Behav 2 Pharm Flashcards
Dementia
Ok
Central ache inhibitors
Tacrine, donepezil, rivastigmine, galantamine, memantine,
Tacrine
• High incidence of hepatotoxicity, newer agents are preferred (no longer used clinically
Addiction vs physical dependency
Physical dependence and tolerance are normal physiologic adaptations
-cant diagnose addiction
Addiction-primary chronic disease of brain reward, motivation, memory and related circuitry so get biological, psychological and behavioral dysfunction
Tolerance and physiological dependence , pain relief ,
Misinterpreted as drug seeking or relapse behavior
Reward defiency syndrome
Dopamine system malfunction
Common pathway for addictive behavior
Addiction genetic
Yes but also environmental
Non substance specific
Addictophrenia model
Assess disease risk severity
Type I alcoholism-mean Nd women need genetic and env predisposition later in life, mild or severe
Type II-sons of male alcoholics, genetic not env, start adolescence , associated with criminal
Addictophrenia type I
Genetic history of addictive disorder-alc
Genetic history of mood disorder
Higher incidence of comorbid mood disorder
Type Ii
Genetic history of addictive disorder-mixed substance and non
Genetic history of personality disorder or criminal behavior
Higher incidence of criminal behavior, risk taking and gambling
Type II
Genetic history of addictive disorder-not a prerequisite, but increases vulnerability
Significant history of trauma-predominantly alchol and benzodiazepine use
Addictophrenia type IV
Genetic history of addictive disorder-not prerequisite but increases vulnerability
Chronic use of high dose drugs known to cause severe physical dependency
High associated with presence of severe psychosocial stressors
Diagnose addictophrenia
Overlaps
Rate scal one to ten one ach category
Predict degree of susceptibility and assist in counseling and treatment planning
Validity and reliability has not been tested
Do ppl die when addicted
Yes. Fifty percent have comorbid psychiatric disorder
-antisocial PD, depression, suicide
Substance use disorder
Using larger amounts for longer
Desire or unsuccessful attempts to cut down or control use
Great deal of time obtaining, using or recovering
Crave, cant fulfill roles, social and interpersonal problems
Stop doing things , tolerance, withdrawal, physical hazard situations
Mild substance use
Two to three symptoms
Moderate substance use
Four to five symptoms
Severe substance use
Six or more symptoms
Early remission
No criteria except craving for over three months but less than twelve
Sustained remission
No criteria for over twelve months except craving
What is substance abuse mental disorder
Symptom of mental disorder
How identify substance abuse mental disorder
Developed one month of substance intoxication or withdraw of med
Involved the substance/med is capable of producing the mental disorder
Not better explained by independent mental disorder (preceded substance, mental disorder stay long after substance gone one month)
Not only in delirium
Distress
Intoxication doe snot apply to what
Tobacco
What has no withdrawal
PCP, inhalants, hallucinogens
Neuroadaptation
CNS changes following repeated use such that person develops tolerance and/or withdrawal
-
Pharmacokinetic neuroadaptation
Adaptation of metabolizing system
Pharmacodynamic neuroadaptation
Ability of cns to function despite high blood levels
Tolerance
Increase amount to get effect or decrease effect same amount
Hospital for withdrawa
Overdose, severe , , suicide, medical comorbidities
Residential withdrawal
No monitoring, restricted env, partial hospitalization
Outpatient withdrawal
No risk and highly motivated
Motivational interventions for withdrawal
Family, relapse prevention, twelve step, alcohol anonymous, CBT< narcotics anonymous
Do a lot of ppl have more than one psychiatric disorder
Yes. Fifty percent
Alcohol intoxication level
.08
Fatal if get to airway issue and cns depression, pulmonary aspiration
Early alcohol withdrawal
Anxiety, irritability, htn, hyperthermia, tachycardia, nausea
Seizures alcohol withdrawal
Twenty four to fort with
Delirium tremendous
Forty eight to seventy two
Three to ten days after
Agitation, confusion, disoriented, fever, HTN, diaphoresis, autonomic hyperactive ,
Hallucinations, autonomic instability, life threatening
Hallmark of delirium tremendous
Profound global confusion
Chronic intake alcohol
Increased opiates, activate GABA A producing GABA inhibition, influx cl, impregnate NMDA which mediates glutamate and interacts with serotonin and dopamine receptors
Withdrawal alcohol
Loss gaba a receptor stimulation causes reduce cl cause tremors, diaphoresis, tachycardia, anxiety, seizures,
Inhibits NMDA receptos
Seizures, delirium
CIWA
