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PHARM250 Nervous system Cheat Sheet by

List of the adverse effects of drugs for Nervous system including diseases and medication treatment

Classi­fic­ation of autonomic drugs

Stimulate parasy­mpa­thetic nervous system
or muscarinic agonists
Inhibit parasy­mpa­thetic nervous system
or muscarinic blockers
Stimulate sympat­hetic nervous system
or adrenergic agonists
Inhibit sympat­hetic nervous system
Adrenergic antagonists
or adrenergic blockers

Classes of autonomic drugs

Stimulate the parasy­mpa­thetic nervous system
Receptor: Acetyl­choline (musca­rinic)
1. Direct acting
2.Indirect acting
Inhibit the parasy­mpa­thetic nervous system, which induces fight-­or-­flight (sympa­thetic)
Stimulate the sympat­hetic nervous system Result depends on type and location of receptor (α or β)
𝛂1 agonist
𝛂2 agonist
𝛃1 agonist
𝛃2 agonist
Adrenergic antagonist
Inhibit sympat­hetic nervous system Action depends greatly on type of receptor (α or β)
𝛂1 antagonist 𝛃1 antagonist 𝛃2 antagonist

Primary neurot­ran­smi­tters in the CNS

The CNS is respon­sible for our percep­tion, mood, consci­ous­ness, behaviour, and cognition Therefore, drugs influence percep­tion, mood, consci­ous­ness, behaviour, and cognition by altering neurot­ran­smitter activity
Serotonin (5HT)
Norepi­nep­hrine (NE)
Dopamine (D)
behaviour & movement

