Pcol 2 Exam 2 Flashcards
Acamprosate
C
NMDA antagonist and GABA A positive allosteric modulator –> Enhances GABA at the GABA A receptor
-Only use for Alcohol use disorder
Campral
Long Acting Benzos
Clonazepam
Clobazam
Clorazepate
Chlordiazepoxide
Diazepam
Flurazepam
Quazepam
1-Klonopin
2-Onfi
3-Tranxene
4-Librium
5-Valium
6-Dalmane
7-Doral
-Enhance GABA at the GABA A receptor in the post-synaptic “bind” to Y2 and A1 Cl- enters hyperpolarize the post synaptic
-Can treat partial and petitmal seizure
Phenobarbital
Enhance GABA at the GABA A receptor any A and B subunit in the post-synaptic . Cl- enters –> Hyperpolarize –> No generation of action potentials
-Can also block AMPA receptors at the post synaptic –> No glutamate binding no excitation
-For partial and Grand mal seizure
Luminal
Primodone
My-
Pro drug when is metabolize is converted to phenobarbital
-Enhance GABA at the GABA A receptors post synaptic bind to GABA A that contain any A and B subunit –> Cl- enters hyperpolarize no generation of impulses
-Can also block AMPA receptors in the post-synaptic when is converted to Phenobarbital
-Treat seizure
Mysoline
Tiagabine
gabit-
Tiagabine (Gabitril)
Inhibit GAT-1 so inhibit GABA reuptake
Enhances GABA
AE:
CNS depression, dizziness, sedation
Vigabatrin
Sa-
Inhibits GABA transaminase so prevent GABA deactivation by transaminase
Sabril
Stiripentol
Diaco-
Stiripentol (Diacomit)
Enhances GABA neurotransmission
AE:
CNS depression
Sedation
Dizzines
Felbamate *
Felb-
Felbamate (Felbatol)
Improve GABA neurotransmission
Block NMDA receptors
AE:
CNS depression
Dizziness
Sedation
Hepatoxicity
Aplastic anemia
Ganaxolone
Zta-
Ganaxolone (Ztalmy)
Improve GABA neurotransmission
AE:
CNS depression
Sedation
Dizziness
Phenytoin
Dil-
Na+ Channel blocker
Dilantin
Cere-
Fosphenytoin
pro drug
na+channel blocker
Cerebyx
Carbamazepine
T-
Na+ channel blocker at the presynaptic glutamagercic neuron
No Na+ enty no impulses generated
-Treat seizure and can treat trigeminal neuralgia
AE:
-Anemia–> decrease WBC count
-Blurry vision
-Increase ADH release –> So can cause fluid retention because increase ADH increases the aquaporins in the collecting duct
-is a enzyme inducer
Tegretol
Oxcarbazepine
T-
na+ Channel antagonist at the pre synapse of the excitatory neuron that is firing and using more often the Na+ channels –> No Na+ entry no impulses generated
Trilipta
Eslicarbazepine
Ap-
Na+ channel blocker at the presynape –> affinity to the excitatory nerve that is using the Na+ channels more often –> preferential affinity to the inactive confirmation
Aptiom
Lamotrigine*
La-
Block Na+ channels of the neuron that is firing rapidly
Treat Partial and grand mal seizure
AE:
-Can cause CNS depression
-Can cause sedation
-Can cause severe skin rxn that can lead to steven johnson syndrome so advice pt to report any skin rashes
Lamictal
Rufinamide
Ban-
Banzel
Na+ channel blocker treat convulsion
AE:
CNS depression
Sedation
Dizzines
Cenobamate
xc-
Xcorpi
Na+ channel blocker
Treat seizure
AE:
Sedation
CNS depression
Dizziness
Zonisamide*
zon-
Block Na+ channels –> Preferential affinity for inactive state
Can block T-type Ca2+ channels in the brain in the post synaptic neuron either GABAergic neuron or Glutamergic neuron
Treat seizure
AE:
Inhibit carbonic anhydrase is good for seizure but also inhibit carbonic anhydrase in the kidney and can cause kidney stones
-Anorexia–> decreases appetite
-CNS depression
-Sedation
Zonegran
Topiramate**
T
Block Na+ channels in the presynaptic –> No Na+ entry no impulses
-Block AMPA receptors in the post synapse–> Can prevent migraines
-Enhances GABA neurotransmission
-Block T-type Ca2+ channels in the post-synapse
Treat partial and grand mal seizure
AE:
CNS Depression
Sedation
Dizziness
Affect taste
Cognitive defects–> Trouble speaking and reading
Inhibit carbonic anhydrase good for seizure but can cause renal stones
Topomax
Lacosamide
Vim-
Vimpat
Na+ channel blocker
Perampanel
Fycom-
Perampanel (Fycompa)
block AMPA receptors
so no glutamate bind no Na+ entry to post synaptic
Treat seizure
AE:
CNS depression
Dizziness
Sedation
***Valproate or Valproic acid
T-Type Ca2+ Channel antagonist in the post synaptic so no Ca2+ entry
and
Inhibits GABA T (gaba transaminase) –>inhibit GABA metabolism so more GABA in the synapse
-Can also block NMDA receptors
AE:
-Increase LFT
-Liver toxicity
-CNS depression
-Sedation
-Dizziness
Depakote, Depakene
Ethosuximide
Zar-
T-type Ca2+ channel blocker
Treat pettit mal seizure
AE:
-Skin rxn
-Anemia
-CNS depression
-Dizziness
-Sedation
Zarontin
Levetiracetam
k
Binds to SV2A protein in that is bound to the vesicles in the presynaptic glutametergic and reduces the release of glutamate
Keppra
Brivaracetam
Brivi-
Bind to SV2A a protein in the vesicle inside the pre synaptic glutametergic neurons and will prevent the vesicle to bind to the membrane so no Glutamate release to the synapse
-Treat convulsion
AE:
-CNS depression
-Dizziness
-Sedation
Briviact
Epidiolex
Reduce glutamate release
is a derivative of THC
-Treat seizure
AE:
Cns depression
Dizziness
Sedation
Cannabidiol
Gabapentin
Neur-
Neurontin
N-type Ca2+ antagonist
N-type Ca2+ are more plentiful in the glutamitergic neurons so will cause less release of glutamate
-for neuropathic pain and convulsion
AE:
Dizziness
CNS depression
Sedation
Pregabalin
Lyri-
Lyrica
Block N-type Ca2+ channels in the presynaps of glutamatergic neurons so no glutamate release
Treat neuropathic pain and convulsion
AE:
Dizziness
CNS depression
Sedation
Lidocaine
Intermediate acting local anasthetic
Block Na+ channels
Prilocaine
Amide derivative
Intermediate local anasthetic
Block Na+ channels
Melpivacaine
Intermediate local anesthetic
Amide derivative
Block Na+ channels
Bupivacaine
Long acting local anasthetic
Amide derivative
Block Na+ channels
Ropivacaine
Amide derivative long acting local anaesthetic
Block Na+ channels in the presynaptic unmyealinated neuron
Dibucaine
Long acting amide derivative local anasthetic
Block Na+ channels
Procaine
Short acting ester derivative local anasthesia
Benzocaine
O, An
Short acting ester derivative local anasthesia
Orajel, Anbesol
Cocaine
Intermediate acting local anasthetic
Block Na+ channels
Ester derivative
Tetracaine
Long acting ester derivative local anasthetic
block Na+ channels in the presynap in the local area
Thiopental
Pent-
Is a parenteral anesthetics general anesthesia agent
-Is use for the induction phase the pt is in a level of unconscious
MOA:
-Enhances GABA at the GABA A it binds to any A and B subunit –> Cl- enters and hyperpolarize the neuron
