Hypertension Cardiovascular Disorders Pathology Notes

Hypertension

WHO definition of hypertension: Hypertension is defined as systolic pressure above 160 mm Hg and/or diastolic pressure above 90.

Hypertension Causes:

• Primary/essential/idiopathic hypertension: It constitutes about 95% of cases.
• Secondary hypertension: It forms about 5% of cases and there is an identifiable cause.

Major causes of hypertension (systolic and diastolic):

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Regulation of Normal Blood Pressure: Normal blood pressure is essential for survival; it causes damage when it increases continuously above the normal range.

Factors Determining Blood Pressure:

• The major factors include age, sex, body mass index, and diet, particularly sodium intake, exertion, emotional state, and others.
• Blood pressure depends on two hemodynamic variables namely cardiac output and peripheral vascular resistance. These two, in turn, are influenced by many genetic, environmental, and demographic factors.
  • Cardiac output: It depends on blood volume, which in turn is influenced by sodium homeostasis.
  • Peripheral vascular resistance: It is determined by functional and anatomic changes in small arteries and arterioles. It is affected by neural and hormonal factors.

Role of Kidney:

The kidneys play an important role in the regulation of blood pressure.

• Renin-angiotensin system: The kidney influences both peripheral vascular resistance and sodium homeostasis (thereby blood volume) through the renin-angiotensin system.
  • Renin: Whenever there is a fall in blood pressure, renin is secreted by the juxtaglomerular cells of the kidney and released into the blood circulation.
  • Angiotensin 2: It raises blood pressure by increasing both peripheral resistance (direct action on vascular smooth muscle cells and causes vasoconstriction) and blood volume.
  • Antihypertensive substances: The kidney also produces substances that cause vasodilation and have an antihypertensive effect. These include prostaglandins and nitric oxide (NO).
• Sodium homeostasis and blood volume:
  • When blood volume is reduced, the glomerular filtration rate falls → leading to increased reabsorption of sodium by proximal tubules of the kidney → thereby conserving sodium and expanding blood volume.
  • When blood volume increases, natriuretic factors (natriuretic peptides) are secreted by the atrial and ventricular myocardium. They inhibit sodium reabsorption in distal tubules and cause excretion of sodium and diuresis.

Morphology of Kidney:

• Gross:
• Involvement: Bilateral.
• Size: Kidneys are either normal or smaller (atrophic).
• Outer surface: It shows a fie, even granularity resembling grain leather.

Pathogenesis of Hypertension:

Write a short note on the pathogenesis of hypertension.

Mechanisms of Essential Hypertension:

• Essential hypertension is a complex and multifactorial disorder. The specific trigger is not known. Probable factors that play a significant role include:
• Decreased renal sodium excretion: It is probably the key feature. Decreased excretion of sodium by the kidney → leads to an increase in fluid volume, cardiac output, and peripheral vasoconstriction → raises blood pressure.
• Raised vascular resistance: Factors that produce vasoconstriction or stimuli that cause structural changes in the vessel wall → result in an increase in peripheral vascular resistance → cause primary hypertension.
• Genetic factors: They play an important role in the development of hypertension. The genetic defects may be in the enzymes involved in aldosterone metabolism, sodium reabsorption, and smooth muscle cell growth.
• Environmental factors: These include stress, obesity, smoking, lack of physical activity, and heavy intake of sodium salt.

Consequences of Hypertension:

• Risk factor: Hypertension is one of the major modifiable risk factors for atherosclerosis.
• Lesions/diseases produced: Cardiac hypertrophy, congestive heart failure (hypertensive heart disease) and ischemic heart disease (IHD), multi-infarct dementia, aortic dissection, stroke, subarachnoid hemorrhage, hypertensive encephalopathy, retinal ischemia/infarction and renal failure.
• Accelerated or malignant hypertension: It is characterized by the rapid rise in blood pressure (i.e. systolic pressure over 200 mm Hg, diastolic pressure over 120 mm Hg) → renal failure, and retinal hemorrhages and exudates, with or without papilloma.
  • It may develop in normotensive individuals but is more common in patients with preexisting benign hypertension (essential or secondary).
  • It develops in ~5% of hypertensive persons. If not treated, death occurs within a year or two.

