Physiological Psych

Question 1

Hindbrain

Answer 1

Located above spinal cord.

Includes medulla, pons, and cerebellum.

Question 2

Medulla

Answer 2

• Involuntary mouth and throat movements involved in swallowing, coughing, and sneezing.
• Regulates survival functions: respiration, heart rate, and blood pressure.
• Brain injury and certain diseases and drugs (especially opioids) can disrupt functioning/cause death.

Question 3

Pons

Answer 3

• Connects two halves of the cerebellum.
• helps coordinate movements on the two sides of the body
• relays messages between the cerebellum and cerebral cortex.
• involved in respiration and the regulation of deep sleep and rapid eye movement (REM) sleep.

Question 4

Cerebellum

Answer 4

• coordinate VOLUNTARY MOVEMENTS
• Also posture and balance.
• Damage –> ataxia (lack of muscle control, impaired balance and coordination, slurred speech, nystagmus/jerky eye movements, blurred/double vision).
• Process/Store PROCEDURAL memories and other IMPLICIT memories.
• some NON-MOTOR COGNITIVE functions (e.g., attention, linguistic processing, and visuospatial abilities).

*if damage, difficulty learning new skills and performing prior ones.

Question 5

Ataxia

Answer 5

characterized by symptoms associated with alcohol intoxication (lack of muscle control, impaired balance and coordination, slurred speech, nystagmus/jerky eye movements, blurred/double vision).

Question 6

Midbrain

Answer 6

connects the hindbrain to the forebrain and includes the reticular formation and substantia nigra.

Question 7

Reticular Formation

Answer 7

• network of neurons from medulla to midbrain.
• regulation of muscle tone, coordination of eye movements, and control of pain.
• contains reticular activating system (RAS/ARAS).

Question 8

reticular activating system (RAS)

Answer 8

AKA ascending reticular activating system (ARAS).
Regulates (1) consciousness and arousal, (2) controls the sleep/wake cycle, and (3) alerts cerebral cortex to incoming sensory signals.
*Lesions = comatose state…direct electrical/sensory stimulation = awaken from sleep/cause alertness

Question 9

Substantia Nigra

Answer 9

• role in reward-seeking, drug addiction, and, through its connection to the basal ganglia, motor control.
• Degeneration of dopamine-producing cells in the substantia nigra = slowed movement, tremors, rigidity, and other motor symptoms of Parkinson’s disease.

Question 10

Subcortical Forebrain

Answer 10

include the hypothalamus, thalamus, basal ganglia, amygdala, and hippocampus.

Question 11

Hypothalamus

Answer 11

-Helps maintain BODY FUNCTIONS like temperature, blood pressure, hunger, thirst, and sleep.
-dev of secondary sex characteristics and sexual behaviors by stimulating the pituitary gland.
-involved in aggression and emotional reactions
*electrical stimulation/damage to different areas can elicit aggression or produce crying or laughter
Contains mammillary bodies, which play a role in memory, and the suprachiasmatic nucleus (SCN)/body’s biological clock

*damage to mammillary bodies = retro/anterograde amnesia

Question 12

suprachiasmatic nucleus (SCN)

Answer 12

serves as the body’s biological clock and regulates the sleep-wake cycle and other circadian rhythms (physiological changes that occur during each 24-hour period).

Question 13

Thalamus

Answer 13

• “relay station” because it receives and then transmits sensory information to the cortex for all of the senses except smell.
• plays an important role in the coordination of sensory and motor functioning, language and speech, and declarative memory.

-Damage can cause retrograde or anterograde amnesia

Question 14

Korsakoff syndrome

Answer 14

Caused by a thiamine deficiency that’s often the result of chronic alcoholism and damages neurons in the thalamus and mammillary bodies.
–symptoms are anterograde amnesia, retrograde amnesia, and confabulation, which involves filling memory gaps (especially gaps in episodic memory) with false information that the person seems to believe is true.

Question 15

Limbic System

Answer 15

Consists of several structures that are involved in emotion. It includes the amygdala, cingulate cortex, and hippocampus.

Question 16

Amygdala

Answer 16

• Emotions, recognition of fear and emotions in facial expressions, acquisition of conditioned fear responses, evaluation of the emotional significance of events, and ATTACHMENT of EMOTIONS to MEMORIES (flashbulb memories).
• hyperactivity plays role in producing distressing memories (PTSD).
• Damage = same level of recall for emotional or nonemotional experiences (should recall emotionally laden memories better).

Question 17

flashbulb memories

Answer 17

vivid and enduring memories for surprising and shocking events. Happen in amygdala.

Question 18

Kluver-Bucy syndrome

Answer 18

• induced from bilateral lesioning of the amygdala
• Symptoms include hyperphagia(increased eating, hyperorality (objects in mouth, reduced fear, hypersexuality, and visual agnosia (which is also known as psychic blindness).

Question 19

Cingulate Cortex

Answer 19

• contains cingulate gyrus and cingulate sulcus
• plays role in motivation, memory, and emotions, including emotional reactions to pain.
• damage –> experience pain but not emotionally distressed by it.
• Abnormalities in the cingulate cortex (and several other areas of the brain including the prefrontal cortex, orbitofrontal cortex, hippocampus, amygdala, and thalamus) have also been linked to major depressive disorder and bipolar disorder

Question 20

Hippocampus

Answer 20

• more in memory and < in emotions than other limbic system structures.
• declarative memories from short-term to long-term memory
• ALSO spatial memory.
• H.M. -> deficits in remote long-term episodic memory.
• damage to hippocampus and entorhinal cortex (an area adjacent to the hippocampus)–> episodic memory and spatial navigation associated with Alzheimer’s disease.
• if PTSD = small hippo

Question 21

Basil Ganglia

Answer 21

• linked to Tourette’s tics
• involved in the initiation and control of voluntary movements, PROCEDURAL memory, and habit learning, cognitive functioning (e.g., attention and decision-making), and emotions.
• consist of the caudate nucleus, putamen, nucleus accumbens, and globus pallidus

*damage=trouble learning new skills and performing prior

Question 22

Cerebral Cortex

Answer 22

Outer layer. Right and Left hemispheres. Contains 4 lobes - frontal, temporal, parietal, and occipital.

