MindMap Gallery local blood circulation disorder
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.
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local blood circulation disorder
congestion and congestion
congestion
concept
arterial congestion
result of dilation of arterioles
Common types
Physiological
slightly
pathological
inflammatory
Inflammation arises early, inflammatory factors trigger vasodilation
Decompression
Reflexive dilation of arteries after long-term pressure contact with local tissue
as a result of
Usually of no consequence, if you have high blood pressure or atherosclerosis, recongestion can cause blood vessels to rupture
congestion
concept
Obstruction of venous return to local tissues or organs
reason
venous compression
Compression of veins leading to obstruction of blood return
venous lumen obstruction
Venous thrombosis or tumor thrombus formation from tumors that invade veins
heart failure
left heart failure pulmonary congestion
Right heart failure and congestion in lower limbs
as a result of
cyanosis
The local tissues and organs where congestion occurs increase in size and are ischemic. Congestion occurring on the body surface causes cyanosis of the skin.
congestion edemacongestive edema
Vascular permeability can be increased
The accumulation of leaked fluid in the serosal cavity is called effusion, such as pleural effusion, ascites, etc.
congestion hemorrhagecongestive hemorrhage
Capillaries further increase permeability or directly rupture, causing red blood cells to flow out and form congestion bleeding.
Occurs on the body surface as petechiae
congestive sclerosis
Local tissue ischemia and hypoxia lead to necrosis, which is repaired by scars, leading to congestion sclerosis
Congestion of vital organs
pulmonary congestion
Caused by left heart failure
There is edema fluid and hemorrhage in the alveolar space
In severe cases, there are a large number of macrophages that engulf hemosiderin particles, which are called heart failure cells.
Macrophages can also phagocytose dust into dust cells
In chronic congestive sclerosis, the texture becomes hard and brown, which is called brown sclerosis of the lungs.
Clinical manifestations include shortness of breath, cyanosis, and coughing up bloody sputum.
Liver congestion
Right heart failure, caused by systemic circulatory failure
Blood accumulates in the central veins of the liver lobules, which may atrophy and become necrotic in severe cases.
Peripheral cells of lobules usually show only steatosis
In chronic liver congestion, the necrotic center of the lobule (red) and the periphery of fatty change (yellow) are arranged in stripes, which is called betel liver (essentially necrosis).
Why isn't it called tabby liver? ? ?
Further development, long-term severe liver congestion leads to congestion cirrhosis.
Bleeding
reason
rupture
mechanical damage
Blood vessel wall or heart disease
Lesion erosion around blood vessel walls
Vein rupture
ruptured capillaries
leakage
damage to blood vessel walls
Increased permeability
Thrombocytopenia or dysfunction
Bleeding occurs when platelets are not enough
coagulation factor deficiency
Pathological changes
internal bleeding
Localized massive bleeding within the tissue is a hematoma
external bleeding
thrombosis
concept
The process of coagulation or aggregation of formed components in the blood in the heart and blood vessels of a living body is called thrombosis
The solid mass is called a thrombus
Conditions and mechanisms of thrombosis
Damage to cardiovascular endothelial cells (major)
Anticoagulation
barrier effect
Anti-platelet adhesion
With prostacyclin PGI2 and NO
Aspirin also inhibits platelet aggregation
Synthetic antithrombin or coagulation factors
Promote fibrinolysis
Procoagulant (damage)
Activate extrinsic coagulation
Assist platelet adhesion
Release vWF
Inhibit fibrinolysis
Abnormalities in blood flow status
Mainly refers to slow blood flow and eddy currents
Slow blood flow forms venous thrombosis, and turbulent flow forms arterial and cardiac thrombosis.
