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**TABLE 9-3.Common management and prevention strategies for catheterization complications are summarized in Table 9-3.It is common to refer to these multiple lesions as diffuse disease. **Figure 9-2. ** Coronary artery circulation with a coronary vessel narrowed with plaque formation. A cineventriculogram is obtained by radiographic imaging during the injection of dye after advancing the catheter from the aorta, through the aortic valve, and into the left ventricle (see Figure 9-1C). The cineventriculogram provides information on ventricular wall motion, ejection fraction, and the presence and severity of mitral regurgitation and aortic regurgitation. Ejection fraction, or the percentage of blood volume ejected from the left ventricle with each contraction, is the gold standard for determining left ventricular function and is helpful in selecting treatment strategies. A left ventricular ejection fractions (LVEF) normal value is 55% to 60%. The LVEF is one of the most important predictors of long-term outcome following acute myocardial infarction (AMI). Patients with ejection fractions less than 20% have nearly 50% 1-year mortality. Another important measurement is the pressure in the left ventricle at the end of diastole. This is called "left ventricular end-diastolic pressure (LVEDP)." It, too, is an important determinant of ventricular function and is considered to be a predictor of morbidity and mortality in patients with heart failure (HF) and those undergoing cardiac surgery. The normal LVEDP is 6-12 mm Hg. ##### **_Complications_** During cardiac catheterization, a number of complications may occur, including arrhythmia; coronary vasospasm; coronary dissection; allergic reaction to the dye; atrial or ventricular perforation resulting in pericardial tamponade; embolus to an extremity, a lung, or, rarely, the brain; acute closure of the left main coronary; myocardial infarction (MI); or death. Common management and prevention strategies for catheterization complications are summarized in Table 9-3. **TABLE 9-3.PTCA, also termed angioplasty or balloon angioplasty, is a cardiac catheterization with the addition of a balloon apparatus on the tip of the catheter for revascularizing the myocardium (Figure 9-3).The catheter tip is advanced, generally over a guidewire, into the coronary artery until the balloon is positioned across the atherosclerotic lesion in the vessel.

Please give any helpful information (danger, cost, etc.)please list them and describe what they did for you.If you have tried any arthritis treatments that most doctors reject (copper bracelet, insect venom, hormone, etc.)you've used for arthritis, and tell what they did for you.**Other Treatments** Please list any over-the-counter remedies (liniments, pills other than aspirin, etc.)Please list other professional treatments you've tried (acupuncture, physical therapy, splints, biofeedback, manipulation, massage, etc.). Of these, what helped the most? What made no difference? Did any treatment injure you? **Surgery** Have you had surgery for arthritis? If no, skip to the section on Exercise. If yes, please name the joint(s) involved and what was done (total knee replacement, partial hip replacement, wrist fusion, etc. ), including the year you had the operation. If you have an artificial joint and know its brand name (Zimmer knee, Techmedica hip, etc.) please give it: How long did it take to fully recover from surgery? What follow-up treatment (physical therapy, exercise advice, etc.) did you receive after your operation(s)? Please tell the outcome (pain relief, greater mobility, infection, etc.) of your operation(s). What advice would you offer someone considering arthritis surgery? **Exercise** Do you exercise (stretch, swim, walk, etc.) for arthritis? If no, please skip to Other Treatments. If yes, please tell _what you do_ and _how much time_ each day you devote to exercise: How did you learn exercises? (Doctor, book, class, etc.) What benefit(s) do you get from exercise? If you have ever been harmed by exercise, please tell what happened: What exercise advice can you offer other arthritis sufferers? **Other Treatments** Please list any over-the-counter remedies (liniments, pills other than aspirin, etc.) you've used for arthritis, and tell what they did for you. If you have tried any arthritis treatments that most doctors reject (copper bracelet, insect venom, hormone, etc.) please list them and describe what they did for you. Please give any helpful information (danger, cost, etc.)**Nutrition** Have you changed the way you eat (avoid some foods, eat more of others, etc.)because of arthritis?If yes, please give details: What has your doctor told you about nutrition and arthritis?Does arthritis affect your food shopping and cooking?If yes, in what way?What vitamins/minerals, if any, do you take, and what do they do for you?

Chronic allograft nephropathy ### Treatment and Prognosis Treatment of chronic TIN is based on the treatment of the primary disease process.5.5.Chronic nephrotoxin exposure, especially the calcineurin inhibitors, lithium, heavy metals (cadmium and lead), chemotherapeutic agents (cisplatinum, ifosfamide), antimicrobials (amphotericin B, antiretroviral drugs), NSAIDs and certain Chinese herbs.4.End-stage kidney disease due to chronic TIN develops between ages 30–60; the rate of progression may be slower in the hyperuricemic patients with the use of allopurinol. Several additional families are now reported with chronic TIN due inherited autosomal dominant mutations in other disease-causing genes.These include the gene encoding renin (REN) [142] mucin-1 (MUC1) [148], hepatocyte nuclear factor - 1B (HNF1B) [149] and SEC61A1 [150]. Together they constituted they newly termed group of Autosomal Dominant Tubulointerstitial Kidney Dieases [151]. There is another rare genetic disease that resembles nephronophthisis histologically except for the presence of hyperchromatic and abnormally enlarged tubular epithelial cell nuclei that causes end-stage kidney disease in the third or fourth decade of life. It was first recognized as a distinct entity and named karyomegalic interstitial nephritis (KIN) in 1979 [143]. In 2012 Zhou et al. [144] identified an autosomal recessive mutation in FAN1 as a cause of KIN. 2. 2. Congenital anomalies of the kidney and urinary tract 3. 3. Inborn error of metabolism, including cystinosis, oxalosis, methylmalonic academia and the mitochondrial cytopathies. 4. 4. Chronic nephrotoxin exposure, especially the calcineurin inhibitors, lithium, heavy metals (cadmium and lead), chemotherapeutic agents (cisplatinum, ifosfamide), antimicrobials (amphotericin B, antiretroviral drugs), NSAIDs and certain Chinese herbs. 5. 5. Chronic allograft nephropathy ### Treatment and Prognosis Treatment of chronic TIN is based on the treatment of the primary disease process.The use of angiotensin converting-enzyme inhibitors and/or angiotensin receptor type 1 blockers are being used with increasing frequency for a variety of chronic renal diseases, especially when associated with hypertension and/or proteinuria.

CONTRAINDICATION: This product is contraindicated in patients who are known to be hypersensitive to it.INDICATIONS: It is used in the treatment of bronchial asthma and reversible bronchospasm.bitolterol mesylate /bitol′t rol mes′ilāt/, an orally inhaled bronchodilator.**Bite wing radiograph** _(Bird and Robinson, 2009)_ _Bithynia_ /b thin′ē· /, a genus of snails, species of which act as intermediate hosts to _Opisthorchis._ biting in childhood, a natural behavior trait and reflex action in infants, acquired at about 5 to 6 months of age in response to the introduction of solid foods in the diet and the beginning of the teething process. The activity represents a significant modality in the psychosocial development of the child, because it is the first aggressive action the infant learns, and through it the infant learns to control the environment. The behavior also confronts the infant with one of the first inner conflicts, because biting can produce both pleasing and displeasing results. Biting during breastfeeding causes withdrawal of the nipple and anxiety in the mother, yet it also serves as a means of soothing teething discomfort. Infants continue to use biting as a mechanism for exploring their surroundings. Toddlers and older children often use biting for expressing aggression toward their parents and other children, especially during play or as a means of gaining attention. Most children normally outgrow the tendency unless they have severe maladaptive or emotional problems. See also **psychosexual development,** **psychosocial development**. bitolterol /bi-tol′ter-ol/, a beta-adrenergic receptor agonist used as a bronchodilator; administered by inhalation as the mesylate salt in the treatment of bronchospasm associated with asthma and the treatment and prophylaxis of bronchospasm associated with chronic obstructive airway disease, including bronchitis and pulmonary emphysema. bitolterol mesylate /bitol′t rol mes′ilāt/, an orally inhaled bronchodilator. INDICATIONS: It is used in the treatment of bronchial asthma and reversible bronchospasm. CONTRAINDICATION: This product is contraindicated in patients who are known to be hypersensitive to it.Bitot's spots /bit z′/ [Pierre Bitot, French surgeon, 1822–1888], white or gray triangular deposits on the bulbar conjunctiva adjacent to the lateral margin of the cornea, a clinical sign of vitamin A deficiency.

American Medical Association (AMA), a professional association whose membership is made up of the largest group of physicians and medical students in the United States, including practitioners in all recognized medical specialties, as well as general primary care physicians.See also **leishmaniasis**.Also called **mucocutaneous leishmaniasis,** **New World leishmaniasis**.See also **Accreditation Review Committee on Education in Surgical Technology**. American Dental Hygienists' Association (ADHA), the largest organization of dental hygienists in the United States. American Hospital Association (AHA), a national organization that represents and serves individuals, institutions, and organizations that work to improve health services for all people. The AHA publishes several journals and newsletters. American Joint Committee on Cancer (AJCC), a nonprofit organization that creates and publishes systems of classification for cancer staging, such as the TNM staging system and Collaborative Stage Data collection systems. American Journal of Nursing, a professional journal containing articles of general and specialized clinical interest to nurses. It is an important resource regarding the profession in the United States. American leishmaniasis, a group of infections caused by various species of the parasitic protozoa _Leishmania_ of Central and South America, characterized by cutaneous lesions at the site of the sandfly bite and transmitting infection and causing disfiguring ulcerative lesions of the nose, mouth, and throat or visceral disease. Illness may be prolonged, rendering patients susceptible to serious secondary infections. Kinds of American leishmaniasis are **chiclero ulcer,** **espundia,** **forest yaws,** and **uta**. Also called **mucocutaneous leishmaniasis,** **New World leishmaniasis**. See also **leishmaniasis**. American Medical Association (AMA), a professional association whose membership is made up of the largest group of physicians and medical students in the United States, including practitioners in all recognized medical specialties, as well as general primary care physicians.

It can also prevent intertrigo (dermatitis caused by friction between opposing surfaces of skin).Adequate support can improve physical appearance and reduce pain in the back, shoulders and neck.The nurse should encourage older women to wear a well-fitting bra.Although initially unilateral, the tender, firm, centrally located enlargement may become bilateral. When gynaecomastia is characterised by a discrete, circumscribed mass, it must be diagnosed to differentiate it from the rarer breast cancer in males. Senescent hyperplasia requires no treatment and generally regresses within 6–12 months. # Breast cancer Breast cancer is the most frequently diagnosed malignancy among females in Australia and New Zealand and, following lung cancer, is the second most common cancer-related cause of female death.1,17 In Australia, the absolute number of new cases of breast cancer is tending to increase from year to year; however, the increase over the last 10 years is considered to be due to changes in the age and size of the population. Mortality rates are declining by an average of 2.2% per year.18 The incidence of breast cancer in the Australian Indigenous population is lower than in the general population, although mortality rates are the same as in the general population. This lower incidence may be related to protective factors such as having children at a younger age and having more pregnancies, while mortality rates may be related to the fact that Indigenous women are less likely to access screening mammography. In contrast in New Zealand, Māori women have a higher incidence of breast cancer than the general population and a 50% higher mortality rate from breast cancer than non-Māori females.19 Gerontological considerations: age-related breast changes Loss of subcutaneous fat and structural support and involution of mammary glands often result in pendulous breasts in the postmenopausal woman. The nurse should encourage older women to wear a well-fitting bra. Adequate support can improve physical appearance and reduce pain in the back, shoulders and neck. It can also prevent intertrigo (dermatitis caused by friction between opposing surfaces of skin).Persistent intertrigo can be treated with an anti-fungal preparation.Surgical lifting of sagging breasts is possible and may be desirable when reconstruction after a **mastectomy** is performed.The decrease in glandular tissue in older women makes a breast mass easier to palpate.This decreased density is probably age-related and occurs even with women on hormone replacement therapy.

A plaster of baking soda moistened with water is also useful.A bath in potassium permanganate may help relieve itching, as will oatmeal baths.Cooling compresses with cold water and vinegar are very useful every 1 to 2 hours.Apply antipruritic skin lotions such as calamine lotion.TREATMENT Wash skin with antiseptic soap as soon after exposure as possible.**L-Histidine*:** 500 mg per day. Blood vessel dilator. Others—Secondary Raw spleen: Anticoagulant. Chlorophyll Wheat germ oil Botanicals—Primary **Gotu kola** **_(Centella asiatica)_** **and Paeonia** **_(P. lactiflora)*_ :** Both have specific anti-fibrin activity, and are specific for this condition. **Ginger** **_(Zingiber officinale)*_ :** Vascular anti-inflammatory. **Horse-chestnut** **_(Aesculus hippocastanum)*_ :** Reduces edema associated with this condition. **Ginkgo** **_(G. biloba)*_ :** Is anti-PAF (Platelet Aggregation Factor) to reduce abnormal clotting of platelets. **Cleavers** **_(Galium aparine)*_ :** A lymphatic stimulant. Botanicals—Secondary • Comfrey _(Symphytum officinale)_ : Poultice • Mullein tea _(Verbascum thapsus)_ : Internal • Plantain _(Plantago lanceolata)_ : Poultice Note: The above therapies are mostly for use with superficial venous thrombophlebitis. Phlebothrombosis of a deep vein is a life-threatening situation and requires treatment in an inpatient facility. # Chapter 103 # Poison Ivy DEFINITION AND SYMPTOMS A contact dermatitis resulting from irritation of the skin by the resin of the poison ivy plant. Within hours (or sometimes several days), the skin begins to itch or burn, followed by the eruption of small blisters, which may coalesce to cover large portions of the body. As the vesicles rupture, crusting forms, overlying a raw, oozing surface. TREATMENT Wash skin with antiseptic soap as soon after exposure as possible. Apply antipruritic skin lotions such as calamine lotion. Cooling compresses with cold water and vinegar are very useful every 1 to 2 hours. A bath in potassium permanganate may help relieve itching, as will oatmeal baths. A plaster of baking soda moistened with water is also useful.Poison ivy _(Rhus toxicodendron)_ and dwarf nettle _(Urtica urens)_ tinctures taken internally at frequent intervals will shorten the course of the rash.Salt-water swimming is very effective therapy.**Therapeutic Agents** Vitamins and Minerals **Vitamin C*:** 1 g per hour.**Vitamin A*:** 25,000 to 50,000 IU one to two times per day.**Vitamin B complex*:** 50 mg two times per day.

Stigma and blame have been ascribed to individuals for centuries, whether we're looking at the slum-dweller who became the prevailing image of the tuberculosis patient in the nineteenth century, the upper-middle-class female patient with fibromyalgia who stands as a symbol of psychosomatic anxiety, or the patient with HIV or Hepatitis C whose infections are the consequences of risky behavior.When applied to diseases like cancer, heart disease, and diabetes, as well as to patients with spinal cord injuries and other conditions, such regeneration could radically alter treatments and outcomes. Since many stem cells are harvested from embryos used in in-vitro fertilization, stem cell research is a hotly contested issue. In previous decades, we had Karen Ann Quinlan and the right to die, and Terry Schiavo and the right to life; and for some, stem cell research is wrapped up in the same conversation about abortion, right to life, and the government's role in shaping science policy. In what some researchers fear as a sign of the return to Bush's "Dark Ages," in 2011, nearly all Republican presidential candidates said they were in favor of limiting President Obama's broadened funding of embryonic stem cell research. For patients and families waiting for a breakthrough, the issue is as intensely personal as it is political for others. Barbara Kivowitz believes the degree to which we view illness as a value itself reflects directly back to our broader cultural priorities. If illness and death are seen as natural processes of living, then we look at patients differently than if illness is seen primarily as a weakness or failing. Stigma and blame have been ascribed to individuals for centuries, whether we're looking at the slum-dweller who became the prevailing image of the tuberculosis patient in the nineteenth century, the upper-middle-class female patient with fibromyalgia who stands as a symbol of psychosomatic anxiety, or the patient with HIV or Hepatitis C whose infections are the consequences of risky behavior.The physical, emotional, and economic toll of chronic disease means prevention will be a constant theme.Yet as we've seen, the factors that go into the prevention and progression of many diseases—health disparities, socioeconomic status, access to health care, environment, and genetics, to name some—make it much more complicated than snap judgments would have it seem.

Hypothermia in an anesthetized patient can occur rapidly and be devastating in such a small patient.Depth of anesthesia in most rodents can be evaluated partially by pinching the toes or gently pinching the ear for reaction to a painful stimulus.The use of dental films or a mammography unit can provide more detailed images in the small patient and may be of greater diagnostic value in these small animals. ## Anesthesia and surgery Most information on anesthesia and surgery is extrapolated from other hystricomorph rodents. Although degus cannot vomit due to their highly developed cardiac sphincter, whenever possible, degus should be fasted 1–2 hours prior to anesthetic administration. Many rodents store food in their oral cavities; cleaning out the oral cavity with a moistened cotton-tipped applicator following induction is recommended to prevent aspiration. Fasting patients for more than 1–2 hours may increase the risks of hypoglycemia and perianesthetic ileus (Richardson 2008). Anesthesia may be accomplished with injectable anesthetic agents and supplemental oxygen or through the delivery of inhalant anesthetic agents via a precision vaporizer (Colby et al. 2012). The small patient size restricts endotracheal intubation in the clinical setting. Anesthetic gases and oxygen may be delivered via an induction chamber, facemask with a non-rebreathing circuit, or commercial rodent anesthetic unit. Any anesthetized patient should be closely monitored from induction through recovery. At a minimum, the patient's heart rate, respiratory rate, temperature, and anesthetic depth should be monitored. Additional anesthetic monitoring to include continuous ECG and pulse oximeter can provide supplemental information about the patient's circulatory and respiratory functions. Depth of anesthesia in most rodents can be evaluated partially by pinching the toes or gently pinching the ear for reaction to a painful stimulus. Hypothermia in an anesthetized patient can occur rapidly and be devastating in such a small patient.Direct heat sources (hot water bottle) should be avoided as they lead to vasodilation, resulting in increased heat loss (Richardson 2008).The patient should be monitored closely on anesthetic recovery and in the perioperative period.When appropriate, the patient may be placed in a small, single-level, solid-wall enclosure for continued observation.

Professional aid is urgently required.First-Aid The owner should bandage the eye with bandage moistened in saline solution (a teaspoonful of ordinary salt to a pint of water).The globe may become trapped by the eyelids which become located behind it.Success has been claimed for treatment involving the injection of 2 ml to 5 ml of an antibiotic preparation into the subconjunctival tissues of the upper eyelid. Antibiotics, parenterally, by subcutaneous injection or by long-acting antibiotic ophthalmic ointment are used in treatment; cortisone is contraindicated. Penicillin, oxytetracycline and chloramphenicol have been reported to give equally good results. A single treatment is usually sufficient. Opacity of the cornea may result from oedema of the cornea following infection with CANINE VIRAL HEPATITIS; see 'Keratitis' above. Ovine infectious keratoconjunctivitis This occurs worldwide. In a field survey carried out by the University of Liverpool's veterinary staff, the microflora of 240 clinically unaffected eyes from sheep in 10 flocks were compared with those of 240 clinically affected eyes from 12 natural outbreaks. Totals of 16 and 17 genera of bacteria were recovered, including Branhamella ovis, E. coli and Staphylococcus aureus. Mycoplasma and acholeplasma were isolated from both groups. Chlamydia psittaci can also be a cause. Pannus is a complication of keratitis in which blood vessels bud out from the margins of the cornea and run in towards the centre of the eye, stopping at the edges of an ulcer if such exists. Pannus is a condition which always takes a long time to clear up, and even months after there may be seen a dullness of the cornea, due to the tiny vessels that still exist but are invisible to the naked eye. Partial displacement Pekingese and other dogs with prominent eyes sometimes suffer a traumatic partial displacement of the eye from the orbit, as a result of being struck by a car or of some other accident. The globe may become trapped by the eyelids which become located behind it. First-Aid The owner should bandage the eye with bandage moistened in saline solution (a teaspoonful of ordinary salt to a pint of water). Professional aid is urgently required.If the cornea, etc., has been badly damaged, the only course is enucleation of the eye.After suturing of the eyelids over the vacant socket, the result will not appear unsightly to the owner.Periodic ophthalmia (see under this heading).(See also OPHTHALMIA.)

That might have been a result of the fever, or it could indicate kidney damage.A urine sample showed no evidence of an infection, but was positive for blood.But the palms of her hands, though rash-free, _were_ red and irritated.The rash didn't itch or hurt.The ones on her arms and chest were larger—the size of nickels—and less well defined.She'd been well until a few days earlier, she told him. She had a little pain when she went to the bathroom, which made her think she had a urinary tract infection, and so she'd increased her fluids. That didn't work, so the next day she came in and saw a different doctor, who started her on an antibiotic and a painkiller. She didn't get better; in fact, that's when she first noticed the itchy palms. The next morning she was so achy she could barely get out of bed. That night, she had shaking chills and a fever of 102°. The rash appeared the following day. It started on her arms, her face, and her chest. She stopped taking the painkiller, thinking the rash could be an allergic reaction to it, she told him. But the rash just kept spreading. Now Sprague was worried. The patient was fifty-seven years old, and other than a back injury a few years ago and some well-controlled high blood pressure, she had always been healthy. Not today. He was glad she was the last patient of the day because he could tell this was going to take some time. On examination she looked tired, and her face was flushed and sweaty. Her short, dark hair lay plastered to her scalp. She had no fever, but her blood pressure was quite low, and her heart was beating unnaturally fast. The rash that now covered her body was made up of hundreds of small, flat red marks. The newest ones, those on her legs, were like red-colored freckles. The ones on her arms and chest were larger—the size of nickels—and less well defined. The rash didn't itch or hurt. But the palms of her hands, though rash-free, _were_ red and irritated. A urine sample showed no evidence of an infection, but was positive for blood. That might have been a result of the fever, or it could indicate kidney damage."You may even need to be admitted to the hospital.I'm not sure what you've got, but I am pretty sure that this is serious."She might have developed an allergy to one of the medicines she was taking, he explained, which could be dangerous and might even require other medications.

"Silver filling" is slang for an amalgam tooth restoration.Worse, it takes the body years to clear even a small amount and it may never clear it entirely.The body unfortunately allows mercury into the brain through the blood-brain barrier, and mercury in the brain and nervous system—even in ultraminute amounts—prevents new and old nerve connections from forming.Most arguments in favour of pesticides rested on the assumption that the exposure was minimal and the pros of consuming fruits and vegetables outweighed the cons. But this argument overlooked the effects of cumulative exposure over time and the truth revealed by recent research: our genetic makeup—and thus our health status—determines how we deal with the exposure. Dioxins, furans, PCBs and pesticides act at the molecular and cellular level, as most free radicals do, to steal electrons from the body's molecules and blow holes in cell membranes. No good can come from these chemicals entering our bodies. Exposure to any or all of them, no matter how minimal, increases our need for antioxidants. ## HEAVY METALS Mercury, arsenic, lead and cadmium are among the metals known to have detrimental effects on humans. All are commonly released by a huge variety of industrial processes. ### Mercury "Quicksilver" is a potent neurotoxin and there is no known safe level of mercury in the human body. New research on the toxic effects of mercury on children has prompted Health Canada to advise Canadians to limit their consumption of certain fish—fresh and frozen tuna, shark, swordfish, escolar, marlin and orange roughy. Mercury toxicity is commonly associated with destruction of nervous system tissue. Women of child-bearing age should be most concerned with mercury contamination, since the mercury may be passed to the fetus, increasing the risk of learning disabilities and neurobehavioural disorders in newborns that may persist through childhood. The body unfortunately allows mercury into the brain through the blood-brain barrier, and mercury in the brain and nervous system—even in ultraminute amounts—prevents new and old nerve connections from forming. Worse, it takes the body years to clear even a small amount and it may never clear it entirely. "Silver filling" is slang for an amalgam tooth restoration.Researchers have measured a daily release of mercury into the body from typical amalgam fillings that is on the order of 10 micrograms.Mercury is a toxic metal; the most minute amount damages cells.The University of Calgary's Faculty of Medicine, Department of Physiology and Biophysics, has recently provided conclusive evidence that _there is no safe level of mercury in the body_.

_cp,_ Cell process; _m,_ mitochondria; _N,_ nucleus.**E,** As osteoblasts reduce their synthetic activity, they flatten, and protein synthetic organelles, particularly the Golgi complex, become reduced.These collagen-containing granules are typically elongated structures with regions of increased electron density.These molecules assemble extracellularly as fibrils and accumulate as a layer of uncalcified matrix called _osteoid_ (prebone) (Figure 6-11, _D_ and _E_). Some debate still continues as to whether the noncollagenous proteins are contained within the collagen secretory granules or in a distinct population of granules. Irrespective of this aspect, noncollagenous proteins also are released mainly along the surface of osteoblasts apposed to osteoid and diffuse from the osteoblast surface toward the mineralization front where they participate in regulating mineral deposition. Near the mineralization front, mineralization foci can be seen within osteoid, and certain noncollagenous proteins, such as bone sialoprotein and osteopontin, accumulate within them (Figure 6-12). FIGURE 6-11 Light level ( **A** ) and electron microscope ( **B** to **D** ) micrographs of active osteoblasts. **A** and **B** are cytochemical preparations for pH-dependent phosphatase activity in the Golgi complex. **B** to **D,** These cells contain an extensive Golgi complex surrounded by abundant rough endoplasmic reticulum _(rER)_ profiles. **C,** The Golgi saccules exhibit spherical _(sd)_ and cylindrical _(cd)_ distentions characteristic of collagen-producing cells. **D,** The cylindrical distentions bud off from the Golgi complex to form secretory granules _(sg)_. These collagen-containing granules are typically elongated structures with regions of increased electron density. **E,** As osteoblasts reduce their synthetic activity, they flatten, and protein synthetic organelles, particularly the Golgi complex, become reduced. _cp,_ Cell process; _m,_ mitochondria; _N,_ nucleus.**C,** Immunolabeling _(black dots)_ reveals the presence of osteopontin _(OPN),_ among other noncollagenous proteins, in these foci.**F,** The linear profiles among the calcified collagen fibrils are mineral crystals.

