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nurs 125 exam 2

gout, adrenergic,Adrenergic-Blocking Drugs, cholinergics and anticholinergics

The stomach secretes: Hydrochloric acid (HCl) Bicarbonate Pepsinogen Intrinsic factor Mucus Prostaglandins
Glands of the Stomach Cardiac Pyloric Gastric The cells of the gastric gland are the largest in number and of primary importance when discussing acid control
Cells of the Gastric Gland Parietal Chief Mucous Endocrine Enterochromaffin
Parietal cells Produce and secrete HCl Primary site of action for many of the drugs used to treat acid-related disorders
Chief cells Secrete pepsinogen, a proenzyme Pepsinogen becomes pepsin when activated by exposure to acid Pepsin breaks down proteins
Mucous cells Mucus-secreting cells (surface epithelial cells) Provide a protective mucus coat Protect against self-digestion by HCl and digestive enzymes
Hydrochloric Acid Secreted by parietal cells when stimulated by food, caffeine, chocolate, and alcohol Maintains stomach at pH of 1 to 4 Acidity aids in the proper digestion of food and defenses against microbial infection via the GI tract
Acid-Related Diseases Peptic ulcer disease (PUD) Gastric or duodenal ulcers that involve digestion of the GI mucosa by the enzyme pepsin
Acid-Related Diseases Helicobacter pylori (H. pylori) Bacterium found in GI tract of 90% of patients with duodenal ulcers and 70% of those with gastric ulcers First-line therapy includes a 10- to 14-day course of a proton pump inhibitor and antibiotics
Acid-Related Diseases (cont’d) GI lesions are a common finding in ICU patients, especially within the first 24 hours after admission Factors include decreased blood flow, mucosal ischemia, hypoperfusion, and reperfusion injury Nasogastric (NG) tubes and ventilators predispose patien
Types of Acid-Controlling Drugs Antacids H2 antagonists Proton pump inhibitors
Antacids Basic compounds used to neutralize stomach acid Salts of aluminum, magnesium, calcium, and/or sodium Many antacid preparations also contain the antiflatulent (antigas) drug simethicone
Antacids: Mechanism of Action Do not prevent the overproduction of acid but instead help to neutralize acid secretions Promote gastric mucosal defensive mechanisms Stimulate secretion of: Mucus: protective barrier against HCl Bicarbonate: helps buffer acidic properties of HCl Pro
Antacids: Drug Effects Reduction of pain associated with acid-related disorders Raising gastric pH 1 point (1.3 to 2.3) neutralizes 90% of the gastric acid Reducing acidity reduces pain as a result of:
Antacids (cont’d) Over-the-counter formulations available as: Capsules and tablets Powders Chewable tablets Suspensions Effervescent granules and tablets
Antacids Used alone or in combination Aluminum salts Magnesium salts Calcium salts Sodium bicarbonate
Antacids: Aluminum Salts Have constipating effects Often used with magnesium to counteract constipation Often recommended for patients with renal disease (more easily excreted)
Antacids: Magnesium Salts Commonly cause diarrhea; usually used with other drugs to counteract this effect Dangerous when used with renal failure—the failing kidney cannot excrete extra magnesium, resulting in accumulation
Antacids: Magnesium Salts (cont’d) Examples Hydroxide salt: magnesium hydroxide (Milk of Magnesia) Carbonate salt: Gaviscon (also a combination product) Combination products such as Maalox, Mylanta (aluminum and magnesium)
Antacids: Calcium Salts Many forms, but carbonate is most common May cause constipation, kidney stones Also not recommended for patients with renal disease—may accumulate to toxic levels Long duration of acid action—may cause increased gastric acid secretion (hyperacidity reb
if someone has renal failure which antacid you should not use one with magnesium because renal can't displaced
Antacids: Sodium Bicarbonate Highly soluble Buffers the acidic properties of HCl Quick onset, but short duration May cause metabolic alkalosis Sodium content may cause problems in patients with heart failure, hypertension, or renal insufficiency
A patient who has chronic renal failure wants to self-treat with an antacid for occasional heartburn. Which medication is the best choice for this patient? A magnesium-containing antacid A calcium-containing antacid An aluminum-containing antacid Beca c
Antacids and Antiflatulents Antiflatulents: used to relieve the painful symptoms associated with gas Several drugs are used to bind or alter intestinal gas and are often added to antacid combination products simethicone
Antacids: Adverse Effects Minimal and depend on the compound used Aluminum and calcium Constipation Magnesium Diarrhea Calcium carbonate Produces gas and belching; often combined
if elderly has heart failure you should not give sodium bicarb - volume, fluid retention
Antacids: Drug Interactions (cont’d) Increased stomach pH Increased absorption of basic drugs Decreased absorption of acidic drugs Increased urinary pH Increased excretion of acidic drugs Decreased excretion of basic drugs
Histamine 2 (H2) Receptor Antagonists Reduce acid secretion All available over the counter in lower dosage forms
