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A conceptual model of cardiac membrane fast sodium and slow calcium ion channels: at rest (A) purchase indapamide 1.5 mg with amex blood pressure chart by time of day, during the initial phases of the fast-response (Band C) buy indapamide 2.5mg blood pressure uk, and the slow-response action potentials (D and E) purchase genuine indapamide online heart attack normal blood pressure. These channels are activated at the end of the repolarization phase and promote a slow sodium and calcium influx that gradually depolarizes the cells during diastole. This slow diastolic depolarization gives the inactivating h gates of many of the fast sodium channels time to close before threshold is even reached (Figure 2-3D). The depolarization beyond threshold during the rising phase of the action potential in these "pacemaker" cells is slow and caused primar ily by the influx of Ca2+ through slow channels (Figure 2-3E). Although cells in certain areas of the heart typically have fast-type action potentials and cells in other areas normally have slow-type action potentials, it is important to recognize that all cardiac cells are potentially capable of having either type of action potential, depending on their maximum resting membrane potential and how fast they depolarize to the threshold potential. As we shall see, rapid depolarization to the threshold potential is usually an event forced on a cell by the occurrence of an action potential in an adjacent cell. A chronic moderate depolarization of the resting membrane (caused, eg, by mod erately high extracellular K+ concentrations of 5-7 mM) can inactivate the fast channels (by closing the h gates) without inactivating the slow Ca2+ channels. Under these conditions, all cardiac cell action potentials will be of the slow type. Large, sustained depolarizations (as might be caused by very high extracel lular K+ concentration such as more than 8 mM), however, can inactivate both the fast and slow channels and thus make the cardiac muscle cells completely inexcitable. Conduction of Cardiac Action Potentials Action potentials are conducted over the surface of individual cells because active depolarization in any one area of the membrane produces local currents in the intracellular and extracellular fuids. These currents passively depolarize immediately adjacent areas of the membrane to their voltage thresholds to initiate an action potential at this new site. In the heart, cardiac muscle cells are branching and connected end to end to neighboring cells by structures called intercalated disks. These disks contain the following: (I) frm mechanical attachments between adjacent cell membranes by proteins called adherins in structures called desmosomes and (2) low-resistance electrical connections between adjacent cells through channels formed by pro teins called connexin in structures called gapjunctions. Figure 2-4 shows sche matically how these gap junctions allow action potential propagation from cell to cell. Cells B, C, and D are shown in the resting phase with more negative charges inside than outside. Cell A is shown in the plateau phase of an action poten tial and has more positive charges inside than outside. Because of the gap junctions, electrostatic attraction can cause a local current flow (ion move ment) between the depolarized membrane of active cell A and the polarized membrane of resting cell B, as indicated by the arrows in the fgure. Local currents and cell-to-cell conduction of cardiac muscle cell action potentials. Because cell B branches (a common morphological characteristic of cardiac muscle fibers), its action potential will evoke action potentials on cells C and D. Thus, an action potential initiated at any site in the myocardium will be conducted from cell to cell throughout the entire myocardium. The speed at which an action potential propagates through a region of car diac tissue is called the conduction velocity. The conduction velocity varies con siderably in different areas in the heart and is determined by three variables. Rapid action potential depolarization favors rapid conduction to the neighboring segment or cell. Electrical characteristics of gap junc tions can be influenced by external conditions that promote phosphorylation/ dephosphorylation of the connexin proteins. Details of the overall consequences of the cardiac conduction system are shown in Figure 2-5. As noted earlier, the specifc electrical adaptations of various cells in the heart are reflected in the characteristic shape of their action potentials that are shown in the right half of Figure 2-5. Both cells have similarly shaped fast response-type action