroids and mechanisms Explanation: ***Decreased production of leukotrienes***
- **Zileuton** is a **5-lipoxygenase inhibitor**. This enzyme is crucial for the synthesis of **leukotrienes** from arachidonic acid.
- By inhibiting 5-lipoxygenase, zileuton directly reduces the overall production of all types of leukotrienes, including LTB4, LTC4, LTD4, and LTE4.
*Decreased signaling via the leukotriene receptor*
- This describes the mechanism of action for **leukotriene receptor antagonists** (LTRAs) like montelukast and zafirlukast, which block leukotriene receptors.
- While zileuton ultimately reduces leukotriene effects, its direct and immediate action is on leukotriene synthesis, not receptor blockade.
*Decreased signaling via the muscarinic receptor*
- This is the mechanism of action for **anticholinergic bronchodilators** (e.g., ipratropium, tiotropium), which block the action of acetylcholine at muscarinic receptors.
- Zileuton does not act on the muscarinic receptor system.
*Decreased mast cell degranulation*
- This is the primary action of **mast cell stabilizers** like cromolyn and nedocromil, which prevent the release of inflammatory mediators from mast cells.
- While leukotrienes are involved in inflammation, zileuton's direct action is not on preventing mast cell degranulation itself but rather on blocking a pathway downstream from initial triggers.
*Decreased IgE-mediated pro-inflammatory activity*
- This describes the mechanism of action for **omalizumab**, a monoclonal antibody that targets IgE, preventing its binding to mast cells and basophils.
- Zileuton acts on the leukotriene synthesis pathway, independent of IgE-mediated processes.
Corticosteroids and mechanisms US Medical PG Question 6: A 47-year-old woman presents to the physician with complaints of fatigue accompanied by symmetric pain, swelling, and stiffness in her wrists, fingers, knees, and other joints. She describes the stiffness as being particularly severe upon awakening, but gradually improves as she moves throughout her day. Her physician initially suggests that she take NSAIDs. However, after a few months of minimal symptomatic improvement, she is prescribed an immunosuppressive drug that has a mechanism of preventing IL-2 transcription. What is the main toxicity that the patient must be aware of with this particular class of drugs?
- A. Pancytopenia
- B. Osteoporosis
- C. Hepatotoxicity
- D. Nephrotoxicity (Correct Answer)
- E. Hyperglycemia
Corticosteroids and mechanisms Explanation: ***Nephrotoxicity***
- The drug described, which prevents **IL-2 transcription**, is likely a **calcineurin inhibitor** like cyclosporine or tacrolimus, often used in autoimmune diseases.
- **Nephrotoxicity** (kidney damage) is a major dose-limiting toxicity of calcineurin inhibitors, causing both acute and chronic kidney injury.
*Pancytopenia*
- While some immunosuppressants can cause **pancytopenia** (e.g., azathioprine, methotrexate), it is not the classic or primary toxicity associated with calcineurin inhibitors.
- Calcineurin inhibitors primarily affect **renal function** and can cause other side effects like hypertension or neurotoxicity.
*Osteoporosis*
- **Osteoporosis** is a known side effect of long-term glucocorticoid use, but not typically a primary toxicity of calcineurin inhibitors.
- Glucocorticoids reduce bone formation and increase bone resorption, leading to bone density loss.
*Hepatotoxicity*
- **Hepatotoxicity** (liver damage) can occur with various immunosuppressants, such as methotrexate, but it is not the most prominent or defining toxicity for calcineurin inhibitors.
- While cyclosporine can cause some liver enzyme elevation, **nephrotoxicity** is far more common and severe.
*Hyperglycemia*
- **Hyperglycemia** can be a side effect of some immunosuppressants, particularly **glucocorticoids** and **tacrolimus** (another calcineurin inhibitor).
- However, for the class of drugs that prevent IL-2 transcription (calcineurin inhibitors), **nephrotoxicity** remains the most significant and common major toxicity to be aware of.
Corticosteroids and mechanisms US Medical PG Question 7: A 43-year-old male with a history of thyroid cancer status post total thyroidectomy presents to his primary care physician after repeated bouts of headaches. His headaches are preceded by periods of anxiety, palpitations, and sweating. The patient says he is unable to pinpoint any precipitating factors and instead says the events occur without warning. Of note, the patient's father and uncle also have a history of thyroid cancer. On exam his vitals are: T 36.8 HR 87, BP 135/93, RR 14, and O2 Sat 100% on room air. The patient's TSH is within normal limits, and he reports taking his levothyroxine as prescribed. What is the next best step in diagnosing this patient's chief complaint?
