Pathophysiology

Clinical Application 2
Name of the Student
Professor’s Name
The appraisal of present case study relates to Mr. J. The individual belongs to African-American ethnicity and is hypertensive for the past two years. He had a history of smoking and suffers from obesity. Moreover, the laboratory findings indicated that Mr. J suffers from dyslipidemia and has a low ejection fraction. The heart of Mr. J is also enlarged, which indicated that he also suffered from left ventricular hypertrophy. Mr. J also suffers from knee pain and mild asthma. He has been taking NSAIDS (NonSteroidal Anti-Inflammatory drugs for the knee pain and inhalers for the management of asthma. The case history also suggests that Mr. J suffered from stress. The stress perhaps developed from recent job loss. Mr. J also had a family history of hypertension. The following questions were related to the dissemination of clinical condition of Mr. J.
How would you classify this pt’s hypertension according to current JNC VIII guidelines?
According to the current JNC VIII guidelines, hypertension in Mr. J could be classified as Stage-2 hypertension (Hernandez-Vila, 2015). JNC VIII guidelines (Joint National Committee) are regulatory guidelines that specify different cardiovascular end-points. Such specifications help to identify the pathological features in an individual and the therapeutic goals associated with such condition. For example, normal blood pressure is specified as <120/80 mmHg.
What is the most clinically significant information related to HTN in this patient’s ROS (review of systems) –explain your thinking.

The most clinically significant information related to HTN in Mr. J is a history of smoking and obesity. Mr. J suffers a low ejection fraction. Mr. J also suffered from left ventricular hypertrophy. The case history also suggests that Mr. J suffered from stress. The job-related stress and the family history of hypertension was certainly the predisposing risk factors for Mr. J’s hypertension. Stress activates the sympathetic nervous system that leads to the release of adrenaline (Meng et al., 2012). Adrenaline acts on alpha-1 receptors on the endothelium of blood vessels to produce vasoconstriction. Vasoconstriction leads to increase in peripheral resistance. Increased peripheral resistance leads to hypertension and left ventricular hypertrophy. The LVH develops from increased afterload on the heart. Obesity might increase the risk of dyslipidemia, which may have further expedited the chances of increased peripheral resistance. Hence, obesity might be considered as another risk factor for Mr. J’s hypertension. The obesity was confirmed through the Body Mass Index. A BMI > 30kg/m2 indicates obesity.
Interpret his lab findings – how do they relate to his hypertension?
The laboratory findings did indicate that Mr. J suffered from dyslipidemia. Dyslipidemia is clinical condition featured by abnormal concentrations of lipids in the serum. The total cholesterol of Mr. J was borderline high (>200-239 mg/dl). Moreover, the LDL concentrations were optimal. However, the HDL concentrations were low. LDL transports cholesterol from the liver to extrahepatic tissues (including endothelium of blood vessels). On the other hand, HDL transports cholesterol from the extrahepatic tissues (including endothelium of blood vessels) to the liver. The LDL/HDL ratio is a determinant of dyslipidemia. As the LDL concentration was high and HDL was low, it leads to atherosclerosis (excess deposition of cholesterol in the endothelium of blood vessels). Atherosclerosis leads to narrowing of blood vessels and is one of the major causes of increased peripheral resistance and the resultant LVH (Ito, McGowan & Moriarty, 2011).
In view of this patient’s history, what is your assessment of his hemoglobin and hematocrit? Is there a need for concern (explain your thinking)?
The hemoglobin concentration is a bit higher, but hematocrit concentration is within the normal range (borderline). Increased Hb and borderline hematocrit increase the viscosity of blood. Increased blood viscosity decreases the flow of blood and leads to increased peripheral resistance. Moreover, the headache and light-headedness may result from decreased perfusion in the brain (reduced supply of blood and oxygen to the brain). There is a need for concern because increased blood viscosity and the resultant increase in peripheral may increase the risk of left ventricular failure (Zubieta-Calleja et al., 2007)
What does this patient’s ejection fraction (EF) results suggest?
The ejection fraction of the patient is quite low, which indicates that the patient has a low cardiac output. Low cardiac output will cause decreased circulation to the peripheral tissues and brain (Kumar, Abbas, & Aster, 2009).
Discuss two signs/symptoms he has of end-organ damage due to his hypertension.
The two end organs that show signs of damage are the heart and the kidneys. Increased peripheral resistance resulted in left ventricular failure, while decreased perfusion led to nephrotoxicity. Nephrotoxicity is evidenced from reduced clearance of creatinine and BUN (Xie et al., 2016) .
Discuss each of the patient’s medications and how they may or may not be impacting the patient’s hypertension? BP = CO x PVR – think about what component of hypertension could they be impacting.
Albuterol (salbutamol) is a beta-receptor agonist. Beta-receptors are present on the myocardium. Increased stimulation of beta-receptors raises the frequency of heart contractions (manifested as increased heart rate) and increases the cardiac output. On the other hand, NSAIDs inhibits cyclooxygenase and prevents prostaglandin formation. Prostaglandins are effective vasodilators. Hence, both drugs predispose the persistence of hypertension (Diao et al., 2012).
References
Diao, D; Wright, JM; Cundiff, DK; Gueyffier, F (2012). “Pharmacotherapy for mild
hypertension.”. The Cochrane database of systematic reviews. 8, 42.
Hernandez-Vila E (2015)A Review of the JNC 8 Blood Pressure Guideline Tex Heart Inst J; 42(3), 226–228.
Ito MK, McGowan MP, Moriarty PM (2011). “Management of familial hypercholesterolemias in adult patients: recommendations from the National Lipid Association Expert Panel on Familial Hypercholesterolemia”. J Clin Lipidol. 5 (3 Suppl),38–45
Kumar, Vinay; Abbas, Abul K; Aster, Jon. (2009). Robbins and Cotran pathologic basis of disease (8th ed.). St. Louis, Mo: Elsevier Saunders,574
Meng, L; Chen, D; Yang, Y; Zheng, Y; Hui, R (2012). “Depression increases the risk of hypertension incidence: a meta-analysis of prospective cohort studies.”. Journal of Hypertension. 30 (5), 842–851
Xie, X; Atkins, E; Lv, J; Bennett, A; Neal, B; Ninomiya, T; Woodward, M; MacMahon, S; Turnbull, F; Hillis, GS; Chalmers, J; Mant, J; Salam, A; Rahimi, K; Perkovic, V; Rodgers, A (2016). “Effects of intensive blood pressure lowering on cardiovascular and renal outcomes: updated systematic review and meta-analysis.”.Lancet. 387 (10017), 435–43
Zubieta-Calleja, G. R.; Paulev, P. E.; Zubieta-Calleja, L; Zubieta-Castillo, G (2007). “Altitude adaptation through hematocrit changes” Journal of Physiology and Pharmacology. 58 Suppl 5 (2), 811–818