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234 Cards in this Set
- Front
- Back
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Describe the food drug and cosmetic act
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born 1938
empowered the food and drug administration to enforce and set premarket safety standards |
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when did the comprehensive drug abuse prevention and control act started
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1970
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Schedule 1 drugs
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High abuse potential
No medical indications Heroin, LSD, Mecaline |
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Schedule 2 drugs
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Highe abuse
accepted medical indications Opium, cocaine, morphine,codeine , oxycodone, methadone, |
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schedule 3 drugs
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less abuse potential
Vicodin or tylenol with codeine |
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schedule 4 drugs
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Low abuse potential
Diazepam, lorazepam, phenobarbital |
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schedule 5 drugs
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lower than schedule 4 for abuse potential
includes limited amounts of opiods for cough aor diarhea |
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6 rights of medication
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right medication
righe dose right time right route right patient right dicumentation |
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Pharmocokinetics
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how a drug is absorbed
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pharmocodynamics
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how a drug interacts with the body
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the Pharmocokinetic processes
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Absorption
Distribution Biotransformation Elimination |
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Enteral route
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delivery of a medication throug the gastrointestinal tract
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Parenteral route
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delivery of a medication outside of the gastrointestinal tract
( needles) |
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efficacy
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a drugs ability to cause the expected response
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summation
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the additive effect
two drugs given together that have the same effect |
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Synergism
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two drugs that both have the same effect are given together to produce a response greater than the sumof their individual responses 1+1=3
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Potentiation
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one drug enhances the effect of another
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Factors affecting drug response relationship
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age
body mass sex environment time of administration Pathology genetics psychology |
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what do alpha 1 receptors do
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cause peripheral vasoconstriction
mild bronchoconstriction and stimulation of metabolism |
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What do the alpha 2 receptors do
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stimulation of these receptors is inhibitory they serve to prevent over release of norepinephrine in the receptors
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What does the Dopaminergic receptors do
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vasodilation (increased blood flow at the kidney)
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how do you figure an infusion rate over time (example 500 ml over one hour
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Volume x drip factor
divide by Time |
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how do you calculate infusion rates example 2mg per
min of lidocane |
Volume x drip x desired dose
divide by dosage on hand |
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what is the antidode for aspirn overdose
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mucamist
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Chemical name
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describes the drugs chemical composition and molecular structure
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Generic name
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name given by the us adopted name council
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trade name
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the drug has a registered trademark , use of the name restricted by he drugs patent owner (usually the manufactruer)
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Pharaceutics
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the study of how various drug forms influence pharmacokinetic and pharacodynamic activities
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Pharmocokinetics
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the study of what the body does to the drug
-absorption -distribution -Metabolism -Excretion |
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Pharmocodynamics
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The study of what the drug does to the body
- the mechanism of drug actions in living tissues |
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Pharaceutical phase
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disintegration of dosage form Dissolution of drug in body
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Pharacodynamic phase
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drug receptor interaction
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Pharmacotherapeutics
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the use of drugs and the clinical indications for drugs to prevent and treat diseases
-Empirical therapeutics -Rational therapeutics |
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Pharmacognosy
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the study of natural (plant and animal) drug sources
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Pharmaceutic
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Dosage form, design affects, dissoulution
pharmaceutic aid substances which are of little or no therapeutic value, but are necessary in the manufacture, compounding, storage, etc., of pharmaceutical preparations or drug dosage forms. They include solvents, diluting agents, and suspending agents, and emulsifying agents. Also, antioxidants; preservatives, pharmaceutical; dyes (colouring agents); flavoring agents; vehicles; excipient; ointment bases. |
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Drug absorption rates for PO administration
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liquids
suspensions powders capsules tablets coated tablets enteric coated tablets |
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Factors that effect absorption
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Food and fluids
Dosage fromulation status of the absorptive surface rate of blood flow to the small intestine acidity of the stomach status of gi motility |
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Routes of drug administration
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enteral (gigu)
parenteral topical |
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Enteral route
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oral
sublingual buccal absorbed through small intestine |
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First pass effet
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the metabolism of a drug and its passage from the liver into the circulation, a high first pass effect would be giving an oral route med, it is processed by liver before reaching target. IV meds prevent first pass effect
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Parenteral route
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IV
IM Sub q ID intrathecal inraarticualr transdermal can be parentaeral too |
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Topicla route
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skin
eyes ears nose lungs rectum vagina |
