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Diagnostic test results or time elements are simply stated without corresponding symbols depression test channel 4 buy 100 mg zoloft. When not stated great depression definition quizlet purchase zoloft, medical follow-up and treatment are presumed with patients receiving levothyroxine (L-T4) which is taken uninterruptedly except when indicated prior to anxiety from alcohol cheap zoloft online particular testing great depression test answer key buy cheap zoloft 100 mg. I therapy detects and treats any areas of residual remain in an isolation room for an average of four days. For at least 1 month prior to I therapy you must not have had Iodine containing preparations (certain! Thyroid hormone medication will also need to be s to pped for approximately 6 weeks before therapy. Before you are discharged you will be brought to the will be arranged by your own doc to r. Department of nuclear medicine where pictures of your body will be taken from various angles. In addition you require certain blood tests on the 131 morning before I administration ( to check whether any residual thyroid tissue is adequately stimulated, and a! When you are discharged home you will be instructed as pregnancy test if you are a woman of childbearing age). Avoid unnecessary trips on public transport and attending public entertainment (you could be sitting next to someone pregnant). If convenient sleep in a single bed if partner is less than given to you prior to I therapy to prevent potential 50 years of age. A doc to r and a technologist will come from the share your utensils with other family members and avoid Department of nuclear medicine to administer the therapy activities which may involve exchange of saliva. The doc to r will check certain details (such as the date of surgery, and the result of any blood tests you may have had). If you are admitted to hospital within 4 weeks of the dose, please arrange for the nuclear medicine department to be notified. This radioiso to pe is accumulated by areas of thyroid tissue and destroys these areas. I understand that rarely complications occur and I accept the possible risks associated with the 131 proposed I therapy. The reported side effects such as salivary gland and neck discomfort, nausea, changes in taste, bone marrow depression, risk of salivary gland tumours and possible risk of leukaemia have been discussed with me. Nuclear Medicine Department, Hammersmith Hospital, London, United Kingdom Alam, F. S Department of Nuclear Medicine, Bach Mai University Hospital, Hanoi, Vietnam Ang, S. Endocrine Research Center and the Division of Cardiology, Taleghani Medical Center, Shaheed Beheshti University of Medical Sciences, Tehran, Islamic Republic of Iran Bal, C. Department of Nuclear Medicine, All India Institute of Medical Sciences, Delhi, India Barrenechea, E. Department of Nuclear Medicine, Veterans Memorial Medical Centre, Manila, Philippines Bauer, D. Department of Nuclear Medicine, La Paz, Bolivia Bo Cho, Y Department of Nuclear Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea Bouyoucef, S. Department of Radiology, Faculty of Medicine Chulalongkorn University, Bangkok, Thailand Calaguas, M. Department of Radiation Oncology, Philippine General Hospital, Manila, Philippines Chari to, C. Department of Nuclear Medicine, Cancer Hospital, Peking Union Medical College, Beijing, China Collins, L. Principal Physicist, Westmead Hospital, Sydney, Australia Demena, S Department of Nuclear Medicine, Addis Ababa, Ethiopia Ekmahachai, M Department of Radiology, Faculty of Medicine Chulalongkorn University, Bangkok, Thailand Ellmann, A Tygerberg Hospital and Stellenbosch University, Cape Town, South Africa 271 Gangadharan, P. Adviser to the Epidemiology Section, Regional Cancer Centre, Delhi, India Geddes, C. Consultant Physician in Nuclear Medicine, Pacific Medical Imaging, Australia Huang, T-S Department of Internal Medicine, National Taiwan University and National Taiwan University Hospital, Taipei, Taiwan Kabir, F. T Department of Nuclear Medicine, Bach Mai University Hospital, Hanoi, Vietnam Konishi, J. Department of Nuclear Medicine, Faculty of Medicine, Kyo to University, Japan Kumar, A. Department of Nuclear Medicine, All India Institute of Medical Sciences, India Lopez, R. Section of Cy to pathology, Faculty of Medicine and Surgery, University of San to Tomas, Philippines Mansberg, R. Department of Endocrinology and Metabolism, University of Siena, Italy Penalonzo, M. Department of General Surgery, Hospital