Drug Treats Mechanism

Anti-Epileptic Drugs (AEDs) - Fitzy

Ethosuximide
Absence seizures
*Narrow spectrum Blocks CaV3.1 ONLY
(Generalized onset)
*Old AED

Valproic Acid (Valproate) Generalized onset seizures

*Broad spectrum (first-line broad spectrum) & Lots
*Old AED Absence seizures

Clonazepam (BZD) DOC for Myoclonic seizures &

*Old AED subcortical myoclonus
All BZDs (Benzodiazepines):
--Binds post-synaptic GABA-A Cl
Status Epilepticus (given IV) channel → allosteric change that
Diazepam and Lorazepam
*IV Fosphenytoin used as potentiates GABA binding (↑ rec.
(BZDs)
backup if these don’t work in 5 sensitivity to GABA)
*Old AED
min

Phenytoin
Tonic-clonic seizures Block NaV channels (prolong fast
*Narrow spectrum
(Generalized or partial onset) inactivation)
*Old AED

Primidone/Phenobarbital
Tonic-clonic seizures Binds post-synaptic GABA-A Cl
(& other Barbiturates)
(Generalized or partial onset) channels → hyperpol / Cl influx
*Old AEDs

Carbamazepine
Tonic-clonic seizures Block NaV channels (prolong fast
*Narrow spectrum
(Partial-onset only) inactivation)
*Old AED

Partial Onset Seizures (simple

Gabapentin Binds CaV channels
and complex)
 Partial Onset Seizures (simple
Pregabalin Multiple mechanisms
and complex)
Partial Onset Seizures (simple Block NaV channels (prolong fast
Oxcarbazepine
and complex) inactivation)

Partial Onset Seizures (simple Block NaV channels (enhance slow

Lacosamide
and complex) inactivation / stabilize slow state)

Partial Onset Seizures (simple

Tiagabine Inhibits GABA reuptake
and complex)
Partial Onset Seizures (simple Inhibits GABA metabolism (by
Vigabatrin
and complex) GABA-T)
Partial Onset Seizures (simple
Ezogabin Opens voltage gated K channels
and complex)

Blocks NaV channels (prolong fast

Lamotrigine (LMT) Broad spectrum; lots
incactivation) & N- / P-type CaV

*Post-synaptic: does 2 things

1. AMPA (glutamate) receptor
Topirimate Broad spectrum; lots antagonist at ligand-gated ion
channels (Na and Ca)
2. GABA-A receptor agonist

Binds synaptic vesicle protein

Levetiracetam Broad spectrum; lots
(SV2A) → dec glutamate release

Zonisamide Broad spectrum; lots Block NaV & T-type Ca channels

Analgesics - Opioids / Narcotics - Fitzy

Morphine is the proto-type (Mu
General
receptor agonist)
Raphe nuclei & Periaqueductal
grey area are good hints you're
talking about opioid receptors

Clinical effects:
*Supra-spinal analgesia
*μ (MOR) binds Endorphins *Euphoria
(peptides) *CNS & resp depression
*Miosis (pupil contraction)
*GI & Uterine motility
Receptors

*Pre- AND Post-synaptic

receptors on dorsal horn of
spinal cord (pain/temp path)
Receptors
Clinical Effects:
*Pre- AND Post-synaptic *κ (KOR) binds Dynorphins *Spinal analgesia
receptors on dorsal horn of (peptides) *Sedation
spinal cord (pain/temp path) *Miosis, GI / uterine motility

*δ binds Enkephalins,
Endorphins (peptides)

*Very LOW oral potency of 20%

Morphine (high 1st pass clearance)
*t1/2 = 2 hours

Group 1 Mu Agoninsts
*Full agoninsts *High oral potency (90%)
Methadone
*Parenteral & Oral *t1/2 = 27 hours

*The "M--ine/one" drugs

*Causes mydriasis (pupil dilation,
Meperidine which is the opposite of other
opioids)
*Subset: Hydromorphone,
Need much lower dose for effect;
Oxymorphone, &
only Levo has high oral potency
Levorphanol

Group 2 Mu Agoninsts
*Full Agoninsts
*Short acting
*100x more potent than
morphine or methadone
*The "-anyl" drugs
Remifentanyl
*Used in anesthesia
Fentanyl *Strong Mu agonist (meperidine
analog)
*Used in induction of general IV
Sufentanil
anesthesia
*VERY short acting; gaining
popularity over meperidine for
childbirth analgesia

