BP from lower extremities

Q: Blood Pressure (BP) obtained from the lower extremity is usually _______________ than the BP obtained from the arm? - select one

A) higher

B) lower

Answer: A

Although undesirable, BP from the lower extremities can be obtained if needed, particularly in End-Stage Renal Disease (ESRD) patients with vascular fistulae. Patients with a known history of coarctation of the aorta may also require that.

The systolic blood pressure in the lower extremity is usually higher than that in the upper extremity (measured from brachial artery). This is true for both the calf and the ankle. In the calf, the difference on average is about 10 mmHg higher, and in the ankle 17 mmHg higher.

While obtaining BP in the lower extremity, the cuff center should align with the popliteal artery. 

#cardiology

#procedures

References:

1. Sheppard JP, Lacy P, Lewis PS, Martin U; Blood Pressure Measurement Working Party of the British and Irish Hypertension Society. Measurement of blood pressure in the leg-a statement on behalf of the British and Irish Hypertension Society. J Hum Hypertens. 2020 Jun;34(6):418-419. doi: 10.1038/s41371-020-0325-5. Epub 2020 Apr 22. PMID: 32322006; PMCID: PMC7299841.

2. McDonagh STJ, Sheppard JP, Warren FC, Boddy K, Farmer L, Shore H, Williams P, Lewis PS, Baumber R, Fordham J, Martin U, Aboyans V, Clark CE; INTERPRESS-IPD Collaborators. Arm Based on LEg blood pressures (ABLE-BP): can systolic leg blood pressure measurements predict systolic brachial blood pressure? Protocol for an individual participant data meta-analysis from the INTERPRESS-IPD Collaboration. BMJ Open. 2021 Mar 19;11(3):e040481. doi: 10.1136/bmjopen-2020-040481. PMID: 33741659; PMCID: PMC7986760.

SJS/TEN and Na

Q: Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) usually causes? - select one

A) hypernatremic dehydration

B) hyponatremic dehydration

Answer: B

Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) is a serious and potentially fatal mucocutaneous drug reaction, characterized by extensive necrosis and detachment of the epidermis due to massive keratinocyte apoptosis. It usually starts as a prodrome of fever and influenza-like symptoms followed in one to three days by an eruption of ill-defined, coalescing, erythematous macules with atypical target lesions. As the disease progresses, vesicles and bullae form, and the skin begins to slough within days. Mucosal involvement occurs in over 90 percent of cases.

Morbidity (and mortality) occurs due to massive loss of fluids, electrolyte imbalance, hypovolemic shock with hyponatremic dehydration, sepsis, and multiple system organ failure (MSOF). These patients are usually managed in a burn unit because of extensive skin detachment. 

#dermatology

References:

1. Hung CC, Liu WC, Kuo MC, Lee CH, Hwang SJ, Chen HC. Acute renal failure and its risk factors in Stevens-Johnson syndrome and toxic epidermal necrolysis. Am J Nephrol. 2009;29(6):633-8. doi: 10.1159/000195632. Epub 2009 Jan 21. PMID: 19155617.

2. Huang SC, Tsai SJ. Hyponatremia and Stevens-Johnson syndrome in a patient receiving carbamazepine. Gen Hosp Psychiatry. 1995 Nov;17(6):458-60. doi: 10.1016/0163-8343(95)90049-7. PMID: 8714810.

3. Shah H, Parisi R, Mukherjee E, Phillips EJ, Dodiuk-Gad RP. Update on Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis: Diagnosis and Management. Am J Clin Dermatol. 2024 Nov;25(6):891-908. doi: 10.1007/s40257-024-00889-6. Epub 2024 Sep 15. PMID: 39278968; PMCID: PMC11511757.

Mx of Delirium Tremens

Q: In refractory delirium tremens(R-DT), phenobarbital should be prescribed ___________ benzodiazepine. - Select one

A) With

B) Without

Answer: A

The probable pathophysiology behind refractory delirium tremens is the low endogenous GABA (gamma-aminobutyric acid) concentrations or acquired conformational changes in the GABA receptor.

Barbiturates and Benzodiazepines work synergistically in R-DT. Barbiturates increase the duration of channel opening, and benzodiazepines increase the frequency of GABA chloride channel opening.

Phenobarbital is the most effective barbiturate in refractory delirium tremens and is often referred to as 'phenobarb-coma.' It should be combined with benzodiazepine and monotherapy with phenobarb should be avoided.

#neurology

#toxicity

#pharmacology

References:

1. Lee CM, Dillon DG, Tahir PM, Murphy CE 4th. Phenobarbital treatment of alcohol withdrawal in the emergency department: A systematic review and meta-analysis. Acad Emerg Med 2024; 31:515.

2. Grover S, Ghosh A. Delirium Tremens: Assessment and Management. J Clin Exp Hepatol. 2018 Dec;8(4):460-470. doi: 10.1016/j.jceh.2018.04.012. Epub 2018 May 5. PMID: 30564004; PMCID: PMC6286444.

3. Kafle P, Mandal AK, Shrestha B, Bhattrai B, Bhandari M, Bhagat S, Shankar Kar B, Sharma D, Gayam V. Twenty-Eight-Day-Long Delirium Tremens. J Investig Med High Impact Case Rep. 2019 Jan-Dec;7:2324709619847228. doi: 10.1177/2324709619847228. PMID: 31053040; PMCID: PMC6505229.

gland enlargement in alcoholic cirrhosis

Q: Which of the following gland enlargement can be seen in advanced alcohol-associated cirrhosis? - select one

A) Parotid gland 

B) Salivary Gland

Answer: A

This question aims to raise awareness of the clinical importance of physical exams and "a physician touch" in clinical medicine.

Even various stigmata of liver failure can guide physicians to the specific etiology of cirrhosis. Three primary organ dysfunctions are highly likely to be seen in advanced alcohol-associated cirrhosis (though they  can be present in other types of cirrhosis)

• Dupuytren contractures
• Parotid gland enlargement
• Testicular atrophy

Although parotid gland enlargement in chronic alcoholism is known since alcohol was known to humankind, it was first reported in present-day literature in 1957 and has been consistently described.

