Irritant contact dermatitis
The irritants direct cytotoxic impact on epidermal keratinocytes causes Irritant contact dermatitis. This disrupts the skin barrier and activates the innate immune system. Keratinocytes in the epidermis can be actually affected by irritants. It is a complicated reaction that is influenced by genetic and environmental elements, both of which have a role in the pathogenesis of the disease. It can be seen in both occupational and non-occupational environments but its more common in the occupations dealing in low humidity conditions. Irritant contact dermatitis (ICD) can be divided into forms caused by chemical irritants, and those caused by physical irritants. Common chemical irritants implicated include: solvents (alcohol, xylene, turpentine, esters, acetone, ketones, and others); metalworking fluids (neat oils, water-based metalworking fluids with surfactants); latex; kerosene; ethylene oxide; surfactants in topical medications and cosmetics (sodium lauryl sulfate); and alkalis (drain cleaners, strong soap with lye residues). Physical irritant contact dermatitis may most commonly be caused by low humidity from air conditioning. Also, many plants directly irritate the skin. Allergic contact dermatitis
Allergic contact dermatitis (ACD) is accepted to be the most prevalent form of immunotoxicity found in humans, and is a common occupational and environmental health problem. By its allergic nature, this form of contact dermatitis is a hypersensitive reaction that is atypical within the population. The development of the disease occurs in two phases, which are induction and elicitation. The process of skin sensitization begins when a susceptible subject is exposed to the allergen in sufficient concentration to elicit the required cutaneous immune response.
Glanzmanns thrombasthenia is an abnormality of the platelets. It is an extremely rare coagulopathy (bleeding disorder due to a blood abnormality), in which the platelets contain defective or low levels of glycoprotein IIb/IIIa (GpIIb/IIIa), which is a receptor for fibrinogen. As a result, no fibrinogen bridging of platelets to other platelets can occur, and the bleeding time is significantly prolonged. Signs and symptoms
Characteristically, there is increased mucosal bleeding:
heavy menstrual bleeding
easy bruising
nosebleeds
Bleeding from the gums
gastrointestinal bleeding
postpartum bleeding
increased postoperative bleeding.The bleeding tendency is variable but may be severe. Bleeding into the joints, particularly spontaneous bleeds, are very rare, in contrast to the hemophilias. Platelet numbers and morphology are normal. Platelet aggregation is normal with ristocetin, but impaired with other agonists such as ADP, thrombin, collagen, or epinephrine. Cause
Glanzmanns thrombasthenia can be inherited in an autosomal recessive manner or acquired as an autoimmune disorder.The bleeding tendency in Glanzmanns thrombasthenia is variable, some individuals having minimal bruising, while others have frequent, severe, potentially fatal hemorrhages. Moreover, platelet αIIbβ3 levels correlate poorly with hemorrhagic severity, as virtually undetectable αIIbβ3 levels can correlate with negligible bleeding symptoms, and 10%–15% levels can correlate with severe bleeding. Unidentified factors other than the platelet defect itself may have important roles. Pathophysiology
Glanzmanns thrombasthenia is associated with abnormal integrin αIIbβ3, formerly known as glycoprotein IIb/IIIa (GpIIb/IIIa), which is an integrin  aggregation receptor on platelets. This receptor is activated when the platelet is stimulated by ADP, epinephrine, collagen, or thrombin.