Universitario Esperanza, Guatemala City, Guatemala Piyasena, R. Radiation Safety Systems Division, Bhabha A to mic Research Centre, Mumbai, India Ranjith, A. Division of Epidemiology and Biostatistics, Tata Memorial Hospital, Mumbai, India Rauf, M. Department of Nuclear Medicine, All India Institute of Medical Sciences, Delhi, India Sirisalipoch, S. Department of Radiology, Faculty of Medicine Chulalongkorn University, Bangkok, Thailand Srivastava, D. Department of Radiodiagnosis, All India Institute of Medical Sciences, Delhi, India Tolentino, R. Department of Molecular Medicine, A to mic Bomb Disease Institute, Nagasaki University, Nagaski, Japan Yorg, J. While all rea sonable efforts have been made to publish reliable data and information, neither the author[s] nor the publisher can accept any legal responsibility or liability for any errors or omissions that may be made. The publishers wish to make clear that any views or opinions expressed in this book by individual edi to rs, authors or contribu to rs are personal to them and do not necessarily reflect the views/opinions of the publishers. The information or guidance contained in this book is intended for use by medical, scientific or health-care professionals and is provided strictly as a supplement to the medical or other professional’s own judgement, their knowledge of the patient’s medical his to ry, relevant manufacturer’s instructions and the appropriate best practice guidelines. Because of the rapid advances in medical sci ence, any information or advice on dosages, procedures or diagnoses should be independently verified. The reader is strongly urged to consult the relevant national drug formulary and the drug companies’ and device or material manufacturers’ printed instructions, and their websites, before administering or utilizing any of the drugs, devices or materials mentioned in this book. Ultimately it is the sole responsibility of the medical professional to make his or her own professional judgements, so as to advise and treat patients appropriately. The authors and publishers have also attempted to trace the copyright holders of all material reproduced in this publication and apologize to copyright hold ers if permission to publish in this form has not been obtained. Copyright Law, no part of this book may be reprinted, reproduced, transmitted, or utilized in any form by any electronic, mechanical, or other means, now known or here after invented, including pho to copying, microfilming, and recording, or in any information s to rage or retrieval system, without written permission from the publishers. Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe. We have not attempted to appraise critically the evidence of effectiveness for different drugs in diseases in order to keep a concise and easy- to -read format Prescribers are advised to check doses in up- to -date formularies and to consult manufacturers for full product information and details of excipients, for use in rare metabolic diseases such as porphyria and Lapp lac to se galac to se defciency this edition attempts to generalize across countries However, each country may have special aspects of prescribing that should be considered Sarah H. Further research led to development of the second generation of retinoids, the monoaromatic retinoids, etretinate and its metabolite, acitretin. Etretinate (which is no longer available) and acitretin are effective treatments for psoriasis and severe congenital disorders of keratinization. A major problem with systemic retinoids is their tera to genicity, and separation of this from their therapeutic effects has never been achieved. Acitretin has a much shorter half-life than etretinate, but a long duration of pregnancy avoidance post-treatment is still advised, as it transpires that acitretin can be converted to etretinate in the presence of alcohol, and the latter is s to red in fat with a half-life of 120 days. Acitretin is an established treatment for psoriasis and, despite development of biological agents (the biologics), it remains an important therapy due to its unique mode of action. Subsequently, the ligand/recep to r complex binds to specifc gene regula to ry regions to modulate gene expression. In the epidermis, acitretin reduces keratinocyte proliferation and normalizes differentiation and cornifcation. It also inhibits production of vascular endothelial growth fac to r and inhibits intraepidermal neutrophil migration. In addition, there is emerging evidence that acitretin may be successfully combined with biologics.

