栓塞多来自静脉血栓脱落

心脑动脉易发生粥样硬化

Detached thrombus or its segments (most common), tumors, parasites

Fat emboli

Nitrogen, air, etc.

Venous system and right ventricular emboli

The resistance in the pulmonary artery increases sharply, causing acute right heart failure

Pulmonary ischemia and hypoxia, reduced blood return to the left heart, and insufficient coronary artery perfusion lead to myocardial ischemia

Pulmonary embolism stimulates the vagus nerve and causes spasm of pulmonary arteries, coronary arteries, bronchial arteries and bronchial smooth muscles through nerve reflexes, leading to acute right heart failure and asphyxia.

Platelets within the thromboembolus release 5-HT and thromboxane A, which can also cause pulmonary vascular spasm.

Patients may suddenly develop symptoms such as difficulty breathing, cyanosis, and shock. In severe cases, death may occur due to acute respiratory and circulatory failure (sudden death)

Aortic system and left ventricular emboli

Easy to emboli

Not easy to embolize

Venous system and right ventricular emboli (rarely)

Mesenteric vein and other portal vein system emboli

Inferior vena cava emboli

Can be phagocytized and absorbed by macrophages, or by Lipase in the blood decomposes and removes it without adverse consequences

Enters the pulmonary circulation in a short period of time, When 75% of the pulmonary circulation area is blocked

Causes pulmonary artery branch, arteriole or capillary embolism

It reaches the systemic circulation through the capillaries of the alveolar wall through the pulmonary veins to the left heart, causing embolism in multiple organs throughout the body.

Free fatty acids released from lipid droplets can also cause local poisoning, damage endothelial cells, and produce a characteristic ecchymotic rash.

Use positive pressure intravenous infusion and artificial pneumothorax or pneumoperitoneum during head, neck, chest wall, and lung surgery or trauma

during childbirth or miscarriage

A small amount of air enters the blood

Large amount of air (>100ml)

Diving operations, caisson operations → The body quickly changes from a high-pressure environment to a normal pressure or low-pressure environment → Gas liberates to form bubbles

Skin and subcutaneous

exercise system

circulatory system

digestive system

nervous system

Pulmonary arterioles and capillaries contain amniotic fluid components (keratinized squamous epithelium, lanugo, vernix, meconium and mucus)

The onset is acute and the consequences are serious. Patients often have difficulty breathing, cyanosis, convulsions, shock, coma, or even death during or after delivery.

Amniotic fluid components enter the blood → multiple pulmonary embolism

Amniotic fluid components enter the blood as antigens

Amniotic fluid has thromboactivase-like effect

Few anastomotic branches, prone to infarction

Dual blood circulation

Rich anastomotic branches

The infarct is cone-shaped, with a fan-shaped or triangular section. Its tip is located at the vascular obstruction, often pointing to the spleen, kidneys, and lungs, and the bottom is the surface of the organ.

Infarction lesions are segmental in shape

The infarction is irregular and map-like

蛋白质多的器官——心、肾、脾、肝,都是凝固性坏死 脂肪多的器官——脑、胰腺、乳房、脊髓,都是液化性坏死

When fresh, due to tissue disintegration, the local colloid osmotic pressure increases and absorbs water, causing local swelling and slight bulges on the surface and cut surface. If the infarction is close to the serosal surface, the serosal surface is often covered with a layer of fibrinous exudate.

Old infarction is slightly dry due to less water content, the texture becomes hard, and the surface is sunken.

It is soft and loose when fresh, and gradually liquefies into a cyst shape over time.

anemic infarction/white infarction

Hemorrhagic infarct/red infarct

Dense tissue and insufficient collateral circulation

spleen, kidney, heart (coagulative necrosis)

brain (liquefied necrosis)

Features

Variety

seen in

Variety

Acute infective endocarditis (emboli are most likely to fall off), bacterial emboli flow into the narrow blood vessel and embolize it

Bacterial clusters and a large number of inflammatory cell infiltrates can be seen in the lesion. If it is a purulent bacterial infection, an abscess can be formed.

platelet adhesion

platelet release

platelet aggregation

Platelets interweave with fibrin to form irreversible aggregates, Formation of platelet thrombus (origin of blood clots)

The blood flow slows down, a vortex is created behind the blood clot, and platelet blood clots are continuously produced.

A fibrin network containing a large number of red blood cells appears between the trabeculae.

Separates platelets and coagulation factors in the blood from the highly procoagulant subendothelial extracellular matrix

Synthetic prostacyclin PCI₂ and nitric oxide NO

Synthesis of thrombomodulin

Synthesis of membrane-associated heparin-like molecules

Synthetic protein S

Synthetic tissue plasminogen activator t-PA

Mediates platelet adhesion reaction

Initiates the intrinsic coagulation process

Initiate the extrinsic coagulation process

Inhibit fibrinolysis

Rheumatic and infective endocarditis, endocardium in the area of ​​myocardial infarction, severe atherosclerotic plaque ulceration, traumatic or inflammatory arterial and venous injury

hypoxia, shock, sepsis and Bacterial endotoxins can cause

Platelets can enter the side stream and increase contact and adhesion with the intima

Local thrombin easily accumulates and reaches the concentration required for coagulation.

like

Features

like

Features

Cancer cells release procoagulant factors, such as tissue factor, etc., resulting in multiple and recurrent thrombotic migratory vasculitis or non-bacterial thromboenditis.

The mucus released by cancer cells contains cysteine ​​proteases, which can directly activate factor X. Plasma coagulation factors such as factor V.VII.VIII and fibrinogen are also often elevated in patients.

Activation of coagulation factors and release of tissue factor induced by a series of factors

Hemoconcentration, increased levels of fibrinogen, prothrombin and coagulation factors Ⅻ and Ⅶ in the blood

A large amount of immature platelets are added to the blood, which increases its viscosity

Long-term ischemia and hypoxia in microcirculatory capillaries leads to extensive cell disintegration and the formation of diffuse intracapillary coagulation.

Increased platelet count and increased viscosity

The origin (head) of persistent thrombus

Heart valves, cardiac chambers, and arteries with faster blood flow

It looks like a small gray-white nodule or vegetation, with a rough surface and a solid texture. It adheres closely to the blood vessel wall and is not easy to fall off.

Platelets Small amounts of fibrin

The most common venous thrombosis

Head downstream (body) of persistent thrombus

Atrial fibrillation or bistenosis causing ball thrombus in the left atrium

Mural thrombi within cardiac chambers, atherosclerotic ulcers, or aneurysms

It has an alternating gray-white and reddish-brown layered structure (alternating gray-white and brown striped structures may appear)

It is rough, dry, and cylindrical in shape, adheres to the blood vessel wall, and is not easy to fall off.

Fibrin RBC WBC plt

tail of persistent thrombus

rarely seen

Thrombus appears dark red

fibrin red white blood cells

Massive coagulation → consumes a large amount of coagulation factors and synthesizes a large amount of fibrin

Fibrin only

process

result

Start in 1~2 days, complete in 2 weeks

Endothelial cells and fibroblasts grow from the blood vessel wall into the thrombus and replace the thrombus

The organized thrombus dries and shrinks or partially dissolves to form a crack. The surrounding new vascular endothelial cells grow into and cover the surface of the crack to form new blood vessels and anastomose and communicate with each other, allowing the partially blocked blood vessels to rebuild blood flow.

Within the thrombus, calcium salt deposition occurs in the fibrous tissue based on vitrification.

Prevent ulcers and tuberculosis from eroding blood vessels and causing heavy bleeding

blocked arteries

venous obstruction

The whole or part of the thrombus breaks off into an embolus. When it travels with the blood flow to a narrow blood vessel, it is blocked and stays, causing thromboembolism.

If the embolus contains bacteria, it can lead to severe septic infarction or abscess formation due to bleeding from the embolized tissue.

rheumatic endocarditis, infective endocarditis

Thrombosis and organization of heart valves may occur repeatedly

depletion coagulopathy

mechanism

mechanism

Compression of local veins causing congestion of corresponding tissues

Compression of the common iliac vein causes congestion in the lower limbs

Compression of mesenteric veins causing intestinal congestion

Compression of hepatic sinusoids and sublobular veins blocks venous return, increases portal venous pressure, and causes congestion of the gastrointestinal tract and spleen.

Patients will experience congestion, edema, and pain in the affected limbs.

There are many venous branches, which can form collateral circulation and blood obstruction is not obvious. Congestion will occur only when a larger venous trunk is blocked or multiple veins are blocked, causing collateral circulation to fail.

Increased pulmonary venous pressure, causing pulmonary congestion

Systemic circulation congestion (liver congestion is common, others include spleen, kidney, gastrointestinal tract and lower limb congestion)

The lungs are enlarged, dark red, and foamy red bloody fluid leaks from the cut surface

The alveolar wall capillaries are dilated and congested, and the alveolar walls become thickened, which may be accompanied by edema of the alveolar septa. Some alveolar cavities are filled with eosinophilic edema fluid, and bleeding can be seen.

Sclerosis of the lungs, showing a tan color (brown sclerosis of the lungs)

The alveolar wall telangiectasias and congestion are more obvious, and the alveolar septa can also be thickened and fibrosed.

In addition to edema fluid and bleeding in the alveolar cavity, a large number of hemosiderin-containing cells, that is, heart failure cells, can also be seen.

The liver increases in size and turns dark red

The central lobular veins and liver sinusoids are dilated and filled with red blood cells. In severe cases, central lobular liver cells may atrophy and necrosis.

Hepatocytes near the periphery of the lobule are close to the hepatic arterioles and suffer from mild hypoxia, so only mild hepatic steatosis may occur.

Betel nut liver

The liver sinusoids in the center of the liver lobules are highly dilated, congestion and bleeding, and the liver cells atrophy or even disappear.

Fatty degeneration of hepatocytes in peripheral liver lobules

Different from portal cirrhosis, its condition is mild and liver lobular reconstruction is not obvious. Usually no portal hypertension or liver failure

The hepatocytes in the center of the liver lobule atrophy and disappear, the reticular fibers collapse and become collagenous, the fat storage cells proliferate next to the liver sinusoids, and the synthesis of collagen fibers increases. Together with the proliferation of fibrous connective tissue in the portal area, the interstitial fibrous tissue of the entire liver increases.

capillary congestion

Capillary permeability↑↑

acute

Chronic

acute

Chronic

Caused by damage to the heart or blood vessel walls, heavy bleeding

Mechanical damage to blood vessels

Blood vessel wall or heart disease

Lesion erosion around blood vessel walls

Vein rupture

ruptured capillaries

The permeability of capillaries and post-capillary veins in the microcirculation increases, and blood leaks out of the blood vessels through the expanded endothelial cell gaps and contracted basement membrane.

damage to blood vessel walls

Thrombocytopenia or dysfunction

coagulation factor deficiency

Such as hemopericardium, hemopleural hemorrhage, hemoperitoneum and hemarthrosis

Such as cerebral subdural hematoma, subcutaneous hematoma, retroperitoneal hematoma, etc.

Under the microscope, red blood cells or hemosiderin can be seen in the tissue

Nosebleeds

Hemoptysis

Vomiting blood

Bloody stools

blood in urine

Petechiae: bleeding points 1 to 2 mm in diameter

Purpura: Bleeding spots 3~5mm in diameter

Ecchymoses: Bleeding spots with a diameter exceeding 1~2cm

The bleeding process is rapid and occurs within a short period of time

May occur when bleeding is widespread

If cirrhosis occurs due to portal hypertension Extensive gastrointestinal mucosal bleeding

ruptured heart

Cerebral hemorrhage (brainstem hemorrhage)

intracerebral cyst hemorrhage

retinal hemorrhage

iron deficiency anemia

Hydrostatic pressure, the plasma exerts force from more water to less water, and if the tissue fluid is more water, the plasma will be reabsorbed Osmotic pressure, plasma exerts force from low concentration to high, and tissue fluid concentration is high, plasma moves to tissue fluid.

right heart failure

left heart failure

Tumor, pregnant uterus compressing veins

Arteriole dilation

Capillary wall permeability↑

Decreased plasma albumin/hypoalbuminemia

Causes subcutaneous tissue edema (orange peel-like appearance)

The axillary lymph nodes were removed, and the lymphatic vessels were also cut and ligated, thereby blocking the lymphatic return path and causing lymphatic return disorder in the upper limbs.

It causes venous occlusion and destruction of lymphatic vessels in the radiation field. It can also compress veins and lymphatic vessels due to local muscle fibrosis, affecting the return flow of the upper limbs.

Tissue fluid retention in the lower limbs, edema of the affected lower limbs and scrotum (elephaniasis)

HE staining shows clear blank area

When the protein content is high (inflammatory edema)

When the protein content is low (cardiac or renal edema)

Often pitting edema

Right heart failure edema

renal edema

Left heart failure, kidney failure, ARDS, lung infections and allergies

Edema fluid accumulates in the alveolar cavity, causing the lungs to become swollen and elastic, become solid, increase the weight ratio, and cause light red foamy fluid to ooze out on the cut surface.

Locally damaged brain tissue

global cerebral edema

naked eye

under the mirror

helpful in diagnosis