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169 Cards in this Set
- Front
- Back
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Pharmacology
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Study of the nature, chemistry, effects and the uses of drugs
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Metrology
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Science of measurements
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Pharmacotherapeutics
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branch of pharmacology that involves using drug to treat, prevent or diagnose diseases.
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Why is pharmacology important?
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Nurses are held personally responsible for every drug they administer or have administered no matter who actually prescribed it.
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Ideal Drug
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There is NONE! No drug is 100% safe because all drugs are chemicals.
*ALWAYS SIDE EFFECTS |
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Drugs need to be:
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Effective-elicits the response for which it is given
Selective-drug that elicits only the response for which it is given. (DOES NOT EXIST!) |
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Properties of drugs:
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-Reversible
-Predictable =Easy to administer -Freedom from interactions with other drugs (DOES NOT EXIST!) -Cheap (generic cheaper) -Chemically stable (store drugs safely) -Simple name that cannot be confused (Name has big letter then it means that it is close to another drug) |
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Drug information sources: Pharmacopeia
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total of all authorized drugs available in a country, containing descriptions, recipes, strenghts, standards of purity, and dosage forms for the drugs. (mainly used by pharmacists)
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Drug information sources:
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-American Hospital Formulary:extensive information on drug classes (published annually)
-FDA Drug bulletin: free, quarterly news letter -USP dispensing information: categories, precautions, side effects, actions, dosage and labeling information (USEFUL FOR NURSES) -Package inserts: provided by manufacturer (made by drug co.) -Physician's Desk Reference (PDR): contains information provided by manufacturer (made by drug co.) -Electronic databases -Hospital Formulary: different for every hospital -Textbooks: reference only |
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Sources of drugs:
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-Synthetic chemicals
-Plants -Animals (only available from other countries) -Mineral products -Genetically engineered chemicals |
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Ways to group drugs:
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-Body system effect
-Chemical characteristics -Therapeutic use -Prototypes |
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Drug nomenclature:
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-Chemical name (used by pharmacist)
-Generic name-all hospitals use generic because they are cheaper and no difference in chemical make up -Trade name: recognized by trademark |
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Legend (prescription drugs)
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prescription drugs require a prescription and must bear the legend "Caution, federal law prohibits dispensing without a prescription"
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Over-the-counter:
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non prescription but signature required. (prevent against meth use)
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New Drug Development:
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-takes many years
-most never make it to market -process monitored by food and drug administration. -US most stringent in the world -average cost to get drug approved: 350 million -Two steps: preclinical-animal testing (3-5 years) and clinical (four phases) |
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Phases of drug development: step 1
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Animal testing:
-two purposes: effect in living tissue and evaluate adverse reactions (toxicity and TI (lethal dose/affective dose)) -investigational new drug application filed for human testing with informed consent by the FDA |
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Phases of drug development: step 2
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Clinical testing:
Phase I: (healthy volunteers) small numbers to determine metabolism and side effects Phase II: (volunteers with disease) evaluate effectiveness and side effects and fine tune dosage Phase III: (larger numbers of patients at research centers) to find rare side effects. -New Drug Application (NDA) to FDA. Marketing begins after NDA approval. Phase IV: post marketing surveillance to gather more information by nurses and physicians |
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Special Circumstances for drugs:
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-Expected drug approval: must still undergo four phases of clincal evaluation and can apply to use drugs in phase 2 or 3 if the patient meets criteria (ex. AIDS)
-Black Box Warning: drug pulled off the market and put back on with warning -Orphan drugs: tax benefits to develop drug affecting 200,000 or less (Drug co's dont want to research drug that wont make them very much money) -Compassionate use: for terminal illness can get certain drugs without FDA approval. |
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Limitations of the testing procedure:
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-limited testing in women and children
-failure to detect all adverse effects |
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Factor's affecting an individual's response to drug:
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-weight
-age -gender -physiologic factors -genetic factors -immunological factors (allergies) -psychological factors -environmental factors -tolerance -drug-drug interaction -drug-food interaction |
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Effects of drugs:
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Desired effect-therapeutic effect of the drug in the body
