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17. A 64-year-old woman has had several episodes of transient ischemic attacks (TIAs).
Aspirin would be a preferred treatment, but she has a history of severe “aspirin
sensitivity” manifest as intense bronchoconstriction. Which group aspirin belongs to?
Side effects of aspirin. What would be a suitable alternative to the aspirin? Mechanism
of action of this drug, indications, routes of administration.

19. A 42-year-old man with an acute MI is treated with alteplase. What is the
mechanism of main desired effect? Which group drug belongs to? Routes of alteplase
administration. Mechanism of action and major indications. Which group and what
drugs may counteract effects of alteplase?
20. A 60-year-old woman with deep-vein thrombosis (DVT) is given a bolus of heparin,
and a heparin drip is also started. 30 min later, she is bleeding profusely from the
intravenous site. The heparin is stopped, but the bleeding continues. Which drug may
reverse the adverse effect of heparin? What is mechanism of heparin action? Side
effects of heparin and routes of administration. Which group heparin belongs to?

1. DIAGNOSIS,
ATHEROSCLEROSIS,
HYPERTENSION,
VASCULITIS
Prof. Volkova L.V.
2010-2011
Kursk

2.  TYPES OF DIAGNOSIS
Diagnosis-medical conclusion about the state of health,
diseases (traumas), cause of death of patient accordion
the 10 International Classification of diseases, traumas and
the causes of death
Nosological diagnosis with reflection of etiology and
pathogenesis of the disease
(staphylococcal sepsis, an anaphylactic shock).
1. Clinical
2. Pathomorphological
3. Pathohistological
 Preliminary -final diagnosis

3. STRUCTURE OF CLINICAL AND
PATHOMORPHOLOGICAL DIAGNOSIS
1) basic disease
2) complications
3)coexistent (associated)diseases
Example:
1) Essential hypertension, cardiac form:hypertrophy of the
heart (weight -500 g, left ventricle wall –1,8 cm, right –0,4
cm), atherosclerosis of coronary vessels (liposclerosis)
2) Arteriolosclerotic nephrocirrhosis, uremia,uremic
gastroenteritis, multiple acute ulcers in stomach, fibrinous
pericarditis, dystrophy of parenchimal organs, edema of
the lung, brain
3) Leiomyoma of the uterus(3cm)

4. MISDIAGNOSIS -DIFFERENCES BETWEEN CLINICAL AND
PATHOMORPHOLOGICAL DIAGNOSIS

 IN BASIC DISEASES:
Hypodiagnostics
Hyperdiagnostics
Later final clinical diagnosis -in the final stage of diseases or
after patient death

In complications and accompanying diseases -
Misdiagnosis is not fixed, however it is marked in clinico-
anatomic epicrysis

5.  IATROGENIC DISEASES
Classification of iatrogenic diseases according the causes
of their development.
I. due to treatment.
A. Drugs
B. Surgical
C. due to physical methods
II. Due to diagnostic researches
III.Due to prophylaxis
IV. Due to information
Surgical (36,3 %)
Infectional-septic (25 %)
Medicamentous (17,2 %)
Toxic epidermal
necrolysis

6. ARTERIOSCLEROSIS -
hardening of the arteries –
thickening and loss of elasticity
of arterial wall
 TYPES:
1) Atherosclerosis–injury of
large elastic or muscular-elastic
type vessels, atheroma
2) Monckeberg medial calcific
sclerosis(after 50 years) -injury
of middle-size, muscular arteries-
calcification of media
3) Artheriolosclerosis-injury of
small arteries and arterioles –
hyaline and hyperplastic
anatomic variants –hypertension
and diabetes mellitus –diabetic
microangiopathy)

7.  ATHEROSCLEROSIS
Atherosclerosis-from words athere (fat) and
sklerosis -hardening
Atherosclerosis is the chronic disease caused
by disturbance of lipids and proteins
metabolism.
It is characterized by the lesions of intima, and
subsequently -media of the elastic and
muscularly-elastic type arteries with formation
of atheromas.
 MORPHOLOGY
Combination of lipid (fatty) dots, streaks,
atheromatous plaques, ulcerations,
calcificationand subsequent complications
are revealed in the vessel walls.
Atherosclerosis is characterized by the injury
of the elastic and muscular-elastic types
arteries, large and middle-size vesselsand less
often -arteries of muscular type. (athermatous
plaques) in the large and medium sized (elastic
or muscular) blood vessels
 Major cause of death -IHD, MI, Stroke

