Selected References

Total Page:16

File Type:pdf, Size:1020Kb

Selected References Selected references BOOKS Markowitz, M. and Cordis, L. (1972). Rheumatic Fever. 2nd Edn. Philadelphia: W. B. Saunders Co. Stollerman, C. H. (1975). Rheumatic Fever and Streptococcal Irifection. New York: Crune & Stratton, Inc. Wannamaker, L. W. and Matsen, J. M. (Eds.) (1972). Streptococci and Streptococcal Diseases. New York: Academic Press, Inc. ARTICLES Aryanpur, K. et al. (1977). Rheumatic heart disease in the developing countries. In Moss, A. J. (ed.) Heart Disease in Infants, Children and Adolescents. Baltimore: Williams & Wilkins Bhayana, J. N. et al. (1974). Mitral steQ.osis in the young in developing countries.]' Thorac. Cardiovasc. Surg., 68, 126 Bravo, L. C. et a!. (1979). Streptococcal infections and rheumatic recurrences in subjects on secondary prophylaxis. Philipp. ]. Intern. Med., 17, 12 Chamovitz, R. et al. (1954). Prevention of rheumatic fever by treatment of previous infections. 1. Evaluation ofbenzathine penicillin C. N. Eng!. ]. Med., 251,466 Chesler, E. (1966). The pattern of rheumatic heart disease in the urbanized Bantu of Johannesburg. S. Afr. Med.]', 40, 899 DiSciascio, C. and Taranta, A. (1980). Rheumatic fever in children: a review. Am. Heart]., 99, 635 Cordis, L. (1973). Effectiveness of comprehensive care programs in preventing rheumatic fever. N. Eng!.]. Med., 289,331 John, S. et al. (1973). Results of mitral valve replacement in young patients with rheumatic heart disease.]. Thorac. Cardiovasc. Surg., 66, 255 Jones, T. D. (1944). The diagnosis of rheumatic fever.]. Am. Med. Assoc., 126, 481 92 SELECTED REFERENCES Lue, H. C. et al. (1979). The natural history of rheumatic fever and rheumatic heart disease in the Orient. jpn. Heart]., 20, 237 Mori, C. et al. (1979). Rheumatic heart disease in childhood: comparative study between Japan and Thailand.jpn. Circ.]', 43, 487 Padmavati, S. (1978). Rheumatic fever and rheumatic heart disease in developing countries. Bull. WHO, 56, 543 Rohde, J. E. and Sadjimin, T. (1979). Elementary school pupils as health educators: role of school health programmes in primary health care. Lancet, 1, 1350 Roy, S. B. et al. (1963). Juvenile mitral stenosis in India. Lancet, 2, 1193 Sanyal, S. K. et al. (1974). The initial attack of acute rheumaticfever during childhood in North India. A prospective study of the clinical profile. Circulation, 49, 7 Shaper, A. G. (1972). Cardiovascular disease in tropics. Br. Med.]., 3, 683 Shrestha, N. K. and Padmavati, S. (1979). Prevalence of rheumatic heart disease in Delhi school children. Indian]. Med. Res., 69, 8"21 Strasser, T. (1978). Recent advances in rheumatic fever control and future prospects. Bull. WHO, 56, 887 Strasser, T. (1980). Community control of rheumatic heart disease in developing countries. WHO Ckron., 34, 336 Strasser, T., Dondog, N., Al Kholy, A. et at. (1981). The community control of rheumatic fever and rheumatic heart disease: Report of a WHO international co-operative project. WHO Bull., 59, 2 Syed, S. A. and Abbasi, A. S. (1966). Rheumaticfeverand rheumatic heart disease: A public health problem.]. Pakistan Med. Assoc., 16, 187 Taranta, A. et al. (1962). 'Chronic' rheumatic fever. Ann. Intern. Med., 56, 367 Taranta, A. et at. (1970). Inter-society Commission for Heart Disease Resources: Prevention of rheumatic fever and rheumatic heart disease. Circulation, 41, A-I-A 15 Taranta, A. and Moody, M. (1971). Diagnosis of streptococcal pharyngitis and rheumatic fever. Pediatr. Clin. N. Am., 18, 125 Tompkins, D. G. et al. (1972). Long term programs of rheumatic fever patients receiving regular intramuscular benzathine penicillin. Circulation, 45, 543 UK and USJ oint Report (1967). The natural history of rheumatic fever and rheumatic heart disease: cooperative clinical trial of ACTH, cortisone and aspirin. Circulation, 32, 457 Wannamaker, L. W., Rammelkamp, C. H. Jr., Denny, F. W., Brink, W. R., Houser, H. B., Hahn, E. O. and Dingle, J. H. (1951). Prophylaxis of acute rheumatic fever by treatment of the preceding streptococcal infection with various amounts of depot penicillin. Am.]