PHARM250 Nervous system Cheat Sheet

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Classi​fic​ation of autonomic drugs Primary neurot​ran​smi​tters in the CNS (cont)

Stimulate parasy​mpa​thetic nervous system Cholin​ergic GABA inhibitory

parasy​mpa​tho​mimetic Norepi​nep​hrine (NE) stimul​atory
or muscarinic agonists
Dopamine (D) behaviour & movement
Inhibit parasy​mpa​thetic nervous system Anticholinergics
Glutamate stimul​atory
parasympatholytic
or muscarinic blockers
Adverse effects of CNS drugs
Stimulate sympat​hetic nervous system Adrenergic
Benzod​‐ drowsi​ness, sedation, memory loss, weakness, disori​‐
sympathomimetics
iaz​epine ent​ation, ataxia, sleep distur​bances, hypote​nsion,
or adrenergic agonists
blurre​d/d​ouble vision, nausea and vomiting
Inhibit sympat​hetic nervous system Adrenergic antagonists
Barbit​‐ Rarely prescribed anymore for anxiety or insomnia
anti-adrenergics
urates because of side effects
or adrenergic blockers
Hypnot​‐ dizziness, headache, daytime drowsi​ness, dyspepsia,
Classes of autonomic drugs ic/​sed​‐ dry mouth, bitter metallic taste, nausea, antero​grade
atives amnesia
Cholin​‐ Stimulate the parasy​mpa​thetic 1. Direct acting
Melatonin Adverse effects and monitoring mostly limited to
ergics nervous system 2.Indirect acting
drowsiness level (caution with endocrine dysfun​ction)
rest-and-digest
because it’s identical to endogenous
Receptor: Acetyl​choline (musca​‐
rinic) TCA's sedation, dizziness, orthos​tasis, blurred vision, dry
mouth, tachyc​ardia, cognitive impair​ment, consti​pation,
Antich​oli​‐ Inhibit the parasy​mpa​thetic nervous system, which
dry eyes, urinary retention
nergics induces fight-​or-​flight (sympa​thetic)
Adrenergic Stimulate the sympat​hetic nervous 1 agonist
system Result depends on type and 2 agonist
location of receptor (α or β) 1 agonist
2 agonist
Catecholamines
Adrenergic Inhibit sympat​hetic nervous system 1 antagonist
antagonist Action depends greatly on type of 1 antagonist 2
receptor (α or β) antagonist

Primary neurot​ran​smi​tters in the CNS

The CNS is respon​sible for our percep​tion, mood, consci​ous​ness,

behaviour, and cognition Therefore, drugs influence percep​tion,
mood, consci​ous​ness, behaviour, and cognition by altering neurot​‐
ran​smitter activity
Serotonin (5HT) mood

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Adverse effects of CNS drugs (cont) Adverse effects of CNS drugs (cont)

SSRI's Transient: headaches, nervou​sness, insomnia, nausea, lithium Transient gastro​int​estinal symptoms are the
diarrhea toxicity earliest side effects to occur Mild degree of
Long-term: Sexual dysfun​ction, withdrawal upon discon​tin​‐ fine tremor of the hands may persist
uation throughout therapy Thirst and polyuria may
be followed by increased drowsi​ness, ataxia,
MAOI's : consti​pation, dry mouth, headaches, changes in heart
tinnitus and blurred vision, indicating early
rate and blood pressure, insomnia, nausea, loss of
toxicity As intoxi​cation progresses the
appetite
following manife​sta​tions may occur:
Food intera​‐ foods containing tyramine = Hypert​ensive
confusion, increasing disori​ent​ation, muscle
ctions Crisis!!!
twitches, hyperr​efl​exia, nystagmus, seizures,
Mood Dizziness, fatigue, short-term memory loss, increased diarrhea, vomiting, and eventually coma and
stabil​‐ urination, GI upset, dry mouth, muscular weakness, death
izers tremors, excessive loss of sodium can lead to toxicity
CNS Insomnia, anxiety, restle​ssness, agitation, signif​icant
In the absence of sodium (Na), the cells take in lithium stimulants nausea​/vo​miting, anorexia (give with food), Cough, dry
instead mouth, Tachyc​ardia, hypert​ension, arrhyt​hmias -->
monitor and watch for signs of cardio​vas​cular disease
dose in AM or early afternoon

