Week 1 Lectures & Topics Not Covered In Tl 1

Front 1

Where in the brain do learning & memory occur?

Back 1

Mainly in the hippocampus & amygdala.

Front 2

How many waking hours are needed for memory to be stabilized & less vulnerable to competing information?

Back 2

about 6

Front 3

Why is sleep important for memory?

Back 3

Sleep helps to consodilate information through simultaneously reviewing the day's events through the hippocampus & visual cortex

Front 4

What is the function of the amygdala?

Back 4

the "gatekeeper" that influences what is perceived, how it is perceived, & how we learn & remember (= emotions are important)

Front 5

Describe short-term memory.

Back 5

lasts minutes to hours
requires temporal lobes

Front 6

Areas of the brain used in semantic, procedural & working memories?

Back 6

Front 7

Area of the brain used in episodic memories?

Back 7

Front 8

How are short & long term memory similar?

Back 8

They are both Ca++ dependent.

Front 9

What is LTP?

Back 9

long term potentiation

Front 10

Discuss the characteristics of LTP. x3

Back 10

1. cumulative: successive episodes of stimulation increase synaptic efficiency
2. cooperativity: greater potentiation when stimulation delivered to a group of axons that terminate in a synaptic field
3. specificity: doesn't induce LTP in all synapses, only locally

Front 11

Discuss long term memory synapses.

Back 11

pre & post-synaptic cells must fire simultaneously.
Glutamate is NT.
AMPA & Ca++ enter NMDA receptors.

Front 12

What happens to DNA w/LTP?

Back 12

new DNA is made.
Hippocampal neurogenesis.

Front 13

Discuss new neurons in the adult brain. x3

Back 13

1. ~1000 neurons formed in dentate gyrus of hippocampus & subventricular zone daily.
2. up to 50% die.
3. May play role in forming temporal associations among memories.

Front 14

Briefly discuss attachment theory.

Back 14

attachment produces affect-laden neural templates; experiences are organized into working models of self/others.

Front 15

What determines who we are & how we view the world?

Back 15

genetic makeup + experiences involving learning & memory

Front 16

Discuss working memory.

Back 16

moment-to-moment awareness & instant retrieval of archived information
"blackboard of the mind"
prefrontal cortex

Front 17

What can promote learning & memory?

Back 17

1. intellectual stimulation
2. maternal behavior
(increase strength & # of hippocampal neurons; increase brain weight)
3. sleep consolidates memory
4. oxytocin plays central role in social bonding & maternal behavior, but also facilitates positive social memories.

Front 18

Discuss appetite hormones & memory.

Back 18

1. ghrelin released by stomach; stim hypothalamus -> triggers appetite
2. leptin produced by fat cells -> antidepressant & enhancement of learning/memory (fat stores depleted -> more leptin produced).
Chronic stress decreases leptin.
Leptin boosts LTP by enhancing glutamate & promoting dendritic growth in hippocampus.

Front 19

What can impede learning & memory?

Back 19

1. amygdala: no amygdala inhibits fear response -> cannot evaluate dangers
2. cortisol: stress & lack of sleep both increase cortisol, inhibits ability to learn & remember
3. excess DA leads to fragmented & disorganized thinking.
4. decreased brain-derived neurotrophic factor important in maintenance of brain; increases frontal DA

Front 20

Discuss interplay between different factors & their biological & behavioral affects.

Back 20

genetics + early adverse life events + current life stress
leads to...
increased CRF
leads to...
ANS activation, depression, anxiety

Front 21

How can the amygdala system of memory affect what happens in the present?

Back 21

something bad happens to a person, don't remember it, but can still have strong feelings about it.
olfactory system is well-connected.

Front 22

Discuss the effects of psychological trauma.

Back 22

1. high levels of NE consolidate emotional memories faster & last longer w/greater likelihood of PTSD.
2. treat w/beta blockers w/in 6 hrs & for 10 days to lessen memories.

Front 23

What role do BG contribute to learning?

Back 23

reward & punishment behavior: DA plays a role in learning/memory & reinforces behavior.

Front 24

What is the most potent predictor of high child cortisol levels & greater psychological symptoms in first grade?

Back 24

maternal depression beginning in infancy

Front 25

Discuss MAOA levels and behavior.

Back 25

low MAOA + abuse ->
antisocial behavior
increased conduct disorders
violent crimes
rape, robbery, assault

Front 26

Discuss abuse & the left brain.

Back 26

abused have:
12% smaller hippocampus
reduced corpus callosum
increased ACTH & cortisol

Front 27

Discuss early adverse events & their affects on the brain.

Back 27

neglect:
increased ACTH & CRF
anhedonia
decreased eating
decreased sleeping
decreased reproduction
increased restless activity
increased withdrawal

Front 28

What is connectomics?

Back 28

imperfect bridge from brain to mind
cellular interactions between brain areas
neural plasticity depenent on intracellular changes, gene transcription, & neurotrophic factors

Front 29

What are Kandel's Principles of Psychiatry's Intellectual Framework?

Back 29

1. All mental processes derive from the brain
2. Genes contribute to the control of behavior
3. Behavior can alter gene expression
4. Learning-based alterations in gene expression alter neuronal connectivity
5. Psychotherapy is effective & produces long-term changes in behavior through learning

Front 30

Contrast REM & NREM.

Back 30

REM NREM
EEG fast, mixed slow
HR variable slow
BP variable low
Resp fast slow
Muscle tone low high

REM is a highly active brain in a paralyzed body.
NREM is an idling brain in a moveable body.

Front 31

How is the REM-NREM cycle controlled?

Back 31

reciprocal action of cholinergic & noradrenergic neurons in pontine reticulum; oscillate out of phase with each other.

REM: high ACh, NE & 5-HT low

Front 32

Which sleep disorders are most commonly seen in primary care?

Back 32

1. breathing-related/sleep apnea
2. periodic limb movements/ nocturnal myoclonus classified as dyssomnia not otherwise specified

Front 33

What are the clinical features of obstructive sleep apnea?

Back 33

1. snoring
2. daytime sleepiness
3. headache, dry throat upon wakening
4. physical findings:
-obesity (BMI>30)
-neck circumference (M>43cm; F>37cm)
-high palate, enlarged tonsils
-HTN
*associated w/greatest morbidity & mortality

Front 34

What are the demographics of sleep apnea?

Back 34

M:F 2-3:1
prevalence increases w/age
under 25yo, more common in African American males than white males
overall U.S. prevalence:
4%M, 2%F

Front 35

Discuss the physiology of sleep apnea.

Back 35

1. Relaxation of muscles in airway; negative inspiratory pressure can collapse airway.
2. Obstruction leads to drop in oxygen saturation.
3. Body increases respiratory effort (more collapse)
4. Increase pulmonary blood flow, increasing BP.
5. Briefly wake, breathe, & fall back to sleep w/o knowing awake.

Front 36

What are some consequences of sleep apnea?

Back 36

repeated episode of sleep apnea -> pulmonary HTN ->
R heart failure OR systemic HTN -> stroke OR CV disease.

The more hypoxic, the greater risk of HTN.

Front 37

Discuss treatment of obstructive sleep apnea.

Back 37

1. surgery or prosthesis: limited usefulness
2. lower pressure gradient by nasal CPAP (continuous positive airway pressure)

Front 38

What is Nocturnal Myoclonus (periodic limb movement disorder (PLMD))?

Back 38

muscle twitches every 20-40s
usually anterior tibialis
periods 4-5 min to hours
15% also have RLS
*but 80% RLS pts have PLMD

Front 39

Discuss treatment of PLMD.

Back 39

*benzodiazepines (raise wakening threshold, doesn't reduce mevements)
*DA agents [ropinorole] may reduce twitches.

Front 40

What is the classic diagnostic tetrad of narcolepsy?

Back 40

Excessive daytime sleepiness:
1. sleep attacks [may progress to full REM sleep]
2. cataplexy - brief, almost imperceptible weakness of isolated muscle groups
3. sleep paralysis - inability to move during sleep onset or wakening [awake but cannot move]
4. hynogogic [sleep onset] or hyponopompic [sleep emergence] hallucinations

Front 41

Discuss narcolepsy & REM latency.

Back 41

REM latency decreased: REM onset w/in 10 minutes of falling asleep, sometimes immediate.
Normal REM latency is 60-90 min.

Front 42

Discuss prevalence & treatment of narcolepsy.

Back 42

0.02-0.09% population
onset b/w 15-25yrs.
1. methylphenidate
2. amphetamine
3. pemoline
4. modafinil
*agents that promote or mimic NE (except modafinil)
5. also sleep hygiene

Front 43

Discuss the pathophysiology of narcolepsy.

Back 43

Probably related to NE system of braintem sleep centers: pontine reticular activating system.
Alpha NE & 5-HT stimulation normally inhibits REM.
Narcoleptics seem to lack this normal REM inhibition.

Front 44

What are physical medical disorders that cause insomnia?

Back 44

1. pain
2. cardiorespiratory disorders (CHF, COPD)
3. GI disorders
4. GU (nocturia, esp. old age)

Front 45

What are neuropsychiatric conditions that cause insomnia?

