Depression Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

What is depression and what are the common symptoms

A

-Depression is a mental health condition characterised by persistent feelings of sadness, emptiness, or hopelessness that interfere with daily life and functioning. It’s more than just a temporary mood swing or feeling blue; it affects how you feel, think, and handle daily activities. Depression requires medical diagnosis and treatment.

Common symptoms include:

-persistent sadness or low mood- Feeling down, tearful, or experiencing a pervasive sense of emptiness.
-Loss of interest or pleasure- A noticeable loss of interest or pleasure in all or most activities, including ones that were previously enjoyed.
-Changes in appetite- Significant weight loss when not dieting, weight gain, or changes in appetite.
-Sleep disturbances- Insomnia (difficulty sleeping) or hypersomnia (oversleeping).
-Fatigue or loss of energy- Feeling unusually tired or a lack of energy to do even small tasks.
-Feeling of worthlessness or excessive guilt-Harsh criticism of perceived faults and mistakes.
-Difficulty concentrating and making decisions- Problems with focus, making decisions, or remembering things.
-Physical symptoms- Unexplained aches or pains, headaches, cramps, or digestive problems without a clear physical cause that do not ease even with treatment.
-Irritability or anger- Feeling agitated, restless, or even violent; the tolerance level might be low, temper short, and everything and everyone may get on your nerves.
-Thoughts of death or suicide- Frequent or recurrent thoughts of death, suicidal ideation without a specific plan, or a suicide attempt or specific plan for committing suicide.

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

What are the different treatments for depression

A

Classification 1:

(SSRIs): These drugs increase the level of serotonin in the brain by inhibiting its reuptake into the presynaptic cell, making more serotonin available to improve transmission of messages between neurons. Examples include fluoxetine (Prozac), sertraline (Zoloft).

(SNRIs): SNRIs work by inhibiting the reuptake of both serotonin and norepinephrine, increasing the concentration of these neurotransmitters in the brain. This helps improve mood and pain perception. Examples include venlafaxine (Effexor XR) and duloxetine (Cymbalta).

(NARI): noradrenaline reuptake inhibitors

(DARI): dopamine reuptake inhibitors

Classification 2:

(TCAs): These older antidepressants work by blocking the reuptake of norepinephrine and serotonin, thus increasing their levels in the brain. They also affect other neurotransmitter systems, which can lead to more side effects. Examples include amitriptyline (Elavil)

(MAOIs): MAOIs increase the levels of norepinephrine, serotonin, and dopamine by inhibiting the enzyme monoamine oxidase, which breaks down these neurotransmitters in the brain. Due to potential side effects and dietary restrictions, they are usually prescribed when other antidepressants haven’t worked. Examples include phenelzine (Nardil) and tranylcypromine (Parnate).

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

Why is it important to stud depression?

A

differentiate between normal and pathological and also because prevalence is high.

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

What is the purpose of feeling depressed and why is prescribing medication not be the best option?

A

purpose: motivational experience and signal that something is going on and should be fixed, it is a warning sign.

why may it not be the best option? sort out your feelings, those feelings are in place for a reason,
but medication can treat the chemical imbalance which can therefore treat the cause.

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

what is the ICD 10 criteria for depression and what are the core symptoms and the difference in severity?

A

-2 weeks persistent symptoms.
-core symptoms low mood and anhedonia (loss of pleasure)
-other symptoms like reduced self esteem and reduced confidence

mild depression: 2 core symptoms and 2 other symptoms
moderate depression: 2 core and 3/4 others
severe depression: 2 core and more than 4 others

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

What is seen in every mental disorder?

A

-loss of self worth and lots of criticism of one’s self.
-disliking one’s self
-Cognitive impenetrability refers to the idea that certain perceptual processes in the brain are not influenced by higher-level cognitive processes such as beliefs, desires, or intentions.
In other words, our perception of the world through these basic sensory processes is direct and unalterable by our thoughts or knowledge.
-when you treat someone with depression you would want to fix this and increase their self worth

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

what is the prevalence of depression? and onset?

A

1in 4 will experience a mental health problem each year
50% more common in women than men

Mental health diagnosis usually increases later in life around 60 years and above.

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

what’s the difference between ICD-10 and DSM-5?

A

ICD-10 is the UK international classification of diseases including all diseases and condition whereas the DMS-5 is the American psychiatric association which focuses primarily on mental health disorders

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

What are the psychotic symptoms of depression?

