This study analyzed the spectrum of nephropathy in proteinuric type 2 diabetic patients through renal biopsies and examined the relationship between nephropathy and retinopathy. The results showed that non-diabetic kidney disease alone or superimposed on diabetic nephropathy was seen in 61.3% of patients. Longer diabetes duration was associated with diabetic nephropathy while isolated non-diabetic disease occurred in those with shorter duration. Retinal lesions were less frequent than in type 1 diabetes and did not reliably predict nephropathy type. Renal biopsy was necessary for accurate diagnosis.
Presentation given to our fellowship program about diabetic kidney disease.
2022 update discussing SGLT2i, MRA (e.g. finerenone), health economics and beyond
Slidedeck of the presentation I gave during the East by Southwest conference, co-organized by the Division of Nephrology (UNM) and the Renal and Electrolyte Division (UPMC)
Presentation given to our fellowship program about diabetic kidney disease.
2022 update discussing SGLT2i, MRA (e.g. finerenone), health economics and beyond
Slidedeck of the presentation I gave during the East by Southwest conference, co-organized by the Division of Nephrology (UNM) and the Renal and Electrolyte Division (UPMC)
Diabetes Mellitus Management in CKD (Clinical Tips) - Dr. GawadNephroTube - Dr.Gawad
- Recorded videos of this lecture:
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My Nephrology Registrar Seminar Talk from September 2013
Topics Covered
Pathogenesis of Diabetic Nephropathy
Other Renal Disease in Diabetes
Treatment of Diabetic Kidney Disease + The Joint Renal Diabetic Clinic
- English version of this lecture is available at:
https://youtu.be/XRD-QqGFP18
- Arabic version of this lecture is available at:
https://youtu.be/c9PoavAtNKM
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- English version of this lecture is available at:
https://youtu.be/lvcXwE0fb-w
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https://youtu.be/r-fG8bSCqZo
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- Recorded videos of this lecture:
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- English version of this lecture is available at: https://youtu.be/WHu05hmExBY
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Diabetes Mellitus Management in CKD (Clinical Tips) - Dr. GawadNephroTube - Dr.Gawad
- Recorded videos of this lecture:
English Language version of this lecture is available at:
https://youtu.be/h3HRvWGUj5A
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My Nephrology Registrar Seminar Talk from September 2013
Topics Covered
Pathogenesis of Diabetic Nephropathy
Other Renal Disease in Diabetes
Treatment of Diabetic Kidney Disease + The Joint Renal Diabetic Clinic
- English version of this lecture is available at:
https://youtu.be/XRD-QqGFP18
- Arabic version of this lecture is available at:
https://youtu.be/c9PoavAtNKM
- Visit our website for more lectures: www.NephroTube.com
- Subscribe to our YouTube channel: www.youtube.com/NephroTube
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- English version of this lecture is available at:
https://youtu.be/lvcXwE0fb-w
- Arabic version of this lecture is available at:
https://youtu.be/r-fG8bSCqZo
- Visit our website for more lectures: www.NephroTube.com
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- Recorded videos of this lecture:
English Language version of this lecture is available at:
https://youtu.be/i_bUFU-p43Q
Arabic Language version of this lecture is available at:
https://youtu.be/RaIP09m4XMY
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- Recorded videos of this lecture:
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https://youtu.be/Zb6WISbvE2k
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https://youtu.be/4IvvrbC31Q4
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- English version of this lecture is available at: https://youtu.be/WHu05hmExBY
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Renal Tubular Pigmentation Associated with Senna-Related MetabolitesEPL, Inc.
“Renal Tubular Pigmentation Associated with Senna-Related Metabolites.” Willson GA (presenter) Malarkey DE, Allison N, Harris N, Miller RA. The 54th Annual Society of Toxicology Meeting. San Diego, CA. March 25, 2015.
