Download Neurophysiology and Psycho-Pharmacology Final Exam General

Neurophysiology and Psycho-Pharmacology Final Exam
General brain structures and their functions
Frontal (exec function, thinking, planning, organizing, prob. solving, emotions, behavior control, personality)
Motor cortex (headband) movement
Temporal (memory, understanding language (Brocha and Werneke) (near ear)
Sensory cortex (sensations) (Behind headband)
Parietal lobe (flat part of my head) perception, making sense of the world, math, spelling, patterns
Occipital (rear, just above cerebellum Vision
Three areas of the frontal lobe and their functions: (exec functions, thinking, planning, organizing, prob. solving)
I.
Ventrolateral - motor inhibition, holding onto info, not impulsive
II.
Orbitofrontal - anticipates a positive or negative response
III.
Dorsolateral - working memory and redall
What 3 things contribute to brain development?
I. genetics (nature)
2. biology (nature)
3. environment (AND nurture) (social interactions influence the construct of reality - crucial during early dev)
* experience alters activity and neuronal connections in the brain, shapes the circuits for memory, emotion,
self-awareness (input of experience from bodily sensations, 5 senses, our ideas and concepts and words)
Left hemisphere
Analytic thought, logic, math
language, reasoning, science,
written, number skills,
Right hand control
Corpus callosum
Right hemisphere (mindfulness activate
Art awareness, creativity,3-D, drive,
imagination, intuition, insight, spatial,
holistic thought, music awareness,
Left hand control
Left
processes more positive and spontaneous emotions
Approach states
Positive affect
Exploration
Sociability
Right
Mediates emot guilt, shy, withdrawal
permits expression of emotions
brings emotions into consciousness
registers facial expressions
Processes unpleasant emotions
Comes online when school begins (due to development of
communication region of brain between 2 hemispheres
Predominant for first 1-3 years
Assertive state motivation, engagement with world
Active motor expression (dopamine)
Dominant for focused attention
Slower activing, logical, linear, sequential, time depen process
Verbal meanings are primary modes of processing
Breaks down info into mentally defined chunks
Primed for externally focused attention and action
Semantic memory representations
Involved in positive emotions such as joy/excitement
Acceptive, receptive, self-regulatory
Focus and responds to novelty
Attentive /reflective states of mind
Dominant for attention, vigilance,
sustained attention, alertness
Autonoetic consciousness/sense of self
Fast acting, holistic processing
Visuospatial perception
Nonverbal meanings are primary
Primed for internally focused attn.
Episodic memory, social cognition
How we receive information from the outside world: neurons send electrical impulses down its axon,
releases a neurotransmitter at the synapse (excites or inhibits the downstream neuron) receptor is influenced
The Limbic System (emotional system) (appraisal, initiation, shutting down)
Amgydala, anterior cingulate, and orbitofrontal cortex
Thalamus - passes along info to amygdala for processing
Hypothalamus activates 3 primary stress response pathways SNS, HPA, or HPP (hypothalamic-pituitary -thyroid
(PNS - parasympathetic Nervous system = helps to de-activate, feeling very mellow) active. by relaxation reduces heart rate, blood pressure, and conserves energy - PNS is mediated by acetylcholine
Anticholinergic effects: to dry everything up (blurry vision, dry mouth, constip, urine retention, dryness)
SNS is mediated by chemical norepinephrine (adrenergic effects (to add fluid) hypotension,
Amgdala = assessment of threat; fight or flight response (assign signific without conscious awareness) (to become
conscious, ext. and int stimuli become connected by the dorsolateral prefrontal cortex (working memory)
Amygdala fires off "danger" signal, establishes an elaborate appraisal that creates fear in the brain. "Neurons that
fire together, wire together"
Hippocampus - reduces arousal, turns off stress response, essential for encoding and retrieving from LTM
Basal ganglia (movement, dopamine defic. = Parkinsons)
Anterior Cingulate gyrus (mirror neurons are here, significance is assigned here)
Orbitofrontal cortex and mid prefrontal cortex coordinate appraisal of complex represents, social cognition
Flight or Fight (3 pathways) HPA Axis (physical, psychological, environmental) In traumatized people, this HPA axis is
highly agitated, leads to heart problems, cholesterol, and high blood pressure, as cortisol in system eats away their
happiness. Cortisol is an enzyme that eats away all your serotonin (so you're depressed. Cortisol is secreted in tears.
Hypothalamus responds to levels of cortisol: reduces CRH if cortisol is high, increases CRH is cortisol is low
Pituitary gland = ACTH
Adrenal glands (located above kidneys) = cortisol
Three types of Memory :
Immediate Short Term Memory
Working (temporary storage and manipulation)
Recent Long Term Memory
Remote - Distant Memory
Implicit memory develops at infancy, explicit at age 2 (speech)
Initial impact of an experience on the brain is called an "engram" (includes somatic, perceptual, emotional, behavior,
semantic, autobiographical (mental model/ mental image)
implicit memory (non declarative) first four levels: somatic, perceptual, emotional, and behavior - generalized "mental
modals" essential for survival, available from infancy; "schemata"
Helps the mind seek out familiar objects/expers
Prior experience shapes anticipatory models ("prospective memory") Implicit memory influences our exper w/others
Transference is the activation of old mental models on current experiences
Explicit memory (declarative) Last two levels Semantic and autobiographical. Develops at AGE 2/speech Two types:
Semantic memory - allows for symbols of external/internal facts to be in graphic / word form (NOESIS)
Episodic memory (autobiographical) knowing the self. (AUTONOESIS) Dependent on devlop of frontal cortical
regions of the brain
Emotional processing. Hippocampus helps us recall the order events occur (Cognitive Mapper). Child develops a sense
of time/sequence. Great for survival.
Items are tagged in STM - rehearsal initiates LTM (lateralized) verbal and nonverbal separate)
Consolidation takes minutes to hours. Storage (short stories are never recalled verbatim)
Attachment (secure, avoidant/depressive, ambivalent/anxiety, disorganized/disoriented)
(caregiver deprivation leads to long term HPA axis mod, and serotonergic/dopaminergic activity (anxiety)
Secure attachments: fluidity of narratives and self-reflection, access to memory (explicit & implicit) emotional)
Insecure attachment: impaired right orbitofrontal region and middle prefrontal cortex
Only access to noetic consciousness (general knowledge and facts, minus sense of ourselves in emot value)
Studies of dismissive mothers demonstrate left hemisphere brain activation inst of right hemispheric active
(consistent with retrieval of autobiographical memories)
Attunement
borrowing caregivers brain to self regulate, in synch with caregiver/baby's needs
Mutual influence of each person on the other = not just alignment of state of mind, but affects
Allows for connection to remain when physical proximity is removed, greater social
environments lead to more complex cortical structures
Transference
transfer younger expectations onto current person (therapist, partner)
Mirror neurons found in the anterior cingulate and ventrolateral region (anterior insula) - allows us to perceive
intentional states of others and imitate their behaviors Mirroring helps child regulate his emotions, vital to brain dev
Affect = what you see
Mood = what gets recorded
Orbitofrontal cortex and middle prefrontal cortex coordinate appraisal of complex representations (social cognition)
(absent in Autism and Asperger's)
NEUROPLASTICITY - brain's ability to stay open for change - grow new synaptic connections, make new myelin, neurons
State of Mind = organization and cohesion of info processing (in the moment reality). Fundamentals:
- to coordinate activity; creates pattern of brain activation for reuse later; repeated activation of the same
state into chronic state of shame or chronic state of optimism. State then becomes a TRAIT
Includes: perceptual bias, emotional tone, emotional regulation, memory processes, mental models, behavior response
patterns (our typical reaction)
When Serotonin and Dopamine fire = happiness
Drive for complexity
Anxious attachment - rejects attempts at closeness
Avoidantly attached infants do NOT have access to external regulatory function (rely on internal function only)
Ambivalently attached infant has access to inconsistent/unreliable external regulatory functions, unable to self soothe
Disorganized attached infants do NOT have access to external OR internal regulatory functions (easily
overwhelmed/dissociate)
The brain's ability to create representations of our reality is heavily influenced by EMOTIONS
Mood Disorders = massively dysregulated emotional state
Anxiety Disorders = flood of arousal causing dysfunction
Bipolar Disorder = "kindling effect" increasing frequency and intensity of dysfunction, becomes stable feature that no
longer needs a triggering effect (don't know where their baseline is, they are so dysregulated)
Aspects of Emotional Regulation Intensity
(because of a previous memory)
Sensitivity - some people feel everything
Specificity - emotional related does to the Amygdala almonds
Windows of tolerance (i.e: hunger, calm in face of crisis)
Anxiety can be masking grief. Or, her anxiety / anger / arousal is keeping depression at bay.