A

Hallucinations can be in any sensory modalities, for example if they have auditory hallucinations they may have negative inner voices, or they may hear screaming-cries for help. The olfactory version could encompass thinking they smell bad, or they may think their own flesh is rotting.

Delusions can be fixed irrational beliefs that out of context with their cultural/ religious views. Some of them think they’ve done something bad, and they don’t know what they’ve done.

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

what are other diagnoses that is similar to depression or may have depressive episodes?

A

Bipolar affective disorder, suffer from different episodes of moods, i.e., they’ll have elevated moods (mania) sometimes hypermania, and suffer from depressive episodes.

Dysthymia- doesn’t necessarily meet criteria for depressive episodes but they have chronic low grade depressive symptoms. with clinical symptoms encompassing: low mood for for 2 years, disturbed appetite and sleep, poor concentration, difficulty making decisions, and hopelessness

So it’s important to differentiate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are other ways in which depression can present that are less obvious?

A

headache
fatigue
weight loss
poor memory
other pain disorders like lower back pain or chest pain

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

what does the biopsychosocial model by George Engel encompass and its purpose

A

Biological: This aspect covers the physiological and genetic factors that can affect health. It includes an individual’s anatomy and biochemistry, the functioning of organs and cells, genetic predispositions, and the impact of diseases or injuries. ie gender, age

Psychological: This includes all aspects of psychological functioning. It involves emotions, thoughts (negative schemas), behaviours, coping mechanisms, personality traits (affectionate), and mental health conditions such as depression or anxiety.

Social: This dimension recognizes the influence of societal factors on an individual’s health. It covers a wide array of elements such as socioeconomic status, culture, family dynamics, social support, education, and environmental factors.

Purpose of the Biopsychosocial Model:
Holistic Care: The model’s primary purpose is to provide a more comprehensive understanding of health care by considering the whole person rather than just the biological symptoms of a disease.

Personalized Medicine: It encourages personalised treatment plans by taking into account the individual differences in lifestyle, belief systems, and social contexts.

Integrated Approach: It promotes an integrated approach to treatment that can include medical interventions, psychological support, and social assistance.

Interdisciplinary Collaboration: It encourages collaboration among healthcare professionals from various disciplines to address the multifaceted needs of patients.

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

what are the biological aetiology of depression?

A

female-male 2:1 prevalence ratio

monoamine theory on chemical imbalance
Caused by monoamine deficiency (serotonin, noradrenaline, and dopamine).
Drugs can reduce abundance of neurotransmitters such as reserpine and can lead to depression. Deficits in MA lead to depression. Most of treatment of antidepressants work by increasing concentration of these neurotransmitters to reduce depression.

against this:
Antidepressants can take up to 3-4 weeks to have therapeutic effect which is a bit problematic.
Cocaine which blocks serotonin and NA transporters and so should increase their abundance between neurones and so you’d expect cocaine to have an antidepressant effect however it doesn’t have an antidepressant effect.

neuroendocrine theory:
Depression is caused by hypersensitivity of HPA axis. Regulation of this axis is critical for healthy stress coping mechanism in person so any dysregulation i.e., hyper or hypo activity can cause problems with stress coping mechanisms such as depression. Stress activates the hypothalamuses releasing CRH acting on pituitary and release ACTH which acts on adrenal glands to release cortisol into the bloodstream. This becomes a problem when is hyperactivates even without stressful stimuli. Increasing cortisol over time. If theory is correct, you’d expect when measuring plasma/urine /saliva cortisol to see higher levels over baseline normal.
There’s evidence that tactile stimulation just after birth can activate 5-HT pathways in hippocampus. So, nurturing a baby has been shown to increase 5-HT in hippocampus which increases glucocorticoid receptors therefore cortisol can now activate hippocampus and regulate HPA activity. So, in case of antidepressants some work by increasing serotonin. So, increasing 5-HT in hippocampus and this will increase glucocorticoid receptors in hippocampus and so cortisol can bind and activate hippocampus and thus supress/regulate HPA activity. Another classic evidence of how genetic and environment predispose depression.Child neglect at very young age predisposes people to develop mental health conditions later in life. The mechanisms underlying this. The HPA is regulated by amygdala and hippocampus. And there are neuronal projections from both these regions to hypothalamus/HPA to regulate its activity and as a result cortisol levels. Activation of amygdala will induce activation of HPA and increase of cortisol levels, whereas activation of hippocampus will supress HPA activity. This would regulate HPA activity and in turn have normal coping mechanisms in place.
So, activation of HPA will release cortisol and this will act on auto-cortisol-receptors on hippocampus that will activate hippocampus which will lead to suppression of HPA activity-feedback.
Problems can arise if there’s too much activation of amygdala or hypoactivity of hippocampus both resulting in increased activation of HPA.
evidence:
Now rat studies has shown that upon child neglect from a rat mother to her children, the rat children hippocampi had lower glucocorticoid genes/receptors (where cortisol binds to). So as a result, the release of cortisol form HPA won’t be able to bind to hippocampus and activate it as usual due to lower levels of glucocorticoid receptors. So, hippocampus is not as activate and supress HPA so there will be increase activation of HPA and predispose rats to develop depression later in life. So, this is how child neglect can influence gene expression/ genetics.
This is good influence of genetic and environment relation to increase depression development.