Histamine 2 (H2) Receptor Antagonists Most popular drugs for treatment of acid-related disorders cimetidine (Tagamet) nizatidine (Axid) famotidine (Pepcid) ranitidine (Zantac)
H2 Antagonists: Mechanism of Action Competitively block the H2 receptor of acid-producing parietal cells Reduced hydrogen ion secretion from the parietal cells Increase in the pH of the stomach Relief of many of the symptoms associated with hyperacidity-related conditions
H2 Antagonists: Drug Effect and Indications Drug effect Suppressed acid secretion in the stomach Indications Gastroesophageal reflux disease (GERD) Peptic ulcer disease (PUD) Erosive esophagitis Adjunct therapy to control upper GI bleeding Zollinger-Ellison syndrome
H2 Antagonists: Adverse Effects Overall, very few adverse effects Central nervous system adverse effects in elderly patients include confusion and disorientation Cimetidine may induce impotence and gynecomastia Thrombocytopenia has been reported with ranitidine and famotidine
H2 Antagonists: Drug Interactions cimetidine (Tagamet) Binds with P-450 microsomal oxidase system in the liver, resulting in inhibited oxidation of many drugs and increased drug levels All H2 antagonists may inhibit the absorption of drugs that require an acidic GI environment for abso
H2 Antagonists: Drug Interactions cimetidine (Tagamet) Binds with P-450 microsomal oxidase system in the liver, resulting in inhibited oxidation of many drugs and increased drug levels All H2 antagonists may inhibit the absorption of drugs that require an acidic GI environment for abso
H2 Antagonists: Drug Interactions Smoking has been shown to decrease the effectiveness of H2 blockers For optimal results, H2 receptor antagonists are taken 1 to 2 hours before antacids
When working with an elderly patient who has been admitted for a possible gastrointestinal bleed, the nurse identifies which drug as having the potential to cause confusion and disorientation? An antacid A proton pump inhibitor An H2 antagonist A muco An H2 antagonist
Proton Pump Inhibitors (PPIs) The parietal cells release positive hydrogen ions (protons) during HCl production This process is called the proton pump H2 blockers and antihistamines do not stop the action of this pump
Proton Pump Inhibitors lansoprazole (Prevacid) omeprazole (Prilosec) rabeprazole (AcipHex) pantoprazole (Protonix) esomeprazole (Nexium)
Proton Pump Inhibitors: Mechanism of Action Irreversibly bind to H+/K+ ATPase enzyme This bond prevents the movement of hydrogen ions from the parietal cell into the stomach Results in achlorhydria—ALL gastric acid secretion is temporarily blocked To return to normal acid secretion, the parietal
Proton Pump Inhibitors: Indications GERD Erosive esophagitis Short-term treatment of active duodenal and benign gastric ulcers Zollinger-Ellison syndrome Nonsteroidal antiinflammatory drug (NSAID)–induced ulcers Stress ulcer prophylaxis Treatment of Helicobacter pylori–induced ulcers
Proton Pump Inhibitors: Adverse Effects PPIs are generally well tolerated Possible predisposition to GI tract infections (Clostridium difficile) Osteoporosis and risk of wrist, hip, and spine fractures in long-term users Pneumonia Depletion of magnesium
Sucralfate (Carafate) Cytoprotective drug Used for stress ulcers, peptic ulcer disease Attracted to and binds to the base of ulcers and erosions, forming a protective barrier over these areas Protects these areas from pepsin, which normally breaks down proteins (making ulce
adrenergic drugs drugs that stimulate the sympathetic nervous system - flight or flight, bronchodilations, elevated bp, elebated pulse, pupils are dilated
sympathetic stimulants adrenergic, adrenominmetics, adrenergic agonists and sympathomimetics
parasympathic stimulants cholinergics, cholinergic agonists and parasympathomimetics
characteristics of adrenergics are mimics the effects of SNS neurotran (catecholamines) NE, EPI and dopamine
Alpha1-adrenergic receptors Located on postsynaptic effector cells (the cell, muscle, or organ that the nerve stimulates)
Alpha2-adrenergic receptors Located on presynaptic nerve terminals (the nerve that stimulates the effector cells) Control the release of neurotransmitters
Beta-Adrenergic Receptors Beta-Adrenergic Receptors postsynaptic effector cells
Beta1-adrenergic receptors—located receptors—located primarily in the heart
Beta2-adrenergic receptors—located in in smooth muscle of the bronchioles, arterioles, and visceral organs
Beta-Adrenergic Agonist Responses Bronchial, GI, and uterine smooth muscle relaxation Glycogenolysis Cardiac stimulation
Dopaminergic Receptors An additional adrenergic receptor Stimulated by dopamine Causes dilation of the following blood vessels, resulting in increased blood flow
Catecholamines Substances that can produce a sympathomimetic response Endogenous Epinephrine, norepinephrine, dopamine Synthetic Dobutamine, phenylephrine
Catecholamines Mechanism of Action Direct-acting sympathomimetic Binds directly to the receptor and causes a physiologic response
Catecholamines Mechanism of Action Indirect-acting sympathomimetic Causes release of catecholamine from storage sites (vesicles) in nerve endings Catecholamine then binds to receptors and causes a physiologic response