Pharmacology principals
Organs associated with metabolizing and excreting the drug
The task of pre and post synaptic neurons
General diagnostic criteria for mental illnesses
Treatment for mental illnesses
Focus on major disorders
Major depression
SSRIs (start low & go slow) 6 mns and psychotherapy
Schizophrenia
Anxiety
Borderline Personality
Common side effects / withdrawal symptoms associated with each class of medications
Side effects
withdrawal symptoms
Neurotransmitters associated with etiology of each diagnosis
Non-pharmacological treatment for each diagnosis
Pharmacodynamics - drug effect on the body
Pharmacokinetics- body's effect on the drug
Absorption
Distribution (lipophyllic - easier for molecules to permeate blood barrier)
BIO TRANSFORMATION - metabolism and excretion of drug
Liver - change chemicals into compounds. Metabolizes only 1 chemical at a time, so they all cue up for liver
Kidney - excreted into urine
Half Life - estimated time required for drug to reach STEADY STATE
THE AMOUNT THE LIVER IS METABOLIZING HAS TO BE EQUAL TO THE AMOUNT THE KIDNEY IS RELEASING
Chemical molecules bind to a receptor (aka LIGANDS) (binding occurs at multiple brain regions)
Agonist = ligand ACTIVATES the receptor
Antagonist - LIGAND BLOCKS the receptor
Antidepressants
Tranquilizers
Benzodiazepine
Librium (non compliant Caucasians complained of side effects, Latinos want quick fix, Asians compliant, felt
side effects were proof medication was cleaning toxins out of body
Valium
Bipolar-
Lithium
Other interferences= hyperthyroidism impacts, drug interactions, endogenous mental illness
DEPRESSION
(not grief, 6-12 mns)
Self esteem intact
BIPOLAR
ANXIETY/OCD
PSYCHOSIS
DEPRESSION:
MDD - Grief episode. 80% of ppl experiencing MDD encounter avg of 6 recurring episodes in lifetime
(PS: medication is ALWAYS warranted in MDD WITH PSYCHOSIS, but ECT is gold standard)
Reactive Depression = mild to moderate, identifiable psych stressors, can be acute/insidious/distant past
psych symptoms but not physical (sleep, energy levels, appetite, sex drive unaffected). Average of 2-6
recurrent depressive episodes
Biological Depression - traced to alternations in neurotransmitter function in limbic system, can be medical
illness, thyroid, sex hormone fluctuation, medication or recr drug use, or endogenous biological depression
Atypical Depression - 15-20% of MDD, cue to assess for bipolar of not sleeping, profound fatigue/not sleeping
or hyposomina, increased appetite, weight gain, sensitivity to interpersonal rejection/separation
SAD - Seasonal Affective Disorder - adaptive to sunlight, (ppl work night shifts, etc)
Premenstrual Dysphoric Disorder (PMDD) and Post Partum Depression (PD) hormone fluctuates destabilize
neurotrans in limbic sys (10% of women experience PD Untreated can last 1-2 yrs
Depression TX: Reduction in Sx 2-4 weeks after initial med TX. 50% relapse within a month. Easy to regress
Stopping is not advised cells are not yet stable. Continue med tx for 6 months, recommended. Combined
antidepressant AND psychotherapy leads to best chance of recovery. (CBT, CBA and Interpersonal psychotherapy)
Tricyclics - considered "dirty" drugs, targets a host of neurotrans, ant9-cholinergic, sex dysfu,
SSRIs (Selective Serotonin Reuptake Inhibitors) - fewer side effects, clean (minimal ineractino with other
receptors other than serotonin, side eff: nausea, sweating, upset stomach, anxiety, insomnia, restlessness, headache,
sexual dysfun, anticholinergic
SNRIs (Serotonin and Norepinephrie Reuptake Inhibitors) - block reupt anxietake of BOTH seroton and norep
Side effects similar to SSRI except minimal sexual dysfunction
