MindMap Gallery cardiovascular system diseases
Pathology summarizes and organizes knowledge points to help learners understand and remember. Straight to the point, it can be used as study notes and review materials to help you systematically review and consolidate the knowledge you have learned. The knowledge points are systematic and comprehensive. I hope it will be helpful to everyone! Suitable for exam review.
Edited at 2024-10-01 23:35:56這是一篇關於《簡愛》人物關係分析的心智圖,幫助你理解和閱讀這本書,本圖關係梳理清楚,非常實用,值得收藏!
This is a mind map about the analysis of the character relationships in "Jane Eyre" to help you understand and read this book. The relationships in this map are clearly sorted out. It is very practical and worth collecting!
An outline of the knowledge points of air and oxygen in Chemistry, including the production of oxygen, catalysts, and reactions. This mind map will help you become familiar with the key points of knowledge and enhance your memory. Students in need can save it.
這是一篇關於《簡愛》人物關係分析的心智圖,幫助你理解和閱讀這本書,本圖關係梳理清楚,非常實用,值得收藏!
This is a mind map about the analysis of the character relationships in "Jane Eyre" to help you understand and read this book. The relationships in this map are clearly sorted out. It is very practical and worth collecting!
An outline of the knowledge points of air and oxygen in Chemistry, including the production of oxygen, catalysts, and reactions. This mind map will help you become familiar with the key points of knowledge and enhance your memory. Students in need can save it.
cardiovascular system diseases
Atherosclerosis AS
concept
arteriosclerosis
Arteriosclerosis generally refers to a disease in which the arterial wall thickens, loses elasticity and hardens.
atherosclerosis
It is characterized by the formation of atherosclerosis or fibrous plaque in the intima of blood vessels, mainly involving large and medium-sized arteries, causing hardening of the wall, narrowing of the lumen and weakening of elasticity, causing ischemic changes in the corresponding organs.
Best place to send hair
abdominal aorta
Causes and pathogenesis
risk factors
hyperlipidemia
Ox-LDL is the most important factor that causes AS and can damage endothelial cells and SMC.
LDL and VLDL cause AS, HDL inhibits
Diseases causing secondary hyperlipidemia
diabetes
hyperinsulinemia
Hypothyroidism and nephrotic syndrome
Gender and age
Premenopausal girls are less likely to develop the disease
Genetic factors, hypertension, smoking, metabolic syndrome
Interference options
High salt diet
Pathogenesis (not yet clear) (order of occurrence from top to bottom)
Lipid penetration theory
Long-term hyperlipidemia causes endothelial damage and lipid infiltration
damage-response theory
The infiltrated lipids are engulfed by monocytes (vascular monocytes infiltrate, not neutrophils) or ingrown SMCs, and become foam cells (lipid droplets are washed away)
Foam cells rupture to form porridge
chronic inflammation theory
The most important biochemical indicator is high-sensitivity C-reactive protein (CRP)
CRP can promote AS
Pathological changes
Basic pathological changes (time from top to bottom)
Fat lines
Features
The earliest visible lesions
nature
Lipid deposition
in general
Dot-like or striped yellow and slightly raised lesions can be seen on the surface of the intima, which are common on the posterior wall of the aorta and the branch openings.
under the mirror
A large number of foam cells accumulated under the intima, and lipid staining was positive.
fibrous plaque
Features
Fatty lines develop from
nature
Lipid organized scar repair
in general
Yellow (lipid damage) or white (fiber repair) raised plaques scattered on the intimal surface
under the mirror
The surface of the lesion is a fibrous cap (mainly collagen fibers), and foam cells, SMC and inflammatory cells can be seen under the cap.
atheromatous plaque
Features
Typical lesions of AS
nature
Cells deep in the fibrous plaque become necrotic and rupture, forming atherosclerotic material
in general
naked eye
Raised yellow-white patches seen in the endometrium
section
The luminal surface is white hard tissue, and the deep part is yellow-white porridge-like material, which is soft.