*Analgesia for moderate pain

Group 3 Mu Agoninsts Codeine &
*Anti-tussive (cough relief - Mu
*Codeine-related Codein related drugs
independent)
*Partial agoninsts (Hydrocodone, Oxycodone)
*Reliable oral absorption (50%)
*Given in combo with
Acetaminophen
Group 3 Mu Agoninsts
*Codeine-related
*Partial agoninsts
*Given in combo with
Acetaminophen
Honorable Mentions
Insoluble Opioid Agoninsts
*Act on Mu rec. in gut
*Anti-diarrheals
Partial / Mixed
(Agoninsts / Antagoninsts)
Illegal Drugs
Opioid Receptor Antagonists
*Used to treat opioid OD
(pinpoint pupils, stupor, &
RR < 12 breaths/min)
Non-narcotic Analgesics
Local Anesthetics - Kruse
*Very safe and effective Anti-
Dextromethorphan
tussive agent
Hydromorphone & *Analgesics
Oxymorphone *NO active metabolite!!
*Moderate Mu agonist
Tramadol *Reliable oral abs. (70%)
*Inhibits catecholamine reuptake
*Low risk due to low CNS/BBB
Loperamide & Diphenoxylate
penetration and low solubility
*Supra-spinal analgesia
*Can precipitate withdrawal (in
Pentazocine
abusers)
*SE: tachy & hallucinations
*Analgesia
*Can precipitate withdrawal (in
Buprenorphine abusers)
*Office-based detox/maintenance in
combo with naloxone
Heroin *Active metabolite is Di-acetylemorphine → Pene
*Occupy but do NOT activate Mu
General Features of Mu receptors
Antagonists *Can precipitate withdrawal
symptoms in the short-term
Naloxone *IV form (ZERO oral absorption)
Naltrexone *P.O. form
Methyl-Naltrexone *GI specific
*"-profen" drugs
NSAIDS / COX inhibitors
*"-ac" drugs
 *Vasoconstrictors (α1) like Epi can
be used to prolong their duration and
Lidocaine (medium)
decrease system absorption &
Mepivacaine (medium)
toxicity
Bupivacaine (long) *Two "i's" = amide class
--NEVER inject Epi into tissues
Ropivacaine (long) *One "i" = ester class
supplied by end-arteries b/c it can
Articaine (medium)
cause gangrene (fingers, toes, ears,
Benzocaine *MOA: block NaV channels
nose, penis)
Cocaine (medium) (@ inner vestibule of channel)
Procaine (short)
*Cocaine has inherent α1 affects &
Tetracaine (long)
does NOT need a vasoconstrictor
with it

CNS
CNS *Low dose: sleepiness, light-
*High conc: nystagmus, headedness, visual/auditory
Side Effects
muscular twitching, and disturbances, restlessness
convulsions --Signs: circumoral (around mouth)
& tongue numbness + metallic taste

Benzocaine *Topical agent only

*Long duration & prolonged

Bupivacaine
anesthesia

*Mostly used as topical anesthetic

Cocaine
of upper resp tract
Local Anesthetics we will
actually use *Use topically due to toxicity with
Dibucaine
injections

Lidocaine *Prototype amide local anesthetic

*Only used for infiltration

anesthesia (inject of anesthetic
Procaine
directly into area of termina nerve
endings)