potentials, but their temporal displacement reflects the fact that i takes some time for the impulse to spread over the atria. Because of sharply rising action potentials and other factors, such as large cell diameters, electrical conduction is extremely rapid in Purkinje fbers. This allows the Purkinje system to transfer the cardiac impulse to cells in many areas of the ventricle nearly in unison. Action potentials from muscle cells in two areas of the ventricle are shown in Figure 2-5. Note in Figure 2-5 that the ventricular cells that are the last to depolarize have shorter duration action potentials and thus are the frst to repolarize. The physiological importance of this behavior is not clear, but it does have an influence on the electrocardiograms discussed in Chapter 4. Electrocardiograms Fields of electrical potential caused by the electrical activity of the heart extend through the extracellular fluid of the body and can be measured with electrodes placed on the body surface. Elctrocardiography provides a record of how the volt age between two points on the body surface changes with time as a result of the electrical events of the cardiac cycle. At any instant of the cardiac cycle, the electrocardiogram indicates the net electrical feld that is the summation of many weak electrical felds being produced by voltage changes occurring on individual cardiac cells at that instant. When a large number of cells are simultaneously depolarizing or repolarizing, large voltages are observed on the electrocardiogram. Because the electrical impulse spreads through the heart tissue in a consistent pathway, the temporal pattern of voltage change recorded between two points on the body surface is also consistent and repeats itself with each heart cycle. The interval between heartbeats (and thus the heart rate) is determined by how long it takes the membranes of these pacemaker cells to spontaneously depolarize during the diastolic interval to the threshold level. Outside influences are required, however, to increase or decrease automaticity from its intrinsic level. The efect of sympathetic and parasympathetic activity on cardiac pacemaker potentials. Activating the cardiac sympathetic nerves (increasing cardiac sympathetic tone) increases the heart rate. Both of these effects increase the time between beats by prolonging the time required for the resting membrane to depolarize to the threshold level. Sympathetic nerves release the transmitter substance norepinephrine on car diac cells. In addition to sympathetic and parasympathetic nerves, there are many {albeit usually less important) factors that can alter the heart rate. These include a num ber of ions and circulating hormones, as well as physical infuences such as body temperature and atrial wall stretch. All act by somehow altering the time required for the resting membrane to depolarize to the threshold potential. An abnor mally high concentration of Ca1+ in the extracellular fuid, for example, tends to decrease the heart rate by shifting the threshold potential. Factors that increase the heart rate are said to have a positive chronotropic efct. Besides their effect on the heart rate, autonomic fbers also infuence the con duction velocity of action potentials through the heart. Increases in sympathetic activity increase conduction velocity {have a positve dromotopic efct), whereas increases in parasympathetic activity decrease conduction velocity {have a negative dromotropic efct). These dromotropic effects are primarily a result of autonomic infuences on the initial rate of depolarization of the action potential and/or influ ences on conduction characteristics of gap junctions between cardiac cells. Students are encouraged to consult current histology references for specifc cellular, morphological details.
Edema is not seen because of the escape mechanism: escape from the sodium retaining effects of hyperaldosteronism 2.5 mg indapamide with mastercard hypertension 10. First of all order 1.5mg indapamide visa hypertension renal failure, read both assertion (A) and reason (R) carefully and independently analyse whether they are true or false buy generic indapamide 2.5 mg on line heart attack jack heart attack. If both A and R are ture, then we have to know whether R is correctly explaining A [answer is (a)] or it is not the explanation of assertion [answer is (b)] 1. Both are stored in secretory granules and equimolar quantities are secreted after β cell simulation. It is associated with the following: • 10% are bilateralQ • 10% are extra-adrenalQ • 10% are malignant Q • 10% occur in children Q • 10% are not associated with hypertensionQ Most of the earlier texts mention that 10% of