Neurology and Psychiatric Drugs Flashcards
Name the centrally acting skeletal muscle relaxants
Diazepam (Benzodiazepene)
Tizanidine (α2 agonist)
Baclofen
Diazepam
-Benzodiazepine (“long tapering flag”)
- increase frequency of oppening of the chloride ion channel
- binds at allosteric site on GABA-A receptor which is a chloride channel and potentiates GABA effects →Cl- influx →hyperpolarization→less neuronal excitation
- indicated for spasticity induced by neurological disorders (e.g. MS)
- produces sedation at required dose for reduction of muscle tone
- can induce withdrawl affects
Tizanidine
-α2 agonist
- inhibits release of excitatory Amino acids thus re-inforcing both pre/postsynaptic inhibition in the spinal cord
- indicated for spasticity induced by neurological disorders (e.g. MS)
- produces sedation at required dose for reduction of muscle tone
- can induce withdrawl affects
Dantrolene
- block RYR1 receptor → decreasing free intracellular calcium concentration.
- treats malignant hyperthermia which is a condition resulting from defective RYR receptors in the Sarcoplasmic reticulum
- useful for spinal injuries ,spasm after stroke
- may cause severe liver toxicity
Botulinum toxin
- exotoxin of clostridium botulinium
- controls release of Ach from vesicles by binding to synaptobrevin
- treats ophthalmic / local muscle spasms
- local facial injection are used for treatment of wrinkles
- present on honey - shouldn’t be given to children < 1 y.o.
- may cause flaccid paralysis
Baclofen
- GABA-B agonist
- GABA-B receptor is a K+ channel →increase K+ influx →hyperpolarization →Ca+2 ion influx decrease → decrease release of excitatory NTs
- rapid ,complete absorbtion after oral adminstration
- used for spasticity induced by neurological disorder (e.g. MS)
- less sedative but also less effective than Diazepam
- enhances sedative/resp dep. effects of opiates
Non depolarizing muscular relaxant
- competitive antagonists preventing Ach to depolarize the muscle cells
- at higher doses they produce more intense motor blockade
1st -muscles of face,eyes
2nd -finger,limbs neck trunk
3rd-intercoastals , diaphragm
- useful for anesthesia and facilitation of intubation
- can be reversed by **Neostigmine
Isoquinolone dervatives -**
- Tubocurarine
- Atra-curium
- Cistra-curium
Steroid dervatives -can be reversed by Neostigmine
-Pan-curonium
-Ro-curonium
*have vagolytic effect +enhance NE release
Depolarizing muscle relaxant
- depolarize muscle cells similarly to Ach however they are more resistant to degradation by AChE therefore n-AChR is incapable of transmitting further impulses because of the resistance to depolarization
- can lead to flaccid paralysis
- During phase I the reaction is irreversible
- useful for rapid endotracheal intubation or during electroconvulsive shock
how are benzodiazepens classified ?
name Benzodiazepens for each category
(“Ben’s Diner”)
-have “PAM-suffix
(“Pam-cakes in Ben’s diner”)
-have “OLAM-suffix”
(“pamcakes offered ALL A.M.”)
——————————————————————————–
Short acting Benzodiazepens -“ATOM”
Triaz-olam
Oxaze-pam (“fast ox”)
Midaz-olam
——————————————————————————–
Intermediate acting Benzodiazpenes “lora the clown”
Loraze-pam
Alpraz-olam
Clonaze-pam
——————————————————————————–
Long acting Benzodiazpenes
Diaze-pam
Fluraze-pam
Benzodiazpenes MOA
(“Ben’s Diner”)
-bind to an allosteric site on GABA-A Receptor
(“Ben’s diner coworker handing the Cab-A driver Pamcakes”)
-GABA-A receptor is a chloride channel, chloride influx hyperpolarizes nerve cells
(“chlo-rider” sign on Cab-A)
-Benzodiazpenes increase the Frequency of opening of the chloride channel
(ben’s diner is :”now open more frequently”)
-potentiates (enhance) transmission of GABA in CNS
(“Red CNS light on Cab-A”)
-GABA is the major inhibitory neurotransmitter in the CNS (the sign on Cab-A says “take it easy” )
-metabolized by the liver and produce long acting active metabolites
(“fast ox has liver spot on him”)
-have addictive potential
(“Ben’s Diner pamcakes have addictive flavour”)
what are Benzodiazepens used for ?
