VMed 151 General Pathology Syllabus PDF

COLLEGE OF VETERINARY MEDICINE Visayas State University Baybay, Leyte Subject: VMed 151 General Pathology - principles of veterinary pathology and necropsy, histopath...

COLLEGE OF VETERINARY MEDICINE Visayas State University Baybay, Leyte Subject: VMed 151 General Pathology - principles of veterinary pathology and necropsy, histopathological diagnosis Prerequisite: VMed 111 (Histology) 6 hrs/wk (3 lec/3 lab) Credit: 4 units Vision: VSU: ‘VSU as the center of excellence in education and research in agriculture and allied fields in the Visayas’ CVM: ‘CVM as the center of excellence in veterinary medicine in the Visayas’ Mission: VSU ‘Attainment of the highest quality of human capital and scientific knowledge for the sustained growth and development of agriculture, fisheries, forestry, and agri-industries’ CVM: ‘Attainment of the highest quality of veterinarians and scientific knowledge for the sustained growth and development of veterinary medicine’ 1. Course Objectives: At the end of the semester the students are expected to know the principles of the disturbances in different body systems, their pathogenesis, gross and microscopic lesions. The specific objectives of the course are the following: 1.1. Know the different disturbances that affect the body systems. 1.2. Learn the pathogenesis of the different disturbances. 1.3. Appreciate the interaction between etiologic agents and cells of the body. 1.4. Understand the gross and microscopic lesions of the different disturbances. COURSE OUTLINE (Lecture) 2. The course deals with the study on the principles of pathology of disturbances affecting the organs of the body systems 2.1. Principles of pathology and disturbances in development and circulation; their pathogenesis gross and microscopic lesions…..Understanding the principles of pathology and pathogenesis of the disturbances in development and circulation can serve as a basis in understanding the gross and microscopic lesions and their significance. (1st Long Exam, 100 pts.) 2.1.1. Introduction 2.1.2. Disturbances in development 2.1.3. Disturbances in circulation 2.2. Disturbances in cell metabolism, necrosis and cell growth and nutrition, their pathogenesis and histopathology….. Understanding the pathogenesis of the disturbances in cell metabolism, necrosis and cell growth and nutrition can serve as basis in understanding the gross and microscopic lesions of organs involved; and their significance, (2nd Long Exam, 100 pts.) 2.2.1. Disturbances in cell metabolism 2.2.2. Necrosis 2.2.3. Disturbances in cell nutrition and growth 1  2.3. Defense against injury, concretions, neoplasms, their pathogenesis and histopathology ……. Understanding the pathogenesis of the defenses against injury, concretions and neoplasms can serve as basis in understanding the gross and microscopic lesions of the organs involved; and their significance. (3rd Long Exam, 100 pts.) 2.3.1. Inflammation 2.3.2. Healing 2.3.3. Fever 2.3.4. Concretions 2.3.5. Neoplasm 3. Basis of Grading 3.1. 3 long exams (300 pts.) 3.2. short quizzes &/or Recitation (115 pts.) 4. References 4.1. Runnells, A., W.S., Monlux and W.A. Monlux. 1977. Principles of Veterinary Pathology. 7th Edition. Iowa University Press, Ames, Iowa: U.S.A. 4.2. Thomson, R.G. 1978. General Pathology. W.B. Saunders Co., Philadelphia: U.S.A. 4.3. Carlton, W.W., M. Donald and M. Garcia. 1995. Thomson’s Special Veterinary Pathology. 2nd Edition. St. Louis, Missouri: U.S.A. 4.4. Jose, T.C. and R.D. Hunt. 1983. Veterinary Pathology. 5th Edition. Lea and Febiger, Philadelphia: U.S.A. 4.5. Jubb, D.C., P.D. Kennedy and N. Palmer. Pathology of Domestic Animals. 4th Edition. Academic Press, Inc., San Diego, California: U.S.A. 4.6. Coles, E.H. 1986. Veterinary Clinical Pathology. W.B. Saunders Co., Philadelphia: U.S.A. Professor: Dr. Tomas J. Fernandez, Jr., DVM, MSC., PhD. 2  INTRODUCTION 1. Cellular Structures 1.1. Plasma Membrane 1.1.1. It has a trilaminar appearance, with 2 electron-dense layer separated by an electron-lucent layer. 1.1.2. It has a coating called glycocolyx, which is a carbohydrate-rich layer, composed of glycoprotein terminals of membrane protein. 1.1.3. It may show a variety of morphological specializations (e.g. microvilli, interdigitations, caveolae & myelin. 1.1.4. It has specialized intercellular attachments such as tight junctions, gap junctions, and desmosomes. 1.1.5. It forms a barrier between the cell with other cells, bacteria, viruses, hormones and other substances involving the cell membrane. 1.1.6. It is critical to the well-being of the cell. 1.2. Nucleus 1.2.1. This is the "brain" of the cell which contains the genetic information that ultimately directs all of the cell activities. 1.2.2. DNA is located and replicated in the nucleus and RNA is synthesized in the nucleus for transport to the cytoplasm. 1.2.3. Structures found in the nucleus: 1.2.3.1. chromatin - contains DNA and associated proteins such as heterochromatin, a condensed and lightly basophilic protein; euchromatin, dispersed, and as a result, stains lightly. 1.2.3.2. Nucleolus - forms a roughly spherical substructure of the nucleus, containing 5-RNA and a little DNA, the balance being mostly protein. It is the site of synthesis of most of the components of ribosomal RNA and cells which are actively synthesizing protein usually have one or more prominent nucleoli. 1.3. Cytoplasm 1.3.1. Mitochondria 1.3.1.1. Site of production of most of the ATP, which forms the cells major source of energy. 1.3.2. Endoplasmic Reticulum 1.3.2.1. These are of two types: rough or granular ER (RER) and smooth reticulum or agranular ER (SER) 1.3.3. Ribosomes 1.3.3.1. Both RER and ribosomes are involved in the synthesis and secretions of proteins. 1.3.3.2. Free ribosomes produce proteins for use in the cell, 1.3.3.3. Ribosomes attached to the ER are involved in the synthesis of protein for export from the cell. 1.3.4. Golgi Apparatus 1.3.4.1. Modifies, concentrates and packages proteins for secretions from the cells. 1.3.5. Lysosomes 1.3.5.1. Membrane-bound organelles that are important in the digestion of biological material in the cell. 1.3.5.2. Peroxisomes are enzyme content of lysosomeswhich suggests that lysosomes may be involved in the destruction of hydrogen peroxide, a substance which may inure cells 3 2. Cell prehension 2.1. Heterophage (phagocytosis) 2.1.1. Extracellular material is taken up by an infolding of the plasma membrane 2.2. Autophage 2.2.1. Effete or injured organelles are initially surrounded by a double- membrane thought to be derived from the ER 2.3. Esotropy 2.3.1. Involves the formation of a membrane-bound structures in which the orientation of the cell membrane is reversed. The inside of such structures is equivalent to the extracellular surface of the plasma membrane 2.3.2. Forward esotropy – includes pinocytosis and phagocytosis, Formation of vesicles from the ER for transport to the Golgi and formation of secretory granules from the golgi. 2.3.3. Reversed esotropy – includes fusion of secretory vesicles with the plasma membrane and the fusions of the phagosome with the lysosome. 2.4. Exotropy 2.4. Maintains the orientation of the membrane and involves the turning of the membrane towards the extracellular space or the cytocavitary space followed by fusion to form a budded-off particle containing cell sap History of Pathology 1. The concept on the cause of disease during the Rennaisance period was put forth by the so-called humoral pathologists. They claimed that the disease is associated with the imbalance of body fluids (humors), which corresponded to imbalance of substances in nature: 1.1. Blood - which was warm and moist like air - heart 1.2. Phlegm - which was warm and moist like water - brain 1.3. yellow bile - which was dry and warm like fire - liver 1.4. black bile - which was dry and cold like earth - spleen Eucrasia (from Greek word eu = well and krasis = mixing) of these humors results in health Dyscrasia (from dys = bad) results in disease 2. Humoral pathology was supported by the following observations: 2.1. Diseases were often characterized by increased discharge of fluid, perspiration and fever, vomition, diarrhea, catarrhal discharge, exudation and transudation to the body cavities. 2.2. Blood was the vital tissue, and individual dies if exsanguinated 2.3. The coagulation of blood was different in healthy and sick individuals 2.3.1. The phlegm of the humoral pathologists is now named Fibrin. What nowadays is considered to be the effect of the disease was considered by the humoral pathologists to be the cause. 3. During the time of Hippocrates, diseases tend to pass through 3 stages: 3.1. A raw preliminary stage 3.2. A ripening staged called the stage of coction or pepsis, and finally 3.3. A stage of crisis in which elimination of the superflous humor or abnormal mixture of humors occurred 4. The following people have contributed something to the study of pathology 4.1. Celsus (30 BC to 30 AD) - recorded the history of the period of humoral pathology. 4  4.2. Claudius Galen (129-201 AD) - considered the greatest medical figure of all times. 4.3. Fernel ( French) - wrote textbooks in pathology, physiology and therapeutics. He was the author of the book PATHOLOGIAE LIBRI, which is considered the first medical work to be called a textbook of pathology. 4.4. William Harvey - published a book on blood circulation, which revolutionized the study of clinical pathology. 4.5. Malphigi - discovered the capillaries and erythrocytes and described in detail the kidneys, lungs and spleen. 4.6. Hans and Zacharias Jansen (Dutch) - invented the first microscope. 4.7. Cornelius Drebel (Dutch) - introduced a better microscope. 4.8. Anton van Leewenhoek (Dutch) - popularized the use of the microscope 4.9. Morgagni (Italian) - began modern pathology with emphasis on correlation between clinical detail and postmortem findings. 4.10. Bichat (French) (1771-1802) - described not just organs, but specific tissues within organs which can be involved separately in disease. He identified 21 different tissues without the aid or use of the microscope. 4.11. Beniviene Malphigi & Valsalva Morgagni- Italy's greatest pathologist in the 19th century 4.12. Fernel & Bichat - France's greatest pathologist in the 19th century 4.13. William Harvey - England's greatest pathologist in the 19th century 4.14. Carl Rokitansky (German) - last of the great contemporary humoral pathologists 4.15. Johannes Mullier (German) - the source of modern histology and cellular pathology 4.16. Rudolf Virchow (German) - disproved the theory of spontaneous generation of cells. He recognized the role of cells in pathology and the biochemical changes in tissues and fluids which forecasted the birth of clinical pathology. By rebuilding pathology on his true conception of the human body as an organized cell state, he deserved the title of the FATHER OF PATHOLOGY. Tools of Pathology.1. The study of pathology involves the examination of tissues called glass slide preparations which are simply very thin (2-5 µm) slices of tissues preserved in formaldehyde or other fixatives and embedded in paraffin wax. These sections are stained with basic stain (hematoxylin, blue) and acid (eosin, red or eosinophilic) which allow various components of the tissue to be visualized. Other stains elucidate the nature of the disease process. 1.1. Hand lens - make an LPO drawing 1.2. Light microscope - basic tool of the pathologist to study sections of tissues. Use the LPO as much as possible. The HPO's is used only for the study of cellular detail. 5 1.3. Histochemistry (histological stain) - after light microscopy, this is the method most often used for the elucidation of pathological processes. These stains are those which react with known specific chemical groups or substances in tissues. 1.3.1. Perl's Method - for hemosiderin, where ferric iron in the tissues combines with potassium ferrocyanide to form Prussian blue. 1.3.2. Congo Red – amyloid 1.3.3. Sudan III or IV – fats 1.3.4. Periodic Acid Schift (PAS) - also known as Hale Method, Mucicarmine, Alcian Blue Method, demonstrates carbohydrate substances e.g. Glycogen. 1.3.5. Toluidine Blue - is specific for mast cell granules. 