-Acute disease -maintenance -supplemental -palliative: pain management -supportive -prophylactic (antibiotics before surgery) Undesired/adverse effect-every drug has one -idiosyncratic: genetically determined abnormal response to ordinary dose of a drug -hypertensive/allergic:immune system recognizes drug as a dangerous foreign substance. Not dose related. -Toxicity (nephrotoxcity, neurotoxicity) -Teratogenic: damage to fetus -Carcinogenic -mutagenic |
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Preventing Adverse Effects
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-verify allergies
-administer at recommended rate, dose. -monitor lab and withold or discontinue if indicated -take appropriate measurements before administering drug (BP, pulse, ect...) |
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Drug-drug Interactions
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two drugs interact and produce an effect
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Drug-drug interactions: Additive
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Two or more "like" drugs (aspirin and codeine)
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Drug-drug interactions: Synergistic
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Two or more "unlike drugs" result in a greater effect (hydroclorathiazide and enalapril)
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Drug-drug interactions: Potentiated effect
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effect of only one of the drugs is increased (meperidine and phenergan)
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Drug-drug interactions: Antagonistic
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Stops the use of a drug (calcium and tetracycline)
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Drug-drug interactions:Incompatible
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-Chemical: structure and pharmacologic properties change
-Physical: precipitate |
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Drug-food interaction
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fats/protein may slow absorption
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Off-label
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use of a drug in ways or purposes other than what was approved by the FDA
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Legislation: Pure Food and Drug Act of 1906
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Establishes USP and NF as official reference
Ingredients must be listed on label. |
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Legislation:Sherley Amendment (1912)
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prohibited fraudulent therapeutic claims
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Legislation: Harrison Narcotic Act of 1914
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Classified certain drugs as narcotics
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Legislation: Food, Drug and Cosmetic Act of 1938
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-Result of 100 deaths from ingestion of diethylene glycol solution of sulfanilamide
-required labeling "Warning may be habit forming" and other labeling on all drug containers -Est. the FDA |
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Legislation: Durham-Humphrey Amendment of the 1938 Act in 1952
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Differentiated drugs that could be sold without prescription from "legend drugs"
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Legislation: Kefauver-Harris Amendment of the 1938 Act in 1962
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-Resulted from thalidamide tragedy
-Protects public by ensuring that adequate preclinical testing is performed. Must prove that drug is safe and effective -Black box warnings |
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Legislation: Comprehensive Drug Abuse and Prevention Act of 1970s
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-Response to misuse and abuse of the 60's
-Classified drugs according to abuse potential |
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Classified drugs according to abuse potential:
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C-I only with approved protocols
C-II writeen script only, no refil C-III script expires in 6 months C-IV same as C-III C-V written script or OTC-varies by state (least strict) |
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Drug Abuse
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use of any drug in a manner that deviates from approved medical or social patterns (it is culturally defined and opinions vary)
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Physical dependence:
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Physiologic reliance on a drug; withdrawal syndrome will occur if drug is discontinued
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Psychological dependence:
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intense subjective need for a particular drug
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Three main drug categories of abuse:
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1. Opioids
2. Stimulants 3. Depressants |
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Drug Tolerance
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need to increase dose to maintain same effect with continued drug use
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Drug Cross tolerance
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Tolerance to one drug confers tolerance to another drug (within the same class)
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Drug withdrawal
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Appearance of physical symptoms due to cessation of drug use; usually opposite to drug effect
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Pharmacokinetics
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what the body does to the drug: absorption, distribution, metabolism, and excretion
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Pharmacodynamics
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What the drug does to the body: mechanism of action
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Pharmacotherapeutics
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clinical use of drugs
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Pharmacokinetics: Absorption
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1. Absorption - drug getting into the bloodstream, bioavailability is the amount of drug that gets into the blood; movement from site of administration to circulation.