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Dustribution
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the trasport of a drug in the body by the bloodstrea to its site of action
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areas of rapid distribution
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muscle
skin fat |
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areas of rapid distribution
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heart
liver kidneys brain |
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Metabolism or biotransformation
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the biochemicla transformaion of a drug into an inactive metabolite, a more soluble compound or a more potent metabolite ,
liver , muscle , kidneys , lungs , plasma ,intestinal mucosa Biologic transformation of a drug into an inactive metabolit more soluble compound more potent metabolite |
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Factors that decrease metabolism
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cardiovascular dysfuncion
renal insufficiency starvation obstructive jaundice slow acetylator erythromycin or ketaconazole drug therapy |
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Factors that increase metabolism
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fast acetylator
barbiturate therapy rifampin therapy |
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areas of rapid distribution
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muscle
skin fat |
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areas of rapid distribution
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heart
liver kidneys brain |
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Metabolism or biotransformation
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the biochemicla transformaion of a drug into an inactive metabolite, a more soluble compound or a more potent metabolite ,
liver , muscle , kidneys , lungs , plasma ,intestinal mucosa Biologic transformation of a drug into an inactive metabolit more soluble compound more potent metabolite |
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Factors that decrease metabolism
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cardiovascular dysfuncion
renal insufficiency starvation obstructive jaundice slow acetylator erythromycin or ketaconazole drug therapy |
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Factors that increase metabolism
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fast acetylator
barbiturate therapy rifampin therapy |
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A Drug
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is any chemical that can affect living processes
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Therapeutics
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the medical use of drugs
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The ideal drug
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Effectiveness
Safety Selectivity |
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Seven important aspects of drug therapy
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Assessment
Dosage and administration Evaluating and Promoting effects Minimizing adverse effects and interactions Prn decisions Managing toxicity |
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three ways that a substance can cross cell membranes
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passing throgh channels and pores for very small molecules
2, transport systems for selective carriers that may or may not use atp 3,direct penetration of the cell membrane (like dissolves like)drugs that are lipid soluble will pass through due to the phospholipid layers of the cells |
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Ph dependent ionization
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the idea that an acid will be unionized in acidic media but will in an alkaline environment
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ion trapping (ph partitioning
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drugs will accumulate on whichever side of the membrane that favors their ionization. with this we can determine which environment a drug will accumulate (using Ph dependent ionization)
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Factors that control Distribution
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1,Blood flow to tissues
2,Exiting the vascular system at capillary beds 3,Typical capillary beds, Drugs pass between cells 4, the blood brain barrier 5,placenta -same as blood brain 6, protein binding, albumin is important drugs that bind stay in the system for a long time and can be a source of drug interaction 7,Some drugs must enter cells to reach sites of action |
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Concepts of metabolism
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1,most drugs are metabolised in the liver
2,Metabolism makes it possible for the kidney to excrete many drugs that otherwise could not 3,Activation of prodrugs, which is a drug that is not active until conversion in the body 4,increased or decreased toxicity |
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Factors that influence rate of metabolism
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Age, hepatic maturation doesnt occur until about a year old
2,induction of drug metabolizing enzymes, which increases the metabolism causing the need for an increased dose for that drug and other drugs given at the same time 3,First pass effect, hepati inactivation of certain oral drugs 4,Nutritional status 5, competition between drugs |
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Concepts of renal drug excretion
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Glomerular filtration and
passive tubular reabsorption,causing drugs that are lipid soluble to undergo passive rabsorption. 2, active tubular secretion |
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Factors that modify renal drug excretion
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Ph dependent ionization, by manipulating urine ph can promote the ionization of a drug can decrease passive rabsorption.
3,competition for active tubular transport 4,Age infants have a limited capacity to excrete drugs 5,time course of drug responses 6,plasma drug levels |
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Non renal routes of drug excretion
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breast milk
bile, lungs, sweat, saliva |
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Describe the significance of drug plasma levels
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used to estimate the concentration of a drug at the action site by checking plasma concentration
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Therapeutic range
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keeping the drug within this range is the goal, a narrow therapeutic range makes things hard
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Drug half life
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the time required for the amount of a drug in the body to decrease by 50%
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Loading doses
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used when a plateau must be reached quickly
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Describe the decline from plateau
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when a drug is discontinued 94% of a drug will be eliminated over an interval of 4 half lives
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Maximal efficacy
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the largest effects that a drug can produce
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relative potency
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the amount of a drug that must be given to elicit an effet
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Drug receptor
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any functional macromolecule in a cell to whic a drug binds to produce its effecs
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what do drugs do at receptors
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mimic or block the action fo the bodys own regulatory molecules
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Describe drug receptors and selectivity of drug action
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if drugs interact with only one kidn of receptor than effects will be limited but it can still produce a variety of effects so selectivity does not guarantee safety
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simple occupancy theory
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the intensity of the response to a drug is proportional to the number of receptors it occupies.
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Affinit
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the strength of the attraction between a drug and its receptor (high affinity makes a very potent drug)
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Agonist
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activate receptors,,
mimics the bodys regulatory processes |
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atagonist
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prevent receptor activation
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noncompetitive antagonist
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bind irreversibly to receptors and reduce maximal response that an agonist can produce
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competitive antagonist
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bind reversibly to receptors competing with agonists for binding sites
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partial agonists
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have moderate intrinsic activity, acts as antagonists as well as agonists
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types of analgesics
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nsaids and opiods
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what is pain
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whatever the patient says it is and where the patient says it is, very unpleasant
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Pain threshold
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the level of stimulus needed to produce the perception of pain , a measure of the physiologic response of the nervous system
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Pain tolerance
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the amount of pain a patient can endure without its interfering with normal function, subjective response
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classification of pain by onset and duration
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Acute pain and chronic pain
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classification of pain
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somatic
visceral superficial vascular referred neuropathic phantom cancer psychogenic central |
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Pain transmission gate theory
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uses the anology of a gate to describe how impulses from damaged tissues are sensed in the brain
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Tissue injury causes the release of what
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bradykinin
histamine potassium prostaglandins serotonin, all of these stimulate nerve endings starting the pain process |
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what are the two types of nerves stimulated
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A and C fibers
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what regulates the type of apin a person feels
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A and C fibers in damaged areas
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where is the location of the gate in reference to pain
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Dorsal horn, which is the point of spinal cord entry to the brain
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What does the gate do in reference to pain and what happens when you shut the gate
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regulates the flow of sensory impulses to the brain
closing it stops the impulses |
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What does activation of large diameter A fibers do
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closes the gate and limits perception of pain
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what does activation of smal diameter C fibers do.
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opens the gate which allows impulse transmission to the brain and causes pain perception
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What dos the nerve fibers from the brain that inervate the gate do with regards to pain perception
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allows the brain to evaluate, identify and localize the pain. It controls the gate before the gate is open.
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what does the body produce to inhibit transmission of a pain.
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Produce Enkephalins and Endorphins that bind to the opoid receptors.
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what does rubbing a painful area do
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Stimulates the large sensroy fibers (A fibers) this closes the gate, pain reduced
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Opioid analgesics
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pain relievers that contain opium form the opium poppy
(Narcotics) |
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Agonist
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bind to opioid pain receptor in the brain (reduction of pain)
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Partial agonist
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bind to pain receptor cause weaker neurologic response (mixed agonist)
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Antagonist
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reverse the effects of these drugs on pain (competitive antagonists)
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What are the five types of opiod receptros
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MU
Kappa Delta Sigma Epsilon |
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What are some other uses for opiod anagesics
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cough suppression
diarrhea balanced anesthesia |
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Analgesics contraindications
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allergy
asthma or resp problems intracranial pressure pregnance |
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Opioid analgesics adverse effects
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pupil constriction
N/V respiratory depression constipation itching flushing urinary retention |
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drugs that bind to opiod receptors and prevent a response
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Naloxone
Naltrexone |
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opiates physical dependence and tolerance
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need larger doses for same effect because of the physical adaptation of the body
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Opiate psychologic dependence
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the need for the drug for effect other than pain relief
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Opioid withdrawal syndrom
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extreme pain and irritability, like a bad flu
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Acetaminophen
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analgesic adn antipyretic effects,
no aniinflammatory effects |
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why use aetaminophen
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great for people that cant have apirin
gets rid of pain by blocking prostiglandin synthisis reduces fever (lethal whith overdose, antidote is acetylcysteine regimen) do not excede 4000 mg per day |
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What are anesthetics
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drugs that depress the central nervous system
muscle relazation depression of consciousness loss of sensory stimulation |
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What is anesthesia
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state of depressd cns activity
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General anesthetics what are the two types
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inhaled (volatile liquids or gasses that are vaporized in oxygen and inhaled and injectable
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What are adjunctive drugs to general anesthetics
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sedative hypnotics (benzoe)
opioids (morphine) Neuromuscular blocking drugs Anticholinergics (atropine) |
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what is general anesthetics used for
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surgical procedures,
unconsciousness muscle relaxation |
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what are the adverse effects of general anesthetics
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myocardial depresson is commonly seen also effects the peripheral circulation, liver, kidneys, respiratory tract.
could also cause malignant hyperthermia ( 104 temp and tachypnea, tachycardia and muscle rigidity) |
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what are local anesthetics for
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block nerve impulses to a certain area
topical parenteral spinal infiltration nerve block topical |
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paralysis occures in what order when using aneshtetcs
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1) autonomic activity is lost
2) pain and other sensory functions are lost 3) motor activity is the last to be lost (when the drug wears off recovery occurs in the reverse order) |
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what are NMBAs
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prevent nerve transmission to certain muscles resulting in paralysis these are used with anesthetic during surgery
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How does succinylcholine work
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it isa the only depolarizing drug, works lik acetylcholine causing depolarization. but the metabolism is slower than ACh. so if it is present repolarization cannot occur
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what do Nondepolarizing NMBAs do
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prevent ACh form acting at the neuromuscular junctions. Nerve cell membrane is not depolarized so the muscle fibers are not stimulated and contraction does not occure
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what is the order of paralysis for NMBAs
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muscle weakness
paralysis of small rapidly moving muscles (fingers and eyes) Paralysis of limbs, neck and trunk Paralysis of intercostal muscles and diaphragm (recovery is in reverse order) flaccid paralysis |
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NMBAs indications
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maintaining controlled ventilation during surgery
ET tube reduce muscle contraciton in an area that needs surgery Diagnostic for myasthenia gravis |
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adverse effects of NMBAs
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hypotension due to the releaseof histamine and tachycardia due to the blockade of muscarinic receptors
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describe moderate sedation or conscious sedation
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combo of benzos and opiates
anxiety and sensitivity to pain are reduceed and patient cannot recal procedure, this is nice because the airway is maintained and patient can follow comands |
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what are some important nursing implications for a patient with sedation
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teach the patient how to breath deep and talk about what they may feel or hear monitor for reacitons and vital signs make sure to orientate during recovery
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Epilepsy
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Chronic recurrent pattern of seizures
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Seizure
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episode of abnormal electrical activity in the nerve cells of the brain
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Convulsions
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involuntary spasmodic contraction of any or all voluntary muscles throughout the body
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describe Primary or idiopathic epilepsy
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the cause cannot be determined
Accounts for more than 50% of cases |
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Describe secondary epilepsy
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Distinct cause identified
trauma, infection, cerebrovascular disorder |
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what is a partial seizure
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short alterations in consciousness
confusion repetitive unusual movements (chewing or swollowing) |
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what is simple seizures
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No impaired consciousness
Face arm and leg motor movements Sensory Hallucinations Personality changes |
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What are complex seizures
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Impaird consciousness
Memory impaiment behavioral effects Aura, chewing and swollowing movements Tonic clonic activity |
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what are generalized seizures
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both ceerebral hemispheres involved
brief loss of consciousness with no confusion head drop or falling down symptoms tonic clonic and spasm possible patient stares off into space |
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Antiepileptic Drugs
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Known as anticonvulsants
usuall life long treatment for control of seizures |
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how do the AEDs work
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prevent generation of spread of electrical discharge and protect surrounding nomal cells, the idea is thought to be that they alter movement of sodium, potassium, adn calcium across neve cells in the brain,
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IV phenytoin should only be used with what iv fluid
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Normal Saline
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What is parkinsons disease
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chronic, progressive, degenerative disorder that effects the dopamine producing neurons in the brain. This is cause by an imbalane of two neurtransmitters (Dopamine and Acetylcholine) DECREASE IN DOPAMINE AND INCREASE IN ACETYLCHOLINE
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When does Parkinsons diseas start showing symptoms
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when about 80% of the dopamine that is stored in the substantia nigra of the basal ganglia is depleted
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what is needed for Parkinsons to be controled (Partially)
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Functioning nerve terminals that can take up dopamine
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Symptoms of Parkinsons Disease
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Bradykinesia (slowness)
Rigidity Tremor Postural instability |
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Dyskinesia
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Difficulty in performing voluntary movements
1 Chorea, irregualr,spasmodic involuntary movements of the limbs or facial muscles. 2.Dystonia, abnormal muscle tone leading to impaired or abnormal movements |
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Describe the on and off phenomenon with PD (Parkinsons Disease)
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rapid mood swings in response to levdopa
PD worsens with too little dopamine Dyskinesia occurs when too much is present This is a progressive disease |
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Describe Levodopa therapy