Back 45

1. Anxiety -sleep onset insomnia
2. Depression
-mid-night wakening
-early morning wakening
-reduced REM latency

Front 46

What are treatments of self-contained depression (sleep pattern resembling anxiety)?

Back 46

short term benzodiazepines or other sedative hypnotics

Front 47

What are treatments for major depression w/sleep disorders?

Back 47

antidepressant should improve sleep - no need for hypnotics

Front 48

How does alcohol affect sleep?

Back 48

-reduces sleep latency
-suppresses REM, especially early in night
-interferes w/slow-wave sleep
-fatigued & irritable upon awakening

Front 49

Of what does the clinical evaluation of the sleepless patient consist?

Back 49

1. sleep history - interview bed partner [if negative for secondary insomnia, ask about sleep-wake habits, sleep schedule, napping, diet & eating schedule, caffeine, meds, alcohol, exercise, activity]
2. ROS to exclude other psychiatric disorders
3. PE
4. labs, X-rays, EEG
5. clinical polysomnography

Front 50

What are non-pharmacologic ways to manage insomnia?

Back 50

1. no etOH w/in 4 hrs of bed
2. no caffeine w/in 6 hrs of bed
3. no heavy meals w/in 3 hrs of bed
4. moderate regular exercise during daytime
5. use bed only for sex & sleep
6. establish bedtime routine
7. relaxation techniques

Front 51

What are the effects of classic benzodiazepines?

Back 51

1. induce sleep BUT suppress REM
2. relieve anxiety
3. anticonvulsant properties
4. muscle-relaxant properties

Front 52

What are the 3 receptor subtypes & drugs that target them?

Back 52

1. BZ-1: responsible for sleep induction
-zaleplon
-zolpidem
-eszopiclone
2. BZ-2: site for anxiolysis, confusion, dependence
3. BZ-3: probably anticonvulsant & muscle relaxant site

Front 53

Discuss melatonin & sleep.

Back 53

-serum levels reduced in insomnia
-improves sleep onset, duration, & quality
-OTC
-long term effects unknown
-Ramelteon (Rozerem) binds to MT-1 & MT-2 melatonin receptors; leaves sleep architecture intact.
-needs more study

Front 54

Discuss pharmacologic treatment of insomnia (see textbook questions).

Back 54

Alprazolam
Lorazepam
Temazepam
Triazolam

Front 55

What determines a person's sexual identity?

Back 55

1. anatomic sex
2. gender identity (self)
3. gender role (public)
4. orientation (toward male, female)
5. intention/sex print (sexual preferences, erotic script)

Front 56

What determines sexual desire?

Back 56

The fluctuating interest a person experiences about behaving sexually:
1. drive (biological)
2. motive (psychological)
3. wish (social)

Front 57

General concepts about sexual history taking?

Back 57

1. basic interviewing techniques: open-ended questions, body language, good listener
2. use language the patient understands
3. "physician has the sanction of society to ask ... extremely personal questions."

Front 58

Typical age at onset of psychosexual disorders?

Back 58

Typically early adulthood (late 20s/early 30s).
Premature ejaculation more commonly begins w/first sexual encounters.
Male Erectile Disorder may begin later in adult life.

Front 59

(1)Typical course, (2)impairments, & (3) prevalence of psychosexual disorders?

Back 59

1. Extremely variable course; may be lifelong or acquired; single episode or recurrent.
2. Impairment of relationship with sexual partner.
3. exact prevalence unknown; common, especially in milder forms

Front 60

Differential diagnosis of sexual dysfunction?

Back 60

1. Sexual dysfunction due to a general medical condition.
2. Substance-induced sexual dysfunction.
3. Sexual dysfunction due to combined factors.

Front 61

Describe sexual drive.

Back 61

Biological component of sexual desire.
Evolves over time; decreases w/increasing age.
Diminished by many psychotropic & antihypertensive medications.
Manifested by the internally stimulated genital sensations & thoughts of sexual behavior.

Front 62

Describe sexual motivation.

Back 62

Psychological component of sexual drive.
Highly contextual in terms of relationship status.
The most socially & psychologically responsive of the 3 components.
Evolves unpredictably over time.
Manifested by a person's willingness to bring his/her body to a specific person for sexual behavior.

Front 63

Describe sexual wish.

Back 63

Social component of sexual desire.
Expectations for sexual behavior based on membership in various subcultural groups (family, religion, gender, region, nation)

Front 64

What is the difference between hypoactive sexual desire disorder & sexual aversion disorder?

Back 64

*Hypoactive sexual desire disorder: persistently or recurrently deficient/absent sexual fantasies & desire for sexual activity.
*Sexual Aversion: persistent or recurrent extreme aversion/avoidance of genital sexual contact w/sexual partner.