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Pathology—Cardiovascular Disease
The focus of the pathology examination summarizes atherosclerosis, hypertension, rheumatism, infective endocarditis, valvular heart disease, cardiomyopathy, etc.
Edited at 2024-01-12 18:49:53
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Pathology—Cardiovascular Disease
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- Outline
Cardiovascular diseases
atherosclerosis
Types of arteriosclerosis
Atherosclerosis of large and medium arteries
medial arterial calcification
Arteriosclerosis (hyalinosis)
concept
lipid deposition in arterial intima
Prevalent site—large and medium-sized arteries
Etiology and pathogenesis
Risk factors (hyperlipidemia, endothelial damage, increased collagen)
Hyperlipidemia (initiating stage)
LDL and VLDL (small and dense) promote the occurrence of AS
Oxidized LDL is the most important atherogenic factor
Causes damage to endothelial cells and smooth muscle cells
Increased permeability of the inner membrane to lipids
Mononuclear (macrophages) cells in the blood and smooth muscle cells in the media migrate into the intima → phagocytose lipids and form foam cells
HDL anti-AS effect
secondary hyperlipidemia
diabetes
hyperinsulinemia
Hypothyroidism, nephrotic syndrome
Hypertension (endothelial damage)
Smoking (endothelial damage, promotion of LDL oxidation, smooth muscle cell proliferation)
genetic factors
LDL receptor gene mutation → familial hypercholesterolemia
other factors
age, gender, obesity
Pathogenesis
Two major sources of foam cells: monocytes (macrophages) and smooth muscle cells
LDL penetrates into the subendothelial space through endothelial cells, and monocytes migrate into the intima
Ox-LDL binds to scavenger receptors on the surface of macrophages and is taken up, forming foam cells.
SMCs in the media migrate into the intima through the windows of the internal elastic membrane to phagocytose lipids and form foam cells.
SMC synthesizes extracellular matrix and forms fibrous cap
Ox-LDL causes necrosis and disintegration of foam cells, forming porridge-like necrosis
Basic pathological changes
Fatty streak stage
naked eye
Yellow spots and stripes
Location—Posterior wall of aorta branch opening
under the mirror
A large number of foam cells under the intima
fibrous plaque stage
naked eye
Gray-yellow or gray-white patches raised on the surface of the intima
under the mirror
Surface - fibrous cap (collagen fibers, derived from smooth muscle cells)
Internal - foam cells, SMC, inflammatory cells
Atheromatous plaque stage (atheroma stage)
naked eye
Intimal surface: gray-yellow plaque
Section: The plaque both bulges toward the surface of the intima and compresses the media deeply.
under the mirror
Fibrous cap aging (hyalinization)
Deep - necrotic material cholesterol crystals
Bottom and edges - foam cells, granulation tissue, inflammatory cells
Media - atrophy and thinning
secondary changes
Vascular lumen narrowing (medium arteries)
Calcification, where blood vessels become hard and brittle (dystrophic calcification)
Bleeding within the plaque, forming a hematoma (most common)
Plaque rupture, forming atheroma-like ulcers Cholesterol emboli
After plaque ruptures and forms an ulcer, collagen is exposed → thrombosis (platelet thrombosis)
Aneurysm formation, which can cause massive bleeding
Diseases of major arteries
aortic atherosclerosis
Predisposed areas
The posterior wall of the abdominal aorta and the openings of its branches
harm
Rupture of aortic aneurysm, rupture of dissecting aneurysm causing massive bleeding
cerebral atherosclerosis
Predisposed areas
basilar artery, circle of Willis, middle cerebral artery
harm
Brain atrophy, cerebral infarction (encephalomalacia), cerebral hemorrhage
renal atherosclerosis
Predisposed areas
The opening of the renal artery or the proximal end of the aorta
harm
Renal atrophy, renal infarction, renal hypertension → AS pyknotic kidney (the infarct is organized to leave a large sunken scar, and multiple scars can shrink the kidney)
Atherosclerosis of extremities
Predisposed areas
lower extremity arteries
harm
intermittent rash
Limb atrophy, limb infarction, dry gangrene
Coronary Atherosclerosis (CHD)
Prevalent site—left anterior descending branch
Features
The plaque is segmental, crescent-shaped in cross section, and eccentric
Luminal stenosis with vasospasm
Only when coronary atherosclerosis causes myocardial ischemia and hypoxia is it called coronary heart disease (CHD).
