restrictive myocardiopathy.pptx
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This document discusses several types of cardiomyopathies including restrictive cardiomyopathy and arrhythmogenic right ventricular dysplasia. Restrictive cardiomyopathy is classified as primary or secondary and can be caused by various infiltrative diseases, storage diseases, or radiation exposure. It presents with signs and symptoms of heart failure and is diagnosed using tests like echocardiogram, MRI, and cardiac biopsy. Treatment involves pharmacological therapies and sometimes surgery. Arrhythmogenic right ventricular dysplasia is a rare genetic disorder causing ventricular arrhythmias and sudden cardiac death in young individuals. It is caused by mutations in genes encoding desmosomal proteins, resulting in fibrofatty replacement of the right ventricular myocardium. Diagnosis involves ECG, MRI, RV
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REVIEW ARTICLE (1).pptx
This document summarizes a review article on arrhythmogenic right ventricular cardiomyopathy (ARVC). It discusses the pathological features and molecular genetic basis of the disease. Mutations in genes encoding desmosomal proteins cause disrupted intercellular junctions and myocyte death. Physical exercise is a critical risk factor. The document reviews clinical presentation, diagnosis, prognosis, and treatment of ARVC. Genetic testing can help identify family members at risk, but results require careful interpretation. Risk of sudden cardiac death is highest in patients with prior arrhythmias or ventricular dysfunction.
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ARVC is a heritable heart muscle disorder that predominantly affects the right ventricle. It is caused by genetic defects in cardiac desmosomes, which are important for cell-to-cell adhesion. This leads to progressive loss of right ventricular myocardium and replacement by fibrofatty tissue. ARVC can cause dangerous ventricular arrhythmias and is a leading cause of sudden cardiac death in young people. Diagnosis involves imaging tests and electrocardiography to detect right ventricular structural abnormalities and arrhythmias.
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Cardiomyopathy is an anatomic and pathologic diagnosis associated with muscle or electrical dysfunction of the heart. It represents a heterogeneous group of diseases that often lead to progressive heart failure and significant morbidity and mortality. The major types are dilated cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy, and arrhythmogenic right ventricular cardiomyopathy. Symptoms are the same as those seen in heart failure and include shortness of breath, fatigue, cough, orthopnea, and edema. Diagnostic studies include BNP levels, electrocardiography, and echocardiography. Treatment is targeted at relieving heart failure symptoms and reducing mortality through pharmacotherapy, devices, and transplantation if needed.
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Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/ARVC) is a genetic heart condition characterized by structural abnormalities and fatty infiltration of the right ventricle, leading to ventricular arrhythmias and sudden cardiac death. It is a common cause of sudden cardiac death in young athletes. Clinical features include palpitations, syncope, chest pain, and dyspnea. Diagnosis relies on a combination of ECG findings, echocardiogram abnormalities of the right ventricle, and genetic testing.
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Cardiomyopathy is a disease of the heart muscle that can cause mechanical and electrical dysfunction. It has many causes including genetic disorders, infections, and metabolic issues.
The prognosis for cardiomyopathy is generally poor if left undiagnosed until advanced stages. Diagnostic tools include echocardiography, chest x-rays, and cardiac catheterization.
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ARVC is a heritable heart muscle disorder that predominantly affects the right ventricle. It is caused by genetic defects in cardiac desmosomes, which are important for cell-to-cell adhesion. This leads to progressive loss of right ventricular myocardium and replacement by fibrofatty tissue. ARVC can cause dangerous ventricular arrhythmias and is a leading cause of sudden cardiac death in young people. Diagnosis involves imaging tests and electrocardiography to detect right ventricular structural abnormalities and arrhythmias.
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3) Restrictive cardiomyopathy stiffens the heart ventricles and impairs filling. Amyloidosis is a common cause.
4) Arrhythmogenic right ventricular dysplasia replaces parts of the right ventricle with fat and fibrosis and can cause arrhythmias or sudden death.
02 2009 - cardiomyopathy - an overview.
Cardiomyopathy is an anatomic and pathologic diagnosis associated with muscle or electrical dysfunction of the heart. It represents a heterogeneous group of diseases that often lead to progressive heart failure and significant morbidity and mortality. The major types are dilated cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy, and arrhythmogenic right ventricular cardiomyopathy. Symptoms are the same as those seen in heart failure and include shortness of breath, fatigue, cough, orthopnea, and edema. Diagnostic studies include BNP levels, electrocardiography, and echocardiography. Treatment is targeted at relieving heart failure symptoms and reducing mortality through pharmacotherapy, devices, and transplantation if needed.
Di Lorenzo Cherubino. Cefalea e vasculopatie genetiche. ASMaD 2011
1. Migraine is associated with several genetic vasculopathies including CADASIL, MELAS, RVCL, CRV, and HIHRATL.
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Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/ARVC) is a genetic heart condition characterized by structural abnormalities and fatty infiltration of the right ventricle, leading to ventricular arrhythmias and sudden cardiac death. It is a common cause of sudden cardiac death in young athletes. Clinical features include palpitations, syncope, chest pain, and dyspnea. Diagnosis relies on a combination of ECG findings, echocardiogram abnormalities of the right ventricle, and genetic testing.
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The prognosis for cardiomyopathy is generally poor if left undiagnosed until advanced stages. Diagnostic tools include echocardiography, chest x-rays, and cardiac catheterization.
Dilated cardiomyopathy is the most common type and is characterized by the enlargement of heart chambers and thinning of the walls. It can lead to heart failure if not properly managed with medications like ACE inhibitors, beta blockers, diuretics, and devices like defibrillators if needed. The prognosis is poor with 50% of patients dying within
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The pathophysiology of cardiomyopathy
This document outlines and defines various types of cardiomyopathies:
- Dilated cardiomyopathy is the most common type and is characterized by dilation and impaired contraction of one or both ventricles.
- Hypertrophic cardiomyopathy is characterized by left ventricular hypertrophy in the absence of another cause. It is often genetic and can cause sudden death.
- Restrictive cardiomyopathy features a rigid ventricle causing severe diastolic dysfunction. It can be idiopathic or caused by conditions like amyloidosis.
- Arrhythmogenic right ventricular cardiomyopathy causes replacement of the right ventricle with fat or fibrosis which can lead to arrhythmias.
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Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is an inherited heart muscle disease characterized by structural abnormalities and fatty replacement of the right ventricle muscle leading to ventricular arrhythmias. It is an important cause of sudden cardiac death in young adults. The disease results from genetic mutations that cause programmed cell death and fibrosis of the right ventricle muscle. Diagnosis is based on ECG findings like inverted T-waves in the right ventricle leads and epsilon waves, along with imaging showing right ventricle structural changes. Treatment involves medications like beta-blockers and implantable defibrillators to prevent arrhythmias.
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The document summarizes arrhythmogenic right ventricular dysplasia (ARVD), a condition where the right ventricle of the heart is replaced by fat and fibrous tissue. It affects mostly young males and can cause sudden cardiac death. Genetic factors are involved in many cases. The condition starts with fatty infiltration of the right ventricle and progresses to include fibrosis, thinning of the ventricular wall, and later involvement of the left ventricle. Diagnosis involves criteria related to structural changes, electrocardiogram abnormalities, arrhythmias, and family history.
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2. Diagnosis involves ECG, cardiac imaging, cardiac biomarkers like troponin and CK-MB. Reperfusion therapy within 6 hours includes PCI or thrombolysis. General treatment measures include aspirin, clopidogrel, anticoagulants, analgesics, beta-blockers, nitrates and oxygen.
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The document discusses several single-gene disorders that can cause ischemic stroke, including:
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This document outlines and defines various types of cardiomyopathies:
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- Hypertrophic cardiomyopathy is characterized by left ventricular hypertrophy in the absence of another cause. It is often genetic and can cause sudden death.
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The document summarizes the classification and characteristics of different types of cardiomyopathies:
1) Cardiomyopathies are classified based on their pathophysiology into dilated, hypertrophic, restrictive, and other types. Specific cardiomyopathies have a distinct disease association like anthracycline toxicity causing dilated cardiomyopathy.
2) Dilated cardiomyopathy has a poor prognosis in children with 60% surviving 5 years. Medical and surgical therapies are improving but transplantation may be required for end-stage cases.
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The document discusses several single-gene disorders that can cause ischemic stroke, including:
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2. Fabry's disease, an X-linked disorder caused by alpha-galactosidase A deficiency, which can cause both large and small vessel strokes in young patients.
3. Sickle cell disease, where strokes typically occur in childhood and are caused by intimal thickening leading to thrombus formation in large arteries or recurrent small subcortical infarcts.
It also briefly mentions other disorders like homocystinuria,
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2. Cardiac amyloidosis typically presents in the 5th to 7th decade with symptoms of severe heart failure such as exertional dyspnea and peripheral edema.
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rheumatic_fever.ppt
1. Acute rheumatic fever is an autoimmune condition that can occur as a consequence of a streptococcal throat infection, causing inflammation in joints, brain, skin, and especially the heart.
2. It is diagnosed using the modified Jones criteria which looks for evidence of prior streptococcal infection and manifestations involving major criteria like carditis or chorea and minor criteria like arthritis or fever.
3. Treatment involves antibiotics to eradicate the streptococcal infection, anti-inflammatory drugs, and long-term antibiotic prophylaxis to prevent recurrent episodes from damaging the heart valves and leading to rheumatic heart disease.
Membrane_Potentials_2021-46887.ppt
Membrane potential is created by a difference in electrical charge across the selectively permeable cell membrane, representing potential energy. This results from ion concentration gradients of sodium, potassium, chloride, and other ions between the extracellular fluid and intracellular fluid. At rest, the membrane potential is around -70mV due to higher potassium and chloride concentrations inside the cell and higher sodium concentration outside. The sodium-potassium pump maintains these gradients by actively transporting ions against their gradients. Graded potentials result from stimuli that do not exceed the threshold, while exceeding the threshold triggers an all-or-none action potential via voltage-gated sodium and potassium channels.
Membrane_transport_2021-46884.ppt
The cell membrane uses a fluid mosaic model with phospholipids, cholesterol, and integral and peripheral proteins that allow for selective transport of molecules. Transport across the membrane can occur through passive diffusion down a concentration gradient or through active transport using membrane proteins like channels and carriers. Channel proteins provide rapid yet less selective transport of small molecules like ions. Carrier proteins provide slower but more selective transport of small molecules and ions through mechanisms like cotransport, vesicular transport, receptor mediated transport, and endocytosis and exocytosis.
Introduction_Lecture_2021-46877.ppt
One of the oldest branches of science, medicine has evolved significantly since Hippocrates first established it as its own field of study separate from religion in 420 BC. Key figures like Galen, Vesalius, William Harvey, Claude Bernard, and Walter Cannon advanced the field through extensive human dissection, quantitative analysis, introduction of scientific methodology, and defining concepts like homeostasis. These pioneers helped transform medicine from a theological pursuit to an evidence-based scientific discipline.
THORAX CLINICAL ANATOMY
The document discusses the anatomy of the lungs and related structures. It describes the structures found at the hilum or root of each lung, including blood vessels, bronchi, and nerves. The root connects the lung to the heart and trachea. The document also briefly mentions surgery for lung cancer infiltrating the mediastinum, which can potentially provide a cure if the tumor is completely resected.
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There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
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The Electrocardiogram - Physiologic Principles
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
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11. Describe the axes of leads (hexagonal reference system)
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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
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Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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restrictive myocardiopathy.pptx
- 4. CLASSIFICATION 1 1primary Primary a) Lofeller's endocarditis b) Endomyocardial fibrosis Secondary a) Infiltrative disease b) storage disease c) Post - radiation disease
- 5. CAUSES
- 7. DIAGNOSIS
- 8. TREATMENT
- 10. PHARMACOLOGICAL
- 11. SURGICAL
- 13. Arrhythmogenic right ventricular dysplasia (ARVD) is a rare familial disorder that may cause ventricular tachycardia and sudden cardiac death in young, apparently healthy individuals. The clinical hallmark of the disease is ventricular arrhythmias, arising predominantly from the right ventricle. The pathological hallmark of the disease is fibrofatty replacement of right ventricular myocardium.
- 14. CAUSE ARVD/C is caused by mutations in genes that encode desmosomal proteins. Desmosomes attach heart muscle cells to one another, providing strength to the myocardium and playing a role in signaling between neighboring cells. Mutations in desmosomal genes impair the function of desmosomes. Without normal desmosomes, cells of the myocardium detach from one another and die, particularly when the heart muscle is placed under stress.These changes primarily affect the myocardium surrounding the right ventricle The damaged myocardium is gradually replaced by fat and scar tissue. As this abnormal tissue builds up, the walls of the right ventricle become stretched out, preventing the heart from pumping blood effectively. These changes also disrupt the
- 15. Arrhythmias Premature Ventricular Contractions Ventricular Tachycardia Syncope Heart failure Sudden cardiac arrest
- 16. DIAGNOSIS ECG MRI CT CARDIAC BIOPSY RV ANGIOGRAM ELECTROPHYSIOLOGY TESTIN G
- 17. TREATMENT oBeta blockers oAntiarrhythmic drugs oACE Inhibitors oImplantable Cardioverter Defibrillator (ICD) oCatheter Ablation
- 18. THANK YOU