Psychiatry Flashcards
Term that describes a fluctuating mood
labile
what is the term for a normal, tranquil mental state or mood.
euthymia
term for loss of enjoyment in life
Anhedonia
what is the definition of a delusion
fixed, false belief that is not understandable within the persons sociocultural setting
What test do you use to assess someones cognition
MoCA
What are hallucinations
Abnormalities of our perception. common features of neurological and psychiatric disorders. External object represented by sensory percept and brain combines memory and experience to produce a meaningful internal percept
What are the different types of perceptual abnormalities
Altered perceptions: sensory distortions and illusions, distorted internal perception of a REAL object
False Perceptions: hallucinations and pseudo hallucinations where there is internal perception without external object
What are the four modalities of hallucinations
- Visual hallucinations
- Auditory hallucinations (can be 1st, 2nd, 3rd person or command)
- Gustatory or olfactory hallucinations
- Tactile hallucinations
what is the difference between hallucinations and pseudo hallucinations
hallucinations: you really believe its there
pseudo-hallucinations: see something but know its not real
What is delirium
organic cerebral syndrome: disturbs consciousness, attention, perception, thinking, memory, emotion, sleep-wake schedule everything
is a psychiatric ,infestation of a physical illness
What causes delirium and what are the risk factors
Risk Factors: infection, environment change, medication, alcholo withdrawal, surgery, pain, stroke, low Na+, depression, advanced age, dementia, immobility, sensory impairment, urinary catheter, malnutrition
Have a critical illness which increases cortisol, starts a systemic inflammatory response and thus causes cerebral hypoxia especially in older patients whose brain is more vulnerable. This causes less ACh synthesis and dysfunction of hippocampal and neocortical areas leading to delirium. Get insanely high dopamine and adrenergic output
How is delirium managed
anticipate that it will happen and modify risk factors
treat the cause.
good nursing: well lit room and familiar faces
medication : want to reduce dopamine without affecting ACh
then give it time
What is the definition of stigma
challenges faced by people with mental illness related to knowledge attitudes and behaviour of people they meet
What is post-stroke psychosis
Neuropsychiatric symptoms forllowing vascular insult to brain, usually right sidded middle cerebral artery lesions which affect frontal and temporal lobes.
causes delusions that are persecutory and Othello’s syndrome (jealousy)
usually auditory hallucinations followed by visual
How is post stroke psychosis managed
Not knows, some respond to antipsychotics but have to be careful giving antipsychotics to dementia patients as can lead to stroke
What is the general interplay between mental and physical health
long term conditions are risk factors for the developement of mental and vica versa
Can be an organic cause like hypothyroidim of cushings causing depression etc, or can be an effect of the medication like steroids, dopamine agonists leading to psychosis
What is the mortality gap
Patients suffering with severe mental illness have a reduced life expectancy compared to general population
can be due to medication affects, increased rates of smoking and alcohol, poor diet and exercise, chaotic lifestyle and low socioeconomic status
How should mental health be managed
Choose medication that minimises impact of physical health
monitor cardiometabolic factors
smokign cessation, dietary advice, drug and alcohol sevices
What factors may affect diagnosis of physical disorders in those with mental health issues
Illness behaviour
Diagnostic overshadowing: think physical symptoms are psychiatric
stigma
lack of resources/ access to services
What is psychosis
difficulty perceiving and interpreting reality
seein in bipolar, Schizoaffective disorder and schizophrenia, depression with psychotic symptoms, delusional disorder, drug induced
What are the types of symptoms psychosis with examples
- Positive Symptoms
halluncinations: perception in absence of a stimulus, any sensory moditality. within auditory can get 1st person which is a thought echo, 2nd or 3rd person, a running commentary or command hallucinations
Delusions: fixed false belief not in keeping with social/cultural norms. Have a theme such as persecutory, grandiosity, religious, nihilistic/guilt, somatic, erotomanic or passivity experiences which are 1st rank symptoms (includes thought broadcasting- others can hear ur thoughts, thought withdrawal- thoughts have been taken, thought insertion- not own thoughts) - Negative Symptoms
Alogia: paucity/pausing in speech, little speech content, slow respond
Avolition/apathy: lack of drive, lack of motivation, poor self care
Anhedonia/asociality: few close friends, few hobbies/interests, impaired social functioning
Affective flattening: unchanging facial expressions, few expressive gesture, poor eye contact, lack of vocal intonations, limited emotional - Disorganisation
Bizzare behaviour: bizarre social behaviour, clothing/appearance, shows aggression/agitation, repetitive/stereotyped behaviour
Formal Thought disorder: lack of logical connection between thoughts such as word salads, derailment, flight of ideas, tangential thought, circumstantial thought
How does psychosis usually present
at any age, usually early 20’s, peaks later later in women
often crhonic and episodic
impacts education, employment, functioning and increases risk of health problems and morbidity
suicide rate higher and mortality rate higher
What symptoms precedes psychosis
Prodronal symptoms: often misdiagnosed as depression
changes in social behaviour and functioning impairments precede onset. Often have had mental disorders previously
What are the risk factors for psychosis
Genetics: Family history of schizophrenia : is highly heritable and highly polygenic (lots of genes, small risk but add up)
Environment: drug use- cannabis, birth complications, maternal infections, migrant status, socioeconomic deprivation, childhood trauma
What symptoms of psychosis might you look for in appearance and behaviour in the MSE?
