Adrenergic agents
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This document discusses adrenergic and cholinergic agents. It describes how adrenergic agents stimulate the adrenergic nervous system through catecholamines like norepinephrine and epinephrine or through non-catecholamines. Common adverse effects of adrenergic agents include palpitations, tachycardia, dizziness and tremors. Cholinergic agents act through the parasympathetic nervous system to slow the heart rate, increase GI motility and secretions, and trigger other effects. Common adverse effects of cholinergic agents include nausea, vomiting, diarrhea, dizziness and hypotension. Both agent types require monitoring of vital signs and clients with certain health conditions are
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Drugs that partially or completely mimic the effects of transmitter substances of the sympathetic nervous system. On the basis of chemical structure we divide Sympathomimetics into
1. Catecholamine
2. Non-Catecholamine
Adrenergic drugs that activate adrenergic receptors are termed
as sympathomimetics, Some sympathomimetics directly activate
adrenergic receptors (direct-acting agonists), while others act
indirectly by enhancing release or blocking reuptake of norepinephrine (indirect-acting agonists). Adrenergic transmission is restricted to the sympathetic division of the ANS. There are three closely related endogenous catecholamine's (CAs).
1. Noradrenaline (NA): It acts as transmitter at postganglionic sympathetic sites (except sweat glands, hair follicles and some vasodilator fibers) and in certain areas of brain.
2. Adrenaline (Adr) It is secreted by adrenal medulla and may have a transmitter role in the brain.
3. Dopamine (DA) It is a major transmitter in basal ganglia, limbic system, CTZ, anterior pituitary, etc. and in a limited manner in the periphery
Mechanism of Action , Therapeutic uses and adverse effects of Adrenergic Agonists
1. Direct-acting agonists:
These drugs act directly on α or β receptors, producing effects similar to those that occur following stimulation of sympathetic nerves or release of epinephrine from the adrenal medulla.
Examples of direct-acting agonists include epinephrine,
norepinephrine, isoproterenol, and phenylephrine.
2. Indirect-acting agonists:
These agents may block the reuptake of norepinephrine or cause the release of norepinephrine from the cytoplasmic pools or vesicles of adrenergic neuron. The norepinephrine then traverses the synapse and binds to α or β receptors.
Examples of reuptake inhibitors and agents that cause norepinephrine release include cocaine and amphetamines,
respectively.
3. Mixed-action agonists:
Ephedrine and its stereoisomer, pseudoephedrine, both stimulate adrenoceptors directly and release norepinephrine
from the adrenergic neuron.
Sympathomimetics
This document discusses sympathomimetic drugs, which mimic the actions of epinephrine and norepinephrine. It describes the sympathetic and parasympathetic nervous systems, defines sympathomimetic drugs, and classifies them based on their mechanisms of action. The document also discusses the synthesis, storage, release, reuptake, and metabolism of catecholamines. It describes adrenergic receptors, where they are located, and provides examples of drugs that act on different receptor types. The actions and uses of epinephrine, norepinephrine, and dopamine are explained. Therapeutic classifications and examples of sympathomimetic drugs are also provided.
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The document discusses catecholamines such as epinephrine, norepinephrine, and dopamine that are produced in the adrenal medulla in response to stress. These catecholamines act on alpha and beta adrenergic receptors to prepare the body for emergency situations by increasing metabolic rate, heart rate, and blood pressure through various cardiovascular and metabolic effects. The adrenal medulla is innervated by preganglionic nerves and stimulated to secrete catecholamines. Glucocorticoids are necessary for normal development of the adrenal medulla. Catecholamines are metabolized to vanillylmandelic acid which is excreted in urine. Pheochromocytoma is a tumor
Anticholinesterases
CONTENTS:
INTRO to Anticholinesterases
MECHANISM OF ACTION
THERAPEUTIC USES
ADVERSE DRUG REACTIONS
OP POISONING- TREATMENT
Congenital adrenal hyperplasia
Congenital adrenal hyperplasia (CAH) is a family of inherited disorders affecting the adrenal glands caused by a deficiency in enzymes involved in cortisol and aldosterone production. The most common type (over 90% of cases) is 21-hydroxylase deficiency, which is autosomal recessive and can cause ambiguous genitalia in females and other symptoms. Clinical manifestations include salt wasting, low blood sugar, and excessive male hormone production leading to virilization. Diagnosis involves blood tests to measure hormone levels before and after stimulation with ACTH. Treatment consists of glucocorticoid and mineralocorticoid hormone replacement, monitoring of hormone levels, and surgery to correct ambiguous genitalia.
