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Fig 1. “Digitus Coeruleus” - “Blue finger”. Analogous to “club finger”, or clubbing of the fingernails, which often ends up with a blue tint at the end of the fingers. Many times clubbing develops in response to inadequate oxygenation of the blood, where there is either a problem in the heart or in the lungs (including the formerly ubiquitous TB), so the blue tint is not unexpected.
Fig 2. Onychomycosis - Fungal nail infection, often characterized by thickened, yellow, crumbly nails.
Fig 3. Onychia maligna - Severe inflammation and ulceration of the matrix and soft parts of the nail bed, accompanied by oozing lymph, purple-red hue surrounding ulcer, nail loss, and pain. Caused by mild trauma in debilitated or immunocompromised patients. Finger becomes bulbous and deformed if not treated. Was known to be caused by strumous or cachetic habits of the insane.
Fig 4. Onychia maligna - Similar to above, longer duration. Bulbous deformation of finger evident.
Fig 5. Arthritis urica Gichtknoten an Finger und Ellenbogen - Gouty arthritis, with gouty deposits in the fingers and elbow. Wow, is that ever some gout.
Die Chiurgischen Krankheiten der Oberen Extremitatan. Paul Vogt, 1881.
The first documentation of gout was in Egypt, in a description of an arthritic big toe with unique symptoms, around 2,600 BC.
Hippocrates knew of gout, and noted its absence in eunuchs and pre-menopausal women.
The realization that the urate crystals found in the urine and joints of gouty patients (first noted by Leeuwenhoek in 1679) was directly related to the symptoms caused wasn’t reached until Alfred Baring Garrod proposed the mechanism of pain in 1848.
Humans and other great apes lost the ability to produce uricase, which is part of the reason that we develop gout, and most other animals don’t…though if the ability to produce that enzyme is interfered with, gout CAN occur. Sue the Tyrannosaurus rex is thought to have been gouty, after all. It’s not known if some larger reptiles did not have the ability to produce uricase in general, or if Sue simply had a genetic defect.