NCM 106 Pharmacology Module 3M PDF

 This has two subdivisions: o Symphatetic nervous system and...

 This has two subdivisions: o Symphatetic nervous system and parasympathetic Autonomic Nervous system Nervous System - Is composed of all nerve tissues, the brain, spinal cord, nerves and ganglia - The purpose of the nervous system is to  Also called as the visceral system receive stimuli and transmit information to  Because this acts on smooth muscles and nerve centers for an appropriate response glands, its functions include control and regulation of the heart, respiratory system, 2 types of nervous systems: gastrointestinal tract, bladder, eyes and glands 1. Central nervous system  Involuntary nervous system over which we  Interprets information sent by impulse from have little or no control the peripheral nervous system and returns  There are two sets of neurons of autonomic the instruction through the peripheral component of the peripheral nervous nervous system for appropriate cellular system which are the afferent or the actions sensory neuron and the efferent or the motor neuron- with 2 pathways. 2. Peripheral Nervous System 1. Afferent or sensory  Consist of two divisions:  Sends impulse to the cns and 1. Somatic nervous system the efferent neuron receives  Voluntary and acts on impulses from the brain and skeletal muscle to produce transmit these impulses locomotion and respiration through the spinal cord to 2. Autonomic nervous system the effector organ  Controls and regulate the 2. Efferent or motor functioning of the heart,  take note that the efferent respiratory system, pathways in the ANS are gastrointestinal system and divided into 2 branches: the glands sympathetic and  Large nervous system that parasympathetic nerves functions without our collectively these two conscious control branches are called the sympathetic nervous system and the parasympathetic nervous  system so take note that each organ is innervated by both sympathetic and parasympathetic nervous system A. Sympathetic Nervous System  also called as the adrenergic system  norepinephrine is the neurotransmitter that innervates smooth muscle on the other Drugs affecting Sympathetic Nervous hand System  has 4 types of adrenergic receptors on an STIMULATE DEPRESS/BLOCK organ cell which are: (the adrenergic 1. alpha₁ neruotransmitters) 2. alpha₂ Adrenergic Agonist/ Adrenergic 3. beta ₁ Adrenergics/Sympathomi Antagonists/Adrener 4. beta₂ metics gic Blockers/Sympathol B. Parasympathetic Nervous system ytics  also called as cholinergic system because it is the neurotransmitter acetylcholine which Adrenergic Agonists stimulates the receptor cells to produce the response  acerylcholine  has cholinergic receptors at organ cells which are either nicotinic or muscarinic Drugs act on sympathetic or parasymphatetic nervous system by either stimulating or  refers to drugs that stimulate the depressing responses. sympathetic nervous system  these drugs are also called adrenergics or sympathomimetics  it is called sympathomimetics because it mimics the neurotransmitters epinephrine and norepinephrine which act on the four main receptors of the effector cells  4 main receptors of effector cells: 1. alpha₁ 2. alpha₂ 3. beta₁ 4. beta₂   If these neurotransmitters act on the the blood vessels and the smooth muscle of receptors, a response is produced. gastrointestinal tract for the blood vessels, it leads to a decrease in vasoconstriction which then leads to Alpha₁ receptor decreased blood pressure because there is vasodilation. For the smooth muscle it leads to the decreased gastrointestinal tone and motility. Beta₁ receptor Alpha₁ receptors are located in the blood vessels in the eye, the bladder and the prostate. Stimulation of the alpha-1 receptor in the blood vessel causes vasoconstriction which leads to increased blood pressure and increased contractibility of the For the heart: heart activation of the alpha-1 receptor in the eye  Beta-1 receptors are located primarily in the leads to mydriasis or pupil dilation for the heart but are also found in the kidneys. bladder its relaxation, and for the prostate its  Stimulation of the beta-1 receptor in the contraction. heart leads to increased heart contraction Alpha₂ receptor thus there is increased heart rate. For the kidneys:  It increases the renin secretion which leads to increased angiotensin and later on increases the blood pressure. Beta₂ receptors Unlike alpha-1 receptors which are located on Beta-2 receptors are found mostly in the smooth specific organs. Alpha-2 receptors are located in the