Exam 2 (Pt. 13) Flashcards
Tolerance and Therapeutic Index - Top Panel
The top panel shows that with early drug use (non-tolerant) the individual experiences mood effects without significant respiratory depression.
Tolerance and Therapeutic Index - Bottom Panel
However, as tolerance develops with repeated use (bottom panel), larger amounts of drug are needed to experience the mood change (the curve shifts to the right) but no change in the dose causing depression of respiration occurs.
Tolerance and Therapeutic Index - Problem
The margin of safety (i.e., therapeutic index) shrinks dramatically in the tolerant individual.
Effect of Chronic Barbiturate Administration on Sleep Architecture - Initial Effect
The panel shows the initial effects of pentobarbital, which include a short onset of sleep and few spontaneous awakenings.
Effect of Chronic Barbiturate Administration on Sleep Architecture - Chronic-Use Effect
Effect The right panel shows the changes after chronic nightly use of the drug. Tolerance is shown by the long onset of sleep (1 hour) and the 12 spontaneously awakenings during the night. Both REM and stages 3 and 4 sleep are suppressed.
Blood Levels of Secobarbital in Mothers and Newborn Infants
Effect of barbiturate on mothers in labor. Blood levels of secobarbital in mothers and their newborn infants after intravenous administration of the drug to the mothers. Each point represents one subject (circles, mothers; asterisks, infants)
Benzodiazepine: Major Therapeutic Uses - Chlordiazepoxide
Benzodiazepine: Major Therapeutic Uses - Diazepam
Benzodiazepine: Major Therapeutic Uses - Oxazepam
The Advantages of Drug “B” Over Drug “A” as Deduced From Dose-Response Curves
Alcohol Content
There is the same amount of alcohol in one regular beer (340 ml/12 oz., 5% alcohol), one glass of wine (140 ml/5oz, 12% alcohol), one glass of fortified wine (85 ml/3oz, 20% alcohol) and one shot of spirits (45 ml/1.5 oz, 40% alcohol).
Time Course of Brain and Venous Ethanol Concentrations
After administration of ethanol (2 g/kg i.p.) to mice, the brain ethanol concentration reached its peak in about 15 min, and did not equate with ethanol levels in venous blood taken from the tip of the tail until 60 min had passed.
Relationship Between Blood Alcohol Concentration and Signs of Intoxication
After three doses of alcohol (1.0 g/kg at time a, and 0.25 g/kg at times b and c), signs of intoxication appeared during the rising phase of the blood alcohol concentration (BAC) curve when the BAC was about 200 mg/dl. However, when the BAC was declining, the subject became sober even though the BAC was about 265 mg/dl.
Metabolism of Ethanol and the Use of the Aldehyde Dehydrogenase Inhibitor, Disulfiram
Ethanol is oxidated by the enzyme alcohol dehydrogenase using NAD+ as a cofactor to form acetaldehyde. A second oxidative step converts acetaldehyde to acetic acid, which, in turn, is broken down to carbon dioxide and water. The first step involving alcohol dehydrogenase is the rate-limiting step. The drug disulfiram (Antabuse) blocks the second step by blocking the activity of aldehyde dehydrogenase.
Dose-Blood Level-Response for Alcohol
Children with Fetal Alcohol Syndrome (FAS) Compared with a Mouse Model of FAS
Normal EEG Patterns and Epileptic EEG Patterns
The top three traces represent normal a (left), q (middle, during drowsiness), and d (right, during deep sleep) activity recorded in the EEG. The bottom two traces illustrate a focal “spike discharge” (circled) and a sudden burst of spike-and-wave activity seen simultaneously in all the leads
Relations Among Cortical EEG, Extracellular, and Intracellular Recordings in a Seizure
The extracellular recording was made through a high-pass filter. Note the high-frequency firing of the neuron evident in both extracellular and intracellular recording during the paroxysmal depolarization shift (PDS).
Pharmacological Treatment of Epilepsy
Antiseizure Drug-Enhanced Na+ Channel Inactivation
Some antiseizure drugs (shown in blue text) prolong the inactivation of the Na+ channels, thereby reducing the ability of neurons to fire at high frequencies. Note that the inactivated channel itself appears to remain open, but is blocked by the inactivation gate (I). A, activation gate.
Drug-Induced Reduction of Current Through T-Type Ca2+ Channels
Some antiseizure drugs (shown in blue text) reduce the flow of Ca2+ through T-type Ca2+ channels, thus reducing the pacemaker current that underlies the thalamic rhythm in spikes and waves seen in generalized absence seizures.
Enhanced GABA Synaptic Transmission
In the presence of GABA, the GABAA receptor (structure on left) is following an influx of Cl-, which in turn increases membrane polarization.
Some antiseizure drugs act by reducing the metabolism of GABA. Others act at the GABAA receptor, enhancing Cl- influx.
Gabapentin acts presynaptically to promote GABA release; its molecular target is currently under investigation. GABA-T, GABA transaminase; GAT-1, GABA transporter.
Categorization of Sleep Disorders - Dysomnias
Categorization of Sleep Disorders - Parasomnias
Comparison of Representative Benzodiazepines for Insomnia Therapy
Non-Benzodiazepine Therapy for Insomnia
Neurotransmitter Systems Affected by General Anesthetics
The main point is only to recognize that different anesthetics act on a wide variety of different neurochemical systems and that they affect these systems in different ways.