Adverse effects of CNS drugs

drowsi­ness, sedation, memory loss, weakness, disori­ent­ation, ataxia, sleep distur­bances, hypote­nsion, blurre­d/d­ouble vision, nausea and vomiting
Rarely prescribed anymore for anxiety or insomnia because of side effects
dizziness, headache, daytime drowsi­ness, dyspepsia, dry mouth, bitter metallic taste, nausea, antero­grade amnesia
Adverse effects and monitoring mostly limited to drowsiness level (caution with endocrine dysfun­ction) because it’s identical to endogenous
sedation, dizziness, orthos­tasis, blurred vision, dry mouth, tachyc­ardia, cognitive impair­ment, consti­pation, dry eyes, urinary retention
Transient: headaches, nervou­sness, insomnia, nausea, diarrhea
Long-term: Sexual dysfun­ction, withdrawal upon discon­tin­uation
: consti­pation, dry mouth, headaches, changes in heart rate and blood pressure, insomnia, nausea, loss of appetite
Food intera­ctions
foods containing tyramine = Hypert­ensive Crisis!!!
Mood stabil­izers
Dizziness, fatigue, short-term memory loss, increased urination, GI upset, dry mouth, muscular weakness, tremors, excessive loss of sodium can lead to toxicity
In the absence of sodium (Na), the cells take in lithium instead
lithium toxicity
Transient gastro­int­estinal symptoms are the earliest side effects to occur Mild degree of fine tremor of the hands may persist throughout therapy Thirst and polyuria may be followed by increased drowsi­ness, ataxia, tinnitus and blurred vision, indicating early toxicity As intoxi­cation progresses the following manife­sta­tions may occur: confusion, increasing disori­ent­ation, muscle twitches, hyperr­efl­exia, nystagmus, seizures, diarrhea, vomiting, and eventually coma and death
CNS stimulants
Insomnia, anxiety, restle­ssness, agitation, signif­icant nausea­/vo­miting, anorexia (give with food), Cough, dry mouth, Tachyc­ardia, hypert­ension, arrhyt­hmias --> monitor and watch for signs of cardio­vas­cular disease
dose in AM or early afternoon
Typical antips­ych­otics
dizziness, drowsi­ness, orthos­tatic hypote­nsion, dry mouth, dry eyes, consti­pation, blood dyscrasias (abnormal lab tests)
EPS and NMS occur with typical antips­ych­otics
Atypical antips­ych­otics (cloza­pine)
signif­icant agranu­loc­ytosis, seizures, tachyc­ardia, NMS • BUT HAS NO EPS
Atypical antips­ych­otics (all the rest)
drowsi­ness, dizziness, dry mouth, hyperg­lyc­emia, changes in choles­terol levels, weight gain, EPS
Barbit­urates for seizures
Soft tissue irritant – avoid injecting if possible IM – inflam­mation; IV – tissue necrosis Can cause vitamin defici­encies (D, B12, folate) • Requires adequate supple­men­tation
dysrhy­thmias, headache, nystagmus, confusion, slurred speech, changes urine colour (red/b­rown), blood dyscra­sias, hyperg­lyc­emia, gingival hypert­rophy, skin reactions, osteop­orosis
Valproic Acid
: sedation, GI upset, prolonged bleeding time, visual distur­bances, ataxia, vertigo, muscle weakness, hepato­tox­icity, pancre­atitis, bone marrow suppre­ssion
mental and physical impair­ment, psychosis, behavi­oural changes, CNS effects, bone marrow suppre­ssion
dopamine agonist
reduced impulse control
Opioid Analgesics
sedation, fatigue, euphoria, confusion, consti­pation, respir­atory depres­sion, nausea, vomiting
Opioid Antagonist
minimal toxicity, however the effect of reversing analgesia will cause increased blood pressure, tremors, hyperv­ent­ila­tion, nausea­/vo­miting and drowsiness (i.e. sudden withdrawal symptoms)
gastric and epigastric discom­fort, increased bleeding time, nausea, possible nephro­tox­icity, cardio­vas­cular events with long term use
possible liver damage (hepat­otoxic metabo­lite), causes less gastric irritation than aspirin, does not affect blood coagul­ation BUT can interact with warfarin
Fatigue, weight gain, heartburn, ataxia, dizziness very common
Pregabalin (Lyrica®)
Dizziness, fatigue, peripheral edema, dry mouth
better tolerated than Gabapentin
infect­ions, hyperg­lyc­emia, hypert­ension, thinning skin, easy bruising, moon face, osteop­orosis, HPA-axis suppre­ssion
Muscle relaxants
sedation, dry mouth, urinary retention (antic­hol­inergic effects)
tingling, mucosal irrita­tion, CNS toxicity, cardio­vas­cular collapse
Duloxetine (Cymba­lta®)
Nausea, dizziness, fatigue all common
dizziness, drowsi­ness, warming & prickling sensation, may experience rebound headache Vasoco­nst­riction =↑ BP
Ergot Alkaloids
leg weakness, muscle pain in extrem­ities, nausea and vomiting
Serotonin Syndrome
↑ risk when >1 drug that increases serotonin in the body
Not always obvious due to promis­cuity – triptans, tramadol, etc.
symptoms: Hypert­ension, tremors, sweating, shivering, confusion, anxiety, restle­ssness, tachyc­ardia, muscle twitching
Anywhere from 30 mins after dose --> weeks after dose of the 2nd drug

Emotional & Mood Disorders

Mood Disorders (Bipolar)
Post-t­rau­matic Stress Disorder (PTSD)
Attention Deficit Hypera­ctivity Disorder (ADHD)
Many more (hundreds)

