Sedatives And Hypnotics Block III Flashcards
What is a sedative
reduces anxiety and exerts a calming effect with little or no effect on motor or mental function
Hypnotic
produces drowsiness and encourages the onset and maintenance of a state of sleep resembling natural sleep
What are the two major classes of Sedatives
BZD and barbiturates
How are most anxiety DO tx acutely
BZD, Barbiturates, SSRIs
What happens when GABA binds to the GABA receptor
When GABA binds to the GABA receptor it results in relaxation and sedation
Major inhibitor receptor
Cl- channel
Barbiturates are no longer indicated for what sleep DO
Insomina
What are the disadvantages of barbiturates
ability to cause coma in toxic doses, physical dependence, and severe withdrawal symptoms
What is methohexital
A barbituate that is shirt acting and used for anesthesia
C-IV
What is Pentobarbital
Short acting barbiturate that is C-II used for anesthesia
What is secobarbital
A short acting barbituate that is PO only and used for anesthesia
What is amobarbital
A short acting barbituate that is used for anesthesia, C-II
What are the ADE of Barbituates
CNS depression, hangover effect, WTHDRAWL
What are the clinical uses of barbituates
Induction of anesthesia, Status epilepticus, Insomina
What are the severe ADE of barbituates
SJS, bone marrow suppression, hepatotoxicity, osteopenia
What medication can be used for generally every SZR type
Phenobarbital
What are the ADE of phenobarbital
Bradycardia, Sex dysfunction, Drowsiness, cognitive impairment
What are the short acting BZD
T.O.M.
Triazolam
Oxazepam
Midazolam
What are the Intermediate acting BZD
T.E.A.L
Temezepam
Estazolam
Alprazolam
Lorazepam
BZD with long half life’s have more or less hangover and break through S/s
Withdrawal symptoms may be less pronounced
Less breakthrough symptoms
More “hangover” symptoms
BZDs with short half lives have more or less break through s/s
Tolerance of the hypnotic effect develops rapidly
Withdrawal is common (breakthrough symptoms)
What are the clinical uses of BZDs
Anxiolytic (Sedative)
Hypnotic: all benzodiazpines induce sleep if high enough doses are given
Muscle Relaxation
Anticonvulsant
Anesthesia/Amnesic actions
Do BZDs effect pain >?
NO !
Which two BZDs are indicated for alcohol withdrawal
Lorazepam and Diazepam
Which BZD is perferred in liver dz
Lorazepam
What should the BZD treatment period be restricted to
3-4 months
If you must use BZD in the elderly which should be used
LOT
Lorazepam
Oxazepam
Temazepam
What is the reversal agent for BZD
Flumazenil
What is the clinical use of busprione
Management of anxiety disorders or short-term relief of the symptoms of anxiety
Slower onset then BZD, but no abuse potential
Appropriate use is to start patient on BZD then switch while tapering BZD
Often used as a second line agent or when BZD should avoided
What is the MOA and clincal use of Zolpidem
acts on the benzodiazepine receptor by enhancing GABA activity (not chemically related to BZD)
Clinical Use:
Only use is for insomnia
IR for difficulty going to sleep
CR for sleep maintenance issues
What are the advantages of zolpidem to BZD
Less dependence and cravings
Lower risk of tolerance and withdrawal
Lacks respiratory depressant properties
What is the clinical use of Eszopiclone
Sleep initiation and maintenance
What are the ADE of the sleep drug eszopiclone
Metallic taste, SI, abnormal thinking (hallucinations)
Causes functional dependence
What is the MOA and clin use of Zaleplon
acts on BZD receptor, but is chemically not related to BZD
Clinical Use:
Short-term treatment of insomnia
Which of the hypnotics is least likes to causes daytime somnolence
Zaleplon
What is the MOA and Clincal use of Surorexant
Mechanism of Action: orexin-receptor antagonist
Clinical Use: treatment of insomnia
In gerenal the ADE of sleep agents and hypnotics are..
SI, somnolence, Hallucinations, abnormal thinking
What is the MOA and clincal use of Ramelton
Mechanism of Action: melatonin receptor agonist.
