2. 2
REVIEW Let us test your recall. Try and answer the following.
__ __ __ __ __ __ = Basic building block of the nervous system.
__ __ __ __ __ __ __ __ __ = Thin, bushy-like structures that receive information from outside the
neuron.
__ __ __ __ = It transmits signal from the cell to a terminal.
__ __ __ __ __ __ __ = it is the space between neurons.
__ __ __ __ __ __ __ __ __ __ __ __ __ __ __ __ __ = It contributes to the regulation of attention,
arousal and memory.
How well did your brain retained the information you read in the
Bluebook? Were you able to guess the words being described by the
aforementioned statements?
NEURON
DENDRITES
NEUROTRANSMITTERS
SYNAPSE
AXON
4. PAIN ACUTE vs CHRONIC PAIN
▫ Acute occurs quickly, is short in
duration, usually can be resolved
▫ Chronic longer lasting, usually at
least 3 months in duration,
possibly will not go away
▫ PAIN IS THE SIXTH (6th) VITAL
SIGN
.
4
5. CAUSES OF PAIN /
DISCOMFORT
▫ Trauma
▫ Tissue damage
▫ Pressure on tissue and nerves
▫ Inflammation of tissues and
nerves
5
7. MECHANISMS
TO CONTROL
PAIN
▫ Massage
▫ Position change
▫ Biofeedback
▫ Exercise
▫ Non-opoid analgesics
▫ Antidepressants
▫ Opioid analgesics
▫ Steroids
7
8. Opioid
Analgesics
▫ Pain relievers that contain opium,
derived from the opium poppy or
chemically related to opium
▫ Very strong pain relievers
▫ Very addicting
8
10. Agonists ▫ Bind to an Opioid receptor in the
brain
▫ Cause an analgesic response
(reduction of pain sensation)
10
11. Opioid
Analgesics
Indications
▫ Main use to alleviate moderate to
severe pain
▫ Often given with adjuvant drugs to
assist primary drugs with pain
relief
▫ Muscle relaxant
▫ Sedative
▫ Alternate with non-narcotic
analgesic
11
13. Opioid
Analgesics
Contraindications
▫ Known drug allergy
▫ Severe asthma
▫ Use with extreme caution if
▫ Respiratory insufficiency
▫ Elevated intracranial pressure
▫ Morbid obesity
▫ Sleep apnea
▫ Paralytic ileus
13
14. Opioid
Analgesics
Adverse
Effects
▫ Euphoria
▫ CNS depression
▫ Leads to respiratory depression
▫ Most serious adverse effect
▫ Nausea and vomiting
▫ Urinary retention
▫ Diaphoresis and flushing
▫ Pupil constriction (miosis)
▫ Constipation
▫ Itching
14
15. Opioids
Opioid
Tolerance
▫ A common physiologic result of
chronic Opioid treatment
▫ Result larger dose is required to
maintain the same level of
analgesia
15
16. Opioids
Physical
Dependence
▫ Physiologic adaptation of the body
to the presence of an Opioid
▫ Opioid tolerance and physical
dependence are expected with
long-term Opioid treatment and
should not be confused with
psychologic dependence
(addiction)
16
17. Opioids
Psychological
Dependence
▫ A pattern of compulsive drug use
characterized by a continued
craving for an Opioid and the
need to use the Opioid for effects
other than pain relief
17
18. Opioids ▫ Misunderstanding of these terms
leads to ineffective pain
management and contributes to
the problem of under treatment
▫ Physical dependence is seen
when the Opioid is abruptly
discontinued or when an Opioid
antagonist is administered
▫ Opioid withdrawal/Opioid
abstinence syndrome
18
19. Antagonists ▫ Reverse the effects of these drugs
on pain receptors
▫ Bind to a pain receptor and exert
no response
▫ Also known as competitive
antagonists
19
20. Toxicity and
Management
of Overdose
ANALEPTICS
▫ naloxone (Narcan)
▫ naltrexone (Revia)
▫ These drugs bind to opiate receptors and
prevent a response
▫ Used for complete or partial reversal of
Opioid-induced respiratory depression
▫ Regardless of withdrawal symptoms, when a
patient experiences severe respiratory
depression, an Opioid antagonist should be
given.
