504 final Flashcards

1
Q

How do drug effects differ from drug actions?

A

Drug actions is the molecular interaction of a drug while the drug effect is the observable physiological changes

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2
Q

What are the four phases of pharmacokinetics? Describe each phase.

A

Absorption – brings drug into circulation
Metabolism – converts drug into one or more other products, metabolites
Distribution – reversible transfer of a drug from one location to another within the body
Excretion – process where a drug is eliminated from the body

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3
Q

What is a dose-effect curve? What is drug tolerance and drug sensitization?

A

Dose effect curve is a curve that shows the magnitude of a drug effect by dose
Drug tolerance refers to decreased effectiveness of drug therefore leading to more administration
Drug sensitization refers to increased effectiveness of drug with repeated administration

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4
Q

Describe each of the ways a drug can alter neurotransmission.

A

Synthesis of a neurotransmitter, storage of a neurotransmission, synaptic release of a neurotransmission, enzymatic breakdown of a neurotransmitter, and reuptake of a neurotransmitter

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5
Q

What does binding affinity mean in the context of drug-receptor interactions?

A

Binding affinity is a drug’s strength of binding to a receptor

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6
Q

What are the differences between agonists and antagonists?

A

Agonist: drug binds to receptor and activate receptor
Antagonist: drug binds to receptor and does not activate receptor

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7
Q

What do the schedule numbers refer to for controlled substances in the U.S.?

A

Refers based on the usefulness and risk of abuse; 1 = high abuse, no medical usefulness, 5 = relatively lower abuse potential, has medical uses

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8
Q

How does the DSM-V define Substance Use Disorder, and what are key features of use disorders?

A

“cluster of cognitive, behavioral, and physiological symptoms indicating that the individual continues using the substance despite significant substance related problems”
Features: powerful drive to use substance, continued use partly to ward off withdrawal symptoms, stimuli and situation associated with drug use become rewarding and command attention, stress enhances frequency and amount of use

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9
Q

Describe how structures of the brain are affected during drug addiction.

A

Intoxication: acute drug effects produce maladaptive and impaired state; reward circuitry
Withdrawal: repeated drug use results in physical or psychological withdrawal effects for both; amygdala, hypothalamus, and ANS
Preoccupation and anticipation: behavior orients from seeking natural reinforcers to seeking drug reinforcers; prefrontal cortex, amygdala, thalamus, and hippocampus

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10
Q

In what similar ways to amphetamine and cocaine produce enhanced dopamine levels.

A

They both increase dopamine levels by effecting the vesicles

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11
Q

In which structure do psychostimulants, as well as many other recreational substances, increase dopamine levels?

A

Nucleus accumbens

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12
Q

What effects do psychostimulants have on psychomotor activity and the sympathetic nervous system?

A

Sympathetic nervous system: increases heart rate, constricts blood vessels, inhibits digestion, relaxes airways
Psychomotor activities: increases activities

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13
Q

How do amphetamines, cocaine, and methylphenidate affect dopamine in the brain?

A

They inhibit dopamine reuptake causing more to be released

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14
Q

What receptor actions by alcohol lead to depressive effects?

A

Activation of GABA causes inhibitory receptor actions

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15
Q

How do benzodiazepines act on GABA receptors? What structures are linked to the actions of benzodiazepines and how do these actions account for the effects of benzodiazepines?

A

Positively modulates GABA
Bind to their own receptors

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16
Q

Does alcohol “kill brain cells?” Does recover occur after abstaining from alcohol use?

A

No it does not kill brain cells, shrinks them
Yes but individual differences can occur

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17
Q

Describe the subjective effects associated with opioid use and the phases of an opioid “high.”

A

Phase 1: Rush, rapid onset of euphoria
Phase 2: High, positive feelings
Phase 3: Nod, reduced anxiety, might include light sleep
Phase 4: straight, period of normalcy

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18
Q

What is beta-endorphin?

A

Naturally occurring hormone produced in the brain that helps manage pain

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19
Q

What is naloxone, and how is it used in opioid overdose situations?

A

Naloxone is an Opioid antagonist, given during overdose to stabilize breathing

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20
Q

How do THC and cannabidiol (CBD) interact with cannabinoid receptors (CB1 and CB2)? What brain structures do cannabinoids act on in the brain (CB1 receptors) and how does this account for the effects of cannabis?

A

THC acts as partial agonists to CB1 and CB2. CB1 receptors located in basal ganglia, nucleus accumbens, substatia nigra, cerebellum, and hippocampus

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21
Q

What is the evidence for cannabis use increasing the risk of schizophrenia?