#hepatology

#physical-exam

References:

1. Stanley J. Wolfe, M.D., W. H. J. Summerskill, D.M., M.R.C.P., and Charles S. Davidson, M.D.- Parotid Swelling, Alcoholism and Cirrhosis, Published March 14, 1957, N Engl J Med 1957; VOL. 256 NO. 11,256:491-495, DOI: 10.1056/NEJM195703142561103

2. Dutta SK, Dukehart M, Narang A, Latham PS. Functional and structural changes in parotid glands of alcoholic cirrhotic patients. Gastroenterology. 1989 Feb;96(2 Pt 1):510-8. doi: 10.1016/0016-5085(89)91578-3. PMID: 2910764.

Onn discovery of cryoprecipitate

A quote from history on the discovery of cryoprecipitate

Cryoprecipitate is cold-insoluble portion of plasma that precipitates when FFP has been thawed between 1- 6 °C. It is rich in fibrinogen and factor VIII. It also contains von Willebrand factor (vWF) and factor XIII.

"I made a mistake in an experiment, and instead of putting frozen plasma back in the freezer at the end of the day's experiment, I instead stuck it in the refrigerator. When I came in the next morning, there was all this junk in the bottom of the tube which I spun out, and I used the plasma for my experiment. My experiment didn't work because there was no Factor VIII in it. And I went back and fished the junk out of the trash and assayed the junk and got these outrageously high values for Factor VIII in the junk, and neither Charlie nor I believed it, and so it was one of those things. And sure enough, about a year later Judith Graham Pool discovered cryoprecipitate".

#hematology

Reference: 

Resnik, Susan (1999). Blood Saga: Hemophilia, AIDS, and the Survival of a Community. Berkeley: University of California Press. pp. 40–41

CGA

Q: What are the six domains of comprehensive geriatric assessment (CGA) in oncology patients?

Answer: More than half of the new cases and 70 percent of mortality from cancer occur in patients ≥65 years of age.

Many oncologists perform comprehensive geriatric assessments (CGAs) and make a shared decision about the extent of oncology treatment. 

Consensus guidelines from the American Society of Clinical Oncology, the National Comprehensive Cancer Network, and the International Society for Geriatric Oncology (SIOG) recommend its use. Over time, there were many modifications done either individually by a physician or by practice groups, but overall, the following domains of CGA should be considered:

• Functional status
• Comorbidity
• Nutrition 
• Medication review
• Psychological state and social support
• Cognitive function

#oncology

References:

1. Decoster L, Van Puyvelde K, Mohile S, et al. Screening tools for multidimensional health problems warranting a geriatric assessment in older cancer patients: an update on SIOG recommendations†. Ann Oncol 2015; 26:288.

2. Mohile SG, Dale W, Somerfield MR, Hurria A. Practical Assessment and Management of Vulnerabilities in Older Patients Receiving Chemotherapy: ASCO Guideline for Geriatric Oncology Summary. J Oncol Pract 2018; 14:442.

3. National Comprehensive Cancer Network. NCCN Clinical Practice Guidelines in Oncology. Older adult oncology. https://www.nccn.org/professionals/physician_gls/pdf/senior.pdf 

4. Hurria A, Gupta S, Zauderer M, et al. Developing a cancer-specific geriatric assessment: a feasibility study. Cancer 2005; 104:1998.

Acetazolamide and Potassium

Q: Diuresis with Acetazolamide causes? - Select one

A) hyperkalemia

B) hypokalemia

Answer: B

Acetazolamide is a carbonic anhydrase inhibitor often used to decrease serum bicarbonate levels in ICU.

Acetazolamide inhibits proximal sodium bicarbonate reabsorption and increases urinary bicarbonate excretion. This increase in sodium bicarbonate delivery to the potassium-secretory site in the collecting tubules generates kaliuresis, leading to clinically significant hypokalemia, which may require potassium repletion.

The usual dose of Acetazolamide is 250 to 500 mg, once or twice a day.

Interestingly, it is used in a wide array of diseases both on and off-label, including:

• Glaucoma
• Idiopathic intracranial hypertension
• Congestive heart failure
• Altitude sickness
• Periodic paralysis
• Epilepsy
• Central sleep apnea
• Marfan syndrome
• Prevention of high-dose methotrexate nephrotoxicity

#nephrology

#electrolytes

#acid-base

References:

1. Prieto de Paula JM, Villamandos Nicás V, Cancelo Suárez P, del Portillo Rubí A, Guillem Ares E, Prada Mínguez A, Sanz de la Fuente H. Eficacia del tratamiento con acetazolamida en pacientes con hipercapnia y alcalosis metabólica sobreimpuesta [Efficacy of acetazolamide treatment of patients with hypercapnia and superimposed metabolic alkalosis]. Rev Clin Esp. 1997 Apr;197(4):237-40. Spanish. PMID: 9254398.

2. Miller PD, Berns AS. Acute metabolic alkalosis perpetuating hypercarbia. A role for acetazolamide in chronic obstructive pulmonary disease. JAMA. 1977 Nov 28;238(22):2400-1. doi: 10.1001/jama.238.22.2400. PMID: 578870.

3. Van Berkel MA, Elefritz JL. Evaluating off-label uses of acetazolamide. Am J Health Syst Pharm. 2018 Apr 15;75(8):524-531. doi: 10.2146/ajhp170279. PMID: 29626002.

4. Farzam K, Abdullah M. Acetazolamide. [Updated 2023 Jul 2]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK532282/

Contraindications of Bupropion

Q: 34 years old overweight male (BMI of 32) with previous history of smoking history, alcoholism, hypertension (HTN), and depression is admitted to ICU with new-onset seizures. Patient acknowledges that recently he used his friend's bupropion to decrease his weight. Name few contraindications for Bupropion?