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It is a precursor of dopamine
Because of the blood brain barrier, exogenously supplied dopamine can not enter but levodopa can. It is taken up by the dopaminergic terminal and converted into dopamine, therapy nonfunctional between 5 and 10 years |
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What is the goal with the drug therapy for Parkinsons
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1)increase levels of dopamine
2) antagonize or block the effects of ACh 3) Slow the progression of the disease |
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What drug catagories are used for parkinsons disease
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Anticholinergic
Antihistamines Dopamine receptor agonist that are direct acting like levodopa and indirect acting like MAO-B inhibitors and COMT inhibitors |
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what does MAOIs like SELEGILINE do for parkinsons disease
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MAOIs break down catecholamines in the CNS
If you block one like MAO-B you get an increase in the levels of dopaminergic stimulation in the CNS (these are used as adjunct therapy) and use can delay unresponsiveness to levodopa therapy |
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MAOIs adverse effects
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usually mild
nausea, lightheadedness, dizziness, abdominal pain, insomnia, confusion, dry mouth (doses higher than 10 mg may cause a hypertensive crusis) |
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Three types of Dopaminergic therapy for parkinsons
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Replacement (presynaptic)
Direct acting/replacement indirect acting |
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Carbidopa
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this is given with levodopa to stop the breakdown of it befor reachin the target in the brain. part of presynaptic therapy
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Indirect acting Dopaminergic therapy causes what
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the release of dopamin from the storage sites at the end of the nerve cells that are still intact and blocks reuptake into the nerve endings (more dopamine will than be available) SYMMETREL is a drug that does this
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why is it important to use COMT inhibitors like TOLCAPONE AND ENTACAPONE
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COMT is the enzyme responsible for the breakdown of levodopa
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Describe direct acting Dopaminergic therapy
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Directly stimulates the dopamine receptors and stimulate the production of more dopamine
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What does Anticholinergic therapy do
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blocks ACH
used to treat muscle tremors and rigidity |
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Why does ACh accumulate in PD
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because of the lack of Dopamine this causes pill rolling and tremors and rigidity
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Anticholinergic therapy indications
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treatment of PD
treatment of drug induced extrapyramidal reaction to certain antipsychotic drugs |
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Anticholinergic side effects
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Drowsiness, confusion, disorientation, constipation, nausea, vomiting,urinary retention,blurred vision, (DILATED PUPILS AND PHOTPHOBIA AND DRY SKIN)decreased salivation
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Patient teaching with regard to PD drugs
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drink plenty of fluids and watch for side effects
Avoid vit B6 in amounts greater than 10mg If taking levodopa with MAOIs watch for hypertensive crisis DO NOT stop drug use suddenly Levodopa may darken the urine and sweat. COMT inhibitor effect only take a few days DRUG HOLIDAYS |
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what are sedatives
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drugs that have an inhibitory effect in the cns
they reduce Nervousness Excitability and Irritability All of this without causing sleep |
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What are Hypnotics
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Cause sleep
A sedative can become a hypnotic if it is given in large enough doses |
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Barbiturates
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Introduced in 1903
used for insomnia and sedation Habit forming Low therapeutic index Replaced with benzodiazepines |
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4 categories of barbiturates
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Ultra short, for short surgery
Short, sedative or hypnotic adn control of convulsive conditions Intermediate, same as short Long, same as intermediate |
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Barbiturates mechanism of action
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site is reticular formation in the brainstem
It inhibits GABA, nerve impulses traveling in the cerebral cortex are also inhibited |
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Barbiturates effects
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Low doses= sedative effects
Highe doses= hypnotic effects (this will lower resp rate) They are notorious enzyeme inducers, that is they stimulate liver enzymes that cause the metabolism or breakdown of many drugs that results in a shortened duration of action. |
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Indications for barbiturates
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hypnotics
sedatives anticonvulsants anesthesia for surgery |
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Barbiturates adverse effects
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CNS depression
Respiratory depression Upset GIGU Agranulocytosis, hypotension Stevens Johnson syndrome Reduced REM sleep causing agitation and stress |
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what can barbiturate overdose lead to
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respiratory arrest
sleep, coma, death |
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What can very large doses of barbiturates be used for
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Anesthesia induction
Uncontrollable seizures (phenobarbital coma) |
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Describe some barbiturate drug interactions
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ETOH, antihistamines, benzos,opioids,tranquilizers will all have additive effects
MAOIs will prolong effects of barbiturates. The increased metabolism will reduce anticoagulant response leading to clot formation. |
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What is the most frequently prescribed sedative hypnotic
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Benzodiazapines because of the favorable drug effects. like not suppressing REM sleep as much and not increasing metabolism of other drugs.
