UTHSC PA Program Podcast

In this episode, we review amaurosis fugax, a transient, painless episode of monocular vision loss caused by temporary retinal ischemia and most commonly associated with embolic disease from carotid atherosclerosis. We discuss the classic description of a "curtain" or "shade" descending over one eye, important vascular risk factors, and why symptoms typically resolve completely within minutes. The segment also covers the urgent diagnostic evaluation—including carotid imaging, vascular imaging, brain MRI, ECG, and echocardiography—to identify carotid or cardiac sources of emboli. We finish with treatment and prevention strategies, emphasizing that amaurosis fugax should be approached as a TIA equivalent and an important warning sign for future ischemic stroke.

References

1. Bushardt RL, Colomb-Lippa DM, Klinger AM, Reed H. The JAAPA QRS Review for PAs: Study Plan and Guide for PANCE and PANRE. 1st ed. LWW; 2021. ISBN: 9781975143817
2. Current management of amaurosis fugax. The Amaurosis Fugax Study Group. (1990). Stroke, 21(2), 201–208. https://doi.org/10.1161/01.str.21.2.201
3. Kaur, K., Najem, K., & Margolin, E. (2025, January 21). Amaurosis Fugax. Nih.gov; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/sites/books/NBK470528/
4. Walker, R. A., & Adhikari, S. (2026). Eye Emergencies. McGraw Hill Medical. https://accessemergencymedicine.mhmedical.com/content.aspx?sectionid=222404436&bookid=2353

In this episode, we review age-related macular degeneration (AMD), a degenerative disease of the macula that causes painless central vision loss while typically preserving peripheral vision. We break down the key differences between dry and wet AMD, including the gradual vision loss, drusen, and retinal atrophy associated with dry disease versus the more sudden visual changes, hemorrhage, and neovascularization seen with wet AMD. The segment also covers important risk factors, diagnostic findings, and treatment strategies, including AREDS2 supplementation for appropriate patients and intravitreal anti-VEGF therapy for wet AMD. We finish with high-yield clinical pearls emphasizing the importance of recognizing metamorphopsia or rapid central vision loss as potential signs of wet AMD requiring urgent ophthalmologic evaluation, along with smoking cessation as an important modifiable risk factor.

References

1. Bushardt RL, Colomb-Lippa DM, Klinger AM, Reed H. The JAAPA QRS Review for PAs: Study Plan and Guide for PANCE and PANRE. 1st ed. LWW; 2021. ISBN: 9781975143817
2. Alkabbani W, Cromer SJ, Patorno E. Neovascular Age-Related Macular Degeneration and GLP-1 RAs. JAMA Ophthalmol. 2025;143(12):1077. doi:10.1001/jamaophthalmol.2025.3720
3. AREDS 2 Supplements for Age-Related Macular Degeneration (AMD) | National Eye Institute.(2021). Nih.gov. https://www.nei.nih.gov/eye-health-information/eye-conditions-and-diseases/age-related-macular-degeneration/nutritional-supplements-age-related-macular-degeneration?utm
4. Kim MS, Nam S, Lee J, Woo SJ. Antithrombotic Medications and Intraocular Hemorrhage Risk in Exudative Age-Related Macular Degeneration. JAMA Netw Open. 2025;8(9):e2531366. doi:10.1001/jamanetworkopen.2025.31366

In this episode, we review cataracts, a common cause of progressive vision loss resulting from opacification of the lens. We discuss important risk factors—including aging, tobacco use, chronic sun exposure, diabetes, ocular injury, and prolonged steroid use—and the classic presentation of painless, progressive blurry vision, increased glare and halos, and difficulty with night vision. The segment also covers the diagnostic evaluation with visual acuity testing, slit-lamp examination, and dilated eye examination, along with nonsurgical strategies for managing mild symptoms. We finish with cataract surgery as the definitive treatment, emphasizing that surgical intervention is based on the degree of functional visual impairment rather than simply the appearance of the lens.

