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abnormal exam 3 Flashcards

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1
Q

what are somatic symptoms and related disorders?

A

Category of disorders in dsm5, related to body (physical), psychological factors underlie or worsen somatic symptoms

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2
Q

somatic symptom disorder

A

one or more somatic symptoms that cause significant distress and/or impairment. chronic stomach pain, chronic headache, excessive worry/anxiety about the symptoms themselves and/or excessive time and energy devoted to health concerns

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3
Q

how long do you have to experience somatic symptom disorder to be diagnosed?

A

persistent for at least 6 months

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4
Q

Illness anxiety disorder

A

significant worry about having or developing a serious illness. somatic symptoms ay or may be present (only mild if present), excessive health-related behaviors or maladaptive avoidance

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5
Q

illness anxiety disorder must persist for ________ to be diagnosed

A

at least 6 months

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6
Q

both somatic and illness anxiety disorder have a prevalence rate of…

A

5-7%

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7
Q

theories of somatic symptom disorder and illness anxiety disorder: genetic

A

health concerns run in families, unclear if result of genetics or modeling

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8
Q

theories of somatic symptoms disorder and illness anxiety disorder: cognitive

A

cognitive factors play a strong role. hyper attentive to physical changes and catastrophize symptoms

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9
Q

theories of somatic symptoms disorder and illness anxiety disorder: trauma

A

experiencing trauma is a risk factor, somatic symptoms frequently seen in PTSD

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10
Q

treatment of somatic and illness anxiety disorders

A

psychodynamic approach: provide insight into connection between emotional and physical symptoms. cognitive behavioral approach: modify catastrophic thinking, exposure to anxiety triggers, reinforce healthy behaviors

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11
Q

what is functional neurological symptom disorder?

A

previously called conversion disorder, altered sensory or motor function (ex: paralysis, blindness, seizures, false pregnancy) symptoms are inconsistent with recognized neurological or medical condition.

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12
Q

what is the lifetime prevalence for functional neurological symptom disorder?

A

.02%

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13
Q

psychogenic non-epileptic seizures

A

specific type of functional neurological symptoms disorder. person experiences epileptic-like seizures but no underlying symptoms

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14
Q

theories of functional neurological symptom disorder: Freudian

A

repressed emotions “transferred” to physical symptoms, primary gain: physical symptoms allow person to avoid anxiety. secondary gain: attention from others, relieved of obligations. still puts blame on the patient, so no no.

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15
Q

theories of functional neurological symptom disorder: behavioral

A

symptoms alleviate stress by removing individual from the environment. “you are stressed, so we are shutting things down so you can take care of yourself”

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16
Q

theories of functional symptom disorder: neurological

A

sensory and motor brain areas impaired by anxiety

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17
Q

treatment of functioning neurological symptom disorder: psychoanalytic

A

helps express painful emotions or memories that are linked to symptoms

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18
Q

treatment of functional neurological symptom disorder: cog-beh

A

reliving the person’s anxiety, alter reinforcements (reduce reinforcements the person is receiving from the symptoms)

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19
Q

dissociation

A

detachment from immediate physical surroundings, physical or emotional reality, your memory, or sense of identity

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20
Q

what is dissociative amnesia?

A

inability to recall important autobiographical information that is inconsistent with normal forgetting. not due to physiological effect of substances or neurological conditions

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21
Q

organic amnesia

A

biological cause, anterograde amnesia, retrograde amnesia

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22
Q

anterograde amnesia

A

inability to remember NEW information

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23
Q

retrograde amnesia

A

inability to remember information from the past

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24
Q

psychogenic amnesia

A

psychological cause, typically only retrograde not anterograde amnesia, retrograde amnesia for personal (not general) information

