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.