Exam 2 Concepts Flashcards
dark outer ring of the brain which is Latin for “bark”
cortex, roughly the size of a pillow case, which is responsible for human intellect and folded
lobes of the brain (4) and their function
- frontal: executive function
- parietal: sensory information, especially tactile (pressure, touch, pain)
- temporal: language and memory
- occipital: visualization
mental disorders in which the frontal lobe is at play
substance abuse
ADHD
limbic system function
controls learning, memory, emotions, and basic drives; hippocampus (memory), hypothalamus (homeostasis), and amygdala (emotion) all part of
how many neurons do we have in our brains?
86 billion and none of them touch
neurotransmitters (NTs) function, creation, and storage
NTs are signaling chemicals which the cell body of the nueron creates and the axon terminal stores within small vesicles
approximately 50 different types
action potential
an electrical charge which travels down the axon between cells of the myelin sheath and causes the release of NTs into the synapse
monoamines (3)
- Dopamine (DA)
- Norepinephrine (NE)
- Serotonin (5HT)
dopamine (DA)
NT which regulates mood, attention, energy, PLEASURE, MOTIVATION, and MUSCLE movements
ex. meds used to increase in clients with depression or ADHD
norepinephrine (NE)
NT involved in mood, attention, energy, and the FIGHT OR FLIGHT response
excessive amounts can cause anxiety or aggitation
ex. meds often used to increase in clients with depression or ADHD
serotonin (5HT)
NT which regulates mood, anxiety, SEXUAL DESIRE, and APPETITE
glutamate
main excitatory NT
“gas pedal”
GABA
main inhibitor NT
“brake pedal”
used in several meds to reduce anxiety, prevent seizures, and induce sleep
acetylcholine
NT which aids in regulation of attention and MEMORY
ex. often increased in pt’s w/Alzheimer’s dz
termination of a neuronal signal
- diffusion
- enzymatic degradation
- reuptake
NT diffusion
NTs float away from the synapse into the cerebrospinal fluid where they cannot activate postsynaptic receptors
NT enzymatic degradation
NTs broken apart by enzymes which end in “-ase”
NT reuptake
presynaptic terminal “pumps” suck NTs back into presynaptic terminal to be stored for future use
functions of psych medications (3)
change release of NTs
change enzymatic regulation
block reuptake
monoamine oxidase inhibitors (MAOIs)
prescribed for major depression, but usually not the first choice
think food AND drug interactions
MAOI food interactions
must AVOID foods w/tyramine (aged/fermented foods)
ex. cheeses, aged/processed meats, anything pickled, overripe fruit
MAOI drug interactions
pts must avoid drugs which increase monoamine NT levels
ex. other antidepressants, cold meds, meperidine (pain med), triptans (migraine meds)
MAOI mechanism of action
block monoamine oxidase which breaks down all three monoamines (DA, NE, 5HT) which increases their levels in the brain’s synapses
MAOI adverse effects
hypertensive crisis: tyramine or NE levels too high –> increased BP
serotonin syndrome: 5HT too high –> altered mental state, fever, sweating, clonus (involuntary rhythmic muscle contraction…foot test)
orthostatic hypotension
tricyclic antidepressants (TCAs)
drugs which help treat major depression, neuropathic pain, and anxiety disorders
ex. diabetes neuropathic pain tx
think LESS selective than SNRIs
TCA mechanism of action
block NE and 5HT REUPTAKE pumps which increases NE and 5HT levels in synapses
TCA adverse effects
anti-cholinergic: block muscarinic cholinergic receptors –> can’t see, spit, pee, sh*t
cardiotoxicity: fatal cardiac dysrhythmias w/overdose; children and pt w/suicidal ideation at risk
orthostatic hypotension
selective serotonin reuptake inhibitors (SSRIs)
first line of drugs for depression and may also be used for anxiety
SSRI mechanism of action
serotonin reuptake pumps blocked which increases 5HT
SSRI adverse effects (5)
“5 s’s”
- S tomach trouble
- S lowed metabolism (weight gain)
- S exual dysfunction
- S uicidal ideation
- S edating (EXCEPT fluoxitine)
serotonin norepinephrin reuptake inhibitors (SNRIs)
prescribed for major depression; duloxetine for neuropathic pain and venlafaxine for anxiety disorders.
SNRIs mechanism of action
blocked reuptake of NE and 5HT; MORE selective than TCAs
SNRI adverse effects
similar to SSRIs plus HTN, especially if dose is high
bupropion
prescribed for depression, smoking cessation, and ADHD
inhibits NO and DA reuptake (NE 5HT effect!!!–>no weight gain)
trazadone
prescribed for depression, but mainly used for insomnia
weak SRI w/ strong sedative and anticholinergic effects
important note about anti-depressants
takes 2-3 weeks for them to kick into action
black box warning for suicidal thoughts, especially pts <18yo
mood stabilizer challenges
treating from above and below
medication adherence, esp w/mania
self-medication w/other substances
mood stabilizer medications
lithium
anti-epileptic
atypical anti-psychotics
lithium benefits and difficulty
pro: highly effective, lowers suicide risk
con: NARROW therapeutic index of 1.5mEq/L
signs of lithium toxicity
A taxia
C oarse tremors
N ausea/vomiting
E ars ringing “tinnitus”
HOLD the drug and call provider
client teaching w/lithium
take w/food to prevent GI upset
maintain fluid and salt intake
avoid strenuous exercise
knows signs of toxicity
normal side effects of lithium
mild nausea/diarrhea
fine hand tremors
polyuria/polydipsia (frequent urination and thirst)
weight gain
anti-anxiety “anxiolytic” medications
benzodiazepines buspirone anti-depressants beta blockers certain anti-histamines
uses of benzodiazepines
anxiety insomnia muscle spasms seizures alcohol w/drawal
benzodiazepine mechanism of action
increase GABA activity “break pedal” which decreases neuronal firing, similar to alcohol
EXTREMELY addictive d/t rapid onset and short half life
benzodiazepine side effects
ataxia
sedation
impaired memory
benzodiazepine precautions
hx of drug abuse
liver dz
elderly d/t possible fall risk
pt must be weaned off benzos after long term use
buspirone mechanism of action
not entirely understood, but binds strongly to 5HT and loosely to DA
benefits and difficulty w/buspirone
pros: no abuse potential, not CNS depressant, no major w/drawal sx
con: long period of onset (weeks)
buspirone food interactions
must AVOID grapefruit juice b/c it is a cyp inhibitor which increases drug levels in the blood–> toxicity
anti-psychotic medications
FGAs “typical”
SGAs “atypical”
uses of FGAs
schizophrenia
aggitation/aggression
nausea/vomiting
intractable hiccups
signs of schizophrenia
"4 D's" D istress D anger D eviant D ysfunction
schizophrenia symptoms
positive: hallucinations, delusions, disorganized speech, bizarre behavior
negative: flat affect, alogia (absence of thought), avolition (lack of motivation), anhedonia (no pleasure), social isolation
FGA mechanism of action
block all dopamine receptors to reduce dopamine activity in the brain
dopamine pathways (4)
mesolimbic: positive sx
mesocortical: negative sx
nigrostriatal: extrapyramidal sx
tuberoinfundibular: endocrine issues
ex. gynecomastia, galactorrhea, amenorrhea
FGA side effects
anticholinergic EPS orthostatic hypotension sedation neuroendocrine photosensitivity
extrapyramidal symptoms d/t FGA
acute dystonia
akathisia
parkinsonism
tardive dyskinesia
neuroleptic malignant syndrome
F ever E levated WBCs and CPK V ital signs unstable E ncephalopathy R igidity
extremely fatal
uses of SGAs
schizophrenia
bipolar disorder
late stage dementia w/psychotic features
SGA mechanism of action
block all dopamine AND serotonin receptors to reduce dopamine activity in the brain in areas w/too much and increases dopamine in areas w/too little
SGA benefit and difficulties
pro: lower extrapyramidal sx
cons: metabolic syndrome, expensive (2-3 times more so than FGAs) while equally effective
metabolic syndrome
may lead to diabetes
central obesity, HTN, high blood sugar, dyslipidemia (bad cholesterol)
mainly caused by clozapine (also causes destrcution of WBCs) and olanzapine
uses of CNS stimulants
ADHD
narcolepsy
CNS stimulants mechanism of action
block reuptake of NE and DA to increase levels at the synapses to increase executive function
CNS stimulant side effects
A ddiction/abuse
A norexia
A rrhythmias
A wake at night (insomnia)
*do NOT combine w/alcohol–>increased BPx2
atomoxetine benefits and risks
pros: NE reuptake inhibitor ONLY, low abuse potential
cons: long period of onset, increased risk of suicide, weight loss, liver toxicity
* not as effective as other CNS stimulants, but option fo pts w/hx of abuse
alcohol cessation medication uses
to help facilitate withdrawal
maintain abstinence
alcohol withdrawal
w/in hrs of last drink: INCREASE all vital signs hallucination illusion N/V seizures tremors
d/t brain compensation for constant GABA increase–> overstimulation w/glutamate
delirium tremens
rare, 2-3 days after last drink: severe disorientation hallucinations severe HTN cardiac dysrhythmias
seizure precautions
pad bedrails
have O2 ready
have suction regulator in case pt begins vomiting; prevent aspiration
disulfiram
causes N/V, sweating, hypotension, headache, palpations w/ANY alcohol ingestion to decrease alcohol temptation
must avoid hidden alcohol in sauces, cough syrup, etc
contraindicated for pts w/CV issues
naltrexone
opioid antagonist which reduces the pleasure derived from alcohol
reduced cravings, reduced buzz
opioid toxicity
C oma
P inpoint pupils
R espiratory depression !!!!
naloxone
powerful opioid antagonist which reverse opioid toxicity
short half life, pain/withdrawal
MUST monitor pt, usually given multiple doses
opioid withdrawal sx
N/V/D yawning rhinorrhea sweating irritability tremor goosebumps muscle spasms/kicking movements "kicking the habit"
methadone
opioid agonist
doses gradually reduced to aid w/withdrawal sx
buprenorphine
PARTIAL opioid agonist
doses gradually reduced to aid w/withdrawal sx
nicotine addiction
HIGHLY lipid soluble so it reaches brain instantaneously and binds to nicotinic N acetylcholine receptors
nicotine N receptors
CV: increased BP and cardiac work
GI: increase motility
CNS: increased alertness, memory, cognition, decreased appetite, pleasure activated
nicotine withdrawal
begins w/in 24h and can last months
abrupt discontinuation best tolerated
cravings, irritability, insomnia, impaired concentration, weight gain
nicotine patches
slower, steadier release of nicotine ONLY which is not carcinogenic itself
CAUTION: increased absorption w/inflammed skin, open wounds, heating pad
varenicline
partial nicotinic agonist to decrease reward of nicotine
side effects: N, mood changes, suicidal ideation!!
activated charcoal mechanism of action
binds to certain drugs to prevent absorption of the drug and allow them to be excreted
lipid soluble drugs such as TCAs, benzos, opioids, NSAIDs, antihistamines, etc
activated charcoal administration
pt must be awake and alert to avoid aspiration
give anti-nausea beforehand !!
mix in 6-8oz water can be w/juice or chocolate to improve taste
NEVER milk
*must be taken w/in 1 hr of drug ingestion
