Autonomic nervous system

Pharmacology is the study of drugs. A drug can be any substance that, when administered to living organisms, produces a change in function. Thus, substances such as water, metals (iron), or insecticides can be classified as drugs. However, the term drug commonly means any medication that is used for diagnosing, curing, or treating disease Every drug produces its intended effect, or therapeutic effect, along with other effects. The therapeutic use(s) of any drug is referred to as the drug indication, meaning indications for use. The term contraindication refers to the situation or circumstance when a particular drug should not be used.

side effects are more of a nuisance than they are harmful Adverse effects are also undesired effects, but these are effects that may be harmful Toxic effects, or toxicity, implies drug poisoning, the consequences of which can be extremely harmful and may be life-threatening. The site of action of a drug is the location within the body where the drug exerts its therapeutic effect Mechanism of action explains how a drug produces its effects. Drugs that bind to specific receptors and produce a drug action are called agonists. Morphine is an example of an agonist.

Drugs that bind to specific receptors and inhibit agonist drug action or cellular functions are called antagonists. Potency is a measure of the strength, or concentration, of a drug required to produce a specific effect therapeutic index (TI) is a ratio of the LD50 to the ED50 of a drug Chapter 2 – Pharmacokinetics and factors of individual variation bioavailability: percentage of the drug dosage that is absorbed. drug absorption: entrance of a drug into the bloodstream from its site of administration. drug distribution: passage of a drug from the blood to the tissues and organs of the body. drug excretion: elimination of the drug from the body.

Drug metabolism: the enzymatic biotransformation of a drug into metabolites. drug microsomal metabolizing system (DMMS): group of enzymes located primarily in the liver that function to metabolize (biotransformation) drugs. enzyme induction: increase in the amount of drug-metabolizing enzymes after repeated administration of certain drugs. half-life: time required for the body to reduce the amount of drug in the plasma by one-half. loading dose: initial drug dose administered to rapidly achieve therapeutic drug concentrations.

Maintenance dose: dose administered to maintain drug blood levels in the therapeutic range. pharmacokinetics: describes the processes of drug absorption, drug distribution, drug metabolism, and drug excretion. Chapter 3 – Geriatric Pharmacology Each of the pharmacokinetic processes—drug absorption, drug distribution, drug metabolism, and drug excretion—is affected to some degree by the aging process. With age there is a decrease in blood flow to the intestinal tract, reduced intestinal absorptive surface area, a decrease in gastric acid secretion, and a decrease in intestinal motility.

The percentage of lean body mass (muscle) and the percentage of total body water decrease The percentage of body fat (adipose tissue) increases with age the rate of drug metabolism decreases with age, although there is much variability. The age-related decreases in liver blood flow and production of some drug microsomal metabolizing enzymes (DMMS) reduce the rate of drug metabolism The elderly are often more sensitive to drugs that depress the central nervous system.

Sedatives, hypnotics, antianxiety agents, antipsychotics, and antidepressant drugs 3940often cause excessive pharmacological and adverse effects in the elderly Pharmacology for the Peripheral Nervous System The peripheral nervous system includes the somatic and autonomic nervous systems. The somatic nervous system is concerned with sensation and voluntary movement. The autonomic nervous system controls blood pressure, heart rate, gastrointestinal activity, and glandular secretions Chapter 5 – intro to Autonomic Nervous System.

The primary function of the central nervous system is to control and coordinate the activity of all the systems in the body. The overall activity of the nervous system at any moment depends on neural communication (via nerve impulses) among many areas of the body. The autonomic nervous system is a subdivision of the central nervous system that regulates the activities of the internal organs and glands. The internal organs and glands are under involuntary or unconscious control ANS is composed of the parasympathetic and sympathetic divisions.

