The concept of atherosclerosis. Etiology and pathogenesis of atherosclerosis
Atherosclerosis of the vessels of the lower extremities is one of the most serious and dangerous diseases of the arteries of the legs. It is characterized by the fact that due to blockage of blood vessels by atherosclerotic plaques or blood clots, there is a partial or complete cessation of blood flow in the lower extremities.
With atherosclerosis, narrowing (stenosis) or complete blockage (occlusion) of the lumen of the vessels that supply blood to the lower extremities occurs, which prevents the normal flow of blood to the tissues. With arterial stenosis of more than 70%, the speed indicators and the nature of blood flow change significantly, there is insufficient blood supply to cells and tissues with oxygen and nutrients, and they cease to function normally.
Damage to the arteries leads to pain in the legs. In case of progression of the disease, as well as with insufficient or incorrect treatment, trophic ulcers or even necrosis of the limbs (gangrene) may appear. Fortunately, this rarely happens.
Obliterating atherosclerosis of the arteries of the lower extremities is a very common disease of the blood vessels of the legs. The largest number of cases is detected in the age group over 60 years - 5-7%, at the age of 50-60 years - 2-3%, 40-50 years - 1%. But atherosclerosis can also be diagnosed in younger people - in 0.3%, people aged 30–40 years get sick with it. It is noteworthy that men suffer from atherosclerosis 8 times more often than women.
Fact: Smoking men over 50 years of age are at the greatest risk of getting atherosclerosis obliterans.
The main causes of atherosclerosis
The main cause of atherosclerosis is smoking. The nicotine contained in tobacco causes the arteries to spasm, thereby preventing blood from moving through the vessels and increasing the risk of blood clots in them.
Additional factors that provoke atherosclerosis of the arteries of the lower extremities and lead to an earlier onset and severe course of the disease:
- elevated cholesterol levels with frequent consumption of foods rich in animal fats;
- high blood pressure;
- excess weight;
- hereditary predisposition;
- diabetes;
- lack of sufficient physical activity;
- frequent stress.
Symptoms of atherosclerosis of the vessels of the legs
The main symptom to look out for is leg pain. Most often, pain occurs when walking in the calf muscles and thigh muscles. When moving, the muscles of the lower extremities increase the need for arterial blood, which delivers oxygen to the tissues. Narrowed arteries during physical exertion cannot fully satisfy the need of tissues for arterial blood, which is why oxygen starvation begins in them, and it manifests itself in the form of intense pain. At the beginning of the disease, the pain disappears quickly enough when physical activity is stopped, but then returns again when moving. There is a so-called intermittent claudication syndrome, which is one of the main clinical signs of obliterating atherosclerosis of the arteries of the lower extremities. Pain in the muscles of the thighs is called high intermittent claudication pain, and pain in the calves of the legs is called low intermittent claudication pain.
In old age, such pains are easily confused with painful sensations in the joints inherent in arthrosis and other joint diseases. Osteoarthritis is characterized not by muscle, but by joint pains, which are most intense at the beginning of the movement, and then somewhat weaken when the patient “walks around”.
In addition to pain in the muscles of the legs while walking, obliterating atherosclerosis of the arteries of the lower extremities can cause the following symptoms in patients (one of them or several at once):
- Chilliness and numbness in the feet, aggravated by climbing stairs, walking, or other exertion.
- Temperature differences between the lower extremities (a leg affected by atherosclerosis of the vessels is usually slightly cooler than a healthy one).
- Pain in the leg in the absence of physical activity.
- Non-healing wounds or sores appear in the area of the foot or lower third of the leg.
- Darkened areas form on the toes and feet.
- Another symptom of atherosclerosis may be the disappearance of the pulse on the arteries of the lower extremities - behind the inner ankle, in the popliteal fossa, on the thigh.
Stages of the disease
According to the existing classification of arterial insufficiency of the vessels of the legs, the above symptoms can be divided into 4 stages of the development of the disease.
- Stage I - pain in the legs that appear only after a lot of physical activity, such as walking long distances.
- Stage IIa - pain when walking over relatively short distances (250-1000 m).
- Stage IIb - the distance of painless walking is reduced to 50–250 m.
- Stage III (critical ischemia) - pain in the legs appears when walking at a distance of less than 50 m. At this stage, pain in the muscles of the lower extremities can begin even if the patient is at rest, this is especially evident at night. To relieve pain, patients usually lower their legs from the bed.
