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Pharmacology and

Therapeutics
Lecturer:
Isaac Amankwaa
COURSE OBJECTIVES
By the end of the course the student will:
Discuss the various sources of drugs
Explain the principles of pharmacology: pharmacokinetics and
pharmacodynamics
Explain the indications, dosages, actions, side effects,
contraindications, drug interactions and nursing implications of
drugs on the various systems of the body
Identify the nursing responsibilities in administering the various
drugs
Apply current drug policies in the country.

COURSE CONTENT
1. Sources of drugs
2. General drug metabolism
3. Analgesics
4. Anaesthesics
5. Tranquilizers: major and minor
6. Antidepressants
7. Anticholinergics
Course content CTD
8. Drugs acting on the cardio-vascular system
9. Haematinics
10.Drugs acting on the respiratory system
11.Drugs acting on the digestive system
12.Drugs acting on the urinary system
13.Drugs used in infections
14.Miscellaneous drugs


Course content CTD
Antimetabolites
Eye preparations
Ear preparations
Drugs acting on the endocrine system
TERMINOLOGIES
Application of Pharm to Nursing
Class to be divided into 4 groups to discuss
1. Role of the nurse in drug therapy
2. Drug administration practices students
observed (good & bad) during their last
clinical placement
3. Why you think nurses must learn pharm in
nursing.
4. The nurse, pharmacist and doctor who plays a
central role in drug therapy and why?

TERMINOLOGIES
PHARMACOLOGY

The study of the interaction of
substances(drugs), other than foods, with
living systems
or
It is the study of effect of drugs on living
organisms.


THERAPEUTICS


The use of drug to diagnose,
prevent or treat diseases or to
prevent pregnancy


Clinical Pharmacology
The study of drugs in humans-
includes the study of drugs in
patients as well as healthy
volunteers

A drug/Medication:
A chemical used in the diagnosis,
treatment, or prevention of disease.
They are used interchangeably.
Sources of drugs
Two main sources:
1. Natural
2. Synthetic
Natural sources
1. Plant sources: digitalis, vincristine &
colchicine.
2. Animal/Human products: E.g. insulin &
adrenaline.
3. Inorganic compounds: E.g. aluminum and
magnesium hydroxide.

Synthetic Sources
Prepared by chemical reactions in the
laboratory.
Majority of drugs prepared by this
method.
One such area is Biotechnology:
manipulation of proteins to permit the large-
scale industrial production of complex
natural substances (e.g. hormones).
Drug names
A drug may have about four names:.
1. Chemical name
2. Generic name (nonproprietary)
3. Official name
4. Trade name
Types of drug names Examples
Chemical name N-Acetyl-para-aminophenol
Generic name acetaminophen
Trade names Paracetamol, Tylenol, EFPAC
Which name to use? Generic or trade?
Disadvantages of using generic names
They are long and complicated
They are difficult to remember
Disadvantages of trade names:
unlimited trade names which create confusion.
Can result in double medication

Controlled substances

Can cause physical or psychological
dependence or both.
Its use is subject to considerable
control.
The nurse has both legal and ethical
responsibilities when administering
these drugs.

Nonprescription or Over-the-counter
drugs (OTCs)

These are drugs that can be purchased
without prescription.
Considered relatively safe for the layperson to
use when taken according to directions
provided by the manufacturer
Medication orders
Patient medications must have an order from
the physician, nurse practitioner or medical
assistant.
Medication orders are written in the form of
PRECRIPTION

Types of Medication orders
1. A standing order: carried out as specified until it is
cancelled by another order. E.g. Caps amoxicillin 500mg
tds for 7 days
2. As needed (p.r.n.) order
3. Single order
Directive is carried out only once at the time
specified by the physician.eg atropine given to
preoperative patients
4. Stat order
Also a single order
Carried out at once

Science
of Pharma-
cology
Pharmacognosy
Pharmacokinetics
Pharmacodynamics
Pharmacotherapeutics
Toxicology
EFFECTS OF DRUGS
Drugs are given for two effects:
Local effects
Systemic effect
Both can further be grouped into
desirable and
Undesirable effects

PRINCIPLES OF PHARMACOLOGY
Chapter Two
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1. Pharmacokinetics
2. Pharmacodynamics
Pharmacokinetics
Processes that affect a drug from the time it
enters the body until it leaves the body
It answers the question: how does the body
handles medications.
Components of PK.
Absorption (A)
Distribution (D)
Metabolism (M)
Excretion (E)
ADME
Absorption
Passage of medication from administrative site till its
entry into the systemic circulation.
Determines how soon a drug becomes available to
exert its action
Factors that influence absorption
1. Route of administration: IM, Oral, IV
2. Drug form e.g. tablet coating, liquid form,
3. Surface area
4. Blood flow
5. Lipid solubility
Absorption of oral drugs

