THE DISEASES OF CARDIOVASCULAR SYSTEM AND RHEUMATIC DISEASES

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THE DISEASES OF CARDIOVASCULAR SYSTEM AND
RHEUMATIC DISEASES
Federal State Budgetary Educational Institution
of Higher Education Perm State Medical
University named after academician E.A. Wagner
of Ministry of Healthcare of Russian Federation
DR.SOURAV DAS, PERM STATE MEDICAL UNIVERSITY,
RUSSIA
Perm, 2017
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CARDIOVASCULAR DISEASES
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ATHEROSCLEROSIS
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DEFINITION

• chronic disease resulting from disruption of
  lipid and protein metabolism, characterized by
  damage to the arteries of the elastic and
  muscular-elastic type in the form of focal
  sedimentation in the inner membrane of lipids and
  proteins and the reactive proliferation of
  connective tissue.

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ETHIOLOGY

• Polyethological disease associated with the
  influence of various exogenous and endogenous
  factors
• - Heredity
• - Environment
• - Food

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RISK FACTORS

• Age
• Sex (male up to 70)
• Heredity
• Hyperlipidemia (hypercholesterolemia)
• Arterial hypertension
• Smoking
• Diabetes mellitus

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HYPOTHESES

• Thrombogenic
• Immune
• Clonal
• Viral
• Reaction to damage
• Lipoprotein
• Neuro-metabolic

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PATHOGENESIS

• In most cases, the development of atherosclerosis
  is preceded by atherogenic dyslipoproteinemia -
  modified lipoprotein s- capture by endothelial
  cells - transferr to the subendothelial space.
• Damage of the endothelium - induction of plasma
  components, including lipoproteins, into the
  inner shell of the vessels.
• The damaged endothelium expresses adhesive
  molecules - adherence (adhesion) of platelets and
  monocytes.

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PATHOGENESIS

• Muscular cells - proliferate, synthesize
  collagen, elastic fibers, protheoglycans - the
  basis of an atherosclerotic plaque.
• Lipoproteins form complexes with proteoglycans
  capture by macrophages - xantom cells.
• Subsequent changes in the plaque capillaries,
  necrosis of central departments, sclerosis,
  hyalinosis, calcification.

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PATHOLOGY PROCESS

• The main morphological expression of
  atherosclerosis is a plaque, the essence of which
  well reflects the name of the disease
• in the center - lipid-protein detritus -
  (athere),
• around - proliferation of connective tissue -
  sclerosis.
• Usually, the arteries of the elastic (aorta) and
  the musculo-elastic type (large organ arteries)
  are affected, and small arteries of the muscular
  type are much less involved in the process.

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ATHEROGENESIS

• Macro
• grease stains and striae
• fibrous plaques
• complicated lesions, represented by fibrous
  plaques with ulceration, hemorrhages and
  overlapping of thrombotic masses
• calcification or atherocalcinosis

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GREASE STAINS AND STRIAE

• areas of yellow or yellow-gray color (spots),
  which sometimes merge and form strips, but do not
  rise above the surface of the inner shell of the
  vessel.
• They contain lipids, revealed by the total
  coloration of the vessel with dyes for fat, for
  example Sudan.
• Earlier fat spots and streaks appear in the aorta
  on the back wall and at the point of divergence
  of its branches, later in the large arteries.

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FIBROUS PLAQUES

• dense oval or rounded, white or yellow-white
  formations, containing lipids and towering above
  the surface of the inner shell of the vessel.
• They often merge together, give the inner surface
  a tuberous appearance and lead to a narrowing of
  the lumen of the vessel (stenotic
  atherosclerosis).
• The most common plaques are located in the
  abdominal aorta, in the arteries of the heart,
  brain, kidneys, lower extremities, carotid
  arteries, etc.
• Most often affected are those areas of the
  vessels that experience hemodynamic (mechanical)
  effects - in the branching and bending of the
  arteries, on their side wall, which has a rigid
  bedding.

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COMPLICATED LESIONS

• Progression of atheromatous changes leads to the
  destruction of plaque carcinomas, ulcerations
  (atheromatous ulcer), hemorrhages in the
  thickness of the plaque (intramural hematoma) and
  the formation of thrombotic overlays at the site
  of ulceration of the plaque.
• Acute clotting of artery and the development of
  an infarction, embolism with both thrombotic and
  atheromatous masses, the formation of an aneurysm
  of the vessel at the site of its ulceration, as
  well as arterial bleeding when the atheromatous
  ulcer is corroded.

