Physiological

pathological

Pathological changes

physiological hypertrophy

pathological hypertrophy

The test points for hyperplasia and hypertrophy are mainly three types of cells in the body: whether they can proliferate

Metaplasia is not caused by the direct transformation of the original mature cells, but by the division, proliferation and multi-directional transformation of the original cells. The result of transdifferentiation of differentiated stem cells or undifferentiated mesenchymal cells in connective tissue

aqueous degeneration

It is mostly due to damage to the mitochondria that the sodium-potassium pump becomes dysfunctional, causing a large amount of sodium ions to accumulate inside the cells, causing cell edema.

Pathological changes: Organelles such as cell mitochondria and endoplasmic reticulum become swollen, forming red-stained fine granules in the cytoplasm under a light microscope.

Commonly occurs in: liver, kidney, heart

Triglycerides accumulate in the cytoplasm of non-fat cells

Fatty infiltration: accumulation of triglycerides in the intercellular matrix

often occurs in

intracellular hyalinization

Hyalinization of fibrous connective tissue

Hyalinization of small arterial walls

hemosiderin

lipofuscin

melanin

Bilirubin

dystrophic calcification

metastatic calcification

coagulative necrosis

liquefaction necrosis

fibrinoid necrosis

caseous necrosis

fat necrosis

Gangrene (area of ​​tissue necrosis and infection by several putrefactive bacteria is called gangrene)

Apoptosis is a manifestation of programmed cell death of individual cells in local tissues in vivo. It is an active cell death mode caused by internal and external factors triggering a pre-existing death program in the cell.

Apoptosis was also known as: pyknotic necrosis in the old days

Common test points

most common

Metamorphosis = degeneration, necrosis

Mild damage is degeneration, while severe damage is necrosis.

Parenchymal cells often appear: cell edema, fatty degeneration, coagulative necrosis, liquefaction necrosis, etc.

Parenchymal cells often appear: cell edema, fatty degeneration, coagulative necrosis, liquefaction necrosis, etc.

The process in which fluid components, cellulose and other proteins, and various inflammatory cells in the blood vessels of local inflammatory tissues pass through the vascular tissue gaps, body cavities, body surfaces, and mucosal surfaces is called exudation. The production of exudate is due to increased blood vessel permeability and leukocytes actively swimming out of the blood vessels.

Exudation is the most characteristic change of inflammation! Text

Including the proliferation of parenchymal and interstitial cells. Inflammatory hyperplasia has the function of limiting the spread of inflammation and repairing damaged tissue

Redness, swelling, heat, pain, dysfunction

Fever, increased peripheral leukocytes, cardiovascular reactions, shock, etc.

Hemodynamic changes

changes in vascular permeability

Leukocyte extravasation

white blood cell activation

vasodilation

Increased vascular permeability

Chemotaxis

fever

pain

tissue damage

There are three basic pathological changes in any inflammation: deterioration, exudation, and proliferation. Each inflammation is called inflammation based on which basic pathological change is the main one. For example: hepatitis. In hepatitis, there is lymphocyte infiltration, massive edema and destruction of liver cells, and hepatocyte regeneration. However, hepatitis is dominated by cell destruction, so hepatitis is a degenerative inflammation.

spoil

ooze

hyperplasia

get well

Migration to chronic inflammation

Spread spread

body death

General chronic inflammation

granulomatous inflammation

Small test points: tumor monoclonal proliferation; Late stage of inflammation: polyclonal proliferation.

During gross observation, attention should be paid to the number, size, shape, color and texture of the tumors

Essence (similar to the moon surrounded by stars)

Interstitium (similar to the stars holding the moon)

Concept: refers to the similarity in morphology and function between tumor tissue and a certain normal tissue.

Degree of differentiation: The more the tissue morphology and function of a tumor are similar to a certain normal tissue, it means the degree of differentiation is high/well, the similarity with normal tissue is small, the degree of malignancy is low, and the prognosis is good. If the similarity to normal tissue is small, the degree of differentiation is lower or poorly differentiated, the degree of malignancy is higher, and the prognosis is poor.