References

1. Bushardt RL, Colomb-Lippa DM, Klinger AM, Reed H. The JAAPA QRS Review for PAs: Study Plan and Guide for PANCE and PANRE. 1st ed. LWW; 2021. ISBN: 9781975143817
2. Chen SP, Woreta F, Chang DF. Cataracts: A Review. JAMA. 2025;333(23):2093–2103. doi:10.1001/jama.2025.159
3. Voelker R. What Are Cataracts? JAMA. 2025;334(14):1308. doi:10.1001/jama.2025.11869
4. Yee H, Wong CMJ, Gupta P, et al. Prevalence, Risk Determinants, and Burden of Undiagnosed Age-Related Eye Diseases Among Older Asian Adults. JAMA Ophthalmol. Published online November 20, 2025. doi:10.1001/jamaophthalmol.2025.4623

n this episode, we review patent foramen ovale (PFO), a common congenital finding caused by incomplete fusion of the septum primum and septum secundum after birth. We discuss why most PFOs are asymptomatic and hemodynamically insignificant, as well as how transient increases in right-sided pressure can permit right-to-left shunting. The segment also covers diagnosis with agitated-saline echocardiography ("bubble study") and the important association between PFO, paradoxical embolism, and cryptogenic stroke, particularly in younger patients. We finish with management considerations after an embolic event and a key distinction between PFO and a true atrial septal defect (ASD).

References

1. Bushardt RL, Colomb-Lippa DM, Klinger AM, Reed H. The JAAPA QRS Review for PAs: Study Plan and Guide for PANCE and PANRE. 1st ed. LWW; 2021. ISBN: 9781975143817
2. Kent DM, Wang AY. Patent Foramen Ovale and Stroke: A Review. JAMA. 2025;334(16):1463-1473. doi:10.1001/jama.2025.10946
3. Koutroulou I, Tsivgoulis G, Tsalikakis D, Karacostas D, Grigoriadis N, Karapanayiotides T. Epidemiology of Patent Foramen Ovale in General Population and in Stroke Patients: A Narrative Review. Front Neurol. 2020;11:281. Published 2020 Apr 28. doi:10.3389/fneur.2020.00281
4. Mojadidi MK, Zaman MO, Elgendy IY, et al. Cryptogenic Stroke and Patent Foramen Ovale. J Am Coll Cardiol. 2018;71(9):1035-1043. doi:10.1016/j.jacc.2017.12.059
5. Warnes CA, Williams RG, Bashore TM, et al. ACC/AHA 2008 guidelines for the management of adults with congenital heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Develop Guidelines on the Management of Adults With Congenital Heart Disease). Developed in Collaboration With the American Society of Echocardiography, Heart Rhythm Society, International Society for Adult Congenital Heart Disease, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol. 2008;52(23):e143-e263. doi:10.1016/j.jacc.2008.10.001

In this episode, we review Kawasaki disease, an immune-mediated vasculitis that primarily affects young children and represents an important cause of acquired coronary artery disease. We discuss the classic "CRASH and BURN" presentation—conjunctivitis, rash, cervical adenopathy, strawberry tongue and oral changes, hand and foot changes, and persistent fever—and the laboratory and echocardiographic findings that support the diagnosis. The segment also covers treatment with IVIG and aspirin, the importance of early therapy, and management considerations for high-risk or IVIG-resistant disease. We finish with the major complication of coronary artery aneurysm and why prompt recognition and treatment are critical to reducing long-term cardiovascular complications.

References

1. Bushardt RL, Colomb-Lippa DM, Klinger AM, Reed H. The JAAPA QRS Review for PAs: Study Plan and Guide for PANCE and PANRE. 1st ed. LWW; 2021. ISBN: 9781975143817
2. Day-Lewis M, Son MBF, Lo MS. Kawasaki disease: contemporary perspectives. Lancet Child Adolesc Health. 2024;8(10):781-792. doi:10.1016/S2352-4642(24)00169-X
3. Gorelik M, Chung SA, Ardalan K, et al. 2021 American College of Rheumatology/Vasculitis Foundation Guideline for the Management of Kawasaki Disease. Arthritis Rheumatol. 2022;74(4):586-596. doi:10.1002/art.420411.
4. Jone PN, Tremoulet A, Choueiter N, et al. Update on Diagnosis and Management of Kawasaki Disease: A Scientific Statement From the American Heart Association. Circulation. 2024;150(23):e481-e500. doi:10.1161/CIR.0000000000001295
5. Newburger JW, Takahashi M, Burns JC. Kawasaki Disease. J Am Coll Cardiol. 2016;67(14):1738-1749. doi:10.1016/j.jacc.2015.12.073

