PHCT F1

• CNS Drugs (Anti-convulsants)

  • Sedative- hypnotic Drugs
  • Barbiturates
  • Benzodiazepines
  • Other sedative-hypnotics
• SEDATIVE

  • refers to a substance that moderates activity and excitement while inducing a calming effect
• SEDATIVE

  • degree of CNS depression is minimum consistent with the therapeutic efficacy
• HYPNOTIC

  • refers to a substance that causes drowsiness and facilitates the onset and maintenance of natural sleep
• HYPNOTIC

  • involves more pronounced depression of the CNS than sedatives
• HYPNOTIC

  • its effect sometimes is called “hypnosis”, but the sleep induced by hypnotic drugs does not resemble the artificially induced passive state of suggestibility also called hypnosis
• hypnosis

  artificially induced passive state of suggestibility
• SEDATIVE-HYPNOTIC DRUGS

  Barbiturates

  Benzodiazepines

  Other sedative-hypnotics
• USES OF SEDATIVE HYPNOTICS

  relief of anxiety

  insomnia

  sedation and amnesia before medical and surgical procedures

  treatment of epilepsy and seizure states

  component of balanced anesthesia (intravenous administration)

  control of ethanol or other sedative-hypnotic withdrawal states

  muscle relaxation in specific neuromuscular disorders

  As diagnostic aids or for treatment in psychiatry
• Barbiturates

  Used as hypnotic and sedative
• Barbiturates

  For induction of anesthesia and for the treatment of epilepsy and status epilepticus
• 4 major groups of barbiturates

  • ultrashort-acting
  • short-acting
  • intermediate-acting
  • and long-acting
• Ultra- short acting BARBITURATES

  Thiamylal

  Thiopental

  Methohexital
• Short acting BARBITURATES

  Pentobarbital (Nembutal Sodium)

  Secobarbital (Seconal)

  Hexobarbital
• Intermediate acting BARBITURATES

  Amobarbital (Amytal)

  Aprobarbital

  Butabarbital

  Butalbital
• Long acting BARBITURATES

  • Phenobarbital (Luminal Sodium)
  • Mephobarbital
• MECHANISM OF ACTION OF BARBITURATES

  • they appear to increase the duration of the GABA-gated chloride channel openings
• MECHANISM OF TOXICITY OF BARBITURATES

  All barbiturates cause generalized depression of neuronal activity in the brain achieved through enhanced GABA-mediated synaptic inhibition
• MECHANISM OF TOXICITY OF BARBITURATE

  Depression of central sympathetic tone and depression of cardiac contractility cause hypotension
• Toxic Dose of Barbiturates

  • dose exceeds 5-10 times the hypnotic dose.
• Fatal Dose of Barbiturates

  shorter-acting agents - 2-3 g

  Phenobarbital - 6-10 g

  Methohexital - IV injections of 1-3 mg/kg of have been reported to cause death in young women undergoing abortion
• Clinical Presentation OF BARBITURATES

  Mild to moderate intoxication

  • slurred speech
  • ataxia
  • Lethargy
  • nystagmus
• Clinical Presentation OF BARBITURATES: With higher doses

  
  

  
  

  • Coma
  • Hypotension
  • Respiratory arrest
• Clinical Presentation OF BARBITURATES: With deep coma

  
  

  
  

  
  

  Pupils are usually small or mid-position

  Hypothermia
• Diagnosis usually based on a history of ingestion.
• • For short-acting barbiturates, coma is likely to happen when the serum concentration exceeds 20-30 mg/L
  • 60-80 mg/L are usually associated with coma
  • 150-200 mg/L with severe hypotension upon use of Phenobarbital.
• useful laboratory studies:

  • arterial blood gases or oximetry
  • BUN
  • chest x-ray
  • creatinine
  • Electrolytes
  • glucose
• Treatment OF BARBITURATES

  
  

  • Emergency and supportive measures
  • Decontamination
  • Prehospital. Administer activated charcoal and ipecac-induced emesis for initial treatment.
  • Hospital. Administer activated charcoal and cathartic
• Treatment OF BARBITURATES

  
  

  1.Alkalinization of urine increases the elimination of phenobarbital but not other barbiturates.

  2. Repeat-dose activated charcoal decreases the half-life Phenobarbital, but there is no evidence that it actually shortens duration of coma.

  3. Hemoperfusion is indicated for severely intoxicated patients not responding to supportive care
• BENZODIAZEPINES

  • contains many compounds that vary widely in potency, duration of effect, presence or absence of active metabolites, and clinical use
• BENZODIAZEPINES

  In general, death from this medication overdose is rare, unless the drugs are combined with other CNS depressant agents such as ethanol or barbiturates.
• MOA of Benzodiazepine

  • they appear to increase the FREQUENCY of the GABA-gated chloride channel openings
• MOT OF BENZODIAZEPINES

  • Cause generalized depression of spinal reflexes and the reticular activating system
  • This may cause coma and respiratory arrest
• BENZODIAZEPINES

  
  

  • Respiratory Arrest- Short-acting triazolobenzodiazepines such as Triazolam (Halcion), Alprazolam (Xanax) and Midazolam (Versed)
  • B. Cardiopulmonary Arrest- Rapid injection of Diazepam
• TOXIC DOSE OF BZD

  toxic-therapeutic ratio for benzodiazepines is very high
• Clinical presentation OF BENZODIAZEPINE TOXICITY

  Lethargy

  Slurred speech

  Ataxia

  Coma

  Respiratory arrest

  Hypothermia may occur

  Patients may have hyporeflexia and midposition or small pupils
• Diagnosis of benzodiazepine is usually based on the history of ingestion or recent injection

  A.Specific levels. Serum drug levels, urine and blood qualitative screening.

  B. Other useful laboratory studies. Glucose, arterial blood gases or pulse oximetry
• drugs and antidotes for bzd toxicity

  Flumazenil is a specific benzodiazepine receptor antagonist that can rapidly reverse coma
• Flumazenil It is administered intravenously with a starting dose of 0.1-0.2 mg, repeated as needed up to a total of no more than 3 mg
• Potential drawbacks in using flumazenil

  
  

  it may induce seizures in patients with cyclic antidepressant overdose.

  
  

  it may induce acute withdrawal

  
  

  Resedation is common when the drug wears off after 1-2 hours, and repeated dosing is usually required