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Essential Hypertension
(High Blood Pressure)

Pathology || Signs and Symptoms || Diagnosis || Treatment || Overview ||
Related Articles || References and Resources || Leave a Comment || Search

Pathology





The pathology of essential hypertension (aka: primary hypertension) is not well understood. However, there are numerous theories, each with supporting evidence.

One theory is based on genetics. Genetic causes are supported by the fact that children of hypertensive parents have an increased risk of developing the disease. However, specific known genetic mutations are not common. When mutations are responsible for essential hypertension they often involve the sodium and chloride channels in kidney cells, or mutations in the genes responsible for producing the proteins and hormones in the renin-angiotensin-aldosterone system. Both of these systems are responsible for maintaining adequate blood pressure. For some reason in hypertensive patients these systems go haywire and overcompensate.

A second theory is that some patients with essential hypertension appear to be "salt sensitive". Salt, or more specifically sodium, appears to play an important role in the development of hypertension. Some patients likely have a genetic predisposition to retain salt.

The result is that the kidneys in "salt sensitive" patients re-absorb more sodium than normal. The re-absorbed sodium enters the blood stream where it exerts an osmotic pull on water in adjacent tissues. Fluid from body tissues is "sucked" into the blood stream resulting in increased blood volumes. The expanded blood volume increases the pressure within the blood vessel causing hypertension.

There are other known causes of hypertension, but they constitute a relatively small proportion of cases. They are discussed in the article on secondary hypertension.

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Signs and Symptoms

Essential hypertension in its earliest stages does not cause any signs or symptoms. In fact many people do not know they have high blood pressure until having it checked at the doctor's office. However, if left untreated hypertension can cause serious long term consequences. These consequences are related to damage of multiple organ systems.

One such consequence is an increase in the risk of cardiovascular disease. The risk of cardiovascular disease doubles with each 20/10 mmHg increase in blood pressure beyond a "baseline" of 115/75 mmHg! After years of pumping at elevated pressures the heart undergoes physical changes. Like a good muscle it becomes larger because it is having to pump harder than normal. The result is a process known as "concentric hypertrophy". The added muscle mass of the heart results in increased oxygen demand and the potential for heart attacks and heart failure.

Overall, nearly a third of heart attacks are attributable to high blood pressure. In addition, the risk of stroke is also dramatically higher in untreated hypertensive patients. The small blood vessels in the kidney and retina can also be damaged by years of high blood pressure resulting in kidney failure (hypertensive nephropathy) and blindness (hypertensive retinopathy).

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Diagnosis

The diagnostic parameters of hypertension are constantly shifting. Currently the diagnosis can be made if a patient presents with a severely elevated blood pressure (systolic blood pressure > 200 and/or a diastolic blood pressure > 120) and/or signs or symptoms referable to the elevated blood pressure.

Severity Classification:
(1) Pre-hypertensive:
       130-140/80-90
(2) Grade 1:
       140-160/90-100
(3) Grade 2:
        >160/>100

In patients with less severe elevations, it is generally recommended that the blood pressure be measured several times over a period of multiple weeks. If the average of these readings is a systolic blood pressure of 140 or greater, or a diastolic blood pressure of 90 or greater than the diagnosis can be made. If the blood pressue stays between 120 and 130 systolic, and 80 to 90 diastolic the diagnosis of "pre-hypertension" is made meaning the patient is at risk of becoming hypertensive.

Some patients may have "white coat" hypertension simply by being in a doctor's office (and the anxiety that this can provoke! Gosh, I hate going to the doctor's office!). If this is the case the patient should be instructed to take their blood pressure at home and keep a log of the results.

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Treatment

Treatment of hypertension consists of lifestyle modifications and/or using medications from several different pharmacologic categories. These medications may be used alone, or in combination depending on the severity and resistance of the high blood pressure to treatment.

