A Case Study Involving Hypertension Case Study

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Hypertension

Essential hypertension or primary hypertension is a highly complex disorder. There are various factors modulating BP or blood pressure in order for adequate tissue perfusion to occur. These include:

Vascular reactivity

Vascular caliber

Humoral mediators

Circulating blood volume

Blood viscosity

Blood vessel elasticity

Cardiac output

Neural stimulation

History of high blood pressure in family

Ethnic background

Aside from these factors, the natural course of primary hypertension is progression from infrequent or occasional to established or frequent hypertension. There is a long, asymptomatic, and invariable period when the persistent hypertension then progresses into complicated hypertension. This means there will be target organ damage to the small arteries and aorta, retina, heart, kidneys, and central nervous system.

The journey to primary hypertension begins with prehypertension from ages 10-30 years. The transition to early hypertension occurs from ages 20-40 years. During this phase peripheral resistance is noticeable. After this stage is established hypertension and this occurs from 30-50 years leading to the last phase, complicated hypertension from ages 40-60 years.

There are various factors that influence BP regulation. Arterial BP can be considered a product of peripheral vascular resistance and cardiac output. Factors that affect cardiac output include renal function, sodium intake, and mineralocorticoids. Peripheral vascular resistance is reliant on humoral factors, the sympathetic nervous system, and local autoregulation. The effects produced by the sympathetic nervous systems are done so via the vasodilator beta effect or vasoconstrictor alpha effect.

Hypertension is an all too common disease, affecting millions. However, research states essential hypertension comes from the body's inability to excrete excess sodium via the kidneys. "Essential hypertension develops when the kidneys become unable to excrete the amount of sodium ingested, unless blood pressure is increased ... shift of the pressure natriuresis relationship toward abnormally high pressure levels is a pathophysiological characteristic of essential hypertension" (Bolivar, 2013, p. 2). While there are several factors that can lead to this, what makes essential hypertension its namesake is when there is no known cause for the hypertension.

Essential hypertension or primary hypertension often has no clearly defined aetiology. While the latest research suggests renal problems as a cause, from a practical standpoint, it is best defined as a level of blood pressure that when treated to lower blood pressure, provides major clinical benefits. The level of positive results changes from patient to patient, depending on absolute cardiovascular risk. Hypertension itself is defined as great than or equal to 140/90 mmHg.

The pathogenesis of primary hypertension has three common causes. They are genetic predisposition, disturbances in neurohumoral control mechanisms and vascular structure, an environmental and lifestyle influences. The first one, genetic predisposition means blood pressure can run in families. Many studies found a consistent level of correlation among first-degree relatives. Meaning, if one relative is found to have deviations from norm BP, then the first-degree relative will also deviate on average by +2 mmHg.

Environmental and lifestyle influences also contribute to a higher prevalence of hypertension, especially in economically developing countries. The "Western" diet of fast food and high salt foods contributes to not only obesity, but also high blood pressure. In terms of pathophysiology, there is appears to be a distinctive find in primary hypertension. That is an inappropriate increase in peripheral vascular resistance, as mentioned earlier, in relation to cardiac output.

What this means is the small arteries or arterioles have been remodeled and are characterized by higher media/lumen ration. There is also a stiffening of large conduit arteries like the aorta influencing the progression and development of hypertension, particularly systolic hypertension (MacGregor & Kaplan, 2010, p. 134). Hypertensions also leads to decreased nitric oxide production and endothelial dysfunction. This could be a consequence of hypertension more so than anything else.

Vascular reactivity or cardiovascular reactivity is commonly understood as a reflection of the physiologic changes of a person's heart from resting/baseline state to a kind of psychological/physical stressor or challenge. An exaggerated cardiovascular response typically indicates hypertension or some other coronary heart disease. Vascular caliber concerns the interactions among the frictional drag produced by the stream, as well as the sensitivity of endothelial cells to such a force. If the drag force put on the endothelial cells reaches a critical set-point, these the cells remain at rest with respect to the factors affecting caliber. Increases in the flow rate also increases the drag, appearing to induce the endothelium to produce a signal triggering relaxation of the subjacent medial smooth muscle. Blood Viscosity is the stickiness and thickness of blood, acting as a direct measure of the capacity of blood to flow through vessels.

