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This can also be seen using high resolution ultrasound or confocal microscopy.If possible through the cloudy cornea, gonioscopy would confirm the presence of a closed angle and a narrow angle in the fellow eye (see Chapter 10).Tonometry would reveal a raised intraocular pressure often has high as 60–70 mmHg (see Chapter 2).These were accompanied by small flashes of light. He has treated hypertension but no other medical problems. The GP examines the eye and finds a normal visual acuity. Dilated fundoscopy reveals no abnormality. #### Questions * What should the GP advise? * What is the diagnosis? * What are the associated risks? #### Answers As the symptoms are acute the GP should arrange for an urgent ophthalmic assessment. The most likely diagnosis is a posterior vitreous detachment. With careful ophthalmoscopy, it will be possible to identify vitreous opacities in keeping with this diagnosis. The flashing lights are caused by traction of the detached vitreous gel on the retina. A specialized examination of the peripheral retina is needed. A tear may occur in the retina, which in turn may lead to a retinal detachment. Laser applied around the tear while it is flat can prevent retinal detachment (see Chapter 11). ### Case 4 A 75-year-old woman attends the main casualty department with nausea and vomiting. She says that her right eye is painful and red and that her vision is blurred. She is long-sighted and wears glasses for near and distance vision. She is generally fit. There is no family history of medical problems. On examination, the casualty officer finds the vision to be reduced to counting fingers in the right eye. The eye is red, the cornea appears cloudy, and the pupil is oval and dilated on the affected side. No view of the fundus is obtained. #### Questions * What is the diagnosis? * How might it be confirmed? * What is the treatment? #### Answers The lady is long-sighted and has acute angle closure (see Chapter 10). Tonometry would reveal a raised intraocular pressure often has high as 60–70 mmHg (see Chapter 2). If possible through the cloudy cornea, gonioscopy would confirm the presence of a closed angle and a narrow angle in the fellow eye (see Chapter 10). This can also be seen using high resolution ultrasound or confocal microscopy.A peripheral iridotomy is then performed, usually with a YAG laser, in both eyes, to prevent further attacks.If she has cataracts then surgical replacement of her lenses with artificial intra-ocular lenses can also help to widen the drainage angle.### Case 5 A 28-year-old man presents to his optician with a painful, red right eye.The vision has become increasingly blurred over the last 2 days.
Lao Tzu said that "what is deeply rooted in nature cannot be uprooted."Because the basic plan of the body, as a physical entity and as an energy system, evolves and exists in an ecological context, what the body needs it obtains from the environment in which it grew.They provide the body with energy in the form of calories and with the material resources to stay healthy and get well.For example, by raising the body's temperature, a fever reduces bacterial reproduction (like an antibiotic, fever is literally bacteriostatic), and sneezing physically expels offending agents (see Figure 1-1 and Chapter 24). Figure 1-1 Relation between rate of cell division for _Bacillus mycoides_ and temperature. (Data from _Encyclopaedia Britannica_ , 1954 ed, s.v. "Bacteriology.") Pathologists know that there are only so many ways that cells can look sick, because cellular reactions have a defined repertoire for manifesting malfunction. We have also learned a great deal over the past 100 years by correlating the appearance of dead tissue cells under the microscope with clinical diagnosis and prognosis. However, studying dead tissue cells for clinical significance does not allow direct observation of the dynamic energy of living cells, systems, organisms, and communities. Although correlation of the appearance of stained tissue cells under a microscope to clinical conditions is a powerful concept in medicine, alternative forms of medicine appear to provide a path to study the energy of living systems for health and healing, perhaps before the development of overt disease, as so often encountered among the many "functional complaints" in modern medicine (see Chapter 2). # NUTRITION AND NATURAL PRODUCTS The reliance on nutrition and natural products is fundamental to CAM and does not play merely a supportive or adjunctive role. Nutrients and plant products are taken into the body and incorporated in the most literal sense. They provide the body with energy in the form of calories and with the material resources to stay healthy and get well. Because the basic plan of the body, as a physical entity and as an energy system, evolves and exists in an ecological context, what the body needs it obtains from the environment in which it grew. Lao Tzu said that "what is deeply rooted in nature cannot be uprooted."# PLANTS Plants are an important part of nature relative to health and a dominant part of the nature in which humans evolved.In addition to producing the oxygen that we breathe, plants are seen as sources of nutrients, medicines (e.g., phytochemicals), and essential oils (e.g., volatiles for inhalation and transdermal absorption); some systems also view plants as sources of vibrational energy.
Most curious, however, was the simple filter to purify water perfected by Charles Chamberland, a collaborator of Louis Pasteur, which allowed for the development of modern virology.In his attempt to grow this mystery virus, Malik Peiris used the MDCK, LLC-Mk2, RDE, Hep-2, and MRC-5 cell lines—or, in simpler terms, dog kidney cells, monkey kidney cells, human muscle cells, human larynx tumor cells, and human embryo lung cells. This is a group of cell lines geared toward growing influenza or other respiratory viruses such as adenovirus, swine fever, and enterovirus. "We're basically going fishing," Peiris told his lab partner, K. H. Chan. "Let's hope we catch some virus." Once the samples were prepared and sealed, they were placed in a slow-rotating incubator and then checked every few hours for signs of cellular damage. For thousands of years, scientists postulated the theory of infectious agents so tiny they could not be observed—couldn't the "bad humors" and "evil spirits" of medieval times have been nothing more than a collective sense of dread at microorganisms so small they seemed to drift in the ether, as scientists would later discover airborne viruses actually did? By the late nineteenth century, the diverse microbial world of bacteria, protozoa, and fungi was established. But as early as 1840, the German anatomist Jacob Henle suggested the existence of microbes, so tiny they could not be observed even by the light microscope, that caused specific illnesses and diseases. Three men—Louis Pasteur, who disproved the theory of spontaneous generation of organisms with his swan-necked flasks that kept yeasts pure; Robert Koch, who demonstrated that specific bacteria caused anthrax and tuberculosis; and Joseph Lister, who developed a technique for obtaining purer cultures of organisms—were instrumental in pushing the study of microorganisms into the modern age. Most curious, however, was the simple filter to purify water perfected by Charles Chamberland, a collaborator of Louis Pasteur, which allowed for the development of modern virology.The filters took the form of hollow, unglazed porcelain cylinders with microscopic pores.The cylinders would be inserted into a tube connected to a hand pump; the entire contraption looked something like a miniature gasoline pump from the 1920s.
It has been proposed however that given many cancer stem cell populations share a large number of molecular features with regular stem cells; direct targeting of these cells could lead to significant deleterious effects on the associated normal tissue homeostasis.## Clinical Significance of Cancer Stem Cells Over the last decades the concept of cancer stem cells has developed from being a hypothesized population to a real definable entity. What is still unclear is what provides a cancer stem cell its unique identity and how prevalent they are throughout tumor development. Indeed, in light of context-dependent plasticity the true prevalence of a cancer stem cell population at any one point in time may be irrelevant as this will be a dynamic and ever changing figure. Importantly, this dictates that classical clinical modes of detecting tumor types such as immunohistochemistry (IHC) will be inappropriate for quantifying cancer stem cell prevalence in this context. Nevertheless, the presence of this unique cell population does provide an important clinical target for therapeutic targeting. In addition to their clonogenic capacity cancer stem cells display many attributes that predispose to drug resistance such as enhanced DNA repair pathways, cellular dormancy, and the expression of multidrug resistance proteins. These faculties suggest that targeting this population may be problematic. Indeed many authors suggest that these attributes may suggest that cancer stem cells are the population responsible for disease recurrence after adjuvant therapy. Late systemic recurrence is not uncommon after apparent complete response. Clearly, for this to occur requires a small, drug resistant and highly clonogenic population to exist – just as cancer stem cells appear to be. It has been proposed however that given many cancer stem cell populations share a large number of molecular features with regular stem cells; direct targeting of these cells could lead to significant deleterious effects on the associated normal tissue homeostasis.Early reports had suggested that Dclk1 marked a putative quiescent intestinal stem cell population; however, others had argued that Dclk1 marked a rare terminally differentiated secretory cell type called a Tuft cell (May _et al._ , 2009; Gerbe _et al._ , 2009).Dclk1 expression has also been described in both murine and human intestinal tumors.
They rush to blend other treatments into the mix and counteract healing.Many failures seem to be the result of parents' impatience with the progress of homeopathic treatment.No more eczema and no asthma or any other systemic condition.In my view, the worst one is mood changes. What would be better: Having clear skin and a depressed mood, or having a good mood and eczema? Can you even answer this question? Recently, the FDA approved the use of _nonsteroidal_ medications, such as Pimecrolimus and Tacrolimus, to treat eczema. These drugs are approved for use in children two years and older. Although I'm not a dermatologist and have never prescribed these drugs, the list of potential complications seems pretty serious to me and includes some systemic conditions. Without a doubt, there are cases of mild eczema that resolve spontaneously, and there are very severe cases that respond beautifully to conventional treatment, with all the symptoms of eczema being completely suppressed. What happens later on with the child's health remains to be seen. _Here's a warning:_ if your child develops significant inflammation of the skin, you should immediately contact your physician or dermatologist. The safety of your child comes as an absolute priority. As I've said many times before, we don't have homeopathic hospitals or full-time pediatric homeopathic clinics in America right now. So at this time, all emergency issues have to be resolved promptly by going to see a conventional physician. ## _Homeopathic Treatment of Eczema_ The paradox in treating this seemingly superficial condition with homeopathy is that it's difficult to treat, but perseverance brings about amazing results—a total cure. No more eczema and no asthma or any other systemic condition. Many failures seem to be the result of parents' impatience with the progress of homeopathic treatment. They rush to blend other treatments into the mix and counteract healing.They also receive suppressive ointments.Parents have real trouble letting go of conventional methods, especially if they've perceived a degree of improvement (suppression).If your child has eczema or any other skin condition, my advice to you is to try to start working on the issue with homeopathic treatment.There are many homeopathic remedies that help cure eczema.
It may or may not come to a head.It feels terribly hot.The boil stings, prickles, and burns.The swelling is red, shiny, and puffy.The following are the most commonly indicated remedies for boils: Apis: This is for a boil in the beginning stages.If your child develops a boil, you should regard it as the immune system working to cleanse the body of unwanted toxins.This anxiety manifests with headaches, difficulty swallowing along with intense thirst, or constriction in the chest. Dosage: Give 2 pellets every day for up to 3 days. If there is improvement after the first dose, you can stop. If there is no response after the third dose, try a different remedy. Repeat the remedy only if there is a return of any symptom. Call your healthcare practitioner if: • Your child is lacking in social skills for maintaining good relationships. • Your child develops a phobia about going to school. BOILS A boil is a skin abscess in which pus accumulates just beneath the surface of an oil gland or hair follicle. Boils develop because of an internal process in which the body needs to rid itself of toxicity. The boil will start out as a small, hard, red bump. As days go by, it becomes more tender, fills with pus, forms a head, bursts open, and then drains. The pus consists of dead white blood cells that have died after killing bacteria. If a boil comes to a head and bursts, it expels the dead bacteria. Sometimes the boil will not burst, and the body will absorb the pus into the system. However, it is best to pop the core out so the boil will fully discharge all the material and resolve itself. If the boils are large, they are called carbuncles, which can leave scars. If there is a lot of toxicity to expel, your child may develop a low-grade fever. If your child develops a boil, you should regard it as the immune system working to cleanse the body of unwanted toxins. The following are the most commonly indicated remedies for boils: Apis: This is for a boil in the beginning stages. The swelling is red, shiny, and puffy. The boil stings, prickles, and burns. It feels terribly hot. It may or may not come to a head.The child is irritable and wants to be left alone to rest or sleep.If there is any sign of redness or heat, look to Hepar Sulph, because Apis will not resolve a boil in the later stages.Belladonna: For a hot, hard, red swelling that may or may not have a head.There is burning heat with dry, swollen, red skin.The onset is rapid and violent.The pains are throbbing and cutting.
Bradykinin increases capillary permeability and is a potent vasodilator considered to be 10 times more effective than histamine.Angiotensin is a potent hormone that results in vasoconstriction and the stimulation of aldosterone causing blood pressure elevation.Ruling out a potential life-threatening process is crucial. Angioedema and anaphylaxis present similarly, are commonly confused for each other, but have differing pathophysiology and significantly different treatments. Simply, anaphylaxis is an acute allergen-mediated reaction, while angioedema is a vascular reaction. More specifically, anaphylaxis is a true systemic hypersensitivity IgE-mediated allergic inflammatory reaction. Angioedema, however, is considered a noninflammatory disease state during which intravascular fluid extravasates secondary to increased capillary permeability into the dermis or submucosa, most commonly in the face, upper airway, and gastrointestinal tract. This vascular reaction results in a deep well-demarcated and asymmetrical nonpitting edema in the subcutaneous dermis thought to be similar to the more superficial wheal-and-flare–type reaction seen in allergic urticaria. Angioedema is most commonly idiopathic but can be ACE inhibitor induced, hereditary or acquired with C1-esterase deficiency. Anaphylaxis on the other hand is most commonly associated with adverse drug reactions and insect stings in adults and food hypersensitivities in children. Both angioedema and anaphylaxis can be life threatening ( _Table 154.1_). Table 154.1 Risk Factors to Developing Clinically Significant Angioedema The mechanism for idiopathic (spontaneous) angioedema is not well understood. ACE inhibitor angioedema however, while rarer with an incidence of 0.1% to 0.7% in patients on pharmacotherapy, accounts for upward of 30% of cases seen in the emergency department. Angiotensin is a potent hormone that results in vasoconstriction and the stimulation of aldosterone causing blood pressure elevation. Bradykinin increases capillary permeability and is a potent vasodilator considered to be 10 times more effective than histamine.The subsequent accumulation of bradykinin most commonly results in bronchospasm, which results in a dry irritating "hacking" cough.The deposition of surplus bradykinin into airway and GI tissue is thought to precipitate clinically significant angioedema.
The goal is to increase the [HCO3–] to 10 meq/L and the pH to 7.20, not to increase these values to normal.Provision of such modest quantities of alkali in this situation seems to provide an added measure of safety, but it is essential to monitor plasma electrolytes during the course of therapy, because the [K+] may decline as pH rises.TABLE 38–4 CAUSES OF HIGH-ANION GAP METABOLIC ACIDOSIS TREATMENT Metabolic Acidosis Treatment of metabolic acidosis with alkali should be reserved for severe acidemia except when the patient has no "potential HCO3–" in plasma. Potential [HCO3–] can be estimated from the increment (Δ) in the AG (ΔAG = patient's AG –10). It must be determined if the acid anion in plasma is metabolizable (i.e., β-hydroxybutyrate, acetoacetate, and lactate) or nonmetabolizable (anions that accumulate in chronic renal failure and after toxin ingestion). The latter requires return of renal function to replenish the [HCO3–] deficit, a slow and often unpredictable process. Consequently, patients with a normal AG acidosis (hyperchloremic acidosis), a slightly elevated AG (mixed hyperchloremic and AG acidosis), or an AG attributable to a nonmetabolizable anion in the face of renal failure should receive alkali therapy, either PO (NaHCO3 or Shohl's solution) or IV (NaHCO3), in an amount necessary to slowly increase the plasma [HCO3–] into the 20–22 mmol/L range. Controversy exists, however, in regard to the use of alkali in patients with a pure AG acidosis owing to accumulation of a metabolizable organic acid anion (ketoacidosis or lactic acidosis). In general, severe acidosis (pH < 7.10) warrants the IV administration of 50–100 meq of NaHCO3, over 30–45 min, during the initial 1–2 h of therapy. Provision of such modest quantities of alkali in this situation seems to provide an added measure of safety, but it is essential to monitor plasma electrolytes during the course of therapy, because the [K+] may decline as pH rises. The goal is to increase the [HCO3–] to 10 meq/L and the pH to 7.20, not to increase these values to normal.
Fatigue is common and is present in almost one-third of patients.Angina pectoris is thought to be due to limited coronary vascular reserve.Twenty to thirty-five percent of patients present with chest pain, mostly during exercise, and the electrocardiogram (ECG) may show pseudoinfarction Q waves.However, DCM is more likely to occur in young individuals with no obvious risk factors for heart failure (other than family history), and a history of chronic skeletal muscle weakness may also be present. The formal diagnosis relies on criteria provided by the World Health Organization/International Society and Federation of Cardiology (WHO/ISFC),1 the Guidelines of the National Heart, Lung, and Blood Institute Workshop on the Prevalence and the Etiology of Dilated Cardiomyopathy,4 and the more recent update contained in the American Heart Association Scientific Statement on Contemporary Definitions and Classification of the Cardiomyopathies.3 Useful and detailed criteria that account for familial forms of DCM as well are described in the Guidelines for the Study of Familial Dilated Cardiomyopathies.2 Patients initially present with typical symptoms and signs of heart failure, because of either volume overload or low cardiac output, or both. Usually, by the time of the diagnosis, probands (the first individual diagnosed within a family) have severe impairment of the left ventricular systolic function. Affected relatives, on the other hand, can be asymptomatic with mild ventricular dilatation and dysfunction. Increasingly, the diagnosis is being made on the basis of family screening of clinically asymptomatic relatives of DCM cases. Educated patients may request such screening on the basis of having an affected family member diagnosed with DCM. Twenty to thirty-five percent of patients present with chest pain, mostly during exercise, and the electrocardiogram (ECG) may show pseudoinfarction Q waves. Angina pectoris is thought to be due to limited coronary vascular reserve. Fatigue is common and is present in almost one-third of patients.Pulmonary and systemic thromboembolisms occur, as first manifestation of the disease, at a rate of 1-6%/year.Most of them can be found in cases with severe left ventricular dilatation and dysfunction.Subtle skeletal muscle disease can complicate DCM, and at times, this is a valuable clinical clue.
Within 10 minutes after giving a dose of toxin, the animals became unsettled and irritable; had congestion of the conjunctivae, ears and other parts of the body and finally developed paralysis of the extremities.Toxicity was so acute and severe that the majority of treated animals succumbed from an anaphylactic-type reaction within 48 hours.It must be emphasized that the study reported here was not designed as a model for human disease, but rather to determine first whether a synergistic effect on a disease process existed between these two pathogens. "† In a presentation entitled, _"T-Lymphocytes and Yeast Flora—Friends or Foes? "_ Max D. Cooper, M.D. (Professor, Pediatrics and Microbiology, Medical School, University of Alabama in Birmingham) discussed immunological factors present in individuals with candidiasis. Then in two one-hour presentations Kazuo Iwata, M.D. (Chairman and Professor of Microbiology, Meiji College of Pharmacy, Tokyo) described his research work on yeast toxins and the types of symptoms and diseases which he had found to be related to _Candida albicans_. Dr. Iwata began studying _Candida albicans_ in 1967. Along with his co-workers he successfully isolated a potent, lethal toxin, _Canditoxin_ , (CT) from a virulent strain of C. albicans. These investigators isolated several high and low molecular weight toxins from _Candida albicans_.† In a published report describing his studies on Canditoxin in mice Dr. Iwata commented, _"Canditoxin_ produced unique clinical symptoms. Immediately after... intravenous injection (of toxin) animals exhibited ruffled fur and unsettled behavior... Toxicity was so acute and severe that the majority of treated animals succumbed from an anaphylactic-type reaction within 48 hours. Within 10 minutes after giving a dose of toxin, the animals became unsettled and irritable; had congestion of the conjunctivae, ears and other parts of the body and finally developed paralysis of the extremities.
The second molar has a large restoration, and the tooth could be fragile leading to fracture.Closed extraction in this case is impossible.8.6 (a) Hypercementosis of the mesial root of the first lower left molar would prompt surgical extraction of this tooth.Fig.## Clinical Evaluation of the Tooth Before Extraction Before starting extraction it is important to evaluate the condition of the crown. Deep caries or a large restoration may indicate a high risk for fracture of the crown during extraction, which would complicate the procedure. A tooth with missing crown will require a special approach. Other factors to consider are tooth/root mobility. Ankylosis, which is often seen with infrapositioned primary teeth or teeth subjected to earlier trauma, often indicates a surgical approach for removal of the primary tooth or, with ankylotic infrapositioned permanent teeth in the anterior region, decoronation to preserve the alveolar bone crest in the anterior region should be chosen. It is also important to assess the status of the adjacent teeth to avoid damage to fragile teeth or teeth with large restorations. The clinical evaluation of the tooth to be removed is done in conjunction with a radiographic assessment. ## Preoperative Radiographic Examination Radiographic examination must always be carried out prior to extraction of teeth to evaluate the degree of difficulty of extraction. Root anatomy, presence of pathology in the root or surrounding bone, vital structures and relation to other roots, neighboring teeth and other factors such as ankylosis with replacement resorption or hypercementosis of the root are taken into consideration (Fig. 8.6). The most common radiograph is a good quality intraoral periapical radiograph. Other techniques, such as panoramic radiographs, scanograms, and cone-beam computer tomography, are more valuable to evaluate the tooth in relation to vital structures such as inferior alveolar nerve and maxillary sinus. Fig. 8.6 (a) Hypercementosis of the mesial root of the first lower left molar would prompt surgical extraction of this tooth. Closed extraction in this case is impossible. The second molar has a large restoration, and the tooth could be fragile leading to fracture.(b) The extent of external root resorption makes extraction of the canine almost impossible due to the risk for fracture.Surgical extraction should be considered.(c) The root configuration of the second lower right molar makes it impossible to remove this tooth without a surgical procedure.(d) The lower first right molar has slender roots that taper towards each other apically.
