Receptor antagonist

1. transdermal route(adhesive patches): A transdermal patch is a medicated adhesive patch that is placed on the skin to deliver a specific dose of medication through the skin and into thebloodstream. Often, this promotes healing to an injured area of the body. An advantage of a transdermal drug delivery route over other types of medication delivery such as oral, topical, intravenous, intramuscular, etc. is that the patch provides a controlled release of the medication into the patient, usually through either a porous membrane covering a reservoir of medication or through body heat melting thin layers of medication embedded in the adhesive.

The main disadvantage to transdermal delivery systems stems from the fact that the skin is a very effective barrier; as a result, only medications whose molecules are small enough to penetrate the skin can be delivered by this method. A wide variety of pharmaceuticals are now available in transdermal patch form. e. g scopolamine for motion sickness 2. advantages and disadvantages of sublingual route: advantages-quick onset of action,action can be terminated by spitting out the tablet,bypasses the first pass metabolism,self administration possible.

Disadvantages: not suitable: for irritantand lipid insoluble drugs,for drug with bad smell and taste,in children. 3. NEW DRUG DELIVERY SYSTEM- Drug delivery is the method or process of administering a pharmaceutical compound to achieve a therapeutic effect in humans or animals. Drug release is from: diffusion, degradation, swelling, and affinity-based mechanisms. The innovative delivery of drugs would not only increase safety and efficacy levels but also improve the overall performance of the drug.

It is value-added features for which companies can charge a premium due to the increased convenience they provide to patients. Macromolecular drugs, which are larger compared to conventional therapies, demand superior delivery platforms for greater efficacy. The goal of all sophisticated drug delivery systems, therefore, is to deploy medications intact to specifically targeted parts of the body through a medium that can control the therapy’s administration by means of either a physiological or chemical trigger.

4., bioavailability-In pharmacology, bioavailability (BA) is a subcategory of absorption and is the fraction of an administered dose of unchanged drug that reaches the systemic circulation, one of the principalpharmacokinetic properties of drugs. By definition, when a medication is administered intravenously, its bioavailability is 100%. [1] However, when a medication is administered via other routes(such as orally), its bioavailability generallyTH[›] decreases (due to incomplete absorption and first-pass metabolism) or may vary from patient to patient.

Bioavailability is one of the essential tools in pharmacokinetics, as bioavailability must be considered when calculating dosages for non-intravenous routes of administration. 5. The volume of distribution (VD), also known as apparent volume of distribution, is a pharmacological, theoretical volume that a drug would have to occupy (if it were uniformly distributed), to provide the same concentration as it currently is in blood plasma.

Therefore, if VD is greater, it shows that the drug is more diluted than it should be (in the blood plasma), meaning more of it is distributed in tissue (i.e. not in plasma).

It is defined as the distribution of a medication between plasma and the rest of the body after oral or parenteral dosing. It is defined as the theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired blood concentration of a drug. [1][2] In rough terms, drugs with high lipid solubility (non-polar), low rates of ionization or low plasma binding capabilities have higher volumes of distribution than drugs which are more polar, more highly ionized or exhibit high plasma binding in the body’s environment.

Volume of distribution may be increased by renal failure (due to fluid retention) and liver failure (due to altered body fluid and plasma protein binding). Conversely it may be decreased in dehydration. 6. Redistribution Highly lipid soluble drugs given by intravenous or inhalation routes are initially distributed to organs with high blood flow. Later, less vascular but more bulky tissues (such as muscle and fat) take up the drug—plasma concentration falls & the drug is withdrawn from these sites.

If the site of action of the drug was in one of the highly perfused organs, redistribution results in termination of the drug action. The greater the lipid solubility of the drug, the faster its redistribution. For example, the anaesthetic action of thiopentone is terminated in a few minutes due to redistribution. However, when the same drug is given repeatedly or continuously over long periods, the low perfusion and high capacity sites are progressively filled up and the drug becomes longer acting. 7.

The blood–brain barrier (BBB) is a separation of circulating blood from the brain extracellular fluid (BECF) in the central nervous system (CNS). It occurs along all capillaries and consists of tight junctions around the capillaries that do not exist in normal circulation. Endothelial cells restrict the diffusion of microscopic objects (e. g. , bacteria) and large or hydrophilic molecules into the cerebrospinal fluid (CSF), while allowing the diffusion of small hydrophobic molecules (O2, CO2, hormones).

