This document discusses corticosteroids and their use in ophthalmology. It begins by describing the basic structure and functions of steroids produced naturally in the body. It then outlines the history of corticosteroid discovery and use in medicine, including their introduction to ocular therapy in the 1950s. The document goes on to explain the mechanisms of action of corticosteroids and their effects on inflammation. It provides details on the administration, pharmacokinetics, efficacy and side effects of systemic corticosteroid use as well as topical ocular administration through eye drops, ointments and injections. Guidelines are given for dosing and monitoring patients on long-term corticosteroid therapy.
Fungal infections of eye cause one of the most dangerious infections. Accurate diagnosis and proper institution of anti-fungal therapy is essential. Here we discuss the various anti-fungal agents available to be used in ophthalmology.
Fungal infections of eye cause one of the most dangerious infections. Accurate diagnosis and proper institution of anti-fungal therapy is essential. Here we discuss the various anti-fungal agents available to be used in ophthalmology.
A surgical procedure featuring a partial thickness scleral flap that creates a fistula between AC and subconjunctival space for filtration of aqueous and creation of conjunctival bleb in an effort to lower IOP
A surgical procedure featuring a partial thickness scleral flap that creates a fistula between AC and subconjunctival space for filtration of aqueous and creation of conjunctival bleb in an effort to lower IOP
The ppt is made for undergraduate students to have a basic understanding on Corticosteroids and its role in all feilds of medicine. This is also useful to Postgraduate students
Corticosteroids in Dentistry| Application and Adverse Effect of CorticosteroidDr. Rajat Sachdeva
Corticosteroids are very similar to Steroid hormones produced naturally in Adrenal Cortex of humans.
Protein, Carbohydrates and Fat metabolism, maintenance of fluid electrolytes and adapting the body to stress.
Corticosteroids are antinflammatory, analgesics, effective on ulceration promotes the healing of nerve injuries.
Oral Sub-mucus Fibrosis, Central Giant Cell Granuloma, Lichen Planus (for 5 min, 0.5% application of Clobetasol Propionates with Nystatin) in a Gingival Tray.
Bullous and Mucous Pemphigoid, Melkerson Rosenthal syndrome, Bell's Palsy, Post-Herpetic neuralgia.
Anti Tubercular Drugs - Mechanism of Action and Adverse effects Thomas Kurian
A brief outline of the mechanism of action and adverse effects of anti tubercular drugs
Only First line and second line drugs are dealt with.First line drugs may be useful for MBBS students and the rest is directed for postgraduate students.
Hope you find it useful.
Fungal infections are more common in men and in women, especially in younger people due to their clothing style. they must be stopped at the budding stage, if not it might spread to multiple areas of body.
Psoriasis is an inflammatory skin disease that is associated with multiple comorbidities and substantially diminishes patients' quality of life. Topical therapies remain the cornerstone for treating mild psoriasis. Therapeutic advancements for moderate to severe plaque psoriasis include biologics that inhibit TNF-α, p40IL-12/23, IL-17, and p19IL-23, as well as an oral phosphodiesterase 4 inhibitor.
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.
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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
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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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
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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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.
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
3. • Steroids are molecules
having GONANE nucleus
• Produced in body from cholesterol
• Adrenal Cortex – Glucocorticoids ( Cortisol ),
Mineralocorticoids ( Aldosterone ), weak Androgens
• Testes – testosterone
• Ovary & Placenta – Oestrogens and progesterone
• Glucocorticoids ( Cortisol ) have a wide range of Physiologic
roles involving metabolism and hemostasis.
