NCM 106 – PHARMACOLOGY
DRUGS ACTING ON THE CENTRAL NERVOUS SYSTEM
NERVOUS SYSTEM
 A complex network of nerves cells that carries the messages
to and from the brain as well as the spinal cord to various
part of the body. It is divided into CNS and the PNS:
 CENTRAL NERVOUS SYSTEM: Made up of the
brain and spinal cord.
 PERIPHERAL NERVOUS SYSTEM: Made up of
nerves (somatic and autonomic nervous systems).
 Somatic Nervous System: Consist of peripheral
fibers that pick up sensory information or sensation
from the peripheral or distant organs and carries
them to the central nervous system.
 Autonomic Nervous Systems: Is a control system
that acts largely, unconsciously and regulates body
function such as the heart rate, digestion,
respiratory rate, pupillary response, urination and
sexual arousal.
 This system is the primary mechanism in control of
the fight response.
NEURON / NERVE CELL
 A very important structure or unit of nervous system.
 These nerve cells send messages by conducting electrical
impulses called action potentials.
Network of Neurons:
 AFFERENT NEURONS: are responsible for taking
information in the CNS.
 EFFERENT NEURONS: carry the responses from the
CNS.
o Synopsis from between the neurons allowing them to
communicate to other neurons or other systems in the body.
o The general flow of information is that the PNS takes in
information through a sensory neurons that sends it to CNS
to be processed and after processing, the CNS tells the PNS
what to do.
o There are about billions of nerve cells which make up the
nervous system:
 This allows movement
 Realization of various sensations
 Response to internal and external stimuli
 Learning, thinking and emotion
o The NS allows organisms to sense, organize and react to
information in the environment. These are responsible for:
 Controlling the functions of human body
 Analyzing incoming stimuli
 Integrating internal and external responses
o Several drugs are used to change the mood or emotional state
of the user. These drugs importantly either promote or
decrease the action of particular neurotransmitter.
NEUROTRANSMITTER:
 This is the chemical messenger that transmits impulses
between neurons.
 Is a chemical messenger that carries, boost and balance
signals between neurons and target cell through the body.
 Several drugs are used as neurotransmitters are the following:
 Acetylcholine
 Norepinephrine and epinephrine
 Dopamine
 Gamma-aminobutyric acid or (GABA)
 Serotonin
→ ACETYLCHOLINE: Chief neurotransmitter this
communicates between nerves and muscles.
→ NOREPINEPHRINE/EPINEPHRINE: these are
catecholamine which functions primarily to increase cardiac
output interest glucose level in the blood
→ DOPAMINE: is sometimes called as the chemical
messenger. It is responsible on how we feel; it is found in
high concentrations in certain areas of the brain; involved in
the coordination of impulses and responses both motor and
intellectual.
→ GAMMA-AMINOBUTYRIC ACID (GABA): is a natural
occurring amino acid that works as neurotransmitter in your
brain; This neurotransmitters functions as chemicals
messenger; GABA is considered an inhibitor of
neurotransmitter because it blocks or inhibits certain brain
signals and decreases activity in your nervous system;
Inhibits nerve activity; Important in preventing over
excitability or stimulation; Example: seizure.
→ SEROTONIN: Key hormone that stabilizes or mood
feelings of well-being and happiness; this hormone impacts
the entire body; it enables cells especially brain cells and
another nervous system cells that communicate each other;
serotonin helps with sleeping and eating and digestion; found
in limbic system and it is important in arousal and sleep as
well as in preventing depression and promoting motivation.
9 CLASSIFICATIONS OF DRUGS ACTING ON THE
NERVOUS SYSTEM
5 Basic Ways In Which The Central Nervous System Drugs
And The Peripheral Nervous System Drugs Act:
1. Drug stimulate the release of neurotransmitter and enhances
action
2. Drugs combines with neurotransmitters preventing their
breakdown and enhancing their action
3. Drugs mimics neurotransmitter and enhance their action
 NCM 106 – PHARMACOLOGY

4. To block the release of neurotransmitter and decreased their prevent hypotension and prevent hypotension and
actions, and respiratory depression. respiratory depression.
5. To blocks receptors so neurotransmitter are unable to act.  Maintain patients in bed  Maintain patients in bed
for at least 3 hours for at least 3 hours
DRUG CLASSIFICATION: because some effects. because some effects.
1. ANXIOLYTIC and HYPNOTIC AGENTS  Flumazenil
 These drugs are used to alter individual’s responses to the (benzodiazepine antidote)
environment. This drug act in the Central Nervous System. – to treat overdosage of
benzodiazepine.
o ANXIOLYTICS prevent feelings of tension or
fear.
2. ANTIDEPRESSANT
o SEDATIVES make calm the patients and make
 All people experience different affective states at various
them unaware of the environment.
times in their lives.
o HYPNOTIC induces sleep.
 These states of minds, which change in particular situations,
usually do not last very long and do often involve extremes of
Anxiety - a feeling of tension, nervousness, apprehension, or fear
happiness or depression.
that usually involves unpleased reactions to stimulus. Anxiety is;
Overwhelming or severe, Interfere activities (in a person), Lead to
Depression - If a person’s mood goes the usual normal ups and
medical problem (most of them), Anxiolytic drugs- is used to lyse
downs, he/she is said to have affective disorder. This refers to the
or break the feelings of anxiety, Some also given a SEDATION.
people’s feelings in response to environment. It is also the time,
when the client feels sad and patients are mostly depressed. They
Sedation - is ANXIOLYTIC and most of the time leads to
may be described as overwhelming feelings of sadness, despair,
drowsiness; Extreme sedation results in further Central Nervous
hopelessness and disorganization. Little energy, sleep
System depression and sleep and also causes of hypnosis thus
disturbances, lack of appetite, limited libido, inability to perform
helping people to fall asleep.
activities and there is a fear of having patients committing suicide.
If left untreated, it can produce multiple physical problems.
 Drugs that are effective hypnotics act on the reticular
activating system (RAS) and block the brain's response to
→ The cause of depression usually is due to:
incoming stimuli. These are connected nuclear in the brains  Deficiency of norepinephrine or (NE)
of the vertebrates that are responsible for regulating the  Dopamine
rightfulness and sleep wake transition then the person no  Serotonin (5 HT) in particular
longer senses or reacts to stimuli. → This is explained in the Biogenic Amine (Theory of
Depression)
1.1 BENZODIAZEPINES – DIAZEPAM (P) → Reasons of Deficiencies:
1.) Monoamine oxidase (MAO)
2.1 BARBITURATES – PHENOBARBITAL (P)
2.) Rapid fire of the neuron
3.) Sensitivity of postsynaptic receptors
ACTION → An enzyme called monoamine oxidase is involved in
BENZODIAZEPINES BARBITURATES removing neurotransmitter, inform the brain. Monoamine
 Most frequent used  Sedative/hypnotic drug of inhibitors are given to prevent this from happening which
anxiolytic. choice. makes more of these brain chemicals available to effect
 Prevent anxiety without  Prevent anxiety without changes in both cells and circuits that have been impacted by
causing much associated causing much associated depression.
sedation. sedation. → ANTIDEPRESSANTS DRUGS WORKS IN THREE
 Less likely to cause  Risk of addiction and WAYS:
physical dependence. dependence is greater that 1. Inhibits the effects of MAO, leading to increased NE
Benzodiazepines. or 5HT.
INDICATION  These 5HT receptors or the 5 hydroxytriptamine
BENZODIAZEPINES BARBITURATES
receptors or Serotonin receptors as well are a
 Act: limbic systems and  General CNS depressant
group of g-protein couple receptors and ligand-
RAS - to make more  Causes sedation, hypnosis,
GABA effective anesthesia, extreme cases gated ion channels found in the central and
 For anxiety disorders of coma. peripheral nervous system. They mediate both
 Alcohol withdrawal  Indicated for relief of excitory and inhibitory neurotransmission.
 Hyperexcitability and signs and symptoms of 2. Block reuptake by the releasing nerve, leading to
agitation anxiety, for sedation, increased neurotransmitter levels.
 Given for preoperative insomnia, preanesthesia
3. Regulate receptor sites, leading to accumulation of
relief of anxiety and and seizures.
tension to aid in balance neurotransmitters.
of anesthesia.
PHARMACOKINETICS 1.1 TRICYCLIC ANTIDEPRESSANTS (TCA) –
BENZODIAZEPINES BARBITURATES IMIPRAMINE (P)
 Absorbed in GI tract  Absorbed in GI tract 2.1 MONOAMINE OXIDASE INHIBITORS (MAOI) –
 Peak: 30 mins – 2 hrs.  Peak: 20-60 mins. PHENELZINE (P)
 Cross the placenta which  Cross the placenta 3.1 SELECTIVE SEROTONIN REUPTAKE INHIBITORS
might affect the fetus.  Enter the breastmilk (SSRI) – FLOUXETINE (P)
 Enter the breastmilk,  Metabolized in the liver 4.1 OTHER ANTIDEPRESSANTS – BUPROPION (P)
therefore this is cautiously  Excreted in the urine
given to clients who are ACTION
breastfeeding. TCA MAOI SSRI
 Metabolized in the liver.  Including  Require  Better choice
 Excreted in the urine. amines, and dietary for many
NURSING CONSIDERATIONS tetracyclics, all regimen to patients; Less
BENZODIAZEPINES BARBITURATES reduces the prevent adverse
 Administer as ordered.  Administer as ordered. reuptake of toxicity. effects; 4
 Do not mix IV drugs in  Do not mix IV drugs in 5HT and NE. weeks- Full
solution with other drugs solution with other drugs therapeutic
because of drug-drug because of drug-drug effect.
interactions. interactions. INDICATION
 Give IV drugs slowly to  Give IV drugs slowly to TCA MAOI SSRI
 NCM 106 – PHARMACOLOGY