20
21. 21
NURSING CONSIDERATIONS WHEN GIVING
NALOXONE
Administer medication very slowly
Anticipate patient response to treatment
Monitor patient very closely
Vital signs, respiratory rate, pulse ox
Continue to monitor closely
½ Life of narcan 60- 90 minutes
½ Life of morphine 2 - 4 hours
22. 22
Toxicity and Management of Overdose
Symptoms of Abstinence Syndrome
Pulmonary edema
Withdrawal symptoms
Nausea
Vomiting
Agitation
Anxiety
Confusion
Pain
23. 23
Opioid Analgesics
Nursing Implications
Oral forms should be taken with food to minimize
gastric upset
Ensure safety measures, such as keeping side rails
up, to prevent injury
Withhold dose and contact physician if there is a
decline in the patients condition or if vital signs are
abnormal, especially if respiratory rate is less than
10 to 12 breaths/min
24. 24
Opioid Analgesics Nursing Implications (contd)
o Check dosages carefully
o Follow proper administration guidelines for
IM
injections, including site rotation
o Follow proper guidelines for IV
administration,
including dilution and rate of administration
25. 25
Opioid Analgesics Nursing Implications (contd)
Constipation is a common adverse effect and may
be prevented with adequate fluid and fiber intake
Instruct patients to follow directions for
administration carefully and to keep a record of
their pain experience and response to treatments
Patients should be instructed to change positions
slowly to prevent possible orthostatic hypotension
26. 26
Monitor for Therapeutic Effects
Decreased complaints of pain
Decreased severity of pain
Increased periods of comfort
Improved activities of daily living, appetite, and sense of
well-being
Decreased fever (acetaminophen)
27. 27
Monitor for Adverse Effects
Contact physician immediately if vital signs change,
patients condition declines, or pain continues
Respiratory depression may be manifested by
respiratory rate of less than 10 breaths/min,
dyspnea, diminished breath sounds, or shallow
breathing
28. 28
Prototype Morphine
Opioid agonist
Schedule II narcotic
Pregnancy Category C
Given orally or parenterally
Half life 2 4 hours
Used for severe pain (chronic or acute)
29. Morphine
▫ Indications
Relief of severe/acute/chronic
pain, analgesia during labor.
▫ Morphine is the drug of choice for
pain due to Myocardial Infarction,
dyspnea from pulmonary edema
not resulting from chemical
respiratory irritant.
29
30. Morphine ▫ Contraindications
▫ Severe respiratory depression,
acute/severe asthma, severe
hepatic/renal impairment. Used
with extreme caution in COPD,
hypoxia, head injury, increased
intracranial pressure
▫
30
31. Morphine Drug-Drug Interactions
▫ Use with EXTREME CAUTION in
patients taking MAOIs
▫ Increased CNS depression and
hypotension with alcohol, sedatives,
hypnotics, barbiturates, tricyclic
antidepressants, antihistamines
▫ May INCREASE the anticoagulant
effect of Warfarin (Coumadin)
31
32. ADVERSE REACTIONS TO NARCOTIC PAIN
MEDICATION
▫ CNS
▫ Impaired judgment
▫ Drowsiness (decrease in LOC)
▫ Decrease in respiratory effort
32
37. ROUTES OF ADMINISTRATION FOR
NARCOTIC ANALGESIA
▫ IV
▫ PO
▫ IM
▫ IN (intra-nasal)
▫ SC (SQ)
▫ TRANSDERMAL
▫ EPIDURAL
▫ RECTAL 37
38. ROUTES OF ADMINISTRATION FOR
NARCOTIC ANALGESIA
▫ INTRAVENOUS
▫ Effective within 5 10 min. Of
administration
▫ Most common route (in hospitalized
patients)
▫ Frequently administered as patient
controlled analgesia (PCA)
38
39. 39
PCA PATIENT CONTROLLED ANALGESIA
▫ DOUBLE LOCK SYSTEM
▫ TIME
▫ AMOUNT
▫ NURSE MUST DOCUMENT
▫ AMOUNT USED
▫ EFFECTIVENESS
▫ VITAL SIGNS INCLUDING RESPIRATIONS
▫ ANY UNTOWARD EFFECTS
▫ TEACH FAMILY ABOUT USE AND ABUSE
40. 40
EPIDURAL PAIN MANAGEMENT
• Catheter is placed into the epidural space to
inject a narcotic or anesthetic drug
• Obstetrics
• Surgical procedures
• Pain management
• Catheter may be left in for follow up
injections by physician or patient controlled
analgesia
41. 41
TRANSDERMAL PATCH
SEVERE PAIN CHRONIC PAIN
FENTANYL PATCH (DURAGESIC) MOST COMMON
Slower onset but more consistent pain relief
Patch usually changed every 72h
Treated just as any other narcotic must account
for every patch
Patch must be dated, timed and signed when
placed
Old patch must be removed when the new one is
placed
42. 42
Nursing Considerations when giving Opioid
Analgesic medication
▫ Assess effectiveness of medication
▫ Use the 0 10 scale to measure intensity of pain
▫ Assess for adverse effects
▫ Assess rate, depth, and rhythm of RESPIRATIONS
▫ Provide for patient safety
44. Overview
▫ This kind of drug is a group of chemically dissimilar
agents that have antipyretic, analgesic and anti-
inflammatory effects.
▫ The structure of this kind of drug differs from that of
steroidal anti-inflammatory drugs.
▫ Nonsteroidal anti-inflammatory drugs NSAIDs
45. History
▫ In ancient Egypt & Greece, dried leaves of myrtle, the bark of
willow & poplar tree
▫ In England, active component from willow bark was identified
as salicin, which is metabolized to salicylate in 1763.
▫ In Germany, salicylic acid was synthesized in 1860.