10.  ETIOLOGY OF ATHEROSCLEROSIS
 Atherosclerosis is polyetiologic disease
which arises due to influence of
exogenous and internal causes.
 Risk factors:
 Non modifiable
1.Age and sex(male)
2.Hereditary and ethnic factors
3.Lipidemia and hypercholesterinemia-
HDL/LDL ratio. Genetic
Hypercholesterinemia
4.Potentially Modifiable
5.High arterial pressure-Tobacco
smoking
6.Hormonal factors (diabetes mellitus,
hypothyroidism)
7.Nervous factors
8.Obesity and hypodynamia, Life Style
THEORIES OF
ATHEROSCLEROSIS.
1. Alimentary or
infiltration theory.
N.N.Anichkov (1913)
2. Immunologic
theory.
3. Thrombogenic
theory.
4. Nervously-
metabolic.
5. Peroxidation
theory.
6. Other theories

11. STAGES OF
PATHOGENESIS
1.Dislipoproteidemia(LDL increase) -
noncontrollable endocytosis of lipids by
the endothelium
2.Damage of the endothelium
3.Infiltration of the plasma components
and lipoproteins into the intimae
4.Adhesionof platelets, monocytes to the
intimae . They release cytokines, growth
factors.
5.Fixation of monocytes to the intima and
their transformation into the foamy cells
–intracellular lipids.

12. 6.Growth factors stimulates proliferation of smooth
muscle cells (SMC) in media. SMC migratesinto the
intima.
7.SMC synthesize proteoglycans, collagen and elastin
fibers –formation of the capof fibrous plaque.
8.Destruction of macrophages, foamy cells, SMC (can
engaf lipids) –formation of the atheromatous debris–
etxtracellular lipids.
9.Capillariesare formed, Т-and B-lymphocytes migrate,
fibrosis, necrosis
10.Extension of lesion and destruction of vessel, deformity,
hardening, calcification and ulceration.
11.Complications-thrombosis, embolism, hemorrhage,
aneurism, dissection and rupture.

13. Structure of Atheroma:
Fibrous Cap
Lipid center
Cholesterol.
Macrophages
and
lymphocytes

14. Formation of atheroma.

15. Pathogenesis of Atheroma: Stage 1.
Endothelial injury:
(increased
permeability,
leukocyte and platelet
adhesion, emigration.

16. Pathogenesis of Atheroma: Stage 2.
Macrophage
activation and
smooth muscle
migration from
media.

17. Pathogenesis of Atheroma: Stage 3.
Lipid
deposition.
Macrophage
and SMC
engulf lipid.

18. Pathogenesis of Atheroma: Stage 4.
Extracellular
lipids,
smooth muscle
proliferation,
Collagen and
ECM deposition.
Central lipid core.
Lympho, Collagen, Fat
Fibro-Fatty Plaque

19. 1.MACROSCOPICAL STAGES OF THE
MORPHOGENESIS OF ATHEROSCLEROSIS
 Macroscopical stages:
1.1) Fatty dots, patches or streaks= Lipoidosis
2.2) Fibrous plaques= Liposclerosis
3.3) Complicated lesions -fibrous plaques with
ulcerations, hemorrhages and thrombosis.
4.4) Atherocalcinosis
 Microscopical stages:
*0) Preliminary (initial) stage, 1-4

22. Atherosclerosis of
aorta

25. CLINICO-
MORPHOLOGICAL
FORMS OF
ATHEROSCLEROSIS
Depend on the
primary lesion of
vessels in the various
topographical zones
1. Atherosclerosis of
aorta
2. Cardiac form
3. Cerebral form
4. Renal form
5. Mesentherial form
6. Atherosclerosis of
arteries of low
extremities