Answer: In the last few years, off-label use of bupropion has risen due to its easy availability and relatively cheaper price. A few of the relative contraindications are

• Seizure disorders, including alcohol withdrawal seizures (bupropion decreases the seizure threshold)
• Bulimia nervosa
• Pregnancy
• Uncontrolled HTN
• Chronic opioid use
• Renal insufficiency
• Hepatic insufficiency
• Use of monoamine oxidase inhibitors within last two weeks

#neurology

#toxicity

#pharmacology

References:

1. Mother To Baby | Fact Sheets [Internet]. Brentwood (TN): Organization of Teratology Information Specialists (OTIS); 1994-. Bupropion. 2023 Jul. Available from: https://www.ncbi.nlm.nih.gov/books/NBK582611/

2. Beyens MN, Guy C, Mounier G, Laporte S, Ollagnier M. Serious adverse reactions of bupropion for smoking cessation: analysis of the French Pharmacovigilance Database from 2001 to 2004. Drug Saf. 2008;31(11):1017-26. doi: 10.2165/00002018-200831110-00006. PMID: 18840021.

3. Stahl SM, Pradko JF, Haight BR, Modell JG, Rockett CB, Learned-Coughlin S. A Review of the Neuropharmacology of Bupropion, a Dual Norepinephrine and Dopamine Reuptake Inhibitor. Prim Care Companion J Clin Psychiatry. 2004;6(4):159-166. doi: 10.4088/pcc.v06n0403. PMID: 15361919; PMCID: PMC514842.

Positive urinary pregnancy test in men

Case: A male undergoing lab tests came out positive for Beta-HCG. What could be the cause of positive Beta-HCG in a male?

Discussion: A positive pregnancy test in a man is a red flag for testicular cancer.

β-hCG is not usually present in males. Its presence suggests a tumor that produces β-hCG, such as Choriocarcinoma, Embryonal carcinoma, and mixed germ cell tumors. Rarely, some seminomas can secrete β-hCG.

Further Testing should be done.

 1. Serum tumor markers:

 • β-hCG (already elevated)

 • Alpha-fetoprotein (AFP) — elevated in NSGCTs except for pure seminomas and choriocarcinomas

 • Lactate dehydrogenase (LDH) — correlates with tumor burden

 2. Testicular ultrasound:

 • First-line imaging to identify testicular masses

 3. Scrotal and physical examination:

 • Palpate for masses or asymmetry

 4. CT scan of chest, abdomen, and pelvis:

 • To evaluate for metastasis (especially lungs, liver, retroperitoneum)

 5. Urology or oncology referral:

 • For surgical exploration (radical inguinal orchiectomy is both diagnostic and therapeutic)

#oncology

#endocrinology

References:

1. Groza D, Duerr D, Schmid M, Boesch B. When cancer patients suddenly have a positive pregnancy test. BMJ Case Rep. 2017 Jul 1;2017:bcr2017220493. doi: 10.1136/bcr-2017-220493. PMID: 28668822; PMCID: PMC5535187.

2. Tsai JR, Chong IW, Hung JY, Tsai KB. Use of urine pregnancy test for rapid diagnosis of primary pulmonary choriocarcinoma in a man. Chest. 2002 Mar;121(3):996-8. doi: 10.1378/chest.121.3.996. PMID: 11888991.

3. Paramore L, Chetwood AS. Role of urinary pregnancy testing in the diagnosis of men with testicular cancer. Ann R Coll Surg Engl. 2025 Jan;107(1):73. doi: 10.1308/rcsann.2023.0029. Epub 2024 Apr 2. PMID: 38563075; PMCID: PMC11658873.

Picture Diagnosis

Q: Patient presents with 10 years of difficulty swallowing food and water. It became worse over the last 3 months. Chest X-ray showed this. What is your diagnosis?

Answer:  The chest X-ray shows a significantly dilated esophagus filled with food and fluid, with an air-fluid level and absence of peristalsis. These findings are highly suggestive of achalasia, a primary esophageal motility disorder characterized by failure of the lower esophageal sphincter (LES) to relax.

Diagnosis: Achalasia

Supporting Features:

• Progressive dysphagia (starting with solids, later affecting liquids)
• Long duration (10 years, worsening over 3 months)
• 
  

Chest X-ray findings:

• Widely dilated esophagus
• Air-fluid level
• Mediastinal widening due to food stasis
• Absence of gastric air bubble (suggesting LES dysfunction)

Next Steps:

1. Confirm with Barium Swallow: "Bird-beak" narrowing at the gastroesophageal junction.

2. Esophageal Manometry: Absent peristalsis, high LES pressure, incomplete relaxation.

3. Endoscopy: Rule out malignancy (pseudoachalasia).

#GI

Further readings:

1. Ribolsi M, Andrisani G, Di Matteo FM, Cicala M. Achalasia, from diagnosis to treatment. Expert Rev Gastroenterol Hepatol. 2023 Jan;17(1):21-30. doi: 10.1080/17474124.2022.2163236. Epub 2023 Jan 1. PMID: 36588469.

2. Cappell MS, Stavropoulos SN, Friedel D. Updated Systematic Review of Achalasia, with a Focus on POEM Therapy. Dig Dis Sci. 2020 Jan;65(1):38-65. doi: 10.1007/s10620-019-05784-3. Epub 2019 Aug 27. PMID: 31451984.

Older age HIV

Q: What age is the cut-off age usually defined for "HIV infections in older adults"? - Select one

A) ≥50 years

B) ≥60 years

C) ≥65 years

D) ≥70 years

Answer: A

As patients with human immunodeficiency virus (HIV) infection are living almost as normal life expectancy as the general population, geriatric care with HIV has itself become a subspecialty of HIV treatment. So far, age ≥50 remains a defining cutoff for such care. Interestingly, more and more patients are getting diagnosed with HIV above this age due to a "taking life easy" attitude and conventional belief that they may have passed the age of practicing protected sex.

HIV care at this age remains complicated due to higher age-related comorbidities and higher risks of polypharmacy. Cumulating older age with HIV also creates a higher risk for malignancy. Other areas include the complex management of different body organs such as bone, liver, and lungs and hormonal changes. 