-Other factors: absorbing surface, blood flow, lipid solubility, rate of dissolution or concentration. form, drug-drug or drug-food interactions |
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Pharmacokinetics: Distribution
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2. Distribution - transport of drug to the site of action in the body (the target tissue)
-many bind to protein (albumin) -only unbound drugs can reach tissues; low unbound=more unbound -two drugs can compete for protein binding sites -lipid solubility -blood flow to area determines rate of distribution (lots of drugs don't pass the blood brain barrier) |
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Pharmacokinetics: Metabolism
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3. Metabolism – breakdown of drug molecule (biotransformation)
-most metabolized by the liver (few are metabolized by the kidney) -Liver metabolism makes drugs water soluble -Body changes drug to a more water soluble or inactive molecule *some inactive drugs change to active drugs (eg. prodrug for morphine is codeine) *some active drugs made more active *some are not metabolized -Metabolism differs by individual, disease, genetics, and drug induced changes |
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Pharmacokinetics: Excretion
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4. Excretion – removal of drug from the body
-Kidney cannot eliminate lipid soluble drugs-must be metabolized first -Kidney primary organ of elimination -many fat-soluble drugs excreted by the bile duct of the liver and leave in the feces-biliary excretion |
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Routes of administration: oral
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slow and variable absorption, (depends on dissolution of dosage form, pH of stomach, presence of food/fluids, rate of GI activity and GI blood flow)
-oral absorbed in GI via hepatic portal system is shunted to liver and then the bloodstream -reduces bioavailability of drugs metabolized by liver (first pass effect) -oral route is only route with first pass effect -can cause local irritation (some drugs not absorbed by the gut) |
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Routes of administration: parenteral
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-No first pass
-Fastest and highest bioavailability -IV direct to blood stream(irreversible and most dangerous) -IM into a muscle with large blood flow (more painful than IV)-good route for drugs that are absorbed slowly over time -IT-intrathecal-into the space between the spinal cord and dura membranes |
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Routes of administration: Topical
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-application to a body surface; bypass first-pass
-eye and ear drops -Dermal:lotions, ointments on skin, slow absorption, low levels of bioavailability -sublingual: rapid absorption -Inhalation -rectal -patches |
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2. Distribution: Volume of distribution
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where the drug can be distributed
-highly water soluble or highly protein bound=low Vd so there is a high blood concentration -highly fat soluble and not protein bound=High Vd so low blood concentration |
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3. Metabolism: Hepatic microsomal enzyme system (P450 system)
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A group of 12 enzyme families
-three of these "families" metabolize drugs *CYP1, CYP2, CYP3 -95% of drugs are metabolized by CYP2 and CYP3 -the other 9 families metabolize endogenous substances (hormones, fatty acids, etc.) |
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3. Metabolism: Phase 1
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-uses P450 system a microsomal enzyme system that makes drugs water soluble so that can be excreted
Drugs can either be: -enzyme inducers -enzyme inhibitors -not involve enzyme system at all -compete with another drug in the enzyme system |
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Enzyme inducers
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increase the metabolism of itself and other drugs, accelerate drug clearance and lower drug level
-may need larger doses to get same effect -inducers may increase the metabolism of some hormones |
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Enzyme inhibitors
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decrease the metabolism of drugs, lower drug clearance and increase drug level.
-usually seen when two or more compete for same enzymes -may need smaller dose to avoid adverse/toxic reaction |
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3. Metabolism: Phase 2
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Drugs go directly to kidneys for excretion after phase 1 and skip phase 2 or be made more water soluble by "conjugation" in phase 2
-some drugs may go directly to phase 2 and then phase 1 |
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3. Metabolism: end result
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-increased drug excretion
-drug inactivation -increased therapeutic action -activation of prodrugs -increased /decreased toxicity |
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Enterohepatic circulation
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bile excreted drugs may be re-absorbed in the bloodstream again and to the liver and out thru the bile duct again
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Pharmacokinetic variables: elimination half-life
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time it takes to reduce the initial plasma concentration by one-half
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steady state:
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amount eliminated=rate of administration
or what is in you=to what your excreting -seen after four or five doses |
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Pharmacokinetic variables: drug effect variables: onset of action
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amount of time until drug produces therapeutic effects
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Pharmacokinetic variables: drug effect variables: peak effect
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time at which drug produces maximum effect (max concentration at target tissue)
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Pharmacokinetic variables: drug effect variables: duration of action
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length of time that drug produces therapeutic effects
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Pharmacodynamics
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The study of the mechanisms of drug actions in the body (what the drug does to the body) The goal is a therapeutic effect.
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Ways drugs produce a therapeutic effect:
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-receptor interaction
-interactins with enzymes involved in metabolic processes -nonspecific interaction (inhibit cell wall) |
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Receptor interactions:
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Drug molecule joins with a reactive site on the surface of the cell or tissue. Proteins embedded in plasma membranes of cells with specific recognition for the drug molecule.
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Classification of drug receptors: agonists
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binds to receptor and there is a response.
