Other competing theories around the turn of the century included one penned by Malcom in 1907, in which the assertion was that prolonged vasoconstriction led to the pathophysiological signs and symptoms of shock. In the following World War I, research concerning shock resulted in experiments by Walter B. Cannon of Harvard and William M. Bayliss of London in 1919 that showed that an increase in permeability of the capillaries in response to trauma or toxins was responsible for many clinical manifestations of shock. In 1972 Hinshaw and Cox suggested the classification system for shock which is still used today. References


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Carney complex and its subsets LAMB syndrome and NAME syndrome are autosomal dominant conditions comprising myxomas of the heart and skin, hyperpigmentation of the skin (lentiginosis), and endocrine overactivity. It is distinct from Carneys triad. Approximately 7% of all cardiac myxomas are associated with Carney complex. Presentation
The spotty skin pigmentation and lentigines occur most commonly on the face, especially on the lips, eyelids, conjunctiva and oral mucosa. Cardiac myxomas may lead to embolic strokes and heart failure and may present with fever, joint pain, shortness of breath, diastolic rumble and tumor plop. Myxomas may also occur outside the heart, usually in the skin and breast. Endocrine tumors may manifest as disorders such as Cushing syndrome. The most common endocrine gland manifestation is an ACTH-independent Cushings syndrome due to primary pigmented nodular adrenocortical disease (PPNAD). The LAMB acronym refers to lentigines, atrial myxomas, and blue nevi. NAME refers to nevi, atrial myxoma, myxoid neurofibromas, and ephelides.Testicular cancer, particularly Sertoli cell type, is associated with Carney syndrome. Thyroid and pancreas cancer may also occur.Although J Aidan Carney also described Carneys triad it is entirely different. Pathophysiology
Carney complex is most commonly caused by mutations in the PRKAR1A gene on chromosome 17 (17q23-q24)
which may function as a tumor-suppressor gene.