-It can also block AMPA receptors
Effects:
-Body is inmobile don’t feel anything
-Analgesia
-Amnesia–> They can block nicotinic receptors in the brain and Ach wont be able to bind amnesia is that they dont remeber anything from surgery
-Vasodilation–> decrease BP , Decrease CO, Decrease HR
-Loss of autonomic reflexes
Emergence phenomenomen:
-When pt is comming out of anesthesia
-HR increase, BP increases
-Body temp is cold so increase shivering
-Nausea and vomiting
Pentothal
Methohexital
Brev-
Methohexital (brevital)
Is a ultra short barbiturate and is use as a general anesthesia for the induction phase
MOA:
-Enhances GABA at the GABA A receptor by binding to any A and B subunit
-It blocks AMPA receptors
Effects:
-The body is immobile –> dont feel pain
-Amnesia–> dont remember anything can be because of block the nicotinic receptors in the brain so ACH wont be able to bind
-Vasodilation–> BP decreases, HR decrease, CO decreases
-Loss of autonomic reflexes–> BP remains low, HR remains low, CO remains low and respiration decreases
Emergence phenomen
Brevital
Propofol
Dipri-
Propofol (diprivan)
General anesthetic parental
MOA:
-Enhances GABA at the GABA A receptor it binds to the B subunit
-It enhances glycine a inhibitory N.s to bind to its receptor in the post synaptic neuron and will allow Cl- to eneter and hyperpolarize the neuron
-It causes opening of K+ channels so K+ leaves and hyperpolarize the post synaptic neuron
-Can block nicotinic receptors in the brain so ACH wont be able to bind
-Is use as a maitenance anesthesia
Effects:
-Analgesia
-Amnesia
-Vasodilation–> Decreases HR, decreases BP, decreases Co
-Respiration decreases
-Loss in autonomic reflexes so BP, HR, Co remains low
-If given as IV it causes damage to the blood vessels
-Has emergence phenomen:
-when pt is waking up from anesthesia: HR and BP increases, body shivering cold, n/v
Diprivan
Fospropofol
Luse-
Fospropofl (Lusedra)
Parental general anesthetic agent
Is a prodrug –> Is the phosphorylated form of Propofol (Diprivan) and once it gets into the bloodstream and the phosphophate is cleave by esterases get propofol and wont cause harm to the bloodstream
MOA:
-It will enhance GABA at the GABA A receptor and it binds to the B subunit
-It enhances glycine (inhibitory n.s) and glycine binds to its receptor in the post-synapse and Cl- will enter and hyperpolarize
-Can open K+ channels in the post synapse
-Can block Nicotinic receptors in the brain so ACH wont be able to bind
Effects:
-Amnesia
-Analgesia
-Vasodilation–> Drop BP, HR decreases, CO decreases, respiration decreases
-Loss in autonomic reflexes so BP remains low, HR remains low and CO remains low
Emergence phenomen
Lusedra
Etomidate
Ami-
Etomidate (amidate):
Generalize parental anesthetic agent
for maitenance phase
MOA:
-It will enhance GABA at the GABA A receptors and it will bind to the B subunit
-It will enhance glycine inhibitory n.s and glycine will bind to its receptor in the post-synaptic neuron and Cl- enters causing hyperpolarization
-It will open K+ channels in the post-synapse so hyperpolarize
-Can block nicotinic receptors in the brain so ACH wont be able to bind –> role in amnesia
Emergence phenomen
Amidate
Ketamine
K-
Ketamine (Ketaclar) is a general parental anesthetic agent
MOA
-It can work as a indirect sympathomimetic–> it will inhibit the reuptake of Norepinephrine so indirectly activating the post synaptic adrenergic receptors –> results in increase HR, increase BP but no change in respiration
-It can enhance GABA at the GABA A receptors it binds to the B subunit so Cl- enters and causes hyperpolarization
-It can enhance glycine (inhibitory n.s) to bind to its receptor in the post synapse so Cl enters hyperpolarize
-Can block NMDA receptors
AE:
-Emergence delirium–> it causes the patient to suffer from hallucinations, dissociatice anesthesia the pt feel like out of body experience
-Increase BP
-Increase HR
-Increase CO
Emergence phenomen:
when pt is waking up from anesthesia it will suffer from:
Increase HR
Increase BP
Increase shivering–> body temperature is cold
Nausea and vomiting
Ketaclar
Isoflurane
-flurane
brand name: -For-
Isoflurane(Forane)
is a inhalation general anesthetic agent
-Is the most potent because the MAC (minimal aveolar concentration) is only 2% so requires only 2% of Isoflurane to be inhaled to cause anesthesia
MOA:
-It will enhance GABA at the GABA A receptor it binds to B subunit –> Cl- enters and hyperpolarize
-It will open k+ channels in the post synaptic
-It will enhance Glycine (inhibitory N.s) to bind to its receptor in the post-synaptic and Cl- enters
AE:
-Malignant hyperthermia reverse it with the antidote dantrolene
Also causes emergence phenomen
if it has high-blood gas partition coefficient –> it will have slow onset of action because move from the aveolar to the blood to the brain slow
It will have also slow emergence phenomen because move slow from the brain to the blood to the aveolar
Forane
Desflurane
Brand name: -Sup-
-Flurane
Inhalation general anesthetic
Least potent –> 10% MAC (minimal aveolar concentration) requires 10% to cause anesthesia
MOA:
-Enhances GABA at the GABA A receptor and binds to B subunit Cl- enters hyperpolarize
-Open K+ channels
-Enhances glycine (inhibitory n.s)–> bind to post synaptic receptor Cl- enters
AE:
-Bronchoconstriction
-Malignant hyperthermia
emergence phenomen
Suprane
Sevoflurane
Brand name: Ult-
-Flurane –> class
Inhaled general anesthetic agent
Is good 4% MAC (Minimal aveolar concentration) requires 4% to produce anesthesia
Is for induced phase
MOA:
-It will enhance GABA at the GABA A receptor it binds to the B subunit so Cl- will enter and causes hyperpolarization
AE:
-Malignant hyperthermia –> increase release of Ca2+ from the SR–> antidote is Dantrolene
Can also cause emergence phenomen when the patient is waking up from the anesthesia
Ultane
Dextroamphetamine + Amphetamine
Ade-, Myday-
Is a indirect sympathomimetic–> It will inderectly increases the activity of the sympathetic N.s
MOA:
-It will work in the CNS and will get into the neuron and will reverse the direction of the VMAT–> So more NE is release to the synapse, followed by DA but some 5-HT
-It can also reversr the direction of the NET (Norepi transporter protein)–> So no reuptake of NE from the synapse to the pre synapse–> Insteade NE stays in the synapse
Treat:
-ADD–> increase levels of NE in the brain will increase attention
-ADHD
-Hypersomnia –> Due to increase levels of NE and DA
