Atherosclerosis. Hypertensive disease. Ischemic heart disease

Август 22, 2022

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Atherosclerosis. Hypertensive disease. Ischemic heart disease

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2. Atherosclerosis (athere – latin gruel) is a chronic disease which is characterized by formation of vascular
3. 1. Age (reducing of sex hormones synthesis and tissue regeneration, i.e. reducing of cholesterol consumption by
4. 1. Development of focal regions of chronic endothelial injury leading to increased vascular permeability and increased
5. 5. Adhesion of platelets to the focal areas of endothelial injury. 6. Release of biologically active
6. 8. Enhanced accumulation of lipids both within cells (macrophages and smooth muscle cells) and extracellularly. 9.
7. Aorta is usually the most involved vessel, the aortic lesions tend to be much more prominent
8. 1. Pre-lipid stage has no gross appearance; microscopically the changes in intima are equal to mucoid
9. 2. In lipidosis stage the accumulation of lipids in the intima leads to formation of fatty
10. Atherosclerosis of aorta, lipidosis stage. Fatty streaks
11. Lipoidosis stage
12. 3. In atheromatosis stage the characteristic plaques are formed. They appear as raised focal areas within
13. Atheromatosis stage
14. Atherosclerosis of aorta, three different degrees of damage
15. Atherosclerosis of coronary artery
16. АТЕРОСКЛЕРОЗ ВІНЦЕВИХ АРТЕРІЙ СЕРЦЯ
17. Atherosclerosis of basilar artery
18. Atheromatosis plague
19. Atherosclerosis of coronary artery, 40 magnification, H&E stain
20. 4. Stage of complications. Atherosclerotic complications may be acute and chronic. It is believed that prominent
21. aneurism
23. 1. Focal rupture or gross ulceration, or both, of the luminal surface of atheromatous plaques may
24. 3. Superimposed thrombosis usually occurs on disrupted lesions (those with rupture, ulceration, erosion, or hemorrhage). Thrombi
25. Dry gangrene of foot Necrosis in heart wall
26. Gangrene of intestine
27. Atherosclerotic nephrosclеrosis
28. Infarction of heart
29. Infarction of brain
30. 1. Atheromas in advanced disease undergo patchy or massive calcification. Arteries may become virtual pipe stems,
32. 3. Uncomplicated atherosclerotic lesions usually cause narrowing of vessel lumen leading to decreasing of blood circulation
33. Dystrophic calcification of aortic valve leaflets
34. Hypertensive disease is a chronic disease which is characterized by chronic elevation of blood pressure that
35. Primary (idiopathic, essential) hypertension (90-95%): benign; malignant (or accelerated). Secondary hypertension that may be caused by:
36. 1. Age. 2. Environmental factors (e.g. frequent stresses, increased salt intake, increased estrogen level). 3. Genetic
37. In hypertensive disease both increased cardiac output and increased peripheral resistance due to constriction of vessel
38. In this stage there are periodical elevations of blood pressure. Morphologically this stage is characterized by
39. In benign hypertensive diseases the prolonged periods of arterioles constriction lead to narrowing of vessels, decreased
40. Hyalinosis of spleen arterioles, medium magnification, H&E stain
41. The muscular-elastic arteries firstly show adaptive changes – thickening and reduplication of the intimal elastic lamina
42. In malignant hypertension rapid and sharp elevation of blood pressure is caused by extremely severe vasoconstriction
43. “Onion-skin” arteriolosclerosis in malignant hypertension, medium magnification, H&E stain
44. Fibrinoid necrosis of renal artery in malignant hypertension, medium magnification, H&E stain
45. “Onion-skin” arteriole, PAS-stain Fibrinoid necrosis of arteriole, PAS-stain
46. Acute complications: - infarction (myocardial, brain); - hemorrhages due to rupture of vessels affected with atherosclerosis).
48. Gross appearance: kidneys are smaller than normal and affected bilaterally. The cortical surface exhibits a fine
49. Benign nephrosclerosis
50. Gross appearance: size of the kidneys varies from small to enlarged, depending on the duration of
51. “Flea-bitten” kidney in malignant hypertension
52. Ischemic heart disease (IHD) is caused by decreasing of coronary blood flow due to atherosclerosis or
53. Transmural infarction
54. 18-24 hours ago
55. 3 – 4 days ago 1- 2 weeks ago Hemopericardium
59. Ischemic brain disease –cerebra-vascular disease
61. Скачать презентацию

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Atherosclerosis (athere – latin gruel) is a chronic disease which is

characterized by formation of vascular intimal lesions called atheromas or fibrofatty plaques in the elastic and muscular arteries with subsequent damage of organs and tissues due to reduced blood supply.

