Last updated on November 23, 2019 at 00:15
The topics about hypertension in pathophysiology are more thorough than this topic. Look there for more details.
Hypertension is a big health problem in developed countries and is known as the silent killer because it’s asymptomatic for many years. Approximately 25 % of the population has some form of it.
We count blood pressures over 139/89 mmHg as benign hypertension (although it’s actually not so benign), and its considered malignant when it reaches 180/110 mmHg.
We distinguish blood pressures into two groups: primary and secondary hypertension.
95 % of all hypertensive cases are primary, and this includes systemic, pulmonary and portal hypertension.
Systemic hypertension is the one always measured in hospitals and at the doctor’s office, and everything above 139/89 is considered hypertension.
You can read about pulmonary hypertension here.
If the pressure difference between the portal vein and the hepatic vein pressure is greater than 5 mmHg, it is considered as portal hypertension.
How does systemic hypertension occur?
The specific triggers are actually unknown but altered sodium retention in kidneys and increased vasoconstriction contribute to this condition.
Sodium retention while blood pressure is normal, leading to a higher blood volume and even higher blood pressure is the key pathologic feature. The pathologic vasoconstriction can result from changes in vessel walls, that happens in the elderly, or increased sympathetic tone as in e.g. obesity. Let’s look at some factors that can alter hypertension.
- Genetic factors
- Increased sympathetic activity that results in frequent vasoconstriction
- Hyperinsulinism, that causes increased sodium and water retention
- Salt intake
- Vasoconstriction increases because it induces stress to our bodies.
- Vitamin D deficiency
This type of hypertension only occurs in 5 % of all hypertensive cases and is due to primary renal disease or adrenal disorders. Let’s take a closer look.
The renal artery narrows, and the perfusion of kidney (RBF) decreases because of this. RAAS will then be activated, and the systemic blood pressure will rise. Usually, this happens in atherosclerosis of renal artery and fibromuscular dysplasia.
- Renoparenchymal hypertension
- Endocrine hypertension
Happens in Conn’s syndrome (hyperaldosteronism), Cushing’s syndrome and pheochromocytoma.
- Aortic coarctation – Narrowing of aorta
- Neurological – Obstructive sleep apnoe and Cushing’s reflex – more about this in pathophys.
- Pregnancy-related – Hypertension related to preeclampsia.
Complications of hypertension
The injuries done by hypertension are many. I’ll just make a quick summary here, but a more detailed list can be found in topic 29 in pathophys.
1. Atherosclerosis – hypertension is a major risk factor for that. For atherosclerosis to occur must the vessels be damaged, which they are in hypertension.
3. Hypertensive heart disease
20 % of cases of hypertension leads to left ventricular hypertrophy and 25 % of heart failures is due to hypertension
Degenerative changes due to injury in the walls of large and medium sized arteries, like hyaline arteriosclerosis where the arteriolar walls thicken due to hyaline and lumen narrows. Hyperplastic arteriolosclerosis is typical in severe hypertension where the vessels undergo concentric laminated thickening of the arteriolar wall, giving them “onion skin”
5. Retinopathy – vascular abnormalities to retina, leading to ischemia and loss of vision
6. Aortic dissection
Injury to the innermost layer of the aortic wall, allowing blood to enter between the layers and forcing them apart.
Nephrosclerosis shows the same changes as in hyaline arteriosclerosis but occurs in the glomeruli (glomerular scarring).
8. Renal failure
Hypertensive nephropathy can lead to proteinuria. Uraemia can also occur due to hypertension.
26. Causes, types and pathomechanisms of shock. Disseminated intravascular coagulation (DIC)
28. Vascular and cellular mechanisms and mediators of acute inflammation