-Narcolepsy–> Is a genetic deficiency of oxerin peptides in the brain so the pt can fall asleen anywhere even while driving
-Obesity and binge eating–> Because the increase levels of NE and DA in the feading center it will reduce the appetite. But amphetamines causes tolerance and when the pt stop using it he will gain weight
Peripheral AE due to the increase levels of NE:
-Increase HR
-Increase BP
-Increase pulse
-Difficulty in urination–> because direct activation of A1 receptors will cause constriction of ther neck of the bladder
-Mydraisis because of activation of A1 receptords
Central AE:
-Insomnia
-Increase respiration
-Loss of appetitie
-Increase motor and speech–> Pt will start talking alot and moving more
-Euphoria due to high levels of DA
-Death from cerebral vasculature
Aderall, Mydaysi
Dextroamphetamine
Dexe-
Indirect acting sympathomimetic:
MOA:
-It will work in the CNS and will get to the neuron and it will reverse the direction of the VMAT –> so more NE and some DA is released in the synapse and some 5-HT
-It will also reverse the direction of NET –> so more NE in the synapse
Thera use:
-Increase attention –> treat ADD and ADHD
-Hypersomnia (pt is always sleeping) but can treat it due to the increase release in NE and DA
-Narcolepsy–> is genetic difference and pt will lack of oxerin peptides in the brain and can easily fall asleep even while driving
-Binge eating and obesity
AE peripheraly:
-Increase HR
-Increase BP
-Increase pulse
-Difficulty in urinating–> Due to the indirect activation of A1 receptors –> so Activating A1 in the bladder will constrict the neck of the bladder
-mydraisis–> dilated pupil so CI= glaucoma
AE centrally:
-Insomnia–> when is use for ADD
-Anorexia–> when is use for ADD
-Increase respiration
-Increase motor and speech–> so pt will be moving and talking more
-Euphoria –> due to release of DA
-Toxicity–> if pt OD it will get a psychosis due to increase lveles of DA in brain–> get psychosis, hallucinations, schizophrenia
-Physical dependence –> if pt suddenly stops will get withdrawal –> fatigue, depresion,, weight gain
Dexedrine
methamphetamine
Des-
Indirect acting sympathimimetics
MOA:
-It will reverse the direction of the VMAT and the NET preferably follow by DA and some 5-HT
-It will also reverse the direction of the VMAT –> so more adrenergic neurons release
Thera use:
-Increase alertness and ability to focus–> treat ADD and ADHD
-Treat hypersomnia
-Treat narcolepsy–> a genetic deficiency in the oxerin peptides in the brain so pt will easily fall asleep even while driving
-Treat obesity and binge eating–> The increase levels of NE and some DA at the feeding center of the brain will cause reduction in appetite. But pt can develop tolerance and eventually gain weight again
AE in the periphery: due to increase NE in the periphery
-Increase HR
-Increase BP
-Increase palpitations
-Difficulty in urinating–> because the increase in NE in the periphery will indirectly cause activation of the A1 receptors—> So activation of the A1 receptor in the neck of the bladder will cause constriction of the neck of the bladder
-mydraisis–> due to indirect activation of A1 receptors
Central AE:
-Insomnia–> When use for ADD
-Anorexia–> When use for ADD
-Increase respiration
-Increase motor and speech–> Pt will be moving more and talking more
Toxicity can be seeing as: a psychosis due to elevated levels of DA in the brain causing hallucinations, paranoia, schizophrenia
physical dependence –> pt become dependent when treating ADD and when suddenly stop suffer from withdrawals–> depression, gain weight, fatigue
-Death can occur by cerebral hemorrage
Desoxyn
Lisdexamphetamine
Vyv-
Indirect sympathomimetic
MOA:
-It will reverse the direction of the VMAT causing more release of NE to the synapse following DA and some 5-HT
-It will also reverse the release majority of the NET so more NE release in the synapse
Therapy use:
-Increase attention–> treat ADD and ADHD
-Treat binge eating and obesity–>Because the high levels of NE in the feeding center of the brain will suppress appetite but the patient can become tolerant and when stop they will gain weight again
-Narcolepsy–> Is a genetic difference in the Oxerin peptider levels in the brain so pt can easily fall asleep–>but high levels of NE in the brain causes wakefullness
-Hypersomnia–> pt is always sleepy but when give Ritalin increases levels of NE and DA in the brain so increases wakefulness
AE in the periphery:
-Increase BP
-Increase HR
-Increase palpitations
-Because of the indirect activation of the A1 receptors –> it can activate A1 receptors in the neck of the bladder constricting the bladder so difficulty urinating
-mydraisis –> dilated pupil
AE in the central:
-Insomnia–> when treat ADD
-Anorexia–> when treat ADD
-Increase respiration
-Increase motor and speach
-Euphoria –> due to increase of DA
toxicity= psychosis due to elevated levels of DA–> hallucinations, paranoia, schizophrenia
-Physical dependence
-Death as cerebral hemorrage
Vyvanse
Ritalin
Indirect sympathomimetic
is a methylphenidate
MOA:
-It will inhibit the reuptake of NE and DA –> so inhibits the NET and DAT
-So accumulation of NE and DA in the synapse
Therapeutic use:
-Increases focus –> Treat ADD and ADHD
-Treat Hypersomnia –> Elevated levels of NE in the brain increases wakefulness
-Treat narcolepsy
-Treat binge eating and obesity–> accumulation levels of NE will suppress appetite in the feeding center–> tolerance can develop and when pt stop med can gain weight again
Periphery AE:
-Increase HR
-Increase BP
-Increase palpitation
-Difficulty urinating –> because accumulation levels of NE can indirectly activate A1 receptors in the bladder and causes constriction of the bladder
Central AE:
-Insomnia–> when treat ADD
-Anorexia–> when treat ADD
-Increase respiration
-Increase motor and speech
Tolerance can develop when treating ADD so thats why increase dose
Physical dependence–> when pt suddenly stop will suffer from withdrawals: fatigue, depression, gain weight
-Death can occur as cerebral hemorrage
-Toxicity–> psychosis due to high levels of DA in brain
Concerta
Methylphenidate indirect sympathomimetic
MOA:
-Will inhibit reuptake of NE and DA by inhibiting NET and DAT so NE and DA will accumulate in the synapse
Thera use:
-Increase Focus –> Treat ADD and ADHD
-Can treat hypersomnia–> bc elevated levels of NE in the brain increases wakefullness
-Can treat narcolepsy
