Central Nervous System Medications

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CENTRAL NERVOUS SYSTEM MEDICATIONS  Control posture, locomotion, and fine

motor coordination
CENTRAL NERVOUS SYSTEM  Lateral hemispheres
Neuron
 Involved with the planning, practice, and
 Receive stimuli and transmit action potentials
learning of complex movements
Axons (Nerve Fibers) Diencephalon
 Slender processes of uniform diameter and may  Located between the brainstem and the
vary in length from a few millimeters to more cerebrum
than a meter
 Consists of the
 Usually, there is only one unbranched axon per
o Thalamus
neuron
o Subthalamus
o Rare branches, if present, are called
o Epithalamus
collateral axons
Action Potential o Hypothalamus
 Electrical impulses due to a temporary shift Hypothalamus
(from negative to positive) in the neuron’s  Main visceral control center of the body and is
membrane caused by ions suddenly flowing in vitally important to overall body homeostasis.
and out of the neuron.
 When action potentials are received:
o Sensory cells: sight, hearing, and touch
o Complex mental activities: conscious
thought, memory, and emotions
o Contraction of muscles and the
secretion of certain glands
Neurotransmitters
 Endogenous chemical messengers which
transmit signals across a chemical synapse,
from one neuron to another "target" neuron,
muscle cell, or gland cell.
 Neurotransmitters are released from synaptic
vesicles in synapses into the synaptic cleft, Cerebrum
where they are received by neurotransmitter  Consists of two hemispheres, left and right,
receptors on the target cells. separated by the longitudinal fissure.
Spinal Cord  Responsible for complex sensory and neural
 Major communication link between the brain and functions and coordination of voluntary body
the PNS (spinal nerves) movements.
 Integration of incoming information and Basal Nuclei
produces responses through reflex mechanisms  Include the corpus striatum (caudate and
Brain lentiform nuclei), subthalamic nuclei, and
 Contained in the cranial cavity substantia nigra
 Is the control center for many of the body’s  Important in controlling motor functions
functions Limbic System
 Parts of the Brain:  Includes parts of the cerebral cortex, basal
o Brainstem nuclei, the thalamus, the hypothalamus, and the
o Cerebellum olfactory cortex
o Diencephalon  Involved in memory, reproduction, nutrition,
o Cerebrum emotional interpretation of sensory input, and
Brainstem emotions in general
 Connects the spinal cord and cerebellum to the
remainder of the brain PAIN
 Contains 10 pairs of cranial nerves Pain
 Damage to small areas of the brainstem can  Unpleasant sensory and emotional experience
cause death. associated with either actual or potential tissue
damage.
Cerebellum  Management should be individualized and has a
 Flocculonodular lobe constant evaluation throughout the treatment to
 Controls balance and eye movements determine the effectiveness of the pain
medication.
 Vermis and medial part of the lateral
hemispheres  Pain is subjective: it involves psychological
experience from the physiologic stimulation.
Pain Threshold Pain Tolerance

 Level of stimulus to  Amount of pain the


produce a painful patient can handle.
sensation.

Remember!
 The ultimate goal of pain management is
freedom from pain
Acute Chronic 