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1. Age (reducing of sex hormones synthesis and tissue regeneration, i.e.

reducing of cholesterol consumption by tissues).
2. Genetic predisposition to hypercholesterolemia.
3. Acquired metabolic disturbances with hyper-cholesterolemia (> 5,2 mmol/l): cholesterol-rich diet, hormonal misbalances, and diabetes mellitus.
4. Hypertension.
5. Smoking.
6. Obesity.
7. Herpesvirus, cytomegalovirus and Chlamydia pneumoniae infection.

Etiology (risk factors)

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1. Development of focal regions of chronic endothelial injury leading to

increased vascular permeability and increased leukocyte adhesion.
2. Insudation of lipoproteins into the vessel wall, mainly LDL and VLDL, and modification of such lipoproteins by oxidation.
3. Adhesion of blood monocytes to the endothelium, their migration into the intima and transformation into macrophages and foam cells.
4. Oxidative modification of lipid by free radicals generated in macrophages or endothelial cells. Oxidized LDL inhibits the motility of macrophages thus favoring the recruitment and retention of macrophages in plaques.

Pathogenesis (steps of development)

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5. Adhesion of platelets to the focal areas of endothelial injury.
6.

Release of biologically active substances that cause migration of smooth muscle cells from media into the intima.
7. Proliferation of immigrant smooth muscle cells in the intima, they gain secretory phenotype and synthesize extracellular matrix, leading to accumu-lation of collagen and proteoglycans in the plaque. Connective tissue is particularly prominent on the intimal aspect, where it produces fibrous cap.

Pathogenesis (steps of development)

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8. Enhanced accumulation of lipids both within cells (macrophages and smooth

muscle cells) and extracellularly.
9. Necrosis of some foam cells with accumulation of extracellular lipids and cellular debris.
10. Mature fibrofatty plaque is composed of central core containing extracellular lipids and lipid-laden cells surrounded by connective tissue. Plaques often undergo disruption with superimposed thrombus.

Pathogenesis (steps of development)

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Aorta is usually the most involved vessel, the aortic lesions tend

to be much more prominent around the ostia of its major branches.
In descending order the most heavily involved vessels are:
thoracic aorta; coronary arteries; popliteal arteries; thoracic aorta; internal carotid arteries; vessels of the circle of Willis.

Localization

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1. Pre-lipid stage has no gross appearance; microscopically the changes in

intima are equal to mucoid swelling.

Morphological stages

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2. In lipidosis stage the accumulation of lipids in the intima

leads to formation of fatty dots and fatty streaks. Fatty dots are usually less than 1 mm in diameter, fatty streaks are 1 cm along. They are yellow and flat, not elevated over intima surface. Microscopically fatty streaks are composed of fat-filled foam cells with lymphocytes and extracellular lipid present in smaller amount than in plaques.
This stage is reversible.

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Atherosclerosis of aorta, lipidosis stage. Fatty streaks

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Lipoidosis stage

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3. In atheromatosis stage the characteristic plaques are formed. They

appear as raised focal areas within intima, having a core of lipid and a covering fibrous cap. They are white or whitish yellow and protrude into vessel lumen. They vary in size from 0.3 to 1.5 cm in diameter but sometimes coalesce to form larger masses.
On section, the superficial portion of these lesions at the luminal surface tends to be firm and white (fibrous cap) and the deep portions yellow or whitish yellow and soft (atheromatous gruel).

