This is a power point presentation titled "Chronic Stable Angina" . For more medical power points, PDFs, ECGs, X-rays, please visit www.medicaldump.com
Its a medical presentation describing how to approach to various cardiac arrhythmias in systematic way. Illustrated with more ECG photographs from standard sources.
Dr Vivek Baliga discusses left atrial myxoma for medical students. Lecture includes a link to MCQs in the video. For access to video, please copy and paste this link --> https://youtu.be/JtkWxbVklgA
Its a medical presentation describing how to approach to various cardiac arrhythmias in systematic way. Illustrated with more ECG photographs from standard sources.
Dr Vivek Baliga discusses left atrial myxoma for medical students. Lecture includes a link to MCQs in the video. For access to video, please copy and paste this link --> https://youtu.be/JtkWxbVklgA
Heart Failure with Preserved Ejection Fraction(HFpEF).ptxSarfraz Saleemi
Heart failure with preserved ejection fraction (HFpEF) is not one disease but a clinical syndrome presenting with symptoms of Heart Failure with a left ventricular ejection fraction (LVEF) ≥50 percent and evidence of cardiac diastolic dysfunction. (abnormal LV filling pattern and elevated filling pressures)
It is more common among older patients and women, and results from abnormalities of active ventricular relaxation and passive ventricular compliance. HFpEF should be part of differential diagnosis in patients with typical symptoms such as fatigue, weakness, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, edema and clinical signs of chronic heart failure. Echocardiography features of normal ejection fraction with impaired diastolic function confirm the diagnosis.
In a myocardial infarction transmural ischemia develops. In the first hours and days after the onset of a myocardial infarction, several changes can be observed on the ECG. First, large peaked T waves (or hyperacute T waves), then ST elevation, then negative T waves and finally pathologic Q waves develop.
Non infarction Q waves
Precise guide for Allied Health Science Students especially cardiac specialty students, DGNM, B.Sc Nursing & M.Sc Nursing Students regarding Non Infarction Q waves
Chronic Stable Angina- Diagnosis & management
By Dr Awadhesh Kumar Sharma
Dr. Awadhesh kumar sharma is a young, diligent and dynamic interventional cardiologist. He did his graduation from GSVM Medical College Kanpur and MD in Internal Medicine from MLB Medical college jhansi. Then he did his superspecilisation degree DM in Cardiology from PGIMER & DR Ram Manoher Lohia Hospital Delhi. He had excellent academic record with Gold medal in MBBS,MD and first class in DM.He was also awarded chief ministers medal in 2009 for his academic excellence by former chief minister of UP Smt Mayawati in 2009.He is also receiver of GEMS international award.He had many national & international publications.He is also in editorial board of international journal- Journal of clinical medicine & research(JCMR).He is also active member of reviewer board of many journals.He is also trainee fellow of American college of cardiology. He is currently working in NABH Approved Gracian Superspeciality Hospital Mohali as Consultant Cardiologist.
Heart Failure with Preserved Ejection Fraction(HFpEF).ptxSarfraz Saleemi
Heart failure with preserved ejection fraction (HFpEF) is not one disease but a clinical syndrome presenting with symptoms of Heart Failure with a left ventricular ejection fraction (LVEF) ≥50 percent and evidence of cardiac diastolic dysfunction. (abnormal LV filling pattern and elevated filling pressures)
It is more common among older patients and women, and results from abnormalities of active ventricular relaxation and passive ventricular compliance. HFpEF should be part of differential diagnosis in patients with typical symptoms such as fatigue, weakness, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, edema and clinical signs of chronic heart failure. Echocardiography features of normal ejection fraction with impaired diastolic function confirm the diagnosis.
In a myocardial infarction transmural ischemia develops. In the first hours and days after the onset of a myocardial infarction, several changes can be observed on the ECG. First, large peaked T waves (or hyperacute T waves), then ST elevation, then negative T waves and finally pathologic Q waves develop.
Non infarction Q waves
Precise guide for Allied Health Science Students especially cardiac specialty students, DGNM, B.Sc Nursing & M.Sc Nursing Students regarding Non Infarction Q waves
Chronic Stable Angina- Diagnosis & management
By Dr Awadhesh Kumar Sharma
Dr. Awadhesh kumar sharma is a young, diligent and dynamic interventional cardiologist. He did his graduation from GSVM Medical College Kanpur and MD in Internal Medicine from MLB Medical college jhansi. Then he did his superspecilisation degree DM in Cardiology from PGIMER & DR Ram Manoher Lohia Hospital Delhi. He had excellent academic record with Gold medal in MBBS,MD and first class in DM.He was also awarded chief ministers medal in 2009 for his academic excellence by former chief minister of UP Smt Mayawati in 2009.He is also receiver of GEMS international award.He had many national & international publications.He is also in editorial board of international journal- Journal of clinical medicine & research(JCMR).He is also active member of reviewer board of many journals.He is also trainee fellow of American college of cardiology. He is currently working in NABH Approved Gracian Superspeciality Hospital Mohali as Consultant Cardiologist.
Comparative effectives of angiotensin-converting enzyme inhibitors and/or angiotensin II receptor blockers added to standard medical therapy for treating patients with stable ischemic heart disease and preserved left ventricular systolic function.
Myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops to a part of the heart, causing damage to the heart muscle. The most common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck, or jaw.
Presentation about heart failure with preserved ejection fraction. Current epidemiology, pathophysiology, diagnostic approac and evidence-based treatment are presented.
go to www.medicaldump.com to download this medical powerpoint presentation. You can find medical templates, medical pdfs and medical powerpoints on all specialties
go to www.medicaldump.com to download this file and check out other medical powerpoints, medical powerpoint templates, medical pdfs and all other medical documents.
go to www.medicaldump.com to download this file and check out other medical powerpoints, medical powerpoint templates, medical pdfs and all other medical documents.
For more free medical powerpoints, visit www. medicaldump.com, Free updates everyday on all specialties including cardiology, nephrology, neurology, pulmonology, etc.
For more free medical powerpoints, visit www. medicaldump.com, Free updates everyday on all specialties including cardiology, nephrology, neurology, pulmonology, etc.
This is a power point presentation titled Hypercalcemia of malignancy. For medical power point, x-rays, CT scans, medical projects or other downloads, visit www.medicaldump.com
These lecture slides, by Dr Sidra Arshad, offer a quick overview of 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 leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
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. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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
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Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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.
2. A 47-year-old man reports a six-month history of intermittent chest discomfort while playing squash. He describes lower substernal tightness with numbness of the left upper arm only during exertion. He does not smoke. His father died suddenly at the age of 49 years. His blood pressure is 138/84 mm Hg. The level of total cholesterol is 261 mg per deciliter (6.7 mmol per liter), of low-density lipoprotein cholesterol 172 mg per deciliter (4.4 mmol per liter), and of high-density lipoprotein cholesterol 50 mg per deciliter (1.3 mmol per liter), and the triglyceride level is 113 mg per deciliter (2.9 mmol per liter). The result of an exercise test is positive, with pain and 1.5 mm of horizontal ST-segment depression at stage 4 of the Bruce protocol. How should the patient's case be managed? Abrams,NEJM,2005;352:2524-2533 Case history
11. Boden WE, ORourke, RA, Teo KK, Hartigan P, Maron D, et al. Optimal Medical Therapy with or without PCI for Stable Coronary Disease. N Engl J Med 2007;356:1503-16.
18. Chronic Stable Angina References 1. Abrams J. Chronic Stable Angina. N Engl J Med 2005;352:2524-33. 2 . Fraker TD Jr, Fihn SD. 2007 Chronic Angina Focused Update of the ACC/AHA 2002 Guidelines for the Management of Patients With Chronic Stable Angina: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Writing Group to Develop the Focused Update of the 2002 Guideline for the Management of Patients with Chronic Stable Angina . J. Am. Coll. Cardiol . 2007;50:2264-2274. 3. Boden WE, ORourke, RA, Teo KK, Hartigan P, Maron D, et al. Optimal Medical Therapy with or without PCI for Stable Coronary Disease . N Engl J Med 2007;356:1503-16. 4. Hochman JS, Steg PG. Does Preventive PCI Work? N Engl J Med 2007;356:1572-1574. 5. Peterson ED, Rumsfeld JS. Finding the Courage to Reconsider Medical Therapy for Stable Angina . N Engl J Med 2008;359:7:751-753. 6. Hochman JS, Lamas GA, Buller CE, Dzavik V, Reynolds HR, et al. Coronary Intervention for Persistent Occlusion after Myocardial Infarction. N Engl J Med 2006;355:2395-407. 7. Mark DB, Pan W, Clapp-Channing NE, Anstrom KJ, et al. Quality of Life after Late Invasive Therapy for Occluded Arteries. N Engl J Med 2009;360:774-83.
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Editor's Notes
Figure 1. Typical Progression of Coronary Atherosclerosis. As the plaque burden increases, the atherosclerotic mass tends to stay external to the lumen, which allows the diameter of the lumen to be maintained; this is known as the Glagov effect, or positive remodeling.1 As plaque encroaches into the lumen, the coronary artery diameter decreases. Myocardial ischemia results from a discordant ratio of coronary blood supply to myocardial oxygen consumption. Luminal narrowing of more than 65 to 75 percent may result in transient ischemia and angina. In acute coronary syndromes, vulnerable plaque is a more important factor than is the degree of stenosis; acute coronary events result from ulceration or erosion of the fibrous cap, with subsequent intraluminal thrombosis. 2, 3 Vulnerable plaque within the vessel wall may not be obstructive and thus may remain clinically silent until it causes rupture and associated consequences. (The figure has been modified from Greenland et al., 4 with permission.)
Figure 2. Kaplan-Meier Survival Curves. In Panel A, the estimated 4.6-year rate of the composite primary outcome of death from any cause and nonfatal myocardial infarction was 19.0% in the PCI group and 18.5% in the medical-therapy group. In Panel B, the estimated 4.6-year rate of death from any cause was 7.6% in the PCI group and 8.3% in the medical-therapy group. In Panel C, the estimated 4.6-year rate of hospitalization for acute coronary syndrome (ACS) was 12.4% in the PCI group and 11.8% in the medical-therapy group. In Panel D, the estimated 4.6-year rate of acute myocardial infarction was 13.2% in the PCI group and 12.3% in the medical-therapy group.
