A study is conducted to investigate the relationship between the development of type 2 diabetes mellitus and the use of atypical antipsychotic medications in patients with schizophrenia. 300 patients who received the atypical antipsychotic clozapine and 300 patients who received the typical antipsychotic haloperidol in long-acting injectable form were followed for 2 years. At the end of the observation period, the incidence of type 2 diabetes mellitus was compared between the two groups. Receipt of clozapine was found to be associated with an increased risk of diabetes mellitus relative to haloperidol (RR = 1.43, 95% p<0.01).
Developed type 2 diabetes mellitus Did not develop type 2 diabetes mellitus
Clozapine 30 270
Haloperidol 21 279
Based on these results, what proportion of patients receiving clozapine would not have been diagnosed with type 2 diabetes mellitus if they had been taking a typical antipsychotic?
Q72
A forty-five-year-old farmer with past medical history of diabetes, hypertension, and possible narrow angles comes into your emergency room confused, diaphoretic, salivating, vomiting and shedding tears. He has pinpoint pupils. You conclude that he is showing effects of acute organophosphate poisoning. While administering the antidote, you should carefully monitor for which of the following side effects?
Q73
A 57-year-old woman comes to the physician for evaluation of a lump in the right breast that she first noticed a week ago. Biopsy of the mass confirms a diagnosis of a pleomorphic lobular carcinoma-in-situ that is estrogen receptor-positive. The patient undergoes lumpectomy, and treatment with tamoxifen is initiated. Which of the following conditions is most likely to occur as a result of tamoxifen therapy?
Q74
A 61-year-old man with a history of type 1 diabetes mellitus and depression is brought to the emergency department because of increasing confusion and fever over the past 14 hours. Four days ago, he was prescribed metoclopramide by his physician for the treatment of diabetic gastroparesis. His other medications include insulin and paroxetine. His temperature is 39.9°C (103.8°F), pulse is 118/min, and blood pressure is 165/95 mm Hg. Physical examination shows profuse diaphoresis and flushed skin. There is generalized muscle rigidity and decreased deep tendon reflexes. His serum creatine kinase is 1250 U/L. Which of the following drugs is most likely to also cause this patient's current condition?
Q75
A 12-year-old boy is brought by his father to a pediatrician for evaluation of stiff jaw and swallowing difficulty. He has also developed painful body spasms triggered by loud noise, light, and physical touch. His father says that a few days ago, his son continued to play football, even after falling and bruising his arms and knees. On examination, the boy had a sustained facial smile, stiff arched back, and clamped hands. The toxin responsible for these clinical manifestations that travel retrograde in axons of peripheral motor neurons blocks the release of which of the following?
Q76
A 59-year-old man comes to the physician because of a 3-month history of frequent urination. He has to urinate every 1–2 hours during the day and wakes up at least 2–3 times at night to urinate. He also reports that over the last 2 months, he has difficulty initiating micturition and the urinary stream is weak, with prolonged terminal dribbling. His pulse is 72/min, and blood pressure is 158/105 mm Hg. Rectal exam shows a smooth, symmetrically enlarged prostate without any tenderness or irregularities. Prostate-specific antigen is within the reference range and urinalysis shows no abnormalities. A postvoid ultrasound shows a residual bladder volume of 110 mL. Which of the following is the most appropriate next step in management?
Q77
A 75-year-old male arrives by ambulance to the emergency room severely confused. His vitals are T 40 C, HR 120 bpm, BP 80/55 mmHg, RR 25. His wife explains that he injured himself about a week ago while cooking, and several days later his finger became infected, oozing with pus. He ignored her warning to see a doctor and even refused after he developed fever, chills, and severe fatigue yesterday. After being seen by the emergency physician, he was given antibiotics and IV fluids. Following initial resuscitation with IV fluids, he remains hypotensive. The ED physicians place a central venous catheter and begin infusing norepinephrine. Which of the following receptors are activated by norepinephrine?
