Download as pdf or txt
Download as pdf or txt
You are on page 1of 18

PHARMACOLOGY

BRANCHES OF PHARMACOLOGY, DRUG NAMES, COMPUTATIONS


PRELIM |2N Ma’am Soraya
Transcribed by: Ochave, Daisy Rey C.

TOPIC OUTLINE  Severe adverse effects


(1) Branches of Pharmacology  Stem from
(2) Drugs  Single large dose
(3) Nursing Process in Pharmacology  small repeated dose
(4) Factors Influencing Drug Action  slow metabolism
(5) Systems Model in Nursing Practice
SITE OF ACTION
 The location within the body where the drug exerts its therapeutic
BRANCHES OF PHARMACOLOGY effect
 abdominal pain = buscopan
BRANCHES OF PHARMACOLOGY
PHARMACOKINETICS  Study of the process of drug absorption, RECEPTOR SITE
distribution, metabolism and excretion  Specific location where the drug attaches itself
(ADME) – movement of drug
 Study of the biochemical and physical  lock and key – initiation of effects after treatment
PHARMACODYNAMICS
effects of drugs on the living organisms  produce action by finding receptor site
 biochemical – inside the body  After attachment to a receptor site a drug may either initiate a
 Physical – MODA
response or prevent a response from occurring
PHARMACOTHERAPEUTICS  Also known as clinical pharmacology, is
general term covering the use of drugs  Receptor cells – composed of Proteins found in the cell membrane
 Not the main responsibility of the nurse
TOXICOLOGY  represents the study of poisons, including CARCINOGENITY
adverse effects of the drug on living
organisms
 Ability of the drug to induce living cells to mutate and become
slow metabolism cancerous
PHARMACOGNOSY  deals with natural drug sources (plant,  chemotherapy
animals, minerals or their products)  Normal cells -> cancer cells

DRUGS TERATOGENICITY
 A substance or mixture of substances used in the diagnosis, cure,  Drug that induces birth defects; causing abnormal development of the
treatment or prevention of disease fetus in the utero

TREATMENT SOURCES OF DRUGS


 Remedy to a health problem PLANTS  Digitalis (purple foxglove)
 Simple manifestations  vincristine (periwinkle)
 Allergy = anti-histamine  morphine (opium poppy)
ANIMALS/ANIMAL  insulin – from pigs and cows
 analgesic = pain  Vaccine- killed attenuated microorganism from horse
 hypertensive = blood pressure PRODUCTS
SYNTHETIC  uses genetic engineering to alter bacteria to produce
chemicals that are therapeutic and effective
CURE VERSION
INORGANIC  these are salts of various elements which can have
 Substance that ends the medical condition therapeutic effects in the human body and are used to
 complete restoration of health COMPOUNDS treat various conditions
 intravenous administration = increase in effectivity  aluminum (antacid for hyperacidity)
 Antibiotics  fluoride (prevention of dental carries and
osteoporosis)
MINERALS AND  Iron
MEHCHANISM OF ACTION
MINERAL
 Explains how a drug produces its effect
PRODUCT
CHEMICAL  Natural sources – insulin; attapulgite (clays);
SIDE EFFECTS laxatives, cardiac drugs, cancer chemotherapeutic drugs
SUBSTANCES
 A secondary, typically tolerable effect/s of a drug or therapy (plants)
MADE IN  Produced semi-synthetically – antimicrobial; human
 actions other than intended therapeutic effects resulting from the
LABORATORY insulin chemically modified
pharmacological action of the drug  Biotechnology – manipulations to permit large-scale
 antihistamine = drowsiness industrial production of complex natural substances or
 usually happens after a few minutes genetically altered biological substances

ADVERSE EFFECTS CLASSFICATION OF DRUGS


 Negative actions resulting from the pharmacological action of a drug,  Drugs classified according to their effects on particular body systems,
among other factors their therapeutic uses, and their chemical characteristics
 Long term effect  E.g. Bronchodilators, anti-histamine, antihypertensives
 Untolerable manifestation (can’t walk, etc.)
 Adverse effects = hold drug CLASSIFICATION OF DRUGS
 Adverse effects = difficulty in breathing, hypersensitivity, increase in PRESCRIPTION  Prescription (℞) is an order (often in written form) by
Cardiac rate DRUGS a qualified health care professional to a pharmacist or
other therapist for a treatment to be provided to their
 Comorbidities – disorders in the body (kidney, etc.) patient.
 Drugs which bear on their labeling the prescription
TOXICITY legend
 Quantity of being poisonous
 Caution – law “prohibits dispensing without  provide valuable background a basic information to help in the understanding of
prescription” pharmacology; it includes related nursing interventions and areas of health
 Medical prescription (Rx) – written order by a teaching
qualified health care professional to a pharmacist or other  Drug facts and comparisons – include comparison of drug cost, patient
therapist for a treatment to be provided to their patient information, section and preparation and administration guidelines
 Theories about the origin: Eye of Horus & Symbol of (5) NURSING TEXTBOOKS
Jupiter  provide valuable background an basic information to help in the understanding
 The symbol Rx – prescription or to write before a drug of pharmacology; it includes related nursing interventions and areas of health
can be prepared, “pre” & “script” teaching
COMPONENTS (6) JOURNALS
 Medical letter – monthly review of new drugs, drug classes, and specific
(1) Drug name
treatment protocols
(2) Drug Dosage
(7) INTERNET INFORMATION
(3) Route of Administration
(4) Frequency and duration of Administration
(5) Signature of the physician
DRUG USES
(1) Symptomatic treatment (relieve)
(2) Preventive – avoid disease
(3) Diagnostic Drugs
(4) Curative
(5) Health Maintenance Drugs
(6) Contraceptive Drugs

DRUG EVALUATION
PURPOSES
 Also known as over the counter drugs  Determine whether they have the presumed effects in living tissue
NON-
 Legally acquired without a prescription  To evaluate any adverse effects
PRESCRIPTION
DRUGS
INVESTIGATIONAL  Drugs that are subjected to clinical studies in order to DRUG EVALUATION PROCESS
evaluate the usefulness of the drug in treating the disease  Using human volunteers to test the drug
DRUGS for which it is claimed to be effected
PHASE 1
 They are informed of the risk
 Used and/or distributed illegally  Paid for participation
 Heroin, stimulants, cocaine  Allows clinical investigators to try the drug in patients which have the
 Subjected to clinical studies in order to evaluate the
PHASE 2
INVESTIGATIONAL disease
usefulness of the drug in treating the disease for which it
DRUGS is claimed to be effected
PHASE 3  Use of drugs in vast clinical market
 Prescribers are informed of all the known reactions & precautions
required for it’s safe use
 FDA
DRUG NAMES  evaluates after Phase 3
CHEMICAL NAME  a systematically derived name which
identifies the chemical structure of the drug;
shows the exact chemical constitution of the BRAND DRUGS VS. GENERIC DRUGS
drug and exact placing of atoms  Protected by a patent
 Eg. N- Acetyl-para-aminophenol
BRAND
 Supplied by single company
GENERIC  given before drug becomes official; reflects DRUGS  Marketed under a brand name
some important pharmacological or chemical  Drug prices are decided by the pharmaceutical companies
NAME/NONPROPRIETARY characteristic of the drug
GENERIC  Low cost version of brand drugs
NAMES Eg. acetaminophen  Produced by generic companies
BRAND NAME  followed by the symbol ®; indicates the DRUGS  Are as safe and effective as brand drugs
name is registered, that its use is restricted to  Drug prices are decided by the pharmaceutical companies
the owner of the drug, who is usually the
manufacturer of the product
GENERIC
 Eg. Tylenol VS GENERIC VS BRANDED
BRANDED (1) Dosage may be identical
EXAMPLE OF A DRUG NAME: (2) Drug formulations are not always the same
 Chemical name: 4-Thia-1-Azabicyclo [3.2.0] heptane-2-carboxylic (3) The two drugs may have different inert
acid, 6 [(aminophenylacetyl) amino]-3,3- dimetyl-7- oxo-, [25-[2,- ingredients
5,6(S*)] ]
 GENERIC NAME: AMPICILLIN
 OFFICIAL NAME: AMPICILLIN, USP
 BRAND NAMES: AMCILL, PRICIPEN, POLYCILLIN
NURSING PROCESS IN PHARMACOLOGY
1. ASSESSMENT
 Forms the basis on which care is planned, implemented & evaluated
SOURCES OF DRUG INFORMATTION  Subjective Data
(1) PHARMACOPEIOA  Objective Data
 is the official source of drug information which contains a list of products used
in medicine, with descriptions of the products, a chemical test for determining for  DRUG HISTORY
identity and purity  to evaluate the patient’s need for medication
(2) FORMULARY  to obtain current and past use of medicines (OTC medicines,
 collection of formulas and prescription prescribed medicines, herbal products, illicit drugs)
(3) PACKAGE INSERT
 to identify problems related to drug therapy
 contains all the chemicals and study information.
(4) REFERENCE BOOKS  to identify risk factors in drug therapy\

