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Analysis of Medical Situations - Assignment Example

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The author of the assignment answers the medical questions and describes the mode of action in different medical situations. The author explains the mechanism of action of heparin, and whether CF is transmitted as a recessive disorder affecting the endocrine gland function …
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Analysis of Medical Situations
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7. What is the mechanism of action of heparin? A. Block prostaglandin synthetase action preventing formation of platelet-aggregating substance thromboxane A2 B. Accelerate formation of antithrombin III-thrombin complex, inactivate thrombin and prevent conversion of fibrinogen to fibrin: correct answer C. Inhibit vitamin K-dependent activation of clotting factors II, VII, IX, and X D. Block adenosine diphosphate-induced platelet-fibrinogen and platelet-platelet binding E. Catalyze conversion of tissue plasminogen to plasmin in the presence of fibrin, producing local fibrinolysis. Answer A. Block prostaglandin synthetase action preventing formation of platelet-aggregating substance thromboxane A2: Heparin does not block prostaglandin synthetase. This mechanism is seen by aspirin like drugs. B. Accelerate formation of antithrombin III-thrombin complex, inactivate thrombin and prevent conversion of fibrinogen to fibrin. Heparin accelerates the inhibition action of anti-thrombin on proteases especially thrombin IIa, IXa and Xa, by forming equimolar stable complexes with them. In the absence of heparin, these reactions are slow, in the presence of heparin, these reactions are accelerated thousand fold. This effect is achieved by heparin binding tightly to antithrombin and causing a conformational change in the inhibitor. Heparin actually acts as a cofactor. Hence this is the correct answer. C. Inhibit vitamin K-dependent activation of clotting factors II, VII, IX, and X: Heparin does not directly inhibit the action of these clotting factors. It actually acts as cofactor in the anti-thrombin- protease complexes. Hence this is not the correct answer. D. Block adenosine diphosphate-induced platelet-fibrinogen and platelet-platelet binding. This mode of action is seen in antiplatelet drugs like aspirin and clopidogrel (Hankey, p.568). E. Catalyze conversion of tissue plasminogen to plasmin in the presence of fibrin, producing local fibrinolysis: This action is seen in fibrinolytics like streptokinase. This is not the mode of action of heparin. References Hankey,Graeme and Eikelboom, John. “Antiplatelet drugs.” MJA 178. 11 (2003): 568-57 Zehnder, J.L., 2004. "Drugs used in the disorders of coagulation." Basic and Clinical Pharmacology. India: McGrawHill Lange, p.547. 8. A 68-year-old patient is brought to the ER with sever, sudden-onset anterior chest pain. He is nauseous and diaphoretic. Vitals are HR 104 (regular) Resp 20 (regular) BP 160/90 T 98.8. He has a history of hypertension and takes a ‘water-pill’. He appears in pain, but hemodynamically stable. The differential diagnosis includes CHF, Angina, MI, aortic dissection, and PE. His ECG shows tachycardia with a regular rate and rhythm and mild left ventricular hypertrophy. There are no q-waves or ST segment changes. CXR shows a slight widening of the mediastinum. Which of the following tests would best discriminate between these differentials? A. MRI B. Angiography C. Cardiac Enzymes E. Spiral CT scan: correct answer A. MRI: The most likely diagnosis in this patient is aortic dissection. Aortic dissection is defined as separation of the layers within the aortic wall. This diagnosis can be presumed in patients with symptoms and signs suggestive of myocardial infarction but without classic ECG findings. This scan has over 90% sensitivity and greater than 95% specificity and infact, is the most sensitive method for diagnosing aortic dissection and has similar specificity to CT scanning. However, it may be difficult to do this scan in a hemodynamically compromised patient. Its use is limited because it is not portable. Also, Spiral CT Scan offers high-quality 2D and 3D reconstructions and is much preferred than MRI (Wiesenfarth, emedicne). B. Angiography: This is still considered as a diagnostic criterion by some surgeons. But the newer imaging modalities have replaced this (Wiesenfarth, emedicne). It is difficult to perform in patients with hemorrhage, shock, and/or cardiac tamponade (Osinuga, emedicine) C. Cardiac Enzymes: This test is of no value in the detection of aortic dissection. Myocardial muscle creatine kinase isoenzyme, myoglobin, and troponin I and T levels are elevated if the dissection has caused myocardial ischemia (Osinuga, emedicne). E. Spiral CT scan: Spiral CT scanning is associated with a good rate of resolution and detection. Also, high-quality 2D and 3D reconstructions are possible with spiral CT scanning, which greatly adds to the usefulness of this imaging modality (Wiesenfarth, emedicne). Hence this is the most appropriate answer. References Osinuga, Oladayo. “Aortic dissection.” eMedicine from WebMD. 