Q78
A 62-year-old woman is hospitalized for an open reduction of a fracture of her right femur following a motor vehicle accident 2 hours prior. She has had rheumatoid arthritis for 12 years. She was hospitalized 1 month ago for an exacerbation of rheumatoid arthritis. Since then, she has been taking a higher dose of prednisone to control the flare. Her other medications include calcium supplements, methotrexate, and etanercept. She has had appropriate nutrition over the years with regular follow-ups with her healthcare providers. Her vital signs are within normal limits. Cardiovascular examination shows no abnormalities. In order to reduce the risk of post-operative wound failure, which of the following is the most appropriate modification in this patient’s drug regimen?
Q79
A neuroscientist is delivering a lecture on the electrophysiology of the brain. He talks about neuroreceptors which act as ion channels in the neurons. He mentions a specific receptor, which is both voltage-gated and ligand-gated ion channel. Which of the following receptors is most likely to be the one mentioned by the neuroscientist?
Q80
A 31-year-old man is brought to the emergency department because of fever and increasing confusion for the past day. He has bipolar disorder with psychotic features and hypothyroidism. Current medications are lithium, haloperidol, and levothyroxine. He drinks one beer with dinner every night. His speech is confused and he is oriented to person only. His temperature is 40°C (104°F), pulse is 124/min, and blood pressure is 160/110 mm Hg. He appears acutely ill. Examination shows diaphoresis and muscle rigidity. Deep tendon reflexes are 1+ bilaterally. There is minor rigidity of the neck with full range of motion. His lungs are clear to auscultation. The abdomen is soft and nontender. His leukocyte count is 15,100/mm3 and serum creatine kinase activity is 1100 U/L. Which of the following is the most likely diagnosis?
Cholinergic/Adrenergic drugs US Medical PG Practice Questions and MCQs
Question 71: A study is conducted to investigate the relationship between the development of type 2 diabetes mellitus and the use of atypical antipsychotic medications in patients with schizophrenia. 300 patients who received the atypical antipsychotic clozapine and 300 patients who received the typical antipsychotic haloperidol in long-acting injectable form were followed for 2 years. At the end of the observation period, the incidence of type 2 diabetes mellitus was compared between the two groups. Receipt of clozapine was found to be associated with an increased risk of diabetes mellitus relative to haloperidol (RR = 1.43, 95% p<0.01).
Developed type 2 diabetes mellitus Did not develop type 2 diabetes mellitus
Clozapine 30 270
Haloperidol 21 279
Based on these results, what proportion of patients receiving clozapine would not have been diagnosed with type 2 diabetes mellitus if they had been taking a typical antipsychotic?
A. 1.48
B. 0.3 (Correct Answer)
C. 0.43
D. 0.03
E. 33.3
Explanation: ***0.3***
- The question asks for the **proportion of patients** receiving clozapine who *would not have been diagnosed* with type 2 diabetes if they had been taking a **typical antipsychotic (haloperidol)**. This is essentially asking for the **attributable risk proportion** among the exposed.
- First, calculate the **incidence of diabetes in the clozapine group**: 30/300 = 0.10. Then, calculate the **incidence of diabetes in the haloperidol group**: 21/300 = 0.07. The difference in incidence (attributable risk) is 0.10 - 0.07 = 0.03. To find the proportion among those exposed, divide this difference by the incidence in the clozapine group: 0.03 / 0.10 = **0.3**.
*1.48*
- This value is close to the **Relative Risk (RR)** of 1.43, which indicates how many times more likely the clozapine group is to develop diabetes compared to the haloperidol group. It does not represent the proportion of patients who would benefit from switching medications.
- The question asks for a proportion that reflects the prevention of diabetes, not a measure of relative risk.
*0.43*
- This value is close to the **attributable risk fraction** (attributable risk percent / 100), which is calculated as (RR - 1) / RR = (1.43 - 1) / 1.43 = 0.43 / 1.43 ≈ 0.30. It's not a direct proportion of patients.
- While related to the increased risk, 0.43 does not directly answer the question about the proportion of patients who would *not* have developed diabetes if they had taken haloperidol.