General Anesthetics (Inhaled & IV) - Kruse

*Anesthetics target synapses of neurons to decrease signaling → by either increasi
General MOA
receptors OR K efflux channels) or decreasing excitatory signals (Ach, AMPA, NM
Stages I to IV: III is the most important (stage of surgical anesthesia) where Pt does
Stages of Anesthesia
reestablished
Inhaled Anesthetics
General Info
*All are "volitile" anesthetics
& are liquids (↑ BP, ↓ vapor
pressure) at room temp except
Nitrous Oxide (is opposite)
*All cause resp depression &
mucociliary fxn (dec resp to
CO & mucus pooling/post-op
infection)
Desflurane
Nitrous Oxide
Sevoflurane
Isoflurane
Enflurane
Halothane
Intravenous (Parenteral/Non-oral) Anesthetics
Dexmedetomidine
Diazepam (Valium)
*A benzodiazepine
Opioid Analgesics as adjunct
treatments
*Blood:Gas partition coefficient:
--Defines the blood solubility of
drug
*Brain:blood partition
--Has inverse relationship with the
coefficient: just shows that all
rate of anesthesia onset (drug w/
the drugs are more solubule in
low blood solubility reach high
the brain than in the blood
arterial pressure rapidly, which
causes equally rapid equilibration to
brain & fast onset of action)
Specific Side Effects Column
*B:G = 0.42 (↓ blood solubility)
*MAC = 6-7% Increased HR
*B:G = 0.47
*MAC > 100%
*B:G = 0.69
Renal toxicity (fluride ion products)
*MAC = 2.0%
*B:G = 1.4
Increased HR
*MAC = 1.4%
*B:G = 1.8
Renal toxicity (fluride ion products)
*MAC = 1.7%
Bradycardia, hepatitis / liver
*B:G = 2.3 (↑ blood solubility)
toxicity (jaundice, arthralgias,
*MAC = 0.75%
myalgias, rash, anorexia)
*Hypnosis & analgesic effects at lvl
*α2 agonist of spinal cord (more resembles a
sleep state)
*Used in perioperative period
*Increase GABA-A receptor
(before surgery) due to amnesia
sensitivity
effect
*IV fentanyl, sufentanil,
*Opioid/Mu receptor agonists
remifentail, and morphone
 *Provides CV stability
*Decreased Steroidogenesis
*Enhances actions of GABA on
Etomidate *Involuntary muscle movements
GABA-A receptors
*Induction of anesthesia and
conscious sedation

*Used in balanced anesthesia &

Fentanyl
conscious sedation
*Reversible by Naloxone
*Prod marked analgesia
*Prodrug that is cleaved to *Effects same as propofol but
Fospropofol
propofol prolonged

*CV stimulation & Symp stim.

*Inc. cerebral blood flow
Ketamine
*Emergency reactions that impair
(Called "Special K" in the *NMDA receptor antagonist
recovery
land of the gays)
*SE: vivid dreams hallucinations,
out of body experiences

Lorazepam (Ativan)
*Preferred over thiopental for
Methohexital
short ambulatory procedures
*Used in balanced anesthesia &
Midazolam (Versed) conscious sedation
*Reversible by Flumazenil *Provides CV stability & marked
amnesia

*Used in induction of anesthesia &

maintenance
*Can cause hypotension

*Has strong anti-emetic (anti-

*Targets GABA-A rec &
Propofol (Piprivan)
potentiates Cl influx current
vomit / nausea) action
*SE: Extreme hypotension / dec in
BP due to profound vasodilation
(also inhibits baroreflex resp)
--Potent respiratory depressent
(causes apnea, useful for intubation)

Increased duration of Cl
Thiopental
channel opening (from GABA- Induce CYP450 enzymes
*A barbiturate
A rec)
Drugs of Movement Disorders - Kruse
*These are mostly to Tx
parkinsonism (TRAP *DA agonists used for Pt < 65 y/o
General
symptoms - tremor, rigidity, *Levodopa/carbidopa for Pt > 65
akinesia, postural instability)

*Precursor to dopamine
*Treats Parkinsonism
*D2 receptor agonist
Levodopa (L-Dopa) --Lowers mortality/symptoms but
*Rapidly absorbed by SI; only
does NOT stop progression
1-3% reaches brain

DOPA decarboxylase inhibitor *Given with L-Dopa to ↑ its life;

Carbidopa
that does not cross the BBB dec. daily requirements by 75%
*History of melanoma
Contra-indications for L- *Monoamine oxidase A
*Pt w/ angle-closure glaucoma
Dopa inhibitors (causes HTN crisis)
*Pt w/ active peptic ulcer

