Workshop 14

  • April 2020
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Workshop nr.14

1.

PATHOLOGY OF THE ARTERIAL SYSTEM Atherosclerosis - ATS a. Aortic atherosclerosis (MA' MI) . Fibro-lipidic plaque b. Coronarian atherosclerosis (MA, MI)

o Fibro-lipidic plaque or fibrotic plaque

with

atheromatous core . Calcified fibrotic plaque o Thrombotic fibrotic plaque c. Cerebral atherosclerosis (MA) 2. Systemic hypertension MI - Benign nephroangiosclerosis

MA

o . o

Concentric hypertrophy of the left ventricle Benignnephroangiosclerosis Cerebral hematoma with ventricular flood 1. Atherosclerosis Atherosclerosis is an arterial disease: o involving large and medium-sized arteries o elastic arteries (e.g., aorta, carotid and iliac arteries) o large and medium sized muscular arteries (e.g., coronary and popliteal arteries, cerebral arteries & lower extremity arteries) o Is characteized by the formation of intimal atherosclerotic plaques (fibrofatty plaques) with secondary involvement of the medial muscular layer. The fundamental lesion in atherosclerosis is fibrolipidic plaque. The lesions have the same morphological appearance regardless of location. a. Aorticatherosclerosis

MA . The lesions are localized in the aortic abdominal segment, at branching or bifurcation of iliac arteries and around the orifices of the emerging collaterals. In severe forms are involved other segments, as well: the thoracic aorta and more rarely ascending aorta. According with American Heart Association (AHA), there are six atherosclerotic lesions: (l) fatty dots, (2) fatty streaks, (3) lipid plaques, (4) atheromatoqs plaques, (5) fibroatheromatous plaques, (6) complicated atherosclprotic plaques (calcification, ulceration, thrombosis and embolism, aneurysm formation).

.

"*l

iTr'[*'

H:ili:'lT,'ffiil]iJ]"J;:Hrany

dots (FD) which are less than 1 mm in diameter. Subsequently they form elongated lesions (l mm width and 1 cm long or longer) proiemining on the intimal aortic surface.

'''.""ff ::#j;Hl[ffi:il",]:ii',1:",j'J;Xxliffi

theintima

lntralumenal prnieminent lesion, whitish-yellow in colour (core of lipids and a covering fibrous cap), of round to oval shape and I-2 cm in diameter.

""',-f:Tl.lilir#ir11tr,:-ffir?Jff

i*o,o,,,u,"deposi,sor

calcium salts leading to a lesional image of egg-shell appearance

'.:-?l$1j-iiii;:i:i**";::*lf;T'nT';."guru,marginsand yellow, granular deposits on the surface By elimination of the atheromatous core are resulting cholesterol emboli

*T-fri,':dftiff,T*:*;ffidffi;;]l";,""., of ulcerated lesions, which are a sourse of emboli MI- Fibro-tipidic plaque Cross section through the aortic wall (Simionescu staining): - At the plaque lsvel the aortic rvall is thickened - The fUro-tip;O plaque is located at the level of the intima with secondarv involvement of the media . The intimalPiaque subendoteliallayer - compact acellular layer composed of coliagen fibers {blue in Simionescu staining)

-

i';:*$i*l f,{fi "'ffim;:F*:u'

"

b.

fibrin (red)

fibrotic base, containing capillary vessels of neoformation Medial atrophy and fibrosis, which affects the elasticity and strenglh of the wall Coronarian atherosclerosis

MA

Coronarian atherosclerosis (fibrotic and fibro atheromatous plaques) has a stenotic feature leading to myocardiai chronic ischemia' branches. on the first 6 cm of " The lesions arslocated on extramyocardial coronaryattery} their origin {anterior descending artety, circumflex . The consequence of coronary ats is coronary stenosis and myocardial chronic ischemia The chronic myocardial ischemia is manifested as myocafiial atrophy and fibrosis in adjacent mYocardium M{ - Coronarian atheroscierosis , Cross section through an extramyocardial coronary artery, r,r'hich presents on 2 . opposite walls 2 ATS plaques: fibro-lipidic plaque and calcified fibrous plaque

,

. .

At the plaque levelthe wall is thickened The plaques are located in the intima, causing secondary medial layer damage by

compression The media becomes thinned and fibrotic (atrophy by compression) and affects the elasticity and strength of the wall The lumen is stenotic I ) Fibro-lipidic plaque Cross section through an extramyocardial coronary artery (HE) The intimal plaque

.

' . .

subendothelial level fibers

-

fibrous cap compact, acellular layer of collagen

""f'ftfi*+i*ff**:y'. ' .

foamy cells

fibrin

the fibrous basis - collagen At the plaque angle, there are present capillaries of neoformation . atrophy and fibrosis of the media 2) Calcified fibrous plaque ' Cross section through an extramyocardial coronary artery (HE) . subendothelial level -accumulation of collagen fibers . in the center of the plaque, there are hematoxilinofil deposits of calcium salts ' atrophy and fibrosis of the media

MI- Fibrous plaque complicated by thrombosis

. . . .

Cross section through an extramyocardial coronary artery (HE) The afiery wall is thickened by a fibrous plaque

The coronary artery lumen is occluded by a recent thrombus, that consists of a fibrin network, white cells and red blood cells The occlusive thrombus causes acute ischemia (myocardial infarction)

c. Cerebral

atherosclerosis Cerebral atherosclerosis appears at approximatively 15 years after the onset of the disease. The most frequent involved cerebral arteries are the polygon Willis vessels.

MA The cerebral arteries of the polygon Willis, located at the brain base, present a thickened wall by the presence of yellowish fibro-lipidic plaques. On the cross section, the cerebral atherosclerotic arteries present a perrnanent opaned lumen, resembling with macaroni (normally, on the cross section, the arteries are collapsed). Cerebral atherosclerosis (fibrotic and fibro atheromatous plaques) has a stenotic feature leading to cerebral chronic ischemia (senile dementia)Cerebral atherosclerotic complications: c Plaque thrombosis i Acute cerebral ischemia (cerebral infarct or cerebral softening )

The rupture wall at the level of the atherosclerotic plaque leading to cerebral hemorrhage

Aneurismal dilatation involving vertebro-basilar artery (aneurysm of underlying media)

-

by thinning

II.

Systemic hypertension Benign HTA: an increase in the arterial blood pressure . It represents the persistent increasing of the systolic and diastolic pressure over normal values . The main target organs: Heart (hypertensive cardiopathy) - concentric hypertrophy of the left ventricle Kidney- benign nephroangiosclerosis Brain- Cerebral hematoma with ventricular flood Arterial system changes . HTA involves arterioles and small arteries. . HTA causes the thickening of the wall and narrow of the lumen (vasoconstriction; damage of the vessel)

MA Heart - concentric hypertrophy of the left ventricle Hypertrophy (HT) is a reaction of cell adaptation characterized by increasing of a or organ volume by increasing in size of cell components. E.g. Concentric tissue hypertrophy of the left ventricle due to HTA (obstacle in front of LV); On the extemal surface the heart is increased in size and volume, and on the cross section, there is a concentric thickening of the left ventricle (over 2 cm in diameter) and a LV stenotic cavity. Brain-Cerebral hematoma with ventricular flood It represents the accumulation of blood in the brain parenchyma. It appears in case of systemic hypertension due to rupture of an aneurysm of middle cerebral artery. Macroscopy: a coagulated blood collection, located in the cerebral parenchyma, adjacent to the lateral cerebral ventricle resulting in ventricular flood and sudden death. Kidney- benign nephroangiosclerosis Benign nephroangiosclerosis is an exemple of ischemic atrophy, consisting ln reducing of arterial circulation in a kidney (chronic ischemia), with consequent loss of cells. The consequence is atrophy of the renal parenchyma in HTA: the two kidneys are atrophic, smaller and paler, with a fine granularity on the external surface. On the cross section, the renal parenchyma is reduced in volume (the cortex and medulla are not distinctive) and is associated with hilar adipose tissue hyperplasia.

MI - Kidney- benign nephroangiosclerosis

. .

Section through the kidney (HE) Afferent arteriole with thick wall, homogenized, eosinophilic (hyalinized) and

stenotic lumen

a

. .

Glomeruli

in different stages of

frbrosis and hyalinization until complete

transformation in spherical structures, homogeneous, eozinofilic without structure and unfunctional Renal tubules: corresponding to affected glomeruli are atrophied or disappeared being replaced by connective scar corresponding to hipertrophied glomeruli are dilated with lumenal hyalin cylinders

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