DRUGS AFFECTING

THE NERVOUS SYSTEM

NEURO-ANAPHY
NEURO-ANAPHY
Nervous System

The nervous system is responsible for controlling the functions

of the human body, analyzing incoming stimuli, and integrating
internal and external responses

Primary Motor Cortex Primary Sensory Cortex

(Frontal Lobe) (Parietal Lobe)
Nervous System

Primary Motor Cortex Primary Sensory Cortex

(Frontal Lobe) (Parietal Lobe)
Nervous System

The nervous system is responsible for controlling the functions

of the human body, analyzing incoming stimuli, and integrating
internal and external responses

Primary Motor Cortex Primary Sensory Cortex

(Frontal Lobe) (Parietal Lobe)
Nervous System
Functions:
● Monitoring changes
- sensory receptors, stimuli, sensory input (information gathering)

● Interpretation of sensory input

- integration: what to do with each input

● Effects responses
- activates muscles (effectors) via motor output

● Mental activity
- consciousness, thinking, memory

● Homeostasis
- stimulate or inhibit the activities to maintain a constant internal environment
NERVOUS SYSTEM OVERVIEW
NERVOUS SYSTEM OVERVIEW
NERVOUS SYSTEM OVERVIEW
Physiology
NEURONS
- structural unit of the nervous system
- 14B neurons: 10B in the brain

Parts:
Soma (Cell body) – nucleus, cytoplasm
Dendrites – short, branch-like projections,
increased surface area for the neuron
Axon – elongated process, carries info from a
nerve to be transmitted to effector cells

This transmission occurs at the end of the

axon, where the axon branches out into what
is called the axon terminal
Physiology: Axons → Fibers

AFFERENT FIBERS: are nerve axons

that run from peripheral receptors
into the CNS (sensory)

Afferent = How it affects the body

EFFERENT FIBERS: are nerve axons

that carry nerve impulses from the
CNS to the periphery to stimulate
muscles or glands (motor)

Efferent = Effects/Exit
Anatomy: Axons → Fibers
Anatomy: Axons → Fibers
Anatomy: Axons → Fibers
Physiology
NEURONS
- unable to reproduce; so, if nerves are
destroyed, they are lost
- If dendrites and axons are lost, nerves
regenerate those structures; however, for
this regeneration to occur, the soma and
the axon hillock must remain intact.

ganglia (groups of nerve bodies)

Physiology
ACTION POTENTIAL
- Nerves send messages by conducting
electrical impulses
-
Physiology

NERVE SYNAPSE
- When the electrical action potential reaches the end of an axon, the
electrical
impulse comes to a halt
- transmission of information between two nerves or between a nerve and a
gland or muscle is chemical
- Nerves communicate with other nerves or effectors at the nerve synapse

Synapse
is made up of a presynaptic nerve, the synaptic cleft, and the postsynaptic
effector cell
 Physiology

Synapse: is made up of a
presynaptic nerve, the
synaptic cleft, and the
postsynaptic effector cell
Physiology

NEUROTRANSMITTERS
- stimulate postsynaptic cells either by exciting or by inhibiting them

- reabsorbed by the presynaptic nerve in a process called reuptake (a

recycling effort by the nerve to reuse the materials and save resources) or
broken down by enzymes in the area
(e.g., monoamine oxidase breaks down the catecholamine neurotransmitters; the
enzyme acetylcholinesterase breaks down the neurotransmitter acetylcholine)
Physiology
Physiology

NEUROTRANSMITTERS
 Physiology
These drugs have several functions:

● blocking the reuptake of neurotransmitters so that they are present in the

synapse in greater quantities and cause more stimulation of receptor sites,

● blocking receptor sites so that the neurotransmitter cannot stimulate the

receptor site,

● blocking the enzymes that break down neurotransmitters to cause an

increase
● in neurotransmitter concentration in the synapse

● stimulating specific receptor sites when the neurotransmitter is not available,

● causing the presynaptic nerve to release greater amounts of the

neurotransmitter
CENTRAL
NERVOUS SYSTEM
ANATOMY
BBB: Blood Brain Barrier
ANATOMY: BLOOD SUPPLY
 ANATOMY: BRAIN

2 cerebral hemispheres,
thalamus, hypothalamus, limbic
system

Contains CN to the specific

senses (SSHBT)
Head and neck muscle activity:
chewing, eye movement
Reticular Activating System:
arousal, awareness, sleep
center
Most primitive area
Contains the brain stem
Controls basic, vital functions:
respiration, regulates BP,
vomiting, swallowing
Cerebellum: balance,
coordination, gait, voluntary
muscle activity
ANATOMY: BRAIN
ANATOMY: Homunculus
 SPINAL CORD

