Phosphodiesterase inhibitors

Phosphodiesterase inhibitors work by preventing the breakdown of cyclic nucleotides like cAMP and cGMP. There are 12 families of PDE enzymes that are involved in breaking down these second messenger molecules. Selective PDE inhibitors have been developed that target specific PDE families for conditions like erectile dysfunction, pulmonary hypertension, heart failure, and asthma. Future research is exploring more selective PDE inhibitors for diseases including sepsis, female sexual dysfunction, cardiovascular issues, and neurological disorders. Read less

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This document summarizes different drugs used for treating diabetes. It discusses the types of diabetes, mechanisms and types of insulin preparations including rapid-acting, intermediate-acting, and long-acting insulins. It also covers oral antidiabetic drugs like sulfonylureas, meglitinides, DPP-4 inhibitors, metformin, thiazolidinediones, alpha-glucosidase inhibitors, and SGLT-2 inhibitors; describing their mechanisms of action, pharmacokinetics and adverse effects. It concludes by listing common oral hypoglycemic agents and their usual daily doses and frequencies.

Piracetam was first synthesized in 1964 and launched clinically in the early 1970s. It has a dual mode of action involving neuroplasticity and anticonvulsant effects. Piracetam has 100% bioavailability and a half life of 4-5 hours, being excreted through urine. Its indications include cognitive disorders like dementia, hypoxia, dysgraphia, vertigo, dyslexia, and sickle cell anemia. The starting adult oral dose is 800mg twice daily, with pediatric dosing ranging from 400mg twice daily to 1 teaspoon 3-4 times daily depending on age.

Oral hypoglycemic agents are classified based on their mechanism of action. Sulfonylureas work by blocking potassium channels in pancreatic beta cells, increasing calcium influx and insulin secretion. Meglitinides like repaglinide have a similar quick-acting mechanism. DPP-4 inhibitors like sitagliptin increase GLP-1 and GIP action. Biguanides like metformin activate AMPK, suppressing glucose production and enhancing uptake. Thiazolidinediones like pioglitazone activate PPARγ, enhancing insulin sensitivity. Other agents include alpha-glucosidase inhibitors, amylin analogues, and SGLT2 inhibitors. While effective at lowering blood glucose,

This document discusses antiarrhythmic drugs used to treat irregular heart rhythms or arrhythmias. It describes the mechanisms that can cause arrhythmias such as enhanced pacemaker activity, after-depolarizations, and reentry. It then covers the major classes of antiarrhythmic drugs including class I sodium channel blockers, class II beta blockers, class III potassium channel blockers, and class IV calcium channel blockers. Specific drugs from each class are discussed, how they work, their therapeutic uses, and potential side effects. Common arrhythmias like atrial fibrillation, atrial flutter, and ventricular tachycardia are also defined.

Digoxin toxicity is caused by digoxin, a plant-derived cardiac glycoside used to treat heart conditions. It has a narrow therapeutic window, so toxicity can easily occur. Common signs of toxicity include arrhythmias such as heart block or tachycardia. Management involves discontinuing digoxin, treating arrhythmias, correcting electrolyte imbalances, and using digoxin antibody fragments for severe toxicity. Factors like renal impairment, hypokalemia, and drug interactions can precipitate or worsen digoxin toxicity.

Dr. D. K. Brahma discusses antiplatelet drugs, which interfere with platelet function and are useful for preventing thromboembolic disorders. The document defines antiplatelet drugs and describes the role of platelets in thrombosis formation. It then discusses the mechanisms of various antiplatelet drugs including aspirin, dipyridamole, ticlodipine, clopidogrel, prasugrel, and GPIIb/IIIa receptor antagonists like abciximab. The uses of these antiplatelet drugs for conditions like heart attacks, strokes, angioplasty and stents are summarized.

