Insulin K lowering effect in renal patients

Q: In kidney failure patients who get treated for hyperkalemia with insulin and glucose, which effect is relatively more resistant? - select one

A) Glucose-lowering effect of insulin

B) Hypokalemic effect of insulin and glucose

Answer: A

Renal failure patients who require emergent treatment for hyperkalemia are usually resistant to the glucose-lowering effect of insulin but not to the hypokalemic effect. This is because their  Na-K-ATPase activity remains elevated.

Glucose/insulin combo starts working in 10 to 20 minutes, peaks at 30 to 60 minutes, and lasts for about 4-6 hours.

#endocrinology

#electrolytes

#nephrology

References:

1. Emmett M. Non-dialytic treatment of acute hyperkalemia in the dialysis patient. Semin Dial 2000; 13:279.

2. Goecke IA, Bonilla S, Marusic ET, Alvo M. Enhanced insulin sensitivity in extrarenal potassium handling in uremic rats. Kidney Int 1991; 39:39.

3. Alvestrand A, Wahren J, Smith D, DeFronzo RA. Insulin-mediated potassium uptake is normal in uremic and healthy subjects. Am J Physiol 1984; 246:E174.

Purulent Pericarditis definition

Q: What is the definition of Purulent pericarditis?

Answer: Purulent pericarditis is defined as a localized infection of the pericardial space characterized either by:

- gross pus in the pericardium 

or 

- microscopic purulence with >20 leukocytes per oil immersion field.

Clinical significance: This distinction is important because purulent and infectious pericarditis are distinct clinical entities that may require different lines of management, and not all infections produce purulent effusions. 

#cardiology

#ID

References:

1. Goodman LJ. Purulent Pericarditis. Curr Treat Options Cardiovasc Med. 2000 Aug;2(4):343-350. doi: 10.1007/s11936-996-0008-8. PMID: 11096539.

2. Lee ES, Lin C, Pizula J, Pandya KA, Mehra AO, Van Herle H. Purulent Bacterial Pericarditis: Rare Yet Lethal. JACC Case Rep. 2024 Mar 4;29(7):102282. doi: 10.1016/j.jaccas.2024.102282. PMID: 38465283; PMCID: PMC10924136.

SQ emphysema after endotracheal intubation

Case: 53 years old patient was intubated in the ICU without any complications. CXR showed an ETT in the right mainstem. Provider pulled the ETT by 3 cm. After adjustment, the patient developed significant SQ emphysema along with periorbital swelling. Almost all cases of postintubation tracheal laceration are reported in? - select one

A) Short female patients

B) Tall male patients

Answer: A

Tracheal tear due to repositioning of the tube without cuff deflation 

Tracheobronchial laceration is a potentially serious complication of endotracheal intubation. It can occur following uneventful intubation. Most injuries are in the lower third of the trachea.

Most common causes include:

• Overinflation of the cuff, resulting in necrosis of the mucosa after prolonged intubation
• Repositioning of the tube without cuff deflation (as may have occurred in the above case)
• Patient movement
• A sudden increase in the intratracheal pressure caused by vigorous coughing in the presence of the endotracheal tube
• Inappropriate tube size
• COPD
• Conditions associated with a weakness of the membranous trachea (eg, elderly patient, steroid therapy)
• Mucosal erosion or perforation of the anterior cartilaginous tracheal wall from the tip of the tube or the stylet.

Interestingly, almost all cases of postintubation tracheal laceration are reported in short female patients.

#procedures

References:

1. A 63-Year-Old Woman With Subcutaneous Emphysema Following Endotracheal Intubation - Chest. 2005;128:434-438

2. Sakamoto A, Kogou Y, Matsumoto N, Nakazato M. Massive subcutaneous emphysema and pneumomediastinum following endotracheal intubation. Intern Med. 2013;52(15):1759. doi: 10.2169/internalmedicine.52.0575. Epub 2012 Mar 1. PMID: 23903518.

Barbeau test

Q: What is the Barbeau test before performing radial artery catheterization?

Answer: When pulse oximetry (pulse-ox) is used to determine the viability of ulnar and radial arteries.

YouTube link: https://www.youtube.com/watch?v=FhjsfgwflxM&t=16s

References:

1. Boncoraglio A, Caltabiano G, Foti PV, Mammino L, Failla G, Palmucci S, Basile A. Distal radial artery: The last extreme rescue arterial access for interventional radiologists? SAGE Open Med Case Rep. 2019 Jan 16;7:2050313X18823918. doi: 10.1177/2050313X18823918. PMID: 30719318; PMCID: PMC6349972.

2. Koury A Jr, Monsignore LM, de Castro-Afonso LH, Abud DG. Safety of ultrasound-guided distal radial artery access for abdominopelvic transarterial interventions: a prospective study. Diagn Interv Radiol. 2020 Nov;26(6):570-574. doi: 10.5152/dir.2020.19543. PMID: 32673202; PMCID: PMC7664746.

3. Diagram source:  Transradial approach and its variations for neurointerventional procedures: Literature review August 2020 - Surgical Neurology International 11:248 DOI: 10.25259/SNI_366_2020 License: CC BY-NC-SA 4.0

Helicobacter pylori infection and esophageal cancer

Q: H. pylori infection may be protective against esophageal adenocarcinoma?

A) True

B) False

Answer: A

Paradoxical to conceptual thinking, H. pylori infection appears to be protective against gastroesophageal reflux disease (GERD), Barrett's esophagus (BE) induced dysplasia, and subsequently to esophageal adenocarcinoma.

The possible explanations for this surprising paradox are two. First, the chronic gastritis from H. pylori infection interferes with the acid production and so protects against BE. Second, H. pylori strains that express cytotoxin-associated gene A (cagA) appear to be especially damaging to the stomach but especially protective for the esophagus. 

