PHARMACOLOGY

FINALS l yey

- Stimulation of beta-1 receptors causes an increase

MODULE 13: AUTONOMIC NERVOUS in the heart rate, and stimulation of beta-2
SYSTEM receptors causes the relaxation of smooth muscle
in the bronchi (bronchodilation), the uterus
(relaxation), and the peripheral arterial blood
vessels (vasodilation).
MODULE 13 Lesson 1 - Stimulation of the dopaminergic receptors in the
brain improves the symptoms associated with
Parkinson's disease.
- Dopamine also increases urine output as a result
ADRENERGIC: Agonists of the stimulation of specific receptors in the
(sympathomimetics) kidneys that results in better renal perfusion.

- Adrenergic drugs are medications that stimulate Nursing Implications for Adrenergic
certain nerves in your body. Agents
- They do this either by mimicking the action of
the chemical messengers epinephrine and
Premedication Assessment:
norepinephrine or by stimulating their release.
1. Obtain baseline vital signs: heart rate and blood
- These drugs are used in many life-threatening
pressure.
conditions, including cardiac arrest, shock,
2. Check for the premedication assessments for
asthma attack, or allergic reaction.
respiratory tract disease, bronchodilators, and
decongestants.
ADRENERGIC ACTION:
Common Adverse Effects:
- The adrenergic nervous system may be
➔ Adverse effects associated with adrenergic agents
stimulated by two broad classes of drugs:
are usually dose related and resolve when the
catecholamines and noncatecholamines.
dosage is reduced or the medication
- The body's naturally occurring neurotransmitter
discontinued.
catecholamines are norepinephrine, epinephrine,
➔ Cardiovascular: Palpitations, tachycardia, skin
and dopamine.
flushing, dizziness, tremors, Orthostatic
- Norepinephrine is secreted primarily from nerve
hypotension.
terminals
➔ Patients who are potentially more sensitive to
- Epinephrine comes primarily from the adrenal
adrenergic agents are those with impaired
medulla
hepatic function, thyroid disease, hypertension,
- Dopamine is found at selected sites in the brain,
and heart disease.
the kidneys and the GI tract.
➔ Patients with diabetes mellitus may also have an
- All three agents are also synthetically
increased frequency of episodes of
manufactured and may be administered to
hyperglycemia.
produce the same effects as those that are
Serious Adverse Effects:
naturally secreted.
➔ Cardiovascular: Dysrhythmias, chest pain, severe
- Noncatecholamines have actions that are
hypotension, hypertension, anginal pain.
somewhat similar to those of the catecholamines;
◆ ACTION: Discontinue therapy
however, they are more selective for certain types
immediately and notify the healthcare
of receptors, they are not quite as fast acting,
provider.
and they have a longer duration of action.
➔ Gastrointestinal Nausea, vomiting.
- The adrenergic side of the autonomic nervous
◆ ACTION: Notify the healthcare provider.
system can be subdivided into the alpha
Ask the patient if there has been a recent
receptors, beta receptors, and dopaminergic
change in his or her regimen of
receptors.
prescription, nonprescription, or herbal
- In general, the stimulation of the alpha-1 receptors
medicines.
causes the vasoconstriction
of blood vessels. The alpha-2 receptors appear to
serve as mediators of negative feedback, thereby
preventing the further release of norepinephrine.
PHARMACOLOGY
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ADRENERGIC AGONISTS (Alpha- and
Beta- Adrenergic Blocking Agents)
ACTION:
- The alpha- and beta-adrenergic blocking agents
act by plugging the alpha or beta receptors,
which prevents other agents—usually the
naturally occurring catecholamines—from
stimulating the specific receptors.
- The beta blockers can be subdivided into
nonselective and selective beta antagonists. The
nonselective blocking agents have an equal
affinity for beta-1 and beta-2 receptors, and they
inhibit both. These agents are propranolol,
nadolol, pindolol, penbutolol, carteolol, sotalol,
and timolol. The selective beta-1 blocking agents
exhibit action against the heart's beta-1 receptors
(cardioselective) and do not readily affect the
beta-2 receptors of the bronchi.
- The selective beta-1 antagonists are esmolol,
metoprolol, acebutolol, betaxolol, bisoprolol, and
atenolol. This selective action is beneficial for
patients in whom nonselective beta blockers may
induce bronchospasm (e.g., those with asthma).
- However, it is important to note that the
selectivity of these agents is only relative. In larger
doses, these agents will also inhibit the beta-2
receptors. There are no selective beta-2 blockers
available. Labetalol and carvedilol exhibit selective
alpha-1 and nonselective beta-adrenergic
blocking activity
USES:
Because one of the primary actions of the alpha-receptor
stimulants is vasoconstriction, it would be expected that
alpha-blocking agents are indicated for patients with
diseases that are associated with vasoconstriction. Alpha
blockers (e.gprazosin, terazosin, doxazosin) are sometimes
used to treat hypertension. Alfuzosin, doxazosin, and
tamsulosin are used to relax the smooth muscle of the
bladder and prostate; they are used to treat urinary
obstruction caused by benign prostatic hyperplasia.
Beta-adrenergic blocking agents (e.g., beta blockers) are
used extensively to treat post–myocardial infarction. They
may also be used for hypertension, angina pectoris,
cardiac dysrhythmias, symptoms of hyperthyroidism, and
stage fright. Nonselective beta blockers must be used
with extreme caution in patients with respiratory
conditions such as bronchitis, emphysema, asthma, or
allergic rhinitis. A beta blockade produces severe
bronchoconstriction and may aggravate wheezing,
especially during pollen season.
Beta blockers should be used with caution in patients
with diabetes and in those who are
susceptible to hypoglycemia. Beta blockers further induce
the hypoglycemic effects of insulin and reduce the
release of insulin in response to hyperglycemia. All beta
blockers mask most of the signs and symptoms of acute
hypoglycemia. Beta-adrenergic blocking agents should
be used only in patients with controlled heart failure.
Further hypotension, bradycardia, or heart failure may
develop.
Nursing Implications for Beta-Adrenergic
Blocking Agents
Premedication assessment:
1. Obtain baseline vital signs: heart rate and
blood pressure.
2. See also the premedication assessments for
patients with antidysrhythmic therapy and
for those with hypertension
Common Adverse Effects:
➔ Most of the adverse effects associated with
beta-adrenergic blocking agents are dose related.
Response by individual patients is highly variable.
Many of the adverse effects that do occur may be
transient. Strongly encourage patients to see their
healthcare providers before discontinuing
therapy. Minor dosage adjustment may be all that
is required to eliminate most adverse effects.
➔ Endocrine: Patients with diabetes.
◆ Monitor for symptoms of hypoglycemia,
including headache, weakness, decreased
coordination, general apprehension,
diaphoresis, hunger, or blurred or double
vision. Many of these symptoms may be
masked by beta-adrenergic blocking
agents.
◆ Notify the healthcare provider if any of the
symptoms described appear
intermittently.
Serious Adverse Effects:
Cardiovascular: Bradycardia, peripheral vasoconstriction
(e.g., purple, mottled skin).
➔ Discontinue further doses until the patient is
evaluated by a healthcare provider.
Heart failure:
➔ Monitor patients for an increase in edema,
dyspnea, crackles, bradycardia, and orthopnea.
Notify the healthcare provider if these symptoms
develop.
Respiratory:
➔ Bronchospasm, wheezing.
 PHARMACOLOGY
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➔ Withhold additional doses until the patient has
been evaluated by a healthcare provider.
MODULE 13 Lesson 2
Cholinergic Agonists
- Drugs that stimulate the parasympathetic
nervous system are called cholinergic agonists, or
parasympathomimetics, because they mimic the
parasympathetic neurotransmitter acetylcholine.
The neurotransmitter located at the ganglions
and the parasympathetic terminal nerve endings
is acetylcholine (ACh). It innervates cholinergic
receptors in organs, tissues, and glands.
Two types of Cholinergic Receptors:
➔ muscarinic receptors, which stimulate smooth
muscle and slow the heart rate, and
➔ nicotinic receptors (neuromuscular), which affect
the skeletal muscles.
Many cholinergic agonists are non selective because they
can affect both the muscarinic and the nicotinic
receptors. However, there are selective cholinergic
agonists for the muscarinic receptors that do not affect
the nicotinic receptors.
Two Types of Cholinergic Agonists:
➔ direct-acting cholinergic agonists act on
receptors to activate a tissue response
➔ indirect-acting cholinergic agonists inhibit the
action of the enzyme cholinesterase (ChE), also
called acetylcholinesterase (AChE), by forming a
chemical complex that allows acetylcholine to
persist and attach to the receptor. Drugs that
inhibit ChE are called cholinesterase inhibitors,
acetylcholinesterase inhibitors, or
anticholinesterases.
Effects of Cholinergic Agonists:
Body Tissue Response
Cardiovascular Decreased heart rate, lowered BP because of
vasodilation, and slowed conduction of
atrioventricular node
Gastrointestinal Increased tone and motility of smooth muscle
of stomach and intestine, increased
peristalsis, and relaxed sphincter muscles
Genitourinary Contraction of muscles of the urinary bladder,
increased tone of ureters, relaxed bladder
sphincter muscles, and stimulated urination
Ocular Increased pupillary constriction or miosis
(pupil becomes smaller) and increased
accommodation (flattening or thickening of
eye lens for distant or near vision)
Glandular Increased salivation, perspiration, and tears
Bronchial (lungs) Stimulation of bronchial smooth muscle
contraction and increased bronchial
secretions
Striated Muscles Increased neuromuscular transmission and
maintenance of muscle strength and tone
➔ Tissue responses to large doses of cholinergic
agonists.
➔ Major tissue responses to normal doses of
cholinergic agonists.
Direct-Acting Cholinergic Agonists:
Many drugs classified as direct-acting cholinergic
agonists are primarily selective to the muscarinic
receptors but are nonspecific because the muscarinic
receptors are located in the smooth muscle of the GI and
genitourinary tracts, glands, and heart.
Bethanechol chloride, a direct-acting cholinergic agonist,
acts on the muscarinic (cholinergic) receptor and is used
primarily to increase urination in the treatment of urinary
retention and neurogenic bladder.
Metoclopramide hydrochloride (HCl) is a direct-acting
cholinergic agonist that is usually prescribed to treat
gastroparesis, nausea, and gastroesophageal reflux
disease (GERD). In low doses, metoclopramide enhances
gastric motility and thus accelerates gastric emptying
time.
Pharmacokinetics
➔ Bethanechol chloride is poorly absorbed from
the GI tract. The percentage of protein binding
and the half-life are unknown. The drug is most
likely excreted in the urine.
Pharmacodynamics
➔ The principal use of bethanechol is to promote
urination by stimulating the muscarinic
cholinergic receptors in the detrusor muscle to
contract the bladder and produce urine output.
Because of the increased tone of the detrusor
muscle
➔ The onset of action is 30 to 90 minutes after
taking an oral dose of bethanechol, and the
duration is 2 hours.
➔ Bethanechol also increases peristalsis in the GI
tract, and the drug should be taken on an empty
PHARMACOLOGY
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stomach 1 to 2 hours before meals to minimize
nausea and vomiting.
Side Effects and Adverse Reactions:
➔ Mild to severe side effects of most muscarinic
agonists, such as bethanechol, include
hypotension, tachycardia, blurred vision, excessive
salivation, increased gastric acid secretion,
abdominal cramps, diarrhea, bronchoconstriction,
and, in some cases, cardiac dysrhythmias. This
group of agents should be prescribed cautiously
for patients with low blood pressure and low heart
rates. Muscarinic agonists are contraindicated for
patients with intestinal or urinary tract
obstruction, severe bradycardia, or active asthma.
Eye
➔ Pilocarpine is a direct-acting cholinergic agonist
that constricts the pupils of the eyes, thus
opening the Schlemm canal to promote drainage
of aqueous humor (fluid). This drug is used to
treat glaucoma by relieving (intraocular) fluid
pressure in the eye and to promote miosis in eye
surgery and examinations.
Indirect-Acting Cholinergic Agonists:
The indirect-acting cholinergic agonists do not act on
receptors; instead, they inhibit or inactivate the enzyme
cholinesterase, permitting acetylcholine to accumulate at
the receptor sites ). This action gives them the name
cholinesterase (ChE) inhibitors, acetylcholinesterase
(AChE) inhibitors, or anticholinesterases, of which there
are two types: reversible and irreversible. The function of
the enzyme cholinesterase is to break down acetylcholine
into choline and acetic acid. A small amount of
cholinesterase can break down a large amount of
acetylcholine in a short
period. A cholinesterase inhibitor drug binds with
cholinesterase, allowing acetylcholine to activate the
muscarinic and nicotinic cholinergic receptors. This action
permits skeletal muscle stimulation, which increases the
force of muscular contraction. Because of this action,
cholinesterase inhibitors are useful to increase muscle
tone for patients with myasthenia gravis (a
neuromuscular disorder). By increasing acetylcholine,
additional effects occur, such as increases in GI motility,
bradycardia, miosis, bronchial constriction, and increased
micturition. The primary use of reversible cholinesterase
inhibitors is to treat myasthenia gravis; another use is to
treat Alzheimer disease. The primary clinical indication for
irreversible cholinesterase inhibitors is glaucoma.
Reversible Cholinesterase Inhibitors:
Reversible cholinesterase inhibitors are used to produce
pupillary constriction in the treatment of glaucoma and
to increase muscle strength in patients with myasthenia
gravis. Drug effects persist for several hours. Drugs used
to increase muscular strength in myasthenia gravis
include neostigmine (short acting), pyridostigmine
bromide (moderate acting), ambenonium chloride (long
acting), and edrophonium chloride (short acting, for
diagnostic purposes). A reversible anticholinesterase drug
is physostigmine, which is used as an antidote for
atropine to reverse anticholinergic toxicity.
Side Effects:
➔ Common side effects from reversible
cholinesterase inhibitors are hypotension,
bradycardia, sweating, hypersalivation, and GI
distress, which includes anorexia, nausea,
vomiting, abdominal pain, and diarrhea.
➔ Caution for reversible cholinesterase inhibitors is
required for patients who have bradycardia,
asthma, peptic ulcers, or hyperthyroidism.
Cholinesterase inhibitors are contraindicated for
patients with intestinal or urinary obstruction.
Irreversible Cholinesterase Inhibitors:
Irreversible cholinesterase inhibitors are potent agents
because of their long-lasting effects. The enzyme
cholinesterase must be regenerated before the drug
effect diminishes, a process that may take days or weeks.
These drugs are used to produce pupillary constriction.
SIGNS OF CHOLINERGIC CRISIS:
D - DIARRHEA
U - URINATION
M - MIOSIS
B - BRADYCARDIA
E - EMESIS
L - LACRIMATION
L - LETHARGY
S - SALIVATION
*NOTE: always remember DUMBELLS for signs of
CHOLINERGIC CRISIS
Cholinergic Antagonists
- Drugs that inhibit the actions of acetylcholine by
occupying the acetylcholine receptors are called
cholinergic antagonists (blocking agents),
muscarinic antagonists, anticholinergics,
cholinergic blocking agents, antispasmodics, or
parasympatholytics. The major body tissues and
organs affected by the anticholinergic group of
drugs are the heart, respiratory tract, GI tract,
urinary bladder, eyes, and exocrine glands. By
blocking the parasympathetic nerves, the
sympathetic (adrenergic) nervous system
 PHARMACOLOGY
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dominates. Anticholinergics and adrenergic
agonists produce many of the same responses.
- Anticholinergic and cholinergic agonists have
opposite effects. The major responses to
anticholinergics are a decrease in GI motility, a
decrease in salivation, dilation of pupils—also
called mydriasis—and an increase in pulse rate.
Other effects of anticholinergics include
decreased bladder contraction, which can result
in urinary retention, and decreased rigidity and
tremors related to neuromuscular excitement. An
anticholinergic can act as an antidote to the
toxicity caused by cholinesterase inhibitors and
organophosphate ingestion. Muscarinic receptors
are a type of cholinergic receptor involved in
tissue and organ responses to anticholinergics
because anticholinergics inhibit the actions of
acetylcholine by occupying these receptor sites.
These drugs may also block the effect of
direct-acting parasympathomimetics, such as
bethanechol and pilocarpine, and of
indirect-acting parasympathomimetics, such as
physostigmine and neostigmine.
Effects of Cholinergic Agonists:
Body Tissue Response
Cardiovascular Heart rate increases w/ large doses, small
doses can decrease heart rate
Gastrointestinal Relaxed smooth muscle tone of GI tract,
decreased GI motility and peristalsis, gastric,
and intestinal secretions are decreased
Urinary Tract Relaxed bladder detrusor muscle and
increased constriction of internal sphincter,
urinary retention can result
Ocular Dilated pupils (mydriasis) and paralyzed ciliary
muscles (cycloplegia) cause a decrease in
accommodation
Glandular Salivation, perspiration, and bronchial
secretion are decreased
Bronchial (lungs) Bronchi are dilated, and bronchial secretions
decrease
Central Nervous Tremors and rigidity of muscles are decreases;
System drowsiness, disorientation and hallucinations
can result from large doses
ATROPINE
➔ Atropine sulfate is a classic anticholinergic—or
muscarinic antagonist—drug.
➔ Scopolamine was the second belladonna
alkaloid produced.
➔ Atropine and scopolamine act on muscarinic
receptors, but they have little effect on nicotinic
receptors except in high doses.
➔ Atropine is useful primarily as a preoperative
medication to decrease salivary secretions and
as an agent to increase heart rate when
bradycardia is present.
➔ Atropine can also be used as an antidote for
muscarinic agonist poisoning caused by an
overdose of a cholinesterase inhibitor or a
muscarinic drug such as bethanechol. However,
if a patient takes atropine or an atropine-like drug
(e.g., an antihistamine), side effects can occur.
Pharmacokinetics:
➔ Atropine sulfate is well absorbed orally and
parenterally. It crosses the blood-brain barrier and
exerts its effect on the central nervous system
(CNS). The protein binding is unknown. It crosses
the placenta. Atropine has a short half-life of 2 to
3 hours, so there is little cumulative effect. Most of
the absorbed atropine is excreted in the urine.
Pharmacodynamics:
➔ Atropine sulfate blocks acetylcholine by
occupying the muscarinic receptor. It increases
the heart rate by blocking vagus stimulation and
promotes dilation of the pupils by paralyzing the
iris sphincter. The two most frequent uses of
atropine are to decrease salivation and
respiratory secretions preoperatively and to
treat sinus bradycardia by increasing the heart
rate.
➔ Atropine also is used ophthalmically for
mydriasis and cycloplegia before eye exams and
to treat inflammation of the iris (iritis) and uveal
tract.
➔ Its onset of action for the intramuscular (IM)
route is 10 to 30 minutes, and it peaks at 30
minutes. The duration is 4 hours.
➔ The onset of action for the IV route is immediate,
and peak action occurs in 5 minutes.
Side Effects and Adverse Reactions:
➔ The common side effects of atropine and
atropine-like drugs include dry mouth, decreased
perspiration, blurred vision, tachycardia,
constipation, and urinary retention.
➔ Other side effects and adverse reactions are
nausea, headache, dry skin, abdominal
distension, hypotension or hypertension,
impotence, photophobia (intolerance of bright
light), and coma.
PHARMACOLOGY
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should not be administered to patients diagnosed