#ID

#epidemiology

References:

1. Wing EJ. HIV and aging. Int J Infect Dis. 2016 Dec;53:61-68. doi: 10.1016/j.ijid.2016.10.004. Epub 2016 Oct 15. PMID: 27756678.

2. Autenrieth CS, Beck EJ, Stelzle D, et al. Global and regional trends of people living with HIV aged 50 and over: Estimates and projections for 2000-2020. PLoS One 2018; 13:e0207005.

3. Li N, Zheng HY, He WQ, He XY, Li R, Cui WB, Yang WL, Dong XQ, Shen ZQ, Zheng YT. Treatment outcomes amongst older people with HIV infection receiving antiretroviral therapy. AIDS. 2024 May 1;38(6):803-812. doi: 10.1097/QAD.0000000000003831. Epub 2024 Jan 12. PMID: 38578958; PMCID: PMC10994140.

Spontaneous, nontraumatic gangrene

Q: Which system amongst the following is more prone to origniate spontaneous (nontraumatic) gas gangrene? - Select one

A) Muscles

B) Genitourinary (GU) tract

C) Respiratory tract

D) Gastrointestinal (GI) tract

E) Hematologic source

Answer: D

Gastrointestinal lesions or undiagnosed adenocarcinoma of the colon should be suspected in patients who develop spontaneous gas gangrene.

The major predisposing factors:

• Colonic malignancy
• Inflammatory bowel disease (IBD)
• Diverticulitis
• GI surgery
• Leukemia
• Lymphoproliferative disorders
• Chemotherapy
• Neutropenia
• Radiation therapy
• Advanced AIDS
• Necrotizing enterocolitis, cecitis, or distal ileitis

#ID

#GI

#oncology

References:

1. Stevens DL, Musher DM, Watson DA, et al. Spontaneous, nontraumatic gangrene due to Clostridium septicum. Rev Infect Dis 1990; 12:286.

2. Johnson S, Driks MR, Tweten RK, et al. Clinical courses of seven survivors of Clostridium septicum infection and their immunologic responses to alpha toxin. Clin Infect Dis 1994; 19:761.

3. Alpern RJ, Dowell VR Jr. Clostridium septicum infections and malignancy. JAMA 1969; 209:385.

4. Srivastava I, Aldape MJ, Bryant AE, Stevens DL. Spontaneous C. septicum gas gangrene: A literature review. Anaerobe. 2017 Dec;48:165-171. doi: 10.1016/j.anaerobe.2017.07.008. Epub 2017 Aug 2. PMID: 28780428.

Torsades de pointes and polymorphic VT

Q: What is the difference between Torsades de Pointes and polymorphic Ventricular Tachycardia (VT)?

Answer: 

Torsades de Pointes, meaning "twisting of points,"  is a rapid and distinct polymorphic VT associated with baseline prolonged QTc interval.

If baseline QTc interval is normal, it is technically called polymorphic VT, not torsades de pointes.

In Torsades de Pointes, continuously changing axis of polymorphic QRS morphologies is observed during each episode. It is typically initiated by bradycardia or, as called, 'pause dependent,' with a short-long-short coupling interval, i.e., PVC (short RR interval), a compensatory pause (long RR interval), and a second PVC (short RR interval).

#cardiology

References:

1. Passman R, Kadish A. Polymorphic ventricular tachycardia, long Q-T syndrome, and torsades de pointes. Med Clin North Am. 2001 Mar;85(2):321-41. doi: 10.1016/s0025-7125(05)70318-7. PMID: 11233951.

2. Tsuji Y, Yamazaki M, Shimojo M, Yanagisawa S, Inden Y, Murohara T. Mechanisms of torsades de pointes: an update. Front Cardiovasc Med. 2024 Mar 5;11:1363848. doi: 10.3389/fcvm.2024.1363848. PMID: 38504714; PMCID: PMC10948600.

3. Rosso R, Hochstadt A, Viskin D, Chorin E, Schwartz AL, Tovia-Brodie O, Laish-Farkash A, Havakuk O, Gepstein L, Banai S, Viskin S. Polymorphic ventricular tachycardia, ischaemic ventricular fibrillation, and torsade de pointes: importance of the QT and the coupling interval in the differential diagnosis. Eur Heart J. 2021 Oct 7;42(38):3965-3975. doi: 10.1093/eurheartj/ehab138. PMID: 33693589.

Harmless Score

Q: The Harmless score applies to? - Select one

A) Acute Aphasia (stroke)

B) Acute Breathing problem

C) Acute Cardiac event

D) Acute Pancreatitis

E) Acute Liver failure

Answer: D

Although the "Harmless acute pancreatitis score" is not a well-known entity, it is an interesting quick-to-do test that can be calculated within 30 minutes of admission to predict mortality/severity. It comprises of three parameters - and if all three are negative, pancreatitis is probably harmless: 

1. Lack of rebound tenderness or guarding
2. Normal hematocrit 
3. Normal serum creatinine

Only one study of 204 patients is available in this regard, but it correctly identified harmlessness with 98 percent accuracy.

#GI

Reference:

Lankisch PG, Weber-Dany B, Hebel K, et al. The harmless acute pancreatitis score: a clinical algorithm for rapid initial stratification of nonsevere disease. Clin Gastroenterol Hepatol 2009; 7:702.

ADEs

Q: Adverse Drug Events (ADEs) are more common in? - Select one

A) Outpatient

B) Emergency Room(ER)

C) Inpatient Ward

D) ICU 

Answer: D

Studies have shown that ICU is the most common place to have ADEs, particularly during night shifts and on weekends. Some of the primary reasons for these mishaps are:

1. ICU patients usually receive more medications than in other medical settings.

2. Many medications are new, and patients' profiles are not yet documented for drug-drug interactions.

3. Most medications in the ICU are given intravenously (IV), which can lead to higher reactions and miscalculations of doses/infusion rates. 

4. ICU patients have multiple severe comorbidities.

5. ICU patients are often sedated and can't check/question/report their own drugs.

6. Upon arrival in the ICU, long-term and often essential drugs are frequently held or discontinued, such as antiplatelets in stent patients or anticoagulants in atrial fibrillation or thrombus patients.

