BY: ANNA ANTOINE

Opioid Analgesics Opioid Antagonists Analgesic Antipyretic Anti-inflammatory drugs Anti-anxiety Sedative-Hypnotic Drugs Anti-Parkinson Skeletal Muscle Relaxants Anesthetics CNS Stimulants

Adrenergic drugs Anti-adrenergic drugs Cholinergic drugs Anti-Cholinergic drugs

Opium is a Greek word meaning juice, or the exudates from the poppy opiate is a drug extracted from the exudates of the poppy opioid is a natural or synthetic drug that binds to opioid receptors producing agonist effects

Examples of Opioid Analgesics are: morphine and codeine As endogenous endorphins

Sedation and anxiolysis Drowsiness and lethargy Apathy Cognitive impairment Sense of tranquility Depression of respiration Main cause of death from opioid overdose Combination of opioids and alcohol is especially dangerous Cough suppression Opioids suppress the cough center in the brain Pupillary constriction pupillary constriction in the presence of analgesics is characteristic of opioid use

Nausea and vomiting Stimulation of receptors in an area of the medulla called the chemoreceptor trigger zone causes nausea and vomiting Unpleasant side effect, but not life threatening
Gastrointestinal symptoms Opioids relieve diarrhea as a result of their direct actions on the intestines Other effects Opioids can release histamines causing itching or more severe allergic reactions including bronchoconstriction Opioids can affect white blood cell function and immune function

Release of pain-signaling neurotransmitters is regulated by endogenous endorphins or by exogenous opioid agonists.

Primary Effect of Opioid Receptor Activation

Reduction or inhibition of neurotransmission, due largely to opioid-induced presynaptic inhibition of neurotransmitter release

Morphine
Heroin Hydromorphone

Fentanyl
Codeine

Naloxone
Naltrexone

Examples: Aspirin and related Nsaids can be used in combination with opiate analgesics NSAIDs have three major actions, all of which are due mainly to the inhibition of arachidonic acid cyclo-oxygenase in inflammatory cells (the COX-2 isoenzyme), and the resultant decrease in prostanoid synthesis.

The decrease in vasodilator prostaglandins (PGE2, PGI2) means less vasodilatation and, indirectly, less oedema.

An Antipyretic effect
This is partly due to a decrease in the mediator prostaglandin that is responsible for elevating the hypothalamic set-point for temperature control in fever.

Some important examples are Aspirin Ibuprofen Naproxen Indomethacin paracetamol (This agent has analgesic and antipyretic effects but little antiinflammatory action).

Usually effective for low- to moderateintensity pain. Integumental pain is relieved better than the pain from hollow visceral areas. Relief of pain occurs through both peripheral and central mechanisms. -Peripherally, it inhibits the synthesis of PGs in inflamed tissues, thus preventing the sensitization of pain receptors to both mechanical and chemical stimuli. -Centrally, the analgesic site exists in close proximity to the antipyretic region in the hypothalamus.

Posttraumatic stress disorder

Social anxiety disorder

Depression
Panic disorder Obsessive-compulsive disorder

Generalized anxiety disorder

Benzodiazepines major class of anxiolytic drugs.

Act primarily via a selective binding sites on the GABA-A receptor. - high-affinity site. - low-affinity site.
POTENTIATE the effects of GABA at the GABA-A receptor.

Generic name

Trade name

Half-life (hrs)

Dosage (mg/day)

Long-acting benzodiazepines Diazepam Valium Chlordiazepoxide Librium Clorazepate Tranxene Estazolam ProSom Prazepam Centrax Quazepam Doral Halazepam Paxipam Clonazepam* Klonopin Flurazepam+ Dalmane Short-acting benzodiazepines Oxazepam Lorazepam Alprazolam Temazepam+ Triazolam+ Midazolam# Serax Ativan Xanax Restoril Halcion Versed

20-80 24-48 100 10-24 100 30-100 15-100

34 100

2-60 15-100 7.5-60 0.5-2.0 20-60 7.5-15 20-160

1.5-20 15-30

8 12 11 2 2

15

30-120 0.5-6 15-30 0.125-0.5 2-4

2-6

Non-benzodiazepine sedative/hypnotics Buspirone (BuSpar) Zolpidem (Ambien) Meprobamate (Miltown) Serotonin 1a agonist binds to benzodiazepine receptor

Example: Valium

Pharmacological Effects:

Reduction of anxiety. Induction of sleep. Anesthesia some benzodiazepines. Respiratory depression not as great as observed with barbiturates.