muscle of the gastrointestinal tract, the lungs, in the post-ganglionic sympathetic nerve endings uterus, and in the liver and the activation of beta-2 receptors in these organs lead to decreased when stimulated they inhibit the release of gastrointestinal tone and motility, bronchodilation, norepinephrine and such change has an effect on relaxation of the uterine smooth muscle and 3. Mixed-acting activation of the glycogenolysis which leads to the  The sympathomimetic medication stimulate increase of blood sugar. the adrenergic receptor sites and also stimulate the release of the norepinephrine After the neurotransmitter has performed its from the terminal nerve endings. Again, as function, the action must be stopped to prevent you can see in the illustration, the D prolonging the effect and it is possible through represents the sympathomimetic drug so it’s neurotransmitter inactivation. considered, to be mixed acting and if it will activate the receptor site and also stimulate Neurotransmitters are inactivated by: the release of the norepinephrine so that the 1. reuptake of the transmitter back into the norepinephrine can bind on the receptor site neuron (nerve cell terminal) after stimulating this receptor, a response is 2. enzymatic transformation or degradation produced. 3. Diffussion away from the receptor  Take note that aside from norepinephrine , epinephrine and dopamine can also produce sympathomimetic response. The mechanism of norepinephrine reuptake plays a more important role in an activation than does Catecholamines the enzymatic action after the reuptake of the  Chemical structures of a substance, transmitter in the neuron, the transmitter may be endogenous or synthetic, that can produce degraded or reused. sympathomimetic response 2 enzymes that inactivate norepinephrine: Endogenous Catecholamines: Epinephrine, 1. Monoamine Oxidase – located inside the neuron norepinephrine and dopamine 2. Catechol-O-Methyltransferase (COMT) – located outside the neuron Examples of Synthetic Catecholamines:  Isoproterenol 3 categories of sympathomimetic drugs:  Dobutamine Examples of Noncatecholamines:  Phenylephrine  Metaproteronol  Albuterol Noncatecholamines 1. Direct- acting  Stimulate the adrenergic receptors and  If it directly stimulates the adrenergic produce sympathomimetic response receptor  For example, in this illustration, this letter D What’s the difference between catecholamines is the drug. This is the sympathomimetic and noncatecholamines especially the synthetic drug. This is considered to be direct acting if ones? this one directly binds or activates the receptor and then a response is produced.  The key difference between catecholamines 2. Indirect-acting and non-catecholamines is that  A sympathomimetic drug is considered to be catecholamines are mainly direct acting indirect acting if it stimulates the release of adrenergic drugs that have catechol while norepinephrine from the terminal nerve non-catecholamines can be direct acting, endings so that the norepinephrine can indirect acting or dual acting adrenergic activate or stimulate the adrenergic receptor drugs that do not have catechol. and then once done, a response id produced.  Adrenergic Agonist:  Drug to drug interaction in the administration 1. Pseudoephedrine of epinephrine when epinephrine is  Stimulates the release of norepinephrine administered concurrently with digoxin from the nerve terminals and acts directly on cardiac dysrhythmia may occur, the nursing the alpha-1 and beta-1 receptors intervention for this one is to monitor the  Over-the-counter drug but controlled patient with the use of ecg or however this is controlled because this electrocardiogram medication can be used in the illegal  Beta blockers can antagonize the action of production of amphetamine and epinephrine methamphetamine  Tricyclic Antidepressants and Monoamine  This medication is helpful in relieving nasal Oxidase Inhibitors intensify and prolong and sinus congestion without rebound epinephrine’s effects congestion  Used with caution to people with diabetes It is important to know the side effects and mellitus because this medication can adverse reactions of epinephrine for us to render increase blood glucose level the appropriate nursing care. Contraindications: hypertension, closed-angle Side effects and Adverse Reactions: glaucoma, bronchitis, emphysema and urinary 1. Hypertension 7.Dizziness retention 2. Tachycardia 8. Urinary Retention 3. Palpitations 9. Nausea 2. Epinephrine 4. Restlessness 10. Vomiting  Epinephrine’s action is non-selective