 Inhibit  Irreversibly  Depression neuron

presynaptic inhibit MAO.  OCD’s stimulation
reuptake of  Panic attacks and response
Neuro  Bulimia  Typical
Epinephrine  PTSD Antipsychotics
and 5HT.  Social Phobias - Dopamine
 The sedative  Social anxiety receptor
effects of these blockers
drugs may (phenothiazine
make them )
more effective  Atypical
in patients Antipsychotics
whose -Block both
depression is dopamine
characterized receptors and
by anxiety and serotonin
sleep receptors.
disturbances. INDICATION
PHARMACOKINETICS CNS
ANTIPSYCHOTIC ANTIMANIC
TCA MAOI SSRI STIMULANTS
 Absorbed: GI  Absorbed: GI  Absorbed: GI  Correct the  Alter sodium  Cortical and
Tract Tract Tract manifestation transport RAS
 Peak: 2-4 hrs.  Peak: 2-3 hrs.  Peak: of  Inhibits NE stimulants
 Bound in  Bound in unknown schizophrenia and dopamine
plasma protein plasma protein  Bound in  Hyperactivity
 Metabolized:  Metabolized: plasma protein  Combative
liver liver  Metabolized: behavior
 Excreted:  Excreted: liver  Agitation -
urine urine  Excreted: elderly
 Cross the  Cross the urine and feces PHARMACOKINETICS
placenta placenta  Cross the CNS
 Enter the  Enter the placenta ANTIPSYCHOTIC ANTIMANIC
STIMULANTS
breast milk breast milk  Enter the  Absorbed: GI 
Absorbed: GI  Absorbed: GI
breast milk Tract Tract Tract
NURSING CONSIDERATIONS  Metabolized:  Peak: 3 hrs.  Peak: 2-4 hrs.
TCA MAOI SSRI liver  Cross the BBB  Metabolized:
 Limit drug  Limit drug  Establish  Excreted: bile  Excreted: liver
access – access – suicide and urine kidney and  Excreted:
overdose suicide precautions –  Cross the 80% urine
(suicide).  Monitor BP – due to over placenta reabsorbed
 Give the major watch for dosage.  Enter the  Cross the
portion of dose hypotension.  Administer breast milk placenta and
at bedtime – drug once a breast milk
prevent injury day in the NURSING CONSIDERATIONS
for elderly. morning – CNS
achieve ANTIPSYCHOTIC ANTIMANIC
STIMULANTS
therapeutic  Do not crush  Monitor  Administer the
optimal or chew lithium daily drug before
effects. sustained-  Give with food 6pm –
released or milk – GI insomnia
3. PSYCHOTHERAPEUTIC AGENTS capsules upset  Provide safety
 These drugs are used to treat psychoses – perceptual and  Parenteral  Maintain – prevent
behavioral disorder. forms: adequate salt injury
o Schizophrenia recumbent for intake
o Mania 30mins –  Arrange for
o Narcolepsy prevents small frequent
o Attention-deficit disorders - Characterized by orthostatic meals.
inability to concentrate on one activity for longer hypotension sugarless
than a few minutes and a state of hyperkinesis.  Monitor CBC lozenges to
Diagnosed in school-aged children. – BM suck –
suppression increase
1.1 ANTIPSYCHOTIC/NEUROPELTIC DRUGS  Provide secretions
a. Typical Antipsychotic Drugs - sugarless
CHLORPROMAZINE & HALOPERIDOL (P) candy and ice
b. Atypical Antipsychotic Drugs – CLOZAPINE, chips for dry
OLANZAPINE, & RISPERIDONE (P) mouth
2.1 ANTIMANIC DRUGS – LITHIUM SALTS (P)  Void before
3.1 CNS STIMULANTS – METHYLPHENIDATE & taking a dose –
DEXTROAMPHETAMINE (P) urinary
retention
ACTION problem
CNS
ANTIPSYCHOTIC ANTIMANIC 4. ANTIEPILEPTIC AGENTS
STIMULANTS
 Dopamine  Opposite of  To treat Epilepsy - The most prevalent of the neurological disorders; is not
receptor depression attention a single disease but a collection of different syndromes.
blockers  Occur with deficit
 Major bipolar disorders and
tranquilizer disorder narcolepsy
 No longer  Ritalin
used –  Lithium salts
action: not
sedation but
 NCM 106 – PHARMACOLOGY

1.1 Generalized Seizures discomfort and painful

a. HYDANTOINS – PHETOIN (P) musculoskeletal
b. BARBITURATES & BARBITURATE-LIKE conditions.
DRUGS – PHENOBARBITAL (P) PHARMACOKINETICS
c. BENZODIAZEPINES - DIAZEPAM (P) CENTRALLY ACTING DIRECT-ACTING
d. SUCCINAMIDES – ETHOSOXIMIDE (P)  Absorbed and metabolized  GI tract
e. GAMMA-AMINOBUTYRC ACID modulator – in the liver.  Liver
VALPROIC ACID  Other relaxants excreted  Urine
2.1 Partial Seizures in the urine.  Enter the breast milk
a. CARBAMAZEPINE (P) NURSING CONSIDERATIONS
CENTRALLY ACTING DIRECT-ACTING
ACTION  If using baclofen, taper  Discontinue the drug at
BARBITURATES/ drug slowly over 1 to 2 any sign of liver
BENZODIAZEPIN
HYDANTOINS BARBITURATE- weeks – to prevent the dysfunction.
ES
LIKE development of psychoses  Discontinue drug at any
 Stabilize nerve membranes throughout the CNS to decrease and hallucination. sign of liver dysfunction.
excitability and hyperexcitability to stimulation.  Provide additional  Periodically discontinue
NURSING CONSIDERATIONS measures to relieve the drug for 2 to 4 days to
HYDANTOIN discomfort. monitor therapeutic effect.
 Discontinue the drug at any sign of hypersensitivity reaction,  Assess for
liver dysfunction, severe skin rash hypersensitivity.
 Administer with food  Taper drug slowly over 1
to 2weeks.
5. ANTIPARKINSONISM AGENTS  Health teachings
Parkinson’s Disease (TRAP) – T: tremor; shaking usually on one
side; R: rigidity; stiffness of the limbs, neck or trunk; A: akinesia: 7. NARCOTICS, NARCOTIG AGONISTS &
loss or impairment in power of voluntary movement; P: posture ANTIMIGRAINE
and balance.  2 Major types of drug:
o Narcotic: the opium derivatives
1.1 DOPAMINERGIC AGENTS – LEVOD0OPA (P) o Antimigraine Drugs: treatment of migraine
2.1 ANTICHOLINERGIC AGENTS – BIPERIDEN (P) headache, a type of severe headache.
3.1 ADJUNCTIVE AGENTS – ENTACAPONE,
SELEGILINE & TOLCAPONE