-full: produces 100% of the maximum possible response -partial: produces less than 100% of the maximum response no matter how high the concentration. |
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Classification of drug receptors: antagonists
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bind to the receptor and there is no response
-competitive antagonist: drug a and drug b compete for same receptor site. If drug b (antagonist) wins then the action of drug a is inhibited. (reversible by increasing agonist) -non-competitive antagonist combines with different parts of the receptor and prevents the action of another drug. (not reversible) -enzyme interaction: Drug interacts with the body's enzymes and inhibits the action of a specific enzyme -nonspecific interaction: drug acts on nonspecific sites with general effects on a wide variety of tissues. (disruption of cell membrane) |
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Monitoring-Factors: therapeutic index
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LD50/ED50 (ratio of benefit and toxic effect)
-greater the TI the safer the drug -narrower the TI the more dangerous the drug ED50: median effective therapeutic dose LD50: dose which leads to death in 50% of patients |
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Monitoring Factor:Serum Drug concentrations
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-Reflects dose, absorption, half-life, rate of metabolism, and excretion
steady state: amount eliminated minimum effective concentration (MEC) onset duration toxic level (peak/trough) |
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Monitoring Factor: Peal and trough Levels
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Peak: time it eakes to reasch maximun drug level through absorption (may take several doses)
Trough: determines minimum plasma concentrations; draw immediately prior to next IV dose being given |
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Loading dose:
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dose of a drug needed to rapidly raise the plasma concentration of a drug
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Monitoring Factor: Patient condition/factors
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-liver and kidney function
-age -gender -ethnicity -weight |
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Monitoring Factor: Tolerance and dependence
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tolerance: decreased response to repetitive drug dose
dependence: physiologic or psychologic need for a drug |
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Pregnancy:
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-first trimester presents greatest danger
-maternal factors (kidney and liver function) may cause more of the drug to cross placenta -breast feeding-may cross into breast milk (concentration is less) |
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Pregnancy safety categories:
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Category A: no risk to fetus
Category B: no risk to animal fetus (info on humans not available) Category C: Adverse effects to animal fetus (info on humans not available) Category D: Possible risk to human fetus; must weigh the risk-benefit Category X: Fetal abnormalities reported (should not use in pregnancy) |
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Pediatric/neonate population
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-75% of drugs have not been approved for pediatric population
-Absorption is immature until 3 years, slowed gastric emptying, reduced first pass due to immature liver -Distribution: total body water content varies with age but greater than an adult, protein binding decreased due to decreased protein production of liver -Metabolism: liver enzymes decreased, older kids have increased metabolism -Excretion: immature kidneys |
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Geriatric:
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-Absorption: decreased production of HCl, perstalsis, gastric blood flow decreased, decreased absorptive properties, laxative use common,decreased cardiac output.
-Distribution: TBW decreased, protein production by liver decreased, decreased cardiac output. -Metabolism: decreased numbers of liver enzymes, blood flow to liver decreased -Excretion: number of nephrons decreased, GFR decreased (give lower doses of meds) -polypharmacy: more than on drug at a time (increased risk of drug interaction) |
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Effects on drug therapy:
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-Beliefs affect compliance
-Diet (high fat affects absorption of some drugs) -Genetic makeup - |
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Hormone
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a substance formed by a tissue in the body and carried in the bloodstream to elicit a response in another part of the body.
-lipid soluble (cholesterol based) -water soluble (protein based) -uses: replacement (gland not producing hormone), pharmacologic (give for purpose other than replacement), diagnostic (looking for specific response) |
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Organs that release hormones:
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-pituitary
-thyroid -adrenals -parathyroids -gonads -pancreatic islet cells |
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Pituitary Gland
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Hypothalamus:releasing hormones and inhibiting factors
Anterior pituitary gland or "master gland": negative feedback, anterior hormones, posterior pituitary gland (storage only) |
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Anterior Pituitary Gland Hormones: Growth hormone (GH)
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-promotes growth of tissue -somatropin and somatrem: treatment of dwarfism, AIDS wasting, not approved as an antiaging drug
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Anterior Pituitary Gland Hormones: Growth Hormone Inhibitor
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-octreotide (somatostatin): synthetic GH release inhibitor
-treatment of GH excess: *acromegaly: excessive GH after growth plates closed *giantism: excess growth hormone before growth plates close -diarrhea secondary to vasoactive tumors (most commonly used for) |
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Anterior Pituitary Gland Hormones: luetenizing hormone
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-ovulation and spermatogenesis
