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Module 4 - Coggle Diagram

- - - - reverse approach relies on identifying the genotype first, then the symptoms that come from this
      - forward approach relies on identifying symptoms, then classifying the schizophrenia based on the groups that share that trait
  - - - heritable features that co-segregate with the disease, and can occur in healthy siblings. These traits are also state dependent, occurring in patient in remission and resistant to drugs
        
        examples include: smooth eye tracking, P50 sensory gating, prepulse inhibition, sustained attention, and working memory
        
        lists of endophenotypes for negative symptoms exists as well, such as reward perception and social communication
        
        no major endophenotype traits exist yet for positive symptoms
  - - - studies here normally fall into two categories, environmental factors or medication causes
        
        environmental focuses on attempting to cause schizophrenia through environmental factors
        
        medication induces symptoms of schizophrenia, although it is only temporary, which makes this difficult to validate, as real schizophrenia is chronic
  - - - the overlap between genetic and environmental factors is ever increasing, making independent approaches to understanding it less useful
  - - - medicine is tested in clinical trials next with schizophrenia to determine if the medication has the intended effect
        
        common issues are false positives or negatives
        
        after testing is finished and gold standard is established, new medicines are able to be used
  - - - instead classified as disorder of connectivity
  - - - recent studies have identified over 40 subtypes of schizophrenia
  - - - negative symptoms; reduction of traits, like apathy
      - cognitive defects
      - positive symptoms; adding traits, like hallucinations
      - usually diagnosed between 18-30
      - two most important environmental periods are perinatal and prepubescent
- - - - patients with depressive issues were shown to have more inflammatory cytokines in their body
    - - humoral pathway- cytokines find leaky spots in the barrier
      - neural pathway- cytokines bind afferent nerve fibers, causing ascending fibers
      - cellular pathway- trafficking of immune cells
    - - cytokines produce reactive oxygen and nitrogen, which reduces the availability of tetrahydrobiopterin, which is used to create monoamines
        
        cytokines enzyme indolamine metabolized tryptophan (used for serotonin) into kynurenine
        
        as tryptophan decreases, depressive symptoms increase
  - - - infusion of BDNF causes more serotonin axons to produde
  - - - prolonged cortisol exposure can cause negative effects on the neurons in the hippocampus, such as reducing dendrite branching and inhibiting neurogenesis
        
        reduced hippocampal volume can cause decreased hippocampal function, exacerbating the negative effects of cortisol even more
      - patients with depressive disorders showed an altered cortisol circadian rhythm
    - - dopamine producers will begin producing less dopamine
  - - - this was discovered for three reasons
        
        second reason was during a study involving Reserpine, an antihypertensive drug, participants showed a decrease in overall mood
        
        third reason was that the same patients who took Reserpine and developed depressive symptoms were given Imipramine, which was able to reverse the depressive symptoms
        
        first FDA approved antidepressant
        
        first reason was that patients with tuberculosis that were treated with monoamine oxidase inhibitor showed improved mood
        
        tuberculosis patients showed euphoria, psycho-stimulation, increased appetite, and improved sleep
        
        when the medicine was used outside of tuberculosis, about 70% of patients saw an improvement with their depression
      - Tryptophan, an amino acid, is used in the synthesis of serotonin. Lacking this is shown to cause depressive symptoms
        
        not all antidepressant medicines that target serotonin f the symptoms, showing that serotonin is not the only factor that causes depression
      - depletion of dopamine and norepinephrine (catecholamines) show similar affects to depletion of serotonin
        
        patients with Parkinson's are more likely to develop depression due to the lack of dopamine
    - - an example would be norepinephrine transporters with polymorphism can be a genetic risk towards depression
    - - has negative side effects of cognitive and memory impairment, schizotypal symptoms, and neurotoxicity
      - showed antidepressant affects after hours, compared to weeks like normal antidepressants
      - hypothesized to work by rapidly increasing neuroplasticity
- - - - largest danger with relapsing is that prior to stopping, a tolerance against the drug has been built, resulting in more amounts taken. When people relapse, they tend to take the amount they did before, but they no longer have that tolerance and overdose
  - - - second stage is the withdrawal and negative effect stage, when the person begins to become irritable for example, when without the substance for a period
        
        final stage is preoccupation and anticipation stage, when the person without drugs after a period begin to think about the drugs incessantly
        
        stages are cyclical. leading back into each other in a loop
    - - compulsivity is defined as repeatedly using the drugs even when aware of the negative effects
  - - - drug abuse can cause or worsen cardiovascular issues, increase chance of stroke. or cause respiratory depression
    - - drug abusers have higher rates of hepatitis B and C, as well as HIV
        
        can increase risks of different types of cancers
  - - - depressants- cause a state of relaxation
        
        other- drugs that can create combinations of these classes
      - hallucinogens- alter perception of reality
      - stimulants- increase energy, cause highs
  - - - treatment revolves around learning to manage drug desires, not remove the desires
    - - treatment from there involves medical intervention and/or behavioral interventions