this was the first lecture which i delivered as a doctor. it was about dyslipidemia. i hope you will find information valuable to you here. please read. let me know about your ideas. comment.
"48 SLIDES???!!", my friends shouted.
A boring "48 slides" is depend on how you arrange it. And this is not the one for sure.
I always love to prepare a short and sweet presentation. Or maybe long but sweet presentation? Oh yeah! Enjoy!
#SLIDESKILLSvsSLIDEKILLS
"48 SLIDES???!!", my friends shouted.
A boring "48 slides" is depend on how you arrange it. And this is not the one for sure.
I always love to prepare a short and sweet presentation. Or maybe long but sweet presentation? Oh yeah! Enjoy!
#SLIDESKILLSvsSLIDEKILLS
Management of hypertensive condition in 2020 according to AHA/ASA guidelines. We will discuss the presentation, clinical assessment, investigations, and management of hypertension along with major randomized controlled trials and guidelines.
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.
AR inherited disorder of impaired copper excretion characterized by excessive deposition of copper in many tissues and organs, principally the liver, brain, and eye. • Discovered by Samuel Alexander kinnier Wilson. Liver fails to excrete sufficient Cu via the bile, and the ability to incorporate Cu into CP is diminished Due to loss of function mutations of the ATP7B gene on chromosome 13, which encodes a copper-transporting ATPase (ATP7B). Most common presentations are with liver disease or neuro- psychiatric disturbances. Kayser–Fleischer ring is the clinical hallmark of WD. caused by deposition of copper in Desçemet’s membrane of cornea. Penicillamine is the of choice.
Diabetes mellitus (DM) has routinely been described as a metabolic disorder characterized by hyperglycemia that develops as a consequence of defects in insulin secretion, insulin action, or both.
Such a deficiency results in increased concentrations of glucose in the blood, which in turn damage many of the body's systems, in particular the blood vessels and nerves.
1. Microvascular (due to damage to small blood vessels).
2. Macrovascular (due to damage to larger blood vessels).
definition of heart failure, classification of heart failure, risk factors for heart failure, clinical features, general physical examination findings in heart failure
Deaths that are caused due to coronary heart disease CHD is a major cause of deaths in most of the population. Even though the mortality rate has been reducing, dyslipidemia is the major known risk factor in pathogenesis of CHD. In this paper we review the role of dyslipidemia and lipid changes that occur in men and women at different stages. We discuss about dyslipidemia causes symptoms and treatments and all the other issues that arise due to dyslipidemia. We talk about different drugs that are used in treating dyslipidemia and their side effects. Yong Yuan | Wen Chen | Lei Luo | Chen Xu "Dyslipidemia: Causes, Symptoms and Treatment" Published in International Journal of Trend in Scientific Research and Development (ijtsrd), ISSN: 2456-6470, Volume-5 | Issue-2 , February 2021, URL: https://www.ijtsrd.com/papers/ijtsrd38594.pdf Paper Url: https://www.ijtsrd.com/pharmacy/pharmaceutics/38594/dyslipidemia-causes-symptoms-and-treatment/yong-yuan
Management of hypertensive condition in 2020 according to AHA/ASA guidelines. We will discuss the presentation, clinical assessment, investigations, and management of hypertension along with major randomized controlled trials and guidelines.
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.
AR inherited disorder of impaired copper excretion characterized by excessive deposition of copper in many tissues and organs, principally the liver, brain, and eye. • Discovered by Samuel Alexander kinnier Wilson. Liver fails to excrete sufficient Cu via the bile, and the ability to incorporate Cu into CP is diminished Due to loss of function mutations of the ATP7B gene on chromosome 13, which encodes a copper-transporting ATPase (ATP7B). Most common presentations are with liver disease or neuro- psychiatric disturbances. Kayser–Fleischer ring is the clinical hallmark of WD. caused by deposition of copper in Desçemet’s membrane of cornea. Penicillamine is the of choice.
Diabetes mellitus (DM) has routinely been described as a metabolic disorder characterized by hyperglycemia that develops as a consequence of defects in insulin secretion, insulin action, or both.
Such a deficiency results in increased concentrations of glucose in the blood, which in turn damage many of the body's systems, in particular the blood vessels and nerves.
