bio Flashcards

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1
Q
  1. Stress activates two biochemical systems
A

• 1) “Fast response” by norepinephrine/epinephrine
• released via the sympathetic nervous system (SNS)
o Effects within seconds, but only lasts minutes (fast-acting & short-term)
o Prepares body for sudden burst of activity
2) “Slow response” by cortisol (the main glucocorticoid) released via the hypothalamic-pituitary-adrenal (HPA) axis
o Activated in minutes to hours and may last hours
o Prepares body for longer-lasting adaptations (occurs later & longer-lasting)
• Cortisol - Restores energy that has been expended
• Shuts down systems not immediately needed to deal with stressor
• Inhibits reproductive system
• Inhibits slow-wave sleep

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2
Q
  1. Chronic overactivity of the HPA-axis leads to the release of high levels of
A

cortisol. This in turn may (a) inhibit the immune and reproductive systems (libido, reproductive hormones); (b) cause appetite/weight gain and glucose intolerance; and (c) increase the risk for depression, anxiety, and cognitive dysfunction

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3
Q
  1. Which receptor is hypothesized to be the major central biological flaw in schizophrenia?
A

The NMDA-glutamate receptor is hypothesized to be the major central biological flaw in schizophrenia

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4
Q
  1. NMDA-R hypofunction in patients suffering from schizophrenia causes
A

(a) hypoactivity of the mesocortical pathway, resulting in cognitive, negative and affective symptoms; and (b) hyperactivity of the mesolimbic pathway, resulting in positive symptoms.

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5
Q
  1. What is the strongest predictor of real-world functioning in patients suffering from schizophrenia?
A

o Cognitive/executive symptoms/signs are the strongest predictor of real-world functioning in patients suffering form schizophrenia

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6
Q
  1. Patients suffering from schizophrenia may have difficulty
A

interpreting social cues and may have distortions in social judgment and reasoning partially because (a) their amygdalae are hyperactive when viewing neutral faces, (b) their amygdalae are hypoactive when viewing scary faces, and (c) they suffer dysconnectivity between emotion and goal-directed behavior.

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7
Q
  1. Neuroimaging and neuropsychological assessment have the potential (hopefully in the not-to-distant future) to
A

identify early, subclinical, or pre- symptomatic patients w/ schizophrenia.

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8
Q
  1. What are the different symptom profiles of major depression that are associated with abnormalities of each of the three main monoamines (5-HT, DA, NE)?
A

o Low “level” of 5-HT system is associated with increased “negative affect.”
o Dysphoria, rumination, guilt/disgust, worthlessness, loneliness, fear/anxiety, irritability, hostility, suicidality
o Particularly affects prefrontal cortex, amygdala, hypothalamus.
o Low “level” of DA system is associated with decreased “positive affect.”
o Dysphoria, anhedonia, loss of motivation & enthusiasm, apathy, anergia or psychomotor retardation, impaired attention & cognition, decreased self-confidence
o Particularly affects prefrontal cortex, nucleus accumbens, basal ganglia, hypothalamus
o Low “level” of NE system is associated with increased “negative affect” and decreased “positive affect.”

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9
Q
  1. Symptoms of fatigue, difficulty concentrating, sleep problems or psychomotor retardation/agitation may occur in someone with
A

an anxiety disorder or a mood disorder.

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10
Q
  1. A major hypothesis is that the biologic basis of bipolar symptoms may be due to
A

unstable “out-of-tune” circuits, resulting in inefficient information processing during both manic and depressive episodes.

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11
Q
  1. Mistakenly diagnosing bipolar depression as
A

being unipolar depression (i.e., major depressive disorder) is a serious mistake.

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12
Q
  1. Fear and panic attacks are associated with
A

dysfunction of circuits that involve the amygdala; and worry and obsession are associated with dysfunction of circuits that involve the cortex, basal ganglia (striatum), and thalamus.

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13
Q
  1. Numerous medical conditions can cause
A

depression, mania, or anxiety even when these affect other body systems in addition to the CNS.

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14
Q
  1. It is currently believed that all drugs of abuse and behavioral addictions cause
A

intense and phasic DA firing in the mesolimbic pathway shortly after taking the drug or engaging in the behavior and hypofunction of the mesolimbic pathway during withdrawal (DA deficit).

