Parovirus 19 fetal severe anemia

Q: A 24-year-old female with 22 weeks of pregnancy is admitted to the ICU with severe symptoms of Parvovirus 19, confirmed with a high IgM titer but a negative IgG titer. There is a severe fetal anemia, and thrombocytopenia is suspected. How should the blood transfusion be given? -select one

A) Slow Intravenous 

B) Intrauterine

C) Plasmapheresis

Answer: B

Usually, a fetus can handle mild to moderate anemia without any major intervention. Severe fetal anemia can lead to hydrops fetalis. Noninvasive methods to detect fetal anemia are:

• Doppler middle cerebral artery (MCA) peak systolic velocity (PSV), and 
• ductus venosus velocity  

Invasively, cord blood sampling can be performed via percutaneous umbilical venous sampling, but is reserved for suspected severe cases requiring intervention.

Interesting, blood transfusions in such situations are given directly via intrauterine. Intrauterine transfusion is possible only after 18 weeks of pregnancy due to the small vessel size prior to it.

The authors of this question highly encouraged students to review reference #4 below.

#Ob-gyn

References:

1. Fairley CK, Smoleniec JS, Caul OE, Miller E. Observational study of effect of intrauterine transfusions on outcome of fetal hydrops after parvovirus B19 infection. Lancet 1995; 346:1335.

2. Rodis JF, Borgida AF, Wilson M, et al. Management of parvovirus infection in pregnancy and outcomes of hydrops: a survey of members of the Society of Perinatal Obstetricians. Am J Obstet Gynecol 1998; 179:985.

3. von Kaisenberg CS, Jonat W. Fetal parvovirus B19 infection. Ultrasound Obstet Gynecol 2001; 18:280.

4. Devlieger R, Vergote S, Van den Eede E, Haenen K, Lewi L. Intrauterine transfusion: Best practices, techniques, and evolving trends. Best Pract Res Clin Obstet Gynaecol. 2026 Feb;104:102686. doi: 10.1016/j.bpobgyn.2025.102686. Epub 2025 Nov 20. PMID: 41289715.

NPPE - MOA

Case: 22 years old atheletic male went through a non-complicated appendectomy under general anesthesia. Patient became agitated on weaning sedation and started biting on the endotracheal tube (ETT). The patient was extubated, but on extubation developed severe pulmonary edema with desaturation. Patient recovered well with supplemental oxygen, non-invasive positive pressure ventilation (NIPPV), diuresis, and infusion of Dexmedetomidine, and was eventually extubated without complications. Why is post-extubation pulmonary edema called negative pressure pulmonary edema (NPPE)?

Answer: Post-extubation pulmonary edema is a common phenomenon in the PACU/ICU if a patient forcibly inhales against a closed glottis. This is also known as the Mueller or reverse Valsalva maneuver. This phenomenon occurs post-extubation due to laryngospasm, pharyngeal obstruction, or biting of the endotracheal tube during extubation. 

Conventional teaching holds that it occurs immediately, though this is not entirely true; a delayed NPPE has been reported up to 12 hours after extubation. People with obesity, short neck, obstructive sleep apnea, or acromegaly are at the highest risk, followed by young, healthy, athletic adults.

The correct term is negative pressure pulmonary edema, which refers to a non-cardiac form of pulmonary edema resulting from the development of negative interstitial pressure around the capillaries, drawing intravascular fluid into the interstitial space.

#procedure

#pulmonary

References:

1. Mulkey Z, Yarbrough S, Guerra D, et al. Postextubation pulmonary edema: a case series and review. Respir Med 2008; 102:1659.

2. Holmes JR, Hensinger RN, Wojtys EW. Postoperative pulmonary edema in young, athletic adults. Am J Sports Med 1991; 19:365.

3. Tsai PH, Wang JH, Huang SC, Lin YK, Lam CF. Characterizing post-extubation negative pressure pulmonary edema in the operating room-a retrospective matched case-control study. Perioper Med (Lond). 2018 Dec 6;7:28. doi: 10.1186/s13741-018-0107-6. PMID: 30534363; PMCID: PMC6282297.

PG

Q: A 43-year-old male with an established history of ulcerative colitis is admitted to the ICU with Lower GI bleed requiring transfusion. On physical exam, chronic ulceration was noted on the lower extremity and diagnosed as Pyoderma gangrenosum (PG). PG, as the name suggests, is an infectious process causing gangrene.

A) True

B) False

Answer: B

Pyoderma gangrenosum (PG) is a misnomer as it is neither an infectious nor a gangrenous condition! The probability of this misnomer arises from its striking, infectious-like appearance.

PG is a neutrophilic dermatosis that presents as an inflammatory, ulcerative skin disorder. The most common presentation of PG is an inflammatory papule or pustule that progresses to a painful ulcer with a violaceous, undermined border and a purulent base. It may also present with bullous, vegetative, peristomal, and extracutaneous lesions.

Clinical Significance: It has high association with an underlying systemic diseases like inflammatory bowel disease, hematologic disorders, and arthritis.

#dermatology

References:

1. Maverakis E, Marzano AV, Le ST, Callen JP, Brüggen MC, Guenova E, Dissemond J, Shinkai K, Langan SM. Pyoderma gangrenosum. Nat Rev Dis Primers. 2020 Oct 8;6(1):81. doi: 10.1038/s41572-020-0213-x. PMID: 33033263.

2. Łyko M, Ryguła A, Kowalski M, Karska J, Jankowska-Konsur A. The Pathophysiology and Treatment of Pyoderma Gangrenosum-Current Options and New Perspectives. Int J Mol Sci. 2024 Feb 19;25(4):2440. doi: 10.3390/ijms25042440. PMID: 38397117; PMCID: PMC10889749.

3. Moltrasio C, Romagnuolo M, Tavoletti G, Maronese CA, Marzano AV. Pyoderma gangrenosum: pathogenetic mechanisms and their implications for treatment. Semin Immunopathol. 2025 Oct 23;47(1):38. doi: 10.1007/s00281-025-01064-7. PMID: 41128863; PMCID: PMC12549756.

iNO and organ dysfunction

Q: Prolonged use of inhaled Nitric Oxide (iNO) is intended to cause more of? - select one

A) Kidney dysfunction

B) liver dysfunction

Answer: A

Prolonged use of iNO beyond 5-7 days may increase the risk of acute kidney injury (AKI). This inference is drawn primarily from trials of its use in patients with ARDS and after cardiac surgery. 