-Can treat binge eating and obesity–> Increase levels of NE will suppress appetitie in the feeding center of the brain but can develop tolerance and pt will gain weight when stop med
Peripheral AE:
-Increase HR
-Increase BP
-Palpitations
-Due to the increase levels of NE in the synapse because of accumulation in the synapse it can indirectly activate A1 receptors –> so activation of A1 in the bladder will cause constriction of the bladder causing difficulty in urination
Central AE:
-Insomnia – when treat ADD
-Anorexia – when treat ADD
-Increase respiration
-Increase motor and speech
-Can develop tolerance when treating ADD so thats why you increase the dose
Physical dependence can also develop and when pt suddenly stops it will cause withdrawal–> gain weight, depression fatigue
_can die from cerebral hemorrage
toxicity = psychosis due to elevated levels of DA
Dexmethylphenidate
F-
Indirect sympathomimetic
methylphenidate
MOA:
-Will inhibit reuptake of NE and DA by inhibiting NET and DAT
So NE and DA will accumulate in the synapse and indirectly activate adrenergic neurons (NE) and dopamergic neurons (DA)
Thera use:
-Increase focus–> treat ADD and ADHD
-Treat Hypersomnia–> Pt is always sleepy so when NE accumulates in the brain it increases wakefulness
-Treat narcolepsy–> genetic difference in the oxerin levels in the brain
-Treat binge eating and obesity–> the accumulation of NE will suppress appetite in the feeding center of the brain. But can develop tolerance and pt can gain weight when stop med
Periphery AE:
-Increase HR
-Increase BP
-Increase palpitations
-Difficulty in urinating –> due to the accumulation of NE in the synapse it will indirectly activate A1 receptors so can activate A1 receptors in the bladder and cause constriction of the bladder
Central AE:
-Insomnia– when treat ADD
-Anorexia– when treat ADD
-Increase respiration
-Increase motor and speech
Tolerance while using it for ADD–> so thats why need to increase the dose
Physical dependece can develop–> So when stop med can suffer from withdrawasl such as: fatigue, gain weight and depression
Toxicity= psychosis due to high levels of DA
Death can occur by cerebral hemorrage
Focalin
Serdexmethylphenidate + Methylphenidate
Azst-
Indirect sympathomimetic
Methylphenidates
MOA:
-It will inhibit the reuptake of NE and DA so it will inhibit NEt and DAT therefore NE and DA will accumulate in the synapse
Thera use:
-Increase focus–> treat ADD and ADHD
-Treat hypersomnia
-Treat narcolepsy
-Treat binge eating and obesity –> the high levels of NE in the synapse will suppress appetite in the feeding center of the brain. But the pt can become tolerant and when stop the drug it will gain weight
Periphery AE due to high levels of NE:
-Increase HR
-Increase BP
-Increase palpitations
-Difficulty in urination –> Because the increase levels in NE it will indirectly activate A1 receptors so A1 receptors in the bladder get active so will constrict the bladder
-Also mydraisis because activation of A1
Central AE:
-Insomnia– when treat ADD
-Anorexia – when treat ADD
-Increase respiration
-Increase motor and speech
Pt can become tolerant when treating ADD so thats why you need to increase the dose
Physical dependence can develop–> and when pt suddenly stops it will suffer from withdrawasl such as: depression, fatigue, gain weight
-Toxiciy OD from methylphenidates–> Psychosis, hallucination, paranoia due to elevated levels of DA
-Can cause death as cerebral hemorrage
Azstarys
Bexamphetamine
Did-
Indirect sympathomimetic
MOA:
-Same as amphetamines but less effective
-So it will reverse the direction of the VMAT –> So increase the release of NE and following DA and some 5-HT
-And will reverse the direction of NET so more NE will be release
-They are schedule 3
Thera:
-They are use as anorexiant as diet pill so treat eating disorders such as obesity and binge eating –> because the increase in NE in the brain will suppress the appetite in the feeding center in the brain
Periphery AE:
-Increase HR
-Increase BP
-Increase palpitation
-difficulty in urination –> due to the increase levels of NE in the synapse it will activate periphery A1 receptors and activation of A1 in the bladder will cause constriction of the neck of the bladder
-Mydriasis
Central AE:
-Insomnia
-Increase respiration
-Increase motor and speech
-Some euphoria due to increase levels of DA in the brain
Didrex
Diethylpropion
ten-
Indirect sympathomimetic
has same MOA as amphetamines but less effective
MOA:
-It will reverse the direction of the VMAT so more NE and DA release to the synapse
-It will also reverse the direction of the NET and DAT so more NE release to the synapse
Thera:
-Is use as a diet pill –> treat eating disorders such as binge eating, obesity because the increase levels of NE will reduce appetite in the feeding center of the brain
Peripheral AE:
-Increase HR
-Increase BP
-Increase palpitations
-Difficulty in urination–> because the increase in NE will indirectly activate A1 receptors and A1 receptors in the bladder when active will constrict the bladder
-Mydriasis – dilated pupil
Central AE:
-Insomnia
-Increase respiration
-Increase motor and speech
-Can cause also tolerance and pt gain weight when stop taking it
Tenuate
Phendimetrazine
Ban-
Indirect sympathomimetic
-Same MOA as amphetamines but less effective
MOA:
-It will reverse the direction of VMAT so more NE release following DA and some 5-HT
-It will reverse the direction of NET and DAT
Thera:
-Is use a diet pill –> treat eating disorders such as obesity and binge eating
Because the increase in NE will suppress appetite in the feeding center
Peripheral AE:
-Increase HR
-Increase BP
-Increase palpitations
-Difficulty in urination –> because the increase in NE can indrectly activate A1 receptors in the bladder and will cause constriction of the bladder
Central AE:
-insomnia
-Increase respiration
-Increase motor and speech
Can cause tolerance and when the pt stop taking it they can gain weight
Bantril
Phentermine
Adi-
Lom- (think omaira)
Indirect sympathomimetic same MOA as amphetamines but less effective
MOA:
-Reverse the direction of VMAT –> so increase release of NE and DA in the synapse
-Reverse direction of NET and DAT
Thera use:
-For eating disorders like obesity and binge eating –> the increase levels of NE will suppress appetite in the feeding center
Peripheral effects and central effects are same as amphetamines
Adipex , lomaira
Phentermine + topiramate
Qsy-
Indirect sympathomimetic
Same MOA of amphetamines but less effective
-Both phentermine and topiramate will supress appetite and treat eating disorders like obesity and binge eating
