gout, adrenergic,Adrenergic-Blocking Drugs, cholinergics and anticholinergics
Quiz yourself by thinking what should be in
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The stomach secretes: | Hydrochloric acid (HCl)
Bicarbonate
Pepsinogen
Intrinsic factor
Mucus
Prostaglandins
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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
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Cells of the Gastric Gland | Parietal
Chief
Mucous
Endocrine
Enterochromaffin
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Parietal cells | Produce and secrete HCl
Primary site of action for many of the drugs used to treat acid-related disorders
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Chief cells | Secrete pepsinogen, a proenzyme
Pepsinogen becomes pepsin when activated by exposure to acid
Pepsin breaks down proteins
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Mucous cells | Mucus-secreting cells (surface epithelial cells)
Provide a protective mucus coat
Protect against self-digestion by HCl and digestive enzymes
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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
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Acid-Related Diseases | Peptic ulcer disease (PUD)
Gastric or duodenal ulcers that involve digestion of the GI mucosa by the enzyme pepsin
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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
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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
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Types of Acid-Controlling Drugs | Antacids
H2 antagonists
Proton pump inhibitors
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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
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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
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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:
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Antacids (cont’d) | Over-the-counter formulations available as:
Capsules and tablets
Powders
Chewable tablets
Suspensions
Effervescent granules and tablets
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Antacids | Used alone or in combination
Aluminum salts
Magnesium salts
Calcium salts
Sodium bicarbonate
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Antacids: Aluminum Salts | Have constipating effects
Often used with magnesium to counteract constipation
Often recommended for patients with renal disease (more easily excreted)
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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
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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)
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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
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if someone has renal failure which antacid you should not use | one with magnesium because renal can't displaced
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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
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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
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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
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Antacids: Adverse Effects | Minimal and depend on the compound used
Aluminum and calcium
Constipation
Magnesium
Diarrhea
Calcium carbonate
Produces gas and belching; often combined
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if elderly has heart failure you should not give | sodium bicarb - volume, fluid retention
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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
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Histamine 2 (H2) Receptor Antagonists | Reduce acid secretion
All available over the counter in lower dosage forms
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Histamine 2 (H2) Receptor Antagonists | Most popular drugs for treatment of acid-related disorders
cimetidine (Tagamet)
nizatidine (Axid)
famotidine (Pepcid)
ranitidine (Zantac)
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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
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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
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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
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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
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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
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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
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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
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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
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Proton Pump Inhibitors | lansoprazole (Prevacid)
omeprazole (Prilosec)
rabeprazole (AcipHex)
pantoprazole (Protonix)
esomeprazole (Nexium)
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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
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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
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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
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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
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adrenergic drugs | drugs that stimulate the sympathetic nervous system - flight or flight, bronchodilations, elevated bp, elebated pulse, pupils are dilated
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sympathetic stimulants | adrenergic, adrenominmetics, adrenergic agonists and sympathomimetics
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parasympathic stimulants | cholinergics, cholinergic agonists and parasympathomimetics
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characteristics of adrenergics are | mimics the effects of SNS neurotran (catecholamines) NE, EPI and dopamine
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Alpha1-adrenergic receptors Located on | postsynaptic effector cells (the cell, muscle, or organ that the nerve stimulates)
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Alpha2-adrenergic receptors Located on | presynaptic nerve terminals (the nerve that stimulates the effector cells)
Control the release of neurotransmitters
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Beta-Adrenergic Receptors Beta-Adrenergic Receptors | postsynaptic effector cells
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Beta1-adrenergic receptors—located | receptors—located primarily in the heart
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Beta2-adrenergic receptors—located in | in smooth muscle of the bronchioles, arterioles, and visceral organs
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Beta-Adrenergic Agonist Responses | Bronchial, GI, and uterine smooth muscle relaxation
Glycogenolysis
Cardiac stimulation
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Dopaminergic Receptors | An additional adrenergic receptor
Stimulated by dopamine
Causes dilation of the following blood vessels, resulting in increased blood flow
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Catecholamines | Substances that can produce a sympathomimetic response
Endogenous
Epinephrine, norepinephrine, dopamine
Synthetic
Dobutamine, phenylephrine
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Catecholamines Mechanism of Action | Direct-acting sympathomimetic
Binds directly to the receptor and causes a physiologic response
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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
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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
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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
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Catecholamines Stimulation of | of beta1-adrenergic receptors on the myocardium, atrioventricular (AV) node, and sinoatrial (SA) node results in cardiac stimulation
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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
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Catecholamines | Treatment of asthma and bronchitis