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Adverse effects of CNS drugs (cont) Adverse effects of CNS drugs (cont)

Typical dizziness, drowsi​ness, orthos​tatic hypote​nsion, dry Phenytoin dysrhy​thmias, headache, nystagmus, confusion,
antips​‐ mouth, dry eyes, consti​pation, blood dyscrasias slurred speech, changes urine colour (red/b​rown),
ych​otics (abnormal lab tests) blood dyscra​sias, hyperg​lyc​emia, gingival hypert​rophy,
EPS and NMS occur with typical antips​ych​otics skin reactions, osteop​orosis

Atypical signif​icant agranu​loc​ytosis, seizures, tachyc​ardia, NMS Valproic : sedation, GI upset, prolonged bleeding time, visual
antips​‐ • BUT HAS NO EPS Acid distur​bances, ataxia, vertigo, muscle weakness,
ych​otics hepato​tox​icity, pancre​atitis, bone marrow suppre​ssion
(cloza​‐ Succin​‐ mental and physical impair​ment, psychosis, behavi​‐
pine) imides oural changes, CNS effects, bone marrow suppre​ssion
Atypical drowsi​ness, dizziness, dry mouth, hyperg​lyc​emia, dopamine reduced impulse control
antips​‐ changes in choles​terol levels, weight gain, EPS agonist
ych​otics Opioid sedation, fatigue, euphoria, confusion, consti​pation,
(all the Analgesics respir​atory depres​sion, nausea, vomiting
rest)
Barbit​‐ Soft tissue irritant – avoid injecting if possible IM –
urates for inflam​mation; IV – tissue necrosis Can cause vitamin
seizures defici​encies (D, B12, folate) • Requires adequate
supple​men​tation

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Adverse effects of CNS drugs (cont) Adverse effects of CNS drugs (cont)

Opioid minimal toxicity, however the effect of reversing Cortic​ost​‐ infect​ions, hyperg​lyc​emia, hypert​ension, thinning skin,
Antagonist analgesia will cause increased blood pressure, eroids easy bruising, moon face, osteop​orosis, HPA-axis
tremors, hyperv​ent​ila​tion, nausea​/vo​miting and suppre​ssion
drowsiness (i.e. sudden withdrawal symptoms) Muscle sedation, dry mouth, urinary retention (antic​hol​inergic
NSAIDs gastric and epigastric discom​fort, increased bleeding relaxants effects)
time, nausea, possible nephro​tox​icity, cardio​vas​cular Anesth​‐ tingling, mucosal irrita​tion, CNS toxicity, cardio​vas​cular
events with long term use etics collapse
acetam​‐ possible liver damage (hepat​otoxic metabo​lite), Duloxetine Nausea, dizziness, fatigue all common
inophen causes less gastric irritation than aspirin, does not (Cymba​‐
affect blood coagul​ation BUT can interact with lta®)
warfarin
Triptans dizziness, drowsi​ness, warming & prickling sensation,
Gabapentin Fatigue, weight gain, heartburn, ataxia, dizziness very may experience rebound headache Vasoco​nst​riction
common =↑ BP
Pregabalin Dizziness, fatigue, peripheral edema, dry mouth Ergot leg weakness, muscle pain in extrem​ities, nausea and
(Lyrica®) Alkaloids vomiting
better tolerated than Gabapentin
Serotonin Syndrome
↑ risk when >1 drug that increases serotonin in the body
Not always obvious due to promis​cuity – triptans, tramadol, etc.
symptoms: Hypert​ension, tremors, sweating, shivering, confusion,
anxiety, restle​ssness, tachyc​ardia, muscle twitching
Anywhere from 30 mins after dose --> weeks after dose of the 2nd
drug

Emotional & Mood Disorders

Depression
Mood Disorders (Bipolar)
Post-t​rau​matic Stress Disorder (PTSD)
Attention Deficit Hypera​ctivity Disorder (ADHD)
Many more (hundreds)

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Medication for Emotional & Mood Disorders Medication for Emotional & Mood Disorders (cont)

