Increased arterial blood input (active)

Physiological congestion: physiological needs, increased metabolism

Pathological congestion: congestion in case state

Cause eliminated →return to normal

Basic diseases such as high blood pressure: emotional excitement → cerebral vascular congestion → more severe stroke

Obstructed venous blood return (passive)

Venous compression → venous lumen stenosis → blood return disorder

Venous thrombosis (or tumor thrombus) → obstruction of venous return

Heart failure → Increased cardiac chamber pressure → Obstructed venous return

Cyanosis

Congestive edema: transudate is retained in the tissue (transudate: capillary congestion → leakage of water, salt and a small amount of protein) Effusion: leakage fluid accumulates in the serosal cavity

Congestive bleeding: leakage of red blood cells (Hemosiderin cells: macrophages phagocytose hemosiderin)

Chronic congestion → tissue hypoxia and nutritional deficiencies → parenchymal cell atrophy → interstitial tissue hyperplasia → reticular fiber collagenization → organ hardening (congestive sclerosis)

pulmonary congestion

Liver congestion

Blood vessel wall damage, dilation

Thrombocytopenia or dysfunction

coagulation factor deficiency

Localized massive bleeding within tissue is called edema

Nasal mucosa→epistaxis

Tuberculosis cavitation, bronchiectasis → oral cavity → hemoptysis

Peptic ulcer, esophageal varices → oral cavity → hematemesis

Colon, stomach bleeding→anus→blood in stool

Urinary tract→blood in urine

Bleeding of skin and mucous membranes, from small to large: petechiae → purpura → ecchymosis Degradation of red blood cells → hemoglobin (red-blue) → bilirubin (blue-green) → hemosiderin (brown-yellow)

Anticoagulant function of endothelial cells

The blood flow slows down and creates vortices in the blood flow → platelet side flow, coagulation factors and thrombin concentration increase

Veins are more likely to form thrombus: ① Slow blood flow in venous valves ② Temporary stagnation of blood flow ③ Increased viscosity ④ Thin walls are easily compressed

There is an increase in platelets and coagulation factors in the blood, or the activity of the fibrinolytic system is reduced, and the blood is in a hypercoagulable state.

Adhesion reaction: platelets adhere to subendothelial collagen

Release reaction: fibrinogen, coagulation factors

Adhesion reaction: thrombin converts fibrinogen to fibrin (platelets intertwined)

Platelet and collagen adhesion → platelet release granules → platelet adhesion (fibrinogen → fibrin) → thrombosis Intravenous thrombosis: blood forms a vortex in the venous valve, and platelets are deposited → forming platelet trabeculae with leukocytes adhering around them → there is a fibrin network between the beams with red blood cells inside → the blood vessel cavity is blocked and the blood coagulates

White thrombi: located in the heart valves, cardiac chambers and arteries with rapid blood flow (acute rheumatic endocarditis)

Mixed thrombosis: persistent intravenous thrombosis

Red thrombus: the tail of a persistent thrombus

Hyaline thrombi: within microcirculatory blood vessels, mainly capillaries (microthrombi)

thrombosis

arterial embolism

arterial spasm

blood vessel compression and occlusion

Blood supply characteristics of organs (whether there is collateral circulation, kidneys, brain, and spleen have no collateral circulation and are prone to infarction)

The degree of sensitivity of local tissues to ischemia: ① Brain oligodendrocytes and nerve cells are the most sensitive ② Skeletal muscle and fibrous connective tissue are the most resistant

Shape: cone → spleen, kidney, lung segmental → intestine Irregular map shape→myocardium

Texture: coagulative necrosis → heart, spleen, kidney Liquefied necrosis → brain

Color: low blood content → off-white → anemic infarction Containing a lot of blood → dark red → hemorrhagic infarction

Anemic infarction: solid organs with insufficient collateral circulation (such as spleen, kidney, heart)

Hemorrhagic infarction: common in organs with dual blood supplies and loose tissue structure (lungs, intestines)

septic infarction

Entering the main pulmonary artery and its branches → pulmonary embolism

Blockage of small arteries in organs → brain, spleen, kidneys and limbs

Emboli from the portal system such as mesenteric vein → intrahepatic portal vein embolism

pulmonary embolism

systemic arterial embolism

Large fat droplets appear in the circulating blood stream and block small blood vessels

Air embolism: A large amount of gas enters the blood circulation and blocks the cardiovascular system. Often due to venous injury and rupture

Decompression sickness: After the high-pressure environment quickly changes to low pressure, the gas originally dissolved in the blood quickly dissociates and forms bubbles (nitrogen embolism)

Amniotic membrane rupture, premature rupture or early placental separation, strong uterine contraction, increased intrauterine pressure, amniotic fluid can enter the venous sinus of the uterine wall, forming an emboli. Embolization of pulmonary artery branches, arterioles and capillaries through blood circulation