Neuro Exam 1 Flashcards
laboratory tests for alcoholism
MCV elevation, high levels of GGT, high levels of liver enzymes, uric acid, triglycerides, ethyl glucuronide and ethyl sulfate (last 2 for ppl who need to get tested for work etc)
ethanol effects on GABA system
interaction with GABA-A receptor and facilitate of GABA transmission = sedative and anxiolytic effects & withdrawal
Wenicke’s encephalopathy symptoms
confusion, loss of muscle coordination, ataxia, let tremor, vision change, nystagmus, diplopia & eyelid drooping
Wernicke’s Syndrome treatment
-usually from severe deficiency of thymine
-admin of IV glucose to pts who are severely malnourished can exhaust their supply of thiamine worsening confusion
thiamine before glucose!
ethanol mechanism of action
-ethanol facilitates GABAergic transmission, GABA id an inhibitory NT
-ethanol blocks glutamate transmission
-glutamate is an excitatory NT
-ethanol results in the release of dopamine in the nucleus accumbens
Symptoms of Korsakoff syndrome
-late/end stage of chronic = irreversible brain damage, anterograde amnesia, loss of memory, confabulation, hallucinations, results from long standing Wernickes
Delirium tremens
-discorded consciousness, life threatening state = medical emergency!
-Hallmarks: hallucinations, disorientation, tachycardia, hypertension, low grade fever, agitation & diaphoresis
-sensorium clouding = pt needs to be hospitalized
Management/prophylaxis of alcohol withdrawal
1- thiamine 50-100mg daily
2- D5 and 0.45 NS (after they are loaded up with thiamine then can give glucose)
3- multivitamin
4-standing order for clonidine & benzos
Disulfiram use & SE
-causes the alcohol/acetyl dehy to build. up = when pts drinks they feel VERY sick
Side effects: drowsiness, headache, fatigue, rash, metallic or garlic-like after taste, impotence, hepatic failure, peripheral neuropathy, optic neuritis
Naltrexone use
-acts as a competitive agonist opioid receptor sites
Acamprosate
-effective in pts who can be trusted to take meds TID
-structurally similar to GABA, increases the activity of the GABA-ergic system
addiction
a primary, chronic, neurobiological diseases, with genetic, psychosocial and environment factors influencing its development and manifestations (5 c’s: chronicity, impaired control over drug use, compulsive use, continued use despite harm, craving)
drug abuse
maladaptive pattern of substance use characterized by repeated adverse consequences related to the repeated use of the substance
agonist
drugs that activate receptors on neurons
antagonist
opiate that binds to receptors but blocks them rather than activating them
partial agonist
drugs that bind to receptors, but not the same degree as full agonists –> ceiling effect
sensitization
increased response to a drug with repeated use, shifting dose response curve to the left: cocaine-induced movement, cataplexy and seizure
tolerance
a state of adaptation in which exposure to a drug induces changes that result in a diminution of one of more the drugs effected over time
-cross tolerance: tolerance to one drug leads to tolerance of other drugs in the same class
physiological dependence
body adapt to presence of drug. needs drugs on broad to maintain homeostasis, specific withdrawal symptoms can be produced by abrupt cessation, rapid dose reduction, decreasing blood level of a drug and/or administration of an antagonist
Withdrawal symptoms
behaviors displayed by a user when drug use ends, typically the opposite of the. drug effect. repeated self-administration: mesolimbic doapmine system, abused drugs all tend to activate this system & has 3 stages: pleasure, associative learning through classical conditioning, incentive salience: craving, get DA release by cues/context alone
creatinine normalize
(urine drug level)/(urine creatinine) x 100
-used to account for how dilute or concentrated the urine is
ethanol effects on the CNS
-facilitates GABAnergic transmission, GABA is an inhibitory NT
-blocks glutamate, glutamate = excitatory NT
-results in dopamine release in nucleus accumbens
-activates opiate peptide system
-blocks NMDA receptors (neuroadapatation & withdrawal)
BAC of 0.10-0.125
-sig impairment of motor coordination, illegal to drive
BAC of 0.13-0.15
(in the cerebellum) gross motor impairment & lack of physical control, blurred vision & major loss of balance, euphoria is reduced and dysphoria is beginning to appear
BAC of 0.25, 0.30 & > 0.40
-needs assistance in walking, total mental confusion
-loss of consciousness
-onset of coma, possible death due to respiratory arrest
-these are toxic levels of alcohol!
