A: It is a malignant cell of B-cell origin buy linezolid in united states online, characterized by: • Large cell with paired mirror image nuclei that resembles ‘Owl’s eye’ appearance buy generic linezolid 600 mg on-line. X: Bulky disease (a widening of the mediastinum by more than 1/3rd or the presence of a nodal mass buy generic linezolid pills. E: Involvement of a single extranodal site that is contiguous or proximal to the known nodal site discount linezolid 600 mg on-line. Staging is done for selection of therapy (radiotherapy or chemotherapy) and also helpful for prognosis. A: If no relapse after 5 years of withdrawal of treatment, it is called cure or disease-free. Skin involvement (T-cell lymphoma) presents as Mycosis fungoides and Sézary syndrome. A: 2 types or grades (depending on the rate at which the cells are dividing): Low grade shows the following characteristics: • Low cell proliferation rate. A:It is a circle of lymphatic tissue in posterior part of oropharynx and nasopharynx, which includes adenoids and tonsils (pharyngeal, tubal, palatine, lingual tonsil). Radiotherapy is also indicated for residual localized site of bulk disease after chemotherapy, for spinal cord and other compression syndrome. Transformation to high grade is associated with poor prognosis, occurs in 3% per annum. In high-grade lymphoma: 75% respond to initial therapy and 50% are disease free for 5 years. Relapse is associated with a poor response to further chemotherapy (,10% 5-year survival), but in patients under 65 years, bone marrow transplantation improves survival. Prognosis High cure rate Low cure rate (low-grade tumours are incurable) mebooksfree. Presentation of a Case (Elderly or Middle Aged): • Present as described in generalized lymphadenopathy. A: Common in the elderly, M:F 5 2:1, involving B lymphocyte, after 45 years (usually 60 to 70 years). A:It is a neoplastic disorder of lymphocyte that usually involves B-lymphocytes and rarely T-lymphocytes (5%). Another staging (Rai staging): • Stage 0: Lymphocytosis, no lymphadenopathy, no hepatosplenomegaly, no anaemia or no thrombocytopenia. A: Treatment depends on stage: • Stage A: No treatment, unless progression occurs. Symptomatic: • For anaemia and thrombocytopenia: Prednisolone and blood transfusion. If refractory or recurrent, splenectomy may be done (also indicated for hypersplenism). Specifc: • Fludarabine alone or with cyclophosphamide or mitoxantrone (with or without steroid) is very helpful. Fludarabine should be avoided in autoimmune haemolytic anaemia as it aggravates anaemia. In combination with chlorambucil, it is superior to either chlorambucil alone or chlorambucil with rituximab. These disorders are grouped together in which one disease may transform to another. Patient may complain of mass or discomfort, or heaviness or pain in left hypochondrium. A: 3 phases: • Chronic phase: In this phase, disease response to treatment and is easily controlled. It can be continued indefnitely, but should be stopped in pregnancy or planning for pregnancy. However, hydroxyurea does not diminish Philadelphia chromosome or affect blastic crisis. Treatment of accelerated phase and blastic crisis: • Treatment is diffcult, imatinib is indicated if the patient has not received it. A: Bone marrow transplantation is indicated if: • The disease is not well controlled. Occurs in 10% per year, relatively refractory to treatment and is the cause of death in majority of cases. Whether they are palpable and painful or not (palpable painful purpura is of vascular origin and non-palpable purpura indicates thrombocytopenia). Presentation of a Case: • There are multiple purpura involving both the legs below the knee, some are red and some are brown or dark and do not blanch on pressure (mention whether palpable or non-palpable). In the elderly, the causes are: • Senile purpura (usually on extensor surface of forearm and leg). History of arthritis, abdominal pain, bloody diarrhoea, haematuria (which are due to Henoch–Schönlein purpura). In any age, mention the causes as follows (if present): • If Cushingoid facies—it is due to steroid. A: As follows: • History of fever—may be dengue haemorrhagic fever or other viral infection, meningococcal septicaemia (the patient looks toxic). Malignant change occurs rarely (suggested by itching, rapid increase in size and increased pigmentation). Campbell de Morgan spot Drug rash Erythema nodosum Q:What investigations should be done in purpura? In this test, a sphygmomanometer cuff is infated over the upper arm between systolic and diastolic blood pressure, kept for 5 minutes and then defated. Again after 5 minutes, look for petechiae in cubital fossa and near the wrist joint. A: It is the spontaneous bleeding or extravasation of blood from the capillary into the skin and mucous membrane that does not blanch on pressure and there is progressive colour change. Q:How to