Transes by: Daisy Rey Ochave | Template by: camillexcar 2


 Cultural Considerations
2. NURSING DIAGNOSIS (5) Check For
 Response To Medications; Observation For S/S Or The Development Of
 Made based on the analysis of assessment data Adverse Effects; Ability To Receive Pt. Education & Self- Administer Meds;
 May be ACTUAL or POTENTIAL Potential For Compliance
 made based on the analysis of assessment data. May be ACTUAL or
POTENTIAL 5. EVALUATION
 Knowledge deficit – about drug action, administration & SE  is an ongoing process that assesses response
 R/T cultural/language barrier or speech articulation problem
 Risk for injury R/T forgetfulness EVALUATION PROCESS
 Ineffective therapeutic regimen management
(1) the effectiveness of the medication prescribed
 R/T lack of finance
(2) observation of signs and symptoms of recurring illness
(3) development of the side/ adverse effects
LIST OF NURSING DIAGNOSES (4) effectiveness of the health teaching or client education
(1) KNOWLEDGE DEFICIT about drug action, administration &
SE SAMPLE NURSING PROCESS
(2) R/T cultural/language barrier or speech articulation problem
(3) RISK for INJURY R/T forgetfulness
(4) INEFFECTIVE THERAEUTIC REGIMEN MANAGEMENT
(5) R/T lack of finances

3. PLANNING
 is characterized by goal setting or expected outcomes which represent
patient goals and state of desired patient behaviors of responses that
should result from the nursing care

INCLUDED ARE
(1) identification of the therapeutic intent for every medication
(2) side effects to be expected and reported
(3) identification of the recommended dosage and route of administration
(4) scheduling of the administration of medication
(5) teaching the patient to keep written records of his responses
(6) additional teaching as needed: eg. techniques of administration, proper storage of
medication

CLINICAL TEACHING EDUCATION


INCLUDES
(1) Administration of drugs
(2) Assessment of drug effectiveness
(3) Self-administration
(4) Diet
(5) Side effects
(6) Cultural considerations

4. INTERVENTION/IMPLEMENTATION
 NURSING ACTIONS necessary to accomplish GOALS or expected
outcomes

NURSING INTERVENTIONS
(1) Dependent Nursing Action
 assist in the admission; orders for diagnostic test; giving medication to the client
(2) Interdependent Nursing Action
 calculations, monitoring effects, establishing nsg interventions or patient’s
education
(3) Independent Nursing Action
 verifies orders, correct transcription of the drug order, makes sound professional
judgment concerning class of drug, therapeutic intent, usual dosage, patent’s
ability to tolerate drug
(4) Client Teaching And Education
 Administration Of Drug
 Assessment Of Drug Effectiveness
 Self-Administration
 Diet
 Side Effects

Transes by: Daisy Rey Ochave | Template by: camillexcar 3


DRUG COMPUTATIONS

Transes by: Daisy Rey Ochave | Template by: camillexcar 4


PHARMACOLOGY

CEPHALOSPORINS
PRELIM |2N Ma’am Soraya
Transcribed by: Ochave, Daisy Rey C.

TOPIC OUTLINE  Cefadroxill, cefazoin, cephalexin

(1) Cephalosporins BACTERIA SUSCEPTIBLE


(2) Pharmacokinetics and Pharmacodynamics  Proteus mirabilis
 Escherrechia coli
(3) Cephalosporins Side Effects  Klebsiella pneumonia [strepto & staph]
(4) Education
2ND GEN  Broader spectrum against gram (-) bacteria (diminished
activity against gram (+) bacteria
“FO”/”FU”  not affected by B-lactamase
CEPHALOSPORINS  Cefuroxime
 Group of antibiotics chemically and pharmacologically related to the  Cefofetam, Cefonicid , Cetaclor – CEFO - syrup given per
penicillin orem sa mga bata, Treats sinusitis
BACTERIA SUCEPTIBLE
 Same with penicillin which are affected by beta-lactamses (second  PEcK + HEN
to the penicillin)  Haemophilus influenza
 Both contain beta-lactamase  enterobacter aerogenes
 Cephalosporins more resistant compared to penicillin  Neisseria gonorrhea/meningitiis
3RD GEN “FT”  Broader gram (-) activity against gram (+) bacteria than 2nd
 First introduced in 1960s; FUNGUS (cephalosporin acremonium) gen
discovered in seawater (1948)  Not affected by B-lactamase
 Effective agains gram + and gram – bacteria  Ceftriaxone, ceftrazidime, cefixime, cefdinir
 Resistant to beta-lactaomase BACTERIA SUSCEPTIBLE
 1960 – cephalosporins used with clinical effectiveness  Serratia marcescens (Hospital infections, gram negative)
 From fungus cephalosporin 4TH GEN “LE”  Greater action than agains (-) and minimal action against
 Disovered from sewerage outlet (sa ilalin ng dagat) gram (+) organisms
 Resistant to most B-lactamases
 Bactericidal or bacteriostatic depending upon  cefepime (Maxipime)
 Susceptibility of the organism being treated  Penetrate the Blood brain barrier and the go through the
 Get the culture and sensitivity testing to identify what kind of cerebrospinal fluid
microorganism is present in the infection of the patient
BACTERIA SUCEPTIBLE
 Dose used  PEcK
 Increase in dosage = bactericidal effect  Staphylococci & Pseudomonas aeruginosa
 Decrease in dosage = bacteriostatic effect
 Tissue concentration of the drug Habang naga saka ang broad spectrum, mas mahal pud siya
 Rate of which bacteria are multiplying
 superinfection of mutant bacteria = have bactericidal effect CEPHALOSPORINS SIDE EFFECTS
ORAL
PHARMACOKINETICS AND  GI: Flatulence, NAVDA (Bloody stool – {stop}
PHARMACODYNAMICS  Best administered with food or milk – increase absorption
PHARMACOKINETICS  Best to be taken on an empty stomach
 [A] P.O. well absorbed (GI Tract)  if with gastric irritation – take with food
 [D] PB (Protein bound) – 75% - 85% (Highly protein bound)
 Must not have hypoalbumenia OTHERS
 [M] SHL – t ½ = 1.5 – 2.5 hr  Fever, rash, pruritus, headaches, vertigo (CNS symptoms) =
 [E] – unchanged in urine 60%-80% hyperssensitiviyy rxn {stop}
 IV/IM
PHARMACODYNAMICS  Prolonged/high doses = phlebitis or thrombophlebitis
 management: use small gauge needle, large veins, alternate
PHARMACODYNAMICS
infusion site
INTRAMUSCULAR ONSET
 Rapid
PEAK ADVERSE REACTIONS
 0.5-2 hours  Nephrotoxicity – renal failure
DURATION
 Unknown  Superinfections
PER OREM ONSET  Anaphylaxis
 Rapid
PEAK
 0.5-1 hr
DRUG INTERACTIONS
DURATION  Cefmetazole (1st) – Disulfuram like interaction
 Unknown  Cefoperazone (3rd) + Alcohol = flushing, dizziness, headache, N/V,
INTRAVENOUS ONSET Muscular cramps
 Immediate
PEAK
 Moxalactam – Chest pain, palpitions, dyspnea, == may lead to
 5-15 hr extreme CV collapse, convulsion and death
DURATION  With aminoglycosides/vancomycin === increased nephrotoxicity
 Unknown  With anticoagulant or thrombolytics/NSAIDS (Non-Seroidal anti
inflammatory drugs) – increased risk of bleeding
CLASSFICATION OF CEPHALOSPORINS  {monitor for blood loss}
1ST GEN  Effective against gram (+) and gram (-) bacteria (BROAD
SPECTRUM)
“TA”/”PHA”  Can be destroyed by B-lactamase produced by bacteria
[PEcK]
 : RI, Skin, GU, bone, my infections
EDUCATION
 Administer on an empty stomach
 Refrigerate oral suspension
 False urine test for glucose with use of clinitest tab or Benedict’s
solution, therefore use blood to check for glucose level

Transes by: Daisy Rey Ochave | Template by: camillexcar 2


PHARMACOLOGY

DRUG INTERACTION AND PRINCIPLES OF DRUG INTERACTION


PRELIM |
Transcribed by: Ochave, Daisy Rey C.