• A major component of response to STRESS Stimulus
• Apart from replacement therapy in Adrenocortical
deficiency, Supra Physiologic doses have been used
extensively in medicine for treatment of spectrum of
disorders (natural & synthetic)
4. • 1930 – Swingle, Pfiffner, Hartman – prepared
adrenocortical extracts
• 1935 – Kendall isolated cortisone in lab
• 1942 – Reichstein and Shoppee – chemical structure of
steroids
• 1949 – Hench – first clinical use of steroids –
Rheumatoid arthritis
• 1950 – Cordon and Mclean – introduced steroids into
ocular therapy
17. VEGF
increase in trancytosis – increased permeability in
inflammed or chronic hypoxic tissues
proliferation of endothelial cells – granulation tissue and
fibrosis
19. MECHANISM OF ACTION
• ..DownloadsVideoAnimation explaining mechanism of action
of glucocorticoids.flv
20. • GLUCOCORTICOID RECEPTOR - Member of nuclear
receptor superfamily
carboxyl end binds ligand ( steroid)
middle region Zn fingers (9 cysteine residues) bind
to pallindromic sequence in GRE
(promotor DNA)
amino terminal activation of Transcription by RNA
polymerase II
21. • COREGULATORS
bridge with other nuclear factors like
NF- kB and AP1 – affect transcription
of other genes – TRANSREPRESSION
enzymes for acetylation / deacetylation of Histones –
altering structure of nucleosomes
• ONSET OF ACTION – 90 to 120 mins
• DURATION - long
22. • Constriction of blood vessels & reduction in permeability
• Inhibition of macrophage recruitment and migration
• Reduction in circulating monocytes, basophils,
eosinophils and lymphocytes. However neutrophilic
leukocytosis occur
• Decrease in expression of adhesion molecules (ICAM)
over endothelium
• Decrease in Diapedesis
• Stability of basophil, mast cell, neutrophil intracellular
granules
23. • Decrease in Antigen Presentation
• T lymphocyte function and proliferation affected more
than B lymphocytes
(cell mediated immunity)
• Suppression of Fibroplasia
24.
25. ROUTES OF DELIVERY
• Topical – skin ointments
eye drops
eye ointments
• Peri Ocular Injections –
sub conjunctival
sub tenon – anterior and posterior
retrobulbar
• Intra Vitreal – injections
implants
• Systemic – Oral
Parenteral – iv, im
27. SYSTEMIC PHARMACOKINETICS
• Well absorbed orally
• i v route – water soluble compounds like Hydocortisone
hemisuccinate, dexamethasone sod phosphate
• i m route – both water soluble or insoluble compounds like
hydrocortisone acetate, triamcinolone acetonide etc given
depending upon duration of effect desired
• Hydrocortisone is 90 % bound to plasma proteins – CBG
and albumin
• Metabolized by hepatic microsomal enzymes –
reduction/hydroxylation/oxidation followed by conjugation.
• Metabolites excreted in urine – major form is 17 keto
compound
• Biologic t ½ is much longer than Plasma t ½
28. • Systemic corticosteroids are the initial drug of choice for
most patients with bilateral endogenous sight threatening
uveitis.