differentiate in bleeding or purpura, whether due to bleeding abnormality or coagulation abnormality? Bleeding into the skin and mucous membrane, purpura is less common or rare purpura is more common 4. Clotting time is normal, but bleeding time is platelet count are normal prolonged and platelet count is low 5. Presentation of a Case: (Present as in Purpura) Q:What is idiopathic thrombocytopenic purpura? A: Varies in child or adult: • In child: Usually acute presentation, previous history of viral infection followed by bleeding or purpura, easy bruising etc. A: As follows: In child: Usually self-limiting, does not require treatment in most cases. Treatment is given for serious bleeding or urgent surgery: • Prednisolone (2 mg/kg), if moderate to severe thrombocytopenia (,10,000) and bruising, epistaxis or other bleeding. First line therapy: • If spontaneous bleeding: prednisolone 1 mg/kg, for 4 to 6 weeks, then taper. After splenectomy, if severe thrombocytopenia with or without signifcant bleeding persists— • Thrombopoietin analogue romiplostim and thrombopoietin receptor agonists eltrombopag may be given. May be needed if persistent or potentially life- threatening bleeding or where emergency splenectomy is done. A: Arthritis, abdominal pain, bloody diarrhoea and urinary complaint (haematuria). A: It is a small vessel vasculitis characterized by purpura or petechial rash, polyarthritis (in big joints), abdominal pain and glomerulonephritis. Common features are (4 systems are involved such as skin, joint, abdomen, kidney): • Skin lesion: Purpura is common in legs and buttock, face and trunk are spared. Due to vasculitis, bowel is oedematous and infamed causing bleeding and obstruction. In adults, 25% cases develop severe crescentic or rapidly progressing glomerulonephritis and renal failure (which are less in children). A: As follows: • Serum IgA is high in 50% cases (IgA-containing immune complex is also high).

Heavy exposure to pollution order linezolid overnight delivery, aller- gens discount linezolid 600 mg otc, or cigarette smoke makes resolution less likely buy linezolid 600 mg with mastercard. An immediate immunoglobulin (Ig) E response to environmental triggers occurs within 15 to 30 minutes and includes vasodilation best 600mg linezolid, increased vascular permeability, smooth-muscle constriction, and mucus secretion. Symptoms result from these changes and may include wheezing, cough (especially if worse at night), difficulty breathing, or chest tightness. These symptoms will be triggered by dust mites, animal dander, cigarette smoke, pollution, weather changes, pollen, upper respiratory infections, or exercise (particularly when performed in a cold environment). The presence of other atopic diseases such as allergic rhinitis, nasal polyps, or atopic dermatitis, may be supportive of the diagnosis. Spirometry should be performed, if possible, whenever a diagnosis of asthma is considered. A chest radiograph is not a required study but can help exclude other diagnoses such as congestive heart failure or in toddlers, foreign-body aspiration. Nonspecific findings of hyperinflation, flattened diaphragms, or increased bron- chial wall markings may be the only abnormalities seen with asthma. Other tests such as sweat chloride testing may be needed to exclude other obstructive diseases of the small airways, such as cystic fibrosis. Viral bronchiolitis is the most com- monly occurring disease of the small airways and usually does not respond to con- ventional asthma therapy. Asthma management involves classifying the baseline disease severity and identi- fying and minimizing exposure to triggers. Classification is made based on spirom- etry and the patient’s symptoms over prior 2 to 4 weeks. The features that are assessed are the frequency of nighttime symptoms, how often the rescue medica- tion is needed, and how much symptoms limit daily activities. Severity is defined as either intermittent or persistent; persistent asthma is further divided into mild, moderate, or severe. Pharmacotherapy for asthma includes quick-relief medications for the acute symptoms and exacerbations, as well as long-term controller medications. These agents also can be used immediately prior to exercise or exposure to allergens to minimize the acute asthmatic response. Increased levels of drug are delivered to the lungs and toxicity is decreased when these medications are delivered through inhalation routes (nebulizer or inhaler). When inhalers are used, a reservoir device (“spacer”) is used to maximize the amount of medication delivered to the lungs. Patients must not over-rely on short-acting inhalers because this practice is associ- ated with death in severe asthma attacks. The most potent available anti-inflammatory drugs are corticosteroids, which are useful for acute exacerbations (oral or intravenous prednisone, prednisolone) and for chronic therapy (inhaled corticosteroids). The inhaled route is best for chronic therapy so that adverse effects on bone mineral density, growth, and immune function are minimized while maximal amounts of the drug can be delivered to the lungs. Other long-term controller medications include mast cell stabilizers (cromolyn, ned- ocromil) and leukotriene modifiers (montelukast), which act by reducing the immune response to allergen exposure. Any chronic condition (such as poorly controlled asthma) may result in failure to thrive. Differentiating asthma from pneumonia (Case 14) requires a thorough personal and family history, careful physical examination, and selected testing such as chest radiographs. Difficult to con- trol or atypical presentations of asthma, especially in a child with failure to thrive, should prompt a consideration of tracheoesophageal atresia (Case 7) or cystic fibrosis (Case 18). Upon reassessment, wheezing increases in all fields, and the child’s color has improved. The albuterol was inadvertently left out of the inhalation treatment, and the girl received only saline. She has been using the albuterol 4 days per week, and about once per week her mother hears her coughing at night and has her use the inhaler. Her improved color indicates reversible symptoms, confirming the diagnosis of asthma. Increased wheezing is auscultated after albuterol treatment because lung areas previously obstructed are now opening, allowing additional airflow. Less-experienced examiners may misinterpret lack of air movement as “clear” breath sounds, further delaying appropriate medical management. Montelukast is a leukotriene modifier that is used in the long-term control of asthma. It is essential to define the severity of every patient’s asthma to determine the appropriate management. This patient’s frequency of daily inhaler use, nighttime use, and level of limitation from symptoms classifies her as mild persistent asthma and a controller medication is indicated. Changing the dose or type of β-adrenergic agonist will not improve her symptoms and are not appropriate management for her severity of asthma. A late-phase reaction typically occurs 2 to 4 hours after an initial wheez- ing episode. National Asthma Education and Prevention Program, Expert Panel Report 3: guidelines for the diagnosis and management of asthma, 2007. Cardio- pulmonary resuscitation was begun by the parents and was continued by para- medics en route to the hospital. You continue to try to revive the child in the emergency center, but pronounce him dead after 20 minutes of resuscitation. You review the history with the family and examine the child, but you are unable to detect a cause of death. Ask the parents if they would like you to call a friend, family mem- ber, religious leader, or other support person. Infanticide must be consid- ered, as well as the possibility of an underlying congenital or metabolic disorder. A coroner will perform an autopsy and police inves- tigators will examine the parents’ home for clues related to the death. Empha- size that these measures can help to bring closure for the family and may yield important information for preventing future child deaths should the couple have more children. Considerations Sudden infant death syndrome is one of the most tragic and frustrating medical diagnoses. When the family is in the emergency center, other possible causes of death (eg, child abuse or inherited disorders) cannot be excluded. Your role is to remain objective about these other possibilities yet sympathetic to the parents’ grieving. Meticulous documentation of the history and physical examination find- ings is imperative. The change will involve either the infant’s breathing, tone, color, or mental status. The investigation of the unexpected infant death includes a clinical history, a postmortem examination, and a death scene investigation. An 18-month-old girl who had a prior sibling that at 1 year of age also died suddenly and unexpectedly. A 5-month-old infant with dysmorphic features and an enlarged heart found on postmortem examination. The mother attempted to give mouth-to-mouth breaths for a few sec- onds and her daughter then began to cry and her breathing and appearance normalized. Reassure the mother that her infant looks healthy and because the symp- toms have resolved, discharge home. Instruct the mother to follow-up with the pediatrician to get an apnea monitor and pulse oximeter so that she will know if similar symptoms occur again and if they are actually life threatening. Infants should sleep in the same bed as the parent or on their chest so they can be closely monitored for apnea. Infants should sleep on their back on a firm mattress with no accompa- nying soft bedding or objects, including no devices advertised to main- tain the sleep position. Pacifiers should be avoided because they can obstruct the baby’s airflow during respiration.

