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Mental Health > MH Patho > Flashcards

MH Patho Flashcards

1
Q

What is stress

A

perceived/anticiapted threat disrupting wellbeing/homeostasis - stimuli may be psychological, physical, or physiologial

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2
Q

What is the physiology of the stress response

A

Stress elicits rapid activation of autonomic nervous system (ANS); two main branches:
1. CNS&hypothalamus release corticotropin releasing hormone (CRH) –> stimulates sympathetic nervous system (SNS)
- sympathoneuronal (SN) releases norepinephrine
- sympatho-adrenomedullary (SAM) releases epinephrine
2. CRH stimltes HPA axis –> pituitary gland to make ACTH –> cortisol

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3
Q

what is general adaptation syndrome (GAS) –> 3 stages

A
  1. alarm stage (stress triggers HPA axis & SNS)
  2. resistance/adaptation stage (actions of cortisol, NE & E) “fight or flight”
  3. exhaustion stage –> allostatic overload due to chronic stress/unsuccessful adaptation –>leads to disorders (impaired immune system/heart failure, kindey failure, death)
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4
Q

What is the SNS

A

sympathetic nervous system

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5
Q

what chemical mediators does the SNS produce

A
  1. catecholamines : epinephrine (E) & norepinephrine (NE)
  2. proinflammatory cytokines
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6
Q

what is the parasympathetic system

A

balances SNS, has antiinflammatory effects and opposes sympathetic catecholamine responses (slows HR)

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7
Q

what effect does epi have on the body

A

stimulats alpha adrenergic response (fight or flight)
-bronchodilation (decrease BP), increase lypolysis, increase CO, decrease insulin, increase glucagon, increase glycogenolysys (increases blood sugar)

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8
Q

what effect does NE have on body

A

stimulates B adrenergic receptors
-increase BP, increase sweat glands, pupil dilation, piloerection, arterile smooth muscle contraction, neuropeptide Y

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9
Q

what effect does cortisol have on the body

A

hydrocortisone synthetic form, used as anti-inflammatory/immunosuppressive agent –> leads to resoluation and repair (if chronic production tolerance may develop leading to inflammation)

abn levels linked to insomnia, obesity, lipid abnormalities, HTN, DM, loss of bone density

cortisol has negative feedback effect on HPA, leads to decreased HPA response

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10
Q

what is allostatis

A

stability through change

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11
Q

what is allostatic overload

A

overaction of adaptive systems –> illness

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12
Q

what is the HPA

A

hypothalamic-pituitary-adrenal axis

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13
Q

what is ACTH

A

adrenocorticotrophic hormone

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14
Q

how is the HPA regulated

A

Hypothalamus secretes CRH –> pituitary releases ACTH –> adrenals secrete cortisol and catecholamines –> cortisol feedsback to pituitary & hypothalamus to terminate HPA response

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15
Q

what is CRH

A

corticotropin-releasing hormone

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16
Q

what are prenatal considerations of stress

A

offspring at higher risk for obesity, HTN, and behavioural issues related to brain alterations

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17
Q

what are childhood considerations of stress

A

decreased growth hormone, altered brain development, HTN, DM, cancer, somatic disorders, behavioural issues, circadian rhythm disruption (altered diurnal cortisol secretion)

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18
Q

what are aging considerations of stress

A

stress-age syndrome: neurohormonal and immune alterations that lead to lower adaptive reserve

may lead to alzheimer disease, limbic system/hypothalamus changes, increased catacholamines, decreased hormones, immunosuppression, inflammation, hypercoagulation of blood, free radical damage

19
Q

how is chronic stress related to depression

A

hypothalamic-pituitary adrenal system dysregulation

chronic HPA activation from stress leads to inflammation which is a risk factor for depression

20
Q

what is the relationship between cancer and stress

A

stress affects g antiviral response, dna repair, and other aspects of cell aging that increase cancer risk

stress leads to inflammation & angiogenesis

21
Q

what is broken heart syndrom

A

acute episode of mental stress has been linked to myocardial ischemia

22
Q

what are GI considerations of stress

A

gut-brain axis connects central and enteric NS, digestive disorders such is IBS coincide with mood disorders

dysbiosis caused by stress - increased gut permeability leads to bacteria leaking into circulation

