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Pathology Chapter 3 Local Blood Circulation Disorders
Pathology Chapter 3 Local blood circulation disorders, such as necrosis of organs or local tissues due to blood vessel obstruction and cessation of blood flow leading to hypoxia, are called infarction.
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Pathology Chapter 3 Local Blood Circulation Disorders
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- Outline
local blood circulation disorder
congestion
The dilation of blood vessels in local organs or tissues and the increase in blood content in the blood vessels is called congestion.
arterial congestion
Due to excessive arterial blood input, the blood volume in the blood vessels of local tissues or organs increases, which is called arterial congestion.
reason
inflammatory hyperemia
Collateral hyperemia (physiological hyperemia)
Postdecompression hyperemia
Pathological changes
Small arteries and capillaries are dilated, and local tissues are bright red in color
as a result of
During arterial congestion, the input of local oxygen and nutrients increases, and metabolism and functional activities are enhanced, which is beneficial to the body. Hot compresses are often used to cause arterial congestion.
venous congestion
Due to obstruction of venous return, blood accumulates in capillaries and venules, increasing the blood content of local tissues or organs, which is called venous congestion.
reason
Venous compression (edema of lower limbs due to pregnancy)
Venous lumen stenosis or obstruction (intravenous thrombosis or intravenous inflammatory thickening)
Heart failure (reduced cardiac output, obstruction of venous return)
Pathological changes
The congestion organ increases in size and weight, the capsule becomes tense, and the texture becomes firm; cyanosis may occur in the skin and mucous membranes.
as a result of
It depends on venous compression, the degree, speed, location, duration of obstruction, and the establishment of local collateral circulation.
Congestive edema (pleural effusion, ascites, or pericardial effusion)
Congestive bleeding
Parenchymal cell atrophy, degeneration, and necrosis
Congestive sclerosis
Congestion of vital organs
Pulmonary congestion (caused by left heart failure, with red or dark red foamy fluid flowing out) ! Heart failure cells: Macrophages phagocytose red blood cells and break down hemoglobin into brown-yellow granular iron-containing hemoglobin. Such phagocytes that engulf hemosiderin are called heart failure cells.
Liver congestion (usually caused by right-sided heart failure or total heart failure) ! Betel nut liver: Alternate red (congestion area) and yellow (fatty degeneration area) stripe-like structures can be seen on the surface and cut surface, which resemble the cut surface of betel nut, and are called "betel nut liver".
Bleeding
The escape of blood from the heart or blood vessels is called hemorrhage. When blood flows outside the body, it is called external bleeding. When blood flows out and collects in tissue spaces or body cavities, it is called internal bleeding.
Causes and types
rupture hemorrhage
Mechanical damage to blood vessels
Destructive lesions that erode blood vessel walls
Diseases of the cardiovascular wall itself
Vein rupture
ruptured capillaries
leakage bleeding
blood vessel wall damage
Thrombocytopenia or platelet dysfunction
Deficiency of coagulation factors (reduced synthesis, excessive consumption, congenital diseases)
Pathological changes
Small bleeding focus (petechiae, petechiae), hematoma
as a result of
Acute massive bleeding can cause hemorrhagic shock. (The blood volume, bleeding speed and location vary)
thrombosis
Concept: The process in which blood components form a solid mass in the cardiovascular system of a living body is called thrombosis. The solid mass formed is called a thrombus.
Conditions and mechanisms of thrombus formation
Cardiovascular endothelial cell damage (prerequisite)
Procoagulant effect of damaged endothelial cells
Activation of platelets (adhesion, release, adhesion)
Changes in blood flow status (slow blood flow or vortex formation)
Platelets enter the side stream, increasing the chance of contact with the endothelium
Activated thrombin or coagulation factors are not easily diluted or washed away
Changes in blood properties (increased blood coagulability)
Postoperative or postpartum (thrombocytosis)
Systemic lupus erythematosus (activated platelets)
Extensive burns (hematoconcentration)
Heterotype transfusion (release of platelet factors and coagulation factors)
certain cancer patients
The process and morphology of thrombosis
Including platelet adhesion and blood coagulation.
