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By A. Ines. Bastyr University.

Gliadin antibodies (IgG or IgA) are not sensitive and specifc and should no longer be used; they are found in a range of bowel diseases and in healthy individuals purchase viagra soft 50mg with visa erectile dysfunction treatment canada. Gliadin antibodies and neurological disease Gluten sensitivity enteropathy is also associated with neurological disease buy viagra soft cheap online erectile dysfunction causes ppt, typically cerebellar ataxia purchase generic viagra soft line erectile dysfunction treatment costs. Saline split- ting of the skin may be used to identify the precise location of the antigenic target to diferentiate between epidermolysis bullosa acquisita (antigen on the dermal side) and pemphigoid (antigen on the epidermal side) purchase viagra soft cheap online erectile dysfunction treatment austin tx. Indications for testing These are restricted to very specifc neurological syndromes. Striated muscle antibodies (immunofuorescence on striated muscle section) strongly associated with underlying thymoma. Anti-Ri (anti-neuronal nuclei) associated with cerebellar ataxia and opsiclonus (small-cell carcinoma, gynaecological or breast tumours associated). Rasmussen’s encephalitis associated with autoantibodies to GluR3 receptor, which cause hyperexcitability of neurones. Distinction between antinuclear and perinuclear staining may require the use of Hep- 2 cells. Indications for testing Acute glomerulonephritis, particularly if associated with pulmonary haemorrhage. Urgent plasmapher- esis is required, and monitoring reduction of antibody with treatment is advisable. Screening for atopic disease; investigation of suspected hyper-IgE syndrome (Job’s syndrome, a rare immunodefciency), Churg–Strauss vasculitis. Interpretation Signifcant allergic disease is possible with low levels of total IgE (including anaphylaxis). Conversely, levels above the normal range are compatible with no clinical allergic disease. IgE >1000 associated with atopic eczema; IgE >50,000 confrms hyper-IgE syndrome (although patients may have lower levels—diagnosis is clinical). Raised levels are also seen in parasitic infections of the bowel, flariasis, lymphoma (especially Hodgkin’s disease), and Churg–Strauss vasculitis. It identifes IgE- mediated reactions (type I) such as inhalant allergy, anaphylaxis, and food allergy. It is dependent on triggering the release of histamine from cutane- ous mast cells. Solution of allergen or controls (histamine or saline) placed on the skin and pierced through by a lancet. Can use factory-prepared allergens; also use double-prick technique with fresh foods (prick food, then the patient)—useful where allergens are labile, e. Interpretation Results can only be interpreted in the context of the clinical history. May need to be followed up by open or blinded challenges where −ve results are obtained in patients with good histories. Many known families of cross-reactivity between biological families • Latex allergy associated with food reactions: banana, avocado, kiwi fruit, chestnut, potato, tomato, cannabis, lettuce. False +ves possible when total IgE is very high due to non-specifc binding (less of a problem with newer assays). Interpretation Raised levels indicate mast cell degranulation and will help distinguish ana- phylactic and anaphylactoid reactions from other causes of reactions (vas- ovagal, hyperventilation, carcinoid, phaeochromocytoma, etc. Drug allergy testing Investigation of severe drug allergy is a specialized feld and all patients should be referred to an appropriate expert for an opinion, usually a con- sultant in allergy or clinical immunology in a regional centre. Testing will usually involve skin prick testing, followed by intradermal testing and patch testing and, if necessary, blind challenge. Allergens in petrolatum jelly are placed in contact with the skin for 48h under occlusion with aluminium cups. Common allergens include metals such as nickel and chromium, dyes and chemical in leather, rubber chemicals (accelerators), and cosmetic chemicals. The tests are labour-intensive and difcult to standardize, with the exception of basic lymphocyte markers. All tests, other than basic lymphocyte markers, should only be requested after discussion with a consultant immunologist. In such cases, urgent referral of the patient to an appropriate paediatric or adult immunologist is more appropriate than fddling around trying to get tests done, as the immunologist will have direct and immediate access to the appropriate tests. Lives have been lost due to delay in transfer, whilst inexperienced clinicians have tried to make diagnoses. Many other surface markers are available to answer more specifc immunological questions, but these will usually be of interest only to clinical immunologists. Investigation of lymphocyte subsets is an important part of the