• Prednisone/prednisolone is the most commonly used oral
corticosteroid
• Initial dose 1-2 mg/kg/day
• Maximum adult oral dose 60 – 80 mg/day
• Maintenance dose (adult) = 10mg/day
• Single morning dose after breakfast, if possible on alternate
days
• Combined with proton pump inhibitors or anti H 2 anti
histaminics
29. SYSTEMIC SIDE EFFECTS
• Sodium and water retention, hypokalaemic hypochloremic
alkalosis
• Rise in BP
• Edema occurs in cases of hypoproteinemia, renal disease,
liver disease
• Heart failure in compromised myocardial function
• Cushing’s Habitus – rounded face (moon face), narrow
mouth, supraclavicular hump, obesity of trunk with relatively
thin limbs –iatrogenic cushing’s syndrome occurs >100 mg
hydrocort / day
• Fragile skin, striae, telangiectasias, hirsutism , acne
• Growth retardation in children
• Diabetes MellitusHyperlipidemia
• Secondary amenorrhoea
31. • Steroids in pregnancy – category C
Fetal abnormalities
• Nursing mothers – secretion into breast milk
Adrenocortical suppression and growth
retardation in child
32. OCCULAR SIDE EFFECTS
• cataract
• occular hypertension and glaucoma
• secondary infections
• retardation of wound healing – post operative
• inhibition of corneal epithelial & stromal
healing – corneal melting
• central serous retinopathy
• exophthalmos
• pseudotumor cerebri
33. HPA AXIS SUPPRESSION
• If systemic steroid given for more than 2-3 weeks
• HPA suppression due to feedback mechanisms
• sudden stoppage precipitates acute adrenocortical
deficiency. Tapering of dose has to be done to avoid this
During tapering, glucocorticoid dependence may
manifest nausea, vomiting, weight loss, lethargy,
headache, fever, muscle pain , postural hypotension
34. • During acute stress, dose has to be increased
even if stressful event occurs months after tapering has
been done
• Many patients achieve normal serum cortisol levels in
less than one year of stopping steroids but in majority of
cases, the ability to respond to stress by increase in
steroid levels remains hampered for upto 2 years
Minor – 2 fold maintenance dose for 24-48 hrs
Major – 10 fold maintenancedose for 48-72 hrs
• If patients on steroids develop systemic infection,
steroids should not be discontinued. Dose needs to be
increased along with addition of specific antimicrobial.
35. GENERAL GUIDELINES
• Use local therapy wherever possible.
• A single dose ( even excessive ) is not harmful – can tide
over mortal crisis even when benefit is not certain
• Short courses ( even high doses ) are not likely to be
harmful in the absence of contradictions
• Long term use is potentially hazardous – duration and dose
to be kept at minimum, which is found by trial and error.
• High doses to begin with, in severe diseases, titrating
downwards acc to response whereas low doses to begin
with, in mild diseases, titrating upwards.
• If chronic use beyond 1 month, addition of immuno -
suppresants to be considered
• No abrupt stoppage after use for 2-3 weeks
36. • TAPERING SCHEDULE for oral prednisolone
> 40mg/day, decrease by 10mg/day every 1-2 weeks
40–20mg/day, decrease by 5mg/day every 1-2 weeks
20–10mg/day, decrease by 2.5mg/day every 1-2 weeks
10-1 mg/day, decrease by 1-2.5mg/day every 1-4 weeks
37. • EVALUATION
Chest X Ray
Tuberculin test
Assessment of DM, osteoporosis, peptic ulcer,
psychological disturbances, cardiovascular status, renal
and hepatic status
• MONITOR-Blood Pressure, Weight, Blood Glucose level
every 3 months and annually.
Measure bone density within first 3 months and annually
thereafter. Supplementary treatment - Calcium 1500 mg
daily andVitamin D 400 IU daily. Bisphosphonates and
Estrogens as needed.
