Arup Kumar Kundu-Bedside Clinics in Medicine, Part 1-Academic Publishers ( ) - Ebook download as PDF File .pdf), Text File .txt) or read book online. ‘clinical methods in medicine’ in questions and answers for MBBS/MD students. Textbook, ‘Clinical Medicine', 7th Edition (Edinburgh) Arup Kumar Kundu MD FICP MNAS. ⇰ File formats: ePub, PDF, site, Audiobook, mobi, ZIP. Download >> Bedside clinics in Medicine Part - 1 (kundu medicine part 1 7th edition December ) How do I download the “Kundu Bedside Clinics” book in a PDF form?.
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Medicine Pdf Bedside Clinics In - bestthing.info bedside clinics in medicine pdf. a place to store memories, thoughts and dreams image c. Clinics in Medicine, Part II 9th Edition by dr Free download Arup Kumar Kundu clinical. Medicine Latest Bedside clinics in Medicine Part -KUNDU 1 PDF. Arup Kumar Kundu is the author of Bedside clinics in Medicine Part - 1 ( avg rating, ratings, 2 reviews), Bedside Clinics in Medicine, Part II (4.
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Views Read Edit View history. Bedside clinics in Medicine Part — 1 kundu medicine part 1 7th edition December Showing of 16 reviews. Sunita Devi. The arthritis was fleeting in nature and not associated with any skin lesion or chorea. Give the summary of the case: Give the short case history from the question discussed above. Sj is palpable. Remember the dictum: Uncommon presentations of common diseases are more common than common presentations of uncommon diseases.
On palpation What is your case? Cough was not associated with rise of temperature. Provisional diagnosis in valvular heart diseases: Two weeks back. On examination. A diastolic thrill is palpable in the mitral area which is best felt in left lateral position and in full expiration. Anatomical — Mitral.
It is a case of mitral stenosis MS of rheumatic origin without any evidence of congestive cardiac failure CCF and the patient is in sinus rhythm at present. There is no deformity of precordium precordial bulging indicates early onset and longer duration cardiac diseases. There is absence of split. Opening snap OS is heard just after S2. Case 1 Mitral Stenosis What is your diagnosis? B Signs: Thyrotoxicosis 6. It is the anterior chest wall which overlies the heart.
Rheumatic fever is the commonest aetiology of MS and it is true in other valvular heart diseases. Opening snap — Audible. There is a diastolic thrill at apex.
Ischaemic heart disease IHD at school 5. Aetiologieal — Rheumatic. Importance of past and family history in CVS: Past history Family history 1.
Some clinicians prefer to add NYHA classification in the provisional diagnosis see page Describe the classical murmur as described in summary.
Why it is a case of mitral stenosis? It is a case of mitral stenosis because of the following: A Symptoms from the history: No murmur.
The different deformities are: There is sustained left parasternal heave as a result of RVH from pulmonary hypertension.
Low or normal. Rheumatic heart disease 4. Any murmur or cardiac lesion detected 4. Normal in position and tapping in character. Bulged precordium. Mitral Stenosis 9 2.
Early onset and longer duration cardiac diseases e. May be associated with dwarfism. Structural abnormality—Stenosis. Recurrent respiratory tract infection 3.
Rheumatic fever 1. Other areas. In health. Complications — Pulmonaiy hypertension. Clubbing with cyanosis plus polycythemia. Hypertension 2.
Arup Kumar Kundu-Bedside Clinics in Medicine, Part 2, 5_e-Academic Publishers (2010)
Rhythm — Sinus rhythm or dysrrhythmia e. There is presence of diastolic thrill. IHD 5. Congenital heart disease 3. Ventricular muscle mass booming Sj is heard in patients with systemic hypertension leading to LVH. Sinus tachycardia due to any cause imcompetence 3.
Prolonged PR interval e. Mitral stenosis. Short PR interval. Wide splitting: During auscultation of heart sounds in different areas. Atrial fibrillation 1. Occasionally along with these.
Arup Kumar Kundu-Bedside Clinics in Medicine, Part 2, 5_e-Academic Publishers (2010)
As low cardiac output in MS produces vasoconstriction.. Cushing's syndrome. Right or left ventricular dysfunction 4. Causes of malar flush: Intervening media between heart valve cusps and the stethoscope e. High altitude.. Complete heart block cannon sound 2. Normally in children wall. Ventricular tachycardia ventricular pacing. Reversed splitting: Multiple extrasystoles right ventricular pacing. Sj tends to be loud as a result of short PR interval.
Table 1: S1 indicates the beginning of ventricular systole and is produced due to closure of atrioventricular valves. Mitral incompetence. Menopausal syndrome 5.