26.  ATHEROSCLEROSIS OF THE AORTA
 2 variants:
1.Lerish’s syndromewith lesion of
abdominal part and bifurcation of aorta
2.Aortic arch syndromewith involving the
arch and thoracic part of aorta.
3.Lerish’s Syndrome -syndrome of
disturbance of blood supply of low
extremity -intermittent claudication, pain,
paleness, weakening of pulsation,
gangreneof extremities.
Aortic arch syndromeand stenosis of
ostium of the branches of aorta: non-
uniform filling of pulse on arms or
absence of pulse, ischemia of the brain
and disturbance of cerebral circulation,
disturbance of vision.
General complications:thrombosis,
thromboembolism and embolism with
atheromatous debris leads to infarctions
(kidneys, gangrene of intestine, extremity)
and aneurysm (rupture, bleeding)

27.  ATHEROSCLEROSIS OF THE AORTA
Aneurysm–abnormal dilation (protrusion) of the wall of aorta or
heart in the place of its lesion.
Aneurysms differ according the form (Saccular, Fusiform), according
the structure of the wall (true and false).
Saccular –essentially spherical (involving only a portion of the
vessel wall) and vary in size from 5 to 20 cm in diameter
Fusiform (involving a long segment -diffuse with complete dilation of
vessels) -vary in diameter (up to 20 cm) and in the length
True aneurysm-wall consists from aorta
False aneurism(pseudoaneurism) -wall is formed by adjoining
tissues and hematomas, (“ pulsating hematoma ”)
Dissection aneurysmis formed after dissection media from intima or
adventitia by blood.

30. Dissection aneurysm

31. SYPHILITIC (LUETIC) ANEURYSM
Tertiary syphilis
Injury of aorta -arc, thoracic part
Media, vasa vasorum in adventitia:
obliterative endartheriitis, infiltrate from
lymphocytes and plasma cells (syphilitic
mesaortitits)–inflammation and scarring
Destrucrion of elastic membranes of media
–loss of elasticity, dilation -Syphilitic
Aneurysm
Macro –contraction of fibrous scar –
wrinkling of intimae –noted grossly as
“tree-barking”
Additional superimposed atheromatousis
of aortic root, coronary ostia, aortic valve
injury –insufficiency -regurgitation –
massive overload hypertrophy (1000 gm –
cor bovinum)
Complications -rupture, heart failure,
complications due to pressure to organs

32. SYPHILITIC
MESAORTITIS

33. SYPHILITIC ANEURYSM
Tertiary syphilis –ascending part of
aorta arch

34. ATHEROSCLEROSIS OF
CORONARY ARTERIES OF
HEART
The atherosclerotic lesion leads
to development of ischemic heart
disease.
1.Acute occlusion of the lumen of
coronary vessels leads to
myocardial infarction
2.Prolonged ischemia cause
diffuse atherosclerotic
cardiosclerosis.

35. CEREBRAL FORM OF
ATHEROSCLEROSIS
atherosclerotic lesion of arteries of
the brain (precerebral and cerebral
vessels). It causes acute and chronic
disturbances of cerebral circulation,
cerebrovascular diseases.
1.Clinical manifestations: transitional
ischemia of the brain or strokes. The
main form is ischemic infarctionof the
brain -area of the grey malacia
caused by thrombosis precerebral
(a.carotis or a.vertebralis)or cerebral
arteries (arteries of the basis of brain,
a. cerebral media). Infarction in sub
cortical area cause paralyses.
2.Chronic ischemia of cortex leads to
dystrophy and atrophy -syndrome of
atherosclerotic dementia.Ischemic infarction
of the brain (focus
of the gray
softening of the
brain) –1
Outcome of
infarction (cyst) -2

36. RENAL FORM OF THE
ATHEROSCLEROSIS.
Plaques in the basic trunk
and large branches of the
renal artery
1.Thrombosis of the artery
cause the infarction of the
kidney
2.Slow atherosclerotic
occlusion leads to
sphenoidal atrophy and
sclerosis –macronodulated
atherosclerotic contracted
kidney (nephrosclerosis).
3.Stenosing atherosclerosis of
renal arteries causes
symptomatic (renal)
hypertension.

37. ATHEROSCLEROSIS OF ARTERIES OF
THE LOW EXTREMITIES
Femoral arteries are often involved, in
connection with development of
collaterals process can be
asymptomatic during long time, then
Lerish’s syndrome can develops.
1.Acute occlusion of the vessel leads to
the gangrene
2.Chronic occlusion–to occurrence of a
Lerish’s syndrome -syndrome of
disturbance of blood supply of low
extremity -intermittent claudication
ATHEROSCLEROSIS OF MESENTERIC
ARTERIES
A. mesenterica sup. is involved:
ischemic colitis, acute occlusion cause
the infarction of the intestine and
gangrene.

38.  GENERAL COMPLICATIONS OF AT
 1) ACUTE:
Thrombosis, Thromboembolism
Rupture –Hemorrhage
Aneurisms
Strokes, Myocardial Infarctions, Renal infarction, Mesentric
thrombosis, gangrene etc.
 2) CHRONIC:
Distrophy, atrophy
Fibrosis in organs
Diffuse cardiosclerosis, atherosclerotic demention, primary
(atherosclerotic -macronodulated) contracted kidney,
intermittent claudication, atrophy of muscles of limbs

39. SYSTEMIC HYPERTENSION -is characterized by elevation of
systemic arterial blood pressure, diastolic pressure more than 90
mm hg, systolic pressure more than 140 mm hg
 TYPES OF HYPERTENSION
1) According the cause (etiology):
primary (essential, idiopathic) -90-95% (unknown etiology)
secondary or symptomatic -arises as symptom of primary
disease and it disappears after its treatment (renal, endocrine,
cardiovascular, neurogenic, others)
2) According clinical duration of hypertension:
benign
malignant

40. SECONDARY OR SYMPTOMATIC HYPERTENSI ON
1. Renal hypertension:renoparenchimal–due to chronic
glomerulonephritis, pyelonephritis, diabetic
glomerulosclerosis, etc., renovascular, due to congenital
anomalies of thekidneys
2. Endocrine hypertension:(due topathology of adrenalglands,
pituitary gland, hyperthyroidism and a hyperparathyreosis, at
climacteric period,carcinoid syndrome).
3. Cardiovascular (hemodynamic hypertension):due to
atherosclerosis of aortic arch, coarctation of aorta
4. Neurogenic hypertension:diseases of nervous system –due
to rising of the intracranial pressure ( trauma, tumour, abscess,
hemorrhage), diseases of the hypothalamus and medulla
oblongata, due to the action of psychogenic factors
5. Other. Medicamental(glucocorticosteroids,
mineralocorticoids, contraceptives, etc.), gestosis, etc.

41. HYPERTENSIVE CRISIS
In HP of any genesis it is possible the
development of hypertensive crisis –
fast, during several hours, additional
significant elevation of BP (diastolic
BP 140 and more)
Hypertensive crisis is usually due to
psychoemotional or physical stress,
excessive uptake of salt or liquid
MORPHOLOGY OF HYPERTENSIVE
CRISIS
1. spasm of arterioles (goffering and
destruction of basal membrane of the
endothelium). Endothelium -in the form
of the palisade
2. Plasmainfiltration of the vessel wall
3. Fibrinoid necrosis of the vessel wall
4.Thrombosis
COMPLICATIONS: INFARCT IONS,
HEMORRHAGES
BININGHHP–is a
chronic and relatively
mild increase in
systemic BP
( diastolic BP not
higher than 110 to
120 mm Hg),may be
primary or secondary
MALIGNANT
(accelerated)HP–
severe and acute
elevation of BP
(diastolic BP higher
than 130-140 mm Hg),
can arise de novo or
as complication of
benign hypertension

42. 
 MALIGNANT( ACCELERATED) HP
1) acute severe elevation of BP (BP 220/140), frequent HP-crisis.
2) diastolic BPhigher than 130-140 mm Hg
3) low rate, can arise due to essential or secondary HP, is typical
for men, age 30-50 years, sometimes –younger than 30 years.
4)groups of high risk:patients with renovascular hypertension,
glomerulonephritis, chronic renal failure, or scleroderma,
pregnant women with toxemia
5) If untreated, leads to death within 1 or 2 years
6) severe clinical manifestation:headache, disturbances of
vision (hemorrhages in retina, papilloedema), hematuria or anuria
( fibrinoid necrosis of vessels of glomerulas in kidneys)
6) secondary manifestations in the organsdevelop very soon


