Scenario 6: A 42-year-old female presented to the dentist complaining intermittent right upper toothache pain
The patient is presenting with symptoms of upper jaw pain that is radiating to the neck, oedema, high blood pressure and urinary retention. The pathophysiological mechanisms of the symptoms include left ventricular hypertrophy, myocardial infarction, cardiac failure, chronic kidney disease (CKD) and hypertension. It should be noted that such factors as ethnic or racial attributes of being from African descent, Asian and Hispanic play a significant role in the pathophysiologic process of the conditions (Deere & Ferdinand, 2020). Fluid buildup in the tissues (oedema) is caused by one or a combination of these conditions (Metra & Teerlink, 2017). There is a need to delve into how the conditions interact leading to the set of symptoms that the patients present with.
One of the major causes of chronic kidney failure in the patient might be hypertension, left ventricular hypertrophy and heart failure which are related. A certain level of proteinuria is common in CKD with the prevalence worsening with increasing severity of CKD (Dan & Lin-Lee, n.d.). Additionally, the patient has urinary incontinence and oedema which points toward reduced kidney function. The most recent research findings show that the majority of the patients with CKD will develop hypertension but the same might be a cause or be caused by kidney disease or both of them (Hamrahian & Falkner, 2016; Ku et al., 2019; Paoletti et al., 2016). Elevated blood pressure exacerbates renal damage and can lead to worsening of CKD.
The levels of serum troponins which result from damage to the myocardial muscle cells are now considered as the most sensitive and specific for diagnosing myocardial infarction (Alkhachroum et al., 2019; Wanamaker et al., 2019). Heart failure complicate myocardial infarction in the vast majority of the patients. Patients that have a myocardial infarction present with jaw pain that radiates to the back of the neck and shoulders which the patient is presenting (Malik et al., 2022). Because of the stress response, the majority of the patients with myocardial infarction experience an increase in their serum glucose levels which is evident in the patient.
Heart failure denotes a clinical condition whereby the body is unable to pump blood sufficient enough to meet the body’s needs. It is caused by any condition which compromises ventricular filling or the ejection of blood to reach systemic circulation (Metra & Teerlink, 2017). Heart failure presents with shortness of breath and fatigue, reduced capacity to tolerate physical exercise, as well as fluid buildup in tissues which can be termed peripheral or pulmonary oedema (Malik et al., 2022). The left ventricular systolic dysfunction is a consequence of cardiac injury, for example, myocardial infarction or overloading the myocardium to a lot work for example in long standing hypertension (Alkhachroum et al., 2019). This leads to such defects in systolic contraction, diastolic relation or both.
One of the predisposing factors to the development of left ventricular hypertrophy, hypertension, chronic kidney failure, and myocardial infarction is race/ethnicity. African Americans, Hispanics and Asians are more prone to the conditions in comparison to the rest of the population (Deere & Ferdinand, 2020). The most recent research findings have it that 47.7% of the non-Hispanic women and 46% of the non-Hispanic men are bound to have some level of cardiovascular disease (Metra & Teerlink, 2017; Wanamaker et al., 2019). This points to the fact that race and ethnicity are predisposing factors to chronic kidney disease and myocardial infarction.
In conclusion, the pathophysiologic processes that contribute to the patient’s symptoms of peripheral oedema, pain in the jaw that radiates to the neck and high blood pressure, elevated troponin levels and urinary retention are left ventricular systolic dysfunction, heart failure, myocardial infarction and reduced kidney function. Ethnicity and race are one of the patient attributes that predispose someone to develop the conditions mentioned.
References
Alkhachroum, A. M., Miller, B., Chami, T., Tatsuoka, C., & Sila, C. (2019). A troponin study on patients with ischemic stroke, intracerebral haemorrhage and subarachnoid haemorrhage: Type II myocardial infarction is significantly associated with stroke severity, discharge disposition and mortality. Journal of Clinical Neuroscience, 64, 83–88.
Dan, L., & Lin-Lee, L. (n.d.). New Understanding on the Role of Proteinuria in Progression of Chronic Kidney Disease | SpringerLink. Retrieved June 19, 2022, from https://link.springer.com/chapter/10.1007/978-981-13-8871-2_24
Deere, B. P., & Ferdinand, K. C. (2020). Hypertension and race/ethnicity. Current Opinion in Cardiology, 35(4), 342–350. https://doi.org/10.1097/HCO.0000000000000742
Hamrahian, S. M., & Falkner, B. (2016). Hypertension in chronic kidney disease. Hypertension: From Basic Research to Clinical Practice, 307–325.
Ku, E., Lee, B. J., Wei, J., & Weir, M. R. (2019). Hypertension in CKD: Core curriculum 2019. American Journal of Kidney Diseases, 74(1), 120–131.
Malik, A., Brito, D., Vaqar, S., & Chhabra, L. (2022). Congestive Heart Failure. In StatPearls. StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK430873/
Metra, M., & Teerlink, J. R. (2017). Heart failure. The Lancet, 390(10106), 1981–1995. https://doi.org/10.1016/S0140-6736(17)31071-1
Paoletti, E., De Nicola, L., Gabbai, F. B., Chiodini, P., Ravera, M., Pieracci, L., Marre, S., Cassottana, P., Lucà, S., & Vettoretti, S. (2016). Associations of left ventricular hypertrophy and geometry with adverse outcomes in patients with CKD and hypertension. Clinical Journal of the American Society of Nephrology, 11(2), 271–279.
Wanamaker, B. L., Seth, M. M., Sukul, D., Dixon, S. R., Bhatt, D. L., Madder, R. D., Rumsfeld, J. S., & Gurm, H. S. (2019). Relationship between troponin on presentation and in-hospital mortality in patients with ST-segment–elevation myocardial infarction undergoing primary percutaneous coronary intervention. Journal of the American Heart Association, 8(19), e013551.