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MindMap Gallery PathologyLocal blood circulation disorder

PathologyLocal blood circulation disorder

This is a mind map about pathological local blood circulation disorders, including bleeding, thrombosis, Infarction, congestion, congestion, etc.

Edited at 2024-03-08 21:03:42

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PathologyLocal blood circulation disorder

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Outline

local blood circulation disorder

Hyperemia (arterial congestion)

big, red, hot

Physiological congestion

Refers to the congestion of local tissues or organs due to physiological needs and enhanced metabolism.

Pathological congestion

inflammatory hyperemia

Congestion (venous congestion)

Big, purple (cyanosis), cool

reason

venous compression

venous lumen obstruction

heart failure

Classification

pulmonary congestion

Caused by left heart failure

acute pulmonary congestion

Foamy red bloody liquid. Under the microscope, the capillaries in the alveolar walls are dilated and congested, the alveoli become thicker, and may be accompanied by edema in the alveolar spaces. Some alveolar cavities are filled with edema fluid, and bleeding can be seen.

chronic pulmonary congestion

Manifestation = acute heart failure cells pulmonary fibrosis

Heart failure cells (macrophages that engulf hemosiderin particles)

The texture becomes hard and tan → the lungs become brown and hardened

Liver congestion

Right heart failure, long-term severe liver congestion: congestion cirrhosis

acute

Under the microscope, the central lobular veins and liver sinusoids are dilated and filled with red blood cells. In severe cases, the central lobular liver cells may atrophy and become necrotic. The hepatocytes near the perilobular portal area are close to the hepatic arterioles and have a mild degree of hypoxia, so only hepatic steatosis may occur.

Chronic

Betel nut liver: The cut surface is red (congestion area) and yellow (liver fatty change area) alternately, the central hepatic sinusoids of the liver lobules are highly expanded with congestion and bleeding, and the liver cells atrophy or even disappear. Fatty degeneration of hepatocytes in peripheral liver lobules

infarction

Reasons: 1. Thrombosis 2. Arterial embolism 3. Arterial spasm 4. Blood vessel compression and occlusion

type

Anemic infarction (solid organs with insufficient collateral circulation, such as spleen, kidneys, heart, and brain tissue)

Hemorrhagic infarction (loose bowel and lung tissue)

Septic infarction (caused by an emboli containing bacteria blocking a blood vessel. Common in acute infective endocarditis)

thrombosis

conditional mechanism

Cardiovascular endothelial cell damage

adhesion reaction

release reaction

sticky reaction

Abnormalities in blood flow status

There are four times more arteries (slower flow) than veins

increased blood coagulability

process

1. Platelets adhere to the exposed collagen surface after intimal injury, and are swollen and deformed after being activated by collagen. 2. Release platelet granules, and then release ADP, thromboxane A, 5-HT, platelet factor IV and other substances from the granules. , so that the platelets in the drug continue to adhere locally and form reversible platelet piles. 3. As the endogenous and exogenous coagulation pathways are activated, it becomes irreversible platelet thrombus and becomes the starting point of thrombus.

type

White thrombus

Located in the heart valves, cardiac chambers and arteries where blood flow is faster

mixed (lamellar) thrombus

Veins have an alternating gray-white and reddish-brown layered structure. The body of the continuous thrombus in the vein is a mixed thrombus, which is rough, dry, cylindrical, and adheres to the blood vessel wall.

red blood clot

In veins, mixed thrombus gradually increases and blocks the vascular cavity. When the local blood flow downstream of the thrombus stops, the blood coagulates and becomes the tail of the continuous thrombus. No adhesion, easy to fall off

hyaline thrombus (fibrinous thrombus)

Capillaries, composed of eosinophilic homogeneous fibrin, most commonly seen in DIC

ending

Soften, dissolve and absorb

The activation of plasmin in the thrombus and the lytic protease released by the disintegration of leukocytes can soften the thrombus and gradually dissolve it.

mechanization and recanalization

The activity of the plasmin system is insufficient and the thrombus will become organized when it exists for a long time.

Calcification (calcium salt deposits)

Influence

block blood vessels

When the arterial lumen is not completely blocked, it can cause ischemia of local organs or tissues and atrophy of parenchymal cells. Complete: infarction. Veins: Complete: congestion, edema, hemorrhage, and even necrosis (such as enterohemorrhagic infarction).

Heart valve deformation

Extensive bleeding (can result from DIC)

embolism

The phenomenon of abnormal substances that are insoluble in the blood and travel with the blood flow to block the lumen of blood vessels is called embolism. Abnormal material blocking a blood vessel is called an emboli (solid, liquid, or gas)

type

Thromboembolism (more than 99%)

Pulmonary embolism (more than 95% comes from the deep veins of the lower limbs above the knee, especially the popliteal vein, femoral vein and iliac vein) right heart failure and vascular smooth muscle spasm

Systemic arterial embolism (80% from the left heart chamber)

fat embolism

When a large number of lipid droplets (9~20g) enter the pulmonary circulation in a short period of time and block 75% of the pulmonary circulation area, it can cause suffocation and death from acute right heart failure.

gas embolism

A large amount of gas (>100ml) quickly enters the veins and flows to the right heart with the blood. Due to the beating of the heart, the air and blood are stirred to form a large number of blood bubbles, causing the blood to become foamy and fill the heart cavity, hindering the return and direction of the venous blood. The output of the pulmonary artery caused severe circulatory disorders. Patients may have difficulty breathing, cyanosis, and sudden death.

Amniotic fluid...

Bleeding

rupture hemorrhage

rupture of the heart or blood vessel wall

Mechanical damage to blood vessels

Blood vessel wall or heart disease

Lesion erosion around blood vessel walls

Vein rupture

ruptured capillaries

leakage bleeding

Increased capillary permeability and enlarged endothelial cell gaps

blood vessel wall damage

Thrombocytopenia or dysfunction

coagulation factor deficiency

endothelial cell function

Anticoagulation

barrier effect

Anti-platelet adhesion effect

Synthetic antithrombin or coagulation factors

Promote fibrinolysis

Promote coagulation

Activates the extrinsic coagulation process,

Assist platelet adhesion

Inhibit fibrinolysis