work-up of any patients with suspected ° or 2° immunodefciency and of patients with unexpected lymphopenia. Samples do not transport well, and results are often abnormal if the patient has an active infection or is on antibiotics. It is preferable to refer patients to a clinical immunologist who will organize testing if appropriate. Indications for testing Patients with deep-seated abscesses, recurrent major abscesses (exclude diabetes, staphylococcal carriage, and hidradenitis suppurativa frst), major oral ulceration, and unusual fungal or bacterial infections (Pseudomonas, Serratia, staphylococci, Aspergillus). Interpretation Interpretation is complex; defects of oxidative metabolism may indicate chronic granulomatous disease; defects of phagocytosis are recognized. After the intro- duction of efective antibiotics during the Second World War, there was great optimism that the fght against infectious diseases had been won. Almost all new diseases are infections, and some of the twenty-frst century’s most pressing problems are pathogens that have only appeared in the 30 years prior to this book being written. New challenges As we proceed through the twenty-frst century, several factors are serv- ing to i the relative importance of infection over other areas of medicine. Infections such as ebola, zika, and avian/swine infuenza are continually emerging and re-emerging. There are more immunosuppressed patients as a result of i use of chemotherapy agents and organ transplantation. Tourists and other travellers are making their way to ever more remote parts of the world. All of these factors mean that the infectious diferential diagnosis—even in the developed world— grows ever longer. It is always worth bearing in mind infection in a diferential diagnosis is often treatable. Accordingly, it is always better not to miss treatable options over incurable ones. A challenge to the clinician The same infection is often capable of causing a wide variety of clinical pictures. This is not so surprising, given the genetic variety of mankind, hence individual responses to a bewil- dering variety of infecting agents. Other diseases can mimic infections non-infectious diseases can resemble infection. Importance of epidemiological factors epidemiology is fundamental to determining which, if any, infecting agents, and therefore investigations, are relevant in a given patient. Travel exposes patients to new infec- tious agents to which they have no immunity. Immunization schedules dif- fer throughout the world, and some groups refuse to have their children vaccinated. Great variation in antibiotic resistance patterns can be observed in diferent parts of the world; this clearly has an impact on the choice of empirical treatment. Finally, travel often has an impact on patterns of sexual and risk-taking behaviour (see Fig. Malaria, which can be life-threatening, is a very common disease in many parts of the world but is not indigenous to most parts of the developed world. Making a diagnosis depends heavily upon the clinician eliciting the clues in the patient’s history. Clinical suspicion should lead to blood flms (on 3 consecutive days) and a platelet count. Bear in mind that the patient may not have been taking adequate prophylaxis, may have been missing tablets, or may not have been absorbing them. The clinician must maintain high clinical suspicion at all times, even and especially when the patient does not ft a social stereotype. Bear in mind that any patient may have a ‘double life’, of which even his/her spouse is unaware. It is danger- ous for the clinician to assume that being married equates to sexual fdelity or even heterosexuality. It may not be immediately obvious that the fever, rash, and hypotension in a woman may be related to her tampon usage (toxic shock syndrome), yet menstruation can be a difcult subject to discuss in some cultural set- tings. The tropical fsh salesman with a chronic rash on his hand could have Mycobacterium marinum infection (aka ‘fsh tank granuloma’). The jaundiced volunteer cleaning out canals at week- ends could have leptospirosis related to contact with rats. The cat owned by the middle-aged lady with recurrent axillary lymphadenopathy may be the key to her problem of cat-scratch disease (Bartonella henselae). The disease in front of you might be the frst ever presentation or the frst in a new outbreak! Almost the only signifcant new human diseases that will appear in the future will be infectious diseases and they will keep appearing till the end of the human species (see Fig. When considering the possibility of an infective process, one should always consider the basic taxonomy • Bacteria (including primitive forms). Investigations available to the infectious diseases or general physician Many tests will be performed with a view to making a diagnosis. Investigation of a patient should be rational and evidence-based, wher- ever possible.

