[资料]病理学英文笔记 [复制链接]

考试前整理的病理英文笔记，由于我没有受过专业的医学英语教育，有错误的地方还请大家批评指正，谢谢啦！

参考资料：中国医科大学病理学英文教学课件
          山医病理学英文教学课件
          人卫6版病理学教材

Introduction to Pathology

1. The core of pathology
  (1) Etiology: causes of the disease
  (2) Pathogenesis: the mechanisms of its development
  (3) Morphologic changes: the structural alteration induced in the cells and organs of the body
  (4) Clinical significance: the functional consequences of the morphologic changes
2. Techniques of Pathology
  ·Human pathology   
  (1) Autopsy
  (2) Biopsy: surgical or diagnostic pathology
  (3) Cytology: smear, fine needle aspiration
  ·Experimental pathology 
  (1) Animal experiment: animal model
  (2) Tissue and cell culture
3. Observation and New Technique of Morphology
  (1) Gross appearance: size, shape, weight, color, consistency, surface, edge, section
  (2) Histologic and cytologic observation: most common and basic formalin fixed → HE (hematoxylin and eosin) stained
  (3) Histochemistry and cytochemistry
  (4) Immunohistochemistry:
      ·Ag-Ab specific reaction
      ·Applications: ①Location analysis: cytokeratin → cell membrane
                      ②Clinical diagnosis and distinguishing: diagnosis of tumor histogenesis
  (5) Ultrastructural observation: TEM (transmitting electron microscope)
                                    SEM (scanning electron microscope)
  (6) Flow cytometry (FCM)
      ·One kind of cells → quantitative
      ·DNA ploidy analysis
      ·Protein nucleus acid → quantitative analysis
      ·Selection of collection of cells
  (7) Image analysis (IA)
  (8) Laser scanning confocal microscope (LSCM) 
      aliving cell → observation in situ or development or quantitative
  (9) Molecular biology technique
      ·Polymerase chain reaction (PCR)
      ·DNA sequencing
      ·Biochip technique: ①Gene chip (DNA chip)
                          ②Protein chip (protein microarray)
                          ③Tissue chip (tissue microarray)

Chapter 1  Adaptation and Injury of Cell or Tissue

§1. Cell adaptation and aging

1. Cell adaptation
  (1) Atrophy
      ①Definition: Normal formed organ or tissue diminished in size due to decrease in the size of the parenchymal cells or in the number of cells
      ②Types: Physiologic atrophy
                Pathological atrophy
                ·Insufficient nutritive atrophy
                ·Atrophy of disuse
                ·Denervation atrophy
                ·Pressure atrophy
                ·Endocrine atrophy
      ③Morphologic changes
        ·Gross appearance: volume↓, weight↓
        ·Histological changes: Decrease in the size and number of cells
                                Lipofuscin → brown atrophy (heart or liver)
  (2) Hypertrophy
      ①Definition: an increase in the size of a tissues or organ due to increased size of individual cells
      ②Types: Physiologic hypertrophy: Pregnancy → uterus↑(endocrine hypertrophy)
                Pathologic hypertrophy: Hypertension → heart hypertrophy
                                        GN → residual nephron hypertrophy
  (3) Hyperplasia
      ①Definition: constitutes an increase in the number of cells in an organ or tissue, which may then have increased volume
      ②Types: Physiologic hyperplasia: Hormonal hyperplasia: SMC of uterus during pregnancy
                                        Compensatory hyperplasia: partial hepatectomy
                Pathologic hyperplasia
  (4) Metaplasia
      ①Definition: a process in which one matured cell type (epithelial or mesenchymal) is replaced by another matured cell type
      ②Types: Epithelial metaplasia
                ·Squamous metaplasia: Barret esophagitis
                ·Glandular metaplasia
                Mesenchymal tissue metaplasia
2. Cellular aging (senescence)
  ·Telomerase activity decreasing and telomere shortening
    Telomeres: short repeated DNA sequences, ensuring the complete replication of chromosomal ends, protecting chromosomal termini from fusion and degradation
  ·DNA damage: DNA damage is repaired by endogenous DNA repair enzymes, some damage persists and accumulates

§2. Injury of cells and tissues

1. Causes
  ·Hypoxia
  ·Chemical agents and drugs
  ·Physical agents
  ·Biologic agents
  ·Immunologic reactions
  ·Genetic defect
  ·Nutritional imbalance
  ·Others: Endocrine, aging, psychological factor
2. Morphologic changes of cell injury
  (1) Reversible injury (Degeneration)
      Definition: Morphologic changes of cell or extracellular stromal damage due of metabolic disorder → the deposition of some abnormal substance, excessive normal substance in cell or stroma
      ·Cellular (hydropic) swelling
        The first manifestation of cell injury
        ①The common site: liver, kidney, heart
        ②Causes: hypoxia, infection, intoxication
        ③Pathologic changes: Gross: increased in the weight of the organ
                                      cutting surface pallor in color
                                      capsule tense
                                      section bulgy
                                      cutting edge bulging
                              LM: cell swelling
                                  fine, red-stained granules within cytoplasm
                                  small clear vacuoles
                                  Ballooned change: clear cytoplasm, cell swelling obviously
                              EM: Mitochondria and ER swelling
      ·Fatty change (steatosis)
        abnormal accumulations of fat (triglyceride, cholesterol, phospholipid) within parenchymal cells
        ①The common site: liver, heart, kidney, muscle
        ②Causes: hypoxia, infection, intoxication, obesity
        ③Morphology: Gross: enlarged, yellow, soft, greasy
                      LM: clear vacuoles in the cytoplasm around the nucleus
                      EM: liposome
        Fatty change of myocardium: The common site: left ventricle subendocardium papilary muscle
                                    Tigered effect: apparent bands of yellowed myocardium alterating with bands of darker, red-brown (uninvolved) myocardium
        Myocardial fatty infiltration: In subpericardial, excessive fat accumulating and inserting among myocardial bandles → Sudden death
        Fatty change of renal tubule epithelium: Causes: lipoprotein↑
                                                          reabsorption of lipoprotein↑
      ·Hyaline change (degeneration)
        an alteration within cells, in the extracellular space and walls of arterioles which gives a homogeneous glassy, pink appearance
        ①Walls of arterioles: Hypertension: walls of arterioles in the kidney, brain, spleen, retina
                                Diabetes: walls of arterioles of all body, especially in the kidney
        ②Within cells: Reabsorbed droplets: varies in size red droplets in proximal tubule cells
                        Mallory bodie (Alcoholic hyaline body): alcoholic liver disease
                        Russell body: within plasma cells
      ·Mucoid change(degeneration)
        deposition of protein and mucopolysaccharide in stroma
        ①The common site: mesenchymal tumor, rheumatism, AS, bone marrow and fat with inadequate nutrition
        ②LM: star-like fibrocyte dotted in gray-blue mucoid matrix
      ·Amyloid change
        amyolid protein deposition in the extracellular space
        ①Sites: among the cells
                  reticular fiber skeleton
                  subBM of small blood vessel
        ②LM: light red (pink), homogeneous
              Congo red stain → red
      ·Pathologic pigmentation
        abnormal deposition of pigment within cytoplasm and extracellularl space
        ①Hemosiderin: hemoglobin-derived
                        Prussian stain → blue
                        LM: golden-brown yellow granules
        ②Lipofuscin: Sites: Aging or with severe malnutrition
                              hepatocyte, myocardial cell, nerve cell
                              Normal conditions: testis stromal cell
                                                nerve cell
                      LM: yellow-brown, fine granules
        ③Melanin: an endogenous, brown-black pigment synthesized by melanocyte (epidermic, mucosal basal layer)
                    Types: Local: nevus, melanoma
                    Systemic: Addison disease (cortex of adrenal gland malfunction)
                              prostate carcinoma treated by large amount of estrogen
      ·Pathologic calcification:
        abnormal deposition of calcium salt within the tissue except bone and teeth
        ①Morphology: psammoma bodies
                      Gross: gray granular or massive, solid, gritty deposits
                      LM: basophilic (blue), amorphous granular or clumped appearance
        ②Types: Dystrophic calcification: Local abnormal deposition of calcium salt in the areas of foreign bodies and necrosis
                                            Sites: foci of caseous
                                                  fatty necrosis
                                                  AS plaque
                                                  thrombosis
                                                  necrotic bodies of parasites
                  Metastatic calcification: calcium salt deposition in some tissues caused by disturbance in calcium metabolism
                                            Sites: pulmonary alveolar wall
                                                  renal tubule BM
                                                  gastric mucosal epithelium
  (2)Cell death
      ·Necrosis
        cell death of living cell, tissue
        ①Basic lesions: Nuclear changes: Pyknosis: nuclear shrinkage, increased basophilia
                                          Karyorrhexis: fragmentation of pyknotic nucleus
                                          Karyolysis
                        Changes of cytoplasm and membrane: Cytoplasm: increased eosinophilia
                                                            Membrane: destroyed
                        Changes of stroma: collagen fiber swelling → lysis → structure disappeared
        ②Types: Coagulative necrosis: Sites: in all tissues except brain such as spleen, kidney, heart
                                      Gross: gray or yellow-white, firm texture
                                      LM: preservation of basic outline
                Liquefactive necrosis: Sites: Pancreas (rich in protease)
                                              Brain (rich in lipid) encephalomalacia (infarct)
                                              Abscess
                Special types: Caseous necrosis: most often in TB
                                                  Gross: white or light yellow, cheesy
                                                  LM: amorphous granular debris tissue, architecture is completely obliterated
                                Gangrene: massive necrosis secondary to saprophyte infection
                                          Types: Dry gangrene: Site: limb, generally the lower leg
                                                              Cause: AS, frostbitten
                                                              Lesion: dry, black, clear border with surrounding normal tissue
                                                Moist gangrene: Site: organ interlinking with outside (lung, intestine, uterus)
                                                                      limb with congestion
                                                                Lesion: no clear border with surrounding normal tissue
                                                Gas gangrene: opening deep trauma combined with clostridium perfringens infection
                                                              Lesion: vague border with normal tissue
                                Fat necrosis: Types: Enzymic: Acute pancreatitis
                                                    Traumatic: Mammary trauma
                                              Gross: chalky gray-white plaque
                                              LM: necrotic fat cells dotted basophilic granules
                                Fibrinoid necrosis: Sites: fibrous connective tissue
                                                          wall of the blood vessel
                                                    Lesion: linear small massive red amorphous substance
                                                    Causes: allergic disease (rheumatism, GN)
                                                            malignant hypertension
        ③Sequences of necrosis: Dissolusion and absorption: Small: leukocyte → hydrolyze tissue
                                                            Debris: phagocytosis
                                                            Large: can't be absorbed → form cyst
                                Detachment and discharging: Lung → trachea → cavity
                                                            Kidney → ureter → cavity
                                                            Skin, mucosa → erosion, ulcer
                                Organization: The process that necrotic tissue, exudates, hematoma, thrombus are replaced by granulation tissue
                                Encapsulation and calcification: Large necrotic foci → encapsulation
                                                                  Necrotic substance → dystrophic calcification
        ④The effect on the body: Physiologic importance of necrotic cell: myocardium, brain
                                  The number of necrotic cell
                                  Regenerative capacity of the affected organ: hepatocyte
                                  Compensatory capacity of the affected organ: kidney, lung
      ·Apoptosis
        programmed cell death, a single cell death in living bodies controled by the genes which is a energy-dependent suicide process
        ①Morphologic: LM: Cell shrinkage: cytoplasm is dense eosinophilically
                          Chromatin condensation: Chromatin aggregates peripherally → producing two or more fragment
                      EM : Apoptotic bodies: apoptotic cell shows surface blebbing
                                              forms a number of membrane-bound bodies
                                              composed of packed cytoplasm, organelles, nuclear fragment
        ②Distinguish between apoptosis and necrosis
                            Necrosis                Apoptosis
          Inducing cause    Pathologic              Physiologic or pathologic
          Scope            Cell gruop              Single cell
          Cytoplasm        Swelling                Shrinkage (dense)
          Mitochondria      Swelling → destroyed  Dense
          Organelle        Swelling → destroyed  Dense
          Chromatin        Aggregated → massive  Dense
          Cell membrane    Break down              Intact, apoptotic bodies
          Inflam-reaction  Exist                  Deficiency
          DNA clearage      Irregular              Internucleosomal cleavage
                            → smearing diffuse    → ladder pattern

