Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PBL Notes > PBL 6 - Depression > Flashcards

PBL 6 - Depression Flashcards

1
Q

What are the Depression related changes in sleep?

A

What are the Depression related changes in sleep?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is part of the limbic system?

A
  • limbic lobe
    • Hippocampus
    • Dendate gyrus
    • Amygdaloid
    • Hypothalamus
    • Anterior thalamus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What happens in the stress response?

A

• fear/anxiety
• Vigilance, avoidance behaviour
• HPA axis activation
Pro-inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the Hippocampal formation ?

A

c shaped
• Retention of short term memory and conversion to long term declarative memory
• Long term potentiation
• Memories are believed to be located in parietal,occipital, temporal and frontal love cortex. Corpus striatum, thalamus and cerebellum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the amygdaloid body?

A

• Several nuclei situated between the anterior end of the temporal horn of the lateral ventricle and ventral surface of the lentiform nucleus
• Has a core function in the fear response and learned fear response
• Electrical stimulation causes vigilance or attention
• Ablation reduces fear and effects aggression and memory
• Sends information to:
○ Hypothalamus to produce an autonomic response
○ Periaqueductal gray matter in the brain stem for a behavioural reaction
○ Cerebral cortex for the emotional experience

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is a synapse?

A

• A chemical junction between two neurons
• Can be inhibitory or excitatory depending on:
○ The nature of the neurotransmitter
○ The type of post synaptic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the steps of synaptic transmission?

A

• Synthesis of a neurotransmitter
○ In the synaptic terminal for small molecules- amino acid and amines
○ In the neuronal body for large molecules like neuropeptide hormones
• Release of a neurotransmitter
○ Action potential triggers calcium entry
○ Synaptic vessels merge with membrane and are expelled via exocytosis
• Interaction of a neurotransmitter with a specific receptor
• Inactivation of a neurotransmitter
○ Can be degraded in the synaptic cleft by ACE
○ Can be actively taken up by the presynaptic terminal and degraded by monoamine oxidase (MAO)
○ Inactivation prevents over excitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the differences between type 1, 2 ,3 and 4 receptors?
What binds to them?

A

Type 1 : Ionotropic receptor
• Neurotransmitters bind to them
• Binding of an agonist causes na/ca and K to be pumped out/into the cell and change the polarisation of the cell

Type 2 : Metabotropic receptor (GPCR)
• Neurotransmitters bind to them
• Binding of an agonist causes activation of G Protein
• This causes generation of a second messenger and activation of cell signalling

Type 3:
• Binding of an agonist causes phosphorylation of tyrosines on key signalling molecules
• Causes activation of cell signalling
• Hormones bind to these

Type 4:
• Agonist enters cell via passive diffusion
• Transported to an intracellular nuclear receptor
• Activation of transcription and translation
• Used by Hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does MAO do?

A

It degrades the Neurotransmitter inside the nerve terminal once it has be re uptaken
• It therefore determines the availability of a transmitter in a synaptic terminal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does a reuptake transporter do? Why is it important?

A
  • It takes up the neurotransmitter from the synapse
    • It determines the time of availability of a transmitter in the synapse
    • If it is blocked the neurotransmitter will be there for longer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the inconsistencies with the old theory of depression?

A

• The long onset of antidepressant effects

Some drugs with enhance monoamine neurotransmission but do not have an antidepressant action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the reward/Pleasure pathway?

A

• Dopamine is sourced from neurons located in the Ventral tegmental area
• The axons of these then release the dopamine in the nucleus accumbens in the Basal forebrain
• This is associated with pleasure and reward
• The dopaminergic neurons are under the control of Serotoninergic neurons in the midbrain raphe
• Effect of serotonin
○ Activates the VTA dopaminergic neurons
○ Enhances release of dopamine in the nucleus accumbens
○ Auto-inhibits the midbrain 5HT neurons
§ Current theory of depression and lag of antidepressant action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the current theory of depression?

A

In the normal situation:
• The serotonergic neuron is spontaneously active
• This activity is inhibited by 5HT1A auto receptors
• This is to prevent excessive firing of the neuron

In depression:
• These receptors are hypersensitive and totally inhibit the neuronal activity
• No 5HT release in VTA and N.Accumbens

After treatment:
• SSRI treatment leads to an increase in extracellular 5HT
• Leads to desensitisation of the inhibitory auto-receptors
• Leads to restoration of neuronal activity and 5HT release in VTA and N.Acc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why is it difficult to study psychoactive drugs?