1. Microvascular (due to damage to small blood vessels).
2. Macrovascular (due to damage to larger blood vessels).
definition of heart failure, classification of heart failure, risk factors for heart failure, clinical features, general physical examination findings in heart failure
Deaths that are caused due to coronary heart disease CHD is a major cause of deaths in most of the population. Even though the mortality rate has been reducing, dyslipidemia is the major known risk factor in pathogenesis of CHD. In this paper we review the role of dyslipidemia and lipid changes that occur in men and women at different stages. We discuss about dyslipidemia causes symptoms and treatments and all the other issues that arise due to dyslipidemia. We talk about different drugs that are used in treating dyslipidemia and their side effects. Yong Yuan | Wen Chen | Lei Luo | Chen Xu "Dyslipidemia: Causes, Symptoms and Treatment" Published in International Journal of Trend in Scientific Research and Development (ijtsrd), ISSN: 2456-6470, Volume-5 | Issue-2 , February 2021, URL: https://www.ijtsrd.com/papers/ijtsrd38594.pdf Paper Url: https://www.ijtsrd.com/pharmacy/pharmaceutics/38594/dyslipidemia-causes-symptoms-and-treatment/yong-yuan
Complications of abnormal lipid levels
Generally, a high total cholesterol level (which includes LDL, HDL, and VLDL cholesterol), particularly a high level of LDL (the "bad") cholesterol, increases the risk of atherosclerosis and thus the risk of heart attack or strok
the aim of sharing this material to help students and provide delayed information regarding topic.You all are most welcome for you suggestion to make i more easy, graspable and attractive.(easy to learn in creative way)
CholesLo shows clinical significance in
helping reduce plasma cholesterol and
homocysteine levels and therefore affects
favourably the risk of subsequent development
of cardiovascular disease. Furthermore, our
findings suggest that the dose required to cause
such improvements in plasma lipid profile is
safe enough to be considered for use in general
population.
this guideline based on recent articles by major education establishments concerned with building national guidelines. please dont be hurry to make comments about use of IV aminophylline. aminiphylline used under some extra care and when other treatment options are failing. benefits of those treatments yet remain controversial. IV aminophylline has its own risks including the possibility of toxicity.
here give the knowledge that you should possess to manage acute and chronic urine retention. the lecture is more concerned about practical patient care and ward setting management. you should minimally be aware about following facts regarding urine retention. the multiple causes of retention will be discussed later in detailed manner. Direction of the lecture seems more toward BPH and acute retention management. beware there are many aspects of a patient present with an AUR. do no harm and always try to keep patient satisfaction. Let me know about your comments an Ideas. try to improve the quality. good luck.
Guidelines on massive blood transfusion(lecture-6)charithwg
it is a very short guideline about massive transfusion. please further read about complications about blood transfusions. and all the recommended reading are mentioned in the last slide. please read.
This is the fifth lecture. it is based on guidelines by NHS UK. the guidelines based are freely available in internet. the source and the used literature are trusted and accurate. i hope this level of a knowledge about the management side of the DKA touches the all areas of patient survival. patho-physiology not discussed here but will be discussed in another lecture in details. to a intern and final year MBBS students or ERPM students must process a level of knowledge described by the lecture. definitely more you read more knowledge you get. get the idea in the lecture and principles of management. so you will be much accurate in a ward. always take superior advice while managing emergencies.
Here i have made an introduction to the notification system in Sri Lanka. it is a component of national disease surveillance system. information here very important to final year MBBS and ERPM students.
This lecture is based on National guidelines(Sri Lanka) and guidelines by NHS UK. all the materials used to prepare the lecture are trusted and high in quality. also the books referred are internationally recognized. both hyper and hypokalemia management included in the lecture. lecture is free and you can even download. i kept no copy rights. i appreciate your support, comments and suggestions. also i would be grateful if you can make these lectures popular. wishing your success.
Organophosphate poisoning national guidelinecharithwg
publication by Dr-C.Here the given information are based on recommendations by sri lankan medical specialists who have dealt with the issue for a long time. it is quite obvious using agro chemical to deliberate self harm is a tendency in developing countries. it is common in agricultural ares.all the information are correct according to my knowledge. all the materials used to publish the slideshow are international publications. you have the full right to download and read. my personal request is to submit your ideas to me. and suggest different topics. i like to see your responses. i hope you would manage patients like these some day though it is so sad to see such incidents. be confident. do good. do not harm. be kind. keep us in your memories.
Lecture 1 tetanus vaccination in sri lankacharithwg
first lecture by Dr-C. its about tetanus immunization and prophylaxis. this will cover the basics of national immunization schedule which follows WHO recommendations and national advisory board for immunization.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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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.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
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
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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
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2. Short definition
◦ Dyslipidemias are disorders of lipoprotein metabolism,
including lipoprotein overproduction or deficiency. These
disorders may be manifested by elevation of the serum total
cholesterol, low-density lipoprotein (LDL) cholesterol and
triglyceride concentrations, and a decrease in the high-
density lipoprotein (HDL) cholesterol concentration.
3. Good and bad fats.
◦ Bad fats- trans fats (risk of atherosclerosis is high)
Artificial trans fats (or trans fatty acids) are created
in an industrial process that adds hydrogen to liquid
vegetable oils to make them more solid
◦ Good-monounsaturated and polyunsaturated fats (including
omega-3s)
Because risk of atherosclerosis is very less.
4. Why we have a strong concern about
dyslipidemias
◦ There is a strong relationship between elevated serum cholesterol levels
and the genesis of coronary heart disease. Coronary artery disease yet
remains one of the major killers in current society.
◦ There are variety of other diseases which have closer relation with
dyslipidemias. dyslipidemia remains major etiological factor of those
diseases.
6. Familial Hypercholesterolemia
◦Also known as primary
Hypercholesterolemia(dyslipidaemias)
◦They are classified in to few classes which is based on
the pattern of lipoproteins on electrophoresis or
ultracentrifugation
10. Diagnosis
◦ Clinical features-
◦ 1) Premature arcus senilis - a white or gray opaque ring in the
corneal margin
◦ 2) Tendon xanthomata - these are hard, non-tender nodular
enlargement of tendons. They are most commonly found on
the knuckles and the Achilles tendons.
◦ 3) Xanthelasmas - fatty deposits in the eyelids.
11. Lipid profile
◦ Traditionally, most laboratories have required patients to fast for 9–12 hours before screening.
However, recent studies have questioned the utility of fasting before lipid panels, and some
diagnostic labs now routinely accept non-fasting samples.
◦ The lipid profile typically includes:
◦ Low-density lipoprotein (LDL)
◦ High-density lipoprotein (HDL)
◦ Triglycerides
◦ Total cholesterol
◦ Using these values, a laboratory may also calculate:
◦ Very low-density lipoprotein (VLDL)
◦ Cholesterol:HDL ratio
12. Cholesterol:HDL ratio
◦Your cholesterol ratio is calculated by dividing your total
cholesterol by your HDL number. For instance, if your
total cholesterol is 180 and your HDL is 82, your
cholesterol ratio is 2.2. According to the American Heart
Association (AHA), you should aim to keep your ratio
below 5, with the ideal cholesterol ratio at 3.5. this
number represents the risk of a CV disease. Risk increase
with the number.
13. Total cholesterol levels in a lipid profile
◦ A total cholesterol level of less than
200 mg/dL (5.17 mmol/L) is normal.
◦ A total cholesterol level of 200 to 239 mg/dL (5.17 to
6.18 mmol/L) is borderline high.
◦ A total cholesterol level greater than or equal to
240 mg/dL (6.21 mmol/L) is high.
14. TG levels
◦ Triglycerides — High triglyceride levels are also associated with an increased risk of
cardiovascular disease
◦ Normal - less than 150 mg/dL (1.69 mmol/L)
◦ Borderline high - 150 to 199 mg/dL (1.69 to 2.25 mmol/L)
◦ High - 200 to 499 mg/dL (2.25 to 5.63 mmol/L)
◦ Very high - greater than 500 mg/dL (5.65 mmol/L)
15. HDL levels
◦ A level greater than or equal to 60 mg/d is exelent level.
◦ while levels of HDL cholesterol less than 40 mg/dL lower than desired.
16. Familial hypecholesterolaemia
◦ Familial hypercholesterolaemia
◦ Suspect familial hypercholesterolaemia where:
◦ Adults have a raised TChol concentration (typically >7.5 mmol/L) and there is
a personal or family history of premature CHD.
◦ Rule out secondary causes of hypercholesterolaemia.
◦ Do not rule out familial hypercholesterolaemia simply because physical signs
such as tendon xanthomata are not present.
◦ Make a diagnosis using the Simon Broome criteria
◦ Check two fasting LDL-C measurements to confirm the diagnosis.