Chapter 2  Tissue Repair

§1. Regeneration

·Complete regeneration
  Incomplete regeneration: fibrous repair → scar
·Physiologic: cell renewing
  Pathologic: cell injury → regeneration
1. Cell cycle and proliferative potential
  (1)Cell cycle: Interphase: G1 (presynthetic)
                              S (DNA synthesis)
                              G2 (premitotic)
                  Mitotic phase (M)
      Go: quiescent cells in a physiologic state
  (2)Types
      ①Labile cells (continuously dividing cell)
        Definition: continue to proliferate → replacing destroyed cells and aged cells
        Cell groups: Stratified squamous cell: epidermis, oral cavity, vagina and cervix
                    The lining mucosa of respiratory and gastrointestinal tract
                    Epithelium of the male and female tract
                    Transitional epithelial of urinary tract
                    Hematopoietic and lymphoid cells
      ②Stable (quiescent) cells
        Definition: not divide or at a very slow rate and undergo rapid division in response to injury
        Cell groups: Parenchymal cells of glandular organ: liver, renal tubule epithelium
                    Mesenchymal cells: fibroblast, SMC
      ③Permanent (nondividing) cells
        Definition: no capacity of regeneration
        Cell groups: Nerve cells: Neurons destroyed are permanent, replaced by the proliferation of glial cell → glial scar
                    Skeletal muscle cells
                    Cardiac muscle cells
2. Regeneration process of various tissues
  (1)Epithelial tissue
      ·Surface epithelium: Squamous cell → basal layer cell
                            Columnar cell → adjacent gland recess cell
      ·Glandular epithelium: Base membrane intact → restored cell
                              Base membrane destroyed → difficult
        Liver: Resected partly → liver cell proliferation
              Necrosis of liver cell, reticular framework intact → hepatocyte proliferation → restore the structure
              Necrosis widely, reticular framework collapsed → hepatocyte nodular regeneration
  (2)Fibrous tissue
  (3)Blood vessel regeneration
      ·Capillary: budding
      ·Large blood vessel
  (4)Cartilage and bone tissue
  (5)Muscle regeneration
  (6)Nervous tissue

§2. Fibrous repair

1. Granulation Tissue
  ①Composition: composed of numerous newly formed capillaries and fibroblast, accompanied with inflammatory cell infiltration
  ②Morphology: Gross: red, soft, granular appearance
                LM: capillaries + fibroblast + inflammatory cells
  ③Functions: Anti-infection and protect wound surface from further injury
                Filling wound and the detect area
                Replacing or encapsule necrosis, thrombus, foreign bodies
2. Scar
  ①Morphology: Gross: contract, pallor, semitransparent, tough less elasticity
                LM: composed of parallel collagen fascicle (hyaline change)
                    less fibrous cells and blood vessel
  ②effect and harm of scar
    ·benefits: filling the wound and ulcer, make tissue and organ intact
                stronger resist pull, lack of elasticity → hernia
    ·disbenefit and harm: contract → obstruction
                            conglutination
                            excess hyperplasia → hypertrophic scar (keloid)

§3. Wound healing

1. process of wound healing
  (1)early change: an acute inflammatory process by the initial injury
  (2)contraction of wound
  (3)proliferation of granulation tissue and formation of scar
  (4)migration and regeneration of epithelium and other tissues
2. types of wound healing
  (1)Healing by first intention (wounds with opposed edges)
      a clean, uninfected surgical incision
  (2)Healing by second intention (wounds with separated edges)
      more extensive loss of cells and tissue, inflammatory ulceration, abscess formation
3. bone fracture healing
  (1)basic process
      ·hematoma formation: 1-2days
      ·fibrous bone scab formation: 2-3days, granulation tissue formation
      ·osteal bone scab formation: osblast → osloid tissue → calcium deposition → woven bone → osteal bone scab
      ·rebuild or remodel: woven bone → ply bone → normal struture
  (2)factors of affect fracture healing?
      ·correct reposition timely
      ·firmly fixation timely
      ·take exercise early, keep local blood supply well

Chapter 3  Hemodynamic Disorder

§1. Hyperemia and Congestion

1. Arterial hyperemia
  (1)Definition: Increased volume of arterial inflow in an organ or tissue (hyperemia)
  (2)Common types
      ·Physiologic: exercise → skeletal muscle
      ·Pathologic: at the foci of inflammation
      ·Hyperemia after reducing pressure
  (3)Sequelae: Restore: if causes abated
                Hemorrhage: hypertension, AS
2. Congestion
  (1)Definition: Resulting from an isolate venous obstruction → accumulation of blood in veinlet and capillary
  (2)Etiology
      ①Veins being pressed: Tumor → press local vein
                            pseudolobule → hepatic sinus
      ②Venous obstruction: thrombosis
      ③Heart failure: left → pulmonary congestion
                      right → hepatic congestion
  (3)Lesions and results
      ①Hydrostatic pressure↑ → congestive edema, hemorrhage
      ②Chronic hypoxia → atrophy or degeneration, fibrosis, sclerosis
  (4)Congestion of important organs
      ·Pulmonary congestion
        ①Cause: left heart failure
        ②Morphology: Gross: volume↑, weight↑, dark red, cut surface, consolidated
                      LM: Aalveolar septa: capillary engorged with blood
                                          become thickened
                                          fibrosis
                          Alveolar spaces: edema fluid
                                          heart failure cells
                                          hemorrhage
                      Brown induration: long period congestion, texture become solid and show brown appearance
      ·Hepatic congestion:
        ①Cause: right heart failure
        ②Morphology: Acute: Gross: enlarged, dark red
                            LM: The central vein and sinusoids: engorged with blood
                                Central hepatocyte: necrosis
                                Peripheral hepatocyte: fatty change
                      Chronic: Gross: nutmeg liver: cut surface shows zones of yellow alternating with zones of red, like nutmeg
                              LM: The central vein and sinusoids: distended with blood
                                  Central hepatocyte: atrophy or necrosis
                                  Peripheral hepatocyte: fatty change
                                  Congestive bands among central vein

