• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/90

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

90 Cards in this Set

  • Front
  • Back
Reduction of anxiety
Sedation
A drug that reduces anxiety, a sedative
Anxiolytic
Induction of sleep
Hypnosis
A reduction in drug effect requiring an increase in dosage to maintain the same response
Tolerance
Removal of drug envokes unpleasant symptoms and opposite effects of drug
Physiologic dependence
A drug taker feels compelled to use the drug and suffers anxiety when separated from the drug
Psychologic dependence
Loss of consciousness with absence of pain response
Anesthesia
Extremely deep anesthesia or depression of brian activity; precursor to respiratory and circulatory failure
Coma
Highest lipid solubility and enters CNS rapidly
Thiopental
Can be used as induction agent in anesthesia, rapidly enters CNS
Thiopental
These drugs undergo extrahepatic conjugation and do not form active metabolites
Lorazepam and oxazepam
Actively metabolized via oxidation at the C5 position
Barbiturates
Only barbiturates that is excreted unchanged via the urine
phenobarbital
Active metabolite of chloral hydrate
trichloroethanol
Reason for zolpidem's short duration of action
Rapid metabolism by the liver
Rapid hepatic metabolism via aldehyde oxidase and P450
Zaleplon
The duration of action of CNS hypnotics ranges few hours to 30 hours ( e.g. list)
zaleplon<zolpidem=triazolam<chloral hydrate
30 hours= chloridiazepoxide, clorazepate, diazepam, phenobarbital
Fast IPSP's are blocked by
GABAa receptor antagonist
Slow IPSP's are blocked by
GABAb receptor antagonist
Primary neurotransmistter mediating IPSP in brain and spinal nuerons
GABA
GABAa receptor activation opens _____
chloride ion channels
GABAb are coupled to G-proteins and activation opens ______ and closes _______
potassium channels
Calcium channels
Glycine receptors are more numerous in
Spine
Increases the frequency of GABA-mediated chloride ion channel opening
Benzodiazepines
An antagonist of BZ receptors and reverses the affects of benzos
Flumazenil
This drug depresses neuronal activity in the midbrain reticular formation prolonging the inhibitory effects of GABA and Glycine
Barbiturates
Interacts with 5HT1 subclass of serotonin receptors but MOA unknown
Buspirone
Exert their effects via BZ receptor but are not BZ's
Zolpidem
Zaleplon
A selective anxiolytic with minimal depressant effects
Buspirone
Anterograde amnesia is more likely with
BZ's
This BZ produces anesthesia
Midazolam
Drug used in high doses causes muscle relaxation. used in cerebral palsy
Diazpem
Selective anticonvulsant action without sedation
Phenobarbital
Clonazepam
Side effects of high doses of sedative-hypnotics
Respiratory arrest, hypotension, CV collapse, depression of medullary center
Only sedative that does not cause dependence
Buspirone
BZ's used for panic attacks and phobia disorders
Alprazolam and clonazepam
Drug used in generalized anxiety disorder + hx of drug abuse
Buspirone
BZ's used for management of sleep disorders and primary insomnia
Estalozam, Flurazepam, Traizolam
Used for the induction of anesthesia
Thiopental
Longer acting drugs used in the management of withdrawal states for ethanol and sedative-hypnotics
Chloradeazpoxide
Diazepam
Cognitive impairment, decreased psyhcomotor skills, and unwanted daytime sedation
AE of Diazepam Flurazepam

B/c of long-lasting active metabolites
What drugs should be avoided when using sedation-hypnotics?
IE Generally speaking
Alcohol
Anithistamines
Antipsychotics
Opioid
TCA
These sedation-hypnotics induce the formation of liver microsomal enzymes
Barbiturates and Carbamates
May displace coumarins from plasma proteins and increase anticouagulants
Chloral hydrate
Precipitate acute intermittent porphyria
Barbiturates
Used at high doses called "date rape" drug
BZ's
Account for low to moderate metabolism of Alcohol ingestion
Alcohol Dehydrogenase ADH
Reason for zero order kinetics in alcohol ingestion
Alcohol dehydrogenase