ANTIPARKINSON-ANTICHOLINERGIC with glaucoma.
DRUGS Side Effects and Adverse Reactions:
➔ Side effects of antihistamines used as
Studies indicate that anticholinergics affect the CNS as
anticholinergics include dry mouth, visual
well as the parasympathetic nervous system.
disturbances (especially blurred vision resulting
Anticholinergics affect the CNS by suppressing the
from pupillary dilation), constipation secondary
tremors and muscular rigidity of parkinsonism, but they
to decreased GI peristalsis, urinary retention
have little effect on mobility and muscle weakness. As a
related to decreased bladder tone, tachycardia
result of these findings, several anticholinergic drugs were
(when taken in large doses), hypotension, skin
developed for the treatment of parkinsonism (e.g.,
rash, muscle weakness, and flushing
trihexyphenidyl hydrochloride, biperiden, and
benztropine). These drugs can be used alone in the early MODULE 14: NEUROLOGIC AND
stages of parkinsonism; they may be used in combination
with levodopa/carbidopa to control parkinsonism, or they NEUROMUSCULAR AGENTS
can be used alone to treat pseudoparkinsonism, which
results from the side effects of the
phenothiazines in antipsychotic drugs. MODULE 14 Lesson 1

Pharmacokinetics:
➔ Benztropine is well absorbed from the GI tract. Its
protein-binding percentage and half-life are
unknown. It is excreted in the urine.
Pharmacodynamics:
➔ Benztropine decreases involuntary movement
and diminishes the signs and symptoms of
tremors and muscle rigidity that occur with
parkinsonism and pseudoparkinsonism. It is
available as an oral tablet and as parenteral IM
and IV injections. Alcohol and other CNS
depressants potentiate sedation. Anticholinergics,
phenothiazines, and tricyclic antidepressants
(TCAs) may increase the anticholinergic effects of
benztropine. The side effects are similar to those
of other anticholinergic drugs.
Anticholinergics for Treating Motion Sickness
➔ The effects of anticholinergics on the CNS benefit
patients who are prone to motion sickness. An
example of such an anticholinergic, classified as
an antihistamine for motion sickness, is
scopolamine. It is available topically as a skin
patch placed behind the ear. Prevention of
motion sickness is also provided via wristbands
and ginger, including ginger gum or candy.
Transdermal scopolamine is delivered over 3 days
and is frequently prescribed for activities such as
flying, cruising on the water, and bus or
automobile trips. Other drugs classified as
antihistamines for motion sickness are
dimenhydrinate, cyclizine, and meclizine
hydrochloride. Dosages may vary according to
age, sex, and weight. Because anticholinergic
drugs can increase intraocular pressure, they
CNS Stimulant and Depressant
***NOTE: AS MUCH AS POSSIBLE, KABISADUHIN DRUGS,
SIDE EFFECTS, ADVERSE EFFECTS AND MGA NURSING
INTERVENTIONS AND MANAGEMENTS (each m14)
PATHOPHYSIOLOGY OF ATTENTION DEFICIT
HYPERACTIVITY DISORDER AND NARCOLEPSY
Narcolepsy is characterized by falling asleep during
normal waking activities, such as driving a
car or talking with someone. Sleep paralysis, the
condition of muscle paralysis that is normal
during sleep, usually accompanies narcolepsy and affects
the voluntary muscles. The narcoleptic is
unable to move and may collapse,
AMPHETAMINES
➔ Amphetamines stimulate the release of the
neurotransmitters norepinephrine and dopamine
from the brain and sympathetic nervous system
(peripheral nerve terminals) and inhibit the
reuptake of these transmitters.
➔ Amphetamines ordinarily cause euphoria and
increased alertness
➔ The half-life of amphetamines varies from 9 to 13
hours.
PHARMACOLOGY
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➔ Amphetamines and dextroamphetamine are • Anorexia

prescribed for narcolepsy and ADHD when • Dry mouth
amphetamine-like drugs are ineffective. • Nausea
• Vomiting
Types of Amphetamines: • Irritability
● Amphetamine Sulfate • Tremors
● Dextroamphetamine Sulfate • Euphoria
● Lisdexamfetamine dimesylate • Blurred Vision
• Headache
SIDE EFFECTS OF AMPHETAMINE: • Abdominal pain
CNS: • Anemia
• Dizziness Adverse Reactions:
• Headache • Tachycardia
• Euphoria • Hypertension
• Confusion • Growth suppression
• Blurred vision • Palpitations
• Restlessness • Seizures
• Insomnia • Transient weight loss
• Seizure • Exfoliative dermatitis
• Tremors • Stroke
Cardiovascular: • Thrombocytopenia
• Tachycardia • Hepatotoxicity
• Hypertension
• Heart palpitations Pharmacokinetics:
• Dysrhythmias ➔ Methylphenidate is well absorbed from the GI
Gastrointestinal: mucosa and is usually administered to children
• Dry mouth twice a day before breakfast and lunch.
• Anorexia ➔ Because food affects its absorption rate, this drug
• Weight loss should be given 30 to 45 minutes before meals.
• Diarrhea ➔ Methylphenidate should be given 6 hours or
• Constipation more before sleep because it can cause
Endocrine: insomnia.
• Erectile Dysfunction ➔ Transdermal patches may be worn for 9 hours
➔ This drug is excreted in the urine, and 40% of
methylphenidate is excreted unchanged.
AMPHETAMINE-LIKE DRUGS FOR Pharmacodynamics:
ATTENTION DEFICIT/HYPERACTIVITY ➔ Methylphenidate helps to correct ADHD by
decreasing hyperactivity and improving attention
DISORDER AND NARCOLEPSY span. It is also a treat for narcolepsy
Methylphenidate ➔ Amphetamine-like drugs are considered generally
➔ the most frequently prescribed drug used to more effective in treating ADHD than are
treat ADHD amphetamines which are generally avoided
➔ Methylphenidate is also used to treat narcolepsy because they have a higher potential for abuse,
Dexmethylphenidate habituation, and tolerance.
➔ Both are given to given to increase a child’s ➔ Methylphenidate potentiates the action of CNS
attention span and cognitive performance stimulants, such as caffeine, and inhibits the
Modafinil metabolism of some barbiturates, such as
➔ Amphetamine-like stimulant that increases phenobarbital, which can lead to increased blood
wakefulness in patients with sleep disorders levels and potential toxicity.
such as narcolepsy
NURSING PROCESS: PATIENT-CENTERED
METHYLPHENIDATE SIDE EFFECTS AND ADVERSE COLLABORATIVE CARE
REACTIONS: Assessment:
Side Effects:
PHARMACOLOGY
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➔ Determine whether the patient has a history of
heart disease, hypertension, hyperthyroidism,
➔ parkinsonism, or glaucoma; in such cases, this
drug is usually contraindicated.
➔ Assess vital signs to be used for future
comparisons. Closely monitor patients with
cardiac
➔ disease because this drug may cause
tachycardia, hypertension, and stroke.
➔ Assess patient mental status, such as mood,
affect, and aggressiveness.
➔ Evaluate height, weight, and growth of children.
➔ Assess complete blood count (CBC), differential
white blood cells (WBCs), and platelets before and
during therapy
Diagnosis:
➔ Health Behavior, Risk-Prone (e.g., impulsiveness,
short attention span, distractibility) that interfere
with peer relationships, learning, and discipline
➔ Family Processes, Interrupted related to
dysfunctional behavior
➔ Development, Risk for Delayed
➔ Knowledge, Deficient related to inexperience with
methylphenidate drug regimen
Planning:
➔ Patient’s hyperactivity will be decreased.
➔ Patient’s attention span will increase.
➔ Patient’s blood pressure and heart rate will be
within normal limits.
➔ Patient will behave in a calm manner.
Nursing Interventions:
➔ Monitor vital signs and report irregularities.
➔ Evaluate height, weight, and growth of children.
➔ Observe patients for withdrawal symptoms such
as nausea, vomiting, weakness, and headache.
➔ Monitor patients for side effects such as
insomnia, restlessness, nervousness, tremors,
irritability, tachycardia, and elevated blood
pressure. Report findings.
Patient Teaching:
➔ Teach patients to take the drug before meals.
➔ Advise patients to avoid alcohol consumption.
➔ Encourage use of sugarless gum to relieve dry
mouth.
➔ Teach patients to monitor weight twice a week
and report weight loss.
➔ Advise patients to avoid driving and using
hazardous equipment when experiencing
tremors, nervousness, or increased heart rate.
➔ Teach patients not to abruptly discontinue the
drug; the dose must be tapered to avoid
withdrawal symptoms. Consult a health care
provider before modifying doses.
➔ Encourage patients to read labels on
over-the-counter (OTC) products because many
contain caffeine. A high plasma caffeine level
could be fatal.
➔ Teach nursing mothers to avoid taking all CNS
stimulants (e.g., caffeine). These drugs are
excreted in breast milk and can cause
hyperactivity or restlessness in infants.
➔ Direct families to seek counseling for children
with ADHD. Drug therapy alone is not an
appropriate therapy program. Notify the school
nurse of the drug therapy regimen.
➔ Explain to patients and family that long-term use
may lead to drug abuse.
Diet:
➔ Advise patients to avoid foods that contain
caffeine (e.g., coffee, tea, chocolate, soft drinks,
and energy drinks).
➔ Encourage parents to provide children with a
nutritious breakfast because the drug may have
anorexic effects.
Side Effects:
➔ Teach patients about drug side effects and the
need to report tachycardia and palpitations.
➔ Monitor children for onset of Tourette syndrome.
Cultural Considerations:
➔ Decrease language barriers by decoding the
jargon of the healthcare environment for those
who have language difficulties or are not in the
healthcare field.
Evaluation:
➔ Evaluate effectiveness of drug therapy, level of
hyperactivity, and presence of adverse effects.
➔ Monitor weight, sleep patterns, and mental status.
➔ Evaluate patient knowledge of methylphenidate
therapy.
ANOREXIANTS AND ANALEPTICS
Anorexiants
➔ Anorexiants cause a stimulant effect on the
hypothalamic and limbic regions of the brain to
suppress appetite
Analeptics
➔ Analeptics, which are CNS stimulants, mostly
affect the brainstem and spinal cord but also
affect the cerebral cortex.
➔ The primary use of an analeptic is to stimulate
respiration
ANOREXIANTS DRUGS FOR OBESITY:
➔ Benzphetamine hydrochloride
➔ Diethylpropion hydrochloride
➔ Phentermine hydrochloride
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➔ Phentermine-topiramate ➔ Children have few REM sleep periods and have