STRATTERA also approved for ADHD (consider if Comorbid dx) Norepin can improve energy and cognition
Causes anxiety, loss of appetite, sedation
Atypical antidepressants= do NOT block re uptake, incrases production of activity of norepinephrine,
increases noradrenergic activity, side effects: anxiety and insomnia, fewer sexual side effects, requires blood testing as
Serzone assoc with liver toxicity (liver puts things in a cue, processes them one at a time)
MAOs (Monamine Oxidase inhibitor) Not first line of defense only when other meds have failed
Has risks - high blood pressure, can't have sausage, salami, soy, wine, smoked salmon, beef bullion , beer or foods high
in tyramine content)
Can be espec. effective treating depression related to Parkinson's (MAO-B inhibitor such as Seligilene)
Over the Counter - St. John's Wort, SAM-e, Omega-3 fatty acids (anti inflame props)
BIPOLAR - 60% of teens, 70% of children with BP will experience serious depression first
Antidepressant meds but BP pts at risk - cause a switch from depression to mania, worsen BP symptoms
Symptoms: hypersomnia, severe fatigue, increased appetite, carb cravings, weight gain), psychotic sx, genetic hx of BP
Poss. etiology - retroflexed rage, loss of attachment, faulty separation (obj relaitons) ; learned helplessness/defeat;
cognitive distortions/expecations, genetic, PTSD, thyroid or viral infections; prescribed/recreat drugs; nurological
disease (Parkinson's , Alzheimers), light/SAD; decreased phys exercise or poor nutrition
Monoamine hypothesis = malfunction of norepinephrine, serotonin and/or dopamine neurons (in limbic/hypothalamus
Excessive reuptake of neurotransmitters, rapid reabsorption from presynaptic cell, decreased postsynaptic receptor, or
decreased release of neurotrans,
BDNF (brain-derived neurotropic factor, brain fertilizer, helps everything grow)
Biological consequences of depression: high sustained level of cortisol leads to cell death in hippocampus, atrophy of
the cingulate, damage artery walls in heart, immune sys (cortisol lets you get sick more often)
BIPOLAR 1
- between episodes, Pts relative asymptomatic, becomes more freq as age increases, mixed episodes
more common in males, more common in youth Antidepressants initate rapid cycling
BIPOLAR II
- less pronounced, no hospitalization, can look like depression with irritable mood
CYCLOTHYMIA - alternating depression/elevation at least 2 yrs, sxs never absent longer than 2 mns
impairment in depression, but not mania
MIXED EPISODE simultan exper both depression at mania or at least in rapid sequence
RAPID CYCLING - 4 or more episodes of mania or depression within one year
Etiology: Dysregulation theory = overactive of mediating brain circuits
chaotic attractor theory - biochem defect leads to dysregulation of neurotran. synthesis
Kindling theory - cumulation of biochem changes in limbic system, buildup causes neurons to become excited
chatecholamine theory - abnormalities in levels of norepinephrine and metabolite MHPG - levels down in depression,
levels up in mania
HPA Axis Theory - over-activation in mixed states and in depressive episode, not seen in manic episode
Protein Signaling Net work Theory and Calcium signaling theory = abnormal levels and signaling
Genetic and familial theories chromosome 22 implicated in bipolar and schizophrenia
Concordance rate in monozygotic twins = 50-60%
4-6 times higher rate assoc w/ first degree relatives
Neuro anatomical theories: decreased CNS volume, cells, neurons, and glia (protector cells)
Cytoprotective protein found in frontal cortex (less of this in bipolar, nourishment for the brain)
Lithium and other mood stabilizers to incrase level in frontal lobe