ethanol absorption
-lipid and protein delay absorption
-water & carbonation speed absorption
-gastric bypass procedures inc absorption
Capacity limited metabolism: *the rate of absorption not only effects the height of the peak, but also the size of the area under the curve
ethanol distribution
-volume of distribution = ~ total body water (males > females > obese)
-rapidly crosses BBB
-zero order metabolism via alcohol dehydrogenase
gender differences in ethanol distribution
-ethanol distributes to total body water & lean mass (women tend to have a small volume of distributing)
-women have less efficient pre-hepatic alcohol dehydrogenase = greater bioavailability
women have less efficient pre-hepatic alcohol dehydrogenase thus there will be greater bioavailability
ethanol distributes largely to total body water and lean mass thus women tend to have a smaller volume of absorption
how do you treat benzo OD?
-Flumazenil 0.2 mg/min up to 3 g
-CI with tricyclic (seizures) or dependent pts
-SEs: N/V & benzo withdrawal s/s
Barbituates
-have similar effects to EToH
-withdrawal can be life threatening: anxiety, N/V, postural hypotension, seizures, delirium, insomnia, hyperexia
-taper: change to longer acting barb & taper, sub with anticonvulsant
GHB/Xyrem
-C3
-used in tx of cataplexy & daytime sleepiness in pts with narcolepsy
-effects: amnesia (used as date rape), hypotonia
-toxicity: coma, seizures, respiratory depression, vomiting
-withdrawals: agitation, mental status changes, elevated BP, HR & tachycardia
what drug is used for opioid overdose?
-naloxone: if pt is unconscious & respiratory depressed
-competes with and displaces narcotics at opioid receptor site
what drugs are used for opioid withdrawal?
-methadone
-buprenorphine
-clonidine
-lofexidine
what drugs are used for opioid maintance?
-methadone
-buprenorphine
what drugs are used for opioid abstinence?
naltrexone
When is methadone used in regards to opioids?
-for detox or maintenance
1) suppresses signs & symptoms of opiate withdrawal
2) extinguish opiate craving
3) block the reinforcing effects of illicit opiates
Sublocade
-monthly injection (do NOT give IV or IM), has BBW for serious harm or death from IV admin
Naltrexone
-used for abstinence maintenance
-pt must be opiate free for 7-10 days!
Vivitrol (Naltrexone XR)
-opiate dependence, recently received opiate detox –> opiate free for at least 7 days
Exclusions: acute hepatic or liver failure, receiving opiate analgesics, w/ current opiate dependence, in acute opiate withdrawal, + urine screen, known allergic reaction to naltrexone
Dextromethorphan (DXM)
-antitussive, at high doses its like PCP and ketamine
Cocaine
-NE and DA re-uptake inhibitor
-effect: euphoria, alertness, mydriasis, sweats/chills, N/V, decreased fatigue, paranoia, aggression
-toxicity: cardiac arrest, MI, stroke, arrhythmia, seizures, hallucinations
-withdrawal: depression, fatigue, nightmares, sleep disturbances, increased appetite, bradyarrhythmia & tremor
-overdose = supportive, lorazepam, holdall, agents PRN cardio complications
amphetamines
-block reuptake of DA and NE, increase release of DAA and NE
-effects: decreased fatigue, alert, decreased appetite, inc activity and respiration, insomnia, anxiety, paranoia, meth mouth
-withdrawal: fatigue, depression, cognitive impairment
-overdose: supportive, haldol, lorazepam (if psychosis)
PCP
-DA, 5HT, NE reuptake inhibitor
effects: euphoria, delusion, hostility, hallucinations, emotional lability
-low dose: sedation, ataxia, nystagmus, slurred speech, paresthesia
-high dose: inc HR, BP, temp, diaphoresis, muscle rigidity, seizures & coma
Ketamine
-anesthetic, CIII, produces a cataleptic-like state in which the pt is dissociated from the surrounding environment by direct action on the cortex + limbic system, reduces poly-synaptic spinal reflexes
effects: increased BP, HR, hallucinations, vivid dreams, delirium, resp. depression, hypertonia, dystonia, seizure
LSD
-stimulate pre-synpatic 5HT1a and 1b + post-synpatic 5HT2
