Action therapeutic effectiveness

Mechanism of Action A centrally-acting skeletal muscle relaxant whose exact mechanism is unknown. Effects may be due to its CNS depressant actions. Therapeutic Effect Relieves muscle spasms and pain. 

Mechanism of Action A phenothiazine that blocks dopamine neurotransmission at postsynaptic dopamine receptor sites. Possesses strong anticholinergic, sedative, and antiemetic effects moderate extrapyramidal effects and slight antihistamine action. Therapeutic Effect Relieves nausea and vomiting improves psychotic conditions controls intractable hiccups and porphyria. 

Mecfianism of Action A recombinant, soluble, long-acting insulin analog that binds to human albumin and provides slow absorption and a prolonged action. Therapeutic Effect Controls glucose levels in diabetic patients. 

Mechanism of Action An antiparkinson agent that irreversibly inhibits the activity of monoamine oxidase type B, the enzyme that breaks down dopamine, thereby increasing dopaminergic action. Therapeutic Effect Relieves signs and symptoms of Parkinson s disease. 

Prolonged Action Parenterals Injections. Intramuscular injections have been developed to achieve prolonged therapeutic effects. This can be accompHshed by suspension of dmg particles in oils or flowable gels, from which the dmg slowly diffuses. Aqueous suspensions can also provide such therapeutic response. In these cases, the soHd dmg crystals generally are quite water insoluble and of a controlled particle size and crystallized form. 

The second-generation antidepressants, particularly RIMAs and SSRJs, are much less toxic ia overdose than the older TCAs and irreversible MAO inhibitors. However, similar to first-generation antidepressants, the therapeutic effect only becomes manifest after several weeks. Up to one-third of depressed patients are nonresponders. Ideally, an antidepressant would combine a more rapid onset of action with greater clinical efficacy and a higher responder rate, as well as even better tolerability. 

All drugs, in addition to their therapeutic effects, have the potential to do harm, i.e. to cause adverse/unwanted reactions (side effects). These may or may not be related to the principal pharmacological action of the drug. Examples of the second category are toxic effects of metabolites of a drug or immunological reactions. 

Hirsh J, Dalen JE, Anderson DR et al (2001) Oral anticoagulants mechanism of action, clinical effectiveness, and optimal therapeutic range. Chest 119 (Suppl.) 8S-21S... 

Pharmacodynamics deals with the drag s action and effect within the body. After administration, most dra enter the systemic circulation and expose almost all body tissues to possible effects of the drug. All dra produce more than one effect in the body. The primary effect of a drag is the desired or therapeutic effect. Secondary effects are all other effects, whether desirable or undesirable, produced by the drag. 

By maintaining low concentrations of cytoplasmic noradrenaline, MAO will also regulate the vesicular (releasable) pool of transmitter. When this enzyme is inhibited, the amount of noradrenaline held in the vesicles is greatly increased and there is an increase in transmitter release. It is this action which is thought to underlie the therapeutic effects of an important group of antidepressant drugs, the MAO inhibitors (MAOIs) which are discussed in Chapter 20. 

PET studies show that at effective therapeutic plasma concentrations most neuroleptics occupy some 80% of brain Dj receptors (in the striatum at least) and this is therefore considered to be a requirement for efficacy (Pilowsky, Costa and Eli 1992 Farde 1996). If that is so then clozapine, which occupies only 20-40% of the Dj receptors at a therapeutic concentration, must have some other action which accounts for its therapeutic effectiveness. 

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