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Adrenergic Agonists
Drugs that stimulate adrenergic receptors and mimic sympathetic nervous system activity
They are also called sympathomimetics
Sympathomimetics
Medications that produce effects similar to the sympathetic nervous system neurotransmitters epinephrine, norepinephrine, and dopamine
Adrenergic Receptors
Receptor sites that respond to the sympathetic neurotransmitters norepinephrine and epinephrine
Adrenergic medications produce different effects depending on which receptor type they stimulate (alpha and beta)
Alpha-Adrenergic Receptors
Adrenergic receptors divided into alpha1 and alpha2 subtypes
Alpha1 stimulation commonly produces vasoconstriction and affects smooth muscle in several body systems
Beta-Adrenergic Receptors
Adrenergic receptors that include beta1 and beta2 subtypes
Beta1 receptors are located primarily in the heart, while beta2 receptors are prominent in bronchial, vascular, and other smooth muscle
Catecholamines
Substances capable of producing a sympathomimetic response
Epinephrine, norepinephrine, and dopamine are endogenous catecholamines, while some medications act as synthetic catecholamines
Dopaminergic Receptor
A receptor activated by dopamine
Stimulation can produce vasodilation in selected vascular beds, including vessels supplying the kidneys, heart, brain, and gastrointestinal tract
Positive Inotropic Effect
An increase in the force of myocardial contraction
Beta1 receptor stimulation can produce this effect and increase stroke volume and cardiac output
Positive Chronotropic Effect
An increase in heart rate
This effect commonly occurs when beta1 receptors in the heart are stimulated
Positive Dromotropic Effect
An increase in conduction of cardiac electrical impulses through the atrioventricular node
Beta1 receptor stimulation can increase this conduction along with heart rate and contractility
Adrenergic Blockers
Act as antagonists at alpha or beta receptors
Sympatholytics
Drugs that inhibit sympathetic nervous system activity
Adrenergic-blocking medications are also called sympatholytics.
First-Dose Phenomenon
A severe and sudden decrease in blood pressure after the first dose of an alpha-adrenergic blocker
Dizziness, syncope, and falls may occur
Orthostatic Hypotension
A drop in blood pressure when moving to a standing position
It can cause dizziness, lightheadedness, or syncope and is common with alpha blockers
Extravasation
Leakage of an IV medication from a blood vessel into surrounding tissue
Extravasated vasopressor can cause intense vasoconstriction and tissue injury
Cardioselective
Describes beta blockers that primarily block beta1 receptors in the heart, reducing heart rate, conduction and contractility
Intrinsic Sympathomimetic Activity
The ability of some beta blockers to block beta receptors while also partially stimulating them
Acebutolol, penbutolol, and pindolol have this property
Pheochromocytoma
A tumor of the adrenal gland that can secrete large amounts of epinephrine and norepinephrine, producing substantial stimulation and hypertension
Lipophilicity
The tendency of a drug to be attracted to and dissolve in lipid or fat
Lipophilic beta blockers such as propranolol can more readily enter the central nervous system
Acetylcholine
The primary neurotransmitter of the parasympathetic nervous system
It binds to cholinergic receptors and produces parasympathetic responses in target tissues
Acetylcholinesterase
The enzyme responsible for breaking down acetylcholine
Inhibiting this enzyme allows acetylcholine to remain available at receptor sites longer
Cholinergic Receptor
A nerve receptor that is stimulated by acetylcholine
The two major types are muscarinic and nicotinic receptors
Muscarinic Receptors
Cholinergic receptors located in smooth muscle, cardiac muscle, and glands supplied by parasympathetic fibers
Many desired effects of cholinergic drugs result from muscarinic receptor stimulation
Nicotinic Receptors
Cholinergic receptors located primarily in the autonomic ganglia where presynaptic and postsynaptic nerve fibers meet
They can also be stimulated by nicotine
Parasympathomimetics
Drugs that mimic parasympathetic nervous system activity
The term is used interchangeably with cholinergic drugs and cholinergic agonists
Direct-Acting Cholinergic Agonist
A medication that binds directly to cholinergic receptors and activates them
Bethanechol and pilocarpine are examples
Cholinesterase Inhibitor
An indirect-acting cholinergic drug that inhibits acetylcholinesterase, increasing the amount of acetylcholine available to stimulate cholinergic receptors
Miosis
Constriction of the pupil
Cholinergic stimulation can produce miosis, which may help reduce intraocular pressure
Cholinergic Crisis
Severe toxicity caused by excessive acetylcholine activity
Findings may include: increased secretions, abd cramping, vomiting, diarrhea, hypotension, bradycardia, respiratory compromise, circulatory collapse, and cardiac arrest
Cholinergic-Blocking Drugs
Drugs that block the actions of acetylcholine at receptor sites and reduce parasympathetic nervous system activity
Parasympatholytics
Drugs that reduce parasympathetic nervous system activity
This is another term for cholinergic-blocking drugs
Anticholinergics
The term most commonly used in clinical practice for drugs that inhibit acetylcholine activity in the parasympathetic nervous system
Antimuscarinic
Describes a drug that blocks acetylcholine at muscarinic receptors
Cholinergic receptors act primarily at these receptors
Competitive Antagonist
A drug that competes with acetylcholine for a receptor site
Once the blocker occupies the muscarinic receptor, acetylcholine cannot produce its usual cholinergic response
Mydriasis
Dilation of the pupil
Blocking cholinergic stimulation prevents contraction of the iris sphincter muscle, allowing the pupil to dilate
Cycloplegia
Paralysis of the ciliary muscle of the eye, which decreases the eye's ability to accommodate for near vision and may contribute to blurred vision
Urinary Retention
Difficulty emptying the bladder
Anticholinergic activity can relax the detrusor muscle and increase internal sphincter constriction, reducing bladder emptying
Anticholinergic Toxicity
Excessive cholinergic blockade that may produce findings such as tachycardia, hot dry skin, urinary retention, confusion, hallucinations, delirium, and cardiac dysrhythmias
Antacids
Basic compounds that neutralize acid already present in the stomach
They do not stop the stomach from producing acid
Gastric Hyperacidity
Overproduction of stomach acid
Persistent hyperacidity can contribute to reflux, mucosal injury, esophagitis, and peptic ulcer disease
Parietal Cells
Stomach cells that produce and secrete hydrochloric acid
They are a major target of acid-suppressing drug therapy.