Each spinal nerve has

two components or roots.
These mixed nerve parts
include a sensory fiber
(called the dorsal root) and a
motor fiber (called the ventral
root). The spinal
sensory fibers bring
information into the CNS from
the periphery. The motor
fibers carry information away
from the brain and cause
movement or
reaction.
 CNS PHYSIOLOGY

SENSORY FUNCTION MOTOR FUNCTION

INTELLECTUAL FUNCTION EMOTIONAL FUNCTION

 NERVOUS SYSTEM

ANATOMY PHYSIOLOGY PATHOLOGY DRUGS

Neurons Action potential of Multiple sclerosis
Schwann cells (auto-immune)
Nerve Synapse Epilepsy Anti-seizure
Neurodegenerative Anti-parkinsonism
(Alzheimer’s, Parkinson’s)

Neurotransmitters Dopamine Parkinson’s Antiparkinsonism

Limbic System Expression of Depression Antidepressant

emotion Anxiety Anxiolytics
ANXIOLYTIC & HYPNOTICS
Anxiolytics and Hypnotic

used to alter an individual’s responses to environmental stimuli

Anxiolytics: reduce or prevent feelings of tension or fear, sedatives because

they can calm patients and make them unaware of their environment

Hypnotics: they can cause sleep,

 Anxiolytics and Hypnotic

ANXIETY SEDATION HYPNOSIS

feeling of tension, loss of awareness and Extreme sedation results

nervousness, reaction to in further central
apprehension, or fear environmental stimuli nervous system (CNS)
that usually involves depression and sleep
unpleasant reactions to a
stimulus
Benzodiazepine

MOA INDICATION
act in the limbic ➢ Anxiety d/o
system and the ➢ Alcohol
RAS to make withdrawal
gamma- ➢ Hyperexcitability
aminobutyric acid ➢ Agitation
(GABA) more
effective, causing
interference with
neuron firing
Benzodiazepine

MOA INDICATION CI / CAUTION A/E

act in the limbic ➢ Anxiety d/o ➢ Allergy CNS: sedation,
system and the ➢ Alcohol ➢ Psychosis drowsiness,
RAS to make withdrawal ➢ Glaucoma, amnesia,
confusion
gamma- ➢ Hyperexcitability shock, coma
CV: BP changes,
aminobutyric acid ➢ Agitation ➢ Pregnancy,
arrythmias
(GABA) more lactating GI: dry mouth,
effective, causing Caution: N/V, constipation
interference with Elderly, debilitated, GU: urinary
neuron firing renal & hepatic retention, loss of
dysfunction libido
Benzodiazepine
Benzodiazepine

NURSING
NURSING RESPONSIBILITIES
PROCESS
Contraindications, baseline status,
ASSESSMENT perform lab tests (renal, liver, CBC)

NURSING r/t CNS effects: disturbed thought

DIAGNOSIS process, risk for injury, sleep pattern
Best therapeutic effect, limited A/E,
PLANNING understands the drug therapy
Proper administration, monitor labs,
INTERVENTION taper dose, comfort measures, health
teaching, support and encouragement
Response to drug, A/E, effectiveness of
EVALUATION teaching plan and comfort measures
Barbiturates

MOA INDICATION
General CNS ➢ Anxiety
depressant: inhibit ➢ Sedation
neuronal impulse ➢ Insomnia
conduction in the ➢ Seizures
ascending RAS,
depress the
cerebral cortex,
alter cerebellar
function, and
depress motor
output
Barbiturates

MOA INDICATION CI / CAUTION A/E

act in the limbic ➢ Anxiety d/o ➢ Allergy CNS: drowsiness,
system and the ➢ Alcohol ➢ Hx of addiction somnolence,
RAS to make withdrawal to the drug class lethargy, ataxia,
vertigo
gamma- ➢ Hyperexcitability ➢ Hepatic & renal
GI: diarrhea, N/V,
aminobutyric acid ➢ Agitation impairment
constipation,
(GABA) more ➢ Respi. Distress epigastric pain
effective, causing ➢ Pregnancy CV: bradycardia,
interference with Caution: hypotension,
neuron firing Pain, seizure, syncope
chronic hepatic, Respi: Respi.
cardiac, respi dses depression
Hypersensitivity
Barbiturates
Barbiturates