ACTION
DOPAMINERGICS ANTICHOLINERGICS
 Block the action of  Increase the levels of
acetylcholine dopamine
 Normalize the
acethylcholine-dopamine
imbalance
PHARMACOKINETICS
DOPAMINERGICS ANTICHOLINERGICS 1.1 NARCOTICS
 Absorbed: GI tract  Absorbed: GI tract a. NARCOTIC AGONIST – MORPHINE (P)
 Metabolized: Liver  Peak: 1 – 4 hrs. b. NARCOTIC AGONIST-ANTAGONIST –
 Excreted: Peripheral cells  Metabolized: liver PENTAZOCINE (P)
 Urine  Excreted: cellular c. NARCOTIC ANTAGONISTS – NALOXONE
 Cross the placenta pathways (P)
 Enter the breast milk  Cross the placenta
 Enter the breast milk ACTION
NURSING CONSIDERATIONS NARCOTIC NARCOTIC NARCOTIC
DOPAMINERGICS ANTICHOLINERGICS AGONISTS AGONISTS – ANTAGONIST
 Administer with food ANTAGONIST
 Provide sugarless lozenges  Reacts with  Stimulate  Bind strongly
 Monitor bowel function opioid certain opioid to opioid
 Advise to void before taking the drug receptors receptors but receptors but
 Establish safety precaution throughout the block other they do not
body to cause receptors. activate the
6. MUSCLE RELAXANTS analgesia,  Less abuse receptors.
sedation, or potential  Play a role in
euphoria. the treatment
1.1 CENTRALLY ACTING SKELETAL MUSCLE
 Develops of narcotic
RELAXANTS – BACLOFEN (P)
physical overdose.
2.1 DIRECT-ACTING SKELETAL MUSCLE
dependence.
RELAXANTS – DANTROLENE (P)
THERAPEUTIC ACTIONS & INDICATION
ACTION NARCOTIC NARCOTIC NARCOTIC
AGONISTS AGONISTS – ANTAGONIST
CENTRALLY ACTING DIRECT-ACTING
ANTAGONIST
 Work in the CNS to  Dantrolene (Dantrium) is
interfere with the reflexes currently available for use
 Act at specific  Relief of  Block opioid
opioid receptor moderate to receptors an
that are causing the in treating spasticity that
sites severe pain reverse the
muscle spasm. directly affects peripheral
 Relief of  Adjuncts to effects of
 Drugs lyse or destroy muscle contraction
severe acute or general opioid
spasm (spasmolytics).
chronic pain anesthesia  Naloxone – is
THERAPEUTIC ACTIONS & INDICATIONS
 Preoperative  Relief pain used to
CENTRALLY ACTING DIRECT-ACTING
medication during labor diagnose
 Tizanidine is an  Dantrolene acts within  Analgesia narcotic
and delivery
alphaadrenergic agonist skeletal muscle fibers, during overdose.
and it is thought to interfering with the release anesthesia  Naltrexone –
increase inhibition of of calcium from the to treat
presynaptic motor neurons muscle tubules. narcotic and /
in the CNS.  This action prevents the or alcoholic
 Indication: relief fibers from contracting.
 NCM 106 – PHARMACOLOGY

dependence. Migraine Headaches – used to describe several different

PHARMACOKINETICS syndromes, all of which include severe, throbbing headaches on
NARCOTIC NARCOTIC NARCOTIC one of the head.
AGONISTS AGONISTS – ANTAGONIST
ANTAGONIST Should be distinguished from:
 IV  Absorbed: IM  Absorbed after  Cluster headaches – usually begin during sleep and involve
administration administration injection. sharp, steady eye pain that lasts 15 to 90 minutes with
is the most  Peak: reach  Metabolized in sweating, flushing, tearing, and nasal congestion.
reliable way to rapidly when the liver  Tension headaches – occur at times of stress, feel like a dull
achieve given IV  Excreted in the band of pain around the entire head and last from 30 minutes
therapeutic  Cross the urine to 1 week. Accompanied by anorexia, fatigue, and mild
levels. placenta  Enter the intolerance to light or sound.
 Cross the  Enter the breast milk  Common migraines – occur without aura, cause severe,
placenta and breast milk unilateral, pulsating pain accompanied by nausea, vomiting,
breast milk sensitivity to light and sound, aggravated by physical
 Oxycodone – activity.
drug of choice  Classic migraines – usually preceded by an aura, or a
during sensation involving sensory or motor disturbances, that occur
pregnancy – about one-half hour before the pain begins.
 Do not crush
or chew ACTION
CONTRAINDICATIONS & CAUTION ANTIMIGRAINE TRIPTANS
NARCOTIC NARCOTIC NARCOTIC  Ergot Derivatives  New class of drug
AGONISTS AGONISTS – ANTAGONIST  Constriction of cranial  Cause cranial vascular
ANTAGONIST blood vessels constriction
 Allergy  Allergy  Allergy  Decrease the pulsation of  Relief of migraine
 Pregnancy  Caution: cranial arteries. headache pain
 Caution: physical THERAPEUTIC ACTIONS & INDICATIONS
respiratory dependence ANTIMIGRAINE TRIPTANS
dysfunction –  Pentazocine –  Block alpha- adrenergic  Bind to selective serotonin
respiratory cause cardiac and serotonin receptor. receptor sites.
depression stimulant  Treatment only for acute
ADVERSE EFFECTS migraine but not prevent
NARCOTIC NARCOTIC NARCOTIC it.
AGONISTS AGONISTS – ANTAGONIST PHARMACOKINETICS
ANTAGONIST ANTIMIGRAINE TRIPTANS
 Respiratory  Respiratory  Most common  Absorbed: many routes  Same
depression depression effect is acute  Onset and action: 15 to 30
 Orthostatic narcotic minutes
hypotension abstinence  Metabolized: liver  Same
 Neurological syndrome:  Excreted: bile  Urine
effects nausea/  Pregnancy: can cause  Cross the placenta
 Genitourinary vomiting, serious adverse effects if  Enter the breast milk
effects sweating, given.
tachycardia,  Excreted in the breast
anxiety milk
DRUG-DRUG INTERACTION CONTRAINDICATIONS & CAUTIONS
NARCOTIC NARCOTIC NARCOTIC ANTIMIGRAINE TRIPTANS
AGONISTS AGONISTS – ANTAGONIST  Presence of allergy  Allergy
ANTAGONIST  CAD
 With  With  To reverse the  Hypertension
barbiturates or barbiturate effects – larger  Peripheral vascular
MAOIs – general doses of disease
respiratory anesthesia – narcotic  Cautions: pruritus and
depression, respiratory antagonists malnutrition
hypotension, depression, may be ADVERSE EFFECTS
sedation or sedation, needed.
coma hypotension, ANTIMIGRAINE TRIPTANS
or coma  Related to druginduced  CNS effects: numbness,
increases. vascular constriction. myalgia, vertigo
NURSING CONSIDERATIONS  CNS effects: numbness,
NARCOTIC NARCOTIC NARCOTIC tingling of extremities
AGONISTS AGONISTS – ANTAGONIST  CV effects: pulselessness,
ANTAGONIST weakness, chest pain, MI
 Provide a  Same  Provide occur.
narcotic artificial  GI upset
antagonist and ventilation  Ergotism: a syndrome -
equipment for  Ensure when severe thirst, BP changes,
assisted giving confusion, drug
ventilation on naltrexone – dependency (prolonged
standby during narcotic free use), drug withdrawal
IV for 7 to 10 syndrome
administration days DRUG-DRUG INTERACTIONS
– for severe ANTIMIGRAINE TRIPTANS
reactions
 If combined with beta- 
Only give triptans after 2
2.1 ANTIMIGRAINE AGENTS blockers – risk for weeks of MAOI
a. ERGOT DERIVATIVES – ERGOTAMINE (P) peripheral ischemia andwithdrawal – if not
b. TRIPTANS – SUMATRIPTAN (P) gangrene is increase. increased vasoconstrictive
effects occur.
NURSING CONSIDERATIONS
ANTIMIGRAINE TRIPTANS
 NCM 106 – PHARMACOLOGY