*0.03*
- This value represents the **absolute difference in risk (attributable risk)**: 0.10 (clozapine incidence) - 0.07 (haloperidol incidence) = 0.03.
- This is the difference in incidence, not the proportion of clozapine users who would avoid diabetes if they were on haloperidol. The question asks for a proportion *among* those receiving clozapine.
*33.3*
- This value is likely derived from incorrect calculations or misinterpretation of the question as an alternative percentage.
- It does not align with any standard epidemiological measure for comparing the impact of switching medications in the context of attributable risk or risk reduction.
Question 72: A forty-five-year-old farmer with past medical history of diabetes, hypertension, and possible narrow angles comes into your emergency room confused, diaphoretic, salivating, vomiting and shedding tears. He has pinpoint pupils. You conclude that he is showing effects of acute organophosphate poisoning. While administering the antidote, you should carefully monitor for which of the following side effects?
A. Barotrauma to middle ear
B. Bronchospasm
C. Hyperkalemia
D. Acute closed-angle glaucoma (Correct Answer)
E. Tinnitus
Explanation: ***Acute closed-angle glaucoma***
- **Atropine**, a common antidote for organophosphate poisoning, can dilate the pupils and **increase intraocular pressure**, precipitating acute closed-angle glaucoma in susceptible individuals.
- The patient's history of "possible narrow angles" indicates a predisposition to this condition, making careful monitoring essential during atropine administration.
*Barotrauma to middle ear*
- **Barotrauma** is typically associated with changes in **ambient pressure**, such as during air travel or diving.
- There is no direct physiological link between organophosphate poisoning treatment and middle ear barotrauma.
*Bronchospasm*
- **Organophosphate poisoning** *causes* bronchospasm due to excessive cholinergic stimulation, while atropine is used to *reverse* it.
- Therefore, bronchospasm would improve, not worsen, with appropriate antidote administration.
*Hyperkalemia*
- **Hyperkalemia** is not a direct side effect of atropine or a common complication of organophosphate poisoning treatment.
- While electrolyte imbalances can occur in critically ill patients, hyperkalemia is not specifically monitored for in this context.
*Tinnitus*
- **Tinnitus** is a perception of noise or ringing in the ears often associated with **auditory system damage** or certain medications.
- It is not a recognized side effect of atropine or a complication to specifically monitor for in organophosphate poisoning.
Question 73: A 57-year-old woman comes to the physician for evaluation of a lump in the right breast that she first noticed a week ago. Biopsy of the mass confirms a diagnosis of a pleomorphic lobular carcinoma-in-situ that is estrogen receptor-positive. The patient undergoes lumpectomy, and treatment with tamoxifen is initiated. Which of the following conditions is most likely to occur as a result of tamoxifen therapy?
A. Ovarian cancer
B. Endometrial cancer (Correct Answer)
C. Osteoporosis
D. Myelosuppression
E. Cardiotoxicity
Explanation: ***Endometrial cancer***
- Tamoxifen acts as an **estrogen receptor agonist** in the **endometrium**, stimulating endometrial proliferation.
- This proliferative effect significantly **increases the risk of endometrial hyperplasia** and **endometrial cancer** in postmenopausal women.
*Ovarian cancer*
- Tamoxifen is not directly linked to an increased risk of ovarian cancer.
- While it affects estrogen receptors, its primary oncogenic risk is specific to the endometrium due to its agonist activity there.
*Osteoporosis*
- Tamoxifen acts as an **estrogen receptor agonist in bone**, which has a protective effect against bone loss.
- Therefore, it typically **reduces the risk of osteoporosis**, especially in postmenopausal women, rather than causing it.
*Myelosuppression*
- Myelosuppression (bone marrow suppression) is a common side effect of many **chemotherapeutic agents**, but it is **not a typical side effect of tamoxifen**.
- Tamoxifen's mechanism of action as a selective estrogen receptor modulator (SERM) does not primarily target rapidly dividing hematopoietic cells.