➔ Phendimetrazine longer periods of stage 3 and 4 NREM sleep
➔ Liraglutide ➔ Older adults experience a decrease in stage 3
➔ Naltrexone and 4 NREM sleep and have frequent waking
◆ Hydrochloride/Bupropion hydrochloride periods.
➔ Serotonin 2C Receptor Agonist
◆ Lorcaserin SEDATIVE-HYPNOTICS
ANALEPTIC DRUGS:
Methylxanthines ➔ Sedative-hypnotics are commonly ordered for
➔ Caffeine Citrate – For neonatal apnea treatment of sleep disorders.
Theophylline ➔ The mildest form of CNS depression is sedation,
➔ For bronchospasm prophylaxis, COPD, asthma, which diminishes physical and mental responses
status asthmaticus and neonatal apnea at lower doses of certain CNS depressants but
Doxapram does not affect consciousness.
➔ For post anesthesia respiratory depression ➔ Because of the many side effects of barbiturates
and their potential for physical and mental
SIDE EFFECT AND ADVERSE REACTIONS: dependency, they are now less frequently
ANOREXIANTS: prescribed
• Nervousness ➔ Hypnotics may be short or intermediate acting.
• Restlessness ◆ Short-acting hypnotics are useful in
• Irritability achieving sleep because they allow the
• Insomnia patient to awaken early in the morning
• Heart Palpitations without experiencing lingering side
• Hypertension effects
ANALEPTICS: ◆ Intermediate-acting hypnotics are useful
• Nervousness Restlessness for sustaining sleep; however, after using
• Tremors one, the patient may experience residual
• Twitching drowsiness, or hangover, in the morning.
• Palpitations SIDE EFFECTS AND ADVERSE REACTIONS:
• Insomnia Hangover
• Diuresis ➔ A hangover is residual drowsiness resulting in
• GI irritation impaired reaction time. The intermediate- and
• Tinnitus long-acting hypnotics are frequently the cause of
• Dysrhythmias drug hangover. The liver bio transforms these
• Convulsions drugs into active metabolites that persist in the
• psychological dependence body, causing drowsiness.
REM Rebound
➔ which results in vivid dreams and nightmares,
CNS DEPRESSANTS
frequently occurs after taking a hypnotic for a
prolonged period then abruptly stopping.
SLEEP CYCLE: However, it may occur after taking only one
➔ Normal sleep is composed of two definite phases: hypnotic dose.
rapid eye movement (REM) and non rapid eye Dependence
movement (NREM) sleep ➔ Dependence is the result of chronic hypnotic
➔ Both REM and NREM sleep occur cyclically at use. Physical and psychological dependence can
about 90-minute intervals during sleep result. Physical dependence results in the
➔ The four succeedingly deeper stages of NREM appearance of specific withdrawal symptoms
sleep end with an episode of REM sleep, and the when a drug is discontinued after prolonged use.
cycle begins again The severity of withdrawal symptoms depends on
➔ If sleep is interrupted, the cycle begins again with the drug and dosage. Symptoms may include
stage 1 of NREM sleep muscular twitching and tremors, dizziness,
➔ Individuals perform better during their waking orthostatic hypotension, delusions,
hours if they experience all types and stages of hallucinations, delirium, and seizures.
sleep.
CHILDREN AND OLDER ADULT SLEEP CYCLE:
PHARMACOLOGY
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Withdrawal symptoms start within 24 hours and
can last for several days.
Tolerance
➔ results when there is a need to increase the
dosage over time to obtain the desired effect. It
is mostly caused by an increase in drug
metabolism by liver enzymes. The barbiturate
drug category can cause tolerance after
prolonged use. Tolerance is reversible when the
drug is discontinued.
Excessive depression
➔ Long-term use of a hypnotic may result in CNS
depression, which is characterized by lethargy,
sleepiness, lack of concentration, confusion, and
psychological depression.
Respiratory depression
➔ High doses of sedative-hypnotics can suppress
the respiratory center in the medulla.
Hypersensitivity
➔ Skin rashes and urticaria can result when taking
barbiturates. Such reactions are rare.
CATEGORIES OF SEDATIVE-HYPNOTICS
➔ Barbiturates
➔ Benzodiazepines
➔ Nonbenzodiazepines
BARBITURATES
➔ Barbiturates are classified under the Controlled
Substances Act as Schedule II for short-acting,
Schedule III for intermediate-acting, and Schedule
IV for long-acting hypnotics.
Classified as long, intermediate, short, and ultrashort
acting.
➔ The long-acting group includes
PHENOBARBITAL and MEPHOBARBITAL, which
are used to control seizures in epilepsy.
➔ The intermediate-acting barbiturates, such as
BUTABARBITAL, are useful as sleep sustainers
for maintaining long periods of sleep.
➔ The short-acting barbiturate SECOBARBITAL
may be used for procedure sedation. Vital signs
should be closely monitored in persons who take
short-acting barbiturates.
Pharmacokinetics
➔ It has a slow absorption rate and is moderately
protein bound. The long half-life is mainly
because of the formation of active metabolites
resulting from liver metabolism.
Pharmacodynamics
➔ Pentobarbital and secobarbital are used
primarily for short-term treatment of insomnia.
Other uses include control of seizures,
preoperative anxiety, and sedation induction. They
have a rapid onset with a short duration of action
and are considered short-acting barbiturates. The
onset of action of pentobarbital is slower when
administered intramuscularly (IM) than when
administered orally (PO).
BENZODIAZEPINES
➔ This drug group is ordered as sedative hypnotics
for inducing sleep.
➔ These drugs are classified as Schedule IV
according to the Controlled Substances Act.
➔ The benzodiazepines increase the action of the
inhibitory neurotransmitter gamma-aminobutyric
acid (GABA) to the GABA receptors. Neuron
excitability is reduced.
➔ Benzodiazepines (except for temazepam) can
suppress stage 4 of NREM sleep, which may result
in vivid dreams or nightmares and can delay REM
sleep.
➔ Benzodiazepines are effective for sleep
disorders for several weeks longer than other
sedative-hypnotics; to prevent REM rebound,
however, they should not be used for longer than
3 to 4 weeks
DRUGS UNDER BENZODIAZEPINES:
➔ Alprazolam –Treat anxiety and panic disorders
➔ Estazolam –Treatment of insomnia
➔ Lorazepam –Used for sedation induction and to
reduce anxiety
➔ Temazepam –Treatment for insomnia
➔ Triazolam – Management of insomnia
NURSING PROCESS: PATIENT-CENTERED
COLLABORATIVE CARE
Assessment:
➔ Obtain a drug history of current drugs and
complementary and alternative therapies that
the patient is taking, especially CNS
depressants, which would potentiate respiratory
depression and hypotensive effects.
➔ Assess baseline vital signs for future comparisons.
➔ Determine whether the patient has a history of
insomnia or anxiety disorders.
➔ Assess renal function. Urine output should be
1500 mL/day. Renal impairment could prolong
drug action by increasing the half-life of the drug.
Diagnosis:
➔ Sleep Deprivation related to adverse effect of
insomnia
➔ Injury, Risk for breathing pattern ineffective
➔ Breathing Pattern, Ineffective related to CNS
depression
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➔ Sexuality Pattern, Ineffective related to adverse
effect of erectile dysfunction
Planning:
➔ Patients will receive adequate sleep when taking
benzodiazepines.
Nursing Interventions:
➔ Monitor vital signs, especially respirations and
blood pressure.
➔ Use a bed alarm for older adults and for patients
receiving a hypnotic for the first time. Confusion
can occur, and injury could result.
➔ Observe the patient for adverse reactions,
especially an older adult or a debilitated patient.
➔ Examine the patient’s skin for rashes. Skin
eruptions may occur in patients taking
benzodiazepines.
Patient Teaching:
➔ Teach patients to use nonpharmacologic
methods to induce sleep such as taking a warm
bath, listening to quiet music, drinking warm
fluids, and avoiding drinks with caffeine for 6
hours before bedtime.
➔ Encourage patients to avoid alcohol and
antidepressant, antipsychotic, and opioid drugs
while taking benzodiazepines. Respiratory
depression can occur when these drugs are
combined.
➔ Warn patients that certain complementary and
alternative therapy products may interact with
benzodiazepines . These products may need to
be discontinued, or the prescription drug dose
may need to be modified.
➔ Advise patients not to drive a motor vehicle or
operate machinery when using
benzodiazepines. Caution is always encouraged.
➔ Encourage patients to check with a health care
provider about OTC sleeping aids. Drowsiness
may result from taking these drugs, therefore
caution while driving is advised.
Side Effects:
➔ Advise patients to report adverse reactions such
as cognitive changes and paradoxical reactions
to their health care provider. Drug selection or
dosage might need to be changed.
➔ Teach patients that benzodiazepines should be
gradually withdrawn, especially if they have been
taken for several weeks. Abrupt cessation may
result in withdrawal symptoms such as tremors
and muscle twitching.
Evaluation:
➔ Assess the effectiveness of benzodiazepines.
➔ Evaluate respiratory status to ensure that
respiratory depression has not occurred.
Pharmacokinetics
➔ Benzodiazepines are well absorbed through the
gastrointestinal (GI) mucosa. They are rapidly
metabolized in the liver to active metabolites.
Benzodiazepines have an intermediate half-life of
usually 8 to 24 hours. These drugs are highly
protein bound, and more free drug is available
when benzodiazepines are taken with other
highly protein-bound drugs, which increases the
risk for adverse effects.
Pharmacodynamics
➔ Benzodiazepines are used to treat insomnia by
inducing and sustaining sleep. They have a rapid
onset of action and intermediate- to long-acting
effects. The normal recommended dose of a
benzodiazepine may be too much for the older
adult, so half the dose is recommended initially
to prevent overdosing.
NONBENZODIAZEPINES
➔ Sometimes referred to colloquially as Z-drugs (as
many of them begin with the letter "z"), are a
class of psychoactive drugs that are very
benzodiazepine-like in nature. They are used in
the treatment of sleep problems.
NONBENZODIAZEPINE DRUGS:
➔ Zolpidem tartrate – treatment of insomnia
➔ Eszopiclone – ultrashort-term treatment of
insomnia
➔ Zaleplon – treatment of insomnia
Pharmacokinetics
➔ Its duration of action is 6 to 8 hours with a short
half-life of 1.4 to 6.73 hours. Zolpidem is
metabolized in the liver to three inactive
metabolites and is excreted in bile, urine, and
feces.
Pharmacodynamics
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NURSING PROCESS: PATIENT-CENTERED

COLLABORATIVE CARE ANESTHETICS
Assessment:
➔ Anesthetics are classified as general and local.
➔ Assess baseline vital signs and laboratory tests
➔ General anesthetics depress the CNS, alleviate
(e.g., aspartate aminotransferase [AST], alanine
pain, and cause a loss of consciousness.
aminotransferase [ALT], bilirubin) for future
➔ The first anesthetic, nitrous oxide (“laughing
comparisons.
gas”), was used for surgery in the early 1800s
➔ Obtain a drug history. Taking CNS depressants
➔ It is still an effective anesthetic and is frequently
with nonbenzodiazepine hypnotics can depress
used in dental procedures and surgery.
respirations.
Pathophysiology
➔ Ascertain the patient’s problem with sleep
➔ Several theories exist regarding how inhalation
disturbance.
anesthetics cause CNS depression and a loss of
Nursing Diagnoses:
consciousness. The differing theories suggest the
➔ Sleep Deprivation related to anxiety
following about inhalation anesthetics:
➔ Fatigue related to insomnia
◆ The lipid structure of cell membranes is
➔ Injury, Risk for
altered, resulting in impaired physiologic
Planning:
functions.
➔ Patient will remain asleep for 6 to 8 hours.
◆ The inhibitory neurotransmitter GABA is
Nursing Interventions:
activated to the GABA receptor that
➔ Monitor vital signs. Check for signs of
pushes chloride ions into the neurons.
respiratory depression (slow, irregular breathing
This greatly decreases the fire action
patterns).
potentials of the neurons.
➔ Use a bed alarm for older adults or patients
◆ The ascending reticular activating system
receiving nonbenzodiazepines for the first time.
is altered, and the neurons cease to
Confusion may occur, and injury may result.
transmit information (stimuli) to the brain.
➔ Observe patients for side effects of
nonbenzodiazepines such as hangover (residual
BALANCED ANESTHESIA
sedation), lightheadedness, dizziness, or
confusion. ➔ Balanced anesthesia is a combination of drugs
Side Effects: frequently used in general anesthesia. Balanced
➔ Advise patients to report adverse reactions such anesthesia may include the following:
as hangovers to a health care provider. Drug 1. A hypnotic given the night before
selection or dosage may need to be changed if a 2. Premedication with an opioid analgesic or
hangover occurs. benzodiazepine (e.g., midazolam) plus an
Evaluation anticholinergic (e.g., atropine) given about 1 hour
➔ Evaluate effectiveness of sedative-hypnotics in before surgery to decrease secretions
promoting sleep. 3. A short-acting nonbarbiturate such as propofol
➔ Determine whether side effects such as hangover 4. An inhaled gas, often a combination of an
occur after several days of taking a sedative inhalation anesthetic, nitrous oxide, and oxygen
hypnotic. Another hypnotic may be prescribed if 5. A muscle relaxant given as needed
side effects persist. ➔ Balanced anesthesia minimizes cardiovascular
problems, decreases the amount of general
MELATONIN AGONISTS anesthetic needed, reduces possible post
anesthesia nausea and vomiting, minimizes the
➔ This drug acts by selectively targeting melatonin
disturbance of organ function, and decreases
receptors to regulate circadian rhythms in the
pain. Because the patient does not receive large
treatment of insomnia.
doses of general anesthetics, fewer adverse
➔ Ramelteon has not been shown to decrease
reactions occur; and recovery is enhanced by
REM sleep. This new drug has a half-life of 1 to 2.6
allowing quicker mobility.
hours. Adverse effects of ramelteon include
drowsiness, dizziness, fatigue, headache,
nausea, and suicidal ideation.
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STAGES OF GENERAL ANESTHESIA Sevoflurane Rapid For induction and maintenance

during surgery

INHALATION GAS ONSET OF INDICATION

ACTION

Nitrous Oxide Very Rapid Must be administered at no less

than a mixture of 21% oxygen;
potency is low

ADVERSE EFFECTS:
• Respiratory depression
• Hypotension
• Dysrhythmias
• Hepatic dysfunction

INTRAVENOUS ANESTHETICS
Intravenous (IV) anesthetics may be used for
➔
general anesthesia or for the induction stage of
anesthesia.
➔ For outpatient surgery of short duration, an IV
anesthetic might be the preferred form of
anesthesia.
MEMORIZE!!!
IV ONSET OF INDICATION
ASSESSMENT BEFORE SURGERY (ULTRASHORT-AC ACTION
➔ The patient’s response to anesthesia may differ TING)
BARBITURATES
according to variables related to the health status
of the individual. These variables include age Methohexital Rapid Frequently used for induction
sodium
(young and older adults), a current health disorder
(e.g. cardiovascular, pulmonary, renal, liver), Thiamylal sodium Rapid Used for induction of anesthesia
pregnancy, history of heavy smoking, and and for electroshock therapy
frequent use of alcohol and drugs. These
BENZODIAZEPINE ONSET OF INDICATION
problems must be identified before surgery S ACTION
because the type and amount of anesthetic
required may need to be adjusted. Diazepam Moderate to For induction of anesthesia; no
rapid analgesic effect