See homeo-.— _homocystinuric, adj._ Homocystinuria: lens dislocation _(Newton, 1995)_ homoeo-.Long-term results of treatment are not available.Treatment may include a diet low in methionine and supplementation with large doses of vitamin B6.It is believed the amino acid may have a toxic effect on cells lining the blood vessels. Studies also indicate that low levels of homocysteine are found in people with high intake of B vitamins. See also homocystine. homocysteine (HCY) test, a blood test used to detect levels of homocysteine, which, if increased, may act as an independent risk factor for ischemic heart disease, cerebrovascular disease, peripheral arterial disease, and venous thrombosis. This test should be considered for screening in individuals with progressive and unexplained atherosclerosis despite normal lipoproteins and in the absence of other risk factors and in those with an unusual family history of atherosclerosis. homocystine /-sis′tin/, a disulfide analog of homocysteine produced by the oxidation of homocysteine. See also homocysteine. homocystinemia /-sis′tinē′mē· /, an amino acid disorder that causes an excess of homocystine in the blood. See also homocystinuria. homocystinuria /h ′m sis′tin r′ē· / [Gk, _homos_ \+ (cystine); Gk, _ouron,_ urine], a rare biochemical abnormality characterized by the abnormal presence of homocystine, an amino acid, in the blood and urine, which is caused by any of several enzyme deficiencies in the metabolic pathway of methionine to cystine. The disease is inherited as an autosomal-recessive trait. Its clinical signs are similar to those of Marfan's syndrome, including mental retardation, osteoporosis leading to skeletal abnormalities, dislocated lenses, and thromboembolism. Treatment may include a diet low in methionine and supplementation with large doses of vitamin B6. Long-term results of treatment are not available. — _homocystinuric, adj._ Homocystinuria: lens dislocation _(Newton, 1995)_ homoeo-. See homeo-.In human beings, the female is the homogametic sex.homogenate /h moj′ nit/, a tissue that is or has been made homogenous, as by grinding cells into a creamy consistency for laboratory studies.A homogenate usually lacks cell structure.Also called broken cell preparation.homogeneous /h ′m jē′nē· s/ Gk, _homos_ \+ _genos,_ kind], 1. consisting of similar elements or parts.**2.
Antiplatelet drugs make platelets less likely to clump and form clots, a common cause of ischemic stroke.If people have had an ischemic stroke, taking an antiplatelet drug can reduce the risk of another ischemic stroke.Having regular checkups enables a doctor to identify risk factors for stroke so that they can be managed quickly.Strokes that cause unconsciousness or that affect a large part of the left side of the brain (which is responsible for language) may be particularly grave. In adults who have had an ischemic stroke, problems that remain after 6 months are likely to be permanent, but children continue to improve slowly for many months. Older people fare less well than younger people. For people who already have other serious disorders (such as dementia), recovery is more limited. If a hemorrhagic stroke is not massive and pressure within the brain is not very high, the outcome is likely to be better after than that after an ischemic stroke. Blood (in a hemorrhagic stroke) does not damage brain tissue as much as an inadequate supply of oxygen (in an ischemic stroke) does. Prevention Preventing strokes is preferable to treating them. The main strategy for preventing a first stroke is managing the major risk factors. High blood pressure (see High Blood Pressure) and diabetes (see Diabetes Mellitus) should be controlled. Cholesterol levels should be measured and, if high, lowered to reduce the risk of atherosclerosis (see discussion of treatment of dyslipidemia). Smoking and use of amphetamines or cocaine should be stopped, and alcohol should be limited to no more than 2 drinks a day. Exercising regularly and, if overweight, losing weight help people control high blood pressure, diabetes, and high cholesterol levels. Having regular checkups enables a doctor to identify risk factors for stroke so that they can be managed quickly. If people have had an ischemic stroke, taking an antiplatelet drug can reduce the risk of another ischemic stroke. Antiplatelet drugs make platelets less likely to clump and form clots, a common cause of ischemic stroke.Aspirin, one of the most effective antiplatelet drugs, is usually prescribed.One adult's tablet or 1 children's tablet (which is about one fourth the dose of an adult aspirin) is taken each day.Either dose seems to prevent strokes about equally well.
Diagnosis * Lab testing.Other major symptoms include diarrhea, weakness, vomiting, jaundice, abdominal mass, migratory thrombophlebitis (recurring blood clots in the leg and pelvic veins), and GI bleeding.Weight loss with poor appetite, occasionally with an aversion to meats and a metallic taste in the mouth.Magnetic sleep systems are believed to improve enzymatic action in the body. The back flex can be worn in the day, over the abdomen, to enhance circulation. Short-Bowel Syndrome A complex condition typically caused by malabsorption that usually accompanies removal of a significant amount of small intestine. Short-bowel syndrome can result from surgery due to Crohn's, cancer, or the clotting of an artery in the digestive tract. This condition often requires intravenous nutrition (hyperalimentation). In some centers, small bowel transplantation is used to address these chronic conditions. A new resource for patients is a center near Boston that uses nutrition to improve regrowth of gut tissue. By supplementing glutamine and growth hormone, they are able to improve patterns of absorption and regrow some tissue while improving absorption in existing tissue. They can be reached at the Nutrition Restart Center, Hopkinton, MA, 01748; (800) 867-6761. PANCREATIC CANCER Pancreatic cancer is now the fifth leading cancer in the United States for both men and women, and appears to be increasing in number as the population grows older. People who have had pancreatitis are more prone to pancreatic cancer. Risk factors include cigarette smoking, alcohol consumption (particularly beer), gallstones, a diet high in animal fats, and diabetes. Symptoms Abdominal pain that is vague and dull in the middle of the abdomen, occasionally going through to the back. Weight loss with poor appetite, occasionally with an aversion to meats and a metallic taste in the mouth. Other major symptoms include diarrhea, weakness, vomiting, jaundice, abdominal mass, migratory thrombophlebitis (recurring blood clots in the leg and pelvic veins), and GI bleeding. Diagnosis * Lab testing.Approximately 85 percent of all pancreatic cancers will have this marker, which is a carbohydrate produced by the cancer cell.* A CAT and MRI scanning.For the CAT scan the tumor must be at least 2 cm to be visualized.* Ultrasound is not as accurate as the scans.
### METABOLISM OF COMPLEX LIPIDS #### TRIACYLGLYCEROL SYNTHESIS Triacylglycerols , commonly referred to as triglycerides, are the predominant storage form of lipids (Chapter 3, Figure 3-2B.Similarly, though, the fatty acid substrate is transported into the peroxisome by a carnitine acyltransferase and the final step in the process is via a similar peroxisomal β-ketothiolase.Treatment for Zellweger syndrome is mainly supportive, including prevention of infections; however, death usually occurs before the first birthday. Some success in the treatment of ALD has been reported with bone marrow transplantation and a diet with low intake of VLCFA and inclusion of Lorenzo's oil , a mixture of 18- and 22-carbon triglycerides. Further research is attempting to provide further support for this treatment and to elucidate the mechanism of Lorenzo's oil. Finally, patients with Refsum disease are maintained on a diet with no phytanic acid (found in beef, lamb, tuna, cod, and haddock); attempts to find alternative/natural therapies are also ongoing. Finally, mitochondria are unable to degrade fatty acids greater than 22 carbons. In the case of very-long-chain fatty acids ( VLCFA ), breakdown occurs in peroxisomes, organelles found in all eukaryotes that provide specialized lipid metabolism as well as processing of toxic substances. Peroxisomes metabolize VLCFA down to an eight-carbon octanyl-CoA, which is then further processed by mitochondria as described above. Peroxisomal oxidation of fatty acids is driven not by ATP but rather by the production of hydrogen peroxide (H2O2), a highly energized molecule, which is converted to water and oxygen by the enzyme catalase found only in peroxisomes. Similarly, though, the fatty acid substrate is transported into the peroxisome by a carnitine acyltransferase and the final step in the process is via a similar peroxisomal β-ketothiolase. ### METABOLISM OF COMPLEX LIPIDS #### TRIACYLGLYCEROL SYNTHESIS Triacylglycerols , commonly referred to as triglycerides, are the predominant storage form of lipids (Chapter 3, Figure 3-2B.As noted previously, triacylglycerol stores 9 kcal/g versus only 4 kcal/g for carbohydrates.Synthesis of triacylglycerols mainly takes place on the smooth endoplasmic reticulum of the liver but can also be generated in adipose (fat) cells.
Kinds of vectors include dogs, which carry rabies; mosquitoes, which transmit malaria; and ticks, which carry Rocky Mountain spotted fever.3.A mechanical vector transmits the infecting organism from one host to another but is not essential to the life cycle of the parasite.A biological vector is usually an arthropod in which the infecting organism completes part of its life cycle.They may transmit nerve impulses at an increasing rate as a joint approaches its maximal range of motion and are believed to have a protective function of signaling the cerebral cortex when a joint has reached the end position of its range. They are the most complicated of the nerve endings. Vater's ampulla. See hepatopancreatic ampulla. VBP, an anticancer drug combination of vinBLAStine, bleomycin, and cisplatin. Also called PVB. VC, abbreviation for vital capacity. VCO2, symbol for carbon dioxide output per unit of time. VCU, abbreviation for voiding cystourethrography. VD, abbreviation for venereal disease. See sexually transmitted disease. V deflection /diflek″shən/ , a deflection on the His bundle electrogram that represents ventricular activation. VDRL, abbreviation for Venereal Disease Research Laboratories. VDRL test, a serological flocculation test for syphilis. It is also positive in other treponemal diseases such as yaws. False-positive and false-negative results may occur. A positive test must be confirmed by further, more definitive testing. Abbreviation for Venereal Disease Research Laboratory test. VDT, abbreviation for video display terminal. V̇ e, symbol for expired volume. V̇ E, symbol for volume expired in 1 minute. Vectibix, a chemotherapeutic agent. Brand name for panitumumab. vector /vek″tər/ [L, carrier] , 1. a quantity having direction and magnitude, usually depicted by a straight arrow. The length of the arrow represents magnitude, and the head represents direction.2. a carrier, especially one that transmits disease. A biological vector is usually an arthropod in which the infecting organism completes part of its life cycle. A mechanical vector transmits the infecting organism from one host to another but is not essential to the life cycle of the parasite. Kinds of vectors include dogs, which carry rabies; mosquitoes, which transmit malaria; and ticks, which carry Rocky Mountain spotted fever.3.Through recombinant deoxyribonucleic acid techniques, genes that cause harmful effects such as cancer are removed and genes that mediate synthesis of essential enzymes are added.The vector then can be injected into a patient who suffers from an enzyme deficiency, such as Lesch-Nyhan syndrome.
By contrast, years of committed meditation practice seem to work from the bottom-up, expanding consciousness by boosting gamma waves, opening up our senses and blurring the boundaries of bodily selfhood.The first is mediated by profuse, high-affinity serotonin 1A receptors and occurs when someone is exposed to mild levels of adversity. It promotes acceptance and resilience. The second is mediated by the more sparse, less sticky 2A receptors and only kicks in when we are faced with extreme, life-threatening situations such as starvation, asphyxia or a lethal adversary. This second stress response promotes brain plasticity: the kind of radical, adaptive thinking that might ensure our long-term survival – assuming, of course, we live to fight another day. In the game of life, fine-tuning the balance between stability and plasticity to match circumstances is the key to success. Over the past decade, as we have learned more about the neuroscience of consciousness, a picture has started to emerge of how altered states – from dreams and trance to psychedelics and meditation – shift the balance in favour of change, shattering the dominance of established, conservative models of thought and behaviour: models that in their most intractable forms are responsible for conditions such as addiction, depression, anxiety and post-traumatic stress disorder (PTSD). In the process, altered states make psychological growth and adaptation possible. We've seen how, for example, drugs such as LSD and psilocybin temporarily stifle alpha waves in the default mode network (DMN), dissolving the ego and promoting communication between brain regions and networks that aren't usually on talking terms, bringing alternative cognitive models to the fore. By contrast, years of committed meditation practice seem to work from the bottom-up, expanding consciousness by boosting gamma waves, opening up our senses and blurring the boundaries of bodily selfhood.In light of these recent advances in the scientific understanding of altered states – and consciousness itself – the future possibilities for medicine and society look exciting.We have an opportunity unprecedented in human history to harness altered states as part of safe, effective new treatments for mental illness and addiction, to enhance general well-being and ease our passing.
5.7B illustrates renal involvement (E-Fig.Fig.This phenomenon is known as metastatic or isolated organ tuberculosis and most commonly involves the kidneys, adrenals, meninges, bone, Fallopian tubes, endometrium and epididymis.These organisms remain viable but quiescent and active tuberculosis may then reappear in tissues remote from the original lesion many years later.Another name for M. tuberculosis which is sometimes used in clinical practice is the eponymous designation Koch's bacillus. Key to Figures B bronchiole Bo bony trabeculae C caseous necrosis D destroyed wall G granuloma L Langhans' giant cell T tubercle Fig. 5.7 Disseminated tuberculosis. (A) Liver (MP); (B) kidney (MP); (C) bone (MP); (D) tuberculous meningitis (MP).If a ruptured tuberculous lymph node (or a rapidly enlarging focus of post-primary tuberculosis) erodes a blood vessel wall, masses of mycobacteria are discharged into the circulation and lodge in the microvasculature. When the eroded vessel is a branch of the pulmonary artery, the organisms pass to other areas of the lung, but when a pulmonary venous tributary is involved, they are spread in the systemic circulation to many organs, notably the liver, kidney and spleen. In this way, vast numbers of new tubercles may be produced throughout the body. Such multiple lesions rarely attain any great size because this occurrence usually produces rapid clinical deterioration and death. Because the gross appearance of individual lesions resembles millet seeds, this condition is known as miliary tuberculosis . Fig. 5.7A shows several miliary tubercles (T) in the liver (E-Fig. 5.4 H ). One of the tubercles exhibits Langhans' giant cells (L) and the larger tubercle shows early central caseous necrosis.It seems that a relatively small number of organisms can be disseminated by the bloodstream to various organs without causing overt disease, only to become reactivated at a later date when the host's immune status is impaired. These organisms remain viable but quiescent and active tuberculosis may then reappear in tissues remote from the original lesion many years later. This phenomenon is known as metastatic or isolated organ tuberculosis and most commonly involves the kidneys, adrenals, meninges, bone, Fallopian tubes, endometrium and epididymis. Fig. 5.7B illustrates renal involvement (E-Fig.Continuation of this process results in destruction of much of the renal cortex and medulla, with eventual rupture of large confluent tubercles into the pelvicalyceal system, which becomes distended with caseous material.This condition is known as tuberculous pyonephrosis .In more advanced cases, infection spreads to involve the ureter and bladder.
Nonoperative management is only indicated in patients who cannot tolerate surgery.Laparoscopy can be used in patients with small MCNs (<4 cm) without mural nodules on imaging.Because of the risk of occult malignancy within the lesion and future malignant transformation, the treatment of choice for all MCNs is complete surgical resection.B, Coronal T2-weighted magnetic resonance image shows a large, multilocular mucinous cystic neoplasm of the pancreas _(arrow),_ displacing the liver, stomach, and spleen. Microscopically, MCNs have an inner columnar epithelial layer and an outer, dense layer composed of ovarian-type stroma, which differentiates them from other cystic neoplasms. Immunohistochemistry of MCNs is frequently positive for estrogen and progesterone receptors. Macroscopically, MCNs appear as round cystic lesions with a smooth surface and fibrous pseudocapsule. Multiple loculi may be present (see Figure 3, _A_ _)_. On CT scan or MRI (see Figure 3, _B_ _),_ MCNs appear as round, well-encapsulated, septated, macrocystic tumors. Calcifications may be visualized within the wall of the tumor and occur more frequently in malignant MCNs. Similarly, mural nodules, biliary obstruction, invasion of vascular structures, extrapancreatic lesions, ascites, and obliteration of fat planes around the pancreas increase the likelihood of invasive malignancy within the MCN. ERCP shows an absence of pancreatic ductal communication in MCNs. An elevated cyst fluid CEA level strongly suggests a mucinous neoplasm (MCN or intraductal papillary mucinous neoplasm [IPMN]) rather than a nonmucinous cyst, and MCNs with malignancy have even higher CEA levels compared with benign MCNs. A cyst fluid CA 19-9 level greater than 37 U/mL suggests a mucinous lesion (either cystadenoma or cystadenocarcinoma) rather than a serous cystadenoma or pseudocyst. Because of the risk of occult malignancy within the lesion and future malignant transformation, the treatment of choice for all MCNs is complete surgical resection. Laparoscopy can be used in patients with small MCNs (<4 cm) without mural nodules on imaging. Nonoperative management is only indicated in patients who cannot tolerate surgery.Prognosis is largely determined by the presence or absence of an invasive component.Recurrence after resection of benign MCN has been reported to be less than 5%, but this increases to as high as 37% in those with invasive carcinoma.
The gate control theory has helped nurses and other health care professionals recognize the _holistic_ nature of pain.When pain occurs, a person's thoughts and emotions can modify one's perceptions as they reach the level of conscious awareness.These areas of the brain regulate thoughts and emotions, including beliefs and values.Pain conduction from C fibers is slow, more diffuse (widespread) and dull, burning, or achy—quite different from the sensations of A delta fibers. In contrast to the intermittent nature of A delta sensations, C fibers usually produce persistent pain. Although many theories of pain have been discussed, the classic gate control theory by Melzack and Wall (1982) still forms the basis of what is believed by most pain researchers today. According to this theory, a gating mechanism occurs in the spinal cord. Nerve fibers (A delta and C fibers) transmit pain impulses from the periphery of the body. These impulses travel to the dorsal horn of the spinal cord, specifically to the _substantia gelatinosa_ , where the gating mechanism occurs. When the gate is opened, pain impulses ascend to the brain; when the gate is closed, the impulses do not get through and pain is not perceived (Fig. 5-1). FIG. 5-1 The gate control theory of pain. Morphine-like substances called endorphins are released when the large-diameter nerve fibers are stimulated. These fibers close the gate and decrease pain transmission. This helps explain why many noninvasive pain management techniques work to relieve pain. Endorphins are thought to be a gene product, and producing them requires a stimulus to the brain. Similar gating mechanisms exist in the nerve fibers descending from the thalamus and cerebral cortex. These areas of the brain regulate thoughts and emotions, including beliefs and values. When pain occurs, a person's thoughts and emotions can modify one's perceptions as they reach the level of conscious awareness. The gate control theory has helped nurses and other health care professionals recognize the _holistic_ nature of pain.### Attitudes and Practices Related to Pain The attitudes of health care professionals toward pain influence the way they perceive and interact with patients in pain.Without adequate assessment skills or knowledge of pain and analgesic therapy, they may not be able to understand their patients' pain.