This ppt will discuss role of oral hypoglycemic agents in management of Diabetes mellitus. Your comments please

Hello friends. In this PPT I am talking about antiepileptic drugs. If you like it, please do let me know in the comments section. A single word of appreciation from you will encourage me to make more of such videos. Thanks. Enjoy and welcome to the beautiful world of pharmacology where pharmacology comes to life. This video is intended for MBBS, BDS, paramedical and any person who wishes to have a basic understanding of the subject in the simplest way.

This ppt is important for UG MBBS, PG Pharmacology and any other healthcare person interested in Antiplatelet drugs.

Electrophysiology of the heart Arrhythmia: definition, mechanisms, types Drugs :class I, II, III, IV Guide to treat some types of arrhythmia

This document provides an overview of stroke, including its definition, types, risk factors, pathophysiology, clinical presentation, diagnosis, treatment both initially and long-term, and management considerations. The two main types of stroke are ischemic (87%) and hemorrhagic (13%). Risk factors include modifiable factors like hypertension and non-modifiable factors like age. Treatment involves stabilizing the patient, diagnosing with imaging, treating the cause, preventing complications, and long-term prevention with medications like aspirin, statins, and anticoagulants depending on the cause of stroke.

Serotonin pharmacology with receptors, agonists and antagonists on these receptors and drug therapy of migraine covered in this lecture

Certain drugs like reserpine, tetrabenazine, haloperidol, and metoclopramide can deplete dopamine or block dopamine receptors, leading to a parkinsonian syndrome within 3 months. The syndrome is symmetric with mild tremor and usually resolves after withdrawing the causative drug. For treatment, antimuscarinic agents are preferred over levodopa, which may worsen symptoms if the neuroleptic drug is continued. MPTP, through its metabolite MPP+, can selectively damage cells in the substantia nigra by inhibiting mitochondrial complex I, leading to parkinsonism through striatal dopamine depletion. MPTP parkinsonism was discovered in individuals who self-administered M

This document discusses paracetamol (acetaminophen) poisoning. It covers the introduction, metabolism, mechanism of toxicity, clinical features, diagnosis, management, postmortem findings, and medicolegal importance of paracetamol poisoning. Paracetamol is metabolized in the liver and can cause toxicity when levels of its toxic metabolite NAPQI exceed levels of glutathione in the liver, leading to liver and sometimes kidney damage. Management involves gastric decontamination and use of the antidote N-acetylcysteine to prevent binding of NAPQI if administered early. Fulminant liver failure may require liver transplantation.

Dopamine is a neurotransmitter that binds to dopamine receptors and influences movement, memory, reward, behavior and other functions. It is synthesized from tyrosine and transported through dopaminergic pathways in the brain. There are two families of dopamine receptors, D1-like and D2-like, which are G protein-coupled receptors that either activate or inhibit the enzyme adenylyl cyclase. Dopamine receptor dysfunction is implicated in diseases like Parkinson’s, schizophrenia and addiction. Dopamine agonists mimic dopamine while antagonists block dopamine receptors.

Educational and therapeutic topic on asthma for MBBS and MD pharmacology students. other students like BDS , BHMS, BAMS etc can use for knowledge. and academic purpose.

Recent advances in the management of parkinson disease

This document discusses Parkinson’s disease (PD), including: – PD is the second most common neurodegenerative disease, characterized by loss of dopaminergic neurons. – Prevalence studies in India show crude prevalence rates ranging from 14-328 per 100,000 depending on the region. – Clinical features include tremors, bradykinesia, muscle rigidity, and postural instability. – UK PDS criteria are used for diagnosis of PD and include supportive criteria like unilateral onset and excellent response to levodopa. – Pharmacological therapies aim to reduce motor symptoms and include levodopa, dopamine agonists, MAO-B inhibitors, and others. Treatment depends on disease stage and goals

This document discusses cardiac glycosides, which are drugs that increase the force of contraction of the heart without increasing oxygen consumption. It specifically focuses on digitalis, which is derived from foxglove. Digitalis increases myocardial contractility in a failing heart, improving cardiac output. It acts by increasing the intracellular calcium levels in cardiac muscle cells. The document covers the chemistry, pharmacology, mechanisms of action, effects on cardiac electrophysiology, pharmacokinetics, uses, and adverse effects of digitalis and other cardiac glycosides in detail over several pages.

