MindMap Gallery local vascular circulation disorder
Pathology, manifestations: 1. Overflow of intravascular components into blood vessels 2. Abnormal blood content in blood vessels in local tissues 3. Abnormal substances appear in blood.
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local vascular circulation disorder
Manifestations: 1. Intravascular components overflow into blood vessels 2. Abnormal blood content in blood vessels in local tissues 3. Abnormal substances appear in blood
congestion
Increased blood input from arteries in the trachea or tissues is called arterial congestion
Active process, telangiectasia of small arteries in local organs and tissues
type
Physiological: Congestion of local organs or tissues due to physiological needs or increased metabolism (after exercise, after eating, in the uterus during pregnancy)
Pathological: inflammatory congestion; when local tissues or organs have been pressurized for a long time, reflex dilation of arterioles occurs after the pressure is relieved (congestion after decompression)
Ischemia-reperfusion injury: In some cases, restoration of blood flow after ischemia can cause peroxidation of surviving tissue, which in turn aggravates tissue damage.
Pathological changes and consequences
Congested organs and tissues mildly enlarged in size
Oxygenated hemoglobin increases in the local microcirculation, and the local tissue is bright red in color
Enhanced metabolism increases local temperature
Hemorrhagic stroke: On the basis of high blood pressure and atherosclerosis, emotional excitement, etc. cause congestion and rupture of the middle cerebral artery.
big, red, hot
congestion
Venous blood return in local tissues or organs is blocked, and blood accumulates in small veins and capillaries, resulting in an increase in blood volume, which is called venous congestion.
Passive process, local or systemic
Causes: venous compression; venous lumen obstruction; heart failure
Pathological changes and consequences
Increased size, swelling, and weight
Congestion on the body surface can be seen in parts of the skin that appear purple-blue, which is called cyanosis.
Local blood flow tissue, capillaries dilate, heat dissipation increases, and body surface temperature decreases
congestion edema, congestion bleeding
Long-term congestion (chronic congestion), due to local tissue hypoxia, accumulation and stimulation of metabolic intermediates, leads to atrophy, degeneration and necrosis of parenchymal cells Interstitial fibrous tissue proliferates, and the network of fibrous collagen in the tissue makes the organs hard (congestive sclerosis)
big, purple, cold
pulmonary congestion
Left heart failure causes an increase in pressure in the left heart chamber, impedes pulmonary venous return, and causes pulmonary congestion.
acute pulmonary congestion
Severe pulmonary edema, coughing up a large amount of pink foamy sputum, and cardiopulmonary failure may occur
telangiectasia
The alveolar spaces are filled with edema fluid and bleeding can be seen
alveolar wall thickening
cardiogenic asthma
chronic pulmonary congestion
acute manifestations
Heart failure cells: Macrophages phagocytose hemosiderin particles (red blood cells)
Alveolar wall fibrosis (brown sclerosis of the lungs)
Clinical manifestations include shortness of breath and cyanosis
Liver congestion
Caused by right heart failure, the hepatic vein return to the heart is blocked, and the central veins of the hepatic lobules and the hepatic steeple are dilated and congested.
acute liver congestion
The liver is enlarged and dark red in color
Central lobular veins and liver sinusoids are dilated and filled with red blood cells
Because peripheral liver cells are close to hepatic arterioles and suffer from mild hypoxia, hepatic steatosis occurs.
chronic liver congestion
Severe congestion in the center, dark red
Perilobular hepatocyte steatosis
Red and yellow stripes appear, betel nut liver
Congestive cirrhosis
Long-term congestion, hepatocyte atrophy, collagenization after the collapse of the reticular fibrous structure, proliferation of fat storage cells near the liver sinusoids, increased synthesis of collagen fibers, proliferation of fibrous connective tissue in the portal area, resulting in hyperplasia of fibrous tissue throughout the liver interstitium
bleeding
rupture hemorrhage
leakage bleeding
thrombus
Thrombosis: The process in which blood coagulates in the living heart and blood vessels or certain formed components in the blood agglomerate to form a solid mass.
