CHAPTER 3
Adverse Effects Of Lithium:
**Nervous & Muscular System:** -Tremor -Ataxia -Confusion -Convulsions **Digestive:** -Nausea -Vomiting -Diarrhea **Cardiac:** -Arrhythmias **Fluid and Electrolyte** -Polyuria -Polydipsia -Edema **Endocrine:** -Goiter -Hypothyroidism
Anti-Depressant Drugs:
**Neurotransmitters that regulate mood:** -Norepinephrine -Serotonin >A Transmission deficiency of one or both of these monamines within the limbic system underlies depression.
Antianxiety and Hypnotic Drugs: Buspirone
>**A drug that reduces anxiety without having a strong sedative-hypnotic property.** >**DOES NOT leave patient sleepish-sluggish; which is better tolerated than Benzo's** >**NOT A CNS DEPRESSANT, so not as dangerous if patient takes with alcohol** >DOES NOT HAVE THE POTENTIAL FOR ADDICTION >Seems to act as a partial serotonin agonist; effects include dizziness and insomnia
Antianxiety and Hypnotic Drugs: Melatonin Receptor Agonists
>**A hormone that is overly excreted at night as part of the normal circadian rhythm.** >**Ramelteon (Rozerem) is a melatonin receptor agonist.** >High selectivity and potency (MT1= regulates sleepiness; MT2= regulate circadian rhythm) >**Treatment of insomnia, but its NOT A CONTROLLED SUBSTANCE or having abuse potential ** >**SE include** -Headache -Dizziness >Long-term use of Ramelteon above therapeutic levels can lead to increased prolactin associated with sexual dysfunction.
Second Generation Antipsychotics: Clozapine
>**An antipsychotic drug that is relatively free of the motor side effects of the phenothiazines and other second generation drugs. ** >**Clozapine has the ability to suppress bone marrow and induce agranulocytosis. Any deficiency in WBC's renders a person prone to serious infections; therefore, regular measurements of WBCs count is required. ** >**Typically, WBC's are measured weekly for the first 6 months, every other week for the next 6 months, and every month thereafter. ** >Clozapine has the potential to induce convulsions. Caution should be used with other drugs that can increase the concentration of clozapine. >Also potential for myocarditis that should be monitored, but most common side effects are drowsiness and sedation, hypersalivation, weight gain, reflex tachycardia, constipation, and dizziness.
Monoamine Oxidase Inhibitors
>**Antidepressant's such as isocarboxazid, phenelzine, and tranylcypromine are MAOIs.** >**Act by inhibiting the enzyme and interfering with the destruction of monoamine neurotransmitters, thereby leaving them more available.** >This increases the synaptic level of the neurotransmitters and makes possible the antidepressant effects of these drugs. >**The problem with inhibiting MAO is that this enzyme is also used by the liver to degrade monoamine substances that enter the body through food. ** >**One monoamine, tyramine, is present in many food substances, such as aged cheeses, pickled or smoked fish, and wine. If the liver cannot breakdown the tyramine from food substances, it can produce SIGNIFICANT VASOCONSTRICTION resulting in elevation of BP and the threat of hypertension. ** >**MAOIs are CONTRAINDICATED WITH CONCURRENT USE OF ANY OTHER ANTIDEPRESSANTS AND SYMPATHOMIMETIC DRUGS. ** >Concurrent use with some OTC produces with sympathomimetic properties (oral decongestants) should be AVOIDED. >**Because of the dangers that result from inhibition of hepatic MAO, patients taking MAOIs must be given a list of foods and drugs that need to be avoided.**
Anticonvulsant Drugs: Lamotrigine
>**Approved by FDA for maintenance therapy of bi-polar disorder, but it is not effective in acute mania. ** >**Lamictal works well in treating the depression of bi-polar disorder with less incidence of switching the patient into mania than anti-depressants. ** >Modulates the release of glutamate and asparate. >Patients should promptly report any rashes which could be signs of life-threatening Stevens Johnson syndrome. This can be minimized by slow titration to therapeutic doses.