§2. Thrombosis

  Definition: within living heart or blood vessel, blood coagulated (clotting) or some components clump form solid mass (thrombus)
1. Conditions and mechanism of thrombosis
  (1)Endothelial injury
      ①Functions of Endothelium
        ·Antithrombotic properties: Screen function of intact endothelium
                                    Antiplatelet adhering
                                    Anticoagulants
                                    Fibrinolytic
        ·Prothrombotic properties: Activate exogenous coagulation process
                                    Promoting adhesion of platelet
                                    Inhibiting fibrinolysis
      ②Functions of Platelets
        ·Adhesion and shape change
        ·Secretion (release reaction)
        ·Aggregation
      ③The common disease
        ·Endocardial injury: myocardial infarction, valvulitis
        ·Vascular injury: traumatic or inflammatory injury (vasculitis), AS → ulcerated plaques
        ·Hypoxia, shock, bacterial endotoxin → DIC → microthrombus
  (2)Alteration in normal blood flow
      ①Refer to stasis or turbulence: Disrupt laminar flow and bring platelets into contact with endothelial cell
      ②Vein is the favored sites
        ·Venous valves → slow, turbulence
        ·Fugacious stasis
        ·Thinner wall → pressed easily
        ·Adherence increased (blood from capillary → vein)
  (3)Blood hypercoagulability
      ①Inherited causes of hypercoagulability
        ·The most common cause: Mutation in the factor V gene
        ·Inherited lack of the anticoagulants: anti-thrombin, protein C, protein S
      ②Acquired causes of hypercoagulability
        ·Widely metastasis of malignant tumor
        ·Loss of blood: severe trauma, large area burn, operation
        ·Hyperlipemia, AS, smoking, obesity
2. The Process and morphology
  (1)The process of thrombosis
      ·Platelets adhere to extracellular matrix at sites of endothelial injury and become activated
      ·Secrete granule products (ADP, 5-HT, TXA2)
      ·Platelets aggregating
      ·The intrinsic and extrinsic pathway activate
      ·Fibrinogen → Fibrin
  (2)Types and morphology
      ·Pale thrombus (Artery thrombus): Sites: Arterial lumen: Coronary Artery
                                                Cardiac valves and chambers
                                                Head of propagating thrombus
                                        Gross: pale nodule or vegetation
                                                rough surface
                                                firmly adherent to arterial wall
                                        LM: Platelet (main) + Fibrin (a little)
      ·Mixed thrombus: Sites: Heart chamber, aneurysm, AS (mural thrombus)
                              Body of propagating thrombus
                        Gross: gray-white alternating with brown
                              dry, rough, adherent to vascular wall
                        LM: Platelet + Fibrin + Erythrocytes
      ·Red thrombus (Venous thrombus): Sites: Tail of propagating thrombus
                                        Gross: dark red
                                              wet → dry friable
                                        LM: Fibrin + RBC + WBC (a little)
      ·Hyaline thrombus (Fibrinous thrombus): Sites: Capillary (microcirculation)
                                              LM: Acidophilic fibrin
                                              Most common cause: DIC
3. Sequelae of thrombus
  (1)Dissolution and absorption
      ①Small → dissolved completely → removed by fibrinolytic system
      ②Large → dissolved partly → detachment → embolism
  (2)Organization and recanalization
      ①Organization: thrombus is replaced by granulation tissue
      ②Recanalization: In process of thrombus organization, thrombus contraction or partly dissolve and forms fissure, newly formed endothelial cell cover the surface of fissure and incorporate to reestablish vascular flow
  (3)Calcification: phlebolith (arteriolith)
4. Affections on the body
  (1)Obstructing blood vessel
      ①Artery thrombosis
        ·Obstructed partly → ischemia hypoxia → parenchymal cell atrophy
        ·Obstructed completely, without effective branch circulation → infarction
      ②Venous thrombosis: without effective branch circulation → congestion, edema, hemorrhage
  (2)Embolism
      Thrombus (deep vein, heart chamber, cardiac valve) → soften, split → detachment → embolism
  (3)Valvular deformation
      Rheumatic or infectious endocarditis → thrombus organized repeatedly → valve thicken
  (4)Extensive hemorrhage
      DIC → microthrombosis

§3. Embolism

·Embolism: In circulation, undissolvable abnormal substances are carried by blood to a site distant from its point of origin and block the lumen
·Embolus: The abnormal substance which block the lumen called embolus, may be solid, liquid, gas
          The most common: dislodged thrombus
          Rare form droplets of fat, bubbles of air, tumor fragment, amniotic fluid
1. The traveling pathways of embolus
  (1)Venous system and right heart
      ·Most: pulmonary artery and its branch
      ·Small embolus with elasticity (fat) → alveolar capillary → left heart → arterial circulation
  (2)Aortic system and left heart
      All the organ (brain, spleen, kidney and extremities)
  (3)Portal venous system
      Mesenteric vein → portal venous braches in liver
  (4)Crossed embolism (paradoxical embolism)
  (5)Retrograde embolism
2. Types and affection
  (1)Thromboembolism
      ①Pulmonary thromboembolism
        ·The origin: Deep leg vein above the level of the knee (popliteal, femoral, and iliac veins)
        ·Sequences: Middle and small embolus: Embolize small branches of pulmonary artery
                                              Dual blood flow into the area from branched circulation → doesn't cause infarction
                                              In the setting of left heart failure → pulmonary congestion → hemorrhagic infarction
                    Large embolus: Pulmonary truncus or large branch → sudden death
                    Multiple small embolus: End-arteriole of pulmonary branches → right heart failure → sudden death
      ②Systemic thromboembolism
        ·The origin: 80% from left heart: Mural thrombus: Subacute infective endocarditis
                                                          Myocardial infarction
                                                          Mitral stenosis
                      Others: AS ulcerated plaque, aneurysm
                      Rare: Crossed embolism
        ·Major sites: Lower extremities (75%), Brain (10%), Intestine, Spleen, Kidney
        ·Results: Depend on: collateral vascular supply
                              tissue's vulnerability to ischemia
                              sites of embolism
  (2)Fat embolism
      ①The origin: Fracture of long bone, adipose tissue injury, burn → enter the circulation by rupture of marrow, vascular sinusoids or vein
      ②Sites
        ·Embolus > 20μm → pulmonary embolism
        ·Embolus < 20μm → capillary → pulmonary vein → left heart → multiple organs
          Brain → edema, hemorrhage → delirium, coma
          Lung → sudden onset of tachypnea, dyspnea, tachycardia
      ③Sequences: Depend on: the sites
                              number of fat globules: small amount → phagocyted
                                                      large amount → pulmonary circulation → acute right heart failure → death
  (3)Gas embolism
      Gas enter the circulation rapidly or bubbles dissolved in the blood out of solution
      ①Air embolism
        ·Causes: Chest wall injury (operation or trauma), obstetric procedure
        ·Sequences: Depend on: the entering speed and volume
                                Small amount → dissolved
                                In excess of 100ml → vein → right heart → a large amount of bubbles with heart pulsating → circulation dysfunction
                                Small bubbles → small branch of pulmonary artery → capillary → left heart → organs
      ②Decompression sickness (caisson disease or diver's disease)
  (4)Amniotic fluid embolism
  (5)Others: Neoplastic cell, Bone marrow cell, Cholesterol crystal in AS foci, Parasite, Bacteria, Fungi

§4. Infarction

  Definition: Ischemic necrosis caused by occlusion of the arterial supply or the venous stasis
1. Causes and conditions of infarction
  (1)Causes
      ·Thrombosis: the most common
                    Coronary artery → myocardial infarct
                    Cerebral artery → cerebral infarct
                    Mesenteric vein → intestine infarct
      ·Arterial embolism: Thromboembolism (common), gas, amniotic fluid, fat embolism → infarct of spleen, kidney, lung, brain
      ·Arterial spasm (vasospasm): Coronary artery with AS → spasm → infarct
      ·Extrinsic compression of a vessel: Tumor, intestine twist, twist of ovary cyst
  (2)Conditions
      ①The nature of the vascular supply
        ·Organs with dual blood supply: Lung: pulmonary artery and bronchial artery
                                        Liver: hepatic artery and portal vein circulation
                                        Hand, forearm: radial artery and ulnar artery
        ·Splenic, renal, cerebral circulations are end arterial → generally cause infarction
      ②Tissue's vulnerability to hypoxia
        ·Nervous cell: undergo irreversible damage when deprived of blood supply for only 3-4 min
        ·Myocardial cell: sensitive and die after only 20-30 min of ischemia
        ·Fibroblast, skeletal cell: many hours
2. Lesions and types of infarct
  (1)Morphologic features
      ①Shape: depend on the distribution of blood vessel
              ·Spleen, kidney, lung: wedge-shape, cut surface → triangle, apex → occluded vessel, base → capsule (organ surface)
              ·Myocardial: irregular map-like shape
              ·Intestine: segmental shape
      ②Texture: depend on the types of necrosis
                ·Heart, spleen, kidney: coagulative necrosis
                ·Brain: liquefactive necrosis
      ③Color: depend on the amount of hemorrhage
              ·Large amount: hemorrhagic infarct (red infarct)
              ·Small amount: anemic infarct (white infarct)
  (2)Types
      ①Anemic infarct (white infarct)
        ·Sites: compact solid organs with less collateral circulation: kidney, spleen, heart
        ·Gross: gray-white
                Margin: narrow rim of hyperemia and hemorrhage
        ·LM: coagulative necrosis
              Nuclear changes and presence of tissue structure outline
              Margin: congestion, hemorrhage, inflammatory response
      ②Hemorrhagic infarct (red infarct)
        ·Conditions: Severe congestion: lung congestion
                                        ovary cyst → twist
                      Loose tissue: lung, small intestine
        ·Common types: Pulmonary hemorrhagic infarct: Site: lower lobe of lung
                                                      Gross: wedge-shape, apex → hilum of lung, base → visceral pleura
                                                      LM: necrosis and outline exist
                                                          Alveolar space: full of RBC
                                                          Margin: congestion, hemorrhage
                        Intestinal hemorrhagic infarct: Causes: mesenteric artery and vein → thrombosis
                                                                intestinal twist, tumor pressed
                                                        Gross: dark-red, segmental
      ③Septic infarct: Embolus: fragmentation of bacterial vegetation from heart valve
                        Morphology: infarct change
                                    abscess formation
3. Affection and consequences
  (1)Affection: depend on organs, size, site, with or without infection
  (2)Consequences: Organization
                    Encapsulation
                    Calcification

