STENCILDENT

  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

                              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