NEET MDS Lessons
Pharmacology
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)
Fourth Generation:
These are extended spectrum antibiotics. They are resistant to beta lactamases.
Cefipime
Types of Neurons (Function)
•There are 3 general types of neurons (nerve cells):
1-Sensory (Afferent ) neuron:A neuron that detects changes in the external or internal environment and sends information about these changes to the CNS. (e.g: rods and cones, touch receptors). They usually have long dendrites and relatively short axons.
2-Motor (Efferent) neuron:A neuron located within the CNS that controls the contraction of a muscle or the secretion of a gland. They usually have short dendrites and long axons.
2-Interneuron or association neurons: A neuron located entirely within the CNS in which they form the connecting link between the afferent and efferent neurons. They have short dendrites and may have either a short or long axon.
Mixed Narcotic Agonists/Antagonists
These drugs all produce analgesia, but have a lower potential for abuse and do not produce as much respiratory depression.
A. Pentazocine
- Has a combination of opiate analgesic and antagonist activity.
- Orally, it has about the same analgesic potency as codeine.
- In contrast to morphine, cardiac workload tends to increase due to an increase in pulmonary arterial and cerebrovascular pressure. Blood pressure and heart rate both also tend to increase.
- Adverse reactions to Pentazocine
• Nausea, vomiting, dizziness.
• Psychotomimetic effects, such as dysphoria, nightmares and visual hallucinations.
• Constipation is less marked than with morphine.
B. Nalbuphine
- Has both analgesic and antagonist properties.
- Resembles pentazocine pharmacologically.
- Analgesic potency approximately the same as morphine.
- Appears to be less hypotensive than morphine.
- Respiratory depression similar to morphine, but appears to peak-out at higher doses and to reach a ceiling.
- Like morphine, nalbuphine reduces myocardial oxygen demand. May be of value following acute myocardial infarction due to both its analgesic properties and reduced myocardial oxygen demand.
- Most frequent side effect is sedation.
C. Butorphanol
- Has both opiate agonist and antagonist properties.Resembles pentazocine , pharmacologically., 3.5 to 7 times more potent than morphine., Produces respiratory depression, but this effect peaks out with higher doses. The respiratory depression that does occur lasts longer than that seen following morphine administration.
- Butorphanol, like pentazocine, increases pulmonary arterial pressure and possibly the workload on the heart.
- Adverse reactions include sedation, nausea and sweating.
D. Buprenorphine
- A derivative of eto`rphine. Has both agonist and antagonist activity. 20 to 30 times more potent than morphine.Duration of action only slightly longer than morphine, but respiratory depression and miosis persist well after analgesia has disappeared.
- Respiratory depression reaches a ceiling at relatively low doses.
- Approximately 96% of the circulating drug is bound to plasma proteins.
- Side effects are similar to other opiates:
- sedation, nausea, vomiting,
- dizziness, sweating and headache.
Chloramphenicol
derived from the bacterium Streptomyces venezuelae
Chloramphenicol is effective against a wide variety of microorganisms, but due to serious side-effects (e.g., damage to the bone marrow, including aplastic anemia) in humans, it is usually reserved for the treatment of serious and life-threatening infections (e.g., typhoid fever). It is used in treatment of cholera, as it destroys the
vibrios and decreases the diarrhoea. It is effective against tetracycline-resistant vibrios.It is also used in eye drops or ointment to treat bacterial conjunctivitis.
Mechanism and Resistance Chloramphenicol stops bacterial growth by binding to the bacterial ribosome (blocking peptidyl transferase) and inhibiting protein synthesis.
Chloramphenicol irreversibly binds to a receptor site on the 50S subunit of the bacterial ribosome, inhibiting peptidyl transferase. This inhibition consequently results in the prevention of amino acid transfer to growing peptide chains, ultimately leading to inhibition of protein formation.
Spectrum of activity: Broad-spectrum
Effect on bacteria: Bacteriostatic
Dental implications of these drugs:
1. Adverse effects: gingival hyperplasia (phenytoin), osteomalacia (phenytoin, Phenobarbital), blood dyscrasias (all but rare)
2. Drug interactions: additive CNS depression (anesthetics, anxiolytics, opioid analgesics), induction of hepatic microsomal enzymes (phenytoin, Phenobarbital, carbamazepine), plasma protein binding (phenytoin and valproic acid)
3. Seizure susceptibility: stress can → seizures
NATURAL ANTICOAGULANTS:
1. PGI-2.
2. Antithrombin.
3. Protein-C.
4. TFPI.
5. Heparin.
6. Fibrinolytic system.