The nerves of the parasympathetic division (also known as the craniosacral division) originate from the brain (cranial nerves 3, 7, 9, and 10) and spinal cord (sacral nerves S2 to S4). The cranial nerves supply the internal organs and glands of the head, thoracic cavity, and upper portion of the abdominal cavity. The sacral nerves supply the lower portion of the abdominal cavity and the pelvic cavity. The origin and distribution of parasympathetic nerves are shown in Figure 5. 1. The nerves of the sympathetic division (known as the thoracolumbar division) originate from the thoracic and lumbar spinal nerves (T1 to L3).

The thoracic nerves supply the internal organs and glands of the head, thoracic cavity, and upper abdominal cavity. The lumbar nerves supply the lower portion of the abdominal cavity and the pelvic cavity. In the parasympathetic nervous system, the neurotransmitter released at the ganglia and the postganglionic nerve endings is acetylcholine (ACH). In sympathetic nerves, the neurotransmitter released at the ganglia is also ACH, but at the postganglionic nerve endings, it is norepinephrine (NE). Nerves that release acetylcholine are referred to as cholinergic, while nerves that release norepinephrine are referred to as adrenergic.

The cardiac and smooth muscle membrane sites where these neurotransmitters act are known as the cholinergic (also known as muscarinic) receptors (ACH) and the adrenergic receptors (NE) sympathetic division, the postganglionic neurons release NE, which stimulates the adrenergic receptors. The adrenergic receptors are divided into alpha and beta receptors The definition or action of alpha-1 receptor stimulation is the contraction of smooth muscle; for example, vasoconstriction of blood vessels. Beta-1 receptors are located mainly on the heart and mediate cardiac stimulation, an increase in heart rate and force of contraction.

Beta-2 receptors are located on smooth muscle and produce relaxation of smooth muscle; for example, relaxation of respiratory smooth muscle (bronchodilation). Chapter 6 – Drugs that affect the sympathetic nervous system adrenergic neuronal blocker: drug that acts at the neuronal nerve endings to reduce the formation or release of NE. alpha-adrenergic drug: drug that stimulates the alpha adrenergic receptors. alpha-1 adrenergic blocker: drug that blocks the alpha-1 effects of NE and EPI. alpha-1 adrenergic receptor: receptor located on smooth muscle that mediates smooth muscle contraction.

Alpha-2 adrenergic receptor: receptor located on adrenergic nerve endings that reduces the release of NE. beta-1 adrenergic receptor: receptor located on the heart that increases heart rate and force of contraction. beta-2 adrenergic receptor: receptor located on smooth muscle that relaxes smooth muscle when stimulated. catecholamine: refers to norepinephrine, epinephrine, and other sympathomimetic compounds that possess the catechol structure. false transmitter: substance formed in nerve endings that mimics and interferes with the action of the normal neurotransmitter.

Nonselective beta-adrenergic blocker: drug that blocks both beta-1 and beta-2 adrenergic receptors. nonselective beta-adrenergic drug: drug that stimulates both beta-1 and beta-2 receptors. selective beta-1 adrenergic blocker: drug that blocks only beta-1 receptors. selective beta-2 adrenergic drug: drug that stimulates only beta-2 receptors at therapeutic doses. sympatholytic: refers to the action of an adrenergic blocking drug or an action that decreases sympathetic activity. sympathomimetic: refers to the action of an adrenergic drug or an action that increases sympathetic activity.

The drugs used to affect sympathetic activity are classified as adrenergic drugs (agonists) that increase sympathetic activity and adrenergic blockers (antagonists) that decrease sympathetic activity. Adrenergic drugs are used to increase blood pressure, stimulate the heart, and produce bronchodilation. Adrenergic blockers are primarily used to lower blood pressure and reduce cardiac stimulation in conditions where there is excessive sympathetic activity. Sympathomimetics are adrenergic drugs (alpha and beta agonists) that produce effects that are similar to stimulating or mimicking the sympathetic nervous system.

7475Sympatholytics refer to adrenergic blocking drugs (alpha, beta, and neuronal blockers) that antagonize or decrease sympathetic activity Sympathomimetic drugs, including NE and EPI, that produce contraction of smooth muscle by stimulating the alpha-1 adrenergic receptors are referred to as alpha-adrenergic drugs. Drugs, including EPI, that both stimulate the heart (stimulate beta-1 receptors) and cause relaxation of smooth muscle (stimulate beta-2 receptors) are referred to as nonselective beta-adrenergic drugs. EPI is one of the few substances that stimulates all alpha and beta receptors.