*Cardiotoxicity*
- **Cardiotoxicity**, such as **cardiomyopathy** or **heart failure**, is a known side effect of certain oncology drugs like **anthracyclines** (e.g., doxorubicin) and some **HER2-targeted therapies** (e.g., trastuzumab).
- Tamoxifen is **not associated with significant cardiotoxicity**.
Question 74: A 61-year-old man with a history of type 1 diabetes mellitus and depression is brought to the emergency department because of increasing confusion and fever over the past 14 hours. Four days ago, he was prescribed metoclopramide by his physician for the treatment of diabetic gastroparesis. His other medications include insulin and paroxetine. His temperature is 39.9°C (103.8°F), pulse is 118/min, and blood pressure is 165/95 mm Hg. Physical examination shows profuse diaphoresis and flushed skin. There is generalized muscle rigidity and decreased deep tendon reflexes. His serum creatine kinase is 1250 U/L. Which of the following drugs is most likely to also cause this patient's current condition?
A. Fluphenazine (Correct Answer)
B. Tranylcypromine
C. Desflurane
D. Methamphetamine
E. Nortriptyline
Explanation: **Fluphenazine**
- The patient's symptoms (fever, confusion, muscle rigidity, elevated CK, autonomic instability like tachycardia and hypertension) after starting metoclopramide are highly suggestive of **neuroleptic malignant syndrome (NMS)**. Metoclopramide is a **D2 receptor antagonist** that can precipitate NMS. Fluphenazine is a **typical antipsychotic** that also blocks D2 receptors and is a classic cause of NMS.
- The combination of **D2 receptor blockade** (by metoclopramide) and another potent D2 blocker like fluphenazine would significantly increase the risk of NMS.
*Tranylcypromine*
- This drug is a **monoamine oxidase inhibitor (MAOI)**. While it can cause **serotonin syndrome** when combined with serotonergic drugs like paroxetine, the clinical picture of NMS (marked rigidity, very high fever, elevated CK) is distinct from typical serotonin syndrome.
- Serotonin syndrome typically involves **hyperreflexia** and **clonus**, whereas this patient presents with **decreased deep tendon reflexes** and generalized **muscle rigidity**, key features of NMS.
*Desflurane*
- Desflurane is an **inhaled anesthetic** that can trigger **malignant hyperthermia** in susceptible individuals. Malignant hyperthermia shares some features with NMS (hyperthermia, muscle rigidity) but is specifically triggered by inhaled anesthetics and succinylcholine, not D2 antagonists.
- Malignant hyperthermia presents acutely during or immediately after anesthesia exposure, which is not consistent with the patient's presentation following metoclopramide initiation.
*Methamphetamine*
- Methamphetamine is a **stimulant** that can cause hyperthermia, tachycardia, and agitation. However, it does not typically cause the profound **muscle rigidity** and significantly elevated **creatine kinase** characteristic of NMS.
- The mechanism of action for methamphetamine is primarily related to increased release of dopamine, norepinephrine, and serotonin, not D2 receptor blockade leading to NMS.
*Nortriptyline*
- Nortriptyline is a **tricyclic antidepressant (TCA)**. While TCAs can have anticholinergic effects and cause some autonomic instability, they are not typically associated with NMS or malignant hyperthermia.
- Long-term use of TCAs can occasionally contribute to **serotonin syndrome** when combined with other serotonergic agents, but NMS is not a direct result.
Question 75: A 12-year-old boy is brought by his father to a pediatrician for evaluation of stiff jaw and swallowing difficulty. He has also developed painful body spasms triggered by loud noise, light, and physical touch. His father says that a few days ago, his son continued to play football, even after falling and bruising his arms and knees. On examination, the boy had a sustained facial smile, stiff arched back, and clamped hands. The toxin responsible for these clinical manifestations that travel retrograde in axons of peripheral motor neurons blocks the release of which of the following?