- A. 24-hour urine free cortisol
- B. Plasma aldosterone/renin ratio
- C. Abdominal CT scan with and without IV contrast
- D. Plasma fractionated metanephrines (Correct Answer)
- E. High dose dexamethasone suppression test
Corticosteroids and mechanisms Explanation: ***Plasma fractionated metanephrines***
- The patient's symptoms of **anxiety, palpitations, sweating, and headaches** occurring in discrete "attacks" are classic for a **pheochromocytoma**, a tumor that secretes catecholamines.
- Given the patient's and his family's history of **thyroid cancer**, specifically likely **medullary thyroid cancer** due to the familial link, there is a high suspicion for **Multiple Endocrine Neoplasia type 2 (MEN2)**, which commonly includes pheochromocytoma. **Plasma fractionated metanephrines** are the most sensitive screening test for pheochromocytoma.
*24-hour urine free cortisol*
- This test is used to detect **Cushing's syndrome**, which involves excessive cortisol production.
- Although Cushing's can cause **hypertension**, the paroxysmal symptoms of anxiety, palpitations, and sweating are not typical of Cushing's syndrome.
*Plasma aldosterone/renin ratio*
- This ratio is used to screen for **primary hyperaldosteronism**, a cause of secondary hypertension.
- While the patient has **hypertension (135/93 mm Hg)**, his symptom complex of episodic anxiety, palpitations, and sweating is not characteristic of primary hyperaldosteronism.
*Abdominal CT scan with and without IV contrast*
- An abdominal CT scan can visualize adrenal masses, but it is typically performed *after* biochemical confirmation of a pheochromocytoma to localize the tumor.
- Performing imaging before biochemical testing risks incidentalomas or missing a biochemically active but small tumor, and it is not the most appropriate *next step* in diagnosis given the strong clinical suspicion.
*High dose dexamethasone suppression test*
- This test is specifically used to differentiate between **Cushing's disease** (pituitary ACTH excess) and other causes of Cushing's syndrome.
- The patient's symptoms are not consistent with excessive cortisol production, making this test inappropriate for his chief complaint.
Corticosteroids and mechanisms US Medical PG Question 8: A 56-year-old woman undergoes open reduction and internal fixation of the distal tibia 1 day after a fall. She has had rheumatoid arthritis for 12 years and diabetes mellitus for 2 years. Her medications over the past year have included metformin, prednisone, calcium supplements, and methotrexate. Prior to surgery, insulin was added to her medications, and the dose of prednisone was increased. She has had appropriate nutrition over the years with regular follow-ups with her healthcare professional. Which of the following is the most appropriate supplement to prevent wound failure in this patient?
- A. Glutamine
- B. Zinc
- C. Vitamin A
- D. Arginine
- E. Vitamin C (Correct Answer)
Corticosteroids and mechanisms Explanation: ***Vitamin C***
- This patient is at high risk for **wound healing complications** due to her comorbidities (diabetes, rheumatoid arthritis) and medications (prednisone, methotrexate). **Vitamin C** (ascorbic acid) is essential for **collagen synthesis** and cross-linking, which is crucial for wound strength and tissue repair.
- While other options play a role in wound healing, Vitamin C is particularly important in patients with **impaired healing** due to chronic inflammation, corticosteroid use, and metabolic disorders, as it counteracts their negative effects on collagen formation.
*Glutamine*
- **Glutamine** is an important fuel for rapidly dividing cells, including immune cells and fibroblasts, and can be beneficial in catabolic states.
- However, its role in directly counteracting the specific challenges of this patient's wound healing (corticosteroid use, diabetes, rheumatoid arthritis) is **less direct** compared to Vitamin C's role in collagen synthesis.
*Zinc*
- **Zinc** is a cofactor for numerous enzymes involved in cell proliferation, immune function, and collagen synthesis.
- While important, zinc deficiency is not explicitly indicated, and its role as a primary intervention to prevent wound failure in a patient with **prednisone-induced healing impairment** is secondary to vitamin C.
*Vitamin A*
- **Vitamin A** can help reverse the negative effects of **corticosteroids** on wound healing by promoting epithelialization and collagen synthesis.
- While relevant due to prednisone use, its overall importance in **collagen formation** and direct wound strength is not as profound or broad as Vitamin C.
*Arginine*
- **Arginine** is a precursor for nitric oxide, which improves blood flow to wounds, and is involved in collagen formation and immune function.
- Although beneficial for wound healing, particularly in critically ill patients, it is **not the most appropriate single supplement** for addressing the specific collagen synthesis impairment seen in this patient's context of corticosteroid use and chronic disease.
