Phenytoin (Dilantin): for tonic-clonic and all partial seizures (not effective against absence seizures)

Mechanism: ↓ reactivation of Na channels (↑ refractory period, blocks high frequency cell firing, ↓ spread of seizure activity from focus)

Side effects: ataxia, vertigo, hirsutism (abnormal hair growth), gingival hyperplasia, osteomalacia (altered vitamin D metabolism and ↓ Ca absorption), blood dyscrasias (rare; megaloblastic anemia, etc)

Drug interactions: induces hepatic microsomal enzymes (can ↓ effectiveness of other drugs); binds tightly to plasma proteins and can displace other drugs

Sufentanil

• A synthetic opioid related to fentanyl.
• About 7 times more potent than fentanyl.
• Has a slightly more rapid onset of action than fentanyl.

Benzodiazepines
All metabolites are active sedatives except the final glucuronide product. Elimination half-life varies a great deal from drug to drug.

?-Hydroxylation is a rapid route of metabolism that is unique to triazolam, midazolam, and alprazolam.
This accounts for the very rapid metabolism and short sedative actions of these drugs.

Pharmacological effects of benzodiazepines

- Antianxiety.
- Sedation.
- Anticonvulsant (including drug-induced convulsions).
- Amnesia, especially drugs like triazolam.
- Relax skeletal muscle (act on CNS polysynaptic pathways).

Indications

- IV sedation, (e.g., midazolam, diazepam, lorazepam).
- Antianxiety.
- Sleep induction.
- Anticonvulsant (e.g., diazepam, clonazepam).
- Panic disorders.
- Muscle relaxation.


Adverse effects

- Ataxia, confusion.
- Excessive sedation.
- Amnesia (not a desired effect with daytime sedation).
- Altered sleep patterns (increase stage 2 and decrease stage 4 sleep).

FUNDAMENTALS OF INJECTION TECHNIQUE

There are 6 basic techniques for achieving local anesthesia of the structures of the oral cavity:

 1. Nerve block

 2. Field block

 3. Infiltration/Supraperiosteal

 4. Topical

 5. Periodontal ligament (PDL)

 6. Intraosseous

 Nerve block- Nerve block anesthesia requires local anesthetic to be deposited in close proximity to a nerve trunk. This results in the blockade of nerve impulses distal to this point. It is also important to note that arteries and veins accompany these nerves and can be damaged. To be effective, the local anesthetic needs to pass only through the nerve membrane to block nerve conduction Field block/Infiltration/Supraperiosteal - Field block, infiltration and supraperiosteal injection techniques, rely on the ability of local anesthetics to diffuse through numerous structures to reach the nerve or nerves to be anesthetized:

  - Periosteum

 - Cortical bone

 - Cancellous bone

 - Nerve membrane

Topical - Topical anesthetic to be effective requires diffusion through mucous membranes and nerve membrane of the nerve endings near the tissue surface

PDL/Intraosseous - The PDL and intraosseous injection techniques require diffusion of local anesthetic solution through the cancellous bone (spongy) to reach the dental plexus of nerves innervating the tooth or teeth in the immediate area of the injection. The local anesthetic then diffuses through the nerve membrane

Anticonvulsant Drugs

A.    Anticonvulsants: drugs to control seizures or convulsions in susceptible people

B.    Seizures: abnormal neuronal discharges in the nervous system produced by focal or generalized brain disturbances

Manifestations: depend on location of seizure activity (motor cortex → motor convulsions, sensory cortex → abnormal sensations, temporal cortex → emotional disturbances)

Causes: many brain disorders such as head injury (glial scars, pH changes), anoxia (changes in pH or CSF pressure), infections (tissue damage, high T), drug withdrawal (barbiturates, ethanol, etc.), epilepsy (chronic state with repeated seizures)

C.    Epilepsy: most common chronic seizure disorder, characterized by recurrent seizures of a particular pattern,  many types (depending on location of dysfunction)

Characteristics: chronic CNS disorders (years to decades), involve sudden and transitory seizures (abnormal motor, autonomic, sensory, emotional, or cognitive function and abnormal EEG activity)

Etiology: hyperexcitable neurons; often originate at a site of damage (epileptogenic focus), often found at scar tissue from tumors, strokes, or trauma; abnormal discharge spreads to normal brain regions = seizure

Idiopathic (70%; may have genetic abnormalities) and symptomatic epilepsy (30%; obvious CNS trauma, neoplasm, infection, developmental abnormalities or drugs)

Neuropathophysiology: anticonvulsants act at each stage but most drugs not effective for all types of epilepsy (need specific drugs for specific types)

Seizure mechanism: enhanced excitation (glutamate) or ↓ inhibition (GABA) of epileptic focus → fire more quickly → ↑ release of K and glutamate → ↑ depolarization of surrounding neurons (=neuronal synchronization) → propagation (normal neurons activated)

Opiate Antagonists

Opiate antagonists have no agonist properties. They are utilized to reverse opiate induced respiratory depression and to prevent drug abuse.

A. Naloxone

 Pure opiate antagonist , Short duration of action,  Only 1/50th as potent orally as parenterally

B. Naltrexone

Pure opiate antagonist, Long duration of action, Better oral efficacy