This document outlines various systemic disorders that can cause corneal changes. It discusses disorders in several categories including carbohydrate metabolism (mucopolysaccharidoses, diabetes mellitus), lipid metabolism (hyperlipoproteinemias, hypolipoproteinemias, shingolipidoses, mucolipidoses), amino acid metabolism, protein metabolism (amyloidosis), immunoglobulin synthesis, connective tissue (Ehlers-Danlos syndrome, Marfan syndrome), nucleotide metabolism (gout, porphyria), and mineral metabolism (Wilson disease). Each section describes the pathogenesis, clinical findings such as corneal clouding, recommended lab evaluations, and management approaches for the conditions.
presentation on intraolcular tumors including detailed explaination on their pathology diagnosis and treatment including details of retinoblastoma. enucleation
presentation on intraolcular tumors including detailed explaination on their pathology diagnosis and treatment including details of retinoblastoma. enucleation
This lecture is part of the yearly Basic Course Lectures in Ophthalmology given by the Dept of Ophthalmology and Visual Sciences at the Philippine General Hospital.
Originally given by Dr Pearl Tamesis-Villalon, it is a 1:30:00 hour lecture on the pathologic lesions seen in the vitreous, retina and choroid. It is meant for the general physician and the beginning ophthalmology resident who is interested in the basics of retinal pathology.
It includes pathologic changes seen in hypertension, diabetes, vaso occlusive disease, vitreous, membranes, choroid, retinal pigment epithelium, retinal detachments, etc. Lesions such as hemorrhages, cotton wool spots, hard exudates and their location in the retinal layers are explained. Fluorescein angiogram and OCT images are also incorporated.
Some images were grabbed from the internet, apologies for not making the necessary acknowledgements.
Epiretinal membrane and vitreomacula traction in updates by Panit Cherdchu, MD.Panit Cherdchu
Epiretinal membrane + Vitreomacula traction in focus of PPP from AAO guidelines includes definition, classification, investigation, treatment (Ocriplasmin,vitrectomy,observation)
This lecture is part of the yearly Basic Course Lectures in Ophthalmology given by the Dept of Ophthalmology and Visual Sciences at the Philippine General Hospital.
Originally given by Dr Pearl Tamesis-Villalon, it is a 1:30:00 hour lecture on the pathologic lesions seen in the vitreous, retina and choroid. It is meant for the general physician and the beginning ophthalmology resident who is interested in the basics of retinal pathology.
It includes pathologic changes seen in hypertension, diabetes, vaso occlusive disease, vitreous, membranes, choroid, retinal pigment epithelium, retinal detachments, etc. Lesions such as hemorrhages, cotton wool spots, hard exudates and their location in the retinal layers are explained. Fluorescein angiogram and OCT images are also incorporated.
Some images were grabbed from the internet, apologies for not making the necessary acknowledgements.
Epiretinal membrane and vitreomacula traction in updates by Panit Cherdchu, MD.Panit Cherdchu
Epiretinal membrane + Vitreomacula traction in focus of PPP from AAO guidelines includes definition, classification, investigation, treatment (Ocriplasmin,vitrectomy,observation)
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
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.
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
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
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.
2. OUTLINE
• Disorders of Carbohydrate metabolism
• Disorders of lipid metabolism and storage
• Disorders of amino acid metabolism
• Disorders of protein metabolism
• Disorders of Immunoglobulin synthesis
• Non-inflammatory disorders of connective tissue
• Disorders of Nucleotide Metabolism
• Disorders of Mineral Metabolism
4. MUCOPOLYSACCHARIDOSES
• rare, inherited lysosomal storage diseases
• can cause corneal clouding from the accumulation of incompletely degraded GAGs
within the keratocytes, corneal epithelium, and endothelium, and also within the
extracellular matrix of the cornea
• Incidence: 1 in 10,000 births.
6. PATHOGENESIS:
• At present, at least 8 MPS syndromes have been described, all of which are autosomal
recessive, with the exception of Hunter syndrome, which is X-linked.
