By A. Rasarus. Bienville University.

This may uncover anxiety that the patient has about a certain symptom and why buy 10mg zetia fast delivery. It may also help to determine severity in a stoic patient who may underestimate or underreport symptoms buy 10 mg zetia visa. Throughout the history buy zetia 10 mg otc, interviewers recognize that patients may forget details generic zetia 10 mg online, so prob- ing questions may become necessary buy zetia 10mg. Moreover, patients sometimes have trouble finding the precise words to describe their complaint. However, good descriptors are necessary to isolate the cause, source, and location of symptoms. Often, the patient must be encouraged to use common language and terminology, to tie a symptom to something common. For instance, encourage the patient to describe the problem to you just as he or she would describe it to a relative or neighbor. The history should include specific components, to ensure that the problem is compre- hensively evaluated. These components are summarized in Table 1-1, and the specific ques- tions to include in each section are described in detail in subsequent chapters. PHYSICAL EXAMINATION The expert diagnostician must also be able to perform a physical assessment accurately. This requires extensive practice with all components of the physical examination and keen Table 1-1. Important to consider using the patient’s terminology. History of Present Illness To provide a thorough description of the chief complaint and current problem. P: precipitating and To identify factors that make symptom worse and/or better; any previ- palliative factors ous self-treatment or prescribed treatment, and response. Q: quality and quantity To identify patient’s rating of symptom (e. R: region and radiation To identify the exact location of the symptom and any area of radiation. S: severity and associated To identify the symptom’s severity (e. T: timing and temporal To identify when complaint was first noticed; how it has changed/pro- descriptions gressed since onset (e. Past Medical History To identify past diagnoses, surgeries, hospitalizations, injuries, allergies, immunizations, current medications. Habits To describe any use of tobacco, alcohol, drugs, and to identify patterns of sleep, exercise, etc. Sociocultural To identify occupational and recreational activities and experiences, liv- ing environment, financial status/support as related to health care needs, travel, lifestyle, etc. Family History To identify potential sources of hereditary diseases; a genogram is help- ful; the minimum includes 1st-degree relatives (parents, siblings, chil- dren), although 2–3 orders are helpful. Review of Systems To review a list of possible symptoms that the patient may have noted in each of the body systems. Extensive, repetitive practice is required to develop physical examination skills, with exposure to a range of normal variants and abnormal findings. Each component of the physical examination must be performed correctly to ensure that findings are as valid and reliable as possible. While performing the physical examination, the examiner must be able to • differentiate between normal and abnormal findings • recall knowledge of a range of conditions, including their associated signs and symp- toms • recognize how certain conditions affect the response to other conditions in ways that are not entirely predictable • differentiate between the importance of varied abnormal findings The aspects of physical examination are summarized in each of the following chapters, using a systems approach. Each of the subsequent chapters also reviews the relevant exami- nation for varied complaints. In addition to the specific skills, it is crucial that vital signs and the patient’s general appearance/condition always be considered in the decision-making. DIAGNOSTIC STUDIES In addition to deciding which questions and physical assessment techniques to implement, the decision-making also guides the selection of any diagnostic studies. Diagnostic studies should be considered if a patient’s diagnosis remains in doubt following the history and physical.

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Paper wasps purchase zetia 10 mg with visa, which often build open nests under windowsills or eaves cheap 10mg zetia overnight delivery, have the ability to sting multiple times Key Concept/Objective: To know general aspects about the behavior of Hymenoptera to appropri- ately counsel a patient regarding avoidance A basic familiarity with the families of the Hymenoptera order can help the clinician to establish the cause of an allergic reaction and to educate patients regarding avoidance cheap 10mg zetia with visa. Many insects are more abundant in warmer climates generic zetia 10 mg online, such as those in the southeastern United States order 10mg zetia overnight delivery; if this patient spends a significant amount of time outdoors, she may be at increased risk of exposure to stinging insects. The three most important families of Hymenoptera in terms of allergic reactions are the bees (including honeybees and bum- blebees), the vespids (including yellow jackets, hornets, and wasps), and imported fire ants. Honeybees are relatively docile and usually do not sting unless provoked. Often, exposure occurs as a result of gardening or stepping on a bee with a bare foot. Africanized honeybees (“killer bees”) are present in the southern United States; they have a tendency to swarm with little provocation and to sting in large numbers. Their venom is identical to that of the common honeybee, and an individual sting is no more potent. Unlike hon- eybees, vespids, such as yellow jackets and wasps, can sting multiple times. Yellow jackets scavenge food and are often found around picnics and garbage cans. They are aggressive and will sting without provocation: thus, allergic persons should be on the lookout for yel- low jackets in the appropriate settings. Paper wasps are abundant in the southeastern United States