Prostaglandin biosynthesis & therapeutic uses of prostaglandin analouges

This document discusses prostaglandin biosynthesis and therapeutic uses of prostaglandin analogues. It describes several prostaglandin analogues including misoprostol, gemeprostol, alprostadil, epoprostenol, latanoprost, carboprost, and dinoprostone. It details their clinical uses such as preventing NSAID-induced ulcers, therapeutic abortion, labor induction, maintaining ductus arteriosus patency in neonates, treating pulmonary hypertension, reducing intraocular pressure, postpartum hemorrhage, and termination or induction of pregnancy. The document also notes some adverse effects and contraindications of the prostaglandin analogues.

This document provides an overview of the pharmacology of dopamine. It discusses dopamine synthesis, receptors, pathways in the brain, and the role of dopamine in conditions like Parkinson’s disease, schizophrenia, and addiction. Dopamine is synthesized from phenylalanine and tyrosine and acts on D1-like and D2-like receptors in the mesolimbic, mesocortical, and nigrostriatal pathways. Imbalances in dopaminergic signaling are implicated in disorders such as Parkinson’s, schizophrenia, and ADHD. Drugs that modify dopamine transmission are used to treat these conditions.

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Similar to Phosphodiesterase inhibitors

This document provides an overview of phosphodiesterases (PDEs), which break down cyclic nucleotides and regulate cell signaling. It discusses the 12 PDE enzyme families, their tissue distribution and substrates. Both non-selective and selective PDE inhibitor drugs are classified, along with their mechanisms and clinical uses in conditions like asthma, heart failure and erectile dysfunction. Emerging research on PDE inhibitors for diseases like Alzheimer’s, stroke and female sexual dysfunction is also summarized.

Phosphodiesterase enzymes (PDEs) regulate intracellular levels of cyclic nucleotides and cell function. There are 11 PDE families with over 50 isoforms. PDE inhibitors prevent degradation of cAMP and cGMP to modulate signal transduction. PDE5 inhibitors like sildenafil, tadalafil, and vardenafil are used to treat erectile dysfunction by prolonging cGMP signaling. They may have other uses such as for pulmonary hypertension, heart failure, and female sexual dysfunction. PDE5 inhibitors are contraindicated with nitrates due to risk of hypotension and require monitoring for potential side effects and drug interactions.

Phosphodiesterase (PDE) enzymes break down cyclic nucleotides like cAMP and cGMP. There are many families of PDEs that regulate these second messenger molecules in different tissues. PDE inhibitors prevent the inactivation of cAMP and cGMP, prolonging their cell signaling effects. Some PDE inhibitors are used to treat conditions like pulmonary hypertension and erectile dysfunction by increasing cyclic nucleotide levels. The document then provides examples of specific PDE inhibitors and their therapeutic applications.

This document discusses phosphodiesterases (PDEs) as drug targets. PDEs play a major role in cell signaling by regulating levels of cyclic nucleotides like cAMP and cGMP. PDE5 inhibitors like sildenafil (Viagra), vardenafil (Levitra), and tadalafil (Cialis) are approved for treating erectile dysfunction by inhibiting PDE5. This increases cGMP levels and blood flow to the penis. Side effects include headaches and flushing. Care must be taken with drug interactions and in patients using nitrates. Selective inhibition of different PDEs is an area of research for conditions like asthma, COPD, heart failure and inflammation. Effective assays are needed to

This document discusses drugs used to treat erectile dysfunction (ED). There are five oral medications that are phosphodiesterase type 5 (PDE5) inhibitors – sildenafil, tadalafil, vardenafil, avanafil, and alprostadil. PDE5 inhibitors work by inhibiting the breakdown of cyclic guanosine monophosphate (cGMP), allowing more blood flow to the penis. Alprostadil is a prostaglandin E1 that works locally in penile tissue through an unknown mechanism. Common side effects of PDE5 inhibitors include headache, flushing and nasal congestion. Proper timing of medication and sexual activity is important.