An interesting paradox is the finding that short-term use (24 hours post-surgery) of iNO in patients who require prolonged cardiopulmonary bypass may have a protective effect for AKI. This short-term benefit is due to the fact that, in prolonged bypass cases, increased hemolysis raises plasma levels of free oxyhemoglobin, which binds and depletes endogenous NO, leading to vasoconstriction, impaired tissue perfusion, and inflammation (reference #3).

#cardiovascular

#nephrology

References:

1. Ruan SY, Huang TM, Wu HY, et al. Inhaled nitric oxide therapy and risk of renal dysfunction: a systematic review and meta-analysis of randomized trials. Crit Care 2015; 19:137.

2. Gebistorf F, Karam O, Wetterslev J, Afshari A. Inhaled nitric oxide for acute respiratory distress syndrome (ARDS) in children and adults. Cochrane Database Syst Rev 2016; :CD002787.

3. Lei C, Berra L, Rezoagli E, et al. Nitric Oxide Decreases Acute Kidney Injury and Stage 3 Chronic Kidney Disease after Cardiac Surgery. Am J Respir Crit Care Med 2018; 198:1279.

The time-relationship of 'osmolal gap' and 'Anion gap' in toxic alcohols

Q: In Methanol and Ethylene Glycol toxicity, the time-relationship of 'osmolal gap' and 'Anion gap' is inversely proportional.

A) True

B) False

Answer: A

After ingestion of Methanol and Ethylene Glycol, the osmolal gap continues to drop as the alcohols are metabolized, while the anion gap rises. The following graph best describes the relationship.

#toxicity

References:

1. Kraut JA, Mullins ME. Toxic Alcohols. N Engl J Med. 2018 Jan 18;378(3):270-280. doi: 10.1056/NEJMra1615295. Erratum in: N Engl J Med. 2019 Jan 10;380(2):202. doi: 10.1056/NEJMx180046. PMID: 29342392.

2. Gallagher N, Edwards FJ. The Diagnosis and Management of Toxic Alcohol Poisoning in the Emergency Department: A Review Article. Adv J Emerg Med. 2019 May 22;3(3):e28. doi: 10.22114/ajem.v0i0.153. PMID: 31410405; PMCID: PMC6683589.

Clinical features of infective endocarditis

Q: A 52-year-old male with a history of End Stage Renal Disease (ESRD) is admitted to the ICU with suspected infective endocarditis (IE). On clinical exam found to have Janeway lesions. Janeway lesions are more common in? - select one

A) acute IE

B) subacute IE

Answer: A

Clinical exam in IE plays an important role. Three hallmark characteristic findings, though relatively uncommon, are highly suggestive of IE:

• Janeway lesions
• Osler nodes 
• Roth spots 

Janeway lesions are nontender erythematous macules on the palms and soles. Histologically, they are microabscesses with neutrophil infiltration of capillaries. Janeway lesions are more common in acute than subacute IE. 

In contrast, Osler nodes and Roth spots occur over a protracted time course of endocarditis. These two entities are sequelae of microthromboembolic occlusion, leading to localized immune-mediated vasculitis. Osler nodes, in contrast to Janeway lesions, are tender and subcutaneous (SQ) violaceous nodules mostly on the pads of the fingers and toes, and may also occur on the thenar and hypothenar eminences. Interestingly, tenderness begins a few days before the nodule appears. Roth spots are exudative, edematous, hemorrhagic lesions of the retina with pale centers.

#physical-exam

#ID

References:

1. Saccente M, Cobbs CG. Clinical approach to infective endocarditis. Cardiol Clin. 1996 Aug;14(3):351-62. doi: 10.1016/s0733-8651(05)70289-7. PMID: 8853130.

2. Loughrey PB, Armstrong D, Lockhart CJ. Classical eye signs in bacterial endocarditis. QJM 2015; 108:909.

3. Abdelgawad H, Azab S, Abdel-Hay MA, Almaghraby A. Clinical features and outcomes of infective endocarditis: a single-centre experience. Cardiovasc J Afr. 2023 May-Jun 23;34(2):82-88. doi: 10.5830/CVJA-2022-027. Epub 2022 Aug 3. PMID: 35924572; PMCID: PMC10512034.

extraocular muscles in CIM

Q: In Critical Illness Myopathy (CIM), the presence of extraocular muscle weakness is diagnostic.

A) True

B) False

Answer: B

CIM has a few characteristic features:

• Flaccid quadriparesis 
• Proximal muscles are affected more than distal muscles.
• Ventilatory failure
• Facial muscle weakness (may or may not present)
• Sparing of extraocular muscles (very rarely involved)
• Intact sensation*
• Intact deep tendon reflexes*

*feature of Critical Illness Polyneuropathy (CIP)

References:

1. Latronico N, Rasulo FA, Eikermann M, Piva S. Illness Weakness, Polyneuropathy and Myopathy: Diagnosis, treatment, and long-term outcomes. Crit Care. 2023 Nov 13;27(1):439. doi: 10.1186/s13054-023-04676-3. Erratum in: Crit Care. 2023 Nov 30;27(1):469. doi: 10.1186/s13054-023-04757-3. PMID: 37957759; PMCID: PMC10644573.

2. Hermans G, Van den Berghe G. Clinical review: intensive care unit acquired weakness. Crit Care. 2015 Aug 5;19(1):274. doi: 10.1186/s13054-015-0993-7. PMID: 26242743; PMCID: PMC4526175.

aortopulmonary angle

Q: On chest X-ray, the aortopulmonary angle can be found on? - select one

A) left side

B) right side

Answer: A

The aortopulmonary angle, also called the aortopulmonary space or window, is a space between the aortic arch and the left pulmonary artery. It contains the ligamentum arteriosum, the left recurrent laryngeal nerve, lymph nodes, and fatty tissue. The space is bounded anteriorly by the ascending aorta, posteriorly by the descending aorta, medially by the left main bronchus, and laterally by the mediastinal pleura.

Clinical Significance: The presence of water radiodensity in this space on radiography may indicate a lymphadenopathy or possible neoplasm.

#pulmonary

#radiology

References:

1. Dewey, Marc; Magid, Donna; Wheeler, Paul S.; Hamm, Bernd (2004). "Aortopulmonary Window or Angle on the Chest Radiograph?". American Journal of Roentgenology. 182 (4): 1085–1086. doi:10.2214/ajr.182.4.1821085. ISSN 0361-803X. PMID 15039195.