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Classification of Benzodiazepines
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sedative-hypnotic
Anxiolytic |
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What are the benzodiazepine types
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long acting
short acting There are also nonbenzodiazepine hypnotics that share many characteristics of benzodiazepines, they are used to treat insomnia |
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Mechanism of action for benzodiazepines
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Depress CNS activity affecting hypothalamic, thalmic and lmbic system.
there are benzodiazepine receptors |
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Benzodiazepines drug effects
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calming the CNS
Inducing sleep Induce skeletal muscle relaxation |
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Benzodiazepine indiations
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Sedation
Sleep induction Skeletal muscle relaxation Anxiety relief treatment of alcohol withdrawal Agitation Depression Epilepsy Balanced anesthesia Moderate conscious sedation |
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Benzodiazepines adverse effects
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Headache
Drowsiness Dizziness Vertigo Lethargy Hangover effect rebound insomnia if for a few days if you quit |
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Muscle relaxants indications
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muscle spasms
Multiple sclerosis,cerebral palsy |
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How do muscle relaxants work
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CNS is the site of action
Acts directly on skeletal muscle Closely resembles GABA |
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dantrolene (Dantrium)
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Malignant hyperthermia crisis
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Muscle relaxant adverse effects
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Euphoria
Lightheadedness Dizziness Drowsiness Fatigue Muscle weakness |
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GABA
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In vertebrates, GABA acts at inhibitory synapses in the brain
Drugs that act as agonists of GABA receptors (known as GABA analogues or GABAnergic drugs) or increase the available amount of GABA typically have relaxing, anti-anxiety and anti-convulsive effects |
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psychotherapeutics
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the treatment of emotional and mental disorders
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psychotherapeutic drug types
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antianxiety drugs
antidepressants antimanic drugs antipsychotics |
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what are the three main emotional and mental disorders
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Psychoses
Affective disorders Anxiety |
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Affective disorders
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(mood disorders)
abnormally pronounced emotions, Bipolar disorder |
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Psychosis
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emotional disorder that impairs the mental function.
loss of contact with reality |
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what is anxiety
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unpleasant state of mind
sense of dread and fear response to negative situations |
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what are the 6 anxiety disorders
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Obsessive-compulsive disorder
Posttraumatic stress disorder Generalized anxiety disorder Panic disorder Social phobia Simple phobia |
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Biochemical ibalance theory
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mental disorders are associated with abnormal levels of endogenous chemicls such as neurotransmitters in the brain
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Catecholamines
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Dopamine
Norepinephrine |
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Indolamines
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Serotonin
Histamine |
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biochemicals necessary for normal mental function
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GABA
Acetylcholine Sodium, potassium, magnesium |
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Treatment for benzodiazepine overdose
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flumazenil
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Drug of choice for treatment of mania
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lithium
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What does antimanic drugs like lithium do
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Thought to potentiate serotonergic neurotransmission
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Biogenic amine hypothesis
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Depression and mania are due to alteration in neuronal an synaptic catecholamine concentration at adrenergic receptor sites in the brain;
Depression=deficiency of catecholamine especially norepinephrine Mania=excess amines |
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Permissive hypothesis
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Affective disorders are due to decreased concentrations of serotonin.