Chapter 4  Inflammation

§1. Introduction

1. Definition: A defensive reaction in living tissue with vascular system to injurious stimuli
              Reaction of blood vessel is the central link
2. Causes
  ·Biologic factors: Bacteria, Virus, Fungi, Parasites
  ·Chemical factors: exogenous, endogenous
  ·Physical agents: trauma, burn
  ·Tissue necrosis
  ·Allergic reaction
3. Basic pathologic changes
  (1)Alteration
      Degeneration, necrosis of local tissue cells
      ·Parenchymal cell: cellular swelling, fatty change, coagulative necrosis, liquefactive necrosis
      ·Mesenchymal cell: mucoid change, amyloid change, hyaline change, fibrinoid necrosis
  (2)Exudation
      In inflammatory foci, the escape of fluid, proteins (fibrin), blood cells from vascular wall into interstitial tissue, body cavities or surface of the body and mucosa
  (3)Proliferation
4. Local manifestation and general reactions
  (1)Local manifestation: Redness, Swelling, Heat, Pain, Loss of function
  (2)General reactions
      ①Fever: Exogenous factors: toxin, virus, Ag-Ab complex
              Endogenous factors: cytokines: IL-1, TNF → PGE
      ②Leukocytosis: Acute purulent inflammation: Neutrophils↑
                      Chronic or virus infection: Lymphocytes↑
                      Allergic disease or parasite: Eosinophils↑
      ③Others: Anorexia, somnolence, malaise
                More synthesis of clotting factors

§2. Acute inflammation

1. Changes of hemodynamics
  Alteration in vascular flow and caliber
  (1)Transient vasoconstriction of arterioles
  (2)Vasodilation and increased blood flow
  (3)Slowing of blood flow
2. Increased vascular permeability
  (1)Mechanism of increased permeability
      ·Endothelial cell retraction: Histamine, Bradykinin, Leukotriene, Substance P
                                    Immediate transient response
      ·Cytoskeletal reorganization: IL-1, TNF, hypoxia
      ·Increased transcytosis: VEGF, Histamine, Bradykinin, Leukotriene, Substance P
      ·Direct endothelial injury: Immediate sustained response: Severe burn, purulent bacteria, result in endothelial cell necrosis and detachment, leakage starts immediately after injury, sustained at a high level for several hours until damaged blood vessel thrombosis and repaired
      ·Delayed prolonged leakage: Mild-to-moderate thermal injury, toxin, x-ray
                                  Increased permeability after a delay of 2 to 12 hours, lasting for several hours or days, involves venules as well as capillary
      ·Leukocyte-mediated endothelial injury
      ·High permeability of new capillary
        ①New vessels sprouts remain leaky until endothelial cells differentiate and form intercellular junctions
        ②Certain factors (VEGF) that cause angiogenesis increase permeability
        ③Increased density of receptor for vasoactive mediators in the surface of endothelial cell
  (2)Fluid exudation
      ①Main causes
        ·Increased vascular permeability → escape of a protein-rich fluid into the interstitium
        ·The loss of protein → reduces intravascular colloid osmotic pressure, increases the colloid osmotic pressure of the interstitial fluid
      ②Distinguish between exudate and transudate
                        Transudate      Exudate
Vascular permeability    Normal          Increased
Protein concentration    0-1.5g/dl      1.5-6g/dl
Protein type            Albumin        Kinds of protein
Rivalta test            Negative (-)    Positive (+)
Fibrin                  No              Have
Gravity                  < 1.018        > 1.018
Cell number              < 0.1×109/L    > 0.5×109/L
Appearance              Clear          Cloudy
3. Leukocyte extravasation and phagocytosis
  (1)Leukocyte extravasation: leukocyte pass through vascular wall into the site of injury
      ①Margination and rolling
      ②Adhesion
        ·Adhesion molecules: Selectin
                              The immunoglobulin family: ICAM-1, VCAM-1
                              Integrins
        ·Mechanisms of adhesive process: Redistribution of adhesion molecules to the cell surface
                                          Induction of adhesion molecules synthesis
                                          Increased avidity of binding
      ③Emigration and chemotaxis
        ·Emigration: leukocytes insert pseudopods into junction between endothelial cells → secrete collagenase → decompose the BM
        ·Chemotaxis: leukocytes emigrate toward the chemical mediators along a chemical concentration gradient
          Chemotactic agent: Exogenous: Bacterial products
                            Endogenous: Complements (C5a), Leukotriene (LTB4), Cytokines (IL-8)
  (2)The roles of leukocytes
      ①Phagocytosis: leukocytes emigrate to inflammatory focus, engulf and kill or degradate the pathogenic organism and tissue debris
        ·Types of phagocytes: Neutrophils, Macrophages, Eosinophils
        ·Process of phagocytosis: Recognition and attachment: Opsonin: a kind of protein in serum which enhances the efficiency of phagocytosis, include Fc fragment of IgG, C3b, collectins
                                  Engulfment
                                  Killing and degradation
      ②Immunological function
      ③Leukocyte-induced tissue injury
4. Inflammatory mediator
  (1)Concept: A series of chemical agents induced inflammation
  (2)General features
      ①Originated from plasma or cells
        ·Cell-derived mediators: Sequestered in intracellular granules
                                  Synthesized in response to a stimulus
        ·Plasma-derived mediators: Present in precursor form → activated by proteolytic cleavage
      ②Most mediators perform their biologic activity by binding to specific receptors on target cells, some have direct enzymatic activity or mediate oxidative damage
      ③A inflammatory mediator can stimulate the release of secondary mediators by target cell → amplifying or opposing activities
      ④A inflammatory mediator can act on one or a few target cell types → different effects depend on cell and tissue types
      ⑤Once activated and released from cell, most of these mediators are short-lived decay, inactivated, scavenged, inhibited
      ⑥Most mediators have the potential to cause harmful effects
  (3)Mediators released by cells
      ·Vasoactive amines
        ①Histamine: Sites: Mast cell granules, Basophils, Platelets
                    Functions: Dilation of arterioles
                                Increase permeability
                    Stimuli that cause histamine release: Physical injury: trauma, cold, heat
                                                          Immune reaction: IgE
                                                          Fragments of complement: C3a, C5a
                                                          Histamine-releasing protein (leukocyte)
                                                          Neuropeptides: substance P
                                                          Cytokines: IL-1, IL-8
        ②5-HT (serotonin): Function: Increase vascular permeability
                            Stimuli that cause 5-HT release: Collagen, Thrombin, ADP, Platelet activating factor (PAF)
      ·Arachidonic acid metabolites
        ①Prostaglandin (PG): Vasodilation (PGE2, PGD2, PGF2, PGI2)
                              Increase permeability
                              Fever and pain
        ②Leukotriene (LT): Chemotactic agent of neutrophils (LTB4)
                            Intense vasoconstriction and bronchospasm (LTC4, LTD4, LTE4)
                            Increased vascular permeability (LTC4, LTD4, LTE4)
        ③Lipoxins (LX)
      ·Leukocyte products and lysosomal components
      ·Cytokines
        Types: Cytokines that regulate lymphocytes function: IL-2, IL-4
              Cytokines involved in natural immunity: TNF-α, IFN-α, IFN-β
              Cytokines that activate macrophages: IFN-γ, TNF-α, TNF-β, IL-5, IL-10, IL-12
              Cytokines that stimulate hematopoiesis: IL-3, IL-7, CSF
              Chemokines: chemotactic activity for leukocyte
      ·Platelet activating factor (PAF)
      ·Nitric oxide (NO)
      ·Nuropeptides
  (4)Mediators from plasma
      ·Kinin system: Bradykinin: Increase vascular permeability
                                  Causes contraction of smooth muscle except blood vessel
                                  Vasodilation
                                  Pain
      ·Complement System: Increase vascular permeability, Vasodilation (C3a, C5a)
                          Chemotaxist (C5a): A powerful chemotactic agent for neutrophils, basophils, eosinophils, monocytes
                          Opsonization (C3b)
      ·Clotting and fibrinolytic system
  (5)Summary of inflammatory mediators
Function          Major mediators
Vasodilation      Histamine, Bradykinin, PGE2, PGD2, PGF2, PGI2, NO
Permeability↑    Histamine, Bradykinin, C3a, C5a, LTC4, LTD4, LTE4, PAF, Substance P
Chemotaxis        C5a, LTB4, Cytokines
Fever              Cytokines (IL-1, IL-6, TNF), PG
Pain              PGE2, Bradykinin
Tissue damage      Lysosomal enzymes, NO
5. Types and morphology
  (1)Serous inflammation
      ①Common sites: mucosa, serosa, loose connective tissue
      ②Lesions: Serous exudation: blood serum (main), albumin (3%-5%), neutrophils, fibrin
      ③Consequence: absorption
                    edema in throat → stifle
  (2)Fibrinous inflammation
      ①Lesions: Fibrinogen exudation: eosinophilic meshwork of threads or amorphous coagulum, necrotic debris, neutrophils
      ②Causes: bacterial toxin, urea, mercury
      ③Sites
        ·Mucosa: Pseudomembranous inflammation: fibrin + necrotic tissue + neutrophils → gray-white, membrane-shaped
                  Common: bacillary dysentery, diphtheria
        ·Serosa: Fibrinous pericarditis → cor villosum
                  Common: pleura, pericardium
        ·Lung: Lobar pneumonia
      ④Consequences: resolution and absorption
                      organization: lung → carnification
  (3)Purulent inflammation
      ①Lesions: Neutrophils exudation, accompanied with tissue necrosis and formation of pus
      ②Types
        ·Surface purulence and empyema: Sites: mucosa and serosa
                                        Surface purulence: superfical infiltration of neutrophils
                                        Empyema: pus deposit in the cavities (gallbladder, appendix)
        ·Phlegmonous inflammation: Concept: diffuse purulent inflammation occurring in loose connective tissue
                                    Pathogen: hemolytic streptococcus
                                    Sites: skin, muscles, appendix
                                    Lesion feature: neutrophils → diffuse infiltration
        ·Abscess: Concept: localized purulent inflammation, accompanied with local tissue necrosis and forming the cavity full of pus
                  Sites: Skin: furuncle, carbuncle
                          Organs: lung, brain, liver, kidney
                  Pathogen: Staphylococcus
  (4)Hemorrhagic inflammation
6. Outcomes of acute inflammation
  (1)Resolution
  (2)Progression of tissue response to chronic
  (3)Extension and spreading
      ①Local dissemination: Pathogen → tissue space or natural tract → surrounding tissue or organ
      ②Lymphatic spread
      ③Hematogenous spread
        ·Toxemia: bacterial toxin or toxic product enter into blood, accompanied with systemic symptoms and injury of solid organs (heart, liver, kidney)
        ·Bacteremia: bacteria enter into blood by local focus and can be checked out from the blood, without systemic symptoms
        ·Septicemia: strong toxic bacteria propagate in blood and release toxin to cause severe systemic symptoms and lesions
        ·Pyemia: septicemia cause by pyogenic bacteria, accompanied with multiple embolic abscess (metastatic abscess) in organs besides manifestation of septicemia

