Behav 2 Pharm Flashcards

(194 cards)

1
Q

Dementia

A

Ok

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Central ache inhibitors

A

Tacrine, donepezil, rivastigmine, galantamine, memantine,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Tacrine

A

• High incidence of hepatotoxicity, newer agents are preferred (no longer used clinically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Addiction vs physical dependency

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Tolerance and physiological dependence , pain relief ,

A

Misinterpreted as drug seeking or relapse behavior

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Reward defiency syndrome

A

Dopamine system malfunction

Common pathway for addictive behavior

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Addiction genetic

A

Yes but also environmental

Non substance specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Addictophrenia model

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Addictophrenia type I

A

Genetic history of addictive disorder-alc
Genetic history of mood disorder
Higher incidence of comorbid mood disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Type Ii

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Type II

A

Genetic history of addictive disorder-not a prerequisite, but increases vulnerability

Significant history of trauma-predominantly alchol and benzodiazepine use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Addictophrenia type IV

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Diagnose addictophrenia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Do ppl die when addicted

A

Yes. Fifty percent have comorbid psychiatric disorder

-antisocial PD, depression, suicide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Substance use disorder

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Mild substance use

A

Two to three symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Moderate substance use

A

Four to five symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Severe substance use

A

Six or more symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Early remission

A

No criteria except craving for over three months but less than twelve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Sustained remission

A

No criteria for over twelve months except craving

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is substance abuse mental disorder

A

Symptom of mental disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How identify substance abuse mental disorder

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Intoxication doe snot apply to what

