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112 Cards in this Set
- Front
- Back
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Three properties of an "ideal" drug
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1. Effectiveness
2. Safety 3. Selective |
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Generic name
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Only ONE generic name
*lower case |
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Trade name
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-Single drug can multiple trade names
-Drugs can have similar trade names *Upper case |
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Dose response relationship
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Relationship between the size of an administered dose and the intensity of the response produced
Determines; -minimum amount of drug we can use -maximum response a drug can elicit -how much we need to increase the dosage to produce the desired increase in response |
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First pass (effect) metabolism
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rapid inactivation of certain oral drugs
if inactivation is complete (100%) then need to give the drug via ANOTHER ROUTE if inactivation is incomplete, then give a higher dose |
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Bioavailability
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the percentage of an administered drug that is available in the bloodstream to act at the target tissue
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Factors that alter drug metabolism
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-age of pt
-route of drug administration/first pass metabolism -dosage of medication -generic disposition of the pt -diet or starvation -preexisting disease |
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Factors that alter drug absorption
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-route of entry
-food in stomach -pH of stomach -blood flow to GI tract or other areas -levels of intestinal flora -body surface area -presence of other drugs -smoking (induces p450; decreases blood flow) -Food (grapefruit juice-inhibits p450 system-leads to overdose) |
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Factors that alter drug excretion
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-glomerular filtration rate (GFR)
small molecular weight is greater then excretion drugs bound to cannot normally pass GFR is affected by bp |
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Factors that alter drug administration
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IV-over 1 min- fastest
IM SubQ Oral (PO) tablets, enteric-coated preparations, sustained-released preparations *sublingual, topical (gels), inhaled, rectal, vaginal, gas |
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Half life
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amount of time required for the plasma concentration of a drug to decrease by 50% after discontinuance of the drug
*in order to obtain a steady state during drug therapy, usually need 3-5 half lives. Steady state- drug in=drug out |
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Therapeutic Index
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a measure of the safety of the drug; calculated by dividing the LD (lethal dose) 50 by the ED (effective dose) 50. LD 50/ED 50
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Receptor Binding
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-usually reversible
-activity regulated with by endogenous compounds -receptor binding will either mimic or block the actions of endogenous regulatory molecules and increase/decrease the rate of physiologic activity controlled by that receptor |
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Properties of receptors
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-normal points of control of physiologic processes
-receptor function is regulated by molecules supplied by the body -Drugs can only mimic or block the body's own regulatory molecules -Drugs cannot give cells new function -Drugs help the body use its preexisting capabilities -it should be possible to make drugs that can alter the rate of any biologic process for which receptors exist |
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Agonist
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Activates receptors (weak, strong, partial)
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Antagonist
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prevents receptor activation; do not have efficacy since they do not produce a response
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Non-competitive
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-binds IRREVERSIBLY to the receptors
-reduce the maximal response |
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Competitive
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-binds reversibly to receptors
-competes with agonist for receptors types -if agonist and antagonist are both present then the receptor will be occupied by whatever is in the higher concentration |
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Drug interactions Terms
Addition |
combination of drugs is EQUAL to the combined responses of the individual drugs
1+1=2 |
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Synergism
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the combined drugs is GREATER THAN the combined responses of the individual drugs
1+1=3 |
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Potentiation
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a drug which has no effect enhances the effect of a second drug
0+1=2 |
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Antagonism
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one drug inhibits the effect of another drug
1+1=0 |
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Drug-drug Interactions
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poly-pharmacy-drug interactions
consequences -intensified effects -reduction of effects/inhibitory effect -unique response creation |
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Drug-food interaction
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-absorption increase/decrease RATE and EXTENT
*TQ*- may decrease drug effectiveness (vK and warfarin) -may increase drug toxicity -timing of drugs with food -Drug-herb interaction -Some drugs cause a depletion of nutrients & minerals -Drugs induce malabsorption -Drugs can change nutrient excretion |
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Adverse drug reactions
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Any noxious, unintended, and undesired effect that occurs at normal drug doses.