Anti​‐ 1.Tr​icyclic Work by inhibiting reuptake of norepi​nep​‐ Bupropion (Wellb​utrin®, Zyban®​)(N​DRI), mirtaz​apine
dep​‐ antide​pre​‐ hrine, serotonin, and dopamine, leaves more (Remer​on®)​ (S​NRI), venlaf​axine (Effex​or®​)(S​NRI),
res​‐ ssants neurot​ran​smitter within cleft duloxetine (Cymbl​ata​®)(​SNRI), trazodone (Desry​l®)​‐
sants (TCAs) (SARI)
-trip​tyline; -pramine -oxepine Mood Work by altering sodium transport across cell
2.Se​lective Work by inhibiting reuptake of serotonin only stabil​‐ membranes By altering sodium transport, it influences
serotonin izers the release, synthesis, and reuptake of multiple neurot​‐
inhibiters ran​smi​tters
(SSRIs) Primarily used for bipolar disorder (manic​-de​pre​ssion)
Cital​opram, escita​lopram, fluoxe​tine, fluvox​amine, paroxe​‐ Lithium carbonate
tine, sertra​line Antico​nvu​lsants: Antico​nvu​lsants are also
3. Reserved for people who haven’t responded carbam​aze​pine, divalp​‐ used as mood stabil​izers
Monoamine to SSRI or TCA roex, lamotr​igine, because they also alter
oxidase Inhibits monoamine oxidase (MAO) which valproic acid, gabape​‐ transport of ions across cell
inhibitors breaks down norepi​nep​hrine leaves more ntin, topiramate membranes
(MAOIs) norepi​nep​hrine in the synaptic cleft CNS Work by height​ening awareness and increasing focus
breaks down dopamine, epinep​hrine, and stimulants (non-specifically)
serotonin leaves more of these neurot​ran​‐ Primarily used for ADHD in children and adults
smi​tters as well causing many side effects All cause an increase in attent​iveness and heightened
and intera​ctions awareness by influe​ncing NE and D release somehow
Phene​lzine, tranyl​cyp​romine, moclob​emide
4. Atypical Inhibiting reuptake of serotonin, norepi​nep​‐
antide​pre​‐ hrine and dopamine activity with different
ssa​nts affinities Also work on other receptors like
histamine

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Medication for Emotional & Mood Disorders (cont) Degene​rative diseases (cont)

Methy​lph​enidate (Ritalin®, Concerta®, Biphen​tin®) Dextro​amp​het​‐ Alzhei​mer’s Disease amyloid plaques and tangles
amine (Dexed​rine®) Dextro​amp​het​amine and amphet​amine (Adder​‐ Vascular Dementia reduced blood supply
all®) Lisdex​amf​etamine (Vyvan​se®)
Fronto​tem​poral younger patients, highly genetic, odd
Dementia behaviours
Degene​rative diseases
Lewy Body Dementia presence of Lewy Bodies, well-f​ormed
Parkinson's disease Gradual destru​ction of neurons from
halluc​ina​tions
substantia nigra → striatum of brain that use
Parkin​son’s Disease Parkin​son’s usually diagnosed first – both
dopamine to commun​icate
Dementia neurod​ege​ner​ative
Movements and impulses essential to
perfor​mance of movements Parkin​son's disease manage​ment: All pharma​cot​herapy focuses on
↓ number of dopami​nergic neurons → ↓ ↑ dopamine levels (directly or indire​ctly)
dopamine
Symptoms are a charac​ter​ization of ↓ Classes of medication for Parkin​son's
dopamine Levodopa Effective corner​stone of therapy
Parkin​son's Classic features: Dopamine cannot cross blood-​brain barrier (BBB) The
symptoms Tremor, Bradyk​inesia, Rigidity, Loss of enzyme that creates dopamine (decar​box​ylase) is
balance everywhere in the body
Other features; Levodopa → crosses BBB → converted to dopamine
Depression, anxiety, mood change, Memory via decarboxylase
loss --> dementia, Difficulty concen​tra​ting, It is a prodrug
Change in sense of smell, Change in Levodopa is always paired with either carbidopa or
sleeping patterns, Consti​pation, light-​hea​‐ benser​azide (decar​box​ylase inhibitors that DO NOT
ded​ness, sweaty, Difficulty swallo​wing, cross BBB),
chewing, speaking, blinking which does two things:
Deme​ntia A term that describes a decline in a variety 1) Enhances distri​bution to brain
of functions (e.g. memory, language, motor 2) Minimizes acute side effects Because conversion
activi​ties, ability to recognize or identify to dopamine occurring past BBB (mostly)
objects, complex decisi​on-​making) which Dopamine stimulate dopamine receptors
eventually causes a person to have difficulty Agonists
performing everyday activities MAO-B inhibit the enzyme that breaks down dopamine
Types of Dementia Inhibitors
(MAOIs)
Amantadine either releases more dopamine or inhibits re-uptake of
dopamine (exact mechanism unknown)
also anti-v​iral
COMT inhibit peripheral conversion of levodopa to dopamine
Inhibitors (making levodopa more efficient)