43. 
 MORPHOLOGY OF MALIGNANT HP
1. Necrotizing arteriolitis-fibrinoid necrosis and hyalinosis of
arterioles in all organs.
2. Hyperplastic arteriolosclerosis-onionskin, concentric,
laminated sclerosis
3.Lesions of kidneys :artheriolonecrosis, fibrinoid necrosis of
capillaries of glomerules, edema and hemorrhages in stroma, in
epithelium of tubules –protein dystrophy
 malignant nephrosclerosis (renal failure)
granular or smoothkidney-may be normal in size or lightly
shrunken, in the cortex can appear small, pinpoint petechial
haemorrhages (peculiar flea-bitten appearance)

44. Malignant hypertension: kidneys.

45. IDIOPATHIC HYPERTENSION OR PRIMARY, ESSENTIAL
HYPERTENSION
1) It is chronic polyetiologicalmultifactorial diseasewith
prolonged and stable elevation of arterial pressure
(hypertension).
major causes -genetic ( polygenic type of inheritance) and
environmental factors.
2) Systolic pressure exceeds 140, and diastolic pressure
–90 mm hg, relatively mild increase in systemic BP,
diastolic BP no more than 110 to 120 mm Hg
3) BP remains at the mild level, is stable during decades
4) at the final stage -serious secondary manifestations
in the organs,complications

46. RISK FACTORS OF
DEVELOPMENT HP
1.Chronic
psychoemotional
efforts
2.Excessive
consumption of salt
3.Obesity
4.Smoking
5.Life style
(hypodynamia)
6.Age, sex, race
7.Level of cholesterol
in the blood, tolerance
to glucose, activity of
rennin
MULTIPLE PATHOGENETIC
FACTORSOF ESSENTIAL HP:
changes between cardiac output
and total peripheral resistance is
altered
The main chains in regulation of
the BP:
1) chronic psychoemotional
stress, nervous and hormonal
influences
2) renal mechanisms-renin-
angiotensin-aldosteron system;
genetic defect of the renal
mechanismsof regulation of the
BP
3) sodium homeostasis
4) calcium metabolism

47. 
 PATHOGENESIS of HP
BP =cardiac output х peripheral resistance( lumen of the
vessel-constrictors + blood volume -sodium, aldosteron +
viscosity of blood + elasticity of the vessel wall + cardiac
factor –heart rate, contractility).
At whole development HP is discribed by following theories
1/ The theory of primary rising of cardiac output (hypervolemia)
1.2/ The theory of vasoconstriction: long action of neurogenic
factors and vasoconstrictors –angiotensin, catecholamins
and ect. Elevation of the sensitivity smooth muscles of
arterioles.
2.These theories supplement each other. The important role in
regulation of BP belongs to the renal mechanism ( secretion
of sodium, balance of vasoconstrictors and vasodilatators).


48.  PATHOGENESIS of HP
 1. homeostasis of sodium:
Increase of cardiac output–due to increase of plasma and blood
volume:
1.Retention of sodium and water, owing to the excessive uptake
of sodium with nutrition
2.Defect of renal excretion of sodium
3.Disturbance of transport of sodium through cellular membranes
-intensifying of permeability of cellular membranes for sodium
2. Nervous and humoral factors of BP regulation:
depends on balance between vasoconstrictorsand vasodilatators
Sympatico-adrenal system
1.Renin-angiotensin-aldosteronsystem, hormones (ACTH,
hydrocortisone, STH, ADH, sex hormones, etc.)
2.Prostaglandin and kallikrein-kinin system, Others
3.3. Generalizedmembranous defect sodium-calcium transport.
Hereditary disturbances of structure and function of cellular
membranes, elevated concentration of sodium and calcium
within the cell owing to disturbance of its input and output from
the cell. It leads to spasmof smooth muscle cells and increase
of their sensitivity to constrictors

50. PATHOGENESIS OF ESSENTIAL
HYPERTENSION

51. PRIMARY, ESSENTIAL HYPERTENSION
BENINGN HP : MORPHOLOGY
1) hyalinosis of the vessels (arterioles)
2) sclerosis of the vessels
3) fibrinoid necrosis
4) aneurisms formation
5) changes in organs:sclerosis, haemorrhages, infarction
6) changes of heart:concentric hypertrophy of the left
ventricle, increase of the weight of the heart
MORPHOLOGY OF BENINGN HYPERTENSION DEPENDS
ON THE STAGE OF THE DISEASE:
1) preclinical( functional,transitional HP)
2) vascular stage -widespread changes of arteries
3) stage of secondary organ changes