2006. 17 December 2007 Wiesenfarth, John. “Dissection, Aorta.” eMedicine from WebMD. 2007. 17 December 2007 14. The physical exam finding most consistent with a diagnosis of atrial septal defect is: A. Blowing systolic murmur in the left axilla. B. Diastolic flow murmur at the lower left sterna border C. High pitched systolic ejection murmur heard best over the pulmonic area: Correct answer D. Rough machinery murmur at the second intercostals space Answer A. Blowing systolic murmur in the left axilla: Atrial septal defect is an abnormally large opening in the atrial septum that enables blood flow between the left and right atria via the interatrial septum. This is mostly due to secundum atrial septal defect usually arising from an enlarged foramen ovale, inadequate growth of the septum secundum, or excessive absorption of the septum primum. Due to this, blood flows from the atria to the ventricles directly during systole. This causes a systolic ejection murmur over the pulmonary trunk in the second left intercostal space (Gessner, emedicine) and not over axilla. B. Diastolic flow murmur at the lower left sterna border. Diastolic murmur starts at or after S2 and ends before or at S1. A medium frequency mid diastolic murmur at the lower left sternal edge occurs with rapid ventricular filling of the right ventricle after the tricuspid valve opens. However, this murmur is heard with great effort and is not a consistent finding (Gessner, emedicine). The murmur which is heard consistently is in systole because the flow occurs through the shunt during systole. Hence this is not the correct answer. C. High pitched systolic ejection murmur heard best over the pulmonic area: The shunt gives rise to high-pitched ejection murmur in systole mainly over the pulmonary trunk in the second left intercostal space. This is the correct answer. Also, there is wide S-2 split which does not change with respiration (Gessner, emedicine). D. Rough machinery murmur at the second intercostals space. This type of murmur is found in patent ductus arteriosus. In patent ductus arteriosus, there is persistence of a normal fetal structure between the left pulmonary artery and the descending aorta and this causes a shunt between the pulmonary artery and the aorta. The continuous or machinery murmur is best heard at the upper left sternal border or left infraclavicular area. (Sethuraman, emedicine). References Gessner, Ira. "Atrial Septal Defect, Ostium Secundum." eMedicine from WebMD. 2006. 17 Dec 2007 Sethuraman, Girish. "Patent Ductus Arteriosus." eMedicine from WebMD. 2006. 17 Dec 2007 15. You are the new instructor for the MD patient assessment course. You are demonstrating cardiac auscultation. Your students are having difficulty differentiating S1 from S2. What instruction will you give them to help them identify S1? A. Determine which sound is softer and lower in pitch in the apical area B. Identify which sound is the softest in every precordial location C. Identify the second heart sound by respiratory splitting D. Palpate the carotid artery while auscultating the heart: Correct answer Answer A. Determine which sound is softer and lower in pitch in the apical area. The first heart S1 is caused by the sudden block of reverse blood flow due to closure of the atrioventricular valves, mitral and tricuspid, at the beginning of ventricular contraction, or systole. The sound arises from the reverberation within the blood associated with the sudden block of flow reversal by the valves. S1 can be heard louder in children and during increased flow through the AV valves as in thyrotoxicosis, anemia, AV fistul, etc (Mehta, p.137). Hence this is not the correct method of identifying S1. B. Identify which sound is the softest in every precordial location. This is a tedious method. It is also unreliable because the first heart sound can be heard louder in some conditions with increased AV flow and second heart sound can be heard softer in aortic atenosis, pulmonary stenosis, pulmonry atresia and fallots tetrology (Mehta, p.137). C. Identify the second heart sound by respiratory splitting. Splitting of second heart sound occurs due to increased blood volume in the right ventricle causing the pulmonary valve to stay open longer during ventricular systole. It is difficult to identify the second sound by respiratory splitting. Infact, in certain conditions, there is the splitting of second sound is fixed. These include atrial septal defect, pulmonary stenosis, myocardial infarction and ventricular septal defect. It is also reversely split in aortic stenosis, patent ductus arteriosus and coarctation of aorta (Mehta, p.137). Hence this is not the correct method of identifying second sound. D. Palpate the carotid artery while auscultating the heart: This is the most appropriate method of identification of first heart sound. It correlates well with the onset of the first sound (Swash, p.87). S1 can be identified by correlation with any pulse in the upper limb, but the most appropriate one is carotid pulse. It is not influenced by any pathological conditions. Hence this is the correct answer. References Mehta, PJ. Practical Medicine. 