#oncology

#GI

#ID

References:

1. Erőss B, Farkas N, Vincze Á, et al. Helicobacter pylori infection reduces the risk of Barrett's esophagus: A meta-analysis and systematic review. Helicobacter 2018; 23:e12504.

2. Castro C, Peleteiro B, Lunet N. Modifiable factors and esophageal cancer: a systematic review of published meta-analyses. J Gastroenterol 2018; 53:37.

bright green cytoplasmic inclusions

Q: What is the importance of bright green cytoplasmic inclusions?

Answer: Usually associated with high mortality (and certain death)

Bright green cytoplasmic inclusions can be seen in neutrophils or monocytes. These patients are usually sick and have high mortality. They are also called "critical green inclusions"

These inclusions usually test negative for iron, bilirubin, and myeloperoxidase on special stains.

Most patients with such findings during COVID-19 died within days of the finding. Similar findings were reported in a septic patient who died.

Most of these patients also have increased transaminases.

#Hematology

#pathology

References: 

1. Jazaerly T, Gabali AM. Green neutrophilic inclusions could be a sign of impending death! Blood 2014; 123:614.

2. Harris VN, Malysz J, Smith MD. Green neutrophilic inclusions in liver disease. J Clin Pathol 2009; 62:853.

3. Cantu MD, Towne WS, Emmons FN, et al. Clinical significance of blue-green neutrophil and monocyte cytoplasmic inclusions in SARS-CoV-2 positive critically ill patients. Br J Haematol 2020; 190:e89.

4. Hodgson TO, Ruskova A, Shugg CJ, et al. Green neutrophil and monocyte inclusions - time to acknowledge and report. Br J Haematol 2015; 170:229.

Anbx after perianal abcess

Q: 73 years old male is admitted to the ICU from a Nursing Home (NH) due to pneumonia. While recovering, the patient also gets diagnosed with a perianal abscess. Surgical service drained it at the bedside. Per American Society of Colorectal Surgery (ASCRS) guidelines, all of the following make him eligible for a course of antibiotics EXCEPT?

A) Signs of systemic infection

B) End Stage Renal Disease

C) Diabetes

D) Valvular heart disease

E) Immunosuppression

Answer: B

Although conventionally all patients with perianal and perirectal abscesses get treatment with a course of antibiotics, to sustain stewardship towards unnecessary use of antibiotics, the American Society of Colorectal Surgery (ASCRS) guidelines suggest a course of empiric antibiotics after drainage of an anorectal abscess only in patients:

• Extensive perianal/perineal cellulitis
• Signs of systemic infection
• Diabetes
• Valvular heart disease
• Immunosuppression

This is because routine antibiotic use after drainage of an anorectal abscess does not protect against fistula formation. Said that clinical judgement supercedes any guidelines!

#ID

#surgical-critical-care

References: 

1. Gaertner WB, Burgess PL, Davids JS, et al. The American Society of Colon and Rectal Surgeons Clinical Practice Guidelines for the Management of Anorectal Abscess, Fistula-in-Ano, and Rectovaginal Fistula. Dis Colon Rectum 2022; 65:964.

2. Sözener U, Gedik E, Kessaf Aslar A, et al. Does adjuvant antibiotic treatment after drainage of anorectal abscess prevent development of anal fistulas? A randomized, placebo-controlled, double-blind, multicenter study. Dis Colon Rectum 2011; 54:923.

CU in OR

Q: 52 years old female with a known history of severe cold urticaria (CU) is admitted for elective ventral hernia repair. Which of the following treatments or preventive measures may not be very effective? - select one

A) Keep patient sufficiently warm throughout the surgery

B) Avoidance of cold intravenous solutions during surgery

C) Keep OR ready for possible anaphylaxis reaction

D) Administer H-1 and H-2 combo before surgery

E) Administer glucocorticoids before surgery

Answer: E

Surgery is a well-known trigger for CU. As expected, and prudently, the first three choices in the above questions should be practiced to avoid any mishap. Also, though it may not be an effective strategy, if the patient's threshold temperature for CU triggers is known, it may help. Many patients with such episodes in the past can report a ballpark figure of their threshold trigger temperature.

Pre-medication with H-1 and H-2 antihistamines may be helpful.

Pre-medication with glucocorticoids is usually ineffective, possibly because of the absence of a late-phase cellular infiltrate.

#allergy-immunology

References:

1. Booth K, Parissis H. Management of cold-induced urticaria during cardiac surgery. J Card Surg 2011; 26:158.

2. De la Borbolla JM, Tapies S, Mbongo C, et al. Cold urticaria: its importance in the operating room. J Investig Allergol Clin Immunol 2010; 20:446.

3. Black AK, Keahey TM, Eady RA, Greaves MW. Dissociation of histamine release and clinical improvement following treatment of acquired cold urticaria by prednisone. Br J Clin Pharmacol. 1981 Sep;12(3):327-31. doi: 10.1111/j.1365-2125.1981.tb01221.x. PMID: 6170299; PMCID: PMC1401800.

4. Siebenhaar F, Staubach P, Metz M, et al. Peltier effect-based temperature challenge: an improved method for diagnosing cold urticaria. J Allergy Clin Immunol 2004; 114:1224.

Dangers of endotracheal intubation in salicylate poisoning

Q: Why is it advisable to avoid intubation as much as possible in a salicylate-toxic patient?

Answer: Intubation exacerbates the salicylate toxicity to unprecedented levels.

A salicylate-toxic patient may die very quickly if intubated just for precaution! They should be intubated -ONLY and ONLY - as a last resort, as if not intubated, they may die, or definitely need airway protection.