• the three "MPS I" disorders (Hurler, Scheie, and Hurler-Scheie) result from different
amino acid substitutions that result in a defect in a-L-iduronidase.
• Hurler syndrome (MPS I-H) is the most severe of the the three, severe cognitive
impairment and with corneal clouding appearing by 1 year of age.
7. CLINICAL FINDINGS:
• Corneal clouding
• Retinopathy
• Optic atrophy
• LAB EVAL: Urine for GAGs. Leukocyte or plasma enzyme assay most precise
• Mgt: PK…
9. DIABETES MELLITUS .”
• PATHOGENESIS: accum of sorbitol alters epi and endo. Leading to thickening of
multilaminar basement membrane, reduced hemidesmosomes and decreased
penetration of anchoring fibrils…. These affect epi-stromal adhesion
• Reduced corneal nerve density and nerve branching related to degree of DM
neuropathy
• CLINICAL FINDINGS: corneal epi surf changes, hypoesthesia
• LAB EVAL: Glycosylated hem related to poor DM control…. Could point to poor
corneal healing
• MGT: Lubs, avoid toxic meds, using therapeutic CLs, minimize epi debridement
surgery, manage Meibomian gland dysfunction, PK
10. DISORDERS OF LIPID METABOLISM
AND STORAGE
• Hyperlipoproteinemias
• Hypolipoproteinemias
• Shingolipidoses
• Mucolipidoses
11. HYPERLIPOPROTEINEMIAS
• Assoc: premature coronary artery and peripheral vascular disease
• Ocular hallmarks: xanthelasma, corneal arcus
• Pathogenesis: extracellular deposits of cholesterol, triglycerides, phospholipids
• O/E: Corneal arcus… in <40yr olds!!!
• LAB EVAL: Fasting and alcohol-restricted lipid profile.
• MGT: Refer for dietary or drug treatment
12. HYPOLIPOPROTEINEMIAS
• 5 disorders: LCAT deficiency, Tangier dx, fish eye dx, familial hypobetalipoproteinemia,
Bassen-Kornzweig syndrome. 3….”
• O/E: LCAT has peripheral arcus and nebular stromal haze. Fish eye dx has corneal
clouding from minute gray-white-yellow dots. Tangier dx has very large orange tonsils;
enlarged liver, spleen and lymph nodes. Corneas have diffuse clouding and opacities
but no arcus.
• LAB EVAL and MGT: Serum lipid profile shows low HDL (lowest in Tangier’s dz).
Appropriate referral and genetic counselling
13. SHINGOLIPIDOSES
• 4 conditions: Fabry dz, multiple sulfatase deficiency, generalized gangliosidosis, Tay
Sachs dz
• Pathogenesis: Fabry caused by deficiency of a-galactosidase A causing accum of
ceramide trihexoside in renal and cardiovascular systems.
• Clinical findings: whorl-like lines in basal layers of corneal epithelium, periorbital edema
(25%), cataracts. Corneal changes resemble those on long-term chloroquine or
amiodarone
• LAB EVAL: In Fabry dz, a-galactosidase A level is markedly decreased in urine and
plasma.
15. MUCOLIPIDOSES
• AR conditions with features common to MPS and lipidoses
• Pathogenesis: inherited disroders of carbohydrate and lipid metabolism combined.
MPS accum in cornea and viscera.
• Dz in this class: ML1, ML2, ML3, ML4, Goldenberg syndrome, mannosidosis,
fucosidosis. {Chr,19.
• O/E: corneal clouding except in mannosidosis and fucosidosis.
• LAB EVAL: Plasma lysosomal hydrolases elevated.
• MGT: Both PK and lamellar keratoplasty (LK) have poor results; allograft limbal stem
cell transplant an option
18. DISORDERS OF PROTEIN
METABOLISM
• Amyloidosis: extracellular accum of amyloid deposits in various tissues and organs
including cornea and conjunctiva.
• Primary localized amyloidosis is the most common form of ocular amyloidosis
• Primary systemic amyloidosis: waxy ecchymotic eyelid papules assoc with vitreaous
veils and opacitites
• Secondary localized amyloidosis: most common form of amyloidosis of the cornea.