Question 23

Frontal Lobe

Answer 23

-Broca’s area, prefrontal cortex, supplementary motor cortex, premotor cortex, primary motor cortex

Question 24

Broca’s area

Answer 24

Major language area. Located in left.

-Damage produces Broca’s aphasia (aka expressive aphasia and confluent aphasia).

Question 25

Broca’s Aphasia

Answer 25

slow, labored speech that consists of primarily nouns and verbs.

• may also exhibit impaired repetition and anomia (inability to recall names of familiar objects).
• comprehension of written and spoken language is intact

Question 26

Prefrontal Cortex (PFC)

Answer 26

• EF aka higher-order cog functioning that includes:planning, decision-making, social judgment, and self-monitoring
• contributes to working memory aspect of short-term memory, prospective memory (memory for future events), attention, and emotional regulation.
• Effects of damage depend on location. Lesions impact event-based prospective (give coworker message when see her) memory more than time-based prospective (take cake out of oven in 30min) memory

Question 27

Dysexecutive syndrome

Answer 27

• Damage to the dorsolateral PFC
• involves deficits in working memory, impaired judgment and insight, lack of planning ability, perseverative responses, and disinterest and apathy.

Question 28

Disinhibited syndrome

Answer 28

• Damage to the orbitofrontal PFC
• characterized by behavioral disinhibition, distractibility, emotional lability and inappropriate euphoria, and “acquired sociopathy.”

Question 29

Apathetic-akinetic syndrome

Answer 29

• damage to the mediofrontal PFC
• involves decreased motor behavior and verbal output, a lack of initiative and motivation (abulia), and flat or diminished affect.

Question 30

Supplementary Motor Cortex

Answer 30

• involved in planning and coordinating self-initiated complex movements
• active when performing AND imagining movements AND watching another perform
• somatotopically organized (each body part controlled by specific cortical area)

-Also involved in PROCEDURAL/IMPLICIT memories. Damage =trouble learning new or performing skills

Question 31

Premotor Cortex

Answer 31

• involved in planning and coordinating complex movements triggered by external (sensory) stimuli
• Active when performing, imagining, and watching others

Question 32

Primary Motor Cortex

Answer 32

• Takes signals from supplementary motor cortex and premotor cortex
• executes movements by sending signals to the muscles
• Damage can result from muscle weakness to paralysis in the opposite (contralateral) side of the body

Question 33

Temporal Lobe

Answer 33

-Contains auditory cortex and Wernicke’s area

Question 34

Auditory Cortex

Answer 34

• Housed in temporal lobe
• involved in processing sound.
• damage could result in auditory agnosia (impairment in sound perception and ID despite intact hearing, cog functioning, and language abilities), auditory hallucinations or cortical deafness (unable to hear sounds)

Question 35

Wernicke’s area

Answer 35

-Major language area usually in dominant (left) hemisphere of the temporal lobe

Question 36

Wernicke’s Aphasia

Answer 36

-aka receptive aphasia and fluent aphasia
-impaired comprehension of written and spoken language, impaired repetition, and anomia (prob w/word finding)
-Speech is fluent but contains word subs and other errors and devoid of meaning
-

Question 37

Conduction Aphasia

Answer 37

• damage to the arcuate fasciculus (connects Broca to Wernicke)
• Intact comprehension with fluent speech but many errors, impaired repetition, and anomia

Question 38

Parietal Lobe

Answer 38

-contains somatosensory cortex

Question 39

Somatosensory Cortex

Answer 39

• Located in parietal lobe

- processes sensory info related to touch, pressure, temperature, pain, and body position

Question 40

Somatosensory Agnosias

Answer 40

• damage to parietal lobe/somatosensory cortex
• types include: tactile agnosia (can’t rec objects by touch), asomatognosia (lack of interest or rec of 1+ parts of own body), and anosognosia (denier of one’s illness)

Question 41

Hemispatial Neglect

Answer 41

• aka unilateral neglect and contralateral neglect
• caused by damage to the right (non dominant) parietal lobe
• neglect of left side of body and stimuli on left side of body

Question 42

Ideomotor Apraxia, Ideational Apraxia, and Gerstmann’s syndrome

Answer 42

• Caused by damage to the left (dominant) parietal lobe
• Ideomotor apraxia: inability to perform motor activity in response to verbal command (e.g., “pretend to comb your hair”)
• Ideational Apraxia: inability to plan and execute task that requires sequence of actions (e.g., steps to make snadwich)
• Gerstmann’s Syndrome: finger agnosia (can’t name fingers), right-left disorientation, agraphia (loss of writing skills), and acalculia (loss of math skills)

Question 43

Occipital Lobe

Answer 43

• contains visual cortex

Question 44

Visual Cortex

Answer 44

• Housed in occipital lobe
• processes visual info
• damage could result in visual agnosia (can see but cannot rec or interpret visual info), visual hallucinations, chromatopsia (loss of color vision) or cortical blindness (loss of vision w/o ophthalmological cause)

Question 45

Prosopagnosia

Answer 45

• caused by bilateral lesions in occipitoemporal junction

- inability to recognize faces of familiar people and in some cases, faces of pets and other familiar animals

Question 46

Nervous System

Answer 46

-Central Nervous System (CNS): brain & spinal cord

Peripheral Nervous System (PNS): transmits between CNS and body…includes SOMATIC and AUTOMATIC nervous systems

Question 47

Somatic Nervous System (SNS)

Answer 47

• VOLUNTARY ACTIONS
• transmits info…body sensory receptors -> CNS
• CNS -> skeletal muscles

Question 48

Automatic Nervous System (ANS)

Answer 48

• INVOLUNTARY actions…although involuntary can be controlled via biofeedback, etc.
• transmits… smooth muscles/organs CNS
• Includes:
  (1) Sympathetic Nervous System: fight or flight; prep for action (e.g., pupil dilation, sweating, increased heart/respiration, inhibit digestion, sexual activity)
  (2) Parasympathetic Nervous System: R&R; pre-emergency state.

