Chloe M. Chhor, MD

• Department of Radiology
• University of California, San Francisco
• San Francisco, California

This is mostly attributed to the improvement in cardiopulmonary bypass techniques prostate cancer ribbon color generic confido 60 caps free shipping, myocardial protection and surgical intensive care prostate cancer natural cures buy confido. With this in mind prostate drainage purchase discount confido line, sicker patients are being referred for surgical treatment androgen hormone use in cattle 60 caps confido order fast delivery, and a proper evaluation of comorbid conditions and risk factors is crucial for stratifying the risk and anticipating the complications prostate cancer breakthrough discount confido 60 caps buy. The cardiac surgical patient should receive a full systems review as well as an evaluation of their functional status and social habits (Table 30. The mechanism leading to clubbing is not completely understood, but it may be related to blood factors that are usually cleared by the lungs but remain elevated in the circulation if there is a right-to-left shunt. Examination of the Cardiovascular System Cyanosis this is the bluish or dusky discoloration of the skin or mucous membranes that results from the presence of unoxygenated Table 30. In healthy and particularly young patients, the rate goes up with inspiration and down with expiration, a phenomenon referred to as sinus arrhythmia. If it is irregular, the next step is to decide whether it is regularly irregular (commonly from dropped beats or extrasysole) or irregularly irregular, as in atrial fibrillation. The pulse deficit is the difference between the pulses detected at the wrist and the apex of the heart. It is seen in, for example, atrial fibrillation, and occurs because not every ventricular contraction results in a transmitted pulse, due to the difference in filling time and filling volumes. This is important in patients with aortic coarctation, aortic dissection or peripheral vascular disease. The pulse usually rises moderately quickly, coinciding with ventricular ejection, and this is then followed by a gradual decrease to the diastolic level. It usually occurs with aortic regurgitation or when the patient has a high cardiac output and low peripheral resistance. The arterial elastic recoil that usually causes the dicrotic notch in diastole is now superimposed on systole and gives the double pulse impression. The premature ventricular contraction has a weaker pulse because of the short filling time. The paradox in pulsus paradoxus is that some beats are heard with a stethoscope over the heart but not felt over the arterial pulse during inspiration. It usually reflects severe heart disease such as cardiac tamponade, constrictive pericarditis or severe lung disease. Atherosclerotic vessels and the vessels of patients with diabetes or renal failure show irregular calcification and in the worst instances feel like rigid pipes. The lack of compressibility can give rise to falsely elevated blood pressure readings. Jugular Venous Pulse Assessment of the jugular venous pulse forms an indirect observation of the right atrial and venous pressure via visualization of the jugular vein. It is an indication of the level of filling and the level of competence of the right heart to receive and deliver blood. The absolute value cannot be measured clinically but can be transduced through a central venous line. Attention should be given to any scars that suggest previous surgery or trauma to the chest. Palpation the cardiac impulse is the result of the heart striking against the chest wall during systole. The point of maximum impulse is the furthermost point laterally and inferiorly from the sternum at which the cardiac impulse can be felt. This location can vary with right and left ventricular hypertrophy or lung disease affecting the location of the heart in the chest. The diameter of the palpated impulse should be less than 3 cm in both the supine and left lateral positions. A value greater than 3 cm is indicative of left ventricular hypertrophy or enlargement. In aortic regurgitation, the ventricle dilates and the resultant impulse is turbulent and hyperdynamic. A slight outward pulsation is occasionally present in children or thin adults with normal hearts. Generally, however, a left parasternal impulse is caused by a dilated or hypertrophied right ventricle, which can occur with pulmonary stenosis or pulmonary hypertension. The most common condition associated with right ventricular dilatation is functional tricuspid regurgitation. Other causes include atrial septal defect, pulmonary insufficiency and ventricular septal defect. Thrills are cardiac murmurs that can be palpated by placing the palm of the hand over the precordium. It can be seen in some forms of heart disease and is usually indicative of limited