Study Psych Drugs

MENTAL HEALTH & PSYCHOTROPIC DRUGS THE BRAIN Functions:

Structure:

Mental disturbances can affect any of these functions of the brain:

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Regulation of skeletal muscle contraction;

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Initiation and regulation of basic drives (sex, hunger, thirst, aggression);

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Conscious sensation;

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Memory;

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Mood;

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Thought;

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Regulation of sleep cycle;

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Language

Since all of these brain functions are carried out by similar mechanisms and are often in similar locations, mental disturbances are often associated with alterations in other brain functions as are the drugs used to treat them. Cerebral Cortex

White Matter

PARIETAL LOBE Sensory & Motor Abstract Thought Proprioception Reading/Math Right/Left Orientation

OCCIPTAL LOBE Vision Visual Association Visual Memory Language Formation

TEMPORAL LOBE Auditory Processes Language Memory Connects with Limbic

CEREBELLUM Balance & Coordination

FRONTAL LOBE Thought Processes Intelligence Social Judgment Voluntary Motor Ability

Maintains Equilibrium Coordinates Skeletal Muscle Contraction

MIDBRAIN Pupilary reflexes Eye movement

PONS Auditory Pathway

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MEDULLA OBLONGATA Reflex Centers Balance Heart rate Respirations Cough, swallow, sneeze Blood pressure Vomiting

NERVOUS SYSTEM Sympathetic

Dominant division of the autonomic nervous system in stress situations. Norepinephrine is the primary neurotransmitter of the sympathetic nervous system. “Fight or Flight” Effects: • Dilated pupils • Increased salivary flow • Increased heart rate • Constricted arterioles • Dilated bronchi • Decreased digestion and intestinal motility • Decreased urinary bladder activity

Parasympathetic

Acetylcholine is the primary neurotransmitter of the parasympathetic nervous system. “Feed and Breed” or “Rest and Digest” Effects: • Undilated pupils • Decreased salivary flow • Decreased heart rate • Dilated arterioles • Undilated bronchi • Increased digestion and intestinal motility • Increased urinary bladder activity

Mental Disturbances

May affect sympathetic and/or parasympathetic nervous systems in nonnormal ways. Stress:

Sympathetic nervous system initiates the release of CRH (corticotropin-releasing hormone), which causes the pituitary to release ACTH (adrenal corticotropin hormone), which causes the adrenal cortex to release cortisol. However, all three hormones influence the functions of the nerve cells in the brain. In mental illness, depression and anxiety, the normal negative feedback loop for these hormones does not appear to work.

Anxiety: May activate both parasympathetic nerves (hypermotility of GI, diarrhea) and sympathetic nerves (vasoconstriction, hypertension) simultaneously.

Nerve Communication Communication of information between neurons is accomplished by movement of chemicals across a small gap called the synapse. Chemicals, called neurotransmitters, are released from one neuron at the presynaptic nerve terminal. Neurotransmitters then cross the synapse where they may be accepted by the next neuron at a specialized site called a receptor. The action that follows activation of a receptor site may be either depolarization (an excitatory postsynaptic potential) or hyperpolarization (an inhibitory postsynaptic potential). A depolarization makes it MORE likely that an action potential will fire; a hyperpolarization makes it LESS likely that an action potential will fire. (Chudler, University of Washington) There are four elements involved in nerve-to-nerve or nerve-to-muscle communication: (1) Production or existence of a neurotransmitter; (2) Release of the neurotransmitter; (3) Reception of the neurotransmitter by another nerve or cell; and (4) Inactivation of the neurotransmitter Changing any one of the four elements can change the results. Neurotransmitter (NT): Definition: A chemical that modifies or results in the transmission of nerve impulses between two synapses. (Mosby’s Dictionary, 7th ed., 2006) Different types of chemicals may act as neurotransmitters: small molecules (like the monoamines such as serotonin), amino acids (such as GABA), neuroactive peptides (such as endorphins), and soluble gases (such as nitric oxide). NT Release:

Neurotransmitters are made in the cell body of the neuron and then transported down the axon to the axon terminal. Molecules of neurotransmitters are stored in small "packages" called vesicles. Neurotransmitters are released from the axon terminal when their vesicles "fuse" with the membrane of the axon terminal, spilling the neurotransmitter into the synaptic cleft. (Chudler, University of Washington)

Reception of NT:

The NT will only bind to post-synaptic cell receptors that recognize them. If these receptors are altered or blocked, then the NT will not bind and the NT action will be prevented.