A. Serotonin
B. Norepinephrine
C. Acetylcholine
D. GABA (gamma-aminobutyric acid) (Correct Answer)
E. Glutamate
Explanation: ***GABA (gamma-aminobutyric acid)***
- The patient's symptoms (stiff jaw, swallowing difficulty, painful body spasms, opisthotonos, sustained facial smile, clamped hands) are classic for **tetanus**, caused by **Clostridium tetani** producing **tetanospasmin**.
- **Tetanospasmin** travels retrograde in peripheral motor neurons to the spinal cord where it blocks the release of **inhibitory neurotransmitters**, primarily **GABA and glycine**, from **Renshaw cells** and inhibitory interneurons.
- Loss of inhibition leads to **unopposed excitation** of motor neurons, causing **sustained muscle contractions** (rigidity) and **spasms**.
- **Glycine** is the major inhibitory neurotransmitter in the spinal cord, while **GABA** predominates in the brain; both are affected in tetanus.
*Serotonin*
- Serotonin is a **monoamine neurotransmitter** involved in mood, sleep, appetite, and other functions, and its release is not directly inhibited by tetanospasmin.
- Disruptions in serotonin pathways are associated with psychiatric disorders or specific syndromes like **serotonin syndrome**, which presents differently with hyperthermia, altered mental status, and autonomic instability.
*Norepinephrine*
- Norepinephrine is a **catecholamine** involved in the sympathetic nervous system and "fight or flight" response.
- While **autonomic instability** with sympathetic overactivity can occur in severe tetanus as a complication, norepinephrine release is not the primary target of tetanospasmin.
- Tetanus primarily affects **inhibitory interneurons** in the spinal cord, not adrenergic neurons.
*Acetylcholine*
- Acetylcholine is the primary **excitatory neurotransmitter** at the **neuromuscular junction**, causing muscle contraction.
- In tetanus, acetylcholine release at the neuromuscular junction is **not blocked**; instead, the problem is **lack of inhibition** of motor neurons, leading to **excessive** acetylcholine release and unopposed muscle contraction.
- Contrast this with **botulism** (botulinum toxin), which *does* block acetylcholine release at the neuromuscular junction, causing flaccid paralysis.
*Glutamate*
- Glutamate is the main **excitatory neurotransmitter** in the central nervous system.
- Tetanospasmin does not directly block glutamate release; rather, the loss of inhibitory neurotransmitters (GABA and glycine) leads to **unchecked excitation** of motor neurons by glutamate, contributing to the muscle rigidity and spasms.
Question 76: A 59-year-old man comes to the physician because of a 3-month history of frequent urination. He has to urinate every 1–2 hours during the day and wakes up at least 2–3 times at night to urinate. He also reports that over the last 2 months, he has difficulty initiating micturition and the urinary stream is weak, with prolonged terminal dribbling. His pulse is 72/min, and blood pressure is 158/105 mm Hg. Rectal exam shows a smooth, symmetrically enlarged prostate without any tenderness or irregularities. Prostate-specific antigen is within the reference range and urinalysis shows no abnormalities. A postvoid ultrasound shows a residual bladder volume of 110 mL. Which of the following is the most appropriate next step in management?
A. Transurethral resection of the prostate
B. Terazosin therapy (Correct Answer)
C. Bladder catheterization
D. Finasteride therapy
E. Cystoscopy
Explanation: ***Terazosin therapy***
- Terazosin is an **alpha-1 adrenergic antagonist** that blocks receptors in the prostate and bladder neck, causing relaxation of the smooth muscle and improving urinary flow. This is a first-line medical treatment for symptomatic **benign prostatic hyperplasia (BPH)**.
- The patient presents with **obstructive and irritative lower urinary tract symptoms (LUTS)**, a symmetrically enlarged prostate, and a postvoid residual volume that indicates bladder outlet obstruction, all consistent with BPH.
- Alpha-blockers provide **rapid symptom relief** (within days to weeks) and may also help with the patient's **elevated blood pressure** (158/105 mm Hg).
*Transurethral resection of the prostate*
- **Transurethral resection of the prostate (TURP)** is a surgical intervention reserved for patients with severe BPH symptoms refractory to medical therapy or those with complications like recurrent urinary retention or renal dysfunction.
