Brain Health 2 Flashcards

1
Q

panic disorder

A

recurring, seemingly unprovoked panic attacks and a persistent worry about having further attacks

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2
Q

agoraphobia

A

severe anxiety about being in situations where escape might be difficult or embarrassing
avoidance of situations irrationally perceived as threatening

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3
Q

obsessive compulsive disorder

A
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
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4
Q

generalized anxiety disorder

A

at least 6 months of persistent and excessive anxiety and worry

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5
Q

specific phobias

A

clinically significant anxiety provoked by exposure to a specific feared object or situation, often leading to avoidance behavior

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6
Q

social phobia

A

clinically significant anxiety provoked by exposure to certain types of social or performance situations, often leading to avoidance behavior

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7
Q

post traumatic stress disorder

A

the re-experiencing of an extremely traumatic event, accompanied by symptoms of increased arousal and the avoidance of stimuli associated with the trauma

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8
Q

what is the HPA axis and what does it control

A

hypothalamic-pituitary-adrenal axis

controls the humoral response and the stress response

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9
Q

HPA steps first half

A
eyes perceive scary stimulus, goes to visual cortex to amygdala
amygdala to hypothalamus
hypothalamus releases CRH
hypothalamus to pituitary
pituitary releases ACTH
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10
Q

HPA steps second half

A

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

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11
Q

Human behavior =

Brain =

A
Product of brain activity 
Product of mutually interacting factors that determines individualism
DNA
Experience 
Environmental Factors
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12
Q

mental illness

A

Diagnosable disorder of thought, mood, or behavior that causes distress or impaired functioning → has biological basis

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13
Q

external biological causes of mental illness

A

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

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14
Q

biological basis of fear/anxiety

A

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

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15
Q

HPA axis slides

A

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

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16
Q

Regulation of the HPA Axis by the Amygdala and Hippocampus

A
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
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17
Q

in anxiety disorder…

A

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

18
Q

new anxiety drugs target

A

CRH receptors

19
Q

benzodiazepines

A

bind to receptor on GABA channels helps to keep open the channel and cause inhibition and reduce anxiety. (quick acting)

20
Q

alcohol

A

can also bind to GABA receptor to help keep it open, some self-medicate for its effects

21
Q

SSRIs

A

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.

22
Q

affective/mood disorders

A

Major Depression:
Depression
Dysthymia

Bipolar Disorder:
Manic-depressive disorder
Mania
Hypomania

23
Q

depression

A

feeling intense sadness, hopeless, or helpless, lasting for prolonged time (4-12 months), severe symptoms that interfere with daily life, often repeated episodes

24
Q

dysthymia

A

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

25
Q

manic depressive disorder

A

alternating episodes of mania & depression

26
Q

mania

A

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

27
Q

monoamine hypothesis

A

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.

28
Q

neuromodulators

A

small group of neurons use one or more neurotransmitters to regulate other groups of neurons throughout the nervous system.

29
Q

diathesis stress response

A

People may have genetic traits (diathesis), but their environmental influences (stressors) determine whether or not a disorder is produced

30
Q

diathesis

stress

A

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

31
Q

genetic vs non genetic

A

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

32
Q

SSRI’s –

A

Selective serotonin reuptake inhibitors

33
Q

SNRI’s –

A

Serotonin-norepinephrine reuptake inhibitors

34
Q

NRI’s –

A

Norepinephrine reuptake inhibitors

35
Q

NDRI’s –

A

Norepinephrine-dopamine reuptake inhibitors

36
Q

MAOI’s

A

Monoamine oxidase inhibitors block MAO so they remain longer in the synapse

37
Q

TCA’s –

A

Tricyclics block both serotonin and norepinephrine transporters but also other NT receptor sites, not selective, more side effects

38
Q

Antidepressants increase

A

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.

39
Q

SSRI side effects

A

first choice today; nausea, nervousness, agitation, dizziness, reduced sexual desire, fatigue, drowsiness, insomnia, weight gain/loss, headaches, dry mouth, vomiting, or diarrhea.

40
Q

tricyclics side effects

A

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