Increased potassium and protein intake
38. I V METHYL PREDNISOLONE PULSE
selected cases where immediate effect is needed
1 g/day or 250 mg q 6 hrly, slow I v infusion X 3 days
Followed by oral prednisolone
Temporarily “switches off ” the IMMUNE SYSTEM
Optic neuritis
Severe corneal graft rejection
Severe sight threatening posterior uveitis
Sympathetic ophthalmitis
VKH
39. PRECAUTIONS
• Should be given under ICU settings
• Monitoring of BP and pulse every 15 – 20 mins
• Electrolyte imbalances and ECG changes likely to occur
41. TOPICAL PHARMACOKINETICS
• Topical – eye drops – solutions and suspensions –
hydrochloride, phosphates, alcohol, acetates
- eye ointments
- drug depots on ocular surface – cotton pledgets
and collagen shields – steady sustained and
slow release
42. EXTENT OF ABSORPTION INTO CORNEA AND
ANTERIOR CHAMBER
time for which drug remains in cul de sac and tear film
flow to lacrimal passage
binding to taer proteins
Metabolism by tear and external tissues
status of corneal epithelium and stroma
type of steroid and its solubility
concentration
osmolarity, pH, viscosity, vehicle, size of particles
dosing frequency
43. • CORNEA TRILAMINAR STRUCTURE
• Corneal and aqueous humor concentrations - Studies in
animal models –
• Keratitis with intact epithelium – Pred acetate > pred
sod phosphate > dexamethasone alcohol. No
dexamethasone sod phosphate was absorbed
• Keratitis with denuded epithelium – Pred sod
phosphate > dexamethasone sod pshpate > pred
acetate
• Intraocular inflammation with intact corneal epithelium
– Pred acetate = pred sod phosphate =
dexamethasone sod phosphate
46. • PREDNISOLONE SOLUTION VS PREDNISOLONE
SUSPENSION
equivalent for intra ocular inflammation models (anterior
uveitis)
rabbit keratitis model shows superiority of prednisolone
acetate over prednisolone sod phosphate
But sophisticated mathematical models show equivalence
in practice efficacy of suspension(pred acetate) is
assumed to be lower due to lack of patient compliance in
shaking well before instillation
47. • OINTMENT VERSUS DROPS
Dexamethasone phosphate ointment had lower
penetration into cornea and aqueous humor than
solution because of slow release of drug molecule
Whereas FML ointment produced similar concentrations
as suspension
• VEHICLE – cyclodextrin (Gate-Dx, Apdrops-Dx)
improves corneal penetration of dexamethasone
48. • TYPE OF STEROID
-FML 0.1 % and 0.25 % has much less corneal
penetration but is comparable to Prednisolone 1% in
alleviating corneal inflammation
gets concentrated in corneal epithelium
-Loteprednol ( modification of prednisolone ) –
undergoes rapid hydrolysis by esterase in anterior
chamber. Effective for corneal and conjunctival
inflammations
-Medrysone 1% – very low penetration of cornea –
discontinued by FDA – used earlier for mild conjunctival
inflammations
49. • SYSTEMIC ABSORPTION after topical treatment is
considerable – through conjunctiva, nasal mucosa and
aqueous humor
By passes hepatic metabolism
suppression of adrenal cortex after 6 weeks of topical
0.1 % dexamethasone phosphate
elevation of blood glucose levels in controlled diabetics
50. OCCULAR SIDE EFFECTS
• occular hypertension and glaucoma
• secondary infections – viral keratitis, fungal keratitis,
toxoplasmosis
• retardation of post operative wound healing
• inhibition of corneal epithelial & stromal
healing – corneal melting
• cataract
• uveitis
• mydriasis
• ptosis
• Toxic to cornea, conjunctiva, skin e g punctate keratopathy
• hypersensitivity
51. PRECAUTIONS AND CONSIDERATIONS
-for initial prescription and renewal beyond 14 days - to rule
out infective pathology especially viral, fungal,
mycobacterial- Slit Lamp biomicroscopy and fluorescein
staining if necessary
-Re evaluate if no improvement in 2 days of start of therapy
-Any drug used beyond 10 days – monitoring of IOP
-Suspicion of fungal infection in long term therapy –
cultures may have to be taken
-To remove contact lens before instillation and re insertion
after 15 mins – absorption of BAK by CL
-Separate bottle for other eye in case of post op treatment
-to be SHAKEN WELL
- Storage b/w 8 – 25 deg celsius
- No abrupt withdrawl – to prevent rebound flaring up
53. High concentrations at site of inflammation without systemic
toxicity
To be given close to site of inflammation
Eliminates daily compliance
Blood – ocular barrier limits diffusion
INDICATIONS – resistent anterior uveitis, intermediate
uveitis, posterior uveitis, CME (mainly unilateral)
especially in patients contraindicated to systemic steroids
CONTRAINDICATIONS – conditions associated with scleral
thinning like scleritis – scleral perforation may occur
PRECAUTIONS – to rule out steroid responders
- and infections
54. SUBCONJUNCTIVAL Inj– absorption directly across the
sclera as compared to sub conjunctival antibiotics
soluble drugs for sub conjunctival inj – insoluble drug will give
unsightly appearance and will lead to irritation
SUB TENON(ANTERIOR and POSTERIOR) – suspensions
are used for better absorption
depot steroids :
Inj Depo Medrone(methyl pred acetate) (0.5ml of 80mg/ml)
Inj Kenalog (triamcinolone acetonide)
effect lasts for 1-2 weeks
55. COMPLICATIONS RELATED TO TECHNIQUE
perforation of globe and intraocular injection
sub conjunctival hemorrhage
retrobulbar hemorrhage
Extraocular muscle fibrosis
scarring between conjunctiva and globe
57. • More targeted delivery
• Controlled and consistent
• Immediate achievement of therapeutic concentration
• By passes BLOOD OCULAR barrier
• Reduced systemic toxicity
• Compliance eliminated
58. Dexamethasone – very short half life – 3-4 hours
Triamcinolone acetonide– longer half life.
4 mg inj : detectable after 3 months
effect upto 6 months
earlier TRICORT and KENACORT Inj – Benzyl alcohal
newer preservative free FDA approved preparations
TRIVARIS (80mg/ml) – 0.05 ml : Uveitis
TRIESCENCE (40mg/ml) – 0.025 to 0.1 ml :
visualization of tissues ILM, ERM in VR
surgery
59. • Off label uses of IVTA
ARMD
Diabetic Retinopathy
Venous Occlusions
Pseudophakic Macular Edema
Proliferative vitreoretinopathy
60. • IVTA Injection
Tranconjunctivally, 3.5 – 4 mm from limbus,
inferotemporally
26 / 27 / 30 guage needle over tuberculin syringe
Under direct visualization : dilated pupils required
Immediately afterwards – CRA pulsations are
checked by IDO
IOP measured after 30 mins
Biomicroscopy after 3 and 7 days
62. • IMPLANTS
RETISERT – 0.59 mg Fluocinolone acetonide
Sustained Release implant for chronic non infectious
posterior uveitis
implanted through pars plana incision, after vitrectomy
lasts for 30 months : has to be removed
ILUVIEN – half of retisert : FAME study for DR : not
approved yet
OZURDEX – 0.7 mg dexamethasone in injectable,
biodegradable implant for macular edema after CRVO
& BRVO and non infectious chronic posterior uveitis.
lasts upto 6 weeks
63.
64. COMPLICATIONS DUE TO TECHNIQUE
Sub conjunctival hemorrhage
vitreous hemorrhage
traumatic cataract
Vitreous detachment
retinal detachment
pseudo endophthalmitis / pseudo hypopyon
(more likely in aphakia and pseudophakia)
sterile endophthalmitis ( benzyl alcohol related )
infective endophthalmitis
dislocation of implant
66. • As Post-operative treatment- In most intraocular & ocular
surface surgeries, topical CSd are usually given
according to the severity of inflammation for few days to
weeks.
Refractive surgery, corneal surgery, intraocular surgery,
glaucoma surgery ( prevents scarring)
Delayed wound healing in cataract surgery may lead to
bleb formation
67. • Periorbital Dermatitis (Atopic, Contact, Irritant,
Seborrheic).
Most patients benefit from short course of CSd ointment
application for 1-2 weeks.
68. • Allergic conjunctivitis (Hay fever, AKC, VKC, GPC,
Phlyctenular)-
Topical CSd are used only as 2nd or 3rd line drugs CSd
bring dramatic improvement with potential side effects..
Use diluted CSd (e.g. 0.01% Dexamethasone or
0.12%Prednisolone) or ‘milder’ CSd (e.g.
Flurometholone, Loteprednol) as pulse therapy (4-8x/day
for 1 week followed by fast tapering).