Thrombus head: white thrombus (grey-white, solid texture)
Mixed thrombus (red and white corrugated thrombus)
Thrombus tail: red thrombus (red blood clot)
Hyaline thrombus (fibrin and few platelets)
outcome of thrombosis
Soften, dissolve, absorb
Mechanization, recanalization
Calcification
The impact of blood clots on the body
Defensive significance of thrombosis (haemostatic effect on ruptured blood)
adverse effects of thrombosis
Blocked blood vessels (myocardial infarction, cerebral infarction, enterohemorrhagic infarction)
embolism
Heart valve deformation
Bleeding (extensive bleeding and shock)
embolism
The phenomenon of insoluble abnormal substances appearing in the circulating blood and traveling to distant places with the blood to block blood vessels is called embolism. Abnormal material that blocks a blood vessel is called an emboli.
The path of travel of emboli
consistent with blood flow direction
Emboli from the right heart and systemic venous system (pulmonary embolism)
Emboli from the left heart, pulmonary veins, or systemic arterial system
Emboli from the portal venous system
Cross-embolism (rare)
Retrograde embolism (rare)
Types of embolism and effects on the body
Thromboembolism
Embolism caused by blood clots is called thromboembolism, which is the most common type of embolism, accounting for more than 90% of all embolisms.
Pulmonary embolism (95% of emboli causing pulmonary embolism come from the deep veins of the lower limbs)
huge plug
pulmonary aorta
A large number of normal-sized emboli
Lung main or branch
few small emboli
no effect
A few very small emboli
Through the blood-qi barrier, it reaches the left ventricle, the brain, the kidneys, etc.
Arterial system embolism (80% of emboli originate from the left heart)
Valvular vegetations in subacute infective endocarditis
Left atrial mural thrombus in mitral stenosis
mural thrombus in myocardial infarction
atherosclerotic ulcer
fat embolism
Traumatic fat embolism
Comminuted fractures of long bones or severe bruises or burns to fatty tissue
non-traumatic fat embolism
Patients with hyperlipidemia, alcoholism, diabetes, and chronic pancreatitis
gas embolism
A large amount of air quickly enters the blood circulation or the gas originally dissolved in the blood quickly dissociates, forming bubbles that block the cardiovascular system, which is called a gas embolism.
air embolism
Due to vein damage and rupture, air enters the blood through the damaged veins (a small amount will dissolve, and more than 100ml will cause circulation disorders)
decompression sickness
Also known as caisson disease or diver's disease
amniotic fluid embolism
Rupture of amniotic membranes - uterine contractions force amniotic fluid into the ruptured uterine wall sinuses - pulmonary systemic circulation - leading to coughing, dyspnea, cyanosis, shock, convulsions, coma and death.
Other types of embolism
Tumor cell embolism, bacterial embolism, parasite embolism
infarction
The necrosis of an organ or local tissue due to blood vessel obstruction and cessation of blood flow leading to hypoxia is called infarction.
Causes and conditions of infarction
reason
Thrombus formation and embolism
blood vessel compression and occlusion
persistent arterial spasm
condition
Type of blood supplying blood vessels (the liver/pulmonary has dual circulation and is not prone to infarction; although the heart and brain have collateral circulation, the lumen is small and is prone to infarction)
How quickly blood flow obstruction occurs
Tissue tolerance to hypoxia (infarction occurs when cerebral hypoxia is interrupted for 3-4 minutes, and infarction occurs when myocardial hypoxia is interrupted for 20-30 minutes)
blood oxygen content
Types and pathological changes of infarction
anemic infarction
It mostly occurs in solid organs with dense tissue structure and insufficient collateral circulation.
The infarct is grayish white, also known as white infarction. The shape is related to the distribution of arterial branches.
hemorrhagic infarction
Often occurs in organs with loose tissue and dual blood circulation, such as lungs and intestines
severe congestion
Dual blood circulation
Loose tissue (loose lung and intestinal tissue)
septic infarction
Caused by emboli containing bacteria blocking blood vessels
Impact and outcome of infarction
dissolve, absorb
Body—scar tissue
Package—calcification
Cyst formation