A

The synaptic mechanisms are complex
○ There are several co-transmitters in the same neuron
○ Complex post-synaptic and pre-synaptic interactions between transmitters
○ There are multiple receptor subtypes for a given neurotransmitter
• Multiple sites of action in the brain
Lack of adequate animal models- subjective experience is difficult to measure without communication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What neuropeptides do we know are involved in mood control?

A
  • TRH
    • Met-ENKEPHALIN
    • Leu-ENKEPHALIN
    • Arginine Vasopressin
    • B-Endorphin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the evidence that 5HT1A receptors are involved in depression

A

Evidence
• There is an efficacy of selective 5HT1A receptor agonists (Buspirone) as an antidepressants
• Brain imaging studies show reduced density of 5HT1A receptors in the brain of depressed patients
○ Also reduced in primates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the theory of Inflammation in depression?

A

• Infection causes activation of immune cells
• Release of pro-inflammatory cytokines (IL-1b, IL-6, TNF-a)
• Sickness behaviour by the brain
○ ? If it is a direct effect
○ ? Via the vagus
○ ? Via receptors in the brain vessels
• Current suspicion of microglial cells
• Usual role of microglial cells:
○ Reuptake of neurotransmitters (especially glutamate)
○ Synaptic plasticity (memory/adaption)
○ Control of the chemical environment (including blood brain barrier)
○ Phagocytosis
○ Release of cytokines
• During chronic stress
○ Activation of microglia
• Effect of antidepressants on microglial cells
○ Suppress the cytokine effect of microglia
Possible that the true effect of antidepressants is to reduce neuroinflammation by inhibiting microglial release of cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the effect of Depression on Cardiac health?

A
  • Increase risk of chronic heart disease 3-4.5 fold
    • Cardiac risk of major depression is comparable to smoking or lack of exercise

Why:
• reason poorly known
• Related to deficiency of 5HT1a receptors
• Effect of 5HT1a receptors in the forebrain
○ When stimulated = anxiolytic
○ When there is a deficiency = causes anxiety
• Effect of 5HT1a receptors in the medullary Raphe
○ When stimulated Inhibits cardiac sympathetic activity
○ When there is a deficiency = tachycardia/cardiac arrhythmias and hypertension

19
Q

What are the physiological changes associated with sleep?

A

Effects of sleep:
• Reduction in sympathetic activity and increase in vagal activity
• Decrease/slowing of vital functions- metabolism, respiratory rate, heart rate, AP, body temperature
• Suppression of voluntary movements
• Changes in EEG: SWS and REM sleep

20
Q

How long is approximately 1 sleep cycle?:

What is it made up of?

A

• ~ 90 minutes
• 80% is Slow wave sleep
20% is REM

21
Q

Which brain structure is involved with turning on/off sleep?

A

• Interconnected groups of neurons with various specialised funcitons
• Suprachiasmatic nucleus of the hypothalamus
○ The brains biological clock
○ Can be modulated by ight via the retino-hypothalamuc tracts
○ Its output controls sleep onset and duration as well as associated bodily changes
• Pineal gland
○ Secretes melatonin
○ Suppressed by light
• Hypothalamus
○ Secretes Orexins
○ Controls arousal and apetite in the dorsal hypothalamus

22
Q

Characteristics of CBT:

A 
• Teaches clients to identify, evaluate and respond to dysfunctional thoughts and beliefs 
	• Emphasises collaboration and active participation
	• Is goal oriented and problem focussed
	• Teaches clients to be their own therapist and aims at relapse prevention
	• Time limited
	• Sessions are structured
		○ Update and check on mood
		○ Bridge from previous session
		○ Setting of agenda
		○ Review of the homework
		○ Discussion of issues , new homework 
		○ Final summary 
		○ Feedback from client
	• Involves homework 
		○ Increasing pleasure and mastery 
		○ Scheduling/structuring activities 
		○ Self-monitoring of feelingsand events
		○ Manipulating behaviour via cues or consequences
		○ Practising alternative behaviours
		○ Increasing information
		○ Will be progressive 
		○ Given with a rational 
	• requires a sound therapeutic alliance
		○ Bond between therapist and patient
		○ Patnership 
		○ Confidence and trust
23
Q

What are the components of the MSE?