TX: pharmaco (you're checking for are they taking meds, side effects, obtained their prescription?) Milieu therapy
(insight and cooperation) Psychotherapy/CBT, Psychoeducation, group therapy for acceptance and med compliance
ECT for med resistance pts, combination med tx is mainstay, multiple mood stabilizers, antidepressants, andjunctive
agents, (benzos and antipsychotics)
LITHIUM = No sedating effect, requires monitoring of blood levels and management of side effects
5-14 days to take effect, full stabilization takes months. Used in manic depression, anxiety in animals
No liver metabolism = relies on kidneys for elimination, LITHIUM HAS NO INTERACTION WITH THE LIVER
Side effects: gastrointes. functional nausea, vomiting, diarrhea, Nervous system (fine hand tremor) Endocrine (thyroid
dysfunction) Renal - relies on kidney for elimination of med
Side effects Hematological - reversible increase in white blood cell count - must monitor their blood
Auto immune like an infection
Dermatological - rash, acne-like lesions, severely painful
Weight gain - common side effect, avg 20 pound gain in 20% (ppl crave sugar and fast foods b/c meds go to stomach
lining) Stomach is irritated, so client craves comfort food
Mechanism of Action - stabilizes cell membranes, reduces dopamine receptor sensitivity in mania
Contributes to serotonin production - for depression
Reduces overactivity of second messenger systems (the supervisor check" messenger)
Increases neuro-protective substances in brain
Terotogenicity - risk during pregnancy, esp 1st trimester, crosses the blood/brain barrier (heart abnormalities)
Anti-convulsant: Depakote/Divalproex considered first line tx for acute mania (side effect: coma and somnolence)
Anti-convulsant: Lamictal/Lamotrigine approved for acute and maintenance tx (second line agent for rapid cycling)
(Possible mechanism: inhib glutamate (cognition/thinking) better decisions about compliance
Second gen antipsychotics: Tx for acute and mixed mania, less risk for extrapyramidal side effects (seizures, cardiac
arthythmia,
Lenth of Tx: long term, lifetime tx. Mood stabilizers continue as routine maint, anti depressants and anti psyuchotics
CBT and Family psychoeducation
Anti depressants
Mood stabilizers
Anti psychotics
anti anxiety meds (Benzos (addictive) Tricyclics, SSRI, SNRIs
OCD SSRIs SROIs
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ANXIETY AND OCD
Neurotic anxiety: overcome by signif emotional issues/conflicts, tight defenses against awareness of issues
sympts manifest as generalized anxiety Approach-avoidance style (afraid to express anger)
Could be redirected or suppressed (grief/loss of relationship or connection
From Psychoanalytic perspective: Freud thought ti was a challenge to defenses which protected the id or super-ego
when defenses failed, experience anxiety
From CBT: over evaluation of danger or underestimation of ability to cope (fight or flight response, false alarms)
Point out "these are just thoughts" More objective
From Biologic perspec: serotonic and norepenephr and dopamine) natural tranq for the brain, negative chloride ions
that stick to the cell and open the gateways, like a stuff room, opening up the window. Dampen the limbic alert syst
Produces a calming affect on the brain. We learn to calm our CNS. We can change this and lower your activation
Cortisol eating up our good neurotrans,. HPA axis activated.
Amygdala - emotional alarm system in limbic system. Neurons that fire together, wire together under threat
Mediates fear, encodes stimulus elements of experience -highly resistant to extinction. Creates memories
Amgydala is next to hippocampus, where memories are stored.