2. Heitzman E, Lane E, Hammack D, Rimmler L (1975). "Radiological evaluation of the aortic-pulmonic window". Radiology. 116 (3): 513–8. doi:10.1148/116.3.513. PMID 1153753.

Enteral free water in high ICP

Q: Patients with elevated Intra-Cranial Pressure (ICP) should not be fed enteral free water.

 A) True

B) False

 Answer: A 

Patients with elevated ICP should be kept euvolemic, rather normo- to hyperosmolar. Any hypotonic fluid administration, including enteral free water, should be avoided whenever possible. Isotonic fluids are usually utilized guided by close monitoring of labs. Serum osmolality is targeted to stay above 280 mOsm/L, between 295 and 305 mOsm/L. Colloids have no specific advantage. 

 Clinicians should be aware that hyponatremia is common in patients with elevated ICP, particularly in patients with subarachnoid hemorrhage SAH). Hypertonic saline in bolus, popularly known as 'salt bomb' can be used per clinical judgement.

 #neurology 

 References: 

 1. Schmoker JD, Shackford SR, Wald SL, Pietropaoli JA. An analysis of the relationship between fluid and sodium administration and intracranial pressure after head injury. J Trauma 1992; 33:476. 

 2. Tranmer BI, Iacobacci RI, Kindt GW. Effects of crystalloid and colloid infusions on intracranial pressure and computerized electroencephalographic data in dogs with vasogenic brain edema. Neurosurgery 1989; 25:173.

 3. SAFE Study Investigators, Australian and New Zealand Intensive Care Society Clinical Trials Group, Australian Red Cross Blood Service, et al. Saline or albumin for fluid resuscitation in patients with traumatic brain injury. N Engl J Med 2007; 357:874.

SCC

Q: Small cell carcinoma in the lungs is considered a neuroendocrine tumor.

A) True

B) False

Answer: A

Small cell carcinoma, large cell neuroendocrine carcinoma, typical carcinoid, and atypical carcinoid all fall under the category of neuroendocrine tumors and share features with carcinoid lesions arising at other body sites. 

Small cell carcinomas and large cell neuroendocrine carcinomas have aggressive courses and, pathologically, exhibit a higher mitotic rate, distinguishing them from pulmonary carcinoids.

#oncology

#pulmonary

References:

1. WHO Classification of Tumours Editorial Board. Thoracic Tumours. In: WHO Classification of Tumours, 5th ed, IARC Publications, 2021. Vol 5.

2. Orlandi R. Neuroendocrine neoplasms of the lung: The latest updates. World J Clin Oncol. 2025 May 24;16(5):106630. doi: 10.5306/wjco.v16.i5.106630. PMID: 40503410; PMCID: PMC12149839.

3. Rekhtman N. Lung neuroendocrine neoplasms: recent progress and persistent challenges. Mod Pathol. 2022 Jan;35(Suppl 1):36-50. doi: 10.1038/s41379-021-00943-2. Epub 2021 Oct 18. PMID: 34663914; PMCID: PMC8695375.

Midazolam as intranasal or buccal route

Q: What is the dose of Midazolam to give intranasally if no IV or IM route is available?

Answer: if its an emergency and no IV line is established or (let say) if no syringe is available even to give intramuscularly (IM), midazolam can be given intranasally using the injectable solution of 5 mg/mL as a metered spray of 0.1 mL containing 0.5 mg, three to five times per nostril, and can be repeated, to a total dose of 10 mg for adults.

It can also be given buccally as 0.2 mg/kg, or a total of 10 mg altogether, once in adults.

#neurology

#pharmacology

References:

1. McKee HR, Abou-Khalil B. Outpatient pharmacotherapy and modes of administration for acute repetitive and prolonged seizures. CNS Drugs 2015; 29:55.

2. Dittrich TD, Vock D, Fisch U, et al. Efficacy and Tolerability of Intranasal Midazolam Administration for Antiseizure Treatment in Adults: A Systematic Review. Neurocrit Care 2024; 41:632.

3. Kay L, Merkel N, von Blomberg A, Willems LM, Bauer S, Reif PS, Schubert-Bast S, Rosenow F, Strzelczyk A. Intranasal midazolam as first-line inhospital treatment for status epilepticus: a pharmaco-EEG cohort study. Ann Clin Transl Neurol. 2019 Dec;6(12):2413-2425. doi: 10.1002/acn3.50932. Epub 2019 Nov 4. PMID: 31682078; PMCID: PMC6917318.

4. Armijo JA, Herranz JL, Pena Pardo MA, Adín J. Midazolam intranasal y bucal en el tratamiento de las convulsiones agudas [Intranasal and buccal midazolam in the treatment of acute seizures]. Rev Neurol. 2004 Mar 1-15;38(5):458-68. Spanish. PMID: 15029526.

CIM

Q: The Critical Illness Myopathy (CIM) affects which group of muscles more? - select one

A) distal 

B) proximal 

Answer: B

CIM, although it causes flaccid quadriparesis, usually affects the proximal muscles more. It is also associated with facial muscle weakness.

A pure exclusive CIM can be distinguished from Critical Illness Polyneuropathy (CIP) by normal sensation and normal or attenuated deep tendon reflexes. Patients with exclusive CIM grimace to pain even when they are encephalopathic.

Unfortunately, most patients suffer from combined CIP and CIM.

#ICU-course

#neurology

References:

1. Lacomis D, Giuliani MJ, Van Cott A, Kramer DJ. Acute myopathy of intensive care: clinical, electromyographic, and pathological aspects. Ann Neurol 1996; 40:645.

2. Z'Graggen WJ, Tankisi H. Critical Illness Myopathy. J Clin Neurophysiol. 2020 May;37(3):200-204. doi: 10.1097/WNP.0000000000000652. PMID: 32358245.

3. Rodriguez B, Larsson L, Z'Graggen WJ. Critical Illness Myopathy: Diagnostic Approach and Resulting Therapeutic Implications. Curr Treat Options Neurol. 2022;24(4):173-182. doi: 10.1007/s11940-022-00714-7. Epub 2022 Mar 28. PMID: 35370393; PMCID: PMC8958813.

4. Friedrich O. Critical illness myopathy: what is happening? Curr Opin Clin Nutr Metab Care. 2006 Jul;9(4):403-9. doi: 10.1097/01.mco.0000232900.59168.a0. PMID: 16778569.

banana bag

Q: Utilizing "Banana bag" plays an integral part in the management of alcohol withdrawal as it contains thiamine.