filling of the right ventricle due to right heart failure, cardiac tamponade or sometimes pericarditis. Physical Examination 461 of the heart is felt with mitral regurgitation, whereas a diastolic thrill in the same location is due to mitral stenosis. Auscultation Auscultation is an invaluable tool in the diagnosis of heart disease, particularly valvular pathologies. Once the examiner reaches the stage of auscultation, they should have a general idea of the disease process affecting the patient, and a stethoscope should be used to confirm the diagnosis. Auscultation of four general areas is essential for the evaluation of heart sounds and murmurs: · the aortic area over the second intercostal space to the right of the sternum. The first heart sound is caused by closure of the mitral (M1) and the tricuspid (T1) valves. The second heart sound is caused by closure of the aortic (A2) and pulmonary (P2) valves. In addition to these normal sounds, a variety of other sounds may be present, including heart murmurs, adventitious sounds and gallop rhythms, also known as the S3 and S4 sounds. The third heart sound (S3) closely follows the second heart sound and is the result of rapid filling of the left ventricle. It is normal in hyperdynamic states and in individuals younger than 30 years of age. The fourth heart sound (S4), which is sometimes audible in an adult, is known as a presystolic gallop or atrial gallop. This gallop is produced by the sound of blood being forced into a stiff or hypertrophic ventricle. It is a sign of a pathological state, usually a failing or hypertrophic left ventricle, as in systemic hypertension, severe valvular aortic stenosis or hypertrophic cardiomyopathy. Additional sounds may also be heard: · the opening snap of mitral stenosis is a soft, low-pitched sound preceding the murmur of mitral stenosis. It can be accentuated by asking the patient to sit up, lean forwards and exhale, bringing the two layers into closer communication. The diaphragm of the stethoscope should be used for highpitched sounds like S1, S2 and most murmurs. The bell of the stethoscope is used for low-pitched sounds such as S3, S4 and the murmur of mitral stenosis. Have the patient turned to left side when listening to the mitral valve and lean forwards when listening to the aortic valve. They may be secondary to a normal flow through an abnormal valve, or to an abnormal flow through a normal valve. Systolic ejection murmurs are seen in: · aortic stenosis; · pulmonary stenosis; · atrial septal defects. Aortic stenosis is associated with a harsh systolic ejection murmur that is heard over the aortic area but also radiates to the carotid arteries. Pulmonary stenosis and the murmurs of an atrial septal defect are best heard at the left sternal edge on inspiration. Pansystolic murmurs are seen in: · mitral regurgitation; · tricuspid regurgitation; · ventricular septal defects. Mitral regurgitation is best heard over the apex and radiates to the axilla, while the murmurs of ventricular septal defects and tricuspid regurgitation are best heard over the left sternal border. Mid-diastolic murmurs occur with: · mitral stenosis; · tricuspid stenosis; · aortic regurgitation (Austin Flint murmurs). The Austin Flint murmur occurs when aortic regurgitation causes a backflow into the left ventricle that closes the mitral valve. Early diastolic murmurs can be heard in: · aortic regurgitation; · pulmonary regurgitation. Aortic regurgitation is best heard over the left edge of the sternum and the apex (in the direction of the regurgitant flow). Pulmonary regurgitation is best heard over the left edge of the sternum and on inspiration. A Graham Steell murmur results from a high-velocity regurgitant flow across the pulmonary valve; this is usually a consequence of pulmonary hypertension. Since the aortic pressure is higher than the pulmonary pressure, a continuous murmur occurs, which is best heard over the left axilla. A high percentage of defects will require some form of medical intervention or surgical correction. Abnormalities of development of the heart can affect the right chambers, the left chambers or the septum between the two sides (atrial and ventral septal defects). They can also affect the heart valves, the venous structures draining into the heart or any combination of these. The pulmonary conus is enlarged, the aortic knuckle is reduced and there are prominent vascular markings. Cyanotic heart diseases are associated with a rightto-left shunt and blood bypassing the pulmonary circulation. A classic and relatively common example is tetralogy of Fallot, which is characterized by pulmonary stenosis, a ventral septal defect, a hypertrophied right ventricle, and an aorta overriding the ventricles. A characteristic feature is that the child adopts a squatting position when tired. Cardiac examination demonstrates