STENCILDENT

 CONSERVATIVE DENTISTRY  Art and science of diagnosis,treatment,prognosis of defense of tooth that do not require full coverage restoration  Such treatment should result in proper tooth form, function ,esthetics ,in harmonious relationship with adjacent hard and soft tissue all of which enhance the general health and welfare of patient DENTAL CARIES: DEFINITION: Is an infectious microbiological disease that result in localized dissolution and destruction of the calcified tissue of teeth -STURDEVANT Is defined as the microbial disease of the calcified tissue of tooth characterized by demineralization of the inorganic protein and destruction of organic substance of tooth -E.A.M.KIDD BASED ON WHO SYSTEM: D1-Non cavitated lesion D2-Cavity limited to enamel  D3-cavity limited to dentin D4-cavity limited to pulp BLACKS CLASSIFICATION: CLASS I CARIES: All pits and fissure caries are class1 caries ,these caries include : Occlusal surface of premolar and molar Occlusal 2/3rd of facial and lingu

                  PROKINETIC DRUGS Drug that promote gastrointestinal transit and hasten gastric emptying METACLOPRAMIDE: They act by blocking D2 dopamine receptor in CTZ -ANTIEMETIC ACTION Enhances acetylcholine release from cholinergic neuron in gut ACTION: GASTROINTESTINAL TRACT: Forward movement of content in upper gastrointestinal tract  Increased gastric emptying Prevent reflux esophagitis CENTRAL NERVOUS SYSTEM: Speeds up gastric emptying USES: Antiemetic Preanesthetic medication In endoscopy ADVERSE EFFECT: Sedation Gynecomastia Diarrhoea Note: Kindly do not consume medication without consulting a physician ,notes on our site is to provide notes for students only.

      FAULTY RADIOGRAPH -PART2                                     EXPOSURE ERROR: STUDENTS CORNER : Hi my dear stencilent family ,sorry for interepting, before moving on to the topic of discussion for today ,we also need to learn more reasons for faulty radiograpgh to occur along with its correction strategies to learn them , do click on the link provided  patient and positioning errors . DARK RADIOGRAPH: REASONS: PROLONGED EXPOSURE TIME (kvp) HIGH KILOWOLTAGE POTENTIAL(MA) Decreased film to source distance CORRECTION: Set exposure time kvp,MAcorrectly Adjust film to source distance LIGHT RADIOGRAPH REASONS : Low kvp -less MA Less exposure  Increased in film to source distance CORRECTION: Set exposure time kvp,MAcorrectly Adjust film to source distance PROCESSING ERROR: DARK RADIOGRAPGH : REASONS: Developing time to long High temperature of developer Inadequate fixation Light exposure before processing CORRECTION: Time -temperature method  68F-5 minute 78F-4 and half munute  LIGHT RAD

             FAULTY RADIOGRAPH ARTIFACT : Unwanted density on the radiograpgh that interfere diagnosis. I)PATIENT AND FILM POSITIONING ERROR: FORESHORTENING: Reasons : increased vertical angulation  correction: angulation maintained to the teeth ELONGATION: reasons:decreased verical angulation correction:angulation to be maintained to respect to teeth CORONAL END CUT: reasons: film not placed sufficient coronally  correction:proper placement of film coronally APICAL END CUT: reasons:film not placed sufficient apically correction:proper placement of film apically CONE CUT: reasons:improper placement of film,improper tube head position  correction:proper placement of film ,tube head  OVERLAPPING: reasons:improper horizontal angulation of tube head  correction:proper anugulation horizontal :0 WRONG SIDE IDENTIFICATION DOT/DOT ARTEFACT: reason:wrong placement of film  correction:dot to be placed towards occlusal surface  FOREIGN BODY : reason:exposure of film with nose ring/ear ring correc

 DYSTROPHIC CALCIFICATION  Pathologic calcification is abnormal tissue deposition of calcium salts together with smaller amounts of iron ,magnesium and other mineral salts Its of two forms : Dystrophic Metastatic Dystrophic calcification : When deposition occurs locally in dying tissue It occurs despite normal serum level of calcium and in the absence of derangement in calcium metabolism Occur in : Area of necrosis Advanced atherosclerosis Damaged heart valve Dead parasite Cancer Students corner : To learn more about  pathogenesis of atherosclerosis  do click on this link to learn more. Pathogenesis: Final step if fomrtaion of crystalline calcium phosphate  INITIATION: Membrane process calcium concentration bind to phospholipid present in membrane ,phosphatase generate phosphate group   PROPAGATION: Cycle of calcium binding phosphate generating micro crystal propagate lead to more calcium deposition  MORPHOLOGY : Calcium salts appear macroscopically fine ,white granules or clum ,gritt

    DISSEMINATED INTRAVASCULAR                                          COAGULATION INTRODUCTION: Complex thrombohemorrhagic disorder Second complication in some disease ETIOLOGY: Massive trauma,surgery Malaria Septicemia Severe burn Snake bite  PATHOGENESIS: Activation of coagulation Thromboitic phase Consumption phase Secondary fibrinolysis CLINICAL FEATURE : Bleeding Organ damage LABORATORY DIAGNOSIS: Platelet count low  Prothrombin and thrombin time is prolonged