Discuss major functions of the brain and how psychotropic drugs can alter these functions: Psychotropic Drugs
>**Associated with disturbance of movement** >**Important to remember that skeletal muscles controlled by the brain include diaphragm, which is essential for breathing, and the muscles of the throat, tongue, and mouth which is needed for speech.** >**Drugs that affect brain function can stimulate or depress respiration or lead to slurred speech.**
Drug Treatment For Alzheimer's Disease
>**Because the disease seems to involve progressive structural degeneration of the brain, there are two major pharmacological directions in its treatment. First attempt to prevent or slow the structural degeneration. Second attempt to maintain normal brain function for as long as possible.** >**Much of the memory loss in this disease has been attributed to insufficient ACh, a neurotransmitter essential for learning, memory, and mood and behavior regulations.** >**Acetylcholinesterase inhibitors slows the rate of memory loss and even improving memory. These drugs work by inactivating the enzyme that breaks down ACh, which leads to less destruction of ACh and, therefore, a higher concentration at the synapse. ** >Most common drug: Aricept. Drug is used for mild to moderate Alzheimer's and become less effective as the brain produces less ACh. >Glutamate, an abundant excitatory neurotransmitter, plays an important role in memory function; however, too much glutamate is thought to be destructive to neurons. Namenda named for the receptor it blocks from glutamate. >Normally, when glutamate binds to NMDA receptors, calcium flows freely and is essential to cell communication; however, pathological gray tangles of amyloid protein that build up in Alzheimer's brains, or amyloid plaques, are associated with excess glutamate. This excess glutamate results in excess calcium, which becomes toxic to surrounding brain cells.
Antianxiety and Hypnotic Drugs: Benzo's
>**Benzo's promote the activity of GABA by binding to a specific receptor on the GABA (a) receptor complex.** >**Binding results in an increased frequency of chloride channel opening causes membrane hyperpolarization, inhibiting cellular excitation. (Cellular excitation decreased= calming effect)** >**When combined with other CNS depressants (alcohol, opiates, TCAs) the inhibitory actions of benzo's can lead to life threatening CNS depression (resp. depression, coma, death)** >Since this drug interferes with electrical activity in the brain, it can lead interference of motor ability, attention, and judgement >Patient on Benzo's must be cautioned about engaging in activities such as construction, and driving a car. >**Benzo's may contribute to falls and broken bones because ataxia is a common side effect secondary to the abundance of GABA receptors in the cerebellum.**
Anticonvulsant Drugs: Carbamazepine
>**Carbamazepine is useful in preventing mania during episodes of acute mania.** >This drug reduces the firing rate of overexcited neurons by reducing the activity of sodium channels. >**Anticholinergic Side Effects: Dry mouth, constipation, urinary retention, blurred vision), orthostasis, sedation, and ataxia**. >**A rash may occur and it should be reported STAT because it could progress to a life-threatening exfoliative dermatitis or Stevens-Johnson syndrome. ** >**Recommended baseline lab work includes liver function tests, CBC, electrocardiogram, and electrolyte levels.** >**Blood levels are monitored to avoid toxicity (>12mcg/mL), but there is no established therapeutic blood levels for carbamazepine in the treatment of bi-polar disorder.**
Antianxiety and Hypnotic Drugs: Doxepin
>**Drug is used for the treatment of insomnia characterized by difficulty in maintaining sleep**. >Mechanism of action is a Histamine-1 blockade. >**Patients with severe urinary retention or on MAOI's should avoid this medication. ** >**Use of other CNS depressants and sedating anti-histamines should also be avoided**.