 Sudden onset  Persistent and


(minutes to hours) recurring (6 weeks
or longer)
Pain Management Ladder
Step 1: Nonopioid (with or without adjuvant medication)
Step 2: Mild to moderate pain; Opioids with or without
non-opioiods and with or without adjuvants
Step 3: Moderate to severe pain; Opioids with or without
non-opioiods and with or without adjuvants
Arachidonic Acid Pathway
 Arachidonic acids are released from
phospholipids in the cell membrane from the
event/injury and metabolized by either
prostaglandin (PG) pathway or leukotriene (LT)
pathway.
 Prostaglandin – induces inflammation and
promotes alteration in vascular responses
Four Processes of Nociception Arachidonic Acid
1. Transduction Prostaglandin (Cyclooxygenase)
 Injured tissue emits chemical mediators  Prostacyclin (PGI2)
to convey the signal of pain.  Thromboxane A2
2. Transmission Leukotriene (Lipoxygenase)
 Pain sensation travels from the spinal  Leukotriene
cord to the brain.
3. Perception of the brain CNS STIMULANTS
 Understanding and interpretation of pain  Drugs that enhances the activities of
by the brain neurotransmitters: dopamine, norepinephrine,
4. Modulation serotonin
 Brain stem releases neurotransmitters Types of CNS Stimulants
that block the pain impulses.  Amphetamines 
 Analeptics
 Anorexiants
Amphetamines
 Action: acts on cerebral cortex*, reticular
activity system**
 Indication:
o ↑wakefulness in narcolepsy***
o ↑attention span, cognition
o ↓hyperactivity, impulsiveness,
restlessness of ADHD
Narcolepsy
 a sleep disorder that affects the control of sleep
and causes overwhelming daytime drowsiness
Examples of Amphetamines
 ADHD
o Methamphetamine (Desoxyn)
o Amphetamine (Adderall)  Sedative-hypnotics
o Dextroamphetamine (Dexedrine) o Low doses: calm the CNS without
o Methylphenidate (Concerta, Ritalin) inducing sleep
 Narcolepsy o High doses: calm the CNS and causes
o Modafinil (Provigil) sleep; also causes respiratory
o Pemoline (Cylert) depression
Classifications of CNS Depressants
Analeptics  Barbiturates 
 Action: stimulates CNS by either increasing  Benzodiazepines
neuronal discharge or inhibiting  Non-benzodiazepines
neurotransmitters Barbiturates
 Indication:  Action: inhibits GABA*, which inhibits nerve
o Reversal of anesthesia-induced impulses in the cerebral cortex; suppresses
respiratory depression REM sleep**
o Stimulate respiration in newborns  Indication: Hypnotics, sedatives,
Examples of Analeptics  anticonvulsants, anesthesia
 Methylxanthines  Habit forming**; low therapeutic index
o Aminophylline
o Theophylline
o Caffeine
 NoDoz
 Doxapram (Dopram)
Anorexiants
 Action: suppress the appetite control center in
the brain
 Indication: obesity
 Ex. Dextroamphetamine (Dexadrine)
CNS Stimulants: Drug Interactions
 +Caffeine = ↑effects
 ↓effects of decongestants, antiHPN,
barbiturates*
 May alter insulin effects
Cns Stimulants: Side Effects/Adverse Effects Types of Barbiturates
 Tachycardia, palpitations, dizziness,  Ultrashort-acting
hypertension o Used as a general anesthetic
 Sleeplessness, restlessness, nervousness, o Ex. thiopental sodium (Pentothal)
tremors, irritability ↑hyperactivity  Short-acting
 Anorexia, dry mouth, vomiting, diarrhea, weight o Induce sleep, controls convulsion, and
loss no residual drowsiness
 Thrombocytopenia* o Ex. pentobarbital (Nembutal),
CNS Stimulants: Contraindications/Precautions secobarbital (Seconal)
 C: Glaucoma, severe CV disease Types of Barbiturates
 P: psychosis, pregnant and breastfeeding  Intermediate-acting
women o Induce and sustain sleep, for
CNS Stimulants: Nsx Action convulsion, but causes residual
 Give before breakfast and lunch* drowsiness (hangover effect)
 Report arrhythmias, seizures, palpitations, liver o Ex. amobarbital (Amytal), butabarbital
problems (Butisol)
 Record ht, wt, and growth of children  Long-acting
 Avoid alcohol, caffeine o Used to control seizures
 Use sugarless gum to relieve dry mouth o Ex. phenobarbital
 Do not stop abruptly; taper** Remember!
 Barbiturates are notorious enzyme inducers; it
CNS DEPRESSANTS stimulate liver enzymes, which speeds up drug
 Action: Drugs that have an CNS inhibitory effect metabolism resulting to shortened duration of
Types of CNS Depressants drug action
 Sedatives Benzodiazepines
o Reduces nervousness,excitability, and  Action: Interacts with GABA to reduce neuron
irritability without causing sleep excitability; do not suppresses REM sleep
 Indication: agitation, anxiety, alcohol  Epilepsy
withdrawal, preoperative sedation, insomnia, o chronic, recurrent occurrence of 2 or
seizure, skeletal muscle relaxation more unprovoked seizure episodes
Types of Benzodiazepines
 Long-acting
o Estazolam (Prosom)
o Flurazepam (Dalmane)
o Others
 Short-acting
o Temazepam (Restoril)
o Triazolam (Halcion)
Remember!
 Benzodiazepines are the most frequently
prescribed sedative-hypnotics because of their
favorable drug effect
Non-benzodiazepines
 Action: neurotransmitter inhibition
 Indication: treat short-term (<10 days) insomnia
 Ex. Zolpidem (Ambien), eszopiclone (Lunesta)
CNS Depressants Drug interactions
 Alcohol, antihistamines, benzodiazepines,
opioids, tranquilizers, CNS depressants, MAOIs
= ↑effect, ↓respirations with
 MAOIs will prolong effects of barbiturates
 ↓anticoagulant response, leading to possible clot
formation
CNS Depressants Side effects/ Adverse effects
 Residual drowsiness (“Hangover effect”)
 Headache, vertigo
 Fall hazard for frail elderly persons
 Drug dependence and tolerance
 Respiratory depression
 Withdrawal symptoms
CNS Depressants: Contraindication
 Pregnancy
 Uncontrolled pain
 Acute intermittent porphyria*
CNS Depressants Nsx Action
 Assess health and drug Hx., monitor VS and I/O:
including supine and erect BPs
 Give 15-30 min before bedtime
 Monitor “hangover effect, ” use with caution in
elderlies, and ensure safety measures (fall risk)
 Avoid alcohol and other CNS depressants
 WOF rebound insomnia 3-4 weeks after drug
being discontinued