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Mark Haas Kidney Summary Banff 2013 in Brazil Kim Solez ,
Kidney summary from 12th Banff Conference on Transplant Pathology from the meeting in Comandatuba-Bahia, Brazil on August 23rd, 2013 http://cybernephrology.ualberta.ca/banff/2013
Immunohistochemistry Antibody Validation Report for Anti-Phospho-JNK1/2/3 (T1...St John's Laboratory Ltd
Serine/threonine-protein kinase involved in various processes such as cell proliferation, differentiation, migration, transformation and programmed cell death. Extracellular stimuli such as proinflammatory cytokines or physical stress stimulate the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway. In this cascade, two dual specificity kinases MAP2K4/MKK4 and MAP2K7/MKK7 phosphorylate and activate MAPK8/JNK1. In turn, MAPK8/JNK1 phosphorylates a number of transcription factors, primarily components of AP-1 such as JUN, JDP2 and ATF2 and thus regulates AP-1 transcriptional activity. Phosphorylates the replication licensing factor CDT1, inhibiting the interaction between CDT1 and the histone H4 acetylase HBO1 to replication origins. Loss of this interaction abrogates the acetylation required for replication initiation.
Anti-Phospho-JNK1/2/3 (T183)-http://www.stjohnslabs.com/phospho-jnk123-t183-antibody
Join our Antibody Validation Project - http://www.stjohnslabs.com/services/antibody-validation
Diabetic nephropathy considered one of the most common complications of DM. This presentation answer the question are some diabetic patient immune to diabetic nephroapthy
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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.
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.
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
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
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
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 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
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.
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
Non‑diabetic renal disease in type 2 diabetes mellitus: Study of renal - retinal relationship
1. Guide : Dr Rekha Patil
Co Guide : Dr Dnyanesh Morkar
Presenter : Dr Prudhvi Krishna
Non-diabetic renal disease in type 2
diabetes mellitus: Study of renal - retinal
relationship
Indian Journal of nephrology August
2015
2. Introduction
▪ The incidence and prevalence of diabetes mellitus
(dm)are increasing
▪ Diabetes still remains the most common cause of ESKD
in the united states and in many other countries.
▪ Diabetic nephropathy (dn) is not the sole renal disease
in diabetic patients. Kidney diseases other than diabetic
nephropathy can occur in type 2 diabetic patients and
such kidney diseases are known as non-diabetic renal
disease (NDRD), either isolated or superimposed on
DN.
3. The occurrence of NDRD in diabetic
patients is reported in several
studies from around the world.[
4. Introduction
▪ DN is hard to reverse.
▪ However, certain NDRD, such as
mesangial-proliferative glomerulonephritis, IgA
nephropathy and membranous nephropathy, are often
treatable, even remittable.
▪ Thus, therapy and prognosis of DN and NDRD are
quite different. Therefore, differential diagnosis of
these two entities in diabetic patients is of
considerable importance.
5. AIM
▪ To analyze spectrum of nephropathy in
proteinuric type 2 diabetic patients and to study
the relationship between nephropathy and
retinopathy in patients with type 2 diabetes
mellitus (T2DM) with proteinuria.
6. AIM
▪ To analyze spectrum of nephropathy in
proteinuric type 2 diabetic patients and to study
the relationship between nephropathy and
retinopathy in patients with type 2 diabetes
mellitus (T2DM) with proteinuria.
7. Methodology
▪ This study was carried in the Department of Nephrology,
Banaras Hindu University, Varanasi, from October 2011
to September 2013.
▪ Diabetes was diagnosed as per WHO criteria.
▪ All type 2 diabetic patients of both gender attending the
nephrology services were screened for proteinuria.
▪ The urine was examined for detection of protein using
dipstick method. The patients with dipstick proteinuria of
1+ or more were subjected to quantitative 24-h urinary
protein.
8. Methodology
▪ Type 2 diabetic patients with proteinuria of more
than 1 g were included in this study.
▪ The duration between diagnosis of DM and
onset of renal manifestations were recorded in
individual patients.
▪ Patients with absence of voluntary consent,
contraindication to kidney biopsy and severe renal
failure (serum creatinine > 5 mg/dl) were excluded
from the study.
9. Methodology
▪ All patients were subjected to detailed
history,physical examination and laboratory
investigations.
▪ Ultrasonography was carried to assess kidney size,
cortical thickness and renal margin in each case.
▪ Single ophthalmologist examined optic fundi for
evidence of diabetic retinopathy (DR).
10. DN was diagnosed in the presence of..
Nodular or diffuse glomerulosclerosis
glomerular hypertrophy,
mesangial (diffuse or nodular) widening
glomerular capillary wall thickening
evidence of exudative lesions or fibrin caps
(i.e. hyaline material heaped up on the inner
side of the glomerular basement membrane)
and the presence of micro aneurysms of
glomerular capillaries.
11. The various NDRDs were diagnosed on the
basis of their characteristic features on light
microscopy.
Membranous nephropathy was diagnosed by
presence of diffuse and global capillary wall
thickening in the absence of significant glomerular
hypercellularity and increase in mesangial matrix.
In few glomeruli, deposits and spikes were also seen
at the outer surface of glomerular basement
membrane.
12. The various NDRDs were diagnosed on the
basis of their characteristic features on light
microscopy.
Focal segmental glomerulosclerosis was
diagnosed on findings of focal areas of consolidation
and otherwise normal pattern elsewhere with no
evidence suggestive of DN.
Amyloidosis was diagnosis was made by the
presence of hyaline material deposits in glomerular
basement membrane and mesangium and confirmed
by positive staining of material with Congo red stain.
13. The various NDRDs were diagnosed on the
basis of their characteristic features on light
microscopy.
Mesangio-proliferative glomerulonephritis was
diagnosed by the presence of increase in number of
mesangial cells and matrix without evidence of other
features of DN such as nodule formation, thickening
of glomerular basement membrane and intertubular
arteriolar hyalinosis or arteriolar hyalinosis.
Isolated NDRD was diagnosed in the absence of
histological features of DN.
Mixed lesions (NDRD superimposed above DN)
were diagnosed in the presence of histological
evidences of DN.
16. NDRD SUPERIMPOSED ON DN
▪ NDRD superimposed on DN was diffuse
proliferative glomerulonephritis (n-2).
▪ The other NDRD in this group included chronic
tubulo-interstitial nephritis, amyloidosis, minimal
change disease and crescentic GN, all consisting of
one case each.
18. ▪ Kidney histology in patients with DR (n-10) revealed
DN in 6 (60%), NDRD in 1 (10%) and mixed lesion
in 3 (30%) patients.
▪ Thus, absence of DR favors NDRD but does not
exclude DN because isolated DN was noted in
28.57% cases in absence of DR.
▪ Similarly biopsy proven NDRD (pure NDRD; 10%
and mixed lesion; 30%) was noted in 40% of cases
in presence of DR.
19. Conclusions
▪ All type 2 diabetic patients with clinical renal disease do
not have classical DN.
▪ Non-diabetic kidney disease either alone or
superimposed on DN were seen in 61.3% of diabetic
patients. We observed that longer duration (>10 years) of
diabetes was the strongest predictor of DN and diabetic
patients having NDRD alone had shorter duration of DM.
▪ DR was absent in 21/31 (67.7%) patients. Thus, retinal
lesion is less frequent in type 2 diabetes in comparison to
type 1 diabetes.
20. Conclusions
▪ Non-diabetic kidney disease was noted in 40% of the
cases in presence of DR and 43% of the cases had
biopsy proven DN in absence of DR.
▪ However, observed that the absence of retinopathy
favors NDRD but does not exclude occurrence of DN.
Therefore, DR does not predict nature of nephropathy in
patients with type 2 diabetes.
▪ Renal biopsy is necessary for precise diagnosis of
diabetic and non-diabetic kidney disease in type 2
diabetic patients with proteinuria.
Editor's Notes
C Congestive heart failure (or Left ventricular systolic dysfunction)1 H Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication)1 A2 Age ≥75 years2 D Diabetes Mellitus1 S2 Prior Stroke or TIA or thromboembolism2 V Vascular disease (e.g. peripheral artery disease, myocardial infarction, aortic plaque)1 A Age 65–74 years1 Sc Sex category (i.e. female sex)1
The European Society of Cardiology (ESC) and National Institute for Health and Care Excellence (NICE) guidelines recommend that if the patient has a CHA2DS2-VASc score of 2 and above, oral anticoagulation therapy (OAC) with a Vitamin K Antagonist (VKA, e.g. warfarin with target INR of 2-3) or one of the non-VKA oral anticoagulant drugs (NOACs, e.g. dabigatran, rivaroxaban, edoxaban, or apixaban) is recommended.
C Congestive heart failure (or Left ventricular systolic dysfunction)1 H Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication)1 A2 Age ≥75 years2 D Diabetes Mellitus1 S2 Prior Stroke or TIA or thromboembolism2 V Vascular disease (e.g. peripheral artery disease, myocardial infarction, aortic plaque)1 A Age 65–74 years1 Sc Sex category (i.e. female sex)1
The European Society of Cardiology (ESC) and National Institute for Health and Care Excellence (NICE) guidelines recommend that if the patient has a CHA2DS2-VASc score of 2 and above, oral anticoagulation therapy (OAC) with a Vitamin K Antagonist (VKA, e.g. warfarin with target INR of 2-3) or one of the non-VKA oral anticoagulant drugs (NOACs, e.g. dabigatran, rivaroxaban, edoxaban, or apixaban) is recommended.
DR was classified into two groups.that is, non‑proliferative DR (NPDR) and proliferative
DR (PDR).
NPDR was diagnosed in the presence of microaneurysm, dot blot or flame‑shaped hemorrhage,
hard exudates, or evidence of macular edema. The PDR was diagnosed in the presence of new vessels formation
or pre‑retinal or vitreous hemorrhage.
C Congestive heart failure (or Left ventricular systolic dysfunction)1 H Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication)1 A2 Age ≥75 years2 D Diabetes Mellitus1 S2 Prior Stroke or TIA or thromboembolism2 V Vascular disease (e.g. peripheral artery disease, myocardial infarction, aortic plaque)1 A Age 65–74 years1 Sc Sex category (i.e. female sex)1
The European Society of Cardiology (ESC) and National Institute for Health and Care Excellence (NICE) guidelines recommend that if the patient has a CHA2DS2-VASc score of 2 and above, oral anticoagulation therapy (OAC) with a Vitamin K Antagonist (VKA, e.g. warfarin with target INR of 2-3) or one of the non-VKA oral anticoagulant drugs (NOACs, e.g. dabigatran, rivaroxaban, edoxaban, or apixaban) is recommended.
C Congestive heart failure (or Left ventricular systolic dysfunction)1 H Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication)1 A2 Age ≥75 years2 D Diabetes Mellitus1 S2 Prior Stroke or TIA or thromboembolism2 V Vascular disease (e.g. peripheral artery disease, myocardial infarction, aortic plaque)1 A Age 65–74 years1 Sc Sex category (i.e. female sex)1
The European Society of Cardiology (ESC) and National Institute for Health and Care Excellence (NICE) guidelines recommend that if the patient has a CHA2DS2-VASc score of 2 and above, oral anticoagulation therapy (OAC) with a Vitamin K Antagonist (VKA, e.g. warfarin with target INR of 2-3) or one of the non-VKA oral anticoagulant drugs (NOACs, e.g. dabigatran, rivaroxaban, edoxaban, or apixaban) is recommended.
C Congestive heart failure (or Left ventricular systolic dysfunction)1 H Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication)1 A2 Age ≥75 years2 D Diabetes Mellitus1 S2 Prior Stroke or TIA or thromboembolism2 V Vascular disease (e.g. peripheral artery disease, myocardial infarction, aortic plaque)1 A Age 65–74 years1 Sc Sex category (i.e. female sex)1
The European Society of Cardiology (ESC) and National Institute for Health and Care Excellence (NICE) guidelines recommend that if the patient has a CHA2DS2-VASc score of 2 and above, oral anticoagulation therapy (OAC) with a Vitamin K Antagonist (VKA, e.g. warfarin with target INR of 2-3) or one of the non-VKA oral anticoagulant drugs (NOACs, e.g. dabigatran, rivaroxaban, edoxaban, or apixaban) is recommended.
C Congestive heart failure (or Left ventricular systolic dysfunction)1 H Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication)1 A2 Age ≥75 years2 D Diabetes Mellitus1 S2 Prior Stroke or TIA or thromboembolism2 V Vascular disease (e.g. peripheral artery disease, myocardial infarction, aortic plaque)1 A Age 65–74 years1 Sc Sex category (i.e. female sex)1
The European Society of Cardiology (ESC) and National Institute for Health and Care Excellence (NICE) guidelines recommend that if the patient has a CHA2DS2-VASc score of 2 and above, oral anticoagulation therapy (OAC) with a Vitamin K Antagonist (VKA, e.g. warfarin with target INR of 2-3) or one of the non-VKA oral anticoagulant drugs (NOACs, e.g. dabigatran, rivaroxaban, edoxaban, or apixaban) is recommended.
C Congestive heart failure (or Left ventricular systolic dysfunction)1 H Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication)1 A2 Age ≥75 years2 D Diabetes Mellitus1 S2 Prior Stroke or TIA or thromboembolism2 V Vascular disease (e.g. peripheral artery disease, myocardial infarction, aortic plaque)1 A Age 65–74 years1 Sc Sex category (i.e. female sex)1
The European Society of Cardiology (ESC) and National Institute for Health and Care Excellence (NICE) guidelines recommend that if the patient has a CHA2DS2-VASc score of 2 and above, oral anticoagulation therapy (OAC) with a Vitamin K Antagonist (VKA, e.g. warfarin with target INR of 2-3) or one of the non-VKA oral anticoagulant drugs (NOACs, e.g. dabigatran, rivaroxaban, edoxaban, or apixaban) is recommended.
C Congestive heart failure (or Left ventricular systolic dysfunction)1 H Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication)1 A2 Age ≥75 years2 D Diabetes Mellitus1 S2 Prior Stroke or TIA or thromboembolism2 V Vascular disease (e.g. peripheral artery disease, myocardial infarction, aortic plaque)1 A Age 65–74 years1 Sc Sex category (i.e. female sex)1
The European Society of Cardiology (ESC) and National Institute for Health and Care Excellence (NICE) guidelines recommend that if the patient has a CHA2DS2-VASc score of 2 and above, oral anticoagulation therapy (OAC) with a Vitamin K Antagonist (VKA, e.g. warfarin with target INR of 2-3) or one of the non-VKA oral anticoagulant drugs (NOACs, e.g. dabigatran, rivaroxaban, edoxaban, or apixaban) is recommended.
C Congestive heart failure (or Left ventricular systolic dysfunction)1 H Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication)1 A2 Age ≥75 years2 D Diabetes Mellitus1 S2 Prior Stroke or TIA or thromboembolism2 V Vascular disease (e.g. peripheral artery disease, myocardial infarction, aortic plaque)1 A Age 65–74 years1 Sc Sex category (i.e. female sex)1
The European Society of Cardiology (ESC) and National Institute for Health and Care Excellence (NICE) guidelines recommend that if the patient has a CHA2DS2-VASc score of 2 and above, oral anticoagulation therapy (OAC) with a Vitamin K Antagonist (VKA, e.g. warfarin with target INR of 2-3) or one of the non-VKA oral anticoagulant drugs (NOACs, e.g. dabigatran, rivaroxaban, edoxaban, or apixaban) is recommended.
C Congestive heart failure (or Left ventricular systolic dysfunction)1 H Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication)1 A2 Age ≥75 years2 D Diabetes Mellitus1 S2 Prior Stroke or TIA or thromboembolism2 V Vascular disease (e.g. peripheral artery disease, myocardial infarction, aortic plaque)1 A Age 65–74 years1 Sc Sex category (i.e. female sex)1
The European Society of Cardiology (ESC) and National Institute for Health and Care Excellence (NICE) guidelines recommend that if the patient has a CHA2DS2-VASc score of 2 and above, oral anticoagulation therapy (OAC) with a Vitamin K Antagonist (VKA, e.g. warfarin with target INR of 2-3) or one of the non-VKA oral anticoagulant drugs (NOACs, e.g. dabigatran, rivaroxaban, edoxaban, or apixaban) is recommended.