PHARMACOLOGY

Prepared by:
Lizette Fortus-Amurao, RN, USRN
DRUG- substance/mixture for diagnosis, cure, treatment, disease
prevention
PHARMACOLOGY- Gk “pharmakon” (drug) & “-logia” (study)
- how drugs interact w/biological systems to affect function
- study of interaction between living org & exogenous
chemicals that alter normal biochemical fx
PHARMACOKINETICS - what body does to the drug
PHARMACODYNAMICS - what drug does to the body
Sources of Drugs
PLANTS- digitalis (purple foxglove); vincristine (periwinkle);
morphine (opium)
ANIMALS- Insulin (pigs & cows); Vaccine (killed/attenuated
microorg from horses)
SYNTHETICS- genetic engineering to alter bacteria for
therapeutic & effective chemicals
INORGANIC COMPOUNDS- salts of various elements
(have therapeutic effects in body)
- aluminum (antacid for hyperacidity); fluoride
(dental carries & osteoporosis)
 3 steps on Developing New Drugs
1. Discovery - candidate compound is picked as possible

therapeutic agent for specific disease

2. Clinical Research - compound tested on cell cultures and

animals; serious harms on living organism??

3. Clinical Development - Clinical trials on human; side effect

is effective and treat diseases.

 Clinical Trials Phases (SEAL)
Phase I - Safety - test in small group and healthy individuals
Safe for humans?
Phase II - Efficacy - How effective the med is? How well it work at
certain dose?
Phase III - Approval - New meds
compared to standard treatment
Just as good or even better on the existing meds
-used by large number of individuals; administered in real life
-basis for approval of regulatory organization for market
Phase IV - Longterm - safety surveillance, side effects? Unsafe? -
Recall/ban
 Drugs Categories:
Agonist - synthesized to look the same and act the same as a
natural or current hormone in the body
Antagonist - to prevent the hormone from interacting with the
receptor in the body
Example: Antidiarrheal
 Anti-
diarrheal
Agoni
st

Drug A
Synthesized to look
the same and act the Receptor A
same as a natural or Any ligand or
current hormone in substrate that binds
the body that normally to receptor A and
slows the gi motility perfectly lead to
slowing the gi motility
Antagoni
st
Dr
ug
Hor B
mo Re
ne ce
Z Drug B, binds to the
pto receptor and
block the active sites
rB to prevent the
hormone z from interactive to the
receptor
Types of Agonist Drugs
1. Full Agonist - drugs that bind to the receptor with complete

response
2. Partial Agonist - unable to induce maximal activation of the

receptor; useful for the treatment and avoidance of drug

dependencies as they induce similar effect but less potent
and addictive
3. Inverse Agonist - Induces the opposite effects; kind of like

antagonist effect but they work directly on the receptor

without blocking the action of a hormone or a substance to
get the effects ex: antihistamines; dipenhydramine;
loratadine
4. Irreversible agonist - full complete response, drug will not be

influenced by anything and will stay bound to the receptor

5. Selective - bind on a specific receptor
Types of Antagonist Drugs
1. Competitive - competition between the hormone and drugs

because they want the same receptor; increasing the

concentration of the drug it will win and bind to the sites
instead of the hormones
2. Non-competitive - bind to allosteric site and changes the
active site; this will change the shape of the active site, so
the hormone will not bind because they are not match
anymore
PHARMACOTHERAPEUTICS
- study of how drugs may best be used in treatment; CHOOSING THE
BEST DRUG
which drug would be most/ least appropriate to use for specific
disease
what dose would be required
PHARMACOGNOSY- study of drugs derived from herbal & natural
resources
TOXICOLOGY- study of poisons & poisonings; toxic effects on living
organism
ANTAGONISTIC- 1 drug interferes w/action of another
- tetracycline + antacid = ↓ tetracycline absorption)
INTERFERENCE- 1 drug inhibits met/excretion of 2 drug ↑ activity of 2
nd nd

