A GABA receptor has multiple sites that have the ability to bind other molecules that
affect the function of the receptor.

Benzodiazepines affect a GABA receptor by.

When GABA receptors become more permeable to Cl- ions, they have what affect on the neuron?

Benzodiazepine receptor binding facilitates GABA receptor binding, which increases the conductance of which ion across nerve cell membranes?

When a neuron is hyperpolarized (further from its resting potential) it:

Benzodiazepines potentiate the effects of GABA.

Barbiturates also bind GABA receptors and affect them almost identically to benzodiazepines.

Barbiturates open the receptor channel directly to Cl- ions thereby hyper-polarizing
the resting potential in a neuron.

Mixing alcohol with benzodiazepines isn’t normally a problem because the two drugs act on different sets of neuronal receptors.

Benzodiazepines are known to cause drug dependency even in therapeutic doses and relatively short courses of treatment.

Increased production of cAMP upon cessation of regular opioid use contributes to the sensation of craving the drug.

Benzodiazepines are effective for all of the following except:

Benzodiazepines react with specific receptors in the:

Benzodiazepines are primarily metabolized where?

Flumazenil is primarily a:

Which drug will produce secondary metabolites in the blood stream and having effect hours after leaving the clinical setting?

Metabolites of the benzodiazepines are excreted mainly in:

Benzodiazepines depress ventilator response to:

Which drug has been associated with increased dementia in the elderly?

In general, large doses of benzodiazepines can cause all of the following except:

How do benzodiazepines lower a patient’s ventilation?

Benzodiazepines are effective for all of the following except:

Which property makes Diazepam a dangerous choice for sedation?

What is the typical midazolam dosing range for oral sedation in adult patients?

What is the maximum midazolam oral dose that most dentists do NOT exceed?

Should a dentist mix midazolam in a cherry flavored over-the-counter Tylenol solution provided it is within the Tylenol dosing guidelines?

IV sedation can be titrated predictably.

A dentist takes 35 minutes to locate the appropriate instruments for his case. N2O (50%) has been delivered for the last 15 minutes. 50 mcg of fentanyl was administered 12 minutes ago. This patient partially obstructs their airway and pulse oximetry reads 89%. What should the primary response be?

What reverses the respiratory effects of midazolam?

What are the appropriate reversal doses for Flumazenil?

What adjuncts to benzodiazepine sedation (medicines combined with benzodiazepines to potentiate sedation) synergistically depress a pediatric patients respiratory drive.

Can standard IV doses of benzodiazepines (within the FDA dosing guidelines) typically cause apnea in patients?

What are the typical midazolam dosing increments used in IV sedation?

Opioids primarily effect all of these receptors except:

Generally, exogenous opioids are medicines and endogenous opioids are neurotransmitters.

Exogenous opioids bind to a different class of receptor in the brain but produce the same result.

Which class of drugs came into use first?

Endogenous opioids include:

Opioid receptors in the brain include all but.

Opioids are most effective at producing:

The pharmacodynamic properties of specific opioids depends on all of the following EXCEPT:

In general, opioids do not seriously impair cardiovascular function:

Endogenous opioids regulate all but.

Which opioid has the lowest lipid solubility and is therefore metabolized more quickly?

Opioids depress respiratory rate primarily by affecting the:

It generally takes a larger dose of which class of drug to render a patient unconscious?

The humane body uses opiate-like substances as neurotransmitters.

In moderate doses, opioids can cause all of the following except:

What are the appropriate reversal doses for Narcan?

Reversal agents such as Narcan and Flumazenil can safely be used to facilitate emergence from oral sedation in order to discharge patients more quickly from dental facilities.

Emergence is the process of awakening from sedation or anesthesia.

Discharge  is the process of allowing the patient to leave the facility safely after treatment.

What is an analgesic?

What is the typical dosing range of Hydrocodone used for post-dental procedure pain relief?

What is the maximum dose that should not be exceeded with Hydrocodone every 4 – 6 hours when administered for oral post dental procedure pain in adults? (Excluding patients with chronic opiate use)

What medicine can be used as a reversal agent when Hydrocodone is administered as an adjunct for sedation?

Increased excitability of neurons produces the euphoric effect of opioids.

What are three life-threatening side effects from high doses of Hydrocodone?

(1) Hypoxia, (2) Dysphoria, (3) Seizures, (4) Apnea

Opioid receptors act through second messengers and affect the permeability of ion channels.

Which of the following drugs are opioids? (Check all that apply.)

Diazepam and Triazolam are in which category of drugs?

Hydrocodone provides amnesia.

Which of the following patients should never be sedated in an office:

It can be said that dopamine is central to many important functions of an organism.

Dopamine is involved in all of these functions except.

All substances that trigger dependencies in humans inhibit the release of dopamine in the nucleus accumbens.

