Author : Dr. Sheldon Fernandes Ophthalmology Resident, Co- Author : Dr. Shubha Nagpal Professor & Head Dept of Ophthalmology Bharati Vidyapeeth University Medical College, Pune.
Rare genetic disorder that occurs worldwide in all races and ethnic groups.
First described by Hebra and Kaposi in 1874.
Photosensitivity and premature onset of all major types of skin cancer .
Inability of a cell to repair damage caused by UV leading to genetic instability and skin cancer.
Responsible for removing the damaged segments of DNA and restoring the original sequence of DNA.
The NER mechanism is composed of two types:
Transcription coupled(TCR): Which rapidly repairs areas of DNA that are "active" and being transcribed into RNA
Global genome(GGR): Which repairs damage in the rest of the genome more slowly
Seven XP genes are central to NER which includes many other accessory proteins
The term “complementation group” is based on cell fusion experiments.
Cells from different XP patients are fused to investigate if the DNA repair defect in the fused cells is corrected.
If DNA repair in the fused cell is increased, each cell provides proteins that the other is lacking and the cells “complement” each other and are in different complementation groups.
If DNA repair in the fused cells is not normalized, the cells do not “complement” each other, meaning that both cells harbor mutations in the same DNA repair gene.
Seven such complementation groups have been identified (XP-A to XP-G), which correspond with mutations in seven distinct genes that can cause XP.
Severity changes is dependent on the amount of sun exposure and the degree of UVR protection
Acute and severe sunburn on minimal sun exposure takes weeks to resolve.
50% of XP patients suffer from severe and prolonged sunburn reactions.
Rest 50% have sunburn reactions that are normal and present with lentigines as well as hypopigmented macules.
Development of many freckles at an early age.
• Rough-surfaced growths (solar keratoses), and skin cancers
• Blistering or freckling on minimum sun exposure
• Telangiectasia (spider veins)
• Limited growth of hair on chest and legs
•
Author : Dr. Sheldon Fernandes Ophthalmology Resident, Co- Author : Dr. Shubha Nagpal Professor & Head Dept of Ophthalmology Bharati Vidyapeeth University Medical College, Pune.
Rare genetic disorder that occurs worldwide in all races and ethnic groups.
First described by Hebra and Kaposi in 1874.
Photosensitivity and premature onset of all major types of skin cancer .
Inability of a cell to repair damage caused by UV leading to genetic instability and skin cancer.
Responsible for removing the damaged segments of DNA and restoring the original sequence of DNA.
The NER mechanism is composed of two types:
Transcription coupled(TCR): Which rapidly repairs areas of DNA that are "active" and being transcribed into RNA
Global genome(GGR): Which repairs damage in the rest of the genome more slowly
Seven XP genes are central to NER which includes many other accessory proteins
The term “complementation group” is based on cell fusion experiments.
Cells from different XP patients are fused to investigate if the DNA repair defect in the fused cells is corrected.
If DNA repair in the fused cell is increased, each cell provides proteins that the other is lacking and the cells “complement” each other and are in different complementation groups.
If DNA repair in the fused cells is not normalized, the cells do not “complement” each other, meaning that both cells harbor mutations in the same DNA repair gene.
Seven such complementation groups have been identified (XP-A to XP-G), which correspond with mutations in seven distinct genes that can cause XP.
Severity changes is dependent on the amount of sun exposure and the degree of UVR protection
Acute and severe sunburn on minimal sun exposure takes weeks to resolve.
50% of XP patients suffer from severe and prolonged sunburn reactions.
Rest 50% have sunburn reactions that are normal and present with lentigines as well as hypopigmented macules.
Development of many freckles at an early age.
• Rough-surfaced growths (solar keratoses), and skin cancers
• Blistering or freckling on minimum sun exposure
• Telangiectasia (spider veins)
• Limited growth of hair on chest and legs
•
This ppt describe about the incidence, diagnosis and management of maculopathy in caaes of pathological myopia.