palpable thrills, abnormal heart sounds and murmurs that are characteristic of each lesion. When the volume of fluid reaches more than 1 L, it interferes with cardiac function, causing cardiac tamponade. It is associated with a characteristic pain that is aggravated by inspiration and leaning forwards. Hypertension develops, and the collateral channels are particularly noted in the intercostal arteries, notching of the ribs being present on radiographs. A radiofemoral delay is detected by the simultaneous palpation of the radial and femoral arteries, the latter being attenuated. There is a globular enlarged cardiac shadow with loss of the normal cardiac contour. Dyspnoea, chest pain and syncope are the most common symptoms and should be investigated thoroughly. Cardiovascular examination requires proper assessment of the pulse and measurement of the jugular venous pressure. Cardiac examination includes inspection and palpation of the chest, but more importantly auscultation of the mediastinum for abnormalities in heart sounds and presence of murmurs. This is related to a mismatch between blood supply and demand that is increased by wall stress during exercise. Aortic stenosis can also manifest with heart failure symptoms that include dyspnoea on exertion, paroxysmal nocturnal dyspnoea and lower extremity oedema. Finally, aortic stenosis can present with syncope that is caused by either low cardiac output or arrhythmia induced by wall stress and ischaemia. Chest pain at rest is not a usual manifestation of aortic stenosis and usually indicates acute myocardial infarction or aortic dissection. Coronary disease manifests with chest pain that is reproducible with exertion, as in stable angina. It can also present with acute chest pain at rest, as in unstable angina or myocardial infarction. Mitral disease does not typically present with chest pain, but rather with dyspnoea and symptoms of heart failure. For each of the following patient histories, select the most likely diagnosis from the list below. Each option may be used once, more than once or not at all: 1 Acute type A aortic dissection 2 Mitral regurgitation 3 Pericarditis 4 Aortic stenosis 5 Coronary artery disease a A 63-year-old woman with dyspnoea on exertion, cough and a systolic murmur heard mostly over the apex b A 55-year-old man with acute, tearing-type, mid-sternal chest pain and a cold left lower extremity c A 66-year-old man with a history of diabetes mellitus, hypertension and hyperlipidaemia. He has chest pain that is induced by walking for half a mile and relieved by rest d A 25-year-old man with chest pain that is relieved by leaning forward. A friction rub is heard on auscultation e A 75-year-old man with progressive worsening of fatigue and dyspnoea on exertion. Physical examination reveals a systolic murmur heard over the right upper sternal border Answers a 2 Mitral regurgitation. For each of the following conditions, select the most likely matches for the presentations given below. It is composed of smooth muscle cells and connective tissue bundles that provide its strength and elasticity. This is lined with an endothelial cell layer that functions both as an interface between the circulating blood and the arterial wall, as well as a source of vasoactive products that prevent thrombosis and regulate the vascular tone by inducing vasoconstriction and vasodilation. It is a degenerative process triggered by endothelial cell dysfunction followed by the adhesion and infiltration of inflammatory cells (macrophages and T lymphocytes), which leads to the formation of fibrocellular plaques. As these plaques continue to grow, they cause an inflammatory reaction that triggers smooth muscle proliferation in the affected area, resulting in luminal narrowing and a reduction of blood flow through the vessel. In addition to genetic predisposition, the risk factors for the development of atherosclerosis include smoking, hypertension, dislipidaemia, diabetes mellitus and coagulation disorders. This process has been shown to start as early as childhood, with endothelial fat streaks being the first manifestations. This chronicity and gradual stenosis usually allows for the formation of collateral arterial channels to the affected organ. As such, the ischaemic symptoms vary depending on the vessel involved, the degree of narrowing and the presence or absence of collaterals.

Syndromes

• Dissociative disorder (not being able to remember a major, traumatic event; the memory loss may be short-term or long-term)
• Electric tooth brushes have been shown to clean teeth better than manual ones.
• Hematoma (blood accumulating under the skin)
• Chronic kidney failure (can cause breath to smell like ammonia)
• Chronically ill, especially who have heart or blood flow problems
• Fainting or feeling light-headed
• What medications do you take?
