✓ Corneal ulcers can have devastating effects on vision if not properly diagnosed and treated. Their etiologies include infectious causes like bacteria, viruses, fungi and parasites, as well as non-infectious causes like trauma, dry eye, exposure, and neurotrophic conditions. Proper management requires controlling infection, inflammation, and promoting re-epithelialization to prevent perforation. Treatment approaches include antibiotics, antifungals, antivirals, bandages, glues, and transplantation depending on the specific cause and presentation of the corneal ulcer.
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.
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.
• Cornea is an avascular, transparent tissue that is an important component of the ocular refractive system.
• It is one of the most densely innervated tissues in the body.
Behind the precorneal tear film there are five layers of cornea:
1. Epithelium and basal lamina
2. Bowman’s layer
3. Stroma
4. Descemet’s membrane
5. Endothelium
Corneal Transparency
The cornea transmits nearly 100% of the light that enters it.
Transparency achieved by Arrangement of stromal lamellae.
Other factors:
Epithelial non-keratinization
Regular & uniform arrangement of corneal epithelium
Junctions between cells & its compactness
Corneal avascularity
Non-myelinated nerve fibers
Once the damaged corneal epithelia are invaded by offending agent, the sequence of pathological changes which occur during development of corneal ulcer can be described under four stages:
1. Progressive infiltration
Grey zone
Localized necrosis
Saucer-shaped ulcer with overhanging edges
2. Active ulceration
Dead material material thrown off
Oedema subsides
Floor and edges are smooth and transparent
3. Regression
From limbus, minute vessels grow in
4. Cicatrization
Formation of fibrous tissue which fill the gap
Opacity generated
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.
orneal ulcer, also called keratitis, is an inflammatory or, more seriously, infective condition of the cornea involving disruption of its epithelial layer with involvement of the corneal stroma. It is a common condition in humans particularly in the tropics and in farming. In developing countries, children afflicted by vitamin A deficiency are at high risk for corneal ulcer and may become blind i
• Cornea is an avascular, transparent tissue that is an important component of the ocular refractive system.
• It is one of the most densely innervated tissues in the body.
Behind the precorneal tear film there are five layers of cornea:
1. Epithelium and basal lamina
2. Bowman’s layer
3. Stroma
4. Descemet’s membrane
5. Endothelium
Corneal Transparency
The cornea transmits nearly 100% of the light that enters it.
Transparency achieved by Arrangement of stromal lamellae.
Other factors:
Epithelial non-keratinization
Regular & uniform arrangement of corneal epithelium
Junctions between cells & its compactness
Corneal avascularity
Non-myelinated nerve fibers
Once the damaged corneal epithelia are invaded by offending agent, the sequence of pathological changes which occur during development of corneal ulcer can be described under four stages:
1. Progressive infiltration
Grey zone
Localized necrosis
Saucer-shaped ulcer with overhanging edges
2. Active ulceration
Dead material material thrown off
Oedema subsides
Floor and edges are smooth and transparent
3. Regression
From limbus, minute vessels grow in
4. Cicatrization
Formation of fibrous tissue which fill the gap
Opacity generated
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.
orneal ulcer, also called keratitis, is an inflammatory or, more seriously, infective condition of the cornea involving disruption of its epithelial layer with involvement of the corneal stroma. It is a common condition in humans particularly in the tropics and in farming. In developing countries, children afflicted by vitamin A deficiency are at high risk for corneal ulcer and may become blind i
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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.
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
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
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.
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
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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
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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.