Data collected and created by Vivek Chaudhary
For queries : vivek977optom@gmail.com
The eye is a mirror which reflect the health of other systems in the human body.
The human eye, as an organ, can offer critical clues to the diagnosis of various systemic illnesses.
Ocular changes are common in various endocrine disorders such as diabetes mellitus and Graves’ disease.
Awareness of the associations between the ocular manifestations and endocrine disorders is the first step in the diagnosis and management of these complex patients.
This ppt describe about the incidence, diagnosis and management of maculopathy in caaes of pathological myopia.
Data collected and created by Vivek Chaudhary
For queries : vivek977optom@gmail.com
The eye is a mirror which reflect the health of other systems in the human body.
The human eye, as an organ, can offer critical clues to the diagnosis of various systemic illnesses.
Ocular changes are common in various endocrine disorders such as diabetes mellitus and Graves’ disease.
Awareness of the associations between the ocular manifestations and endocrine disorders is the first step in the diagnosis and management of these complex patients.
The presentation was made under the wise guidance of my professor DR.(prof) P. Rawat (MGMMC & M.Y. HOSPITAL, INDORE).It covers the essential aspects of optic neuritis & optic atrophy.
This lecture is based on medical students those are preparing for postgraduate degree namely FCPS/MS/MD/ any any subject coz hypertension is a systemic disease and by seeing the ocular fundus we can asses the general condition of blood vessels in major organ.
This lecture is based on post-graduate students of Ophthalmology (DO, DCO, MCPS, FCPS, MS) and optical principle of LASER, construction of laser and laser tissue interaction has cover the lecture
This lecture is based on post-graduate students of Ophthalmology (DO, DCO, MCPS, FCPS, MS) and optical principle of GAT has to know for a student to use the instrument friendly
This lecture is based on post-graduate medical students of all subject those who are students MS/MD/FCPS of different subject on Central Tendency and Dispersion.
This is the 5 th lecture on "Research Methodology through zoom. The lecture was based on postgraduate Medical students those are different courses of FCPS/MS/MD/PhD (any Specialty)
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
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
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
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.
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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.
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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
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.
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.
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
2. Optic Nerve
Each optic nerve carries about 1.2 million fibers that arise from the retinal
ganglion cells. The optic nerve has the following parts:
Intraocular nerve head 0.7 mm
Intraorbital 30 mm
Canalicular 6 mm
Intracranial 10 mm
Total 46.7 mm
3. Diseases of the optic nerve
a) Congenital anomalies
b) Oedema: Papilloedema
c) Inflammation: Optic neuritis
d) Atrophy: Optic atrophy
e) Tumours
4. Optic atrophy
• Optic atrophy refers to the death of the retinal ganglion cell axons that comprise
the optic nerve
• Optic atrophy is an end stage that arises from myriad causes of optic nerve
damage anywhere along the path from the retina to the lateral geniculate.
• Optic atrophy is somewhat of a misnomer as atrophy implies disuse,
and thus optic nerve damage is better termed optic neuropathy.
5. Optic atrophy:
Optic atrophy: Degeneration of optic nerve
There are 3 types of optic atrophy
a) Primary optic atrophy
b) Secondary optic atrophy
c) Consecutive optic atrophy
d) There is another type of optic atrophy which is called glaucomatous optic
atrophy
6. Primary optic atrophy
In conditions with primary optic atrophy (eg, pituitary tumor, optic nerve tumor,
traumatic optic neuropathy, multiple sclerosis), optic nerve fibers degenerate in an
orderly manner and are replaced by columns of glial cells without alteration in the
architecture of the optic nerve head.
7. Primary Optic atrophy
The disc is chalky white and
sharply demarcated, and
the retinal vessels are normal.
Lamina cribrosa is well
defined.
8. Secondary optic atrophy
In conditions with secondary optic atrophy (eg, papilledema, papillitis), the
atrophy is secondary to papilledema.
Optic nerve fibers exhibit marked degeneration, with excessive proliferation of
glial tissue.