*D2 agonist / Ergot alkaloid

derivative
*Also Tx endocrine disorders
Dopamine Receptor Agonists Bromocriptine (hyperprolactinemia, acromegaly)
*H/L of 15 hours
*Pt wont respond well to these *Extensive first pass metabolism
if he does not respond to L- by CYP3A4
Dopa
*Used in addition to L-dopa *D3 receptor agonist
for end-dose akinesia or on- *Also Tx RLS (restless leg
off phenomenon Pramipexole syndrome)
*All peak in conc within 1-3 *H/L of 8 hours; 90% excreted in
hours (2hrs on average) urine
*Treat Parkinsonism if Pt <
age 65
for end-dose akinesia or on-
off phenomenon
*All peak in conc within 1-3
hours (2hrs on average)
*Treat Parkinsonism if Pt <
age 65
Monoamine oxidase (MAO)
inhibitors
*"-giline" drugs
COMT Inhibitors
*Prolong effects of levodopa
by inhibiting peripheral
metabolism
*"-capone" drugs
Apomorphine
Amantadine
Anti-cholinergic agents
Tremor Treatments
*D2 receptor agonist
*Tx RLS
Ropinirole
*Metabolized by hepatic CYP1A2
*H/L of 2 hours
*MAO-A: metabolizes NE and Serotonin
*MAO-B: metabolizes phenylethylamine and benzyl
Monoamine Oxidases --Dopamine and tryptamine are metabolized equally
*Use of L-Dopa + non-selective MAO inhibitor ca
accumulation of NE --> this MUST BE AVOIDED
Irreversible MAO-B inhibitor
Selegiline (Deprenyl)
(also inhibits MOA-A @ high concs)
Irreversible MAO-B inhibitor
Rasagiline
(more potent than selegiline)
COMT (Catechol-O- *Metabolizes L-Dopa to 3-O-methyldopa (competes
methyltransferase) across intestinal mucosa & BBB)
Both central & peripheral effects
Tolcapone *Can cause hepatotoxicity & inc.
liver enzymes
Entacapone Peripheral effects only
*Dopamine agonist @ post- *Subcutaneous injection for quick
synaptic D2 receptors in temp relief of off-periods of
caudate-putamen akinesia (works w/in 10 min)
*Can cause livedo reticularis
*Anti-viral drug; MOA in (vascular condition w/ purplish
parkinsonism tx is unknown mottled discoloration of skin,
usually on legs)
Benztropine, biperiden,
orphenadrine, procyclidine, mAchR antagonists
trihexyphenidyl
Metoprolol & propranolol β1 receptor antagonists
Primidone Anti-epileptic drug
Topirimate Serotonin receptor agonist
Alprazolam BZD
Intramuscular injection of
botulinum toxin A

Huntingtons Disease
Treatments
Riluzole
Wilson's Disease Tx
*Copper storage disease due
to reduced ceruloplasmin
(shows high Cu in brain &
viscera)
Pharmacology of the Eye - Fitzy
Glaucoma
Open Angle Glaucoma
*Most common type
Themes
Drugs that Tx Glaucoma:
β2 agoninsts
*Isoproterenol & salbutanol
β1 antagoninsts
*Timolol
α2 agonists
*Brimonidine
*Apraclonidine / clonidine
Carbonic anhydrase
inhibitors (topical/eyedrops)
*Dorzolamide
*Acetazolamide
Reserpine *Impair dopaminergic
neurotransmission to alleviate
chorea by blocking vesicular
Tetrabenazine monoamine transporter
*Inhibits glutamate release and
blocks post-synaptic NMDA- and
Treats ALS
kainite-type glutamate receptors
*Inhibits NaV channels
Chelating agents that complexes
Penicillamine
with Cu and is excreted easily
Potassium disulfide Reduces intestinal absorption of Cu
Trientine Chelating agent
Increase fecal excretion of Cu by
Zinc acetate & zinc sulfate
decreased GI absorption
Due to ↑ IOP (intraocular pressure) from 2 modalities:
1. Increased inflow/secretion (creation of aqueous humor from pigmented iris epi
2. Decreased outflow of aqueous humor from trabechular meshwork / Schlemm's
↑ IOP due to ↓ outflow *Tx by ↓ inflow or ↑ outflow
*Adrenergics & "-amide's" decrease inflow / aqeuous humor secretion
*Muscarinics increase outflow from meshwork
*Prosta- drugs increase Uveoscleral outflow (which decreased in elderly)
Secretion (inflow) Trabecular outflow
↓ (decrease) ↑ (increase)
↓ (decrease) no change
↓ (decrease) no change
↓ (decrease) no change
mAchR agonists
no change ↑ (increase)
*Pilocarpine (M3 agonist)

Prostanoid FP receptor
agoninsts
no change no change
*Latanoprost
*Travoprost (fluprostenol)
Prostamines
no change ↑ (increase)
*Bimatoprost
Migraines and Headache Stuff - Fitzy
Process: Brainstem dysfxn sparks wave of excitatio
(CSD) --> stimulates H+ & K+ discharge causing va
*Migraine = neurovascular
reflex/blood shunting away from brain stimulates rel
headache due to dilation of
& nerves, causing dilation --> releases neuropeptid
Physiology / Patho-phys cranial blood vessels → causes
+ inflammatory agents (NO, histamine, PGs) → in
pain, sensory, & central nerve
nerve & transmits migraine pain thru TG system (d
activation
which are the key two mediators in the system)
**Organic nitrates (NO) used to tx CAD can prov