neurogenesis/neuroplasticity theory:
Neuroplasticity theory of depression proposes that neuronal loss, will cause depression specifically in hippocampus and prefrontal cortex. Decreased neurogenesis in those regions is associated to cause depression and shown in animal models. In prefrontal cortex is associated with decision making and judgment, and the lack of this is one of the characteristics seen present in depressed individuals. So, this impairment in decision making is due to hypo frontality/ neuronal loss in this region. Antidepressants and electroconvulsive therapy (induce electrical stimulation to the brain) are known to induce neurogenesis in this region. Which supports this theory that neuronal loss is associated with depression. 5-HT is known to promote neurogenesis and increasing brain derived neurotrophic factor found in prefrontal cortex and hippocampus.
Evidence suggests increased release of glutamate can happen due to stress in prefrontal cortex can lead to neuronal loss and as a result, depression. As it activates NMDA receptor causes excitotoxicity in excess causing neuronal loss. Blocking this receptor by ketamine it will induce and antidepressant effect, which works immediately, suggesting glutamate is associated with neuronal death and leads to depression

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

what is the psychological aetiology of depression?

A

a) cognitive
i) Cognitive triad by Aaron Beck: negative self-view (things are bad because I’m bad), negative interpretations of experiences (everything has always been bad), negative view of future (anticipation of failure)
ii) They’re more likely to focus on negative aspect of a situation ignoring positives and so they can distort and misinterpret situations- cognitive bias (polar reasoning-All or nothing, Abstraction- success is ignored, overgeneralisation- if this went badly, everything else will)
b) Negative self-schemas
i) Schemas- package of knowledge that stores info about ideas, ourselves and the world around us. This is developed during childhood. Beck proposes that depressed individuals have negative self-schemas that’s originates possibly from negative childhood experiences (criticism from parents or bullying at school). So those with negative self-schemas interpret everything in a negative way as will lead to cognitive bias
c) Personality
i) Those who have affectionate traits, can lead to anxiety and depression as they often blame themselves and can lead to problems with coping skills, and unable to deal with events that life throws at us.
d) Adverse childhood experiences
i) All types of abuse, witnessing domestic violence, parental separation/divorce, imprisonment of household member, mental health problems in household, substance abuse in household.
ii) Parental style: lack of care/neglect or overprotection and bullying that may occur to child.

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

what is the social aetiology of depression?

A

a) Vulnerability factors which increased risk of depression if provoking agent is present such as major difficulties i.e., divorce (Brown and Harris): 3+ children under age of 14, not working outside the home, lack of confiding relationship.
b) Poverty
c) Physical illness (ongoing health problems like cancer, diabetes can lead to depression)-they might lose will in life, and may always have to depend on others which can be frustrating even have discrimination/prejudice and therefore can impact their thinking pattern< some physical illness such as hyperthyroidism can directly lower moods which is biological
d) Low education

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

sum all causes and which it results in for depression

A

Repeated stress is causality for depression will induce activation of HPA and release of cortisol. This release of cortisol can lead to detrimental gene transcription responses and lead to neuronal apoptosis and that can lead to depressive symptoms.
Excessive release of glutamate in brain will hyperactivate NMDA receptors and lead to neuronal loss due to excitotoxicity.
Noradrenaline via acting on alpha2 receptors or serotonin acting on 5-HT receptors can activate signal transduction pathways that inhibit detrimental gene transcription response thereby preventing neuronal apoptosis. Instead activates beneficial transcription responses that lead to neurogenesis- antidepressant effect. Low level of serotonin and noradrenaline will cause less activation of its receptors, less beneficial transcription response, less increase in neurogenesis. Increasing BDNF induces neurogenesis in prefrontal cortex and hippocampus decreasing depressive symptoms.