Depression & ADHD Flashcards

1
Q

Diagnostics for Major Depressive Episode:

A
  • prolonged & cause SIGNIFICANT distress/dysfunction
  • incl. depressed mood or anhedonia
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2
Q

What are the common Fx’s of a Major Depressive Episode (MDE)?

A

Depressed most of the day, Anhedonia, Weight Change, Sleep Disturbance etc.

  • diagnosed when a change from baseline & sustained for 2 weeks or longer
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3
Q

What is the prevalence of major depression?

A

Yearly prevalence ~ 6-7%

Lifetime prevalence of about 16%, almost 1 in 6

leading cause of disability worldwide

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4
Q

What is the Neuropathology & Neuroimaging of Depression?

A
  • small reduction in hippocampal size
  • increased activation of the amygdala by (-) stimuli
  • reduced activation of the nucleus accumbens by rewarding stimuli (+ events)
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5
Q

How is the presentation of depression often misleading?

A
  • often complain of stomach upset, pain sensitivity, fatigue, fibromyalgia
  • anxiety/insomnia often co-exist (req BZDs/Z drugs)
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6
Q

What is the global Pt assessment for depression?

A
  • Medical - low thyroid, anemia, chronic pain, infections, electrolytes, liver, CV, epilepsy, PD’s, AD’s, Malignancy
  • Substance-related - EtOH, THC, Nicotine, Opiate, Stimulant
  • Drugs/Hormones
  • Stresses/Losses

MUST include Thyroid Function!! - hard to get depression to improve if this is low

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7
Q

Use of BZD’s?

A

may be useful to reduce distress, anxiety, insomnia - esp. early in Tx

do NOT really treat the illness

consider potential for dependence & non-adherence

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8
Q

Antidepressants

What do they target?

Why don’t they work fast?

Why take them when things are going better?

Can you become addicted?

A

take several weeks to work (3-6 ish)

can get relapse?

cannot get addicted to them

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9
Q

Can you use St. John’s Wort for Depression?

A
  • multiple active components which impact many NT’s/targets
  • effective for MILD to MODERATE depression
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10
Q

____ is a key cause of depression

A

NT dysfunction

  • altered communication b/t brain neurons & neuron tracts/systems
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11
Q

What are the 2 key potential sites for drug action?

A
  1. REUPTAKE into the nerve ending or UPTAKE into a glial cell
  2. Degradation
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12
Q

Antidepressants

Immediate effects vs Long-term effects

A

Immediate effects:
- enhance “impact” or signalling of NT across synapse (esp. 5HT, NE, & DA)

  • IMMEDIATE BENEFITS UNLIKELY, SE’s ARE LIKELY

Over 2-4 weeks & beyond:
- sustained enhanced signalling
- DO NOT CAUSE ADDICTION, DEPENDENCY

Long-term admin is NEEDED for FULL & OPTIMAL BENEFITS

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13
Q

Ketamine for Depression?

A

lower dose of IV may produce Antidepressant effects within 4hrs

how? NO SPECIFIC EFFECTS ON NTs

RAPID effects on G proteins (like a flood of NT)

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14
Q

Try use something that targets more than 1 NT b/c…

A

if any of these are under-preforming, it can affect there effects

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15
Q

What is consistent with better outcomes?

A
  • access to supports
  • adherence to tx
  • a history of “more rapid” response
  • lower life stressors are consistent with better outcomes
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16
Q

If we don’t treat depression, ppl tend to…

A

get better

17
Q

What is the Pharmacist’s role?

A
  • Adherence
  • Education
  • Support & adverse effect reduction/management
18
Q

Who is susceptible/vulnerable to depression?

A
  • genetics
  • pyscho-social elements like feeling connected, feeling valued & supported
  • life events & stressors, socio-economic factors
  • overall physical/medical health
  • out “psych immune system”
19
Q

ADHD main Sx

A
  • inattention
  • distractibility
  • impulsivity
  • hyperactivity
20
Q

How many months are req’d for diagnose?

A

6 months (req’s thorough assessment)

21
Q

What is seen with ppl with ADHD?

A
  • more injuries
  • lower grades
  • worse driving record
  • higher risk of drug abuse
  • more antisocial
  • lower job status & performance

COMORBITIES are common

22
Q

What are the ADHD symptoms that are usually mixed?

A

Inattentive cluster
- distractibility
- forgetfulness
- poor organization
- lack persitence
- mistake-prone
- work avoidant

Hyperactive cluster
- fidgetiness
- intrusiveness
- restlessness
- noisiness
- talkativeness
- inappropriate activity

23
Q

What is the ADHD course look like?

A

variable

  • onset by 12 yoa, but usually earlier
  • hyperkinesis improves 1st, inattention spectrum is last & least to remit
  • (+) family Hx & comorbid disorders
24
Q

What predominates in adults?

A

Sx often move away from the Hyperactive domains
- DISTRACTIBILITY & INATTENTION may predominate in adults

25
Q

What is the etiology of ADHD?

A

multifactoral
- genetics!!!! (~80%)
- right-sided hypofrontality
- Locus Ceruleus “underperforms” (OPPOSITE FROM ANXIETY)
- more evident once they start school

26
Q

What is the neuropathology & neuroimaging of ADHD?

A
  • small increase in cerebrum growth at age 1-3 yoa
  • reduced #’s of cerebellar Purkinje neurons
  • reduced cell size & increased cell density in the limbic areas of the brain
27
Q

What are the risk factors of ADHD?

A
  • high risk in 1st degree relatives
  • risk increases with diff situations during pregnancy
  • D4 allele abnormalities

= response inhibition &/or arousal regulation deficits!

28
Q

What is the multimodal approach for ADHD?

A
  • behavioural - structure, checklists, attainable goals
  • avoiding triggers, if known
  • chiropractic approach
  • use combo Tx DRUGS WITHOUT SUPPORT = LOW SUCCESS RATE
29
Q

What are the Tx goals for ADHD?

A
  • Collaborative: Support System & School
30
Q

What are the ADHD deficits?

A
  • inhibition of the ability to: control behaviour, resist distractions, maintain an awareness of space & time
  • arousal dysregulation - leads to insufficient alertness, often alternating with overarousal
31
Q

What are the neurochemical targets for ADHD?

A
  • underperformance of DOPAMINERGIC & NORADRENERGIC tracts is consistent with the deficits seen in ADHD
  • STIMULANTS, which increase BOTH of these systems, are considered 1st line Tx
  • the improvement in “gating” ability can improve behaviour control, executive function & regulate arousal
32
Q

What are ADHD’s stimulant targets?

A
  • to SELECT restraint & to mentally FOCUS
  • regulated arousal = IMPROVED PERFORMANCE
  • increased control = reduced hyperactivity & distractibility, &/or aggression
33
Q

What psychostimulants could be used?

A

Methylphenidate, Amphetamines

ALL block NE & DA reuptake

  • INCREAED NE/DA ACTIVITY in Locus Ceruleus improves attention, ability to FOCUS or SELECT
  • Amphetamines also promote DA & NE release from presynaptic neurons
34
Q

What are the adverse effects of stimulants?

A
  • may decrease appetite
  • may increase BP, anxiety, irritability, difficulty falling asleep, stomach complaints, headache

etc.

35
Q

What is recommended in terms of ADHD medication?

A

drug holidays
- to reassess tx/minimize growth effects