There are also beta-adrenergic drugs that selectively stimulate only the beta-2 receptors at therapeutic doses. These drugs are referred to as the selective beta-2 adrenergic drugs and are used primarily as bronchodilators Sympatholytic drugs that block the alpha effects of NE and EPI are known as the alpha-adrenergic blockers. Most alpha blockers available today only block the alpha-1 receptor (relaxation of smooth muscle). Drugs that block both the beta-1 and beta-2 effects of EPI are known as the nonselective beta-adrenergic blockers.

Drugs that block only beta-1 receptors are known as selective beta-1 adrenergic blockers. The effect of these alpha- and beta-blockers is to decrease sympathetic activity, especially in the cardiovascular system. The blocking drug competes with NE or EPI for the receptor sites Drugs that act at the adrenergic nerve endings to reduce the formation or release of NE are known as the adrenergic neuronal blockers The most important clinical effect produced by the alpha-adrenergic drugs is stimulation of the alpha-1 receptors to cause contraction of smooth muscle.

This includes vasoconstriction of most blood vessels, contraction of sphincter muscles in the gastrointestinal (inhibits movement of intestinal contents) and urinary (restricts passage of urine) tracts, and contraction of ocular muscles that causes dilation of the pupil of the eye (mydriasis). Alpha drugs are administered intravenously in hypotensive states; for example, after surgery, to increase 7576blood pressure and maintain circulation.

Vasoconstriction of blood vessels in mucous membranes of the nasal sinuses produces a decongestant effect The beta-adrenergic drugs have a selective action to stimulate beta receptors. With the exception of NE and EPI, most beta drugs produce very few alpha effects. The most important actions of the beta drugs are stimulation of the heart (beta-1) and bronchodilation (beta-2). Epinephrine is the drug of choice for the immediate treatment of acute allergic reactions, such as anaphylaxis The alpha-blockers compete with NE and EPI for binding to the alpha-adrenergic receptors.

When the alpha-blocker binds to the receptors, it prevents NE and EPI from producing the alpha sympathetic responses. The alpha-blockers are used in the treatment of hypertension, especially when excessive vasoconstriction is present. The alpha-blockers are also used in peripheral vascular conditions (poor blood flow to skin and extremities) such as Raynaud’s disease, where the vasodilation increases blood flow to the skin and extremities.

Alpha-blockers are used in the treatment of pheochromocytoma, a tumor of the adrenal medulla where excessive catecholamine levels cause severe hypertension Beta-blocking drugs bind to beta-adrenergic receptors and antagonize the beta effects of EPI and NE.

Patients with hypertension, angina pectoris, and cardiac arrhythmias often have increased sympathetic activity, with excessive amounts of EPI and NE being released. By occupying beta receptors, the beta-blockers antagonize and reduce the effects of EPI and NE on beta receptors. The heart (beta-1) is one of the most important beta organs and the main clinical use of beta-blockers is to decrease the activity of the heart.

Blockade of the beta-1 receptors produces a decrease in heart rate, force of contraction, and impulse conduction through the conduction system of the heart. These effects are useful in patients with fast heart rates (tachycardia), cardiac arrhythmias, and other cardiac conditions where excessive sympathetic activity is present. Decreasing cardiac function also decreases blood pressure and beta-blockers are used in the treatment of hypertension The main activity that occurs inside the adrenergic nerve endings is the formation and storage of NE.

Norepinephrine is synthesized from amino acids, either phenylalanine or tyrosine. Several drugs interfere with the formation or the storage of NE. Such drugs are called adrenergic neuronal blockers. Chapter 7 – Drugs affecting Parasympathetic Nervous system The autonomic nervous system regulates the functions of the internal organs and glands. As previously discussed, the sympathetic division controls activity during physical exertion and stress (fight or flight). The parasympathetic division regulates body functions mainly during rest, digestion, and waste elimination.