The document discusses drugs used to treat erectile dysfunction (ED). There are five oral phosphodiesterase type 5 inhibitors (PDE5Is) including sildenafil, tadalafil, vardenafil, avanafil, and alprostadil. PDE5Is work by inhibiting the PDE5 enzyme and increasing blood flow to the penis to facilitate erection. Alprostadil is a prostaglandin E1 injection or suppository that works locally in the penis. All drugs have similar side effects like headaches and flushing but differ in how long their effects last and if they interact with food. Proper use and understanding the mechanisms and pharmacokinetics of these drugs is important for

This document discusses drugs used to treat erectile dysfunction. It begins with an introduction to erectile dysfunction and benign prostatic hyperplasia. The main drugs discussed are PDE5 inhibitors including sildenafil, tadalafil, vardenafil and avanafil, as well as alprostadil. These drugs work by inhibiting the PDE5 enzyme and increasing levels of cGMP in the penis to produce an erection. The document provides details on the mechanism of action, pharmacokinetics, molecular structures, adverse effects and uses of these erectile dysfunction drugs.

PDE-5 inhibitors like sildenafil revolutionized erectile dysfunction treatment by increasing cGMP. They work by inhibiting the PDE-5 enzyme, allowing cGMP to enhance erectile function with sexual stimulation by causing smooth muscle relaxation and blood flow into the penis. Common side effects include headache and flushing. Serious risks include myocardial infarction, especially with underlying heart conditions. PDE-5 inhibitors are contraindicated with nitrates due to the risk of severely low blood pressure. Dosage and drug interactions vary between PDE-5 inhibitors.

This document discusses erectile dysfunction and oral phosphodiesterase type 5 (PDE5) inhibitors for its treatment. It provides information on: 1) Currently available PDE5 inhibitors like sildenafil and those in development like tadalafil and vardenafil which are potent and selective for the PDE5 isoenzyme. 2) The mechanism of action of PDE5 inhibitors in inhibiting the PDE5 isoenzyme and increasing cGMP levels in the corpus cavernosum for improved erectile function. 3) Clinical trial results showing PDE5 inhibitors like tadalafil can provide successful intercourse for over 24 hours, improving erections, with a generally well tolerated safety profile

Phosphodiesterase-5 (PDE-5) inhibitors like sildenafil revolutionized erectile dysfunction treatment by inhibiting the PDE-5 enzyme and increasing cGMP levels. They work by enhancing smooth muscle relaxation in the penis during sexual stimulation. Common side effects include headache, flushing and stomach pain. Use with nitrates is dangerous and may cause low blood pressure or heart attack. Proper dosing and not exceeding one pill per day is important. PDE-5 inhibitors have been safely used to treat other conditions like pulmonary hypertension as well.

This slides were prepared for My Post Graduation activities and seminar most of them are from sources such as slide share, Pub Med, Standard Pharmacology Textbooks . Feel free to comment/correct/suggest Thank you

Tadalafil is a phosphodiesterase type 5 inhibitor used to treat erectile dysfunction. It has a longer duration of action than other PDE5 inhibitors like sildenafil and vardenafil, remaining effective for 36 hours after dosing. Studies show tadalafil significantly improves erectile function in men with diabetes and may provide additional benefits like improved beta-cell function and metabolic syndrome. Tadalafil is also being investigated for treating conditions like pulmonary arterial hypertension.

Emergency drugs used_in_o.s.___common_drug_interactions_in_o.s._practice__ora.