In this episode, we review central venous line placement, including the major indications for central access and the three primary insertion sites: the internal jugular, subclavian, and femoral veins. We walk through the essential steps of sterile central line insertion using the Seldinger technique, from patient positioning and venous access to guidewire placement, dilation, catheter insertion, and securing the line. The segment also highlights important complications—including arterial injury, pneumothorax, hemothorax, arrhythmias, thrombosis, infection, and air embolism—along with appropriate post-procedure management.

References

1. Bushardt RL, Colomb-Lippa DM, Klinger AM, Reed H. The JAAPA QRS Review for PAs: Study Plan and Guide for PANCE and PANRE. 1st ed. LWW; 2021. ISBN: 9781975143817
2. Dariushnia SR, Wallace MJ, Siddiqi NH, et al. Quality improvement guidelines for central venous access. J Vasc Interv Radiol. 2010;21(7):976-981. doi:10.1016/j.jvir.2010.03.006
3. Dunne H, Abou-Abdallah M, Robinson M, Kenyon O, Brassett C. Should Sedillot's triangle be used for central venous cannulation? A cadaveric study. Clin Anat. 2023;36(6):881-886. doi:10.1002/ca.24020
4. Kehagias E, Galanakis N, Tsetis D. Central venous catheters: Which, when and how. Br J Radiol. 2023;96(1151):20220894. doi:10.1259/bjr.20220894
5. Vegas A, Wells B, Braum P, et al. Guidelines for Performing Ultrasound-Guided Vascular Cannulation: Recommendations of the American Society of Echocardiography. J Am Soc Echocardiogr. 2025;38(2):57-91. doi:10.1016/j.echo.2024.12.004

In this episode, we review transposition of the great arteries (TGA), a critical cyanotic congenital heart defect in which the aorta arises from the right ventricle and the pulmonary artery from the left ventricle, creating two parallel circulations. We discuss why survival depends on mixing through an ASD, VSD, or patent ductus arteriosus, and highlight the classic neonatal presentation of cyanosis that does not improve with supplemental oxygen. The segment also covers diagnosis with echocardiography, the classic "egg on a string" chest X-ray appearance, and initial stabilization with prostaglandin E1 and balloon atrial septostomy when needed to improve mixing. We finish with definitive surgical management, including the arterial switch procedure, and key clinical pearls for recognizing this life-threatening congenital heart defect early.

References

1. Bushardt RL, Colomb-Lippa DM, Klinger AM, Reed H. The JAAPA QRS Review for PAs: Study Plan and Guide for PANCE and PANRE. 1st ed. LWW; 2021. ISBN: 9781975143817
2. Canan A, Ashwath R, Agarwal PP, François C, Rajiah P. Multimodality Imaging of Transposition of the Great Arteries. Radiographics. 2021;41(2):338-360. doi:10.1148/rg.2021200069
3. Haas NA, Driscoll DJ, Rickert-Sperling S. Clinical Presentation and Therapy of d-Transposition of the Great Arteries. Adv Exp Med Biol. 2024;1441:663-670. doi:10.1007/978-3-031-44087-8_38
4. Martins P, Castela E. Transposition of the great arteries. Orphanet J Rare Dis. 2008;3:27. Published 2008 Oct 13. doi:10.1186/1750-1172-3-27
5. Zbrzycki M, Schramm R, Costard-Jäckle A, Morshuis M, Gummert JF, Zubrzycka M. Pathogenesis and Surgical Treatment of Dextro-Transposition of the Great Arteries (D-TGA): Part II. J Clin Med. 2024;13(16):4823. Published 2024 Aug 15. doi:10.3390/jcm13164823

In this episode, we review bradycardia, focusing on how abnormalities in cardiac impulse generation or conduction can produce a heart rate below 60 beats per minute and, when severe, compromise cardiac output. We distinguish physiologic from pathologic bradycardia and discuss symptoms of impaired perfusion, including fatigue, dizziness, syncope, dyspnea, hypotension, altered mental status, and shock. The segment also covers the diagnostic approach with ECG, cardiac monitoring, and evaluation for reversible causes, as well as management of unstable bradycardia with atropine, cardiac pacing, dopamine, or epinephrine when indicated.