NURSING
NURSING RESPONSIBILITIES
PROCESS
ASSESSMENT Contraindications, baseline status (PE)
r/t CNS effects: disturbed thought
NURSING
process, risk for injury; impaired gas
DIAGNOSIS exchange r/t respiratory depression
Best therapeutic effect, limited A/E,
PLANNING understands the drug therapy
Proper administration, monitor labs,
INTERVENTION taper dose, comfort measures, health
teaching, support and encouragement
Response to drug, A/E, effectiveness of
EVALUATION teaching plan and comfort measures
Barbiturates

MOA INDICATION
General CNS ➢ Anxiety
depressant: inhibit ➢ Sedation
neuronal impulse ➢ Insomnia
conduction in the ➢ Seizures
ascending RAS,
depress the
cerebral cortex,
alter cerebellar
function, and
depress motor
output
ANTIDEPRESSANTS
Antidepressants

Affect: people’s feelings in response to their environment, whether positive

and pleasant or negative and unpleasant.

All people experience different affective states at various times in their lives.

These states of mind, which change in particular situations, usually do not

last very long and do not often involve extremes of happiness or sadness.

If a person’s mood goes far beyond the usual normal “ups and downs,” he or
she is said to have an affective disorder.
DEPRESSION

For 2 weeks or more, > 5 of the following at least one is either (1) depressed
mood or (2) anhedonia:
● Depressed mood (can be irritable in children or adolescents)
● Sleep: Insomnia or hypersomnia
● Interest loss (anhedonia)
● Guilt (worthlessness)
● Energy loss (fatigue)
● Cognition/concentration difficulties (distractibility)
● Appetite loss and/or weight loss (not dieting) or weight gain (>5% change
in body weight in a month)
● Psychomotor agitation or retardation
● Suicidal ideations (passive: thoughts, felt like better off dead; or active:
plan, attempt; preoccupation with death)
DEPRESSION

depression results from a deficiency

of biogenic amines in key areas of the brain; these biogenic amines include
norepinephrine (NE), dopamine, and serotonin (5HT)

Both NE and 5HT are released throughout the brain by neurons that react
with multiple receptors to regulate arousal, alertness, attention, moods,
appetite, and sensory processing
DEPRESSION

Deficiencies of these neurotransmitters may develop for three

known reasons:
1) Monoamine oxidase (MAO) may break them down to be
recycled or restored in the neurons
2) Rapid fire of the neurons → depletion
3) Increased number or sensitivity of postsynaptic receptors →
depleting neurotransmitter levels
Drug Therapy

Causes of Deficiencies DRUG MOA

monoamine oxidase (MAO) may break inhibit the effects of MAO,

them down to be recycled or restored leading to increased NE or 5HT in the
in the neurons synaptic cleft)

may block reuptake of these

rapid fire of the neurons → depletion
Increased number or sensitivity of
postsynaptic receptors → depleting
neurotransmitter levels
neurotransmitters by the releasing nerve,
leading to increased neurotransmitter
levels in the synaptic cleft
regulate receptor sites and the
breakdown of neurotransmitters, leading
to an accumulation of neurotransmitter in
the synaptic cleft.
Drug Therapy

Causes of
DRUG MOA DRUG CLASS
Deficiencies
monoamine oxidase inhibit the effects of MAO MAO Inhibitors (MAOI)
(MAO) may break them
down
block reuptake of these SSRI: Selective serotonin
rapid fire of the neurons neurotransmitters by the reuptake inhibitors
→ depletion releasing nerve TCA: tricyclic
antidepressants
Increased number or regulate receptor sites and COMT: catecholamine-O-
sensitivity of postsynaptic the breakdown of methyltransferase
receptors → depleting neurotransmitters
neurotransmitter levels
Sites of Action
Sites of Action
Sites of Action
Drug Therapy

Causes of
DRUG MOA DRUG CLASS
Deficiencies
monoamine oxidase inhibit the effects of MAO MAO Inhibitors (MAOI)
(MAO) may break them
down
block reuptake of these SSRI: Selective serotonin
rapid fire of the neurons neurotransmitters by the reuptake inhibitors
→ depletion releasing nerve TCA: tricyclic
antidepressants
Increased number or regulate receptor sites and COMT: catecholamine-O-
sensitivity of postsynaptic the breakdown of methyltransferase
receptors → depleting neurotransmitters
neurotransmitter levels
ANTISEIZURE
SEIZURE

EPILEPSY, the most prevalent of the neurological disorders, is not a single

disease but a collection of different syndromes characterized by the same
feature:

Sudden discharge of excessive

electrical energy from nerve
cells located within the brain
→ SEIZURE
SEIZURE

This release stimulates motor nerves → convulsions, with tonic–

clonic muscle contractions → potential to cause injury, tics, or
spasms

May stimulate autonomic or sensory nerves → cause different

effects: barely perceptible, temporary lapse in consciousness or
a sympathetic reaction

Because epilepsy involves a loss of control, it can be frightening

to patients when they are first diagnosed.
SEIZURES

PRIMARY SEIZURES: no underlying cause can be identified

SECONDARY SEIZURES: outside factors—head injury, drug

overdose, environmental exposure, and so on—may precipitate
seizures.
SEIZURES
SEIZURES
SEIZURES
Antiepileptic

● Antiepileptics, or antiseizure agents;

anticonvulsants

● DOC: any given situation depends on

the type of epilepsy, patient age,
specific patient characteristics such
as cultural variations, and patient
tolerance for associated adverse
effects.

● Can be used to treat more than one

type of seizure
SEIZURES: Generalized

1. Tonic-clonic: muscle contraction → aggressive spasm; LOC, post-ictal state

(confusion), exhaustion
2. Absence: abrupt, brief periods of LOC (3-5 secs); no muscle contractions
3. Myoclonic: short, sporadic periods of muscle contraction; often secondary
4. Febrile: r/t high fevers, tonic-clonic
5. Jacksonian: one area in the brain → one part of the body → other parts
6. Psychomotor: LOC, no memory of the event; emotional outburst,
psychological disurbance
7. Status Epilepticus: seizures rapidly recur again and again with no recovery
between seizures.
SEIZURES: Focal

Simple partial: single brain area involving single muscle movement or sensory
changes

Complex partial: series complex sensory and motor changes

Sensory: Hallucinations, mental distortion, personality changes, LOC
Motor: involuntary urination, chewing motions, diarrhea
Generalized Seizure

DRUG CLASS INDICATION CI ADVERSE EFFECTS

Hydantoins Tonic-clonic; Allergy, CNS depression; liver toxicity,
(phenytoin) prevent status pregnancy, gingival hyperplasia,
epilepticus (SE), lactating, dermatologic reactions
Tx of seizures elder,
after neurosx impaired
Barbiturates Long-term tx of renal or liver CNS depression, sedation,
(phenobarbital) tonic-clonic hypnosis, anesthesia;
seizures (cortex) dependence and withdrawal
Benzodiazepines Severe; clonic- CNS depression, dependence
(Diazepam) tonic; SE and withdrawal
Succinimides DOC for Absence CNS depression, decreased GI
(ethosuximide) seizures effects, bone marrow
suppression
Generalized Seizure

NURSING PROCESS NURSING RESPONSIBILITIES

Contraindications, seizure characteristics, baseline status (PE,
ASSESSMENT
ECG), assess labs (renal, liver)
NURSING CNS: disturbed thought process, risk for injury
DIAGNOSIS Acute discomfort: GI, CNS, GU effects
Best therapeutic effect, limited A/E, understands the drug
PLANNING therapy
Proper administration, monitor labs, taper dose, comfort
INTERVENTION measures, health teaching, support and encouragement
Response to drug, A/E, effectiveness of teaching plan and
EVALUATION comfort measures
Focal Seizure
Partial Seizure

NURSING PROCESS NURSING RESPONSIBILITIES

Contraindications, seizure characteristics, baseline status (PE,
ASSESSMENT
EEG), assess labs (renal, liver)
CNS: disturbed thought process, risk for injury
NURSING
Acute pain: GI, CNS effects
DIAGNOSIS Risk for infection: bone marrow suppresion
Best therapeutic effect, limited A/E, understands the drug
PLANNING therapy
Proper administration, prevent S/E, taper dose, comfort
INTERVENTION measures, health teaching, support and encouragement
Response to drug, A/E, effectiveness of teaching plan and
EVALUATION comfort measures
ANTIPARKINSONISM
ANTIPARKINSONISM
PARKINSON’S DISEASE

debilitating disease: degeneration of

dopamine-producing cells in the substantia nigra
→ progressive loss of coordination and function

Substantia nigra: a part of the brain rich in dopamine and dopamine

receptors; site of degenerating neurons in Parkinson disease

Parkinsonism: Parkinson disease–like extrapyramidal symptoms that are

adverse effects associated with particular drugs or brain injuries
PARKINSON’S DISEASE

Rhythmic tremors (1st)

→ rigidity or weakness

Bradykinesia: postural
instability, extreme slowness or
sluggishness, difficulties in
performing intentional
movements

Shuffling gait: hallmark

Mask-like face: CN defects
Dysphagia: aspiration
pneumonia
Dopaminergic Agents: Levodopa

