The document discusses the anatomy and examination of the cornea. It provides details on:
- The 5 layers of the cornea including the epithelium, Bowman's membrane, stroma, Descemet's membrane, and endothelium.
- Common conditions that may be observed during examination of the cornea such as nebula, leucoma adherent, and keratoconus.
- Procedures like keratoplasty that are used to treat opaque areas of the cornea by replacing the diseased tissue with healthy donor corneal tissue.
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
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
Vitreous hemorrhage is the extravasation, or leakage, of blood into the areas in and around the vitreous humor of the eye.[1] The vitreous humor is the clear gel that fills the space between the lens and the retina of the eye. A variety of conditions can result in blood leaking into the vitreous humor, which can cause impaired vision, floaters, and photopsia.
It's an indepth presentation by Dr. Shah-Noor Hassan.
Vitreous hemorrhage is the extravasation, or leakage, of blood into the areas in and around the vitreous humor of the eye.[1] The vitreous humor is the clear gel that fills the space between the lens and the retina of the eye. A variety of conditions can result in blood leaking into the vitreous humor, which can cause impaired vision, floaters, and photopsia.
It's an indepth presentation by Dr. Shah-Noor Hassan.
Classification of Eye Movements Using Electrooculography and Neural NetworksWaqas Tariq
Electrooculography is a technique for measuring the cornea-retinal potential produced by eye movements. This paper proposes algorithms for classifying eleven eye movements acquired through electrooculography using dynamic neural networks. Signal processing techniques and time delay neural network are used to process the raw signals to identify the eye movements. Simple feature extraction algorithms are proposed using the Parseval and Plancherel theorems. The performances of the classifiers are compared with a feed forward network, which is encouraging with an average classification accuracy of 91.40% and 90.89% for time delay neural network using the Parseval and Plancherel features.
A comprehensive summary of all the common corneal diseases starting from different types infective keratitis, non infective keratitis, corneal dystrophies, corneal ectasias to corneal degenerations.
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.
direct ophthalmoscope
fundoscopy course
fundus examination
medical students
ophthalmology
faculty of medicine
kafrelsheikh university
new mansoura university
delta university
Acute Limb Weakness
case presentation
PBL session
3rd year
neuro ophthalmology
new mansoura university
A 54-year-old man, Mr. Stephen Smith, was brought by ambulance to the Emergency Department. He had woken up from sleep with slurring of speech and weakness of his right arm and leg. His wife was extremely distressed as Mr Smith had been perfectly well the previous night when he went to sleep. Within 20 minutes after the initial call was made Mr. Smith was admitted to the Emergency Department and was reviewed by the SpR covering the Regional Specialist Stroke Unit. Mr. Smith had been on regular antihypertensive medication (lisinopril) for 8 years. He smoked 5-8 cigarettes a day and was a social drinker consuming about 6 units of alcohol a week. He was not diabetic.
His Serum lipids were checked and was advised to reduce weight and started on a Statin (Simvastatin). There was no family history of hyperlipidaemia but his grandfather died after a Stroke. Mr. Smith had an urgent appendectomy 1 week and made an uneventful recovery. He lives with his wife in a 4-bedroom detached house.
Neurological examination showed that Mr. Smith was fully conscious and alert. He had an upper motor neuron facial palsy on the right side. He had expressive dysphasia but appeared to comprehend speech. He was just able to lift his right arm off the bed for a short period but had no grip. His right leg was weak.
Reflexes on the right side were exaggerated and his right plantar was extensor. He responded to touch and pin prick equally on both sides. He either had visual inattention or a visual field defect on the right side. He had no papilloedema His blood pressure was 164/96, pulse 84 per min, regular. Other systems were entirely normal.
ECG and all routine blood tests were performed. An emergency CT scan was requested and even though the scan was normal the SpR ruled out emergency thrombolysis in this instance. Mr. Smith was admitted to the Acute Stroke Unit and was seen by the Stroke Consultant. Mr. Smith remained fully conscious and alert but had some difficulty in swallowing. Hence an intravenous infusion was commenced and an alternate strategy was adopted for providing his nutritional requirements. A carotid Doppler scan was requested.