Position of valve cusps mitral or tricuspid at the onset of ventricular systole: Factors influencing the intensity of Sl: MI or TI. Carcinoid syndrome. Heart rate — In tachycardia. Fibrosis of the lung. Chronic alcoholism. Paget's disease.. How loud Sj in MS can be explained? Due to persistent diastolic gradient across the mitral valve. Hyperkinetic circulation e. Pliability of the valve cusps e. It has two components: What is mitral fades? It is the pinkish purple patches on cheeks.
Big left atrial thrombus. Longer duration of mid-diastolic murmur. Features of severe MS are: Atrial fibrillation produces varying intensity of S. Absent presystolic accentuation in MS: When MS is associated with: Artrial fibrillation.
Diastolic murmur of MS is heard as soon as the blood flows from the left atrium to left ventricle after opening of the mitral valve i. If the apex goes outward. Left atrial failure. The last part of ventricular diastole last rapid filling phase actually coincides with atrial systole. Narrow S2-OS gap the smaller the gap.. LVH is not a feature of isolated MS.
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It is: Mitral valve calcification.. Mitral incompetence MI or severe aortic incompetence AI.
Comment on apex beat in MS: Usually the apex is in normal position. Presence of opening snap. There is no blood flow in the isovolumetric relaxation period and this is why the murmur of MS is mid-diastolic. Active rheumatic carditis due to prolonged PR interval.
Atrial systole increases the blood flow across the stenotic valve and thus. What is an opening snap mitral? A Opening snap is produced due to bellowing down of the closed mitral valve cusps at the onset of ventricular diastole i. Why the murmur is mid-diastolic in MS? Recognition of pliable mitral valve cusps: Digitalis overdose due to prolonged PR interval.
Left atrial failure LAF. B It indicates: Other signs of severity are: Acute myocardial infarction. Presystolic accentuation of the diastolic murmur disappears.. Varying intensity of S. Irregularly irregular pulse with varying volume. MS results from shortening of chordae tendineae and fusion of commissures. Symptoms due to low cardiac output—fatiguability.
Button hole. Pathological types oj MS: Common symptoms of MS: Symptoms due to left atrial failure i. Fish mouth. Congestive cardiac failure may precipitate and embolic manifestations may appear CVA.
Absent a-wave in the neck veins or JVP. Changes occuring after left atrial failure in MS producing pulmonary oedema: Funnel type. Changes noticeable when atrial fibrillation develops in MS: Opening snap is not heard. Symptoms due to RVF—swelling of legs oedema. Symptoms due to arrhythmia—palpitation. Aetiology of MS: As standing reduces the venous return. The criteria for diagnosis are: Which chamber of heart fails first in MS?
The left atrium. Pulmonary apoplexy — Due to rupture of thin-walled. Acute pulmonary oedema — Profuse. Winter bronchitis chronic bronchitis — Blood-streaked mucoid sputum. Atrial fibrillation is rare. Presystolic component of the murmur disappears. The common causes are. Lumbar canal stenosis patient often stoops forward during walking to reduce symptoms.
Atheroma or severe atherosclerosis of lower limb arteries. If he continues to walk. Valve calcification is uncommon. What is juvenile mitral stenosis: This type of MS is usually found in India. Pulmonary infarction — Frank haemoptysis. Pulmonary haemosiderosis — Rare. Common risk factors are diabetes.
What is damped MS? Development of pulmonary hypertension diminishes the cardiac output throttle effect and results in temporary symptom-free period period of illusion. Pin-point mitral valve. Most significant finding in your case: The mid-diastolic rumbling murmur. Often the mid-diastolic murmur is not audible and thus known as silent MS.
What is tight or severe MS? Normal cross-sectional area of mitral valve orifice is cm2 average 5 cm2. Common in South-East Asia. Venous claudication bursting pain on walking. Occurs below 18 years of age. Haemoptysis in MS: The possible mechanisms are — 1. Overdose of anticoagulant therapy rare — Often required for embolic manifestation. What is intermittent claudication?
This is a cramp-like pain. Coarctation of aorta. Mitral Stenosis 13 3. Cold legs. MS develops earlv in contrast to the west where the patient experience disability in the 4th decade. In India. Palpation of peripheral pulses in legs. Chamber involvement in MS: Needs immediate operation. Which ventricle fails first in MS? Presence of bilateral basal crepitations fine.
Austin Flint murmur — It is a functional low-pitched. Oedema of the matral valve cusps produce obstruction and gives rise to diastolic murmur. Functional mid-diastolic murmur — Found in increased left-to-right shunt in ventricular septal defect VSD. Echocardiography and cardiac catheterisation are diagnostic. Increased flow through the normal mitral valve also occurs in severe MI. Peripheral signs of AI are present. Features of RVH are never present.