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ATHEROCALCINOSIS

• the final phase of atherosclerosis, which is
  characterized by the deposition of calcium salts
  in fibrous plaques, i.e. their calcification.
• Plaques acquire a stony density (petrification of
  plaques), the wall of the vessel at the place of
  petrification is sharply deformed.

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IMPORTANT

• Different types of atherosclerotic changes are
  often combined in the same vessel, for example,
  in the aorta, one can see simultaneously fatty
  spots and bands, fibrous plaques, atheromatous
  ulcers with thrombi and atherocatalcinosis, which
  indicates a wavy course of atherosclerosis.

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ATHEROGENESIS

• Micro
• before lipidosis
• lipoidosis
• liposclerosis
• atheromatosis
• ulceration
• atherocalcinosis

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BEFORE LIPIDOSIS

• increased permeability and damage to the inner
  shell of the vessel. Lipid droplets appear in
  endothelial cells, sometimes occupying up to 50
  of the cytoplasm.
• Characterized by edema of endothelial cells, the
  disappearance of glycocalyx, damage to the
  cytomelemma, the disclosure of interendothelial
  contacts, the appearance in the subendothelial
  layer of droplets of fat, plasma proteins,
  fibrinogen (fibrin).

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LIPOIDOSIS

• focal infiltration of the inner shell of the
  vessel, especially its surface areas, lipids
  (cholesterol), lipoproteins, proteins, which
  leads to the formation of fat spots and bands.
• Lipids diffusely impregnate the inner membrane
  and accumulate in the muscular cells and
  macrophages, which turn into xantom cells.
  Expressed swelling and destruction of elastic
  membranes.

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LIPOSCLEROSIS

• proliferation of connective tissue elements of
  the inner shell of vessels in the areas of
  deposition and decomposition of lipids and
  proteins, what leads to the formation of fibrous
  plaque.
• At the edges of the plaque, a new formation of
  thin-walled vessels takes place, which also
  become an additional source of lipoprotein and
  plasma protein intake.

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ATHEROMATOSIS

• the lipid masses that make up the central part of
  the plaque, as well as the adjacent collagen and
  elastic fibers, decay. At the same time, an
  amorphous mass is formed in which cholesterol
  crystals are detected (atheromatous detritus).
• Atheromatous masses are delimited from the lumen
  of the vessel by a layer of mature, sometimes
  hyalineized connective tissue (plaque cover).
• The muscular membrane often atrophies, sometimes
  undergoes atheromatous decay, as a result of
  which the plaque reaches in some cases the outer
  shell of the vessels.

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ULCERATION

• With the progression of atheromatosis, in
  connection with the destruction of newly formed
  vessels, a hemorrhage into the thickness of the
  plaque (intramural genome) occurs.
• In case of destruction of the plaque cover, an
  atheromatous ulcer is formed.
• The defect of the inner shell of the vessel is
  often covered by thrombotic masses.

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ATHEROCALCINOSIS

• the final stage of morphogenesis of
  atherosclerosis, although lime deposition begins
  already in the stage of atheromatosis and even
  liposclerosis.

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CLINICOPATHOLOGIC TYPES

• atherosclerosis of the aorta
• atherosclerosis of the coronary arteries of the
  heart (cardiac form, cardiac ischemia)
• atherosclerosis of the cerebral arteries (brain
  form of fibrovascular disease)
• atherosclerosis of renal arteries (renal form)
• atherosclerosis of the intestinal arteries
  (intestinal form)
• atherosclerosis of arteries of lower extremities

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WHAT HAPPENS

• Slow narrowing of the feeding artery by an
  atherosclerotic plaque leads to chronic
  insufficiency of blood supply and ischemic
  changes - dystrophy and atrophy of the
  parenchyma, diffuse or fine-sclerotic sclerosis
  of the stroma.
• Acute occlusion of the feeding artery, usually
  due to complicated lesions (plaque hemorrhage,
  thrombosis), leads to acute blood supply
  insufficiency and development of necrosis -
  infarction, gangrene.
• In addition, in some cases, deep atheromatous
  ulcers can lead to the development of an
  aneurysm, i.e. the bulging of the artery wall in
  the lesion site followed by a rupture and a
  hemorrhage.