References

1. Bushardt RL, Colomb-Lippa DM, Klinger AM, Reed H. The JAAPA QRS Review for PAs: Study Plan and Guide for PANCE and PANRE. 1st ed. LWW; 2021. ISBN: 9781975143817
2. Cejin MC, Koyfman A, Long B. Pearls and Pitfalls: Severe Bradycardia. J Emerg Med. 2026;80:297-316. doi:10.1016/j.jemermed.2025.11.002
3. Kusumoto FM, Schoenfeld MH, Barrett C, et al. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation. 2019;140(8):e382-e482. doi:10.1161/CIR.0000000000000628
4. Mangrum JM, DiMarco JP. The evaluation and management of bradycardia. N Engl J Med. 2000;342(10):703-709. doi:10.1056/NEJM200003093421006
5. Tannenbaum L, Long B. Electrocardiogram essentials: Bradycardia. Am J Emerg Med. 2025;97:58-64. doi:10.1016/j.ajem.2025.07.030

In this episode, we review postrenal acute kidney injury (AKI), an acute decline in kidney function caused by urinary outflow obstruction that creates backpressure and decreases glomerular filtration. We discuss common causes—including BPH, nephrolithiasis, malignancy, urethral strictures, and neurogenic bladder—and why significant AKI typically requires bilateral obstruction, obstruction of a solitary functioning kidney, or a distal bladder outlet or urethral obstruction. The segment also covers the diagnostic role of renal ultrasound, hydronephrosis, bladder scanning, and CT, along with treatment focused on promptly relieving the obstruction. We finish with high-yield pearls on infected obstruction as a urologic emergency and monitoring for postobstructive diuresis after urinary drainage is restored.

References

1. Bushardt RL, Colomb-Lippa DM, Klinger AM, Reed H. The JAAPA QRS Review for PAs: Study Plan and Guide for PANCE and PANRE. 1st ed. LWW; 2021. ISBN: 9781975143817
2. Ronco C, Bellomo R, Kellum JA. Acute kidney injury. Lancet. 2019;394(10212):1949-1964. doi:10.1016/S0140-6736(19)32563-2.
3. Lameire N, Van Biesen W, Vanholder R. Acute renal failure. Lancet. 2005;365(9457):417-430. doi:10.1016/S0140-6736(05)17831-3.
4. Mercado MG, Smith DK, Guard EL. Acute kidney injury: diagnosis and management. Am Fam Physician. 2019;100(11):687-694.

In this episode, we review prerenal acute kidney injury (AKI), an acute decline in kidney function caused by decreased renal perfusion without initial structural damage to the kidneys. We break down the major causes—including volume depletion, decreased cardiac output or effective circulating volume, and medication-related changes in renal hemodynamics—and explain how activation of the RAAS and ADH systems produces the classic laboratory findings of prerenal AKI. The segment also highlights diagnostic clues, volume assessment, treatment aimed at restoring renal perfusion, and why prolonged hypoperfusion can progress to ischemic acute tubular necrosis and intrinsic AKI.

References

1. Bushardt RL, Colomb-Lippa DM, Klinger AM, Reed H. The JAAPA QRS Review for PAs: Study Plan and Guide for PANCE and PANRE. 1st ed. LWW; 2021. ISBN: 9781975143817
2. Lameire NH, Bagga A, Cruz D, et al. Acute kidney injury: an increasing global concern. Lancet. 2013;382(9887):170-179. doi:10.1016/S0140-6736(13)60647-9.
3. Ostermann M, Lumlertgul N, Jeong R, See E, Joannidis M, James M. Acute kidney injury. Lancet. 2025;405(10474):241-256. doi:10.1016/S0140-6736(24)02385-7.
4. Thadhani R, Pascual M, Bonventre JV. Acute renal failure. N Engl J Med. 1996;334(22):1448-1460. doi:10.1056/NEJM199605303342207.