which 5. Tremors 11. Dyspnea means it stimulates more than one 6. Dysrhythmia 12. Pulmonary Edema adrenergic receptor  Acts on alpha-1 , beta-1, beta-2 adrenergic receptor sites  Unlike epinephrine which is non-selective,  Is frequently used in emergencies to treat albuterol is a selective beta-2 agonist which anaphylaxis or anaphylactic reaction which means this medication stimulates beta-2 means a life-threatening allergic response receptor sites  A potent inotropic drug which means this  This medication relaxes bronchial smooth medication can strengthen the myocardial muscle and promotes bronchodilation thus contraction this medication is therapeutic to condition  Administered through / Administration: like asthma subcutaneous/ly, IM  Again take note: Albuterol is a selective (intramuscular/ly),IV(intravenous/ly), beta-2 agonist however when administered inhaled/ inhalation this is not given orally in high doses it can also affect beta-1 and because it is rapidly metabolized in the remember beta-1 is found in the heart and gastrointestinal tract and the liver which when beta-1 receptor site is activated it can results in unstable serum level increase heart rate thus with the  Increases cardiac output, promotes administration of high doses of albuterol it vasoconstriction, and systolic blood pressure can also increase the heart rate elevation, increases heart rate , and  Most common SE of oral/inhalation albuterol; produces bronchodilation tremors, nervousness and restlessness  Take note: high doses of epinephrine can  Take note: When albuterol is taken cause cardiac dysrhythmia thus an concurrently with monoamine oxidase electrocardiogram monitoring is important inhibitor -> hypertensive crisis may occur  Can cause renal vasoconstriction which leads  Take note: Beta antagonist or beta blocker to renal perfusion and output with this being may inhibit the action of albuterol because said, it is important to monitor the urine albuterol is a beta-2 agonist which is a direct output of the patient opposite of beta antagonist  Adrenergic Agonists  Determine baseline glucose level. Patient Problems (In a client who need to receive Drug Target Indications adrenergic agonists include): receptor  Hypotension s  Decreased gas exchange Epinephrine alpha₁,  Dyspnea beta₁,  Hypoxemia beta₂ Epinephrine alpha₁, Hypotensive Planning (Agonists are administered in order to): HCI beta₁, states,  Patient’s vital signs will be within acceptable beta₂ bronchoshospas ranges. m, asthma  Patients will experience therapeutic effects Norepinephrine alpha₁, Acute by improved blood pressure, breathing bitartrate beta₁ Hypotension, pattern and cardiac output cardiogenic and septic shock Nursing Interventions: Dopamine HCI alpha₁, Hypotension,  Administer epinephrine 1mg for cardiac beta₁ Heart Failure, resuscitation; may repeat every 3-5 minutes. septic and Follow each does with 20-mL saline flush to cardiogenic shock ensure proper delivery. Normally, Midodrine HCI alpha₁ Orthostatic epinephrine is administered 1mg IV over 1 hypotension minute or more. Phenylephrine alpha₁ Sinus and nasal  Monitor IV site frequently when HCI congestion, administering norepinephrine bitartrate or hypotension/shoc dopamine this is because extravasation of k, PSVT, these drugs cause tissue damage and glaucoma, necrosis within 12 hours. These drugs should pupillary dilation be diluted sufficiently in IV fluids. Pseudoephedri alpha₁, Nasal congestion  To administer the antidote, phentolamine ne HCI alpha₂, mesylate, 5-10 milligrams diluted in 10-15 beta₁ mL of normal saline infiltrated into the area Albuterol beta₂ for IV extravasation of norepinephrine and dopamine. Metaproterenol beta₂ Acute  Check blood pressure every 3-5 minutes if sulfate bronchospasm, alpha-adrenergic agonist is administered IV asthma and and monitor ECG. COPD  Cold medications by spray or drops must be Dobutamine beta₁ Heart failure, administered with the head in upright HCI cardiogenic shock position. and for cardiac  Encourage patient to have an EpiPen readily surgery available at all times and to store in cool, Terbutaline beta₂ Asthma, COPD, dark place. Refrigeration of epipen is not sulfate and prophylaxis recommended. and treatment of  Teach patient and family that EpiPen must be bronchospasm used immediately upon the initial occurrence of difficulty breathing, wheezing, Adrenergic Agonist hoarseness, hives, itching, or swelling of the Assessment: lips and tongue.  