MOA INDICATION
Increase ➢ Relief of s/sx of
Dopamine levels in idiopathic
the substantia Parkinson
nigra; stimulate disease
dopamine
receptors; restore
balance between
inhibitory and
stimulating
neurons
Dopaminergic Agents: Levodopa

MOA INDICATION CI / CAUTION A/E

Increase ➢ Relief of s/sx of ➢ Allergy CNS effects:
Dopamine levels in idiopathic ➢ Pregnancy, anxiety,
the substantia Parkinson lactating nervousness,
headache,
nigra; stimulate disease ➢ Suspicious skin
malaise, fatigue,
dopamine lesions
confusion,
receptors; restore (melanoma) mental changes,
balance between blurred vision,
inhibitory and ataxia, twitching
stimulating GI, CVS
neurons
Dopaminergic
NURSING
NURSING RESPONSIBILITIES
PROCESS
Contraindications, baseline status
ASSESSMENT (PE), assess labs (renal, liver)
r/t CNS effects: disturbed thought
NURSING process, risk for injury
DIAGNOSIS Dopaminergic: urinary retention,
constipation
Best therapeutic effect, limited A/E,
PLANNING understands the drug therapy
Proper administration, monitor labs,
taper dose, comfort measures,
INTERVENTION
health teaching, support and
encouragement
Response to drug, A/E, effectiveness
EVALUATION of teaching plan and comfort
measures
MUSCLE RELAXANT
Neuromuscular Abnormalities

Muscle Spasm

Muscle Spasticity
Centrally Acting Skeletal Muscle Relaxants

MOA INDICATION
interfere ➢ relief of
with the reflexes discomfort
that are causing associated with
the muscle spasm; acute, painful
spasmolytics musculoskeletal
conditions as an
adjunct to rest,
physical therapy,
and other
measures
Centrally Acting Skeletal Muscle Relaxants

MOA INDICATION CI / CAUTION A/E

interfere ➢ relief of ➢ Allergy CNS depression
with the reflexes discomfort GI disturbances
that are causing associated with Caution use: Hypotension
Arrhythmias
the muscle spasm; acute, painful ➢ Hx of Epilepsy
Urinary
spasmolytics musculoskeletal ➢ Cardiac
frequency/urgen
conditions as an dysfunction cy, enuresis
adjunct to rest, ➢ Hepatic/renal
physical therapy, dysfunction
and other
measures
Centrally Acting

NURSING
NURSING RESPONSIBILITIES
PROCESS
Contraindications, baseline status (PE)
ASSESSMENT

NURSING r/t CNS effects: disturbed thought

DIAGNOSIS process, risk for injury, acute pain
Best therapeutic effect, limited A/E,
PLANNING understands the drug therapy
Proper administration, monitor labs,
INTERVENTION taper dose, comfort measures, health
teaching, support and encouragement
Response to drug, A/E, effectiveness of
EVALUATION teaching plan and comfort measures
Direct-Acting Skeletal Muscle Relaxants

MOA INDICATION
directly affects ➢ reduces painful
peripheral muscle and disabling
contraction spasticity

acts within skeletal

muscle fibers,
interfering with the
release of calcium
from the muscle
tubules
Direct-Acting Skeletal Muscle Relaxants

MOA INDICATION CI / CAUTION A/E

directly affects ➢ reduces painful ➢ Allergy CNS depression
peripheral muscle and disabling ➢ Active liver GI disturbances
contraction spasticity disease Hepatocellular
damage*
➢ Pregnancy,
acts within skeletal lactating
Botulinum
muscle fibers, toxins:
interfering with the Caution use: anaphylactic
release of calcium ➢ Women over reactions
from the muscle 35y.o.*
tubules ➢ Liver, cardiac
disease
Direct-Acting

NURSING
NURSING RESPONSIBILITIES
PROCESS
Contraindications, baseline status (PE)
ASSESSMENT

NURSING r/t CNS effects: disturbed thought

DIAGNOSIS process, risk for injury, acute pain
Best therapeutic effect, limited A/E,
PLANNING understands the drug therapy
Proper administration, monitor labs,
taper dose, comfort measures, health
INTERVENTION
teaching, support and
encouragement
Response to drug, A/E, effectiveness of
EVALUATION teaching plan and comfort measures
PAIN & MIGRAINE
PAIN & MIGRAINE
PAIN & MIGRAINE
PAIN

unpleasant sensation and emotional experience → SUBJECTIVE

Pain occurs whenever tissues are damaged.→ cell injury releases many
chemicals (kinins and prostaglandins) → stimulate specific sensory nerves.

