Unlike phototoxic reactions which resemble exaggerated sunburns, photoallergic reactions can cause intense itching and can lead to thickening of the skin. Phytophotodermatitis: UV radiation induces inflammation of the skin after contact with certain plants (including limes, celery, and meadow grass). Causes pain, redness, and blistering of the skin in the distribution of plant exposure. Polymorphic light eruption: Recurrent abnormal reaction to UVR. It can present in various ways including pink-to-red bumps, blisters, plaques and urticaria. Solar urticaria: UVR-induced wheals that occurs within minutes of exposure and fades within hours. Other skin diseases exacerbated by sunlight: Several dermatologic conditions can increase in severity with exposure to UVR. These include systemic lupus erythematosus (SLE), dermatomyositis, acne, atopic dermatitis, and rosacea.Additionally, since sunburn is a type of radiation burn, it can initially hide a severe exposure to radioactivity resulting in acute radiation syndrome or other radiation-induced illnesses, especially if the exposure occurred under sunny conditions. For instance, the difference between the erythema caused by sunburn and other radiation burns is not immediately obvious. Symptoms common to heat illness and the prodromic stage of acute radiation syndrome like nausea, vomiting, fever, weakness/fatigue, dizziness or seizure can add to further diagnostic confusion. Prevention
The most effective way to prevent sunburn is to reduce the amount of UV radiation reaching the skin.
The caffeine molecule is structurally similar to adenosine, and is capable of binding to adenosine receptors on the surface of cells without activating them, thereby acting as a competitive antagonist.In addition to its activity at adenosine receptors, caffeine is an inositol trisphosphate receptor 1 antagonist and a voltage-independent activator of the ryanodine receptors (RYR1, RYR2, and RYR3). It is also a competitive antagonist of the ionotropic glycine receptor. Effects on striatal dopamine
While caffeine does not directly bind to any dopamine receptors, it influences the binding activity of dopamine at its receptors in the striatum by binding to adenosine receptors that have formed GPCR heteromers with dopamine receptors, specifically the A1–D1 receptor heterodimer (this is a receptor complex with 1 adenosine A1 receptor and 1 dopamine D1 receptor) and the A2A–D2 receptor heterotetramer (this is a receptor complex with 2 adenosine A2A receptors and 2 dopamine D2 receptors). The A2A–D2 receptor heterotetramer has been identified as a primary pharmacological target of caffeine, primarily because it mediates some of its psychostimulant effects and its pharmacodynamic interactions with dopaminergic psychostimulants.Caffeine also causes the release of dopamine in the dorsal striatum and nucleus accumbens core (a substructure within the ventral striatum), but not the nucleus accumbens shell, by antagonizing A1 receptors in the axon terminal of dopamine neurons and A1–A2A heterodimers (a receptor complex composed of 1 adenosine A1 receptor and 1 adenosine A2A receptor) in the axon terminal of glutamate neurons.