Fuchs heterochromic iridocyclitis (FHI) is a chronic unilateral uveitis appearing with the triad of heterochromia, predisposition to cataract and glaucoma, and keratitic precipitates on the posterior corneal surface. Patients are often asymptomatic and the disease is often discovered through investigation of the cause of the heterochromia or cataract. Neovascularisation (growth of new abnormal vessels) is possible and any eye surgery, such as cataract surgery, can cause bleeding from the fragile vessels in the atrophic iris causing accumulation of blood in the anterior chamber of the eye, also known as hyphema. Presentation
This condition is usually unilateral, and its symptoms vary from none to mild blurring and discomfort. Signs include diffuse iris atrophy and small white keratic precipitates (deposits on the inner surface of the cornea), cells presenting in the anterior chamber as well as the anterior vitreous. Glaucoma and cataract occur frequently. Complications
Glaucoma
Cataract
Decreased visual acuity (vision loss)
Iris atrophy

Causes
According to recent research, not a single theory is able to explain the cause fully. However current plausible theories include infection with Toxoplasma gondii, Herpes simplex virus, Rubella, neurogenic causes, and autoimmune pathology. Diagnosis
Diagnosis is made by an ophthalmologist or optometrist based on the clinical presentation. One indication can be the Amsler sign, which is the presence of blood (hyphema) in the aspirated vitreous fluid, in paracentesis of the anterior chamber. This is caused due to iris atrophy usually seen in FHI and exposure of the fragile iris vasculature to the vitreous fluid.
Licorice and closely related plants are perennial shrubs, the roots of which are used in medicine as well as making candies and in cooking other desserts because of the sweet taste. Through inhibition of 11-beta-hydroxysteroid dehydrogenase type 2 (11-beta-HSD2), glycyrrhizin allows cortisol to activate mineralocorticoid receptors in the kidney. This severely potentiates mineralocorticoid receptor-mediated renal sodium reabsorbtion, due to much higher circulating concentrations of cortisol compared to aldosterone. This, in turn, expands the extracellular volume, increases total peripheral resistance and increases arterial blood pressure. The condition is termed pseudohyperaldosteronism.Secondary hyperaldosterone can also be caused by a genetic mutation in the kidneys which causes sodium and potassium wasting. These conditions can be referred to syndromes such as Bartter Syndrome and Gitelman Syndrome. Treatment
Treatment includes removing the causative agent (such as licorice), a high-potassium, low-sodium diet (for primary) and high-sodium diet (for secondary), spironolactone and eplerenone, potassium-sparing diuretics that act as aldosterone antagonists, and surgery, depending on the cause. Secondary hyperaldosteronism may also be treated with cox2 inhibitors which cause water retention, sodium retention and potassium retention as well as raising blood pressure. Bartter and Gitleman syndrome tend to cause low blood pressure in significant populations and treatment with blood pressure medications tend to lower the blood pressure even more. Other animals
Cats can be affected by hyperaldosteronism. The most common signs in cats are muscle weakness and loss of eyesight, although only one of these signs may be present.