Record baseline vital signs for future  Do not use Epipen if particles are pink to comparisons brown. In the administration of epinephrine  Determine patient’s health history. through the use of epipen take care to inject  subcutaneously and not intradermally and pressure. Adrenergic agonist are centrally acting be sure to apply sufficient pressure to or those that activate or stimulate the alpha-2 activate the epipen while holding the device receptors. in place for 5-10 seconds. The epipen should be inserted into the outer thigh after the Central – Acting Alpha Agonists administration, massage the injection site for  These medications are used to control 10 seconds to promote absorption and hypertension reduce vasoconstriction and tissue irritation.  Take note: That high doses of clonidine and  Again before using the epipen check for pink methyldopa can cause sodium and water to round particles of the epinephrine retention; frequently administered with through this part of the EpiPen diuretics. These medications must not be abruptly discontinued because rebound hypertensive crisis may result however that is less likely to happen with the use of guanfacine Examples:  Clonidine  Methyldopa  Guanfacine Clonidine  For hypertension / hypertensive medication  Alpha-2 adrenergic agonist that’s why its considered a central acting alpha agonist  Do not administer the epinephrine if  This medication is available in oral tablet or particles are pink to brown in color. transdermal patch form which is replaced every 7 days; skin irritation may occur with Pseudoephedrine this route of aministration.  Alpha-1 and beta1  This medication is not used if pregnant or the Epinephrine woman is contemplating of pregnancy  Alpha-1, beta-1 and bet-2 because clonidine is considered as pregnancy Albuterol category C which means that this medication  Beta-2 may pose a risk to the fetus Alpha-2 receptor is located in the post-ganglionic  This medication may produce bradycardia, sympathetic nerve ending and when stimulated hypotension, sedation and dry mouth at very they inhibit the release of norepinephrine which low doses leads to the decrease in vasoconstriction which then results in vasodilation and decrease in blood Methyldopa  Another example of central acting alpha agonist  This is used for chronic or pregnancy induced hypertension.  This medication must not be used in patients with impaired liver function. Side effects and Adverse Reactions:  Drowsiness  Dry mouth  Dizziness  Slow heart rate (bradycardia)  Headache  Nasal congestion   Nightmares bladder, neck and  Constipation prostate gland  Edema Beta₁ Decreases Heart rate, reduces force of Adrenergic Antagonist (Adrenergic Blocker) contraction  Drugs that block the effect of adrenergic Beta₂ Constricts bronchioles, neurotransmitters contracts uterus;  Also called as adrenergic blockers or inhibits glycogenolysis symoatholytics which can decrease  Most adrenergic antagonost block either the blood glucose alpha receptor or the beta receptor  These medications block the effect of Alpha- Adrenergic Antagonist neurotransmitters either by :  Drugs that block or inhibit a response at the  Directly occupying the receptors or alpha-adrenergic receptor site  Indirectly by inhibiting the release of  They are also called adrenergic blocker or the neurotransmitters norepinephrine alpha blocker and this group of medication and epinephrine is divided into two subgroups: 1. selective alpha blockers(which Remember that receptor sites in the adrenergic blocks only the alpha-1) system are: 2. nonselective alpha blockers (which blocks both alpha-1 and Alpha₁ Alpha-adrenergic alpha-2 receptor sites ) antagonist  Can promote vasodilation causing a Alpha₂ Adrenergic Neuron decrease in blood pressure (promote Antagonist vasodilation -> dec. BP) Beta₁ Beta- Adrenergic  If vasodilation is long-standing, Antagonist hypotension may result (long-standing Beta₂ Beta- Adrenergic vasodilation -> orthostatic hypotension) Antagonist  Dizziness may be a symptom of decrease in blood pressure as blood pressure decreases, Drugs that block the effect of the adrenergic pulse rate usually increase to compensate neurotransmitters are collectively called as for the low blood pressure and inadequate adrenergic antagonists. Those adrenergic blood flow. antagonists that block alph-1 and alpha-2 are  Alpha antagonist can be used to treat called alpha-adrenergic antagonists and peripheral vascular disease such as those that specifically block alpha-2 are called Raynaud disease this is because adrenergic antagonists. Adrenergic antagonist vasodilation occurs permitting more blood that block beta-1 and beta -2 are beta – flow to the extremities. adrenergic antagonist.  