 Avoid prolonged used –  Arrange for safety ventilation + CNS  Shock

prevent severe adverse precautions if CNS or depression)
effect. visual changes occur.  Cautions: severe
 Assess extremities cardiovascular diseases,
carefully – if decubitus hypotension, shock, ICP,
ulcer/gangrene is present myasthenia gravis
(causes by peripheral ADVERSE EFFECTS
vasoconstrictions). GENERAL ANESTHESIA LOCAL ANESTHESIA
8. GENERAL & LOCAL ANESTHETICS  Depressive effects - 
Local blocking sensation
Circulatory depression, 
CNS effects: headache,
Anesthetics – are drugs that are used to cause complete or partial Hypotension, Shock, restlessness, anxiety,
loss of sensation. Decreased cardiac output,dizziness, tremors, blurred
Respiratory depression, vision
Can be subdivided into: Delirium  GI upsets
 General Anesthetics - are CNS depressant to produce loss of  Cardiovascular effects:
pain sensation and consciousness. Blocks body reflexes. Peripheral vasodilation,
 Local Anesthetics - are drugs used to cause loss of pain myocardial depression,
sensation without the systemic effects associated with severe arrhythmias
CNS depression. DRUG-DRUG INTERACTIONS
GENERAL ANESTHESIA LOCAL ANESTHESIA
1.1 General Anesthetic Agents  If ketamine and  With succinylcholine –
a. BARBITURATES – THIOPENTAL (P) halothane are combined: increased and prolonged
b. NON-BARBITURATES – MIDAZOLAM (P) severe cardiac depression Neuromuscular blockage
c. GASES – NITROUS OXIDE (P) occurs occurs.
d. VOLATILE LIQUIDS – HALOTHANE (P)
 Barbiturates and
2.1 Local Anesthetic Agents narcotics – produce apnea
a. ESTERS – BENZOCAINE (P)
NURSING CONSIDERATIONS
b. AMIDES – BUPIVACAINE & LIDOCANE (P)
GENERAL ANESTHESIA LOCAL ANESTHESIA
c. OTHERS – PRAMOXINE & DYCLONINE
 Have equipment on  Same
standby to maintain  Same
TYPES & MODE OF ADMINISTRATION
airway (ventilator)  Spinal anesthesia: ensure
GENERAL ANESTHETIC LOCAL ANESTHETIC
 Check vital signs the patient is well
 Barbiturate - IV drugs to  Topical - To traumatized hydrated and lying down
induce rapid anesthesia skin for 12hrs. –minimize
 Nonbarbiturate - IV  Infiltration - Injecting the headache.
administration with a wide tissues directly to prevent
variety effects them from transmitting
9. NEUROMUSCULAR JUNCTION BLOCKERS
 Gases - Enter the bronchi nerve impulses
and alveoli, pass quickly  Field Block - Injecting all  Affect the normal functioning of muscles by interfering with
into the brain and cause around the area, more the normal processes that occur at the junction of nerve and
CNS depression. intense than infiltration muscle cell.
 Volatile Liquids -  Nerve Block - Injecting  Sarcomere - The functional unit of a muscle.
Unstable at room the nerves to cause loss of
temperature and release pain sensation or muscle
gases. paralysis is desired.
 Intravenous Regional -
Injecting anesthetic into
the vein of the arm or leg
using tourniquet to
prevent from entering the
general circulation.
THERAPEUTIC ACTIONS & INDICATIONS
GENERAL ANESTHESIA LOCAL ANESTHESIA
 Depression of reticular  Temporary interruption
activating system and  Affect the permeability of
cerebral cortex. nerve membranes (sodium
 Indications: sedation, ions)
anesthesia, amnesia,  Indications: infiltration
unconsciousness (painful anesthesia, peripheral
surgical procedures) nerve block, spinal
anesthesia, local pain
relief.
PHARMACOKINETICS
GENERAL ANESTHESIA LOCAL ANESTHESIA
 Lipid soluble (throughout  Broken down in the
the body) plasma
 Liver  Amide (slowly The normal muscle function involves the arrival of a nerve
 Cross the placenta metabolized in the liver) impulse at the motor nerve terminal, followed by the release of
 Note: 4-6 hrs. nursing the  Note: they should be used Ach into the synaptic cleft.
women after recovery during pregnancy and
before nursing the baby. lactation only if the
benefit outweighs any
potential risk to the fetus
or neonate that could
occur if the drug is
inadvertently absorbed
systematically
CONTRAINDICATIONS & CAUTIONS
GENERAL ANESTHESIA LOCAL ANESTHESIA
 Status asthmaticus  Allergy
(difficulty in providing  Heart block
 NCM 106 – PHARMACOLOGY