• Vivid and unpleasant dreams
• Endocarditis
• Signs of fluid in the space around the lungs (pleural effusion), such as decreased breath sounds

Turnover time for the hard palate is of the order of about 3­4 weeks androgen hormone response element order 60 caps confido amex, whereas that for buccal mucosa is nearer 2 weeks prostate 25 cost of confido. The turnover time of gingival collagen is about three times slower than that of the periodontal ligament prostate cancer 2 causes purchase discount confido on line. The presence of a basal lamina on its external and internal surfaces makes this epithelium unique prostate yellow sperm cheap confido 60 caps free shipping. Due to the presence of cytokeratins man health check discount confido 60 caps with amex, Merkel cells can be identified by immunohistochemical techniques using antibodies for cytokeratins 8/18 and 20. This keratin layer is thin and translucent and, as underlying blood capillaries lie close to its surface, the vermilion assumes a red coloration. The serous glands (of von Ebner), by draining into the trenches surrounding the circumvallate papillae, bring ingested material into solution for tasting. The protein filaggrin eventually binds keratin filaments together into a stable network. The junctional epithelium has fewer desmosomes, larger intercellular spaces, two basal lamina, a higher turnover rate, is more permeable, contains more organelles associated with the synthesis and extracellular secretion of protein and has a different cytokeratin profile. The thin, keratinized layer, the absence of skin appendages, the pronounced dermal papillae and the absence of minor salivary glands indicate that this is the vermilion zone of the lip. The clear cells in the basal layer represent nonkeratinocytes (melanocytes and Merkel cells). They generally lack the tonofilaments and the many desmosomes of typical keratinocytes, and do not stain as readily as them when visualized in routine haematoxylin and eosin preparations. The lamina lucida and lamina densa are products of the basal cells (stratum germinativum) of the epithelium. The parasympathetic innervation of minor mucous glands is the greater petrosal branch of the facial nerve via the pterygopalatine ganglion and greater palatine nerve. Because of the keratinized layer and the prominent epithelial rete, it is likely to come from the masticatory mucosa of the hard palate or gingiva. Skin would show sweat glands and hair follicles, and may contain an extra layer near the surface, the stratum lucidum. As the attachment has migrated on to the cementum, this must represent an older patient. The apical migration of the junctional epithelium on to cementum, together with an obvious infiltration of inflammatory cells, indicates this to be diseased tissue. Because of the presence of muscle and glandular tissue, and because of the absence of bone, skin and masticatory mucosa, this section is probably from the soft palate. D = respiratory (ciliated) epithelium lining the nasal surface of the soft palate. They probably derive their parasympathetic nerve supply from the facial nerve (via the pterygopalatine ganglion), which is distributed in branches emanating from this ganglion. The muscles of the palate (C) are innervated by the cranial accessory nerve (via the pharyngeal plexus), except for the tensor veli palatine muscle, which is supplied by the mandibular branch of the trigeminal nerve. Outline essay answers Question 1 the junctional epithelium is the epithelial collar that surrounds the tooth and extends from the region of the cement­enamel junction to the bottom of the gingival crevice. In its basic histological appearance, the junctional epithelium is a lining epithelium in that it is a stratified squamous epithelium comprising two main layers: a single basal layer, above which are a variable number of layers comprising what may be termed the prickle cell layer. Cervically, where it is continuous with the crevicular epithelium, it may be 15­30 cells thick (up to 100 m), whilst apically it narrows to only 1­3 cells thick. Unlike masticatory epithelium, lining epithelium lacks the granular and keratinized layers. Like all epithelium, the junctional epithelium is separated from the underlying lamina propria by a basal lamina. Unlike other types of lining mucosa, where this interface shows some degree of folding, that associated with the junctional epithelium is remarkably flat. Like other lining epithelia, junctional epithelium contains stem cells situated in the basal layer that give rise to daughter cells that pass to the superficial layers and are eventually shed into the gingival crevice. However, the rate of proliferation and turnover within the junctional epithelium is the highest within oral epithelium, the complete cycle being in the order of days rather than weeks. Whereas those that characterize lining epithelia are cytokeratins 4 and 13, those found in junctional epithelium are the cytokeratins found in odontogenic tissue, such as cytokeratin 19, reflecting its origin from the reduced enamel epithelium. The basal layer of the junctional epithelium is separated by a basal lamina (external basal lamina) from the underlying lamina propria. However, uniquely, the junctional epithelium is also joined to the enamel at its free surface by a second basal lamina (internal basal lamina). As the internal basal lamina can only be produced by the superficial cells of the prickle cell layer, this is reflected in the morphology of the cell which, unusually, contains numerous free ribosomes, cisternae of rough endoplasmic reticulum and prominent Golgi material. As with the prickle cell layer in lining