(“Ben’s Diner”)
-IV adminstration of Benzodizapenes are useful in managment of alcohol withdrawl , seizures , anesthesia (“Ivy on pole”)
-IV adminstration of Benzos can be used for general anesthesia
(“green shirt sedated customer with straw in mouth”)
-IV adminstration of Benzos is useful to induce
conscious sedation for minor procedures ,e.g.-colonoscopy
(cup saying “lite” infront of sedated customer)
——————————————————————————–
-useful for treatment of status epilepticus
(“coworker unplugging jackhammer”)
- can treat insomnia (“customer sleeping on table”)
- **not 1st line due to physical dependence**
-can treat Parasomnias in children
(“crying kid in pajamas”)
-benzos are muscle relaxants used to treat Spasticity cause by upper motor neuron disorders
(“red shirt blacky relaxed on diner’s bench”)
- useful in treatment of General Anxiety Disorder {G.A.D}
- *SSRIs/SNRIs are 1st line
(“Anxious cutsomer not sure if he can pay for the date lool”)
- Benzos are useful for treating Panic disorder
- *SSRIs/SNRIs are 1st line
Benzodiazepens side effects
-can potentially cause addiction
(pam-cakes have “addictive flavour”)
-can cause tolerance (“all are welcome” sign in Ben’s Diner)
-Benzodiazepens can cause Anterograde Amnesia and learning impairment
(“question mark hat on sedated customers head”)
- useful for conscious sedation so patient will follow orders but will forget unpleasant procedure afterwards
- Benzos can cause Central Ataxia causing elderly patient to fall
(“unbalanced stack of pamcakes infront of old fart”)
-elderly patients are more sensitive for Benzos side effects (“disoriented man sitting infront of stack of unbalanced pamcakes”)
- adminstration of Benzos should be avoided with other CNS depressants such as 1st generation antihistamines
(“coworker with bee swatter smacks old fart customer”)
what are the alcohol withdrawal symptoms
? what role do Benzos have in treating alcohol withdrawal
-alcohol also binds GABA-A receptor but on a different allosteric site
(“alcoholic guy is on back of Cab-A”)
-Benzos are useful in treatment of alcohol withrdawl symptoms (“hangover special pamcakes”)
- especially long acting Benzos such as Diazepam and Chlordiazepoxide
(“Long tapering flag on hangover special pamcakes”) - for patients with hepatic insufficiency use short-acting Benzos
Alcohol Withdrawal symptoms -“3 alcohol specialists”
1st specialist (8-12 hours) - insomnia ,tremulousness , anxiety , autonomic instability
2nd specialist (12-48 hours) - Seizures
_3rd specialist (_48-96 hours)-**delirium tremens** (fever ,disorientation , severe agitation )
what is the key difference between Benzodiazepens and Barbiturates
-the difference between them is that Barbiturates bind different allosteric site on GABA-A receptors
(“barber shop located on other side of Cab-A”)
How can you reverse Benzodiazepens-induced sedation
-Flumazenil is a competitive antagonist at the BZD receptor and can reverse Benzos-induced sedation
(“violent-antagonizing fluffy muzzled dog”)
Name the non-Benzodiazepine hypnotics
(“catching some Z’s”)
the 3 Z’s
Zolpidem
Zaleplon
esZopiclone
non-Benzodiazepine hypnotics MOA
-bind same allosteric site as Benzodiazepines at GABA-A receptor
(“ben’s diner coworker and zzz mattresses coworker are grabbing the same Cab-A handle”)