1.1 NONDEPOLARIZING NEUROMUSCULAR DRUGS ACTING ON THE AUTONOMIC NERVOUS

BLOCKERS – PANCURONIUM (P) SYSTEM (PNS)
2.1 DEPOLARIZING NEUROMUSCULAR BLOCKER –
SUCCINYCHOLINE (P) Autonomic Nervous System (ANS):
 also called “involuntary or visceral nervous system” Because
 Nondepolarizing NMJs - Act as antagonists to acetlycholine it mostly functions with little conscious awareness of its
at the NMJ and prevent depolarization of muscle cells. activity.
 Depolarizing NMJs - Act as an Ach agonist at the junction,  Working closely with the endocrine system.
causing stimulation of the muscle cell and then preventing it  Helps to regulate and integrate the body’s internal functions
from repolarizing. within in a relatively narrow range of normal.
 Integrates parts of the central and peripheral nervous system
ACTION to automatically react to changes in the internal and external
NONDEPOLARIZING NMJ DEPOLARIZING NMJ environment.
BLOCKERS BLOCKERS  Functions:
 Curare – first discovered.  Succinylcholine – only o Main nerve centers (ANS) are located in the
 Occupy the muscular drug used. hypothalamus, the medulla, and the spinal cord.
cholinergic receptor sites.  Attaches to the Ach o Nerve impulses that arise in peripheral structures
 Do not cause activation of receptor site on the muscle are carried by the afferent nerve fibers.
muscle cells. cell, depolarizing the o These integrating centers in the CNS respond by
muscle. sending out efferent impulses along the autonomic
THERAPEUTIC ACTIONS & INDICATIONS nerve pathways.
NONDEPOLARIZING NMJ DEPOLARIZING NMJ o These impulses adjust the functioning of various
BLOCKERS BLOCKERS internal organs in ways that keep the body’s
 Hydrophilic, instead of lipophilic internal environment constant, or homeostasis.
 Do not cross the BBB (blood-brain barrier) o ANS works to regulate blood pressure, heart
 Block the acetylcholine  Prevent muscle movement rate, respiration, body temperature, water
receptor ( It cannot be (By prohibiting the balance, urinary excretion, and digestive
stimulated) depolarization) functions.
PHARMACOKINETICS o The control exerted by this system results from an
interrelationship between opposing divisions of the
NONDEPOLARIZING NMJ DEPOLARIZING NMJ
autonomic systems: the sympathetic and the
BLOCKERS BLOCKERS
parasympathetic divisions.
 Metabolized: serum
 Excreted: urine
 Note: Succinylcholine is often used during CS (however,
does cross the placenta)
CONTRAINDICATIONS & CAUTIONS
NONDEPOLARIZING NMJ NONDEPOLARIZING NMJ
BLOCKERS BLOCKERS
 Allergy
 Myasthenia Gravis – because blocking of the Ach
cholinergic receptors aggravates the neuromuscular disease.
 Cautions: family history of malignant hyperthermia –
serious adverse effect (extreme muscle rigidity, severe
hyperpyrexia, acidosis, and death)
 Caution: Succinylcholine should NOT be used with caution
in patients with fractures – might lead to additional trauma.
 Narrow-angle glaucoma/penetrating eye injuries – intraocular
pressure increases
 Paraplegia/spinal cord injury – cause loss of potassium from
overstimulated cells and hyperkalemia
ADVERSE EFFECTS COMPARISON:
SYMPATHETIC PARASYMPATHETIC
NONDEPOLARIZING NMJ NONDEPOLARIZING NMJ
CNS NERVE ORIGIN
BLOCKERS BLOCKERS
 Thoracic  Cranium
 Associated with the paralysis of muscles – depression  Lumbar spinal cord  Sacral spinal cord
 Gastrointestinal dysfunction – if prolonged drug used
PREGANLIONIC NEURON
 Decubitus ulcer – loses of reflex muscle movement
 Short axon  Long axon
DRUG-DRUG INTERACTIONS
PREGANGLIONIC NEUROTRANSMITTER
NONDEPOLARIZING NMJ NONDEPOLARIZING NMJ  Acetylcholine  Acetylcholine
BLOCKERS BLOCKERS GANGLIA LOCATION
 Drug combinations result in an increased neuromuscular  Next to spinal cord  Within or near effector
effect. organs
 Calcium channel blockers – may also greatly increase the POSTGANGLIONIC NEUROTRANSMITTER
paralysis  Norepinephrine  Acetylcholine
 With cholinesterase inhibitors – the effect of NMJ blockers is  Epinephrine
decreased. NEUROTRANSMITTER TERMINATOR
NURSING CONSIDERATIONS  Monoamine oxidase  Acetylcholinesterase
NONDEPOLARIZING NMJ DEPOLARIZING NMJ (MAO)
BLOCKERS BLOCKERS  Catechol-O-
 Monitor VS methyltransferase
 Maintain Dantrolene on standby (COMT)
 Arrange for a small dose of nondepolarizing NMJ blocker GENERAL RESPONSE
before the use of Succinylcholine – reduce adverse effects  Fight or flight  Rest and digest
 Maintain a cholinesterase inhibitor on standby – overcome
excessive neuromuscular blockag
 NCM 106 – PHARMACOLOGY

catecholamines
 Epinephrine is a
natural
catecholamine
THERAPEUTIC ACTIONS & INDICATION
ALPHA- & BETA- ALPHA-SPECIFIC BETA-SPECIFIC
 Increased: heart  Stimulate  Stimulate
rate, myocardial alphaadrenergic betaadrenergic
contractility receptors receptors
 Bronchi dilate  Used to treat  Used to manage
and respirations shock or shock- bronchial spasm,
increase in rate like states asthma
and depth  Clonidine-  Isoproterenol –
 Vasoconstrictio essential increase heart
n occurs with hypertension rate,
increase in BP  Phenylephrine - conductivity,
 Intraocular (cold and allergy contractility
pressure products) for  Treatment of
decreases constricting shock – increase
 Glycogenolysis topical vessels cardiac activity.
-breakdown of  Midodrine –
glucose stores orthostatic
that the glucose hypotension
can be used as
energy
PHARMACOKINETICS
ALPHA- & BETA- ALPHA-SPECIFIC BETA-SPECIFIC
 Absorbed  Widely  Isoproterenol
rapidly after distributed in - rapidly
injection or the body distributed
passage  With a short after injection
ADRENERGIC RECEPTORS through period (20-
Alpha1 Beta1 mucous 45mins)
 Found in blood vessels,  Found in cardiac tissue membranes
iris, and urinary bladder.  Stimulate increased  Metabolized:  Liver  Liver
 Cause vasoconstriction myocardial activity liver  Urine  Urine
 Increase peripheral  Increased heart rate  Excreted:
resistance  Increased lipolysis urine
 Thus, rising blood  Breakdown of fats in  Note: Because the sympathomimetic drugs stimulate the
pressure peripheral tissues SNS, they should be used during pregnancy and lactation
Alpha2 Beta2 only if the benefits to the mother clearly outweigh any
 Located on nerve  Found in the smooth potential risks to the fetus or neonate.
membranes muscle in blood vessels, CONTRAINDICATIONS
 Acts as modulators of bronchi, periphery, uterine ALPHA- & BETA- ALPHA-SPECIFIC BETA-SPECIFIC
norepinephrine release muscle  Pheochromocy-  Allergy  Allergy
 Causes a reflex decrease  Leads to vasodilation toma (overload of  Severe  Pulmonary
in norepinephrine release  Relaxes uterine smooth catecholamines - hypertension hypertension/d
 Prevent overstimulation of muscle. fatal) /tachycardia uring
effector sites  Tachyarrhythmias (additive anesthesia
CHOLINERGIC TRANSMISSION / ventricular effects) (severe
Muscarinic Receptors Nicotinic Receptors fibrillation  Narrow-angle reaction)
 Stimulated by muscarine  Located in the adrenal (exacerbate the glaucoma  Eclampsia
 Found in visceral effecator medulla, autonomic conditions) (exacerbated /uterine
organs, sweat glands, ganglia, neuromuscular  Hypovolemia by arterial hemorrhage
muscular smooth muscle junctions (fluid constriction) /intrauterine
 Pupil constriction,  Muscle contraction replacement -  Pregnancy death
increased GI motility &  Release of NE and treatment of (potential (complicated
secretion , increased epinephrine hypotension) adverse effects by relaxation,
urinary bladder  Halogenated on the fetus) increase BP)
contraction, slowing heart hydrocarbon  Pregnancy
rate general /lactation
anesthetics
1. ADRENERGIC AGONIST CAUTION
 Also called sympathomimetic drugs because they mimic ALPHA- & BETA- ALPHA-SPECIFIC BETA-SPECIFIC
the effects of the sympathetic nervous system (SNS). The  Should be used  Cardiovascular  Diabetes
therapeutic and adverse effects associated with these drugs of peripheral disease  Thyroid
are related to their stimulation of adrenergic receptor sites. vascular disease /vasospasm disease
(ex. (aggravated by  Vasomotor
1.1 ALPHA- & BETA-ADRENERGIC AGONISTS – atherosclerosis, vascular effects) problems
DOPAMINE (P) Raynaud’s  Thyrotoxicosis  Degenerative
2.1 ALPHA-SPECIFIC ADRENERGIC AGONISTS – disease or /diabetes heart disease
PHENYLEPHRINE (P) diabetes (thyroidstimulati  History of
3.1 BETA-SPECIFIC ADRENERGIC AGONISTS – endaritis- ng/glucose – stroke
ISOPROTERENOL (P) exacerbated by elevating effects) (exacerbated
systemic  Lactation (may by the
ACTION vasoconstrictio be passed to the sympathomim
ALPHA- & BETA- ALPHA-SPECIFIC BETA-SPECIFIC n) infants) etic effects of
 Stimulate all of  Bind primarily  Used to treat  Hepatic /renal the drug)
the adrenergic to alpha obstructive impairment
receptors receptor pulmonary (could interfere
 Some drugs are conditions. with metabolism
preparations of / excretion of the
 NCM 106 – PHARMACOLOGY