15th edition. India: PJ Mehta publishers, 2001. pg,137. Swash, Michael. Hutchinsons Clinical Methods. London: W.B. Sauders, 2002, p.87-89 16. An echocardiogram will measure pressures within the heart and great vessels. Which of the following statements is FALSE about measures of pulmonary artery pressure? A. Echocardiogram pulmonary artery pressures, if done well, will correlate very well to pulmonary capillary wedge pressure. B. An echocardiogram pulmonary artery pressure of 50-60 mm Hg at rest is far above normal. C. The mean pulmonary artery pressure is always closer to the diastolic pressure rather than the systolic pressure D. Exercise can cause a three times increase in pulmonary artery systolic pressure with no change in pulmonary diastolic pressure. E. Blood flowing to the lungs encounters greater resistance than blood flowing to the body: correct answer Answer A. Echocardiogram pulmonary artery pressures, if done well, will correlate very well to pulmonary capillary wedge pressure: ECHO allows for extensive noninvasive assessment of the right ventricular function. Though it will not take the place of right heart catheterizations in defining and assessing pulmonary artery pressures, when done properly, it can be used to monitor and assess response to therapies and predict the overall prognosis of patients with pulmonary artery hypertension (Stenbis, Medscape Today). B. An echocardiogram pulmonary artery pressure of 50-60 mm Hg at rest is far above normal: The normal pulmonary artery pressure is about 14 mmHg when the person is resting. If it is more than 25 mmHg, it is known as pulmonary arterial hypertension, a condition where in there is narrowing of pulmonary arteries causing the right side of heart to work harder to pump blood through the lungs (What Is Pulmonary Arterial Hypertension?, National Institute of Health). C. The mean pulmonary artery pressure is always closer to the diastolic pressure rather than the systolic pressure: This is wrong because, the diastolic pressure depend on the pulmonary vascular resistance. D. Exercise can cause a three times increase in pulmonary artery systolic pressure with no change in pulmonary diastolic pressure. This is true. Degre et al (2004) studied the normal pulse pressure relationship with exercise in sitting position in middle aged male healthy persons. They found that at rest in the sitting position the mean pulmonary artery pressure is 10.8 ± 4.3 mm Hg. But during exercise, the mean pulmonary artery pressure reaches 22.5 ± 4.6 mm Hg, which is about two and half times at rest. The total pulmonary resistance decreases during exercise and hence there is no change in pulmonary diastolic pressure. E. Blood flowing to the lungs encounters greater resistance than blood flowing to the body: This is not true because, blood flowing through the lungs encounters the least resistance in the body. References Degre, S, de Coster, A, Messin, R, Denolin, H. "Normal pulmonary pressure-flow relationship during exercise in the sitting position." European Journal of Applied Physiology, 31 (1), p.53-59. "What Is Pulmonary Arterial Hypertension?" National Institute of Health, US Department of Health and Human Services, 2006. 17 December, 2007 Steinbis, Susan. "Pulmonary Hypertension." Medscape Today. 2005. 17 December, 2007 18. Your patient is a 15 year old female. She has a systolic murmur that is difficult to hear. You suspect it is a murmur due to mitral valve prolapsed. What could you ask a patient to do to accentuate the positive cardiac findings of mitral valve prolapsed? A. Squat. B. Hop on one foot C. Kneel D. Perform a Valsalva maneuver: Correct answer Answer A. Squat. In mitral valve prolapse, the mitral valve leaflet prolapses into the left atrium which cause abnormal ventricular contraction and mitral regurgitation. The murmur heard is a late systolic murmur due to mitral regurgitation. Squatting causes increase in the blood flow to the lungs. In squatting from standing position, the click and murmur may move back to late systole. This is because, prompt squatting from standing position increases venous return and left ventricular volume. Also, while the patient is standing from squatting position, the murmur moving back to early systole on a beat-to-beat basis as the heart rate accelerates. Sometimes, squatting may be associated with an increase in peripheral vascular resistance, causing increase in the tension on the mitral valve apparatus and directing blood flow mainly into the left atrium, rather than to the