*both active and cooperative e.g., para for erection and symp for ejaculation

Question 49

Neurons

Answer 49

• dendrites (receive info), soma (cell body, fluid inside - @rest then + when excited), and axon (release; action potential)
• Some axons have myelin (insulation) to speed conduction…

Question 50

Synaptic Transmission

Answer 50

• Begins when action potential reaches axon terminal
• neurotransmitter released into synaptic cleft
• intensity of stimulus has to do with frequency of action potentials or number of neurons engaged (all action potentials the same)
• neurotransmitters can have inhibitory or excitatory effect

Question 51

Dopamine

Answer 51

• both excitatory and inhibitory functions
• movement, personality, mood, sleep
• mesolimbic dopaminergic pathway: “reward circuit” (e.g., drugs); ventral tegmental -> ventral striatum/nucleus accumbens
• mesocortical dopaminergic pathway: emotion, motivation, EF; ventral tegmental -> PFC
• tuberoinfundibulnar dopaminergic pathway: hormone regulation (e.g., inhibition of prolactin); hypothalamus -> pituitary gland
• nigrostraital dopaminergic pathway: Purposeful movement; substantia nigra -> dorsal striatum/caudate nucleus, putamen
• low in substantia nigra=Parkinson’s
• excess in caudate nucleus=Tourette’s
• hypo in cortical, hyper in subcortical = schizo

Question 52

Acetylcholine (ACh)

Answer 52

• excitatory and inhibitory
• movement (muscles contract), arousal, attention, memory
• Myasthenia gravis (autoimmune disorder): destroys ACh receptors@neuromuscular junctions
• Low ACh in hippocampus/entorhinal cortex = early memory loss in Alzheimer’s

Question 53

Glutamate

Answer 53

• excitatory
• movement, emotions, learning, and memory
• too much =cell damage/death AKA glutamate-induced excitotoxicity
• involved in stroke, seizure disorders, neurodegenerative diseases (Huntington’s and Alzheimer’s)

Question 54

Norepinephrine

Answer 54

• Excitatory
• involved in arousal, attention, learning, memory, stress, and mood
• Per catecholamine hypothesis…
  (1) deficit = depression
  (2) excessive = mania

Question 55

Serotonin

AKA 5-hydroxytryptamine or 5-HT

Answer 55

• Inhibitory
• arousal, sleep, sex, mood, appetite, pain
• low in brain = depression, suicidality, bulimia nervosa, OCD, migraines
• high in brain = anxiety, obsessive thinking…anorexia nervosa (food restriction helps lower serotonin)
• high in blood = ASD, chronic schizo (w. enlarged cerebral ventricles/atrophy)

Question 56

Gamma-Aminobutyric Acid (GABA)

Answer 56

• inhibitory
• memory, mood, arousal, sleep, motor control

-low=insomnia, seizures, anxiety (benzodiazepines reduce anxiety and induce sleep by +GABA effects
)
-degeneration (along with ACh) in basal ganglia –> Huntington motor sx

Question 57

Endorphins

Answer 57

• inhibitory…similar effect to opioid drugs
• pleasure and well-being, analgesic effects
• acupuncture may stimulate

Question 58

Drug Effects on Neurotransmitters

Answer 58

(1) Agonists: mimic or increase effect of NP
(2) Partial agonists: produce similar but weaker effects than NP
(3) Inverse agonists: Opposite of effect of NP/agonists
(4) Antagonists: No effects but block or reduce effect of NP/agonist

Question 59

Sensation v. Perception

Answer 59

• Sensation: Process by which sensory receptors & nervous system receive & represent stimulus energies.
• Perception: Process of organizing&interpreting sensory info which allows to recognize objects&events.

*Bottom-up (data driven: begin w/incoming sensory info and continues up to brain)/Top-down (concept-driven: begins in brain’s use of knowledge/expectations to interpret incoming sensory info) Processing explain how they’re integrated.

Question 60

Vision

Answer 60

-physical stimuli are light waves absorbed by photoreceptors (light-sensitive receptors) in retina.

• 2 types of photoreceptors:
  (1) cones (work best in bright light) for visual acuity (sharpness and precise detail) and color.
  (2) rods for peripheral vision and help vision in dim light (more sensitive to light).

Question 61

Theories of Color Vision

Answer 61

Trichromatic theory: Retina contains 3 types of color receptors/cones (red, blue, green). Applies to initial retinal processing.

Opponent-process theory: 3 types of opponent-process cells (red/green, blue/yellow, white/black). Applies to beyond retina processing and explains afterimages and colorblindness.

Question 62

Color Blindness

Answer 62

• Usually bc of genetic mutation but also bc of injury/disease (e.g., diabetes, MS).
• If genetic: affect both eyes. abnormal recessive gene on X chromosome.Affects males more. red/green most common.

Question 63

Depth Perception

Answer 63

Depends on:
(1) binocular: both eyes, close objects, include retinal disparity (objects from 2 diff views..closer object = +disparity) and convergence (eyes turn inward when object close).

(2) monocular: 1 eye. Objects@farther away. Relative size, overlap/interposition, linear perspective, texture gradients, relative motion/motion parallax.

Question 64

Pain

Answer 64

-Caused by various stimuli (e.g., extreme temps, mechanical pressure, electrical stimulation) and perception moderated by emotional state and past experience.

Gate control theory:

• small unmyelinated fibers in spinal cord transmit pain to brain.
• large myelinated fibers in spinal cord transmit other sensory signals.
• pain transmission affected by incoming pain signals but closed by other sensory signals (e.g., pain relief through heat or cold, distraction techs, guided imagery, hypnosis).

Question 65

Synesthesia

Answer 65

• Sensations in 1 sensory modality trigger associated sensation in another.
• Most common is grapheme-color synesthesia (#’s or letters are associated w/specific colors).
• Genetic component…increased cross-activation and cross-connectivity between brain sensory areas.