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ATHEROSCLEROSIS OF THE AORTA

• It is more sharply expressed in the abdominal
  part and is characterized by usually complicated
  lesions and calcification. In this regard, most
  often accompanied by thrombosis, thromboembolism
  and embolism atheromatous masses with the
  development of infarcts and gangrene (intestines,
  lower limbs).
• Often an aortic aneurysm develops, which can be
  cylindrical, saccular or herniated. The wall of
  an aneurysm in some cases forms aorta (true
  aneurysm), in others - adjacent organs and
  hematoma (false aneurysm).

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ATHEROSCLEROSIS OF THE CORONARY ARTERIES OF THE
HEART

• lies at the heart of coronary heart disease, the
  morphological expression of which is focal
  ischemic dystrophy, myocardial infarction,
  large-focal (post-infarction) and diffuse
  small-focal cardiosclerosis.

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ATHEROSCLEROSIS OF THE CEREBRAL ARTERIES

• is the basis of cerebrovascular diseases, the
  most characteristic manifestations of which are
  ischemic and hemorrhagic cerebral infarction
  (stroke).
• Prolonged ischemia of the cerebral cortex due to
  stenosing atherosclerosis leads to atrophy of the
  cerebral cortex, the development of
  atherosclerotic dementia.

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ATHEROSCLEROSIS OF RENAL ARTERIES

• or wedge-shaped areas of atrophy of the
  parenchyma with collapse and sclerosis of the
  stroma, or develop heart attacks followed by the
  formation of retracted scars.
• As a result of ischemia of the kidney tissue with
  steno-scintillating atherosclerosis, symptomatic
  (renal) hypertension occurs.

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ATHEROSCLEROSIS OF THE INTESTINAL ARTERIES

• Atherosclerosis of the intestinal arteries,
  complicated by thrombosis, leads to gangrene of
  the gut.
• Stenosing atherosclerosis of the mesenteric
  arteries can lead to the development of ischemic
  colitis, in which the splenic angle and the
  rectosigmoid parts of the colon are more often
  affected.

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ATHEROSCLEROSIS OF ARTERIES OF LOWER EXTREMITIES

• Atherosclerosis of arteries of the extremities
  femoral arteries are more often affected.
• Stenosing atherosclerosis in the absence of
  collateral circulation leads to muscle atrophy
  and a characteristic symptom of intermittent
  claudication (pain that occurs in the legs when
  walking).
• If atherosclerosis is complicated by thrombosis,
  then atherosclerotic gangrene develops.

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HYPERTENSIVE DISEASE
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DEFINITION

• According to the WHO, it is a persistent increase
  in blood pressure systolic above 140 and
  diastolic - above 90 mm Hg.

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THE DEGREE OF INCREASE IN BLOOD PRESSURE AND
CLINICAL COURSE

• benign hypertension, characterized by a slow
  development and a moderate increase in blood
  pressure (the level of diastolic pressure does
  not exceed 110-120 mm Hg).
• malignant hypertension, which is characterized by
  a significant increase in blood pressure (the
  level of diastolic pressure exceeds 110-120 mm
  Hg) and a rapidly progressive course leading to
  death in 1-2 years - occurs initially or as a
  complication of benign hypertension.

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CLASSIFICATION

• Primary essential - chronic disease, the main
  clinical manifestation of which is a prolonged
  and persistent increase in blood pressure
  (hypertension)
• Secondary symptomatic

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SECONDARY

• Renal hypertension associated with kidney disease
  (nephrogenic hypertension) or renal vessels
  (renovascular hypertension).
• Endocrine Hypertension
• in case of excess of glucocorticoids - illness or
  syndrome of Itsenko-Cushing
• with an excess of catecholamines -
  pheochromocytoma
• with renin-producing kidney tumors.

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SECONDARY

• Neurogenic hypertension
• increased intracranial pressure (trauma,
  opaquehol, abscess, hemorrhage)
• b) with damage to the hypothalamus and brainstem
• c) associated with psychogenic factors.
• Other hypertension due to coarctation of the
  aorta and other anomalies of blood vessels,
  increase in volume circulate blood transfusion
  with excessive transfusion, polycythemia, etc.

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RISK FACTORS

• The greatest importance in the development of
  hypertension are given to the chronic
  psychological and emotional overstrain (frequent
  stresses, conflict situations, etc.) and
  excessive consumption of table salt.

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PATHOLOGY

• Malignant hypertension often occurs after a
  period of benign course, the average duration of
  which is about 10 years. Less often malignant
  course is observed from the very beginning.
• More often malignant course is observed in men
  aged 35-50 years, sometimes up to 30 years.
• The most characteristic sign of malignant
  hypertension is arteriolar necrosis.

