This document provides information on vascular disorders of the retina. It begins with the anatomy and blood supply of the retina. It then discusses diabetic retinopathy in detail, including pathogenesis, signs, diagnosis and treatment. It also briefly covers hypertensive retinopathy and retinal vein occlusion, describing their pathophysiology, classification systems, clinical presentation and management. The document focuses primarily on providing an overview of diabetic retinopathy and its various stages and complications.
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.
This presentation describes the background of the cornea and the corneal diseases in general, also it describes in detailed manner how to manage the corneal ulcer with its different causes
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.
This presentation describes the background of the cornea and the corneal diseases in general, also it describes in detailed manner how to manage the corneal ulcer with its different causes
Congenital Glaucoma is one of the most common causes of irreversible childhood blindness. This presentation covers this topic in detail that can aid physicians in effective patient care.
PS: The slides in the preview look skewed, download the presentation to view the font used in Office 2012 and upwards.
Congenital Glaucoma is one of the most common causes of irreversible childhood blindness. This presentation covers this topic in detail that can aid physicians in effective patient care.
PS: The slides in the preview look skewed, download the presentation to view the font used in Office 2012 and upwards.
Hypertensive Retinopathy (HTN-R) for undergraduate MBBS Students.
Covers the basics of Aetiology, pathophysiology, clinical features, Classification and management of HTN-R.
Also encompasses salient points for PGMEE
The retina is the tissue layer located in the back of your eye. This layer transforms light into nerve signals that are then sent to the brain for interpretation.
When your blood pressure is too high, the retina’s blood vessel walls may thicken. This may cause your blood vessels to become narrow, which then restricts blood from reaching the retina. In some cases, the retina becomes swollen.
Over time, high blood pressure can cause damage to th
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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
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
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3. ANATOMY OF RETINA
The retina is a thin,
semitransparent, multilayered
sheet of neural tissue that lines
the inner aspect of the posterior
two-thirds of the wall of the
globe.
4. LANDMARKS OF RETINA
1. Optic Disc
2. Retinal Blood
Vessels
3. Area centralis with
fovea and foveola
4. Peripheral retina
and ora serrata
5. Thickest near the
optic disc
6. Thin towards the
peripheral
6. BLOOD SUPPLY OF THE RETINA:
•Outer 4 layers of retina is supplied by (till outer nuclear layer)
choriocapillaries.
•The inner six layers gets its supply from central retinal artery which
is a branch of ophthalmic artery.
•The outer plexiform layer gets partly by both the above arteries.
•The fovea is avascular and is mainly supplied by choriocapillaries.
•The inner portion of the retina is perfused by branches of the central
retinal artery.
•In 30% of eyes ,a cilioretinal artery,branching from the ciliary
circulation ,supplies part of inner retina mainly The Macula Region.
•The retinal blood vessels maintain the inner blood-retinal barrier.This
physiological barrier is due to single layer of non-fenestrated
endothelial cells,whose tight junctions are impervious to tracer
substances such as fluorescein.
7.
8. •Retinal blood vessels lack an internal elastic lamina & a
continuous layer of smooth muscle cells.
•The retinal arteries are end arteries & have no
anastomoses.The only place where the retinal system
anastomoses is in the neighbourhood of lamina cribrosa.
•The veins of the retina unite to form Central retinal vein at the
disc, which follows the corresponding artery.
•The terminal fundus arterioles bend sharply and dip almost
vertically into the retina.
•In most of the Extramacular fundus- two retianal capillary
networks- a superficial and a deep.
•In parafoveal zone it is well developed and in 3 layers.
•A capillary free zone of 500miceo metre diameter in foveal
zone- FAZ.
9. VASCULAR DISORDERS OF
RETINA
1.DIABETIC RETINOPATHY
2.HYPERTENSIVE RETINOPATHY
3.RETINAL VEIN OCCLUSION
4.RETINAL ARTERY OCCLUSION
5.RETINOPATHY OF PREMATURITY
10. DIABETIC RETINOPATHY
• Diabetic retinopathy is a disorder of the retinal
vessels that eventually develops to some
degree in nearly all patients with long-
standing diabetes mellitus.