Medication for Emotional & Mood Disorders

1.Tric­yclic antide­pre­ssants (TCAs)
Work by inhibiting reuptake of norepi­nep­hrine, serotonin, and dopamine, leaves more neurot­ran­smitter within cleft
-tript­yline; -pramine -oxepine
2.Sele­ctive serotonin inhibiters
Work by inhibiting reuptake of serotonin only
Citalo­pram, escita­lopram, fluoxe­tine, fluvox­amine, paroxe­tine, sertraline
3. Monoamine oxidase inhibitors (MAOIs)
Reserved for people who haven’t responded to SSRI or TCA
Inhibits monoamine oxidase (MAO) which breaks down norepi­nep­hrine leaves more norepi­nep­hrine in the synaptic cleft
breaks down dopamine, epinep­hrine, and serotonin leaves more of these neurot­ran­smi­tters as well causing many side effects and intera­ctions
Phenel­zine, tranyl­cyp­romine, moclob­emide
4. Atypical antide­pre­ssants
Inhibiting reuptake of serotonin, norepi­nep­hrine and dopamine activity with different affinities Also work on other receptors like histamine
Bupropion (Wellb­utrin®, Zyban®­)(N­DRI), mirtaz­apine (Remer­on®­)(S­NRI), venlaf­axine (Effex­or®­)(S­NRI), duloxetine (Cymbl­ata­®)(­SNRI), trazodone (Desry­l®)­(SARI)
Mood stabil­izers
Work by altering sodium transport across cell membranes By altering sodium transport, it influences the release, synthesis, and reuptake of multiple neurot­ran­smi­tters
Primarily used for bipolar disorder (manic­-de­pre­ssion)
Lithium carbonate
Antico­nvu­lsants: carbam­aze­pine, divalp­roex, lamotr­igine, valproic acid, gabape­ntin, topiramate
Antico­nvu­lsants are also used as mood stabil­izers because they also alter transport of ions across cell membranes
CNS stimulants
Work by height­ening awareness and increasing focus (non-specifically)
Primarily used for ADHD in children and adults
All cause an increase in attent­iveness and heightened awareness by influe­ncing NE and D release somehow
Methyl­phe­nidate (Ritalin®, Concerta®, Biphen­tin®) Dextro­amp­het­amine (Dexed­rine®) Dextro­amp­het­amine and amphet­amine (Adder­all®) Lisdex­amf­etamine (Vyvanse®)

Degene­rative diseases

Parkinson's disease
Gradual destru­ction of neurons from substantia nigra → striatum of brain that use dopamine to commun­icate
Movements and impulses essential to perfor­mance of movements
↓ number of dopami­nergic neurons → ↓ dopamine
Symptoms are a charac­ter­ization of ↓ dopamine
Parkin­son's symptoms
Classic features:
Tremor, Bradyk­inesia, Rigidity, Loss of balance
Other features;
Depression, anxiety, mood change, Memory loss --> dementia, Difficulty concen­tra­ting, Change in sense of smell, Change in sleeping patterns, Consti­pation, light-­hea­ded­ness, sweaty, Difficulty swallo­wing, chewing, speaking, blinking
A term that describes a decline in a variety of functions (e.g. memory, language, motor activi­ties, ability to recognize or identify objects, complex decisi­on-­making) which eventually causes a person to have difficulty performing everyday activities
Types of Dementia
Alzhei­mer’s Disease
amyloid plaques and tangles
Vascular Dementia
reduced blood supply
Fronto­tem­poral Dementia
younger patients, highly genetic, odd behaviours
Lewy Body Dementia
presence of Lewy Bodies, well-f­ormed halluc­ina­tions
Parkin­son’s Disease Dementia
Parkin­son’s usually diagnosed first – both neurod­ege­ner­ative
Parkin­son's disease manage­ment: All pharma­cot­herapy focuses on ↑ dopamine levels (directly or indire­ctly)