Carey-Coombs murmur — Soft mid-diastolic murmur of active rheumatic valvulitis.
The cough becomes productive with profuse. Echocardiography is essential for final diagnosis.. Conducted murmur of AI — Early diastolic.. There is absence of loud S. The murmur varies in intensity from day to day and usually disappears after the acute attack.
The patient is awakened from sleep with a feeling of apprehension. Murmur increases at the height of inspiration. There is absence of diastolic thrill.
Tricuspid stenosis — Mid-diastolic murmur with presystolic accentuation which is loudest at lower left sternal edge. Acute pulmonary oedema is the severe form of cardiac asthma due to marked increase in pulmonary capillary pressure leading to alveolar oedema.
Describe the classical attack of paroxysmal nocturnal dyspnoea PND: It is the sudden and dramatic development of acute dyspnoea occuring in the early hours of night. He sits upright gasping in the bed with the legs hanging by the side of the bed to reduce left atrial pressure by gravitational pooling or rushes to an open window in the hope that cool fresh air will relieve him.
When the aortic regurgitant jet of blood impinges on the anterior mitral leaflet thereby stenosing the mitral orifice relatively. Left atrial myxoma— a Alteration of physical signs murmur with change of posture. These are accompanied by a dry. Ball valve thrombus — The thrombus usually floats in the left atrium and obstructs the mitral orifice in diastole. An old case of MS usually does not suffer from PND because of the development of protective mechanisms mentioned above.
Broncho-pulmonary venous shunts. Diffuse pulmonary infections viral. Narcotic heroin. Inhalation of toxins and irritants phosgene. Why dyspnoea occurs in MS? The events in MS go like this: Aspiration of vomitus. Capillary-alveolar-interstitial barrier. PND is a symptom of decompensation of the left heart. Acute haemorrhagic pancreatitis. High pulmonary vascular resistance pulmonary hypertension.
Protective mechanisms to prevent pulmonary oedema in MS: As the disease progresses to chronic mitral stenosis.
Sir William Osier (18491919)
Miscellaneous — Cardio-pulmonary bypass. The causes of non-cardiogenic type are— 1.
Cardiogenic— engorged neck veins. Severe sepsis. Pulmonary oedema is of two types. Probable theories are: How do you like to investigate a case of MS? Elevation of left atrial pressure and fall in Pa02 during sleep.. Complications of MS: Recurrent broncho-pulmonary infections. Venous return increases in recumbency. Adrenergic drive is reduced during sleep. Sudden death may be caused by ball valve thrombus where the LA outlet is blocked by large pedunculated thrombus.
Infective endocarditis — Very rare more common in milder form of MS than in severe form. Acute left atrial failure and acute pulmonary oedema. Pulmonary hypertension.
Reduction of vital capacity in supine position. Mobilisation of oedema fluid from extravascular to intravascular compartment on lying. Heart rate increases during rapid eye movement REM sleep.
Atrial fibrillation AF. Rationality of nervous system examination in MS i. Cardiac cachexia in severe chronic heart failure. Rheumatoid arthritis or ankylosing spondylitis MI or AI. Hydrothorax from CCF. Liver — Soft and tender liver with mild enlargement due to CCF. The external features for congenital heart diseases are: Fundoscopy — Roth spot.
Crepitations at lung bases due to left-sided heart failure. Spleen — In the presence of SBE. Rationality of skeletal system examination in cardiac disorders: F Echocardiography M-Mode and 2-D to see chamber enlargement. May be propped-up. Rationality of G.
Mesenteric embolism. In acquired heart diseases. Kyphoscoliosis shifting of apex beat. Dwarfism in cyanotic congenital heart diseases. Polydactyly or syndactyly congenital heart disease. H Doppler study — To know the functional status.
Ascites may develop from CCF.
Important points in general survey in CVS: Respiration tachypnoea. Oesophagus is pushed or curved backward sickling of oesophagus by the enlarged LA. Rationality of respiratory system examination in MS i. C Chest X-ray lateral view —Obliteration of retrosternal space in left lateral view with slight increase in transverse diameter of heart PA view indicates RVH.
Sydenham's chorea. Hemiplegia or monoplegia may occur in a patient with MS commonly with atrial fibrillation. Artificial valves may work for more than 20 years.. Asymptomatic patients with a single attack of thromboembolic manifestation.
Left atrium is free of clots. Treatment of CCF by restriction of physical activity. Extremely tight stenosis. Valve and sub-valvular apparatus are free of calcification. Valvular calcification. Neck vein. MS with complications as mentioned earlier e. MS with significant MI. Cyanotic congenital heart disease. Loud S.
MS with pregnancy where previous pregnancy was symptomatic. Secondary prevention of acute rheumatic fever is done. Prosthesis is done in grossly damaged valve and sub- valvular structures. Elevated in SBE.
Significant symptomatic MS. Criteria for mitral valvuloplasty: Contraindications of closed valvotomy: Open valvotomy needs open heart surgery with cardio-pulmonary by-pass. Progressive symptomatic deterioration inspite of medical treatment.
Present in SBE remember. MS with left atrial thrombus. Treatment done in MS with Ml: Mitral valve replacement prosthesis.
Treatment of MS: Mild MS may need no treatment. Pure MS may have trivial MI. Eisenmenger's syndrome. Medical treatment in MS: Very important clue to diagnosis in different cardiovascular disorders. Indications of valvotomy: Reflects central venous pressure. Mitral valve distorted by previous operation 3. The different modalities of treatment are: Presence of active rheumatic carditis. Anticoagulation in the presence of atrial fibrillation or big left atrial clot to reduce the risk of systemic embolism.
Cyanotic congenital heart diseases. One should search for thyrotoxic features in all CVS disorders. Mechanical prosthesis like Starr-Edwards valve or Bjork- Shiley valve. Must be seen in all patients: Ionescu- Shiley. If MS is associated with pulmonary hypertension. A metallic sound is audible in mitral area which coincides with S. Metallic mitral valve prosthesis in MS—auscultatory findings: Symptomatology consists of exertional dyspnoea..
Complications of prosthetic valve: Thromboembolism needs anticoagulation. Increased bed rest. Case 2 Mitral Incompetence What is your diagnosis? This is a case of organic mitral incompetence regurgitation of rheumatic origin with features of congestive cardiac failure and pulmonary hypertension.
Mitral valvotomy—in symptomatic tight MS. Mitral Incompetence 19 4. MS with pregnancy: The book is indispensable for not only undergraduates and postgraduate students but also for teachers and practitioners in Medicine as well.
Kiranmoy Mitra, Ex-Assoc. Ravishankar and S. A purist pedagogue, a massive mentor, and an exemplary exponent engrossed with an expansive professional expertise and competency, he has probed deeply into several cases along with history, diagnosis and management invariably in an easy-to-understand question-answer form.
This lucidity, sometimes in a literary, and mostly in a highly scientific manners, has made this work an invaluable medical contribution-cum-anthology for undergraduate and postgraduate students.
Moreover a beginner may find it a crutch to have a naive rendezvous into this area of medicine. The diagnostic procedures and methodologies are nicely delineated. This book will be a constant concise companion for all, students and teachers alike, in different Indian Universities and Medical Colleges as this treasure will elicit the clinical spirit of approach from a modest conventional way to highly sophisticated method.
It was nice and quite interesting I can recommend the book to my students as a ready reckoner I found that there is a wealth of information in the book which is difficult to get from other books I have been an ardent reader of both of your textbooks on clinical medicine, since the first day of my ward duty.
To be very honest I have learnt more from your books than from Kamaalchand M, P. The book has in fact satisfied the need of a long awaited reference book for examinee being complete by itself in all respects Nath Barbhuiya Retd. Bedside Clinics in Medicine, Part I, which is highly informative, well-written with latest additions It definitely provides so much of knowledge and information, that everytime I close the book after reading it, I do so with an extreme sense of happiness and confidence of knowing so much It is unequivocal opinion that the book is outstanding and entirely removes the need to study multiple books in clinical medicine For my final year exams I just had to quote them to be appreciated by the examiners.
I wish to explain my gratitude as a student of medicine for your valuable contribution which is unfathomable The chapters on radiological diagnosis and ECG interpretations will certainly help all concerned. Emergency tackling of different cases also, will help the young professionals The book is likely to be well accepted and the second edition of the book supports that expectation.
Looking back, recollecting my MD days, I repeat my words I owe you my MD. Pradeep Kumar Shenoy C, Ex-clinical fellow and registrar. Department of Rheumatology, Manipal Hospital, Bangalore. I am very happy to inform you that I have got selected for MD I owe my success to your book, and your in time valuable suggestion and advice.
You have been my behind the scene teacher and educator and inspiration Bhushan Madke, student of Indira Gandhi Govt. Medical College, Nagpur, Maharashtra. You have donated breath to me I feel it is a very good book and very informative George K.
I read your book on bedside clinical examination The book is really wonderful. Hats of sirHe is best known. CSF is absorbed by arachnoid villi. Atay - Cankaya 5 Cilt. Instruments and Procedures 15 commonly or is really uncooperative.
Dehydration due to any cause e. Samuel P.