• Most Common cause of bilateral severe visual
loss in working age group in US
11. RISK FACTORS
• Age at diagnosis of diabetes
• Duration
• Poor control of diabetes
• Pregnancy
• Hypertension
• Nephropathy
• Hyperlipidemia
• Obesity
• Anemia
• Smoking
• Cataract surgery
12. PATHOGENESIS
MICROVASCULAR LEAKAGE
1. LOSS OF PERICYTES
2. MICRO ANEURYSM
3. BLOOD RETINAL BARRIER
BREAKDOWN
IT CAUSES
1. RETINAL OEDEMA
2. HARD EXUDATE
3. RETINAL HEMORRHAGES
• SUPERFICIAL(FLAME
SHAPED)
• DEEP(DOT AND BLOT)
MICROVASCULAR OCCLUSION
1. THICKENING OF BASEMENT
MEMBRANE
2. ENDOTHELIAL DAMAGE
3. STICKNESS AND AGGREGATION OF
PLATELETS
4. FIBRINOLYTIC SYSTEM IS DEFECTIVE
5. RED CELL AGGREGATION
6. DEFECTIVE OXYGEN TRANSPORT
IT CAUSES
1. RETINAL ISCAEMIA(COTTON WOOL
SPOTS)
2. NEOVASCULARIZATION ON THE
SURFACE OF RETINA,OPTIC NERVE
HEAD AND IRIS(RUBEOSIS IRIDIS)
3. ARTERIO VENOUS SHUNTS
17. 3. HARD EXUDATES
• LOCATED
BETWEEN INNER
PLEXIFORM AND
INNER LAYER OF
RETIINA
• COMPOSED OF
PLASMA PROTEINS
AND LIPID
• YELLOW WAXY
APPEARANCE WITH
DISTINCT MARGINS
19. PREPROLIFERATIVE CHANGES
1. VASCULAR CHANGES
• VENOUS CHANGES IN THE FORM OF
BEADING,LOOPING AND SAUSAGE LIKE
SEGMENTATION
• ARTERIOLES BECOME NARROW
28. DIAGNOSIS
1. FUNDUS EXAMINATION WITH
• DIRECT OPHTHALMOSCOPE
• INDIRECT OPHTHALMOSCOPE
• SLIT LAMP BIMICROSCOPY WITH CONTACT LENS
AND NON CONTACT LENS
2. FUNDUS FLUORESCEIN ANGIOGRAPHY FOR
ASSESSMENT OF:
• LEAKING AREAS
• OCCLUSION AREAS
3. OPTICAL COHERENCE TOMOGRAPHY IS USEFUL
TO ASSESS RETINAL OEDEMA
29. TREATMENT
MEDICAL
1. CONTROL OF RISK FACTORS
• DIABETES MELLITUS
• HYPERTENSION,ANAEMIS,NEPHROPATHY,HYPERLIPI
DEMIA
2. ANTIVASCULAR ENDOTHELIAL GROWTH FACTOR
3. INTRAVITREAL STEROIDS ARE USEFUL TO REDUCE
THE MACULAR OEDEMA (INTRAVITREAL INJECTION OF
TRIAMCINOLONE)
30. LASER PHOTOCOAGULATION
OBJECTIVES
1. TO DESTROY THE HYPOXIC
RETINA ,STOP THE RELEASE
OF VASOFORMATIVE
SUBSTANCE AND CAUSE
INVOLUTION OF NEW VESSEL
2. TO DESTROY THE LEAKAGE
AREAS AND ENHANCE THE
ABSORPTION OF OEDEMA
AND EXUDATE
TYPES
1. FOCAL TREATMENT
FOR FOCAL MACULAR
OEDEMA
2. GIRD TREATMENT
FOR DIFFUSE
MACULAR OEDEMA
3. PANRETINAL
PHOTOCOAGULATION
31.
32. SURGERY
PARS PLANA VITRECTOMY IS
INDICATED FOR:
1. DENSE PERSISTENT
VITREOUS HAEMORRHAGE
2. TRACTIONAL RETINAL
DETACHMENT
3. EPIRETINAL MEMBRANES
36. 1. The cardinal funduscopic feature of malignant hypertension is disk swelling, which appears as
blurring and elevation of disk margins. The top image also shows a characteristic star-shaped
macular lesion caused by leaking retinal vessels; the bottom image also shows a characteristic
flame-shaped hemorrhage and dilated veins.
2. Moderate hypertensive retinopathy is characterized by thinned, straight arteries; intraretinal
hemorrhages; and yellow hard exudates (top). Cotton-wool spots (bottom) are an additional
feature of moderate hypertensive retinopathy. They are caused by focal axonal swelling of the
retinal nerve fiber layer as a result of small-vessel occlusion.
37. Retinal arteriolar narrowing due to thickening and opacification of arteriolar
walls (copper wiring) caused by hypertensive arteriosclerosis. Image also
shows macular edema.