§3. Chronic inflammation

1. Causes
  (1)Persistent infections by certain microorganisms with lower toxicity: Tubercle bacilli (TB)
  (2)Prolonged exposure to exogenous or endogenous toxic agents
  (3)Autoimmunity caused by autoantigens: Rheumatoid arthritis, Systemic lupus erythematosus
2. Classification
  (1)Chronic non-specific inflammation
      ①Morphologic features
        ·Infiltrative cells: Lymphocyte, Plasma cell, Monocyte
        ·Tissue destruction: induced by inflammatory cells
        ·Proliferation: Fibrous connective tissue, Blood vessel, Epithelial cell, Gland, Parenchymal cell
      ②Chronic inflammatory cells
        ·Mononuclear phagocyte system: Blood: Monocyte
                                        Tissue: Macrophage: Liver: Kupffer cells
                                                            Spleen, Lymph node: Sinus histocyte
        ·Lymphocyte: produce lymphokines (IFN-γ)
        ·Mast cell: parasite infection, anaphylactic reaction to drugs
        ·Eosinophils: parasite infection
      ③Some characteristic changes
        ·Inflammatory polyp: under the stimulation of inflammatory agents, local mucosal epithelium, glands, fibrous connective tissue proliferate, form protrudent mass
                              Common sites: nasal polyp
                                            cervical polyp
                                            intestinal polyp
        ·Inflammatory pseudotumor: a clear edge, tumor-like mass, formed by tissue inflammatory proliferation, often occur in eyes and lung
  (2)Chronic specific inflammation (Chronic granulomatous inflammation)
      ①Granulomatous inflammation: a distinctive chronic inflammation, characterized by formation of granuloma
        Granuloma: Monocytes exude, macrophages proliferate, form clear nodular focus
      ②Types
        ·Infectious granuloma: caused by insoluble particles that are capable of inducing a cell-mediated immune reaction
                                Formation: macrophages engulf insoluble particles → present antigen to T-lymphocytes → cytokines (IL-2, IFN-γ) → Epithelioid cell and Multinucleate giant cell
                                The common diseases: TB, Leprosy, Rheumatism, Typhoid fever, Syphilis
                                For example: Tubercle: Central: Caseous necrosis
                                                      Periphery: Epithelioid cells, Langhans giant cells, Lymphocytes, Fibrous connective tissue
        ·Foreign body granuloma

Chapter 5  Neoplasm

§1. Definition and morphology of tumor

1. Concept: Tumor (neoplasm): under the stimulation of tumorigenic agents, a single cell of local tissue lost the controlling to its growth at the gene level, excessive hyperplasia to form neoplasm
2. Distinguish between neoplastic and nonneoplastic proliferation
                          Neoplastic proliferation    Nonneoplastic proliferation
Proliferation            Monoclonality              Polyclonality
Morphology and function  Abnormal                    Normal
Differentiation          Abnormal                    Matured
Growth                    Persistent, autonomy        Limited
Influence                Harmful                    Beneficial
3. Morphology and structure
  (1)Macropathology: Number, Size, Shape, Color, Texture
  (2)Histological structure
      ①Parenchyma: Neoplastic cell: determine the biologic feature and differentiation
      ②Stroma: Connective tissue, Blood vessel, Lymphocyte infiltration

§2. Neoplastic differentiation and atypia

1. Differentiation
  (1)Definition: Refer to the extent to which neoplastic cells resemble comparable its originated normal cells, both morphologically and functionally
  (2)Degree of differentiation: well differentiated, poorly differentiated, undifferentiated
2. Atypia: Neoplastic tissue has various extent of differences with its originated normal tissue, both cell morphologically and tissue architecturally
  Anaplasia: Lack of differentiation of malignant neoplastic cell, with obvious atypia
  Anaplastic neoplasm: Composed of undifferentiated cell, with obvious atypia
  Pleomorphism: Obvious variation in size and shape, with obvious atypia
  (1)Architectural atypia
      Refer to difference between neoplastic tissue and its originated normal tissue on arrangement (polarization, organ-like structure, the relationship with stroma)
  (2)Cellular atypia
      ①Pleomorphism of neoplastic cells
        ·Variation in size and shape
        ·Generally larger than normal cells (tumor giant cells)
      ②Pleomorphism of nucleus
        ·Increased nucleus: The nuclear-to-cytoplasmic ratio may approach 1:1 instead of the normal 1:4-1:6
        ·Variation in size, color and shape: Size: Huge, two or more nuclei, bizarre nuclei
                                              Color: DNA↑, hyperchromasia
                                              Shape: The chromatin is coarsely clumped and distributed along the nuclear membrane
                                                    Increased mitotic figures: atypical, bizarre, multipolar mitotic figures
      ③Changes of cytoplasm
        ·Basophilia → nucleoprotein increased
        ·Abnormal products or secretion: Mucus, glycogen, lipid → helpful to determine histogenesis of tumor
      ④Ultrastructural changes
        Organelles: signs of histogenesis
        ·Neuroendocrine granules → neuroendocrine tumor
        ·Tonofilament and desmosomes → squamous cell carcinoma
        ·Myofilament and dense body → SMC

§3. Growth and spread of tumor

1. Biology of tumor growth
  (1)Monoclonality: Tumor is formed by a transformed cell proliferation
  (2)The natural history of most malignant tumors
      ①Malignant transformation in the target cell
      ②Clonal growth of the transformed cell
      ③Local invasion
      ④Distant metastasis
  (3)The multiple factors that influence tumor growth:
      ①Kinetics of tumor cell growth
        ·Doubling time of tumor cells: In reality, cell cycle time for many tumors is equal to or longer than that of corresponding normal cells, growth of tumor is not associated with a shortening of cell doubling time
        ·Growth fraction: The proportion of cells within the tumor population that are in the proliferative pool (S + G2 phase)
        ·Tumor cell production and loss: Growth of tumors are determined by the excess of cell production over cell loss
      ②Tumor angiogenesis
        Angiogenesis factors: tumor cells, infiltrated Macrophages → VEGF, FGF
      ③Tumor progression and heterogeneity
        ·Tumor progression: Malignant tumor become more aggressive in the process of growth, including accelerated growth, local invasion, distant metastasis
        ·Tumor heterogeneity: In the process of growth, monoclonal tumor cells generate subclones with different characteristics, such as invasiveness, rate of growth, hormonal responsiveness, susceptibility to antineoplastic drugs
2. Growth pattern of tumor
  (1)Expansile growth: The mode of most benign tumor, well demarcated, intact capsule
  (2)Exophytic growth: The mode of both benign and malignant tumor (also grow by infiltrating)
                        Sites: surface of body, body cavities, tract organs
                        Shape: papillary, polypoid, cauliflower
  (3)Infiltrating growth: The mode of most malignant tumor, absence of capsule, infiltrate and destroy surrounding tissue
3. Spread of tumor
  (1)Local invasion and direct spreading
      ①Cell adhesion molecules↓, detachment of the tumor cells from each other
      ②Attachment to BM↑
      ③Degradation of extracellular matrix
      ④Migration of tumor cells
  (2)Metastasis
      Malignant tumor cells invade into lymphatics, blood vessles and body cavities from primary site, reach remote site, continue growth to form the same type tumor
      ①Lymphatic metastasis
        ·The most common pathway for the initial dissemination of carcinoma
        ·Common sites: Lung, Gastrointestinal tract → Left supraclavicular lymph node
      ②Hematogeneous metastasis
        ·The favored pathway of sarcoma
        ·Common sites: Lung (most), Liver, Bone
        ·Features of metastatic tumor: Clear border, scattered in distribution, multiple, close to surface of organ
        ·Carcinoma umbilicus: Metastatic tumor located surface of the organ form umbilication because of central hemorrhage and necrosis
      ③Transcoelomic metastasis
        ·Definition: Malignant tumor of organ in body cavity (pleural, peritoneal cavity) penetrate into the surface of the organ, tumor cells drop to seed in the surface of the other organs of body cavity and form majority of metastatic tumor
        ·Krukenberg tumor: Gastric carcinoma destroy gastric wall, tumor cells seed in the ovaries to form metastatic tumor

§4. Grading and staging of tumor

1. Grading of tumor
  ·Grade Ⅰ: well differentiated
  ·Grade Ⅱ: moderately differentiated
  ·Grade Ⅲ: poorly differentiated
2. Staging of tumor
  TNM classification
  ·T: primary tumor: T1-T4
  ·N: regional lymph node involved: N0; N1-N3
  ·M: metastasis: M0; M1

§5. Effects of tumor on host

1. Benign tumor: Local oppression and obstruction
2. Malignant tumor
  (1)Local oppression and obstruction, pain, fever, weight loss
  (2)Cachexia: Refer to the state of progressive loss of weight, anemia, weakness and systemic failure
  (3)Ectopic endocrine syndrome: Some non-endocrine tumors elaborate hormones or hormone-like substance (ACTH, PTH, ADH, insulin), give rise to endocrine disorder and show homologous symptoms
  (4)Paraneoplastic syndrome: Neoplastic products (ectopic hormones) or abnormal immune reaction or other unclear causes lead to lesions of endocrine, nervous, digestive system and so on

§6. Difference between benign and malignant tumor

                    Benign                            Malignant
Differentiation    well, unobvious atypia            poor, obvious atypia
Mitotic figures    no or rare                        numerous                           
                    no pathologic mitosis              pathologic mitosis
Growth speed        slow                              rapid
Growth pattern      Expansile or exophytic growth      Infiltrating or exophytic growth                             
Secondary changes  rare                              common (hemorrhage, necrosis, ulcer)
Metastasis          never                   frequent
Recurrence          rare                              often
Effects on host    unobvious                          obvious
                    local oppression and obstruction  infiltrate the surrounding normal tissues
                                                      secondary changes, cachexia

§7. Nomenclature and classification

1. Nomenclature
  (1)Benign tumor
      Histogenesis + "oma": Fibroma, Adenoma
  (2)Malignant tumor
      ·Carcinoma: Arising in epithelial cell: Squamous cell carcimnoma, Adenocarcinoma
      ·Sarcoma: Arising in mesenchymal tissue: Fibrosarcoma, Liposarcoma, Leiomyosarcoma, Rhabdomyosarcoma
      ·Carcinosarcoma
  (3)Others
      ·Arising in totipotential cells: Teratoma
      ·-blastoma: Neuroblastoma, Medulloblastoma
      ·Malignant-: Malignant melanoma, Malignant meningioma
      ·Custom: Leukemia, Seminoma
      ·Name: Ewing's sarcoma, Hodgkin lymphoma
      ·Tumor cell morphology: Clear cell sarcoma
      ·-omatosis: Neurofibromatosis, Lipomatosis
2. Classification
  ·/0: benign
  ·/1: borderline, unspecified, uncertain
  ·/2: carcinoma in situ, grade Ⅲ intraepithelial neoplasia, noninvasive
  ·/3: malignant

§8. Precancerous lesions, dysplasia and carcinoma in situ

1. Precancerous lesions
  (1)Concept: Certain benign lesions possess the possibility of cancerization, which progress to cancinoma with duration
  (2)Common precancerous lesions
      ①Adenoma of large intestines
      ②Chronic cervicitis and cervical erosion
      ③Mammary fibrocystic disease
      ④Chronic atrophic gastritis and intestinal metaplasia
      ⑤Ulcerative colitis
      ⑥Chronic ulcer of skin
      ⑦Leukoplakia: oral cavity, vulva
2. Dysplasia (atypical hyperplasia)
  Proliferative epithelium possess a certain extent of atypia, commonly arise in squamous epithelium and glandular epithelium
3. Carcinoma in situ
  Severe dysplasia totally involved to the mucosa or epidermis, without penetration of the basement membrane

§9. Introduction of common tumors

1. Epithelial tumor
  (1)Benign epithelial tumor
      ①Papilloma
        ·Origin: Squamous epithelium, Transitional epithelium
        ·Sites: Skin, Urinary tract
        ·Gross: Papillary mass (exophytic) with pedicle
        ·LM: Papillary epithelium, connective tissue core → Finger-like structure
      ②Adenoma
        ·Origin: Glandular epithelium
        ·Sites: Thyroid gland, Ovary, Breast, Intestines
        ·Gross: Polypoid, Papillary, Nodular
        ·Types: Tubular adenoma and villous adenoma: Sites: Rectum, Colon
                                                      Character: Multiple (liable to canceration)
                Cystadenoma: Site: Ovary
                              Types: Serous papillary cystadenoma (liable to canceration)
                                    Mucinous cystadenoma
                Fibroadenoma: Site: Breast
                Pleomorphic adenoma: Origin: Glandular epithelial cells and myoepithelial cells
                                      Sites: Parotid, Salivary gland
                                      Lesion: Epithelial tissue + Mucoid tissue + Cartilage-like tissue
                                      Character: liable to recurrence
  (2)Malignant epithelial tumor
      ①Squamous cell carcinoma
        ·Sites: Skin, Oral cavity, Esophagus, Larynx, Cervix, Vulva
        ·Gross: Cauliflower
        ·LM: Well differentiated: Keratin pearl, Intercullular bridge
      ②Adenocarcinoma
        ·Tuburlar adenocarcinoma: Sites: Gastrointestinal tract, Thyroid gland, Gallbladder, Uterus body
        ·Papillary adenocarcinoma: Sites: Thyroid gland, Ovary
        ·Solid carcinoma: Sites: Breast, Thyroid gland, Stomach
                          Types: Carcinoma simplex: parenchyma ≈ stroma
                                  Scirrhous carcinoma: parenchyma < stroma
                                  Medullary carcinoma: parenchyma > stroma
        ·Mucinous (colloid) carcinoma: Sites: Stomach, Large intestine
                                        Lesion: signet-ring cell
      ③Basal cell carcinoma
        ·Sites: Commonly in the face of old man, such as eyelid, nosewing
        ·Gross: Ulcer, growth slowly
        ·LM: Cancerous cells like basal cells
        ·Character: Less metastasis, sensitive to radiotherapy
      ④Transitional cell carcinoma
        Sites: Bladder, Ureter, Renal pelvis
2. Mesenchymal tumor
  (1)Benign mesenchymal tumor
      ①Fibroma
        ·Origin: Fibrous connective tissue
        ·Sites: Subcutis of extremities and trunk
        ·Gross: Intact capsule, nodular, gray, pliable and tough
        ·LM: Well differentiated tumor cells are spindle shape and arrange in a crisscross pattern
      ②Lipoma
      ③Hemangioma
      ④Leiomyoma
        ·Sites: Uterus, Gastrointestinal tract
        ·Gross: Nodular, intact capsule, gray, firm
        ·LM: Fascicles of spindle cells arrange in a crisscross pattern, blunt-ended elongated nuclei
      ⑤Chondroma
  (2)Malignant mesenchymal tumor
      ①Fibrosarcoma
        ·Origin: Fibrous connective tissue (fibroblast)
        ·Sites: Subcutis of extremities
        ·Gross: Soft, fish-fleshy, with hemorrhage and necrosis
      ②Liposarcoma
        ·Origin: Original mesenchymal tissue
        ·Sites: Retroperitoneum, deep soft tissue of extremities
        ·Gross: Nodular, lobular
        ·LM: Lipoblast
        ·Age: Adult (>40)
      ③Rhabdomyosarcoma
        ·Age: Children (<10) and infant
        ·Sites: Head, Neck, Genitourinary tract             
        ·Lesions: Rhabdomyoblast
      ④Leiomyosarcoma
        ·Sites: Uterus, Gastrointestinal tract, Retroperitoneum, Mesentery
        ·Gross: fish-fleshy, with hemorrhage and necrosis
        ·LM: Spindle cells arrange in interweaving fascicle
      ⑤Angiosarcoma
        ·Origin: Endothelium of blood vessel
        ·Sites: Skin (common), organs
        ·Gross: Nodular, papular, commonly necrosis and hemorrhage
      ⑥Chondrosarcoma
        ·Age: 40-70
        ·Site: Pelvis
        ·Gross: Semitransparent, spotty calcification
        ·LM: Cartilage cell with atypia scattered in cartilage matrix
      ⑦Osteosarcoma
        ·Age: Adolescent
        ·Origin: Osteoblast
        ·Sites: Lower part of thighbone, Upper part of shankbone 
        ·Gross: Gray-white, fish-fleshy, with hemorrhage and necrosis
        ·LM: Tumor bone
3. Difference between carcinoma and sarcoma
                                      Carcinoma                  Sarcoma
Origin                                Epithelial tissue          Mesenchymal tissue
Incidence                              Common, adult (>40)        Less, the young
Gross                                  Hard, gray-white, dry      Soft, gray-red, wet, fish-fleshy
Histology                              Cancerous nests            Diffuse arrangment
Border between parenchyma and stroma  Clear                      Unclear
Reticulum fiber                        Abscence                  Presence
Immunohistochemistry                  Epithelial marker CK (+)  Mesenchymal marker Vimentin (+)
Metastasis                            Lymphatic                  Hematogeneous
4. Neuroectoderm derived tumor
  (1)Central nervous system tumor
  (2)Peripheral nervous system tumor
  (3)Diffuse neuroendocrine system tumor
  (4)Retinoblastoma
      ·Age: Infant (<3)
      ·Origin: Embryo of retina
      ·LM: Composed of roundlet cells, arrange in chrysanthemum pattern
  (5)Pigmented nevus
  (6)Malignant melanoma

§10. Molecular basis of oncogenesis

1. Oncogene
  (1)Proto-oncogene: Cellular genes that promote normal cells growth and differentiation, exist in normal cells, in the form of inactivity
  (2)Activation of proto-oncogene
      ·Concept: Proto-oncogene → Cellular oncogene
      ·Mode: Point mutation
              Gene amplification
              Chromosomal translocation
2. Tumor suppressor gene
  ·Concept: Cellular genes that exist in normal cells, inhibit normal growth, cause cells to malignant transform when they are inactive
  ·Examples: Rb, p53, P16
3. Genes that regulate apoptosis and DNA repair
  ·Bcl-2: inhibit apoptosis
  ·Bax: induce apoptosis
4. Telomere and tumor

§11. Environmental factors of oncogenesis

1. Chemical carcinogenic agents
  (1)Indirect-acting agents
      ①Polycyclic hydrocarbons
      ②Aromatic amines and azo dyes
      ③Nitrosamines
      ④Aflatoxin
  (2)Direct-acting agents
2. Physical carcinogenic factors
  (1)Ionizing radiation: X-ray, γ-ray
  (2)UV
3. Biologic carcigenic agents
  (1)RNA virus
      HTLV-1: Adult T-cell leukemia/lymphoma
  (2)DNA virus
      ①Human papilloma virus (HPV)
      ②Epstein-Barr virus (EBV)
      ③Hepatitis virus B (HBV)

