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NECROSIS -pathology notes

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  NECROSIS  DEFINITION: Its defined as the morphological changes taking place in a tissue after cell death due to degradative action f enzymes on irreversibly injured cell. TYPES OF NECROIS : A)CASEOUS NECROSIS B)LIQUEFACTIVE NECROSIS C)COAGULATIVE NECROSIS D)FIBRINIOD NECROSIS E)FAT NECROSIS F)GANGEROUS NECROSIS CYTOPLASMIC CHANGES : Increased eosinophilia of cytoplasm  Vacuolation and moth eaten appearance of cytoplasm  Calcification of cell membrane and intracellular structures  Formation of myelin figures  NUCLEAR CHANGES : KARYOLYSIS : Fading of basophilia of nucleus PYKNOSIS: Nuclear shrinkage due to condensation of chromatin  KARYORRHEXIS -Nuclear fragmentation  A)CASESOUS NECROSIS : Its seen in tuberculosis and occurs due to both enzymatic degradation of tissue and denaturation of cellular proteins  The tissue architecture is lost and replaced by soft ,creamy cheese like material  Microscopically ,there is amorphous granular debris seen  Examples : tuberculosis lymph node ,tube

AGE ESTIMATION DEMIRJIANS METHOD

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  AGE ESTIMATION  INTRODUCTION : Radiology plays an important role in human age determination Dental radiography is a non-destruction and simple technique used daily in dental practice  Age estimation in children can be based on radiographic analysis of developmental stages of dental elements since: Strong genetic control More reliable in predicting chronological age than other osteological indicators NEED FOR IDENTIFICATION: A competent forensic death investigation of human remains has 4 goals : Determination of the means Manner Cause of death Identification of the remains METHODS: DEMIRJIANS METHOD: To assess the developmental stages of third molars from the mandible . Eight stages (A-H) Plus 0 - absence  CONCLUSION : Teeth represent useful material for age estimation  Development of each individual can be effected by : Genetic  Nutritional Climatic  Hormonal Environmental  It has been reported that dental mineralisation is less affected by external factors when compared to bone mine

Epidemiology of oral cancer

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  EPIDEMIOLOGY OF ORAL CANCER  INTRODUCTION: One of the major threats to public health in the developed world-cancer 2nd most common cause of death According to world health report :9.6 million death in 2018 its estimated that new cases will rise by 50% in the next 20 years . Cancer is defined by 4 characteristic trait: Clonality Autonomy Anaplasia Metastasis  International classification of disease (ICD) WHO (9TH version) Oral cancer is classified under rubrics  Lip-140 Tongue-141 Gingiva-143 Floor of mouth-144 Other parts of mouth-145  CANCER REGISTRATION IN INDIA: National cancer registry program(NCRP)was commenced by Indian council of medical research  3 (PBCRPS )  Population based cancer registries : Bangalore  Chennai  Mumbai 3 Hospital based cancer registries : Chandigarh, Dibrugarh, Thiruvanthapuram  Commenced from January 1 in 1982  Currently there are 36 (PBCRS) and 236 (HBCR) under NCRP. ETIOLOGY AND RISK FACTOR : Tobacco and alcohol -2020 WHO fact sheet :1.3 billion tobacco

Principles of tooth preparation at glance

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 PRINCIPLES OF TOOTH PREPARATION DEFINITION : Tooth preparation is defined as the process of removal of diseased and or healthy enamel ,dentin and cementum to shape a tooth to receive a restoration (GPT8). BIOLOGIC : 1)PREVENTION OF DAMAGE  Adjacent teeth Soft tissue Pulp  2)CONSERVATION OF TOOTH STRUCTURE  3)MARGIN INTEGRITY Placement  Geometry  Adaptation  MECHANICAL : 1)RETENTION FORM  Magnitude of dislodging forces Geometry of preparation Path of insertion Roughness of fitting surface of casting  Materials being cemented Type of luting agent  2)RESISTANCE FORM Magnitude of dislodging forces Geometry of preparation Type of luting agent  3)STRUCTURAL DURABILITY  Occlusal reduction Functional cusp bevel Axial reduction  AESTHETIC : 1)Partial veneer restoration 2)Metal ceramic restoration 3)All ceramic restoration  AIM OF THIS POST : Hello my dear stencildent viewers hope you glanced through the principles of tooth preparation this is just a introductory post the upcoming post will be

Anti-tubular action ,pharmacokinetics,adverse effects of Rifampicin

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  RIFAMPICIN : Its a semi-synthetic derivative of Rifamycin  1st line drug used in tuberculosis  Rifampicin is bactericidal to M.tuberculosis,M.leprae Inhibits most gram positive and gram negative bacteria like staphylococcus aureus,N.meningitidis,E.coli,klebsiella,pseudomonas,proteus and legionella ANTI-TUBULAR ACTION: Tuberculocidal :treatment for tuberculosis  Acts on intra and extracellular organism and drug resistant organism hence called - STERILISING AGENT  Inhibit DNA dependent RNA synthesis if used alone it develops drug resistance                                                    Rifampicin             Bind with beta subunit of DNA dependent RNA polymerase                                          Inhibition of MRNA synthesis                                            Tuberculocidal effect PHARMACOKINETICS: 1)ABSORPTION:Given orally 2)DISTRIBUTION:Penetrate cavities,caseous masses,placenta and meninges 3)METABOLISM :Liver 4)EXCRETION:Bile and urine  T 1/2 : 2 hours  INTERACT

LEUKOPLAKIA - oral medicine notes

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 LEUKOPLAKIA  POTENTIALLY MALIGNANT DISORDER :  R isk of malignancy being present in a lesion or condition either during the time of initial diagnosis or at future date  PRECANCEROUS LESION :  Benign morphological altered tissue in which cancer is more likely to develop than its normal counterpart : leukoplakia  Erythroplakia  Tobacco pouch keratosis  Palatal lesion in reverse smokers  PRECANCEROUS CONDITION :  Generalized state or a disease which can be associated with greater than  normal risk of cancer development  OSMF Lichen planus  Epidermolysis bullosa  LEUKOPLAKIA :  White plaque of questionable risk having excluded (other)known disease or disorder that carry no risk for cancer  PLAQUE-  Raised lesion that are greater than 1 cm in diameter ,they are essentially large papules  PAPULE:  Lesion raised above skin or mucosal surface that are smaller than  1 cm in diameter  WHO DEFINITION : Non scrapable white patch or plaque that cannot be characterized clinically or pathologically

DO YOU KNOW ABOUT CRUSH SYNDROME?

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 CRUSH SYNDROME  INTRODUCTION : It is due crushing of muscles causing : Extravasation of blood Release of hemoglobin into circulation leading to acute tubular necrosis and acute renal failure CAUSES ; Road traffic accident  Earthquake Mining ,industrial accident  Air crash Tension increases in muscle that results in increased ischemic damage  3 days :urine discolored,scanty  Life threatening  EFFECTS : Renal failure  Toxemia,septicemia Gas gangrene  Disability with extensive tissue loss TREATMENT : Tension in muscle compartment is relieved by placing multiple ,parallel,deep incision in limb Mannitol is given to improve urine output Alkalisation of urine is done using sodium citrate /sodium bicarbonate  Hemodialysis is done - life saving procedure  Other measures : Oxygen therapy  Antibiotics Blood transfusion  Bladder catheterization  AIM OF THIS POST : Hello stencildent family ,the title is definitely not a click bait it is clearly not related with CRUSH !The aim of this post is to gi