Inactivation of NT:

There are three mechanisms for inactivating a NT. (1) Diffusion: The unbound NT molecules drift away from the synaptic cleft to sites that do not recognize them. (2) Enzymatic Deactivation: Specific enzymes bind with the NT molecules and change their shape so they will no longer be recognized by the receptors.

(3) Reuptake: The neuron that released the NT can take back the whole NT molecule removing it from the cleft. The NT will then be destroyed by an intracellular enzyme (such as monoamine oxidase) or be recycled for use later.

Neurotransmitters Neurotransmitter

Receptor

Action

Decreased

Dopamine (DA)

D1, D2

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Fine muscle movement

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Parkinson’s

(Synthesized from Tyrosine)

Deactivated by Monoamine Oxidase

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Integration of emotions and thoughts

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Depression

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Involved with decision-making

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Stimulates hypothalamus to release hormones (sex, thyroid, adrenals)

α1, α2

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Level in brain affects mood

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Depression

β1, β2

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(Catecholamine)

Deactivated by Monoamine Oxidase

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Serotonin

5-HT

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Actual name is “5-hydroxytryptamine”

Deactivated by Monoamine Oxidase

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Most of 5-HT’s function is vasoconstriction in cardiovascular, respiratory and GI systems.

Elevated

MONOAMINES

(Catecholamine) Norepinephrine (NE) (Synthesized from Dopamine)

(5-HT) (Synthesized from Tryptophan)

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Schizophreni a

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Mania

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Mania

Plays a part in sleep/wake cycle

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Anxiety

Stimulates sympathetic branch of ANS for “fight or flight”

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Schizophreni a

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Anxiety

Most prevalent neurotransmitter in the Central Nervous System. Used by more that 50% of neurons

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Depression

Glutamate is the most important excitatory (EPSP) neurotransmitter, exciting about 90% of the postsynaptic terminals to which it contacts

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Suicide

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Multiple sclerosis

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Reduces Anxiety

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Depression

Plays a role in sleep regulation, dreaming, hunger, mood, pain perception, aggression and sexual behavior Is found in platelets and plays a role in platelet aggregation

AMINO ACIDS Glutamate

NMDA

(Derived from αketoglutarate)

mGluR1,2

Gammaaminobutyric Acid (GABA) (Synthesized directly from glutamate)

Deactivated by Glial Cells in CNS (Astrocytes)

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As an excitatory neutrotransmitter, it binds to ionotropic receptors, causing depolarization by opening Na+ ion channels

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At metabotropic receptors, it is modulatory; Plays a major role in cellular metabolism

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Principle excitatory amino acid in CNS

GABAA

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The most important inhibitory (IPSP) neurotransmitter

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Anxiety

GABAB

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Present in high concentrations in the CNS, preventing the brain from becoming overexcited

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Schizophrenia

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Huntington’s Chorea

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As an inhibitory neutrotransmitter, it binds to both ionotropic and metabotropic receptors, causing hyperpolarization by opening Cl- ion channels

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Used by inhibitory interneurons in the spinal cord

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Plays a role in inhibition; reduces aggression, excitation and anxiety

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May play a role in pain perception

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Has anticonvulsant and muscle-relaxing properties

Neurotransmitter

Receptor

Action

Decreased

Elevated

NEUROPEPTIDES CRH Corticotropin Releasing Hormone

Endorphins

Acts on Pituitary to release ACTH

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Initiates the CRH-ACTH-Cortisol reaction in stress

Opiate receptors

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Substance P and enkephalins: Active during inflammation and pain transmission in the PNS

o

Endorphins: Endogenous opiates which cause euphoria, suppress pain, or regulate responses to stress

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Are either excitatory or inhibitory, and can also act as neuromodulators, affecting the amount of neurotransmitter released

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Some form part of the neuroendocrine system by functioning both as hormones and neurotransmitters

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Plays a part in physiological processes including euphoric feelings, appetite modulation, and the release of sex hormones.

