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Chapter 6 Cardiovascular System Diseases
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Chapter 6 Cardiovascular System Diseases
- DeepSeek User Guide Collection
In order to help everyone use DeepSeek more efficiently, a collection of DeepSeek guide mind map was specially compiled! This mind map summarizes the main contents: Yitu related links, DS profile analysis, comparison of DeepSeek and ChatGPT technology routes, DeepSeek and Qwen model deployment guide, how to make more money with DeepSeek, how to play DeepSeek, DeepSeek scientific research Application, how to import text from DeepSeek into MindMaster, the official recommendation of DeepSeek Wait, allowing you to quickly grasp the essence of AI interaction. Whether it is content creation, plan planning, code generation, or learning improvement, DeepSeek can help you achieve twice the result with half the effort!
- DeepSeek 30 feeding level instructions
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- Voice recognition commercial solution
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cardiovascular system diseases
Section 1 Atherosclerosis atherosclerosis,AS
Features
Most common cardiovascular diseases
Mainly affects large and medium arteries
More common in middle-aged and elderly people, with the fastest development among 40-50 years old
Basic lesions:
Intimal lipid deposition, focal fibrosis, wall thickening, lumen stenosis and weakened elasticity
1. Risk factors for atherosclerosis
Dyslipidemia (hyperlipidemia) Major risk factors for atherosclerosis
Lipids are transported in the blood in the form of lipoproteins
CM, VLDL, LDL, IDL, HDL
hypertension
reason
Strong blood flow impact and mechanical pressure
Causes endothelial damage and increases intimal permeability to lipids
Affects arterial wall connective tissue metabolism
Renin, catecholamines, and angiotensin related to hypertension influence arterial wall metabolism
Lipid penetrates into the intima and foam cells form
smoking
reason
Increased blood CO concentration and hypoxic damage to endothelial cells
LDL oxidation
Activate certain mutagenic substances
Diabetes and hyperinsulinemia
diabetes
Triacylglycerol, VLDL increases, HDL decreases; hyperglycemia causes LDL glycosylation and hypertriglyceridemia
hyperinsulinemia
The higher the insulin levels, the lower the HDL levels
other
Genetics, age, gender, weight, infection
2. The pathogenesis of AS (understand)
Lipid factors
hyperlipidemia
endothelial cell damage Increased endothelial permeability
Lipids are deposited within the membrane
Macrophage clearance response and medial smooth muscle cell proliferation
AS
endothelial cell damage
The role of monocytes and macrophages
Smooth muscle cells migrate and proliferate
3. Pathological changes of AS (key points)
site of occurrence
Large and medium arteries throughout the body
Arterial bifurcations, branch openings, and convex curved surfaces of blood vessels are areas where plaques are likely to occur.
Basic pathological changes
Fatty streak
naked eye
Dot-like or striped yellow lesions that are not raised or slightly raised in the intima
Often located at the opening of a blood vessel branch
light microscope
There are a large number of foam cells under the intima of the lesion. Foam cells are large in size and round or oval in shape. Contains a large number of small vacuoles
fibrous plaque
naked eye
Irregular raised patches are scattered on the intimal surface, and the color changes from light yellow or gray-yellow to porcelain white.
under the mirror
fiber cap
lipid domain
base
atheromatous plaque
naked eye
Gray-yellow plaques on the intima surface, compressing the upper and lower structures. A fibrous cap can be seen on the surface of the cut surface, and yellow or yellow-white porridge material is found in the deep layer.
under the mirror
A large amount of amorphous necrosis, cholesterol crystals and calcium salt deposition under the fibrous cap; the media becomes thinner
secondary lesions
intra-plaque bleeding
plaque rupture
thrombosis
Calcification
aneurysm formation
vascular lumen stenosis
AS of vital organs
aortic atherosclerosis
parts
It occurs most often at the openings of the posterior wall of the aorta and its branches.
Lesions: fibrous and atheromatous plaques, secondary atherosclerotic ulcers, aortic aneurysm
Impact: Vascular obstruction generally does not occur, but aneurysm rupture can cause fatal bleeding.
Coronary AS and coronary AS heart disease
Carotid artery and brain AS
parts
Commonly found at the origin of the internal carotid artery, basilar artery, middle cerebral artery and circle of Willis
Diseases and effects
Arterial wall thickening, hardening, narrowing, and decreased elasticity
Brain atrophy, cerebral infarction, cerebral hemorrhage
Renal AS
parts
It usually occurs at the opening of the renal artery and the proximal end of the aorta, the interlobar artery and the arcuate artery may be affected.
