Neurology class 2 Flashcards
norepinephrine/epinephrine
mainly excitatory; drives motivation
dopamine
mainly excitatory; reward and pleasure
serotonin
inhibitory; does not require enzyme for transport; balances mood
GABA
inhibitory; decreases cell activity
Glutamate
excitatory; memory and learning
substance P
excitatory; deals with synaptic communication
monoamines
dopamine, epinephrine, norepinephrine
- recycled in the synapse by monoamine oxidase
alzheimer’s disease
64% of all dementia
- cannot cure but treat with increasing ACh through cholinesterase inhibitors
cholinesterase inhibitors
decrease Ach breakdown
Rivastigmine, Galantamine
cholinesterase inhibitors
alzheimer’s pathophysiology
breakdown and recycling of amyloid proteins–> accumulation of amyloid deposits–> amyloid plaques which interfere with communication–> loss of neurons
Parkinsons
2nd most common form of dementia
- no cure but can treat with increasing dopamine
levodopa, Rotigotine
dopamine agonists
parkinson’s pathophysiology
destruction of dopamine receptors leading to reduced transmission in basal ganglia which filters extra and purposeful movement
hypothalamic SCN
generates hormones and is the “computer” of the brain
melatonin
secreted from pineal gland located in the epithalamus
tryptophan–> serotonin–> melatonin
sleep cycle
circadian rhythm input from hypothalamic SCN–> decreased RAS and cortical stimulation–> decreased excitatory neurotransmitter stimulation
REM sleep stage
“wakeful” vital signs but in very deep sleep
Insomnia
difficulty falling and staying asleep which can be caused by high cortisol
- often at least one ADL is altered alongside
Flurazepam (Dalmane), Temazepam (Restoril), Triazolam
benzodiazepines for insomnia
- will cause pupil dilation due to PNS block
Sonata, Ambien, Lunesta
non-benzodiazepines for insomnia
- bind with GABA but from different angle
will cause pupil constriction
opioids
will cause pupil dilation
stimulants
obstructive sleep apnea
has nothing to do with neurotransmitters it deals with collapse of airways; common in obese patients
- common in REM stage
- common due to increased pressure on diaphragm which decreases mobility
obstructive sleep apnea pathophysiology
pharynx collapse–> pharyngeal wall collapse–> tongue obstruction of oropharynx
cerebral apnea
deficit in the brain stem and respiratory centres
migraine
must occur for at least 15 days within a month for 3 months
- higher incidence in adult women due to estrogen levels
migraine pathophysiology
trigeminal nerve irritation–> inflammation within meningeal
migraine without aura
most common form of migraine
serotonin agonists
treat migraines to balance brain activity
triptans (sumatriptan, zolmitriptan)
serotonin agonists
botox as treatment for migraines
acts as an antiinflammatory to decrease neurotransmitter hyperstimulation
anxiety
intense fear due to SNS and HPA axis stimulation leading to S&S of anxiety
- women more affected but present in 12% of the population
excessive and uncontrollable worry with systemic symptoms and unable to modulate with present coping mechanisms
generalized anxiety
intense fear with systemic symptoms
- CNS involves major emotional centers (amygdala, hippocampus, prefrontal cortex)
- SNS stimulation
panic
benzodiazepines for anxiety
increase inhibitory neurotransmitter GABA
Alprazolam (Xanax), diazepam (Valium), Lorazepam (ativan), Midazolam (Versed)
benzodiazepines for anxiety
hallucinations
abnormalities of sensory perception
- perception without real time input
sensory block (hallucinations)
stored images replace the intel coming in
neuronal dysfunction (hallucinations)
hyperactivity or deficit creates dysfunction and images
delusions
abnormalities of thought
- false beliefs in facts and or personal status
psychosis
state of perceptive loss of reality
- hallucinations and delusions
schizophrenia
dysfunction of thoughts and language expression which is chronic
- cause is unknown but will show up on MRI
- dopamine excess
incomprehensible speech, disconnected thought process
disorganized behaviour of schizophrenia
hallucinations, delusions, paranoia, agitation
psychotic (positive) behaviour of schizophrenia
schizophrenia diagnosis
at least 2 S&S plus 2 other functional alterations
antipsychotics
target limbic system D2 receptors which deals with emotions; decrease hyperexcitation of the brain
D2 antagonism in basal ganglia cause issues with tongue movement, muscle rigidity, tremors, restlessness , and muscle spasms
Extrapyramidal side effects of antipsychotics
neuroleptic malignant syndrome
VS crisis characterized by hyperthermia, unstable BP, incontinence, and diaphoresis
schizoaffective disorder
schizophrenia accompanied with another disorder
‘typical’ antipsychotic drugs
high efficacy for ‘positive’ (psychotic) symptoms
phenothiazines and non-phenothiazines
‘typical’ antipsychotic drugs
chlorpromazine
type of phenothiazine (antipsychotic)
haloperidol
type of non-phenothiazine (antipsychotic)
olanzapine (zyprexa), quetiapine (seroquel), clozapine (clozaril), risperidone (risperdal)
‘atypical’ antipsychotic drugs
‘atypical’ antipsychotic drugs
high efficacy for ‘positive’ and negative symptoms and cause less sedation
depression
lack of serotonin and norepinephrine, may be accompanied by hallucination and delusions
** make sure to rule out hypothyroidism due to similar symptoms
SSRI’s
“ine” ; 1st line drugs that take 1-2 weeks to take effect
Fluoxetine (prozac), sertraline (zoloft), paroxetine (Paxil)
SSRI’s
SNRI (atypical antidepressants)
increase serotonin and norepinephrine
Mirtazapine (Remeron), Bupropion (Wellbutrin)
SNRI
tricyclic antidepressants
serotonin, norepinephrine, and dopamine reuptake inhibitors
Imipramine (Impril)
tricyclic antidepressants
MAO inhibitors
inhibit monoamine oxidase enzyme which increases neurotransmitter presence
ketamine
dissociative anesthetic; its receptors are glutamate, serotonin and opioid
- when used for anesthetic the dose is 10x lower
Esketamine
type of ketamine
Lithium
sodium channel blocker that increases serotonin and decreases sodium to decrease impulsivity and mood swings
- narrow TI, toxicity, slow onset, drug interactions
loss of sensation in a focused area of the body
- used for minor procedures such as sutures
local anesthesia
loss of sensation in a body region
- used in dental procedures
regional anesthesia
systemic; loss of consciousness and combines many drugs for an optimal effect
- used for major procedures such as abdominal surgery
general anesthesia
systemic; low level sedation to maintain VS without intubation
monitored anesthesia care (MAC)
sleepy, able to awaken, able to respond when prompted, maintain VS without assistance
conscious sedation
sedation of a patient for the purposes of a medical procedure/intervention
anesthesia
“sodium channel blockers”
- impede action potential so cell cannot depolarize leading to decreased sensory impulses to other cells
- work on efferent and afferent pathways
- lipophilic, cleared through circulation, hepatic metabolism, no BBB significance
local anesthetics
“caine”
- Prilocaine, Lidocaine, Bupivacaine, Ropivacaine, Cocaine
local anesthetics or “sodium channel blockers”
shortest acting local anesthetic
Lidocaine
longest acting local anesthetic
Bupivacaine
known to be systemic, very lipophilic, vasoconstriction at local level
cocaine
topical, infiltration, nerve block, epidural, spinal
local anesthetic routes
solarcaine
topical anesthetic
used as an adjunct in anesthesia
- localizes vasoconstriction which helps with bleeding control and increases the duration of the anesthetic
Epinephrine
used as an adjunct in anesthesia
- helps neutralize the pH of a tissue in case of a bacterial infection
sodium bicarbonate
location ensured by no CSF return in needle
- there will be a loss of sensation to the spinal nerves as the anesthetic bathes the nerves
- onset will be in 20-30 min and there will be a continuous infusion through an indwelling catheter
- dosage is higher than spinal route
epidural
location ensured by CSF return in needle drawback
- always injected below L2
- quick onset
spinal anesthetic route
very little side effects, can use small amounts due to its potency, analgesic
fentanyl
cause good analgesia without euphoric effects, has depressive symptomologies, good for patients with previous addictions
Dilaudid
“thane”; decrease action potentials, increase GABA
inhaled general anesthetics
nitrous oxide, halothane, isoflurane
inhaled general anesthetics
propofol (diprivan)
IV anesthetic
increase GABA and has a rapid onset of action as well as a short half life
- requires continuous infusion for effect and requires intubation as well as VS support
Propofol (Diprivan)
dissociative anesthetic that is also a CNS depressant
ketamine
block Ach binding at nicotinic receptors; “nium”
- no BBB penetration just PNS
- muscle paralysis including the diaphragm
- ideal for complex procedures
neuromuscular blocking agents
vecuronium, rocuronium, pancuronium
neuromuscular blocking agents