Photographs (j, k) demonstrate a white pale irregular inner surface of the cystic mass after removal of the germinating membranes (arrows).Intraoperative photographs demonstrate (e–f) clear fluid being aspirated from the cystic mass (arrows).Note the extraction of the fluid with a surgical aspirator (g), and removal of the germinating membrane from the hydatid cyst (h, i) (arrows).* CT: "2-tone duct" sign in which the pancreatic duct shows two different densities on CT: lower density representing fluid (dilated duct without any tumor), and an area of slightly higher density representing a tumor growing in the duct. * MR: T2WI: the dilated pancreatic duct shows two different signal intensities, an area of high signal intensity that represents fluid and an area of slightly higher intensity that represents tumor growing in the duct. * Other findings on CT/MR: branch duct dilation, hypoenhanced areas (tumor necrosis), calcification, and infiltrative or invasive growth. * MRCP/ERCP: abrupt disruption of the pancreatic duct and the intraductal tumor, recognized as the "cork-of-wine-bottle" sign, wherein the tumor is surrounded by fluid in the dilated duct and is easily recognized. ### 13.16.6 Differential Diagnosis * Intraductal papillary mucinous neoplasm, IPMN, neuroendocrine tumor, acinar cell carcinoma, solid cystic pseudopapillary neoplasm, and tumor metastases ### 13.16.7 Treatment * Surgical resection ## 13.17 Hydatid Cyst of the Pancreas (Figs. 13.34–13.36) Fig. 13.34 Hydatid cyst of the pancreas. A 19-year-old male from Argentina with history of epigastric pain, weight loss, and a palpable epigastric mass. CECT axial (a–d) images demonstrate a large cystic mass with a thick capsule in the pancreatic head (arrows). Intraoperative photographs demonstrate (e–f) clear fluid being aspirated from the cystic mass (arrows).Note the extraction of the fluid with a surgical aspirator (g), and removal of the germinating membrane from the hydatid cyst (h, i) (arrows). Photographs (j, k) demonstrate a white pale irregular inner surface of the cystic mass after removal of the germinating membranes (arrows).13.35 Hydatid cyst of the pancreas.A 20-year-old male patient with history of chronic epigastric pain.Transferred from the mountains of Peru (Ancash).Past medical history non-contributory.CECT axial (a, b) and coronal (c, d) images reveal an ovoid cystic mass with a thick capsule involving the pancreatic head (arrows).This pancreatic cystic mass was removed.
In the resting cell DNA is wound tightly around core histones, excluding the binding of the enzyme RNA polymerase II, which activates gene transcription and the formation of messenger RNA.Each core histone has a long N-terminal tail that is rich in lysine residues, which may become acetylated, thus changing the electrical charge of the core histone.Most of these inflammatory proteins are regulated by increased gene transcription, which is controlled by proinflammatory transcription factors, such as nuclear factor-κB (NF-κB) and activator protein-1 (AP-1), that are activated in asthmatic cells.6 For example, NF-κB is markedly activated in epithelial cells of asthmatic patients, and this transcription factor regulates many of the inflammatory genes that are abnormally expressed in asthma. NF-κB may be activated by rhinovirus infection and allergen exposure, both of which exacerbate asthmatic inflammation. Chromatin remodelling Chromatin consists of DNA and basic proteins called histones, which provide the structural backbone of the chromosome. It has long been recognized that histones play a critical role in regulating the expression of genes and determine which genes are transcriptionally active and which ones are suppressed (silenced). The chromatin structure is highly organized as almost two metres of DNA have to be packed into each cell nucleus. Chromatin is made up of nucleosomes, which are particles consisting of 146 base pairs of DNA wound almost twice around an octamer of two molecules each of the core histone proteins H2A, H2B, H3 and H4.7 Expression and repression of genes is associated with remodelling of this chromatin structure by enzymatic modification of the core histone proteins, particularly by acetylation. Each core histone has a long N-terminal tail that is rich in lysine residues, which may become acetylated, thus changing the electrical charge of the core histone. In the resting cell DNA is wound tightly around core histones, excluding the binding of the enzyme RNA polymerase II, which activates gene transcription and the formation of messenger RNA.Gene transcription only occurs when the chromatin structure is opened up, with unwinding of DNA so that RNA polymerase II and basal transcription complexes can now bind to DNA to initiate transcription.
When the external tone is turned off, you will be asked if your tinnitus has become softer or gone away and to indicate when it returns to its usual state.In the residual inhibition test, you will listen to a tone that is a little louder than your tinnitus for one minute.• How loud is the sound on a 10-point scale (0 = not heard; 10 = like a plane taking off in your head)? • What is your state of mind (that is, are you feeling anxious or sad and tired)? • How would you describe the quality and length of your sleep? • Do you have any other medical problems? • What medications do you take? • Have you or other family members had ear problems in the past (exposure to noise, hearing aids, surgery)? • Do you have associated symptoms, such as hearing loss, ear pain, or ear stuffiness? Hint: even if you have filled out a questionnaire, be sure to mention any of the above issues directly to the doctor or assistant who does the intake. Bring notes! Avoid telling your doctor a long story about Aunt Rose's tinnitus, because you want your doctor to focus on _you_ and on the problem you are having right now. #### Physical Examination The examination will focus on the head, neck, brain, and cardiovascular system. Your ENT will listen for pulsatile tinnitus using a stethoscope over the ear canal, major blood vessels of the head and neck, and the heart. He or she may put pressure on the blood vessels in your neck or ask you to turn your head and say whether these maneuvers change the loudness of your tinnitus. #### Hearing Tests Your hearing will be tested during your first visit. This test can provide important diagnostic information even if you do not suffer from hearing loss. Advanced testing can also detect pulsations of the eardrum. Specific tests for tinnitus include pitch matching to determine the frequency of your tinnitus, loudness matching to determine loudness of your tinnitus, and a test for _residual inhibition_. In the residual inhibition test, you will listen to a tone that is a little louder than your tinnitus for one minute. When the external tone is turned off, you will be asked if your tinnitus has become softer or gone away and to indicate when it returns to its usual state.Most people with subjective tinnitus will not require any imaging tests, but if your ENT is concerned about the possibility of a benign tumor, he or she may order an MRI.For those who have objective tinnitus, a CT scan or MRI is often necessary to rule out a benign middle ear tumor, vascular malformation, or stroke.
39.15 Photomicro graph showing tissue from gross total resection (H&E stain) What is the diagnosis?39.14 Photom icrograph showing tissue from gross total resection (H&E stain) Fig.39.13 Phot omicrograph showing tissue from gross total resection (H&E stain) Fig.39.12 Pho tomicrograph showing tissue from gross total resection (H&E stain) Fig.Fig.No additional stains were performed.* MRI studies disclosed a large, solid intracerebral lesion involving the right temporoparietal region. The lesion had a minor cystic component, focal necrosis, was isointense to gray matter on both T1- and T2-weighted images, and enhanced with contrast. There was some peritumoral edema and mass effect. The lesion was not in close proximity to the ventricular system. ### 39.2.2 Pathology Findings * Figures 39.7 and 39.8 are representative photomicrographs of routine H&E stained sections of tumo r from partial surgical excision. Immunohistochemical studies for glial fibrillary acidic protein (GFAP) and ep ithelial membrane antigen (EMA) are depicted in Figs. 39.9 and 39.10. Fig. 39.7 Photo micrograph from partial surgical excision (H&E stain) Fig. 39.8 Photo micrograph from partial surgical excision (H&E stain) Fig. 39.9 Imm unohistochemical study: glial fibrillary acidic protein (GFAP) Fig. 39.10 Imm unohistochemical study: epithelial membrane antigen (EMA) What is the diagnosis? ## 39.3 Case Study C ### 39.3.1 History Summary * A 10-year-old boy presented with headaches and "clumsiness." According to his parents, these symptoms have been slowly progressive over the course of a year. * MRI studies rev ealed a large posterior fossa lesion; Figure 39.11 shows a representative T1-weighted postcontrast image. Fig. 39.11 T1-weighted postcontrast MR image ### 39.3.2 Pathology Findings * Figures 39.12, 39.13, 39.14, and 39.15 are representative photomicrographs of routine H&E stained sections from tissu e obtained at gross total resection of this lesion. No additional stains were performed. Fig. 39.12 Pho tomicrograph showing tissue from gross total resection (H&E stain) Fig. 39.13 Phot omicrograph showing tissue from gross total resection (H&E stain) Fig. 39.14 Photom icrograph showing tissue from gross total resection (H&E stain) Fig. 39.15 Photomicro graph showing tissue from gross total resection (H&E stain) What is the diagnosis?* A large, right post erior parasagittal lesion was detected on MR imaging studies.A representative T1-weighted postcontrast image is shown in Fig.39.16.Of note, a smaller lesion was present more anteriorly (not shown); this lesion was also parasagittal and was solid with diffuse contrast enhancement.Fig.
The left brachiocephalic vein runs diagonally down the upper mediastinum from the patient's left to right.Left sided internal jugular or subclavian vein lines need to run through the left brachiocephalic vein before entering the superior vena cava.See p22 for an example X-ray of correctly positioned right and left sided central venous lines.If there is a only a single lumen, it is usually best not to use it for venepuncture, as this can cause the line to become blocked, preventing it from being used for IV fluids/medications. 5. Reviewing the post insertion chest X-ray, you think that the central venous line may have been mistakenly placed into an artery. What is the most appropriate initial step? * * * The correct answer is C) Analyse a sample taken from the line on an arterial blood gas machine to confirm whether venous or arterial. --- * * * Accidental placement within a central artery, such as the common carotid artery at the neck or the subclavian artery, is a potential complication of central venous catheters. Instilling IV medication, such as total parenteral nutrition, into an arterial line has serious consequences, including stroke. Knowledge of the normal venous and arterial anatomy on chest X-ray is thus needed to determine if a venous catheter is misplaced line. Right sided internal jugular or subclavian vein lines should traverse the right brachiocephalic vein, which forms the superior right border of the mediastinum, directly down into the superior vena cava. If a right sided central line crosses the midline of the mediastinum, you must consider whether it is within an artery (subclavian or common carotid) and is passing into the aortic arch. See p22 for an example X-ray of correctly positioned right and left sided central venous lines. Left sided internal jugular or subclavian vein lines need to run through the left brachiocephalic vein before entering the superior vena cava. The left brachiocephalic vein runs diagonally down the upper mediastinum from the patient's left to right.A) As long as it bleeds and flushes it is safe to use – Incorrect.Arterially placed lines will bleed and flush, so this does not tell you whether the line is venous or arterial.B) Immediately remove and resite – Incorrect.If the line is arterial, it will need removal and resiting.
The leaves are harvested for medicinal use in summer, when the plant is in flower.Growing to a height of six feet (two meters), it bears upward-growing stems with pale, smooth, green leaves and small, yellow flowers.Anyone who uses any type of a sleeping aid, especially a barbiturate, should be careful of the additive effects of sleeping pills and corydalis. COUCH GRASS Latin names: _Elymus repens, Graminis rhizoma,_ or _Agropyron repens_ (Poaceae [haygrass] family) Other common names: dog grass, quackgrass General Description Couch grass is an invasive weed found in the Americas, northern Asia, Australia, and Europe. It is similar to, and sometimes misidentified as, Johnson grass. A vigorous perennial growing to a height of three feet (one meter), couch grass has long, creeping rhizomes, slender leaves, and erect flower spikes bearing green flowers in two rows. The rhizome and the seeds are used in herbal medicine. Evidence of Benefit Couch grass is a rich source of healing mucilages that soothe and relieve inflamed sore throat. It has been used to treat difficult urination and kidney stones since the time of the Roman Empire. Benefits of couch grass for specific health conditions include the following: • _Kidney problems_. Couch grass is useful for inflammatory diseases of the urinary tract and for prevention of kidney stones. Considerations for Use Couch grass is used as a tea or used to irrigate the kidneys. When used as an irrigant, it is important to consume copious amounts of water. No irrigations should be done in those with edema due to heart or kidney failure. The bulk herb is available from online retailers and in herb shops. Herb gardeners attempting to grow couch grass should exercise caution, since it easily becomes an uncontrollable weed. DAMIANA Latin name: _Turnera diffusa_ (Turneraceae [damiana] family) General Description Damiana is an aromatic shrub of the hot and humid reaches of Texas, Mexico, Central America, and Namibia. Growing to a height of six feet (two meters), it bears upward-growing stems with pale, smooth, green leaves and small, yellow flowers. The leaves are harvested for medicinal use in summer, when the plant is in flower.Animal studies indicate that the herb has blood sugar–lowering effects and is an anti-inflammatory.It also seems to bind progesterone but not estrogen and may be helpful in menopause formulas and to increase sexual function.Damiana has been associated with improved sexual function for both men and women.
• More women than men suffer from PTSD.• A traumatic event is an extreme event, such as a rape, stabbing, road traffic accident, robbery, natural disaster or medical emergency.Key messages • PTSD is an anxiety disorder that develops in some people after a traumatic event.Other helpful resources are listed in the Appendices.Additionally, people may turn to alcohol or drugs to try to cope with the distressing feelings and memories and can develop alcohol- or drug-use problems. It is important to recognize your symptoms as early as possible and seek professional help. When PTSD is the primary problem, then once your treatment is under way your mood, panic, and sleep will improve and you will feel less inclined to turn to substances to help you cope. If possible, avoid alcohol and other substances. Recognize your desire to cope with alcohol or substances as a sign that you need help with your PTSD. ### How long does treatment last for? Trauma-focused CBT is a short-term therapy that lasts for about three months depending on your needs. Typically between eight and twelve sessions are offered; these may last sixty to ninety minutes each session. If you have had more than one trauma, treatment is likely to last longer so that the therapist can help you come to terms with everything that has happened to you. ### What should I do if I think I have PTSD? If you are in the UK, go to your GP and ask for a referral for trauma-focused psychological therapy. Depending on where you live, you may have access to the Improving Access to Psychological Therapies Programme (IAPT), which offers trauma-focused CBT for PTSD sufferers. Other helpful resources are listed in the Appendices. Key messages • PTSD is an anxiety disorder that develops in some people after a traumatic event. • A traumatic event is an extreme event, such as a rape, stabbing, road traffic accident, robbery, natural disaster or medical emergency. • More women than men suffer from PTSD.• PTSD can be treated.• Trauma-focused CBT has the best evidence for helping people to recover.
TFFC is a ligamento-cartilagenous complex separating the proximal row of the carpus and ulna.(c) Triangular fibrocartilage complex (TFCC) injuries: The TFFC transmitting about one fifth of the axial load from the wrist to the forearm plays a pivotal role as a stabilizer of the distal radioulnar joint.(d) Intersection syndrome: Is defined as an inflammation at the crossing points of the tendons of the first dorsal compartment and the extensor radialis longus and brevis. This point is typically 2-3 in. proximal to the radio-carpal joint. This entity is seen in sports involving repetitive wrist extension. ##### 3.3.1.1 Ligamentous Injuries of the Wrist (a) Scapholunate injuries: Are considered to be the most common ligamentous injury of the wrist. In its typical pattern, the injury is the result of abnormally large forces causing wrist extension, ulnar deviation and supination at the carpal bones. In extreme situations seen with complete scapholunate rupture, the normal alignment between scaphoid, lunate and triquetrum is lost: a characteristic appearance of scapholunate dissociation is seen on plain radiographs. This injury pattern is seen in collision with the fellow sports personnel and fall on an outstretched hand, with the hand held in the above position at the time of the impact in both instances. (b) Lunotriquetral injuries: Are less common compared to scapholunate injuries and usually do not progress to arthrosis and collapse of the architecture of proximal row of carpal bones. These injuries occur as the result of forces that cause wrist extension, radial deviation and pronation at the carpal bones. Unlike scapholunate ruptures, insufficiency of lunotriquetral ligament does not disrupt the normal alignment of the lunate and triquetrum due to presence of extrinsic dorsal and volar ulnar ligaments stabilizing these carpal bones. (c) Triangular fibrocartilage complex (TFCC) injuries: The TFFC transmitting about one fifth of the axial load from the wrist to the forearm plays a pivotal role as a stabilizer of the distal radioulnar joint. TFFC is a ligamento-cartilagenous complex separating the proximal row of the carpus and ulna.The TFCC is completed on the ulnar side by the ulnar collateral ligament, and the extensor carpi ulnaris sheath.Principally, TFCC injuries are divided into traumatic (class I) and degenerative tears (class II), the former being more common in athletes.Each class is further subdivided into A, B, C, and D, with IB being the commonest type of injuries in the athletes.
In addition, the AG may increase with an increase in anionic albumin, because of either increased albumin concentration or alkalosis, which alters albumin charge.An increase in the AG is most often due to an increase in unmeasured anions and, less commonly, is due to a decrease in unmeasured cations (calcium, magnesium, potassium).TABLE 38–2 EXAMPLES OF MIXED ACID-BASE DISORDERS APPROACH TO THE PATIENT Acid-Base Disorders A stepwise approach to the diagnosis of acid-base disorders follows (Table 38–3). Care should be taken when measuring blood gases to obtain the arterial blood sample without using excessive heparin. Blood for electrolytes and arterial blood gases should be drawn simultaneously prior to therapy, because an increase in [HCO3–] occurs with metabolic alkalosis and respiratory acidosis. Conversely, a decrease in [HCO3–] occurs in metabolic acidosis and respiratory alkalosis. In the determination of arterial blood gases by the clinical laboratory, both pH and PaCO2 are measured, and the [HCO3–] is calculated from the Henderson-Hasselbalch equation. This calculated value should be compared with the measured [HCO3–] (total CO2) on the electrolyte panel. These two values should agree within 2 mmol/L. If they do not, the values may not have been drawn simultaneously, a laboratory error may be present, or an error could have been made in calculating the [HCO3–]. After verifying the blood acid-base values, the precise acid-base disorder can then be identified. CALCULATE THE ANION GAP All evaluations of acid-base disorders should include a simple calculation of the AG; it represents those unmeasured anions in plasma (normally 10 to 12 mmol/L) and is calculated as follows: AG = Na+ –(Cl– \+ HCO3–). The unmeasured anions include anionic proteins, (e.g., albumin), phosphate, sulfate, and organic anions. When acid anions, such as acetoacetate and lactate, accumulate in extracellular fluid, the AG increases, causing a high-AG acidosis. An increase in the AG is most often due to an increase in unmeasured anions and, less commonly, is due to a decrease in unmeasured cations (calcium, magnesium, potassium). In addition, the AG may increase with an increase in anionic albumin, because of either increased albumin concentration or alkalosis, which alters albumin charge.A fall in serum albumin by 1 g/dL from the normal value (4.5 g/dL) decreases the AG by 2.5 meq/L.Know the common causes of a high-AG acidosis (Table 38–3).
ONGOING CARE FOLLOW-UP RECOMMENDATIONS Patient Monitoring • Frequent monitoring is required for relapse, disease progression, and for detecting signs of toxicity of medical management. • Reevaluate for azotemia, urine protein, hypertension, edema, loss of renal function, cholesterol, and weight. DIET • Normal protein (1 g/kg/day) • Low fat (cholesterol) • Reduced sodium (<2 g/day) • Supplemental multivitamins and minerals, especially vitamin D and iron • Fluid restriction if hyponatremic PATIENT EDUCATION • Printed material for patients: National Kidney Foundation, 30 E. 33rd Street, Suite 1100, New York, NY 10016; 800-622-9010 – Childhood nephrotic syndrome – Diabetes and kidney disease – Focal glomerulosclerosis • Web site: National Institutes of Health: nephrotic syndrome PROGNOSIS Nephrotic syndrome in children (MCD) is typically self-limited and carries a good prognosis. In the adult, the prognosis is variable. Complete remission is expected if the basic disease is treatable (infection, malignancy, drug-induced); otherwise, a relapsing and remitting course is possible, with progression to dialysis seen in more aggressive forms (diabetic glomerulosclerosis). COMPLICATIONS • Thromboembolism: – Deep vein, renal vein, or central venous thrombosis may occur. – The risk appears to be greater the lower the serum albumin. – Pulmonary embolism is a known complication. • Pleural effusion • Symptomatic hypovolemia • Ascites • Hyperlipidemia, cardiovascular disease • Acute renal failure, progressive renal failure • Protein malnutrition/muscle wasting • Infection secondary to low serum IgG concentrations, reduced complement activity, and depressed T-cell function: peritonitis, pneumonia, or cellulitis • Loss of vitamin D (vitamin D–binding protein loss in urine) leading to bone disease • Proximal tubular dysfunction resulting in glucosuria, aminoaciduria, phosphaturia, bicarbonaturia, and vitamin D deficiency REFERENCES 1.Am Fam Physician.2009;80(10):1129–1134.2.Crew RJ, Radhakrishnan J, Appel G. Complications of the nephrotic syndrome and their treatment.Clin Nephrol.2004;62(4):245.3.Fried LF, Orchard TJ, Kasiske BL.Effect of lipid reduction on the progression of renal disease: a meta-analysis.Kidney Int.2001;59(1):260–269.4.Kunz R, Friedrich C, Wolbers M, et al.