-GABA-A receptor is a chloride channel,chloride influx hyperpolarizesnerve cells
(“chlo-rider” sign on Cab-A)
-potentiates (enhance) transmission of GABA in CNS
(“Red CNS light on Cab-A”)
-GABA is the major inhibitory neurotransmitter in the CNS (the sign on Cab-A says “take it easy” )
-Barbiturates bind different allosteric site on GABA-A receptors
(“barber shop located on other side of Cab-A”)
-alcohol also binds GABA-A receptor but on a different allosteric site
(“alcoholic guy is on back of Cab-A”)
Pharmakokinetics of Zolpidem Zaleplon es-Zopiclone
-Zolpidem and Zaleplon are fast acting non-Benzos with rapid onset (sheeps sign says :”fall asleep FAST”)
-Non-benzos hypnotics have short duration of action
(“sheeps quick jump and fall on sign”)
-Zolpidem and Zaleplon are metabolised by the liver
(“sheeps on sign have liver spot on them”)
Side effects on non-Benzos
-elderly are more sensitive to the side effects
-can cause Central Ataxia
(“unbalanced stack of pillows”)
-avoid use with other CNS depressants
(“cannot combine with other CoupoNS”)
- e.g.- 1st Gen. Antihistamines
(“bee swatter coworker hitting old fart”)
what are non-Benzodiazepene hypnotics used for ?
-useful in treatment of insomnia
- Zolpidem and Zaleplon are short-acting and therefore useful in treating Sleeep onset insomnia and not for maintaining sleep
- esZopiclone has longest half life and is therefore effective for both falling asleep and maintaining sleep
-less likely to cause withdrawal symptoms
(“sale sign says break those bad sleeping habits”)
-non-benzos are less likely to cause tolerance
(sale sign says “returns not tolerated”)
how can you reverse non-benzos sedation ?
Flumazenil - BZD Competitive antagonist
(“fluffy muzzled dog biting on zzz matresses red arrow sign”)
what other drugs can be used to treat insomnia ? MOA?
(“let your sleepless nights melt away”)
- *Melatonin**
- *Ramelteon/Agomelatin** (melatonin receptor agonists)
-MT1 and MT2 melatonin receptors are found in the suprachiasmatic nucleus of the hypothalamus and are activated by Ramelteon
(“nucleus above x shaped ceiling fan”)
- **-Ramelteon has no direct effects on GABA-ergic transmission in the CNS **
- melatonin receptors maintain the Circadian rythm (“light and dark spotlights”)
-Ramelteon/Melatonin have fewer side effects and are safer in Geriatric patients
(peacefully sleeping old fart below “melt-away sign”)
Name Barbiturates
Thiopental
(“The Ol’ quick shave”)
Primidone
(“Perm is done!” primadona)
Phenobarbital
Barbiturates MOA
-GABA-A receptor is a chloride channel,chloride influx hyperpolarizes nerve cells
(“chlo-rider” sign on Cab-A)
-potentiates (enhance) transmission of GABA in CNS
(“Red CNS light on Cab-A”)
-GABA is the major inhibitory neurotransmitter in the CNS (the sign on Cab-A says “take it easy” )
-binds to a separate allosteric site on GABA-A Receptor
(“barber opening dooe on other side of Cab-A driver Pamcakes”)
-Barbiturates increase the duration of opening of the GABA-A receptor chloride channel
(sign at entrance of shop saying :”long hair? now open longer”)
-Barbiturates have long duration of action and therefore “hangover” effects are more common
(“long tapering flag outside barber shop”)
Barbiturates Pharmacokinetics
(mainly Thiopental here?)