Adverse Effects primarily observed at plasma concentrations exceeding anxiolytic range.

Expected side effects: sedation, ataxia, dependence. Impaired cognition and motor function. Confusion. Amnesia. Fatal overdose is uncommon, except when taken with alcohol

Benzodiazepines may induce tolerance in some individuals.

Discontinuation of benzodiazepine therapy in tolerant patients MUST be gradual.

Benzodiazepines - Indications
Anxiety and Insomnia Sedation Drug-induced hyperexcitability PCP intoxication. Spasticity Cerebral Palsy Tetanus toxin toxicity. Anesthesia Alcohol withdrawal syndrome. Seizures.

Parkinsons disease (PD) is a progressive disorder of movement that occurs mainly in the elderly. Degenerative disease of the basal ganglia causing tremor at rest, muscle rigidity hypokinesia, often with dementia. Often idiopathic, but may follow stroke, virus infection, can be drug-induced (neuroleptic drugs).

Associated with marked loss of dopamine from basal ganglia. Can be induced by MPTP, a neurotoxin affecting dopamine neurons in the corpus striatum.

Drugs that replace dopamine (e.g. levodopa, usually used concomitantly with peripherally acting dopa decarboxylase inhibitor, e.g. carbidopa) Drugs that mimic the action of dopamine (e.g. bromocriptine, pergolide and others in development) MAO-B inhibitors (e.g. selegiline)

Drugs that release dopamine (e.g. amantadine)

Acetylcholine antagonists (e.g. artane)

Mechanism of action: Levodopa is rapidly decarboxylated in the gastrointestinal tract. Prior to the advent of decarboxylase inhibitors (carbidopa), large oral doses of levodopa were required; thus, toxicity from dopamine was a limiting factor. Pharmakokinetics: Levodopa is well absorbed from the small bowel; however, 95% is rapidly decarboxylated in periphery.

Peripheral dopamine is metabolized in the liver to dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), which are then excreted in urine.

Pharmacologic effects:

The effects on bradykinesia and rigidity are more rapid and complete than the effects on tremor. Other motor defects in PD improve. The psychological well-being of patient is also improved. Tolerance to both beneficial and adverse effects occurs with time. Levodopa is most effective in the first 2-5 years of treatment. After 5 years of therapy, patients have dose-related dyskinesia, inadequate response, or toxicity.

Adverse effect:
Principal adverse effects include:

Anorexia, nausea, and vomiting upon initial administration, which often limit the initial dosage. Cardiovascular effects, including tachycardia, arrhythmias, and orthostatic hypotension. Mental disturbances, including vivid dreams, delusions, and hallucination. Hyperkinesia

Drug interactions:

Vit B6 reduces the beneficial effects of Levodopa by enhancing its extracerebral metabolism. Phenothiazines, reserpine, and butyrophenones antagonize the effects of levodopa because they lead to a junctional blockade of dopamine action.

Carbidopa is an inhibitor of dopa decarboxylase. Because it is unable to penetrate the blood-brain barrier, it acts to reduce the peripheral conversion of levodopa to dopamine. As a result, when carbidopa and levodopa are given concomitantly.

A selective inhibitor of MAO-B, It enhances and prolongs the antiparkinsonism effect of levodopa. It may reduce mild on-off or wearing-off phenomena.

Amantadine is an antiviral agent used in the prophylaxis of influenza A2 . It was found to improve parkinsonian symptoms by stimulating the release of dopamine from dopaminergic nerve terminals in the nigrostriatum and delaying its reuptake.

Amantadine may be more efficacious in Parkinsonism than the anticholinergic atropine derivatives but is less effective than levodopa. It has been used alone to treat early PD and as an adjunct in later stages.

Mechanism:

Since the deficiency of dopamine in the triatum augments the excitatory cholinergic system in the striatum, the blockade of this system by anticholinergic agents, such as artane, helps to alleviate the motor dysfunction.

Therapeutic uses:

Although not as effectives as levodopa or bromocriptine, it may have an additive therapeutic effect at any stage of the disease when taken concurrently.

Adverse effects:

Mental confusion and hallucinations. It can occur as can peripheral atropine-like toxicity (e.g. cycloplegia, urinary retention, constipation)