7. In ICUs, patients' levels of care remain the same during night shifts and on weekends, but there is less staffing and supervision.

#pharmacology

#patient-safety

References:

1.Wilmer A, Louie K, Dodek P, et al. Incidence of medication errors and adverse drug events in the ICU: a systematic review. Qual Saf Health Care 2010; 19:e7.

2. Kane-Gill S, Weber RJ. Principles and practices of medication safety in the ICU. Crit Care Clin 2006; 22:273.

3. Bell CM, Brener SS, Gunraj N, et al. Association of ICU or hospital admission with unintentional discontinuation of medications for chronic diseases. JAMA 2011; 306:840.

4. Miller AD, Piro CC, Rudisill CN, et al. Nighttime and weekend medication error rates in an inpatient pediatric population. Ann Pharmacother 2010; 44:1739.

Dental trauma during intubation

Q: 52 years old male has an accidental tooth avulsion during intubation in a small rural town where no emergency dental help is available on short notice. An attempt should be made to reimplant. 

A) Yes

B) No

Answer: A

Although it is true that, ideally, a dentist, oral-maxillofacial surgeon, or trauma surgeon should perform tooth reimplantation, dentists are generally unavailable in acute ICU/ER/trauma-field situations. In minor, partial, or lateral avulsion (not major facial trauma), where reimplantation seems easy, it should be attempted. A tooth reimplanted within one hour has a better chance of healing and becoming functional over a period of time. This advantage is lost once the three-hour markup is over. A few precautions that need to be taken care of are:

• Try not to disturb the socket 
• Handle the tooth by the crown 
• Root should not be wiped or even handled
• Rinse the tooth and socket with tap water or saline
• Attempt to replace the tooth in the socket (it may "click" into place!)

If an operator seems uncomfortable or reimplantation seems complicated, the tooth should be preserved preferably in a culture medium (Hank's Balanced Salt Solution) or in milk if the culture medium is not available. 

If a tooth is intruded, reimplantation should not be attempted; instead, it should not be manipulated, as this may lead to significant trauma. Reimplantation can be painful, so 1% lidocaine WITHOUT epinephrine should be applied to the region. If doable, a regional dental block is preferred.

If an avulsed tooth cannot be located, a CXR should be performed. It should be retrieved via scope if it's found in the bronchus or esophagus. The probability of salvaging is low if it is below the diaphragm.

In any case, a dentist, trauma surgeon, or oral-maxillofacial surgeon should be called as soon as possible.

#trauma

#procedures

#dental-medicine

References:

1. Belmonte FM, Macedo CR, Day PF, et al. Interventions for treating traumatised permanent front teeth: luxated (dislodged) teeth. Cochrane Database Syst Rev 2013; :CD006203.

2. Jones LC. Dental Trauma. Oral Maxillofac Surg Clin North Am 2020; 32:631.

3. Schatz JP, Hausherr C, Joho JP. A retrospective clinical and radiologic study of teeth re-implanted following traumatic avulsion. Endod Dent Traumatol 1995; 11:235.

4. Petrovic B, Marković D, Peric T, Blagojevic D. Factors related to treatment and outcomes of avulsed teeth. Dent Traumatol 2010; 26:52.

B symptoms

Q: Which of the following is not considered a "B" symptom in lymphoma? - Select one

A) Fever

B) Night sweats 

C) Weight loss

D) Pruritus

Answer: D

The criteria for B symptoms is the presence of all of the following symptoms:

• Unexplained fever >38°C during the previous month
• Recurrent drenching night sweats during the previous month
• Weight loss >10 percent of body weight within six months of diagnosis

Less known is that if patients don't meet any of the above-mentioned, then they are categorized as "A."

These patients may have other symptoms such as fatigue, pruritus, pain (mainly when drinking ETOH), or any other symptoms, but are not considered B symptoms.

#oncology

References:

1. Shadman M. Diagnosis and Treatment of Chronic Lymphocytic Leukemia: A Review. JAMA. 2023 Mar 21;329(11):918-932. doi: 10.1001/jama.2023.1946. PMID: 36943212.

2. Mamgain G, Singh PK, Patra P, Naithani M, Nath UK. Diffuse large B-cell lymphoma and new insights into its pathobiology and implication in treatment. J Family Med Prim Care. 2022 Aug;11(8):4151-4158. doi: 10.4103/jfmpc.jfmpc_2432_21. Epub 2022 Aug 30. PMID: 36353039; PMCID: PMC9638643.

3. Dehghani M, Haddadi S, Vojdani R. Signs, Symptoms and Complications of Non-Hodgkin's Lymphoma According to Grade and Stage in South Iran. Asian Pac J Cancer Prev. 2015;16(8):3551-7. doi: 10.7314/apjcp.2015.16.8.3551. PMID: 25921177.

melanoptysis

Q; What is Melanoptysis?

Answer: Black pigmented  airway secretions

This question aims to guide students to use proper medical terms when describing, writing, and presenting patients, reports, and scientific papers.

Melena and Ptysis are Greek words meaning black and to spit.

The quality and density of soot-containing airway secretions during fire exposure, smoke inhalation, or pollution exposure can give a clinician clue to the level of exposure. Clinically, this is an important term to understand, as dense soot-containing airway secretions during fire and smoke may call for early intubation. Delay may cause vocal cord edema and lead to fatal airway collapse.

Melanoptysis is often described as exposure to pollution, coal dust, and smog. It is usually accompanied by Pneumoconiosis, as these patients typically have long-term lung exposure, which causes lung parenchyma to become pathologically blackened.

Other symptoms of fire exposure besides melanoptysis are cough, wheezing, hyperventilation followed by hypoventilation, erythema, hyperemia, and increased pulmonary shunting from lobar collapse or atelectasis.

#fire

#pulmonary

References/further readings:

1. Rehberg S, Maybauer MO, Enkhbaatar P, et al. Pathophysiology, management and treatment of smoke inhalation injury. Expert Rev Respir Med 2009; 3:283.

