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MINISTRY OF PUBLIC HEALTH OF UKRAINE

BUKOVINIAN STATE MEDICAL UNIVERSITY


Approval on methodological meeting

of the department of pathophisiology

Protocol №

Chief of department of the pathophysiology,

professor Yu.Ye.Rohovyy

“___” ___________ 2008 year.


Methodological Instruction

to Practical Lesson



Мodule 1 : GENERAL PATHOLOGY.

Contenting module 3. Typical disorders of metabolism.


Theme18: Pathology of lipide metabolism.Atherosclerosis.


Chernivtsi – 2008

1.Actuality of the theme. Atherosclerosis – exceptionally widespread disease. On data WHO, mortalitis of the patients in the age 35-44 years for damages of heart and vessels connected with atherosclerosis, increased lately by 60 %. The knowledge of the reasons and mechanisms of atherosclerosis development is necessary for the doctors of various profession for prophylaxis and treatment of this disease. According to modern notions, main etiological factors of atherosclerosis is dyslipoproteinemia and increased permeability arterial wall for lipoproteins. The primary prophylaxis foresee realization of such methods, as organization of rational nutrition, early preventing obesity, increase of physical activity, revealing and treatment arterial hypertension and diabetes mellitus, fighting with smoking and abusing by alcohol.

^ 2.Length of the employment – 2 hours.

3.Aim:

To khow: there are following disturbances of lipide metabolism:

1. Hyperlipemia (essential, genotypic, retention, transport types)

2. Atherosclerosis, arteriosclerosis

3. Obesity

4. Fatty infiltration and dystrophy (liver and oth. organs), fatty degeneration.

To be able: to analyse of the pathogenesis of the atherosclerosis. Arteriosclerosis is a chronic disease of the arterial system characterized by abnormal thickening and hardening of the vessel walls. Smooth muscle cells and collagen fibers migrate into the tunica intima causing it to stiffen and thicken; this decreases the artery's ability to change lumen size.

^ I stage is deposition of lipids ? irritation of the histiocytes ? proliferation of the histiocytes. II stage is xanthomatosis ? histiocytes ? capture of lipids —> irritation of fibroblasts ? thickening of the subendothelium, deformation of the elastic tissue ? consolidation of the connective fibers. III stage - patches, nutrient material is received by histiocytes with difficulty, necrosis. IV stage is atheromatosis, formation of ulcers, which can perforate thrombi are formed.

^ To perform practical work: to analyse the sequence of cellular interactions in atherosclerosis. Hyperlipidemia and other risk factors are thought to cause endothelial injury, resulting in adhesion of platelets and monocytes and release of growth factors, including platelet-derived growth factor (PDGF), which lead to SMC migration and proliferation. Foam cells of atheromatous plaques are derived from both macrophages and SMCs-from macrophages via the very-low-density lipoprotein (VLDL) receptor and low-density lipoprotein (LDL) modifications recognized by scavenger receptors (e.g., oxidized LDL), and from SMCs by less certain mechanisms. Extracellular lipid is derived from insudation from the vessel lumen, particularly in the presence of hypercholesterolemia, and also from degenerating foam cells. Cholesterol accumulation in the plaque reflects an imbalance between influx and efflux, and high-density lipoprotein (HDL) probably helps clear cholesterol from these accumulations. SMCs migrate to the intima, proliferate, and produce ECM, including collagen and proteoglycans




4. Basic level.

The name of the previous disciplines


The receiving of the skills

  1. histology

  2. biochemistry

  3. physiology

Lipids and lipoproteins of blood plasma

Transport of lipids.

Intermediate metabolism of fat.

Sources cholesterol of blood plasma and it metabolism.

Anatomic-physiological features of vessels.





^ 5. The advices for students.

  1. The role fat in the organism.

1. Fat is a source of reserve energy, its supplies are 10%.

2. Fat is a source of endogenous metabolic water.

3. Fat participates in heat production and saving one as it conducts heat poor.

4. Cholesterol participates in:

  1. construction of the cellular membrane and consequently in its permeability;

  2. being the dielectric it provides the conduction of impulses in the definite direction ( without myelin coat may be “chaos” in n.s.)