Step 4: Compute the value of test statistic “Z” viagra soft 50 mg free shipping impotence stress, (Z = Observed difference/ Standard error) cheap viagra soft 50 mg amex zma impotence. Confidence interval: The 95 % confidence interval for population mean is sample mean ± 1 discount viagra soft amex erectile dysfunction non prescription drugs. In a city A order viagra soft online pills impotence nasal spray, 20% of a random sample of 900 school boys had defective eye sight, in another city B, 15. Find out whether the proportion of girl students is 40% of all Students (boys & girls) for all the years i. Test Regarding Single Mean This test is used for testing the significance of difference between sample mean and population mean or whether sample has been drawn from the population or not. In case of small sample (n<30), the test statistics is: 2 X −µ (x x) t = where S2 = S/ n n − 1 The test statistics ‘t’ has degrees of freedom, i. If calculated value of ‘t’ is greater than table value, then it rejects the null hypothesis and if less, then H0 may be accepted. Unpaired t test x − x 2 2 12 2 ∑( )( )x 1 −x +∑x 2 −x t = where S = 1 1 n n 2 S + 12 n12n Degree of freedom (df) df = (n1 – 1) + (n2 – 1) = n1 + n2 – 2 b. Paired t-test dn – ∑ di t = where d = x – y , d = , S i i i n 2 ∑ ()di d S = n − 1 examples Calculate‘t’ test for the following data: 1. Repaglinide: following results showed the values of blood glucose in mg% before and after the medication. Apgar scores in two groups of newborns, one group born to high-risk mothers and the other to normal mothers, are given below. Comment whether there is significant difference in the Apgar scores of these two groups. Newborns of high-risk mothers (x): 5 3 2 4 7 6 3 Newborns of normal mothers (y): 1 1 2 1 1 3 5 Mean for x = 4. Following are the results of weight gain by pigs that were on two different diets A and B. Diet a 25 32 30 34 24 14 32 24 30 31 Diet b 44 34 22 10 47 31 40 30 32 35 Mean of diet ‘A’ = 27. In other words, whether there is an association between the row and the column variable. Compute the values of chi-square test statistic = χ2 = Σ(O–E) /E2 2 2 (Observed Expected) χ = Expected 4. If calculated value of χ2 is greater than table value of χ2, reject the null hypothesis otherwise accept it. Comments whether the good attendance (more than 75%) has any effect on the results of examination. The chi­square test of significance is useful as a tool to determine whether or not it is worth the researcher’s effort to interpret a contingency table. A significant result of this test means that the cells of a contingency table should be interpreted. A non­significant test means that no effects were discovered and chance could explain the observed differences in the cells. Fisher exact test: Sometimes Chi-squared test and normal tests for 2 × 2 tables may not be valid if sample size is very small. Fisher’s exact test is recommended, when • The overall total of table is less than 20 or • The overall total is between 20 and 40 and smallest of the four expected numbers is less than 5. In correlation, change in the value of one variable will change the value of another variable. Negative correlation Positive Correlation When the increase /decrease in the value of one variable may increase / decrease the value of another variable such a correlation is called positive correlation. Negative Correlation If the value of one variable increases then the value of the other variable decreases and vice­versa, e. Karl Pearson’s Coefficient of Correlation The coefficient of correlation is calculated by using the formula: Karl-Pearson’s coefficient Cov (x,y) (xi x) (yi y) r = = σ. Interpretation of the Correlation Coeffcient Correlation analysis is a measure of relationship between two variables. The higher value of V establishes high degree of relationship only and it should not be taken as a measure of cause and effect relationship. In some cases a casual relation may exist between two variables whereas in others a relationship may exist between two variables because both are related to a third variable. Sometimes the relationship may be purely due to chance, if another set of data is collected and a Pearson V is calculated, the resulting V may be meaningless. Computation of the correlation coefficient: – – – X Y (X–X) (Y–Y) (X –X) (Y–Y) 8 12 1 0 0 3 9 -4 -3 12 4 10 -3 -2 6 10 15 3 3 9 6 11 -1 -1 1 7 12 0 0 0 11 15 4 3 12 Σx = 49 84 0 0 40 n = 7 ∑ x ∑ y – – x = = 7 y = = 12 n n ∑ (x xy y) ( ) 40 Covariance (xy) = = = 6. Age of husband: 18 19 20 21 22 23 24 25 26 Age of wife: 17 17 18 18 18 19 19 20 21 Answer = r = 0. Temperature: 98 99 100 101 102 103 104 105 100 Pulse rate: 72 80 92 111 116 128 132 130 90 Answer = r = 0. It is customary to denote the independent variable by x and dependent variable by y. The formula for obtaining the regression coefficient is as follows: y = b0+ b1x where, y = Mean of y1, y2,. If one of the regression coefficients is