The amount of drug reaching the systemic
circulation is considerably less than the
amount absorbed due to the extraction and
metabolism of the drug by a process called
first pass effect.
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Some of the drug is inactivated and not all will
be available for use at its intended site of
action.
Drugs are therefore formulated to account for
this difference in availability to the tissues.
This is why different forms of drugs are not
equal
Bioavailability

The portion of a dose that reaches
the systemic circulation and is
available to act on body cells.

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IV drugs- 100% bioavailability
Absorption is rapid and 100% bioavailable.
Avoids problems with stomach acid and
intestinal absorption issues.
IM drugs
Not as rapid as IV.
Better absorption if there is a good blood
supply.
Oral drugs
<100% bioavailability because
Some not absorbed
1
st
pass effect


Routes that avoid 1
st
pass effect
Sublingual and Bucal routes
Absorbed into the highly vascularized tissue under
the tongue or between the cheek and the gum-
the oral mucosa
Bypass the liver
Rapidly absorbed.

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Distribution
After a drug is absorbed, the transportation of
that drug from the bloodstream to the body
tissues and intended site of action is called
distribution.
Factors Affecting Distribution

Blood supply to site of action: drug is distributed in
this order:
a. Extensive blood supply: heart liver, kidney
b. Areas of slower distribution: skin, fat
c. Bones and brain
Protein binding
Degree of first pass effect.

Metabolism
Series of chemical reactions that inactivates a
drug by converting it into watersoluble
compound so that it can be excreted by the
body.

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It takes place mainly in the liver and produces:
1. An inactive metabolite
2. A more soluble compound
3. A more potent metabolite e.g. prodrugs.
Levodopa is a prodrug of dopamine
hydrochloride

Other organs or body tissues responsible for metabolism

Liver (mainly)
Skeletal muscle
Kidneys
Lungs
Plasma
Intestinal mucosa

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Factors that decrease (delay) metabolism

Cardiovascular dysfunction
Renal insufficiency
Starvation
Obstructive jaundice
Erythromycin or ketoconazole drug therapy

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Excretion
Removal of drugs from the body.
Drugs and their metabolites can exit the body
in urine, bile, sweat, saliva, breast milk, and
expired air.
The most important organ for drug excretion
is the kidney.
Drug excretion
Some drugs are excreted unchanged
Patients who may require dosage
reduction:
Patients with kidney disease
Children
older adults
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Half-life of a drug
Time required for the serum
concentration of a drug to decrease by
50% or half of its original concentration.
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Half-life of a drug
Knowledge about drug half-life help in
determining dosing interval

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Pharmacodynamics
Study of what drugs do to the body and how
they do it.
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Drug actions
Drugs usually work in one of four ways:
1. To increase cellular activities.
2. To replace missing chemical
3. To slow cellular activities
4. To interfere with the functioning of
foreign cells.
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Receptor theory of drug action
A drug will not act unless it is bound
Most drugs cause their effects by interacting
with specific drug receptors
What are receptors
Structures on a cell
Have chemical structure that matches the shape
and charge of the drug.
Like the relationship btnx a key and lock


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Types of drug-receptor interactions
1. Agonist drug
Able to interact and activate receptors
Have two properties
Affinity: ability of a drug to bind to a receptor
Efficacy: tendency of a drug to activate a
receptor once it is bound

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Antagonist drug

Able to interact with receptor but do not change
the receptor
Properties
Have affinity
Have no efficacy


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Types of antagonist drugs
Competitive antagonist
Compete with the agonist drug for the same
receptor site.
Prevents the agonist from binding and therefore
prevents the agonist from causing effect
Effect of competitive antagonist can be overcome
by giving greater dose of the agonist
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Types of antagonist drugs
Non-competitive antagonist
Permanently occupy or change the receptor so
that the agonist cant interact with it.
The effect of non-competitive antagonist cannot
be overcome by increasing the dose of the
agonist.
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The Dose-response relationship
The bigger the dose of a given drug, the
greater the effect
Dose response relationship is dependent on
A. Affinity
B. Efficacy
C. Potency
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Efficacy

The maximum effect produced by a drug.
E.g. if 1 gm of drug A and B are administered to
reduce patients pain and drug A does it at 80%
and drug B does it at 50%, then drug A is said to
be more efficacious than drug B.

Potency
Amount of drug that is given to elicit an effect.
A potent drug produces its effect at low doses.
E.g. if 10 mg of drug A is administered and the
effect is 60% and 20mg of drug B produces
same 60% effect, then drug A is said to be
more potent than B.

Pain
Definition
Pain is an unpleasant sensory or emotional
experience related to actual or potential tissue
damage
Stimulus for pain
Chemical
Mechanical
electrical
thermal
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Classification of Pain

Based on duration
Acute pain: a sharp, intense pain of rapid onset
occurring over a short period.
Chronic pain: persistent or intermittent usually
defined as lasting at least 6 months.
Base on location
Somatic pain: pain arising from body walls
Visceral pain: pain arising from organs in the
abdominal and thoracic cavities
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Classification of pain
Referred pain: pain that occurs at the site distant
from the source of the disease or injury, usually of
visceral source.
Phantom limb pain: pain associated with a
missing limb
Emotional or psychogenic pain


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Pathophysiology of pain
1.Transduction
2.Transmission
3.Modulation
4.Perception

Transduction

Nociceptors detect pain stimuli;
convert them into electrical
impulse .
Histamine, bradykinin,
acetylcholine & serotonin
increase the transmission of
pain.
Prostaglandins: increase the
sensitivity of pain receptors.




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Transmission

Movement of pain stimulus from site of injury
to the spinal cord.
This signal travels along:
1. A-delta fibers:
smaller, myelinated & transmit pain signals rapidly
produces the first fast or acute pain
2. Type C fibres
are larger, unmyelinated
transmit the second pain that is normally dull, aching
and burning in quality.
The pain also last longer


Modulation

In the spinal cord, the signal
Produce a reflex
gets sent the CNS to be
perceived.
Endogenous opioids (endorphins
and encephalin) modulate intensity
of the signal sent up to the brain.

Perception

Final stop
Occurs in the brain
It is also conscious subjective and emotional.


Analgesics
Drugs that relieve or reduce pain
without producing
unconsciousness.
2 types
Non-narcotic/NSAIDs
Narcotic analgesics


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Non-narcotic analgesics
AKA Cyclooxygenase inhibitors
Group of drugs that relieve pain, fever, and/or
inflammation
E.g. include:
Salicylates
NSAIDs
Acetaminophen

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Classification of non-narcotic
analgesics

1. Nonsteroidal anti-inflammatory drugs
Have anti-inflammatory properties
E.g. aspirin, ibuprofen, naproxen, diclofenac
2. Acetaminophen
Reduce pain and fever but cant suppress
inflammation
E.g. Tylenol or paracetamol


Mechanism of action
Inactivates cyclooxygenases (enzyme required
for prostaglandin formation)
Two forms of cyclooxygenases
COX-1
COX-2
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Cox-1
Present in all tissues/cells
Functions:
blood clotting
protect stomach lining,
Decrease gastric secretion,
increase mucus secretion.
Inhibition: adverse effects of NSAIDs

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Cox-2
Active at sites of trauma, or injury and is
associated with pain and other signs of
inflammation.
Inhibition of COX-2 results in therapeutic
effects

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Non-steroidal anti-inflammatory
drugs (NSAIDs)
Introduction
A non-narcotic analgesic
So named because they dont belong to the
steroids group
Yet have anti-inflammatory & analgesic
properties

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Classification of NSAIDs
First-generation NSAIDs
Inhibit COX-1 and COX-2
E.g. aspirin, ibuprofen and naproxen.
Second Generation NSAIDs:
Inhibit COX-2 only.
Inhibit pain and inflammation with minimal risk
of serious side effects.
E.g. celecoxib.

Examples of NSAIDs
Salicylates
Ibuprofen
Naproxen
Diclofenac sodium
Indometacin
Celecoxib
perixicam
Salicylates
Pharmacologic Effects
1. Analgesic
2. Antipyretic
3. Anti-inflammatory

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Types of Salicylates
Aspirin (acetylsalicylic acid)
Magnesium salicylate
Sodium salicylate
All have similar in pharmacologic activity ( aspirin
has greater anti- inflammatory effect

Aspirin (acetylsalicylic acid): a
prototype
Generic name: aspirin
Trade names: Ecotrin,
Classification: Antipyretic, Analgesic (non-
opioid), anti-inflammatory, anitrheumatic,
antiplatelet, salicylate and NSAID
Therapeutic actions
1. Suppression of inflammation: rheumatoid arthritis and
osteoarthritis.
2. Analgesia: mild to moderate pain e.g. headache &
dysmenorrhea
3. Reduction of fever: Inhibits pyrogen-induced synthesis
of prostaglandins.

