This document provides an overview of dyslipidemia. It defines dyslipidemia as abnormal levels of lipids in the blood such as total cholesterol, LDL cholesterol, triglycerides, and others. The document then discusses the epidemiology of dyslipidemia, noting that over half of US adults over age 20 have total cholesterol levels at or above 200 mg/dL. It also summarizes the Fredrickson classification system for different types of hyperlipidemias based on abnormal lipid levels and lipoproteins. The document concludes by listing some of the primary genetic causes of hypercholesterolemia and hypertriglyceridemia.
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)
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#SLIDESKILLSvsSLIDEKILLS
Dyslipidemia
Disorder of Lipid & Lipoprotein Metabolism
A common form of Dyslipidemia is characterized
by three lipid abnormalities:
Elevated triglycerides,
Elevated LDL and
Reduced HDL cholesterol.
Important Modifiable Risk Factor for CAD
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)
"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
Dyslipidemia
Disorder of Lipid & Lipoprotein Metabolism
A common form of Dyslipidemia is characterized
by three lipid abnormalities:
Elevated triglycerides,
Elevated LDL and
Reduced HDL cholesterol.
Important Modifiable Risk Factor for CAD
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.
The high risks of lipids and its relevance towards the development of different cardiovascular diseases has been known to all where this present slide focuses on that only along with the different treatment procedures,.
Hyperlipidemia , dyslipidemia , and drug therapy
also Fat transport and metabolisim and pathophysiology of lipoprotein
clincal importance of
1. Hypertriglycredemia
2. Hypercholesterolemia
3.Combined hyperlipidemia
4. Some other lipoprotein disorders
Including disorder of HDL_C
Diabetic Dyslipidemia
By Dr. Usama Ragab Youssif
ISMA CME Activity 2021
In Tolip EL Galala Hotel
-----------
Introduction
Physiology of lipid metabolism
Pathophysiology of diabetic dyslipidemia
Statin therapy (+/- ezetimibe) evidence and translation of evidence
Residual CV risk: excess TG
EPA therapy evidence and translation of evidence
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.
The high risks of lipids and its relevance towards the development of different cardiovascular diseases has been known to all where this present slide focuses on that only along with the different treatment procedures,.
Hyperlipidemia , dyslipidemia , and drug therapy
also Fat transport and metabolisim and pathophysiology of lipoprotein
clincal importance of
1. Hypertriglycredemia
2. Hypercholesterolemia
3.Combined hyperlipidemia
4. Some other lipoprotein disorders
Including disorder of HDL_C
Diabetic Dyslipidemia
By Dr. Usama Ragab Youssif
ISMA CME Activity 2021
In Tolip EL Galala Hotel
-----------
Introduction
Physiology of lipid metabolism
Pathophysiology of diabetic dyslipidemia
Statin therapy (+/- ezetimibe) evidence and translation of evidence
Residual CV risk: excess TG
EPA therapy evidence and translation of evidence
Definition:
Many childhood conditions are caused by gene mutations that encode specific proteins. These mutations can result in the alteration of primary protein structure or the amount of protein synthesized.
The functional ability of protein, whether it is an enzyme, receptors, transport vehicle, membrane, or structural element, may be relatively or seriously compromised.
These hereditary biochemical disorders are collectively termed as ‘’Inborn errors of metabolism’’
The prolong complications of coronary artery disease such as angina pectoris, myocardial infarction, cardiac heart failure, its management and surgical mgt.
Management Of Nephrotic Syndrome
Objectives
To briefly review the definition & etiology of nephroticsyndrome.
To understand the terminology pertaining to clinical course of nephroticsyndrome.
To understand the management of nephroticsyndrome:Specific management & Supportive care and management of complications
Management of congenital nephrotic syndrome
Comprehensive description of various primary dyslipidemias, cholesterol transport and molecular mechanisms involved.
View in slideshow after downloading for better experience.
