IMD Handout (2024-2025) PDF

CHAPTER 1: Cell Injury Causes of Cell Injury: 1- Hypoxia (loss of aerobic oxidative respiration or ischemia, loss of blood supply) 2- Infectious agents. 3- Physical agents (temperature, trauma, radiation). 4- Chemical agents & drugs. 5- Immunologic reactions. 6- Nutritional imbalance 7- Gen...

CHAPTER 1: Cell Injury Causes of Cell Injury: 1- Hypoxia (loss of aerobic oxidative respiration or ischemia, loss of blood supply) 2- Infectious agents. 3- Physical agents (temperature, trauma, radiation). 4- Chemical agents & drugs. 5- Immunologic reactions. 6- Nutritional imbalance 7- Genetic factors. Types of Cell Injury: Reversible Cell Injury (Degeneration) Irreversible cell injury ( Necrosis and Apoptosis) Reversible Cell Injury (Degeneration) (In case of mild injury of short duration) 1-Hydropic degeneration (cloudy swelling): Definition: Cell swelling due to water accumulation Gross Pictures: The organ is swollen & pale Microscopic Picture: (nucleus is normal) Cloudy swelling: cells are swollen with pale eosinophilic granular cytoplasm Hydropic changes: Cells are swollen with clear vacuole or vacuoles 2-Fatty change (Steatosis): Definition: Excess fat in parenchymal cells. Sites: Common in liver, but can occur in other organs. Causes of hepatic steatosis: Alcohol, malnutrition, diabetes mellitus, obesity Special stain for fat:  Black with osmic acid  Orange red with Sudan III Irreversible cell Injury (Necrosis & Apoptosis) (In case of severe injury or injury of long duration) 1- Necrosis: Definition: Necrosis is death of a group of cells within a living body Types of Necrosis 1-Coagulative Necrosis: in infarction of all organs except brain 2-Liquefied Necrosis: in brain and abscess 3-Caseous Necrosis: in tuberculosis. 1  4- Fat Necrosis: Two subtypes: a) Enzymatic Fat Necrosis: In acute pancreatitis, forming calcium soaps. b) Traumatic Fat Necrosis: in female breast caused by trauma 5- Fibrinoid Necrosis: in autoimmune diseases as rheumatic myocarditis Causes & Pathogenesis: (same as cell injury) Gross Picture:  Necrotic tissue appears opaque & yellow.  The surrounding tissue appear hyperaemic due to inflammation. Microscopic Picture: 1- Cellular Changes: a) Nuclear Changes: o Pyknosis: The nucleus becomes small & dark o Karyorrhexis: Nuclear fragmentation o Karyolysis : Faint dissolved nucleus b) Cytoplasmic Changes: o The cells may appear swollen (cytomegaly) 2- Architecture Changes: a) Protein denaturation (coagulation) b) Necrotic tissue may appear structureless 2-Apoptosis: Definition: It is programmed cell death or cell suicide, that usually involve few or single cells o It is regulated by Bcl-2 gene. o It is not associated with release of chemical mediators or inflammation. o It can be physiological or pathological. Examples 1-Physiological (normal) such as  During embryogenesis  Endometrium during menstruation 2-Pathological:  Liver cells in hepatitis  Some malignant tumour cells 2 Morphological features of Apoptosis: o Shrinkage of cell size o Nuclear chromatin condensation, followed by fragmentation of DNA o Formation of membrane blebs, followed by their separation= apoptotic bodies. o The apoptotic bodies consist of a dark nuclear fragmented cytoplasm. They become engulfed by phagocytic cells. 3  Intracellular Accumulation & Extracellular Deposition -Intracellular Accumulation: Cells may accumulate water, fat, glycogen, protein (in hyalinosis), and pigments (endogenous and exogenous) Pigments: A-Endogenous Pigments: 1-Melanin: (normally present as in skin, hair)  Increased melanin is observed in: o Prolonged exposure to sun o Chloasma: Brown patches in skin in pregnancy  Decreased melanin in albinism hereditary condition. 2. Lipochrome pigment Yellow brown pigment In Old age it increase in the tissues as a result of wear and tear. Examples: Heart  Brown atrophy of heart 3. Haemoglobin Derived Pigments A- hemosiderin: a) Haemosiderosis  Localized hemosiderin deposition in haemorrhage ( eg :trauma)  Generalized hemosiderin deposition as in excess iron in diet b) Haemochromatosis:  It is the most common form of iron overload. It is a congenital disorder due to a gene defect on chromosome 6.  - In advanced disease hemosiderin is deposited in many tissues as: Liver (causing liver cirrhosis) Heart (causing heart failure). Pancreas (Bronze diabetes is due to iron–induced damage of pancreatic islets) Microscopically: Iron pigment appears as a golden pigment In the cytoplasm. It can be visualized in tissues by the special stain (Prussian blue) 4  Exogenous Pigment 1- Inhalation Of carbon particles lead to black pigment in the lung ( anthracosis). 2- Ingestion: Chronic ingestion of lead  deposited in gum mucosa 3- Inoculation: Tattoo -Extracellular deposition: 1- Calcium: a- Dystrophic calcification: Deposition of calcium salt in injured and necrotic tissue with normal blood calcium level Gross: appears white & hard with granular surface Microscopic: Stained dark blue with haematoxylin Examples: Atherosclerosis, old scar, fat necrosis, dead ova b- Metastatic Calcification: Deposition of calcium salts in normal living tissue due to high blood calcium level Examples: Hyperparathyroidism 2- Amyloidosis Definition: Extra cellular deposition of abnormal protein (amyloid) mainly in the wall of blood vessels & basement membranes. Microscopic staining: 1) Hematoxylin & eosin stain: Amyloid appears homogenous & eosinophilic 2) Congo red stain (stain of choice): Amyloid stains orange red and when examined by polarized light, the amyloid appears as an apple- green birefringence Preferred site of biopsy: from kidney, rectum or gingiva 5 Classification of Amyloidosis: A-Systemic Amyloidosis: Amyloid is deposited in many organs 1-Primary amyloidosis: Plasma cell tumors 2- Secondary amyloidosis: in chronic inflammatory disorders: as tuberculosis. B. Localized Amyloidosis: Amyloid is deposited in one organ. Examples: Medullary carcinoma of the thyroid gland. 6  CHAPTER 2: Inflammation Definition: It is a protective mechanism of living tissue against injury. Its aim is to localize and destroy the causative agents and starts the process of repair. It may itself cause tissue damage. NB: Suffix (itis) = Inflammation (appendicitis) Types of Inflammation Acute Inflammation Chronic inflammation Onset: Rapid onset, short Gradual onset, prolonged duration (minutes or hours) duration( weeks to years) Injury: Mild, self-limited Severe & prolonged Types of inflammatory cells: Acute inflammatory cells: Neutrophils & Macrophages in acute inflammation Eosinophils: in allergic inflammation Lymphocytes & plasma cells: in viral infection Chronic inflammatory cells: Lymphocytes, Plasma cells & Macrophages in chronic inflammation Giant cells: Commonly seen in granulomas Acute Inflammation Steps of Acute Inflammation Local vascular Events (steps): 1- Temporary vasoconstriction: (First to occur to few seconds) 2- Arteriolar Vasodilatation: leads to redness and warmth of the inflamed area. 3- Increased vascular permeability: leads to formation of fluid rich in protein called (exudate) 4- Vascular Slowing (Stasis) 5- Formation of Inflammatory Fluid Exudate Functions of inflammatory fluid exudate: 1- Brings antibodies to inflammatory area 2- Brings leukocytes, chemical mediators, nutrients 3- Contain Fibrin threads: a)Helps localization of infection 7  b) Forms network helps in movement of phagocytic cells and fibroblasts 4- Dilute bacterial toxins 5- Drain products of inflammation Local Cellular Events (steps) 1) Margination & Rolling: leukocytes settle then roll on endothelial surface. 2) Pavementing: leukocytes adhere to endothelial surface. 3) Emigration: leukocytes leave the blood to extravascular space. 4) Chemotaxis: leukocytes are directed to move towards the inflamed area 5) Phagocytosis: mechanism a) Recognition & attachment of the particle to the phagocytic cel b) Engulfment c) Killing & Degradation of ingested particles occurs via: Oxygen dependent:* Reactive Oxygen Species (ROS) and * Nitrogen Oxide (NO) Oxygen independent: lysosomal enzymes Signs & Symptoms of acute Inflammation 1- Redness: vascular dilatation 2- Warmth: vascular dilatation 3- Swelling: due to: accumulation of exudate 4- Pain Systemic changes of acute inflammation: Fever Leukocytosis: blood leukocytes over 10,000/cmm Lymphangitis & lymphadenitis Fate of Acute Inflammation: 1-Resolution 2- Healing 3-Spread: Direct, lymphatic & blood spread 4-Chronicity Chemical Mediators Role in Inflammation: Reactions of Principal mediator inflammation Vasodilatation and Increased vascular Histamine permeability Chemotaxis, Chemokines, C3a, C5a Fever TNF Pain Prostaglandins Tissue damage Lysosomal enzymes of leukocytes Reactive Oxygen species, NO 8  Types of Acute Inflammation A- Acute Suppurative Inflammation (Pus) Localized Diffuse 1- Abscess 1- Cellulitis 2- Boil (Fruncle) 2- Acute Suppurative appendicitis 3- Carbuncle 3- Peritonitis B- Acute non Suppurative Inflammation (No Pus) 1- Serous inflammation 2- Fibrinous inflammation 3- Serofibrinous inflammation 4- Catarrhal inflammation 5- Pseudomembranous inflammation 6- Allergic inflammation Abscess Definition: A localized suppurative inflammation result in the formation of a cavity containing pus. Aetiology: Caused by staphylococcus aureus infection. Pathology of Abscess: Gross: Cavity filled with pus which is thick creamy yellowish material Microscope: large number of neutrophils, pus cells ( dead neutrophils), necrotic material and, bacteria Complication of Abscess: 1-Spread: a) Direct spread abscess enlarge b) Lymphatic spread  lymphadenitis c) Blood spreadpyaemia, septicaemia, bacteraemia 2-Chronic abscess 3- Gangrene 4- Complication of healing: a) Chronic ulcer: (loss of surface epithelium) b) Sinus : (blind ended tract between abscess & skin) c) Fistula: ( tract between abscess cavity & hollow organ) d) Keloid: ( large scar due to over healing) Carbuncle Definition: Multiple deep subcutaneous abscesses communicating with each other & opened through multiple points in skin. Common in diabetics. Sites: back of neck, scalp 9  Abscess Versus Cellulitis Abscess Cellulitis Localized suppurative inflammation Diffuse suppurative inflammation Staph aureus Streptococcal haemolyticus Any organ or tissue loose subcutaneous tissues ,orbit Spread: less common Spread: more common Acute Non Suppurative Inflammation :(NO PUS) 1-Catarrhal inflammation: Mild inflammation with mucus secretion. E.g : common cold 2-Pseudomembranous Inflammation: Severe Inflammation with secreted bacterial toxins e.g Diphteria lead to pseudomembrane in throat. 3-Serous inflammation: Accumulation of fluid poor in protein, e.g: pleural & pericardial effusion burn blister 4-Fibrinous inflammation: Accumulation of fluid exudate rich in protein (fibrin) e.g: fibrinous pericarditis and lobar pneumonia 5-Serofibrinous inflammation: Exudate rich in both fluid & fibrin e.g: Serofibrinous pericarditis 6-Allergic: excess eosinophils, e.g: Allergic rhinitis & Urticaria Chronic Inflammation Aetiology: 1- Chronic inflammation may follow acute 2- Chronic from the start: Microscopic picture: 1- Fibrosis 2- Chronic Inflammatory cells: lymphocytes, plasma cells &macrophages: 3- Thick wall arteries Types: 1- Chronic Non specific inflammation: (chronic inflammatory cells, fibrosis, thick wall arteries) 2- Granulomatous inflammation (Granuloma): Definition: Special form of chronic inflammation characterized by localized aggregate of: o Macrophages, Lymphocytes o Epithelioid cells: modified macrophages o Giant cells: collection of macrophages Types : a) Infective granuloma: Bacterial: Tuberculosis Parasitic: Bilharzial Fungal b) Foreign body granuloma: Surgical sutures or glass particles c) Unknown aetiology. 10  Tuberculosis (TB): Definition: Chronic granulomatous inflammation caused by tubercle bacilli Tubercle is the basic lesion = (Granuloma+ Caseous necrosis) Gross Picture: Tubercles fuse & form small follicle 1-2 mm in diameter. Caseous necrosis is yellow and cheesy Microscopic Picture: Tubercles are Granuloams formed of Epithelioid cells, Langhans' giant cells, Lymphocytes and Caseous necrosis A) Primary Pulmonary Tuberculosis Etiology: First infection in the lung by inhalation of human tubercle bacilli. It is child hood type Pathology: Primary TB complex 1-Ghon's focus: initial tuberculous lung ; lesion subpleural (lower part of upper lobe or upper part of lower lobe) 2-Tuberculous lymphangitis: 3-Tuberculous lymphadenitis:  Enlarged  Caseous  Matted together Gross and microscope: as tubercle (see above) Fate of primary TB infection: 1-Localization With adequate immunity Heal by fibrosis (+/- dystrophic calcification) Small lesions are totally replaced by fibrosis Larger becomes surrounded by fibrosis (encapsulation). Some bacilli may however remain alive  If later the body resistance is lowered , the dormant bacilli lead to reactivation of tuberculosis →Secondary pulmonary TB 2- Spread of TB due to failure of localization a) Direct to surrounding tissue b) Lymphatic spread to hilar LN c) Blood spread: 1- Small number→ No effects (destroyed by phagocytic cells) 2- Moderate number→ Isolated organ TB: (one organ ) 3- Large number caseous destruction of of vessels) → miliary tuberculosis 11  CHAPTER 3: Repair (Healing)  Definition: Is the replacement of damaged tissue by new healthy one.  Types of repair:  Regeneration: Replacement of injured cells by cells of the same type.  Fibrosis: Replacement of injured cells by fibrosis, any part of the body except brain.  Gliosis: Replacement of injured cells by gliosis in brain.  Types of cells according to proliferative activity: Labile Cells Stable Cells Permanent Cells Continuously dividing Limited capacity of division Non dividing cells Skin Parenchymatous cells Myocardium, Mucous membranes Liver, Spleen, Pancreas. Skeletal muscles Hemopoietic cells Mesenchymal cells CNS cells (neurons) Osteoblast, Chondroblast Factors affecting efficiency and type of repair: 1. General factors: (a) Age. (healing better in young age) (b) Nutritional deficiencies ( vit.c, zink & proteins). (c) Drugs as corticosteroids (d) Chronic diseases as Diabetes mellitus 2. Local factors: (a) Types of cells. (b) Blood supply. (c) Persistent infection or foreign body (d)Extent of tissue damage. Factors controlling the mechanism of repair: 1) Growth Factors Recruit cells of G0 into the cell cycle. It includes: 1)Epidermal Growth Factor (EGF) 2)Platelets derived growth factor (PDGF) 3)Fibroblastic growth factors (FGFS) 2- Cell to cell interaction (Contact inhibition signals) 10  In case of tissue damage  cell loss  loss of contact inhibition  stimulate cells to divide until establish contact again. 3- Extracellular Matrix (ECM) (Cell Matrix Interactions) The ECM proteins include (fibronectin and laminin). ECM play important roles in cell migration, proliferation, differentiation and adhesions. Healing Of Bone Steps: see figure below Stage 1: Hematoma and granulation tissue formation (made of capillaries & mesenchymal cells). Stage 2: Soft callus = (cartilaginous callus) Some mesenchymal cells differentiate into cartilage, others into osteoid. Osteoid undergoes gradual calcification forming non lamellar bone ( temporary callus). Stage 3: (Permanent/ Hard callus): Formation of lamellar bone Stage 4: (Bone Remodeling) Removal of unnecessary internal and external callus (by osteoclast). Bone marrow regenerates inside the medullary canal. Causes of Imperfect Bone Healing: A- Local causes: 1. Inadequate immobilization. 2. Pathological fracture eg: due to bone tumour or osteoporosis. 11  3. Soft tissue interposition between the fracture ends. 4. Ischaemia & Infection B- General causes: 1. Corticosteroid therapy. 2. Malnutrition &Vitamin deficiency. 3. Old age.(delayed healing) 4. Systemic disease e.g. diabetes mellitus. Healing By Fibrosis Definition: Replacement of damaged tissue by granulation tissue which matures to fibrous tissue (scar). Granulation tissue is red granular & highly vascular formed of fibroblasts & capillaries Scar is pale, nearly avascular & smaller in size. Steps of granulation tissue & fibrosis: 1- Angiogenesis: Formation of new blood vessels. 2- Fibrogenesis: Migration and proliferation of fibroblasts. 3- Maturation and Remodeling: to form permanent scar through.  