A) True

B) False

Answer: B

Although in the United States, use of "banana bag" is almost an integral part of management in alcohol withdrawal, there is no evidence that it prevents or contributes much to preventing Wernicke's encephalopathy or Delirium Tremens (DTs). It is called a banana bag due to its yellow color and contains

• thiamine
• folate
• multivitamin (MVI)
• isotonic saline with 5% dextrose

It is true that thiamine (given first) and glucose should be administered to prevent or treat Wernicke encephalopathy in the early phase of management, but preparing or specifically requesting a banana bag is not supported by evidence! 

Electrolytes, vitamins, and volume should be administered as needed per clinical and laboratory values.

#toxicity

References:

1. Flannery AH, Adkins DA, Cook AM. Unpeeling the Evidence for the Banana Bag: Evidence-Based Recommendations for the Management of Alcohol-Associated Vitamin and Electrolyte Deficiencies in the ICU. Crit Care Med. 2016 Aug;44(8):1545-52. doi: 10.1097/CCM.0000000000001659. PMID: 27002274.

2. LoVecchio F. Multivitamin "banana bags" provide little value in emergency department patients. Ann Emerg Med. 2012 May;59(5):414-5. doi: 10.1016/j.annemergmed.2011.11.007. PMID: 22525531.

3. Wells C, Butcher R, McCormack S. Intravenous Multivitamin Therapy Use in Hospital or Outpatient Settings: A Review of Clinical Effectiveness and Guidelines [Internet]. Ottawa (ON): Canadian Agency for Drugs and Technologies in Health; 2020 Oct 15. Available from: https://www.ncbi.nlm.nih.gov/books/NBK567072/

Kt/V

Q: What is the target Kt/V in patients with peritoneal dialysis? - select one

A) ≥ 1.3/week

B) ≥ 1.7/week

Answer: B

The objective of this question is to introduce students to the concept of Kt/V in dialysis patients, which is used to indicate dialysis adequacy. The K, t, and V stand respectively for:

K – dialyzer clearance of urea

t – dialysis time

V – volume of distribution of urea*

Per the US National Kidney Foundation, in hemodialysis (HD), the target is ≥1.3^, and in peritoneal dialysis, the target is ≥1.7/week. Although there are various criticisms against its use, it remains a vital concept for clinicians to know.

Clinical significance: It correlates with survival.

There are online calculators available to determine Kt/V

*approximately equal to the patient's total body water

^ Per Centers for Medicare and Medicaid Services (CMS): the minimum required is ≥1.2 per session

References/further reading:

1. Churchill BM, Patri P. The Nitty-Gritties of Kt/Vurea Calculations in Hemodialysis and Peritoneal Dialysis. Indian J Nephrol. 2021 Mar-Apr;31(2):97-110. doi: 10.4103/ijn.IJN_245_19. Epub 2021 Apr 2. PMID: 34267430; PMCID: PMC8240937.

2. Gotch FA. Kt/V is the best dialysis dose parameter. Blood Purif. 2000;18(4):276-85. doi: 10.1159/000014449. PMID: 10965068.

3. Maliha G, Weinhandl ED, Reddy YNV. Deprescribing the Kt/V Target for Peritoneal Dialysis in the United States: The Path Toward Adopting International Standards for Dialysis Adequacy. J Am Soc Nephrol. 2023 May 1;34(5):751-754. doi: 10.1681/ASN.0000000000000101. Epub 2023 Feb 14. PMID: 36787755; PMCID: PMC10125636.

PCS and sleep

Q: The postconcussion syndrome (PCS) is associated with daytime sleepiness.

A) True

B) False

Answer: A

Almost all patients who went through Traumatic Brain Injury (TBI) experience PCS with a wide variety of symptoms.

One common symptom is a sleep-wake disorder characterized by increased daytime sleepiness and insomnia at night. The cause is circadian rhythm disturbances. The associated symptoms include abnormal behaviors during sleep, such as sleep talking, bruxism, and dream enactment, as well as sleep-disordered breathing. 

#neurology

#trauma

References:

1. Duclos C, Dumont M, Wiseman-Hakes C, et al. Sleep and wake disturbances following traumatic brain injury. Pathol Biol (Paris) 2014; 62:252.

2. Sandsmark DK, Elliott JE, Lim MM. Sleep-Wake Disturbances After Traumatic Brain Injury: Synthesis of Human and Animal Studies. Sleep 2017; 40.

3. Baumann CR. Traumatic brain injury and disturbed sleep and wakefulness. Neuromolecular Med 2012; 14:205.

Adenosine and numbness

Q: A 47-year-old male in the ICU went into supraventricular tachycardia (SVT) and was successfully converted to Normal Sinus Rhythm (NSR) with a total of 18 mg of Adenosine. On the telemetry strip, total Asystole time was 8 seconds. The patient now complains of numbness in the upper extremities. What should be your next step? - select one

A) Repeat EKG 

B) CT scan of the head

C) Limited EEG

D) MRI

E) Observation

Answer: E 

Adenosine may make patients' limbs feel numb for a few minutes after administration intravenously. Usually, it happens when the patient requires more than 12 mg of Adenosine. It usually resolves without any complication.

There may be concern for some central effect, but it would be appropriate to observe rather than indulging in a 'million-dollar' workup (choices B, C, and D).

EKG (choice A) can be performed to confirm NSR and rule out underlying coronary ischemia, but observation precedes any workup.

#cardiology 

#pharmacology 

References/further reading: 

1. Gupta A, Lokhandwala Y, Rai N, Malviya A. Adenosine-A drug with myriad utility in the diagnosis and treatment of arrhythmias. J Arrhythm. 2020 Dec 18;37(1):103-112. doi: 10.1002/joa3.12453. PMID: 33664892; PMCID: PMC7896475.

2. Biaggioni I, Killian TJ, Mosqueda-Garcia R, Robertson RM, Robertson D. Adenosine increases sympathetic nerve traffic in humans. Circulation. 1991 May;83(5):1668-75. doi: 10.1161/01.cir.83.5.1668. PMID: 2022024.

3. Rae CP, Mansfield MD, Dryden C, Kinsella J. Analgesic effect of adenosine on ischaemic pain in human volunteers. Br J Anaesth. 1999 Mar;82(3):427-8. doi: 10.1093/bja/82.3.427. PMID: 10434828.