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Few studies have been done to depression symptoms lashing out order zoloft on line assess the incidence and prevalence of defeca to the great depression definition wikipedia buy discount zoloft 100mg online ry dysfunction anxiety nausea order generic zoloft online. Defeca to depression and exercise cheap zoloft on line ry Dysfunction the term defeca to ry dysfunction often is used synonymously with the symp to m of constipation. Constipation is an imprecise term used by patients to report a variety of symp to ms, including infrequent s to ols, dyschezia, straining, variation in s to ol consistency and caliber, incomplete emptying, bloating, and abdominal pain. The most common symp to ms associated with constipation are straining and hard s to ols (2,3). Defeca to ry dysfunction is defined by many physicians as infrequent s to ols, typically fewer than three bowel movements per week. This definition is based on s to ol frequency studies in which 95% of women have more than three bowel movements per week. However, the prevalence of constipation has been estimated to range from 2% to 28%, depending on the definition applied (5–7). There is an increased prevalence of constipation among women and elderly individuals, nonwhite individuals, and those with low income and low education levels (5–7). An estimated 85% of physician visits results in a prescription; including drug costs would increase this amount substantially (8). Fecal Incontinence the reported prevalence of fecal incontinence varies between 2% and 3% for community-dwelling individuals, 3% to 17% for those of increased age, and 46% to 54% for nursing home residents (12). A prevalence of 28% has been reported among patients seeking benign gynecologic care and 36% of primary care patients surveyed (13,14). The prevalence of fecal incontinence in the United States is expected to increase 59% from 10. Epidemiologic studies of fecal incontinence are compromised by social stigmata and the lack of a uniform definition. Definitions of fecal incontinence vary with respect to the type of material passed (solid, liquid, or gas), the frequency and duration of events (once in a lifetime to twice a week), and the impact on quality of life. Most authors agree that the true prevalence of this condition is underestimated in the current scientific literature. A large health survey in the United States found age, female gender, physical limitations, and poor general health to be independent risk fac to rs associated with fecal incontinence (16). Fecal incontinence has tremendous psychosocial and economic implications for individuals and society as a whole. The loss of such a basic function can be emotionally devastating, leading to poor self-esteem, depression, social isolation, and decreased quality of life (13,14,17). Fecal incontinence is the second leading reason for nursing home placement in the United States, even though less than one-third of individuals with this condition seek medical attention (13,17). The overall annual cost to treat fecal incontinence is difficult to pinpoint, but accounts for more than $400 million per year in the cost of adult incontinence products alone (17). Symp to m-Based Approach to Colorectal Disorders Several medical conditions cause defeca to ry dysfunction, fecal incontinence, or combined symp to ms. Following is the differential diagnosis—a proposed classification system based on systemic fac to rs, ana to mic and structural abnormalities, and functional disorders. Differential Diagnosis Disordered Defecation Causes of defeca to ry dysfunction have traditionally been divided in to systemic disorders and idiopathic constipation (all nonsystemic causes). Idiopathic constipation can be subdivided in to ana to mic and structural abnormalities and functional disorders (Table 28. In one study, gastrointestinal symp to ms were present in 76% of patients with diabetes, including constipation, which occurred in 60% (18). In patients with diabetes, constipation is believed to be secondary to intestinal au to nomic neuropathy, resulting in delayed or absent gastrocolic reflex and decreased bowel motility. Although diabetes has been classified with the endocrinologic causes, it should also be grouped with the enteric neuropathies. Pregnancy is not considered a disease state; however, there is an 11% to 38% prevalence of constipation that is believed to result from the effect of progesterone on smooth muscle (19,20). Iron supplements and prior constipation treatment are also associated with constipation during pregnancy (20). The neurologic systemic fac to rs can be divided in to central and peripheral processes. Spinal cord lesions, multiple sclerosis, and Parkinson disease affect the au to nomic nervous system. Trauma to the sacral nerves often leads to severe constipation from decreased left-sided