Patients who are pre-hypertensive or have stage 1 hypertension should be started on "lifestyle" modification therapy for at least 6 months prior to starting medicines (assuming there are no other health issues like diabetes or coronary artery disease). Lifestyle therapy consists of increasing aerobic exercise, as well as adhering to the "DASH" diet. DASH stands for "dietary approaches to stop hypertension" and consists of eating fruits, vegetables, low-fat dairy, whole grains, poultry and fish while reducing (or eliminating) red meat and sugars. This intervention alone can decrease systolic pressures over 10 mmHg and diastolic pressures over 5 mmHg.

Sometimes diet and exercise aren't enough so we may have to resort to medications to control blood pressure. The first category of medications are known as diuretics, most commonly of the thiazide class. Thiazide diuretics work by inhibiting the re-absorption of sodium at the distal convoluted tubule of the kidney. Less sodium means less circulating blood volume, and therefore decreased blood pressure. Hydrochlorothiazide is a commonly used thiazide diuretic; it is considered first line therapy for most patients.

The second category of medications is known as β-blockers. β-blockers lower blood pressure by slowing the heart rate, and indirectly lowering the amount of angiotensin II, a potent natural blood vessel constrictor, produced by the body. This effect of β-blockers is due to a reduction in renin synthesis by specialized cells in the kidney.

A third category of medications known as angiotensin converting enzyme inhibitors (ACEIs) interfere with the formation of angiotensin II. ACEIs inhibit an enzyme present in the lung, which converts angiotensin I into the more potent vasoconstrictor angiotensin II. Interestingly, ACEIs also increase the level of bradykinin; this molecule causes blood vessels to dilate, which helps to further lower pressure.

There are also medications called direct angiotensin receptor blockers (ARBs), which inhibit the actions of angiotensin II. They do this by blocking angiotensin IIs ability to bind to its normal receptor sites.

Some medications, the calcium channel blockers (CCBs), lower blood pressure by inhibiting the contraction of smooth muscle cells that line the blood vessel walls. A specific subcategory of calcium channel blockers known as dihydropyridines block calcium from flowing into vascular smooth muscle cells. This results in decreased contraction of the muscle surrounding the vessel. As a result the vessel remains dilated, which lowers pressure.

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Overview

The pathology of essential hypertension is not well understood. Several theories have been postulated, but it is likely a combination of genetic predispositions that result in this type of high blood pressure. Years of elevated blood pressure lead to cardiovascular disease including heart failure, heart attacks, and stroke, as well as damage to the kidneys and retinas. Treatment is with lifestyle modifications, diuretics, β-blockers, calcium channel blockers, angiotensin converting enzyme inhibitors, and angiotensin receptor blockers.

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Related Articles

- Heart attack (myocardial infarction)

- Stroke (cerebrovascular accident)

- Atherosclerosis

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References and Resources

(1) Drenjančević-Perić I, Jelaković B, Lombard JH, et al. High-Salt Diet and Hypertension: Focus on the Renin-Angiotensin System. Kidney Blood Press Res. 2010 Nov 12;34(1):1-11.

(2) Sanada H, Jones JE, Jose PA. Genetics of Salt-Sensitive Hypertension. Curr Hypertens Rep. 2010 Nov 9.

(3) Lilly LS, et al. Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty. Fourth Edition. Lippincott Williams and Wilkins, 2006.

(4) Le T, Bhushan V, Grimm L. First Aid for the USMLE Step 1. New York: McGraw Hill, 2009.

(5) Kumar V, Abbas AK, Fausto N. Robbins and Cotran Pathologic Basis of Disease. Seventh Edition. Philadelphia: Elsevier Saunders, 2004.

(6) Savica V, Bellinghieri G, Kopple JD. The effect of nutrition on blood pressure. Annu Rev Nutr. 2010 Aug 21;30:365-401.

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Renin is a hormone released by the kidney when it senses decreased blood pressures. Renin cleaves a liver-produced protein called angiotensinogen into a smaller fragment called angiotensin I. Angiotensin I gets further cleaved into angiotensin II by an enzyme called angiotensin converting enzyme (ACE, see the section on ACE inhibitors) in the lung. Angiotensin II then circulates around the body where it causes blood vessels to constrict (thus raising pressure) and the kidney to retain sodium (leading to increased blood volume).