Cells of the barrier actively transport metabolic products such as glucose across the barrier with specific proteins. This barrier also includes a thick basement membrane and astrocytic endfeet. 8. placental barrier term sometimes used for the placental membrane, because it prevents the passage of some materials between the maternal and fetal blood. The semipermeable layer of tissue in the placenta that serves as a selective membrane to substances passing from maternal to fetal blood. 9. Biotransformation is the chemical modification (or modifications) made by an organism on a chemical compound.

If this modification ends in mineral compounds like CO2, NH4+, or H2O, the biotransformation is called mineralisation. Biotransformation means chemical alteration of chemicals such as (but not limited to) nutrients, amino acids, toxins, and drugs in the body. It is also needed to render nonpolar compounds polar so that they are not reabsorbed in renal tubules and are excreted. Biotransformation of xenobiotics can dominate toxicokinetics and the metabolites may reach higher concentrations in organisms than their parent compounds 10.

Pharmacogenetics refers to genetic differences in metabolic pathways which can affect individual responses to drugs, both in terms of therapeutic effect as well as adverse effects. [1]In oncology, pharmacogenetics historically refers to germline mutations (e. g. , single-nucleotide polymorphisms affecting genes coding for liver enzymes responsible for drug deposition andpharmacokinetics), whereas pharmacogenomics refers to somatic mutations in tumoral DNA leading to alteration in drug response (e. g. , KRAS mutations in patients treated with anti-Her1biologics).

11. A prodrug is a pharmacological substance that is administered in an inactive (or less than fully active) form, and is subsequently converted to an active pharmacological agent (drug) through normal metabolic processes (bioactivation). A prodrug serves as a type of ‘precursor’ to the intended drug. Prodrugs can be used to improve how the intended drug is absorbed, distributed, metabolized and excreted (ADME). [1][2] Prodrugs are often designed to improve oral bioavailability in cases where the intended drug is poorly absorbed through the gastrointestinal tract.

A prodrug may also be used to improve how selectively the intended drug interacts with cells or processes that are not its intended target. This reduces the adverse or unintended effects of the intended drug, especially important in treatments like chemotherapy, which can have severe unintended and undesirable side effects. 12. An agonist is a chemical that binds to a receptor of a cell and triggers a response by that cell. Agonists often mimic the action of a naturally occurring substance.

Whereas an agonist causes an action, an antagonist blocks the action of the agonist and an inverse agonist causes an action opposite to that of the agonist. 13. antagonist is a type of receptor ligand or drug that does not provoke a biological response itself upon binding to a receptor, but blocks or dampens agonist-mediated responses. [1] In pharmacology, antagonists have affinity but no efficacy for their cognate receptors, and binding will disrupt the interaction and inhibit the function of an agonist or inverse agonist at receptors.

Antagonists mediate their effects by binding to the active site or to allosteric sites on receptors, or they may interact at unique binding sites not normally involved in the biological regulation of the receptor’s activity. Antagonist activity may be reversible or irreversible depending on the longevity of the antagonist–receptor complex, which, in turn, depends on the nature of antagonist receptor binding. The majority of drug antagonists achieve their potency by competing with endogenous ligands or substrates at structurally defined binding sites on receptors.

14 partial agonists are drugs that bind to and activate a given receptor, but have only partial efficacy at the receptor relative to a full agonist. They may also be considered ligands which display both agonistic and antagonistic effects – when both a full agonist and partial agonist are present, the partial agonist actually acts as a competitive antagonist. Some currently common drugs that have been classed as partial agonists at particular receptors include: buspirone, aripiprazole, buprenorphine, andnorclozapine. inverse agonist is an agent that binds to the same receptor as an agonist but induces a pharmacological response opposite to that agonist. A prerequisite for an inverse agonist response is that the receptor must have a constitutive (also known as intrinsic or basal) level activity in the absence of any ligand. An agonist increases the activity of a receptor above its basal level while an inverse agonist decreases the activity below the basal level. 16. drug potency,the amount of drug required to produce a given percentage of its maximal effect, irrespective of the size of maximal effect.

A drug can have high potency but poor efficacy, meaning that response is seen at very low doses and remains small even at high doses. Drug potency is seldom an important clinical consideration. 17. drug efficacy indicates the capacity for beneficial change (or therapeutic effect) of a given intervention (e. g. a drug, medical device, surgical procedure, or a public health intervention). If efficacy is established, an intervention is likely to be at least as good as other available interventions, to which it will have been compared.

