Tag: arteriosclerosis

Quick look at Aneurysms and Dissection

Quick look at Aneurysms and Dissection

Aneurysms are permanent and abnormal dilation of a part of a blood vessel or heart due to an attenuated intact arterial wall, or thinned out wall of a heart, mainly ventricles. This is also known as a “True aneurysm”. The difference between a true and a false aneurysm is the intact wall in a true  aneurysm. A false aneurysm is actually formed due to a defect in vascular wall, which leads to extra-vascular hematoma which freely communicates with the inside of the vessel. This is formed when blood is contained by the surrounding connective tissue after a complete breach in the vascular wall.

Eg :- as an acute complication after a Myocardial infarction, Cardiac rupture can occur. The blood in ventricles will be escaped into the pericardial space and the pericardial adhesions can limit this breach to a single focus.

Due to constant hemaodynamic stress a vessel wall is facing, it is in a continous process of synthesizing, degrading and remodelling/repairing the connective tissue. Any defect in this cycle would disrupt the intergrity of the vessel wall and lead to an aneurysm. All these reasons can be categorized mainly in to 3 main topics, as follows;

  1. Defective synthesis of connective tissue
    • Marfan syndrome —-> defective synthesis of scaffolding protein —> Aberrant TGF – beta activity—-> Weakening of elastic tissue
    • Loeytz-Dietz Syndrome —-> Mutation in TGF-beta —-> Defective synthesis of collagen I and III and elastin
    • Scurvy—-> Vitamin C deficiency —–> Defective cross linking of collagen
  2. Increased Degradation of connective tissue.
    • Increase degradation normally occurs when there is an inflammation going on in the wall. During atherosclerosis abnormal activity of macrophages will lead to increased levels of Matrix Metello Proteases(MMP) which would accelerate the degradation of vascular wall, over the synthesis. Also  Production of certain inflaaotory cytokines will lead to stimulation of macrophages to release MMPs. Vasculitis is another example
  3. Weakening of the vascular wall due to loss of smooth muscles or disposition of non collagenous/elastic substances. (Explained in Quick look at Aortic aneurysms and dissections)

In contrast to aneurysms, Dissections have a distinct breach in the vessel wall, which leads to accumulation of blood, from the intravascular space between the laminar planes of media. This forms a blood filled channel within the media and blood do not communicate with the outside of the vessel as in false aneurysms.

Although even if we say there is a breach in the vessel wall, aortic dissections sometimes can occur without any intimal tear. Aorta is a large artery. It has a very large Tunica media. This layer is so thick, that small blood vessels called, “Vasa Vasorum”are present to supply blood to this layer to provide their nutritional and oxygen requirements. During hypertension due to medial thickening  in the arterioles (Quick look at Pathology in hypertension) and loos of their integrity, these can rupture leading to accumulation of blood within the laminar planes of media of aorta.

Quick look at Pathology in hypertension

Quick look at Pathology in hypertension

Normal cutoff values for blood pressure are 120/80 mmhg (systolic/diastolic). A person with sustained and persistent elevated blood pressure levels  than the cutoff values is said to be having Hypertension.

Generally hypertension is categorized into two depending on the etiology as follows;

  1. Primary Hypertension (Essential Hypertension)
  2. Secondary Hypertension

Primary hypertension is said to be developing mainly due to 2 reasons. First is the genetic make- up. It is said that familial aggregation or the genetic make up would explain the  occurrence of hypertension among twins. Second would be the vascular causes which would result in vasoconstriction. It could be an inbuilt cause which would stimulate constriction of vessels, or stimuli from outside such as smoking, obesity, stress, etc.

Secondary hypertension develops as a result of malfunction in another system. Depending on the etiology, causes for above, can be discussed under 4 main categories;

  • Renal 
    • there are 3 main factors which would influence in increase in blood pressure such as activation of renin-angiostensin-aldesterone system, retention of sodium and water and Release  of vasopressor materials. (Discussed mainly under “Quick look at physiology of Blood pressure regulation”)
  • Endocrine
    • Hormonal imbalances causing elevated blood pressure levels are included under this topic. Eg :- Cushing’s syndrome, Primary aldosteronism, phaeochromocytoma, oral contraceptives, etc.
  • Coartctation of Aorta
  • Neurogenic 
    • Eg:- polyneuritis, Raised Intracranial pressure, etc..

There are various pathological changes occurring in hypertension in  various organs. Many of these can be explained using the basic changes occurring in blood vessels, specially in arterial system.

In hypertension, due to increased haemodynamic stress,  degenerative changes occurring in the large and small sized arteries will lead mainly to atherosclerosis. Also it would lead to aortic dissection, cerebrovascular hemorrhages and aneurysms.

Many of the pathological changes occurring in other oragns can be expalined using the changes occuring in arterioles.

  1. Hyaline arteriolosclerosis 
  2. Hyperplastic arteriolosclerosis

Due to gradual elevation of blood pressure, over a long period would cause degenerative changes in the endothelial cells, which would lead to leakage of plasma proteins in to the intimal layer, causing aggregation of pink, glass like proteinacious material in the intimal layer of blood vessels, leading to intimal thickening, which would in turn cause luminal narrowing. Along with this as there would be an increase in synthesis of matrix of smooth muscle cells, in the Tunica media as a response to increased haemodynamic stress also contributes for luminal narrowing. These changes are called “Hyaline arteriolosclerosis”. Normally these changes occur in patients who have “Benign hypertension”, which develops slowly and gradually over years. These changes are mostly widespread and  affects almost all the organs.

If the blood pressure suddenly and markedly elevated over 200/140mmhg, it is called “Malignant Hypertension”. Most acute change expected would be fibrinoid necrosis of blood vessels, due to marked increase in blood pressure. This would cause leakage of massive amount of fluid out in to the organs causing edema. If patient suffers from this type elevations in blood pressure, for a reasonable amount of time to call it a chronic condition, arterioles will show an adaptation where concentric laminated thickening of smooth muscles occurs with re-duplication of basement membranes. This would mimic the arrangement of an onion-skin. Therefore it is also called an Onion-Skin type thickening. These changes are known as “Hyperplastic Arteriolosclerosis”.