When?Over 140,000 cases and 4000 deaths were reported, mainly in adolescents and adults.A massive reemergence of diphtheria occurred in the newly independent states of the former Soviet Union during the 1990s. Mostly in India, Nepal, Bangladesh and other areas where vaccine coverage is low.Where? Mainly children aged 4–6.Who dies?Moderate dehydration causes thirst, restlessness, irritability, decreased skin elasticity and sunken eyes. Severe dehydration causes worsening symptoms with clinical shock (rapid weak pulse, low blood pressure, cool pale skin, confusion and reduced consciousness). ### What are the chances of survival? With appropriate fluid and electrolyte replacement, and antibiotics where indicated, the chance of survival is excellent. Very young children, elderly people and those debilitated by other serious disease are most at risk. HOW TO AVOID IT • Access to safe drinking-water, sanitation and good personal and food hygiene are vital. • Exclusive breastfeeding for the first 6 months of life helps to protect infants. • Vaccination is available against some pathogens (e.g. rotavirus, cholera). • When traveling, drink only bottled water from reputable sources (check it isn't just filled from a tap) or use water-purifying tablets. • Probiotic supplements offer some protection against diarrheal infections. • Zinc supplements can reduce stool volume by 30% and duration of illness by 25%. ## 27 Diphtheria Diphtheria is a disease caused by the bacterium _Corynebacterium diphtheriae,_ which is usually inhaled. On its own, it produces a mild sore throat. But if the bacterium is itself infected with a promiscuous virus (a bacteriophage), it acquires the ability to kill. How common is it? Once a leading cause of death among children, the global burden has now decreased to between 5000 and 10,000 deaths per year. Who dies? Mainly children aged 4–6. Where? Mostly in India, Nepal, Bangladesh and other areas where vaccine coverage is low. A massive reemergence of diphtheria occurred in the newly independent states of the former Soviet Union during the 1990s. Over 140,000 cases and 4000 deaths were reported, mainly in adolescents and adults. When?Cyclical epidemics occurred every 7–10 years.Why? Exposure to a toxigenic strain of _Corynebacterium diphtheriae_.The virus impregnates the bacterial cell with a gene that codes for a powerful toxin.In non-immune people, this toxin causes the larynx and tonsils to swell alarmingly.
Older people are also more likely to already have disorders that limit treatment of stroke.SPOTLIGHT ON AGING After a stroke, older people are more likely to have problems, such as pressure sores, pneumonia, permanently shortened muscles (contractures) that limit movement, and depression.In such cases, the outlook is very good.Diagnosis If people have a sudden, severe headache that peaks within seconds or that is accompanied by any symptoms suggesting a stroke, they should go immediately to the hospital. Computed tomography (CT—see page 2037) is done to check for bleeding. A spinal tap (lumbar puncture—see page 635) is done if CT is inconclusive or unavailable. It can detect any blood in the cerebrospinal fluid. A spinal tap is not done if doctors suspect that pressure within the skull is increased. Cerebral angiography (see Angiography) is done as soon as possible to confirm the diagnosis and to identify the site of the aneurysm or arteriovenous malformation causing the bleeding. Magnetic resonance angiography (see page 2041) or CT angiography (see page 2038) may be used instead. Prognosis About 35% of people die when they have a subarachnoid hemorrhage due to an aneurysm because it results in extensive brain damage. Another 15% die within a few weeks because of bleeding from a second rupture. People who survive for 6 months but who do not have surgery for the aneurysm have a 3% chance of another rupture each year. The outlook is better when the cause is an arteriovenous malformation. Occasionally, the hemorrhage is caused by a small defect that is not detected by cerebral angiography because the defect has already sealed itself off. In such cases, the outlook is very good. SPOTLIGHT ON AGING After a stroke, older people are more likely to have problems, such as pressure sores, pneumonia, permanently shortened muscles (contractures) that limit movement, and depression. Older people are also more likely to already have disorders that limit treatment of stroke.Some treatments, such as endarterectomy, are more likely to cause complications in older people.Nonetheless, treatment decisions should be based on the person's health rather than on age itself.Some disorders common among older people can interfere with their recovery after a stroke, as in the following: People with dementia may not understand what is required of them for rehabilitation.
He can speak but doesn't have conversations, and he doesn't play with toys typically the way his peers do.One boy is already falling well behind his peers.It's not uncommon for parents to get two different opinions about the severity of their child's autism or even if it's autism at all.He is the author of _Challenging the Myths of Autism_ , which has inspired educators and parents to consider a radical reframing of how we think about and treat people diagnosed with autism. His book has been honored with the Mom's Choice Gold Award, the American Non-Fiction Authors' Association Silver award, and the 2012 International Book Award for Best Parent-Resource. MOVING PAST HISTORICAL STEREOTYPES OF AUTISM The medical pathologist focuses the microscope to sharpen his view on the odd-looking cells. Using a special stain to color them, with a closer look, he positively identifies adenocarcinoma. There's no mystery or guess work. The cells meet the globally accepted characteristics of this well-defined type of cancer. Within a few hours, the family is called into the doctor's office for the devastating news. At the same time, he is able to give them clear treatment options, answer their questions, and explain the statistical probability of beating it. In a different part of the hospital, a less certain diagnosis is being made with an even less certain course of treatment. Unlike the pathologist staring straight at the cancer cells, autism is not a cell we can see. We can't measure it like insulin in blood for diabetes or as a biomarker in urine. Autism doesn't have a certain temperature like a fever or a specific blood pressure. Instead, autism is made up of a group of behavioral symptoms that the doctor observes and then decides, subjectively, if they look "autistic enough." It's not uncommon for parents to get two different opinions about the severity of their child's autism or even if it's autism at all. One boy is already falling well behind his peers. He can speak but doesn't have conversations, and he doesn't play with toys typically the way his peers do.The psychiatrist is looking for a specific yet broad set of behaviors (or absence of typically present behavior) that may add up to the necessary group of symptoms for a diagnosis.It's a complex process.Typically, a diagnosing physician or psychologist has a fairly limited time to observe a young three-year-old's range of behaviors.In some cases, an hour or less.
### Activities of the Lipoxins The lipoxins are potent anti-inflammatory eicosanoids and counteract the actions of the pro-inflammatory eicosanoids (primarily LTB4 but also PGE2 and TXA2). Reproduced with permission of themedicalbiochemistrypage, LLC.FIGURE 24-2: Pathways for the synthesis of LXA 4 and LXB4.FIGURE 24-1: Structures of LXA 4 and LXB4. Lipoxin A4 (LXA4) and lipoxin B4 (LXB4) were the first-recognized eicosanoid-related mediators that display both potent anti-inflammatory and pro-resolving actions in animal models of disease. The LX act as agonist ligands for specific GPCR resulting in the activation of cellular responses important to inflammation and inflammatory resolution. The LX and their analogs exert important activities related to airway inflammation, asthma, arthritis, cardiovascular disorders, gastrointestinal disease, periodontal disease, kidney diseases and graft-versus-host disease (GVHD), and many other diseases/disorders where uncontrolled inflammation is a key mediator of disease pathogenesis (Figure 24-1). The synthesis of the lipoxins occurs via 3 distinct pathways, one of which is triggered via the actions of aspirin. The 2 "classical" pathways for the synthesis of the lipoxins are the result of the concerted actions of 15-LOX acting on arachidonic acid in epithelial cells (eg, airway epithelia) and 5-LOX in leukocytes or through the actions of 5-LOX in leukocytes followed by 12-LOX action in platelets (Figure 24-2). This latter activity requires that platelets interact directly with adherent neutrophils as occurs only following platelet activation. Activated leukocytes that adhere to epithelial cells as a consequence inflammation (such as gastrointestinal, airway, or kidney epithelia) induce the production of lipoxins. An additional stimulus that leads to production of lipoxins is epithelial cell conversion of LTA4 that is released from airway epithelia. FIGURE 24-2: Pathways for the synthesis of LXA 4 and LXB4. Reproduced with permission of themedicalbiochemistrypage, LLC. ### Activities of the Lipoxins The lipoxins are potent anti-inflammatory eicosanoids and counteract the actions of the pro-inflammatory eicosanoids (primarily LTB4 but also PGE2 and TXA2)._ALXR_ is a multirecognition receptor involved in immune responses, which was originally identified as the formyl peptide receptor-like 1 (FPRL1) protein; a member of the formyl peptide receptor (FPR) family of receptors that bind _N_ -formulated peptides derived by the degradation of bacteria or host cells.The FPR family of receptors is involved in mediating immune responses to infection.
Keep in mind, though, that corticosteroids can weaken tendons.This helps ensure that the medication gets where it belongs.If a steroid injection seems to be the best option to calm a painful joint, request that it be done under ultrasound guidance.It is little wonder that when rofecoxib (Vioxx) and comparable drugs were developed, patients and doctors alike were enthusiastic. Although there never was any evidence that Vioxx offered more effective pain relief, people were hopeful. Doctors were convinced that the digestive tract protection such drugs were supposed to provide would be well worthwhile. It wasn't until years later that studies revealed these drugs increased the risk of dying from heart attacks and strokes., What can someone do for joint pain that undermines the quality of life? Despite the problems with NSAID pills, it is possible to use NSAIDs topically. They may kick in a bit more slowly with pain relief, but after two or three weeks, the relief they offer is pretty similar. The Food and Drug Administration has approved three forms of diclofenac to be applied to the skin on or near the sore joint: Voltaren Gel, Flector patch, and Pennsaid Topical Solution. Putting medicine on the skin might trigger a rash in sensitive individuals, but it is less likely to cause serious digestive tract problems. Adverse reactions are still possible, so patients using one of these topical pain medicines need to stay in touch with their physicians. Another approach that the doctor may offer a desperate patient is a steroid injection into the joint. Although this treatment often eases pain in the short term, it does not provide reliable long-term relief for tendinitis. Steroid injections may offer many patients relief from arthritis joint pain for a few months, but the pain relief appears to fade more quickly with each subsequent injection. If a steroid injection seems to be the best option to calm a painful joint, request that it be done under ultrasound guidance. This helps ensure that the medication gets where it belongs. Keep in mind, though, that corticosteroids can weaken tendons.Arthritis expert Joanne Jordan, MD, MPH, Herman and Louise Smith Distinguished Professor of Medicine and director of the Thurston Arthritis Research Center at the University of North Carolina, reminds us that both doctors and patient make a big mistake if they overlook all the nondrug approaches that can be helpful.
* Although usually found in defined ranges, serologic evidence suggests E. canis and A. phagocytophilum occur in all 48 contiguous states.); (2) A. platys: tropism for platelets; shares serologic cross-reactivity with A. phagocytophilum.SEE ALSO * Hypothyroidism * Myopathy, Inflammatory–Masticatory Muscle Myositis and Extraocular Myositis Suggested Reading Stades FC, Gelatt KN. Diseases and surgery of the canine eyelid. In: Gelatt KN, ed., Veterinary Ophthalmology, 4th ed. Ames, IA Blackwell, 2007, pp. 583–594. Author J. Phillip Pickett Consulting Editor Paul E. Miller E Ehrlichiosis BASICS DEFINITION Caused by Ehrlichia spp.—tick-borne rickettsial disease Dogs * Within the family Anaplasmataceae—three pathogenic genera: Ehrlichia, Anaplasma, and Neorickettsia. * Ehrlichia spp.—divided into three groups: (1) E. canis: ehrlichiosis found intracytoplasmically in circulating leukocytes; (2) E. ewingii: canine granulocytic ehrlichiosis; like A. phagocytophilum, infects granulocytic cells in dogs, but differs in geographic distribution (mainly found in southeastern and south-central United States); (3) E. chaffeensis: like E. canis, tropism for mononuclear cells; mainly a human pathogen but causes disease in dogs; disease distribution based on vector (mainly Amblyomma americanum) range. * Anaplasma spp.—two organisms of importance: (1) A. phagocytophilum: infects mainly horses but also the granulocytic cells of dogs; mainly found in northeastern and upper midwestern states and California based on distribution of vectors (hard ticks Ixodes spp. ); (2) A. platys: tropism for platelets; shares serologic cross-reactivity with A. phagocytophilum. * Although usually found in defined ranges, serologic evidence suggests E. canis and A. phagocytophilum occur in all 48 contiguous states.Cats * Feline mononuclear ehrlichiosis.* Extremely rare.* E. risticii and A. phagocytophilum.* Serologic evidence—suggests a species that cross-reacts with E. canis can cause illness.
Almost everyone who has this disorder recovers completely.The diagnosis is based on the symptoms, on whether the person has been exposed to any of the known causes, and on an examination of the cornea with a slit lamp (a device used by a doctor to examine the eye with magnification—see Figure: :What Is a Slit Lamp?).A doctor may apply eye drops that contain a dye called fluorescein, which temporarily stains areas of the cornea where cells are damaged, making these areas easier to identify. Superficial Punctate Keratitis Superficial punctate keratitis is death of small groups of cells on the surface of the cornea. The eyes become red, watery, and sensitive to light. Most people recover fully. Symptoms can be relieved. The cause of this disorder may be any of the following: A viral infection A bacterial infection (including trachoma) Dry eyes Strong chemicals splashed in the eye Exposure to ultraviolet light (sunlight, sunlamps, or welding arcs) Prolonged use of contact lenses An allergy to eye drops Blepharitis (eyelid inflammation) A side effect of certain drugs taken by mouth or vein (intravenously) In superficial punctate keratitis, the eyes are usually painful, watery, sensitive to bright light, and bloodshot, and vision may be slightly blurred. Often there is a burning, gritty feeling or a feeling as if a foreign object is trapped in the eye. When ultraviolet light causes the disorder, symptoms usually do not occur until several hours after exposure and last for 1 to 2 days. When a virus causes the disorder, a lymph node in front of the ear on the affected side may be swollen and tender. The diagnosis is based on the symptoms, on whether the person has been exposed to any of the known causes, and on an examination of the cornea with a slit lamp (a device used by a doctor to examine the eye with magnification—see Figure: :What Is a Slit Lamp?). Almost everyone who has this disorder recovers completely.When the cause is a bacterial infection or prolonged use of contact lenses, antibiotics are used, and the wearing of contact lenses is temporarily discontinued.When the cause is dry eyes, ointments and artificial tears are effective.
Data gained in cases of simple starvation and refeeding were different from those seen in anorexia nervosa and recovery from the disease.However, since most of these alterations were normalized after special feeding and recovery [141], the changes may also be regarded as consequences rather than causes of the disease.Activation of incretin peptide hormones (GLP-1, GIP) is important not only in the decrease of body weight but also in the improvement of glucose metabolism: some derivatives of exogenous agonist exendin-4 versus structural analogs of GLP-1 (eg, exenatide versus liraglutide) or blockers of its degrading dipeptidyl-peptidase-4 enzyme (eg, sitagliptin) are already used in the medical practice treating type 2 diabetes and obesity. Some other surgical interventions (eg, sleeve gastrectomy, adjustable gastric banding) cause much smaller changes in incretin functions—these are less effective than RYGB in reducing body weight and hyperglycemia. However, _ob/ob_ mice failed to maintain low body mass after RYGB [137]. Apparently, this raises the idea that in the background of massive obesity and diabetes not only gluttony but also some primary disorder of such incretin mechanisms [42] might play a role. ### Anorexia—Eating Disorders—Calorie Restriction—Chronic Diseases #### Signaling Feeding State in Eating Disorders, Anorexia Nervosa In anorexia nervosa the baseline PYY3-36, PP, CCK, and insulin plasma levels were high (although with great heterogeneity) [99,136–139], and the postprandial CCK rise started earlier and reached higher peak values than in controls [140]. These seem to suggest that abnormalities of the GI peptides may be responsible for the anorexia. However, since most of these alterations were normalized after special feeding and recovery [141], the changes may also be regarded as consequences rather than causes of the disease. Data gained in cases of simple starvation and refeeding were different from those seen in anorexia nervosa and recovery from the disease.Bulimia nervosa is accompanied by elevated CCK level in the "urge to vomit" stage [145], but not earlier.
Any _Salmonella_ serotype can probably cause any of these clinical manifestations under appropriate conditions, but in practice the _S enterica_ serotypes are associated primarily with gastroenteritis.This may be due to the downregulation of innate toll-like receptor responses in the intestinal mucosa by the Vi antigen. Macrophage oxidative burst inhibited Infection spreads through RES Eventually, the increasing bacterial population begins to overflow into the bloodstream (Figure 33–8). The entry of Gram-negative bacteria and their LPS endotoxin into the blood starts the fever, which slowly increases and persists with the continued seeding of _S_ Typhi. This sometimes results in metastatic infection of other organs including the urinary tract and the biliary tree. The latter causes reinfection of the bowel. This cycle beginning and ending in the small intestine takes approximately 2 weeks to complete. RES sites seed the bloodstream and other organs Endotoxin produces the fever #### IMMUNITY Natural infection with _S_ Typhi confers immunity, and reinfection is rare unless the course was shortened by early administration of antimicrobials. The immune response is both TH1- and TH2 mediated. In nonfatal cases, antibody and activated macrophages eventually subdue the untreated infection over a period of about 3 weeks. Which antigens stimulate this immunity is not clearly understood. The Vi antigen is usually credited, but various surface proteins are also candidates. Immunity follows natural infection SALMONELLOSIS: CLINICAL ASPECTS #### MANIFESTATIONS The clinical patterns of salmonellosis can be divided into gastroenteritis, bacteremia with and without focal extraintestinal infection, enteric fever, and the asymptomatic carrier state. Any _Salmonella_ serotype can probably cause any of these clinical manifestations under appropriate conditions, but in practice the _S enterica_ serotypes are associated primarily with gastroenteritis._S enterica_ = gastroenteritis Typhi = enteric fever ##### Gastroenteritis Typically, the episode begins 24 to 48 hours after ingestion, with nausea and vomiting followed by, or concomitant with, abdominal cramps and diarrhea.Diarrhea persists as the predominant symptom for 3 to 4 days and usually resolves spontaneously within 7 days.Fever (39°C) is present in about 50% of the patients.
In parallel, tetracyclines stimulate growth of disease-causing Candida fungus, Staphylococci and Clostridia in the digestive tract.First, it makes the gut wall anatomically vulnerable to invasion by pathogenic microbes; second, it alerts the immune system to attack these changed proteins, starting an auto-immune reaction in the body against its own gut.This in turn does two things.A good example is tuberculosis, where wide use of antibiotics has created new varieties of the Mycobacterium Tuberculosis resistant to all existing antibiotics. • Antibiotics have a direct damaging effect on the immune system, making us more vulnerable to infections, which leads to a vicious cycle of more antibiotics and more infections. Let us have a look at what different groups of antibiotics do to the gut flora. Penicillins In this group we have very widely used Amoxicillin, Ampicillin, Flucloxacillin and all other antibiotics with "-cillin" at the end of their name. These drugs have a damaging effect on two major groups of our beneficial resident bacteria: Lactobacilli and Bifidobacteria, while promoting growth of the pathogenic Proteus family, Streptococci and Staphylococci. This particular group of antibiotics allow bacteria normally found only in the bowel to move up to the intestines, which predisposes the person to development of IBS (Irritable Bowel Syndrome) and other digestive disorders. Tetracyclines (Tetracycline, Doxycycline and other "-cyclines") This group of drugs is routinely prescribed to teenagers for acne as a long course, lasting from three months to two years. Tetracyclines have a particular toxic effect on the gut wall by altering protein structure in the mucous membranes. This in turn does two things. First, it makes the gut wall anatomically vulnerable to invasion by pathogenic microbes; second, it alerts the immune system to attack these changed proteins, starting an auto-immune reaction in the body against its own gut. In parallel, tetracyclines stimulate growth of disease-causing Candida fungus, Staphylococci and Clostridia in the digestive tract.A prolonged course of treatment can completely eliminate these bacteria from the digestive system, leaving it open to invasion by pathogenic species of E.coli and other microbes.Antifungal antibiotics (Nystatin, Amphotericin, etc.)These drugs lead to selective stimulation of growth of the Proteus family and lactose-negative E.coli species, capable of causing serious disease.
PIC enhanced S1PR1 expression in CLL cells and their migratory response toward S1P [33].Activated CLL cells displayed reduced expression of S1PR1 and the migratory response toward S1P.The exit of normal lymphocytes from lymphoid tissues depends on the presence of sphingosine-1 phosphate (S1P) and the expression of S1P receptor-1 (S1PR1).PIC attenuated MMP-9 gene expression via the suppression of NF-κB activity. Furthermore, TNF-α-induced Akt phosphorylation was significantly attenuated in the presence of PIC [30]. PIC suppressed both the proliferation and invasion of cultured AH109A hepatoma cells [31]. PIC, at lower concentrations (25–50 μM), induced cell cycle arrest at G2/M phase, while it caused apoptosis at a higher concentration (100 μM). PIC suppressed invasive capacity of hepatoma cells by scavenging reactive oxygen species (ROS). PIC also suppressed the tumor growth and metastasis in hepatoma-bearing rats [31]. ### 9.2.6 Multidrug Resistance (MDR) Modulation The identification of compounds that overcome the resistance to cancer cell apoptosis that frequently accompanies MDR is of great therapeutic importance. PIC effectively inhibited the multidrug resistance-associated protein, MRP1 as assessed by its ability to suppress the efflux of the fluorescent MRP1 substrate (BCECF) from human erythrocytes [32]. ### 9.2.7 Modulation of Tumor Microenvironment Chronic lymphocytic leukemia (CLL) is characterized by the progressive accumulation of clonal B lymphocytes. Proliferation occurs in lymphoid tissues upon interaction of leukemic cells with a supportive microenvironment [33]. Therefore, the mobilization of tissue-resident CLL cells into the circulation is a useful therapeutic strategy to minimize the reservoir of tumor cells within survival niches. The exit of normal lymphocytes from lymphoid tissues depends on the presence of sphingosine-1 phosphate (S1P) and the expression of S1P receptor-1 (S1PR1). Activated CLL cells displayed reduced expression of S1PR1 and the migratory response toward S1P. PIC enhanced S1PR1 expression in CLL cells and their migratory response toward S1P [33].PIC treatment reduced tumor growth.
The upper extremity, or arm, has two compartments containing primarily the deltoid and biceps brachii muscles anteriorly and the triceps muscle posteriorly.Early débridement leads to loss of muscle that probably would have survived.There are areas of ischemia of the muscle that are allowed to demarcate with superficial débridement at 2 to 3 weeks.The manometer is set so that its top is level with or slightly below the compartment, and the stopcock is opened. The manometer is gradually raised until the meniscus is seen to fall. The measurement is expressed in centimeters of water or divided by 1.4 to equal millimeters of mercury. Muscle compartmental pressure is normally less than 20 mm Hg. The authors tend to perform compartment decompression in a patient with suspected compartment syndrome whose muscle compartment pressure is greater than 35 mm Hg. FIGURE 1 The Stryker pressure monitor is a handheld solid-state transducer device that can be used to directly measure muscle tissue pressure. The syringe and manometer are housed in a special chamber, and the directions for use are engraved on the back of the chamber. ## Treatment: Compartment Decompression The definitive treatment of compartment syndrome is release of the constricting tissue. Nonoperative therapies have no role in the treatment of compartment syndrome. Release of the constricting tissues almost always requires a long incision that involves the skin, subcutaneous tissues, and underlying fascia. Subcutaneous fasciotomy is best avoided. Débridement of ischemic muscle should be conservative because many segments of muscle that appear necrotic actually survive, and the negative or detrimental systemic effects of ischemic muscle are avoided once the compartment is decompressed and the products of dead muscle escape onto the dressing (Figure 2). FIGURE 2 A fasciotomy was performed for muscle ischemia of the calf after repair of a popliteal artery injury with ligation of the injured vein. There are areas of ischemia of the muscle that are allowed to demarcate with superficial débridement at 2 to 3 weeks. Early débridement leads to loss of muscle that probably would have survived. The upper extremity, or arm, has two compartments containing primarily the deltoid and biceps brachii muscles anteriorly and the triceps muscle posteriorly.The resultant extensive cellulitis compromises perfusion, necessitating a long incision beginning just distal to the deltoid to just above the elbow, staying lateral to the brachial artery and median nerve.
During this process, the ovaries cease to produce eggs, and, more important, the production of the two sex hormones, estrogen and progesterone, declines to a very low level.##### A Woman's Aging Body Menopause generally takes place between ages 35 and 55.Consult with your pharmacist or physician to explore whether any medications you are taking might have potential sexual side effects.Drugs that commonly affect sexual function (arousal, erectile function, or achieving orgasm) include antidepressants used to treat depression and anxiety disorders other psychiatric medications, such as antipsychotic drugs and lithium antihistamines for allergies, such as pseudoephedrine (Sudafed) high blood pressure medications and heart medications, such as digitalis (Digoxin) medications for treating the symptoms of Parkinson disease (although dopamine-increasing medications can sometimes increase libido, too) stomach acid blockers, such as the H2 blockers Tagamet, Zantac, and Pepcid some chemotherapy medications hormone medications, such as steroids, which can cause mood changes that affect sexual function hormone-blocking medications, such as those used in the treatment of breast and prostate cancers arthritis pain medications, such as ibuprofen (Motrin) opiate painkillers alcohol, nicotine, and other recreational drugs If a prescription drug causes sexual difficulty as a side effect, it may be possible to reduce the dose, take a "vacation" from using the drug, or switch to another drug in order to preserve sexual function. None of these decisions should be made, however, without consulting the doctor who prescribed the medication. Consult with your pharmacist or physician to explore whether any medications you are taking might have potential sexual side effects. ##### A Woman's Aging Body Menopause generally takes place between ages 35 and 55. During this process, the ovaries cease to produce eggs, and, more important, the production of the two sex hormones, estrogen and progesterone, declines to a very low level.
On three separate visits, your doctor should measure your blood pressure while you are relaxed and not talking, at least twice on each visit and at least once on both arms.DO YOU HAVE HIGH BLOOD PRESSURE?In order to get a complete picture, your doctor will have to do specific tests and will have to see you regularly.On the other hand, evidence from studies of both experimental animals and human beings indicates that even if your blood vessels have become so damaged that your blood pressure can't come down, this program can still extend your life. So stick with the program even if your blood pressure doesn't come down. After all, what you really care about is your sense of wellbeing and your living a long, healthy life. > > You _can_ reload the dice; you can change the odds of your suffering or dying from high blood pressure. > > You are the one who is ultimately responsible for your own health. To keep on top of this program, you should monitor your own progress, using the chart in Part Four. CHAPTER 9 Step One: See Your Doctor The very first step you should take is to see your doctor. Please do not get involved with the other steps of this program before you do this. The results could be disastrous. Your doctor needs to examine you to verify that you do indeed have high blood pressure, and if you do, to determine just what type of high blood pressure it is. Then, if certain types of hypertension are ruled out, your doctor should do the following: * Advise you about any changes in whatever drugs you may currently be taking. * Evaluate your risk of coronary artery disease to determine the type and amount of exercise that is safe or you. * Monitor your progress with our program as a whole. GET A COMPLETE PHYSICAL EXAM Get a complete physical examination. Your doctor should carefully evaluate your blood pressure and test for other specific disease conditions that may cause high blood pressure. In order to get a complete picture, your doctor will have to do specific tests and will have to see you regularly. DO YOU HAVE HIGH BLOOD PRESSURE? On three separate visits, your doctor should measure your blood pressure while you are relaxed and not talking, at least twice on each visit and at least once on both arms.Because of this, a 1986 editorial in the journal _Hypertension_ recommended that if the initial diastolic pressure is above 90 mm Hg, the blood pressure should be remeasured on at least two more occasions during the next four weeks.If during this time the diastolic blood pressure falls below 90 mm Hg, the recommendation is that further measurements be made at three-month intervals for a year.
In people at risk for familial pancreatic cancer, routine endoscopy can be used to monitor changes in pancreatic tissue.Because COX-2 plays a role in inflammation and mediates tumour growth and development, it is a valuable target for the development of drugs used in the prevention and treatment of several cancers, including breast cancer, colorectal cancer, and pancreatic cancer.Chemotherapy is generally used when pancreatic cancers have spread to distant organs and may be required so that as many cancer cells as possible can be sought out and destroyed. Endocrine or islet cell tumours may be treated with hormone therapy, in which specific hormones are used to stop or slow the growth of the cancer in the endocrine cells. Targeted drug therapies that block cellular processes driving cancer cell proliferation have been used in combination with chemotherapy in some pancreatic cancer patients. For example, a drug called erlotinib (Tarceva) blocks the activity of a kinase (a type of enzyme) associated with the epidermal growth factor receptor (EGFR), which stimulates unregulated cell division when mutated in cancer cells. When erlotinib is given in combination with the chemotherapeutic agent gemcitabine (Gemzar), an antimetabolite that inhibits the synthesis of genetic material in dividing cells, patient survival is improved, although only modestly. Several other targeted drugs such as cetuximab (Erbitux), a monoclonal antibody that binds to EGFR and thus prevents kinase activation and cell division, are being developed and tested in clinical trials for pancreatic cancer. In most cases, pancreatic cancer cannot be completely prevented, but risk can be decreased by reducing or eliminating cigarette smoking and following a diet low in animal products and high in fruits and vegetables. Researchers are also investigating anti-inflammatory therapeutic agents that inhibit an enzyme called cyclooxygenase-2 (COX-2). Because COX-2 plays a role in inflammation and mediates tumour growth and development, it is a valuable target for the development of drugs used in the prevention and treatment of several cancers, including breast cancer, colorectal cancer, and pancreatic cancer. In people at risk for familial pancreatic cancer, routine endoscopy can be used to monitor changes in pancreatic tissue.## ## CONCLUSION The digestive system is relatively simple in anatomic terms—it is a tube through which food passes and is broken down into useful components.The physical and chemical processes that underlie the passage of food and the extraction and absorption of nutrients are relatively recent discoveries, having been made primarily in the 20th century.
The signal is the same as in the spleen.There is a 15 mm sized lesion (arrow) in the tail of the pancreas that has higher signal than the pancreas.(a) T2W haste.12.3 Accessory spleen within the pancreatic tail.This indicates that this mass too is an accessory spleen Fig.(e) Same as (d) reveals RES uptake in the other mass.If torsion of such a (long) vascular pedicle occurs, this may lead to occlusion of the vessels with subsequent infarction of the accessory spleen (Fig. 12.2). They may be mistaken for tumors or large glands. Very rarely an accessory spleen is located within the pancreas and may then be misinterpreted as a pancreatic tumor leading to laparotomy and resection (Fig. 12.3). When an accessory spleen is suspected, the most important diagnostic criterion is to identify its complete similarity with the ordinary spleen. When still in doubt, nuclear scintigraphy with technetium-99m sulfocolloid is useful. Fig. 12.2 Wandering accessory spleen. The patient had been splenectomized a few years earlier due to a lacerated spleen after blunt abdominal trauma. He now presented with abdominal pain. An MR enterography was performed showing normal small bowel. (a) T2 haste. There is a 3 cm solid mass (arrow) in the left lower quadrant. (b) TIW fat sat after intravenous injection of gadolinium. There is an irregular contrast medium uptake in the mass. The mass is supplied with long vessels from the left upper quadrant (small arrows). It was assumed that these vessels were prone to torsion and that the irregular contrast medium uptake was due to intermittent ischemia causing fibrosis in the mass. (c) T1W fat sat after intravenous injection of gadolinium reveals a second mass (arrow) in the left upper quadrant close to the left kidney with homogeneous contrast medium uptake. (d) Technetium scintigraphy using an albumin colloid shows uptake in the reticuloendothelial system (RES). This reveals the uptake in the accessory spleen located close to the left kidney. (e) Same as (d) reveals RES uptake in the other mass. This indicates that this mass too is an accessory spleen Fig. 12.3 Accessory spleen within the pancreatic tail. (a) T2W haste. There is a 15 mm sized lesion (arrow) in the tail of the pancreas that has higher signal than the pancreas. The signal is the same as in the spleen.On fat sat sequence the accessory spleen (arrow) has lower signal than the surrounding pancreatic tissue.(c) Surgical specimen shows the accessory spleen (*) within the resected tail of the pancreas.(courtesy of Katarina Håkansson, MD, Kalmar, Sweden) ## 12.5 Splenic Cysts Splenic cysts are often found incidentally (Fig.12.4).They may be secondary to trauma infarction or infection.
Huge, heavily loaded commercial barges, with very limited ability to manoeuvre, were bearing down on us.This canal is a major shipping route and it was extremely busy.I vividly remember the time I was sailing a small yacht up the Ijmuiden canal to Amsterdam and debris became entangled around our propeller, rendering the engine useless.This is caused by the 'fight or flight' hormone adrenaline, which primes the body to cope with an adverse situation by increasing both the rate and the force of contraction. It does so by opening additional calcium channels in heart cell membranes. This speeds up the rate at which the sinus node cells fire, so that the heart rate is increased, and it also boosts the amount of calcium that is released from the intracellular stores and thereby enhances the strength of contraction. Adrenaline is made by the adrenal glands that lie just above the kidney, and is secreted into the bloodstream in response to stress or exercise; a related substance with a similar action, noradrenaline, is released from nerves that innervate the heart. Although an increased heart rate during exercise is essential in order to ensure that the limb muscles are adequately supplied with fuel and oxygen, too fast a rate is deleterious. This is because the heart muscles themselves cannot be supplied with oxygen fast enough. The consequence is angina – a severe incapacitating chest pain that can extend down the left arm. Angina is more easily precipitated in people whose coronary blood vessels are narrowed as a result of atherosclerotic plaques (fatty deposits in the vessel walls). Consequently, an exercise test, which increases the heart rate and thus its oxygen demand, is often used to test the health of the coronary vessels. Angina is not only brought on by exertion: it can also be triggered by anger, excitement or emotional stress. I vividly remember the time I was sailing a small yacht up the Ijmuiden canal to Amsterdam and debris became entangled around our propeller, rendering the engine useless. This canal is a major shipping route and it was extremely busy. Huge, heavily loaded commercial barges, with very limited ability to manoeuvre, were bearing down on us.He retired below deck to crush a glass capsule of amyl nitrate (nitroglycerin) under his nose and inhale the vapour.This eased his pain by dilating the coronary vessels and increasing blood flow to his heart.Nitroglycerin acts by releasing a natural gas called nitric oxide, which stimulates the production of a chemical called cyclic GMP that causes blood vessels to relax.
15.10 and discussion that follows).It is important to note that Purkinje cell axons arising from the cerebellar cortex of the vermis, paravermal zone, or the hemispheric zone overlying the deep cerebellar nuclei project to the corresponding deep cerebellar nucleus (see Fig. The Purkinje cell axons always form _inhibitory synapses_.The trigeminal nerve nuclei also send projections (trigeminocerebellar fibers) relaying sensory input from orofacial structures and the stretch receptors of the muscles of mastication. These fibers pass into the cerebellum via the inferior cerebellar peduncle where they terminate as mossy fibers. ## Efferents (Output) from the Cerebellum > Efferent fibers from the cerebellum arise from the Purkinje cells of the cerebellar cortex and the cells of the deep cerebellar nuclei Efferent fibers from the cerebellum arise from two sources (see Fig. 15.9): 1. Purkinje cells , which constitute the ultimate integrating terminal within the cerebellar cortex. 2. Cells of the deep cerebellar nuclei. These nuclei house the nerve cells whose _axons form the principal cerebellar output_ (see discussion that follows). ### Efferent Fibers from Purkinje Cells > The majority of the Purkinje cell axons terminate locally in the deep cerebellar nuclei. A small extracerebellar projection terminates in the vestibular nuclei The Purkinje cell axons of the cerebellar cortex have two destinations. The only extracerebellar destination is as follows: the axons of the Purkinje cells located in the cortex of the vestibulocerebellum go past the deep cerebellar nuclei, exit the cerebellum, to end in the vestibular nuclei. The majority of Purkinje cell axons, though, terminate locally at their main targets (destination) – the deep cerebellar nuclei. The Purkinje cell axons always form _inhibitory synapses_. It is important to note that Purkinje cell axons arising from the cerebellar cortex of the vermis, paravermal zone, or the hemispheric zone overlying the deep cerebellar nuclei project to the corresponding deep cerebellar nucleus (see Fig. 15.10 and discussion that follows).#### Output from the flocculonodular lobe to the Vestibular Nuclei > Purkinje cells of the flocculonodular lobe project to the vestibular nuclei Purkinje cell axons arising from the cortex of the flocculonodular lobe (vestibulocerebellum) form a small extracerebellar projection as they exit the cerebellum via the juxtarestiform body to terminate in the vestibular nuclei** (see Fig.
water purification, emergency, methods of purifying unclean water for drinking purposes in emergencies.The contamination may result in unsafe and/or unsanitary water supplies.water pollution, the contamination of lakes, rivers, and streams by industrial or community sources of substances.See cottonmouth.water moccasin, a snake.See waterbed.water mattress.It requires immediate emergency treatment, hospitalization, and intensive care. Emergency treatment includes vasopressor drugs, IV fluids, plasma, and oxygen. No sedatives or narcotics are given. Specific treatment is intensive antibiotic therapy, given parenterally and continued for several days after symptoms subside. Care includes close observation and adequate provision of fluids and nutrients. water hemlock, (Cicuta douglasii) a highly poisonous plant commonly found in wet meadows and pastures and along the banks of streams. Water hemlock (Dobbs, 2009) watering can perineum (WCP), (Informal) a perineum with numerous fistulas leaking urine owing to abscesses or sometimes strictures of the urethra. water-in-oil emulsion, a mixture in which water or aqueous solution is the dispersed phase and oil or an oily substance is the continuous phase, resulting in water droplets dispersed in oil. water intoxication, an increase in the volume of free water in the body, resulting in dilutional hyponatremia. Common causes are excessive ingestion of water, increased infusions of hypotonic IV solutions, or excess secretions of antidiuretic hormone. Clinical manifestations are abdominal cramps, nausea, vomiting, lethargy, and dizziness. It can potentially lead to convulsions and coma. See also syndrome of inappropriate antidiuretic hormone secretion. water mattress. See waterbed. water moccasin, a snake. See cottonmouth. water pollution, the contamination of lakes, rivers, and streams by industrial or community sources of substances. The contamination may result in unsafe and/or unsanitary water supplies. water purification, emergency, methods of purifying unclean water for drinking purposes in emergencies.When purifying chemicals are added, they should be thoroughly mixed with the water, and the mixture should be allowed to stand for 30 minutes.Also called emergency preparation of safe drinking water.waters.(Nontechnical) See amniotic fluid.watershed infarct /wô″tərshed/ , an area of necrosis in the brain caused by an insufficiency of blood where the distributions of cerebral arteries overlap.
The immune system reaction to oral microflora that are deleterious to wound healing coupled with compromised osseous integrity and the lack of osteoclastic remodeling may be particularly devastating for the development of clinical ONJ.A multi‐step trajectory to clinical ONJ likely includes (i) underlying osseous compromise; (ii) trauma exposing the osseous tissue, and (iii) infection. There are several studies that suggest antiresorptive treatment may lead to areas of bone necrosis and/or altered biomechanical integrity long before clinical ONJ presents [8–10]. Notably, empty osteocyte lacunae are found in cortical bone after long‐term treatment with zoledronate in the absence of clinical ONJ. This is one of the underlying premises supporting the categorization of stage 0 ONJ [4], yet similar findings have not been convincingly verified in humans. Suppression of bone turnover, through inhibition of osteoclastic activity, is at the core of the underlying necrosis and altered biomechanical integrity; however, suppression of bone turnover alone is not sufficient to cause ONJ. It is likely that inhibition of osteoclastic function compromises the ability of the alveolar bone to respond to extrinsic local factors and maintain a normal homeostasis [11]. Trauma features prominently in the pathogenesis of ONJ with 46% to 79% of ONJ patients having dentoalveolar trauma preceding ONJ clinical presentation, and specifically dental extraction [12]. Spontaneous incidence of ONJ may also be attributed to the trauma associated with normal masticatory function or dental prosthetic devices coupled with a very thin oral mucosa overlying the bone. Once the osseous tissue is exposed, infection is likely a key factor [13]. More than 750 species of bacteria are found in the oral cavity and comprise complex communities existing primarily in biofilms on the surfaces of teeth, prostheses, gingiva, and tongue [14]. The immune system reaction to oral microflora that are deleterious to wound healing coupled with compromised osseous integrity and the lack of osteoclastic remodeling may be particularly devastating for the development of clinical ONJ.Recent evidence suggests that bisphosphonate therapy results in significant differences in the expression of genes regulating immune function, barrier functions, tissue remodeling, and lymphangiogenesis [16, 17].
As a result, more water is _reabsorbed_ by these tubules and returned to the blood, decreasing blood osmolarity by making it more dilute.ADH acts directly on kidney tubules and collecting ducts, making them more permeable to water.28-year-old female cousin who has type 1 diabetes mellitus C. 72-year-old grandmother who is 15 pounds overweight D. 72-year-old grandfather who takes 81 mg of aspirin daily ## Hormonal Regulation of Fluid Balance The endocrine system helps control fluid and electrolyte balance. Three hormones that help control these critical balances are aldosterone, antidiuretic hormone (ADH), and natriuretic peptide (NP). _Aldosterone_ is a hormone secreted by the adrenal cortex whenever sodium levels in the extracellular fluid (ECF) are decreased. Aldosterone prevents both water and sodium loss. When aldosterone is secreted, it acts on the kidney nephrons, triggering them to reabsorb sodium and water from the urine back into the blood. This action increases blood osmolarity and blood volume. Aldosterone prevents excessive kidney excretion of sodium. It also helps prevent blood potassium levels from becoming too high. _Antidiuretic hormone (ADH)_ , or vasopressin, is produced in the brain and stored in the posterior pituitary gland. ADH release from the posterior pituitary gland is controlled by the hypothalamus in response to changes in blood osmolarity. The hypothalamus contains specialized cells (osmoreceptors) that are sensitive to changes in blood osmolarity. Increased blood osmolarity, especially an increase in the level of plasma sodium, results in a slight shrinkage of these cells and triggers ADH release from the posterior pituitary gland. ADH acts directly on kidney tubules and collecting ducts, making them more permeable to water. As a result, more water is _reabsorbed_ by these tubules and returned to the blood, decreasing blood osmolarity by making it more dilute.Less water is then reabsorbed, and more is lost from the body in the urine.As a result, the amount of water in the extracellular fluid (ECF) decreases, bringing osmolarity up to normal._Natriuretic peptides (NPs)_ are hormones secreted by special cells that line the atria of the heart (atrial natriuretic peptide [ANP]) and the ventricles of the heart.
A weak or uncoordinated tongue can result in early entry of a liquid or food bolus into the pharynx and an open airway.In addition, there must be adequate sensation to detect the bolus as it moves through the mouth and pharynx to assist with triggering the swallowing and maintaining airway protection.The airway status of the child is an important consideration and a pharyngeal flap is generally contra-indicated when it is compromised in conditions like sleep apnea or in laryngeal anomalies. Indications for referral to a speech pathologist for children with resonance disorders are summarized in Fig. 5. Fig. 5 Referral considerations to a speech language pathologist for resonance problems ## 3.5 Feeding and Swallowing ### 3.5.1 Developmental Nature of Feeding and Swallowing in Children Children develop feeding abilities and swallowing coordination, much like they acquire other developmental milestones. Feeding milestones start with sucking and progress to cup drinking, spoon feeding, and chewable table foods over the first year of life. Feeding is differentiated from swallowing primarily by voluntary versus involuntary motor control. Feeding involves the process of taking food into the mouth and preparing the food to be swallowed in a coordinated fashion. This is also considered the oral preparatory stage of the swallow. Once food reaches the base of the tongue and begins to propel into the hypopharynx, the reflexive nature of swallowing comes into play. The swallow transports the food or liquid bolus through the pharynx, into the esophagus, and is completed when the bolus moves into the stomach. Coordinated swallowing requires sequencing breathing with swallowing in conjunction with controlled movement of the liquid or food from the mouth to the pharynx (39). In addition, there must be adequate sensation to detect the bolus as it moves through the mouth and pharynx to assist with triggering the swallowing and maintaining airway protection. A weak or uncoordinated tongue can result in early entry of a liquid or food bolus into the pharynx and an open airway.Also, when the sensory system is muted, such as when GERD is present, there can be a compromise of swallow coordination and an aspiration risk.### 3.5.2 Disordered Feeding and Swallowing Typical concerns with feeding and swallowing involve efficiency, coordination, and safety.
UCSF developed a 3-D convolutional neural network for chest CT in more than 1,600 patients, of whom 320 had confirmed lung cancer.Multiple reports from academic medical centers have shown the power of deep learning to sort through a variety of scans, including CT scans for liver and lung nodules and bone age, adding to the expanding evidence that machines can accomplish accurate diagnostic work.A Mayo Clinic team showed that the texture of brain MRI images could predict a particular genomic anomaly, specifically 1p/19q co-deletion, that's relevant to surviving certain types of brain cancer. Similarly, using deep learning algorithms to read MRI scans of patients with colon cancer could reveal whether a patient has a critical tumor-gene mutation, known as KRAS, awareness of which should significantly influence treatment decisions. Machine learning of mammography images from more than 1,000 patients, coupled with biopsy results indicating a high risk of cancer, showed that more than 30 percent of breast surgeries could be avoided. Applying deep learning to X-ray images of hip fractures can lead to diagnoses as accurate as those derived from the more advanced—and so more expensive—image techniques, including MRI, nuclear bone scans, or CT, which doctors otherwise turn to when analyses of X-rays give uncertain results. Using a convolutional neural network with 172 layers, trained with over 6,000 X-rays (with a total of 1,434,176 parameters), and validated in more than a thousand patients, the accuracy of the algorithm was shown to be greater than 99 percent, quite comparable to performance by experienced radiologists. Multiple reports from academic medical centers have shown the power of deep learning to sort through a variety of scans, including CT scans for liver and lung nodules and bone age, adding to the expanding evidence that machines can accomplish accurate diagnostic work. UCSF developed a 3-D convolutional neural network for chest CT in more than 1,600 patients, of whom 320 had confirmed lung cancer.Geisinger Health in Pennsylvania used nearly 40,000 head CT scans to show high accuracy of machine diagnosis of brain hemorrhage.Radboud University in the Netherlands found that a deep neural network trained on more than 1,400 digital mammograms gave similarly accurate readings as those performed by twenty-three radiologists.
If rectal preparations are not available, many oral formulations can be given rectally if the patient is unable to take medications by mouth.Analgesics that are available as rectal suppositories include hydromorphone, oxymorphone, morphine and paracetamol.Although morphine is commonly administered to patients with cancer pain via the sublingual route, little of the drug is actually absorbed from the sublingual tissue. Instead, most of the drug is dissolved in saliva and swallowed, making its metabolism the same as that of oral morphine. Fentanyl citrate is administered transmucosally. The fentanyl dose is embedded in a flavoured lozenge on a stick. The drug is absorbed by the permeable buccal mucosa after being rubbed actively over it (not sucked as a lollipop), allowing the drug to enter the bloodstream and travel directly to the CNS. Pain relief typically occurs within 5–7 minutes after administration. This agent should be used only for patients who are already receiving and who are tolerant to opioid therapy. An oromucosal spray delivery of cannabinoid extract (Sativex) shows promise in treating chronic, neuropathic pain conditions. It has been approved in Canada for the treatment of pain in multiple sclerosis. ##### Intranasal route Intranasal administration allows delivery of medication to highly vascular mucosa and avoids the first-pass effect. Butorphanol is one of the few intranasal analgesics currently available. This drug is indicated for acute headache and other intense, recurrent types of pain. Intranasal delivery of other opioids is being investigated. ##### Rectal route The rectal route is often overlooked but is particularly useful when the patient cannot take an analgesic by mouth, such as those patients with severe nausea and vomiting. Analgesics that are available as rectal suppositories include hydromorphone, oxymorphone, morphine and paracetamol. If rectal preparations are not available, many oral formulations can be given rectally if the patient is unable to take medications by mouth.This delivery system is useful for the patient who cannot tolerate oral analgesic drugs.Absorption from the patch is slow and it takes 12–17 hours to reach full effect with the first application.Therefore, transdermal fentanyl is not suitable for rapid dose titration, but it can be effective if the patient's pain is stable and the dose required to control it is known.
spinales) or from the trunci plexus brachialis in the regio cervicalis lateralis.anteriores of the nn.The supraclavicular branches of the plexus brachialis arise directly from the radices plexus brachialis (rr.28.12_ Supraclavicular branches Right shoulder.### Pars Supraclavicularis & Fasciculus Posterior _Fig.28.11_ Plexus brachialis Right side, anterior view._Fig.Lymph from the upper limb and mamma drains to the nll. axillares. The superficial lymphatics of the upper limb lie in the subcutaneous tissue, while the deep lymphatics accompany the arteries and deep veins. Numerous anastomoses exist between the two systems. _Fig. 28.8_ Lymphatics of the upper limb Right limb. _Fig. 28.9_ Lymphatic drainage of the hand Right hand, radial view. Most of the hand drains to the nll. axillares via nll. cubitales. However, the pollex, index, and dorsum manus drain directly. _Fig. 28.10_ Nodi lymphoidei axillares Right side, anterior view. For surgical purposes, the nll. axillares are divided into three levels with respect to their relationship with the m. pectoralis minor: lateral (level I), posterior (level II), or medial (level III). They have major clinical importance in breast cancer (see p. 77 ). ### Nerves of the Upper Limb: Plexus Brachialis Almost all muscles in the upper limb are innervated by the plexus brachialis, which arises from segmenta C5–T1 medullae spinalis. The rr. anteriores of the nn. spinales give off direct branches (pars supraclavicularis of the plexus brachialis) and merge to form three trunci, six divisiones (three anteriores and three posteriores), and three fasciculi. The pars infraclavicularis of the plexus brachialis consists of short branches that arise directly from the fasciculi and long (terminal) branches that traverse the limb. _Fig. 28.11_ Plexus brachialis Right side, anterior view. ### Pars Supraclavicularis & Fasciculus Posterior _Fig. 28.12_ Supraclavicular branches Right shoulder. The supraclavicular branches of the plexus brachialis arise directly from the radices plexus brachialis (rr. anteriores of the nn. spinales) or from the trunci plexus brachialis in the regio cervicalis lateralis.rhomboidei major et minor N. suprascapularis \| C4–C6 \| M. supraspinatus M. infraspinatus N. subclavius \| C5–C6 \| M. subclavius N. thoracicus longus \| C5–C7 \| M. serratus anterior _Fig.28.13_ Fasciculus posterior plexus brachialis: Short branches Right shoulder.
###### Ethnicity There is a racial predilection, being 10 times more common in white than in black children.###### Sex There is no sex predilection; although male preponderance was much higher (male : female 12 : 1) in children with multiple skin lesions [4].Lesions may occur at birth and very rarely in adults [3].Clinically, they can be further stratified into two major groups: (i) those that predominantly affect the skin but may have a systemic component (e.g. juvenile xanthogranuloma, reticulohistiocytoma); and (ii) those such as Erdheim–Chester disease and sinus histiocytosis with massive lymphadenopathy (Rosai–Dorfman disease) that are primarily systemic diseases where the skin may be involved. ## DENDRITIC CELL ORIGIN #### Disorders with mainly skin involvement with/without a systemic component ### Juvenile xanthogranuloma ###### Definition and nomenclature Juvenile xanthogramuloma (JXG) is a benign proliferative disorder of histiocytes occurring in early infancy and childhood that spontaneously regresses. * * * Synonyms and inclusions * Naevoxanthoendothelioma * Xanthoma multiplex * Juvenile xanthoma * Multiple eruptive xanthoma in infancy * Congenital xanthoma tuberosum * Xanthoma naeviforme * Juvenile giant cell granuloma * * * ###### Epidemiology ###### Incidence and prevalence Juvenile xanthogranuloma is the commonest of the non-LCH, non-HLH histiocytic disorders. The incidence of JXG is unknown and is likely underestimated due to its natural history of spontaneous involution. ###### Age JXG occurs predominantly during infancy with median ages at onset ranging from 5 months to 1 year as reported in two large series [1, 2]. Lesions may occur at birth and very rarely in adults [3]. ###### Sex There is no sex predilection; although male preponderance was much higher (male : female 12 : 1) in children with multiple skin lesions [4]. ###### Ethnicity There is a racial predilection, being 10 times more common in white than in black children.Patients with JXG and NF1 have a significantly higher risk of developing myeloid leukaemia than normal [6].###### Pathophysiology ###### Pathology JXG is characterized by a dense infiltrate of small histiocytes in the dermis, which stain positively for factor XIIIa, CD68, CD163, CD14 and fascin (Figure 136.8a, b).Stains for S100 and CD1a are negative.
* Topical application of THC was found to decrease allergic inflammation in a model of contact dermatitis (eczema).* Synthetic topical cannabinoids relieved pain experienced by patients suffering with post-herpetic neuralgia.* Five major phytocannabinoids showed potent activity against MRSA.* Topical extracts were shown to have anti-inflammatory properties in laboratory animal experiments.Pediatric patients and patients with disabilities may not be able to cooperate with certain delivery methods. I have found that tinctures work well for these patients as they can be taken by mouth, hidden in food, or even given through a gastrostomy tube. Concentrated tinctures are also advised as a larger milligram dose in a smaller volume is easier for patient compliance. ### Dermal/Topical Cannabis can be made into ointments, salves, lotions and alcohol preparations and applied to the skin to treat local pain (such as in arthritis) or rashes (such as psoriasis or eczema). These preparations have been used in India and Latin America for hundreds of years with reports of significant pain relief, especially for joint pain and for relief of certain skin rashes. There is evidence that topical cannabis is effective treatment for skin infections such as MRSA, a resistant type of bacterial skin infection. Psychoactivity with topical cannabis use is rare. Preparations are currently available that are THC-rich, CBD-rich or a combination of both cannabinoids. A number of scientific studies researching the effects of topical preparations of cannabis demonstrated the following: * Topical applications of THC helped mice heal faster from skin allergies. * Topical extracts were shown to have anti-inflammatory properties in laboratory animal experiments. * Five major phytocannabinoids showed potent activity against MRSA. * Synthetic topical cannabinoids relieved pain experienced by patients suffering with post-herpetic neuralgia. * Topical application of THC was found to decrease allergic inflammation in a model of contact dermatitis (eczema).Many of my patients use topical preparations successfully for arthritis, especially on the smaller joints, such as hands, feet, elbows, and knees.Some patients report relief of bursitis pain, plantar fasciitis pain and scar tissue pain.A few patients even find relief of neck and low back pain and a few report that nerve pain responds as well.
■ Continued frequency of home visits depends on patient condition, degree of independence with infusion care, and ongoing needs.This may involve two visits per day to coincide with initiating and discontinuing the infusion.The most commonly administered 118isotonic fluids include 0.9% sodium chloride and 5% dextrose in water. In an older study that included 30 long-term care residents from 24 to 90 years of age, who received SC infusions from 1 to 2 days for dehydration, all infusions were completed without adverse effects except for one incidence of local edema at the site (Walsh, 2005). PATIENT SELECTION CONSIDERATIONS * * * ■ The patient and family are motivated and willing and capable of participating in infusion management. ■ The patient is clinically stable. The patient is exhibiting signs of mild to moderate dehydration; treatment of severe dehydration would not be appropriate in the home. The patient is at known risk for dehydration (e.g., expected side effects with chemotherapy, and hyperemesis gravidarum). ■ An appropriate infusion route is selected. Short peripheral IV catheters, midline peripheral catheters, or PICCs are common VADs that may be used for fluid replacement. SC route is appropriate for older adults or other adults with limited venous access and no existing VAD. ■ The home environment is safe, clean, with adequate refrigeration space, and the patient has ready access to a telephone. ■ Reimbursement is verified. Private third-party payers vary in coverage. COMPREHENSIVE CARE, ASSESSMENT, AND MONITORING * * * Plan for Home Care and Visit Frequency ■ Schedule home visits to coincide with the time of fluid administration with the infusion pharmacy and the patient. This may involve two visits per day to coincide with initiating and discontinuing the infusion. ■ Continued frequency of home visits depends on patient condition, degree of independence with infusion care, and ongoing needs.The infusion rate for fluid replacement varies widely.For patients without any cardiac or other conditions that increase the risk of fluid overload, the infusion rate may be high (e.g., infuse a liter of fluid over 3 to 4 hours).For older adults and others at risk, slow infusion rates are appropriate.
The Answer is 1 and 2 The nurse is taking care of an elderly client with left-sided heart failure.11.The child should not be totally immobile because it can lead to post-op respiratory complications.4.Repositioning is a comfort intervention.CORRECT: Elevating the extremity and applying an ice pack will help to reduce swelling and may reduce pain.3.The nurse knows that this client is at risk for autonomic dysreflexia. Which of the following measures should this nurse take to keep the client comfortable, manage his elimination needs, and prevent common causes of autonomic dysreflexia? _Category:_ Elimination 1. Turning is necessary to prevent decubitus ulcers and promote comfort, but it does not necessarily prevent an increase in blood pressure as seen with autonomic dysreflexia. 2. Sleeping 8–10 hours is not related to autonomic dysreflexia. 3. Offering fluids is a nursing measure but may not be related to autonomic dysreflexia because a client with a spinal cord injury may have a fluid restriction to help control blood pressure. 4. CORRECT: Bladder distension and bowel impaction can result in autonomic dysreflexia, causing a critical increase in blood pressure. 10. The Answer is 3 The nurse is taking care of a child after an open reduction of the radius and ulna of her right arm. The child is now immobilized in a plaster cast splint reinforced with an Ace wrap. Which of the following non-pharmacological nursing interventions will promote comfort for this child? _Category:_ Non-pharmacological comfort interventions; Mobility/immobility 1. Heat would not be appropriate, because it could cause, rather than reduce, swelling. 2. The cast should be elevated for the first 24–48 hours and not be left flat on the mattress. 3. CORRECT: Elevating the extremity and applying an ice pack will help to reduce swelling and may reduce pain. Repositioning is a comfort intervention. 4. The child should not be totally immobile because it can lead to post-op respiratory complications. 11. The Answer is 1 and 2 The nurse is taking care of an elderly client with left-sided heart failure.Select all that apply. _Category:_ Rest and sleep 1.CORRECT: Taking short walks may provide distraction and increase mobility, circulation, and overall well-being if tolerated.2.CORRECT: Allowing the client to sit in an armchair makes it easier to breathe and is a safe alternative to an armless chair.
In contrast with these 2 studies, the investigators of the CARE-2 study were unable to confirm that sevelamer and calcium-acetate phosphate binders affect CAC progression differently and showed an approximate 30 % progression at the end of 1 year for both treatment arms [64].However, the changes in calcium score severity seen at 52 weeks were independent of the levels of LDL cholesterol, HDL cholesterol and C-reactive protein. Additionally, sevelamer therapy was accompanied by a simultaneous improvement in bone mineral density [59]. Interestingly, an inverse relationship between CAC and bone mineral density has also been observed in non-uremic individuals [60, 61] and suggests an interaction between bone and vascular health. Fig. 6.3 Extensive cardiovascular calcification in a patient suffering from end-stage renal disease. The soft tissues have been removed and only the calcified portion of the aorta and coronary arteries are shown. AA aortic arch, LAD left anterior descending coronary artery, CX circumflex coronary artery, RCA right coronary artery, TA thoracic aorta Fig. 6.4 Median percentage calcium score change for coronary arteries and aorta in end-stage renal disease patients randomized to 1-year treatment with sevelamer or calcium-based salts. The progression was significant for both coronary arteries and aorta only in the calcium salt treated patients [58] A second randomized study was performed with the same primary end-point of CAC progression in patients randomized to sevelamer or calcium-based phosphate binders within a few weeks of beginning hemodialysis [62]. At the end of 18 months of follow-up calcium treated patients again showed a significant 11-fold greater progression of CAC than sevelamer treated patients (p < 0.002). The secondary end point of this study was long-term mortality; at the end of 4.5 years of follow-up the mortality of calcium treated patients was double that of sevelamer treated subjects (hazard ratio: 3.2; p < 0.02) [63]. In contrast with these 2 studies, the investigators of the CARE-2 study were unable to confirm that sevelamer and calcium-acetate phosphate binders affect CAC progression differently and showed an approximate 30 % progression at the end of 1 year for both treatment arms [64].However, 80 % of the sevelamer treated patients also received statins and this may have caused CAC progression in both arms as shown in the general population (see above).Furthermore, the PTH level of sevelamer treated patients was double that of prior studies [58, 62], suggesting a very poor control of mineral metabolism.
C AUTION: In recent years, _Castanea dentata_ has been extensively damaged by an imported blight.Clinically: Extracts used for bleeding hemorrhoids, varicose veins, arteriosclerosis.Folk medicine: It is valued and used for arthritis, rheumatism, female bleeding, hemorrhoids, and chronic inflammation of the intestines.The chestnut is low in protein, high in carbohydrates and starch; contains minerals such as phosphate of potash, magnesia, some sodium, and iron. M EDICINAL PARTS: Leaves, inner bark. S OLVENTS: Boiling water, alcohol (partial solvent). B ODILY INFLUENCE: Mild sedative, astringent, tonic. U SES: Culpeper said the inner skin that contains the nut "is of so binding a quality that a scruple of it being taken by a man or ten grains by a child, soon stops any flux whatsoever." The green or dried leaves can be used, and it is considered a specific for whooping cough or nagging distressing coughs, controlling the paroxysm; and in frequent hiccups and other irritable and excitable conditions of the respiratory organs. Fevers, ague respond to the soothing of the mucous surfaces and the nervous system; acts as an antispasmodic. _Lobelia inflata_ (lobelia), and _Caulophyllum thalictroides_ (blue cohosh) are most successfully combined for the above mentioned. D OSE: 1 ounce to 1 pint of boiling water, infused for 15 minutes. A wineglassful three times a day, children half that amount. The fluid extract is convenient: dose 10 drops three times a day; 5 drops for children. H OMEOPATHIC CLINICAL: Tincture of leaves gathered in summer for diarrhea, whooping cough. R USSIAN EXPERIENCE: _Konsky cashtan_ (horse chestnut) does not grow wild but has long been cultivated in European Russia, middle Asia, and Caucasia. Folk medicine: It is valued and used for arthritis, rheumatism, female bleeding, hemorrhoids, and chronic inflammation of the intestines. Clinically: Extracts used for bleeding hemorrhoids, varicose veins, arteriosclerosis. C AUTION: In recent years, _Castanea dentata_ has been extensively damaged by an imported blight.CHICKWEED _Stellaria media_ C OMMON NAMES: Stitchwort, scarwort, satin flower, adder's mouth, starweed.F EATURES: There are about twenty-five species native and naturalized on the American continent.The Native Americans used native chickweed for many years but also adopted naturalized species.
It can be hypothesized that the control of body weight and composition depends on an axis with interrelated, and possibly self-controlled, components of food intake, metabolic rate, body fat stores and physical activity.2015).Key pathways of fetal programming include those mediated through glucocorticoids, with their vital role in developmental regulation of adipose tissue, appetite regulation and energy homeostasis regulated by the hypothalamus, and the neurohormones insulin and leptin influencing the actions of neuropeptides in the hypothalamic nuclei. A better understanding of these processes may provide opportunities for the prevention of obesity and improved public health. Keywords ObesityAdipose tissueNutritional programmingPregnancy nutritionBMIGrowthMetabolic syndrome Overweight and obesity are defined by abnormal or excessive fat accumulation which may impair health and obesity and have significant repercussions on health, being related to various cardiovascular causes of mortality, cancer, Type 2 diabetes, musculoskeletal disorders, work disability and sleep apnoea (Visscher and Seidell 2001). Obesity, once established, is infamously difficult to reverse and, therefore, the solution to obesity related health problems may lie in its prevention. Traditionally, obesity has been thought to result from an imbalance of energy intake and expenditure, resulting if the intake of energy exceeds its expenditure over a significant period of time. It is intriguing to consider why energy balance occurs in some individuals despite the same obesogenic environmental conditions prevalent in the developed world which in others leads to obesity (Ojha et al. 2015). It can be hypothesized that the control of body weight and composition depends on an axis with interrelated, and possibly self-controlled, components of food intake, metabolic rate, body fat stores and physical activity.Although the energy balance equation between food intake and energy expenditure may appear deceptively simple, it seems that these variables have a much more complex relationship (Budge et al.2005).Moreover, recently there is increasing evidence that factors in the periconceptional period, in utero and in early neonatal life may determine later obesity.
Since this process was not affected by inhibitors of ABC transporters (Cyclosporin A, MK571, PSC-833, GF120918, Ko143), the authors concluded that hesperetin could move transcellularly by passive diffusion.145 However, this conclusion should be supported by the experimental demonstration that influx transporters were indeed not involved.Since the permeability of both quercetin and naringenin was higher in the basolateral-to-apical than in the opposite direction, it was reasonable to assume the involvement of a carrier-mediated transport efflux system. Using specific ABC inhibitors, it has been shown that the quercetin efflux is mediated by MRP2 but not by P-gp. Naringenin, on the other hand, was both an MRP2 and a P-gp substrate. Figure 37.2 Scheme showing extensive distribution of cell membrane transporters as potential routes for flavonoid cell transport, in both the central compartment and different peripheral tissues (brain, kidney, liver, intestine, and vascular endothelium). ABC transporters are indicated by pentagons ( ); solute carriers by triangles ( ) (one direction transport), or diamonds (♦) (bidirectional transport). BCRP, breast cancer-resistant protein; BTL, bilitranslocase; GLUT1, glucose transporter 1; MCT1, monocarboxylate transporter 1; MRPs, multidrug-resistance-related proteins; OATs, organic anion transporters; OATPs, organic anion transporting proteins; P–gP, P-glycoprotein; SGLT1, sodium/glucose co-transporter 1. Another similar study addressed the metabolism and transport of hesperetin (the aglycone of hesperidin, the major flavanone present in sweet oranges and orange juice), and its metabolites across the intestinal epithelium, using the same Caco-2 cell monolayer model.145 Apically applied hesperetin permeated the monolayer and was found in the basolateral compartment. Since this process was not affected by inhibitors of ABC transporters (Cyclosporin A, MK571, PSC-833, GF120918, Ko143), the authors concluded that hesperetin could move transcellularly by passive diffusion.145 However, this conclusion should be supported by the experimental demonstration that influx transporters were indeed not involved.
The presence of APA interferes with hemostatic mechanisms and can interfere with anticoagulants.• Newer oral anticoagulants (dabigatran, apixaban, and rivaroxaban) may be alternatives to warfarin with few drug interactions and no need for monitoring.• Danaparoid, fondaparinux, and argatroban can be considered in APS patients with heparin-induced thrombocytopenia.Test Interpretation Usual finding is thrombosis and minimal vascular or perivascular inflammation: • Acute changes: capillary congestion and noninflammatory fibrin thrombi • Chronic changes: ischemic hypoperfusion, atrophy, and fibrosis TREATMENT MEDICATION First Line • Primary thromboprophylaxis: Low-dose aspirin is indicated in asymptomatic carriers of APAs with SLE and in pregnancy. It may be considered in other asymptomatic carriers. Hydroxychloroquine is recommended in all antiphospholipid-positive SLE patients. • Secondary thromboprophylaxis: All symptomatic, nonpregnant patients with APS need indefinite anticoagulation. The target INR depends on the severity and type of thrombosis: – Venous thrombosis (first episode): warfarin with target INR of 2.0 to 3.0 – Arterial thrombosis or recurrent venous thrombosis despite anticoagulation: warfarin with target INR 3.0 to 4.0 – LMWH and fondaparinux are alternatives. • New oral anticoagulants such as rivaroxaban, apixaban, and dabigatran; all have been approved for treatment of DVT/PE; studies in APS are lacking; a prospective randomized controlled trial of warfarin versus rivaroxaban in patients with thrombotic APS and with a target INR of 2.5 is underway. – Rituximab may be an option in severe cases, possibly in those with hematologic and microthrombotic/microangiopathic manifestations (3,4)[B]. • Danaparoid, fondaparinux, and argatroban can be considered in APS patients with heparin-induced thrombocytopenia. • Newer oral anticoagulants (dabigatran, apixaban, and rivaroxaban) may be alternatives to warfarin with few drug interactions and no need for monitoring. The presence of APA interferes with hemostatic mechanisms and can interfere with anticoagulants.• Statins can decrease proinflammatory and prothrombotic state in APS.They are not recommended in the absence of hyperlipidemia; some APA-positive patients with recurrent thrombosis while adequately anticoagulated may benefit from statin therapy.• B-cell inhibition may help in recalcitrant APS cases.• Complement inhibition may be useful in refractory cases, but utility is being unclear.
The nailbed is on the right and the bone of P3 on left of photomicrograph.Figure 4.27 (A) Normal nailbed.Invasion and destruction of the phalangeal bones is common (Figure 4.27A–C).The subepithelial cells are as described previously for malignant melanoma but in most cases the neoplastic cells have an epithelioid morphology with prominent nucleoli and intracytoplasmic melanin granules.## NAILBED (SUBUNGUAL) NEOPLASMS ## Subungual malignant melanoma This is a malignant neoplasm of melanocytes of the nailbed epithelium. ##### Incidence, age, breed, and sex This neoplasm is commonly found only in dogs and accounts for approximately 8% of all cases of malignant melanoma. The peak incidence is between 8 and 12 years of age. Breeds at increased risk are Scottish terrier (9.9), giant schnauzer (9.8), rottweiler (6.8), miniature schnauzer (5.9), and standard schnauzer (5.5). Other breeds cited in the literature have the following OR values based on our database: doberman pinscher (2.4), golden retriever (2.2), Labrador retriever (1.3), and cocker spaniel (1.6). No sex predilection has been noted (53% female, 47% male). ##### Gross morphology Because the neoplasm arises in the nailbed it may not be visible on external evaluation. Dogs may present with paronychia, nail deformity, or nail loss and lameness. Radiographic examination of the affected digit shows lysis of P3. The gross and radiographic findings are very similar to those seen with cases of subungual squamous cell carcinoma. On cut section the neoplasm may appear variably pigmented brown/black, with invasion and destruction of P3. ##### Histological features There is often an intraepithelial component of neoplastic melanocytes, either as single cells or as nests in the basal layer of the nailbed. The subepithelial cells are as described previously for malignant melanoma but in most cases the neoplastic cells have an epithelioid morphology with prominent nucleoli and intracytoplasmic melanin granules. Invasion and destruction of the phalangeal bones is common (Figure 4.27A–C). Figure 4.27 (A) Normal nailbed. The nailbed is on the right and the bone of P3 on left of photomicrograph.The neoplastic melanocytes extend between the nailbed epithelium and bone of P3 with focal invasion of bone.(C) Nests of neoplastic melanocytes are present within the nailbed epithelium and adjacent tissue.By convention, all subungual melanomas were considered malignant.
The NBT dye test is negative in the X-linked type of CGD (NBT dye is _not_ converted to a blue dye), because the NADPH oxidase enzyme complex is dysfunctional.In this test, leukocytes in a test tube are incubated with the NBT dye, which turns blue if superoxide FRs are present, indicating that the respiratory (oxidative) burst is intact (considered to be a positive test).The X-linked type is characterized by a mutation in the _CYBB_ gene that encodes for a component in the NADPH oxidase enzyme complex (PHOX system) rendering the complex dysfunctional. The reduced production of O2•– results in an absent respiratory (oxidative) burst. Catalase-positive organisms that produce H2O2 (e.g., _Staphylococcus aureus, Nocardia asteroides, Serratia marcescens, Aspergillus_ species, and _Candida_ species) are ingested but _not_ killed, because the catalase degrades the H2O2 produced by these pathogens. Myeloperoxidase is present, but HOCl• is _not_ synthesized because of the absence of H2O2. However, catalase-negative organisms (e.g., _Streptococcus_ species) that produce H2O2 are ingested and can be killed when myeloperoxidase combines H2O2 (derived from the bacteria) with Cl– to form HOCl•. Granulomatous inflammation occurs in tissue, because the neutrophils, which can phagocytose bacteria but not kill most of them, are eventually replaced by cells associated with chronic inflammation, mainly lymphocytes and macrophages. Macrophages fuse to form multinucleated giant cells, which is a characteristic feature of granulomatous inflammation. Patients with CGD have severe infections involving the lungs (pneumonia is the most common presentation), skin, visceral organs, and bones. The classic screening test for CGD is the nitroblue tetrazolium (NBT) dye test. In this test, leukocytes in a test tube are incubated with the NBT dye, which turns blue if superoxide FRs are present, indicating that the respiratory (oxidative) burst is intact (considered to be a positive test). The NBT dye test is negative in the X-linked type of CGD (NBT dye is _not_ converted to a blue dye), because the NADPH oxidase enzyme complex is dysfunctional.Treatment of CGD involves prophylaxis and treatment of infections and bone marrow transplantation.Myeloperoxidase (MPO) deficiency differs from CGD in that both O2•– and H2O2 are produced (normal respiratory burst).However, the absence of MPO prevents synthesis of HOCl•.(7) Deficiency of NADPH (e.g., glucose-6-phosphate dehydrogenase [G6PD] deficiency) produces a microbicidal defect.
Fulminant hepatitis due to hepatitis C is very rare in the United States.The infection is usually asymptomatic or mild and anicteric in 75%, but it results in a chronic carrier state in up to 85% of adult patients.Several extrinsic factors, such as alcohol abuse and smoking, are related to progression of chronic hepatitis C. The influence of age, gender, and race due to genetic factor variation has been implicated with progression of hepatitis C. Coinfection with other viruses such as HIV, HBV, HAV, and human T-lymphotropic virus influence the outcome of HCV disease. Host factors play important role in hepatitis C disease progression Alcohol abuse and smoking influence hepatitis severity HCV-infected patients may develop cirrhosis of liver with increased risk of HCC. It has also been suggested that alcoholism increases the rate of HCC in HCV-infected patients. It is also believed that HCC is probably caused by long-term damage followed by rapid growth rate of hepatocytes during regeneration of liver, which may be mediated by some cytokines. Recent studies suggest that various HCV protein–host-cell interactions may play a role in the development of HCC, including disturbance in the cell cycle, upregulation of oncogenes, and loss of tumor suppressor gene functions. HCV core protein has been shown to perturb and modify the growth of the cell cycle. HCV core interacts directly or indirectly with components or pathways that lead to oncogenesis such as tumor suppressor genes ( _p53, p73_ ), protein kinase, cell cycle, and cell proliferation and differentiation. In addition, HCV nonstructural proteins, NS3 and NS5A, and HCV core protein play a role in cell transformation, differentiation, and oncogenesis. Increased risk of HCC with chronic hepatitis C HCV core and NS3 and NS5A implicated with oncogenesis CLINICAL ASPECTS #### MANIFESTATIONS The incubation period of hepatitis C averages 6 to 12 weeks. The infection is usually asymptomatic or mild and anicteric in 75%, but it results in a chronic carrier state in up to 85% of adult patients. Fulminant hepatitis due to hepatitis C is very rare in the United States.Cirrhosis and HCC are late sequelae of chronic hepatitis.Chronic hepatitis tends to wax and wane, is often asymptomatic, and may be associated with either elevated or normal ALT values in serum ( Figure 13–14 ).Chronic hepatitis C is the leading infectious cause of chronic liver disease and liver transplantation in the United States.**FIGURE 13–14.
These can occur because of peristaltic motion, but can be limited if spasmolytic drugs are given.The HASTE sequence can be sensitive to intraluminal flow-void artifacts.Normal bowel wall has low signal intensity on HASTE sequences, an increased signal intensity can be seen in edematous lesions (inflammation).In a study that investigated this subject, prone scanning position did lead to improved small bowel distension but not to improved lesion detection (Cronin et al. 2008). We perform MR enterography in supine position, as this is more comfortable. Patient acceptance of MR enterography MR enterography is generally tolerated well by patients. In a study that evaluated patient acceptance of MR enterography and MR enteroclysis in 38 patients, MR enterography was preferred by patients and these patients experienced less abdominal pain and discomfort associated with the procedure (Negaard et al. 2008). Also, more patients were willing to repeat the MR enterography than the MR enteroclysis. Other advantages of MR enterography are the shorter image time when compared with MR entero-clysis (fixed protocol for MR enterography while the length of the MR enteroclysis is dictated by obtaining optimal distension) and favorable logistics (the naso-duodenal tube has to be placed under fluoroscopic guidance before the MR enteroclysis). ### 8.3.1 Sequences For adequate assessment of the small bowel, multiple sequences have to be performed. This section gives an overview of sequences useful for MR enterogra-phy. For more details on sequences, the reader is referred to Chap. 1. #### 8.3.1.1 Half-Fourier Single Shot RARE (HASTE) The Half-Fourier single shot RARE (Half Fourier Single Shot Turbo Spin-Echo, HASTE) sequence is often performed in the axial and coronal plane. This sequence generates images with a strong T2-weighting. Because of short acquisition times (less than 1 s per slice), breathing artifacts are minimal. Normal bowel wall has low signal intensity on HASTE sequences, an increased signal intensity can be seen in edematous lesions (inflammation). The HASTE sequence can be sensitive to intraluminal flow-void artifacts. These can occur because of peristaltic motion, but can be limited if spasmolytic drugs are given.HASTE images can be performed using fat suppression.Fat and edema (intramural edema of the bowel wall is indicative of inflammation) both have high signal intensity on T2-weighted images.To visualize the difference between both entities, a sequence with fat suppression is recommended.For more functional information, a dynamic thick slab T2-weighted TSE hydrography sequence can be performed.
In my clinic, the most common reason I recommend CoQ10 to my patients is if they are taking a statin medication for heart disease or cholesterol indications, since taking a statin decreases normal CoQ10 production.Some items—like Prevagen (see box "The Problem with Prevagen")—are aggressively marketed for brain health, but do they really work? We don't have enough research to say. (In the case of Prevagen, the research seems to be highly flawed.) Still, the following supplements—coenzyme Q10, phosphatidylserine, huperzine A, and alpha lipoic acid—stand out for their fascinating theoretical possibilities. You'll notice I don't include specific Better Brain action steps for these supplements, but still my suggestion is to learn as much as you can about them, discuss them with your physician, and decide if they're worth adding to your regimen. ## _Coenzyme Q10 (Ubiquinone) (potentially promising, not ready for prime time)_ Coenzyme Q10 (CoQ10, also called ubiquinol or ubiquinone) is commonly recommended and marketed as a compound to help memory, yet I can find no solid evidence that it improves cognitive function. At high dosages, more than 200 mg per day, it is one of the only agents available that has been shown to slow the progression of Parkinson's disease. CoQ10 has also been helpful in reducing symptoms for people with congestive heart failure. With extensive study, it has been shown to be very safe and have few side effects. Because memory loss is associated with decreased brain cell mitochondrial function, and CoQ10 has been shown to improve mitochondrial energy production, in theory it could help prevent memory loss. In my clinic, the most common reason I recommend CoQ10 to my patients is if they are taking a statin medication for heart disease or cholesterol indications, since taking a statin decreases normal CoQ10 production.They interconvert rapidly (meaning that ubiquinol turns into ubiquinone and vice versa), so I don't see a compelling reason to pick one form over the other, especially if you are asked to pay extra for the reduced form since ubiquinol is generally more expensive.A major limitation with CoQ10 supplements is their absorption.
Abalone is difficult to digest and does not feature in any of our remedies.The last, however, is not commonly found outside China.Other popular fish are eel, clams, crab, and abalone.Shrimp are among the most prized fish, however, so accorded for their strong Yang energy.The most commonly eaten fish in China is carp; they are plentiful, as they breed with ease in ponds and rice paddies.Protein, 22.3 g; Fat, 26.1 g; Fiber, 0 g; Carbohydrate, 0 g; Vitamin A, 8 IU; Vitamin B1, 0.52 mg; Vitamin B2, 0.3 mg; Niacin, 3.9 mg; Vitamin C, 0 mg; Calcium, 8 mg; Phosphorus, 206 mg; Iron, 1.19 mg Mutton _Sweet (Earth), warm, Yang_ Mutton nourishes qi and the blood. It is considered a good tonic for conditions of general weakness and fatigue. Mutton is the preferred meat for curing male sexual weaknesses such as frequent nocturnal emission and premature ejaculation. It is also prescribed for indigestion, pains in the abdomen, and all cold-syndrome ailments. Protein, 21.5 g; Fat, 16.1 g; Fiber, 0 g; Carbohydrate, 0 g; Vitamin A, –; Vitamin B1, 0.13 mg; Vitamin B2, 2.3 mg; Niacin, 4.7 mg; Vitamin C, 0 mg; Calcium, 9 mg; Phosphorus, 177 mg; Iron, 1.4 mg FISH In China, fish is considered to be one of the most wholesome foods. Fish is also considered to be a symbol of wealth and abundance; the word for fish _(yu)_ is pronounced just like the word meaning "abundance." The golden carp, or goldfish _(yu jing),_ is particularly auspicious because the word sounds similar to the words meaning "abundant gold"—hence the great number of goldfish images one sees on the walls of many Chinese restaurants around the world. Fish are also a positive symbol in Buddhist iconography. For Buddhists they represent freedom from the chains of the material world. The most commonly eaten fish in China is carp; they are plentiful, as they breed with ease in ponds and rice paddies. Shrimp are among the most prized fish, however, so accorded for their strong Yang energy. Other popular fish are eel, clams, crab, and abalone. The last, however, is not commonly found outside China. Abalone is difficult to digest and does not feature in any of our remedies.Carp _Sweet (Earth), cold, Yang_ Carp meat nourishes the blood and qi and affects the stomach, kidneys, and spleen.It is a diuretic.Carp also promotes lactation after childbirth.
anencephalus /an′ən·sef′ə·ləs/ ,a fetus whose embryonic development proceeds with the lethal defect of an absence of a major portion of the brain and skull.anemo-,a prefix meaning "airflow" or "wind": anemophobia.Also called pale infarct, white infarct.anemic infarct,tissue necrosis from arterial occlusion.Depending on the kind of anemia, treatment includes providing supplements of the deficient component, eliminating the cause of the blood loss, or alleviating the hemolytic component. The latter may involve administration of adrenal corticosteroids or splenectomy. Appropriate laboratory tests are repeated at intervals to monitor the response and need for continued therapy. Erythropoietin injections may be used to stimulate erythrocyte production when anemia is secondary to chronic renal failure, the anemia of chronic disease, or chemotherapy. -anemia, -anaemia, -nemia,suffixes meaning "(condition of) erythrocyte deficiency": achlyanemia, melanemia. anemia of chronic disease,a decrease in the erythrocyte count as a result of a chronic inflammatory state. anemia of pregnancy,an Hct < 30% or Hgb < 10g/dL. Physiologic anemia of pregnancy results from dilution because on average there is a 1,000-mL increase in plasma volume and a 300-mL increase in red blood cell (RBC) volume. Iron deficiency anemia is the most common nonphysiologic anemia of pregnancy because endogenous iron stores are insufficient to meet the increased iron requirements of pregnancy. Treatment is exogenous iron supplementation, generally 60 to 180 mg of elemental iron per day. Associated with anemia of pregnancy is a folate deficiency, which increases the risk of neural tube defects (NTDs). Treatment is exogenous folate of 0.4 to 1.0 mg per day. anemic, See anemia. −anemic, adj. anemic anoxia,a condition characterized by an oxygen deficiency in body tissues, resulting from a decrease in the number of erythrocytes or in the amount of hemoglobin in the blood. anemic infarct,tissue necrosis from arterial occlusion. Also called pale infarct, white infarct. anemo-,a prefix meaning "airflow" or "wind": anemophobia. anencephalus /an′ən·sef′ə·ləs/ ,a fetus whose embryonic development proceeds with the lethal defect of an absence of a major portion of the brain and skull.The cranium does not close, and the vertebral canal remains a groove.It is thought to be caused by a combination of genetic and environmental factors.It can be detected early in gestation by amniocentesis and analysis or by ultrasonography.See also neural tube defect.−anencephalous, adj.
##### Management.Fractures of the posterior alveolar process may involve the floor of the maxillary sinus and result in abnormal thickening of the sinus mucosa or the accumulation of blood and sinus secretions, in which case an air-fluid level may be appreciated.If the fracture plane is truly associated with the tooth, the line should not shift relative to the tooth.The teeth in the fragment have a recognizable dull sound when percussed, and the attached gingiva may have lacerations. The detached bone may include the floor of the maxillary sinus, in which case bleeding from the nose on the involved side may occur as well as ecchymosis of the buccal vestibule. ##### Imaging Features. Periapical images, if they can be made, often do not reveal fractures of a single cortical wall of the alveolar process, although evidence exists that the teeth have been luxated. However, a fracture of the anterior labial cortical plate may be apparent on an occlusal image or on a lateral extraoral image of the mandible if bone displacement has occurred and the x-ray beam is oriented at near right angles to the direction of bone displacement. Fractures of both cortical plates of the alveolar process are usually apparent (Fig. 30-18). FIGURE 30-18 A and B, Two images demonstrate an alveolar process fracture extending from the distal aspect of the mandibular right cuspid in an anterior direction _(arrows)_ and through the tooth socket of the right central incisor. The closer the fracture is to the alveolar crest, the greater the possibility that root fractures are present. It may be difficult to differentiate a root fracture from an overlapping fracture line of the alveolar bone. Several images produced with different projection angles may help with this differentiation. If the fracture plane is truly associated with the tooth, the line should not shift relative to the tooth. Fractures of the posterior alveolar process may involve the floor of the maxillary sinus and result in abnormal thickening of the sinus mucosa or the accumulation of blood and sinus secretions, in which case an air-fluid level may be appreciated. ##### Management.Gingival lacerations are sutured.If the luxated permanent teeth are splinted and stable, intermaxillary fixation may be unnecessary.Teeth that have lost their vascular supply may eventually require endodontic treatment.A soft diet for 10 to 14 days is recommended.Antibiotic coverage is provided because of communication with tooth sockets.
#### Single- Versus Dual-Chamber Implantable Cardioverter-Defibrillators Presently, expert consensus does not provide guidelines for the selection of single- versus dual-chamber ICDs.sedentary lifestyle) and in those in whom technical issues such as limitations in vascular access preclude or increase the risk associated with inserting an atrial lead.Dual-chamber pacemakers should be programmed to minimize right ventricular pacing in patients with intact AV conduction. Rate-adaptive pacing is recommended for patients with significant symptomatic chronotropic incompetence who demonstrate improvement in symptoms after rate-adaptive pacing is programmed. Single-chamber atrial pacing is not generally recommended because many patients with sinus node disease are at risk for AV block, but it may be considered in patients with normal AV and ventricular conduction. ##### Atrioventricular Block and Bifascicular/Trifascicular Block Dual-chamber pacing is recommended instead of single-chamber ventricular pacing in patients with these blocks based on expert consensus. However, randomized controlled trials performed exclusively or primarily in elderly, sedentary patients did not support the superiority of dual-chamber pacing for major endpoints other than pacemaker syndrome (e.g., AF, stroke, heart failure). Early, acute randomized studies demonstrated that dual-chamber pacing improves exercise tolerance when compared with fixed-rate ventricular pacing, but benefit over rate-adaptive ventricular pacing has been inconsistent. Thus single-chamber ventricular pacing is an acceptable alternative to dual-chamber pacing in patients with AV block who have clinical conditions that limit the benefits of dual-chamber pacing (e.g. sedentary lifestyle) and in those in whom technical issues such as limitations in vascular access preclude or increase the risk associated with inserting an atrial lead. #### Single- Versus Dual-Chamber Implantable Cardioverter-Defibrillators Presently, expert consensus does not provide guidelines for the selection of single- versus dual-chamber ICDs.Disadvantages of dual-chamber ICDs include higher cost, atrial lead complications, and decreased longevity.Dual-chamber pacing modes that minimize ventricular pacing are important in ICD patients because of their high prevalence of left ventricular dysfunction, and they reduce the risk for heart failure as a result of obligatory right ventricular pacing in ICD patients.
As the bacteria increase in numbers, the level of the autoinducer peptide increases, stimulating toxin production.S. aureus coordinately regulates virulence factors by secreting autoinducer peptides.This may allow bacteria growing in discrete host sites, such as an abscess or consolidated pneumonia, to overcome host defenses.All Salmonella strains that infect humans are closely related enough to form a single species, meaning that they share many "housekeeping" genes. Differences in a relatively small number of pathogenicity genes determine whether an isolate of Salmonella causes life-threatening typhoid fever or self-limited enteritis. Virulence genes are frequently found grouped together in clusters called pathogenicity islands. Mobile genetic elements such as plasmids and bacteriophages can transmit functionally important genes to bacteria, including genes that influence pathogenicity and drug resistance. Genes for toxins are sometimes found in plasmids but are more often found in the genomes of bacteriophages, including the genes that encode the toxins responsible for the pathogenesis of cholera, diphtheria and botulism. Genes for acquired antibiotic resistance traits are more frequently found on plasmids, which can spread not only within bacterial species but also between more distantly related organisms. For example, a plasmid with genes for vancomycin resistance can spread not only between species of Enterococcus, but also to more distantly related (and virulent) S. aureus. Many bacteria coordinately regulate gene expression within a large population by a process called quorum sensing. For example, bacteria can induce expression of virulence factors as they grow to high concentration in tissue. This may allow bacteria growing in discrete host sites, such as an abscess or consolidated pneumonia, to overcome host defenses. S. aureus coordinately regulates virulence factors by secreting autoinducer peptides. As the bacteria increase in numbers, the level of the autoinducer peptide increases, stimulating toxin production.Thus, because of quorum sensing, unicellular bacteria acquire some of the more complex properties of multicellular organisms, in which different cells perform different functions.
The success of this treatment holds promise for the use of the active stem cells residing in the neurogenic niches.Three months post retransplantation of this cell suspension into the patient, they could observe a significant increase in dopamine uptake within the transplanted putamen and an improved motor function up to 5 years.Taken into consideration that overexpression of BDNF in the SVZ progenitors itself could not replicate these benefits, underlines the importance of paracrine regulation on SVZ progenitors [88]. Next, overexpression of transcription factors, such as NeuroD1 enhanced the neuronal fate, maturation, differentiation, and synaptic integration of newborn neurons leading to a rescue of dendritic spine density and spatial memory [89]. Further, compounds acting on the Wnt3a pathways have shown to be beneficial as well. Chronic overexpression or activation of Wnt3a was able to enhance DG neurogenesis and rescue behavioral impairments in triple transgenic AD mice [90,91]. #### Cell transplantation The use of the endogenous stem cell pool as a source for transplantation overcomes the ethical problems associated with fetal tissue and the detrimental response of the innate immune system. The feasibility of SVZ progenitor cell isolation, subsequent neurosphere culture and differentiation followed by transplantation in the affected region has already been demonstrated [92,93]. Nevertheless, no studies have been performed using this stem cell source in a clinically relevant setting. However, Lévesque et al. were able to isolate dormant stem cells from cortical samples of a PD patient, expand them in vitro and differentiate them to dopaminergic and GABAergic neurons [94]. Three months post retransplantation of this cell suspension into the patient, they could observe a significant increase in dopamine uptake within the transplanted putamen and an improved motor function up to 5 years. The success of this treatment holds promise for the use of the active stem cells residing in the neurogenic niches.First, we have to grasp, how to direct the newly generated neurons to the lesioned area, second how to differentiate them into a specific neuronal fate, and third how functional synaptogenesis and long-term survival is induced.One of the hurdles of cell therapy today is the limited ability of grafted neurons to migrate through the adult brain from the site of injury.
refractive error /rifrak″tiv/ , a defect in the ability of the lens of the eye to focus an image accurately, as occurs in nearsightedness and farsightedness.refraction of eye [L, refringere, to break apart; AS, eage] , the deflection of light from a straight path through the eye by various ocular tissues, including the cornea, lens, aqueous humor, and vitreous body.−refractive, adj.reflex vasodilation [L, reflectere, to bend back, vas, vessel, dilatare, to spread out] , any blood vessel dilation that results from stimulation of vasodilator nerves or inhibition of vasoconstrictors of the sympathetic nervous system, including by epinephrine-type drugs. reflux /rē″fluks/ [L, refluere, to flow back] , an abnormal backward or return flow of a fluid. Kinds include gastroesophageal reflux, hepatojugular reflux, vesicoureteral reflux. reflux esophagitis, esophageal irritation and inflammation that result from reflux of the stomach contents into the esophagus. See also gastroesophageal reflux. Reflux esophagitis: endoscopic view (Goldman et al, 2012) reflux laryngitis, a burning sensation in the hypopharynx and larynx caused by nocturnal gastric reflux. It occurs most commonly in older patients who sleep in the recumbent position. refracting angle. See angle of refraction. refracting medium, the transparent tissues and fluid of the eye that refract light. refraction /rifrak″shən/ [L, refringere, to break apart] , 1. n., the change of direction of energy as it passes from one medium to another of different density.2. n., an examination to determine and correct refractive errors of the eye.3. n., (in ultrasonography) the phenomenon of bending wave fronts as the acoustic energy propagates from the medium of one acoustic velocity to a second medium of differing acoustic velocity.4. adj., pertaining to the recovery period after an action potential either in muscular or nervous tissue. −refractive, adj. refraction of eye [L, refringere, to break apart; AS, eage] , the deflection of light from a straight path through the eye by various ocular tissues, including the cornea, lens, aqueous humor, and vitreous body. refractive error /rifrak″tiv/ , a defect in the ability of the lens of the eye to focus an image accurately, as occurs in nearsightedness and farsightedness.The refractive index is related to the number, charge, and mass of vibrating particles in the material through which light is passing and may be used as a measure of the total solids in a solution.
The test usually involves the use of a vaginally inserted probe so that the uterus can be examined from within the bowl of the pelvis.The pelvic ultrasound scan is a non-invasive examination that can provide very useful information.Imaging tests and biopsy Because the uterus and ovaries are deep organs, imaging tests are very often necessary to provide more information.The cervical screening test is offered to all women in the UK between the ages of 25 and 65 at regular (three-yearly and then five-yearly) intervals as part of a national screening program. Cervical screening is not wholly reliable, in that many women who have no physical abnormality will have unclear smear test results and will have to be recalled for re-examination (false-positive results), and some cervical cancers will be missed (false-negative results). Many women are recalled for the more invasive colposcopy treatments on the basis of slight abnormalities that may never have developed into cancer. There is ongoing debate over whether the cost of the program and its inconvenience to many women is outweighed by the advantages of the early detection of cancer in a few. However, it has been estimated that the UK cervical screening program saves about 3000 lives per annum by preventing the development of advanced cervical cancer. There was a 43 percent reduction in cervical cancer incidence from 1987 to 1997 in the UK that followed the introduction of the screening program. The introduction of HPV vaccination in teenage girls is likely to impact positively on the incidence of cervical cancer in the long term. It may be possible that the rates of this cancer may drop to such an extent that there will no longer be a need for the screening program. Imaging tests and biopsy Because the uterus and ovaries are deep organs, imaging tests are very often necessary to provide more information. The pelvic ultrasound scan is a non-invasive examination that can provide very useful information. The test usually involves the use of a vaginally inserted probe so that the uterus can be examined from within the bowl of the pelvis.The formation of the Graafian follicle can be seen, and so ultrasound can give an indication of healthy ovulation.Endoscopy of the vagina (colposcopy) is a test that requires the insertion of a vaginal speculum.A colposcope (a form of endoscope) is used to provide detailed images of the surface of the cervix, and permits the removal of cervical biopsies and treatment of the cervix.
Many people find that the ancient arts of acupuncture and acupressure or the application of hot and cold compresses can relieve pain, as does exercise—which not only helps maintain strength and flexibility, but actually changes muscle cells, making them less sensitive to pain.Transcutaneous electrical nerve stimulation (TENS) and ultrasonic stimulation may also be viable options.These medications—which include steroids; bone-forming, antidepressant, and anticonvulsant medications; antihistamines; and sedatives—are often useful in treating opioid-resistant pain. For whatever reason, they do relieve pain, although they are not usually labeled as pain relievers. A simple measure such as aspirin or acetominophen, with or without codeine, or ibuprofen (Motrin, Advil) may do the job well enough. But when pain is severe, the dosage has to be increased or the drug has to be taken more frequently. If these simple measures don't help, then it is important to increase the strength or potency of the medication. Sometimes, just the addition of an adjuvant medication is all that is needed. Other Pain-Relief Options For the 5 to 10 percent of people who do not receive adequate pain control under WHO's guidelines, there are other options. Pain specialists can prevent pain stimuli from reaching the central nervous system by the delivery of local anesthetic procaine (Novocain) or lidocaine (Xylocaine), steroids, toxins, or nerve-destroying agents. They can also use an alternative delivery system, such as the administration of opioids and other drugs subcutaneously or into the spine, or use a local spinal anesthetic. Transcutaneous electrical nerve stimulation (TENS) and ultrasonic stimulation may also be viable options. Many people find that the ancient arts of acupuncture and acupressure or the application of hot and cold compresses can relieve pain, as does exercise—which not only helps maintain strength and flexibility, but actually changes muscle cells, making them less sensitive to pain.Anticonvulsants such as carbamazepine (Tegretol), phenytoin (Dilantin), and gabapentin (Neurontin) may help in pain relief, especially neuropathic pain.Other techniques include epidural spinal injections, peripheral nerve blocks, radiofrequency neurolysis to destroy nerves with radio waves, or alcohol nerve injections.
Next, the transducer must be rotated in this position to identify the smallest transverse diameter (typically the luminal profile will change from elliptical to circular), thus avoiding an oblique cross-sectional scan plane through the aorta, which would lead to an overestimation of the diameter.A6.32 a–c Aortic aneurysm a The therapeutic management of an aortic aneurysm is mainly dictated by its diameter, involvement of the iliac artery, presence of thrombosis, and infrarenal extent, including the distance to the renal artery origins, which is important when stenting is contemplated. Since the renal artery origins are best seen transversely, and the segment between the origins and the end of the aneurysm longitudinally, it is helpful to first identify the superior mesenteric artery in the longitudinal view and then use it as a guiding structure. The renal arteries arise 1–2 cm distal to the origin of the mesenteric artery. The segment between the end of the aneurysm and the superior mesenteric artery origin can thus be measured in longitudinal orientation. This value minus 2 cm is the distance between the renal artery origin and the aneurysm.b Whether stenting is an option depends on the diameter of the aneurysm. Since a dilated aorta is also elongated (mostly with a left lateral convexity), imaging modalities with data acquisition in standardized transverse sections such as CT will lead to overestimation when the longest diameter of the elliptical lumen is measured (right section). To eliminate this source of error and perform a precise and reproducible cross-sectional diameter measurement (with little inter- and intraobserver variation) in repeat examinations, the sonographer must first identify the site of the largest diameter of the aneurysm. Next, the transducer must be rotated in this position to identify the smallest transverse diameter (typically the luminal profile will change from elliptical to circular), thus avoiding an oblique cross-sectional scan plane through the aorta, which would lead to an overestimation of the diameter.The transverse lower abdominal scan reveals a contained perforation with complete thrombosis of the spilled blood at the time of the examination.The contour of the thrombosed aneurysm (arrow) is distinct from the clotted perivascular blood.The site of perforation is indicated by the contour disruption anterolaterally.
A schematic summary outlining the progression in development of the cell heterogeneity within neural tissue and highlights the reaction of parenchymal astrocytes to injury with focus on the molecular characteristics they share with radial glial cells and adult neural stem cells (NSCs), but absent in mature astrocytes in the adult healthy brain.This prompted the analysis of their stem cell potential by dissociating the tissue surrounding an invasive injury site and culturing the cells in neurosphere conditions as described above. Indeed, in this assay a limited fraction of reactive astrocytes shows long-term self-renewal and multipotency, suggesting that pathophysiological stimuli may trigger dedifferentiation of some mature astrocytes into NSCs [148, 211, 212, 218, 225–228, 235]. Interestingly, this potential to form self-renewing and multipotent neurospheres occurs in a time-dependent manner progression closely correlating to the proliferative reaction of astrocytes described above. For instance in response to acute injury (such as stab wound and focal laser lesion) or ischemia, the ability of reactive astrocytes to form neurospheres strongly increases during early post-injury stages (3–5 days after injury), but rapidly declines thereafter, such that neurospheres can be no longer observed as 14 days after injury [148, 211, 212, 228, 235]. Most importantly, genetic fate mapping using GLAST::CreERT2 mice revealed that neurosphere-forming cells originate from grey matter astrocytes both after stab wound injury and in amyloidosis conditions [211, 217, 235]. These cells exhibit stem cell hallmarks as they self-renew for many passages [211, 212] and approximately half of them are multipotent, since they are able to generate some neurons as well as astrocytes and oligodendrocytes in vitro [235]. Fig. 3 Progression in development of the cell heterogeneity within neural tissue and the reaction of parenchymal astrocytes to brain injury. A schematic summary outlining the progression in development of the cell heterogeneity within neural tissue and highlights the reaction of parenchymal astrocytes to injury with focus on the molecular characteristics they share with radial glial cells and adult neural stem cells (NSCs), but absent in mature astrocytes in the adult healthy brain.As development proceeds, some of radial glial cells persist into the adult brain and act as adult NSCs in the adult SVZ and hippocampal SGZ, where they proliferate to produce both neurons and glia.

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Multilingual Medicine: Model, Dataset, Benchmark, Code

Covering English, Chinese, French, Hindi, Spanish, Hindi, Arabic So far

👨🏻‍💻Github •📃 Paper • 🌐 Demo • 🤗 ApolloCorpus • 🤗 XMedBench
中文 | English

🌈 Update

[2024.03.07] Paper released.
[2024.02.12] ApolloCorpus and XMedBench is published！🎉
[2024.01.23] Apollo repo is published！🎉

Results

Apollo-0.5B • 🤗 Apollo-1.8B • 🤗 Apollo-2B • 🤗 Apollo-6B • 🤗 Apollo-7B

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Data: Huge, Diverse, Clean, Multilingual

Usage

Zip File
Data category
- Pretrain:
  - json_name: {data_source}_{language}_{data_type}.json
    - data_type: medicalBook, medicalGuideline, medicalPaper, medicalWeb(from online forum), medicalWiki
    - language: en(English), zh(chinese), es(spanish), fr(french), hi(Hindi)
    - data_type: qa(generated qa from text)
  - data item:
    - data_type==text: list of string
```
[
  "string1",
  "string2",
  ...
]
```
    - data_type==qa: list of qa pairs(list of string)
```
[
  [
    "q1",
    "a1",
    "q2",
    "a2",
    ...
  ],
  ...
]
```
- SFT:
  - json_name: {data_source}_{language}.json
    - data_type: code, general, math, medicalExam, medicalPatient
  - data item: list of qa pairs(list of string)
```
  [
    [
      "q1",
      "a1",
      "q2",
      "a2",
      ...
    ],
    ...
  ]
```

Citation

@misc{wang2024apollo,
   title={Apollo: Lightweight Multilingual Medical LLMs towards Democratizing Medical AI to 6B People},
   author={Xidong Wang and Nuo Chen and Junyin Chen and Yan Hu and Yidong Wang and Xiangbo Wu and Anningzhe Gao and Xiang Wan and Haizhou Li and Benyou Wang},
   year={2024},
   eprint={2403.03640},
   archivePrefix={arXiv},
   primaryClass={cs.CL}
}

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