these tumors are familialQ but Robbins 8th/1159 clearly says that it has been modifed. The most reliable feature of follicular cancer is demonstration of capsular invasion or vascular invasion. It presents as a painless enlargement of the thyroid and transient hyperthyroidism (lasting about 2-8 weeks). Clinical features are pain in neck, sore throat, fever, fatigue, anorexia, myalgia, enlarged thyroid and the presence of transient hyperthyroidism lasting for 2-6 weeks. It may be followed by asymptomatic hypothyroidism but recovery is seen in most of the patients. Capillary dysfunction in target organs leads to microvascular disease (not macrovascular disease) leading to diabetic retin- opathy, neuropathy and nephropathy. These patients don’t develop ketoacidosis and its symptoms (nausea, vomiting, respiratory diffculties) because of elevated portal insulin levels. The ‘fat sparing’ effect of insulin prevents the formation of ketone bodies by inhibiting the fatty acid oxidation in the liver. It is because of the deposition of the altered form of calcitonin which gets deposited in the thyroid stroma. The extracellular components of bone consist of a solid mineral phase (consisting of calcium and phosphate) and an organic matrix consisting of type I collagen (90–95%), serum proteins such as albumin, cell attachment/signaling proteins such as thrombospondin, osteopontin and fbronectin, calcium-binding proteins such as matrix glial protein and osteocalcin and proteoglycans such as biglycan and decorin. The mineral phase of bone is deposited initially in intimate relation to the collagen fbrils and is found in specifc locations in the “holes” between the collagen fbrils. This architectural Cleidocranial dysplasia is caused arrangement of mineral and matrix results in a two-phase material well suited to withstand by heterozygous inactivating mechanical stresses. As an osteoblast secretes matrix, which is then mineralized, the cell becomes an osteocyte. Mineralization is a carefully regulated process dependent on the activity of osteoblast-derived alkaline phosphatase, which probably works by hydrolyzing inhibitors of mineralization. The process of bone and activity by this indirect remodeling is initiated by contraction of the lining cells and the recruitment of osteoclast mechanism. These precursors fuse to form multinucleated, active osteoclasts that mediate Calcitonin, in contrast, binds to bone resorption. After osteoid mineralization, osteoblasts fatten and form a layer of lining cells over new bone. Hydroxyproline (not very specifc) bone and so, it is used as a marker of bone growth for biopsies in humans. Paget’s disease (osteitis deformans) can be characterized as a collage of matrix madness. It is Tetracycline is incorporated into marked by regions of furious osteoclastic bone resorption, which is followed by a period of hectic mineralizing bone and can be detected by its fuorescence. It that interval can be calculated by has been linked to slow virus infection by paramyxovirus. It can be involving one bone or measuring the distance between monostotic (tibia, ilium, femur, skull, vertebra, humerus) in about 15% of cases and affecting the two fuorescent labels. On radiography, the Pagetic bone is typically enlarged with thick, coarsened cortices and cancellous bone. There is increased serum alkaline phosphatase and increased urinary excretion of hydroxyproline. Bone overgrowth in the craniofacial skeleton may produce leontiasis ossea and the weakened Pagetic bone may lead to invagination of base of skull (platybasia). The histologic hallmark is the mosaic pattern of lamellar bone which is produced by prominent cement lines that anneal haphazardly oriented units of lamellar bone. Secondary osteoarthritis and chalk-stick type fractures are the other complications in Paget’s disease. Osteoid osteoma and osteoblastoma Osteoid osteoma and osteoblastoma are terms used to describe benign bone tumors that have identical histologic features but that differ in size, sites of origin, and symptoms. Osteoid Concept osteoma is less than 2 cm in size and usually affects patients in their teens and twenties. They usually involve the femur or tibia, where they commonly arise in the cortex and less Osteoblastoma differs from osteoid frequently within the medullary cavity. The pain is osteoma in that it more frequently involves the spine; the pain is characteristically nocturnal, and is dramatically relieved by aspirin. X-ray shows the presence of central radiolucency surrounded by a induce a marked bony reaction. It is seen in adolescent males as a frm, solitary growth at the end of long bones. Multiple osteochondromas occur in multiple hereditary exostosis, which is an autosomal dominant hereditary disease. Chondroma Chondromas are benign tumors of hyaline cartilage that usually occurs in bones of endochondral origin. These can be • Enchondroma: When origin is intramedullary • Subperiosteal or juxtacortical: Originate from the surface of bone Enchondromas are most common intraosseous cartilage tumors. Enchondromas are composed of well-circumscribed nodules of cytologically benign Ollier’s disease is a syndrome hyaline cartilage. The center of the nodule can calcify whereas peripheral portion may of multiple enchondromas (or undergo enchondral ossifcation. The unmineralized nodules of cartilage produce well- enchondromatosis) circumscribed oval lucencies that are surrounded by a thin rim of radiodense bone (O ring sign). Maffuci’s syndrome is associa Patients with Ollier’s disease may undergo malignant transformation to chondrosarcoma whereas tion of soft tissue hemangiomas those with Maffuci’s syndrome have increased risk of ovarian cancer and brain gliomas. It has a bimodal age distribution with almost 75% occurring in patients younger than age 20. The second peak occurs in the elderly with conditions like Paget disease, bone infarcts, and prior irradiation. It is more commonly seen in the males with increased risk of the development in patients with familial retinoblastoma. It arises from the metaphysis of the long bones with the knee being the most commonly affected site. Microscopically, there is presence of anaplastic cells producing osteoid and bone. The tumor frequently breaks through the cortex and lifts the periosteum, resulting in reactive periosteal bone formation. The triangular shadow between the cortex and raised The formation of bone by the tumor cells is characteristic of ends of periosteum is known radiographically as Codman’s triangle. Spotty calcifcations may be present and central necrosis may create cystic Codman’s triangle.
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Check the femoral pulse in infants and young children order indapamide with a mastercard hypertension vs preeclampsia, or Evaluate the brainstem by checking the responses in each the carotid pulse in an older child or adolescent buy indapamide 2.5 mg visa heart attack queen. A normal pupil will constrict is felt order cheapest indapamide and indapamide blood pressure chart for age and weight, and there are no, or minimal signs of life, commenced after a light stimulus. Normal blood pressure values in children vary • If the child is crying or speaking, is this strong or weak? A low blood pressure indicates • Does the child fx their gaze on the carer(s), or does he/she decompensated shock. An easy formula for determining the lower limit of • Is the child’s behavior normal for their developmental age? Be careful to avoid Age Systolic blood Diastolic blood rapid heat loss, especially in infants and children in a cold pressure (mmhg) pressure (mmhg) environment. Neonates (1st day) 60–74 60–74 31–45 31–44 • Is there a nonblanching rash present? Neonates (4th day) 76–83 68–84 37–53 35–53 Infant (1 month) 73–91 74–94 36–56 37–55 Secondary Assessment Infant (3 months) 78–100 81–103 44–63 45–65 The secondary assessment focuses on advanced lifesupport Infant (6 months) 82–102 87–105 46–66 48–68 interventions and management. Generally, the initial Categorization by Severity assessment is aimed at detecting immediate lifethreatening problems that can compromise basic life functions, as in the Respiratory Distress primary survey. Shock Laboratory and Radiological Diagnostic Testing Compensated • Establishing a clinical diagnosis: obtain a quick random • Tachycardia blood sugar • Cool pale diaphoretic skin • Performing laboratory investigations and imaging. Always reassess the patient; the purpose is to assess the efectiveness of the emergency interventions provided and Hypotensive identify any missed injuries or conditions. This should be • All features of compensated shock and blood pressure performed in every patient after the detailed physical exami below the 5th percentile 193 nation and after ensuring completion of critical interventions. Do the following regardless of diagnosis: • Start oxygen Clinical Pearls • If respiratory distress {{ Ensure airway open by head tilt, chin lift, jaw thrust • Cardiac arrest can be prevented in most children if respiratory {{ If not maintainable, intubate distress is assessed and treated {{ If cannot intubate, ventilate with bag and mask. Part 12: Pediatric Advanced Life circulation (capillary refll, color, heart rate, pulse, blood Support: 2015 American Heart Association Guidelines Update for Cardiopulmonary pressure, mental status, urine output). Pediatric