STENCILDENT

  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

  LOCAL ANAESTHETICS Drugs that block peripheral nervous tissue when applied locally to nerve tissue in appropriate concentration,without loss of consciousness CLASSIFICATION: A) INJECTABLE : SHORT ACTING : Procaine  Chloroprocaine  INTERMEDIATE ACTING  Lignocaine  Prilocaine LONG ACTING Bupivacaine  Ropivacaine tetracaine  B) SURFACE ANAESTHETIC: Lignocaine  Cocaine Tetracaine MECHANISM OF ACTION : Primary mechanism of action: blockade of voltage gated sodium channel  local anaesthesia diffuse through cell membrane to bind the voltage sensitive sodium channel to prevent generation of action potential and conduction  DIFFERENTIAL BLOCKADE: 1)Autonomic (1st blocked )followed by sensory fibres,pain temperature ,touch ,pressure,vibration  Non myelinated fibres are blocked readily than myelinated  FEATURES OF LOCAL ANAESTHETICS: 1) It should have quick onset of action  2)It should not be irritating to skin and mucous membrane  3)Duration of action must be long enough to allow desired surge

  CATECHOLAMINES Neurotransmitter that take part in adrenergic transmission Catecholamines are synthesised from adrenal medulla ,from a specialised cell:chromaffin cell  The catecholamine includes : Adrenaline Nor -adrenaline Dopamine SYNTHESIS : 1)AT BLOOD : Phenylalanine 

ANGIOTENSIN CONVERTING ENZYME INHIBITOR COVID -19 (CORONAVIRUS 2019 DISEASE)a current pandemic infection caused by   RNA virus  Its mainly transmitted by droplet generated when an infected person coughs,sneezes or inhales. Symptoms:fever ,dry cough,tiredness.  Less common symptoms :headache,sore throat,diarrhoea,loss of taste or smell. Even if you notice mild symptoms don't hesitate to ask your doctor.  Get vaccinated at your chance  Getting vaccinated is very important to save us as well as your close ones , to learn more about herd immunity and its importance do check it out through this link  HERD IMMUNITY ANGIOTENSIN CONVERTING ENZYME INHIBITOR CAPTOPRIL: Dipeptide ace inhibitor Orally active Prototype drug Sulfhydryl containing dipeptide surrogate of proline  Abolish pressor action of angiotensin 1 without affecting angiotensin 2 Increase plasma kinin level : responsible for cough ,angioedema,hypotensive action. Decrease blood pressure is seen more in sodium depleted subject a

  PROTON PUMP INHIBITOR  Peptic ulcer occurs due to the imbalance between acid -pepsin secretion and mucosal defense factor  Proton pump inhibitor act by inhibiting the gastric acid secretion  Its a efficacious inhibitor omeprazole is a drug that's commonly use MECHANISM OF ACTION: The parietal cells of stomach secrete :H + with the help of enzyme H+K+ATPase present in the plasma membrane Omeprazole and other proton pump inhibitor are produrg get activated in the acidic environment of the stomach to sulfenamide which binds covalently with H+K+ATPase   The binding is irreversible Single dose can almost (95%)inhibit gastric secretion Acid secretion start only after new H+K+ATPase enzyme is synthesises . Ulcer heals rapidly even in resistant cases. PHARMACOKINETICS; Given as enteric coated granules to avoid degradation by acid in stomach Effect of 1 dose remains for 2 to 3 days Microsomal enzyme inhibitor Increases level of benzodiazepine,warfarin  ADVERSE EFFECT : Headache Nausea Pai

  PEPTIC ULCER  - Part 1  Peptic ulcer is result from imbalance between acid pepsin secretion and mucosal defense factor Stomach secrete 2.5 litre of gastric juice daily MECHANISM OF ACTION: Chief cell secrete pepsinogen Parietal  cell secrete   hydrochloric  acid and intrinsic factor Gastric acid secretion regulated by  Acetylcholine   - muscarinic  receptor Gastrin - g receptor Histamine- h2 receptor Acetylcholine and gastrin act on parietal  cell Act indirectly on enterochromaffin cells releasing  histamine Mucosa secretes mucus  which forms the protective layer ,bicarbonate and prostaglandin Prostaglandin  stimulate mucus and bicarbonate that leads to vasodilation  and thereby inhibit gastric  secretion  CLASSIFICATION : DRUG FOR PEPTIC ULCER : A) GASTRIC ACID SECRETION INHIBITOR : H2 antihistamine - CIMETIDINE,RANITIDINE Proton pump inhibitor - OMEPRAZOLE,LANSOPRAZOLE B) GASTRIC ACID NEUTRALIZER : Systemic - sodium bicarbonate,sodium citrate Non systemic - magnesium hydroxide,calc

 ANTI-DIABETIC DRUG Diabetes mellitus: C hronic disorder characterised by hyperglycemia  and altered metabolism of carbohydrate,lipid,and protein. oral antidiabetic drug lowers blood glucose level CLASSIFICATION:                               ANTI- DIABETIC DRUG 1) ENHANCE INSULIN SECRETION: A)POTASSIUM ATP CHANNEL BLOCKER:      a1) Sulfonylurea :Gliclazide,Glipizide       a2)Phenylalanine analogue : Nateglinide B) DIPEPTIDYL PEPTIDASE INHIBITOR 2) OVERCOME INSULIN RESISTANCE: a)Biguanide : Metformin b)Thiazolidinedione: Pioglitazone  3) MISCELLANEOUS DRUG: a) Alpha glucosidase inhibitor :Acarbose,Voglibose b) Amylin analogue : Pramlintide c) Dopamine agonist :Bromocriptine  INSULIN  Its used in insulin dependent diabetes mellitus  and non-insulin dependent diabetes mellitus Pharmacological action: 1) CARBOHYDRATE METABOLISM: Reduces blood glucose level promote glycogenesis in muscle 2) PROTEIN METABOLISM :  Promote protein synthesis inhibit protein breakdown 3) DECREASE URA OUTPUT FRO

 CORTICOSTEROID: PHARMACOLOGY  Corticosteroid are hormone produced in the cortex of the adrenal gland. CLASSIFICATION: A)  GLUCOCORTICOID: Short acting glucocorticoid:   CORTISOL,HYDROCORTISONE Intermediate acting glucocorticoid: PREDNISOLONE,METHYLPREDNISOLONE Long acting glucocorticoid: BETAMETHASONE,DEXAMETHASONE B ) MINERALOCORTICOID: ALDOSTERONE FLUDROCORTISONE STRUCTURE AND SYNTHESIS: Corticosteroid have cyclopentanoperhydrophenanthrene ring  They are synthesized in the adrenal cortex from cholesterol under the influence of ACTH. Everyday about 10 to 20 mg of hydrocortisone maximum in the early morning and 0.125mg of aldosterone are secreted in response to stress.  MECHANISM OF ACTION :  Steroid hormone enter inside the cell of target organ Hormone bind to specific receptor inside the cytoplasm Activation of steroid  receptor complex  Steroid receptor complex enter inside the nucleus Complex bind to specific site on double stranded nucleic acid Protein synthesis  USES : Cortico