7. Three Layers
Epithelium & its Basement. 1
(Stroma & its ant condensation ( Bowman Zone. 2
( Endothelium & its Basement (Descemet Membrane.3
Structure
10. Superficial
Punctate epithelial erosions.1
Tiny ,slightly depressed, epithelial defects
which stain with flourescein but not with
rose Bengal
PEE are non specific and may develop in a
wide variety of keratopathies
Signs of Corneal Disease
21. Def: Corneal ulcers are defect in the corneal epithelium
.with or without stromal infiltration
:Types
A) Infectious ulcerative keratitis
B)Non infectious ulcerative keratitis
Corneal ulcers
23. :Causes
:Local causes
Punctate marginal keratitis: Staphylococci, Streptococci, hypersensitivity to
medications
Peripheral keratitis associated with blepharitis:
:Systemic causes
Generally manifestation of systemic, immune-mediated disease
Most common: Rheumatoid arthritis, Wegener’s granulomatosis and
polyarteritis nodosa
Non Infectious Ulcerative Keratitis
24. INFECTIOUS Non INFECTIOUS
Pain No pain
Discharge No discharge
AC reaction: present A C reaction: absent
Central Peripheral
: ++++Trauma : -------Trauma
28. ✓A corneal ulcer is anocular emergency that
raises high stakes of questions about
diagnosis and management.
✓When a large corneal ulcer is staring you in
the face time isn't in your side.
✓Despite varying etiologies and presentations,
as well as different treatment approaches ,
corneal ulcers have one thing in common : the
potential to cause devastating loss of vision.
Important Facts
29. Control of infection- 1
Control of inflammation- 2
–- 3
– lid
– bandage
- 4
Promotion of re-epithelialization
lubrication
closure
soft contact lens
Prevention of perforation
– tissue adhesive glue
– conjunctival flap
– systemic immunosuppressive agents
Corneal grafting
PRINCIPLES OF MANAGEMENT
OF CORNEAL DISEASE
39. Greyish-white ulcer with indistinct margins
Surrounded by feathery infilterates
Ring infilterate
Endothelial plaque
Hypopyon
History of vegetable matter
inj ury
40. ✓Dull grey infiltrate.
✓Satellite lesions.
✓Awareness of those ulcers resembling bacterial
keratitis
✓Awareness of those caused by yeast better
defined borders
✓Real flags
Differentiators
54. Opaque cells arranged in a course punctate
or stellate pattern
Central desquamation leads to a linear
–Fluorescein
– Rose Bengal stain
–Diminished corneal
branching ulcer.
stain
sensitivity
Anterior stromal infilterates
Geographical or amoeboid ulcer
DENDRITIC ULCER
55.
56.
57. Herpes zoster keratitis
Healing corneal abrasion
Pseudodendrites due to soft contact lens
Acanthamoeba keratitis
Drug toxicity
Differential diagnosis
58. ✓Dentritic ulcer.
✓Loss of corneal sensation.
✓Photophobia.
Types of HSV keratitis:
✓Primary
✓Recurrent
✓Dentritic , Geographic , Metaherptica
✓Diabetic foot in the eye Neurotrophic
Differentiators
63. Conjunctival: Pinkish-white nodule surrounded by
hyperaemia
Corneal: May resolve spontaneously or extend
radially to the cornea. May cause severe ulceration or
.perforation
SIGNS
64.
65. Short course of topical steroids
Topical antibiotics
TREATMENT
66. (:keratoconjunctivitis sicca (KCS
Or
keratitis sicca: is a multifactorial disease of the tears and
the ocular surface disturbance with corneal
manifestations
:Causes
Dry eye- 1
Vitamin A deficiency- 2
Keratoconjunctivitis
Sic ca
67.
68. Exposure keratopathy (EK) is the cornea damage that
occurs from prolonged exposure of the ocular surface to
. the outside environment
EK can lead to ulceration, microbial keratitis, and
permanent vision loss from scarring
:Causes
Lagophthalmos -1
Proptosis-2
Lid malposition- 3
Exposure Keratopathy
69.
70. is a degenerative disease of the cornea caused by
damage of the trigeminal nerve which results in
impairment of corneal sensitivity, spontaneous corneal
epithelium breakdown, poor corneal healing and
development of corneal ulceration, melting and
perforation
:Diagnosis
by placing a cotton wad or cotton thread in contact with
:the corneal surfaceCorneal sensitivity test
Neurotrophic keratitis