▫ In 1875, acetylsalicylic acid was synthesized.
46. Common pharmacological effects
These drugs show the same pharmacological effects
▫ -- antipyretic effect
▫ -- analgesic effect
▫ -- anti-inflammatory effect
47. Antipyretic
Effects
▫ "normal" temperature: slightly
affected
▫ "elevated" temperature: reduced
▫ The higher temperature, the more
potent
▫ Mechanisms of Antipyretic Action
Blocks pyrogen-induced
prostaglandin production in
thermoregulatory center (CNS)
49. Analgesic
Effects
Effective to mild to moderate pain
0.5g of aspirin is a weak or mild analgesic
that is effective in short, intermittent types
of pain as encountered in neuralgia, myalgia,
toothache.
50. Analgesic Effects
▫ Pain may arise from:
Musculature, dental work , vascular , postpartum
conditions, arthritis , bursitis
▫ Sites of action:
peripherally -- sites of inflammation
subcortical sites
52. Anti-inflammatory Effects
▫ NSAIDs only inhibit the symptoms of
inflammation
▫ But they neither arrest the progress of
the disease nor do they induce
remission
54. Mechanism of action
The principal pharmacological effect of NSAIDs is due
to their ability to inhibit prostaglandin synthesis by
blocking the cyclooxygenase （COX） activity of
both COX-1 and COX-2.
NSAIDs----- acetylation of COX
(reversible or irreversible)
58. Pharmacokinetics
▫ Rapidly absorbed: stomach and upper small
intestine
▫ Distribution：through the body
rapidly hydrolyzed --------- acetic acid +
salicylate, catalyzed by tissue/blood
esterases
59. Elimination-----Pharmacokinetics
▫ metabolite in liver
dose ＜1g/day：one-order elimination T1/2: 3--5 hrs
dose ＞1g/day：zero-order elimination
＞4g/day T1/2:
▫ Excretion: kidney, influenced by pH of urine
60. Pharmacodynamics
1. Analgesic Effects (300-600mg)
2. Antipyretic Effects (300-600mg)
3. Anti-inflammatory Effects (3-6g)
do not influence the progress of disease
4. Effects on Platelets (40-100mg)
Reduced platelet aggregation
reduces thromboxane A2 (TXA2) formation
61. Low doses 40-100mg/day
▫ Platelets
▫ No nuclei
▫ No new COX1
produce
▫ TXA2 production ↓
▫ Lifetime:
8-11 days
▫ Endothelial cell
▫ Has nuclei
▫ New COX1 produce
62. Pharmacodynamics
5. Other effects
▫ Immune inhibition
▫ Effect on metabolism of
connective tissue
▫ Effects on metabolism of
glucose, fat, protein ----
catabolism ↑
▫ ACTH release ↑
63. Clinical Uses
1. Commonly used for management of mild to moderate pain
(300-600mg)
2. Combination agents (cold)
3. Used for reducing fever (300-600mg)
4. Useful in treatment of:
(high doses 3-6g) T1/2 > 12 hours
0 rheumatic fever
0 rheumatoid arthritis
0 other inflammatory joint diseases
64. Clinical Uses
5. Antiplatelet: (low doses) 40-100mg
reduce incidence of transient ischemic
attacks (prophylaxis)
reduce incidence of unstable angina
(prophylaxis)
may reduce incidents of coronary artery
thrombosis
65. Clinical
Uses
6. Hypertension in pregnancy :
(low doses) 60-100mg
TXA2↓
7. Local indication
GI inflammation : 5-amido-
salicylic acid
66. SIDE
EFFECTS
1. CNS: excitation----inhibition
salicylic acid reaction:
Headaches; confusion;
hallucinations; tremors; vertigo;
behavior disturbance
2. GI effects: direct stimulation
PGE2 & PGI2 ↓
Esophagitis; gastric
ulcerations; GI hemorrhage
67. SIDE
EFFECTS
3. Liver & renal toxicity
Dose dependence toxicity
Reye's syndrome
a potentially fatal disease that
causes numerous detrimental
effects to many organs, especially
the brain and liver.
The disease causes hepatitis with
jaundice and encephalopathy
69. Acetaminophen ▫ Rapidly absorbed from GI
▫ Phenacetin is largely converted to
Acetaminophen
▫ Similar antipyretic, analgesia to aspirin
▫ Weak anti-inflammatory properties
▫ used to reduce fever and pains (a major
ingredient in numerous cold and flu
medications) (choice for child)
▫ used appropriately, side effects are rare
70. Indomethacin
▫ More potent than aspirin
▫ As an anti-inflammatory
agent
▫ More adverse reaction
Ibuprofen
▫ Fewer adverse reaction
▫ Brufen；Benzeneacetic
acid； Fenbid； Emodin；
Motrin
71. Phenylbutazone ▫ Powerful anti-inflammatory effects
▫ Weak analgesic & antipyretic
activities
▫ Promote excretion of uric acid
▫ Used for acute gout, rheumatic &
rheumatoid arthritis
▫ More adverse reaction
▫ Can induce activities of drug
metabolize-E
▫ Can displace other drugs from
plasma proteins
75. Skeletal Muscle Relaxants (SMRs)
• Drugs that act peripherally at neuromuscular
junction/muscle fiber or centrally in the cerebrospinal axis
to reduce muscle tone or cause paralysis
• A muscle relaxants is a drug that affects skeletal muscle
function and decreases the muscle tone.