Parasympathetic stimulation increases the activity of the gastrointestinal and genitourinary systems and decreases the activity of the cardiovascular system. Drugs that increase parasympathetic activity (cholinergic) are used in the treatment of Alzheimer’s disease, glaucoma, myasthenia gravis, and urinary and intestinal stasis. Drugs that decrease parasympathetic activity (anticholinergics) are indicated for the treatment of overactive urinary and intestinal conditions, asthma and COPD, motion sickness, and during various ophthalmic procedures.

The cholinergic receptors at the parasympathetic postganglionic nerve endings (as shown in Figure 7. 2(a)) are known as muscarinic receptors. The term muscarinic is derived from the drug muscarine, which is an alkaloid obtained from a particular type of mushroom. One of the first drugs used to establish the function of the autonomic nervous system (ANS), muscarine produces effects that are similar to those of ACH, but only at these particular receptor sites.

Consequently, early pharmacologists referred to these receptors as muscarinic, and the terminology is still in use. Drugs that act like ACH 9293 9394or muscarine at these receptors are referred to as either cholinergic or muscarinic. Drugs that block ACH at the muscarinic receptors are referred to as anticholinergic or antimuscarinic The cholinergic receptors at the neuromuscular junction (NMJ) of skeletal muscle (seen in Figure 7. 2(c)) are known as nicotinic-muscle (Nm) receptors. Nicotine also stimulates or acts like ACH at the skeletal neuromuscular junction.

Drugs that block the effects of ACH at the NMJ are referred to as neuromuscular blockers or skeletal muscle relaxants The direct-acting cholinergic drugs primarily increase GI secretions and motility, increase urinary tract function (urination), and cause pupillary constriction (miosis). Cholinergic drugs are used locally during ophthalmic examinations as miotics to constrict the pupils and in the treatment of glaucoma reversible anticholinesterase drugs are more widely used than the direct-acting cholinergic drugs.

They are used in the treatment of glaucoma, myasthenia gravis, urinary retention, intestinal paralysis, Alzheimer’s disease and as antidotes to the curare-type skeletal muscle blockers and the anticholinergic drugs. Myasthenia gravis is a disease of the skeletal muscle endplate where ACH functions to stimulate muscle tone and contraction Chapter 8 – Drugs affecting Autonomic Ganglia ganglionic blocker: drug that blocks the nicotinic-neural (Nn) receptors and reduces the activity of the autonomic nervous system.

ganglionic stimulant: drug that stimulates the nicotinic-neural (Nn) receptors to increase autonomic nervous system activity. nicotine: alkaloid drug in tobacco that stimulates ganglionic receptors. nicotinic-neural (Nn) receptor: cholinergic receptor at the autonomic ganglia. Ganglionic stimulants – use to stop smoking Ganglionic blockers bind to and block Nn receptors. Since the sympathetic division has greater control over regulation of blood pressure, the ganglionic blockers cause a reduction in blood pressure and are primarily used in the treatment of severe hypertension Chapter 9 – Skeletal muscle relaxants.

Many drugs inhibit skeletal muscle contraction by interfering with neuromuscular function. Drugs that inhibit skeletal muscle contraction by blocking conduction within the spinal cord are known as centrally acting skeletal muscle relaxants. In contrast, peripheral skeletal muscle relaxants inhibit muscle contraction at the NMJ Skeletal muscle relaxation is desirable in spastic diseases (multiple sclerosis and cerebral palsy), conditions in which the spinal cord has been damaged (trauma, paraplegia), and injuries in which pain accompanies overexertion of the muscles.

In addition, surgical and orthopedic procedures and intubation (for example, bronchoscopy) are often facilitated by the use of skeletal muscle relaxants The peripheral neuromuscular blockers are used primarily before (premedication) and during surgical procedures (surgical relaxation) to relax abdominal or intrathoracic skeletal muscles Neuromuscular blockers are used in an ICU setting with critically ill patients who are compromised by their existing conditions of bronchospasm or chronic obstructive pulmonary disease (COPD), making it difficult for them to be properly externally ventilated.

