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Co-Director, University of Puerto Rico School of Medicine

Administration of blocking agents is aimed at preventing the entrance of radioactive materials into tissues. Examples include antithyroid drugs, glucocorticoids, ammonium chloride, diuretics, expectorants, and inhalants. It is useful to characterize the chest pain as (1) new, acute, and ongoing; (2) recurrent, episodic; and (3) persistent, sometimes for days. Myocardial Ischemia Angina Pectoris Substernal pressure, squeezing, constriction, with radiation typically to left arm; usually on exertion, especially after meals or with emotional arousal. Mediastinal Emphysema Sharp, intense, localized to substernal region; often associated with audible crepitus. Oppressive, constrictive, or squeezing; may radiate to arm(s), neck, back Less severe, similar pain on exertion; + coronary risk factors "Tearing" or "ripping"; may travel from anterior chest to mid-back Hypertension or Marfan syndrome (Chap. Chest Wall Pain Due to strain of muscles or ligaments from excessive exercise or rib fracture from trauma; accompanied by local tenderness. Esophageal Pain Deep thoracic discomfort; may be accompanied by dysphagia and regurgitation. Emotional Disorders Prolonged ache or dartlike, brief, flashing pain; associated with fatigue, emotional strain. Figure 33-2 presents clues to diagnosis and workup of acute, life-threatening chest pain. Evaluation of acute pain requires rapid assessment of likely causes and early initiation of appropriate therapy. Physical exam may be unrevealing or misleading, and laboratory and radiologic exams delayed or unhelpful. Visceral pain (due to distention of a hollow viscus) localizes poorly and is often perceived in the midline. Intestinal pain tends to be crampy; when originating proximal to the ileocecal valve, it usually localizes above and around the umbilicus. Pain from biliary or ureteral obstruction often causes pts to writhe in discomfort. Associated Symptoms Look for fevers/chills (infection, inflammatory disease, infarction), weight loss (tumor, inflammatory disease, malabsorption, ischemia), nausea/vomiting (obstruction, infection, inflammatory disease, metabolic disease), dysphagia/odynophagia (esophageal), early satiety (gastric), hematemesis (esophageal, gastric, duodenal), constipation (colorectal, perianal, genitourinary), jaundice (hepatobiliary, hemolytic), diarrhea (inflammatory disease, infection, malabsorption, secretory tumors, ischemia, genitourinary), dysuria/hematuria/vaginal or penile discharge (genitourinary), hematochezia (colorectal or, rarely, urinary), skin/joint/eye disorders (inflammatory disease, bacterial or viral infection). Predisposing Factors Inquire about family history (inflammatory disease, tumors, pancreatitis), hypertension and atherosclerotic disease (ischemia), diabetes mellitus (motility disorders, ketoacidosis), connective tissue disease (motility disorders, serositis), depression (motility disorders, tumors), smoking (ischemia), recent smoking cessation (inflammatory disease), ethanol use (motility disorders, hepatobiliary, pancreatic, gastritis, peptic ulcer disease). Rectal examination assesses presence and location of tenderness, masses, blood (gross or occult). General examination: evaluate for evidence of hemodynamic instability, acid-base disturbances, nutritional deficiency, coagulopathy, arterial occlusive disease, stigmata of liver disease, cardiac dysfunction, lymphadenopathy, and skin lesions. In selected cases, percutaneous biopsy, laparoscopy, and exploratory laparotomy may be required. Consider obstruction, perforation, or rupture of hollow viscus; dissection or rupture of major blood vessels (esp. Brief History and Physical Examination Historic features of importance include age; time of onset of the pain; activity of the pt when the pain began; location and character of the pain; radiation to other sites; presence of nausea, vomiting, or anorexia; temporal changes; changes in bowel habits; and menstrual history. Pain localized to the epigastrium may be of cardiac origin or due to esophageal inflammation or perforation, gastritis, peptic ulcer disease, biliary colic or cholecystitis, or pancreatitis. Pain localized to the right upper quadrant includes those same entities plus pyelonephritis or nephrolithiasis, hepatic abscess, subdiaphragmatic abscess, pulmonary embolus, or pneumonia, or it may be of musculoskeletal origin. Additional considerations with left upper quadrant localization are infarcted or ruptured spleen, splenomegaly, and gastric or peptic ulcer. Left lower quadrant pain may be due to diverticulitis, perforated neoplasm, or other entities previously mentioned. Traditionally, narcotic analgesics were withheld pending establishment of diagnosis and therapeutic plan, since masking of diagnostic signs may delay needed intervention. Ruptured aneurysm (instant onset), cluster headache (peak over 3­5 min), and migraine (onset over minutes to hours) differ in time to peak intensity. The psychological state of the patient should also be evaluated since a relationship exists between pain and depression. Onset usually in childhood, adolescence, or early adulthood; however, initial attack may occur at any age.