These patients have a high tendency to have peri-procedural cardiovascular collapse. Once a neuromuscular blocking agent (NMBA) terminates the salicylate-induced primary respiratory alkalosis, an acidosis acutely and substantially worsens, followed by salicylate anions protonating to uncharged salicylic acid, redistributing into vulnerable tissue, and exacerbating toxicity. On the other end of the spectrum, severe metabolic acidosis is considered a "physiologically difficult airway" because induction agents and NMBAs make the apneic phase of rapid sequence intubation physiologically intolerable. 

In situations where intubation is ABSOLUTELY NEEDED, many experts advise administration of 'one to two amps of bicarb.' Another option is to do awake intubation without NMBA to avoid an apneic period. In such cases, Ketamine is a good choice because it maintains respiratory drive. If NMBA is administered, the apneic time should be minimized.

After intubation, high minute ventilation (MV) should be maintained to counter severe acidosis expected post-intubation in salicylate poisoning. The rule of thumb is to apply the same MV as the patients had before intubation. Again, it is advisable to avoid long-acting NMBAs.

The eventual goal is to take control of acid-base balance via more definitive treatment, such as hemodialysis or CRRT.

#toxicology

#procedures

#acid-base

References:

1. Stolbach AI, Hoffman RS, Nelson LS. Mechanical ventilation was associated with acidemia in a case series of salicylate-poisoned patients. Acad Emerg Med 2008; 15:866.

2. Greenberg MI, Hendrickson RG, Hofman M. Deleterious effects of endotracheal intubation in salicylate poisoning. Ann Emerg Med 2003; 41:583.

PAC balloon inflation

Q: To measure Pulmonary artery pressure (wedge) via pulmonary artery catheter (PAC), when the balloon is inflated, it should not be inflated beyond the tip of the catheter.

A) True

B) false

Answer: B

While wedging the Swan-Ganz catheter (PAC), the balloon should be fully inflated to cover the tip of the catheter; otherwise, the risk of pulmonary artery rupture increases. Also, the measurement would not be correct.

#hemodynamics

#procedures

References:

1. Ennala S, Melillo CA, Lane JE, Tonelli AR. Effect of pulmonary artery catheter balloon inflation on pulmonary hemodynamics. Cardiovasc Diagn Ther. 2022 Feb;12(1):37-41. doi: 10.21037/cdt-21-515. PMID: 35282667; PMCID: PMC8898684.

2. Durbin CG Jr. The range of pulmonary artery catheter balloon inflation pressures. J Cardiothorac Anesth. 1990 Feb;4(1):39-42. doi: 10.1016/0888-6296(90)90445-l. PMID: 2131854.

Adapting to a loved one death

Q: The process of adapting to the loss of a loved one and integrating grief is called? - Select one

A) Bereavement

B) Grief

C) Mourning 

D) Prolonged grief disorder 

Answer: C

It is essential to understand four responses that may occur after the loss of a loved one.

Bereavement (choice A) is simply the situation in which a loved one dies.

Grief  (choice B) is the natural response to that loss, expressed through thoughts, feelings, behaviors, and physiologic reactions, influenced by personal, cultural, and religious rituals.

Mourning (choice C) is the process of adapting to a loss and integrating grief. Adaptation involves accepting the finality and consequences of the loss and a changed relationship with the deceased, restoring the capacity to thrive, and re-envisioning the future with the possibility for happiness and meaning in a world without the deceased. Like grief, mourning is influenced by personal, cultural, and religious beliefs and rituals.

Prolonged grief disorder (choice D) is a prolonged grief disorder is a form of grief that is unusually intense, protracted, and disabling. It is maladaptive thoughts, dysfunctional behaviors, dysregulated emotions, and/or serious psychosocial problems that impede adaptation to the loss. It is also named as chronic grief, complex grief, complicated grief, pathological grief, persistent complex bereavement disorder, traumatic grief, and unresolved grief.  Please note: For many experts, it is not a psychiatric disorder in its purest form,

#palliative care

#psychiatry

References:

Zisook S, Shear K. Grief and bereavement: what psychiatrists need to know. World Psychiatry 2009; 8:67.

Boelen PA, Smid GE. Disturbed grief: prolonged grief disorder and persistent complex bereavement disorder. BMJ 2017; 357:j2016.

ICD-11 for Mortality and Morbidity Statistics (Version: 05/2021) https://icd.who.int/browse11/l-m/en#/http://id.who.int/icd/entity/1183832314 (Accessed on August 31, 2025).

Prigerson HG, Boelen PA, Xu J, et al. Validation of the new DSM-5-TR criteria for prolonged grief disorder and the PG-13-Revised (PG-13-R) scale. World Psychiatry 2021; 20:96.

Lactulose MoA

Q: What are the 3 mechanisms by which lactulose improves hepatic encephalopathy?

Answer: 

Although lactulose use is usually synonymous with a simple cathartic intervention to 'flush out' colonic bacteria, its mechanism of action (MoA) is relatively more complex:

1. The conversion of Lactulose to lactic acid results in acidification of the gut lumen. This favors the conversion of NH4+ + to NH3 and the passage of NH3 from tissues into the lumen.

2. Gut acidification inhibits ammoniagenic coliform bacteria, leading to increased levels of nonammoniagenic lactobacilli.

3. Lactulose also works as a cathartic, reducing colonic bacterial load.

Also, in contrast to conventional belief, lactulose does not significantly alter colonic water content; rather, its effect is due to stimulation of motility (reference # 2)

#GI

#pharmacology

#hepatology

References:

1. Bloom PP, Tapper EB. Lactulose in cirrhosis: Current understanding of efficacy, mechanism, and practical considerations. Hepatol Commun. 2023 Oct 12;7(11):e0295. doi: 10.1097/HC9.0000000000000295. PMID: 37820287; PMCID: PMC10578757.