Runs out of NAD+
ADH converts alcohol to
Acetaldhyde
Induction of this system is thought to cause tolerance in alcohol ingestion
MEOS
Acetaldehyde is metabolized to______ via ______
Acetate

Acetaldehyde dehydrogenase
Account for low to moderate metabolism of Alcohol ingestion
Alcohol Dehydrogenase ADH
Reason for zero order kinetics in alcohol ingestion
Alcohol dehydrogenase

Runs out of NAD+
ADH converts alcohol to
Acetaldhyde
Induction of this system is thought to cause tolerance in alcohol ingestion
MEOS
Acetaldehyde is metabolized to______ via ______
Acetate

Acetaldehyde dehydrogenase
Account for low to moderate metabolism of Alcohol ingestion
Alcohol Dehydrogenase ADH
Reason for zero order kinetics in alcohol ingestion
Alcohol dehydrogenase

Runs out of NAD+
ADH converts alcohol to
Acetaldhyde
Inhibits aldehyde dehydrogenase
Disulfiram
Others: Metronidazole, oral hypoglycemics, cephalosporins
The MEOS system uses ______ for the oxidation of alcohol
NADPH and O2
Impairment of driving occurs at
60mg/dl and 80mg/dl
Levels greater than ______ can lead to loss of consciousness, anesthesia, and coma
300mg/dl
Alcohol levels that are considered lethal
> 500 mg/dl
Although the CNS effects of ethanol are not known, the MOA is probably thru
GABAa action receptors
And glutamate inhibition
How does alcohol ingestion lead to depress heart rate and hypothermia
Relaxes vascular smooth muscle
NAD depletion leads to
Reduced gluconeogenesis
Hypoglycemia
Fat accumulation
The most common neurologic abnormality
Peripheral Neuropahty
Syndrome defined as ataxia, confusion, and paralysis of extraocular muscles
Wernicke-Korsakoff syndrome
Syndrome caused by thiamine deficiency
Wernicke-Korsakoff
The reason chronic ethnaol ingestion causes gynecomastia, testicular atrophy, and slat retention
Altered metabolism of steroids in liver
Excessive use causes hypertension, anemia, and MI
Chronic ethanol ingestion
A common neoplasia incidence is increased in chronic ethanol ingestion
Breast carcinoma
Used to protect against CNS effects in chronic alocholics
thiamine
Syndrome caused by thiamine deficiency
Wernicke-Korsakoff
The reason chronic ethnaol ingestion causes gynecomastia, testicular atrophy, and slat retention
Altered metabolism of steroids in liver
Excessive use causes hypertension, anemia, and MI
Chronic ethanol ingestion
A common neoplasia incidence is increased in chronic ethanol ingestion
Breast carcinoma
Used to protect against CNS effects in chronic alocholics
thiamine
What do you use for the management of abstinence syndrome for chronic alcholics?
Thiamine admis
Electrolyte correction
Diazepam with dose tapering
Discontinuance leads to insominia, tremor, anxiety, DT's and life-threatening seizures
Ethanol
Used to treat alcoholics and causes nausea, headache, flushing, and hypotension when alcohol is used
Disulfiram
Opioid used in the TX of alcoholism
Naltrexone
SSRI used in the Tx of alcoholism
Fluoxetine
Drug is Metabolized to formaldehyde and formic acid by Alcohol DH
Methanol
The major side effects of methonal ingestion
Blindness, Severe acidosis, Retinal damage
Used in the Tx of ethanol ingestion
Ethanol
Side effects of ehtylene glycol ingestion
Severe acidosis and Renal damage
Alcohol dehydrogenase metabolzies ethylene glycol to ______
Oxalic acid
Tx for the acute ingestion of ethylene glycol
Ethanol or Fomepizole