(Derived from secretory proteins formed in the cell body)

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Plays a role in mental activity

Depression

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Stress

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Anxiety

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Depression

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Premature ejaculation

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Hyperactivit y

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Obsessivecompulsive disorder

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Phobias

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Depression

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Suicidal thoughts

CHOLINERGICS Acetylcholine (ACh)

Nicotinic

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The only small molecule NT that is not an amino acid or derived from one

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Alzheimer’s

(N1, N2)

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Precursor choline cannot be synthesized by the body and must be obtained from external food sources

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Huntington’s Chorea

(Synthesized from Choline)

Muscarinic

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Used by motor neurons as an excitatory neurotransmitter in the spinal cord

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Parkinson’s

(M1, M2)

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Used at neuromuscular junctions as an excitatory neurotransmitter to influence muscle activation

Deactivated by Cholinestera se

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Used by the Autonomic Nervous System, such as smooth muscles of the heart, as an inhibitory neurotransmitter in preganglionic neurons and postganglionic parasympathetic neurons

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Used everywhere in the brain. For example, memory systems of the CNS (may be related to Alzheimer's Disease).

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Female sexual dysfunction

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Paranoia

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Ideas of grandeur

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Mania

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Auditory hallucination

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Most receptors for acetylcholine are ionotropic

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Plays a role in learning, memory

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Mood regulator: manic, sexual behavior

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Primary regulator of alertness

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Used in control of smooth muscle, exocrine glands and vasculature.

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High concentration in hypothalamus, which regulates hormone secretion

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Inflammatory response (local blood flow)

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Stimulates gastric secretions

AMINO ACIDS DERIVATIVES Histamine (Synthesized from Histadine)

H1, H2W

www.columbia.edu/cu/psychology/courses/1010/mangels/neuro/transmission/transmission.html http://faculty.washington.edu/chudler/chnt1.html http://web.indstate.edu/thcme/mwking/nerves.html

Receptors “Dopaminergic”

Known as D1 or D2. (D2 is implicated in addiction.) They bind specifically with dopamine and are active in many areas of the CNS: Basal ganglia: MOVEMENT Limbic: MOOD, EMOTIONS Pituitary: INHIBITION OF PROLACTIN Medulla Oblongata: VOMITING Hypothalamus:

“Adrenergic”

ERECTION

Think “ADRENALIN”. They bind with the catecholamines (dopamine, norepinephrine, epinephrine) and are active in the sympathetic response. Alpha1: VASOCONSTRICTION; located on blood vessels in the skin, vas deferens and GI tract… the effect is reduced blood flow to these areas. Beta1:

INCREASED HEART RATE; located in the heart where stimulation results in enhanced myocardial contractility.

Beta2:

BRONCHIAL DILATION; located in the lungs

“Serotonergic”

Bind with serotonin. Serotonin affects mood, anxiety, arousal, aggression, impulse control, and thinking abilities; but also contributes to physiological effects such as vasoconstriction, GI motility and smooth muscle contractions. 5-HT1: CNS inhibitor affecting sleep, appetite, thermoregulation, anxiety, pulmonary vasoconstriction. 5-HT2: CNS excitation affecting behavior, learning and smooth muscle contraction (including stomach contraction) 5-HT3: Affects anxiety and vomiting mechanism in the intestines 5-HT4 Increases GI motility

“Cholinergic”

Bind with acetylcholine. The effects of cholinergic receptor stimulation include: vasodilation of blood vessels; slower heart rate; constriction of bronchioles and reduced secretion of mucus in the respiratory tract; intestinal cramps; secretion of salvia; sweat and tears; and constriction of eye pupils. Nicotinic:

Located at the neuromuscular junction and affect skeletal muscles.

Muscarinic:

Located throughout the CNS and PNS and affect smooth muscles.

M2:

“Histaminergic”

In parasympathetic fibers, it reduced heart rate; in sympathetic fibers it causes vasodilation in skeletal muscle

Bind with histamine. Histamine is a chemical involved in local immune responses as well as regulating physiological function in the gut and acting as a neurotransmitter. New evidence also indicates that histamine plays a role in chemotaxis of white blood cells. It also maintains ALERTNESS. H1:

Found on smooth muscle, endothelium, and central nervous system tissue; causes vasodilation, bronchoconstriction, smooth muscle activation, and separation of endothelial cells (responsible for hives), and pain and itching due to insect stings; the primary receptors involved in allergic rhinitis symptoms and motion sickness. In stomach, it stimulates secretion of gastric acid.

H2:

Located on parietal cells, which primarily regulate gastric acid secretion

H3:

Decreases neurotransmitter release of histamine, acetylcholine, norepinephrine, serotonin

PSYCHOTROPIC DRUGS Pharmacokinetics “Agonists”:

Drugs that enhance or potentiate the effects of a neurotransmitter or hormone. May be accomplished by mimicking the effects, activating the receptors, increasing the amount of NT in the synapse, or inhibiting the deactivation of the NT.