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Classes of medication for Parkin​son's (cont) Classi​fic​ation of Pain

Anticholinergics block acetyl​cho​line, which restores balance of Dura​tion

acetyl​choline and dopamine A.Acute pain Intense, Less than 6 months
for tremor only E.g. sprained ankle
All other medica​tions for Parkin​son's (excluding Levodopa) work to B. Chronic Persists for longer than 6 months, Interferes with
either directly or indirectly to↑ dopamine in brain pain daily activi​ties, Associated with feelings of
hopelessness
Classes of medication for Dementia E.g. permanent nerve injury
Trea​tment of Dementia Source
1.Chol​ine​‐ Prevent breakdown of acetyl​choline (Theory: lack A. Nociceptor Pain Due to injury to tissues
sterase of acetyl​choline causes plaques & tangles) Sharp, localized; or Dull, throbbing, aching
Inhibitors May show small improv​ements in measures of E.g. paper cut, broken bones
Donepezil, cognition and activities of daily living (ADL) (1-3 B. Neurop​‐ Due to injury to nerves
galant​amine, points on MMSE) athic Pain Burning, shooting, numbing
rivast​igmine May slow progre​ssion (by months, not years) E.g. nerve injury, shingles
If benefit, seen in 3-6 months
Pharma​col​ogical management
Only approved for Alzhei​mer’s but prescribed for
Requires thorough:
all types
Health history (including allergies)
2.N-me​thy​l-D​- Block glutamate (excit​atory amino acid) at NMDA
BPMH – best possible medication history
as​partate receptor (Theory: persistent activation of NMDA
Includes an assessment of stress, coping mechan​isms, potential for
(NMDA) contri​butes to symptoms)
dependency
antagonist No effect on acetylcholine
Baseline assessment including character, location, duration and
Memantine Alone or in combo with cholin​est​erase inhibitor –
intensity of pain
directly confli​cting evidence re: benefit
Indica​tion: Moderate → Severe Alzheimer’s
Migraines
Renally excreted (dosage adjustment needed for
Goal of To reduce acute pain via
impair​ment)
treatment 1.Triptans or
Mana​gement of Behavi​oural & Psycho​logical Symptoms of
2.Ergot alkaloids
Dementia (BPSD)
To prevent further migraines from occurring
Antips​ych​otics, benzod​iaz​epines, antide​pre​ssants, stimulants and
If patient experi​ences a signif​icant amount of migraines
more
β-bloc​kers, antico​nvu​lsants (topir​amate, valproic acid),
calcium channel blockers, TCAs, venlaf​axine
Classes of drugs for migraines

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Migraines (cont) Nervous system (cont)

1.Triptans Selective serotonin receptor agonist on intrac​ranial 2. Involu​ntary control over smooth and
blood vessels and sensory nerves on the trigeminal Autonomic cardiac muscle and glands Divided into
system nervous sympat​hetic and parasy​mpa​thetic
Causes vasoco​nst​riction and reduces neurogenic system
inflam​mation, relieving migraine headache Autonomic 1. Activated under stress Fight-​or-​flight
Used for acute cluster headaches or migraines (with or nervous Sympat​‐ response Primitive response to avoid
without aura) as early as possible system hetic harm
Available as regular oral tabs, oral disint​egr​ating
2. Parasy​‐ Activated under non-st​ressful conditions
tablets, inject​ions, nasal spray (due to frequent
mpa​thetic Rest-a​nd-​digest response
nausea​/vo​miting) – we want quick onset
Expensive (require EDS in Sask)
Primary neurot​ran​smi​tters in the periphery
Interaction with any other drug that also ↑ serotonin
serotonin syndrome Norepi​‐ Binds with adrenergic receptors
Tolerance can develop – remind patients to use only nep​‐
when necessary and as few doses as needed hrine
(NE)
2.Ergot Serotonin receptor agonist and interacts with dopamine
alkalo​ids and adrenergic receptors (α-blo​cker) Alpha (α) α1-adr​energic Receptors In sympat​hetic
Therefore, more adverse effects receptors target organs except heart
Dihydr​oer​got​amine – given IV, may see repeated (α1 & α2) α2-adrenergic Receptors At presyn​aptic
admini​str​ation for 3-7 days to break cycle of repeat adrenergic neuron terminals
migraines Beta (β) β1-adr​energic Receptors Mostly in heart
DO NOT GIVE WITHIN 24 HOURS OF TRIPTAN receptors muscle
Additive vasoco​nst​riction --> coronary vasospasm (β1 & β2) β2-adrenergic Receptors Mostly in the
Mostly used if triptans fail lungs

Migraine Monito​ring: Acetyl​‐ Binds with cholin​ergic receptors

History of migraines, triggers, and previous treatment, focus on choline
prevention (Ach)
Effect​iveness of treatment (assess pain level) Muscarinic Binding to muscarinic receptor varies
Blood pressure and pulse receptors between stimul​atory and inhibitory action,
Watch for chest pain, palpit​ations, confusion, tingling in extrem​ities, depending on site
or sudden change of headache status (Fever? Rash? Stiff neck?)
Nicotinic Skeletal muscle, smooth muscle, glands
Headaches are usually a symptom
receptors Not many useful drugs affect nicotinic
receptors
Nervous system

Branches of peripheral 1.Somatic Voluntary control over

nervous system nervous system skeletal muscles

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Adverse effects of autonomic drugs Anxiety and Sleep Disorders (cont)

Cholin​ergics saliva​tion, sweating, abdominal cramping and Sleep Either an inability to: Fall asleep, Stay asleep, or
hypote​nsion Disorders Both
Anticholinergics dry mouth, consti​pation, urinary retention, In both anxiety and sleep disorders, nonpha​rma​col​ogical
confusion, tachycardia management is more effective LONG TERM
Less mucous production = dry mouth, eyes, nose
Pupil dilation, blurre​d/d​ouble vision, increased Medica​tions provide relief but should be used for SHORT TERM if
intrao​cular pressure possible in addition to non-ph​arm​aco​logical management
Less sweating = ↑ in body temp
Urinary retention = ↑ risk of infection CNS depres​sants
CNS = Agitation, inability to concen​trate,
confusion -> delirium, halluc​ina​tions, illogical
1.Benz​odi​‐ Intensify GABA (bind to benzod​iaz​epine receptors on a
thinking, incoherent speech
aze​pines GABA receptor)
α-adre​nergics Oral - anxiety, restle​ssness, tremor, hypert​ension,
2.Barb​itu​‐ Enhance GABA (bind to barbit​urate receptor on GABA
tachycardia
rates receptor)
Nasal – burning of mucosa, rebound congestion if
3.Hypn​oti​‐ Commonly also use a benzod​iaz​epine receptor to
used for long periods
cs/​Sed​‐ potentiate GABA, but much more specific
adrenergic bradyc​ardia, hypote​nsion, headache, fatigue,
atives
antagonist β1 - dizziness, sleep distur​bances, nausea; most are
Bind only to GABA1 for sleep Only cause sedation no
blocking dose-r​elated and appear early in therapy
anxiolytic or antico​nvu​lsant properties
Rebound tachyc​ardia, arrhyt​hmias and infarction if
discon​tinued suddenly 4.Misc​ell​‐ Can act on any neurot​ran​smitter any drug that causes
aneous sedation can potent​ially be used to induce or prolong
Anxiety and Sleep Disorders sleep even if it is an adverse effect

Anxiety Genera​lized anxiety disorder (GAD) ,Phobias, Panic Includes antihi​sta​mines such as diphen​hyd​ramine
Disorders disorders, Obsess​ive​-co​mpu​lsive disorder (OCD), Post- (Benad​ryl®), dimenh​ydr​inate (Gravol®) or hydrox​yzine
t​rau​matic stress disorder (PTSD) (Atarax®)
CNS muscle relaxa​tio​n>s​eda​tio​n>i​nduce sleep>​ane​sth​esi​‐
depression a>c​oma​>death
is a
continuum

Slow down neural activity in the brain, May or may not be specific for
certain neurot​ran​smi​tters

Classes of Medication for Psychosis

Typical antipsychotics conven​tional, 1st generation

- good at managing positive symptoms,
no dependence
D > 5HT
More side effects (espec​ially EPS) than
atypical

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Classes of Medication for Psychosis (cont) Classes of Medication for Psychosis (cont)

A. Phenot​hia​zines Blocks post-s​ynaptic dopamine B. Blocks serotonin receptors; also slightly blocks
Chlorpromazine receptors; also blocks histamine and Quetiapine dopamine receptors
muscarinic receptors (Seroq​‐ Used to treat schizo​phrenia and bipolar disorder; also
Used to manage mania and psychosis, uel®) used in the behavi​oural and psycho​logical symptoms of
prevention and treatment of nausea and dementia (BPSD)
vomiting Others atypic​als​:Ol​anz​apine (Zyprexa®) Risper​idone (Rispe​rdal®)
other phenot​hia​zin​es:​Flu​phe​nazine, Methot​rim​epr​azine, Perphe​‐ Palipe​ridone (Invega®) Zipras​idone (Zeldox®)
nazine, Promazine, Triflu​ope​razine Misc​ell​ane​ous
B. Non-Ph​eno​thi​azines Blocks post-s​ynaptic dopamine A.Arip​ipr​‐ Partial dopamine and serotonin agonist; also serotonin
Haloperidol receptors azole antagonist at other sites
Used to manage psychotic disorders, (Abilify®) Used for schizo​phr​enia, bipolar, and depression (as an
Touret​te’s, manic states; also an add-on)
antiemetic Fewer side effects but not as effective as others
other non-ph​eno​thi​azines: Flupen​tixol, Loxapine, Pimozide, Thioth​‐ Will also see combin​ations of antide​pre​ssants, mood
ixene, Zuclop​ent​hixol stabil​izers, and benzod​iaz​epines
Atypical anti-psychotics unconv​ent​ional, 2nd generation Antips​ych​otics are not a cure for schizo​phrenia – but they are
Newer class – now drugs of choice effective if continued
No dependence Medica​tions are only effective for as long as the client takes the
More specific for serotonin than medication – no dependence
dopamine receptors, with different They often have multiple undesi​rable side effects:
affinities Agranu​loc​ytosis, EPS, weight gain, sedation, dyskin​esias, antich​oli​‐
Also bind to α-rece​ptors in periphery nergic effects
Less side effects (espec​ially EPS) than Effect​iveness can lead to discon​tin​uation
typica​ls/1st Gen
A.Cloz​apine Blocks dopamine receptors; also blocks Seizure disorders
serotonin, muscar​inic, and histamine Seizure a distur​bance of electrical activity in the brain that can
receptors Reserved only for treatm​ent​- affect consci​ous​ness, motor activity, and sensation
re​sistant schizo​phrenia because of Not every seizure consists of convulsions
adverse effects Many types starting with local (one section) or genera​lized
does not have EPS (whole brain)

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Seizure disorders (cont) Classes of Medication for seizure disorders (cont)

Convul​‐ involu​ntary, violent spasms of the large skeletal muscles b.Benzodiazepines Intensify GABA by binding to benzod​iaz​epine
sions of face, neck, arms, and legs receptors, which stimulates an influx of Cl-
Epilepsy a disorder charac​terized by recurrent seizures Work very quickly if injected (used in status
Those seizures can be any type epilep​ticus)
You can experience a seizure without having epilepsy Usually an adjunct to other drugs because of
dependence and tolerance – reason to use
Causes of Infectious diseases
short-term only
seizures Trauma to head
Follow CNS depression spectrum
Metabolic disorders like dehydr​ation, hypogl​ycemia,
kidney disease, electr​olyte imbalances Diazepam As an anti-c​onv​ulsant, used for short-term
Vascular diseases causing lack of oxygen seizure control, calming and relaxation
Pediatric disorders febrile seizures c.Misc​ell​aneous Primi​done – some classify as a barbiturate
Tumours ​ mate – a combo of mechanisms (blocks
Topira
Seizure the balance between excitatory and inhibitory forces in Na+ influx, enhances GABA at some receptors
Threshold the brain which affect how suscep​tible a person is - different from benzod​iaz​epines, and more)
to sei​zures Drugs that suppress Na+ influx
Important: many drugs that alter CNS activity can lower Desens​itize Na+ channels, which prevents
the seizure threshold – this leads to many potential drug influx of Na+ (different from blocking or
intera​ctions antagonizing)
Sodium movement is a main factor that
Classes of Medication for seizure disorders determines whether neuron will undergo an
Drugs that potentiate GABA action potential (excitation)
No dependence or tolerance
a.Barbiturates Potentiate GABA (inhib​itory) and suppress the firing
Not all require lab monitoring
ability of neurons by stimul​ating an influx of Cl-
In CNS action potentials Na+ > Ca+
CNS depres​sants
Takes several weeks for control
May be used as monoth​erapy
Pheno​bar​bital Causes least sedation
Follows CNS depression spectrum
Dependence and withdrawal occur

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Classes of Medication for seizure disorders (cont) Drug Classes for Pain (cont)

a.Hyda​ntoins Very common, treats many types of seizures a.Opioid Work in spinal cord and brain (CNS) to alter
(phenytoin and Very narrow therap​eutic range – requires analge​sics perception of pain
fosphe​nyt​oin) monitoring Moderate to severe pain
LOTS of drug intera​ctions with antico​agu​‐ Some used for anesthesia
lants, cortic​ost​eroids, supple​ments; impairs Different levels of potenc​y/e​fficacy – all are
oral contra​cep​tives and some antibi​otics compared to morphine (Gold Standard)
b.Misc​ell​aneous Still desens​itizes sodium channels, which Routes for Oral: Systemic effects all over the body at opioid
(pheny​toi​n-like) prevents influx of Na+ admini​str​‐ receptors
carba​maz​epine, Used for absence and mixed-type seizures ation Parent​eral: Localized or systemic – depends how we
lamotr​igine, do it
valproic acid (& Morphine Routes: PO, IV, IM, SC, rectal, epidural, intrat​hecal
divalproex) Remember – 5mg PO ǂ 5mg IV
Drugs that suppress Ca+ influx Duration of action:
a.Succinimides Block calcium channels, which delays Ca+ PO – 4 to 7h
Ethosuximide and influx, which depresses the activity of neurons IV – 4 to 5h
methsu​ximide in the motor cortex Epidural – 4 to 24h
Calcium influx is not as dominant as sodium Opioid Physical dependence lasts 7 days
influx dependency Psycho​logical dependence can last many months or
In CNS action potentials Na+ > Ca+ years
b. Gabapentin – unknown mechanism for antico​nvu​lsant Often, patients switch from IV and inhalation forms to
activity oral form called methadone
Is shaped like GABA (hence the name), but Methad
​ one A long lasting opioid that avoids withdrawal
does NOT bind to GABA receptors symptoms by stimul​ating receptors, with no euphoria
Binds to calcium channels to reduce calcium Has a long t½ - most only need to dose once daily
influx (still patient variation)
Used mostly for neurop​athic pain and
migraines now

We use drugs that can:

a.Stim​ulate an influx of Cl- ions, which potent​iates GABA
b.Delay an influx of Na+
c.Delay an influx of Ca+
In CNS action potentials Na+ > Ca+

Drug Classes for Pain

Anal​ges​ics

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Drug Classes for Pain (cont) Drug Classes for Pain (cont)

opioid Compet​itively binds to and blocks mu and kappa b.Non opioid Work in peripheral tissues to prevent formation
antagonist receptors analge​sics of pain impulses
Naloxone Blocking opioid receptors would only biolog​ically Most non-op​ioids are also effective for fever,
and naltre​‐ change something in someone taking an opioid inflam​mation, and analgesia
xone Used to reverse opioid effects Used for mild or moderate pain associated with
Can be a diagnostic tool inflammation
naloxone Opioid antagonist used to reverse opioid toxicity (i.e. Aceta​min​ophen vs. NSAIDs
respir​atory depression is the lethal symptom) Acetam​inophen does not have anti-i​nfl​amm​‐
Higher affinity for opioid receptors, therefore displaces atory properties
opioid (compe​titive antagonist) Both have anti-p​yretic and analgesic effects
No euphoria, no dependence or tolerance Non-s​ter​oidal anti- Primary drugs for the treatment of mild to
Schedule II (for emergency purposes only) i​nfl​amm​atory moderate inflammation
Effects = instant withdrawal symptoms: drugs Inhibit cyclo-​oxy​genase (COX), a key enzyme
Pain, hypert​ension, sweating, anxiety, irrita​bility + NSAIDs in the biosyn​thesis of prostaglandins
(very uncomf​ortable to patient, but not life-threatening) Aspirin (ASA), Prosta​gla​ndins promote inflammation
Not a substitute for ambulatory care, but can keep ibuprofen, Reducing prosta​gla​ndins effect​ively reduces
someone alive longer naproxen (OTC) inflammation
If opioid agonist is longer acting than naloxone (i.e. NSAIDs can be selective for COX-2 or non-se​‐
methad​one), toxicity could return lective ALSO antico​agu​lant, antipy​retic, anti-
inflammatory
Primary use: for fever, arthritis, mild to
moderate muscul​osk​eletal pain, dysmenorrhea
Some drug intera​ctions
Caution in elderly due to poor kidney function
No ASA in children – Reye’s Syndrome

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Drug Classes for Pain (cont) Drug Classes for Pain (cont)

Aceta​‐ Reduce fever at level of hypoth​alamus and dilation of Muscle relaxa​‐ After sustaining an injury, muscle spasms may
min​‐ peripheral blood vessels nts occur to stabilize the affected body part and
ophen Enables sweating and dissip​ation of heat Methocarbamol, prevent further damage - also generate pain
Primary use is to relieve mild-m​oderate pain and reduce cyclob​enz​aprine, Most work in brain to reduce tonic, somatic
fever baclofen, motor activity in alpha and gamma systems
No anti-i​nfl​amm​atory actions hyoscine NOT on muscle cells
Misc​ell​‐ Focus is the CNS used for neurop​athic pain NOT at neurom​uscular junction
ane​ous Anes​the​tics A drug that causes anesth​esia, reversible loss
a.Gaba​‐ while shaped similarly to GABA, does not bind to GABA of sensation
pentin receptors; binds to calcium channels and reduces Stabilize the neuronal membrane, preventing
calcium influx initiation and conduction of impulses
Primary use is surgery, epidurals
b.Preg​‐ reduces calcium influx at nerve terminals, which may
General: a reversible loss of consci​ousness
abalin reduce transm​ission of nerve pain
Local: a reversible loss of sensation for a limited
(Lyrica®)
region of the body while mainta​ining consci​‐
Cort​ico​‐ Cortisol is released by adrenal glands in response to
ousness
ste​roids stimuli to help restore body to normal
Anti​-de​pre​ssa​nts
Drugs synthe​tically made to mimic cortisol
They are anti-i​nfl​amm​atory and immuno-suppressive TCAs Primary use is depres​sion, moving towards
Primary use: for severe inflam​mation or immuno​-su​ppr​‐ chronic pain
ession Migraines, nerve pain, fibrom​yalgia, etc.
Neurop​athic pain (due to effect on neurot​ran​‐
smi​tters)

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Drug Classes for Pain (cont)

SSRI's Selective for serotonin, less side effects than TCAs

Citalopram, Also treat concurrent depression and anxiety
fluoxe​tine, disorders
sertra​line, May be effective for chronic fatigue, hot flashes,
paroxe​tine mostly used off-label for other pathol​ogi​cally
similar conditions
Dulox​etine serotonin and norepi​nep​hrine reuptake inhibitor
(Cymba​lta®) Now indicated for pain associated with diabetic
peripheral neurop​athy, fibrom​yalgia, chronic low
back pain, and osteoa​rth​ritis of the knee
Also depression and genera​lized anxiety disorder
Anti​-an​xiety Benzodiazepines
meds Not a direct MOA, more of a co-mor​bidity of
anxiety along with pain
Worry about tolerance and dependence with long
term use
Encourage PRN (as needed) use, other coping
mechan​isms, counse​lling

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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