  3. the corticosteroids, sex hormones, bile acids, vit.D are formed from cholesterol

  1. Name types of hyperlipoproteinemias due to HWO’s classification.

According to classification of HWO hyperlipoproteinemias are following:

Types

Hereditary origin

Acquared

Type I - ?ChM

Deficiency lipoproteinlipase

Systemic lupus erythomatosus (SLE)

Type IIa - ?LDL

Family hypercholesterinemia (deficiency receptors to LDL)

Hypothyroidism
^

Type IIb - ?LDL+?VLDL


Combine familial hypercholisterinemia

Nephritic syndrome

Type III - ?remnaht particles of ChM+?IDL


Family hyperlipoprotein emia the IIId type

Obesity
^

Type IV - ?VLDL


Combine family hyperlipidemia

Diabetes mellitus

Type V - ?ChM+?VLDL


Family hypertriglycerides

Alcohol intoxication

Legend: ? - increase Ch – chylomicrons, LDL – low density lipoproteides, VLDL – very low density lipoproteides, IDL – intermediate density lipoproteins.


^ 3. Disturbances of lipide metabolism

1. Hyperlipemia (essential, genotypic, retention, transport types)

2. Atherosclerosis, arteriosclerosis

3. Obesity

4. Fatty infiltration and dystrophy (liver and oth. organs), fatty degeneration.


^ 4. Characterize atherosclerosis, the main risk factors and pathogenesis.

Arteriosclerosis is a chronic disease of the arterial system characterized by abnormal thickening and hardening of the vessel walls. Smooth muscle cells and collagen fibers migrate into the tunica intima causing it to stiffen and thicken; this decreases the artery’s ability to change lumen size.

Atherosclerosis is a form of arteriosclerosis in which the thickening of the vessel walls is caused by hardening of soft deposits of intraarterial fat and fibrin that reduce lumen size. Atherosclerosis can take several forms depending on the anatomic vessel location, the individual’s age, genetic and physiologic status, and the risk factors to which each individual may have been exposed. It is the leading contributor to coronary artery and cerebrovascular disease.

Lipid deposition is an early event in atherogenesis and occurs with excessive influx and deposition of macrophages containing oxidized low-density lipoproteins (LDL) into the arterial wall. This event occurs subsequent to endothelial injury. The lesions of atherosclerosis occur primarily within the tunica intima or the innermost layer. These lesions include the fatty streak, fibrous plaque, and complicated lesion. The early fatty streak is a flat, yellow, lipid-filled smooth muscle cell that causes little or no obstruction of the affected vessel.

^ Fibrous plaque is the characteristic lesion of advancing atherosclerosis and consists of lipid-laden smooth muscle cells surrounded by a fibrous matrix. The lesion is elevated and protrudes into the lumen of the artery. The core of the fibrous plaque consists of lipids and debris from cellular necrosis caused by insufficient blood supply. If the lesion progresses sufficiently, it occludes the arterial lumen at arterial bifurcation, curves, or regions where the arteries taper.

Complicated lesions occur as the fibrous plaques are altered by hemorrhage, calcification, cellular necrosis, and blood clots throughout the intimal layer. As the altered complex structure becomes rigid, it causes extensive vascular occlusion.

High blood pressure develops if arteriosclerosis elevates systemic vascular resistance. Cerebral or myocardial ischemia is a life-threatening manifestation of atherosclerosis that occurs in the vessels of the brain or heart.

Dietary modifications are always the first treatment for atherosclerosis. Fat intake should be reduced to less than 30 % of daily caloric consumption. Daily cholesterol intake must be reduced to 250 to 300 mg. Total blood cholesterol levels of less than 200 mg/dl, with low-density lipoproteins (LDL) less than 130 mg/dl and high-density lipoproteins (HDL) more than 35 mg/dl, are desirable. Drugs that decrease lipidemia are prescribed if serum lipoproteins are not reduced by dietary modifications or if lipid levels are dangerously elevated in an individual requiring a lengthy time for significant dietary change and weight reduction.

    1. ^ Describe obesity. What is the role of genital, constitutional and environmental factors in their development?

Three basic pathogenetic factors are important in the development of obesity: increased intake of food, which doesn't correspond to the energy expenditures; insufficient mobilization of fat from the depots; surplus formation of fat from carbohydrates (S.M. Leites).

The surplus consumption of food, which is provoked by increased appetite, can be stipulated by increased excitability of the "nutritional center", which is situated in the anteriolateral nuclei of the posterior hypothalamic region. The changes, to which the nutritional center is reacting, can be the cause of prolonged nutritional excitation and as a result of alimentary obesity. So, all states, which decrease the level of glucose in blood, stead fastly for example, some increase of the function of the pancreatic islands, are accompanied by feeling of hunger, which stipulates the possibility of overeating. The signals from the receptors of die alimentary tract are also important in activity of the nutritional center. A definite degree of extension of the stomach inhibits the activity of the nutritional center. In decrease of sensitivity of the nervous endings in the wall of the stomach the inhibition develops only in excessive extension of (lie stomach, diat also creates die preconditions to overeating and obesity. Dysbalance of energy is possible in transition from the physical labour to the way of life without physical loading if the former degree of excitability of die nutritional center is preserved. Obesity can be connected with disturbance of fat mobilization from fat depots as a source of energy in normal function of die nutritional center.