A

Heavy use and age of use

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22
Q

What are the main categories of psychedelics?

A

Cholinergics, entactogens, serotonergics, glutaminergics, and opioid kappa receptor agonists

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23
Q

How does LSD act on serotonin receptors? Which receptor is key for visual hallucinations?

A

Acts as an agonist
5-HT2A receptor is key for visual hallucinations

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24
Q

What is “ego-dissolution,” for psychedelics?

A

They lose their sense of self

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25
Q

What are the two primary effects of MDMA on neurotransmitter systems?

A

Inhibits serotonin and dopamine storage in vesicles
Reverse direction of 5-HT and dopamine reuptake transporters

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26
Q

How might ketamine disrupt long-term potentiation? On the otherhand, how might ketamine lead to increased dendritic spine growth?

A

Decreased power of alpha and theta waves, increased gamma waves, reduced depressive symptoms

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27
Q

What types of neurotransmitter balances occur in depression? Is serotonin deficiency linked to depression?

A

There is a lack of support for role of serotonin deficiency
Balances of serotonin, norepinephrine, and dopamine

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28
Q

What is the glucocorticoid theory of depression, and what may this condition lead to?

A

Abnormal activation of HPA and excess cortisol are crucial for MDD
May lead to major depressive disorder

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29
Q

What is the neurotrophic theory of depression?

A

Reduced expression of neurotrophins occurs in depression

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30
Q

What are the primary types of antidepressants, and what neurotransmitter systems do they target?

A

Elevate serotonin levels, increase dopamine transmission
MAO inhibitors, tricyclic antidepressant drugs, SSRI, SNRI, Atypical antidepressant drugs

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31
Q

What are the side effects associated with serotonin reuptake inhibitors, as presented in lecture?

A

Affective blunting and alexithymia
Serotonin syndrome
Serotonin discontinuation syndrome

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32
Q

What neurobiological changes are associated with bipolar disorder?

A

Abnormal signaling between amygdala and cingulate cortex

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33
Q

What is the role of lithium in treating bipolar disorder, and what are its major treatment limitations?

A

enters neuron, interferes with second messengers, neuroprotective effects against neurodegeneration
Major limitation is the adverse side effects, renal failure and nausea etc.

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34
Q

What types of other drug treatments are used for bipolar disorder?

A

Mood stabilizers, antipsychotic + antidepressant, anticonvulsant + antidepressant

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35
Q

How does dysregulation of the HPA axis contribute to PTSD symptoms?

A

PTSD causes dysregulation by compromising negative feed back system which is caused by cortisol activating sympathetic nervous pathways

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36
Q

What changes in neurotransmitter levels are seen in PTSD?

A

Increased norepinephrine, decreased serotonin, decrease GABA and increased glutamate

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37
Q

Describe the pathway for corticotropin-releasing hormone and adrenocorticotropin for the HPA axis and creating a stress response.

A

Hypothalamus secretes CRH during stress, which binds to receptors on pituitary cells
Pituitary cells produce/release ACTH
ACTH circulates to the adrenal gland where adrenal hormones such as cortisol are produced/released
Cortisol activates sympathetic nervous pathways and generates negative feedback to both the hypothalamus and the anterior pituitary

38
Q

Be able to describe three neurotransmitter changes in PTSD. What neuroanatomical changes occur in PTSD?

A

Neuroanatomical: reduced volume and activity in hippocampus; increased activity in amygdala, reduced prefrontal and anterior cingulate cortex volume

39
Q

Describe the function of the cortico-striato-thalamo-cortical (CSTC) circuit and how this may be dysregulated in obsessive-compulsive disorder.

A

Important for reward and motivation related processes, executive function, motor and response inhibition, can cause either or decrease cortical excitation with thalamus
Overactivity of this pathway to thalamus associated with OCD

40
Q

For reducing anxiety, how does a benzodiazepine’s effects differ from a beta blocker’s effects?

A

beta blockers do not impair cognitive performance, benzos do impair cognitive performance

41
Q

Describe the general outcomes of MDMA treatment for PTSD.

A

Reduced resistance to discussing causative events, enhanced insight on negative emotions

42
Q

Describe the cortical axonal organization and hippocampal cellular organization in schizophrenia.

A

Reduced volume and white matter

43
Q

In what regions of the brain may dopamine levels be altered in schizophrenia?

A

Prefrontal cortex

44
Q

Name four examples of physiological features of emotions.

A

Heart rate changes, cutaneous blood flow, piloerection, gastrointestinal mobility

45
Q

How are the following structures involved in reward?

A

Lateral hypothalamus – motivates/regulates feeding, motivates/regulates drinking, enhances wakefulness
Amygdala – associates stimuli with reward
Frontal cortex – integration of sensory information with reward; assesses value of reward
Nucleus accumbens – mediates emotion response to reward; motivational aspects of reward

46
Q

What is the role of the amygdala in fear and anxiety? Compare the information shared to the amygdala via the short loop versus the long loop

A

The amygdala is the main structure processing fear and anxiety related stimuli. Information processed in the short loop processed fast while the long loop is the slow path to information processing

47
Q

What is the role of the hippocampus in emotion?

A

The hippocampus mediates integration of information from memory into cognition for emotional processing

48
Q

What is the role of the anterior cingulate cortex in emotion?

A

Integrates emotional and cognitive information, emotional conflict resolution

49
Q

What is the role of the prefrontal cortex in emotion?

A

Prefrontal cortex: involved in cognitive reappraisal and regulation of emotional responses facilitating top-down control over emotions

50
Q

Regarding lateralization, describe the “right-hemispheric dominance hypothesis” and the “valence hypothesis.”

A

Right-hemispheric dominance hypothesis: All emotions are processed in the right hemisphere
Valence hypothesis: left hemisphere dominance for positive stimuli and right for negative stimuli

51
Q

How do higher levels of CO2 affect inhalation? What psychological effect can this cause?

A

CO2 changes firing rate due to activation of chemoceptors. Can cause psychological effects such anxiety and panic attacks

52
Q

How does damage to the 1) ventromedial region of the hypothalamus and 2) lateral region of the hypothalamus affect eating?

A

Damage to ventromedial: causes more eating than normal
Damage to lateral region: causes less eating than normal

53
Q

How do GLP-1 agonists lower body weight?

A

Increases metabolism and insulation excretion

54
Q

How does osmotic thirst differ from hypovolemic thirst?

A

Osmotic thirst increases when salts and minerals in blood increase (eating salty food)
Hypovolemic thirst occurs when volume of extracellular fluid decreases (losing water and electrolytes during exercise)

55
Q

What is the approximate length of time that sensory memory is maintained? Where does sensory memory reside?

A

Maintained 1-2 secs but up to 10 sec. Resides in cortical areas specialized for processing sensory modalities

56
Q

About how long does it take for visual information to reach to the prefrontal cortex?

A

About 370 ms

57
Q

To present a concept about memory processes and memory testing, describe a delayed non-match to position task and how state the timing of drug treatment can be used to assess encoding, consolidation, or retrieval

A

Behavior test used to study memory processes, includes encoding, consolidation, and retrieval
Giving the drug at different times can show how the drug might be affecting the different stages depending on when it is given

58
Q

What cortical structure is critical for working memory?

A

The prefrontal cortex, dopamine levels

59
Q

What structures of the brain are important for declarative memory?

A

Entorhinal cortex
Hippocampus

60
Q

What structure of the brain is critical for trained movements?

A

Basal ganglia

61
Q

What are the features of the dentate gyrus that make it important for memory formation?

A

Neurons from the entorhinal cortex???
What features or types of memory are mediated by the mammillary nuclei?
Recollective memory, behavioral reactions to memory

62
Q

Describe the process of long-term potentiation regarding NMDA receptors and AMPA receptors.

A

Synapses become stronger through the coordinated activation of NMDA receptors, allowing calcium influx into the postsynaptic neuron, leading to the increased sensitivity of AMPA receptors, ultimately enhancing synaptic transmission

63
Q

What is a reflex?

A

An unlearned functional relation between a specific type of stimulus and a specific type of response

64
Q

What is kinesis? What are the symptoms of tardive dyskinesia?

A

Kinesis is an unlearned functional relation between a stimulus condition and the speed of movement. Symptoms include uncontrollable and repetitive movements of the face and body.

65
Q

What does the term “taxis” mean? What does “thigmotaxis” mean?

A

Taxis means an unlearned functional relation between a stimulus and movement toward or away from the stimulus. Thigmotaxis is the motion or orientation of an organism in response to a touch stimulus

66
Q

What is a fixed action pattern?

A

An unlearned sequence of responses that once started, continues to occur regardless of the effects of separate responses on the environment

67
Q

What is a central pattern generator?