Chapter 6  Diseases of Cardiovascular System

§1. Atherosclerosis (AS)

1. Etiology and pathogenesis
  (1)Risk factors
      ①Hyperlipidemia
      ②Hypertension
      ③Smoking
      ④Diabetes and hyperinsulimemia
      ⑤Heredity: LDL-receptor gene mutation → LDL↑ → familial  hypercholesterolemia
      ⑥Others: Age, Sex, Obesity
  (2)Pathogenesis
      ①Response to injury hypothesis
      ②Lipid infiltration hypothesis
      ③The role of macrophage hypothesis
2. Morphology
  (1)Basic pathologic changes
      ①Fatty streak
        ·Gross: yellow flat spots or streaks, slightly raised
        ·LM: composed of lipid-filled foam cells (Macrophage, SMC)
      ②Fibrous plaque
        ·Gross: irregular grey-white raised plaque
        ·LM: Fibrous cap: hyaline degeneration of collagen, SMC embed in ECM
              foam cells, lipid, inflammatory cells
      ③Atheromatous plaque (atheroma)
        ·Gross: whitish yellow irregular elevated plaque
        ·LM: Surface: fibrous cap
              Center: amorphous necrotic substance, lipid, cholesterol crystal, calcification
              Surrounding: granulation tissue, lymphocytes, foam cells
              Media: become thin
  (2)Complicated lesion
      ①Hemorrhage in plaque
      ②Rupture of plaque
      ③Thrombosis → infarction
      ④Calcification
      ⑤Aneurysm formation
3. Lesions in principal arteries
  (1)Aorta: aneurysm
  (2)Coronary artery: coronary heart disease
  (3)Carotid artery and Cerebral artery
      ·Ischemic atrophy of brain
      ·Infarction: thrombosis
      ·Hemorrhage: aneurysm (Willis circle)
  (4)Renal artery
  (5)Artery of extremities: claudication, gangrene
  (6)Mesenteric artery

§2. Coronary atherosclerosis and coronary heart disease

1. Coronary atherosclerosis
  (1)Distribution: Left anterior descending coronary artery > Right coronary artery > Left coronary artery > Left circumflex coronary artery
  (2)Features: crescent plaque of myocardial side, eccentric stenosis
  (3)Grades: Ⅰ < 25%         
              Ⅱ 26%-50%
              Ⅲ 51%-75% 
              Ⅳ > 76%
2. Coronary heart disease (CHD)
  (1)Angina pectoris
      ·Pathogenesis: Acute, temporarily, comparatively coronary arterial blood supply↓
                      Cardiac oxygen demand↑
      ·Clinical types
        ①Stable angina pectoris
        ②instable angina pectoris
        ③Variant angina pectoris (Prinzmetal angina pectoris)
  (2)Myocardial infarction (MI)
      ①Subendocardial myocardial infarction
        ·Concept: the area of ischemic necrosis limited to the inner 1/3 and involves papillary muscle, trabeculae carnae
        ·Circumferential infarction
      ②Transmural myocardial infarction (regional myocardial infarction)
        ·Concept: the area of ischemic necrosis involves the full or nearly full (>2/3) thickness of the ventricular wall
        ·Lesion: Anemic infarct
        ·Lab: CPK↑, LDH↑, SGPT↑, SGOT↑
      ③Complication
        ·Heart failure
        ·Myocardial rupture
        ·Ventricular aneurysm
        ·Mural thrombosis
        ·Cardiogenic shock
        ·Acute pericarditis
        ·Arrhythmias
  (3)Myocardial fibrosis
      ·Cause: moderate-severe stenosis of the coronary artery
      ·Van Gieson stain: fibrosis (red), myocardium (yellow)
  (4)Sudden coronary death

§3. Hypertension

1. Etiology and pathogenesis
  (1)Etiology
      ①Genetic factors
      ②Diet: intake of sodium↑
      ③Psychological factors: stress
      ④Others: obesity, smoking, age↑
  (2)Pathogenesis
      ①Renal retention of excess sodium
      ②Functional vasoconstriction
      ③Structural hypertrophy
2. Pathologic changes
  (1)Benign hypertension (Chronic hypertension)
      ①Stage of functional disturbance
        ·Arteriole: temporal spasm, without structural changes
        ·Clinical features: BP variation, headache
      ②Stage of arterial changes
        ·Arteriolosclerosis: characteristic changes, arteriolar hyaline degeneration
                              Sites: afferent artery, spleen central artery, retina artery
        ·Small artery sclerosis: collagenous fiber↑, elastic fiber↑, internal elastic membrane break, SMC↑
                                  Sites: interlobular artery, arch artery, brain artery
        ·Large artery sclerosis: accompanied with AS
      ③Stage of organic changes
        ·Heart: compensative hypertrophy of left ventricle, weight↑
                left ventricular wall: 1.5-2cm
                papillary muscle and trabeculae carnae: thick
                ventricular chamber: not dilative
                Concentric hypertrophy → Eccentric hypertrophy
        ·Kidney: Primary granular atrophy of the kidney
                  Gross: bilateral, symmetric small
                        weight↓, hard, fine granular
                        cortex: thin
                  LM: glomeruli: fibrosis and hyaline degeneration
                      corresponding tubules: atrophy
                      interstitial fibrous tissue↑
                      remained: glomeruli: compensative hypertrophy
                                corresponding tubules: compensative dilation
        ·Brain: Hypertensive encephalopathy: edema, Hypertensive crisis
                Softening of brain: microinfarct
                Cerebral hemorrhage: severe complication
                                      Favorite sites: basal ganglia, internal capsule
        ·Retina: central artery sclerosis
  (2)Malignant hypertension (Accelerated hypertension)
      mainly affecting the kidney
      ①Hyperplastic arteriolosclerosis: intima: thick
                                        SMC↑, collagenous fiber↑
                                        concentric thickening: onionskinning
      ②Necrotizing arteriolitis: intima, media: fibrinoid necrosis

§4. Rheumatism

1. Etiology and pathogenesis
  (1)Etiology
      related to the infection of group A beta-hemolytic streptococci
  (2)Pathogenesis
      Ag-Ab cross reactions
2. Basic pathologic changes
  (1)Alterative and exudative phase
      ·Sites: heart, serosa, joint, skin
      ·Lesions: connective tissue stroma: mucoid degeneration
                collagenous fiber: fibrinoid necrosis
                infiltrative cells: Lymphocytes, Plasma cells, Monocytes
  (2)Proliferative phase (granulomatous phase)
      ·Sites: myocardial interstitium (beside blood vessel)
              subendocardium
              subcutaneous connective tissue
      ·LM: Aschoff body: center: fibrinoid necrosis
                          nearby: Aschoff cell: awl-eye cell, caterpillar cell
                          periphery: Lymphocytes
  (3)Fibrous phase (healed phase)
3. Lesions of organs
  (1)Rheumatic heart disease
      ①Rheumatic endocarditis
        ·Sites: heart valve (Mitral valve)
        ·Lesions: Gross: Verrucous vegetations: grey-white, semitransparent, miliary, alone the line of closure of the mitral valve, firmly adhere to valve
                  LM: Pale thrombus
                  Mc Callum patch: back wall of left antrum, endocardium irregular thickening
        ·Results: repeated organization of the vegetations → valve thicken, harden, adhere → chronic valvular vitium of the heart
      ②Rheumatic myocarditis
        Sites: myocardial mesenchymal connective tissue, near small blood vessel
      ③Rheumatic pericarditis
        ·Lesions: Serous or fibrinous pericarditis
                  Cor villosum: a lot of fibrin exude and form a heavy shaggy coat with adhesion between the layers of the pericardium
        ·Results: absorption → recovery
                  organization → constrictive pericarditis
  (2)Rheumatic arthritis
      Sites: the large joints, such as knee, shoulder, wrist, elbow, coxa
  (3)Rheumatic lesions of the skin
      ①erythema annulare
      ②subcutaneous nodules
  (4)Rheumatic arteritis
  (5)Rheumatic encephalopathy

§5. Infective endocarditis

1. Acute infective endocarditis
  (1)Cause: organisms (high virulence)
  (2)Sites: mitral or aortic valve
  (3)Lesion: Gross: affects previously normal valves
                    vegetations: bulky, gray-yellow, fragile, fall off easily → septic infarct
                    valve: ulceration, perforation
              LM: vegetations are composed of purulent exudate, thrombi, necrotic tissue, bacteria
2. Subacute infective endocarditis
  (1)Cause: organisms (lower virulence)
  (2)Pathologic changes
      ①Heart
        ·Sites: mitral or aortic valve
        ·Gross: affects previously abnormal valves
                vegetations: different in size, single or in group, gray-yellow, papillary or cauliflower-like, friable, fall off easily
                valve: deformation, ulceration, perforation
        ·LM: vegetations are composed of platelets, fibrin, bacteria, necrotic tissue, neutrophiles
              bottom of ulcer: granulation, lymphocytes, monocytes
      ②Blood vessel: embolism (brain, kidney, spleen), vasculitis (osler nodule)
      ③Kidney: microembolism → local or diffuse GN
      ④Septicemia: fever, anemia, spleen enlarged, Roth point

§6. Valvular vitium of the heart

1. Mitral stenosis
  (1)Causes: majority: rheumatic endocarditis
              minority: subacute infective endocarditis
  (2)Lesion: "fish-mouth" deformity
  (3)Clinical features: X-ray: "pear shaped heart"
2. Mitral insufficiency
  (1)Causes: majority: rheumatic endocarditis
              minority: subacute infective endocarditis
  (2)Clinical features: X-ray: "spherical heart"
3. Aortic valve stenosis
  (1)Causes: majority: rheumatic aortic valvulitis
              minority: congenital dysplasia, AS
  (2)Clinical features: X-ray: "boot shaped heart"
4. Aortic valve insufficiency
  Causes: majority: rheumatic aortic valvulitis
          minority: infective endocarditis, AS, syphilitic aortitis

