The correct answer is E. Vascular endothelial growth factor (VEGF) is a heparin binding glycoprotein that increases endothelial cell proliferation in vitro and capillary growth (i.e., angiogenesis) in vivo. Unlike most other growth factors, VEGF has unique target cell specificity for vascular endothelial cells, i.e., it does not directly stimulate growth of other types of cells. VEGF mRNA expression is increased in human skeletal muscle within an hour following intensive exercise. This increase in VEGF mRNA expression is followed by increased VEGF protein levels, which can initiate angiogenesis in the muscles. Growth of new blood vessels decreases diffusion distances between capillaries and muscle fibers, thereby improving oxygen transport to the tissues.

Basic fibroblast growth factor (bFGF) (choice A) is a heparin-binding growth factor capable of stimulating angiogenesis. However, bFGF mRNA expression is not increased following an exercise routine such as that described in the vignette.

Exercise decreases myoglobin oxygen saturation (choice D) as well as intracellular pO₂(choice B).

Endurance exercise training can stimulate growth of mitochondria in human skeletal muscle and thereby increase mitochondrial volume density (choice C) (i.e., volume of mitochondria per unit volume of muscle); however, growth of new mitochondria will not occur within an hour after exercise.

The correct answer is A. Cholecystokinin, or CCK, is synthesized in the duodenal and jejunal mucosa and stimulates gallbladder contraction and pancreatic enzyme secretion. Other functions include slowing of gastric emptying, an atrophic effect on the pancreas, and secretion of antral somatostatin, which in turn, decreases gastric acid secretion.

Gastrin (choice B) prepares the stomach and small intestine for food processing, including stimulating secretion of HCl, histamine, and pepsinogen, increasing gastric blood flow, lower esophageal sphincter tone, and gastric contractions.

Gastric inhibitory peptide, or GIP (choice C), stimulates pancreatic insulin secretion at physiologic doses and inhibits gastric acid secretion and gastric motility at pharmacologic doses.

Secretin (choice D) stimulates secretion of bicarbonate-containing fluid from the pancreas and biliary ducts.

Vasoactive intestinal polypeptide, or VIP (choice E), relaxes intestinal smooth muscle and stimulates gut secretion of water and electrolytes.

The correct answer is C. The vast majority of sweat glands in the body are innervated by sympathetic cholinergic neurons. Sympathetic cholinergic neurons are sympathetic postganglionic neurons that happen to release acetylcholine instead of norepinephrine.

Bradycardia (choice A), bronchoconstriction (choice B), and increased gastrointestinal motility (choice D) would all result from stimulating parasympathetic cholinergic neurons.

Increased peripheral vascular resistance (choice E) would result from stimulating sympathetic adrenergic neurons.

The correct answer is D. The key symptom is hyperventilation. Hyperventilation results in hypocapnia, alkalosis, increased cerebrovascular resistance, and decreased cerebral blood flow. Carbon dioxide plays an important role in the control of cerebral blood flow. An increase in arterial PCO₂ dilates blood vessels in the brain and a decrease in PCO₂ causes vasoconstriction. The anxious, hyperventilating woman is "blowing off" carbon dioxide, which lowers her arterial PCO₂. This decrease in PCO₂ has caused the cerebrovascular resistance (choice E) to increase, thereby decreasing cerebral blood flow. The decrease in cerebral blood flow has caused the woman to feel faint and to have blurred vision. Other symptoms commonly associated with the hyperventilation of anxiety states are feelings of tightness in the chest and a sense of suffocation.

Hyperventilation increases the arterial oxygen content (choice A) and PO₂(choice B) in a normal person.

A decrease in arterial PCO₂ causes the arterial pH (choice C) to increase, i.e., the patient becomes alkalotic.

The correct answer is D. Motilin is a hormone released by the small intestine during the fasting state. Its waxing and waning blood levels correlate with the initiation and ending of migrating motor complexes (MMC). Furthermore, injection of motilin has been shown to evoke MMC activity. The MMC typically begins in the stomach, and over a 90-120 minute period, migrates to the ileum, where it dies out. As one complex dies out in the ileum, another complex begins in the stomach provided the fasting state continues. Eating a meal interrupts the MMC activity.

Cholecystokinin (choice A) is released during the intestinal phase of the digestive period (not during a fast). Its secretion is evoked by the presence of fat and protein digestion products in the duodenum. It induces contraction of the gall bladder and relaxation of the sphincter of Oddi.

Gastrin (choice B) is released from G cells in the antrum, mostly during the gastric phase of the digestive period (not during a fast). It tends to increase stomach motility, although the rate of emptying is decreased because gastrin also causes the pyloric sphincter to contract. It also may contribute to the increase in ileal and colonic motility as part of the gastroileal and gastrocolic reflexes, respectively.

Gastrin-releasing peptide (choice C) mediates the neural release of gastrin. Antral enteric neurons that are activated by vagal efferents or by local reflexes release gastrin-releasing peptide, which stimulates the G cells to secrete gastrin.

Secretin (choice E) is a duodenal hormone that is released during the intestinal phase of the digestive period (not during a fast). Its secretion is evoked by a duodenal pH less than 4.5. Secretin tends to decrease the rate of stomach emptying.

Somatostatin (choice F) is released by delta cells in the stomach mucosa. It mediates the inhibition of gastrin secretion that occurs when the pH of the gastric juice falls below 3. It also acts directly on the parietal cell to decrease acid secretion.

The correct answer is B. Chylomicrons are produced by enterocytes (intestinal epithelial cells), using gut luminal triglycerides for the source of the lipid. The chylomicrons are secreted into the gut lymphatic system, and from there drain eventually into the systemic venous system from the thoracic duct, and hence into the serum portion of the blood. They are initially large and have a very high triglyceride content. With time, lipoprotein lipase releases triglycerides from the chylomicron core by hydrolyzing them to more easily absorbed fatty acids. The enzyme is located on the external surface of the vascular endothelium of tissues with triglyceride needs such as skeletal muscle, cardiac muscle tissue, and lactating breast. The result of lipoprotein lipase activity is that the chylomicrons shrink in size.

While adipose tissue can utilize chylomicrons, lipoprotein lipase is located on the endothelial cells rather than adipocytes (choice A). Adipocytes have an adipose tissue lipase, which is an intracellular enzyme that can cleave triglycerides to glycerol and fatty acids, allowing them to be released into the circulation when chylomicrons are low.

Enterocytes (choice C) have the ability to pick up mixed micelles from the gut lumen for repackaging in the smooth endoplasmic reticulum as chylomicrons.

Hepatocytes (choice D) pick up the chylomicron remnants after the lipoprotein lipase shrinks them.

Myocytes (choice E) are not involved in chylomicron metabolism.

The correct answer is A. Tingible body macrophages are characteristic of a reactive follicular center in benign reactive lymphadenitis. Within the lymph node, the germinal center is the major site of antigen-dependent B-lymphocyte selection and maturation. Certain B cells are selected, and those that are less suited for a particular antigen are eliminated by apoptosis. The apoptotic debris is ingested by macrophages that then appear as "tingible body macrophages." The tenderness is also suggestive of benignity.

Hodgkin's disease (choice B) is a type of lymphoma that spreads from node to node in contiguity. There are four main subtypes of the disease. Histologically, the characteristic cell finding is the Reed-Sternberg cell. Hodgkin's disease usually presents with painless cervical adenopathy and fever, chills, night sweats, and weight loss.

Malignant histiocytosis (choice C) is a common subtype of non-Hodgkin's lymphoma. The characteristic cell appears large with a vesicular nucleus and prominent nucleolus. The disorder can present with nodal enlargement (usually non-tender) or with extranodal involvement.

Non-Hodgkin's lymphoma (choice D) is the name for a varied group of lymphomas that are not associated with Reed-Sternberg cells. They usually present with lymphadenopathy and splenomegaly. They do not spread in contiguity and 30% present extranodally. The histologic presentation varies, but all contain atypical lymphocytes.

Sézary syndrome (choice E) is a type of cutaneous T-cell lymphoma. Neoplastic T cells are found in the upper dermis and also within the peripheral blood. Patients present with lymphadenopathy, pruritic erythroderma, and exfoliation.

The correct answer is A. The right lymphatic duct drains the right arm, the right side of the chest, and the right side of the head. The thoracic duct drains the rest of the body. Both the right lymphatic duct and the thoracic duct dump into the large venous channels at the base of the neck. Occlusion of this drainage can produce intractable edema in sites feeding these ducts.

The left side and right leg would be affected, rather than the right side and left leg (choice B).

The entire left side (rather than just the left arm, choice C) and right leg drain into the thoracic duct.

The right arm and the right half of the head (choices D and E) drain to the right lymphatic duct.

The correct answer is E. Von Willebrand factor (vWF) is a self-polymerizing clotting protein present in the serum and the subendothelial basal lamina, which has binding sites for collagen, platelets, and fibrin. At a site of injury, vWF forms the bridge between the exposed collagen fibers and platelets in circulation, stimulating platelet degranulation and initiating the cellular component of the clotting cascade. An equally important role for vWF is binding platelets to the newly formed fibrin strands in a blood clot.

Factor VIII (choice A) and Factor IX (choice B) are clotting proteins of the intrinsic pathway. Factor VIII acts in concert with activated Factor IX (IXa) to cleave Factor X to Xa. Xa is the prothrombin activator central to both the intrinsic and extrinsic pathways.

Fibronectin (choice C) is a serum protein that acts as an opsonin for phagocytic cells in clots. Fibronectin binds non-specifically to bacteria and other materials in the newly forming clots, and draws the cell membrane of phagocytes into contact with these substances.

Tissue factor (choice D) is a protein released from injured tissues that works in concert with Factor VII to initiate the extrinsic pathway of coagulation. Like Factors VIII and IX, tissue factor and Factor VII cleave Factor X to Xa.