2. Gunn D, Yeldho C, Hoad C, Menys A, Gowland P, Marciani L, Spiller R. Mechanisms underlying the laxative effect of lactulose: A randomized placebo-controlled trial showing increased small bowel water and motility unaltered by the 5-HT3 receptor antagonist, ondansetron. Neurogastroenterol Motil. 2024 Apr;36(4):e14754. doi: 10.1111/nmo.14754. Epub 2024 Feb 5. PMID: 38316636.

In emergent management of hyperkalemia

Q: All of the following can be used in emergent management of hyperkalemia EXCEPT? - Select one

A) Intravenous Epinephrine 

B) Nebulized Albuterol

C) Intravenous Albuterol

D) Subcutaneous Terbutaline

E) Insulin with glucose 

Answer: A

Beta-2-adrenergic agonists (B2AA) are used as adjuvant treatment in emergent hyperkalemia. Although 'Epi' (choice A) is a B2AA, it can induce angina. A large proportion of patients who developed hyperkalemia usually have renal failure/insufficiency and are prone to have underlying subclinical coronary disease.

Mechanism of Action (MoA): The B2AA drives potassium into the cells by increasing the activity of the Na-K-ATPase pump in skeletal muscle. Beta-2-adrenergic receptors in skeletal muscle also activate the inwardly directed Na-K-2Cl cotransporter, which may account for as much as one-third of the uptake response to catecholamines. B2AA in the acute treatment of hyperkalemia lowers the serum potassium concentration by 0.5 to 1.5 mEq/L. The reason B2AA is used only as an adjuvant treatment is that it takes approximately 30 minutes to achieve peak effect with intravenous infusion and 90 minutes with nebulization.

Albuterol (choices B and C) is relatively selective for the beta-2-adrenergic receptors. The dose for emergent hyperkalemia administered via nebulizer is 4 to 8 times the dose for bronchodilation, i.e., 10 to 20 mg in 4 mL of saline, administered over 10 minutes by nebulization. Less well known is the fact that Albuterol can be given IV in a dose of 0.5 mg. Similarly, SQ terbutaline (choice D) is a suitable option when an IV line or nebulizer is unavailable or the patient can't tolerate them.

Insulin (choice E) is not a B2AA, but it drives potassium inside the cell and decreases the extracellular potassium transiently. Glucoce is added to insulin to avoid hypoglycemia.

Emergent dialysis is an effective way of lowering K, but arrangements may take time.

#electrolytes

References:

1. Clausen T, Everts ME. Regulation of the Na,K-pump in skeletal muscle. Kidney Int 1989; 35:1.

2. Gosmanov AR, Wong JA, Thomason DB. Duality of G protein-coupled mechanisms for beta-adrenergic activation of NKCC activity in skeletal muscle. Am J Physiol Cell Physiol 2002; 283:C1025.

3. Sowinski KM, Cronin D, Mueller BA, Kraus MA. Subcutaneous terbutaline use in CKD to reduce potassium concentrations. Am J Kidney Dis 2005; 45:1040.

4. Palmer BF, Carrero JJ, Clegg DJ, Colbert GB, Emmett M, Fishbane S, Hain DJ, Lerma E, Onuigbo M, Rastogi A, Roger SD, Spinowitz BS, Weir MR. Clinical Management of Hyperkalemia. Mayo Clin Proc. 2021 Mar;96(3):744-762. doi: 10.1016/j.mayocp.2020.06.014. Epub 2020 Nov 5. PMID: 33160639.

K and HTN

Q: The relationship of potassium (K) level and hypertension (HTN) is ____________ proportional? - select one

A) directly

B) inversely 

Answer: B

Although sodium intake remains an essential target in hypertension management, considerable evidence suggests that a higher-normal K level significantly lowers blood pressure in patients with HTN (but has an insignificant effect on normotensive patients). Several mechanisms have been proposed to explain this relationship. 

Firstly, low K-intake reduces sodium excretion by activating the chloride-sensitive WNK (With-No-Lysine kinase) pathway, thereby activating the thiazide-sensitive NaCl cotransporter. Conversely, a high intake of potassium increases sodium excretion. Potassium "sensing" via basolateral potassium (K+) channels in the distal convoluted tubule plays a key role in these pathways.

Secondly, potassium modulates the renin angiotensin system, which is upregulated in the setting of hypokalemia.

Thirdly, hypokalemia causes vascular calcification and promotes arterial stiffness by inducing autophagy and promoting vascular smooth muscle calcification.

All forms of K, i.e., bicarbonate, citrate, and chloride, produce the same effect. None is superior to others.

#electrolytes

#CVS

#hemodynamics

References:

1. Aburto NJ, Hanson S, Gutierrez H, et al. Effect of increased potassium intake on cardiovascular risk factors and disease: systematic review and meta-analyses. BMJ 2013; 346:f1378.

2. Binia A, Jaeger J, Hu Y, et al. Daily potassium intake and sodium-to-potassium ratio in the reduction of blood pressure: a meta-analysis of randomized controlled trials. J Hypertens 2015; 33:1509.

3. Poulsen SB, Fenton RA. K+ and the renin-angiotensin-aldosterone system: new insights into their role in blood pressure control and hypertension treatment. J Physiol 2019; 597:4451.