17. The Simon Broom diagnostic criteria
for diagnosing familial
hypercholesterolemia
◦ Definite familial hypercholesterolaemia is diagnosed if an individual has:
◦ A TChol level in an adult of >7.5 mmol/L (>6.7 mmol/L in a child) and an LDL-C of >4.9 mmol/L
(>4.0 mmol/L in a child); PLUS
◦ Tendon xanthomata or evidence of these signs in a first-degree or second-degree relative; OR
◦ DNA evidence of an LDL receptor mutation, familial defective apo-B-100 or a PCSK9 mutation.
◦ Possible familial hypercholesterolaemia should be diagnosed if the cholesterol concentrations fit
these criteria and the individual has at least one of the following:
◦ A family history of myocardial infarction in a second-degree relative aged 50 years or younger,
or in a first-degree relative aged 60 years or younger.
◦ A family history of raised TChol greater than 7.5 mmol/L in adult first-degree or second-degree
relatives or greater than 6.7 mmol/L in a child, brother or sister aged younger than 16 years.
18. Familial combined hyperlipidaemia
◦ This is the most common genetic dyslipidaemia, occurring in about 1
in 100 people but is usually polygenic in origin.
◦ Lipid phenotypes in familial combined hyperlipidaemia vary
considerably but suspect where:
◦ There is family history of hyperlipidaemia or premature CHD not due
to familial hypercholesterolaemia.
◦ Moderate-to-severe mixed hyperlipidaemia (typically TChol 6.5-8.0
mmol/L and TG 2.3-5.0 mmol/L).
19. Short description about lipoproteins
◦ VLDL Very-low-density lipoprotein
◦ Makes up 10%-15% of total cholesterol
◦ With LDL, the main form of "bad" cholesterol
◦ A precursor of LDL.
◦ LDL Low-density lipoprotein
◦ Makes up 60%-70% of total cholesterol
◦ Main form of "bad" cholesterol
◦ Causes build up of plaque inside arteries.
20. continued
◦ HDL High-density lipoprotein
◦ Makes up 20%-30% of total cholesterol
◦ The "good" cholesterol
◦ Moves cholesterol from arteries to the liver.
21. Atherosclerosis
◦ Atherosclerosis, or hardening of the arteries, is a condition in
which plaque builds up inside the arteries. Plaque is made of
cholesterol, fatty substances, cellular waste products, calcium
and fibrin (a clotting material in the blood).
Atherosclerosis is a type of arteriosclerosis. Arteriosclerosis is
a general term for the thickening and hardening of arteries.
22. Pathology
◦ 1)endothelial damage-(smoking,hypertension,elevated blood
cholesterols.)
◦ 2)fatty streak formation in the vessel wall.
◦ 3) These accumulations contain both living, active WBCs
(producing inflammation) and remnants of dead cells,
including cholesterol and triglycerides.
◦ 4)Calcification of the lesion.
◦ 5)reduction in the arterial wall diameter and elasticity.
26. Risk factors for atherosclerosis
◦ increasing age
◦ gender (At younger ages, males are more at risk. Premenopausal women are relatively
protected; after menopause the risk in women increases and eventually exceeds the risk in
males.)
◦ family history
◦ genetic abnormalities (yet fully not explained)
◦ Hyperlipidemia
◦ Hypertension
◦ Cigarette smoking (smoking potentiates the other risk factors)
◦ Diabetes
◦ C-reactive protein level (increased in atherosclerosis)
27. Lesser or uncertain risk factors
◦ Obesity
◦ Physical inactivity
◦ Stress
◦ Postmenopausal estrogen deficiency
◦ High carbohydrate intake
◦ Lipoprotein (a) (an altered form of LDL that seems to be independently associated with
increased risk of atherosclerosis)
◦ Trans-fat intake
28. Diseases associated with atherosclerosis
◦Most common disease is IHD
◦Carotid artery disease.
◦PVD+/_leriche Xd
◦Chronic kidney disease due to atherosclerosis of renal
artery.
29. Total cardiovascular risk assessment.
◦Total cardiovascular risk estimation means the
likelihood of a person developing an atherosclerotic
CV event over a defined period of time.
◦Most guidelines use risk estimation systems based on
either the Framingham or the SCORE(Systemic
Coronary Risk Estimation) projects
30. Basics-when to use a risk estimation
system
(1) Those with
◦ † known CVD
◦ † type 2 diabetes or type 1 diabetes with
◦ microalbuminuria
◦ † very high levels of individual risk factors
◦ † chronic kidney disease (CKD)
They are automatically categorized in high risk group. While they need prompt medical
management to cover all the risk factors.
31. Basics-when to use a risk estimation
system
◦ All the other patients not falling in above mentioned criteria
should assessed with a risk estimation system like SCORE.
32. ◦ Risk estimation systems including firmingham and SCORE are
somewhat similar. Once you are familiar with one system you
can easily adapt other system. As an example here we are
using SCORE system to calculate risk.(risk estimation systems
will change with the dynamics of the medical knowledge and
newer recommendations by clinicians)
33. SCORE (developed in EU)
◦ The SCORE system estimates the 10 year risk of a first fatal
atherosclerotic event, whether heart attack, stroke, or other
occlusive arterial disease, including sudden cardiac death.
34.
35.
36. SCORE
◦The SCORE data indicate that the total CVD
event risk is about three times higher than the
risk of fatal CVD for men, so that a SCORE risk
of 5% translates into a CVD risk of 15% of total
(fatal plus non-fatal)
37. SCORE
◦Clinicians often ask for thresholds to trigger
certain interventions, but this is problematic
since risk is a continuum and there is no
threshold at which, for example, a drug is
automatically indicated,
38. Risk groups depending of SCORE
system-Very High Risk
◦ Subjects with any of the following falls this category.
◦ Documented CVD by invasive or non-invasive testing (such as coronary
angiography, nuclear imaging, stress echocardiography, carotid plaque on
ultrasound), previous myocardial infarction (MI), ACS, coronary
revascularization [percutaneous coronary intervention (PCI), coronary artery
bypass graft (CABG)] and other arterial revascularization procedures, ischaemic
stroke, PAD.
◦ Patients with type 2 diabetes, patients with type 1 diabetes with
◦ Patients with moderate to severe CKD
◦ A calculated 10 year risk SCORE ≥10%.
39. Risk groups depending of SCORE
system-High Risk
◦ Subjects with any of the following:
◦ † Markedly elevated single risk factors such as familial
dyslipidaemias and severe hypertension.
◦ † A calculated SCORE ≥5% and ,10% for 10 year risk of fatal
CVD.
40. Risk groups depending of SCORE
system-Moderate Risk
◦ Subjects are considered to be at moderate risk when their
SCORE is ≥1% and ,5% at 10 years.
41. Risk groups depending of SCORE
system-Moderate Risk
◦The low risk category applies to individuals with
SCORE ,1%.
42. About What the patient should be
adviced?
◦ 1)lifestyle-diet, exercise
◦ 2)Controlling the causes of secondary hyperlipidemia.
◦ 3)Controlling DM.
◦ 4)timely medical assessments.
◦ 5)importance of drug compliance.
◦ 6)well know side effects of therapy.
◦ 7)adequate knowledge about IHD.
43. Which patients should be treated?
◦ The most important factor to consider is a person's long-term
risk of experiencing a heart attack or stroke. If the risk is very
low, there is probably no need for statins, unless the LDL is
above 190 mg/dL (4.9 mmol/L). If the risk is very high — for
example, someone who has had a heart attack in the past —
the person may benefit from statins, even if his or her
cholesterol is not elevated.
44. New guidelines from the American
College of Cardiology
◦ People who already have cardiovascular disease. This group includes people who have had
heart attacks, strokes caused by blockages in a blood vessel, mini-strokes (transient ischemic
attacks), peripheral artery disease, or prior surgery to open or replace coronary arteries.
◦ People who have very high LDL (bad) cholesterol. This group includes adults who have LDL
cholesterol levels of 190 mg/dL (4.9 mmol/L) or higher.
◦ People who have diabetes. This group includes adults who have diabetes and an LDL between
70 and 189 mg/dL (1.8 and 4.9 mmol/L), especially if they have evidence of vascular disease.
◦ People who have a higher 10-year risk of heart attack. This group includes people who have
an LDL above 100 mg/dL (1.8 mmol/L) and whose 10-year risk of a heart attack is 7.5 percent or
higher.
45. Manage hypertriglyceridaemia
◦ Controlling triglyceride levels decrease risk of IHD.
◦ Also prevents Pancreatitis.
