An important message to the people of the united states of america. This applies to over 3 million people in american and 1/300 people worldwide. Familial hypercholesterolemia is a very serious disorder. In this presentation you will see statements from valid sources such as the United States national Library of Medicine.
Personalized medicine in Familial HypercholesterolaemiaDr. Julius Kwedhi
Familial hypercholesterolemia (FH) is an autosomal-dominant genetic disease present in all racial and ethnic groups and has long been recognized as a cause of premature atherosclerotic coronary heart disease.1–3 Heterozygous FH has the highest prevalence of genetic defects that cause significant premature mortality (≈1:200 to 1:500 or higher in founder populations).
The genetic basis of the disorder, impaired functioning of the low-density lipoprotein (LDL) receptor, was first recognized by Goldstein and Brown4 in their Nobel Prize–winning work.
Studies of LDL receptor function have identified additional mechanisms for the pathogenesis of FH (defects in apolipoprotein [apo] B impairing binding with the LDL receptor and gain-of-function mutations in proprotein convertase subtulisin/kexin type 9 [PCSK9] that enhance LDL receptor degradation).
FH leads to elevated LDL concentrations, with levels in heterozygous FH generally in untreated adults >190 mg/dL LDL cholesterol (LDL-C) and in untreated children or adolescents >160 mg/dL LDL-C. Long-term exposure to elevated plasma concentrations of LDL-C begins in utero, leading in heterozygotes to premature ischemic heart disease in mid adulthood and in homozygotes to ischemic heart disease in childhood or early adulthood.
An important message to the people of the united states of america. This applies to over 3 million people in american and 1/300 people worldwide. Familial hypercholesterolemia is a very serious disorder. In this presentation you will see statements from valid sources such as the United States national Library of Medicine.
Personalized medicine in Familial HypercholesterolaemiaDr. Julius Kwedhi
Familial hypercholesterolemia (FH) is an autosomal-dominant genetic disease present in all racial and ethnic groups and has long been recognized as a cause of premature atherosclerotic coronary heart disease.1–3 Heterozygous FH has the highest prevalence of genetic defects that cause significant premature mortality (≈1:200 to 1:500 or higher in founder populations).
The genetic basis of the disorder, impaired functioning of the low-density lipoprotein (LDL) receptor, was first recognized by Goldstein and Brown4 in their Nobel Prize–winning work.
Studies of LDL receptor function have identified additional mechanisms for the pathogenesis of FH (defects in apolipoprotein [apo] B impairing binding with the LDL receptor and gain-of-function mutations in proprotein convertase subtulisin/kexin type 9 [PCSK9] that enhance LDL receptor degradation).
FH leads to elevated LDL concentrations, with levels in heterozygous FH generally in untreated adults >190 mg/dL LDL cholesterol (LDL-C) and in untreated children or adolescents >160 mg/dL LDL-C. Long-term exposure to elevated plasma concentrations of LDL-C begins in utero, leading in heterozygotes to premature ischemic heart disease in mid adulthood and in homozygotes to ischemic heart disease in childhood or early adulthood.
"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
the study was a pilot study done at National Institute of Ayurveda under the Phd Research Programme with an aim to find out new avenues in the managegement of Dyslipidemia - Medoroga and Coronary Heart Disease - Hridroga, thus initiating a new concept of Preventive Cardiology through Ayurveda & Panchakarma
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.
Etiopathogenesis and pharmacotherapy of hyperlipidemias
a. the pathophysiology of selected disease states and the rationale for drug therapy;
b. the therapeutic approach to management of these diseases;
c. the controversies in drug therapy;
d. the importance of preparation of individualised therapeutic plans based on diagnosis;
e. needs to identify the patient-specific parameters relevant in initiating drug therapy,
and monitoring therapy (including alternatives, time-course of clinical and laboratory
indices of therapeutic response and adverse effects);
f. describe the pathophysiology of selected disease states and explain the rationale for
drug therapy;
g. summarise the therapeutic approach to management of these diseases including
reference to the latest available evidence;
h. discuss the controversies in drug therapy;
i. discuss the preparation of individualised therapeutic plans based on diagnosis; and
j. identify the patient-specific parameters relevant in initiating drug therapy, and
monitoring therapy (including alternatives, time-course of clinical and laboratory indices of therapeutic response and adverse effects).
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
"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
the study was a pilot study done at National Institute of Ayurveda under the Phd Research Programme with an aim to find out new avenues in the managegement of Dyslipidemia - Medoroga and Coronary Heart Disease - Hridroga, thus initiating a new concept of Preventive Cardiology through Ayurveda & Panchakarma
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.
Etiopathogenesis and pharmacotherapy of hyperlipidemias
a. the pathophysiology of selected disease states and the rationale for drug therapy;
b. the therapeutic approach to management of these diseases;
c. the controversies in drug therapy;
d. the importance of preparation of individualised therapeutic plans based on diagnosis;
e. needs to identify the patient-specific parameters relevant in initiating drug therapy,
and monitoring therapy (including alternatives, time-course of clinical and laboratory
indices of therapeutic response and adverse effects);
f. describe the pathophysiology of selected disease states and explain the rationale for
drug therapy;
g. summarise the therapeutic approach to management of these diseases including
reference to the latest available evidence;
h. discuss the controversies in drug therapy;
i. discuss the preparation of individualised therapeutic plans based on diagnosis; and
j. identify the patient-specific parameters relevant in initiating drug therapy, and
monitoring therapy (including alternatives, time-course of clinical and laboratory indices of therapeutic response and adverse effects).
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
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)
Lipids are a heterogenous group of
water –insoluble ( hydrophobic ) organic
molecules. Presentation on how they affect the body and what to do to prevent their effects.
The Roman Empire A Historical Colossus.pdfkaushalkr1407
The Roman Empire, a vast and enduring power, stands as one of history's most remarkable civilizations, leaving an indelible imprint on the world. It emerged from the Roman Republic, transitioning into an imperial powerhouse under the leadership of Augustus Caesar in 27 BCE. This transformation marked the beginning of an era defined by unprecedented territorial expansion, architectural marvels, and profound cultural influence.
The empire's roots lie in the city of Rome, founded, according to legend, by Romulus in 753 BCE. Over centuries, Rome evolved from a small settlement to a formidable republic, characterized by a complex political system with elected officials and checks on power. However, internal strife, class conflicts, and military ambitions paved the way for the end of the Republic. Julius Caesar’s dictatorship and subsequent assassination in 44 BCE created a power vacuum, leading to a civil war. Octavian, later Augustus, emerged victorious, heralding the Roman Empire’s birth.
Under Augustus, the empire experienced the Pax Romana, a 200-year period of relative peace and stability. Augustus reformed the military, established efficient administrative systems, and initiated grand construction projects. The empire's borders expanded, encompassing territories from Britain to Egypt and from Spain to the Euphrates. Roman legions, renowned for their discipline and engineering prowess, secured and maintained these vast territories, building roads, fortifications, and cities that facilitated control and integration.
The Roman Empire’s society was hierarchical, with a rigid class system. At the top were the patricians, wealthy elites who held significant political power. Below them were the plebeians, free citizens with limited political influence, and the vast numbers of slaves who formed the backbone of the economy. The family unit was central, governed by the paterfamilias, the male head who held absolute authority.
Culturally, the Romans were eclectic, absorbing and adapting elements from the civilizations they encountered, particularly the Greeks. Roman art, literature, and philosophy reflected this synthesis, creating a rich cultural tapestry. Latin, the Roman language, became the lingua franca of the Western world, influencing numerous modern languages.
Roman architecture and engineering achievements were monumental. They perfected the arch, vault, and dome, constructing enduring structures like the Colosseum, Pantheon, and aqueducts. These engineering marvels not only showcased Roman ingenuity but also served practical purposes, from public entertainment to water supply.
2024.06.01 Introducing a competency framework for languag learning materials ...Sandy Millin
http://sandymillin.wordpress.com/iateflwebinar2024
Published classroom materials form the basis of syllabuses, drive teacher professional development, and have a potentially huge influence on learners, teachers and education systems. All teachers also create their own materials, whether a few sentences on a blackboard, a highly-structured fully-realised online course, or anything in between. Despite this, the knowledge and skills needed to create effective language learning materials are rarely part of teacher training, and are mostly learnt by trial and error.
Knowledge and skills frameworks, generally called competency frameworks, for ELT teachers, trainers and managers have existed for a few years now. However, until I created one for my MA dissertation, there wasn’t one drawing together what we need to know and do to be able to effectively produce language learning materials.
This webinar will introduce you to my framework, highlighting the key competencies I identified from my research. It will also show how anybody involved in language teaching (any language, not just English!), teacher training, managing schools or developing language learning materials can benefit from using the framework.
Students, digital devices and success - Andreas Schleicher - 27 May 2024..pptxEduSkills OECD
Andreas Schleicher presents at the OECD webinar ‘Digital devices in schools: detrimental distraction or secret to success?’ on 27 May 2024. The presentation was based on findings from PISA 2022 results and the webinar helped launch the PISA in Focus ‘Managing screen time: How to protect and equip students against distraction’ https://www.oecd-ilibrary.org/education/managing-screen-time_7c225af4-en and the OECD Education Policy Perspective ‘Students, digital devices and success’ can be found here - https://oe.cd/il/5yV
How to Split Bills in the Odoo 17 POS ModuleCeline George
Bills have a main role in point of sale procedure. It will help to track sales, handling payments and giving receipts to customers. Bill splitting also has an important role in POS. For example, If some friends come together for dinner and if they want to divide the bill then it is possible by POS bill splitting. This slide will show how to split bills in odoo 17 POS.
We all have good and bad thoughts from time to time and situation to situation. We are bombarded daily with spiraling thoughts(both negative and positive) creating all-consuming feel , making us difficult to manage with associated suffering. Good thoughts are like our Mob Signal (Positive thought) amidst noise(negative thought) in the atmosphere. Negative thoughts like noise outweigh positive thoughts. These thoughts often create unwanted confusion, trouble, stress and frustration in our mind as well as chaos in our physical world. Negative thoughts are also known as “distorted thinking”.
How to Create Map Views in the Odoo 17 ERPCeline George
The map views are useful for providing a geographical representation of data. They allow users to visualize and analyze the data in a more intuitive manner.
4. Lipoproteins Packages to transport insoluble lipids in the blood Chylomicrons (carry TG from gut to adipose tissues and skeletal muscle) Chylomicron remnants VLDL (carries TG from liver) LDL (carries cholesterol fromliver) IDL HDL (carries cholestero to the liver)
8. Causes 3 major mutations LDL-R ApolipoproteinB An enzyme involved in the degradation of the receptor PCSK9
9. Diagnosis On 4 clinical criteria Possible FH Definite FH These patients are screened for DNA mutation If DNA mutation found in index case then 100% sensitive and specific Cascade testing (first and second degree)
10. Cascade Screening Relatives of FH should be screened before age 10 with Genetics if mutation known LDLC if mutation unknown Do not use Framingham risk
11. Management High intensity statin therapy for all FH lifelong add in ezetemibe Specialist referral Advice RE pregnancy Aim to reduce LDL C by 50% from baseline Lifestyle advice Homozygous FH Consider referral to cardiologist
13. Lipid management in Type I diabetes Patients with Increased ACR, or 2 or more features of metabolic syndrome BP>135/80 HDL < 1.2 (women) and 1.0 (men) TG > 1.8 Waist circumference 80cm (women) 100cm (Men) Evidence of insulin resistance (>1 Unit/kg/day) Smoking, age, FH of CVD Should be assumed to be at high arterial risk and started on statin
14. Lipid management in type II Diabetes IF >40 years consider high risk of CVD unless Not overweight Normotensive (<140/80mm/Hg) No microalbuminuria Non-smoker No high risk lipid profile No history or FHx of CVD Then use UKPDS risk engine http://www.dtu.ox.ac.uk/riskengine/
15.
16. Lipid management in type II Diabetes If <40 years use statins if at high risk of CVD Once started on cholesterol lowering therapy Simvastatin 40mg Reassess after 3 months Yearly measurement thereafter Aim for LDL< 2.0mmol/L TC < 4mmol/L
17. Case study 1 50 year-old male Type II diabetic Obesity (BMI 36) Recurrent pancreatitis Treatments NR 80 units tds Glargin 180 units at night Fenofibrate 267mg Metformin 850mg bd Aspirin
18. Case study 2 HbA1C 9.5% TC 8.3 TG 20.66 HDL 1.0 LDL not result
19. TG and type II diabetes If high TG perform full fasting sample Assess secondary causes EtOH Hypothyroidism Renal impairment Hyperglycaemia If TG remain>4.5mmol/Lstart fenofibrate
20. Primary prevention In those aged 40-75 If CV risk is >20% in next 10years treat after modifying other risk factors GPs should screen their population and use risk assessment Treatment with simvastatin 40mg and no need to recheck or treat to target LDL Do not use fibrate, ezetemibe or anion exchange resins
23. Other drugs Niacin/nicotinic acid (Niaspan) Decreases hepatic VLDL production Reduces LDL and TG Fibrates Increase lipoprotein lipase activity Both increase HDL Ezetemibe Reduces cholesterol absorption from gut Reduces LDL (no effect on HDL)
24. Omacor (omega 3 fatty acids) Reduces TG Reduced death - secondary prevention of MI
25. Dietary advice Fat should make up<30% of calorie intake Saturated fat <10% of calorie intake Cholesterol <300mg/day 5 a day 2 portions oily fish per week
27. Summary Statins are an effective treatment for hypercholesterolaemia Treat patients if C risk >20% over 10years Almost all type II diabeteics are considered high risk and should be treated to targets of TC <4mmol/L LDL <2mmol/L