Diseases and effects
Plaques cause lumen stenosis, renal tissue ischemia and necrosis, parenchymal atrophy, and interstitial fibrous tissue proliferation. AS pyknotic kidney
Limb AS
parts
Arteries of the lower limbs are common, such as the iliac artery, femoral artery, and anterior and posterior tibial arteries.
Diseases and effects
intermittent claudication
Limb atrophy
dry gangrene
Mesenteric AS
Influence
Common infarction, paralytic ileus, shock
Section 2 Coronary Atherosclerosis and Coronary Atherosclerotic Heart Disease
coronary atherosclerosis
parts
The left anterior descending coronary artery is the most common The rest are the right main trunk, left main trunk or left circumflex branch, and posterior descending branch. in
left anterior descending coronary artery
right coronary artery
Left circumflex branch
Pathological changes
It mostly occurs on the heart wall side of blood vessels. The plaques are crescent-shaped and eccentric. The blood vessel walls are thickened, hardened, and narrowed.
Stenosis grade (1-25-50-75-75) Level 1, 2, 3 and 4
clinical manifestations
coronary heart disease
concept
Myocardial dysfunction and/or organic disease caused by coronary artery stenosis and insufficient blood supply is also called ischemic heart disease, or coronary heart disease for short. Coronary atherosclerosis accounts for the majority of coronary heart disease.
Performance
Angina pectoris, myocardial infarction, sudden cardiac death
Causes and pathogenesis
Cause
Coronary atherosclerosis, the most common
coronary artery spasm
Pathogenesis
coronary artery insufficiency
Luminal stenosis greater than 50%, secondary lesions and coronary artery spasm
Increased myocardial oxygen consumption
Increased myocardial load caused by various reasons
Clinical manifestations and types
Angina pectoris
concept
clinical manifestations
type
stable angina
Mild angina pectoris occurs when excessive physical activity increases and myocardial oxygen consumption increases
Blockage greater than 75%
unstable angina
Unstable, can occur during load or rest; attack frequency and duration are progressively aggravated
Often triggered by coronary atherosclerotic plaque rupture and thrombosis
variant angina
There is usually no obvious trigger, and it often occurs when resting or waking up from a dream.
Significant stenosis of the coronary arteries, or caused by episodic spasm
myocardial infarction
concept
It refers to a large-scale myocardial necrosis caused by the sudden reduction or interruption of coronary blood supply, causing persistent ischemia in the blood supply area.
Clinical manifestations:
Severe and long-lasting retrosternal pain that cannot be completely relieved by nitrate preparations or a short rest can lead to arrhythmia, shock or heart failure.
type
subendocardial myocardial infarction
lesion site
1/3 of the myocardium on the chamber side of the ventricular wall, and also affects the carotid columns and papillary muscles
Morphological characteristics
Multiple and small focal necrosis, which may coalesce and form severe circular infarcts
The necrotic area is not limited to a certain branch area, but is irregularly distributed around the ventricle.
regional myocardial infarction
scope
Transmural myocardial infarction, involving the entire thickness of the ventricular wall, the infarct site and the occluded coronary artery branch supply blood The area is consistent. The scope is generally large, the shape is irregular, and the infarct area is 2.5-10 square centimeters. Infarction that does not involve the entire thickness but is more than 2/3 deep is called thick-walled infarction.
Predisposed areas
Left anterior descending coronary artery (50%) Right coronary artery (25%-30%) Left circumflex coronary artery (15%-20%)
Pathological changes
Gross: anemic infarction
Under the mirror:
Blood biochemical indicators
Decreased glycogen in myocardial cells
Increased levels of myoglobin, myosin and troponin in serum
Increased aspartate aminotransferase GOT, creatine phosphokinase CPK, and lactate dehydrogenase LDH in the blood
Complications and consequences
ruptured heart
aneurysm formation
Abdominal wall thrombosis changes
acute pericarditis
Arrhythmia
cardiac insufficiency
cardiogenic shock
Myocardial fibrosis (understand) myocardial fibrosis
The result of persistence of myocardial fibers and repeated aggravation of ischemia and hypoxia caused by moderate and severe coronary atherosclerotic stenosis.
Pathological changes
naked eye
light microscope
Sudden coronary death (sudden cardiac death)
Atherosclerosis is the most common form of sudden cardiac death. In adults aged 30-49 years, men are more common than women, and it mostly occurs on the basis of coronary atherosclerosis.
Section 3 Hypertension
Overview
One of the most common cardiovascular diseases, it is a clinical syndrome mainly characterized by sustained elevation of systemic arterial blood pressure. Sustained elevation of arterial blood pressure can lead to a clinical syndrome of cardiac, cerebral, renal, and vascular changes.
