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Modern pharmacology with clinical applications

Description: this book address drugs affecting the autonomic nervous system, cardiovascular system and CNS, drugs used to treat inflammatory disorders, chemotherapy, drugs affecting the endocrine system and additional, important drugs such as histamines and vitamins.

Author name: Charles R. Craig, Robert E. Stitzel

Number of pages: 832

Language: English

Edition: 5^th edition

ISBN no.: 0316159344, 978-0316159340

Publishing country: USA

DOXACURIUM

Doxacurium  binds competitively to cholinergic receptors on the motor end-plate to antagonize the action of acetylcholine, resulting in a block of neuromuscular transmission (non-depolarizing). This action is antagonized by acetylcholinesterase inhibitors, such as neostigmine. Doxacurium  is a long-acting, nondepolarizing skeletal muscle relaxant. The neuromuscular block produced by doxacurium  may be antagonized by anticholinesterase agents. As with other nondepolarizing neuromuscular blocking agents, the more profound the neuromuscular block at reversal, the longer the time and the greater the dose of anticholinesterase required for recovery of neuromuscular function. Doxacurium  is approximately 2.5 to 3 times more potent than pancuronium and 10 to 12 times more potent than metocurine.

REFERENCE-KD TRIPATHI, JAYPEE BROTHERS MEDICAL PUBLISHERS PVT.LTD 7^TH EDITION, REPRINT 2001,PG NO.:347,352,353.

DOXAZOCIN

The mechanism of action of DOXAZOCIN  selective blockade of the alpha1 (postjunctional) subtype of adrenergic receptors. Studies in normal human subjects have shown that doxazosin competitively antagonized the pressor effects of phenylephrine (an alpha1 agonist) and the systolic pressor effect of norepinephrine.

REFERENCE-KD TRIPATHI, JAYPEE BROTHERS MEDICAL PUBLISHERS PVT.LTD 7^TH EDITION, REPRINT 2001,PG NO.:142,144,565.

DOXEPIN

The acute effects of antidepressant treatments on brain norepinephrine (NE) and serotonin (5-HT) systems cannot account fully for their delayed therapeutic action.  The effects of long-term antidepressant treatment on biogenic amine metabolism and on various indexes of presynaptic and postsynaptic receptor function. In contrast to variable effects on NE and 5-HT turnover and on presynaptic receptor Doxepin treatments produce consistent alterations in a number of measures of postsynaptic amine receptor sensitivity. Longterm treatment of Doxepin  has been found to reduce β-adrenergic sensitivity while enhancing responses to serotonergic and α-adrenergic stimulation, suggesting that modulation of receptor sensitivity may be a mechanism of action common to tricyclic antidepressants, "atypical" antidepressants, monoamine oxidase inhibitors, and electroconvulsive therapy.

REFERENCE-KD TRIPATHI, JAYPEE BROTHERS MEDICAL PUBLISHERS PVT.LTD 7^TH EDITION, REPRINT 2001,PG NO.:458,465.

doxycycline

Doxycycline inhibits bacterial protein synthesis by binding to the 30S ribosomal subunit. Doxycycline has bacteriostatic activity against a broad range of Gram-positive and Gram-negative bacteria.

Among the tetracycline group of compounds, doxycycline  blocked and reversed both spontaneous and interleukin 1β-induced OA-NOS activity in ex vivo conditions. Similarly,  doxycycline inhibited  lipopolysaccharide- and interferon-γ-stimulated iNOS in RAW 264.7 cells in vitro, as assessed by nitrite accumulation. Although both these enzyme isoforms could be inhibited by doxycycline , their susceptibility to this drugs was distinct.

REFERENCE-KD TRIPATHI, JAYPEE BROTHERS MEDICAL PUBLISHERS PVT.LTD 7^TH EDITION, REPRINT 2001,PG NO.:733,735,736,737,738.