  PATHOGENESIS OF ATHEROSCLEROSIS INTRODUCTION: Lipid plaque form on the inside wall of arteries Arteries :narrowed and becomes hardened Atherosclerosis is caused when endothelial wall get damaged by hypertension ,smoking,hyperglycemia Increased permeability of arterial wall -allowing LDL cholesterol to get in  White blood cells like monocyte ,move freely through blood vessel Endothelial cell express adhesion protein molecule when an irritating stimuli ,tat capture monocyte ,undergo morphologic changes ,enter between cell -DIAPEDIESIS White blood cell (engulf )produce free radical in contact with LDL  gets oxidized resulting in positive feedback situation  Foam cell produced ,saturated with LDL die and release content ,that's taken by other white blood cell Fragment of dead cell produce area with lipid core to form plaque This plaque accumulate more calcium salt and dead cell leading to atherosclerosis Blood clot form on endothelial wall thrombus Flow through blood stream called em

  VIRCHOWS TRIAD  THROMBOSIS : Process of formation of solid mass in circulation from flowing blood ,this mass itself is called thrombus According to virchows three things/factors essential for blood clot ,"thrombus formation". 1)Endothelial cell injury 2)Hemostasis 3)Hypercoagulality STUDENTS CORNER : Welcome back to our site ,if you are our new subscriber then do consider checking out our  posts by either clicking on the subject you want to learn or you can start by searching the topic of your interest ,coming back to the content so today the topic of discussion is on virchows triad ,previously we have discussed on  PLATELET , FATE OF THROMBI , when this question is asked do give a short introduction on platelet and proceed by mentioning all three in the virchows triad that is the endothelial injury,hemostasis( click on the link to learn about hemostasis ) followed by hypercoaguability and conclude your answer with fate of thrombi . ENDOTHELIAL INJURY: Increases the risk

                PARACETAMOL Analgesic ,anti-pyretic ,week anti inflammatory properties. Brain:Active cyclo-oxygenase -anti-pyretic action Gastric irritation mild STUDENT CORNER: HI!my dear stencildent family welcome back to our website ,if your knew to our site please do consider checking out our other posts to ,now moving on to our topic of discussion for today its about a very well and often used,and misused drug paracetamol it belongs to non -steroidal antiinflammatory drug click on this link to learn about  NSAID CLASSIFICATION  . PHARMACOKINETICS: Orally well absorbed Thirty percent protein bound Metabolised by microsomal enzyme  ADVERSE EFFECT: Nausea Rashes Large dose:  Acute paracetamol poisoning  Hepatotoxic Jaundice Nephrotoxicity - renal failure USES: Analgesic:tooth ache ,head ache  Antipyretic Chronic pulpitis,periodontal abscess,post extraction MECHANISM OF ACTION: Small portion: metabolised to -N-acetyl benzoquinone gets detoxified ,conjugation to glutathione large doses

                       METRONIDAZOLE INTRODUCTION: Antiameobic drug useful in infection caused by protozoa Entamoeba histolytica Its a tissue amoebicidal used for both extraintestinal and intra intestinal amoebiasis Metronidazole belongs to class nitroimidazole which is the first line drug for all forms of amoebiasis They are active against other protozoa ( TRICHONOMAS VAGINALIS, GIARDIA LAMBIA AND ANEROBIC INFECTION) MECHANISM OF ACTION: Metronidazole as a pro drug enter in the organism  Nitro group present in the drug accept electron from ferredoxin  Nitro group converted to highly reactive nitro radical Highly reactive nitro radical damage microbial DNA  Leads to death of organism produce cidal effects PHARMACOKINETICS: ABSORPTION: Orally ,Intravenous, Topical  DISTRIBUTION: Diffuse into tissue METABOLISM: liver EXCRETION: Urine  ADVERSE EFFECT : GASTROINTESTINAL :Nausea,vomiting ,abdominal cramps ALLERGIC REACTION: skin rashes -urticaria ,flushing  CENTRAL NERVOUS SYSTEM : ataxia,d

                        LUDWIG ANGINA STUDENTS CORNER : HI !my dear stencildent family ,today we will be discussing about a very important topic ,yes its about Ludwig angina here we given a sample as to how you can present this answer when asked first of all do start by listing out table of content ,then move on to describing the surgical anatomy ,reason for Ludwig angina existence and how it gets precipitated ,pathology ,clinical features ,management -surgery point of view and conclude with complications.                         TABLE OF CONTENT : INTRODUCTION SURGICAL ANATOMY ETIOLOGY PRECIPITATAING FACTOR PATHOLOGY CLINICAL FEATURES MANAGEMENT  SURGERY COMPLICATION INTRODUCTIO N: Ludwig angina refers to serious ,potentially life threatening polymicrobial cellulitis of submental ,submandibular region combined with inflammatory edema of mouth Organism commonly isolated : STAPHYLOCOCUS AUREUS ,STREPTOCOCUS VIRIDAN ANEROBE :Fusiform bacilli,diptheroid  Cellulitis:  Diffuse inflammation