MH Patho Flashcards
What is stress
perceived/anticiapted threat disrupting wellbeing/homeostasis - stimuli may be psychological, physical, or physiologial
What is the physiology of the stress response
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
what is general adaptation syndrome (GAS) –> 3 stages
- alarm stage (stress triggers HPA axis & SNS)
- resistance/adaptation stage (actions of cortisol, NE & E) “fight or flight”
- exhaustion stage –> allostatic overload due to chronic stress/unsuccessful adaptation –>leads to disorders (impaired immune system/heart failure, kindey failure, death)
What is the SNS
sympathetic nervous system
what chemical mediators does the SNS produce
- catecholamines : epinephrine (E) & norepinephrine (NE)
- proinflammatory cytokines
what is the parasympathetic system
balances SNS, has antiinflammatory effects and opposes sympathetic catecholamine responses (slows HR)
what effect does epi have on the body
stimulats alpha adrenergic response (fight or flight)
-bronchodilation (decrease BP), increase lypolysis, increase CO, decrease insulin, increase glucagon, increase glycogenolysys (increases blood sugar)
what effect does NE have on body
stimulates B adrenergic receptors
-increase BP, increase sweat glands, pupil dilation, piloerection, arterile smooth muscle contraction, neuropeptide Y
what effect does cortisol have on the body
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
what is allostatis
stability through change
what is allostatic overload
overaction of adaptive systems –> illness
what is the HPA
hypothalamic-pituitary-adrenal axis
what is ACTH
adrenocorticotrophic hormone
how is the HPA regulated
Hypothalamus secretes CRH –> pituitary releases ACTH –> adrenals secrete cortisol and catecholamines –> cortisol feedsback to pituitary & hypothalamus to terminate HPA response
what is CRH
corticotropin-releasing hormone
what are prenatal considerations of stress
offspring at higher risk for obesity, HTN, and behavioural issues related to brain alterations
what are childhood considerations of stress
decreased growth hormone, altered brain development, HTN, DM, cancer, somatic disorders, behavioural issues, circadian rhythm disruption (altered diurnal cortisol secretion)
what are aging considerations of stress
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
how is chronic stress related to depression
hypothalamic-pituitary adrenal system dysregulation
chronic HPA activation from stress leads to inflammation which is a risk factor for depression
what is the relationship between cancer and stress
stress affects g antiviral response, dna repair, and other aspects of cell aging that increase cancer risk
stress leads to inflammation & angiogenesis
what is broken heart syndrom
acute episode of mental stress has been linked to myocardial ischemia
what are GI considerations of stress
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
what are adiposity considerations of stress
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
what are PTSD/stress considerations
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
what are 4 symptoms of PTSD
re-experiencing, avoidance, negative congnitions and mood, and arousal (insomia, hypervigilance)
what are the 4 main types of ADHD
- predominantly inattentive
- predominantly hyperactive
- combined
- unspecified
what neurotransmitters are thought to be involved in ADHD
Epi & NE
what receptors in the brain are involved in ADHD
may be a defect in dopamine receptor D4 (DRD4) and over expression of dopamine transporter 1 (DAT-1)
what are the functions of DRD4 and DAT-1
DRD4 - uses dopamine and NE to modulate response to environment
DAT-1 takes dopamine and NE into presynaptic nerve terminal
what are clinical manifestations of ADHD
inattention, impulsivity, hyperactivity
what is the diagnostic criteria for ADHD in adults
5 or more symptoms present for >6month in more than one setting and have been present since age 12
what is the diagnostic criteria for ADHD in children
6 or more symptoms present for at least 6 months both at home and at school, behaviours not due to other comorbidity
what medications are used for ADHD
diazepam (valium), lorazepam (Ativan), Alprazolam (Xanax)
*all are controlled substances
what is the MOA for ADHD medications
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
what are AEs related to ADHD medications
CNS depression, anterograde amnesia, sleep driving/sleep disorder, paradoxical effects, resp depression, abuse
what are some side effects of ADHD meds
constipation, dizziness, dry mouth, HA, NV
are ADHD meds safe in pregnancy
because of high lipid solubility can cross placenta and enter breast milk –> contraindicated in pregnancy and BF
what are some drug interactions with ADHD meds
very few, don’t take with other CNS depressants (barbituates, alcohol, opioids)
what monitoring is required with ADHD meds
none, assess for therapeutic effect
what are special considerations for ADHD meds
caution with OSA/snoring, substance use, COPD, geriatric, paediatrics (contraindicated in neonates), hepatic impairment, renal impairment
explain withdrawal from benzodiazepines after short term use
withdrawal generally mild, may even go unnoticed (anxiety, insomnia, sweating, tremors, dizziness)
explain withdrawal from benzodiazepines after long term use
risk of serious withdrawal syndrome (panic, paranoia, delirium, HTN, twitching, seizures)
explain the process for d/c benzodiazepines
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
why does extra caution need to be taken when prescribing benzos to older adults
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)
