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Professor, West Virginia School of Osteopathic Medicine

Atypical lymphocytes resembling leukemic lymphoblasts are characteristic of these viral illnesses. These tumor cells usually are found in clumps in the normal marrow but occasionally replace the marrow completely. Almost half of the children with newly diagnosed leukemia have total leukocyte counts less than 10,000/mm3. Therefore, the diagnosis of leukemia is established by examination of bone marrow, most commonly aspirated from the posterior iliac crest. A normal marrow contains less than 5% blasts; a minimum of 25% blasts confirms the diagnosis. African-American and Hispanic populations have lower remission and higher relapse rates. Higher leukocyte counts, especially if higher than 50,000/mm3, have an unfavorable prognosis. The karyotypes of leukemic cells have diagnostic, prognostic, and therapeutic significance. Patients with hyperdiploidy generally have a more favorable prognosis; those with hypoploidy and pseudodiploidy do less well. Bone radiographs may show altered medullary trabeculation, cortical defects, or transverse radiolucent lines; these radiologic findings lack prognostic significance and usually are unnecessary. Consolidation treatment, aimed at further reducing residual leukemia, delivers multiple chemotherapies in a relatively short period of time. Maintenance therapy with methotrexate and 6-mercaptopurine, vincristine, and prednisone is given for 2 to 3 years to prevent relapse; therapy is discontinued for children who remain in complete remission for 2 to 3 years. The school will not allow the child to register until his immunizations are up-to-date. Call the school nurse or principal to inform him or her that this child should not receive immunizations while he is taking chemotherapy. Call the school nurse or principal to inform him or her that this child will never receive immunizations because of the alteration in his immune system. A mother brings to the clinic her 4-year-old son who began complaining of right knee pain 2 weeks ago, is limping slightly, is fatigued, and has had a fever to 100. Laboratory testing reveals a normal hemoglobin, hematocrit, and white blood cell count and differential. A high susceptibility to leukemia is associated with certain heritable diseases (Klinefelter syndrome, Bloom syndrome, Fanconi syndrome, ataxia telangiectasia, neurofibromatosis) and chromosomal disorders such as Down syndrome. Children with Down syndrome have a 10- to 15-fold increased risk for developing leukemia. Although the viruses in the vaccine are attenuated, immunosuppression from treatment can be profound and viral disease can result. Immunizations without live virus (diphtheria, tetanus, inactivated poliovirus vaccine, hepatitis A and B) are not absolutely contraindicated in this case, but the immunosuppression with chemotherapy often inhibits antibody responses. The platelet count frequently is less than 20,000/mm3, but other laboratory test results are normal, including the bone marrow aspiration (which may show an increase in megakaryocytes). Acute lymphoblastic leukemia has a peak incidence at age 4 years, and boys are affected more frequently. Acute lymphoblastic leukemia is often called the "great imitator" because of its nonspecific symptoms of anorexia, irritability, lethargy, pallor, bleeding, petechiae, leg and joint pain, and fever. Combination chemotherapy is the principal therapy for childhood acute lymphoblastic leukemia. Induction therapy (prednisone, vincristine, and asparaginase) produces remission within 4 weeks in approximately 98% of children with average-risk acute lymphoblastic leukemia. This page intentionally left blank Case 18 You are called to the operating room to manage an infant recently born by emergency cesarean delivery. The mother, an 18-year-old with one previous child, received no prenatal care and arrived at the hospital approximately 1 hour prior to delivery. At delivery you find a large (4500 g), grayish-colored infant with poor tone, no spontaneous respirations, and a pulse of 100 beats per minute (bpm). If these simple measures fail, bag-and-mask ventilation and endotracheal intubation may be required. Considerations Fetal hyperinsulinism is a response to poorly controlled maternal hyperglycemia resulting in fetal macrosomia and increased fetal oxygen requirements.

Jaundice, which causes yellowish discoloration of skin, is caused by abnormal bilirubin metabolism or by retention of bilirubin. It can occur in newborns and in people with hemolytic anemia or ineffective erythropoiesis. This disorder exhibits increases in both unconjugated and conjugated bilirubin levels. Hepatitis is defined as inflammation of the liver and subsequent hepatocellular damage caused by bacterial infection, drugs, toxins, or viral infections. Hepatitis B is transmitted through parenteral injection or through exchange of bodily secretions, as occurs during sexual intercourse. Gastric fluid analysis serves to: (1) Determine pH of gastric fluid, with low pH (achlorhydria) indicative of pernicious anemia (2) Detect hypersecretion of gastric fluid caused by a secreting tumor. Lactose intolerance test examines whether lactose is formed normally in gastric cells. The procedure involves ingestion of a lactose cocktail followed by glucose analysis. The pancreas is a highly vascularized organ connected to the small intestine by the ampulla of Vater. It is considered both an endocrine gland that synthesizes hormones and an exocrine gland that provides digestive enzymes to aid in digestion. These cells produce the following enzymes: (1) Amylase, which breaks down starch and glycogen and is used to diagnose acute pancreatitis; (2) Lipase, which hydrolyzes fats to produce alcohols and fatty acids with elevated levels present in people who have acute pancreatitis; and (3) Trypsin, which is a proteolytic enzyme (functions in protein breakdown). Pancreatic disorders typically result in decreased secretion of enzymes or hormones. Cystic fibrosis is an autosomal recessive genetic disorder characterized by pulmonary disease and intestinal malabsorption caused by lack of pancreatic enzyme secretion. Pancreatitis (inflammation of the pancreas) is associated with alcohol abuse or gallbladder disease and also occurs in patients with lipid disorders and is caused by the release of pancreatic enzymes from cells into the surrounding pancreatic tissue. Diabetes mellitus is a multifactorial disease that occurs when the pancreas can no longer produce insulin, which leads to hyperglycemia. Insulinoma is a tumor of the cells in the islets that leads to increased circulating insulin and hypoglycemia. It involves intubation and gathering of pancreatic fluid after stimulation with secretin, followed by measurement of fluid volume. Quantitative fecal fat examination determines the presence of increased fats in feces (steatorrhea), which is a disorder almost always associated with exocrine pancreatic insufficiency. A 72-hour fecal specimen is collected, and the fats extracted with ether and weighed. A screening procedure involves mixing a small amount of fecal specimen with a fat-soluble stain and examining the specimen microscopically for lipid droplets. Pilocarpine nitrate is used to stimulate sweating on skin which is collected on a small disc. Newborn screening programs and genetic tests that assess the presence of genetic alterations in a number of genes related to cystic fibrosis are also available (see Chapter 10). Enzyme testing for amylase and lipase is performed using a variety of methodologies. Some include the pulmonary system because of the extensive connections between the heart and lungs. Blood passes first through the right, or pulmonary, side of the heart to be oxygenated in the lungs and then is returned to the left, or systemic, side that boosts pressure for the circuit of blood around the body. The microscopic anatomy of the heart includes the myocardium that is made up of cardiac muscle fibers. Myocardium is composed of cardiac muscle fibers interspersed with blood vessels, lymphatics, and nerves. Cardiac muscle fibers synthesize specific proteins (troponin for example) that can be assessed in blood following muscle cell injury. Cardiac dysfunction involves many parts of the heart and can begin in an area other than the heart itself. Heart failure takes many forms, such as congestive heart failure, coronary artery disease, and myocardial infarction (heart attack).

In dry gangrene the coagulative pattern is predominate, while in wet gangrene the liquefactive pattern is predominate. Primary lysosomes are cytoplasmic vacuoles that contain numerous acid hydrolases produced by the Golgi. These vacuoles combine either with vacuoles containing cellular components (autosomes) or with clathrin-coated endocytic vesicles that contain extracellular material (phagosomes). This fusion forms the secondary lysosome (multivesicular body, or phagolysosome) in which the macromolecules are degraded. The products of the normal lysosomal function are usually reutilized by the cell, but if the material is not digestible. Examples of hypertrophy include enlarged skeletal muscle in response to repeated exercise or anabolic steroid use and enlarged cardiac muscle in response to volume overload or hypertension. Examples of physiologic hyperplasia include the increased size of the female breast or uterus in response to hormones. Pathologic hyperplasia may be compensatory to some abnormal process, or it may be a purely abnormal process. Examples of compensatory pathologic hyperplasia include the regenerating liver, increased numbers of erythrocytes in response to chronic hypoxia, and increased numbers of lymphocytes within lymph nodes in response to bacterial infections [follicular (nodular) hyperplasia]. Examples of purely pathologic hyperplasia include abnormal enlargement of the endometrium (endometrial hyperplasia) and the prostate (benign prostatic hyperplasia). Examples of atrophy include decreased size of limbs immobilized by a plaster cast or paralysis, or decreased size of organs affected by endocrine insufficiencies or decreased blood flow. Metaplasia is a term that describes the conversion of one histologic cell type to another. Examples of metaplasia include respiratory epithelium changing to stratified squamous epithelium (squamous metaplasia) in response to prolonged smoking, the normal glandular epithelium of the endocervix changing to stratified squamous epithelium (squamous metaplasia) in response to chronic inflammation, or the normal stratified squamous epithelium of the lower esophagus changing to gastric-type mucosa in response to chronic reflux. In contrast to metaplasia, dysplasia refers to disorganized growth and is characterized by the presence of atypical or dysplastic cells. Dysplasia can be seen in many organs, such as within the epidermis in response to sun damage (actinic keratosis), the respiratory tract, or the cervix (cervical dysplasia). These 100 Pathology substances can cause proliferation of many types of epithelial cells and fibroblasts. Celsus originally described four cardinal signs of inflammation: rubor (redness), tumor (swelling), calor (heat), and dolor (pain). Redness (rubor) and heat (calor) are primarily the result of increased blood flow secondary to vasodilation of arterioles. This vasodilation is mainly the result of prostaglandins (prostacyclin) and nitric oxide, but histamine and bradykinin also participate in this response. Swelling (tumor) results from fluid leaking into the interstitium, while pain (dolor) results from the secretion of bradykinin. This increased vascular permeability results from either direct endothelial injury or contraction of endothelial cells. Substances that cause the latter include histamine (secreted from mast cells, basophils, and platelets), bradykinin, complement components (C3a and C5a), and leukotrienes (C4, D4, and E4). The result of this increased vascular permeability is that large amounts of fluid and cells from the blood can leak into the interstitial tissue. This inflammatory edema fluid, called an exudate, is characterized by a high protein content, numerous inflammatory cells (mainly neutrophils), abundant cellular debris, and a specific gravity greater than 1. In contrast to exudates, transudates result from either increased intravascular hydrostatic pressure or decreased osmotic pressure and are characterized by a low protein content, few cells, and a specific gravity less than 1. The most significant chemotactic agents for neutrophils include bacterial products, complement components (particularly C5a), products of the lipoxygenase pathway (mainly leukotriene B4), and cytokines (particularly interleukin 8). These reactions result in increased calcium levels in the cytoplasm of neutrophils, which then stimulates the assembly of contractile elements in the cytoplasm of leukocytes (actin and myosin), causing movement. These same chemotactic factors activate leukocytes, which results in increased production of arachidonic acid metabolites, activation of the respiratory (oxidative) burst, degranulation and secretion of lysosomal enzymes, and modulation of the leukocyte adhesion molecules. Abnormal formation of melanosomes in these individuals results in oculocutaneous albinism. Most of these patients eventually develop an "accelerated phase" in which an aggressive lymphoproliferative disease, possibly the result of an Epstein-Barr viral infection, results in pancytopenia and death. Ataxia-telangiectasia is a chromosome instability syndrome that is characterized by increased sensitivity to x-rays (causing a markedly increased risk of lymphoid malignancies), recurrent infections, oculocutaneous telangiectasias (dilated blood vessels), and cerebellar ataxia.