Prodrome phase Tx *5HT-1B/1D receptor agoninsts

Triptans:
--12-36 hours *Sub-Q injections (fastest), nasal
*Sumatriptan
spray, or tablet form
*Zolmitriptan
*Symptoms: yawning, --Only sumatriptan can be injection
depression, lethargy,
excitability, craving, distase
--This is a treatment for
prodrome problems and is *Less specific → interacts w/ α rec,
Ergot alkaloids
NOT entirely preventative dopamine rec, various 5HT rec
*Dihydroergotamine (DHE)
--Act as agonists, partial agonists,
*Ergotamine & caffeine
and antagonists

Headache phase Tx *Breakthrough headaches that have

*Photophobia, Phonophobia, vomiting should be treated with
NSAIDS & Acetaminophen
nausea, vomiting Ketorolac b/c it is the only
--4 to 72 hours injectiable NSAID!
 Propanolol & Timolol Beta blockers

Amitriptylene & Imipramine Tricyclic antidepressants

Topirimate & Valproate Anticonvulsants
Preventative Agents
Verapamil Ca channel blockers

Botox Cleaves SNAP-25

 Side effects
BAD: Weight gain, tremor, hair loss, neural polydactyly
tube defects in prego moms
Gingival hyperplasia, Hirsutism,
Hypocalcemia & Osteoporosis
*Powerful, non-specific CNS depression
*Causes increased duration in Cl channel opening
*Significant sedation & lethal respiratory
*High doses are GABA-independent
depression
*General: aplastic anemia, leukopenia,
neutropenia, thrombocytopenia,
Hypocalcemia and Osteoporosis
*Probs when STARTING CBZ:
--Inc clearance of oral contraceptives
--Inc clearance of warfarin (inc clotting)
*Life threatening allergic reaction / rash
No significant drug interactions
Notes
*Absence seizures are mediated by T-Type Ca ion
channels (CaV3.1), which mediate 3 Hz spikes and
wave activity in the thalamus
*Class D teratogen: can cause spina bifida, atrial
septal defect, cleft palate, hypospadias, &
*If used with Lamotrigine, will inhibit
glucuronidation of drugs by the UGT system &
cause parent drug buildup
*Causes Cl channels to open with greater frequency
*Is always GABA-dependent
*Status Epilepticus: caused by abrupt withdrawal of
AEDs, sedatives, etc. Often during Natural Disasters
*Contrast to Barbiturates: BZD's only increase
sensitivity/potentiation of GABA binding!
*Induces Hepatic CYP450 enzymes
*Class D teratogen: can cause spina bifida, atrial
septal defect, cleft palate, hypospadias, &
polydactyly
*Zero-order pharmacokinetics (doubling dose does
NOT double serum lvl)
*Induces Hepatic CYP450 enzymes
*Class D teratogen: can cause spina bifida, atrial
septal defect, cleft palate, hypospadias, &
polydactyly
*Rash reaction often due to Steven-Johnson
syndrome (rare disorder of mucous membranes)
*100% clearance is renal
 *100% clearance is renal

Hyponatriemia (esp in elderly) → inc resp *50% clearance is renal

of CT's to ADH (considered SIADH) *Analogue of carbamazepine

Reduces the amplitudes & freq of sustained

repetitive firing spikes when stimulus was prolonged

Urinary retention

*Rash reaction often due to Steven-Johnson

*Life threatening allergic reaction / rash
syndrome (rare disorder of mucous membranes)

*50% clearance is renal

Nephrolithiasis
*Memory: A good Top can Amp up the fun

*50% clearance is renal

*Well tolerated, no CYP interaction *Memory: Gotta use the LEVEr to pull up the
vesicles

*50% clearance is renal

*Can cause miosis (pin-point pupils) &

*Opioids also constrict Sphincter of Odi (controls
extreme constipation!! → look for these
bile!!)
in ER for opioid drug overdose

