Week 2 Flashcards
How is schizophrenia diagnosed?
Schizophrenia spectrum disorders, as the symptoms exists on a spectrum.
It is diagnosed using the DSM-5
It is considered a neurodevelopmental disorder - these are disorders where the nervous system is disturbed in some way.
What are some of the positive symptoms of schizophrenia?
HIDD
Hallucinations - experiencing a sensory experiences in the absence of an external stimuli. Can be of any 5 senses, auditory is most common.
Inappropriate affect - emotional response - crying from a joke
Delusions - Firmly held beliefs that are not grounded in reality. There is a greater power controlling their thoughts.
Disorganised speech/though - bizzare connections between ideas, trouble organising words into sentences others understand.
What are some of the negative symptoms of schizophrenia?
FAAAC
Flat affect - lack of emotional expression
Avolition - lack of motivation or interest in engaging in routine activities.
Alogia - poverty in speech
Anhedonia - loss of pleasure in activities previously enjoyed.
Catatonia - catatonic schizophrenia - motor abnormalities. Waxy flexibility.
DSM-5
The Diagnostic and Statistical Manual of the American Psychiatric Association .
What we currently use to match symptoms with a particular disorder to arrive at a diagnosis.
What evidence supports genetic factors in the development of schizophrenia?
Genetics play a large role in the development of schizophrenia. The more shared genetic material, the more likely schizophrenia can be developed.
Monozygotic twins
What evidence supports environmental factors in the development of schizophrenia?
Dizygotic twins - share the same amount of genetic material as siblings, but are more likely to develop schizophrenia than siblings, as they share the same prenatal environment, and are likely to share the same environment given their similarity in age.
Environmental risk factors of schizophrenia
Environment is thought to have an epigenetic effect - meaning environmental factors may turn genes off or on.
Environmental risk factors of schizophrenia
Environment is thought to have an epigenetic effect - meaning environmental factors may turn genes off or on.
- maternal stress, prenatal nutrition and prenatal infections
- Birth complications and childhood adversity
- Being born and raised in urban areas
- Exposure to toxins like marijuana or harmful alcohol use
- Highly stressful situations
Agonist
An agonist is drug that activates the receptor it binds to e.g. opium - stimulations
Creates a certain action
Produces a chemical reaction
Cocaine and amphetamines
Antagonist
A drug that binds to a receptor but does not activate it. The binding of an antagonist to a receptor can then block other substances from binding to, and activating, that receptor e.g. ip
Blocks the drug from activating
Opposes a certain action
Reduces stimulation
What is the dopamine theory of schizophrenia and how has it developed over time?
- Antipsychotic drugs had side effects that resembles Parkinson’s disease.
- Schizophrenia patients were given reserpine which had side effects that mimicked Parkinson’s
- The next discovery was that Parkinson’s is partly caused by low levels of dopamine.
- Stimulant drugs like cocaine and amphetamines, which are agonists, increase dopamine in the brain and in high doses can produce a state that closely resembles symptoms of schizophrenia.
In short, excess levels of dopamine cause schizophrenia, where as antipsychotic medication, such as reserpine reduces dopamine in the brain, subsequently reducing schizophrenia symptoms.
How has the treatment of schizophrenia developed over time?
- Indian snake root - reserpine - reduces dopamine in the brain.
- Chlorpromazine (claw-pro-ma-zeen) - didnt change the levels of dopamine in the brain. Antagonist - blocked the receptors in the brain. This changed the finding of the the dopamine theory of schizophrenia.
- Haloperidol an effective antipsychotic belonging to a group of drugs called butyrophenones
Chlorpromazine (claw-pro-ma-zeen)
Anti-psychotic Antagonist Blocks the D1 and D2 dopamine receptors From the group of drugs called phenothiazines (Feen-o-thigh-a-zeens)
Chlorpromazine (claw-pro-ma-zeen)
Anti-psychotic Antagonist Blocks the D1 and D2 dopamine receptors From the group of drugs called phenothiazines (Feen-o-thigh-a-zeens)
Haloperidol (hello-perri-doll)
Anti-psychotic Antagonist Only blocks D2 dopamine receptors From the group of drugs called butyrophenones (bu-tear-o-phen-ens)
Tardive dyskinesia
Tar-div dis-con-nee-sia
Involuntary movement within the body. Caused by antipsychotic medication. Can be irreversible. Known as extrapyramidal
Atypical antipsychotics
Second generation
Developed to improve issues associated with first generation medications
The first atypical antipsychotic to be developed - Clozapine D1, D4 and seotonin receptors
D2 D4
Glutamate and glycine
currently being studied investigating its role in schizophrenia
Monozygotic tiwns
1 egg, divides into 2
Identical Twins
Dizygotic Twins
Fraternal twins
2 separate eggs
Enlarged lateral ventricles
The larger ventricles along with the larger fissures often found in the brains of individuals suffering from schizophrenia signifies a loss in brain volume.
Loss of Brain Volume
Grey and white matter - found in pre-frontal cortex and temporal cortices, such as the hippocampus, amygdala, thalamus, anterior cingulate and nucleus accumbens.
Although brain volume reduces, the number of neurons does not, they are tightly packed together and it is believed the dendrites are compromised, the positive symptom of schizophrenia, disorganised thoughts and speech is thought to be a product of this. Dendritic branches and spines.
Aetiology
The cause of..or the history of
Polygenetic
Many genes associated with schizophrenia. ANd many of the same genes associated with major depression, autism, bipolar have also been linked to schizophrenia.
Synaptic pruning
The brains natural process of removing connections within the brain to make room for more useful connections as we get older. As seen in patients with schizophrenia , lack of connection in the brain as an increased elimination of synapses occurs.
Structural abnormalities
Synaptic pruning
Stem cells not developing into neurons or neurons migrate into irregular areas of the brain
Classic Psychedelic’s
LSD, psilocybin
Can produce symptoms similar to positive schizophrenia, such as HIDD
Agonist, bind to our serotonin receptors
Dissociative Hallucinogen (other class of psychedelics)
Ketamine and phencyclidine (fen-sick-li-dine)
Produce negative symptoms PCP of schizophrenia FAAAC
Ketamine is an antagonist, binds to our glutamate receptors and blocks them from activating
Glutamate is the excitatory neurotransmitter within a synapse, because ketamine stops this firing, we see the negative symptoms of schizophrenia.
Reactive Depression
Triggered by a negative experience
Endogenous (en-dodge-enous) Depression
Seems to begin without any trigger
Symptoms of depressions
- Sleeping too much or too little
- Feelings of worthlessness
- Excessive guilt
- Withdrawing socially
- Anhedonia
- Change in appetite
- Loss of energy - in some cases even the basic task as personal hygiene
- Negative rumination (roomie-nation) can extend to thoughts of self-harm, dead or suicide
- Anxiety
Comorbid condition
Medical conditions that co-occur with others, e.g. anxiety and depression
Monoamine Oxidase Inhibitors
Momo-aye-meen
The first anti depressants developed
Are not as popular today, as others have been created which are safer with less side effects Discovered accidentally in the 50’s when it failed to treat tuberculosis, however it left patients feeling less concerned about their illness.
- Iproniazid.
It works by inhibiting the activity of monoamine oxidase, an enzyme which breaks down monoamine neurotransmitters so there is more serotonin in the neuron.
Iproniazid (i-pre-ni-a-zid)
Monoamine Oxidase
Seasonal Affective Disorder (SAD)
Depression is linked to seasons, usually winter. Reduction in light.
Peripartum Depression
Can effect women during and after pregnancy
Tricyclic Antidepressants 3
try-sic-lick
Work by blocking reuptake of both serotonin and no-re-pi-ne-phrine (nuh-reh-puh-NEH-fruhn).
Nu-reh-puh-neh-fruhn, is a stress hormone and neurotransmitter. Try-sic-lick works to ensure there is more of this in the brain as well as serotonin.
3 rings of atoms gives it its name
Norepinephrine- Sympathetic nervous system - body prepares for fight or flight response
What are the 5 major classes of antidepressants?
MANTS
Monoamine Oxidase Inhibitors
(Momo-aye-meen)
Atypical Antidepressants
NMDA-Receptor Antagonist
Tricyclic Antidepressants 3
(try-sic-lick)
Selective Monoamine-Reuptake Inhibitors
NMDA-Receptor Antagonist
This drug is an antagonist. It works by blocking the receptor and preventing the agonist molecules from binding to it and activating it.