§7. Cardiomyopathy and myocarditis

1. Cardiomyopathy
  (1)Dilated cadiomyopathy
      Pathologic changes: progressive hypertrophy of the heart, dilatation of all chambers, systolic dysfunction
  (2)Hypertrophic cardiomyopathy
      Pathologic changes: left ventricle and interventricular septum thicken, abnormal diastolic filling
  (3)Restrictive cardiomyopathy
      Pathologic changes: fibrosis of the endocardium and endomyocardium → restriction of ventricular filling
  (4)Keshan disease
      Pathologic changes: severe degeneration and necrosis of the myocardium, formation of repairing scar
2. Myocarditis

Chapter 7  Diseases of Respiratory System

§1. Pneumonia

1. Bacteria pneumonia
  (1)Lobar pneumonia
      ·Etiology: pathogens: pneumococcus
                  inducing factors: cold, excessive tired, anaesthesia
      ·Pathologic changes
        ①Congestion stage: Gross: swollen, red
                            LM: alveolar wall: capillary: diffuse dilation and congestion
                                alveolar space: serous exudate, a few RBC, neutrophils, macrophages, numerous bacteria
        ②Red hepatization: Gross: red, solid, liver-like consistence
                            LM: alveolar wall: capillary: dilation and congestion
                                alveolar space: full of fibrin, lots of RBC, a few neutrophils and macrophages, numerous bacteria
                                                fibrinous nets pierce through cohn's pores from one alveolus into adjacent alveoli
        ③Gray hepatization: Gross: gray-white, solid, liver-like consistence
                            LM: alveolar wall: capillary: compressed
                                alveolar space: fibrin↑, connection among fibrinous nets↑, lots of neutrophils
        ④Resolution stage: enzymatic digestion of fibrin
      ·Complication
        ①Pneumonary carnification: neutrophils↓ → incomplete resolution → organization of exudate → diffuse fibrosis
        ②Lung abscess and empyema
        ③Thickening and adhesion of pleura: fibrinous pleurisy
        ④Septicemia or pyemia
        ⑤Infectious shock
  (2)lobular pneumonia (bronchopneumonia)
      ·Etiology: pathogens: staphylococcus, pneumococcus
      ·Pathologic changes: Gross: scattered gray-yellow foci of consolidation are centered on bronchioles
                                  severe: Confluent bronchopneumonia
                            LM: suppurative, neutrophil-rich exudate fills the bronchi, bronchioles and adjacent alveolar spaces
      ·Complication
        ①Respiratory failure
        ②Heart failure
        ③Pyemia
        ④Lung abscess and empyema
2. Viral penumonia
  ·Etiology: pathogens: influenza virus
  ·Pathologic changes: LM: interstitial pneumonia
                            alveolar septum: widen obviously, edema, dilation and congestion of blood vessels, infiltrated with lymphocytes and monocytes
                            Hyaline membrane
                            Viral inclusion: round or oval, erythrocyte-like in size, surrounded with a transparent halo

§2. Chronic obstructive pulmonary disease (COPD)

1. Chronic bronchitis
  (1)Etiology
      ①Infection: virus, bacteria
      ②Smoking
      ③Air pollution and allergic reaction
      ④Internal factors
  (2)Pathologic changes
      ①Bronchial epithelium: degeneration and necrosis, goblet cells↑, squamous metaplasia
      ②Hypertrophy and hyperplasia of submucosal glands, mucous glandular metaplasia, secretion of mucus↑
      ③Bronchial wall: congestion and edema, infiltrated with lymphocytes and plasma cells
      ④SMC, cartilage
2. Bronchial asthma
  Pathologic changes
  ·Gross: mucous plugs
  ·LM: BM: thicken obviously, hyaline degeneration
        submucosa: edema, hyperplasia of mucous glands, goblet cells↑
        SMC: hypertrophy and hyperplasia
        infiltrated with eosinophils, monocytes, lymphocytes and plasma cells
        Charcot-Leyden crystals
3. Bronchiectasis
  Pathologic changes
  ·Gross: bronchi: dilation, purulent exudate
  ·LM: bronchial wall: thicken obviously, destroyed, fibrosis
        submucosa: dilation and congestion of blood vessels, infiltrated with lymphocytes, plasma cells, even neutrophils
4. Pulmonary emphysema
  (1)Etiology and pathogenesis
      ①Obstructive ventilative dysfunction
      ②Elasticity of respiratory bronchioles and alveolar wall↓
      ③α1-antitypsin↓
  (2)Types
      ①Alveolar emphysema (Obstructive emphysema)
        ·Centriacinar emphysema
        ·Periacinar emphysema
        ·Panacinar emphysema
      ②Interstitial emphysema
      ③Others
        ·Paracicatricial emphysema: bullae lung
        ·Compensatory emphysema
        ·Senile emphysema
  (3)Pathologic changes
      ·Gross: volume↑, pale, blunt margin, soft, elasticity↓
      ·LM: alveolus: enlarged
            alveolar septum: narrow, rupture, capillary↓

§3. Pneumoconiosis

1. Silicosis
  (1)Definition: Inhale a lot of crystalline SiO2 for a long time, cause the formation of silicotic nodules and diffuse interstitial fibrosis of lung
  (2)Pathologic changes
      ①Silicotic nodule
        ·Gross: clear border, round or oval, gray-white, hard, sand-like feeling
        ·LM: Cellular silicotic nodule: macrophages engulf SiO2 and assemble
              Fibrous silicotic nodule: fibrosis, concentric circular or vortiginous arrangement
              Hyaline silicotic nodule: hyaline degeneration of collagenous fiber
      ②Diffuse interstitial fibrosis of lung
  (3)Stages
      ·stageⅠ: pulmonary hilar lymph nodes: enlarged, formation of silicotic nodules, fibrosis
      ·stageⅡ: silicotic nodules↑, obvious fibrosis, lesions < 1/3 of the whole lung
                weight↑, hardness↑, volume↑
                pleura: thickened
      ·stageⅢ: density of silicotic nodules↑, confluent
                weight and hardness↑↑
                pleura: diffuse fibrosis, thickened
                silicotic cavity
  (4)Complications
      ①Tuberculosis                   
      ②Chronic cor pulmonale
      ③Pulmonary infection
      ④Obstructive emphysema: bullae lung → autopneumothorax

§4. Chronic cor pulmonale

1. Etiology and pathogenesis
  (1)Pulmonary diseases: COPD
      hypoxia → pulmonary arterioles spasm → resistance of pulmonary circulation↑ → pressure of pulmonary artery↑ → hypertrophy and dilation of right heart
  (2)Disorder affecting chest movement
  (3)Diseases of pulmonary vessels
2. Pathologic changes
  (1)Lesions of lung
      ·Pro-existed lesions
      ·Changes of pulmonary arterioles: hyperplasia and thickening of media, hyperplasia of elastic fiber and collagenous fiber
  (2)Lesions of heart
      Right ventricle: wall: thicken, hypertrophy
                      chamber: dilate
                      papillary muscle and trabeculae acrneae: thicken

§5. Tumors of respiratory system

1. Nasopharyngeal carcinoma
  (1)Etiology
      ①EB virus
      ②Heritable factors
      ③Chemical carcinogen
  (2)Pathologic changes
      ·Gross: nodular, cauliflower-like, infiltrating, ulcerative
      ·Histology
        ①Squamous cell carcinoma: Keratinizing squamous cell carcinoma (well differentiated)
                                  Nonkeratinizing squamous cell carcinoma (poorly differentiated)
                                  Undifferentiated squamous cell carcinoma: Vesicular nucleus cell carcinoma: round or oval vesicular nucleus, 1-2 large nucleoli, infiltrated with lymphocytes
        ②Adenocarcinoma
2. Carcinoma of the lung
  (1)Etiology
      ①Smoking
      ②Air pollution
      ③Occupational factors
  (2)Pathologic changes
      ·Gross types
        ①Central type
        ②Peripheral type
        ③Diffuse type
        Early stage carcinoma of the lung: Central type: limited in bronchial lumen or infiltrate the bronchial wall but without penetration of outside membrane and not infiltrate pulmonary parenchyma, without lymphatic metastasis
                                          Peripheral type: nodular, tumor mass <2cm, without lymphatic metastasis
        Occult carcinoma of the lung: Cytology: tumor cells (+)
                                      Clinical examination: (-)
                                      X-ray: (-)
                                      Biopsy: carcinoma in situ or early infiltrative carcinoma, without lymphatic metastasis
      ·Histologic classification
        ①Squamous cell carcinoma
        ②Adenocarcinoma
        ③Adeno-squamous carcinoma
        ④Small cell carcinoma: most malignant, oat cell carcinoma, neurosecretory granules
        ⑤Large cell carcinoma
        ⑥Sarcoid carcinoma

排版变乱了，凑合看吧

东西太多，lz应该发善心弄到一个记事本里，大家都方便。

引用第9楼blueblood于2008-05-07 11:53发表的  :东西太多，lz应该发善心弄到一个记事本里，大家都方便。

好啊，我整理整理

平时去别的论坛查找资料时，都是非会员不能下载附件，注册后还有权限限制，考虑到这点，就这样发了，方便新人浏览，呵呵

word版下载

现在的病理学考试好像只有名解用英文出题，其他的都用中文诶，还是中文答题的。

引用第13楼twinkle于2008-05-07 16:15发表的  :现在的病理学考试好像只有名解用英文出题，其他的都用中文诶，还是中文答题的。

恩，谢谢！
这是准备研究生复试时整理的，虽然只有笔试的五个英文名解和面试的一段翻译，但我在医学英语这方面很薄弱哦，呵呵，实践证明效果还是比较明显滴，以后还要继续努力啊