Bizarre or inappropriate clothing, agitation, abnormal movements, self-neglect, self-harm injuries, facial expression range, echo phenomena like echopraxia 9repeating movements), echolalia), eye contact, if able to establish rapport, looking around the room
What symptoms of psychosis may you see in speech?
Reduced volume, reduced intonations, normal rate
Why must mood be assessed in someone with psychosis?
Other mental disorders can cause psychosis, depression often comes with schizophrenia. Schizophrenia patients are at risk of suicide
What cognitive impairments are associated with schizophrenia
dementa praecox : described as dementia of the young so :
working memory and executive function impairments
poorer educational attainment
cognitive impairments are stable over time and independent of psychotic symptoms, are difficult to treat too
What difficulties may there be when treating someone with psychosis
may have poor insight into this and thinks there is nothing wrong with them: this leads to less follow up appointments, not staying in hospital, not getting treated, impacts ability to have capacity to consent
How would schizophrenia be diagnosed
cannot diagnose on one consultation would be an acute and transient psychotic episode
have to look for heterogenity within disorder categories
observe
What antipsychotics are used to treat psychosis and how do they work?
Dopamine antagonists or partial agonists to block dopamine receptors as there is more dopamine and elevated presynaptic dopamine in the striatum which causes psychotic symptoms. Using an agonists can cause psychotic symptoms as enhances effect
Example: risperidone
What are the side effects of anti psychotics?
Extrapyramidal side effects, as reduced dopamine everywhere.
Dopamine blockade in the nigrostriatal (extrapyramidal) dopamine system (helps to maintain posture and tone).
Can lead to
- Parkinsonism : bradykinesia. Postural instability, rigidity, slow and shuffling gait : destination, lack of arm swing, pill-rolling tremor (move thumb across other fingers)
- Acute dystonic reactions : involuntary contractions of muscles
- Tardive dyskinesia : face and body make irregular movements that you can’t control
- Akathisia : cannot remain still
- Sedation
- Constipation
- Higher prolactin releases suppressing dopamine
- Dysrhythmia - long QT
- Increased appetite, weight gain and diabetes
- Agranulocytosis
- Neutropenia
What is the difference between typical and atypical antipsychotics?
Typical have an increased risk of extrapyramidal side effects, atypical are less likely to cause
How should psychosis be managed?
Lowest therapeutic dose of atypical antipsychotics, change the medication, anticholinergic medications may help. Counsel patients about risks
Should follow up, usually have episodic courses with periods of wellness and relapse, could recover completely. Keep managing the side effect and use health promotion to try to stop smoking and fix diet,
What treatment options are there for someone who as been experiencing psychosis
Pharmacological: antipsychotic medications
Psychological: CBT for psychosis, avatar therapy
Social support: supportive environments, housing benefits, budgeting and employment support
What are the two disease classification books
US manual: DSM
WHO manual: ICD
Definition for mood disorders
change in mood to depression or elation activity level usually changes with it, usually recurrent and related to stressful events
What is the criteria for depressive episode
2 weeks or more of depressed mood
4 of the following: appetite change, sleep change, anhedonia, less concentration, low energy, guilt, agitation/retardation, suicidal thoughts.