“Antagonists:

Drugs that decrease or limit the effects of a neurotransmitter or hormone. May be accomplished by blocking the receptors, preventing the NT from binding with the receptors (changing its shape, for example), preventing the NT’s release, or increasing the rate of the NT’s deactivation.

It is thought that some of the symptoms of psychosis are the result of too much or not enough neurotransmitter. Therefore, drugs try to counter the effects of this imbalance by “correcting” or modulating the action. However, because the nervous system is complex in its interconnectedness, changing the action at one transmission/receptor site has effects in other areas. This is why psychotropic drugs have such debilitating side effects. Modulation of NTs Receptor Blocking

(Decreases NT action)

Example: Dopamine Receptor Blocking In schizophrenia, the victim suffers from excess Dopamine. Blocking the dopamine receptors prevents the NT from binding with its receptors and thereby reduces the effects of the NT with the goal of reducing the effects of the schizophrenia. However…dopamine not only effects mood and thought processes, it also controls the modulation and fine-tuning of motor activity and inhibits the release of prolactin in the pituitary. This results in the movement dysfunctions knows as extrapyramidal effects and in galactorrhea (production of breast milk) in females and gynecomastia (femalelike breasts) in males. Additionally, dopamine blockers also bind to the acetylcholine muscarinic receptors (smooth muscle, cardiac muscle and exocrine glands used in the parasympathetic response) and the norepinephrine alpha1 receptors (used in vasoconstriction). This results in antiparasympathetic effects known as “anticholinergic” effects (blurred vision, dry mouth, constipation, urinary retention) due to the blocking of ACh and in orthostatic hypotension and failure to ejaculate due to the blocking of NE. Enzyme Inhibitors

(Increases NT action) Example: Monoamine Oxidase Inhibitors (MAOI) Again, in depression, the goal of antidepressants is to elevate the level of NTs. Besides blocking the reuptake, another strategy is to prevent the destruction of the NT once it has been re-absorbed by the neuron that released it. The monoamines (dopamine, norepinephrine, epinephrine and serotonin) are destroyed by an enzyme called monoamine oxidase (MAO) inside the neuron. An enzyme inhibitor prevents the MAO from destroying the NT. However…MAOs are also located in the liver and are responsible for breaking down all monoamines, including food substances and drugs. Tyramine, for

example (found in aged cheese, pickled and smoked herring, and wine) is a monoamine that must be broken down by MAOs. If not broken down, tyramine can cause life-threatening hypertension. Reuptake Inhibition

(Increases NT action)

Example: Tricyclic Antidepressants In depression, the NTs norepinphrine and serotonin are thought to be decreased. To elevate the levels of NT in the synapse, reuptake inhibitors block the pre-synaptic receptors preventing the reabsorption of the NT by the cell that released it. However…the molecules that bind to the pre-synaptic receptors, also tend to bind with the muscarinic receptors for acetylcholine, the alpha-1 receptors for norepinephrine and the H-receptors for histamine. This results in the anticholinergic effects of dry mouth, blurred vision, constipation and urinary retention; the orthostatic hypotension and erectile dysfunction associated with norepinephrine blockage; and sedation and weight gain associated with histamine blockage. Selective Reuptake Inhibition

(Increases NT action)

Example: SSRIs (Selective Serotonin Reuptake Inhibitors) To counter the side effects of general reuptake inhibition, some drugs preferentially block the uptake of certain NTs. SSRIs target only serotonin pre-synaptic receptors and therefore do not bind with the muscarinic, adrenergic or histaminergic receptors, and thereby reduce the anticholinergic and antihistamine side effects. However…in depression, a decrease in norepinephrine is accompanied by the decrease in serotonin. SSRIs do not elevate levels of NE, and are therefore not as effective as other antidepressants that elevate levels of both NTs. Autoreceptor Blockage

(Increases NT action)

Example: Buspirone Another way to elevate levels of NT at the synapse is to deactivate the mechanism for shutting off its release. Pre-synaptic cells contain an autoreceptor that binds with the NT. When the autoreceptor is bound, the release of the NT is stopped. Autoreceptor blockers prevent the NT from binding with the autoreceptors, and as a result, the NT continues to be released into the synapse.