The regulation of process of mobilization and deposition of fat is accomplished by die nervous and endocrine systems. So decrease of the tonus of the sympathetic nervous system can provoke die delay of mobilization and going out of fat from the adipose tissue. Disappearance of fat from the adipose tissue on the head and thorax with simultaneous deposition of it in lower half of body is observed in.

Barraquer - Simons disease - progressive lipodystrophy connected with lesion of the centers of the diencephalon, spinal cord and nodes of the sympathetic trunk. Disturbance of mobilized fat influence of hormones is observed in pathology of the pituitary, thyroid gland, adrenal and sexual glands. Obesity, which is characterized by hyperinsulinism, resistance to insulin and hyperglycernia, can be observed. It is considered that basic damages are at the level of target cells. They are connected with decrease of quantity of receptors for insulin stipulating the resistance to insulin and compensatory hyperinsulinism. Now the peculiarities of the adipose tissue, quantity and size of fatty cells - adipocytes are taken into account in pathogenesis of obesity. The quantity of the adipose cells is genetically stipulated factor and their size depend on the age, sex, influence of the regulatory and metabolic factors. Quantity of the adipose cells is relatively constant and doesn't change with age. It is more in women than in men. The quantity of die adipose cells in young people is 3*1010, contents of fat in the adipocyte are 0.6 mcg, total quantity of fat in the organism is about 18 kg. There are cases of obesity with total quantity of fat more than 70 kg, in normal quantity of adipocytes, however the mass of one cell is 1.6 mcg. In other cases die mass of adipocytes remains normal and their quantity reaches 9*10 . Total quantity of fat can be equal to 100 kg and more.

    1. Distinguish between hypertrophic and hyperplastic obesity.

Pathogenetical classification based on the criterion of size and quantity of adipocytes distinguishes two types of obesity: hypertrophic and hyperplastic.

Hypertrophic obesity depends on the quantity of fat in each adipocyte that is connected with increased concentration of insulin, hyperlipemia, decrease of the tolerance to glucose. Not infrequently this form of obesity is complicated by development of atherosclerosis and diabetes mellitus at in a young age.

Hyperplastic obesity is connected with increase of quantity of adipocytes, which depends on the genetic factors or the environment regulating the morphogenesis of the adipose tissue in the embryonal period and at early age. Obesity influence the organism unfavorably. The negative influence of obesity is manifested in less degree at young age, when adaptational possibilities are expressed better. And the quantity of complications connected with obesity increases with age. The mortality of people with obesity at 20-24 years old 30 % higher than in persons with normal body mass, and it is by 50°'o higher in persons of 40-55 years old. The prolonged obesity provoke a number of functional changes in the vitally important organs and also the disturbance of metabolism in connection with deposition of large quantity of fat and increase of the loading on most of vitally important organs. First of all the metabolism in the adipose tissue is disturbed, where the speed of synthesis of triglycerides and lipoproteins is increased, ability to mobilization of the adipose reserves is disturbed, hyperlipemia, increase of free fatty acid level, hypercholesterinemia are observed. Disturbances in carbohydrate metabolism are manifested in limitation of glucose metabolism, increase of glycogen content in the liver. Utilization of glucose is impaired in the muscular tissue in spite of hyperinsulinism. Respiratory coefficient, equal to 0.7-0.74, is evidence mat fatty acids are used as a source of energy.

Deposition of fat in the myocardium decreases significantly the contractile function of the heart. Obesity is often accompanied by atherosclerosis, increase of the arterial pressure, blood coagulation, development of thrombosis. The pulmonary venlilation is deteriorated, vital capacity is decreased, predisposition to the congestion and development of chronic inflammation in the respiratory tracts appear. Dyspnoe arises even in small physical loading. The circulatory and respiratory hypoxias appear.

Combination of obesity with diabetes mellitus arises in the case of insulinoresistance connected with decrease of the number of receptors t| insulin on the surface of the adipose cells.