What is the criteria for major depressive disorder
depressive episode but no manic or hypomanic episodes cave 3 subtypes:
- atypical features: inc sleep and appetite with heightened mood
- melancholic features: no mood reactivity with marked psychomotor retardation and anhedonia
- psychotic features : delusions and halllucinations
Describe the cycle of low mood
Thoughts, Feelings, Physiological symptoms, Behaviours all changed to negative
How are manic and hypomanic episodes diagnosed
For one week with fucntional impairment
euphoric or irritable mood, 3/7 of following: decreased need for sleep with increased energy, distractibility, gradnsiosity/inflated self esteem, racing thoughts, increased talkativeness, increased goal directed activities, impulse behaviour = MANIC
4 days with symptoms, without functional impairment = HYPOMANIC
Difference between type 1 bipolar, type II bipolar and unspecified bipolar disorder and cyclothymia diagnosis
Bipolar I: manic and hypomanic episodes (one week with functional impairment) usually starts with hypomaniac/depressive first episode
Bipolar II= four days with no functional impairment, no manic episodes only hypomanic with at least one major depressive episode
Cyclothymia: swings in mood but not enough to meet thresholds
^ these three cycle more than four times per year
Unspecified bipolar disorder= symptoms for less than four days , thresholds for manic or hypomanic episodes not met
How can manic episodes be characterised
manic will have hallucinations, hospitalisation or psychotic features that affect daily life, hypomanic will not
What is the difference in heritability and insight between bipolar disorder and depression
Bipolar highly heriditary, depression not
Insight preserved in depression, impaired in mania (will deny any mania= more hypomanic or manic they are the more they will deny)
why can insight cause misdiagnosis in bipolar disorder and why is this important
Will deny as lack insight so easy to miss diagnosis, if dignose with MDD and give antidepressants then may trigger and episode and worsen the long term course
What biases are seen in patients with depression
Attention biases: typical of anxiety more. but maintaining/shifting attention bias in depressed people, harder to disengage from negative material, and less attention to positive material.
Memory biases: recall negative more than positive
Perceptual biases: recognise negative/sad faces more than happy or any other
What area of the brain is affected in maintaining/shifting attention biases
Amygdala response prolonged to negative stimuli
Prefrontal cortex: anterior cingulate cortex mediates attentional biases, lateral inferior frontal cortex impairs ability to divert attention from task irrelevant negative info
What area of the brain is affected in perception bias
Amygdala response to negative stimuli is prolonged
What is the amygdalas role
perception and encoding of stimuli, exhibits a bias to detecting cues that signal threats, like fear expressions
How do different types of antidepressants work
Single Dose
Noradrenergic: recognise happy faces more
Serotinergic: recognise sad/fearful less
both increase and decrease amygdala response.
Week
Both types: less recognition of anger and feat
reduced amygdala and prefrontal cortex response to fear
How can clinical responses to antidepressants be predicted
early change in positive processing predicts later response
elevated baseline anterior cingulate cortex in tasks that probe it predict positive response
What is the proposed hypothesis for depression
Monoamine deficiency hypothesis : low 5-HT, Norepinephrine or dopamine
only indirect evidence
How would monoamine oxidase A and tryptophan hydroxylase inhibitors affect serotonin
Monoamine oxidase A: breaks dow serotonin
Trypyophan hydroxylase inhibitors : prevent serotonin synthesis
so need high monoamines and tryptophans for serotonin
What modality of imaging is most useful to investigate brain pharmacology
PET imaging : is selective, use a tracer or ligand that binds to target, it accumulates in those areas and can see where in the brain the effect took place
Compare and contrast fMRI and PET scans
fMRI: measure brain O2 and activity so less selective, less invasive
PET: selective and invasive as radioactive, expensive
How are dopamine receptors quantified
Use [11C]Raclopride which is a dopamine antagonist will bind and take up dopamine receptors, can see where the effect happens
Then use an amphetamine challenge to increase dopamine release from presynaptic
Can then see how much dopamine released in response to that dose of amphetamine
Why cant a double PET scan be used for definitive serotonin evidence
serotonin antagonists are not sensitive enough for pharmacological challenges, agonist may be used
How do psychedelics differ from SSRIs
psychedelics act on the post synaptic 5HT receptor, SSRIs work on the presynaptic reuptake receptor.
