1. Mental Health

2. Note:
Really basic general layout/overview
All information is taken straight from sources

3. Mental health in the balance between all aspects of life, physical, social, emotional and spiritual.
A mental disorder is a psychological or behavioural pattern in an individual that can cause distress of disability that is not expected as part of normal development.

4. Anxiety Disorders Anxiety is the inappropriate expression of fear.
Panic Disorder
Sudden onset, short lasting (30 min), fearfulness, terror, palpitations, sweating, trembling, chest pain, nausea, chills, blushing. In 2% of population. More common in women. 50% with major depression. 25% develop substance abuse.

5. Obsessive-Compulsive Disorder
Recurrent intrusive thoughts perceived as inappropriate. Germs, doing harm, sex, violence. Compulsions are behaviors performed to reduce anxiety as hand washing, counting, checking on things. 2% of population. Equal men and women

6. Biological Basis
Stressors are normal and normally handled by experience and learning. Anxious people have stressors at the wrong time or place.
The Stress Response - The hypothalamic-pituitary-adrenal (HPA) axis
Avoidance behavior
Increased vigilance and arousal
Activation of Sympathetic Nervous System
Increase cortisol release.

7. Increased cortisol release is controlled by a part of the hypothalamus -> ACTH releasing hormone -> ACTH from anterior pituitary -> Cortisol from adrenal cortex.
The hypothalamus is controlled by the Amygdala and Hippocampus
The central nucleus of the amygdala is responsible for the stress response. The basolateral nucleus of the amygdala gathers information from sensory areas and projects to the central nucleus.

8. Hippocampal activity suppresses CRH
Hippocampal activity suppresses CRH. The hippocampus contains cortisol receptors and normally regulates this hormone. Prolonged stress and high cortisol levels can cause these cells in the hippocampus to wither and die. Imaging shows decreased activity of this area in people with post-traumatic stress syndrome and hyperactive prefrontal cortex.

9. Treatment for anxiety disorders
Psychotherapy sometimes works. Therapist tries to lessen fears by slowly introducing the fear stimulant and making the stimulant appear harmless - as in phobia of airplane travel.

10. Anxiolytic Medications
Benzodiazipines (Classified as hypnotics and sedatives these chemicals target mostly CNS GABAA receptors which are direct and fast acting Cl- gates causing inhibition in cells. The benzodiazipines potentiate the effects of GABA and do not work without GABA present.) (Includes Valium, Xanax, Librium, Halcion). Their effects are, in many ways, similar to Alcohol. Alcohol acts in the same way and this may account for the common use of alcohol. It is believed, but not proven that Diazipines are substituting for a natural modulating chemical that is unknown. Results are swift.

11. Serotonin-selective reuptake inhibitors (SSRIs) as (Prozac)
Serotonin-selective reuptake inhibitors (SSRIs) as (Prozac). Serotonin is a modulatory neurotransmitter diffusely found in the brain. Serotonin works on a G-protein-coupled receptor and the SSRIs block reuptake of serotonin, thus making it more influential. It requires weeks to get a useful response to SSRIs therapy. The increase in brain serotonin is immediate - so it is thought that the therapy comes from a brain adaptation to increases of serotonin. One of the effects that correlates with therapy is the reduction of CRH receptors. CRH is a neurotransmitter in the amygdala and injecting it in this area causes stress response and anxiety.

12. Mood Disorders = Insert definition
30% will have a bout within their lifetime.
Major Depression
Untreated depression can last 4-12 months. There is no logical cause of the depression and the person can not control it.
Symptoms
Loss or increase of appetite
Insomnia or hypersomnia
Fatigue
Feelings of worthlessness and guilt
Diminished ability to concentrate
Recurrent thoughts of death

13. Bipolar Disorder
Also called Manic-depression. Periods of depression interspersed with periods of mania or frenzy.
Symptoms of Mania
Inflated self-esteem or grandiosity (anyone in authority that enjoys it)
Decreased need for sleep
Increased talkativeness or feelings of pressure to keep talking
Flight of ideas
Distractibility
Increased goal-directed activity. (Many of our most productive ancestors had this disorder)

14. Biological Basis Monoamine Hypothesis
Reserpine used to treat high blood pressure by interfering with loading catechol amines (epinephrine, norepinephrine, and catechol) into vesicles. It depleted catechols in the brain and body. It also caused psychotic depression in 20% of patients. Another drug used to treat tuberculoses caused mood elevation. They are both inhibitors of the enzyme monoamine oxidase (MAO) which is the enzyme that destroys the monoamines including serotonin.