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Blood viscosity is greater in hypertensive patients. Blood vessel elasticity diminishes in a hypertensive patient. This is due to a thickening of the vessels. With regards to ethnic background, African-Americans are more likely than Caucasians or Hispanics to get high blood pressure earlier in life. Family history also plays a part because if family members develop high blood pressure, the person could also develop based on lifestyle, genetics, and weight.

Pathophysiology of Symptoms

Dry Skin:

While dry skin is not common among those suffering from hypertension, it is a common symptom of hypothyroidism. As it will be discussed in the lab section, Mr. Irving's lab results indicate hypothyroidism. What causes dry sin in hypothyroidism? Reduction in circulation. With cases of hypothyroidism, the skin may receive as little as one-fifth the normal blood supply, leading to chronic dry sin, dry, brittle hair, and in some cases, eczema.

Fatigue:

Fatigue symptoms are a hallmark of hypothyroidism. Because thyroid hormone is essential to a person's metabolism and energy output, low thyroid hormone levels lead to fatigue. Fatigue can also be connected to high blood pressure as fatigue and high blood pressure often go hand-in-hand. If a person goes for a prolonged period of time with chronic high blood pressure and does not receive treatment, fatigue may show up as a symptom. Medications used to treat high blood pressure also may present with fatigue as a side effect. Lisinopril causes drowsiness so this may also contribute to the fatigue experienced by Mr. Irving.

Constipation:

Constipation can be another symptom of hypothyroidism. As the body receives less thyroid hormone, colon contractions within the body become slower, weaker, and more sluggish. This leads to the body's inability to move waste to the colon for defecation to take place. Lifestyle may also contribute as constipation alleviate requires proper hydration and intake of fiber-rich foods.

Weight Gain:

Weight gain can come from a myriad of things, but most of the time it comes from poor lifestyle choices. When people overeat and do not maintain a daily exercise regimen, high blood pressure, obesity, and constipation can become a problem. Weight gain directly contributes to higher blood pressure. The ten pound weight gain Mr. Irving experienced could come from poor lifestyle choices and from hypothyroidism. An underactive thyroid slows down the metabolism, increase fatigue and constipation in a person. This leads to less overall movements, and ineffective removal of waste from the body.

Persistent Cough:

Lisinopril may cause a cough in some patients. Patients with hypertension, taking medications to treat hypertension, sometimes complain of a dry cough. This is especially common with ACE inhibitors. "Although all 3 classes of antihypertensive drugs have been associated with cough as a side effect, the causal explanation differs between classes, and the level of evidence is strongest with angiotensin-converting enzyme (ACE) inhibitors -- a first-line antihypertensive drug class for many patients" (Van Amburgh, 2011). Lisinopril is an ACE inhibitor.

How ACE inhibitors may cause a dry cough is by the medication preventing the breakdown of substance P and bradykinin, resulting in accumulation of protussive mediators within a person's respiratory tract. This means that a person taking Lisinopril or medications like it, have a chance of experience dry cough. Coughing is the most common symptom of ACE inhibitors. Therefore, it will be the most likely cause of Mr. Irving's persistent dry cough.

Relationship to Primary Hypertension:

Hypothyroidism produces various symptoms in an adult. From low energy to chronic dry skin, it decreases the body's ability to process food and be energized. Poor diet and little to no exercise leads to weight gain and constipation and exacerbates hypothyroidism symptoms. Weight gain increases the likelihood of getting high blood pressure. Hypertension medications taken to treat BP may create a persistent dry cough.

Lab Results:

Mr. Irving had several blood tests done. The first one was a TSH test along with a free T4 test. Doctors frequently use the TSH test to assess thyroid function as well as any symptoms that could show a thyroid disorder that include hypothyroidism and hyperthyroidism. The pituitary gland helps maintain a stable amount of T# or triiodothyronine and T4 or thyroxine. Doctors order a TSH test when patients complain of constipation, dry skin, and fatigue (Podzolkov & Fadeyev, 2009).

Mr. Irving noted he has dry skin, gained weight, and had constipation. These are symptoms of hypothyroidism. High TSH results often mean the patient tested has chronic or acute thyroid dysfunction….....

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