ACUTE PAIN: occurs in response to recent tissue damage or injury

CHRONIC PAIN: constant or intermittent pain that keeps occurring long past
the time the injured area would be expected to heal
 PAIN ASSESSMENT

O - onset
L - location
P – precipitating/provoking
D - duration
Q - quality
C - characteristic
R - relieving
A – associating/aggravating
S - scale
R - relieving
T - timing
T - timing
S – scale (0-10)
 PAIN ASSESSMENT

O - onset
L - location
P – precipitating/provoking
D - duration
Q - quality
C - characteristic
R - relieving
A – associating/aggravating
S - scale
R - relieving
T - timing
T - timing
S – scale (0-10)
PAIN MANAGEMENT

Nonpharmacological: warmth, massage, positioning,

acupuncture, meditation

Pharmacological: NSAIDs, Acetaminophen, Narcotics (Opioids)

GOAL: Achieve maximum pain relief

Opioid receptors: peptides, endorphins, enkephalins

*endorphins & enkephalins: modulate pain information coming into the

brain; endorphins are released during stress to block pain sensation
Narcotic Agonist

MOA INDICATION
react with the ➢ relief of severe
opioid acute or chronic
receptors pain,
throughout the preoperative
body to cause medication,
analgesia, sedation, analgesia during
or euphoria anesthesia

Controlled
substance
Narcotic Agonist

MOA INDICATION CI / CAUTION A/E

react with the ➢ relief of severe ➢ Allergy Respiratory
opioid acute or chronic ➢ Diarrhea by toxic depression:
receptors pain, poisons apnea, cardiac
arrest, shock
throughout the preoperative ➢ After biliary
Orthostatic
body to cause medication, surgery or
hypotension
analgesia, sedation, analgesia during surgical GI effects
or euphoria anesthesia anastomoses CNS:
➢ Pregnancy, lightheadedness,
Controlled lactating dizziness, fear,
substance anxiety
Narcotic Agonist-Antagonist

MOA INDICATION
act at specific ➢ relief of mod. To
opioid receptor severe pain
sites in the ➢ adjunct to gen.
CNS to produce anesthesia
analgesia, sedation, ➢ pain relief during
euphoria, and labor and
hallucinations delivery
Narcotic Agonist-Antagonist

MOA INDICATION CI / CAUTION A/E

act at specific ➢ relief of mod. To ➢ Allergy Respiratory
opioid receptor severe pain depression:
sites in the ➢ adjunct to gen. Caution: apnea,
suppression of
CNS to produce anesthesia ➢ Physical
cough reflex
analgesia, sedation, ➢ pain relief during dependence
CTZ stimulation:
euphoria, and labor and ➢ COPD, respi. N/V, constipation
hallucinations delivery Dysfunction CNS: anxiety,
lightheadedness,
dizziness
Narcotics Agonist(-Antagonist)
NURSING
NURSING RESPONSIBILITIES
PROCESS
Contraindications, pain assessment,
ASSESSMENT general PE, assess labs (renal, liver)
CNS: Disturbed sensory perception,
NURSING
risk for injury; GI: Constipation;
DIAGNOSIS Impaired gas exchange: respi. dep.
Best therapeutic effect, limited A/E,
PLANNING understands the drug therapy
Proper administration, monitor
respiratory status, comfort
INTERVENTION
measures, health teaching, support
and encouragement
Response to drug, A/E, effectiveness
EVALUATION of teaching plan and comfort
measures
Narcotic Antagonist

MOA INDICATION
block opioid ➢ reversal of A/E
receptors and ➢ Tx of narcotic
reverse the effects overdose
of opioids:
respiratory
depression,
sedation,
psychotomimetic
effects,
and hypotension
Narcotic Antagonist

MOA INDICATION CI / CAUTION A/E

block opioid ➢ reversal of A/E ➢ Allergy Acute narcotic
receptors and ➢ Tx of narcotic ➢ Pregnant, abstinence
reverse the effects overdose lactating syndrome: N/V,
sweating,
of opioids:
tachycardia,
respiratory
HTN, tremors,
depression, anxiety
sedation,
psychotomimetic
effects,
and hypotension
Narcotics Antagonist

NURSING PROCESS NURSING RESPONSIBILITIES

Contraindications, pain assessment, neuro PE, ECG
ASSESSMENT

CV: acute pain, decreased cardiac output

NURSING DIAGNOSIS CNS: risk for injury
Best therapeutic effect, limited A/E, understands the drug
PLANNING therapy
Proper administration, continuous monitoring, comfort
INTERVENTION measures, health teaching, support and encouragement
Response to drug, A/E, effectiveness of teaching plan and
EVALUATION comfort measures
MIGRAINE HEADACHE

debilitating disease: degeneration of

dopamine-producing cells in the substantia nigra
→ progressive loss of coordination and function

Substantia nigra: a part of the brain rich in dopamine and dopamine

receptors; site of degenerating neurons in Parkinson disease

Parkinsonism: Parkinson disease–like extrapyramidal symptoms that are

adverse effects associated with particular drugs or brain injuries
 ANTI-MIGRAINE

ERGOT DERIVATIVES:
Block alpha-adrenergic and
serotonin receptor sites in the
brain → vasoconstriction →
decrease cranial artery pulsation
→ decrease in hyperperfusion of
the basilar artery bed

CI: Allergy
A/E: CNS – numbness, tingling,
muscle pain;
CV – pulseless, weakness, chest
pain, MI
GI: CTZ stimulation
 ANTI-MIGRAINE

TRIPTANS:
Binds to SSR sites →
vasoconstriction → pain relief

CI: Allergy, pregnancy, lactating

elderly, hepatic/renal dysfunction

A/E: CNS – numbness, tingling,

burning sensation. dizziness
CV – BP changes, chest tightness
GI: dysphagia, discomfort
Ergot Derivatives & Triptans

NURSING PROCESS NURSING RESPONSIBILITIES

Contraindications, physical examination, monitor lab results
ASSESSMENT

CV: acute pain, decreased cardiac output

NURSING DIAGNOSIS CNS: risk for injury, disturbed sensory perception
Best therapeutic effect, limited A/E, understands the drug
PLANNING therapy
Proper administration, continuous monitoring, comfort
INTERVENTION measures, health teaching, support and encouragement
Response to drug, A/E, effectiveness of teaching plan and
EVALUATION comfort measures
PAIN & MIGRAINE
AUTONOMIC
NERVOUS SYSTEM
ADRENERGIC | CHOLINERGIC (Agonist, Antagonist)
ANS
ANS
ANS
SYMPATHETIC NS

referred to as the “fight-or-flight” system or the

system responsible for preparing the body to respond to stress

Stress can be
either internal, such as cell injury or death, or external, such as a perceived or
learned reaction to various external situations or stimuli.
PARASYMPATHETIC NS

craniosacral system because the CNS neurons that originate

parasympathetic impulses are found in the cranium (one of the
most important being the vagus or 10th cranial nerve) and in the
sacral area of the spinal cord

The terms “cholinergic,” “muscarinic,” and “vagal” are often used

interchangeably when discussing the parasympathetic system
PARASYMPATHETIC NS

Parasympathetic system stimulation results in the following actions:

● Increased motility and secretions in the GI tract to promote digestion and

absorption of nutrients

● Decreased heart rate and contractility to conserve energy and provide rest
for the heart
● Constriction of the bronchi, with increased secretions

● Relaxation of the GI and urinary bladder sphincters, allowing evacuation of

waste products

● Pupillary constriction, which decreases the light entering the eye and
decreases stimulation of the retina
Cholinergic Receptors

MUSCARINIC RECEPTORSS
stimulated by muscarine; found in visceral effector organs, such as
the GI tract, bladder, and heart, in sweat glands, and in some vascular smooth
muscle.

Stimulation: pupil constriction, increased GI motility and secretions (including

saliva), increased urinary bladder contraction, and a slowing of the heart rate.

NICOTINIC RECEPTORS
CNS, the adrenal medulla, the autonomic ganglia, and the neuromuscular
junction

Stimulation: skeletal muscle contractions, autonomic responses such as

signs and symptoms of a stress reaction, and release of norepinephrine and
epinephrine from the adrenal medulla.
ANS
ADRENERGIC AGONIST
ADRENERGIC AGONIST

adrenergic agonist is also called a sympathomimetic drug because it

mimics the effects of the sympathetic nervous system (SNS)

Adrenergic agonists also can affect both the alpha- and beta-receptors, or
they can act at specific receptor sites
Adrenergic Agonist

MOA INDICATION
mediated by the ➢ Hypotensive or
adrenergic shock
receptors in target ➢ Bronchospasm
organ ➢ Asthma
Adrenergic Agonist