DRUG CLASSES ANTIPSYCHOTICS Traditional:

Atypical:

Phenothiazides, thioxanthenes, butyrophenones

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All block dopamine receptors (and muscarinic, alpha-1, and H receptors)

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Treat positive symptoms of schizophrenia

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All cause extrapyramidal (EPS) side effects that may not be reversible

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Parkinsonism, akinesia, alcathisia, dyskinesia, tardive dyskinesia

Block serotonin and dopamine receptors. Have fewer side effects than traditional.

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Clozapine (Clozaril) •

Blocks dopamine in the limbic system only (no motor dysfunction)

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Side Effects: Bone marrow suppression (agranulocytosis); convulsions; myocarditis; sedation, hypersalivation, tachycardia, dizziness.

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Not a first choice drug because of side effects.

Risperidone (Risperdal) •

Treats both positive and negative symptoms of schizophrenia.

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No motor dysfunction at normal doses.

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Elderly at increased risk of CVA with dementia and agitation

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Side Effects: weight gain, sexual dysfunction

Quetiapine (Seroquel) •

Binds with broad range of receptors (dopamine, serotonin, histamine, norepinephrine, acetylcholine)

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Best with Lewy Body Dementia

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Not for use with Alzheimer’s or vascular dementia

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Side effects: weight gain, sedation

Olanzapine (Zyprexa) •

A derivative of clozapine

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Antagonist of serotonin, dopamine, histamine, norepinephrine and muscarinic receptors.

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Side effects: anticholinergic effects, sedation, hyperglycemia and Type II diabetes mellitus

Ziprasidone (Geodon) •

Affects serotonin and norepinephrine

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Acts as both a reuptake inhibitor and binds serotonin, dopamine, norepinephrine and histamine receptors

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Side effects: anticholinergic effects, sedation and can prolong the QT interval (may be fatal with a history of arrhythmia).

Aripiprazole (Abilify) •

Partial agonist at dopamine receptor site (stabilizes dopamine system)

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Can decrease dopamine if too much is released, or it can stimulate receptors to increase dopamine levels if not enough.

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Side effects: sedation, hypotension, anticholinergic effects

ANTIDEPRESSANTS All antidepressants carry an FDA warning for children/adolescents and suicide. Tricyclic (TCA):

MAOIs

SSRIs

Atypical/Novel

Amitriptyline (Elavil); imipramine (Tofranil); nortriptyline (Pamelor) 

Block reuptake of norepinephrine and serotonin (to a lesser degree) preventing their destruction and increasing their level at the synapse

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Also block muscarinic and histamine receptors

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Unsure about mechanisms for helping depression, but they do work.

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Side effects: sedation, anticholinergic effects, seizures, arrhythmias, heart block, CVA, hypoglycemia.

Isocarboxazid (Marplan); phenelzine (Nordil); tranylcypromine (Parnate) •

Prevents monoamine oxidase from destroying dopamine, norepinephrine, and serotonin after reuptake.

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Increases synaptic level of neurotransmitters resulting in anti-depressant effects.

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Avoid foods containing tyramine because MAO is prevented from breaking down this amino acid. May result in fatal hypertensive crisis.

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Prevents the liver from breaking down other drugs containing monoamines, thereby increasing the risk for toxicity.

Fluoxetine (Prozac); sertraline (Zoloft); paroxetine (Paxil); citalopram (Celexa); escitalopram (Lexapro) •

Block the reuptake and destruction of serotonin only

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Has a decreased ability to block the muscarinic and histamine receptors than the TCAs, therefore fewer anticholinergic/sedative effects MAOIs

Venlafaxine (Effexor); duloxetine (Cymbalta); mirtazapine (Remeron) •

SNRIs: Serotonin and norepinephrine reuptake inhibitors

Bupropion (Wellbutrin); •

Dopamine and norepinephrine reuptake inhibitor

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Seems to block nicotinic receptors

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Effective antidepressant and first-line smoking cessation drug

Trazodone (Desyrel) •

Probably a serotonin reuptake inhibitor

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Most common side effect is sedation

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Not used often because of it sedative effects.

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May potentiate digoxin.

ANTIANXIETY (“Anxiolytics”) Benzodiazapines:

Diazepam (Valium); clonazepam (Klonopin); alprazolam (Xanax) •

All bind to (benzodiazepine) receptors adjacent to GABA receptors, potentiating the effects of GABA.

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Benzodiazapines do not inhibit neurons in the absence of GABA.