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PATHOLOGY

• In benign hypertension, taking into account the
  duration of the development of the disease, three
  stages are distinguished
• 1) preclinical
• 2) common changes in the arteries
• 3) changes in organs due to changes in arteries
  and violation of intraorganic circulation.
• These stages are in good agreement with the
  stages of "benign" hypertension, proposed by WHO
  experts Stage I - mild course, II stage -
  moderate severity and stage III - hypertensive
  disease with severe course.

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PRECLINICAL STAGE

• Characterized by episodes of a temporary increase
  in blood pressure (transient hypertension).
• At this stage, hypertrophy of the muscular layer
  and the elastic structures of the arterioles and
  their small branches, the morphological signs of
  arteriolar spasm or their deeper changes in cases
  of hypertensive crisis are found.
• There is moderate compensatory hypertrophy of the
  left ventricle of the heart.

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STAGE OF COMMON CHANGES IN THE ARTERIES

• Characterizes the period of persistent increase
  in blood pressure, the degree of myocardial
  hypertrophy increases, the heart mass can reach
  900-1000 g, and the thickness of the wall of the
  left ventricle - 2-3 cm (cor bovinum - bovine
  heart).
• Changes in the arteries of the elastic,
  muscular-elastic and muscular types are
  represented by elastofibrosis and
  atherosclerosis.
• Plasmatic impregnation and its outcome -
  hyalinosis, or arteriolosclerosis - develop in
  connection with hypoxic injuries, which leads to
  vasospasms.
• Similar changes appear in small arteries of the
  muscular type. Most often, arteriologinosis is
  noted in the kidneys, brain, pancreas, intestine,
  retina, capsule of the adrenal glands.

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STAGE OF CHANGES IN ORGANS

• Secondary changes in organs due to changes in
  arteries and violation of intraorganic
  circulation.
• Secondary organ changes can develop slowly
  against the background of arterioles of o- and
  atherosclerotic occlusion of vessels, leading to
  atrophy of the parenchyma and sclerosis of the
  stroma.
• In case of thrombosis, spasm, fibrinoid necrosis
  (more often during a crisis) acute changes occur
  - hemorrhages, infarcts.
• Hyalinosis and fibrinoid necrosis with the
  development of microaneurysms are especially
  often found in the vessels of the brain, leading
  to intracerebral hemorrhages.

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STAGE OF CHANGES IN ORGANS

• Changes in the kidneys with chronic benign
  hypertension are caused by arteriolar hyalinosis
  (arteriolosclerosis), which is accompanied by
  collapse of capillary loops and glomerulus
  sclerosis (glomeruloskelethrosis), canal atrophy,
  compensatory hypertrophy of the remaining
  nephrons, which give the kidney surface a
  granular appearance.
• The kidneys in this case decrease, become dense,
  the cortical substance becomes thinner. Such
  kidneys, which are the outcome of their sclerosis
  against the background of arteriolar hyalinosis
  (arti-rilosclerotic nephrosclerosis), are called
  primary-wrinkled.
• Arteriolosclerotic nephrosclerosis can lead to
  the development of chronic renal failure.

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CLINICOPATHOLOGIC TYPES

• The cardiac form of hypertensive disease, like
  the cardiac form of atherosclerosis, is the
  essence of ischemic heart disease.
• The cerebral form of hypertensive disease (like
  atherosclerosis of the brain vessels) underlies
  most cerebrovascular diseases.
• The renal form of hypertension is characterized
  by both acute and chronic changes.

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PROGNOSIS AND DEATH

• The mortality rate of men over 40 years with
  blood pressure 150/100 mmHg. exceeds the average
  death rate by 125, women by 85.
• Most people with benign form of hypertension die
  from heart failure, myocardial infarction,
  cerebral stroke (ischemic or hemorrhagic), or
  intercurrent diseases.
• Approximately 5 of hypertensive patients develop
  malignant hypertension and they die from renal
  failure.

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CARDIAC ISCHEMIA
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CARDIAC ISCHEMIA

• group of diseases caused by absolute or relative
  deficiency of coronary circulation. In the vast
  majority of cases, coronary heart disease (CHD)
  develops with atherosclerosis of the coronary
  arteries, so there is a synonym for the name -
  coronary disease.

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RISK FACTORS

• The most important risk factors of the first
  order are hyperlipidemia, tobacco smoking,
  arterial hypertension, decreased physical
  activity, obesity, nutritional factor
  (cholesterol diet), stress, decreased glucose
  tolerance, male sex, alcohol consumption.
• Among the risk factors of the second order - the
  violation of the content of trace elements
  (zinc), increased water hardness, increased
  levels of calcium and fibrinogen in the blood,
  hyperuric acid,mia and others.