epithelium, desmosomes link the same cells in the junctional epithelium. However, they are fewer in number and this is correlated with larger intercellular spaces that may comprise up to 5% of the volume of the tissue in the junctional epithelium. This renders the junctional epithelium permeable to tissue fluid derived from underlying capillaries in the lamina propria, known as gingival crevicular fluid. Indeed, even healthy gingival tissue may exhibit neutrophils in the intercellular spaces, indicative of its protective role. The lack of membrane-coating granules may also assist the permeability of the cell layer. Question 2 As many as 10% of the cells in the oral epithelium are non-keratinocytes. The three main non-keratinocytes are melanocytes, Langerhans cells and Merkel cells. All (except for the Merkel cells) lack the tonofilaments and desmosomes characteristic of keratinocytes. Non-keratinocytes may appear as clear cells in sections stained routinely with haematoxylin and eosin. Lacking the typical cytokeratins associated with normal keratinocytes, they remain unstained in sections of epithelium stained for cytokeratins. They are derived from the neural crest and are present in the skin by about 8 weeks of intrauterine life. Once located in the epithelium, they are assumed to be long-lived, but with some powers of self-replication, and are seen to divide in vitro. Melanocytes have long processes that extend in several directions and across several epithelial layers. As suggested by their name, melanocytes produce the pigment melanin, using the enzyme tyrosinase. Their presence in the oral mucosa would appear to have little obvious functional significance. The long processes of the melanocyte extend between adjacent keratinocytes and each melanocyte establishes contact with about 30­40 keratinocytes. Keratinocytes release numerous mediators that are essential for normal melanocyte function. Ultrastructurally, the cytoplasm of melanocytes characteristically contains pigment that is packaged in small, dark granules termed melanosomes. As the melanosomes mature under the activity of tyrosinase, their melanin content increases. The pigment is passed to adjacent keratinocytes as the tips of the dendrites are actively phagocytosed by the keratinocytes. Melanin pigmentation is usually not pronounced in the buccal mucosa, tongue or hard palate. The number of melanocytes varies in different regions, but the difference in the degree of pigmentation between populations is the result of a combination of the size and degree of branching of the cells (rather than the absolute number), the size of the melanosomes, the number and degree of dispersion of the melanosomes, the degree of melanization of the melanosomes, and the rate of degradation of the pigment. Langerhans cells are dendritic cells situated in the layers of epithelium above the basal layer. They are derived from bone marrow precursors that are probably related to the monocyte lineage and leave the blood stream to enter the lamina propria, before penetrating the basal lamina to reach the epithelium. Such migration may relate to certain chemokines released by keratinocytes, with surface receptors on the Langerhans cells. Indeed, lymphocytes present within the oral epithelium are commonly associated with Langerhans cells. Ultrastructurally, the Langerhans cell contains characteristic trilaminar, rod-shaped granules called Birbeck granules. These may be up to 50 nm long and 4 nm wide, and have a vesicular swelling at one end, resembling a tennis racquet. The Merkel cell is found in the basal layer, often closely apposed to nerve fibres. As the Merkel cells contain cytokeratin, they can be identified by immunohistochemical techniques using antibodies for cytokeratin 8 and 18. They are common in masticatory epithelia such as gingiva, but less frequent in lining mucosa such as the buccal mucosa. The cytoplasm contains numerous mitochondria, abundant free ribosomes and a collection of electron-dense granules (80­180 nm in diameter), adjacent to the nerve terminal, and these may liberate a transmitter towards the terminal, giving the cell a sensory function. D cells associated with the inflammatory response are present within the epithelium. Cells associated with the inflammatory response are present within the epithelium. Lymphocytes are the most common type of inflammatory cell, although polymorphonuclear leukocytes and plasma cells are also seen. Lymphocytes are retained within the epithelial layer by binding to integrins (that may increase in disease). The greater degree of permeability of non-keratinized epithelium may account for the larger number of inflammatory cells said to occur there compared with masticatory epithelium. In inflamed tissues, the fluid flow rate increases, leading to a greater osmotic gradient. Fluid flows across a weakened basement membrane, as there is loose organization of the junctional and sulcular epithelium. There is also increased fluid flow from capillaries into connective tissues as a consequence of the host response. It washes away potentially harmful cells and molecules from the gingival sulcus and may contain antibacterial substances. It also contains high calcium and phosphate concentrations important for remineralization. Its value as a biomarker may be as an indicator of current disease metabolic activity, involving both soft and mineralized periodontal tissue, as it is non-invasive and site-specific. It may be used as a prognostic or diagnostic indicator of disease progression or future disease activity, or as an indicator of response to therapy. It may also provide information regarding the mechanisms