- Given that the patient has not yet tried medical therapy, and his symptoms are not immediately life-threatening, surgery is not the most appropriate first step.
*Bladder catheterization*
- **Bladder catheterization** is indicated for acute urinary retention or in cases of severe bladder obstruction leading to renal impairment.
- While the patient has significant LUTS and a postvoid residual volume, he is not in acute urinary retention, so immediate catheterization is not necessary as a long-term management strategy.
*Finasteride therapy*
- **Finasteride** is a **5-alpha reductase inhibitor** that reduces prostate size by inhibiting the conversion of testosterone to dihydrotestosterone. It is more effective in patients with larger prostate volumes and takes several months to show its full effect.
- Though a valid treatment for BPH, alpha-blockers like terazosin provide faster symptomatic relief by addressing dynamic obstruction and are generally preferred as initial therapy, often in combination with 5-alpha reductase inhibitors for larger prostates.
*Cystoscopy*
- **Cystoscopy** is an invasive procedure used to visualize the bladder and urethra directly. It is typically reserved for cases where there is suspicion of other pathologies like bladder stones, strictures, or bladder cancer, or for preoperative planning.
- The patient's symptoms and examination findings are consistent with BPH, and his PSA is normal, so primary cystoscopy is not indicated as the next step in management.
Question 77: A 75-year-old male arrives by ambulance to the emergency room severely confused. His vitals are T 40 C, HR 120 bpm, BP 80/55 mmHg, RR 25. His wife explains that he injured himself about a week ago while cooking, and several days later his finger became infected, oozing with pus. He ignored her warning to see a doctor and even refused after he developed fever, chills, and severe fatigue yesterday. After being seen by the emergency physician, he was given antibiotics and IV fluids. Following initial resuscitation with IV fluids, he remains hypotensive. The ED physicians place a central venous catheter and begin infusing norepinephrine. Which of the following receptors are activated by norepinephrine?
A. Alpha 1, Alpha 2, Beta 1, Beta 2
B. Alpha 1, Alpha 2, Beta 1 (Correct Answer)
C. Alpha 2
D. Alpha 1, Beta 1, Dopamine 1
E. Alpha 1, Beta 1
Explanation: ***Alpha 1, Alpha 2, Beta 1***
- **Norepinephrine** primarily activates **alpha-1** (peripheral vasoconstriction), **alpha-2** (presynaptic inhibition and some vasoconstriction), and **beta-1** (increased heart rate and contractility) adrenergic receptors.
- These are the **primary receptors** responsible for norepinephrine's clinical effects: vasoconstriction (alpha-1, alpha-2) and positive inotropic/chronotropic effects (beta-1).
- This receptor profile makes norepinephrine an ideal **vasopressor** in septic shock, as seen in this patient.
*Alpha 1, Alpha 2, Beta 1, Beta 2*
- While **norepinephrine** does activate alpha-1, alpha-2, and beta-1 receptors, it has **negligible affinity for beta-2 receptors**.
- **Epinephrine** (not norepinephrine) is the catecholamine with significant **beta-2 activity**, causing bronchodilation and vasodilation in skeletal muscle.
- Including beta-2 is a common mistake when confusing norepinephrine with epinephrine.
*Alpha 2*
- This option is far too incomplete as **norepinephrine** has significant action on **alpha-1** and **beta-1** receptors, which are crucial for its vasoconstrictive and inotropic effects.
- Activating only alpha-2 receptors would primarily lead to presynaptic inhibition and limited vasoconstriction, not the broad cardiovascular support required in septic shock.
*Alpha 1, Beta 1, Dopamine 1*
- While **norepinephrine** does activate **alpha-1** and **beta-1** receptors, it does **not** activate **dopamine 1 (D1) receptors**.
- Only **dopamine** itself or specific **dopamine agonists** stimulate D1 receptors, leading to renal and mesenteric vasodilation.
- This option incorrectly attributes dopaminergic activity to norepinephrine.