Comparisons of this type are typically made in ‘explanatory’ randomized controlled trials, whereas ‘pragmatic’ trials are used to establish the effectiveness of an intervention. 18. A placebo is a simulated or otherwise medically ineffectual treatment for a disease or other medical condition intended to deceive the recipient. Sometimes patients given a placebo treatment will have a perceived or actual improvement in a medical condition, a phenomenon commonly called the placebo effect. In medical research, placebos are given as control treatments and depend on the use of measured deception.

Common placebos include inert tablets,sham surgery,[3] and other procedures based on false information. [1] However, placebos can also have a surprisingly positive effect on a patient who knows that the given treatment is without any active drug, as compared with a control group who knowingly did not get a placebo. [4] 19. Drug synergy occurs when drugs can interact in ways that enhance or magnify one or more effects, or side-effects, of those drugs. This is sometimes exploited in combination preparations, such as codeine mixed with acetaminophen or ibuprofen to enhance the action of codeine as a pain reliever.

Some drugs users frequently utilize 5-HTP, a serotonin precursor often used as anantidepressant, prior to and after ingestion of MDMA. It is said to increase the “high” and decreases the “comedown” stages of MDMA use, although most anecdotal evidence has pointed to 5-HTP significantly altering the effect of MDMA when used at the same time, as well as potentiating the side effects associated with serotonin syndrome[Other examples include the use of Cannabis with LSD, where the active chemicals in cannabis have been reported to enhance the hallucinatory experience of LSD. 20 .

Physiological antagonism describes the behavior of a substance that produces effects counteracting those of another substance (a result similar to that produced by an antagonist blocking the action of an agonist at the same receptor) using a mechanism that does not involve binding to the same receptor.

There are several substances that have antihistaminergic action despite not being ligands for the histamine receptor. For instance, epinephrine raises arterial pressure through vasoconstriction mediated by A1-adrenergic receptor activation, in contrast to histamine, which lowers arterial pressure.

Thus, despite not being true antihistamines because they do not bind to and block the histamine receptor, epinephrine and other such substances are physiological antagonists to histamine. 21. The therapeutic index (also known as therapeutic ratio) is a comparison of the amount of a therapeutic agent that causes the therapeutic effect to the amount that causes death (in animal studies) or toxicity (in human studies) Quantitatively, it is the ratio given by the lethal or toxic dose divided by the therapeutic dose.

In animal studies, the therapeutic index is the lethal dose of a drug for 50% of the population (LD50) divided by the minimum effective dose for 50% of the population (ED50). Lethality is not determined in human clinical trials; instead, the dose that produces a toxicity in 50% of the population (TD50) is used to calculate the therapeutic index. While the lethal dose is important to determine in animal studies, there are usually severe toxicities that occur at sublethal doses in humans, and these toxicities often limit the maximum dose of a drug.

A higher therapeutic index is preferable to a lower one: a patient would have to take a much higher dose of such a drug to reach the lethal/toxic threshold than the dose taken to elicit the therapeutic effect. in animal studies, or for humans, 22. Physiological tolerance or drug tolerance is commonly encountered in pharmacology, when a subject’s reaction to a specific drug and concentration of the drug is progressively reduced, requiring an increase in concentration to achieve the desired effect. [1] Drug tolerance can involve both psychological drug tolerance and physiological factors.

Characteristics of drug tolerance: it is reversible, the rate depends on the particular drug, dosage and frequency of use, differential development occurs for different effects of the same drug. Physiological tolerance also occurs when an organism builds up a resistance to the effects of a substance after repeated exposure. This can occur with environmental substances, such as salt or pesticides. A rapid drug tolerance is termed tachyphylaxis 23.

An adverse drug reaction (abbreviated ADR) is an expression that describes harm associated with the use of given medications at a normal dosage during normal use.

ADRs may occur following a single dose or prolonged administration of a drug or result from the combination of two or more drugs. The meaning of this expression differs from the meaning of “side effect”, as this last expression might also imply that the effects can be beneficial. [1]The study of ADRs is the concern of the field known as pharmacovigilance. An adverse drug event (abbreviated ADE) refers to any injury caused by the drug (at normal dosage and/or due to overdose) and any harm associated with the use of drug (e. g.discontinuation of drug therapy). [2] ADRs are a special type of ADEs.

24. An idiosyncrasy is an unusual feature of a person (though there are also other uses, see below). It also means odd habit. The term is often used to express eccentricity or peculiarity. [1][2] A synonym may be quirk. 25 Type I hypersensitivity is also known as immediate or anaphylactic hypersensitivity. The reaction may involve skin (urticariaand eczema), eyes (conjunctivitis), nasopharynx (rhinorrhea, rhinitis), bronchopulmonary tissues (asthma) and gastrointestinal tract (gastroenteritis).