of periodontal tissue destruction. Question 4 the oral surface of the hard palate is exposed to significant forces during mastication. It also has important sensory functions and is a source for the secretion of saliva from minor salivary glands. In its capacity to resist masticatory loads, the oral surface of the hard palate is covered by a keratinized, masticatory mucosa, whose structure shows the relevant adaptations. Its epithelium consists of keratinized (or parakeratinized), stratified, squamous epithelium. Cells are generated from stem cells in the proliferative basal layer and, over a period of about 3 weeks, these migrate to the surface where they are shed. Normal desquamation of the epithelial cells will be accompanied by the loss of bacteria adhering to the cells on the surface. In their passage from the basal layer, the cells increase in size and undergo differentiation, acquiring cytokeratin microfilaments. Initially they become prickle cells that contact via numerous desmosomes, providing a system of mechanical support within the epithelial layer (eventually coming to occupy about 50% of the intercellular space). In the more superficial layers of the stratum spinosum, the granules come to lie close to the cell membrane. It gathers in the gingival sulcus and may be collected by non-invasive means at the gingival margin. In healthy tissues, small amounts of subgingival plaque give rise to macromolecular plaque and this is usually removed by desquamating epithelial cells or phagocytosis. The membrane-coating granules first seen in the prickle cell layer move towards the superficial surface of the keratinocyte and discharge their lipid-rich contents into the extracellular space. The cells are larger and flatter, but most significantly now contain large numbers of small granules (0. These contain profilaggrin, the precursor to the protein filaggrin that eventually binds the keratin filaments together into a stable network. Synthesis of additional proteins, loricrin and involucrin, which will help form a more resistant cell wall (envelope), is evident in the granular layer. In the superficial layer of the epithelium, the continued maturation of the epithelial cells results in the loss of all organelles (including nuclei and keratohyaline granules). The cells of the keratinized layer become filled entirely with closely packed tonofilaments surrounded by the matrix protein filaggrin. The keratin is also strongly cross-linked by disulphide bonds, contributing to the mechanical and chemical resistance of the layer. In the cornified layer, involucrin becomes cross-linked (by the enzyme transglutaminase) to form a thin (10 nm), highly resistant, electron-dense, cornified envelope just beneath the plasma membrane. Although only constituting 5% of the cell envelope, involucrin is an important component on the internal aspect, acting as a binding site for lipids that are extruded to form a water-insoluble barrier.

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Note that a false positive anterior drawer test may be elicited if the posterior cruciate ligament is already ruptured prostate size cheap 60 caps confido fast delivery. The examiner holds the foot internally rotated in one hand and applies a valgus stress to the knee with the other mens health zucchini carbonara purchase 60 caps confido fast delivery. If there is a rupture of the anterior cruciate ligament prostate cancer vs breast cancer statistics purchase confido 60 caps amex, this manoeuvre will lead to a forward subluxation of the lateral tibial condyle on the femur prostate oncology kansas confido 60 caps on line. A positive test result occurs if there is a palpable clunk at about 20­30° as the tibia reduces into its normal position prostate urine test quality confido 60 caps. The knees are observed from the lateral side: a posterior sag of the tibia on the femur of the involved extremity indicates that there has been a rupture of the posterior cruciate ligament. A posteriorly directed force on the tibia is confirmatory, and an anterior force on the tibia should reduce the tibia to its normal position. The Arcuate Ligament Complex the arcuate ligament is a thickening of the posterior capsule. It arises from the fibular head and diverges such that one limb is attached to the femoral condyle and popliteus tendon, while the other limb curves over the popliteus and is attached to the back of the lateral meniscus. Posterolateral rotatory instability of the knee results from disruption of the arcuate ligament complex, which is made up of the arcuate ligament, the lateral collateral ligament, the tendoaponeurotic portion of the popliteus muscle and the lateral head of the gastrocnemius. The external rotation recurvatum test is positive in posterolateral rotatory instability. With the patient supine, the legs are elevated from the examining table by grasping the great toes and lifting them. The test is positive if the involved knee falls into external rotation, varus and recurvatum. The tibia is pushed posteriorly, a positive test result occurring when the lateral side of the tibial plateau is subluxed posteriorly in relation to the femoral condyle. The knee is taken from a position of abduction and external rotation to adduction and internal rotation by applying force to the foot. The test is positive if there is a palpable click in the appropriate compartment of the knee as the torn meniscus becomes entrapped within the knee. A comparative test should be carried out on the normal knee to rule out the presence of a non-pathological click. The examiner then exerts an axial downward force over the flexed knee while externally and internally rotating the foot. A sharp pain is indicative of a tear in the medial meniscus on external rotation and the lateral meniscus in internal rotation. The Thessaly test has recently been designed to detect the presence of a meniscal tear with a high sensitivity and specificity. The patient then rotates his knee, internally and externally, at 5° and then 20° of flexion. The patient presents with pain, swelling and a limited range of motion of the knee. In the case of injury during a sporting event, it is useful to know whether the patient was able to finish the event; if so, it is less likely that there is a serious injury. The menisci transmit a significant proportion of the body weight through the knee, and meniscal tears are the most common injuries to the knee that necessitate surgery. These injuries occur most commonly in athletes where there is sudden twisting motion of the flexed weight-bearing knee, leading to a tear in the substance of the meniscus. When the displaced fragment crosses or gets settled in the intercondylar notch, true locking of the knee usually occurs. The locked knee is one of the few conditions in which a reasonable presumptive diagnosis can be made after an acute knee injury. Passive knee extension by the examiner comes up against a firm elastic resistance, preventing full extension. The other causes of a locked knee are a loose body, a torn remnant of the anterior cruciate ligament and a symptomatic discoid meniscus. In middle age, however, the menisci undergo degenerate change with loss of elasticity whereby the slightest trauma can cause a tear. It is important to know the time period between the injury and the onset of swelling. Immediate swelling of the knee usually results from bleeding into the joint cavity ­ haemarthrosis ­ due to tearing of the vascularized structures inside the knee. There could be a tear of a cruciate ligament or peripheral detachment of the meniscus, but an intra-articular fracture may have occurred and radiographs should therefore be taken. The fluid can be investigated to detect the presence of globules of fat as this strongly suggests a fracture. An effusion that occurs some hours after the injury is suggestive of a traumatic synovitis, which usually does not involve any major structure in the knee, although this scenario may mask the presence of a meniscal tear in the avascular zone. In these circumstances, it is important to re-examine the knee some days later when a more accurate assessment can be made. In certain cases, however, there is interference with movement between the joint surfaces due to a loose meniscal fragment, especially when the knee is flexed and twisted during normal activities. The patient may be able to overcome the locking by shaking the limb or twisting the knee, resulting in a sudden freeing of knee movement. Only 40 per cent of all meniscal tears are displaced into the joint, causing locking of the knee. Other symptoms include pain at the joint line, especially on twisting or kneeling, repeated swelling and giving way of the knee. Rupture of the posterior cruciate ligament results from a violent injury such as striking the dashboard of a car in an accident, hyperflexion or hyperextension. The knee exhibits more hyperextension than the uninjured side when the legs are lifted off the couch by holding the heels. The posterior drawer test reveals a posterior sag of the tibia, which can be increased by a posteriorly directed force and reduced to normal by an anterior force. Injury to the arcuate ligament complex and the posterior cruciate ligament gives rise to posterolateral rotatory instability of the knee. Loose Bodies Loose bodies may appear after long-term osteoarthritis, osteochondral defects, synovial chondromatosis and rarely traumatic events. The patient often describes something moving in the joint and can sometimes even feel the loose body. The physical findings are often non-specific unless the joint is locked at the time of consultation. Rupture of the Ligaments Ligamentous rupture requires a considerable degree of violence following direct trauma such as a traffic accident or a sportsrelated injury. There is usually haemarthrosis if the ligament is intra-articular, or bruising if the ligament is extra-articular. Rupture of the medial collateral ligament results from vigorous ball games and skiing, in which a severe valgus force is applied to the knee. If the knee is examined a few days after the injury, there may be visible swelling and bruising on the medial side of the knee. There is tenderness over the ligamentous attachments, the medial aspect of the knee and the joint line. When a valgus stress is applied to the knee at 30°, there is excessive laxity and pain. Incomplete injuries are often more painful than complete ruptures on valgus stress, due to stretching of the remaining injured but intact ligament fibers, but marked instability is noted with complete injuries. Rupture of the lateral collateral ligament of the knee occurs when severe varus forces are applied to a knee in 30° of flexion. The discrete cord-like ligament runs from the femoral condyle to the head of the fibula. When it is torn, there may be swelling and bruising laterally, tenderness over the ligamentous attachments and lateral joint line, and excessive movement when a varus stress is applied to the knee. Rupture of the anterior cruciate ligament occurs in hyperextension injuries, when the ligament is tented over the intercondylar notch in the femur. The site of the lesion is usually the medial femoral condyle, adjacent to the intercondylar notch. There is an area of osteonecrosis and partial detachment of articular cartilage