Question 66

Psychophysics

Answer 66

Weber’s Law: just noticeable diff (JND) is constant proportion, regardless of intensity of OG stimulus. (e.g., always 2% for weight). Better for mid-range intensities.

Fechner’s Law: AKA Fechner-Weber law. Predicts logarithmic relationship btwn psychological sensation and magnitude of physical stimulus. JND grows w/ intensity. Better for extreme intensities.

Stevens’ Power Law: Most accurate. Exponential relationship btwn psychological sensation & magnitude of physical stimulus. Exponent varies for different stimuli. Based on magnitude estimation.

Question 67

Long-Term Potentiation (LTP)

Answer 67

• short-term storage of info = +neurotransmitter release, while long-term storage = dev. of new synapse and changes in neuron structure.
• Result of rapid and/or high-frequency stimulation. Plays essential role in learning and memory formation.
• Changes in synapses associated with the formation of long-term memories depends on the synthesis of RNA, which is necessary for protein synthesis (inhibiting RNA can block long-term formation).

Question 68

Sleep Function theories

Answer 68

Theories either (1) recovery/restoration or (2) adaptive/evolutionary (e.g., conserve energy)

Question 69

Stages of Sleep

Answer 69

Stage 1: Transition. low frequency, high amplitude alpha waves (drowsiness) replaced by low frequency, low amplitude theta waves
Stage 2: Theta waves w/ sleep spindles (burst of fast waves) and K-complexes (large slow waves).
Stage 3: After 20m. Low frequency, high amplitude delta waves. Slow-wave/deep sleep.
Stage 4: Delta waves w/ even higher amplitude. Slow-wave/deep sleep.
REM: After 80-90min of sleep. EEG similar to Stage 1. AKA paradoxical sleep due to active brain and physiological arousal. Most dreams and more likely to be weird. After 10 min of REM, cycle through non-REM and REM stages repeat until REM sleep increases and Stage 3/4 shorten.

Question 70

Lifespan Changes in Sleep

Answer 70

• Newborn infants sleep longer, more REM, and begin sleep w/active/REM sleep followed by quiet (non REM) sleep.
• Newborn sequence reverses @3mo.
• 4 stages of non-REM evident @6mo.
• Sleep time decreases from 14-16 to 8 hours in adulthood.
• If old, trouble w/sleep onset and maintenance, less deep sleep (Stage 4), more even REM throughout night, and advanced sleep/circadian phase advance (aka sleeping early and waking up earlier).

Question 71

Antipsychotics AKA neuroleptics: First Generation

Answer 71

First-get antipsychotics (FGAs) AKA conventional/traditional antipsychotics.
INCLUDE: chlorpromazine (Thorazine; low potency), haloperidol (Haldol; high potency), thioridazine (Mellaril; low potency), and fluphenizine (Prolixin; high potency).
Tx: Schizophrenia and other psychotic sx. Most effective for positive sx. Block dopamine receptors (D2).

Side effects:

(a) Anticholinergic. Likely w/low potency FGA. Include: dry mouth, blurred vision, urinary retention, constipation, and tachycardia (rapid heart rate).
(b) Extrapyramidal. Likely w/high potency FGAs. Include: Parkinsonism (resting tremor, muscle rigidity, slowed movement), dystonia (sp. muscle contractions), akathisia (sense of inner restlessness), TARDIVE DYSKINESIA (life threatening, after long-term drugs use, MORE COMMON IN OLDER WOMEN. Involuntary movements of tongue, face, jaw, maybe limbs and trunk. Sometimes irreversible, treated w/gradual drug withdrawal and benzodiazepine or switch to SGA.
(c) Neuroleptic malignant snydrome (NMS). Rare. Life-threatening. Includes muscle rigidity, high fever, autonomic dysfunction (sweating, unstable blood pressure, tachycardia), altered mental state (e.g., confusion, combativeness). Tx w/ stop drug and provide supportive therapy (e.g., hydration, cooling).

Question 72

Antipsychotics AKA neuroleptics: Second Generation

Answer 72

Second gen antipsychotics (SGAs) AKA atypical antipsychotics. INCLUDE: clozapine (Clozaril), risperidone (Risperdal), olanzapine (Zyprexa), quetiapine (Seroquel), and aripiprazole (Abilify).
Tx: Schizophrenia. As or more effective for pos. sx and more effective for neg. sx (compared to FGA).

SGA (like clozapine) may be used when FGA ineffective. For pos sx, block dopamine receptors (D3 and D4). For neg sx., block serotonin receptors.

SGA’s less likely to cause extrapyramidal side effects, but can cause anticholinergic, neuroleptic malignant syndrome, and metabolic syndrome.

(metabolic syndrome: weight gain, high blood pressure, insulin resistance, hyperglycemia, increase diabetes mellitus risk and heart disease risk).

Clozapine (and other SGA’s to lesser extent) can cause agranulocytosis (life threatening, low white blood count and requires monitoring).

Question 73

Serotonin Reuptake Inhibitors (SSRI’s)

Answer 73

INCLUDE: fluoxetine (Prozac, Sarafem), fluvoxamine (Luvox; may also +dopamine and norepinephrine), paroxetine (Paxil), sertraline (Zoloft), and citalopram (Celexa).

-Most frequently prescribed antidepressants; first-line pharmacological treatment for MDD and persistent depressive disorder. (some also tx premenstrual dysphoric disorder, OCD, panic disorder, GAD, PTSD, bulimia nervosa, and premature ejaculation).

Tx effects by blocking the reuptake of serotonin at nerve synapses.

SSRIs comparable to TCAs re: efficacy.
SSRIs have fewer side effects, safer in overdose (e.g., are less cardiotoxic), and safer for older adults.

Side effects: mild anticholinergic effects, gastrointestinal disturbances, insomnia, anxiety, and sexual dysfunction, and abrupt cessation of an SSRI can cause discontinuation syndrome, which involves headaches, dizziness, mood lability, impaired concentration, sleep disturbances, and flu-like symptoms.

