Cryoglobulins cause tissue damage by three mechanisms; they can:

a) increase blood viscosity thereby reducing blood flow to tissues to cause the hyperviscosity syndrome (i.e., headache, confusion, blurry or loss of vision, hearing loss, and epistaxis;
b) deposit in small arteries and capillaries thereby plugging these blood vessels and causing infarction and necrosis of tissues including in particular skin (e.g., ears), distal extremities, and kidneys;
c) in type II and type III disease, deposit on the endothelium of blood vessels and activate the blood complement system to form pro-inflammatory elements such as C5a thereby initiating the systemic vascular inflammatory reaction termed cryoglobulinemic vasculitis. Essential cryoglobulinemic disease
The signs and symptoms in the increasingly rare cases of cryoglobulinemic disease that cannot be attributed to an underlying disease generally resemble those of patients suffering Type II and III (i.e., mixed) cryoglobulinemic disease. Type I cryoglobulinemic disease
Signs and symptoms due to the cryoglobulins of type I disease reflect the hyperviscosity and deposition of cryoglobulins within the blood vessels which reduce or stop blood perfusion to tissues. These events occur particularly in cases where blood cryoglobulin levels of monoclonal IgM are high in patients with IgM MGUS, smoldering Waldenströms macroglobulinemia, or Waldenströms macroglobulinemia and in uncommon cases where the levels of monoclonal IgA, IgG, free κ light chains, or free λ light chains are extremely high in patients with non-IgM MGUS, non-IgM smoldering multiple myeloma, or multiple myeloma. The interruption of blood flow to neurological tissues can cause symptoms of confusion, headache, hearing loss, and peripheral neuropathy.
Keratosis follicularis may refer to:

Dariers disease
Focal palmoplantar keratoderma with oral mucosal hyperkeratosisSee also:

Isolated dyskeratosis follicularis
Keratosis follicularis spinulosa decalvans