drug
- probenecid + spectinomycin = prolonged spectinomycin antibacterial
activity d/t blocking renal excretion by probenecid
INCOMPATIBILITY- not mixed together/administered at same site
- haziness, precipitate, change of solution color when mixed
- ampicillin + gentamicin = amp inactivates gentamicin
DESIRED ACTION- expected response
SIDE EFFECT- d/t pharmacological effect; when meds is administered
regardless of dose
ADVERSE EFFECT- undesirable event at normal dose/correct administration
TOXICITY- severe adverse effect/poisonous
CARCINOGENICITY- induce cells to mutate & become malignant
TERATOGENICITY- induce birth defect
 NURSING RESPONSIBILITIES
• Administering drugs
• Assessing drug effects
• Intervening to make the drug regimen more tolerable
• Providing patient teaching about drugs and the drug regimen
•Monitoring the overall patient care plan to prevent medication
errors
 Drug Evaluation
FDA - Food and Drug Authority
Drugs must pass through several stages of development
Drug Classifications
PRESCRIPTION- written order by qualified health professional to a pharmacist/
therapist for a specific treatment for patient
Components: - date & time drug was written - drug name - drug dosage
- route of administration - administration frequency & duration
- physician signature
NON-PRESCRIPTION- OTC medications
INVESTIGATIONAL- subjected to clinical studies to evaluate usefulness
ILLICIT/STREET- illegal; non-medical, alter mood/feeling (heroin, nubain, Cytotec)
ORPHAN- for rare disease (affect < 200,000 in US)
- neglected because sales profit may not be enough to cover costs of dev’t
Drug Names
CHEMICAL- systemically derived name showing
chem structure; chem constitution; exact atoms placing
- N-Acetyl-para-aminophenol
GENERIC- given before drug turns official; reflect
important
pharmacological/chem characteristic;
acetaminophen
BRAND- followed by ®; name is registered; its use is
restricted to drug owner (manufacturer); Tylenol
REMEMBER
Generic drugs are drugs no longer protected by patent and can be produced
by companies other than the one that developed it.
OTC drugs are available without a prescription and are deemed safe when
used as directed.
• Orphan drugs are drugs that have been discovered but that are not financially
viable because they have a limited market or a narrow margin of safety. These
drugs may have then been adopted for development by a drug company in
exchange for tax incentives.
Reaction to Drug
PHOTOSENSITIVITY- skin, eyes
HYPERSENSITIVITY- exaggerated immunologic response to drug
considered as foreign
IDIOSYNCRATIC- during 1 intake (d/t metabolism differences)
st