After 3 weeks, Mr. Smith seemed to make good progress and the MDT meeting recorded a consistent improvement in his Barthel Index. The Stroke Team met him with his wife and discussed arrangements for discharge home. His wife was keen to know what support measures were available to them when Mr. Smith returned home. She also wanted to know about the risk of a future stroke and how this could be cut down.
ILOs:-
1- Consider the differential diagnosis of speech.
2- Discuss the risk factors for stroke and primary prevention of stroke.
3- Discuss the overall management of a patient with an acute stroke.
4- Complications of stroke
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.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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.
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.
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
3. Anterior 1Anterior 1/6 of outer coat/6 of outer coat
Curved & Domshaped
Fibrous, Transparent & No BVsFibrous, Transparent & No BVs
Diameter : Horizontal 12mmDiameter : Horizontal 12mm
Vertical 11mmVertical 11mm
Thickness: Central 0.5 - 0.6mmThickness: Central 0.5 - 0.6mm
Peripheral 0.8 – 1.0mmPeripheral 0.8 – 1.0mm
Refractive Power : 42 DRefractive Power : 42 D
( What is The LIMBUS ?)( What is The LIMBUS ?)
4. 5 Layers of the Cornea
a.Epithelium: 5-6 layers of cells
b.Bowman’s membrane: clear acellular layer
c.Stroma: 90% of corneal thickness
collagen fibrils that are parallel to each other
d.Descemet’s membrane: basal lamina of corneal
endothelium
e.Endothelium: single layer of cells which act as a
“pump”
5. NERVE SUPPLY OF THE CORNEANERVE SUPPLY OF THE CORNEA
55THTH
C.NC.N
OPHTH. division NASOCILIARY N 2 LongOPHTH. division NASOCILIARY N 2 Long CILIARY NCILIARY N
PAIN & COLD & SUPERFICIAL TOUCHPAIN & COLD & SUPERFICIAL TOUCH
12. SUPPURATIVE SUPERFICIALSUPPURATIVE SUPERFICIAL
KERATITSKERATITS
(CORNEAL ULCERS)(CORNEAL ULCERS)
DEFINITIONDEFINITION
Localized Necrosis of Sup. StromaLocalized Necrosis of Sup. Stroma
with destruction of overlying Epith.with destruction of overlying Epith.
ETIOLOGYETIOLOGY
Predisposing FactorsPredisposing Factors
Causative OrganismsCausative Organisms
13. Predisposing FactorsPredisposing Factors
LocalLocal
a) Traumaa) Trauma
- Abrasion- Abrasion
-- FB , Rubbing lashes , PTDs , CLFB , Rubbing lashes , PTDs , CL
b) Loss of corneal sensationsb) Loss of corneal sensations
c) Ocular causesc) Ocular causes (( xerosis, A deficiency, Lagoph.).)
d) Prolonged use of Steroidsd) Prolonged use of Steroids
GeneralGeneral
malnutrition Pregnancymalnutrition Pregnancy
Diabetes Liver & Renal FailureDiabetes Liver & Renal Failure
14. CAUSATIVE ORGANISMSCAUSATIVE ORGANISMS
a) Bacterial e.g. Gono, Diphth., Pneumo,a) Bacterial e.g. Gono, Diphth., Pneumo, Staph, StreptStaph, Strept….….
b) Fungal ( not common )b) Fungal ( not common )
c) Viral e.g. Herpes Simplex and Zosterc) Viral e.g. Herpes Simplex and Zoster
d) Acanthamoeba (C.L.)d) Acanthamoeba (C.L.)