. Med., 10,673 Wood, H. F. et al. (1964). Rheumatic fever in children and adolescents. A long term epidemiologic study. Ann. Intern. Med., 60 (Supp!. 5), 31 93 Index abdominal pain 39, 59 treatment of 62-64 acute phase reactants and the Jones Aschoff body 12, 28 Criteria 46 atrioventricular conduction distur­ age bances 33 and incidence of rheumatic fever 23, 24 bacitracin test 22 and recurrences 23, 24 bed rest, in treatment of rheumatic anemIa 55 fever 61 antibiotics benzathine penicillin G 75, 87, 88 and prevention of recurrences 75-78 and treatment of rheumatic fever 61 carditis 30-34 and treatment of streptococcal arrhythmias in 33 infections 86-88 bed rest for 61 antibodies differential diagnosis of 55-58 heart 26 electrocardiogram in 3l streptococcal, and diagnosis of murmurs in 30 rheumatic fever 41-43, 59 prognosis of 66-70 streptozyme test 43 silent 33 anti-inflammatory drugs 62-64 steroids in 62-64 antistreptolysin 0 (ASO) 23, 26, treatment of 60-65 41-43,46,47 viral 57 arrhythmias 33 Carey Coombs murmur 31 arthralgia 34 chorea, Sydenham's 35-37 differential diagnosis 51-55 clinical findings 36 and Jones Criteria 45-50 differential diagnosis 58 arthritis treatment of 65 differential diagnosis of 51-55 congenital heart disease 56 infectious 53 congestive heart failure treatment of reactive 53 62-65 in rheumatic fever 34, 35 C-reactive protein 44, 64 94 INDEX crowding, and incidence of rheumatic J ones Criteria 45-47 fever 18-21 application of 47-50 cultures, throat, for streptococcal maj or manifestations 46 infections 85 minor manifestations 46 juvenile mitral stenosis 68 diagnosis of rheumatic fever laboratory findings criteria for 45-47 antistreptococcal antibodies 41-43 differential 51-59 C-reactive protein 44 errors in 58, 59 erythrocyte sedimentation rate (ESR) of streptococcal infections 84, 85 44 digitalis 64 Legg-Calve-Perthes 52 diuretics 64 leukemia 55 limb pain, in differential diagnosis electrocardiogram 33 51, 52 environment, and rheumatic fever Lyme arthritis 54 18-21 epistaxis 39 McCallum patch 27 erythema marginatum 38 mitral stenosis 68 erythrocyte sedimentation rate (ESR) mortality 69 40, 44, 59 murmurs erythromycin in streptococcal infections of aortic regurgitation 31 87,88 Carey Coombs 31 etiology, of acute rheumatic fever innocent 55 18-25 of mitral regurgitation 31 of mitral stenosis 31 family studies 24, 25 in rheumatic carditis 30 fever 38 myocarditis pathology of 27 genetic factors 24 viral, in diagnosis of rheumatic fever glomerulonephritis, and skin infections 57 25, 26 growing pains 52 nodules see subcutaneous nodules nutrition, and etiology of rheumatic health education 90 fever 21 healthworkers, non-physician, for rheu- matic fever prevention 89-91 onset, rheumatic fever, mode of 29 heart antibodies 26 overcrowding and rheumatic fever heart block 33 incidence 18-21 heart disease, congenital, and diagnosis of rheumatic fever 56 pathogenesis 25-27 heart murmurs, in rheumatic fever 31 pathology 27, 28 heart sounds 32 penicillin hemichorea 36 noncompliance in use of 79-82 Henoch-Sch6nlein purpura 54 oral 77 host factors, and the etiology of rheu­ parenteral (benzathine penicillin) matic fever 23-25 75-77 Huntington's chorea 58 for prevention of initial rheumatic attacks 86-88 incidence, of rheumatic fever 14, 15 for prevention of rheumatic recur­ and