A

Tobacco

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What has no withdrawal

A

PCP, inhalants, hallucinogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Neuroadaptation
CNS changes following repeated use such that person develops tolerance and/or withdrawal -
26
Pharmacokinetic neuroadaptation
Adaptation of metabolizing system
27
Pharmacodynamic neuroadaptation
Ability of cns to function despite high blood levels
28
Tolerance
Increase amount to get effect or decrease effect same amount
29
Hospital for withdrawa
Overdose, severe , , suicide, medical comorbidities
30
Residential withdrawal
No monitoring, restricted env, partial hospitalization
31
Outpatient withdrawal
No risk and highly motivated
32
Motivational interventions for withdrawal
Family, relapse prevention, twelve step, alcohol anonymous, CBT< narcotics anonymous
33
Do a lot of ppl have more than one psychiatric disorder
Yes. Fifty percent
34
Alcohol intoxication level
.08 Fatal if get to airway issue and cns depression, pulmonary aspiration
35
Early alcohol withdrawal
Anxiety, irritability, htn, hyperthermia, tachycardia, nausea
36
Seizures alcohol withdrawal
Twenty four to fort with
37
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
38
Hallmark of delirium tremendous
Profound global confusion
39
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
40
Withdrawal alcohol
Loss gaba a receptor stimulation causes reduce cl cause tremors, diaphoresis, tachycardia, anxiety, seizures,
41
Inhibits NMDA receptos
Seizures, delirium
42
CIWA
Numerical value to symptoms with points >ten severe withdrawal
43
Treat withdrawal alcohol
Benzodiazepines GABA agonist Anticonvulsants for seizure risk -carbamazepine or valproic acid Thiamine supp
44
Meds for staying off alc
Disulfiram, naltrexone, acamprosate
45
Disulfiram
No work more harm than good Inhibits aldehyde DH Can cause death if alcohol given Psychiatric AE, dermatological rashes, polyneuropathy, hepatotoxicity
46
Naltrexone
Opioid antagonist Check LFT
47
Acamprosate
Unknown moa check kidney function
48
Benzodiazepine
Similar to alc but less cognitive impaired More lipophilic shorted action
49
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
50
Opioid intoxication
Pinpoint pupils, constipation, bradycardia, hypotension, decreased rr
51
Withdrawal opioids
Not life threatening unless severe medical illlness but uncomfortable, dilated pupils lacrimation, goosebumps, nv
52
Treat opioid with
Anti-emetic, antacids, NSAIDS< BZd
53
Treat
Support education, skills, methadone, naltrexone, buprenorphine
54
Methadone
From methadone assisted treatment program Oral High risk deadly when used with benzodiazepine, or 3a4 substrate Mu agonist
55
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
56
Naltrexone
Opioid blocker, mu antagonist
57
Buprenorphine
Partial mu agonist Need to take ASAM course to give prescription If highly motivated
58
Stimulate acute intox
Euphorias, vigor, gregariousness, hyperactivity, restlessness, interpersonal sensitivity, anxiety tension, anger, impaired judgement, Tachycardia HTN NV
59
Chronic stimulant
Blunting, fatigue, sadness, withdrawal hypotension bradycardia Psychosis Withdrawal suicide risk and depression
60
Cocaine
CVA and MI get EKG Rhabdomyolysis with compartment syndrome Neuroadaptation prevent reuptake of DA
61
Amphetamine
Neurotoxicity from chronic from glutamate and axonal degeneration Fatal in brugada syndrome Psychosis Neuroadaptation inhibits reuptake of da, ne, se, mainly da
62
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
63
Withdrawal tobacco
Dysphagia, irritability, anxiety, decreased conc, insomnia, increased appetite
64
Med tobacco
Bupropion Varenicline
65
Hallucinogens
Natural peyote Synthetic LSDD DMT, STP, MDMA,
66
MDMA
Enhanced empathy, personal insight, euphoria, increased energy, Illusions, hyperacusis, sensitivity to touch, taste/smell altered, Tolerance quick and teeth grinding if continue use
67
Fever MDMA
HIHGH up to forty three Tachycardia, sweating, muscle spasms Rhabdomyolysis, renal failure, seizures, DIC, arrhythmia, death
68
Neuroadaptation mdma
Serotonin, da, ne, but mainly 5HT2 agonist
69
Psychosis mdma
Hallucinations, paranoid, serotonin neural injury
70
Withdrawal mdma
Unclear
71
Cannabis
Increase appetite, tachycardia, panic, psychosis, color sound taste change, relaxation
72
Neuroadaptation
Cb1 cb2 receptors coupled with G protein and AC to Ca channel inhibiting calcium influx Decrease uptake gaba and da
73
Who has high risk psychosis cannabis
MALES
74
Withdrawal cannabis
Insomnia, irritability, anxiety, poor appetite, expression,
75
Treat cannabis
Detox, behavioral model, no pharmacological treatment
76
PCP
Vertical nystagmus and horizontal Severe dissociative reactions HTN
77
Treat pcp
Antipsychotic drugs or BZd Low stimulation env Acidity urine
78
Neuroadaptation pcp
Opiate receptor effects Allosteric modulator of glutamate NMDA receptor No tolerance or withdrawal
79
Adhd
Ok
80
Increasing ADHD
Increasing awareness and access to services
81
Comorbid ADHD
Mood disorders, anxiety, substance disorders, explosive,
82
Tourettes is associated with what
OCD and ADHD
83
Tourettes triad
TS, ADHD, OCD
84
Chronic tic disorder
Higher in ADHD
85
ADHD suicide
Yes up
86
What is executive function
Information processing dysfunction within prefrontal cortex Defiency of dopamine and NE
87
What area of the rain is dysfunction in ADHD
Dorsal anterior midcingulate cortex
88
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
89
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,
90
Attention task increased activation
Left cuneus and right cerebellum
91
DSM-V diagnostic criteria for ADHD
Children still should have six or more symptoms 17 and up at least 5
92
Inattentative ADHD
Can’t give close attention and sustaining attention, not listening, avoids thinking, distracted
93
Hyperacute type ADHD
Fidgets, cant stay still, driven by a motor, talks a lot, blurts out answers, cant wait
94
What history get ADHD
``` History of disease Developmental history Medical history Family history Screen for comorbid disorders ```
95
TOVA
Test of variables of attention | Test is shorter in kids
96
Conners continuous performance test
Task oriented computerized assessment of attention related problems in 8 and older Related to attention
97
How give conners continuous performance test
15 min computer test
98
Conners adult adhd rating scales
Correlates with the measures believed to measure related constructs
99
Treat adhd
Don’t yell or cticize less harsh parenting
100
Treat med 4-5
Methylphenidate if behavior therapy no work
101
Treat adhd 6-11
Stimulant and BHT
102
Treat adhd 12-18
BHT and med
103
12-18
Get assent from adolescent BHT and med
104
Alternative to stimulant for adhd
Guanfacine and clonidine A2 adrenergic agonists
105
Bupropion
Antidepressant with catecholamines gif effects Increase seizure but lack abuse liability, single daily dosing, and efficacy for co occurring anxiety and depression
106
Atomoxetine
Inhibits presynaptic ne reuptake resulting in increased synaptic NE and DA Long QT Caution with CVD
107
Modafinil
Binds da transporter, inhibiting reuptake Dermatological and psychiatric reactions
108
Methylphenidate
Reuptake inhibitor of da
109
Amphetamine
Reuptake inhibitor of catecholamines and releases
110
Why methylphenidate good
Betwe CPT response, Bette with tourettes, visuomotor disorder, less anorexia and sleep delay not there
111
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
112
Integration
Happening!
113
What is integrated care
Systematic coordination of general and behavioral healthcare Substance abuse and mental health and primary are