TOPIC OUTLINE  change in color


 Toxic for the patient
(1) Drug Interactions  ampicillin + gentamicin = amp.
(2) Principles of Drug Action Inactivates gentamicin
 Change in the physical property of
the medications
DRUG INTERACTIONS DISPLACEMENT  The displacement of the first drug by a
 Drug interaction is a reaction between two (or more) drugs or between second drug increases the activity of the
first drug
a drug and a food, beverage, or supplement. Taking a drug while having  Warfarin + valproic acid = increased
certain medical conditions can also cause a drug interaction. For anticoagulant effect
example, taking a nasal decongestant if you have high blood pressure
may cause an unwanted reaction OTHER TERMINILOGIES
 A drug interaction is said to occur when the action of one drug is  Expected response
DESIRED ACTION
altered by the action of another drug  Effects which result from
SIDE EFFECTS
pharmacological effects of the drug
DRUG INTERACTIONS  Actions other than intended therapeutic
effects resulting from the pharmacological
 Caffeine/coffee – causes arrhythmia
action of a drug
 Taking 5 medications  A range of undesirable effects
ADVERSE EFFECTS
 drug to drug medications -> might be adverse effect (unintended and occurring at normal
doses) of drugs that cause mild to severe
reactions
DRUG INTERACTIONS ARE ILLICITED IN TOXICITY  Severe adverse effect; quality of being
poisonous
TWO WAYS CARCINOGENICITY  Ability of the drug to induce living
(1)  Agents that when combined increase the action of one or both drugs cells to mutate and become cancerous
(2)  Agents that when combined, decrease the effect  Chemotherapy
TETRATOGENICITY  Drug that induces birth defects;
causing abnormal dev. Of a fetus in utero
DRUG INTERACTIONS PHOTOSENSITIVITY  Skin reaction d/t exposure to sunlight
 2 drugs with similar actions are taken  Advice patients to wear long sleeves,
ADDITIVE EFFECT have umbrella
for a doubled effect
 2 drugs must have the same effect  Can lead to contact dermatitis (sugat
 propoxyphene + aspirin = added sugat ang mukha)
analgesic effect HYPERSESITIVITY/ALLERGIC  Hypersensitive response of the client’s
immunological system in the presence of
 Propoxyphene = for pain in the liver REACTION a drug
 aspirin pain reliever
 caffeine + paracetamol = terrible  In every medication/procedure, always
headache due to kainit, dehydration ask if the patient has any allergies or not.
IDIOSYNCRATIC REACTION  may occur when the client is first
Aspirin is not anymore considered for exposed to the drug; result of abnormal
pain reliever. It is a blood thinner reactivity to a drug caused by genetic
which is prone to bleeding tendencies differences between the client and no
 The combined effect of 2 drugs is > the reacting individuals
SYNERGISTIC EFFECT  Severe hypersensitivity
sum of the effect of each drug given alone
 Helping out the other drug to be  Stem’s Johnson’s Disease
effective (they are different drugs)  Start Clinical tests of medication
 Ampicillin + sulbactam = prolonged
action of the antibiotic
 Ampicillin is an antibiotic PRINCIPLES OF DRUG ACTION
 subactan is a synthetic antimicrobial
 subactan protects the other drug to
avoid resistance in the bacteria PRINCIPLES OF DRUG ACTION
 1 drug interferes with the action of DRUGS DO NOT  Alters only existing cells except chemotherapy
ANTAGONISTIC EFFECT
another CREATE NEW  Antibiotics
(ANTIDOTE)  One drug becomes ineffective CELLULAR FUNCTIONS  Alters microorganism
 Known as to be the antidote (panlaban BUT RATHER AFTER  Slows the growth of microbial organism
sa toxicity na mangyari) EXISTING ONES  Antibiotic slows the growth and/or reproduction of
 Tetracycline + antacid = decrease microbial organisms
absorption of the tetracycline Drug action is relative to the physiological state which
 Vitamin K + warfarin existed when the drug was administered
 Heparin + protamine SO4  Treatments done
 1 drug inhibits the met. /excretion of a  alleviating symptoms
INTERFERENCE
2nd drug, causing increase activity of the
second drug EXAMPLE
 Can inhibit metabolism  An anti-hypersensitive agent is successful in the
 Wastes cannot be exerted/cleansed patient’s blood pressure is lower during therapy than
 Cumulative effect before therapy
 Dili dyud dapat isabay DRUGS MAY INTERACT  The relationship between a drug and a receptor is
 Probenecid + spectinomycin = WITH THE BODY IN similar to that between a key and a lock
prolonged antibacterial activity from SEVERAL DIFFERENT
spectinomycin due to blocking renal WAYS ALTER THE CHEMICAL COMPOSITION OF A
excretion by probenecid BODY FLUID
 Should not be mixed together or  Antacid – for the acidity of the stomach
INCOMPATABILITY  Laxatives – for defecating
administered at the same site
 Strong coffee causes constipation so drink lots of
SIGNS water
 Precipitate/clouding
ACCUMULATE IN CERTAIN TISSUES BECAUSE
OF THEIR AFFINITY FOR A TISSUE
COMPONENT
 Iron supplement makes our teeth black
 When a child is give a lot of tetracycline, the child’s
teeth will turn yellow due to the yellow composition of
tetracycline
 Anesthesia to lower the nerve for numbness
BY FORMING A  lock and key method
CHEMICAL BOND WITH  Once the drug finds its receptor site, the drug will then
SEPCIFIC RECEPTORS go to the part of the body
WITH IN THE BODY  Antacids for heart burn
DIFFERENT DRUGS  Hormones
WHOSE MOLECULES  Insulin, from the outside source madali lang malocate
PRECISELY FIT INTO A ang receptor site since the insulin knows where to go
GIVEN RECEPTOR
ELICIT; THOSE WHICH
DO NOT PERFECTLY
FIR PRODUCE ONLY A
WEAK OR NO REPONSE
AT ALL
MOST DRUGS HAVE  Lock and Key
SEVERAL DIFFERENT
ATOMS WITHIN EACH
MOLECULE THAT
INTERLOCK INTO
VARIOUS LOCATIONS
ON A RECEPTOR
DRUGS THAT  Drugs that in interact with a receptor to stimulate a
INTERACT WITH A response are known as agonists
RECEPTOR  Drugs that interact with a receptor but do not stimulate
a response are called antagonists

ONCE DRUG  ADME


ADMINISTERED, ALL  Absorption
DRUGS GO THROUGH  Distribution
FOUR STAGES  Metabolism
 Excretion

AGONIST VS ANTAGONIST
 Agonist – Antagonist drugs exert some agonist as well as antagonist
action

AGONIST
 Drugs which interact with a receptor to produce a response

ANTAGONIST
 Drugs interact to inhibit or prevent the action of an agonist

EXAMPLE
 depression of CNS by narcotic agonists – morphine reversed by
Narcotic Antagonist – Narcan (naloxone)
 morphine has narcotic antagonist which is known to be an antidote,
narcan (naloxone)
 Antagonist is common with anesthesia

PRINCIPLES APPLIED TO PHARMACOLOGY

PRINCIPLES OF DRUG ACTION


C Check why the medication is given and know the classification of the drug
H How will you know if the medication is effective? What are your assessment
parameters in monitoring the effects of the drug?
 check for baseline data
 take cues
 check nausea or vomiting
E Exactly what time should the medication be given
C Client teaching tips. What are the therapeutic and side effects of the medication
K Keys to giving it safely. You should be able to identify interventions to counteract
the adverse effects of the drug

Transes by: Daisy Rey Ochave | Template by: camillexcar 2


PHARMACOLOGY

INTRODUCTION TO ANTIBIOTICS
PRELIM |2N Ma’am Soraya
Transcribed by: Ochave, Daisy Rey C.

