Medical. Pharmacology. Seventh Edition. KD TRIPATHI MD. Ex-Director- Professor and Head of Pharmacology. Maulana Azad Medical College and associated. (tripathi) essentials of medical pharmacology 1, Pages··48 KD TRIPATHI MD. Ex-Director-Professo. Load more similar PDF files. PDF Drive. pharmacologyunitedvrgpdf&ved=2ahUKEwj2-pePrMfbAhXbdn0KHU3.

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    The subject is highly dynamic. Developments are occurring both in defining molecular targets for drug action and finding targeted drugs, as well as in accruing credible evidence regarding the impact of different treatment modalities on therapeutic outcomes. These efforts have begun to crystallize into evidence based medicine and clear cut therapeutic guidelines. The present edition endeavours to amalgamate the developments with the core content of the subject. While the primary theme of the book outlined in the preface to the first edition is maintained, the successive editions have become more descriptive and more comprehensive. In preparing this edition, all chapters have been revisited and extensively updated. Recent innovations have been highlighted, notably in antidiabetic drugs, psychopharmacological agents, antiplatelet drugs, treatment of inflammatory bowel disease, drugs affecting renin-angiotensin system, anticoagulants, antiviral including anti-HIV drugs, targeted anticancer drugs, etc. New drugs released in India have been included. Infrequently used drugs and those not available in India are presented briefly in extract type. Important points are summarized in boxes. Use of distinctive headings in a hierarchical order makes the text highly systematic. Representative trade names of drugs with available dosage forms are mentioned. Due emphasis is given to diseases prevalent in India and similar tropical countries, along with their current drug therapy. The most important objective of medical pharmacology is to train medical students in therapeutic decision making according to specific clinical problems in individual patients.

    Carries greater risk of anaphylactic reaction p. Intra arterial injection B. Intrathecal injection C. Intravenous injection D. Intramuscular injection p. Weakly basic drugs B.

    Weakly acidic drugs C. Strong electrolytes D. Nonpolar drugs p.

    KD Tripathi 7th Edition Essentials Of Medical Pharmacology

    Passive diffusion B. Facilitated diffusion C. Active transport p. Pinocytosis 2. Is dependent upon metabolic activity of the cell B. Is competitively inhibited by chemically related drugs C. Is affected by extent of ionization of drug molecules D. Exhibits saturation kinetics p.

    Morphine sulfate B. Diclofenac sodium C. Hyoscine hydrobromide D. Quinine dihydrochloride p. Atropine sulfate B. Chloroquine phosphate C. Ephedrine hydrochloride p. Phenytoin sodium 2. Blood flow through the capillary B. Lipid solubility of the drug C. It is specific B. It is pH dependent C. It is saturable D. It requires metabolic energy p.

    Complexing with the other drug in the intestinal lumen B. Altering gut motility C. Altering gut flora D. Damaging gut mucosa p. Percentage of administered dose that reaches systemic circulation in the unchanged form B.

    Ratio of oral to parenteral dose C. Ratio of orally administered drug to that excreted in the faeces D. Ratio of drug excreted unchanged in urine to that excreted as metabolites p. Is freely water soluble B. Is completely absorbed C. Is incompletely absorbed D. Undergoes little first-pass metabolism p. Molecular weight of the drug B. Site of application C. Lipid solubility of the drug D.

    Nature of the base used in the formulation p. High lipid solubility B.

    Low ionisation at physiological pH values C. High plasma protein binding D. High tissue binding p. Highly lipid soluble drugs B.

    Poorly lipid soluble drugs C. Depot preparations D.

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    Highly plasma protein bound drugs 2. On intravenous injection it produces general anaesthesia for 10 min. Which process is responsible for termination of its action: A. Metabolism in liver B. Plasma protein binding C.

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    Excretion by kidney D. Redistribution p. P-glycoprotein efflux carriers in brain capillary cells B. Tight junctions between endothelial cells of brain capillaries C. Enzymes present in brain capillary walls D.

    All of the above p. It is constituted by tight junctions between the endothelial cells of brain capillaries and the glial tissue B. It allows passage of lipid soluble drugs into the brain C. It limits entry of highly ionized drugs into the brain D. It regulates passage of substances from brain into blood p.

    Are excreted faster in alkaline urine C. Are highly ionized in the gastric juice D. Do not cross blood-brain barrier p. Increases volume of distribution of the drug B. Facilitates glomerular filtration of the drug C. Minimises drug interactions p. Generally makes the drug long acting 2. Contributes to the response at the given moment B.

    Remains constant irrespective of the total drug concentration C.

    Remains constant irrespective of the disease state D. Is not available for metabolism unless actively extracted by the liver p. Activate the drug B. Inactivate the drug C. Convert lipid soluble drugs into nonlipid soluble metabolites D.

    Convert nonlipid soluble drugs into lipid soluble metabolites p. Hydralazine B. Clonidine C. Captopril D. Enalapril p. The prototype member of a class of drugs B. The oldest member of a class of drugs C. An inactive drug that is transformed in the body to an active metabolite D. A drug that is stored in body tissues and is then gradually released in the circulation p. CYP 3A4 B. CYP 2C9 C.

    CYP 2E1 D. CYP 1A2 p. It generates the hepatotoxic metabolite N-acetyl benzoquinone immine from paracetamol B. It is involved in demethylation of codeine into morphine C.

    Its altered form is responsible for poor capacity to hydroxylate many drugs including metoprolol p.

    It is inhibited by quinidine 2. Glucuronidation B. Acetylation C. Methylation p. Glutathione conjugation 2.

    Tolerance B. Physical dependence C. Psychological dependence D.

    Idiosyncrasy p. Glucuronide conjugation B. Oxidation D. Reduction p. Microsomal enzymes B. Nonmicrosomal enzymes C. Both microsomal and nonmicrosomal enzymes p.

    Mitochondrial enzymes 2. A conformational change in the enzyme protein to favour binding of substrate molecules B. Expression of enzyme molecules on the surface of hepatocytes C.

    Enhanced transport of substrate molecules into hepatocytes D. Increased synthesis of enzyme protein p. Phenobarbitone B. Propranolol C. Phenylbutazone D. If you are unable to locate the links, please refresh the page. Read Online. Read online. Please note these are external links and we do not host any downloads on our website. If you are the owner of the content or have disputes regarding the terms, please read our complete Disclaimer page or leave us a message via our Contact Us page.

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    KD Tripathi Pharmacology PDF FREE Download [Direct Link]

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