tropical countries 14 rences 75-78 95 RHEUMATIC FEVER reactions 81 fatalities 69 for streptococcal infections 86-88 rheumatoid arthritis 52 for treatment of acute rheumatic rubella, and arthritis 55 fever 61 pericarditis 32 St Vitus' dance see chorea, Sydenham's pharyngitis see streptococcal infections salicylates in rheumatic fever 62-64 physical activity and acute rheumatic serum sickness 54 fever 61 sequelae, of rheumatic fever 66-70 pneumonia, rheumatic 39 sickle cell disease 55 polyarthritis see arthritis socioeconomic factors 18-21 prevalence of rheumatic heart disease steroids, recommended regimen of 16 62-64 prevention streptococcal antibodies see antibodies duration of prophylaxis 78 streptococcal pharyngitis of initial rheumatic attacks 83-88 cultures for 85 obstacles to 79-82 diagnosis of 84 of recurrent rheumatic attacks treatment for 86-88 75-82 streptococci, group A prognosis see sequelae antibodies to 23 prophylaxis see prevention and etiology of rheumatic fever public health aspects 16, 17,89-91 21-23 serologic groups 22 rebound phenomena 64 serologic types 22 recurrences, rheumatic 71-74 streptozyme test 43 clinical ;'anifestations 73; 74 subcutaneous nodules 37 prevention of 75-82 sulfonamides, for prevention of rheu- relation to age and interval 71-73 matic recurrences 76-78 rheumatic fever Sydenham's chorea see chorea clinical manifestations in different synovitis of the hip 53 countries 48-50 definition of 11 tachycardia 32 differential diagnosis of 51-59 throat cultures 85 duration of attack 39, 40 tics, in diagnosis of chorea 58 history of 12, 13 severity, importance of 14, 15 viral infections sequelae 66-70 and arthritis 54 treatment of 60-65 carditis 57 rheumatic heart disease definition of 12 Yersinia enterocolitica, polyarthritis in 54 96 .
Recommended publications
  • Rheumatic Heart Disease in Children: from Clinical Assessment to Therapeutical Management
    European Review for Medical and Pharmacological Sciences 2006; 10: 107-110 Rheumatic heart disease in children: from clinical assessment to therapeutical management G. DE ROSA, M. PARDEO, A. STABILE*, D. RIGANTE* Section of Pediatric Cardiology, *Department of Pediatric Sciences, Catholic University “Sacro Cuore” – Rome (Italy) Abstract. – Rheumatic heart disease is presence of valve disease or carditis can be still a relevant problem in children, adolescents easily recognized through echocardiographic and young adults. Molecular mimicry between examinations, but the combination of clinical streptococcal and human proteins has been pro- posed as the triggering factor leading to autoim- tools and echocardiography consents the munity and tissue damage in rheumatic heart most accurate assessment of heart involve- disease. Despite the widespread application of ment2. It is well known however that minimal Jones’ criteria, carditis is either underdiagnosed physiological mitral regurgitation can be or overdiagnosed. Endocarditis leading to mitral identified in normal people and might over- and/or aortic regurgitation influences morbidity diagnose the possibility of carditis. Only in and mortality of rheumatic heart disease, whilst myocarditis and pericarditis are less significant 30% patients serial electrocardiogram studies in determining adverse outcomes in the long- are helpful in the diagnosis of acute RF with term. Strategy available for disease control re- non-specific findings including prolonged PR mains mainly secondary prophylaxis with the interval, atrio-ventricular block, diffuse ST-T long-acting penicillin G-benzathine. changes with widening of the QRS-T angle and inversion of T waves. Carditis as an ini- Key Words: tial sign might be mild or even remain unrec- Rheumatic heart disease, Pediatrics.
