The amygdala is responsible for threat detection and the conditioned and unconditioned fear responses that are carried out as a response to a threat.The HPA axis is responsible for coordinating the hormonal response to stress. Given the strong cortisol suppression to dexamethasone in PTSD, HPA axis abnormalities are likely predicated on strong negative feedback inhibition of cortisol, itself likely due to an increased sensitivity of glucocorticoid receptors. PTSD has been hypothesized to be a maladaptive learning pathway to fear response through a hypersensitive, hyperreactive, and hyperresponsive HPA axis.Low cortisol levels may predispose individuals to PTSD: Following war trauma, Swedish soldiers serving in Bosnia and Herzegovina with low pre-service salivary cortisol levels had a higher risk of reacting with PTSD symptoms, following war trauma, than soldiers with normal pre-service levels. Because cortisol is normally important in restoring homeostasis after the stress response, it is thought that trauma survivors with low cortisol experience a poorly contained—that is, longer and more distressing—response, setting the stage for PTSD. It is thought that the locus coeruleus-noradrenergic system mediates the over-consolidation of fear memory. High levels of cortisol reduce noradrenergic activity, and because people with PTSD tend to have reduced levels of cortisol, it has been proposed that individuals with PTSD cannot regulate the increased noradrenergic response to traumatic stress. Intrusive memories and conditioned fear responses are thought to be a result of the response to associated triggers. Neuropeptide Y (NPY) has been reported to reduce the release of norepinephrine and has been demonstrated to have anxiolytic properties in animal models.
Uveitis–glaucoma–hyphaema (UGH) syndrome, also known as Ellingson syndrome, is a complication of cataract surgery, caused by intraocular lens subluxation or dislocation. The chafing of mispositioned intraocular lens over iris, ciliary body or iridocorneal angle cause elevated intraocular pressure (IOP) anterior uveitis and hyphema. It is most commonly caused by anterior chamber IOLs and sulcus IOLs but, the condition can be seen with any type of IOL, including posterior chamber lenses and cosmetic iris implants. Pathophysiology
The mechanical irritation of mispositioned intraocular lens over iris, ciliary body or iridocorneal angle cause spectrum of iris transillumination defects including anterior uveitis, hyphema and elevated intraocular pressure (IOP). Uveitis results from mechanical breakdown of the blood–aqueous barrier and resultant intraocular inflammation. A hyphema results from damage to vascular tissue of the iris, ciliary body, or angle by mispositioned IOL. Elevated intraocular pressure can be caused by pigment dispersion, uveitis, hyphema or direct blocking of aqueous humor drainage system.UGH syndrome is most commonly caused by anterior chamber IOLs and sulcus IOLs, but it can be seen with any type of IOL, including posterior chamber lenses and cosmetic iris implants. The condition has significantly reduced due to increased use of posterior chamber IOLs, advancements in lens design, IOL material and surgical techniques etc. Currently, majority of IOLs are implanted in the capsular bag, minimizing the chance of IOL contacting uveal structures.