The architecture is lost, resulting in indistinct margins.
On visual fields, progressive contraction of visual fields may be seen
9. The disc is grey or dirty
grey,
the margins are poorly
defined,
Lamina cribrosa is obscured due to proliferating fibroglial tissue.
Hyaline bodies (corpora amylacea) or drusen may be observed.
Peripapillary sheathing of arteries as well as tortuous veins may be observed.
Secondary Optic atrophy
10. Consecutive optic atrophy
Consecutive atrophy is an ascending type of atrophy (eg,
chorioretinitis, pigmentary retinal dystrophy, cerebromacular
degeneration) that usually results from diseases of the choroid or the
retina.
11. Consecutive optic
atrophy due to PRP.
The disc is waxy pale with
a normal disc margin,
Marked attenuation of
arteries, and
A normal physiologic cup.
12. Glaucomatous optic atrophy
Characteristics include
vertical enlargement of cup,
visibility of the laminar pores (laminar dot sign),
backward bowing of the lamina cribrosa,
bayoneting and nasal shifting of the retinal vessels, and peripapillary halo and
atrophy.
Splinter hemorrhage at the disc margin may be observed.
13.
14.
15. Primary optic
Atrophy
Secondary
Optic Atrophy
Consecutive
Optic Atrophy
Glaucomatous
optic Atrophy
Optic disc Chalky white or
white
Dirty white in
colour
Disc appears
yellow waxy
Pale disc
Margin Margins are
sharply outlined
Edges are
blurred
Edges are not so
sharply defined
Edges are well
define
Blood vessels Major retinal
blood vessels
and surrounded
retina are
normal
Vessels are
attenuated and
perivascular
sheathing
Vessels are
attenuated
Normal
16. Important causes of primary OA
a) Optic neuritis RBN
b) Compression by tumours and aneurysms.
c) Hereditary optic neuropathies.
d) Toxic and nutritional optic neuropathies; these may give temporal pallor,
particularly in early/milder cases when the papillomacular fibers are
preferentially affected
21. Inflammation of the Optic Nerve (Optic Neuritis)
An inflammation of the optic nerve is known as optic neuritis. The optic nerve
may be affected by inflammation in any part of its course, but for clinical
convenience it is usual to divide inflammatory conditions into two categories:
Those affecting the part of the nerve ophthalmoscopically visible at the disc and
therefore showing obvious signs of disease:
a) Papillitis, or
b) Neuroretinitis, and
22. Inflammation of the Optic Nerve (Optic Neuritis)
Those which attack the nerve proximal to this region and therefore show no
ophthalmoscopic changes, so that the diagnosis has to be made on the basis of
symptoms alone:
Retrobulbar neuritis.
23. Papillitis
• Papillitis is characterized by hyperaemia and oedema of the optic disc, which may
be associated with peripapillary flame-shaped haemorrhages.
• Cells may be seen in the posterior vitreous.
• Papillitis is the most common type of optic neuritis in children, but can also affect
adults
24. Papillitis is characterized by hyperaemia and
oedema of the optic disc,
associated with peripapillary flame-shaped
haemorrhages
Cells may be seen in the posterior vitreous.
Papillitis is the most common type of optic
neuritis in children, but can also affect adults
25. Difference between Papillitis & Papilloedema
1) Inflammation or infarction of
optic nerve head
2) Usually unilateral
3) At beginning
4) Central/paracentral scotoma to
complete blind
5) Disc hyperemic and elevated
better to see with + 2D
6) Engorged, tortuous vessels
7) Near or on disc
8) RAPD
9) Steroid
1) Swelling of optic nerve head due
to increased ICP
2) Bilateral
3) Late stage
4) Enlarged blind spot
5) Disc hyperemic and elevated
better to see with >+4 D
6) Engorged, tortuous vein
7) Around disc not periphery
8) No
9) Control ICP
1) Definition
2) Unilateral/bilateral
3) Vision impairment
4) VF
5) Fundus appearance
6) Vessels appearance
7) Hemorrhage
8) Pupillary light reflex
9) Treatment
Comments Papillitis Papilloedema
27. Toxic, Nutritional and Hereditary Optic Neuropathy
(Parson’s): Aetiopathogenesis
Many nutritional deficiencies, toxic and hereditary optic neuropathies produce a
very similar clinical picture because there are common pathways by which these
vitamins work and by which many of these toxins interact
Vitamin deficiencies associated with poor diet may be compounded by the
ingestion of cassava and elevated levels of cyanide.