5. adrenergic drugs
This document discusses adrenergic drugs and their mechanisms of action. It describes how adrenergic receptors are classified into alpha and beta receptors, which have subtypes. It explains how various drugs like adrenaline, isoprenaline, dopamine, dobutamine, phenylephrine, and alpha methyl dopa act as agonists at these receptor subtypes, and outlines their therapeutic uses and adverse effects. Selective beta-2 agonists like salbutamol are also covered, which are used for conditions like bronchial asthma and premature labor.
Digitalis toxicity vijay
Digoxin toxicity can occur due to various predisposing factors and causes that increase digoxin levels like drug interactions and electrolyte imbalances. Manifestations include cardiac, gastrointestinal, neurological and other symptoms. Diagnosis involves evaluating symptoms, past digoxin use, ECG changes, electrolyte and renal status, and plasma digoxin levels. Treatment focuses on stopping digoxin, decreasing absorption, correcting electrolyte imbalances, and using medications like potassium, beta blockers, antiarrhythmics or digoxin antibodies in severe cases.
Digoxin toxicity
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.
Antidrenergic Drugs (updated 2016) - drdhriti
Antiadrenergic drugs, also known as alpha blockers or alpha antagonists, work by blocking the effects of adrenaline and other related drugs at receptor sites. They occupy both alpha-1 and alpha-2 adrenergic receptors without activating them. Clinically, they are used to modify the responses of endogenous catecholamines like adrenaline and noradrenaline in both physiological and pathophysiological conditions. Common uses include treating pheochromocytoma, hypertension, Raynaud's disease, and benign prostatic hyperplasia. Individual drugs vary in their selectivity and duration of action at different receptor subtypes. Side effects may include postural hypotension, nasal congestion, and inhibition of ejac
Digoxin and its Toxicity
Digoxin is a cardiac glycoside commonly used to treat heart failure. It works by inhibiting the sodium-potassium pump in cardiac cells, increasing intracellular calcium levels and improving cardiac contractility. The main indications for digoxin are heart failure with reduced ejection fraction and atrial fibrillation or flutter with rapid ventricular response. Clinical trials have shown that discontinuing digoxin in stable heart failure patients can lead to worsening symptoms and reduced exercise capacity. Digoxin has a long half-life, requires dosage adjustments in renal impairment, and interacts with several other drugs. Therapeutic drug monitoring is important to avoid toxicity.
L5: Adrenergic agonists; sympathomimetics
This document discusses adrenergic agonists, which are drugs that act on pathways mediated by the endogenous catecholamines norepinephrine and epinephrine. These drugs target various steps in catecholamine synthesis, storage, release, binding, and removal and are used to treat conditions like hypertension, depression, shock, asthma, and angina. Adrenergic agonists are classified as direct-acting if they act directly on receptors, or indirect-acting if they increase catecholamine levels in the synapse. The document also describes the subtypes of alpha and beta adrenergic receptors, their locations, mechanisms of action, and the effects of prolonged receptor stimulation.
Adrenergic receptors and its modulators
This document discusses adrenergic receptors and modulators. It describes the sympathetic nervous system and neurotransmitters like norepinephrine, epinephrine, and dopamine. Norepinephrine is stored in synaptic vesicles and released via calcium-dependent fusion. Release can be modulated by prejunctional autoreceptors and heteroreceptors. There are alpha and beta adrenergic receptors which are G-protein coupled and have various effects. Drugs can affect receptors as agonists or antagonists and are used to treat conditions like hypertension and heart failure.
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Cholinergic Antagonist Agents
This document discusses cholinergic antagonist agents, which block the actions of acetylcholine in the parasympathetic nervous system. It describes their uses in conditions like myasthenia gravis and drug overdoses. The document outlines the agents' mechanisms of action as competitive antagonists that bind muscarinic receptors. It also details their therapeutic uses in treating conditions of the CNS, cardiovascular, respiratory, gastrointestinal and genitourinary systems. Potential side effects and interactions are presented.