- does not occur at any dose in most patients and develop mostly
unpredictable in susceptible individuals only
Principles of Drug Actions
1. Drug don’t create new cellular fx but only alter
- antibiotic slows growth/reproduction of microbial organism
- drug action is relative to physiological state when drug was administered
2. Drug may interact w/body in many ways
- alter body fluid chem composition
- accumulate in tissues bc affinity for tissue component (form chem bond
w/receptors)
3. Drug response/effect strength depend on drug molecule’s fit in receptor site
- precise fit à strong effect loose fit à weak effect
4. Agonist-Antagonist drug exert both agonist & antagonist response
- agonist (produce response); antagonist (counter/depress response; in antidote
therapy)
Guiding Principles
C- heck why meds is given & know drug classification
H – ow to know if med is effective? Assessment parameters in
monitoring effects?
E- xactly what time should med be given
C – lient teaching tips. What therapeutic & side effects
K – eys to giving it safely. Identify interv to counteract adverse effects
 THE PRESCRIPTION
- written order/instruction of valid physician/dentist/veterinarian for specific drug use
- doctor’s order on px chart for use of specific drug
- basis: Rules & Regulations to Implement Prescribing Requirement under
Generics Act of 1988 (RA 6675)
PRESCRIPTIONS NOT ALLOWED
1. Violative
- generic name isn’t written - generic name not legible; legible
brand name is written
- brand name is indicated & instructions added (“no substitution”)
which obstruct/ hinder/ prevent generic dispensing
2. Erroneous
- brand name precedes generic name - generic name is inside
parenthesis
- brand name isn’t in parenthesis - > 1 drug prescribed on 1
prescription form
3. Impossible
- only generic name is written but not legible
- generic name doesn’t correspond to brand name
Factors Influencing Drug Action
Age- extremes most sensitive (newborn, infant, elderly)
Body Wt- ↑ dosage = overweight; ↓ dos = underwt (pediatrics use mg/kg)
Metabolism/Genetics- susceptibilities metabolize meds differently
- lack enzymes prolong plasma level & ↑ toxicity risk
- pharmacogenomics (how drugs interacts w/inherited genes)
Illness- pathologic condition alter rate of absorption, distribution, metabolism, excretion
- short gut syndrome (↓ absorption capacity)
Psychological- attitude/expectation; willingness to take meds (compliance)
Dependence/Addiction/Habituation- withdrawal (physical); emotional attachment
Tolerance- ↑ dose needed to produce same effect lower doses once provided
- may be caused by psycho dependence
Cumulative Effect- if next doses are administered before previous dose is fully metabolized
- result to drug toxicity; consumption rate exceeds metabolism rate
Drugs & the Body
Drugs usually work in one of four ways:
To replace or act as substitutes for missing chemicals
To increase or stimulate certain cellular activities
To depress or slow cellular activities
• To interfere with the functioning of foreign cells, such as
invading microorganisms or neoplasms (drugs that act in
this way are called chemotherapeutic agents).
PHARMACODYNAMICS- study of drug biochemical & physiological
effects
- mechanism of action; WHAT DRUG DOES TO BODY
PHARMACOKINETICS- study of absorption, distribution,
biotransformation(metabolism) & excretion; WHAT BODY DOES TO
DRUG
PHARMACODYNAMICS —— WHAT DRUG DOES TO BODY
drug response cause: primary physiologic effect (desirable) secondary (un/desirable)
ex: Diphenhydramine HCL (1st generation antihistamine)
Treats allergies (primary); CNS depression (secondary)
Receptor Theory- drugs act on receptors by binding to receptor to produce (initiate)/block
(prevent) a response
 Drug Receptors:
Cell surface or intracellular regulatory proteins – mediate the effects of
endogenous chemical signals such as neurotransmitters and hormones.
e.g. adrenoreceptors, steroid receptors, acetylcholine receptors.
Enzymes – cell surface, membrane-spanning or intracellular proteins
inhibited (or less commonly activated) by the binding of a drug. e.g.
Na+K
+ATPase is the cell surface receptor for cardiac glycosides such as
digitalis
Structural proteins – extra- or intracellular proteins inhibited (or less
commonly activated) by the binding of a drug. e.g.tubulin is the
receptor for colchicine - an anti-inflammatory agent
Drug Actions- replace/act as substitutes for missing chemicals
- Increase/stimulate certain cellular activities
- Depress/slow cellular activities
- Interfere w/functioning of foreign cells (invading microorganisms)
Onset of Action- Time to reach min effective concentration (MEC) after drug is
administered
Peak of Action- Condition when drug reaches its highest blood/plasma conc
Duration of Action- length of time drug exerts a pharmacological effect
Agonists- Drugs that produce a response
Antagonists- block a response
Therapeutic Index- Measures margin of safety of drug
- narrow MOS (low therapeutic index) wide MOS (high
therapeutic index)
- closer ratio is to “1” = greater toxicity danger
Therapeutic Range (therapeutic window)- between min
effective concentration in plasma & min toxic
concentration
- ex: Paracetamol (10 mg to 15 mg /kg)
Peak Drug Level- Highest drug plasma concentration at a
specific time
Trough Level- lowest drug plasma conc & measure rate where
drug is eliminated
PHARMACOKINETICS- study of absorption, distribution,
biotransformation(metabolism) & excretion; WHAT BODY DOES TO
DRUG
 Proces
s:
1. ABSORPTION- from GI tract to body fluids by passive/active absorption/ pinocytosis
Passive - higher to lover concentration w/o requiring energy
Active - uses energy to actively move a molecule across a cell membrane
- Pinocytosis (Cell Drinking) - engulfing drug particles
factors
o Blood flow o Pain o Stress & food o Exercise
o Drug solubility o pH o Drug concentration o Dosage form
o Nature of absorbing surface- single cell layer faster than multi-layered skin
- respiratory epithelium (steroids); intestinal epithelium (carb)
o Hepatic first-pass effect- drug inactivation by hepatic enzymes before drug reaches
systematic circulation for distribution
- bioavailability: % administered drug dose reaching system circulation
o Enterohepatic recycling- absorption from bile to small bowel then into circulating system
o Route of administration- linked to blood supply (vascularity)
Factors affecting Absorption
Intravenous- blood volume (vascularity)
Intramuscular & Subcutaneous - perfusion fat content,
temp
Oral - stomach activity; time length in stomach,
bloodflow to GIT, presence of interacting food/drug
Mucous Membrane - perfusion, integrity, food presence,
smoking,
time length in area
2. DISTRIBUTION- drug becomes available to body fluids & body tissues
Factors: Blood flow, Affinity to body tissues; Protein-binding effect
Manner
Protein-binding- protein REGULATE drug; bind w/specific protein components such as:
Bound portion is inactive (doesn’t exert pharmacologic response)
Unbound portion is active (free drug)
Toxicity: excess free-circulating drug (when 2 highly-protein bound drugs are given to
px w/liver disease/low albumin)
Blood-brain Barrier- protective system (keep foreign invaders/poisons away from CNS)
Highly lipid-soluble drugs
Antibiotics can’t pass through
CNS effects by med result from indirect processes & not by actual CNS to drug
Placenta & Breastmilk- drugs readily pass through (can affect developing fetus)
- Secreted into breastmilk
Category A NO RISK evident
B NO RISK in human/animal
studies
C RISK can’t be ruled out
D + evidence of risk
X CONTRAINDICATED in
pregnancy
3. METABOLISM- chem changes substance undergo in body (by enzymatic action)
- Drugs are metabolized in GI tract & liver
- most drugs inactivated by liver enzymes & converted into water-soluble
substances (for renal excretion)
Half-life (t ½) -time for ½ of drug concentration to be eliminated
- decrease drug into half through time
- First order: proportional rate of elimination to concentration
- Zero order: constant rate of elimination regardless of conc
T½ TIME ELAPSED DOSAGE (at 20mg start) PERCENTAGE LEFT

1 2 hrs 10 mg 50%

2 4 hrs 5 mg 25%

3 6 hrs 2.5 mg 12.5%

4 8 hrs 1.25 mg 6.25%

4. EXCRETION
- by organs/tissues (part of natural metabolic activity)
• Kidneys (main route; [free, water-soluble, unbound drugs])
• Urine pH (influences drug excretion)
Acidic (for weak base drugs)
Alkaline (for weak acid drugs)
• Others (bile, feces, lungs, saliva, sweat, breastmilk)