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Psychopathology > Biological Perspectives > Flashcards

Biological Perspectives Flashcards

1
Q

Major aspects of the biological perspective of psychology

A
  • Diathesis Stress Model (Meehl, 1962; Zubin & Spring, 1977)
  • Twin Studies (Plomin et al., 1994; 2001; many others!)
  • Brain abnormalities /differences may play a role
  • Neurological testing can be done/MRIs
  • Disturbance in hormone levels may play a role which could warrant use of medication
  • Substances can exacerbate symptoms
  • Caffeine/amphetamines – anxiety
  • Alcohol – depression
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2
Q

Depression basics

A
  • twin studies: MZ twins have higher concordance rate for MDD than DZ twins
  • adoption studies: persons adopted into new familiars are more likely to experience depression if biological parent did
  • biologically: in past, monoamine hypothesis
    biologically: 5HT
  • Diathesis stress model
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3
Q

Treatment for depression

A

MAOs, TCAs, SSRIs

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4
Q

More evidence for depression in family, twin studies:

A
  • higher concordance for MZ twins (54-59) than DZ twins (13)
  • close familial relationships = higher risk for depression
  • heritability seems to be about 20-40%
  • genes seem to have some interaction with neurotransmitters as well
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5
Q

Monoamine hypothesis/ cathecholoamine hypothesis of depression

A
  • Low levels of monoamines (serotonin, norepinephrine, dopamine) are correlated with depression (Sachar and Baron, 1979)
  • SSRIs and SNRIs help reduce depression by blocking reuptake of monoamine agonists
  • Typtophan depletion suggests that low levels of serotonin cause people with personal or family history of depression to become depressed but not in otherwise healthy subjects (Delgado, 1990)
  • Respirine (for BP) which interferes with storage of monoamines in synaptic vesicles, thus reducing the amount, resulting in depression (Sachar & Baron, 1979)
  • Seems to be more than just low levels of monoamines, may be fundamental brain differences in the depressed persons brain
  • Significant improvement in depression as a result of drug therapy
  • Lower levels of serotonin in the cerebral spinal fluid of depressed individuals implies less produced in brains (Traskmann et al, 1981)
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6
Q

Cortisol and depression

A
  • high levels of cortisol is excreted during times of stress

- released by adrenal cortex above the kidney

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7
Q

Brain abnormalities in depression

A
  • Prefrontal cortex, amygdala, hippocampus, anterior cingulated cortex (Drevets et al, 1992; Soares & Mann, 1997; Davidson, Pizzagalli & Nitschke, 2002)
  • Evidence for a decreased amount of tissue in prefrontal cortex (Elkis et al, 1996)
  • Decreased volume of hippocampus (Videbeen & Ravnkilde, 2004)
  • Hippocampus and limbic system (Drevets, 2001)
  • Increased metabolic activity in orbitofrontal cortex and amygdala- areas associated with emotional processing (Drevets, 2000; Siegle et al 2002)
  • May reflect depressed persons attempt to suppress unpleasant thoughts and emotions (Siegle et al 2002)
  • Decreased activity and reduction in size of cingulate cortex during depression and increased activity there during mania (Drevets, 2000)
  • Abnormal sleep EEG in 40-60% of outpatients and 90% of inpatients
  • Few disorders have biological bases in one defined area of the brain
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8
Q

serotonin and depression

A
  • Promoter portion of 5HT transporter gene can be short or long, short alleles of this region’s transporter genes in one or both chromosomes results in less 5HT productions which makes one more likely to develop depression
  • Caps et al (2003) did a longitudinal study showing life events and the short alleles of the 5HT transporter gene interacted and caused the highest risk for depression
  • Short alleles also seem to contribute to reduction in size of the cingulate cortex, causing a malfunction in feedback loop designed to help regulate activity in the amygdala
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9
Q

Diathesis-stress model

A

genetic predisposition (diathesis) toward depression when combined with environmental stressors produces depression

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10
Q

Family studies for anxiety

A
  • twin studies for panic disorder and OCD
  • MZ twins concordance rates are 34% higher in natural vs. adoptive parents
  • higher concordance rate for MZ twins in panic disorder
  • Crowe et al (1983) found first degree relatives of anxious people with panic disorder have 17% morbidity risk as compared to 2% risk for controls, theory that this is caused by a single dominant gene
  • NIMH (1999): 6-8x greater risk for first degree relatives
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11
Q