Midazolam

Midazolam- it is thought that the action of  benzodiazepenes such as midazolaam are mediated through the inhibitory neurotransmitter gamma-aminobutyric acid(GABA), which is one of the major inhibitory neurotransmitter in the brain. BZD’s increase the activity of  GABA, thereby producing a calming effect, relaxing skeletal muscles and inducing sleep. BZD’s bind to the benzodiazapene site on GABA-A receptors, which potentiates the effect of  GABA by increasing the frequency of chloride channel opening.

Reference: Tripathi K.D; Essentials of Clinical Pharmacology; Jaypee Brothers Medical Publishers; Seventh edition; Page no.378, 383, 405

Miconazole

Miconazole interacts with 14-alpha demethylase, a cytochrome P450 enzyme necessary to convert lanosterol to ergosterol. As ergosterol is an essential component of the fungal cell membrane, inhibition of its synthesis results in increased cellular permeability causing leakage of cellular contents. Miconazol may also inhibit endogeneous respiration, interacts with membrane phospholipids, inhibit the transformation of yeast to mycelia forms, inhibit purine uptake and impaired triglyceride and phospholipid biosynthesis.

Reference: Tripathi K.D; Essentials of Clinical Pharmacology; Jaypee Brothers Medical Publishers; Seventh edition; Page no. 787, 792

Metyrapone

Metyrapone blocks cortisol synthesis by reversibly inhibiting steroid-11 beta hydroxylase. This stimulates ACTH secretion, which in turn increases plasma 11-deoxycortisol levels. It is an adrenal steroid synthesis inhibitor.

Reference: Tripathi K.D; Essentials of Clinical Pharmacology; Jaypee Brothers Medical Publishers; Seventh edition; Page no. 295

Ezetimibe

Ezetimibe inhibits the absorption of cholesterol from the small intestine and decreases the amount of cholesterol normally available to liver cells, leading them to absorb more from circulation and thus lowering levels of circulating cholesterol the exact mechanism is not known, but it appears that ezetimibe blocks the critical mediator of cholesterol absorption the Niemann-Pick C1-like1 (NPC1C1) protein on the gastrointestinal tract epethilial cells as well as hepatocytes, blocks aminopepetidase N, and interrupts a Caveolin 1-Annoxin A2 complex involved in trafficking cholesterol.

Reference: Tripathi KD; Essentials of Clinical Pharmacology; Jaypee Brothers Medical Publishers; seventh edition; Page no: 635

Falodipine

Felodipine decreases arterial smooth muscle contractility and subsequent vasoconstriction by inhibiting the influx of calcium ions through voltage-gated L-type calcium channels. It reversibly competes against nitrendipine and other DHP CCBs for DHP binding sites in vascular smooth muscle and cultured rabbit atrial cells. Calcium ions entering the cell through these channels bind to calmodulin. Calcium-bound calmodulin then binds to and activates myocin light chain kinase (MLCK). Activated MLCK catalyzes the phosphorylation of the regulatory light chain subunit of myocin, a key step in muscle contraction. Signal amplification isachieved by calcium-induced calcium release from the sarcoplasmic reticulum through ryanodine receptors. Inhibition of the initial influx calcium decreases the contractile activity of arterial smooth muscle cells and results in vasodilation. The vasofilatory effects of felodipine result in an overall decrease in blood pressure. Felodipine may be used to treat mild to moderate essential hypertension.

Reference: Tripathi KD; Essentials of Clinical Pharmacology; Jaypee Brothers Medical Publishers; seventh edition; Page no:

Febuxostat

Febuxostat is a non-purine-selective inhibitor of xanthine oxidase. It works by non-competitively blocking the molybdenum pterin center which is the active site on xanthine oxidase. Xanthine oxidase is needed to successively oxidase both hypoxanthine and xanthine to uric acid. Hance, febuxostat inhibits xanthine oxidase, therefore reducing production of uric acid. Febuxostat inhibits both oxidised as well as reduced form of xanthine oxidase because of which febuxostat can't be easily displaced from the molybdenum pterin site.