28. Cassava is the third-largest source of food
carbohydrates in the tropics,
after rice and maize. Cassava is a
major staple food in the developing world,
providing a basic diet for over half a
billion peoples. Nigeria is the world's
largest producer of cassava, while Thailand
is the largest exporter of cassava starch.
It must be properly prepared before
consumption, as improper preparation of
cassava can leave enough
residual cyanide to cause acute cyanide
intoxication
Cassava
29. Toxic, Nutritional and Hereditary Optic Neuropathy
(Parson’s): Aetiopathogenesis
• Within the mitochondria, oxidative phosphorylation involves the process of
electron transfer to oxygen at one end and the production of adenosine
triphosphate (ATP) at the other end.
• Vitamins such as B12 and folic acid are crucial to this process.
• Agents such as cyanide or formate (a metabolic product of methanol) block this
electron transport.
30. Toxic, Nutritional and Hereditary Optic Neuropathy
(Parson’s): Aetiopathogenesis
• The net result of these deficiencies and toxins is the decreased production of ATP
by mitochondria within all the cells of the body, most of which have compensatory
mechanisms to cope with this metabolic stress, such as muscle cells, which can
produce more mitochondria.
• Neurones with very low, very thin or unmyelinated axons, such as the
papillomacular bundle, are at a great disadvantage and more prone to be damaged
by these disorders.
31. Clinical Features
Usually, there is a sudden or rapid painless bilateral vision loss.
Simultaneous involvement of both eyes is more common with nutritional
deficiency, toxic and some hereditary disorders,
but monocular onset and fellow eye involvement occurring later (days, weeks or
months) is more common with Leber hereditary optic neuropathy.
Visual loss occurs, ranging from mild [6/7.5 (20/25)] to severe (finger-counting).
32. Clinical Features
Other clinical signs include disturbed colour perception and field defects typically
characterized by a centrocaecal scotoma.
Later, a temporal pallor of the disc becomes evident.
Associated neurological features such as paraesthesiae, ataxia and impaired
hearing may be seen
33. Differential Diagnosis
Leber hereditary optic neuropathy
Kjer autosomal dominant optic neuropathy
Compressive optic neuropathy (pituitary adeno ma or craniopharyngioma
compressing the optic chiasma)
Bilateral optic neuritis
34. Treatment
Avoidance of smoking, improvement of diet, nutritional supplementation and
administration of vitamins (B1, B6, B12) may show good results if the diagnosis is
made early and treatment instituted.
Vision can return to normal or near normal over several months. However, visual
loss is permanent in chronic, long-standing nutritional or toxic optic neuropathy
35. Toxic Optic Neuropathies
These include a number of conditions in which the optic nerve fibres are damaged
by exogenous poisons. Previously, these were called the toxic amblyopias, which is
a misnomer going by the modern definition of amblyopia.
36. The most common of these poisons are
tobacco,
ethyl alcohol,
methyl alcohol,
arsenic,
lead,
thallium,
carbon disulphide,
stramonium and
Cannabis indica
In some of them (tobacco, methyl
alcohol), the disease is primarily retinal
and follows poisoning of the ganglion
cells of the retina which results in
degeneration of the nerve fibres.
Others are due to a direct effect on the
nerve fibres themselves.
37. The neuropathy produced by diabetes, carbon disulphide (seen in the rayon
industry), and iodoform resembles that of tobacco.
38. Tobacco-induced Optic Neuropathy: Pathogenesis
This results from the excessive use of tobacco, either pipe smoking or chewing,
and from the absorption of dust in tobacco factories. Cigars suffer the most;
cigarette smokers are rarely affected.
In many cases there is also an over-indulgence of alcohol but this is not invariable.
Patients, usually 35–50 years of age, may have smoked excessively for years with
digestive disturbance.
The potent factor is cyanide in tobacco associated with a deficiency of vitamin B12.
39. Tobacco-induced Optic Neuropathy: Symptoms
Pathologically, the condition is due to degeneration of the ganglion cells of the retina,
particularly of the macular area. In the nerve, the papillomacular bundle is degenerated
Clinically, the patient complains of increasing fogginess of vision, usually least marked in
the evening and in dull light.
Central vision is greatly diminished, so that reading and near work become difficult.
Although the condition is bilateral, one eye is usually more affected.
40. Tobacco-induced Optic Neuropathy: Diagnosis
The fundus is normal or a slight temporal pallor may be seen in the disc
but the diagnosis is made from the characteristic defects in the central fields.
These primarily involve the centrocaecal area between the fixation point and the
blind spot.
The scotoma gradually extends to involve the fixation area itself so that central
vision may be lost but the peripheral field remains unaffected.
41. Tobacco-induced Optic Neuropathy: Treatment
Consists of abstaining from tobacco and alcohol.
If this is done the prognosis is eventually good
Improvement may be hastened by intramuscular injections of 1000 mg
hydroxycobalamine. This dose should be repeated five times at intervals of 4 days
then at 2-weekly intervals for a few months.
Recovery may be monitored by the VEPs.
42. Optic Neuropathy: Ethyl Alcohol
Although alcohol is usually an adjuvant in tobacco-induced optic neuropathy,
it may cause a similar neuropathy in the absence of the latter.
Such patients frequently suffer from alcoholic peripheral neuritis.
The disease, characterized by a central scotoma,
may be due essentially to avitaminosis owing to chronic lack of nourishment.
43. Optic Neuropathy: Ethyl Alcohol
No specific therapy is available.
General measures such as stopping alcohol intake,
improved diet and
injections of hydroxycobalamine as outlined above can be tried.
Steroid therapy has not been found to be of any benefit.
44. Optic Neuropathy: Methyl Alcohol
Poisoning from drinking wood alcohol has always been common in countries
during prohibition, and occurs sporadically from drinking methylated spirit.
Individual susceptibility is marked.
It may occur in an acute or chronic form.
In the acute form there may be severe metabolic acidosis with nausea, headache
and giddiness followed by coma.
45. Optic Neuropathy: Methyl Alcohol
If the patient survives, vision fails very rapidly, passing through the stages of
contracted fields and
absolute central scotomata to
blindness.
The vision may improve, but usually relapses, becoming gradually abolished by
progressive optic atrophy.
Restoration of sight is rarely complete.
46. Optic Neuropathy: Methyl Alcohol
Ophthalmoscopically, there may be:
blurring of the edges of the discs and
diminution in the size of the vessels in the early stages.
Later there are signs of optic atrophy, usually of the primary type.
Pathologically:
there is widespread degeneration of the ganglion cells
47. Optic Neuropathy: Methyl Alcohol
Treatment
in the acute stage includes intra-venous bicarbonate and ethyl alcohol.
In the chronic form there is a gradual, progressive loss of vision with the
development of optic atrophy.
48. Optic Neuropathy: Arsenic
This is especially liable to cause optic atrophy, usually total.
Manifestations of acute toxicity include
burning in the throat, difficulty in swallowing,
nausea, vomiting, diarrhoea and abdominal pain,
with cyanosis, hypotension, delirium, seizures and haemolysis.
49. Optic Neuropathy: Arsenic
Manifestations of chronic poisoning include
erythroderma, hyperkeratosis,
hyperpigmentation, exfoliative dermatitis,
skin carcinoma,
bronchitis and polyneuritis.