*They are coupled to G-proteins but have very little

to do with AC, cAMP, etc. These just stop Ca influx
MECHANISM:
pre-synaptically (NMDA rec) and cause K efflux
*Pre-synaptic: Opioid agoninsts bind
post-synaptically to decrease overall neural
receptors & prevent Ca influx = no
signaling
glutamate discharge & no action
potential carried thru NMDA rec
*Remember: respiratory depression from opioids
activation
can cause a respiratory acidosis! (shallow
breathing = keep CO2 --> increase H+)
*Post-synaptic: opioid agonist binds → K
---This also causes hyperkalemia
efflux & hyperpolarization
*On top of pain (trauma/cancer/etc), opioids are used
*Contra-indications: brain injury,
to treat Sickle Cell crisis, severe diarrhea, &
emphysema
dyspnea caused by pulmonary edema from left
ventricular failure
 to do with AC, cAMP, etc. These just stop Ca influx
MECHANISM:
pre-synaptically (NMDA rec) and cause K efflux
*Pre-synaptic: Opioid agoninsts bind
post-synaptically to decrease overall neural
receptors & prevent Ca influx = no
signaling
glutamate discharge & no action
potential carried thru NMDA rec
*Remember: respiratory depression from opioids
activation
can cause a respiratory acidosis! (shallow
breathing = keep CO2 --> increase H+)
*Post-synaptic: opioid agonist binds → K
---This also causes hyperkalemia
efflux & hyperpolarization
*On top of pain (trauma/cancer/etc), opioids are used
*Contra-indications: brain injury,
to treat Sickle Cell crisis, severe diarrhea, &
emphysema
dyspnea caused by pulmonary edema from left
ventricular failure

*Active metabolites are M-3-glucuronide,

M-6-glucuronide, & hydromorphone
--These are hepatically created by UGT
1A1 and UGT 2B7

*Can cause prolonged QT-interval in acute

*Used for Withdrawal/maintenance and
Detoxification
overduse or during long-term methadone treatment
--Not due to Mu receptors but w/ K+ HERG
channels in heart
--Memory: Doing Meth in the QT bathroom takes
longer

*Normeperidine (a toxic metabolite) can

accumulate and cause seizures
*Used for analgesia during childbirth

*Rapid onset & distribution (lipophilic)

*Transmucosal (given as lollipop) to help *Pt can heat up the Fentanyl patches at home and
breakthru pain while on morphine use a bunch at once to abuse them → watch for
*Transdermal patches are given to Pt for acute respiratory depression
home use (slows delivery/onset)

*It is metabolized in tissue (liver not

needed) and can be immediately cut off due
to its fast-acting nature

*Metabolized by CYP 2D6 - HY!!

--CYP 2D6 has a lot of gene allelic *Its active metabolite is morphine, which is why Pt
variation amongst the population (some can OD and die from codeine if they have an ultra
ppl metabolize ultra fast, normal, or fast CYP 2D6 allele
slow)
 *Opioid related but does NOT act on Mu
receptors

*If pt is put on these and then has morphine *Memory device: Water and Oxygen morph into
or other metabolite in system, suspect abuse no active metabolites

*Analgesia for moderate pain

*Associated with seizures
*Memory: Cats don't ride the Tram
*Caution use in Pt on tricyclic or SRI anti-
depressants
*Of course all opioids treat diarrhea, but
this is used OTC because of low abuse
potential

*κ agonist + μ partial agonist + δ antagonist

*μ partial agonist + κ & δ antagonist

acetylemorphine → Penetrates BBB rapidly → exaggerated euphoria & addiction potential

*Competitively displaces heroin,

morphine, fentanyl, etc

*Use for emergency settings: can reverse

coma & respiratory depression to
stabalize Pt and get read for oral doses of
Naltrexone
*Long duration of action (48 hrs for single *Memory: NalTrexone has a "T" because you can
oral dose) Take it by mouth
*Can treat opioid-induced constipation
without taking away the Pt's opioids
*Ketorolac is the only injectable NSAID
--VERY important for Pt who have emetic
issues and need an NSAID
 *Amides = metabolized in CYP450 in liver
--Typically more lipophilic w/ longer
*Quickly block Type A delta fibers (pain/temp)
duration
and Type C fibers (diffuse pain) because they are so
small (2-5μm)
*Esters = metabolized in plasma
--This is why it is harder to block Type A alpha
(hydrolyzed by butyrylcholinesterase)
fibers (motor & prop) since they are very large (12-
--Procaine is shortest duration; Tetracaine is
20 μm)
an exception and has long duration;
Benzocaine is surface use only

*CV: can cause systemic hypotension

(blocks cardiac Na channels = decrease
contractility, conduction rate, & arteriolar
dilation) *Allergic reactions are common to ester-type (one
*IV Lidocaine is Class 1b anti- "I") but very rare with amide-type local anesthetics
arrhythmic
*Bupivacaine most cardiotoxic due to long
duration

*Hemorrhoids, premature ejaculation,

anesthetic lube (NG tubes, catheters)
*Provides more sensory block than motor
block
*Blocks nerve impulses, causes *Can cause euphoric properties in CNS due to
vasoconstriction, & inhibits local NE re- inhibition of catecholamine reuptake (esp
uptake Dopamine)

*Gives faster, more intense, longer lasting

*Used as an antiarrhythmic agent
anesthesia than equal dose procaine

*Compared to newer agents, is less potent, *Metabolized to a para-aminobenzoic acid, which

slower onset, and shorter duration of action inhibits action of sulfonamide antibiotics

aling → by either increasing inhibitory signals (Chloride influx based channels w/ GABA and Glycine
signals (Ach, AMPA, NMDA, or 5-HT → blocks Na or Ca influx)
anesthesia) where Pt does not responsd to painful stimuli (trapezius squeeze) and breathing is
 MAC (Minimum alveolar concentration): the
*Factors that determine alveolar conc: anesthetic potency (ED50) of a drug → shows
1. Partial pressure / inspired conc (Fa) amount of drug required to prevent a response to
2. Alveolar ventilation (Fi) surgical incision in 50% of Pt
--The faster FA/FI approaches 1, the faster --Described as vol % (the percentage of atmosphere
the anesthesia will occur that is anesthetic at the MAC)
*↑ CO = ↓ FA & lowers rate of anesthesia --So, 1 MAC causes anesthesia in a Pt that will
(it increases drug uptake to blood & dilutes prevent movement so surgical incision, this means a
it in alveoli) dose of 1.4% atmosphere of isoflurance OR 0.75%
atmospheres for halothane

General Inhaled Anesthetic Side Effects

*Nausea and vomiting

Malignant Hyperthermia: can be caused if

inhaled volitile anesthetics are given with
succinylcholine (sudden onset tachy,
hyperthermia, hyperkalemia, acidosis)
--Tx is dantrolene

*Principally used for short-term sedation

of intubated and ventilated patients in
ICU setting or as adjunct to general
anesthesia

*Reversed by Flumazenil

*Used w/ large dose of BZD's to achieve

general aneshetic state
*Rapid onset, moderate recovery

Slow onset & recovery

*Causes paresthesias and pruritus (severe

itching) in genitals/perineal

*Can be drug of abuse → causes dissociated

anesthetic state of catatonia (inability to move
Moderately rapid onset and recovery normally), amnesia, and analgesia w/ or w/o loss
of consciousness (Pt's eyes remain open with
nystagmic gaze)

Rapid onset and recovery

Slow onset & recovery

*Rapidly metabolized in liver; also has

~30% metabolism outside of liver (mostly
lung)
*Most common parenteral anesthetic in US
*Water insoluble → infused using emulsion of
*Rapid onset and recovery (15-30 sec)
soybean oil, glycerol, and lecithin (solution is milky
white)
*Context-sensative half-life: dependent on
--This composition means it has potential to cause
rate of redistribution, accumulation in fat, &
allergic reactions
metabolic rate all w/ continuous infusion.
Propofols effects do not last long even after
continous infusion

*Induction agents, but usually you use

propofol or methohexital
Side Effects:
*GI: Nausea, anorexia, and/or vomiting in
80% of patients (chemo rec. trigger in brain)

*CV: postural hypotension, HTN (lg doses)

*"On-off Phenomenon" = while taking drug, Pt has
*Dyskinesias: Choreoathetosis off periods of marked akinesia alternate over course
(intermediate speed btwn twitchy motions of a few hours with on-periods of improved mobility
of chorea and writhing movements of but marked dyskinesia
athetosis) --Can also be due to dose wearing off before next
dose is taken
*Behavior: depression, anxiety, agitation, --Apomorphine can help tx Pt with bad off-periods
insomnia, confusion, delusions,
hallucinations, nightmares, euphoria, others
--Can be helped with anti-psychotic agents
like clozapine, olanzapine, quetiapine,
risperidone

*Drastically ↓ GI side effects of L-Dopa

*Do not give L-Dopa to psychotic

patients!