2. Kurahara Y, Shimatani Y. Melanoptysis. QJM. 2023 Jul 28;116(7):540-541. doi: 10.1093/qjmed/hcad042. PMID: 36944265.

3. Martínez-Girón R, Mosquera-Martínez J, Martínez-Torre S. Black-pigmented sputum. J Cytol. 2013 Oct;30(4):274-5. doi: 10.4103/0970-9371.126667. PMID: 24648674; PMCID: PMC3945631.

FTDs

Q: Which symptom is most common in frontotemporal dementias (FTDs)? - Select one

A) Visual disturbances

B) Aphasia

C) Metallic taste

D) Cochlear degeneration

E) Temperature deregulation

Answer: B

Although FTD occurs as frequently as Alzheimer disease (AD), it remains one of the most under diagnosed neurodegenerative disorders, due to its early occurrence with mean age of 58 and as most patient either have changes in social behavior and personality or become somnolent with ptimary progressive aphasia (PPA), and get refer to psychiatry service. 

It involves the frontal and/or temporal lobes. To complicate matters, many patients simultaneously develop concomitant parkinsonism or motor neuron disease (MND). The underlying etiology is genetic.

It is usually classified into three subtypes:

• Behavioral variant FTD (bvFTD) 
• Nonfluent PPA or "agrammatic PPA." 
• Semantic PPA

Patients need a neurology consult and may undergo various imaging and neuropsychiatric testing. Social support and speech therapy are the mainstays of the treatment, though trazadone and citalopram may help.

#neurology

#psychiatry

References:

1. Antonioni A, Raho EM, Lopriore P, Pace AP, Latino RR, Assogna M, Mancuso M, Gragnaniello D, Granieri E, Pugliatti M, Di Lorenzo F, Koch G. Frontotemporal Dementia, Where Do We Stand? A Narrative Review. Int J Mol Sci. 2023 Jul 21;24(14):11732. doi: 10.3390/ijms241411732. PMID: 37511491; PMCID: PMC10380352.

2. Kirshner HS. Frontotemporal dementia and primary progressive aphasia, a review. Neuropsychiatr Dis Treat. 2014 Jun 12;10:1045-55. doi: 10.2147/NDT.S38821. PMID: 24966676; PMCID: PMC4062551.

3. Neylan KD, Miller BL. New Approaches to the Treatment of Frontotemporal Dementia. Neurotherapeutics. 2023 Jul;20(4):1055-1065. doi: 10.1007/s13311-023-01380-6. Epub 2023 May 8. PMID: 37157041; PMCID: PMC10457270.

4. Magrath Guimet N, Zapata-Restrepo LM, Miller BL. Advances in Treatment of Frontotemporal Dementia. J Neuropsychiatry Clin Neurosci. 2022 Fall;34(4):316-327. doi: 10.1176/appi.neuropsych.21060166. Epub 2022 May 17. PMID: 35578801.

nsNSAIDs, other drugs and GI bleed

Q: 58 years old male with previous history of osteoarthritis, and chronic depression is admitted to ICU with gastrointestinal bleed (GIB). The risk of GIB increases in the patient who takes Nonselective nonsteroidal anti-inflammatory drugs (nsNSAIDs) along with selective serotonin reuptake inhibitors (SSRI).

A) True

B) False

Answer: True

Although nsNSAIDs can indeed increase GI symptoms such as dyspepsia, peptic ulcer disease (PUD), and GIB, these symptoms get augmented due to other drugs on the patient's profile. These include concurrent use of glucocorticoids, antiplatelet agents (eg, aspirin, clopidogrel and anticoagulants. It is less known that SSRIs also increase such risk.

The other risk factors of GIB from nsNSAIDs are prior history of GI ulcer or GIB, older age, taking high NSAID dose, and underlying Helicobacter pylori infection.

#pharmacology

#GI

References:

1. Alam SM, Qasswal M, Ahsan MJ, Walters RW, Chandra S. Selective serotonin reuptake inhibitors increase risk of upper gastrointestinal bleeding when used with NSAIDs: a systemic review and meta-analysis. Sci Rep. 2022 Aug 24;12(1):14452. doi: 10.1038/s41598-022-18654-2. PMID: 36002638; PMCID: PMC9402708.

2. de Jong JC, van den Berg PB, Tobi H, de Jong-van den Berg LT. Combined use of SSRIs and NSAIDs increases the risk of gastrointestinal adverse effects. Br J Clin Pharmacol. 2003 Jun;55(6):591-5. doi: 10.1046/j.0306-5251.2002.01770.x. PMID: 12814454; PMCID: PMC1884264.

3. Loke YK, Trivedi AN, Singh S. Meta-analysis: gastrointestinal bleeding due to interaction between selective serotonin uptake inhibitors and non-steroidal anti-inflammatory drugs. Aliment Pharmacol Ther. 2008 Jan 1;27(1):31-40. doi: 10.1111/j.1365-2036.2007.03541.x. Epub 2007 Oct 5. PMID: 17919277.

Citrate for CRRT

Q: What's the rationale behind using citrate (when heparin is not used) to avoid filter clotting in continuous renal replacement therapy (CRRT)?

Answer: Citrate combines with calcium resulting in extracorporeal chelation, which blocks calcium-dependent steps of clotting cascade. When extracorporeal blood mixes with venous blood, the ionized calcium level is restored, and systemic anticoagulation is avoided. 

Citrate is also metabolized via the liver, and chelated calcium is released back into circulation, which prevents hypocalcemia (though frequent checks are required, particularly in liver insufficiency).

#nephrology

#procedures 

Recommended readings: 

1. Honoré PM, Rimmelé T, Joannes-Boyau O. Citrate anticoagulation for continuous renal replacement therapy. Intensive Care Med. 2024 Sep;50(9):1553-1556. doi: 10.1007/s00134-024-07531-3. Epub 2024 Jul 22. PMID: 39037609.