Definitions -side effect-nearly unavoidable secondary drug effect produced at therapeutic doses -toxicity-adverse drug reaction caused by excessive dosing -Allergic reaction-immune response-there must be prior sensitization of the immune system -Idiosyncratic effect-uncommon drug response resulting from a genetic predisposition -Iatrogenic disease- disease produced by a physician (produced by drugs) -Physical dependence-long term use of certain drugs usually associated with "narcotics". Centrally acting drugs can promote dependence. -Carcinogenic effect-ability of certain medications and environmental chemicals to cause cancer -Teratogenic effect-drug induced birth defect |
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Adverse reaction prevention
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-Reducing ADR's is everyone (dealing with drug production and usage) responsibility
-Anticipation of ADR to minimize them -Liver, kidney, bone marrow are important sites of drug toxicity |
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Adverse reaction intervention
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-ADRs can be reduced by individualizing therapy
-Take steps to promote adherence -Monitor clinical response/plasma drug level -Take thorough drug history -Avoid drugs on the Beer's list |
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Indications
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Reasons a person would take a medication
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Contraindication
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Reason NOT to take medication
Ex-Allergy |
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Role of genetics in drug responses
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Special chemicals in the body that most drugs interact with to produce effects-more to come-
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Role of genetics in drug responses
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Genetics can alter metabolism of drugs and predispose a pt to unique interactions
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Patient Adherence
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Ways to reduce non adherence
-use large print -keep it simple -organize drug regime -reminders -improve access -Education (pt and caregiver) |
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Cytochrome P450 system
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a liver enzyme system (made up of 12 or more systems) which metabolize medications
-has INDUCERS and INHIBITORS |
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P450 drug INDUCERS
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-increase enzyme activity
(can increase or decrease drug effectiveness) |
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P450 drug INHIBITORS
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-decrease enzyme activity
(can increase or decrease drug effectiveness) |
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Schedule of Drug
I II III IV V |
I-NO accepted medical use/ hi abuse potential (heroin, LSD)
II-valid medical use/ hi abuse potential III-Potential for abuse less then # II IV-Low abuse potential/ possible psych dependency/ limited physical dependency V-Least abuse potential |
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Def-Tolerance
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Decreased responsiveness to a drug as a result of repeated drug administrations
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Def- Dependence (physical)
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-not the same as addiction
-drugs they need. when they stop then it leads to withdrawal. Not addicted-physically need it |
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Def-Withdrawal
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-the act or process of ceasing to use an addictive drug.
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Def-Addiction
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-more psychological in nature
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OTC drugs
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-Drugs purchased without prescription. Account for 60% of all doses of medication administered.
Advantages Disadvantages -cheap -Drug-drug interactions -effective -dependency -increases autonomy -difficult to monitor -convenient -may delay seeking help |
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OTC herbals
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-Derived from plants
-No FDA approval required before 1962 -Correct labeling required by FDA in 1994 |
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Individual responses to drugs
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physiological variables
-age, gender, weight, body composition Pathological variables -diminished function of kidneys and liver, etc Genetic variables -alter metabolism, and predispose pt to unique interactions -decrease responsiveness to drug d/t repeated administration -placebo effect -variability in absorption -non adherence to therapy -drug interactions -diet |
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Drugs and pregnancy
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-physiologic changes during pregnancy impact drugs
-placental drug transfer -adverse reactions -teratogenesis-dangerous in 1st tri. -drug therapy during breast feeding |
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Teratogenic agents
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"to produce a monster"-alcohol, warfarin, drugs, etc.