This document discusses various emergency drugs used in oral surgery. It provides classifications of emergency drugs as injectables, non-injectables, primary and secondary advanced cardiac support drugs. It then discusses 20 individual emergency drugs in detail including their introduction, indications, contraindications, trade names, dosages and adverse effects. The drugs discussed include adrenaline, atropine, dopamine, metoclopramide, phenaramine maleate, hydrocortisone, dexamethasone, diazepam, fortwin-pentazocin, furosemide, pancuronium bromide, styptochrome, and ethamsylate.

Sildenafil citrate, commonly known as Viagra, was originally developed as a treatment for hypertension and angina but was found to cause unwanted side effects of prolonged erections. It works by inhibiting phosphodiesterase type 5, allowing for increased blood flow to cause an erection. It is prescribed for erectile dysfunction and pulmonary hypertension. Common side effects include headache, flushing, and nasal congestion. It should not be taken with nitrates due to the risk of dangerously low blood pressure.

A 59-year-old male presented with cough, expectoration, fever for 2 days, and shortness of breath on exertion for 3 days. He has a history of anemia, congestive heart failure, and chronic liver disease with ascites. On examination, he had a temperature of 101F, oxygen saturation of 90%, and bilateral wheezing. Laboratory tests showed elevated white blood cell count and liver enzymes. He was diagnosed with lower respiratory tract infection and pneumonia. He was treated with antibiotics, nebulizers, steroids, and other medications. The pharmacist intervened due to some drug interactions and provided counseling to the patient.

Dr Himali Perera Consultant Venereologist Coordinator Training and Capacity Building, National STD /AIDS Control Programme

This document provides an overview of schizophrenia and antipsychotic drugs. It discusses the history and classification of schizophrenia, as well as hypotheses for its mechanisms. It then describes the classification, mechanisms of action, uses, and adverse effects of various antipsychotic drugs, including first-generation antipsychotics/neuroleptics and newer second-generation atypical antipsychotics. Recent research advances discussed include studies on adjunctive treatments using drugs like raloxifene, N-acetyl cysteine, and estrogen to improve outcomes of antipsychotic treatment.

This document provides an overview of anti-hypertensive medications. It discusses the different classes of anti-hypertensive drugs including thiazide diuretics, ACE inhibitors, ARBs, calcium channel blockers, beta blockers, and other classes. For each class, it covers indications, mechanisms of action, pharmacokinetics, dosing, adverse effects, drug interactions and other key points. The document is intended as an educational presentation on the treatment of hypertension with pharmacological therapies.

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More from Elza Emmannual

Transgenic animals are created through recombinant DNA technology by inserting foreign genes into the animal’s genome. This is done to improve livestock, use animals as bioreactors for pharmaceutical production, and for research purposes. The main methods of creating transgenic animals are DNA microinjection, retrovirus-mediated gene transfer, embryonic stem cell transfer, and sperm-mediated gene transfer. Examples include transgenic cows that produce more nutritious milk, pigs with genes to reduce environmental pollution, and mice used widely as model organisms. While transgenic animals have benefits, there are also ethical concerns regarding animal welfare and unintended environmental impacts.

This document provides information about guinea pigs, hamsters, and rabbits as experimental animals. It discusses their biological characteristics, handling techniques, uses in research, and methods of injection and blood collection. Guinea pigs are herbivorous and ideal models for studying various diseases. Hamsters have cheek pouches and are used for transplant and virus research. Rabbits are docile, have simple cardiac tissues, and are widely used in pharmaceutical and toxicology testing. Proper animal handling and use of appropriate injection sites and needle sizes are emphasized.

This document summarizes various inotropic drugs used to increase cardiac contractility including cardiac glycosides like digoxin, catecholamines like dopamine and dobutamine, phosphodiesterase inhibitors like milrinone, and calcium sensitizers like levosimendan. It provides details on their mechanisms of action, pharmacokinetics, uses, dosages, and side effects. The document focuses on the inotropic and hemodynamic effects of these drugs and their roles in treating low cardiac output states and heart failure.