Consider this possible experiment: the subject is told to look at a screen with a black dot in the middle (a fixation point). The subject has been instructed to push a button if the photograph is of someone they recognize. The photograph might be of a celebrity, so the subject would press the button, or it might be of a random person unknown to the subject, so the subject would not press the button. Neurons are the primary type of cell that most anyone associates with the nervous system. Neurons are important, but without glial support they would not be able to perform their function. They are responsible for the electrical signals that communicate information about sensations, and that produce movements in response to those stimuli, along with inducing thought processes within the brain. The threedimensional shape of these cells makes the immense numbers of connections within the nervous system possible. It is the axon that propagates the nerve impulse, which is communicated to one or more cells. The other processes of the neuron are dendrites, which receive information from other neurons at specialized areas of contact called synapses. Myelin acts as insulation much like the plastic or rubber that is used to insulate electrical wires. A key difference between myelin and the insulation on a wire is that there are gaps in the myelin covering of an axon. Each gap is called a node of Ranvier and is important to the way that electrical signals travel down the axon. The first way to classify them is by the number of processes attached to the cell body. Using the standard model of neurons, one of these processes is the axon, and the rest are dendrites. Multipolar cells have more than two processes, the axon and two or more dendrites. True unipolar cells are only found in invertebrate animals, so the unipolar cells in humans are more appropriately called "pseudo-unipolar" cells. Unipolar cells are exclusively sensory neurons and have two unique characteristics. The axon projects from the dendrite endings, past the cell body in a ganglion, and into the central nervous system. They are found mainly in the olfactory epithelium (where smell stimuli are sensed), and as part of the retina. Neurons can also be classified on the basis of where they are found, who found them, what they do, or even what chemicals they use to communicate with each other. Some neurons referred to in this section on the nervous system are named on the basis of those sorts of classifications (Figure 12. Glial Cells Glial cells, or neuroglia or simply glia, are the other type of cell found in nervous tissue. The name glia comes from the Greek word that means "glue," and was coined by the German pathologist Rudolph Virchow, who wrote in 1856: "This connective substance, which is in the brain, the spinal cord, and the special sense nerves, is a kind of glue (neuroglia) in which the nervous elements are planted. Astrocytes have many processes extending from their main cell body (not axons or dendrites like neurons, just cell extensions). Generally, they are supporting cells for the neurons in the central nervous system. One oligodendrocyte will provide the myelin for multiple axon segments, either for the same axon or for separate axons. Ependymal cells line each ventricle, one of four central cavities that are remnants of the hollow center of the neural tube formed during the embryonic development of the brain. The choroid plexus is a specialized structure in the ventricles where ependymal cells come in contact with blood vessels and filter and absorb components of the blood to produce cerebrospinal fluid. Satellite cells are found in sensory and autonomic ganglia, where they surround the cell bodies of neurons. Schwann cells are different than oligodendrocytes, in that a Schwann cell wraps around a portion of only one axon segment and no others. Oligodendrocytes have processes that reach out to multiple axon segments, whereas the entire Schwann cell surrounds just one axon segment.

Causes include the following: primary (idiopathic) or secondary due to gastroesophageal reflux disease, emotional stress, diabetes, alcoholism, neuropathy, radiation therapy, ischemia, or collagen vascular disease. An important variant is nutcracker esophagus: high-amplitude (>180 mmHg) peristaltic contractions; particularly associated with chest pain or dysphagia, but correlation between symptoms and manometry is inconsistent. If heart disease has been ruled out, edrophonium, ergonovine, or bethanechol can be used to provoke spasm. Rare pts require surgical intervention: longitudinal myotomy of esophageal circular muscle. Oral valganciclovir (900 mg bid) is an effective alternative to parenteral treatment. Candida Esophagitis In immunocompromised hosts, or those with malignancy, diabetes, hypoparathyroidism, hemoglobinopathy, systemic lupus erythematosus, corrosive esophageal injury, candidal esophageal infection may present with odynophagia, dysphagia, and oral thrush (50%). Diagnosis is made on endoscopy by identifying yellow-white plaques or nodules on friable red mucosa. Candida Esophagitis Oral nystatin (100,000 U/mL), 5 mL q6h, or clotrimazole, 10-mg tablet sucked q6h, is effective. Predisposing factors include recumbency after swallowing pills with small sips of water and anatomic factors impinging on the esophagus and slowing transit. Pill-Related Esophagitis Withdraw offending drug, use antacids, and dilate any resulting stricture. Eosinophilic Esophagitis Mucosal inflammation with eosinophils with submucosal fibrosis can be seen especially in pts with food allergies. Treatment involves a 12-week course of swallowed