Classes of medication for Parkin­son's

Effective corner­stone of therapy
Dopamine cannot cross blood-­brain barrier (BBB) The enzyme that creates dopamine (decar­box­ylase) is everywhere in the body
Levodopa → crosses BBB → converted to dopamine via decarboxylase
It is a prodrug
Levodopa is always paired with either carbidopa or benser­azide (decar­box­ylase inhibitors that DO NOT cross BBB),
which does two things:
1) Enhances distri­bution to brain
2) Minimizes acute side effects Because conversion to dopamine occurring past BBB (mostly)
Dopamine Agonists
stimulate dopamine receptors
MAO-B Inhibitors (MAOIs)
inhibit the enzyme that breaks down dopamine
either releases more dopamine or inhibits re-uptake of dopamine (exact mechanism unknown)
also anti-viral
COMT Inhibitors
inhibit peripheral conversion of levodopa to dopamine (making levodopa more efficient)
block acetyl­cho­line, which restores balance of acetyl­choline and dopamine
for tremor only
All other medica­tions for Parkin­son's (excluding Levodopa) work to either directly or indirectly to↑ dopamine in brain

Classes of medication for Dementia

Treatment of Dementia
1.Chol­ine­sterase Inhibitors
Donepezil, galant­amine, rivast­igmine
Prevent breakdown of acetyl­choline (Theory: lack of acetyl­choline causes plaques & tangles)
May show small improv­ements in measures of cognition and activities of daily living (ADL) (1-3 points on MMSE)
May slow progre­ssion (by months, not years)
If benefit, seen in 3-6 months
Only approved for Alzhei­mer’s but prescribed for all types
2.N-me­thy­l-D­-as­partate (NMDA) antagonist
Block glutamate (excit­atory amino acid) at NMDA receptor (Theory: persistent activation of NMDA contri­butes to symptoms)
No effect on acetylcholine
Alone or in combo with cholin­est­erase inhibitor – directly confli­cting evidence re: benefit
Indica­tion: Moderate → Severe Alzheimer’s
Renally excreted (dosage adjustment needed for impair­ment)
Management of Behavi­oural & Psycho­logical Symptoms of Dementia (BPSD)
Antips­ych­otics, benzod­iaz­epines, antide­pre­ssants, stimulants and more

Classi­fic­ation of Pain

A.Acute pain
Intense, Less than 6 months
E.g. sprained ankle
B. Chronic pain
Persists for longer than 6 months, Interferes with daily activi­ties, Associated with feelings of hopelessness
E.g. permanent nerve injury
A. Nociceptor
Pain Due to injury to tissues
Sharp, localized; or Dull, throbbing, aching
E.g. paper cut, broken bones
B. Neurop­athic Pain
Due to injury to nerves
Burning, shooting, numbing
E.g. nerve injury, shingles
Pharma­col­ogical management
Requires thorough:
Health history (including allergies)
BPMH – best possible medication history
Includes an assessment of stress, coping mechan­isms, potential for dependency
Baseline assessment including character, location, duration and intensity of pain


Goal of treatment
To reduce acute pain via
1.Triptans or
2.Ergot alkaloids
To prevent further migraines from occurring
If patient experi­ences a signif­icant amount of migraines
β-bloc­kers, antico­nvu­lsants (topir­amate, valproic acid), calcium channel blockers, TCAs, venlaf­axine
Classes of drugs for migraines
Selective serotonin receptor agonist on intrac­ranial blood vessels and sensory nerves on the trigeminal system
Causes vasoco­nst­riction and reduces neurogenic inflam­mation, relieving migraine headache
Used for acute cluster headaches or migraines (with or without aura) as early as possible
Available as regular oral tabs, oral disint­egr­ating tablets, inject­ions, nasal spray (due to frequent nausea­/vo­miting) – we want quick onset
Expensive (require EDS in Sask)
Interaction with any other drug that also ↑ serotonin  serotonin syndrome
Tolerance can develop – remind patients to use only when necessary and as few doses as needed
2.Ergot alkaloids
Serotonin receptor agonist and interacts with dopamine and adrenergic receptors (α-blo­cker)
Therefore, more adverse effects
Dihydr­oer­got­amine – given IV, may see repeated admini­str­ation for 3-7 days to break cycle of repeat migraines
Additive vasoco­nst­riction --> coronary vasospasm
Mostly used if triptans fail
Migraine Monito­ring:
History of migraines, triggers, and previous treatment, focus on prevention
Effect­iveness of treatment (assess pain level)
Blood pressure and pulse
Watch for chest pain, palpit­ations, confusion, tingling in extrem­ities, or sudden change of headache status (Fever? Rash? Stiff neck?)
Headaches are usually a symptom

