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Pharmacology 110
Chapters 1-7
Question | Answer |
---|---|
Pharmacology | the study of drugs |
Pharmacogenetics | study of genetically determined variations in responses to drugs |
Pharmacokinetics | study of how a drug enters, circulates and leaves the body |
Pharmacy | act of preparing and dispensing drugs |
Toxicology | study of the harmful effects of drugs on living tissues |
Types of Drug Names: | Chemical, Generic, Brand/Trade |
Food and Drug Administration (FDA) | Insures the public that drugs are safe and effective |
Federal Trade Commission (FTC) | functions to regulate trade practices of drug companies and false advertising of nonprescription drugs, foods, & cosmetics |
Drug Enforcement Administration (DEA) | Administers the Controlled Substance Act of 1970 and regulates the manufacture and distribution of substances with potential for abuse |
Omnibus Budget Reconciliation Act (OBRA) | 1990 Mandates: In 1993, pharmacists consul and review drug history with patients about their prescriptions |
Drug | any chemical substance that affects biological systems (living organisms) |
Sources of Drugs | Plant, Animal, Minerals, Synthetic |
Potency | related to the amount of the drug needed to produce effect |
ED50 | dose of drug that produces effect in 50% of subjects |
LD50 | median lethal dose, one half of subjects die |
Efficacy | related to the maximum effect of drug-regardless of dose |
Drugs interact at the _______ level | cellular |
Chemical signaling between cells releases what? | neurotransmitters, local substances, and hormone secretions |
What must the drug bind with to produce pharmacolgic effect? | receptor |
Drug receptors | macromolecular chemical structures involved in transport processes, metabolic and regulatory pathways |
What happens when a drug combines with a receptor | a chemical mechanism of action occurs and it alters the function of the organism |
Agonist | drug has affinity and combines with receptor - produces an effect |
Antagonist | counteracts the action of an agonist - produces no effect |
Which route of administration has the most rapid drug response | Intravenous Route IV |
List the different routes of administration | IV, IM, Subcutaneous, and Oral administration |
Enteral Route | drug goes through the GI tract |
Parenteral | bypass the digestive system - GI tract |
What are two examples of Enteral Route | Oral and Rectal |
What are three examples of Parenteral Route | Injection, Inhalation, and Topical |
What are two advantages of Oral Route | Safest, and least expensive |
What are two disadvantages of Oral Route | slow onset of action, and less predictable |
What are two advantages of Rectal Route | use for the unconscious or vomiting patient, use for systemic (antivomiting) effect |
What are two disadvantages of Rectal Route | poor and irregular absorption, and poor patient acceptance |
What are two advantages of Parenteral IV Route | rapid drug response, more predictable response |
What are two disadvantages of Parenteral IV Route | irretrievability of drug, local irritation - phlebitis |
What are two advantages of IM Route | irritating drugs better tolerated in skeletal muscles, and provides a sustained effect |
What is a disadvantage of IM Route | uncomfortable injection (usually in deltoid or gluteus) |
What are two advantages of Inhalation Route | rapid onset and absorption, no needles |
What are two disadvantages of inhalation route | limited to substances that can be introduced into trachea, nausea may occur |
What are two advantages of topical route | used for local or systemic effects |
What are two disadvantages of topical route | local irritation, edema |
Is the dental hygienist allowed to administer IV or IM drugs | no |
What factors influence the rate of absorption | physicochemical, site of absorption, and drug's solubility |
lipid solubility | lipid soluble (non-ionized) compounds readily pass through membranes |
If infection is present (high acidity) & local anesthetic is used there is _________ penetration of the membrane and ______________ action of the anesthetic | deceased; decreased |
List the steps involved in Oral Absorption | 1. Disruption 2. Disintegration 3. Dispersion 4. Dissolution |
Drug Half-Life (T1/2) | time for the concentration of drug to fall to one half of its blood level. The longer the half life, the slower its removed from the body and the longer the action of the drug |