peripheral circulation. In such a situation, the murmur may become accentuated in the squatting position. Thus, squatting can increase the murmur, but it is more practical, common and easy to hear the murmur with Valsalva maneuver. B. Hop on one foot. This is the wrong answer. Hopping only causes tachycardia. It does not accentuate the murmur. C. Kneel. This is the wrong answer. Kneeling does not have effect on the murmur. D. Perform a Valsalva maneuver: This is the correct answer. Valsalva maneuver is performed by forcibly exhaling against closed lips and pinched nose, forcing air into the middle ear. During this maneuver, initially when there is expiratory force, there is increased pressure in the chest and this causes blood to go out of the pulmonary circulation and thus enter the left atrium. Then, again, pressure in the chest also reduces venous return to the heart and consequently the cardiac output decreases. When the pressure in the chest is released, the pulmonary vessels and aorta re-expand and cause further decrease in the pressure due to decreased left ventricular return. Then there is rapid increase in cardiac output and of blood pressure. These physiological changes at the left atrium accentuate the late systolic murmur of mitral valve prolapse. References Plewa, Michael. “Mitral Valve Prolapse.” eMedicine from WebMD. 2006. 17 December, 2007 Venugopalan, Poothirikovil. “Mitral Valve Prolapse.” eMedicine from WebMD. 2007. 17 December, 2007 http://www.emedicine.com/ped/topic1465.htm 20. A pediatric patient has a grade 2/6 medium pitched blowing midsystolic murmur located in the 2nd left intercostals space near the left sternal border with no radiation when the patient is in the recumbent position. It is not discernable when the patient sits up. The echo results are back. What are the results MOST likely to be? A. Atrial septal defect B. Hypertrophic cardiomyopathy C. Mitral valve prolapsed D. No cardiac or valvular defect: Correct answer Answer A. Atrial septal defect: In this condition, the murmur is ejection systolic and is found over the pulmonary trunk in the second left intercostal space. It peaks in mid systole and is never more than grade 2-3/6. It is indistinguishable from an innocent pulmonic flow murmur (Gessner, emedicine). But in an innocent murmur, the murmur is blowing, not ejection type. Hence, though this answer can be correct, it is not the most appropriate answer. B. Hypertrophic cardiomyopathy: In this condition, holosystolic murmur of mitral regurgitation is heard at the apex and left axilla in patients with systolic anterior motion of the mitral valve and significant LV outflow gradients. In some, diastolic decrescendo murmur of aortic regurgitation is heard. These murmurs are usually more than 2/6 and are discernable when the patient sits up (Berul, eMedicine). C. Mitral valve prolapse: In mitral valve prolapse, the murmur heard is a late systolic murmur due to mitral regurgitation. The murmur radiates along the left sternal border to the aortic area. In significant mitral regurgitation, the murmur may be holosystolic. This murmur is accentuated with valsalva manouver and squatting (Venugopalan, emedicine). D. No cardiac or valvular defect. The murmur discussed is an innocent murmur. These are sounds made by the blood circulating through the hearts chambers and valves or through blood vessels near the heart. They are common in children. They are less than or equal to 2/6 grade. They do not radiate and are not discernable when the patient sits up. They are not associated with other signs and symptoms suggestive of cardiac disease (Innocent Heart Murmurs, AHA). This is the most appropriate answer. References Berul, Charles. "Cardiomyopathy, Hypertrophic." eMedicine from WebMD. 2006. 17 Dec 2007 Gessner, Ira. "Atrial Septal Defect, Ostium Secundum." eMedicine from WebMD. 2006. 17 Dec 2007 “Innocent Heart Murmurs.” American Heart Association (AHA). 17 Dec 2007 Venugopalan, Poothirikovil. “Mitral Valve Prolapse.” eMedicine from WebMD. 2007. 17 December, 2007 http://www.emedicine.com/ped/topic1465.htm 21. Which condition does not produce a dull percussion note? A. Tension pneumothorax: correct answer B. Pleural effusion C. Atelectasis D. Pneumonia Answer A. Tension pneumonthorax: In this condition, there is accumulation of air under pressure in the pleural space. It occurs when injured tissue forms a 1-way valve, allowing air to enter the pleural space and preventing the air from escaping naturally (Bjerke, eMedicine). The air in the pleura causes tympanic note on percussion. B. Pleural effusion: In pleural effusion, there is increased fluid accumulation in between the pleurae. The normal pleural space contains approximately 1 mL of fluid. The fluid causes dull note on percussion, decreased breath sounds, decreased tactile fremitus and friction rub (Rubin, eMedicine). C. Atelectasis: Pulmonary atelectasis refers to collapse of part of the lung. Physical examination reveals decreased breath sounds and a dull percussion note over the part of the lung collapsed (Bye, eMedicine). D. Pneumonia: In this condition, there is consolidation of the lungs where in there is accumulation of fluid in the affected segments. Dull note to percussion may not be appreciated in all cases of pneumonia. Infact, decreased air entry and bronchial breathing are better signs consistent with pneumonia (Stephen, eMedicine). References Bjerke, Scott. “Tension Pneumothorax.” eMedicine from WebMD. 