4. Furusho T, Uchida S, Sohara E. The WNK signaling pathway and salt-sensitive hypertension. Hypertens Res 2020; 43:733.

Supplemental Vitamin & Kidney Stones

Case: 53 years old male who recently became conscious of his health, and started taking multiple different vitamins, after subscribing to health-related social media videos, is admitted to the ICU with severe sepsis and flank pain associated with crepitus over the same area. The patient gets diagnosed with severe emphysematous pyelonephritis. Which of the following 'over the counter' (OTC) vitamins may cause these symptoms? - select one

A) Vitamin A

B) Vitamin B

C) Vitamin C

D) Vitamin D

Answer: C

Higher than recommended dietary allowance of Vitamin C (ascorbic acid), i.e., 90 mg/day, may lead to the formation of urinary calcium oxalate stones. High-dose vitamin C results in increased oxalate generation as the ascorbic acid is metabolized. For every 1000 mg of vitamin C ingested above 500 mg/day, urinary oxalate excretion rises 6 to 13 mg/day. Ingestion of 2000 mg/day of vitamin C significantly increases urinary oxalate excretion, carrying an extremely high risk of calcium oxalate stone formation. 

This risk appears to be higher in males (Reference #2).

#nephrology

#vitamins

References: 

1. Massey LK, Liebman M, Kynast-Gales SA. Ascorbate increases human oxaluria and kidney stone risk. J Nutr 2005; 135:1673.

2. Thomas LD, Elinder CG, Tiselius HG, et al. Ascorbic acid supplements and kidney stone incidence among men: a prospective study. JAMA Intern Med 2013; 173:386.

3. Ferraro PM, Curhan GC, Gambaro G, Taylor EN. Total, Dietary, and Supplemental Vitamin C Intake and Risk of Incident Kidney Stones. Am J Kidney Dis 2016; 67:400.

Proximal vs distal DVT

Q: Deep Venous Thrombosis (DVT) located in the popliteal vein is designated as? - select one

A) Proximal DVT

B) Distal DVT 

Answer: A

DVT is labelled as proximal if it occurs in the vein at:

• popliteal
• femoral
• iliac 

DVT  is labelled as distal if it occurs in isolation in calf veins or below the knee, as in:

• peroneal
• posterior tibial
• anterior tibial
• gastrocnemius 
• soleal

#CVS

#hematology

Further readings:

1. Kabashneh S, Singh V, Alkassis S. A Comprehensive Literature Review on the Management of Distal Deep Vein Thrombosis. Cureus. 2020 May 10;12(5):e8048. doi: 10.7759/cureus.8048. PMID: 32537267; PMCID: PMC7286578.

2. Nishiwaki S, Morita Y, Yamashita Y, Morimoto T, Amano H, Takase T, Hiramori S, Kim K, Oi M, Akao M, Kobayashi Y, Toyofuku M, Izumi T, Tada T, Chen PM, Murata K, Tsuyuki Y, Saga S, Sasa T, Sakamoto J, Kinoshita M, Togi K, Mabuchi H, Takabayashi K, Shiomi H, Kato T, Makiyama T, Ono K, Inoko M, Kimura T; COMMAND VTE Registry Investigators. Impact of no, distal, and proximal deep vein thrombosis on clinical outcomes in patients with acute pulmonary embolism: From the COMMAND VTE registry. J Cardiol. 2021 Apr;77(4):395-403. doi: 10.1016/j.jjcc.2020.10.019. Epub 2020 Nov 18. PMID: 33218901.

Steroids in HELLP

Q: Dexamethasone is one of the mainstay treatments in HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets).

A) True

B) False

Answer: B

In contrast to previous beliefs and earlier studies, dexamethasone failed to show any improvement in HELLP syndrome. Larger studies have been unable to show any benefits in improving maternal outcome or perinatal/infant death, despite the improvement in platelet count in the steroid group.

#ob-gyn

#hepatology

References:

1. Fonseca JE, Méndez F, Cataño C, Arias F. Dexamethasone treatment does not improve the outcome of women with HELLP syndrome: a double-blind, placebo-controlled, randomized clinical trial. Am J Obstet Gynecol 2005; 193:1591.

2. Katz L, de Amorim MM, Figueiroa JN, Pinto e Silva JL. Postpartum dexamethasone for women with hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome: a double-blind, placebo-controlled, randomized clinical trial. Am J Obstet Gynecol 2008; 198:283.e1.

3. Woudstra DM, Chandra S, Hofmeyr GJ, Dowswell T. Corticosteroids for HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome in pregnancy. Cochrane Database Syst Rev 2010; :CD008148.

Lasix effects - beside diuresis

Q: Besides diuresis, describe 2 more effects of furosemide (Lasix)?

Answer: Lasix is a diuretic that acts on the loop of Henle and inhibits the reabsorption of both sodium and chloride ions. Besides this basic function of diuresis

1. Lasix also causes peripheral vasodilation (mostly venodilatation) and an increase in systemic venous capacitance. Obviously, this helps with the CHF patients.

2. Lasix reduces ICP and can be used in conjunction with Mannitol by interfering with the Na transport, which in turn slows the production of CSF fluid from the choroid plexus.

#pharmacology

#hemodynamics

References:

1. de Berrazueta JR, González JP, de Mier I, Poveda JJ, García-Unzueta MT. Vasodilatory action of loop diuretics: a plethysmography study of endothelial function in forearm arteries and dorsal hand veins in hypertensive patients and controls. J Cardiovasc Pharmacol. 2007 Feb;49(2):90-5. doi: 10.1097/FJC.0b013e31802e3c39. PMID: 17312449.

2. Roberts PA, Pollay M, Engles C, Pendleton B, Reynolds E, Stevens FA. Effect on intracranial pressure of furosemide combined with varying doses and administration rates of mannitol. J Neurosurg. 1987 Mar;66(3):440-6. doi: 10.3171/jns.1987.66.3.0440. PMID: 3102698.

3. Samson D, Beyer CW Jr. Furosemide in the intraoperative reduction of intracranial pressure in the patient with subarachnoid hemorrhage. Neurosurgery. 1982 Feb;10(2):167-9. PMID: 7070614.

