HTN leading to hyperplastic arteriolosclerosis?

[MudPhud20XX]

Hi all,

So one of the consequences of malignant hypertension is hyperplastic arteriolosclerosis. According to Pathoma, this is due to the thickening of vessel wall by hyperplasia of smooth muscle which is often described as "onion-skin" appearance.

So can anyone explain the mechanism of this adaptation? Is it similar to the Lt. ventricle hyperplasia due to HTN? I am not sure if this would apply to hyperplasia of the smooth muscle of blood vessel though...

Many thanks in advance.

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[tranquilo]

Hi all,

So one of the consequences of malignant hypertension is hyperplastic arteriolosclerosis. According to Pathoma, this is due to the thickening of vessel wall by hyperplasia of smooth muscle which is often described as "onion-skin" appearance.

So can anyone explain the mechanism of this adaptation? Is it similar to the Lt. ventricle hyperplasia due to HTN? I am not sure if this would apply to hyperplasia of the smooth muscle of blood vessel though...

Many thanks in advance.

Myocytes are considered nondiving cells and as such they undergo hypertrophy (not hyperplasia) and most likely due to hemodynamic overload. In the case of hyperplastic arteriolosclerosis, you have some form of insult to kidney vasculature (endothelial activation) -> bunch of GFs, blah blah that stimulate SMC hyperplasia -> tunica intima thickens from migration of proliferated SMCs

You will probably find a nice chart of this somewhere online. Hope this gets you started

 

[Apoplexy__]

Lt. ventricle hyperplasia due to HTN?

Yeah like tranquilo said, this is NOT hyperplasia. It's hypertrophy. Very important - cardiac myocytes are non-dividing cells.

Smooth muscle cells, on the other hand, can proliferate in the face of physiological stress. Examples: uterine smooth muscle in pregnancy (both hyperplasia and hypertrophy) and bronchiolar smooth muscle in asthma. A pathological example: endometriosis.

I've heard of board questions that give you a clinical example and ask you what the growth alteration is. For example: clogged pancreatic ducts in cystic fibrosis, the cells are atrophic pre-obstruction (pressure atrophy). Renal artery stenosis, the kidney is atrophic post-obstruction (chronic ischemia), and the non-obstructed kidney is hypertrophied. Important stuff.

 

[MudPhud20XX]

Thank you so much guys! I really appreciate it.