STENCILDENT

                              ODONSETRON  Pro type of anti-emetic drug Controls cancer chemotherapy /radiotherapy ,drug induced vomiting. MECHANISM OF ACTION: It blocks depolarization of 5 HT through 5-HT3 receptor on vagal  afferent in gastro intestinal tract. Cytotoxic drugs/chemotherapy causes cellular damage there by induce vomiting ,thereby release of mediator of 5-HT from intestinal mucosa,activation of vagal afferent in gut and sends emetogenic impulse to NTS. Odonsetron blocks emetogenic impulses both at peripheral and central relay  PHARMACOKINETICS: Oral bio availability :60-70% Eliminated in urine ,faceces SIDE EFFECTS : Headache Mild constipation Rashes  Allergic reaction  CONCLUSION: Hi stencildent family hope you all liked this short notes on odonsetron if it helped you learn then do let me know in the comment section below as this would motivate me to post more such content .                                   Thank you  NOTE: pharmacology notes are for purely educational

      REACTIONARY HEMORRHAGE  INTRODUCTION: The term hemorrhage refers to excess loss of blood due to rupture of blood vessel STUDENTS CORNER : Start your answer by giving a short introduction to the topic followed by table of contents ,it can be visa versa to ,under the table of content mention etiology ,precipitating factors, pathophysiology ,clinical features and end it with treatment plan . Now let me give you a mnemonic that I used while preparing in order to remember etiology remember HTC MTC where: H-HYDROCELE SURGERY   T-THYROID SURGERY   C-CHOLECYSTECTOMY  M-MAJOR ABDOMINAL SURGERIES T-TONSILLECTOMY  C-CIRCUMSICION .  To remember precipitating factors the mnemonic as:   PBS ,CVS P(SILENT )  B- BLOOD PRESSURE  S-STRAING   C-CLOT DISLODGEMENT   V- VOMITING  S - SLIPPING OF LIGATURE . Clinical feature CDC TROPHY   C-CYANOSIS  D-DRY FACE,DRY MOUTH   C-COLD CLAMMY SKIN   T- TACHYPNEA,TACHYCARDIA  R- RAPID THREADY PULSE  O-OLIGURIA  P-PALLOR  H- HYPOTENSION  Y (SILENT )  Hope thes

  NON -STEROIDAL INFLAMMTORY DRUG STUDENTS CORNER: Hello VANAKKAM!,my dear stencildent family members this is a continuation of previous blog on introduction to non-steroidal anti inflammatory drug where in we learnt classification, mechanism of action of NSAID in detail along with a short notes on ASPIRIN if we haven't learnt about it yet then do click on the link to  NSAID -PART 1 learn more. Now lets get inside our content on propionic acid derivative drug-ibuprofen ,acetic acid derivative drug -ketorolac and fenamate derivative mephenamic acid.  PROPIONIC ACID DERIVATIVE : IBUPROFEN Better tolerated alternative to aspirin ,safest NSAID  Antiplatelet  action is short lasting  Weaker anti-inflammatory drug USES: Analgesic ,anti-pyretic Rheumatoid arthritis Tooth extraction(aspirin +codeine) Soft tissue injury ADVERSE EFFECTS : Nausea Vomiting CENTRAL NERVOUS SYSTEM: Headache ,dizziness, blurring of vision ,rash ,itching  PHARMACOKINETICS AND INTERACTION: ABSORPTION-Well absorbed

  CLAUDICATION PAIN IN LEG WHILE WALKING  INTRODUCTION: Claudio means to limp (Latin word) Crampy pain in muscle seen in limbs  Site of pain depends on site of arterial occlusion Due to arterial occlusion Metabolites -lactic acid Substance p accumulate in muscle and cause pain common site -calf muscle Pain in foot - block in lower tibial and plantar vessel Pain in calf-block in femoropopliteal site Pain in thigh - block in superficial femoral artery  Pain in buttocks'-block in common iliac - LERICHE SYNDROME Pain commonly develops when muscles are exercising  During exercise: increase perfusion and increased opening of collateral wash the metabolites away BOYD CLASSIFICATION: GRADE 1: Pain after walking distance which pain develop CLAUDICATION DISTANCE  If patient continues to walk pain subsides -metabolites causing pain are washed away in the circulation due to increased blood flow in muscle and also opening of collateral GRADE2: Pain still persist on continuing walk ,but can walk