2. Jacobs R, Verbrugghe W, Dams K, Roelant E, Couttenye MM, Devroey D, Jorens P. Regional Citrate Anticoagulation in Continuous Renal Replacement Therapy: Is Metabolic Fear the Enemy of Logic? A Systematic Review and Meta-Analysis of Randomised Controlled Trials. Life (Basel). 2023 May 17;13(5):1198. doi: 10.3390/life13051198. PMID: 37240843; PMCID: PMC10221969.

3. Poh CB, Tan PC, Kam JW, Siau C, Lim NL, Yeon W, Cui HH, Ding HT, Song XY, Yan P, Chea KL, Liu JS, Chionh CY. Regional Citrate Anticoagulation for Continuous Renal Replacement Therapy - A Safe and Effective Low-Dose Protocol. Nephrology (Carlton). 2020 Apr;25(4):305-313. doi: 10.1111/nep.13656. Epub 2019 Sep 16. PMID: 31469465.

4. Oudemans-van Straaten HM, Ostermann M. Bench-to-bedside review: Citrate for continuous renal replacement therapy, from science to practice. Crit Care. 2012 Dec 7;16(6):249. doi: 10.1186/cc11645. PMID: 23216871; PMCID: PMC3672558.

Antipsychotic med and side effects

Q: 24 years old male recently started on an antipsychotic medicine presented to ER with choking sensation and difficulty breathing, requiring emergent intubation. Patient's friend acknowledged that patient used cocaine before taking his antipsychotic med. ED physician reports difficult intubation while advancing the Endotracheal tube. What could be the possible cause?

Answer: Antipsychotic-induced laryngospasm

A few forms of dystonia after starting antipsychotics could be life-threatening, including laryngospasm. Unfortunately, the onset is usually rapid and may involve other symptoms such as 

• torticollis
• retrocollis
• oculogyric crisis, and 
• opisthotonos

Young male patients with history of substance abuse, specifically cocaine, are more prone to develop laryngospasm. 

This should be treated by 50 mg IV Diphenhydramine every four to six hours till the symptoms resolve. Alternatively, IV or IM 1-2 mg Benztropine can be used.

#toxicity

#pharmacology

#psychiatry

References:

1. O'Neill JR, Stephenson C. Antipsychotic-Induced Laryngeal Dystonia. Psychopharmacol Bull. 2022 Feb 25;52(1):61-67. PMID: 35342202; PMCID: PMC8896750.

2. Maguire PA, Brazel M, Looi JCL. Antipsychotic-induced acute laryngeal dystonia: A systematic review of case reports. Schizophr Res. 2024 Feb;264:248-262. doi: 10.1016/j.schres.2023.12.032. Epub 2024 Jan 6. PMID: 38185029.

HES

Q: Cannabinoids are? - Select one

A) Hydrophilic

B) Lipophilic

Answer: B

Cannabinoids accumulate in adipose tissues, including central and peripheral adipose tissues, due to their lipophilic nature.

Clinical significance: In patients who are long-term users of cannabinoids, when exposed to fasting, lipolysis occurs in the body, and degradation of cannabinoid into pro-emetic agents precipitates hyperemesis, leading to Cannabinoid Hyperemesis Syndrome (HES). Moreover, if the patient has genetic differences in his cytochrome P450 system, it causes the accumulation of cannabinoid metabolites, making HES worse/intense.

#toxicity

#drug-abuse

#GI

References:

1. Wightman RS, Metrik J, Lin TR, et al. Cannabis Use Patterns and Whole-Blood Cannabinoid Profiles of Emergency Department Patients With Suspected Cannabinoid Hyperemesis Syndrome. Ann Emerg Med 2023; 82:121.

2. Russo EB, Spooner C, May L, et al. Cannabinoid Hyperemesis Syndrome Survey and Genomic Investigation. Cannabis Cannabinoid Res 2022; 7:336.

3. Burillo-Putze G, Richards JR, Rodríguez-Jiménez C, Sanchez-Agüera A. Pharmacological management of cannabinoid hyperemesis syndrome: an update of the clinical literature. Expert Opin Pharmacother. 2022 Apr;23(6):693-702. doi: 10.1080/14656566.2022.2049237. Epub 2022 Mar 20. PMID: 35311429.

Clonidine and Eye

Q: Clonidine causes? - Select one

A) Miosis

B) Mydriasis

Answer: A

Clonidine is an alpha-2 adrenergic agonist. It was invented decades ago as a topical nasal decongestant. Later, many of its on- and off-label uses were utilized. Clonidine is now widely used for:

• Hypertension 
• Adjunctive for anesthetic sedation and analgesia
• Spinal anesthesia
• Opioid detoxification
• Alcohol withdrawal
• Smoking cessation
• Postmenopausal hot flashes
• Prevention of perioperative myocardial ischemia
• Attention deficit disorder with hyperactivity
• Refractory conduct disorder
• Tourette syndrome 
• Sleep disturbances

The classic clonidine "toxidrome” consists of four symptoms:

1. Depressed mental status
2. Miosis
3. Depressed respirations
4. Bradycardia and hypotension

#toxicity

#pharmacology

References:

1. Nishina K, Mikawa K, Uesugi T, et al. Efficacy of clonidine for prevention of perioperative myocardial ischemia: a critical appraisal and meta-analysis of the literature. Anesthesiology 2002; 96:323.

Glassman AH, Stetner F, Walsh BT, et al. Heavy smokers, smoking cessation, and clonidine. Results of a double-blind, randomized trial. JAMA 1988; 259:2863.

2. Clayden JR, Bell JW, Pellard P. Menopausal flushing: double-blind trial of a non-hormonal medication. Br Med J 1974; 9:490.

3. Manzon L, Nappe TM, DelMaestro C, Maguire NJ. Clonidine Toxicity. 2023 Jun 26. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan–. PMID: 29083752.

Amiodarone and Eye

Q: If corneal microdeposits are noted in patients on Amiodarone therapy, it should be considered serious, and Amiodarone should be stopped immediately to avoid blindness.