if exposed during 1st tri.(embryonic period)-gross malformations 2nd/3rd tri.(fetal period)-disrupts function |
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Functions of the autonomic nervous system (involuntary functions)
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Regulation of
1. the heart 2.secretory glands (salivary, gastric, sweat, & bronchial) 3. smooth muscle (muscles of the bronchi, blood vessels, urogenital, and GI tract) |
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Parasympathetic regulatory functions
(Cholinergic) |
Seven functions
1. Slowing the heart rate 2. Increased gastric secretion 3. Emptying the bladder 4. Emptying the bowel 5. Focusing the eye for near vision 6. Constricting the pupil 7. Contracting bronchial smooth muscle |
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Sympathetic regulatory functions
(Adrenergic) |
1. Regulation of cardiovascular
-maintaining blood flow to the brain -redistribution of blood (important to organs) -compensation for loss blood 2. Regulation of body temperature -regulates blood flow to the skin -promotes secretion of sweat -induces piloerection 3. Implemention of "fight or flight" reaction -increases heart rate and blood pressure -shunting blood away from the skin -dilating the bronchi -dilating the pupils -mobilizing stored energy (break down glucose) |
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Neurotransmitters of the Parasympathetic (Cholinergic) system
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Acetylcholine
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Neurotransmitters of the Sympathetic (Adrenergic) system
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Epinephrine
Norepinephrine Dopamine |
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Parasympathetic (Cholinergic) Receptors
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Nicotinic N
Nicotinic M Muscarinic |
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Sympathetic (Adrenergic) Receptors
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Alpha 1
Alpha 2 Beta 1 Beta 2 Dopamine |
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Functions of the parasympathetic (Cholinergic) receptor
-Nicotinic N -Nicotinic M -Muscarinic |
Nicotinic N- Release of epinephrine from the adrenal gland
Nicotinic M- Contraction of skeletal muscle Muscarinic- Eye- contraction of the ciliary muscle and decrease pupil diameter Heart-Decrease rate Lung-Constriction of bronchi and promotion of excretions Bladder-Contraction of detrusor increases bladder pressure, allows urine to leave the body through detrusor contraction with trigone/sphincter relaxation GI tract-Salivation, increase gastric secretions and intestinal tone/mobility Sweat glands-generalized sweating Sex organs-erection Blood vessels-vasodilation |
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Functions of the sympathetic (Adrenergic) receptor
-Alpha 1 -Alpha 2 -Beta 1 -Beta 2 -Dopamine |
Alpha 1
Eye-Contraction of radial muscle of iris causing mydriasis (increase pupil size) Arterioles-Constriction Veins-Constriction Sex organs-Ejaculation Prostate capsule-Contraction Bladder-Contraction of trigone/sphincter Alpha 2 Presynaptic nerve terminals-Inhibtion of transmitter release Beta 1 Heart-Increase rate, force, AV conduction velocity Kidney-Renin release Beta 2 Arterioles- Dilation Bronchi-Dilation Uterus-Relaxation Liver-Glycogenesis Skeletal muscle-enhanced contraction Dopamine Kidney-Dilation of kidney vasculature |
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Drugs that BLOCK Parasympathetic Nervous system (PNS) and functions
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-Parasympatholytics
-Anticholinergics -Cholinergic Antagonists -Antimuscarinics |
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Drugs that MIMIC Parasympathetic Nervous system (PNS) and functions
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-Parasympathomimetics
-Cholinergic drugs -Cholinergic agonists -Muscarinic Drugs |
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Drugs that BLOCK Sympathetic Nervous system (SNS) and functions
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-Sympatholytics
-Antiadrenergics -Adrenergic Antagonists -Adrenergic Blockers |
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Drugs that MIMIC Sympathetic Nervous system (SNS) and functions
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-Sympathomimetics
-Adrenergics -Adrenergic Agonists |
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Def-Sympathomimetic
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Adrenergic agonist
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Muscarinic Agonist- Bethanechol
-Function -Uses -Side effects |
Activate muscarinic receptor
-Used for acute urinary retention -May need to catheterize in 30 min if no response -Never give with mechanical obstruction or immediately after GI surgery -Atropine counteracts effect -Contra indication=pt with asthma & bladder infection |
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Muscarinic Agonist- Pilocarpine
-Function -Uses -Side effects |
-Constricts pupil and ciliary muscle to help in drainage (Glaucoma)
-Side effects=dizziness, flushing, bronchospasm, decreased vision, increased tearing -Contra indication= pt with asthma and PUD (Peptic Ulcer Disease) |
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Muscarinic Antagonist- Atropine
-Function -Uses -Side effects |
-Decrease secretions
-Pupil dilation -Tachycardia -Decreased voiding and GI motility -Receptor blocker -Side effects=Xerostomia (dry mouth), blurred vision, urinary retention, constipation, anhidrosis (no sweating), tachycardia, asthma |
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Anticholinergic drugs- Oxybutinin
-Function -Uses -Side effects |
AKA Ditropan
-Used to treat overactive bladder -Side effects=slows GI tract, urinary retention, tachycardia -Contra indication- pt with glaucoma |
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Functions of cholinesterase inhibitors
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-Prevent the degradation of acetylcholine by acetylcholinesterase
-Viewed as indirect-acting cholinergic agonist -Lack selectivity -Limited therapeutic applications |
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Neostigmine-Cholinesterase inhibitor
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-Reversible
-Used for reversal of non depolarizing neuromuscular blockade (used post operatively, treatment of overdose) |
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Myasthenia Gravis
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-Fluctuating muscle weakness and predisposition to rapid fatigue (this is an autoimmune process where antibodies attack Nicotinic M receptors on skeletal muscle
-Symptoms=ptosis (droppy eye), dysphagia (weakness swallowing) *CHECK SWALLOWING FOR SIGNS OF MYASTHENIA GRAVIS*, and weakness of skeletal muscle -Give medication in SMALL DOSES and ADJUST to pt response |
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Function and uses of Neuromuscular Blockers
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Function
-Prevent acetylcholine from activating nicotinic m -Cause muscles to relax -NO ORAL FORMS! -Cannot cross the BBB or placenta Uses -Muscle relaxation during surgery -Facilitation of mechanical ventilation -Adjunct to electroconvulsive -Endotracheal intubation -Diagnosis of myasthenia gravis |
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Succinylcholine-Depolarizing Neuromuschlar Blockers
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-Prolongs depolarization
-IRREVERSIBLE -Very short acting time -Used for surgery, endotracheal intubation, ventilatory control -Side effects=Malignant hyperthermia, postoperative muscle pain, hyperkalemia |
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Def-Adrenergic agonist
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-Produce effects by activating adrenergic receptors
-Sympathomimetic -Lots of applications |
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Effects of Adrenergic receptor activation
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Alpha 1
-increase pupil size -Constriction of arterioles and veins -Ejaculation of sex organs -Contraction of prostate capsule -Contraction of trigone and sphincter muscle in the bladder Alpha 2 -Inhibition of transmitter release Beta 1 -Increased heart rate, force of heart contraction, and AV conduction velocity -Release of renin from kidneys Beta 2 -Dilation of arterioles and bronchi -Relaxation of uterus -Glycogenolysis in liver -Enhanced contraction of skeletal muscle Dopamine -Dilation of kidney vasculature |
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Therapeutic applications of Alpha 1 agonist
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-Hemostasis (stops bleeding via vasoconstriction)
-Nasal decongestion -Adjunct to local anesthesia -Mydriasis (dilating pupils) |
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Therapeutic applications of centrally acting Alpha 2 Agonist
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-Reduce the firing of sympathetic neurons
-Used primarily for hypertension -Effects similar to those of the direct-acting adrenergic receptor blockers |
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Clonidine- Centrally acting Alpha 2 agonist
*IMPORTANT-WILL BE ON THE TEST* |
-Potent Alpha 2 receptor blocker
-Mechanism of antihypertensive action -reduces sympathetic outflow to blood vessels and heart by selective activation of Alpha 2 receptors in the CNS -Used for hypertension -Pharmacologic effects/side effects-Bradycardia and decrease in cardiac output, drowsiness, xerostomia (dry mouth), rebound hypertension, not recommended with pregnancy, constipation, impotence -Apply transdermally every 7 days to hairless upper arm/torso |
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Effect and consequences of Beta 1 receptors
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Effect-Mainly in the heart (you have 1 heart)
-Increase- heart rate contractility conduction velocity automaticity renin secretions Consequences/therapeutic applications -Cardiac arrest (not preferred drug of choice) -Heart failure -Shock -Atrioventricular heart block |
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Effect and consequences of Beta 2 receptors
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Effect-mainly in the lungs (you have 2 lungs)
-Relaxation of tracheal and bronchial smooth muscle -asthma -Delay of pre-term labor -Dilates veins and arterioles (not in skin) Consequences -Hyperglycemia -Tremor |
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Def- Epinephrine
-Adrenergic agonist |
Therapeutic uses
-Delay absorption of local anesthetic -Control superficial bleeding -Elevate blood pressure -Overcome AV block -Nasal decongestant -Decreases GI activity Adverse effects -Hypertensive crisis -Angina pectoris -Hyperglycemia |
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Def- Dopamine
-Adrenergic agonist |
Therapeutic uses
-Shock (increases cardiac output and renal perfusion) -Heart failure (increases myocardial contractility) -Acute renal failure (if it works then it increases urine output) Adverse effect -Tachycardia, dysrhythmias, anginal pain, necrosis |
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Def- Terbutaline
-Adrenergic agonist (Beta 2) |
Therapeutic uses
- Asthma (replaced isoproterenol in treatment) -Delay of preterm labor (relaxes muscle) Adverse effects -Minimal therapeutic doses -Tremor most common (tachycardia) |
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Adrenergic antagonist
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Cause direct blockade of adrenergic receptors
*with one exception, ALL produce reversible blockade* |
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Prazoin (MInipress)
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Alpha 1 blocker (adrenergic antagonist)
-use has decreased due to reflex tachycardia |
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Tamulosin (Flomax)