MOA INDICATION CI / CAUTION A/E

mediated by the ➢ Hypotensive or ➢ Allergy CV: Arrythmias,
adrenergic shock ➢ Ventricular HPN,
receptors in target ➢ Bronchospasm fibrillation palpitations,
angina, dyspnea
organ ➢ Asthma ➢ Hypovolemia
GI
➢ PVD
Hypokalemia –
➢ Pregnancy, aldosterone
lactation release d/t SNS
stimulation
(muscle cramps)
Adrenergic Agonist
NURSING
NURSING RESPONSIBILITIES
PROCESS
Contraindications, V.fib,
ASSESSMENT hypovolemia

NURSING CV: Decreased cardiac output;

DIAGNOSIS Ineffective tissue perfusion
Best therapeutic effect, limited A/E,
PLANNING understands the drug therapy
Proper administration, monitor
respiratory status, comfort
INTERVENTION
measures, health teaching, support
and encouragement
Response to drug, A/E, effectiveness
EVALUATION of teaching plan and comfort
measures
Alpha-Specific Adrenergic Agonist

MOA INDICATION
Stimulator of ➢ Shock, shock-
alpha-receptors like states
➢ Maintain BP
Alpha-Specific Adrenergic Agonist

MOA INDICATION CI / CAUTION A/E

Stimulator of ➢ Shock, shock-like ➢ Allergy CV: Arrythmias,
alpha-receptors states ➢ Ventricular HPN,
➢ Maintain BP fibrillation palpitations,
angina, dyspnea
➢ Hypovolemia
GI
➢ PVD
Hypokalemia –
➢ Pregnancy, aldosterone
lactation release d/t SNS
stimulation
(muscle cramps)
Alpha-Specific Adrenergic Agonist
NURSING
NURSING RESPONSIBILITIES
PROCESS
Contraindications, V.fib,
ASSESSMENT hypovolemia

NURSING CV: Decreased cardiac output;

DIAGNOSIS Ineffective tissue perfusion
Best therapeutic effect, limited A/E,
PLANNING understands the drug therapy
Proper administration, monitor
respiratory status, comfort
INTERVENTION
measures, health teaching, support
and encouragement
Response to drug, A/E, effectiveness
EVALUATION of teaching plan and comfort
measures
Beta-Specific Adrenergic Agonist

MOA INDICATION
Stimulator of beta- ➢ Bronchospasm
adrenergic ➢ Shock
receptors
Beta-Specific Adrenergic Agonist

MOA INDICATION CI / CAUTION A/E

Stimulator of beta- ➢ Bronchospasm ➢ Allergy CNS: restless,
adrenergic ➢ Shock ➢ Pulmonary HTN anxiety, fear,
receptors ➢ Eclampsia tremor, fatigue,
headache
CV: tachy, MI,
angina,
DOB
GI upset
Hypokalemia
Beta-Specific Adrenergic Agonist
NURSING
NURSING RESPONSIBILITIES
PROCESS
Contraindications, PE, CV status,
ASSESSMENT urine output, lab test
CV: Decreased cardiac output;
NURSING
Ineffective tissue perfusion, acute
DIAGNOSIS pain
Best therapeutic effect, limited A/E,
PLANNING understands the drug therapy
Proper administration, monitor
respiratory status, comfort measures,
INTERVENTION
health teaching, support and
encouragement
Response to drug, A/E, effectiveness
EVALUATION of teaching plan and comfort
measures
ADRENERGIC ANTAGONIST
ADRENERGIC ANTAGONIST

also called sympatholytic drugs because they lyse, or block, the effects of the
sympathetic nervous system (SNS).

By occupying the adrenergic receptor site, they prevent

norepinephrine released from the nerve terminal or from the adrenal
medulla
from activating the receptor, thus blocking the SNS effects

adrenergic receptor–site
specificity
ADRENERGIC ANTAGONIST

NONSELECTIVE
- Alpha-adrenergic Blockers: phentolamine
- Beta-adrenergic Blockers: propanolol

SELECTIVE
- Alpha1-Selective Adrenergic Blockers: tamsulosin, doxazosin
- Beta1-Selective Adrenergic Blockers: atenolol, metoprolol, esmolol
NONSELECTIVE ADRENERGIC ANTAGONIST
SELECTIVE ADRENERGIC ANTAGONIST
ANS
CHOLINERGIC AGENTS
CHOLINERGIC

act at the same site as the neurotransmitter

acetylcholine (ACh) and increase the activity of the ACh receptor
sites throughout the body

their stimulation produces a response similar to what is seen

when the parasympathetic system is activated
DIRECT INDIRECT
INDIRECT
ANTICHOLINERGICS
ANTICHOLINERGIC

drug that opposes the effects of acetylcholine at

acetylcholine receptor sites; they are also called
parasympatholytic agents
ANTICHOLINERGIC
ANS
- END -