Nervous system

Branches of peripheral nervous system
1.Somatic nervous system
Voluntary control over skeletal muscles
2. Autonomic nervous system
Involu­ntary control over smooth and cardiac muscle and glands Divided into sympat­hetic and parasy­mpa­thetic
Autonomic nervous system
1. Sympat­hetic
Activated under stress Fight-­or-­flight response Primitive response to avoid harm
2. Parasy­mpa­thetic
Activated under non-st­ressful conditions Rest-a­nd-­digest response

Primary neurot­ran­smi­tters in the periphery

Norepi­nep­hrine (NE)
Binds with adrenergic receptors
Alpha (α) receptors (α1 & α2)
α1-adr­energic Receptors In sympat­hetic target organs except heart
α2-adrenergic Receptors At presyn­aptic adrenergic neuron terminals
Beta (β) receptors (β1 & β2)
β1-adr­energic Receptors Mostly in heart muscle
β2-adrenergic Receptors Mostly in the lungs
Acetyl­choline (Ach)
Binds with cholin­ergic receptors
Muscarinic receptors
Binding to muscarinic receptor varies between stimul­atory and inhibitory action, depending on site
Nicotinic receptors
Skeletal muscle, smooth muscle, glands
Not many useful drugs affect nicotinic receptors

Adverse effects of autonomic drugs

saliva­tion, sweating, abdominal cramping and hypote­nsion
dry mouth, consti­pation, urinary retention, confusion, tachycardia
Less mucous production = dry mouth, eyes, nose
Pupil dilation, blurre­d/d­ouble vision, increased intrao­cular pressure
Less sweating = ↑ in body temp
Urinary retention = ↑ risk of infection
CNS = Agitation, inability to concen­trate, confusion -> delirium, halluc­ina­tions, illogical thinking, incoherent speech
Oral - anxiety, restle­ssness, tremor, hypert­ension, tachycardia
Nasal – burning of mucosa, rebound congestion if used for long periods
adrenergic antagonist β1 -blocking
bradyc­ardia, hypote­nsion, headache, fatigue, dizziness, sleep distur­bances, nausea; most are dose-r­elated and appear early in therapy Rebound tachyc­ardia, arrhyt­hmias and infarction if discon­tinued suddenly

Anxiety and Sleep Disorders

Anxiety Disorders
Genera­lized anxiety disorder (GAD) ,Phobias, Panic disorders, Obsess­ive­-co­mpu­lsive disorder (OCD), Post-t­rau­matic stress disorder (PTSD)
Sleep Disorders
Either an inability to: Fall asleep, Stay asleep, or Both
In both anxiety and sleep disorders, nonpha­rma­col­ogical management is more effective LONG TERM

Medica­tions provide relief but should be used for SHORT TERM if possible in addition to non-ph­arm­aco­logical management

CNS depres­sants

Intensify GABA (bind to benzod­iaz­epine receptors on a GABA receptor)
Enhance GABA (bind to barbit­urate receptor on GABA receptor)
Commonly also use a benzod­iaz­epine receptor to potentiate GABA, but much more specific
Bind only to GABA1 for sleep Only cause sedation no anxiolytic or antico­nvu­lsant properties
Can act on any neurot­ran­smitter any drug that causes sedation can potent­ially be used to induce or prolong sleep even if it is an adverse effect
Includes antihi­sta­mines such as diphen­hyd­ramine (Benad­ryl®), dimenh­ydr­inate (Gravol®) or hydrox­yzine (Atarax®)
CNS depression is a continuum
muscle relaxa­tio­n>s­eda­tio­n>i­nduce sleep>­ane­sth­esi­a>c­oma­>death
Slow down neural activity in the brain, May or may not be specific for certain neurot­ran­smi­tters

Classes of Medication for Psychosis

Typical antipsychotics
conven­tional, 1st generation
- good at managing positive symptoms,
no dependence
D > 5HT
More side effects (espec­ially EPS) than atypical
A. Phenot­hia­zines
Blocks post-s­ynaptic dopamine receptors; also blocks histamine and muscarinic receptors
Used to manage mania and psychosis, prevention and treatment of nausea and vomiting
other phenot­hia­zin­es:­Flu­phe­nazine, Methot­rim­epr­azine, Perphe­nazine, Promazine, Triflu­ope­razine
B. Non-Ph­eno­thi­azines
Blocks post-s­ynaptic dopamine receptors
Used to manage psychotic disorders, Touret­te’s, manic states; also an antiemetic
other non-ph­eno­thi­azines: Flupen­tixol, Loxapine, Pimozide, Thioth­ixene, Zuclop­ent­hixol
Atypical anti-psychotics
unconv­ent­ional, 2nd generation
Newer class – now drugs of choice
No dependence
More specific for serotonin than dopamine receptors, with different affinities
Also bind to α-rece­ptors in periphery
Less side effects (espec­ially EPS) than typica­ls/1st Gen
Blocks dopamine receptors; also blocks serotonin, muscar­inic, and histamine receptors Reserved only for treatm­ent­-re­sistant schizo­phrenia because of adverse effects
does not have EPS
B. Quetiapine (Seroq­uel®)
Blocks serotonin receptors; also slightly blocks dopamine receptors
Used to treat schizo­phrenia and bipolar disorder; also used in the behavi­oural and psycho­logical symptoms of dementia (BPSD)
Others atypic­als­:Ol­anz­apine (Zyprexa®) Risper­idone (Rispe­rdal®) Palipe­ridone (Invega®) Zipras­idone (Zeldox®)
A.Arip­ipr­azole (Abilify®)
Partial dopamine and serotonin agonist; also serotonin antagonist at other sites
Used for schizo­phr­enia, bipolar, and depression (as an add-on)
Fewer side effects but not as effective as others
Will also see combin­ations of antide­pre­ssants, mood stabil­izers, and benzod­iaz­epines
Antips­ych­otics are not a cure for schizo­phrenia – but they are effective if continued
Medica­tions are only effective for as long as the client takes the medication – no dependence
They often have multiple undesi­rable side effects:
Agranu­loc­ytosis, EPS, weight gain, sedation, dyskin­esias, antich­oli­nergic effects
Effect­iveness can lead to discon­tin­uation

Seizure disorders

a distur­bance of electrical activity in the brain that can affect consci­ous­ness, motor activity, and sensation
Not every seizure consists of convulsions
Many types starting with local (one section) or genera­lized (whole brain)
involu­ntary, violent spasms of the large skeletal muscles of face, neck, arms, and legs
a disorder charac­terized by recurrent seizures
Those seizures can be any type
You can experience a seizure without having epilepsy
Causes of seizures
Infectious diseases
Trauma to head
Metabolic disorders like dehydr­ation, hypogl­ycemia, kidney disease, electr­olyte imbalances
Vascular diseases causing lack of oxygen
Pediatric disorders febrile seizures
Seizure Threshold
the balance between excitatory and inhibitory forces in the brain which affect how suscep­tible a person is to sei­zures
Important: many drugs that alter CNS activity can lower the seizure threshold – this leads to many potential drug intera­ctions