Peripheral neuromuscular blockers can reduce chest wall resistance (muscle relaxation), thereby increasing compliance and ventilation (oxygen/carbon dioxide exchange). DIRECT-ACTING SKELETAL MUSCLE RELAXANTS – treatment of malignant hyperthermia and spastic conditions. Muscle spasms associated with multiple sclerosis, cerebral palsy, and spinal cord injuries may reduce patients’ ability to function or perform activities required for daily living CENTRALLY ACTING SKELETAL MUSCLE RELAXANTS (SPASMOLYTICS) – Drugs that inhibit or interrupt painful intermittent muscle contractions are called spasmolytics.

Anesthetics Anesthesia is the loss of feeling or sensation, and it may be induced by drugs that will bring about partial or complete loss of sensation. When a patient receives local anesthesia, the patient is fully awake but does not feel pain in the area that has been anesthetized. When general anesthesia is administered, the patient is unconscious. Chapter 10 – local anesthetics General anesthetics abolish the response to pain by depressing the CNS and producing loss of consciousness.

Local anesthetics, as their name suggests, produce a temporary loss of sensation or feeling in a confined area of the body. The most common clinical use of local anesthetics is to abolish painful stimulation prior to surgical, dental (tooth extraction), or obstetric (delivery) procedures Local anesthetics are valuable because they block sensory nerves at doses that do not inhibit motor nerve function two classes of local anesthetics: ester local anesthetics and amide local anesthetics.

The ester local anesthetics have a short or moderate duration of action because they are metabolized by enzymes (cholinesterases) that are present in the blood and skin amide local anesthetics are usually the longer-acting drugs because these agents must be metabolized in the liver All of the other local anesthetics used today produce vasodilation; All of the local anesthetics can affect the CNS Pharmacology of the Central Nervous System.

The central nervous system includes the brain and spinal cord. It processes information to and from the peripheral nervous system and serves to coordinate and control our bodies. You will learn about drugs that are used for their sedative effect, antianxiety drugs, antidepressants, antiepileptic drugs, opioid and non-opioid analgesics and drugs used to treat patients with Parkinson’s disease. Chapter 19 – Opioid Analgesics.

Sympathetic nervous system mobilize the body’s fight-or-flight response & constantly active at a basic level to maintain homeostasis. Parasympathetic nervous system responsible for stimulation of “rest-and-digest” or “feed and breed” WE WILL WRITE A CUSTOM ESSAY SAMPLE ON ANY TOPIC …

Diffusion Equation Diffusion is proportional to change in pressure x surface area x solubility / thickness x square root of molecular weight Dyspnea Shortness of breath, difficulty breathing. WE WILL WRITE A CUSTOM ESSAY SAMPLE ON ANY TOPIC SPECIFICALLY FOR …

What does dual innervation mean? Dual innervation means that a body organ receives neural innervation from both sympathetic and parasympathetic neurons on the ANS. Which division, sympathetic or parasympathetic, has longer preganglionic axons? Why? Most parasympathetic preganglionic axons are longer …

Overview The autonomic nervous system (ANS), along with the endocrine system, coordinates the regulation and integration of bodily functions. The endocrine system sends signals to target tissues by varying the levels of blood-borne hormones. In contrast, the nervous system exerts …

Know general characteristics of signal-transducing receptors: Bind to a ligand (drug or endogenous molecule) Participate in a signaling cascade Distinguish from non-receptor-mediated drug action Graded or Dose-Response effects (vs. all-or-none) Understand “occupational theory” of drug action Molecular basis (ligand-receptor interaction) …

Objectives After reading this chapter, the student should be able to: Describe and diagram the three divisions (sympathetic, parasympathetic, and enteric) of the autonomic nervous system and list their functions. Describe and diagram the anatomy of the sympathetic pathways, including …

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