INHALATION ANESTHETICS Midazolam Rapid For induction of anesthesia and for

endoscopic procedures
➔During the third stage of anesthesia, inhalation
OTHERS ONSET OF INDICATION
anesthetics—that is, gas or volatile liquids ACTION
administered as gas—are used to deliver general
anesthesia. Droperidol and Moderate to Neuroleptic Analgesic
fentanyl rapid
➔ Inhalation anesthetics typically provide smooth
induction Etomidate Rapid For short-term surgery
MEMORIZE!!!!
Ketamine Rapid Used for short-term surgery or for
INHALATION ONSET OF INDICATION hydrochloride induction of anesthesia
VOLATILE LIQUID ACTION
Propofol Rapid For induction of anesthesia, may be
Halothane Rapid Highly potent anesthetic used for general anesthesia

Methoxyflurane Slow Used during labor Fospropofol Rapid For induction and maintenance of
anesthesia
Enflurane Rapid for surgery, can depress respiratory
function ADVERSE EFFECTS:
• Respiratory and Cardiovascular depression
Desflurane Rapid Volatile Liquid Anesthetic • Propofol supports microbial growth and may increase
the risk for bacterial infection.
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TOPICAL ANESTHETICS Dibucaine

hydrochloride
Amide For topical use (creams &
ointments) to affect areas

➔ Use of topical anesthetic agents is limited to Etidocaine Amide For peripheral nerve block,
mucous membranes, broken or unbroken skin hydrochloride infiltration, caudal, and epidural
anesthesia
surfaces, and burns. Topical anesthetics come in
different forms: solutions, liquid sprays, ointments, Tetracaine Ester For spinal anesthesia (high & low
creams, gels, and powders. Topical anesthetics hydrochloride saddle block); also for topical use to
affected areas, such as the eye to
decrease the sensitivity of nerve endings in the anesthetize cornea, the nose and
affected area. the throat for bronchoscopy, and
the skin for relief and pain and
pruritus (itching)
LOCAL ANESTHETICS
➔ Local anesthetics block pain at the site where SPINAL ANESTHESIA
the drug is administered by preventing
➔ Spinal anesthesia requires that a local anesthetic
conduction of nerve impulses.
be injected into the subarachnoid space below
➔ Local anesthetics are useful in dental
the first lumbar space (L1) in adults and the third
procedures, suturing skin lacerations, short term
lumbar space (L3) in children.
(minor) surgery at a localized area, blocking
➔ If the local anesthetic is given or spreads too high
nerve impulses (nerve block) below the
in the spinal column, the respiratory muscles
insertion of a spinal anesthetic, and diagnostic
could be affected, and respiratory distress or
procedures such as lumbar puncture and
respiratory failure could result.
thoracentesis.
Types of Spinal Anesthesia:
➔ Local anesthetics may also be used to perform
1. Nerve Block - Various sites of the spinal column
regional blocks—such as brachial plexus, axillary,
can be used for local anesthetics
femoral, or sciatic blocks—to provide analgesia for
2. Spinal Block - results from the penetration of the
surgery of the upper or lower extremities.
anesthetic into the subarachnoid space, which is
➔ Most local anesthetics are divided into two
the space between the pia mater membrane and
groups, the esters and the amides, according to
the arachnoid membrane.
their basic structures. The amides have a very
3. Epidural Block - the placement of the local
low incidence of allergic reaction.
anesthetic in the epidural space just posterior to
the spinal cord or the dura mater. The epidural
ANESTHETICS TYPE INDICATION space is located between the posterior
longitudinal ligament on the anterior side and the
Short acting (30 min to 1 hr)
ligamentum flavum posteriorly
Chloroprocaine Ester For infiltration caudal, and epidural 4. Caudal Block is an epidural block placed by
hydrochloride anesthesia; onset of action is 6 to 12
mins
administering a local anesthetic through the
sacral hiatus
Procaine Ester For nerve block, infiltration, 5. Saddle block is given at the lower end of the
hydrochloride epidural, and spinal anesthesia;
useful in dentistry; use w/ caution spinal column to block the perineal area
in patients allergic to ester-type ADVERSE REACTION:
anesthetics.
• Postdural-puncture headache
Moderate Acting (1 to 3 hrs) • Hypotension
NURSING PROCESS: PATIENT-CENTERED
Lidocaine Amide For nerve block, infiltration, COLLABORATIVE CARE
hydrochloride epidural, and spinal anesthesia;
allergic reaction is rare. Lidocaine is Assessment:
used to treat cardiac dysrhythmias. ➔ Assess baseline vital signs.
➔ Obtain a drug and health history, noting drugs
Mepivacaine Amide For nerve block, infiltration, caudal,
hydrochloride and epidural anesthesia; may be that affect the cardiopulmonary system.
used in dentistry
Nursing Diagnoses:
Long Acting (3 to 10 hrs)
➔ Pain, Acute related to injury
➔ Breathing Pattern, Ineffective related to CNS
Bupivacaine Amide For peripheral nerve block, depression
hydrochloride infiltration, caudal, and epidural
anesthesia Planning:
PHARMACOLOGY
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➔ Patients will participate in preoperative
preparation and will understand postoperative
care.
➔ Patient’s vital signs will remain stable following
surgery.
Nursing Interventions
➔ Monitor the postoperative state of sensorium.
Report if a patient remains excessively
unresponsive or confused.
➔ Observe preoperative and postoperative urine
output. Report deficit of hourly or 8-hour urine
output.
➔ Monitor vital signs following general and local
anesthesia; hypotension and respiratory
depression may result.
➔ Administer an analgesic or a narcotic-analgesic
with caution until the patient fully recovers from
the anesthetic. To prevent adverse reactions, the
dosage might need to be adjusted if the patient is
under the influence of an anesthetic.
Patient Teaching
➔ Explain to patients the preoperative preparation
and postoperative nursing assessment and
interventions.
Evaluation
➔ Evaluate the patient’s response to the anesthetics.
Continue to monitor for adverse reactions.
ANTISEIZURE DRUGS
➔ Drugs used for epileptic seizures are called
antiseizure drugs, anticonvulsants, or
antiepileptic drugs
➔ Antiseizure drugs stabilize nerve cell membranes
and suppress the abnormal electrical impulses
in the cerebral cortex
➔ These drugs prevent seizures but do not
eliminate the cause or provide a cure.
➔ Antiseizure drugs are classified as central
nervous system (CNS) depressants.
➔ Antiseizure drugs are not indicated for all types of
seizures. For example, phenytoin is effective in
treating tonic-clonic and partial seizures but is
not effective in treating absence seizures.
Pharmacophysiology
Antiseizure drugs work in one of three ways:
1. by suppressing sodium influx through the drug
binding to the sodium channel when it is
inactivated, which prolongs the channel
inactivation and thereby prevents neuron firing;
2. by suppressing the calcium influx, which prevents
the electric current generated by the calcium ions
to the T-type calcium channel; or
3. by increasing the action of gamma-aminobutyric
acid (GABA), which inhibits neurotransmitters
throughout the brain.
HYDANTOINS
➔ The first antiseizure drug used to treat seizures
was phenytoin, a hydantoin discovered in 1938
and still commonly used for controlling seizures
➔ Hydantoins inhibit sodium influx, stabilize cell
membranes, reduce repetitive neuronal firing,
and limit seizures
➔ By increasing the electrical stimulation threshold
in cardiac tissue, it also acts as an
antidysrhythmic.
➔ It has a slight effect on general sedation, and it is
nonaddicting
➔ However, this drug should not be used during
pregnancy because it can have a teratogenic
effect on the fetus.
Pharmacokinetics
➔ Phenytoin is slowly absorbed from the small
intestine. It is a highly protein-bound (90% to 95%)
drug, therefore a decrease in serum protein or
albumin can increase the free phenytoin serum
level. With a small to average drug dose, the
half-life of phenytoin is approximately 24 hours,
but the range can be from 7 to 42 hours.
Phenytoin is metabolized to inactive metabolites,
and this portion is excreted in the urine.
Pharmacodynamics
➔ The pharmacodynamics of orally administered
phenytoin include onset of action within 30
minutes to 2 hours, peak serum concentration in
1.5 to 6 hours, steady state of serum
concentration in 7 to 10 days, and a duration of
action dependent on the half-life of up to 45
hours. Oral phenytoin is most commonly
ordered as a sustained-release (SR) capsule. The
peak SR concentration time is 4 to 12 hours.
➔ Intravenous (IV) infusion of phenytoin should be
administered by direct injection into a large vein
via a central line or peripherally inserted central
catheter (PICC). The drug may be diluted in
saline solution; however, dextrose solution
should be avoided because of drug
precipitation. The manufacturer recommends
use of an in-line filter when the drug is
administered as an infusion. IV phenytoin, 50 mg
or a fraction thereof, should be administered over
1 minute for adults and at a rate of 25 mg/min for
older adults. Infusion rates of more than 50
mg/min may cause severe hypotension or cardiac
dysrhythmias, especially for older and debilitated
PHARMACOLOGY
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patients. Local irritation at the injection site may
be noted, and sloughing—formation of dead
tissue that separates from living tissue—may
occur. The IV line should always be flushed with
saline before and after each dose to reduce
venous irritation. Intramuscular (IM) injection of
phenytoin irritates tissues and may cause
damage. For this reason, and because of its erratic
absorption rate, phenytoin is not given by the IM
route.
Side effects and Adverse Reactions:
• Depression
• suicidal ideation
• Stevens-Johnson syndrome
• ventricular fibrillation
• blood dyscrasias, such as thrombocytopenia (low
platelet count), leukopenia (low white blood cell count),
and purple glove syndrome (swollen, discolored, and
painful extremities that may require amputation)
• Hyperglycemia
• Less severe side effects are nausea vomiting, gingival
hyperplasia (overgrowth of gums or reddened gums
that bleed easily), constipation, drowsiness, headaches,
slurred speech, confusion, alopecia, hirsutism, and
nystagmus
DRUG DRUG INTERACTIONS:
➔ The hydantoins displace anticoagulants and
aspirin, causing more free-drug availability and
increasing their activity
➔ Barbiturates, rifampin, and chronic ingestion of
ethanol increase hydantoin metabolism.
➔ Drugs like sulfonamides and cimetidine can
increase the action of hydantoins by inhibiting
liver metabolism, which is necessary for drug
excretion.
➔ Antacids, calcium preparations, sucralfate, and
antineoplastic drugs also decrease the
absorption of hydantoins
➔ Antipsychotics and certain herbs can lower the
seizure threshold, the level at which seizure may
be induced, and they increase seizure activity
BARBITURATES
➔ Phenobarbital, a long-acting barbiturate, is
prescribed to treat tonic-clonic, partial, and
myoclonic seizures and status epilepticus, a
rapid succession of epileptic seizures.
➔ Barbiturates reduce seizures by enhancing the
activity of GABA, an inhibitory neurotransmitter.
Possible teratogenic effects and other side effects
related to phenytoin are less pronounced with
phenobarbital. The therapeutic serum range of
phenobarbital is 20 to 40 mcg/mL.
➔ Risks associated with the use of phenobarbital
include sedation and tolerance to the drug.
Discontinuance of phenobarbital should be
gradual to avoid recurrence of seizures.
SUCCINIMIDES
➔ The succinimide drug group is used to treat
absence seizures. Succinimides act by
decreasing calcium influx through the T-type
calcium channels.
➔ The therapeutic serum range of ethosuximide is
40 to 100 mcg/mL.
➔ Adverse effects include blood dyscrasias, renal
and liver impairment, and systemic lupus
erythematosus.
BENZODIAZEPINES
➔ The benzodiazepines that have anti seizure
effects are clonazepam, clorazepate
dipotassium, lorazepam, and diazepam.
➔ Clonazepam is effective in controlling absence
and myoclonic seizures, but tolerance may occur
6 months after drug therapy starts;
consequently, clonazepam dosage must be
adjusted. Clorazepate dipotassium is
administered for treating partial seizures.
➔ Diazepam is administered by IV to treat status
epilepticus. The drug has a short-term effect;
thus other antiseizure drugs, such as phenytoin or
phenobarbital, must be given during or
immediately after administration of diazepam.
IMINOSTILBENS
➔ Carbamazepine, an iminostilbene, is used to
control tonic-clonic and partial seizures.
➔ Carbamazepine is also used for psychiatric
disorders (e.g., bipolar disorder), trigeminal
neuralgia 527 (as an analgesic), and alcohol
withdrawal.
➔ The therapeutic serum range of carbamazepine
is 4 to 12 mcg/mL.
➔ A potentially toxic interaction can occur when
grapefruit juice is taken with carbamazepine,
and drug concentrations must be carefully
monitored.
VALPROATE
➔ Valproic acid is prescribed for tonic-clonic,
absence, and mixed types of seizures, although
the safety and efficacy of this drug has not been
PHARMACOLOGY
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established for children younger than 2 years of 12. Ezogabine

age.
➔ Care should be taken when giving this drug to
very young children and to patients with liver
disorders because hepatotoxicity is one of the
possible adverse reactions. Liver enzymes should
be monitored.
➔ The therapeutic serum range for a patient with
seizures is 50 to 100 mcg/mL.
ANTISEIZURE DRUGS AND
PREGNANCY
➔ Phenytoin and carbamazepine have been linked
to fetal anomalies such as cardiac defects and
cleft lip and palate.
➔ It has been reported that valproic acid is known
to cause major congenital malformations in
infants in 4% to 8% of pregnant women who
take the drug
13. Felbamate
14. Perampanel
PRECAUTIONS:
➔ Antiseizure drugs tend to act as inhibitors of
vitamin K, contributing to hemorrhage in infants
shortly after birth.
◆ Frequently, pregnant women taking
antiseizure drugs are given an oral vitamin
K supplement during the last week or 10
days of the pregnancy, or vitamin K is
administered to the infant soon after
birth.
➔ Antiseizure drugs also increase the loss of folate
(folic acid) in pregnant women, thus pregnant
individuals should take daily folate supplements.
ANTISEIZURE DRUGS AND
PREGNANCY

