The patient described suffers from scurvy, due to a deficiency of dietary vitamin C. Absence of vitamin C leads to impaired hydroxylation of proline residues in the nascent procollagen chains, leading to weakness of blood vessel walls. Clinically, the deficiency syndrome is characterized by perifollicular hemorrhages, fragmentation of hairs, purpura, ecchymoses, splinter hemorrhages, and hemorrhages into muscle. In patients with normal dentition, gum changes (swelling, bleeding, loosening of teeth) are also noted. Without supplementation with vitamin C, death may eventually occur. Administration of factor VIII would be indicated for factor VIII deficiency, which would also lead to a prolonged PTT (paial thromboplastin time), which was not noted. Administration of iron would be of benefit in iron-deficiency anemia, but there is no indication of a hypochromic, microcytic anemia in this patient. The anemia of scurvy is typically normochromic and normocytic, due to bleeding. Administration of vitamin B12 would be indicated for a megaloblastic anemia. Although a macrocytic anemia may be observed in scurvy (due to concomitant dietary folate deficiency or peurbations in the folate pool), this patient did not show macrocytosis. Ref: Bender D.A. (2011). Chapter 44. Micronutrients: Vitamins & Minerals. In D.A. Bender, K.M. Botham, P.A. Weil, P.J. Kennelly, R.K. Murray, V.W. Rodwell (Eds),Harper's Illustrated Biochemistry, 29e.