fluticasone (440 g bid) using a metered-dose inhaler. Intestinal water absorption passively follows active transport of Na+, Cl­, glucose, and bile salts. Proximal small intestine: iron, calcium, folate, fats (after hydrolysis of triglycerides to fatty acids by pancreatic lipase and colipase), proteins (after hydrolysis by pancreatic and intestinal peptidases), carbohydrates (after hydrolysis by amylases and disaccharidases); triglycerides absorbed as micelles after solubilization by bile salts; amino acids and dipeptides absorbed via specific carriers; sugars absorbed by active transport. Intestinal Motility Allows propulsion of intestinal contents from stomach to anus and separation of components to facilitate nutrient absorption. Propulsion is controlled by neural, myogenic, and hormonal mechanisms; mediated by migrating motor complex, an organized wave of neuromuscular activity that originates in the distal stomach during fasting and migrates slowly down the small intestine. Mediated by one or more of the following mechanisms: Osmotic Diarrhea Nonabsorbed solutes increase intraluminal oncotic pressure, causing outpouring of water; usually ceases with fasting; stool osmolal gap > 40 (see below). Lactase deficiency can be either primary (more prevalent in blacks and Asians, usually presenting in early adulthood) or secondary (from viral, bacterial, or protozoal gastroenteritis, celiac or tropical sprue, or kwashiorkor). Secretory Diarrhea Active ion secretion causes obligatory water loss; diarrhea is usually watery, often profuse, unaffected by fasting; stool Na+ and K+ are elevated with osmolal gap < 40. Exudative Inflammation, necrosis, and sloughing of colonic mucosa; may include component of secretory diarrhea due to prostaglandin release by inflammatory cells; stools usually contain polymorphonuclear leukocytes as well as occult or gross blood. A sudden, acute course, often with nausea, vomiting, and fever, is typical of viral and bacterial infections, diverticulitis, ischemia, radiation enterocolitis, or drug-induced diarrhea and may be the initial presentation of inflammatory bowel disease. A longer (>4 weeks), more insidious course suggests malabsorption, inflammatory bowel disease, metabolic or endocrine disturbance, pancreatic insufficiency, laxative abuse, ischemia, neoplasm (hypersecretory state or partial obstruction), or irritable bowel syndrome. Parasitic and certain forms of bacterial enteritis can also produce chronic symptoms. Fecal impaction may cause apparent diarrhea because only liquids pass partial obstruction. Several infectious causes of diarrhea are associated with an immunocompromised state (Table 53-1). Physical Examination Signs of dehydration are often prominent in severe, acute diarrhea. Certain signs are frequently associated with specific deficiency states secondary to malabsorption. Are there features to suggest underlying autonomic neuropathy or collagenvascular disease in the pupils, orthostasis, skin, hands, or joints?

Syndromes

• Chest MRI
• Head MRI scan
• Severe hypothyroidism (underactive thyroid gland) 
• Grow body hair
• MRI scans
• Is often "on the go," acts as if "driven by a motor"

The mass transfer coefficient is specific for the membrane used and the solute being considered; for dialyzers, this is usually represented as KoA, where A is the effective surface area of the specific dialyzer. Manufacturers generally provide the KoA of the different solutes for the specific dialyzer, and the clearance of specific solutes at different blood and dialysate can be calculated from such values. However, it is important to keep in mind that these KoA values are determined by manufacturers in aqueous solutions, and will result in a higher calculated value for these solute clearances than is observed clinically. Another important caveat in the relationship between higher clearance and higher blood flow rate is the fact that, in the clinical setting, blood flow rate measured by the blood pump may not accurately represent the actual blood flow rate flowing through the hollow fibers of the dialyzer. A practical implication of these observations is that, although the clearance of most solutes theoretically increases with higher blood and dialysate flow rates, in practice the maximum prescribed blood flow rate should not exceed a rate at which the negative pre-pump pressure. Finally, although these limitations to blood flow rate do not apply to dialysate flow, there are also practical limits to increasing the dialysate flow rate; not only is the expense of preparing water for dialysate preparation increased, but, because of the limitation of the mass transfer coefficient for specific solutes and specific dialysis membranes, the optimal combination of dialysate flow is approximately 1. Thus, if the maximum blood flow rate (above which the negative arterial pressure prepump exceeds -250 mm Hg) is 350 mL/min, then the optimal dialysate flow is around 600 to 700 mL/min. Assessing the Dialysis Dose where Cpost is the urea concentration at the completion of dialysis, and Cpre is the urea concentration before the start of dialysis. The other variable that determines the net impact of solute removal from the patient by hemodialysis is the volume of distribution of the solute. Thus, the dose of dialysis is usually defined as Kt/V, where V is the volume of distribution of that particular solute. Urea has been the index molecule used to define the dose of dialysis, because it is easily measured, it is small and therefore diffuses readily across a dialysis membrane, and, importantly, its volume of distribution (total body water) can be calculated from the weight of the patient. Thus, the dose of dialysis traditionally Although solute clearance by diffusion is dependent on the size of the solute molecule, other considerations, such as the electrical charge of the molecule and its effective size, also impact the net transfer of uremic solutes across the membrane. Although phosphate has a low molecular weight and, based on its molecular size, would be expected to be easily cleared by high-flux dialysis membranes, in reality phosphate is cleared rather poorly during dialysis because of its high negative charge and the large number of water molecules that circulate with the phosphate moiety; additionally, because of the large intracellular reservoirs of phosphate and slow transfer from the intracellular to the plasma compartment, net phosphate clearance by dialysis is poor. This results in a time-dependent slow clearance during conventional dialysis, with moderate clearance and declining removal during the first 2 hours of standard hemodialysis, and negligible removal afterward. However, as discussed later, the removal of phosphates is higher during longer dialysis treatments, such as occurs with nocturnal dialysis (approximately 8 hours), because the longer dialysis time allows the timedependent transfer of phosphate from intracellular to the plasma compartment; accordingly, patients treated with nocturnal dialysis often require fewer or no phosphate binders. Extracellular Volume Control (Ultrafiltration) Another important function of hemodialysis is the removal of excess fluid that accumulates in the absence of effective kidney function. Modern dialysis equipment adjusts these hydrostatic pressure gradients by varying the negative ("suction") pressure in the dialysate compartment rather than increasing the pressure in the blood compartment; this avoids the potential for increased lysis of red blood cells. However, as this rapid transfer of plasma water occurs at the inlet of the dialyzer, the concentration of protein (oncotic pressure) rapidly rises in the blood compartment; because these proteins are also negatively charged, there is a corresponding development of a "concentration polarization," whereby there is a rapid increase in negatively charged plasma protein concentration at the membrane surface (inside the blood compartment). This has the effect of disproportionately increasing the oncotic pressure at the interface between the blood compartment and the surface of the membrane. The high oncotic pressure at the surface of these high-flux membranes inhibits further ultrafiltration to the extent that, toward the blood outlet of high-flux dialysis membranes, "reverse filtration" may occur, with dialysate solutions moving across the membrane into the blood compartment. Although there are numerous abnormalities in the concentration of various metabolites that result from kidney failure, acid-base (bicarbonate) balance and potassium concentration are examples of the use of various dialysate solutions to correct such abnormalities. One of the functions of dialysis is to compensate for this metabolic acidosis by replenishing blood bicarbonate. Most often, this is accomplished using formulations of dialysate solutions with bicarbonate concentrations, generally between 30 and 32 mEq/L. However, this product cannot simply be added as a component of dialysate, because the presence of other electrolytes needed in the dialysate (specifically calcium and magnesium) would result in their precipitation as carbonates, thereby reducing the concentration of all three components. Current dialysate delivery technology requires the preparation of two separate dialysate streams, one called "acid concentrate," which combines all the ingredients of dialysate except sodium bicarbonate, and a second stream that contains sodium bicarbonate and sodium chloride. One important detail in the choice of dialysate bicarbonate levels is the presence of acetate in the formulation of the "acid concentrate" mentioned earlier. Depending on the manufacturer and whether the concentrate is liquid or powder, most "acid concentrates" contain 4 to 8 mEq/L of acetate (acetic acid) to maintain an acidic milieu and to prevent precipitation of calcium and magnesium salts. It is important that the prescription for the dialysate bicarbonate take into consideration the concentration of the acetate, because the acetate is rapidly metabolized (Krebs cycle) to bicarbonate on a 1:1 ratio. Thus, when the dialysate prescription is for a "bicarbonate level of 35 mEq/L," the effective total buffer in the dialysate may be as high as 42 mEq/L, depending on the amount of acetate; this may result in marked postdialysis alkalemia. There are ongoing studies about the optimal concentration of total buffer, but most observation data suggest that a total buffer of around 35 to 37 mEq/L is optimal; ideally, such a concentration should be adjusted for each patient, depending on their dietary intake, protein catabolic rate, and the resulting predialysis and postdialysis bicarbonate level. In the absence of kidney function, potassium (and other electrolytes such as magnesium) accumulates in the blood; accordingly, an important function of dialysis is to reduce the potassium concentration between dialysis episodes to a level that prevents significant predialysis hyperkalemia while avoiding significant hypokalemia after dialysis. Because potassium removal depends on the difference in potassium concentration between the blood and the dialysate, in concept the simplest way in which potassium removal can be maximized is to use a dialysate potassium concentration of 0 mEq/L.