-infertility certain drugs are given to stimulate LH release. |
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Anterior Pituitary Gland Hormones: Follicle stimulating horomone
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infertility treatment along with LH-stimulates growth of ovarian follicle and spermatogenesis
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Anterior Pituitary Gland Hormones: Prolactin
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-responsible for milk production in nursing mothers
-no replacement drug |
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Anterior Pituitary Gland Hormones: Adrenocorticotropic Hormone (ACTH)
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-tells adrenal gland to make cortisol and cortisone
-limited therapeutic use; mainly diagnostic |
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Anterior Pituitary Gland Hormones: Thyroid stimulating hormone
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Diagnostic
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Posterior Pituitary Hormones: Vasopressin (ADH)
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-release prevents loss of water from kidneys
-treatment of diabetes insipidis -unlabeled use in bed wetting -acute GI hemorrhage |
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Posterior Pituitary Hormones: Oxytocin (Pitocin)
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-only used to induce labor
-level increases at term and labor starts -Tocolytic: drug that inhibits contractions |
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Thyroid Hormones:
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T3, T4 (regulates body metabolism)
-T3: physiologically active -T4: physiologically inactive -levothyroxine (synthroid): T4 -Liothyronine (Cytomel): T3 -Both used to treat hyporthyroidism |
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Antithyroid agents: Thioamides
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propylthiouracil (PTU): used most often
-methimazole: not used often -both used to treat hyperthyroidism -blocks synthesis of thyroid hormone by thyroid |
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Antithyroid agents: strong iodine solution
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used short term treatment of hyperthyroidism
-blocks the release of thyroid hormone temporarily -use pre-op to take out thyroid (prevents hemmorhaging) |
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Adrenal gland hormones: corticosteroids
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hormones produced by the adrenal cortex: "sugar", "water", "sex"
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Corticosteroids: glucocorticoids
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-cortisol and cortisone: "sugar"
-CHO, Protein, and lipid metabolism -inflammatory and immune response -nerve excitability -bone formation and growth -maintains viscosity of gastric mucous -use: replacement (addisons disease), allergic reactions, dermatologic conditions, inlammatory diseases, cerebral edema, suppression of immune response -side effects: cushingoid features, elevated BP, bone demineralization, suceptibility to infection, poor healing, thin an easily bruised skin. |
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Adrenal gland hormones: Mineralocorticoids
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-Aldosterone
-sodium retention and potassium excretion -use: replacement and idiopathic hypotension -SE: hypernatremia, hypokalemia -Fludrocortisone (Florinef) The drug given |
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Calcium regulating Hormones: Parathyroid Hormone
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-Released when Ca+ levels drop and acts on bone, gut, kidneys to increase calcium level; only used diagnostically for:
*chronic hypocalcemia (treated with oral calcium salts and Vit. D) *Acute hypocalcemia (treated with IV calcium gluconate) *Recombinant DNA version of PTH increases bone building cells |
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Calcium regulating Hormones: Calcitonin
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-made in specialized cells of thyroid gland
-acts opposite parathyroid hormone to regulate serum Ca+ levels. (ie. lowers Ca+ levels and prevents lose from bones) -Calcitonin used in the reatment of hypercalcemia, osteoporosis Paget's disease |
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Calcium regulating Hormones: Bisphosphonates
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-NOT HORMONES
-bind to bone and prevent bone resorption -poorly absorbed from GI and must be taken on empty stomach with full glass H2O -Main use is in treatment/management of osteoporosis -long term use linked to hip fractures (+4) |
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Womens health agents: Estrogen
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-secreted by the ovaries
-natural and synthetic forms -necessary for development and maintenance of female reproductive system and development of secondary sex characteristics -elevated at delivery to prevent hemorrhage -Prevents postmenopausal bone loss -uses: contraception, uterine bleeding, dysmenorrhea, delayed sexual development, prevention of osteoporosis, symptoms of menopause, treatment of prostate cancer. -SE: most serious is thromboembolism, fluid retention, nausea, hypertension, sore breats -Prototype: conjugated estrogen (Premarin) -Does not prevent CVD in postmenopausal, increases risk of uterine and ovarian cancer if used alone, increases risk of certain types of breast cancer, increased risk of MI, stroke, PE, DVT |
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Womens health agents: Progestins (progesterone)
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-secreted by the ovaries and placenta
-available as natural and synthetic -readies uterus for implantation and nourishment of fertilized ovum, maintains pregnancy if ovum fertilized; suppresses uterine contractions -uses: contraception with estrogen, prevent miscarriage, brest and endometrial cancer, hormone replacement therapy, endometriosis, treatment of endometrial caner. -SE: nausea, edema, wt gain, insomnia, blood clots -Prototype: medroxyprogesterone (provera) |
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Womens health agents: Selective Estrogen Receptos Modulators (SERM's)
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-act as estrogen receptor agonsts on estrogen receptors located on bones and simultaneously block estrogen receptors on breasts.