The plaque enlarges, bulges toward the surface and compresses the media
under the mirror
A large number of cells under the fibrous cap undergo necrosis and collapse, releasing intracellular substances, cholesterol deposition (crack-like), calcium salt deposition, etc., and the media of the blood vessel is compressed and atrophied.
secondary lesions
intra-plaque bleeding
Rupture of new capillaries within the plaque
plaque rupture
The material in the plaque flows into the bloodstream and can easily cause blood clots
thrombosis
Plaque ruptures, collagen is exposed, and thrombus forms
Calcification
Calcium salt deposition in fibrous plaque
aneurysm formation
The blood vessels where AS occurs have reduced elasticity and thin walls. They are squeezed and expanded by blood pressure and are prone to rupture and massive bleeding.
vascular lumen stenosis
Expanded and narrowed by atheromatous material, corresponding to organ ischemia
Major arterial pathological changes
aortic atherosclerosis
The obstruction is not obvious, but an aneurysm may rupture and cause massive bleeding.
coronary artery
coronary atherosclerosis
Have all the changes of atherosclerosis
Most commonly occurs in the left anterior descending artery
Plaque lesions occur on the side of the heart wall and are crescent-shaped
Eccentric lumen stenosis
coronary atherosclerotic heart disease
Coronary heart disease (CHD)
Caused by coronary artery stenosis leading to myocardial ischemia
Causes of myocardial hypoxia
Atheromatous plaques cause luminal stenosis and reduce blood volume during coronary perfusion.
Increased myocardial load, increased oxygen consumption, and relative insufficient blood supply to the coronary arteries
clinical manifestations
Angina pectoris
Mechanism
Myocardial hypoxia causes the accumulation of acidic products from incomplete metabolism, stimulating local nerve endings in the heart and producing pain.
Angina pectoris is a reflex symptom of myocardial ischemia
clinical manifestations
Precordial pain, which can radiate to the left upper limb, can be relieved with nitroglycerin or rest
Myocardial infarction MI (myocardial infarction)
Overview
anemic infarction
type
Subendocardial MI
The lesion mainly affects the inner third of the myocardium of the ventricular wall, and also affects the carotid columns and papillary muscles. It often manifests as multiple and small focal necrosis.
The distribution of lesions is not limited to the blood supply range of a certain coronary artery, but is irregularly distributed around the left ventricle.
In severe cases, the lesions expand and fuse to involve the entire subendocardial myocardium, causing circular infarction.
transmural MI
Is a type of typical MI, also called regional MI
The location of MI is consistent with the blood supply area of the occluded coronary artery branch. The lesion is large and involves more than 2/3 of the ventricular wall. It mostly occurs in the left anterior descending artery and its location corresponds to the left ventricle.
Pathological changes
2h
Recognizable by light microscope
6h
Beginning to be discernible, the infarct is pale in color
8-9h
naked eye
khaki infarction
under the mirror
Parenchymal coagulation infarction, homogeneous red staining of the cytoplasm or irregular coarse granular shape (shrinkage zone)
Interstitial edema with neutrophil infiltration
24h
Myophosphate kinase CPK and lactate dehydrogenase LDH were significantly increased in the blood
4d
Congestive and hemorrhagic bands appear around the infarct
7-14d
Granulation tissue appears in the marginal zone, which can grow into the infarct and appears red.
21d
Granulation tissue begins to organize and form scar tissue
MI complications
heart failure
When MI involves the papillary muscles, it can cause mitral valve insufficiency and induce acute left heart failure, which then affects the whole heart.
ruptured heart
Predisposed areas
Lower 1/3 of the left ventricle, interventricular septum and left ventricular papillary muscles
Cause of rupture
As the infarct loses elasticity, ruptured neutrophils and monocytes release a large amount of proteases to dissolve the infarct.
cause of death
People who die from the anterior wall of the left ventricle die from cardiac compression caused by the influx of blood into the pericardium; people who die from the interventricular septum die from acute right ventricular dysfunction caused by the influx of blood from the left ventricle into the right ventricle.
ventricular aneurysm
Occurrence time
Mostly the healing period of MI
reason
Infarcted myocardium or scar tissue bulges under pressure
Predisposed areas
The anterior wall of the left ventricle near the apex
other
Mural thrombosis, cardiogenic shock (the heart cannot beat), acute pericarditis (necrosis involving the epicardium), arrhythmia (necrosis involving the conduction system)
myocardial fibrosis
Coronary artery stenosis leads to repeated myocardial ischemia, repeated fibrosis repair, and gradually develops into chronic ischemic heart disease of heart failure.