TX: GAD stress management, relax training, meditation, CBT, Yoga, Qi gong, dancing (GABA, amino acid)
and benzos (addictive) magnify the work our negative ions do for us naturally
TX: Social Phobias : CBT (no med tx) relaxation training
Panic Disorder: Meds are important, tx is meds and psychotherapy, stop/reduce panic first, then CBT, then insight
oriented tx
OCD: (dirtiness, safety, symmetry, excessive self doubt, intense worry) 2/3 also experience depression, emerges in
late childhood and remains steady. 2.5% gen pop, 7% in genetic relatives
PT knows their thoughts are irrational, no pleasure = ego dystonic
vs
Impulse control issues (gambling, overeating) = ego syntonic
Anorexia - believe that worries and rituals regarding food are rational
Traditional Psychoanalytic theory: early parenting overly strict, did not let pt individualize, no autonomy
Biologic: signif increase in basal ganglia and frontal lobe activity, dysfunc. inhibition response to primitive inst urges
Impairment in neural pathway function
OCD TX: Behavioral expos and response prevention , and medication with SROIs and SSRI's effective 50-65%
95% relapse if meds are discontinued
Benzos - high density of receptors in limic system, enhances GABA, increases chloride neg ions
Must phase out SLOWLY, 1-2 mns tapered off, or it could kill them. withdrawal anxiety, insomnia, nightmares, seizure
Do NOT use with alcohol, advise against abrupt discontinuation, offer support for meds that take longer to be effective
Atypical benzos show less cognitive impairment side effects, reduced risk of dependency, greater specificity in binding
receptors, suppresses REM and Stage III : for athletes, sleep is very important to restore body ,
Anti-colinergic and impacts memory (i.e. People who take Ambien have foggy memory, less deep sleep)
PS: Stage 4 sleep is where our emotional tone/baseline is set.
Meds: Buspirone: works well with smokers as it acts like nicotine ("take the edge off")
delayed onset, similar to antidepressants, reduced anxiety within 1-2 weeks
Reduced risk of tolerance or dependence, no psychomotor impairment side effect
Side effect: nausea, dizziness, anxiety
Medications: antihistamines (Benadryl) Has a 4 hour window, PT can build up a tolerance, anti-collinergic system:
targets histamines in the brain, blocks histamine receptors, producing sedation and reduction in anxiety
Side effects: drowsiness, impaired performance
Experience effect in 30 minutes, lasts 4 hours, narrow window of effect, non habit forming, but tolerance develops
Betablockers: Used for hypertension, calms body, has a physiologic effect on the body
Blocks effects of norepinephrine at the receptor, reduces peripheral manifestations of anxiety, performance anxiety
Side effects: dizziness, lowered blood pressure, can cause depression with prolonged use
Effective adjunctive tx for panic disorder, must discontinue slowly 1-2 month taper
Clonidine and Tiagabine:
Clonidine focuses on NE (its presynaptic inhibitor of NE, typ used to treat hypertension and opiate withdrawal
Tiagabine: works with reuptake / recycling of GABA: anticonvulsant, GABA reuptake inhib, researched for possible PTSD
and panic disorder
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PSYCHOSIS; cognitive impairment, social impairments, affected frontal lobe (doesn't come online until teens)
Brief Psych Disorder
Delusional Disorder
Schizophrenia
Schizophreniform Disorder
Schizoaffective Disorder (you may only see mood, no psychosis)
Shared Psychotic Disorder (weak boundaries, takes on another's illness)
Psychotic Disorder not otherwise specified (atyp)
Major Depression with psychotic Features
Bipolar, Mania
Biolog: theory: enlarged lateral ventricals, smaller anterior hippocampi, decreased metabolic active in prefrontal
cortex, positive assn between levels of dopamine metabolite and clinical severity
Dopamine model: Too much activity, overactive and hyperactive dopamine neurons, drugs that increase dopamine,
produce paranoid psychosis, exacerbate positive sympt. (Opposite of Parkinson's)
Hyperdopaminergic active in mesolimbic tracts are associated with POSITIVE SYMPTOMS
Decreased active in prefrontal cortex assoc with NEGATIVE symptoms
Glutamate model: Blocking of glutamate at the N-methyl-D-aspartate (NMDA) receptor in brain (respon for
neuroplasticity), induces negativism, apathy, disorg thinking)
Theory suggests primary dysreg of glutamate system, cognitive deficits, dopaminergic hyperactivity
Neuro-developmental/neurodegenerative model
Defective in utero, abnormal devel later (during synaptic pruning in adolescence)
Progressive loss of neurons and cognitive function, early intervention and tx is key
TX: antipsychotics (relapse is common), psychosis damages the brain, (neurons that wire together, fire together)
Both typ and atyp meds are effective, family therapy/education, social skills training, cognitive remediation
First gen antipsychotics: dopamine blockers (side effects: extrapyramidal, shuffling gait, tremor, decreased facial
expression, muscle spasms, akathisia)
Anticholinergic ) drying of the membranes
antiadrendergic - dropping of blood pressure
Tardive dyskinesia - invol. movement, atypical effects: weight gain, lower seizure threshold, temperature dysreg,
lactation.