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DIRECT REASONS

• Immediate causes of ischemic myocardial damage in
  CHD include thrombosis of coronary arteries,
  bohemia thrombosis, prolonged spasm, functional
  myocardial overstrain under conditions of
  stenosing arteriosclerosis of coronary arteries
  and insufficient collateral circulation.

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ISCHEMIA

• Reversible ischemic lesions develop in the first
  20-30 minutes of ischemia and in the event of
  termination of the effect of the factor causing
  them, completely disappear. Morphological changes
  are found mainly in electron microscopy - the
  swelling of mitochondria, deformation of their
  cristae, relaxation of myofibrils.

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MYOCARDIAL INFARCT

• Irreversible ischemic damage to cardiomyocytes
  begins after ischemia lasting more than 20-30
  minutes.
• After 18-24 h of ischemia, a necrosis zone is
  formed, visible micro- and macroscopically, i.e.
  a myocardial infarct is formed.

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MYOCARDIAL INFARCT

• Types of necrosis
• coagulation - necrotic masses are removed by
  phagocytosis by macrophages
• coagulation with subsequent myocytolysis -
  necrosis is located in the peripheral parts of
  the infarct and is caused by the action of
  ischemia and reperfusion
• myocytolysis - colliquated necrosis necrotic
  masses are eliminated by lysis and phagocytosis

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MYOCARDIAL INFARCTION

• The form of acute ischemic heart disease,
  characterized by the development of ischemic
  necrosis of the myocardium. It develops 18 hours
  after the onset of ischemia, when the necrosis
  zone becomes visible micro- and macroscopically.
• Macroscopically the infarct of the wrong form,
  white with a hemorrhagic aureole.
• Microscopically determined zone of necrosis,
  surrounded by a zone of demarcation inflammation,
  separating the first from the preserved tissue of
  the myocardium. In the necrosis zone, coagulation
  necrosis in the center, coagulation myocytolysis
  and colliquated necrosis along the periphery are
  determined.
• The zone of demarcation inflammation in the first
  days of the infarction is represented by the
  leukocyte shaft and full blood vessels with
  diapedesis, and from the 7th to the 10th day - a
  young connective tissue gradually replacing the
  necrosis and ripening zone. Scarring of the
  infarction occurs by the 6th week.
• During the infarct, two stages are distinguished
  necrosis and scarring

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CLASSIFICATION OF MYOCARDIAL INFARCTION

1. By time of occurrence
2. Primary (first emerged)
3. Recurrent (developing within 6 weeks after the
   previous one)
4. Repeated (developed more than 6 weeks after the
   previous one
5. By localization
6. The anterior wall of the left ventricle and the
   anterior parts of the interventricular septum
7. Posterior wall of left ventricle
8. The lateral wall of the left ventricleInterventric
   ular septum
9. Extensive heart attack
10. In the prevalence
11. Subendocardial
12. Intramural
13. Subendocardial
14. Transmural

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COMPLICATIONS

• cardiogenic shock, ventricular fibrillation,
  asystole, acute heart failure, myomation and
  heart rupture, acute aneurysm, parietal
  thrombosis with thromboembolic complications,
  pericarditis.
• Mortality with myocardial infarction is 35 and
  develops most often in the early, preclinical
  period of the disease from lethal arrhythmias,
  cardiogenic shock and acute heart failure. In a
  later period - from thromboembolism and heart
  rupture, often in the area of acute aneurysm with
  a tamponade of the pericardial cavity.

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LARGE-FOCAL (POST-INFARCTION) CARDIOSCLEROSIS

• develops in the outcome of the transferred
  infarct and is represented by a fibrous tissue.
• The stored myocardium undergoes regenerative
  hypertrophy. In the event that large-scale
  cardiosclerosis occurs after transmural
  myocardial infarction, a complication can occur-a
  chronic aneurysm of the heart.
• Death comes from chronic heart failure or
  thromboembolic complications.

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DIFFUSE SMALL-FOCAL CARDIOSCLEROSIS

• As a form of chronic ischemic heart disease,
  diffuse small-focal cardiosclerosis develops as a
  result of relative coronary insufficiency with
  the development of small foci of ischemia.
• It can be accompanied by atrophy and
  lipofuscinosis of cardiomyocytes.