colonic motility, decreased rectal to ne and sensation, and increased distention. These findings are also seen in patients with meningomyelocele, damage to the lumbosacral spine, and pelvic floor trauma (21,22). Higher spinal cord lesions result in delayed sigmoid transit and decreased rectal compliance. In these upper mo to r neuron lesions, colonic reflexes are intact, and defecation can be initiated by digital stimulation of the anal canal (23,24). Individuals with multiple sclerosis can have no gastrocolic reflex, decreased colonic motility, decreased rectal compliance, and even rec to sphincteric dyssynergia (25,26). Constipation worsens with the duration of illness and may be compounded by the side effects of medical therapy. Similar findings of rec to sphincteric dyssynergia and medication side effects are present with Parkinson disease. The absence of intramural ganglion cells in the submucosal and myenteric plexuses of the rectum causes loss of the rec to sphincteric inhibi to ry reflex. Patients with this illness usually present with functional obstruction and proximal colonic dilation. In most patients, the condition is diagnosed within 6 months of age, although milder cases can be seen later in life. Importantly, some of the most commonly used prescription and over-the-counter medications, including aluminum antacids, beta-blockers, calcium channel blockers, anticholinergics, antidepressants, and opiates, cause defeca to ry dysfunction (Table 28. Lifestyle issues, such as inadequate fiber intake and insufficient fluid intake, can exert similar effects independently or in conjunction with other disorders. Functional disorders are those that do not have an identifiable ana to mic or systemic etiology. Most functional disorders are motility disorders, such as slow-transit constipation or colonic inertia, irritable bowel syndrome (constipation predominant), and functional constipation. Patients also may have functional limitations, such as decreased mobility and cognition. It is important to understand that this classification system is somewhat arbitrary, and several of these conditions are interrelated. Fecal Incontinence Anal continence depends on a complex interaction of cognitive, ana to mic, neurologic, and physiologic mechanisms. The continence mechanism can often compensate for a deficiency in one of these processes, but it can be overwhelmed with increased severity or decreased function over time. Systemic etiologies of fecal incontinence often are due to disease states that cause diarrhea. The rapid transport of large volumes of liquid s to ol to the rectum can produce urgency and incontinence even in healthy individuals (28). Fecal incontinence frequently results from infectious diarrhea caused by bacteria. Numerous medications and dietary items cause diarrhea and fecal incontinence (Table 28. Endocrine fac to rs that can lead to fecal incontinence include diabetes mellitus and hyperthyroidism. With diabetes, diarrhea can develop from au to nomic dysfunction, bacterial overgrowth, osmotic diarrhea with sugar substitutes, and pancreatic insufficiency. Inflamma to ry bowel disease is considered an idiopathic or au to immune systemic fac to r. Ulcerative colitis and Crohn disease cause fecal incontinence during exacerbations with bouts of bloody diarrhea. Inflamma to ry bowel disease can also result in structural abnormalities, such as anal fissures, fistulas, abscesses, and operative complications that lead to fecal incontinence.

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One study showed an increasing risk with increasing number of cigarettes per day in current smokers depression definition clinical order genuine zoloft. Some studies were limited to depression definition nhs discount zoloft 25mg overnight delivery women; in other studies depression symptoms cognitive buy discount zoloft, the number of men was relatively small (20% of the to mood disorder support group buy generic zoloft 25mg tal sample). Nevertheless, there was some indication in the two studies that allowed sex-specific analyses that the association was stronger in women than in men. Stronger associations for never smokers and current smokers were seen with Graves disease with ophthalmopathy (for never smokers, the odds ratio was 4. The only study that presented sex-specific analyses reported a stronger effect in women than in men. Fewer studies are available regarding smoking and hypothyroidism (defined as Hashimo to thyroiditis, clinical hypothyroidism, subclinical hypothyroidism, or au to immune thyroiditis), and the overall association with hypo thyroidism was weaker (odds ratio around 1. Several prospective studies provided data regarding the risk of developing multiple sclerosis in relation to smoking his to ry in women (Table 12). Villard Mackin to sh & Vessey (1993) also found an association with smok ing his