less than unity, then other must be greater than unity. Arithmetic mean of regression coefficient is greater than the correlation coefficient provided r > 0. The data is collected through open-ended questions in an interview, self-administered questionnaires, in-depth interviews, key informant information, and focus group discussions or through observations during fieldwork. The data collected through testimonials (reactions and comments), log books (free flowing text and procedures), journals, diaries, documents, reports, stories, case studies, etc. Since the qualitative data consist of words and observations, not the numbers, hence the analysis requires a systematic approach. To establish clear links between the research objectives and the summary findings derived from the raw data and to ensure these links are both transparent and defensible. To develop a model or theory about the underlying structure of experiences or processes, which are evident in the text data. There are various methods of analyzing qualitative data but none of the methods is perfect, however, the most commonly used methods are described as under: 1. Content analysis This is the most commonly used method in the medical and health research. Understanding the data: Read data carefully so as to understand in the context of the research objectives and goal to be achieved. Codes have tags or labels, which are assigned to whole Analysis of Qualitative Data 173 documents or segments of documents (i. The coding process includes development, finalization, and application of the code structure. The development of the code structure is an iterative and lengthy process, which begins in the data collection phase. Coding may be inductive or deductive but a well-framed, clear, and comprehensive code structure promotes the quality of subsequent analysis. Grounded Theory Approach to Developing Code Structure The recommended approach to developing a set of codes is purely inductive. This approach limits researchers from erroneously “forcing” a preconceived result. Data are reviewed line by line in detail and as a concept becomes apparent, a code is assigned. Upon further review of data, the analyst continues to assign codes that reflect the concepts that emerge, highlighting and coding lines, paragraphs, or segments that illustrate the chosen concept. As more data are reviewed, the specifications of codes are developed and refined to fit the data. To ascertain whether a code is appropriately assigned, the analyst compares text segments to segments that have been previously assigned the same code and decides whether they reflect the same concept. Using this ‘‘constant comparison’’ method, the researchers refine dimensions of existing codes and identify new codes. Through this process, the code structure evolves inductively, reflecting ‘‘the ground,’’ i. Deductive Approaches to Developing Code Structure Miles and Huberman (1994) have described a more deductive approach, which starts with an organizing framework for the codes. In this approach, the initial step defines a structure of initial codes before line-by-line review of the data. Preliminary codes can help researchers integrate concepts already wellknown in the extant literature. For example, a deductive approach of health service use might begin with predetermined codes for predisposing, enabling, and need factors based on the behavioral model. Great care must be taken to avoid forcing data into these categories because a code exists for them; however such a ‘‘start list’’ does allow new inquiries to benefit from and build on previous insights in the field. An Integrated Approach to Developing Code Structure An integrated approach employs both inductive development of codes as well as a deductive organizing framework for code types (start list). These code types are: • Conceptual codes and subcodes identifying key concept domains and essential dimensions of these concept domains. Applying the Finalized Code Structure First approach in applying the finalized code structure to the data is to have two to three members of the research team which re-review all the data, applying independently the codes from the finalized code structure. The second approach is to establish the reliability of multiple coders from the research team with a selected group of data. Once coders have been established to be reliable with one another, one of the coders completes the remainder of the coding independently. Generating outcome Researcher should focus on three types of output from qualitative studies i. These outputs may be helpful in improving the measurement of multifaceted interventions; the generation of hypotheses about causal links among service quality, cost, or access; and revealing the context of events those might influence various health- related outcomes. Taxonomy: It is a system for classifying multifaceted, complex phenomena according to common conceptual domains and dimensions.