15. CLINICAL PICTURECLINICAL PICTURE
SymptomsSymptoms
Pain Severe ( FB or pricking sensation )Pain Severe ( FB or pricking sensation )
Irritation of nerve endingsIrritation of nerve endings
PhotophobiaPhotophobia
LacrimationLacrimation
BlepharospasmBlepharospasm
Diminution of visionDiminution of vision
SignsSigns
Lids: OedemaLids: Oedema
Conj.: Ciliary injectionConj.: Ciliary injection
Cornea: Loss of luster, Grey infilt., Oedema & +ve FTCornea: Loss of luster, Grey infilt., Oedema & +ve FT
Iris: Tender CB, Const. pupil & Aqueous flareIris: Tender CB, Const. pupil & Aqueous flare
16. COMPLICATIONS OF CORNEAL ULCERSCOMPLICATIONS OF CORNEAL ULCERS
A) Non Perforated corneal ulcer
Early Complications
(1)(1) 2ry Iridocyclitis : ( Toxins )2ry Iridocyclitis : ( Toxins )
(2) 2ry Glaucoma(2) 2ry Glaucoma : Open angle glaucoma: Open angle glaucoma
(3) Descematocele :
Late Complications (Healing abnormalities)
(1) Corneal opacity ( Nebula, Macula or Leucoma non adherent )
(2) Keratectasia:( weak corneal scar)
(3) Pseudoptregium
17. B) COMP. OF PERFORATED CORNEAL ULCERSB) COMP. OF PERFORATED CORNEAL ULCERS
Early Complications
(1) Iris Prolapse
(2) Anterior synechia ( Small periph. Perforation)
(3) Corneal Fistula ( Small central perforation )
Lost AC IOP River Green Sign
(4) Malposition of the Lens
Sublaxation Ant. Dislocation Extrusion
(5) Intra-ocular Hge
Hyphema Vit., Ret. And choroidal hges
(6) Macular and Optic Disc Oedema
(7) Endo or Panophthalmitis
18. Late complications
(1) Ant.Polar Cataract (Toxins )
(2) Leucoma Adherent ( Large Peripheral Perforation )
- AC irregular
- Pupil pear shaped
(3) Ant. Staphyloma ( partial or total )
(4) 2ry Glaucoma (closed angle by PAS )
(5) Atrophia bulbi ( atrophy of the cil. processes )
B) COMP. OF PERFORATED CORNEAL ULCERS (cont.)B) COMP. OF PERFORATED CORNEAL ULCERS (cont.)
19. MANAGEMENT OF CORNEAL ULCERSMANAGEMENT OF CORNEAL ULCERS
INVESTIGATIONS + TREATMENT
A) Corneal Scrapping ( Culture & Sensitivity )
Gram Stain for Bacteria
Geimsa Stain for Trachoma & Acanthamoeba
Silver Stain for Fungi
B) Local ttt (1) Atropine sulphate 1%
(3) Bandage or Dark Glasses
(4) Counter irritant
(2) Dressings ( Antibiotic dps & oint )
C) Systemic ttt
Antibiotics Analgesics
Vitamins A & C
22. Signs ( Acute Serpiginous ulcer )
- Ulcer Near the centre
Central advancing Edge
Crescentic, undermined,
preceded by dense infiltration
Peripheral Healing Edge
Flat, Epithelialized, Vascularized
- Posterior Abscess :
Dense infiltration in front of D M
- Hypopyon in the Anterior Chamber
( Sterile Pus )
23. Fungal UlcerFungal Ulcer
Predisposing Factors
Trauma with green plant
Use of Steroids
Contact Lenses
Causative Agent
Fusarium ( Filamentary fungi )
Candida ( Yeast forming fungi )
24. Acanthamoeba keratitisAcanthamoeba keratitis
Aetiology
Protozoa ( Tap water and Swimming pools )
70% of cases are C L wearers
Clinical Picture
Punctate or Dendritic K
Partial or Complete ring of Infiltration
25. Dendritic Corneal UlcerDendritic Corneal Ulcer
Herpes Simplex Virus ( Epitheliotropic )
1ry infection in early childhood
Dormant in 5th
Ganglion
Recurrence with body resistance
Predisposing factors
Fevers (Influenza, Common cold and Pneumonia)