Peripheral AE same as amphetamines
Central AE same as amphetamines
Qsymia
Atomoxetine
St-
Indirect sympathomimetic
Also referred as NERI
MOA:
-It will inhibit the reuptake of NE it will inhibit NET
-Is not a stimulant so will not cause difficulty for the kid to fall asleep and will not increase motor and speech
Thera:
-Is use for ADD in kids
-It takes 6 weeks to see effects
AE:
-Increase HR
-Increase BP
-Increase palpitations
-Increase LFT–> causes hepatotoxicity
-Reduce appetite
-Difficulty in urinating
DDi:
-Atomoxetine is metabolize by CYP 2D6 –> if the pt is a poor metabolizer the levels of atomoxetine will increase in the blood and is toxic
-Avoid SSRI because they are CYP 2D6 inhibitors
Strattera
Viloxazine
Qel-
Indirect sympathomimetic
also known as NORI
MOA:
-It will inhibit the reuptake of NE it will inhibit NET
-So more NE in the synapse accumulated
Thera:
-Treat ADD in kids but it takes 6 weeks to see effects
-it not a stimulant so it will not increase Motor and speech and will not cause difficulty for the kid to fall asleep
-Is less effective than methylphenidates and is not schedule
AE:
-Increase HR
-Increase BP
-Increase palpitations
-Difficulty urinating
-Decrease appetite
Qelbree
Ephedrine
Brok
Pri tabs
Mixed acting sympathomimetic
MOA:
It has direct activation of A1, B1 , B2 receptors
It has indirect effect of reversing the VMAT so more NE release in the synapse
Thera use:
-Use as bronchodilator and nasal decongestian –> when OTC
-Use to treat hypotension–> IV in hospital
AE:
-Increase BP–> effect of A1 activation
-Increase HR–> effect of B1 activation
-Increase Blood glucose–> effect on B2
-Increase Aq humor production–> effect on B2
-Insomnia–> indirect effect of increasing NE release
-Anorexia –> indirect effect of increasing NE release
Bronkaid , primatene tabs
Solriamfetol
Sun-
Is also known as a DNRI
MOA:
It will inhibit the reuptake of DA and NE like methylphenidates
Thera use:
-Treat narcolepsy
-Can treat hypersomnia
AE:
-Increase BP
-Increase HR
-Reduction in appetetite
Sunosi
Modafinil
Pro-
Treat narcolepsy
MOA:
-It will increase levels of Histamine and oxerin in the brain increasing wakefullness
AE:
-Reduction in appetite–> can be because of high levels of Histamine
Provigil
Armodafinil
-vigil
Treat narcolepsy
MOA:
-Increase levels of histamine and oxerin in the brain causes wakefullness
AE:
-Reduction in appetite can be because of high levels of histamine
Nuvigil
Sodium Oxybate
Xy-
Treat narcolepsy:
MOA:
-It will activate GABA B that is Gi and will decrease CNS activity
-Can also activate GHB that will decrease CNS activity
Thera:
-Take it at bedtime because it causes the pt to fall asleep and the pt will get such a goodnight sleep that will remain awake during the day is likea “rebound daytime insomnia”
AE:
-CNS depression
-Respiratory depression
-Sedation
-Death if mix wil alcohol
Xyrem
Pitolisant
Waki-
Block H3R autoreceptors in the presynapse
MOA:
-It will block H3R in the presynapse and H3R are autoreceptor that will reuptake Histamine from the synapse back to the presynapse but because is block by Pitolisant (Wakix) more Histamine is release to the synapse and can activate H1 receptors in the post synapse causing wakefulness
Treat narcolepsy
AE:
-Skin rash
-Itching
-Reduce appetite
Wakix
Fibanserin
A-
5-HT 1A receptor agonist
MOA:
-5-HT1A recepto is in the presynapse and when active it will cause less release of 5-HT to the synapse
Thera use:
-Treat female hypoactive sexual desire disorder –> fibanserin addyi will increase libido in those women
AE:
-CNS depression
-Sedation
avoid alcohol
Addyi
Imipramine
T-
TCA
MOA:
-Inhibit reuptake of NE and 5-HT so inhibit NEt and SERT and they can activate adrenergic receptors
Thera:
-Treat depression takes weeks to months
-Treat neuropathic pain –> inhibit reuptake of 5-HT and NE in the spinal cord (like tramadol with the adrenergic descending neurons)
-Treat nocturnal enuresis–>befcause block Muscarinic receptors so bladder is relax and can hold more urine
AE:
-Drop in BP–> because vasodilation–> because block A1 receptors
-Xerostomia–> block muscarinic
-Tachycardia–;. block muscarinic
-Mydriasis–> dilate pupil –:> block muscarinic
-Hold more urine–> block mucarinic bladder relax
-Sedation–> block H1 and histamine wont be able to bind
-increase appetitie so gain weight–> block H1 receptors
-Seizure
-Cardiac arrythmia
-CNS depression –> Respiratory depression followed by coma then death
CI:
-Glaucoma
-Seizure hx
-arrythmia hx
Serotonin syndrome:
-Akathisia –> restlesness
-Tremors
-Clonus
-Muscle hypertonic
-Hyperthermia
-Death
Tofranil
Clomipramine
Ana-
TCA
MOA:
Inhibit reuptake of NE and 5-HT so inhibit NET and SERT
activate adrenergic receptors (indirectly)
Thera:
-Treat depression takes weeks to months to see improvement in mood in clinically depressed pt
-Treat nocturnal enuresis due to block muscarinic receptors
-Treat neuropathic pain –> inhibit reuptake of NE and 5-HT in the spinal cord
AE:
-Xerostomia–. block musca
-Tachycardia–. bloc musca
-Mydriasis–> block musca
-Hold more urine bladder relax–> block musca
-Drop in BP–> vasodilation–> block A1
-Sedation–> block H1
-Increase weight increase appetite–> block H1
-Seizure
-Cardiac arrythmia
-CNS depression–> respiratory depression–> coma–> death
-Sexual effects–> dificulty in maintain erection
CI:
-Glaucoma
-Seizure HX
-Arrythmia HX
Serotonin syndrome
Anafranil
Desimipramine
Nor
TCA
MOA:
-Inhibit reuptake of NE and 5-HT inhibit NET and SERT
Thera:
-Takes weeks to months to see improvement in mood in clinically depressed pt
-Treat neuropathic pain
-Treat nocturnal enurisis
AE:
-Drop bp–> vasodilatio –> block A1
-Tachycardia–> block Musca
-Xerostomia–. block musca
-Mydriasis–.block musca
-bladder relax hold more urine–.block musca
-Seizure
-Cardiac arrythmia
-Sedation–> block H1
-Increase weight–. block h1
-CNS depression–. respiratory depression–. coma death
-Sexual effects–. difficulty in maitaining erection
CI:
-Glaucoma
-Seizure hx
-arrythmia hx
Serotonin syndrome
Norpramin
Amtriptyline
E
TCA
MOA:
-Inhibit reuptake of NE and 5-HT inhibit NET and SERT
Thera:
-Takes weeks to months to see improvement in mood in clinically depressed pt
-Treat neuropathic pain
-Treat nocturnal enurisis
AE:
-Drop BP–> vasodilation–> bloc A1
-Xerostomia, mydriasis -dilate pupil, hold more urine, tachycardia–> block Muscarinic
-Sedation and increase weight–> block h1
-Seizure
-Cardiac arrythmia
-Sexual effects–> difficulty in maintaining erection