Corticosteroids and mechanisms US Medical PG Question 9: A 65-year-old woman with COPD comes to the emergency department with 2-day history of worsening shortness of breath and cough. She often has a mild productive cough, but she noticed that her sputum is more yellow than usual. She has not had any recent fevers, chills, sore throat, or a runny nose. Her only medication is a salmeterol inhaler that she uses twice daily. Her temperature is 36.7°C (98°F), pulse is 104/min, blood pressure is 134/73 mm Hg, respiratory rate is 22/min, and oxygen saturation is 85%. She appears uncomfortable and shows labored breathing. Lung auscultation reveals coarse bibasilar inspiratory crackles. A plain film of the chest shows mild hyperinflation and flattening of the diaphragm but no consolidation. She is started on supplemental oxygen via nasal cannula. Which of the following is the most appropriate initial pharmacotherapy?
- A. Albuterol and montelukast
- B. Albuterol and theophylline
- C. Prednisone and albuterol (Correct Answer)
- D. Roflumilast and prednisone
- E. Prednisone and salmeterol
Corticosteroids and mechanisms Explanation: ***Prednisone and albuterol***
- This patient is experiencing an **acute exacerbation of COPD** (AECOPD) characterized by worsening dyspnea, increased sputum purulence (yellow sputum), and elevated respiratory rate, despite no fever or chills. AECOPD is managed with **systemic corticosteroids** (like prednisone) and **short-acting bronchodilators** (like albuterol).
- Prednisone reduces **airway inflammation**, while albuterol provides rapid **bronchodilation** to relieve bronchospasm and improve airflow.
*Albuterol and montelukast*
- **Montelukast** is a leukotriene receptor antagonist used for chronic asthma management and sometimes for COPD patients with an asthmatic component, but it is not a first-line agent for acute exacerbations.
- While **albuterol** is appropriate, montelukast works too slowly to be the primary acute anti-inflammatory agent needed for an AECOPD.
*Albuterol and theophylline*
- **Theophylline** is a phosphodiesterase inhibitor that can improve lung function but has a narrow therapeutic index and significant side effects, making it a less preferred option, especially in acute settings.
- While **albuterol** is appropriate, theophylline is not generally used as an initial agent for AECOPD given safer and more effective alternatives like corticosteroids.
*Roflumilast and prednisone*
- **Roflumilast** is a phosphodiesterase-4 inhibitor used to reduce exacerbations in patients with severe COPD and chronic bronchitis, but it is a chronic medication and not indicated for acute management.
- While **prednisone** is appropriate, roflumilast is not an acute bronchodilator for immediate relief.
*Prednisone and salmeterol*
- **Salmeterol** is a **long-acting beta-agonist (LABA)**, which is part of the patient's maintenance therapy for COPD. In an acute exacerbation, **short-acting bronchodilators** like albuterol are preferred for rapid relief.
- While **prednisone** is appropriate, continuing salmeterol alone as the bronchodilator in an acute setting is insufficient without a short-acting agent.
Corticosteroids and mechanisms US Medical PG Question 10: A previously healthy 30-year-old man comes to the physician because of a 2-week history of lesions on his elbows. He has no history of serious illness and takes no medications. Physical examination shows skin lesions on bilateral elbows. A photograph of his right elbow is shown. Which of the following is the most appropriate treatment for this patient's skin condition?
- A. Diphenhydramine
- B. Ketoconazole
- C. Dapsone
- D. Terbinafine
- E. Calcipotriene (Correct Answer)
Corticosteroids and mechanisms Explanation: ***Calcipotriene***
- The image shows **erythematous plaques with silvery scales on the elbow**, which is characteristic of **psoriasis**.
- **Calcipotriene** (a vitamin D analog) is a topical medication commonly used to treat localized psoriasis by inhibiting keratinocyte proliferation and promoting their differentiation.
*Diphenhydramine*
- **Diphenhydramine** is an antihistamine primarily used for allergic reactions and insomnia.
- It would not address the underlying inflammatory and hyperproliferative pathology of psoriasis.
*Ketoconazole*
- **Ketoconazole** is an antifungal medication used to treat fungal infections of the skin.
- The presented skin lesions are consistent with psoriasis, not a fungal infection.
*Dapsone*
- **Dapsone** is an antibacterial and anti-inflammatory drug used for conditions like leprosy, dermatitis herpetiformis, and some autoimmune skin conditions.
- It is not a first-line treatment for typical plaque psoriasis as seen in this patient.
*Terbinafine*
- **Terbinafine** is an antifungal medication, primarily used for dermatophyte infections such as ringworm or athlete's foot.
- It would be ineffective for psoriasis, which is an autoimmune inflammatory condition.
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