-Barbiturates have long duration of action and therefore “hangover” effects are more common
(“long tapering flag outside barber shop”)
- Thiopental has rapid onset and short duration of action because it’s highly lipid soluble
- plasma levels of Thiopental decrease rapidly due to redistribution to skeletal muscle and adipose
(“barber cuts hair and redistributes it to arms and belly of customer”)
Redistribution graphof Thiopental (on customer’s chest)
Decay line - rapid decay of plasma Thiopental
Brief peak - rapid accumulation of thiopental in brain and rapid redistribution
Growth line-rapid accumulation of Thiopental in skeletal muscle and adipose(recovery from anesthesia)
Barbiturates side effects
-chronic use of barbiturates leads to tolerance
(“all are welcome” sign in entrance of barbershop)
-chronic barbiturates use leads to physical dependence
(“addicted to curls” sign)
-can cause hypotension
(“fainted old fart sitting on hair dryer chair”)
-can cause profound cardiac and respiratory depression
(“old fart has collapsed heart and lungs t-shirt”)
-can cause severe CNS depression (coma) ,should be avoided in elderly
(“brain shaped hair dryer”)
-barbiturates are potent inducers of the CYP450 which may increase metabolism of drugs such as warfarin
(activated chrome bumper plate saying “CYP450”)
what are Barbiturates used for ?
IV-adminstration of Barbiturates (“Ivy on pole”)
-IV adminstration of Thiopental can be used for induction of anestehsia since its highly lipid soluble and enters the CNS quickly.
(intubated customer getting “The Ol’ quick shave”)
-IV adminstration of Phenobarbital can be used to treat Seizures
(“coworker outside unplugging jackhammer”)
-Primidone (“perm is done!”) can be used to treat seizures and essential tremors - 1st line with propanolol
(“prima dona’s barber has tremulous hand”)
name the IV Anesthetics
(“Ivy on all damn poles”)
Propofol
(Introducing Prospero “fall asleep” the hypnotist)
Etomidate
(Introducing the beast from the east “THE INTIMIDATOR”)
Ketamine
(Introducing “snaKE TAMINg” nomad )
Benzodiazepines
(“Ben’s Diner”)
Thiopental
(“The ol’ quick shave”)
Propofol
(prospero “fall asleep” the hypnotist)
-potentiate chloride current through the GABA-A receptor complex
(“old Cab-A behind prospero’s stand”)
-can be used for induction of anesthesia
(introducing prospero “fall asleep” the hypnotist)
-can be used for maintenance of anesthesia
(sign next to prospero says :”try to MAINTAIN your sanity!”)
-propofol cause profound vasodilation (arterial+venous)
Etomidate
(“introducing the beast from the east the INTIMIDATOR”)
-potentiates chloride current through the GABA-A receptor complex
(“old Cab-A behind the INTIMIDATOR stand”)
-is an IV anesthetic for induction
(“introducing the intimidator”)
-Etomidate preserves cardiovascular stability
(“the buffy intimidator stabilizes the patient “)
Ketamine
(“snaKE TAMINg)
-inhibits the NMDA receptor complex which is a glutamate receptor and ion channel
(“hitched nomadic camel”)
-can be used for induction of anesthesia
(“introducing the snaKE TAMINg nomad”)
-causes “dissociative anesthesia”
(“man looking in snakes eye causing dissociative trance”)
-can cause unpleasant emergence reactions
- vivid colorful dreams
(“colorful steam from snakes bucket”) - hallucinations
- out of body experiences
-can cause cardiovascular stimulation{Incr.BP HR CO}
(“stimulated cobra’s head shaped like heart”)
Benzodiazepines
(“Ben’s Diner”)
Midaz-olam ,
Loraze-pam
-IV anestheic used preoperatively
-used for conscious sedation for minor procedures such as colonoscopy
(“bowel water pump outside Ben’s Diner”)
Barbiturates
(“Barber’s shop)
-Thiopental has rapid onset and short duration of action since it is highly lipid soluble
(“The Ol’ quick shave”)
-IV Anesthetic used for induction of anesthesia