Reference: Tripathi KD; Essentials of Clinical Pharmacology; Jaypee Brothers Medical Publishers; seventh edition; Page no: 213

Exenatide

Exenetide is a functional analog of the human incretin glucagon-like peptide-1(GLP-1). Incretin enhance glucose-dependent insulin secretion and exhibit other antihyperglycemic actions following their release into the circulation from the gut. The GLP-1 system increases insulin secretion only in the presence of elevated plasma glucose levels, avoiding inappropriately high insulin levels during fasting. The drug also moderates peak serum glucagon levels during hyperglycemic periods following meals, but does not interfere with glucagon release in response to hypoglycemia. Secondary effects to drug administration reduces the rate of gastric emptying and decreases food intake, mitigating the potential severity of hyperglycemic events after meals.

Reference: Tripathi KD; Essentials of Clinical Pharmacology; Jaypee Brothers Medical Publishers; seventh edition; Page no: 270

Title -Principles of pharmacology

AUTHOR- HL Sharma, K.K sharma

Edition - Third

Publisher - Paras Medical Publisher

ISBN NO. - 9788181914644

Length -995

Description -This textbook primarily target towards undergraduate medical students special topics such as pediatrics and geriatric pharmacology and pharmacology of radio contact media and drug schedules have been included. The strength of this book lies in the topic in general pharmacology.

Language -English

Publishing country - U. S

Publishing Year - 2017

Title - Pharmacology For Medical Graduate

Author-Tara Shanbhagy,  Smita Shenoy

Edition - Third

Publisher - Elsevier Health. INR

ISBN NO. - 9788131242391

Length - 452

Description - Each chapter in this book presents a therapeutic problem with physiocial or biochemical system, followed by a discussion of physiology and pathophysiology of the system.

Language - English

Publishing country - New York

Publishing Date -10 Oct 2015

Title - Pharmacology success

Author- Ray A. Hargrove Huttel, Kathryn Cadenhead Colgrove

Edition - Second

Publisher - F. A Davis Company

ISBN NO. -  928-0803639058 , 928-0803639058

Length - 512

Description - Each chapter in this book presents a clinical vignette illustrating a Therapeutic problem within a physiologic or biochemical system ,followed by a discussion of the biochemistry, physiology and pathophysiology of the system.

Language - English

Publishing country - New York

Goodman and Gilmans: The Pharmacology Base of Therapeutics

Title - Goodman and Gilmans The Pharmacology Base of Therapeutics

Author - Alfred Gillan Sr., Louis S. Goodman

Edition -Thirteenth

Publisher- Mc Craw Hill education

ISBN NO. - 978-1259584739, 978-1259584732

Length - 1419

Description - Goodman and Gilman describes the action and uses of therapeutic agents in relation to physiology and pathophysiology. It provide a clear understanding of the drugs essential to preventing,  diagnosing and treating disease.

Language - English

Publishing country - New York

Rang and Dales Pharmacology

Title - Rang and Dales pharmacology

Author - H. P Rang, M. Maureen Dale

Edition - seventh, reprint

Publisher -Elsevier / Churchill living stone, 2012

ISBN NO. - 9780702053627

Length - 777 Pages

Description - rang and dales pharmacology provides knowledge of pharmacology course and provides a clear and approach to the analysis therapeutic agents at the cellular and molecular level through detailed diagrams.

Language - English

Publishing country - London

mechanism of action of metamizol

•  metamizole is a anti inflammatory drug.
•  basic machanism of action of metomizol is yet unknown.
•  some people have noted that inhibiting brain and prostaglandin [fat life moleculars that are involved   in inflamation, pain, and fever]synthesis might be involved.
•  recantlly researchers gave potential mechanism involving metamizole being a prodrug.

reference:Tripathi K.D., “Essentials of Medical Pharmacology”, Jaypee brothers medical publishers, Seventh edition, New Delhi, page no.203.