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examples of bronchildilators are | Examples: albuterol (works the fastest), ephedrine, epinephrine, formoterol, levalbuterol, metaproterenol, pirbuterol, salmeterol, and terbutaline*
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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
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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
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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
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Vasoactive Sympathomimetics (Pressors, Inotropes): Examples | dopamine
epinephrine
phenylephrine
norepinephrine,
dobutamine
ephedrine
fenoldopam
midodrine
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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)
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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
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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
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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
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Salmeterol is indicated for | for prevention of bronchospasms, not management of acute symptoms
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Overuse of nasal decongestants may cause | rebound nasal congestion or ulcerations
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Administering two adrenergic drugs together may precipitate severe cardiovascular effects such | tachycardia or hypertension
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when someone is having an asthma attack there is no what? | GAS EXCHANGE - no alveoli is open -
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Monitor for therapeutic effects (cardiovascular uses) | Decreased edema
Increased urinary output
Return to normal vital signs
Improved skin color and temperature
Increased LOC
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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
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REMEMBER!! TO listen for everything so you can know a patient change of status | lungs, belly heart
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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
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adrenergic blockers are also known as | Adrenergic antagonists
Sympatholytics
Alpha blockers, beta blockers, or alpha-beta blockers
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adrenergic blockers are classified by what? | type of adrenergic receptor they block
Alpha1 and alpha2 receptors
Beta1 and beta2 receptors
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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
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adrenergic blocker drugs effects and indication, alpha blockers | Used to control and prevent hypertension in patients with pheochromocytoma
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what reverse the potent vasocontstrictive effects of extravaseted vasopressors such as norepinephrine or epinephrine | Phentolamine - Restores blood flow and prevents tissue necrosis
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the tumor in the adrenal gland will release catecholimes and catecholmies will do what | vasoconstriction - high blood pressure
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Common Alpha Blockers | phenoxybenzamine HCl (Dibenzyline)
phentolamine (Regitine)
prazosin (Minipress)
terazosin (Hytrin)
alfuzosin (UroXatral)
tamsulosin (Flomax)
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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
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Beta1 receptors Located primarily on | he heart
Beta blockers selective for these receptors are called cardioselective beta blockers
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Beta2 receptors Located primarily on | smooth muscle of bronchioles and blood vessels
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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
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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
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beta 2 | 2 lungs
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beta 1 | 1 heart
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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
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Adverse Effects: Beta Blockers | Agranulocytosis, thrombocytopenia
AV block, bradycardia, heart failure
Dizziness, depression, unusual dreams, drowsiness
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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
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Beta Blockers: Examples | metoprolol (Lopressor)
propranolol (Inderal)
sotalol (Betapace) atenolol (Tenormin)
carvedilol (Coreg)
esmolol (Brevibloc)
labetalol (Normodyne)
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Remember that alpha blockers may | precipitate hypotension
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Remember that some beta blockers may | precipitate bradycardia, hypotension, heart block, heart failure, and bronchoconstriction
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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
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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
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coreg effects whats? | Alpha and beta blocker!!!
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alpha blockers might do what | hypotension
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BPH, vasodilation in more then one area |
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The sympathetic nervous system is also called | the adrenergic system
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the parasympathetic nervous system is called the | cholinergic system
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Why is the parasympathetic nervous system called the cholinergic system? | because the neurotransmitter at theend of the neuron that innervates the muscle is acetylcholine
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the cholinergic receptors at organs cells ar either | nicotinic or muscarinic meaning that they are stimulated by the alkaloid nicotine and muscarine
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acetylcholine stimulates | the receptor cells to produce a response but the enzyme actylcholinesterase may inactivate acetycholine b4 it reaches the receptor cel
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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
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alpha 2 | inhibits release of of norepinephrine; dilates blood vessels; produces hypotension; decreases gastrointestinal motility and tone
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beta 1 | increases heart rate and force of contraction; increases renin secretin, which increases blood pressure
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beta 2 | dilates bronchioles; promotes gastrointestinal and uterine relaxation; promotes increase in blood sugar thorugh glycogenolysis in liver; increases blood flow in skeletal muscles
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catecholamines | are the chemical structures of a substance that can produce a sympathomimetic response: example: epinephrine, norepinephrine and dopamine
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Epineprhine | = Catecholamine = Adrenalin = Acts on Alpha 1, Beta 1, Beta 2. Used in Anaphylaxis - Strengthens Myocardial contraction
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albuterol | selective for Beta 2 - purely bronchodilation
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Clonidine and Aldomet are | selective Alpha 2 drugs to treat htn
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alpha blockers are helpful in decreasing symptoms of | benign prostatic hypertrophy
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alpha blockers promote vasodilation causing a | decrease in bp
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beta adrenergic blockers are called | beta blockers
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beta blockers * Some beta blockers are nonseletctive | decrease heart rate, decrease bp
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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
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What is inderal contraindicated for? | asthma or second, 3rd degree heart block ALSO many drug interactions! Dilantin, NSAIDS.
