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98 Cards in this Set
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Psychoses |
A group of psychological disorders in which patients experience a loss of contact with reality. |
Loss of something |
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Schizophrenia |
A psychotic disorder which produces disturbance in reality, cognition, interpersonal relations, and mood |
What type of disorder and what does it disturb? |
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Comorbid |
Additional disease or condition which co-occurs with the primary diagnosis |
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Schizophrenia- "Positive category" |
Symptoms not experienced by non-affected individuals |
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Schizophrenia- "Negative category" |
Behavioural deficits or impairments |
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Schizophrenia- "disorganized category" |
Erratic changes in speech, motor behaviour, and emotions |
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Delusions |
Strongly held beliefs despite overwhelming evidence to the contrary. (Positive symptom) |
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Persecutory delusions |
Most common type of delusion. Belief that that the individual is being targeted, followed, harassed, and conspired against. (Positive symptom) |
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Hallucinations |
Perception in the absence of an actual sensory stimulus. Ex: hearing voices (positive symptom) |
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Apathy or avolition |
Inability or lack of desire to "get started" |
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Schizophrenia- autism |
Tendency to keep to oneself and lose interest in other people or the surroundings (negative symptom) |
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Anhedonia |
The inability to enjoy activities that are normally considered pleasurable (negative symptom) |
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Affect flattening |
Overall reduction in the range and intensity of emotional expression (negative symptom) |
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Psychotic break |
The first appearance of psychotic symptoms |
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The birth month effect |
People born in winter/early spring have a 5-8% increase risk of developing schizophrenia |
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Schizophrenia- neuroanatomical findings |
Reduction in brain weight and an enlargement of the ventricles |
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Neurodegeneration |
Process which leads to neuronal damage and/or death |
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Schizophrenia- dopamine hypothesis |
Proposes that schizophrenic symptoms are due to excess activity of dopamine |
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Cell bodies of dopaminergic neurons |
Ventral tegmental area (VTA) |
Where are they found? |
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What does activation of neuronal cell bodies in the VTA lead to? |
Leads to the release of dopamine at the cortex, hippocampus, and the nucleus accumbens |
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Schizophrenia- overstimulation of the D2 receptor leads to? |
Positive symptoms |
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Schizophrenia- under-stimulation of D1 receptors leads to? |
Negative and cognitive symptoms |
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Antipsychotic agents |
Used to treat schizophrenia |
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Conventional antipsychotics |
Improves positive symptoms by blocking the D2 receptor |
What does it improve and how? |
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Atypical antipsychotics |
Improves both the positive and negative symptoms by weakly blocking the D2 receptors as well as blocking serotonin 5-HT2 receptors |
What does it improve and how? |
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Hyperprolactinemia |
Without dopamine, cannot release prolactin. This leads to breast development and milk production. |
Side effect to antipsychotics |
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Extrapyramidal symptoms |
Continuous muscle spasms, motoric restlessness, ridgidy, tardive dyskinesia |
Antipsychotic side effect |
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Neuroleptic malignant syndrome |
Muscle stiffness, difficulty breathing, altered mental status, renal failure, fluctuations in blood pressure, tremors, dehydration, racing heartbeat, very high fever that can be fatal. |
Antipsychotic side effect |
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Resilience |
The ability to maintain psychbiological allostasis, and to adapt successfully to severe and chronic stress |
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Stress inoculation |
"Good stress" helps practice the use of active coping strategies and gain confidence |
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Cingulum |
A white matter tract within the cingulate cortex that connects the frontal lobe with the temporal lobe. This connects the reasoning circuitry with the emotional circuitry. |
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Neuropeptide Y (NPY) |
A hormone release in the brain during stress. It acts at receptors in the amygdala, prefrontal cortex, hippocampus, and brainstem to shut down the stress response by inhibiting the secretion of ACTH and norepinephrine. NPY levels are higher in those who are resilient. |
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Neurodevelopmental disorders |
A group of disorders in which the development of the CNS is impaired and whose symptoms appear during the early developmental period (before 6) |
Definition |
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Autism spectrum disorder |
Characterized by deficits in social communication, social interaction, restricted repetitive behaviours, interests, and activities |
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ASD- impairments |
Verbal communication, social communication, social cognition/imagination, lack of flexible thinking |
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The corpus callosum |
Connects the cerebellar hemispheres |
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The caudate |
Associated with motor processes |
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The amygdala |
Generates fear |
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The frontal temporal lobes |
Important for the understanding and perception of social interactions, the interpretation of facial expressions and theory of mind |
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De novo mutations |
"Glitches" in the genetic code that occur spontaneously in a sperm or egg cell and are not genetically inherited from either parent |
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Types of eating disorders |
Anorexia Nervosa (AN) Bulimia Nervosa (BN) Binge-Eating Disorder (BED) |
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Anorexia Nervosa |
Dangerous levels of weight loss that are not explainable by a particular medical condition. They show an intense fear of gaining weight. |
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Lepin |
Signal telling your body how much adipose tissue it has, as well as signals your body that you are full. Those with anorexia have very low levels of lepin. |
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Ghrelin |
Hormone that is associated with hunger. Circulating ghrelin levels are very high in patients with anorexia, because of their constant state of starvation. Individuals with AN seem to be ghrelin-resistant |
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Distorted body image |
Extremely common symptom of anorexia- Individuals insist they are fat even when they are not |
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Parietal lobe and AN |
Certain regions of the lobe seem to be involved in body image |
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Interoception |
The ability to sense/perceive the physiological condition of the body. Interoception is needed to be able to perceive/register hunger, fullness, heart rate, soreness, ect. AN patients have little to no insula and interoception |
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Homeostatic component |
Concerns eating food to maintain physical health |
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Hedonic component (pleasure) |
Concerned with eating for enjoyment, taste, and pleasure |
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Drugs |
Chemical compounds that when administered produce a physiological change in the body. They can be naturally occurring or synthetic |
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Psychoactive drugs |
Substances that act to alter mood, thought, or behaviour. Most psychoactive drugs exert their effects by influencing chemical signaling in the synapse |
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CNS Depressants |
General suppression and relaxation; tend to suppress mental functions; at low doses they may be calming, but at high doses result in intoxication leading to sedation, coma, or death. E.g. alcohol, opiates (morphine, heroin), anxiolytics (benzodiazepine, barbiturates) |
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CNS Stimulants |
Drugs that stimulate arousal; give a rapid but temporary boost of energy or clarity. E.g. amphetamine (meth, speed), cocaine, caffeine, nicotine |
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Hallucinogens |
Altered perceptual experiences; disturb ones sense of reality and cause hallucinations e.g. marijuana, LSD, MDMA (ecstasy) |
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Mesocorticolimbic dopamine system |
When rewarding stimulus is detected, dopamine neurons in the ventral tegmental area are activated. They release dopamine into the prefrontal cortex, nucleus accumbens, and hippocampus |
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Fitness and math and reading |
Specific brain regions are involved in each function: Math- PFC and intraparietal sulcus Reading- PFC and posterior cingulate cortex Aerobic exercise- the network connecting the frontal lobe and the parietal lobe |
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How is exercise good for the brain? |
Cardiovascular- increasing the blood and oxygen flow to the brain Enhance neurotransmission- increasing neurotransmitter concentrations promoting communication Enhanced neuroplasticity- increasing growth factors promoting synaptic plasticity and neurogenesis |
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Neurotransmitters |
Serotonin, dopamine, GABA, glutamate and norepinephrine |
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Vascular endothelial growth factor (VEGF) |
Promotes vascular growth |
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Brain-derived neurotrophic factor (BDNF) |
Promotes neurogenesis and axonal growth |
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Mood disorders |
Are pathological disorders characterized by pathological extremes of certain moods |
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Psychotherapy |
Cognitive behavioural therapy is most widely studied |
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Pharmacotherapy |
-Serotonin and/or Noadrenaline Reuptake Inhibitors -tricyclic antidepressants -monoamine oxidase inhibitors |
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PFC |
Responsible for complex mental tasks such as self-control and planning |
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Amygdala |
Part of the limbic system, is involved in emotional processing |
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CBT and the brain |
Depressed individuals have reduced activity of the PFC allowing the amygdala and emotions to go unchecked. CBT reverses this disparity |
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Monoamine hypothesis of depression |
Proposes that the underlying biological or neuroanatomical basis for depression is a decreased availability of noradrenaline and/or serotonin |
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Monoamine oxidase |
An enzyme which degrades monoamine neurotransmitters such as dopamine, noradrenaline, and serotonin |
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Monoamine oxidase inhibitors (depression drug treatment) |
Block the enzyme MAO from degrading neurotransmission. Leads to an increased availability of the neurotransmitters. Increases neurotransmission. |