  NON -STEROIDAL ANTI INFLAMMATORY DRUG  They are non-opioid analgesics  They have anti-pyretic ,uricosuria properties CLASSIFICATION  A)NON SELECTIVE COX-INHIBITOR : ACETIC ACID ACID :   KETOROLAC,INDOMETHACIN,NABUMETONE ENOLIC ACID : PIROXICAM PYRAZOLONE : PHENYLBUTAZONE OXYPHENBUTAZONE FENAMATE : MEPHENAMIC ACID PROPIONIC ACID : IBUPROFEN KETOPROFEN NAPROXEN FLURBIPROFEN SALICYLATE: ASPIRIN B)PREFERENTIAL COX-2 INHIBITORS  : DICLOFENAC ACECLOFENAC ETODOLAC NIMESULIDE MELOXICAM C)SELECTIVE COX - 2 INHIBITOR : PARECOXIB CELECOXIB ETORICOXIB D)ANALGESICS WITH ANTI-PYRETIC WITH POOR ANTI-INFLAMMATORY ACTION: PARA AMINOPHENOL DERIVATIVE :PARACETAMOL (ACETAMINOPHEN) PYRAZOLONE DERIVATIVES:METAMIZOL PROPIPHENAZONE BANZOXAZOCINE DERIVATIVE :NEFOPAM MECHANISM OF ACTION: When any infectious agent (stimuli)enters the  body it affect phospholipid bilayer ( important component of cell membrane)it stimulate enzyme phospholipase A2  ,it destroys phospholipids to arachidonic acid it enters two path

                  DENTIN BONDING AGENTS  1) FIRST GENERATION DENTIN BONDING AGENT: It consist of surface active co-monomer NPG-GMA  MECHANISM OF ACTION:  This co -monomer could chelate with calcium on tooth surface to generate chemical bond of resin to calcium  example: SS WHITE BURS,CREVIDIENT  It had poor strength ,hence when used in non-carious lesion without mechanical retention 2) SECOND GENERATION: They were based on phosphorous esters of methyl acrylate derivative  MECHANISM OF ACTION: Adhesion was by means of iconic interaction between the negatively charged phosphate groups and positively charged calcium smear layer ADVANTAGE: Bond strength was high  DISADVANTAGE: Due to bond instability in the net oral environment and there one degree bonding to the smear layer and not dentin  EXAMPLE: Clearfin bonding system 3) THIRD GENERATION: It was phosphate based material contain HEMA and 10  carbon molecule ,10-MDP MECHANISM OF ACTION: The concept of phosphoric acid etching of dentin b

                         CIPROFLOXACIN Its a first generation fluoroquinolones anti microbial drug Active against gram negative bacilli especially Enterobacteriaceae and Neisseria Its highly susceptible to salmonella ,shigella, Enterobacter Rapid bactericidal activity activity by digesting DNA It has low frequency of resistance MECHANISM OF ACTION: Fluoroquinolone does 2 roles :  Inhibit topoisomerase in gram positive bacteria ,there by inhibit separation of DNA Strands  Inhibit DNA Gyrase enzyme in gram negative bacteria ,thereby resealing strands of DNA  Ultimately both block synthesis of bacterial DNA and produce bactericidal effect. PHARMACOKINETICS: ABSORPTION: Oral, Intravenous ,topical  DISTRIBUTION: Kidney ,lung ,bile METABOLISED: Liver  EXCRETION: Urine USE: Anthrax Bacterial diarrhea Chancroid Conjunctivitis Typhoid fever : first choice Tuberculosis: component for chemotherapy Urinary tract infection : upper urinary tract infection ADVERSE EFFECTS : GASTROINTESTINAL TRACT: Na