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15
Q
  1. Compulsive drug use is linked to
A

(a) neuroplastic changes with the DA reward circuit down-regulating (tolerance) and the compulsive (habit) circuit getting stronger, (b) craving caused by classical conditioning to associated stimuli, and (c) associative learning/conditioning.

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16
Q
  1. Associative learning/conditioning is one of the major reasons why
A

why the benefits of drug rehab programs often do not last unless there is follow-up treatment designed to offset this effect.
• Associative learning/conditioning — Drug effects & withdrawal become linked w/ cues & mood states
• A major factor in the “failure” of many in-patient drug rehab programs, unless there is sufficient follow-up treatment designed to offset this effect

17
Q
  1. Which type of neurocognitive disorder (NCD) is most associated w/ beta-amyloid (neuritic) plaques and neurofibrillary tangles in addition to impairments in declarative memory, language, and other cognitive impairments?
A
  • Alzheimers?

* The “amyloid cascade hypothesis”

18
Q
  1. NCD due to
A

frontotemporal lobar degeneration (“frontotemporal dementia”) is associated w/ primarily executive dysfunction and changes in mood and behavior.

19
Q
  1. Patients w/ Alzheimer’s disease (AD) eventually have
A

severe memory and other cognitive impairments in addition to emotional, behavioral, or perceptual abnormalities.

20
Q
  1. The “gold standard” for diagnosing AD in a living pt requires
A

a medical workup (H&P, labs, neuroimaging) and neuropsychological assessment.

21
Q

Dr. Burke clearly expressed his belief (and supported that belief with many examples)

A

that psychiatric sx’s that occur during neurological or other medical illnesses/conditions are often due to the pathology of the illnesses/conditions and not just psychological reactions to having such illnesses/conditions. However, there may also be psychological reactions superimposed on the primary sxs.

22
Q
  1. Before beginning individual psychotherapy with a client with a mood or anxiety disorder, a therapist should
A

review past medical records and recommend a current medical evaluation (unless a recent one within the last several months has already been performed).

23
Q
  1. What is the best technique/method for predicting real-world functioning after a CNS injury?
A

• Neuropsychological assessment, including being the best technique/method for predicting real-world functioning after a CNS injury

24
Q
  1. Lesions in which region of the prefrontal cortex may cause cognitive inflexibility and perseveration?
A

• Cognitive inflexibility and perseveration may occur with dysfunction of the dorsolateral prefrontal cortex (DLPFC).

25
Q
  1. Lesions in which region of the prefrontal cortex may cause significant behavioral disinhibition (e.g., angry outbursts); inappropriate social interactions with fellow employees; and decreased concern for social rules?
A

• Oribtal Prefrontal Cortex

26
Q
  1. Which period is the most critical for a woman to avoid drugs, stress, or toxins?
A

• 1st trimester

27
Q
  1. The benefits of complex environments for offspring may occur if
A

the offspring themselves were raised in complex environments or if the mothers were exposed to complex environments during pregnancy; and the benefits include larger, more adaptable brains.

28
Q
  1. ADHD patients may suffer from dysfunction of the
A

dorsal portion of the ACC, prefrontal cortex, and basal ganglia (including loops that connect these structures).

29
Q
  1. ADHD has been associated with
A

genetic factor(s) or maturational delay.

30
Q
  1. Abnormal attention and executive functioning are the usual causes of
A

the academic and interpersonal difficulties experienced by ADHD patients, not primary dysfunction of such structures as the hippocampus.

31
Q
  1. The most significant negative outcomes caused by closed-head injury (CHI) are
A

executive, emotional, personal, social, and vocational difficulties. However, they also may suffer from deficits in attention, information processing speed, and memory. Most of these are due to lesions in the frontal and temporal lobes; but damage to axons and edema may cause disconnection between areas and overall decreased efficiency.

32
Q
  1. Due to the potential severity and complexity of impairment, X is more important for patients who have suffered a CHI, compared to patients who have suffered a penetrating head injury or postconcussive syndrome with no previous head injury.
A

comprehensive neuropsychological assessment