Classes of Medication for seizure disorders

Drugs that potentiate GABA
Potentiate GABA (inhib­itory) and suppress the firing ability of neurons by stimul­ating an influx of Cl-
CNS depres­sants
Takes several weeks for control
May be used as monoth­erapy
Causes least sedation
Follows CNS depression spectrum
Dependence and withdrawal occur
Intensify GABA by binding to benzod­iaz­epine receptors, which stimulates an influx of Cl-
Work very quickly if injected (used in status epilep­ticus)
Usually an adjunct to other drugs because of dependence and tolerance – reason to use short-term only
Follow CNS depression spectrum
As an anti-c­onv­ulsant, used for short-term seizure control, calming and relaxation
Primidone – some classify as a barbiturate
Topiramate – a combo of mechanisms (blocks Na+ influx, enhances GABA at some receptors - different from benzod­iaz­epines, and more)
Drugs that suppress Na+ influx
Desens­itize Na+ channels, which prevents influx of Na+ (different from blocking or antagonizing)
Sodium movement is a main factor that determines whether neuron will undergo an action potential (excitation)
No dependence or tolerance
Not all require lab monitoring
In CNS action potentials Na+ > Ca+
(phenytoin and fosphe­nytoin)
Very common, treats many types of seizures
Very narrow therap­eutic range – requires monitoring
LOTS of drug intera­ctions with antico­agu­lants, cortic­ost­eroids, supple­ments; impairs oral contra­cep­tives and some antibi­otics
b.Misc­ell­aneous (pheny­toi­n-like)
carbam­aze­pine, lamotr­igine, valproic acid (& divalproex)
Still desens­itizes sodium channels, which prevents influx of Na+
Used for absence and mixed-type seizures
Drugs that suppress Ca+ influx
Ethosu­ximide and methsu­ximide
Block calcium channels, which delays Ca+ influx, which depresses the activity of neurons in the motor cortex
Calcium influx is not as dominant as sodium influx
In CNS action potentials Na+ > Ca+
b. Gabapentin
– unknown mechanism for antico­nvu­lsant activity
Is shaped like GABA (hence the name), but does NOT bind to GABA receptors
Binds to calcium channels to reduce calcium influx
Used mostly for neurop­athic pain and migraines now
We use drugs that can:
a.Stim­ulate an influx of Cl- ions, which potent­iates GABA
b.Delay an influx of Na+
c.Delay an influx of Ca+
In CNS action potentials Na+ > Ca+

Drug Classes for Pain

a.Opioid analgesics
Work in spinal cord and brain (CNS) to alter perception of pain
Moderate to severe pain
Some used for anesthesia
Different levels of potenc­y/e­fficacy – all are compared to morphine (Gold Standard)
Routes for admini­str­ation
Oral: Systemic effects all over the body at opioid receptors
Parent­eral: Localized or systemic – depends how we do it
Routes: PO, IV, IM, SC, rectal, epidural, intrat­hecal
Remember – 5mg PO ǂ 5mg IV
Duration of action:
PO – 4 to 7h
IV – 4 to 5h
Epidural – 4 to 24h
Opioid dependency
Physical dependence lasts 7 days
Psycho­logical dependence can last many months or years
Often, patients switch from IV and inhalation forms to oral form called methadone
A long lasting opioid that avoids withdrawal symptoms by stimul­ating receptors, with no euphoria
Has a long t½ - most only need to dose once daily (still patient variation)
opioid antagonist
Naloxone and naltrexone
Compet­itively binds to and blocks mu and kappa receptors
Blocking opioid receptors would only biolog­ically change something in someone taking an opioid
Used to reverse opioid effects
Can be a diagnostic tool
Opioid antagonist used to reverse opioid toxicity (i.e. respir­atory depression is the lethal symptom)
Higher affinity for opioid receptors, therefore displaces opioid (compe­titive antagonist)
No euphoria, no dependence or tolerance
Schedule II (for emergency purposes only)
Effects = instant withdrawal symptoms:
Pain, hypert­ension, sweating, anxiety, irrita­bility + (very uncomf­ortable to patient, but not life-threatening)
Not a substitute for ambulatory care, but can keep someone alive longer
If opioid agonist is longer acting than naloxone (i.e. methad­one), toxicity could return
b.Non opioid analgesics
Work in peripheral tissues to prevent formation of pain impulses
Most non-op­ioids are also effective for fever, inflam­mation, and analgesia
Used for mild or moderate pain associated with inflammation
Acetam­inophen vs. NSAIDs
Acetam­inophen does not have anti-i­nfl­amm­atory properties
Both have anti-p­yretic and analgesic effects
Non-st­eroidal anti-i­nfl­amm­atory drugs