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Skeletal muscle relaxants work by blocking acetylcholine receptors at the neuromuscular junction, relaxing muscles. There are two main types - depolarizing and non-depolarizing. Succinylcholine is the only depolarizing drug used clinically. It causes initial fasciculations before prolonged muscle relaxation. Non-depolarizing drugs like tubocurarine and vecuronium are competitive antagonists that do not activate acetylcholine receptors, preventing muscle contraction. They have short, intermediate, or long durations of action and differ in side effects and metabolism. Dantrolene works via a different mechanism by preventing calcium release in muscles.
skeletalmusclerelaxants-161103031625.pdf
Skeletal muscle relaxants work by blocking acetylcholine receptors at the neuromuscular junction, relaxing muscles. There are two main types - depolarizing and non-depolarizing. Succinylcholine is the only depolarizing drug used clinically. It causes initial fasciculations before prolonged muscle relaxation. Non-depolarizing drugs like tubocurarine and vecuronium are competitive antagonists that bind acetylcholine receptors without activating them, preventing muscle contraction. Their effects can be reversed with acetylcholinesterase inhibitors. Dantrolene acts via a different mechanism by preventing calcium release in muscle cells.
REPORT
Noradrenaline is a neurotransmitter that acts on alpha-1, alpha-2, and beta-1 receptors. It is used intravenously as a vasopressor agent to raise blood pressure in hypotensive states. Isoprenaline acts predominantly on beta-1 and beta-2 receptors and is used as a bronchodilator. Dopamine acts on dopaminergic, alpha, and beta receptors. At low doses it causes renal and mesenteric vasodilation, while at higher doses it causes vasoconstriction. It is used to treat cardiovascular shock. Adrenergic drugs include pressor agents, cardiac stimulants, bronchodilators, and drugs that act on the uterus
report
Noradrenaline is a neurotransmitter that acts on α1, α2, and β1 receptors. It increases blood pressure through vasoconstriction and is used as a vasopressor agent. Isoprenaline acts mainly on β1 and β2 receptors and is used as a bronchodilator. Dopamine acts on D1, D2, α1, and β1 receptors. Low doses cause renal and mesenteric vasodilation while moderate doses have positive inotropic effects. Dobutamine is a derivative that predominantly acts on β1 receptors to increase contractility without affecting heart rate. Ephedrine, phenylephrine, and other sympathomimetic drugs have various adrenergic
Inotropic agents
Inotropic agents work by increasing the force and velocity of cardiac muscle contraction. They are used to improve myocardial function and support circulation in heart failure. Common inotropic agents include cardiac glycosides like digoxin which inhibit Na+-K+-ATPase, beta-adrenergic agonists like dobutamine which stimulate beta-1 receptors, and phosphodiesterase inhibitors like milrinone which increase cAMP levels. While inotropes can provide short-term hemodynamic support, long-term use does not improve survival and may increase mortality in heart failure patients.
Cholinergic antagonist agents
This document discusses cholinergic blocking agents, which are drugs that block the actions of acetylcholine in the parasympathetic nervous system. It describes their uses in treating conditions like asthma, Parkinson's disease, and peptic ulcers. The document outlines the agents' mechanisms of action as competitive antagonists that bind to muscarinic receptors. It also details their therapeutic effects on organ systems and potential side effects like increased heart rate, urinary retention, and decreased secretions. Drug interactions that can cause additive cholinergic effects are also noted.
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This document discusses anticholinergic agents, which are drugs that inhibit the action of acetylcholine at cholinergic receptors in the central and peripheral nervous system. It describes the different types of cholinergic receptors, including muscarinic (M1-M5) and nicotinic (N1, N2) receptors. It provides examples of anticholinergic drugs that act as antagonists at these receptors, such as atropine, scopolamine, ipratropium, and ganglionic blockers. The document also discusses the clinical uses of anticholinergic agents for conditions like bradycardia, gastrointestinal disorders, and as pre-operative medications to reduce secretions. The main
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This document discusses adrenergic blockers, including their classification, mechanisms of action, effects and uses. It describes how alpha and beta blockers work by preventing the interaction of neurotransmitters like norepinephrine with corresponding adrenergic receptors. Common alpha blockers mentioned are prazosin, terazosin and doxazosin. Beta blockers discussed include metoprolol, atenolol, propranolol and esmolol. Their effects on the cardiovascular, respiratory and other systems are summarized. Therapeutic uses for conditions like hypertension, heart failure and prostate issues are also highlighted.
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This document summarizes various classes of drugs acting on the cardiovascular system. It discusses cardiotonic drugs that increase heart contraction including cardiac glycosides like digoxin. It also covers antihypertensive drugs such as diuretics, ACE inhibitors, calcium channel blockers, and vasodilators that are used to treat hypertension. Digitalis is discussed in depth, outlining its mechanism of inhibiting sodium-potassium pumps to increase calcium in cardiomyocytes and thus strengthen heart contractions.