(“Introducing the BARBER SWEENY PENTAL”)
Neurolept Analgesia
Neuroleptanalgesia
- a state of analgesia ,sedation, muscle relaxation BUT no loss of consciousness
- Fentanyl + Droperidol
- contraindicated in parkinsonism
- useful during diagnositc procedures requiring cooperation of the patient
Neuroleptanesthesia
- Fentanyl+Dorperidol, Nitrous oxide
- addition of NO improves amnesia
Peri-operative medications
Before surgery
-IV. Barbiturates - Thiopental (“the ol’ quick shave”)
-Sedative/Anxiolytic Benzodiazepine -Diazepam (“long tapering flag”)
-Antimuscarinic - parasympatholytic agent -Atropine(“alice”)
-Analgetics - Opiods (fentanyl) non opioids
—————————————————————————————————
During surgery
-NMB- Succinylcholine (depolarizing) / Curare derivatives ( non-depolarizing)
-Pressors in case of shock - Norepinephrine
—————————————————————————————————
After surgery
-If opioids were used before surgery - non-opioids should be used
-antagonism of NMB -Neostigmine
-antagonism for opioids if respiration is too slow - Naloxone
Gaseous anesthetic
Nitrous Oxide (N2O)
Volatile anesthetics
Enflurane
Isoflurane
Halothane
Volatile anesthetics pharmacodynamics
-volatile anesthetics are liquid at room temperature
(e.g. enflurane, isoflurane, halothane)
(“Air tank in water”)
-volatile anesthetics are fluorinated
(e.g. enflurane, isoflurane,halothane)
(“Balloon flower”)
-highly soluble inhaled anesthetic (e.g. halothane)
(“Moving freely in ball pit”)
more soluble inhaled anesthetics (e.g. halothane) have a slower onset of action
(“Passed out later”)
-more soluble inhaled anesthetics (e.g. halothane) have a longer duration of action (“Long tapering flag”)
- Partition>>>: higher blood:gas partition coefficient
(e. g. halothane) → higher solubility → **slower onset of action - ———————————————————————————**
Less steep arterial tension curve (e.g. halothane) → higher blood:gas partition coefficient→higher solubility → slower onset of action
Nitrous Oxide Pharmacodynamics
less soluble inhaled anesthetic
(“Impeded by ball pit”)
(e.g. N2O)
less soluble inhaled anesthetics (e.g. N2O) have a faster onset of action
(“Passed out earlier”)
less soluble inhaled anesthetics (e.g. N2O) have a faster recovery
(“Immediate rescue” )
Steeper arterial tension curve (e.g. N2O)→ lower blood:gas partition coefficient→ lower solubility → faster onset of action
Volatile Anesthetics side effects
-inhaled anesthetics can cause respiratory depression (leading to decreased minute ventilation and hypercapni a)
(“Deflating lung balloons”)
-myocardial depression →hypotension
(“deflating heart balloon”)
-fluorinated anesthetics increase cerebral blood flow (decrease cerebral vascular resistance)(“Red brain wig”)
halothane can be hepatotoxic
(e.g. massive hepatic necrosis) (“Cracked liver”)
enflurance can be nephrotoxic (“Smacked in the flank”)
enflurance can induce seizures (“Shaking”)
-malignant hyperthermia
(skeletal muscle hypersensitivity to volatile anesthetics) (“Magnificent birthday”)
MAC
minimum alveolar concentration (MAC)
MAC corresponds to the dose of anesthetic that causes 50% of patients to become unresponsive to painful stimuli
(“1 out of 2 unresponsive”)
1/MAC corresponds to the potency of an inhaled anesthetic (“Inverted bowl of potent mac and cheese”)
what is the treatment of malignant hyperthermia
Dantrolene
———————————————————————————–
Blocking Ryan: dantrolene blocks ryanodine receptors
-treats malignant hyperthermia
malignant hyperthermia
-succinylcholine (depolarizing muscle relaxant) can also causes malignant hyperthermia
malignant hyperthermia is related to a defect in ryanodine receptors (RyR) in the sarcoplasmic reticulum
-excess heat production and consumption of ATP induces rhabdomyolysis
what is the mechanism of action of SSRIs ?
-inhibit presynaptic reuptake of Serotonin
(“worker in sitcom keeps post-it stick notes out of the drawer”)
name the SSRIs
(“travel posters behind expreSS tRIps”)
Selective Serotonin Re-uptake Inhibitors
Paroxetine
(“Parrot air” poster)
Fluoxetine
(“Fly out”poster)
Sertraline
(“Desert Airline” poster)
Citalopram
(“the City” poster)
MOA of SNRIs
-inhibit presynaptic re-uptake of Norepinephrine and Serotonin
(“North and South compass poster above dual copy machine “)
Name the SNRIs
SNRIs
-Venlafaxine
(“fax machine infront of compass poster”)
-Duloxetine
(“Dual copy machine below compass poster”)
what can SSRIs AND SNRIs be used for ?
- 1st line treatment for depression {M.D.D}
- *slower onset than Benzos so not useful for treatment of acute symptoms *
-1st line treatment of G.A.D
(Anxious coworker holding “preformance repot”)
-useful for treatment of panic disorder
(“the scream saver”)
-useful for treatment of PTSD
(coworker holding dog tags saying “PT” and SD”)
(“happy/sad masks logo on right edge of sitcom”)
what can SSRIs specifically be used for?
-useful in managment of OCD
(“obsessively neat coworker re-arranging his table”)
-
useful in treatment of Bulimia
(blonde coworker opening “binge snack drawer”)
-useful in treatment of Social Anxiety Disorder
(“shy coworker hiding behind desk “)
what can SNRIs specifically be used for?
-useful for treatment of Diabetic Neuropathy
(“coworker feeling pain from Diasweeties machine”)
-useful in treatment of chronic pain (neuropathic)
(“chronically frayed wires from diasweeties machine”)
-useful in treatment of fibromyalgia
(“fiber bars at top shelf in diasweeties machine” )
how long should you wait before considering an alternative treatment for SSRIs/SNRIs ?
-SSRIs and SNRIs take 1-2 months to achieve maximum effect
(“2 months calendar behind shy guy”)
what are the Side effects of SSRIs ?
-hyponatremia as a result of SIADH {incr. ADH}
(“inappropriately wet head of blacky coworker”)
-SSRIs can cause Sexual Dysfunction
(“patty rejects and throws paper clips in ugly guy’s face”)
-SSRIs can cause weight gain
(“fat guy next to expreSS tRIps counter”)
-SSRIs can cause Drowsiness
(“purple shirt coworker sleeping on the job”)
what condition may percipitate as a result of SSRIs and SNRIs abuse ? what are the characterisitc findings of this condition ?
-SSRIs and SNRIs may cause Serotonin Syndrome
(“excessive smiley post-it sticky notes in back office”)
-combination of SSRIs/SNRIs with other drugs may also cause serotonin syndrome {e.g. TCAs,MAOis}
(“Tricycle and mouse traps in smiley backoffice”)
-serotonin syndrome is characterized by hyperthermia and hypertension
(“michelle boss of the office is hot and has steam coming out of his ears”)
-characterized by neuromuscular hyperactivity , hyperreflexia , clonus
(“boss of office hyperactive foot tap”)
what is the treatment for Serotonin Syndrome ?
Cyproheptadine (5-HT2 blocker)
(boss of the office holding sign saying “silly pranks prohibited”)
what are the side effects of SNRIs?
-SNRIs can cause hypertension
(“hypertensive coworker has steam coming out of his ears because of the fax machine”)