Therapeutic actions
4. Dysmenorrhea: Inhibits prostaglandin
synthesis in the uterine smooth muscles.
5. Suppression of platelet aggregation
Synthesis of thromboxane A
2
(TXA
2
) in the
platelet promotes aggregation.
Aspirin causes an irreversible inhibition of COX-1,
the enzyme that makes TXA
2.

Dosages
Aches and pains; fever: 325-650mg q 4 hrs.
Acute rheumatic fever: 5-6gm/day/ divided doses
Rheumatoid arthritis: 3.6-5.4mg /day/divided doses
Acute MI: 160mg once a day
Ischemic stroke/TIAs 50-325mg once a day
Routes: Oral and Rectal

Adverse effects
GIT disturbances: e.g. dyspepsia and
vomiting.
Bleeding: due to inhibition of platelet
aggregation.
Renal impairment: inhibits synthesis of
prostaglandins that cause vasodilation. The
resultant vasoconstriction decreases renal
blood flow to the kidneys
Allergy:
Adverse effects
Salicylism
A syndrome: occurs when aspirin levels climb just
slightly above therapeutic levels. The symptoms
include: Dizziness & Tinnitus
Reyes syndrome (rare but serious)
Characterized by encephalopathy and fatty liver
degeneration.
Observed in children with influenza or chickenpox
& taking aspirin.


Contraindication
1. Hemophilia
2. Children under 12 years
3. GIT ulceration
4. aspirin intolerance
5. breastfeeding
Adverse effects
GIT disturbances
Salicylate toxicity produces a condition called
salicylism. The symptoms include:
Dizziness
Tinnitus
Impaired hearing
Nausea
Vomiting
Mental confusion.

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contraindication
Heamophillics
Chdn under 12 yrs
GIT ulceration
Breastfeeding

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Ibuprofen
Generic Name: ibuprofen
Trade/brand name: ????
Classification: NSAID, Analgesic (non-opioid),
priopionic acid derivative
Dosage

Therapeutic action
Exhibits anti-inflammatory, analgesic and
antipyretic properties
Has both central and peripheral effects
Indications
Relief S/S of rheumatoid arthritis
Relief of mild to moderate pain
Fever reduction


Side effects

Dyspepsia
vomiting,
abdominal pains,
heartburns,
nausea,
Diarrhoea
Severe GI bleeding and Unceration

Contraindications
1. Peptic Ulcer disease
2. Hypersensitivity
3. Neonates with congenital heart disease
4. Active bleeding
Acetaminophen
Generic name acetaminophen
Trade/Brand name Paracetamol, Tylenol,
Panadol
Mechanism of action
Inhibition of prostaglandins by Paracetamol
occurs ONLY IN THE CNS.
Has no effect on prostaglandin synthesis in the
peripheral sites.
This may explain the absence of anti-
inflammatory effects and gastric ulceration.



Indications

Relief of pain and fever
It is preferred to NSAIDs for use in children
suspected of having chicken pox and influenza
Good replacement for patients with aspirin
toxicity


Dosages:
Adult and children over 12 yrs
325mg to 650mg q 4 to 6 hrs.
Pediatric patients
0-3 months 62.5mg
4-11 months 125mg
12-23 months 187.5mg
2-3 years 250mg
4-5yrs 375mg
6-7 yrs 500mg

Metabolism of acetaminophen

Acetaminophen can be metabolized in two ways;
1. Major pathway:
Acetaminophen undergoes conjugation with glucuronic acid to form nontoxic metabolites.
At therapeutic doses, practically the entire drug is converted to nontoxic compounds via the
major pathway.
2. Minor pathway :
Acetaminophen is oxidized by P450-containing enzyme into highly reactive and toxic
compound.
Only a small fraction is converted into toxic metabolite via the minor pathway.
Under normal conditions, the toxic metabolite undergoes rapid conversion to a nontoxic
form; glutathione is required for the conversion.
When an overdose of acetaminophen is taken, a larger than normal amount is processed via
the minor pathway; hence, a large quantity of toxic metabolite is produced.
As the liver attempts to detoxify the metabolite, glutathione is rapidly depleted, and further
detoxification stops. As a result, the toxic metabolite accumulates, causing damage to the
liver.

Opioids (Narcotic) Analgesics
Two classes:
Narcotic analgesics obtained from raw opium
Synthetic narcotic analgesics
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Narcotic Analgesics
Terminologies
Opiates: compounds extracted from the opium
poppy flower
opioids: chemical compounds that are wholly
synthesized, but which resemble the opiates in
their actions e.g. meperidine
Other Examples: morphine and codeine.


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General properties of narcotic analgesics
They have capacity to reduce pain and pain
perception
Able to alter ones reaction to the pain
They have sedative properties
They cause profound feeling well-being
(euphoria)
Addictive properties (physical and
psychological dependence)
Examples of Narcotic Analgesics
(Opiates & Opioids)
Strong opioid
Morphine sulfate
Pethidine Hydrocloride (meperidine)
Fentanyl
butorphanol,
Levophanol
Mild opioid
Tramadol HCL
Codeine phosphate

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Prototype: Morphine sulfate
Generic name
Morphine sulfate
Trade name:
???
Classification:
Opioid agonist analgesic

Dosage and route
Oral
15mg PO daily, as a single dose in the evening
IM or Subcutaneous
5-20mg/70kg as directed by physician
IV
2.5-15/70kg of body weight



Effects of morphine

analgesia,
sedation,
euphoria,
respiratory depression, cough suppression and
suppression of bowel motility.

105
Indication

Severe acute pain or severe chronic pain.
Preoperative sedation and adjunct to anesthesia
control of pain associated with acute myocardial
infarction
Relieve of severe, persistent cough
Treatment of severe diarrhea and intestinal cramping.

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Contraindication

Hypersensitivity
Addiction
Hemorrhage
Bronchial asthma
Increased intracranial pressure

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Adverse Effects

Read from hand out
108

DRUGS USED IN THE PERIOPERATIVE
PERIOD

109
Introduction
These drugs are CNS depressants.
Classified into:
General anesthetic agents,
Narcotic analgesics
Sedative-Hypnotics.

110

Preoperative agents: Sedative-hypnotics

Definitions
Anxiolytics: drugs that prevent feeling of tension or fear.
Sedatives: provide a calming effect on patients
Hypnotics: induces sleep.
Sedative-hypnotic: Produces calming effect at lower doses
and induce sleep at higher doses.
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Sedative-hypnotics are grouped as:
barbiturates
benzodiazepines
Barbiturates
They are powerful CNS
depressants
Rarely used because of:
side effects
risk of psychological
and physical
dependence.


Mechanism of action

Act on the brainstem in the reticular activating
system (RAS) by:
inhibiting nerve cell function
reducing nerve impulse transmission to the
cerebral cortex.
Raising the seizure convulsive threshold.

Drug
name
Dosage/Route Adverse effects
Pheno
barbita
l
(lumin
al)
Sedative: oral; 30-120mg /day
IV/IM; 100-200mg/day
Drowsiness, vitamin
deficiency (vit. D;
folate, or B
12
)
Pentob
arbital
Sedative: oral; 20-30mg bid or qid
Hypnotic: oral; 120-200mg;IM,
150-200mg
Respiratory
depression,
laryngospasm
OVERVIEW
Drugs given for therapeutic purposes are
called medications.
Administering medications-an important
nursing responsibility
The basic requirements for accurate drug
administration are often called the five
rights and the three checks
THE THREE CHECKS
The label on the medication container should
be checked three times during medication
preparation.
The label should be read:
when the nurse reach for the container
Immediately before pouring or opening the
medication
When replacing the container to the drawer or
shelf
The five rights
The right medication to the
Right patient in the
Right dosage through the
Right route at the
Right time



LEGAL RESPONSIBILTIES
Registered Nurses are legally empowered, to
give medications ordered
When giving medications, the nurse is legally
responsible for safe and accurate administration.
She may be held liable for not giving a drug or for
giving a wrong drug or a wrong dose.
she is expected to have sufficient drug knowledge
to recognize and question erroneous orders.
LEGAL RESPONSIBILTIES
The nurse also is legally responsible for actions
delegated to people who are inadequately
prepared for or legally barred from
administering medications (such as nursing
assistants).
nurses are expected to
monitor clients responses to drug therapy.
to teach clients safe and effective self-
administration of drugs when indicated

All substances are poisons;
there is none that is not a
poison. The right dose
differentiates a poison from
a remedy.