to ry and multiple sclerosis in the Oxford Family Planning Association cohort. In a small study using self-reported multiple sclerosis in a population-based study in Norway, the overall asso ciation with ever smokers (risk ratio 1. Two recent reviews have summarized studies of smoking his to ry in relation to risk of developing rheuma to id arthritis (Albano et al. The association with smoking his to ry appears to be stronger in patients positive for rheuma to id fac to r than in patients negative for rheuma to id fac to r and stronger in men than in women. There is also some evidence of associations with pack years or smoking duration, but more variable effects have been seen with the amount smoked per day (Albano et al. The severity of rheuma to id arthritis may be increased in smokers, as evidenced by increased disability and risk of extra articular manifestations, including vasculitis and interstitial lung disease, but not of joint swelling (Albano et al. A recent meta-analysis examined the association between smoking and the risk of systemic lupus erythema to sus in seven case– control and two cohort studies (Costenbader et al. Larger studies specifically designed to assess sex differences are needed to understand the effect of smoking across the spectrum 144 Chemical/Physical Agents and Au to immunity of au to immune diseases. Although a positive correlation between alcohol intake and the degree of liver injury has been reported, there is a high degree of variability in the development and severity of disease between individuals with similar levels of abusive ethanol consumption, and only a small percentage of alcoholic patients develop cirrhosis or hepatitis. Heavy drinkers without significant liver disease had significantly lower titres of IgA antibodies against acetaldehyde modified erythrocyte protein and IgG antibodies against oxidized or malondialdehyde-modified low-density lipoproteins, compared with patients with alcoholic liver disease (Viitala et al. These studies suggest that multiple mechanisms or genetic fac to rs may be involved in the disease process. In support of this, two studies using the National Academy of Sciences – National Research Council twin registry in the United States concluded that there was genetic predisposition to organ-specific complications of alcoholism based on the significant concordance rates in monozygotic twins (Hrubec & Omenn, 1981; Reed et al. Gene polymorphisms encoding for the enzymes responsible for ethanol metabolism, oxidative stress, and proinflamma to ry/immune responses have been investi gated (Bataller et al. A genetic analysis of individuals participating in a study evaluating liver disease in northern Italy suggested that heavy drinkers with cirrhosis or alcoholic liver disease had a higher frequency (0. A study in alcoholic patients in Japan reported an increase in the frequency of individuals homozygous for the C1 allele in men with alcoholic cirrhosis (Yamauchi et al. In contrast, there was no difference in either C1 or C2 allelic distribution in an earlier study conducted in Caucasian men (Carr et al. Cy to kine gene polymorphisms have also been suggested to play a role in the pathogenesis of alcoholic liver disease. The i511 146 Chemical/Physical Agents and Au to immunity allele 2 was found at a higher frequency in patients with cirrhosis than in heavy drinkers without liver disease. Jarvelainen and colleagues (2001) demonstrated that in Finnish males, expression of one T allele was associated with both alcoholic hepatitis and cirrho sis. There is conflicting evidence as to whether variations in the genes encoding for manganese superoxide dismutase represent a risk fac to r for alcoholic liver disease (Degoul et al. The data on cy to kine and metabolic enzyme gene polymorph isms in the human population as well as experimental studies with ethanol-fed rodents are indicative of the importance of inflamma tion, oxidative stress, and endo to xin in the pathogenesis of alcohol induced liver damage. Chronic ethanol exposure has been associ ated with the formation of alcohol-modified proteins, leading to au to antibody formation and immune-mediated damage to the liver. Circulating antibodies recognizing acetaldehyde–malondialdehyde adducts have been found in Wistar rats fed an ethanol-containing liquid diet (Xu et al. Immunization with acetaldehyde adducts in conjunction with ethanol feeding stimulated ex vivo lymphocyte proliferation in B6 mice, but not in several other strains (Shimada et al. The antibodies generated by these alcohol-modified proteins may also respond to unmodified self-proteins, leading to a breaking of to lerance and au to immune pathology. Obese strain chickens spon taneously develop a disease very similar to Hashimo to thyroiditis. They were the first model that showed that exposure to iodine affects the course of disease. Depletion of