Antipsychotic Drugs: First Generation
>**First generation antipsychotic drugs is also referred to as conventional antipsychotics, typical antipsychotics, and standard psychotics.** >**These drugs are strong antagonists (blocking the action) of the D2 receptors for dopamine. ** >**It has been postulated that an overactivity of the dopamine system in certain areas of the mesolimbic system may be responsible for at least some of the symptoms in schizophrenia.; thus blockage of dopamine may reduce these symptoms. ** >**This is thought to be particularly true of the "positive" symptoms of schizophrenia, such as delusions (paranoid and grandiose ideas) and hallucinations (hearing, or seeing things not present in reality). ** >These drugs are also antagonists----to varying degrees---of the muscarinic receptors of ACh which are receptors for norepinephrine and histamine. >**Because dopamine (D2) in the basal ganglia plays a major role in the regulation of movement, it is not surprising that dopamine blockage can lead to motor abnormalities (extrapyramidial side effects) such as parkinsonism, akinesia, akathisia, dyskinesia, and tardive dyskinesia** >**Nurses and physicians often monitor patients for evidence of involuntary movements after administration of the first generation antipsychotic agents**. >An important physiological function of dopamine is that it acts as the hypothalamic factor that inhibits the release of prolactin from the anterior pituitary gland; thus blockage of dopamine transmission can lead to increased pituitary secretion of prolactin. In women, this hyperprolactinemia can result in amenorrhea (absence of menses) or galactorrhea (breast-milk flow), and in men can lead to gynecomastia (development of the male mammary glands) >**ACh is the neurotransmitter released by the post-ganglionic neurons of the parasympathetic nervous system. Through its attachment to the muscarinic receptors on internal organs, it serves to help regulate internal function. Blockage of the muscarinic receptors by phenothiazines and a wide variety of other psychiatric drugs can lead predictable effects based on the knowledge of the parasympathetic nervous system. Side effects include: Blurred vision, dry mouth, constipation, and urinary hesitancy. These drugs can also impair memory since ACh is important for memory function.** >**In addition to blocking dopamine and muscarinic receptors, many of the first-generation antipsychotic drugs act as antagonists at the receptors for norepinephrine. The ability of sympathetic nerves to constrict blood vessels is dependent on the attachments of norepinephrine receptors; thus blockage of these receptors can bring vasodilation and a consequent drop in BP. ** >These types of receptors above this are also found on the vas deferens and are responsible for the propulsive contractions leading to ejaculation. Potent antagonists of this type with little anti-cholinergic effects, such as trazodone, can lead to priapism, a painful prolonged erection that is caused by the inability of the erection to subsidize. >Finally, many of the first generation antipsychotic agents, as well as a variety of other psychiatric drugs, block the H1 receptors for histamine. The two most significant side effects of blocking these receptors are sedation and substantial weight gain. Nonadherence to the medication regimen is a significant issue because of these troublesome side effects, and second generation antipsychotic drugs have consequently become the drugs of choice.
Antianxiety and Hypnotic Drugs:
>**GABA is the major inhibitory (calming) neurotransmitter in the CNS. ** >3 types of GABA receptors -GABA (a) [target of benzo, barbituates, & alcohol) -Gaba (b) [coupled to potassium/calcium channels are associated with pain, memory, mood, and other CNS functions] -Gaba (c)---role is not defined >**Drugs that enhance GABA (a) receptors exert a sedative hypnotic action on brain function. The most commonly used anti-anxiety agents are benzo's.**
Anti-Depressant Drugs: SNRIs
>**INCREASE BOTH SEROTONIN AND NOREPINEPRHINE** >Venlafaxine is more of serotonergic agent at lower therapeutic doses, and norepinephrine reuptake blockade occurs at higher doses, leading to the dual SNRI action. >**Hypertension may be induced in patients because of a dose dependent effects based on norepinephrine reuptake blockade. Doses higher than 150 mg/ day can increase diastolic BP 7-10 mmgh.** >Pristiq works the same as Effexor. >**Duloxetine is an SNRI indicated for both depression and GAD as well as diabetic neuropathy and fibromyalgia**. >Like TCAs, SNRI's have a therapeutic effects on neuropathic pain by activating the descending norepinephrine and 5-HT pathways to the spinal cord, thereby limiting pain signals ascending to the brain.
