Week 13 - Mood Disorders Flashcards
(37 cards)
What are emotions
Short-lived, intense, linked to specific cause. Can have indicative facial expressions and body language
What does affect mean
Encompasses a broad range of sensations that people can experience, embodies both emotions and moods
What is mood
Longer-lasting emotional state, often with no clear cause.
“a disposition to respond emotionally in a particular way that may last for hours, days or even weeks, perhaps at a low level and without the person knowing what prompted the state”
What can mood disorders cause - dent related
- Stress, pain, bruxism, TMJ disorders, periodontal disease.
- Poor hygiene due to low motivation. More susceptible to infection and illness
- Medications can cause xerostomia, acid reflux – from anxiolytics (anxiety reducing medication) and antidepressants
- Loss of taste perception (ageusia) – desire for comfort food
- Dental anxiety leads to avoidance and worsened oral health.
What is depression
state of Profound sadness;
- may be reactive or endogenous.
what is reactive depression
depression in response to a life event or experience
What is endogenous depression
depression due to no apparent trigger
What is clinical depression
depression that continues for longer than normal
What are the 2 main types of clinical depression
Unipolar and bipolar.
* Linked to suicide, CVD, cancer.
* Reciprocal effect with oral health and depression
What are the emotional related symptoms of depression
- misery, apathy, pessimism, sadness
- low self esteem
- guilt
- social withdraw
- decreased ability to function
- indecisiveness, loss of interest/pleasure and motivation
- suicidal ideas
What are biological symptoms of depression
- retardation of though and action, poor memory
- loss of libido (desire for sexual activity)
- sleep disturbance and loss of appetite or hyperphagia
- reduced energy; general aches and pains
What are the 2 theories for the cause of depression
- Monoamine hypothesis
- Neuroplasticity theory
What is the monoamine hypothesis of depression
- Depression from deficiency in monoamine a group of neurotransmitters that regulate mood, arousal and emotions
- serotonin and noradrenaline
Problems with treatment
- No drugs that increase monoamine
* Limitations: 2–4-week latency, partial efficacy.
*Suggests the drugs induce adaptive changes in the brain rather than direct pharmacological effects
A serotonin deficiency causes what
emotion related symptoms of depression
Noradrenaline deficiency causes what
Biological symptoms of depression
What is the neuroplasticity theory of depression
- Depression involves neuronal loss in the hippocampus, Prefrontal cortex and amygdala
Neuronal loss – a combination of neurodegeneration and apoptosis linked to reduced neurogenesis and neuroplasticity
- Antidepressants may reverse this by stimulating neurogenesis and inhibiting apoptosis.
**Normal mood depends on the right balance between the 2 processes of neurodegeneration/apoptosis and neurogenesis.
What are the factors which alter neuroplasticity
- Chronic inflammation
- Stress
- Neurotrophic factors (BDNF)
How does chronic inflammation alter neuroplasticity
Increases cytokines, apoptosis.
- Increased levels of pro inflammatory cytokines –> increased neuronal apoptosis
- Immunoregulatory effects of antidepressants –> decreased production of pro-inflammatory cytokines
How does stress alter neuroplasticity
Raises cortisol and glutamate, causing neuronal atrophy.
- Elevated cortisol and excessive glutamate –> causing altered gene expression, reduced neurogenesis, acute and chronic neural injuries and reduced autophagy
- Atrophy in some brain regions and remodelled synaptic activity in the amygdala – negative emotions and fear
- Antidepressants promote neurogenesis and stimulate autophagy
How do neurotrophic factors (BDNF) alter neuroplasticity
Decreased in depression; enhanced with healthy lifestyle.
- Lower levels in depression and anxiety
- BDNF supports survival of neurons, promotes synaptic connections, is essential for learning and memory and suppresses inflammation
- Diet low in processed foods, reduced stress, sufficient sleep and exercise can improve BDNF levels
What is the possible mechanisms of action of antidepressants
- Inhibition of the presynaptic monoamine reuptake pump – prolongs duration of NT in the synaptic gap increasing chance of signaling
- Blockage of presynaptic receptor – removes the inhibition of NT release from the nerve terminal – level of NT in the synaptic gap increases
*the receptor prevents excess releases of NT, we can unblock it to increase release - Inhibition of monoamine oxidase – enables release of more NT when the terminal is stimulated
- Change in the sensitivity of postsynaptic receptors to its NT – alters the magnitude of the response to stimulation
What are the different types of first generation antidepressants
- Monoamine oxidase inhibitors (MAOIs) (selective and non selective)
- Tricyclic tetracyclic antidepressants (TCAs and TeCAs)
What are monoamine oxidase inhibitors (MAOIs)
- First generation antidepressants
Inhibit all monoamine breakdown by blocking the enzyme monoamine oxidase (MAO) which normally breaks down neurotransmitters like serotonin, noradrenaline and dopamine
o Adverse: Hepatoxic (Liver toxicity), drug/food interactions, xerostomia. lethal drug interactions
o Types: Non-selective, MAO-A (antidepressant), MAO-B (Parkinson’s).
What are the different types of monoamine oxidase (MAO)
- MAO-A
- MAO-B
