Pcol 2 Exam 2 Flashcards

Question

Brivaracetam | Brivi-

Answer 1

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

Answer 2

Reduce glutamate release is a derivative of THC -Treat seizure AE: Cns depression Dizziness Sedation | Cannabidiol

Answer 3

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

Answer 4

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

Answer 5

Intermediate acting local anasthetic Block Na+ channels

Answer 6

Amide derivative Intermediate local anasthetic Block Na+ channels

Answer 7

Intermediate local anesthetic Amide derivative Block Na+ channels

Answer 8

Long acting local anasthetic Amide derivative Block Na+ channels

Answer 9

Amide derivative long acting local anaesthetic Block Na+ channels in the presynaptic unmyealinated neuron

Answer 10

Long acting amide derivative local anasthetic Block Na+ channels

Answer 11

Short acting ester derivative local anasthesia

Answer 12

Short acting ester derivative local anasthesia | Orajel, Anbesol

Answer 13

Intermediate acting local anasthetic Block Na+ channels Ester derivative

Answer 14

Long acting ester derivative local anasthetic block Na+ channels in the presynap in the local area

Answer 15

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

Answer 16

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

Answer 17

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

Answer 18

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

Answer 19

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

Answer 20

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

Answer 21

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

Answer 22

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

Answer 23

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

Answer 24

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

Answer 25

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

Answer 26

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

Answer 27

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

Answer 28

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

Answer 29

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

Answer 30

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

Answer 31

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

Answer 32

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

Answer 33

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

Answer 34

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

Answer 35

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

Answer 36

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

Answer 37

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

Answer 38

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

Answer 39

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

Answer 40

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

Answer 41

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

Answer 42

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

Answer 43

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

Answer 44

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

Answer 45

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

Answer 46

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

Answer 47

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

Answer 48

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

Answer 49

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

Answer 50

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

Answer 51

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

Answer 52

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

Answer 53

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

Answer 54

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

Answer 55

TCA MOA: -Inhibit reuptake of NE and 5-HT inhibit NET and SERT | Asendin

Answer 56

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

Answer 57

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

Answer 58

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

Answer 59

SSRI | Lexapro

Answer 60

Celexa SSRI

Answer 61

Zoloft SSRI

Answer 62

Trintellix SSRI

Answer 63

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

Answer 64

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

Answer 65

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

Answer 66

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

Answer 67

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

Answer 68

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

Answer 69

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

Answer 70

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

Answer 71

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

Answer 72

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

Answer 73

Atypical antidepressant Inhibit NET and SERT But can block H-1, Muscarinic receptors and A1 receptors can cause serotonin syndrome | Desyrel

Answer 74

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

Answer 75

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

Answer 76

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

Answer 77

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

Answer 78

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

Answer 79

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

Answer 80

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

Answer 81

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

Answer 82

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

Answer 83

Samidorphan is a mu antagonist some kappa agonist When combine olanzepine a antipsychotic with samidorphan there is less risk of gain weight | Lybalvi

Answer 84

Atypical antipsychotic block D2 , H1 , 5-HT2a AE Hyperglycemia hypercholesterolemia gain weight sedation prolong qt - arrythmia Seizure | Seroquel

Answer 85

Atypical antipsychotic Block D2 but less strong than typical Can block H1 AE Gain weight Hypercholesterolemia Hyperglycemia Seizure Prolong Qt -arrythmia Sedation | Risperdal

Answer 86

Atypical antispsychotic block D2 H1 and 5-HT 2a AE Hyperglycemia Hypercholesterolemia Gain weight Sedation Seizure Prolong QT-arrythmia | Fanapt

Answer 87

Atypical antipsychotic Block D2 Block H1 Block 5-HT 2a AE Gain weight Hypercholesterolemia Hyperglycemia Sedation Seizure prolong QT-arrythmia | Latuda

Answer 88

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

Answer 89

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

Answer 90

atypical antipsychotic | Vraylar

Answer 91

atypical antipsychotics | Caplyta

Answer 92

5-HT2a inverse agonist Block 5-HT2a Treat psychosis and parkinson AE: Edema | Nuplazin

Pcol 2 Exam 2 Flashcards

(116 cards)