Tear substitutes, Antihistamine vasoconstrictor
combination, Mast cell stabilizers are the first line drugs
generally.
69. • Chronic Adenoviral Keratoconjunctivitis-
Topical CSd only temporarily resolve the subepithelial
infiltrates without affecting the clinical course.
• Herpetic (H. simplex) stromal keratitis-
CSd contraindicated in any form of active epithelial
keratitis while topical diluted CSd (1:10 dexamethasone)
bd/tds is useful for stromal disease (immunological
basically)
given along with prophylactic antiviral treatment.
70. • Scleritis-
Topical steroids are not effective unlike in episcleritis.
Periocular steroids are contraindicated (chances of
scleral thinning & perforation).
oral Prednisolone is given for 2-3 weeks followed by
slow tapering.
71. • Corneal chemical injury-
topical steroids, qid to 2 hourly depending upon the
severity) for the first week only followed by shifting to
topical NSAIDs.
Risk of corneal melting/ulceration is very minimal in the
first week of chemical injury. After which corneal stromal
repair is inhibted
72. • Herpes Zoster Keratitis-
Topical CSd are used for stromal keratitis & uveitis.
Sometimes also used for epithelial keratitis, cautiously
topical CSd don’t increase viral replication in Zoster
epithelial keratitis.
Pseudodendrites are present (elevated mucous plaques)
that are fluorescein stain negative.
73. • Corneal graft rejection-
Topical CSd every hourly for endothelial rejection.
Topical CSd 4x/day for epithelial rejection (relatively
benign).
Systemic CSd, if topical CSd fail or recurrence occurs.
For severe rejection (generalised corneal edema), IV
methyl Pred (pulse steroid therapy) is given along with
intensive topical CSd (1 hourly).
• Also as prophylaxis
74. • Anterior uveitis-
In acute non-granulomatous uveitis, topical pred acetate
drops every 1-6 hourly depending on the severity.
Periocular steroids are used for noncompliant patients.
75. • Intermediate uveitis
i) Topical CSd are not much effective. Might be given
along with periocular CSd.
ii) Periocular CSd (posterior subtenon’s injection of
combination of steroid depot
iii) Systemic CSd is required in bilateral cases or those
with severe inflammation.
Generally no treatment is required if visual acuity is >/=
6/12..
76. • Posterior uveitis-
Non-specific posterior uveitis needs oral prednisolone
Very severe cases may need IV Methylpred pulse.
posterior subtenon depot inj,
IVTA(TRIVARIS),
Depot CSd implants (RETISERT & OZURDEX)
• VKH, sarcoidosis, sympathetic ophthalmitis – systemic
(oral) therapy. I v methyl prednisolone pulse may haveto
be given
77. • Postoperative endophthalmitis)
i)In early endophthalmitis, along with antibiotics, give
topical prednisolone 1-2 hrly or I-Vit Dexamethasone
(0.4 mg) with antibiotic.(role controversial)
ii) Late endoph (starting after a week) - Avoid all CSd
until fungus infection is ruled out & patient is definitely
responding to antibiotics.
78. • Thyroid eye disease-
oral Prednisolone 1-2mg/kg/ D for significant proptosis
causing exposure keratopathy, significant diplopia or
vision loss because of optic neuropathy..
79. • Orbital pseudotumour-
Early & aggressive systemic therapy is the mainstay of
treatment.
For recurrent & non-responding cases, retrobulbar or
intralesional CSd injection may be tried.
Low dose orbital irradiation & immunosuppressives are
the alternatives
80. • Optic neuritis-
If patient seen early, IV methyl prednisolone pulse
therapy followed by oral prednisolone 1 mg/kg/D
X11days with tapering over a week.
Oral CSd not recommended, recurrences become
commoner (ONTT study).
IV CSd offers- Reduced recurrence rate, Shortened
visual recovery time, But no long term visual benefit
Only observe, in cases of recurrent ON or known case of
multiple sclerosis.