Common causes of venous thrombosis
Slow and swirling blood flow in venous valves
Temporary stagnation of blood flow
Veins have thin walls and are easily compressed
Blood viscosity is high
increased blood coagulability
hereditary hypercoagulable state
acquired hypercoagulable state
surgery, trauma
DIC
antiphospholipid antibody syndrome
Formation process
Formation of sticky accumulations of platelets
platelet trabeculation
Cellulose network formation
blood clotting
form
White blood acid
Platelets and a small amount of fibrin
Parts with faster blood flow, such as the heart and arteries; the starting point of venous thrombosis
Small gray-white nodules, rough
red blood clot
Intravenous, tail of mixed thrombus
Fibrin mesh and filled with red blood cells (coagulated blood)
Dark red, easy to fall off and form embolism
mixed thrombus
Heart (globular) and blood vessels (lamellar)
White red thrombus with neutrophils at the edge
Spherical shape in the atrium
hyaline thrombus
intravascular microcirculation
fibrin
Can't see
ending
Soften, dissolve and absorb
Small thrombi are easily absorbed, while large thrombi tend to fall out and form embolism as soon as they soften.
mechanization and recanalization
The replacement of thrombus by granulation tissue is called thrombus organization
Because the organized thrombus will become dehydrated and become smaller, it is prone to cracks. The new vascular endothelium will grow into the anastomosis to form a new blood vessel. The partially blocked blood vessel will re-establish blood flow, which is called recanalization.
Calcification
Calcified phleboliths or arterial stones
Influence
block blood vessels
Causes ischemic atrophy until infarction
embolism
When softened, it falls off to form an embolus.
Heart valve deformation
Recurrent clots form in the heart valves, which thicken as they become organized
Generalized hemorrhage (DIC)
It can lead to extensive tissue necrosis and bleeding, consuming a large amount of coagulation factors, and coagulation disorders, leading to widespread bleeding and death from shock.
embolism
The path of travel of emboli
Venous system and right heart emboli
block lungs
Aortic system and left heart emboli
obstruction of small arteries in organs
Commonly found in the brain, spleen, kidneys, and limbs
Portal venous system emboli
Block the liver
cross obstruction
Seen in patients with atrial septal defect
Reverse sexual obstruction
rare
type
Thromboembolism
pulmonary artery
Usually no serious consequences unless the number of emboli is extremely large or blocks a large blood vessel
leading to acute right heart failure and asphyxia
Combined stimulation of the vagus nerve, leading to sudden death
Hemorrhagic infarction of the lungs
systemic arteries
Wherever it is blocked, it will cause
fat embolism
Often derived from long bone fractures and fatty tissue damage
Most commonly blocks cerebral blood vessels, causing cerebral edema and perivascular spotting.
A large number of lipid droplets entering the lungs can cause right heart failure and suffocation
gas embolism
caused by air
When more than 100ml of gas enters the veins and enters the right heart, the mixed blood becomes foamy, hindering venous return and causing suffocation.
Gas can also block pulmonary arteries and cause DIC
Decompression sickness (N2 embolism)
Due to low pressure and then high pressure, nitrogen cannot be quickly integrated into the blood, causing different diseases depending on the location.
Subcutaneous emphysema, joint and muscle pain, located within local blood vessels leading to ischemia and infarction
amniotic fluid embolism
Fetal metabolites causing anaphylactic shock
Amniotic fluid emboli blocks the pulmonary artery and the amniotic fluid contains vasoactive substances causing reflex vasospasm
Amniotic fluid has the function of thromboplastin and causes DIC
infarction
The shape of the infarct
tapered
spleen
kidney
lung
segmental
intestinal
map shape
Heart
Necrosis type
coagulative necrosis
Heart
spleen
kidney
liquefaction necrosis
brain
Infarction type
anemic infarction
Visible congestion and bleeding bands
Brain, heart, spleen, kidney
hemorrhagic infarction
Occurrence conditions
severe congestion
loose tissue
site of occurrence
lung
Blood congestion is a prerequisite
Coagulative necrosis of infarction (more protein, less enzymes)
Patient presents with chest pain due to infarct pleurisy
intestinal
Features
The infarction is dark red and the boundaries are blurred
septic infarction
Caused by emboli containing bacteria that block blood vessels, such as acute infective endocarditis