The document discusses the history, clinical overview, pathophysiology, neurochemistry, and treatment of Alzheimer’s disease. It notes that Dr. Alois Alzheimer first identified the disease in 1906 in a patient named Auguste Deter. The clinical features include progressive loss of memory and cognitive decline. Pathologically, it involves amyloid plaque formation and neurofibrillary tangles. Current treatment focuses on augmenting cholinergic transmission using cholinesterase inhibitors as first-line treatment, along with memantine which is a NMDA receptor antagonist. Lifestyle changes and antioxidants may also help slow progression.

The document outlines the International Council for Harmonisation (ICH) Good Clinical Practice (GCP) guidelines, which provide an international ethical and quality standard for clinical trials involving human subjects. The guidelines seek to protect the rights, safety, and well-being of trial subjects, and help ensure that clinical data is credible. They were established in 1996 and harmonize standards across the European Union, Japan, and United States. The ICH GCP guidelines outline principles for ethical conduct of research, risk identification, informed consent, qualifications of investigators and staff, monitoring, record keeping, and roles of sponsors and investigators.

Monoclonal antibodies are produced by a single clone of B lymphocytes and are directed against a single antigenic determinant. They are made using hybridoma technology, which involves fusing B lymphocytes with myeloma cells to produce hybridomas that secrete antibodies against a specific antigen. Georges Köhler and Cesar Milstein developed this technique in 1975 and won the Nobel Prize in 1984. Monoclonal antibodies are classified as murine, chimeric, humanized, or human depending on their source and can be armed or unarmed. They have various therapeutic uses for treating cancer, autoimmune diseases, and asthma through mechanisms like ADCC, CDC, and immunomodulation.

This document discusses GABA modulators. It begins by introducing GABA as the major inhibitory neurotransmitter in the mammalian central nervous system. It then discusses the three main types of GABA receptors: GABAA, GABAB, and GABAC. The GABAA receptor is an ionotropic receptor that opens chloride channels, while the GABAB receptor is a metabotropic G protein-coupled receptor. The document outlines the biosynthesis and mechanism of action of the different GABA receptor subtypes. It also discusses several drugs that act on GABA receptors, including benzodiazepines, barbiturates, baclofen, vigabatrin, tiagabine, valproate

Fibrinolytics such as streptokinase, urokinase, alteplase, reteplase, and tenecteplase activate the natural fibrinolytic system and lyse thrombi to recanalize occluded blood vessels. They are used to treat myocardial infarction, deep vein thrombosis, pulmonary embolism, and peripheral arterial occlusion. Antifibrinolytics like epsilon amino-caproic acid and tranexamic acid inhibit plasminogen activation and clot dissolution to prevent or control bleeding caused by fibrinolytics or surgical procedures. The timing of fibrinolytic administration is critical for heart attack treatment, with better outcomes seen within 1-3 hours of symptom onset.

This document provides information on general anaesthetics including their cardinal features, history, stages of anaesthesia, measurement of potency, mechanisms of action, classification, inhalational anaesthetics, intravenous anaesthetics, and conscious sedation. It discusses key figures and discoveries in the history of anaesthesia such as Humphry Davy, Horace Wells, William Morton, and John Snow. It also summarizes the stages of anaesthesia, factors that determine anaesthetic potency including oil-gas and blood-gas partition coefficients, and the pharmacokinetics and mechanisms of action of various inhalational and intravenous anaesthetic agents.

The document discusses cholinergic transmission in the nervous system. It describes how acetylcholine (ACh) acts as a neurotransmitter at neuromuscular junctions and autonomic ganglia. It outlines the synthesis, storage, release and termination of ACh through choline transporters and choline acetyltransferase. Various toxins that affect cholinergic transmission are also mentioned. The document further discusses muscarinic and nicotinic receptors, and the actions of ACh through these receptors in different organ systems. Finally, it covers cholinomimetic drugs, anti-choline esterase drugs and their mechanisms and uses, as well as treatment for organophosphate poisoning.

The document discusses various classes of antifungal drugs including their mechanisms of action, spectrum of activity, pharmacokinetics and clinical uses. It describes polyenes like amphotericin B and nystatin, azoles including imidazoles and triazoles, allylamines like terbinafine, antimetabolites like flucytosine and griseofulvin. It also discusses newer antifungals like echinocandins including caspofungin.

Left heart failure can present with several symptoms: 1. Dyspnea that progresses from exertional to at rest due to decreased lung compliance, increased airway resistance, and respiratory muscle fatigue. 2. Orthopnea relieved by sitting up due to fluid redistribution increasing pulmonary capillary pressure and elevating the diaphragm. 3. Paroxysmal nocturnal dyspnea, episodes of dyspnea and coughing at night even when sitting up due to depressed respiratory center and reduced adrenal stimulation at night.

A 63-year-old man presented with right abdominal pain. He was diagnosed with subhepatic appendicitis based on ultrasound findings and treated conservatively. When his pain did not improve with antibiotics, he was admitted. He later developed right epididymitis, pneumonia, and an abdominal abscess. Exploratory surgery found necrosis of right cord structures and an abscess, which were treated by removing the infected tissue. The patient was discharged after his wound had fully healed.

This document describes the case of a newborn baby boy delivered via normal vaginal delivery at 40 weeks gestation who experienced neonatal hypoglycemia. He was found to have a blood glucose of 40 mg/dL at 14 hours of life. He was treated with IV dextrose but had issues maintaining peripheral IV access, with four cannulas needing placement within 48 hours. His blood glucose levels fluctuated before being successfully breastfed on the sixth day of life and discharged on the seventh day.

This document summarizes the mechanisms of action of various protein synthesis inhibitors in bacteria. It discusses how these inhibitors target different stages of mRNA translation in the bacterial ribosome, including initiation, elongation, and termination. Some key inhibitors mentioned are aminoglycosides, spectinomycin, linezolid, tetracyclines, chloramphenicol, macrolides, clindamycin, streptogramins, and mupirocin. They act by binding to different sites on the bacterial ribosomal subunits and disrupting proper formation of initiation complexes, misreading of mRNA, peptide bond formation, and translocation during translation.

This document discusses the mechanisms of action of antimicrobial drugs. It explains that antimicrobials work by inhibiting microbial growth and multiplication through various targets, including the cell wall, cell membrane, protein synthesis, intermediary metabolism, and nucleic acid metabolism. It provides examples of specific drugs that act on these various targets, such as betalactams which inhibit cell wall synthesis, polymixins which disrupt the cell membrane, and fluoroquinolones which inhibit DNA gyrase. The document aims to describe how antimicrobials are able to selectively kill pathogens while sparing host cells.

This document discusses different types of alpha adrenergic blockers, including their classification, mechanisms of action, effects, uses, and examples. It covers reversible nonselective alpha blockers like phentolamine and tolazoline, irreversible nonselective blockers like phenoxybenzamine, and reversible selective alpha-1 blockers like prazosin. These drugs cause vasodilation and reduce blood pressure by blocking alpha receptors. They are used to treat conditions like hypertension, Raynaud’s disease, prostate issues, and pheochromocytoma. The document also briefly mentions alpha-2 blockers, ergot alkaloids, and other miscellaneous agents that have alpha blocking properties.

This document discusses drug interactions and teratogenicity. It defines drug interaction as the modification of response to one drug by another when administered simultaneously. Drug interactions can occur via pharmacokinetic or pharmacodynamic mechanisms. Teratogenicity refers to a drug’s ability to cause fetal abnormalities. Several factors determine a drug’s teratogenic effects, including the developmental stage of exposure and dose. Common teratogens include alcohol, warfarin, isotretinoin and thalidomide. Thalidomide caused over 10,000 birth defects in the 1960s, demonstrating the need for careful preclinical testing of drugs in pregnancy.

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This presentation, authored by Dr. Faiza, Assistant Professor of Physiology at CIMS Multan, delivers an in-depth analysis of heart valves, heart sounds, valvular heart diseases, and congenital heart defects. It begins by distinguishing between normal and abnormal heart sounds, elucidating the timing and causes of the four heart sounds—S1, S2, S3, and S4—and their clinical significance. Detailed explanations are provided on the auscultation sounds that define conditions such as mitral stenosis, mitral insufficiency, aortic stenosis, and aortic insufficiency, with a focus on how these pathological changes affect cardiac mechanics and blood pressure. The presentation delves into abnormal heart sounds, known as murmurs, categorizing them by their causes, which include valvular lesions, rheumatic fever, aging, congenital heart diseases, viral infections during pregnancy, and hereditary factors. It explores the various types of murmurs, their timing within the cardiac cycle, and their association with specific valvular heart diseases such as stenosis and regurgitation. The intricate relationship between systolic and diastolic murmurs and conditions like anemia and ventricular septal defects is also highlighted. Further, the presentation covers the pathophysiology of congenital heart diseases, offering a comprehensive review of conditions such as Tetralogy of Fallot and Patent Ductus Arteriosus. It explains the mechanisms of these diseases, their impact on cardiac function, and the clinical manifestations observed in affected individuals. The physiological adjustments of the circulatory system during exercise in patients with valvular lesions are discussed, emphasizing the reduced cardiac reserve and the risk of acute pulmonary edema. Special attention is given to the compensatory mechanisms of the heart in response to valvular diseases, including the development of concentric and eccentric hypertrophy, increased venous return, and the eventual progression to heart failure. The presentation also examines rheumatic valvular lesions, aging-related aortic stenosis, and the specific challenges posed by these conditions, such as reduced stroke volume and increased metabolic demand. This thorough exploration of heart sounds, valvular diseases, and congenital defects is designed to enhance understanding and clinical acumen, making it a valuable resource for medical students, healthcare professionals, and educators in the field of cardiology and physiology.

Certainly! The cranial nerve examination is a crucial part of assessing neurological function. Let’s break it down step by step: Gather Equipment: Pen torch Snellen chart Ishihara plates Ophthalmoscope and mydriatic eye drops (if needed) Cotton wool Neuro-tip Tuning fork (512 Hz) Glass of water General Inspection: Observe the patient for any signs of underlying pathology: Speech abnormalities (glossopharyngeal or vagus nerve issues) Facial asymmetry (facial nerve palsy) Eyelid abnormalities (ptosis may indicate oculomotor nerve problems) Pupillary abnormalities (mydriasis in oculomotor nerve palsy) Strabismus (may indicate oculomotor, trochlear, or abducens nerve palsy) Note any limb abnormalities (spasticity, weakness, wasting, tremor, fasciculation) that suggest neurological syndromes. Look for walking aids (associated with various neurological conditions) #health #medicine # cranial #brain health #cranial nerves #examination # tools # nerves # explore

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Prostatitis Severity- How to Determine if You Have Mild Symptoms.pptx

Do you know how to determine if you have mild prostatitis symptoms. Whether it is mild or severe, natural medicine Diuretic and Anti-inflammatory Pill can help you get rid of it.

STRATEGIES FOR RATIONALISING/REDUCING CAESAREAN SECTION RATE BY USE OF “SION .

The journey to reduce/rationalise the C-section rate started in June 2023 and it’s an ongoing study been carried out at #SionHospital #LTMMC Mumbai. It’s going to revolutionise the journey of motherhood for safer, predictable maternal and fetal outcome. The SION model is a structured and networked approach to promoting vaginal deliveries. By integrating education, support, policy implementation, and continuous improvement, it aims to enhance maternity care and reduce unnecessary C-sections through collaborative efforts among healthcare providers and patients. Encouraging trials of labor after previous C-sections (TOLAC) and fostering a multidisciplinary team approach in maternity care are crucial. Regular training for healthcare providers and establishing supportive hospital policies further promote vaginal births.

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