Metabolism (Biotransformation) | the body's process of changing drug so it can be excreted by the kidneys |
Hepatic microsomal enzymes | enzymes responsible for metabolism of drugs |
Metabolite | compound that is produced when a drug is metabolized |
What is the most important means of excretion | the kidneys |
Distribution | the passage of drugs into various body fluid compartments |
Therapeutic Effect | all desirable actions of a drug |
Adverse Effect | all undesirable reactions of a drug |
Toxic Reaction | extension of pharmacologic effect; amount of desired effect is excessive (poisoning) - dose related |
Side Effect | dose related reaction, not part of desired therapeutic outcome |
Idiosyncratic reaction | genetically related abnormal drug response certain populations mores susceptible to adverse reactions |
Drug Allergy | an unusual or exaggerated reaction of the body, such as a rash, that is not predictable or dose related |
Drugs (reduce/increase) the body's ability to fight infection | reduce |
Teratogenic Effect | congenital abnormalities |
Local Effect | local tissue irritation caused by injectable, topical or oral drugs |
Drug Interactions | effect of one drug is altered by another drug |
Hypersensitivity (Allergic Reaction) | individuals immune system responds to drug |
anaphylactic shock | respiratory symptoms, skin rash |
anaphylaxis | acute, life-threatening (lowers BP, respiratory depression and heart irregularities) |
Therapeutic Index | a measurement used for evaluation of drug safety |
the larger/wider the TI, the ________ the drug | safer |
What are the evaluation of drugs for toxicity based on | experiments in animals and clinical trials in humans |
What does the Central Nervous System consist of | the spinal cord and brain |
What does the Peripheral Nervous System consist of | the spinal and cranial nerves, includes the autonomic nervous system |
What does the Autonomic Nervous System do | it regulates BP, heart rate, GI tract mobility, salivary glands secretions, and bronchial smooth muscle |
What does the Autonomic Nervous System rely on to initiate responses | neurotransmitters and receptors |
The SANS is involved in what type of responses | fight or flight |
What responses are included in the SANS | heart rate increase, skin cold and clammy, stomach feels in a "knot", mouth is dry |
What chemical is released to help the heart beat faster, and allow more O2 to muscles to meet stressful situations | adrenaline/epinephrine |
What type of response is the Parasympathetic autonomic nervous system (PANS) involved in | rest or digest |
What responses does the PANS have | responses opposite the SANS, heart rate and respiration decrease, increase of blood to digestive system, stimulation of secretion of salivary glands |
What do the PANS and SANS have in common | both contain sensory and motor nerves |
Mydriasis | dilation of the pupil |
Myosis | constriction of the pupil |
What are neurotransmitters | chemicals released to send messages between nerve-nerve, or nerve-tissue |
What are neurotransmitters released in response to | nerve action (drug agents) to react with receptor (a membrane component) |
Interaction of neurotransmitter and receptor occurs by | enzyme and metabolic processes |
drugs can alter the events associated with the | neurotransmitters |
What are the drug groups in the PANS | cholinergic agents and anticholinergic agents |
Cholinergic agents | act at location where acetylcholine is neurotransmitter |
Anticholinergic agents | cholinergic blocking agents; blocks action acetylcholine |
What are the drug groups in the SANS | adrenergic agents, and adrenergic blocking agents |
Adrenergic agents | act at location where norepinephrine is neurotransmitter |
Adrenergic blocking agents | sympathetic blocking agents |
What is the major neurotransmitter of the PANS | acetylcholine |
Cholinergic Direct Agents | act on receptor; acetylcholine and choline derivatives, pilocarpine |
Cholinergic Indirect Agents | cholinesterase inhibitors, physotigmine |
cholinesterase inhibitors | acts by inhibiting enzyme, "cholinesterase" and allow the build up of acetylcholine |
Physostigmine | used to treat drug overdose |
Pharmacologic affects of cholinergic agents | Cardiovascular: decrease in cardiac output, GI: increase secretion activity, and Effects on the eye: myosis |