Morphological stages

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Atheromatosis stage

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Atherosclerosis of aorta, three different degrees of damage

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Atherosclerosis of coronary artery

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АТЕРОСКЛЕРОЗ ВІНЦЕВИХ АРТЕРІЙ СЕРЦЯ

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Atherosclerosis of basilar artery

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Atheromatosis plague

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Atherosclerosis of coronary artery, 40 magnification, H&E stain

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4. Stage of complications.
Atherosclerotic complications may be acute and chronic.

It is believed that prominent dyslipidemia favor excessive accumulation of lipids in the plaque causing arising of acute complication, subtle dyslipidemia favor minor accumulation of lidips and prominent collagen and extracellular matrix accumulation in the plaque causing narrowing of the vessel lumen thus leading to chronic complications.

Morphological stages

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aneurism

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1. Focal rupture or gross ulceration, or both, of the luminal

surface of atheromatous plaques may result in exposure of highly thrombogenic substances that induce thrombus formation or discharge of debris into the bloodstream, producing microemboli (cholesterol emboli or atheroemboli).
2. Hemorrhage into a plaque may occur, especially in the coronary arteries. The source of blood is ruptured vessels of overlying fibrous cap or the thin-walled capillaries that vascularize the plaque. An enlarging hematoma may induce plaque rupture.

Acute complications

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3. Superimposed thrombosis usually occurs on disrupted lesions (those with rupture,

ulceration, erosion, or hemorrhage). Thrombi may partially or completely occlude the lumen; they may become incorporated within the intimal plaque by organization.
Complete thrombosis of vessel can cause infarction of heart, brain, kidney and other organs, gangrene of limbs and intestine. Myocardial infarction and stroke are the most common causes of death in patients with advanced atherosclerosis.
4. Complicated atherosclerotic lesions may lead to rupture of affected vessel.

Acute complications

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Dry gangrene of foot
Necrosis in heart wall

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Gangrene of intestine

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Atherosclerotic nephrosclеrosis

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Infarction of heart

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Infarction of brain

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1. Atheromas in advanced disease undergo patchy or massive calcification. Arteries

may become virtual pipe stems, and the aorta may assume an eggshell brittleness.
2. Although atherosclerosis is initially an intimal disease, in severe cases, particularly in large vessels, the underlying media may undergo considerable atrophy with loss of elastic tissue, causing sufficient weakness to permit aneurysmal dilation.

Chronic complications

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3. Uncomplicated atherosclerotic lesions usually cause narrowing of vessel lumen

leading to decreasing of blood circulation in organs and tissues. Chronic ischemia leads to parenchymal atrophy and stromal sclerosis. Examples:
cardiosclerosis,
nephrosclerosis,
cerebral sclerosis (appearing as senile dotage)
muscle atrophy,
intermittent lameness,
atrophy of intestinal mucosa (appearing as malabsorption syndrome).
4. Deposition of atheromatous masses in heart valves can cause valve dysfunction.

Chronic complications

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Dystrophic calcification of aortic valve leaflets

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Hypertensive disease is a chronic disease which is characterized by chronic

elevation of blood pressure that affects both the function and the structure of blood vessels, predominantly small muscular arteries and arterioles.

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Primary (idiopathic, essential) hypertension (90-95%):
benign;
malignant (or accelerated).
Secondary hypertension that may be

caused by:
- renal diseases;
- narrowing of the renal artery (due to hypoplasia, fibro-muscular dysplasia, or atheromatous plaque);
- hyperproduction of glucocorticoids, adrenaline, thyroxin, and other hormones.

Classification

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1. Age.
2. Environmental factors (e.g. frequent stresses, increased salt intake, increased

estrogen level).
3. Genetic predisposition (deregulation in genes which are responsible for increased renal sodium reabsorption, blood level of pressor substances such as angiotensin II, reactivity of vascular smooth muscle to pressor agents etc).

Etiology (risk factors)

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In hypertensive disease both increased cardiac output and increased peripheral resistance

due to constriction of vessel muscle cells contribute to the increased pressure.
There are 3 clinical-morphological stages:
- functional;
- prominent morphological changes in vessels;
- secondary changes in internal organs.