Prepared in Dec 2013.
What are lipoproteins?
Structure of lipoprotein complex.
Classification of lipoproteins.
Important enzyme and protein involved in lipoprotein metabolism.
Apolipoprotein.
Lipoprotein metabolism.
Clinical disorders
Importance of lipoprotein.
Conclusion
Reference.
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.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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.
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
- 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
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
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
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MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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.
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
1. DYSLIPIDEMIA
Integrated Therapeutics I Seminar
Msc, Clinical Pharmacy PG Study
School of Pharmacy, JU
Moti Deressa hundera
Jimma, Oromia, Ethiopia
September 2009
3. Cholesterol – A Hot Topic
CVD & death
Prevalence of CVD is worldwide.
Major,independent risk factors of
ajor,i
atherosclerosis
Hypertriglyceridemia :acute pancreatitis
Robs dollar: 17% of total direct health care
costs
Huge profit: WOW! PROVE-IT Trial 4
4. CHD Risk Factors ranking - PROCAM Study
Risk factor Relative risk P Value
Smoking 2.3 0.001
LDL cholesterol (mg%)
> 100 but < 160 1.9 0.01
> 160 4.3 0.001
Hypertension (SBP > 140; DBP > 90) 1.8 0.001
HDL cholesterol (mg%)
40 to 55 1.7 0.01
< 40 2.7 0.001
Triglycerides (mg%)
105- 167 1.6 0.01
>167 2.6 0.001
Fasting blood glucose (mg%)
110 - 126 1.4 0.05
> 126 1.9 0.01
Family history of MI 1.4 4
0.05
5. 5
Why much concern…?
Relative risk of CHD
Additive Effect
4.5 3
1.6
Smoking 16 SBP >160
6
5
4
Dyslipidemia
With DM all risks are doubled
5
6. Definition: Hyperlipidemia
abnormal levels of lipids in blood
TC, LDL-cl, TG, apo-B, or Lp(a) above the 90th
percentile
,Or HDL-c or apo A-1 <10th percentile
several forms:
– Hyperlipoproteinemia: lipoprotein
– Hyperlipidemia: TG & cholesterol
– Hypertriglyceridemia: TG only
– Hypercholesterolemia: cholesterol 6
1
7. Major Plasma & lipoproteins:
Typetypes
Source Major lipid Apoproteins ELFO
Athero-
genicity
–
Chylomicr Dietary A-I, B-48, no
Gut
ons TGs C-I, C-III, E mobility (pancreat
itis)
Endogeno B-100, E,
VLDL Liver us C-II, C- Pre-β +
TGs III,
VLDL Ch esters, B-100, C- Slow
IDL +
remnant TGs III, E pre- β
VLDL, 7
LDL Ch esters B-100 β +++ 7
IDL
anti-
8. Epidemiology
Prevalence ???
2002 audit of GP practices in England >50% US adults > 20 yrs have
TC ≥200 mg/dL.
Patients with CVD
Detected & Controlled > 1/2 of borderline to high risk
remain unaware
Detected & Uncontrolled <1/2 of highest-risk are on
drug therapy
only 1/3 are achieving their
LDL goal
Undetected <20% of CHD patients are at
their LDL goal
NHANES, : 199-2000
Br J Cardiol 2006;13:145
9. 9
Intestinal Cholesterol Absorption
Intestinal Biliary Dietary
epithelial cell cholesterol cholesterol
Through
lymphatic
system to
the liver MTP
CM Cholesteryl esters
Luminal
cholesterol
ACAT excretion Bile
(esterification)
acid
ABCG5 Micellar
ABCG8
cholesterol
Free
cholesterol uptake
Bays H et al. Expert Opin Pharmacother 2003;4:779-790.
20. Screening
Diagnosis: ATP III of NCEP
- For all above 20 yrs
Symptoms: once in q 5 years
– asymptomatic,
– xanthomas, enlargement of
liver or spleen, pancreaitis, - For those above 45
Atherosclerosis yrs – once in 2 years
FMH
- For those with
PE already known lipid
abnormality follow-up q
lipid panel 3-6 months
LDL = TC– (HDL +
TG/5)
21. Management: principle
Treat according to global risk level, not only cholesterol value
Achieve at least a 30% to 40% reduction in LDL-C
Initial therapy for any lipoprotein disorder is therapeutic
lifestyle changes, TLC
TLC in all patients with lifestyle-related risk factors regardless of
LDL-C level
any potential underlying medical problems
Initiation & Selection of Drug therapy
Monitor for efficacy and safety
22. Mgt: Goals for Lipids
LDL HDL
– < 100 →Optimal
– < 40 → Low
– 100-129 → Near optimal
– 130-159 → Borderline – ≥ 60 → High
– 160-189→ High Serum Triglycerides
– ≥ 190 → Very High – < 150 → normal
Total Cholesterol – 150-199 →
– < 200 → Desirable Borderline
– 200-239 → Borderline – 200-499 → High
– ≥240 → High
– ≥ 500 → Very High
23. 23
Treatment Strategy
Lipid Profile, Risk Assessment
LDL > 100 Look For Sec. Causes
Treat the cause, if found
Treatment
NO CHD
CHD +
Primary Prevention
Sec. Prevention
LDL < 130
2 or more < 2 RF
RF
High Risk Low Risk
LDL > 100 LDL <160
25. Updated NCEP ATP III: Risk Categories,
LDL-C Goals, Treatment Cutpoints
LDL-C goal Initiate TLC* Consider drug Tx
Risk category (mg/dL) (mg/dL) (mg/dL)
High risk
CHD and CHD <100 ≥100 ≥100
risk equivalents (optional goal: <70) (<100: drug optional)
(10-year risk >20%)
Moderately high risk
≥2 risk factors <130 ≥130 ≥130
(10-year risk 10%-20%) (optional goal: <100) (100-129: drug optional)
Moderate risk
≥2 risk factors ≥130 ≥130 ≥160
(10-year risk <10%)
Lower risk
0–1 risk factor† <160 ≥160 ≥190
(160-189: drug optional)
*TLC=therapeutic lifestyle changes
†Almost all people with a 0–1 risk factor have a 10-year risk 25
<10%; thus, risk calculations are not necessary Grundy SM et al. Circulation. 2004;110:227-239.
26. Therapeutic Lifestyle Changes ,TLC
TLC Nutrient Recommended Intake
TLC Diet Saturated fat < 7% of calories
PUFA fat Up to 10% of calories
MUFA fat Up to 20% of calories
Weight Total fat 25–35% of calories
reduction Carbohydrate 50–60% of calories
Fiber 20–30 grams per day
Protein Approx. 15% of calories
physical Cholesterol Less than 200 mg/day
activity
DIETARY THERAPY
26
28. Progression of Drug Therapy for
LDL-C Lowering
Visit 1 Visit 2 Visit 3 F/U
q
6 6 Visits
Initiate LDL-
LDL- If LDL goal If LDL goal 4–6 Monitor
lowering wks not achieved, wks not achieved, mo response &
drug intensify LDL-
LDL- drug therapy adherence
therapy lowering or refer to a to therapy
therapy lipid specialist
Start statin Consider If LDL goal
or bile acid higher dose of has been
resin or the statin or achieved,
nicotinic add a bile acid treat other
acid resin or lipid risk
nicotinic acid factors
Expert Panel on Detection, Evaluation, and Treatment of High Blood
Cholesterol in Adults. JAMA 2001;285:2486-2497.
29.
30. 30
Treatment of ↓ HDLc
Low HDLc
Therapeutic Lifestyle Change
Drug Therapy
Therapy of Choice : Niacin
Add on drug - Finofibrate
31. 31
Treatment of ↑ TG
High TG
Therapeutic Lifestyle Change
Drug Therapy
Therapy of Choice : Fibrate
Add on drug – Statin, Niacin
32. Treatment of Mixed Hyperlipidemia
High LDL-C and TGs
LDL-
Therapeutic Lifestyle Change
Drug Therapy
STEP 1 Achieve the LDL-C goal: statins
LDL-
Therapy of Choice : Statin + Fibrate
Achieve the non-HDL-C goal
non-HDL-
STEP 2 Increase LDL-C lowering or
LDL-
Add a fibrate, niacin or fish oils
Expert Panel on Detection, Evaluation, and Treatment of High Blood
Cholesterol in Adults. JAMA 2001;285:2486-2497.
33. ATP III: The Metabolic Syndrome
Diagnosis is established when ≥3 of these risk factors are present.
Risk Factor Defining Level
Abdominal obesity
(Waist
circumference) >102 cm (>40 in)
Men >88 cm (>35 in)
Women
TG ≥150 mg/dL
HDL-C
Men <40 mg/dL
Women <50 mg/dL
Blood pressure ≥130/≥85 mm Hg
Expert Panel on Detection, Evaluation, and Treatment of High 33
≥110
Cholesterol in Adults. JAMA 2001;285:2486-2497. mg/dL
Blood Fasting glucose
34. 34
Statins – Mechanism of Action
Cholesterol VLDL
synthesis LDL receptor–mediated
receptor–
LDL receptor Apo
VLDLR
B hepatic uptake of LDL& VLDL
HMGCoA (B–E receptor)
(B– Apo remnants
E Serum LDL-C
LDL-
Intracellular synthesis Apo
Cholesterol LDL Serum VLDL remnants
B
Serum IDL
Hepatocyte Systemic Circulation
1. Reduce hepatic cholesterol synthesis (HMG CoA),
CoA),
2. lowering intracellular cholesterol,
3. Upregulation of LDL receptor and
4. ↑ the uptake of non-HDL from circulation.
non-
35. The LDL-C–Lowering Efficacy of the
Currently Available Statins
Daily Atorv
Dose a Fluva Lova Prava Simva
10 mg –39% –22% –30%
20 mg –43% –22% –27% –32% –38%
40 mg –50% –25% –32% –34% –41%
80 mg –60% –36% –42% –47%
Physician’s Desk Reference. 55th ed. Montvale, NJ: Medical 35
Economics, 2001.
36. 36
CHD Risk Reduction – Statin Therapy
Relative Risk Reduction (%)
Endpoints +20 0 –5 –10–15–20–25–30–35–40–45–50
Major coronary events
Coronary deaths
Cardiovascular deaths
Non_CV events
Total mortality
Strokes
Intermittent
claudication
Angina
La Rosa JC et al. JAMA 1999;282:2340-2346.
37. Fibrates
⇑ FA oxidation in muscle and liver and lipogenesis in the liver
Most effective at reducing VLDL (TG); smaller ↓ in LDL-chol but
useful ↑ in HDL-chol
α
Act as PPARα ligands (cf glitazones) -
38. Fibric Acid Derivatives
Indications: Adjunctive therapy to diet
Hypertriglyceridemia (Type IV and V)
Combined hyperlipidemia (Type IIb) with low
HDL-C who do not respond to nicotinic acid
Mechanism of Increase peripheral lipolysis and decrease
Action: hepatic TG production
Efficacy: Decrease TG 25–50%
LDL-C decreases, remains the same, or increases
Increase HDL-C 15–25% in hypertriglyceridemia
Side Effects: GI upset (8%), cholelithiasis, myositis, abn LFTs
Contraindications: Hepatic or renal dysfunction
Pre-existing gallbladder disease
Intervention Trials: HHS, VA-HIT, BIP, LOCAT, BECAIT, DAIS
38
39. 39
Bile Acid Resins: Mechanism of Action
↑↑ Cholesterol 7-α
7-
Gall Bladder hydroxylase
Bile Acid ↑ Conversion of
cholesterol to BA
Enterohepatic Recirculation
↑ BA Secretion Liver
Terminal Ileum
↑ LDL Receptors
Reabsorption
of bile acids ↑ VLDL and LDL removal
↑ BA
Excretion
Net Effect - ↓ LDL-C
LDL-
40. 40
Nicotinic Acid – Mechanism of Action
Mobilization of FFA
Apo B
Serum VLDL
results in reduced
VLDL VLDL lipolysis to LDL
TG
synthesis VLDL Serum LDL
secretion
LDL
HDL
Liver Circulation
Hepatocyte Systemic Circulation
Decreases hepatic production of VLDL and of apo B
41. 41
Effect of Niacin on Lipoproteins
35%
HDL-
HDL-C with crystalline niacin
25%
HDL-
HDL-C with Niaspan®
12.5%
Baseline LDL-
LDL-C with Niaspan®
-15% LDL-
LDL-C with crystalline niacin
TG with Niaspan®
-30% TG with crystalline niacin
0 1g/d 2g/d 3g/d
Adapted from Knopp RH. N Engl J Med 1999;341:498-511..
43. Fish Oils
Indication Adjunctive therapy to diet
s: Hypertriglyceridemia (Type IV and
V)
With statins or other LDL-C–
lowering drugs in mixed
hyperlipidemia
Efficacy: Decrease TG 30–40%
LDL-C remains the same or
increases
No change in HDL-C
Side
GI upset and a “fish burp”
Effects:
43
Interventi Lyon Heart Study (dietary), GISSI
on Trials: Prevenzione Trial, others
45. Dyslipidemia and DM
Elevated TG
Elevated VLDL Type Rx used Effect on lipids
Insulin Favourable
Reduced HDL-C Metformin Mildly favourable
Increase in SD-LDL Sulfonylureas Not favourable
Decrease in Apo A I Glitazones Favourable
Acarbose No effect
Increase in Apo B
Apo A I / Apo B < 1
All Diabetics must be given STATIN 45
46. 46
Hypertension Treatment and Lipids
Type Rx used Effect on lipids
1. Diuretics Unfavourable
2. Indapamide Mildly favourable
3. ACEi and ARB Very favourable
4. Betablockers Unfavourable
5. Ca channel blockers No effect
47. Special consideration
Elderly: Women
– Start slow & go slow HDL > LDL ?
– ↓ absolute risk More responsive than
reduction ?? men
Children: Pregnancy: Not
– < 10 years: No drug recommended
therapy!
- High risk: BAR,
– 10-20: d/t guideline
Ezetimibe?
– First line: BAR→
statins Menopause?
48. BOTTOM LINE
Hyperlipidemia is a modifiable risk factor for
IHD and stroke
1° & 2° prevention of ASCVD are
possible!
TLC is a must !
Intervention with a statin is highly effective and
can reduce risk by ~ 1/3rd
Follow up
49. Where are we heading ? ?
20000 B.C. 2004
Paleolithic sup. age Neolithic age 19th century 21st century
Technology has changed a lot in the way we live
Processed
Hunting-gathering foods
subsistence
- Animal fats
and glucides
High level of
¯ Dietary fibre
physical activity Sedentary
But, we have not altered our life style
life
Thrifty genotype Susceptibility genotype
Journal of internal medicine 2003:254(2):114-25
50. References
Joseph T. DiPiro, Pharmacotherapy,A
Pathophysiologic Approach,Seventh Edition, 2008
Harrison's PRINCIPLES OF INTERNAL
MEDICINE, Seventeenth Edition, 2008
NCEP, www.
www.lipidsonline.org
51. Thanks for your Attention!
Questions are guaranteed in life; Answers aren’t!!