The reaction may cause a range of symptoms from minor inconvenience to death. The reaction usually takes 15 – 30 minutes from the time of exposure to the antigen, although sometimes it may have a delayed onset (10 – 12 hours). Immediate hypersensitivity is mediated by IgE. The primary cellular component in this hypersensitivity is the mast cell or basophil. The reaction is amplified and/or modified by platelets, neutrophils and eosinophils. A biopsy of the reaction site demonstrates mainly mast cells and eosinophils. 26. Drug dependence means that a person needs a drug to function normally.

Abruptly stopping the drug leads to withdrawal symptoms. Drug addiction is the compulsive use of a substance, despite its negative or dangerous effects. A person may have a physical dependence on a substance without having an addiction. For example, certain blood pressure medications do not cause addiction but they can cause physical dependence. Other drugs, such as cocaine, cause addiction without leading to physical dependence. 27. A drug interaction is a situation in which a substance (usually another drug) affects the activity of a drug when both are administered together.

This action can be synergistic (when the drug’s effect is increased) or antagonistic (when the drug’s effect is decreased) or a new effect can be produced that neither produces on its own. Typically, interactions between drugs come to mind (drug-drug interaction). However, interactions may also exist between drugs and foods (drug-food interactions), as well as drugs and medicinal plants or herbs (drug-plant interactions). People taking antidepressant drugs such asmonoamine oxidase inhibitors should not take food containing tyramine as hypertensive crisis may occur (an example of a drug-food interaction).

These interactions may occur out of accidental misuse or due to lack of knowledge about the active ingredients involved in the relevant substances. 28Neostigmine (Prostigmin, Vagostigmin) is a parasympathomimetic that acts as a reversible acetylcholinesterase inhibitor. By interfering with the breakdown of acetylcholine, neostigmine indirectly stimulates both nicotinic and muscarinic receptors. Unlike physostigmine, neostigmine has a quaternary nitrogen; hence, it is more polar and does not enter the CNS. Its effect on skeletal muscle is greater than that of physostigmine, and it can stimulate contractility before it paralyzes.

Neostigmine has moderate duration of action, usually two to four hours. [3]Neostigmine binds to the anionic site of cholinesterase. The drug blocks the active site of acetylcholinesterase so the enzyme can no longer break down the acetylcholine molecules before they reach the postsynaptic membrane receptors. This allows for the threshold to be reached so a new impulse can be triggered in the next neuron. In myasthenia gravis there are too few acetylcholine receptors so with the acetylcholinesterase blocked, acetylcholine can bind to the few receptors and trigger a muscular contraction. 29.

Edrophonium is a readily reversible acetylcholinesterase inhibitor. It prevents breakdown of the neurotransmitter acetylcholine and acts by competitively inhibiting the enzyme acetylcholinesterase, mainly at the neuromuscular junction. It is sold under the trade names Tensilon and Enlon 30. Pilocarpine is a parasympathomimetic alkaloid obtained from the leaves of tropical American shrubs from the genus Pilocarpus. It is a non-selectivemuscarinic receptor agonist[2] in the parasympathetic nervous system, which acts therapeutically at the muscarinic acetylcholine receptor M3 due to its topical application,[3] e.g. , in glaucoma and xerostomia.

31. sialagogue an agent that stimulates the flow of saliva. Herbs with sialagogue action include:Bloodroot (Sanguinaria Canadensis), Blue Flag (Iris versicolor), Cayenne pepper (Capsicum minimum),Centaury (Centaurium erythraea),Great Yellow Gentian (Gentiana lutea)Ginger (Zingiber officinale),Northern Prickly-ash (Zanthoxylum americanum), Senega (Polygala senega) Mayapple (Podophyllum peltatum) 32. PHYSOSTIGMINE| NEOSTIGMINE| Natural source| Synthetic source| Tertiary amine| Quaternary amine| High lipid solubility| Low lipid solubility| More CNS toxic| Less CNS toxic|.

Doesn’t have a direct action on skeletal muscle junction (on nicotinic receptor)| Has also direct action on skeletal muscle junction| | | | | 33. anticholinergic drugs: 1 pertaining to a blockade of acetylcholine receptors that results in the inhibition of the transmission of parasympathetic nerve impulses. 2 an anti-cholinergic agent that functions by competing with the neurotransmitter acetylcholine for its receptor sites at synaptic junctions. Anticholinergics are used to treat spastic disorders of the GI tract, to reduce salivary and bronchial secretions before surgery, or to dilate the pupil.