ANTICONVULSANTS
Seizure
 Abnormal electric discharges from neurons
characterized by loss of consciousness and
convulsive movements

Seizure Disorders
 Convulsion
o sudden, violent, irregular movement of a Anticonvulsants*
limb or of the body, caused by  Action: Suppress abnormal neuron firing,
involuntary contraction of muscles and inhibiting seizure activities
associated especially with brain
disorders
 Indications: Tonic-clonic seizure*, status
epilepticus**, complete partial seizures***,
arrhythmias, trigeminal neuralgia****
Classifications of Anticonvulsants
 Suppress Na influx
o Phenytoin (Dilantin)
 Suppress Ca influx
o Valproic acid (Depakane), divalproex
(Depakote)
 Enhance action of GABA*
o Clonazepam (Klonopin), gabapentin
(Neurontin)
 Inhibit GABA degradation
o Vigabatrin (Sabril)
Types of Anticonvulsants
 Hydantoin 
 Barbiturates  Anticonvulsants: Side Effect/Adverse Reactions
 Benzodiazepines  SE: Gingivitis, gingival hyperplasia, nystagmus,
 Succinimides  diplopia, dizziness, slurred speech, decreased
 Carbamazepine coordination, alopecia
Hydantoin  AE: Thrombocytopenia, Stevens-Johnson
 Most commonly-used drug for seizure control: syndrome*
phenytoin Anticonvulsants: Contraindications
 Lesser toxic effects; non-addicting  Pregnancy, sinus bradycardia, sinoatrial block,
 Should NOT be used in pregnancy second- and third-degree AV block, Adam-
Stokes syndrome**
 Has a narrow therapeutic range
Anticonvulsants: Drug interactions
Barbiturates
 +Cimetidine (Tagamet), INH, sulfonamides =
 For grand mal* acute episodes of status
↑effects
epilepticus
 +Folic acid, antacids, calcium, sucralfate,
 Use long-acting barbiturate: phenobarbital
antineoplastics, antipsychotics, primrose, ginkgo
 Lesser teratogenic** effects than phenytoin
= ↓effects
Benzodiazepines
 ↓Effects of anticoagulants, oral contraceptives,
 Primary treatment for acute seizures: diazepam
antihistamines, dopamine, theophylline
 Short term effect; not for maintenance Anticonvulsants: Nsx Action
 For petit mal seizures: clonazepam  Monitor serum drug levels (toxicity), glucose
 High degree of tolerance* levels in DM, liver enzymes, CBC (platelet),
 Adjunctive therapy for treatment of partial ECG
seizures: clorazepate  Administer with food
Succinimides  Ensure safety during usage (fall risk)
 Used to treat absence or petit mal seizures*  Avoid certain herbs, alcohol, and other CNS
 May be used in combination with other depressants
anticonvulsants Anticonvulsants: Contraindications: Nsx Action
Carbamazepine  For women taking oral contraceptives, advise to
 It works by decreasing nerve impulses that consider other methods
cause seizures and nerve pain, such as  Promote oral hygiene and dental check-ups
trigeminal neuralgia and diabetic neuropathy.
 Must be taken at same time every day, taper
 Also used to treat bipolar disorder. drug
 Warn of harmless pinkish red or brown urine