A 
• Appearance
		○ Distinctive features
		○ Clothing
		○ Grooming
		○ hygiene
	• Behaviour
		○ Facial expression
		○ Body language
		○ Eye contact
		○ Posture
		○ Response to the assessment itself
		○ Level of arousal 
		○ Rapport and social engagement
		○ Ancxious or aggressive behaviour
		○ Psychomotor activity and movement 
		○ Unusual features
	• Speech
		○ Rate 
		○ Volume 
		○ Tonality
		○ Quantity
	• Mood and Affect
		○ Patients own words
		○ Observed expression of emotion
		○ Range - flat -expansive
		○ Appropriateness
		○ Stability or labile
	• Thought content
		○ Delusions
		○ Overvalued ideas
		○ Preoccupations
		○ Depressive thoughts/ruminations
		○ Self harm, suicidal, aggressive or homicidal ideation
		○ Obsessions
		○ Anxiety- general or specific
	• Thought form
		○ Formation and coherance of thoughts
		○ Highly irrelevant comments 
		○ Frequent changes in topic
		○ Excessive vagueness
		○ Nonsense words
		○ Pressured or halted speech
		○ Poverty of thought or content
	• Perception
		○ Hallucinations
		○ Illusions
		○ Dissociative symptoms 
		○ Derealisation
		○ depersonalisation
	• Cognition
		○ Level of consciousness (alert, drowsy, intoxicated)
		○ Orientation to reality 
		○ Memory functioning 
		○ Literacy and arithmetic skills
		○ Visuospatial processing (copying a diagram)
		○ Attention and concentration
		○ General knowledge
		○ Language (naming objects)
		○ Ability to deal with abstract concepts 
	• Insight
		○ Awareness of abnormal symptoms
		○ Awareness that this is due to MH
		○ Need for treatment
		○ Awareness of contributing factors ie drugs 
	• Judgement
		○ Refers to problem solving ability 
		○ Give them a practical dilemma to see what the outcome is.
24
Q

What are the typical symptoms of depression?

A 
Mood:
	•  low mood 
	• Tearfulness
	• Irritability
	• Feelings of hopelessness
	• Helplessness
Thoughts/Cognition
	• Worthlessness/guilt
	• Burden to others
	• Suicidal thoughts
	• Indecision
	• Poor concentration
	• Complaints of memory loss
Behaviour
	• Withdrawal and avoidance of others
	• Marked loss of interest, motivation
	• Dispropotionate diability
	• Disproportionate physical symptoms 
	• Signs of depression: appearance and reactions
Biological symptoms
	• Weight change
	• Appetite change
	• Sleep patterns
	• Fatigue
	• Physical complaints- pain
25
Q

What is mania?

A
  • Mood is elevated, irritable and agitated
    • Increased activity
    • Risk taking
    • Sexual disinhibition
    • Inflated self esteem “gradiosity”
    • Poor sleep
    • Increased energy
    • Psychotic symptoms consistant with mood
26
Q

What can cause mania?

A
  • primary: bipolar affective disorder
    • Substance withdrawal
    • Medication effects
    • Organic mood disorder due to CNS disease ie frontal lobe syndrome
27
Q

What are the risk factors for depression?

A 
○ Genetics 
			§ 1/3 genetic cause
			§ 2-3 x risk if FDR has hx of depression
		○ Early Loss
		○ Adversity
		○ Other psychiatric disorders
		○ Lack of social support
		○ Medical illness
		○ Biological triggers
		○ Drug and alcohol abuse 
		○ Chronic stress especially if unresolvable 
		○ Personality factors
			§ Obsessionalism
			§ Perfectionism
			§ High negative affectivity
			§ Low self esteem
28
Q

What is hypomania?

A

Bipolar features without psychosis

29
Q

What are the genetic considerations for Bipolar?

A
  • 50% of patients have at least one parent with Bipolar
    • If one parent has bipolar there is a 25 % chance that any child will have a mood disorder
    • If both parents have bipolar then the risk for the child is 50-75%
30
Q

What are some secondary causes of mood disorders?

A
  • Parkinsons disease - especially for depression
    • CVA
    • Head injury
    • Infections- HIV especaially mania
    • Steroids- especially mania
    • Epilepsy
    • Endocrine - hypo/hyperthyroid
31
Q

What is the epidemiology of depression?