Aspirin (ASA), ibuprofen, naproxen (OTC)
Primary drugs for the treatment of mild to moderate inflammation
Inhibit cyclo-­oxy­genase (COX), a key enzyme in the biosyn­thesis of prostaglandins
Prosta­gla­ndins promote inflammation
Reducing prosta­gla­ndins effect­ively reduces inflammation
NSAIDs can be selective for COX-2 or non-se­lective ALSO antico­agu­lant, antipy­retic, anti-inflammatory
Primary use: for fever, arthritis, mild to moderate muscul­osk­eletal pain, dysmenorrhea
Some drug intera­ctions
Caution in elderly due to poor kidney function
No ASA in children – Reye’s Syndrome
Reduce fever at level of hypoth­alamus and dilation of peripheral blood vessels
Enables sweating and dissip­ation of heat
Primary use is to relieve mild-m­oderate pain and reduce fever
No anti-i­nfl­amm­atory actions
Focus is the CNS used for neurop­athic pain
while shaped similarly to GABA, does not bind to GABA receptors; binds to calcium channels and reduces calcium influx
b.Preg­abalin (Lyrica®)
reduces calcium influx at nerve terminals, which may reduce transm­ission of nerve pain
Cortisol is released by adrenal glands in response to stimuli to help restore body to normal
Drugs synthe­tically made to mimic cortisol
They are anti-i­nfl­amm­atory and immuno-suppressive
Primary use: for severe inflam­mation or immuno­-su­ppr­ession
Muscle relaxants
Methoc­arb­amol, cyclob­enz­aprine, baclofen, hyoscine
After sustaining an injury, muscle spasms may occur to stabilize the affected body part and prevent further damage - also generate pain
Most work in brain to reduce tonic, somatic motor activity in alpha and gamma systems
NOT on muscle cells
NOT at neurom­uscular junction
A drug that causes anesth­esia, reversible loss of sensation
Stabilize the neuronal membrane, preventing initiation and conduction of impulses
Primary use is surgery, epidurals
General: a reversible loss of consci­ousness
Local: a reversible loss of sensation for a limited region of the body while mainta­ining consci­ousness
Primary use is depres­sion, moving towards chronic pain
Migraines, nerve pain, fibrom­yalgia, etc.
Neurop­athic pain (due to effect on neurot­ran­smi­tters)
Citalo­pram, fluoxe­tine, sertra­line, paroxetine
Selective for serotonin, less side effects than TCAs
Also treat concurrent depression and anxiety disorders
May be effective for chronic fatigue, hot flashes, mostly used off-label for other pathol­ogi­cally similar conditions
Duloxetine (Cymba­lta®)
serotonin and norepi­nep­hrine reuptake inhibitor
Now indicated for pain associated with diabetic peripheral neurop­athy, fibrom­yalgia, chronic low back pain, and osteoa­rth­ritis of the knee
Also depression and genera­lized anxiety disorder
Anti-a­nxiety meds
Not a direct MOA, more of a co-mor­bidity of anxiety along with pain
Worry about tolerance and dependence with long term use
Encourage PRN (as needed) use, other coping mechan­isms, counse­lling
Pain management is subjective and difficult to manage due to consistent change of condition, tolerance, and dependence – and racism
Patient is guide to treatment
Difficult to know when to encourage more or less use of analgesics


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