2006. 17 December, 2007 Bye, Michael. “Atelectasis, Pulmonary.” eMedicine from WebMD. 2006. 17 December, 2006 Rubin, Jeffrey. “Pleural Effusion.” eMedicine from WebMD. 2007. 17 December, 2007 Stephen, James. “Pneumonia, Bacterial.” eMedicine from WebMD. 2007. 17 December, 2007 25. A chest x-ray of a patient with dyspnea reveals an area of increased density in the right lower lung field that obscures the costo-phrenic angle. Which of the following findings would help confirm your diagnosis of pleural effusion? A. Decreased vocal fremitus in the right lower lung field B. Hyporesonance on percussion of the right lower lung field C. Right lateral decubitus x-ray view showing layering along right chest wall: Correct answer D. Fine crackles at the right lung base on auscultation E. None of the above Answer A. Decreased vocal fremitus in the right lower lung field: This condition is seen in pleural effusion. But it also seen in other conditions like pneumothorax, consolidation, fibrosis and collapse of the lung (Mehta, p.103). Hence this is not the most appropriate diagnosis. B. Hyporesonance on percussion of the right lower lung field: This is also seen in pleural effusion. Other conditions like consolidation, fibrosis, collapse and atelectasis have similar findings (Mehta, 107) and this cannot confirm the diagnosis. C. Right lateral decubitus x-ray view showing layering along right chest wall: This test allows layering of fluid due to gravity (Rubin, emedicine). It can be compared with an anterio-posterior view to assess the amount of fluid. Other conditions like consolidation, fibrosis, atelectasis, etc., which demonstrate common findings like dull note to percussion, decreased breath sounds and decreased vocal fremitus do not demonstrate layering in decubitus position. Hence this is the most appropriate diagnostic finding. Infact, shifting dullness is more appropriate and can differentiate pleural effusion from empyema. D. Fine crackles at the right lung base on auscultation: These are usually seen in consolidation. In pleural effusion secondary to pneumonia, these sounds can be heard on auscultation. But in increased accumulation of fluid, the sounds may not be clear. This is not the appropriate diagnostic feature. E. None of the above: This is not the correct answer because C is the correct answer. References Mehta, PJ. Practical Medicine. 15th edition. India: PJ Mehta publishers, 2001. pg,103, 107. Rubin, Jeffrey. “Pleural Effusion.” eMedicine from WebMD. 2007. 17 December, 2007 http://www.emedicine.com/MED/topic1843.htm 27. Which of the following physical exam findings would be most likely in a patient who has isolated lobar pneumonia? A. Ipsilateral tympany to percussion and diminished tactile fremitus B. Ipsilateral increased tactile fremitus and dullness to percussion: correct answer C. Ipsilateral dullness to percussion and reduction in tactile fremitus D. Bilateral tympany to percussion and diminished tactile fremitus E. Localized wheezing best auscultated anteriorly Answer A. Ipsilateral tympany to percussion and diminished tactile fremitus: This condition is seen in pneumothorax and is not the correct answer. In pneumothorax, there is accumulation of air in the pleural space. It occurs when injured tissue forms a 1-way valve, allowing air to enter the pleural space and preventing the air from escaping naturally (Bjerke, eMedicine). The air in the pleura causes tympanic note on percussion. Since there is decreased conduction of sound, the tactile fremitus is diminished. B. Ipsilateral increased tactile fremitus and dullness to percussion: This is the correct answer. In lobar pneumonia, there is dullness over the affected part of the lung due to consolidation. Tactile vocal fremitus increases because of increased conduction of sound and sound vibrations from the larynx pass down the bronchi and cause lungs and chest wall to vibrate (Mehta, p.102). Hence this is the correct answer. C. Ipsilateral dullness to percussion and reduction in tactile fremitus: This is seen in pleural effusion. In pleural effusion, there is increased fluid accumulation in between the pleurae. The fluid causes dull note on percussion, decreased breath sounds, decreased tactile fremitus and friction rub (Rubin, eMedicine). D. Bilateral tympany to percussion and diminished tactile fremitus: This is not the correct answer. This is seen in bilateral pneumothorax. This is not the correct answer. E. Localized wheezing best auscultated anteriorly: This is not the correct answer. These auscultatory findings are seen in bronchitis or bronchial asthma. References Bjerke, Scott. “Tension Pneumothorax.” eMedicine from WebMD. 2006. 17 December, 2007 Mehta, PJ. Practical Medicine. 15th edition. India: PJ Mehta publishers, 2001, pg, 102. Rubin, Jeffrey. “Pleural Effusion.” eMedicine from WebMD. 2007. 17 December, 2007 28. Which of the following is TRUE regarding a tension pneumothorax? A. It is a result of air entering the pleural space due to a rupture of a bleb on the pleural surface B. It occurs when air enters the pleural space during inspiration but does not escape during expiration: correct answer C. Tracheal deviation toward the affected side occurs D. It occurs most commonly in tall, thin young men. Answer A. It is a result of air entering the pleural space due to a rupture of a bleb on the pleural surface. Rupture of bleb on the pleural surface causes pneumothorax, but not tension pneumothorax. Tension pneumothorax is the accumulation of air under pressure in the pleural space and develops when injured tissue forms a 1-way valve, allowing air to enter the pleural space and prevents the air from escaping naturally (Bjerke, eMedicine). B. It occurs when air enters the pleural space during inspiration but does not escape during expiration: This is the correct answer. Air that has entered the pleural space does not have an exit route. Hence, this condition rapidly progresses to respiratory insufficiency, cardiovascular collapse, and, ultimately, death if unrecognized and untreated (Bjerke, eMedicine). The air trapping in the pleural cavity causes shifts of the intrathoracic structure (Bjerke, eMedicine). C. Tracheal deviation toward the affected side occurs: The airtrapping in the pleural cavity causes shifts of the intrathoracic structure (Bjerke, eMedicine). The trachea is deviated to the opposite side due to increasing pressure. The heart and mediastinal structures are pushed to the contralateral side. Trachea is deviated to the same side in fibrosis and collapse of the lung. D. It occurs most commonly in tall, thin young men. Tension pneumothrax occurs mostly due to injury, hence is not dependent on age and sex.. Spontaneous pneumothorax most frequently occurs in tall, thin men aged 20-40 years (Bowman, eMedicine). References Bjerke, Scott. “Tension Pneumothorax.” eMedicine from WebMD. 2006. 17 December, 2007 Bowman, Glenn. “Pneumothorax, Tension and Traumatic.” eMedicine from WebMD 2006. 17 December, 2007 30. Which of the following electrocardiographic changes is typical of acute pericarditis? A. Diffuse ST segment depression B. Diffuse ST segment elevation: correct answer? C. Q wave in anterior leads D. Increased T wave amplitude E. Mildly elevated ST segments in II III and AVF with no reciprocal changes Answer A. Diffuse ST segment depression. This is not the correct answer. Diffuse ST segment in inferior and precordial leads on ECG is mainly seen in myocardial ischemia, mainly due to left main coronary artery stenosis (Sclarovsky, 575). B. Diffuse ST segment elevation: In acute pericarditis, there is diffuse concave upward ST elevation, except in aVR and V1 in which the ST segment is usually depressed. T waves are upright in the leads with ST elevation, and the PR segment deviates opposite to P-wave polarity. This is the most appropriate ECG finding in acute pericarditis (Gentlesk, eMedicine). C. Q wave in anterior leads: This is suggestive of anterior wall infarction. D. Increased T wave amplitude: This si caused by some anesthetic drugs like lidocaine, bupivacaine which enter the circulation accidentally and atropine (Tanaka, p.915) E. Mildly elevated ST segments in II III and AVF with no reciprocal changes: This is not the correct answer because; these findings are not seen in acute pericarditis. References Gentlesk, Phillip. “Pericarditis, Acute.” eMedicine from WebMD. 2005. 17 December, 2007 Tanaka, Makata, Nitta, Rie, Nishikawa, Toshiaki. “Increased T-Wave Amplitude After Accidental Intravascular Injection of Lidocaine Plus Bupivacaine Without Epinephrine in Sevoflurane-Anesthetized Child.” Anesth Analg 92 (2001):915–7 Sclarovsky, Samuel, Kjell, Nikus & Birnbaum, Y. “Manifestation of left main coronary artery stenosis is diffuse st depression in inferior and precordial leads on ECG.” J Am Coll Cardiol, 40 (2002): 575-576 31. CF is transmitted as recessive disorder affecting the endocrine gland function. A. True B. False: correct answer Answer A. True. This is not the correct answer because cystic fibrosis is an autosomal recessive disorder affecting exocrine gland function and not endocirne function (murray, eMedicine). B. False: This is the correct answer. CF is an autosomal recessive disorder. It affects exocrine gland function. It affects multiple organ systems and chiefly resulting in chronic respiratory infections, pancreatic enzyme insufficiency, and associated complications in untreated