Catecholamines Mechanism of Action Mixed-acting sympathomimetic Directly stimulates the receptor by binding to it and Indirectly stimulates the receptor by causing the release of stored neurotransmitters from vesicles in the nerve endings
Catecholamines Stimulation of alpha-adrenergic receptors on smooth muscles results in Vasoconstriction of blood vessels Relaxation of GI smooth muscles (decreased motility) Constriction of bladder sphincter Contraction of uterus Male ejaculation Contraction of pupillary muscles
Catecholamines Stimulation of of beta1-adrenergic receptors on the myocardium, atrioventricular (AV) node, and sinoatrial (SA) node results in cardiac stimulation
Catecholamines Drug Effects (cont’d) Stimulation of beta2-adrenergic receptors on the airways results in Bronchodilation (relaxation of the bronchi) Other effects of beta2-adrenergic stimulation Uterine relaxation Glycogenolysis in the liver
Catecholamines Treatment of asthma and bronchitis
examples of bronchildilators are Examples: albuterol (works the fastest), ephedrine, epinephrine, formoterol, levalbuterol, metaproterenol, pirbuterol, salmeterol, and terbutaline*
catecholamines are used for what? treatment of asthma and bronchitis, treatment of nasal congestion, temporary relief of conjunctival congestion (eyes), reduction of intraocular pressure & dilation of pupils
catecholamines are used for treatment of nasal congestion -- HOW so? Intranasal (topical) application causes constriction of dilated arterioles and reduction of nasal blood flow, thus decreasing congestion Alpha1-adrenergic receptors Examples: ephedrine, naphazoline, oxymetazoline, phenylephrine, and tetrahydrozoline
Vasoactive Adrenergics (Pressors, Inotropes) - big hitters! seen usually in the ER Also called cardioselective sympathomimetics Used to support the heart during cardiac failure or shock; various alpha and beta receptors affected
Vasoactive Sympathomimetics (Pressors, Inotropes): Examples dopamine epinephrine phenylephrine norepinephrine, dobutamine ephedrine fenoldopam midodrine
Alpha-Adrenergic Adverse Effects CNS Headache, restlessness, excitement, insomnia, euphoria Cardiovascular Palpitations (dysrhythmias), tachycardia, vasoconstriction, hypertension Other Loss of appetite, dry mouth, nausea, vomiting, taste changes (rare)
Beta-Adrenergic Adverse Effects CNS Mild tremors, headache, nervousness, dizziness Cardiovascular Increased heart rate, palpitations (dysrhythmias), fluctuations in BP Other Sweating, nausea, vomiting, muscle cramps
Nursing Implications for individuals with chronic lung disease Instruct patients to avoid factors that exacerbate their condition Encourage fluid intake (up to 3000 mL/day) if permitted Educate patients about proper dosing, use of equipment (metered-dose inhaler [MDI], spacer, nebulizer), and equipment care
what to do with intravenous administration Check IV site often for infiltration Use clear IV solutions Use an infusion pump Infuse drug slowly to avoid dangerous cardiovascular effects Monitor cardiac rhythm
Salmeterol is indicated for for prevention of bronchospasms, not management of acute symptoms
Overuse of nasal decongestants may cause rebound nasal congestion or ulcerations
Administering two adrenergic drugs together may precipitate severe cardiovascular effects such tachycardia or hypertension
when someone is having an asthma attack there is no what? GAS EXCHANGE - no alveoli is open -
Monitor for therapeutic effects (cardiovascular uses) Decreased edema Increased urinary output Return to normal vital signs Improved skin color and temperature Increased LOC
Monitor for therapeutic effects (asthma) Return to normal respiratory rate Improved breath sounds, fewer crackles Increased air exchange Decreased cough Less dyspnea Improved blood gases Increased activity tolerance
REMEMBER!! TO listen for everything so you can know a patient change of status lungs, belly heart
adrenerigic blocking drugs, what do u expect from it? Decrease bronchildilators, pupil constrict - Bind to adrenergic receptors, but inhibit or block stimulation of the sympathetic nervous system (SNS) Have the opposite effect of adrenergic drugs Inhibit—or lyse—sympathetic stimulation
adrenergic blockers are also known as Adrenergic antagonists Sympatholytics Alpha blockers, beta blockers, or alpha-beta blockers
adrenergic blockers are classified by what? type of adrenergic receptor they block Alpha1 and alpha2 receptors Beta1 and beta2 receptors
adrenergic blocker drugs effects and indication, alpha blockers Cause both arterial and venous dilation, reducing peripheral vascular resistance and BP Used to treat hypertension Effect on receptors on prostate gland and bladder decreases resistance to urinary outflow, thus reducing urinary obstruction and relieving
adrenergic blocker drugs effects and indication, alpha blockers Used to control and prevent hypertension in patients with pheochromocytoma
what reverse the potent vasocontstrictive effects of extravaseted vasopressors such as norepinephrine or epinephrine Phentolamine - Restores blood flow and prevents tissue necrosis