drugs)  Tamsulosin  Propranolol

ADVERSE EFFECTS  Terazosin  Sotalol
ALPHA- & BETA- ALPHA-SPECIFIC BETA-SPECIFIC  Timolol
 Arrhythmias  Anxiety  Anxiety BETA1-SELECTIVE ADRENERGIC BLOCKING AGENTS
 Hypertension  Restlessness  Restlessness  Acebutolol
 Palpitations  Depression  Fear  Atenolol
 Dyspnea  Fatigue  Tremor  Betaxolol
 Related to  Strange dreams  Fatigue  Bisopropolol
depressant  Blurred vision  Headache  Esmolol
effect  Cardiovascular  Cardiovascular  Metoprolol
effects effects
 Depressant  Pulmonary ADRENERGIC BLOCKERS
effects effects: dyspnea ALPHA- & BETA- ALPHA BETA
 GI upset  Used to treat  More specific  Used to treat
DRUG-DRUG INTERACTION cardiac-related and safer cardiovascular
ALPHA- & BETA- ALPHA-SPECIFIC BETA-SPECIFIC conditions. drug. problems:
 TCAs and  MAOIs (can  With other Hypertension,
MAOIs cause severe sympathomim Angina,
(increased hypertension, etic drugs Migraine
norepinephrine headache, (increased THERAPEUTIC ACTIONS & INDICATIONS
levels or hyperpyrexia) effects) ALPHA- & BETA- ALPHA BETA
increased  Phenylephrine  Combined Blocked the effects  Phentolamin  Decreased
receptor with TCAs with beta- of norepinephrine blocks the heart rate,
stimulation) (increased adrenergic at alpha-and postsynaptic contractility,
 Drugs that effects) blockers betareceptors alpha1 – excitability
cause  Clonidine with (decreased decreasing the  Leads to: -
hypertension TCAs (decreased therapeutic sympathetic Decreased
(increased risk hypertensive effects). tone in the arrhythmias,
of effect) vasculature cardiac
hypertension)  Clonidine with and causing workload,
propanolol vasodilation oxygen
(paradoxical (lowering BP) consumption.
hypertension PHARMACOKINETICS
occur) ALPHA- & BETA- ALPHA BETA
 Midodrine  Well absorbed  Absorbed  Absorbed
(precipitate throughout the after injection from the GI
increased drug body tract and
effects of  Metabolized in undergo
digoxin, beta- the liver hepatic
blockers)  Excreted in the metabolism
NURSING CONSIDERATIONS feces and urine  Excreted in
ALPHA- & BETA- ALPHA-SPECIFIC BETA-SPECIFIC  Note: not the urine
 Extreme  Do not  Beta-blocker recommended  Note: should
caution in discontinue on standby for use in not be used
calculating abruptly –taper when giving children during
and over 2-4 days parenteral younger than 18 lactation
preparing (rebound isoproterenol years.
doses (small hypertension, (in case of CONTRAINDICATIONS & CAUTIONS
errors – flushing, severe ALPHA- & BETA- ALPHA BETA
serious effects arrhythmias, reactions).  In patients with Allergy  Allergy
 Always dilute hypertensive  Use minimal bradycardia or CAD  Bradycardia
drug (prevent encephalopathy, dose of heart blocks  MI  Heart blocks
tissue irritation death). isoproterenol  Shock or CHF  Cautions: in  Shock
on injection)  If given to achieve  With cautions: pregnancy and  CHF
 Phentolamine Phenylephrine desired effects. diabetes – lactation  COPD
on standby (in IV – Alpha- aggravates the  Acute asthma
case blocking agent response  Caution:
extravasation on standby (in Bronchospasm – Diabetes and
occurs) case of severe respiratory hypoglycemia;
reactions). distress due to the Hepatic
loss of dysfunction
2. ADRENERGIC ANTAGONIST norepinephrine’s
 Are also called sympatholytics because they lyse, or block bronchodilating
the effects of the sympathetic nervous system. actions
 The therapeutic and adverse effects are related to their ability ADVERSE EFFECTS
to react with specific adrenergic receptor sites without ALPHA- & BETA- ALPHA BETA
activating them.  Dizziness  Hypotension  Dizziness
 They prevent norepinephrine released from the terminal or  Paresthesia  Orthostatic  Paresthesia
from the adrenal medulla, thus blocking the SNS effects.  Insomnia hypotension  Insomnia
 Depression  Angina  Depression
ALPHA- & BETA-ADRENERGIC ALPHAADRENERGIC  Fatigue  MI  Fatigue
BLOCKING AGENTS BLOCKING AGENTS  Vertigo  CVA  Vertigo
 Carvedilol  Phentolamine  Flushing  Memory loss
 Guanadrel  Tachycardia  Disorientation
 Guanethidine  Arrhythmia
 Labetalo DRUG-DRUG INTERACTIONS
ALPHA1-SELECTIVE ALPHA- & BETA- ALPHA BETA
BETA-ADRENERGIC
ADRENERGIC BLOCKING  Risk of excessive  Ephedrine  Parodoxical
BLOCKING AGENTS
AGENTS hypotension if and hypertension
 Alfuzosin  Carteolol combined with epinephrine – rebound
 Doxazosin  Nadolol enflurane, – decreased hypertension if
 Prazosin  Pindolol halothane, or hypertensive with clonidine
 NCM 106 – PHARMACOLOGY

isoflurane effects  NSAIDS – have little or no effect at the neuromuscular junction

anesthetics 
Hypotension decreased THERAPEUTIC ACTIONS & INDICATIONS
if combined hypertensive  Atropine is used to depress salivation and bronchial
with alcohol effects secretions and to dilate the bronchi.
NURSING CONSIDERATIONS  To relax GI and genitourinary tracts: - to cause Mydriasis
ALPHA- & BETA- ALPHA BETA (relaxation of the pupil), Cyclopegia (inhibition of the ability
 Do not  Monitor heart  Do not of the lens to accommodate to near vision.
discontinue rate and blood discontinue  Scopolamine is also used to decrease the nausea and
abruptly after pressure abruptly after vomiting associated with motion sickness.
chronic therapy chronic PHARMACOKINETICS
 Monitor for therapy  Well absorbed after administration
hypotension  Cross the BBB
 Excreted in the urine
ALPHA1-SELECTIVE BETA1-SELECTIVE CONTRAINDICATIONS & CAUTIONS
 are drugs that have 
Have an advantage over  Allergy
specific affinity for alpha1 the nonselective beta-  Glaucoma – possibility increased pressure with pupil dilation
blockers in some cases.  Peptic ulcer, ulcerative colitis, intestinal atony, paralytic
 They do not usually ileus, toxic megacolon – intensified with further slowing GI
block beta2- receptor activity.
sites  Cautions: breastfeeding, spasticity and damage
 They do not block the ADVERSE EFFECTS
sympathetic  CSN effects: blurred vission, pupil dilation, photophobia,
bronchodilation cyclopegia, IOP
(important in lungs  Weakness, dizziness, insomnia, mental confusion
diseases or allergic  Dry mouth
rhinitis)-for smoker  Altered taste perception, nausea, heartburn, constipation,
THERAPEUTIC ACTIONS & INDICATIONS bloated feelings, and paralytic ileus
 Decreased in vascular tone  decreased heart rate, DRUG-DRUG INTERACTION
and vasodilation – which contractility, excitability  If with antihistamines, antiparkinsonism drugs, MAOIs,
leads to a fall in blood  Decreased arrhythmias TCAs – increases effects.
pressure  Decreased cardiac work  The effectiveness of phenothiazines decreases if they are
load combined with anticholinergic drugs, and the risk of paralytic
 Decreased oxygen ileus increases.
consumption NURSING CONSIDERATIONS
PHARMACOKINETICS  Ensure proper administration of the drug.
 Well absorbed and  Absorbed from the GI
undergo extensive hepatic tract CHEMOTHERPEUTIC AGENTS
metabolism  Metoprolol is increased if  These are drugs used to DESTROY ORGANISMS that and
 Excreted in the urine is taken with food. ABNORMAL CELLS that invade THE BODY.
 Metabolized in the liver
excreted in the urine
CONTRAINDICATIONS & CAUTIONS
 Allergy  Allergy
 Lactation  Diabetes, thyroid disease ,
 Caution: CHF, renal or COPD
failure
 Hepatic impairment
 Pregnancy
ADVERSE EFFECTS
 CNS effects: - Dizziness,  CNS, CV, +Genitourinary  Anti-Infective Agents
Weakness, Fatigue, Effects: - Decreased libido  Antibiotics
Drowsiness, Depression - Impotence - Dysuria -  Antiviral Agents
 Cardiovascular effects: - Peyronie’s disease  Antifungal Agents
Arrhythmias,  Antiprotozoal Agents
Hypotension, Edema,  Antihelmintic Agents
CHF, Angina  Antineoplastic Agents
DRUG-DRUG INTERACTIONS
 Increased hypotensive  Decreased effect with
effects if combined with clonidine, NSAIDs,
other vasodilating or rifampin, barbiturates
antihypertensive drugs
NURSING CONSIDERATIONS
 Monitor BP, pulse,  Do not stop abruptly –
rhythm, cardiac output taper the dose over 2
regularly weeks
 Give oral forms with food
– facilitate absorption