ANTICONVULSANTS DRUGS
BARBITURATES:
1. Phenobarbital – most common
2. Primidone
BENZODIAZEPINES:
1. Clonazepam
2. Clorazepate
3. Diazepam
4. Lorazepam
HYDANTOINS:
1. Fosphenytoin
2. Phenytoin –most common
IMINOSTILBENE:
1. Carbamazepine
2. Oxcarbazepine
3. Eslicarbazepine
SUCCINIMIDES:
1. Ethosuximide
VALPROATE:
1. Valproic acid
MISCELLANEOUS:
1. Gabapentin
2. Acetazolamide
3. Lamotrigine
4. Levetiracetam
5. Brivaracetam
6. Tiagabine
7. Topiramate
8. Zonisamide
9. Magnesium sulfate
10. Pregabalin
11. Lacosamide
PHARMACOLOGY
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Nursing Interventions:
➔ Monitor serum drug levels of antiseizure
medication to determine therapeutic range (10 to
20 mcg/mL).
➔ Encourage patient’s compliance with medication
regimen.
➔ Monitor patient’s complete blood count (CBC)
levels for early detection of blood dyscrasias.
➔ Use seizure precautions (environmental
protection from sharp objects, such as table
corners) for patients at risk for seizures.
➔ Determine whether the patient is receiving
adequate nutrients; PHENYTOIN may cause
anorexia, nausea, and vomiting.
➔ Advise female patients who are taking oral
contraceptives and antiseizure drugs to use an
additional contraceptive method.
Patient Teaching:
➔ Teach patients to shake suspension-form
medications thoroughly before use to
adequately mix the medication to ensure
NURSING PROCESS: PATIENT-CENTERED
accurate dosage.
COLLABORATIVE CARE
➔ Advise patients not to drive or perform other
Assessment:
hazardous activities when initiating anti seizure
➔ Obtain a health history that includes current
therapy as drowsiness may occur.
drugs and herbs the patient uses. Report and
➔ Counsel female patients contemplating
document any probable drug-drug or herb-drug
pregnancy to consult with a health care provider
interactions.
because phenytoin and valproic acid may have a
➔ Assess the patient’s knowledge regarding the
teratogenic effect.
medication regimen.
➔ Monitor serum phenytoin levels closely during
➔ Check urinary output to determine whether it is
pregnancy because seizures tend to become
adequate (>1500 mL/d).
more frequent due to increased metabolic rates.
➔ Determine laboratory values related to renal and
➔ Warn patients to avoid alcohol and other CNS
liver function. If both blood urea nitrogen (BUN)
depressants because they can cause an added
and creatinine levels are elevated, a renal
depressive effect on the body.
disorder should be suspected. Elevated serum
➔ Explain to patients that certain herbs can
liver enzymes (alkaline phosphatase, alanine
interact with antiseizure drugs and dose
aminotransferase, gamma-glutamyl transferase,
adjustment may be required.
59-nucleotidase) indicate a hepatic disorder.
➔ Encourage patients to obtain a medical alert
Nursing Diagnoses:
identification card, medical alert bracelet, or tag
➔ Injury, Risk for
that indicates their diagnosis and drug regimen.
➔ Oral Mucous Membranes, Impaired related to
➔ Teach patients not to abruptly stop drug therapy
blood dyscrasias
but rather to withdraw the prescribed drug
➔ Nutrition, Imbalanced: Less than Body
gradually under medical supervision to prevent
Requirements related to anorexia
seizure rebound (recurrence of seizures) and
➔ Falls, Risk for
status epilepticus.
Planning:
➔ Counsel patients about the need for preventive
➔ Patient’s seizure frequency will diminish.
dental checkups.
➔ Patients will adhere to antiseizure drug therapy.
➔ Warn patients to take their prescribed antiseizure
➔ Patient’s side effects from phenytoin will be
drug, get laboratory tests as ordered, and keep
minimal.
follow-up visits with health care providers.
➔ Teach patients not to self-medicate with
over-the-counter (OTC) drugs without first
consulting a health care provider.
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➔ Advise patients with diabetes to monitor serum

glucose levels more closely than usual because DRUGS FOR PARKINSON’S DISEASE AND
phenytoin may inhibit insulin release, causing ALZHEIMER DISEASE
an increase in glucose level.
➔ Inform patients of the existence of national, state,
and local associations that provide resources,
PARKINSON’S DISEASE
current information, and support for people with
epilepsy. Three symptoms were described for Parkinson’s Disease:
Diet: 1. involuntary tremors of the limbs,
➔ Coach patients to take antiseizure drugs at the 2. rigidity of muscles, and
same time every day with food or milk. 3. slowness of movement
Side Effects: ➔ The cardinal symptoms are rigidity, tremors, gait
➔ Tell patients that urine may be a harmless disturbance, and bradykinesia.
pinkish red or reddish brown color. ➔ Normally the symptoms have a gradual onset and
➔ Advise patients to maintain good oral hygiene are usually mild and unilateral in the beginning.
and to use a soft toothbrush to prevent gum ➔ There are different types of parkinsonism
irritation and bleeding. ◆ Parkinson’s disease is the most common
➔ Teach patients to report symptoms of sore type, which is a degeneration of
throat, bruising, and nosebleeds, which may dopaminergic neurons leading to a lack
indicate a blood dyscrasia. of dopamine.
➔ Encourage patients to inform health care ◆ Pseudoparkinsonism frequently occurs
providers of adverse reactions such as gingivitis, as an adverse reaction to
nystagmus, slurred speech, rash, and dizziness. chlorpromazine, haloperidol, lithium,
(Stevens-Johnson syndrome begins with a rash.) metoclopramide, methyldopa, and
Evaluation: reserpine.
➔ Evaluate effectiveness of drugs in controlling
seizures. ANTICHOLINERGICS
➔ Monitor serum phenytoin levels to determine
whether they are within the desired range. High ➔ Anticholinergic drugs reduce the rigidity and
serum levels of phenytoin are frequently some of the tremors characteristic of
indicators of phenytoin toxicity. Parkinson’s disease but have a minimal effect
➔ Monitor patients for hydantoin overdose. Initial on bradykinesia.
symptoms are nystagmus and ataxia (impaired ➔ The anticholinergics are parasympatholytic that
coordination). Later symptoms are hypotension, inhibit the release of acetylcholine.
unresponsive pupils, and coma. Respiratory and ➔ Anticholinergics are still used to treat
circulatory support, as well as hemodialysis, are drug-induced parkinsonism, or
usually used in the treatment of phenytoin pseudoparkinsonism, a side effect of the
overdose. antipsychotic phenothiazine drug group.
Examples of anticholinergics used for
ANTISEIZURE DRUGS AND STATUS Parkinson’s disease include trihexyphenidyl and
benztropine.
EPILEPTICUS ANTIPARKINSON DRUGS: ANTICHOLINERGICS
➔ Benztropine mesylate- For Parkinson’s disease,
➔ Status epilepticus, a continuous seizure state, is
tremor, and drug-induced PARKINSONISM.
considered a medical emergency. If treatment is
➔ Trihexyphenidyl hydrochloride - For Parkinson’s
not begun immediately, death could result. The
disease and drug-induced
choices of pharmacologic agents are diazepam
PSEUDOparkinsonism.
administered by IV or lorazepam followed by IV
NURSING PROCESS: PATIENT-CENTERED
administration of phenytoin. For continued
COLLABORATIVE CARE
seizures, midazolam or propofol and then
Assessment
high-dose barbiturates are used. These drugs
➔ Obtain a health history. Report any history of
should be administered slowly to avoid
glaucoma, gastrointestinal (GI) dysfunction,
respiratory depression.
urinary retention, angina, or myasthenia gravis. All
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anticholinergics are contraindicated if a patient

has glaucoma. DOPAMINERGIC CARBIDOPA AND
➔ Obtain a drug history. Report any probable LEVODOPA
drug-drug interactions, such as with
phenothiazines, tricyclic antidepressants (TCAs), ➔ Levodopa was effective in diminishing
and antihistamines, which increase the effect of symptoms of Parkinson’s disease and increasing
trihexyphenidyl. mobility; this is because the blood-brain barrier
➔ Assess baseline vital signs for future admits levodopa but not dopamine.
comparisons. The pulse rate may increase. ➔ The enzyme dopa decarboxylase converts
➔ Assess the patient’s knowledge regarding the levodopa to dopamine in the brain, but this
medication regimen. enzyme is also found in the peripheral nervous
➔ Determine usual urinary output as a baseline for system and allows 99% of levodopa to be
comparison. Urinary retention may occur with converted to dopamine before it reaches the
continuous use of anticholinergics. brain.
Nursing Diagnoses: ➔ Therefore only about 1% of levodopa taken is
➔ Mobility, Impaired Physical related to muscle available to be converted to dopamine once it
rigidity, tremors, and bradykinesia reaches the brain, and large doses are needed to
➔ Elimination, Impaired Urinary related to urinary achieve a pharmacologic response.
retention ➔ Because of the side effects of levodopa and the
➔ Knowledge, Deficient related to unfamiliarity with fact that so much levodopa is metabolized before
drug regimen it reaches the brain, an alternative drug,
Planning: carbidopa, was developed to inhibit the enzyme
➔ Patients will have decreased involuntary dopa decarboxylase.
symptoms caused by Parkinson’s disease or ➔ By inhibiting the enzyme in the peripheral
drug-induced parkinsonism. nervous system, more levodopa reaches the brain.
Nursing Interventions: ➔ The advantages of combining levodopa with
➔ Monitor vital signs, urine output, and bowel carbidopa are that more dopamine reaches the
sounds. Increased pulse rate, urinary retention, basal ganglia and that smaller doses of levodopa
and constipation are side effects of are required to achieve the desired effect.
anticholinergics. ➔ The disadvantage of the carbidopa-levodopa
➔ Observe involuntary movements. combination is that with more available levodopa,
Patient Teaching: more side effects may occur
➔ Advise patients to avoid alcohol, cigarettes, SIDE EFFECTS AND ADVERSE REACTION
caffeine, and aspirin to decrease gastric acidity. • Nausea
➔ Encourage patients to relieve a dry mouth with • Vomiting
hard candy, ice chips, or sugarless chewing • Dystonic movement (involuntary abnormal movement)
gum. Anticholinergics decrease salivation. • Psychotic behavior
➔ Suggest that patients use sunglasses in direct • Angioedema
sunlight because of possible photophobia. • Palpitations
➔ Advise patients to void before taking the drug to • Orthostatic hypotension
minimize urinary retention.
➔ Counsel patients who take an anticholinergic for COMPARISON OF LEVODOPA (ALONE) TO COMBINATION
control of symptoms of Parkinson’s disease to OF CARBIDOPA AND LEVODOPA
have routine eye examinations because A. When levodopa is used alone, only 1% reaches the
anticholinergics are contraindicated in patients brain because 99% converts to dopamine while in
with glaucoma. the peripheral nervous system.
➔ Encourage patients to ingest foods high in fiber B. By combining carbidopa with levodopa,
and to increase fluid intake to prevent carbidopa can inhibit the enzyme decarboxylase
constipation. in the periphery, thereby allowing more levodopa
Evaluation to reach the brain.
➔ Evaluate the patient’s response to trihexyphenidyl NURSING PROCESS: PATIENT-CENTERED
or benztropine mesylate to determine whether COLLABORATIVE CARE
Parkinson’s disease symptoms are controlled. Assessment:
➔ Obtain vital signs to use for future comparisons.
PHARMACOLOGY
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➔ Assess patients for signs and symptoms of
Parkinson’s disease, including stooped forward
posture, shuffling gait, masked facies, and
resting tremors.
➔ Obtain a patient history that includes glaucoma,
heart disease, peptic ulcers, kidney or liver
disease, and psychosis.
➔ Obtain a drug history. Report if drug-drug
interaction is probable. Drugs that should be
avoided or closely monitored are
carbidopa-levodopa, bromocriptine, and
anticholinergics
Nursing Diagnoses:
➔ Mobility, Impaired Physical related to dizziness
➔ Activity Intolerance, Risk for
➔ Falls, Risk for
➔ Knowledge, Deficient related to unfamiliar
medications
Planning:
➔ Patient’s symptoms of Parkinson’s disease will be
decreased or absent after 1 to 4 weeks of drug
therapy.
Nursing Interventions:
➔ Monitor vital signs and electrocardiograms.
Orthostatic hypotension may occur during early
use of carbidopa-levodopa and bromocriptine.
Instruct patients to rise slowly to avoid
faintness.
➔ Observe weakness, dizziness, or syncope, which
are symptoms of orthostatic hypotension.
➔ Administer carbidopa-levodopa with low-protein
foods. High-protein diets interfere with drug
transport to the central nervous system (CNS).
➔ Observe symptoms of Parkinson’s disease.
Patient Teaching:
➔ Urge patients not to abruptly discontinue the
medication. Rebound Parkinson’s disease
(increased symptoms of Parkinson’s disease)
can occur.
➔ Inform patients that urine may be discolored and
will darken with exposure to air. Perspiration
may also be dark. Explain that both are
harmless, but clothes may be stained.
➔ Advise patients to avoid chewing or crushing
extended-release tablets.
➔ Encourage patients to report side effects and
symptoms of dyskinesia. Explain that it may take
weeks or months before symptoms are
controlled.
➔ Suggest to patients that taking
carbidopa-levodopa with food may decrease GI
upset, but food will slow the rate of drug
absorption.
➔ Urge patients who take high doses of selegiline
to avoid foods high in tyramine such as aged
cheese, red wine, cream, yogurt, chocolate,
bananas, and raisins to prevent hypertensive
crises.
Amantadine and Bromocriptine:
➔ Urge patients taking amantadine to report any
signs of skin lesions, seizures, or depression. A
history of these health problems should have
been previously reported to a health care
provider.
➔ Advise patients taking bromocriptine to report
symptoms of lightheadedness when changing
positions, a symptom of orthostatic
hypotension.
➔ Warn patients to avoid alcohol when taking
bromocriptine.
➔ Teach patients to check their heart rate and
report rate changes or irregularity.
➔ Counsel patients not to abruptly stop the drug
without first notifying a health care provider.
Evaluation:
➔ Evaluate effectiveness of drug therapy in
controlling symptoms of Parkinson’s disease.
➔ Determine if there is an absence of side effects.
➔ Determine if the patient and family have
increased knowledge of the drug regimen.
DOPAMINE AGONISTS
➔ Other dopamine agonists, also called
dopaminergics, stimulate the dopamine
receptors.
◆ For example, amantadine hydrochloride is
an antiviral drug that acts on the
dopamine receptors.
➔ It may be taken alone or in combination with
carbidopa-levodopa or an anticholinergic drug
➔ Initially, amantadine produces improvement in
symptoms of Parkinson’s disease and
parkinsonism in approximately two-thirds of
patients, but this improvement is usually not
sustained because drug tolerance develops.
Amantadine can also be used to treat
drug-induced parkinsonism
➔ Bromocriptine mesylate acts directly on
dopamine receptors in the CNS, cardiovascular
system, and GI tract
➔ Bromocriptine is more effective than amantadine
and the anticholinergics; however, it 545 is not as
effective as carbidopa-levodopa in alleviating
Parkinson’s disease symptoms.
➔ Patients who do not tolerate carbidopa-levodopa
are frequently given bromocriptine.
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DOPAMINE AGONISTS DRUGS • Confusion