    [Show full text]
  • CARDIOLOGY Section Editors: Dr
    2 CARDIOLOGY Section Editors: Dr. Mustafa Toma and Dr. Jason Andrade Aortic Dissection DIFFERENTIAL DIAGNOSIS PATHOPHYSIOLOGY (CONT’D) CARDIAC DEBAKEY—I ¼ ascending and at least aortic arch, MYOCARDIAL—myocardial infarction, angina II ¼ ascending only, III ¼ originates in descending VALVULAR—aortic stenosis, aortic regurgitation and extends proximally or distally PERICARDIAL—pericarditis RISK FACTORS VASCULAR—aortic dissection COMMON—hypertension, age, male RESPIRATORY VASCULITIS—Takayasu arteritis, giant cell arteritis, PARENCHYMAL—pneumonia, cancer rheumatoid arthritis, syphilitic aortitis PLEURAL—pneumothorax, pneumomediasti- COLLAGEN DISORDERS—Marfan syndrome, Ehlers– num, pleural effusion, pleuritis Danlos syndrome, cystic medial necrosis VASCULAR—pulmonary embolism, pulmonary VALVULAR—bicuspid aortic valve, aortic coarcta- hypertension tion, Turner syndrome, aortic valve replacement GI—esophagitis, esophageal cancer, GERD, peptic OTHERS—cocaine, trauma ulcer disease, Boerhaave’s, cholecystitis, pancreatitis CLINICAL FEATURES OTHERS—musculoskeletal, shingles, anxiety RATIONAL CLINICAL EXAMINATION SERIES: DOES THIS PATIENT HAVE AN ACUTE THORACIC PATHOPHYSIOLOGY AORTIC DISSECTION? ANATOMY—layers of aorta include intima, media, LR+ LRÀ and adventitia. Majority of tears found in ascending History aorta right lateral wall where the greatest shear force Hypertension 1.6 0.5 upon the artery wall is produced Sudden chest pain 1.6 0.3 AORTIC TEAR AND EXTENSION—aortic tear may Tearing or ripping pain 1.2–10.8 0.4–0.99 produce
    [Show full text]
  • Cardiology 2
    Ch02.qxd 7/5/04 3:06 PM Page 13 Cardiology 2 FETAL CARDIOVASCULAR PHYSIOLOGY The ‘basic science’ nature of this topic – as well as the potential pathological implications in paediatric cardiology – makes it a likely viva question. Oxygenated blood from the placenta returns to the fetus via the umbilical vein (of which there is only one). Fifty per cent traverses the liver and the remaining 50% bypasses the liver via the ductus venosus into the inferior vena cava. In the right atrium blood arriving from the upper body from the superior vena cava (low oxygen saturation) preferentially crosses the tricus- pid valve into the right ventricle and then via the ductus flows into the descending aorta and back to the placenta via the umbilical arteries (two) to reoxygenate. The relatively oxygenated blood from the inferior vena cava, however, preferentially crosses the foramen ovale into the left atrium and left ventricle to be distributed to the upper body (including the brain and coro- nary circulation). Because of this pattern of flow in the right atrium we have highly oxygenated blood reaching the brain and deoxygenated blood reach- ing the placenta. High pulmonary arteriolar pressure ensures that most blood traverses the pulmonary artery via the ductus. Changes at birth 1. Occlusion of the umbilical cord removes the low-resistance capillary bed from the circulation. 2. Breathing results in a marked decrease in pulmonary vascular resistance. 3. In consequence, there is increased pulmonary blood flow returning to the left atrium causing the foramen ovale to close. 4. Well-oxygenated blood from the lungs and the loss of endogenous prostaglandins from the placenta result in closure of the ductus arteriosus.
    [Show full text]
  • Rheumatic Heart Disease
    RHEUMATIC HEART DISEASE Rheumatic fever is an acute immunologically mediated multisystem inflammatory disease that occurs few weeks after an attack of group A beta- hemolytic streptococcal pharyngitis. It is not an infective disease. The most commonly affected age group is children between the ages of 5-15 yearsQ. The disease is a type II hypersensitivity reaction in which antibodies against ‘M’ protein of some streptococcal strains (1, 3, 5, 6, and 18) cross-react with the glycoprotein antigens in the heart, joints and other tissues (molecular mimicry). CLINICAL FEATURES It presents with fever, anorexia, lethargy and joint pain 2-3 WEEKS after an episode of Streptococcal Infection is required for diagnosis Migratory Polyarthritis is the commonest major manifestation. Q Salient feature`s of the major criteria Carditis All the layers of the heart namely pericardium, myocardium and endocardium are involved, so this is called pancarditis. The pericarditis is associated with fibrinous/serofibrinous exudate and is called as ‘bread and butter’ pericarditis. It may manifest as breathlessness (due to heart failure or pericardial effusion), palpitations or chest pain (usually due to pericarditis or pancarditis). Other features include tachycardia, cardiac enlargement and new or changed murmurs. A soft mid-diastolic murmur (the Carey Coombs murmur) is typically due to valvulitis, with nodules forming on the mitral valve leaflets. Aortic regurgitation occurs in 50% of cases but the tricuspid and pulmonary valves are rarely involved. Pericarditis may cause chest pain, a pericardial friction rub and precordial tenderness. Cardiac failure may be due to myocardial dysfunction or valvular regurgitation. Valvular involvement is common in rheumatic heart disease.
    [Show full text]
  • Cardiovascular Pathology the Perfect Preparation for USMLE® Step 1
    Cardiovascular Pathology The Perfect Preparation for USMLE® Step 1 2021 Edition You cannot separate passion from pathology any more than you can separate a person‘s spirit from his body. (Richard Selzer) www.lecturio.com Cardiovascular Pathology eBook Live as if you were to die tomorrow. Learn as if you were to live forever. (Mahatma Gandhi) Pathology is one of the most-tested subjects on the USMLE® Step 1 exam. At the heart of the pathology questions on the USMLE® exam is cardiovascular pathology. The challenge of cardiovascular pathology is that it requires students to be able to not only recall memorized facts about cardiovascular pathology, but also to thoroughly un- derstand the intricate interplay between cardiovascular physiology and pathology. Understanding cardiovascular pathology will not only allow you to do well on the USMLE® Step 1 exam, but it will also serve as the foundation of your future patient care. This eBook... ✓ ...will provide you with everything you need to know about cardiovascular pathology for your USMLE® Step 1 exam. ✓ ...will equip you with knowledge about the most important diseases related to the cardiovascular system, as well as build bridges to the related medical sciences, thus providing you with the deepest understanding of all cardiovascular pathology topics. ✓ ...is specifically for students who already have a strong foundation in the basic sciences, such as anatomy, physiology, biochemistry, microbiology & immunology, and pharmacology. Elements of this eBook High-yield: Murmurs of grade III and above are High-yield-information will help you to focus on the most important facts. usually pathological. (...) A number of descriptive pictures, mnemonics, and overviews, but also a reduction to the essentials, will help you to get the best out of your learning time.
    [Show full text]
  • 11 Valvular Heart Disease and Rheumatic Fever
    Chapter 11: Valvular Heart Disease and Rheumatic Fever 375 11 Valvular Heart Disease and Rheumatic Fever CONTENTS AORTIC STENOSIS AORTIC REGURGITATION MITRAL STENOSIS MITRAL REGURGITATION MITRAL VALVE PROLAPSE RHEUMATIC FEVER BIBLIOGRAPHY AORTIC STENOSIS Aortic stenosis is the most common valvular lesion in the United States. This lesion is common because approximately 2% of individuals are born with a bicuspid valve which is prone to stenosis, and the aging population is increasing, and calcific aortic stenosis progresses with advancing years. Rheumatic aortic stenosis is now uncommon, except in Asia, Africa, the Middle East, and Latin America. The patient’s age at the time of diagnosis usually gives a reasonable assessment of the underlying disease. • Diagnosis before age 30 is typical of congenital aortic stenosis. • In patients over age 70, calcific aortic sclerosis owing to degenerative calcification is common, and significant stenosis develops in up to 5% of these individuals. Aortic sclerosis is common in the elderly, and although the lesion is significant, it is hemody- namically not important. Stenosis develops particularly when there is associated hyper- cholesterolemia. Importantly, the progression of stenosis can be significantly retarded by statin therapy. • A bicuspid valve occurs in approximately 2% of the population, with a male to female ratio of 4:1, and is predisposed to degenerative calcification and stenosis. Between ages 30 and 70, calcification of a bicuspid valve is the most common cause of aortic stenosis, and much less frequently, cases of rheumatic valvular disease are encountered. The causes of aortic stenosis can be seen in Table 11.1. From: Contemporary Cardiology: Heart Disease Diagnosis and Therapy: A Practical Approach, Second Edition Edited by: M.