sudden coronary death
The most common form of sudden cardiac death
carotid and cerebral arteries
Predisposed areas
The origin of the internal carotid artery, the basilar artery, the middle cerebral artery and the circle of Willis
as a result of
Brain atrophy, dementia, encephalomalacia
Aneurysm forms, ruptures and causes brain hemorrhage
renal artery
AS pyknotic kidney
Renal artery plaque leads to luminal stenosis, renal ischemia, parenchymal atrophy, and mesenchymal tissue hyperplasia
Merger of plaques leads to renal tissue infarction. After organization, the plaques become large and sunken. The adhesion of multiple plaques causes the kidney to shrink.
arteries of extremities
Predisposed areas
Lower extremity arteries, buttock arteries
Intermittent claudication, narrowing of arteries in lower limbs, inability to walk, recovery can be achieved with rest
Complete occlusion, resulting in dry gangrene
Hypertension
definition
Systolic blood pressure is 140 points higher, diastolic blood pressure is 90 points higher
reason
risk factors
genetic factors
Obesity, high-salt diet and alcohol consumption
Psychosocial factors, physical activity and neuroendocrine factors
Pathogenesis
genetic mechanism
Born with high blood pressure
production mechanism
renin-angiotensin-aldosterone system RAAS
Strongly constrict arterioles and increase peripheral resistance
Promote proto-oncogene expression, increase SMC proliferation, and increase peripheral resistance
Activate sympathetic nerves
Promote reabsorption and increase circulating blood volume
sympathetic nervous system
NE excites cardiac beta receptors, causing heart rhythm and contraction to increase
NE acts on blood vessels, causing contraction
Sympathetic nerves act on the kidneys, reducing their blood flow and increasing aldosterone release
endothelial dysfunction
Endothelial NO levels or activity are downregulated and local RAAS is overactivated.
insulin resistance
Insulin can protect cardiovascular systems. When obese people develop AS, insulin levels increase significantly.
increased insulin
Promote renal tubuleworms to absorb Na and water
leading to endothelial cell dysfunction
Increase sympathetic nerve activity
Sensitize cells to growth factors and promote SMC production
type
benign hypertension
dysfunctional period
Fluctuating blood pressure increases, which can recover after treatment and rest
Arteriopathy stage
Arteriosclerosis
Characteristics of major diseases such as hypertension
Hyalinization of small arteries
The renal afferent arterioles, retinal arteries, and central splenic arteries are most likely to be involved
Resulting in arterial wall thickening and lumen narrowing to occlusion
Arteriolar sclerosis
Most likely to involve small muscular arteries, such as renal interlobular arteries
Causes thickening of the tube wall and narrowing of the tube lumen
Arteriosclerosis
No obvious lesions or complicated by AS
visceral disease stage
Heart (hypertensive heart disease)
naked eye
The left ventricular wall is thickened to 1.5cm (normal 1cm). The left ventricular papillary muscles and columns are thickened, and the cardiac chambers are not dilated (central hypertrophy)
Late decompensation, increased contractility, and passive expansion of the heart are called eccentric hypertrophy, which continues to develop into heart failure.
under the mirror
Myocardial cells become thicker, longer, and have more branches. Myocardial cell nuclei are hypertrophied and deeply stained
Kidney (granular pyknotic kidney)
First, there is hyalinization of the afferent arteriole, leading to glomerular ischemia. Secondly, hyalinization of the glomerulus leads to atrophy of the glomerular ischemia, mesenchymal tissue hyperplasia, and lymphocyte infiltration.
Kidney atrophy on the affected side and compensatory enlargement on the contralateral side
The renal section of the affected side shows that the renal cortex becomes thinner, the corticomedullary boundary is blurred, and the renal pelvis and perirenal fat tissue increase.
brain
Cerebral edema or hypertensive encephalopathy
Hypertensive crisis: severe headache, disturbance of consciousness, convulsions, etc.
The cause of cerebral edema is hyaline degeneration of brain capillaries, which increases permeability
Encephalomalacia
Liquefied necrosis (microinfarction) caused by local cerebral ischemia caused by small artery disease
Under the microscope, liquefaction necrosis appears as mesh-like lesions with loose texture; later scars are repaired to form colloid scars.
cerebral hemorrhage
The most serious complications are often fatal
Most commonly occur in basal ganglia and internal capsule
The lenticulostriate arteries in this area are directly impacted by the middle cerebral artery.
retina
central retinal arteriosclerosis
malignant hypertension
More common in teenagers
Characterized by proliferative arteriolar sclerosis (fibrinoid necrosis) and necrotizing arteritis
Mainly affects the kidneys
Rapidly rising blood pressure may lead to hypertensive encephalopathy, renal failure, retinal hemorrhage, etc.
