increased motility and diarrhea due to the stimulation by mast cell con-
tents. Periportal fibrosis of the liver often occurs in systemic mastocytosis
due to the extensive infiltration of mast cells into the liver. Melanocytes
(answer b)are not affected. Anemia and osteoporosis (answers c and d)
would occur in either multiple myeloma or plasmacytosis, where there are
excessive numbers of plasma cells. The excessive production of plasma
cells in the bone marrow disrupts normal hematopoiesis including the
production of RBCs, causing anemia. Plasma cells release interleukins (IL-
1 and IL-6) and tumor necrosis factor-alpha (TNF-α) that stimulate osteo-
clastic activity and induce osteoporosis (see clinical case questions in
the chapter on bone and cartilage).
The positive Darier’s sign is a red wheal and surrounding erythema
around the lesions after rubbing due to the release of histamine.
100.The answer is a.(Alberts, pp 872–874, 1015. Kumar, pp 42, 95, 110,
1198, 1204. Rubin, pp 86–88, 103.)Platelet-derived growth factor (PDGF)
stimulates chemotaxis of monocytes and macrophages as well as fibroblasts
to the site of a wound. PDGF also induces proliferation of vascular smooth
muscle cells (answer b)to facilitate blood vessel repair and fibroblasts
(answer c)to synthesize type I collagen. PDGF stimulates the formation of
granulation tissue (answer d)consisting of new connective tissue and
small blood vessels that form in the wound site. Type II collagen (answer e)
is synthesized by chondrocytes in hyaline and elastic cartilage. Wound
healing is a complex process initiated by damage to capillaries in the der-
mis. The clot forms through the interaction of integrins on the surface of
blood platelets with fibrinogen and fibronectin. Fibrin is the primary pro-
tein that constructs the three-dimensional structure of the clot. A scar is
formed as a very dense region of type I collagen fibers. Macrophages
remove debris at the wound site and are also involved in the remodeling of
the scar. All wound healing processes are slower in diabetics, and the pres-
ence of advanced-glycation end products (AGE) and their interaction with
the receptor for AGE (RAGE) as well as the endogenous ligand for RAGE
(ENRAGE) appear to contribute to inhibited healing in diabetes. AGE are
produced by the nonenzymatic glycation and oxidation of proteins/lipids
and alter those molecules and therefore the function and structure of tissues
and organs such as the kidney (diabetic nephropathy), peripheral nerves
(neuropathy), and the retina (diabetic retinopathy).
Connective Tissue Answers 189