WE in dialysis

Q: What's the reason behind the increased risk of Wernicke Encephalopathy (WE) in renal dialysis patients?

Answer: Loss of the water-soluble vitamins, including thiamine 

It is a misconception that WE occurs only in heavy alcohol abuse. WE can occur in a wide range of causes, including poor nutrition, malabsorption, increased metabolic requirements, systemic illnesses, and/or increased loss of water-soluble vitamins.

Thiamine is a water-soluble vitamin that may be lost either in hemodialysis or peritoneal dialysis.

#neurology

#nephrology

#vitamins

References:

1. Hung SC, Hung SH, Tarng DC, et al. Thiamine deficiency and unexplained encephalopathy in hemodialysis and peritoneal dialysis patients. Am J Kidney Dis 2001; 38:941.

2. Jagadha V, Deck JH, Halliday WC, Smyth HS. Wernicke's encephalopathy in patients on peritoneal dialysis or hemodialysis. Ann Neurol 1987; 21:78.

3. Descombes E, Dessibourg CA, Fellay G. Acute encephalopathy due to thiamine deficiency (Wernicke's encephalopathy) in a chronic hemodialyzed patient: a case report. Clin Nephrol 1991; 35:171.

4. Oudman E, Wijnia JW, Severs D, Oey MJ, van Dam M, van Dorp M, Postma A. Wernicke's Encephalopathy in Acute and Chronic Kidney Disease: A Systematic Review. J Ren Nutr. 2024 Mar;34(2):105-114. doi: 10.1053/j.jrn.2023.10.003. Epub 2023 Oct 13. PMID: 37838073.

Smoking and HP

Q: Cigarette smoking may have a preventive effect on hypersensitivity pneumonitis (HP).

A) True

B) False

Answer: A

Cigarette smoking has a paradoxical effect on HP, meaning it is associated with a decreased risk of HP! This was found universal on all forms of HP, including farmer's lung, pigeon breeder's disease, contaminated air conditioners induced HP, and Japanese summer-type HP (Trichosporon cutaneum). 

This paradox gets trickier in the sense that once HP occurs, smoking does not attenuate its severity, but rather may cause a more chronic and severe course. This predisposition to a chronic course appears to be associated with a less pronounced production of IgG antibody in smokers.  Fortunately, this effect of smoking is reversible.

#pulmonary

#immunology

References:

1. Murin S, Bilello KS, Matthay R. Other smoking-affected pulmonary diseases. Clin Chest Med 2000; 21:121.

2. Arima K, Ando M, Ito K, et al. Effect of cigarette smoking on prevalence of summer-type hypersensitivity pneumonitis caused by Trichosporon cutaneum. Arch Environ Health 1992; 47:274.

3. McSharry C, Banham SW, Boyd G. Effect of cigarette smoking on the antibody response to inhaled antigens and the prevalence of extrinsic allergic alveolitis among pigeon breeders. Clin Allergy 1985; 15:487.

4. Ohtsuka Y, Munakata M, Tanimura K, et al. Smoking promotes insidious and chronic farmer's lung disease, and deteriorates the clinical outcome. Intern Med 1995; 34:966.

Myxedema madness

Q: What is myxedema madness?

Answer: When myxedema presents with psychotic features, it is called myxedema madness. 

The actual cause of psychosis in these patients is not clear, but concomitant hyponatremia is suspected to be the cause. Seizure is also not uncommon. Progressively, these patients progress to altered consciousness, confusion, lethargy, and obtundation. Focal or generalized seizures may progress to status epilepticus. Lumbar puncture (LP) may reveal elevated protein levels (typically <100 mg/dL).

#endocrinology

#neurology

#psychiatry

References:

1. Westphal SA. Unusual presentations of hypothyroidism. Am J Med Sci 1997; 314:333.

2. Mavroson MM, Patel N, Akker E. Myxedema Psychosis in a Patient With Undiagnosed Hashimoto Thyroiditis. J Am Osteopath Assoc 2017; 117:50.

3. Jansen HJ, Doebé SR, Louwerse ES, et al. Status epilepticus caused by a myxoedema coma. Neth J Med 2006; 64:202.

4. Haupt M, Kurz A. Reversibility of dementia in hypothyroidism. J Neurol 1993; 240:333.

Digitalis induced Ventricular Tachycardia

Q: Which of the following is more effective in Digitalis-induced Ventricular Tachycardia (V.Tach.)? - select one

A) Lidocaine

B) Phenytoin

Answer: B

Ventricular tachycardia (V.Tach.) is common in Digitalis toxicity and may respond well to Phenytoin (Dilantin). Lidocaine is another practical choice, but phenytoin depresses the enhanced ventricular automaticity without significantly slowing AV conduction. Phenytoin may reverse digitalis-induced prolongation of AV nodal conduction. Phenytoin has been shown to dissociate the inotropic and dysrhythmic action of digitalis, thus suppressing digitalis-induced tachydysrhythmias without diminishing the contractile effects. In addition, phenytoin can terminate supraventricular dysrhythmias induced by digitalis, whereas lidocaine may not be as effective.

Phenytoin has been administered in boluses of 100 mg every 5-10 minutes up to a loading dose of 15 mg/kg.

#cardiology

#pharmacology

References:

1. Alvarado-Alvarado JA, Salas-Villela RA, Reyes-Guerrero JA, Ezquerra-Osorio A. Phenytoin as treatment for bidirectional ventricular tachycardia in a patient with anterior myocardial infarction and digoxin toxicity. Arch Cardiol Mex. 2022;92(4):550-552. doi: 10.24875/ACM.21000262. PMID: 36413700; PMCID: PMC9681520.