Pharmacology of the Autonomic Nervous System
The document discusses the autonomic nervous system and pharmacology of its sympathetic and parasympathetic divisions. It describes the pre- and post-ganglionic fibers, neurotransmitters, and receptors involved. Catecholamines, adrenergic receptors, and drugs that target the sympathetic system like agonists, antagonists, and their effects are summarized. Parasympathetic muscarinic and nicotinic receptors, cholinergic drugs like direct and indirect agonists, and anticholinergic drugs are also outlined.
Cns stimulants & drugs of abuse
This document discusses CNS stimulants and drugs of abuse. It classifies CNS stimulants based on their site of action in the brain and effects. It describes convulsants and respiratory stimulants, psychomotor stimulants, and psychotomimetic drugs. It covers specific stimulants like amphetamines, cocaine, caffeine, and hallucinogens. It also discusses mechanisms of action, clinical uses, toxicity, and classifications of drugs of abuse. Addiction is described as compulsive drug use despite negative consequences due to adaptive changes in the brain's reward system.
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Anticholinergic drugs work by competitively blocking acetylcholine receptors in the parasympathetic nervous system. They inhibit nerve transmission at muscarinic receptors. Atropine is a prototypical anticholinergic that causes dilation of the pupils, decreased secretions, and tachycardia. Anticholinergics have therapeutic uses for conditions like asthma, COPD, Parkinson's disease, peptic ulcers, and overactive bladder. However, they can cause adverse effects like dry mouth, constipation, blurred vision, urinary retention, and CNS effects like agitation. Individual drugs have specific indications and contraindications must be considered like glaucoma and prostate issues.
cholinergicdrugs-160304092118.pptx
The document discusses the parasympathetic nervous system and cholinergic drugs. It describes how the parasympathetic nervous system works to rest and digest functions like decreasing heart rate and increasing GI motility. It then explains cholinergic drugs, which mimic acetylcholine, as either direct acting agonists that bind receptors or indirect acting drugs that inhibit acetylcholinesterase. Side effects result from overstimulation of the parasympathetic nervous system and can include things like increased secretions, bronchospasm, and bradycardia.
Sympathomimmetics
This document summarizes adrenergic agonists and antagonists. It describes the synthesis and metabolism of catecholamines like dopamine, norepinephrine, and epinephrine. It also discusses the different adrenergic receptor types (alpha and beta), their locations and functions. Various adrenergic drugs are classified and their mechanisms, effects, uses, and adverse effects outlined, including epinephrine, norepinephrine, dopamine, dobutamine, dopexamine, fenoldopam, phenylephrine, clonidine and others.
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Adrenergic agents
- 1. Final Exam
- 2. Adrenergic Agents • Adrenergic nervous system stimulated by 2 classes of drugs: – Catecholamines – Noncatecholamines • Neurotransmitter catecholamines – Norepinephrine—secreted at nerve terminals – Epinephrine—adrenal medulla – Dopamine—brain, kidney, GI tract • Non-catecholamines – Selective – Not quite fast acting – Longer duration of action
- 3. Adrenergic Agents • Assess VS—HR & BP • Adverse effects are dose related • Adverse effects resolve when dose is reduce or discontinued • Client sensitive are: • Impaired liver function • Thyroid disease • HTN • Heart disease • DM have increase episodes of Hyperglycemia
- 4. Adrenergic Agents • Common Adverse Effects – Palpitations – Tachycardia – Dizziness – Tremors – Orthostatic hypotension • Serious Adverse Effects—w/cardiac d/c immediately & notify provider – Dysrhythmias – Chest pain – Severe hypotension – HTN – Angina pain – N/V—notify providers • Interactions: MAOI, TCA, atropine & halothane, OTC meds
- 5. Cholinergic Agents • Parasympathomimic • Produce effects of acetylcholine • Other can inhibit acetyl cholinesterase (metabolize ACH)-- indirect-acting cholinergic agent • PNS can be directly stimulated by some agents • Actions: – Slow heartbeat – Increase GI motility – Increase GI secretions – Increased contraction of urinary bladder w/relaxation of muscle sphincter – Increase contractility of bronchial smooth muscle – Sweating – Miosis of eye which decrease intaocular pressure – Increased force of contraction of skeletal muscle – Sometimes decrease blood pressure
- 6. Cholinergic Agents • VS: HR & BP • The higher the doses the greater the likelihood for adverse effects • CAE: • N/V/D/AC • Dizziness • Hypotension (monitor orthostatic pressures) • Bronchospasm & wheezing • Bradycardia (withhold the next dose) • Interactions: atropine, antihistamines