and along the Gulf Coast; they build nests under overhangs. Imported fire ants have become an increasing hazard; their sting induces a unique sterile pustule that is readily recognized. A mother and her 14-year-old son are in your office. He subsequently developed severe swelling at the site of envenomation; the swelling increased over 24 hours and persisted for several days. He did not, however, develop generalized urticaria, dyspnea, dys- phonia, or weakness. The mother is concerned about the possibility of his having a life-threatening reac- tion to stings and wants to know what to look for and what tests can be done to determine his risk. Involvement of the pulmonary and circulatory systems distinguishes a systemic allergic reaction from a severe localized cutaneous reaction B. RAST must be interpreted in light of the patient’s allergic history because venom-specific IgE antibodies may be present in patients who have never demonstrated an allergic reaction to stings C. RAST is less sensitive than skin testing, and up to 15% to 20% of patients with a documented anaphylactic reaction and positive skin- test results may have undetectable levels of venom-specific IgE anti- bodies 20 BOARD REVIEW D. The degree of reaction to a venom skin test (as measured by the size of the wheal and flare) closely correlates with the severity of a patient’s allergic reaction to stings Key Concept/Objective: To be able to use clinical and laboratory information to diagnose allergic reactions to Hymenoptera stings Allergic reactions to stings are IgE mediated and may be local or systemic. Local reactions are late-phase reactions consisting of swelling at the site of the sting: they may be massive and cause considerable pain. Systemic reactions, although sometimes localized to the skin (especially in children, who may develop only generalized urticaria), may also involve the pulmonary, circulatory, and gastrointestinal systems and are a medical emergency. Skin testing and RAST can help establish the diagnosis of allergy in a patient with a history that suggests the patient is at risk. Skin testing is more sensitive for detecting allergy (up to 20% of patients with a positive skin test and documented allergic reaction to a sting may not have detectable IgE with RAST), but the size of the wheal and flare reaction has absolute- ly no relation to the severity of the allergic response to a sting. RAST should not be per- formed as a screening test in patients without an appropriate clinical history, because adults who never develop allergic reactions may demonstrate venom-specific IgE antibod- ies. A 25-year-old woman with a history of eczema presents to the emergency department 2 hours after being stung by a bee while gardening. Initially, swelling occurred at the site of the sting; this was followed by a diffuse urticarial eruption, dyspnea, wheezing, and dizziness. At the triage station, she is awake but somewhat lethargic. Her blood pressure is 94/32 mm Hg, and her heart rate is 112 beats/min. Which of the following statements concerning this patient is false? Epinephrine is the initial drug of choice for anaphylactic reactions and may be lifesaving B. If the patient demonstrates initial improvement after treatment, it is safe to discharge her home after observing her for 2 to 4 hours C. Corticosteroids such as hydrocortisone are appropriate to administer, although their ability to prevent late-phase reactions is debated D.

No appreciable difference in the properties of bone growing adjacent to the different polymers was noted at the first three time periods (6 10mg zetia for sale, 12 buy zetia 10 mg without a prescription, and 24 weeks) 10 mg zetia visa. All chambers demonstrated good bone ingrowth and a trend toward increasing impedance zetia 10 mg visa. However cheap 10mg zetia with visa, 48 weeks post-implantation there was a marked decrease in the impedance of the bone in the PLA chambers in comparison to the 24-week PLA data. This was in direct contrast to the bone growing near the tyrosine-derived polymers which was still increasing in impedance at 48 weeks. Very little bone is observed growing into the PLA chamber and the impedance is significantly lower than the impedance at 48 weeks for polyDTE. In contrast, well-mineralized bone is observed filling the channels of the DTE bone chamber. Using acoustic microscopy, a quantitative micromechanical analysis of bone growing adjacent to biodegradable polymers was possible. The decrease in the elastic properties of the bone juxtaposed to PLA from 24 to 48 weeks possibly reflects the effect of PLA degradation products. Hypothetically, PLA degradation results in a more acidic local environment, causing bone resorption (seen histologically) and consequently a reduction in the impedance of the surrounding bone. On the other hand, bone growing into the tyrosine-derived polycarbonate implants continued to calcify out to 48 weeks and approached 75% of the impedance for normal canine cortical bone. This methodology works quite well for the character- ization of this type of bony specimen. However, the properties thusly determined are by definition averaged over the specimen’s entire cross section and length. Similar testing protocols have been imple- mented for cores of cancellous bone67,68 and individual trabeculae. Relatively little bone is found within the chamber and the impedance is significantly lower. A well-mineralized bone is found adjacent to the polymer coupons. The tissue in such instances is highly heterogeneous and anisotropic. Conventional testing procedures that measure bulk specimen properties cannot easily deal with this type of specimen. Bone has a very irregular and delicate structure, making the fabrication and testing of specimens difficult. Numerous researchers have attempted to overcome these obstacles using other techniques. Spatial variations in material hardness can be investigated using a host of indentation tests (Vickers, Brinell, and Rockwell). Each technique uses indentors