Second Generation Antipsychotics
>**Known as atypical antipsychotics which produce fewer extrapyramidial side effects and target both negative and positive symptoms of schizophrenia.** >**Often chosen as first-line treatments over the first generation antipsychotics because of their lower risk of EPS. ** >**Most of second generation drugs can increase the risk of metabolic syndrome with increased weight, glucose, and triglycerides. ** >Simultaneous blockade of receptors of 5-HT2x and H1 is associated with weight gain from increased appetite stimulation via the hypothalamic eating centers. >Strong antimuscarinic properties at the M3 receptor on the pancreatic beta cells can cause insulin resistance leading to hyperglycemia. >Clozapine and olanzapine have the highest risk of causing metabolic syndrome/ Aripiprazole and ziprasidone have the lowest risk. >**Second generation antipsychotics are predominantly D2 (dopamine) and Serotonin (5-HT2a) antagonist (blockers). The blockade at the mesolimbic dopamine pathway decreases psychosis, similar to the mechanism by which first-generation antipsychotics work.** >Decreasing D2 can decrease psychosis but cause adverse effects elsewhere. Decreased D2 in the nigrostriatal area can cause the movement side effects of EPS; decreased D2 in the mesocortical area can worsen cognitive and negative symptoms of schizophrenia; decreased D2 in the tuberoinfundibular area can increase the hormone prolactin leading to gynecomastia, galactorrhea, amenorrhea, and low libido.
Anti-Depressant Drugs: 3 Hypotheses mechanism of action
>**Monoamine hypothesis of depression** -**A deficiency in one or more of the three neurotransmitters; serotonin, norepinephrine, or dopamine. The theory is that increasing these neurotransmitters alleviates depression. ** >Monamine receptor hypothesis of depression -Low levels of neurotransmitters cause post-synpatic receptors to be up-regulated (increased in sensitivity or number). Increasing neurotransmitters by antidepressants results in down-regulation (desensitization) of key neurotransmitter receptors. >Another hypothesis for the mechanism of anti-depressant drugs is that with prolonged use they increased production of neurotrophic factors. These factors regulate the survival of neurons and enhance the sprouting of axons to form new synpatic connections.
Mood Stabilizers: Lithium
>**Mood stabilizer in patients with bi-polar (manic-depressive) disorders. ** >Mechanism of action not understood, but lithium may well act by affecting electrical conductivity in neurons. >It may be that an overexcitement of neurons in the brain underlies bipolar disorder and that lithium interacts in some complex way with sodium and potassium at the cell membrane to stabilize electrical activity. >Also, lithium may reduce excitatory neurotransmitter glutamate and exert an anti-manic effect. >By altering electrical conductivity, lithium represents a potential threat to all body functions that are regulated by electrical currents. Foremost among these functions is cardiac contraction; lithium can induce, although not commonly, sinus bradycardia. >**Extreme alteration of cerebral conductivity with overdose can lead to convulsions. ** >**Alteration in nerve and muscle conduction can commonly lead to tremor at therapeutic doses or more extreme motor dysfunction with overdose.** >**Sodium and potassium play a strong role in regulating fluid balance, and the distribution of fluid in various body compartments explains the disturbances in fluid balance that can be caused by lithium. This include polyuria (output of large volumes of urine) and edema (accumulation of fluid in the interstitial space)** >**Long-term use of lithium can cause hypothyroidism in some patients, which is secondary to interfering with the iodine molecules affecting the formation and conversion to its active form (T3) thyroid hormone.** >**In addition, hyponatremia can increase the risk of lithium toxicity because increased renal reabsorption of sodium leads to increased reabsorption of lithium as well. ** >Lithium has a low therapeutic index. This means that the blood level of a drug that can cause death is not far above the blood level required for drug effectiveness. >**Blood level of lithium needs to be monitored on a regular basis to be sure that the drug is not accumulating and rising to dangerous levels.**
Anti-Depressant Drugs: Tricyclic Anti-Depressants
>**NO LONGER FIRST LINE MEDICATIONS SINCE THEY HAVE MORE SIDE EFFECTS, TAKE LONGER TO REACH OPTIMAL DOSE, AND ARE FAR MORE LETHAL IN OVERDOSE** >**Act primarily by blocking the reuptake of norepinephrine for the secondary amines (nortriptlyine) and both norepinephrine and serotonin for the tertiary amines (amitriptyline).** >**Blockage prevents norepinephrine from coming in contact with its degrading enzyme MAO, and thus increases the level of norepinephrine in the synapse. ** >**Also block the muscarinic receptors that normally bind acetylcholine. This blockage leads to typical anti-cholinergic effects such as blurred vision, dry mouth, tachycardia, urinary retention, and constipation.** >Depending on the individual drug, these agents can also block H1 receptors in the brain. Blockage of these receptors by any drug causes sedation and drowsiness. >**People taking TCAs often have adherence issues because of their adverse reactions. ** >**TCA overdose can be fatal secondary to cardiac conduction disturbances from excessive sodium channel blockade.**
Antianxiety and Hypnotic Drugs: Short Acting Sedative-Hypnotic Agents
>**Newer class called "Z" Drugs** -Zolpidem -Zaleplon >**They have sedative effects without the anti-anxiety, anticonvulsant, or muscle relaxant effects of BZD's. ** >**Onset of action is faster than most BZDs. ** >**It is important to inform patients taking non-benzo hypnotic agents about the quick onset and to take them when they are ready to go to sleep. ** >Eszopiclone has the longest duration of action (7-8 hours); unpleasant taste upon awakening.
Second Generation Antipsychotics: Risperidone
>**Risperidone has a low potential for inducing agranulocytosis or convulsions. However, high therapeutic dosages (>6mg/day) may lead to motor difficulties.** >**As a potent D2 antagonist, it has the highest risk of EPS among the second-generation antipsychotics and may increase prolactin which may lead to sexual dysfunction. ** >**Risperidone can cause orthostatic hypotension and sedation. Keep in mind that orthostatic hypotension can lead to falls, which are a serious problem among older adults. ** >**Weight gain, sedation, and sexual dysfunction are adverse effects that may affect adherence to treatment regimen and should be discussed with patients.** >Risperidal consta is an injectable form of the drug that is administered Q2 weeks. A rare but serious side effect is an increased risk of CVA in older adults with dementia who are being treated for agitation.
Anti-Depressant Drugs: Serotonin-Norephinephrine Disinhibitors
>**SNDIs represented ONLY BY ONE DRUG WHICH IS REMERON/MIRTAZAPINE** >Increases norepinpehrine and serotonin transmission by antagonizing (blocking) pre-synpatic alpha 2 noradrenergic receptors. >**Mirtazapine offers both anti-anxiety and anti-depressant effects with minimal sexual dysfunction and improved sleep.** >This anti-depressant is particularly suited for the patient with nausea because it is an anti-emetic. >**Most common SE are sedation and weight gain secondary to potent H1 blockade and 5-HT2c blockade.**
Second Generation Antipsychotics: Quetiapine
>**Seroquel is a strong blockage of H1 receptors accounts for the high sedation.** >The combination of H1 and 5-HT2c blockage leads to the weight gain associated with use of this drug and also to a moderate risk of metabolic syndrome. >**Also causes orthostatic hypotension. Has a low risk for EPS or prolactin elevation from low D2 binding due to rapid dissociation at D2 receptors.**
Treating Anxiety Disorders with Anti-Depressants
>**The symptoms, neurotransmitters, and circuits associated with anxiety disorders overlap extensively with those of depressive disorders, and many antidepressants have proven to be effective treatments for anxiety disorders.** >**SSRIs are often used to treated OCD, social anxiety disorders (SAD), generalized anxiety disorders (GAD), and panic disorders (PD)** >**Venlafaxine is used to treat GAD, SAD, and PD. ** >**Duloxetine (Cymbalta) has FDA approval for GAD**
Anticonvulsant Drugs:
>**Valproate (Depakote) and Valproic Acid (Depakene) and Carbamazepine (Tegretol) and lamotrigine (Lamictal) demonstrated efficacy in treatment of bi-polar disorder. ** >These drugs reduce the firing rate of very-high-frequency neurons in the brain. >Other proposed mechanisms as mood stabilizers are glutamate antagonists and GABA agonist.
