This document discusses various types of heart disease including hypertensive heart disease, cardiomyopathies, valvular heart disease, and infective endocarditis. It provides details on the criteria, morphology, causes, and clinical features of each condition. Specifically, it describes how hypertensive heart disease can cause left or right ventricular hypertrophy and heart failure. It also explains the differences between dilated, hypertrophic, and restrictive cardiomyopathies and their causes and features.
Endomyocardial fibrosis (EMF) is a disease that is characterized by fibrosis of the apical endocardium of the right ventricle (RV), left ventricle (LV), or both.
The clinical manifestations are largely related to the consequences of restrictive ventricular filling, including left and right sided heart failure.
The heart failure is associated with atrioventricular-valve regurgitation.
Endomyocardial fibrosis is a major cause of illness and death in areas where it is endemic, and in its severest form carries a very poor prognosis, with an estimated survival of 2 years after diagnosis.
Endomyocardial fibrosis (EMF) is a disease that is characterized by fibrosis of the apical endocardium of the right ventricle (RV), left ventricle (LV), or both.
The clinical manifestations are largely related to the consequences of restrictive ventricular filling, including left and right sided heart failure.
The heart failure is associated with atrioventricular-valve regurgitation.
Endomyocardial fibrosis is a major cause of illness and death in areas where it is endemic, and in its severest form carries a very poor prognosis, with an estimated survival of 2 years after diagnosis.
Pulmonary edema is often caused by congestive heart failure. When the heart is not able to pump efficiently, blood can back up into the veins that take blood through the lungs. As the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs.
Pulmonary edema is often caused by congestive heart failure. When the heart is not able to pump efficiently, blood can back up into the veins that take blood through the lungs. As the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs.
Epidemiology , diagnosis and treatment of Hypertension Toufiqur Rahman
Hypertension, Blood pressure, Systolic Hypertension, Diastolic Hypertension, Epidemiology, Classification of hypertention, Type of hypertension, aetiology of hypertension, Clinical features, complications of hypertension, ambulatory blood pressure monitoring, Resistant hypertension, anti hypertensives,
Best Ayurvedic medicine for Gas and IndigestionSwastikAyurveda
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
2. Hypertensive Heart Disease
SYSTEMIC (LEFT-SIDED) HYPERTENSIVE HEART
DISEASE:
Criteria for diagnosis :
(1) left ventricular hypertrophy ( concentric)
(2) history or pathologic evidence of hypertension.
Asymptomatic and suspected only by ECG or
Echocardiographic indications of left ventricular
enlargement.
3. Atrial fibrillation (owing to left atrial enlargement),
or C.H.F with cardiac dilation, or both.
Effective control of hypertension can prevent or
lead to regression of cardiac hypertrophy and
its associated risks.
Morphology:
Left ventricular hypertrophy .
Left ventricular wall thickness may exceed 2 cm
and heart weight may exceed 500 gm.
4. Microscopically:
o The earliest change is increase in transverse
diameter of myocytes.
o At more advanced stage cellular and nuclear
enlargement becomes more irregular with
variation in cell size , and interstitial fibrosis.
5. PULMONARY (RIGHT-SIDED) HYPERTENSIVE HEART
DISEASE (COR PULMONALE):
Right ventricular ( hypertrophy, dilation, and failure )
secondary to pulmonary hypertension caused by
disorders of lungs or pulmonary vasculature .
Those caused by diseases of left side of heart, or
congenital heart diseases are excluded.
7. Cor pulmonale may be acute or chronic,
depending on suddenness of development
of pulmonary hypertension:-
Acute cor pulmonale: can follow massive
pulmonary embolism.
Chronic cor pulmonale: usually secondary to
prolonged pressure overload caused by
obstruction of pulmonary arteries or arterioles.
8. Morphology:
Acute cor pulmonale: marked dilation of right
ventricle without hypertrophy.
Chronic cor pulmonale: right ventricular wall
thickens up to 1.0 cm or more, and may even
approximate that of left ventricle.
9. Cardiomyopathies:
Heart disease resulting from a primary
abnormality in myocardium.
Three patterns:
o Dilated cardiomyopathy.
o Hypertrophic cardiomyopathy.
o Restrictive cardiomyopathy.
The dilated form is most common (90% of cases),
and the restrictive is least prevalent.
10. DILATED CARDIOMYOPATHY:
Also called congestive cardiomyopathy.
Causes:
Familial (genetic) : autosomal dominant.
Toxicities: chronic alcoholism.
Myocarditis.
pregnancy-associated nutritional deficiency.
Immunologic reaction.
In some patients: unknown ( idiopathic ).
11. Morphology:
Heart is large and flabby, with dilation of all
chambers.