3. ANTICHOLINERGIC AGENTS NURSING CONSIDERATIONS

 Are used to block the effects of acetylcholine. Also called  Resistance to anti-infective occurs
parasympatholytics agents. These classes of drugs were
very widely used to decrease gastrointestinal (GI) activity
and secretions in the treatment of ulcers.
 ATROPINE (P)

ANTICHOLINERGIC
AGENTS/PARASYMPATHOLYTICS
 Atropine (generic) has been used for many years and is
derived from the plant belladonna.
 Atropine and Scopolamine work by blocking only the
muscarinic effectors in the parasympathetic nervous system.
 They do not block the nicotinic receptors and therefore
 NCM 106 – PHARMACOLOGY

1. ANTI-INFECTIVE AGENTS 2. Fluoroquinolones (2nd, 3rd and 4th Gen): modified

Use of Anti-infectives: 1st gen quionolones; not highly protein bound;
 Treatment of systemic infections wide distribution to urine and other tissues; limited
 Prophylaxis CSF penetration.

TREATMENT OF SUPERINFECTION
 Identification of pathogens
 Combination therapy

Reasons of Use:
 Smaller dose of each drug (fewer adverse effects)
 Synergistic effect

ANTIBIOTICS: refer to the chemical which inhibits specific

bacteria.
 Living microorganisms
 Synthetic
 Genetic engineering
GOAL OF ANTIBIOTIC THERAPY
→ To decrease the population of invading bacteria
o Gram positive – bacteria whose cell wall
retains a stain.
o Gram negative – cell was looses a stain
→ Aerobic and Anaerobic bacteria
1.1 AMINOGLYCOSIDES
 Group of powerful antibiotics used to treat infections caused
by gram negative aerobic bacilli (bacterial).
 G.N.A.T.S. – Gentamicin, Neomycin, Amikacin,
Tobramycin, Streptomycin
 Indications: Gram-negative microorganisms that cause
urinary tract infections, meningitis, wound infections, and
life - threatening septicemias.
2.1 CEPHALOSPHORINS
4.1 PENICILLIN AND PRAS
 Penicillin’s beta-lactam structure (beta-lactam ring)
interferes with bacterial cell-wall synthesis by inhibiting the
bacterial enzyme that is necessary for cell division and
cellular synthesis.
 Prolonged use of Penicillin will lead to resistance.
 4 CATEGORIES OF PENICILLINS:
1. Basic Penicillins (BP)
2. Broad-Spectrum Penicillin (BSP)
3. Extended-Spectrum (ESP)
4. Penicillin-Resistant Antibiotics (PRAs)
 THERAPEUTIC CLASSIFICATION AND
INDICATIONS:
 Has bactericidal effects (interferes with cell wall
building) by preventing biosynthesis of the cell
wall framework (bacteria burst).
 Treatment of gram-positive bacteria: streptococcal
infections including pharyngitis, tonsillitis, scarlet
fever and endocarditis, pneumococcal infections;
staphylococcal infections, rat-bite fever, anthrax
etc.
 PHARMACOKINETICS:
 rapidly absorbed in the GI tract (peak of 1hr) but
sensitive to gastric juices (taken on empty
stomach)
 excreted unchanged in urine
 crosses breast milk and can cause adverse
reactions
 Contraindications:
 Patients with allergy to the drug
 Use with caution to patients with renal disease.

1.1 PENICILLINS:
o Penicillin G benzathine (Zalpen, Penadur)
o Penicillin G potassium (Pfizerpen)
o Penicillin G procaine (crysticillin – AS)
o Penicillin V (Veetids)
2.1 BROAD SPECTRUM PENICILLINS: used to treat both
gram-positive and gram-negative bacteria.
3.1 FLUOROQUINOLONES o Amoxicillin (Amoxil, Himox)
 Actions: o Amoxicillin-clavulanate(Augmentin)
1. enters bacterial cell by passive diffusion and o Ampicilin (Ampicin)
interfere with DNA enzymes action o Ampicillin-sulbactam (Unasyn)
2. Little cross-resistance but misuse may lead to 3.1 EXTENDED SPECTRUM PENICILLINS: also broad
resistant strains spectrum; Effective against Pseudomonas aeruginosa, a
gram-negative bacillus; Action is similar to Aminoglycosides
but are less toxic.
o Piperacill-tazobactam
o Mezlocillin sodium (Mezlin)
o Ticarcillin-clavulanate (Timentin)
4.1 PENICILLIN RESISTANT ANTOBIOTICS-PRAS:
Effective against gramnegative organisms; also called
"Antistaphylococcal Penicillin".
o CLOXACILLIN (Secloxin)
o Dicloxacillin (Dyapen, Dycill)
o Oxacillin (Prostaphlin)
o Nafcillin

 Classification: 5.1 SULFONAMIDES

1. Quinolones (1st Gen): Highly protein bound;  PHARMACOKINETICS: Also called sulfa drugs
mostly used in UTIs o Sulfadiazine
 NCM 106 – PHARMACOLOGY

oSulfisoxazole  Amantidine is slowly absorbed in the GIT, half-life of 15hrs.

oSulfasalazine - a sulfapyradine (Arthritis)
oCotrimoxazole - a combi-drug (famethoxazole and
trimethoprim)
 THERAPEUTIC ACTIONS AND INDICATIONS:
o They competitively block para-aminobenzoic acid
(PABA) to prevent the synthesis of folic acid.
o Used to treat gram-positive and gram-negative
bacteria (Chlamydia trachomatis and Nocardia; H.
influenza, E.coli and P. Mirabilis)
o Emergence of resistant bacterial strains
 PHARMACOKINETICS:
o Teratogenic in nature and distributed in breatmilk.
o Given orally abosrobed in the GI and excreted in
urine.
o Time of peak level and half-life varies from every
individual
o OTITIS MEDIA, PNEUMONITIS,
BRONCHITIS, UTI
6.1 Others (in coursepack)
DRUG THERAPY ACROSS THE LIFESPAN
CHILDREN:
 Use anti-infective with caution; early exposure may lead to
early sensitivity.
 Habitual use has contributed greatly to the development of
resistant strains.
 Monitor hydration and nutritional status – increased
susceptibility to GIT and nervous system effects.
ADULTS:
 Drug allergies and the emergence of resistant strains because
these groups demands anti-infectives for a “quick cure” of
various signs and symptoms.
 Pregnant and nursing women must use extreme caution
because this can affect the fetus.
OLDER ADULTS:
 Susceptible to severe adverse GI, renal and neurological
effects.
 Possible host poisoning
3. ANTI-VIRAL AGENTS
VIRUSES
 causes a variety of conditions ranging from warts, to
common cold and “flu” to diseases like chickenpox and
measles.
 must enter the human cell to survive
 replicates inside the human cell
 have no cell wall and made up of nucleic acid components
 do not have a metabolic machinery of their own – uses host
enzymes
 Oseltamivir is readily absorbed in the GIT
 Ribavirin is inhaled
 Zanamivir is delivered via a Diskhaler device
 Excreted in urine
Considerations:
 Not proven safe and effective in children
 Taken for a longer period of time
 Older patients are susceptible to adverse effects
 Patients with renal dysfunction
Adverse Effects:
 May be related to dopamine levels in the brain:
o light-headedness, dizziness, and insomnia;
o nausea,
o orthostatic hypotension, and urinary retention
2.1 Agents for Herpes and Cytomegalovirus
 TA: inhibit viral DNA replication by competing with viral
substrates
 • Acyclovir (Zovirax) • Valacyclovir (Valtrex) • Cidofovir
(Vistide) • Famciclovir (Famvir) • Foscarnet (Foscavir) •
Ganciclovir (Cytovene) • Valganciclovir (Valcyte)
3.1 Agents for HIV and AIDS
 Goals of Antiretroviral therapy: SUPPRESS VIRAL
REPLICATION to slow the decline in the number of CD4
cells (Helper T cells)
 Reduce the incidence of opportunistic infections
 Classes of Anti-retroviral Drugs
1. Nonnucleoside Reverse Transcriptase
Inhibitors
 TA: bind directly to HIV reverse
transcriptase
 Nevirapine (P)
2. Nucleoside Reverse Transcriptase Inhibitors
 Zidovudine (P)
3. Protease Inhibitors
 Fosamprenavir (P)
4. Fusion Inhibitor
 Enfuvirtide (Fuzeon)
5. CCR5 Coreceptor Antagonist
 Maraviroc (P)
6. Integrase Inhibitor
4.1 Anti-Hepatitis B AGENT
 Hepa B Agents O Vaccination of Hepa B
 In the past, treatement ( ADEFOVIRHepsera)
 In 2004 and 2005 - Adefovir and Entecavir (Baraclude)
 In 2006- neocleoside NRTI Telbivudine (Tyzeka) was found
effective
4. ANTIFUNGAL AGENTS
 Also called ANTIMYCOTIC DRUGS
 prevents replication and eventually death of fungi
 Drugs which are used to treat:
1. Systemic mycoses
2. Superficial/topical mycoses

SYESTEMIC ANTIFUNGALS
Azoles Ichinocandin Others
Fluconazole (P) anidulafungin amphotericin B
itraconazole caspofungin nystatin
posaconazole micafungin
terbinafine (P)
voriconazole
clotrimazole (P)
1.1 Agents for Influenza A and Respiratory Viruses Binds to sterols and Inhibits glucan Work by causing
• Vaccines to stimulate immunity can cause cell death synthesis fungal death or
• Common drugs: (fungicidal) or prevent fungal
 AMANTADINE (Symmetrel) interfere with cell replication
 OSELTAMIVIR (Tamiflu) replication
 RIBAVIRIN (Virazole) (fungistatic).
 RIMANTADINE (Flumadine)
 ZANAMIVIR(Relenza) TOPICAL ANTIFUNGALS
Azoles Ichinocandin
Therapeutic Actions and Indications: Clotrimazole Butenafine
 Exact mechanism of action is UNKNOWN. Ketoconazole Ciclopitox
 Beliefs: prevents shedding of the viral protein coat and entry Miconazole Gentian violet
of virus into the cell. Terbinafine Tionaftate

Pharmacokinetics:
 NCM 106 – PHARMACOLOGY

Adverse Effects:
 allergy Other Agents
 burning sensation  Gold Compounds
 skin irritation Chrysotherapy - use of gold salts
>Auranofin (Ridaura)
>Aurothioglucose(Solganal)
5. ANTIPROTOZOAL AGENTS >gold sodium thiomalate (Aurolate)
>Anakinra(Kineret)
1.1 Antimalarials
 usually given in combination form to attach the Plasmodium Nursing Considerations:
at various stages.  Chronic use of Ibuprofen may damage the kidneys
 Quinine, Chloroquine (Aralen), Primaquine(Daraprim), (renal evaluation is necessary)
Hydroxychloroquine (Plaquenil), Mefloquine (Lariam)  Watch for GI bleeding
 Nursing responsibilities:
o Assess hearing status of patient 4. IMMUNO MODULATORS
o Monitor urine output  are drugs which either suppress the immune system
o Check visual changes (Immunosuppressants) or stimulate the immune system
o Not given to pregnant women (Immunostimulants).
 Other Protozoal infections:
o Amebiasis 1.1 IMMUNOSUPPRESANT
o Leishmaniasis  Used in conjunction with corticosteroids to block
o Tryposomiasis inflammatory reaction and decrease initial damage to cells.
o Trichomoniasis  USES:
o Giardiasis o Autoimmune diseases
o Organ/tissue transplantation
6. ANTIHELMINTICS AGENTS o Common Class of Immunosuppresants:
 T- and B-Cell Suppressors
 Interleukin-Receptor Antagonist
 Monoclonal Antibodies
 Common Drugs: Cyclosporine (P)

2.1 IMMUNOSTIMULANTS
 Used to energize the immune system
 Includes: interferons and interleukins
 USES:
1.1 ABENDAZOLE  Immunodeficiency Disorders
 Broad spectrum  Chronic Infections
 Drug of choice for treatment of hydatid disease and  Cancer
cysticercosis.  Common immunostimulants
 Used for the treatment of ( intestinal nematodes ) e.g.  Interferon alfa-2b
ascariasis, tricurasis and strongyloidiasis, pinworm,  Aldesleukin
hookworm  Interferon alfacon-1
 Peginterferon alfa-2b
2.1 MEBENDAZOLE (Vermox)  Interferon alfa-n3
 Synthetic benzimidazole  Aprelvekin
 Wide spectrum and safer than albendazole  Nursing Considerations :
 Mechanism of action: As albendazole It kills hookworm, pin  check for adverse effects for patients using
worm, ascariasis and trichuris eggs. interleukins .
 Children are given higher doses of
3.1 PYRANTEL PAMOATE immunosuppressants.
 Broad spectrum  Not given to pregnant women and lactating
 Pharmacokinetics: Poorly absorbed orally; Half of the drug is mothers (fetal abnormalities, susceptibility to
excreted unchanged in the feces. infection and will cross placental barrier).
 Mechanism of action: Neuromuscular blocking drug leads to  Use with cautions to clients with:
paralyzes of worms.  cardiac disease
 myelosuppresion
DRUGS ACTING ON THE IMMUNE SYSTEM  central nervous system dysfunction
 Inform clients that they may manifest a "flue"-like
1. ANTI-INFLAMMATORY, ANTIARTHRITIS AND symptoms while on therapy (fever, myalgia,
RELATED AGENTS fatigue, arthralgia).
Focus of Tx:
 Accelerate renal excretion of Uric Acid VACCINES
 Reduce the conversion of purine to uric acid  Active Immunity – Natural or Artificial
 Inhibits prostaglandin synthesis  Passive Immunity -

1. SALICYLATES (ASA) IMMUNE SERA

 block inflammatory response, antipyretic and analgesic  Refer to sera that contain antibodies to specific bacteria or
actions viruses.
 inhibits prostaglandin synthesis  Provide passive immunity
 Aspirin Bayer (P) o Tetanus immunoglobulins
 may cause GI problems o Rabies immunoglobulins
o ANTITOXINS AND ANTIVENINS
2. NSAIDs
 provides strong anti-inflammatory and analgesic effects NURSING RESPONSIBILTIES:
 Ibuprofen (Dolan, Advil) (P)  time of diluting vaccines
 place vaccines in their proper places (bioref)
3. ANTIGOUT DRUGS  keep vaccine away from heat
 Uric acid inhibitor: ALLOPURINOL -inhibits the final steps  give Paracetamol
of uric acid biosynthesis.
 Uricosurics – increase the rate of uric acid excretion by
inhibiting its reabsorption.
 Colchicine – inhibits migration of leukocytes to the inflamed
site.