Also helpful in decreasing symptoms of Benign Prostatic Hyperplasia (BPH) Take note: That the following receptors Drug Target Indications happen when alpha-1 receptor site is blocked. Receptors Receptor Responses Phentolamine Alpha₁ Antidote for Alpha₁ *Vasodilation: mesylate dopamine, decreases BP; reflex dobutamine, tachycardia might phenylephrine, result; epinephrine, *mydriasis (dilation of NE, and pupils), catecholamine *suppresses ejaculation extravasation *reduces contraction of smooth muscle in Doxazosin Alpha₁ Hypertension mesylate and BPH Prazosin HCL Alpha₁ Hypertension Terazosin Alpha₁ Hypertension HCI and BPH Another example of alpha blockers however these medications are nonselective because these medications do not only target alpha-1 but also target beta receptors. Drug Target Indications Receptors  Or the adrenergic antagonists that target Carvedilol Alpha₁ and Antidote for beta-1 and beta-2 beta₁ and dopamine,  These medications are also called as beta beta₂ dobutamine, blockers phenylephrine,  Decrease heart rate and decrease in blood epinephrine, pressure usually follows NE, and  Useful in treating mild to moderate catecholamine hypertension, angina, heart failure, and extravasation myocardial infarction Labetalol Alpha₁ and Acute/chronic  You need to remember that beta blockers beta₁ and hypertension should not be abruptly discontinued instead beta₂ it must be tapered off over 1-2 weeks. Because if not it can lead to tachycardia, hypertension myocardial infarction. 2. Beta- Adrenergic Antagonist  Could be selective and non-selective  Nonselective beta blockers block both beta- 1 (decrease heart rate) and beta-2 (leads to bronchoconstriction) receptors  This beta blocker is contraindicated in asthma also non selective beta blockers are used with extreme caution in patient with Chronic Obstructive Pulmonary Disorder (COPD)  Remember that electrolyte imbalances such as hypomagnesemia and hypokalemia should be corrected before initiating beta blocker therapy Drug Examples of Nonselective Beta Adrenergic Antagonist  This medications block beta-1 and beta -2  Bet-2 receptors are mostly located in the lungs  Can cause bronchoconstriction Drug Target Indications Receptors Propanol beta₁ and beta Hypertension, ₂ angina, MI,  HF,  Onset of action for oral preparation is 1 dysrhythmia hour, peak time is 2-1 hours and duration of and migraine action is 24 hrs. prophylaxis  Effective for once-daily dosing Nadolol beta₁ and beta Hypertension  Contraindication: Bradycardia, heart block, ₂ and angina cardiogenuc shock, acute heart failure, Pindolol beta₁ and beta Hypertension asthma and sick sinus syndrome ₂  NSAIDS decrease the hypotensive effect of Sotalol beta₁ and beta For ventricular atenolol ₂ dysrhythmia,  Hypotension can be potentiated when taken atrial flutter concurrently with another antihypertensive and atrial medication fibrillation  When atenolol is administered concurrently Timolol beta₁ and beta Hypertension, with atropine or other anticholinergics that maleate ₂ glaucoma leads to increased absorption of atenolol treatment, and for migraine Side effects and adverse reactions: prophylaxis 1. Bradycardia 7. Cardiac dysrhythmia 2. Hypotension 8. Flushing Selective Beta – Adrenergic Antagonist 3. Headache 9. Fatigue  Only target one type of beta receptor 4. Dizziness 10. Erectile dysfunction 5. Cold extremities 11. Depression Drug Target Indications 6. Bronchospasm Receptors Metoprolol beta₁ Hypertension, 3. Adrenergic Neuron Antagonist tartate angina. HF, and  Adrenergic neuron blockers acute MI  Block the release of NE from the Atenolol beta₁ sympathetic terminal neurons Acebutolol beta₁ Hypertension and  Used to decrease blood pressure HCI dysrhythmia Ex. Reserpine Betaxolol beta₁ Hypertension and  Resembles alpha and beta adrenergic glaucoma blockers  Reduces the serotonin and catecholamine Bisoprolol beta₁ Hypertension transmitters, depletion of which may lead to fumarate severe mental depression Esmolol HCI beta₁ Supraventricular  Withhold the administration of reserpine if tachydysrhythmia heart rate (HR) of the patient is 60 and hypertension beats/min  Advise the patient that the therapeutic Atenolol effects of adrenergic neuron antagonist may  Selective beta-1 blocker not occur for two to three weeks after  This medication decreases the sympathetic initiation of therapy outflow to the periphery and suppresses the renin- angiotensin- aldosterone system Autonomic Nervous system (RAAS) response 1. Sympathetic Nervous System  Blocks beta-1 receptors -> decreases heart  Also called as the adrenergic system rate peripheral vascular resistance, force of  Norepinephrine cardiac contraction and cardiac output and  4 types of adrenergic receptors on organ reduces both systolic and diastolic blood cells: pressure 1. alpha₁  This medication is available in tablets and in 2. alpha₂ parenteral form for IV administration 3. beta₁  4. beta₂ 2 types of cholinergic receptors: 1. Muscarinic receptors  (stimulate the smooth muscle and slow the heart rate) 2. Nicotinic receptors  (neuromuscular, affects the skeletal muscles) 2 types of cholinergic agonists: 1. Direct-acting 2. Parsympathetic Nervous System  act on the receptors to activate a tissue  also called as cholinergic system response  acetylcholine 2. Indirect acting  Cholinergic receptors at organ cells:  inhibit the action of the enzyme nicotinic or muscarinic cholinesterase/ acetylcholinesterase and  Acetylcholinesterase enzyme may inactivate by forming a chemical complex that acetylcholine before it reaches allows acetylcholine to persist and attach to the receptor Drugs affecting Parasympathetic Nervous system STIMULATE DEPRESS/BLOCK Cholinergic Agonist Cholinergic Antagonist Cholinergic Agonists  Drugs that stimulate parasympathetic nervous system  Also called as parasympathomimetics 1. Direct-Acting Cholinergic Agonist  They are called parasympathomimetics  Many drugs classified as direct-acting because they mimic the parasympathetic cholinergic agonists are primarily neurotransmitter acetylcholine, the selective to the muscarinic receptors but neurotransmitter located at the ganglions are nonspecific because the muscarinic and the parasympathetic terminal nerve receptors are located in the smooth endings is acetylcholine muscle of the gastrointestinal tract, the  Stimulate the parasympathetic nervous genital urinary tract, the glands and the system by mimicking the parasympathetic heart. neurotransmitter acetylcholine  Drug examples of direct-acting  This neurotransmitter innervates cholinergic agonists which acts on the cholinergic receptors in the organs, tissues muscarinic receptors: and glands o Bethanecol o Metaclopramide Hydrochloride (HCI)   What you need to remember in of possible problems in a client who need to receive administering these medications are the bethanecol include : following: Patient Problems o Should be prescribed cautiously to  Urinary Retention patients with low blood pressure and  Hypotension chronic obstructive pulmonary disease or COPD  Take note: Muscarinic agonists are contraindicated for patients with intestinal of Planning: urinary tract obstruction, severe bradycardia  The objective of administering bethanecol or active asthma such as methanical and to the client is to promote voiding (patient methylclopramide are contraindicated to will void more frequently after taking patients with intestinal or urinary tract cholinergic agonists) obstruction, severe bradycardia or active asthma Nursing Interventions: A. Bethanecol That the nurse must carry out an administering  This medication is direct-acting cholinergic bethanecol will include the following: agonist  Monitor the vital signs (heart rate, blood  Acts on the muscarinic receptor pressure decrease when large doses of  This medication is used in a treatment of cholinergics are taken) urinary retention and neurogenic bladder  orthostatic hypotension is a side effect of  Principal use is to promote urination by cholinergic agonists such as mechanical stimulating the muscarinic cholinergic record fluid intake and output decreased receptors in the detrusor muscle to contract urinary should be reported because it may the bladder and produce urine output be related to urinary obstruction  This medication can also increase peristalsis  Give cholinergic agonists 1 hour before or 2 in the gastrointestinal tract (GIT) and hrs after meals to minimize nausea and increase gastric emptying time vomiting  This drug should be taken on an empty  If a patient complains of gastric pain the stomach 1-2 hours before meals to minimize drug may be given with meals nausea and vomiting  Check serum amylase, lipase, aspartate aminotransferase (AST), and bilirubin levels Side effects and adverse reactions  These laboratory values may increase 1. Hypotension slightly in a patient taking cholinergic 2. Tachycardia agonists 3. Excessive salivation  The nurse must also auscultate breath 4. Increased gastric acid secretion sounds for rails, crackling sounds or rhonchi 5. Abdominal cramps because cholinergic agonists can increase 6. Diarrhea bronchial secretions. 