50. Optic Neuropathy: Arsenic
The condition is diagnosed by the detection of arsenic in the hair and nails and the
measurement of arsenic levels in the blood (normal ,3 mg/dl) and urine (normal
,100 mg/L).
Acute ingestion is treated as a medical emergency. with gastric lavage and
dimercaprol.
D-penicillamine is useful in the treatment of chronic poisoning.
51. Optic Neuropathy: Lead
Lead poisoning is rarely seen nowadays since precautions have been taken to
eliminate salts of this metal from pottery glazes, children’s paints, painted toys,
etc.
However, it may still be a major problem due to vehicular pollution in some part
of the world.
Indigenous systems of medicine may include therapy with heavy metals for
prolonged periods.
52. Optic Neuropathy: Lead
• The ocular signs are optic neuritis or optic atrophy, which may be primary or post-
neuritic.
53. Optic Neuropathy: Ethambutol
Is used in the treatment of tuberculosis,
but acute or chronic optic neuritis, of uncertain mechanism, can occur.
Toxicity is broadly dose- and duration-dependent; the incidence is as high as 18%
at a daily dose over 35 mg/kg, but is rare (<1%) with a standard daily dose of 15
mg/kg or lower.
Toxicity typically occurs between 3 and 6 months of starting treatment,
54. Optic Neuropathy: Ethambutol
Symptoms may be absent.
but typically include painless bilateral blurring,
usually central though sometimes paracentral or peripheral.
Impairment of colour vision may be noticed
55. Optic Neuropathy: Ethambutol (Signs)
Minimal to severe reduction in VA,
normal or slightly swollen optic discs with splinter-shaped haemorrhages,
normal or sluggish pupils.
Red–green dyschromatopsia is the most common objective abnormality of colour
vision,
but subtle (undetectable on Ishihara testing) blue–yellow defects may be an early
finding.
56. Optic Neuropathy: Ethambutol
Visual field defects can be central or peripheral.
Prognosis is good following cessation of treatment, although recovery can be
prolonged.
A minority sustain permanent visual impairment, with optic atrophy.
57. Optic Neuropathy: Ethambutol (Screening)
Baseline VA and Ishihara testing are prudent prior to starting ethambutol, and the
patient should be advised of the necessity of reporting any visual disturbance.
Repeat testing should be performed frequently – possibly monthly – when the
dose is more than 15 mg/kg, and every 3–6 months with lower doses.
Ethambutol should be stopped immediately if toxicity develops, with
consideration also given to discontinuation of isoniazid if being used
synchronously.
59. Optic Neuropathy: Amiodarone
Optic neuropathy, probably demyelinative, affects 1–2% of patients on
long-term amiodarone treatment.
It is almost certainly not dose-related.
Distinction from non-arteritic anterior ischaemic optic neuropathy
(NAION), which also affects patients with systemic vascular disease, may
be difficult; it has been suggested that NAION is more common in patients
on amiodarone.
60. Optic Neuropathy: Amiodarone
Differentiation is clinically important as it is key to a decision about whether to
discontinue the drug.
The presence of a crowded optic disc,
speed of onset,
bilaterality,
duration of disc swelling and features of systemic amiodarone toxicity may be
helpful in this regard.
61. Optic Neuropathy: Amiodarone
• Presentation is with sudden or insidious unilateral or bilateral visual impairment,
after a mean period of 6–9 months taking the drug. About one-third of patients are
asymptomatic.
• Signs in a majority are unilateral or bilateral optic disc swelling that may persist
for a few months after medication is stopped. Corneal is Vortex keratopathy
(cornea verticillata)
62. Optic Neuropathy: Amiodarone
Investigation: Cranial imaging may be indicated when bilateral disc swelling is
present.
• Visual field defects are of varied configuration and severity, and may be reversible
or permanent
Prognosis is variable; cessation of the drug usually improves vision, but 20% may
deteriorate further. Final VA of worse than 6/60 occurs in around 20% of eyes.
Screening: Patients should be warned of the risk and cautioned to report visual
symptoms immediately