*Alpha 1, Beta 1*
- This option correctly identifies two of the main receptors activated by **norepinephrine**: alpha-1 (vasoconstriction) and beta-1 (positive inotropy and chronotropy).
- However, it **omits alpha-2 receptors**, which norepinephrine also activates, contributing to both presynaptic feedback inhibition and additional vasoconstriction.
- While not completely wrong, this is an incomplete answer.
Question 78: A 62-year-old woman is hospitalized for an open reduction of a fracture of her right femur following a motor vehicle accident 2 hours prior. She has had rheumatoid arthritis for 12 years. She was hospitalized 1 month ago for an exacerbation of rheumatoid arthritis. Since then, she has been taking a higher dose of prednisone to control the flare. Her other medications include calcium supplements, methotrexate, and etanercept. She has had appropriate nutrition over the years with regular follow-ups with her healthcare providers. Her vital signs are within normal limits. Cardiovascular examination shows no abnormalities. In order to reduce the risk of post-operative wound failure, which of the following is the most appropriate modification in this patient’s drug regimen?
A. Replacing prednisone with hydrocortisone
B. Applying topical vitamin C
C. Adding zinc supplementation (Correct Answer)
D. Discontinuing steroids before surgery
E. Increasing prednisone dose initially and tapering rapidly after 3 days
Explanation: ***Adding zinc supplementation***
- **Zinc** plays a crucial role in **collagen synthesis**, immune function, and **wound healing**, making supplementation beneficial for reducing post-operative wound failure, especially in patients with chronic inflammatory conditions or those on corticosteroids.
- Chronic inflammation from **rheumatoid arthritis** and long-term **corticosteroid use** can impair zinc absorption and lead to deficiency, which exacerbates wound healing issues.
*Replacing prednisone with hydrocortisone*
- Both **prednisone** and **hydrocortisone** are corticosteroids, and switching between them does not inherently reduce the risk of wound failure.
- While prednisone is converted to prednisolone in the liver, hydrocortisone is directly active; both have similar immunosuppressive and anti-inflammatory effects that can impair wound healing.
*Applying topical vitamin C*
- **Topical vitamin C** is primarily used for its antioxidant properties and role in collagen synthesis in the skin, but its systemic effect on deep surgical wound healing is limited.
- **Systemic vitamin C deficiency** can impair wound healing, but the patient's history of appropriate nutrition suggests this is less likely to be the primary issue.
*Discontinuing steroids before surgery*
- Abruptly discontinuing **prednisone**, especially in a patient on a higher dose for an **RA flare**, carries a high risk of causing an **adrenal crisis**, which is life-threatening.
- Steroids are typically continued at a stress-dose equivalent during surgery to prevent **adrenal insufficiency**, not discontinued.
*Increasing prednisone dose initially and tapering rapidly after 3 days*
- Increasing the **prednisone dose** pre-operatively could further suppress the immune system and impair wound healing, increasing the risk of infection and dehiscence.
- While a **stress-dose steroid** regimen is appropriate, the goal is to provide physiological replacement, not to significantly increase the dose beyond what is necessary to prevent adrenal crisis.
Question 79: A neuroscientist is delivering a lecture on the electrophysiology of the brain. He talks about neuroreceptors which act as ion channels in the neurons. He mentions a specific receptor, which is both voltage-gated and ligand-gated ion channel. Which of the following receptors is most likely to be the one mentioned by the neuroscientist?
A. NMDA receptor (Correct Answer)
B. GABAA receptor
C. AMPA receptor
D. Nicotinic acetylcholine receptor
E. Glycine receptor
Explanation: ***NMDA receptor***
- The **NMDA receptor** is unique among ionotropic glutamate receptors as it functions as both a **ligand-gated** and **voltage-gated** ion channel.
- It requires both the binding of an excitatory neurotransmitter (like **glutamate**) and a sufficient **depolarization** of the postsynaptic membrane to remove a **magnesium ion (Mg2+) block** from its pore.
*GABAA receptor*
- The **GABAA receptor** is a **ligand-gated ion channel** that opens upon binding of the neurotransmitter **GABA**, leading to an influx of chloride ions and neuronal hyperpolarization.
- It is primarily responsible for **inhibitory synaptic transmission** in the central nervous system.
*AMPA receptor*
- The **AMPA receptor** is an ionotropic glutamate receptor that is primarily **ligand-gated**, opening swiftly upon binding of **glutamate** to allow sodium and potassium ion flow.
- While it contributes to depolarization, it is generally not considered to have a significant **voltage-gating** mechanism like the NMDA receptor.
*Nicotinic acetylcholine receptor*
- The **nicotinic acetylcholine receptor** is a **ligand-gated ion channel** that opens in response to the binding of **acetylcholine**, initiating fast excitatory synaptic transmission.
- It is **not voltage-gated** in the same manner as the NMDA receptor; its opening is primarily dependent on neurotransmitter binding.
*Glycine receptor*
- The **glycine receptor** is a **ligand-gated chloride channel** that mediates fast inhibitory synaptic transmission in the spinal cord and brainstem.
- Its activation by **glycine** leads to an influx of chloride ions, causing hyperpolarization, and it does not exhibit significant voltage-gating properties.
Question 80: A 31-year-old man is brought to the emergency department because of fever and increasing confusion for the past day. He has bipolar disorder with psychotic features and hypothyroidism. Current medications are lithium, haloperidol, and levothyroxine. He drinks one beer with dinner every night. His speech is confused and he is oriented to person only. His temperature is 40°C (104°F), pulse is 124/min, and blood pressure is 160/110 mm Hg. He appears acutely ill. Examination shows diaphoresis and muscle rigidity. Deep tendon reflexes are 1+ bilaterally. There is minor rigidity of the neck with full range of motion. His lungs are clear to auscultation. The abdomen is soft and nontender. His leukocyte count is 15,100/mm3 and serum creatine kinase activity is 1100 U/L. Which of the following is the most likely diagnosis?
A. Delirium tremens
B. Neuroleptic malignant syndrome (Correct Answer)
C. Bacterial meningitis
D. Herpes simplex encephalitis
E. Lithium toxicity
Explanation: ***Neuroleptic malignant syndrome***
- The patient presents with **fever (40°C)**, **muscle rigidity**, **altered mental status (confusion)**, **autonomic instability (tachycardia, hypertension, diaphoresis)**, and **elevated creatine kinase**, all classic features of **Neuroleptic Malignant Syndrome (NMS)**.
- The use of **haloperidol**, a high-potency antipsychotic, is a significant risk factor for NMS.
*Delirium tremens*
- While delirium tremens can cause altered mental status, autonomic instability, and fever, it is typically preceded by a history of **heavy chronic alcohol intake** followed by acute withdrawal, which is not indicated by "one beer with dinner every night."
- **Muscle rigidity** and **marked elevation of creatine kinase** are not typical features of delirium tremens.
*Bacterial meningitis*
- Although bacterial meningitis presents with fever and altered mental status, it would typically involve **nuchal rigidity** that limits range of motion, which is not fully present here, and **CSF findings** (e.g., pleocytosis, low glucose) would be diagnostic.
- **Profound muscle rigidity** and **markedly elevated creatine kinase** are not characteristic features of bacterial meningitis.
*Herpes simplex encephalitis*
- This condition presents with fever, altered mental status, and often **focal neurological deficits** or **seizures**, which are not described.
- Diagnosis relies on **characteristic MRI findings** and **CSF PCR for HSV DNA**, and it would not typically cause diffuse **muscle rigidity** or **elevated creatine kinase**.
*Lithium toxicity*
- **Lithium toxicity** typically presents with neurological symptoms like **tremors**, **ataxia**, **nystagmus**, and altered mental status, but it is less commonly associated with **severe muscle rigidity**, **very high fever (40°C)**, or **markedly elevated creatine kinase** unless complicated by severe dehydration or NMS-like features.
- A **high lithium level** would be expected, which is not mentioned as present.