-CNS depression–> resp depression–. coma death
-Low therapeutic index
CI:
-Glaucoma
-Seizure hx
-Arrythmia hx
-ED
Serotonin syndrome
Elavil
Nortriptyline
P and A
TCA
MOA:
inhibit reuptake of NE and 5-HT inhibit NET and SERT
Thera:
-Treat depression
-Nocturnal enurisis
-Neuropathic pain
AE:
-Drop bp–> vasodilation–> block A1
-Tachycardia, xerostomia, mydraisis, bladder relax and hold more urine–. block muscarinic receptors
-Sedation and gain weight–> block H1 receptors
-Seizure
-Cardiac arrythmia
-Sexual effects–> difficulty in maintain erection
-CNS depression–> resp depression–> coma–> death
CI:
-Glaucoma
-Seizure hx
-Arrythmia hx
Serotonin syndrome
Pamelor, Aventil
Doxepin
Sil-
TCA
MOA:
-Inhibit reuptake of NE and 5-HT inhibit NET and SERT
Thera:
-takes weeks to months to see improve in mood in clinically depressed pt
-Treat neuropathic pain due to inhibit reuptake of 5-HT and NE in the spinal cord
-Treat nocturnal enurisis
AE:
-Drop BP–> vasodilation–.block A1
-Xerostomia, tachycardia, hold more urine because bladdrr is relax, Mydraisis dilate pupil, –> block muscarinic receptors
-Sedation and gain weight–. block H-1
-Seizure
-Cardiac arrythmia
-Sexual effects–> difficulty in maintain erection
-CNS depression–> resp depression–> coma death
-Low thera index
CI:
-Glaucoma
-Seizure hx
-ED
-Cardiac arrythmia hx
Serotonin syndrome
Silenor
Protriptyline
Viva-
TCA
MOA:
-Inhibit reuptake of NE and 5-HT inhibit NET and SERT
Thera use:
-takes weeks to months to see improvement in mood in pt clinically depressed
-Treat neuropathic pain
-Treat nocturnal enurisis
AE:
-Drop BP–> vasodilation–> block A1
-Xerostomia, tachycardia, bladder relax and hold more urine, mydraisis dilate pupil–> block muscarinic receptors
-Sedation and gain weight–> block H-1
-Seizure
-Cardaic arrythmia
-Sexual effects–> difficulty in maitainin erection\
-CNS depression–> resp depression–> coma death
CI:
-Glaucoma
-ED
-Seizure hx
-Arrythmia hx
Serotonin syndrome
Vivactil
Trimipramine
Sur
TCA
MOA:
-Inhibit reuptake of NE and 5-HT inhibit NEt and SERT
Thera:
-Takes weeks to months to see improvement in mood in clinically depressed pt
-Nocturnal enurisis
-Neuropathic pain
AE:
-Drop in BP–> vasodilation–> block A1
-Xerostomia, tachycardia, bladder relax and hold more urine, mydraisis dilate pupil–>block muscarinic receptors
-Sedation and gain weight–> block H1 receptors
-Seizure
-Cardiac arrythmia
-Sexual effects–> difficulty in maintaining erection
-CNS depression–> resp depression–> coma –death
-Low thera index
-Serotonin syndrome
Surmontil
Maprotiline
Lu
TCA
MOA:
-Inhibit reuptake of NE and 5-HT inhibit NET and SERT
thera:
-takes weeks to months to see improvement of mood in clinically depressed pt
-Nocturnal enurasis
-Neuropathic pain
AE:
-Drop in BP–> vasodilation–> block A1
-Xerostomia, tachycardia, bladder relax hold more urine, mydriasis–>block muscarinic receptors
-Sedation and gain weight–>block H-1 receptors
-Sexual effects–> difficulty in maitaining erection
-Seizure
-Cardaic arrythmia
-CNS depression–. resp depression–> coma death
-Low thera index
CI
-Glaucoma
-ED
-Seizure
-Arrythmia
Serotonin syndrome
Ludiomil
Amoxapine
Ase
TCA
MOA:
-Inhibit reuptake of NE and 5-HT inhibit NET and SERT
Asendin
Fluvoxamine
L
SSRI
MOA:
Selective 5-HT receptor inhibitor will inhibit SERT
Treat depression
Benefits over TCA:
-Less risk of seizure
-Less risk of cardiovascular events
-Less risk of arrythmia
-More selective to SERT
-Is a strong 2D6 inhibitor
AE:
-Insomnia
-Anorexia
-Agitation
-Nausea and vomiting–> due to the inhibition of SERT there is accumulation levels of 5-HT in the synapse it will cause activation of 5-HT3 receptors in the GIT
-Sexual effects–> difficulty to maitain erection
Luvox
Fluoxetine
P
SSRI
is a strong 2D6 inhibitors
MOA:
-Selective seratonin reuptake inhibitor is selective to inhibit SERT
-treat depression
Benefits compared to TCA
-Less risk of seizure
-Less risk of cardiovascular events
-And are more selective
AE:
-Insomnia
-Agitation
-Anorexia
-Nausea and vomitng–> because inhibition of SERT will cause accumulation of 5-HT levels in the synapse therefore it can activate5-HT3 in the GIT
-Sexual effects
Prozac
Paroxetine
P
SSRI
-Strong 2D6 inhibitor
MOA:
-Is a selective serotinin inhibitor it will inhibit SERT so 5-HT accumulates in the synapse
-Treats depression
Advantages:
-More selective
-Less risk of cardiovascular events
-Less risk of seizure
AE:
-Insomnia
-Agitation
-nausea and vomiting –> because it can activate the 5-HT3 in the GIT do to the accumulation of 5-HT in the synapse
Paxil
Escitalopram
L
SSRI
Lexapro
Citalopram
c
Celexa
SSRI
Setraline
z
Zoloft
SSRI
Vortioxetine
Tri
Trintellix
SSRI
Venlafaxine
E
SNRI
MOA:
Inhibit NET and SERT –> inhibit reuptake of NE and 5-HT
-is more selective than TCA and does not block H1 no block muscarinic so no changes in CO
Thera:
-Treat depression
-Treat peripheral neuropathy–> inhibit reuptake of 5-HT and NE will cause indirect activation of 5-HT receptors and A2 receptors in the presynaptic primary efferent neuron so when activate A2 (gi) K+ leaves hyperpolarize and will cause less release of glutamate and substance P onto post synaptic ascending neurons so no pain impulses from spinal cord
-Treat fibromyalgia
-When increase dose of venlafaxine (effexor) can increase BP
AE:
-Insomnia
-Agitation–> increase alertness
-Decrease appetite
Serotonin syndrome
Effexor
Desvenlafaxine
P
SNRI
MOA:
-Inhibit NET and SERT inhibit reuptake of NE and 5-HT so more in the synapse
-Better than TCA because is more selective and does not block H-1, and no block on muscarinic receptors no change in CO
Thera:
-Treat depression
-Treat peripheral neuropathy–> inhibit reuptake of 5-HT and NE in the spinal cord will indirect activate 5-HT and A2 receptors on the primary efferent presynaptic sensory neuron so when A2 is active (gi) will cause K+ to leave hyperpolarize so no release of glutamate and substance P onto post synaptic ascending neuron so no pain impulses
-Treat fibromyalgia
AE:
-Insomnia
-Agitation–. increase alertness
-Decrease appetite–anorexia
Serotonin syndrome
Pristiq
Duloxetine
C
SNRI
MOA:
-Inhibit NET and SERT–> inhibit reuptake of NE and 5-HT so more in the synapse
-More selective than TCA so will not block h-1 and muscarinic receptors so no change in CO
Thera:
-Treat depression
-Treat peripheral neuropathy–> inhibit reuptake of 5-HT and NE in the spinal cord will indirect activate A2 receptors and 5-HT receptors in the primary presynaptic afferent neuron and when A2 is active (Gi) will open K+ channels K+ leaves and hyperpolarize therefore no release of glutamate and substance P onto post synaptic ascending neurons so no pain impulses