SQ unf-Heparin in pregnancy

Case: 32-year-old newly pregnant patient admitted to the ICU with Pulmonary Embolism, and now getting discharged. The clinician decided to keep her on unfractionated heparin with a dose of 5000 units every 12 hours. As the pregnancy progresses, the dose of unfractionated heparin should be increased proportionally.

A) True

B) False

Answer: A

The unfractionated heparin dose should be increased as pregnancy progresses, as Heparin prescription is weight-based. A general rule of thumb is every 12 hours dose of:

• 5000 to 7500 units in the first trimester
• 7500 to 10,000 units in the second trimester
• 10,000 units in the third trimester

That said, clinical judgment and close monitoring of bleeding risks are required.

#ob-gyn

#hematology

References:

1. American College of Obstetricians and Gynecologists' Committee on Practice Bulletins—Obstetrics. ACOG Practice Bulletin No. 196: Thromboembolism in Pregnancy. Obstet Gynecol 2018; 132:e1. Reaffirmed 2022.

2. Barbour LA. Current concepts of anticoagulant therapy in pregnancy. Obstet Gynecol Clin North Am 1997; 24:499.

3. Mok T, Nguyen AV, Kwan L, et al. Prophylactic Unfractionated Heparin in Antepartum Hospitalizations: A Randomized Controlled Trial. Obstet Gynecol 2024; 144:118.

Bromocriptine treatment in PPCM

Q: The cardiology team decided to start Bromocriptine for a postpartum cardiomyopathy patient. Which one other intervention should be considered with bromocriptine?

Answer: Anticoagulation

Although bromocriptine or antiprolactin therapy is not yet a standard of care in PPCM, many experts have used it based on clinical judgment, on the premise that prolactin potentiates PPCM. So far, the evidence is very weak, though.

Bromocriptine is thrombogenic, and anticoagulation is warranted.

The recommended dose is 2.5 mg once daily for at least one week in uncomplicated cases. In those with LVEF less than 25 percent and/or in shock, 2.5 mg twice daily for two weeks, then 2.5 mg once daily for six weeks. It may also improve right ventricular function.

Cabergoline can be substituted if bromocriptine is not available.

#cardiology

#pharmacology

References:

1. Hilfiker-Kleiner D, Haghikia A, Berliner D, et al. Bromocriptine for the treatment of peripartum cardiomyopathy: a multicentre randomized study. Eur Heart J 2017; 38:2671.

2. van der Meer P, van Essen BJ, Viljoen C, et al. Bromocriptine treatment and outcomes in peripartum cardiomyopathy: the EORP PPCM registry. Eur Heart J 2025; 46:1017.

3. Attachaipanich T, Attachaipanich S, Kaewboot K. Efficacy and safety of bromocriptine in peripartum cardiomyopathy: A systematic review and meta-analysis. Int J Cardiol 2025; 427:133105.

4. Tremblay-Gravel M, Marquis-Gravel G, Avram R, et al. The effect of bromocriptine on left ventricular functional recovery in peripartum cardiomyopathy: insights from the BRO-HF retrospective cohort study. ESC Heart Fail 2019; 6:27.

5. Haghikia A, Schwab J, Vogel-Claussen J, et al. Bromocriptine treatment in patients with peripartum cardiomyopathy and right ventricular dysfunction. Clin Res Cardiol 2019; 108:290.

6. Maurel C, Abhay K, Schaeffer A, Lange F, Castot A, Melon E. Acute thrombotic accident in the postpartum period in a patient receiving bromocriptine. Crit Care Med. 1990 Oct;18(10):1180-1. doi: 10.1097/00003246-199010000-00026. PMID: 2209050.

Clinical exam in acute opioid toxicity

Q: Which of the following is a more reliable sign of acute opioid toxicity? - select one

A) Depressed mental status

B) Decreased respiratory rate

C) Miotic pupils

Answer: B

In acute opioid toxicity, pupils are expected to be constricted, but they can be normal or even larger. It also depends on the type of opioid, like meperidine, overdose tends to present with normal pupils. The co-ingestion of sympathomimetics or antimuscarinics can cause pupils to be larger on exam. In comparison, a decreased respiratory rate of less than 12 by manual counting on the best side is a better toxicity of acute opioid toxicity.

Bradycardia or hypotension from histamine release may occur, but it can't predict opioid toxicity unless the history is very clear. Similarly, normal capnography or hypothermia should not be relied on too much.

Mental status can range from coma to euphoria. The occurrence of a seizure should raise the possibility of tapentadol, tramadol, or meperidine overdose.

Hypoxia and traumatic brain injury (TBI) can be the cause, result, or simultaneously occurring features and require prompt address.

#toxicity

References:

1. Fahmy NR, Sunder N, Soter NA. Role of histamine in the hemodynamic and plasma catecholamine responses to morphine. Clin Pharmacol Ther 1983; 33:615.

3. Viglino D, Bourez D, Collomb-Muret R, et al. Noninvasive End Tidal CO2 Is Unhelpful in the Prediction of Complications in Deliberate Drug Poisoning. Ann Emerg Med 2016; 68:62.

4. Palkovic B, Marchenko V, Zuperku EJ, Stuth EAE, Stucke AG. Multi-Level Regulation of Opioid-Induced Respiratory Depression. Physiology (Bethesda). 2020 Nov 1;35(6):391-404. doi: 10.1152/physiol.00015.2020. PMID: 33052772; PMCID: PMC7864237.

COPD - cardinal symptoms

Q: The presence of two out of three cardinal symptoms of COPD exacerbation helps to justify? - select one

A) Start antibiotics

B) Admit to hospital

C) Start IV steroids

D) Order chest X-ray

E) perform bronchoscopy

Answer: A

The three cardinal symptoms of COPD exacerbation are:

• Increased dyspnea
• Increased sputum volume/viscosity
• Increased sputum purulence

The presence of 2 out of 3 cardinal symptoms is a clinical indication for empiric antibiotic therapy; otherwise, antibiotics can be held off to balance the fine line between minimizing resistance and stewardship. The only other justification for starting antibiotics is radiographic or microbiologic evidence of pulmonary infection. That said, antibiotic initiation in COPD exacerbations remains a clinical decision based on the clinician's judgment. Various algorithms and guidelines have been described.

Admitting to the hospital (choice B) depends on the severity and clinical deterioration of the symptoms. Oral steroids and IV steroids (choice C) usually have similar efficacy. Getting C-X-ray (choice D) or performing 'bronch' (choice E) depends solely on the indications and suspicion of infections.