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RHEUMATIC DISEASES
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DEFINITION

• are a group of diseases characterized by
  affection of connective tissue due to a violation
  of the body's immune homeostasis (connective
  tissue disease with immune disorders).

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WHO ARE IN GROUP

• rheumatism, rheumatoid arthritis
• systemic lupus erythematosus
• Bekhterev's disease (Strumpell-Miarie disease)
• systemic scleroderma
• nodular periarteritis
• dematomyositis

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PATHOGENIC MECHANISM

• The focus of chronic infection causes tension and
  perversion of the immune reaction of the body,
  resulting in autoimmunization, toxic immune
  complexes and immunocompetent cells that damage
  the micro-circulatory channel of certain organs
  or tissues.

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COMMON SIGNS

• presence of chronic focal infection
• pronounced impairment of immunological
  homeostasis
• generalized vasculitis
• chronic undulating course
• systemic progressive disorganization of the
  connective tissue

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PRESENCE OF CHRONIC FOCAL INFECTION

• It is known that B-hemolytic streptococcus group
  A is the cause of rheumatism.
• Autoantogens antigens form the same immune
  complexes with autoantibodies, damaging various
  tissues and walls of blood vessels.

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GENERALIZED VASCULITIS

• The immediate-type hypersensitivity reaction is
  realized in the microcirculatory bed (capillary,
  venule, arteriola). As a result, destruction
  (fibrinoid necrosis), plasmorrhagia, thrombosis,
  endothelial proliferation and perithelium occur.
• Morphologically, destructive-proliferative
  thrombovasculitis is identified, which can be
  endo-, meso-, peri-, and panvasculitis. The
  delayed-type hypersensitivity reaction is
  represented in this case by the proliferative
  component.

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SYSTEMIC PROGRESSIVE DISORGANIZATION OF THE
CONNECTIVE TISSUE

• is composed of 4 phases
• - mucoid swelling
• fibrinoid changes (manifestation of an immediate
  hypersensitivity reaction)
• inflammatory cell reactions (expression of
  hypersensitivity reaction of immediate and
  delayed types)
• - sclerosis

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RHEUMATISM
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DEFINITION

• an infectious-allergic disease with a predominant
  lesion of the heart and vessels, undulating
  course, periods of exacerbation and fading.

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ETHIOLOGY

• The causative agent is (i-hemolytic group A
  streptococcus, which causes sensitization of the
  body (repeated angina).
• Genic factors and age are of great importance in
  the onset of the disease.

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CLINICOPATHOLOGIC TYPES

• cardiovascular
• polyarthritis
• nodosa
• cerebral

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CARDIOVASCULAR TYPE

• most frequent, occurs in both adults and
  children.
• Endocarditis is the main manifestation of this
  form of rheumatism.
• Localization distinguishes valvular, chordal,
  parietal endocarditis.
• The most pronounced changes usually develop in
  the valves of the left atrioventricular (mitral)
  and aortic valves.
• There are 4 types of rheumatic valvular
  endocarditis diffuse (or valvulitis), acute
  warty, fibroplastic, recurrently warty.

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ENDOCARDITIS

• Diffuse endocarditis - mucoid swelling, swelling
  of the connective tissue base of the valve, and
  the fullness of the capillaries. Endothelium is
  not affected, thrombotic overlap is absent.
• Acute warty endocarditis - mucoid swelling,
  fibrinoid necrosis of the connective tissue and
  endothelium of the valves. The edges of the
  valves suffer particularly badly. As a result of
  the destruction of the endothelium, conditions
  are created for the formation of thrombi, which
  are located at the edge of the valve and are
  represented mainly by fibrin (white thrombus).
  Thrombotic overlays on the valves are called
  warts.

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ENDOCARDITIS

• Fibroplastic endocarditis develops as a
  consequence of the two previous forms of
  endocarditis and is characterized by a
  predominance of sclerosis and scarring.
• Recurrent-warty endocarditis - disorganization of
  connective tissue in sclerotized valves -
  endothelial necrosis and the formation of warts
  on valves (thrombotic overlap of various sizes).
  In the outcome - sclerosis, hyalinosis of the
  valves.

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MYOCARDITIS

• one of the frequent manifestations of rheumatism.
  
• There are 3 forms of myocarditis nodular
  (granulomatous), diffuse interstitial
  (interstitial) exudative, focal interstitial
  (interstitial) exudative.
• Nodular myocarditis - granulomas in the
  perivascular connective tissue of various parts
  of the heart. Granulomas might be in various
  phases of development "blossoming," "fading,"
  "scarring." In myocytes, protein or fatty
  degeneration is noted to varying degrees. Nodular
  myocarditis is terminated by diffuse small-focal
  cardiosclerosis.