Menstruation
Drugs ( Immunosuppressive drugs or Steroids)
Clinical Picture
1ry Ocular infection Dermato-blepharitis
Follicular Conjunctivitis
Epithelia Keratitis
26. Recurrent Ocular Infection (C/P of H. Keratitis)
(A) Blepharoconjunctivitis
(B) Epithelial Keratitis: Dendretic Herpetic Corneal Ulcer
Dendritic appearance
Long course with tendency to Recurrence
Superficial ( never perforate except in … )
Never Vascularised
Hypothesia
Double Stain Test
C) Amoeboid Ulcer
due to immunity or local Steroids
27. Herpes Zoster OphthalmicusHerpes Zoster Ophthalmicus
Varicella-Zoster (Neurotropic) Virus
Old age - Immunity
Clinical Picture :
Lids : Dermatoblepharitis ( pain and rash )
Keratitis : ( Hutchinson’s rule )
Epithelial Keratitis ( Punctate or dendritic )
Interstitial Keratitis
28. Ulcer with LagophthalmosUlcer with Lagophthalmos
Bell’s phenomena
Symptoms
as usual corneal ulcer ( of vision is not marked..why?)
Signs
Incomplete lid closure
Ciliary injection & +ve flurorescein
Ulcer in lower 1/3 with straight upper border
Treatment
Usual ttt
Methyl cellulose drops 0.5% several times/day
29. KeratomalaciaKeratomalacia
Non infective ulceration and melting of the cornea
Vitamin A (malnourished infants or malabsorption in adults)
Clinical Picture
Loss of corneal luster
Melting of the cornea
Corneal hypothesia
Conjunctiva: dry with Bitot’s spots
Treatment
Vit. A injection (200,000 IU/day)
Topical vit. A in early cases
Surgical ttt in late cases : Conj. Flap
Therapeutic CL
PK
30. Neurotrophic (Neuroparalytic) KeratitisNeurotrophic (Neuroparalytic) Keratitis
Corneal Sensation
Aetiology
Herpes Zoster
Clinical Picture
Symptoms No pain
vision (central ulcer)
Signs
Large deep ulcer perforation
Treatment
Usual ttt of corneal ulcer
Long term Bandage
Tarsorraphy ( median )
32. Degenerative ConditionsDegenerative Conditions
ARCUS SENELIS
Bilateral peripheral Fatty degeneration
Common in old age
Symptoms non
Signs
Clear zone between the opacity and Limbus (Lucid interval of vogt)
NB ARCUS JUVENILIS may occur in hyperlipidemia or juv. DM
33. Band Shaped keratopathyBand Shaped keratopathy
Horizonal opacity ( in the interpalpebral area )
Hyaline degeneration + Ca deposition
34. KERATOCONUSKERATOCONUS
Definition
Progressive conical protrusion of the cornea
Starts at Puberty
Weakness of central part
Incidence
Bilateral
+ve family history
Symptoms
Gradual of vision - Myopia ( Curvature & Axial )
- irregular Astigmatism
- Opacity at the apex of the cone
Sudden of vision (Acute Hydrops i.e. acute edema due to rupture of DM)
35. Signs of Keratoconus
A) Early
Retinoscopy ( RR is spinning or scissoring )
placido disc: ring distortion
Keratometer
B) Late
- Cone shaped central cornea
Notching of the L.L. on looking down Manson’
Slit Lamp Thin apex and deep A.C.
- Fleisher ring: brown ring the cone base ( hemosidren deposition )
37. KERATOPLASTYKERATOPLASTY
Aim: Replacing the opaque part by a clear cadaveric cornea
Types:
- Lamellar ( Superficial )
- Deep ( Penetrating )
NB: Both of them may be partial or total
Indications:
- Optical a) Central corneal opacities
b) Keratoconus
- Therapeutic a) Resistant corneal ulcer
b) Corneal fistula