Rheumatism
Causes and pathogenesis
Group A strep infection
M protein has a similar structure to the surface of heart valves and is a marker of rheumatoid origin
Hypersensitivity reaction in infected persons
genetic susceptibility
streptococcal toxin theory
Pathological changes
Deterioration and exudation stage
Early changes in rheumatism, myxoid degeneration and fibrinoid necrosis of connective tissue
Proliferative phase (granulomatous phase)
The appearance of rheumatic bodies (Aschoff bodies) is a characteristic of rheumatism.
Composition: Composed of groups of rheumatoid cells and a small amount of lymphocytes and plasma cells gathered in fibrinoid necrosis lesions
Rheumatoid cells: proliferating macrophages engulf fibrinoid necrosis
Fibrosis stage (hardening stage)
Aschoff cells transform into fibroblasts to repair tissue scars
Can be formed repeatedly
Organ disease
rheumatic heart disease
rheumatic endocarditis
The essence is that the endocardium is destroyed, causing white thrombus
The mitral valve is most commonly affected, followed by the combined involvement of the mitral valve and aortic valve
The formation of verrucous growths on the valve surface, especially on the obturator border
The vegetation adheres firmly and is not easy to fall off
Microscopically, the vegetation is composed of platelets and fibrin (white thrombus), accompanied by small focal fibrinoid necrosis, surrounded by a small number of rheumatoid cells.
Later intervalvular adhesion, valve orifice stenosis, causing intimal hyperplasia, called Macallum spots
rheumatic myocarditis
Interstitial myocarditis with rheumatoid bodies present
rheumatic epicarditis
Serous or fibrinoid inflammation of the epicardium leading to villous heart disease
pericardial rub sound
develop pericarditis
rheumatoid arthritis
Often attacks large joints, with good prognosis
skin lesions
annular erythema
exudative lesions
subcutaneous nodules
proliferative lesions
infective endocarditis IE
concept
Pathogenic microorganisms directly invade the endocardium from menstrual blood, causing inflammation and the formation of vegetations.
Pathogenesis
native valve infective endocarditis
Streptococcus
acute infective endocarditis
Staphylococcus aureus
subacute infective endocarditis
viridans streptococci
clinical changes
acute infective endocarditis
Verrucous growths on the affected heart valves, consisting mainly of a mixture of purulent exudate, thrombus, necrotic tissue, and large bacterial colonies (larger than rheumatic endocarditis)
Mainly affects mitral and aortic valves
subacute infective endocarditis
heart
Mainly affects mitral and aortic valves
Vegetation often forms on diseased valves
Composition of platelets, fibrin, colonies, necrosis combination, and neutrophils
The vegetations are polyp-like or cauliflower-like and are easy to fall off. Ulcers or even perforations may form on the valves.
Blood vessel
Shedding of vegetations, formation of arterial thrombosis and vasculitis
Embolism is most common in the brain
allergy
Involves the kidneys, leading to nephritis
septicemia
Long-term fever, splenomegaly, leukocytosis, small bleeding spots in mucous membranes, etc.
valvular heart disease
mitral stenosis
The cause is rheumatic fever, caused by repeated attacks of rheumatic endocarditis caused by group A streptococcal infection.
Valve adhesion (signature lesion), the opening is reduced to 0.5cm, and the valve is fish-shaped.
Early left atrial compensatory hypertrophy, late left atrial decompensation, and pulmonary congestion
Long-term pulmonary congestion leads to compensatory hypertrophy of the right ventricle, followed by decompensation, followed by right heart failure and venous congestion.
Late X-ray shows pear-shaped heart
Mitral valve insufficiency
Consequences of a single episode of rheumatic endocarditis
X-ray shows left ventricular hypertrophy and spherical heart
aortic stenosis
Caused by rheumatic aortitis
X-ray, heart boot shape
aortic valve insufficiency
Caused by rheumatic aortitis
Compensatory enlargement of the left ventricle, leading to left heart failure
The heart will become hypertrophic except for the left atrium.