Combo w/MAOI, lithium, or other serotonergic drug can cause (life threatening) serotonin syndrome–> extreme agitation, confusion, autonomic instability, hyperthermia, tremor, seizures, and delirium. Tx serotonin syndrome =immediate withdrawal of the serotonergic drugs and providing appropriate medical tx for sx.

*Like other antidepressants, the SSRIs have a delayed onset of therapeutic effects on depressive symptoms of about two to four weeks (Antidepressant Medication, 2017).

Question 74

Serotonin and Norepinephrine Reuptake Inhibitors (SNRI’s)

Answer 74

INCLUDES: venlafaxine (Effexor), duloxetine (Cymbalta), and desvenlafaxine (Pristiq).
Tx: MDD, social anxiety disorder, and neuropathic pain and other pain disorders.

SNRIs similar to the SSRIs in terms of efficacy
Evidence SNRI more effective for severe depression (e.g., Thronson & Pagalilauan, 2014).

Tx effects are due to inhibition of the reuptake of serotonin and norepinephrine at synapses.

The side effects of the SNRIs are similar to those of the SSRIs and, like the SSRIs, they can cause discontinuation syndrome when abruptly stopped and serotonin syndrome when combined with other serotonergic drugs.

Because of effects on norepinephrine, can elevate blood pressure…not good if have hypertension or heart problems.

Question 75

Norepinephrine Dopamine Reuptake Inhibitors (NDRI’s)

Answer 75

INCLUDES: bupropion (Wellbutrin, Zyban).
Tx: MDD and assist with smoking cessation.

Tx effects by inhibiting the reuptake of norepinephrine and dopamine at synapses.

Side effects: skin rash, decreased appetite and weight loss, agitation, insomnia, dizziness, and seizures.

Advantages: few anticholinergic effects, does not cause sexual dysfunction, and is not cardiotoxic. Note that bupropion and other antidepressants that increase levels of norepinephrine and dopamine have an energizing effect, which means they’re useful for patients who have low energy and motivation but not for those who have insomnia or are very anxious.

Question 76

Tricyclic Antidepressants (TCA’s)

Answer 76

INCLUDE: amitriptyline (Elavil; neuropathic pain), imipramine (Tofranil), clomipramine (Anafranil; for OCD), nortriptyline (Pamelor; neuropathic pain), desipramine (Norpramin), and doxepin (Sinequan).
Tx: MDD, panic disorder, OCD, and neuropathic pain.

Tx effects by inhibiting the reuptake of norepinephrine, serotonin, and dopamine at synapses.

side effects: cardiovascular effects (e.g., hypertension, tachycardia, orthostatic hypotension), anticholinergic effects, sedation, weight gain, and sexual dysfunction.

Because cardiotoxic and lethal in overdose, MUST be prescribed with caution for patients who have heart disease or are suicidal.

Question 77

Manoamine Oxidase Inhibitors (MAOI’s)

Answer 77

INCLUDE: phenelzine (Nardil), isocarboxazid (Marplan), and tranylcypromine (Parnate).
Tx: treatment-resistant depression or atypical depression, which involves reversed vegetative symptoms such as hypersomnia, increased appetite, and reactive dysphoria.

Tx effects by increasing norepinephrine, serotonin, and dopamine, by inhibiting the activity of monoamine oxidase enzyme (which deactivates these neurotransmitters).

Side effects: anticholinergic effects, orthostatic hypotension, sedation, and sexual dysfunction. Also hypertensive crisis when taken in conjunction with certain drugs (e.g., amphetamines, antihistamines) or food containing tyramine (e.g., aged cheese and meat, soy products, beer, red wine, sauerkraut, fava beans, ripe bananas).

(hypertensive crisis sx: severe throbbing headache, neck pain or stiffness, rapid heart rate, nausea and vomiting, sweating, sensitivity to light, confusion, and delirium)

Question 78

James-Lange Theory (Emotions)

Answer 78

Exposure to stimulus (growling bear) -> physiological reaction (rapid heart rate/breathing) -> perceived as an emotion (feels afraid)

I.E., EMOTION FOLLOWS PHYSIOLOGICAL AROUSAL

-Facial feedback hypothesis: mimicking facial expression associated w/specific emotion causes us to then experience that emotion (e.g., smiling is contagious/makes us feel happy)

Question 79

Cannon-Bard Theory (Emotions)

Answer 79

Emotion and Physiological Arousal occur TOGETHER.

Exposure to stimulus -> Thalamus then send signals to both cerebral cortex and sympathetic nervous system

Says: ALL EMOTIONS INVOLVE SIMILAR PHYSIOLOGICAL AROUSAL…such that, differences in emotional reactions aren’t due to differences in arousal.

Question 80

Schachter and Singer’s Two-Factor Theory (Emotions; AKA Cognitive Arousal Theory)

Answer 80

Physiological Arousal is similar for all emotions. Differences in emotions DUE TO ATTRIBUTIONS (cognitive label) FOR THE AROUSAL. DEPENDENT on EXTERNAL CUES.
MISATTRIBUTION OF AROUSAL: Mislabeling arousal when cause is unknown (epinephrine studies - look to environment for cues on how to feel)

Zillman’s (1971) EXCITATION TRANSFER THEORY: Assumes - physical arousal decays slowly and continue following event, residual arousal can intensify arousal caused by another unrelated event, people have limited insight into arousal cause and may misattribute arousal solely to SUBSEQUENT UNRELATED EVENT (e.g., watching scary movie makes you feel more sexually attracted).

Question 81

Lazarus’s Cognitive Appraisal Theory (Emotions)

Answer 81

People respond with different emotions to same events bc differences in APPRAISAL.
Unlike other theories, says PHYSIOLOGICAL AROUSAL FOLLOWS COGNITIVE APPRAISAL.

Three Types of Appraisal:

(1) Primary: Determine if irrelevant, benign-positive, or stressful. (if stressful, determines if threat, challenge, or harm/loss). Impacted by beliefs, values, motivations, etc.
(2) Secondary: If stressful, then ID coping options and effectiveness to deal w/event.
(3) Reappraisal: Monitor event and adjust primary and/or secondary appraisal accordingly.