Mural thrombi are common and may be a source
of thromboemboli.
Mitral or tricuspid regurgitation results from
ventricular chambers dilation (functional
regurgitation).
Muscle cells are attenuated, stretched, and irregular.
Interstitial and endocardial fibrosis of variable
degree is present
12. Clinical Features:
Occur at any age, but usually between 20 and 50 y’s.
Slowly progressive signs and symptoms of CHF
such as shortness of breath, and easy fatigability.
Secondary mitral regurgitation and abnormal
cardiac rhythms are common.
Death is due to progressive cardiac failure or
arrhythmia and can occur suddenly.
Embolism from dislodgment of an intracardiac
thrombus may occur.
Cardiac transplantation is only hope.
13. HYPERTROPHIC CARDIOMYOPATHY :
characterized by: myocardial hypertrophy,
abnormal diastolic filling, and in one third of cases
intermittent ventricular outflow obstruction.
Morphology:
Massive myocardial hypertrophy without
ventricular dilation.
disproportionate thickening of ventricular septum
as compared with free wall of left ventricle (ratio
greater than 3:1) termed asymmetrical septal
hypertrophy.
14. On cross-section: ventricular cavity has
"banana-like" configuration by bulging of
ventricular septum into lumen.
Microscopically:
(1) Extensive myocyte hypertrophy with
transverse myocyte diameters greater than 40 µm
(normal 15 µm).
(2) Haphazard disarray of myocytes.
(3) Interstitial and replacement fibrosis.
15.
16. Pathogenesis:
H.C.M caused by a mutation in any one of
several genes that encode proteins that are
part of sarcomere.
Sarcomere is the contractile unit of cardiac and
skeletal muscle.
Most cases are familial and pattern of transmission
is autosomal dominant with variable expression.
Remaining cases appear to be sporadic.
17. Mutations are found in at least 12 sarcomeric genes.
Including: β-myosin heavy chain (β-MHC),
cardiac troponinT, α-tropomyosin, and
myosin-binding protein C (MYBP-C).
Of these, mutation in β-MHC gene is most common .
18. Clinical Features:
Impaired diastolic filling of massively
hypertrophied left ventricle.
25% of patients have dynamic obstruction to
left ventricular outflow.
Limitation of cardiac output and secondary
increase in pulmonary venous pressure cause
exertional dyspnea.
Harsh systolic ejection murmur, caused by
ventricular outflow obstruction .
19. Owing to massive hypertrophy: myocardial ischemia
commonly results, even in absence of concomitant
CAD, and thus anginal pain is frequent.
The major clinical problems in H.C.M are:
o atrial fibrillation with mural thrombus formation ,
and possibly embolization.
20. o infective endocarditis of mitral valve.
o intractable cardiac failure.
o ventricular arrhythmias , and sudden death.
Hypertrophic cardiomyopathy is one of the most
common causes of sudden, otherwise unexplained,
death in young athletes.
21. RESTRICTIVE CARDIOMYOPATHY :
Decrease in ventricular compliance, resulting in
impaired ventricular filling during diastole.
The contractile (systolic) function of left ventricle
is usually unaffected.
Idiopathic ; or associated with distinct diseases
that affect myocardium: radiation fibrosis,
amyloidosis, sarcoidosis, or metastatic tumor.
22. Morphology:
Ventricles are of normal size or slightly enlarged.
Cavities are not dilated, and myocardium is firm.
Microscopically: patchy or diffuse interstitial fibrosis,
which can vary from minimal to extensive.
amorphous deposits of pale pink material between myocardial fibers.
This is characteristic for amyloid. Amyloidosis is a cause for restrictive cardiomyopathy.
23. Valvular Heart Disease:
Valvular involvement by disease causes stenosis,
insufficiency (regurgitation or incompetence), or both.
Stenosis is failure of a valve to open completely,
thereby impeding forward flow.
Insufficiency, in contrast, results from failure of a valve
to close completely, thereby allowing reversed flow.
Valvular abnormalities may be caused by congenital
disorders , or by a variety of acquired diseases.
The most important causes of acquired heart valve
diseases are:
24. VALVULAR DEGENERATION CAUSED BY CALCIFICATION :
due to calcific deposits (composed of calcium phosphate
mineral).
The most frequent calcific valvular diseases are:-
Calcific Aortic Stenosis:
It is the consequence of calcification owing to progressive
and advanced age-associated "wear and tear“ injury
Morphology:
The morphologic hallmark of calcific aortic stenosis is
heaped-up calcified masses within the aortic cusps.
( a heavily calcified aortic valve removed at the time of surgical valve replacement )
25. Clinical Features:
obstruction to left ventricular outflow leads to
gradually increasing pressure gradient across the
calcified valve.
cardiac output is maintained by development of
concentric left ventricular (pressure overload)
hypertrophy.
The hypertrophied myocardium tends to be ischemic
and angina pectoris may appear.
There may be impairment of both systolic and diastolic
myocardial function, with symptoms of CHF.
such patients require prompt relief of obstruction by
surgical valve replacement.
26. Mitral Annular Calcification:
Degenerative calcific deposits can develop in fibrous
ring (annulus) of mitral valve.
The process generally does not affect valvular function.
however, it may lead either to:
o regurgitation by interfering with systolic contraction of
mitral valve ring.
o stenosis by impairing opening of mitral leaflets.
o arrhythmias and occasionally sudden death by calcium
deposits penetrating sufficiently deeply to impinge on
atrioventricular conduction system.
27. Mitral annulus calcification: pathology specimen
This autopsy specimen demonstrates thickened mitral valve leafelts, with marked stenosis.
The mitral annulus calcification is seen as pale white 'lumps' under the endothelium around
the margins of the valve
28. MYXOMATOUS DEGENERATION OF MITRAL VALVE
(MITRAL VALVE PROLAPSE):
one or both mitral leaflets are "floppy" and prolapse, or
balloon back into left atrium during systole.
most often in young women.
Usually an incidental finding on physical examination.
may lead to serious complications in minority of cases.
Morphology:
ballooning (hooding) of mitral leaflets.
leaflets are often enlarged, redundant, thick, and
rubbery.
Chordae tendineae are elongated, thinned, and
occasionally ruptured.
29. Slide Description: This is floppy mitral valve seen from above (left).
Note also the thickened, distorted tricuspid valve, probably
rheumatic in origin.
30. Pathogenesis:
there is developmental defect of connective tissue,
possibly systemic.
So it is a common feature of Marfan syndrome (caused
by mutations in gene encoding fibrillin-1 )
Clinical Features:
Most patients are asymptomatic, discovered on routine
examination by presence of a midsystolic click .
when mitral regurgitation occurs, there is a late systolic
or sometimes holosystolic murmur.
A minority of patients have chest pain mimicking
angina, dyspnea, and fatigue.
31. RHEUMATIC FEVER AND RHEUMATIC HEART DISEASE :
Rheumatic fever ( RF ) is an acute, immunologically
mediated, multisystem inflammatory disease that
occurs a few weeks following an episode of group A
streptococcal pharyngitis.
Acute rheumatic carditis during active phase of RF may
progress to chronic rheumatic heart disease (RHD).
The most important consequence of RV is chronic
valvular deformities, characterized principally by
deforming fibrotic valvular disease (particularly mitral
stenosis)
32. Morphology:
During acute RF, focal inflammatory lesions are found
within heart called Aschoff bodies ( rheumatic
granuloma ).
Aschoff bodies consist of foci of degenerated collagen
surrounded by lymphocytes (primarily T cells),
occasional plasma cells, and plump macrophages called
Anitschkow cells (pathognomonic for RF).
Anitschkow cells have abundant cytoplasm and central
round-to-ovoid nuclei in which the chromatin is
disposed as a central, slender, wavy ribbon (hence the
designation "caterpillar cells").
Some of larger macrophages become multinucleated to
form Aschoff giant cells.
33.
34.
35. Aschoff bodies may be found in any of three layers of
heart ( pericardium, myocardium, or endocardium )
hence the lesion is called pancarditis.
involvement of endocardium and left-sided valves
results in fibrinoid necrosis within cusps or along
chordae tendineae .
on which sit small (1- to 2-mm) vegetations (verrucae)
along lines of closure.
These irregular, warty projections (verrucae ) arise from
precipitation of fibrin at sites of erosion, related to
underlying inflammation and collagen degeneration.
36.
37. Chronic RHD is characterized by organization of acute
inflammation and subsequent fibrosis.
valvular leaflets become thickened and retracted,
causing permanent deformity.
Microscopically there is diffuse fibrosis and often
neovascularization that obliterate the originally
avascular leaflet architecture.
In chronic rheumatic mitral valvulitis the valve leaflets and chordae tendineae are
thick, rigid, and interadherent.
38. Pathogenesis:
acute rheumatic fever is a hypersensitivity reaction
induced by group A streptococci.
antibodies directed against M proteins of certain strains
of streptococci cross-react with glycoprotein antigens
in heart, joints, and other tissues.
The onset of symptoms 2 to 3 weeks after infection and
the absence of streptococci from the lesions support
the concept that RF results from an immune response
against the offending bacteria.
39. Clinical Features:
RF is characterized by major manifestations:
(1) migratory polyarthritis of large joints,
(2) carditis.
(3) subcutaneous nodules.
(4) erythema marginatum of skin.
(5) Sydenham chorea ( neurologic disorder with
involuntary purposeless, rapid movements ).
The diagnosis is established by so-called Jones criteria:
the presence of two of major manifestations, or one
major and two minor manifestations ( fever, arthralgia,
or elevated blood levels of acute phase reactants-CRP).
40. Acute RF appears most often in children between
ages 5 and 15, but about 20% of first attacks occur
in middle to later life.
Although pharyngeal cultures for streptococci are
negative by the time the illness begins, antibodies
to one or more streptococcal enzymes, such as
streptolysin O and DNAse B are present and can be
detected in sera of most patients.
41. INFECTIVE ENDOCARDITIS (IE ):
is characterized by colonization or invasion of heart
valves or endocardium by a microbe, leading to
formation of bulky friable vegetations composed of
thrombotic debris and organisms, often associated with
destruction of underlying cardiac tissues.
Although fungi, rickettsiae (Q fever), and chlamydiae
have been responsible for these infections, most cases
are bacterial (bacterial endocarditis).
42. Etiology and Pathogenesis:
classified on clinical grounds into acute and subacute
forms.
Acute endocarditis: destructive infection of a previously
normal heart valve with a highly virulent organism
(S. aureus ) as in intravenous drug abusers.
Subacute endocarditis: organisms of low virulence
(Streptococcus viridans )can cause infection in
a previously deformed valves.
Prosthetic valve endocarditis is caused most commonly
by coagulase-negative staphylococci ( S. epidermidis).
43. Morphology:
In both subacute and acute forms friable, bulky, and
destructive vegetations containing fibrin, inflammatory
cells, and bacteria or other organisms are present on
heart valves .
The aortic and mitral valves are most common sites of
infection
The vegetations may be single or multiple and may
involve more than one valve.
Vegetations sometimes erode into underlying
myocardium to produce an abscess cavity (ring abscess).
Fungal endocarditis tends to cause large vegetations
than does bacterial infection.
44. Systemic emboli may occur because of friable nature of
vegetations, and may cause infarcts in brain, kidneys,
myocardium, and other tissues.
Because the embolic fragments contain large numbers of
virulent organisms, abscesses often develop at sites of
such infarcts (septic infarcts).
With passage of time, fibrosis, calcification, and chronic
inflammatory infiltrate may develop.
45. Mitral vegetation in a 78-year-old man with infective endocarditis.
Intraoperative photograph shows a large vegetation (arrow) adhering to posterior
mitral leaflet (arrowhead).
46. Diagnostic Criteria for Infective Endocarditis
Pathologic Criteria:
Microorganisms, demonstrated by culture or histologic examination, in a vegetation, embolus from a
vegetation, or intracardiac abscess.
Clinical Criteria:
Major:-
Positive blood culture(s) indicating characteristic organism.
Echocardiographic findings ; including valve-related or implant-related mass or abscess, or partial
separation of artificial valve.
New valvular regurgitation.
Minor:-
Predisposing heart lesion or intravenous drug use.
Fever.
Vascular lesions ; including arterial petechiae, subungual/splinter hemorrhages , emboli, septic infarcts,
mycotic aneurysm, intracranial hemorrhage, Janeway lesions.
Immunologic phenomena ; including glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor.
Microbiologic evidence ; including single culture showing uncharacteristic organism.
Echocardiographic findings consistent with but not diagnostic of endocarditis ; including new valvular
regurgitation, pericarditis.
47. Diagnosis by Duke Criteria, requires either pathologic or
clinical criteria; if clinical criteria are used, 2 major, or 1
major + 3 minor, or 5 minor criteria are required for
diagnosis.
Janeway lesions are small erythematous lesions on
palms and soles.
Osler nodes are small subcutaneous nodules in pulp of
digits.
Roth spots are oval retinal hemorrhages with pale
centers.
Prevention of IE is done by prophylactic use of
antibiotics in patient with cardiac anomaly or artificial
valve who is about to have a dental, surgical, or other
invasive procedure.
50. Nonbacterial Thrombotic Endocarditis (NBTE):
NBTE is characterized by deposition of small masses
(1 to 5 mm) of fibrin, platelets, and other blood
components on leaflets of cardiac valves.
In contrast to vegetations of IE, the valvular lesions of
NBTE are nondestructive , sterile and do not contain
microorganisms.
NBTE is often encountered in debilitated patients,
such as those with cancer or sepsis ( hence previously
termed marantic endocarditis).
NBTE may producing emboli and resultant infarcts in
brain, heart, or elsewhere.