Pathogenesis

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In this stage there are periodical elevations of blood pressure. Morphologically

this stage is characterized by arising of adaptive processes: hypertrophy of vessel smooth muscle cells in arterioles due to prolonged periods of contraction. Rarely the reversible dystrophic changes in the vessel walls occur. At this stage the initial features of myocardial hypertrophy are evident. In malignant hypertension this stage is usually omitted.

Functional stage

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In benign hypertensive diseases the prolonged periods of arterioles constriction lead

to narrowing of vessels, decreased blood flow and hypoxia. Hypoxia leads to dystrophic changes similar to mucoid swelling. Increased vascular permeability leads to leakage of blood proteins into vessel wall (plasmatic impregnation) which eventually progresses to hyalinosis. Such vessels are unable to dilate, so these changes lead to constant elevation of blood pressure.

Prominent morphological changes in vessels

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Hyalinosis of spleen arterioles, medium magnification, H&E stain

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The muscular-elastic arteries firstly show adaptive changes – thickening and reduplication

of the intimal elastic lamina - elastosis. As time passes the progressive increase of connective tissue in intima occurs - fibroelastosis. At final stage elastic fibers disappears leaving prominent intimal sclerosis - intimal fibrosis. Such changes lead to sharpening of diastolic and systolic changes of blood pressure.

Prominent morphological changes in vessels

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In malignant hypertension rapid and sharp elevation of blood pressure is

caused by extremely severe vasoconstriction of small muscular arteries leading to severe hypoxia.
The fibrinoid necrosis of small muscular arteries is the most prominent feature of malignant hypertensive disease. The period of acute injury is rapidly followed by smooth muscle proliferation and a striking concentric increase in the number of layers of smooth muscle cells, which yields the so-called onion-skin appearance.

Prominent morphological changes in vessels

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“Onion-skin” arteriolosclerosis in malignant hypertension, medium magnification, H&E stain

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Fibrinoid necrosis of renal artery in malignant hypertension, medium magnification, H&E

stain

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“Onion-skin” arteriole, PAS-stain
Fibrinoid necrosis of arteriole, PAS-stain

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Acute complications:
- infarction (myocardial, brain);
- hemorrhages due to rupture of vessels

affected with atherosclerosis).
Chronic complication:
parenchymal atrophy and interstitial sclerosis in most organs. The most prominent changes are seen in kidneys.

Secondary changes in internal organs

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Gross appearance: kidneys are smaller than normal and affected bilaterally. The

cortical surface exhibits a fine granularity, but coarse scars are also encountered. On cut section, the cortex is thinned – primary reduced kidney.
Microscopic appearance: many glomeruli appear normal, whereas others show varying degrees of ischemic change. Initially, the glomerular capillaries are thickened and shriveled. Cells of the glomerular tuft are progressively lost. Collagen and matrix material are deposited within Bowman's space opposite the hilus. Eventually, the glomerular tuft is obliterated by a dense, eosinophilic globular mass inclosed in a scar, all within Bowman's capsule. Tubular atrophy is associated with fibrosis of the related interstitium.

Kidney changes in benign hypertensive disease

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Benign nephrosclerosis

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Gross appearance: size of the kidneys varies from small to enlarged,

depending on the duration of preexisting benign hypertension. The cortical surface characteristically displays petechiae, accounting for the name "flea-bitten" kidney. The cut surface is mottled red and yellow and occasionally exhibits small cortical infarcts.
Microscopic appearance: in addition to changes seen in benign HD the glomeruli frequently show fibrinoid necrosis, sometimes in continuity with the same process in the afferent arterioles. Subtotal infarction of glomeruli, with dilated capillaries stuffed with erythrocytes, is common. Usually fewer than half of the glomeruli show acute, necrotizing, inflammatory lesions.

Kidney changes in malignant hypertensive disease

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“Flea-bitten” kidney in malignant hypertension

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Ischemic heart disease (IHD) is caused by decreasing of coronary blood

flow due to atherosclerosis or hypertensive disease.
Classification:
Acute IDH:
1. Angina pectoris.
2. Myocardial infarction.
Chronic IHD:
1. Diffuse tiny-focal cardiosclerosis;
2. Massive post-infarction cardiosclerosis.

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