Side Effects:
*Same as L-Dopa except for:
--GI but add constipation, dyspepsia, and
reflux esophagitis
--Bromocriptine only: Digital vasospasm,
Contra-indications:
pleural & retroperitoneal fibrosis
*Pt with history of psychotic illness
--Same mental disturbances but more
*Recent MI or active peptic ulcure
severe than with L-Dopa
*Bromocriptine specifically in Pt with peripheral
--Misc: headache, nasal congestion,
vascular disease (vasoconstricting effects)
increased arousal, pulmonary infiltrates
**Rarely, Pt taking pramipexole or
ropinirole may feel uncontrollable
tendency to fall asleep at inappropriate
times
 severe than with L-Dopa
*Bromocriptine specifically in Pt with peripheral
--Misc: headache, nasal congestion,
vascular disease (vasoconstricting effects)
increased arousal, pulmonary infiltrates
**Rarely, Pt taking pramipexole or
ropinirole may feel uncontrollable
tendency to fall asleep at inappropriate
times

E and Serotonin
enylethylamine and benzylamine
e are metabolized equally by MAO-A and -B
lective MAO inhibitor can cause HTN crisis due to
his MUST BE AVOIDED

*Slows breakdown of dopamine, prolongs *Contra-indicated in Pt taking meperidine, tricyclic

anti-parkinsonism effect of L-Dopa antidepressants, or SRI

*Used as neuroprotective agent and for

early symptomatic treatment of PD
-O-methyldopa (competes w/ L-Dopa for transport
BBB)

Side Effects (SE):

*Orange discoloration of urine
*Diarrhea, abdominal pain, and sleep
disturbances

*SE: nausea (can pre-treat w/

trimethobenzamide), dyskinesias,
drowsiness, sweating, hypotension, and
injection brusing

*Can cause heart failure, urinary retention,

and GI issues
--Do not give to Pt with history of seizures
or heart failure!

*Can help w/ tremor and rigidity

*Can cause typical sympathetic SE's
(constipation, urinary retention, blurred
vision)
 *HD note: GABA & glutamic acid
decarboxylase (the enzyme that makes
GABA) are markedly reduced in basal
ganglia of HD patients → loss of inhibitory
signaling

Symptoms of Wilson's Disease:

*Neuro & hepatic
--Tremor, choreiform movements, rigidity,
hypokinesia, dysarthria, dysphagia
**Kayser-Fleischer ring (brown ring on
the edge of the iris of the eye)

r from pigmented iris epithelial cells)

ar meshwork / Schlemm's canal onto the eye

umor secretion

reased in elderly)

Uveoscleral outflow

no change

no change Bad in resp disease cases

↑ (increase) Also protects against loss of retinal ganglion cells

no change
 *Contracts ciliary muscle & widens spaces in the
trabecular meshwork

*Causes miosis (sphincter muscle contraction)

no change
--M3 antagonists (cyclopentolate, atropine,
scopolamine) cause mydriasis!!

--α1 agonists (phenylephrine, dipivefrin, NE) also

cause mydriasis! - from radial muscle contraction

↑ (increase) *Remodel the ciliary body & form partially

organized intermuscular tubes → involves matrix
metalloproteinases (MMP's) and tissue inhibitors of
metalloproteinases (TIMPS)
↑ (increase)

n sparks wave of excitation/depression in cortex Serotonin: has a vasoconstricting effect

& K+ discharge causing vasoconstriction -->
y from brain stimulates release of NO from TG vessels
n --> releases neuropeptides (CGRP & substance P)
NO, histamine, PGs) → inflammation irritates TG
e pain thru TG system (done by CGRP & NO,
iators in the system)
used to tx CAD can provoke migraine
*5HT-1B rec are on cranial vasculature & 5HT-
1D on peripheral nerves
Future reference:
*5HT2 (serotonin itself): aggregates blood platelets
*5HT-1A agoninsts: anxiolytic & anti-depression
*5HT3 antagoninsts: anti-emesis
*5HT4 agonist: gastrointestinal disorders

*Be aware of what other meds Pt is taking (Serotonin

Syndrome?)
*Contra-indications:
*Mimics serotonin = vasoconstriction by
--Pt w/ ischemic or vasospastic coronary diseases,
lowering cAMP
other CV disorders, & also uncontrolled HTN
*Inhibits pre-synaptic release of CGRP
--Also in Pt taking MAO inhibitors (b/c they are
metabolized by MAO)
*Partially contraindicated in prego Pt (be cautious)

*Gives profound vasoconstriction

*Never use a Triptan and a DHE together!!!
response outside of just cranial vessels
*VERY bad in CAD cases
--Be aware of this causing dry gangrene!
*Completely contraindicated in prego Pt
(called St. Anthony's Fire)
*Contraindicated for pt asthmatics (causes
bronchoconstriction)

*Inhibits Ach release at motor end plate

*LAST resort if absolutely nothing else
works for over a year