Exam 2 Dr Langford Review Flashcards

1
Q

What are the key causes and mechanisms of depression?

A

✔ Monoamine Dysfunction: Imbalance in serotonin (5-HT), norepinephrine (NE), dopamine (DA)
✔ HPA Axis Dysregulation: Overactive stress response = excessive cortisol, hippocampal shrinkage
✔ Neuroinflammation: Increased cytokines reduce BDNF & neuroplasticity
✔ Neurodegeneration: Chronic stress leads to neuronal loss & volume reduction in key areas
✔ Genetic & Epigenetic Factors: Genetic predisposition + environmental stress

Mnemonic: “H.I.G.S.” → Hormonal, Inflammatory, Genetic, Stress-related

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2
Q

Why is the Monoamine Hypothesis considered incomplete?

A

Antidepressants increase neurotransmitters immediately, yet symptom relief takes weeks.
Direct neurotransmitter level changes aren’t consistently found in depressed patients. Neuroplasticity plays a major role in recovery (BDNF & structural changes)

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3
Q

What role does serotonin (5-HT) play in depression?

A

Regulates mood, anxiety, and impulsivity

Part of the Monoamine Model.

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4
Q

What is the function of norepinephrine (NE) in relation to mood disorders?

A

Controls alertness, energy, & stress response

Part of the Monoamine Model.

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5
Q

What is the role of dopamine (DA) in mood regulation?

A

Governs motivation, pleasure, & reward processing

Part of the Monoamine Model.

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6
Q

Which brain regions are commonly affected in depression?

A

✔ Prefrontal Cortex (PFC)
✔ Amygdala
✔ Nucleus Accumbens
✔ Thalamus
✔ Striatum

Mnemonic: “PANTS” → Prefrontal Cortex, Amygdala, Nucleus Accumbens, Thalamus, Striatum

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7
Q

What happens to the Prefrontal Cortex (PFC) in depression?

A

Underactive, leading to poor decision-making & executive dysfunction

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8
Q

How does the amygdala change in depression?

A

Overactive, contributing to increased anxiety & negative emotional bias

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9
Q

What is the effect of a reduced Nucleus Accumbens in depression?

A

Reduced reward response, leading to anhedonia

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10
Q

What imaging findings are associated with depression?

A

✔ MRI: Reduced hippocampal volume, prefrontal cortex thinning
✔ fMRI: Overactivity in amygdala, default mode network hyperconnectivity (rumination)

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11
Q

What is the impact of chronic stress on the HPA axis in depression?

A

Chronic stress leads to an overactive HPA axis, increasing cortisol & damaging the hippocampus

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12
Q

What is the Dexamethasone Suppression Test (DST) used for?

A

To assess HPA axis function; depressed patients fail to suppress cortisol

It is not specific enough for diagnosis.

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13
Q

What are the effects of antidepressants on neuroplasticity?

A

✔ Increase BDNF → Supports neurogenesis
✔ Reduce glucocorticoids which restores HPA function by upregulating the glucocorticoid receptors→ Protects hippocampus from stress damage
✔ Restore neurotransmitter balance → 5-HT, NE, DA, Glutamate

Mnemonic: “BIG N” → BDNF, Inflammation, Glucocorticoids, Neurogenesis

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14
Q

What differentiates unipolar depression from bipolar disorder?

A

✔ Unipolar Depression: Consistent underactivity
✔ Bipolar Disorder: Fluctuating hyper/hypoactivity

Mnemonic: “Bipolar = Rollercoaster Brain”

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15
Q

What are key interventions that can increase BDNF?

A

✔ Sleep regulation
✔ High-intensity exercise
✔ Electroconvulsive Therapy (ECT)
✔ Social interaction & environmental enrichment
✔ Antidepressants (increase BDNF over time, but this isn’t their primary mechanism of action).
✔ Nutrition (Omega-3s, flavonoids, and curcumin).
✔Lithium may support neuroplasticity but is not a primary BDNF booster.

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16
Q

What are the symptoms associated with the Nucleus Accumbens?

A

Anhedonia (no pleasure) due to dopamine dysfunction.

17
Q

What is the role of the hypothalamus in depression?

A

Appetite and sleep issues caused by regulation disruption.

18
Q

What occurs in the striatum in depression?

A

Motor agitation due to hyperactivation.

19
Q

What are neurobiological changes that occur in Bipolar Disorder?

A

✔ PFC and Limbic System Dysregulation: Abnormal connectivity between the amygdala & PFC.

✔ Gray Matter Changes:
Increased amygdala volume.
Decreased gray matter volume in PFC.
✔ Mania = Dopamine & Glutamate Excess
✔ Depression Phase = Low Dopamine & Underactive PFC

20
Q

What is the role of the dorsolateral PFC in depression?

A

Cognitive impairment due to executive function deficits.

21
Q

What occurs in the amygdyla during depression?

A

Anxiety, stress, and suicidality (emotions) are overactivated due to the stress response.

22
Q

What occurs in the basal forebrain due to depression?

A

fatigue and low energy due to NE and DA reduction.

23
Q

How does Ketamine work for depression?

A

Ketamine (NMDA antagonist) → Immediate effects via glutamate modulation.

24
Q

How do SSRIs/SNRIs work in depression?

A

SSRIs/SNRIs → Gradual increase in BDNF & neuroplasticity.

25
Q

How does the HPA axis release cortisol?

A

Hypothalamus → Releases CRH
Pituitary → Releases ACTH
Adrenal Gland → Releases cortisol