-use: breast cancer treatment and osteoporosis -SE: blood clots, leg cramps, hot flashes |
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Donoprostone
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-Cervidil
-prostaglandin to induce abortion (RU-486-progesterone antagonist to induce abortion) |
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Womens health agents: Birth Control Pills (BCP)
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-Act by inhibiting ovulation (negative feedback mechanism)
-Combination of estrogen and progesterone or only progesterone -numerous adverse effects: thromboembolism, hypertension, cancers, teratogenic |
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Men's Health Agents: Androgens
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-Testosterone
-produced by testes -androgenic effects: growth and development of primary and secondary male sex charcteristics; spermatogenesis -anabolic effects: growth of bone and muscle tissue; stimulate production of red blood cells (RBCs) -uses: delayed puberty in male, anemias, sexual dysfunction, infertility, breast and uterine cancer in females, endometriosis -SE: acne, gynecomastia, virilization, water retention, mood swings, aggression, liver disorders, increased RBC production, testicular atrophy-sterility |
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Men's Health Agents: Androgen inhibitors
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-used in treatment of BPH, some used in prostate cancer
-androgen receptor blockers -gonadotropin releasing hormone analogs -alpha 1 adrengeric blockers are also used in BPH (not hormones) Work by relaxing the prostate capsule. |
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Insulin and oral hypoglycemic agents: Type 1 and 2 diabetes
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-both result in hyperglycemia
-significantly different in onset, course, treatment and pathology -type 1 ALWAYS treated with insulin; type 2 may or may not be treated with insulin |
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Insulin
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-must be given sub q
-increases glucose transport to liver, heart, skeletal muscle, adipose tissue; must be present for muscle and fat tissue to utilize glucose for energy; provides glucose for cellular energy -storage of fat in fat cells (lipid levels increase if insulin not available) -lack of insulin results in protein depletion; protein used for energy |
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Insulin types
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-immediate (onset within 15 miniutes)
*onset: immediate *peak: 1.5 hrs *duration: 3-4 hours -short acting or regular insulin *onset: .5-1 hr *peak:2-3 hrs *duration: 3-6 hrs -intermediate of "NPH" insulin *onset: 1-1.5 hrs *peak: 4-10 hrs *duration: 10-16 hrs -long-acting *onset:1-2 hrs *no peak *24 hr. duration (HS administration) -insulin mixtures: 70/30 (70% NPH, 30% regular); 50/50 (50% NPH, 50% regualr) |
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Type 2 diabetes: sulfonylureas
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increase secretion of insulin, decrease liver glucogenolysis, increase sensitivity to insulin
-may see hypoglycemic SE |
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Type 2 Diabetes: meglitinides
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a nonsulfonylurea that stimulates pancreas to produce more insulin
-may see hypoglycemic SE -need to eat within 30 minutes of taking |
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Type 2 Diabetes: biguanide
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decreases hepatic glucose production and increases use of glucose by muscle and fat cells
-no hypoglycemic SE -may see lactic acidosis and has GI SE -must be off for a period of time before dye studies -not recommended for people with kidney, liver, disease, heavy alcohol use, over 80. |
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Type 2 Diabetes: alpha-glucosidase inhibitors
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-block alpha glucosidase in gut thereby delaying glucose absorption
-causes severe gas -take with first bite of food |
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Type 2 diabetes: thiazolidinediones
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-"glitazones"
-TZD's (insulin sensitizers) -decrease insulin resistance by action on receptor cells of muscles and fat cells -associated with weight gain and fluid retention -takes 4-6 weeks to see effect on glucose |
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Newer Drugs for diabetes
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-Amylinomimetic or amylin analogue: that slows gastric empyting; and suppresses appetite; suppresses postpriandial hepatic glucose production. It is released at same time as insulin. For postmeal glucose control.
-Incretin mimetic/GLP- 1 analogue: hormone of the gut that regulates release of insulin in response to fluctuations in blood sugar. Signals pancreas to make right amount of insulin to lower blood sugar; when normal level reached, signals pancreas to stop insulin release -DPP-4 inhibitors: enzyme that deactivates GLP-1 (an incretin that slows gastric emptying and stimulates that production of insulin in response to eating) |
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Glucose elevating hormone
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-Glucagon
-half-life of 3-10 minutes -IM, IV, Subq |
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Central Nervous system
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-Spinal cord and brain
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Peripheral Nervous System
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-Afferent fibers carry sensory information to the brain
-Efferent fibers carry information form CNS *Somatic-innervates voluntary or skeletal muscle contractions *Autonomic-innervates involuntary smooth muscle, cardiac, glands -sympathetic branch -parasympathetic branch |
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Neurotransmitters:
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Chemical substances that transmit nerve signals or impulses from one neuron to another
-excitatory neurotransmitters: stimulate neurons -inhibitory neurotransmitters: inhibit the neuron |
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Autonomic Nervous System Drugs
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-Sympathomimetic or adrenergic
*direct -acting *indirect-acting -sympatholytic or adrenergic blocking *block alpha or beta receptors, deplete stores of norepinephrine or inhibit sympathetic activity by direct action on CNS -parasympathomimetic or cholinergic *direct acting *indirect acting -parasympatholytic or anticholinergic (block receptors at NM junction or ganglia) *specific *non-specific |
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Sympathetic Nervous System (adrenergic)
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-promotes self-preservation: "fight-or-flight"
-norepinephrine, epinephrine are neurotransmitters |
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Parasympathetic Nervous System (cholinergic)
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-acts opposite SNS-"rest and digest"
-acts to conserve energy -neurotransmitter is acetylcholine -acetylcholine receptors are muscarinic and nicotinic |
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Cholinergics, cholinergic agonists, parasympathomimetics, cholinergic agents, muscarinics, nicotinics:
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Drugs that stimulate receptors of the parasympathetic nervous system.
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Types of cholinergic receptors: Nicotinic
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stimulated by nicotine and acetylcholine
-nicotinic N-located on cell bodies and postganglionic neurons of sym. and para. and adrenal medulla -nicotinic M-located mainly on skeletal muscle (skeletal contraction) -nicotinic CNS-brain and spinal cord |
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Types of cholinergic receptors: muscarinic
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stimulated by muscarinic and acetylcholine
-located postsynaptically on cells in smooth and cardiac muscle |
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Action of Cholinergic agonists: Direct
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directly: bind directly to cholinergic receptor and activate them.
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Action of Cholinergic agonists
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Indirectly: make more acetylcholine available at receptor site by inhibiting acetylcholinesterase
-reversible inhibitors -irreversible inhibitors |
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Muscarinic drug effect
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-same as PSNS stimulation
-rest and digest -SLUDGEM: salivation, lacrimation, urinary incontinence, diarrhea, gastrointestingal cramps, emesis, and miosis -decreased heart rate, vasodilation, bronchoconstriction |
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Use of Direct acting cholinergics:
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-poorly absorbed orally
-relaxes bladder and GI -used for dry mouth (xerostomia) -topical eye drops for glaucoma |
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Use of Indirect Cholinergics:
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-treatment of Myasthenia Gravis
-Reversal of NM blockade -Alzheimer's Disease: increased ACh in brain preserves memory and learning |
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Overdose management of cholinergics
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-rarely seen with topical administration
-Atropine is antidote (anticholinergic) |
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Irreversible Cholinesterase Inhibitors (TOXINS): organophosphate agents
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-used in pesticides and nerve gas to irreversibly block acetylcholinesterase activity
-common in rural areas -Antidote is Atropine -similar symptoms of excess muscarinis and nicotinis stimulation |
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Cholinergic Antagonists
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Drugs that block or inhibit the action of ACh at the muscarinic receptors in the PSNS
-cholinergic blockers -anticholinergics -antimuscarinic -muscarinic antagonists -parasympatholytics Block the PSNS allowing the SNS to predominate. Have many of the same effects as the adrenergics one of the oldest groups of drugs Atropine is prototype may be natrually derived from belladonna plant readily crosses the blood brain barrier Action is opposite cholinergics |
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Anticholinergic overdose effects
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-Hot as a hare
-mad as a hatter (confusion) -red as a beet (flushed face) -dry as a bone (decreased secretions) -blind as a bat (pupil dilation) |
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Pharmacologic effects
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-eyes dilate
-slows GI motility and decreases secrections and salivation -low doses slow heart rate and large doses increase heart rate -decreased bladder contraction -broncho dilation |
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Therapeutic uses of anticholinergics:
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-Ocular uses: mydriasis, cycloplegia, inflammation, adhesions (with miotics to break)
-Cardiovascular: treatment of bradycardia -Respiratory uses: acute rhinitis, COPD, chronic bronchitis, emphysema -GI: IBS as an antispasmodic -Bladder: Overactive bladder, incontinence -CNS: Parkinsons disease(restor balance btw dopamine and Ach in brain to decrease tremor), motion sickness (reduces neurotransmission from vestibular apparatus to brain |
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Teaching for anticholinergics:
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-chew gum for dry mouth
-caution driving (blurred vision) -dark glasses if light sensitivity -check before using OTC -watch for heat strok |
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Action of Nicotine
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-stimulates all sns and psns ganglia in the ans
-has adrenergic and cholinergic effects |
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Adrenergic Agonists (alpha adrenergics, beta adrenergics, sympathomimetics)
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Large group of synthetic and natural occuring drugs
-catecholamines (natural is norepinephring and synthetic is dobutamine) -noncatecholamines (phedrine) -stimulate the SNS-fight or flight -increased heart rate -bronchial dilation -pupil dilation -mobilizes stored energy |
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Catecholamines
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-Cannont cross BBB
-cannot take by mouth (destroyed by MOA and COMT); must be IV -brief duration |
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Noncatecholamines
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-cross BBB
-can be taken orally; longer half-life |
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Neurotransmitters of SNS
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-epinephrine-released by medulla