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MYOCARDITIS

• Diffuse interstitial exudative myocarditis
  (mainly in children) - infiltration of stroma
  with lymphocytes, histiocytes, neutrophilic and
  eosinophilic leukocytes. Vessels full-blooded,
  pronounced edema of the stroma. The myocardium
  loses its tone, becomes flabby, the heart
  cavities expand, so the clinical manifestation of
  this myocarditis is always severe cardiovascular
  failure. In the outcome in the myocardium
  develops diffuse cardiosclerosis.
• Focal interstitial exudative myocarditis has the
  same morphological manifestations as diffuse,
  only the process is focal. Clinically, it usually
  takes place latently. At the end there is focal
  cardiosclerosis.

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PERICARDITIS

• Pericarditis in rheumatism is serous, fibrinous
  and serous-fibrinous.
• Pericarditis results in the formation of
  adhesions in the pericardial cavity.
• Sometimes complete obliteration of the
  pericardial cavity and even calcification of
  fibrinous superimposed (palpable heart) are
  possible.

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VASCULITIS

• Rheumatic vasculitis, especially the
  microcirculatory bed, is very characteristic.
• Arteries and arterioles develop fibrinoid
  necrosis, thrombosis, proliferation of
  endothelial and adventitial cells.
• The permeability of the walls of the vessels is
  increased.
• Diapedemic hemorrhages and sometimes larger
  hemorrhages are possible.
• Arteriosclerosis arises in the outcome of
  rheumatic vasculitis.

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POLYARTHRITIS TYPE

• Occurs in 10-15 of patients.
• Mostly small and large joints are affected -
  serous-fibrinous inflammation.
• The synovial membrane is full-blooded, vasculitis
  is expressed, the synoviocytes proliferate, the
  connective tissue undergoes mucoid swelling, and
  exudate (usually serous) forms in the joint
  cavity.
• Articular cartilage is not involved in the
  process, therefore, with rheumatism, joint
  deformities are usually not observed.

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NODOSA TYPE

• Characterized by the phenomena of disorganization
  of connective tissue in the periarticular region
  and along the tendons - large foci of fibrinoid
  necrosis are found, surrounded by a cellular
  reaction (lymphocytes, macrophages, histiocytes)
  - nodosa erythema develops.

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CEREBRAL TYPE

• It is caused by the development of rheumatic
  vasculitis.
• If occurs in children, called small chorea.
• In addition to rheumatic vasculitis, especially
  at the level of microcirculation, there are
  dystrophic and necrobiotic changes in the brain
  tissue, small hemorrhages.
• The defeat of other organs and tissues is poorly
  represented, although it is always detected with
  a purposeful examination.

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COMPLICATIONS

• most often associated with the development of
  thromboembolic syndrome caused by warty
  endocarditis.
• With heart disease, cardiovascular failure
  develops, which is associated with myocardial
  decompensation.
• Sometimes various complications can cause
  adhesion in the cavities of the pericardium,
  pleura, abdominal cavity.

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PRACTICAL PART
112
GROSS SPECIMENS
113
? 143. ATHEROSCLEROSIS OF THE AORTA

• From the intima side multiple foci of
  atherosclerotic lesions of the aorta are visible
  fat spots and bands, uncomplicated fibrous
  plaques, ulcerated plaques and plaques with
  thrombotic overlays and calcification.

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? 148A. RUPTURE OF THE HEART WALL (RUPTURA
CORDIS) IN THE ACUTE STAGE OF MYOCARDIAL
INFARCTION

• In the lateral wall of the left ventricle of the
  heart there is a through defect of a slit shape
  up to 3 cm long.

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? 149. CHRONIC ANEURYSM OF THE HEART

• The anterior and lateral walls of the left
  ventricle of the heart are thinned, forming
  protrusion (aneurysm). Wall of an aneurysm of
  dense-elastic consistency, whitish-gray color
  (due to scar tissue). In the aneurysmal cavity,
  parietal thrombi are visible.

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? 150. SCARRING OF THE KIDNEY DURING
ATHEROSCLEROSIS (ATHEROSCLEROTIC SHRIVELED KIDNEY)

• The size of the organ is usually unchanged the
  kidney tissue is densified. Its surface with
  numerous, intertwined narrow deep cicatricial
  depressions.