Collagen deposition  Obliteration of blood vessels Wound contraction by the action of myofibroblast. Finally the scar is pale, nearly avascular &smaller in size. Examples of Healing by Fibrosis: A. Wound healing: Primary and secondary union B. Healing of Serofibrinous inflammation. C. Fibrous organization of thrombus D. Healing of Infarctions. Wound Healing Types of Wound Healing: 1) Healing by Primary Union. 2) Healing by Secondary Union. Comparison between types of wound healing Primary Union (Intension) Secondary Union (Intension) 1- Clean, minimal tissue damage. 1- Infected, gapping wound. 2- Shorter healing time. 2- Longer time healing. 3- Less granulation tissue. 3- More granulation tissue. 4- Smaller pale linear scar. 4- Large scar. 5-Early epidermal regeneration. 5- Delayed epidermal regeneration. 6-Less wound complication. 6-More wound complication. 12 Complications of wound healing: 1. Cosmetic deformities: due to extensive scarring 2. Function loss: Excessive scar contraction may lead to contracture (limitation of movement). 3. Keloid Formation: (overdone repair) Genetically determined and common in dark skin people. A firm mass covered by stretched skin may follow surgery or burns. 4-Chronic: Ulcer : loss of epithelial continuity Sinus: cyst opening on surface. Fistula: opening tract between 2 hollow Sinus Fistula organs. 5- Implantation epidermoid cyst: Cyst lined by squamous epithelium filled with keratin due to epithelial cells trapped within the wound. 6- Rarely carcinoma: Marjolin’s ulcer: mainly scars of burn. 13  CHAPTER 4: Cellular adaptation & Growth disturbances Atrophy Definition: Cellular Atrophy: It is acquired shrinkage of cell size due to decreased cell anabolism and/ or increased cell catabolism. Tissue or organ atrophy: Is decrease in its size and weight, either due to cell atrophy or cell loss. Etiology and Types: 1-Physiological atrophy: Atrophy of thymus after puberty & atrophy of mammary gland and ovaries after menopause due to diminished hormone stimulation. 2-Pathological atrophy: -Disuse atrophy e.g. Atrophy of the muscles of a limb; in prolonged immobilization after bone fracture. -Neuropathic atrophy e.g. Atrophy of muscles of a limbs; in case of nerve injuries. Hypertrophy Definition: Hypertrophy is an increase in the size of the cell leading to increase in the size of the affected organ. It is due to increased protein synthesis. Aetiology & Types: 1- Physiological hypertrophy: a- Pregnant uterus due to hormone stimulation. b- Hypertrophy of striated muscles in muscle builders. 2- Pathological hypertrophy: A) Adaptive type: Left ventricular hypertrophy due to hypertension. B) Compensatory type: If one of a paired organ is out of function or surgically removed , the other organ undergoes compensatory hypertrophy e.g. kidney enlargement when the other kidney is surgically removed. 14  Hyperplasia Definition: Hyperplasia is an increase in the number of cells, leading to increase in the size of the affected tissue or organ. Etiology and types: 1- Physiological hyperplasia: Hormonal hyperplasia e.g. mammary glands at puberty. 2- Pathological hyperplasia: A- Hormonal hyperplasia e.g. Endometrial & mammary hyperplasia due to excessive estrogen stimulation. B- Compensatory hyperplasia Hyperplasia of the liver after partial hepatectomy. Bone marrow hyperplasia following hemorrhage. Metaplasia Definition: It is the transformation of one mature cell type into another of the same category. It is due to chronic irritation. It is reversible process Aetiology and types: 1). Epithelial metaplasia: Most common examples Squamous Metaplasia: Transformation of columnar or transitional cells into stratified squamous epithelium. E.g: Bronchial respiratory epithelium in cigarette smokers. 2- Mesenchymal Metaplasia: Fibroblast may become transformed into chondroblasts or osteoblasts that producing bone or cartilage in abnormal sites.E.g: Localized Myositis Ossificans. Leukoplakia Definition: Hyperkeratotic stratified squamous epithelium  Thick irregular white mucosal patches, common in tongue  It is a precancerous lesions that may be squamous cell carcinoma. Dysplasia Definition:  Dysplasia is a non-neoplastic proliferation of cells.  Dysplastic cells shows atypia, they show pleomorphism, enlarged dark (hyperchromatic ) nuclei and increased mitotic activity.  