-norepinephrine-released by postganglionic neurons of SNS -dopamine |
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SNS receptors:
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-alpha
-beta -domaminergic |
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Effects of adrenergic agonists:
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-depend on selectivity for alpha or beta receptors and whether it is a catecholamine or a noncatecholamine
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Therapeutic uses of adrenergics
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depends on selectivity for alpha or beta receptors
-asthma -preterm labor -allergies -pupil dilation -vasopressor effect (shock) |
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Adrenergic receptors: alpha 1
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-located blood vessels, eyes, bladder, prostate capsule
-uses: vasoconstriction |
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Adrenergic receptors: alpha 2
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located on the end of the nerve itself
-uses: stimulation INHIBITS NE release |
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Adrenergic receptors: beta 1
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heart mainly
-use: increases heart rate, contractility, and conduction through AV node |
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Adrenergic receptors: Beta 2
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lungs uterus, liver
use: bronchial dilation, uterine relaxation, gluconeogenesis |
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+/- chronotropic
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increases/decreases heart rate
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+/- inotropic
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decrease or increase force of contraction
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Nonselective adrenegics
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-prototype: epinephrine (a catecholamine)
-stimulates all receptors so wide range of use -SE: increased pulse, elevated BP, palpitations, vision changes, hyperglycemia, tremor (in high doses) -epinephrine is available over the counter |
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Selective adrenergic agonists: alpha 1
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-prototype: phenylephrine
-use: vasoconstriction for eye procedures, shock, allergies -SE: hypertension, bradycardia, H/A, restlessness, insomnia -contraindications: hypertension, history of stroke, glaucoma |
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Selective adrenergic agonists: alpha 2
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-prototype is clonidine
-use: management of hypertension -SE: drowsiness, rebound hypertension if suddenly withdrawn |
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Nonselective Beta Agonist:
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-adrenergic agonists with affinity for beta receptors
-first choice is ALWAYS selective agent -prototype is isoproterenol -use: CHF, shock, asthma -Effects: increase heart rate, palpitations, H/A, dizziness, bronchodilation, sweating ,elevated blood sugar |
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Selective adrenergic agonist: beta 1
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-in heart mainly
-increased heart rate, contractility, and conduction through AV node -prototype: dobutamine -use: shock, CHF, cardiac arrest -SE: dysrhythmia, tachycardia, chest pain |
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Selective adrenergic agonist: beta 2
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-use: asthma, bronchitis, uterine relaxation for preterm labor.
-SE: hyperglycemia, tremor -Most life threatening ar seizure and arrhymias and stroke -overdose: give adrenergic blocking agent |
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Adrenergic antagonists
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drugs that block adrenergic receptors thereby blocking stimulations of SNS
-sympatholytics, alpha blockers, beta blockers |
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Use of Alpha blockers:
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-hypertension; causes vasodilation and decreased BP
-Raynaud's disease and frostbite -migraines -BPH: relaxes prostate |
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Alpha blockers:
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-never alpha 2 blockers: dont need to increase noepinephrine
-Prototype: prazosin -SE: orthostatic hypertension, nasal congestion, tachycardia, incontinence |
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Beta Blockers: Nonselective
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-prototype: propanolol
-induce asthma attack -some nonselective beta blockers also block alpha |
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Beta Blockers: Beta 1
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-no beta 2 blockers: never want to stop breathing
-large doses of beta 1 blockers can cause beta 2 blockage -Prototype: metoprolol -SE: bradycardia, lethargy, CHF, depression, hypotension |
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Uses of beta blockers:
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-angina pectoris (chestpain): increases "rest time" of the heart to get more O2
-hypertension -dysrhythmias: slows conduction through heart -MI, heart failure: inhibits effects of catecholamines (blocks increase heart rate and contractile force) -glaucoma -hyperthyroidism and stage fright -should not be stopped abruptly and may maske signs of hypoglycemia -ALWAYS check heart rate and BP prior |
