KAKAIBANG ALTAPRESYON Secondary Hypertension

KAKAIBANG ALTAPRESYON

Secondary Hypertension: Unveiling the silence of the’ Silent Killer’

Secondary Hypertension: Pay attenti~n – this is “essential” the pathophysiology of it all.
Pete de la Pefla, MD, FPCp, DPSEM

Hypertension is an intermittent or sustained elevation of diastolic or systolic blood pressure. At least one of the following two criteria is present.

a. Systolic blood pressure>= 140 mmHg on two separate occasions b. Diastolic blood pressure >= 90mmHg on two separate occasions

The two major types of hypertension are essential, also called primary or diopathic and secondary, majority of which are endocrine in nature.

To discuss the pathophysiology of secondary hypertension, one must know how hypertension happens.

ESSENTIAL HYPERTENSION:
Hypertension may be caused by an increase in cardiac output, total peripheral resistance or both.

Cardiac output may be increased by conditions that increase the heart rate or stroke volume.

Peripheral resistance may be increased by conditions that increase blood viscosity or a reduction of the lumen of the blood vessels.

Strong family history, race, gender, stress, obesity, a diet high in sodium or fat, use of tobacco, a sedentary lifestyle and aging may all play a role. Why does it all happen?

Some speculations help explain the development of hypertension.

• Abnormally increased tone in the sensory nervous system causing increased peripheral resistance

Always remember that hypertension usually doesn’t produce signs and symptoms until vascular changes in the heart, brain, or kidneys occur. Complications occur late in the disease and can lead to organ damage.

• Changes in the arteriolar wall causing resistance
• Increased blood volume resulting from
• Increase in arteriolar thickening which may be caused by genetic factors
• Abnormal renin release resulting to the formation of angiotensin II, which constricts the vessel wall and increases blood volume

SECONDARY HYPERTENSION:
Hypertension that is related to the underlying disease. As discussed in the previous issue, secondary hypertension may be caused by the following:
*renal parenchymal disease
*renovascular disease
*pheochromocytoma
*primary aldosteronism
*cushings syndrome
*dysfunction of the thyroid, pituitary, parathyroid

WHY? WHY? WHY? – for secondary hypertension.

1. Chronic renal disease – Damage to the kidney either from chronic glomerulonephritis/ renal artery stenosis interferes with sodium excretion. It also disrupts the renin-angiotensin-aldosterone system and renal perfusion causing rise in blood pressure.
2. Cushing’s Syndrome – An excess of cortisol levels also lead to increase in blood pressure by increasing renal sodium retention, angiotensin I levels and increased vascular response to norepinephrine.
3. Primary aldosteronism – An excess of aldosterone levels may also lead to an increased intravascular volume, altered sodium concentration in vessel walls. This may also lead to increased peripheral resistance.
4. Pheochromocytoma – This is due to increased secretion of epinephrine and norepinephrine. Epinephrine increases cardiac contractility and rate while norepinephrine increases peripheral resistance.

It is important to know why hypertension happens. Knowing the pathophysiology of hypertension whether’ essential’ or ‘secondary’ leads to proper treatment.

Always remember that hypertension usually doesn’t produce signs and symptoms until vascular changes in the heart, brain, or kidneys occur. Complications occur late in the disease and can lead to organ damage.

If only your heart can speak, Pay attention – “Stop pushing so hard! I don’t need all this pressure. “

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