TOPIC OUTLINE  Interferes with CHON synthesis w/o affecting normal cells
= prevent normal growth and reproduction (host defenses
(1) Anti-bacterial eradicate organism)
(2) Pharmacokinetics of antibacterial
DRUGS
(3) Pharmacodynamics  Aminoglycosides
(3) Resistance to antibacterial  Tetracycline
(4) Antibiotic Combination  Erythromycin
(5) Categories of Antibacterials  Lincomycin
INHIBITION OF EFFECT
 Bacteriostatic
Drugs face numerous obstacles in reaching their target cells. For SYNTHESIS OF  Interferes with steps of metabolism of the cell
most medications that we give to the patient, the greatest barrier is BACTERIAL  Essential for normal function and/or growth of bacterial cell
crossing the many membranes that separate the drug from its target RNA AND DNA (Both)
cells. We always have to consider that drugs would need to be in a DRUG
solution first so that it can be absorbed properly by the body  Sulfonamides
 In the environment, we are surrounded with microorganisms  INH
 Rifampicin
 Bacteria produces toxins that causes cell lysis/ cell death
 Bacteria invades the cells and targets the nucleus
 Check the frequency because antibacterials have to be precise kasi ang BACTERIA CELL
kalaban ng katawan ay microorganism
 Stock desired = doctor’s order
 Stock on hand = what you have
 Body weight of the patient can vary the medication dose
 SD X SH = quantity

ANTI-BACTERIALS
ANTIMICROBIAL/ANTIBACTERIAL
 Inhibit the growth of or kill bacteria/microorganisms
 There are 10 types of antibacterials
 Anti = Against
 Penicillin is the oldest type of antimicrobial
 Bactericidal – antimicrobial has the capacity to kill the bacteria
 More dosage compared to bacteriostatic
 Causes cell lysis
 Bacteriostatic – inhibit the growth of the microorganism
 Prevents the normal growth and reproduction
 Bacteriostatic becomes bactericidal once the dosage increases

ANTIBIOTICS
 Chemicals that are produced by 1 kind of microorganism that inhibits MECHANISM OF ACTION
the growth of or kills another
 Antimicrobial and antibiotic can be used interchangeably

DIFFERENT MECHANISMS OF ACTIONS OF


ANTIBACTERIALS
INHIBITION OF EFFECT
 Bactericidal
CELL WALL  Enzyme breakdown of cell wall
SYNTHESIS  Inhibition of the enzyme in the synthesis of the cell wall =
loss of structural integrity of the bacterial cell and death of the
organism

DRUG
 Penicillin
 Cephalosporin
 Vancomycin
ALTERATION EFFECT
 Both
IN
MEMBERANE
 Membrane permeability is increase PHARMACOKINETICS OF ANTIBACTERIAL
 Loss of cellular substances causes lysis of cell = permitting
EPRMEABILITY leakage of intracellular components = bactericidal PHARMACOKINETICS – WHAT THE BODY DOES TO THE
DRUG (ANTIMICROBIAL)
DRUG  Must only penetrate the bacterial cell wall in sufficient concentration;
 Amphoterin B must have affinity to the binding sites
 Nystatin
 Polymyxin  Binding sites are for bacteria
INHIBITION OF EFFECT  time drug remains at the binding site = increase effect; controlled by
PROTEIN  Bacteriostatic distribution, half-life & elimination
SYNTHESIS
 most are not highly chon bound = longer half- life --greater  development of antibiotic resistant disablers
concentration at binding sites  Disable antibiotic-resistant mechanism in the bacteria
 mostly eliminated from the body through urine after the 7th half-  Not an antibiotic but a compound
life  Shuts off the valve in the pathogen’s DNA to avoid replication
 The longer the half-life, the greater the concentration  bacterial vaccine – against pneumococcus – pneumonia & meningitis
 pharmacodynamics drug concentration & affinity is needed to achieve  Injections usually for the children
mec necessary to halt growth of microorganism.  flu vaxx
 constant increase drug concentration above mec =bactericidal effect  prevent antibiotic abuse
 Prescription of doctor
PHARMACODYNAMICS  Di mag skip ug dose
 Drug concentration and affinity is needed to achieve MEC necessary  normally 7 days kahit mayo na on the third day, tulo pa din
to halt growth of microorganism according to prescription
 Affinity to its receptor site  compliance and multi antibiotic Therapy
 Minimum effective concentration
 Constant increase drug concentration above MEC = Bactericidal effect ANTIBIOTIC COMBINATIONS
 Daily use of antibiotics, delay the development of the microorganisms
FREQUENCY, DOSE AND DURATION OF creates resistance as well
DRUG ADMINISTRATION DEPENDS ON
(1) Severity infection ANTIBIOTIC COMBINATIONS
 Intravenously = Malala na masyado (sepsis) – naka drip ADDITIVE  An additive effect occurs when two or more “like” drugs
 Don’t give P.O. are combined
EFFECT  An additive effect may be intentional or may
(2) Site of infection
unintentionally cause harm
(3) Type of pathogen
POTENTIATIVE  Exposure to one chemical results in the other chemical
 there are pathogens that have different sensitivity/resistance to antibiotics
producing an effect greater than if given alone
 Get the culture and the gram stain first before administering EFFECT
(4) Immunocompetence of the host ANTAGONISTIC  Combination of a drug that is bactericidal penicillin + drug
 inherent, natural immunity that us bacteriostatic. Tetracycline = desired effect may be
 There are medications that should only be bacteriostatic to help the immune reduced
system
(5) Adverse effects
SPECTRUM
 Check dosage and frequency to avoid drug effects
(6) Continuous infusion regimen vs. intermittent dosing SPECTRUM
 Continuous infusion = constant drug concentration and the time of exposure is
NARROW  Against one type of organism
longer compared to intermittent dosing
 Penicillin and Erythromycin – For Gram (+) bacteria
(7) Once daily dosing = less severe adverse reactions; increase adherence SPECTRUM
 Azithromycin (3-5 once a day) BROAD  Against both gram (+) and Gram (-)
 Pneumonia type of diseases  Tetracycline and Cephalosporins
 Less severe adherence
SPECTRUM

RESISTANCE TO ANTIBACTERIAL GENERAL ADVERSE REACTIONS


HYPERSENSITIVITY  Refers to the undesirable reactions produced by the
 Resistance continue to grow despite the antibiotics normal immune system, including allergies and
autoimmunity
RESISTANCE OF ANTIBACTERIAL DUE TO:  These reactions may be damaging, uncomfortable, or
occasionally fatal
(1) INHERENT TO NATURAL  Rash, pruritus and hives (Manifestations)
 Occurs without previous exposure to the antibacterial drug  Severe anaphylactic shock
 Gram (-) pseudomonas aeruginosa resistant to Pen G  Tachycardia
 consideration: kasi matagal na masyado ang penicllin  Bronchospasms = cardiac arrest
(2) ACQUIRED (PERMANENTE NA NAGA INOM)  General adverse effects
 Responsible for causing penicillin resistance = penicillinase; enzyme that
metabolizes PenG = drug is ineffective PREVENTION
 Caused by prior exposure to antibacterial  Antihistamine
 Responsible for causing penicillin resistance = penicillinase  Epinephrine
 PENICILLINASE - Enzyme that metabolizes PenG = drug is ineffective  Bronchodilators
(beta-lactamase)  Appearance of bacteriological and clinical evidence
SUPERINFECTION
CAUSES OF ACQUIRED RESISTANCE of new infection during the AMT of a primary one
 Therapeutic doses of AMA the normal microbial
(1) Mutant bacteria
population of intestinal, respiratory, and urinary tracts;
 Grown a thicker cell wall
as a result, some develop super infection
(2) Transfer of genetic Instruction to another species
 Microorganism responsible for the new infection can
be drug-resistance strain of enerobacteriaceae,
HOW TO BEAT THE PROBLEM? pseudomonas, and candida
 The broader the AM spectrum, and the longer the
 New antibiotics are developed. ==linezolid (zyvox) period of AM treatment, the grater is the possibility of
 Used for mutant bacteria super infection produced by a typical drug-resistant
 methicillin-resistant staphylococcus microorganism
 vre- vancomycin-resistant enterococci & penicillin-resistant  An infection on top of infection
 die to removal of inhibitory mechanisms
streptococci  Alteration in normal flora which results to
 quiniupristin/dalfopristin (synercid) against vre and treatment of superinfection
bacteremia (nasa blood na sepsis), s. Aureus & strepotoccus pyrogenes  Secondary infection due to disturbed normal flora
 Occur with the use of broad spectrum antibiotics
 Zynox and synercid are developed  Oral thrush, stomatitis, diarrhea, bladder pain, etc.

Transes by: Daisy Rey Ochave | Template by: camillexcar 2


ORGAN TOXICITY  Chemicals that can cause adverse effects or disease
states manifested in specific organs of the body
 the liver and kidney are particularly susceptible to
organ toxicity as they are the sites of toxic filtration and
toxin metabolic breakdown
 Almost any organ or tissue in the body can be
affected by anti-microbial toxicity
 Damage to organs that are involved in drugs
metabolism and excretion (liver and kidneys)
 Aminoglycosides = ototoxic and nephrotoxic

CATEGORIES OF ANTIBIOTICS
(1) PENICILLINS
 Penicillins are used to treat infections caused by bacteria. They work by
killing the bacteria or preventing their growth. There are several different kinds
of penicillins. Each is used to treat different kinds of infections
(2) CEPHALOSPORINS
 Cephalosporins are beta-lactam antimicrobials used to manage a wide range of
infections from gram-positive and gram-negative bacteria. The five generations
of cephalosporins are useful against skin infection, resistant bacteria, meningitis,
and other infections
(3) TETRACYCLINES
 Tetracyclines are used to treat infections and to help control acne.
Demeclocycline, doxycycline, and minocycline also may be used for other
problems as determined by your doctor. Tetracyclines will not work for colds,
flu, or other virus infections
(4) AMINOGLYCOSIDES
 Aminoglycosides are used in the treatment of severe infections of the
abdomen and urinary tract, as well as bacteremia and endocarditis. They are also
used for prophylaxis, especially against endocarditis. Resistance is rare but
increasing in frequency
(5) MACROLIDES AND LINCOSAMIDES
 Macrolide and lincosamide antibiotics are bacteriostatic agents that block
protein synthesis in bacteria by binding to the 50S subunit of the bacterial
ribosome
 Macrolide and lincosamide antibiotics are chemically distinct but share a
similar mode of action. They have a spectrum of activity limited to gram-positive
cocci (mainly staphylococci and streptococci) and bacilli, to gram-negative cocci,
and intracellular bacteria (Chlamydia and Rickettsia species)
(6) VANCOMYCIN
 Vancomycin is in a class of medications called glycopeptide antibiotics. It
works by killling bacteria in the intestines. Vancomycin will not kill bacteria or
treat infections in any other part of the body when taken by mouth
(7) CHLORAMPHENICOLS
 Chloramphenicol is a medication used in the management and treatment of
superficial eye infections such as bacterial conjunctivitis, and otitis externa. It has
also been used for the treatment of typhoid and cholera. Chloramphenicol is an
antibiotic and is in the class of antimicrobials that inhibits protein synthesis
(8) FLUOROQUINOLONES
 The fluoroquinolones are indicated for treatment of several bacterial
infections, including bacterial bronchitis, pneumonia, sinusitis, urinary tract
infections, septicemia and intraabdominal infections, joint and bone infections,
soft tissue and skin infections, typhoid fever, anthrax, bacterial gastroenteritis
(9) SULFONAMIDES
 Sulfonamides, or "sulfa drugs," are a group of medicines used to treat
bacterial infections. They may be prescribed to treat urinary tract infections
(UTIs), bronchitis, eye infections, bacterial meningitis, pneumonia, ear
infections, severe burns, traveler's diarrhea, and other conditions
(10) PEPTIDES
 Polypeptide antibiotics target bacterial cell membranes, more specifically
prevents the transport of peptidoglycan precursors synthesised in the cytoplasm,
to components that have a major function in the growth of bacteria cell walls
 These peptides penetrate the bacterial membranes, accumulate inside bacteria
and then block bacterial functions and induce cell death via interacting with
intracellular DNAs and RNAs. The antimicrobial function of these cationic
AMPs is mainly to target DNAs and induce DNA damage

Transes by: Daisy Rey Ochave | Template by: camillexcar 3


PHARMACOLOGY

INTRODUCTION TO PHARMACOLOGY
PRELIM |
Transcribed by: Ochave, Daisy Rey C.

TOPIC OUTLINE 65 AND  Everything else

(1) Pharmacology ABOVE

“Health is a condition in which all parts and subparts are in FACTORS INFLUENCING DRUG ACTION
harmony with the whole of the client.”
FACTORS INFLUENCING DRUG ACTION
PHARMACOLOGY (1) AGE
 From Greek pharmakon, “drug”; and -logia, “study”  Most sensitive to the response of drugs – infants and elderly
 Deals with all aspects regarding drugs (2) BODY WEIGHT
 Overweight – increase dosage
 Suspensions – for pediatric patients, incorporated with water or in  Underweight – decrease in dosage
food  Pediatrics – calculated ml of drug / kgBW
 modes of administrations – routes, p.o. (3) METABOLIC RATE/GENETIC FACTORS
 Concerned with the history, physical and chemical properties of drugs (4) ILLNESS
 pathologic conditions alter rate of absorption, distribution, metabolism and
including ways in which drug affecting living systems excretion
 Study of drugs  eg. clients: in shock, who are vomiting, with nephrotic syndrome or
 How drugs will interact with the biological system (affects systems of malnutrition, with kidney failure
the body) (5) PSYCHOLOGICAL ASEPECTS
 Attitudes and expectations
 Different medications, has different effects and concerns  Willingness to take medicines as prescribed
 In San Pedro College, a protective environment is given to the patients (6) DEPENDENCE
especially when taking their medicines  Also known as addiction or habituation
 Interactions = living organisms and exogenous chemicals  Physical dependence – develops withdrawal symptoms
 Psychological dependence – emotionally attached to the drug
 Pharmacology affects the kidneys, brain, and interactions of people
(7) TOLERANCE
 occurs when higher doses are required to produce the same effect that lower
REVIEW: 10 RIGHTS IN DRUG ADMINISTRATION doses once provided
 can be caused by psychological dependence
10 RIGHTS IN DRUG ADMINISTRATION (8) CUMULATIVE EFFECT
PATIENT  refers to the patient, know its name and if it is the right  if the next doses are administered before previously administered doses have
patient been metabolized or excreted
DRUG  checking the medical order, medicine, medication  may result in drug toxicity
ticket  rate of consumption exceeds rate of metabolism (eg. alcohol)
DOSE  certain amount needed for medication with respect to
everything in the patient (age, gender, conditions, etc.)

TIME  Consider the frequency and interval


 Antibiotics - 3x – 6 hours, 3x in 12 hours – depends
on the doctors order
 Biogesic – 30 minutes onset, 1 hour at peak of
medication (mawawala na headaches mo)
ROUTE  mode of transmission
SITUATION: A nurse gave a polyamp (nebulization
medicine) to a patient but the nurse was about to give it in
per orem
ASSESSMENT  investigate, take baseline data, take vital signs
 kurog = temperature
 have a quick interview at the patient
 interview before medication, during medication and
after medication
 Pose checking condition
EDUCATION  educate the patient
 read a lot of books and search for effects of drugs

REFUSE  every individual has the right to refuse


 know the reason why the patient refuses the medication
and document it for evidence
 investigate why the patient refuses the medication
 have the patient sign forms and waivers
EVALUATE  Do assessments first

DOCUMENTATION  NO WRITTEN DOCUMENTATION, TASK NOT


DONE

PHARMACOLOGY CHART USED BY


PEOPLE
0-4  Amoxycilin
4-12  Rotalin
12-18  Appetite Suppressants

18-24  No – DoZ (for brain development, caffeine)


24-38  Prozoac
38-65  Viagra
PHARMACOLOGY

PENICILLIN
PRELIM |2N Ma’am Soraya
Transcribed by: Ochave, Daisy Rey C.