Substances modulate dopamine in the brain in all of these ways except:

Chronic use of opioids reduces the production of which of the following?

Substances like morphine that imitate natural neuromediators do so by:

When a neuron is hyperpolarized (further from its resting potential) it:

Benzodiazepines potentiate the effects of GABA.

Barbiturates also bind GABA receptors and affect them almost identically to benzodiazepines.

Barbiturates open the receptor channel directly to Cl- ions thereby hyper-polarizing
the resting potential in a neuron.

Mixing alcohol with benzodiazepines isn’t normally a problem because the two drugs act on different sets of neuronal receptors.

Benzodiazepines interact with which receptor?

In a nerve, the dendrite:

GABA:

To reverse an opiate, administer:

To reverse a benzodiazepine, administer:

BENZODIAZEPINE RECEPTOR QUESTION

Benzodiazepines are used as sedatives, hypnotics, anxiolytics, anticonvulsants and muscle relaxants.  Benzodiazepines are similar in pharmacological action but have different potencies.  Some benzodiazepines work better in the treatment of particular conditions.  The useful clinical effects of benzodiazepines are sedation, hypnosis, anti-anxiety, amnesia, muscle relaxation, and a potent anti-seizure effect.  Their detrimental clinical effects are respiratory depression, rapid physical dependence, and an absence of analgesia.

Mechanisms of Action:

Benzodiazepines are a class of agents that work on the central nervous system, acting selectively on gamma-aminobutyric acid-A (GABA-A) receptors in the brain. It enhances response to the inhibitory neurotransmitter GABA, by opening GABA-activated chloride channels and allowing chloride ions to enter the neuron, making the neuron negatively charged and resistant to excitation.

The GABA(A) receptors are membrane protein complexes that are composed of α, β, and γ subunits. The membrane receptors are mainly expressed in the brain but can also be found in different tissue such as muscle and immune cells. γ-aminobutyric acid (GABA) is the endogenous ligand for the GABA(A) receptors inhibiting the signaling transduction mediated by these receptors by hyper-polarization (increase of chloride ion efflux). Other molecules are known to modulate GABA(A) receptor actions such as alcohol, steroids and barbiturates.

Where are the GABA receptors mainly distributed in the human body?

Clinical Receptor Summary:

The GABA receptor is the major molecular target for the action of many drugs in the brain.  Among these are benzodiazepines, intravenous anesthetics (barbiturates and propofol), volatile anesthetics, and ethanol.  GABA receptors have been identified electrophysiologically and pharmacologically in all regions of the brain.  The complex includes five major binding domains with binding sites localized in or near the Cl− channel.  Benzodiazepines, barbiturates as well as anesthetic steroids (propofol) bind to sites on the GABA receptor.  The domains modulate the receptor response to GABA stimulation. In addition, other drugs, including volatile anesthetics and ethanol have been reported to have an effect on this receptor.  An integral part of this complex is the Cl− channel. The GABA specific ­binding site is directly responsible for opening the Cl− channel.

Benzodiazepine agonists represent the largest group of agents in this general class of depressant drugs.  They show anticonvulsant, anxiolytic and sedative—hypnotic activity. Well­ known examples include diazepam and Xanax, which often are prescribed for their anti­-anxiety effects. Halcion is known for its sedative and anxiolytic properties.  The mechanism of action of benzodiazepine agonists is to enhance GABAergic transmission.  The advantage of benzodiazepines is that they do not open the Cl- channels directly.  Instead they act more subtly by potentiating the effect of GABA.

Barbiturates comprise another class of drugs commonly used therapeutically for anesthesia and control of epilepsy.  Barbiturates bind to another site on the GABA receptor.  This opens the Cl- channels directly and causes similar clinical effects.  Phenobarbital and pentobarbital are two of the most commonly used barbiturates. Phenobarbital was used to treat patients with epilepsy since 1912. Pentobarbital is also an anticonvulsant and has useful sedative properties.

A variety of agonists bind to this site and elicit GABA­-like responses. One of the most useful agonists is the compound muscimol, a naturally occurring GABA analog isolated from the psychoactive mushroom Amanita muscaria. It is a potent and specific agonist at GABA receptors and has been a valuable tool for pharmacological and radioligand ­binding studies.

Which of the following statements is true?

Clinical Receptor Summary:

The GABA receptor is the major molecular target for the action of many drugs in the brain.  Among these are benzodiazepines, intravenous anesthetics (barbiturates and propofol) volatile anesthetics, and ethanol.  GABA receptors have been identified electrophysiologically and pharmacologically in all regions of the brain.  The complex includes five major binding domains with binding sites localized in or near the Cl− channel.  Benzodiazepines, barbiturates as well as anesthetic steroids (propofol) bind to sites on the GABA receptor.  The domains modulate the receptor response to GABA stimulation. In addition, other drugs, including volatile anesthetics and ethanol have been reported to have an effect on this receptor.  An integral part of this complex is the Cl− channel. The GABA specific ­binding site is directly responsible for opening the Cl− channel.

