Pharm Psyc

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positive symtoms

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• generally regarded as manifestations of psychosis
• delusions
• auditory hallucinations, hearing voices, false ideas/thories 

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negative symtoms

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• absence of normal trais or abilities
• flat of blunted affect and emotion
• alogia- poverty of speech 
• anhedonia- inability to experience pleasrue
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Dopamine

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• catecholamine (like epi and noreipi)
• synthesied from the amino acid tyrosine
• can be inhibiory or excitatory 
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MOA of chlorpromazine

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• increase metabolism of dopamine, resulting in signifcantly lower brain dopamine levels
• drops dopamine in the brain --> a lot of psychotic symptosm of schizophrenia would disapear. 
• Led to dopamine hypothsis 

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Phenothiazines

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• Dopamine D2 receptor antagonist
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1st generation antipsychotics

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• antipschotic effects occur in presence of 70% occupancy of the D2 receptors
• works well with positive symptoms but may make negative symtoms worse

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Adverse effects of 1st generation drugs

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• Extrapyramidal side effects--> parkinsonism tremors, rigidity, slowness of movement
• Dystonia- involunatry and usually painful muscle contractions
• akathisia- inability to resist the urge to move 
• tardive dyskinesia 

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Butyrophenones

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• Haldol --> 1st generation drug
• minial anticholinergic effects- can be used in PT with delirium
• associated iwth more neurolgocial disturbacnes that casue EPS and tartive dyskinesia 
• Block the dopamine receptors

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Thioxanthine

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• thiothixene --> 1st generation drug
• replacement of nitrogen in the central ring
• increased potency compared to chlorpromazine, less sedating, fewer anticholinergic side effects
• Associated with more neurolgoical disturances that cause EPS

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Muscarinic receptor antagomis (anticholinergic)

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• conteracts extrapyramidal side effects but gives dry mouth, constipatin, other anticholinergic effects
• will somtimes offset the EPS 

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Later generation antipsychotics

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• sometimes called atypical antipsychotics
• target dopamine and serotonin --> more loosely bound to D2 receptors then typical
• broader spectrum of treatment effects (positive and negative symptoms)
• better tollerated, lower occurrence of adverse effects

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5-HT seotonin receptors 

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• decreases negative symtoms and EPS
• serotonin inhibits dopamine release
• + symptoms associated with hyperdopaminergic condition in limbic lobe - more D2 receptors there
• - symtoms assocaited with hypodopaminergic condtion in frontal lobe- more 5- HT receptors there and serotonin inhibts dopamines release

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Clozapine

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• atypical 2nd generation
• most effective (last resort) durg in controlling treatment - resistnat schizophrenia
• most dangerous 5 black box warnings risk of agrnulocytosis
• most effective in reducing negative symtoms 
• strong antagonism of 5-HT 2A receptors 
• highest antcholinergic effects, hypotension, sedation, weight gain

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Risperidone

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Predominantly blocks D2, then 5-HT

• lacks anticholnergic activity
• increases prolactin levels ( don't give to breast cancer PT)
• increased EPS (dose dependent)
• weigth gain and sedation
• highest cance of EPS, diabetes, prolactin elation

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Ziprasidone

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• Clinically significant QT prolongation in susceptible PT
• may cause hyperprolactinemia
• not associated with weigth loss 

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Aripiprazole 

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• Abilify
• unique mechanism of action as a D2 partial agonist
• low EPS, no QT prolongation, no sedation 
• could cause potential intolerability due to akathisia/activation
• not associated with weight gain

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Anticholinergic side effects

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• constipation, urinary retention, exacerbation of narrow angle glucoma
• benefical effects: counter acts parkinsonian SE of antipsychotic drugs 

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antiadrenergic Side effects

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• orthostatic hypotension
• acute high doses may produce cardiovascular collapse, death
• q

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Neuroleptic malignant syndrone

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• mental status- catatonia, vital signs (tackycardic, unstable BP, hyperthermia
• Appearance - muscle rigidity
• stop drug, reversal of the dopamine blockade (bromocriptine) relax the muscles (dantrolene)

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GABA receptor

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• work by opening Cl or K channels (inhibitory effect) which makes the nuronla membrane less responsive to stimulation which lowers the magnitude of response if stimulation does occur
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barbiturates

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• have generally been replaced by benzodiaxepine for clinical treatmetn b/c barbituates are lethal in OD, have low margin of safty, have a high tolerance and abuse

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MOA of barbiturates

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• enhances acitivity (agonist) at the GABA (A) receptor increase inhbition by increasing chlorine influx, activity does not need an action potential also diminshed the effects of glutamate
• glucose and oxygne consuptom in the brain decrease 
• stablized nurons by increasd outflow of K
• can exert their actions in the absence of GABA

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Benzodiazepine

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• reduces anxiety w/o prodcuing excessive sdation- compound spcific balance of sedation/ muscle relazation/ anxiolytic effects
• less derpession of respiratory centers in teh medulla but respiratory depression still occurs anc eb by syndergistically incresed in the presence of other drugs or alcohol 

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bariturates adverse effects

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• promote non resfult sleep by reducing early REM and causing late REM rebound 
• Cognitive depression is strong

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Benzodiazepine MOA

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• they are GABA A agonists, binding to that reeptor site
• when bound, bezos increase the number of tiems teh chloride channel opens in reponse to GABA
• important note: benzo require the presence of GABA at the receptor to elicit action 