7. bronchospasm  Have (IV) atropine sulfate (0.6 – 1.2 mg) available as an antidote for cholinergic Cholinergic Agonist, Direct Acting: Bethanecol overdose Assessment:  Early signs of overdosing includes flushing,  Assess baseline vital signs salivation, sweating, nausea and abdominal  Assess urine output (should be> 1500 cramps mL/day)  Increase bathing frequency and linen  Obtain patient history of health problems change when needed because diaphoresis such as peptic ulcer, urinary obstruction or or excessive perspiration may occur asthma  Monitor for possible cholinergic crisis of Cholinergic Agonist such as methanical can which symptoms will include muscular aggravate symptoms of these conditions examples weakness and increased salivation Evaluation:  The function of the enzyme cholinesterase is  Determine effectiveness of the cholinergic to break down acetylcholine into choline and agonist or anticholinesterase acetic acid.  A small amount of cholinesterase can break B. Metoclopramide HCI down a large amount of acetylcholine in a  Also an example of direct-acting cholinergic short period. agonist  A cholinesterase inhibitor binds with  Acts on muscarinic receptor cholinesterase allowing acetylcholine to  This medication is usually prescribed to activate muscarinic and nicotinic cholinergic treat gastroparesis, nausea and receptors. gastroesophageal reflux disease (GERD)  This action permits skeletal muscle  In low doses, metoclopramide enhances stimulation which increases the force of gastric motility and thus accelerates gastric muscular contraction because of this action, emptying time the cholinesterase inhibitors are useful to increase muscle tone for patients with Direct-Acting Cholinergic Agonist but this myasthenia gravis by increasing time acts on nicotinic receptor acetylcholine additional effects occur such as increase in GI motility bradycardia, miosis, or Drug examples of these medications: constriction of the pupils, bronchial  Pilocarpine constriction and increased micturition  Carbachol Reversible Cholinesterase Inhibitors Pilocarpine  Primary use: to treat myasthenia gravis  Direct-acting cholinergic agonist: eye  This medications are used to produce  Used to treat glaucoma by relieving pupillary constriction in the treatment of (intraocular) fluid pressure in the eye and to glaucoma and to increase muscle strength promote miosis (dilation) in eye surgery and in patients with myasthenia gravis examinations  Drug effects persist for several hours  Constricts the pupils of the eyes which leads to the opening of the Schlemm canal to Drug examples: promote drainage of aqueous humor Neostigmine  Oral form of pilocarpine is used to relieve Pyridostigmine bromide xerostomia (dry mouth) Ambenonium Chloride Edrophonium Chloride Indirect Cholinergic Agonists Physostigmine  Which have an interaction with either – antidote for atropine, for nicotinic or muscarinic receptors, the anticholinergic toxicity indirect cholinergic agonists do not act on cholinergic receptors Contraindications:  Do not have an interaction on the Asthma cholinergic receptors Diabetes  Inhibit or inactivate the enzyme Cardiovascular disease cholinesterase -> permitting acetylcholine Intestinal/ urinary obstruction to accumulate at the receptor sites  This action gives them the name Must be used with Caution: cholinesterase (CHE) inhibitors or Bradycardia acetylcholine inhibitors (acetylcholinesterase Peptic ulcer (AChE) inhibitors ) or anticholinesterase Seizure o Reversible Dysrhythmia o Irriversible Side effects: Hypotension Bradycardia  Sweating Hypersalivation GI distress (can be manifested: anorexia, nausea, vomiting, abdominal pain, and diarrhea) Irreversible Cholinesterase Inhibitors  Indirect Cholinergic Agonists: Cholinesterase Inhibitors  Primary clinical indication : glaucoma  This medication is used to produce pupillary constriction.  