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25
dissociative fugue
subtype of dissociative amnesia. sudden, unexpected travel. confused or new identity. very rare. most cases are short distance, no new identity, and brief (hours or days)
26
what is DID
two or more distinct personality states (alters) that offer discontinuity of sense of self and alteration in affect, behavior, cognition, and other functioning. recurrent gaps in memory inconsistent with ordinary forgetting. not a normal part of accepted cultural or religious practice
27
lifetime prevalence of DID
around 1%
28
common types of alters
host (true identity), child (most common, may be created during trauma), persecutor (may inflict self harm), protector (perform tasks host cannot perform)
29
DID: alters may:
be aware or unaware of one another, like or dislike each other, work together or have conflicting goals
30
how does DID develop: genetics
likely genetic predisposition for heightened dissociation
31
how does DID develop: environment
high rates of childhood abuse/trauma. dissociative reaction to trauma, trauma memories stored in alter, compartmentalization of memories/experiences
32
how is DID treated?
goal is to "integrate" all personalities. determine function of each personality, review and understand trauma history
33
controversy of DID, left side of argument
prevalence increased dramatically after 1980 - concerns that alternate identities may be reinforced by therapists, concern that people are faking/exaggerating
34
controversy of DID, right side of argument
DID patients can be reliably diagnosed and exist across cultures/religions of the world. neuroimaging studies have shown brain activation distinct from "acting"
35
what is anorexia nervosa?
restriction of energy intake relative to requirements leading to significantly low weight. intense fear of gaining weight or persistent behaviors to avoid weight gain. disturbance in perception of weight or influence of weight on self evaluation.
36
two types of anorexia nervosa
restricting type, or binging type
37
lifetime prevalence of anorexia nervosa in females
up to 4%
38
lifetime prevalence of anorexia nervosa in males
0.3%
39
health complications due to anorexia
heart failure, low bone density, kidney damage, death (5-9%)
40
what is bulimia nervosa?
recurrent episodes of binge eating, recurrent compensatory behavior to prevent weight gain. self induced vomiting, laxatives, fasting, excessive exercise. binging/purging occurs at least once a week.
41
lifetime prevalence of bulimia nervosa in females
up to 2.6%
42
lifetime prevalence of bulimia nervosa in males
up to 1.6%
43
what is binge eating?
eating an unusually large amount of food (1200-1400 cals in 1-2 hours). lack of control, often food high in fat or carbs, often at home alone at night accompanied by negative emotions
44
comparison of AN and BN
common to move between diagnoses
45
AN vs bn
significantly underweight, very disturbed perception and fixation on weight/shape, in binge/purge type only
46
an vs BN
often normal weight or underweight, more realistic perception of shape/weight but still overconcern with weight/shape, binging and purging at least once per week
47
atypical anorexia
all criteria are met for AN except individual's weight is within or above normal weight range
48
AN more common along:
asian/white americans
49
BN more common among
hispanic and white americans. also, men. higher rates in sexual minority men
50
sociocultural factors of eating disorders: social pressures and norms
exposure to thin-ideal, friends attitudes discussing body dissatisfaction, athletics involvement (sports where weight matters)
51
sociocultural factors of eating disorders: family dynamics
parent - conflict and control, negative emotional expression discouraged, messages to lose weight. child is then - perfectionist, focused on pleasing others. maternal eating pathology increases risk - body dissatisfaction, internalization of thin-ideal, dietary restraint, eating disorder symptoms
52
biological factors of eating disorders
genetic risk. heritability is 56% for anorexia, and 41% bulimia. in brain functioning, low serotonin levels may lead to cravings for BN. disturbances in both serotonin and dopamine, reduced hypothalamus activity for AN.
53
psychological factors of eating disorders: emotions
depression symptoms --> eating disorder.
54
psychological factors of eating disorders: cognitive
overvaluation of shape or weight, internalization of thin ideal, perfectionism, low self esteem
55
how are eating disorders treated?
AN can be particularly difficult to treat. first step: achieve medically stable weight. next step, psychological intervention. typically CBT and/or family therapy for 6-12 months.
56
what are substance use disorders?
impaired control, social impairment, risky use, pharmacological. distinguished between abuse and dependence
57
12 month prevalence of alcohol use disorder:
10%
58
12 month prevalence of other SUD's
2-3%
59
central nervous system depressants
alcohol, prescription pills (benzos, barbiturates), gas, glue, paint thinners
60
substance use disorder: alcohol
slows cns, increased GABA activity. low doses include a euphoric feeling and confidence. high doses impair cognition, heightened depression/aggression, poor coordination, fatigue, respiratory paralysis, death/coma. long term consequences include heart disease, cancer, dementia
61
1st stage to third stage alcohol withdrawals
shakes, weakness, headache, nausea. seizures. delirium tremens (hallucinations and delusions, fever, irregular heartbeat)
62
CNS stimulants
cocaine, amphetamines, nicotine, caffeine, opiods
63
cocaine
blocks dopamine reuptake, more dopamine available. initial effects: euphoria, high self esteem, high energy. high/repeated doses: grandiosity, impulsiveness, compulsive behavior. long term consequences: heart attack, stroke, gastrointestinal problems, risky behaviors to obtain it, HIV from needle sharing
64
cocaine withdrawal
dysphoria, fatigue, sleep problems, increased appetite
65
amphetamines
prescription pills prescribed for ADHD and other problems, diverted for illegal use/abuse, manufactured illegally
66
nicotine
chemical in tobacco, "fight or flight" like response, withdrawal: depressed, anxious, restless, hungry
67
caffeine
high doses: agitation, seizures, respiratory problems. withdrawal: flu like, headache, fatigue, low mood
68
opioids
oxycontin, heroin, fentanyl
69
opioid use and withdrawal
initial effects: rush of euphoria, followed by lethargy, slurred speech, cognitive slowing. high doses: coma, seizure, respiratory suppression, death. withdrawal: dysphoria, achiness, nausea, sweating, diarrhea, fever
70
substance use disorder: biological factors. genetics
around 50% risk for disorder development. general inherited vulnerability for addiction. variations in genes related to: impulsivity, the metabolism of different substances, dopamine system functioning (how rewarding a person finds a substance)
71
substance use disorder: biological factors. brain functioning
drugs of abuse affect the reward system in the brain and affect dopamine either directly or indirectly. example: amphetamines and cocaine --> increase dopamine levels directly
72
SUD psychological factors: mental illness
you can't treat one or the other, (mental illness and substance use disorder) they work hand in hand
73
SUD psychological factors: cognitions
"alcohol helps me relax" "easier to openly express love and affection" "alcohol improves sex"
74
SUD social and cultural factors
social learning, chronic stress, culture/age, gender (males at higher risk compared to females. higher rates among gender minorities)
75
SUD stages of treatment
assessment and diagnosis, assess and increase motivation, determine level of care (inpatient detox, residential program, outpatient group) treatment, maintenance
76
how do you assess/increase motivation for SUD?
motivational interviewing
77
motivational interviewing for SUD
can be used on its own or in context of other treatment, empathetic non confrontational approach, elicit and solidify motivation and commitment to change, focus on client's ambivalence and desire to change
78
different levels of treatment for SUD (low to high)
outpatient services, intensive outpatient, residential, intensive inpatient
79
outpatient services level (SUD)
lowest level, no risk of medical complications, in a supportive home environment
80
intensive outpatient level
low middle, minimal risk of medical complications, less supportive home environment, needs structure
81
residential level SUD
high middle, has medical risk, unable to control use in outpatient care
82
intensive inpatient services level SUD
highest level, acute withdrawal, 24 hour medical care required
83
what substance is used to treat alcohol withdrawal
benzos
84
what substance is used to treat heroin withdrawal
methadone
85
is nicotine used for SUD withdrawal
yes, replacement therapy
86
what is an antagonist for SUD
meds to block effects. naltrexone is an antagonist for opioids and alcohol. naloxone is used to treat opioid overdose
87
what is aversive conditioning
meds that make you sick if you drink alcohol for example. antabuse for alcohol
88
treatment for SUD
CBT, AA
89
what is health psychology
study of psychological and behavioral factors to physical health, illness, and healthcare
90
increasing relevance of health psychology. why?
chronic illnesses are increasingly common. people now live longer with illness. increased understanding of how important psychological/behavioral factors are to health
91
how does chronic stress affect health?
lowered immune functioning, more susceptible to infections, suppressed immune system cells (for the higher stress levels)
92
Love hurts, couples interaction and wound healing takeaways
on average it took a day longer for wounds to heal after conflict conversation compared to supportive. couples with higher hostile behaviors during interactions took 2 days longer on average to heal. showed larger increases in proinflammatory cytokines following conflict conversation
93
how does chronic stress affect blood pressure?
increased risk for high blood pressure and coronary heart disease
94
how does personality and mental health factors like hostility and depression impact health?
increased risk for high blood pressure and coronary heart disease (less healthy behaviors)
95
aerobic exercise has _____ __________ effects on adults with _____
large antidepressant, MDD
96
four stages of sleep every 90 mins
non-REM1, non-REM2, non-REM3, REM
97
non-REM1
slowed breathing, sometimes sensations of floating/falling
98
non-REM2
clearly asleep
99
non-REM3
slower brain waves, harder to awaken, sleepwalking, sleep talking can occur
100
REM
fast eye movements, dreaming
101
why do we sleep?
sleep protects us, recuperates, restore and rebuild fading memories of the day's experience, feeds creative thinking, supports growth
102
how does sleep affect mental health?
lack of sleep can lead to irritability, poor emotion regulation (more reactive to emotional stimuli), perceptual distortions, impairs memory learning decision making creative thinking.
103
insomnia is a risk factor for what
psychiatric disorders
104
what is insomnia?
persistent difficulty falling or staying asleep, and/or early wakening with inability to return to sleep
105
insomnia must persist for ___ nights per week for ____ months
at least 3 (both)
106
lifetime prevalence for insomnia
10-15%
107
how is insomnia treated?
medications (benzos, ambien, melatonin) but these only last as long as person takes meds. cognitive behavioral therapy for insomnia
108
what does CBT look like for insomnia treatment?
identify what is influencing person's sleep, address behaviors and cognitions that may be negatively influencing sleep
109
what influences sleep?
sleep drive, circadian rhythm, conditioning, hyperarousal
110
what is sleep drive
the biological need for sleep that increases as you stay awake
111
what is circadian rhythm?
body's internal clock, a roughly 24 hour cycle that regulates sleep-wake patterns
112
what is conditioning (sleep)
the pairing of sleep with other stimuli
113
what is hyperarousal?
more anxiety/stress --> worse sleep
114
improving sleep in CBT-insomnia: sleep drive
eliminate naps during the day, exercise, wake up at a regular time each day
115
improving sleep in CBT-insomnia: circadian rhythm
go to bed and wake up at the same time each day, get exposure to natural light during the day
116
improving sleep in CBT-insomnia: conditioning
use bed for sleep and sex (no tv, phone, etc) dont sleep other places, dont stay in bed unless youre asleep, have a bedtime routine
117
improving sleep in CBT-insomnia: hyperarousal
have a comfortable sleep environment, eliminate use of substances and very large meals before bed, treat other medical conditions, address maladaptive beliefs about sleep, set aside a "worry time" that is well before bed

Abnormal Psych (3 decks)

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