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action of benzodiazepine

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• int he amygdala, frontal cortex and insula, their effects reduce: response to fearful stimuli, anxiety, panic and agitation
• in spinal cord, cerebellum and brain stem their effects result in muscle relazation and mild sedation

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Benzos are not recommend for

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• PT who rely on fine motor or cognitive skills
• PT who must remain mentally allert
• PT receiving other CNS depressign agents for pain, sizure control, muscle spasm, 
• elderly PT

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Benzodiazepines can be reversed by using

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Flumazenil since it competeitivley binds to the GABA receptor and has not other signifcant effects in humans

many benzos have longer half lifes than flumazenil, so repeated dosing may be required

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Buspirone

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• Serotonin receptor partial agonist, effects are gardual, usually apparetn within 14 days
• reduces aggression, anxiety and irritability
• can't be mixed with MAO-I profound hypotension occurs

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Kava

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• A beverage prepared from teh oceanic kava plant
• can reduce anxiety but there are many reports of hepatotoxicity
• acts of the GABA A receptors, has been shown to block NA channels which blocks gluatmate activity

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Ramelteon

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• Selective melatonin receptor agonist
• acts on the suprachiasmatic nucleus (SCN) the SCN sends signals to the penal gland to influence release of melatonin

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antihistamines

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• diphenhydramine and doxylamine
• postsynaptic histaminic and muscarinic blockade
• FDA approvd for insomnia treatment
• most common OTC sleep aid ingredients

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resperpine

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• alkaloid from root of indian snake plant
• found to interact with storage vesicles and deplete norepinephrine and serotonin in the CNS and PNS
• induced severe depression, suicide was common with early use of high doses
• first indication that depressin may have a biochemical basis

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Impipramine

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• developed as an antihistamine and was investigated as a schizophrenia treatment since it had anticholinergic effects
• no effective as an antipsychotic
• mechanism was determiend to be inhibition of the reuptake of norepinephrine and serotonin by blocking their transport across membraens within the CNS, thus making their levels higher

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Trazodone

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• 1st serotonergic agent- antidepressant effects may be dueto agonist action at the 5_HT 1A receptor and inhibiton of the serotonin reuptake transporter, alogn with antagonism of 5-HT2A

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Serotonin deficiency

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anxiety, panic, phobia, obsession and compulsions

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norepiephrine deficiency

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decreased concentratiosn, diminished memory, impaired information processing, fatiuge

 

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Norepinephrine and dopamine

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decreased attention, pschomotor retartation

 

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dopamine deficiency

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cognative slowing, carvings, hypersomnia, adhedonia 

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SSRI

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• 1st line treatment for depression b/c it has has equal efficacy, wide margin of sfety in OD, less evere side effects
• useful in anxiety disorder, bulemia, borderline persoinality disorder

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Adverse effects of SSRI

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• anxiety, tremors, insomina, GI symptoms, increased appetie, HA, rash, sexaul dysfunction

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Serotonin syndrome

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• interaction when serotonergic drugs are taken together eg SSRI and MAOI, TCA
• symtoms: mental status chagnes- agitation, confusin, hyperpyrexia, motor abnormalites
• can lead to sizzure, coma or dath
• treatment: benozos, supprotive care
• dantrolnene for muscle rgidity

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TCA side effects

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• antimuscarinic: dry mouth, constipation, urinary retetion
• antihistaminic: sedation
• Na channel clockage: increase QRS, arrhymias
• alpha bockade: orthostatic hypotension, tachycardia, sexual dysfunction
• doesn't cause tardive dyskinesia
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MAOI MOA

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block the breakdown of neurotransmitters but also block metabolism of related compounds

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MAOI adverse effects

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HA, CNS stimulation, dry mouth, weight gain, hypotension, sexual disturbances

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antidepressents dicontinuation

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• can produce withdrawl symptoms --> crying 
• may be more severe in SNRI discontinuation
• most common with shrot half life drugs
• washout peroid of several weeks may be need before starting another drug
• SSRI and SNRI should be tapered slowly

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ADHD diagnostic critera

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• 6 or more symptoms of inattention for six months or more and/ or 6 or more symptoms of hyperactivity- impulsivity for 6 or more
• must also have onset prior to age 7 and impariment in ore then on setting

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Drugs approved for ADHD

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• stimulatns--> methylphenidate, dexmethylphenidate, amphetamine
• these medications cause release of presynaptic norepinephinrine and dopamine, and block reuptake of noreip and epi

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Atomoxetine

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• another druge for ADHD
• NE reuptake inhibitor
• adverse effects: hepatotoxciity, suicidal evetns, CV, gowth sloing
• approved for adult ADHD

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Modafinil

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• Stimulant
• approved for excessive sleepiness
• adverse efect profile resulted in rejection by the FED for ADHD use but is stil used off labe for ADHD

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Adverse effects of stimulants

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• loss of appetite, weight loww, sleeping problems, irritability, stomachache, HA, 
• symptoms of depresion (particularly with missed doses)
• intensification of ticks 9muscle twitches of the face and other parts of tthe body
• hyptension (guanfacine)

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Acute dystonia

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• occus suddenly and is painful--> extreme muscle spasms common in children and yong males 
• common with highpotency drugs or combo medications
• rapidly reversible with anticholinergics

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Drugs to treat EPSE

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• Antichoinergics 9benztropine, trihexyphenidyl)
• Antihistamines--> diphendydramine
• dopamine agonists (amantadine)
• Benzodiasepines (diazepam)