Includes ketamine which has undesirable side effects.
Selective Monoamine-Reuptake Inhibitors
SSRI’s - selective serotonin reuptake inhibitors.
Works by blocking the reuptake of serotonin so there is more serotonin in the neuron.
SNRI’s - Selective Norepinephrine-Reuptake Inhibitors
Atypical Antidepressants
Made up of a range of antidepressants which has a range of modes of action.
Dopamine, melatonin agonist and antagonists
Monoamine Theory of Depression
This theory is based on the evidence that depression is caused by an underactivity of serotonin and norepinephrine. Antidepressants act as an agonist to increase these neurotransmitters.
More support came from the process of up regulation. This is when the number of receptors for a neurotransmitter increase to compensate for a lack of neurotransmitter. Found during autopsies.
Many antidepressant drugs increase the levels of serotonin and norepinephrine in the brain fairly rapidly, yet the effects are only seen weeks later, suggesting that some other change is happening down stream.
Neuroplasticity Theory of Depression
The neuroplasticity theory of depression holds that depression is a result of decreased neuroplasticity processes in the brain. This leads to neuron loss and other pathology.
Depression disrupts neuroplastic processes such as neurogenesis in the hippocampus.
Antidepressants increase the neuroplastic processes in the brain, hippocampal neurogenesis.
Brain-derived neurotropic factor (BDNF) plays an important role in neuronal survival and growth and has been found in patients who have shown improvements in depression. Both drug treatment and therapies have shown to increase BDNF
Neuroplasticity
The ability of neural networks in the brain to change through growth and reorganization.
Neurogenesis
The process by which new neurons are formed in the brain
rTMS
Repetitive Transcranial Magnetic Stimulation
Electromagnetic pulses which stimulate the brain
Stimulates the nerves or nerve cells that have been deactivated or damaged.
rTMS re-creates the nerve pathways again and we call that a neuroplasticity effect
rTMS is usually applied to specific areas of the brain - usually the prefrontal cortex.
DBS
Deep brain stimulation
Electrical currents are used to target abnormal brain activity. This method triggers blood flow and a series of chemical reactions that leads to the release of neurotransmitters
These actions help to correct malfunction and connections in the brain.
Doctor surgically implant electrode on the targeted areas of ta patients brain
Bipolar disorder type II
People who experience bouts of
- depression
- hypomania
Bipolar disorder type I (2+1) = 3 symptoms
People who experience bouts of
- depression
- hypomania
- mania
Hypomania
A reduced need for sleep
High energy
Positive affect
Mania
Delusions of grandeur Overconfidence Impulsivity Distractibility Psychosis (loss of touch with reality)
Lithium
Mood stabilizer
metallic ion
Brain differences associated with bipolar
Reduction in gray matter Specific brain structures being smaller - medial pre frontal cortex - anterior cingulate - temporal gyrus - hippocampus
Anxiety
Chronic fear that persists in the absence of any direct threat
fear and worrying
When it becomes so severe that it disrupts functioning, it is referred to as an anxiety disorder
4 Anxiety disorders
General anxiety
Phobias
Agoraphobia
Panic disorder
Mood stabilizers
Without the use of mood stabilizers, the recurrence of mood episodes become more severe and more frequent if left untreated.
Many mood stabilizers are also effective in the treatment of both epilepsy and schizophrenia.
Bipolar - brain differences
Reduction in gray matter volume
Specific brain structures being smaller - medial prefrontal cortex, anterior cingulate, hippocampus
Benzodiazepines
valium/diazepam
prescribed as antidepressants, relaxants, sleep.
Addictive
Agonistic action on GABA receptors
Muscle relaxant
Serotonin Agonist
Buspirone
Serotonin receptor
It produces anxiolytic (antianxiety) effects without the common side effect of ataxia - muscle relaxation.
It does however have other common side effects of anti depressants
Tourette’s disorder
A disorder of tics
involuntary, repetitive, stereotyped movements or vocalizations.
synaptic pruning
causes increased elimination of synapses
Epigentics
Stressful or traumatic life events can change how genes are read by cells
Neurogensis
the process by which new neurons are formed in the brain