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? 151 (91). HYPERTROPHY OF THE MYOCARDIUM OF THE
LEFT VENTRICLE WITH ARTERIAL HYPERTENSION

• The heart is enlarged by the left ventricle. The
  thickness of the myocardium of the left ventricle
  at its base is 1.5 cm (or more). The thickness of
  the myocardium of the right ventricle within the
  norm (less than 0.5 cm).

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? 152. PRIMARILY WRINKLED KIDNEY
(CICATRICIAL-WRINKLED KIDNEY WITH PRIMARY
ARTERIAL HYPERTENSION)

• The kidneys are reduced, compacted. Fibrous
  capsules are easily removed, exposing the
  fine-grained surface.

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? 153. ACUTE WARTY ENDOCARDITIS OF THE MITRAL
VALVE IN RHEUMATISM

• Valve leaflets slightly thickened, soft,
  translucency reduced. On the surface of the
  leaflets at the closing edge there are small
  thrombotic overlays in the form of towering knots
  ("warts").

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? 154. RECURRENT-WARTY ENDOCARDITIS OF THE MITRAL
VALVE IN RHEUMATISM

• Valves are thickened, compacted, whitish-gray,
  opaque, fused together. On the surface of the
  deformed valve flaps, fresh thrombotic overlays
  are located.

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? 156. HEART WITH RHEUMATIC MITRAL STENOSIS

• Valves are thickened, compacted, whitish-gray,
  opaque, fused together. The left atrioventricular
  aperture is narrowed (mitral stenosis). On the
  surface of the valves, a fresh thrombotic overlap
  is located along the closing edge, giving the
  mitral opening the appearance of a "fish mouth".

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? 157. HEART WITH DECOMPENSATED RHEUMATIC
MALFORMATION

• The heart is enlarged, its cavities are dilated,
  the walls are thinned (in comparison with the
  compensated state). Myocardium looks clayey
  (flabby, yellowish-gray).

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SLIDES
124
? 32. ATHEROSCLEROTIC PLAQUE OF THE AORTA IN THE
STAGE OF ATHEROMATOSIS

• Staining with Sudan III.
• A cut of the aortic wall through the center of
  the atherosclerotic plaque. The central sections
  of the plaque occupy a rich fat detritus, colored
  by Sudan III in orange. The plaque cover is
  preserved. Nearby the wall of the normal aorta is
  visible.

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? 222A. MYOCARDIAL INFARCTION, NECROTIC (ACUTE)
STAGE

• Staining with hematoxylin and eosin.
• The site of myocardial necrosis is formed by
  hypereosinophilic detritus. In some preparations,
  contours of the destroyed muscle fibers are
  visible (heterogeneous phase of necrosis),
  however, the cell nuclei in these areas are not
  detected. In the preserved tissue near the
  infarct, the microvessels are surrounded by cells
  of the inflammatory infiltrate, primarily
  neutrophilic granulocytes and macrophages
  (demarcation inflammation).

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? 222?, 222?. MYOCARDIAL INFARCTION, STAGE OF
ORGANIZATION

• Staining with hematoxylin and eosin.
• The area of ??necrosis is replaced by a fibrous
  connective tissue granulation can be seen in the
  preparation ? 222c and coarse-fiber (scar) in the
  preparation ? 222?. Cardiomyocytes, located
  around the cicatrix, are thickened their nuclei
  are enlarged, irregularly shaped, hyperchromic
  (signs of hypertrophy).

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? 148. RECURRENT-WARTY ENDOCARDITIS

• Staining with hematoxylin and eosin.
• Tissues show vessels (normally they are absent),
  severe fibrosis, fibrinoid necrosis foci
  (amorphous acellular eosinophilic masses), focal
  lymphohystiocytic infiltrate. On the surface of
  the valve with endothelium devotion, there are
  thrombotic overlays in the form of eosinophilic
  amorphous masses. Part of the thrombotic overlap
  is partially or completely replaced by fibrous
  tissue.

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? 149. GRANULOMATOUS RHEUMATIC MYOCARDITIS

• Staining with hematoxylin and eosin.
• In the myocardium between the bundles of muscle
  fibers there are numerous fading rheumatic
  granulomas Áshoff-Talalayeva.

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? 150. CARDIOSCLEROSIS IN THE OUTCOME OF
RHEUMATIC MYOCARDITIS

• Staining with van Gieson.
• In the stroma of the myocardium, mainly around
  small vessels, interlayers of dense fibrous
  tissue are found, the collagen fibers of which
  are colored red with acid fuchsin.