#pulmonary

#stewardship

References:

1. Sethi S, Murphy TF. Acute exacerbations of chronic bronchitis: New developments concerning microbiology and pathophysiology--impact on approaches to risk stratification and therapy. Infect Dis Clin N Am 2004; 18:861.

2. Vollenweider DJ, Frei A, Steurer-Stey CA, Garcia-Aymerich J, Puhan MA. Antibiotics for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2018 Oct 29;10(10):CD010257. doi: 10.1002/14651858.CD010257.pub2. PMID: 30371937; PMCID: PMC6517133.

3. Balser E, Neher JO, Safranek S, Taraday J. Clinical inquiries: When are antibiotics indicated for acute COPD exacerbations? J Fam Pract. 2006 Dec;55(12):1079-80. PMID: 17137546.

4. Laue J, Reierth E, Melbye H. When should acute exacerbations of COPD be treated with systemic corticosteroids and antibiotics in primary care: a systematic review of current COPD guidelines. NPJ Prim Care Respir Med. 2015 Feb 19;25:15002. doi: 10.1038/npjpcrm.2015.2. PMID: 25695630; PMCID: PMC4373494.

Acidic PH of pleural fluid

Q: All of the following pathologies will cause pleural fluid acidosis EXCEPT? - select one

A) Malignancy

B) Tuberculosis

C) Urinothorax 

D) Misplaced central line

E) urease-splitting organisms 

Answer: E

Pleural effusion analysis remains an integral part of the differential diagnosis in most of the pulmonary pathologies with pleural effusion. Identifying the pH of pleural fluid is a valuable way to narrow down the cause of the underlying disease. Pleural fluid acidosis, particularly if combined with low glucose, is a given complicated parapneumonic pleural effusion or empyema, proven otherwise, EXCEPT for urease-splitting organisms such as Proteus species, which usually cause a spuriously elevated pleural PH.

The other causes of acidic pleural effusion are all the other choices in the question, i.e., malignancy, tuberculosis, urinothorax, misplaced central venous catheter infusing isotonic saline, along with rheumatoid pleuritis and lupus pleuritis.

Putting pleural fluid analysis in context with the history and other findings almost always led clinicians to the right diagnosis.

#procedures

#pulmonary

#laboratory-analysis

References:

1. Pine JR, Hollman JL. Elevated pleural fluid pH in Proteus mirabilis empyema. Chest 1983; 84:109.

2. Sahn SA. State of the art. The pleura. Am Rev Respir Dis 1988; 138:184.

3. Houston MC. Pleural fluid pH: diagnostic, therapeutic, and prognostic value. Am J Surg. 1987 Sep;154(3):333-7. doi: 10.1016/0002-9610(89)90623-5. PMID: 3307471.

4. Bowmaster SM, Merrill AE, Manning NL, Wilson JS, Gross TJ. Improving Pleural Fluid pH Accuracy: A Quality Improvement Initiative. J Appl Lab Med. 2025 Nov 4;10(6):1593-1599. doi: 10.1093/jalm/jfaf118. PMID: 40891251.

Abdominal pain with bowel wall edema

Q: A 68-year-old male whose blood pressure medicines have recently been changed presented to the Emergency Room with severe colicky abdominal pain associated with nausea and vomiting. CT of the abdomen showed bowel wall edema. Acute care surgery was consulted for possible "ex-lap", but the only advice offered was to discontinue his home BP medicine. Which anti-hypertensive is highly suspected? - Select one

A) ACE inhibitor

B) Beta-Blocker

C) Calcium Channel Blocker 

D) Diuretic (Furosemide)

E) Vasodilator (hydralazine)

Answer: A

The objective of this question is to emphasize that well-known angioedema associated with ACE-I is not limited to the face, lips, mouth, throat, larynx, uvula, but also the extremities, genitalia, and bowel wall are also common. Appearance of bowel wall edema on abdominal computed tomography (CT) or ultrasound, including in POCUS, when combined with history and symptoms, can avoid undue further workup or even unneeded "exploratory laparotomy". Elderly patients are more prone to bowel wall angioedema.

#surgical-critical-care

#GI

#pharmacology

References:

1. Dobbels P, Van Overbeke L, Vanbeckevoort D, Hiele M. Acute abdomen due to intestinal angioedema induced by ACE inhibitors: not so rare? Acta Gastroenterol Belg 2009; 72:455.

2. Chase MP, Fiarman GS, Scholz FJ, MacDermott RP. Angioedema of the small bowel due to an angiotensin-converting enzyme inhibitor. J Clin Gastroenterol 2000; 31:254.

3. Arakawa M, Murata Y, Rikimaru Y, Sasaki Y. Drug-induced isolated visceral angioneurotic edema. Intern Med 2005; 44:975.

Meatal Care and CAUTI

Q: In the ICU, using antibacterial urethral lubricants at the meatal site prevents catheter-related urinary tract infections (CAUTIs).

A) True

B) False

Answer: B

Applying disinfectants or antibacterial urethral lubricants at the meatal site does not prevent CAUTI and may instead lead to the development of resistant bacteria at the meatus. Cleansing the peri-urethral area with soap and water during daily bathing is adequate to prevent CAUTI.

#ID

#ICU-care

References:

1. Koskeroglu N, Durmaz G, Bahar M, et al. The role of meatal disinfection in preventing catheter-related bacteriuria in an intensive care unit: a pilot study in Turkey. J Hosp Infect 2004; 56:236.

2. Willson M, Wilde M, Webb ML, et al. Nursing interventions to reduce the risk of catheter-associated urinary tract infection: part 2: staff education, monitoring, and care techniques. J Wound Ostomy Continence Nurs 2009; 36:137.

3. . Classen DC, Larsen RA, Burke JP, et al. Daily meatal care for prevention of catheter-associated bacteriuria: results using frequent applications of polyantibiotic cream. Infect Control Hosp Epidemiol 1991; 12:157.

Systemic endotoxins and mastication

Q: Mastication ____________ the release of bacterial endotoxins of oral origin into the bloodstream. (select one)

A) decreases

B) increases

Answer: B

Oral health is highly associated with cardiovascular and cerebrovascular risk, with a hazard ratio of 2.12 in men less than 60 years of age, even after adjustment for known cardiovascular disease risk factors. Chronic periodontitis with radiographic bone loss is a significant risk factor.

The probable mechanism is chronic systemic inflammation. Interestingly, mastication has shown intermittent bacteremia and release of bacterial endotoxins of oral origin into the bloodstream, particularly in patients with poor oral health.