Thrombus: a solid mass that forms
forming conditions
Cardiovascular endothelial cell damage (most common cause)
Abnormal blood flow status
Common in veins, slowed blood flow and swirling blood flow
increased blood coagulability
Tumors synthesize coagulation factors, severe injuries, burns, DIC
Types and forms
White thrombus
Faster blood flow, heart valves, chambers, and arteries
Small gray-white nodules or vegetations, rough, solid and not easy to fall off
Platelets, a small amount of fibrin, white blood cells, red blood cells
acute rheumatic endocarditis, systemic lupus erythematosus
mixed thrombus
Slow blood flow, heart chambers, atherosclerotic walls, aneurysms
Alternating gray-white and reddish-brown layered structure
Platelets under the trabeculae, the trabeculae are filled with red blood cells
Atrial fibrillation, ventricular aneurysm, aneurysm
red blood clot
Local blood flow stops, veins
Dark red, moist and elastic when fresh
Fibrin network, few white blood cells, many red blood cells
Femoral vein thrombosis tail → pulmonary embolism
hyaline thrombus
Capillaries, which can only be observed under a microscope
Endothelial damage, coagulation abnormalities
eosinophilic homogeneous fibrin
DIC (disseminated intravascular coagulation)
ending
Soften, dissolve and absorb
mechanization and recanalization
Recanalization: New vascular endothelial cells grow into and cover the surface of the crack to form new blood vessels, anastomose and communicate with each other, allowing the partially blocked blood vessels to rebuild blood flow (the blood vessels are smaller than before)
Calcification
Thrombus calcifies to form phleboliths or arterial stones
Effect on the body
block blood vessels
red, mixed thrombus
embolism
red, mixed thrombus
pulmonary embolism
Heart valve deformation
White thrombus
Rheumatic endocarditis and infective endocarditis
extensive bleeding
hyaline thrombus
DIC, first hypercoagulable and then hypocoagulable
embolism
Abnormal substances that are insoluble in blood appear in the circulating blood flow and travel with the blood flow to block the lumen of blood vessels.
Abnormal substances that block blood vessels are called emboli
Emboli can be solid, liquid or gas
Operation path
Venous system and right cardiac cavity emboli——Pulmonary embolism
Aortic system and left ventricular emboli
Commonly found in the brain, spleen, kidneys and limbs
Portal system emboli
cross embolism
Congenital atrioventricular septal defect, patent ductus arteriosus
retrograde embolism
type
Thromboembolism 99%
pulmonary embolism
Most come from deep veins in the lower limbs above the knee
as a result of
Small and medium-sized emboli often block small branches of the pulmonary artery and do not cause serious consequences.
Large thromboembolic embolism in the main or large branches of the pulmonary artery
Straddle embolism: Blocks the bifurcation of the main pulmonary artery, and the patient may have difficulty breathing, cyanosis, shock, and in severe cases, death from acute respiratory and circulatory failure (sudden death)
The emboli are small and numerous, and can be widely distributed and embolize most small branches of the pulmonary artery.
Sudden death from right heart failure
systemic arterial embolism
Left ventricular chamber 80%
The main parts are lower limbs, brain, intestine, kidney and spleen
Liver infarction rarely occurs
fat embolism
Sources of emboli: long bone fractures, severe contusions and burns of fatty tissue, fatty liver, disease leading to unstable blood lipids
A small amount of lipid droplets entering the blood has no adverse effects, but a large amount of lipid droplets entering the pulmonary circulation in a short period of time can cause suffocation and death from acute right heart failure.
gas embolism
air embolism
Neck and chest injuries
During labor or miscarriage, the uterus contracts strongly and air is squeezed into the venous sinuses that have ruptured the uterine wall.