1.3.6. Gridley's and Grocott Silver Methenamine - for fungi 6 2. Enzyme histochemical 2.1. Identify the presence of specific enzymes in the stained tissues, particularly useful in the study of muscle lesions to distinguish different types of muscle fibers. For this purpose, fresh, frozen tissues rather than fixed tissues, are required. 2.2. Enzymes in cells and tissues are also demonstrated by histochemical methods. The tissue slice is incubated with a substrate; the enzyme then acts on the substrate and liberates a component that is made visible in the section by forming either a colored compound or an insoluble precipitate. For example, alkaline phosphatase is shown by treating a section with glycerophosphate. The liberated PO4 is then treated with cobalt nitrate to produce cobalt PO4 that is finally converted to cobalt sulphide. The presence of the enzyme is thus indicated by a black precipitate over and around the cells containing the particular enzyme 3. Dark field, Phase Contrast 3.1. Useful in immunopathology where deposits of & Fluorescent Microscope Ig's, complement or other substances can be & Immunochemistry detected. Fluorescence depends upon either the fact that some tissue components fluoresce naturally in UV light (primary fluorescence) or the fact that certain components can be made to fluoresce by treating a section with certain dyes called fluorochromes such as auramine O and tetracycline (secondary fluorescence) 4. Electron Microscope (EM) 4.1. EM is a major tool for examining the morphological changes in diseased tissues. EM has illuminated the study of cellular disorder mainly by linking organelles with particular function. This enables the histopathologist to translate the morphological alteration into functional disturbances. This is especially true if the only detectable lesions or changes are demonstrable by EM, since the morphological alterations are very slight to be seen by light microscopy (LM). Its advantage is its high resolution, which far exceeds that of LM. Issues in the Study of Pathology 1. Conflicts in Understanding Pathology arise from the following: 1.1. The host defense linked together in inflammation, is also the major pathway of tissue injury 1.2. The same factor producing the beautiful life-saving hemostatic plug, is also responsible for the ugly and life-threatening thrombus 1.3. Macrophages that perform phagocytosis heroics release enzymes which degrade or injure tissues 2. The Pathologist studies tissues obtained by: 2.1. Biopsy - tissue samples taken from an alive animal 2.1. Necropsy (Autopsy)- postmortem examination of animals in which tissues can be obtained and processed 7 3. Diagnosis in Pathology has three forms: 3.1. Morphologic Diagnosis - describes the predominant lesion in the tissue; the most important of the three forms. e.g. suppurative enteritis 3.2. Etiological Diagnosis -gives the specific causes of the disease. e.g. Parvoviral enteritis 3.3. Definitive Diagnosis -gives the specific disease entity. e.g. Johne's disease Morphological Diagnosis Etiologic Diagnosis Definitive Diagnosis 1. Subacute non-suppurative L. canicola nephritis Leptospirosis Interstitial nephritis 2. Chronic granulomatous Mycobact. paratob. Johne's disease enterocolitis 3. Subacute catarrhal enteritis E. coli enteritis Collibacillosis 4. Non-suppurative meningo- Viral meningoencephalitis Rabis encephalitis Levels of Structural and Functional Example for Diabetes Mellitus Organization 1. Whole organism dog 2. Organ systems endocrine system 3. Organ pancreas 4. Tissues islet of Langerhans 5. Cells beta cells 6. Subcellular organelles endoplasmic reticulum 7. Biochemical-molecular insulin (this level is not known in other diseases) DEFINITIONS OF TERMS Pathology 1. The word pathology comes from two Greek words: patho, means disease or alteration; and logos, which means study. 2. It is the study of the anatomical, chemical and physiological alterations in an organism. 3. Terms that are related in the study of pathology: 3.1. General Pathology - basic alterations in tissues as the result of disease. 3.2. Special Pathology - application of what is general pathology to the various specific diseases that involve the individual as a whole. 3.3. Experimental Pathology - production of lesions by experimental method. 3.4. Macroscopic (gross) Pathology - examination of tissue alterations with the naked eyes. 3.5. Microscopic Pathology, Histopathology or Cellular Pathology- examination of alterations with the aid of a magnifying lens such as the microscope. 3.6. Clinical Pathology - laboratory methods used to aid in arriving at a diagnosis. 3.7. Humoral Pathology - alterations in antibodies that occur in an individual as a result of disease. 3.8. Chemical Pathology -chemical alterations of the body fluids and tissues that result from disease. 3.9. Physiological Pathology - deals with functions of organs. 8  3.10. Necropsy, Autopsy or Postmortem - Examination of an individual after death by systematic dissection. 3.10.1. Necropsy - applicable to veterinary medicine. 3.10.2. Autopsy - applicable to human medicine. 3.11. Morbid Changes - alterations in tissues found at necropsy that are the result of disease. 3.12. Biopsy - removal and elimination of tissue obtained from the living animal. 3.13. Health - state of an individual living in complete harmony with his environment. 3.14. Disease - condition in which an individual shows an anatomical, chemical, or physiological deviation from the normal. Aspects of Veterinary Pathology 1. Etiology – causation of a disease 1.1. Extrinsic causes 1.2. Intrinsic cause 1.3. Predisposing causes 2. Pathogenesis 3. Lesion 3.1. Macroscopic Lesions - Alterations that can be seen with the naked eyes. 3.2. Microscopic Lesions - Alterations that can only be seen with the aid of a magnifying lens. 3.3. Pathognomonic Lesion - Alteration that indicate without doubt the cause of a particular disease. 4. Alteration of Body Fluid Biochemistry 5. Symptoms - Clinical sign manifested by the living individual as the result of tissue changes. 6. Result or Termination of a disease 6.1. Recovery - damage by the disease is repaired. 6.2. Invalidism - damage by the disease not completely repaired. 