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In high-risk populations such as those with hip or knee replacement discount 50 mg viagra soft otc impotence lifestyle changes, a combination of mechanical and pharmacologic therapies should be considered purchase viagra soft 50 mg mastercard erectile dysfunction drugs and glaucoma. For example order discount viagra soft on-line beer causes erectile dysfunction, extended prophylaxis for up to 28 to 35 days is recommended for patients who have had a hip fracture or who undergo total hip replacement surgery purchase 50 mg viagra soft fast delivery erectile dysfunction vegan. Conditions that predispose persons to an increased risk of thrombosis are referred to as hypercoagulable states or thrombophilia. These conditions are being identified more frequently and may be classified as inherited or acquired. Therefore, routine screening for these mutations is not warranted in most patients with arterial thrombosis. There are no clear evidence-based guidelines for managing patients with thrombosis in the setting of these thrombophilias. In general, acute thrombosis should be managed in a standard fashion, but the duration of therapy is less clear, and the benefits of long-term anticoagulation must be weighed against the risks of bleeding. Deficiency of any of the three natural anticoagulants is associated with an increased risk of venous thrombosis. All are inherited as autosomal dominant defects and are further subclassified based on reduction in their levels or defective quality of the protein. It may be inherited, and genetic defects causing a deficiency of cystathionine β-synthase or a mutation in methylenetetrahydrofolate reductase have been reported. Acquired causes include deficiencies in vitamin B , B , or folate; smoking; and liver or12 6 renal failure. Therefore, the initiation of an alternative anticoagulant, unless contraindicated, is recommended. Once platelet counts are more than 100,000 to 150,000 mm , warfarin may be started at a low dose (2. Early introduction or higher doses of warfarin may lead to venous limb gangrene or warfarin-induced skin necrosis. Antiphospholipid antibodies are a heterogeneous group of autoantibodies that, if present in a patient with thrombosis, lead to the antiphospholipid syndrome. Antiphospholipid antibodies can be divided into three groups: (a) anticardiolipin antibodies, (b) lupus anticoagulants, and (c) β -glycoproteins. They are often associated with other2 autoimmune conditions and can cause recurrent pregnancy loss, as well as arterial or venous thrombosis. Anticardiolipin antibodies are detected and quantified using an enzyme-linked immunosorbent assay and may be IgG, IgM, or IgA. Lupus anticoagulants prolong phospholipid-dependent blood clotting times, and it has been reported that there is about a fivefold increased risk of thrombosis in patients with this finding. Once a thrombotic event occurs, long-term therapy with warfarin must be considered. Predictive value of compression ultrasonography for deep vein thrombosis in symptomatic outpatients: clinical implications of the site of vein noncompressibility. Fondaparinux or enoxaparin for the initial treatment of symptomatic deep venous thrombosis: a randomized trial. Subcutaneous fondaparinux versus intravenous unfractionated heparin in the initial treatment of pulmonary embolism. A comparison of two intensities of warfarin for the prevention of recurrent thrombosis in patients with the antiphospholipid antibody syndrome. Guidelines for the use of retrievable and convertible vena cava filters: report from the Society of Interventional Radiology multidisciplinary consensus conference. Comparison of fixed-dose weight-adjusted unfractionated heparin and low-molecular-weight heparin for acute treatment of venous thromboembolism. Importance of cardiac troponins I and T in risk stratification of patients with acute pulmonary embolism. Apixaban versus enoxaparin for thromboprophylaxis after knee replacement: a randomized double-blind trial. Meta-analysis: outcomes in patients with suspected pulmonary embolism managed with computed tomographic pulmonary angiography. Usefulness of clinical prediction rules for the diagnosis of venous thromboembolism: a systematic review. Effectiveness of managing suspected pulmonary embolism using an algorithm combining clinical probability, D-dimer testing, and computed tomography. Brain natriuretic peptide as a predictor of adverse outcome in patients with pulmonary embolism. Underuse of venous thromboembolism prophylaxis for general surgery patients: physician practices in the community hospital setting. Color-flow duplex scanning for the surveillance and diagnosis of acute deep venous thrombosis. Echocardiography Doppler in pulmonary embolism: right ventricular dysfunction as a predictor of mortality rate. Diagnosis of deep-vein thrombosis: comparison of clinical evaluation, ultrasound, plethysmography, and venoscan with X-ray venogram. Value of the 12-lead electrocardiogram at hospital admission in the diagnosis of pulmonary embolism. Clinical, laboratory, roentgenographic, and electrocardiographic findings in patients with acute pulmonary embolism and no pre- existing cardiac or pulmonary disease. Increased risk of venous thrombosis in oral- contraceptive users who are carriers of factor V Leiden mutation. Value of assessment of pretest probability of deep- vein thrombosis in clinical management. The aorta is the principal conductance vessel in the body and is divided into the ascending, arch, descending thoracic, and abdominal components. The ascending aorta includes the aortic root, which contains the sinuses of Valsalva. The left and right coronary arteries arise from the left and right coronary sinuses, respectively. These include the brachiocephalic (innominate), the left common carotid, and the left subclavian arteries. The point at which aortic arch joins the descending aorta is called the isthmus, marked by ligamentum arteriosum. The aortic isthmus is often the site of origin of dissection tear because the aorta is relatively fixed to the thoracic cage in this region. The descending thoracic aorta provides the intercostal vessels as it courses through the posterior mediastinum. The vascular supply to the anterior spinal artery is included among these vessels. It provides the splanchnic and renal arteries before bifurcating to become the common iliac arteries. It consists primarily of laminar layers of elastic tissue and smooth muscle in varying amounts. This structure allows for the high tensile strength and elasticity required to withstand the pressure changes of each heartbeat throughout the life of the individual. The adventitia is the thin outer layer that anchors the aorta within the body, in addition to providing nourishment to the outer half of the wall through the vasa vasorum. The elasticity of the aortic wall allows it to distend under the pressure created during ventricular systole. In this way, the kinetic energy that was developed during ventricular systole is stored as potential energy in the distended aortic wall. Then, during ventricular diastole, the potential energy is converted back to kinetic energy by elastic recoil of the wall. Pressure receptors in the ascending aorta and aortic arch signal the vasomotor centers of the brain via the vagus nerve. Aortic dissection classically occurs when a tear in the intima results in separation of the intima from the media (90% of cases). This aortic tear then propagates anterograde or less commonly, retrograde typically creating a false lumen in the aortic wall. In either case, acute aortic dissection results from a pathologic weakening of the aortic wall because of medial necrosis, atherosclerosis, or inflammation. Surgery is often recommended for patients exhibiting unstable symptoms or lesions involving the ascending aorta. Otherwise, medical management and frequent radiologic follow-up for signs of progression are recommended. There are many risk factors for aortic dissection, although the most common is a history of systemic hypertension as evidenced in over 70% of cases. The following list includes the most common conditions associated with aortic dissection: a. These patients require comprehensive aortic imaging at diagnosis and heightened surveillance to follow aortic diameter owing to the increased risk of complications related to aortic disease. Marfan syndrome is a genetic disorder with high penetrance and variable expression affecting connective tissue. The principal features of Marfan syndrome involve the cardiovascular, ocular, and skeletal systems, with patients at exceedingly high risk for aortic disease. In fact, nearly all patients with Marfan syndrome demonstrate some form of aortic disease during their lifetime. Vascular disease among these patients is highly prevalent, with 98% demonstrating aortic root aneurysms, and portends a grim prognosis. Early reports of Loeys–Dietz syndrome suggested a particularly aggressive disease process with arterial complications occurring at a mean age of 26 years. However, subsequent data have revealed less aggressive phenotypes with later presentations, and a mean age of death closer to the fifth decade among less severe phenotypes. Clinical features include easy bruising and rupture of the uterus, intestines, and arteries. Gravid women with this condition have a particularly poor prognosis during childbirth because of the high risk of arterial and uterine rupture.