1. Amantadine hydrochloride – For Parkinson’s • urinary retention
disease, drug induced parkinsonism • Constipation
2. Bromocriptine mesylate – For Parkinson’s BROMOCRIPTINE:
disease • GI disturbances (nausea)
3. Pramipexole dihydrochloride – For Parkinson’s • orthostatic hypotension
disease and restless leg syndrome • Palpitations
• chest pain
MONOAMINE OXIDASE B INHIBITORS • lower extremity edema
• Nightmares
(MAOI)
• Delusion
➔ The enzyme MAO-B causes catabolism • Confusion
(breakdown) of dopamine. SELEGILINE:
➔ Selegiline inhibits MAO-B and thus prolongs the • Hypertensive crises can occur if foods high in
action of levodopa. tyramine—such as aged cheese, red wine, and
➔ It may be ordered for patients newly diagnosed bananas—are ingested concurrently.
with Parkinson’s disease or parkinsonism. TOLCAPONE:
➔ The use of selegiline could delay • severe liver damage
carbidopa-levodopa therapy by 1 year • urine can have a dark discoloration
MAOI DRUGS: • uncontrollable urges (sex, gambling, spending money)
1. Selegiline hydrochloride – for Parkinson’s • suddenly falling asleep
disease and parkinsonism ENTACAPONE:
2. Rasagiline – For Parkinson’s disease • urine can have a brownish orange discoloration
• uncontrollable urges (sex, gambling, spending money)
CATECHOL-O-METHYLTRANSFERASE • suddenly falling asleep
CONTRAINDICATIONS:
INHIBITORS(COMT INHIBITORS) ➔ Anticholinergics or any drugs that have
➔ The enzyme COMT inactivates dopamine anticholinergic effects are contraindicated for
➔ When taken with a levodopa preparation, COMT patients with glaucoma. Those with severe
inhibitors increase the amount of levodopa cardiac, renal, or psychiatric health problems
concentration in the brain. should avoid levodopa drugs because of adverse
COMT INHIBITORS DRUGS: reactions.
1. Tolcapone – For Parkinson’s disease ➔ Patients with chronic obstructive lung diseases
2. Entacapone – For PD such as emphysema can have dry, thick mucous
SIDE EFFECTS AND ADVERSE REACTIONS: secretions caused by large doses of
ANTICHOLINERGICS: anticholinergic drugs.
• Dry secretions DRUG-DRUG INTERACTIONS:
• urinary retention ➔ Antipsychotic drugs block the receptors for
• constipation, dopamine.
• blurred vision ➔ Carbidopa-levodopa taken with a monoamine
• increase in heart rate oxidase inhibitor (MAOI) antidepressant can
CARBIDOPA-LEVODOPA: cause a hypertensive crisis.
• GI disturbances
• nausea and vomiting ALZHEIMER DISEASE
• Dyskinesia
➔ Alzheimer disease is an incurable dementia
• orthostatic hypotension
illness characterized by chronic, progressive
• increased heart rate
neurodegenerative conditions with marked
• Nightmares
cognitive dysfunction. Onset usually occurs
• sudden sleep onset
between 45 and 65 years of age.
• impulse control symptoms
Pathophysiology
• mental disturbances
➔ Many physiologic changes contribute to
• suicidal tendencies
Alzheimer disease. Currently, theories related to
AMANTADINE:
• Orthostatic hypotension
PHARMACOLOGY
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the changes that cause Alzheimer disease include

the following: ACETYLCHOLINESTERASE/CHOLINEST
◆ Degeneration of the cholinergic neuron ERASE INHIBITORS
and deficiency in acetylcholine
◆ Neuritic plaques that form mainly ➔ The cure for Alzheimer disease is unknown
outside of the neurons and in the ➔ FDA-approved medications to treat Alzheimer
cerebral cortex disease symptoms include acetylcholinesterase
◆ Apolipoprotein E4 (apo E4) that (AChE) inhibitors
promotes formation of neuritic plaques, ➔ AChE is an enzyme responsible for breaking
which binds beta-amyloid in the plaques down ACh and is also known as cholinesterase
◆ Beta-amyloid protein accumulation in ➔ These AChE inhibitors increase cognitive
high levels that may contribute to function for patients with mild to moderate
neuronal injury • Presence of Alzheimer disease.
neurofibrillary tangles with twists inside
the neurons RIVASTIGMINE
➔ The etiology of Alzheimer disease is unknown,
➔ Rivastigmine, an AChE inhibitor, is prescribed to
although factors thought to influence the
improve cognitive function for patients with
occurrence of Alzheimer disease are genetic
mild to moderate Alzheimer disease.
predisposition, virus, infection, or inflammation
➔ This drug increases the amount of ACh at the
that attacks brain cells as well as nutritional,
cholinergic synapses.
environmental, and immunologic factors.
➔ Rivastigmine tends to slow the disease process
➔ Alzheimer disease has three stages that include
and has fewer drug interactions than donepezil.
mild, moderate, and severe
PHARMACOKINETICS
◆ Mild stage, which is the early-stage, the
➔ Rivastigmine is absorbed faster through the GI
person has memory lapses, difficulty
tract without food. It has a relatively short
concentrating, misplaces objects,
half-life and is given twice a day. The dose is
forgets what was just read, and has
gradually increased. The protein-binding power is
increased problems with planning and
average.
organizing
PHARMACODYNAMICS
◆ Moderate stage (middle-stage) is the
➔ Rivastigmine has been successful in improving
longest stage and may last many years.
memory in mild to moderate Alzheimer disease.
The person may be irritable, moody,
The onset of action is 0.5 to 1.0 hour for topical
withdrawn, display frustration and
application; peak action is 8 to 16 hours. When
anger, have personality and behavioral
given orally, the peak is 1 hour.
changes (may refuse to bathe), has
➔ This drug is contraindicated for patients with
changes in sleep pattern, confusion
liver disease because hepatotoxicity may occur.
regarding what day it is, inability to
Cumulative drug effect is likely to occur in older
recall personal information (phone
adults and in patients with liver and renal
number and address), may wander and
dysfunction.
become lost, inability to perform routine
ACETYLCHOLINESTERASE INHIBITORS FOR ALZHEIMER
tasks, and difficulty controlling
DISEASE:
bowels/bladder
1. Donepezil
◆ Severe stage the person forgets recent
2. Rivastigmine
experiences and previously known
3. Memantine
individuals, requires high levels of
4. Galantamine
assistance with activities of daily living,
NURSING PROCESS: PATIENT-CENTERED
inability to respond to their environment
COLLABORATIVE CARE
or converse, inability to walk, sit, or
Assessment:
swallow, becomes vulnerable to
➔ Assess the patient’s mental and physical
infections, especially pneumonia
abilities. Note limitation of cognitive function and
selfcare.
➔ Obtain a history that includes any liver or renal
disease or dysfunction.
PHARMACOLOGY
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➔ Assess for memory and judgment losses. Elicit
from family members a history of behavioral
changes such as memory loss, declining interest
in people or home, difficulty in following through
with simple activities, and a tendency to wander
from home.
➔ Observe signs of behavioral disturbances such as
hyperactivity, hostility, and wandering. • Examine
the patient for signs of aphasia or difficulty in
speech.
➔ Note motor function.
➔ Determine family members’ ability to cope with
the patient’s mental and physical changes.
Nursing Diagnoses:
➔ Self-Care Deficit, Feeding related to memory loss
➔ Self-Care Deficit, Bathing related to memory loss
➔ Self-Care Deficit, Toileting related to memory loss
➔ Confusion, Chronic related to memory loss
➔ Family Processes, Interrupted related to
decreased cognition
➔ Coping, Compromised Family related to
overwhelming disruption of lifestyle
➔ Injury, Risk for
➔ Nutrition, Imbalanced: Less than Body
Requirements related to anorexia, nausea, and
vomiting
Planning:
➔ Patient’s memory will be improved.
➔ Patient will maintain self-care of body functions
with assistance
Nursing Intervention:
➔ Maintain consistency in care.
➔ Assist the patient in ambulation and activity.
➔ Monitor for side effects related to continuous
use of acetylcholinesterase inhibitors.
➔ Record vital signs periodically. Note signs of
bradycardia and hypotension.
➔ Observe any patient behavioral changes, and note
any improvement or decline.
Patient Teaching:
➔ Explain to the patient and family the purpose for
the prescribed drug therapy.
➔ Clarify times for drug dosing and schedule for
increasing drug dosing to the family member
responsible for the patient’s medications.
➔ Teach family members about safety measures
such as removing obstacles in the patient’s path
to avoid injury when the patient wanders.
➔ Inform family members of available support
groups such as the Alzheimer Disease and
Related Disorders Association.
➔ Inform patients and family members that the
patient should rise slowly to avoid dizziness and
loss of balance.
➔ Monitor routine liver function tests because
hepatotoxicity is an adverse effect.
➔ Inform family members about foods that may be
prepared for the patient’s consumption and
tolerance.
Evaluation:
➔ Evaluate effectiveness of the drug regimen by
determining whether the patient’s mental and
physical status shows improvement from drug
therapy.
DRUGS FOR NEUROMUSCULAR
DISORDERS AND MUSCLE SPASMS
MYASTHENIA GRAVIS
➔ MG is a chronic autoimmune neuromuscular
disease that affects approximately 20 in 100,000
persons
➔ MG can occur in people of any ethnicity and sex;
however, MG peaks in women around the
childbearing years, whereas the peak onset in
men is between 50 and 70 years.
➔ MG can also occur in people outside of this age
range. Although it is not a genetic disorder, a
familial tendency may be apparent.
Pathophysiology
➔ MG results from a lack of acetylcholine receptor
(AChR) sites
➔ This autoimmune disorder involves an antibody
response against an alpha subunit of the
AChRsite at the neuromuscular junction.
➔ Antibodies attack the AChRsites, obstructing the
binding of AChand eventually destroying the
receptor sites.
➔ When AChaR sites are reduced, AChmolecules are
prevented from binding to receptors and
stimulating normal neuromuscular transmission
➔ The result is ineffective muscle contraction and
muscle weakness.
➔ MG is characterized primarily by weakness and
fatigue of the skeletal muscles.
➔ The patient may experience ptosis and diplopia
➔ Other characteristics of MG include dysphagia
(difficulty chewing and swallowing), dysarthria
(slurred speech), and respiratory muscle weakness
➔ When muscular weakness in the patient with MG
becomes generalized, myasthenic crisis may
occur.
➔ This complication is a severe, generalized muscle
weakness that may involve the muscles of
respiration, such as the diaphragm and intercostal
muscles
PHARMACOLOGY
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➔ Overdosing with AChEinhibitors may cause
another complication of MG called cholinergic
crisis, which is an acute exacerbation of
symptoms.
➔ A cholinergic crisis usually occurs within 30 to 60
minutes after taking anticholinergic drugs
➔ This complication is due to continuous
depolarization of postsynaptic membranes that
creates a neuromuscular blockade.
➔ The patient with cholinergic crisis often has
severe muscle weakness that can lead to
respiratory paralysis and arrest
ACETYLCHOLINESTERASE INHIBITORS
➔ The first drug used to manage MG is
NEOSTIGMINE
➔ It is a short-acting acetylcholinesterase inhibitor
with a half-life of 0.5 to 1 hour.
➔ The drug must be given on time to prevent
muscle weakness.
➔ The AChEinhibitor pyridostigmine has an
intermediate action and is given every 4 to 6
hours
ACETYLCHOLINESTERASE INHIBITORS FOR
MYASTHENIA GRAVIS
1. Edrophonium – for diagnosing MG
2. Neostigmine – for Controlling MG
3. Pyridostigmine – For controlling MG
Pharmacokinetics
➔ Pyridostigmine is poorly absorbed from the
gastrointestinal (GI) tract. Half of the
sustained-release capsule is absorbed readily, but
the balance is poorly absorbed. The half-life of
oral pyridostigmine is 3 to 7 hours, and it is 2 to 3
hours for intravenous (IV) administration.
Because of its short halflife, pyridostigmine
must be administered several times a day. The
drug is metabolized by the liver and is excreted in
the urine.
Pharmacodynamics
➔ Pyridostigmine increases muscle strength in
patients with muscular weakness resulting from
MG. The onset of action of oral pyridostigmine is
30 to 45 minutes, the peak is 1 to 3 hours, and
the duration is 3 to 4 hours. Overdosing of
pyridostigmine can result in signs and
symptoms of cholinergic crisis. This crisis
requires emergency medical intervention
because of respiratory muscle weakness.
➔ Overdosing and underdosing of AChEinhibitors
have similar symptoms: generalized muscle
weakness, which can include the muscles of
respiration, the diaphragm, and the intercostal
muscles resulting in dyspnea (difficulty
breathing), and dysphagia. Additional symptoms
that may be present with overdosing are
increased salivation (drooling), sweating, and
bronchial secretions, along with miosis,
bradycardia, and abdominal pain. All doses of
AChEinhibitors should be administered on time
because late administration of the drug could
result in muscle weakness.
➔ Underdosing can result in myasthenic crisis, and
overdosing can result in cholinergic crisis.
Edrophonium is an ultra–short-acting
AChEinhibitor that may be used to distinguish
between myasthenic crisis and cholinergic crisis.
These two crises have a similar major symptom:
severe muscle weakness.
SIDE EFFECTS AND ADVERSE REACTIONS
• GI disturbances
• Nausea
• Vomiting
• Diarrhea
• abdominal cramps
• increased salivation and tearing
• miosis (constricted pupil of the eye)
• blurred vision
• Bradycardia
• Hypotension
NURSING PROCESS: PATIENT-CENTERED
COLLABORATIVE CARE
Assessment:
➔ Obtain a drug history from the patient that
includes all current medications.
➔ Observe the patient’s drug profile for possible
drug interactions.
➔ Patients should avoid atropine, atropine-like
drugs, and muscle relaxants.
➔ Record baseline vital signs.
➔ Assess patients for signs and symptoms of
myasthenic crisis, such as muscle weakness
with difficulty breathing and swallowing.
Nursing Diagnoses:
➔ Breathing Pattern, Ineffective related to weak
respiratory muscles
➔ Activity Intolerance related to fatigue
➔ Anxiety related to possible recurrence of
myasthenic crisis and dyspnea
➔ Knowledge, Deficient related to unfamiliar
medications
Planning:
➔ Patient’s symptoms of muscle weakness and
difficulty breathing and swallowing caused by MG
will be eliminated or reduced in 2 to 3 days
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Nursing Intervention:
➔ Monitor effectiveness of drug therapy
(AChEinhibitors). Muscle strength should be
increased. Both depth and rate of respirations
should be assessed and maintained within
normal range.
➔ Administer prescribed acetylcholinesterase
inhibitor following dosage recommendations
and nursing guidelines.
➔ Observe patients for signs and symptoms of
cholinergic crisis caused by overdosing, such as
muscle weakness, respiratory failure, increased
salivation, sweating, and bronchial secretions
along with miosis.
➔ Have an antidote for cholinergic crisis
(ATROPINE SULFATE) readily available.
Patient Teaching:
➔ Teach patients to take drugs as ordered to avoid
recurrence of symptoms.
➔ Encourage patients to wear a medical
identification bracelet or necklace that indicates
health problems.
➔ Teach patients about the side effects of
medication and when to notify the health care
provider.
➔ Advise patients to report recurrence of symptoms
of MG to the health care provider.
➔ Inform patients to take the drug before meals for
best absorption. If gastric irritation occurs, take
the drug with food.
Evaluation:
➔ Evaluate effectiveness of the drug therapy to
maintain muscle strength.
➔ Determine the absence of respiratory distress.
➔ Evaluate the correct use of the drug by the
patient.
MULTIPLE SCLEROSIS
➔ Multiple sclerosis (MS) is an autoimmune
disorder that attacks the myelin sheath of nerve
fibers in the brain and spinal cord, which results
in lesions called plaques
➔ Although the cause of MS is unknown, it is
thought that the disease develops in a
genetically susceptible person as a result of
environmental exposure, like an infection
➔ The onset of MS is usually slow.
➔ It is a condition in which there are remissions and
exacerbations of multiple symptoms.
➔ Common manifestations of MS are motor,
sensory, neurologic, cerebellar, and emotional
problems.
➔ MS is difficult to diagnose. Most physicians use at
least one other test besides the medical history
and neurologic exam, such as MRI, visual evoked
potential (VEP) testing, or analysis of
cerebrospinal fluid (CSF), to confirm the diagnosis
➔ Motor symptoms include weakness or paralysis of
the limbs, muscle spasticity, and diplopia
➔ Patients with MS experience sensory
abnormalities, including numbness and tingling,
blurred vision, vertigo, and tinnitus.
➔ Patients may experience neuropathic pain
particularly in the low thoracic and abdominal
areas.
➔ Cerebellar signs include nystagmus, ataxia,
dysarthria, and dysphagia
➔ If the sclerotic plaque is located in the central
nervous system (CNS), problems with bowel and
bladder function and sexual and cognitive
dysfunction can occur.
FOUR CLASSIFICATIONS OF MULTIPLE SCLEROSIS
1. Relapsing remitting MS (RRMS): The patient
experiences relapse with full recovery and
residual deficit on recovery (affects 85%).
2. Primary progressive MS (PPMS): Slowly
worsening neurologic function is evident from
the beginning with no relapses or remissions
(affects 10%).
3. Secondary progressive MS (SPMS): The initial
course is relapsing remitting, followed by
progression with or without occasional relapses,
minor remissions, and plateaus (about 50% of
people with RRMS develop SPMS within 10
years).
4. Progressive relapsing MS (PRMS): This form is
progressive from the onset, with clear acute
relapses with or without full recovery (affects
5%). There is no known cure for MS.
IMMUNOMODULATORS
➔ Immunomodulators are disease-modifying drugs
(DMDs), also called disease-modifying therapies
(DMTs), and they are the first line of treatment
for patients with MS
➔ DMDs can slow the progression of the disease
and prevent relapses.
➔ No two cases of MS are alike, so the drugs are
tailored to the disease pattern and manifestations
of the patient.
DRUGS FOR MULTIPLE SCLEROSIS
IMMUNOMODULATORS:
1. Beta Interferon –has been shown to decrease
both the number and severity of MS attacks
(Relapses) and to significantly slow the
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progression of physical disability associated ➔ Centrally acting muscle relaxants are used in
with relapsing remitting MS cases of spasticity to suppress hyperactive reflex
a. Mode of action – Antiviral and and for muscle spasms that do not respond to
immune-regulatory properties are anti-inflammatory agents, physical therapy, or
produced by interacting with specific other forms of therapy.
receptor sites on cell surfaces. It is not
exactly known how interferon works with SPASTICITY
MS. Beta interferon is produced by
recombinant DNA Technology ➔ Skeletal muscle spasticity is muscular
2. Interferon beta-1a hyperactivity that causes contraction of the
3. Interferon beta-1b muscles, resulting in pain and limited mobility.
4. Glatiramer citrate – Treatment of ➔ Centrally acting muscle relaxants act on the spinal
Relapsing-Remitting MS cord.
5. Teriflunomide– Treatment of ➔ Examples of centrally acting muscle relaxants
Relapsing-Remitting MS used to treat spasticity are baclofen, dantrolene,
DRUGS FOR MULTIPLE SCLEROSIS and tizanidine.
IMMUNOSUPPRESSANTS: ➔ Diazepam, a benzodiazepine, has also been
1. Mitoxantrone –Treatment of secondary (chronic) effective for treating spasticity
progressive, progressive relapsing or worsening
relapsing remitting MS MUSCLE SPASMS
2. Dimethyl fumarate – Treatment of relapsing ➔ Various centrally acting muscle relaxants are used
forms of MS for muscle spasm to decrease pain and increase
DRUGS FOR MULTIPLE SCLEROSIS SPHINGOSINE range of motion.
1-PHOSPHATE RECEPTOR MODULATORS: ➔ They have a sedative effect and should not be
1. Fingolimod – Treatment of relapsing forms of taken concurrently with CNS depressants such as
MS barbiturates, narcotics, and alcohol.
DRUGS FOR MULTIPLE SCLEROSIS MONOCLONAL ➔ These agents, with the exception of
ANTIBODY: cyclobenzaprine, can cause drug dependence.
1. Alemtuzumab –used for second treatment ➔ Examples of this group of centrally acting muscle
2. Natalizumab –Treatment to reduce frequency of relaxants are
exacerbations of relapsing MS ◆ Carisoprodol
◆ Chlorzoxazone
SKELETAL MUSCLE RELAXANTS ◆ Cyclobenzaprine
➔ Muscle relaxants relieve muscular spasms and ◆ Metaxalone
pain associated with traumatic injuries and ◆ Methocarbamol
spasticity from chronic debilitating disorders ◆ Orphenadrine citrate
(e.g., MS, stroke [CVA], cerebral palsy, head and
spinal cord injuries). Pharmacokinetics
➔ Spasticity results from increased muscle tone ➔ Cyclobenzaprine is well absorbed from the GI
from hyperexcitable neurons; this is caused by tract, and its half-life is moderate.
increased stimulation from the cerebral neurons Cyclobenzaprine is metabolized in the liver and
or lack of inhibition in the spinal cord or at the excreted in urine
skeletal muscles. Pharmacodynamics
➔ The centrally acting muscle relaxants depress ➔ Cyclobenzaprine alleviates muscle spasm
neuron activity in the spinal cord or brain, or they associated with acute painful musculoskeletal
enhance neuronal inhibition on the skeletal conditions.
muscles. ➔ When cyclobenzaprine is taken with alcohol,
kava, valerian, sedative-hypnotics, barbiturates,
or tricyclic antidepressants (TCAs), increased
CENTRALLY ACTING MUSCLE
CNS depression occurs.
RELAXANTS ➔ The onset of action, peak concentration time, and
duration of action for cyclobenzaprine are short.
➔ The mechanism of action of centrally acting
SIDE EFFECTS AND ADVERSE REACTIONS:
muscle relaxants is not fully known.
• Drowsiness
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• Dizziness enzymes such as alkaline phosphatase (ALP),

