Class 6 Flashcards

1
Q

Catecholamines, name them + associated with

A

dopamine, norepinephrenine, epinephrenine

Energy, excitement, pleasure

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2
Q

Idolamines, name them + associated with

A

serotonin, melatonin

sleep, social affiliation, well-being

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3
Q

advanced monoamine hypothesis supposes that serotonin or norepinephrine concentrations in the brain are regulated by

A

MAO A activity

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4
Q

Monoamine hypothesis: severity of symptoms linked to

A

changes in the activity of monoamine transporters in specific brain regions

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5
Q

Other neurotransmitters involved

A

dysfunctional muscarinic acetylcholine system

glutamate is involved in neurotransmission, brain energy
metabolism, astrocyte function, neurotoxicity, neuroplasticity, and learning (increase)

Decrease in GABA

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6
Q

central to abnormalities in neurotransmission

A

balance of excitatory/inhibitory neurotransmission

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7
Q

hypercortisolism has

A

neurocytotoxic effects

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8
Q

manic episodes may be preceded by

increased concentrations of

A

adrenocorticotropic (ACTH) hormone and

cortisol

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9
Q

HPA axis: variations in pathway are genetic or environmental

A

environmental risk factors

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10
Q

Chronobiology

A

circadian rhythms abnormalities may play a role in

precipitating periodic episodes of depression and mania

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11
Q

melatonin secretion modulates the production of

A

thyrotropin and tuberalin hormone and induces synthesis of triiodothyronine (T3). excessive hypothalamic T3 may mediate mania, whereas insufficient hypothalamic T3 may cause depression

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12
Q

Neuroimaging

A

previous mild traumatic brain injury has been identified as a risk factor

disruption to cortico–striatal–limbic circuits: disconnect between emotional and executive functioning

enlargement of lateral and third ventricles after several manic episodes= more space, more fluid, less cortex, happens after several manic episodes

progressive decline in hippocampal, fusiform, and cerebellar gray matter density after repeated episodes

gray matter volume reductions in the prefrontal cortex

decrease volumes in hippocampus and thalamus

grey matter reductions occur in anterior limbic regions, which may be related to executive control and emotional
processing abnormalities

increased rates of deep white matter hyperintensities

excessive activation in brain regions associated with emotional regulation

going from cortex to limbic system is different

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13
Q

Neuroimmunity

A
 alterations in pro-inflammatory cytokines
and anti-inflammatory cytokines were
mania and depression
 changes tend to disappear in euthymia,
indicating that inflammation may be
associated with acute phases
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14
Q

Mania criteria

A
Specific Symptom
(4 out of 7 sxs for 1 week)
Feeling
1. elevated, expansive, or irritable mood 
Physical
2. decreased need for sleep
3. talkative/pressured speech
4. psychomotor agitation
Thinking
4. Increased goal-directed activity
5. flight of ideas/racing thoughts
6. distractibility
7. pleasurable, but risky behaviour 

Clinical Significant Distress
or
Impairment Occupational Social Other

Exclusions: subs, GMC

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15
Q

Hypomania criteria

A
Specific Symptom
(3/4 out of 7 sxs for 4 days)
Feeling
1. elevated, expansive, or
irritable mood
Physical
2. decreased need for sleep
3. talkative/pressured speech
4. psychomotor agitation
Cognitive/Thinking
4. Increased goal-directed activity
5. flight of ideas/racing thoughts
6. distractibility
7. pleasurable, but risky behaviour 

Uniequivocal change in functioning, observable by other
but
Not severe enough to cause impairment

Excusions: subs, GMC

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16
Q

Bipolar I

A
  • Manic Episode

- Major Depressive Episode

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17
Q

Bipolar II

A
  • Hypomanic Episode

- Major Depressive Episode

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18
Q

Cyclothymia

A
  • minimum of 2 years
  • Hypomanic symptoms
  • Depressive symptoms
  • symptoms present most of the time
  • no period of 2 months symptom free
  • no full episodes
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19
Q

Epidemiology

A

In Canada
 Bipolar I - 1%
 Bipolar II - 4%
 Depression is ranked the #1 cause of disability
in globally
 Burden is caused by early age of onset and years of potential full-life productivity lost