52.  1. PRECLINICAL STAGE OF HP
Incidental elevation of BP and change in small-size arteries
and arterioles
1 -hypertrophy of a muscular layer and elastic structures of
small-size arteries and arterioles
2 -spasm of arterioles
3 -moderate compensatory hypertrophy of the left ventricle of
heart


53. 
2. STAGE OF THE WIDESPREAD CHANGES OF ARTERIES:
Stable elevation of BP and change of the vessels -arterioles,
elastic-type, muscular-elastic and muscular-type arteries and
heart
ARTERIOLES AND SMALL -SIZE ARTERIES OF MUSCULAR
TYPE:
1. Plasmainfiltrationinto the walls of arterioles and small-size
muscular-type arteries.
2. Hyalinosis, arteriolosclerosis
4. Arteriolonecrosis, hemorrhages(incrisis)
ELASTIC-TYPE, MUSCULAR-ELASTIC –TYPE AND
MUSCULAR TYPE ARTERIES :
1. elastofibrosis-hyperplasia and dissection of the internal
elastic membrane
2. sclerosis -growth of connective tissue between dissection
of the membranes
3. stenosing atherosclerosis-" goes down " in arteries of
muscular type, circular localization of fibrous plaques
 HEART:
1. Hypertrophy of myocardium: 900-1000 gm, thickness of the
wall of left ventricle -2-3 sm -Cor bovinum)

54. HYALINE ARERIOLOSCLEROSIS IS A MAIN
MORPHOLOGIC CHARACTERISTIC OF BENINGN HP
homogeneous, pink, hyaline thickening of the walls of
arterioles with loss of underlying structural detail, with
narrowing of the lumen

55. 3. STAGE OF SECONDARY
CHANGES IN THE ORGANS
Due to disturbances of organ
circulation
CHRONIC DURATION -
atrophy and sclerosis in the
organs)
ACUTE CHANGES -
thrombosis,spasm leads to
fibrinoid necrosis –
hemorrhages and infarcts.
CLINICO-MORPHOLOGICAL
FORMS OF HP
1. Cardiac form (ischemic
heart disease)
2. Cerebral (cerebrovascular
diseases -hypertensive
encephalopathies)
3. Renalform

56. CLINICO-MORPHOLOGICAL
FORMS OF HP
1. Renal form: primary
contracted kidney
(nephrosclerosis), infarction
2. Cardiac form:
cardiosclerosis, MI, acute and
chronic IHD
3. Cerebral form:hypertensive
encephalopathy, cerebral
vascular disease (strokes –
infarctions and
haemorrhages)
Clinical manifestation and
complications:infarctions,
haemorrhages, failure of
functions ( renal failure, heart
failure)

57. RENAL FORM: PRIMARY
CONTRACTED KIDNEY
symmetrical atrophy of both
kidneys (110-130g)
diffuse, fine granularity that
resembles grain leather
 microscopical changes:
hyalinosis and sclerosis of
the vessels,
glomerulosclerosis and
hyalinosis, atrophy of cortex
and medulla , interstitial
fibrosis
hyaline arteriosclerosis is a
major morphologic
manifestation of benign
nephrosclerosis.

58. Primary contracted kidney

59. CEREBROVASCULAR DISEASES :
CEREBRAL FORMS OF ATHEROSCLEROSIS
AND HYPERTENSION.
ACUTE DISTURBANCES OF THE CEREBRAL
CIRCULATION:
1. Transitional ischemiaof the brain
2. Strokes-acute local disturbances of the
cerebral circulation with damage of the tissue
and disturbances of function.
 Kinds of strokes:
Hemorrhagic-hematoma, hemorrhagical
imbibition, subarachnoidal hemorrhage
Ischemic- grey encephalomalacia
(ischemic infarction, hemorrhagicinfarction,
mixed)
CHRONIC DISTURBANCES OF THE CEREBRAL
CIRCULATION:
Atherosclerotic aphrenia, demention.
Hypertensiveencephalopathy.
Complications of strokes –paralyses, edema of
the brain, dislocation of a brain, blood in the
ventricular system of the brain

