PAPILLOEDEMA
- Oedema of the optic disc caused by increased intracranial pressure. This blocks axoplasmic transport, causing swelling of the optic nerve head.
- Symptoms include blurred vision, visual field defects, and over time potential blindness if not treated.
- Diagnosis is made through examination showing blurred disc margins, venous congestion, retinal exudates, and imaging showing disc swelling. Treatment aims to relieve intracranial pressure through surgical or medical means to prevent permanent nerve damage.
Ischemic optic neuropathy constitutes one of the major causes of blindness or seriously impaired vision among the middle-aged and elderly population.
Ischemic optic neuropathy is due to acute ischemia of the optic nerve. it can be classified into two, depending upon the part of the optic nerve involved:
1.Anterior ischemic optic neuropathy (AION)
-AION is due to acute ischemia of the front (anterior) part of the optic nerve (also called optic nerve head), which is supplied mainly by the posterior ciliary arteries.
-AION is divided into two types, depending on what causes it:
1.Arteritic AION: This is the most serious type and is due to a disease called giant cell arteritis or temporal arteritis.
2. Non-arteritic AION: This is the usual, most common type, with many different causes but not associated with giant cell arteritis.
2.Posterior ischemic optic neuropathy (PION). -
-PION is a much less common type. It is due to acute ischemia of the back (posterior) part of the optic nerve, located some distance behind the eyeball; this part of the optic nerve is NOT supplied by the posterior ciliary arteries
(Hayreh, 2009)
Ischemic optic neuropathy constitutes one of the major causes of blindness or seriously impaired vision among the middle-aged and elderly population.
Ischemic optic neuropathy is due to acute ischemia of the optic nerve. it can be classified into two, depending upon the part of the optic nerve involved:
1.Anterior ischemic optic neuropathy (AION)
-AION is due to acute ischemia of the front (anterior) part of the optic nerve (also called optic nerve head), which is supplied mainly by the posterior ciliary arteries.
-AION is divided into two types, depending on what causes it:
1.Arteritic AION: This is the most serious type and is due to a disease called giant cell arteritis or temporal arteritis.
2. Non-arteritic AION: This is the usual, most common type, with many different causes but not associated with giant cell arteritis.
2.Posterior ischemic optic neuropathy (PION). -
-PION is a much less common type. It is due to acute ischemia of the back (posterior) part of the optic nerve, located some distance behind the eyeball; this part of the optic nerve is NOT supplied by the posterior ciliary arteries
(Hayreh, 2009)
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anatomy of optic nerve and its blood supply and clinical corelation
Presentation Layout: optic nerve anatomy
Embryology of optic nerve
Introduction
Parts of optic nerve
Blood supply
Clinical significance
For Further Reading
Wolff’s Anatomy of the eye and orbit by Bron, Tripathi and Tripathi
Anatomy and Physiology of eye by A.K. Khurana 2nd edition
Comprehensive Ophthalmology by A.K. Khurana 5th edition
AAO- Fundamentals & Principles of Ophthalmology : sec 2
Walsh and Hoyt’s Clinical Ophthalmology
Internet
Direct Download Link ❤❤https://healthkura.com/eye-ppt/28/❤❤
Dear viewers Check Out my other piece of works at ❤❤❤ https://healthkura.com/eye-ppt/❤❤❤
anatomy of optic nerve and its blood supply and clinical corelation
Presentation Layout: optic nerve anatomy
Embryology of optic nerve
Introduction
Parts of optic nerve
Blood supply
Clinical significance
For Further Reading
Wolff’s Anatomy of the eye and orbit by Bron, Tripathi and Tripathi
Anatomy and Physiology of eye by A.K. Khurana 2nd edition
Comprehensive Ophthalmology by A.K. Khurana 5th edition
AAO- Fundamentals & Principles of Ophthalmology : sec 2
Walsh and Hoyt’s Clinical Ophthalmology
Internet
Disc oedema is a common entity in ophthalmology. Different causes and differential diagnosis are described in the ppt. Pathogenesis, clinical features,signs, symptoms and treatment options are described. Papilloedema should be differntiated from optic neuritis. Papilloedema has different stages in its clinical courses. Different stages has its separate appearance. Different clinical tests are done to see the progress of the disease.
Also called Disc oedema
Passive disc swelling associated with increased intra cranial pressure
Bilateral and asymmetrical
Inflammations such as papillitis, neuroretinitis, papillophlebitis and uveitis.
Ocular hypotony
CRVO, AION (anterior ischemic optic neuropathy) and uremia
Orbital causes – tumors, grave’s orbitopathy and orbital cellulitis
Leukemia and lymphomas
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
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
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
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.
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.
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Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
2. PAPILLOEDEMA
• Oedema of the optic disc or
nerve head due to raised
intracranial pressure.
• Optic nerve is enclosed up to the
lamina cribrosa within the
meningeal sheaths common to
the brain.
– Rise in ICT is equally evident
around the nerve.
– Development of oedema at the optic
disc.
– Hydrostatic, non inflammatory
phenomenon.
3. AETIOLOGY
• Increased intracranial pressure.
Due to intracranial space
occupying lesion, mainly
tumours of the midbrain,
parieto-occipital region and
cerebellum.
Brain abscess
Thrombosis of cavernous
sinus or other intracranial
veins Aneurysm
Subarachnoid haemorrhage
Pseudotumour cerebri
Malignant
hypertensio
n
4. (a) Left optic nerve sheath meningioma with disc edema and shunt vessels.(b)Axial computed
tomography of the orbits with contrast showing enhancement along the left optic nerve (arrows).
6. PATHOLOGY
• Passive oedema without
evidence of infammation.
• Small blood vessels are engorged
and tortuous.