resulting from intraarticular impingement upon movement. The patient has symptoms of pain and recurrent effusion; catching and locking can occasionally occur if a loose body detaches in the joint. A false-positive patellar grind test is usually present due to rubbing of the patella against the lesion upon flexion and extension of the knee. This condition is rarely seen in the patella, in which it gives rise to anterior knee pain. Changes in the articular cartilage of the patella and trochlea are the primary problems. The spectrum ranges from minor cartilage fibrillation via chondromalacia to frank patellofemoral arthritis. Anterior knee pain can also present as well in the younger population due to different underlying aetiologies, described below. Patellar Malalignment Patients may show an altered quadriceps angle (Q angle), that is, the angle between the line joining the anterior superior iliac spine to the centre of the patella and the line joining the centre of the patella to the tibial tuberosity. Other causes are weakness of the vastus medialis muscle and tightness of the hamstring muscles. These conditions can alter the mechanics of the patellofemoral Anterior Knee Pain 261 joint, leading to excessive forces across it and producing anterior knee pain. Chondromalacia Patellae this is a usually self-limiting condition that is seen in young adults and adolescents. There is softening and fibrillation involving the articular cartilage of the patella. Synovial Shelf Syndrome the medial synovial shelf or fold is an embryological remnant. Impingement of this synovial shelf on the femoral condyle can cause abrasions affecting the condylar cartilage and thus anteromedial knee pain. It should be suspected when tenderness can be elicited along the medial patellar retinaculum during flexion and extension of the knee. Lateral Facet Compression Syndrome this condition is due to a tight lateral patellar retinaculum and excessive lateral tilt. Patellofemoral tenderness is exacerbated when the lateral facet of the patella is pushed laterally against the femur, and is reduced when the examiner pushes it medially. It occurs in adolescents during their growth spurt and is most common in athletic youngsters. Sinding-Larsen­Johansson Disease this occurs predominantly in children under 10 years of age and is characterized by tenderness of the lower pole of the patella and the adjacent patellar tendon. Patellar Instability In normal circumstances, the patella engages the trochlear groove at 30­40° of flexion, and when the quadriceps muscle contracts with the knee in the extended position, the patella should be pulled superiorly in a straight direction. At terminal extension with an unstable patella, however, the patella may be seen to sublux laterally out of the trochlear groove. As the knee goes into flexion again, the patella may be noted to jump back into the groove. This is called the patellar J sign and indicates abnormal tracking of the patella. The examiner then attempts to displace the patella medially ­ excursion of the patella of less than one-quarter of its maximum width is considered a positive result, while 10 mm of displacement medially is considered normal, and 5 mm or less abnormal. The patellar apprehension test is indicative of dynamic instability and recurrent dislocations. Patients with instability fire their quadriceps in response to the painful gliding motion of the patella. The quadriceps (Q) angle indicates the relative angle of insertion of the quadriceps mechanism. It is measured, as described above, by drawing two imaginary lines connecting the centre of the patella to the anterior superior iliac spine proximally and the tibial tuberosity distally. A Q angle greater than 20° is considered abnormal and is associated with patellar instability. Patellar Dislocation Many factors can contribute to patellar instability and ultimately recurrent lateral dislocations. These can include, for example, abnormal patellar tracking and an increased Q angle due to excessive femoral anteversion, genu valgum and a wide pelvis. Other factors are related to poor patellofemoral contact due to hypoplasia affecting the condylar groove or the patella itself. Tight lateral structures or lax medial structures may contribute to lateral patellar dislocation. Acute dislocations also occur laterally and are usually the result of a traumatic event in an athlete. Radiographs should be carefully examined for evidence of a fracture of the patella or lateral femoral condyle. Not infrequently, an osteochondral fragment is sheared off during the dislocation and should be removed or fixed back into place. Examine the lateral radiograph for evidence of a lipohaemarthrosis, that is, fat floating on top of the effusion, seen in the suprapatellar bursa. If in doubt, aspirate the knee and look for fat globules floating on the haemarthrosis. If a penetrating injury has occurred, this bursa may be infected with pyogenic organisms, leading to a surrounding cellulitis. The range of movement in the knee should, however, be well preserved, differentiating this condition from septic arthritis. This may be injured by direct trauma to the knee, with resulting fibrosis and oedema. In the chronic condition, there is pain when the knee is fully extended as the fat pad is compressed between the articular surface of the femur and tibia.

Diseases

• Epidermolysis bullosa, junctional
• Cervical cancer
• Francheschini Vardeu Guala syndrome
• Marphanoid syndrome type De Silva
• Factor V deficiency
• Paraphilia
• Abnormal systemic venous return
• Glycosuria
• Brachydactyly Smorgasbord type

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