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Inderal and Digoxin (Or calcium blocker) is BAD!!! Because? | Atrioventricular (AV) block may occur
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drugs that block the release of norepinephrine from the sympathetic terminal are called | adrenergic neuron blockers
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What are the two groups of drugs that affect the parasympathetic nervous system? | Cholinergics(parasympathomimetics) and anticholinergics(parasympatholytics
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Drugs that stimulate the parasympathetic nervous system are called | Cholinergics/parasympathomimetics
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Drugs that stimulate the parasympathetic nervous system are called Cholinergics/parasympathomimetics because | Mimic the parasympathetic neurotransmitter acetylcholine
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Acetylcholine is the | neurotransmitter located at the ganglions and the parasympathetic terminal nerve endings. It innervates the receptors in organs tissues and glands
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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!!
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Direct acting cholinergic drugs act on the | receptors to activate a tissue response
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Indirect acting cholinergic drugs inhibit the action of the enzyme | cholinesterase (ChE) by forming a chemical complex thus permitting acetylcholine
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The major responses of cholinergic drugs are to stimulate | bladder and gastrointestinal tone, constrict pupils of the eyes (miosis) and increase neuromuscular transmission.
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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
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Bethanechol chloride ( urecholine) a direct acting cholinergic receptor and is used | primarily to increase urination
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Metoclopramide HCL (raglan) is a | direct acting cholinergic drug that is usually prescribed to treat gastroesophageal reflux disease (GERD)
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Metoclopramide | increases gastric emptying time
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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
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The function of enzyme cholinersterase | is to beak down into choline and acetic acid
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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
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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.
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The primary use of cholinesterase inhibitors is to | treat myasthenia gravis, other uses are to treat glaucoma, alzheimers disease and muscarinic antagonist poisoning.
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Drugs that inhibit the actions of acetylcholine by occupying the acetylcholine receptors are called | anticholinergics/parasympatheolytics
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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.
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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
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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
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Drugs that stimulate the parasympathetic nervous system (PSNS) | Cholinergic Drugs
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Cholinergic Drugs Also known as | cholinergic agonists or parasympathomimetics
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cholinergic receptors have 2 types | location and action once stimulated
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what are the two types of cholinergic receptors | nicotinic receptors and muscarinic recptors
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nicotinic receptors are located in | the ganglia of both the psns and sns
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what are they names nicotinic | because they can be stimulated by alkaloid nicotine
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muscarinic receptors are located | postsynaptically in the effector organs of the PSNS
Smooth muscle
Cardiac muscle
Glands
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names muscarinic because | because they can be stimulated by the alkaloid muscarine
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Cholinergic Drugs: Mechanism of Action:Direct-acting cholinergic agonists | Bind to cholinergic receptors, activating them
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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
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Indirect-Acting (Cholinesterase Inhibitors):Reversible | Bind to cholinesterase for a period of minutes to hours
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Indirect-Acting (Cholinesterase Inhibitors)Irreversible | Bind to cholinesterase and form a permanent covalent bond
The body must make new cholinesterase to break these bonds
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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
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Cholinergic Drug Effects | Cardiovascular effects
Decreased heart rate
Vasodilation
Respiratory effects
Bronchial constriction, narrowed airways
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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
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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
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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
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cholinergic drug indications | cholinergic drug indications
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memantine (Namenda) | memantine (Namenda)
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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
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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
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adverse effects of cholinergic | Respiratory
Increased bronchial secretions, bronchospasms
Other
Lacrimation, sweating, salivation, miosis
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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)
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what do you give to reverse a neuromuscular blocking agent - the antidote | physostigmnine & pyridstigmine
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|
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Interactions | Anticholinergics, antihistamines, sympathomimetics
Antagonize cholinergic drugs, resulting in decreased responses
Other cholinergic drugs
Additive effects
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Herbal Products: Gingko: Common uses | Prevent memory loss
Vertigo
Tinnitus
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|
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Herbal Products: Gingko | May cause GI upset, headache, bleeding
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|
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Herbal Products: Gingko:Potential interactions | Aspirin
NSAIDs
Anticoagulants
Anticonvulsants
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|
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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)
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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
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|