OCD and biological perspective

A

-evidence for neurobiological deficits in OCD comes from relationship of OCD to a variety of disorders with known neurological basis in basal ganglia, high instance of OCD noticed following Tourette’s syndrome
-OCD (Carlson, 2013)- Damage to basal ganglia
Increased activity to frontal lobe
-Natural human tendencies that go overboard
-Possible that people with OCD don’t have enough serotonin (treated SSRIs)
–Riggs and Foa (1993) most prevalent neurochemical implicated is 5HT as critical in expression of symptoms
-studies have directly investigated 5HT have been inconclusive
-most of the support has come from studies of 5HT and drug efficacy (Zohler & Insel, 1987)
-5HT deficiency (Lavoie & Parent, 1990) show that 5HT agonists block reuptake and lead to improvement, 5HT antagonists worsen symptoms, 5HT has inhibitory effect on species typical behaviors thru input from 5HT terminals in the orbiofrontal cortx and basal ganglia
-typically treated with SSRIs
-first line of defense in panic disorder and OCD (APA, 1998)

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12
Q

PTSD and biological perspective

A

-Volume of hippocampus shrinks (true of all extreme, chronic stress)
Increased cortisol
-Cortisol is released when someone is stressed
-Released by adrenal cortex, above the kidney
Opposite for amygdale (gets larger)
Greater activity in amygdala when preented with pictures of threatening stimuli

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13
Q

Neurochemical abnormalities and anxiety

A
  • diminished number of benzodiazepine receptors or by secretion of a neuromodulator that blocks the benzo binding site at the GABA receptor, benzos that bind to the receptor site increase sensititivty and lead to an anxiolitic effect
  • benzos increase GABA and cause anxiolytic effects and benzo antagoinists cause anxiety (Nutt et al 1990)
  • low 5HT may play a role
  • SSRIS help reduce anxiety (Santarelli, 2003)
  • GABA seems to be implicated (Maddux & Winstead, 2008)
  • medications, like valium, act to stimulate the GABA receptors
  • GABA system (inhibitory): Decreased GABA leads to decreased firing of neurons, drug studies with benzo agonists bind to GABA-A receptors and increase sensitivity, decrease in number of receptors or secretion of a neuromodulator that blocks binding and leads to anxiety (Stahl, 2010)
  • GABA is the major inhibatory neurotransmitter (relaxes)
  • Benzodiazapines are agonists, enhances the relax person
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14
Q

Brain abnormalities and OCD

A
  • PET scans suggest that deficits in orbitofrontal cortex functioning and caudate nucleus found (Behar et al 1984) (Saxena et al 1998)
  • fMRI scans showed increased activity in orbitofrontal cortex and cingulated cortex when holding contaminated objects (Breiter et al 1996)
  • symptoms may be the result of imbalance in direct and indirect pathway from the cerebral cortex thru caudate to basal ganglia (Saxena et al 1998)
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15
Q

anxiety as fight or flight

A

basic structure of response to a threat is:

Freeze –> Flight –> Fight –> tonic immobility

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16
Q

4 response stages occur in the successive flight or fight

A
  • pre-encounter stage
  • encounter stage
  • post-encounter stage
  • tonic immobility
17
Q

Pre-encounter stage

A

the defense cascade, predators have yet to be encountered. Thus, target-specific defense behavior is not yet engaged and appetitive motivation may be simultaneously present

18
Q

encounter stage

A

a predator has been detected and the immediate response is for the prey animal to cease all movement (freeze). Additional responses during this stage include focused attention, sustained cardiac deceleration, defensive analgesia, and potentiated startle. These responses orient the animal toward potential threat and prepare it for action. Freezing also minimizes detection as many predators are highly dependent on movement for prey identification (see Gallup, 1977)

19
Q

post-encounter stage

A

Continued approach by the predator sets in motion a sequence of active defensive postures (e.g., flight or fight) that characterize the postencounter, or circa strike, stage. Here, most prey will first attempt to escape. When escape is not possible or thwarted (as indicated by tactile contact with a predator), a prey animal will subsequently fight or resist. Clear evidence that the organism has changed to a defensive posture is first seen in the startle reflex response, a response that is often potentiated during this stage, coupled with rapid acceleration in heart rate and electrodermal activity. These behavioral action tendencies are associated with the multicomponent emotional response known as fear (LeDoux, 2000)

20
Q

Tonic immobility

A

Unsuccessful escape or resistance typically results in the prey entering a state of TI. The most obvious feature of TI is profound but reversible physical immobility and muscular rigidity. This immobilized state includes a sustained and largely involuntary pattern of neuromuscular activity (i.e., cataleptic–catatonic) and sympathetic and parasympathetic responses. Additional characteristics of the response include intermittent periods of eye closure, fixed, unfocused gaze or stare, Parkinsonian-like tremors in the extremities, suppressed vocal behavior, analgesia, and waxy flexibility (Gallup, 1974a; Gallup & Rager, 1996).

