Introduction To Pharmacology

 

INTRODUCTION TO PHARMACOLOGY

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HISTORY •

Early drug – plants, animals & minerals

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2700 BB – earliest recorded drug use found in Middle East & China

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1550 BC – Egyptians created Ebers Medical Papyrus Castor oil – laxative Opium – pain Moldy bread – wounds & bruises

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Galen (131-201 AD) Roman physician; initiated common use of   prescriptions

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1240 AD – introduction of apothecary system (Arab doctors) 1st set of drug standards & measurements (grains, drams, minims), currently being phased out

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15th century – apothecary shops owned by barber, surgeons, physicians, independent merchants

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18th century – small pox vaccine (by Jenner) Digitalis from foxglove plant for strengthening & slowing of  heartbeat Vitamin C from fruits

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19 century – morphine & codeine extract from opium Introduction of atropine & iodine Amyl nitrite used to relieve anginal pain Discovery of anesthetics (ether, nitrous oxide)

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Early 20th century – aspirin from salicylic acid Introduction of Phenobarbital, insulin, sulforamides

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Mid 20th century 1940 – Discovery antibiotics (penicilline, tetracycline, streptomycin), antihistamines, cortisone

 

1950 – discovery antipsychotic drug, antihypertensives, oral contraceptives, polio vaccine

2.

DEFINITION & SUBDIVISIONS

Drug – chemical introduced into the body to cause some changes WHO def: any product/subs used to modify/explore physiologic • system/pathologic states for the benefit of the patient Pharmacology – study of the manner in which the function of living system is affected by chemical agents/drugs •

Science concerned with history, history, sources, physical ph ysical & chemical properties of drugs & the way in which drug affects living system

Subdivisions of pharmacology: 1. pharmacodynamics – study of the biochemical & physiological ph ysiological effects of drugs & mechanisms of action •

what the drug does to the body

2. pharmacokinetics – deals with the absorption, distribution, biotransformation & excretion of drugs •

what the body does to the drug

3. pharmacotherapeutics – study of drugs used in the diagnosis, prevention, suppression, & treatment of diseases deals with beneficial effects of the drugs (medicines) • 4. pharmacognosy – study of drugs in their original unaltered state; origin of drugs d rugs •

source of drugs

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ex: penicillin from penicillium (fungi)

5. Toxicology – study of biologic toxins: study of poison & its effects deals with deleterious effects of physical & chemical agents (including drugs) in human

Pharmacoeconomics – study of relationship of drugs & economics e conomics

 

Pharmacovigilance – science of collecting,researching, analyzing, & evaluating set of  information about adverse drug effects. Receptor – a component of the cell that interacts with drug, initiating a chain of   biochemical events leading to drugs’ observed effects •

Human body works through complicated series of chemical c hemical reactions & processes

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Important aspects of nursing: understanding how drug ant on body to cause changes & apply that knowledge in clinical setting Patients take complicated drug regimen & receive potentially toxic drug Some manage their own care at home

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 Nursing responsibilities regarding drug therapy: Administering drugs Assessing drug effects Intervening to make drug regimen more tolerable Provide patient teachings about drugs & drug regimen

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Knowing how drug works --- easier to handle --- enhances drug therapy

DRUG NOMENCLATURE 1. CHEMICAL CHEMICAL NAME – atomic/m atomic/molecul olecular ar structur structuree of drug 2. GENERIC GENERIC NAME/NONNAME/NON-PROP PROPER ERTY TY NAME NAME – original original designati designation on given to the the drug when the drug company applies for approval patents -

univer universal sally ly accept accepted ed & not capi capital talize ized; d; before before drug drug becomes becomes offic official ial,, used in all countries

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prot protect ected ed by la law; w; not ca capi pita tali lized zed

3. TRADE/BRAN TRADE/BRAND/PRO D/PROPRIE PRIETY TY NAME NAME – name name given by the drug drug company that developed it -

fol followe lowed d by the the sy symb mbol ol R or TM, 1st letter is capitalized

chemical name – acetylsalicylic acid generic name – aspirin trade name – aspilet

 

COMMON SOURCES /4 MAJOR SOURCES (ORIGINS) OF DRUGS:

1. Animal sources sources – from organs, organs, organ organ secretion secretion or organ cells •

Used to replace human chemical not produces because of disease or 

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genetic problems Thyroid drugs & growth hormones preparations – from animal thyroid & hypothalamus tissue (many of these preparations are now created synthetically – safer & purer)

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Insulin – from pancreas of animals (hog, cattle, sheep): thru genetic engineering – cld produce human insulin by altering E. coli bacteria making it a better product without impurities that come with animal  products

2. vegetable/pl vegetable/plant ant sources sources – roots, roots, bark, sap, sap, leaves, leaves, flowers, flowers, seeds of medicinal medicinal  plants •

digitalis from wildflower, purple foxglove, dried leaves of plant

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active principles of plants 

alkaloids – alkaline in reaction, bitter in taste, powerful in  physiologic activity

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atropine & scopolamine

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morphine sulfate, cocaine, quinine, nicotine, caffeine

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 procaine

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glycosides – digitalis

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resin – soluble in alcohol; example – colonic irritant found in laxative cascara

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gums – used in bulk-type laxatives: some used in certain skin preparations for their soothing relief 

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oils – castor oil, oil of wintergreen

3. Mineral Mineral sources sources – from free elements, elements, both both metallic metallic & non-meta non-metallic llic usually usually in in form of acids bases, salts found in food

 

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Dilute HCI – control/prevent indigestion

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Calcium, aluminum, fluoride, iron, gold, potassium

4. synthetic synthetic sources sources – many many drugs developed developed synthetica synthetically lly after after chemical chemical in plants, plants, animals, or environment have been screened for signs of therapeutic activity •

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more potent, more stable, less toxic steroids – arthritis & other diseases

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sulfonamides/chemotherapeutic agents – kill microorganism slow their growth

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meperidine HCI (Demerol)

DRUG CLASSIFICATION A. by acti action on •

Anti infectives – antiseptics, disinfectants, sterilants

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Antimicrobials, metabolic, diagnostic materials, vitamins & minerals

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Vaccine & serums, antifungals, antihistamines, antineoplastics, an tineoplastics, antacids

B. By body body syst system em •

CNS – (+)/(-) actions of neural pathways & centers: Phenobarbital

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ANS – governs several severa l bodily functions so that drugs that affect ANS will at the same time affect other systems functions

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GIT – acts on mascular & glandular tissues: leperamide

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RESPIRATORY SYSTEM – act on resp. tract, tissues, cough center, suppress, relax, liquefy & stimulate depth & rate of respiration

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Urinary system – act on kidney & urinary tract

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Circulatory system – act on heart, blood vessels, blood; metoprolol

KINDS OF DRUGS Prescription/legend drug – can be dispensed d ispensed if with prescription order; with specific name of drug & dosage regimen to be used by patient

 

non-prescription drug – can be dispensed over –the-counter/without prescription order  -

forr self fo self tre treat atme ment nt of varie variety ty of of comp compla lain ints ts

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vitami vitamin n suppleme supplements nts,, cold/cou cold/cough gh remedies remedies,, analgesi analgesics, cs, antaci antacids, ds, herbal herbal  products

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ca caut utio ions ns in us usee of of OTC OTC drug drugs: s: 1. delay delay in pro profes fessio sional nal diagno diagnosis sis & treat treatmen mentt of  serious/potentially serious condition may occur  2. symptom symptomss may be mask masked ed making making the diagno diagnosis sis more more complicated 3. clients’ clients’ health care care provider/ provider/pharma pharmacist cist should should be consult consulted ed  before OTC preparations are taken 4. labels/inst labels/instructi ructions ons should be follow followed ed carefully carefully 5. ingredients ingredients in OTC drug may may interact interact with prescribed prescribed drug 6. inactive inactive ingredien ingredients ts may may result result in adverse adverse reactions reactions 7. po pote tent ntia iall for for ov over erdo dose se 8. multiple multiple medicati medication on users users are are at risk risk as as more more medications medications are added to therapy regimen 9. interaction interactionss of medications medications are potenti potentially ally dangerous dangerous

Investigational drug – new drugs undergoing unde rgoing clinical trails Illicit/street drug – used/distributed illegally for non-medical purposes to alter mood of  feeling

**when drug is taken by mouth, it undergoes 3 phases: 1. ph phar arma mace ceut utic ic/d /dis isso solu luti tion on 2. ph phar arma maco coki kine neti tics cs 3. ph phar arma maco cody dyna nami mics cs

I. PHAR PHARMA MACE CEUT UTIC IC/D /DIS ISSO SOLU LUTIO TION N -

Drug Drug goes goes into into solut solution ion so so that that it can can cross cross the biol biologic ogic membra membrane ne

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Not Not foun found d in drug drug admi admini nist ster ered ed par parent enter eral ally ly

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1st phase of drug action of agents taken by mouth

 

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Addi Additi tive ve enh enhan ances ces ab abso sorb rbabi abili lity ty of dru drugs gs

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EXCI EXCIPI PIEN ENTS TS:: filt filter erss & iine nert rt subs substa tance ncess

Allows drugs to take on particular size & shape Enhance drug dissolution – potassium (K) --- losartan K (cozaar); sodium (Na) ---cloxacillin Na (Prostaphlin-A) 2 phases: -

Disint Disintegr egrati ation on – brea breakdo kdown wn into into smal smaller ler parts parts

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Dissol Dissoluti ution on – futhe futherr breakd breakdown own into into smal smaller ler parts parts in in GIT –  absorption; dissolved into liquid

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rate limiting: limiting: time it takes takes drug to disinte disintegrate grate & dissolv dissolvee to become available available for  for   body to absorb it

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fact factor orss affe affect ctin ing g diss dissol olut utio ion n form of drug (LIQUID VS. SOLID) – liquid more absorbed than solid,

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already in solution, rapidly available for GI absorption Gastric ph (acid vs alkaline) – acidic media (ph=1.2) faster disintegration &

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absorption 

Age – young vs elderly – inc ph. Dec absoption

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Enteric coated drugs – resist disintegration in gastric acid •

Disintegration occurs only in alkaline environment (intestine)

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Should not be crushed

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Presence of food – interfere with dissolution & absorption, enhance absorption of other drugs, may be protectants of gastric g astric mucosa

I. PHARMA PHARMACOK COKINE INETIC TICS S – action action of body body to the the drug: drug: 

Study of absoption (taken into the body), bod y), distribution (moved into various tissues), metabolism/biotransformation (changed into a form that can be excreted) & excretion (removed from the body) of drugs

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What happens to the drug when it enters the body “kinetics” movement: deals with drugs actions as it moved through the body

 

Also concerned with a drug’s onset of action, peak concentration concen tration level, &

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duration of action

4 processes involved: I. Absorption Absorption – route route of drug takes takes from from the time time it enters enters the body until it it is absorbed absorbed in circulating fluids 

Movement of drug molecules from site of administration to circulatory system

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Movement of drug particles from GIT to body fluids involve 3 processes 

Passive absorption (diffusion) – movement from higher  concentration o

 No energy required: occurs when smaller molecules diffuse across membrane

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Stops when drug concentration on both sides of the membrane is equal

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Major process through which drugs are absorbed into the body

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Active absorption – needs carrier (enzymes or protein) to move against a concentration gradient o

Energy is required: from lower concentration to higher  concentration

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Used to absorb electrolytes (i.e. sodium, potassium) & some drugs (levodopa)

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Pinocytosis – engulfs the drug to carry it across the membrane o

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Transport fat-soluble vitamins (vit.A,D,E,K)

Factors affecting absorption: •

Drug solubility – lipid soluble drugs pass readily through GI membrane, Water – soluble drugs need an enzyme or protein

 

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Local condition at site of absorption – weak acids less ionized in stomach

- - - readily pass through the SI •

Pain / stress / solid foods / fatty or hot foods – slows down gastric emptying time

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Drug concentration – drugs can take several hours/days to reach peak concentration levels (slow rate: rectal administration or sustained – release drugs)

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Circulation at site of absorption – poor circulation hampers ha mpers absorption (i.e. shock) 

The more blood vessels, the faster the absorption

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Exercise – decrease blood flow to GI – slows absorption

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Application of heat/massage increases blood flows at site

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Muscles area selected for IM administration: •

Blood flows faster through deltoid muscle (upper arm) vs gluteal muscle (buttocks)

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Gluteal muscle can accommodate larger  volume of drug than deltoid muscle

3. Metabolism – biotransformation: essential for termination of a drug’s drug’s biologic activity so can be easily excreted •

Sites of metabolism o

Liver – main organ for drug metabolism 

Through the drug metabolizing enzymes (microsomal enzymes, non-microsomal enzymes)

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1st pass effect hepatic 1st pass – some drugs do not directly go into circulation but pass thru intestinal lumen to liver via portal vein - - drug metabolized in liver into inactive form - - decrease

 

amount of active drugs - - - increase incr ease recommended dose for  oral drugs Lidocaine – extensive 1st pass – not given orally

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Plasma

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Kidneys

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Membranes of intestine

Process by which body changes a drug from its dosage form to a more watersoluble form that can then be excreted

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Can be metabolized in several ways: o

Most drugs metabolized into inactive metabolites (products of  metabolism), which are then excreted

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Other drugs converted to active metabolites – capable of exerting their  own pharmacologic action 

May undergo further metabolism or may be excreted from  body unchanged

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Prodrugs – some drugs administered as inactive drugs which don’t become active until they’re metabolized

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Permits the body to inactive a potent drug before it accumulates &  produces toxic effects

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Phases of drug metabolism: o

Phase 1: endoplasmic reticulum; introduce/expose a functional group on the parent compound (i.e. alkylation, alipathic hydroxylation, oxidation, deamination, hydrolysis h ydrolysis,, microsomal oxidases) 

Cytochrome p450 inducer – inc drug metabolism, dec  bioavailability

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Cytochrome p450 inhibitor – dec drug metabolism, inc levels of drug prolonged effect & inc toxicity

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Phase 2 – conjugation reactions that lead to formation of covalent linkage between parent compound with glucoronic acid, sulfate,

 

glutathione or acetate (glucoronidation, sulfation, acetylation); synthetic reactions •

Factors affecting biotransformation: o

Genetic – some people metabolize drugs rapidly, other more slowly

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Physiologic Liver diseases (cirrhosis), heart failure – dec circulation in liver  

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Infants – immature livers – dec rate of metabolism

Area of absorbing surface to which a drug is exposed – (+) chemical agents may destroy the drug

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Types Ty pes of transport – diffusion, active, pinocytosis

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Routes of administration – skin absorption slower than IM

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Absorption with in seconds/minutes: sublingual, IV, IV, by

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inhalation route Slower rate absorption: oral, IM SC routes

Bioavailability – consideration of highest importance in drug effectiveness & safety 

Subcategory of absorption

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% of administered drug does that reaches systemic circulation

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Oral route 89% 8 9% of drug is bound to protein •

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Diazepam, piroxicam, valproic acid

Moderately highly protein bound drugs – (61-89% bound  protein) •

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Moderately protein – bound drugs – 30-60% •

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Erythromycin, phenytoin

Aspirin, lidocaine, pindolol, theophyliine

Low protein-bound drugs - < 30% bound to protein (amikacin, amoxicillin)

DISTRIBUTION

PROTEINBINDING

BLOOD FLOW

BODY TISSUE AFFINITY

PHARMACOLOGIC EFFECT

 

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Elderlies – dec liver size, blppd flow, enzyme production - - - slows metabolism

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Environment – cigarette smoke may affect rate of some drugs o

Stressful environment – prolonged illness, surgery, injury

III. Excretion/el Excretion/elimina imination tion – removal removal of drug drug from the the body: drug drug is changed changed into inactive form & excreted by the body

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Routes: o

Kidney – main organ for drug elimination: leaves the body through urine

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Free/unbound/water soluble drugs – filtered in kidney

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Protein bound drug – cannot be filtered in kidney

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(+) kidney dose – dose must be decreased

Lungs, exocrine (sweat, salivary, salivary, mammary) glands, skin, intestinal tract

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Factors affecting drug excretion o

Urine ph – normal: 4-5.8 

Acid urine – promotes elimination of weak base drugs •

i.e. cranberry juice – dec urine ph - - - (-) elimination of  aspirin

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alkaline urine – (+) elimination of weak acid drug •

overdose aspirin - - - give Nabicarbonate – inc urine ph - - - (+) excretion of drug

 

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glomerular filtration rate (GFR) – dec GFR - - - drug excretion slowed/impaired 

can result to drug accumulation

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extent of filtration directly proportional to GFR & to fraction of  unbound drug to plasma ratio of clearance = fu x GFR - - - cleared by filtration • •

ratio of clearance < fu x GFR - - - cleared tubular  reabsorption

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ratio of clearance > fu x GFR - - - cleared by tubular  secretion

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creatinine clearance – most accurate test to determine renal function 

creatinine – excreted in kidney

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dec renal GFR – inc serum creatinine level & dec urine creatinine clearance 

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12-24 hrs urine collection & blood sample  Normal – 85-135 ml/min; elderly – 60ml/min

Renal clearance – amount of substance removed from the blood by the kidneys

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Half-life/elimination half-life (t ½) – time it takes for one half of drug concentration to be eliminated o

Short t ½ = 4-8 hrs: given several times a day (i.e. penicillin G)

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Long t ½ = > 12 hrs: given 2x or 1x / day (digoxin)

II. PHARMACODY PHARMACODYNAMIC NAMICS S – refers refers to action action of drug to to the body body 

What happens to the body in response to the drug

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Effects of drugs on the cell’s cell’s biological & physiological functions & mechanisms of action

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Interactions between chemical components of living systems & foreign chemicals including drugs that enter these system

 

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Mechanism of action: means by which a drug produces alteration in function of their action

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Drug actions: a. To replace/a replace/act ct as substitute substitute for missing missing chemical chemicalss  b. To inc or stimula stimulate te certain certain cellular cellular activiti activities es c. To depress depress/sl /slow ow cellul cellular ar activi activitie tiess d. To interfere interfere with with functioni functioning ng of foreign foreign cells cells (i.e. (i.e. invading invading microorganisms/neoplasms) – chemotherapeutic Agents

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Theories of Drug Actions a. Drug-recept Drug-receptors ors interact interaction ion – certain certain portion portion of drug molecule molecule (active (active site) selective combines with some molecular structure (reactive site) on the cell to produce a biologic effect 

Receptor site – drugs act at specific areas on cedil memb.; react with certain chemicals to cause an effect with in cell

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“lock & key theory” – specific chemical (key key)) approaches a cell membrane & finds a perfect fit (the ( the lock) at receptor site –  affects enzymes system within a cell – produce certain effects

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Specificity – selectivity theory

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Drug action may be: •

Agonists Agonis ts – drugs that produce a response o

insulin reacts with specific insulin receptor site to change cell membrane permeability pe rmeability - - - (+) movement of glucose into cell

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competitive compe titive antagonist antag onist – act with receptor recepto r sites to block  normal stimulation producing no effect o

curare – use on spear in Amazon to paralyze  prey & cause death: occupies receptor sites for  Acetylcholine (needed in muscle contraction & movement) - - - prevents nerve stimulation causing paralusis

 

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noncompetitive antagonist - prevent reaction of  another chemical with different receptor site on that cell

 b. drug-enzym drug-enzymes es interaction interaction – interf interferes eres with with enzyme enzyme systems systems that act act as catalyst from various chemical reations 

enzyme systems – cascade effect; one enzyme activating another - - - causing cellular reaction

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if single step in one of enzyme enz yme system is blocked – normal cell function is disrupted

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ex: acetazolamide (diamox) – diuretic that block carbonic anhydrase – alters H+ & H2O exchange exchang e systems in kidneys & eye

c. nonspecific nonspecific drug interact interaction ion – act by biophysical biophysical means means that that do not affect cellular enzymatic reactions d. selective selective toxicity toxicity – all chemothe chemotherapeut rapeutic ic agent would act act only on 1 enzyme system needed for life of a pathogen or neoplastic cell & will nor affect healthy cells 

ex: penicillin

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unfortunately most of it cause destruction of normal human cells

Drug response may be: 1. primary primary – always desirable desirable / physiologi physiologicc effects effects 2. second secondary ary – desira desirable ble or or undesi undesirab rable le ex: diphenhydramine (benadryl) – 1 st effect: antihistamine, treat symptoms of  allergy; 2: CNS depression - - - drowsiness desirable: when given at bedtime: undesirable: when client is driving

Classification of drug action: 1. rapid – few seconds seconds to minutes minutes (IV, (IV, SL, inhalation) inhalation) 2. intermediate intermediate – 1-2 hrs after after administrat administration ion (IM, (IM, SC)

 

3. Delayed/sl Delayed/slow ow – several several hrs hrs after administrat administration ion (rectal, (rectal, oral)

Parameters of Drug Action: 1. onset of action action – latent latent period: period: interval interval between between time time drug is is administer administered ed & 1st sign of its effect •

time it takes to reach the minimum effective e ffective concentration (MEC) after a drug is administered

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time from drug administration to 1st observable effect _T0 – T1)

2. duration duration of action action – period period from from onset onset until drug effect effect is is no longer longer seen seen •

length of time the drug exerts ex erts pharmacologic effect (T1 – T3)

3. peak action action – drug drug reaches reaches its highest highest blood / plasma plasma concentrati concentration on (T0 – T2)

Termination of action – point from onset at a t which drug effect is no longer seen Minimal effective concentration – lowest plasma concentration that produces the desire effect Peak plasma level – highest plasma concentration attained from a dose Toxic level – plasma concentration at which a drug produces adverse effects Therapeutic range – range of plasma concentration that produces the desire effect without toxicity (range between minimal effective concentration & toxic level) Loading dose – bolus of drug given initially to attain rapidly a therapeutic plasma concentration •

large initial dose; when immediate drug response is desired

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given to achieve a rapid MEC in the plasma

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i.e. digoxin - - - requires LD

Maintenance dose – amount of drug necessary to maintain a steady therapeutic plasma concentration Dose response – relationship between minimal vs. maximal amount of drug dosed needed to produce desired drug response •

i.e. some clients respond to lower drug dose d ose while others need a high dose

 

Maximal efficacy (maximum drug effect) – all drugs give a maximum drug effect (maximal efficacy) •

i.e. simvastatin 40mg vs rouvastatin 10mg

Drug-response relationship: Biologic half-life (t1/2) = time required to reduce to ½ amount of unchanged drug d rug that is in the body •

short t1/2 drugs need to be administered more often than one with a longer t1/2

Lethal dose (LD50) – dose lethal to 50% of animals tested Effective dose (ED50) – dose required to produce produ ce therapeutic effect on 50% animals tested Therapeutic index (TI) – ratio between LD50 and ED50; the closer the ratio is to 1, the greater the danger involved in giving the drug to humans •

estimates the margin of safety of a drug through the use of a ratio that measures the effective (therapeutic or concentration) dose (ED) in 50% of persons/animals (ED50) & lethal dose in 50% of animals (LD50) TI=LD50/ED50

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low therapeutic index: narrow margin of safety; might need to adjust drug dose & plasma drug levels need to be monitored

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high therapeutic index: wide margin of safety less danger of producing produc ing toxic effects

4 Categories of Drug Action: 1. stim stimul ulat atio ion/ n/de depr pres essi sion on •

stimulation – inc rate of cell activity/secretion from the gland

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depression – dec cell activity & function of a specific organ

2. replacement replacement – replaces replaces essenti essential al body compounds; compounds; i.e. i.e. insulin insulin 3. inhibition/ inhibition/killi killing ng of organi organism sm – interfere interfere with with bacterial bacterial cell growth growth ; i.e. antibiotic antibioticss

 

4. irritation irritation – i.e. i.e. laxative laxative – irritate irritate inner inner wall wall of colon - - - inc peristals peristalsis is - - - inc defecation

Drug potency – relative amount of drug required to produce desired response •

also used to compare a drug

dose response curve – graphical representation of relationship between dose of drug & response it produces •

low dose – low response

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dosage increased produce slight increase response, as dose further increases, drug response increases markedly, at certain point however, inc dose yield little or no inc in response - - - drug have reached Maximum Effectiveness

Factors Affecting Affecting Dose Response Curve: -

nurse nurse must must be be aware aware that that human human factor factor has has trem tremendo endous us infl influenc uencee on what actually happens when it enter the body

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no 2 peop people le react react in exact exactly ly the the same same way way to to any given given drug drug

1. weight heavier heavier patient patient – large largerr dose to get get therapeutic therapeutic effect effect (more (more tissue tissue to  perfuse & inc receptor site in some reactive tissues) -

dec we weigh ghtt – de dec do dose

2. age – children children (immune (immune system system for handling handling drugs) drugs) & older older adults adults -

older older patien patients: ts: lless ess abso absorpt rption ion,, distrib distributi ution on between between fewe fewerr plasma plasma

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 proteins & less efficient perfusion: geriatric dosages nurse nurse shoul should d monitor monitor closel closely y for desi desired red effec effects ts (may (may adjus adjustt dose) dose)

3. toxicity 4. pharmacogenet pharmacogenetics ics – effect effect of a drug drug action that that varies varies from a predicte predicted d drug response because of genetic factors or hereditary he reditary influence •

 people have different genetic makeup – do not always respond identically to a drug dosage or planned drug therapy

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ex: African – Americans do not respond as well as whites to some classes of  antihypertensive medications

5. rout routee of ad admi mini nist stra rati tion on

 

6. emot emotio iona nall fac facto tors rs 7. pre-ex pre-exist isting ing disea disease se state state – liver liver disea disease se 8. drug history history – drug interactio interaction n – synergi synergistic/ stic/excret excretion ion 9. tolerance 10. cumulative cumulative effect effect 11. drug- drug interact interaction ion 12. BMR – inc BMR – inc drug metaboli metabolism sm & excretion excretion

Drug Interaction 1. Additive Additive effect effect – 2 drugs drugs with simila similarr actions actions are taken taken for a doubled doubled effect effect (desirable/undesirable) (1 + 1 = 2) •

Ibuprofen + paracetamol + added analgesic effect

2. Synergist Synergistic ic – combined combined effect effect of 2 drugs drugs is greater greater than than sum of the the effect effect or each drug given alone (1 + 1 = 3) •

Aspirin + codeine = greater analgesic effect

3. potentiatio potentiation n – a drug that that has no effect effect enhances enhances the the effect effect of a 2nd drug (0 + 1= 2) 4. Antagonisti Antagonisticc – one dr drug ug inhibits inhibits the the effect effect of another another drug drug (1 + 1 = 0) •

Tetracycline + antacid = dec absorption of tetracycline

SIDE EFFECTS •

Physiologic effects not related to desired drug effects

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All drugs have side effects 

Desirable: diphenhydramine (Benadryl) at bedtime – s/e: drowsiness

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Undesirable

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Result mostly from drugs that lack specificity

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Might be used interchangeably with adverse reactions

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 Not a reason to discontinue drug therapy

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 Nurse’ss role: teach clients  Nurse’ c lients to report any side effects

 

ADVERSE REACTIONS •

More severe than side effects

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Range of untoward effects (unintended, occurring at normal doses) of drug that cause mild-severe side effects: anaphylaxis (cardiovascular collapse)

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Always undesirable Must always be reported & documented because they represent variances from planned therapy. therapy.

TOXIC EFFECT/TOXICITY •

Can be identified by monitoring the plasma (serum) therapeutic range of the drug

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 Narrow TI (aminoglycoside & antibiotics) – therapeutic range is monitored When drug level exceeds therapeutic range, toxic effects are likely to occur  from overdosing or drug accumulation.