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Alpha 1 blocker (adrenergic antagonist)
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Beta adrenergic antagonist
-Functions- -Uses- |
Cause blockade of adrenergic receptors
-*with one exception, ALL produce reversible blockade* Used with anginal pectoris, migraine, stage fright, glaucoma, hyperthyroidism, etc |
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Nonselective vs. selective beta adrenergic antagonist
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Nonselective Selective
-Uses- -Uses- Hypertension More selective in nature? Angina MI Stage fright Migraines Hyperthyroidism |
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Nursing considerations when using non selective beta blockers
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-Don't stop using abruptly, taper over 2 weeks
-Atropine is the antidote for bradycardia -Epi. is the antidote for bronchoconstriction and hypoglycemia |
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Propranolol- Non-selective beta blocker
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Uses
-Decreases- heart rate contractility automaticity conduction myocardial workload and O2 demand Contra indications -pt with diabetes -pt with severe allergies -pt with cardiac disorders Adverse side effects -Bradycardia -AV heart block -heart failure -bronchoconstriction -CNS effects |
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Metoprolol- Cardio-selective beta blocker
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Primarily blocks Beta 1 receptors
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Effects when drugs are taken chronically
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-Different effects possible for drugs taken chronically verse initially use
-Increase therapeutic effect (may take weeks to build up) -Decrease side effects over time -Tolerance (decrease response over time) verse physical dependence (abrupt stop will show withdrawal symptoms) |
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Parkinson's Disease
-Therapeutic goals- |
-Ideal (reverse neuronal degeneration or prevent further damage) doesn't exist
-Improve pt ability to carry out ADL -Drug selection is determined by the extent that Parkinson's Disease (PD) interferes with ADLs |
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Levodopa
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Drug for PD treatment
-Dopamine replacement drug |
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Levodopa-Carbidopa
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Drug for PD
-Levodopa=promotes dopamine synthesis (highly effective, but benefits diminish over time- "on off" phenomena) -Carbidopa=Blocks destruction of levodopa in periphery (no adverse effects on its own) -Both are used for more severe symptoms *Diets high in B6 are NOT good since it enhances the activity of enzymes that breakdown dopamine* |
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Mirapex -Nonergot Dopamine Agonist
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-Used in early PD and with Levodopa in advancing PD
-max. benefits take weeks -Associated with "sleep attacks" |
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"On-off" phenomenon
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Loss of symptom relief may last for minutes or hours.
-Avoiding high protein meals may help in reducing |
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Levodopa
-Drug interactions- -Adverse effects- -Food interactions- |
-Highly effective
-Combined with carbidopa Adverse effects -Nausea -Psychosis -May darken sweat and urine -can activate malignant melanoma -cardiovascular effects-postural hypotension and dysthythmias High protein and B6 diets are NOT good since they reduce therapeutic effects (enhance the breakdown of dopamine) |
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Advantages of carbidopa
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-No adverse effects of its own
-increase the available levodopa in the CNS and allows for a 75% decrease in needed Levodopa in the body therefore decreasing the potential adverse effects |
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Mirapex
-Uses- -Adverse effects- |
Used alone in early PD and with Levodopa in advancing PD
Adverse effects -Monotherapy- -nausea, dizziness, insomnia, constipation, weakness, hallucinations -Combined- -orthostatic hypotension and dyskinesas |
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"Wearing off"
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-Develops near the end of the dosing interval and may just mean the drug level has dropped below therapeutic level
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Management of non-motor symptoms
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-90% of pt develop non-motor symptoms (depression, dementia, psychosis, etc)
-Depression is in 50% of pt -Dementia happens in 40% of pt |
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Parkinson's and Pyridoxine (B6)
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Pt should avoid multivitamins that contain Pyridoxine since it decreases the amount of Levodopa that reaches the CNS.
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Drugs to be avoided with the administration of Levodopa
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-Pyridoxine (B6)
-Antipsychotic -MAO inhibitors |
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Alzheimer's Disease (AD)
-Risk factors- -Symptoms- |
Progressive memory loss and inability to perform routine daily tasks
Risk factors -Advancing age 65+ -Family history -female -head injury -low education level -low levels of folic acid Symptoms -Behavior problems (wandering, pacing, screaming etc) -Inability to recognize family members -Inability to communicate in final stages -Complete loss of self-identity |
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Drug therapy for AD
-recommended and not recommended |
-5 drugs have been approved (Neuronal receptor blocker (1) and cholinesterase inhibitor (4)).