TOPIC OUTLINE PENICILLINASE-  Used to treat penicillinase-producing S.


aureusgram (+); not effective against gram (-)
(1) Penicillin RESISTANT organisms
(2) Pharmacodynamics PENICILLIN/  Not effective with gram negative organisms
(3) Pharmacokinetics ANTISAPHYLOCOCCAL  Resistant to penicillanse
PENICILLIN  Doa culture and sensitivity test to determine the
(4) Drug Effects the microorganism in the wound of the patient
(5) Drug-Lab-Food Interactions
(6) Nursing Considerations EXAMPLES
 [Oral] cloxacillin (Prostaphlin-A),
dicloxacillin(Dynapen)
PENICILLIN  [Parenteral] methicillin (Staphcillin),
nafcillin(Vigopen)
 Natural antibacterial agent from mold genus called penicillium  Less effective than Pen G against gram (+)
notatum (1928, alexander fleming) organism (resistance)
 moldy bread used on wounds to treat infection (3500 yrs. Ago)  MRSA – Methicillin-resistant
staphylococcus aureus (resistance)
 Natural, mold genus
 referred to as beta-lactam – inactivated by penicillinase (Enzyme  Effective against Pesudomonas
EXTENDED SPECTRUM
being produced by microorganism) PENICILLIN/ aeroginosa[gram (-)]
 Penicillin has a beta-lactarine  Not penicillinase-resistant; effective against
ANTIPSEUDOMONAL gram (–) organism- == Proteus, Klebsiella
 both bactericidal and bacteriostatic – mode of action PENICILLIN pneumoniae, Enterobacter
 interferes with the bacterial cell wall synthesis by inhibiting  Less toxic than aminoglycosides
bacterial enzyme  Less toxic
 Do not disrupt existing bacterial cell wall, but only newly forming
EXAMPLES
and actively growing cell wall  Piperacillin, ticarcillin disodium
BETA-LACTAMASE  Penicillinase sensitive penicillin + Beta-
Lactamase inhibitors
BASIC PENICILLIN GROUP INHIBITORS  combination of penicillin type of antimicrobial
PENICLLIN G  primarily bactericidal; doc for treating many so beta lactamse is added due to penicillinase
infections caused by penicillin- sensitive organisms sensitive
 first penicillin administered orally and by
injection (oral –only 1/3 of the dose is absorbed; EXAMPLES
im/iv—more effective in achieving a therapeutic  [O] amoxicillin (BSP) + clavulanic acid
serum per level ==Augmentin, Amoxyclav
 Acquired resistance  [P] ampicillin (BSP) + sulbactam== Unasyn
 Drug of choice – DOC  [P} piperacillin (ESP) + tazobactam== Tazocin
 1/3 of the dose if taken orally – bioavailability  The clavulanic, sulbactan, and tozobactam are
(lesser percentage compared through systemic beta lactamase inhibitors making the antibiotic
approach) effective and extending its antimicrobial effect
 Serum – blood/systemic circulation
PROCAINE PENICLLIN  extends the drug’s action; has milky color; less
painful during injection
G (WYCILLIN)  Stay long inside the body
 More concentrated but less painful
PHARMACODYNAMICS
 short duration of action; IM route is very painful  What does it do to the body
AQUEOUS PEN G
 Di masyado concentrated
 Given at a slower rate once given intravenously MODE OF ACTION
PENICLLIN V  preferred for ORAL
 2/3 absorbed in GIT, but is less POTENT
 BACTERICIDAL – interfere with the ability of susceptible bacteria to
 effective against mild-mod Infection, including build their cell walls –weaken the walls = swell then burst from osmotic
ANTHRAX. (Respiratory infection) ONSET: 0.5 HR
 Penoxymethyl penicillin - generic name PEAK: 1-2 hr
 tablet form
 Can be given systemically DURATION: 6-8 HR
 Drug of choice  diri ginakuha ang interval on how often gina administer ang
BROAD SPECTRUM  Used to treat both gram (+) and gram (-) medication
bacteria (E. Coli, H. Influenzae, Shigella
PENICILLINS/ dysenteriae, Proteus mirabilis, Salmonella)
AMINOPENICILLIN  Costlier than penicillin; not PENICILLINASE PHARMACOKINETICS
RESISTANT  [A] rapidly in the git
 Treat respiratory conditions, hand to mouth
infections – are enterobacters (affects the  peak level in 1 hr
gastrointestinal tract)  sensitive to gastric acid levels in the stomach taken on empty
 Mas mahal stomach
 Not penicillinase resistant
 Ineffective with staphylococcus
 [ + 1 glass of water, 1 hr ac (before meals) or 2-3 hrs pc (after
meals) ]
EXAMPLES  Best take on an empty stomach
 ampicillin (Ampicin); amoxicillin (Amoxin)  [e] unchanged in the urine
(most prescribed for adults & children)
 Maraming nagiging resistant to these types  If seen, it means it did not undergo biotransformation to
of penicillns, due to resistance and the penicillinase increase its water soluble, and not readily filtered.
enzyme  Penicillin crosses into the urine
 bacampicillin (Penglobe) amoxicillin-
clauvanate (Amoxyclav, Augmentin)
 Medication can still be noticed or manifested with the urine
 Penicillin was already overused and became output of the clients
resistant due to the enzyme  enter in breastmilk
 can cause diarrhea & adverse reaction to the baby
AMOXICILLIN  Alcohol is OUT!/ ask about allergies
BORAD  Well absorbed in GIT  Take full course of meds
SPECTRUM  Evaluate cultures,
CHON BOUND  Short in half-life
 Lesser of the protein type bound
= 25%  Excreted in urine 70%
90%  SHL
 In bite and urine

CLOXACILLIN
PENICILLINASE  Partially absorbed
RESISTANT
CHON BOUND  high protein bound, pagpasok sa katawan, dapat maka hanap
ng protein agad
= 90%  SHL – frequency of the medication is shorter compared to
HHL, easily excreted
 In bile and urine (excretion – entero-hepatic)

CONTRAINDICATIONS AND CAUTIONS


CONTRAINDICATIONS AND CAUTIONS
(1) Allergies to penicillin, cephalosporins, other allergens - Most Common
 Common hypersensitivity reactions due to the microorganism being used as cure
 Take history taking
(2) CAUTIONS
 With RENAL disease
 Lower the dose kasi mahirapan mag ihi
 Pregnant & lactating women – diarrhea & superinfections in infant

DRUG EFFECTS
DRUG EFFECTS
MAJOR  involve in GIT = N,V,D {mgt: SFF} (Nausea,
Vomiting and Diarrhea)
 Lower the dose If nasusuka, rest the bowel for an
hour
 glossitis, stomatitis, sore mouth, furry tongue
 [mgt: ice chips, sugarless candy}
 r/t loss of bacteria from normal flora =
superinfection
 Fungal infections
HYEPRSENSITIVITY  rash, fever, wheezing
 Anaphylactic shock
PAIN &  Phlebitis
 {mgt: administer slowly, remove IV line (pag di nag
INFLAMMATION wowork), warm compress, gentle massage}
AT INJECTION SITE Giving the medication intravenously, always check the
injection site

DRUG-LAB-FOOD INTERACTIONS
DRUG-LAB-FOOD INTERACTIONS
DRUG  Increase effect with aspirin (Antidote) , probenecid (Anti platelet) - do not
combine with penicillin
 decrease effect with tetracyclines, erythromycin – antagonistic {should be
avoided or increase dosage of penicillin, but increase ae} – do not combine
with penicillin
 if taken with contraceptive pills – OCP less effective
 Pwede ma buntis ang mama due to decrease effect in contraceptive pills
 Increase dosage alternatives but adverse reactions will come out
LAB  elevate AST, ALT
 Can be hepatotoxic
 Elevate blood levels of patient
FOOD  decreased effect with acidic foods or juices

NURSING CONSIDERATIONS
 Monitor for superinfections
 Evaluate renal [BUN & creatinine] &liver [AST,ALT] functions
 Diarrhea r/t superinfections
 {mgt: take yogurt, more fluids}
 Inform physician before taking other meds
 Cultures- prior to 1st dose

Transes by: Daisy Rey Ochave | Template by: camillexcar 2


PHARMACOLOGY

PHASES OF DRUG ACTION


PRELIM |2N Ma’am Soraya
Transcribed by: Ochave, Daisy Rey C.