◦ (elevated triglycerides also cause hepatomegaly and splenomegaly)
◦ Treatment options-Fibrates, Niacine, Omega-3 fatty acids.
◦ Statins may use as a combined therapy. (statin and a
◦ fibrate, particularly fenofibrate, bezafibrate, or ciprofibrate)
◦ Better management of triglycerides helps to lower the VLDL levels.
46. How to manage low HDL levels.
◦ Low HDL levels increase the risk of IHD.
◦ Low HDL levels can be treated with-
◦ 1) Statins produce modest elevations in HDL-C
◦ 2)nicotinic acid-Nicotinic acid appears to increase HDL-C by partially reducing HDL
catabolism and mainly by increasing apo A1 synthesis by the liver.
◦ (fibrates has a small ability to elevate HDL levels though there is no therapeutic
advantage)
◦ 3)Cholesteryl ester transfer protein inhibitors(new drug group and very effective)
torcetrapib, dalcetrapib, and anacetrapib
47. Management of LDL levels
◦ Statins-Statins reduce synthesis of cholesterol in the liver by competitively inhibiting HMG-CoA
reductase activity.
◦ Commonly used statins-
◦ atorvastatin (Lipitor),
◦ fluvastatin (Lescol, Lescol XL),
◦ lovastatin (Mevacor, Altoprev),
◦ pravastatin (Pravachol),
◦ rosuvastatin (Crestor),
◦ simvastatin (Zocor), and
◦ pitavastatin (Livalo).
48. Statins are widely used in sri lanka. What
do we need to know about statins?
◦ Usually statins are metabolized in liver.
◦ There are two serious sideeffects which a clinican must be aware of.
◦ 1)myopathy which may progress in to rhabdomyolysis. (myoglobin levels will be increased
causing acute renal failure.) one of the signs of myopathy and muscle damage elevated CPK.
◦ 2)hepatocellular damage.(clinicians usually assess this condition by periodical measurement
of ALT levels. If the AST levels are elevated a repeat AST must be done. And if the AST levels
are high as three folds that of normal statins will be discontinued.
Statins may elevate blood sugar levels mildly.(though statins shouldn’t omit).
Combining statins with fibrate increases the possibility of myopathy.
49. Cholesterol absorption inhibitors.
◦ intestine absorbs the cholesterol from your diet and releases it into your bloodstream. The drug
ezetimibe (Zetia) helps reduce blood cholesterol by limiting the absorption of dietary
cholesterol. Ezetimibe can be used in combination with a statin drug.
◦ Ezetimibe is the first lipid-lowering drug that inhibits intestinal uptake of dietary and biliary
cholesterol
◦ And the advantage this drug will not interfere with absorption of other lipid soluble nutrients.
50. Bile-acid-binding resins (Bile acid
sequestrants)
◦ cholestyramine
◦ Colestipol
◦ these are bile acid binding exchange resins.
51. Nicotinic acid
◦ Nicotinic acid has a broad lipid modulating action. In can
increase the HDL levels, decrease the LDL levels and
triglyceride levels.
◦ This can be used with statins.
52. Diet.
◦ There are many internet resources regarding diet therapy and food for dyslipidaemic patients.
◦ As a overview there is a huge encouragement toward use of vegetables and fruits.
◦ Indeed a good diet plays a major role in managements of atherosclerosis.
◦ Role dietician is very important.
53. Resources and references.
◦ Dyslipidaemia management guidelines by European society of cardiology.
◦ Web portal of American association of family physicians.
http://www.aafp.org/afp/1998/0501/p2192.html
◦ Hyperlipidaemia- http://patient.info/health/hyperlipidaemia-leaflet
◦ Web page myoclonic USA.-http://www.mayoclinic.org
◦ Atherosclerosis-
http://www.heart.org/HEARTORG/Conditions/Cholesterol/WhyCholesterolMatters/Atherosclerosis_UC
M_305564_Article.jsp#.WDpbdUVlSs0
◦ Hyperlipidaemia-http://www.rightdiagnosis.com/h/hyperlipidaemia/complic.htm
◦ GP notebook fedrickson classification
http://www.gpnotebook.co.uk/simplepage.cfm?ID=x20020617063512021840
◦ Primary dyslipidaemias Maersk manual http://www.merckmanuals.com/professional/endocrine-and-
metabolic-disorders/lipid-disorders/dyslipidemia