Pulmonary arteriolar gas embolism: A large amount of gas (more than 100ml) enters the veins, hindering the return of venous blood and its output to the pulmonary artery, causing serious obstacles
Decompression sickness (nitrogen embolism)
When the human body changes from high pressure to low pressure, the gas originally dissolved in the body fluid quickly dissociates into bubbles. Oxygen and carbon dioxide can be redissolved in the body fluid. However, nitrogen dissolves slowly in the body fluid, and many bubbles appear in the blood, causing gas embolism.
Symptoms: Muscle pain, necrosis of the femoral head (avascular necrosis)
amniotic fluid embolism
The uterus contracts strongly, the amniotic fluid enters the venous sinuses of the ruptured uterine wall, and the menstrual blood circulates into the pulmonary artery branches, small arteries and capillaries.
Ingredients: keratinized squamous epithelium, lanugo, vernix, meconium and mucus
mechanism
Fetal metabolites in amniotic fluid enter the blood and cause anaphylactic shock
Amniotic fluid emboli blocks the pulmonary artery and amniotic fluid contains vasoactive substances causing reflex vasospasm
Amniotic fluid has the effect of thromboplastin causing DIC
infarction
Necrosis of organs or local tissues due to blood vessel obstruction and stagnant blood flow leading to hypoxia.
Arterial obstruction causes ischemic necrosis of local tissue
Venous obstruction causes tissue hypoxia
reasons and conditions
reason
thrombosis
Mainly seen in myocardial infarction and cerebral infarction caused by coronary artery and cerebral atherosclerosis combined with thrombosis.
arterial embolism
arterial spasm
When coronary atherosclerosis is combined with bleeding, coronary artery spasm
blood vessel compression and occlusion
Formative factors
Organ blood supply characteristics
Sensitivity of local tissue to ischemia
Brain, nerve cells (3-4min)>cardiac cells (20-30min)>skeletal muscle, fibrous connective tissue
Lesions and types
Morphological characteristics
shape
The infarction is cone-shaped, with a fan-shaped or triangular section, and the tip points toward the "door"
Spleen, kidney, lung
segmental
intestinal
map shape
myocardial infarction
texture
coagulative necrosis
heart, spleen, kidney
liquefaction necrosis
brain
color
anemic infarction/white infarction
Hemorrhagic infarct/red infarct
type
anemic infarction
Solid organs with dense tissue structure and insufficient collateral circulation
Spleen, kidney, heart and brain (no infarction)
Naked eye: Early stage: white congestion zone Late stage: scar Under the mirror: Early stage: polycoagulative necrosis Late stage: granulation tissue or scar
subtopic
hemorrhagic infarction
Conditions: Severe congestion; loose tissue
Anemic infarction: When the lungs become consolidated due to inflammation
Lungs, intestines, ovaries
Pulmonary hemorrhagic infarction: pulmonary embolism on the basis of pulmonary congestion
enterohemorrhagic infarction
Often occurs in mesenteric arterial embolism and venous thrombosis, or intussusception, volvulus, incarcerated hernia, tumor
septic infarction
Emboli containing bacteria block blood vessels
Bacteria and a large number of inflammatory cells can be infiltrated in the infarct. If there is purulent infection, an abscess will be formed.
Impact and outcome
The magnitude of the effect depends on the organ infarcted, the size and location of the infarct, and the presence or absence of bacterial infection.
Irreversible lesions, infarcts can be dissolved, absorbed, or organized, wrapped, and calcified
Venous thrombosis is common
Blood flow at the venous valve is slow and whirlpools appear
Venous blood flow sometimes temporarily stops
Vein walls are thin and susceptible to pressure
As blood passes through capillaries and into veins, blood viscosity increases
Endothelial cells
anticoagulant effect
barrier effect
Anti-platelet adhesion effect
Synthetic antithrombin or coagulation factors
Promote fibrinolysis
Procoagulant effect
Activates extrinsic coagulation process
Assist platelet adhesion
Inhibit fibrinolysis