A
  • life time risk is 15%
    • 3rd highest burden of disease
    • F>M
    • 80% will have more than 2 recurrences in their lifetime
    • 12-15% will fail to recover and have chronic, unremitting illness
32
Q

What is Melancholia and why is it relevant to treatment?

A

• features:
○ Psychomotor change
○ Anhedonia
○ Affective non-reactivity
○ Vegetative changes- sleep/mood/energy/diurnal variation
• Relevance
○ Indicator that biological treatment is indicated

33
Q

How can we distinguish between depression and grief?

A
  • There is an overlap in symptoms
    • Melancholic symptoms are rare in grief but can have sdisturbed sleep and appetite
    • Cognitive symptoms of worthlessness and hopelessness are more typical of depression
    • Can have regret and guilt in BOTH
34
Q

What are the types of Bipolar?

A

• Type 1 = severe depression and severe Mania
○ Females more than males
○ Lifetime prevalence is 0.6%
○ Depressive episodes more common then manic episodes
○ 50% recurrance within 2 years
○ Risk of suicide is 30-60 x the general population
• Type 2 = Severe depression and mild mania
○ Life time prevalence is 0.4%
○ Females more than males
○ Depressive episodes more common than manic episodes but are more severe
○ Hypomania rather than manic
○ Increased risk of suicide is the same as type I

35
Q

What are the symptoms of Mania?

A
  • Mood elevation
    • +/- irritability
    • Increased speed of thinking
    • Increased confidence and grandiosity
    • Ideas +++
    • Incresed positive outlook
    • Distractible
    • Risk-taking
    • Disinhibition
    • Overbearing
    • Overactive, poor task completion
    • Increased amount and speed of activiyt
    • Reduced need for sleep
    • Appetite increases or descreases
    • Increased energy
36
Q

Can delusions occur in depression or mania?

A

• yes and this does not mean it is schizoaffective disorder
• Auditory hallucinations can occur- voices of condemnation
• Mania
○ Grandiose
○ Persecutory
○ God speaking to them

37
Q

Why is psychotic mood symptoms relevant in bipolar and depression

A 
• Pharmacotherpay or ECT indicated 
	• Mania
		○ Antipsychotic alone or with mood stabiliser
	• Depression
		○ Antipsychotic plus antidepressant
38
Q

Who is at increased Risk of suicide?

A
  • Male gender
    • Indigenous people (twice as likely)
    • Northern territory
    • Mental health problems
    • Family history of suicide
    • Family discord, violence or abuse
    • Alcohol use or other substances
    • Social or geographical isolation
    • Financial stress
    • Bereavement
    • Prior suicide attempt
    • Old age
39
Q

What are some warning signs of someone who may be suicidal?

A
  • Hopelessness
    • Feeling trapped- like there is no way out
    • Increasing alcohol or drug use
    • Withdrawing from friends, family or society
    • No reason for living, no sense of purpose in life
    • Uncharacteristic or impaired judgement of behaviour
40
Q

What could be a “tipping point” for someone at risk of commiting suicide?

A
  • Relationship ending
    • Loss of status or respect
    • Debilitating physical illness or accident
    • Death or suicide of relative or friend
    • Suicide of someone famous or member of peer group
    • Argument at home
    • Being abused or bullied
    • Media report on suicide or suicide methods
41
Q

What are signs that someone is at imminent risk?

A
  • Expressed intent to die
    • Has plan in mind
    • Has access to lethal means
    • Impulsive, aggressive or antisocial behaviour
42
Q

What are some protective factors in relation to suicide risk?

A
  • being connected or belonging to a family
    • Having at least one person to relate to and bond with
    • Having the skills to deal with difficult situations
    • Spirituality and beliefs
    • Good physical and mental health
    • Effective treatment for mental illness and emotional problems
43
Q

What are the public health measures that can prevent suicide?

A

• primary prevention
○ Building stronger more resilient people
○ Preventing incidence of risk factors
• Secondary prevention
○ Interventions to provide additional support to people with risk factors and warning signs
• Early intervention
○ Interventions with people at high risk
• Interventions
○ Interventions with those who are suicidal
• Postvention
○ Minimise harm to other post suicide event

44
Q

Is a history of self harm create a higher risk for the patient to commit suicide?

A
  • YES
    • 50% of those who commit suicide have a history of self harm
    • Risk of suicide increased 30-50 fold

PBL Notes (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions