Pathophysiology of Bipolar Disorder

Type of Bipolar

Bipolar 1 which is severe manic epsidoes with depressive episodes. Bipolar 2 which is hypomaniac with major depressive episodes. Cyclothymia which are milder mood swings

Patho of Bipolar

Neurotransmitter Imbalances (DA, NE, serotonin), genetic factors, neuroplasticity due to reduced neurogenesis, and environmental factors

Lithium

1) MOA

2) Clinical Use

3) SE

Modulates neurotransmitter release to stabilize mood. Used for acute mania or as a long-term mood stabilizer. Side effects are weight gain, tremor, thyroid dysfunction, and renal impairment

Lithium signaling pathways

Lithium inhibits PIP2 which decreases PKC activation thus decreasing neuronal excitability. Lithium is a direct competitive inhibitor of GSK3 which inhibits various signaling cascades

Considerations with Lithium pharmacotherapy

Mechanism is not clearly understood. Small therapuetic index. Acute doses are high and chronic doses are low. Lag time effectiveness if 5-7 days after start. Loading dose required

Anticonvulsants

1) examples + their respective MOA

Carbamazepine blocks NA channels, Lamotrigine blocks Na and Ca channels, and Topiramate blocks Na channels, enhances GABA, and inhibits AA/Glutamate receptors

MOA of agomelatine

melatonin agonist which regulates circardian clock and serotonin antagonist which enhances the release of NE and DA

nAch: what it stands for, moa, and effect

nicotinic Ach receptor that is activated by nicotine which causes the influx of Na and Ca causing neuronal excitation.

mAch: what it stands for, example, moa, and effect

muscarinic Ach receptor, scopolamine is an example, is an M1-M5 subtype, and causes smooth muscle contraction