TOPIC OUTLINE
(1) Three Important Phases of Drug Action  the tablet goes into disintegration then goes to granules and is
(2) Pharmaceutic Phase disintegrated again forming into small particles
(3) Pharmacokinetic Phase  Patients with a problem in absorption will result to very limited
(4) Pharmacodynamic Phase dissolution. Comparing it to granules and small particles, it became
limited until the best dissolution
Drugs face numerous obstacles in reaching their target cells. For  These are cases that you need to do these for a better dissolution
most medications that we give to the patient, the greatest barrier is process: a patient which has absorption therefore, turn it into drug in
crossing the many membranes that separate the drug from its target solution for best dissolution.
cells. We always have to consider that drugs would need to be in a
solution first so that it can be absorbed properly by the body DRUG EXAMPLES
 K+ -> Penicillin (antibiotic that is fully absorbed in the GI tract due to
the gastric acid)
THREE IMPORTANT PHASES OF DRUG  Addition of excipients, Sodium and Potassium ions so it becomes
ACTION Penicillin potassium
 Na+ -> Pen G Sodium
THREE IMPORTANT PHASES OF DRUG
ACTION PHARMACOKINETIC PHASE
PHARMACEUTIC  What happens upon taking the drug  The process of drug movement to achieve drug action
PHASE  What the body does to the drug
 What the body does to the drug  Most oral medications are absorbed in small intestine through the
PHARMACOKINETIC
action of extensive mucosal villi in the gastro-intestinal tract
PHASE
PHARMACODYNAMIC  Wherein what the drug does to the body
PHASE 4 PROCESSES OF PHARMACOKINETICS
(1) ABSORPTION
 First process in the Pharmacokinetics
PHARMACEUTIC PHASE  The movement of drug particles from the GI tract to body fluids y passive
 Has 2 phases which are: Disintegration and Dissolution absorption, active absorption, or pinocytosis
 Lipid-soluble and non-ionized are absorbed faster than water and ionized drugs
 disintegration – breakdown of a tablet into smaller particles  non-ionized drugs = weak drugs; no positive or negative charge that could
 dissolution – dissolving process of the smaller particles in the GIT repel it in the cell membrane for the absorption process
fluid prior to absorption TYPES OF ABSORPTION
 Depends on rate limiting and excipients PASSIVE  Drug molecule move form a region of relatively
 Rate limiting – time it takes for the drug to disintegrate and high to low concentration without requiring energy
ABSORPTION  Passive transport/passive diffusion
dissolve and become available for the body to absorb (Mechanical and  if mas maluwag, lilipat don
Chemical Digestion)  Lipid soluble and weak ionized drugs can be
 Excipients – Fillers or inert substance (additives) used in absorbed faster
drug preparation to take on a particular size and shape to enhance the ACTIVE  Process that uses energy to actively move a
molecule across a cell membrane
drug’s dissolution; Increases absorbability of a drug ABSORPTION  requires a carrier or protein enzyme like the ATP
 A tablet form of medication is not a hundred percent of the (Adenosine Triphosphate) to cross the drug in the
drug components it contains excipients and fillers to enhance the drug’s membrane
PINOCYTOSIS  Process by which cells carry drug across the
dissolution process and promotes more absorbency of the drugs. They membranes engulfing the drug particles
also give the form of the drug (ex. Capsule, tablet, tablet)  Endocytosis – pinocytosis
 Remember that other routes in taking the medications has no  medications that goes inside the nucleus by
pharmaceutic phase. Only the PO medications will undergo the 2 phases pinocytosis
 Cancer medications or chemotherapeutic
medications

FACTORS AFFECTING ABSORPTION


(1) BLOOD FLOW
 Greater blood supply enhances absorption
 Poor circulation = poor absorption process
 Poor circulation problems: Diabetes mellitus (problem with the
blood being thick and lower blood supply)
(2) PAIN
 Slow gastric emptying way
 Drug remains in the stomach longer
 Sometimes might vomit or nausea
(3) STRESS AND FOOD
 Slow gastric emptying way
 Drug remains in the stomach longer
 Faster peristaltic movement = diarrhea
 Taking in of too much hot/cold foods with medications can
become a factor
(4) EXERCISE
 When a person is exercising, the movement of the extremities will
decrease circulation in the gastro-intestinal tract because more blood
flow will go to the peripheral muscles, decreasing blood flow in the
gastro-intestinal tract
 The more rapid the absorption the faster the onset of drug action
(5) NATURE OF ABSORBING SURFACE  Is the process by which the drug becomes available to body fluids and body
 Transport of drug molecules is faster through a single later of tissues
cells (intestinal epithelium) than the transverse layers of the cells  Where the drug reaches the reactive tissues
(skin)  Molecules travel over the body via the vascular/lymphatic system (routes in the
 madaming daanan na layer if sa skin distribution of the drug)
 Surgery – application of creams over the area being operated FACTORS AFFECTING DRUG DISTRIBUTION
(6) DRUG SOLUBILITY
(1) BLOOD FLOW
 non-ionized drugs are more absorbable
 Liquids are more soluble (2) AFFINITY TO THE BODY TISSUES
 The principles of drug action
(7) pH
 alkalinity and Acidity (3) PROTEIN-BINDING EFFECT
 Calcium carbonate needs an acidic environment has to be taken
with reduced stimulation of gastric acid
(8) DRUG CONCENTRATION HOW ARE DRUGS DISTRIBUTED
 Absorption increase if the tablet is taken with a glass of water as to PROTEIN  Drugs that bind with specific protein component
dilute the solution such as albumin and globulin
BINDING  EXAMPLE
 Enhances absorption
(9) DOSAGE FORM  anticonvulsants – albumin (where they have
 Physical form of the drug = mg/mcg to bind)
 Route of IM = faster absorption than SC injection  antidysrhythmics – globulin (where they
have to bind)
(10) HEPATIC FIRST-PASS EFFECT
 The portion of the drug that is bound to protein is
 Inactivation of drug by enzymes in the liver before the drug
reaches that systemic circulation for distribution inactive (do not cause pharmacologic response)
 Bioavailability  The portion of the drug that us unbound is called
 the percentage of the administered drug dose that reaches the free drug which is an active drug (causes
systemic circulation pharmacologic response)
 Taking oral medication, the bioavailability occurs after  When 2 highly protein bound drugs are given
absorption and hepatic drug metabolism and always less than a concurrently, drug toxicity may result
hundred percent  consider the patient’s protein level
 Intravenous medication has a bioavailability of 100% (diretso  Receptor sites and sites of action are composed of
na siya or available for the circulation) protein
 With absorption process it goes inside the stomach and being  Too many medications are given to a particular
absorbed in the small intestine but before it goes in the circulation, it client, they need to have the protein in order to have
goes in the portal circulation (the liver) its action so they must not be hypoalbuminemia, they
 Most metabolism in the liver is accomplished by the hepatic will go to the blood flow all over the body which can
microsomal enzyme system lead to drug toxicity
 chemical alteration, resulting more acting in the original then
being excreted DRUG TOXICITY
 Activate muna para ma deliver and maipalabas  Too much of free drug released in the circulation
 EXAMPLE: two highly CHON-bound drugs and
(11) ENTEROHEPATIC RECYCLING
low albumin)
 Absorption of drug from the bile into the small bowel and then
into the circulating system BLOOD-  Is a protective system of cellular activity that keeps
 There is a capacity of the liver to store some components of the foreign invaders/poisons away from the CNS
BRAIN  High lipid soluble drugs are more likely to pass the
drug inside the bile, when times comes it is needed in the body, it will
be ejected from the gallbladder all the way to the circulation
BARRIER blood brain barrier
 bile stores components of the drug which can be readily passed on  Our blood is composed of lipid
 Antibiotics cannot pass this BBB
(12) ROUTE OF ADMINISTRATION
 CNS effects by medications are result of indirect
 Linked to blood supply
drug effects and not the actual reaction of the drug to
ROUTES OF ADMINISTRATION the CNS
IV  Blood Volume  composed of tight walls which will limit movement
 absorption is instantaneous because of the of drug molecule in the brain tissue, Hindi lahat ng
blood volume itself gamut nakaka punta sa CNS to avoid irreversible brain
 If there are problems such as the disease damage
problems then it will have a problem with  Drugs readily pass trhough the placenta and affect
absorption
PLACENTA
the developing fetus
IM  perfusion AND  Drugs are secreted into breast milk and therefore
 fat content BREASTMILK have the potential to affect the neonate
 temperature  Side effects = kung okay siya sa adult it doesn’t
 When we give intramuscular do the mean na okay siya sa baby din
massaging of the are to increase the rate of  Always categorize the medicines first
absorption process  Found in package inserts
SQ  Perfusion
 fat content
FDA PREGNANCY
 temperature CATEGORY
 Consider the fat content as high CATEGORY No risk evident
 Lesser blood circulation or perfusion A  no risk to the fetus according
ORAL  Acidity of the stomach to studies
 Length of time in the stomach (decreased CATEGORY  no risk evident in human
motility) B studies or animal studies
 Blood flow to the GIT CATEGORY  Risk cannot be ruled out
 Exercise = lesser absorption C  hindi pwede tanggalin si risk
 Presence of interacting food or drug  checking out on the benefits
 The drug being exposed sa loob ng more than the risks itself
stomach  Pwede pa din ibigay but the
MUCOUS  Perfusion patient has to be evaluated all the
MEMBRANE  Integrity time
 Presence of food – smoking (respiratory CATEGORY  (+) evidence of risk exists
mucous membrane) D  Risk vs benefit of the drug
 Length of time in the area must be determined
(2) DISTRIBUTION

Transes by: Daisy Rey Ochave | Template by: camillexcar 2


 Used in life threatening  Depress or slow cellular activities
conditions  Patient is being given anesthesia – decreases function of CNS
CATEGORY  Contraindicated in pregnancy
X  Drug should be avoided in
 Interfere with the functioning of foreign cells such as invading
pregnancy organisms
(3) METABOLISM/BIOTRANSFORMATION  Inhibition/Killing of microorganism (Antibiotics)
 chemical changes a substance undergoes in the body such as by the action of
enzymes
 Drugs are metabolized in both the GI tract and liver (primary site of PHARMACODYNAMIC PHASE OF DRUG
metabolism)
 Most drugs are inactivated by liver enzymes and are converted to water soluble ACTION
substances (inactive metabolites for renal excretion) ONSET OF ACTION  Time it takes to reach the minimum effective
 Liver is the primary site for metabolism concentration (MEC) after a drug is administered
 MEC – Minimum Effective Concentration is the
HALF LIFE least amount drug plasma concentration in order to
 Time it takes for ½ of the drug concentration to be eliminated start exerting a pharmacologic effect
 Slowly eliminated by the kidneys  Where the onset of action takes place
 The drug is already delivered in the site of action
EXAMPLE: PEAK OF ACTION  Condition that occurs when the drug reaches its
HALF LIFE = q 20 hrs highest blood or plasma concentration
DOSAGE: 20 mg  Pumpasok pag nasa highes blood or centration na
HOURS DOSAGE %  Nasa circulatory system na ang drug molecule
2 hours 10 mg 50% DURATION OF  Length of time the drug has a pharmacological
4 hours 5 mg 25% effect
ACTION
6 hours 2.5 mg 12.5%  Drugs that produce a response
8 hours 1.25 mg 6.25%
AGONISTS
ANTAGONISTS  Drugs that block a response
HALF LIFE OF 650mg ASPIRIN
#t ½ TIME OF DOSAGE % LEFT
ELIMINATION REMAINING
1 3hrs 325 mg 50%
2 6hrs 162 mg 25%
3 9hrs 81 mg 12.5%
4 12hrs 40mg 6.25%
5 15hrs 20mg 3.1%
6 18hrs 10MG 1.55%
(4) EXCRETION/ELIMINIATION PROCESS
 Kidneys are responsible for filtering the free water/soluble or other drugs
 Process of eliminating substances by body organs or tissues, as part of a natural
metabolic activity
 Kidneys – main route of elimination (free, water soluble, unbound drugs)
 Others – bile (enterohepatic cycle), feces, lungs (As we breathe out air),
saliva, sweat and breastmilk
 Urine pH influences drug’s excretion
 Acid urine – elimination of weak base drugs
 Alkaline urine – elimination of weak acid drugs
 Be careful in handing drugs especially with dealing the patient to avoid cellular
destruction (feces)
 Dapat hindi aabot sa blue kasi pupunta sa toxic concentration
PHARMACODYNAMIC PHASE
 Is the study of drug concentration and its effects on the body ADDITIONAL INFORMTION TO THE
 Drug response can cause a primary and secondary physiologic effect
 The primary effect is desirable and the secondary effect may be
PHARMACODYNAMICS
desirable or undesirable Pharmacodynamics – what the drug does to the body, how the drug
 What the drug does to the body would respond (primary or secondary effect)
 Known also as the mode of action
EXAMPLE  Peak drug level is important to check for toxicity levels
 Diphenhydramine (Benadyl) – Anti-histhamine drugs  P.O. medications – peak drug level
 1st effect = treats allergy  1-3 hours after administration
 2nd effect central nervous system depression (drowsiness)  Intravenous administration – peak drug level
 10 min
RECEPTOR THEORY  Mas mabilis compared to P.O.
 Drugs act through receptors by binding to the receptor to produce
(initiate) a response or to block (prevent) a response THERAPEUTIC INDEX – TAKEN BY BLOOD SAMPLES
 The better the drug fits at the receptor site, the more biologically  Measures the margin of safety of a drug (effective: dose: lethal dose)
active the drug is  Low TI: narrow margin of safety
 Masyadong makipot, so need bantayan ang patient
DRUG ACTIONS (The drug may act in 4 ways)  High TI: Wide margin of safety
 Replace or act as substitutes for missing chemicals  Mas safe
 Becomes as a replacement (Insulin, patient lacking insulin)  The close the ration is to the 1 the great the danger of toxicity
 Increase or stimulate certain cellular activities  ang gamot once taken, it is a toxic substance so it undergoes different
 Laxative – increases the peristalsis movement, increases water phases
absorption in GIT – enables to for smooth elimination

Transes by: Daisy Rey Ochave | Template by: camillexcar 3


 Ratio given by the pharmacist/chemist na need Makita ang margin of
safety ng gamut since drugs are toxic
 Ratio of effectivity of the medication
 Seen in blood levels
 Done if madami nang gamot kinukuha ang patient

THERAPEUTIC RANGE (THERAPEUTIC WINDOW) – TAKEN


BY BLOOD SAMPLES
 Between the minimum effective concentration in the plasma and the
minimum toxic concentration
 EXAMPLE: digoxin (0.5 to 2 ng/ml) - cardiovascular disorders
 Taken out with drug samples

PEAK DRUG LEVEL – TAKEN BY BLOOD SAMPLES


 Highest plasma concentration of drug at a specific time
 Indicate the rate of absorption of the drug
 PO medication – peak time (1-3 hours)
 Intravenous (systemic) – peak time (10 min)

TROUGH LEVEL (PRONOUNCED AS “TROFF”) – TAKEN BY


BLOOD SAMPLES
 Is the lowest plasma concentration of a drug and measures the rate at
which the drug is eliminated
 Indicare the rate of elimination of the drug
 Pababa ang concentration ng gamot = elimination of the drug
 Plasma = blood

Transes by: Daisy Rey Ochave | Template by: camillexcar 4

You might also like