GENERAL PHARMACOLOGY.pdf

GENERAL PHARMACOLOGY Pharmacology is the science about drugs. It studies their properties and use. The main task of pharmacology is to create new more effective medicinal drugs for treatment and prophylaxis of diseases. GENERAL PHARMACOLOGY is a divis...

GENERAL PHARMACOLOGY Pharmacology is the science about drugs. It studies their properties and use. The main task of pharmacology is to create new more effective medicinal drugs for treatment and prophylaxis of diseases. GENERAL PHARMACOLOGY is a division of Pharmacology which studies general concepts of this science. These concepts are connected with pharmacokinetics and pharmacodynamics. PHARMACOLOGY = PHARMACOKINETICS + Definition of Terms: Clinical Pharmacology: It evaluate the pharmacological action of drug preferred route of administration and safe dosage range in human by clinical trials. Drugs: Drugs are chemicals that alter functions of living organisms. Drugs are generally given for the diagnosis, prevention, control or cure of disease. Pharmacy: It is the science of identification, selection, preservation, standardization, compounding and dispensing of medical substances. Pharmacodynamics: The study of the biological and therapeutic effects of drugs (i.e, “what the drug does to the body”). Pharmacokinetics: Study of the absorption, distribution metabolism and excretion (ADME) of drugs (“i.e what the body does to the drug”). Pharmacotherapeutics: It deals with the proper selection and use of drugs for the prevention and treatment of disease. Toxicology: It’s the science of poisons. Many drugs in larger doses may act as poisons. Poisons are substances that cause harmful, dangerous or fatal symptoms in living substances. Chemotherapy: It’s the effect of drugs upon microorganisms, parasites and neoplastic cells living and multiplying in living organisms. Pharmacopeia: An official code containing a selected list of the established drugs and medical preparations with descriptions of their physical properties and tests for their identity, purity and potency. Pharmacognosy: concerned with the identification of crude effect of natural occurring drugs. Posology: study of drug dosage Potency: lowest concentration of the drugs to produced the desired pharmacologic effects Efficacy: highest concentration of the drugs to produce the desired pharmacologic effects Drug product: finished dosage form of the drug containing active ingredients. Active Ingredients: chemical components responsible for claimed therapeutic effects of the drug product/s. Generic Drug: drug product whose patent has been expired or never been patented. Generic Name: shortened scientific name base on active ingredient, widely used Chemical Name: complete description of chemical structure of drug, not used. Brand, Trade, Propriety Name: name given by pharmaceutical company to distinguished their drug products from other competitors although it contains the same active ingredients. Half life: time it takes for ½ of the drug to be eliminated at constant rate 0.693/t 0.5 - Amount of time required for plasma concentration of a drug to decrease by 50% after discontinuance of the drug. Hypersensitivity/Hyperreactive: drug produces usual effect at unexpected low dosage Supersensitivity: increase sensitivity as a result of denervation allergy Hyporeactive: drug produces usual effect at unexpected large dosage Tolerance: decrease sensitivity acquired as a result of prior exposure to the drug due to enzyme induction metabolizing more drugs thus decrease plasma effect. A. Tachyphylaxis – tolerance rapidly develop after administration of only few doses of drugs B. Immunity - reduced sensitivity as a result of antibody formation.  Idiosynchratic reactions: any other untoward reactions to pharmaceutical administration that has no obvious logical pharmacodynamic cause and can not be attributed to hypersensitivity reactions. Placebo: substance without intrinsic pharmacologic activity but may yield valuable therapeutic effect. Types of Drugs for Ocular Diseases: 1. Prophylactic Drugs: deal with agents used to prevent ocular diseases. 2. Diagnostic Drugs: agents used to diagnose or detect ocular diseases. 3. Therapeutic Drugs: agents used to treat ocular disease a. Curative – reverses a basic pathologic process b. Protective – limit the damage caused by pathologic process c. Palliative – relieves symptoms without modifying the causal process. According to mechanism of action: Rational drug – therapeutic mechanism is understood Empirical Drug – rests upon clinical and statistical evidence of effectiveness PHARMACOKINETICS Pharmacokinetics is the section of Pharmacology that studies how the body acts on the drug. It studies: a. Routes of Administration b. Absorption c. Distribution d. Biotransformation e. Elimination f. Excretion ROUTES OF DRUGS ADMINISTRATION Enteral routes Parenteral routes Topical application 1. Sublingual (under the tongue) 1. Injections 1. On the surface of skin 2. Oral (by mouth, per os) 2. Inhalations (through the 2. On the surface of mucous 3. Rectal (in rectum) respiratory pathways) membrane 3. Intranasal 4. Transcutaneous 5. Intravenous  For IV administration: the drug has rapid onset and short duration of action. For oral administration: it has slow onset of action, lower concentration, and more durative effect. DRUGS ABSORPTION Absorption is the enter of a drug into the blood from the site of administration. First- pass metabolism can occur with orally administered drugs. Drugs administered orally are fist exposed to the liver and may be extensively metabolized before reaching the rest of the body Drugs administered IV enter directly into the systemic circulation and has direct access to the rest of the body. During the absorption drug crosses cell membranes. There are such kinds of this crossing as: passive diffusion, filtration, active transport, and endocytosis. Passive diffusion is directed down concentration gradient. It does not require energy or carrier and is not saturable. Facilitated diffusion (or filtration) also is down gradient and energy independent, but needs carrier and is saturable. Active transport is against gradient, needs energy ATP and carrier, it is saturable. Factors influencing absorption are: 1. Chemical structure Water- or lipid-solubility Ionization 2. A medicinal form 3. The route of administration 4. State of tissues in the site of administration. Bioavailability is the fraction of administered drug that reaches the systemic circulation. Factors that influence bioavailability are solubility of a drug, nature of a drug, chemical instability, first-pass hepatic metabolism. Factors that affect Bioavailability: 1. Solubility of the drug in the contents of the stomach 2. Dietary pattern 3. Tablet size 4. Quality control in the manufacturing and drug formulation Formulations of drug depend on: a. barrier d. stability of drug b. setting in which the drug is used e. first pass effect/pre-systemic elimination c. urgency of medical situation *First order kinetic of drug absorption: constant fraction of the drug reaches the blood circulation after any routes except IV, IA, IC. *Zero order kinetic of drug absorption: 100% of the drug reaches the blood circulation after IV, IA, IC.  