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cardiovascular system diseases
Clinical Medicine Undergraduate Pathology, including atherosclerosis, hypertension, rheumatism, infective endocarditis, and valvular heart disease Myocarditis etc.
Edited at 2024-03-08 10:15:45
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cardiovascular system diseases
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- Outline
cardiovascular system diseases
atherosclerosis
Overview
arteriosclerosis
feature
Thickening, stiffening, and loss of elasticity of arterial walls
type
atherosclerosis
Mainly affected
Large and medium arteries
Lesion characteristics
Lipid in the plasma is deposited on the intima of large and medium-sized arteries, causing the formation of intimal fibrous plaques and atherosclerotic plaques, hardening the arterial walls and narrowing the lumen.
medial arterial calcification
Rarely, medium muscular arteries in the elderly, medial calcium salt deposition → may ossify
Arteriosclerosis
Diabetes, hypertension → hyaline degeneration of small arteries
Predisposed areas
Abdominal aorta>Coronary artery>Descending aorta>Carotid artery>Basic cerebral artery Circle of Willis
Etiology and pathogenesis
risk factors
Hyperlipidemia
The sustained increase in plasma LDL and VLDL levels and the decrease in HDL levels are positively correlated with the incidence of AS.
hypertension
Strong impact on blood vessel walls, endothelial damage, and changes in vessel wall metabolism
smoking
Endothelial loss, blood Co concentration, LDL oxidation
Diseases causing secondary hyperlipidemia
diabetes
hyperinsulinemia
Hypothyroidism and nephrotic syndrome
genetic factors
Gender, age, weight, infection, etc.
HDL in premenopausal women, low prevalence
metabolic syndrome
Pathogenesis
Lipid penetration theory
damage-response theory
The role of arterial SMC
chronic inflammation theory
Pathological changes
Fat lines
naked eye
Small yellow spots or stripes, flat or slightly raised on the surface of the intima, obvious at the openings of blood vessels
under the mirror
There are a large number of foam cells FC gathered in the endothelium of the fat streaks, and the cytoplasm is vacuolated.
fibrous plaque
naked eye
It initially appears as a gray-yellow plaque raised in the intima; later, due to the increase in surface collagen and glass-like change, it becomes porcelain white, like wax droplets.
under the mirror
fiber cap
lipid region
base
atheromatous plaque
Main ingredients
Cells, ECM, extracellular and intracellular lipids
naked eye
A gray-yellow patch that is obviously raised on the surface of the intima. The surface layer is a fibrous cap, and the deep part is a yellow porridge-like substance.
under the mirror
fiber cap hyalinization
There are a large number of necrotic cells under the fibrous cap
Adventitial capillaries, CT hyperplasia, lymphocyte infiltration
secondary lesions
intra-plaque bleeding
Plaque rupture and ulceration
thrombosis
Calcification
aneurysm formation
vascular lumen stenosis
important atherosclerosis
aorta
It mostly occurs in the openings of the posterior wall of the aorta and its branches, with the abdominal aorta the most serious disease, which can easily lead to aneurysm formation.
coronary artery
Predisposed areas
The left anterior descending coronary artery is the most common, followed by the right main coronary artery
According to the degree of stenosis of the vascular lumen, it is divided into 4 levels.
Coronary atherosclerosis
coronary atherosclerotic heart disease
Main clinical manifestations
Angina pectoris
mechanism
myocardial infarction
type
subendocardial MI
transmural MI
Pathological changes
MI complications
heart failure
ruptured heart
ventricular aneurysm
mural thrombosis
cardiogenic shock
acute pericarditis
Arrhythmia
chronic ischemic heart disease
carotid and cerebral arteries
Most commonly found at the origin of the carotid artery, the basilar artery
renal artery
AS type pyknotic kidney
arteries of extremities
Common arteries in lower limbs
mesenteric artery
intestinal infarction
hypertension
standard
Adult systolic blood pressure ≥140mmHg/18.4Pa or diastolic blood pressure ≥90mmHg/12.0kpa
Classification
Essential hypertension/idiopathic hypertension/hypertension
Systemic disease with systemic arteriosclerosis as the basic lesion
Cause
genetic and genetic factors
Overweight and obesity, high-salt diet and alcohol consumption
social psychological factors
physical activities
neuroendocrine factors
Pathogenesis
Long-term negative mental stimulation
Subcortical vasoconstrictor center predominates
Sympathetic nervous excitement
Renal vasoconstriction → renal ischemia → RAAS → blood volume ↑ → blood pressure ↑
sodium and water retention
Extracellular fluid↑, CO↑, arteriolar wall water content↑, peripheral resistance↑, arterial smooth muscle contractility↑→blood pressure↑
Types and pathological changes
Benign hypertension/progressive hypertension
installment
dysfunctional period
The basic disease is intermittent spasm of small arteries throughout the body; no organic disease; headache in the morning
arterial system disease stage
Arteriosclerosis
Hyalinization of arterioles is a characteristic morphological change of hypertension; it is found in arterioles of various organs throughout the body.