6.3. Death - loss of body functions. Etiology 1. Extrinsic Causes 1.1. Physical - influences of mechanical nature 1.1.1. Trauma - sudden, violent, physical force which results in crushing or separation of tissues. 1.1.1.1. Contusion -integument not broken 1.1.1.2. Abrasion -integument broken 1.1.1.3. Incision -smooth, long, narrow, clean type wound 1.1.1.4. Laceration - tearing of tissues 1.1.1.5. Perforation -point of entry of mechanical force narrow 1.1.1.6. Rupture -tissues stretched until fibers part 1.1.1.7. Fracture - simple fracture, compound fracture, comminuted fracture, impacted, etc. 1.1.1.8. Concussion - injury of the brain in which the skull is not broken 1.1.1.9. Sprain or strain - injury of joint in which anatomic relation of bones is maintained 1.1.1.10. Luxation or Dislocation - injury of joint in which anatomic relation of bones is not maintained 1.1.2. Pressure -less violent physical force over long period and causes compression of tissues 1.1.3. Obstruction - lumen of hollow organ closed 1.1.4. Malposition - organs rotate around their attachment or long axes. 9  1.1.4.1. Torsion - around long axis 1.1.4.2. Intussusception - telescoping 1.1.4.3 Hernia - protrusion of an organ through natural or artificial body opening 1.1.4.4. Strangulation - blood vessels of an organ are compressed 1.1.4.5. Volvulus - around mesentery 1.1.4.6. Prolapse - appearance of organ or portion of organ of body Opening. Terms related to prolapse 1.1.4.6.1. Eversion - rectum turns inside out & protrudes through anus 1.1.4.6.2. Eventration - portion of intestine or other organ protrudes through vent in ventral abdominal wall 1.1.4.6.3. Ptosis - drooping or falling of dorsal eyelid 1.2. Thermal 1.2.1. Excessive Heat 1.2.1.1. Among animals sheep tolerates heat loss followed by in order cow, dog, cattle, pig and cat. 1.2.1.2. Heatstroke is the result of heat retention. 1.2.1.3. Burn is a lesion produced by heat. 1.2.1.4. Grades of Burn 1.2.1.4.1. First Degree – reddening of the skin, mild inflammation followed by slight peeling of superficial layers of skin. 1.2.1.4.2. Second Degree - characterized by formation of blister or vesicle and destruction of epidermal cell in the area of the vessel. 1.2.1.4.3. Third Degree - characterized by complete necrosis and severe inflammation. Dead tissues slough, leaving an ulcer which heals slowly by formation of connective tissues rich with blood vessels (granulation tissues). 2.1.2.4. Fourth Degree - Tissue is blackened and charred. 1.2.1.5. Effects of Burn 1.2.1.5.1. If 1/4 - 1/3 of the surface of body is burned, even if only first or second degree burn, death occurs within 24 hours. 1.2.1.5.2. Death is due to release of histamine and histamine-like substances which produce the cardiovascular reaction known as shock. 1.2.2. Excessive Cold 1.2.2.1. Local effects of excessive cold resemble those by excessive heat: 1.2.1.1.1. There is contraction of the blood vessel (local anemia) 1.2.1.1.2.. At this point if heat loss is prevented, the area returns to normal. 1.2.1.1.2. If the area is not protected and the temperature of the tissue remains for a short time slightly under the freezing point, the vessel wall suffers injury and inflammation of the tissue develops. 10  1.2.2.2. Mechanism of Freezing 1.2.2.2.1. Crystals form in the cells and cause mechanical tearing of cells. 1.2.2.2.2. Upon freezing, the water in the cells forms crystals around which salt concentrates; water is withdrawn from the cell to form colloids; and this colloidal change is reversible so long as the colloids do not coagulate. 1.3. Atmospheric Pressure 1.3.1. Exemplified by two conditions: 1.3.1.1. Caison's disease (excessive atmospheric pressure) 1.3.1.2. Brisket’s disease (low atmospheric pressure). 1.4. Light 1.4.1. Over exposure to sunlight (sunburn): Carcinoma of the vulva and eyelid of cattle 1.4.2. Photosensitization: porphyria (phylloerythrin), fagophyrism (buckwheat poisoning), hypericism (St. John's wort) 1.5. Electricity 1.5.1. This is exemplified by electrocution due to strong electrical current; and electrocution due to lightning. The latter is manifested by a lesion on the skin characterized by tree-like arborization. 1.6. Ionizing Radiation 1.6.1. Types of nuclear radiation most often utilized: 1.6.1.1. Particles designated as alpha, beta (electron, proton and neutron) 1.6.1.2. Rays called gamma, x-rays (Roentgen rays) 1.6.1.3. Effects produced by the radiation: 1.6.1.3.1. Rate and degree of exposure 1.6.1.3.2. Energy of the ionizing agents 1.6.1.3.3. Lapse of time existing since the exposure 1.6.1.3.4. Kind of tissue involved 1.6.1.3.5. Extent of body exposure 1.6.1.3.6. Species of mammals involved 1.7. Chemicals 1.7.1. Endogenous poisons 1.7.1.1. Originate in the body 1.7.2. Exogenous poisons 1.7.2.1. Inorganic bases, acids and salts and those derived from plants, molds and bacteria 1.7.3. Effects of poisons: 1.7.3.1. Exert corrosive or caustic action; produce degenerative changes in parenchymatous organs; excite, depress or paralyze the nerve and heart; alter blood 1.8. Excess of Food This is not much of a problem in animals, as they are raised to be fattened. However, excessive intake of water may overhydrate the animals which may be bad to the cells or tissues. 11  1.9. Deficiency of Food 1.9.1. Quantitative or qualitative lack of food. Any of the nutrients that may be lacking in amount or quality may cause adverse effects on the well being of animals 1.10. Viable Influences 1.10.1. Microorganisms such as bacteria, viruses, molds and fungi, rikettsia and etc. 1.10.2. Parasites such as insects, ticks and mites, protozoa, helminths and acanthocephala 1.11. Stress 1.11.1. Any form of stresses may cause alteration in the blood of animals which in turn may result in shock. Intrinsic 1. Genus 1.1. Hog cholera is a disease of pig 2. Race and Breed 2.1. Dairy cattle are more susceptible to various diseases than are beef cattle. 2.2. Within dairy breeds, the Jersey and Guernsey are less resistant to various diseases than the Holstein 2.3. German Shepherd, Great Dane, and St. Bernard are more severely affected with bone disease and canine distemper 3. Family 3.1. Certain families of animals have various lethal genes or other undesirable character that bring about the destruction of an individual. 4. Age 4.1. Tumors are more frequently observed in older animals. 4.2. Strangles in the horse is a disease of young horses rather than old horses. 4.3. Nutritional anemia in swine is a disease of piglet. 5. Sex 5.1. Reproductive diseases are more common in female than in the male. 5.2. Metritis, mastitis, acetonemia and milk fever are more confined to the female. 5.3. Nephritis in the dog is two or three times more common in the male than in the female. 6. Color 6.1. Melanosarcomas are very common in gray and white horses but are seldom observed in brown or black horses. 6.2. Animals with nonpigmented skin are much more susceptible to photosynthetic diseases. 12  DISTURBANCE IN DEVELOPMENT Teratology 1. Anomalies 1.1. Disturbances of development that involve an organ or a portion of an organ 1.2. They are transmitted in accordance with the Mendelian Laws of Inheritance. 2. Monsters 2.1. A disturbance of development that involves several organs and causes great distortion of the individual Heritable Anomalies 1. Lethal Hereditable Defects 1.1. Shortleggedness in Dexter Cattle 1.1.1. Dexter cattle mated interse never bred true but follow the Mendelian ratio of 1ne bulldog (always stillborn): two Dexter (shortleggedness): one kerry (normal) 1.1.2. Explanation 1.1.2.1. Shortleggedness in Dexter is due to a dominant lethal gene which, if inherited both from the sire & dam, causes their offspring to be stillborn. 1.2. Latent lethal defect (recessive gene) in a form of dwarfism 1.2.1. A dwarf-gene-carrier bull when mated to a dwarf-gene-free cattle will not get dwarfs in F1 calves, but 50% of the calves will be dwarf-gene-carriers 1.2.2. In F2, dwarf-gene-carrier females, which are mated with dwarf-gene-carrier males, produce dwarfs according to the characteristic Mendelian ratio of !:2:1 (stillborn:dwarfs:normal) 1.3. Hemophilia 1.3.1. Sex-linked recessive character, characterized by defect in coagulation. 1.3.2. Transmitted through female carriers 1.4. Congenital porphyria 1.4.1. Defect in formation of hemoglobin, the enzyme system responsible for the conversion of porphyrin to heme is defecdtive. 1.4.2. Defect lies in the enzyme system of the bone marrow cells which forms porphyrin. 2. Nonlethal Hereditable Defects 2.1. Cryptochidism 2.1.1. A condition in which the testicles of pigs are undescended. Pigs having this condition are worthless breeders. Pork derived from their carcasses is likely to have an undesirable sex odor 2.2. Scrotal hernia 2.2.1. Protrusion of intestine through the umbilical canal 2.3. Deafness in white collies 13 Nonheritable Anomalies 1. Lethal nonheritable anomalies 1.1. Causes could be due abnormal influences during intrauterine life such as: 1.1.1. Separation of the embryo from its attachment 1.1.2. Abnormal pressure upon the fetus due to deficiency in amount of amniotic fluid (hemicephalis, hydrocephalus, fissure formation) 1.1.3. Adhesion between the amnion and the surface of the embryo. 1.1.4. Disturbances in endocrine system which may directly affects growth and development Classification of Anomalies 1. Disturbance in Development 1.1. Arrest of Development 1.1.1. Agenesis - incomplete and imperfect development of organ or part. 1.1.2. Aplasia - requires further development 1.1.3. Acrania - absence of most or all the bones of the cranium 1.1.4 Anencephalia - absence of the brain 1.1.5 Hypocephalia - incomplete development of the brain 1.1.6. Hemicrania - absence of the half of the head 1.1.7. Exencephalia- defective skull with brain exposed or extruded 1.1.8. Hydrencephalocele - an exencephalia in which the protruding brain contains a locale ventricle which is filled with excessive amount of fluid 1.2. Fissures on the Median Line 1.2.1. Cranioschisis - skull 1.2.2. Cheiloschisis - lip (harelip) 1.2.3. Palatoschisis - oral cavity (cleft palate) 1.2.4. Rachischisis - spinal column (spina bifida) 1.2.5. Schistorrachis - thorax or sternum 1.2.6. Schistosomus - abdomen 1.2.7. Schistocormis - thorax, neck or abdomen 1.3. Fusion of Paired Organs 1.3.1. Cyclopia - eyes 1.3.2. Ren Arcuatus - kidney (horse shoe kidneys) 2. Excess of Development 2.1. Congenital 2.1.1 Congenital hypertrophy 2.1.1.1. Hemihypertrophy 2.2. Increase in the number of a part 2.2.1. Polyotia - ears 2.2.2. Polyodontia - teeth 2.2.3. Polymelia - limbs 2.2.4. Polydactylia- digits 2.2.5. Polymastia - mammary gland 2.2.6. Polythelia - teats 3. Displacement During Development 3.1. Organs 3.1.1. Dextrocardi 3.1.2. Ectopia cordis cervicalis 14  3.2. Tissues 3.2.1. Teratoma 3.2.2. Dermoid cyst 3.2.3. Odontoid cyst 3.2.4. Dentigerous cyst 4. Persistence of Fetal Structures 4.1. Foramen Ovale 4.2. Ductus Arteriosus 4.3. Urachus 4.4. Wolffian Ducts (Mesonephric ducts) 4.5. Vitelline ducts 4.6. Brachial clefts 5. Fusion of Sexual Characteristics 5.1. Hermaphrodite 5.1. An individual having both testicular and ovarian tissues 5.2. Pseudohermaphrodite 5.2.1. An animal with a unisexual development of sex glands, either testicular or ovarian tissues, but also having either a unisexual or bisexual development of either parts of the genitalia 5.3. Freemartin 5.3.1. A female calf having arrested development of sex organs and being a twin of a perfect male. Classification of Monster 1. Twins entirely separate 1.1. Although separate these twins are in a single chorion. 1.2. One twin is well developed the other is malformed (acardius) 1.3. In the malformed fetus there is arrested development of heart, lungs and trunk. Such monster may lack head (acephalus), limbs and other recognizable features (amorphus) or trunk (acormus). 2. Twins United 2.1. Anterior Twinning 2.1.1. Pygopagus 2.1.1.1. United in the pelvic region 2.1.2. Ischiopagus 2.1.2.1. United in the pelvic region with the bodies at an obtuse angle 2.1.3. Dicephalus 2.1.3.1. Two separate heads. Added designations: tetrapus, tripus, dipus, tetrabrachius, tribrachius, bibrachius 2.1.4. Diprosopus 2.1.4.1. Doubling in the cepahlic region without complete separation of heads, only the face double. Added designations depend on the number of eyes - tetraphthalmus, triophthalmus, diopthalmus; ears tetrotus, triotus, diotus; mouths-distomus, monostomus; forelimbs tribachius, dibrachius. 15 2.2. Posterior Twinning 2.2.1. Craniopagus 2.1.1.1. Union of head (brain usually separate) 2.2.2. Cephalothoracopagus 2.1.2.1. Union of head and thorax 2.2.3. Dipygus 2.2.3.1. Doubling of posterior extremities and posterior part of the body 2.3. Twinning Almost Complete 2.3.1. Thoracopagus 2.3.1.1. United only by the thorax 2.3.2. Prosopothoracioagys 2.3.2.1. Besides the union of the abdomen and thorax, the head and neck are united 16  DISTURBANCE IN CIRCULATION Hyperemia 1. Definition 1.1. An increase amount of blood in any portion of the circulatory system. 2. Types of hyperemia 2.1. Active Hyperemia 2.1.1. Acute General Active Hyperemia 2.1.1.1. Causes 2.1.1.1.1. Systemic disease such as erysipelas and pasteurellosis 2.1.1.1.2. Renal disease where there is retention of body fluid 2.1.1.1.3. Repeated intravenous medication with electrolyte solution, blood or plasma 2.1.1.2. Microscopic Appearance 2.1.1.2..1. Difficult to determine 2.1.1.2.2. There is an increase amount of blood within the arteries and capillaries 2.1.1.3. Macroscopic Appearance 2.1.1.3.1. Arteries throughout the body are distended with blood. The organs and tissues have fleshed appearance. 2.1.2. Acute Local Active Hyperemia (most common type of hyperemia) 2.1.2.1. Causes 2.1.2.1.1. Physiological 2.1.2.1.2. Pathological 2.1.2.2. Microscopic 2.1.2.2.1. Arteries/arterioles/capillaries are distended. 2.1.2.2.2. Difficult to detect in dead animals. 2.1.2.3. Macroscopic 2.1.2.3.1. Part of the organ is enlarged, swollen, and is heavier than normal due to the increase amount of blood. 2.1.2.3.2. Color is more intense red. 2.2. Passive Hyperemia 2.2.1. Acute General Passive Hyperemia 2.2.1.1. Causes 2.2.1.1.1. Degeneration and necrosis of the myocardium 2.2.1.1.2. Sudden myocardial accidents such as myocardial infarction resulting from thrombus or embolus in a coronary vessels 2.2.1.1.3. Pneumonia 2.2.1.1.4. Pulmonary thrombosis or embolism 2.2.1.1.5. Hydropericardium, hemopericardium or pyopericardium 2.2.1.1.6. Hydrothorax, hemothorax and pyothorax 2.2.2.2. Microscopic Appearance 2.2.2.2.1. Veins and capillaries are distended with blood. 2.2.2.3. Macroscopic Appearance 2.2.2.3.1. Organs throughout the body have intense bluish-red (cyanotic) color & enlarged. 2.2.2.3.2. Veins are distended with blood 17 2.1.2. Chronic General Passive Hyperemia 2.1.2.1. Cause 2.1.2.1.1. Heart: 2.1.2.1.1. Stenosis of a valvular opening 2.1.2.1.2. Valvular insufficiency 2.1.2.1.3. Myocardial Failure 2.1.2.1.4. Anomalies of the heart such as persistent foramen ovale, interventricular defects, or dextro-position of aorta, or valves or portion of valves not formed 2.1.2.1.5. Constrictive lesions of the pericardium/epicardium 2.1.2.1.2. Lungs: 2.1.2.1.2.1. Obliteration of the capillary bed 2.1.2.1.2.2. Compression of major pulmonary vessels by tumors, cysts or abscesses 2.1.2.2. Microscopic Appearance 2.1.2.2.1. Veins/capillaries are distended with blood 2.1.2.2.2. Cells/tissues are separated by a transudate which stains slightly pink with eosin 2.1.2.2.3. Parenchymatous cell undergo atrophy. 2.1.2.2.4. Hyperplasia of the interstitial tissues of organ and supporting white fibrous connective tissues 2.1.2.3. Macroscopic Appearance 2.1.2.3.1. Veins throughout the body engorged with blood 2.1.2.3.2. Blood within the veins as well as the tissues of body is cyanotic 2.1.2.3.3. Edema of tissues of body 2.1.2.3.4. Atrophy of parenchyma of organs (liver) 2.1.3. Acute Local Passive Hyperemia 2.1.3.1. Cause 2.1.3.1.1. Malposition of the viscera (intussusception, volvulus, torsion) in which veins are compressed. 2.1.3.1.2. Thrombi within a vein 2.1.3.1.3. External pressure from ligation, torniquets, bandages, rubber bands 2.1.3.2. Microscopic Appearance 2.1.3.2.1. Veins/capillaries are distended with blood 2.1.3.2.2. Interstitial tissues/lumen of involved organ distended with blood 2.1.3.2.3. Edema 2.1.3.2.4. Necrosis, suppurative inflammation 2.1.3.3. Macroscopic Appearance 2.1.3.3.1. Necrosis of endothelial cells 2.1.3.3.2. Hemorrhage by rhexis and diapedesis occurs 2.1.3.3.3. If bacteria present, putrefactive organisms invade dead tissues and cause gangrene 2.1.3.3.4. Veins distended with blood 2.1.3.3.5. Involved tissues have a bluish-red color 18  2.1.4. Chronic Local Passive Hyperemia 2.1.4.1. Cause 2.1.4.1.1. External pressure upon the veins by enlarging neoplasms, nodes, abscess upon veins, and thrombus. 2.1.4.1.2. Scar tissue contract with age 2.1.4.1.3. Fibrosis of liver compressed hepatic sinusoids 2.1.4.2. Microscopic Appearance 2.1.4.2.1. Veins and capillaries are distended with blood 2.1.4.2.2. Edema 2.1.4.2.3. Hyperplasia of white fibrous connection tissues is a permanent alteration. 2.1.4.3. Macroscopic Appearance 2.1.4.3.1. Organ larger than normal (first appearance of condition) 2.1.4.3.2. Atrophy (later) 2.1.4.3.3. Veins engorged with blood 2.1.4.3.4. Edematous (involved tissues) Hypostatic Congestion 1. Definition 1.1. Accumulation of blood in the ventral portion of the body due to the influence of gravity. 2. Cause 2.1. Heart cannot maintain efficient blood pressure to overcome the force of gravity. 2.2. Agonal congestion - type of hypostatic congestion which occurs at the time of death. 2.3. Postmortem Congestion - a form of hypostatic congestion which is observed after death. 2.4. When the heart ceases to beat there is no longer a force which will maintain the circulation of the blood and overcome gravity. 3. Microscopic Appearance 3.1. Veins and capillaries are distended with blood 3.2. Complicating alteration: edema, hemorrhage, inflammation and necrosis. 3.3. Section of the portion of ventral blood vessel contains: erythrocyte (ventral), narrow zone of leukocytes (dorsal) and zone of plasma (middle) 4. Macroscopic Appearance 4.1. Veins in ventral portion of an organ are distended with blood Ischemia 1. Definition 1.1. Also known as local anemia, is a deficiency of arterial blood in a portion of an organ or ion. 2. Cause: 2.1. External pressure upon an artery 2.2. Narrowing of the lumen of an artery due to thrombus or embolus or pressure upon the vessel 19 3. Microscopic Appearance: 3.1. Necrosis 3.2. Atrophy of organ if obstruction is partial 4. Macroscopic Appearance 4.1. Paleness of a portion of an organ Hemorrhage 1. Definition 1.1. The escape of all of the constituents of the blood from any portion of the blood vascular system. 2. Types (according to how blood escape from vessel wall) 2.1. Rhexis 2.1.1. Blood escapes through a break in the wall of vessel. 2.2. Diapedesis 2.2.1. Blood leaves vessel through an intact vascular wall. 3. Cause 3.1. Physiologic 3.1.1. Parturition 3.1.2. Menstruation 3.1.3. Rupture of the graffian follicle 3.1.4. Rupture of umbilical cord. 3.2. Mechanical 3.2.1. Exemplified by laceration, contussion, rupture 3.3. Necrosis & Disturbance in metabolism in the vessel wall 3.4. Bacterial and viral diseases 3.5. Neoplasm - destroys vessel wall 3.6. Toxic chemical agents - cyanide, arsenic 3.7. Hemophilic disease 3.8. Passive hyperemia 4. Classification of Hemorrhages 4.1. Source of blood 4.1.1. Examples: cardiac, arterial, venous, capillary 4.2. Size or shape 4.2.1. Petechial hemorrhage 4.2.1.1. Tiny and punctate, having a diameter not larger than 1 mm. 4.2.2. Ecchymotic hemorrhage 4.2.2.1. Circumscribed hemorrhage a few mm in diameter 4.2.3. Linear hemorrhage 4.3.3.1. Hemorrhages appear in line 4.2.4. Suffusions 4.2.4.1. Diffuse, flat, often irregular shape areas of bleeding 4.2.5. Haematoma 4.2.5.1. If the extravasated blood collects in a spherical-shaped mass in the tissue 20  4.3. Location 4.3.1. Epitaxis - nose bleed 4.3.2. Hemoptysis - spitting blood 4.3.3. Hematamesis - vomiting blood 4.3.4. Enterorrhagia - intestinal hemorrhage 4.3.5. Metrorrhagia - uterine bleeding 4.3.6. Hematuria - discharging bloody urine 4.3.7. Hemopericardium- blood in the covering of heart 4.3.8. Hemothorax - blood collects in the thoracic cavity 4.3.9. Hemoperitoneum- presence of blood in the peritoneal cavity 4.4. Color 4.4.1. Varies depending on the vessel involve. 4.4.2. Red cells are visible in tissue outside of vessel 4.4.3. Hemosiderin-laden macrophages ("heart failure cells") & erythrophagocytosis is indication of former hemorrhage. 5. Microscopic Appearance 5.1. Presence of erythrocytes outside of vascular system 5.2. Length of time hemorrhage has persisted in tissues can be determined: 5.2.1. Recent hemorrhage - RBC intact and stain sharply 5.2.2. Long-standing hemorrhage - outline of RBC cannot be determined, not stain well, crophages phagocytizing the cells 6. Macroscopic Appearance 6.1. Presence of blood outside vessels Anemia 1. Definition 1.1. Quantitative or qualitative decrease in the amount of blood in the vascular system. 2. Two types of Anemia 2.1. General - reduction in the total number of RBC and/or of hemoglobin 2.1.1. Terms related to General Anemia 2.1.1.1. Characteristic of number of RBC 2.1.1.1.1. Oligomia - reduction in the total blood volume 2.1.1.1.2. Hydremia - quality of blood becomes thinner 2.1.1.1.3. Oligocythemia - number of RBC diminished 2.1.1.1.4. Oligochomemia - quality of hemoglobin decreases 2.1.1.2. Size of RBC 2.1.1.2.1. Normocytic 2.1.1.2.2. Macrocytic 2.1.1.2.3. Microcytic 2.1.1.3. Characteristic of Hemoglobin: 2.1.1.3.1. Normochromic 2.1.1.3.2. Hypochromic 2.2. Local anemia (also referred to as- ischemia) 2.3. Types of Anoxia that occurs in Tissue 2.3.1. Stagnant - Results from reduced flow of oxygenated blood, as in shock or heart failure 21  2.3.2. Anoxia - Results from insufficient oxygenation of blood, as in severe pneumonia 2.3.3. Anemia - Caused by low hemoglobin or reduced capacity to carry hemoglobin 2.3.4. Histotoxic - Results from inability of cells to use oxygen, as in a toxic damage to cells 3. Classes of Anemia According to Etiology 3.1. Anemia due to decreased blood formation 3.1.1. Insufficient bone marrow (myelophthisic anemia) i.e. anemia associated with leukemia & anemia associated with avian leukosis complex 3.1.2. Depression of bone marrow - function of hypoplastic and aplastic anemia. i.e anemia of ionizing radiation; aplastic anemia of cattle fed with trichloroethylene-extracted soybean meal 3.1.3 A deficiency of materials for the formation of erythrocytes (hypoplastic or nutritional anemia) i.e. hypochromic anemia of iron & copper deficiency; hypochromic anemia of cobalt deficiency. 3.2. Anemia Due to Increased Blood Loss 3.2.1. Extravascular, resulting from hemorrhage (hemorrhagic) 3.2.2. Intravascular, resulting from hemolysis (hemolytic anemia) 3.3. Other Types as Seen Morphologically 3.3.1. Changes in blood film: 3.3.1.1. Anisocytosis - RBC are not of sufficiently uniform size 3.3.1.2. Poikilocytosis -RBC have bizzare and abnormal shapes being elongated, angular, ovoid or distorted 3.3.1.3. Nucleated RBC - Hurriedly produced from bone marrow 3.3.1.4. Basophilic - Minute dark specks appear in Stippling RBC. This common following acute loss of blood 3.3.1.5. Polychromatophilia - RBC do not stain uniformly 3.3.2 Changes in Tissue 3.3.2.1. Hyperplasia of bone marrow 3.3.2.2. Section of spleen/liver may rarely show erythropoietic Centers 4. Microscopic Appearance: 4.1. Paleness of tissue; RBC count is below normal 5. Macroscopic Appearance 5.1. Paleness of mucous membrane 5.2. Anoxia or Hypoxia Sludged Blood 1. Definition 1.1. Conglutination of erythrocytes within the vascular system of the living individual 2. Cause 2.1. Diseases that agglutinate RBC 22 3. Microscopic Appearance 3.1. Cannot be demonstrated 4. Macroscopic Appearance 4.1. Clumping of RBC Thrombosis 1. Definition 1.1. Formation of a clot within the vascular system 2. Cause 2.1. Injury to the endothelium: mechanical factor, parasitic factor, tumor and bacteria 2.2. Roughness of vessel lining (scar) 2.3. Stasis of blood flow 2.4. Disruption of the laminar flow of blood 2.5. Alteration in the composition of the blood 2.6. Increased amount of fibrinogen and a more rapid clotting time. This are associated with the use of ether and chloroform as general anesthetics. 