Tumor tissue structure and cell morphology are different to varying degrees from corresponding normal tissues, which is called tumor atypia.

Add one after tissue and cell type The word "tumor" can be used; no distinction is made between epithelial or mesenchymal

Malignant tumors of epithelial origin

Malignant tumors of mesenchymal origin

myoblastoma

lipoblastoma

chondroblastoma

osteoblastoma

Tips: Chicken cartilage in juice

Expansive growth

exophytic growth

infiltrative growth

The growth rates of different tumors vary greatly. Benign tumors generally grow slowly, while malignant tumors grow faster.

After the tumor diameter reaches 1~2mm, it cannot continue to grow without the formation of new blood vessels to provide nutrients. Tumors have the ability to induce angiogenesis. Tumor cells themselves and inflammatory cells (mainly macrophages) can produce angiogenic factors, such as vascular endothelial growth factor (VEGF) to induce the formation of new blood vessels.

During the growth process of malignant tumors, the phenomenon of increased invasiveness is called tumor evolution, which can be manifested as accelerated growth, infiltration into surrounding tissues and distant metastasis. Tumor evolution is associated with its acquisition of increasing heterogeneity

It is an indicator that describes the degree of malignancy. It is an indicator of benignity and malignancy. It is an indicator of how good it is and how bad it is.

According to the tumor: degree of differentiation, atypia, number of mitotic figures

Grade I--highly differentiated, well differentiated, small atypia, and low degree of malignancy

Grade Il - moderately differentiated, moderately malignant

Grade III—poor differentiation, large atypia, and high degree of malignancy

Staging describes the tumor’s growth range, lymph node spread, and distant metastasis. TNM is commonly used internationally.

T: size of primary tumor and depth of invasion

N: Lymph node metastasis and fusion

M: Whether there is distant metastasis

Local compression and obstruction (main symptoms)

secondary changes

secretion of too many hormones

body death

secondary changes

Cachexia

ectopic endocrine syndrome

paraneoplastic syndrome

Although certain diseases (or lesions) are not malignant tumors themselves, they have the potential to develop into malignant tumors, and patients are at increased risk of developing corresponding malignant tumors. These diseases or lesions are called precancerous diseases or precancerous lesions. It should be noted that precancerous diseases (or lesions) do not necessarily develop into malignant tumors. Summary: Precancerous lesions are not cancer.

Leukoplakia (oral cavity, vulva) [Oral ulcer NO!]

Breast fibroplasia【Breast fibroadenoma NO!】

Chronic atrophic gastritis with intestinal metaplasia

chronic ulcerative colitis

Colorectal adenoma/polyposis

chronic skin ulcers

Dysplasia is a term used to describe atypical growths associated with tumor formation. Dysplastic epithelium has cellular and structural atypia, but it does not always progress to carcinoma. Some dysplasia that does not involve the full thickness of the epithelium may reverse regression when the causative factor is removed.

The term carcinoma in situ (CIS) is usually used for epithelial lesions. It refers to dysplastic cells that are the same as cancer cells in morphology and biological characteristics. They often involve the entire thickness of the epithelium but do not break through the basement membrane and infiltrate downward. It is sometimes also called It is intraepithelial carcinoma.

Benign tumors of epithelial tissue (not important

Epithelial malignant tumors

mesenchymal tissue tumors

thrombosis

arterial embolism

arterial spasm

blood vessel compression and occlusion

Depends on the vascular distribution pattern of the infarcted organ

cone distribution

stage distribution

map shape

Depends on the type of cell necrosis in the tissue

For example: cerebral infarction, due to interruption of blood flow, leads to ischemia and hypoxia of brain tissue. Since the death of brain cells is liquefaction necrosis, the texture of cerebral infarction is relatively soft, which is also called softening focus.

It depends on whether there are a large number of red blood cells in this tissue after infarction

Divided into: anemic infarction (white infarction) hemorrhagic infarction (red infarction)

anemic infarction

Hemorrhagic infarction is a red infarction. The infarction focus is dark red and the amount of bleeding is large. It occurs on the basis of severe congestion and is often found in organs with loose tissue, dual blood supply or abundant anastomotic branches.

Commonly found in: lung, intestine, ovarian cyst pedicle twist

Venous system and right heart emboli

Aortic system and left heart emboli

pulmonary embolism

systemic arterial embolism

fat embolism

non-traumatic fat embolism

air embolism

decompression sickness

amniotic fluid embolism

Physiological congestion

Pathological congestion

Congested organs: large, red, hot

Mostly pathological congestion

Organs with congestion: big, purple, cool

Long-term organ congestion will cause congestion sclerosis (excessive cell tissue necrosis, resulting in fibrous repair and eventual sclerosis)

Congestion of vital organs

Damage to vascular endothelial cells is most important

Abnormalities in blood flow status

increased blood coagulability

thrombus

embolus

embolism

ischemia

infarction

White thrombus

mixed thrombus

red blood clot

hyaline thrombus

outcome of thrombosis

coated epithelium blood cells

Glandular epithelium Smooth muscle cells Hepatocytes Renal tubular epithelial cells

Neuronal cells, cardiomyocytes, bones muscle cells

new capillaries

fibroblasts

inflammatory cells

myofibroblasts

Anti-infection and wound protection

Fill wounds and other tissue defects

Organized or encapsulated necrosis, thrombosis, inflammation Penetration of metal and other foreign matter

Mature into fibrous connective tissue (Scar tissue)

The morphological signs of scar tissue are

It is seen in wounds with few tissue defects, neat wound edges, no infection, and tight wound surfaces after bonding or suturing. This kind of wound has only a small amount of blood clots, a mild inflammatory reaction, and epidermal regeneration can cover the wound within 24 to 48 hours. Granulation tissue can grow from the edge of the wound on the third day and quickly fills the wound. Collagen fibers will appear on both sides of the wound in 5 to 7 days. At this time, the sutures of the incision can be removed, and the incision reaches clinical healing standards.

It is seen in wounds with large tissue defects, irregular wound edges, open wounds, inability to neatly join together, or wounds with infection. This type of wound healing has an obvious inflammatory response, a large wound, obvious wound shrinkage, a longer healing time, and a larger scar.

Both bone tissue and bone marrow are rich in blood vessels. There will be massive bleeding at and around the two ends of the fracture, forming a hematoma, which will solidify after a few hours. At the same time, a mild inflammatory reaction often occurs.

2 to 3 days after the fracture, the hematoma begins to be replaced by granulation tissue and organized, and then fibrosis occurs to form fibrous callus, or temporary callus. The naked eye and X-ray examination show spindle-shaped swelling in the fracture area. In about 1 week, the proliferated granulation tissue and fibrous tissue can further differentiate to form hyaline cartilage. The formation of hyaline cartilage is generally more common in the callus area of ​​the periosteal membrane, but less common in the callus area of ​​the bone marrow.

The above-mentioned fibrous callus gradually differentiates into osteoblasts and forms osteoid tissue. Later, calcium salt deposition occurs, and the osteoid tissue transforms into woven bone. The cartilage tissue in the fibrous callus also evolves into bone tissue through the process of chondrification bone. , thus forming bony callus.

Real bone tissue appears during this period, but the bone tissue is disordered and not dense.

Because the structure of woven bone is not dense enough and the trabecular bone is arranged disorderly, it still cannot meet the needs of normal function. In order to adapt to the stress during bone activity, woven bone is further remodeled into mature lamellar bone. The normal relationship between cortical bone and medullary cavity and the normal arrangement of trabecular bone are also restored. Remodeling is completed under the coordinated action of bone resorption by osteoclasts and new bone formation by osteoblasts.

During this period, the soft and disorderly arranged bone tissue is remodeled to form lamellar bone.

age

Nutrition

Infection and foreign bodies

local blood circulation

Innervation and ionizing radiation

Timely and correct reduction of the fracture end is a necessary condition for fracture healing.

Timely and firm fixation of fracture ends is an important factor in healing.

Actively performing functional exercises early and maintaining good local blood supply can promote the healing process.