That's 40 more calories and 5 more grams of fat than a glass of fat-free milk.A cup of full-fat soy milk contains 127 calories and 5 grams of fat.Soy foods can also be high in fat and calories.If you've been diagnosed with thyroid dysfunction, exert caution in consuming soy products.Furthermore, a team of Italian researchers showed that 7S globulin also affects beta-VLDL liver receptors, leading to increased clearance of these final-stage LDL precursor compounds. Method of Attack #6. By adding soy protein to your diet, you tend to eliminate some animal protein, which is loaded with saturated fat and cholesterol. Cut your saturated fat and cholesterol intake and you automatically lower LDL cholesterol. A diet high in animal protein can actually induce high LDL cholesterol, at least according to animal research. Rabbits fed an animal protein chow (high in the milk protein casein) showed a higher rate of production of Apo B protein (the type that encircles LDL particles) and LDL cholesterol compared with rabbits fed chow high in soy protein. ## SOY CAUTION The American Cancer Society recommends that breast cancer survivors consume only moderate amounts of soy foods and cautions against intentionally ingesting more concentrated sources of soy, such as soy-containing pills, powders, or supplements. Aside from this, any additional disadvantages of eating soy foods appear to affect only individuals with known food allergies or individuals diagnosed with some type of thyroid dysfunction. Soy does tend to be a highly allergenic food, particularly in children, so if you're sensitive to soy, avoid eating soy products. Soy may also cause problems with thyroid function by deactivating the enzyme responsible for synthesizing thyroid hormones. Some scientific evidence even suggests a link between soy consumption and goiter, but the consensus is that in healthy individuals, soy consumption does not adversely affect thyroid function. If you've been diagnosed with thyroid dysfunction, exert caution in consuming soy products. Soy foods can also be high in fat and calories. A cup of full-fat soy milk contains 127 calories and 5 grams of fat. That's 40 more calories and 5 more grams of fat than a glass of fat-free milk.Soy cereals taste great—but beware, they are often sugar-coated.## FILLING THE PRESCRIPTION Americans should include soy foods in their diet on a daily basis, to the tune of _20–25 grams of soy protein per day._ My patients find it easiest to simply replace cow's milk with soy milk.

There has been a trend in recent years toward the development of more proximal cancers, which may relate to changes in epidemiologic risk factors.Finally, there is evidence that there are important differences in the epidemiologic risk factors associated with different subtypes of CRC.Diets with a high calorie intake and those rich in meat, particularly animal fat, have been implicated in many studies.- Possible mechanisms for this effect include the production of heterocyclic amines, stimulation of higher levels of fecal bile acids, production of reactive oxygen species, and elevated insulin levels., In addition to high-risk factors, there are inverse associations with vegetable and fiber consumption, although fiber falls out of some multivariate analyses when adjusted for other dietary risk factors.- This effect could be related to anticarcinogens, antioxidants, folate, induction of detoxifying enzymes, binding of luminal carcinogens, fiber fermentation to produce volatile fatty acids, or reduced contact time with epithelium because of faster transit., Several studies, including a large pooled multivariate analysis, have found that high folate intake is associated with a decreased risk of CRC, providing some of the most direct evidence of dietary risk factor relationships., Finally, alcohol intake has been associated with an increased risk of CRC. There is an inverse association between use of nonsteroidal antiinflammatory drugs and CRC risk. Smoking exposure is associated with CRC, although the relative risk is less than for many other tobacco-related cancers, and some studies consider cigarette smoking only a suggestive risk factor. Sedentary lifestyle, long-standing IBD (see Colitis-Associated Neoplasia), pelvic irradiation, and ureterosigmoidostomy are also associated with an increased risk of CRC. Finally, there is evidence that there are important differences in the epidemiologic risk factors associated with different subtypes of CRC. There has been a trend in recent years toward the development of more proximal cancers, which may relate to changes in epidemiologic risk factors.Furthermore, there are molecular biologic differences between right- and left-sided CRCs that would support different epidemiologic associations.More recently, research has focused on the complex interactions of hormones, energy balance, intestinal flora, and inflammation.Genetic polyposis syndromes account for fewer than 0.5% of all incident CRCs (Table 27.4).

(A) H&E (HP); (B) immunohistochemical staining for MelanA (MP).21.19 Lentigo maligna.Fig.21.17).The Breslow thickness of this lesion is much greater than 1 mm and the prognosis is poor, with a high chance of metastatic spread.More advanced tumours can have nodular areas and sometimes show surface ulceration because the expanding mass of tumour cells destroys the overlying epidermis. Occasional lesions are not pigmented and these are termed amelanotic melanomas . These tumours are more difficult to recognise and may be confused with other lesions such as intradermal naevi and basal cell carcinomas. Complete excision is the initial treatment of choice in cases of melanoma. Fig. 21.17 Superficial spreading malignant melanoma: dermal invasion. (A) LP; (B) HP.As in the superficial spreading malignant melanoma in situ shown in Fig. 21.16, there are nests of atypical melanocytes in all layers of the epidermis (AM), but in this example malignant cells have broken through the epidermal basement membrane to invade the dermis (D) in a radial/horizontal growth pattern. Again, there are prominent melanophages (M), and some lymphocytic inflammatory cells (I) are also present in the surrounding dermis.In Fig. 21.17B, the infiltrating cells show obvious nuclear pleomorphism and are seen to have prominent nucleoli. In contrast to Fig. 21.16, the malignant cells lie between dermal collagen fibres and there is no basement membrane around them. Fig. 21.18 Malignant melanoma: nodular (LP).The low-power image in Fig. 21.18 shows the architectural pattern of a malignant melanoma with a nodular (vertical) growth phase component, which invades into the deep dermis (D).In this case, there is no melanocyte proliferation at the dermo-epidermal junction (compare with Fig. 21.17).The Breslow thickness of this lesion is much greater than 1 mm and the prognosis is poor, with a high chance of metastatic spread. Fig. 21.19 Lentigo maligna. (A) H&E (HP); (B) immunohistochemical staining for MelanA (MP).Fig.21.19A shows an almost continuous line of single, atypical melanocytes (AM) in the basal layer.The cells show pleomorphism with enlarged, hyperchromatic nuclei.Typically, these abnormal melanocytes extend down the basal layer of skin appendages such as hair follicles (H).This is illustrated in Fig.21.19B, using an immunohistochemical method to highlight melanocytes (stained brown).

Medications that may contribute to or cause syncope are listed in Table 45-2.(Adapted from Go AS, Mozaffarian D, Roger VL, et al; American Heart Association Statistics Committee and Stroke Statistics Subcommittee: Heart disease and stroke statistics—2013 update: a report from the American Heart Association. Circulation 127:e6–e45, 2013.) Figure 45-3 Causes of syncope by age. (From Parry SW, Tan MP: An approach to the evaluation and management of syncope in adults. BMJ 340:c880, 2010.) ##### Multifactorial Causes. Previously, up to 40% of patients with recurrent syncope remained undiagnosed, despite extensive investigation, particularly older patients, who have marginal cognitive impairment and for whom a witnessed account of events is often unavailable. More recently, diagnostic yield for all ages has improved with the application of guidelines.28 Although diagnostic investigations are available, the high frequency of unidentified causes in clinical studies may occur because patients failed to recall important diagnostic details,14,29 because of the stringent diagnostic criteria used in clinical studies or, probably most often, because the syncopal episode resulted from a combination of chronic and acute factors rather than from a single obvious disease process.22 A multifactorial cause likely explains most cases of syncope in older adults who are predisposed because of multiple chronic diseases and medication effects superimposed on the age-related physiologic changes described earlier.30 Common factors that in combination may predispose to or precipitate syncope include anemia, chronic lung disease, chronic heart failure, and dehydration. Medications that may contribute to or cause syncope are listed in Table 45-2.Common causes of syncope are listed in Box 45-1.The most frequent individual causes of syncope in older patients are neurally mediated syndromes, including CSS, orthostatic hypotension, and postprandial hypotension, as well as arrhythmias, including tachyarrhythmias and bradyarrhythmias.These disease processes are described in the next section.

Regeneration of blood cells such as T-cells involved in immune response are also being studied.To this end, the patient's cell were transformed into iPS cells, expanded in so-called cell sheets and implanted into the patient.**Properties and risks. ** iPS cells and embryonal stem cells (ESC) (→78) have quite similar properties. Their behavior in differentiation, gene expression and methylation (epigenetics) (→66) is similar. Compared to ESC, iPS are artificially modified by transcription factors. As some of these factors are known to be involved in the formation of cancer cells, the safety of iPS-derived somatic cells is not yet resolved. **Expansion of iPS cells. ** iPS cells are adherent cells. They are usually grown on surfaces to which growth-promoting substances such as cadherin, an adhesion protein, are supplied. Complex but serum-free media are used for growth. They contain glucose, amino acids, _γ_ -aminobutyric acid, inorganic salts, and recombinant proteins such as growth factors. After expansion, the cells are harvested from the surface by soft detachment, using, e. g., EDTA. The whole process can be carried out within robot-assisted work stations. **Applications. ** The two most important applications are in regenerative medicine (→308) and in the personalized testing of drugs. Both applications are expected to lead to innovative and large markets. In regenerative medicine, clinical studies are already being carried out with individualized iPS cells. In Japan, human patients with macular degeneration are treated with retinal pigment epithelium; patients suffering from Parkinson's disease are being treated with dopamine neuron progenitor cells; and patients with heart insufficiency are being treated with cardiomyocytes. To this end, the patient's cell were transformed into iPS cells, expanded in so-called cell sheets and implanted into the patient. Regeneration of blood cells such as T-cells involved in immune response are also being studied.## Tissue Engineering **General.** Tissue engineering aims at the functional regeneration of tissues through implantation of tissue cultured _in vitro._ Initial efforts on skin replacement for treating burns have been followed after several decades by tissueengineered bone, blood vessels, liver, cartilage, ligaments, cornea, muscle, and nerve cells.

Constipation for many patients can also alternate with diarrhea and abdominal cramps in a common condition known as irritable bowel syndrome.Dr. Donovan notes that many older patients' dependence on laxatives and enemas leads to relaxed gut muscles, which make elimination more difficult.In contrast, Dr. Chaitow has found that lean individuals whose diets are more vegetarian often have a sluggish and slow bowel pattern. He notes that people are different biochemically and emotionally and must be treated on an individualized basis. Regardless of such individual differences, however, it is now known that irregular bowel movements are directly related to serious health conditions. A study published in The Lancet reported that women who have fewer than three bowel movements per week have four times the risk of breast disease than those who have one or more bowel movements per day. Furthermore, colon cancer accounts for over 56,000 deaths each year. Nutritionist Lindsey Duncan, C.N., of Santa Monica, California, says, "I've consulted with 8,000 clients, who come to me with a variety of health problems ranging from fatigue, depression, impaired immune function, and obesity to gas, acne, and lower back pain. The vast majority of these complaints and symptoms are alleviated by cleansing, healing, and supporting the intestinal system." ## Causes of Constipation According to Patrick Donovan, N.D., of Seattle, Washington, constipation can be caused by a number of different factors and conditions, including poor diet and nutrition, dehydration, food allergies, lack of exercise, poor posture, emotional upsets and anxiety, imbalances of estrogen and progesterone, imbalances in the autonomic nervous system, drugs and medications, and the misuse of laxatives. Dr. Donovan notes that many older patients' dependence on laxatives and enemas leads to relaxed gut muscles, which make elimination more difficult. Constipation for many patients can also alternate with diarrhea and abdominal cramps in a common condition known as irritable bowel syndrome.Today, many have a seriously delayed transit time of 50-70 hours.One reason transit times have increased is that our diets now include less fiber from fresh fruits and vegetables.As fiber is indigestible, it helps give stools bulk, while also making them soft and flexible.

(6) Pneumonia can occur in postoperative patients or following viral respiratory infection, especially influenza.epidermidis_ are the most common causes of infections at the site where cardiac pacemakers are installed.aureus_ and _S.For example, _S.aureus_ is the most common cause._S.(5) Postsurgical wound infections are an important cause of morbidity and mortality in hospitals.(Used with permission from Wolff K, Johnson R (eds): _Fitzpatrick's Color Atlas & Synopsis of Clinical Dermatology_. 6th ed. New York: McGraw-Hill, 2009. Copyright © 2009 by The McGraw-Hill Companies, Inc.) Severe necrotizing skin and soft tissue infections are caused by MRSA strains that produce P-V leukocidin. These infections are typically community-acquired rather than hospital-acquired. These community-acquired, methicillin-resistant strains of _S. aureus_ (CA-MRSA) are a common cause of infection among the homeless and intravenous drug users. Athletes who engage in close personal contact such as wrestlers and football players are also at risk. Note that hospital-acquired MRSA (HA-MRSA) causes approximately 50% of all nosocomial _S. aureus_ infections. Molecular analysis reveals that the CA-MRSA strains are different from the HA-MRSA strains. (2) Septicemia (sepsis) can originate from any localized lesion, especially wound infection, or as a result of intravenous drug abuse. Sepsis caused by _S. aureus_ has clinical features similar to those of sepsis caused by certain gram-negative bacteria, such as _Neisseria meningitidis_ (see Chapter 16). (3) Endocarditis may occur on normal or prosthetic heart valves, especially right-sided endocarditis (tricuspid valve) in intravenous drug users. (Prosthetic valve endocarditis is often caused by _S. epidermidis_.) (4) Osteomyelitis and septic arthritis may arise either by hematogenous spread from a distant infected focus or be introduced locally at a wound site. _S. aureus_ is a very common cause of these diseases, especially in children. (5) Postsurgical wound infections are an important cause of morbidity and mortality in hospitals. _S. aureus_ is the most common cause. For example, _S. aureus_ and _S. epidermidis_ are the most common causes of infections at the site where cardiac pacemakers are installed. (6) Pneumonia can occur in postoperative patients or following viral respiratory infection, especially influenza.In many hospitals, it is the most common cause of nosocomial pneumonia in general and especially of ventilator-associated pneumonia in intensive care units.CA-MRSA causes a severe necrotizing pneumonia.(7) Conjunctivitis typically presents with unilateral burning eye pain, hyperemia of the conjunctiva, and a purulent discharge.The organism is transmitted to the eye by contaminated fingers._S.

Therefore, constant blood flow is required to maintain cerebral metabolism._St Louis, MO: Mosby; 2002:702._ ) #### **Cerebral Blood Flow** The brain cannot store oxygen or glucose in significant quantities.In: Urden LD, Stacy KM, Lough ME, eds._ Thelan's Critical Care Nursing: Diagnosis and Management.Neurologic therapeutic management.( _Reprinted from: Mendez KA.The body is able to compensate for a limited amount of increased intracranial volume by displacement of intracranial venous blood, decreased production of CSF, or displacement of CSF into the spinal subarachnoid space. ICP rises when these compensatory mechanisms have been exceeded (Figure 12-6). Compliance refers to the change in volume needed to result in a given change in pressure and reflects the effectiveness of the compensatory mechanisms. With decreased compliance, a small increase in volume results in a large increase in ICP. Compliance is based on several factors, including the amount of volume increase and the time over which the increase occurs. Smaller increases in volume result in less increase in pressure. Increases in volume that occur over a long period of time are better tolerated than rapid increases because there is time for compensation to occur. Older adults typically have increased compliance because of cerebral atrophy. Increased ICP can result in cerebral hypoperfusion, ischemia, herniation, and eventually death. **Figure 12-6. ** Intracranial volume-pressure curve. **(A)** Pressure is normal, and increases in intracranial volume are tolerated due to compensatory mechanisms. **(B)** Increases in volume may cause increases in pressure. **(C)** Small increases in volume may cause large increases in pressure (compensatory mechanisms have been exceeded). ( _Reprinted from: Mendez KA. Neurologic therapeutic management. In: Urden LD, Stacy KM, Lough ME, eds._ Thelan's Critical Care Nursing: Diagnosis and Management. _St Louis, MO: Mosby; 2002:702._ ) #### **Cerebral Blood Flow** The brain cannot store oxygen or glucose in significant quantities. Therefore, constant blood flow is required to maintain cerebral metabolism.CBF is determined by blood pressure and cerebral vascular resistance.Autoregulation refers to the ability of cerebral blood vessels to maintain consistent CBF by dilating or constricting in response to changes in blood pressure.Vasodilation occurs in response to decreased blood pressure; increased blood pressure results in vasoconstriction.

Patients with upper airway infections should be kept in a position of comfort.Deep space cellulitis is difficult to differentiate from deep space abscess and may require needle aspiration after CT or MRI.Key Concepts A severe sore throat with surprisingly minimal findings on examination of the oropharynx suggests serious soft tissue infection, such as epiglottitis or retropharyngeal abscess.Patients who appear toxic, who are immunocompromised, or who have poor home resources require hospital admission and intravenous antibiotics. Infectious processes of the sinuses can spread to the orbit or central nervous system and can be fulminant. Sinusitis may extend to involve the bones and soft tissues of the face and orbit. Facial and periorbital cellulitis, periorbital abscess, optic neuritis, blindness, and orbital abscess may develop. Patients with orbital complications may have marked swelling, proptosis, decreased ocular motility, and decreased visual acuity. Sinusitis may also lead to intracranial complications. Meningitis, cavernous sinus thrombosis, epidural or subdural empyema, and brain abscess occur. Intracranial involvement may result in headache, decreased sensorium, or focal neurologic deficits and has a rapidly progressive course. Acute fulminant fungal sinusitis requires intravenous antifungal therapy and aggressive surgical débridement.36,37,39 Complications of mucormycosis are directly related to delay in diagnosis and treatment. This opportunistic fungal infection rapidly progresses to involve the central nervous system and is associated with high morbidity and mortality rates. Sinusitis is associated with an increased incidence of bronchitis and asthma. Key Concepts A severe sore throat with surprisingly minimal findings on examination of the oropharynx suggests serious soft tissue infection, such as epiglottitis or retropharyngeal abscess. Deep space cellulitis is difficult to differentiate from deep space abscess and may require needle aspiration after CT or MRI. Patients with upper airway infections should be kept in a position of comfort.Posterior parapharyngeal abscess may involve the cervical sympathetic chain, carotid artery, or internal jugular vein.Posterior to the retropharyngeal space lies the danger space, which extends from the base of the skull to the superior mediastinum at about the level of T2.

Activate the organs.**3.Find the pulses of the stomach, pancreas, and spleen on the left side of the abdomen.7.21.Pulse points of the stomach, pancreas, and spleen Fig.7.20.Fig.If the pulse feels slower or blocked on one side, use the Dragon Pulsing techniques to clear and activate it.The pulse can be felt as a vibration at the surface, gradually becoming deeper and resonating with your hand.The pancreas secretes digestive juices and enzymes that help digestion and absorption of nutrients in the small intestine. It is also an endocrine gland, producing several important hormones such as insulin, which regulates blood-sugar levels in the body. While holding a fundamental role in balancing the functions and energy levels of the body, the pancreas is also very reactive to stress factors. Because unbalanced activity and/or blood flow in the pancreas can easily deregulate many body functions, directing and balancing its blood supply is important. The spleen is situated in the upper left region of the abdomen, between the stomach and the diaphragm. It receives and filters arterial blood from the splenic artery, removing debris and old red blood cells that can be recycled. Acting as a lymph node, the spleen contains immune cells—macrophages and lymphocytes—that treat this recycling blood. The spleen filters fluid out of the blood, passing it into outgoing lymph vessels, which drain into the thoracic duct and the left subclavian vein. Balancing the Pulse of the Stomach, Pancreas, and Spleen **1. Find the pulse points of the stomach, pancreas, and spleen** (fig. 7.20). Place one hand over the stomach and spleen on the left side of the rib cage and the other hand over the pancreas underneath the ribs (fig. 7.21). Gently rock and hold, pressing and releasing the area around the organs until you feel the pulses. **2. Hold. ** Hold the pulse points of the spleen, pancreas, and stomach with your Lao Gung points. The pulse can be felt as a vibration at the surface, gradually becoming deeper and resonating with your hand. If the pulse feels slower or blocked on one side, use the Dragon Pulsing techniques to clear and activate it. Fig. 7.20. Pulse points of the stomach, pancreas, and spleen Fig. 7.21. Find the pulses of the stomach, pancreas, and spleen on the left side of the abdomen. **3. Activate the organs.**4.Healing sound.** Take time to connect to the stomach, pancreas, and spleen.Ask your student to breathe deeply into these organs, exhaling with the sound "who-o-o-o-o-o" to let go of any tension or negative feelings such as worry, anxiousness, or mistrust.

Antitachycardia pacing (ATP) to terminate AF consists of a burst of rapid atrial pacing at the onset of AF.When these pacing algorithms have been evaluated in rigorous fashion, they have been found to be ineffective or at best minimally effective in reducing the AF burden.However, omega-3 PUFAs did prevent recurrent AF after cardioversion of persistent AF in two prospective randomized studies in which patients were pretreated with 2 to 6 g/day of fish oil for 1 month before cardioversion.43,44 Almost all patients in these studies also received amiodarone or sotalol. The rationale for pretreatment with the fish oil was to allow enough time for the omega-3 PUFAs to become incorporated into cell membranes and exert their ion channel effects. These data suggest that fish oil can be helpful in preventing recurrent AF when used in combination with an antiarrhythmic drug after cardioversion of persistent AF. ## Nonpharmacologic Management of Atrial Fibrillation ### Pacing to Prevent Atrial Fibrillation Randomized clinical trials comparing dual-chamber (DDD) pacing with right ventricular pacing have concluded that atrial pacing prevents AF. Studies suggest that the higher incidence of AF during ventricular pacing than during DDD pacing may be at least partially due to a proarrhythmic effect of ventricular pacing, not only to a suppressive effect of atrial pacing. Studies involving small numbers of patients have suggested that dual-site right atrial pacing or pacing of the interatrial septum near the Bachmann bundle prevents AF. Although it is possible that these atrial pacing techniques decrease the propensity for AF, the magnitude of the effect appears to be minimal. Some antibradycardia pacemakers are designed to prevent and terminate AF. Pacing algorithms to prevent AF consist of atrial pacing to prevent suppression of postextrasystolic pauses and acceleration of the atrial pacing rate when repetitive premature atrial complexes are sensed. When these pacing algorithms have been evaluated in rigorous fashion, they have been found to be ineffective or at best minimally effective in reducing the AF burden. Antitachycardia pacing (ATP) to terminate AF consists of a burst of rapid atrial pacing at the onset of AF.Because of insufficient evidence to support its use, atrial pacing is not indicated for prevention of AF in patients without bradycardia.In patients with a bradycardia indication for a pacemaker and paroxysmal AF or recurrent episodes of persistent AF, the data available clearly support the use of atrial-based pacing and programming to minimize the amount of ventricular pacing.

This swelling can cause pain, but it is generally temporary.Although the treatment itself is painless, radiation does cause some short-term swelling in soft tissues.Inflammation.This will subside over the course of about a month, but I encourage people to think about how they will manage this fatigue so they are prepared.Each Gy is equivalent to one joule of energy absorbed per kilogram of tissue. The total amount of Gys that are required to kill a tumor is dependent on the individual tumor, but many tumors require 40 to 70 Gy to be killed. By comparison, a CT scan has 16 mGy, or 0.16 Gy. The amount of radiation delivered with each dose is called a fraction, and this is also measured in Gy. You will typically need to arrive for radiation at the same time each day, and you will usually have the same radiation therapist to position you on the table and direct the radiation based on the location of your small tattoo. The radiation itself will be over in just a few minutes, but the entire visit to the radiation oncology department will generally take thirty to forty-five minutes. Like everything else, you will get used to the routine, and the staff will be able to get you in and out pretty quickly. I have had many patients tell me that they become friendly with the other patients getting radiation at the same time because you do see each other every day for up to several weeks. You become radiation buddies. When you complete a course of radiation at MGH, you get to ring a bell in the waiting room if you want. It becomes a celebratory moment to mark completion of the course. Side Effects of Radiation There are both short- and long-term side effects to radiation. Fatigue. This is the most common immediate side effect of radiation. I tell my patients to expect to be exhausted beginning about two weeks after the radiation starts and lasting until two weeks after it ends. People who never needed an afternoon nap before will find themselves napping regularly. This will subside over the course of about a month, but I encourage people to think about how they will manage this fatigue so they are prepared. Inflammation. Although the treatment itself is painless, radiation does cause some short-term swelling in soft tissues. This swelling can cause pain, but it is generally temporary.If a tumor is close to the skin, you may develop what looks like a sunburn in that area.If radiation hits the gastrointestinal tract, you may develop nausea or diarrhea.Scarring.The normal tissues in the path of radiation beams can sustain long-term damage.For women who receive radiation to the underarm for breast cancer, this scarring can cause the affected arm to swell.