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Neurotransmitter transporters |
Transmembrane proteins which act to transport neurotransmitters across the cell membrane |
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Reuptake inhibitors (depression drug treatment) |
Block these neurotransmitter transporters, leading to continued presence of neurotransmitters in the synaptic cleft |
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Tricyclic antidepressants |
First generation antidepressant. Block the reuptake of norepinephrine, serotonin and/or dopamine. Has been largely replaced by more specific reuptake inhibitors |
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Selective serotonin reuptake inhibitors (SSRIs) |
Specifically inhibits serotonin transporters. Increases serotonin concentrations in the synaptic cleft. I.e. fluoxetine aka Prozac |
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Norepinephrine reuptake inhibitors (NRIs) |
Specifically inhibits norepinephrine transporters. I.e. reboxetine aka vestra |
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Serotonin-Norepinephrine reuptake inhibitors |
Inhibits both serotonin transporters and norepinephrine transporters. I.e venlafaxine aka effexor |
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Neuroplasticity theory of depression |
Proposes that depression occurs as a result of decreased neuroplasticity |
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Immune hypothesis of depression |
Proposes that the immune reaction plays a causal role in the origin of depression |
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Glucocoticoid hypothesis of depression |
Proposes that dysfunctional regulation of the HPA axis in the stress response plays a key role in causing depression |
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Resistant depression- ketamine |
NMDA receptor antagonist, blocks the binding of glutamate to it's receptor. Administered at sub-anesthetic doses it has a remarkably fast onset |
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Resistant depression- electroconvulsive therapy |
Induces a controlled but generalized seizure while the patient is anesthetisized and is delivered in short bursts that are repeated over several weeks. Major side effect- memory loss |
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Transmagnetic stimulation |
Induces an electrical current in the brain using a magnetic coil placed over the scalp. |
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Broadmann area 25 |
(The subcallosal cingulate area) moderates fear and other emotions, plays a significant role in expectation, reward processing, error assessment, learning and decision making, regulates memory, regulate stress and arousal. This area is hyperactive in depressive patients. |
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Deep brain stimulation |
Following surgical implantation of electrodes, small electric pulses are applied to specific brain regions. A battery powered pacemaker is placed in the chest and stimulates the target area continuously with 130 pulses/second |
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Hypercortisolemia |
Elevated levels of cortisol in the blood, even during non-stressful times. |
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Antidepressant side effects |
Increased anxiety Sexual dysfunction Weight gain Dry mouth Blurred vision Memory impairment |
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Fear in the brain |
The amygdala is responsible for emotional and motivated behaviours. It receives input from all of the sensory systems. It outputs to the hypothalamus which in turn regulates the stress response |
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PFC and the stress response |
One of the major connections of the amygdala. Involved in the final stages of reacting to danger. It is our conscious control over anxiety |
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Neurobiology of panic |
Increased activation in the cingulate cortex and parahippocampal gyrus. The amygdala is often hypersensitive Decreased activity in the PFC Overall excessive excitatory neurotransmission may enhance anxiety |
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Treating anxiety- CBT |
Focuses on challenging the reality of patients obsessions and the behavioural necessity for their compulsions. As effective as medications in treating chronic anxiety disorder. |
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Pharmacological treatments (anxiety) |
Drugs with anti-anxiety properties are called anxiolytics. Since excessive excitatory neurotransmission is thought to enhance anxiety, most strategies seek to increase inhibitory signalling. |
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Signs of PTSD |
1) recurring and frightening memories 2) avoidance of potential triggers 3) a heightened state of arousal |
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Long term potential (LTP) |
Is the process by which synapses are strengthened in two or more neurons that fire simultaneously, or in close sequence. This makes them more likely to fire together in the future |
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Neurogenesis |
The birth of new neurons from stem cells. This process occurs in two regions within the adult mammalian brain 1) the subventricular zone (SVZ) of the lateral ventricles 2) the subgranular zone (SGZ) of the dentate gyrus of the hippocampus |
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Pattern separation |
The recording of events such that we can distinguish separate yet similar events. This occurs in the dentate gyrus |
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Pattern completion |
The ability to recall and complete a memory based on a limited set of sensory inputs. Pattern completion occurs in the CA3 |
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Obsessions |
Recurrent and persistent thoughts, urges, or images that are experienced as intrusive and unwanted |
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Compulsions |
Repetitive behaviours or mental acts aimed at preventing or reducing anxiety or distress |
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Theory of embodied cognition |
The notion that the brain maintains a dynamic relationship with the rest of the body |
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