Mydriasis drugs causing

Eye The radial pupillary dilator muscle of the iris contains alpha-receptors activation by drugs causes mydriasis. 

Cycloplegic mydriatics cause mydriasis and cyclople-gia (paralysis of the ciliary muscle, resulting in an inability to focus the eye). These drugs (see Chap. 25) are used in the treatment of inflammatory conditions of the iris and uveal tract of the eye and for examination of the eye... 

Medications with anticholinergic properties induce mydriasis, which can lead to angle closure in pupillary block and plateau iris. Pupillary block may also be induced by drugs that cause miosis.12... 

Antimuscarinic drugs block contraction of the iris sphincter and ciliary muscles of the eye produced by ACh. This results in dilation of the pupil (mydriasis) and paralysis of accommodation (cycloplegia), responses that cause photophobia and inability to focus on nearby objects. Ocular effects are produced only after higher parenteral doses. Atropine and scopolamine produce responses lasting several days when applied directly to the eyes. 

In the eye, the radial pupillary dilator muscle of the iris contains oo receptors activation by drugs such as phenylephrine causes mydriasis (see Figure 6-9). Alpha stimulants also have important effects on intraocular pressure. Alpha agonists increase the outflow of aqueous humor from the eye and can be used clinically to reduce intraocular pressure. In contrast, agonists have little effect, but antagonists decrease the production of aqueous humor. These effects are important in the treatment of glaucoma (see Chapter 10), a leading cause of blindness. 

Eye. Atropine and similar antimuscarinics block the acetylcholine-mediated contraction of the pupillary sphincter muscle, thus causing dilation of the pupil (mydriasis).1 During an ophthalmologic exam, these drugs may be applied topically in order to dilate the pupil, thus allowing a more detailed inspection of internal eye structures such as the retina. 

FIGURE 14.6 Miosis and mydriasis caused by autonomic drugs. N = nerve. 

At higher concentrations, atropine causes block of all parasympathetic functions. However, atropine is a remarkably safe drug in adults. Atropine poisoning has occurred as a result of attempted suicide, but most cases are due to attempts to induce hallucinations. Poisoned individuals manifest dry mouth, mydriasis, tachycardia, hot and flushed skin, agitation, and delirium for as long as a week. Body temperature is frequently elevated. These effects are memorialized in the adage, "dry as a bone, blind as a bat, red as a beet, mad as a hatter."... 

This is caused by excessive stimulation of CNS and peripheral serotonin receptors and is characterized by changes in mental state, autonomic hyperactivity (hypertension, tachycardia, hyperthermia, may be up to 4l°C, hyperactive bowel sounds, mydriasis, excessive sweating) and neuromuscular abnormality (tremor, clonus, ocular clonus, hypertonicity, hyperreflexia) the latter may lead to rhabdomyolysis with consequent risk of renal failure, hyperkalaemia and hypocalcaemia. Symptoms usually occur within 6 hours of taking the provoking drug, Tremor, akathisia and diarrhoea are early features. 

Topical instillation of a 1% solution in eyes with normal adrenergic innervation causes mydriasis and also some vasoconstriction. However, hydroxyamphetamine is used only as a mydriatic agent. After topical application onset occurs within 15 minutes, maximum dilation occurs within 60 minutes, and the duration of mydriasis is approximately 6 hours. The U.S. Food and Drug Administration has labeled this drug as a Pregnancy Category C. 

When used for routine mydriasis, hydroxyamphetamine appears to be effective while causing Uttle, if any, ocular irritation. It has been suggested that, due to the indirect action of this drug, it may be a safe mydriatic to use in eyes with shallow anterior chambers, and it may be more readily counteracted with miotics. In patients with open-angle glaucoma, hydroxyamphetamine elevates lOP minimally, if at all. Reductions of lOP have also been reported. 

Central nervous system depressants include the barbiturates, such as phenobarbital, and the antianxiety drugs, including diazepam (VaUum), chlordiazepoxide Odbrium), oxazepam (Serax), flurazepam hydrochloride (Dalmane), and lorazepam (Ativan). The benzodiazepines, including diazepam, occasionally cause mydriasis, presumably because of their anticholinergic side effects. 

Early signs of tricyclic antidepressant toxicity are due to anticholinergic effects and include tachycardia, mydriasis, dry mouth, low-grade fever, diminished bowel sounds, CNS excitation, and delirium. More serious toxicity is manifested by coma, respiratory depression, seizures, and cardiovascular toxicity including conduction disturbances, hypotension, ventricular arrhythmias, and asystole. Seizures cause hyperthermia, rhabdomyolysis, and metabolic acidosis. Clinical deterioration can be rapid and catastrophic in patients with tricyclic antidepressant overdose. Death most often occurs due to dysrhythmia and circulatory collapse. The typical therapeutic dose of a tricyclic antidepressant is 2-4 mg kg day Doses of 15-20 mg kg are potentially lethal. Therapeutic drug levels for most tricyclic antidepressants range from 100 to... 

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