76. Common Symptoms/Conditions in which SMRs are used
• In conjunction with GA:
– Facilitate intubation of the trachea
– Facilitate mechanical ventilation
– Optimized surgical working conditions
• In Muscle spasm: a sudden involuntary contractionof one or more muscle
groups and is usually an acute condition associated with muscle strain
(partial tear of a muscle) or sprain
– Musculoskeletal Injury or Sports Injury
– Low Back pain or neck pain
– Fibromyalgia, tension headaches
• It may be used to improve symptoms such as muscle spasms, pain, and
hyperreflexia.
77. History:
From Fun
hunting in
Jungles to
Operation
theatre
Curare: The arrow poison
Source: Chondrodendrone tomentosum
andStrychnos toxifera
Derived from: "ourare“ meaning arrow poison in
South American Indian
Tubocurarine name: Because of packing in
“hollow bamboo tubes”
81. Classification: Peripherally acting SMRs
1. Neuromuscular Junction (NMJ)Blockers :
A. Nondepolarizing (Competitive) blockers:
a. Long acting: d-Tubocurarine, Pancuronium, Doxacurium,
Pipecuronium, Gallamine and Metocurine
b. Intermediate acting: Vecuronium, Atracurium, Cisatracurium,
Rocuronium,
Rapacuronium
c. Short acting: Mivacurium
A. Depolarizing blockers: Succinylcholine (suxamethonium),
Decamethonium
B. Botulinum Toxin
1. Directly acting: Dantrolene
82. Nondepolarizing (Competitive) blockers
• Nondepolarizing (Competitive) Blockers having no intrinsic activity
(antagonist)
• These are of 3 types based on their activity:
a. Long acting: d-Tubocurarine, Pancuronium, Doxacurium,
Pipecuronium, Gallamine and Metocurine
b. Intermediate acting: Vecuronium, Atracurium,
Cisatracurium, Rocuronium, Rapacuronium
c. Short acting: Mivacurium
83. Nondepolarizing (Competitive) blockers
Pharmacological actions:
• Skeletal muscles: Intravenous injection of nondepolarizing
blockers rapidly produces muscle weakness followed by flaccid
paralysis.
• Autonomic ganglia: produce some degree of ganglionic blockade
• Histamine release: d-TC releases histamine from mast cells.
Histamine release contributes to the hypotension produced by d-
TC. Flushing, bronchospasm and increased respiratory secretions are
other effects.
84. Pharmacological actions (Cont.,)
• Cardiovascular system: d-Tubocurarine produces significant fall in
BP.This is due to
– Ganglionic blockade
– Histamine release and
– Reduced venous return
• Gastrointestinal tract: The ganglion blocking activity of
competitive blockers may enhance postoperative paralytic ileus after
abdominal operations.
• Central nervous system: All neuromuscular blockers are quaternary
compounds— do not cross blood-brain barrier.
85. Nondepolarizing blockers - Individual compounds
• d-Tubocurarine: 1st agent to undergo clinical investigation
– 1-2 hr. duration of action
– Histamine releaser (Bronchospasm, hypotension)
– Blocks autonomic ganglia (Hypotension)
• Clinical Use:
– Not clinical used do to its histaminic effects.
– Long duration of action(60 to 120 mins) and CVS effects restricted
its use
86. Nondepolarizing blockers - Individual compounds
• Pancuronium:
– It is a synthetic steroidal compound, ~5 times more potent
than d-TC. use is now restricted and longer acting
– Because of longer duration of action, needing reversal, its
to prolonged operations, especially neurosurgery.
▫
• Pipecuronium:
▫ – Muscle relaxant with a slow onset and long
duration of action; steroidal in nature;
recommended for prolonged surgeries.
87. Nondepolarizing blockers - Individual compounds
• Vecuronium:
– It is a most commonly used muscle relaxant for routine surgery and
in intensive care units..
• Atracurium:
– Four times less potent than pancuronium and shorter acting.
• Rocuronium:
– Muscle relaxant with a rapid onset and intermediate duration of
action which can be used as alternative to SCh for tracheal
intubation without the disadvantages of depolarizing block and
cardiovascular changes.
88. Depolarizing Blockers - Succinylcholine
• Succinylcholine have affinity and sub-maximalintrinsic activity at Nm
receptor.
• It acts on sodium channels, open them and causes initial twitching
and fasciculation.
• It does not dissociate rapidly from the receptors resulting in
prolonged depolarization and inactivation of Na+ channels.
90. Advantages of Succinylcholine
• Most commonly used for Tracheal intubation
• Rapid onset (1-2 min)
• Good intubation conditions – relax jaw, separated vocal
chords with immobility, no diaphragmatic movements
• Short duration of action (5-10 minutes)
• Dose 1-1.5mg/kg
• Used as continuous infusion occasionally
91. Side effects of Succinylcholine
• Cardiovascular: unpredictable BP, heart rate and arrhythmias
• Fasciculation
• Muscle pain
• Increased intraocular pressure
• Increased intracranial pressure
• Hyperkalemia: k+ efflux from muscles, life threatening in Cardiac
Heart Failure, patient with diuretics etc.
• Malignant hyperthermia
92. What is Malignant hyperthermia
Rare genetically determined reaction to susceptible persons having
abnormal RyR receptor Ca+ channel
Caused by Halothane and manifests as high temperature due to
persistent muscle contraction
Increased intracellular Ca+
Succinylcholine accentuates this condition
Treatment:
Rapid external cooling – ice pack
Bicarbonate infusion
100% oxygen inhalation
Injection of dantrolene: Direct acting muscle relaxant
93. Indication of Neuro Muscular Junction Blockers
• Adjuvant to General anesthesia
• Assisted ventilation
• Convulsion and trauma from
electroconvulsive therapy
• Status epilepticus
Vocal cord
94. Directly acting relaxants - Dantrolene
Different from neuromuscular blockers, no action on
neuromuscular transmission
Mechanism of Action: Ryanodine receptors (RyR) calcium
channels – prevents depolarization – no intracellular release
of Ca++
Absorbed orally, penetrate brain and produces sedation,
metabolized in liver, excreted in kidney. T1/2 8-12 hrs
Dose: 25-100mg - 4 times daily
Uses: Upper Motor Neuron disorders – paraplegia, hemiplegia,
cerebral palsy and malignant hyperthermia (drug of choice 2.5-
4 mg/kg)
Adverse effects – Sedation, malaise, light headedness,
muscular weakness, diarrhea and hepatotoxicity
96. MOA: Centrally acting Muscle relaxants
• Drugs that reduce skeletal muscle tone by selective
action on cerebrospinal axis
• Depress the spinal and supraspinal reflexes of muscle tone
• Also depresses polysynaptic reflexes of ascending reticular
formation – wakefulness disturbed (sedation)
• No effect on NM junction but reduce Upper Motor
Neuron spasticity and hyperreflexia
97. Mephenesin (Relaxyl/medicreme)
• Mephenesin (Relaxyl/medicreme)
–Modulation of reflexes in spinal internuncialneuron
–Cannot be used systemically
–Irritant rather than relaxant – topical preparations
• Carisoprodol, Chlorzoxazone (Mobizox), Methocarbamol
(Robinax/Robiflam) and Chlormezanone – similar but can
be used orally
98. Benzodiazepines as muscle relaxant
• Very potent centrally acting muscle relaxant – supraspinal
• Mechanism of action is via “GABAA receptor Cl- complex”
enhancement
• Inhibitory in nature
• Diazepam and Clonazepam are the most potent ones
• Diazepam is the prototype of BZDs
99. Baclofen- GABAB agonist
• Mechanism of action: GABA B agonist
– Hyperpolarization of neurons by increasing K+
conductance and alteration of Ca++ flux
– Does not affect to Cl- conductance
• Site of action: spinal chord – depresses polysynaptic and
monosynaptic reflexes
• Clinical effects: decreased hyperreflexia; reduced painful
spasms; reduced anxiety
• Dose: orally 5 mg three times daily, gradually increase to
20 mg four times daily or higher
• Intrathecally initially 50 mcg/day increase to 300-800 mcg/day
100. Tizanidine/ clonidine
• Mechanism of action: alpha-2 receptor agonist –
inhibits the release of excitatory amino acids in spinal
interneurons
• Clinical effects: reduced tone, spasm frequency, and
hyperreflexia
• Doses: tizanidine initial 4 mg three times daily
increase to 36 mg/day; clonidine initial 0.1 mg twice
daily increase to 2.4 mg/day
101. Uses of Centrally acting relaxants
• Acute muscle spasms
• Backache and neuralgias
• Anxiety and tension
• Spastic neurological disorders
• Tetanus
• Electroconvulsive therapy
• Orthopedic manipulations
102. Centrally acting Vs Peripherally acting
Centrally acting Peripherally acting
• Decrease muscle tone
but no reduction in
power
• Polysynaptic reflexes in
CNS
• CNS depression
• Orally and parenterally
• Spastic conditions, muscle
spasm
• Cause muscle paralysis
• Block NM transmission
• No CNS effect
• Given IV
• Short term surgical
procedures
103. Non-pharmacologic interventions to relieve muscle spasm
and spasticity
Non-pharmacologic interventions include:
• Physical interventions (stretching, passive movements)
• Transcutaneous electric nerve stimulation (TENS)
• Transcranial direct current stimulation (tDCS)
• Shock wave
• Vibratory stimulation (whole body vibration)
• Electromyography biofeedback
• Repetitive transcranial magnetic stimulation (TMS)
• Therapeutic ultrasound & Acupuncture
• Orthotics (splints, casts)
• Thermotherapy & Cryotherapy
104. Nursing Role
• Monitor patient response to therapy (improvement in muscle spasm
and relief of pain; improvement in muscle spasticity).
• Monitor for adverse effects (e.g.CNS changes, GI depression,
urinary urgency, etc).
• Discontinue drug at any sign of liver dysfunction to prevent adverse
effects.
• Monitor patient compliance to drug therapy.
• Provide safety measures (e.g. adequate lighting, raised side rails,
etc.) to prevent injuries.
• Educate client on drug therapy to promote understanding and
compliance.
106. SEDATIVE AND HYPNOTIC DRUGS
Sedative effect
Given during waking hours
May cause drowsiness
Hypnotic effect
Given at bedtime with the purpose of inducing sleep
MAY BE THE SAME DRUG GIVEN AT DIFFERENT
DOSAGES
107. 111
Benzodiazepines
Prototype
Diazepam (Valium)
Antianxiety, anticonvulsant, sedative/hypnotic, skeletal muscle
relaxant
Schedule IV drugs Moderate potential for abuse
Pregnancy category D
Half-life 20-50 hours (metabolites also cause sedation up to 100
hours)
Drug of choice to treat status epilepticus (sustained seizures)
109. 113
BENZODIAZEPINES
MECHANISM OF ACTION
Binds with benzodiazepine receptors in nerve cells of the
brain these cells also have binding sites for GABA (gamma-
aminobutyric acid) which is an inhibitory neurotransmitter.
Excitatory v. Inhibitory transmitters
Excitatory Norepinephrine
Inhibitory - GABA
113. 117
BENZODIAZEPINES
Drug-Drug interactions
Cimetidine, hormonal contraceptives, disulfiram, fluoxetine,
isoniazid, ketoconazole, metoprolol, propoxyohene,
propranolol, and valproic acid may enhance the effects of
sedatives by decreasing their metabolism.
May decrease the efficacy of levodopa
Rifampin, barbiturates may increase the metabolism of
benzodiazepines, decreasing their effectiveness.
114. 118
BENZODIAZEPINES
Herbal products to avoid when using benzodiazepines
Kava kava
Valerian root
Camomile
CAN INCREASE SEDATION
THIS APPLIES TO ALL CNS DEPRESSANTS
116. 120
BENZODIAZEPINES
REVERSAL AGENT FOR OVERDOSE OF
BENZODIAZEPINES
FLUMAZENIL
INDICATED FOR THE REVERSAL OF MODERATE
SEDATION OR GENERAL ANESTHIA
117. 121
NURSING CONSIDERATIONS
ASSESS PATIENT WITH FOCUS ON REASON FOR GIVING
SEDATION
ANXIETY
NERVOUSNESS
REASSESS PATIENT FOR RESPONSE TO DRUG
SEDATIVE Q 4-6 H
HYPNOTIC AT BEDTIME
MONITOR VS AND POTENTIAL FOR DEPRESSION
118. 122
CONTRAINDICATIONS TO SEDATIVES
AND HYPNOTICS
Patient with a history or current use of
recreational drugs or alcohol abuse
Respiratory compromise
Pregnancy or lactation
119. 123
NURSING IMPLICATIONS
Administer accurately
Teach patient about expected effects and
possible side effects
Provide for patient safety
Observe for therapeutic effects
Decrease in anxiety
Positive signs of sleep
120. 124
NURSING IMPLICATIONS
Observe for adverse effects
Excessive sedation
Hypotension
Observe for drug interactions
Concurrent use of other CNS depressants
121. 125
Barbiturates Used as Anxiolytic-Hypnotics
These were once the sedative-hypnotic
drugs of choice but newer anxiolytics
have replaced them. Barbiturates have
high risk for addiction and dependency.
122. 12
Therapeutic Action
These are general CNS depressants that
inhibit neuronal impulse conduction in the
ascending RAS, depress the cerebral cortex,
alter cerebellar function, and depress motor
output. Therefore, they can cause sedation,
hypnosis, anesthesia, and even coma.
123. 127
Indications
•Generally indicated for anxiety, sedation,
insomnia, paresthesia, and seizures.
•Parenteral forms may be used for treatment
of acute manic reactions.
124. 128
Route Onset Peak Duration
Oral 15 min 30-60 min 10-16 h
IM, subcutaneous – 10-30 min 4-6 h
IV Up 10 15 min 5 min 4-6 h
Pharmacokinetics
125. Contraindications
and Cautions
▫ Allergy to barbiturates. Prevent severe
hypersensitivity reactions.
▫ History of addiction to sedative-hypnotic
drugs: barbiturates are more addicting than
most other anxiolytics
▫ Latent or manifest euphoria. May be
exacerbated by drug effects
▫ Marked hepatic impairment or
nephritis. May alter the metabolism and
excretion of drugs
▫ Respiratory distress and
dysfunction. Exacerbated by CNS
depression caused by drugs.