Degree of dysplasia: It is mainly in the epithelium. Dysplasia is graded into: mild, moderate and severe according to: 15  Degree of cell atypia Extent of involvement. Severe dysplasia corresponds to carcinoma in situ, it involves the entire epithelial thickness.  Example of dysplasia: 1- Cervical dysplasia in females with chronic cervicitis. 2- Urothelial dysplasia in patients with bilharzial cystitis.  Prognosis of dysplasia: 1-Mild and moderate grades of dysplasia Do not involve the entire thickness of the epithelium Commonly reversible when the cause is removed 2-Severe dysplasia (carcinoma in situ) is highly precancerous (premalignant). Almost all cases progress to INVASIVE CANCER. Carcinoma In Situ  Definition: It is an intraepithelial carcinoma or preinvasive carcinoma, represent a severe form of epithelial atypia WITHOUT invasion of the BASEMENT MEMBRANE.  Fate: Progression to invasive carcinoma after variable times (Usually years). 16  CHAPTER 5: Neoplasia Definition:It is a new growth (Tumor) forming an abnormal mass due to cell proliferation which is uncontrolled, autonomous, irreversible, unlimited, and has NO useful function. Classification of tumors According to tissue of origin (Histological classification). 1. Epithelial tumors. 2. Mesenchymal tumors. 3. Others According to their behavior (Biological classification). 1. Benign Neoplasm. 2. Malignant Neoplasm. 3. Locally Malignant Benign tumors Malignant tumors Rate of growth Slow Rapid Mode of growth Expansile Infiltrative Gross:  Margins Regular Irregular  Cut Section No hemorrhage or Hemorrhage & necrosis  In a solid organ necrosis Irregular & Non capsulated Globular/Ovoid, & Capsulated Fungating Polypoid Ulcerative with raised  From surface Polyp/Papilloma everted edges epithelium Infiltrative 17 Microscopic Cell differentiation: Cells perfectly Cells show anaplasia/atypia (Extent to which tumor differentiated (resemble 1-Cellular pleomorphism: cells resemble normal normal cells) 2-Nuclear pleomorphism: cells) 3-Nuclear enlargement and hyperchromatism 4-Prominent Nucleoli 5-Increased mitoses Histologic Carcinoma may be graded differentiation: (Extent to Architecture resemble according to degree of which tumor structure normal tissues differentiation to: resemble normal structure Well differentiated (grade of tissue) I), Moderately differentiated (grade II), Poorly differentiated (grade III) Undifferentiated(grade IV). BETTER differentiated tumors as grade I tend to show less marked cellular anaplasia & grows slower Behavior & Prognosis DO NOT Spread SPREAD (Direct, lymphatic & blood ) Do NOT Recur RECUR after excision Dangerous if: DANGEROUS & CAUSE DEATH In brain or In hollow organ as intestine causing obstruction In endocrine glands producing hormones 18 Tissue of Origin Benign Malignant A) Epithelium 1. Surface epithelium. a) Stratified Squamous cell Squamous cell carcinoma b) squamous papilloma a) Transitional Transitional cell Transitional cell carcinoma papilloma a) Ducts of glands Duct papilloma Duct carcinoma a) Mucosa of GIT Adenomatous polyp Adenocarcinoma 1. Glandular epithelium Endocrine & Exocrine glands Adenoma Adenocarcinoma A) Mesenchyme 1. Connective tissue a) Fibrous Fibroma Fibrosarcoma b) Adipose Lipoma Liposarcoma d) Bone Osteoma Osteosarcoma. &osteoblasloma e) Cartilage Chondroma, Chondrosarcoma osteochondroma 1. Smooth muscle Leiomyoma Leiomyosarcoma 2. Striated muscle Rhabdomyoma Rhabdomyosarcoma 3. Endothelium Angioma Angiosarcoma 4. Mesothelium Rare Mesothelioma 5. Synovium Synovial sarcoma A) Others 1. Melanocytes Nevus Malignant melanoma 2. Totipotent cells Teratoma ,mature Teratoma, immature (malignant) 3. Embryonic cells Embryonic rumors 4. Lymphoid & Lymphoma &leukemia hemopoeitic 5. Schwann cells Schwannoma Malignant peripheral sheath tumor 6. Trophoblast Vesicular mole Choriocarcinoma 19 Carcinoma Sarcoma Definition: Malignant tumor of Definition: Malignant tumor of epithelium. mesenchyme. Incidence: Most common form of Incidence: Less common form of malignancy. malignancy Age: Usually old age: >40 years. Age: Usually young age: