ANIMAL CASTRATION: A BOOK FOR THE USE OF STUDENTS AND PRACTITIONERS

By Q. GAURE

1 INTRODUCTION TO PATHOLOGY 1 1 INTRODUCTION 1 2 HISTORY OF PATHOLOGY 1 3 MAKING A DIAGNOSIS 1 4 DIAGNOSTIC INVESTIGATIONS IN PATHOLOGY 1 4 1 GROSS PATHOLOGY 1 4 2 BIOPSY 1 4 3 HISTOPATHOLOGY 1 4 4 CYTOPATHOLOGY 1 4 5 HAEMATOPATHOLOGY 1 4 6 HISTOCHEMISTRY 1 4 7 IMMUNOHISTOCHEMISTRY (IHC) 1 4 8 IMMUNO?UORESCENCE (IF) 1 4 9 MOLECULAR PATHOLOGY 1 4 10 CYTOGENETICS (CLINICAL GENETICS) 1 4 11 BIOCHEMICAL METHODS 1 4 12 MEDICAL MICROBIOLOGY 1 4 13 MICROBIAL CULTURE 1 4 14 FLOW CYTOMETRY 1 4 15 ELECTRON MICROSCOPY 1 4 16 FORENSIC PATHOLOGY/AUTOPSY 1 4 17 ORAL AND MAXILLOFACIAL PATHOLOGY 1 5 SUMMARY BIBLIOGRAPHY 2 HOMEOSTASIS 2 1 INTRODUCTION 2 2 HOMEOSTASIS AT THE CELLULAR, TISSUE, AND ORGAN LEVELS 2 3 REGULATION AND MECHANISMS OF HOMEOSTASIS 2 4 HOMEOSTATIC MECHANISMS (FEEDBACK MECHANISMS) 2 4 1 POSITIVE FEEDBACK 2 4 2 NEGATIVE FEEDBACK 2 5 ORAL HOMEOSTASIS 2 6 HOMEOSTASIS AND AGEING 2 7 NUTRITION AND HOMEOSTASIS 2 8 ENVIRONMENT AND HOMEOSTASIS 2 9 SUMMARY CONTENTS 3 DISEASE, DISORDER, AND DISABILITY 3 1 INTRODUCTION 3 2 DISEASE: DE?NITION AND CHARACTERISTICS 3 2 1 AETIOLOGY 3 2 2 PATHOGENESIS 3 2 3 MORPHOLOGICAL, FUNCTIONAL, AND CLINICAL MANIFESTATIONS 3 3 EPIDEMIOLOGY 3 4 CLASSI?CATION OF THE DISEASE 3 5 NUMERICAL DISEASE-CODING SYSTEMS 3 6 DISORDER (MEDICAL DISORDER) 3 6 1 MENTAL DISORDER 3 6 2 PHYSICAL DISORDER 3 6 3 GENETIC DISORDER 3 6 4 EMOTIONAL AND BEHAVIOURAL DISORDERS (EBDS) 3 7 DISABILITY 3 8 SUMMARY 4 CELL STRUCTURE AND FUNCTION, CELL DIVISION AND CELL CYCLE, CELL TYPES AND STEM CELLS 4 1 INTRODUCTION 4 2 CELL STRUCTURE AND FUNCTION 4 2 1 THE PLASMA MEMBRANE 4 2 2 CYTOPLASM 4 3 INTERCELLULAR JUNCTIONS 4 3 1 TIGHT JUNCTIONS 4 3 2 GAP JUNCTIONS 4 3 3 DESMOSOMES/HEMIDESMOSOMES 4 4 CELL COMMUNICATION (CELL SIGNALLING) 4 5 SIGNALLING PATHWAYS 4 5 1 AUTOCRINE SIGNALLING 4 5 2 ENDOCRINE SIGNALLING 4 5 3 PARACRINE SIGNALLING 4 5 4 JUXTACRINE SIGNALLING 4 6 INTERACTION WITH EXTRACELLULAR MATRIX 4 7 CELL DIVISION AND THE CELL CYCLE 4 7 1 INTERPHASE 4 7 2 MITOTIC PHASE 4 8 CONTROL AND REGULATION OF THE CELL CYCLE 4 9 CELL TYPES IN THE HUMAN BODY 4 10 STEM CELLS 4 10 1 TOTIPOTENT STEM CELLS 4 10 2 PLURIPOTENT STEM CELLS (PSCS) 4 10 3 MULTIPOTENT STEM CELLS 4 10 4 UNIPOTENT STEM CELLS 4 10 5 OLIGOPOTENT STEM CELLS 4 11 SUMMARY 5 CELLULAR PATHOLOGY 5 1 INTRODUCTION 5 2 CELL INJURY 5 3 CAUSES OF CELL INJURY 5 3 1 HYPOXIA (OXYGEN DEPRIVATION) 5 3 2 MECHANICAL TRAUMA 5 3 3 EXTREME HEAT (THERMAL BURN) 5 3 4 EXTREME COLD (CRYOGENIC BURN) 5 3 5 IONISING RADIATION 5 3 6 NON-IONISING RADIATION 5 3 7 ELECTRICAL SHOCK 5 3 8 CHEMICAL INJURY 5 3 9 THERAPEUTIC AND ILLICIT DRUG INJURY 5 3 10 INJURY DUE TO INFECTIOUS AGENTS 5 3 11 NUTRITIONAL IMBALANCES 5 3 12 IMMUNOLOGICALLY MEDIATED CELL INJURY 5 3 13 GENETIC AND METABOLIC CELL INJURY 5 3 14 INJURY FROM FREE RADICALS 5 4 MECHANISMS OF CELL INJURY 5 4 1 PLASMA MEMBRANE DAMAGE 5 4 2 MITOCHONDRIAL DAMAGE 5 4 3 ADENOSINE TRIPHOSPHATE (ATP) DEPLETION 5 4 4 CYTOSOLIC CALCIUM DERANGEMENT 5 4 5 NUCLEIC ACID DAMAGE 5 5 RESPONSES TO CELL INJURY 5 5 1 REVERSIBLE CELL INJURY 5 5 2 IRREVERSIBLE CELL INJURY 5 6 CELLULAR ADAPTATION 5 6 1 HYPERTROPHY 5 6 2 HYPERPLASIA 5 6 3 ATROPHY 5 6 4 METAPLASIA 5 6 5 DYSPLASIA 5 7 CELLULAR DEGENERATION 5 7 1 HYDROPIC DEGENERATION (CLOUDY SWELLING/VACUOLAR DEGENERATION) 5 7 2 FATTY CHANGE (FATTY DEGENERATION) 5 7 3 HYALINE CHANGE 5 7 4 MUCOID DEGENERATION (MUCINOUS DEGENERATION, MYXOMATOUS DEGENERATION) 5 7 5 FIBRINOID DEGENERATION (FIBRINOID NECROSIS) 5 8 CELLULAR ACCUMULATIONS AND PATHOLOGIC CALCI?CATION 5 8 1 ABNORMAL ACCUMULATIONS OF LIPIDS 5 8 2 ABNORMAL ACCUMULATION OF PROTEINS 5 8 3 ACCUMULATION OF GLYCOGEN 5 8 4 ACCUMULATION OF PIGMENTS 5 8 5 PATHOLOGIC CALCI?CATION 5 9 CELL DEATH 5 9 1 APOPTOSIS 5 9 2 NECROSIS 5 10 SUMMARY 6 INFLAMMATION: AN OVERVIEW 6 1 INTRODUCTION 6 2 AETIOLOGY 6 3 CARDINAL SIGNS OF INFLAMMATION 6 4 CELLS OF THE INFLAMMATORY RESPONSE, THEIR LOCATION, AND PRIMARY ROLE 6 5 CLASSIFICATION OF INFLAMMATION 6 5 1 ACUTE INFLAMMATION 6 5 2 CHRONIC IN?AMMATION 6 5 3 TYPES OF CHRONIC IN?AMMATION 6 6 MORPHOLOGIC PATTERNS OF INFLAMMATION 6 6 1 FIBRINOUS INFLAMMATION 6 6 2 SUPPURATIVE (PURULENT) INFLAMMATION 6 6 3 SEROUS INFLAMMATION 6 6 4 ULCERATIVE INFLAMMATION 6 6 5 CATARRHAL INFLAMMATION 6 6 6 PSEUDOMEMBRANOUS IN?AMMATION 6 6 7 GRANULOMATOUS IN?AMMATION 6 7 SUMMARY 7 HEALING: TISSUE REGENERATION AND REPAIR 7 1 INTRODUCTION 7 2 TYPES OF CELLS AND TISSUES INVOLVED IN THE HEALING PROCESS 7 3 HEALING BY REGENERATION 7 4 HEALING BY REPAIR 7 5 THE ROLE OF CYTOKINES, GROWTH FACTORS, AND EXTRACELLULAR MATRIX 7 6 WOUND HEALING 7 7 CATEGORIES OF CUTANEOUS WOUND HEALING 7 7 1 HEALING BY FIRST INTENTION (PRIMARY UNION) 7 7 2 HEALING BY SECOND INTENTION (SECONDARY INTENTION) 7 8 HEALING OF ORAL MUCOSAL WOUNDS 7 9 FRACTURE HEALING 7 9 1 STAGES IN FRACTURE HEALING (BONE REGENERATION) (FIG 7 2) 7 10 TOOTH EXTRACTION SOCKET HEALING 7 11 FACTORS THAT IN?UENCE WOUND HEALING 7 11 1 LOCAL FACTORS 7 11 2 SYSTEMIC FACTORS 7 12 COMPLICATIONS OF WOUND HEALING 7 13 SUMMARY 8 GENETIC AND DEVELOPMENTAL PATHOLOGY 8 1 INTRODUCTION 8 2 CHROMOSOMES AND GENES 8 3 GENOTYPE AND PHENOTYPE 8 4 INHERITANCE PATTERNS 8 4 1 SINGLE-GENE INHERITANCE (MENDELIAN INHERITANCE) 8 4 2 SEX-LINKED INHERITANCE 8 4 3 MITOCHONDRIAL INHERITANCE 8 4 4 MULTIFACTORIAL INHERITANCE 8 5 GENETIC DISORDERS 8 5 1 MONOGENIC DISORDERS 8 5 2 POLYGENIC DISORDERS (MULTIFACTORIAL INHERITANCE DISORDERS) 8 5 3 CHROMOSOMAL DISORDERS (CYTOGENETIC DISORDERS) 8 6 MUTATIONS 8 7 CONGENITAL AND DEVELOPMENTAL DISORDERS 8 8 SUMMARY 9 INFECTIOUS AND COMMUNICABLE DISEASES: AN OVERVIEW 9 1 INTRODUCTION 9 2 THE CONCEPT OF CHAIN OF INFECTION 9 3 ROUTES AND MODES OF ENTRY OF MICROBES 9 3 1 DIRECT TRANSMISSION 9 3 2 INDIRECT TRANSMISSION 9 4 HOST DEFENCES AGAINST INFECTION 9 5 TYPES OF INFECTIOUS AGENTS AND MECHANISM OF INFECTIONS 9 5 1 BACTERIA 9 5 2 VIRUSES 9 5 3 FUNGI 9 5 4 PROTOZOA 9 5 5 HELMINTHS 9 5 6 PRIONS 9 6 SUMMARY 10 AN INTRODUCTION TO IMMUNOLOGY AND IMMUNOPATHOLOGY 10 1 INTRODUCTION 10 2 THE IMMUNE SYSTEM: INNATE AND ADAPTIVE IMMUNITY 10 2 1 INNATE IMMUNITY 10 2 2 ADAPTIVE IMMUNITY 10 2 3 T CELLS AND ANTIGEN PRESENTING CELLS(APCS) 10 2 4 B CELLS 10 3 ANTIBODY-MEDIATED VERSUS CELL- MEDIATED IMMUNITY 10 4 PASSIVE VS ACTIVE IMMUNISATION 10 5 IMMUNOPATHOLOGY 10 5 1 HYPERSENSITIVITY REACTIONS 10 5 2 AUTOIMMUNITY 10 5 3 IMMUNODE?CIENCY 10 6 IN?AMMATION 10 7 CONCLUSIONS AND SUMMARY 11 NEOPLASIA AND CARCINOGENESIS 11 1 INTRODUCTION 11 2 CLASSI?CATION OF NEOPLASMS 11 2 1 BENIGN NEOPLASMS 11 2 2 MALIGNANT NEOPLASMS 11 3 OTHER TUMOUR TERMINOLOGIES 11 4 NON-NEOPLASTIC TUMOUR-LIKE LESIONS 11 5 EPIDEMIOLOGY OF CANCER 11 6 AETIOLOGY OF CANCER 11 6 1 CHEMICAL CARCINOGENS 11 6 2 PHYSICAL CARCINOGENS 11 6 3 VIRAL CARCINOGENS (ONCOGENIC VIRUSES) 11 6 4 BACTERIA, FUNGI, AND PARASITES AS CARCINOGENS 11 7 ROLE OF HOST FACTORS IN CARCINOGENESIS 11 8 CLINICAL EFFECTS OF NEOPLASMS 11 9 CANCER STAGING 11 9 1 PRIMARY TUMOUR (T) 11 9 2 REGIONAL LYMPH NODES (N) 11 9 3 DISTANT METASTASIS (M) 11 10 SPREAD OF CANCER: METASTASIS 11 11 CANCER DIAGNOSIS: INVESTIGATIONS 11 11 1 HISTOPATHOLOGY AND CYTOPATHOLOGY 11 11 2 HISTOLOGICAL GRADING OF CANCER 11 11 3 TUMOUR MARKER TESTS 11 11 4 HISTOCHEMISTRY 11 11 5 IMMUNOHISTOCHEMISTRY (IHC) 11 11 6 FLOW CYTOMETRY 11 11 7 MOLECULAR DIAGNOSIS 11 11 8 IMAGING TESTS 11 11 9 DIAGNOSTIC SURGERY: SENTINEL NODE MAPPING 11 12 CARCINOGENESIS 11 12 1 HOST DEFENCE AGAINST CANCER 11 12 2 STAGES OF CANCER DEVELOPMENT 11 12 3 MOLECULAR AND GENETIC BASIS OF CANCER 11 12 4 HALLMARKS OF CARCINOGENESIS 11 12 5 ROLE OF TUMOUR SUPPRESSOR GENES, CELLULAR PROTO- ONCOGENES, AND GROWTH FACTORS IN CARCINOGENESIS 11 13 SUMMARY 12 ENVIRONMENTAL AND NUTRITIONAL PATHOLOGY 12 1 INTRODUCTION 12 2 ENVIRONMENTAL POLLUTION 12 3 EFFECTS OF TOBACCO, ALCOHOL, AND SUBSTANCE ABUSE 12 4 EFFECTS OF RADIATION 12 5 NUTRITION AND MALNUTRITION 12 5 1 NUTRITIONAL DE?CIENCIES 12 5 2 NUTRIENT EXCESSES 12 6 SUMMARY 13 HEMODYNAMIC DISORDERS 13 1 INTRODUCTION 13 2 HYPEREMIA AND CONGESTION 13 3 HAEMORRHAGE 13 4 HAEMOSTASIS 13 5 DISORDERS OF HAEMOSTASIS 13 6 LABORATORY DIAGNOSIS OF HAEMOSTATIC DISORDERS 13 7 THROMBOSIS 13 8 ARTERIAL OR VENOUS BLOOD STASIS AND TURBULENCE 13 9 HYPERCOAGULABLE STATE 13 10 ARTERIAL THROMBOSIS 13 11 DISSEMINATED INTRAVASCULAR COAGULATION (DIC) 13 12 EMBOLISM 13 13 PULMONARY EMBOLISM 13 14 SYSTEMIC THROMBOEMBOLISM 13 15 INFARCTION 13 16 OEDEMA 13 17 SHOCK 13 18 SUMMARY 14 IMBALANCES IN FLUIDS AND ELECTROLYTES, ACIDS AND BASES: AN OVERVIEW 14 1 INTRODUCTION 14 2 FLUID BALANCE 14 3 ELECTROLYTE BALANCE 14 4 ACID-BASE BALANCE 14 5 ABNORMALITIES IN ACID-BASE BALANCE 14 5 1 ALKALOSIS 14 6 SUMMARY 15 AGEING 15 1 INTRODUCTION 15 2 THEORIES OF AGEING 15 2 1 THE PROGRAMMED THEORIES 15 2 2 THE ERROR (DAMAGE) THEORY 15 3 NORMAL AGEING 15 4 AGE-RELATED DISEASES 15 5 SUMMARY 16 PAIN: BASIC CONCEPTS 16 1 INTRODUCTION 16 2 PATHOPHYSIOLOGY OF PAIN 16 3 CLASSI?CATION OF PAIN 16 3 1 NOCICEPTIVE PAIN 16 3 2 NEUROPATHIC PAIN 16 3 3 MIXED PAIN 16 3 4 PSYCHOGENIC PAIN 16 4 CONDITIONS ASSOCIATED WITH PERIPHERAL AND CENTRAL NEUROPATHIC PAIN 16 5 SUMMARY 17 DENTAL, ORAL, MAXILLOFACIAL AND SALIVARY GLAND DISEASES: AN OVERVIEW 17 1 INTRODUCTION 17 2 COMMON DEVELOPMENTAL DISORDERS 17 3 DENTAL CARIES AND PATHOLOGY OF THE DENTAL PULP 17 4 OTHER ACQUIRED DENTAL DISORDERS 17 5 PERIODONTAL DISEASES 17 6 MUCOSAL DISEASES 17 7 DISEASES OF THE JAW BONES 17 7 1 JAW CYSTS 17 7 2 JAW TUMOURS 17 7 3 FIBRO-OSSEOUS LESIONS 17 8 DISEASES OF THE SALIVARY GLANDS 17 8 1 MEDICATION-INDUCED HYPOSALIVATION AND XEROSTOMIA 17 9 SUMMARY 18 PATHOLOGY OF ORGAN SYSTEMS OF THE BODY 18 1 INTRODUCTION 18 2 GASTROINTESTINAL DISEASES 18 2 1 GASTROESOPHAGEAL RE?UX DISEASE (GORD) 18 3 LIVER DISEASES 18 3 1 VIRAL HEPATITIS 18 4 CARDIOVASCULAR DISEASES 18 5 RESPIRATORY DISEASES 18 6 DISEASES OF THE BLOOD AND BLOOD- FORMING ORGANS 18 6 1 ANAEMIAS 18 6 2 HAEMOGLOBINOPATHIES (SICKLE CELL ANAEMIA AND THALASSEMIA) 18 6 3 DISORDERS OF COAGULATION 18 7 DISORDERS OF THE IMMUNE SYSTEM 18 7 1 HYPERSENSITIVITY REACTIONS 18 8 DISEASES OF THE RENAL SYSTEM 18 9 DISEASES OF THE ENDOCRINE SYSTEM AND METABOLISM 18 10 DISEASES OF THE NERVOUS SYSTEM 18 11 DISEASES OF BONE AND JOINTS 18 12 PSYCHIATRIC DISORDERS 18 13 SUMMARY HISTORY OF PATHOLOGY IN PREHISTORIC TIMES, THE DISEASE WAS ASSOCIATED WITH RELIGION, MAGIC (“EVIL EYE OF THE SPIRITS”), AND DIVINE IN?UENCES (“CURSE FROM GOD”) HEROPHILUS, ONE OF THE GREAT GREEK PHYSICIANS, ALONG WITH ERASISTRATUS, PROVIDED A BEGINNING FOR ANATOMICAL PATHOLOGY AND AUTOPSY GREEK PHILOSOPHERS SOCRATES, PLATO, AND ARISTOTLE INTRODUCED PHILOSOPHICAL CONCEPTS TO MEDICINE HIPPOCRATES WAS AN EMINENT GREEK PHYSICIAN WHO DISASSOCI- ATED MEDICINE FROM MAGIC AND RELIGION HE BELIEVED IN SYMPTOMS FROM PATIENTS’ HISTORIES AND DESCRIBED METHODS OF DIAGNOSIS HE IS ALSO INSTRUMENTAL IN FORMING RATIONAL AND ETHICAL PRINCIPLES IN MEDICAL PRACTICE (HIPPOCRATIC OATH) ROMAN PHYSICIAN CORNELIUS CELSUS IS CREDITED WITH INTRODUC- ING CARDINAL SIGNS OF IN?AMMATION (RUBOR, TUMOUR, CALOR, AND DOLOUR), AND CLAUDIUS GALLEN POSTULATED HUMORAL THEORY AROUND 200 AD, INDIAN PHYSICIANS CHARAKA AND SUSHRUTA DESCRIBED ASPECTS OF DISEASE AND MEDICAL AND SURGICAL REME- DIES IN BOOKS CHARAKA SAMHITA AND SUSHRUTA SAMHITA, RESPECTIVELY PATHOLOGY DEVELOPED ONLY AS SCIENCE ADVANCED SOME PROMINENT INDIVIDUALS CONTRIBUTED TO THE DEVELOPMENT OF PATHOLOGY IN THE SEVENTEENTH AND EIGHTEENTH CENTURIES ANTONY VAN LEEUWENHOEK (1632–1723) INVENTED THE ?RST MICROSCOPE, AND MARCELLO MALPIGHI (1624–1694) USED THE MICROSCOPE TO STUDY SKIN AND LYMPHOID TISSUE IN THE SPLEEN AND HAS BEEN CREDITED AS THE FATHER OF HISTOLOGY GIOVANNI MORGAGNI (1682–1771) LAID THE FOUNDATION FOR CLINICOPATHO- LOGIC METHODS IN THE STUDY OF DISEASE OTHER NOTABLE CLINI- CIANS RESPONSIBLE FOR THE ADVANCEMENT OF PATHOLOGY AND THE HAEMATOPATHOLOGY THIS BRANCH OF PATHOLOGY DEALS WITH ABNORMALITIES OF THE BLOOD CELLS, AND THEIR PRECURSORS IN THE BONE MARROW ARE INVESTIGATED TO DIAGNOSE THE DIFFERENT KINDS OF DISEASES 1 INTRODUCTION TO PATHOLOGY MOLECULAR PATHOLOGY MOLECULAR PATHOLOGY REVEALS DEFECTS IN THE CHEMICAL STRUC- TURE OF MOLECULES IN THE GNOME MOLECULAR PATHOLOGY CAN MANIFEST IN DISORDERS SUCH AS SICKLE CELL DISEASE, OSTEOGENE- SIS IMPERFECTA, AND THE DEVELOPMENT OF NEOPLASMS THIS TECH- NIQUE IS COMMONLY USED IN THE DIAGNOSIS OF CANCER AND INFECTIOUS DISEASES COMMON METHODS INCLUDE POLYMERASE CHAIN REACTION (PCR) AND IN SITU HYBRIDISATION (ISH) IN THE PCR TEST, MINUTE AMOUNTS OF NUCLEIC ACIDS CAN BE AMPLI?ED USING OLIGONUCLEOTIDE PRIMERS SPECI?C TO THE GENES BEING STUDIED ISH IS A TECHNIQUE THAT ALLOWS FOR THE PRECISE LOCALI- SATION OF A PARTICULAR NUCLEIC ACID SEGMENT WITHIN A HISTO- LOGIC SECTION ISH IDENTI?ES SPECI?C GENES OR THEIR MESSENGER RNA IN TISSUE SECTIONS OR CELL PREPARATIONS 1 4 10 CYTOGENETICS (CLINICAL GENETICS) THIS METHOD INVESTIGATES INHERITED CHROMOSOMAL ABNORMALI- TIES IN THE GERM CELLS OR ACQUIRED CHROMOSOMAL ABNORMALITIES IN SOMATIC CELLS USING MOLECULAR BIOLOGY TECHNIQUES 1 4 11 BIOCHEMICAL METHODS BIOCHEMICAL TECHNIQUES REFER TO ASSAYS AND PROCEDURES THAT ENABLE INVESTIGATORS TO ANALYSE THE SUBSTANCES FOUND IN LIVING ORGANISMS AND THEIR CHEMICAL REACTIONS THIS IS A METHOD BY WHICH THE METABOLIC DISTURBANCES OF DISEASE ARE INVESTIGATED BY ASSAY OF VARIOUS NORMAL AND ABNORMAL COMPOUNDS IN THE BLOOD, URINE, SALIVA, ETC 1 4 12 MEDICAL MICROBIOLOGY MEDICAL MICROBIOLOGY, ALSO KNOWN AS CLINICAL MICROBIOLOGY, IS A SUBDISCIPLINE DEALING WITH STUDYING MICROORGANISMS (PARASITES, FUNGI, BACTERIA, VIRUSES, AND PRIONS) CAPABLE OF INFECTING AND CAUSING HUMAN DISEASES 1 4 13 MICROBIAL CULTURE MICROBIAL CULTURE IS ONE OF THE PRIMARY DIAGNOSTIC METHODS IN MICROBIOLOGY MICROBIAL CULTURE IS A METHOD OF GROWING A MICROBIAL ORGANISM TO DETERMINE WHAT IT IS, ITS ABUNDANCE IN THE TESTED SAMPLE, OR BOTH THE TOOL IS OFTEN USED TO DETER- MINE THE CAUSE OF INFECTIOUS DISEASE BY LETTING THE AGENT MUL- TIPLY IN PREDETERMINED MEDIA IN THE LABORATORY IN THE CASE OF BACTERIAL INFECTIONS, THE MOST APPROPRIATE ANTIBIOTIC CAN BE SELECTED BY DETERMINING THE BACTERIA’S SENSITIVITY TO VARIOUS ANTIBACTERIAL AGENTS 1 4 14 FLOW CYTOMETRY THIS TECHNIQUE IS COMMONLY USED TO DIAGNOSE CANCERS OF THE BLOOD CELLS, SUCH AS LEUKAEMIAS 1 4 15 ELECTRON MICROSCOPY THE STANDARD MICROSCOPES USED BY PATHOLOGISTS ARE NOT POW- ERFUL ENOUGH TO SEE THE SMALLEST PARTS THAT MAKE UP A CELL SOME DISEASES CAN ONLY BE DIAGNOSED AT THIS SUBCELLULAR LEVEL 1 4 DIAGNOSTIC INVESTIGATIONS IN PATHOLOGY SUMMARY PATHOLOGY IS CONCERNED WITH THE CAUSE, DEVELOPMENT, STRUC- TURAL, AND FUNCTIONAL CHANGES, AND NATURAL HISTORY ASSOCIATED WITH DISEASES IT IS THE FOUNDATION FOR CLINICAL PRACTICE, INCLUDING DENTISTRY CLINICAL PATHOLOGY AND DIAGNOSTIC PATHOLOGY ARE TWO MAJOR DIVISIONS OF PATHOLOGY BIOPSY AND HISTOPATHOLOGY ARE THE MOST COMMONLY USED DIAGNOSTIC PRO- CEDURES IN DENTAL PRACTICE THESE PROCEDURES ARE EXTENSIVELY USED TO DIAGNOSE MUCOSAL, JAWBONE, AND SALIVARY GLAND DIS- EASES HISTOCHEMICAL, IMMUNOLOGICAL, BIOCHEMICAL, AND MOLECULAR PATHOLOGY TECHNIQUES ARE USED FOR THE CON?RMA- TION OF DIAGNOSIS OF DISEASES OF IMMUNOLOGICAL AND NEOPLAS- TIC ORIGIN BIBLIOGRAPHY FUNKHOUSER WK JR PATHOLOGY: THE CLINICAL DESCRIPTION OF HUMAN DISEASE MOLECUL PATHOL 2018:217–29 HTTPS://DOI ORG/10 1016/ B978- 0- 12- 802761- 5 00011- 0 MELROSE RJ, HANDLERS JP, KERPEL S, SUMMERLIN DJ, TOMICH CJ AMERICAN ACADEMY OF ORAL AND MAXILLOFACIAL PATHOLOGY THE USE OF BIOPSY IN DENTAL PRACTICE THE POSITION OF THE AMERICAN ACADEMY OF ORAL AND MAXILLOFACIAL PATHOLOGY GEN DENT 2007;55(5):457–61 MOHAN H, MOHAN S INTRODUCTION TO PATHOLOGY ESSENTIAL PATHOLOGY FOR DENTAL STUDENTS 5TH ED NEW DELHI: JAYPEE BROTHERS MEDICAL PUBLISHERS; 2017 P 1–8 PENA GP, ANDRADE-FILHO JS HOW DOES A PATHOLOGIST MAKE A DIAG- NOSIS? ARCH PATHOL LAB MED 2009;133(1):124–32 HTTPS://DOI ORG/10 5858/133 1 124 PMID SIMON HC APPLICATIONS OF PATHOLOGY IN: SIMON HERRINGTON C, EDITOR MUIR’S TEXTBOOK OF PATHOLOGY 15TH ED LONDON: CRC PRESS; 2014 P 3–10 WILTSE LL HEROPHILUS OF ALEXANDRIA (325–255 BC): THE FATHER OF ANAT- OMY SPINE 1998;23:1904–14 1 INTRODUCTION TO PATHOLOGY REGULATION AND MECHANISMS OF HOMEOSTASIS HOMEOSTASIS IS REGULATED BY NEGATIVE FEEDBACK LOOPS AND POSITIVE FEEDBACK LOOPS BOTH HAVE THE SAME STIMULUS COM- PONENTS: SENSOR (ALSO REFERRED TO AS RECEPTOR), CONTROL CENTRE, AND EFFECTOR (FIG 2 1) NEGATIVE FEEDBACK LOOPS PREVENT AN EXCESSIVE RESPONSE TO THE STIMULUS, WHEREAS POSITIVE FEED- BACK LOOPS INTENSIFY THE RESPONSE UNTIL AN ENDPOINT IS REACHED THE SENSOR COLLECTS INFORMATION FROM THE SURROUND- INGS AND REPORTS FURTHER TO THE CONTROL CENTRE THE CONTROL CENTRE MONITORS AND PROCESSES THE RECEIVED INFORMATION AND CONVEYS A SIGNAL TO THE EFFECTOR THE EFFECTOR PRODUCES A REAC- TION BASED ON THE SIGNAL PROVIDED BY THE CONTROL CENTRE CONTROL CENTRES IN THE BRAIN AND OTHER BODY PARTS MONITOR AND REACT TO DEVIATIONS FROM HOMEOSTASIS THE EFFECTOR IS AN ORGAN, GLAND, MUSCLE, OR ANOTHER STRUCTURE THAT ACTS ON THE SIGNAL FROM THE CONTROL CENTRE TO MOVE THE VARIABLE BACK TOWARD THE SET POINT A SET POINT IS A PHYSIOLOGICAL VALUE AROUND WHICH THE NORMAL RANGE ?UCTUATES AS THE BODY WORKS TO MAINTAIN HOMEOSTASIS, ?UCTUATIONS ARE NORMAL IF THEY DO NOT BECOME TOO EXTREME THE NORMAL BODY TEMPERATURE RANGE IS THE SPREAD OF VALUES WITHIN WHICH SUCH ?UCTUATIONS ARE CONSIDERED INSIGNI?CANT (E G THE NORMAL RANGE FOR AN ADULT IS ABOUT 36 5–37 5 °C (97 7–99 5 °F) POSITIVE FEEDBACK POSITIVE FEEDBACK AMPLI?ES CHANGES AND INTENSI?ES A RESPONSE UNTIL AN ENDPOINT IS REACHED CHILDBIRTH AND BLOOD CLOTTING ARE TWO EXAMPLES OF POSITIVE FEEDBACK MECHANISMS (SEE BELOW) EXAMPLES OF POSITIVE FEEDBACK MECHANISMS: – CHILDBIRTH POSITIVE FEEDBACK IN CHILDBIRTH NORMALLY BEGINS WHEN THE HEAD OF THE INFANT PUSHES AGAINST THE CER- VIX THIS STIMULATES NERVE IMPULSES, WHICH TRAVEL FROM THE CERVIX TO THE HYPOTHALAMUS IN THE BRAIN IN RESPONSE, THE HYPOTHALAMUS SENDS THE HORMONE OXYTOCIN TO THE PITUITARY GLAND, WHICH SECRETES IT INTO THE BLOODSTREAM SO THAT IT CAN BE CARRIED TO THE UTERUS OXYTOCIN STIMULATES UTERUS CON- TRACTIONS, WHICH PUSH THE BABY HARDER AGAINST THE CERVIX IN RESPONSE, THE CERVIX DILATES IN PREPARATION FOR THE BABY’S PASSAGE THIS POSITIVE FEEDBACK CYCLE CONTINUES WITH INCREASING LEVELS OF OXYTOCIN, MORE MUSCULAR UTERINE CONTRACTIONS, AND WIDER CERVIX DILATION UNTIL THE BABY IS PUSHED THROUGH THE BIRTH CANAL AND OUT OF THE UTERUS (FIG 2 2) – BLOOD CLOTTING (HAEMOSTASIS) THE MECHANISM OF HAEMO- STASIS CAN BE DIVIDED INTO FOUR STAGES: (1) CONSTRICTION OF THE BLOOD VESSEL (2) FORMATION OF A TEMPORARY “PLATELET PLUG ” (3) ACTIVATION OF THE COAGULATION CASCADE (4) FORMATION OF “?BRIN PLUG” OR THE ?NAL CLOT HAEMOSTASIS FACILITATES A SERIES OF ENZYMATIC ACTIVATIONS THAT LEAD TO CLOT FORMATION WITH PLATELETS AND ?BRIN POLYMER THIS CLOT SEALS THE INJURED AREA AND CONTROLS AND PREVENTS FURTHER BLEEDING WHILE TISSUE REGENERATION OCCURS ONCE THE INJURY STARTS TO HEAL, THE PLUG SLOWLY REMODELS, AND IT DISSOLVES WITH THE RESTORATION OF NORMAL TISSUE AT THE SITE OF THE DAMAGE – MENSTRUAL CYCLE THE OVARIES RELEASE THE HORMONE OESTROGEN AT THE START OF THE MENSTRUAL CYCLE THE OESTROGEN OPERATES AS A POSITIVE FEEDBACK LOOP STIMULATION THE INFORMATION IS DELIVERED TO THE BRAIN, WHICH PROMPTS THE HYPOTHALAMUS TO RELEASE THE GONADOTROPIN-RELEASING HORMONE AND THE PITU- ITARY TO RELEASE THE LUTEINISING HORMONE THE CONTROL UNIT RELEASES THESE HORMONES IN RESPONSE TO THE STIMULATION THESE HORMONES THEN CAUSE THE OVARIES TO RELEASE OESTROGEN, 2 HOMEOSTASIS NEGATIVE FEEDBACK NEGATIVE FEEDBACK IS A MECHANISM THAT REVERSES A DEVIATION FROM THE SET POINT THUS, NEGATIVE FEEDBACK MAINTAINS BODY PARAMETERS WITHIN THEIR NORMAL RANGE THE MAINTENANCE OF HOMEOSTASIS BY NEGATIVE FEEDBACK GOES ON THROUGHOUT THE BODY AT ALL TIMES SOME EXAMPLES ARE GIVEN BELOW EXAMPLES OF NEGATIVE FEEDBACK MECHANISMS: – REGULATING BODY TEMPERATURE (THERMOREGULATION) A TYPI- CAL NEGATIVE FEEDBACK MECHANISM IN THE HUMAN BODY IS REGULATING BODY TEMPERATURE WHEN THE BODY’S TEMPERA- TURE RISES ABOVE NORMAL, THE BRAIN SENDS SIGNALS TO VARIOUS ORGANS, INCLUDING THE SKIN, TO RELEASE HEAT IN THE FORM OF SWEAT THESE PHYSIOLOGICAL ACTIONS CAUSE THE TEMPERATURE TO DROP TO THE POINT WHERE THE NEGATIVE FEEDBACK MECHA- NISM’S PATHWAYS ARE SHUT DOWN WHEN THE BODY’S TEM- PERATURE DROPS BELOW NORMAL, THE BLOOD ?OW TO THE SKIN DECREASES, AND THE PERSON MIGHT START SHIVERING SO THAT THE MUSCLES GENERATE HEAT AND WARM THE BODY (FIG 2 3) – BLOOD SUGAR REGULATION: BLOOD GLUCOSE CONCENTRATION RISES AFTER A MEAL (THE STIMULUS) THE PANCREAS RELEASES THE HORMONE INSULIN AND SPEEDS UP GLUCOSE TRANSPORT FROM THE BLOOD INTO SELECTED TISSUES (THE RESPONSE) BLOOD GLUCOSE CONCENTRATION THEN DECREASES, WHICH IN TURN REDUCES THE ORIGINAL STIMULUS AND CAUSES A REDUCTION IN THE SECRETION 2 4 HOMEOSTATIC MECHANISMS (FEEDBACK MECHANISMS) NUTRITION AND HOMEOSTASIS VARYING LEVELS OF UNDERNUTRITION OR OVERNUTRITION CAN ALTER HOMEOSTATIC INTERACTIONS BETWEEN NUTRITION AND METABOLISM UNDERNUTRITION CAN RESULT FROM INADEQUATE INGESTION OF NUTRI- ENTS, MALABSORPTION, IMPAIRED METABOLISM, LOSS OF NUTRIENTS DUE TO DIARRHOEA, OR INCREASED NUTRITIONAL REQUIREMENTS, AS 2 7 NUTRITION AND HOMEOSTASIS GODLEWSKI M, KOBYLI?SKA A PROGRAMMED CELL DEATH-STRATEGY FOR MAIN- TENANCE CELLULAR ORGANISMS