3. Classification of Thrombi 3.1. According to location within the blood vascular System: cardiac, arterial, venous, capillary, lymphatic 3.2. According to location within the heart or vessel: 3.2.1. Mural - Attached to wall of heart or blood vessel 3.2.2. Valvular - Attached to heart valves 3.2.3. Lateral - Attached to one side of vessel wall 3.2.4. Occluding - Attached to the entire endothelial circumference of vessel 3.2.5. Canalized - Results when intravascular clots have been partially repaired and new blood channels have been formed through the clot 3.3. According to the infectious agents 3.3.1. Septic - Contains bacteria 3.3.2. Parasitic - Contains parasites (Dirofilaria immitis, Strongylus vulgaria 3.3.3. Aseptic- Do not contain bacteria or parasites 3.4. According to Color 3.4.1. Pale or White - Composed entirely of platelets 3.4.2. Red - Composed of platelets, fibrin, RBC, WBC 3.4.3. Mixed - Composed of white and red clots 3.4.4. Laminated - Composed of alternating layers of white and red constituents 3.5. Fate of Thrombi 3.5.1. Contraction 3.5.2. Liquefaction by autolytic enzymes 3.5.3. Disintegration by enzymes of leukocytes 3.5.4. Abscessation 3.5.5. Organization 3.5.6. Canalization 3.5.7. Mineralization 23 4. Comparison of Thrombus and Postmortem Clot 4.1. Thrombi Postmortem Clot Dry in consistency Moist Granular or rough surface Smooth & glistening surface White or buff in color Intense red or yellow Stratified in structure Uniform in structure Attached to vessel wall Not attached to vessel wall Vascular endothelium below Undamaged, smooth and glistening the thrombus is damaged & rough Composed primarily of Composed primarily of fibrin thrombocytes Forms in a flowing stream of blood Forms in a stagnant column of blood Found in living animal Found in dead animal May be partially organized No indications of organization Caused by endothelial injury Initiated by thromboplastin 5. Types of Postmortem Clot 5.1. Red or Current Jelly Clot 5.1.1. Occurs when the components of the blood are mainly distributed throughout the clot 5.1.2. Occurs when there is rapid clotting of blood and the composition of blood is normal 5.2. Yellow or Chicken-fat Clot 5.2.1. Occurs when the components of the blood are not evenly distributed throughout the clot 5.2.2. The ventral portion of the clot is red, while the dorsal portion is yellow and is composed of fibrin and serum Embolism 1. Definition 1.1. Presence of a foreign body in the circulatory system causing obstruction 1.2. Emboli do not lodge in a vein because the flow of blood in a vein is always into a vessel of increasing diameter 2. Cause 2.1. Thrombus 2.1.1. Disintegrated fragments are carried by the flowing blood as embolus 2.2 Fibrin 2.2.1. Introduced in the circulatory system by means of blood transfusion blood is improperly defibrinated or when inadequate amounts of anticoagulants are used 2.3. Parasitic 2.4. Bacteria - Clumps 2.5. Neoplasms 2.6. Clumps of normal body cells 2.7. Fat emboli 2.8. Gas emboli - Caisson disease 3. Microscopic Appearance 3.1. Characteristic appearance of embolus 3.2. Coagulative necrosis of tissue 3.3. Inflammatory reaction is present 24 4. Macroscopic Appearance 4.1. Tissues are pale or grays in color due to necrosis Infarction 1. Definition 1.1. An infarct is a local area of necrosis resulting from an unusual obstruction in the arterial tree 2. Cause 2.1. Thrombi 2.2. Emboli 2.3. Contraction of musculature of arterial walls by drug poisoning (ergot) 3. Microscopic Appearance 3.1. Infarcts have a cone-shaped appearance with the apex of the cone at the point of arterial obstruction and the base of the cone at the periphery of an organ 3.2. Area of necrosis 4. Macroscopic Appearance 4.1. Cone-shaped appearance with apex of the cone at the point of arterial obstruction and the base of cone at the periphery of the organ 4.2. Commonly observed in kidney/spleen 4.3. Red or hemorrhagic infarcts bulge above surrounding surface of organ 4.4. Pale or anemic infarcts usually have a slightly depressed surface. In this case hemoglobin and other substances have diffused out of the area 4.5. When an infarct has been organized, contraction of connective tissue causes a depressed surface and pocketing of the organ Jaundice 1. Definition 1.1. A condition in which there is an excessive amount of either hemobilirubin or chlebilirubin, or both in the circulating blood and tissue fluids causing them to become yellow in color. 2. Types of Jaundice 2.1. Hemolytic or prehepatic 2.1.1. Cause: 2.1.1.1. Various protozoan diseases such as piroplasmosis, babesiosis, anaplasmosis or bartonellosis 2.1.1.2. Viral infections such as viral equine anemia, toxins of Clostridium hemolyticus bovis 2.1.1.3. Incomplete blood typing 2.1.1.4. Hemolytic anemia of a new born baby - Rh negative mother develops antibodies against the fetus which is Rh positive 2.2. Toxic or intrahepatic 2.2.1. Causes 2.2.1.1. Infectious or noninfectious agents which are capable of injuring hepatic cells: 2.2.1.2. Salmonella 2.2.1.3. Infectious canine hepatitis 25  2.2.1.4. Plant toxins (Seneco, Crotalaria, Actra actragalus) 2.2.1.5. Inorganic poison (phosphorus) 2.2.1.6. Organic compounds (clay pigeons) 2.3. Obstructive or posthepatic jaundice 2.3.1. Cause 2.3.1.1. Parasites such as Ascaris lumbricoides, Thysanosoma actinoides, Fasciola hepatica, etc. 2.3.1.2. Gallstone is the common cause of obstruction of biliary duct of man 2.3.1.3. Tumors 2.3.1.4. Inflammatory alteration within hte wall of ducts (cholangitis) or the gall bladder (cholecystitis) or pancreatitis which may close hepatic duct 3. Diagnosis 3.1. Icteric Index 3.2. Van Den Bergh Reaction 3.2.1. Technique 3.2.1.1. The test consists of mixing Ehrlich's reagent (diazotized sulfanilic acid) with plasma or serum 3.2.1.2. The bilirubin reacts with the reagent to form a colored compound – azorubin or azobilirubin 3.2.2. Interpretation of Van Den Bergh Reaction 3.2.2.1. Direct Reaction 3.2.2.2. Indirect Reaction 3.2.2.3. Biphasic Reaction 3.3. Comparison of 3 types of Jaundice Hemolytic Toxic Obstructive A. Color of Tissue slight to moderate slight to moderate intense & Blood Plasma B. Color of Feces increased normal hypopigmentation Pigmentation (gray) C. Consistency normal normal greasy of Feces D. Color of Urine light yellow intense yellow intense yellow E. Icteric Index low to moderate moderate high F. Van Den Bergh indirect biphasic direct Reaction 26  RBC destruction (worn out RBC) Heme + Globin > iron and globin RE Cells Porphyrin Biliverdin