• Lightheadedness aspartate aminotransferase (AST), alanine
• Headaches aminotransferase (ALT), and gamma-glutamyl
• GI sensitivity (e.g., nausea, vomiting, abdominal transferase (GGT).
distress) ➔ Record vital signs. Report abnormal results.
• Cyclobenzaprine and orphenadrine have ➔ Observe for CNS side effects (e.g., dizziness).
anticholinergic effects Patient Teaching
MUSCLE RELAXANTS DRUGS: ➔ Teach patients that the muscle relaxant should
ANXIOLYTICS: not be abruptly stopped. The drug should be
1. Diazepam tapered over 1 week to avoid rebound spasms.
CENTRALLY ACTING MUSCLE RELAXANTS: ➔ Advise patients not to drive, operate dangerous
1. Baclofen machinery, or make important life-changing
2. Tizanidine decisions when taking muscle relaxants. These
3. Dantrolene Sodium drugs have a sedative effect and can cause
4. Carisoprodol drowsiness.
5. Chlorzoxazone ➔ Inform patients that most of the centrally acting
6. Methocarbamol muscle relaxants for acute spasms are usually
7. Metaxalone taken for no longer than 3 weeks.
8. Orphenadrine ➔ Teach patients to avoid alcohol and CNS
DEPOLARIZING SKELETAL MUSCLE RELAXANT: depressants. If muscle relaxants are taken with
1. Succinylcholine these drugs, CNS depression may be intensified.
NEUROMUSCULAR BLOCKING AGENT: ➔ Advise patients that these drugs must be used
1. Pancuronium Bromide cautiously when pregnant or nursing.
2. Vecuronium bromide ➔ Patients should always check with the health care
NURSING PROCESS: PATIENT-CENTERED provider prior to stopping medications.
COLLABORATIVE CARE ➔ Encourage patients to report side effects of the
Assessment muscle relaxant: nausea, vomiting, dizziness,
➔ Obtain a medical history. Cyclobenzaprine is fainting, headache, and diplopia can occur.
contraindicated if the patient has cardiovascular Dizziness and fainting are most likely caused by
disorders, hyperthyroidism, or hepatic orthostatic (postural) hypotension.
impairment or is taking concurrent monoamine ➔ Advise patients to take muscle relaxants with
oxidase inhibitors (MAOIs). food to decrease GI upset.
➔ Obtain baseline vital signs. Evaluation
➔ Assess the patient’s health history to identify ➔ Evaluate the effectiveness of the muscle relaxant,
the cause of muscle spasm and determine and determine whether the patient’s muscular
whether it is acute or chronic. pain or spasms have decreased or disappeared.
➔ Observe the patient’s drug history for possible
drug interactions. PSYCHOPHARMACOLOGY
➔ Note whether the patient has a history of
narrow-angle glaucoma or MG. Cyclobenzaprine AGONISTS
and orphenadrine are contraindicated with ➔ Drugs that occupy receptors and activate them
these health problems. ANTAGONISTS
Nursing Diagnoses ➔ Drugs that occupy receptors but do not activate
➔ Physical Mobility, Impaired related to dizziness them. Antagonists block receptor activation by
and hyperactive reflexes agonists.
➔ Activity Intolerance related to drowsiness and Pharmacodynamics
hyperactive reflexes Down regulation
Planning ➔ Drug causes receptor to change
➔ The patient will be free of muscular pain within 1 ◆ Ex. Consistent use of antidepressant
week. causes postsynaptic receptor to decrease
Nursing Interventions in number
➔ Monitor serum liver enzyme levels of patients Pharmacodynamic tolerance
taking dantrolene and carisoprodol. Report to ➔ Used to describe a reduction in receptor
the health care provider elevated levels of liver sensitivity (desensitization)
PHARMACOLOGY
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Drug Drug Interaction
➔ Pharmacokinetics interactions
◆ Occurs when one of the 4 processes is
inhibited or induced
➔ Pharmacodynamics interactions
◆ Ex. 2 drugs with same properties
synergistic or addictive effects
◆ 2 drugs with opposing effects reducing
their effectiveness
****NOTE: DI KO NA SINAMA ROLES OF DIFFERENT
NEUROTRANSMITTERS
ANTIANXIETY / ANXIOLYTICS/
MINOR TRANQUILIZERS
ANXIETY AND SLEEP DISTURBANCES
➔ Amongst the most frequently occurring
psychiatric conditions.
➔ Anxiety is an unpleasant experience of
something unknown
➔ A sub-symptom of a number of different
psychiatric conditions such as depression and
psychosis
ANXIETY
➔ OCD, Panic Anxiety, Social Phobia, specific
Phobias, PTSD
SLEEP DISTURBANCES
➔ Difficulties in Falling Asleep
➔ Poor quality of sleep or premature awakening
Pathophysiology
➔ GABA is important in understanding the mode of
action of anxiolytics drugs and sedatives, GABA
binds to GABA A receptors. These are chloride
channels and increase the Cl flow into the cell,
thereby hyperpolarizing the postsynaptic
membrane. This causes inhibition of impulse
traffic and reduced anxiety and wakefulness.
➔ Area of CNS related to anxiety with abundant
supply of GABAergic neurons and GABA receptors
as well as neurons that release other transmitters
is the AMYGDALA. Stimulation causes release of
GABA, inhibition of impulse transfer to other parts
of the brain and reducing anxiety.
➔ BENZODIAZEPINE receptors are distributed are
distributed in the CNS in a similar way to GABAa
receptors, and are found in high density in the
amygdala, especially in the parts that distribute
anxiety conditioned fear reaction in experimental
animals Neuropsychological basis of sleep is
complicated. Stimulation of the brain stem (PONS
and RAS) can induce sleep
Indications:
➔ Used to treat anxiety and anxiety disorders,
insomnia, obsessive compulsive disorders,
depression, PTSD and alcohol withdrawal
Mechanism of Action:
➔ Benzodiazepines mediate the actions of the
amino acid GABA
➔ Buspirone acts as a partial agonist at serotonin
receptors which decreases serotonin turnover
SIDE EFFECTS
• Can cause physical dependency
• Drowsiness
• Sedation/next day sedation
• Poor coordination
• Impaired memory
• Clouded sensation
MANAGEMENT:
• Advise client not to drink alcohol because
benzodiazepines potentiate its effects
• Advise client to be aware of decreased response time,
slower reflexes and possible sedative effects
• Advise not to discontinue the drug abruptly and
without order from the physician
ANTIPSYCHOTICS (NEUROLEPTICS,
MAJOR TRANQUILIZERS)
➔ All antipsychotic drugs tend to block D2 receptors
in the dopamine pathways of the brain
➔ Dopamine released in these pathways has less
effect.
➔ Excess release of dopamine in the mesolimbic
pathway has been linked to psychotic
experiences. It is the blockade of dopamine
receptors in this pathway that is thought to
control psychotic experiences.
DOPAMINE
➔ In the brain, dopamine functions as a
neurotransmitter, a chemical released by nerve
cells to send signals to other nerve cells.
➔ The human brain uses five known types of
dopamine receptors, labeled D 1 , D 2 , D 3 , D 4 ,
and D 5 . Dopamine is produced in several areas
of the brain, including the substantia nigra and
the ventral tegmental area
*****NOTE: DI KO NA DIN SINAMA YUNG MGA REWARD
CIRCUIT AND PATHWAYS
ANTIPSYCHOTIC DRUGS
(NEUROLEPTICS)
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TYPICAL ANTIPSYCHOTICS:
1. Chlorpromazine -
a. 25 mg, 50 mg, 100mg, and 200mg tablet OCCURRENCE:
b. 25 mg/mL solution ➔ First week of treatment
2. Haldol ➔ Younger than 40 years old
a. 5 mg/mL solution ➔ Males
3. Haloperidol ➔ Receiving high potency drugs e.g. haloperidol &
a. 20 mg tablet thiothixene
ATYPICAL ANTIPSYCHOTICS: MANAGEMENT:
1. Clozapine ➔ Give anticholinergic medications such as
a. 25 mg, 50 mg, 100 mg, and 200 mg benztropine mesylate cogentin) IM or
tablet diphenhydramine benadryl) IM or IV
ADVERSE EFFECT PROFILE:
First Generation antipsychotics AKATHISIA
- Higher risk of neurological side effects
➔ REPORTED BY THE CLIENT AS AN INTENSE NEED
Second Generation antipsychotics
TO MOVE ABOUT
- Higher risk of metabolic side effects
Manifestations
➔ Restless or anxious & agitated
EXTRAPYRAMIDAL SIDE EFFECTS
➔ w/ rigid posture or gait
➔ Acute Dystonia ➔ Inability to sit still
◆ Abnormal postures caused by involuntary Management
spasm ➔ Change medication
Manifestations ➔ Oral meds of beta blocker, anticholinergics or
➔ Muscular rigidity & cramping benzodiazepines
➔ Stiff or thick tongue w/ difficulty of swallowing
➔ Laryngospasm & respiratory difficulties AKINESIA/BRADYKINESIA
➔ Opisthotonus ; tightness in the entire body w/ the
➔ ABSENCE OF MOVEMENT / SLOWED MOVEMENT
head back and arched neck
Manifestation
➔ Oculogyric crisis; eyes rolled back in a locked
➔ Weakness
position
➔ Fatigue
➔ Torticollis; twisted head & neck
➔ Painful muscles
➔ Writer’s cramp; fatigue spasm affecting a hand
➔ Anergia
Management
➔ Give anticholinergic medications such as
benztropine mesylate cogentin) IM or
diphenhydramine benadryl) IM or IV
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long term use of conventional typical

PSEUDOPARKINSONISM antipsychotics
➔ Irreversible
➔ RESEMBLES PARKINSON'S DISEASE
➔ No effective treatment
Manifestations
MANAGEMENT
➔ Stooped posture
➔ No substantial management available yet.
➔ Mask like facies
➔ Vitamin E has helped improve the condition in
➔ Decrease arm swing
minority of patients
➔ Shuffling gait
CHARACTERISTICS
➔ Cogwheel rigidity
➔ Tongue writhing
➔ Drooling
➔ Tongue protrusion
➔ Tremors
➔ Teeth grinding
➔ Coarse pill rolling movements of the thumb &
➔ Lip smacking
fingers while at rest
➔ Symptoms stop w/ sleep
Management
ANTICHOLINERGIC SIDE EFFECTS
➔ Change medication to an antipsychotic drug
➔ Affects cranial nerves III, VII, IX, X
with lower incidence of EPS
◆ Dry mouth
➔ Add oral anticholinergic
◆ Constipation
➔ Give amantadine (dopamine agonist)
◆ Urinary hesitance or retention
◆ Blurred near vision
NEUROLEPTIC MALIGNANT
◆ Dry eyes
SYNDROME ◆ Photophobia
◆ Nasal congestion
➔ POTENTIALLY FATAL IDIOSYNCRATIC REACTION
◆ Decreased memory
TO A NEUROLEPTIC
◆ Tachycardia
Manifestation
◆ Decreased sweating
➔ Rigidity
MANAGEMENT
➔ High fever
➔ Calorie free beverages or hard candy and taking
➔ Unstable BP
frequent sips of water
➔ Diaphoresis
➔ For blurring of vision avoid tasks that are
➔ Pallor
dangerous such as driving and operating
➔ Delirium
machine
➔ Elevated CPK
◆ Reassure that normal vision will return in
➔ Confused & mute
a few weeks
➔ Agitated or stuporous
◆ Pilocarpine eye drops may be used
OCCURRENCE
➔ Avoid exposure to extreme heat if there is
➔ First two weeks of therapy
decreased sweating
➔ After an increase in dosage
➔ Advise wearing of sunglasses outdoors for those
➔ Dehydration
w/ photophobia
➔ Poor nutrition
➔ For urinary retention, encourage frequent
➔ Concurrent medical illness
voiding and voiding when urge is present
MANAGEMENT
➔ Stool softeners, increase OFI and inclusion of
➔ Immediately discontinue medication
grains and fruits in the diet
➔ Treat dehydration & hyperthermia
ANTI-ADRENERGIC SIDE EFFECTS
➔ May change medication
➔ Hypotension
➔ Dantrolene (Dantrium) and Bromocriptine
➔ Reflex Tachycardia : compensatory mechanism for
(Parlodel) are the drugs of choice
lower extremity
➔ Antipsychotics should not be administered at
➔ Ask pt to get out of bed or change position slowly
least two weeks after symptom resolution
➔ Management of hypotension resolves this
ENDOCRINE SIDE EFFECTS
TARDIVE DYSKINESIA ➔ INHIBITION OF DOPAMINE CAUSES
➔ A syndrome of permanent involuntary HYPERPROLACTINEMIA
movements that is most commonly caused by MEN
➔ Impotence
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➔ Loss of libido
➔ Gynecomastia SELECTIVE SEROTONIN REUPTAKE
➔ Low sperm count
INHIBITORS (SSRI)
➔ Feminization
WOMEN
➔ Amenorrhea
➔ Loss of libido
➔ Galactorrhea
➔ Risk for osteoporosis
➔ Change in menstrual cycle
METABOLIC SYNDROME OR INSULIN
RESISTANCE LEADING TO TYPE 2 DM
➔ Hyperglycemia
➔ Obesity
➔ Elevated lipid levels
➔ Coagulation abnormalities
➔ Hypertension SIDE EFFECTS
SEXUAL SIDE EFFECTS ➔ Anxiety
➔ Decreased libido ➔ Agitation
➔ Impotency ➔ Akathisia
➔ Impaired ejaculation ➔ Nausea
GI SIDE EFFECTS ➔ Insomnia
➔ Weight gain atypical antipsychotics specially with ➔ Sexual dysfunction
clozapine and olanzapine; except with ziprasidone ➔ Headache
➔ Carbohydrate craving ➔ Diarrhea
MANAGEMENT: ➔ Diminished sexual drive
➔ Choose an appropriate diet ➔ Difficulty achieving orgasm
➔ Advise not to take diet pills ➔ or erection
OTHER SIDE EFFECTS ➔ Weight gain
1. CLOZAPINE ➔ Sedation (paroxetine)
a. Can cause Agranulocytosis which is ➔ Sweating
characterized by leukopenia, malaise, ➔ hand tremors
sore throat and fever MANAGEMENT
b. Obtain patient’s baseline WBC count ➔ For akathisia give propranolol (inderal) or a
and differential before initiation of benzodiazepine
treatment ➔ For insomnia, a sedative hypnotic or low dose
c. WBC count should be done weekly for 4 trazodone may be given
weeks after discontinuation of the drug ➔ Sweating and Continued Sedation indicate the
need for change in medication
DEPRESSION
SEROTONIN NOREPINEPHRINE
Pathophysiology
➔ Monoamine theory depression stems from a REUPTAKE INHIBITORS (SNRIs)
defective monoaminergic transmission in the
➔ Serotonin Norepinephrine Reuptake inhibitors
CNS, with regard to too little noradrenaline and 5
(SNRIs) include desvenlafaxine (Pristiq)
HT in some central nervous synapses.
duloxetine (Cymbalta) venlafaxine (Effexor),
◆ Theory is based on the observation that
venlafaxine XR (Effexor XR), milnacipran (Savella),
antidepressants TCA and MAOI’s increase
and levomilnacipran (Fetzima)
monoaminergic transmission.
SIDE EFFECTS
◆ Patients who received reserpine became
➔ Most common to the class of SNRIs include
depressed. Reserpine acts by depleting
nausea, dizziness, and sweating. SNRIs,
the stores of monoaminergic transmitters.
particularly duloxetine, venlafaxine, and
desvenlafaxine may cause sexual dysfunction.
ANTI-DEPRESSION DRUGS
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Other side effects include tiredness, constipation, advised before prescribing these drugs to young
insomnia, anxiety, headache, and loss of appetite. people
SIGNIFICANT WARNINGS MANAGEMENT
➔ Abnormal bleeding ➔ Caution when driving or performing activities
➔ Suicidal thoughts or behavior: All requiring sharp and alert reflexes
antidepressants may increase the risk of suicidal ➔ Calorie free beverages or hard candy and taking
thoughts or behavior in children, adolescents, and frequent sips of water for dry mouth
young adults (18 to 24 years of age). ➔ Stool softeners, increase fluid intake, and inclusion
CONTRAINDICATIONS of grains and fruits in the diet for constipation
➔ Duloxetine and milnacipran should not be used ➔ Avoid exposure to extreme heat if there is
in patients with uncontrolled narrow angle or decreased sweating
angle closure glaucoma ➔ For patients w/ blurred vision, advise pt to avoid
potentially dangerous tasks. Reassure that normal
TRICYCLIC COMPOUNDS (TCA) vision will return in a few weeks. Pilocarpine eye
drops may be used.
➔ INHIBIT reuptake of both noradrenaline and 5 HT ➔ Advise wearing of sunglasses outdoors for those
in nerve terminals with photophobia
➔ Results in increase of the neurotransmitter in the ➔ For urinary retention, encourage frequent
synaptic cleft. voiding & voiding when urge is present
➔ For urinary hesitancy, provide the patient privacy

MONOAMINE OXIDASE INHIBITORS

➔ There are two forms of the MAO enzyme (MAO A)
and MAO B
➔ Moclobemide is a reversible and specific MAO A
inhibitor that increases 5 HT, noradrenaline and
dopamine in the synaptic cleft by a reduction of
presynaptic breakdown of these transmitters.
➔ By inhibiting MAO the amount of
neurotransmitter in the synaptic cleft is increased.
➔ MAO A inhibitors have a good antidepressant
effect, generally few adverse
➔ effects
➔ Older MAO inhibitors such as tranylcypromine,
inhibit tyramine breakdown in the liver leading to
higher levels of tyramine, which is an indirectly
acting sympathomimetic. Resulting to severe
hypertensive crisis
SIDE EFFECTS ***NOTE: MEMORIZE THE DRUGS!!!!
➔ Dry mouth
➔ Constipation
➔ Urinary retention
➔ Dry nasal passage
➔ Blurred near vision
➔ Sedation
➔ Orthostatic hypotension
➔ Weight gain
INDICATIONS
➔ Tachycardia
Treatment
➔ Sexual dysfunction
➔ Major depressive disorder
ADVERSE EFFECTS
➔ Anxiety disorder
➔ Because of an increase in aggression, violence
➔ Depressed phase of bipolar
and suicides by teenagers treated with
➔ disorder
monoamine reuptake inhibitors, great care is
➔ Psychotic depression
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➔ Panic disorder ANTIDEPRESSANTS TAKE EFFECT IN

➔ Eating disorder ➔ SSRI - 2-3 weeks
Given: ➔ CYCLIC COMPOUNDS - 4-6 weeks
➔ Early in the morning ➔ MAOI - 2-3 weeks
MANAGEMENT
➔ Advise wearing of sunglasses outdoors for those MOOD STABILIZING DRUGS
with photophobia
➔ For urinary retention, encourage frequent
voiding & voiding when urge is present
➔ For urinary hesitancy, provide the patient privacy
SIDE EFFECTS
➔ Daytime sedation
➔ Insomnia
➔ Weight gain
➔ Dry mouth
➔ Orthostatic hypotension
➔ Sexual dysfunction
➔ Hypertensive Crisis
MANAGEMENT: MAOI
➔ Inform client of the possibility of hypertensive INDICATION
crisis ➔ Treatment of Acute Episode of Mania
➔ Implement dietary restrictions by giving the MECHANISM OF ACTION
client a food list of what to avoid ➔ Lithium normalizes reuptake of serotonin,
➔ Instruct client not to take any OTC without norepinephrine, acetylcholine and dopamine
consulting the consultant or pharmacist ➔ Valproic acid & topiramate increase GABA level
➔ Valproic & carbamazepine stabilize mood through
HYPERTENSIVE CRISIS KINDLING PROCESS (snowball like effect that
raises the level of threshold to minor manic
➔ Results when the client who is taking MAOI episodes thus preventing full blown mania
ingested tyramine containing food such as the
following: LITHIUM
◆ Mature or aged cheese
◆ Aged meats like pepperoni, salami, meat ➔ Gold standard for the treatment of bipolar
extracts, sausages disorder
◆ tofu, over ripe fruit, avocado ➔ Dosage & blood lithium levels should be
◆ All tap beer monitored
◆ Soy Sauce , or soybean condiments THERAPEUTIC SERUM LEVEL
◆ Yogurt, sour cream, peanuts MSG ➔ 0.6 - 1.2 mEq/L (normal range)
HYPERTENSIVE CRISIS SIGNS & SYMPTOMS MILD-MODERATE TOXIC REACTIONS
➔ Hypertension ➔ 1.5 - 2 mEq/L
➔ Hyperpyrexia MODERATE TO SEVERE TOXIC REACTIONS
➔ Tachycardia ➔ 2 - 3 mEq/L
➔ Diaphoresis TOXIC EFFECTS:
➔ Cardiac dysrhythmias ➔ >3 mEq/L
FATAL DRUG INTERACTIONS ➔ severe diarrhea, vomiting
➔ Another MAOI ➔ Drowsiness, muscle weakness & lack of
➔ TCA ➔ Coordination, coma & death if serum
➔ Demerol LITHIUM SIDE EFFECTS
➔ Antihypertensives ➔ Nausea
➔ General anesthesia ➔ Diarrhea
➔ SSRI ➔ Anorexia
◆ Serotonergic syndrome: agitation, fever, ➔ Fine hand tremor
tachycardia,hypotension, hyperreflexia, ➔ Polydipsia
rigidity) ➔ Polyuria
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FINALS l yey

➔ Metallic taste in the mouth ➔ Acts as cortical and RAS stimulants by increasing
➔ Fatigue the release of norepinephrine, dopamine and
➔ Lethargy serotonin from the presynaptic neurons and block
➔ Weight gain their reuptake
CARBAMAZEPINE SIDE EFFECTS ➔ Paradoxical effect of calming by hyperexcitability
➔ Drowsiness through CNS stimulation is related to increase
➔ Sedation stimulation of an immature RAS
➔ Dry mouth ADVERSE EFFECTS
➔ Blurred vision ➔ Nervousness
➔ Orthostatic hypotension and rashes ➔ Insomnia
(carbamazepine) ➔ Dizziness and headache
➔ Weight gain, alopecia, tremor ( valproic acid) ➔ Blurred vision and difficulty with
TOPIRAMATE SIDE EFFECTS accommodation
➔ Dizziness ➔ GI effects nausea and vomiting
➔ Sedation ➔ CV effects hypertension, arrhythmias and
➔ Weight Loss angina
➔ Increased incidence of renal calculi SIDE EFFECTS
MANAGEMENT ➔ Anorexia
➔ Monitor blood levels periodically, time of the last ➔ Weight loss
dose must be accurate so that plasma levels can ➔ Nausea
be checked 12 hours after the last dose has been ➔ Irritability
taken ➔ Growth and weight suppression (long term)
➔ Take medication w/ meals to prevent nausea MANAGEMENT
➔ Advise client not to drive until dizziness, lethargy, ➔ Advise to take medications w/ meals to avoid
fatigue or blurring of vision has subsided anorexia and nausea
TOXIC EFFECTS ➔ Clients should avoid caffeine, sugar & chocolates
1. VALPROIC ACID 1. AMPHETAMINES & METHYLPHENIDATE
➔ Can cause hepatic failure, liver function test a. Potential for abuse is high
before start of therapy & frequent intervals 2. PEMOLINE
specially for the first six months a. Cause life threatening liver failure
➔ Can produce teratogenic neural tube defects (
spina bifida)
➔ Can cause pancreatitis
2. CARBAMAZEPINE
➔ Can cause aplastic anemia & agranulocytosis.
Monitor WBC & platelet counts
3. LAMOTRIGINE
➔ Can cause Stevens Johnson syndrome and
rarely, toxic epidermal necrolysis
STIMULANTS

INDICATIONS
➔ For treatment of ADHD and narcolepsy
MECHANISM OF ACTION