Elevation of Blood Pressure Because of their ability to cause vasoconstriction discount 600mg linezolid free shipping, alpha agonists can elevate1 blood pressure in hypotensive patients purchase generic linezolid. Please note buy 600 mg linezolid visa, however order generic linezolid line, that alpha agonists1 are not the primary therapy for hypotension. Rather, they are reserved for situations in which fluid replacement and other measures either are contraindicated or have failed to restore blood pressure to a satisfactory level. Mydriasis Activation of alpha receptors on the radial muscle of the iris causes mydriasis1 (dilation of the pupil), which can facilitate eye examinations and ocular surgery. Note that producing mydriasis is the only clinical use of alpha activation that is1 not based on vasoconstriction. Adverse Effects of Alpha Activation1 All of the adverse effects caused by alpha activation result directly or indirectly1 from vasoconstriction. Hypertension Alpha 1 agonists can produce hypertension by causing widespread vasoconstriction. The cause is lack of blood flow to the affected area secondary to intense local vasoconstriction. If extravasation occurs, the area should be infiltrated with an alpha -blocking agent (e. The mechanism is this:1 alpha -mediated vasoconstriction elevates blood pressure, which triggers the1 baroreceptor reflex, causing heart rate to decline. In patients with marginal cardiac reserve, the decrease in cardiac output may compromise tissue perfusion. However, their ability to activate alpha2 2 receptors in the periphery has little clinical significance because there are no therapeutic applications related to activation of peripheral alpha receptors. By activating central alpha receptors, we can2 produce two useful effects: (1) reduction of sympathetic outflow to the heart and blood vessels and (2) relief of severe pain. The central alpha agonists used for2 effects on the heart and blood vessels, and the agents used to relieve pain, are discussed in Chapters 15 and 22, respectively. Clinical Consequences of Beta Activation 1 All of the clinically relevant responses to activation of beta receptors result from1 activating beta receptors in the 1 heart; activation of renal beta receptors is not1 associated with either beneficial or adverse effects. Therapeutic Applications of Beta Activation1 Heart Failure Heart failure is characterized by a reduction in the force of myocardial contraction, resulting in insufficient cardiac output. Because activation of beta1 receptors in the heart has a positive inotropic effect (i. Shock This condition is characterized by profound hypotension and greatly reduced tissue perfusion. By increasing heart rate and force of contraction, beta stimulants can1 increase cardiac output and can thereby improve tissue perfusion. Cardiac Arrest By activating cardiac beta receptors, drugs have a role in initiating contraction1 in asystole or pulseless ventricular rhythms. Initial management focuses on cardiopulmonary resuscitation, external pacing, or defibrillation (whichever is applicable), and identification and treatment of the underlying cause (e. When a beta agonist 1 is indicated, epinephrine, administered intravenously, is the preferred drug. Adverse Effects of Beta Activation1 All of the adverse effects of beta activation result from activating beta receptors1 1 in the heart. Altered Heart Rate or Rhythm Overstimulation of cardiac beta receptors can produce 1 tachycardia (excessive heart rate) and dysrhythmias (irregular heartbeat). Angina Pectoris In some patients, drugs that activate beta receptors can precipitate an attack of1 angina pectoris, a condition characterized by substernal pain in the region of the heart. Anginal pain occurs when cardiac oxygen supply (blood flow) is insufficient to meet cardiac oxygen needs. The most common cause of angina is coronary atherosclerosis (accumulation of lipids and other substances in coronary arteries). Because beta agonists increase cardiac oxygen demand (by1 increasing heart rate and force of contraction), patients with compromised coronary circulation are at risk for an anginal attack. Clinical Consequences of Beta Activation 2 Applications of beta activation are limited to the 2 lungs and the uterus. Drugs used for their beta -activating ability include epinephrine, isoproterenol, and2 albuterol. Therapeutic Applications of Beta Activation2 Asthma Asthma is a chronic condition characterized by inflammation and bronchoconstriction occurring in response to a variety of stimuli. Because drugs that activate beta receptors in the lungs promote bronchodilation, these drugs can2 help relieve or prevent asthma attacks. For therapy of asthma, adrenergic agonists that are selective for beta2 receptors (e. This is especially true for patients who also suffer from angina pectoris or tachycardia because drugs that can activate beta receptors would1 aggravate these cardiac disorders. It should be noted, however, that inhalation does not guarantee safety: Serious systemic toxicity can result from overdosing with inhaled sympathomimetics, so patients must be warned against inhaling