What are some examples of tryptamine psychedelics
Smoing DMT
Psilocin/Psilocybin oral
Ayahuasca oral
LSD
What are the effects, positives and risks of psychedelics
effects: blissful state, spiritual experience, deeply positive mood, mystical type experiences
is non addictive, low brain toxicity, good theraputic index
risk: anxiety, nausea, headache,
What is the potential use of psychedelics- psilocybin in medicine
increased well being, less OCD, addiction, depression and suicidality
produces a rapid, sustained response
What are the three core symptoms of depression
Low mood
Anhedonia
Low energy/anergia
Describe the biological and cognitive symptom triad of depression
Biological: sleep, appetite, libido
Cognitive: views about oneself, the world and the future
In older patients who present with low mood what differential is important to consider
Pseudodementia
What does the risk assessment include
risk to self:suicide, self harm, self care neglect
risk to others: plans to harm others, command hallucinations
risk from others: vulnerable to exploitation, risk of retaliation from others
What is the definition of a personality disorder
maladaptive patterns of behaviour, cognition and inner experience
How to differentiate between bipolar affective disorder ad borderline personality disorder
BPAD: episodic days/weeks, heritable so in families, associated with grandiosity, mood states not affected by environment, hallucinations
BPD: mood changes over hours/days, poor self image, fear of abandonment, self harm, trauma/disrupted attachment
Both will have mood swings, unstable interpersonal relationships, impulsive sexual behaviour and suicidality
How to differentiate between BPAD and schizophrenia
BPAD: episodic delusions/hallucinations
Schizophrenia: chronic hallucinations
both have hallucinations, cognitive impairment, depression and negative symptoms
What is the difference between schioaffective disorder and schizophrenia
Schizoaffective: more of a mood component get bipolar mood swings with a psychotic aspect
Schizophrenia : hallucinations and delusions (all the psychosis)
How is BPAD and ADHD/attention deficit hyperactivity disorder differentiated
BPAD: not always in childhood, episodic, family history, depressive episodes, amphetamines worse
both: hyperactivity, impulsivity, concentration impaired, executive function impaired, abnormal working and short term memory
What disorders are usually comorbid with bipolar disorder
Anxiety disorder
Substance use disorder
What organic causes of depression are possible
Endocrine
Systemic: HIV, cancer, infections, lupus
Deficiencies in B12 or folic acid
Neurological: MS, Azheimers
Medications
Vascular Depression: late life depression, white matter hyperintensities : more vulnerable to stressors, should treat vascular risk factors like diabetes, hypertension, addictions
Poststroke depression: retardation in thinking and behaviour, lesion in left frontal lobe or basal ganglia, more frontal the more severe
Give some examples of why a person may use a drug, categorise into positive reinforcement, negative reinforcement and other
Positive: gain a positive state: escapism, feel high, stay awake, enjoy it
Negative: overcome a bad state: boredom, to get to sleep, stop anxiety, feel better
Other: to try, rebel, why not
How does ICD-10 define harmful substance use
Damage to the health of the user without diagnosis of dependence syndrome : e.g get chest infections from smoking
What is the difference between hazardous use and harmful use
Hazardous : Likely to cause harm
Harmful: already caused harm
Define Dependence Syndrome
3/6 of following:
- strong desire to take
- difficult in controlling substance intake
- get withdrawal state
- has tolerance
- neglects alternative interests
- persist despite evidence of harmful concequences
What is the difference between addiction and dependence
Addiction/ dependence syndrome: compulsive drug use despite harm, cant stop using, cant keep up with family, work or life, have tolerance and withdrawal
Dependence : the physical adaptation - only the tolerance
What are the elements involved in brain addiction
Pre-existing vulnerabilities like Fx and Age, leads to neuroadaptations to maintain brain function after exposure to the drug, results in cycles of remission and relapse
How does alcohol alter the brain system in
1) Acutely
2) Chronically with alcohol in system
3) Chronically without alcohol
Alters the balance between GABA-A (GABA-benzodiazepine) the inhibitory system and the Glutamate/excitatory NMDA receptors.