- IV stage - at this stage, the occurrence of trophic ulcers. As a rule, areas of blackening of the skin (necrosis) appear on the fingers or heel areas. In the future, this can lead to gangrene.
In order not to bring obliterating atherosclerosis to an extreme stage, it is important to diagnose it in time and treat it in a medical institution.
Treatment of atherosclerosis of arteries of the lower extremities
This disease requires an individually designed treatment regimen for each individual patient. Treatment of atherosclerosis of the vessels of the lower extremities depends on the stage of the disease, its duration, the level of damage to the blood arteries. In addition, when diagnosing and compiling a clinical picture, the presence of concomitant diseases in the patient is also taken into account.
If obliterating atherosclerosis is detected at the initial stage, it may be sufficient to improve the condition by eliminating risk factors. In this case, help:
- Compulsory cessation of smoking and other bad habits.
- Compliance with a diet low in animal fats and lowering cholesterol levels in the blood.
- With excessive fullness or obesity - weight correction.
- Maintaining normal blood pressure at a level not exceeding 140/90 mm Hg. Art.
- Regular physical activity (walking, swimming pool, exercise bike, etc.).
- For patients with diabetes - control of blood sugar levels.
With vascular atherosclerosis, the use of the following products is strictly prohibited: butter, margarine, lard, margarine, fatty meat, sausages, pates, offal, high-fat dairy products, fried potatoes, ice cream, mayonnaise, flour buns.
Important: A sedentary lifestyle makes blood vessels less elastic and accelerates the progression of the disease.
At other stages, the following methods are used to treat atherosclerosis of the vessels of the lower extremities:
- Conservative;
- Endovascular (minimally invasive);
- Operational.
Conservative treatment
It can also be used at the initial stage of the disease, as well as in cases where the patient's condition does not allow the use of other methods (with complications of concomitant pathology). Conservative treatment involves the use of medications, physiotherapy and includes pneumopressure therapy, dosed walking and exercise therapy.
Unfortunately, there are no medications that completely restore normal blood circulation in a clogged artery and cure atherosclerosis. Drug treatment can only provide support and affect the small vessels that carry blood around the blocked portion of the artery. Drug treatment aims to widen these "detours" and compensate for poor blood circulation.
To relieve spasm from small arterial vessels, thin the blood and protect the walls of the arteries from further damage, special medications are used, some of which need to be drunk in courses, while others should be taken constantly.
In addition to medicines, patients are prescribed pneumopress therapy - massage of the soft tissues of the leg with the help of special equipment. With the help of alternating low and high pressure in the cuff worn on the limb, peripheral arteries expand, blood flow to the skin, muscles and subcutaneous tissue increases, and vessels are stimulated.
Endovascular treatment
The most common methods of treatment for atherosclerosis of the vessels of the legs are endovascular methods - arterial stenting, balloon dilatation, angioplasty. They allow you to restore normal blood circulation through the vessel without surgery.
Such procedures are carried out in the X-ray operating room, on special equipment. At the end, a pressure bandage is applied to the patient's leg, and he must remain in bed for 12-18 hours.
Surgery
If the clogged arteries in the legs are too long for endovascular techniques, one of the following types of surgery is used to restore blood circulation in the legs:
- Prosthetics of an artery section with an artificial vessel (alloprosthesis);
- Shunting is the restoration of blood flow by redirecting the movement of blood through an artificial vessel (shunt). A segment of the saphenous vein of the patient himself can be used as a shunt;
- Thrombendarterectomy is the removal of an atherosclerotic plaque from an affected artery.
Surgical methods can be combined or supplemented with other types of operations. If the operation is performed at the IV stage of the disease, when dead zones have already appeared, these areas are surgically removed and the trophic ulcers are closed with a skin flap.
If obliterating atherosclerosis has passed into the extreme stage, when the patient has developed gangrene of the lower extremities, and it is no longer possible to restore blood flow, amputation of the leg is performed. Sometimes this becomes the only way to save the patient's life.
How to avoid the disease?
Prevention of atherosclerosis includes primarily:
- To give up smoking.
- Proper nutrition, cholesterol-free diet.
- Physical exercise.
These are three whales that will reduce the risk of atherosclerosis of the vessels of the lower extremities. It is not necessary to exhaust yourself with physical exercises, you can just take daily walks and do gymnastics for the legs. In addition, special acupressure and traditional medicine recipes help as a prophylactic.
Read more about the comprehensive prevention of atherosclerosis here.
Video: atherosclerosis of the vessels of the legs, presentation
Step 2: after payment, ask your question in the form below ↓ Step 3: You can additionally thank the specialist with another payment for an arbitrary amount
slide number 1
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slide number 2
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Atherosclerosis is a chronic disease of the arteries, accompanied by the formation of single and multiple lipid, mainly cholesterol, deposits or plaques in the inner lining of the arteries.
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Atherosclerosis, or rather, increased blood cholesterol, is one of the main risk factors for the development of cardiovascular diseases ... this is the "RUT OF LIFE"
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The term "atherosclerosis" comes from two Latin words: athere - which means gruel, and sclerosis - hard, dense, which reflects the stages of development of an atherosclerotic plaque. Atherosclerosis occurs in all people. The first signs of atherosclerosis are found at the age of five. "Atherosclerosis is a natural aging process" A. Davydovsky
slide number 5
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Causes of atherosclerosis The causes of atherosclerosis are high blood pressure, smoking, diabetes, high cholesterol. But the main cause of atherosclerosis lies in the violation of cholesterol metabolism.
slide number 6
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Risk factors for atherosclerosis Gender. Men are more prone to developing atherosclerosis than women. The first signs of this pathology can appear already from the age of 45 or even earlier, in women from the age of 55. Perhaps this is due to a more active participation in the exchange of estrogen cholesterol and low and very low density lipoproteins.
slide number 7
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Age. This is a natural risk factor. With age, atherosclerotic manifestations worsen.
slide number 8
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Heredity. This is one of the causes of atherosclerosis. Atherosclerosis is a multi-causal disease. Therefore, the level of hormonal levels, hereditary disorders of the plasma lipid profile, and the activity of the immune system play important roles in accelerating or slowing down the development of atherosclerosis.
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Bad habits. Smoking is a poison to the body. This habit is another reason for the development of atherosclerosis. As for alcohol, there is an interesting relationship: the use of small doses of alcohol daily is an excellent prevention of atherosclerosis. True, the same dose contributes to the development of cirrhosis of the liver. In addition, large doses of alcohol accelerate the development of atherosclerosis.
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Excess weight. This factor has a very negative effect on atherosclerosis. Excess weight can lead to diabetes mellitus, and this pathology is very malignant for the development of atherosclerosis.
slide number 11
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Nutrition. Our future health will depend on how useful our food is, how much it contains the chemical compounds we need. Few people know that no diet, other than therapeutic, is approved by the World Food Hygiene Council. You need to eat rationally and adequately to your needs and energy costs.
slide number 12
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Symptoms of atherosclerosis are often cold, bluish-white extremities; frequent heart problems; memory loss; violation of blood supply; poor concentration; the patient becomes irritable and feels tired. People with high blood pressure, as well as weak kidneys and diabetes, are most susceptible to atherosclerosis.
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Doctors consider atherosclerosis to be the most typical today: aorta, causing angina pectoris; kidneys; limbs; coronary arteries (ischemic heart disease); extracranial vessels, mainly the carotid artery, leading to cerebrovascular disease and cerebral stroke.
slide number 16
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How to treat atherosclerosis? Smoking cessation Physical activity Normalizing body weight Maintaining normal blood pressure Changing dietary habits
slide number 17
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"sclerosis" - solid) is a disease that affects the walls of blood vessels, mainly arteries of the muscular and musculo-elastic type, which is based on disorders of fat and protein metabolism, primarily cholesterol metabolism, manifested by imbibition of the vascular wall by proteins and lipids, followed by development around of these deposits 3. Dynamics of mortality of the population of Russia from diseases of the circulatory system for the period 1980–2002. 4. The dynamics of mortality in Russia for various classes of causes refers to arterial sclerosis, regardless of the cause and mechanism of its development.
Pathophysiology of atherosclerosis - online presentation
"sclerosis" - solid) is a disease,
affecting the walls of blood vessels
way, the arteries of the muscular and musculo-elastic type, which is based on
lie violations of fat and protein
metabolism, especially cholesterol metabolism,
manifested by imbibition of the vascular
walls with proteins and lipids, followed by
development around these deposits
3. Dynamics of mortality of the population of Russia from diseases of the circulatory system for the period 1980–2002.
4. Dynamics of mortality in Russia for various classes of causes
designate arterial sclerosis regardless of cause and mechanism
its development. Atherosclerosis is just a type
arteriosclerosis, reflecting disorders of lipid metabolism
and proteins (metabolic arteriosclerosis). In such an interpretation
The term "atherosclerosis" was introduced in 1904 by Marchand and
substantiated by experimental studies by N.N. Anichkov.
Therefore, atherosclerosis is called Marchand-Anichkov disease.
Depending on the etiological, pathogenetic and
morphological features distinguish types of arteriosclerosis:
1) atherosclerosis (metabolic arteriosclerosis);
2) arteriosclerosis, or hyalinosis (for example, with hypertensive
3) inflammatory arteriolosclerosis (for example, syphilitic,
4) allergic arteriosclerosis (for example, with nodular
5) toxic arteriosclerosis (for example, adrenaline);
6) primary calcification of the middle lining of the arteries
7) age-related (senile) arteriosclerosis.
response to damage (R. Ross, A. Glomset, A. Gotto, R. Jackson, 1976).
macrophages and some lipoproteins occurs
first intracellular and then extracellular accumulation of lipids
(cholesterol). In turn, alteration of the vascular wall
promotes both inflammation and
proliferation of smooth muscle cells and their synthesis of collagen,
glycosaminoglycans that form the tire and other
connective tissue elements of an atherosclerotic plaque. Growth,
development, and subsequently, the rupture of atherosclerotic
plaque contributes to the formation and separation of blood clots, the release
atheromatous masses into the vessel lumen, initiation of thromboembolic
8. Damage to the vascular endothelium - a trigger for the development of atherosclerosis
9. The role of hypertension in damage to the vascular endothelium
endothelial injury factor
vessels, especially in places
their bifurcations. This phenomenon is good
illustrates the following
In section ≪a≫ blood pressure
greatest, shear stress
maximum. Right here
and destruction occurs
endotheliocytes and their desquamation
(peeling) from the surface
vessel. In section ≪b≫ pressure
least blood. Damage
endothelium in these areas
happening. As is known,
hypertension and
atherosclerosis is two
processes that are closely related
themselves, or, more precisely, contributing
each other's development
10. Damage to the vascular endothelium is a trigger for the development of atherosclerosis
20-NETE (20-hydroxyeicosotetraenoic acid)
low density lipoproteins (LDL, β-lipoproteins, β-LP),
very low density lipoproteins (VLDL, pre-β-LP),
HDL-transfer of cholesterol from cells of various organs and tissues to liver cells, where it and
play apoproteins that are embedded in the lipid monolayer of the membrane
lipoprotein micelles. It is the molecules of apoproteins that micelles of lipoproteins are
ligands that bind the corresponding lipoprotein to its receptor. They are in a row
cases also play the role of cofactors for the corresponding enzymes. Currently
Four types of apoproteins have been identified:
Apo-A - provides a connection between HDL and the corresponding receptor apparatus.
Apo-B - provides communication between LDL and the receptor apparatus of liver cells and
Apo-C-II is a cofactor for lipoprotein lipase, due to which triglycerides
removed from chylomicrons and VLDL;
Apo-E - ensures the connection of lipoproteins with the receptor apparatus of hepatocytes.
Another type of apoprotein, the so-called apoprotein (a), has also been described.
attribute the greatest atherogenicity and being a part of LDL. The atherogenicity of this
apoprotein is explained by several of its properties. First, it is easily oxidized and
taken up by macrophages. Secondly, hepatic cells have the least amount
receptors for LDL containing lipoprotein (a). And finally, thirdly, there are data on
that LDL containing lipoprotein (a) have increased
activated platelets stimulate the release of factor from the endothelium
growth. The latter stimulates the proliferation of smooth muscle cells of the arterial
wall, which leads to its thickening and creates conditions for the formation of
further atherosclerotic plaques. activation of leukocytes, which have
increased adhesion to the endothelium, leads to its damage and promotes
penetration of lipids into the vascular wall. increased endothelial permeability
and vascular intima for coarse plasma proteins and lipids. Through the endothelium
through pinocytosis, globulins, albumins, fibrinogen and
lipids. In addition, the permeability of the vascular intima to monocytes increases. When
monocytes penetrate the vascular wall, they are transformed
macrophages, which begin to actively capture lipids and accumulate them in
vascular wall. increased activity of serum hyaluronidase, which leads to
depolymerization of hyaluronic acid contained in the vessel wall, and
increase in vascular tissue permeability. Cholesterol split off in the cell
from LDL by acting on this complex of lysosomal enzymes, through
regulation of the activity of the 3-hydroxy-3-methylglutaryl-coenzyme A-reductase enzyme contained in the cells, which is responsible for controlling the rate
limiting reaction of biosynthesis of endogenous cholesterol, reduces the synthesis
the last one. Hypercholesterolemia in the dolipid period has one important
feature: the chemical structure of cholesterol changes. If in intact
body cholesterol esters contain unsaturated fatty acids and such
cholesterol is easily utilized, then against the background of the development of atherosclerosis in these esters
saturated fatty acids appear. This cholesterol is poorly utilized and
retained in the blood serum.
At this stage of atherosclerosis,
vascular intima appear yellow
spots. Lipolytic Activity
vascular wall is sharply reduced, in
intimacy is delayed a lot
the amount of lipids (result
mechanism), proteins. For these products,
also into decaying acidic
mucopolysaccharides reaction develops
from the side of the vascular wall in the form
proliferation of connective tissue.
In the vascular wall around deposits
proteins and lipids there is a rapid
proliferation of connective tissue. AT
intimacy there is a large number
fat-laden macrophages (so
called xanthoma cells)
which partly go into the lymph, and
partly disintegrate, increasing the
the highest amount of detritus in the vascular
wall, where a dense plaque is formed,
protruding into the lumen of the artery.
in liposclerotic plaque
Two processes run in parallel:
increased sclerosis, that is, growth
connective tissue, and strengthening
breakdown of protein and lipid masses, then
there is detritus formation.
atherosclerotic plaque in this
the period on the cut is
dense connective tissue
capsule containing
masses of detritus and cholesterol crystals.
At this stage, intimacy becomes thinner,
capsule, the plaque adsorbs on itself
calcium salts and
6. Atheromatous ulcer
The plaque shell becomes very
thin, the plaque ulcerates, and
atheromatous masses enter
play the so-called
which are synthesized in
receptors and disrupt
which was already
more foam cell death
spurs inflammation by
(interleukin 1, necrosis factor
tumors, etc.). In the same
period of time is activated
smooth muscle cells. Under
influence of a number of growth
factors and pro-inflammatory
they acquire cytokines
mobility, migrate from the media
into the intima and subendothelial layer and
there they become secretory. Produced
they form collagen
enters its own cycle
PDGF, α-FGF, TGF-β, IGF - growth factors, IL-1 -
22. Mechanisms of atherosclerotic plaque formation
a - elastic "yellow" plaque with a large lipid core and a thin cap; b - rupture of the "yellow" plaque c
detritus falling into the lumen of the vessel (red dots) and the formation of a parietal thrombus; c - the structure of the "white"
fibrous plaque with a relatively small lipid core and a thick, durable fibrous capsule.
MECHANISMS OF ATHEROGENIC ACTION
Hypercholesterolemia, increased cholesterol and LDL
Elevation of cholesterol and LDL levels in the postmenstrual period
Decreased HDL content and increased VLDL
Increase in cholesterol and LDL, decrease in HDL
Decreased HDL, endothelial damage
Genetically determined dyslipidaemias
Endothelial damage, atherogenic changes in lipid
spectrum of blood, disorders of the trophism of the vascular wall
Endothelial damage, increased lipolysis
Atherogenic changes in the blood lipid spectrum, endothelial damage
27. Research on primary prevention of atherosclerosis
primary prevention of atherosclerosis
Primary prevention of atherosclerotic diseases in the population
implies a set of government measures aimed at
prevention of atherosclerosis of vessels of vital organs and complications with
using non-drug methods to combat risk factors (arterial
hypertension, smoking, hyper- and dyslipidemia, overweight,
hypodynamia) and medications (under the secondary
Prevention refers to measures taken to
inhibition of the progression of the disease and the reverse development of the existing
The study was devoted to the study of the possibility of implementing
primary prevention of coronary artery disease with an anti-atherosclerotic diet and
smoking cessation. The research program has been carried out since 1972.
in the city of Oslo (Norway). Of 16,202 apparently healthy men aged 40–49, there were
1232 people were selected with a high risk of coronary artery disease, but with a normal level of blood pressure
Particular importance was attached to the assessment of the actual nutrition of persons in the group
interventions, educating them on an anti-atherosclerotic diet and monitoring it.
compliance. The smoking weaning intervention consisted of conversations about the dangers
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