The correct structure of the tear film ensures the appropriate degree of hydration of the eye surface, and has a protective and nourishing function. Irregularities in the structure of one of the three layers of the tear film can contribute to dry eye syndrome. In recent studies, scientists have focused on dysfunction of the Meibomian gland and on deficiencies in the lipid layer of the tear film, which led to the evolution of preparation complementing the tear film. Dry eye syndrome is a multifactorial disease of the ocular surface. Symptoms vary from itching, burning, irritation, eye strain and eye inflammation to potential complications that include damage to the cornea, conjunctiva, and even loss of vision.  Blurred vision is a component of the definition of DSO (apart from discomfort, tear film instability, changes in tear osmolarity, changes in neurosensory and specific inflammation on the surface of the eye). Changes in the thickness of the tear film translate into changes in the breaking power of the eye. It is believed that for every 0.1 mm change in tear film thickness, there is 0.5 D in the "+" or "-" direction. The result of aberration is the lack of a sharp, dotted image.Treatment is adjusted individually for each patient, based on the underlying disease mechanism. Recent studies have shown that dry eye is an inflammatory disease that shares many characteristics with autoimmune diseases. The main goal of this work is to present an outline of epidemiology, pathogenesis, risk factors and treatment methods.

Central serous chorioretinopathy (CSCR) is a disease characterized by serous detachment of the neurosensory retina in the macular area, caused by increased choroidal vascular permeability. The disease is more common in young and middle-aged men (20-50 years old), it has been shown to be highly correlated with an increased level of stress in patients. Other risk factors for the central serous chorioretinopathy are: type A personality (ambitious, nervous and emotional people), use of steroids, Cushing’s syndrome, helicobacter pylori infection, gastroesophageal reflux, hypertension, sleep apnea. The disease leads to visual impairment: metamorphopsia, blurred vision, color vision impairment, impaired contrast and vision in the dark. CSCR diagnostics include funduscopic examination of the eye through the Volk lens revealing focus of circular retinal elevation, optical coherence tomography (OCT), which is a quick and non-invasive test that allows the diagnosis and monitoring of the disease. In the past, the diagnosis was based on fluorescein angiography, the dye spilling out fills the detachment space, revealing the leak center. In most cases the shunt stops spontaneously and spontaneous resorption of the subretinal fluid occurs without the need for treatment. The chronic form of CSCR ongoing more than 4 months requires initiation of therapeutic procedures. The first- line treatment is laser therapy. Micropulse laser therapy of the retina stimulates the pigment epithelium to produce anti-angiogenic factors and inhibit the inflammatory process, as a consequence, the resorption of the subretinal fluid occurs with minimal damage to the retina.