[Melatonin maintains circadian rhythm (sleep-wake cycle)]
Clinical Use:
Treatment of insomnia characterized by difficulty with sleep onset
Not limited to short-term use
In studies only showed a 4.6min improvement in sleep latency and 7.3min increase in total sleep time
What is the MOA of clinical use of Tasimelteon
melatonin receptor agonist
Clinical Use:
Non-24-hour sleep-wake disorder that is generally present in blind patients due to lack of stimulus from the sun
What sleep DO is useful to blind pts.
Tasimelteon
What is the non Pham approach to insomnia
Improve sleep hygiene
Sleep restrictive therapy
CBT
What TCA can be used for insomnia
Amitryptyline
What SRAs can be used for insomnia
Trazadone
Mirtazapine
What are the DOC for anxiety DO
BZDs
What drugs can be used in monotherapy of GAD if antidepressant meds are not necessary
Busprione and Pregabalin
What are 1st line agents in social anxiety
What are second line
1: SSSRI, SNRI
2: Gabapentin and pregablin
What anticonvulsants can be used in PTSD
Tiagabine, Topiramate, divalproex
What is the most severe form of alcohol withdrawal
Delirium termens
What is teh 1st line for prevention of SZR in alcohol withdrawal
BZDs
What is the most frequently used medication in outpatient alcohol detox
Chlordiazepoxide
What is wernickes encephalopathy
Presence of neurological symptoms, a triad of confusion, ataxia and ophthalmoplegia associated with ethanol withdraw due to chronic alcoholism
How do we treat wernickes encephalopathy
IV mixture used to treat acute alcohol intoxication
Banana Bag – Multi Vitamins, Thiamine and Folic Acid in 1L NS
Electrolytes: monitor level
Vitamins: Folic acid and vitamin B12
Fluid Therapy
What are the 1st line agents in alcohol abuse?
What are the second line
First Line:
Naltrexone (Vivitrol)
Acamprosate (Campral)
Second Line: Disulfiram (Antabuse) Topiramate (Topamax) Gabapentin (Neurontin) Baclofen (Lioresal) SSRI’s
How does naltrexone effect the liver
Liver toxicity (5x increase in liver enzymes)
What is the MOA and clincal use of Acamprosate
Structurally similar to GABA; principal effect is believed to come from antagonism of glutamate neurotransmission.
Clinical Use:
Maintenance of abstinence from alcohol
Must be taken three times a day
How is Acamprosate metabolized
Not metabolized by the liver
Excreted by kidneys; reduce or stop if renal insufficiency
What is the MOA of disulfiram
Inhibits aldehyde dehydrogenase (ALDH), blocking the metabolism of ethanol at the acetaldehyde step.
If a patient drinks alcohol while taking disulfiram, it will cause them to have a “Disulfram Reaction”
How does Disuflram effect alcohol cravings
Does NOT reduce cravings for alcohol, high relapse rate
How should disulfiram be used
Has not shown better efficacy compared to placebo
Direct observed therapy: was effective
Only for patients who are motivated
Counseling, monitoring and support programs should be used in conjunction with disulfiram therapy
What is the most common psych DO in children
ADHD
What is the non-pharm approach to ADHD
Food additives, Refined Sugar, Food Sensitivity
What should be checked prior to starting Pharm Tx on a ADHD child
Prior to initiating pharmacologic treatment check BP, HR, & Ht/Wt
What are the non stim for ADHD
Atomoxetine
Clonidine
Guanfacine
All amphetamine and stimulant derivatives are schedule what?