Hydrochloric Acid
Acid secreted by parietal cells that maintains the stomach's highly acidic environment and supports digestion and protection against microorganisms
H2 Receptor Antagonists
Acid-suppressing drugs that competitively block H2 receptors on parietal cells, reducing hydrogen ion secretion and increasing gastric pH.
Proton Pump
The hydrogen-potassium ATPase pump in parietal cells
It performs the final step in moving hydrogen ions into the stomach to form gastric acid
Proton Pump Inhibitors
Drugs that irreversibly inhibit the proton pump, greatly reducing hydrogen ion secretion and gastric acid production.
Mucosal Protectant
A drug that protects damaged GI tissue by forming a local barrier over ulcers or erosions rather than primarily suppressing acid production
Acid Rebound
A return of increased gastric acidity associated with overuse, misuse, or rapid discontinuation of some high acid-neutralizing antacids
Milk-Alkali Syndrome
A complication associated with excessive calcium-containing antacid use, characterized by hypercalcemia, alkalosis, headache, and nausea
Antidiarrheal Drugs
Medications used to counter or control diarrhea.
Different classes work by binding substances in the GI tract, reducing intestinal motility, decreasing secretions, or restoring normal intestinal flora
Diarrhea
The abnormally frequent passage of loose stools
Nursing assessment includes the frequency, amount, consistency, associated symptoms, hydration status, and possible cause before medication therapy is selected
Constipation
A condition involving abnormally infrequent or difficult passage of stool
Possible contributing factors include medications, inadequate fluid or fiber intake, inactivity, metabolic conditions, and neurologic disorders.
Peristalsis
The coordinated wavelike contraction and relaxation of GI smooth muscle that moves intestinal contents through the gastrointestinal tract
Several bowel medications work by either slowing or increasing this movement.
Irritable Bowel Syndrome (IBS)
A recurring intestinal disorder characterized by abdominal discomfort, bloating, flatulence, diarrhea, constipation, or alternating bowel patterns
Medication therapy differs depending on whether diarrhea or constipation predominates.
Laxatives
Medications that promote bowel evacuation by increasing stool bulk, softening or lubricating stool, increasing intestinal water, or stimulating peristalsis
Absorbents
A class of antidiarrheal medications that coat the GI tract and bind substances such as bacteria or toxins to their surface so they can be eliminated in the stool
Because they can also bind medications, drug interactions are an important consideration
Probiotics
Products containing microorganisms that help restore the balance of normal intestinal flora
They may be useful when normal GI bacteria have been disrupted, such as during antibiotic therapy
Bulk-Forming Laxatives
Laxatives that absorb water and increase the bulk of intestinal contents
The increased bulk distends the bowel and promotes reflex peristalsis.
Adequate fluid intake is essential to reduce the risk of obstruction or impaction.
Hyperosmotic Laxatives
Laxatives that increase the water content of the stool, producing intestinal distention, increased peristalsis, and bowel evacuation
Fluid and electrolyte status are important nursing considerations with this class
Nausea
An unpleasant sensation that often produces the urge to vomit and may precede emesis
Emesis
The forcible emptying of gastric and sometimes intestinal contents through the mouth; another term for vomiting
Antiemetic Drugs
Medications used to prevent or relieve nausea and vomiting
Different classes act at different points in the vomiting pathways
Chemoreceptor Trigger Zone (CTZ)
A brain region involved in detecting nausea-producing substances and sending signals that help trigger vomiting
Vomiting Center
The brain area responsible for coordinating the physiologic events that produce nausea and vomiting
Anticholinergic Antiemetics
Drugs that block acetylcholine receptors in vestibular and related pathways
They are especially useful for motion-related nausea and vomiting
Antidopaminergic Antiemetics
Drugs that block dopamine receptors in the CTZ
Their safety profile includes risks such as orthostatic hypotension and extrapyramidal symptoms.
Prokinetic Drugs
Medications that increase GI motility and promote gastric emptying
Some also reduce nausea by blocking dopamine receptors in the CTZ
5-HT3 Receptor Blockers
Serotonin-blocking antiemetics that act at 5-HT3 receptors in the GI tract, CTZ, and vomiting center
They are commonly used for chemotherapy- and postoperative-related nausea and vomiting
Neurokinin-1 Antagonists
Antiemetics that block substance P at neurokinin-1 receptors in the brain stem
They are often combined with other antiemetic classes for chemotherapy-induced nausea and vomiting