38. Classification
• Keith-Wagener-Barker classification
Grade Description
Grade 1 Slight narrowing, sclerosis, and tortuosity of the retinal arterioles; mild,
asymptomatic hypertension
Grade 2 Definite narrowing, focal constriction, sclerosis, and AV nicking; blood
pressure is higher and sustained; few, if any, symptoms referable to blood
pressure
Grade 3 Retinopathy (cotton-wool patches, arteriolosclerosis, hemorrhages); blood
pressure is higher and more sustained; headaches, vertigo, and
nervousness; mild impairment of cardiac, cerebral, and renal function
Grade 4 Neuroretinal edema, including papilledema; Siegrist streaks, Elschnig
spots; blood pressure persistently elevated; headaches, asthenia, loss of
weight, dyspnea, and visual disturbances; impairment of cardiac, cerebral,
and renal function
41. Retinal Vein Occlusion
• Definition:
o It is a common vascular disorder characterized by retinal vein
occlusion resulting in edema and hemorrhages on retina in the
affected region with potential blinding complications
• Types:
o Central retinal vein occlusion
o Branch Retinal vein occlusion
• Etiology and Risk Factors:
o Age of age of above 50 years
o Systemic diseases like hyperlipidemia, Diabetes, Chronic Renal
Failure
o Chronic Open Angle Glaucoma
42. Retinal Vein Occlusion
• Clinical Presentation:
o Sudden painless loss of vision
o Persistent decreased central vision
• Clinical Examination:
o Visual Acuity- Severe visual loss, up to 20/200
o Intra Ocular Pressure- Raised
o Fundus Examination- dilated, tortuous veins, retinal and macular
edema, flame shaped hemorrhages, and cotton wool spots
43. Central retinal vein occlusion
Clinical manifestation
• Non-ischemic type
– Mild fundus change :
retinal hemorrhage and
tortuous vein
– Mild VA decrease
– capillary nonperfusion rare
– Visual field defect (retinal
hemorrhage)
44. • Ischemic type:
– More common
– Extensive retinal
hemorrhage and
tortuous vein,Multiple
cotton-wool spots
– Severe VA decrease
– Widespread capillary
nonperfusion, 60%
cases present iridal
neovascularization.
45. BRANCH RETINAL
VEIN OCCLUSION
• MORE COMMON THAN
CRVO
• OEDEMA AND
HAEMORRHAGE
LIMITED TO THE
AFFECTED VEIN
• VISSION AFFECTED
ONLY MACULAR AREA
IS INVOLVED
• SECONDARY
GLAUCOMA OCCURS
RARELY
• PROGNOSIS IS
REASONABLY GOOD
46. Retinal Vein Occlusion
• Investigations:
o Fluorescein Angiography
o ECG
o Blood CP
o ESR
o Blood Glucose level
• Complications:
o Chronic Macular Edema
o Conversion from Non-Ischemic to Ischemic type
o Retinal Neovascularization
o Neovascular Glaucoma
47. Retinal Vein Occlusion
• Treatment:
o Macular Laser Photocoagulation
o Intra Vitreal injections anti-VEGF and steroids
o Intra Vitreal triamcinolone injections
48. Retinal Artery Occlusion
• Definition:
o Vascular disorder of retina resulting in sudden painless loss of
vision, with antecedent transient visual loss
• Types:
o Central Retinal Artery Occlusion
o Branch Retinal Artery Occlusion
• Etiology:
o Thrombosis due to atherosclerosis
o Embolism
o Raised Intra Ocular Pressure
o Giant Cell Arteritis
o Angiospasm- Retinal Migraine
51. BRANCH
RETINAL
ARTERY
OCCLUSION
• DUE TO LODGMENT OF
EMBOLI AT
BIFURCATION OF
RETINAL ARTERY
• RETINAL DISTAL TO
OCCLUSION BECOMES
OEDEMATIOUS WITH
NARROWED
ARTERIOLES
• INVOLVED AREA
ATROPHIED CAUSING
SECTORIAL VISUAL
FIELD DEFFECT
PERMANANTLY.
52. Retinal Artery Occlusion
• Treatment:
o Intraocular pressure lowered immediately by anterior chamber
paracentasis or I.V Acetazolamide
o Inhaled oxygen and carbon dioxide mixture to improve oxygen
delivery to retina
o Thrombolytic therapy
53. Retinopathy Of Prematurity
• Definition:
o It is a bilateral vasoproliferative retinopathy occurring in
premature infants with low birth weight and exposed to high
concentration of oxygen
• Etiology and Risk Factors:
o Low birth weight
o Exposure to high concentrations of oxygen
o Premature birth
• Pathology:
o THE TEMPORAL RETINAL VASCULARIZATION IS
COMPLETED 1 MONTH AFTER BIRTH
o TOXIC LEVEL OF OXYGEN INTERFERES WITH
REVASCULARIZATION BY DAMAGING THE ENDOTHELIUM
AND OBLITERATING NEWLY FORMED CAPILLARIES.
59. Retinopathy Of Prematurity
• Treatment:
o Peripheral retinal laser in stage 2
o Ablation of avascular retina in stage 3
o Vitreotomy in stage 4 & 5