129
126. Contraindications
and Cautions
▫ Pregnancy. Associated with congenital
abnormalities
▫ Lactation. Has potential for adverse effects
on the infant.
▫ Acute or chronic pain. Can cause
paradoxical excitement which can mask
other symptoms
▫ Seizure disorder. Abrupt withdrawal of
barbiturates can precipitate status
epilepticus
▫ Chronic hepatic, cardiac, and respiratory
diseases. Can be exacerbated by the
depressive effects of these drugs.
130
128. Nursing
Considerations
These are vital nursing interventions
done in patients who are taking
anxiolytic-hypnotics:
▫ Administer intravenous diuretics slowly
because rapid administration may cause
cardiac problems.
▫ Do not mix intravenous drugs in solution
with any other drugs to avoid potential
drug-drug interactions.
▫ Taper dose as ordered because abrupt
withdrawal can precipitate seizure attacks.
132
129. Nursing
Considerations
▫ Provide comfort measures (e.g.
small, frequent meals, access to
bathroom facilities, orientation, etc.)
to help patient tolerate drug effects
▫ Provide safety measures (e.g.
adequate lighting, raised side rails,
etc.) to prevent injuries.
▫ Educate client on drug therapy to
promote compliance.
133
131. 135
Anxiety Disorders
A group of mental disorders characterized by a
vague uneasy feeling of discomfort or dread. The
symptoms of anxiety prevent the individual from
normal functioning . can be an exaggerated
response to an actual event or anxiety unrelated
to an identifiable event or condition.
134. 138
BUSPIRONE (BuSpar)
Mechanism of action unknown
Interacts with serotonin and dopamine in
the brain
No muscle relaxant effects
No anticonvulsant effects
Does not cause sedation
135. 139
BUSPIRONE (BuSpar)
Uses / indications
Short term management of anxiety
disorders
Not appropriate for immediate relief may
take
several weeks to see effects
136. 140
BUSPIRONE (BuSpar)
Side effects
Dizziness, nausea, headache, anxiety, fatigue,
Insomnia
Contraindications
Renal/hepatic failure
Use of MAOIs
138. 142
ETIOLOGY OF DEPRESSION
Monoamine neurotransmitter dysfunction
Deficiency of norepinephrine and/or
serotonin.
Balance, integration and interactions
among
norepinephrine, serotonin, and other
neurotransmission systems is an
important
etiological factors.
139. 143
ETIOLOGY OF DEPRESSION
Neuroendocrine factors
AN INCREASE IN CRF (corticotropin releasing
factor/hormone) HAS BEEN NOTED IN
PATIENTS WITH DEPRESSION.
142. 146
TRICYCLIC ANTIDEPRESSANTS(TCAs)
First generation of antidepressant therapy
Mechanism of action
Corrects the imbalance in the neurotransmitter
concentrations of serotonin and norepinephrine at
the nerve endings in the CNS. This is done by
blocking the reuptake of the neurotransmitters and
thus causing these neurotransmitters to accumulate
at the nerve endings.
Also have nonselective receptor antagonism
causing many side effects.
145. 149
TRICYCLIC ANTIDEPRESSANTS
Interactions
WHEN TAKEN WITH MAOIs MAY RESULT IN
INCREASED THERAPEUTIC LEADING TO
TOXIC EFFECTS (HYPERPYRETIC CRISIS)
TCAs can inhibit the metabolism of
warfarin,resulting in an increase in
anticoagulation
146. 150
TRICYCLIC ANTIDEPRESSANTS
Toxicity and management of overdose
TCA overdoses are fatal 70 - 80 of the time
Death usually results from seizures or
dysrhythmias
THERE IS NO SPECIFIC ANTIDOTE FOR TCAs
147. 151
MONOAMINE OXIDASE INHIBITORS
(MAOIs)
First generation of antidepressant drugs
Highly effective
Many side effects and drug/drug, drug/food
interactions
Disadvantage potential to cause hypertensive crisis
when taken with tyramine
149. 153
MAOIs Mechanism of Action
Inhibit the MAO enzyme system in the CNS
Amines (dopamine, serotonin, norepinephrine)
are not broken down, resulting in higher levels in
the brain
Result alleviation of symptoms of depression
150. 154
MAOIs Indications
Depression, especially types characterized by
symptoms such as increased sleep and appetite
depression that does not respond to other drugs
such as tricyclics
152. 156
MAOIs Overdose
Symptoms appear 12 hours after
ingestion
Tachycardia, circulatory collapse,
seizures, coma
Treatment protect brain and heart,
eliminate toxin
153. 157
Hypertensive Crisis and Tyramine During
MAOI Therapy
Ingestion of foods and/or drinks with the
amino acid tyramine leads to hypertensive
crisis, which may lead to cerebral
hemorrhage, stroke, coma, or death
155. 159
Antidepressants MAOIs
Concurrent use of MAOIs and SSRIs may lead to
serotonin syndrome
If the decision is made to switch to an SSRI, there
must be a 2- to 5-week wash-out period between
