Brain Health 2 Flashcards
panic disorder
recurring, seemingly unprovoked panic attacks and a persistent worry about having further attacks
agoraphobia
severe anxiety about being in situations where escape might be difficult or embarrassing
avoidance of situations irrationally perceived as threatening
obsessive compulsive disorder
obsessions = recurrent, intrusive thoughts, images, ideas, or impulses that are perceived as being inappropriate, grotesque, or forbidden compulsions = repetitive bx or mental acts to reduce anxiety
generalized anxiety disorder
at least 6 months of persistent and excessive anxiety and worry
specific phobias
clinically significant anxiety provoked by exposure to a specific feared object or situation, often leading to avoidance behavior
social phobia
clinically significant anxiety provoked by exposure to certain types of social or performance situations, often leading to avoidance behavior
post traumatic stress disorder
the re-experiencing of an extremely traumatic event, accompanied by symptoms of increased arousal and the avoidance of stimuli associated with the trauma
what is the HPA axis and what does it control
hypothalamic-pituitary-adrenal axis
controls the humoral response and the stress response
HPA steps first half
eyes perceive scary stimulus, goes to visual cortex to amygdala amygdala to hypothalamus hypothalamus releases CRH hypothalamus to pituitary pituitary releases ACTH
HPA steps second half
pituitary (releases ACTH) to adrenal glands
adrenal glands release cortisol
body prepared for fighting or fleeing
cortisol circulates throughout body
glucocorticoid receptors on the hippocampus
Human behavior =
Brain =
Product of brain activity Product of mutually interacting factors that determines individualism DNA Experience Environmental Factors
mental illness
Diagnosable disorder of thought, mood, or behavior that causes distress or impaired functioning → has biological basis
external biological causes of mental illness
Syphilis: infection, Mania, cognitive deterioration
B vitamin deficiency: agitation, impaired reasoning, depression
HIV infection in brain: progressive loss of cognition and behavior
Toxoplasmosis: found in cats and cat owners, usually asymptomatic, but loose links to ADHD, Schizophrenia, OCD
biological basis of fear/anxiety
Fear evoked by threatening stimulus: Stressor Presented (or not) (Ex. Exam, divorce, loss of job, death of loved one)
Stress response activated
Stimulus-response relationship strengthened (or weakened) by experience
HPA axis slides
Amygdala interprets stimulus as a threat, activates hypothalamus
Hypothalamus releases corticotropin-releasing hormone (CRH)
Pituitary receives CRH and releases adrenocorticotropic hormone (ACTH) into bloodstream
Adrenal glands on kidneys receive ACTH and release cortisol (stress hormone) which activates sympathetic response
Regulation of the HPA Axis by the Amygdala and Hippocampus
Both regulate CRH neurons Amygdala activates the HPA axis Hippocampus deactivates the HPA axis Glucocorticoid receptors for cortisol Signals Hypothalamus - Feedback loop to decrease CRH release Push-pull style regulation
in anxiety disorder…
Overly responsive to ACTH, CRH, or Cortisol
Amygdala responds to non-dangerous stimuli
Insufficient glucocorticoid receptors on hippocampus, diminished activity to inhibit CRH
Generalized Anxiety Disorder, OCD, PTSD, Phobias, Social Phobia, Panic Disorder
new anxiety drugs target
CRH receptors
benzodiazepines
bind to receptor on GABA channels helps to keep open the channel and cause inhibition and reduce anxiety. (quick acting)
alcohol
can also bind to GABA receptor to help keep it open, some self-medicate for its effects
SSRIs
Bind to serotonin transporter proteins, without reuptake serotonin stays in synapse (acts slowly over weeks)
As serotonin levels are elevated for a long period of time, the nervous system adapts and reduces anxiety
Number of Glucocorticoid receptors in the hippocampus increases with elevated serotonin, better able to signal hypothalamus to reduce output of CRH and inhibiting the stress response.
affective/mood disorders
Major Depression:
Depression
Dysthymia
Bipolar Disorder:
Manic-depressive disorder
Mania
Hypomania
depression
feeling intense sadness, hopeless, or helpless, lasting for prolonged time (4-12 months), severe symptoms that interfere with daily life, often repeated episodes
dysthymia
persistent depressive disorder, not as severe as major depression but chronic, lose interest in daily life, lack productivity, low self-esteem, feel hopeless, irritable, worry a lot, difficulty sleeping or sleep for excessive amounts, lack energy
manic depressive disorder
alternating episodes of mania & depression
mania
abnormal elated mental state, feelings of euphoria, inflated self-esteem, talkativeness, desire to embark on goal-oriented activities, as well as lack of inhibition, impulsive, racing thoughts, diminished need for sleep, risk-taking, impaired judgment, and irritability
Equally common in women and men
monoamine hypothesis
Problems arise with the modulatory systems for serotonin, norepinephrine, and/or dopamine causing deficits in the CNS
In Early Studies, drugs that decreased monoamines caused severe depression (Reserpine-for Blood Pressure interferes with loading serotonin into vesicles)
Drugs that increased monoamines improved patient mood
Drug for Tuberculosis inhibits MAO (Monoamine Oxidase – enzyme that destroys serotonin and norepinephrine)
More complicated than just too little of serotonin and norepinephrine because antidepressant drugs that elevate levels do not work for several weeks.
neuromodulators
small group of neurons use one or more neurotransmitters to regulate other groups of neurons throughout the nervous system.
diathesis stress response
People may have genetic traits (diathesis), but their environmental influences (stressors) determine whether or not a disorder is produced
diathesis
stress
genetic predisposition for a disease; runs in families.
early childhood abuse or neglect, traumatic event, major loss, or biological trigger (disease or toxin) and other stresses in life are risk factors in the development of mood disorders
genetic vs non genetic
genetic: Severely depressed patients have increased CRH in CSF, elevated blood cortisol due to hyperactive HPA Axis (enlarged Adrenal Glands), a hippocampus with decreased number of glucocorticoid receptors and less grey matter, overactive Amygdalas.
non genetic: Tactile stimulation in early childhood increases glucocorticoid receptors
SSRI’s –
Selective serotonin reuptake inhibitors
SNRI’s –
Serotonin-norepinephrine reuptake inhibitors
NRI’s –
Norepinephrine reuptake inhibitors
NDRI’s –
Norepinephrine-dopamine reuptake inhibitors
MAOI’s
Monoamine oxidase inhibitors block MAO so they remain longer in the synapse
TCA’s –
Tricyclics block both serotonin and norepinephrine transporters but also other NT receptor sites, not selective, more side effects
Antidepressants increase
monoamine transmission leading to changes in gene expression in the neurons targeted by the monoamines, which are long-term. This includes desensitization of neurotransmitter receptors, leading to both therapeutic action and tolerance to side effects.
SSRI side effects
first choice today; nausea, nervousness, agitation, dizziness, reduced sexual desire, fatigue, drowsiness, insomnia, weight gain/loss, headaches, dry mouth, vomiting, or diarrhea.
tricyclics side effects
more side effects but still used when other treatments do not work; similar effects including dry nose, blurry vision, lowered gastrointestinal motility or constipation, urinary retention, cognitive and/or memory impairment, increased body temperature, sedation, and adverse cardiovascular effects