Irreversible cholinesterase inhibitors are potent agents because of their long- lasting effects  Take note that pralidoxime chloride – antidote for irreversible and reversible cholinesterase inhibitors NCM 106: Pharmacology Module 3M: ANS Part 3 → Drug examples: Atropine Sulfate Scopolamine CHOLINERGIC Atropine Sulfate ANTAGONISTS → First derived from a belladonna plant → Drugs that inhibit the action of → Atropine sulfate acts on muscarinic acetylcholine by occupying the receptors and have little effect on acetylcholine receptors nicotinic receptors except in high doses → These medications are also → Atropine sulfate is useful primarily in pre-operative medication to decrease called as muscarinic salivary secretions antagonists, anticholinergics, → This medication also acts as an agent cholinergic blocking agents, to increase heart rate when bradycardia antispasmodics, or is present parasympatholytics → This medication is also used as an antidote for miscarriage agonist → These medications affect the poisoning caused by overdose of heart, respiratory tract, GI tract, cholinesterase inhibitor of a muscarinic urinary bladder, eyes and drug such as bethanechol exocrine glands → Atropine sulfate blocks acetylcholine → Major Responses: by occupying muscarinic receptor Decrease in GI motility → This medication increases the heart rate by blocking vagus stimulation and Decrease salivation promotes dilation of the pupils by Promote mydriasis paralyzing the iris sphincter Increase in pulse rate → Two most frequent uses of → Other Effects: Atropine Sulfate Decrease bladder 1. To decrease salivation and respiratory secretions contraction (results to preoperatively urinary retention) 2. To treat sinus bradycardia by Decrease rigidity and increasing the heart rate tremors related to the → Atropine sulfate is also useful neuromuscular ophthalmically because of its property to excitement cause mydriasis or dilation of the pupils → This medication can also cause → NOTE: Anticholinergics and cycloplegia or paralysis of the adrenergic agonists produce ciliary muscle of the eye which many of the same responses are necessary before an eye → A cholinergic antagonist can act examination and in the treatment as an antidote to the toxicity of the iris (iritis) and uveal tract caused by cholinesterase Common Side Effects: Xerostomia (dry mouth) inhibitors and organophosphate Nasal dryness Organophosphate is an Blurred vision example of an irreversible Tachycardia cholinesterase inhibitor Constipation → May also block the effect of the Urinary retention direct-acting and indirect-acting Other Side Effects and Adverse parasympathomimetics Reactions: Nausea Headache Dehydration Yuson, Drea NCM 106: Pharmacology Seizure CHOLINERGIC ANTAGONIST: Hypotension or hypertension Antiparkinson Photophobia (intolerance to Anticholinergics bright light) → Affect the CNS by suppressing Coma the tremors and muscular rigidity of parkinsonism but has little CHOLINERGIC AGONIST, DIRECT ACTING: ATROPINE effect on mobility and muscle weakness Assessment: → As a result, several Before administering atropine sulfate, anticholinergic drugs were the nurse must: developed for the treatment of ✓ Assess baseline vital signs parkinsonism such as (drug ✓ Assess urine output Patient Problems: examples): ❖ Urinary retention Trihexyphenidyl ❖ Hypertension hydrochloride (HCl) Planning: Biperiden Atropine sulfate is administered to the Benztropine client in order: ✓ To decrease secretions before Benztropine surgery → Decreases the involuntary and ✓ To increase heart rate will be diminishes the signs and symptoms of increased tremors and muscle rigidity that occur Nursing Interventions: with parkinsonism and ✓ Monitor vital signs pseuoparkinsonism ✓ Determine fluid intake and output → Available as oral tablet and as ✓ Assess bowel sounds parenteral IM and IV injections ✓ Teach patient with narrow-angle → NOTE: Alcohol and other CNS glaucoma to avoid atropine-like depressants potentiate sedation drugs → Anticholinergics, phenothiazines and Evaluation: tricyclic antidepressants may increase ✓ Evaluate response to the anticholinergic effect anticholinergic medications → Side effects of benztropine are similar to anticholinergic drugs Cholinergic Antagonists are also used as Antiparkinson / Anti-parkinson medications CHOLINERGIC ANTAGONIST: Studies indicate that anticholinergics affect Motion Sickness the central nervous system as well as the parasympathetic nervous system. → The effect of anticholinergics on the CNS benefit patients who are prone to motion sickness → Drug Examples: (antihistamines) Scopolamine Dimenhydrinate Cyclizine Meclizine Hydrochloride (HCl) → Most of the mentioned drugs can be purchased over-the-counter Yuson, Drea NCM 106: Pharmacology with the exception of scopolamine → NOTE: Cholinergic antagonists are contraindicated to glaucoma Scopolamine → Available topically as a skin patch; placed behind the ear → Scopolamine is frequently prescribed for activities such as flying, cruising on the water and bus for automobile trips → Side Effects and Adverse Reactions: Xerostomia Drowsiness Visual disturbances Constipation Tachycardia (when taken in large doses) Hypotension Dysphagia Anhidrosis Flushing Yuson, Drea