reason
Plaque causes lumen stenosis and secondary spasm → insufficient blood supply to the coronary arteries (less blood supply)
Increased myocardial load → increased myocardial oxygen consumption (more use)
clinical manifestations
Angina pectoris
S-T segment decreases
clinical manifestations
Paroxysmal precordial pain, radiating to the left upper limb, lasting several minutes
mechanism
Hypoxia causes accumulation of metabolic substances, stimulating afferent nerves and causing pain
type
stable angina pectoris
unstable angina
variant angina
ending
Relief after taking nitrates, multiple attacks can cause myocardial infarction
Myocardial infarction MI
clinical manifestations
Severe and persistent substernal pain
Nitrates cannot relieve
Complicated arrhythmia, heart failure
mechanism
Coronary atherosclerosis
Additional triggers (overexertion, tachycardia, shock) lead to cardiac overload
Classification
Subendocardial MI
S-T segment is not elevated
transmural MI
S-T segment elevation (myocardial damage), pathological Q wave (myocardial necrosis), late inverted "V" T wave (early towering) (myocardial ischemia)
Pathological changes—anemic infarction
in general
6 hours ago—no visible changes
6 hours later—the infarct becomes pale and irregular in shape.
After 8 to 9 hours - earthy color
Light microscopy
Early stage—myocardial coagulative necrosis
Day 4—Inflammatory congestion zone appears around the infarct
Day 7—Granulation tissue
3 weeks—the infarct becomes organized and scarring forms
Biochemistry-myocardial enzyme spectrum
Glycogen reduction
Elevated myoglobin
Aspartate aminotransferase SGOT, alanine aminotransferase SGPT, creatine phosphokinase CPK, lactate dehydrogenase increase LDH
MI complications
heart failure
ruptured heart
ventricular aneurysm
mural thrombus
cardiogenic shock
acute pericarditis
Arrhythmia
myocardial fibrosis
Pathological changes
naked eye
White fibrous strips on the heart wall, enlargement of the heart, dilation of the cardiac chambers, and thickening of the endocardium
under the mirror
Extensive myocardial fibrosis and scarring
Diffuse vacuolation of subendocardial cardiomyocytes
sudden coronary death
two conditions
Except suicide and homicide
Moderate to severe AS in more than one coronary artery, may have complex lesions, but no other fatal diseases → acute myocardial ischemia, severe arrhythmia
hypertension
Basic lesions
systemic arteriosclerosis
Diagnostic criteria
Systolic blood pressure ≥140mmHg and/or diastolic blood pressure ≥90mmHg
risk factors
family inheritance
Obesity, excessive sodium intake, alcohol consumption
social psychological factors
physical activities
neuroendocrine
Pathogenesis
genetic mechanism
Mechanism of high blood pressure
Blood pressure is mainly determined by cardiac output and peripheral vascular resistance of the systemic circulation
Cardiac output—heart rate, myocardial contractility
total peripheral resistance
vasomotion state
Resistance small vessel structural status
acute regulation of blood pressure
Achieved through sympathetic nerve activity and baroreceptors
Sympathetic neurotransmitters excite cardiac and renal B1 receptors
Sympathetic-adrenomedullary system, catecholamine release
chronic regulation of blood pressure
Kidney regulation of total body fluid volume
RAAS regulation (AngII is a central link in the pathogenesis of hypertension)
mechanism
Strong contraction of arterioles increases peripheral resistance, strong contraction of venules increases blood return to the heart
Acts on sympathetic nerves and promotes vasoconstriction
Promote aldosterone release and increase circulating blood volume
Promote the release of antidiuretic hormone and increase circulating blood volume
Directly acts on renal vasoconstriction, decreases urine output, and increases blood volume
endothelial dysfunction
Insulin resistance
vascular remodeling mechanism
Classification
Essential hypertension (90-95%)
benign hypertension
Pathological changes
dysfunctional period
No morphological changes
Intermittent spasm and contraction of small arteries throughout the body
clinical
Intermittent headaches and fluctuating increases in blood pressure
Treatment is most effective during this period, but is often overlooked
Arteriopathy stage
systemic arteriosclerosis
Arteriosclerosis (hyalinosis)
Arterioles most commonly affected
renal afferent arteriole
retinal artery
mechanism
Long-term spasm of arterioles, increased blood pressure → endothelial damage, increased permeability → penetration of plasma proteins into the subendothelial space
Long-term spasm of arterioles and elevated blood pressure → hypoxia of medial smooth muscle cells → cell degeneration and necrosis → increased secretion of collagen fibers
Glassy substance → Thickening of arteriole wall → Small lumen
Plasma proteins Extracellular matrix Collagen fibers Proteoglycans
under the mirror
The lumen of the arterioles becomes smaller and the walls are thickened and stained homogeneously red.
muscular arteriosclerosis
Proliferation of collagen fibers and elastic fibers in the intima, and rupture of the internal elastic membrane
Medial smooth muscle cells proliferate and hypertrophy, secreting large amounts of collagen fibers and elastic fibers
Large and medium-sized arteries have no obvious changes or are complicated by AS
visceral disease stage
heart
Compensatory phase—concentric hypertrophy (complicated by angina)
Heart weight reaches more than 400g
Left ventricular wall thickness 1.5~2cm
Thickening of nipple muscle column
The heart chambers are not dilated
Decompensation – eccentric hypertrophy (heart failure)
Increased load on the left ventricle → Gradual decompensation of the heart leading to left ventricular dilation → Severe heart failure
kidney
under the mirror
Hyalinization of the glomerular afferent artery: the glomerulus atrophies → fibrosis → hyalinization, and the renal tubule atrophies and disappears
Interstitial fibrous tissue proliferation and lymphocyte infiltration
Compensatory hypertrophy of glomeruli and compensatory dilation of renal tubules
naked eye
primary granular pyknotic kidney
Kidney size decreases, weight decreases, texture becomes hard, surface is covered with numerous uniform red fine particles
On the cut surface, the renal cortex becomes thinner, the corticomedullary junction is unclear, and the renal pelvis and perirenal adipose tissue proliferate significantly.
clinical
Mild to moderate proteinuria
Polyuria, nocturia, low specific gravity urine
Increased blood creatinine and urea nitrogen → uremia
brain
Cerebral edema/hypertensive encephalopathy
Hypertension → increased permeability of small arteries in the brain → large amounts of fluid entering the brain tissue → increased intracranial pressure → sharp rise in blood pressure, severe headache, nausea and vomiting (hypertensive crisis)
Encephalomalacia (liquefied necrosis)
mechanism
Cerebral arteriosclerosis and spasm → ischemia of blood supply area and infarction
in general
Most microinfarcts
Light microscopy
Liquefied necrosis of infarction, mesh-like
cerebral hemorrhage
High blood pressure is the most serious and fatal complication
Predisposed areas
Basal ganglia, internal capsule
reason
Cerebral arteriosclerosis makes the walls of the arteries brittle → blood pressure increases and blood vessels rupture
Decreased elasticity of blood vessel walls → formation of micro-aneurysms → increased blood pressure, rupture and bleeding
Lenticulostriate arteries are prone to rupture (most common in the basal ganglia)
Clinical symptoms
Internal capsule hemorrhage → contralateral hemiplegia and sensory loss
Left cerebral hemorrhage → aphasia
Bleeding breaks into the brain ventricle → sudden coma and death
retinal arteriopathy
Arteriosclerosis of the central retinal artery
It can be observed through an ophthalmoscope, so it is often used clinically as a representative of systemic small arteriosclerosis.
Mild - blood vessels tortuous, enhanced reflection
Moderate - indentation at arteriovenous intersection
Severe—retinal hemorrhage, blurred vision
malignant hypertension
Common in young adults
Blood pressure value exceeds 230/130mmHg
Acute onset, death from renal failure, cerebral hemorrhage, or heart failure within more than one year
lesions
arteriolar fibrinoid necrosis
proliferative arteriosclerosis
secondary hypertension
Secondary to other diseases (renal artery stenosis, nephritis)
Rheumatism
Lesion characteristics
Rheumatic corpuscles (Ashaofu corpuscles)
clinical manifestations
More common in teenagers
Acute phase—rheumatic fever
fever
Heart and joint damage
Annular erythema, subcutaneous nodules
minor chorea
Chronic phase—rheumatic valvular heart disease
Cause
Related to beta-hemolytic streptococcus infection, there are cross-antigens (antigen-antibody cross-reactions) in tissues such as heart valves and brain
Not a direct result of streptococci
Pathological changes
Deterioration and exudation period (1 month)
spoil
degeneration - myxoid degeneration of connective tissue
Necrosis - fibrinoid necrosis of collagen fibers
ooze
Serum, cellulose
Macrophages, lymphocytes, plasma cells (no neutrophils)
Proliferative/Granulomatous Phase (2-3 months)
Characteristic granulomatous lesions—rheumatic bodies/Ashauf bodies (diagnostic significance)
parts
Myocardial interstitial, subendocardial, subcutaneous connective tissue
Element
Central—fibrinoid necrosis
Peripheral—rheumatoid cells, rheumatoid giant cells
Mostly located next to small blood vessels in the myocardial interstitium
The cells are large in size and have large nuclei (owl-eye-shaped in cross-section and caterpillar-like in longitudinal section).
Peripheral—macrophages, lymphocytes, plasma cells, fibroblasts
Fibrosis stage/sclerosis stage/scar stage/healing stage (2-3 months)
Rheumatoid bodies transform into small spindle scars
Fibrinoid necrosis is absorbed
Rheumatoid cells transform into fibroblasts, which produce collagen fibers
Rheumatic diseases of various organs
rheumatic endocarditis
Predisposed areas
Mitral valve
Features
acute phase
Vegetation formation on the valve atretic margin (with small focal fibrinoid necrosis)
under the mirror
White thrombus
naked eye
Off-white, translucent, millet-sized, arranged in a single row like beads, firmly attached
Chronic phase
McCallum spots
Valvular disease—valvular stenosis, insufficiency
clinical
Fever, anemia, cardiac murmur
rheumatic myocarditis
parts
left ventricle, ventricular septum, left atrium, left atrial appendage
Myocardial interstitium, near blood vessels
Typical basic lesions of rheumatism
rheumatic epicarditis
Mainly serous/cellulose exudation - villous heart →
→Recover, absorb
→Organization→Constrictive pericarditis
rheumatoid arthritis
big joint
serous inflammation
migratory pain
Does not cause joint deformity
skin lesions
Diagnostic significance—Annular erythema (exudative lesion)
Diagnostic significance—subcutaneous nodules (subcutaneous on the extensor side of large joints) (proliferative lesions)
rheumatic arteritis
parts
arteriole
lesions
acute phase
Myxoid degeneration of arterial wall, fibrinoid necrosis, rheumatic bodies
later stage
Fibrosis and thickening of the blood vessel wall, narrowing of the lumen, and thrombosis
rheumatic encephalopathy
Children, more common in girls
chorea minor
infective endocarditis
acute infective endocarditis
Cause
Pyogenic bacteria - Staphylococcus aureus
infection process
Pathogenic bacteria infect a certain part of the body (purulent osteomyelitis) → bacteria enter the blood and cause sepsis → invade the originally normal aortic valve and mitral valve → acute suppurative valvulitis
naked eye
Huge vegetation on valve atresia margin
Large, soft, grayish-yellow, easy to fall off, and can damage chordae tendineae
under the mirror
Purulent exudate, white thrombus, necrotic tissue, bacterial colony
clinical
The onset is sudden, the course is short, and the condition is severe. Most patients die within days or weeks.
Acute valvular insufficiency, septic infarction and abscess, death
subacute infective endocarditis
Cause
viridans streptococci
infection process
Pathogenic bacteria cause tonsillitis, osteomyelitis/iatrogenic procedures → bacteremia → vegetations form on the diseased mitral valve/aortic valve, which can destroy the chordae tendineae
Pathological changes
The heart is the main thing, not just the heart
heart
naked eye
Vegetation forms on the atretic edge of the diseased valve: polyp-shaped or cauliflower-shaped, crispy in texture and easy to fall off
under the mirror
white thrombus, necrotic tissue, bacterial colony, neutrophils
Granulation tissue hyperplasia at the base of ulcer
lesions
Valvular orifice stenosis, insufficiency
Blood vessel
Vegetation falls off and forms emboli (brain, kidney, spleen) → aseptic infarction
allergy
Glomerulonephritis, Osler's nodes
septicemia
Fever, splenomegaly, small bleeding spots in skin and mucous membranes, anemia
clinical
The course of the disease is long, lasting several months or even more than a year.
valvular heart disease
Lesion characteristics
Hemodynamic changes
Classification
valve orifice stenosis
Valvular insufficiency
combined valvular disease
Mitral stenosisMS
Cause
Rheumatic fever (major), infective endocarditis
naked eye
Early stage - mild valve thickening - septum-like
Late stage - valve thickening and hardening - fish mouth shape
landmark lesions
Adhesions between adjacent valve leaflets
Does not involve the left ventricle
Hemodynamics and cardiac changes
Early days
Diastolic rumble murmur
Mitral valve stenosis → Obstruction of blood flow from the left atrium to the left ventricle → Compensatory dilation and hypertrophy of the left atrium → Blood quickly passes through the stenosis under pressure
later stage
Left heart failure - dyspnea, cyanosis, coughing up bloody frothy sputum
Left atrial decompensation, blood stasis → obstruction of pulmonary venous return → pulmonary congestion, pulmonary edema
Increased pulmonary venous pressure → reflex pulmonary arteriole contraction and spasm → increased pulmonary artery pressure → compensatory right ventricular hypertrophy → right ventricular decompensation and dilatation = relative tricuspid valve insufficiency → right heart failure, systemic circulation congestion
clinical manifestations
Heart failure - jugular vein distention, liver congestion and enlargement, lower limb edema
Apical diastolic rumble murmur
X-ray - pear-shaped heart: dilated hypertrophy (late shrinkage) of the left atrium, increased dilatation of the right ventricle
Mitral valve insufficiency
Cause
Rheumatic endocarditis (major), infective endocarditis
Hemodynamics and cardiac changes
Apical global systolic blowing murmur
Mitral regurgitation → left ventricular systole: part of the blood refluxes into the left atrium
Compensatory left atrial hypertrophy
The left atrium receives both blood from the pulmonary veins and blood from the left ventricle
compensatory left ventricular hypertrophy
Increased volumetric load
After decompensation of the left heart → pulmonary congestion → pulmonary hypertension → compensatory hypertrophy of the right heart and then failure, congestion of the systemic circulation
clinical manifestations
Apical global systolic blowing murmur
X-ray - spherical heart: dilated hypertrophy of the four cardiac chambers
aortic stenosis
Cause
Degenerative diseases of the elderly, AS
Hemodynamics and cardiac changes
Rough, ejection systolic murmur
Aortic stenosis → Obstruction of blood discharge from the left ventricle → Compensatory hypertrophy of the left ventricle (concentric hypertrophy) → Decompensation of the left heart, left heart failure
clinical manifestations
Rough, ejection systolic murmur
X-ray—boot-shaped heart: left ventricular concentric hypertrophy
Angina pectoris (main stenosis comes with angina pectoris)
aortic valve insufficiency
Cause
Rheumatism, infective endocarditis
Hemodynamics and cardiac changes
Aortic valve insufficiency → part of the blood refluxes back to the left ventricle during diastole → compensatory hypertrophy of the left ventricle
clinical
Auscultation of aortic valve area: diastolic blowing murmur
Increased pulse pressure difference (= blood flow is intermittent = carotid pulse)
Cardiomyopathy
type
dilated (congestive) cardiomyopathy
Most common, sudden death in young adults, more men than women
Features
Progressive heart enlargement, highly dilated ventricular chambers, and reduced myocardial contractility
hypertrophic cardiomyopathy
family inheritance
Features
Ventricular hypertrophy, the ventricular cavity becomes smaller
restrictive cardiomyopathy
Features
Restricted ventricular filling and progressive myocardial fibrosis
Arrhythmogenic right ventricular cardiomyopathy
Keshan disease
Features
Severe degeneration and necrosis of the myocardium, scar formation, and enlargement of the heart into a spherical shape
Endemic cardiomyopathy, associated with low selenium