NEUROMUSCULAR MEDICATIONS
Myasthenia Gravis (MG)
 Autoimmune disease caused by lack of nerve
impulses and muscle responses at myoneural
junction due to lack of acetylcholine reaching
cholinergic receptors
 Characteristics:
o Muscular weakness and
fatigue 
o Respiratory muscle paralysis,
ptosis, difficulty chewing and
swallowing
Cholinesterase Inhibitors
 Action: transmission of neuromuscular impulses
by preventing destruction of Ach – allows
adrenergic response
 Indication: control and treat MG
Short-acting
 Neostigmine (Prostigmin)
Ultrashort-acting for diagnosing MG
 Edrophonium (Tensilon)
Intermediate acting
 Pyridostigmine (Mestinon)

Myasthenia Cholinergic
crisis crisis Muscle Relaxants
 Provides relief of painful musculoskeletal
 Underdosed  Overdosed conditions:
 Severe muscle  Severe muscle o Muscle spasms
weakness cramping o Management of spasticity of severe
 Improves after chronic disorders
edrophonium* o Multiple sclerosis, cerebral palsy
 Work best when used along with physical
therapy
Cholinesterase Inhibitors: Side effects/Adverse Muscle Relaxants
effects Central acting: CNS Direct acting: Skeletal
 Pupil constriction muscle
 GI distress, abdominal cramps
 Excess saliva, sweating  Baclofen (Lioresal)  Dantrolene
 Headache, dizziness, seizures  Diazepam sodium
 Hypotension, bradycardia, dysrhythmias  Carisoprodol (Soma)  Quinine
 Bronchospasm, respiratory depression  Cyclobenzaprine
CholinesteraseInhibitors: Nsx Action (Flexeril)
 Administer doses on time  Methocarbamol
 Take drug before meals (Robaxin)
 Monitor drug effectiveness
 Antidote for cholinergic crisis: atropine
Multiple Sclerosis (MS)  Muscle Relaxants: Side Effects/ Adverse Effects
 Autoimmune disorder that attacks myelin sheath  Drowsiness, sedation, dizziness, headaches, GI
of nerve fibers distress, fatigue, drug dependence
 Characteristics: Muscle Relaxants: Nsx Action
o Weakness or spasticity in extremities  Take with food
o Diplopia  • Monitor VS, liver function
 Do not allow to drive
 Do not take longer than 3 weeks
 Do not stop abruptly: discontinue over 1 week to
avoid rebound spasms
 Avoid alcohol and other depressants