A

They are neuronal circuits that when activated can produce rhythmic motor patterns such as walking, breathing, flying, and swimming

68
Q

Compare and contrast smooth and striated muscle fibers.

A

Smooth muscle is used for involuntary movements, autonomic nervous system. Striated muscle, voluntary control

69
Q

Describe a neuromuscular junction. What neurotransmitter is released from motor neurons? How does the size of a motor neuron relate to muscle fiber type?

A

Neuromuscular junction is the area where the motor neuron connects to muscle fibers releasing Ach-causing muscles to contract, motor neuron size correlates with type of muscle fiber

70
Q

Name the role for the following frontal lobe areas for movement:

A

Prefrontal cortex – integration of sensory information, planning movement
Premotor cortex – preparation of movements, external stimuli guide behavior
Supplementary cortex – Sequences of movements and coordinating bilateral movements
Motor cortex – Execution of voluntary movements

71
Q

When generally to mirror neurons become activated?

A

Become activated when another neuron makes specific movements

72
Q

What is the role of the corticospinal tract in motor signaling?

A

Caries signals from primary motor cortex to muscles in the limbs and trunks

73
Q

What is the role of the basal ganglia in movement?

A

Plays a role in determining the amplitude and direction of movement

74
Q

Describe the symptoms of Parkinson’s Disease. What is the neuropathology behind PD?

A

Bradykinesia (loss of voluntary motor activity), rigidity, tremors.
Neuropathology: caused by abnormal connections, loss of 70-80% of dopamine neurons in substantia nigra (MPTP converted to MPP+ - a neurotoxin that destroy DA neurons)

75
Q

What are the symptoms of Huntington’s Disease? What is the cause of this disease?

A

Symptoms: jerky arm movements, facial twitch, late tremors, chorea
Cause: Genetic

76
Q

What are the symptoms of amyotrophic lateral sclerosis?

A

Lou Gehrig disease
Atrophy, muscle weakness, paralysis

77
Q

What characteristics might differ in intersex individuals?

A

Differences might be for chromosomes, genitals, reproductive organs, secondary sex traits, hormonal patterns, hormone production, and hormone response

78
Q

How common is genital ambiguity in children born in the United States?

A

1 out of 100 children

79
Q

How can mutations in the SRY gene impact the development of male or female characteristics?

A

XY – develop female structures but ovaries are underdeveloped and not functional
XX – develop male sex characteristics

80
Q

What are the characteristics of congenital adrenal hyperplasia and androgen insensitivity in intersex individuals?

A

In congenital adrenal hyperplasia: over development of adrenal glands, elevated testosterone in females, intermediate and underdeveloped sex characteristics
Androgen insensitivity: XY chromosome may develop female genital appearance

81
Q

What is the difference between cisgender and transgender identities?

A

Cisgender matches assigned sex at birth while transgender differs from assigned sex

82
Q

At what age do children typically develop gender self-categorization?

A

Physical characteristics around age 3 and gender realization by age 6 (most of the time)

83
Q

When was homosexuality removed as a mental disorder from the DSM, and what were the contributing factors to its removal from the DSM?

A

Removed in 1973, factors were scientific research and activism, had no basis

84
Q

What is gender dysphoria?

A

“significant distress or impairment related to gender incongruence, desire to change primary or secondary sex characteristics”

85
Q

What is the purpose of gender-affirming therapy, and who can receive it?

A

Anyone can receive gender affirming care (e.x. plastic surgery)
Purpose is to affirm a patients gender orientation

86
Q

What types of gender-affirming care are available (including non-surgical and surgical interventions)?

A

Feminizing hormone therapy (estrogen), masculinizing hormone therapy (testosterone), puberty blockers, facial reconstructive surgery, top surgery, bottom surgery

87
Q

What is the sexually dimorphic nucleus, and how does its size differ across genders and orientations?

A

It is a group of cells in hypothalamus that involves sexual behavior
Larger in males compared to females, homosexual males may have smaller dimorphic nucleus

88
Q

How does the anterior hypothalamus respond to pheromones in homosexual men compared to heterosexual men and women?

A

Activates male pheromones similar between homosexual men and heterosexual women, less active in heterosexual males

89
Q

What evidence does congenital adrenal hyperplasia (CAH) provide regarding testosterone’s role in behavior?

A

Shows that early testosterone exposure contributes to male typical behaviors in girls with CAH

90
Q

What is the role of the “fruitless” (fru) gene in male fruit fly behavior?

A

males won’t display typical courtship behavior and will instead court other males