    [Show full text]
  • CHAPTER E13 Approach to the Patient with a Heart Murmur
    S1 S2 CHAPTER e13 A Approach to the Patient With a Heart Murmur B Patrick T. O’Gara C Joseph Loscalzo CHAPTER e13 A2 P2 D Ⅵ INTRODUCTION The differential diagnosis of a heart murmur begins with a careful assessment of its major attributes and response to bedside maneu- vers. The history, clinical context, and associated physical examina- E tion findings provide additional clues by which the significance of a heart murmur is established. Accurate bedside identification of a OS Approach to the Patient With a Heart Murmur heart murmur can inform decisions regarding the indications for F noninvasive testing and the need for referral to a cardiovascular specialist. Preliminary discussions can be held with the patient regarding antibiotic or rheumatic fever prophylaxis, the need to S3 restrict various forms of physical activity, and the potential role for G family screening. Heart murmurs are caused by audible vibrations that are due to increased turbulence from accelerated blood flow through normal or abnormal orifices, flow through a narrowed or irregular orifice H into a dilated vessel or chamber, or backward flow through an incompetent valve, ventricular septal defect, or patent ductus arte- Figure e13-1 Diagram depicting principal heart murmurs. riosus. They traditionally are defined in terms of their timing within A. Presystolic murmur of mitral or tricuspid stenosis. B. Holosystolic (pansystolic) the cardiac cycle ( Fig. e13-1 ) . Systolic murmurs begin with or after murmur of mitral or tricuspid regurgitation or of ventricular septal defect. the first heart sound (S1 ) and terminate at or before the component C. Aortic ejection murmur beginning with an ejection click and fading (A2 or P2 ) of the second heart sound (S2 ) that corresponds to their before the second heart sound.
    [Show full text]
  • Pediatric and Adolescent Care
    CHAPTER 11 – CARDIOVASCULAR SYSTEM First Nations and Inuit Health Branch (FNIHB) Pediatric Clinical Practice Guidelines for Nurses in Primary Care. The section on Rheumatic Fever (Carditis) has been updated as of December 2017. The remaining content of this chapter was reviewed in September 2011. Table of Contents INTRODUCTION ....................................................................................................11–1 ASSESSMENT OF THE CARDIOVASCULAR SYSTEM .......................................11–1 In Infants ..........................................................................................................11–1 In Children ........................................................................................................11–2 Medical History (Specific to Cardiovascular System) ......................................11–2 Physical Findings .............................................................................................11–2 COMMON PROBLEMS OF THE CARDIOVASCULAR SYSTEM ..........................11–3 Heart Murmurs .................................................................................................11–3 Innocent Heart Murmur ....................................................................................11–4 EMERGENCY PROBLEMS OF THE CARDIOVASCULAR SYSTEM ...................11–5 Cardiac Failure .................................................................................................11–5 Cyanosis in the Newborn (Birth to 6 Weeks) ...................................................11–6
    [Show full text]
  • Cardiovascular
    Notes compiled for Pediatrics Cardiovascular (Med I, Block 3, CV) Contents CV 036 Valvular Heart Disease A CV Dr. J Tam CV 042 Valvular Heart Disease II T1 CV Dr. J Tam CV 044 Development of the Heart and Lung L AN Dr. M Torchia CV 045 Valvular Heart Disease III T5 CV Dr. J Tam CV 046 Congenital Heart Disease I A PD Dr. R Soni CV 048 Development of the Heart and Lung A AN Dr. M Torchia CV 049 Congenital Heart Disease II L PD Dr. R Soni CV 050 Congenital Heart Disease III T1 PD Dr. R Soni CV 075 Genetic Aspects of Cardiomyopathy L GN Dr. A Chudley CV 076 Acquired Pediatric Heart Disease L PD Dr. R Soni CARDIOVASCULAR COURSE: MED I BLOCK III Valvular Heart Disease I & II (CV036) OBJECTIVES: Assigned Reading to be completed prior to CV042 University of Manitoba –Faculty of Medicine Instructor: Dr. J. Tam Objectives: At the completion of these sessions, the student will be able to: 1. Describe the common etiology, pathology and pathophysiology of: a) aortic stenosis b) aortic regurgitation c) mitral stenosis d) mitral regurgitation e) tricuspid regurgitation 2. Apply the above knowledge to describe the clinical manifestations and physical findings of the above valvular abnormalities. 3. Describe the laboratory findings (chest x-ray, ECG, echocardiogram) that assist in the diagnosis of the above entities. 4. Relate the pathophysiology to therapeutic approaches (both medical and surgical). 5. Briefly discuss the indications for surgical intervention of valvular heart disease. 6. List the various surgical options – repair, mechanical replacement, bioprosthetic replacement, homograft replacement, autograft replacement.
    [Show full text]
  • Rheumatic Heart Disease
    PLEASE CHECK Editing file BEFORE! ​ ​ ​ ​ Rheumatic Heart Disease ★ Objectives: ​ 1. Know that RHD is prevalent in our region, and economic burden 2. Know how to diagnose the disease and how to approach a patient with RHD 3. Know the principles of management 4. Know how to prevent RHD; Who needs prophylaxis and for how long 5. Recognize complications and how to manage it ★ Resources Used in This lecture: Slides, Kumar, Class notes, 433 teamwork. ​ ​ ​ ​ ​ Done by: Razan Alsubhi & Rasha Bassas Contact us at: [email protected] ​ ​ ​ Epidemiologic Background ● Globally rheumatic heart disease is the commonest CVD in young people 25 yrs old ● The overall incidence of ARF from 5-51 per 100000 population with a mean of 19 per 100000 population ● In children 5-14 yrs old 0.8-5.7 per 1000 children with a median of 1.3 per 1000 ● The incidence of RF and the prevalence of RHD has declined substantially in developed nations. ● This decline has been attributed to: ✓ Improved hygiene. ✓ Reduced household crowding. ✓ Improved medical care. ● A disease of poverty1 and low socioeconomic status ● In underdeveloped countries RHD is the leading cause of CV death during the first five decades of life. Global Burden of RHD ● Total cases with RHD: 20 Millions ● 3 Million have CHF. ​ ​ ● 1 Million require valve surgery. ​ ​ ● Annual incidence of RF: 0.5 Million, nearly half develop carditis ​ ● Estimated deaths from RHD: 230,000 per year. ​ ​ ■ Imposes a substantial burden on healthcare systems with limited budgets VS ARF ​ ​ RHD : ✓ Acute Rheumatic Fever (ARF): Is a systemic inflammatory disorder that occurs in children ​ ​ between 5 and 15 years of age as a result of group A beta hemolytic streptococcal throat infection ​ ​ ​ “Pharynx is the most common site for infection leading to RF”.
