Cause

Classification

Heart atrophy is usually maltrophic atrophy

Cause

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Cause

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Cause

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Cause

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The atrophy of nerve cells and cardiomyocytes is a common cause of aging of the brain and heart muscle.

chronic inflammation

apoptosis

The heart blood vessels are tortuous (blood vessels are interstitial cells and do not shrink), and the capsule is relaxed

Cerebral gyri become narrower and cerebral sulci become deeper

Myocardial fibers become thinner and narrower

widening of intermuscular distance

Lipofuscin granules can be seen in cardiomyocytes

Skeletal muscle thickening and hypertrophy in athletes

Under the action of estrogen and progesterone during pregnancy, uterine smooth muscle cells hypertrophy and increase in number (hypertrophy with hyperplasia)

? Senile prostatic hyperplasia? ?

Increased cardiac afterload or partial left ventricular myocardial necrosis during hypertension → left ventricular hypertrophy (simple hypertrophy, myocardial inability to proliferate)

Loss of renal function due to unilateral nephrectomy or renal artery occlusion → contralateral renal hypertrophy

Increased secretion of thyroxine in hyperthyroidism → hypertrophy of thyroid follicular epithelial cells

Pituitary basophiloma Increased secretion of adrenotropin → Adrenocortical cell hypertrophy

Concentric cardiac hypertrophy: thickening of the left ventricular wall and interventricular septum, significant thickening of the papillary muscles, and relatively small left ventricular cavity

Activation of proto-oncogenes, increased DNA content, and active mRNA expression lead to

Hyperplasia of remaining liver cells after partial liver resection

In high altitude areas, the body's bone marrow red blood cells and peripheral blood red blood cells increase.

Lobular gland epithelial hyperplasia of adolescent female breasts

Endometrial gland hyperplasia during the menstrual cycle

After tissue injury, wound healing, fibroblasts and capillary endothelial cells are stimulated by growth factors to proliferate.

Chronic inflammation or long-term exposure to physical and chemical factors, covering cell proliferation

Granulation tissue organizes to form scars

The most common cause of pathological hyperplasia is excess hormones or growth factors

increased estrogen

Androgen metabolite dihydrotestosterone

Epithelial classification

metaplastic type

Fibrous tissue (fibroblasts) transform into osteoblasts and chondrocytes

The affected organs increase in size, have blunt edges, tense capsules, ectropion of the cut surface, and become lighter in color (for example, the liver cord becomes larger and thicker, and congestion decreases, resulting in lighter color)

Turbidity and swelling

Early stage: Swelling of organelles such as mitochondria and endoplasmic reticulum → red-stained fine granular matter

Water and sodium further accumulate, the cells swell significantly, the cell matrix is ​​highly loose and vacuolated, and the cell nuclei may also swell.

Granular degeneration, watery degeneration, ballooning degeneration

Lipid droplets of varying sizes appear in the cytoplasm. Large ones can fill the cell and push the nucleus to one side.

In paraffin sections, fat is dissolved and lipid droplets appear vacuolated.

In frozen sections, Sudan 3/4 can be used to dye orange/red respectively.

Can be dyed black with osmic acid

Chronic liver congestion: centrilobular steatosis

Phosphorus poisoning: fatty changes around the lobules

The center is susceptible to hypoxia and the periphery is sensitive to phosphorus

Lipid droplet component of hepatocellular steatosis: neutral fat

Mechanisms of hepatocellular steatosis

Summary of causes: ischemia and hypoxia, phosphorus poisoning, carbon tetrachloride poisoning, starvation, high-fat diet, (sepsis??), hepatitis A virus

Chronic alcoholism or hypoxia (anemia)

Commonly confused with: fatty infiltration of myocardium (fatty heart)

Location: Mainly located at the base of proximal convoluted tubule cells, only in severe cases does it involve the distal convoluted tubule

Ingredients: Excessive reabsorption of lipoproteins in raw urine

Site of occurrence: In the cytoplasm

Deposition materials: various proteins

Pathological changes

Example

Site of occurrence: intercellular matrix (fibrous tissue)

Deposit material: collagen

Features

Pathological changes

Example

Site of occurrence: interstitium (arterial wall)

Deposit material: plasma proteins

Pathological changes: plasma proteins penetrate into the arterial wall, coupled with the deposition of basement membrane metabolites, the arterial wall thickens and narrows, the blood vessel elasticity weakens, and it is easy to rupture and bleed.

Example

Alzheimer's disease, Hodgkin's disease (Hodgkin's lymphoma), elderly, tuberculosis, multiple myeloma, medullary thyroid cancer

Tip: The foodie lady has many marrows

primary

Secondary

Hyaluronidase activity decreases in hypothyroidism, leading to accumulation of hyaluronic acid

Source: Macrophage phagocytosis. Produced by degradation of RBC hemoglobin

Ingredients: Combining Fe3 and protein

Under the microscope: golden yellow or brown particles, which can be stained blue by Prussian blue. This pigment can also be seen outside the cells after macrophage rupture.

Example

Source: Undigested organelle fragments in autophagic lysosomes

Ingredients: Mixture of phospholipids and proteins

Under the microscope: yellowish brown microgranular

Example

Source: melanocytes

Ingredients: Tyrosine is oxidized and polymerized by levodopa

Example

Source: The product of RBC aging and destruction, it is the main pigment in the bile duct

Ingredients: Derived from hemoglobin, but does not contain iron

Under the microscope: Rough, golden particles in the cytoplasm

Example

Fine particles or agglomerates, feeling gritty or hard to the touch

Large calcifications can cause deformation and hardening of tissues and organs

Calcium carbonate and cholesterol can form stones in the gallbladder, renal pelvis, bladder, ureter, etc.

Note: Blue can also be stained for amyloidosis, gray-blue matrix of myxoid change, etc. Inflammatory cells can also be stained blue-purple.

Features: Normal calcium and phosphorus metabolism in the body

Deposition site: necrotic or imminent necrotic tissue or foreign body

Example

Characteristics: Systemic calcium and phosphorus metabolism disorder (hypercalcemia)

Deposition site: within normal tissue

Example

Naked eye: grayish-yellow, dry, solid, with clear boundaries with healthy tissue

Under the microscope: The fine cell structure disappears, but the tissue outline remains. Congestion, hemorrhage and inflammatory reaction zones are formed around the necrotic area, and the boundary is clear.

Commonly occurs in solid organs: heart, liver, spleen, kidney

Ischemia and hypoxia, bacterial toxins, chemical corrosion

Caseous necrosis is complete coagulative necrosis, and some gangrene also contains coagulative necrosis.

Less coagulable protein in tissue

Necrotic cells themselves and neutrophils release large amounts of hydrolases

Tissues are rich in water and phospholipids

Dissolution and liquefaction are prone to occur after necrosis

Under the microscope: dead cells are completely digested and local tissues are rapidly dissolved

Abscess: Fungal infection, neutrophils release large amounts of proteases

Encephalomalacia: ischemia and hypoxia

Lytic necrosis developing from cellular edema

viral hepatitis

spinal cord

Note: Although liver abscess caused by amoeba is not an abscess in the conventional sense, it can also cause liquefaction necrosis.

To the naked eye: Fibrinoid necrosis is necrosis that cannot be determined by the naked eye.

Under the microscope: Formation of filamentous, granular, small strips of fast structureless material

Be honest and lively, feed the wolves and eat your kidneys

Fibrinoid necrosis occurs only in nephritis but not in nephropathy

The acute phase of autoimmune reaction is fibrinoid necrosis, and the chronic phase is fibrosis.

To the naked eye: the necrotic area is yellow, like cheese

Under the microscope: It is granular red stain without structure, which is complete coagulative necrosis.

Necrotic lesions contain substances that inhibit hydrolase activity and are difficult to dissolve and absorb.

tuberculosis

Occasionally seen in some infarcts, tumors, and tuberculoid leprosy

The typical manifestation of granulomatous inflammatory center is caseous necrosis: "The schoolgirl without a horse goes to school to catch cats"

Naked eye: gray-white calcium lesions

Also belongs to the category of liquefaction necrosis

acute pancreatitis

breast trauma

dry gangrene

wet gangrene

gas gangrene

Such as chronic cervicitis, local mucosal epithelial necrosis and shedding

Memory: The structure of the word "guan", with a vertical line in the middle connecting two "mouths", just like a fistula connecting two organs

Such as: pulmonary tuberculosis