Effects On Various Organs

Write a short note on vascular pathology in hypertension.

Vascular Pathology:

1. Large and Medium Vessel Disease: Atherosclerosis

• Hypertension is one of the major modifiable risk factors for thermogenesis.
• Causes degenerative changes in the walls of large and medium arteries.
• Predisposes to:
  • Aortic dissection and
  • Cerebrovascular hemorrhage.

2. Small Vessel Diseases:

Two forms can occur in hypertension:

1. Hyaline arteriosclerosis, and
2. Hyperplasia arteriosclerosis.

1. Hyaline arteriosclerosis: It is seen in the arterioles in patients with benign hypertension.

Microscopy of Hyaline arteriosclerosis:

It shows thickening of the wall due to homogeneous, pink hyaline material and narrowing of the lumen.

A consequence of Hyaline arteriosclerosis: The arterioles narrowing → impaired blood supply to the kidney → produces ischemia and glomerular scarring. The kidney changes in benign hypertension are called benign nephrosclerosis.

2. Hyperplastic arteriosclerosis: It occurs in severe (malignant) hypertension.

Microscopy Hyperplastic arteriosclerosis :

The blood vessels show “onion-skin,” concentric, laminated thickening of the walls of the arterioles and narrowing of the lumen of the arteriole. It may also show fibroid deposits and necrosis of the vessel wall (necrotizing arterioles), particularly in the kidney.

Hypertensive Heart Disease

Systemic hypertension can increase the demands on the heart and cause pressure overload and left ventricular hypertrophy. It is termed hypertensive heart disease (HHD).

Systemic (left-sided) hypertensive heart disease:

• Hypertrophy of the heart develops as an adaptive response to the pressure overload produced by chronic hypertension. However, compensatory hypertrophy can ultimately lead to myocardial dysfunction, cardiac dilation, and congestive heart failure (CHF).
• Pathologic criteria for the diagnosis of HHD
  • Left ventricular hypertrophy
  • Clinical history or pathologic evidence of hypertension in other organs (for example, Kidney).

Morphology of heart:

• Hypertension produces left ventricular pressure overload hypertrophy. The left ventricular wall is thickened and may exceed 2.0 cm.
• Microscopically, there is an increase in the size of myocardial fibers and their nuclei.

Nephrosclerosis of the heart:

Nephrosclerosis is the term used for the renal pathology associated with sclerosis of renal arterioles and small Arteries. It is strongly associated with hypertension and can be divided into benign and malignant nephrosclerosis.

Benign Nephrosclerosis

Definition of Benign nephrosclerosis:

Benign nephrosclerosis is defined as the renal pathology associated with sclerosis of renal arterioles and small arteries. Benign nephrosclerosis is associated with hypertension. However, it may also be observed in diabetes mellitus and increasing age in the absence of hypertension.

Malignant Hypertension And Accelerated Nephrosclerosis:

Definition of Malignant Nephrosclerosis:

Malignant nephrosclerosis is defined as a renal disease associated with the malignant or accelerated phase of hypertension.

The malignant or accelerated phase of hypertension is relatively uncommon. It is often superimposed on preexisting essential benign hypertension, secondary forms of hypertension, or an underlying chronic renal disease, particularly glomerulonephritis or reflux nephropathy.

Morphology of Malignant Nephrosclerosis:

• Gross:
  • The size of the kidney depends on the duration and severity of the hypertension.
  • Flea-bitten kidney: It is characterized by the presence of small, pinpoint petechial hemorrhages on the cortical surface due to the rupture of arterioles or glomerular capillaries.
• Microscopy:
  • Histological changes of blood vessels → narrowing of vascular lumens→ ischemic atrophy.
  • Fibroid necrosis of arterioles: It is characterized by eosinophilic granular change in the wall of the blood vessel.
  • Onion skinning (hyperplastic arterioles): It is seen in the interlobar arteries and arterioles. It is characterized by intimal thickening due to concentric proliferation of smooth muscle cells + fie concentric layering of collagen, proteoglycans, and plasma proteins.

Hypertensive Cerebrovascular Disease:

The most important effects of hypertension on the brain are

• Lacuna infarcts
• Slit hemorrhages
• Hypertensive encephalopathy
• Massive hypertensive intracerebral hemorrhage.