basic and advanced Other Supportive Therapy life support: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Waiting for {{ –1 Thrombocytopenia (platelet count <100,000 μL ) confrmatory laboratory tests is discouraged. However, during {{Hyperbilirubinemia (plasma total bilirubin >4 mg/dL or intubation and mechanical ventilation, increased intrathoracic 70 μmol/L) pressure and drugs used for sedation can reduce venous return • Tissue perfusion variables and lead to worsening shock if the patient is not adequately {{Hyperlactatemia (>1 mmol/L) volume-loaded. Mechanical ventilation should be done using {{Decreased capillary refll or mottling (normal flling in early lung protective strategies (tidal volume 4–6 mL/kg of ideal warm shock) body weight, plateau pressure ≤30). T ereafter, central venous oxygen saturation (ScvO2) Any of the is following thought to be due to infection: greater than or equal to 70% and cardiac index between 3. Noninvasive • Acute lung injury with PaO2/FiO2 <200 in the presence of pneumonia as infection source measures, such as echocardiography, may be utilized to assess • Creatinine >2. Rapid fuid boluses of 20 mL/kg can be started through peripheral or intraosseous line till the (isotonic crystalloid or colloids) can be administered by push central line is established. Shock is further defned into warm or rapid infusion device (pressure bag) while observing for or cold shock, catecholamine resistant, and refractory shock as signs of fuid overload (i. Children commonly require 40–60 mL/ Antibiotics and Source Control kg in the frst hour (some children may require 180–200 mL/ kg). Any site of localized pus on suspected community acquired or hospital-acquired collection or any other source of infection should be taken care infection, local resistance pattern of organism, site of infection, of once child is stable enough for procedure. Antibiotics may and whether immune-compromised or immune-competent de-escalated later according to culture sensitivity report. The choice of empiric drugs should also take into consideration the ongoing epidemic and Steroid Therapy endemic (e. Hydrocortisone may be administered as There is no role of deep vein thrombosis and stress ulcer an intermittent or continuous infusion (preferable in view of prophylaxis in prepubertal children with severe sepsis. Glycemic Control Diuretics and Renal Replacement Therapy Hypoglycemia should be prevented by providing appropriate glucose delivery rate to the child. Associations have been Fluid overload in severe sepsis has been associated with reported between hyperglycemia and an increased risk of increased risk of mortality, so efort to reverse fuid overload death and longer length of hospital stay. Two consecutives with diuretics when shock has resolved and if unsuccessful, values of more than or equal to 180 mg/dL should be then continuous venovenous hemofltration or intermittent managed with insulin infusion in addition to glucose to avoid dialysis to prevent greater than 10% of total body weight fuid hypoglycemic episodes. Blood products and plasma Therapies Extracorporeal Membrane Oxygenation Packed cell transfusion may be given to maintain hemoglobin Extracorporeal membrane oxygenation may be used to of 10 gm/dL if child is hemodynamically unstable (ScvO2<70% support children and neonates with septic shock or sepsis- during resuscitation) and target of 7–9 g/dL is reasonable associated respiratory failure. The survival of septic patients after stabilization and recovery from shock and hypoxemia. Higher platelet counts (≥50,000/mm3 [50 × H1N1 pediatric patients with refractory respiratory failure. Early diagnosis, allowing Providing early enteral nutrition to maintain gut integrity and rapid therapeutic intervention, is essential in improving the to prevent gut translocation of bacteria should be the goal outcome of these patients. Partial or complete fuid resuscitation, early appropriate antibiotics, tailored use of total parenteral nutrition can be given, where enteral feeding inotropes and vasopressors, lung protective strategy for acute cannot be established. Early recognition protein C and Activated protein Concentrate of organ failure and supportive therapy especially renal No beneft of recombinant human activated protein C in replacement therapy to prevent further injury helps in reversal patients with septic shock. Initial resuscitation • For respiratory distress and hypoxemia, start with face mask oxygen, or if needed and available, high fow nasal cannula oxygen or nasopharyngeal continuous positive airway pressure. For improved circulation, peripheral intravenous access or intraosseous access can be used for fuid resuscitation and inotrope infusion when a central line is not available. If mechanical ventilation is required then cardiovascular instability during intubation is less likely after appropriate cardiovascular resuscitation • Initial therapeutic endpoints of resuscitation of septic shock: capillary refll of ≤2 s, normal blood pressure for age, normal pulses with no diferential between peripheral and central pulses, warm extremities, urine output >1 mL/kg/h, and normal mental status. Antibiotics and source • Empiric antibiotics be administered within 1 h of the identifcation of severe sepsis. Blood cultures should be control obtained before administering antibiotics when possible but this should not delay administration of antibiotics. The empiric drug choice should be changed as epidemic and endemic ecologies dictate (e. Fluid resuscitation • In the industrialized world with access to inotropes and mechanical ventilation, initial resuscitation of hypovolemic shock begins with infusion of isotonic crystalloids or albumin with boluses of up to 20 mL/kg crystalloids (or albumin equivalent ) over 5–10 minutes, titrated to reversing hypotension, increasing urine output, and attaining normal capillary refll, peripheral pulses, and level of consciousness without inducing hepatomegaly or rales. If hepatomegaly or rales exists then inotropic support should be implemented, not fuid resuscitation. In nonhypotensive children with severe hemolytic anemia (severe malaria or sickle cell crises) blood transfusion is considered superior to crystalloid or albumin bolusing D. Inotropes/ • Begin peripheral inotropic support until central venous access can be attained in children who are not vasopressors/ responsive to fuid resuscitation vasodilators • Patients with low cardiac output and elevated systemic vascular resistance states with normal blood pressure be given vasodilator therapies in addition to inotropes E. Corticosteroids • Timely hydrocortisone therapy in children with fuid refractory, catecholamine resistant shock, and suspected or proven absolute (classic) adrenal insufciency G. During resuscitation of low superior vena cava oxygen plasma therapies saturation shock (<70%), hemoglobin levels of 10 g/dL are targeted. Mechanical ventilation • Lung-protective strategies during mechanical ventilation J. Sedation/analgesia/ • We recommend use of sedation with a sedation goal in critically ill mechanically ventilated patients with sepsis drug toxicities • Monitor drug toxicity labs because drug metabolism is reduced during severe sepsis, putting children at greater risk of adverse drug-related events K. Glycemic control • Control hyperglycemia using a similar target as in adults ≤180 mg/dL. Glucose infusion should accompany insulin therapy in newborns and children because some hyperglycemic children make no insulin whereas others are insulin resistant l.
All movements cheap 2.5mg indapamide hypertension renal disease, both active and passive It is the second most common type (afer • If treatment is started at this are limited in all directions purchase indapamide 1.5 mg visa arteria femoralis superficialis. Tere is apparent shortening of the acquired by hematogenous spread from Stage 3: (Stage of erosion and bone destruc- limb on the right side order indapamide 2.5 mg free shipping toprol xl arrhythmia. Purely synovial tuberculosis as seen in the dislocated to dorsum illi (posterior Systemic examination does not reveal any knee joint is uncommon in the hip. Tere is pain, stifness and limp on the For convenience it is described in three d. General symptoms like fever, anorexia Stage 1: (Stage of synovitis or Stage of sinus and wasting of muscles. It is due to friction between the dam- aged articular surfaces of acetabulum and head of femur following disappear- ance of protective muscle spasm during sleep. In primary or synovial type, the bacilli in the bloodstream are deposited in the synovium. In secondary or osseous type, the infec- tion starts in the bony part (Metaphysis) of the joint and then involves synovial membrane. It is an imaginary semicircular line joining medial cortex of femoral neck to lower border of the superior pubic ramus. Any break in continuity of this indicates dislocation or sublaxation of femoral head (Fig. Frame knee: Premature fusion of distal femoral epiphysis in patients who are on plaster for a long time (usually more than a year). Prolonged plastering of the limb, usually more than a year, may result in fusion of Fig. Stage 1: The affected hip is in a position of flexion, in marked shortening of the limb with abduction and external rotation. Stage 2: The affected hip is in a position of flexion adduction and internal rotation. What