Question 82

Brain Mechanisms of Emotions

Answer 82

Paper (1937) -> Paper Circuit involved hippocampus, mammillary bodies, thalamus, and cingulate gyrus. Now circuit thought to be more involved w/memory than emotion.

Cerebral Cortex:

• Left (dominant) hemisphere: POSITIVE EMOTIONS…damage = “catastrophic reaction”…depression, anxiety, fear, paranoia.
• Right (non dominant) hemisphere: NEGATIVE EMOTIONS…damage = “indifferent reaction”….inappropriate indifference and/or euphoria.

Amygdala: Part of limbic system. Recognize fear in facial expressions, attaching emotions to memories, eval incoming info to determine emotional significance, mediate emotional reaction. ELECTRICAL STIMULATION = fear or rage response. DAMAGE =loss of fear response w/o loss of other emotional responses.

Hypothalamus: Regulates PHYSICAL SIGNS of emotions by communicating w/autonomic nervous system and pituitary gland. DAMAGE = rage. ELECTRICAL STIMULATION = other emotions such as pleasure or fear.

Question 83

Stress

Answer 83

Selye’s GENERAL ADAPTATION SYNDROME: Stress response always the same w/

(1) initial ALARM REACTION STAGE: engages sympathetic nervous system to give body energy to respond w/ flight-or-flight.
(2) RESISTANCE STAGE: If stressor persists. Some functions return to normal but CORTISOL continues to be elevated to help body cope and provide high energy level.
(3) EXHAUSTION STAGE: If stress or effects not resolved. Physiological processes begin to break down.

McEwen’s ALLOSTATIC LOAD MODEL (stress response not always the same and depend on nature/nurture factors, etc.).

• Amygdala, hippocampus, and PFC are primary mediators in appraising stress and determining response.
• ALLOSTASIS -> body adapts to achieve stability (e.g., elevated blood pressure/cortisol may be necessary). ALLOSTATIC STATE: When body adapts (e.g., produces cortisol). Can be maintained for limited time. ALLOSTATIC LOAD: Chronic stressors don’t allow body to bounce back so maintain adaptations that cause wear and tear. ALLOSTATIC OVERLOAD: Adverse effects on physical/mental health. E.g., dysregulated immune system, PTSD, MDD, substance use disorder.
• Allostasis and consequences of extended load vary person to person.

Question 84

Cerebrovascular Accident (CVA) AKA Stroke

Answer 84

Risks: hypertension, atherosclerosis (artery hardening), heart disease, diabetes, cigs, booze, obesity, old, male, Black, and fam hx.

Ischemic/Thrombotic Stroke: Blockage in cerebral artery due to blood clot in the brain. Most common. Blockage for less than 5 min = TRANSIENT ischemic stroke (TIA), which could signal future bigger stroke.

Embolic Stroke: Cerebral artery blockage due to blood clot in heart or elsewhere.

Hemorrhagic Stroke = rupture in cerebral artery. Can be Intracerebral Hemorrhage (within brain) or Subarachnoid Hemorrhage (between brain and brain membrane).

Stroke sx by Cerebral Artery:
(a) Middle Cerebral: contralateral sensory loss/hemiparesis/hemiplegia/homonymous hemianopsia, dysarthria…AND* aphasia -> dominant hemisphere or Apraxia/contralat neglect -> non-dominant.

(b) Posterior Cerebral: Contralateral sensory loss, hemiparesis, contralat. homonymous hemianopsia (or other visual thing), dysarthria, NAUSEA & VOMITING, AND MEMORY LOSS.*
(c) Anterior Cerebral: Contralateral sensory loss/hemiparesis (leg), IMPAIRED INSIGHT/JUDGEMENT, MUTISM, APATHY, CONFUSION, and URINARY INCONTINENCE.*

Question 85

TBI

Answer 85

Open or Closed Head Injuries.

Closed head injuries:

• more damage. May lose consciousness.
• emotional, cog, bx, and physical sx when wake up.

Cog sx usually include anterograde (post-traumatic amnesia) and retrograde amnesia.

• duration of anterograde am predicts recovery/other sx.
• re: retrograde, recent long-term affected more. Most distant memories recover first.

Most recovery from TBI within 3mo and first year. May have indefinite sx.

Question 86

Motor Disorders: Huntington’s Disease

Answer 86

Cause: autosomal dominant gene. 50% change of passing on.
Brain: abnormal basal ganglia, GABA, glutamate
Sx: Onset 30-50yo. Worsen over time. AFFECTIVE SX (depression, mood swings) PRECEDE COG AND MOTOR SX.
-Cog sx=short-term memory loss, impaired concentration/judgement. Later may meet criteria for
mild or major neurocog disorder.
-Motor sx=clumsiness, fidgety, involuntary movements, facial grimacing. Later get athetosis and chorea. Then trouble speaking, swallowing.

Question 87

Motor Disorders: Parkinson’s Disease

Answer 87

Cause: Genetic and environmental. Variants of ApoE gene for increased risk.
Brain: loss of dopamine-producing cells in substantia nigra & basal ganglia (motor sx). Excessive glutamate. Degeneration of norepinephrine neurons in locus coeruleus (non-motor sx).
Sx: Prominent motor sx (tremors in hand w/pill rolling, impaired balance, muscle rigidity, bradykinesia (slowed voluntary movement). Also depression (50%)…precede motor sx in 20% of cases. Also mild/major neurocog. disorder.
Tx: no cure. L-dopa for motor sx in early stages to increase dopamine.

Question 88

Focal Onset Seizures

Answer 88

One localized area in one hemisphere and affect one side of body (may spread to other parts of brain)

Focal onset aware/partial seizures -> no loss of consciousness
Focal onset IMPAIRED/complex partial seizures –> loss of consciousness w/aura.

Temporal Lobe: Most common. Genetic, TBI, tumor/infection, cerebrovascular accidents. Stress frequent trigger.