A) True

B) False

Answer: B

Corneal microdeposits and/or lenticular opacities are common in patients on amiodarone therapy. This is due to the secretion of amiodarone by the lacrimal gland, which accumulates on the corneal surface. It is popularly known as cat's whiskers and is visible at the juncture of the lower one-third and upper two-thirds of the cornea. This is a dose-dependent effect and gets resolved a few months after stopping the drug. This more extended resolution is due to the longer half-life of Amiodarone. It does not have profound side effects except that it can be annoying cosmetically. It does not affect visual acuity, though it may cause halo vision with colored rings around lights, especially at night. Some photophobia and blurred vision may occur. These symptoms may get better with lowering the dose. 

Though serious side effects like optic neuropathy or papillopathy may occur but are scarce, other reasons besides Amiodarone toxicity should be ruled out first.

#pharmacology

#toxicity

#cardiology

References:

1. Mäntyjärvi M, Tuppurainen K, Ikäheimo K. Ocular side effects of amiodarone. Surv Ophthalmol 1998; 42:360.

2. Ingram DV. Ocular effects in long-term amiodarone therapy. Am Heart J 1983; 106:902.

3. Passman RS, Bennett CL, Purpura JM, Kapur R, Johnson LN, Raisch DW, West DP, Edwards BJ, Belknap SM, Liebling DB, Fisher MJ, Samaras AT, Jones LG, Tulas KM, McKoy JM. Amiodarone-associated optic neuropathy: a critical review. Am J Med. 2012 May;125(5):447-53. doi: 10.1016/j.amjmed.2011.09.020. Epub 2012 Mar 3. PMID: 22385784; PMCID: PMC3322295.

4. Gittinger JW Jr, Asdourian GK. Papillopathy caused by amiodarone. Arch Ophthalmol. 1987 Mar;105(3):349-51. doi: 10.1001/archopht.1987.01060030069028. PMID: 3827710.

Frog sign

Q: What is Frog sign?

Answer: In Paroxysmal Supra-Ventricular Tachycardia (PSVT), a rapid and regular bulging is seen in the neck. These are prominent jugular venous A waves due to atrial contraction against the closed tricuspid valve, termed as "frog sign".

 

#physical-exam

#cardiology

References:

1. Brief report: the hemodynamic mechanism of pounding in the neck in atrioventricular nodal reentrant tachycardia - N Engl J Med. 1992 Sep 10;327(11):772-4.

2. Evaluation of Patients with Palpitations - NEJM, May, 1998, Volume 338:1369-1373

Tuberculous pleuritis and HIV

Q: In HIV patient with tuberculous pleural effusion, CD4 count can remarkably affect the pleural fluid cell count and composition.

A) True

B) False

Answer: B

Tuberculous pleural fluid is usually a straw-colored exudate with protein concentration of>3.0 g/dL (30 g/L). LDH is commonly above 500 international units/L. The pH stays lower than 7.40 in most cases. Glucose is between 60 and 100 mg/dL but can be lower. An abundance of mesothelial cells may be present.

The nucleated cell count in pleural exudate is usually between 1000 and 6000 cells/mm3. It is primarily lymphocyte-predominant but can be neutrophil-predominant in the early phase.

There is no major correlation between the peripheral CD4 count and pleural exudate cell count or composition in HIV patients.

A less known fact is that TB pleural effusion accounts for about 5 percent of eosinophilic pleural effusions.

#pulmonary

#ID

References:

1. Frye MD, Pozsik CJ, Sahn SA. Tuberculous pleuritis and HIV disease. Chest 1995; 108:102S.

2. Riantawan P, Chaowalit P, Wongsangiem M, Rojanaraweewong P. Diagnostic value of pleural fluid adenosine deaminase in tuberculous pleuritis with reference to HIV coinfection and a Bayesian analysis. Chest 1999; 116:97.

3. McNally E, Ross C, Gleeson LE. The tuberculous pleural effusion. Breathe (Sheff). 2023 Dec;19(4):230143. doi: 10.1183/20734735.0143-2023. Epub 2023 Dec 19. PMID: 38125799; PMCID: PMC10729824.

4. Shaw JA, Diacon AH, Koegelenberg CFN. Tuberculous pleural effusion. Respirology. 2019 Oct;24(10):962-971. doi: 10.1111/resp.13673. Epub 2019 Aug 16. PMID: 31418985.

ISCLS

Q: Name at least three laboratory findings that may help diagnose Idiopathic Systemic Cappilary Leak Syndrome (ISCLS)?

Answer: Although ICLS is a clinical diagnosis and is considered a diagnosis after all other etiologies are ruled out, few labs are highly suggestive of ISCLS.

It includes:

• Very high hematocrit (55 to 73 percent)
• Leucocytosis around 30 cells/mm3 
• Hypoalbuminemia, around 1.7 ± 0.7 gm/dL
• Lactic acidosis above normal

The clinical signs of ISCLS are hypotension, generalized edema, ascites, bilateral pleural effusions, pericardial effusions, cerebral edema, restlessness, encephalopathy, systemic hypoperfusion with cool and vasoconstricted skin, oliguria/anuria, and diminished pulses. 

The acute right axis deviation on the EKG and the above findings favour ISCLS.

Luckily, it resolves quickly within 3-4 days.

#hemodynamics

#vascular

References:

1. Kapoor P, Greipp PT, Schaefer EW, et al. Idiopathic systemic capillary leak syndrome (Clarkson's disease): the Mayo clinic experience. Mayo Clin Proc 2010; 85:905.

2. Dhir V, Arya V, Malav IC, et al. Idiopathic systemic capillary leak syndrome (SCLS): case report and systematic review of cases reported in the last 16 years. Intern Med 2007; 46:899.

3. Druey KM, Parikh SM. Idiopathic systemic capillary leak syndrome (Clarkson disease). J Allergy Clin Immunol 2017; 140:663.

4. Eo TS, Chun KJ, Hong SJ, et al. Clinical Presentation, Management, and Prognostic Factors of Idiopathic Systemic Capillary Leak Syndrome: A Systematic Review. J Allergy Clin Immunol Pract 2018; 6:609.