ADHD Drugs
>ADHD shows symptoms of short attention spans, impulsivity, and overactivity. >Methylphenidtes, adderall, and vyvanse are helpful in these conditions. >These drugs are sympathomimetic amines and have been shown to function as direct and indirect agonists at adrenergic receptor sites. >Psychostimulants act directly at the postsynaptic receptor by mimicking the effects of norepinpehrine and dopamine into the presynaptic neuron, and increasing the release of these monoamines into the extraneuronal space. >Side Effects: Agitation, exacerbation of psychotic thought processes, hypertension, and growth suppression, as well as their potential for abuse. >FDA approve 3 non stimulants for treatment of ADHD: Straterra, Guanaficine, and Clonidine. >Straterra is a norepinephrine reuptake inhibitor approved for use in children 6+. Common Side Effects: Decreased appetite and weight loss, fatigue, and dizziness. Contraindicated for patients with severe cardiovascular disease due to its potential to increase BP and HR. >Guanfacine and Clonidine are centrally acting alpha2 adrenergic agonists that have traditionally been used for hypertension. FDA approved forms for ADHD are used in children ages 6-17. Both should be increased slowly and should not be D/C'd abruptly. Guanfacine's most common SE include sleepiness, trouble sleeping, low BP, nausea, stomach pain, and dizziness. >Clonidine can be used alone or in combination with ADHD drugs. Common SE are fatigue, irritability, throat pain, insomnia, nightmares, emotional disorder, constipation, increased body temp, dry mouth, ear pain.
Third Generation Antipsychotic: Aripiprazole
>Abilify is a unique antipsychotic known as a dopamine system stabilizer. >Partial agonist at the D2 receptor. In areas of the brain with excess dopamine, it lowers the dopamine level by acting as a receptor antagonist; however in regions with low dopamine, it stimulates receptors to raise the dopamine level. >Lacks the sedation and weight gain properties >Side Effects: Insomnia and Akathisia.
Herbal Treatments
>Among the major concerns of HCP are the long-term effects (nerve, kidney, and liver damage) of some herbal agents and the possibility of adverse chemical reactions when herbal agents are taken in combination with other substances, including conventional medications. >Another key concern regarding the use of alternative herbs and nutrients is the quality of herbal supplements on the mark. Many brands are poor quality, having dosing inconsistencies, or are questionable purity and stability. >It is important that nurses explore the patient's use of herbal supplements in a non judgemental manner by asking "What OTC meds or herbs do you take to help your symptoms? Do they help? How much are you taking? How long have you been taking them?" . >Individuals taking medications or other supplements need to be aware of drug-substance interactions and product safety. Such discussion should be apart of the initial and ongoing interviews with patients.
Anti-Depressant Drugs: Other Anti-Depressant's
>Buproprion (Wellbutrin) is an anti-depressant that is also used for smoking cessation (zyban) >Seems to act as a norepinpehrine-dopamine reuptake inhibitor and also inhibits nicotonic ACh receptors to reduce the addictive action of nicotine. >Side Effects include: Insomnia, Tremor, Anorexia, and weight loss >Contraindicated in patients with seizure disorder, in patients with a current or prior diagnosis of bulimia or anorexia nervosa, and patients undergoing abrupt discontinuation of alcohol or sedatives (including benzo's) due to the potential of seizures.