I—Inflammatory disorders include vulvitis and bartholinitis (often related to gonorrhea) order viagra soft 100mg with mastercard erectile dysfunction pump australia, various forms of vaginitis (bacterial buy viagra soft with a visa erectile dysfunction statistics uk, trichomoniasis order viagra soft 50mg with amex blood pressure drugs erectile dysfunction, and moniliasis) 100mg viagra soft mastercard impotence after 60, and salpingo-oophoritis. Thus, a urethral carbuncle, urethritis, cystitis, hemorrhoids, and anal fissures can cause dyspareunia. N—Neoplasms causing dyspareunia are leukoplakia vulvitis, kraurosis vulvae, carcinoma of the vulva and vagina, ovarian cysts, and carcinoma. When uterine and cervical carcinomas extend beyond the genital tract, dyspareunia is present. Any neoplasm of the bladder and rectum that has extended into the genital tract will undoubtedly cause dyspareunia. Introduction of the male organ before adequate foreplay has created a lubricated vagina is another cause. Women in menopause may require lubricants to prevent local trauma, because the vagina remains dry even after sexual excitement because of lack of hormonal secretion. Incest, guilt from masturbation, and latent homosexuality are a few of the problems that may be encountered. A few other2 mechanisms that produce hyperventilation and tachypnea will be discussed later on in this chapter. The best basic science for developing a list of the causes of dyspnea and tachypnea is pathophysiology. Disorders of oxygen intake: In this category are the conditions that may block the respiratory passages such as laryngitis, foreign bodies, an aortic aneurysm or mediastinal tumor pressing on the trachea or bronchi, bronchial asthma, acute infectious bronchitis, and pulmonary emphysema. Also considered in this category are conditions that interfere with the “respiratory pump” (thoracic cage, thoracic and diaphragmatic muscles, and respiratory centers in the brain) such as kyphoscoliosis, Pickwickian syndrome, myasthenia gravis, Muscular dystrophy and other neuromuscular diseases, peritonitis, encephalitis, and brain tumors. Disorders of oxygen absorption: Lobar pneumonia, sarcoidosis, silicosis, berylliosis, and various causes of pulmonary fibrosis, and pulmonary edema are considered here. Oxygen diffusion across the alveolocapillary membrane is affected in all of these. Alveolar proteinosis, shock lung, and the adult respiratory distress syndrome must also be considered here. Disorders of perfusion of the pulmonary capillaries: Pulmonary emboli, hemangiomas of the lungs, and congenital heart increases such as tetralogy of Fallot belong in this category. Also included in this category 298 are diseases with a ventilation–perfusion defect. In other words, some alveoli are being ventilated but not perfused with blood, while at the same time some alveoli are being perfused but not ventilated. Pulmonary emphysema and the various conditions associated with pulmonary fibrosis (e. In methemoglobinemia and sulfhemoglobinemia, there may be enough blood, but it is unable to carry the oxygen. Increased tissue oxygen demand: During exercise and nervous stress, and in febrile states, leukemia and other malignancies, and hyperthyroidism there is an increase in tissue metabolism; consequently, tachypnea may develop to increase the supply. Other wastes of tissue metabolism may cause an acidosis and stimulate the respiratory centers in this fashion. From the above discussion, it should be evident that the clinician can develop an excellent list of the causes of dyspnea and tachypnea with an understanding of the pathophysiology involved. A few conditions cannot be recalled with this method: hyperventilation syndrome, ingestion of acids (e. Approach to the Diagnosis The history and physical examination will almost invariably disclose the cause of dyspnea. To confirm pulmonary disease one will order pulmonary function studies, a chest roentgenogram, and arterial blood gases. If routine pulmonary function studies are normal, more sophisticated studies such as the nitrogen washout test and perfusion and ventilatory scans may be necessary. A determination of the erythrocytes’ methemoglobin, arterial oxygen saturation, and diaphorase I test must be done. Case Presentation #19 A 55-year-old white male electrician calls you asking if you would order an antibiotic for a cough he has had for 10 days. Utilizing the methods discussed above, what are the possible causes of the cough and shortness of breath at this point? On examination, you find that the patient is expectorating frothy, slightly blood-tinged sputum, has crepitant rales at both lung bases, cardiomegaly, and a rapid irregular heart rhythm with a pulse deficit. An abnormally long labor may result from inadequate abdominal muscle or uterine muscle contractions, obstruction of the birth canal, abnormalities of the fetus or placenta, and unusual positions of the fetus in the abdomen and pelvis. Inadequate abdominal muscle contractions: This may be due to diastasis recti, ventral hernias, and obesity. Inadequate uterine muscle contractions: This may result from malformations of the uterus, such