Part III - jpck.zju.edu.cnjpck.zju.edu.cn/jcyxjp/files/dao/04/PPT/042.pdf · Apoptosis Conception:...

ZHOU REN周韧

Prof., M.D., Ph.D.

Institute of Pathology & Forensic MedicineDepartment of Pathology & Patho-physiology

Zhenjiang University Judicial Evidence & Evaluation Center

Zhejiang University School of Medicine

General Curriculum

Cell injury and AdaptationPart III

Chapter 1. Cell injury and AdaptationPart III

Course of Basic Medical Sciences Chapter 1

2. Cell DeathI. Necrosis

Def. Necrosis may be defined as the morphology of cell death in living body.

AutolysisHeterolysis

Fundamental changes①Nuclear changes: Pyknosis, karyorrhexis, Karyolysis.

②Cytoplasmic changes: acidophilic, granular, opaque mass.

Gross appearances of necrosis in earlier stage

Classification of necrosisDifferent classifications of necrosis type

①Coagulative necrosis②Caseous necrosis③Liquefactive necrosis④ Fat necrosis

Fibrinoid necrosis (Fibrinoid change )Gangrene

a)Dry gangreneb)Moist gangrenec)Gas gangrene

① Coagulative necrosis② Liquefactive necrosis③ Types of Special necrosis

Caseous necrosisGangrene

a) Dry gangreneb) Moist gangrenec) Gas gangrene

Fat necrosisFibrinoid necrosis (Fibrinoid change )

Types of necrosis.①Coagulative necrosisConception: Coagulative necrosis implies preservation of the basic outline of the coagulated cell for some days with the disappearance of fine structures (cellular details) within cell.

Mechanism: Intracellular acidosis denatures not only structural proteins but also enzymic proteins and so blocks the proteolysis of the cell.

Morphology:②Caseous necrosis

Conception: A distinctive form of coagulative necrosis, most often occurs in tuberculosis. The term “caseous” is derived from the gross appearance of the necrotic area. i.e. white and cheesy. Characteristic morphology: disappearance of both basic outline and fine structures (cellular details) within cell of the affected cell.

③Liquefactive necrosisConception: The damaged cells are lysed by autolysis or heterolysis leaving amorphous, fluid or semifluid material.Morphology:

④ Fat necrosisa)Enzymatic fat necrosis: In acute pancreatitis, activated pancreatic enzymes are released from pancreas resulting in destruction of fat tissue.b)Traumatic fat necrosis: Trauma induce rupture of fat cells. The released fat causes chronic inflammation and foreign body reaction.

Fibrinoid necrosis(Fibrinoid change) Conception: Accumulation of pink staining homogenous masses of fibrin, immunoglobulins, and other plasma proteins within the vascular wall, connetive tissue is known as fibrinoid change.

GangreneDef. Massive necrosis of body surface or organs with a passage to the body surface with putrefaction superadded is known as gangrene.

Classification:a)Dry gangrene

Conception: Dry gangrene occurs in the extremities due to occlusion of large artery with intact venous returns. The necrotic area is well dermacated black and mummification.

Morphology:Course of Basic Medical Sciences Chapter 1

b)Moist gangreneConception: Blockage of venous return and artery supply→massive necrosis followed by liquefaction caused by bacterial enzyme→purplish black color with fouelsmelling.

c)Gas gangreneConception: A serious complication of war wounds. deep contaminated wound(massive necrosis) + clostridia group bacterial infection→gas production through the action of saccharolytic and proteolytic enzyme released from bacteria.

Cellular aging

functional alterationmorphorlogy

Aging clock•telomeres: its length ∝ life span• telomerase: control of the length

II. ApoptosisConception: Apoptosis is a distinct type of cell death(cell suicide). It usually involves single cells, or cluster of cells. It is thought to be responsible for numerous physiologic events as well pathologic including the programmed destruction of cells during embryo-genesis..

Course of Basic Medical Scie ter 1nces Chap

Biochemical Characteristics of Apoptosis：

• 由基因调控，是耗能的主动过程

• Ca2+/Mg2+依赖的核酸内切酶活化

• DNA断裂以核小体为单位

• DNA电泳呈阶梯状图谱

Molecular Mechanism of Apoptosis：

I. Physiology of Apoptosis :

Biological significances of Apoptosis：

1. Programmed cell death in embryo-development for shaping the body morphology.

2. Hormone-depended cell retrogrades in adult.

e.g. uterus endomembrane in menses cycle, ovary follicle occlusion in manopause, post-feed breast gland retrogrades.

3. Relative balance of cell number in cellular dynamics, e.g. epithelium in crypt of small intestine.

4. The remove of post-life cell: neutrophils post-acute inflammation, lymphocytes post-immune reactions,

5. The remove of harmful cell: self-reaction lymphocytes, post-reaction Tc cell after virus infection and neoplasm.

The diseases caused by abnormal increment of apoptosis :

Alzheimer’s disease /neuron cell

AIDS/ MΦ,TH

some virus infection: Councilman body in viral hepatitis

post-radio injury or drug injuryprotected from mutation of DNA

infarction of myocardium or stroke (apoplexy)

Biological significances of Apoptosis：II. Pathology of Apoptosis :

some types of pathological atrophy due to duct occlusion of pancreas, parotid or kidney

post-gonadectomy atrophy: post-testectomy prostate gland

The diseases caused by abnormal decrement of apoptosis :

Some type of neoplasia

Some type of Autoimmune diseases: e.g. SLE

Key words in this chapter

NecrosisCoagulative necrosisCaseous necrosisLiquefactive necrosisFat necrosisFibrinoid necrosis Gangrenea)Dry gangreneb)Moist gangrenec)Gas gangrene

ApoptosisAdaptationAtrophyHypertrophyHyperplasiaMetaplasia

Degeneration Cellular swellingFatty changeHyaline changeAmyloid change(amyloidosis)Mucoid degenerationIntracellular pigment accumulationPathological calcification

Chapter 2 Regeneration and Repair

REGENERATION

Control of Cell GrowthMolecular events in cell growthDifferentiation at site of injuryExtracellular matrix and Cell-Matrix interactions

1. Labile cells continue to multiply throughout the life to replace those shed or destroyed cells during physiologic processes, including epidermis, alimentary, respiratory and urinary epithelium, hemopoietic cells, lymphoid cells.

2. Stable cells normally cease multiplication but retain mitotic ability during adult life. e.g. liver cell, kidney tubular cells, endocrine cells.

3. Permanent cells loss mitotic ability, comprise neurons and skeletal and cardiac muscle cells.

Regeneration: The migration and proliferation of specialized cells re- establishing the anatomical and functional integrity of an organ or tissue. These processes may ac t a lone, but usua l ly found incombination.

Molecular events of cell growthCourse of Basic Medical Sciences Chapter 2

Extracellular matrix and Cell-Matrix interactionsCourse of Basic Medical Sciences Chapter 2

REPAIRRepair: the migration and proliferation of connective tissue cells

leading to scar formation.(Organization)

1. Angiogenesis2. Fibrosis3. Maturation and organization of the scar (remodeling)

Organization is the replacement of dead tissue or inert material by granulation tissue—immature fibrovasculartissue. It is seen in infarct, hematoma, thrombi, and fibrinous exudates.

Granulation tissue is formed by proliferative (novel) fibroblasts and capillaries.

WOUND HEALINGHealing is the replacement of dead tissue by

viable tissue. In considering the healing of skin wound,two types of healing are usually distinguished.

1. Healing by first intention which occurs in a clean wound with a minimum space between the margins——incised wound.Stages in healing may be as follows: (1) Escape of blood and exudate(2) Acute inflammation during the first 24hr

(3)Proliferation and migration of epithelial cells of the epidermis which undermine the blood clot superficial forming a scab. This regeneration is usually complete 24 to 36 hr after injury.(4) Migration and proliferation of fibroblasts and endothelial cells (organization is seen 48 to 72 hr).

(5) Appearance of collagen fibers coated with ground substance 4 to 5 days.

(6) Scar formation during the second week.

2. Healing by second intention which occurs in open or excised wound.

Comparison of two types of healing

characteristic Primary union Secondary union (1st intention) (2nd intention)

defect size small largesuture usually yes noamount of necrotic tissue small large

PMN/monocyte less moreamount of granulation tissue small largescar size very small largerate of hearing rapid slowcomplication rarely, if any more

Fracture healing

(1) Formation of hematoma (2) Formation of fiber bone(3) Formation of osteo-bone(4) Reconstruction of novel bone

FACTORS INFLUENCING WOUND HEALING

1. local factors retarding the processes of healing

(1)infections (2)foreign bodies(3)poor blood supply

2. general factors retarding the processes of healing

(1)aging(2)poor nutrition(3)diseases (diabetes)(4)endocrine factors: adrenal

corticosteroid hormone inhibits proliferation of fibroblasts and collagen synthesis

Key words and points in this chapterRepairOrganizationGranulation tissue1st intention2nd intentionFACTORS INFLUENCING WOUND HEALING

ZHOU REN周韧

Prof., M.D., Ph.D.

Institute of Pathology & Forensic MedicineDepartment of Pathology & Patho-physiology

Zhenjiang University Judicial Evidence & Evaluation Center

Zhejiang University School of Medicine

General Curriculum

Disorder of vascular flow

Structure and function of blood vesicle

Disorder of vascular flowmay be divided into general and local categories.

The local disorders contain:①Derangement of local blood volume: hyperemia and

ischemia,②Derangement of blood properties and content:

thrombosis, embolism and infarction.③Derangements of vascular permeability and anatomic

integrity: edema, hemorrhage.

Hyperemia

Def. Hyperemia refers to a local increased volume of blood caused by dilatation of the small vessels.

1. Arterial hyperemia (active hyperemia)It results from an augmented arterial inflow, such as occurs in the muscles during exercise, at sites of inflammation, and in the pleasing neurovascular dilatation termed blushing.

Active hyperemia causes increase of the volume of local tissue, of the metabolism and function of the organ. It is beneficial to the organism. Active hyperemia of body surface shows red in color and increase in local temperature.

2. Venous hyperemia (passive hyperemia, congestion)

It results from diminished venous flow such as follows cardiac failure or obstructive venous disease.

Etiology

(1)Compression on vein(2)Intravenous obstruction(3)Cardiac failure

Morphology

Congested organ increases in size and weight, solidifies in consistence, and shows dark color and capsular stiffness.

Chronic congestion of lung

Chronic congestion of liver

Hemorrhage

Def. Hemorrhage refers to extravasation of blood caused by rupture of blood vessel.

Hematoma:

Accumulation of large amount of blood within the tissue of the body.

Hemothorax, hemopericardium,hemoperitoneum, hemarthrosis:

blood accumulation in body cavities asthoracic cavity, pericardial cavity,Peritoneal cavity and arthritic cavityrespectively.

Petechiae: Minute hemorrhage into skin, mucous

membrane or serosal surface.

Purpura: Slight larger hemorrhage.

Ecchymosis: A large subcutaneous hematoma.

Part III - jpck.zju.edu.cnjpck.zju.edu.cn/jcyxjp/files/dao/04/PPT/042.pdf · Apoptosis Conception:...

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