21
Q

How is tonic immobility different from freezing behavior seen in the encounter stage?

A

). Early encounter stage freezing is associated with increased responsivity to stimuli, an alert posture, and volitional action tendencies (Marks, 1987), whereas TI involves a catatonic-like motionless posture and unresponsiveness

22
Q

Mania and genetic factors

A 
Twin studies (Bartleson et al., 1977)
	MZ= 74
	DZ=17
-Close relatives with the disorder leads to greater risk; First degree relatives with manic episode leads to 6-8 times greater risk (Tsuang & Falone, 1990)
-May be a single dominant gene
-Adoption Studies: 31% of bio parents and 12% of adopted parents had affective disorder (Mendlewicz & Rainier, 1977)
-Evidence for a single dominant gene on x chromosome being responsible for susceptibility (Spence et al., 1995)
23
Q

mania and brain abnormalities

A
  • 39% reduction in size of particular area medial prefrontal cortex
  • cerebellum abnormalities
24
Q

mania and biochemical explanations

A
  • Monoamine Hypothesis
  • excess of amines (NE & 5HT) occurs at critical synapses in CNS, no conclusive evidence for neuro-physio basis (Carlson 1998)
  • Drug therapy: lithium is effective in treating bipolar disorder, underlying mechanism unknown, but lithium helps with both depressed and manic episodes
25
Q

Schizophrenia and “Schizotaxia, schizotypy, and schizophrenia” (Meel, 1962)

A

-content is learned but is fundamentally a neurological disease of genetic origin
-felt that if you impose social learning history on the individual, they will socially learn the four behaviors:
cognitive slippage
anhedonia
ambivalence
interpersonal aversion
-most important causal influence was schizophrenogenic mother (Maternal ambivalence, aversion inputs to child so many are schizotypes who pass this on to their child)
-Schizotaxia is a vulnerability (Necessary condition) to express a phenotype

26
Q

schizophrena and genetics

A

-may be a multifactorial polygenetic link of chromosomes, so that once a threshold is reached, schizophrenia occurs

27
Q

schizophrenia and twin studies

A
  • corroborated that there is a heritable aspect of schizophrenia
  • reports that concordance rates have been as high as
  • 65% MZ and 14% DZ, where estimated risk in general population is 1%
  • overall, MZ=35%, DZ=7% for schizophrenia
  • MZ=58%, DZ=19% for schizotypic
  • Concordance Rates in MZ twins about 50%
  • Family studies and twin studies (Gotteman & Shield, 1982; Sweeney, Haas, & Nimgoankar, 2000)
  • higher concordance in 1st and 2nd degree relatives (overall risk 5-15% greater)
  • concordance rates for MZ at least 4 times greater (MZ: 48, DZ: 17)
28
Q

schizophrenia and adoption studies

A
  • supports the idea that the environment does play a role
  • parent with schizophrenia but child adopted into healthy environment leads to better outcomes, less chance of child developing schizophrenia
  • child with schizophrenic parents adopted into a family that is healthy has 0% chance of developing, disturbed family 38% and very disturbed 92%
29
Q

schizophrenia and diathesis-stress model

A
  • person inherits a vulnerability to schizophrenia (diathesis), interacts with the environment
  • genotype is necessary but not sufficient
  • depending on the intensity of the stress, the genes may or may not get triggered
  • interaction between nature and nurture
  • shift emphasis from role of dynamic factors in etiology to their role in facilitating and preventing the expression of schizophrenia
  • vulnerability to schizophrenia is seen as an enduring proclivity toward depressive symptoms
  • it’s a stable trait, present premorbidly, at onset, during symptoms, and in remissions
  • aspects of vulnerability are genetic, and some may be acquired biologically thru intra uterine, birth, and post natal complications
  • coping strengths or supports minimize the expression of vulnerability
  • schizophrenia is determined by nature of vulnerability and stress and by ones strengths and environmental supports
  • interaction of sufficient stress with sufficient vulnerability can lead to immediate states of dysfunction that amplify existing cognitive, affective, and social coping deficits
  • this interacts negatively with stressors and magnifies their effect in downward deterioration that culminates in full clinical symptoms
  • vulnerabilities to schizophrenia include:
  • deficits in processing complex info, maintaining attention, distinguishing between relevant and irrelevant stimuli
  • dysfunctions in physiology such as deficits in sensory inhibition and poor control over autonomic responsibilities
  • impairments in social competence, such as processing interpersonal stimuli, assertiveness, or conversational capacity
  • coping deficits such as over evaluating threats, underestimating internal resources, and excessive use of denial
30
Q

schizophrenia and neurochemical factors

A
  • eye movement studies – schizophrenics have abnormal smooth pursuit eye movements (SPEM)
  • Dopamine seems to be implicated (Maddux & Winstead, 2008)
  • D2 Dopamine receptors are more numerous in several brain areas of many but not all schizophrenics
  • underactivity in areas of the prefrontal cortex
  • progressive loss of cortical tissue thru adolescence
  • no current consensus on the cause of schizophrenia
  • seems to be a genetic predisposition
  • all studies on this topic are quickly out of date
  • schizophrenia seems to be multidetermined, because no one theory explains it fully
  • Carlson 2007 states that because concordance rate is not 100%, there must be other factors outside of heritability
31
Q

dopamine hypothesis of schizophrenia

A
  • Enlarged ventricles
  • seems to be overactivity in the mesolimbic pathway, which projects from VTA to nucleus accumbens and amygdale
  • excess DA leads to positive symptoms (doesn’t account for negative and cognitive symptoms)
  • DA agonists (amphetamines) can produce symptoms of schizophrenia
  • DA antagonists (antipsychotics) which block D2 and D4 receptors reduce symptoms
32
Q

theory of cognitive dysmetria in schizophrenia

A
  • Too much dopamine being produced
  • Ventricles are enlarged
  • The frontal lobe is too small
  • Mis-communication between the difference brain regions
  • No one knows what the miscommunication is
33
Q

brain abnormalities in schizophrenia

A
  • enlarged ventricles
  • reduced density in frontal and temporal regions
  • hypoactivity in frontal lobes so increase negative signs (poorer executive functioning)
  • hypofrontality hypothesis
  • brain damage theories
34
Q

hypofrontality hypothesis of schizophrenia

A
  • seems to be decreased activity in the frontal lobes, especially dorsolateral prefrontal cortex
  • appears to be responsible for negative symptoms
  • Schizophrenic patients show decreased activation in the prefrontal cortex when compared to controls, especially when performing tasks that require prefrontal cortex
  • hypofrontality is likely caused by lack of DA in prefrontal cortex (Carlson, 2007)
  • decrease in DA neuron activity in prefrontal cortex seems to increase DA release in nucleus accumbens (Jentsch et al., 1998), the reverse is also true, thus decrease in one can cause increase in another
  • this explains why negative symptoms are not responsive to antipsychotics because they reduce DA
  • some medications such as ariprazole serve to reduce DA in the nucleus accumbens where there is too much and increase DA in prefrontal cortex where it is needed, seems to reduce both pos and negative symptoms
35
Q

brain damage theories of schizophrenia

A
  • PET scans show decreased glucose metabolism in frontal and temporal loves which leads to information processing deficits
  • CTs and MRIs indicated that brain damage in frontal and temporal loves are associated with negative symptoms
  • Viral Infection Hypothesis (Mednick 1988, 1995)
  • exposure to virus in the 2nd trimester of pregnancy
  • High prevalence in winter months (controversial)
36
Q

Dimensional Model of schizophrenia

A 
Type I vs Type II
-type I 
	abrupt positive symptoms
	 intact intellect
	good response to meds
	related to  DA system – biochemical
-type II
	gradual onset, negative symptoms
	 predominate, chronic course, 
	intelligence impaired
	poor response to meds
	related to structural abnormalities
37
Q

treatment considerations for schizophrenia

A
  • traditionally antipsychotics have been used to treat symptoms
  • most antipsychotics are dopamine receptor blockers (Wong et al, 1986)
  • side effects of antipsychotics include tardive dyskenisia (i.e., involuntary, repetitive movements), tremors
38
Q

Individuals who possess _________ (short or long) ____________ (monoamine) transporter allele have to be more likely to experience depression.

A

Short

Serotonin

Psychopathology (12 decks)

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