too much drug. Delay of Preterm Labor Activation of beta receptors in the uterus relaxes uterine smooth muscle. Adverse Effects of Beta Activation2 Hyperglycemia The most important adverse response to beta activation is hyperglycemia2 (elevation of blood glucose). The mechanism is activation of beta receptors in2 the liver and skeletal muscles, which promotes breakdown of glycogen into glucose. As a rule, beta agonists cause hyperglycemia only in patients with2 diabetes; in patients with normal pancreatic function, insulin release will maintain blood glucose at an appropriate level. If hyperglycemia develops in the patient with diabetes, medications used for glucose control will need to be adjusted. It occurs because2 activation of beta receptors in skeletal muscle enhances contraction. This effect2 can be confounding for patients with diabetes because tremor is a common symptom of hypoglycemia; however, when due to beta activation, it may be2 accompanied by hyperglycemia. Fortunately, the tremor generally fades over time and can be minimized by initiating therapy at low doses. Clinical Consequences of Dopamine Receptor Activation Activation of peripheral dopamine receptors causes dilation of the renal vasculature. This effect is employed in the treatment of shock: by dilating renal blood vessels, we can improve renal perfusion and can thereby reduce the risk for renal failure. It should be noted that, when dopamine is given to treat shock, the drug also enhances cardiac performance because it activates beta receptors in1 the heart. Multiple Receptor Activation: Treatment of Anaphylactic Shock Pathophysiology of Anaphylaxis Anaphylactic shock is a manifestation of severe allergy. The reaction is characterized by hypotension (from widespread vasodilation), bronchoconstriction, and edema of the glottis. Although histamine contributes to these responses, symptoms are due largely to release of other mediators (e. Anaphylaxis can be triggered by a variety of substances, including bee venom, wasp venom, latex rubber, certain foods (e. Treatment Epinephrine, injected intramuscularly or intravenously, is the treatment of choice for anaphylactic shock. Benefits derive from activating three types of adrenergic receptors: alpha, beta, and beta. By activating these receptors, epinephrine can1 1 2 reverse the most severe manifestations of the anaphylactic reaction. Activation of beta receptors increases cardiac output, helping elevate blood pressure. Blood1 pressure is also increased because epinephrine promotes alpha -mediated1 vasoconstriction. In addition to increasing blood pressure, vasoconstriction helps suppress glottal edema. Individuals who are prone to severe allergic responses should carry an epinephrine autoinjector (e. Antihistamines are not especially useful against anaphylaxis because histamine is only one of several contributors to the reaction. Properties of Representative Adrenergic Agonists Our aim in this section is to establish an overview of the adrenergic agonists. The information is presented in the form of “drug digests” that highlight characteristic features of representative sympathomimetic agents.

Murmur is produced by either normal volume of blood passing through abnormal valve or increased volume of blood pass- ing through a normal valve or congenital defect discount linezolid 600 mg free shipping. Late systolic: Found in mitral valve prolapse and also in papillary muscle dysfunction generic linezolid 600mg online. Innocent murmur: Benign cost of linezolid, usually soft systolic order 600mg linezolid amex, present in upper sternal edge (commonly pulmonary area), found in some normal people without heart problem. Pericardial Rub: • It is superfcial, harsh, scratchy, creaking, grating, leathery sound. Opening snap is better heard in left lower sternal edge in between mitral and tricuspid area. Venous Hum: It is a continuous murmur due to kinking and partial obstruction of one of the large veins in the neck. It is found in the neck above the clavicle and upper part of chest, more on the right side of sternum. Venous hum can be obliterated by pressure on the neck or lying down or altering the position of neck (as there is reduction of venous obstruction). It is accentuated by sitting with head extended and turned to the side opposite to that auscultated. This will increase the heart rate, increase the fow across the mitral valve and murmur will be prominent. There may be history of fever, weight loss, myalgia, arthralgia, skin rash, Raynaud’s phenomenon. Other causes are (very rare, do not mention unless asked): congenital, calcifcation of valve (usually in elderly), carcinoid syndrome. A: It is occurs in atrial systole, due to increased fow across the stenosed valve from left atrium to left ventricle. A: It is the rosy colouration of cheeks, may be bluish tinge, due to arteriovenous anastomosis and vascular stasis on the cheeks. It is not pathognomonic, may be present in normal person, also in hypothyroidism, polycythaemia. A: Cerebral embolism, causing cerebral infarction, usually with right sided hemiplegia. A: Involvement of the lenticulostriate branch of left middle cerebral artery causing lesion in the internal capsule. A: Chest X-ray shows: • Upper lobe veins are dilated (early feature): Upper lobe diversion (normally, ratio between upper and lower lobe veins is 1:3, which is altered to 1:1). A: As follows: • Thick mitral valve leafet (with restricted opening), diastolic doming of anterior mitral leafet and restricted movement of posterior mitral leafet. A: As follows: • Valvuloplasty (percutaneous balloon mitral valvuloplasty) is the treatment of choice. If it is not possible and in severe case, can undergo successful surgery, preferably in the third trimester. A: As follows: • Rupture of anterior leafet of chorda tendineae—murmur radiates to axilla and back. A: Mitral valve prolapse may be primary (common) or secondary to other diseases, such as: • Marfan’s syndrome. My diagnosis is Mitral stenosis with Mitral regurgitation (mixed mitral valve disease). My diagnosis is Mitral regurgitation with Mitral stenosis (mixed mitral valve disease). Occasionally, diffculty arises, when the patient has loud frst heart sound and apex beat is also displaced. In such cases, you should say that, ‘it is diffcult to be sure clinically about the dominant lesion. Presentation of a Case: • Pulse: 76/min, low volume, slow rising, normal in rhythm. A: Plateau or anacrotic pulse which is slow rising, small volume (pulsus parvus) or late peaking (pulsus tardus). It may be associated with characteristic face such as broad forehead, widely set eyes and pointed chin, mental retardation and hypercalcaemia called ‘Williams syndrome’. A: It is a degenerative disorder characterized by thickening of aortic valve cusps. Risk factors like hyperlipidaemia, diabetes mellitus, smoking, hypertension which may cause aortic calcifcation. Young adults to middle aged: • Calcifcation and fbrosis of congenitally bicuspid aortic stenosis. Enlarged left ventricle and dilated ascending aorta, calcifcation of valve on lateral view). In mild or asymptomatic cases with valvular pressure gradient,50 mmHg: • Follow up (periodic echocardiogram should be done). Anticoagulant is necessary if associated with atrial fbrillation or mechanical valve prosthesis is used. A: Biological or tissue valve is preferred than mechanical one, as biological valve does not require anticoagulation. Presentation of a Case: • Pulse: 92/min, high volume, collapsing type, normal in rhythm. Mention, if the following fndings are present: • Ejection systolic murmur in aortic area, which radiates to right side of neck. A: As follows: • Eye: Argyll Robertson pupil (in syphilis), dislocated lens, irregular pupils, iridodonesis (in Marfan’s syndrome). A: As follows: • X-ray chest (shows cardiomegaly, dilated ascending aorta, pulmonary oedema). Transoesophageal echocardiography may provide additional information about the valves and aortic root. A: The name was originated from a Victorian toy, ‘Consisted of a sealed tube, half flled with water and half is vacuum. Inversion of the tube causes the fuid to fall rapidly without air resistance, which strike the other end with a noise like hammer blow’. A: Due to regurgitant fow from aortic valve causing vibration of anterior leafet of mitral valve. A: As follows according to suspicion of cause: • In syphilis—Argyll Robertson pupil. There is left ventricular enlargement and hypertrophy that causes increased stroke volume, so cardiac output is maintained. Tissue valves are preferred in the elderly and when anticoagulants must be avoided. On auscultation: • First heart sound: Soft in tricuspid area, normal in other areas. A: As follows: • Functional, secondary to other disease (pulmonary hypertension, cor pulmonale, right heart failure). In drug addicts with infective endocarditis of tricuspid valve: • Surgical removal of the valve is done to eradicate the infection. A: It is a congenital heart disease associated with downward displacement of tricuspid valve into the right ventricle. Characteristically, multiple clicks occur due to asynchronous closure of tricuspid valve. On auscultation: • 1st heart sound: Normal in all the areas, soft on tricuspid area. Presentation of a Case: (Usually, the Patient is an Adult or Elderly) • Pulse: 70/min, normal in volume, rhythm and character. A: As follows: • Chest X-ray—(shows enlarged pulmonary conus with post-stenotic dilatation, oligaemic lung felds in valvular stenosis). In metallic valve replacement, there is metallic sound on auscultation and in tissue valve replacement, there is click). My diagnosis is Metallic mitral valve prosthesis which appears to be functioning well. My diagnosis is Metallic aortic valve prosthesis which appears to be functioning well. A: It is detected in the following ways: • There is a vertical midsternal scar mark of thoracotomy. Mitral valve prosthesis is detected by: • Over the mitral valve, there is metallic sound coincides with frst heart sound (sharp closing). Aortic valve prosthesis is detected by: • Over the aortic valve, metallic sound is present, coincides with second heart sound (sharp closing).

U. Givess. Graceland University.

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