START HERE WITH MEDICATION TREATMENT, CONTINUED…… (second gen antipsychotics) (3 more pages!)
Then 11 and 12 and you’re ready to print on Friday and study on Sat and Sunday! Good job, Audrey!
Serotonin and Dopamine blockers (associated with mood/negative symptoms)
Less side effects than first gen meds and more tolerable
signif. reduces tardive dyskinesia, improves cognition as it works on frontal lobe
Produces weight gain, increased heart disease/stroke
Agranulocytosis: decreases white blood cell count
Side effect of first and second gen meds, severe blood disorder, causes several deaths, requires weekly monitoring
After 6 mns of normal levels, reduce to biweekly, blood tests and meds costly
Choosing an antipsychotic - first gen effective for positive symps, ineffective for neg sympts
Second gen effective for negative sympts/ mood bc serotonin is there., but only in 30% of cases
Weight the efficacy of the drug agains the side effects (weight gain) has it been successful in past?
patients motor state / dyskinesia, stroke?
Length of Tx: short period of kicking in. Some side effects subside w/n few hours/days of tx
Some pts show improvement in pos symptoms 1-2 wks\ STAY ON MEDS FOR AT LEAST 1 YR
Type of Dx is a factor: for Schizophrenia, recommend 1 yr (onset and severity of side effects will influence length of TX
Relapse is a big factor - education regarding prodromal sympt is crucial, early intervention is key/pre-teen onset
Pt and family ed about dx, meds, side effects, relapse, med compliance should be a goal of TX
Make symptoms ego-dystonic with pt, strong rapport is necess, esp for paranoia, CBT is effective
Social skills training, If pt enjoys their pos symptoms, you will want ot use motivational psch to show disconnect
11 PTSD, Substance Abuse, Personality Disorders
Recurring trauma more devastating than single episode; age of exposure to trauma is important, impacts personality
People with mental illness are more vulnerable to PTSD
Attachment and repetition compulsion - early abuse alters neurobiology
Attachment and impaired affect modulation - poor affect regulation and permanent alternations of nervous system
Hyperarousal - expos to trauma initiates hypervigilance and withdrawal patterns depleting norepinephrine
Intrusive symps flashbacks traced to stress induced reaction of hippocampus/amygdala pathways (NE & Serotonin)
NE is good for plasticity. SE needed for memory - that cushions or make us feel soothed from anxiety
Glutamate good for calming down body, but during stress, it goes away. Then a lot of cortisol starts eating up
neurotransmitters.
Acute toxic levels of glutamate and cortisol damage part of grain assoc with affect regulation
Kindling - repeated episodes change brain functioning, progressively increases intensity of affective sympts
Therefore, PTSD induced by environment, both psych and physiological impact
TX Psychotherapy if first choice - exposure based cognitive therapy (journaling, articulating helps them process what
happened to them and desensitizes it.)