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Side effects: sedation

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Flurazepam (Dalmane) and triazolam (Halcion) create a hypnotic effect and increase sedation

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Lorazepam (Ativan) and alprazolam (Xanax) decrease anxiety without sedation.

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Atypical:

Antidepressants:

Used alone, these drugs rarely result in respiratory depression, coma or death. However, used in conjunction with other CNS depressants (alcohol, opiates), they can be life-threatening. Buspirone (BuSpar) •

Seems to act as a serotonin autoreceptor blocker, thereby increasing synaptic level of serotonin.

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Does not have a strong sedative effect.

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Is not a CNS depressant

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Does not have an addiction potential

Some antidepressants may also treat anxiety disorders.

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Imipramine (Tofranil)—a TCA—is used to treat panic attacks.

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SSRIs are used to treat obsessive/compulsive disorder

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Sertraline (Zoloft)—an SSRI—is used to treat social phobias.

ATTENTION DEFICIT Psychostimulants: Methylphenidate (Ritalin); dextroamphetamine (Adderall)

Non-stimulant:

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Attention deficit results from an overactive limbic system.

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Drugs seem to work by increasing the release and blocking the reuptake of monamines.

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Side effects: agitation; increased psychotic thought processes; hypertension; longterm growth suppression; abuse potential.

Atomoxetine HCl (Strattera) •

Acts as a norepinephrine reuptake inhibitor

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May be used in children over 6 years of age

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Side effects: decreased appetite; weight loss; fatigue; dizziness

ALZHEIMER’S DISEASE Anticholinesterase:

Tacrine (Cognex); donepezil (Aricept); rivastigmine (Exelon); galantamine (Reminyl) •

Memory loss in Alzheimer’s is related to decrease in acetylcholine, resulting in plaques and nerve tangles in the brain.

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Drugs cannot cure the disease, but may slow the symptoms and increase memory function

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Work by disrupting the enzyme acetylcholinesterase (which destroys acetylcholine in the synapse).

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Tacrine (Cognex) has lots of side effects: nausea, abdominal distress, increased heart rate, liver toxicity. Need to perform liver function tests regularly.

• NMDA Receptor Blocker:

Donepazil (Aricept) has fewer side effects than tacrine. However, it causes sedation, nausea and diarrhea. Memantine HCl (Namenda) •

Antagonizes N-methyl-D-aspartate (NMDA) receptors, the persistent activation of which seems to increase Alzheimer’s symptoms.

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Is the only drug for moderate to severe dementia related to Alzheimer’s.

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Renal impairment may be a side effect.

MOOD STABILIZERS (BIPOLAR DISORDER) Lithium:

Anticonvulsants:

Lithium (Escalith; Lithobid)

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Lithium is a charged ion (electrolyte)

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It may act by affecting the electrical conduction of the neuron

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May interact with sodium and potassium

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Its interaction/disruption to normal sodium/potassium processes makes it a threat to all body functions •

Cardiac contractions (arrhythmias)

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Brain conductivity (seizures)

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Nerve/muscle impulses (motor side effects like tremors or weakness)

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Can affect fluid balance (polyruia, edema)

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Long term use increases risk to kidneys and thyroid

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Has the lowest therapeutic dose of all psych drugs.

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Side effects: tremor, ataxia, confusion, convulsions, N/V, diarrhea, arrhythmias, polyruia, polydipsia, edema, goiter, hyperthyroidism

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Monitor blood levels closely!

Carbamazepine (Tegretol); valproic acid (Depakote); lamotrigine (Lamictal); Lamotrigine •

All are used to calm the manic client before long-term stabilization with lithium

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Valproic acid and carbamazepine may be used long-term when lithium cannot be tolerated.

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Carbamazepine is similar to TCAs in structure and serves as a neuron analgesic (calms excited nerves).

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Side effects are nausea, sedation, ataxia, rash, possible liver effects

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Regularly check liver functioning, CBC, ECG and electrolytes

Valproic acid is probably first choice over lithium and carbamazepine because it is better tolerated. •

Is recommended for mixed episodes and rapid cycling

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Side effects: alopecia, tremor, weight gain, sedation

Newest approved anticonvulsant for use for bipolar is Lamotrigine. •

Used for acute and long-term management of mania/bipolar

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Has well-tolerated side effects; but may have a rare life-threatening dermatologic effect.

Calcium channel blockers and thyroid hormones have also been used to treat manic/bipolar disorder.