15. So the theory went that mood is an abnormal influence of these modulators. However, other drugs that affect monoamines such as amphetamines and cocaine were not good at treating depression. It also took several weeks of medication to work although the drugs carried out their activities immediately. So the conclusion is that the change in catecholamine concentrations causes adaptation in the CNS that are useful.

16. The Diathesis-Stress Hypothesis
Diathesis refers to a genetic component to the predisposition of disease states.
Anxiety is due to hyperactivity of the HPA axis. Anxiety and depression, however, coexist most of the time. Blood cortisol levels are high, CRH levels are high in the CSF. Injecting CRH into animal brains can mimic severe depression and anxiety.

17. Anxious patients have fewer glucocorticoid receptors
Anxious patients have fewer glucocorticoid receptors. Genes, early childhood experience, and monoamines regulate the number of these receptors.
Rats which have more maternal care or tactile input from other pups, have more cortisol receptors. The cortisol receptors provide negative feedback and reduce the amount of CRH. Ignored rats have fewer cortisol receptors and are more likely to be anxious.

18. Treatment for Mood Disorders
Electroconvulsive Therapy
The patient is given anesthesia and muscle relaxants and a shock with electrodes on the scalp to the temporal lobes. Gives quick relief, but also causes memory loss that can extend back to 6 months.
Psychotherapy
Works with mild to moderate depression

19. Antidepressants
All of the drug types elevate the levels of monoamine neurotransmitters in the brain. It takes weeks to be effective. There is an increase in glucocorticoid receptors. Drugs with anti CRH activity are being sought.
Lithium
Lithium was discovered accidentally to stabilize and calm rats. It works well with humans with bipolar disease also.
Lithium interferes with PIP formation, a second messenger, and cAMP. It requires weeks to be effective and its mechanism of action is really unknown. It can enter nerve cells through Na+ gates, but is not pumped out by the Na+-K+ pump. SO it accumulates in nerve and muscle cells.

20. Schizophrenia A loss of reality. Negative Symptoms Positive Symptoms:
Delusions
Hallucinations
Disorganized Speech
Grossly disorganized or catatonic behavior
Negative Symptoms
Reduced expression of emotion
Poverty of Speech
Difficulty in initiating goal-directed behavior

21. Paranoid Schizophrenia has delusions that powerful forces are out to get you. Also in toxic psychosis. These tend to be the most dangerous to others, but are more readily treated.
Disorganized Schizophrenia = a "flat affect". Incoherent speech and disorganized behavior. Usually deteriorate with time.
Catatonic Schizophrenia = immobility, stupor, bizarre posturing

22. Biological Basis
Genes and the environment. Genes play a large part Fig But no genes or environmental factors have been found that explain its incidence.
There are physical changes in the brain in some cases that indicate a loss of brain cells.

23. Dopamine Hypothesis
Possibly damage to the mesocorticolimbic system.
Too much amphetamine or cocaine can lead to typical symptoms temporarily. Chlorpromazine was used and prevented the positive symptoms. It was originally developed as an antihistamine, but now is classed as a neuroleptic These are now known to be potent blockers of dopamine receptors, especially the D2 receptor. Some new drugs have been developed that do not significantly block D2 receptors and yet work.

24. Glutamate Hypothesis
Phencyclidine (PCP) was used as an anesthetic. It is still used on animals. It produces a dissociation of the mind so that one does not remember pain.
It also can produce paranoia, hallucinations and an insensitivity to pain. A bad combination. PCP is thought to block NMDA receptors.
Mice were developed with fewer NMDA receptors and their behavior suggests schizophrenia.

25. Treatment
Neuroleptics reduce the positive effects of schizophrenia, but side effects over the long term are awful. Tardive dyskinesia is an involuntary movement especially in jaw and lips. Side effects are especially bad in women.
Atypical neuroleptics can be used as a substitute and also work on negative schizophrenic effects.