"Mad cow disease" is one of these transmissible spongiform encephalopathies that infects cattle but may be transmitted to humans by consuming infected beef.These unusual infectious agents cause several universally fatal diseases of the central nervous system, characterized by loss of coordination, inability to move, emotional disturbances, dementia, and finally death.Introduction Almost all infectious agents fall into several well-defined categories, including bacteria, viruses, fungi, and protozoan (unicellular) or metazoan (multicellular) parasites. All of these agents are considered by at least some authorities as alive (although others do not classify viruses as such), and all use a nucleic acid, either DNA or RNA, as their hereditary information. Prions are different from any other known infectious agent: they are not living and are composed solely of a single protein without any nucleic acid. Prion hereditary information used during reproduction appears to be contained in the shape of the protein. These agents may pass from one individual to another via an infectious route or may be transmitted to offspring through an inherited mutation in the gene that encodes a normal cellular form of the protein. Table 28.1 Infectious agents of humans Prion proteins are found primarily on the surface of neurons but are also present on glial cells, platelets, and some leukocytes, including hematopoietic stem cells. The exact function of the normal protein is not clear, but it may function in copper ion transport, in blocking the formation of amyloid plaques associated with Alzheimer's disease, during T lymphocyte activation, during blood cell production, or in synaptic transmission. These unusual infectious agents cause several universally fatal diseases of the central nervous system, characterized by loss of coordination, inability to move, emotional disturbances, dementia, and finally death. "Mad cow disease" is one of these transmissible spongiform encephalopathies that infects cattle but may be transmitted to humans by consuming infected beef.Iatrogenic transmission may also occur because normal decontamination procedures, including autoclaving, do not inactivate these hardy infectious agents.History Scrapie, a transmissible spongiform encephalopathy (TSE) of sheep, was reported in 1730 in Europe, and in 1936 it was found to be transmissible between sheep.

For one thing, it is vitally important that you work with a health-care provider who can ensure the diagnosis, track your symptoms, and monitor your recovery—so long as you find the _right_ health-care provider.On the contrary.Does this mean that traditional medicine has no role in your recovery?Or suppose you lean over to lift a heavy box from the floor, or to move the armchair, or to pick up your baby from the crib, and—ouch!—your back goes out. Again, you know what to do: bend your knees and straighten up slowly, apply ice, rest as best you can, and pop an over-the-counter pill. Again, in most cases, that will do it, but if not, you know to go to an orthopedist or physical therapist for relief. But when you suddenly feel that you will not make it to a bathroom in time, so severe is your urinary urgency, or when you feel a pain in your pelvic area but can't quite pinpoint where, or when you feel bloated and uncomfortable and as if you are straining to move your bowels, you're not sure what to do to find relief. Your first thought is probably that you have a bacterial infection in some internal organ. Or you might rush to the Internet to check out your symptoms and look for a diagnosis. A disorder in your pelvic floor muscles is probably the last thing most people think of. Yet a musculoskeletal disorder—that is, a problem in the muscles, connective tissue, nerves, or in your body's alignment—is a likely cause of your pain, as you have now learned. You also now know that your pain can be relieved and your condition healed through the natural healing of this book—the exercises, massage, nutrition, self-care, and relaxation techniques you've been learning and practicing. Does this mean that traditional medicine has no role in your recovery? On the contrary. For one thing, it is vitally important that you work with a health-care provider who can ensure the diagnosis, track your symptoms, and monitor your recovery—so long as you find the _right_ health-care provider.Under no circumstances does it mean, however, that you should turn to the Internet.Like most health-care professionals, I despair at what patients do to themselves when they self-diagnose and self-medicate as a result of Internet searches.

This results in a loss of space and asymmetric axial inclinations of the adjacent teeth and subsequent asymmetric molar occlusion.When primary molars are ankylosed, the adjacent teeth continue to erupt as a part of dentoalveolar development and appear to tip over the crown of the ankylosed tooth.In the absence of dental compensations, this often produces midline deviations. Even if the glenoid fossae are symmetrically positioned, the maxilla can undergo certain degree of rotational growth change relative to the cranial base with resultant asymmetric occlusal relationship. In addition to asymmetric mandibular positioning, morphological variations between the right and left sides of the mandible like differences in the length of the body of the mandible or height of the developing ramus, can lead to asymmetries. Moulding of the parietal and facial bones due to intrauterine pressure during pregnancy and significant pressure in the birth canal during parturition can result in facial asymmetry. These changes are usually considered as transient which undergo rapid restoration of the normal skull relationships within a few weeks to several months.3 Trauma and/or infection within the temperomandibular joint can cause ankylosis of the condyle to the temporal bone.4 The loss of muscle function and tone as a result of damage to a nerve may indirectly lead to asymmetry. Various pathological conditions, not necessarily congenital in nature, cause craniofacial asymmetries. Osteochondroma of the mandibular condyle leads to facial asymmetry, mandibular deviation and open bite on the involved side.5 Asymmetries within the maxillary or mandibular arch lead to significant differences in the interarch relationships on the right and left sides. When primary molars are ankylosed, the adjacent teeth continue to erupt as a part of dentoalveolar development and appear to tip over the crown of the ankylosed tooth. This results in a loss of space and asymmetric axial inclinations of the adjacent teeth and subsequent asymmetric molar occlusion.Any unilateral partial loss of the leeway space results in an asymmetric molar relationship.Such molar occlusion is often encountered in patients with arch length loss as a result of interproximal caries or premature loss of a primary or permanent tooth.Congenitally missing teeth, supernumerary teeth or ectopic eruptions are common causes for developing occlusal asymmetries.

It is often useful to compare the measure being validated to relevant outcomes of interest.With regression, different variances may be observed depending on the assignment of measures to independent and dependent variables.Correlation coefficients suggest a relationship between the two measures, and do not necessarily infer that the measures capture the same parameter.In aging research, reclassification methods have been used to test the validity of biomarkers [62] and risk models for predicting cardiovascular disease risk, such as the Framingham Risk Score, [61, 63, 75] and risk of osteoporotic fracture, such as FRAX model [64]. Additional options for validating a measure that does not have a dichotomous outcome include comparing the measure to an alternative measure using correlation coefficients or using regression to estimate the amount of variance one explains of the other (captured by the coefficient of determination [R 2]). One advantage of using regression is the ability to account for other parameters that may affect results of the measure. Guralnik et al. [57] used multiple linear regression to estimate the amount of variance of the SPPB summary score that was accounted for by an alternative method of measurement, self-reported function, adjusting for age and sex. They found that self-reported function alone accounted for 42% of the variance and that adding age and sex to the model accounted for an additional 4%, which illustrates that while the proportion of variance explained by self-reported function was high, there was still a considerable proportion of variance that remained unexplained. From this, the authors concluded that self-reported function may not adequately capture all of the parameters of physical function, and that an additional performance measure, such as the SPPB, provides a more complete assessment. However, correlation and regression analyses should be used with caution, given that they both have weaknesses [76, 77]. Correlation coefficients suggest a relationship between the two measures, and do not necessarily infer that the measures capture the same parameter. With regression, different variances may be observed depending on the assignment of measures to independent and dependent variables. It is often useful to compare the measure being validated to relevant outcomes of interest.Using Cox proportional hazards regression, Guralnik et al.[57] tested the association of SPPB summary scores and self-reported function measures with two outcomes that are highly salient to older adults: nursing home admission and mortality.

Figure 25-5 Potential steps of tumor progression in dysplastic nevi.The diagnosis is based on this constellation of features, rather than any single finding.One possible suspect is germline mutations that increase the expression of TERT, the gene that encodes the catalytic subunit of telomerase (described later under Melanoma). Morphology Dysplastic nevi are larger than most acquired nevi (often greater than 5 mm across) and may number in the hundreds in those with the dysplastic nevus syndrome (Fig. 25-6A). They are flat macules, slightly raised plaques with a "pebbly" surface, or target-like lesions with a darker raised center and irregular flat periphery. They can be recognized by their size, variability in pigmentation (variegation), and irregular borders. Most seem to be acquired rather than congenital. Unlike ordinary moles, dysplastic nevi occur on both sun-exposed and protected body surfaces. Microscopically, dysplastic nevi usually involve both the epidermis and the dermis and exhibit architectural and cytologic atypia (Fig. 25-6A, B). Nevus cell nests within the epidermis may be enlarged and often fuse or coalescence with adjacent nests. As part of this process, single nevus cells begin to replace the normal basal cell layer along the dermoepidermal junction, producing lentiginous hyperplasia. Cytologic atypia takes the form of nuclear enlargement, irregular, often angulated, nuclear contours, and hyperchro­masia (Fig. 25-6C). Associated alterations in the superficial dermis include lymphocytic infiltrates (usually sparse); release of melanin from dead nevus cells into the dermis (melanin incontinence), where it is phagocytosed by dermal macrophages; and a peculiar linear fibrosis surrounding the epidermal rete ridges that are involved by the nevus. The diagnosis is based on this constellation of features, rather than any single finding. Figure 25-5 Potential steps of tumor progression in dysplastic nevi.B, Lentiginous junctional nevus.C, Lentiginous compound nevus with abnormal architectural and cytologic features (dysplastic nevus).D, Early melanoma, or melanoma in radial growth phase (large dark cells in epidermis).E, Advanced melanoma (vertical growth phase) with malignant spread into the dermis and vessels.

FIGURE 1 Flow diagram representing three-staged approach to management of the open abdomen.The three stages are (1) prosthetic insertion and attempt at delayed primary closure, (2) staged split-thickness skin grafting for planned ventral hernia, and (3) definitive reconstruction with a modification of the components separation technique (Figure 1).2010; 251(4):604–614. Williams-Johnson, JA, McDonald, AH, Strachan, GG, et al. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomized, placebo-controlled trial The CRASH-2 Collaborators. _Lancet_. 2010; 376(9734):23–32. # The Abdomen That Will not Close Jordan A. Weinberg, MD and Timothy C. Fabian, MD The appreciation of abdominal compartment syndrome (ACS) in the 1980s ultimately led to a fundamental change in the management of the laparotomy wound. The "open abdomen" has become the standard treatment both for the management of ACS, by decompressive laparotomy, and for the prevention of ACS, by leaving the abdomen open after operations in the setting of shock. Although the open abdomen has contributed to the salvage of patients who may otherwise have died, the surgeon is then faced with the subsequent management of this open wound, with its inherent acute and chronic challenges. The acute challenge involves prevention of potential collateral damage, including the disastrous complication of intestinal fistulae. The chronic challenge created by the successful avoidance or treatment of ACS is that of definitive reconstruction of the large abdominal wall defect in the patients who recover from the acute insult. At the authors' institution, a fairly standardized staged approach for managing the abdominal wound has developed. The three stages are (1) prosthetic insertion and attempt at delayed primary closure, (2) staged split-thickness skin grafting for planned ventral hernia, and (3) definitive reconstruction with a modification of the components separation technique (Figure 1). FIGURE 1 Flow diagram representing three-staged approach to management of the open abdomen.

**2.** Pulmonary stenosis is narrowing at the entrance to the pulmonary artery.**D.** Pulmonary stenosis **1.In addition, bounding pulses in the arms, weak or absent femoral pulses, and cool lower extremities may be present.With coarctation of the aorta, the blood pressure is higher in the upper extremities than in the lower extremities.** Children show signs of exercise intolerance, chest pain, and dizziness when standing for long periods. **6. ** Management **a. ** Dilation of the narrowed valve may be done during cardiac catheterization. **b. ** Surgical aortic valvotomy (palliative) may be done; a valve replacement may be required at a second procedure. **C.** Coarctation of the aorta **1. ** Coarctation of the aorta is localized narrowing near the insertion of the ductus arteriosus. **2. ** Blood pressure is higher in the upper extremities than the lower extremities; bounding pulses in the arms, weak or absent femoral pulses, and cool lower extremities may be present. **3. ** Signs of HF may occur in infants. **4. ** Signs and symptoms of decreased cardiac output may be present. **5. ** Children may experience headaches, dizziness, fainting, and epistaxis resulting from hypertension. **6. ** Management of the defect may be done via balloon angioplasty in children; restenosis can occur. **7. ** Surgical management **a. ** Mechanical ventilation and medications to improve cardiac output are often necessary before surgery. **b. ** Resection of the coarcted portion with end-to-end anastomosis of the aorta or enlargement of the constricted section, using a graft, may be required. **c.** Because the defect is outside the heart, cardiopulmonary bypass is not required, and a thoracotomy incision is used. With coarctation of the aorta, the blood pressure is higher in the upper extremities than in the lower extremities. In addition, bounding pulses in the arms, weak or absent femoral pulses, and cool lower extremities may be present. **D.** Pulmonary stenosis **1. ** Pulmonary stenosis is narrowing at the entrance to the pulmonary artery. **2.**3.** Pulmonary **atresia** is the extreme form of pulmonary stenosis in that there is total fusion of the commissures and no blood flows to the lungs.**4.** A characteristic murmur is present.**5.** Infants or children may be asymptomatic.**6.** Newborns with severe narrowing are cyanotic.**7.** If pulmonary stenosis is severe, HF occurs.**8.

Blue staining illustrates neural crest cells, visualized using lacZ staining.** ( _A_ ) Cranial neural crest cell migration to the prospective cranial, facial, and neck region in a mouse embryo at embryonal day 10 (lineage tracing using R26 reporter assay).116.2.**Fig.Congenital defects in tissues derived from the neural crest form a diverse class of disorders called neurocristopathies [16].## FORMATION OF CRANIOFACIAL ECTOMESENCHYME (NEURAL CREST) A critical step in early craniofacial development is the formation, migration, and differentiation of the neural crest [12]. This multipotent cell population forms in the interphase between neural and non‐neural ectoderm at all axial levels. Upon induction, neural crest cells undergo epithelial to mesenchymal transdifferentiation, delaminate from dorsal ridges of the neural tube just before it closes, and migrate ventrolaterally along stereotypical migration paths to their target tissues, where they differentiate to multiple different cell types (eg, melanocytes, ganglia of peripheral nerves, and cells of the adrenal medulla) [13, 14]. Neural crest cells formed in the anterior embryo from the midbrain to the hindbrain level migrate to the cranial, facial, and neck region, where they give rise to the cranial neural crest (CNC) (Fig. 116.2) [15]. These cells, which are collectively called ectomesenchyme, populate the mesenchyme of the frontonasal process (FNP), maxillary process (MXP), and mandibular process of the first pharyngeal arch (Figs 116.2 and 116.3), and form most of the cranial and facial connective tissues (eg, chondrocytes, osteocytes, pericytes, and dermal cells). Most of the cranial and facial bones are derived from the CNC (Fig. 116.2). Congenital defects in tissues derived from the neural crest form a diverse class of disorders called neurocristopathies [16]. **Fig. 116.2. ** ( _A_ ) Cranial neural crest cell migration to the prospective cranial, facial, and neck region in a mouse embryo at embryonal day 10 (lineage tracing using R26 reporter assay). Blue staining illustrates neural crest cells, visualized using lacZ staining.Green arrows depict the patterns of cranial neural crest (CNC) migration.(B) Schematic illustration of newborn (human) craniofacial bones.Gray color depicts the bones derived from the CNC.

###### Genetics A pharmacogenetic predisposition exists as drug-specific HLA associations have been reported for certain medications.Expanded and activated cytotoxic T cells are removed by apoptosis but a small population is prevented from apoptosis by keratinocyte derived interleukin (IL)-15 and remain as skin-resident memory T cells until the next activation cycle [98, 110, 111].* * * ### Box 118.6 Drugs associated with fixed drug eruption * Non-steroidal anti-inflammatory drugsa * Paracetamola * Co-trimoxazolea * Tetracyclinesa * Penicillins * Metronidazole * Rifampicin * Erythromycin * Carbocisteine * Pseudoephedrine * Phenolpthalein * Barbiturates * Carbamazepine * Sulphasalazine * Penicillins * Metronidazole * Rifampicin * Erythromycin * Calcium-channel blockers * Angiotensin-converting enzyme inhibitors * Omeprazole * Iodinated contrast * Azole systemic antifungals * Complementary medicines * Food, e.g. cashew nuts, asparagus From [98–100, 102, 103, 106, 116, 120, 121]. aCommon reported agents. * * * ###### Pathophysiology FDE is a form of classical delayed-type hypersensitivity reaction and skin resident T cells are believed to be the key mediators in eliciting FDE. Long after clinical resolution, 'resting' FDE lesions contain CD8+ T cells with an effector/memory phenotype. These cells are located at the dermal–epidermal junction and remain quiescent until drug re-challenge. On re-exposure to the drug, there is activation and expansion of these CD8+ lymphocytes with the release of interferon (IFN)-γ and cytotoxic granules resulting in keratinocyte apoptosis. At the end of the immune response, regulatory T cells are recruited into the lesions and limit further damage by inhibiting the cytotoxic T cells. Expanded and activated cytotoxic T cells are removed by apoptosis but a small population is prevented from apoptosis by keratinocyte derived interleukin (IL)-15 and remain as skin-resident memory T cells until the next activation cycle [98, 110, 111]. ###### Genetics A pharmacogenetic predisposition exists as drug-specific HLA associations have been reported for certain medications.###### Pathology Early biopsy specimens show an interface dermatitis reaction pattern with vacuolar degeneration of basal keratinocytes, dermal oedema and a perivascular lymphocytic infiltrate of the upper dermis.Eosinophils may be present.Resolved or healing lesions are characterized by pigment-laden macrophages in the upper dermis [98, 114] (Figure 118.11).

Management of this problem is described on p. 1382.If the drug is stopped, even for a day or two, the atrophied adrenal glands cannot produce the glucocorticoids and the patient develops acute adrenal insufficiency, a life-threatening condition.As a result, the patient completely depends on the exogenous drug.Monitor the patient's daily complete blood count (CBC) with differential WBC count and absolute neutrophil count (ANC). Inspect the mouth during every shift for lesions and mucosa breakdown. Assess the lungs every 8 hours for crackles, wheezes, or reduced breath sounds. Assess all urine for odor and cloudiness. Ask about any urgency, burning, or pain on urination. Take vital signs at least every 4 hours to assess for fever. A temperature elevation of even 1° F (or 0.5° C) above baseline is significant for a patient who is immunosuppressed and indicates infection until it has been proved otherwise. Skin care is important for preventing infection because the skin may be the patient's only intact defense. Teach him or her about hygiene, and urge daily bathing. If the patient is immobile, turn him or her every hour and apply skin lubricants. Perform pulmonary hygiene every 2 to 4 hours. Listen to the lungs for crackles, wheezes, or reduced breath sounds. Urge the patient to cough and deep breathe or to perform sustained maximum inhalations every hour while awake. ### Preventing Acute Adrenal Insufficiency The patient most at risk for acute adrenal insufficiency is the one who has Cushing's syndrome as a result of glucocorticoid drug therapy. The exogenous drug inhibits the feedback control pathway (see Fig. 64-3 in Chapter 64), preventing the hypothalamus from secreting corticotropin-releasing hormone (CRH). The lack of CRH inhibits secretion of ACTH from the anterior pituitary gland. Without normal levels of ACTH, the adrenal glands atrophy and completely stop production of any of the corticosteroids. As a result, the patient completely depends on the exogenous drug. If the drug is stopped, even for a day or two, the atrophied adrenal glands cannot produce the glucocorticoids and the patient develops acute adrenal insufficiency, a life-threatening condition. Management of this problem is described on p. 1382.She has been prescribed 45 mg of prednisone daily to slow the progression of this disease and has been adherent to this therapy for the past 12 weeks.She now has a moon face, buffalo hump, acne, thinning scalp hair, and muscle weakness.Today, her blood pressure is elevated and she is being started on an antihypertensive drug, along with an H2 histamine blocker.

This buys time for the cell to repair the damage to its DNA or to complete S phase.The phosphorylated form of Cdc25 is inactive, and without active Cdc25 cells are unable to activate CDK1-cyclin B and enter M phase.To prevent entry into mitosis, Chk1 and Cds1 phosphorylate Cdc25.When active, these kinases prevent cells passing both the G2/M and the G1/S control points.Figure 18.9 Retinoblastoma protein Rb sequesters E2F, the critical transcription factor controlling entry into S phase. Checkpoints Tell the Cell Cycle When To Stop and When To Go The cell cycle has built-in safety devices to ensure that each cell division results in a perfect copy of the parental cell's genome being passed on to its progeny. These were termed checkpoints by Leland Hartwell, who shared with Paul Nurse and Tim Hunt the 2001 Nobel Prize for Physiology or Medicine for their pioneering work on the molecules that control the cell cycle. A checkpoint pathway detects errors and passes a message on down the line to stop the cell cycle until the problem has been attended to. Checkpoints are like the air bags on a car; they serve no purpose whatsoever for most of the journeys that you take but can save your life in the event of a crash. Similarly, checkpoint proteins have no function during normal cell growth but are activated only in response to trauma. The best-characterized cell cycle checkpoints are those that respond to DNA damage or the failure to complete DNA replication. Both situations result in the activation of the protein kinase ATM. In response to DNA damage, for example by ultraviolet light , ATM activates two more protein kinases, Chk1 and Cds1 (Fig. 18.10). In the case of incomplete DNA replication only Chk1 is activated. When active, these kinases prevent cells passing both the G2/M and the G1/S control points. To prevent entry into mitosis, Chk1 and Cds1 phosphorylate Cdc25. The phosphorylated form of Cdc25 is inactive, and without active Cdc25 cells are unable to activate CDK1-cyclin B and enter M phase. This buys time for the cell to repair the damage to its DNA or to complete S phase.18.9).p53 is produced all the time in cells but is broken down rapidly, so its concentration is usually low.However, phosphorylated p53 is not destroyed so its concentration increases.In turn, the systems that repair DNA are activated and expression of a number of new proteins is induced.One of these is p21CIP1, a member of a class of proteins called CKIs for cyclin dependent kinase inhibitors.

The venous anatomy of this region is variable and not well characterized.##### Veins Submucosal and intramural veins give rise to small veins that accompany corresponding named arteries.The fourth part of the duodenum therefore receives a potential collateral supply from the coeliac trunk and superior mesenteric artery, which means that it is not commonly affected by ischaemia.###### Inferior pancreaticoduodenal artery The inferior pancreaticoduodenal artery usually arises from the superior mesenteric artery or its first jejunal branch, near the superior border of the third part of the duodenum (Bertelli et al 1996). It crosses behind the superior mesenteric vein and passes behind the uncinate process of the pancreas, where it divides into anterior and posterior branches. The anterior branch passes to the right, immediately inferior and then anterior to the lower border of the head of the pancreas, and runs superiorly to anastomose with the anterior superior pancreaticoduodenal artery. The posterior branch runs posteriorly to the right behind the head of the pancreas, and anastomoses with the posterior superior pancreaticoduodenal artery (Bertelli et al 1997). Both branches supply the pancreatic head, its uncinate process, and the second and third parts of the duodenum. Occasionally, the anterior and posterior branches arise separately from the superior mesenteric or first jejunal artery. ###### Jejunal artery branches Branches from the first jejunal branch of the superior mesenteric artery supply the fourth part of the duodenum and frequently anastomose with a terminal branch of the anterior superior pancreaticoduodenal artery. The fourth part of the duodenum therefore receives a potential collateral supply from the coeliac trunk and superior mesenteric artery, which means that it is not commonly affected by ischaemia. ##### Veins Submucosal and intramural veins give rise to small veins that accompany corresponding named arteries. The venous anatomy of this region is variable and not well characterized.The inferior pancreaticoduodenal vein runs inferiorly and usually drains into the superior mesenteric vein or its first jejunal tributary.Small veins from the first and upper second parts of the duodenum drain directly into the portal vein, and veins from the third and fourth parts may drain directly into the superior mesenteric vein.

If hearing loss is still detected, children may be fitted with hearing aids and may benefit from placement in an educational setting responsive to children with impaired hearing.If results of the ABR are abnormal, the test is repeated in 1 month.It can be used in children of any age.The ABR is painless and usually done while children are sleeping.Less severe hearing impairment can be more subtle and lead to behavior that is misinterpreted by parents and doctors, such as the following: Ignoring people who are talking to them some but not all of the time Being able to talk and hear well at home but not in school (mild or moderate hearing impairment may cause problems only in the midst of the background noise of a classroom) In general, if children are developing well in one setting but have noticeable social, behavioral, language, or learning difficulties in a different setting, they should be screened for hearing impairment. Screening and Diagnosis Because hearing plays such an important role in a child's development, many doctors recommend that all newborns be tested for hearing impairment by the age of 3 months. This testing is required by law in many states. Newborns are usually screened in two stages. First, children are tested for echoes produced by healthy ears in response to soft clicks made by a handheld device (evoked otoacoustic emissions testing). If this test raises questions about a child's hearing, a second test is done to measure electrical signals from the brain in response to sounds (the auditory brain stem response test, or ABR). The ABR is painless and usually done while children are sleeping. It can be used in children of any age. If results of the ABR are abnormal, the test is repeated in 1 month. If hearing loss is still detected, children may be fitted with hearing aids and may benefit from placement in an educational setting responsive to children with impaired hearing.If children ignore people who are talking to them some but not all of the time, their hearing may be impaired.Treatment Treating some causes of hearing loss can restore hearing.For example, ear infections can be treated with antibiotics or surgery, earwax can be manually removed or dissolved with ear drops, and cholesteatomas can be surgically removed.

My parents took her to the vet, and the next thing they knew she was having emergency surgery to remove an infected uterus.She suddenly stopped eating but drank all the water she could get, and just generally acted sick.#### AN INFECTED UTERUS **"My parents have had a Collie mix for ages.When a dog is spayed, the ovaries and the uterus—which is Y-shaped—are removed.A dog who won't let the incision alone will need to wear an Elizabethan collar (see page 427) until she forgets about the incision or it has healed completely. The most serious potential risk in spaying a dog is death from an unpredictable anesthetic reaction, excessive bleeding, or an abdominal infection. But it is exceedingly rare for a healthy young dog to die as a result of being spayed. Careful monitoring of a dog's heart rate, breathing, blood pressure, and body temperature is the best safeguard against an allergic reaction to anesthetic. Many vets check a dog's blood-clotting ability before surgery to make sure the dog doesn't have an unsuspected bleeding disorder (see page 358). Sterile instruments, sterile surgical garb, and careful skin preparation minimize the possibility of infection. Other potential surgical complications—pain, fever, or skin irritation from the sutures or a minor skin infection—are slightly more common but fortunately not life-threatening. Those are the basics of how a dog is spayed. Your own vet will be happy to discuss the details as they pertain to your dog: what blood tests the vet recommends before surgery, what kind of anesthesia is used and how it's monitored, whether dogs usually or sometimes are given pain medication after a spay, whether the dog stays overnight or goes home the same day, and so on. Knowing what to expect is the best way to put your mind at ease. When a dog is spayed, the ovaries and the uterus—which is Y-shaped—are removed. #### AN INFECTED UTERUS **"My parents have had a Collie mix for ages. She suddenly stopped eating but drank all the water she could get, and just generally acted sick. My parents took her to the vet, and the next thing they knew she was having emergency surgery to remove an infected uterus."** Pyometra is the veterinary term for an infected uterus.The condition is very common in older unspayed dogs and can be fatal if the infected uterus isn't removed quickly.In fact, a veterinary adage—"Never let the sun set on a pyometra"—emphasizes the need to get the dog into surgery sooner rather than later.

Other lymph nodes in the armpit, the groin and so forth may become enlarged as a consequence of infection in different parts of the body.A small child may be irritable after being vaccinated, and lethargy and 'swollen glands' in the neck are a familiar feature of respiratory infections.The excess lymphokines spill over into the blood and are then carried to the brain.The presence of bound antibody neutralises viral infectivity by a variety of different mechanisms, including the attachment of an additional, toxic (for the virus) molecule called complement, signalling to macrophages that the antigen/antibody complex with the attached virus should be eaten and destroyed, or by simply preventing virus entry into the epithelial cells or nerve cells where it likes to grow. In the case of polio, antibodies in the blood stop the virus from getting to the brain and spinal cord. This prevents the paralytic symptoms of poliomyelitis, which result directly from the virus-induced destruction of irreplaceable nerve cells, particularly the large motor neurons. The antibody molecules are themselves proteins that are made by large production 'factories' called plasma cells. The plasma cells are the progeny of a small subset of white blood cells called B lymphocytes, or B cells, that bear a juvenile form of the anti-poliovirus antibody on their surface and multiply rapidly after vaccination. This process of specific cell division, or clonal expansion, goes on in the lymphoid tissue, the lymph nodes and spleen that provide a 'nurturing' environment for the optimal development of immunity. Any immune response, whether caused by immunisation or infection, is likely to be associated with lymph node distension and effects such as drowsiness resulting from the secretion of various chemicals (called lymphokines) that are normally made by the responding cells. The excess lymphokines spill over into the blood and are then carried to the brain. A small child may be irritable after being vaccinated, and lethargy and 'swollen glands' in the neck are a familiar feature of respiratory infections. Other lymph nodes in the armpit, the groin and so forth may become enlarged as a consequence of infection in different parts of the body.Infectious mono-nucleosis is an example of an immune response that is, for a time, out of control, though it generally resolves.Almost everyone is infected with EBV and, though most of us live happily with this persistent virus for life, it can cause lymphomas in people who are severely immunosuppressed.

#### **Enteral nutrition** The ESPEN Guidelines on Enteral and Parenteral Nutrition 2006 and 2009 state that preoperative fasting from midnight is unnecessary in most patients, and that patients undergoing elective surgery who do not have specific risk of aspiration may drink clear fluids and eat solids until 2 and 6 hours before anaesthesia, respectively.These trials have shown that TPN in these settings is useless or deleterious. Now we are aware that a possible adverse effect of postoperative TPN may be the potentiation of a hyperglycaemic status due to the abrupt load of glucose in conditions where there is already a condition of glucose intolerance and an insulin resistance. On the other hand, at least two randomised controlled trials in cancer patients with a weight loss ≥10% have shown that pre- and postoperative TPN was able to reduce complications, and in one study mortality too, when compared with isotonic fluids administration. It is noteworthy that no apparent correlation was found between reduction of postoperative complications and preoperative improvement of the standard nutritional markers of nutritional risk. A prospective randomised study involving cirrhotic patients who were submitted to wide hepatic resections for hepatocarcinoma reported that perioperative BCAA-enriched parenteral nutrition can reduce postoperative complications. However, these conclusions have to be accepted with some reservation because the control group may have been treated with an excessive load of fluid and sodium and there is now evidence that an excessive perioperative load of fluid may be deleterious. **Table 22.16** Effects of total parenteral and enteral nutrition on daily protein turnover in cancer patients. UGI, upper gastrointestinal; BEE, basal energy expenditure; C/N, kcal/nitrogen; GI, gastrointestinal. Adapted from Bozzetti (1989), copyright © 1989 by SAGE Publications. Reprinted by permission of SAGE Publications. #### **Enteral nutrition** The ESPEN Guidelines on Enteral and Parenteral Nutrition 2006 and 2009 state that preoperative fasting from midnight is unnecessary in most patients, and that patients undergoing elective surgery who do not have specific risk of aspiration may drink clear fluids and eat solids until 2 and 6 hours before anaesthesia, respectively.Since an inadequate oral intake for more than 14 days is associated with higher mortality, enteral nutrition (tube feeding or oral nutritional supplementation (ONS)) is indicated even in patients without obvious malnutrition, if it is anticipated that the patient will be unable to eat for more than 7 days perioperatively.

As a result, you don't see many hospitals featuring "preventive care units."In many cases, this is a holdover from the days when there were few effective preventive strategies for heart disease or, for that matter, many other diseases.Insurance policies typically pay for procedures—not prevention.The reimbursement policies of our health-care system clearly favor the plumbing approach.The fact that people aren't being treated with the appropriate noninvasive medical therapies, whether that means a statin drug, a blood pressure medication, a heart-healthy diet, an exercise program, or smoking cessation, helps explain our persistently high rates of angioplasty and bypass surgery. This is costing us dearly from both a human and economic perspective. It has been the rule rather than the exception that new medical approaches, even those that have solid scientific backing, are slow to be integrated into everyday practice. Today, if surgeons went from patient to patient without washing their hands or sanitizing their instruments, you would be appalled. Yet back in the mid-1800s, this was standard practice, and as a result, nearly half of all surgery patients died from postoperative infection. One would think that when, in the 1870s, renowned British physician Joseph Lister demonstrated that measures such as hand-washing, sterilizing surgical equipment, and cleaning wounds could reduce patient death rates dramatically, his fellow physicians would have readily adopted his lifesaving techniques. In fact, most physicians in his own country refused to believe him. Two decades would pass before aseptic surgery would become standard practice in his native England. I mention this because, when it comes to the willingness and speed of the medical community to embrace new approaches, things haven't changed all that much. FOLLOW THE MONEY There are strong economic incentives for physicians and hospitals to cling to the old way of doing things. The reimbursement policies of our health-care system clearly favor the plumbing approach. Insurance policies typically pay for procedures—not prevention. In many cases, this is a holdover from the days when there were few effective preventive strategies for heart disease or, for that matter, many other diseases. As a result, you don't see many hospitals featuring "preventive care units."Doctors are being paid to treat disease, not to prevent it.In contrast, insurers and health plans pay woefully little to primary-care doctors who practice preventive medicine.Physicians who sit down with their patients and take the time to educate them and work out individual treatment plans are reimbursed for a standard office visit whether they spend 5 minutes or much longer with a patient.

The PET image was developed through administration of a radioactive tracer (a radioactive compound whose activity, represented by the movement of the emitted _positrons_ , are detectable by a scanner), along with a natural body compound.In humans, synaptic densities appear to remain at these elevated levels until puberty, when some mechanism that is apparently under genetic control causes synapses to be eliminated, reducing them to the lower adult levels. As the child grows, the brain selectively strengthens or "prunes" connections based on experience. Failure to eliminate excess neurons would be akin to having unneeded or redundant circuits on a computer chip (Huttenlocher, 1979). Thus, the folk wisdom that a loss of brain cells is necessarily accompanied by a loss of adaptive capacity is confuted by an extensive literature documenting the benefits of programmed cell death. Considering the billions of brain cells affected by programmed cell death, both before and after birth, apoptosis qualifies as perhaps the most extensive evidence of neural plasticity. VIEWING PLASTICITY IN ACTION (1973) The most graphic evidence of brain plasticity has come from brain imaging studies. In earlier imaging studies, the brain was visualized by constructing images derived from computerized analysis of brain electrical activity, using the electroencephalograph (EEG), or by computerized tomography (CT), which takes X-rays of the brain in multiple slices. A remarkable breakthrough in imaging took place in 1973, when positron emission tomography (PET) was introduced by Michael Phelps, at Washington University in St. Louis. The PET image was developed through administration of a radioactive tracer (a radioactive compound whose activity, represented by the movement of the emitted _positrons_ , are detectable by a scanner), along with a natural body compound.Brain cells at work use glucose as their fuel.Consequently, through measuring the activity of the emitted positrons, the neuroscientist is able to identify brain activity of conscious, alert subjects, showing detailed biochemical changes that occur with various experiences.

These malignant tumors present as round to oval solid masses with well-demarcated borders.This lipase hypersecretion syndrome generally correlates with advanced disease, usually liver metastasis.66 ##### Imaging Features.A significant clinical clue occurring in about 15% of patients is the presence of multinodular panniculitis and polyarthralgia from lipase hypersecretion.Nonetheless, to distinguish well-differentiated tumors from poorly differentiated, high-grade carcinomas, these tumors are classified as neoplasms distinct from malignancies. This rationale supports the proposal by the Papanicolaou Society of Cytopathology to classify FNAs of PanNETs in the "Neoplastic–Other" category rather than the "positive" or "malignant" category of a five-tiered cytological grading system. Such a classification clearly distinguishes PanNETs from the much more common, and much more lethal, pancreatic ductal adenocarcinoma. Small neoplasms without adverse prognostic features are curable by surgical resection; prognosis is related to tumor size, mitotic rate, necrosis, extrapancreatic invasion, vascular invasion, and nodal or distant metastases. Survival is significantly better than that of pancreatic adenocarcinoma. In patients with tumors limited to the pancreas, survival is 61% after 5 years. In patients with distant metastases, survival is 15% after 5 years.60 ### Acinar Cell Carcinoma Acinar cell carcinoma is an aggressive malignancy representing less than 2% of all pancreatic exocrine tumors. ##### Clinical Features. These carcinomas generally occur in older adults (mean age 62 years), but occasionally they occur in children and adolescents. Males are four times more likely to be affected than females. A significant clinical clue occurring in about 15% of patients is the presence of multinodular panniculitis and polyarthralgia from lipase hypersecretion. This lipase hypersecretion syndrome generally correlates with advanced disease, usually liver metastasis.66 ##### Imaging Features. These malignant tumors present as round to oval solid masses with well-demarcated borders.The loss of the organized "grape-like" clustering with solid, irregularly shaped cell clusters is a clue to the malignant nature of cells that resemble acinar cells (Papanicolaou, ×600).Figure 30-34 Acinar cell carcinoma.Rosette formation, naked tumor nuclei, and loose granules in the background are clues to the diagnosis (Hema III, ×600).##### Differential Diagnosis and Ancillary Studies.

It evolves from chronic damage to healthy cells and tissue in which both the localized tissue and the wider microenvironment demonstrate abnormalities ranging from genetic deletions, to p53 mutations, to cellular anoxia (Goldberg & Diamandis, 1993).Cancer is a multistage, stepwise, and cumulative disease.■ Cancer-preventive bioactive compounds are found predominantly in foods of plant origin and many have several biological activities associated with reduced cancer risk. ■ Diet alters carcinogenesis through a variety of cellular and molecular pathways including immune modulation, modulation of growth factors/signals, methylation, apoptosis, antioxidation, and anti-inflammatory effects. ■ Specific dietary recommendations for risk reduction are available from the American Cancer Society and the American Institute for Cancer Research/World Cancer Research Fund. These recommendations reflect the need for significant behavioral change for most Americans and sufficient support for adopting healthier food choices should be provided. ■ Cancer will be diagnosed in 50% of males and over one-third of females in their lifetime; thus most Americans are "at-risk" for this disease and should be encouraged to adopt a cancer-preventive diet; select populations have even greater risk—cancer survivors, family members of cancer patients, smokers, obese individuals, those with high UV light or other environmental exposures and those with compromised immunity—these subgroups should be specifically targeted for cancer-risk-reduction education. What one chooses to eat can have profound effects on his/her health, particularly when it comes to reducing the risk of cancer. In fact, food selections throughout the lifespan likely have relevance in terms of lifetime cancer risk. Cancer is a multistage, stepwise, and cumulative disease. It evolves from chronic damage to healthy cells and tissue in which both the localized tissue and the wider microenvironment demonstrate abnormalities ranging from genetic deletions, to p53 mutations, to cellular anoxia (Goldberg & Diamandis, 1993).Diet and the constitutive nutrients and bioactive food components (BAFC) play a vital role in enhancing the host response against cancer.Further, diet is a _modifiable_ cancer risk factor.Unlike age or genetic predisposition, dietary choices can be changed by the individual with the goal of reducing cancer risk.

Other postoperative complications include skin ulceration, hypertrophic scar formation, intercostal neuralgia and wound infection.Prevention of the problems that cause excessive capsule formation is critical.Surgeons differ in their approaches to the prevention of contracture formation, although gentle manual massage around the implant is routine.When there is insufficient skin tissue to support an immediate placement, a tissue expander can be used to stretch the skin and muscle at the mastectomy site before inserting implants (see Fig 51-9). Placement of the expander can be performed at the time of mastectomy or at a later date. The tissue expander, which is minimally inflated at the time of surgery, is gradually filled by weekly injections of sterile water or saline solution, which stretch the skin and muscle. Once the tissue is adequately stretched and the anticipated breast size is reached, the expander is surgically removed and a permanent implant is inserted. Some expanders are designed to remain in place and become the implant, eliminating the need for a second surgical procedure. Tissue expansion does not work well in individuals with extensive scar tissue from surgery or from radiation therapy. Figure 51-9 **A** , Tissue expander with gradual expansion. **B** , Tissue expander in place after mastectomy. The body's natural response to the presence of a foreign substance is the formation of a fibrous capsule around the implant. If excessive capsular formation occurs as a result of infection, haematoma, trauma or reaction to a foreign body, a contracture can develop, resulting in a deformed breast. Surgeons differ in their approaches to the prevention of contracture formation, although gentle manual massage around the implant is routine. Prevention of the problems that cause excessive capsule formation is critical. Other postoperative complications include skin ulceration, hypertrophic scar formation, intercostal neuralgia and wound infection.Musculocutaneous flaps can be taken from the back (latissimus dorsi muscle) or the abdomen (transverse rectus abdominis muscle).In the latissimus dorsi musculocutaneous flap, a block of skin and muscle from the patient's back is used to replace tissue removed during mastectomy.48 A small implant may be needed beneath the flap to gain reasonable breast shape and size.

Dysfunction of the facial nerve leads to a characteristic abnormality of the anterior segment of the eye, "keratoconjunctivitis or lagophthalmic keratitis".Therefore, maintaining the function of the nerve and potential restoration of nerve function are responsible roles of the physician.63.52 Removal of the orbital plate and screws that fix the dislocated position are visible behind the soft tissues. Placement of the implant Fig. 63.53 Pre- and postoperative photographs: the face is symmetric and the diplopia is gone Fig. 63.54 Gunshot wound with extensive orbital floor and maxillary defect. The 'bridging' plate placed without supporting the eyeball perforated the soft tissues. After removing the plate, performing fistuloplasty and reconstructing the buccal soft tissues, a CAD-CAM implant is placed. The diplopia is gone and the contours of the face are restored. # Part VII Neuro-Ophthalmological Considerations of the Facial Nerve 64. Tumor Lesions of the Facial Nerve © Springer International Publishing Switzerland 2016 Judit Somlai and Tibor Kovács (eds. )Neuro-Ophthalmology10.1007/978-3-319-28956-4_64 # 64. Tumor Lesions of the Facial Nerve Ildikó Gádor1 (1) Unit of Otoneurology, Department of Otorhinolaryngology, National Institute of Neurology, Budapest, Hungary Ildikó Gádor Email: gadorildi@gmail.com Muscles and motor nerves of the facial mimics, the facial nerves are important tools of non-verbal communication in human relationships. Functional disorder of this nerve – in addition to organic and esthetic disadvantages – significantly affects the psychic condition of the patient as well. Therefore, maintaining the function of the nerve and potential restoration of nerve function are responsible roles of the physician. Dysfunction of the facial nerve leads to a characteristic abnormality of the anterior segment of the eye, "keratoconjunctivitis or lagophthalmic keratitis".Determining the reason for the condition and the treatment of it may be performed with interdisciplinary cooperation (Figs.64.1 and 64.2).Fig.64.1 Late postoperative stage of a large cerebellopontin angle tumor occurring in early childhood, leading to facial paralysis with consequent keratoconjunctivitis Fig.

(These two methods of drug administration are discussed earlier in this chapter.)Orencia can be given as either an IV infusion or by subcutaneous (sub-Q) injection.What is important is that this is a very different class of medications than the ones that we have previously reviewed.More about the precise function of these agents is given below, in the description of the only T cell modulator so far approved, Orencia. ##### _Abatacept (Orencia)_ _Generic available_ : no _Intravenous dose_ : dependent on weight; weeks 0, 2, and 4, followed by a monthly dose _Subcutaneous dose_ : 125 mg per week self-injected; dosage the same, regardless of weight _Delivery options:_ _Intravenous_ : Orencia is available for intravenous infusion _Subcutaneous_ : single-dose, prefilled glass syringe _Effective within:_ four weeks to six months Orencia came to market in 2005. First introduced as an IV infusion drug, it became available for self-injection in 2011. As noted above, the T cell is an immune cell involved early in the process of the inflammation cascade of RA. To participate in the inflammatory process, the T cell has to be "activated" or "stimulated." You will recall from Chapter 1 that an _antigen-presenting cell_ (APC) presents an _antigen_ (foreign substance) to the T cell to activate it (as shown in Figure 4). The activation of T cells is, in itself, a complex process that requires two signals from another immune cell. Because there are two signals needed, the T cell is activated in a process called "co-stimulation" (see Figure 21A). It is this process that Orencia disrupts (Figure 21B). Hence, Orencia is formally considered a "T cell selective co-stimulation modulator," since it interferes with the second signal required to fully activate the T cell. Don't be concerned if this seems a lot to take in. It may be useful to you to be familiar with the science behind the terminology, since you will see these terms in your reading. What is important is that this is a very different class of medications than the ones that we have previously reviewed. Orencia can be given as either an IV infusion or by subcutaneous (sub-Q) injection. (These two methods of drug administration are discussed earlier in this chapter.)It takes approximately 30 minutes to receive the full infusion.After your initial dose, you receive Orencia two weeks later, then two weeks after that, and then every four weeks thereafter.The dosage is adjusted according to your weight.The subcutaneous form is given weekly by self-injection, just below the skin using a prefilled syringe.The dosage is the same for everyone regardless of weight.

** the rate at which an illness occurs in a particular area or population.**3.** (in statistics) the rate at which an illness or abnormality occurs, calculated by dividing the number of people who are affected within a group by the entire number of people in that group.**2.** an illness or an abnormal condition or quality.morbidity /môrbid′itē/ [L, _morbidus,_ diseased], **1.The theory was developed from a standard of care created by expert nurses to manage the care of patients with terminal illness. 8-MOP. See **methoxsalen**. MOPP /mop/, abbreviation for a combination drug regimen used in the treatment of cancer, containing three antineoplastics, _M_ ustargen (mechlorethamine hydrochloride), _O_ ncovin (vinCRIStine sulfate), Matulane ( _p_ rocarbazine hydrochloride), and _p_ redniSONE (a glucocorticoid). MOPP is prescribed in the treatment of Hodgkin's disease. _Moraxella_ , a genus of the Neisseriaceae family of gram-negative nonmotile cocci. They are found as pathogens and parasites on the mucous membranes of warm-blooded animals. _Moraxella catarrhalis_ , a species of aerobic nonmotile bacteria found in both the normal and the diseased nasopharynx. It is a cause of otitis media and respiratory diseases. It is a significant pathogen in children and patients with underlying conditions. Formerly called **_Neisseria catarrhalis._** _Moraxella lacunata_ , a species of nonmotile cocci that causes corneal infections and subacute conjunctivitis or angular conjunctivitis in humans. morbid [L, _morbidus,_ diseased], **1. ** pertaining to a pathological or diseased condition, either physical or mental. **2. ** preoccupied with unwholesome ideas. morbid anatomy. See **pathological anatomy**. morbidity /môrbid′itē/ [L, _morbidus,_ diseased], **1. ** an illness or an abnormal condition or quality. **2. ** (in statistics) the rate at which an illness or abnormality occurs, calculated by dividing the number of people who are affected within a group by the entire number of people in that group. **3. ** the rate at which an illness occurs in a particular area or population.It is published by the Centers for Disease Control and Prevention in Atlanta, Georgia.The publication also includes information on accident rates and important international health data.morbidity rate [L, _morbidus,_ diseased, _ratum,_ calculation], the number of cases of a particular disease occurring in a single year per a specified population unit, as _x_ cases per 1000.

In addition to inhibiting the enzyme, the binding of glucose exposes the covalently bound phosphate to the action of the protein phosphatase.Glucose is an inhibitor of glycogen phosphorylase in the liver.In hypoxia, it is the major substrate of anaerobic glycolysis.This ensures that glycogen is rapidly degraded in metabolic emergencies.It ensures that excess carbohydrate is stored away as glycogen after a meal. Through the protein kinase B cascade (see Fig. 16.18 in Chapter 16 and Fig. 19.4 in Chapter 19), it regulates glycogen metabolism by at least three mechanisms: • It reduces the level of cAMP by activating the cAMP-degrading phosphodiesterase PDE3B. • It inhibits glycogen synthase kinase-3 (GSK3), one of the protein kinases that phosphorylate and inactivate glycogen synthase. • It stimulates protein phosphatase-1, which reverses the cAMP-induced phosphorylations. Protein phosphatase-1 dephosphorylates glycogen synthase, glycogen phosphorylase, and phosphorylase kinase. As a result, protein phosphatase-1 switches the cell from glycogen breakdown to glycogen synthesis. Phosphatase-1 is activated by an insulin-triggered phosphorylation and inactivated by the phosphorylation of a different site by protein kinase A. In addition it is allosterically inhibited by the cAMP-activated phosphoprotein inhibitor-1 (see Fig. 24.19, B). Glucose-6-phosphate is an allosteric activator of glycogen synthase b and phosphatase-1 and an inhibitor of glycogen phosphorylase in muscle. Thus glycogen synthesis is favored when substrate is available. AMP is an allosteric activator of glycogen phosphorylase in muscle and other extrahepatic tissues. This ensures that glycogen is rapidly degraded in metabolic emergencies. In hypoxia, it is the major substrate of anaerobic glycolysis. Glucose is an inhibitor of glycogen phosphorylase in the liver. In addition to inhibiting the enzyme, the binding of glucose exposes the covalently bound phosphate to the action of the protein phosphatase.The effects of the second messengers on glycogen metabolism are similar in muscle and liver, but the stimuli that control them are different.

We will need to use our expertise and authority to advocate for services to meet children's needs and to educate parents and caregivers to achieve the goal of optimal rehabilitation for every patient.While renal development is completed during term gestation, cognitive development is incomplete at birth and continues for at least two decades, thus the full effects of such defects may not be manifest until young adulthood and its associated expectations and stressors; (4) serial insults to the maturing brain including uremia, stroke, shock, hypoxemia, intermittent dialysis treatments, hypertension and medications; (5) interruption of schooling with consequent lack of engagement in education and limitation in adult potential as measured by educational attainment and employment; (6) interruption or impairment of age-appropriate social and emotional experiences with limitation of usual life goals including interpersonal relations, independence from family unit and child-rearing. CKD is a lifelong condition that will require different treatment phases, including dialysis and transplant, with ongoing effects on neurocognitive function. Whenever possible, our goals for affected children include an ability to be responsible for their own treatments, medications, and healthcare decisions, as well as an acceptable quality of life. Nephrologists will need to remain aware of the burden of managing chronic disease at a young age and how that differs from the experience of adults who develop CKD later in life. It is important that nephrology services incorporate a psychologist as part of the treatment team. Understanding how mild, moderate and severe CKD impact neurodevelopment can inform treatment decisions, evaluation methods, accommodations and interventions, and allow us to provide parents and caregivers with more accurate information about a child's potential for rehabilitation. We will need to use our expertise and authority to advocate for services to meet children's needs and to educate parents and caregivers to achieve the goal of optimal rehabilitation for every patient.If major comorbidities are present or patients return to dialysis, the risks increase substantially.Awareness of these challenges and early and comprehensive efforts to improve educational outcomes are important in promoting more complete rehabilitation and the best possible quality of life for children with CKD.References 1.

The wire is blunted to prevent inadvertent cortical penetration as the wire is inserted.For the metacarpal fracture with unacceptable deformity, our preferred technique is closed reduction and internal fixation, using a pre-bent, blunted 1.6 mm Kirschner wire.Treatment strategies should thus be aimed at pain relief and early mobilisation.In addition, pseudoclawing of the finger, as a result of dynamic imbalance of the surrounding soft tissues, is sometimes observed [93] (Fig. 10.13). However, the functional impact of malunion of the little finger metacarpal neck or shaft fractures, has been questioned [94]. Patients should thus be assessed and counselled carefully before embarking on corrective osteotomy. Fig. 10.12 Malunion of fifth metacarpal. Note the evidence of previous pinning Fig. 10.13 Appearance of pseudoclawing as a result of a boxer's fracture Angulation deformity can be corrected with a closing wedge, opening wedge or a pivot osteotomy [11]. The effect on the soft tissues as a result of shortening (closing wedge) or lengthening (opening wedge) has to be taken into consideration. There is a general consensus that a rotational deformity is not acceptable and it may be corrected with a step osteotomy [95] or a rotational osteotomy [96]. ## Conclusions and Personal Views Management of metacarpal fractures should focus on restoring the skeletal stability and hand function. The optimal treatment is determined by the extent of injury to the bone and surrounding soft tissues. Current evidence would support that no specific immobilisation is required for the uncomplicated boxer's fracture (up to 70° angulation), as satisfactory results, without significant functional restriction, have been reported [25, 26, 28, 97]. Treatment strategies should thus be aimed at pain relief and early mobilisation. For the metacarpal fracture with unacceptable deformity, our preferred technique is closed reduction and internal fixation, using a pre-bent, blunted 1.6 mm Kirschner wire. The wire is blunted to prevent inadvertent cortical penetration as the wire is inserted.A gentler bow is created in the wire to effect three-point fixation, once within the canal.A small incision is made at the base of the metacarpal, on either its radial or ulnar corner.Blunt dissection is carried out, taking care not to damage the tendons and cutaneous nerves.A 2 mm drill or sharp awl is used to open the medullary canal.

MISCELLANEOUS SEE ALSO * Melanocytic Tumors, Skin and Digit * Squamous Cell Carcinoma, Skin Suggested Reading Wobeser BK, Kidney BA, Powers BE, Withrow SJ, Mayer MN, Spinato MT, Allen AL.* Prognosis for cats is poor with median survival times of 2–3 months and metastatic rates of approximately 25%; survival times are similar in cats with primary and metastatic squamous cell carcinoma.* Benefit of chemotherapy has not been established; however, in patients with advanced stage of disease, chemotherapy as used for squamous cell carcinoma of other sites could be considered. MEDICATIONS DRUG(S) Piroxicam (dogs) 0.3 mg/kg PO q24h for analgesia; (cats) no established dosages; however, 0.3 mg/kg PO q48h has been used anecdotally. CONTRAINDICATIONS/POSSIBLE INTERACTIONS None FOLLOW-UP PATIENT MONITORING * Complete surgical excision of the primary lesion and no evidence of metastasis—additional treatment may not be required. * Recheck with physical examination, thoracic radiographs, lymph node evaluation, ± abdominal ultrasound at 1 month, then every 3 months after treatment (complete surgical excision). EXPECTED COURSE AND PROGNOSIS * Survival time following complete surgical excision depends upon location of the tumor on the digit—squamous cell carcinoma originating from subungual epithelium: 95% 1-year and 74% 2-year survival; squamous cell carcinoma originating in other parts of the digit: 60% 1-year and 44% 2-year survival. * In one recent report, survival at 1 year and 2 years was 50% and 18%, respectively, while in another recent retrospective study less than half the dogs died of squamous cell carcinoma and the median survival time was not reached. * Surgery to amputate affected digit, regardless of presence of metastases, provides positive impact on survival in the dog; however, dogs with metastatic disease at the time of presentation were more likely to have local recurrence in one small study. * Prognosis for cats is poor with median survival times of 2–3 months and metastatic rates of approximately 25%; survival times are similar in cats with primary and metastatic squamous cell carcinoma. MISCELLANEOUS SEE ALSO * Melanocytic Tumors, Skin and Digit * Squamous Cell Carcinoma, Skin Suggested Reading Wobeser BK, Kidney BA, Powers BE, Withrow SJ, Mayer MN, Spinato MT, Allen AL.Vet Pathol 2007, 44(3): 355–361.Author Jackie M. Wypij Consulting Editor Timothy M. Fan S Squamous Cell Carcinoma, Ear BASICS OVERVIEW * Malignant tumor of squamous epithelium occurring on the pinna, external ear, and/or middle ear.* Pinna—most common location in cats; tumors of the pinna in dogs are rarely squamous cell carcinoma.

If hypotension occurs, reduce infusion rate or discontinue.##### Side-effects Intravenous injection may cause CNS, cardiovascular (hypotension, heart block, arrhythmias) and respiratory depression.at intervals of 6–8 hours monitored by measurement of plasma conentration.Maintenance dose 100 mg i.v.Drug concentration in plasma does not correlate with therapeutic effect and monitoring is only necessary to assess complications of suspected toxicity. ##### Cautions/contraindications Acute liver disease, porphyria. Monitor liver biochemistry 6-monthly in those most at risk of severe liver damage (check with a _National Formulary_ ). Many drug interactions with antiepileptics and other drugs (check with a _National Formulary_ ). #### Phenytoin ##### Mechanism of action Inhibit sodium influx across the cell membrane, reduce cell excitability. ##### Indications All forms of epilepsy except absence seizures, but used much less in developed countries. Also used in management of status epilepticus and in trigeminal neuralgia. ##### Preparations and dose _Capsules: 25 mg, 50 mg, 100 mg, 300 mg; suspension: 30 mg/5 mL; injection: 50 mg/mL._ Oral 150–300 mg daily (single dose or two divided doses) increased gradually as necessary (with plasma-phenytoin concentration monitoring); usual dose 200–500 mg. Reference range for concentration 40–80 µmol/L (10–20 mg/L) immediately before the next dose. IV Give with blood pressure and ECG monitoring. 18 mg/kg diluted to 10 mg/mL in 0.9% sodium chloride at a rate not exceeding 50 mg/min (average-sized adult 1000 mg over 20 min) as a loading dose. Maintenance dose 100 mg i.v. at intervals of 6–8 hours monitored by measurement of plasma conentration. ##### Side-effects Intravenous injection may cause CNS, cardiovascular (hypotension, heart block, arrhythmias) and respiratory depression. If hypotension occurs, reduce infusion rate or discontinue.##### Cautions/contraindications Contraindicated in sinus bradycardia, heart block and porphyria.Many drug interactions (check with a national formulary).Highly protein bound and can be displaced by valproate and salicylates, which therefore enhance the effect.

Simply listening to music (see here) can help, too.Numerous studies have shown the benefits of yoga (see here), qigong (see here) and other forms of exercise that involve slow, deep breathing for lowering high blood pressure.Relaxation (see here) Methods that encourage slow, deep, rhythmic breathing may be as effective as some medications in treating high blood pressure.It consists of two numbers; the first is your systolic blood pressure (the pressure in your arteries when your heart contracts) and the second is your diastolic blood pressure (the pressure as your heart relaxes). Blood pressure of less than 120/80 is considered normal, and between 120/80 and 140/90 is classified as high-normal. High blood pressure (also known as hypertension) is diagnosed when blood pressure is consistently greater than 140/90, and is considered severe when it exceeds 180/110. High blood pressure doesn't always cause symptoms, and may be present even if you feel well. Nevertheless, it increases your risk of developing some serious health problems (including heart attack, stroke and kidney disease) and requires ongoing treatment by your doctor. The following remedies may help you manage your blood pressure. ### Suggested remedies Lifestyle factors If you have high blood pressure, your doctor may recommend that you quit smoking, eat more fruit and vegetables, cut back on salt and alcohol and/or reduce your body weight. You should also follow a healthy diet. Meditation (see here) Regular meditation–transcendental meditation in particular—has been shown in numerous studies to reduce blood pressure, most likely by reducing stress and balancing the autonomic nervous system. Relaxation (see here) Methods that encourage slow, deep, rhythmic breathing may be as effective as some medications in treating high blood pressure. Numerous studies have shown the benefits of yoga (see here), qigong (see here) and other forms of exercise that involve slow, deep breathing for lowering high blood pressure. Simply listening to music (see here) can help, too.Coenzyme Q10 (see here) In a review of the scientific evidence for a range of natural therapies for hypertension published in 2008, CoQ10 supplements were shown to lower blood pressure more significantly than any other therapy studied.Garlic (see here) Extensive research suggests that garlic may be of some help in lowering blood pressure in people with hypertension.

Serving Size: one serving, 4 large shrimp—22 g. Per serving: calories—22, calories from fat—2, total fat—0 g (0% daily value), saturated fat—0 g (0%), trans fat—, cholesterol—43 mg (14%), sodium—49 mg (2%), total carbs—0 g (0%), dietary fiber—0 g (0%), sugars—0 g, protein—5 g, vitamin A—1%, vitamin C—1%, calcium—1%, iron—4%.Shrimp— *Properties—antioxidant, anti-inflammatory *High in vitamin B12 (cobalamin), protein, choline, iodine, selenium, phosphorus, copper, cholesterol *Low in calories, fat *Contains carotenoids, vitamins A, B3 (niacin), B5 (pantothenic acid), B6 (pyridoxine), B9 (folate), C, E, calcium, iron, magnesium, potassium, sodium, zinc, Omega-3 fatty acids, Omega-6 fatty acids Beneficial Effects— *beneficial for heart health *beneficial for muscles *beneficial for energy *provides anti-cancer benefits *beneficial for the nervous system *beneficial for skin health *beneficial for eye health *beneficial for thyroid gland health Possible Adverse Effects— *shrimp is high in cholesterol. Individuals that need to limit their cholesterol intake may wish to limit shrimp consumption. *Note: Some individuals may have sensitivities or allergies to fish and shrimp. Reactions may range from simple skin itching to severe anaphylactic reactions, such as difficulty breathing. People with known allergies are advised to avoid this food item. *Note: Some fish are considered unsafe for pregnant or nursing mothers, or young children to eat. If individuals have concerns regarding mercury levels, pollutants, pesticides in fish, it may be wise to limit or avoid eating specific varieties of fish. *Note: Some individuals may experience adverse reactions to sulfite preservatives in certain foods. Individuals with known sensitivities to sulfites may wish to question the store's meat or fish manager about the presence or absence of sulfites in fresh and prepackaged foods. Serving Size: one serving, 4 large shrimp—22 g. Per serving: calories—22, calories from fat—2, total fat—0 g (0% daily value), saturated fat—0 g (0%), trans fat—, cholesterol—43 mg (14%), sodium—49 mg (2%), total carbs—0 g (0%), dietary fiber—0 g (0%), sugars—0 g, protein—5 g, vitamin A—1%, vitamin C—1%, calcium—1%, iron—4%.Serving Size: one ounce sorghum grain (2 tablespoons) —28 g. Per serving: calories—95, calories from fat—8, total fat—1 g (1% daily value), saturated fat—0 g (1%), trans fat—, cholesterol—0 mg (0%), sodium—2 mg (0%), total carbs—21 g (7%), dietary fiber—2 g (7%), sugars— g, protein—3 g, vitamin A—0%, vitamin C—0%, calcium—1%, iron—7%.

Traumatic wounds comprise such diverse damage as deep cuts, compound fractures, frostbite necrosis, and thermal burns.The latter include the endometrial surface, after separation of the placenta, and the umbilical stump in the neonate.##### Wound Infections Wounds subject to infection can be surgical, traumatic, or physiologic.Blockage of ducts with inspissated sebum, as in acne vulgaris, predisposes to the condition. **Acne vulgaris** also involves inflammation of hair follicles and associated sebaceous glands. ##### Furuncles The furuncle is a small abscess that develops in the region of a hair follicle. Furuncles may be solitary or multiple and may constitute a troublesome recurrent disease. Spread of infection to the dermis and subcutaneous tissues can result in a more extensive multiloculated abscess, the **carbuncle. ** ##### Impetigo Pyoderma, also termed impetigo, is a common, sometimes epidemic, skin lesion. The initial lesion is often a small vesicle that develops at the site of invasion and ruptures with superficial spread characterized by skin erosion and a serous exudate, which dries to produce a honey-colored crust. ##### Erysipelas Erysipelas is a rapidly spreading infection of the deeper layers of the dermis. It is associated with edema of the skin, marked erythema, pain, and systemic manifestations of infection including fever and lymphadenopathy. ##### Cellulitis Cellulitis is not a skin infection as such, but it can develop by extension from skin or wound infections. It usually manifests as an acute inflammation of subcutaneous connective tissue with swelling and pain and often with marked constitutional signs and symptoms. ##### Wound Infections Wounds subject to infection can be surgical, traumatic, or physiologic. The latter include the endometrial surface, after separation of the placenta, and the umbilical stump in the neonate. Traumatic wounds comprise such diverse damage as deep cuts, compound fractures, frostbite necrosis, and thermal burns.**TABLE S–1** Major Causes of Skin and Wound Infections ### **II.BONE AND JOINT INFECTIONS** ##### Osteomyelitis The onset of acute hematogenous osteomyelitis is usually abrupt, but can sometimes be insidious.It is classically characterized by localized pain, fever, and tenderness to palpation over the affected site.

A careful patient history should be obtained prior to any imaging, and confirmation of MRI compatibility should be confirmed.However, the valves used in the TAVI procedure (transcatheter aortic valve implantation) are noted to be MRI-conditional.The majority of artificial heart valves are considered MRI-safe.These characteristic findings can be evident on non-contrast MR angiography using time-of-flight imaging technique [71]. Confirmation with conventional angiography or CT angiography can be obtained postpartum if needed. ### 17.6.4 Amniotic Fluid Embolism Amniotic fluid embolism, also known as anaphylactoid syndrome of pregnancy, is a devastating clinical condition. If a communication forms between the uterine veins and the amniotic sac, then amniotic fluid can enter into venous circulation. This can precipitate anaphylaxis- and shocklike symptoms resulting in dramatic circulatory collapse and hypoxemia, carrying with it high maternal mortality and morbidity risks [36]. Should a patient survive the acute presentation, MRI can be a useful tool for evaluation of myocardial damage following the acute presentation. Evidence of late gadolinium may be present, indicating presence of focal myocardial damage [45]. Through analysis of a case report, Hosoya and colleagues [45] proposed that the finding of late gadolinium enhancement supports the theory that cardiac complications seen in amniotic fluid embolism may be due to direct left ventricular myocardial injury due to immune reactions and not due to pulmonary embolism. ## 17.7 Evaluation of Postsurgical Cardiovascular Diseases ### 17.7.1 Artificial Heart Valves Although the topic of MRI safety with regard to the developing fetus is discussed extensively elsewhere in this book, there are specific safety considerations with regard to artificial valves. The majority of artificial heart valves are considered MRI-safe. However, the valves used in the TAVI procedure (transcatheter aortic valve implantation) are noted to be MRI-conditional. A careful patient history should be obtained prior to any imaging, and confirmation of MRI compatibility should be confirmed.MRI allows for detailed assessment of both native and prosthetic valves.Similar to assessment of native valves, MRI can be used to evaluate structure and function of the prosthesis.It is of particular importance to accurately diagnose prosthetic valve endocarditis.

Thalidomide sparked scientific interest in the field of transplacental teratogenesis (see Glossary item, Teratogenesis).Current theory holds that thalidomide kills cells that are needed for limb development, with embryotoxicity highest in weeks 3 and 8 following conception [13].By that time, over 10,000 children were affected worldwide [13].The drug was removed from the European market in 1961.• **Mad hatter disease** **→** occupational exposure to heavy metals (mercury) Beginning in the seventeenth century, European hatters used mercury in the preparation of felt from animal fur. Mercury vapors induced tremors in the hatters, and the disease came to be known, callously, as mad hatter disease. Occurrences of the disease among hatters continued for at least two more centuries. By the mid-nineteenth century, the link between mercury exposure and tremors was a scientific certainty. England passed laws to protect hatters from mercury exposure, and the incidence of disease declined. Though a rarity, new cases of mad hatter disease have occurred in the twentieth century. Today, mercury is used in gold extraction. As a result, mercury contamination has increased in gold mining areas, and new cases of occupational tremors are occurring among gold workers [12]. • **Phocomelia** **→** medication-induced teratogenesis via thalidomide Thalidomide was first marketed in 1957 as a treatment for morning sickness. Thalidomide was used in many countries, but not in the U.S., where it was denied Food and Drug Administration (FDA) approval. Extreme cases of phocomelia characterized by congenital absences of one or more limbs were reported for the first time in Germany. Soon thereafter large numbers of congenital limb malformations were reported throughout Europe. The occurrences of limb malformations were traced to a common exposure: thalidomide. The drug was removed from the European market in 1961. By that time, over 10,000 children were affected worldwide [13]. Current theory holds that thalidomide kills cells that are needed for limb development, with embryotoxicity highest in weeks 3 and 8 following conception [13]. Thalidomide sparked scientific interest in the field of transplacental teratogenesis (see Glossary item, Teratogenesis).Many workers in this industry developed disfiguring, disabling, and life-threatening necrotic lesions extending from gingiva into underlying bone (i.e., mandible or maxilla).It took nearly a half-century to associate the jaw condition (eventually called "phossy jaw") with phosphorus exposure, and to eliminate phosphorus in the manufacture of matches [14].

A scope with a camera directly visualizes, and forceps inserted through it can sample, the small intestine.Enteroscopy— , $$$$, Y.If you have sedation, you should have nothing by mouth for four hours before the test, except for necessary medications (check with your GI doctor).Often bleeding can be treated at the time of the procedure.Breath tests— / , $, N. Tests that measure gas that you breathe out in a tube to evaluate poor absorption of sugars, which indicates the presence of Helicobacter pylori or bacterial overgrowth. Lactose or fructose is ingested to evaluate malabsorption of those compounds. If you don't absorb the sugars, they can cause intestinal gas, bloating and pain due to the release of hydrogen gas and the production of fatty acids by the bacteria. Lactulose is ingested to look for bacterial overgrowth in the small intestines (hydrogen and methane gases are measured). For H. pylori testing, a labeled carbon isotope, C-13 or C-14, is given by mouth (C-13 is not radioactive), and the bacteria incorporate this substance into carbon dioxide when they break down urea. The carbon dioxide is measured. The breath test for H. pylori can be used to look for active disease and assess that treatment of the bacteria was successful. Upper endoscopy— , $$$–$$$$, Y. A scope with a camera directly visualizes, and forceps inserted through it can sample, the esophagus, stomach and duodenum. The back of your throat is anesthetized with a spray or gargle. Most people want to have conscious sedation or, more recently, propofol sedation. This test is useful to evaluate GERD that is not responding to therapy, trouble swallowing, possible ulcer disease, gastritis, celiac disease, and causes for bleeding, diarrhea or anemia. Often bleeding can be treated at the time of the procedure. If you have sedation, you should have nothing by mouth for four hours before the test, except for necessary medications (check with your GI doctor). Enteroscopy— , $$$$, Y. A scope with a camera directly visualizes, and forceps inserted through it can sample, the small intestine.Depending on the type of test, a preparation may or may not be needed.If you have sedation, you should have nothing by mouth for four hours before the test, except for perhaps your necessary medications (check with your GI doctor).Colonoscopy— / , $$$–$$$$$, Y/N.

However, it does not record plaque levels or details of attachment loss and recession.It assesses and codes for the presence of bleeding, calculus or plaque retention factors, and pockets (see Fig 4-1b).It is intended to determine which patients will benefit from a more detailed periodontal examination and may require more complex periodontal therapy.Xerostomia can be associated with increased gingivitis due to lack of the innate defensive functions of saliva. It may also be a feature in HIV-positive children. ### _Anatomical Features_ Enamel projections and pearls (Fig 4-10), proximal and palatogingival grooves (Fig 4-11) are all developmental dental features and have been associated with gingivitis and attachment loss. Cemental tears are defined as complete separation of the cement from the dentine or partial separation within the cement layer and these may be associated with attachment loss. The prevalence of these tears in the young has not been documented. **Fig 4-10** Enamel projection into bifurcation in association with buccal attachment loss on stained extracted mandibular molar. **Fig 4-11** Palatal root groove. ### Periodontal Screening Since the recommendation of the British Society of Periodontology in 1986 to introduce periodontal screening into general dental practice using the Community Periodontal Index of Treatment Needs (CPITN), the index has been reconfigured as the Basic Periodontal Examination. The BPE provides a quick and simple method of screening all patients for periodontal problems. It is comfortably tolerated and gives the practitioner an indication of the need for periodontal treatment and the level of further periodontal examination required for differing periodontal disease levels. The BPE is not intended as a replacement for periodontal indices designed to measure "periodontal status", such as the six-point per tooth measurement of probing pocket depths (Chapter 8). It is intended to determine which patients will benefit from a more detailed periodontal examination and may require more complex periodontal therapy. It assesses and codes for the presence of bleeding, calculus or plaque retention factors, and pockets (see Fig 4-1b). However, it does not record plaque levels or details of attachment loss and recession.The ball end on this probe is very useful for detecting subgingival calculus deposits.This procedure can be comfortably undertaken on young individuals provided the recommended probing force of 20–25g (0.20–0.25N) is not exceeded.Additional marks at 8.5mm and 11.5mm are present on the WHO "C-type" probe version for clinical use (Fig 4-12).

Duration: 2 hours.The shell is then filled with a saline solution.The expander is removed and replaced in the pocket with a permanent implant that is an unfilled silicone rubber shell.When the expander has been inflated to the desired size, there is a second outpatient procedure (often under local anesthesia and intravenous sedation, though it may also be done under general anesthesia).3.A long horizontal incision is made from one side of the abdomen to the other above the pubic area. A large ellipse of tissue is cut from mostly below the belly button. The tissue that's been cut is left attached to the underlying muscle and blood supply. 3. The surgeon makes a tunnel deep in the fat from the abdomen up to the breast. The tissue is then pulled up through the tunnel, rotated into its new position in the chest, and reshaped into a breast. 4. In some cases, the tissue for reconstruction may be removed completely from the underlying tissue and then must be reattached in the chest area using microsurgery. Duration: 4 hours. For a reconstruction using an implant: 1. A breast expander (a balloonlike device made from silicone rubber) is placed in a deflated state under the tissue that remains from the breast that's been removed. 2. For several months thereafter, the patient goes to the doctor's office for repeated injections of small amounts of sterile saline (salt water) by means of a small needle through the skin. The saline gradually expands the device and the tissue over it begins to stretch. This creates a breast-shaped pocket for a breast implant. A patient may feel pressure or discomfort, which subsides as the tissue expands. 3. When the expander has been inflated to the desired size, there is a second outpatient procedure (often under local anesthesia and intravenous sedation, though it may also be done under general anesthesia). The expander is removed and replaced in the pocket with a permanent implant that is an unfilled silicone rubber shell. The shell is then filled with a saline solution. Duration: 2 hours.The nipple is reconstructed with flaps of skin at the site, and the nipple and areola are tattooed to the appropriate color.Occasionally, skin grafts may be used in the procedure.What to expect when it's over: If a patient's tissue is used, she remains in the hospital for about 4 days.When an expander is placed, hospitalization is slightly shorter.Patients are usually walking by the second day.

**980.** "Foods and fluids that will increase urine alkalinity should be consumed."**4.** "My fluid intake should be increased to at least 3000 mL daily."**3.** "The prescribed medication must be taken until it is finished."**2.** "I need to urinate frequently throughout the day."** **1.Which client statement indicates to the nurse the **need for further instruction?** Remain with the client and sit in silence; this will encourage the client to verbalize feelings. **976. ** The nurse has just admitted to the nursing unit a client with a basilar skull fracture who is at risk for increased intracranial pressure. Pending specific health care provider prescriptions, the nurse should safely place the client in which positions? **Select all that apply. ** **1. ** Head midline **2. ** Neck in neutral position **3. ** Head of bed elevated 30 to 45 degrees **4. ** Head turned to the side when flat in bed **5. ** Neck and jaw flexed forward when opening the mouth **977. ** The nurse reviews the arterial blood gas results of an assigned client and notes that the laboratory report indicates a pH of 7.30, Pco2 of 58 mm Hg, Po2 of 80 mm Hg, and HCO3 of 27 mEq/L. The nurse interprets that the client has which acid-base disturbance? **1. ** Metabolic acidosis **2. ** Metabolic alkalosis **3. ** Respiratory acidosis **4. ** Respiratory alkalosis **978. ** The nurse has admitted a client to the clinical nursing unit after undergoing a right mastectomy. The nurse should plan to place the right arm in which position? **1. ** Elevated on a pillow **2. ** Level with the right atrium **3. ** Dependent to the right atrium **4. ** Elevated above shoulder level **979. ** On the second postpartum day, a client complains of burning on urination, urgency, and frequency of urination. A urinalysis indicates the presence of a urinary tract infection. The nurse instructs the client regarding measures to take for the treatment of the infection. Which client statement indicates to the nurse the **need for further instruction? ** **1. ** "I need to urinate frequently throughout the day." **2. ** "The prescribed medication must be taken until it is finished." **3. ** "My fluid intake should be increased to at least 3000 mL daily." **4. ** "Foods and fluids that will increase urine alkalinity should be consumed." **980.At what time should the nurse plan to assess the client for a hypoglycemic reaction?**1.** 10:00 **2.** 11:00 **3.** 17:00 **4.** 23:00 **981.** The nurse is the first responder after a tornado has destroyed many homes in the community.Which victim should the nurse attend to **first?** **1.** The 32-year-old pregnant woman who exclaims, "My baby is not moving."**2.

b.Most commonly involve the first metatarsophalangeal joint (MTP; called podagra; joint in the foot with the most trauma) • Polyarticular involvement occurs in 10% to 15% of cases.Acute gout: 1st MTP joint most often involved a.Recurrent acute attacks of gout are the rule.Polyarticular JRA (40% of cases) • Disabling arthritis predominates. JRA, polyarticular: disabling arthritis predominates 4. Pauciarticular JRA (40% of cases) a. Arthritis limited to a few joints. b. Uveitis with the potential for blindness JRA, pauciarticular: limited arthritis; uveitis and potential for blindness I **Gouty arthritis** 1. Epidemiology a. Definition—tissue deposition of monosodium urate (MSU) due to prolonged hyperuricemia Gout: MSU in tissue; prolonged hyperuricemia b. Occurs more often in men >30 years of age (95% of cases) Gout: male dominant disease c. Uncommon in women _before_ menopause (5% of cases) d. Primary gout arises from inborn errors of metabolism involving purine metabolism. • Example—deficiency of hypoxanthine-guanine phosphoryltransferase (HGPRT) in Lesch-Nyhan syndrome (refer to Chapter 6) e. Secondary causes are more common causes of gout. (1) Underexcretion of uric acid (UA) in kidneys (80%–90% of cases) Gout: most cases result from UA underexcretion • Examples—lead (Pb) poisoning, alcoholism, diets rich in red meat, seafood, beer, thiazides (2) Overproduction of uric acid (increased nucleated cell turnover; 10%–20% of cases) • Examples—treating leukemia, psoriasis f. Clinical conditions commonly associated with gout (1) Urate nephropathy, renal stones (refer to Chapter 20) (2) Hypertension (HTN), coronary artery disease (CAD) (3) Lead poisoning Gout associations: urate nephropathy, renal stones, HTN, CAD, Pb poisoning • Produces interstitial nephritis, which interferes with uric acid excretion 2. Recurrent acute attacks of gout are the rule. Acute gout: 1st MTP joint most often involved a. Most commonly involve the first metatarsophalangeal joint (MTP; called podagra; joint in the foot with the most trauma) • Polyarticular involvement occurs in 10% to 15% of cases. b.(1) Activate synovial cells, leukocytes, and the complement cascade; the latter releases C5a, which attracts neutrophils into the joint producing acute inflammation • Neutrophils also phagocytose uric acid crystals.Acute gout: free UA crystals in joint responsible for initiating the attack (2) Another common site for acute gout is the extensor tenosynovium on the dorsum of the midfoot.

Microvascular complications are related to the direct impact of high glucose levels, but elevated blood pressure contributes to excretion of protein and renal complications.The risk of complications increases with longer duration of diabetes and poorer metabolic control.The duration of diabetes is an important component in the development of diabetic complications.Factors associated with increased risk of hypoglycemia include intensive therapy, better glycemic control, irregular schedule, and alcohol consumption (especially if combined with exercise or decreased carbohydrate intake). Counter-regulatory hormones responded to the stress of her illness resulting in a release of glucose from her liver. MN's pancreatic beta cells were unable to respond by producing insulin to facilitate tissue uptake of the excess glucose. Chronic microvascular complications that affect smaller blood vessels in the eyes and kidneys and neurological functioning are closely related to elevation of blood glucose. The Diabetes Control and Complications Trial (DCCT) demonstrated that intensive treatment of patients with type 1 diabetes dramatically reduces the risk of progression to retinopathy, nephropathy, and neuropathy by 50 to 75 percent. The DCCT intensified diabetes management by including self-monitoring of blood glucose at least 4 times a day and the use of multiple insulin injections or the use of a continuous insulin infusion pump to reduce hemoglobin A1C from approximately 9 to 7 percent. The DCCT intensive treatment was, however, associated with an increased risk of hypoglycemia and weight gain. Use of nutritional strategies, such as more regular meal times, use of snacks, and adjustments to match insulin dosage to carbohydrate intake were stressed as an essential component of behavior modification. Because weight gain will adversely affect glycemia, lipid levels, blood pressure, and general health, prevention of weight gain should be advised. The duration of diabetes is an important component in the development of diabetic complications. The risk of complications increases with longer duration of diabetes and poorer metabolic control. Microvascular complications are related to the direct impact of high glucose levels, but elevated blood pressure contributes to excretion of protein and renal complications.Diabetes, especially when accompanied by insulin resistance, is associated with increased triglycerides and cholesterol (very low density lipoprotein [VLDL] and low density lipoprotein [LDL]).The DCCT showed 25 percent less hypercholesterolemia with tight control.Control of blood pressure and lipid levels is essential to prevent or ameliorate the macrovascular complications of diabetes.

However, multiple chromosomes have been identified in various studies conducted over the last decade.Genetic linkage studies are complex and difficult to replicate.Even though the risk factor association in first-degree relatives is four to six times higher than in the general population, the exact mode of transmission has yet to be identified.Research continues, with potential promising findings with nimodipine. * **Neuroanatomical Theories: Cellular Resiliency. ** As in schizophrenia research, efforts have been made to explore neuroanatomical abnormalities in mood disorders from a causational approach, as well as from a disease-consequence approach. To date, neuro-imaging and postmortem studies have shown enough positive results that research in this area is likely to expand greatly (Soares and Mann 1997; Manji et al. 2000). Key initial findings point to a decrease in CNS volume and cell numbers, neurons, and/or glia in mood disorders. Some results apply to major depression and some to bipolar disorder. An unexpected finding of these studies is the identification of a cytoprotective protein in the frontal cortex. This finding has sparked interest in defining the mechanism by which lithium and other mood stabilizers increase levels of this protein (see chapter 17 for further discussion). The existence of neuroprotective proteins holds great promise for furthering the understanding of mood disorders and for developing effective treatments. * **Genetic and Familial Theories. ** Familial, twin, and adoption studies support the theory that bipolar disorder is heritable. Bertelsen's early Danish twin studies have been supported in the intervening years, and it is generally accepted that the concordance rate for monozygotic twins is 50 to 60 percent for bipolar disorder (Tsuang and Faraone 1990). Even though the risk factor association in first-degree relatives is four to six times higher than in the general population, the exact mode of transmission has yet to be identified. Genetic linkage studies are complex and difficult to replicate. However, multiple chromosomes have been identified in various studies conducted over the last decade.2001).In summary, the neurobiology of bipolar disorders is thought to encompass both functional and structural abnormalities at multiple levels of the CNS.Molecular and cellular alterations, systems and pathway disruptions, and compensatory processes are all areas of interest, either as independent factors or as elements of a cascade effect.

Some experts claim that the manufacture of various chemicals, such as chlorofluorocarbons used as propellants in aerosol sprays, and the effects of high-flying jet aircraft are destroying this protective layer and allowing excessive amounts of ultraviolet radiation to penetrate the earth's atmosphere, thus subjecting humans to increased dangers of skin cancer and other health problems.Therefore, other tests of fetal well-being are recommended before performing an emergency cesarean section or induction of labor. oxyuriasis. See **enterobiasis**. oxyuricide /ok′sē· ′ris d/, an agent that destroys pinworms. **_Oxyuris vermicularis_**. See **_Enterobius vermicularis._** oz, abbreviation for **ounce**. oz ap [L, _uncia_ ], abbreviation for _apothecary ounce,_ a unit of weight equal to 31.1035 grams. ozena / zē′n / [Gk, _ozein,_ to have an odor], a condition of the nose characterized by atrophy of the nasal conchae and mucous membranes. Symptoms include crusting of nasal secretions, discharge, and, especially, a very offensive odor. Ozena may follow chronic inflammation of the nasal mucosa. ozone (O3) [Gk, _ozein,_ to have an odor], an allotropic form of oxygen consisting of molecules containing three oxygen atoms. Ozone is formed when oxygen is present in an electric discharge, as might occur in a lightning storm. Ozone is used as a bleaching, cleaning, and oxidizing agent and has a faint, chlorinelike odor. ozone hole, a seasonal depletion of the steady-state ozone concentration in the stratosphere, particularly over Antarctica. ozone shield, the layer of ozone that hangs in the atmosphere from 20 to 40 miles above the surface of the earth and protects the earth from excessive ultraviolet radiation. Some experts claim that the manufacture of various chemicals, such as chlorofluorocarbons used as propellants in aerosol sprays, and the effects of high-flying jet aircraft are destroying this protective layer and allowing excessive amounts of ultraviolet radiation to penetrate the earth's atmosphere, thus subjecting humans to increased dangers of skin cancer and other health problems.The ozone shield is implicated in certain health problems that affect some air travelers.See also **ozone sickness**.ozone sickness, an abnormal condition caused by the inhalation of ozone that may seep into jet aircraft at altitudes over 40,000 feet.It is characterized by headaches, chest pains, itchy eyes, and sleepiness.Exactly why and how ozone causes this condition is not known.

The most important allosteric regulator of both glycolysis and gluconeogenesis is fructose 2,6-bisphosphate, **F2,6BP**.The inhibition of PFK1 by ATP is overcome by AMP, which binds to the R state of the enzyme and, therefore, stabilizes the conformation of the enzyme capable of binding F6P.**FIGURE 10-5: Alternative pathway of glycolysis is carried out in highly proliferative cells such as one observed in cancer cells. Cancer cells express the PKM2 isoform of pyruvate kinase, which is much less active than other isoforms and is also negatively regulated by binding to tyrosine-phosphorylated proteins. The dashed arrow for the PKM2 reaction is to demonstrate that this reaction is inefficient compared to the transfer of phosphate from PEP directly to PGAM1. PGAM1: phosphoglycerate mutase. PEP: phosphoenolpyruvate. 3-PG: 3-phosphoglycerate, 2-PG: 2-phosphoglycerate. 2,3-BPG: 2,3-bisphosphoglycerate. His11 refers to the catalytic site histidine that is phosphorylated by phosphate donation from PEP. ** Reproduced with permission of themedicalbiochemistrypage, LLC. _PFK1_ is a tetrameric enzyme that exists in 2 conformational states termed R and T that are in equilibrium. ATP is both a substrate and an allosteric inhibitor of PFK1. Each subunit has 2 ATP-binding sites, a substrate site and an inhibitor site. The substrate site binds ATP equally well when the tetramer is in either conformation. The inhibitor site binds ATP essentially only when the enzyme is in the T state. F6P is the other substrate for PFK1 and it binds preferentially to the R state enzyme. At high concentrations of ATP, the inhibitor site becomes occupied and shifts the equilibrium of PFK1 conformation to that of the T state, thereby decreasing the ability of PFK1 to bind F6P. The inhibition of PFK1 by ATP is overcome by AMP, which binds to the R state of the enzyme and, therefore, stabilizes the conformation of the enzyme capable of binding F6P. The most important allosteric regulator of both glycolysis and gluconeogenesis is fructose 2,6-bisphosphate, **F2,6BP**.The PFK2 enzyme in mammals exists as a homodimer.The PFK2 kinase domain is related to the catalytic domain of adenylate kinase.The F-2,6-BPase domain of the enzyme is structurally and functionally related to the histidine phosphatase family of enzymes.

The reticular dermal plexus is located in the middle portion of the dermis and is primarily venous.7.20).The subpapillary plexus is located at the junction of the papillary and reticular layers of the dermis and gives off small branches that form perpendicular capillary loops in the dermal papillae (usually one loop per papilla) (see Figs 7.1, 7.4; Fig.The blood supply to the skin originates from three main sources: the direct cutaneous, musculocutaneous and fasciocutaneous systems. The direct cutaneous system of vessels is derived from the main arterial trunks and accompanying veins. These vessels course in the subcutaneous fat parallel to the skin surface and are confined to certain areas of the body, e.g. the supraorbital artery, the superficial circumflex iliac artery and the dorsalis pedis artery. The musculocutaneous perforators arise from the intramuscular vasculature, pass through the surface of the muscle, and pierce the deep fascia to reach the skin by spreading out in the subcutaneous tissues. The fasciocutaneous system consists of perforating branches from deeply located vessels (deep to the deep fascia) that pass along intermuscular septa and then fan out at the level of the deep fascia to reach the skin. Examples include the fasciocutaneous perforating vessels from the radial and ulnar arteries. The direct cutaneous vessels, musculocutaneous perforators and fasciocutaneous perforators each contribute to six anastomosing horizontal reticular plexi of arterioles (Fig. 7.19), which have vascular connections between them and which ultimately provide the blood supply to the skin. Three plexi are located in the skin itself and supply all elements including the sweat glands and pilosebaceous units. The subpapillary plexus is located at the junction of the papillary and reticular layers of the dermis and gives off small branches that form perpendicular capillary loops in the dermal papillae (usually one loop per papilla) (see Figs 7.1, 7.4; Fig. 7.20). The reticular dermal plexus is located in the middle portion of the dermis and is primarily venous.The close association between arteriolar and venous plexi allows the countercurrent heat exchange between bloods at different temperatures.Fig.7.19 Vascular supply to the skin.A, Note the various horizontal plexuses fed by direct cutaneous, fasciocutaneous and musculocutaneous arteries.Compare with Figure 79.6.B, Higher magnification of vascular supply.

Signs and symptoms Reactive arthritis typically involves pain and swelling in the knees, ankles, feet and hips.Having this gene also doesn't guarantee that you'll get reactive arthritis when you experience an infection.Reactive arthritis is thought to occur in people who are genetically predisposed to it – many people with the condition carry the HLA-B27 gene.≈≈≈≈≈≈≈ #### ARTHRITIS AND INFLAMMATORY BOWEL DISEASE An estimated 1.4 million Americans have Crohn's disease or ulcerative colitis, the two common forms of inflammatory bowel disease (IBD) that cause chronic inflammation of the digestive tract. As many as 25 percent of people with IBD also experience enteropathic arthritis. Some researchers believe this form of arthritis may result from an immune response to intestinal bacteria in the inflamed bowel. Because people often experience pain and swelling in multiple joints, especially the knees and ankles, as well as stiffness in the spine, the condition is considered a form of spondyloarthritis. ≈≈≈≈≈≈≈ Reactive arthritis Reactive arthritis is when an inflammatory condition occurs as a reaction to an infection elsewhere in your body. Many different types of infectious organisms can trigger the joint inflammation. Reactive arthritis was formerly known as Reiter's syndrome. What's considered the classic form of reactive arthritis is caused by a bacterial infection in the intestines, genitals or urinary tract. The intestinal form is caused by foodborne infections from salmonella, campylobacter, shigella or yersinia. Chlamydia, a sexually transmitted infection, can cause the genital form. Overall, men between the ages of 20 and 40 are most likely to develop reactive arthritis. Having a bacterial infection does not mean you'll get arthritis. Reactive arthritis is thought to occur in people who are genetically predisposed to it – many people with the condition carry the HLA-B27 gene. Having this gene also doesn't guarantee that you'll get reactive arthritis when you experience an infection. Signs and symptoms Reactive arthritis typically involves pain and swelling in the knees, ankles, feet and hips.Inflammation of the tendons (tendinitis) or at places where tendons attach to bones (enthesitis) is common.This often results in pain at the heel or back of the ankle (Achilles tendinitis).There may be pain in the lower back and buttocks.

**postanesthesia care unit (PACU)** Recovery room.The isotope emits activity in the form of positrons, which are scanned and converted into a color image by a computer.The patient is injected with the molecule _deoxyglucose,_ which is tagged to an isotope.**polymyositis** A diffuse inflammatory disease of skeletal (striated) muscle that causes symmetric weakness and atrophy. **polyp** An abnormal outgrowth from a mucous membrane. **polypectomy** Surgical removal of a polyp, such as a nasal polyp. **polyphagia** Excessive eating. **polypharmacy** The use of many drugs to treat multiple health problems for older adults. **polyuria** Frequent and excessive urination. **pores** Openings or spaces. **portal hypertension** An abnormal persistent increase in pressure within the portal vein; a major complication of cirrhosis. **portal hypertensive gastropathy** A complication that can occur in patients with portal hypertension, with or without esophageal varices. Slow gastric mucosal bleeding may result in chronic slow blood loss, occult positive stools, and anemia. **portal-systemic encephalopathy (PSE)** A clinical disorder seen in hepatic failure and cirrhosis; it is manifested by neurologic symptoms and is characterized by an altered level of consciousness, impaired thinking processes, and neuromuscular disturbances; also called "hepatic encephalopathy" and "hepatic coma." **positive deflection** In electrocardiography, the flow of electrical current in the heart (cardiac axis) toward the positive pole. **positive inotropic agents** Drugs that increase myocardial contractility and are prescribed to improve cardiac output. **positron emission tomography (PET)** A diagnostic tool that provides information about the function of the brain, specifically glucose and oxygen metabolism and cerebral blood flow. The patient is injected with the molecule _deoxyglucose,_ which is tagged to an isotope. The isotope emits activity in the form of positrons, which are scanned and converted into a color image by a computer. **postanesthesia care unit (PACU)** Recovery room.**post-concussion syndrome** A group of clinical manifestations following a concussion that consist of personality changes, irritability, headaches, dizziness, restlessness, nervousness, insomnia, memory loss, and depression.The prolonged pattern is classified as post-trauma syndrome.

See atrophic gastritis.gastric atrophy.gastric areas, small patches of gastric mucosa, 1 to 5 mm in diameter, separated by the plicae villosae and containing the gastric pits.Also called watermelon stomach.It may result in chronic blood loss and anemia.Total gastrectomy (Rothrock, 2015) -gastria, suffix meaning "(condition of) possessing a stomach or stomachs": atretogastria, macrogastria, megalogastria. gastric /gas″trik/ [Gk, gaster, stomach] , pertaining to the stomach. -gastric, suffix meaning a "type of stomach or number of stomachs": endogastric, paragastric, trigastric. gastric acid pump inhibitor. See proton pump inhibitor. gastric analysis, examination of the contents of the stomach, primarily to determine the quantity of acid present and incidentally to ascertain the presence of blood, bile, bacteria, and abnormal cells. It may also be done to detect acid-fast bacillus in a client with undiagnosed tuberculosis. A sample of gastric secretion is obtained via a nasogastric tube. The technique used varies according to the information desired. The total absence of hydrochloric acid is diagnostic of pernicious anemia. Patients with gastric ulcer and gastric cancer may secrete less acid than normal whereas patients with duodenal ulcers secrete more. The composition and volume of the secretions may also provide diagnostic information. This procedure is rarely performed. gastric antacid. See antacid. gastric antral vascular ectasia, a rare vascular anomaly of the gastric antrum consisting of dilated and thrombosed capillaries and veins that form lines in the antrum that radiate toward the pylorus, resembling the stripes on a watermelon, seen most often in elderly women or patients with chronic liver disease. It may result in chronic blood loss and anemia. Also called watermelon stomach. gastric areas, small patches of gastric mucosa, 1 to 5 mm in diameter, separated by the plicae villosae and containing the gastric pits. gastric atrophy. See atrophic gastritis.gastric bypass, bariatric surgery performed to reduce stomach capacity and allow food to bypass part of the small intestine.gastric cancer, a malignancy of the stomach.Approximately 97% of stomach tumors are adenocarcinomas, which may be ulcerating, polypoid, diffuse, and fibrous, or superficial spreading lesions.Lymphomas and leiomyosarcomas account for less than 3%.

Alcoholics Anonymous (AA), an international nonprofit organization, founded in 1935, consisting of abstinent alcoholics whose purpose is to stay sober and help others recover from the disease of alcoholism through a 12-step program, including group support, shared experiences, and faith in a higher power.It is characterized by brain damage or dysfunction that results from excessive alcohol use.alcoholic hepatitis, an acute toxic liver injury associated with excess ethanol consumption. It is characterized by necrosis, inflammation caused by the accumulation of polymorphonuclear leukocytes, and in many instances Mallory bodies. **Alcoholic hepatitis** _(Kumar et al, 2007)_ alcoholic hepatopathy, a liver disease resulting from alcoholism, progressing in time to fibrosis and cirrhosis. alcoholic ketoacidosis, the fall in blood pH (acidosis) sometimes seen in alcoholics and associated with a rise in the levels of serum ketone bodies. alcoholic neuropathy, damage to the peripheral nerves as a result of alcohol consumption. Also called **alcoholic paralysis**. alcoholic-nutritional cerebellar degeneration, a sudden, severe incoordination in the lower extremities characteristic of poorly nourished alcoholics. The patient walks, if at all, with an ataxic or a wide-based gait. Treatment consists of improved nutrition, abstinence from alcohol, and physical therapy. See also **alcoholism**. alcoholic paralysis [Ar, _alkohl,_ essence; Gk, _paralyein,_ to be palsied]. See **alcoholic neuropathy**. alcoholic psychosis, any of a group of severe mental disorders in which the ego's functioning is impaired, including pathological intoxication, delirium tremens, Korsakoff's psychosis, and acute hallucinosis. It is characterized by brain damage or dysfunction that results from excessive alcohol use. Alcoholics Anonymous (AA), an international nonprofit organization, founded in 1935, consisting of abstinent alcoholics whose purpose is to stay sober and help others recover from the disease of alcoholism through a 12-step program, including group support, shared experiences, and faith in a higher power.Meetings are held at convenient times in public locations such as factories, schools, churches, hospitals, and other community buildings.Similar groups who work with the children, relatives, friends, and associates of alcoholics are **Al-Anon** and **Alateen.** alcoholic trance, a state of automatism resulting from ethanol intoxication.

A solution containing procaine is frequently injected (subcutaneously)" (Pschyrembel Naturheilkunde).**Note:** Neural therapy according to Dr. Ferdinand Huneke (1891–1966): "Therapeutic local anesthesia with the aim of healing sites of chronic irritation (e.g., scars, chronically inflamed tonsils, devitalized teeth).• Injuries to the **malleoli** and the **calcaneus** are related to the pelvic organs and hip joints via the zones and can cause problems and diseases there. #### 11.2.2 Tissue of the Foot Lymphatic and venous **congestion** and **edema** are found especially in the region of the ankles, the Achilles tendon, and on the dorsal part of the feet near the five metatarsophalangeal joints, particularly in women. Retraction or sluggishness of the tissue can be observed both on the plantar and medial sides of the feet, often clearly circumscribed. **From My Practice** In my experience, sportsmen and women with poorly healed injuries or fractures of the ankle joints or with scars on the medial or lateral malleoli later tended to suffer from pelvic or hip problems, partly of a structural–muscular nature and partly of a functional nature, which they had not had before. Every now and then I noticed that the nailing through the calcaneus that was necessary for extension treatment where fracture of the lower leg occurred, was directly related to the subsequent development of malfunctions, and even acute inflammatory processes in the pelvic organs of such patients who had been involved in accidents. After treatment of these small scars with neural therapy on the medial and lateral sides of the calcaneus (precisely the zones of the pelvic organs) and a few treatments of the zones of the foot, the problems usually vanished as quickly as they had appeared. **Note:** Neural therapy according to Dr. Ferdinand Huneke (1891–1966): "Therapeutic local anesthesia with the aim of healing sites of chronic irritation (e.g., scars, chronically inflamed tonsils, devitalized teeth). A solution containing procaine is frequently injected (subcutaneously)" (Pschyrembel Naturheilkunde).During a series of treatments and/or through a change in eating habits and improvement of the intestinal flora, we observe that these "swellings" often decrease, at least partially, in line with the patient's improved bowel function.

The use of MTA combined with infrared LLLT resulted in a more advanced and better quality bone repair.28 Fractures have different etiologies and treatment may or may not be associated with bone loss.It was concluded that the combination of MTA with LLLT and/or with GBR resulted in a better bone repair.Increased new bone formation was observed when the LED light was used alone or combined with the use of MTA + GBR, MTA + BMP, and MTA + BMP + GBR. These results indicate that the use of LED light alone or in combination with MTA, MTA + BMP, MTA + GBR, and MTA + BMP + GBR caused less inflammation, and an increase of both collagen deposition and bone deposition, as observed on both histological and morphometric analysis **. ** Our team has used Raman analysis to assess bone repair in these different models. Benefits of the isolated or combined use of MTA, BMPs, GBR, and laser on bone repair have been reported. Peaks of hydroxyapatite and CH groups on defects grafted with MTA, treated with or without laser, BMPs, and GBR, were studied. Laser irradiation (850 nm) was applied every other day for 2 weeks. Raman readings were taken at the surface of the defect. Statistical analysis showed significant differences between all groups ( _P_ = 0.001) and between Group 2 and all other groups ( _P_ <0.001), with the exception of group 10 ( _P_ = 0.09). At day 21, differences were seen between all groups ( _P_ = 0.031) and between groups 8 and 10 when compared with groups 6 ( _P_ = 0.03), 5 ( _P_ <0.001), 4 ( _P_ <0.001), and 9 ( _P_ = 0.04). At the end of the experimental period, no significant differences were seen between the groups. With regards to CH groups, significant differences were seen by the 15th day ( _P_ = 0.002) between group 2 and all other groups ( _P_ <0.0001), but not with the control. Advanced maturation of irradiated bone is due to increased secretion of calcium hydroxyapatite (CHA), which is indicative of greater bone calcification and resistance. It was concluded that the combination of MTA with LLLT and/or with GBR resulted in a better bone repair. The use of MTA combined with infrared LLLT resulted in a more advanced and better quality bone repair.28 Fractures have different etiologies and treatment may or may not be associated with bone loss.We aimed to assess, through Raman spectroscopy, the level of CHA (~958 cm−1) in complete tibial fracture animals treated with infrared irradiation combined with or without LPT, BMPs, and GBR.Animals with complete tibial fractures were divided into five treatment groups.

It is thought that viruses cause asthma exacerbations by activating the immune system.Increased airway responsiveness can last from 2 to 8 weeks after the infection in both normal and asthmatic persons.Therefore, they increase the hyperresponsiveness of the bronchial system.Infections cause inflammatory changes in the tracheobronchial system and alter the mucociliary mechanism.Physical training (aerobic exercise) had to be undertaken for at least 20–30 minutes, two to three times a week, over a minimum of 4 weeks. • No adverse effects were noted on lung function and wheeze in asthmatic patients. • Physical training was found to have no effect on resting lung function or the number of days of wheeze. • Physical training can improve cardiopulmonary fitness in individuals with asthma. #### Conclusions • Physical training can improve cardiopulmonary fitness without changing lung function. • The benefit of improved fitness on quality of life is unknown. #### Implications for nursing practice • Patients with asthma should be encouraged to engage in regular physical exercise. • Patients should be advised about prevention and treatment of exercise-induced asthma. P, patient population of interest; I, intervention or area of interest; C, comparison of interest or comparison group; O, outcome(s) of interest; T, time. Reference for evidence Ram FS, Robinson SM, Black PN, et al. Physical training for asthma. Cochrane Airways Group. _Cochrane Database Syst Rev_. (4):2005. CD001116. ### Respiratory infections Respiratory infections (especially viral infections) are one of the most common precipitating factors of an acute asthma attack. Influenza and rhinovirus are the major pathogens in older children and adults. Infections cause inflammatory changes in the tracheobronchial system and alter the mucociliary mechanism. Therefore, they increase the hyperresponsiveness of the bronchial system. Increased airway responsiveness can last from 2 to 8 weeks after the infection in both normal and asthmatic persons. It is thought that viruses cause asthma exacerbations by activating the immune system.### Nose and sinus problems Allergic rhinitis is a major predictor of adult asthma.Treatment of allergic rhinitis may reduce the frequency of asthma exacerbations.Some patients with asthma have chronic sinus problems that cause inflammation of the mucous membranes.Although the cause is usually non-infectious (e.g.allergies), bacterial infections may also be a cause.

In most cases these do not need to be three consecutive days.You will need to complete the bladder diary for at least three days before the investigations.Therefore, if you are unsure about whether you need to stop taking them, do contact the clinic or hospital where the testing will take place, or your GP.### _What conditions can be identified with urodynamic testing?_ As this type of investigation looks at the function of your bladder, conditions that are caused by differences in the way the bladder works can be evaluated by urodynamic testing, such as: * in men, an enlarged prostate gland (benign prostatic hyperplasia) * unstable detrusor muscle * stress incontinence * urge incontinence * mixed stress and urge incontinence. Investigations such as urodynamic testing can also provide important information about the severity of a bladder problem, particularly if you don't fit the usual criteria for a condition: The hospital I went to sort of poo-pooed me – they said, 'You're too young to have a bladder condition as severe as that.' Then they gave me a test where I sat on a toilet and I remember after the test the doctor said to me, 'I can't believe that it is quite so severe,' and he apologised that he had thought I was, well, sort of making it up really. _Denny_ ### _How do I prepare for urodynamic testing?_ If you take medication for your bladder symptoms, your doctor may ask you to stop taking this for five days before your testing session. (Examples of bladder medications can be reviewed in Chapter 12.) It is important that you know for certain if you do need to stop taking these medicines as in some cases your doctor will need to perform the urodynamic tests when you are taking the tablets as prescribed. Therefore, if you are unsure about whether you need to stop taking them, do contact the clinic or hospital where the testing will take place, or your GP. You will need to complete the bladder diary for at least three days before the investigations. In most cases these do not need to be three consecutive days.If you do experience constipation in the days before your appointment, see page on how to deal with this problem and discuss these treatments with your doctor.### _What will happen on the day of the urodynamic testing?_ As mentioned above, urodynamic investigation consists of a flow rate test and a filling cystometry test.

Note the continuity between the rough and the smooth endoplasmic reticulum (arrows).Newstead, unpublished electron micrograph_ ) Plate 202 An area of smooth endoplasmic reticulum hypertrophy from the liver of a hamster that had received phenobarbitone.×54 000 ( _Dr J.D.1_; _Plate 202_), they are morphologically and functionally distinct ( _see_ reviews by Porter, 1961, and Fawcett, 1981). The smooth endoplasmic reticulum usually presents as a meshwork of branching tubules and/or vesicles. Relatively thick sections are needed to demonstrate the tubular pattern. Unlike the rough endoplasmic reticulum, the smooth endoplasmic reticulum rarely forms cisternae. It is worth noting that this is a delicate system which, at least in some cell types (e.g. steroid-producing cells), is easily affected by preparative procedures. Glutaraldehyde fixation is, as a rule, more likely to preserve the tubular formations while in osmium-fixed material the tubules tend to break up into vesicles. The smooth endoplasmic reticulum in hepatocytes, however, is not so sensitive to preparative procedures. In the tubular epithelial cells of rat kidney fixed by glutaraldehyde perfusion many focal aggregates of branching smooth-membrane-bound tubules are found ( _Plate 183, Fig. 2_), but kidney tissue preserved by immersion in fixatives usually shows scant smooth endoplasmic reticulum (Newstead, personal communication). Plate 183 _Fig. 1._ Cow hepatocyte, showing cytoplasmic zones occupied by rough (R) and smooth (S) endoplasmic reticulum. Glycogen rosettes (G) occur almost exclusively in association with the smooth endoplasmic reticulum. Continuity between the rough and smooth endoplasmic reticulum can just be discerned (arrow) at this low magnification. ×36 000 _Fig. 2._ Numerous smooth-membrane-bound ramifying tubules are seen in this tubular epithelial cell of a rat kidney perfused with glutaraldehyde. ×54 000 ( _Dr J.D. Newstead, unpublished electron micrograph_ ) Plate 202 An area of smooth endoplasmic reticulum hypertrophy from the liver of a hamster that had received phenobarbitone. Note the continuity between the rough and the smooth endoplasmic reticulum (arrows).In the liver the smooth endoplasmic reticulum occupies focal areas of cytoplasm, usually in company with glycogen rosettes ( _Plate 183, Fig.1_).If the glycogen is abundant then the smooth endoplasmic reticulum is difficult to visualize.The smooth endoplasmic reticulum becomes somewhat more prominent and its association with glycogen more evident in animals fasted for a day or two.

The conjunctiva helps protect the eye by keeping small foreign objects and infection-causing microorganisms out and by contributing to the maintenance of the tear film.Often a tiny, yellowish spot develops at the center of the swollen area, usually at the edge of the eyelid. The stye tends to rupture after 2 to 4 days, releasing a small amount of pus and ending the problem. With an internal stye, pain and other symptoms are usually more severe than with an external stye. Pain, redness, and swelling tend to occur underneath the eyelid. Occasionally, inflammation is severe and may be accompanied by fever or chills. Treatment Although antibiotics are sometimes used to treat styes, they usually do not really help much. The best treatment is to apply hot compresses for 5 to 10 minutes 2 to 3 times a day. The warmth helps the stye come to a head, rupture, and drain. Because an internal stye rarely ruptures by itself, a doctor may have to open it to drain the pus. Internal styes tend to recur. Trichiasis Trichiasis is misalignment of eyelashes, which rub against the eyeball, in a person who does not have entropion. The cause of trichiasis is usually unknown. The eye becomes red and irritated, has a foreign body sensation, and develops tearing and sensitivity and sometimes pain when exposed to light. If the condition persists, scarring can occur. A doctor bases the diagnosis on the symptoms and an examination. Trichiasis differs from entropion in that the eyelid position is normal. An eye doctor can remove the eyelashes with forceps. If eyelashes grow back, other methods can be used to remove them, such as electrolysis or cryosurgery (use of extreme cold to destroy the hair follicle). CHAPTER 223 Conjunctival and Scleral Disorders The conjunctiva is the thin, transparent lining that covers the back of the eyelid and loops back to cover the sclera (the white of the eye), right up to the edge of the cornea (see Structures That Protect the Eye). The conjunctiva helps protect the eye by keeping small foreign objects and infection-causing microorganisms out and by contributing to the maintenance of the tear film.There are many causes of inflammation, including infections by bacteria (including chlamydia), viruses, or fungi; allergic reactions; chemicals or foreign bodies in the eye; and overexposure to sunlight.Conjunctivitis tends to be relatively short-lived, although it sometimes lasts for months or years.

Pregnancies at increased risk of fetal abnormality need to beidentified: * previous child with congenital anomaly * family history of an inherited disorder, consanguineous * parents known carriers of an autosomal recessive disorder * parents from ethnic group with specific risk, e.g.* Optimize management of pre–existing maternal medical conditions such as diabetes and hypertension.## Neonatal Networks The different levels of care required by newborn infants are shown in Fig 3.4. As it is not possible or efficient to provide all levels of care in every hospital, neonatal or perinatal (including maternity) networks working across hospital boundaries have been developed. Their aim is to improve care for mother and baby by facilitating collaborative working, unified protocols and minimizing geographic variations in care. **Fig. 3.4** Levels of neonatal care. # 4 Prepregnancy care, prenatal screening and fetal medicine * * * # Prepregnancy care To optimize the chances of a healthy baby, mothers are advised: * Attend clinic for prenatal care. * Avoid or cease maternal smoking, alcohol, drug misuse,medication (unless essential) prior to conception. * Toxoplasmosis exposure – avoid eating undercooked meat (and wear gloves when handling cat litter). * _Listeria_ infection – avoid unpasteurized dairy products and soft ripened cheeses, e.g. brie. * Folic acid supplements preconceptually to 12 weeks – to reduce risk of neural tube defects and cardiac malformations in countries without folic acid fortification of foods, as in the UK and Europe. Higher dose if previous baby with neural tube defect. * Avoid eating shark, swordfish, marlin and limit tuna as high levels of mercury. Limit oily fish as contain pollutants. * Optimize management of pre–existing maternal medical conditions such as diabetes and hypertension. Pregnancies at increased risk of fetal abnormality need to beidentified: * previous child with congenital anomaly * family history of an inherited disorder, consanguineous * parents known carriers of an autosomal recessive disorder * parents from ethnic group with specific risk, e.g.* * * * * * # Prenatal screening ## Maternal blood The routine screening tests vary geographically, but include: * maternal blood group, antibodies against rhesus (D) and other red cell incompatibilities * hepatitis B (surface and e-antigen status) * syphilis serology, * rubella, * HIV infection * screening for chromosomal anomalies (see below) * hemoglobin electrophoresis.

Upon initial diagnosis, parents are left with a near infinite amount of resources to sift through in order to determine the best course of action for treating their child.This allows for discussion of the child's presentation throughout the evaluation when observations are still fresh in everyone's minds and when parents' presenting concerns can be readily addressed.Beck Anxiety Inventory (BAI; Beck & Steer, 1993), the Child Behavior Checklist (CBCL; Achenbach & Rescorla, 2001), and the Behavior Assessment Scale for Children, Second Edition (BASC-2; Reynolds & Kamphaus, 2003). ; 13. ASD and psychosis; limited socialization, unusual behaviors, odd language. Psychosis is more likely, however, as the onset was in early adulthood, although there may have been some prodromal symptoms in childhood due to limited social relations; individual has nonsensical and tangential speech, again beginning in adulthood, as opposed to early childhood as seen in ASD. ; 14. False Chapter 8 Case Conceptualization and Integrated Report Writing The Parent Conference The presentation of results of the comprehensive diagnostic evaluation is two-fold: it begins with a parent/caregiver conference that allows for dissemination and discussion of findings, and it ends with a written report. Many clinicians choose to withhold having a parent conference until the report is written. However, it is our experience, particularly when conducting the initial diagnostic evaluation where parents are understandably extremely anxious about what their child's diagnosis might be, that providing immediate feedback is not only beneficial but also necessary. This allows for discussion of the child's presentation throughout the evaluation when observations are still fresh in everyone's minds and when parents' presenting concerns can be readily addressed. Upon initial diagnosis, parents are left with a near infinite amount of resources to sift through in order to determine the best course of action for treating their child.The parent conference also allows for discussions about evidence-based practices and how best to seek out, evaluate, and make informed decisions about the treatment and intervention approaches that, although readily available, may not be the most appropriate given the specific needs of their child.

• Do not wear contact lenses (may increase risk of keratitis).• Do not eat 1 hr before or 2 hrs after dose.• Immediately report eye problems (pain, swelling, blurred vision, vision changes) or skin blistering/redness.• Minimize exposure to sunlight.• Report any yellowing of skin or eyes, abdominal pain, bruising, black/tarry stools, dark urine, decreased urine output.Interstitial lung disease (ILD), including pulmonary infiltration, pneumonitis, ARDS, allergic alveolitis, reported in 2% of pts. Hepatotoxicity reported in 10% of pts. Keratitis such as eye inflammation, lacrimation, light sensitivity, blurred vision, red eye occur in 1% of pts. ##### NURSING CONSIDERATIONS BASELINE ASSESSMENT Obtain baseline CBC, BMP, visual acuity. Obtain negative pregnancy test before initiating therapy. Question current breastfeeding status. Screen for history/co-morbidities, contact lens use. Receive full medication history including vitamins, herbal products. Assess skin for lesions, ulcers, open wounds. INTERVENTION/EVALUATION Monitor renal/hepatic function tests, urine output. Encourage PO intake. Assess for hydration status. Offer antidiarrheal medication for loose stool. Report oliguria, dark or concentrated urine. Immediately report skin lesions, vision changes, dry eye, severe diarrhea. Obtain chest X-ray if ILD suspected. PATIENT/FAMILY TEACHING • Most pts experience diarrhea and severe cases may lead to dehydration or kidney failure; maintain adequate hydration. • Avoid pregnancy; contraception should be used during treatment and up to 2 wks after discontinuation. • Report any yellowing of skin or eyes, abdominal pain, bruising, black/tarry stools, dark urine, decreased urine output. • Minimize exposure to sunlight. • Immediately report eye problems (pain, swelling, blurred vision, vision changes) or skin blistering/redness. • Do not eat 1 hr before or 2 hrs after dose. • Do not wear contact lenses (may increase risk of keratitis).**Do not confuse albiglutide with exenatide, dulaglutide, or liraglutide.** ##### ♦ CLASSIFICATION **PHARMACOTHERAPEUTIC:** Glucagon-like peptide-1 (GLP-1) receptor agonist.**CLINICAL:** Antidiabetic.##### USES Adjunct to diet and exercise to improve glycemic controls in pts with type 2 diabetes mellitus.

Fig.6.14).The cervical spine has the most canal width compared to the vertebral body width (Fig.The cervical spine and L5 have the greatest transverse diameter with growth, possibly related to the need for both volume and motion in these areas of the spine.The growth of the canal area for all vertebral bodies and ages is approximately 6.2 mm2/year.Besides the canal becoming wider with growth, the pedicles also increase their transverse width with age. The increase in pedicle size occurs lateral to the spinal canal through remodeling (Fig. 6.12). The implication of this outer pedicle wall remodeling is that this allows the medial pedicle wall to become thicker and more resilient to inadvertent medial pedicle wall implant penetration and also provides for increased canal transverse diameter as the pedicles enlarge. Human and animal studies have shown that unilateral surgical closure of the neurocentral synchondrosis can cause asymmetric growth and scoliosis [25]. However, these procedures do not cause significant spinal canal stenosis, likely due to preserved posterior element appositional growth. Fig. 6.12 Specimen showing relatively large canal dimensions compared to the width of the vertebral body. The neurocentral synchondrosis (NCS) is still open. Most of the increase in canal area seen into adolescence occurs through increase in the lateral inter-pedicular distance and pedicle remodeling ### 6.4.2 Canal Width and Area For the 32 specimens, we noted that the lateral canal width increased with age and also varied by the spine level (Fig. 6.13). We have shown that canal area increases proportional to the lateral canal width but is independent of the AP width (area vs. lateral width r 2 = 0.68–0.83 but r 2 is only 0.22 for AP canal width). By age 5 years, the canal was 71 % of its final size, and by age 10 years, 95 %. After age 5 years, the increase in canal area is almost completely through an increase in lateral canal width, not AP width. The growth of the canal area for all vertebral bodies and ages is approximately 6.2 mm2/year. The cervical spine and L5 have the greatest transverse diameter with growth, possibly related to the need for both volume and motion in these areas of the spine. The cervical spine has the most canal width compared to the vertebral body width (Fig. 6.14). Fig.One-way analysis of vertebral canal width.The spread for each vertebral level indicates increasing canal width with age from 1 to 18 years.C1 and C2 data are not included.Canal width is greatest in the cervical and lower lumbar spine.Younger subjects (aged 1 and 3 years) are at the bottom and older subjects (aged 17–18 years) are at the top Fig.

This effect is especially felt on the energy channel supplied by the liver—that is, the external genitalia, the breasts, the centers of the eyes, the spleen, and the crown of the head.In the theory of TCM, when emotions build up beyond the liver's capacity to contain them, they cause the body and mind to "shake."This stops the production of quantities of stomach acid large enough to aggravate or cause ulcers. The somatostatin that the body releases in response to the formula also puts a brake on excessive acid production. Higher levels of motilin ensure that the digested food passes out of the stomach quickly, further ensuring that the stomach produces a minimal amount of acid. In addition to helping stop production of excess acid in the stomach, this formula promotes the smooth transit of digested food through the intestine. Astragalus may also help to maintain healthy bacteria in the intestine, but this was accomplished in an animal model—not in humans. The traditional use of this formula in treating vitiligo has not been investigated, but it is known that the formula causes the immune systems of animals to produce more of an immune factor known as interleukin-2 (IL-2), which is sometimes used in the medical treatment of vitiligo. Traditional Chinese medicine (TCM) recommends this formula as gentle and effective, especially appropriate for children's use. There are no reports of toxicity associated with this formula. AUGMENTED RAMBLING POWDER This widely used formula from traditional Chinese medicine (TCM) contains white atractylodis, bupleurum, dong quai, gardenia, hoelen, licorice, moutan, and white peony. _Rambling_ refers to a free spirit, and an _augmented_ powder was especially effective. This combination of herbs was devised by ancient Chinese herbalists who believed that the combination could free the user from the effects of trapped vital energies of emotion stored in the liver. In the theory of TCM, when emotions build up beyond the liver's capacity to contain them, they cause the body and mind to "shake." This effect is especially felt on the energy channel supplied by the liver—that is, the external genitalia, the breasts, the centers of the eyes, the spleen, and the crown of the head.Modern research has found that Augmented Rambling Powder lowers estrogen levels.This makes it effective against disorders affected by estrogen, such as breast cancer, and other disorders of the breast and female reproductive tract.As a complementary treatment for cancer, the formula is used to increase the effectiveness of estrogen-binding drugs, such as tamoxifen (Nolvadex).

FIGURE 39.12A-B(A) Exostosis of humerus, (B) X-ray—exostosis humerus.• Retarded growth and dwarfism are seen in diaphyseal aclasis.39.12A).#### Clinical presentation • A circumscribed hard swelling near a joint (Fig.• Malignant change is more common in multiple familial exostoses (15%).• May affect several bones at a time.• Multiple in diaphyseal aclasis (multiple exostoses).• Chondromata of long bones occur in dyschondroplasia (multiple chondromatosis or Ollier disease). • Malignant change is not uncommon, usually of the major bones. **_DD:_** Chondrosarcoma, fibrous dysplasia, chondroblastoma, giant cell tumour. #### Clinical presentation • **_Ecchondroma_** : hard swelling on the affected bone. • **_Enchondroma_** : expansion of affected bone (Fig. 39.10). FIGURE 39.10Enchondroma middle finger. #### Relevant investigations **X-rays are diagnostic. ** • Centrally or eccentrically placed medullary osteolytic tumour. • Stippled or punctate matrix calcification is seen throughout the lesion in 50% of cases. • **_Ecchondroma_** : bony outgrowth from the bone (Fig. 39.11). • **_Enchondroma_** : lesion inside the bone expanding the cortex. FIGURE 39.11X-ray—chondroma of humerus. #### Treatment • **_No treatment_** is necessary, in general. • **_Excision_** may be done for unsightly swellings. • **_Follow up is_** required for patients with Ollier disease for fear of malignancy. ### Osteochondroma #### Incidence and aetiology • The commonest benign tumour of bone. • Arises from the growing epiphyseal cartilage plate, but gets left behind at the centre as the bone grows. • Grows outwards like a mushroom, and it is capped by a cartilage. • Usually single. • Multiple in diaphyseal aclasis (multiple exostoses). • May affect several bones at a time. • Malignant change is more common in multiple familial exostoses (15%). #### Clinical presentation • A circumscribed hard swelling near a joint (Fig. 39.12A). • Retarded growth and dwarfism are seen in diaphyseal aclasis. FIGURE 39.12A-B(A) Exostosis of humerus, (B) X-ray—exostosis humerus.39.12B).The capping cartilage is not seen.#### Treatment **_Excision_** when required.Surgical margin should include the entire cartilaginous cap to prevent malignant change.### Giant cell tumour (osteoclastoma) #### Incidence and aetiology • Potentially malignant tumour.• Behaves like a malignant tumour by recurrence and metastasizing through blood.

The role of stress is difficult to gauge.I had remarried in 2003, but the second marriage had also had its difficulties.I had been through a divorce, counseling for a number of years, and a longish relationship that ended stressfully.I had been under a lot of stress in the fifteen years prior to my diagnosis.I wonder about the role that stress plays in bringing on illness.I have never been religious, but I am certainly an Ashkenazi Jew. I have one biological son, and three biological grandchildren, as well as a brother, sister, and many cousins. I solicited as much information as I could from my sister, brother, and uncle. There had not been any pancreatic cancer in my immediate family that anyone knew of. However, both of my parents had had other types of cancer. My mother died with chronic leukemia. My father had been successfully treated for colon cancer. I had never thought about this before. When I did, it made sense that eventually I might also be diagnosed with some form of cancer. I had smoked when I was a teenager. Not heavily, and I had stopped in my late twenties, but there it was, I had smoked. Overall, I had not led an unhealthy life, but I guess I could have tried harder to reduce my risks for cancer. I worried about my biological son and my grandchildren. I told him about all the things that might make a difference. Not smoking was the most important. Being aware that unexplained symptoms, like those I had noticed in the year before my diagnosis, might be a clue. Letting the doctor know the family history. Much later, I decided to undergo genetic testing for the most common type of mutant genes, BRCA 1 and 2. The results were negative. I wonder about the role that stress plays in bringing on illness. I had been under a lot of stress in the fifteen years prior to my diagnosis. I had been through a divorce, counseling for a number of years, and a longish relationship that ended stressfully. I had remarried in 2003, but the second marriage had also had its difficulties. The role of stress is difficult to gauge.I have read that there is no clear evidence that stress can lead directly to cancer.This makes sense to me, intuitively.After all, many people who live under tremendous strain do not develop cancer.Still, I wonder.However, all I could do as I embarked on cancer therapy was deal with the present.None of this other stuff really mattered in the short term.

As cyclin D–CDK4 complexes accumulate in mid-G1, p27KIP1 and p21CIP1 are redistributed from cyclin E–CDK2 to cyclin D–CDK4/6 complexes, leading to the activation of cyclin E–CDK2, which completes the phosphorylation of RB, as described above.Cdk4 kinase activity is induced by binding to D-type cyclins, its phosphorylation by the cyclin-dependent kinase (CAK) and p27Kip1 that serves as an assembly factor. The active cyclin D–Cdk4/6 holoenzyme initiates the phosphorylation of Rb. Binding of p27Kip1 to increased levels of cyclin D–Cdk4/6 complexes relieve the inhibition of cyclin E–Cdk2 complexes that complete the phosphorylation of Rb and phosphorylate p27Kip1, which is then degraded by the proteasome machinery. Phosphorylation of Rb releases E2F1, 2, and 3a that transactivate the expression of E2F-responsive genes, including cyclin E, cyclin A, and E2F1 and genes required for the initiation of DNA replication (S phase). These holoenzymes are themselves regulated by inhibitory proteins called cyclin-dependent kinase inhibitory proteins (CKIs) that comprise two families: the INK4 family and the CIP/KIP family. INK4 proteins bind to and specifically negatively regulate the activity of the cyclin D-dependent kinases CDK4 and CDK6. The family consists of four members – p16INK4a, p15INK4b, p18INK4c, and p19INK4d – two of which, p16INK4a and p18INK4c, act as tumor suppressors. The CIP/KIP family has three members: p21CIP1/WAF1, a p53-responsive gene (see below), and p27KIP1 and p57KIP2, two tumor suppressors. All three members of this family are negative regulators of cyclin E– and cyclin A–CDK2 and of cyclin B–CDK1, while p27KIP1 and p21CIP1 also act as positive regulators of cyclin D–CDK4/6 by stimulating complex assembly. As cyclin D–CDK4 complexes accumulate in mid-G1, p27KIP1 and p21CIP1 are redistributed from cyclin E–CDK2 to cyclin D–CDK4/6 complexes, leading to the activation of cyclin E–CDK2, which completes the phosphorylation of RB, as described above.7.6).Figure 7.6 The cyclin-dependent kinase inhibitory (CKI) proteins from the Ink4 and Cip/Kip protein families collaborate to enforce cell cycle arrest.In mid-G1 and in response to antiproliferative signals, Ink4 proteins are induced.Ink4 proteins bind to Cdk4/6 and free cyclin D that is rapidly degraded.p27KIP1 is reassorted to cyclin E–Cdk2 complexes to inhibit their kinase activity.