OPIOID ANALGESICS
Opioid Drugs
 Derived from opium plant that imitates natural
narcotics.
 Utilized to relieve and decrease pain without
causing the patient to lose consciousness.
 Further, it also has antitussive and antidiarrheal
properties.
Opioid Drugs: Action
 Liver metabolizes the opioid drugs, thus
terminal and toxic occupying
increasing the liver enzymes.
illnesses. effects the receptor
 Also acts on the medulla oblongata which sites.
controls the respiration and coughing • Treatment
Agonist Mixed Antagonist for opioid
overdose
 Binds to  Weakly  These are
opiate receptor antagonize not pain
sites in the the effects medications; Opioid Drugs: Contraindications
peripheral of agonists however, it  Drug allergy
nervous system and others blocks the
 Severe asthma
and in the CNS. exert effect of the
 Hypotension
 When agonist to opioid agonist
the other and being  Severe renal disease
attached, the
drug mimics the receptors. used for  Increased ICP – decreased respiratory rate
effects of  Weaker reversal of  Head injuries
natural neurologic / drug
biochemical pain reliever reactions.
compounds response as  In effect, it Opioid Drugs: Side Effects/ Adverse Effects
that produce compared to also reverses  Constipation
the body's agonists. the analgesic  Hypotension
natural pain  i miss effect of the  Nausea and vomiting
reliever such as you opioid  Sedation and mental clouding
endorphins.  i miss u agonist.  Respiratory Depression
most  Subacute overdose
mommy  Urinary retention
 i miss u  Pupil constriction
mostest *Opioids are HIGHLY ADDICTIVE NARCOTICS
daddy] commonly prescribed to treat pain. 

Opioid Drugs: Examples Analgesic Ceiling Effect for Opioid Analgesics


 Opioid Tolerance
Agonists Mixed Antagonist o Increases tolerance that makes the
doses higher to main the therapeutic
 Morphine  Nalbuph  Naloxone effect.
 Fentanyl ine  Naltrexon  Physical Dependency
 Meperidine  Pentazo e o Physiologic adaptation of the body to the
 Codeine cine opioids
 Methadone Opioid Withdrawal Syndrome
Anxiety Irritability

Hot Flushes Joint Pain

Rhinorrhea  Diarrhea 

Opioid Drugs: Drug Interaction


 Opioid depresses the respiratory status.
 Alcohol, antihistamines, barbiturates,
benzodiazepines, phenothiazine, and CNS
depressants will INCREASE the respiratory
depressant effects.
 Monoamine oxidase inhibitors (MAOI) will
increase respiratory depression and
Opioid Drugs: Indication hypotension.
Agonists Mixed Antagonist o MAOI + Meperidine = deep coma and death
Remember!
Severe pain • Given to • Block the  Withdrawal symptoms’ onset on prolonged use
in acute, limit effect of of opioids will depend on the half-life of the
chronic and dependency opioids by medication.
Opioid Drugs: Nsx Action
 Monitor Vital Signs (Respiratory Rate) including Non-Opioid Drugs:Indication
Pain Scale  Relieves mild to moderate pain
 Oral forms should be taken with food. o Rheumatoid and osteoarthritis
 Encourage DOB to promote lung expansion o (Most common – Ibuprofen)
 Instruct to change position slowly  Antipyretics, anti-inflammatory
 Increase fluid intake and fiber to soften the stool  Vascular headaches
Remember!  Platelet inhibitions
 For patients on opioids, keep naloxone and
resuscitation equipment at bedside all the time. Non-Opioid Drugs: Contraindication
 Allergies with NSAIDs.
NON-OPIOID ANALGESICS  High risk for bleeding
Non-Opioid Drugs: Action  Not advised to pregnant women
 AKA Non-steroidal Antiinflammatory Drugs Non-Opioid Drugs: Side Effects/Adverse Effects
(NSAIDs)  Bleeding (Internal)
 Inhibit cyclooxygenase (COX) enzymes to  Nephrotoxicity
prostaglandins.  Diarrhea, Nausea, vomiting, anorexia
 Peripheral – acting (gastrointestinal distress)
 Inhibits pain receptors  Hepatotoxicity
 Promotes peripheral vasodilation to reduce Remember!
fever.  Chronic salicylate intoxication also known as
Non-Opioid Drugs: Types salicylism. Clinical manifestations are:
o Tinnitus and hearing loss
Acetic Acids Salicylates Para-
(Nonselective COX (Nonselective aminophenol o Metabolic Acidosis and Respiratory
Inhibitors) COX Alkalosis
Inhibitors) o Nausea, vomiting, and diarrhea
 Treatment: to remove the salicylate from the GIT
and prevent further absorptions
Diclofenac sodium Aspirin Acetaminophen Reye’s Syndrome
(Voltaren) Paracetamol  When aspirin (salicylates) is given to children
Indomethacin with chicken pox or flu-like symptoms
 Life threatening: causes neurologic deficits that
can lead to coma and liver dysfunction.
COX-2 Inhibitors Fenamic Acids Propionic Acids
(Selective COX (Nonselective (Nonselective Non-Opioid Drugs: Drug Interactions
Inhibitor) COX COX  Amplify the effects of anticoagulants, oral
Inhibitors) Inhibitors) hypoglycemic agents
 High risk of toxicity with Calcium channel
Celecoxib Mefenamic Acid Naproxen blockers
(Celebrex) Ibuprofen  Alcohol, corticosteroids increase GIT effects.
Ketorolac Non-Opioid Drugs: Nsx Action
 Stop aspirin for 1 week before surgery
 Cautiously administer salicylates to asthmatics
because of the risk of having bronchospasm.
 Cautiously administer NSAIDs to high risk of
thrombotic events such as Myocardial Infarction
or Stroke
 Watch out for drug allergies.
 Watch out for signs and symptoms of bleeding.
 Assess auditory functions.
 Monitory CBC, platelet, Prothrombin time and
hepatic and Renal functions.
 Administer NSAIDs with food.
 Do not chew or crush enteric coated tablets.

ANESTHESIA
Anesthesia
Remember!
 Depresses central nervous system (CNS) or
 All NSAIDs are absorbed in the GIT,
peripheral nervous system (PNS) which
metabolized in the liver, and excreted by the
produces:
kidneys.
o Loss of consciousness
 Surgeries  Shorter  Reliev
o Loss of responsiveness to stimuli
– rapid onset surgical e or
o Muscle relaxation procedures prevent
Anesthesia: Action (outpatient pain (minor
General Local surgeries) burn pain)
 Ketamine –  Reliev
 Anesthesia absorbed  Absorption varies induced profound e itchiness
by the blood through widely. sense of and
the lungs.  Metabolites are dissociation from irritation
 Rapid distribution to excreted in the urine. environment  Anest
organs  Blocks nerve  Benzodiaze hetize
 Primarily works by impulses at the point pines – produce before
depressing the CNS of contact. sedation or giving
amnesia but does injection
not relief  Numb
Parenteral Topical mucosal
surface
 Lipid-soluble and  Applied over the (urinary
well distributed to the intact skin or mucous catheter)
body membrane
 Crosses placenta  Little systemic
and enter breast milk absorption, however, General Anesthesia:  Contraindication
 Occupy sites on with impaired skin  Inhalation:
receptors on the integrity, it increases o Hypersensitivity
CNS and modifying the systemic o Liver disorder
release of absorptions.
o Malignant hyperthermia
neurotransmitters  Excreted in the urine
 Parenteral:
 Depresses CNS,  Absorbed by the skin
o Drug allergy
skeletal muscle and acts on the
relaxation nerve cell membrane o Pregnant
and blocks o Narrow angle glaucoma
transmission o Malignant Hyperthermia
Anesthesia: Side Effects/Adverse Effects
 Respiratory depression
Overton-Meyer Theory  Myocardial depression
 The greater the drug’s lipid solubility, the greater  Malignant Hyperthermia – sudden and lethal
the effect. increase in body temperature.
Anesthesia: Types
 Failure of calcium uptake by the muscle.
General Local Anesthesia
Ketamin Propofol Thiopent Fentanyl Midazola
Anesthesia
e al m
Inhalation Intravenous Amide Ester
Prolong Respirator Respirato CNS and CNS and
(with (with
ed y ry respirator respiratory
nitrogen) oxygen)
recovery, depressio depressio y depressio
 Sevofl  Barbitu irrational n, n depressio n,
urane rates behavior, bradycardi n, hypotensi
 Desflu (thiopental)  Bup  Pr excessive a, Arrhythmi on
rane  Benzo ivacaine ocaine salivation hypotensio as
 Nitrou diazepines  Lev  C and n
s oxide (midazolam) obupivac hloropr tearing
(laughing  Dissoci aine ocaine
gas) atives  Lid  T
(ketamine) ocaine etracai Local: Topical:
 Opiate ne
s (fentanyl)  Anxiety,  Hypersensitivity
apprehension, reactions 
Anesthesia: Indication restlessness,  Skin irritations
nervousness Frostbite
Inhalation: Parenteral: Topical: disorientation,
confusion
 Spinal headache – Angiotensin II 
from spinal
anesthesia Epinephrine 
 Relieve by bedrest
and conventional
analgesics

Anesthesia: Drug Interaction


 Inhalation - Combination with other CNS,
Cardiac or respiratory depressants will increase
depressant effects.
 Anesthesia: Drug Interaction - Ketamine and
nondepolarizing drugs increase neuromuscular
effect and prolonged respiratory depression
 Barbiturates or opioids + Ketamine: prolong
anesthesia time
 Anticholinergics – increases potential for
confusion, tachycardia, constipation
Anesthesia: Drug Interaction
 Co-administered with Epinephrine – to constrict
blood vessels and this in return control local
bleeding and reduces anesthesia absorption
(due to vasoconstriction) which prolongs
anesthetic action at site.
Balance Anesthesia
 Usage of minimal doses of multiple anesthesia
to achieve desired effects Rheumatism
Anesthesia: Nsx Action  General term for disorders that are characterized
 Encourage deep breathing exercises, coughing, by inflammation. degeneration or metabolic
early ambulation as postoperatively derangement of connective tissues.
 Monitor vital signs and LOC, respiratory status,
and pain status.
 Promote safety measures and precautions
Remember!
 Local anesthesia is the safer choice than
general anesthesia for elderly patients,
respiratory disorders such as COPD and
myasthenia gravis.

ANTI-INFLAMMATORY MEDICATION
Inflammation
 Reaction to tissue injuries
 Caused by the release of histamine, serotonin,
bradykinin, leukotrienes and prostaglandins Anti-inflammatory Medications
 The symptoms were caused by the vascular NSAIDs Steroids
responses such as capillary, artery and venous
dilation.  Disease- Modifying  Anti-Gout
 Fluids and leukocytes migrate towards the injury  Antirheumatic
site.  Drugs
 Induced by Phospholipase A2
Phospholipase A2 Stimulation
Corticosteroids: Action
Tissue Injury  Suppresses immune responses and reduces
inflammation, anti-stress and anti-allergic
Thrombin  Prevents the leakage of plasma from the
capillaries and the migration of leukocytes
Bradykinin 
 Inhibit inflammation by the means of inhibiting  Indication:
the release of phospholipase A2 enzymes o Rheumatoid arthritis
(which frees the phospholipid)  Contraindication:
o Inhibit arachidonic acids o Active bacterial infection, active herpes
Corticosteroids:  zoster,active or latent tuberculosis,
 Indication: acute or chronic hepatitis B or C.
o Severe inflammations Disease-Modifying Antirheumatic Drugs (DMARDs)
o Immunosuppression
Non – Biologic Biologic DMARDs Gold Drug
 Contraindication: DMARDs (Immunomodulators) Therapy
o Drug allergy
o Fungal infections
Corticosteroid: Side Effects/Adverse Effects Methotrexate Adalimumab Auranofin
 Hyperglycemia Leflunomide Anakinra (Ridaura)
 Infection Etanercept
 Weight gain and edema
 Cushing’s Syndrome
Disease-Modifying Antirheumatic Drugs (DMARDs)
Corticosteroid: Drug Interaction
 Side Effects / Adverse Effects
 Aspirin and NSAIDS + Corticosteroids =
o Pancytopenia
increases risk of GIT bleeding and ulceration
o Infections
 Corticosteroids + Potassium losing diuretics =
o Fatigue, nausea and vomiting and flu-
hypokalemia
like symptoms
 Dexamethasone decreases the effect of
anticoagulants and antidiabetic medications  Drug Interaction:
o Should not be used with other DMARDs
 Prednisone + Barbiturates, phenytoin and
rifampin = decrease the effect of prednisone. immunosuppressants
Corticosteroids: Nsx Action Disease-ModifyingAntirheumatic Drugs (DMARDs):
Nsx Action
 Live vaccines should not be given with this
treatment.  Report signs and symptoms of infections to
physicians.
 Avoid individuals with infections
 Do not administer live vaccines.
 Monitor for electrolytes, blood glucose levels,
daily weight, and hypertension.  Monitor for complete blood count and liver
enzymes
 Taper after a long-term use.
 Monitor injection site for pain, swelling and
 Give the medications during the morning.
irritation.
 Administer with food to prevent GIT irritation.
Anti-Gout Medications
 Encourage food high in potassium.
 Action:
Remember!
o Minimize inflammation by blocking uric
 Abrupt withdrawal of corticosteroids can cause
acid absorptions and increasing the uric
rebound inflammation, fever, depression,
acid excretion.
hypotension, hypoglycemia and adrenal
 Indication:
insufficiency.
o Hyperuricemia
Disease-Modifying Antirheumatic Drugs (DMARDs): o Gout
Action  Contraindication:
 Slows the progression of disease associated o Renal or hepatic disease
with arthritis. Anti-Gout Medications
 Exhibit anti-inflammatory, antiarthritic, and Colchicine Allopurinol Probenecid
immunomodulating effects and works by
inhibiting the movement of the cells into the Anti-gout by Uric acid Uricosurics
damaged tissue. reducing inhibitors
Remember! inflammatory
 Abrupt withdrawal of corticosteroids can cause responses
rebound inflammation, fever, depression,
hypotension, hypoglycemia and adrenal
insufficiency.
Disease-Modifying Antirheumatic Drugs (DMARDs) 
 have a slow onset of action that takes up to Anti-Gout Medications: Side Effects / Adverse
several weeks and usually take 3 to 6 months to Effects
see full effects. (Slow-acting antirheumatic drugs  Bone marrow suppression
(SAARDs))  Uric acid stones
Disease-Modifying Antirheumatic Drugs (DMARDs):  Metallic taste
 Diarrhea
diarrhea) because of the actions
 Nausea and vomiting withhold risk of having
Anti-Gout Medications: Drug Interaction medications kidney stones.
 Aspirin can trigger the gout attack; aspirin with • It can cause • Limit exposure
anti gout medications causes elevated uric acid renal failure to sunlight
levels.
Anti-Gout Medications: Nsx Action
 Avoid alcohol, foods high in purine.
 Encourage increased fluid intake to prevent
kidney stones.
 Monitor liver functions.
Anti-Gout Medications: Nsx Action
Colchicine Allopurinol Probenecid

Use cautiously • Increases the Mild GIT distress


with cardiac, effect of warfarin may occur; take
renal, GIT and oral with food to
diseases hypoglycemic lessen distress.
• If GIT symptoms • Do not take • Aspirin
occur (vomiting, large doses of interfere
nausea, vitamin C with uricosuric

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