2. Garan H, Ruskin JN, Powell WJ Jr. Centrally mediated effect of phenytoin on digoxin-induced ventricular arrhythmias. Am J Physiol. 1981 Jul;241(1):H67-72. doi: 10.1152/ajpheart.1981.241.1.H67. PMID: 7246790.

3. O'Reilly MV, MacDonald RT. Efficacy of phenytoin in the management of ventricular arrhythmias induced by hypokalaemia. Br Heart J. 1973 Jun;35(6):631-4. doi: 10.1136/hrt.35.6.631. PMID: 4712468; PMCID: PMC458670.

4. Regina AC, Rehman R, Hai O. Cardiac Glycoside and Digoxin Toxicity. [Updated 2025 Mar 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459165/

Extent of Anbxs for MRSA resistance

Q: All methicillin-resistant isolates of Staphylococcus aureus (MRSA) should also be considered resistant to all cephalosporins and carbapenems.

A) True

B) False

Answer: B

The answer used to be true, but since the advent of ceftaroline and ceftobiprole (fifth-generation cephalosporins), the answer is now false, as both ceftaroline and ceftobiprole retain activity against MRSA.

As a general rule, all methicillin-resistant isolates should be considered resistant to all beta-lactam antibiotics, including beta-lactamase inhibitor combinations, cephalosporins, and carbapenems, regardless of in vitro susceptibility results.

Other potential available agents are Linezolid, Telavancin, Teicoplanin, and Daptomycin. 

Numerous trials have shown larger efficacy with the combination of different drugs.

#ID

#pharmacology

References:

1. Chambers HF. Methicillin-resistant staphylococci. Clin Microbiol Rev 1988; 1:173.

2. Chang J, Tasellari A, Wagner JL, Scheetz MH. Contemporary pharmacologic treatments of MRSA for hospitalized adults: rationale for vancomycin versus non-vancomycin therapies as first line agents. Expert Rev Anti Infect Ther. 2023 Jul-Dec;21(12):1309-1325. doi: 10.1080/14787210.2023.2275663. Epub 2023 Nov 24. PMID: 37876291.

3. Cosimi RA, Beik N, Kubiak DW, Johnson JA. Ceftaroline for Severe Methicillin-Resistant Staphylococcus aureus Infections: A Systematic Review. Open Forum Infect Dis 2017; 4:ofx084.

4. Soriano A, Morata L. Ceftobripole: Experience in staphylococcal bacteremia. Rev Esp Quimioter 2019; 32 Suppl 3:24.

Stages of AF

Q: There are how many stages of Atrial Fibrillation (AF)? - select one

A) Three

B) Four

Answer: B

In 2023, the American College of Cardiology/American Heart Association/American College of Clinical Pharmacy/Heart Rhythm Society and 2024 European Society of Cardiology (ESC) guidelines have been updated to recognize the "disease continuum" aspect of AF. This new classification is clinically significant, with distinct management strategies for each stage.

Stage 1: At risk for AF 

– This stage is identified by either modifiable or nonmodifiable risk factors for AF:

1. Modifiable – such as Obesity, lack of fitness, hypertension, sleep apnea, alcohol, diabetes mellitus

2. Non-modifiable risk factors – Genetics, male sex, and age

Stage 2: Pre-AF

– This stage is identified by structural or electrical findings or clinical conditions predisposing AF:

1. Structural findings – such as Atrial enlargement

2. Electrical findings – Frequent atrial ectopy, short bursts of atrial tachycardia, or atrial flutter

3. High-risk clinical conditions – Heart failure, valve disease, coronary artery disease, hypertrophic cardiomyopathy, neuromuscular disorders, or hyperthyroidism

Stage 3: AF

 – This stage is further categorized under four substages:

1. 3A: Paroxysmal AF – AF that is intermittent and terminates in ≤7 days from onset. 

2. 3B: Persistent AF – AF that is continuous for >7 days and often requires intervention. A patient who presents with persistent AF and later has paroxysmal AF with treatment are still considered to have persistent AF, as this designation is more helpful in defining their AF substrate and clinical outcomes. Chronic or Lone AF is no more used as a term.

3. 3C: Long-standing persistent AF – AF that is continuous for >12 months.

4. 3D: Successful AF ablation – Freedom from AF after catheter (percutaneous) or surgical intervention to eliminate AF.

Stage 4: Permanent AF

 – This term is used when the patient and clinician make a joint decision to stop further attempts to restore and/or maintain sinus rhythm (ie, rhythm control). This stage represents a therapeutic decision and an inherent attribute of AF. 

#cardiology

References:

1. Joglar JA, Chung MK, Armbruster AL, et al. 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation 2024; 149:e1.

2. Van Gelder IC, Rienstra M, Bunting KV, et al. 2024 ESC Guidelines for the management of atrial fibrillation developed in collaboration with the European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J 2024; 45:3314.

3. Wyse DG, Van Gelder IC, Ellinor PT, et al. Lone atrial fibrillation: does it exist? J Am Coll Cardiol 2014; 63:1715.

Ketofol

Q: For Procedural Sedation and Analgesia (PSA), in Ketofol, "Ketamine and Propofol" are premixed in the combination of? - select one

A) 1:1 

B) 1:2

Answer: A

"Ketofol" has been used by many clinicians to get the best of both drugs and reduce the side effects of both drugs, e.g., reducing the propofol-induced hypotension and ketamine-induced vomiting and emergence reactions. The other advantage is that both drugs act synergistically. Commonly, 10 mg/mL ketamine and 10 mg/mL propofol are mixed into a 20-mL syringe. The initial dose is 0.375 to 0.5 mg/kg (0.0375 to 0.05 mL/kg of this mixture). Half of this dose can be repeated.

Although theoretically this is a great approach, studies have failed to bring any strong evidence.