Meds for targeted symps only - must restore sense of control over turbulent emotions
short term tx for severe intrusive sxs and psychosis
Co occurring depression or panic treated with mds - 9-12 mns recom.
Borderline Personality Disorder :: ACT therapy (Acceptance and commitment therapy)
Hysteroid - dysphoric - lability extreme sensitivity to abandonment - needy threats, " If you leave me, I'll kill myself"
Schizotypal (exhaustive) Schizophren magical thinking "something about your aura " clinging
Angry-impulsive - challenging, impulsivity and anger, low frustration tolerance - any sign you're not enjoying them, they
will lash out, hostility, you're the worst person
Etiology of Borderline PD - inborn defective ability to absorb early interpersonal experience adequately - not reading
the right cues from others - temperament, early severe trauma alter brain development
TX for BPD - meds do not directly target symptoms, but can reduce targeted sympts, adjunct to psychotherapy
DBT (individual, group, telephone check in, Therapist needs consult group and support
Substance Abuse - rapidly absorbed, crosses blood-brian barrier, CNS depressant, metab by liver, monopolizes the liver,
all else cues up. Gastirc irritant and toxic to liver cells and neurons
Considered a genetic condition but mechanism unclear
Polymorphism of D2 Dopamine receptor gene, strong assoc with schizophren, mania, and APD, depressive sx during
intoxication (dampens everything in body), produces anxiety sxs during withdrawal.
Tx: meds can be effective (Antabuse - causes unpleasant reaction) Naltrexone has been showing promise, reduces
cravings, Campral for maintenance (takes edge off - helps with detox)
Psychotherapy - Motivational Interviewing (going through their reasons and excuses) Stages, goal is to create ambiv
Group Therapy and Support Groups (AA, process groups)
Subst abuse - stimulants (Meth amphetamines) blocks off post synaptic nerves absorbing serotonin so it is all out in the
system - feels really good
Acts on the dopaminergic system - activates reward system in limbic system, increases release of Dopamine and NE,
decreases reuptake
Euphoria, paranoia, hyperexcitability
Crack cocaine has more intense effect, more addictive, withdrawal reduces availability of neurotrans, pushes a lot of
Dopa into system, but "I need more, I need more") Dopa tricks the body "I'll make you suffer" (like you have a cold)
Withdrawal reduces availability of neurotrans, intense feelings of cravings, depression, restlessness
NE- memory and learning. X: Benzos and Betablocker (Methadone) Tx varies per stage of TX
Initial use blocks effects of DOPA and NE, during withdrawal, meds are used to reduce craving
Treat intox and withdrawal first, psychother 2nd and for maintenance
Heroin is the most abused substance - associated receptors involved in sensation of pain and pleasure
Synthetic opioids can lead to dependency (morphine heroine, oxycodone, hydrocodone, codeine)
Acute opiate intox leads to sedation, respiratory depression, can be fatal. Tolerance builds up.
Withdrawal effects: anxiety, agitation, sweating, runny nose, trembling (hard to shake on your own, need detox clinic
Substance relationed disorders: OPIATES
TX: different meds prescribed at various phases of use: Naloxone and Naltrexone address acute intox. Methadone and
others used to treat withdrawal sxs. Strategies for treating dependence: Methadone reduces craving (blocking)
produces less of a high - less prone to abuse
Opiate antagonist (Naltrexone) creates a neg effect, so it doesn't feel as great, effect of opiate will be blocked if it is used
Hallucinogens for Substance related disorders: drug stays in system for 24 hours
Produce transient psychotic states, visual, auditory, olfactory hallucinations
Not assoc with dependence or withdrawal
Can produce florid psychosis during acute intox, 12-24 hours to run course,
Anti anxiety or anti psychotics can be use dto decrease sxs, some pts exper flashback hallucins, if severe, anti anxiety or
antipsychotics can be used
Overdose of PCP can lead to convulsions
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Children Dx and Tx
Collinergic = keeps things lubricated
Anti-Collinergic - dries things up (i.e. Benadryl) but it will dry up the neurotransmitters, too