Cause
Repeated spasms → endothelial damage → plasma proteins penetrate into the endothelium and the tunica media secrete ECM from SMC → SMC apoptosis → hyaline degeneration of the wall
under the mirror
The tube wall is homogeneously red-stained, the tube wall is thickened, and the official cavity becomes smaller or even occluded.
Arteriolar sclerosis
Intimal fibrous thickening, media SMC proliferation, vessel wall thickening, and lumen stenosis
Aortic disease
May be accompanied by AS lesions
visceral disease stage
heart
Mainly manifested as left ventricular hypertrophy
Compensatory period - concentric hypertrophy Decompensation - eccentric hypertrophy, heart failure
kidney
Afferent and muscular small A sclerosis → nephron ischemia → atrophic fibrosis-granular pyknotic kidney
Primary granular pyknosis/arteriosclerosis
naked eye
Bilateral kidney symmetry decreases in size, weight, and texture becomes hard
Fine particles are evenly distributed on the surface
The cortex becomes thinner and the cortex-medullary boundary becomes blurred
perirenal adipose tissue
under the mirror
Glomerular arterial hyalinization, myotype small A sclerosis; glomerular atrophy, fibrosis, hyalinization due to ischemia
Compensatory hypertrophy of peripheral relatively intact glomeruli
brain
Brain edema
Hypertensive encephalopathy
Encephalomalacia
Cerebral hemorrhage/stroke/stroke
Often occurs in basal ganglia, internal capsule
retina
Fine sclerosis occurs in the central retina
Retinal edema, exudation, hemorrhage, optic disc edema
malignant hypertension/rapidly progressive hypertension
More common in young adults, with acute onset, early onset of renal failure, and death from heart failure, uremia, and cerebral hemorrhage within 1 year.
Lesion characteristics
necrotizing arteritis
Arteriolar wall fibrinoid necrosis
proliferative arteriosclerosis
Intima thickening, concentric layer thickening of blood vessel wall like onion
The lesions are most obvious in the kidneys and cerebral arteries
Rheumatism
Overview
Associated with Group A B-hemolytic Streptococcus infection
Allergy-autoimmune diseases
Mainly affects connective tissues and blood vessels throughout the body: main heart and joints; subcutaneous, brain, and blood vessels
Lesion characterized by rheumatic granuloma formation
Cause
cross-reactivity
Pathogenesis
Antigen-antibody cross-reaction mechanism
Basic lesions
Deterioration and exudation stage
Myxoid change and fibrinoid necrosis at the lesion site
With a small amount of lymph, plasma, neutrophils, and mononuclear cell infiltration
Proliferative/Granulomatous Phase
Features
Characteristic rheumatic bodies are formed on the basis of metamorphic exudation.
rheumatic body
The center is fibrinoid necrotic material, surrounded by rheumatoid cells, lymphocytes, and plasma cells
Rheumatic cells are large in size and can be single or multinucleated, with owl-eye or nematode-like nuclei.
Rheumatoid cells originate from macrophages adjacent to the lesion
Rheumatoid bodies are mainly distributed in the myocardial interstitium, subendocardium, and subcutaneous CT
fibrosis/sclerosis stage
Fibrin-like necrotic material is absorbed; rheumatoid cells → fibroblasts → produce collagen-rheumatoid body fibrosis → spindle scar
Diseases of various organs
rheumatic heart disease
rheumatic endocarditis
parts
Mainly involved heart valves: main mitral valve/mitral valve and aortic valve simultaneously
lesions
acute phase
naked eye
The valve becomes swollen, thickened, and loses its luster; the atretic edge of the valve is easily damaged → a bead-like, single-row, gray-white, translucent, wart-like excrescence is formed, as big as a millet, which is firmly adhered to the valve and is not easy to fall off.
under the mirror
Valvular collagen swelling, myxoid change, fibrinoid necrosis
The vegetation is a white thrombus composed of platelets and fibrin, with many inflammatory cells infiltrating at its base.