Anticholinergic agents | prevent the action of acetylcholine by blocking the receptor site, block the action of acetylcholine on smooth muscle, glandular tissues and the heart, and antimuscarinic agent (block muscarinic receptors) |
Pharmacologic effects of anticholinergic agents | CNS: depression/stimulation, Exocrine glands: reduce secretion (saliva, respir, GI, urinary), Smooth muscle: relaxes, bronchial dilation, Eye: dilates pupils, Cardio: produces tachycardia |
Uses for cholinergic direct agents, acetylcholine, and choline derivatives | urinary retention, and myasthenia gravis (muscle weakness) |
uses for cholinergic direct agent pilocarpine | glaucoma, and xerostomia |
uses for cholinergic indirect agents cholinesterase inhibitors | glaucoma, and myashenia gravis (muscle weakness) |
uses for cholinergic indirect agents physostigmine | to treat drug overdose (especially for anticholinergic agents-atropine) |
Uses for anticholinergic agents | preoperative medication, treatment of repiratory and GI disorders, opthalmologic examination, reduction of parkinson-like movements, motion sickness and OTC sleep aids, Dentistry: reduce saliva |
Anticholinergic agent adverse reactions | xerostomia, blurred vision, sensitive to light (photophobia), fever, tachycardia, urinary and GI stagnation |
Contraindications of anticholinergic agents | Glaucoma, Prostatic hypertrophy, intestinal or urinary obstruction, cardiovascular disease |
What is the major neurotransmitter of the SANS | epinephrine, and norepinephrine |
Where is epinephrine released from | the adrenal medulla (kidney) |
Norepinephrine is | the major substance released at nerve endings |
What are the Sympathetic Nervous system receptors | alpha, & beta receptors |
alpha receptors are located | in skin and skeletal muscles |
stimulation of alpha receptors results in | smooth muscle excitation/contraction |
What is the primary site of alpha receptors | arteries, causes vasoconstriction |
What are the two types of beta receptors | B1 & B2 |
B1 beta receptors stimulate the | heart muscle, increase rate & strength, stimulates glycogen formation |
B2 beta receptors | relaxes smooth muscle (affects lungs), vasodilation and bronchodilation |
B-adrenergic blocking agents | agents that block Beta receptors |
Adrenergic Agents Pharmacologic effects | CNS, Cardio, Eye:mydriasis, Respiratory: relax of muscle, Increase metabolism, Reduce flow of saliva |
What are some precautions with epinephrine in local anesthetics | patients with angina, hypertension, hyperthyroidism, could cause tachycardia |
Hypertension untreated produces | no symptoms, termed "silent killer" |
Why are adrenergic agents used in dentistry regarding vasoconstriction | 1. it is added to local anesthetics for prolonged effect 2. it is used to control bleeding by producing hemostasis |
How are adrenergic agents used in dentistry regarding cardiac effects | for the treatment of shock and cardiac arrest |
How are adrenergic agents used in dentistry regarding bronchodilation | they are used to treat asthma, emphysema and for the treatment of anahylaxis |
How are adrenergic agents used in dentistry regarding CNS stimulation | they are used for diet control - amphetimine-like agents, because they cause an increase in metabolic rate; ADHD/ADD |
What are the four uses of Adrenergic agents in dentistry | Vasoconstriction, Cardiac effects, Bronchodilation, and CNS stimulation |
What are the 6 names of adrenergic agents | Epinephrine (Adrenaline), Dopamin (Intropin), Phenylephrine (Neo-Synephrine), Levondordefrin (Neo-Cobefrin), Isoproterenol (Isuprel), Amphetamine |
What properties does Epi have | a & B stimulating properties |
What is Epinephrine (adrenaline) used for | asthmatic attacks, anaphylaxis, it is put in local anesthetics to delay absorption, and reduce systemic reactions |
What is Dopamine (Intropin) used for | it is used in the treatment of shock |
What is Phenylephrine (Neo-Synephrine) used for | used in nose sprays for the constriction of vessels to reduce swelling of membranes |
What is Levonordefrin (Neo-Cobefrin) used for | it is used as a vasoconstrictor in local anesthetics |
What is Isoproterenol (Isuprel) used for | it has been used in the past for asthma |
What adrenergic agent is currently being used to treat asthma | albuterol (Proventil, Ventolin) |
What is Amphetamine and amphetamine-like drugs used for | for CNS excitation and alertness |