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Patients should notify their physician if they experience muscle weakness, abdominal cramps, diarrhea, or difficulty breathing |
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|
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cholinergic will increase peptic acid bad for peptic ulcer |
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|
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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
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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 thereceptor site and cause a cholinergic effect:Once these drugs bind to receptors, they inhibit nerve transmission at these re
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Cholinergic-Blocking Drugs: Examples | atropine
dicyclomine (Bentyl) - gi
glycopyrrolate (Robinul)
oxybutynin (Ditropan)
scopolamine (Transderm-Scōp) - n/v
tolterodine (Detrol) - urinary
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|
||||
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
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|
||||
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
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|
||||
Cholinergic-Blocking Drugs: Drug Effects | Genitourinary
Relaxed detrusor muscle
Increased constriction of internal sphincter
Result: urinary retention
Glandular
Decreased bronchial secretions, salivation, sweating
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|
||||
Cholinergic-Blocking Drugs: Drug Effects | Respiratory
Decreased bronchial secretions
Dilated bronchial airways
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|
||||
Cholinergic-Blocking indication Drugs: CNS | Decreasing muscle rigidity and muscle tremors
Parkinson’s disease
Drug-induced extrapyramidal reactions
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|
||||
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
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|
||||
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)
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|
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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
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|
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Cholinergic-Blocking indication Drugs:Respiratory | Cholinergic blockers are used to treat:
Exercise-induced bronchospasms
Chronic bronchitis
Asthma
Chronic obstructive pulmonary disease
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|
||||
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
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|
||||
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
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|
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cholinergics block interactions | Amantadine, antihistamines, phenothiazines, tricyclic antidepressants, digoxin
When given with other cholinergic blocking drugs, cause additive cholinergic effects, resulting in increased effects
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|
||||
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
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|
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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
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|
||||
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
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|
||||
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
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|
||||
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
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|
||||
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
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|
||||
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
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|
||||
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)
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|
||||
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
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|
||||
if a patient is taking psych meds - what can happen | they can have drug induced extrapyriamidal reactions
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|
||||
benadryl is a | anticholinergic
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|
||||
insuline | protein hormone used to control deiabetes
🗑
|
||||
insulin | a protein secreted from beta cells of the pancreas, is necessary for carbohydrate metabolism
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|
||||
the beta cells make | up 75% of the pancreas
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|
||||
and the alpha cells that secrete | glucagon a hyperglycemic substance occupy approximately 20
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|
||||
oral hypoglycemic drugs also known as oral antidiabetic drugs | are synthetic preparation that stimulate insulin release or otherwise alter teh metabolic response
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|
||||
Diabetes Mellitus | chronic diseae resulting from deficient glucose metabolism, is caued by insufficient insulin secretion from beta cells
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|
||||
diabetes mellitus is characterized by the three P's | polyuria, polydipsia and polyphagia (increased hunger)
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|
||||
diabetes mellitus is | a disorder of pancrease
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|
||||
diabetes insipidus is disorder of | posterior pituitary gland
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|
||||
insulin is | released from the beta cells of the islets of langerhans in reposne ot an increase in blood glucose
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|
||||
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
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|
||||
NPH | neutral protamine hagedorm
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|
||||
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
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|
||||
drugs that decrease insulin are | tricyclic antidepressants, monoamine oxidase, aspirin and oral anticoagulants
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|
||||
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
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|
||||
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
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|
||||
Major Long-Term Complications of DM (Both Types) | Macrovascular (atherosclerotic plaque) & Microvascular (capillary damage)
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|
||||
Type 1 | Insulin therapy
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|
||||
Type 2 | Lifestyle changes
Oral drug therapy
Insulin when the above no longer provide glycemic control
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|
||||
Insulins Function as | a substitute for the endogenous hormone
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|
||||
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
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|
||||
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
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|
||||
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)
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|
||||
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
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|
||||
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
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|
||||
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
🗑
|
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