as bicornuate uterus; multiple 304 fibroids and other neoplasms of the uterus; drugs that inhibit uterine contractions, such as morphine and other sedatives; and primary uterine inertia. Obstruction of the birth canal: Look for ovarian cysts, uterine fibroids, cervical stenosis, deformities of the pelvis, impacted feces, and an enlarged bladder in this category. Abnormalities of the fetus: This category includes large babies, polyhydramnios due to diabetes mellitus, hydrocephalus, abdominal neoplasms or ascites in the fetus, and twins or additional multiple births. Abnormal position of the fetus: Breech presentation, transverse lie, face or brow presentation, and occipitoposterior presentations are included in this category. Approach to the Diagnosis Thorough examinations, sonograms, x-rays of the abdomen for fetal size and position, and amniocentesis are all useful procedures to assist in the diagnosis. One could cover most of the causes simply by considering the inflammatory lesions of the genitourinary tract in ascending order. Thus, there may be urethritis or urethral carbuncle, trigonitis or prostatitis, cystitis, or pyelonephritis with associated cystitis. This would not, however, cover the disorders that frequently cause associated inflammation of the urinary tract or are associated with difficulty in voiding. M—Malformations would bring to mind meatal stricture, bladder neck obstruction by prostatic hypertrophy, median bar, and urethral strictures. N—Neoplasms of the prostate and bladder may cause difficulty in voiding or painful urination when secondary infection sets in. T—Trauma suggests cystitis and trigonitis (honeymoon cystitis) caused by frequent or traumatic intercourse or by introduction of foreign bodies into the bladder, such as catheters. In women with “negative” cultures, Chlamydia urethritis must be considered and treated. In men with negative cultures, prostatic examination, massage, and evaluation of discharge are done. All patients with persistent dysuria should be given a therapeutic trial of antibiotics even when the urinalysis is negative. Applying the above methods, what would be your list of possible causes for this young man’s problem? History reveals that he was treated with penicillin 2 months ago for a urethral discharge that developed after a casual sexual encounter. Thus, otitis externa would be like urethritis, otitis media like cystitis, and so forth. Foreign bodies in the ear, like foreign bodies in the bladder, must always be looked for. Referral to an otolaryngologist or neurologist is probably best for the busy physician who is unable to find the cause on a routine examination. However, 308 what if the heart and chest sound normal and there is a negative Homans sign? Obviously, before the physician questions the patient the clinician needs a more complete list of diagnostic possibilities. Fluid is passing from the blood compartment into the subcutaneous tissues and back again all the time. The pressure in the veins may be so high that it overcomes the oncotic pressure of the albumin and other proteins in the blood. The pressure in the arteries may be so high that more fluid is pushed out than can be reabsorbed with normal oncotic pressure. The level of serum albumin may be so low that the oncotic pressure drops to a point where it cannot reabsorb all the fluid being driven out by the forward pressure of the arteries or backward pressure of the veins. This is seen in conditions in which either too little albumin is produced (cirrhosis of the liver) or too much albumin is lost in the urine (nephrotic syndrome of diabetes mellitus, lupus erythematosus, amyloidosis, and several other disorders of the kidney). The lymphatic channels that pick up any excess fluid that the veins cannot pick up may be blocked. This occurs notably in filariasis, Milroy disease, and lymphedema following mastectomy, but other conditions may also block the lymphatics. An abnormal protein (mucoprotein) may be deposited in the tissues and lead to edema. A reduction in tissue turgor pressure may be responsible for the edema in older people and beriberi (vitamin B deficiency). Retention of salt as in primary and secondary aldosteronism is a minor factor, because most cases of aldosterone-secreting adenomas do not have significant edema. It would be a serious omission not to mention local conditions such as cellulitis, ruptured Baker cysts, burns (especially sunburn), contusions, and urticaria that may cause edema, but these are usually obvious. If there is nephrosis, there will be significant lowering of the serum albumin level and proteinuria. Liver function studies will usually confirm cirrhosis or liver disease, but ultrasonography can reveal ascites to assist in the diagnosis. Unilateral edema of the lower extremities suggests deep vein thrombosis, which can be confirmed by Doppler ultrasound studies, plethysmography, or contrast venography. Spirometry and arterial blood gas analysis will diagnose pulmonary emphysema with cor pulmonale. She admitted to consuming one to two glasses of wine before dinner almost daily for many years.

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