What adrenergic agent is used to treat attention deficit disorders | Ritalin, Dexedrine |
a-adrenergic blocking agents | inhibit vasoconstricting effects decrease blood pressure |
B-adrenergic blocking agents | generic names end in -olol; produce bradycardia and bronchoconstriction |
Nonselective propranolol (Inderal) | depresses the heart (bradycardia) used for arrythmias, angina, hypertension, migraines |
Selective Tenormin | more activity on heart and blood vessels (B1 receptors) (bradycardia) few side effects because it is selective, less drug interactions |
Why should you use caution when using epinephrine with local anesthesia | variations in blood pressure or epinephrine reversal (lowering of BP, rather than increase) |
Epinephrine reversal results from | patients pretreated with alpha blocking agents then given epinephrine |
What are 5 uses of adrenergic blocking agents | Hypertension: decrease BP, Peripheral vascular disease, Treatment of benign prostatic hypertrophy, Cardiac effects, Produces or causes bronchoconstriction |
Where are Adrenergic receptors found | in most tissues of the body |
What are the types of adrenergic receptors | alpha & Beta |
What does the stimulation of alpha adrenergic receptors cause | vasoconstriction of smooth muscle, results in increase BP |
What does the stimulation of Beta adrenergic receptors cause | cardiac stimulation, bronchodilation and vasodilation |
What does the stimulation of Beta 1 cause | cardiac stimulation, results in increase heart rate and strength of contractions |
What does the stimulation of Beta 2 cause | bronchodilation of the lungs and vasodilation of vascular beds uterus |
Epinephrine is both a ________ & ________ agonist | alpha & Beta |
Epinephrine can produce these effects because it is both an alpha and a Beta agonist | it can increase BP, heart rate, and produce bronchodilation |
What are the two components of pain | Perception and Reaction |
Perception of pain | the physical component (remains constant) signal from the site of pain to the CNS |
Reaction of pain | psychological component of pain (variation) individuals vary greatly in their reaction to pain |
With what factors is pain threshold altered | age, gender, race, ethnic group, fatigue, fear |
Placebo Effect | giving a placebo; sometimes effective for pain control |
What are the Divisions of Analgesic Agents | Nonopioid (nonnarrcotic) and Opioid (narcotic) |
Nonopioids act at which site of action | peripheral nerve endings |
What is the mechanism of action of Nonopioids | inhibit prostaglandin synthesis |
Are Nonopioids addictive | NO |
Opioids act at which site of action | they act within the CNS |
What is the mechanism of action of Opioids | depress the CNS |
Categories of Nonopioids | Salicylates (Aspirin), Nonsteroidal Anti-inflammatory Drugs (NSAIDS), Acetaminophen (Tylenol) |
How do Salicylates (aspirin) effect pain | peripherally by inhibiting production of prostaglandins |
How do Salicylates inhibit production of prostaglandins | by inhibiting the enzyme cyclooxygenase |
What are the Effects (3 A's) of Salicylates | Analgesic, Antipyretic, and Anti-inflammatory |
Analgesic | reduces pain |
Antipyretic | reduces elevated body temperature (fever) |
Anti-inflammatory | reduces inflammation |
Anitplatelet | prevents clotting, helpful in prevention of mycardial infarction, used in suspected heart attacks |
How is Aspirin most effective in dentistry | for throbbing pain and inflammation |
How is Aspirin most effective in medicine | for pain and inflammation with arthritis |
Why should you never place Aspirin on oral mucosa | a painful ulceration occurs |
What are the adverse reactions of Aspirin | GI, Bleeding, Toxicity, Reye's Syndrome, Allergies |
How many days should the patient stop taking aspirin before a procedure | 2-3 days |
What is the name of the toxicity of aspririn, and what does it cause | salicyclism; brain damage |
Why should you not give children with chickenpox, or influenza aspirin | can cause Reye's syndrome which leads to brain damage |
If a patient is allergic to aspirin what other medications should be avoided | NSAIDS |
List the four medications that can interact with aspirin | Warfarin (coumadin), Probenecid, Sulfonhylureas, Methotrexate |
If a patient is currently taking aspirin, what will happen if they take Warfarin before a procedure | it will increase bleeding |
Does aspirin cause xerostomia | NO |
What is the regular dosage of aspirin | 1 aspirin = 325 mg (5 grain) child's dose or preventive adult dose |
What are the components of pain | Perception & Reaction |
Perception | the physical component (remains constant) signal from the site of pain to the CNS |
Reaction | psychological component of pain (variation) individuals vary greatly in their reaction to pain |
What factors alter the pain threshold | age, gender, race, ethnic group, fatigue, fear |
Nonopioid analgesic agents | are nonnarcotic, act at peripheral nerve endings (site of action), inhibit prostaglandin synthesis (mechanism of action) and are nonaddictive |
Which component triggers pain and inflammation | prostaglandins |
Opioid analgesic agents | narcotic, act within the CNS (site of action), depress the CNS (mechanism of action) addictive |
What do you think of when you hear Nonopioids | Salicylates (Aspirin), Nonsteroidal Anti-inflammatory drugs (NSAIDs), Acetaminophen (Tylenol) |
How do Salicylates (Aspirin) effect pain | peripherally |
What do Salicylates inhibit | production of prostaglandins |
What does the use of Salicylates result in | reduction of painful perception |
What are the 3 A's (Effects and Uses) of Salicylates (Aspirin) | 1. Analgesic: reduces pain, 2. Antipyretic: reduces elevated body temperature (Fever), 3. Anti-inflammatory: reduces inflammation |
How can Salicylates (Aspirin) be used regarding antiplatelet | prevents clotting, helpful in prevention of myocardial infarction, used in suspected heart attacks |
How is Aspirin most effective in dentistry | for throbbing pain & inflammation most common |
How is Aspirin most effective in medicine | for pain & inflammation with arthritis |
Where should Aspirin NEVER be placed | on oral mucosa because it will cause a painful ulceration |
What are the five adverse reactions of Aspirin | 1. Gastrointestinal, 2. Bleeding, 3. Toxicity (salicylism), 4. Reye's Syndrome, 5. Allergies: true allergy-avoid NSAIDS |
What are some Aspirin interactions to be aware of | Warfarin (Coumadin): will cause increase in bleeding if used with Asprin, Probenecid, Sulfonylureas, Methotrexate |
What is the regular dosage of Aspirin | 1 aspirin=325 mg (5 grain) or 81mg=child's dose or preventive adult dose |
Does Aspirin cause xerostomia | NO |
What do Nonsteroidal Anti-Inflammatory Drugs (NSAIDS) inhibit | the production of prostaglandins - inhibits enzyme cyclooxygenase (like aspirin) |
What are the effects (3 A's) and uses of NSAIDs | 1. Analgesic 2. Antipyretic 3. Anti-inflammatory |
In dentistry what are NSAIDs widely used for | most used for dental pain (stronger than aspirin) & as effective as medium strength narcotics (codeine) |
What are NSAIDs most widely used for in medicine | rhumatoid arthritis, dysmenorrhea (painful menstruation) |
What are some examples of NSAIDs | Ibuprofen (Advil, Motrin), Naproxen sodium (Aleve), Naproxen (Naprosyn) |
What are some adverse reactions of NSAIDs | 1. Gastrointestinal, 2. CNS-dizziness, seadation, 3. Blood clotting-prolongs bleeding, 4. Pregnancy- contraindicated, problems occur |
What are some drug interactions with NSAIDs | Decreases the effect of BP medications, Reduces the effects of antihypertensive drugs, diuretics, ACE inhibitors, and & B-blockers |
What do COX II specific inhibitors do | they inhibit only COX II enzyme; zero in on specific site |
What are COX II specific inhibitors | agents that block prostaglandins involved in inflammation, celecoxib (Celebrex) |
Why do the newer NSAIDs differ from the other NSAIDs | because they have a decrease in side effects |
NSAIDs decrease the effects of antihypertensive drugs, TRUE or FALSE | TRUE |
NSAIDs increase the effects of B-Blockers TRUE or FALSE | FALSE |
Propanyolol B-Blocker contraindicates NSAIDs TRUE or FALSE | TRUE |
What are two other names of Ibuprofen | Advil and Motrin |
What are two other names for Naproxen sodium | Aleve, Naprosen |
What are two other names for COX II inhibitors | Celebrex, Vioxx |
What are the effects (2 A's) of Acetaminophen (Tylenol) | Analgesic, & Antipyretic |
How is Tylenol different from Aspirin | it is NOT an anti-inflammatory |
Why are aspirin and NSAIDs more effective than Tylenol in dentistry | most dental problems are inflammatory and they have anti-inflammatory action |
What are three uses of Tylenol | 1. aspirin hypersensitive patients (allergy), 2. Patients who get gastric irritation with aspirin, 3. young children- to avoid Reye's Syndrome |
What are the adverse reactions of Tylenol | Liver damage and kidney damage |
What are drug interactions of Tylenol | Alcoholics |
What is gout | disease usually in men, involving joint (usually big toe) due to excess uric acid |
What drugs are used for the treatment of gout | probenecid (Benemid), & Colchincine |
How is Benemid used to treat gout | it increases the excretion of uric acid |
How is Colchincine used to treat gout | it is used in acute gout attacks |
What is the drug of choice used to treat gout with moderate pain | Acetominophen |
What is an Opioid | Narcotic, have morphine-like action |
When are opioids useful | when history of allergy is known |
Describe the chemical structure of opioids | natural and semisynthetic |
How are opioids classified | by chemical structure, and efficacy |
Which receptors are used by opioids | Mu, kappa, & delta |
How do opioids differ from one another | they act differently depending on which receptor they bind to and the receptor action effect |
In which part of the body do opioids act | CNS |
Which opioid is the prototype in which all other opioids are measured | Morphine |
List the opioids from stongest to weakest | Morphine, oxycodone, hydrocodone, codeine |
Describe the uses of opioids in dentistry | generally only used if NSAIDs are ineffective, begin with codeine or hydrocodone combinations & used only for short periods of time |
Which opioid is most commonly used in dentistry | Codeine |
List four therapeutic uses of opioids | 1. Pain relief, 2. Sedation & anxiety relief, 3. Cough suppression, 4. Diarrhea (symptomatic relier) |
Can opioids be used during pregnancy | yes, but not towards the end of the pregnancy |
Which opioid is used for sedation & anxiety relief | meperkline (Demerol) |
What opioids are used for cough suppression | codeine cough syrups |
How do opioids help give symptomatic relief of diarrhea | they decrease contraction/ motility in intestinal tract |
What are the adverse reactions of Opioids | 1. Sedation/euphoria, 2. Respiratory depression, 3. GI symptoms (nausea, vomiting), 4. Constipation, 5. Abuse can occur |
What are some of the signs to look for of possible addiction to Opioids | Myosis & Constipation |
What are the drug interaction of Opioids and their cause | alcohol & sedative-hypnotics which will result in respiratory depression |
What are the contraindications of Opioids | 1. Alcoholic or addict -greater potential for abuse, 2. Head injury- increases intracranial pressure, 3. Chronic pain (TMJ)- addiction potential, 4. Respiratory disease- respiratory depression can occur |
Which type of medication should be used to avoid possible addiction when a patient has chronic pain (TMJ) | NSAIDs and muscle relaxants |
What are 5 ways to recognize signs of addiction | 1. request certain drugs, 2. claims allergies & pain medications don't work, 3. cancels appointments-needs refills, 4. complains of pain days after treatment, 5. claims "low pain threshold" |
How are Opioids grouped | by action at receptor sites |
List the 3 Groups of Opioids | 1. Agonist Opioids, 2. Agonist-antagonist, 3. antagonists |
What is the most common agonist opioids | morphine |
Which agonist opioid is most commonly abused by staff members | Vicodin |
What is the most commonly used pain combination of agonist opioids | vicodin-hydrocodone-acetaminophen |
Which agonist opioid is most potent orally effective opioid | hydromorphone (Dilaudid) |
What are Agonist-Antagonist opioids | mixed opioids that have a lower abuse potential |
What is the antagonist of opioids and what is it used for | Naloxone (Narcan) combines with opioid receptor and produces no effect; used to treat opioid overdose; counteracts respiratory depression; works at all 3 receptor sites |
What is the antagonist for Anticholenergics | physostigmine |
What is the antagonist of Benzodiazepinese | flumazen 1 |
What is the antagonist for opioids | Narcan |
What is the most commonly used narcotic in dentistry | Codeine |
The efficacy in opioids is | variable |
What is the major sign in diagnosing an opioid OD, or identifying an addict | Myosis |
When can NSAIDs NOT be used | in pregnancy |
What is a major symptom of Opioid overdose and how can it be treated | Respiratory depression which can be treated with the antagonist naloxone |