Compensatory hypertrophy and hyperplasia of the pancreatic islands providing the increased secretion of insulin (hyperinsulinism) for overcoming resistance, is followed by exhaustion. In this case it is supposed that obesity is etiological factor of diabetes mellitus.

^ 5.1. Content of the theme. The role fat in the organism. Name types of hyperlipoproteinemias due to HWO’s classification. Disturbances of lipide metabolism. Characterize atherosclerosis, the main risk factors and pathogenesis. Describe obesity. What is the role of genital, constitutional and environmental factors in their development? Distinguish between hypertrophic and hyperplastic obesity.

^ 5.2. Control questions of the theme:

  1. The role fat in the organism.

  2. Name types of hyperlipoproteinemias due to HWO’s classification.

  3. Disturbances of lipide metabolism

  4. Characterize atherosclerosis, the main risk factors and pathogenesis.

  5. Describe obesity. What is the role of genital, constitutional and environmental factors in their development?

  6. Distinguish between hypertrophic and hyperplastic obesity.


^ 5.3. Practice Examination.

1. Atherosclerosis raises the systolic blood pressure by:

A. Increasing arterial distensibility and vessel lumen radius or diameter.

B. Increasing arterial distensibility and decreasing vessel lumen radius or diameter.

C. Decreasing arterial distensibility and increasing vessel lumen radius or diameter.

D. Decreasing arterial distensibility and lumen radius or diameter.

E. None of the above is correct.

2. ^ Events in the development of atherosclerotic plaque include all of the following except:

A. Accumulation of LDL ( low-density lipoprotein ).

B. Smooth muscle proliferation.

C. Calcification.

D. Decreased elasticity.

E. Complement activation.

3. Which is «good cholesterol»?

A. Very low-density lipoproteins — VLDL.

B. High-density lipoproteins —HDL.

C. Low-density lipoproteins — LDL.

D. Intermediate density lipoproteins — IDL.

4. ^ What is true (T)/ false (F)?

A. Fatty acids from dietary lipids are reesterified in intestinal cells and exported as protein-containing chylomicrons.

B. Lipoprotein lipase from endothelial cells catalyzes the release of triglycerides from the chylomicrons.

C. The chylomicron remnants are taken up by the liver and these form the major source of cholesterol for the tissues.

D. HDL carry cholesterol from tissue to the liver for excretion in the bile.

E. LDL receptors in the liver take up VLDL, IDL and LDL, lowering circulating cholesterol.

5. ^ As we well know, obesity is associated with different syndromes except:

A. Atherosclerosis.

B. Myxedema.

C. Hyperthyroidism.

D. Cushing`s syndrome ( hyperfunction of adrenal cortex ).

E. Hypogonadism.

F. Non-insulin dependent diabetes ( NIDDM).

6. ^ What is true (T). What is false (F)?

A. Cholesterol is a product which is difficult to metabolize.

B. The subendothelium of the vessels is a bradytrophism of tissue.

C. Cholesterol is formed in the liver from fats, carbohydrates, proteins.

D. Cholesterol is a hydrophobic substance, its connection with protein (and with lipids) is necessary for the transformation into the hydrophilic state.

E. A lot of cholesterol is contained in B-lipoproteins (70–75 %).

F. B-lipoproteins are increased in the body of elderly persons.

G. Hypodynamia and hypoxia predispose to atherosclerosis because of the decreased oxydation of lipids and promote accumulation of cholesterol in subendothelium.

H. Hyperlipemia is associated with atherosclerosis and obesity.

L. Obesity may occur without atherosclerosis.

7. ^ Obesity may be connected with the following causes except.

A. Brain injury.

B. Encephalitis.

C. Meningitis.

D. Overeating.

E. Insulin insufficiency.

F. Hereditary predisposition.

8. Match the correct answer. What is hormone increasing (8a) lypolisis and what promotes (8b) lypogenesis.

A. Adrenalin, noradrenalin. B. STH. C. ACTH. D. TTH. E. Insulin. F.Prolactin.


Literature:

1. Gozhenko A.I., Makulkin R.F., Gurcalova I.P. at al. General and clinical pathophysiology/ Workbook for medical students and practitioners.-Odessa, 2001.

2. Gozhenko A.I., Gurcalova I.P. General and clinical pathophysiology/ Study guide for medical students and practitioners.-Odessa, 2003.

3. Robbins Pathologic basis of disease.-6th ed./Ramzi S.Cotnar, Vinay Kumar, Tucker Collins.-Philadelphia, London, Toronto, Montreal, Sydney, Tokyo.-1999.

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