Anti-Depressant Drugs: Monoamine Oxidase Inhibitors
>MAOIs are a group of anti-depressant drugs that illustrate the principle that drugs can have a desired beneficial effect in the brain while at the same time having possibly dangerous effects elsewhere in the body. To understand actions of these drugs, keep in mind following definitions: -**Monoamines: a type of organic compound; includes the neurotransmitters; norepinephrine, epinephrine, dopamine, serotonin, and may different food substances and drugs** -**Monoamine Oxidase (MAO): An enzyme that destroys monamines ** -**Monoamine Oxidase Inhibitors (MAOIs): drugs that prevent the destruction of monoamines by inhibiting the action of MAO** >**Monoamine neurotransmitters, as well as any monamine food substance or drugs, are degraded (destroyed) by the enzyme MAO, which is located in neurons and in the liver.**
Anti-Depressant Drugs: Other Anti-Depressant's: Vilazodone
>Mechanism of action includes enhancing the release of serotonin by inhibiting the serotonin transporter and by stimulating serotonin receptors via partial agonism (similar to the anxiolytic medication buspirone). >Common adverse reactions include: diarrhea, nausea, insomnia, vomiting. >DO NOT TAKE AT BEDTIME >SHOULD BE TAKEN WITH FOOD TO INCREASE BIOAVAILABILITY >Trazodone was not used for anti-depressant treatment for many years, but was given, along with another agent, for the treatment of insomnia, as sedation is one of the common side effects. >Common side effects are orthostatic hypotension and sedation.
Discuss major functions of the brain and how psychotropic drugs can alter these functions: :Functions
>Monitor changes in the external world >Monitor the composition of body fluids >Regulate contractions of the skeletal muscles >Regulate the internal organs >Initiate basic drives; hunger, thirst, sex, aggressive self-protection. >Mediate conscious sensation >Store and retrieve memories >Regulate mood (affect) and emotions >Think perform intellectual functions >Regulate the sleep cycle >Produce and interpret language >Process visual and auditory data
Anticonvulsant Drugs: Other Anticonvulsants
>Other anti-convulsants used as mood stabilizers are gabapentin, topiramate, and oxcarbazepine. >None of these drugs has FDA approval as a mood stabilizer and are lacking evidence for the primary treatment of bi-polar disorder. >Antipsychotic medications and anti-anxiety meds such as clonazepam are used for their calming effects during mania.
Anti-Depressant Drugs: SSRI
>Prozac, Zoloft, Paxil, Celexa, Lexapro and Luvox preferentially block the reuptake and degradation of serotonin, but they have different effects on neurotransmitters >**Fluoxetine 5-HT2c antagonist, can lead to the anorexic and antibulmic effects at higher doses.** >**Paxil is the MOST ANTICHOLINERGIC among the SSRI's due to its muscarinic-1 antagonist property. Although it is less anti-cholinergic than TCAs, paxil may not be the best choice for patients with contraindications with anti-cholinergic agents (ex: narrow-angle glaucoma)** >**SSRIs as a group, have less ability to block the muscarinic and histamine receptors than do the TCAs. As a result of their more selective action, they seem to show comparable efficacy without eliciting the anti-cholinergic and sedating side effects resulting from stimulation of different receptors.** > 5-HT2a & HT2c stimulation of receptors in the spinal cord may inhibit spinal reflexes of orgasm >Stimulation of 5-HT2a receptors in the mesocortical area may decrease dopamine activity in this area, leading to apathy and low libido. >5-HT3 receptors stimulation in the hypothalamus or brainstem may cause nausea or vomiting, while GI side effects are secondary to the 5-HT3 and or 5-HT4 receptors in the GI tract.
Anticonvulsant Drugs: Valproate
>Valproate (Depakote & Depakene) is structurally different from other anticonvulsants and psychiatric drugs that show efficacy in the treatment of bi-polar disorder. >**Divalproex is recommended for mixed episodes and has been found useful for rapid cycling.** >**Common side effects include: Tremor, Weight gain, and Sedation. ** >**Occasional serious side effects are: Thrombocytopenia, pancreatitis, hepatic failure, and birth defects. ** >**Baseline levels are measured for liver function indicators and CBC before an individual is started on this medication, and measurements are repeated periodically. In addition, the therapeutic blood level of the drug is monitored.**
LOOK AT PAGE 54 IN PSYCH BOOK
HAS SIDE EFFECTS FOR EACH DRUG MAKE SURE YOU COPY THIS CHART!!!