23
Q

what are adiposity considerations of stress

A

chornic glutocorticoids (cortisol) leads to metabolic syndrom (increased BP, blood glucose, fat around waist, and cholesterol)
may lead to increased viseral fat, decreased bone mass, and inflammatory cytokine release leading to insulin resistance and DM

24
Q

what are PTSD/stress considerations

A

patients with PTSD may have high cortisol levels initially, but low over time as the body adapts to prevent deleterious effects of chronically high cortisol - glucocorticoid sensitivity may be increased and feedback to HPA altered

25
Q

what are 4 symptoms of PTSD

A

re-experiencing, avoidance, negative congnitions and mood, and arousal (insomia, hypervigilance)

26
Q

what are the 4 main types of ADHD

A
  1. predominantly inattentive
  2. predominantly hyperactive
  3. combined
  4. unspecified
27
Q

what neurotransmitters are thought to be involved in ADHD

A

Epi & NE

28
Q

what receptors in the brain are involved in ADHD

A

may be a defect in dopamine receptor D4 (DRD4) and over expression of dopamine transporter 1 (DAT-1)

29
Q

what are the functions of DRD4 and DAT-1

A

DRD4 - uses dopamine and NE to modulate response to environment
DAT-1 takes dopamine and NE into presynaptic nerve terminal

30
Q

what are clinical manifestations of ADHD

A

inattention, impulsivity, hyperactivity

31
Q

what is the diagnostic criteria for ADHD in adults

A

5 or more symptoms present for >6month in more than one setting and have been present since age 12

32
Q

what is the diagnostic criteria for ADHD in children

A

6 or more symptoms present for at least 6 months both at home and at school, behaviours not due to other comorbidity

33
Q

what medications are used for ADHD

A

diazepam (valium), lorazepam (Ativan), Alprazolam (Xanax)

*all are controlled substances

34
Q

what is the MOA for ADHD medications

A

depress CNS - reduce anxiety, induce muscle relaxation
potentiate GABA by amplifying actions of endogenous GABA (limit to how much CNS depression can take place unlike barbiturates)
high lipid solubility - crosses BBB

35
Q

what are AEs related to ADHD medications

A

CNS depression, anterograde amnesia, sleep driving/sleep disorder, paradoxical effects, resp depression, abuse

36
Q

what are some side effects of ADHD meds

A

constipation, dizziness, dry mouth, HA, NV

37
Q

are ADHD meds safe in pregnancy

A

because of high lipid solubility can cross placenta and enter breast milk –> contraindicated in pregnancy and BF

38
Q

what are some drug interactions with ADHD meds

A

very few, don’t take with other CNS depressants (barbituates, alcohol, opioids)

39
Q

what monitoring is required with ADHD meds

A

none, assess for therapeutic effect

40
Q

what are special considerations for ADHD meds

A

caution with OSA/snoring, substance use, COPD, geriatric, paediatrics (contraindicated in neonates), hepatic impairment, renal impairment

41
Q

explain withdrawal from benzodiazepines after short term use

A

withdrawal generally mild, may even go unnoticed (anxiety, insomnia, sweating, tremors, dizziness)

42
Q

explain withdrawal from benzodiazepines after long term use

A

risk of serious withdrawal syndrome (panic, paranoia, delirium, HTN, twitching, seizures)

43
Q

explain the process for d/c benzodiazepines

A

d/c gradually, slowly taper for several weeks/months. sub short half life med in if possible - do not stop abruptly - and monitor for withdrawal for 3 weeks post d/c

44
Q

why does extra caution need to be taken when prescribing benzos to older adults

A

long term use should be avoided due to minimal efficacy and possible harm (risk of cognitive impairment/delirium/falls, apnea, hypotension, bardycardia, cardiac arrest, polypharmacy interactions)

Mental Health (2 decks)

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