of a particular size and geometry, from which a measure of material stiffness can be determined. Several investigators71,72 have successfully used microindentation methods to assess local property variations in various well-mineralized tissues. Additional research efforts have employed similar methods toward the characterization of local prop- erty variations in partially mineralized bone and fracture callus. The spacing of indents must be rather large due to the effect of each indent on the surrounding area since the material is damaged (work-hardened) for some distance from the point of indentation. The response of the material at the indent site is also dependent on the properties of the adjacent material buttressing the deformed material. Indentation techniques are not well suited for heterogeneous materials. They are also time consuming and cause permanent damage to the specimen. The mineral density of irregularly shaped and partially calcified bone can also be determined using dual X-ray energy absorptiometry (DEXA). This can be done in vivo; however, the resolving capability of most systems is relatively low (approximately 100 µm), and interpreting the results is difficult due to averaging across specimen thickness.

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Knee OA is more than five times more prevalent than hip OA buy zetia 10 mg fast delivery, and together they affect 10–25% of people over the age of 65 10 mg zetia mastercard. In the developed world OA ranks fourth in health impact among women and eighth among men zetia 10mg line. A current view of the nature of osteoarthritis The traditional view of OA is that it is a degenerative disease of articular cartilage cheap zetia 10mg line, the inevitable consequence of ageing purchase zetia 10 mg without a prescription, that once symptomatic always progresses, and for which nothing definitive can be done other than surgery. This pessimistic view is widely held not just by the general public but also by many of the healthcare professionals who manage patients with OA. In the last decade, however, it has become increasingly apparent that such a negative perspective is unfounded. For example: G Study of the pathophysiology of OA shows it to be a metabolically active, dynamic process involving synthetic as well as degradative processes. Although there is localised loss of articular cartilage there is accompanying new tissue production, especially new bone, and adaptive remodelling of joint shape. G There are a wide variety of effective non-pharmacological and drug interventions that can significantly reduce the pain and disability of OA. A more appropriate view of OA is that it reflects the dynamic repair process of synovial joints (Figure 5. Often the initiating insult is unclear (“primary OA”) but sometimes there is an obvious cause such as a torn ligament (“secondary OA”). The tissues that comprise a joint – cartilage, bone, synovium, capsule, ligament, muscle – depend on each other for their normal health and function. Insult to one tissue will impact on the others resulting in a common OA phenotype affecting the whole joint. The process of OA involves production of new bone, especially at the joint margin (osteophyte), thickening of the synovium and capsule, and remodelling of joint shape. Often the OA process can compensate for an insult, resulting in an anatomically altered but pain free functioning joint – “compensated OA”. Sometimes, however, it fails, resulting in slowly Insults Outcome traumatic inflammatory metabolic?? Such a perspective readily explains the marked clinical heterogeneity of OA and the variable outcomes observed. Currently a number of risk factors are recognised that associate with the development of OA. They include constitutional factors, such as heredity, gender, ageing or obesity, and local mechanical factors such as trauma, instability and occupational and recreational usage. We also recognise some negative, possibly “protective” associations such as osteoporosis (hip OA) and smoking (knee OA). Risk factors for the development of OA may differ from those relating to the progression of OA (prognosis). For example, obesity and osteoporosis are minor risk factors for the development of hip OA but may be important risk factors for its more rapid progression. An important realisation in the last decade is that risk factors for pain and disability may differ from those for structural OA. Again, the mechanisms for such correlation are unclear. Importantly, however, such observations have shifted the research focus not just to joint tissues other than cartilage but also to factors outside the joint. Increasing realisation that “knee pain is the malady, not OA”4 has encouraged a more holistic approach to the study of regional musculoskeletal pain, with x ray evidence of OA a secondary rather than primary feature of interest. Inclusion of pain and disability within the research agenda of “OA” has extended the range of questions from: G “what are the mechanisms of joint damage and repair in OA? The latter questions, of course, are of immediate relevance to clinical assessment and to healthcare delivery. Questions at all three levels, however, merit equal attention. They should be studied together, in parallel rather than in sequence. Any management plan must be individualised and patient centred and take into account holistic factors such as the patient’s daily activity requirements, their work and recreational aspirations, their perceptions and knowledge of OA, and the impact of pain and disability on their life. Although management is individualised there are currently evidence-based interventions,9–11 largely life-style changes, that should be considered in all OA patients, especially those with large joint OA. Every doctor should inform their OA patients regarding the nature of their condition and its investigation, treatment and prognosis. However, in addition to being a professional responsibility, education itself improves outcome.