#dental

#cardiology

References: 

1. Chen F, Song Y, Li W, et al. Association between periodontitis and mortality of patients with cardiovascular diseases: A cohort study based on NHANES. J Periodontol 2024; 95:175.

2. Petrenya N, Hopstock LA, Holde GE, et al. Relationship between periodontitis and risk of cardiovascular disease: Insights from the Tromsø Study. J Periodontol 2022; 93:1353.

3. Geerts SO, Nys M, De MP, et al. Systemic release of endotoxins induced by gentle mastication: association with periodontitis severity. J Periodontol 2002; 73:73.

Ketamine-induced sclerosing cholangitis

Case: 72-year-old male ventilated in ICU after severe community-acquired pneumonia has been sedated on Ketamine infusion. On the fifth day of infusion, the patient's alkaline phosphatase is markedly elevated, and a liver ultrasound is negative for calculi or acalculous cholecystitis. What's the probable diagnosis?

Answer: Ketamine induced sclerosing cholangitis

In the last few years, ketamine has become widely popular in ICUs as a sedative agent. Less appreciated is ketamine induced sclerosing cholangitis and liver injury, particularly in ventilated patients who may require prolonged sedation, as it appears to be a dose-dependent effect. Ketamine infusion may be associated with sclerosing cholangitis, jaundice, decompensated cirrhosis, and even fatal acute liver failure (ALF).

#toxicity

#pharmacology

References:

1. Keta-Cov research group. Electronic address: vincent.mallet@aphp.fr, Keta-Cov research group. Intravenous ketamine and progressive cholangiopathy in COVID-19 patients. J Hepatol 2021; 74:1243.

2. de Tymowski C, Dépret F, Dudoignon E, et al. Ketamine-induced cholangiopathy in ARDS patients. Intensive Care Med 2021; 47:1173.

3. Vanrusselt A, Nijs J, Van den Bergh L, Schoofs N, Smets S, Strybol D, Rappaport A. Ketamine-induced sclerosing cholangitis: a case series. Acta Gastroenterol Belg. 2025 Jul-Sep;88(3):271-276. doi: 10.51821/88.3.13914. PMID: 41083171.

feeding in prone position

Q: Patients should not be fed in prone positioning, and tube feeding should be stopped.

A) True

B) False

Answer: B

Conventionally, it was thought that in the prone position, the chances of aspiration or emesis go high, but tube feeding in the prone position is safe, particularly if placed post-pyloric. The only precaution needed is to keep the patient's head in a slightly elevated position (about 25 degrees). 

Said that high residual volumes should be monitored. Adjuvant use of Prokinetic agents (like erythromycin) is helpful.

#nutrition

#pulmonary

References:

1. Reignier J, Thenoz-Jost N, Fiancette M, et al. Early enteral nutrition in mechanically ventilated patients in the prone position. Crit Care Med 2004; 32:94.

2. Saez de la Fuente I, Saez de la Fuente J, Quintana Estelles MD, et al. Enteral Nutrition in Patients Receiving Mechanical Ventilation in a Prone Position. JPEN J Parenter Enteral Nutr 2016; 40:250.

3. Reignier J, Dimet J, Martin-Lefevre L, et al. Before-after study of a standardized ICU protocol for early enteral feeding in patients turned in the prone position. Clin Nutr 2010; 29:210.

4. Linn DD, Beckett RD, Foellinger K. Administration of enteral nutrition to adult patients in the prone position. Intensive Crit Care Nurs 2015; 31:38.

absolute contraindications for laparoscopic cholecystectomy.

Q: Advanced cirrhosis with portal hypertension is an absolute contraindication for laparoscopic cholecystectomy.

A) True

B) False

Answer: B

The objective of this question is to emphasize that there are very absolute contraindications to laparoscopic cholecystectomy 

• Inability to tolerate general anesthesia
• Peritonitis with hemodynamic compromise
• Refractory coagulopathy 

Previous extensive abdominal surgery, advanced cirrhosis with portal hypertension, active cholangitis, CHF, or compromised respiratory status - all are relative contraindications. Although it should be kept in mind that patients with poor reserve may not tolerate pneumoperitoneum and may have a higher likelihood of conversion to open operation.

#surgical-critical-care

#GI

References:

1. Keus F, Broeders IA, van Laarhoven CJ. Gallstone disease: Surgical aspects of symptomatic cholecystolithiasis and acute cholecystitis. Best Pract Res Clin Gastroenterol 2006; 20:1031.

2. Chin X, Mallika Arachchige S, Orbell-Smith J, Wysocki AP. Preoperative and Intraoperative Risk Factors for Conversion of Laparoscopic Cholecystectomy to Open Cholecystectomy: A Systematic Review of 30 Studies. Cureus 2023; 15:e47774.

3. Nathaniel J Soper, Preeti Malladi - Laparoscopic cholecystectomy - https://www.uptodate.com/contents/laparoscopic-cholecystectomy (last access: March 30, 2026) UpToDate®

Chiari and Chiari-like Malformations

Q: Chiari malformations by definition is _________________ displacement of the cerebellum. - select one

A) downward 

B) upward

Answer: A

Chiari malformations are a heterogeneous group of disorders characterized by anatomic anomalies of the cerebellum, brainstem, and craniocervical junction, with downward displacement of the cerebellum, either alone or with the lower medulla, into the spinal canal.

#neurology

# neurosurgery

References:

1. Sarnat HB. Disorders of segmentation of the neural tube: Chiari malformations. Handb Clin Neurol 2008; 87:89.

2. Schijman E. History, anatomic forms, and pathogenesis of Chiari I malformations. Childs Nerv Syst 2004; 20:323.

3. Sahuquillo J, Moncho D, Ferré A, López-Bermeo D, Sahuquillo-Muxi A, Poca MA. A Critical Update of the Classification of Chiari and Chiari-like Malformations. J Clin Med. 2023 Jul 11;12(14):4626. doi: 10.3390/jcm12144626. PMID: 37510741; PMCID: PMC10380265.

'Livedo reticularis' and 'livedo racemosa'

Q: What's the difference between 'Livedo reticularis' and 'Livedo racemosa'?

Answer: Although Livedo reticularis and Livedo racemosa have been used interchangeably, technically, there is a subtle difference between them. Both have a violaceous mottling or reticular pattern of the skin of the extremities, mostly legs, and usually with circles.