DRUGS DISTRIBUTION Distribution is the process by which a drug leaves the blood stream and enters the intersticium (extracellular fluid or the cells of the tissues). Factors that affect Drug Distribution: A. PROTEIN BARRIERS Forms of Drug Distribution: 1. Free or Unbound form – active and reaches the site of action producing desired effect. 2. Bound Form – binds to albumin and remains in the blood circulation until excreted by the kidneys leading to drug termination of drug action. 3. Metabolite – drug that have pass thru the hepatic microsomal enzymes and have undergone biotransformation into other form of drug either active or inactive (mostly). 4. Pro-drug form (inactive) – requires metabolism to be activated B. BLOOD FLOW C. TISSUE PERMEABILITY D. SIZE OF ORGAN E. PRESENCE OF RECEPTOR Receptor – specific molecular protein or macromolecule (DNA) which is a component of cells, biologic system, microorganisms, other foreign bodies, into which the drug interacts to initiate chain of biochemical events leading to the drug desired effect. - Follows the “lock and key” principles of drug interactions - Should be selective and modifiable to bring about the effect Affinity – amount of attraction between drug and receptor *Drug with high affinity binds to receptor even at low concentration while moderate to low affinity requires higher drug concentration. Receptor Sites: i. Type I – at cell membrane ii. Type II – at cytoplasm iii. Type III – at nucleus Binding forces between drug and receptor (Bond): 1. Covalent Bond – strongest bond and produced irreversible effect. 2. Van der Waals Bond – weakest bond and most important because most of drugs contain cationic and anionic groups. 3. Hydrogen Bond 4. Ionic Bond 5. Hydrophobic Bond *Drug Selectivity – affect only one type of receptor and produces a specific response. Different Types of Drug Ligands AGONIST - refers to an agent that activates a receptor to produce an effect similar to that of the physiologic signal molecule. It has both high affinity as well as high intrinsic activity, therefore can trigger the maximal biological response. PARTIAL AGONIST - an agent that activates a receptor to produce a submaximal effect but antagonizes the actions of a full agonist. It has full affinity but with low intrinsic activity and hence is only partly as effective as an agonist. INVERSE AGONIST - decreases the number of activated receptors to below that observed in the absence of drug. Thus, inverse agonists have an intrinsic activity less than zero, reverse the activity of receptors, and exert the opposite pharmacological effect of agonists. ANTAGONIST - an agent that prevents the action of an agonist on a receptor but doesn’t have any effect of its own. It has only affinity but no intrinsic activity. This drug binds to the receptor and blocks the binding of an endogenous agonist. - has no effect in the absence of an agonist but can decrease the effect of an agonist when present. - Bind to receptor without initiating changes - Efficacy is zero - Inhibits or blocks responses caused by agonist Antagonism: Based on MOA Chemical antagonism – antagonist neutralizes the effect of agonist (e.g. neutralization reaction, chelation of heavy metals) Physiologic antagonism – antagonist may act at a completely separate receptor, initiating effects that are functionally opposite those of the agonist Pharmacologic antagonism – antagonist acts at a similar receptor causing competitive antagonism Antagonism: Based on Surmountability Competitive (surmountable) antagonism – both agonist & antagonist compete with the same active site in the receptor causing prevention of an agonist from binding to its receptor Non-competitive (non-surmountable) antagonism – antagonist acts at a site beyond the active site of the agonist’s receptor Antagonism: Based on bond interaction Reversible antagonism – forms non-covalent bond specifically intermolecular forces of interaction Irreversible antagonism – binds covalently to the active site of the receptor, thereby reducing the number of receptors available to the agonist. Pharmacodynamic Drug Interaction by Enhancement of drug effect Addition: The response elicited by combined drugs is EQUAL to the combined responses of the individual drugs (1 + 1 = 2) Synergism: The response elicited by combined drugs is GREATER than thecombined responses of the individual drugs (1 + 1 = 3) Potentiation: A drug which has no effect on the system enhances the effect of the other (0 + 1 = 2) Dose-Response Relationships 1. Graded Dose-Response Relationship - It plots the magnitude of response against increasing doses of a drug. - It is characterized by the magnitude of response increasing continuously with greater concentration of unbound drug at the receptor site. POTENCY: Refers to the concentration (EC50) or dose (ED50) of a drug required to produce 50%of that drug’s maximal response EFFICACY: The relationship between receptor occupancy and its ability to initiate a response. - Graded dose-response curve indicates maximal efficacy of a drug - “Intrinsic Activity” - Measured by Emax 2. Quantal Dose Response Relationship - Graphically plots the percent of the population that responds to a drug versus the drug dose - Used to generate information regarding the margin of safety to be expected from a particular drug used to produce a specified effect.  - Often characterized by stating the: MEDIAN EFFECTIVE DOSE (ED50): The dose at which 50% of the individual exhibit the specified quantal effect MEDIAN TOXIC DOSE (TD50): The dose required to produce a particular toxic effect in 50% of animals MEDIAN LETHAL DOSE (LD50): The dose with which the toxic effect is death to 50% of the population Therapeutic index (TI) of a drug is the ratio of the dose that produces toxicity in half the population to the dose that produces a clinically desired or effective response in half the population TI is a measure of a drug’s safety (margin of safety) - A larger value indicates a wide margin between doses that are effective and doses that are toxic. BIOTRANSFORMATION OF DRUGS Biotransformation is metabolism of drugs in the body. The main organ for drugs metabolism is the liver. Biotransformation is realized in two stages: PURPOSES: 1. Transform drugs from bound (inactive) to free (active) or vice versa. 