Depression results from decreased serotonin and catecholamine levels Mania results from increased catecholamin but decreased serotonin levels |
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Dysregulation hypothesis
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Depression and other affective disorders result from a failure in the regulation of catecholamine activity
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How do selective serotonin reuptake inhibiters work
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increase serotonin concentrations at nerve endings, no cardio effect
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New gereration antidepressants indications
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Depresson
Bipolar disorder Obesity eating disorders OCD anxiety disorders |
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Newer generation antidepressants adverse effects
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H/A, dizziness, tremor, nervousness, insomnia, FATIGUE
GIGU problems WEIGHT GAIN AND WEIGHT LOSS sexual dysfunction |
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Serotonin Syndrome causes
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Delirium
agitation, Tachycardia, sweating, hyperreflexia, muscle spasms, shivering, course tremors, Hyperthermia, seizures, renal failure, rhabdomyolysis, Dysrhythmias, DIC |
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Newer generation antidepressant drug interactions
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bound to plasma proteins
Compete with other protein binding drugs. inhibition of cytochrome p-450 system MAOIs |
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Mechanism of action of tricyclics
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block reuptake of neurotransmitters, causing accumulation at the nerve endings. It is thought that increasing concentrations of neurotransmitters will correct abnormally low levels that lead to depression
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increasing norepinephrine when you block the reuptake of it will cause
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antidepressant effect and tremors, tachycardia etc
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increasing serotonin when you block the reuptake of it causes
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antidepressant effect and H/A anxiety, nausea, sexual dysfunction
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An overdose of first generation antidepresants )(cyclics)results in what
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death CNS and cardio systems are affected death results from seizures or dysrhythmias
there is no specific antidote, just BLS and charcoal |
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MAOIs
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considered second line treatment for depression not responsive to cyclics but has potential to cause hypertensive crisis when taken with tyramine
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MAOIs mechanism of action
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inhibit the MAO enzyme system in the CNS, because of this amines like dopamine, serotonin, and norepinephrine are not broken down. which may help depression
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MAOIs adverse effects
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ORTHOSTATIC HYPOTENSION
tachy, dizziness, insomnia, blurred vision, nausea, drowsiness, |
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MAOIs overdose treatment
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symptoms appear 12 hours after ingestion,
tachycardia, shock, seizures, coma. Protect brain and heart with gastric lavage, urine acidification, hemodialysis |
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What should you avoid when taking MAOIs
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Tyramine, it can cause a hypertensive crisis...
Some foods to avoid mature cheese smoked meat yeast red wines italian broad beans |
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what could concurrent use of MAOIs and SSRIs lead to
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Serotonin syndrome
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How do you avoid serotonin syndrome
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there should be a 2 to 5 week wash out period
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Antipsychotics
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drugs used to treat serous mental illness
behavioral problems or psychotic disorders |
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How do Antipsychotics work
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they block dopamine receptors in the brain(limbic system, basal ganglia) areas associated with emotion, cognitive function, motor function.
Because of the lower Dopamine levels in the CNS a tranquilizing effect is caused |
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What do newer antipsychotics do
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block specific dopamine receptors, D2
Block specific serotonin receptors S2 this improves the safety profile and efficacy |
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Antipsychotics indications
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serious mental illnesses
Movement disorders (tourettes Nausea intractable hiccups |
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Adverse effects, for antipsychotics
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sedation, delirium
orthostatic hypotension syncope, dizziness, EKG changes, photosensitivity, skin rash, hyperpigmentation, pruritus. Dry mouth, constipation, leukopenia and agranulocytosis. |
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Neuroleptic malignant syndrome, regarding antipsychotics
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High fever, unstable BP
myoglobinemia |
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Extrapyramidal symptoms, regarding antipsychotics
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involuntary muscle symptoms similar to parkinsons.
Akathisia(muscle restlessness) Dystonia (painful muscle spasms) Tardive dyskinesia, (involuntary contractins of oral and facial musles) Choreoathetosis(wavelike movements of extremities) |
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When taking tricyclics what may you need to do before surgery
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be weaned and discontinue due to the possible reactions with anesthetic drugs
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when should you wear sunscreen
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when taking anipsychotics
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Stimulants are
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sympathomimetic drugs
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Analeptics are used for
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CNS stimulant
appetite suppressant (anorexiant) treatment of ADHD Narcolepsy Migraine H/A |
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Adverse effects of stimulants include
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palpitations, nausea, dry mouth, urinary frequency, insomnia
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Uses for caffeine
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Neonatal apnea
respiratory depression in adults enhance effects of analgesics and migraine medications CNS stimulation |
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Rules for taking drugs for ADHD
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should be given at least 6 hours before bedtime to reduce insomnia
may cause dry mouth take on empty somach 45 min before meals may need drug holidays keep jounal of response |
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Rules for serotonin agonist
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avoid food cntaining tyramine
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