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Which of the following statements regarding the molecular genetics of CML is false? The chromosomal translocation in CML involves the c-myc gene B buy zetia 10mg with visa. The accelerated or blast phase of CML is often associated with duplica- tion of the Philadelphia chromosome D cheap zetia 10mg overnight delivery. Imatinib mesylate is directed against the tyrosine kinase produced by the Philadelphia chromosome and is therefore used in the treatment of CML Key Concept/Objective: To understand the molecular genetics of CML The first specific chromosomal translocation identified in human cancer was the Philadelphia chromosome order zetia 10mg on-line, which underlies CML buy zetia 10mg free shipping. The fusion of chromosomes 9 and 22 leads to the joining of two unrelated genes buy 10mg zetia free shipping, the c-abl gene, which encodes a tyrosine kinase and is located on chromosome 9, and the gene bcr (for breakpoint recombination), locat- ed on chromosome 22. A chimeric protein with novel transforming properties is formed from this specific chromosomal rearrangement. The accelerated or blast phase of CML is often associated with duplication of the Philadelphia chromosome, suggesting that increased copies of this aberrant gene confer a dose-dependent transforming effect. The recent discovery of an effective inhibitor of the bcr-abl kinase, imatinib mesylate (former- ly STI571), has led to dramatic responses in CML and has revolutionized treatment of this leukemia. In Burkitt lymphoma, the chromosomal locus containing the c-myc gene is rearranged such that the upstream negative regulatory regions (i. Deregulation of c-myc expression in these cells is thus a potent force driving cellular pro- liferation. A 31-year-old female patient comes to your office with concerns about her family being “predisposed” to cancer. She says that her son was recently diagnosed with retinoblastoma. She wants to know if future children will also develop cancer. Which of the following statements regarding the Knudson model of human cancer genetics is false? Children with familial tumors have inherited an initial genetic hit (i. Tumor suppressor gene mutations are gain-of-function mutations; they are dominant mutations C. Both retinoblastoma and Wilms tumor follow the Knudson model of human cancer genetics D. Children with sporadic tumors need to acquire two independent genet- ic hits within the same cell Key Concept/Objective: To understand the Knudson model of human cancer genetics Alfred Knudson proposed the model that now forms the foundation of human cancer genetics. The Knudson model predicts that children with familial tumors have inherited an initial genetic hit (i. In contrast, children with sporadic tumors need to acquire two independent genetic hits within the same cell, an unlikely event that explains the less frequent, unilateral presentation and later onset of sporadic cancers. Subsequent genetic studies in two of the tumors studied by Knudson identified these so-called genetic hits as the sequential inactivation of the two alleles of a critical tumor suppressor gene: RB1 in retinoblastoma and WT1 in Wilms tumor. The Knudson model also explains the paradox that tumor suppressor gene mutations are loss-of-func- tion or recessive mutations, yet familial cancer presents as an autosomal dominant trait. Although loss of a single allele of a tumor suppressor gene may be functionally silent in the presence of a normal second allele, the frequency of spontaneous mutations is suffi- ciently high to ensure that at least one cell within the target tissue is likely to lose the sec- ond allele and initiate malignant transformation. A 57-year-old man presents to the hospital with generalized weakness, weight loss, and worsening con- stipation. A colonoscopy is performed, and a large intraluminal mass is seen. Results of biopsy indicate adenocarcinoma of the colon. Which of the following statements regarding p53 is false? Genetic injuries trigger the stabilization and activation of p53 protein C. High levels of p53 protein in tumor specimens are commonly taken as evidence of a mutation in p53 Key Concept/Objective: To understand the basic principles of the p53 genomic stability gene p53 plays a critical role in the maintenance of genomic integrity—hence its popular des- ignation as “guardian of the genome. However, genetic injuries, such as those that occur through ionizing radia- tion, trigger the stabilization and activation of p53 protein. Activation of p53 leads to arrest in the G1 phase of the cell cycle, enabling cells to repair DNA damage before proceeding into S phase and DNA replication.

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8 of 10 - Review by A. Rasarus
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