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MindMap Gallery Repair of damage, local blood circulation disorder (pathology)

Repair of damage, local blood circulation disorder (pathology)

This is a mind map about damage repair and local blood circulation disorders (pathology), including hemorrhage, thrombosis, infarction, congestion, congestion (venous congestion), etc.

Edited at 2024-03-14 17:45:13

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Repair of damage, local blood circulation disorder (pathology)

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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 intestinal and lung tissue, severe congestion)

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

Dust cells, macrophages swallowing dust, silicosis Foam cells Macrophages lipid phagocytosis Atherosclerosis Heart failure cells, macrophages, hemosiderin-laden red blood cells, left heart failure Typhoid cells Macrophages phagocytose Typhi bacilli Enterotyphoid fever Betel nut liver, blood stasis and fatty change coexist

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

Repair of damage

regeneration

Classification

pathological regeneration physiological regeneration

mechanism

epithelial tissue

Covering epithelial regeneration: squamous epithelial defect, wound edge or bottom basal layer cells divide and proliferate → tissue stem cells differentiate and proliferate and move to the defect → form a single layer of epithelium → proliferate and differentiate into squamous epithelium Mucous membrane: similar, first becomes cuboidal and then becomes taller and becomes columnar cells

Glandular epithelial regeneration (if the gland structure, including the basement membrane, is completely destroyed, it cannot regenerate): Hepatocyte regeneration: partial liver resection: proliferation through hepatocyte division Hepatocellular necrosis: the liver lobule mesh scaffold is intact, extending along the scaffold from the edge zone Extensive necrosis of liver cells: reticular fibers transform into collagen fibers or massive proliferation of fibrous tissue.

Fibrous tissue regeneration: Injury stimulates fibroblasts (which can be transformed from quiescent fibroblasts/undifferentiated mesenchymal cells) to divide and proliferate.

Regeneration of cartilage tissue and bone tissue: Cartilage regeneration begins with the proliferation of perichondrium Bone tissue has strong regeneration ability and can be fully recovered after a fracture

Blood vessel

Regeneration of capillaries (blood vessel formation): sprouting method

Repair of large blood vessels: The disconnection requires surgical anastomosis. The severed muscle layer is not easy to completely regenerate and is connected by connective tissue hyperplasia and scar repair.

Muscle tissue: extremely weak regeneration ability, The muscle fibers are completely disconnected and the membrane is not broken → scar healing The entire muscle fiber (including the sarcolemma) is destroyed → difficult to regenerate

nervous tissue

Destruction in the brain and spinal cord cannot regenerate → Repair of glial cells and their fibers: glial scars When peripheral nerves are damaged → if the nerve cells connected to them are still alive: they can be completely regenerated →If the separation is too far or there is scar obstruction: traumatic neuroma, intractable pain

fibrous repair

First, the granulation tissue proliferates, dissolves, absorbs the necrotic tissue and other foreign matter in the damaged area, and fills the tissue defect. Then the granulation tissue → scar tissue mainly composed of collagen fibers, and the repair is completed.

Granulation tissue: composed of new capillaries and proliferated fibroblasts, accompanied by infiltration of inflammatory cells. It is bright red, granular, soft and moist to the naked eye.

Granulation tissue function

Anti-infection and wound protection

Fill wounds and other tissue defects

Organize or encapsulate necrotic thrombi, inflammatory exudates and other foreign bodies

scar tissue effects

Refers to the fibrous connective tissue formed after the granulation tissue has been remodeled and matured.

Fills connection defects and maintains organ integrity and strength

The scar shrinks, restricting movement, and excessive protrusion of the skin is called keloid.

wound healing

skin

Skin appendages (hair follicles, sweat glands, sebaceous glands) are completely destroyed and cannot be completely regenerated, but scar repair The initial stage of tendon rupture is also scar repair

Early bleeding, redness, swelling, clots and scabs

Wound shrinkage

Granulation tissue proliferation and scarring

Regeneration of epidermis and other tissues

Fracture healing: complete regeneration

process

Hematoma formation: massive bleeding at both ends of the fracture and around it

Fibrous callus formation: the hematoma begins to be replaced by granulation tissue and organized

Bone callus formation: calcium salt deposition → woven bone

Callus reconstruction or remodeling: lamellar bone

Influencing factors

age nutrition

Infection and foreign bodies, local blood circulation, innervation, ionizing radiation

type

Primary healing: a wound with few tissue defects, neat wound edges, no infection, and strict wound closure after bonding or suturing.

Second-stage healing: The defect is large and the edges of the wound are irregular and cannot be neatly aligned, resulting in a large scar.

Cells (strong regeneration ability→weak)

Unstable cells (continuously dividing cells) have strong regenerative ability, and stem cells are a necessary condition

epidermal cells Gastrointestinal and respiratory tract mucosal lining cells germ cell lumen lining cells

Stable cells (resting cells)

Parenchymal cells of various glands: pancreas, salivary glands, endocrine glands, sebaceous glands, sweat glands, epithelial cells of renal tubules, etc.

Permanent cells (non-dividing cells) have extremely weak regenerative potential

Nerves, skeletal muscles, cardiomyocytes