60.  CEREBROVASCULAR DISEASES
They arise due to atherosclerosis and hypertension.
 Classification:
1. The diseases of the brain due to to ischemic damages:
Ischemic encephalopathy
Ischemic and hemorrhagic infarcts of brain
2. Intracraneal hemorrhages:
Intracerebral –hematoma, hemmorhagical imbibition
Subarachnoidal
Mixed
3. Hipertension cerebrovascular diseases:
Lacunar changes –set of small cysts in the cerebral tissue
Subcortical leukoencephalopathy –subcortical loss of axons
and demyelination
Hypertensiveencephalopathy –patients with malignant form of
HP -fibrinoid necrosis of the vessel wall, petechial
hemorrhages and edema

62. Subarachnoid
Haemorrhage:

64.  VASCULITES
inflammation of the vessels (often with necrosis of the
vascular wall).
 Classification:
Due to spreading of the process: local, systemic
Due to etiology: primary, secondary
Due to inflammatory reaction:
•destructive
•destructive-productive
•productive
Due to lesion of the vessel wall:
•endovasculitis
•mesovasculitis
•perivasculitis
•endomesovasculitis
•panvasculitis

65.  CLASSIFICATION OF PRIMARY VASCULITES
1. With lesion of aorta and its large branches and giant
cell reaction:
nonspecific aortoarteriitis –Takayasu disease
temporal (giant cell) arteriitis.
2. With lesion of middle-size and small-size arteries and
destructive-productive reaction:
Polyarteritis nodosa
Kawasaki disease
Wegener granulomatosis
3. With primary lesion of medium-size and small-size
arteries and capillaries and veins:
Thrombangiitis obliterans (Buerger disease)-upper and
low extremities

67.  TYPES OF SECONDARY VASCULITES:
Infectious processes: syphilis, tuberculosis, sepsis,
etc.
Systemic diseases of connecting tissue: rheumatic fever,
rheumatoid arthritis, SLE
Vasculites of "hypersensitivity"
Vasculites at malignant neoplasms.

 CLINICAL MANIFESTATIONS
Depending on topography of the process and its
prevalence -various clinical symptoms and pathology
(infarctions in organs, sclerosis, atrophy, gangrene,
hemorrhages).Due to lesion of vessels of kidneys -renal
hypertension, lungs -pulmonary hypertension, vessels
of the skin-hemorrhagic diathesis, ect.

68.  POLYARTERITIS NODOSA
rheumatic disease or primary systemic destructive-
productive vasculitis with systemic lesion of the connecting
tissue of middle-size and small-size arteries.
systemicarteriitis with lesion of the kidneys and fast
progressing, loss of functions.
basic manifestations -formation of nodules in the vessels
(aneurysmal diverticulums), “thickenings“, microscopically –
fibrinoid necrosis and proliferative reactions.
Renal, coronary, mesenteric, hepatic vessels and arteries of the
brain can be involved
Etiology: unknown
Provoke factors -infections, insolation, trauma, stress, ect.
Pathogenesis: immune complexes -vasculites -fibrinoid
necrosis of the media –exudation -proliferation of adventitia
-sclerosis -formation of nodular thickenings of the wall

69. POLYARTE -
RIITIS NODOSA

70. POLYARTERITIS NODOSA

71.  POLYARTERITIS NODOSA
 ORGANOPATHOLOGY
in kidneys -subacute or chronic glomerulonephritis
muscular –joint injuries (syndrome)
dermal lesions (urticaria, spotty hemorrhages)
cardiovascular symptoms
lesion of organs of the abdominal cavity ( pain, necrosises,
ulcers)
pulmonary pathology
neurologic symptoms
 DURATION:
acute (myocardium infarction, disturbance of cerebral
circulation, hypertensive crisis, destructive pneumonia
chronic–slow progression with fever, muscular and artritis
pains, polyneuritis.
Outcomes:acute duration -ischemia, infarctions,
hemorrhages , chronic -sclerosis, dystrophy, hemorrhages
with loss of functions

72. Takayasu
arteritis

73. Vascu-
litis

74. Buerger
disease

75. DIAGNOSIS,
ATHEROSCLEROSIS,
HYPERTENSION,
VASCULITIS
Prof. Volkova L.V.
2010-2011
Kursk