114
Team based care
At least 2 providers who work with patient and their caregivers
115
Behavioral health
Behavioral factors in medical care -mental health, lifestyle
116
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,
117
Benefits of integrated care
Improved experience, outcomes, expenditures, satisfaction
118
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
119
Triple aim
Population health, experience, per capita cost
120
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
121
Quadruple aim
Reduce care costs, satisfied patients, improved population health, satisfied providers
122
Interprofessional education
When 2 or more professions learn from , about and with each other
123
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
124
PCBH
Improves access rates
125
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
126
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)
127
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
128
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
129
BHC chronic medical conditions
HA, insomnia, HTN, asthma, diabetes, obesity, chronic pain
130
Lifestyle modifications BHC
Tobacco, cessation , weight, alcohol misuse, nonadherence, PA
131
Areas commonly addressed by BHC
Depression, GENERALISTS PERSPECtIVE, anxiety
132
Motivational interviewing
Helps ambivalence | -mixed feelings; feeling two ways about something; desire to do two opposing or conflict things
133
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
134
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,
135
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
136
Conceptual system of language
Broadly distributed set of structures that provides the concepts underlying our language.
137
0-6 months
Language universalists recognize all sounds that might be language as distinct sounds
138
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
139
When language complete/the language acquisition pathway
1 year Babbling converted to language
140
Second language learned during language acquisition phase
Activates adjacent region of brocabut same pathway as first language
141
What is social cognition
Function in interpersonal and social situations Emotion comrpeshension and theory of mind
142
Social cognition
Ability to infer emotional state of another from observable information such as prosody and facial expression
143
Emotion comprehension
Neural circuits for recognizing emotion in others are also involved in producing that emotion in ourselves
144
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)
145
The __ controls the use of the eyes and directs the gaze to that triangle (particularly the eyes) when looking at human faces
Amygdala
146
How see face if damage to amygdala
Spends little time looking at the eyes of another and doesnt methodically scan face
147
Mirror neuron system
Mirror neurons fire both when do something (smile) and see someone else do same Imitative learning
148
Anterior mirror system
Identifies the goal of the action
149
Posterior mirror neuron system
Identifies the motor actions
150
Posterior sector of the superior temporal sulcus
Provides the visual input
151
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
152
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)
153
Steps of prosody
1. Primary auditory cortex is required for the basics of sound processing, including identity of pitch, loudness, and other characteristics of the sound 2. 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 3. Perception of prosody The judgement of the emotional stimulus is then determined int he frontal cortex
154
Theory of mind
Ability to understand the mental states of others and to appreciate how these differ from our own
155
Core pathway of theory of mind
Amygdala and connections to the medial temporal lobes and orbitofrontal areas
156
Decision making: stimulus encoding system
Orbitofrontal cortex Ventromedial prefrontal cortex Striatum
157
Action selection system
Anterior cingulate cortex Learns and encodes the subjective value of the results. Error detection
158
Expected reward system: predicts expected reward
Basal ganglia Amygdala Insular cortex-Processing of social emotions Intraparietal cortex-somatosensory processing and planning/intent
159
A decision in which the risks are explicit relies most heavily on the
Stimulus encoding system
160
Ambiguous risk decisions in which the risks are unknown rely most heavily ont he _
Expected reward system and eventually the action selection system
161
Neurophysiology of Limbic system
Ok
162
Limbic system
Fighting, feeling, feeding, fleeing, fucking Emotion and motivational drives
163
Hypothalamus
Physiological responses connection to ANS
164
Olfactory areas
Olfaction and emotion strongly linked Parts of Limbic system deal with olfaction (in addiction to emotion)
165
Thalamus
Anterior nucleus part of papez circuit Other regions involved in both input and output of Limbic system
166
Basal ganglia
Nucleus accumbens Putamen Each plays a different role in emotion
167
Hippocampus
Another part of the papez circuit Memory and emotion are strongly linked Parahippocampal regions linked to surprise
168
Amygdala
Association with emotion recognized very early Particularly fear and anger
169
Cingulate cortex
Mostly paleocortex Many of these neurons show after discharge
170
Circuits that allow us to experience an emotional re the same as what
Circuits that allow us eat identify emotion in others
171
When do mirror neurons fire
When smile and see other smile
172
Innate fear
Fear that requires no experience
173
Learned fear
Learned Indirect or direct
174
Amygdala
Processing and recognition of social cues related to fear Emotional conditioning in response to fear Memory
175
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
176
Learned fear inputs arrive where
Lateral nucleus of the amygdala
177
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
178
Hypothalamus learned fear
Hypothalamus is important in generating physiologic response Decides what responses are required and relays information appropriately
179
Damage to amygdala
Fear is not perceived, therefore conditioning related to fear does not occur
180
Anger
Amygdala and dopamine receptors
181
Inhibiting anger
Neocortex, ventromedial hypothalmic, septal nuclei
182
Avoidance
Opposite pleasure/reward-prevent the occurrence of a behavior that has short term rewards but long term negative consequences
183
Avoidance substrate
Lateral posterior hypothalamus, dorsal midbrain, entorhinal cortex
184
Sadness anatomical substrate
Lower sector of the anterior cingulate cortex Strongly activated when recalling sad events
185
Disgust
Insular cortex/putamen Processing and recognition of social cues related to disgust Damage abolishes
186
Surprise
Strongly associated with parahippocampal gyrus Parahippocampal gyrus is important in detecting novelty or unexpected events
187
Anterior cingulate cortex
2 regions Ventral-affective Dorsal-cognitive
188
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
189
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
190
Ventromedial prefrontal cortex receives input from
Amygdala, hippocampus, temporal visiual association area, dorsolateral prefrontal cortex
191
Three roles of cortical emotion
Reward processing, integration of bodily signals, top down regulation
192
Reward processing
With the amygdala, we link new stimulus to a primary reward
193
Integration of bodily signals
Gut feeling -decision when logical analysis is unable to help
194
Top down regulation
Espicially towards delayed gratification