    [Show full text]
  • Manual of Cardiology
    MANUAL OF CARDIOLOGY MANUAL OF CARDIOLOGY V Jacob Jose MD DM card, MS Univ of Penn, FCCP, FACC, FIAE Professor of Cardiology Department of Cardiology Christian Medical College Hospital Vellore, Chennai JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD New Delhi Published by Jitendar P Vij Jaypee Brothers Medical Publishers (P) Ltd B-3 EMCA House, 23/23B Ansari Road, Daryaganj New Delhi 110 002, India Phones: +91-11-23272143, +91-11-23272703, +91-11-23282021, +91-11-23245672, Rel: 32558559, Fax: +91-11-23276490, +91-11-23245683 e-mail: [email protected], Visit our website: www.jaypeebrothers.com Branches 2/B, Akruti Society, Jodhpur Gam Road Satellite Ahmedabad 380 015, Phones: +91-079-26926233, Rel: +91-079-32988717, Fax: +91-079-26927094, e-mail: [email protected] 202 Batavia Chambers, 8 Kumara Krupa Road Kumara Park East, Bangalore 560 001 Phones: +91-80-22285971, +91-80-22382956, Rel: +91-80-32714073, Fax: +91-80-22281761, e-mail: [email protected] 282 IIIrd Floor, Khaleel Shirazi Estate, Fountain Plaza Pantheon Road, Chennai 600 008, Phones: +91-44-28193265, +91-44-28194897, Rel: +91-44-32972089, Fax: +91-44-28193231, e-mail: [email protected] 4-2-1067/1-3, 1st Floor, Balaji Building, Ramkote Cross Road Hyderabad 500 095, Phones: +91-40-66610020, +91-40-24758498, Rel:+91-40-32940929, Fax:+91-40-24758499, e-mail: [email protected] No. 41/3098, B & B1, Kuruvi Building, St. Vincent Road Kochi 682 018, Kerala, Phones: 0484-4036109, +91-0484-2395739, +91-0484-2395740, e-mail: [email protected] 1-A Indian Mirror Street, Wellington Square Kolkata 700 013, Phones: +91-33-22451926, +91-33-22276404, +91-33-22276415, Rel: +91-33-32901926, Fax: +91-33-22456075, e-mail: [email protected] 106 Amit Industrial Estate, 61 Dr SS Rao Road, Near MGM Hospital, Parel, Mumbai 400 012, Phones: +91-22-24124863, +91-22-24104532, Rel: +91-22-32926896, Fax: +91-22-24160828, e-mail: [email protected] “KAMALPUSHPA” 38, Reshimbag, Opp.
    [Show full text]
  • 186923 3 En Bookfrontmatter 1..20
    2 CARDIOLOGY Section Editors: Dr. Mustafa Toma and Dr. Jason Andrade Aortic Dissection DIFFERENTIAL DIAGNOSIS PATHOPHYSIOLOGY (CONT’D) CARDIAC DEBAKEY—I ¼ ascending and at least aortic arch, MYOCARDIAL—myocardial infarction, angina II ¼ ascending only, III ¼ originates in descending VALVULAR—aortic stenosis, aortic regurgitation and extends proximally or distally PERICARDIAL—pericarditis RISK FACTORS VASCULAR—aortic dissection COMMON—hypertension, age, male RESPIRATORY VASCULITIS—Takayasu arteritis, giant cell arteritis, PARENCHYMAL—pneumonia, cancer rheumatoid arthritis, syphilitic aortitis PLEURAL—pneumothorax, pneumomediasti- COLLAGEN DISORDERS—Marfan syndrome, Ehlers– num, pleural effusion, pleuritis Danlos syndrome, cystic medial necrosis VASCULAR—pulmonary embolism, pulmonary VALVULAR—bicuspid aortic valve, aortic coarcta- hypertension tion, Turner syndrome, aortic valve replacement GI—esophagitis, esophageal cancer, GERD, peptic OTHERS—cocaine, trauma ulcer disease, Boerhaave’s, cholecystitis, pancreatitis CLINICAL FEATURES OTHERS—musculoskeletal, shingles, anxiety RATIONAL CLINICAL EXAMINATION SERIES: DOES THIS PATIENT HAVE AN ACUTE THORACIC PATHOPHYSIOLOGY AORTIC DISSECTION? ANATOMY—layers of aorta include intima, media, LR+ LRÀ and adventitia. Majority of tears found in ascending History aorta right lateral wall where the greatest shear force Hypertension 1.6 0.5 upon the artery wall is produced Sudden chest pain 1.6 0.3 AORTIC TEAR AND EXTENSION—aortic tear may Tearing or ripping pain 1.2–10.8 0.4–0.99 produce
    [Show full text]