2. Transform drugs from non-polar (lipid soluble) to polar (water soluble). 3. Excretion of drug by kidneys by making the drugs more polar (less lipophilic). 4. Formation of metabolites by the active hepatic microsomal enzyme (cytochrome P450) leading to termination of drug action. Phases of Biotransformation: A. Stage I - reactions are non-synthetic and include oxidation, reduction, hydrolysis. Microsomal oxidation/reduction with participation of enzymes of cytochrome P-450 system is an important way of biotransformation of many drugs. The result of stage I is the formation of active or inactive products which enter the stage II reactions. Oxidation – most common, involves addition of O2 or removal of Hydrogen. Reduction – involves addition of Hydrogen or removal of Oxygen.  Hydrolysis – original drug is broken into separate parts. B. Stage II reactions are synthetic (conjugation with glucuronic and sulfuric acids, methylation, acethylation). They lead to the formation of inactive metabolites excreted from the body. *Drugs which increase the activity of microsomal enzymes in the liver are named the inductors of microsomal oxidation (e.g. phenobarbital, chlorpromazine). *Drugs which decrease the activity of microsomal enzymes in the liver are named the inhibitors of microsomal oxidation (e.g. metronidazole). EXCRETION – the process by which drug leaves the body. Drugs excreted are in non-polar (water soluble) metabolites thru the action of liver metabolism. ELIMINATION – disappearance of active molecule of drug from blood circulation thus related to termination of drug action. *First Order Elimination – rate of elimination is proportionate to the concentration of drugs in plasma *Zero Order Elimination – implies elimination at a constant rate regardless of the concentration of drugs in the plasma. PHARMACOKINETIC METRICS Pharmacokinetics is the mathematical description of the rate and extent of uptake, distribution of drugs in the body. The following are the most commonly measured pharmacokinetic metrics: Volume of distribution is the apparent volume in which a drug is distributed (i.e., the parameter relating drug concentration to drug amount in the body) total amount of drug Formula: Vd in the body Elimination half-life is the time required for the concentration of the drug to reach half of its original value Steady state concentration is the concentration at steady state, the situation where the overall intake of a drug is fairly in dynamic equilibrium with its elimina-tion. Steady state  is reached when a time of 4 to 5 times the half-life for a drug after regular dosing is started. Area under the curve is the integral of the concentration-time curve after a single dose or in steady state. Clearance is the volume of plasma cleared of the drug per unit time. *Bioavailability is the systemically available fraction of a drug. It is a subcategory of absorption and is the fraction of an administered dose of unchanged drug that reaches the systemic circulation. - When a medication is administered intravenously, its bioavailability is 100%. - When the medication is administered via other routes, its bioavailability decreases. *Absolute bioavailability compares the bioavailability of the active drug in systemic circulation following non-intravenous administration with the bioavailability of the same drug following intravenous administration. *Relative bioavailability measures the bioavailability of a formulation of a certain drug when compared with another formulation of the same drug, usually an established standard, or through administration via a different route. It is one of the measures used to assess bioequivalence between two drug products. PRESCRIPTION A medical prescription (℞) is an order (often in written form) issued by a qualified health care professional (e.g. physician and dentist) to a pharmacist or other therapist for a treatment (medicine or device) to be provided to their patient. There are two broad legal classifications of medications:  The medications which can be obtained only by prescription which are referred as prescription drugs or legend drugs. The medications which may be purchased without a prescription, which are termed non prescription drugs or over-the-counter (OTC). COMPONENTS OF PRESCRIPTIONS Generally, a prescription consists of the following parts: (1) Prescriber’s name, degree, address and telephone number. In the case of prescriptions coming from a hospital or a multicenter clinic, the hospital or clinic’s name, address and telephone numbers appear at the top. In such a case, the physician’s name and degree would appear near his/her signature. (2) Patient’s name, address, age, and the date of prescription. (3) The Superscription, which is represented by the Latin sign. (℞). This sign represents ‘‘take thou’’ or ‘‘you take’’ or ‘‘recipe.’’ Sometimes, this sign is also used to denote the pharmacy itself. (4) The Inscription is the general content of the prescription. It states the name and strength of the medication, either as its brand (proprietary) or generic (nonproprietary) name. In the case of compounded prescriptions, the inscription states the name and strength of active ingredients. (5) The Subscription represents the directions to the dispenser and indicates the type of dosage form or the number of dosage units. For compounded prescriptions, the subscription is written using English or Latin abbreviations. A few examples are provided as follows: - M. et ft. sol. Disp vi (Mix and make solution. Dispense six) - Ft. ung. Disp ii (Make ointment and dispense two) - Ft. cap. DTD xii (Make capsules and let twelve such doses be given) (6) The Signal, also known as transcription represents the directions to the patient. These directions are written in English or Latin or a combination of both. Latin directions in prescriptions are declining, but since they are still used, it is important to learn them. A few examples are present: - ii caps bid, 7 days (Take two capsules twice daily for seven days) - gtt. iii a.u. hs (Instill three drops in both the ears at bedtime) - In rect. prn pain (Insert rectally as needed for pain) (7) The prescriber’s signature. (8) The refill directions, in which the information about how many times, if authorized, a prescription can be refilled is provided.  (9) Other information, such as ‘‘Dispense as Written.’’ BFAD CONTROLLED SUBSTANCES Schedule/Classificati Definition Examples Prescribing Guidelines ons Schedule 1 (C-I) High abuse potential and Marijuana, Heroin, Lysergic Not available for no accepted medical use Acid Diethylamide (LSD), therapeutic use Mescaline and Tetrahydrocannabinols Schedule 2 (C-II) High abuse potential and Meperidine (Demerol), Only available by a written abuse lead to severe Cocaine, Morphine, prescription signed by psychic or physical Methadone, Amphetamine, prescriber and must be dependance Pentobarbital, Secobarbital supplied within 72 hours. Can not be refilled unless in case of emergency. Schedule 3 (C-III) Less abuse potential and Codeine, Hydrocodone May not be refilled more abuse may lead to than 6 months after the moderate or low physical date of PO is issued. dependence or high psychological dependence. Schedule 4 (C-IV) Less abuse potential and Diazepam, Alprazolam, May not be refilled more limited physical or Clorazepate, Phenobarbital than 6 months after the psychological dependence date of PO is issued. Schedule 5 (C-V) Limited physical or Loperamide, Robitussin AC Only loperamide are psychological abuse (guaifenesin + codeine) dispensed without the potential Prescription order (PO), Robitussin AC needs PO Drug Development and Approval Testing Phase Purpose Subjects Time Period A. Preclinic Testing Determine drug effects and Lab animals 1-2 years safety Investigational New Drugs (IND) Application B. Clinical Testing Determine the drug effects, safe Small number of < 1 year 1. Phase One dosage and pharmacokinetics. healthy volunteers 2. Phase Two Assess drug effectiveness in 200-300 patients 2 years treating a specific disease or with target disease disorder. or disorder 3. Phase Three Assess drug effectiveness and 1,000 – 3,000 3 years safety in a larger disease or patients with target disorder population disease or disorder New Drug Application (NDA) Approval 4. Phase Four Monitor any problems that General population Indefinite occurs after NDA approval with target disease or disorder LOCAL ANESTHETIC AGENTS o Anesthesia – loss of pain with loss of consciousness o Analgesia – loss of pain without loss of consciousness Mechanism of Action: (base on two theories): A. Specific Receptor Theory – blocks the sodium channel o Block nerve conduction by decreasing the permeability of nerve cell membrane to Na+ ions by blocking the openings of the Na+ channels thus interfere with the depolarization process. Block the channels by: Blocking the external openings – in ionized form of anesthetic agent Blocking the internal openings – in ionized form of anesthetic agent once absorb in uncharged form Compete with calcium ions. *Calcium has regulatory role for movement of Na+ ions across the cell membrane. B. Membrane Expansion Theory o In uncharged or an-ionized form, the anesthetic agent is absorbed at the cell membrane and becomes part of cell membrane structure at the Na+ channel which altering the channel configuration. Structural Components: 1. Aromatic unsaturated (lipophilic) acid – essential for its anesthetic activity 2. Intermediate alkyl chain 3. Tertiary amino (ionizing) group ▪ In unmyelinated fibers, 8-10mm segment of fibers must be block and least amount of anesthetic agent are required to prevent conduction of impulse. ▪ In myelinated fiber at least 3 nodes of Ranvier must be block and highest concentration of anesthetic agent are required to prevent conduction of nerve impulse. ▪ Changes in structural components, alter the potency and toxicity of these agents. Compounds with ester linkage are least toxic and less allergic reactions than amide group. The longer the length of alkyl chain, the greater is the potency but the greater is also the toxicity of the drug. ▪ Some of anesthetic agents have vasodilating property e.g., Bupivacaine and Etidocaine ▪ Most of the anesthetic agents are synthetic except cocaine. Physiochemical Characteristics: 1. All local anesthetics exist in solution: a. uncharged amide – lipophilic b. positively charged ammonium cation 2. Degree of ionization: a. only non-ionized form readily passes the cell membrane b. local anesthetics are weak base tend to ionized in acid solution; enhance stability and shell life c. uncharged form dominates (more lipid soluble) d. in the presence of infection, the ionized form increases Characteristics of Local Anesthetics 1. Relatively low ocular and systemic toxicity 2. Do not alter pupillary size and accommodation 3. Long duration 4. Cheap 5. Stable in solution 6. Will not interfere with other drugs Classification of Anesthetic Agents ESTER GROUP AMIDE GROUP nd 1. Procaine – 2 discover, used for short procedure 1. Lidocaine – most common 2. Tetracaine 2. Etidocaine 3. Benoxinate 3. Mepivacaine 4. Proparacaine – most common 4. Bupivacaine  5. Benzocaine 5. Prilocaine 6. Cocaine – 1st discover, the only natural drug Distinguishes between the esters and the amides Esters Amides Have short action Have long action Are metabolized by esterases of blood Are metabolized in the liver Are not active at acid pH (in the site of purulent Are active at acid pH (in the site of inflammation) purulent inflammation) Decrease the effect of sulfa drugs. Do not interact with sulfa drugs. Routes of Local Anesthetic Agents 1. Topical local anesthetic agents o Benoxinate 0.4% o Cocaine 1%-10% : alters pupil size o Proparacaine 0.5% - rapid onset (15 seconds) and shortest duration of action (20 minutes) o Tetracaine 0.5% Indications of Local Anesthetics: I. Examination technique – uses topical a. Forced Duction Test – used cocaine or lidocaine b. ERG – use tetracaine c. Goldmann Applanation Tonometry – use proparacaine or benoxinate d. Gonioscopy – use proparacaine or benoxinate e. Corneal Epithelial debridement – use cocaine f. Contact lens fundus examination II. Surgical Procedures – uses injectable a. lacrimal duct irrigation e. laser trabeculoplasty b. foreign body and suture removal f. probing c. laser iridotomy g. minor eyelid surgery d. paracentesis – aspiration of aqueous humor h. corneal scraping (can be topical) Ocular Side Effects of Topical Anesthetics: 1. Mild stinging and burning sensation – most common 7. Corneal edema 2. Vasodilation 8. Slowed epithelial healing 3. Shortening of TBUT 9. Punctate Epithelial Keratitis 4. Decreases reflex tearing 10. Epithelial desquamation 5. Decrease blinking 11. Allergy at lids and conjunctiva 6. Decrease epithelial mitosis and migration Systemic Side Effects of Local Anesthesia: I. CNS A. Early Excitatory Effects 1. Restlessness 5. Miosis 2. Anxiety 6. Tremors 3. Dizziness 7. Convulsive seizures – most serious 4. Tinnitus (ringing at the ear) B. Depressive Effects 1. Drowsiness 4. Coma 2. Sedation 5. Respiratory Failure 3. Unconsciousness 6. Death II. CVS 1. Hypertension 2. Bradycardia then tachycardia – results to arrythmia 3. Decrease cardiac output 4. Peripheral vasodilation – results to hypotension 5. A-V heart block 6. Circulatory collapse (shock) 7. Methemoglobinemia – results to cyanosis due to hypoxia *Hypersensitivity/Allergic reaction are very rare. Peculiarities of preparations 1. Procaine (Novocainum) is an ester; dilates blood vessels; is used for infiltration, conductive and spinal anesthesia; other indications are spasms of blood vessels and smooth muscles, pain syndromes, arrhythmia, toxicosis of pregnancy; may cause allergic complications including anaphylaxis, collapse, hypotension, seizures (in overdose). 2. Tetracaine (Dicainum) is an ester; dilates blood vessels; is more active and more toxic than procaine; is used only for surface anesthesia. 3. Benzocaine (Anaesthesinum) is an ester; is less active than procaine; is not dissolved in water; is used only for surface anesthesia in burns, wounds, diseases of skin and mucous membranes; is not toxic, but may cause methemoglobin formation when is used on large areas of skin lesions. 4. Lidocaine (Xycainum) is the amide; acts longer than procaine; is more active; is suitable for all types of anesthesia; is used for the treatment of ventricular tachyar-rhythmia (IV). 5. Trimecaine is an amide; pharmacological properties are similar to lidocaine. Bupivacaine (Marcaine) is an amide; is one of the most active local anesthetics; is used for infiltration, conductive and spinal anesthesia; has toxic action on the heart. 6. Articaine is an amide; more active than lidocaine and procaine; acts during 1-5 hrs; is used for infiltration and conductive anesthesia; is widely used in dentistry. Combination of articaine with vasoconstrictor is known as Ultracaine. Other Anesthetic Agents ▪ 0.5% - 1% Proparacaine: - Most common used because of very few side effects. - Most rapid onset f action (5 minutes) and short duration of action (20 minutes) - Less irritating and allergic anesthetic agent - Does not penetrate the cornea and conjunctiva Uses: for tonometry and gonioscopy, minor conjunctival and corneal procedures ▪ Tetracaine (0.5% solution or ointment): - Hydrolyzed by AchE - 10x as potent as cocaine and 10x toxic as procaine Uses: a. foreign body removal e. gonioscopy b. corneal scraping f. tonometry c. suture removal g. paracentesis d. ERG Side Effects: transient stinging and burning sensation, conjunctival redness ▪ Cocaine (2%, 4%, 10%): - Alkaloids from Erythroxylon coca - Potent but not commonly used because it is highly toxic - Common abuse (addicting property) - Not used during tonometry because it softens the cornea which give lower value in patient with glaucoma - Has also adrenergic (mydriatic and vasoconstrictive) effects - Combined with epinephrine, phenylephrine, homatropine or atropine for resistant eyes to mydriasis Onset of Action: 2-5 minutes Duration of Action: 30 minutes to 2 hours Uses: a) Diagnosis of Horner’s syndrome – using 4% - 10% b) Forced duction test c) Corneal epithelial debridement – loosed the corneal epithelium d) Dacryocystorhinostomy – using nasal spray e) Deepens anterior chamber after cataract surgery f) Breaks posterior synechiae Side effects: a) Corneal epithelial toxicity – grayish pits erosion b) Narcotics – addicting property  c) CVS – bradycardia followed tachycardia, arrythmia, hypertension Contraindications: Hypertension and angle closure glaucoma ▪ Benoxinate (0.4%): - Para-aminobenzoic acid ester of cocaine (substitute for cocaine) - Has antibacterial property to Pseudomonas Aeruginosa Uses: applanation tonometry Side Effects: stinging and burning sensation 2. Injectable local anesthetics – given by retrobulbar/periocular injection, tissue infiltration A. Esters Onset (seconds) Duration (hours) 1. Procaine 15-25 sec. 0.5-1 hrs. 2. Tetracaine 20-30 sec. 3-5 hrs. B. Amide 1. Prilocaine 5-15 sec. 1-3 hrs. 2. Lidocaine 5-15 sec. 1-3 hrs. 3. Mepivacaine 5-15 sec. 1-3 hrs. 4. Bupivacaine 10-20 sec. 3-5 hrs. 5. Etidocaine 5-15 sec. 3-5 hrs. ▪ Lidocaine (1%, 2%) – injectable, most common, 50% more toxic than procaine, effects last for 1 hour. ▪ Procaine (0.5% - 4%) – potent, non-toxic injectable anesthetic agent Added to prolong the anesthetic effects: 1. Epinephrine: vasoconstrictive effect 2. Hyaluronidase/ Spreading factor: enhance infiltration and dispersion of drug giving more effective motor block. 3. Bicarbonate: increases the percentage of anesthetic in non-ionized form thus enhances its absorption. DRUGS ACTING ON CARDIOVASCULAR SYSTEM (CVS) I. ANTI-HYPERTENSIVE AGENTS  o Side Effects: orthostatic hypotension (HPoN) except diuretics and antihyperlipidemic agents A. Diuretics: agents that enhances renal output of water and electrolytes MOA: inhibit renal tubular reabsorption of NA+ and water Side Effects: electrolytes imbalance and dehydration (DHN) 1A. Thiazide Diuretics – most commonly used anti-hypertensive diuretic agent ▪ Hydrochlorothiazide (HCT) – most commonly used - Combine with other anti-hypertensive agents e.g., ACE inhibitors, beta blockers and angiotensin receptor II blockers. 1B. Loop Diuretics – more potent diuretics but weaker anti-hypertensive effect - Severe electrolytes imbalance ▪ Furosemide, Bumetanide, Ethacrynic Acid 1C. K+ Sparing Diuretics – has modest anti-hypertensive effect with minimal K+ loss - Useful for mineral corticosteroids excess with HPN ▪ Spironolactone, Amiloride, Triamterene B. Beta-Blockers: also used as anti-angina and anti-arrhythmic agents, also combined with other anti-hypertensive agents e.g., calcium channel blocker and ACE inhibitors. o Side Effects: Bradycardia B1. Non-selective Beta Blockers – act on both alpha and beta receptors o Contraindications: chronic obstructive pulmonary diseases (COPD or COLD) and diabetic using insulin or oral hypoglycemic agents ▪ Propranolol (1st to be discover), Timolol, Alprenolol, Metipranolol, Nadolol, Bunolol, Labetalol IV, Pindolol B2. Cardio-selective Beta-blockers – safe with COPD and DM with insulin ▪ Practolol (1st to be discover), Metoprolol, Betaxolol, Atenolol, Esmolol, Acebunolol C. Calcium Channel Blocker (CCB) – also used as anti-angina and anti-arrhythmic, also combined with beta blockers and diuretic agents (HCT) ▪ Nifedipine, Felodipine, Amlodipine, Lercanidipine, Verapamil (for arrhythmia and angina also), Diltiazem (also used for arrhythmia)  D. Angiotensin Converting Enzyme (ACE) Inhibitors – inhibit Na+ and water retention. It also combines with diuretics and beta blockers. ▪ Captopril, Enalapril, Imidapril, Linisopril, Perindopril, Trandolapril E. Angiotensin II antagonists – also combined with diuretics ▪ Losartan, Telmisartan, Olmesartan, Valsartan, Candesartan, Irbesartan F. Arteriolar Vasodilators – causes Na+ and water retention due to increase rennin secretion thus should be combined with diuretics and beta blockers ▪ Hydralazine – safe for pre-eclampsia and eclampsia ▪ Minoxidil – also as hair grower ▪ Diazoxide IV G. Central-acting Sympatholytic agents – acts by stimulating alpha2 (inhibitory) decreasing sympathetic outflow from the brain. ▪ Clonidine and Methyldopa H. Pre-ganglionic Adrenergic Blockers ▪ Guanetidine – displaces NE at the presynaptic ends and released as “false” neurotransmitter ▪ Guandrel ▪ Reserpine – inhibit the storage and release of NE I. Anti-hyperlipidemic Agents I1. Fibric Acids – for elevated triglycerides and LDL in the blood MOA: increase lipase in peripheral tissue ▪ Clofibrate, Fenofibrate, Bezafibrate, Ciprofibrate ▪ Gemfibrozil – causes cholelithiasis I2. Hydroxymethylglutaryl Co-enzyme (HMG-CoA) reductase inhibitor - for hypercholesterolemia *MOA: inhibit HMG-CoA reductase (enzyme which catalyzed cholesterol synthesis in liver) o Side Effects: elevates ALT or SGOT ▪ Atorvastatin, Simvastatin, Fluvastatin, Lovastatin, Pravastatin II. DRUGS FOR CONGESTED HEART FAILURE (CHF) *3D’s management of CHF: Diet, Diuretics and Digitalis A. Cardiac Glycosides (Digitalis) – has (+) inotropic (inc. C.O.) and (-) chronotropic effects (dec. Heart Rate direct effect on SA node) MOA: inhibit sodium potassium pump on myocardial cell membrane ▪ Deslanatoside  ▪ Digoxin – commonly used as maintenance drug ▪ Digitoxin Side Effects: Digitalis Intoxication o Signs and Symptoms for Digitalis Intoxication: - GIT: anorexia (Earliest sign), nausea, vomiting, diarrhea - CNS disturbances: drowsiness, fatigue, confusion, visual disturbances - Cardiac Effects: arrhythmia, PVC, AV heart block, paroxysmal atria, tachycardia, and ventricular tachycardia. Ocular Side Effects: - Xanthopsia: blue-yellow color defect - Colored borders to object - Flickering vision - “Glare phenomenon” – object appears covered with brown-orange color or white snow - Scotoma - Decrease vision - Diplopia - Mydriasis Treatment of Digitalis intoxication: - Discontinue medication - Give K+ sparing diuretics - K+ administration - Give anti-arrhythmic agents e.g., lidocaine, phenytoin, propranolol, procainamide B. K+ sparing diuretics: Spirinolactone, Amiloride, Triamterene C. ACE inhibitors D. ARB E. Catecholamines – stimulate B1 receptors (Dopamine, Dobutamine) F. Vasodilators – Prazosin (Alpha1-blocker), hyrdralazine and minoxidil, nitroglycerine (Organic Nitrates) G. Others – Amrinone and Milrinone (for short term treatment of CHF). III. DRUGS FOR ANGINA PECTORIS Angina Pectoris – chest pain due to myocardial ischemia due to imbalance between myocardial demand and supply. Pain is due to accumulation of acid metabolites (lactic acids) in the myocardium. Pain is characterized as compression and tightness in the retro-sternal region radiating to the left shoulder, left arm and numbness at the digits. Types of Angina Pectoris 1. Stable (Exertional) Angina Pectoris  - Most common form of ischemic heart disease (IHD) - Due to myocardial oxygen demand greatly exceeds the oxygen supply usually precipitated by physical exertion due to presence of coronary artery atherosclerosis or stenosis. o Treatment: a) Organic Nitrates b) Beta Blockers c) Calcium channel blockers (CCB) 2. Variant or Prinzmetal Angina Pectoris - Oxygen supply to myocardium decreases due to coronary artery vasospasm and pain occurs even at rest. o Treatment: a) Calcium Channel Blockers -drug of choice b) Organic Nitrates – may be added 3. Unstable Angina Pectoris - Serious and life threatening forms of Myocardial Infarction characterized by increase oxygen demand and decrease oxygen supply due to presence of coronary artery thrombosis or vasoconstriction thus this is a combination of stable and Prinzmetal angina pectoris - Pain is manifested by minimal level of exertion or spontaneously even at rest. o Treatment: a) CCB + Organic Nitrates b) CCB + Beta Blockers Medical Treatment: A. Organic Nitrates – vasodilators NO3 is a precursors of Nitrous Oxide (has vasodilating property) which acts by increasing the production of cyclic GMP (2nd messenger that inhibit smooth muscles contraction) within the cardiac muscles. *Long-acting Nitrates a) Nitroglycerines b) Isosorbide Dinitrate (IDN) c) Isosorbide Mononitrate (IMN) d) Erythrityl Tetranitrate e) Pentaerythritol Tetranitrate B. Beta Blockers – decrease heart rate (decrease workload) thus decreases myocardial oxygen demand. ▪ B.1 selective – propranolol ▪ B.2 non-selective – metoprolol C. Calcium Channel Blockers (CCB) – decrease the workload, decrease myocardial oxygen demand  o Nifedipine, Verapamil, Diltiazem D. Dipyridamole Mode of Action (MOA): 1. Inhibit uptake of adenosine (vasodilating effect at coronary arteries) by the rbc. 2. Inhibit platelet aggregation E. NSAID Acetyl salicylic acid (ASA) or Aspirin - inhibit platelet aggregation Non-pharmacologic Management ▪ Identify potentiating factors that exacerbate anginal attack (e.g. HPN, CHF, anemia, Thyrotoxicosis) – direct the management to these causes. ▪ Lifestyle changes – avoid smoking, exercise, weight control, stress management ▪ Surgery – coronary artery bypass and coronary artery angioplasty IV. DRUGS FOR ARRHYTHMIA Arrhythmia – abnormal in heart rate and rhythm due to irregularity on site of origin of cardiac impulse or disturbance/faulty in initiation of conduction of impulse. A. Class I (Na+ channel blockers) MOA: block Na+ at the channel preventing spreading of depolarization ▪ Subclass A – Procainamide, Quinidine, Disopyramide (alternative to the first two) ▪ Subclass B – Lidocaine (drug of choice), Phenytoin, Tocainide ▪ Subclass C – Flecainide, Eucainide B. Class II (Beta Blockers) ▪ Non-selective beta blockers – propranolol ▪ Cardio-selective beta blockers – metoprolol C. Class III (drugs that prolong repolarization) ▪ Amiodarone ▪ Bretylium – adrenergic blocker (Vasodilator) *Side Effect: orthostatic hypotension D. Class IV (Calcium Channel Blocker) ▪ Verapamil – more effective ▪ Diltiazem ANTI-INFECTIVE (ANTIMICROBIAL) AGENTS Chemical substances which can be natural, semi-synthetic or synthetic (artificial) which can  inhibit the growth or kill the microorganism. Types of Anti-infective Agents: I. Antibiotics - Chemical substances which can be natural, semi-synthetic or synthetic (artificial) which can inhibit the growth (bacteriostatic) or kill (bactericidal) the bacteria. Classifications of Antibiotics: A. According to Mechanism of Action (MOA) ▪ Inhibit the synthesis of bacterial cell wall. o example: Penicillin, Bacitracin, Vancomycin, Cephalosporins ▪ Alters the function and permeability of bacterial cell membrane. o Example: Polymixin B ▪ Inhibit the translation of genetic information and protein synthesis. o Example: Tetracycline, Aminoglycosides, Macrolides, Chloramphenicol ▪ Inhibit the synthesis of bacterial nucleic acid. o Example: Quinolone, Rifampicin ▪ Inhibit the synthesis of essential metabolite necessary for the synthesis of folic acid. o Example: Sulfonamide B. According to Antimicrobial Activity ▪ Bactericidal – actual killing effect of the drug ▪ Bacteriostatic – inhibit the bacterial replication or growth C. According to Spectrum of Activity ▪ Narrow Spectrum – kill or inhibit limited varieties of bacteria o Example: Penicillin, Chloramphenicol, Erythromycin ▪ Broad Spectrum – kill or inhibit wide varieties of bacteria o Example: Amoxicillin, Cephalosporins, Aminoglycosides D. According to absorbability of site of administration ▪ Local-acting – absorbed at site of application or injection with little systemic absorption ▪ Systemic Acting – reaches the general circulation Factors that confer Bacterial Resistance to Antibiotic: 1. Bacteria developed enzymes that destroy the active drug (e.g., Penicillinase or Beta Lactamase) 2. Bacteria change the permeability of the drug. 3. Bacteria developed an altered structural target (receptor) for the drug. Routes of Antibiotic Administration 1. Topical – solution or ointment, most common 2. Periocular Injections o Subconjunctival or Sub Tenon’s injection  o Retrobulbar injections 3. Intraocular injection o Intracameral injections o Intravitreal injections 4. Systemic Routes o Alimentary – oral o Parenteral – IV, IM Ocular Indications of Antibiotics a. stye g. uveitis b. bacterial conjunctivitis h. retinitis c. endophthalmitis i. optic neuritis d. keratitis and corneal ulcer j. orbital cellulitis e. dacryocystitis k. meibomitis f. sinusitis l. blepharitis Major Group of Antibiotics 1. Sulfonamide a) Sulfamethoxazole – combined with trimethoprim (co-trimoxazole) b) Sulfacetamide – topical c) Sulfadiazine 2. Quinolones a) Nalidixic acid b) Pipemidic acid c) Oxolinic acid 3. Fluoroquinolones a) Ciprofloxacin f) Enoxacin b) Ofloxacin g) Sparfloxacin c) Norfloxacin h) Grapafloxacin d) Levofloxacin i) Trovafloxacin e) Lomefloxacin *a-d have ocular preparation 4. Penicillin – from penicillium (mold), discovered by Alexander Fleming a) Penicillin B and Penicillin V b) Penicillinase-resistant Penicillin o Example: Cloxacillin, Dicloxacillin, Oxacillin, Nafcillin C) Broad-spectrum Penicillin o Example: Ampicillin, Amoxicillin, Bacampicillin d) Anti-Pseudomonas Penicillin o Example: Carbenicillin, Ticarcillin, Azlocillin, Mezlocillin, Piperacillin 5. Cephalosporins a) 1st generation – good for gram positice bacteria  o Example: Cefalexin, Cefazolin nd b) 2 generation – effective for PEcK o Example: Cefuroxime, Cefaclor rd c) 3 generation – effective for PEcKS o Example: Cefotaxime, Ceftriaxone d) 4th generation – effective for HENPEcKS o Example: Cefditoren, Cefepine, Cefpirone 6. Aminoglycosides – effective for gram negative bacteria a) Streptomycin – oldest e) Neomycin – also for Acanthamoeba b) Spectinomycin f) Amikacin c) Gentamycin g) Kanamycin d) Tobramycin ▪ Side Effects: Ototoxicity and Nephrotoxicity – if used for>5 days Vestibulotoxic – vertigo and loss of balance 7. Tetracycline – DOC for Trachoma and inclusion conjunctivitis A. Short-acting Oral Tetracycline o Tetracycline and Oxytetracycline B. Intermediate acting Tetracycline o Methacycline and Demeclocycline C. Long-acting Tetracycline o Doxycycline and Minocycline 8. Chloramphenicol – drug of choice for typhoid fever 9. Macrolides – useful for patient allergic to other antibiotics o Erythromycin, Clarithromycin, Roxithromycin and Azithromycin 10. Bacitracin 11. Polymixin B II. Anti-Protozoal Agents 1. Metronidazole Uses: ✔ Entamoeba coli and histolytica ✔ Trichomonas vaginalis 2. Itraconazole – for Acanthamoeba and combined with neomycin III. Anti-Malarial Agents 1. Chloroquine and Hydroxychloroquine – for uncomplicated malaria Side Effects:  a.) “whorl-like” pattern of pigment deposits at corneal epithelium b.) “halos around light” c.) “bull’s eye” maculopathy pattern d.) pallor/pale optic disc e.) abnormal ERG f.) decrease visual acuity – most common early manifestation g.) central and secocentral scotoma h.) narrowing of arterioles i.) changes in color vision j.) nyctalopia 2. Quinine – for Plasmodium falciparum 3. Pyrimethamine + sulfadoxine – for Plasmodium Falciparum IV. Antimycotic Agents – preparations are mostly topical used for Fusarium, Candida, and Aspergillus Side Effects: hepatotoxic 1) Nystatin – drug of choice for oral candidiasis 2) Amphotericin B (IV) – for systemic fungal infection Ocular Side Effects: a. Greenish corneal discoloration b. Corneal clouding c. Chemosis 3) Griseofulvin – for Taenia (ringworm) 4) Topical preparations: a. Miconazole c. Clotrimazole b. Ketoconazole d. Tioconazole Ocular Anti-fungal/Anti-Mycotic Agents 1. Polyenes 3. Imidazole a. Amphoterecin B a. Miconazole b. Natamycin b. Ketoconazole 2. Pyrimidine 4. Triazoles a. Flucytosine a. Fluconazoles b. Itraconazoles V. Anti-viral Agents Common Viruses: a. Herpes Virus c. Cytomegalic Virus (CMV) b. Varizella-zoster virus d. HIV Classifications: 1. Amantidine – drug of choice for influenza A 2. Idoxuridine – 1st approved anti-viral agent 3. Anti-Herpes agent – Acyclovir, Famciclovir, Ganciclovir, Valaciclovir 4. Anti-Retroviral agents – for HIV (Zidovudine, Didanosine, Lamivudine, Zalcitabine, Stavudine) 5. Oseltamivir – for bird’s flu (H5N1) 6. Inosiplex – for chickenpox 7. Methisoprinol – for Mumps virus 8. Methisazole – prophylactic for small pox Ocular Antiviral Agents A. TOPICAL B. ORAL C. INTRAVENOUS D. INTRAVITREAL 1. Vidarabine 1. Acyclovir 1. Ganciclovir 1. Formivirsen 2. Trifluridine 2. Valaciclovir 2. Foscarnet 3. Ganciclovir 3. Cidofovir VI. Anti-tuberculotic Agents 1. 1st line of drugs: a. Isoniazid (INH) Side Effects: i. Peripheral neuritis ii. Optic neuritis iii. Hepatotoxic b. Rifampicin c. Ethambutol Side effects: Optic Neuritis d. Streptomycin – IM Side effect: Ototoxicity and Nephrotoxicity nd 2. 2 line of drugs a. Pyrazinamide – 2 months duration of medication, can cause hepatotoxic VII. Anti-leprotic Agents 1. Sulfone – derivatives of Dapsone 2. Rifampicin 3. Clafazimine – for resistant strains VIII. Anti-Helmentic Agents A. For Ascarasis, Enterobius, Hookworm: 1) Pyrantel Pamoate or embonate 4) Tetramisole  2) Mebendazole 5) Piperazine 3) Albendazole B. For Tapeworms: 1) Niclosamine Ocular Anti-infective Agents I. Antibacterial Agents A. Topical A.1. Solution A.2. Ointment Bacitracin Polymixin B Polymixin B Chloramphenicol Neomycin Bacitracin Tobramycin Gramicidin Oxytetracycline Erythromycin Sulfacetamide Neomycin Gentamicin Chloramphenicol Gentamicin Levofloxacin Gentamicin Tobramycin Norfloxacin Tobramycin Fucidic Acid Ofloxacin Framycetin Erythromycin Ciprofloxacin Ofloxacin Framycetin Lomefloxacin Ofloxacin Ciprofloxacin Antibiotics with solution and suspension preparation: 1. Neomycin 4. Tobramycin 2. Polymixin B 5. Oxytetracycline 3. Gentamicin 6. Chloramphenicol IX. Anti-Inflammatory Agents ❖ Corticosteroids – may combine with antibiotics 1) Dexamethasone 4) Hydrocortisone 2) Betamethasone 5) Fluorometholone 3) Prednisolone CORTICOSTEROIDS Effects: 1) Anti-inflammatory activity – most important to ophthalmologist 2) Restore toward normal excessive permeability of inflamed capillary 3) Decrease cellular and fibrinous exudation (edema) and tissue formation 4) Inhibit fibroblastic and collagen forming activity (Keloid) 5) Retard epithelial and endothelial regeneration (retard healing) 6) Mydriasis ) Blepharoptosis  ❖ Mode of administration in Anterior segment diseases: Topical (most effective) ❖ Mode of administration in Posterior segment diseases: Systemic, Periocular, Intravitreal Indications: I. Eyelids a. allergic blepharitis d. Hemangioma b. contact dermatitis e. chemical burns c. chalazion f. Herpes Zoster (shingles) II. Conjunctiva a. allergic conjunctivitis c. Herpes Zoster Keratitis b. vernal conjunctivitis d. mucocutaneous lesions III. Sclera a. Episcleritis b. Scleritis IV. Cornea a. epithelial punctate keratitis f. marginal ulcers b. Herpes simplex disciform g. interstitial keratitis c. keratitis h. acne rosacea keratitis d. Herpes zoster keratitis i. chemical burns e. immune graft rejection *Side Effects: 1.) Mental changes – euphoria to psychosis 2.) Activation of infection – serious in tuberculosis 3.) temporary increase severity of diabetes and hypertension 4.) GI ulceration – PUD 5.) Osteoporosis – leads to fractures 6.) Electrolytes imbalance – causing edema 7.) Impaired wound healing – due to delay fibroblastic or scar formation 8.) “Moon Facie” – manifestation of Cushing syndrome 9.) Ocular Complications: a. Secondary Open angle Glaucoma – due to accumulation of glycosaminoglycans at the trabecular meshwork after 6 weeks use of topical dexamethasone. After 18 months of therapy, it causes permanent glaucoma. b. Posterior Subcapsular lens Opacity (cataract) f. Papilledema c. Secondary Keratomycosis g. Mild Exophthalmos d. Mild Ptosis h. Edematous Eyelids e. Mydriasis 10.) Reduced local tissue immunity A. Glucocorticoids – has an effect on glucose metabolism causing hyperglycemia 1) Short-medium acting: a. Prednisolone d. hydroxycortisone or cortisol b. Prednisone e. Methylprednisolone c. Cortisone f. Meprednisone 2) Intermediate-acting: a. triamcinolone c. Paramethasone b. Fluprednisolone 3) Long-acting: a. Betamethasone b. Dexamethasone B. Mineralocorticoids – has an effect on electrolytes a. Fludrocortisone b. Desoxycorticosterone Synthetic Corticosteroids Potency 1. Prednisone (10x more potent than cortisone) 4% 2. Prednisolone (10x more potent than cortisone) 5% 3. Methyprednisolone 4. Triamicrolone 4% 5. Dexa and Betamethasone (30-50x more potent than cortisone) 25-30% 6. Cortisone (least potent) 0.8% 7. Hydrocortisone 1% 8. Fluoromethalone 40-50% 9. Fluocinolone 240% ❖ Non-steroidal Anti-inflammatory Drugs (NSAIDs) – inhibit cyclooxygenase thus decrease prostaglandins production. a. Fluriprofen – inhibit cell mitosis thus delay wound healing b. Diclofenac Na+ - decrease intraocular inflammation after surgery c. Ketorolac – potent analgesic (180x) and has an anti-puritic effect. Used on Allergic conjunctivitis d. Indomethacin e. Oxyphenbutazone f. Phenylbutazone ❖ Anti-Histamine Agents – prevent histamine by acting on H1-receptor site. It is used for allergic conditions affecting conjunctiva and eyelids a. Naphazoline d. Antazoline  b. Lodoxamide e. Phenylephrine – sympathomimetic amines c. Tetrahydrozoline Common Over The Counter (OTC) Drugs I. Acetaminophen (Paracetamol) – analgesic and antipyretic agent (NSAID). - causes liver dysfunction in overdose ❖ Antidote: N-acetylcysteine (effective if given 8-24hrs after ingestion) II. Acetylsalicylic Acid (Aspirin) – analgesic, antipyretic, anti-inflammatory and anti-arthritic agent (NSAID) - Causes metabolic acidosis and respiratory alkalosis, fever and coma in an overdose. ❖ Antidote: NaHCO3 Most commonly Drugs of Abused present in Urine (DAO) A. Stimulants i. Amphetamine – benzoic acid and p-hydroxyamphetamine is the metabolite ii. Metamphetamine – amphetamine is metabolite iii. Cocaine – benzoyl ecgonine is the metabolite B. Hallucinogens i. Phencyclidine ii. Delta-9-tetra-hydrocannabinol (THC) – also known as Marijuana/Hashish C. Hypnotic Sedatives i. Barbiturates a. Amobarbital d. Butalbital b. Secobarbital e. Pentobarbital c. Phenobarbital ii. Benzodiazepines a. Alprazolam c. Flurazepam b. Chlordiazepoxide d. Diazepam D. Narcotic Analgesic (Opoids) – use as post operation analgesia a. Meperidine e. Fentanyl Citrate b. Codeine f. Nalbuphine c. Morphine g. Hydromorphone  d. Methadone h. Oxycodone and Hydrocodone *Side Effects: Miosis Decrease visual acuity Decrease accommodation Myopia *Naloxone – treatment of acute opoid overdose *Naltrexone – maintenance drug for opioid addicts in treatment program MEDICAL ABBREVIATIONS LATIN ABBREVIATIONS MEANING Ad ad Up to, to Ad move Ad mov. apply Alternis horis Alt. hor. Every other hour Ante a before Ante Cibus a.c. Before meal Bis in die B.I.D. 2x a day Ter in die T.I.D. 3x a day Quarter in die Q.I.D. 4x a day Capsula Cap. Capsule Cum c with Debus Alternis Debus alternis Every other day gram g., gm gram gutta gt., gtt A drop hora h. An hour Hora somni h.s. At bedtime nocte Noct. At night Oculo utro O.U. Each eye Oculo uterque O.U. both eyes Oculus dexter O.D. Right eye Oculus Sinister O.S. Left eye Per os p.o. By mouth Pro re nata p.r.n. When needed quaque q Each, every Quaque hora q.h. Every hour recipe Rx Take, you take signatura Sig. Write, you write Sine s without solutio Sol. solution Tabella Tab. tablet Unguentum Ung. ointment Ut dictum Ut. dict As desired Unus i. one duo ii two tres iii three quattuor iv four quinque v five