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20
Q

course

A

 Age of onset in teens with depression and/or irritability
 Diagnosed officially in 20s or 30s
 Longer delays in diagnosis if BPII
 Initial mood episodes associated with stressors, less so over time
 Manic episodes are more common at beginning of illness course
 Most cases, mania tends to diminish in severity and intensity over time
 Depressive episodes cause the most burden, particularly in BPII

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21
Q

Worse prognosis if associated with:

A
  • substance misuse/abuse/dependence
  • medical comorbidity
  • psychiatric comorbidity (personality, anxiety, PTSD)
  • family history of BP and suicide
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22
Q

Risk factors

A

Age: risk of decreases with age
Sex
 Depression, Bipolar II - F:M ratio = 2:1
 Bipolar I- F:M ratio = 1:1
Family psychiatric history:  Depression genetic (2 to 4-fold increasedrisk), Bipolar genetic (10-fold increased risk)
familial non-genetic – exposure to depressed parent, compromised parenting, neglect
Lack of social support
Stressful life events
Emotional coping: ruminating
Sleep-wake cycle disturbances
Personality style:
 Neuroticism:
 Greater problems adapting life difficulties/transitions
 High interpersonal dependence
Anxiety disorders or sx of it, SUD (cannabis increases chance of depression 2 fold and suicidal thinking and attempts 4 fold), personality disorders, PTSD (more common in BPII), suicide attempts

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23
Q

Protective factors

A

Married
working
higher income
higher level of education

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24
Q

Rx champix

A

promotes impulsivity

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25
Q

Bipolar/mania rating tools

A

 Mood Disorder Questionnaire (MDQ)
 self- report
 screening for mania/hypomania

 Young-Mania Rating scale (YMRS)
 clinician-rated
 once on medication

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26
Q

Medical Investigations, labs

A

Biochem: LFTs, creatinine, urea, lipid profile, egfr (liver +kidney)
 Urine: elderly - UTI (can become manic); young - beta-HCG; osmolality (li can cause diabetes insipidus)
 Endo: Vit D (low vit D = depression), thyroid profile, prolactin, as indicated – catecholamines
 Systems – CBC, ferritin, iron profile, vitamin D, bleeding times, platelets, B12, folate

27
Q

Imaging

A

if psychosis/head trauma, CT head

28
Q

If pain, labs

A

autoimmune markers, inflammatory markers

29
Q

Best mood stabilizer

A

Li

30
Q

Li

A

Effective in: manic episodes, prevention of mania and to a lesser degree depressive episodes
 Also an augmenting agent for unipolar depression
 Equal or better efficacy in bipolar disorder compared to valproate for manic, depressive, or mixed episodes
 well-established to prevent suicide in mood disorders (not the case for other mood stabilizers)

31
Q

Lithium – common side effects

A
 GI symptoms: dyspepsia, N/V, diarrhea, especially at the beginning
 Weight gain
 Hair loss: give zn and selenium
 Tremor
 Sedation
 Decreased cognition
 Ataxia
 Long-term adverse effects upon thyroid, kidneys (monitor regularly, lowest therapeutic dose)
Goes though the kidney
32
Q

Valproic Acid

A

 Effective in: acute mania, prevention of mania
 Does not treat acute bipolar depression
 May not prevent bipolar depression
 Could be more effective than lithium for rapid cycling and mixed episodes of mania

33
Q

Valproic Acid – mechanisms

A

 By inhibiting voltage-sensitive sodium channels (VSSCs) – and having less sodium passing into neurons therefore indirectly diminishing the release of glutamate – thus less excitatory neurotransmission
 By boosting the actions of GABA – thus more inhibitory neurotransmission
 By inhibiting, regulating, or activating various downstream signal transduction cascades – ultimately promoting neuroprotection and long-term plasticity

34
Q

Valproic Acid – side effects

A

 Hair loss, weight gain, sedation
Goes through the liver
 liver & pancreatic effects (monitor regularly)
 Female reproductive: amenorrhea, polycystic ovary syndrome, fetal toxicities, such as neural tube defects

35
Q

Carbamazepine

A

 Effective in: acute mania, prevention of mania
 Does not treat acute bipolar depression
 May not prevent bipolar depression

36
Q

Carbamazepine – mechanism

A

Blocking voltage-sensitive sodium channels (VSSCs) – perhaps at the alpha subunit of the channel

37
Q

Carbamazepine – side effects

A
  • Sedation
  • The potential to cause fetal toxicity such as neural tube defects
  • Induction of the cytochrome P450 (CYP) enzyme 3A4 – can result in the reduction of blood and brain levels of certain antipsychotics such as clozapine, quetiapine, ziprasidone, aripiprazole, and lurasidone
     Need to monitor blood counts (CBC, WBCs) due to suppressant effects upon the bone marrow
38
Q

Lamotrigine

A

 Effective in: acute bipolar depression and prevents bipolar depression
 Not as effective for acute mania
 Unclear if effective for mania prevention
Has an interaction with epical: double the does of lamotrigine

39
Q

Lamotrigine – mechanism

A

 May work by reducing the release of the excitatory neurotransmitter glutamate – not clear whether this action is secondary to blocking the activation of voltage-sensitive sodium channels (VSSCs) or to some additional synaptic action
start at 12,5 increase 2 weeks

40
Q

Lamotrigine – side effects

A

 Generally well tolerated, but propensity to cause rashes, including the life-threatening Stevens-Johnson
syndrome (toxic epidermal necrolysis)
 Start low, go slow

41
Q

Psychological Treatments- Principles

A

 Stress-diathesis model; all PT trials are combined with medication use
 Prevent relapse, promote social functioning
 Reduce symptoms, mood fluctuations
 Promote good coping, enhance medication compliance, promote family communication
 Efficacy has been shown in prevention of relapse mainly, therefore patients are not in acute phases of illness
 Therapists should be knowledgeable in bipolar disorder and pharmacological treatments

42
Q

Psychological Treatments- Types of Approaches

A
  1. Early warning
  2. Cognitive Behavioural Therapy (CBT)
  3. Psychoeducation
  4. Focused family therapy
  5. Interpersonal and social rhythm therapy (IPSRT)
43
Q

Psychological Treatments- Common factors

A

 Psychoeducation about illness
 Promote medication compliance
 Promote regular daily routine and sleep
 Monitor early warnings
 Develop strategies to prevent full episodes
 General coping strategies including problem solving

44
Q

Manic warning signs:

A

decreased need for sleep, increased activities, more sociable, racing thoughts

45
Q

Depression warning signs:

A

loss of interest, can’t get worries off their mind, interrupted sleep

46
Q

Interpersonal and social rhythm therapy (IPSRT)

A

 identify the effects of key problematic areas related
to: interpersonal conflicts, role transitions, grief and
loss, social skills
 links above to current symptoms, feelings states
and/or problems
 seeking to reduce symptoms by learning to cope
with or resolve these interpersonal problem areas
 seeking to improve the regularity of daily life in
order to minimize relapse.

47
Q

Psychoeducation

A

 illness awareness
 treatment compliance
 early detection of prodromal symptoms and relapse
 lifestyle regularity

48
Q

physical activity promotes

A

neurogenesis

49
Q

monoamine hypothesis now includes

A
the role of neurotransmitter receptors, transporters,
catabolizing enzymes (monoamine oxidase [MAO], and COMT), and other brain neurobiological systems
50
Q

Dopamine in mania, high or low

A

high

51
Q

When in mania, what could explain that the mood stabilizer is low even though they are compliant

A

pt is in high catabolic state

52
Q

Ach

A

main neurotransmitter in the parasympathetic system

53
Q

glutamate

A

excitatory transmitter, learning, neuroplasticity, astrocyte function

54
Q

too much glutamate

A

cellular death

55
Q

bipolar patients, they have lower level of melatonin when they’re euthimic true or false

A

true

56
Q

melatonin is not released in the presence of

A

light

57
Q

Order of depressive sx

A

physical sx, feelings, thinking

58
Q

How much physical activity to prevent depression

A

30 min 3 times or more per week

59
Q

Depression, what symptoms improve first

A

physical

60
Q

How much sleep needed

A

5 straight hours

61
Q

Levodopa

A

manic

62
Q

corticosteroids

A

manic or depressed

63
Q

Medical History bipolar

A
 Parkinson’s disease
 epilepsy
 diabetes
 migraine
 stroke
 lupus
 cancers
 Crohn’s disease
 chronic illnesses (pain, irritable bowel syndrome, fibromyalgia)