Some anticholinergics reduce parkinsonian symptoms but are never considered primary agents for therapy. Atropine in large doses stimulates the central nervous system and in small doses acts as a depressant. Among numerous cholinergic blocking agents are atropine, belladonna, glycopyrrolate, hyoscyamine, methixene hydrochloride, trihexyphenidyl hydrochloride, and scopolamine. Also calledcholinergic-blocking agent, parasympatholytic. 34. atropine is used as a pre anaesthetic agent: Used as pre-anesthetic medication with wide safety margin for stimulation of cardiac and respiratory functions, and inhibition of salivary and bronchial secretions.

Used prior to wide verity of anesthetic agents (barbiturates, or inhalation anesthetics), sedatives, and narcotics. 35. use of atropine for organophosphate poisoning Atropine is not an actual antidote for organophosphate poisoning. However, by blocking the action of acetylcholine at muscarinic receptors, atropine also serves as a treatment for poisoning byorganophosphate insecticides and nerve gases, such as tabun (GA), sarin (GB), soman (GD) and VX.

Troops who are likely to be attacked with chemical weapons often carry autoinjectors with atropine and obidoxime, which can be quickly injected into the thigh. Atropine is often used in conjunction with pralidoxime chloride. 36. scopolamine, also known as levo-duboisine and hyoscine, is a tropane alkaloid drug with muscarinic antagonist effects. It is among thesecondary metabolites of plants from Solanaceae (nightshade) family of plants, such as henbane, jimson weed, Angel’s Trumpets (Datura orBrugmansia), and corkwood (Duboisia).

[2][3] 37. Tubocurarine (also known as D-tubocurarine or DTC) is a skeletal muscle relaxant in the category of non-depolarizingneuromuscular-blocking drugs, used adjunctively in anesthesia to provide skeletal muscle relaxation during surgery ormechanical ventilation. Unlike a number of other related skeletal muscle relaxants, it is now rarely considered clinically to facilitate endotracheal intubation. Tubocurarine is classified as a long-duration,[1] antagonist for Nicotinic acetylcholine receptor. [2] It is the active agent of curare.

Currently, tubocurarine is rarely used as an adjunct for clinical anesthesia because safer alternatives, such as cisatracuriumand rocuronium, are available 38. Suxamethonium chloride (INN), also known as suxamethonium or succinylcholine, is a nicotinic acetylcholine receptor agonist, used to induce muscle relaxation and short-term paralysis, usually to facilitate tracheal intubation. Suxamethonium is sold under the trade names Anectine,Quelicin, and Scoline. It is used as a paralytic agent for euthanasia/immobilization of horses. It is colloquially referred to as “succs” in hospitalsettings.

[1]Suxamethonium acts as a depolarizing neuromuscular blocker. It acts on nicotinic receptors resulting in persistent depolarization of the motor end plate. It is degraded by butyrylcholinesterase, a plasma cholinesterase. This hydrolysis by butyrylcholinesterase is much slower than that of acetylcholine by acetylcholinesterase. 39. Suxamethonium (succinylcholine) apnoea occurs when a patient has been given the muscle relaxant suxamethonium, but does not have the enzymes to metabolise it. Thus they remain paralysed for an increased length of time and cannot breathe adequately at the end of an anaesthetic.

40. Botulinum toxin is a protein and neurotoxin produced by the bacterium Clostridium botulinum. [1][2] It is the most acutely toxic substance known, with an estimated human median lethal dose of 1. 3–2. 1 ng/kg intravenously or intramuscularly and 10–13 ng/kg when inhaled. [3] Botulinum toxin can cause botulism, a serious and life-threatening illness in humans and animals. Popularly known by one of its trade names, Botox, it is used for various cosmetic and medical procedures 41. A muscle relaxant is a drug which affects skeletal muscle function and decreases the muscle tone.

It may be used to alleviate symptoms such as muscle spasms, pain, and hyperreflexia. The term “muscle relaxant” is used to refer to two major therapeutic groups: neuromuscular blockers and spasmolytics. Neuromuscular blockers act by interfering with transmission at the neuromuscular end plate and have no central nervous system (CNS) activity. They are often used during surgical procedures and in intensive care and emergency medicine to cause paralysis. Spasmolytics, also known as “centrally acting” muscle relaxants, are used to alleviate musculoskeletal pain and spasms.

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