• Aura w/strange taste or odor.
• Rising sensation in stomach, sudden fear/emotion, sense of deja vu or jamais vu.
• sweating, dilated pupils, tachycardia, autonomic sx (lip-smacking, chewing/swallowing, fidgeting, picking clothes), trouble speaking and impaired comprehension.

Frontal Lobe: 2nd most common. During sleep. Last < 30.

• kicking, rocking, bicycle pedaling, other rep movements
• abnormal body posturing, explosive screams/laughter,
• trouble sleeping with INTACT comprehension
• autonomic sx.

Parietal Lobe: tinging, numbness, pain, abnormal sensations, feelings of movement (floating), distortions in body image (body part shrunk, absent)

Occipital Lobe: Rapid eye blinking, eyelid flutter, involuntary eye movements, flashing/stationary bright lights, multi-colored circular patterns, simple visual hallucinations, partial blindness, impaired visual acuity, etc.

Question 89

Generalized Onset Seizures

Answer 89

Affect both hemispheres.
Generalized onset motor/tonic-clonic/grand mal seizures -> change in consciousness. Tonic phase = stiffening face/limbs followed by clonic phase = jerky rhythmic movements in arms and legs. May be depressed/confused/fatirgued/ no memory following seizure.

Generalized onset NON-motor/absence/petit mal seizures -> brief loss of consciousness w/ blank or absent stare (eyes may turn upward/eyelids flutter)

Question 90

Migraine Headache

Answer 90

Intense, throbbing pain (usually one side), may have nausea, vomiting, sensitivity to light or other stimuli.

Can be w/ aura (Classic Migraines) or w/o aura (Common Migraines).

Triggers: emotional stress, relax after stress, weather change, booze, certain foods, skipping meal, etc. May worsen w/ bend forward, walking, other physical activity.

Link to low level of serotonin.

Tx: nonsteriodal anti-inflammatory drugs, ergot alkaloids, SSRIs, SSRI agonists, beta blockers, biofeedback/autogenic training.

Question 91

Hypertension

Answer 91

Primary: Cause unknown. 90% of cases. Asymptomatic. Risks = obesity, tobacco, excessive salt, stress, male, older, black, fam hx.

Secondary: Secondary to other disease.

Tx: lifestyle change, diuretic, beta blocker, ACE inhibitor, biofeedback/relaxation training, etc.

Question 92

Endocrine Disorders (thyroid gland)

Answer 92

(disorders of thyroid gland most common)

Hyperthyroidism: caused by hypersecretion of thyroid hormones. Sx = increased metabolism, elevated body temp, heat intolerance, increased appetite w/weight loss, accelerated heart rate, insomnia, emotional lability, reduced attention span.

Hypothyroidism: caused by hyposecretion of hormones. Sx = decreased metabolism, reduced appetite w/weight gain, slowed heart rate, lowered body temp, cold intolerance, depression, lethargy, decreased libido, confusion, impaired concentration & memory.

Question 93

Endocrine Disorders (pituitary gland and pancreas)

Answer 93

Pituitary gland -> Antidiuretic hormone (ADH) AKA vasopressin = responsible for water excreted in urine. Low ADH = central diabetes insipidus. Sx=peeing often, extreme thirst, dehydration, constipation, weight loss, low blood pressure. (if due to kidneys, referred to as nephrogenic diabetes insipidus).

Pancreas….maintains blood glucose balance
Hypoglycemia: when too much insulin. Sx=nervousness, shaking, sweating, hunger, dizziness, irritability, confusion/disorientation, weakness, sleepiness, pallor, blurred vision, tingling/numb lips and tongue, headaches, fast/irregular heartbeat, clumsiness, seizures, loss of consciousness.
Risk: high dose of insulin, skipping meals, exercising too much, booze, hepatitis, cirrhosis of liver, adrenal/pituitary gland dis

Diabetes Mellitus;
Type 1: autoimmune disease that destroys insulin-producing cells in the pancreas. Genetic predisposition. Can be caused by viral infection, etc.
Type 2: More common. When not producing enough insulin. Risks: genetic predisposition, overweight, sedentary lifestyle, over 45 years, Native American, black, Latino.

Sx of Type 1 and 2 include: extreme hunger, thirst, frequent urination, unexplained weight loss, blurred vision, numbness/tingling in handset, frequent infections.

Question 94

Neurological Diagnostic Tests

Answer 94

EEG: electrodes on head to measure brain electrical activity. Good for dx seizures, brain injury, tumors, sleep disorders, confirming brain death. Neuropsychiatric EEG-Based Assessment Aid (NEBA) for 6-17yo dx tool for ADHD eval (theta/beta waves). Microelectrodes for single neuron activity.

Neuroimaging: Structural techniques (CT, MRI), and Functional techniques (rCBF), single photon emission computed tomography (SPECT), positron emission tomography (PET), and fMRI.

• PET and SPECT use radioactive tracers injected in bloodstream.
• fMRI use magnetic fields and radio waves
• fluoredeoxyglucose PET (FDG-PET) assesses glucose metabolism. Useful for Alzheimer’s differential (e.g., w/frontotemporal neurocog disorder)

*MRI preferred over CT bc produces 3D image.

Question 95

Sedatives, Hypnotics, Anxiolytics

Answer 95

Benzodiazepines:

• diazepam(Valium), alprazolam(Xanax), and lorazepam(Ativan).
• Increase GABA activity.
• Tx: anxiety, insomnia, seizures, alcohol withdrawal.
• Side effects: drowsiness/sedation, weakness, unsteadiness, impaired memory/concentration, anticholinergic effects (inhibit acetylcholine), sexual dysfunction, and disorientation/confusion (if old).
• Can have PARADOXICAL EFFECT (excitability, anxiety). Chronic use = tolerance, dependence, and withdrawal sx (rebound anxiety, depression, anorexia, delirium, seizures). Combo w/alcohol can be lethal (synergistic depressant effect).

Barbiturates:

• thiopental (Pentothal), amobarbital (Amytal), and secobarbital (Seconal)
• Increase GABA. Used as general anesthetic.
• Tx: anxiety, insomnia, seizures.
• Side effects: drowsiness, dizziness, confusion, ATAXIA, COG IMPAIRMENT, and paradoxical excitement.
• Can lead to tolerance/dependence. Withdrawal sx: seizures, delirium, death. Lethal w/alcohol.

Azapirones:

• buspirone (BuSpar)
• Tx: GAD, other anxiety
• Side effects: sissiness, dry mouth, sweating, nausea, headache.
• does not cause sedation, dependence, or tolerance

Question 96

Narcotic-Analgesics (Opioids)

Answer 96

Mimic body’s natural analgesics (endorphins/enkephalins).

Include: natural opioids (opium, morphine, heroin, codeine) and synthetic and semi-synthetic opioids (methadone, oxycodone, hydrocodone, fentanyl).

Use: pre-surgery anesthetic. Tx pain. METHADONE for heroin detoxification (reduces craving and withdrawal w/o pleasure effect).
Side effects: dry mouth, nausea, pupil constriction, postural hypotension, drowsiness, dizziness, constipation, respiratory depression.
OVERDOSE = convulsions, coma, death.
Can lead to dependence/tolerance and withdrawal sx (similar to flu but also insomnia, abdominal cramps, vomiting, diarrhea, rapid heartbeat, high blood pressure).

DRUG OVERDOSE (OPIOIDS MOST FREQUENT) IS LEADING CAUSE OF ACCIDENTAL DEATHS IN US.

Question 97

Beta-Blockers

Answer 97

Inhibit sympathetic nervous system activity.
Include: Propranolol (Inderal).
Tx: hypertension, cardiac arrhythmia, migraine, essential tremor. ALSO anxiety (but just somatic sx and not psychological).
Side effects: hypotension, tremors, headaches, confusion, cardiac arrhythmia

Question 98

Mood Stabilizers

Answer 98

Lithium: (Eskalith, Lithobid). First line for acute mania/classic bipolar (euphoric mania w/o rapid cycling). Side effects: nausea, vomiting, diarrhea, metallic taste, thirst, weight gain, hand tremor, fatigue, impaired memory/concentration. Needs monitoring to avoid lithium toxicity (results in seizures, coma, death).

Anticonvulsant Drugs: (carbamazepine/Tegretol and valproic acid/Depankene). For acute mania and bipolar w/mixed episodes. Sid effects: nausea, dizziness, sleepiness, lethargy, ataxia, tremor, visual disturbance, impaired concentration. Monitor for liver failure and to avoid agrunlocytosis (low white blood cells) and aplastic anemia (for carbamazepin

Question 99

Drugs for Alzheimer’s

Answer 99

Cholinesterase inhibitors: Delay breakdown of acetylcholine. All approved for mild/moderate Alzheimer’s. Include tacrine (Cognex, no longer bc risk for liver failure, etc.), donepezil (Aricept, also approved for severe cases), rivastigmine (Exelon), and galantamine (Razadyne).

NMDA receptor antagonist: Regulates activity of glutamate. Includes memantine (Namenda)

Question 100

Psychostimulants

Answer 100

Include: methylphenidate (Ritalin, Concerta), premoline (Cylert), and amphetamine-dextroamphetamine (Adderall).
-Increase attention, reduce hyperactivity/impulsivity. Unclear how they impact academics when sole tx.

How? Increase dopamine and norepinephrine in prefrontal cortex.
Side effects: insomnia, nervousness, decreased appetite, weight loss, abdominal pain. May also suppress growth but reversed w/drug holidays.

-College students: evidence increase attention/pos mood but not reading comprehension/fluency and may have neg effect on working memory/academic performance

Question 101

Other Drugs for ADHD

Answer 101

Prescribed when stimulants don’t work or unable to tolerate side effects.

Include:
atomoxetine (Strattera): Norepinephrine re-uptake inhibitor. Most common. Better for pts w/ADHD and tic, sleep, anxiety, or depression.
guanfacine (Intuniv) and clonidine (Kapvay): alpha-2-adrenergic agonists. OG for high blood pressure. Good when pt also has Tourette’s/tic disorder.

Antidepressants -> 3rd line of tx. Include tricyclic (desipramine/Norpramin) and NDRI (buproprion/Wellbutrin) which increase brain levels of dopamine/ norepinephrine

Question 102

Drugs for Alcohol Use Disorder

Answer 102

disulfiram (Antabuse): Tx alcoholism by causing unpleasant sx w/ alcohol consumption. Causes nausea and vomiting, shortness of breath, tachycardia, a throbbing headache, dizziness, etc.

naltrexone (ReVia): opioid antagonists. reduces the pleasurable effects of and cravings for alcohol.

acamprosate (Campral): opioid antagonists. Just reduces cravings.

Question 103

Other Psychopharm Terms

Answer 103

Drug Half-Life: Many drugs have longer half-life for older adults due to age-related changes in metabolism, etc. (e.g., long half life benzodiazepines eliminated in 24hrs may take 72 hours in older pops). Ideal to start low and increase.

Drug Tolerance: repeated drug use = gradual reduction in effect, which requires titration.
Cross-Tolerance: when tolerance for one drug = tolerance to other drug in same class. E.g., tolerance to alcohol = tolerance to benzodiazepines and barbiturates (all central nervous system depressants).

Therapeutic Index (TI): Measures drug safety.

• for animals, divide LethalDose50 by EffectiveDose50 (LD50/ED50).
• LD50=minimum drug dose w/lethal effect in 50%. Low LD50= MORE LETHAL.
• ED50=effectiveness/minimum drug dose for therapeutic effect in 50%.

-in HUMANS…TD50/ED50 (TD50 = minimum dose w/toxic effect in 50%).

• **When ED50 is same or higher than LD50 or TD50, TI = 1.0 or less which means NARROW THERAPEUTIC WINDOW
• dose for therapeutic effect is equal to or higher than dose for lethal/toxic effect.
• HOWEVER, when ED50 is LOWER…TI is larger than 1.0 and drug has WIDE THERAPEUTIC WINDOW. More desirable bc safer; dose for desired effect is LOWER than dose that’s lethal/toxic.