Paracelsus, 1493-1541
Ideal Drug
Effectiveness
Safety
Selectivity
Reversible
Predictability
Ease of administration
Freedom from drug interactions

Ideal Drug
Low cost
Chemical Stability
Possession of a simple generic name

PHARMACOKINETICS

Therapeutic Objective
Maximum benefit with minimum harm


The intensity of the response to a drug is
directly related to the concentration of the
drug at its site of action
Intensity of Drug responses
Administration dosage and route
Pharmacokinetics
Pharmacodynamics
Individual variation
Nursing Responsibilities
Last line of defense against errors!!!!!!!!!


Patient education

Utilize the nursing process
Drug Legislation
1906 drugs should be free of adulterants
1938 testing for toxicity
1962 proof of effectiveness
1970 Controlled Substance Act Scheduled
drugs
1997 Food and Drug Administration
Modernization Act
New Drug Development
Preclinical testing prior to testing on humans
Clinical testing
I normal volunteers except maybe patients
who have disease
II and III patients
IV released for general use
Be neither the first to adopt the new nor the
last to abandon the old!
Drug Names
Chemical
Generic Name
Trade Name


OTC drugs
Pharmacokinetics
Drug movement throughout the body
Absorption movement of drug from its site of
administration into blood
Dissolve must dissolve before being absorbed
Surface area the larger the faster
Blood flow most rapid where blood flow is high
Lipid solubility - the higher the faster
pH partitioning
Absorption - Routes
IV no barriers to absorption
Intramuscular good for poorly soluble drugs, time
released
Subcutaneous again no significant barriers
Oral must pass through cells of epithelium, enteric
coating
Safer but highly variable absorption enteric,
sustained-release, tablets
Distribution
Blood flow to tissues
Exiting the vascular system once it has been
delivered pass through pores in capillary
wall
Protein - binding
Drugs can bind with proteins
Parts of drugs will be bound during any given
time period
Impedes drugs ability to reach sites of action,
metabolism, or excretion

Metabolism
LIVER
Enzymatic alteration of drug structure
Consequences of metabolism
Accelerated renal excretion kidney cannot
excrete highly lipid soluble
Drug inactivation
Increased therapeutic action
Activation of prodrugs
Increased or decreased toxicity
Considerations in Metabolism
Age
Induction of drug metabolizing enzymes
First-pass effect Nitroglycerin
Nutritional status
Competition between drugs
Excretion
KIDNEY
Glomerular filtration blood to tubular urine
Tubular reabsorption
Active tubular secretion pumps for organic
acids and organic bases to urine

Monitoring drug levels
Plasma drug levels


Therapeutic range
Drug Half-life
Time requires for the amount of drug in the
body to decrease by 50%
Will determine dosing requirements
Goal - plateau
Dosing
Loading doses when plateau must be
achieved quickly
Routine smaller doses maintenance doses
Peak and trough levels
Maximal efficacy largest effect a drug can
produce


Potency one that produces its effects at
lower dosages
Receptors
Drugs bind to receptors to produce effects

Reversible
All that drugs can do is mimic the physiological
activity of the bodys own molecules
Block the physiological activity of the bodys
own molecules
Agonists
Mimic the bodys own regulatory molecules
Antagonists
Drugs that block the actions of endogenous
regulators
Partial agonists
Mimic the actions but with reduced intensity
Drug Interactions
Can have varying effects

Direct chemical or physical IV preparation
Drug Food Interactions
Frequently decreased rate of absorption

Grapefruit juice can inhibit metabolism

with food with or shortly after meal
empty stomach one hour prior to meal or
two hours after
Adverse drug reactions
Side effect
Toxicity
Allergic reaction
Idiosyncratic effect
Iatrogenic disease
Physical dependence
Carcinogenic effect
Teratogenic effect induce birth defect


Ways to minimize
Variation in drug responses
Age
Body composition
Gender
Pathophysiology
Tolerance
Placebo effect
Genetics
Variability in absorption bioavailability oral
ability to reach circulation
Compliance
What does the term adverse reaction refer to?
A. A life-threatening response to a response
to a drug
B. A drug-induced allergy
C. A harmful, undesirable response to a drug
D. An unpredictable response to a drug
What is an idiosyncratic response?
A. a toxic reaction
B. an allergic reaction
C. a reaction peculiar to the patient
D. an anaphylactic reaction
Which statement accurately characterizes geriatric
patients compliance with prescribed drug regimens?
A. compliance decreases with age
B. compliance increases with age
C. compliance increases with multiple health
problems
D. compliance decreases when more than three
drugs are prescribed


END
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