• Secondary systemic amyloidosis: seen in many conditions like RA. Amyloid doesn’t
deposit in the cornea in secondary systemic amyloidosis
20. DISORDERS OF IMMUNOGLOBULIN
SYNTHESIS
• Watch in MM, WM, BMG.. Have excess synthesis of Ig by plasma cells; assoc with
crystalline corneal deposits
• Pathogenesis: direct tissue invasion or hyperviscosity syndrome
• O/E: Crystalline deposition in all layers of cornea, copper deposition in cornea,
sludging of blood flow in conjunctiva and retina, pars plana proteinaceous cysts,
infiltration of sclera, orbital bony invasion with proptosis.
• LAB EVAL: Serum electrophoresis, CBC and general screening for albumin/globulin
and Ca2+ levels,
• Mgt: No ophthal Rx needed except when depositions interfere with vision… LK
21. NON-INFLAMMATORY DISORDERS OF
CONNECTIVE TISSUE
• Ehlers-Danlos Syndrome: hyperextensibility of joints and skin, easy bruisability and
formation of “cigarette paper” scars.
• Pathogenesis: AD, AR, and X-linked variants. 20 types. Specific defects occur in collagen
type I and III synthesis, and there can be lysyl hydroxylase deficiency.
• Clinical findings: EDS type VI is ocular-scoliotic type, AR, assoc with only moderate joint and
skin extensibility, brittle cornea easily ruptured on minor trauma, blue sclera, keratoconus
keratoglobus and severe scoliosis.
• Lab eval: altered urinary ratio of lysysl pyridinoline to hydroxylysyl pyridinoline that is x-tic of
EDS VI.
• MGT: Be aware of condition and associations: MVP
, SBR, ..brittle cornea mimics child
abuse!!!.. Use patch grafts to repair corneoscleral ruptures. Genetic counselling
22. MARFAN SYNDROME
• Common AD disorder associated with disorders of the eye (ectopia lentis), heart and
skeletal system. Maps to fibrillin gene.
• Pathogenesis: defects in fibrillin synthesis
• O/E: thinning of sclera, subluxation of lens, flattening of cornea
• Mgt: Complete cardiac eval. CTR during cataract surgery in case of lens subluxation.
23. DISORDERS OF NUCLEOTIDE
METABOLISM
• Gout: results from deposition of urate crystals in the joints or kidney
• Pathogenesis: RFs… obesity, cytotoxic chemotherapy, myeloproliferative disease,
diuretic therapy, excessive alcohol intake
• O/E: fine corneal epithelial and stromal deposits . Rarely an orange-brown band
keratopathy or typical whitish band keratopathy
• LAB EVAL: Serum uric acid level typically elevated.
• Mgt: Indomethacin, Colchicine or phenylbutazone… allopurinol… superficial deposits
can be scrapped off or keratectomy done
24. PORPHYRIA
• Excess production and excretion of porphyrins, pigments involved in synthesis of heme
• Pathogenesis: Porphyria cutanea tarda, form most commonly associated with ocular
surface disease. Is sporadic or AD.
• o/e: corneal thinning and perforation at limbus
• Lab eval: urine turns dark on standing. Reduced liver and red cell uroporphyrinogen
decarboxylase activity is confirmatory.
• Mgt: protection from UV light and reduction of iron by phlebotomy or subcut
desferrioxamine are the principal treatments. No specific ocular treatment. Artificial
tears helfpful.
25. DISORDERS OF MINERAL
METABOLISM
• Wilson disease: (hepatolenticular degeneration).
An AR disorder caused by multiple allelic substitutions or deletions in an ATPase,
Pathogenesis: Copper deposited in liver, then in kidneys and eventually in brain and
cornea at Descemet membrane.
O/E: Copper deposition in posterior Descemet membrane (Kayser-Fleischer ring).
Gonioscopy helpful in seeing this ring.
Lab eval: low serum ceruloplasmin, high urinary copper suggestive of dx
Mgt: Penicillamine. KF ring used to monitor progress of therapy.