Pathophysiology and Clinical Presentation – Correct Diagnosis

Hypertension is a consistent elevation of systemic arterial blood pressure. Specifically, hypertension is caused by any condition that increases the systemic vascular resistance (increased blood viscosity or decreased blood vessel diameter), cardiac output, or a combination thereof (Brashers, 2014).

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Hypertension is the most common primary diagnosis in the United States. Approximately 1/3rd of adults over the age of 20 have hypertension and this number increases to 2/3rds of adults over the age of 60. The prevalence of hypertension is nearly equal between men and women (Table 3). African American adults have among the highest rates of hypertension in the United States, at approximately 44% (Table 4). Upwards of 80% of adults are aware of their hypertension, and 71% are on an anti-hypertensive medication, but only 48% of those have their hypertension controlled (Centers for Disease Control and Prevention [CDC], 2014).

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The pathogenesis of primary hypertension, also known as essential hypertension, is a highly complex and multifactorial interaction between the environment and genetics (Fig. 7). Combined, these increase vascular tone (increased peripheral resistance), and blood volume, thus resulting in sustained increases in blood pressure (Brashers, 2014). Multiple pathophysiologic mechanisms mediate these effects and include the RAAS (Renin-Angiotensin-Aldosterone System), SNS (Sympathetic Nervous System), natriuretic peptides and mutations in the gene Adducin. Inflammation, endothelial dysfunction, obesity-related hormones, and insulin resistance also contribute to both increased peripheral resistance and increased blood volume.

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Insulin Resistance:
Damage and dysfunction of endothelial cells results in decreased production of vasodilators (nitric oxide), resulting in hypertension. Insulin can increase blood pressure by activating the SNS, increasing renal sodium reabsorption, hypertrophy of resistance vessels, and/or alteration of transmembrane ion transport. Conversely, hypertension can cause altered delivery of insulin and glucose to the skeletal muscle cells, leading to insulin resistance (Salvetti, Brogi, Legge, & Bernini, 1993).

Natriuretic hormones (Adducin):
Modulate (lowers) renal sodium excretion, increasing vascular resistance, leading to hypertension (Brashers, 2014).

Overactive SNS:
Increased production of catecholamines (epinephrine and norepinephrine) results in SNS overactivity. This results in an increased heart rate, increased peripheral vascular resistance due to systemic vasoconstriction, and hypertension. Additionally, an overactive SNS effects insulin resistance, vascular remodeling, has procoagulant effects, which can lead to neospasm and narrowing of the blood vessels (Brashers, 2014).

Pressure-Natriuresis Relationship Shift:
Commonly known as “Shift in Pressure-natriuresis relationship.” Caused by increased vascular volume related to a decrease in renal excretion of salt in the urine, leading to hypertension (Brashers, 2014).

Inflammation:
Commonly known as “Shift in Pressure-natriuresis relationship.” Caused by increased vascular volume related to a decrease in renal excretion of salt in the urine, leading to hypertension (Brashers, 2014).

Overactive RAAS:
Contributes to salt and water retention, leading to increased vascular resistance and hypertension (Brashers, 2014).

Mutation of the gene Adducin:
Adducin is an essential component of the sodium-potassium pump, and mutations cause an increased tubular renal retention of sodium, increasing vascular volume, causing hypertension (Brashers, 2014).

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