patients. Most carriers of the gene are asymptomatic. It is caused by defects in the gene for cystic fibrosis transmembrane conductance regulator (CFTR). CFTR encodes for a protein that functions as a chloride channel. Mutations in the gene for CFTR result in abnormalities of cAMP-regulated chloride transport across epithelial cells on mucosal surfaces. This causes decreased secretion of chloride and increased reabsorption of sodium and water across epithelial cells. The decreased hydration of mucus results in mucus that is stickier to bacteria, which results in infection and inflammation. Also, secretions in the respiratory tract, pancreas, gastrointestinal tract, sweat glands, and other exocrine tissues also become thickier. This makes the secretions difficult to clear (Sharma, eMedicine) References Murray, Nicole. “Cystic Fibrosis.” eMedicine. 2007. 17 December, 2007 Sharma, Girish. “Cystic Fibrosis.” eMedicine. 2006. 17 December, 2007 http://www.emedicine.com/ped/topic535.htm 35. You culture the sputum of an 18 month old CF patient. What are the most likely infective organisms? A. streptococcus pneumonia and staphylococcus aureus B. Moreaxella catarrhalis and Haemophilus influenzae C. Streptococcus pneumoniae and Haemophilus influenzae D. Pseudomonas aeruginosa and staphylococcus aureus: Correct answer Answer A. Streptococcus pneumonia and staphylococcus aureus. The bacteria most commonly isolated from CF sputum include Staphylococcus aureus, Haemophilus influenzae and Pseudomonas aeruginosa. Hence this is not the correct answer (Govan, p.912). B. Moraxella catarrhalis and Haemophilus influenzae. This is also not the correct answer because of above stated reasons. C. Streptococcus pneumoniae and Haemophilus influenzae. This is also not the correct answer. D. Pseudomonas aeruginosa and staphylococcus aureus: This is the correct answer. In cystic fibrosis, the commonly isolated organisms are Staphylococcus aureus, Haemophilus influenzae and Pseudomonas aeruginosa. Colonisation of the airways by mucoid, alginate-producing variants of P. aeruginosa is recognised as a major cause of pulmonary deterioration (Govan, p.912). Staphylococcus aureus also causes chronic respiratory tract infections in patients with cystic fibrosis. The organism adheres primarily to mucus components of the respiratory epithelium and that significant differences do not exist in binding of S. aureus to CF or non-CF cells (Ulrich, p. 83). These infections often need treatment through intravenous antibiotics. The mucus encourages the development of bacterial microenvironments that are difficult for immune cells to penetrate. These infections lead to bronchiectasis. Development of resistance to commonly used antibiotics is common. References Govan, JRW & Nelson, JW. “Microbiology of lung infection in cystic fibrosis.” British Medical Bulletin 48 (1992):912-930 Ulrich, Martina et al. “Localization of Staphylococcus aureus in Infected Airways of Patients with Cystic Fibrosis and in a Cell Culture Model of S. aureus Adherence.” Am. J. Respir. Cell Mol. Biol., 19.1, (1998): 83-91 39. An IgA deficiency can cause a higher incidence of infections predominantly in the respiratory, gastrointestinal, and urogenital tracts. This antibody is first detected in about the thirteenth postnatal day. At what age are adult levels of IgA achieved? A. 1-2 years B. 6-7 years: Correct answer C. 10-12 years D. 16-18 years Answer A. 1-2 years: This is not the correct answer. Though, the development of B-lineage cells begins in the fetal liver, serum IgA levels reach adult levels only after 4 years of age. Hence, the deficiency can be diagnosed reliably only after 4 years of age (shah, pediatric oncall). B. 6-7 years: This is the correct answer. Serum IgA deficiency is the most common immunglobulin deficiency. Though, many patients are asymptomatic, some patients with IgA deficiency have increased risk for upper respiratory tract infection, allergies, celiac like enteropathies and autoimmune disorders. The normal range of IgA levels are 80 - 350 mg/dl. these levels are reached beyond 4 to 5 years of age. In those with deficiency, the levels are < 7mg/dl but with normal S.IgG and IgM levels (Bascom, eMedicine). C. 10-12 years. This is not the correct answer. In a study by Buckley et al (1968), they found that there was significant relationship between age and both IgG and IgA concentrations up to ages 6 and 7 years. No correlation was present between age and immunoglobulin concentrations beyond that time, suggesting that the adult concentrations of IgG and IgA are normally reached and maintained after ages 6 and 7 years. D. 16-18 years. This is not the correct answer References Bascom, Rebecca. “Immunoglobulin A Deficiency.” eMedicine from WebMD. 2006. 17 December, 2007. Buckley, Rebecca, Dees, Susan, OFallon, Michael. “Serum Immunoglobulins: Levels in normal children and in uncomplicated Childhood allergy.” Pediatrics, 41.3, (1968): 600-611 Shah, Ira. “IgA deficiency-Case Report.” 17 December, 2007. 46. Which of the following mechanisms prevents occlusion in a normal coronary artery? A. Endothelial affinity for low density lipoproteins B. Monocytes in the intimal layer which are quick to phagocytize lipids C. Release of cytokines to intitiate an inflammatory response D. Angiogenesis and proliferation of smooth muscle cells in the area of plaque formation E. Activation of Proteins C and S by luminal endothelial cell surface molecules: Correct answer Answer A. Endothelial affinity for low density lipoproteins. This is the wrong answer because, affinity of endothelial cells to LDL proteins causes atherosclerosis. B. Monocytes in the intimal layer which are quick to phagocytize lipids. This is the wrong answer. Monocytes play a central role in the inflammatory disease atherosclerosis and they produce proinflammatory cytokines. Infact, patients with coronary artery disease have increased levels of CD14+CD16+ monocytes and these are associated with coronary atherosclerosis. hence it can be said that these monocytes play a role in athrosclerosis (Schitt, p.419). C. Release of cytokines to intitiate an inflammatory response. Cytokines signal immune cells such as T-cells and macrophages to travel to the site of infection. They also activate these cells, stimulating them to produce more cytokines. They are involved in a variety of immunological, inflammatory and infectious diseases.Inflammation causes swelling of the vascular endothelium and infact, narroes the blood vessels. Hence this is not the correct answer. D. Angiogenesis and proliferation of smooth muscle cells in the area of plaque formation. This is not the correct answer because this leads to worsening of stenosis. E. Activation of Proteins C and S by luminal endothelial cell surface molecules: This is the correct answer. These are physiological anticoagulants activated by thrombin. They are activated following thrombin generation after heparin neutralization. Infact, post-coronary bypass grafting, protein C activation during reperfusion is associated with hemodynamic recovery or postoperative myocardial damage. (Raivo, p.44). References Raivo, Peter et al. “Activation of protein C and hemodynamic recovery after coronary artery bypass surgery.” J Thorac Cardiovasc Surg , 133 (2007):44-51 Schitt, Axel et al. “CD14+CD16+ monocytes in coronary artery disease and their relationship to serum TNF- levels.” Thrombosis and Haemostasis, Schattauer. 92 (2004): 419 – 424. 17 December, 2007. 49. A 60 year old male presents with severe chest pain he describes as ‘sharp and tearing’. It radiates to his mid-back. He has a history of HTN and presents with a BP of 170/104 in the right arm. Blood pressure in the left arm is ten points lower. His right radial pulse is stronger than the left. Neither change in position nor deep breathing affects his panel level. What is the most likely diagnosis? A. Perforated peptic ulcer: Correct answer B. Aortic dissection C. Acute pericarditis D. Aortic stenosis E. Pleuritis Answer A. Perforated peptic ulcer: This is the correct answer. The patients with perforated peptic ulcer present with sudden onset of epigastric pain and rapid generalization of pain. The heart rate and blood pressure may increase due to the intensity of pain and peritonitis. B. Aortic dissection. In this condition, there is tear in the intimal layer, followed by formation and propagation of a subintimal hematoma. The pain is sudden in onset and is ripping or tearing. Some patients present with only mild pain, often mistaken for musculoskeletal conditions, located in the thorax, groin, or back. Anterior chest pain occurs in anterior arch or aortic root dissection. Pain in the neck or jaw indicates that the dissection involves the aortic arch and intrascapular pain involves the descending aorta (Wiesenfarth, eMedicine). C. Acute pericarditis. in acute pericarditis, the patient presents with sharp, dull, aching, burning, or pressing chest pain associated with dyspnoea and sometimes fever. The intensity of pain varies from barely perceptible to severe (Gentlesk, eMedicine). D. Aortic stenosis: This is not the correct answer. Obstruction of blood flow across the aortic valve is known as aortic stenosis. The patient may present with palpitation, angina, exertional syncope, fatigue and symptoms of left ventricular failure (Balentine, eMedicine). E. Pleuritis. Pain due to inflammation of the pleura can cause painful respiration. The patient has sharp chest pain with breathing. The pain can limit the movement on the side of the chest. References Balentine, Jerry. “Aortic Stenosis.” eMedicine from WebMD. 2007. 17 December, 2007 Gentlesk, Phillip. “Pericarditis, Acute.|” eMedicine from WebMD. 2005. 17 December, 2007 http://www.emedicine.com/med/topic1781.htm Wiesenfarth, John. “Dissection, Aorta.” eMedicine from WebMD. 2007. 17 December 2007 Read More
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