Folate acid deficiency Red cell indices reveal an MCV greater than 100 f/L, folate levels less than 4 ng/mL, and erythrocyte folate activity less than 20 ng/mL.What red cell indices, laboratory results, and characteristics on a peripheral blood smear indicate this anemia**?**What is the most common cause of macrocytic anemia in pregnancy?If anemia is severe, IV iron may be used.With anticoagulation antepartum continuing for 6 weeks postpartum ##### **Anemias and Hemoglobinopathies** **What is physiologic anemia of pregnancy**? During the course of pregnancy, there is an expansion in plasma volume greater than that of the RBC mass. This reflects in a decrease in hematocrit during pregnancy; however, it is not a true anemia. **How is true anemia in pregnancy defined**? It is generally defined as an Hct less than 30% or a hemoglobin less than 10 g/dL **What are the effects of maternal anemia on pregnancy**? Preterm birth Fetal growth restriction **What are the two most common causes of anemia during pregnancy**? 1. **Iron deficiency anemia** 2. Anemia from acute blood loss **What red cell indices, laboratory results, and characteristics on a peripheral blood smear indicate an iron deficiency anemia**? Mean cell volume (MCV) less than 80 f/L. Mean corpuscular hemoglobin concentration (MCHC) less than 30% Serum iron is decreased (< 50 mg/dL). Total iron-binding capacity (TIBC) is increased. Serum ferritin is decreased (a level < 15 ug/L is confirmatory of iron deficiency anemia). Blood smear findings include small, pale erythrocytes (microcytic and hypochromic). **What is the treatment of iron deficiency anemia**? Treatment is iron therapy consisting of ferrous sulfate 325 mg bid. If anemia is severe, IV iron may be used. **What is the most common cause of macrocytic anemia in pregnancy? What red cell indices, laboratory results, and characteristics on a peripheral blood smear indicate this anemia**? Folate acid deficiency Red cell indices reveal an MCV greater than 100 f/L, folate levels less than 4 ng/mL, and erythrocyte folate activity less than 20 ng/mL.**What is the recommended folate level in pregnant women and what is the treatment for folate deficiency anemia**?A recommended level of folate during pregnancy is 400 ug/d and treatment is 1 mg of folic acid PO once daily.**What are examples of hereditary hemolytic anemias**?

( _Reproduced, with permission, from the University of Texas Health Science Center Houston Medical School_.)Be able to describe the anatomy of the four cardiac valves ### DEFINITIONS **MURMURS:** Soft or harsh abnormal heart sounds, often caused by turbulent blood flow, and described in relation to the phase of the cardiac cycle in which they are heard **ATRIAL FIBRILLATION:** Rapid, uncoordinated muscular twitching of the atrial wall **TACHYCARDIA:** A heart rate of at least 100 beats/min ### DISCUSSION #### _Cardiac Conduction System_ The **conduction system of the heart** is composed of specially modified cardiac muscle cells. It initiates and rapidly conducts cardiac impulses throughout the heart to produce cardiac muscle contraction. The system ensures the simultaneous contraction of both atria, followed by a similar coordinated contraction of both ventricles. The **SA node,** composed of these modified cardiac muscle cells, lies within the **atrial wall on the right side** of its junction with the **superior vena cava** (SVC). This can be located at the superior end of the external landmark, the **sulcus terminalis. ** The SA node spontaneously depolarizes to initiate the cardiac conduction impulse and thus is often referred to as the **heart's pacemaker. ** The impulse generated by the SA node spreads through the atrial wall to converge on the **AV node** and produces simultaneous atrial contraction. **Anterior, middle, and posterior internodal pathways** of very rapid conduction are described (Figure 13-1). **Figure 13-1. ** Cardiac conduction system: 1 = sinoatrial node, 2 = anterior internodal pathway, 3 = middle internodal pathway (Wenckebach bundle), 4 = posterior internodal pathway, 5 = atrioventricular node, 6 = atrioventricular bundle of His, 7 = moderator band, 8 = right bundle branch, 9 = terminal conducting fibers of Purkinje, 10 = left bundle branch. ( _Reproduced, with permission, from the University of Texas Health Science Center Houston Medical School_.)** The **AV bundle (of His)** arises from this node and lies within the **membranous portion of the interventricular septum.** It courses toward the apex of the heart, and at the upper portion of the muscular portion of this septum, it divides into **right and left bundle branches.** The bundle branches lie on their respective sides of the septum just beneath the endocardium.

When administering the calcium channel blocker, it is important to prevent hypotension.It may act to limit vasospasm but also likely prevents ischemia-induced cerebral injury as well.The mechanism of action is not clear.Efforts to prevent vasospasm include administration of nimodipine 60 mg orally every 4 hours.CT angiography may be used as an alternative for localization but does not provide the opportunity for intervention. Lumbar puncture will also evaluate for meningitis and encephalitis, which are also possible in this case. Appropriate culture and polymerase chain reaction diagnostic tests should be included in the diagnostic evaluation. **113. The answer is A**. ( _Chap. 35_ ) This patient presents with an SAH caused by a ruptured anterior cerebral artery and has evidence of increased intracranial pressure with midline shift on a CT scan of the head. He has undergone aneurysm repair, and the care now should focus on the medical management of SAH. Some of the principles of the medical management of SAH include treatment of intracranial hypertension, management of blood pressure, prevention of vasospasm, and prevention of rebleeding. A patient who is unresponsive with evidence of intracranial hypertension should immediately undergo emergent ventriculostomy, which allows measurement of intracranial pressure (ICP) and can treat elevated ICP. Other strategies for treatment of elevated ICP include hyperventilation, mannitol, sedation, and hypernatremia. If a patient survives the initial aneurysmal bleed and the aneurysm is treated, the leading cause of morbidity and mortality after SAH is development of cerebral vasospasm. Vasospasms occur in about 30% of patients after SAH, typically between day 4 and 14, peaking at day 7. Efforts to prevent vasospasm include administration of nimodipine 60 mg orally every 4 hours. The mechanism of action is not clear. It may act to limit vasospasm but also likely prevents ischemia-induced cerebral injury as well. When administering the calcium channel blocker, it is important to prevent hypotension.In addition, most patients also receive volume expansion.This therapy has commonly been known as "triple H" therapy for hypertension, hypervolemia, and hemodilution.Glucocorticoids are not used in the treatment of SAH.There is no evidence that they reduce cerebral edema or have a neuroprotective effect.**114.The answer is D**.( _Chap.

## Applications Piezocision can be used in a generalized, localized, or sequential manner.Courtesy of Dr Eleni Kanasi.(b) Improvement of the labiomental fold after grafting.Courtesy of Dr Eleni Kanasi.**Figure 5.11** (a) Deep labiomental fold.By grafting the mandibular anterior region, a deep labiomental fold can be corrected and the profile can be enhanced (Figure 5.11).When the movement was studied at 10 weeks the canine distalization was two times more on the Piezocision side than the control side, and the canine rotation was similar on both sides. The study concluded that Piezocision is a minimally invasive alternative to corticotomies, significantly shortening the orthodontic treatment time. ## Grafting: increasing the scope of tooth movement and improvement of the periodontium The orthodontic treatment of teeth beyond the limits of the labial or lingual alveolar plate can lead to dehiscence formation (McComb, 1994; Wennstrom, 1996; Joss-Vassalli _et al._ , 2010) and predispose the patient to recession (Zachrisson, 1996; Melsen and Allais, 2005). Bone grafting increases alveolar volume, thereby increasing the scope of orthodontic tooth movement. Crowding cases can be treated without extraction by the expansion of the alveolus with bone augmentation (Ferguson _et al._ , 2006). When Piezocision is used, the graft can be placed without the need of a flap elevation. The area where bone graft is needed can be tunneled, the graft material can be placed with a syringe and sutured, and the alveolus of that area can be expanded. Another positive effect of bone augmentation during alveolar decortication is that it improves the patient's profile. By grafting the mandibular anterior region, a deep labiomental fold can be corrected and the profile can be enhanced (Figure 5.11). **Figure 5.11** (a) Deep labiomental fold. Courtesy of Dr Eleni Kanasi. (b) Improvement of the labiomental fold after grafting. Courtesy of Dr Eleni Kanasi. ## Applications Piezocision can be used in a generalized, localized, or sequential manner.Certain cases can benefit from a sequential approach, where the RAP effect is induced at certain areas of the arch at a specific time.And once the desired tooth movement is achieved at these specific locations, the other areas are decorticated to induce the RAP.

In the Bristol cohort [36] the association was with Herberden's nodes.#### OA in Other Joints Studies have suggested that risk of knee OA might be related to the presence of hand OA [36–38].NHANES III did not find either education level or income to be associated with risk of RKOA [22].With the aging of the US population, the burden of OA is expected to increase throughout the coming years. ## 29.7 Risk Factors OA is a complex disorder with identifiable risk factors that include biomechanical, metabolic or inflammatory processes; congenital or developmental deformities of the joint; and genetic factors. As noted above, age, sex and race are prominent risk factors for OA. Biomechanical contributors include repetitive or isolated joint trauma related to certain occupations or physical activities that involve repeated joint stress. These can predispose an individual to early OA. Obesity may contribute from a biomechanical perspective, or from a systemic perspective related to a subacute metabolic syndrome. Certain metabolic disorders (e.g., hemochromatosis, ochronosis) are also associated with OA. High bone mineral density (BMD) has been shown to be associated with hip or knee OA. Estrogen deficiency may also be a risk factor for hip or knee OA. Inflammatory joint diseases, such as rheumatoid arthritis, may result in cartilage degradation and biomechanical factors that lead to secondary OA. Candidate gene studies and genome-wide scans have identified a number of potential genetic markers of OA. ### 29.7.1 Non-Modifiable Risk Factors #### Demographic Risk Factors Prior studies have reported an increase in the risk of radiographic knee OA (RKOA) with advancing age, as well as an increased risk of RKOA in women compared to men. Data from the NHANES III and the Johnston County OA Study have reported an increased risk of RKOA among African-Americans compared to whites, particularly among African-American women [21, 22]. NHANES III did not find either education level or income to be associated with risk of RKOA [22]. #### OA in Other Joints Studies have suggested that risk of knee OA might be related to the presence of hand OA [36–38]. In the Bristol cohort [36] the association was with Herberden's nodes.In the Croatian study [37], the association was greater in women compared to men, and was greater for OA in the distal interphalangeal joints compared to the proximal interphalangeal joints.That study also found an increased risk of RKOA with carpometacarpal involvement in men.

These masses, which can range in size from that of lead shot to large marbles, are known as gallstones.This is more likely to occur if cholesterol is present in excess in the bloodstream, a result, in part, of the rich Western diet.In some people the composition of this rich mixture in the gallbladder becomes unbalanced, so that some of the substances come out of solution and form solid masses.This syndrome requires urgent medical management * Notifiable diseases: notification of a number of specified infectious diseases is required of doctors in the UK as a statutory duty under the Public Health (Infectious Diseases) 1988 Act and the Public Health (Control of Diseases) 1988 Act, and, more recently, the Health Protection (Notification) Regulations 2010. The UK Health Protection Agency (HPA) Centre for Infections collates details of each case of each disease that has been notified. This allows analyses of local and national trends. This is one example of a situation in which there is a legal requirement for a doctor to breach patient confidentiality. Diseases that are notifiable include: acute encephalitis, acute infectious hepatitis, acute poliomyelitis, anthrax, cholera, diphtheria, enteric fevers (typhoid and paratyphoid), food poisoning, infectious bloody diarrhea, leprosy, malaria, measles, meningitis (bacterial and viral forms), meningococcal septicemia (without meningitis), mumps, plague, rabies, rubella, scarlet fever, severe acute respiratory syndrome (SARS), smallpox, tetanus, tuberculosis, typhus, viral hemorrhagic fever, whooping cough, yellow fever. Important diseases of the gallbladder Gallstones As described in Section 3.1a, the gallbladder is a storage vessel for bile, which is manufactured in the liver. Bile consists of some waste products, including bilirubin, and also chemicals called bile salts, which are essential for the digestion of fats. In addition, bile contains the fatty substance cholesterol. In some people the composition of this rich mixture in the gallbladder becomes unbalanced, so that some of the substances come out of solution and form solid masses. This is more likely to occur if cholesterol is present in excess in the bloodstream, a result, in part, of the rich Western diet. These masses, which can range in size from that of lead shot to large marbles, are known as gallstones.It is estimated that up to one-fifth of adults in the West have gallstones and less than one in five of these will develop any problem from them.They are twice as common a finding in women as in men, and seem particularly common in overweight Western women of late childbearing age.

TENS units operate by producing small-intensity currents.Cutaneous stimulation includes such methods as massage, pressure, heat, cold and transcutaneous electrical nerve stimulation (TENS).Equipment that has adjustable features, such as reclining chairs, height-adjustable toilet seats and alternating pressure mattresses, may assist in achieving temporary pain relief.People who experience pain from cancer often protect themselves from pain by lying down or staying in certain positions for long periods of time. Gentle exercise plays an important role in reducing pain related to immobility through maximizing the use of stiff joints and developing muscle strength. Further exercise can prevent painful contractures through non-use of painful limbs. Exercise may range from a regular walking programme through to sitting out of bed in a chair or simple movements while lying in bed. Family members can encourage participation in any functional activities that also incorporate movement. Generally, some level of exercise is possible for all people with cancer throughout the varying stages of their disease but its use needs to be monitored so as not to contribute to breakthrough pain, and altered to suit individual needs. Exercise is also effective in the management of pain due to specific nerve or tissue damage. For example, patients with head and neck cancer who have shoulder disability and pain due to spinal accessory nerve damage have been shown to benefit from progressive resistive exercise (McNeely et al 2008). Finally, exercise has been found to improve mood and in turn this may make it easier for people to cope with chronic pain (Duijts et al 2010). Pain may be exacerbated by pressure in the region of the tumour or from being in one position for prolonged periods of time. Attention to positioning, correct body alignment, and use of pillows and supports may relive pressure-related pain. Equipment that has adjustable features, such as reclining chairs, height-adjustable toilet seats and alternating pressure mattresses, may assist in achieving temporary pain relief. Cutaneous stimulation includes such methods as massage, pressure, heat, cold and transcutaneous electrical nerve stimulation (TENS). TENS units operate by producing small-intensity currents.They appear to produce stimulation that 'overrides' or 'negates' the pain stimuli.A systematic review of the efficacy of TENS in chronic pain found that it conferred some pain relief, but there was uncertainty as to what method of use was most efficacious (Nnoaham & Kumbang 2008).The stimulation may be applied to the painful area if the skin is not compromised.

Price framed dental disease in a way that, while not counterintuitive to me, lay outside the scope of my learning.The words on the pages rang out with startling clarity, echoing my experiences with my own patients.From the very first lines of _Nutrition and Physical Degeneration_ , I was transfixed.As in _Weston A. Price, DDS_. It's rare to come across a book about dentistry on _any_ shelf, let alone one in a vacation setting. (I don't have the exact numbers, but I don't think most people pack dentistry books when they go on holiday. Not even dentists.) Even though I was in Turkey to get away from dentistry, I couldn't resist pulling it off the shelf. The book was called _Nutrition and Physical Degeneration: A Comparison of Primitive and Modern Diets and Their Effects_. It was a reprint of a book originally published in 1939. I had never heard of Price, but it turned out he was a dental professor, author, and clinician with a practice in Cleveland. In the beginning, Price talked about his experiences as a dentist in the 1920s and '30s. He described how, over the years, more and more people with chronic disease came to his clinic and how they all seemed to suffer from oral disease, too. He sensed a relationship there. Over a 10- to 15-year period, more and more of the children who came to him had deformed dental arches and tooth decay. And these children suffered from an alarming number of chronic diseases, like tuberculosis. Price had a hunch that the rise in TB was somehow tied to the rise in oral disease. He suspected that there was a direct link between how bad a child's teeth were and how poor their overall health was. From the very first lines of _Nutrition and Physical Degeneration_ , I was transfixed. The words on the pages rang out with startling clarity, echoing my experiences with my own patients. Price framed dental disease in a way that, while not counterintuitive to me, lay outside the scope of my learning.He wrote, "I am entirely serious when I suggest that it is a very myopic medical science which works backward from the morgue rather than forward from the cradle."Price had an uncanny ability to evaluate a person's overall health just by looking at their face and jaw.He didn't just see teeth when he looked into a mouth.He saw the structures forming the human face, airways, and digestive system.

This scenario of a loss of consciousness followed by a lucid interval and a second loss of consciousness is very typical for epidural hematoma.The ipsilateral pupil was affected by compression of the oculomotor nerve (CN III) by the temporal lobe of the brain.Over time, the hematoma formed, putting pressure on the underlying brain tissue.He lost consciousness briefly but woke up after about 45 s and had no neurological deficits. He was taken to the emergency room and seemed to be in good condition. Four hours later, while being observed, he complained of an increasing headache and had a seizure. On examination, the patient's right pupil appeared dilated and reacted sluggishly to light. The emergency physician is concerned about increased intracranial pressure. What is the most likely diagnosis? What is the anatomical explanation for this condition? * * * ### ANSWER TO CASE 44: #### Epidural Hematoma _Summary:_ A 15-year-old boy was hit by a baseball to the right temple area. He lost consciousness briefly and had a lucid interval. Four hours later, he developed an increasing headache, a dilated and sluggish right pupil, and had a seizure, consistent with increased intracranial pressure. • **Most likely diagnosis:** Epidural hematoma resulting in increased intracranial pressure • **Anatomical explanation for this condition:** Disruption of a branch of the middle meningeal artery, which causes a growing hematoma between the dura and cranium and puts pressure on the underlying brain ### CLINICAL CORRELATION This 15-year-old baseball player underwent significant blunt trauma to the right temple area by a baseball. He briefly lost consciousness, likely due to the concussion of the baseball. After waking up, he had no neurological deficits; however, after 4 h, there were signs of increased intracranial pressure. The most likely explanation is disruption of the middle meningeal artery, which underlies the temporal bone. Over time, the hematoma formed, putting pressure on the underlying brain tissue. The ipsilateral pupil was affected by compression of the oculomotor nerve (CN III) by the temporal lobe of the brain. This scenario of a loss of consciousness followed by a lucid interval and a second loss of consciousness is very typical for epidural hematoma.Emergent cerebral decompression and surgical control of the bleeding are paramount.### APPROACH TO: #### Meninges and Arterial Supply to Brain ### OBJECTIVES 1.Be able to list the meningeal layers 2.Be able to identify the dural folds and associated dural sinuses 3.

It is best to take it with food since food can increase its absorption and, thereby, increase plasma levels with more "bang for the buck."Geodon has FDA approval for the treatment of schizophrenia and for acute mania or mixed bipolar episodes.It is very highly protein bound.It is metabolized by CYP450 3A4.In addition to antagonizing 5HT2 and D2 receptors, it also blocks the reuptake of serotonin and norepinephrine as well as being a 5HT1A agonist. Therefore, it has properties of an antidepressant. It does not, however, have an FDA indication for use in treating major depression. When Geodon first came onto the market, there was concern that it prolonged the QTc interval. This is a measurement on the EKG that reflects the time it takes for depolarization and repolarization of the left atrium and ventricle to occur, that is, how long it takes the heart to be able to beat again. A prolongation of the QTc interval increases the risk that a premature beat can occur, leading to the development of an arrhythmia. This problem was found during the development of Geodon when it was administered to beagle dogs. The problem appears to be relatively unique to beagles and clinically has not been found in humans. However, physicians have been wary of using Geodon. Consequently, it is often underdosed. Geodon has a half-life of about 7 hours, so b.i.d. dosing is necessary. Doses of 20–40 mg b.i.d. may be more activating than higher doses. There may be more D2 antagonism with higher doses. Doses of 120–160 mg daily, divided, are typically necessary to fully treat psychosis. It has alpha-1 antagonism, but does not antagonize M1 or H1 receptors so it is less likely to cause weight gain, sedation, metabolic syndrome, and insulin resistance than other S2D2s. It is metabolized by CYP450 3A4. It is very highly protein bound. Geodon has FDA approval for the treatment of schizophrenia and for acute mania or mixed bipolar episodes. It is best to take it with food since food can increase its absorption and, thereby, increase plasma levels with more "bang for the buck."It is available as a capsule and as a short-acting injectable but not in a depot form.Invega Invega is the active metabolite of Risperdal.It is the only medication approved by the FDA for the acute treatment of schizoaffective disorder either as monotherapy or as an adjunct to mood stabilizers and/or antidepressants.It is also FDA approved for the treatment of schizophrenia.

In previous chapters, I have explored why treatment complications sometimes do not come to the attention of clinicians and researchers.It also presents a key puzzle for scholars interested in medical knowledge and a critical challenge for those who stake their hopes in evidence-based medicine.It reflects the recognition of idiosyncrasy in medical practice: all patients are different. Multivariate analysis helps doctors to ferret out which differences might be the most important determinants of treatment response. It enables them to provide patients with a nuanced prognosis and with the individualized risk assessment needed for informed consent. The intent is not to blame but to understand. But blame may be an inevitable and unfortunate consequence. Multivariate analyses and genetic studies each suggest that the problem is not what surgery does to patients, but what liabilities patients bring into the operating theater. Physicians must consciously ensure that such displacement of risk and responsibility onto patients never undermines the assiduity with which they work to optimize the safety of their therapies. ### **CHAPTER SIXTEEN Competition's Complications** **I** magine a conversation that takes place a thousand times each day in this country. A cardiac surgeon recommends that a patient undergo coronary artery bypass surgery. The patient asks if there will be any complications. The clinical evidence supports a wide range of possible answers. One surgeon could say, "Yes, we have to put you on a heart-lung machine; this is an imperfect substitute for the heart and introduces the risk of stroke, cognitive decline, and personality change." Another surgeon could say, "Long-term cognitive outcomes are just as good in patients who have surgery as in those who do not, and sometimes even better." The fact that each claim is well supported by recent research on the cerebral complications of bypass surgery poses a dilemma for patients and doctors. It also presents a key puzzle for scholars interested in medical knowledge and a critical challenge for those who stake their hopes in evidence-based medicine. In previous chapters, I have explored why treatment complications sometimes do not come to the attention of clinicians and researchers.Beginning in the mid-1990s, the cerebral complications of bypass surgery received unprecedented attention in certain arenas.Motivation for this effort came from therapeutic competition.As angioplasty, especially with stents, surged past bypass surgery in the 1990s, one of its selling points was its lower rate of cerebral complications.

When people find out that I am a veterinarian, they usually ask me when I decided on that career path.sounds like a great gig.Sometimes they don't know what it means, but becoming an animal saver or a pet-erinarian (so cute!)I think most children decide that they are going to become a veterinarian at some point.I call it a "neck neuter" because the mass looks like a testicle as it is being removed. The mass is submitted for histopathology and the preliminary results are available within twenty-four hours. The dogs recover in the intensive care unit (ICU) and go home the following day. In ten to fourteen days they will return for suture removal and an appointment with a medical oncologist to discuss the histopathology results and whether or not we recommend chemotherapy. Chemotherapy can start the same day. And that is why I wish I were a dog. Because I would take better care of me. I have clients who tell me this all the time. They say that if they get sick, they want to check themselves in to our animal hospital, because the care is so much better, so much faster, and we care so much more. It's a joke. Sort of. I will spend the next year dividing my time between having and treating cancer, between being the doctor and being the patient. It is a perspective I would never have asked for, and I don't mean to be critical but, well, I just can't help myself. I'm a little critical of the human system. We need to do better. We need to care more. We need to advocate more. We need to cherish ourselves the way we do our most perfect companions — our dogs. BEFORE I TELL YOU more about my thyroid situation, I should tell you a little about myself. I am a veterinary surgical oncologist, but more simply, I am a small animal veterinarian. I think most children decide that they are going to become a veterinarian at some point. Sometimes they don't know what it means, but becoming an animal saver or a pet-erinarian (so cute!) sounds like a great gig. When people find out that I am a veterinarian, they usually ask me when I decided on that career path.This isn't technically true, but I did write it down at school when I was six, and it's the earliest documentation available that I wanted to help animals for a living.I can't remember ever deciding to be a vet; it was just something I had always known.This is a feeling a lot of us in the profession share.It is part of our fabric to love and understand animals and want to help them.

## The central nervous system During embryonic development of the CNS, a hollow neural tube forms from the ectodermal layer of the inner cell mass of the embryo.Stimuli are carried by somatic sensory nerves towards the CNS and nerve impulses are carried by somatic motor nerves to skeletal muscles, where they initiate a response.• Motor nerves carry impulses away from the CNS. • Mixed nerves carry both sensory and motor fibres. An intercalated neuron is one that lies between a sensory neuron and a motor neuron. Such neurons may not always be present within a nerve pathway. • Afferent nerves carry impulses towards a structure, usually in the CNS. • Efferent nerves carry impulses away from a structure, usually in the CNS. Afferent and efferent are also terms used within other systems (e.g., the blood vascular system) to describe blood and lymphatic capillaries going to and leaving organs. Nerve fibres may be further classified according to the organ with which they are associated. • Visceral sensory and motor nerves are associated with the visceral body systems – the heart, digestive, respiratory, urinary and reproductive systems. Stimuli are carried by visceral sensory nerves from blood vessels, mucous membranes and the visceral organs to the CNS. Impulses are transmitted from the CNS by visceral motor nerves to smooth muscle and glandular tissue, where they initiate a response. • Somatic sensory and motor nerves are associated with the somatic structures in the body – receptors in the skin, muscles, joints and tendons and in specialised somatic organs such as the ear and eye. Stimuli are carried by somatic sensory nerves towards the CNS and nerve impulses are carried by somatic motor nerves to skeletal muscles, where they initiate a response. ## The central nervous system During embryonic development of the CNS, a hollow neural tube forms from the ectodermal layer of the inner cell mass of the embryo.The anterior end of the tube becomes the brain and the remaining tube becomes the spinal cord.The brain and spinal cord are hollow and are filled with CSF.### The brain The function of the brain is to control and coordinate all the activities of the normal body.The brain is a hollow, swollen structure lying within the cranial cavity of the skull, which protects it from mechanical damage.