Marijuana
cannabinoid receptors, release dopamine
inhalants
glues, solvents, butane, gasoline etc –> rapidly absorbed via capillaries in the lungs, penetrate BBB
Krokodil
-homemade formulation of potent, short-acting opioid, desomorphine, derived from cocaine
-contains gasoline, lighter fluid, iodine, hydrochloric acid, red phosphorus
bath salts
-synthetic stimulants known as “cathinones”, belongs to phenyethalmine, enhance release and block reuptake and breakdown of NE, DA, 5HT
Synthetic cannabinoid
-analogs of naturally occuring chemicals found in mj (THC, CBD, CBN), cannibis like effects
Kratom
-legal plant product that acts as a stimulant at lower doses and opiate effects at higher doses
-can cause addiction, withdrawal, psychosis & death
-13x more potent than morphine
causes of non epileptic seizures
-extreme metabolic disruption, deficiency state or local effect of a brain tumor, withdrawal from sedative/hypnotic drugs including ethanol, infection, renal failure, hypoxic encephalopathy, febrile convulsions
non epileptic seizures (4 causes)
-metabolic
-toxic
-hemodynamic
-psychogenic
partial seizures
-begin at discrete + relatively limited foci; motor function w or w/o march
simple seizures
-spread limited; uncomplicated, affects only limited aspects of neural function, motor symptoms or sensory symptoms, consciousness + memory undisturbed
complex partial seizures
-alteration of consciousness follows initial simple seizure, typically appears confused or preoccupied, may exhibit automatisms (lip smacking, fumbling with clothes etc) –> 70% arise from focus in temporal lobe
absence seizures (petit mal seizures)
-minor impairment of neural function b/s of short duration of seizures, blank stare or other facial expression indicate impaired consciousness, 2-10 secs
–> disruption in intentional behavior, consciousness + memory but not posture, muscle tone or ongoing autonomic behavior (walking), can occur 100s times/day
Tonic-clonic seizures (grand mal)
–maximal seizure response of brain in which all brain systems can be recruited into paroxysmal discharge, may have 1-2 myclonic jerks upon waking on day of seizure (~50% have aura before they start)
Tonic-clonic seizures (tonic, clonic, terminal) phases
-tonic: 10-15 secs of muscle extension, bladder may empty, breathing stops & pupils unresponsive to light
-clonic: violent muscle spams, respiration resumes but ineffective (cyanosis)
-terminal: limp + quiet w/ normal breathing, may become conscious w/ no recollection of seizure
Status epilepticus: after finishing one seizure, starts another = medical emergency
signs of immediate medical attention
-seizure lasts longer than 10 secs or occurrence of second seizure
-difficulty in arousing at 10 min intervals
-complaints of difficulty with vision
-vomiting
-persistent headache after a rest period
-unconsciousness with failure to respond
-unequal size pupils or excessively dilated
which AEDs inc the clearance of estrogen and dec OC effectiveness
-phenobarbital
-phenytoin
-primidone
-carbamazepine
–> divalproex sodium does not effect OC but bad for tx
–> do NOT use Ocs with higher estrogen concentration = higher risk of stroke
Pregnancy & epilepsy- what a prego bish gotta do*
*-she should establish a pt provider relationship with experienced OBGYN & neurologist + do this before conception
*-not d/c her own anticonvulsant (seizures are a greater risk to fetus)
*-if she was treated with VA or carbamazepine (before she knew she was prego) inquire about amniocentesis
*-if she is treated w/ phenobarbital throughout her prego, neonatal phenobarbital withdrawal is likely but manageable
-diet should include folate & folate supps
**carbamazepine and VA –> neural tube defects
breastfeeding and epilepsy
Ethosuximide, zonisamide, clonazepam + diazepam are CI during breast feeding
levetiracetam
-go to drug used for all seizure types
-dose adjustment based on GFR
AEs: some weight gain & enhances CNS depressants
