Diabetic retinopathy is caused by chronic hyperglycemia leading to progressive dysfunction of the retinal vasculature. This causes vascular leakage, focal ischemia, retinal hypoxia and neovascularization as well as thickening of the basement membrane and loss of pericytes impairing oxygen and nutrient flow. The stages include non-proliferative diabetic retinopathy characterized by microaneurysms and hemorrhages, and proliferative diabetic retinopathy characterized by new vessel growth. Macular edema can also occur from fluid leakage causing vision loss.
Retinal vein occlusion (RVO) is an obstruction of the retinal venous system by thrombus formation and may involve the central, hemi-central or branch retinal vein.
The most common aetiological factor is compression by adjacent atherosclerotic retinal arteries.
Other possible causes are external compression or disease of the vein wall e.g. vasculitis.
Retinal vein occlusion (RVO) is an obstruction of the retinal venous system by thrombus formation and may involve the central, hemi-central or branch retinal vein.
The most common aetiological factor is compression by adjacent atherosclerotic retinal arteries.
Other possible causes are external compression or disease of the vein wall e.g. vasculitis.
Branched Retinal Vein Occlusion (BRVO) for undergraduate MBBS Students.
Covers the basics of Aetiology, pathophysiology, clinical features, types, associated conditions and management of BRVO.
Also encompasses salient points for PGMEE
Leukocoria ( or white pupillary reflex) is an abnormal white reflection from the eye.
Leukocoria is a medical sign for a number of several conditions.
- this presentation at annual conference of the Ophthalmic department, faculty of medicine - Al-Azhar University in association with DOS & EOS Cairo, Egypt January 2017
Branched Retinal Vein Occlusion (BRVO) for undergraduate MBBS Students.
Covers the basics of Aetiology, pathophysiology, clinical features, types, associated conditions and management of BRVO.
Also encompasses salient points for PGMEE
Leukocoria ( or white pupillary reflex) is an abnormal white reflection from the eye.
Leukocoria is a medical sign for a number of several conditions.
- this presentation at annual conference of the Ophthalmic department, faculty of medicine - Al-Azhar University in association with DOS & EOS Cairo, Egypt January 2017
Diabetic retinopathy presentation intended to refresh the knowledge of ophthalmic nurses, ophthalmic clinical officers and other mid level ophthalmic personnel, and read initially for the self-support diabetes patients group.
An Android Application
It does the embedding of AR based library content into the natural environment to generate a 3D model of the product which is tracked thus displaying it on the mobile screen.
SAGE | IOB CORPORATE - MAPEAMENTO DE RISCOS - REVISÃO TRIBUTÁRIAMartcom Digital
Conheça a Revisão Tributária
Consiste na avaliação da qualidade e assertividade no cumprimento das obrigações fiscais principais e acessórias da empresa no âmbito Federal, Estadual e Municipal, considerando todos os tributos diretos e indiretos, inclusive ajustes tributários aos impactos da EC Nº 87/2015. São certificadas as bases de cálculos, créditos, débitos e obrigações acessórias da empresa. Podem revelar eventuais créditos não aproveitados, assim como permitirá a empresa antecipar-se em caso de eventuais inconsistências.
Se presenta una concepción sistémica del hombre en la ecosfera dinámica, y como parte de un universo razonablemente inexplicable sus limites y sostenibilidad.
A premature newborn is a baby delivered before 37 weeks of gestation. Depending on when they are born, premature newborns have underdeveloped organs, which may not be ready to function outside of the uterus.
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.
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.
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
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
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
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.
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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.
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
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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.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
- 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
2. Diabetic retinopathy
• Prevalence increases with
– duration of diabetes
– Poor control of diabetis
– Pregnancy
– Hypertension
– nephropathy
3. PATHOGENESIS
• Aldose reductase
• Enzyme that converts sugar to alcohol (ie: glucose to
sorbitol)
• Sarbitol cannot diffuse out of the cell easily – increase
intracellular concentration.
• Osmotic forces draw water into the cell causing
electrolyte imbalance.
• The resultant damage to lens epithelial cells, which have
a high concentration of aldose reductase, is responsible
for the cataracts seen in children with galactosemia and
in animals with experimental diabetes mellitus.
4. • Because aldose reductase is also found in high
concentration in retinal pericytes and Schwann
cells, some investigators suggest that diabetic
retinopathy and neuropathy may be caused by
aldose reductase-mediated damage.
5. VASOPROLIFERATIVE FACTORS
• Hypoxic retina produces a “vasoproliferative factor” that
diffuses to nearby blood vessels inducing
neovascularization.
• Vascular endothelial growth factor (VEGF) has been
implicated in diabetic retinopathy.
• VEGF is found in the vitreous of patients with diabetic
retinopathy and decreases after PRP.
• Experimental intravitreal injections of VEGF produce
retinal ischemia and microangiopathy in primates.
• The use of anti-VEGF compounds in patients with
diabetic retinopathy.
6. PLATELET AND BLOOD VISCOSITY
• Platelet abnormalities in diabetics may contribute to
retinopathy.
• It has been shown that the platelets in diabetic patients
are “stickier” than platelets of patients without diabetes.
• Once some platelets adhere to the basement membrane
or to damaged cell walls, they secrete prostaglandins
which cause other platelets to adhere to them
(aggregation).
• Arachidonic acid -> prostaglandin (thromboxane A2)
• Thromboxe A2 – potent vasoconstrictor and platelet
aggregating agent.
7. • It has been postulated that abnormal platelet adhesion
and aggregation causes focal capillary occlusion and
focal areas of ischemia in the retina, which in turn
contribute to the development of diabetic retinopathy.
8. PATHOGENESIS OF DR
• Progressive dysfunction of the retinal
vasculature secondary to chronic
hyperglycemia
• Leads to vascular leakage, focal ischemia,
retinal hypoxia and neovascularisation
• Thickening of BM and loss of pericytes,
impairing oxygen and nutrient flow
• Final metabolic pathway unknown
9. STAGES OF DR
• Non-proliferative DR
– Mild
– Moderate
– Severe
• Proliferative DR
– Mild - moderate
– High risk
• Macula edema
– Early macula edema
– CSME
10. MILD NPDR
– Microaneurysm are the first ophthalmoscopically
detectable change in diabetic retinopathy.
– Histologically, thickening of the capillary basement
membrane and pericytes dropout.
– Pericytes are mesothelial cells that surround and
support the retinal capillary endothelial cells. Normally
there is one pericyte per endothelial cell.
– the pericytes dies off and are decreased in number.
– Their absence weakens the capillaries and permits thin-
walled dilatations, called microaneurysms, to develop.
11. MICROANEURYSM
– Focal dilatation of the retinal capillaries due to loss of
pericytes
– 10-100 μm in size.
– Appear as a red dot on the superficial retinal layer.
– Fibrin and RBC can accumulate within aneurysms.
– Despite the multiple layers of basement membrane,
microaneurysms are permeable to water and large
molecules, allowing the transudation of fluid and lipid
into the retina.
14. RETINAL HEMORRHAGE
• When the wall of a capillary or microaneurysm is thin, it
may rupture, giving rise to an intraretinal hemorrhage.
• If the hemorrhage is deep
( ie; in the inner nuclear layer or the outer plexiform layer )
• Dot or blot hemorrhage
• Superficial hemorrhage (ie; nerve fiber layer)
• Flame or splinter- shape
17. Hard exudates
• Yellow deposit of lipid
and protein within the
sensory retinal layer.
• Due to leaking from the
microaneurysm.
• Outer plexiform and inner
nuclear layer.
• Accumulation may cause
a circinate pattern
– it accumulates in a ring
around a group of leaking
microaneurysms.
18. COTTON WOOL SPOT
• Nerve fiber layer infarcts.
• Also known as soft exudates.
• Result from occlusion of the pre-capillary arterioles that
supply the nerve fiber layers.
• Local ischemia causes effective obstruction of
axoplasmic flow in the nerve fiber layer.
• Subsequent swelling of the nerve fibers gives a
characteristic white fluffy appearance to the cotton wool
spot.
• Flourescein angiography shows no capillary perfusion in
the area corresponding to the cotton wool spot.
20. VENOUS BEADING
• Saccular bulges of the wall of retinal veins .
• Indicates sluggish retinal circulation and are nearly
always adjacent to extensive areas of capillary
nonperfusion.
• May represent an area of endothelial proliferation that
fail to develop into new vessels.
• Capillaries next to areas of nonperfusion that dilate and
function as collaterals are referred to as IRMA.
21. IRMA
• Remodelled capillary bed without any
proliferative changes
• Collateral vessels seen on FFA, no leakage
• Usually found in borders of non-perfused retina
22. • IRMA are frequently difficult to differentiate from
surface retinal neovascularization.
• Fluorescein, however, does not leak from IRMA
but leaks profusely from neovascularization.
24. SEVERE NPDR
• All of the above plus 4:2:1 rule from
ETDRS
– DH / BH in all 4 quadrants.
– Venous beading in 2 quadrants or more.
– IRMA in 1 quadrant or more.
25. PDR
• Mild / moderate PDR
– mild NVD / NVE
• High risk PDR
– NVD about 1/3 Disc
area
– Any NVD plus VH
– NVE > ½ DD with VH
26. What happens in PDR
• New blood vessels arise from the
endothelial cells of post-capillary venules
• Evolve in 3 stages
– Fine NV formation with minimal fibrous tissue
extend beyond ILM
– NV increase in size and fibrous component
– NV regress, leaving fibrovascular proliferation
along post hyaloid
27. • In new vessel formation, the endothelial
cells have to
– become activated
– be released from its surroundings
– migrate
– proliferate
28. Endothelial cell activation
• Ischaemic retina release local growth factors
that activate endothelial cells in healthy
capillaries at the edge of the ischaemic area
• VEGF is released by the retinal pigment
epithelial cells in response to hypoxia
• Also produced by RPE in response to
hyperglycaemia through activation of the protein
kinase C pathway
• Other sources include the platelets and white
blood cells that occlude the capillaries
29. • Breakdown of BM causes migration of
endothelial cells
• Laminin, a major component of the
basement membrane, causes angiogenesis
when degraded
• Breakdown of collagen, found in BM, also
has to occur for angiogenesis
30. Migration and proliferation
• Endothelial cells then migrate from the post-capillary
venules into the surrounding tissue
• As they migrate, more cells and tubes are formed
• Pairs of tubes join together thus forming loops
• The top of the loop then forms further tubes that go
through the same process producing further loops
• Controlled by urokinase-type plasminogen activator
(UPA) and TGF beta
• In response to VEGF
– UPA stimulates cells to migrate
– TGF beta matures the proliferated cells into capillary tubes
31. • New vessels grow from
the walls of post-capillary
venules
• Always form loops, and
loop back to the
originating vessel
• The diameter is often
bigger than the vessel
they originated from
• Grow between the inner
surface of the retina and
the vitreous
32. • May grow into the
posterior hyaloid face
• Results in an
inflammatory response
and scar formation
• Contraction results in
– NV being pulled forward
and appearing to stand up
– NV tearing , leading to
hemorrhage
– combination of both
33. • New vessels always grow on a platform of glial cells
• If the new vessel component predominates then vitreous
haemorrhage occurs
• Sometimes the glial cells predominate.
• Glial cells associated with new vessels growing along the
major vascular arcades are particularly at risk
• The reaction between the glial cells and the vitreous
results in scar formation
• These scars contract, causing retinal folds and
eventually TRD
34. MACULAR EDEMA
• Intercellular fluid from leaking
microaneurysms or diffuse capillary
incompetence
• The fluid initially located between the outer
plexiform layer and inner nuclear layer.
• Later, it may also involve the inner plexiform
and nerve fiber layers,until the entire full
thickness of the retina becomes edematous.
35. CLINICALLY SIGNIFICANT MACULAR EDEMA
• Retinal thickening within 500micrometer of the centre of
the macula.
• Exudate within 500 micrometer of the centre of macula.
• Retinal thickening one disc area (1500 micrometer) or
larger,any part of which is within one disc diameter of the
centre of the macula.
38. Advanced Diabetic Eye Disease
• Serious vision- threatening complication of DR that occur
in patients in whom treatment has been inadequate or
unsuccessful.
• Clinical feature :
• Hemorrhages – may be preretinal (retrohyaloid),intragel
or both.
• Tractional retinal detachment – cause by progressive
contraction of fibrovascular membranes over areas of
vitroretinal attachment.
• Rubeosis iridis – iris neovascularization (NVI)
• May lead to glaucoma
• NVI particularly common in eyes with severe retinal
ischemia.