-Treat fibromyalgia
AE:
-Insomnia
-Agitation
-Anorexia - decrease appetite
-Hepatotoxicity
Serotonin syndrome
Cymbalta can cause hepatoxicity
Milnacipram
Sev
SNRI
MOA:
-Inhibit reuptake of NE and 5-HT inhibit NET and SERT
-More selective than TCA so it will not block H1 and no block muscarinic so no change in CO
thera:
-Treat depression
-Treat peripheral neuropathy–> inhibit reuptake of 5-HT and NE in the spinal cord will indirect activate 5-HT and A2 receptors on the primary afferent presynaptic neuron so when activate A2 (Gi) will cause opening of K+ channels K+ leaves hyperpolarize and will cause no release of glutamate and substance P onto postsynaptic ascending neurons so no pain impulses
-Treat fibromyalgia
AE:
-Insomnia
-Agitation
-Anorexia
Serotonin syndrome
Sevella
Levomilnacipram
Fet
SNRI
MOA:
-Inhibit NET and SERT –> inhibit reuptake of NE and 5-HT
-More selective than TCA because it will not block H1 and Muscarinic receptors so will not change CO
Thera:
-Treat depression
-Peripheral neurpathy
-Fibromyalgia
AE:
-Insomnia
-Agitation
-Anorexia
-Serotonin syndrome
Fetzima
Phenelzine
PheNar TranPar SelEm
Monoamine oxidase inhibitor
MOA:
-Is non selective irreversiblle inhibitors MAO-A that is responsible for breaking down NE, 5-HT, epi, DA, tyramine –> MAO-A has a role in depression
-And also inhibit MAO-B –> breaks down DA and tyramine
-So by inhibiting MAO when the monoamines are taken back up to the presynapse there will be no destruction of the monoamines so there will be increase levels of monoamines in the presynapse (either adrenergic neuron or serotonergic neuron) and when they are stimulated there will be even more NE release from adrenergic neurons to the synapse and activate adrenergic neurons in post synapse or more 5HT release from the serotenergic presynaptic neuron to the synapse
thera use:
-Treat depression
AE:
-Hypotension drop in BP
-Seizure
-Serotonin syndrome
DDi:
-Avoid taking indirect sympathomimetics the ones that can increase release of NE, 5-HT and DA to the synapse:
Amphetamines–> Dextroamphetamine + amphetamine (Aderall, Mydaysis), Dextroamphetamine (Dexedrine), Methamphetamine (Desoxyn), Lisdexamfetamine (Vyvanse)
-Ephedrine (Brokaid, primatine tabs)–> has direct and indirect activity
-Pseudoephedrine (Sudafed)
-Benzamphetamine (Didrex)
-Diethylpropion (Tenuate)
-Phendimetrazine (Bontil)
-Phentermine (Adipex, lomaira)
-Phentermine + topiramate (Qsymia)
Because the indirect sympathimimetic the ones that work like amphetamines will reverse the direction of VMAT and NET and will cause the release of more NE to the synapse and when the pt is also taking a MAOi they have elevated levels of NE in the presynaptic so when combine with indirect sympathomimetic there will be abnormal elevated levels of NE activating adrenergic neurons causing:
Hypertension crisis
Tachycardia
Arrythmia
-Palpitations
Food-drug interaction:
-Avoid tyramine containing foods like cheese, fermented wine because they have high tyramine
-Tyramine is metabolize by MAO-A in the GIT
But in a patient taking MAOi and take tyramine food the tyramine will not be broken down in the GIT andget to the blood stream to the presynaptic adrenergic neurons and act as a indirect sympathomimetic and cause abnormal release of NE therefore causing hypertension crisis, tachycardia, palpitaitons, arrythmia
Nardil
Tranylcypromine
PheNa TranPar SelEm
Phenelzine (Nardil)
Tranylcypromine (P
Selegiline (E
Non selective irriversible Monoamine oxidase inhibitor
-So the effects will persist longer time even when stop taking drug because it takes time for the body to increase the levels of MAO after taking the drug
MOA:
-Irriversible inhibits MAO-A –> has a role in depression because metabolize NE, Epi, DA, 5-HT and tyramine
and also inhibits MAO-B –> metabolize DA and tyramine
So the monoamines when taken back up to the presynapse there will not be broken down by MAO when getting to the vesicle so the patient will have elevated levels of monoamines in the presynapse and when the adrenergic receptors are activated there will be more release of NE to the synapse or when the seratonergic neurons are activated there will be more release of 5-HT to the synapse
Thera:
-Treat depression
AE:
-Hypotension
-Seizure
DDi:
Avoid indirect sympathomimetics the ones that work like amphetamines and cause increase release of NE and 5HT and DA to the synapse because when the patient is on MAOi has elevated levels of NE in the presynaptic and the indirect sympathomimetic will cause the excessive release of NE to the synapse activating adrenergic receptors in the post-synapse causing severe hypertension crisis, increase BP, increase HR, tachycardia, palpitations, arrythmia
avoid:
-Amphetamines–> Dextroamphetamine + amphetamine (Aderall, mydaysis), Dextroamphetamine (Dexedrin), Methamphetamine (Desoxyn), Lisdexamfetamine (Vyvanse)
-Benzamphetamine (Didrex)
-Diethylpropion (tenuate)
-Phendimetrazine (Bontril)
-Phentermine (Adipex, lomaira)
-Phentermine + topiramate (Qsymia)
Avoid tyramine containing food osea fermented food like cheese, wine, beer
Because normally tyramine is metabolize by MAO-A in the GIT but when taking Tranylcypromine (Parnate) tyramine will not be broken down in the GIT and get into the blood stream to the presynaptic adrenergic neuron and act as a indirect sympathomimetic and cause excessive release of NE to the synapse causing: hypertension crisis, tachycardia, palpitations
-Serotonin syndrome
Parnate
Selegiline
PheNar TranPar Selem
Is more selective for the MAO-B –> the one responsible for metabolism of DA and tyramine
Is given as a transdermal patch and when the levels in the blood increase it can eventually inhibit MAO-A and treat depression
AE:
Hypotension
Seizure
DDi:
-Avoid indirect sympathomimetics that work like amphetamines and increase the release of NE and 5-HT to the synapse because when also taking Selegiline (Emsam) the levels of monoamines in the presynapse will be high because no MAO therefore there will be no destruction of NE, 5-HT, DA when getting stored in the vesicles. But if co-admin a indirect sympathomimetic that works like amphetamines will cause excessive release of NE to the synapse causing: hypertension crisis, palpitations, tachycardia, arrythmia
Avoid drugs like amphetamines:
Amphetamine–> Dextroamphetamine + amphetamine (Aderall, mydaysis), Dextroamphetamine (dexedrine), Methamphetamine (Desoxyn), Lisdexamfetamine (vyvanse)
Amphetamine like–> Benzamphetamine (Didrex), Diethylpropion (Tenuate), Phendimetrazine (Bontril), Phentermine (Lomaira, Adipex), Phetermine + topiramate (Qsymia)
-Pseudoephedrine –sudafed a 1 agonist
-Ephedrine –> brokaid, primatine tabs mixed acting
Food-drug interactions:
Avoid tyramine contaning foods like cheese, wine, beer fermented food
Because normally tyramine is broken down by MAO-A in the GIT
but when pt is on MAOi and consume cheese there is increase levels of tyramine and is not broken down by MAO-A in the GIT insteade gets to the bloodstream to the presynaptic adrenergic neuron and acts as a indirect sympathomimetic
Emsam
Bupropion
W
Atypical antidepressant
MOA:
Inhibit NET and DAT –> so inhibit reuptake of NE and DA
Thera:
-Treat depression
-For smoking cessation therapy because the increase in DA has a role in pleasure
AE:
-Insomnia
-Agitation
-Decrease appetite
-Increase risk of seizure
Wellbutrin
Mirtazepine
R
Atypical antidepressant
MOA:
-It will antagonize A2 receptors in the nerve ending of presynaptic adrenergic receptors there is called autoreceptors so block it therefore causes more release of NE to the synapse
-Antagonize A2 receptors in the nerve ending of presynaptic 5-HT neurons is called heteroreceptor but because is block there is more NE release to synapse
-Blocks H-1 receptor therefore results in sedation and gain weight
AE:
-Sedation
-CNS depression
-Gain weight
Remeron
Trazodone
D
Atypical antidepressant
Inhibit NET and SERT
But can block H-1, Muscarinic receptors and A1 receptors
can cause serotonin syndrome
Desyrel
Vilazodone
v
Atypical antidepressant
MOA
Inhibits SERT so can treat depression-> can cause serotonin syndrome
Can also work as a 5-HT1a partial agonist and will cause less release of 5-HT from the presynapse treating anxiety
Viibryd
Gepirone
Ex
Atypical antidepressant
MOA:
5-HT1a partial agonist –> so will cause less release of 5-HT from the presynaptic
Gepirone metabolite has A2 antagonist activity
Block A2 autoreceptors in the nerve ending of presynaptic adrenergic neuron
Block A2 heteroreceptor in nerve ending of presynaptic seratonergic neuron so more NE release treat depression
AE:
-Prolong the QT can cause arrythmia
CI
-Arrythmia
Exxua
Esketamine
S
Novel antidepressant
MOA:
-Inhibits NMDA receptors in the gabaergic interneuron therefore reducing the release of GABA
As a result glutamate will be release form presynaptic glutamaergic receptors and because NMDA is block it will activate AMPA receptors in the post synaptic receptors
The activation of AMPA receptors will lead to the increase release of BDNF
The increase in BDNF will increase neuronal grow and increase synapses
Treat resistant depression
Sprivator
Zuranolone
Zur
Novel antidepressants
MOA:
Will increase allopregnolone that is a neuronal steroid and allopregnolone will enhance GABA at the GABA A receptor at the delta subunit
Treat postpartum depression becuase when mom gave birth the levels of allopregnolone drop
Zurzuvae
Lithium
Inhibit Inocetol phosphate pathway
Inhibit the release of NE from adrenergic neurons
Inhibits protein kinases
-Decrease adrenergic activity
Treat mania depression –> bipolar disorder
-Avoid giving to pt that suffers from hyponatreamia because they will absorb and retain more lithium and lithium has a low therapeutic index
DDi –> diuretics because they lower Na+ levels
AE:
-Skin rashes
-Muscle tremors
-Polyuria–> affect ADH
Aripiprazole
A
Atypical antipsychotic
Works as a partial agonist
Less likely to cause gain weight and hypercholesterolemia
AE:
-Prolong QT-arrythmia
-Seizure
-Sedation-block h1
-Hyperglycemia
-Less risk of abnormal muscle movement because works as a partial agonist
Abilify
Ziprasidone
G
Atypical antipsychotic
MOA
-Blocks D2 receptors but less potent as traditional antispsychotic
-Block 5-HT2a receptor and H1 receptors
-Ziprasidone (geon) is less likely to increase weight and hypercholesterolemia
AE:
-Sedation
-QT prolongation
-Seizure
-Hyperglycemia
-Some gallocteria in female and gynecomastiab in male
-Some dystonia, pseudoparkinson, akathisia, TD
Geon
Clozapine
Cloz
Atypical antipsychotic
MOA
-Block D2, D1,D4 and can block alpha 1, muscarinic receptors and histamine h1 receptor\
-WORST OFFENDER IN INCREASING WEIGHT AND CAUSING HYPERCHOLESTEROLEMIA
-Can decrease suicide thougths and behavior and has 0 risk of TD
AE:
-Hypercholesterolemia
-Agranularcytosis– reduction in wbc pt can die from infection
-Myocarditis- infection of myocardium
-Prolong qt - arrythmia
-Seizure
-Sedation
-Dizziness drop bp
-Xerostomia, tachy, mydraiss, hold more urine–> musca
Clozaril
Olanzepine
Z
Atypical antipsychotic
MOA
-Block D2 receptors
Can block 5-HT2a and H1
-Increase weight significantly and hypercholesterolemia
-prolong qt
-Seizure
-Hyperglycemia
-Sedation
Less risk of the prolactin effects less risk of dystonia, pseudoparkinson, akathesia, tardive diskenisia
Zyprexa
Olanzepine + Samidorphan
Ly
Samidorphan is a mu antagonist some kappa agonist
When combine olanzepine a antipsychotic with samidorphan there is less risk of gain weight
Lybalvi
Quetiapine
s
Atypical antipsychotic
block D2 , H1 , 5-HT2a
AE
Hyperglycemia
hypercholesterolemia
gain weight
sedation
prolong qt - arrythmia
Seizure
Seroquel
Risperidone
R
Atypical antipsychotic
Block D2 but less strong than typical
Can block H1
AE
Gain weight
Hypercholesterolemia
Hyperglycemia
Seizure
Prolong Qt -arrythmia
Sedation
Risperdal
Iloperidone
f
Atypical antispsychotic
block D2
H1 and 5-HT 2a
AE
Hyperglycemia
Hypercholesterolemia
Gain weight
Sedation
Seizure
Prolong QT-arrythmia
Fanapt
Lurasidone
Atypical antipsychotic
Block D2
Block H1
Block 5-HT 2a
AE
Gain weight
Hypercholesterolemia
Hyperglycemia
Sedation
Seizure
prolong QT-arrythmia
Latuda
Paliperidone
I
Atypical antipsychotic
MOA
Block D2 but not that strong
Block 5-HT2a
Block H1
AE
Gain weight
Sedation
Hypercholesterolemia]
Hyperglycemia
Seizure
Prolong QT - arryhtmia
less risk of dystonia, pseudoparkinson, akathisia, td, prolactin
Invega
Asenapine
S
Atypical antipsychotic
Block D2, H1 and 5-HT2a
AE:
Less prolacting, less dystonia less psedoparkinson, less akithesia, less td
-Gain weight
-Hypercholesterolemia
-Hyperglycemia
-Seizure
-Prolong qt -arrythmia
Saphris
Cariprazine
V
atypical antipsychotic
Vraylar
Lumateperone
c
atypical antipsychotics
Caplyta
Pimavanserin
5-HT2a inverse agonist
Block 5-HT2a
Treat psychosis and parkinson
AE:
Edema
Nuplazin