the tumor in the adrenal gland will release catecholimes and catecholmies will do what vasoconstriction - high blood pressure
Common Alpha Blockers phenoxybenzamine HCl (Dibenzyline) phentolamine (Regitine) prazosin (Minipress) terazosin (Hytrin) alfuzosin (UroXatral) tamsulosin (Flomax)
Beta Blockers - Block stimulation of beta receptors in the SNS Compete with norepinephrine and epinephrine Can be selective or nonselective Nonselective beta blockers block both beta1 and beta2 receptors
Beta1 receptors Located primarily on he heart Beta blockers selective for these receptors are called cardioselective beta blockers
Beta2 receptors Located primarily on smooth muscle of bronchioles and blood vessels
Mechanism of - Cardioselective beta blockers (beta1) Reduce SNS stimulation of the heart Decrease heart rate Prolong sinoatrial (SA) node recovery Slow conduction rate through the AV node Decrease myocardial contractility, thus reducing myocardial oxygen demand
Mechanism of Action - Nonselective beta blockers (beta1 and beta2) Cause same effects on heart as cardioselective beta blockers Constrict bronchioles, resulting in narrowing of airways and shortness of breath Produce vasoconstriction of blood vessels Other effects
beta 2 2 lungs
beta 1 1 heart
beta blockers (beta1 and beta2) - indications Angina Decreases demand for myocardial oxygen Cardioprotective Inhibits stimulation from circulating catecholamines Dysrhythmias Class II antidysrhythmic Migraine headache Lipophilicity allows entry into CNS Antihypertensive Heart failure Glauc
Adverse Effects: Beta Blockers Agranulocytosis, thrombocytopenia AV block, bradycardia, heart failure Dizziness, depression, unusual dreams, drowsiness
Nonselective beta blockers may interfere with normal responses to hypoglycemia (tremor, tachycardia, nervousness) May mask signs and symptoms of hypoglycemia Use with caution in patients with diabetes mellitus
Beta Blockers: Examples metoprolol (Lopressor) propranolol (Inderal) sotalol (Betapace) atenolol (Tenormin) carvedilol (Coreg) esmolol (Brevibloc) labetalol (Normodyne)
Remember that alpha blockers may precipitate hypotension
Remember that some beta blockers may precipitate bradycardia, hypotension, heart block, heart failure, and bronchoconstriction
Adrenergic-Blocking Drugs - Possible drug interactions may occur with: Antacids (aluminum hydroxide type) Antimuscarinics/anticholinergics Diuretics and cardiovascular drugs Neuromuscular blocking drugs Oral hypoglycemic drugs
A patient with type 2 diabetes is taking a beta blocker as part of treatment for hypertension. Which complication is most likely to develop? Hypoglycemia
coreg effects whats? Alpha and beta blocker!!!
alpha blockers might do what hypotension
BPH, vasodilation in more then one area
The sympathetic nervous system is also called the adrenergic system
the parasympathetic nervous system is called the cholinergic system
Why is the parasympathetic nervous system called the cholinergic system? because the neurotransmitter at theend of the neuron that innervates the muscle is acetylcholine
the cholinergic receptors at organs cells ar either nicotinic or muscarinic meaning that they are stimulated by the alkaloid nicotine and muscarine
acetylcholine stimulates the receptor cells to produce a response but the enzyme actylcholinesterase may inactivate acetycholine b4 it reaches the receptor cel
alpha 1 increases force of heart contraction, vasocontriction increases blood pressure, mydriasis (dilation of pupils), salivary glands decrease, increases urinary bladder relaxation and urinary sprinter conraction
alpha 2 inhibits release of of norepinephrine; dilates blood vessels; produces hypotension; decreases gastrointestinal motility and tone
beta 1 increases heart rate and force of contraction; increases renin secretin, which increases blood pressure
beta 2 dilates bronchioles; promotes gastrointestinal and uterine relaxation; promotes increase in blood sugar thorugh glycogenolysis in liver; increases blood flow in skeletal muscles
catecholamines are the chemical structures of a substance that can produce a sympathomimetic response: example: epinephrine, norepinephrine and dopamine
Epineprhine = Catecholamine = Adrenalin = Acts on Alpha 1, Beta 1, Beta 2. Used in Anaphylaxis - Strengthens Myocardial contraction
albuterol selective for Beta 2 - purely bronchodilation
Clonidine and Aldomet are selective Alpha 2 drugs to treat htn
alpha blockers are helpful in decreasing symptoms of benign prostatic hypertrophy
alpha blockers promote vasodilation causing a decrease in bp
beta adrenergic blockers are called beta blockers
beta blockers * Some beta blockers are nonseletctive decrease heart rate, decrease bp
propranolol hydrochloride (inderal) was the first beta blocker prescribed to treat angina, cardiac dysrhythmias, hypertension and heart failure. BUT has a lot of SE bc of nonselective response for beta 1 & beta 2. Contraindicated for people for asthma
What is inderal contraindicated for? asthma or second, 3rd degree heart block ALSO many drug interactions! Dilantin, NSAIDS.
Inderal and Digoxin (Or calcium blocker) is BAD!!! Because? Atrioventricular (AV) block may occur
drugs that block the release of norepinephrine from the sympathetic terminal are called adrenergic neuron blockers
What are the two groups of drugs that affect the parasympathetic nervous system? Cholinergics(parasympathomimetics) and anticholinergics(parasympatholytics
Drugs that stimulate the parasympathetic nervous system are called Cholinergics/parasympathomimetics
Drugs that stimulate the parasympathetic nervous system are called Cholinergics/parasympathomimetics because Mimic the parasympathetic neurotransmitter acetylcholine
Acetylcholine is the neurotransmitter located at the ganglions and the parasympathetic terminal nerve endings. It innervates the receptors in organs tissues and glands
The two types of cholinergic receptors are muscarinic receptors and which stimulate smooth muscle and slow the heart rate and nicotinic recptors (neuromuscular) which affect the skeletal muscles. *many cholinergic drugs are nonselective!!
Direct acting cholinergic drugs act on the receptors to activate a tissue response
Indirect acting cholinergic drugs inhibit the action of the enzyme cholinesterase (ChE) by forming a chemical complex thus permitting acetylcholine
The major responses of cholinergic drugs are to stimulate bladder and gastrointestinal tone, constrict pupils of the eyes (miosis) and increase neuromuscular transmission.
Direct acting cholinergics are primarily selective to the muscarinic receptors but are non specific because the muscarinic recprots are locatd in the smooth muscles of the GI and genitourinary tacts, glands and heart
Bethanechol chloride ( urecholine) a direct acting cholinergic receptor and is used primarily to increase urination
Metoclopramide HCL (raglan) is a direct acting cholinergic drug that is usually prescribed to treat gastroesophageal reflux disease (GERD)
Metoclopramide increases gastric emptying time
Pilocarpine is a direct acting cholinergic drug that constricts the pupils of the eys thus opening the canal of schlemm to promote drainage of aqueous humor. This drug is used to treat glaucoma by relieving fluid
The function of enzyme cholinersterase is to beak down into choline and acetic acid
A cholinestersase inhibitor drug binds with cholinesterase allowing acetylcholine to activate the muscarinic and nicotinic cholinergic receptors. This action permits skeletal muscle stimulation which increases the force of muscular contraction
Cholinesterase inhibitors are useful to increase muscle tone for clients with myasthenia gravis ( a neuromuscular disorder) by increasing acetylcholine additional effets occur such as increase in GI motility, bradycardia, miosis, bronchial constriction and increased micturition.
The primary use of cholinesterase inhibitors is to treat myasthenia gravis, other uses are to treat glaucoma, alzheimers disease and muscarinic antagonist poisoning.
Drugs that inhibit the actions of acetylcholine by occupying the acetylcholine receptors are called anticholinergics/parasympatheolytics
The major body tissues and organs affected by anticholinergic group of drugs are the heart, respiratory tract, GI tract, urinary bladder,eyes and exocrine glands.
The major responses to anticholinertics are a decrease in GI motility, a decrease in salivation, dilation of pupils( mydriasis) and an increase in pulse rate, decrease bladder contraction which can result in urinary retention and decrease rigidity and tremors
Atropine is useful as a preoperative medication to decrease salivary secretion, as an antispasmodic drug & 2 treat peptic ulcers bc it relaxes the smooth muscles of the GI tract & decrease peristalsis & as an agent to increase the heart rate when bradycardia is present
Drugs that stimulate the parasympathetic nervous system (PSNS) Cholinergic Drugs
Cholinergic Drugs Also known as cholinergic agonists or parasympathomimetics
cholinergic receptors have 2 types location and action once stimulated
what are the two types of cholinergic receptors nicotinic receptors and muscarinic recptors
nicotinic receptors are located in the ganglia of both the psns and sns
what are they names nicotinic because they can be stimulated by alkaloid nicotine
muscarinic receptors are located postsynaptically in the effector organs of the PSNS Smooth muscle Cardiac muscle Glands
names muscarinic because because they can be stimulated by the alkaloid muscarine
Cholinergic Drugs: Mechanism of Action:Direct-acting cholinergic agonists Bind to cholinergic receptors, activating them
cholinergic drug: mechanism of action: Indirect-acting cholinergic agonists Inhibit the enzyme acetylcholinesterase, which breaks down ACh Results in more ACh available at the receptors
Indirect-Acting (Cholinesterase Inhibitors):Reversible Bind to cholinesterase for a period of minutes to hours
Indirect-Acting (Cholinesterase Inhibitors)Irreversible Bind to cholinesterase and form a permanent covalent bond The body must make new cholinesterase to break these bonds
Drug Effects of cholinergic Stimulate intestine and bladder Increased gastric secretions Increased gastrointestinal motility Increased urinary frequency Stimulate pupils Constriction (miosis) Reduced intraocular pressure Increased salivation and sweating
Cholinergic Drug Effects Cardiovascular effects Decreased heart rate Vasodilation Respiratory effects Bronchial constriction, narrowed airways
Cholinergic Drug Effects At recommended doses, cholinergics primarily affect muscarinic receptors. At high doses, cholinergics stimulate nicotinic receptors Desired effects are from muscarinic receptor stimulation. Many undesirable effects are caused by stimulation of nicotini
cholinergic drug indications Direct-acting drugs Reduce intraocular pressure Useful for glaucoma and intraocular surgery echothiophate carbachol pilocarpine Topical application because of poor oral absorption
cholinergic drug indications Direct-acting drug—bethanechol Increases tone and motility of bladder and GI tract Relaxes sphincters in bladder and GI tract, allowing them to empty Helpful for postsurgical atony of the bladder and GI tract Oral dose or subcutaneous injection
cholinergic drug indications cholinergic drug indications
memantine (Namenda) memantine (Namenda)
adverse effects of cholinergic Adverse effects are a result of overstimulation of the PSNS-Cardiovascular-Bradycardia, hypotension, syncope, conduction abnormalities (AV block and cardiac arrest) CNS-Headache, dizziness, convulsions, ataxia Gastrointestinal,Abdominal cramps, increase
adverse effects of cholinergic Adverse effects are a result of overstimulation of the PSNS Cardiovascular-Bradycardia, hypotension, syncope, conduction abnormalities (AV block and cardiac arrest) CNS-Headache, dizziness, convulsions, ataxia Gastrointestinal-Abdominal cramps, increas
adverse effects of cholinergic Respiratory Increased bronchial secretions, bronchospasms Other Lacrimation, sweating, salivation, miosis
neuromusclar blocking agents when to use when someone having a high asthma attack!!! need to intubate them, but the body will do a gag reflex. need to settle them down. Another one is Epidural ( A BLOCKING AGENT)
what do you give to reverse a neuromuscular blocking agent - the antidote physostigmnine & pyridstigmine
Interactions Anticholinergics, antihistamines, sympathomimetics Antagonize cholinergic drugs, resulting in decreased responses Other cholinergic drugs Additive effects
Herbal Products: Gingko: Common uses Prevent memory loss Vertigo Tinnitus
Herbal Products: Gingko May cause GI upset, headache, bleeding
Herbal Products: Gingko:Potential interactions Aspirin NSAIDs Anticoagulants Anticonvulsants
Encourage patients with myasthenia gravis to take medication 30 minutes before eating to help improve chewing and swallowing When cholinergic drugs are prescribed for Alzheimer’s disease, be honest with caregivers and patients that the drugs are for management of symptoms (not a cure)
Therapeutic effects of anti-Alzheimer’s drugs may not occur for up to 6 weeks Atropine is the antidote for cholinergics, and it should be available in the patient’s room for immediate use if needed
Patients should notify their physician if they experience muscle weakness, abdominal cramps, diarrhea, or difficulty breathing
cholinergic will increase peptic acid bad for peptic ulcer
Cholinergic-Blocking Drugs Drugs that block or inhibit the actions of acetylcholine (ACh) in the parasympathetic nervous system (PSNS) Also known as anticholinergics, parasympatholytics, and antimuscarinic drugs
Mechanism of Action Cholinergic-Blocking Drugs Competitive antagonists:Compete with ACh for binding at muscarinic receptors in the PSNS:As a result, ACh is unable to bind to the receptor site and cause a cholinergic effect:Once these drugs bind to receptors, they inhibit nerve transmission at these re
Cholinergic-Blocking Drugs: Examples atropine dicyclomine (Bentyl) - gi glycopyrrolate (Robinul) oxybutynin (Ditropan) scopolamine (Transderm-Scōp) - n/v tolterodine (Detrol) - urinary
Cholinergic-Blocking Drugs: Drug Effects Cardiovascular Small doses: decrease heart rate Large doses: increase heart rate CNS Small doses: decrease muscle rigidity and tremors Large doses: drowsiness, disorientation, hallucinations
Cholinergic-Blocking Drugs: Drug Effects Eye Dilated pupils (mydriasis) Decreased accommodation caused by paralysis of ciliary muscles (cycloplegia) Gastrointestinal Relax smooth muscle tone of GI tract Decrease intestinal and gastric secretions Decrease motility and peristalsis
Cholinergic-Blocking Drugs: Drug Effects Genitourinary Relaxed detrusor muscle Increased constriction of internal sphincter Result: urinary retention Glandular Decreased bronchial secretions, salivation, sweating
Cholinergic-Blocking Drugs: Drug Effects Respiratory Decreased bronchial secretions Dilated bronchial airways
Cholinergic-Blocking indication Drugs: CNS Decreasing muscle rigidity and muscle tremors Parkinson’s disease Drug-induced extrapyramidal reactions
Cholinergic-Blocking indication Drugs:cardiovascular Affects the heart’s conduction system Low doses: slow the heart rate High doses: block inhibitory vagal effects on sinoatrial (SA) and atrioventricular (AV) node pacemaker cells Results in increased heart rate
Cholinergic-Blocking indication Drugs:cardiovascular Atropine Used primarily for cardiovascular disorders Diagnosis of sinus node dysfunction Symptomatic second-degree heart block Severe sinus bradycardia with hemodynamic compromise (advanced life support)
Cholinergic-Blocking indication Drugs:Respiratory Blocking the cholinergic stimulation of the PSNS allows unopposed action of the SNS Results Decreased secretions from nose, mouth, pharynx, bronchi Relaxed smooth muscles in bronchi and bronchioles Decreased airway resistance Bronchodilation
Cholinergic-Blocking indication Drugs:Respiratory Cholinergic blockers are used to treat: Exercise-induced bronchospasms Chronic bronchitis Asthma Chronic obstructive pulmonary disease
Cholinergic-Blocking indication Drugs:Gastrointestinal PSNS controls gastric secretions and smooth muscles that produce gastric motility Blockade of PSNS results in: Decreased secretions Relaxation of smooth muscle Decreased GI motility and peristalsis
cholinergic block adverse effects cardiovascular - increse hr dysrhythmias, cns restlessness, irritability, disorientation, dilated pupils, GI decreased salivation, genitourinary - urinary retention, glandular decreased sweating, respiratory decresed bronchial secretions
cholinergics block interactions Amantadine, antihistamines, phenothiazines, tricyclic antidepressants, digoxin When given with other cholinergic blocking drugs, cause additive cholinergic effects, resulting in increased effects
cholinergic blocking nursing implications Keep in mind that these drugs block the action of ACh in the PSNS. Assess for allergies, presence of BPH, urinary retention, glaucoma, tachycardia, MI, HF, hiatal hernia, and GI or GU obstruction Perform baseline assessment of vital signs and systems ov
cholinergic blocking nursing implications Medications should be taken exactly as prescribed to have the maximum therapeutic effect Overdosing can cause life-threatening problems Blurred vision will cause problems with driving or operating machinery
cholinergic blocking nursing implications Patients may experience sensitivity to light and may want to wear dark glasses or sunglasses When giving ophthalmic solutions, apply pressure to the inner canthus to prevent systemic absorption
cholinergic blocking nursing implications Patients may experience sensitivity to light and may want to wear dark glasses or sunglasses When giving ophthalmic solutions, apply pressure to the inner canthus to prevent systemic absorption
cholinergic blocking nursing implications Dry mouth may occur; can be handled by chewing gum, frequent mouth care, and hard candy Check with physician before taking any other medication, including over-the-counter medications Antidote for atropine overdose is physostigmine
cholinergic blocking nursing implications Anticholinergics taken by the elderly patient may lead to higher risk for heatstroke because of the effects on heat-regulating mechanisms
cholinergic blocking nursing implications Teach patients to limit physical exertion and avoid high temperatures and strenuous exercise Emphasize the importance of adequate fluid and salt intake
cholinergic blocking nursing implications Patients should report the following symptoms to their physician: urinary hesitancy and/or retention, constipation, tachycardia, palpitations, tremors, confusion, sedation, hallucinations, decreased sweating (leading to hot, dry skin)
Nursing Implications (cont’d) Monitor for therapeutic effects For patients with Parkinson’s disease: fewer tremors and decreased salivation and drooling For patients with urologic problems: improved urinary patterns, less hypermotility, increased time between voiding Monitor for
if a patient is taking psych meds - what can happen they can have drug induced extrapyriamidal reactions
benadryl is a anticholinergic
insuline protein hormone used to control deiabetes
insulin a protein secreted from beta cells of the pancreas, is necessary for carbohydrate metabolism
the beta cells make up 75% of the pancreas
and the alpha cells that secrete glucagon a hyperglycemic substance occupy approximately 20
oral hypoglycemic drugs also known as oral antidiabetic drugs are synthetic preparation that stimulate insulin release or otherwise alter teh metabolic response
Diabetes Mellitus chronic diseae resulting from deficient glucose metabolism, is caued by insufficient insulin secretion from beta cells
diabetes mellitus is characterized by the three P's polyuria, polydipsia and polyphagia (increased hunger)
diabetes mellitus is a disorder of pancrease
diabetes insipidus is disorder of posterior pituitary gland
insulin is released from the beta cells of the islets of langerhans in reposne ot an increase in blood glucose
glucose is converted to glycogen for future glucose need int he liver and muscle
intermediate acting insulin are cloudy and may contain protamine a protein that prolongs the action of insuilne or zinc which also slows the onset of actions and prolongs durations
NPH neutral protamine hagedorm
intermediate insulin onset is 1 to 2 hours and peak 6-12 hours,and duration is 18-24 hrs
drugs that increase blood sugar is? thiazide diuretics, glucocorticoids, thyroid agents and eztrogen
drugs that decrease insulin are tricyclic antidepressants, monoamine oxidase, aspirin and oral anticoagulants
Type 2 Diabetes Mellitus Caused by insulin deficiency and insulin resistance
Type 2 Diabetes Mellitus Many tissues are resistant to insulin Reduced number of insulin receptors Insulin receptors less responsive
Type 2 Diabetes Mellitus- Several comorbid conditions Obesity Coronary heart disease Dyslipidemia Hypertension Microalbuminemia (protein in the urine) Increased risk for thrombotic (blood clotting) events
Major Long-Term Complications of DM (Both Types) Macrovascular (atherosclerotic plaque) & Microvascular (capillary damage)
Type 1 Insulin therapy
Type 2 Lifestyle changes Oral drug therapy Insulin when the above no longer provide glycemic control
Insulins Function as a substitute for the endogenous hormone
Insulins Function as Restores the diabetic patient’s ability to: Metabolize carbohydrates, fats, and proteins Store glucose in the liver Convert glycogen to fat stores
Human insulin Derived using recombinant DNA technologies Recombinant insulin produced by bacteria and yeast
Rapid-acting Most rapid onset of action (5 to 15 minutes) Shorter duration Patient must eat a meal after injection Insulin lispro (Humalog) Similar action to endogenous insulin Insulin aspart (NovoLog) Insulin glulisine (Apidra
Short-acting Regular insulin (Humulin R) Onset 30 to 60 minutes The only insulin product that can be given by IV bolus, IV infusion, or even IM
Intermediate-acting Insulin isophane suspension (also called NPH) Cloudy appearance Slower in onset and more prolonged in duration than endogenous insulin
Long-acting glargine (Lantus), detemir (Levemir) Clear, colorless solution Usually dosed once daily Referred to as basal insulin
Sliding-Scale Disadvantage: delays insulin administration until hyperglycemia occurs; results in large swings in glucose control
Biguanides metformin (Glucophage
Sulfonylureas Second generation: glimepiride (Amaryl), glipizide (Glucotrol), glyburide (DiaBeta, Micronase)
Glinides repaglinide (Prandin), nateglinide (Starlix)
Thiazolidinediones pioglitazone (Actos) rosiglitazone (Avandia) Only available through specialized manufacturer programs
Alpha-glucosidase inhibitors acarbose (Precose), miglitol (Glyset)
Biguanides Decrease production of glucose by the liver Decrease intestinal absorption of glucose Increase uptake of glucose by tissues Do not increase insulin secretion from the pancreas (does not cause hypoglycemia)
Sulfonylureas Stimulate insulin secretion from the beta cells of the pancreas, thus increasing insulin levels Beta cell function must be present Improve sensitivity to insulin in tissues Result in lower blood glucose levels
Glinides Action similar to sulfonylureas Increase insulin secretion from the pancreas
Alpha-glucosidase inhibitors Reversibly inhibit the enzyme alpha-glucosidase in the small intestine Result in delayed absorption of glucose Must be taken with meals to prevent excessive postprandial blood glucose elevations (with the “first bite” of a meal)
Biguanides (metformin) Primarily affects GI tract: abdominal bloating, nausea, cramping, diarrhea, feeling of fullness May also cause metallic taste, reduced vitamin B12 levels Lactic acidosis is rare but lethal if it occurs Does not cause hypoglycemia
Sulfonylureas Hypoglycemia, hematologic effects, nausea, epigastric fullness, heartburn, many others
Glinides Headache, hypoglycemic effects, dizziness, weight gain, joint pain, upper respiratory infection or flulike symptoms
Thiazolidinediones Moderate weight gain, edema, mild anemia Hepatic toxicity—monitor alanine aminotransferase (ALT) levels
Alpha-glucosidase inhibitors Flatulence, diarrhea, abdominal pain Do not cause hypoglycemia, hyperinsulinemia, or weight gain
Amylin agonist Mimics the natural hormone amylin Slows gastric emptying Suppresses glucagon secretion, reducing hepatic glucose output Centrally modulates appetite and satiety Used when other drugs have not achieved adequate glucose control Subcutaneous injection
Oral antidiabetic drugs Always check blood glucose levels before giving Usually given 30 minutes before meals Alpha-glucosidase inhibitors are given with the first bite of each main meal Metformin is taken with meals to reduce GI effects Metformin will need to be discontinue
If hypoglycemia occurs: Administer oral form of glucose, if the patient is conscious Give the patient glucose tablets or gel, corn syrup, honey, fruit juice, or nondiet soft drink or have the patient eat a small snack, such as crackers or a half sandwich Deliver D50W or glucag
Created by: starr8904