Benzodiazepine agonists represent the largest group of agents in this general class of depressant drugs.  They show anticonvulsant, anxiolytic and sedative—hypnotic activity. Well­ known examples include diazepam and Xanax, which often are prescribed for their anti­-anxiety effects. Halcion is known for its sedative and anxiolytic properties.  The mechanism of action of benzodiazepine agonists is to enhance GABAergic transmission.  The advantage of benzodiazepines is that they do not open the Cl- channels directly.  Instead they act more subtly by potentiating the effect of GABA.

Barbiturates comprise another class of drugs commonly used therapeutically for anesthesia and control of epilepsy.  Barbiturates bind to another site on the GABA receptor.  This opens the Cl- channels directly and causes similar clinical effects.  Phenobarbital and pentobarbital are two of the most commonly used barbiturates. Phenobarbital was used to treat patients with epilepsy since 1912. Pentobarbital is also an anticonvulsant and has useful sedative properties.

A variety of agonists bind to this site and elicit GABA­-like responses. One of the most useful agonists is the compound muscimol, a naturally occurring GABA analog isolated from the psychoactive mushroom Amanita muscaria. It is a potent and specific agonist at GABA receptors and has been a valuable tool for pharmacological and radioligand ­binding studies.

Anxiolysis is best described by which of the following statements:

THE OPIOID RECEPTOR

Opioids are among the world’s oldest known drugs; the therapeutic use of the opium poppy predates recorded history.  The analgesic (painkiller) effects of opioids are due to decreased perception of pain, decreased reaction to pain as well as increased pain tolerance.  The human body naturally produces its own opiate-like substances and uses them as neurotransmitters. These substances include endorphins, enkephalins, and dynorphin, often collectively known as endogenous opioids. Endogenous opioids modulate our reactions to painful stimuli. They also regulate vital functions such as hunger and thirst and are involved in mood control, immune response, and other processes. The reason that medicine based opiates affect us so powerfully is that these exogenous substances bind to the same receptors as our endogenous opioids.

Medicine based opioids bind to specific receptors located throughout the central nervous system and other tissues.  Four major types of opioid receptor have been identified: mu, kappa, delta, and sigma.  While opioids provide some degree of sedation, they are most effective at producing analgesia.  The pharmacodynamic properties of specific opioids depend upon which receptor is bound, the binding affinity, and whether the receptor is activated.

These four receptors, through second messengers, influence the likelihood that ion channels will open, which in certain cases reduces the excitability of neurons. This reduced excitability is the likely source of the euphoric effect of opiates and appears to be mediated by the mu and delta receptors. This euphoric effect also appears to involve another mechanism in which the GABA-inhibitory interneurons come into play. By attaching to their mu receptors, exogenous opioids reduce the amount of GABA released. Normally, GABA reduces the amount of dopamine released in the nucleus accumbens. By inhibiting this inhibitor, the opiates ultimately increase the amount of dopamine produced and the amount of pleasure felt.

Which of the following statements best describes a clinical benefit of opioids?

CLINICAL EFFECTS OF OPIOIDS

Cerebral:

• Opiates produce a potent analgesic effect.  Intravenous opioids have been the mainstay of pain control for more than a century.
• Opiates are very predictable when used as a primary or secondary sedative.  Mild to moderate dose dependent sedation occurs with all opiates . Unlike barbiturates or benzodiazepines, relatively large doses of opioids are required to render patients unconscious.
• Regardless of the dose, opioids do not reliably produce amnesia.

Respiratory:

• Opioids depress ventilation, particularly respiratory rate.  Resting PaCO2 increases and the response to a CO2 challenge is blunted, resulting in a shift of the CO2 response curve downward and to the right.  These effects are mediated through the respiratory centers in the brainstem.  The apneic threshold, the highest PaCO2 at which a patient remains apneic, is elevated, and hypoxic drive is decreased.
• Morphine and meperidine can cause histamine-induced bronchospasm in susceptible patients.
• Opioids (particularly fentanyl, Sufentanil, and Alfentanil) can induce chest wall rigidity severe enough to prevent adequate ventilation.  This centrally mediated muscle contraction is most frequent after large drug boluses and is effectively treated with muscle relaxants.
• Opioids can effectively blunt the broncho-constrictive response to airway stimulation such as that occurring during intubation.

Opioids decrease ventilation in the human body through which mechanism?

Nitrous Oxide is:

Nitrous Oxide reduces the drive to breathe.

Opiates can stimulate a nauseous reaction.

To help reduce a patient’s nauseous reaction, you can: