The guidelines provide recommendations for screening, risk assessment, treatment goals, and management of dyslipidemia to prevent cardiovascular disease. Key points include screening adults based on age and risk factors, using LDL-C and other lipid levels to determine risk stratification and treatment goals, and employing lifestyle changes and pharmacologic therapies like statins and fibrates to manage lipid levels and reduce risk. The guidelines aim to optimize dyslipidemia treatment to lower cardiovascular disease risk.
Management of CAD in Diabetes the cardiovascular equivalent is challenging.The slides take you from the epidemiology,ADD,and CV benefit and how to manage CAD
SGLT2 inhibitors in Heart failure: A prized addition to HF treatment optionsahvc0858
Early Diabetes and Dyslipidaemia Treatment Optimisation.
Presentation by Dr Chan Wan Xian
Cardiologist, Echocardiologist
Heart Failure Intensivist
Asian Heart & Vascular Centre
www.ahvc.com.sg
Goal attainments and their discrepancies for low density lipoprotein choleste...Paul Schoenhagen
Purpose: Low density lipoprotein cholesterol (LDL-C) is primary treatment target for patients with dislipidemia. The apolipoprotein B (apo B), an emerging biomarker for cardiovascular risk prediction, appears to be superior to the LDL-C. However, little is known about goal attainments and their discrepancies for LDL-C and apo B in Chinese patients with known CAD or DM.
Management of CAD in Diabetes the cardiovascular equivalent is challenging.The slides take you from the epidemiology,ADD,and CV benefit and how to manage CAD
SGLT2 inhibitors in Heart failure: A prized addition to HF treatment optionsahvc0858
Early Diabetes and Dyslipidaemia Treatment Optimisation.
Presentation by Dr Chan Wan Xian
Cardiologist, Echocardiologist
Heart Failure Intensivist
Asian Heart & Vascular Centre
www.ahvc.com.sg
Goal attainments and their discrepancies for low density lipoprotein choleste...Paul Schoenhagen
Purpose: Low density lipoprotein cholesterol (LDL-C) is primary treatment target for patients with dislipidemia. The apolipoprotein B (apo B), an emerging biomarker for cardiovascular risk prediction, appears to be superior to the LDL-C. However, little is known about goal attainments and their discrepancies for LDL-C and apo B in Chinese patients with known CAD or DM.
Reduciendo eventos cardiovasculares en pacientes con DM2: nuevas evidencias
23/06/16 18:00h Casa del Corazón, Madrid
http://ecvdm2.secardiologia.es
#ECVDM2
Resultados de nuevos estudios: más allá de la no inferioridad
Dr. Luis Masmiquel Comas, Endocrinólogo. Hospital Son Llàtzer (Palma de Mallorca)
La aterosclerosis como enfermedad sistémica una visión integral de la enfermedad cardiovascular
Miércoles, 22/06/16 18:00h-20:00h Casa del Corazón, Madrid
http://cvvt.secardiologia.es
#CVVT
La enfermedad aterosclerótica en cardiología: particularidades y novedades
Dr. Leopoldo Pérez de Isla. Hospital Universitario Clínico San Carlos, Madrid
SGLT2 Inhibitor therapy has opened up an exciting avenue for the Physicians to manage the patients with CKD . The slide set highlights the major trials on the drug showing remarkable benefits.
Reduciendo eventos cardiovasculares en pacientes con DM2: nuevas evidencias
23/06/16 18:00h Casa del Corazón, Madrid
http://ecvdm2.secardiologia.es
#ECVDM2
Resultados de nuevos estudios: más allá de la no inferioridad
Dr. Luis Masmiquel Comas, Endocrinólogo. Hospital Son Llàtzer (Palma de Mallorca)
La aterosclerosis como enfermedad sistémica una visión integral de la enfermedad cardiovascular
Miércoles, 22/06/16 18:00h-20:00h Casa del Corazón, Madrid
http://cvvt.secardiologia.es
#CVVT
La enfermedad aterosclerótica en cardiología: particularidades y novedades
Dr. Leopoldo Pérez de Isla. Hospital Universitario Clínico San Carlos, Madrid
SGLT2 Inhibitor therapy has opened up an exciting avenue for the Physicians to manage the patients with CKD . The slide set highlights the major trials on the drug showing remarkable benefits.
Diabetes and heart two sides of the same coinSunil Wadhwa
This ppt presented in a CME of doctors in March 2017 discusses-if all Diabetics should be treated aggressively for prevention of coronary artery disease & SHOULD IT BE PRESUMED AS IF THEY ARE ALREADY PATIENTS OF CAD?
This presentation is updated till March 2017
Dyslipidemia, specially high LDL cholesterol is the key risk factor for cardiovascular diseases. The presentation discusses metabolism and structure of lipoproteins, their screening and interpretation, risk assessment methods, targets for various lipoproteins and its step by step treatment.
Dyslipidemia and CVS by Mohit Soni and Chandan KumarOlgaGoryacheva4
My students Mohit Soni and Chandan Kumar had presented this topic in our 22nd Student Scientific Society Conference in the department of Propaedeutic of Internal Diseases No.2
This lecture presents the 1-Updated recommendations regarding definition and proper diagnosis of HTN. 2-Updated guidelines for threshold of BP to start treatment and targets of treatment. 3- Updated recommendations on CV risk assessment and management. 4-Hypertension and comorbidities: updated guidelines
Ponencia realizada por el Prof. Alberto Zambon en la segunda sesión de CardioVascular Virtual Topic 2022, titulada Residual cardiovascular risk. What is the role of icosapent ethyl?
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
- 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
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.
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
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
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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
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
1. American Association of Clinical Endocrinologists
and American College of Endocrinology
Guidelines for Management of Dyslipidemia
and Prevention of Cardiovascular Disease
Writing Committee
Chair: Paul S. Jellinger, MD, MACE
Co-Chair: Yehuda Handelsman, MD, FACP, FACE
Members:
David S. H. Bell, MD, FACP, FACE
Zachary T. Bloomgarden, MD, MACE
Eliot A. Brinton, MD, FAHA, FNLA
Michael H. Davidson, MD, FACC, FACP, FNLA
Sergio Fazio, MD, PhD
Vivian A. Fonseca, MD, FACE
Alan J. Garber, MD, PhD, FACE
George Grunberger, MD, FACP, FACE
Chris K. Guerin, MD, FNLA, FACE
Jeffrey I. Mechanick, MD, FACP, FACE, FACN, ECNU
Rachel Pessah-Pollack, MD, FACE
Paul D. Rosenblit, MD, PhD, FNLA, FACE
Donald A. Smith, MD, MPH, FACE
Kathleen Wyne, MD, PhD, FNLA, FACE
Reviewers:
Michael Bush, MD
Farhad Zangeneh, MD
2. Mục lục
I. Sàng lọc
II. Các xét nghiệm cần phải làm
III. Các yếu tố nguy cơ
IV. Phân tầng nguy cơ
V. Mục tiêu điều trị
VI. Phương pháp điều trị
VII. Theo dõi điều trị
4. SÀNG LỌC
Familial Hypercholesterolemia
• Individuals should be screened for FH when there is a family history of:
• Premature ASCVD (definite MI or sudden death before age 55 years in father
or other male first-degree relative or before age 65 years in mother or other
female first-degree relative) or
• Elevated cholesterol levels (total, non-HDL, and/or LDL) consistent with FH
Adults With Diabetes
• Annually screen all adult individuals with T1DM or T2DM for dyslipidemia
Young Adults (Men Aged 20-45 Years, Women Aged 20-55
Years)
• 5 years
Recommendationsassociatedwiththis
question:
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497.
Abbreviations: ASCVD, atherosclerotic cardiovascular disease; FH, familial hypercholesterolemia; HDL, high-density lipoprotein; LDL, low-density lipoprotein; MI, myocardial
infarction; T1DM, type 1 diabetes mellitus; T2DM, type 2 diabetes mellitus.
5. Middle-Aged Adults (Men Aged 45-65 Years, Women Aged 55-65 Years)
• every 1 to 2 years.
Older Adults (Older Than 65 Years)
• every year.
Children and Adolescents
• In children at risk for FH (e.g., family history of premature cardiovascular disease or
elevated cholesterol): 3; 9-11; 18 years of age
• >16 years: every 5 years; if they have
• ASCVD risk factors
• overweight or obesity
• insulin resistance syndrome
• family history of premature ASCVD
Recommendationsassociatedwiththis
question:
SÀNG LỌC
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497.
Abbreviations: ASCVD, atherosclerotic cardiovascular disease; FH, familial hypercholesterolemia.
9. Additional Screening Tests
Coronary artery calcification
•the need for more aggressive treatment strategies
hsCRP
•a standard risk assessment that is borderline
•intermediate or higher risk: LDL-C concentration less than 130 mg/dL
Lp-PLA2
•specificity than hsCRP, especially in the presence of hsCRP elevations
Homocysteine
•The routine measurement of homocysteine, uric acid, plasminogen activator inhibitor-1, or
other inflammatory markers is not recommended because the benefit of doing so is not
sufficiently proven (Grade D).
Carotid intima media thickness
•R34. Carotid intima media thickness may be considered to refine risk stratification to
determine the need for more aggressive ASCVD preventive strategies (Grade B; BEL
2).
Recommendationsassociatedwiththis
question:
Abbreviations: ASCVD, atherosclerotic cardiovascular disease; hsCRP, highly sensitive C-reactive protein; LDL-C, low-density lipoprotein cholesterol.
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497.
10. CÁC XÉT NGHIỆM
Coronary artery calcification
• the need for more aggressive treatment strategies
hsCRP
• a standard risk assessment that is borderline,
• an intermediate or higher risk with an LDL-C concentration less than 130 mg/dL
Lp-PLA2
• more specificity than hsCRP, especially in the presence of hsCRP elevations
Homocysteine
• homocysteine, uric acid, plasminogen activator inhibitor-1, or other
inflammatory markers is not recommended
Carotid intima media thickness
• the need for more aggressive ASCVD
Recommendationsassociatedwiththis
question:
Abbreviations: ASCVD, atherosclerotic cardiovascular disease; hsCRP, highly sensitive C-reactive protein; LDL-C, low-density lipoprotein cholesterol.
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497.
12. CÁC YẾU TỐ NGUY CƠ
family history of coronary artery disease (in male,first-degree relative
younger than 55 years; in female, first-degree relative younger than 65
years)
cigarette smoking
polycystic ovary syndrome
hypertension
low HDL-C (<40 mg/dL)
high LDL-C
chronic renal disease (CKD) stage 3/4,
evidence of coronary artery calcification and age (men =45; women =55
years).
Subtract 1 risk factor if the person has high HDL-C.
21. MỤC TIÊU ĐIỀU TRỊ
Risk category Risk factors/10-year risk
Treatment goals
LDL-C
(mg/dL)
Non-HDL-C
(mg/dL)
Apo B
(mg/dL)
Extreme risk
– Progressive ASCVD including unstable angina in individuals after
achieving an LDL-C <70 mg/dL
– Established clinical cardiovascular disease in individuals with DM,
stage 3 or 4 CKD, or HeFH
– History of premature ASCVD (<55 male, <65 female)
<55 <80 <70
Very high risk
– Established or recent hospitalization for ACS, coronary, carotid or
peripheral vascular disease, 10-year risk >20%
– DM or stage 3 or 4 CKD with 1 or more risk factor(s)
– HeFH
<70 <100 <80
High risk
– ≥2 risk factors and 10-year risk 10%-20%
– DM or stage 3 or 4 CKD with no other risk factors
<100 <130 <90
Moderate risk ≤2 risk factors and 10-year risk <10% <100 <130 <90
Low risk 0 risk factors <130 <160 NR
Barter PJ, et al. J Intern Med. 2006;259:247-258; Boekholdt SM, et al. J Am Coll Cardiol. 2014;64(5):485-494; Brunzell JD, et al. Diabetes Care.
2008;31:811-822; Cannon CP, et al. N Engl J Med. 2015;372(25):2387-2397; Grundy SM, et al. Circulation. 2004;110:227-239; Heart Protection Study
Collaborative Group. Lancet. 2002;360:7-22; Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497; Lloyd-Jones DM, et al.
Am J Cardiol. 2004;94:20-24; McClelland RL, et al. J Am Coll Cardiol. 2015;66(15):1643-1653; NHLBI. NIH Publication No. 02-5215. 2002; Ridker PM, J
Am Coll Cardiol. 2005;45:1644-1648; Ridker PM, et al. JAMA. 2007;297(6):611-619; Sever PS, et al. Lancet. 2003;361:1149-1158; Shepherd J, et al.
Lancet. 2002;360:1623-1630; Smith SC Jr, et al. Circulation. 2006;113:2363-2372; Stevens RJ, et al. Clin Sci. 2001;101(6):671-679; Stone NJ. Am J
Med. 1996;101:4A40S-48S; Weiner DE, et al. J Am Soc Nephrol. 2004;15(5):1307-1315.
Abbreviations: ACS, acute coronary syndrome; apo, apolipoprotein; ASCVD, atherosclerotic cardiovascular disease; CKD, chronic kidney disease; DM, diabetes mellitus;
HeFH, heterozygous familial hypercholesterolemia; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; NR, not recommended.
22. MỤC TIÊU ĐIỀU TRỊ
TG category TG concentration (mg/dL) TG goal
Normal <150
<150 mg/dL
Borderline high 150-199
High 200-499
Very high ≥500
TG levels that are even moderately elevated (≥150 mg/dL) may identify individuals at
risk for the insulin resistance syndrome. TG levels ≥200 mg/dL may indicate a
substantial increase in ASCVD risk. Hypertriglyceridemia is also commonly associated
with a procoagulant state and hypertension.
Einhorn D, et al. Endocr Pract. 2003;9:237-252; Frick MH, et al. NEJM. 1987;317:1237-1245; Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr
Practice. 2017;23(4):479-497; Keech A, et al. Lancet. 2005;366:1849-1861; NHLBI. NIH Publication No. 02-5215. 2002; Tenaknen L, et al. Arch Intern
Med. 2006;166:743-748.
Abbreviations: ASCVD, atherosclerotic cardiovascular disease; TG, triglycerides.
25. PHƯƠNG PHÁP ĐIỀU TRỊ
Treatment categories for dyslipidemia:
Lifestyle changes
Physical activity
Medical nutrition therapy
Smoking cessation
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497.
Abbreviations: apo, apolipoprotein; MTP, microsomal transfer protein; PCSK9, proprotein convertase subtilisin/kexin type 9.
Pharmacologic therapy
Statins
Fibrates
Omega-3 fish oil
Niacin
Bile acid sequestrants
Cholesterol absorption inhibitors
PCSK9 inhibitors
MTP inhibitor
Antisense apo B oligonucleotide
Combination therapies
26. PHƯƠNG PHÁP ĐIỀU TRỊ
Physical Activity
• at least 30 minutes of moderate-intensity physical activity [consuming 4-7
kcal/min] 4 to 6 times weekly, with an expenditure of at least 200 kcal/day)
• 10 minutes minimum per session
• aerobic activity, muscle-strengthening activity: at least 2 days/week
Medical Nutrition Therapy
• a reduced-calorie diet consisting of fruits and vegetables (combined ≥5
servings/day), grains (primarily whole grains), fish, and lean meats
• saturated fats, trans-fats, and cholesterol should be limited,
• plant stanols/sterols (~2 g/ day) and soluble fiber (10-25 g/day)
• Primary preventive nutrition consisting of healthy lifestyle habits is
recommended in all healthy children
Smoking Cessation
Recommendationsassociatedwiththis
question:
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497.
Abbreviation: LDL-C, low-density lipoprotein cholesterol.
27. PHƯƠNG PHÁP ĐIỀU TRỊ
Statins
Fibrates
• Fibrates should be used to treat severe hypertriglyceridemia (TG >500 mg/dL)
• Fibrates may improve ASCVD outcomes in primary and secondary prevention when
TG concentrations are 200 mg/dL and HDL-C concentrations <40 mg/dL
Recommendationsassociatedwiththis
question:
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497.
Abbreviations: ASCVD, atherosclerotic cardiovascular disease; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol;
TG, triglycerides.
28. Bile Acid Sequestrants
• reducing LDL-C and apo B and modestly increasing HDL-C, but they may increase TG
Omega-3 Fish Oil
• 2 to 4 g daily, should be used to treat severe hypertriglyceridemia (TG >500 mg/dL).
• Dietary supplements are not FDA-approved for treatment of hypertriglyceridemia and
generally are not recommended for this purpose
Combination Therapy
• Combination therapy of lipid-lowering agents should be considered when the LDL-C/ non-
HDL-C level is markedly increased with monotherapy
Recommendationsassociatedwiththis
question:
PHƯƠNG PHÁP ĐIỀU TRỊ
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497.
Abbreviations: apo, apolipoprotein; FDA, Food and Drug Administration; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein
cholesterol; TG, triglycerides.
29. PCSK9 Inhibitors
•combination with statin therapy for LDL-C lowering in individuals with FH.
•PCSK9 inhibitors: maximally tolerated statin therapy.
•They should not be used as monotherapy except in statin-intolerant individuals
Cholesterol Absorption Inhibitors
•Ezetimibe may be considered as monotherapy in reducing LDL-C and apo B, especially in statin-
intolerant individuals.
•Ezetimibe can be used in combination with statins
Niacin
•Niacin therapy: reduce TG
•Niacin therapy should not be used with statin
Recommendationsassociatedwiththis
question:
PHƯƠNG PHÁP ĐIỀU TRỊ
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497.
30. children and adolescents > 10 years old
LDL-C ≥190 mg/dL
LDL-C ≥160 mg/dL and
the presence of 2 or more cardiovascular risk factors, even
after vigorous intervention
having overweight or obesity,
or having other elements of the insulin resistance syndrome;
a family history of premature ASCVD (before age 55 years).
Statins, Fibrat, Ezetimibe
32. THEO DÕI ĐIỀU TRỊ
6 weeks after therapy initiation
6-week intervals until the treatment goal is achieved.
stable lipid therapy: 6- to 12-month
Liver transaminase: before and 3 months after niacin or fibric acid treatment.
Liver transaminase levels should be measured periodically thereafter (e.g., semiannually or annually)
Creatine kinase: myalgias or muscle weakness on statin therapy
Recommendationsassociatedwiththis
question:
Jellinger P, Handelsman Y, Rosenblit P, et al. Endocr Practice. 2017;23(4):479-497. Abbreviation: ASCVD, atherosclerotic cardiovascular disease.
polycystic ovary syndrome HỘI CHỨNG BUỒNG TRỨNG ĐA NANG
HeFH = heterozygous familial hypercholesterolemia tăng cholesterol máu gia đình dị hợp tử
Learn meat thịt nạc
Chế độ ăn
Lượng và loại lipid trong thức ăn
Tổng lượng lipid trong thức ăn nên khoảng 25-35% calo thu nhập. Khi lượng lipid >35% calo thu nhập thường liên quan đến tăng acid béo bão hòa và tăng calo thu nhập. Ngược lại, nếu lượng lipid quá thấp có nguy cơ làm giảm hấp thu vitamin E và các acid béo thiết yếu, góp phần làm thay đổi bất lợi trên HDL.
Loại lipid trong thức ăn
. Cơ thể người hấp thu lipid chủ yếu dưới dạng các acid béo tự do, và một phần nhỏ hơn là cholesterol
. Lượng acid béo bão hòa nên < 6 % calo thu nhập
. Lượng acid béo chuyển hóa <1% calo thu nhập
. Lượng cholesterol trong chế độ ăn lý tưởng nên < 150mg/ngày
. Nên ăn loại chứa nhiều acid béo không bão hòa đơn và acid béo không bão hòa đa n-3, n-6 (omega-3, omega-6)
. Lượng acid béo không bão hòa đa n-6 nên < 10% calo thu nhập
Bảng 3. Loại lipid và ảnh hưởng lên chuyển hóa, tim mạch[6]
Loại lipid
Ảnh hưởng lên chuyển hóa
Ảnh hưởng lên tim mạch
Acid béo bão hòa (SFA: saturated fatty acids)
-Tăng HDL-C và LDL-C
-Có thể thúc đẩy tạo huyết khối
-Tăng tỷ lệ bệnh ĐMV
-Có thể tăng nguy cơ ung thư tiền liệt tuyến, đại tràng
Acid béo không bão hòa đơn (MUFA: monounsaturated fatty acids)
-Giảm LDL-C nhẹ
-Tăng HDL-C
-Có thể cản trở quá trình oxy hóa
-Có thể giảm thấp bệnh ĐMV
Acid béo không bão hòa đa n-3 (PUFA: polyunsaturated fatty acids)
-Có thể giảm tạo huyết khối
-Quan trọng trong phát triển võng mạc và não
-Tăng tỷ lệ n-3/n-6 có thể giảm tỷ lệ bệnh ĐMV
-n-3 có thể tăng trọng lượng sinh
-Có thể ngừa đột tử tim
Acid béo không bão hòa đa n-6 (PUFA: polyunsaturated fatty acids)
-Acid arachidonic, chất quan trọng trong viêm
-Có thể giảm bệnh ĐMV
-Lượng nhiều có thể sinh ung thư
Acid béo chuyển hóa
(trans fatty acids) , chủ yếu từ hydrogen hóa PUFA trong công nghiệp thực phẩm
-Tăng LDL-C
-Giảm HDL-C
-Tăng Lp(a)
-Cản trở chuyển hóa PUFA
-Tăng tỷ lệ bệnh ĐMV
Carbonhydrate trong chế độ ăn
Lượng carbonhydrate nên chiếm khoảng 45-55% calo thu nhập. Khuyến khích ăn nhiều rau, trái cây, hạt, và ngũ cốc nguyên hạt.
Lượng đường cần giảm < 10%. Hạn chế các loại nước ngọt. Cần tiết chế chặt chẽ hơn với bệnh nhân có tăng cân hay tăng triglyceride máu.
Protein
Nên ăn các loại thịt trắng, thịt nạc,gia cầm, cá
Hạn chế thịt đỏ
Chất xơ
Những thực phẩm nhiều chất xơ hòa tan thường được dung nạp tốt, có hiệu quả giảm LDL-C. Liều khuyến cáo 5-15 g chất xơ hòa tan mỗi ngày.Để điều trị tốt mỡ máu, chế độ ăn cần 25-40g chất xơ, tối thiểu 7-13 g chất xơ hòa tan.
Nên ăn theo chế độ DASH (Dietary Approaches to Stop Hypertension)
Bảng 4. Chế độ ăn DASH cho người có nhu cầu 2100 calo/ngày
Tổng lượng mỡ
27% calo
Natri
2300 mg
Mỡ bão hòa
6% calo
Kali
4700 mg
Protein
18% calo
Calcium
1250 mg
Carbonhydrate
55% calo
Magne
500 mg
Cholesterol
150 mg
Chất xơ
30 g
Rượu
Lượng rượu tối đa mỗi ngày mà không làm tăng triglyceride là 20-30g với nam, và 10-20g ở nữ. Đối với người tăng triglyceride, khuyến cáo bỏ rượu.
Trường hợp bệnh nhân đáp ứng với điều trị
. Tiếp tục điều trị cùng loại và liều lượng statin đã cho trong 3-12 tháng
. Xem xét giảm liều statin khi LDL-C hai lần thử liên tiếp < 40 mg/dL
. Ngưng statin khi LDL-C < 20 mg/dL