C-II
What are the clin uses of stimulant and amphetamines
ADHD, narcolepsy, Obesity
What are the ADE of Amphetamines and Stimulants
Insomina, SZR, tremor, INC. BP, HR, NVD anorexia
Decreased growth rate
Priapism in children and adults
What is the contraindications for amphetamines and stimulants
Contraindicated in patients with hypertension, CV diseases, hyperthyroidism, and glaucoma
Nonstimulants are 1st line therapy in pts with ADHD if…
There is a concern for medication abuse
A strong family/patient preference not to use a stimulant
The patient has a condition in which stimulants are not recommended (e.g. cardiac disease, glaucoma, loss of appetite)
What is the MOA and Clin use of Atomoxetine
Not a controlled substance
First non-stimulant drug approved for ADHD
Mechanism of Action: blocks the reuptake of norepinephrine
Clinical Use:
Monotherapy for the treatment of ADHD in patients six years and older
Proven effective but not better or worse than stimulants
May be used as a first line agent
What is a first line non stimulating monotherapty drug for ADHD in chlidren older than 6 yo
Atomoxetine
What is the MOA and Clin use of Clonidine
Not a controlled substance
Mechanism of Action: central α2 agonist
Clinical Use:
Alternative for children who are intolerant to stimulants especially those with tics
FDA approved for monotherapy or as an add-on to stimulants
Concurrent disease treatment:
Impulsive behavior
Tourette’s Syndrome
What non stimulant can be used for impulsive behavior and Tourette’s
Clonidine
What is the MOA and Clin use of guanfacine
Not a controlled substance
Mechanism of Action: central α2 agonist
Clinical Use:
FDA approved for monotherapy or as an add-on to stimulants
Alternative for children who are intolerant to stimulants
Indicated for children with tic disorders
Are SSRI useful in ADHD
NO!
Which TCAs can be used in ADHD
Imipramine, and desipramine
What is the clin use of Modafinil and Armodafinil
Mechanism of Action: Not fully known; May decrease GABA-medicated neurotransmission
Clinical Use: improve wakefulness in adult patients with excessive sleepiness associated with obstructive sleep apnea (OSA), narcolepsy or shift work disorder (SWD)
What drugs can be used in obstructive sleep apnea and, narcolepsy, and shift work DO
Modafinil and Armodafinil
What is the MOA and clin uses of caffeine
Caffeine is a methylxanthine (theophylline is a derivative)
Mechanism of Action: (multiple possible explanations)
Antagonist of adenosine receptors
Increases of cAMP by inhibiting phosphodiesterase
Increases medullary response to CO2
Clinical Use:
For migraine headaches in combination with other medications
Apnea of prematurity (neonates)
Non clinical uses:
Overcoming sleep deprivation, mental acuity and physical performance
What is an overweight BMI
Greater than 25,
Greater than 40 is obesity
What is the non pharm approach to Obesity
Behavior modification
Diet and Excercise
Who is bariatric surgery indicated for
BMI greater than 35
What is the pharm approach to obesity
Used to support non-pharmacologic therapy for patients with a BMI > 30kg/m2, OR BMI >27kg/m2 with a comorbidity (e.g. dyslipidemia, hypertension, type 2 diabetes)
In general, advise discontinuing medication if at least 5% weight loss is not achieved after 12 weeks of use
How are amphetamines used in obesity control
Increase norepinephrine and dopamine release which suppresses appetite and increases thermogenesis
The dopaminergic activity is linked to their addictive properties (C-II)
These can lead to rebound binge eating, weight gain and depression when stopped
Rarely used specifically for obesity
How are SSRIs used in obesity Tx
(fluoxetine and sertraline)
Suppress appetite and have been shown to be effective in weight loss but after one year but regaining weight is likely
What is the MOA and Clin use of Phentermine/ Topiramate in Obesity
Mechanism of Actions:
Phentermine: promotes appetite suppression and decreased food intake secondary to its sympathomimetic activity
Topiramate: unknown regarding weight loss, but may cause appetite suppression and satiety through enhanced GABA activity
Should be taken in the morning to avoid insomnia
Taper to avoid seizures
What ADE of topiramte
advanced atherosclerosis, cardiovascular disease, moderate to severe hypertension, hyperthyroidism
What is the MOA and clin use of orlistat
Lipase Inhibitor: reduces fat absorption by inhibiting GI lipase activity in the small intestine
30% of ingested fat is excreted in the feces
Obestity
What is the MOA of liraglutide
Type 2 Diabetic Agent (Victoza)
Mechanism of Action: GLP-1 agonist
Can liraglutide be used in obese pts that are pregnant
NO
What are the ADE of Liraglutide used for obesity
Pancreatitis
Symptomatic hypoglycemia is rare in patients without diabetes, but more in patients with diabetes
Suggest reducing the insulin dose by ≥ 20%
Suggest reducing sulfonylurea doses by ≥ 50%