Syndromes

• You may be asked to stop taking aspirin, ibuprofen (Advil, Motrin), warfarin (Coumadin), and any other drugs that make it hard for your blood to clot.
• Skin infection (from scratching)
• Is it better after you sleep?
• If there is pain, is it in the muscles, joints, spine, or other location?
• Seizures
• Photodynamic therapy, in which a special drug is injected into the tumor and is then exposed to light. The light activates the medicine that attacks the tumor.

The orange color is the result of the combined effects of the red and yellow heterozygotes. An allele is incompletely dominant if the phenotype of the heterozygote is an intermediate of the phenotypes of the homozygotes. Seemingly small changes to the genetic code can result in disastrous, life-altering, life-threatening, even life-incompatible alterations to protein structure and function. As protein function necessarily depends on protein structure, protein structure necessarily depends upon the genetic code. One of the clearest examples of this-and a clear example of the dire results of even the smallest errors in the genetic system-is the molecular basis for the pathophysiology of sickle cell disease, also called sickle cell anemia. A disease most prevalent in people of tropical or subtropical origin, sickle cell anemia is a genetic disorder that results in abnormally shaped red blood cells. Rather than having the normal flexible biconcavity, these red blood cells assume a shape that is rigid and sickle shaped (like the curved blade used to cut tall grasses). Sickle cell disease is caused by a point mutation in the gene for the -globin chain of hemoglobin. In this particular mutation, a thymine nucleotide is substituted for an adenine nucleotide, resulting in the substitution of valine for glutamic acid at the sixth position from the amino terminus of the -globin chain. Individuals with sickle cell disease are homozygous for the mutated allele, which is autosomal recessive. The substitution of a nonpolar amino acid for an acidic (charged) amino acid has no effect on the secondary, tertiary, and even quaternary structure of hemoglobin: Under normal physiological conditions, this is a totally benign mutation! However, Under low-oxygen conditions, the deoxy form of hemoglobin exposes a hydrophobic patch on the protein with which the nonpolar valine residue can interact by way of hydrophobic interactions. These interactions cause the hemoglobin molecules (called hemoglobin S, for the sickle cell mutation) to aggregate and form precipitates that distort the shape of the red blood cell and decrease its elasticity. Under conditions of low oxygen tension, the aggregation of hemoglobin and the resulting shape change lead to damage of the erythrocyte membrane. Repeated sick-ling causes accumulated membrane damage and significantly decreased elasticity. These damaged cells do not return to their normal shape even after oxygen levels have been restored. We saw that for traits to be inherited, the genes that code for the traits must be passed from one generation of individuals to the next. Each cell in the human body contains the complete blueprint for all the proteins that are necessary for life and that make each person unique. We will primarily examine the eukaryotic mechanisms of gene replication, although a review of some bacterial and viral genetics is included for Test Day completeness. Its basic unit is a nucleotide, which has three basic parts: a deoxyribose sugar, a nitrogenous base, and a phosphate group (see Figure 15. There are four nitrogenous bases in two categories: cytosine and thymine are single-ringed pyrimidines, whereas adenine and guanine are double-ringed purines. Take a glance at the sidebar for a quick way to remember this distinction on Test Day. First, two linear molecules are wound together in a spiral orientation, making it a double-stranded helix. This allows for base pairing through hydrogen bonding of the side chains, giving greater stability to the overall molecule. A pairs with T, forming two hydrogen bonds and C with G, making three hydrogen bonds. This A/T versus C/G ratio tells us how high this temperature needs to be, with more C/G requiring a higher temperature. This allows each of the parent strands to act as a template for generation of a daughter strand. In the days before printing presses, monks used to carry out the same process with ancient tomes. They would copy a book from an existing manuscript (parent strand), generating a new one (daughter strand). Origin of Replication the human genome has about 3 billion base pairs; it is truly amazing to think that all of those base pairs are in every single one of our cells (with the exception of gametes, which have half the genetic complement).