MAOI therapy and SSRI therapy
157. 161
SSRIs Newer-Generation
Antidepressants
Fewer adverse effects than tricyclics and
MAOIs
Very few drug-drug or drug-food
interactions
Still takes about 4 to 6 weeks to reach
maximum clinical effectiveness
158. SSRIs
Mechanism of action
▫ Selectively inhibits serotonin reuptake
▫ Little or no effect on norepinephrine or
dopamine reuptake
▫ Result in increased serotonin
concentrations at nerve endings
▫ Advantage over tricyclics and MAOIs
little or no effect on cardiovascular
system
162
160. SSRI
Antidepressants
Adverse Effects
▫ Body System Effects
▫ CNS Headache, dizziness,
tremor, nervousness,
insomnia, fatigue
▫ GI Nausea, diarrhea, constipation,
dry mouth
▫ Other Sexual dysfunction,
▫ weight gain, weight loss, sweating
▫ Most common and bothersome
164
163. SNRIs
Drug Interactions
Highly bound to plasma proteins
Compete with other protein-binding drugs, resulting in
more free, unbound drug to cause a more pronounced
drug effect
Inhibition of cytochrome P-450 system
164. OTHER ANTIDEPRESSANTS NOT CLASSIFIED
bupropion
Wellbutrin, zyban
Commonly prescribed for smoking cessation
maprotiline
Similar to TCAs
Mirtazapine
Remeron
Often prescribed to enhance appetite
165. NURSING CONSIDERATIONS WHEN PATIENTS
ARE TAKING ANTIDEPRESSANTS
Comprehensive patient history
Complete medication history
Monitor patient for therapeutic effects
Monitor patients for adverse effects
Education of patient on drug expectations and adverse
effects
Educate patient regarding drug-drug, drug-food and drug-
herbal interactions
167. NURSING CONSIDERATIONS
Monitor serum lithium levels
Therapeutic levels are 1.0 1.5 meq/L
Lithium is eliminated intact by the kidneys.
Encourage fluids to completely eliminate the drug
Monitor for therapeutic and adverse effects
168. PSYCHOSIS
A severe mental disorder characterized by disordered
thought process and often bizarre thinking.
Hypoactivity or hyperactivity
Agitation
Aggressiveness
Hostility
Social withdrawal
169. Antipsychotic Drugs
Antipsychotic AKA Neuroleptic
Any drug that modifies or treats psychotic
behaviors usually by blocking dopamine receptors
in the brain
171. HALDOL- FIRST GENERATION
ANTIPSYCHOTIC
Schizophrenia
Long half-life facilitates better
compliance by patients
Long-term treatment of psychosis
Can be given either IV or po
174. Mechanism of Action
▫ Block dopamine receptors in
the brain (limbic
system, basal ganglia)areas
associated with
emotion, cognitive function,
motor function
▫ Dopamine levels in the CNS
are decreased
▫ Result tranquilizing effect in
psychotic patients
175. ADVANTAGES OF NEWER GENERATION
ANTIPSYCHOTICS
Reduced effect on Prolactin levels
Stimulates mammary glands to produce milk
Lower risk of
o Neuroleptic malignant syndrome
o Extrapyramidal adverse effects
o Tartive dyskinesia
176. 180
Indications
Treatment of serious mental illnesses
Bipolar affective disorder
Depressive and drug-induced psychoses
Schizophrenia
Autism
Movement disorders (such as Tourettes
syndrome)
Some medical conditions
Nausea, intractable hiccups
178. 182
Adverse Effects (contd)
Body System Adverse Effects
GI Dry mouth, constipation
GU Urinary hesitancy or retention,
impaired erection
Hematologic Leukopenia and
agranulocytosis
179. 183
Adverse Effects (contd)
Body System Adverse Effects
Metabolic/endocrine Galactorrhea,
irregular menses, increased appetite,
polydipsia
180. 184
Nursing Implications
Before beginning therapy, assess both
the physical and emotional status of
patients
Obtain baseline vital signs, including
postural BP readings
Obtain liver and renal function tests
181. 185
Nursing Implications (contd)
Assess for possible contraindications to
therapy, cautious use, and potential drug
interactions
Assess LOC, mental alertness, potential for
injury to self and others
Check the patients mouth to make sure oral
doses are swallowed
182. 186
Nursing Implications (contd)
Provide simple explanations about the
drug, its effects, and the length of time
before therapeutic effects can be
expected
Abrupt withdrawal should be avoided
Advise patients to change positions
slowly to avoid postural hypotension and
possible injury
183. 187
Nursing Implications (contd)
The combination of drug therapy and psychotherapy
is emphasized because patients need to learn and
acquire more effective coping skills
Only small amounts of medications should be
dispensed at a time to minimize the risk of suicide
attempts
Simultaneous use of these drugs with alcohol or
other CNS depressants can be fatal