Numerical value to symptoms with points
> ten severe withdrawal
Treat withdrawal alcohol
Benzodiazepines GABA agonist
Anticonvulsants for seizure risk -carbamazepine or valproic acid
Thiamine supp
Meds for staying off alc
Disulfiram, naltrexone, acamprosate
Disulfiram
No work more harm than good
Inhibits aldehyde DH
Can cause death if alcohol given
Psychiatric AE, dermatological rashes, polyneuropathy, hepatotoxicity
Naltrexone
Opioid antagonist
Check LFT
Acamprosate
Unknown moa check kidney function
Benzodiazepine
Similar to alc but less cognitive impaired
More lipophilic shorted action
Withdrawal benzodiazepines
Similar to alcohol can get from tapering too fast
Sconvert short to long half life then slowly taper
Decrease does every week or two
If rapid give valproic acid or carbamazepine
Or gabapentin and tizanidine
Opioid intoxication
Pinpoint pupils, constipation, bradycardia, hypotension, decreased rr
Withdrawal opioids
Not life threatening unless severe medical illlness but uncomfortable, dilated pupils lacrimation, goosebumps, nv
Treat opioid with
Anti-emetic, antacids, NSAIDS< BZd
Treat
Support education, skills, methadone, naltrexone, buprenorphine
Methadone
From methadone assisted treatment program
Oral
High risk deadly when used with benzodiazepine, or 3a4 substrate
Mu agonist
What do if not MAT and in er for pain
Call service at methadone clinic then give dose
If need mroe dont use another 3a4 substrate
Naltrexone
Opioid blocker, mu antagonist
Buprenorphine
Partial mu agonist
Need to take ASAM course to give prescription
If highly motivated
Stimulate acute intox
Euphorias, vigor, gregariousness, hyperactivity, restlessness, interpersonal sensitivity, anxiety tension, anger, impaired judgement,
Tachycardia HTN NV
Chronic stimulant
Blunting, fatigue, sadness, withdrawal hypotension bradycardia
Psychosis
Withdrawal suicide risk and depression
Cocaine
CVA and MI get EKG
Rhabdomyolysis with compartment syndrome
Neuroadaptation prevent reuptake of DA
Amphetamine
Neurotoxicity from chronic from glutamate and axonal degeneration
Fatal in brugada syndrome
Psychosis
Neuroadaptation inhibits reuptake of da, ne, se, mainly da
Tobacco
CYP1a2 induced
Stop olanzapine
No intoxication diagnosis
Neuroadaptation-nicotine acetylcholine receptors on da neurons in ventral tegmental area release da in nucleus accumbens
Rapid tolerance
Withdrawal tobacco
Dysphagia, irritability, anxiety, decreased conc, insomnia, increased appetite
Med tobacco
Bupropion
Varenicline
Hallucinogens
Natural peyote
Synthetic LSDD
DMT, STP, MDMA,
MDMA
Enhanced empathy, personal insight, euphoria, increased energy,
Illusions, hyperacusis, sensitivity to touch, taste/smell altered,
Tolerance quick and teeth grinding if continue use
Fever MDMA
HIHGH up to forty three
Tachycardia, sweating, muscle spasms
Rhabdomyolysis, renal failure, seizures, DIC, arrhythmia, death
Neuroadaptation mdma
Serotonin, da, ne, but mainly 5HT2 agonist
Psychosis mdma
Hallucinations, paranoid, serotonin neural injury
Withdrawal mdma
Unclear
Cannabis
Increase appetite, tachycardia, panic, psychosis, color sound taste change, relaxation
Neuroadaptation
Cb1 cb2 receptors coupled with G protein and AC to Ca channel inhibiting calcium influx
Decrease uptake gaba and da
Who has high risk psychosis cannabis
MALES
Withdrawal cannabis
Insomnia, irritability, anxiety, poor appetite, expression,
Treat cannabis
Detox, behavioral model, no pharmacological treatment
PCP
Vertical nystagmus and horizontal
Severe dissociative reactions
HTN
Treat pcp
Antipsychotic drugs or BZd
Low stimulation env
Acidity urine
Neuroadaptation pcp
Opiate receptor effects
Allosteric modulator of glutamate NMDA receptor
No tolerance or withdrawal
Adhd
Ok
Increasing ADHD
Increasing awareness and access to services
Comorbid ADHD
Mood disorders, anxiety, substance disorders, explosive,
Tourettes is associated with what
OCD and ADHD
Tourettes triad
TS, ADHD, OCD
Chronic tic disorder
Higher in ADHD
ADHD suicide
Yes up
What is executive function
Information processing dysfunction within prefrontal cortex
Defiency of dopamine and NE
What area of the rain is dysfunction in ADHD
Dorsal anterior midcingulate cortex
What regions of brain have decreased activation in patients with adhd
Right inferior prefrontal cortex
Supplementary motor area
Anterior cingulate cortex
Left caudate into putamen and insula and right mid thalamus
Attention tastes
Decreased activation right dorsolateral prefrontal cortex, left putamen and globus pallidus, right posterior thalamus, caudate tail , right inferior parietal lobe, precuneus and superior temporal lobe,
Attention task increased activation
Left cuneus and right cerebellum
DSM-V diagnostic criteria for ADHD
Children still should have six or more symptoms
17 and up at least 5
Inattentative ADHD
Can’t give close attention and sustaining attention, not listening, avoids thinking, distracted
Hyperacute type ADHD
Fidgets, cant stay still, driven by a motor, talks a lot, blurts out answers, cant wait
What history get ADHD
History of disease Developmental history Medical history Family history Screen for comorbid disorders
TOVA
Test of variables of attention
Test is shorter in kids
Conners continuous performance test
Task oriented computerized assessment of attention related problems in 8 and older
Related to attention
How give conners continuous performance test
15 min computer test
Conners adult adhd rating scales
Correlates with the measures believed to measure related constructs
Treat adhd
Don’t yell or cticize less harsh parenting
Treat med 4-5
Methylphenidate if behavior therapy no work
Treat adhd 6-11
Stimulant and BHT
Treat adhd 12-18
BHT and med
12-18
Get assent from adolescent BHT and med
Alternative to stimulant for adhd
Guanfacine and clonidine
A2 adrenergic agonists
Bupropion
Antidepressant with catecholamines gif effects
Increase seizure but lack abuse liability, single daily dosing, and efficacy for co occurring anxiety and depression
Atomoxetine
Inhibits presynaptic ne reuptake resulting in increased synaptic NE and DA
Long QT
Caution with CVD
Modafinil
Binds da transporter, inhibiting reuptake
Dermatological and psychiatric reactions
Methylphenidate
Reuptake inhibitor of da
Amphetamine
Reuptake inhibitor of catecholamines and releases
Why methylphenidate good
Betwe CPT response, Bette with tourettes, visuomotor disorder, less anorexia and sleep delay not there
Advantages to amphetamine
More consistent response day to day
Higher proportion of patients with good/excellent response
Better with comorbid conduction disorder/oppositional defiant
Less depression/apathy
Fewer stomachaches
May be better with higher
Integration
Happening!
What is integrated care
Systematic coordination of general and behavioral healthcare
Substance abuse and mental health and primary are
Team based care
At least 2 providers who work with patient and their caregivers
Behavioral health
Behavioral factors in medical care -mental health, lifestyle
3 factors driving the integrated healthcare movement
Hig prevelance of behavioral health conditions in primary care
Most behavioral health conditions remain undetected and untreated
Cost of untreated behavioral health conditions is exorbitant
Poor follow through on referrals to outside speciality
Poor health outcome when compared ot other wealthy country’s-excessive expenditure, policy changes, disparities, provider burnout,
Benefits of integrated care
Improved experience, outcomes, expenditures, satisfaction
Triple aim
Framework for an approach to optimizing health system performance. New design must be developed to simultaneously pursue
1. Improving patient experience, improving health of populations, reducing per capita cost
Triple aim
Population health, experience, per capita cost
Provider burn out
Less likely with BHC get improved job satisfaction, can address behavior, more likely to continue able to see more patients in 20, recognize behavior
Quadruple aim
Reduce care costs, satisfied patients, improved population health, satisfied providers
Interprofessional education
When 2 or more professions learn from , about and with each other
Interprofessional education
Core curriculum prepares us to function collaboratively on health care teams by making each year of curriculum, to learn in academic and/or clinical environments that permit interaction with students enrolled in other profession
PCBH
Improves access rates
Primary care behavioral health SH
SHARES MANY COMMON AIMS AND FEATURES OF PATIENT CENTERED MEDICAL HOMES AND WHOLE PERSON CARE
RECOGNITION OF ASSISTANCE FOR OVERBURDENED PRIMARY CARE PROVIDERES AND SYSTEMS
GENERALIST AND POPULATION-HEALTH BASED MODEL
DESCRIBE WHAT AN EFECTIVE FULLY INTEGRATED ARE TEAM LOOKS LIKE
Shared treatment space
Systemspathways: shared care provision, medical records
Type of collaboration: full and reciprocal
Composition-entire clinic staff
————approach/function
-hudDlEs before clinic
Treatment plans: shared and mutually supported
-scope of problems targeted (targeted vs. non targeted)
Describe what an effective fully integrated care team looks like
Allows for immediate warm hands off
PCP retains full responsibility for the patient and possesses the final decision makeing authority for patients
Explain four functions that a behavioral health consultant can provide to assist a physician in his or or her day to day practice
Assessment, education, brief intervention, referral, warm hands off, chronic illness, mental health disorders, prevention, quality improvement, early intervention, stress mediated disease/symptoms, chronic pain management program chronic care registries, SUBSTANCE MISUSE. IMPROVED COMMUNICATION BETWEEN PROVIDER AND PATIENTS
BHC chronic medical conditions
HA, insomnia, HTN, asthma, diabetes, obesity, chronic pain
Lifestyle modifications BHC
Tobacco, cessation , weight, alcohol misuse, nonadherence, PA
Areas commonly addressed by BHC
Depression, GENERALISTS PERSPECtIVE, anxiety
Motivational interviewing
Helps ambivalence
-mixed feelings; feeling two ways about something; desire to do two opposing or conflict things
Biopsychosocial
A patien resists colonoscopy , patients asthma and co occurring depression get worse despite evidence based treatment , dying patient in unwilling to let go of interventions, even thought he acknowledges that they are futile
How BHC help
Prioritize concerns and clarify issues, address stresss, lifestyle and cultural and family variables related to. Sleep
-connect patient with social work, increase disease self management
Education about condition
Help prioritize concerns,
What area surrounds broca, wernicke, and arcuate fasciculus
Mediation also system for language, including a number or areas int her temporal, parietal and frontal association areas. This relays information to the language implementation system from the third system in language production
Conceptual system of language
Broadly distributed set of structures that provides the concepts underlying our language.
0-6 months
Language universalists recognize all sounds that might be language as distinct sounds
6-9 mo
Brains change and start to recognize the specific language sounds of their native language. Drop use of phenomena that dont occur in their language
When language complete/the language acquisition pathway
1 year
Babbling converted to language
Second language learned during language acquisition phase
Activates adjacent region of brocabut same pathway as first language
What is social cognition
Function in interpersonal and social situations
Emotion comrpeshension and theory of mind
Social cognition
Ability to infer emotional state of another from observable information such as prosody and facial expression
Emotion comprehension
Neural circuits for recognizing emotion in others are also involved in producing that emotion in ourselves
Steps one through threeemotional compression
Perception of facial expressions requires that we identify a face as something
Bring in the emotional component
-same circuit recognizes it in someone else bc facial details that cue us as to what emotion we are seeing in another person are concentrated in very specific areas in a triangle of eyes, nose mouth! (Normal person gaze scans another persons face in a triangle eyes to mouth)
The __ controls the use of the eyes and directs the gaze to that triangle (particularly the eyes) when looking at human faces
Amygdala
How see face if damage to amygdala
Spends little time looking at the eyes of another and doesnt methodically scan face
Mirror neuron system
Mirror neurons fire both when do something (smile) and see someone else do same
Imitative learning
Anterior mirror system
Identifies the goal of the action
Posterior mirror neuron system
Identifies the motor actions
Posterior sector of the superior temporal sulcus
Provides the visual input
Imitative behavior is crucial to developing social cognitive skills=we tend to imitate emotional state/behavior as well as motor behavior. The circuit for imitating is believed to interact with Limbic structures via the _
Insula
Prosody
Study of the tine and rhythm of speech and how these features contribute to meaning. Study of aspects of speech that typically apply to a level above that of the individual phoneme and very often to sequences of words )prosodic phrase)
Steps of prosody
- Primary auditory cortex is required for the basics of sound processing, including identity of pitch, loudness, and other characteristics of the sound
- That information is then sent to the right posterior superior temporal sulcus where, along with other acoustical information rom secondary auditory processes, we begin to piece together the meaning of the loudness, pitch, etc of the focalization
- Perception of prosody
The judgement of the emotional stimulus is then determined int he frontal cortex
Theory of mind
Ability to understand the mental states of others and to appreciate how these differ from our own
Core pathway of theory of mind
Amygdala and connections to the medial temporal lobes and orbitofrontal areas
Decision making: stimulus encoding system
Orbitofrontal cortex
Ventromedial prefrontal cortex
Striatum
Action selection system
Anterior cingulate cortex
Learns and encodes the subjective value of the results.
Error detection
Expected reward system: predicts expected reward
Basal ganglia
Amygdala
Insular cortex-Processing of social emotions
Intraparietal cortex-somatosensory processing and planning/intent
A decision in which the risks are explicit relies most heavily on the
Stimulus encoding system
Ambiguous risk decisions in which the risks are unknown rely most heavily ont he _
Expected reward system and eventually the action selection system
Neurophysiology of Limbic system
Ok
Limbic system
Fighting, feeling, feeding, fleeing, fucking
Emotion and motivational drives
Hypothalamus
Physiological responses connection to ANS
Olfactory areas
Olfaction and emotion strongly linked
Parts of Limbic system deal with olfaction (in addiction to emotion)
Thalamus
Anterior nucleus part of papez circuit
Other regions involved in both input and output of Limbic system
Basal ganglia
Nucleus accumbens
Putamen
Each plays a different role in emotion
Hippocampus
Another part of the papez circuit
Memory and emotion are strongly linked
Parahippocampal regions linked to surprise
Amygdala
Association with emotion recognized very early
Particularly fear and anger
Cingulate cortex
Mostly paleocortex
Many of these neurons show after discharge
Circuits that allow us to experience an emotional re the same as what
Circuits that allow us eat identify emotion in others
When do mirror neurons fire
When smile and see other smile
Innate fear
Fear that requires no experience
Learned fear
Learned
Indirect or direct
Amygdala
Processing and recognition of social cues related to fear
Emotional conditioning in response to fear
Memory
Learned fear
A direct thalmo-amygdaloid pathway to the lateral nucleus of the amygdala:mediates rapid response
An indirect thalami cortico amygdaloid pathway to the lateral nucleus of the amygdala: this pathway mediates later responses
Learned fear inputs arrive where
Lateral nucleus of the amygdala
Lateral nucleus of amygdala
Integrates the inputs for learned fear so paired information is sent to basal and intercalated nuclei for additional processing then sent to central nucleus of the amygdala
Hypothalamus learned fear
Hypothalamus is important in generating physiologic response
Decides what responses are required and relays information appropriately
Damage to amygdala
Fear is not perceived, therefore conditioning related to fear does not occur
Anger
Amygdala and dopamine receptors
Inhibiting anger
Neocortex, ventromedial hypothalmic, septal nuclei
Avoidance
Opposite pleasure/reward-prevent the occurrence of a behavior that has short term rewards but long term negative consequences
Avoidance substrate
Lateral posterior hypothalamus, dorsal midbrain, entorhinal cortex
Sadness anatomical substrate
Lower sector of the anterior cingulate cortex
Strongly activated when recalling sad events
Disgust
Insular cortex/putamen
Processing and recognition of social cues related to disgust
Damage abolishes
Surprise
Strongly associated with parahippocampal gyrus
Parahippocampal gyrus is important in detecting novelty or unexpected events
Anterior cingulate cortex
2 regions
Ventral-affective
Dorsal-cognitive
Cortical role in emotion
Integration of visceral, attentional and emotional input
Regulation of affect-particularly top-down control
Monitors or detects conflict between our functional state and new information that has potential or motivational consequences. It does not decide what to do, but relays the information to the 2 divisions
Dorsolateral division receives input of
Received input from
Motor areas, basal ganglia, pre and supplementary motor cortex
Cingulate cortex, espicially parts related ot performance monitoring
Several cortical association areas
Ventromedial prefrontal cortex receives input from
Amygdala, hippocampus, temporal visiual association area, dorsolateral prefrontal cortex
Three roles of cortical emotion
Reward processing, integration of bodily signals, top down regulation
Reward processing
With the amygdala, we link new stimulus to a primary reward
Integration of bodily signals
Gut feeling -decision when logical analysis is unable to help
Top down regulation
Espicially towards delayed gratification