investigations will you do to con- affected hip has the same deformity as in stage 2 but in an exaggerated form. Kanamycin - 10 to 20 mg/kg, up to a shown in Xray painless movement maximum of 1 gm. Ethionamide - 15 to 30mg/day upto a giving no chance for reactivation or maximum of 1gm/day. During acute symptoms: Traction and • The frst 6 weeks of ambulation is Earliest sign. The aim months partial weight bearing, next • In advanced stage, when there is is to restore movement and protect the 3 to 6 months full weight bearing dislocation of hip, Shenton’s line is joint from stress. Stage of cure: When pain and deformity • Unprotected full weight bearing • Diminished joint space due to des has been corrected, achieving a painless walking is allowed around 1½ to truc tion of cartilage. The diseased focus in the acetabular advent of modern day chemotherapy, Tis is a case of crushing osteochondritis region is approached and thoroughly irra- extraarticular arthrodesis was the of right femoral head epiphysis or Perthes diated. The joint is then thoroughly washed geons presently prefer the combination abduction and internal rotation. No general features of fever, loss of • A long period of follow up is necessary 24. Absence of general features like fever, enough giving no chance for reactiva- Tis is done when bony ankylosis of hip loss of weight, anorexia, night sweats. Dramatic response to bed rest and skin • A certain proportion of hips may require A subtrochanteric osteotomy, an extra traction for relief of pain during irrita- arthrodesis later, but many will have capsular procedure is usually performed. Failure of conservative treatment to of the acetabulum and the upper end tects the epiphyseal cartilage, e. What is the pathogenesis and pathology of Case Summary The aim of arthrodesis operation is to Perthes disease? A male child aged 7 years, was admitted with Tis is a form of crushing osteocondritis a. Intraarticular arthrodesis with mod- a limp on the right side and pain in the right where the disease afects the femoral head. Pathogenesis Tis joint is opened, diseased tis- Tere is no history of fever, loss of weight Vascular jeopardy is the most important sue removed, the head of femur and and anorexia. No history of tuberculosis in factor in the pathogenesis of Perthes disease acetabulum are made raw to expose the family is present. Deformed and fattened head, short neck angled that it is adducted about 20 degrees sular arteries. What will happen if the patient is not supply only from the capsular arter- scan) has been devised by Catterall in treated? Hence avascularity develops at this which increasing amounts of femoral Osteoarthrosis will occur. What are other causes of avascular necro- an efusion into the hip joint following ing outcome. Stage 1: Bone death - due to avascu- ischemic and necrotic and of Caries Spine larity, part of the bony femoral head there is severe collapse. If a small part of epiphysis is involved and whole idea behind treatment is to keep 2. Chief complaints: there is rapid repair, the bony architecture fattening and distortion of the head a. When half or less than half of the head later stages fbrous or osseous ankylosis involved or the repair process is slow, is involved by the disease, prognosis is causing rigidity of the spine. When there is more than twothirds of pain and paraplegia of sudden or grad- plana) but enlarged (coxa magna) and the head is involved containment treat- ual onset. It has been seen that for better vasculari- indicates prolapsed intervertebral The radiological picture varies with the zation, femoral head should be well con- disk. Type and the amount of head which has been achieved by conservative methods (plas- i. What is the commonest site of skeletal • Inspection: (Tuberculosis of Spine) tuberculosis? Gait: Patient walks with short steps in Spine is the commonest site of skeletal Case Summary caries of dorsal spine to avoid jerks. Cervical spine-The child sup- in the back and deformity (gibbus) for last two ment of spine? The thoracolumbar spine is the common- under the chin and twists his Pain was gradual in onset, with occasional est site of involvement. Toracolumbar spine is the most vides support placing his hands history is present. Central type: Here the central part of located by applying gentle blows on Tis is a case of tuberculosis of spine. Adolescent male child with pain in the the weakened vertebrae giving rise to sure on the side of the spinous proc- back and deformity, i. Appendicial or posterior type: In this • Percussion: Over the spine is ofen per- • Kyphosis: Tis is excessive posterior type the posterior complex of the ver- formed to elicit tenderness.