HOMEOSTASIS POSTEPY HIG MED DOSW (ONLINE) 2016;70:1229 KILIAN M, CHAPPLE I, HANNIG M, ET AL THE ORAL MICROBIOME–AN UPDATE FOR ORAL HEALTHCARE PROFESSIONALS BR DENT J 2016;221:657–66 QIU H, SCHLEGEL V IMPACT OF NUTRIENT OVERLOAD ON METABOLIC HOMEOSTA- SIS NUTR REV 2018;76(9):693–707 SMITH SA, TRAVERS RJ, MORRISSEY JH HOW IT ALL STARTS: INITIATION OF THE CLOTTING CASCADE CRIT REV BIOCHEM MOL BIOL 2015;50(4):326–36 2 HOMEOSTASIS MORPHOLOGICAL, FUNCTIONAL, AND CLINICAL MANIFESTATIONS THE AETIOLOGIC AGENT PRODUCES MORPHOLOGICAL, FUNCTIONAL, AND CLINICAL CHANGES THROUGH A PATHOGENETIC PATHWAY THE FOLLOWING ARE SOME FEATURES OF CLINICAL INTEREST: – SYMPTOM: A SYMPTOM IS EXPERIENCED BY AN INDIVIDUAL, SUCH AS FEELING FEVERISH, HAVING A HEADACHE, OR HAVING SHORTNESS OF BREATH WHEN AN ILLNESS OR DISEASE IS EVI- DENCED BY SYMPTOMS, IT IS KNOWN AS SYMPTOMATIC SOME CONDITIONS, INCLUDING EARLY CANCERS, HYPERTENSION, AND INFECTIONS, MAY BE PRESENT BUT SHOW NO SYMPTOMS; THESE ARE ASYMPTOMATIC – SIGN: A SIGN IS AN OBJECTIVE, OBSERVABLE INDICATION OF A DISEASE, INJURY, OR ABNORMAL PHYSIOLOGICAL STATE THAT MAY BE DETECTED DURING A PHYSICAL EXAMINATION OR DIAGNOSTIC PROCEDURE – VITAL SIGNS INCLUDE FOUR CLINICAL SIGNS THAT CAN IMMEDI- ATELY MEASURE THE BODY’S OVERALL FUNCTIONING AND HEALTH STATUS THEY ARE BODY TEMPERATURE, HEART RATE, BREATHING RATE, AND BLOOD PRESSURE THE RANGES OF THESE MEASURE- MENTS VARY WITH AGE, WEIGHT, GENDER, AND GENERAL HEALTH – PATHOGNOMONIC FEATURES: SOME DISEASES MANIFEST WITH SPECI?CALLY DISTINCTIVE FEATURES DENOTING SIGNS AND SYMP- TOMS ON WHICH A DIAGNOSIS CAN BE MADE THESE ARE CALLED PATHOGNOMONIC FEATURES PILL-ROLLING TREMORS ARE PATHOG- NOMONIC FOR PARKINSON’S DISEASE NUMERICAL DISEASE-CODING SYSTEMS UNDERSTANDING DISEASES IN WAYS THAT ENABLE PREVENTION, TREAT- MENT, AND THE ALLOCATION OF RESOURCES REQUIRES A RELIABLE MEA- SUREMENT THAT ALLOWS VALID COMPARISONS BETWEEN PLACES AND OVER TIME CLASSI?CATION OF DISEASES AND RELATED THINGS IS ESSENTIAL FOR SUCH MEASUREMENT THE INTERNATIONAL CLASSI?CATION OF DISEASES (ICD) OF THE WORLD HEALTH ORGANISATION IS ONE OF THE MAIN BASIS FOR COMPARABLE STATIS- TICS ON CAUSES OF DEATH AND NON-FATAL DISEASE EACH DISEASE OR A GROUP OF DISEASES IS DESIGNATED A SPECI?C NUMBER IN THE ICD CLASSI?CATION THE WORLD HEALTH ASSEMBLY ADOPTED THE MOST RECENT ICD-11 IN MAY 2019 SYSTEMATISED NOMENCLATURE OF MEDICINE (SNOMED) IS THE OTHER CODED CLASSI?CATION AVAILABLE SNOMED CT STANDS FOR SYSTEMATIZED NOMENCLATURE OF MEDICINE – CLINICAL TERMS IT IS A STAN- DARDISED, INTERNATIONAL, MULTILINGUAL CORE CLINICAL HEALTHCARE TERMINOLOGY THAT CAN BE USED IN ELECTRONIC HEALTH RECORDS (EHRS) ICD WAS ADOPTED BY THE 72ND WORLD HEALTH ASSEMBLY IN 2019 AND CAME INTO EFFECT ON 1 JANUARY 2022 AS A CLASSI?CA- TION AND TERMINOLOGY, ICD-11 ALLOWS THE SYSTEMATIC RECORD- ING, ANALYSIS, INTERPRETATION, AND COMPARISON OF MORTALITY AND MORBIDITY DATA COLLECTED IN DIFFERENT COUNTRIES OR REGIONS AT DIFFERENT TIMES IT ENSURES SEMANTIC INTEROPERABILITY AND REUS- 3 DISEASE, DISORDER, AND DISABILITY