• In Livedo reticularis – the circles are usually unbroken
• In Livedo racemosa - the circles are usually broken

Livedo reticularis can be seen in many clinical situations, such as Raynaud's phenomenon and cold exposure. The finding is benign and reversible with rewarming. 

Livedo racemosa (though commonly referred to as livedo reticularis) occurs in vasculitis, occlusive vascular disease (athero-emboli or thrombosis), or antiphospholipid syndrome (APS). This can be a sign of an underlying devastating clinical process.

#rheumatology

#clinical-exam

References:

1. Choi E, Henkin S. Raynaud's phenomenon and related vasospastic disorders. Vasc Med 2021; 26:56.

2. Uthman IW, Khamashta MA. Livedo racemosa: a striking dermatological sign for the antiphospholipid syndrome. J Rheumatol 2006; 33:2379.

3. Sajjan VV, Lunge S, Swamy MB, Pandit AM. Livedo reticularis: A review of the literature. Indian Dermatol Online J. 2015 Sep-Oct;6(5):315-21. doi: 10.4103/2229-5178.164493. PMID: 26500860; PMCID: PMC4594389.

4. Pincelli MS, Echavarria AMJ, Criado PR, Marques GF, Morita TCAB, Valente NYS, de Carvalho JF. Livedo Racemosa: Clinical, Laboratory, and Histopathological Findings in 33 Patients. Int J Low Extrem Wounds. 2021 Mar;20(1):22-28. doi: 10.1177/1534734619896938. Epub 2020 Jan 29. PMID: 31996060.

CVP and bed level

Q: 68-year-old patient admitted with CHF. Now, with diuresis, the patient is clinically stable and ready for transfer to the floor. Patient's last CVP noted was 12. The patient's bed is raised to perform a portable chest x-ray. With elevation of the bed, CVP will? (select one)

A) Fall

B) Rise

C) No change

Answer: B

The CVP transducer and intravascular volume at the "zero" point act as a balance of fluids. If the transducer drops below zero (such as when the bed is elevated), CVP will rise. It's similar to a seesaw.

Bed up  - CVP falsely down

Bed down  - CVP falsely up

#hemodynamics

References:

1. Zhou J, Zuo X, Liu S, Chu M, Tian Y. [Discussion on the zero-calibration and the zero line in the measurement of central venous pressure and invasive arterial blood pressure]. Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2023 Mar;35(3):316-320. Chinese. doi: 10.3760/cma.j.cn121430-20220926-00862. PMID: 36916347.

2. Lloyd-Donald P, Fujino M, Waldman B, Miles LF. Measurement and interpretation of central venous pressure: a narrative review. Anaesthesia. 2025 Sep;80(9):1093-1102. doi: 10.1111/anae.16633. Epub 2025 Jun 3. PMID: 40457939; PMCID: PMC12351226.

3. Figg KK, Nemergut EC. Error in central venous pressure measurement. Anesth Analg. 2009 Apr;108(4):1209-11. doi: 10.1213/ane.0b013e318196482c. PMID: 19299788.

Pentad of Graves' disease

Q: What is the pentad of Graves' disease?

Answer: A full-blown ideal Graves' disease usually consists of five features:

1. Hyperthyroidism
2. Goiter
3. Oorbitopathy
4. Dermopathy
5. Tachycardia

Other features may also be present, including heat intolerance, tremor, palpitations, anxiety, weight loss despite a normal or increased appetite, increased bowel frequency, and shortness of breath. Skin exam may have some remarkable and striking onycholysis, softening of the nails, hyperpigmentation, pruritus and hives, vitiligo, alopecia areata, and thinning of the hair.

A large number of patients may not have all of these features overtly. Diagnosis is based on clinical signs and symptoms and laboratory work-up.

Graves' disease, by definition, is an autoimmune disease. It is caused by thyroid-stimulating hormone (TSH, thyrotropin) receptor antibodies (TRAb) that activate the receptor, thereby stimulating thyroid hormone synthesis and secretion, as well as thyroid growth (diffuse goiter).

#endocrinology

#clinical-exam

References:

1. Toro-Tobon D, Stan MN. Graves’ Disease and the Manifestations of Thyrotoxicosis. [Updated 2024 Sep 24]. In: Feingold KR, Adler RA, Ahmed SF, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK285567/

2. Lee SY, Pearce EN. Hyperthyroidism: A Review. JAMA. 2023 Oct 17;330(15):1472-1483. doi: 10.1001/jama.2023.19052. PMID: 37847271; PMCID: PMC10873132.

3. Davies TF, Andersen S, Latif R, Nagayama Y, Barbesino G, Brito M, Eckstein AK, Stagnaro-Green A, Kahaly GJ. Graves' disease. Nat Rev Dis Primers. 2020 Jul 2;6(1):52. doi: 10.1038/s41572-020-0184-y. PMID: 32616746.

MOA of clopidogrel

Q: Clopidogrel (and other platelet P2Y12 receptor blockers) causes gastrointestinal bleed (GIB) due to its ulcerogenic characteristic.

A) True

B) False

Answer: B

Aspirin (ASA) and other nonsteroidal antiinflammatory drugs (NSAIDs) are directly ulcerogenic, but Platelet P2Y12 receptor blockers are not. They actually impair ulcer healing! This is the reason some experts believe in "GI-bleeders" only monotherapy with Platelet P2Y12 receptor blockers can be used.

In GI ulceration (caused by ASA, NSAIDs, or other causes), platelet aggregation leads to the release of platelet-derived growth factors, such as vascular endothelial growth factor (VEGF), which promote angiogenesis and endothelial cell proliferation, processes required for ulcer healing. Platelet P2Y12 receptor blockers prevent this healing.

#pharmacology

#cardiology

References:

1. Cryer B. Reducing the risks of gastrointestinal bleeding with antiplatelet therapies. N Engl J Med 2005; 352:287.

2. Ma L, Elliott SN, Cirino G, et al. Platelets modulate gastric ulcer healing: role of endostatin and vascular endothelial growth factor release. Proc Natl Acad Sci U S A 2001; 98:6470.

3. Waqas SA, Imran Z, Bilal AR, Ahmed S, Gaba H, Chew NWS, Greene SJ, Khan MS. Efficacy of clopidogrel monotherapy versus aspirin monotherapy after percutaneous coronary intervention. J Thromb Thrombolysis. 2025 Oct 10. doi: 10.1007/s11239-025-03185-0. Epub ahead of print. PMID: 41071255.