iodine after hatching, achieved by injections of potassium chlorite, reduced thyroid infiltration. In contrast, the onset of spontaneous thyroiditis was hastened by adding sodium iodide to the diet. This effect, however, was reduced by administration of antioxidants, suggesting that reactive oxygen intermediates are one mechanism by which iodine contributes to cell injury. The Biobreeding/Worcester rat has been widely used as a model for studying spontaneous diabetes mellitus, but it also develops au to immune thyroiditis. Administration of excess iodine accelerates the appearance of the lymphocytic infiltration of the thyroid and the production of thyroid-specific au to antibodies. The incidence of diabetes is very low, but many of the animals develop au to immune thyroiditis. Iodinated thyroglobulin is more antigenic than the same molecule lacking iodine, suggesting another mechanism by which iodine enhances thyroiditis. Several studies have evaluated the effects of excessive iodine intake in humans, and antithyroid antibodies and iodine-induced hypo and hyperthyroidism have been reported following long-term iodine treatment for endemic goitre (Boyages et al. Although a few epidemiological analyses have been published, they are often confounded by the absence of a clear-cut diagnosis. Clinical outcomes can be the result of immunoallergic, pseudoallergic, or au to immune-like mechanisms. However, a comprehensive review of adverse au to immune responses and au to immune diseases associated with therapeutic agents is beyond the scope of this monograph, and only a few examples will be discussed below. Table 13 provides an abbreviated list of therapeutic drugs that have reportedly been associated with au to immune reactions. When considering drug-induced au to immunity, it is important to differentiate two situations. On the other hand, one given agent is associated with only one given type of au to immune disease. In the latter case, the disease can be organ specific and then closely mimic the spontaneous disease, except that cessation of the offending agent leads to the progressive recovery of clinical and then biological manifestations of the disease. The disease can also be systemic and consists of clinical manifestations and biological/immunological changes markedly different from those of spontaneous diseases. Interestingly, drug-induced systemic au to immune-like reactions often resemble systemic hypersensitivity reactions, and this further illustrates overlapping mechanisms between immunoallergic and au to immune-like reactions. Hydralazine inhibits the covalent 150 Chemical/Physical Agents and Au to immunity binding reaction of the complement protein C4, and susceptibility to hydralazine-induced lupus, as in idiopathic systemic lupus erythema to sus, may depend partly upon genetically determined C4 levels (Sim & Law, 1985; Speirs et al. Adoptive transfer of T cells made au to reactive by treatment with either hydralazine or procainamide causes a lupus like disease (Yung et al. The possibility of a lupus-inducing effect of the drug on T cell development in the thymus has been suggested (Quddus et al. Studies of the specificities of B cells that respond to chroma tin-reactive T cells at the initiation of this au to immune process demonstrated a rapid and robust expansion of anti-chromatin-secret ing B cells, thus indicating the presence of a normal immune reper to ire that includes non- to lerant au to reactive B cells that respond to strong T cell drive and are readily manifested if Fas-mediated activation-induced cell death is inhibited (Ayer et al. Because of a high incidence of adverse events and the strong association with several au to immune-like phenomena, including myasthenia, pemphigus, and Goodpasture disease, the clinical use is limited. The adverse effects of D-penicillamine in animals are similar to those observed in humans. A study on the effects of D-penicillamine in various strains of mice indicated that D-penicillamine facilitates the induction of au to antibodies in animals with an inherent suscep tibility to au to immunity (Brik et al.

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It is tropical depression definition buy cheap zoloft 25mg, rather depression definition tumblr generic zoloft 50mg without prescription, a serious attempt to mood disorder teenager 100 mg zoloft overnight delivery present important facts about many disease processes in the hope that the student will read much further in major textbooks and journals and will receive some assistance in passing medical school depression symptoms lack of emotion order 25 mg zoloft mastercard, licensure, or board examinations. Each question is accompanied by an answer, a paragraph explanation, and a specific page reference to an appropriate textbook or journal article. A bibliography listing sources can be found following the last chapter of this text. Each multiple-choice question in this book contains four or more possible answer options. By following this suggestion, you approximate the time limits imposed by the Step 1 exam. After you finish going through the questions in the section, spend as much time as you need verifying your answers and carefully reading the explanations provided. Pay special attention to the explanations for the ques tions you answered incorrectly—but read every explanation. The author of this material has designed the explanations to reinforce and supplement the information tested by the questions. If you feel you need further information about the material covered, consult and study the references indicated. The High-Yield Facts added for this edition are provided to facilitate rapid review of pathology to pics. It is anticipated that the reader will use the High-Yield Facts as a “memory jog” before proceeding through the questions. Reversible Cell Injury • swelling of cell organelles and entire cell • dissociation of ribosomes from endoplasmic reticulum • decreased energy production by mi to chondria • increased glycolysis > decreased pH > nuclear chromatin clumping b. Irreversible Cell Injury • irreversible damage to cell membranes and mi to chondria • influx of calcium in to mi to chondria; forms dense bodies (flocculent densities in heart) • release of cellular enzymes. Increased delivery of free fatty acids to liver • starvation • corticosteroids • diabetes mellitus 2. Decreased formation of apoproteins • carbon tetrachloride • protein malnutrition (kwashiorkor) 1 Copyright © 2007 by the McGraw-Hill Companies, Inc. Mechanisms/phases a) initiation phase > caspases are activated b) execution phase > cell death occurs i. Characteristics • cause > hypoxia or to xins (irreversible injury) • many cells or clusters of cells • cells swell • inflammation present High-Yield Facts 3 2. Cellular Adaptation • hypertrophy > increase in the size of cells • hyperplasia > increase in the number of cells • atrophy > decrease in the size of an organ • aplasia > failure of cell production • hypoplasia > decrease in the number of cells • metaplasia > replacement of one cell type by another • dysplasia > abnormal cell growth b. Abnormal Organ Development • anlage > primitive mass of cells • aplasia > complete failure of an organ to develop (anlage present) • agenesis > complete failure of an organ to develop (no anlage present) • hypoplasia > reduction in the size of an organ due to a decrease in the number of cells • atrophy > decrease in the size of an organ due to a decrease in the size or number of preexisting cells 5. Products • C3b > opsonin • C5a > chemotaxis and leukocyte activation • C3a, C4a, C5a > anaphyla to xins • C5–9 > membrane attack complex b. Deficiencies • deficiency of C3 and C5 > recurrent pyogenic bacterial infections • deficiency of C6, C7, and C8 > recurrent infections with Neisseria species • deficiency of C1 esterase inhibi to r > hereditary angioedema • deficiency of decay-accelerating fac to r > paroxysmal nocturnal hemoglobinuria 8. Thromboxane (TxA2) • produced by platelets • causes vasoconstriction • stimulates platelet aggregation b. Caseating Granulomas • aggregates of activated macrophages (epithelioid cells) • tuberculosis b. Noncaseating Granulomas • sarcoidosis • fungal infections • foreign-body reaction High-Yield Facts 5 10. Composition • increased protein • increased cells • specific gravity greater than 1. Examples • inflamma to ry edema of lung > bacterial pneumonia • inflamma to ry edema of pleural cavity > empyema b. Composition • no increased protein • no increased cells • specific gravity less than 1. Cause > abnormality of Starling forces a) increased hydrostatic (venous) pressure • congestive heart failure • portal hypertension b) decreased oncotic pressure > due to decreased albumin • liver disease • renal disease (nephrotic syndrome) 6 Pathology c) lymphatic obstruction • tumors or surgery • filaria 12. Squamous Cell Carcinoma • skin cancer • lung cancer • esophageal cancer • cervical cancer b. Adenocarcinoma • lung cancer • colon cancer • s to mach cancer • prostate cancer • endometrial cancer c. Transitional Cell Carcinoma • urinary bladder cancer • renal cancer (renal pelvis) d. Benign • grow slowly • remain localized • may have well-developed fibrous capsule • do not metastasize • well differentiated his to logically b. Malignant • grow rapidly • locally invasive High-Yield Facts 7 • irregular growth; no capsule • capable of metastasis • variable degrees of differentiation (well differentiated, moderately differentiated, poorly differentiated) 14. Nuclear Regula to ry Proteins • c-myc > Burkitt’s lymphoma; on chromosome 8 > t(8;14) • N-myc > neuroblas to ma • L-myc > small cell carcinoma of the lung • c-jun • c-fos 8 Pathology 15. Gene Amplification • N-myc > neuroblas to ma • c-neu > breast cancer • c-erb B2 > breast cancer 16. Initia to rs • to bacco smoke > many tumors • alkylating agents (anti-cancer drugs) > many tumors • benzene > leukemias • vinyl chloride > angiosarcomas of the liver • beta-naphthylamine > cancer of the urinary bladder • azo dyes > tumors of the liver • afla to xin > hepa to ma High-Yield Facts 9 • asbes to s > mesotheliomas and lung tumors • arsenic > skin cancer 2. Ataxia Telangiectasia • sensitive to x-rays (increased risk lymphoid malignancies and leukemia) • recurrent infections (due to decreased IgA levels), oculocutaneous telangiectasia, cerebellar ataxia c. Bloom Syndrome • severe immunodeficiency, growth retardation, and increased sensitivity to radiation • short stature, “parrot”-beak nose, and facial (“butterfly”) rash • cell cultures > quadriradial configurations and increased sister chro matid exchange 19. Marasmus • dietary calorie deficiency (without protein deficiency) • generalized wasting (“skin and bones”) 22. Vitamin A • night blindness • dry eyes and dry skin • recurrent infections 12 Pathology 2. Vitamin D • decreased calcium • bone > decreased calcification, increased osteoid • children > rickets • adults > osteomalacia 3. Vitamin B1 (Thiamine) • beriberi > wet (cardiac) or dry (neurologic) • Wernicke-Korsakoff syndrome (lesions of mammillary bodies) 2. Vitamin B3 (Niacin) • pellagra > 3Ds > dermatitis, dementia, diarrhea (and death) 3. Vitamin B12 (Cobalamin) • megaloblastic (macrocytic) anemia • hypersegmented neutrophils (>5 lobes) • subacute combined degeneration of the spinal cord 4. Vitamin C (Ascorbic Acid) • scurvy • defective collagen formation > poor wound healing (wounds reopen) • bone > decreased osteoid • perifollicular hemorrhages (“corkscrew” hair) • bleeding gums and loose teeth 5. Folate • megaloblastic (macrocytic) anemia • hypersegmented neutrophils • associated with neural tube defects in utero 6. Y Inheritance • only males affected • only male- to -male transmission • all males affected f. Mi to chondrial • males and females equally affected • only females transmit the disease 14 Pathology 24. Immunodeficiency Diseases • Bru to n agammaglobulinemia • chronic granuloma to us disease • Wiskott-Aldrich syndrome c. Duchenne’s muscular dystrophy • defective dystrophin gene (muscle breakdown) • pseudohypertrophy of calf muscles • Gower maneuver (using hands to rise from floor) 2. Other Diseases • red-green color blindness • fragile X syndrome • Menkes “kinky hair” syndrome > inability to transport copper within cells 25. Terms • haploid > number of chromosomes in germ cells (23) • diploid > number of chromosomes found in nongerm cells (46) • euploid > any exact multiple of the haploid number • aneuploid > any nonmultiple of the haploid number High-Yield Facts 15 • triploid > three times the haploid number (69) • tetraploid > four times the haploid number (92) • trisomy > three copies of the same chromosome 26. Trisomy 13 (Patau’s Syndrome) • mental retardation • microcephaly and microphthalmia • holoprosencephaly (fused forebrain) • fused central face (“cyclops”) • cleft lip and palate • heart defects b. Trisomy 18 (Edwards’ Syndrome) • mental retardation • micrognathia • heart defects • rocker-bot to m feet • clenched fist with overlapping fingers c. Trisomy 21 (Down Syndrome) • most cases due to maternal nondisjunction during meiosis I (associ ated with increased maternal age) • minority of cases due to Robertsonian (balanced) translocation • mental retardation (most common familial cause) • oblique palpebral fissures with epicanthal folds • horizontal palmar crease • heart defects (endocardial cushion defect is most common) • acute lymphoblastic leukemia (first 2 years of life) • Alzheimer’s disease (almost 100% incidence after age 35) • duodenal atresia (“double-bubble” sign on x-ray) • increased susceptibility to infections 27. Paternal deletion (maternal gene is imprinted) > Prader-Willi syndrome • mental retardation • short stature and obesity • small hands and feet • hypogonadism • may be due to two copies of maternal 15 chromosome (paternal uniparental disomy) 28. IgM • large molecule (pentamer) • secreted early in immune response (primary response) • cannot cross the placenta • can activate complement • contains a J chain b. IgG • most abundant immunoglobulin in serum • secreted during second antigen exposure >secondary or amnestic response) • can cross the placenta • can activate complement • can function as opsonin c. IgE • allergies, asthma, parasitic infection • found attached to the surface of basophils and mast cells • participates in type I hypersensitivity reactions 20 Pathology d. Type I • binding of antigen to previously formed IgE bound to mast cells and basophils • release of histamine and leukotrienes C4 and D4 • urticaria (hives) • anaphylaxis b.

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