Acutely: boosts GABA-benzodiazepine cou[pling so get anxiolysis and sedation. blocks the NMDA excitatory system so get impaired memory
Chronic: reduced the sensitivity of GABA-A receptor system so the brain can walk and talk despite the alcohol, it changes the subunits. Also upregulates the excitatory system so alcohol cant switch ever NMDA receptor off (dont blackout).
Chronic use without alcohol: still have upregulation of excitatory system due to the neuroadaptation. NMDA is a calcium channel so more floods inside as no alcohol switching of any causing hyperexcitability : seizures and cell death. GABA-A function also still reduced so, effect of the inc NMDA receptor is even more pronounced
What medication boosts GABA function
Benodiazepines: reduces glutamate by inc GABA-A
What medication is used to help people stay away from alcohol
Acamprosate: reduced NMDA function, so less glutamate
What sites of the brain do drugs affect
Levels of dopamine
Dopaminergic projections in the brain stem to the ventral tegmental area and project to the ventral striatum and frontal cortex. The drug changed dopamine levels
Opioid system - mu especially mediate pleasurable effects
Describe the different interactions between substances of abuse and dopamine
Cocaine and Amphetamine: block dopamine reuptake
Amphetamine: stimulate dopamine release
Alcohol, Opiates, Nicotine: all indirectly increase dopamine neurone firing by alteringinhibition in ventral tegmental area.
How do levels of D2 receptors relate to addiction probability
Higher D2 receptors: reward system sufficient so inc too much more likely to feel uncomfortable
Less D2 receptors: reward system deficient so helps to feel normal
Who are more vulnerable to problematic drug use
Those with blunted brain activation in striatum, or less D2 receptors. Makes them more likely to relapse too
What brain regions are associated with
1) binge/intoxication
2) withdrawal
3) anticipation/ craving
1) thalamus: form habits in the dorsal striatum
2) Amygdala
3) Prefrontal cortex, hippocampus, ventral striatum
How does reinforcement change with the development of addicition
Intially get positive reinforcement and feels good with a big high , then when brain adapts, high isnt as much so negative reinforcement takes over as have to take it just to feel normal/homeostatic
What brain regions are associated with negative emotional states in addiciton
Reduced dopamine and mu opiod function
Dysregulation in amygdala: inc activity in kappa opioid, NA etc
How does the amygdalas response differ between drug users and alcohol users
In drug users the amygdala responds strongly to aversive images but in alcohol it doesnt
How does your body change from voluntary drug use to habitual and compulsive
Prefrontal to striatum modifies : switches the other way striatum to prefrontal. Switches from ventral striatum which is limbic or emotional to dorsal striatum (putamen) which is involved in habits.
There is also a memory role from the hippocampus to cause craving
who will have a greater prefrontal cortex/inferior frontal gyrus out of : healthy controls, abstinent alcoholics and abstinent polydrug users
Abstinent alcoholics, then control then polydrug
Greater frontal lobe response : can inhibit better
What drug is used to block heroin use in opioid addicts and to modulate reward in alcoholism
Naltrexone
Define intoxication, withdrawal state, tolerance and harmful use
Intoxication: transient syndrome due to recent substance ingestion
Withdrawal state: symptoms when drug is reduced
Tolerance: after repeated use, drug produces a decreased effect
Harmful use: pattern of substance use that is damaging to health has to have physical or mental affect, social concequences, includes binges
Instead of alcohol abuse or drug abuse what are these named
Opioid use disorder
Alcohol use disorder
How are units calculated
(%strength X ml)/1000
What is the excretion rate of alcohol
1 unit/8g alcohol per hour
Describe the absorption, pharmocodynamics and metabolism of alcohol
Absorption: max blood conc reached in 1 hour, food slows, bubbly soda increases, is hydrophilic so widely distributed
Pharmaco: enhances GABA-A transmission causing sedation and anxiolysis, stimulated dopamine release, inhibits NMDA glutamate release
Metabolism: alcohol dehydrogenase oxidises ethanol to acetylaldehyde. Acetalaldehyde dehydrogenase turns to CO2 and H2O. Liver does this.