Adult circulatory systolic blood pressure ≥140 mmHg (18.4kPa) or/and diastolic blood pressure ≥ 90 mmHg (12.0kPa)
Essential hypertension (90%-95%)
Main clinical manifestations
Increased systemic arterial blood pressure
Basic lesions
systemic arteriosclerosis
More common in middle-aged and elderly people
Secondary hypertension (5%-10%)
Increased blood pressure that occurs with certain medical conditions
Such as chronic glomerulonephritis, renal artery stenosis, pyelonephritis, mineralocorticoidism, adrenal tumors
Causes and pathogenesis
Cause
genetic factors
dietary factors
Occupational and psychosocial stress factors
neuroendocrine factors
other factors
Pathogenesis
genetic mechanism
The mechanism of hypertension
Types and pathological changes
Benign hypertension (slowly progressive hypertension) Slow onset and long course of disease
dysfunctional period
In the early stage of the disease, small arteries throughout the body spasm intermittently and blood pressure rises. There are no organic changes in the blood vessels, and clinical blood pressure fluctuates.
arterial system disease stage
Arteriosclerosis
Main pathological features of hypertension: hyaline degeneration of arterioles
Light microscopy: Arteriole wall thickening
Arteriolar sclerosis
Mainly involves renal interlobular arteries, arcuate arteries and small arteries of the brain
Arteriosclerosis
Blood pressure continues to rise and loses its volatility
visceral disease stage
heart disease
compensatory period
naked eye
The left ventricular wall is thickened, the papillary muscles and columns are thickened, and the cardiac chamber is not dilated but is relatively narrowed, which is called concentric hypertrophy.
decompensation period
naked eye
The heart enlarges, the ventricular wall becomes thinner, the ventricular cavity is significantly expanded, and the flesh column and Papillary muscles become flattened, forming eccentric hypertrophy
light microscope
Myocardial cells become thickened and elongated, and their nuclear hypertrophy and deep staining
nephropathy
Gross: primary granular pyknotic kidney
The volume is reduced, the surface is diffusely granular, the cortex on the cut surface is thinned, and the adipose tissue around the renal pelvis increases.
Light microscopy: showing changes in the two sets of nephrons
Some glomeruli have fibrosis and hyaline degeneration, and the corresponding renal tubules shrink and disappear. Other glomeruli enlarge due to compensation, and the tubules also expand compensatoryly.
brain lesions
cerebral edema
Hypertensive encephalopathy
Encephalomalacia
cerebral hemorrhage
Location: Commonly found in the basal ganglia and internal capsule, followed by the white matter of the brain, pons and cerebellum
Retinopathy (understanding) mainly refers to the heart, brain and kidneys
Arteriosclerosis of the central arteries is divided into four levels
Malignant hypertension (rapidly progressive hypertension)
Basic features
It tends to occur in young people and can be malignant at the beginning or evolve from a slow-progressing type.
If blood pressure rises sharply above 230/130mmHg in a short period of time, hypertensive encephalopathy and early renal failure may occur.
Pathological changes
The characteristic lesions are proliferative endarteritis and necrotizing arteritis, mainly affecting the kidneys.
Section 4 Rheumatism
Overview
Rheumatism is an allergic disease associated with Group A B-hemolytic Streptococcus infection
The lesions mainly involve the connective tissue and blood vessels throughout the body, forming characteristic rheumatic granulomas, which most often invade the heart and joints. Heart disease is the most serious, mostly occurring between the ages of 5 and 15, with the peak incidence between the ages of 6 and 9.
Cause and pathogenesis
Cause
Associated with group A B-hemolytic Streptococcus infection
in accordance with
A history of upper respiratory tract infection before onset of illness
The anti-“O” titer in the patient’s blood increases when the patient becomes ill
No streptococci were detected in the lesions
Certain components of Streptococcus cross-react with certain components in the body
Pathogenesis
Antigen-antibody cross-reaction theory
Pathological changes
Basic lesions
It mainly occurs in the collagen fibers of anterior connective tissue, and the lesions are most obvious in the heart, blood vessels, serosa, etc.
Characteristic lesions: rheumatoid bodies
Divided into three stages according to the course of the disease
Deterioration and exudation stage
Early stage of rheumatism
Myxoid degeneration and fibrinoid necrosis occur in the connective tissue at the lesion site
Accompanied by transverse fibrin exudation and infiltration of lymphocytes, plasma cells and monocytes
The secondary lesion lasts for one month
Proliferative phase (granulomatous phase)
Characteristic rheumatoid bodies can be seen in the connective tissue on the basis of deterioration and exudation.
rheumatoid body concept
Groups of rheumatoid cells gather in fibrinoid necrosis lesions, and are spindle-shaped or oval nodular lesions composed of a small number of lymphocytes and plasma cells, called rheumatoid bodies (Aschoff bodies).