Typical rheumatic bodies are rare
Late stage of disease
Vegetation organization → scar → valve thickening, hardening, curling, shortening, valve leaflet adhesion → valvular heart disease
rheumatic myocarditis
Mainly involves myocardial interstitial connective tissue, especially around small blood vessels CT
lesions
Early days
Myocardial interstitial CT myxoid degeneration, fibrinoid necrosis → rheumatic bodies, focal distribution, spindle shape
later stage
Rheumatic corpus fibrosis→scarring
rheumatic epicarditis
Often accompanied by the first two, mainly exudation
serous effusion→pericardial effusion
Fibrinous exudation→Villous heart→A large amount of fiber cannot be absorbed, organized adhesions→Constrictive pericarditis
rheumatoid arthritis
Clinical features
Often involves large joints, manifesting as migratory joint pain
under the mirror
serous inflammation
May have Aschoff body formation
Generally no sequelae
rheumatic arteritis
Can involve large and small arteries
rheumatic lesions of the skin
annular erythema
exudative lesions
subcutaneous nodules
proliferative lesions
rheumatic disease of the brain
Involving brain/intracerebral arteries
Extravertebral system → chorea minor
infective endocarditis
Overview
Inflammatory diseases caused by direct invasion of the endocardium by pathogenic microorganisms such as bacteria or fungi
Characterized by the formation of vegetations containing bacteria or other pathogenic microorganisms on the heart valves
Pathogenesis
Can occur in patients without underlying heart disease
90% occur in patients with structural heart disease
Pathological changes and clinicopathological connections
acute infective endocarditis
subacute infective endocarditis
myocarditis
viral myocarditis
Primary myocarditis caused by cardiomyocyte-tropic virus
isolated myocarditis
diffuse interstitial myocarditis
A large number of lymphocytes, plasma cells and macrophages infiltrate. Myocardial cell necrosis is less
Idiopathic giant cell myocarditis
Focal necrosis and granuloma formation in the myocardium with red staining in the center and no structural necrosis, surrounded by infiltration of lymph, plasma, mononuclear and eosinophils, and a large number of multinucleated giant cells.
immunoreactivity
myocardial interstitial inflammation
Infiltration of eosinophils, lymphocytes, and monocytes can be seen in the myocardial interstitium and next to small blood vessels, and granuloma formation is encountered. Myocardial cells have varying degrees of deformation and necrosis.
valvular heart disease
concept
Organic lesions of the heart valve caused by congenital developmental abnormalities or acquired diseases, manifested as valve orifice stenosis or insufficient closure
Cause
The vast majority are rheumatic endocarditis and infective endocarditis. Atherosclerosis and syphilitic aortitis can affect the aortic valve. A few cases include valve degeneration, calcification and congenital developmental abnormalities.
mitral stenosis
Early days
Compensatory dilatation and hypertrophy of left atrium
Late stage
Left atrial decompensation, obstruction of pulmonary venous return, pulmonary congestion, edema or leakage bleeding - manifestations of left heart failure; long-term recurrence, triggering arterial hypertension, compensatory right ventricular hypertrophy - relative tricuspid valve insufficiency, right ventricular dysfunction , systemic venous congestion
Mitral valve insufficiency
Early days
Compensatory dilatation and hypertrophy of left atrium
Late stage
Compensated and decompensated hypertrophy of the left ventricle, followed by pulmonary congestion, pulmonary hypertension, right ventricular and atrial decompensation - right heart failure and systemic venous congestion
aortic valve insufficiency
Early days
Regurgitation of blood through aortic valve orifice
Late stage
Left heart failure, pulmonary congestion, pulmonary hypertension and right heart failure occur in sequence
aortic stenosis
Early days
Obstruction of blood removal from the left ventricle
Late stage
Left heart failure, pulmonary congestion, pulmonary hypertension and right heart failure occur in sequence