Recommended -Donepezil, Galatamine, rivastigmine (CI) and Memantine (NRB). Not recommended Tacrine d/t liver damage *Cholinesterase inhibitors should be avoided with asthma and COPD pt because they cause broncho constriction. |
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Memantine
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Neuronal receptor blocker
-Used for moderate to severe AD -Better tolerated then the other drugs Adverse effects -Dizziness -Headache -Confusion -Constipation |
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Tacrine
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Cholinesterase Inhibitor used to treat AD
-Avoid use due to liver damage |
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Other treatments for AD
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-Vitamin E and selegiline
-NSAIDs (ibuprofen) -Estrogen -Ginkgo biloba -Drugs for neuropsyciatric symptoms -SSRIs for depression |
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Multiple Sclerosis (MS)
-Signs- -Symptoms- |
chronic inflammatory, autoimmune disorder that damages the myelin sheath of neurons in the CNS
Varying depending on where CNS damage occur and the size of the region -paresthesias-numbness -muscle/motor problems -visual impairment -bladder/bowel symptoms -sexual dysfunction -disabling fatigue -emotional lability -depression |
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Drug therapy for MS
Interferon Beta -Use- -Adverse effects- -Drug interaction- |
Used to modify disease process, treat acute relapse, and manage symptoms. NO CURE.
Interferon Beta- a naturally occurring glycoprotein with antiviral, anti proliferative, and immunomodulatory actions. Use -Reduces frequency/severity of attacks -Reduces # and size of lesions -Delays progression of disability Adverse effects -Flu-like symptoms -Hepatotoxicity -Myelosuppression -Injection-site interactions -Depression -Neutralizing (antibodies) -Drug interaction Drug interaction -Immunosupressants increase the risk for opportunistic infections to occur. These drugs should be discontinued 3 months before natalizumab is started. Rotate the injection sites. |
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Glatiramer Acetate (Copaxone)- Drug for MS
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-Used for long-term therapy of relapsing-remitting MS
-Protects myelin by inhibiting immune response to myelin basic protein |
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Mitoxantrone monitoring- Drug for MS
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-Perform CBC at baseline and after treatment
-Perform liver test at baseline and after treatment -Determine left ventricular ejection fraction (LVEF) |
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Epilepsy
-Phenytoin- -Carbamazepine- -Valproic Acid- |
Group of disorders characterized by excessive excitability or neurons in the CNS (can produce a variety of symptoms)
Phenytoin, Carbamazepine, and Valproic Acid are all traditional antieplepitic drugs (AED) |
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Phenytoin (Dilatin)
-Therapeutic level- -Adverse effects- -Drug interactions- -Pregnancy use- |
Selective inhibition of sodium channels
Therapeutic level=10-20 mcg/ml Adverse effects -Sedation -Ataxia (staggering gait) -cognitivie impairment -skin rash -gingival hyperplasia (excessive gum tissue growth) Drug interactions -Decreases the effects of oral contraceptions, warfarin, and glucocorticoids -Alcohol and CNS-depressants will add to the effects of Dilantin Pregnancy use -teratogenic (bleeding tendencies in newborns) |
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Management of Status epilepticus
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-Continous series of tonic-clonic seizures, lasting at least 20 to 30 min with loss of consciousness
-Tachycardia, increase blood pressure, hyperthermia -Medical emergency Goals of treatment=maintain ventilation, correct hypoglycemia, terminate seizures |
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Drugs used for spasticity
-Baclofen- -Diazepam- -Dantrolene- |
Movement disorders of CNS origin
Baclofen-Acts on CNS. Decreases flexor and extensor spasms. Suppresses resistance to passive movement. NOT with stroke. ASE=no antidote for overdose, urinary retention, CNS depressant Diazepam-Acts on CNS. Mimics action of GABA. Only benzodiazepine labeled to treat spasticity. ASE=sedation Dantrolene-Acts directly on skeletal muscle. Suppresses release of calcium from sarcoplasmic reticulum. Used to treat malignant hyperthermia. ASE=Hepatic toxicity, muscle weakness, drowsiness, diarrhea, acne-like rash |