This lesion lasts for 2-3 months
Fibrosis phase (healing phase)
The fibrinoid necrosis in rheumatoid granuloma is gradually absorbed, and fibroblasts gradually appear to produce collagen fibers.
Rheumatoid bodies gradually become fibrotic, forming spindle-shaped scars
February-March
Diseases of various organs
rheumatic heart disease
rheumatic endocarditis
Site: Mainly invading valves
Mitral valve
Mitral valve Aortic valve
Tricuspid and pulmonary valves are rarely affected
Valvular pathological changes can be divided into two stages
Early stage
Gross: Verrucous endocarditis
Microscopically: composed of platelets and fibrin, accompanied by small focal fibrinoid necrosis, and may have a small number of Asauf cells.
later stage
chronic valvular heart disease McCallum spots
rheumatic myocarditis
Location: Myocardial interstitial connective tissue, commonly found in the left ventricle, septum, left atrium and left atrial appendage
Lesion: rheumatic body
rheumatic pericarditis
Location: Visceral layer of epicardium
Lesions: serous and fibrinous exudates
Serous epicarditis-epicardial effusion
Fibrinous epicarditis - villous heart
clinical manifestations
Outcome: constrictive epicarditis
rheumatoid arthritis
Location: Often involving large joints, shoulders, wrists, elbows, knees, and ankles
lesions
clinical manifestations
rheumatic arteritis
Location: Both large and small arteries can be affected, with small arteries being more common.
lesions
acute phase
later stage
skin lesions
In the acute stage of rheumatism, annular erythema and subcutaneous nodules may appear on the skin, which has diagnostic significance.
annular erythema
Site: Skin of trunk and limbs
lesions
Naked eye: The center of the lesion is normal in color and surrounded by a red ring or semi-ring.
Microscopically: exudative lesions
Disappears in about 1-2 days
subcutaneous nodules
Location: Commonly found in the subcutaneous connective tissue on the sides of elbows, wrists, knees, ankles and other joints, round or oval, 0.5-2cm in diameter
Lesion: proliferative lesion
rheumatic encephalopathy
Rheumatoid arteritis and subcortical encephalitis
Location: Cerebral cortex, basal ganglia, thalamus and cerebellar cortex
Lesions: nerve cell degeneration, glial cell proliferation and glial nodule formation.
Clinical: chorea minor with extrapyramidal involvement
Section 5 Infectious Endocarditis (Understanding) (infective endocarditis)
acute infective endocarditis
subacute infective endocarditis
Overview
Mainly caused by infection with less virulent viridans streptococci. Vegetation often forms on existing diseased areas of the valve
Main pathological changes
heart
Location: Mitral valve and aortic valve
To the naked eye: vegetations form on the valves, looking dirty and grayish-yellow.
Under the microscope: composed of platelets, fibrin, neutrophils, necrosis and bacteria
Clinical: cardiac signs and sepsis
Blood vessel
Arterial embolism: more common in the brain, followed by the kidney, spleen, and heart
Vasculitis:
clinical manifestations
Bleeding of skin, mucous membranes and fundus
European summary
nephropathy
Allergy: focal or diffuse glomerulonephritis
septicemia
long-term fever
Bleeding of skin, mucous membranes and fundus of eyes
Splenomegaly, hypersplenism, leukocytosis
Section 6 Heart Valvular Disease
Concept: Refers to organic lesions of the cardiac membrane caused by damage or congenital developmental abnormalities, manifested as valve orifice stenosis and/or insufficiency, eventually leading to cardiac insufficiency and systemic blood circulation disorders.
Etiology and pathogenesis
Common pathological types
mitral stenosis
lesions
Narrow type
Diaphragm type
funnel type
Hemodynamic and cardiac changes
compensatory dilation of left atrium
Pulmonary congestion, edema, leakage hemorrhage
Compensatory hypertrophy and dilation of the right ventricle, tricuspid regurgitation, right atrial congestion, and signs of large circulation congestion
Mild narrowing of the left ventricle
clinicopathological link
Mitral valve insufficiency
aortic valve insufficiency
Hemodynamic changes
clinicopathological link
aortic stenosis
Hemodynamic changes
clinical contact pathology
Angina pectoris, which can cause sudden death in severe cases
Decreased pulse pressure
Aortic systolic blowing murmur
X-ray "boot-shaped heart"