#procedures

#pharmacology

References:

1. Messenger DW, Murray HE, Dungey PE, et al. Subdissociative-dose ketamine versus fentanyl for analgesia during propofol procedural sedation: a randomized clinical trial. Acad Emerg Med 2008; 15:877.

2. Willman EV, Andolfatto G. A prospective evaluation of "ketofol" (ketamine/propofol combination) for procedural sedation and analgesia in the emergency department. Ann Emerg Med 2007; 49:23.

3. Miner JR, Moore JC, Austad EJ, et al. Randomized, double-blinded, clinical trial of propofol, 1:1 propofol/ketamine, and 4:1 propofol/ketamine for deep procedural sedation in the emergency department. Ann Emerg Med 2015; 65:479.

4. Ferguson I, Bell A, Treston G, et al. Propofol or Ketofol for Procedural Sedation and Analgesia in Emergency Medicine-The POKER Study: A Randomized Double-Blind Clinical Trial. Ann Emerg Med 2016; 68:574.

Sarcomatoid renal cell carcinoma

Q: 44 years old male is admitted to the ICU after partial Renal Cell Carcinoma (RCC) removal, as some parts were found to be unresectable perioperatively. Patient is designated as having RCC with Sarcomatoid features. It is considered a good sign with a good prognosis for chemotherapy later.

A) True

B) False

Answer: B

Sarcomatoid dedifferentiation in RCC (clear or non-clear) consists of cell components that are spindled or resemble sarcoma cells. These tumors are recognized for their distinctive molecular and biological characteristics, including their clinical response to therapies.

The prognosis of patients with advanced, unresectable, or metastatic sarcomatoid RCC is usually poor. There is hope that with the arrival of checkpoint inhibitor immunotherapy, prognosis may improve, as newly emerging data show some evidence of a good response.

#oncology

#surgical-critical-care

References:

1. Delahunt B, Cheville JC, Martignoni G, et al. The International Society of Urological Pathology (ISUP) grading system for renal cell carcinoma and other prognostic parameters. Am J Surg Pathol 2013; 37:1490.

2. Fontes-Sousa M, Calvo E. First-line immune checkpoint inhibitors in advanced or metastatic renal cell carcinoma with sarcomatoid features. Cancer Treat Rev. 2022 Apr;105:102374. doi: 10.1016/j.ctrv.2022.102374. Epub 2022 Mar 10. PMID: 35303549.

3. Su H, Yu C, Ma X, Yu X, Sun G. Immunotherapy treatment for sarcomatoid renal cell carcinoma: case report and literature review. Ann Med Surg (Lond). 2024 Feb 28;86(9):5471-5475. doi: 10.1097/MS9.0000000000001647. PMID: 39239004; PMCID: PMC11374251.

BIA-BCL and BIA--SCC

Q: Breast implant-associated squamous cell carcinoma (BIA-SCC) and breast implant-associated B-cell lymphoma (BIA-BCL) are usually benign diseases. 

A) True

B) False

Answer: B

BIA-BCL and BIA-SCC, if they occur, are aggressive tumors, which may require surgical en bloc excision of the implant, capsule, and tumor, followed by chemotherapy as well as radiation therapy.

BIA-BCL seems to be more responsive to chemotherapy, whereas BIA-SCC is found to be less responsive to chemotherapy.

They can occur with any type of implant and typically develop late, with a mean time of around 22-23 years. BIA-BCL usually presents as erythema and a periprosthetic effusion, while BIA-SCC presents as a late-onset seroma or mass.

#oncology

References:

1. Goldberg MT, Llaneras J, Willson TD, et al. Squamous Cell Carcinoma Arising in Breast Implant Capsules. Ann Plast Surg 2021; 86:268.

2. Buchanan PJ, Chopra VK, Walker KL, et al. Primary Squamous Cell Carcinoma Arising From a Breast Implant Capsule: A Case Report and Review of the Literature. Aesthet Surg J 2018; 38.

3. Fracol ME, Rodriguez MM, Clemens MW. A Spectrum of Disease: Breast Implant-Associated Anaplastic Large Cell Lymphoma, Atypicals, and Other Implant Associations. Clin Plast Surg 2023; 50:249.

American Society of Plastic Surgeons statement on breast cancer-associated squamous cell carcinoma. 09/08/2022. https://www.plasticsurgery.org/for-medical-professionals/publications/psn-extra/news/asps-statement-on-breast-implant-associated-squamous-cell-carcinoma (last accessed on October 2, 2025.

Gender difference in SLE

Q: Having a 'male sex' is considered a poor prognostic factor associated with increased mortality in systemic lupus erythematosus (SLE).

A) True

B) False

Answer: A

Conventionally, SLE is considered a disease more common in African American females. The prognosis associated with increased mortality gets worse if a patient is affected. Other poor prognostic factors are:

• Kidney disease
• Hypertension
• Presentation at extreme ages
• Low socioeconomic status
• Being a Black person
• Presence of antiphospholipid antibodies
• Antiphospholipid antibody syndrome
• High overall disease activity

#rheumatology

References:

1. Albrecht K, Troll W, Callhoff J, Strangfeld A, Ohrndorf S, Mucke J. Sex- and gender-related differences in systemic lupus erythematosus: a scoping review. Rheumatol Int. 2025 Jun 27;45(7):160. doi: 10.1007/s00296-025-05910-7. PMID: 40576834; PMCID: PMC12204902.

2. Lee YH, Song GG. Mortality in patients with systemic lupus erythematosus: A meta-analysis of overall and cause-specific effects. Lupus 2024; 33:929.

3. Sutton EJ, Davidson JE, Bruce IN. The systemic lupus international collaborating clinics (SLICC) damage index: a systematic literature review. Semin Arthritis Rheum 2013; 43:352.