What is illicit brew and what is it broken down into
Laced with methanol:is broken into formaldehyde and causes toxicity for retina
How should alcohol be assessed- (liver)
look for jaundice, bruising, clubbing, oedema
Wernikes encephalopathy, Korsakoffs syndrome (memory impairment)
Investiate: US of liver, bloofs, brathalyser, urine drug screen
What assessment tools are used for alcohol
CAGE: cut down, annoyed, guilty, eye-opener(need in morning)
AUDIT : score over 8 give brief advice, over 20 then refer to specialist
Describe the pattern of alcohol withdrawal
6-12hrs: Minor withdrawal symptoms : tremulousness, anxiety, nausea
12hrs- 1 day: Alcoholic hallucinosis
12-48hrs: withdrawal seizures
48-72hrs: delirium tremens: auditory and visual hallucination, confusion, hypertension, tachycardia, fever,
Describe the types of opioids
Opiates/Natural/Alkaloids: Morphine, Codiene, Thebaine
Opioid/Synthetic: Methadone, Pethidine, Tramadole
Opiod/Semi-synthetic: Hydrocodone, Hydromorphone, Oxycodone
What is the difference between opiates and opioids
Opiate : natural opioids only
Opioids: All of them
What is the name of the antagonist to the opioid receptors mu, delta and kappa
Naltrexone
What signs are seen in opiate assessment, what investigations should be done
Collapsed vein/track marks
Endocarditis
Skin abscesses
HIV/Hep
Investigate: Bloods, breathalyser, urine drug, blood cultured for endocarditis
What symptoms are seen in opiate withdrawal and what scale is used to measure
Tachycardia, sweating, restlessness, dilated pupils, bone pain,
COWS
What are symptoms of an opiate overdose
Slow/no breathing, choking, gurgling, blue lips and nails, tiny pupils, clammy/cold skin
What dugs are used for alcohol abstinance
Acamprosate (inc GABA-A), Naltrexone, Disulfiram (Inhibits acetaldehyde), Nalmefene
What medications are used for alcohol detox
Benzodiazepines : chlordiazepoxide
What drugs are used for opioid abstinence and how is a detox regime made
Methadone or Buprenoprhine
Detox: maintenance treatment
What treatment is used for benzos dependence
Diazepam, slowly reduce
What are the two types of GABA receptor
GABA-A is a postsynaptic ionotrophic receptor, Cl- travels thru
GABA-B is a presynaptic receptor that regulates release
What two medications target GABA-A and B receptors
GABA-A: Alprazolam - binds to the postsynaptic to keep the NT within the synapse, partial agonist
GABA-B: Baclofen is an agonist so inc release
Where can medications choose to target in the body
1) Enzyme targeting: MAOIs to stop serotonin breakdown, etc
2) Receptor targeting: antagonists to block receptor or agonists to mimic substrate and bind to enhance receptor
3) Reuptake site targetin : SSRI, to inc NT conc in synapse, some also enhance release like amfetamine
4) Ion targeting medicines: affects sodium channels : block to stop Ap passing down in epilepsy. Or slowing Ca2+ uptake to block Nt release
What are the fast and slow neurotransmitters
FAST: glutamate is excitatory in pyramidal cells, GABA is inhibitory : for memory and movement
SLOW/Modulators: dopamine, serotonin, noradrenaline: emotions, drives
Describe what disorders are usually associated with imbalances of : glutamate, GABA, 5-HT, Dopamine, NA, ACh
Glutamate excess= epilepsy and alcoholism
GABA- deficiency : anxiety
5HT deficiency: depression
Dopamine excess: Psychosis
NA excess: Nightmares
ACh deficiency: dementia
Why are partial agonists used
Lower effect than full agonists :used in overdose.
In high NT or agonist medication can be an antagonist.
Has a plateau unlike full agonist or antagonist e.g too much dopamine can cause psychosis and too little depression etc
What are inverse agonists
Opposite effect to agonist but not an antagonist. They dont block but work in the opposite way e.g. if alcohol has turned on GABA-A then use inverse agonist to reverse effect
What is allosteric modulation
Drugs bind to allosteric receptor and alter the channel.
e.g GABA binds to GABA receptor to inhibit neurones, benzodiazepines acts on allosteric sites to enhance GABA action
What is another term for the active site
orthosteric site