7. • Nerve fibres in ONHare swollen and
axoplasmic stasis is noted.
• Physiological cup gets filled in and
internal limiting membrane israised.
• Nerve fibres become swollen and
varicose and ultimately degenerate.
• Numerous cystoid bodies in frontof
lamina cribrosa.
• Engorgement of axons.
Swollen axonsare filled with
mitochondria.
Mitochondria are structurallyswollen
and disrupted.
Cotton-wool spots. A, Clinical appearanceof cotton-wool spots. B,Microinfarct of nerve
fiber layer produces aggregates of ruptured and enlarged axons(cytoid bodies). Cytoid
bodies, observed clinically ascotton-wool spots, lie just under internal limiting
membrane. C,Nucleoid of cytoid body consistsof dense massof filamentous material, the
edgeof which is more detailed in inset. D, Marked swelling of axon (a) in nerve fiber layer
two hours after experimental central retinal arteryocclusion (m, axonal mitochondrion).
8. PATHOLOGICALCHANGES IN SURROUNDING RETINA AND MACULAR REGION
• Oedemain the nerve fibrelayer
raises the internal limiting
membrane in folds.
• Retinal exudates distributed
radially along the folds,present
in the macular region- Macular
fan or Macularstar.
9. STAGESOFPAPILLOEDEMA
• EARL
YST
AGE
Fullness and tortuosity of veins
Venouspulsation on optic disc is
absent
• LA
TEST
AGE
Hard exudates on retina between
disc and macula
Macular star and macularfan
10. SYMPTOMS
• Early stages-Asymptomatic
• Ontime- Constant compression
leading to transient ischemia
without obscuring visual
functions (4-6 weeks)
• >6weeks- Nerve fibres
degenerate
Transient obscuration of vision
Enlargement of blind spot
Contraction of visualfield
Relative scotoma
• Transient attacks of blurred
vision- Bilateral or monocular
black outs lasting for afew
secondsoften precipitated by
changesin posture.
• Chronic papilloedema- Severe
loss of central visualacuity.
11. • Asatrophy sets in-
– Complete blindness
– Pupils are large and
immobile
– Headachewhich is worse in
arecumbent position
– Nauseaand vomiting
– Diplopia (Non specific
paresis of the sixthnerve)
This7-year-old boy with abrain stem glioma presented with diplopia associatedwith bilateral
sixth nerve palsiesthat had started gradually about 2 months before and more recent symptoms
of raised intracranial pressure. Theoptic discs are grossly elevated with markedly dilated
capillaries and veins, numerous cotton wool spots, and the right eye hasamacular star, asaresult
of protein/lipid accumulation from transudation from disc capillaries.Although the blind spots
were very large on Goldmann fields, the visual acuity was 0.1 (6/7.5, 20/25, 0.8) right and 0.0 left.
12. SIGNS
• Blurring of optic discmargins-
– Starts at upper and lower margins
and extends around the nasalside,
temporal side usually visible and
sharp
– Hyperaemic
– Progressive edema reduces sizeof
the physiologicalcup
• Veinsbecome congested and
turgescent (absentpulsations)
13. • Small arterioles become
prominent, appearing asred
streaks.
• Eventually the disc becomes
elevated into amound higher
than the surrounding retinaand
mushrooms out sothat the
vesslesbends sharply over its
margins
Definite parallax elicited with IDO
• Flameshaped and punctate
hemorrhages
• Surface of the disc losesits
reddish hue, now opaque.
Note circumferential retinal folds a.k.a Paton’slines.
Veinsthat are enormously dilated may be buried for large
tracts of their course in theswolen and oedematous retina.
14. • Macular star- Radiating,
oedematous folds around the
macula (incomplete)
• Macular fan- fan shaped folds on
the side towards the disc
• Cotton wool spots due to retinal
microinfarcts- scattered
throughout posterior half of
fundus
• Longstanding cases-Atrophic
changeswhen the nerve fibres
canno longer withstand the
pressure and degenerate.
Optic atrophy secondary to long standingpapilloedema
15. • Usually bilateral, not necesssarily
equal on both sides.
• Foster-Kennedy syndrome- U/L
papilledema with or without optic
atrophy on groove or orbitalsurface
if the frontal lobe or of the pituitary
body.
• DIAGNOSIS:
Indirect ophthalmoscopy-difficult
to assessin early casesfor disc
changes
Fluorescien angiography
demonstrates dilatation of the
surface capillaries and leakageof
the dye (vertically oval pool
surrounding the nervehead)
(a) Truediscedemawith (b) leakageon fluorescein angiography (latephase).
16. DIFFERENTIALDIAGNOSIS
• ISCHAEMICOPTICNEUROP
A
THY
-
– Arteritic a/w GCAor NonArteritic a/w
vasculopathy
– Profound, sudden visual loss
– Swollen disc, characteristic pallid
appearance
– Selflimiting disease, >55 years,women
– Non arteritic ischaemic opticatrophy,
involvement of short posterior ciliary
branches leading to swelling of optic
nerve head and later to atrophy and
sometimes cupping.
(a) Right anterior ischemic optic neuropathy with mild disc edemaand afew
peripapillary hemorrhages. (b) Corresponding inferior altitudinal visual field
defect on a30–2 Humphrey visual field test.
17. TREATMENT
• Relief of causalpressure
• Timely decompression or
removal of tumour- Relief of
general symptoms of raisedICT,
vision improves rapidly if the
nerves have not been
irretrievably damaged and
papilledema subsides
• Surgical option for
pseudotumour cerebri-
Lumbar peritoneal shunt, or local
decompressionby making
multiple slits or cutting awindow
in the optic nerve sheaths (dura
and arachnoid) in the orbit.