81. • Arteritic Ischemic optic neuropathy-
suspicion of Giant Cell Arteritis in a case of AION,
immediately start pulse steroid therapy, followed by oral
prednisolone for 2- 4 weeks if temporal artery biopsy is
positive, thereafter maintaining for 6 months to a year
(monitor ESR).
Blindness from GCA is usually permanent & CSd
basically help to prevent it in the other eye as the
contralateral eye can get involved within 24 hours
82. • Optic nerve injury-
Immediately institute ‘Mega’ intravenous methyl-pred
doses like that for spinal cord injuries. Loading dose of
30mg/kg by slow IV infusion followed by maintenance
dose of 5.4mg/kg every hour for 48 hours. Followed by
oral prednisolone
Monitor the visual acuity & relative afferent pupillary
defect (RAPD) closely.
83. OCULAR HYPERTENSION
• Increase in IOP when applied locally or given systemically.
• IOP elevation may lead to optic nerve damage & changes in
visual field similar to POAG.
• Incidence of ocular hypertension – 5 % in patients with no
family history of POAG ; upto 90% in patients with positive
history
• Mostly reversible on stopping, but long term usage may lead
to permanent elevations.
• Mucopolysaccharide deposition in trabecular meshwork.
• Gene involved – GLC1A / TIGR / MYOC on ch 1q21 – 1q31
84. • Development of softer topical steroids –
FML (0.1 % and 0.25 %)
Loteprednol (0.2 % and 0.5 %)
Rimexolone
Less percentage of patients developing ocular HTN and
that too after longer duration compared to
dexamethasone 0.1% or prednisolone 1%
structure activity studies indicate close relationship
between anti inflammatory potency and occular
hypertensive effect
85. • PRECAUTIONS
Regular IOP and Optic Disc monitoring, if steroids are
used for than 10 days, INCLUDING ‘SOFTER’ TOPICAL
DRUGS
Analysis of Risk Benefit ratio in cases already diagnosed
with POAG
Identification of steroid responders before PERIOCULAR
and INTRAVITREAL injections – effect of 6 weeks of
therapy with topical Dexamethasone 0.1 %
• MANAGEMENT
Require concurrent anti glaucoma medication
Removal of implants/periocular depot, vitrectomy in case
of IVTA, and trabeculectomy may have to be
undertaken.
86. CATARACT
• Development of posterior subcapsular cataract reported
more commonly in literature with long term systemic
therapy
• Recent Advances - intravitreal implants(RETISERT and
OZURDEX) and multiple intravitreal injections (IVTA) -
upto 100 % incidence
• Incidence correlates with the dose and duration of
systemic therapy
• 75 % patients >16mg/day prednisolone develop PSC
• Dose of 10 mg/day for 1 year have minimal risk
• Long term topical therapy also at risk e.g. vernal & atopic
Keratoconjunctivitis, keratoplasty for keratoconus
• Irreversible changes in lens due to binding of steroid
molecules with lens fibres and biochemical alterations
• Enhanced by concomitant Diabetes Mellitus
87. • Children are particularly at risk
• Cataract progresses despite stopping treatment
• Periodic slit lamp examination is recommended
88. CONCLUSION
• 2 edged swords
• Effect of Steroids are non specific, palliative and never
curative
• Concomitant specific treatment has to given
• Appropriate Use relies on good clinical judgement and
close watch on complications
• Newer molecules having higher selectivity for anti
inflammatory activity
• Newer methods of drug delivery
89. REFERENCES
• Goodman and Gilman : Pharmacological Basis of
therapeutics – 12th ed (2011)
• Katzung : Basic & Clinical Pharmacology – 11th ed (2011)
• K D Tripathi : Pharmacology - 6th Ed (2010)
• Albert Jakobiec : Principles & Practice of Ophthalmology in
ch 23 Corticosteroids in practice – 3rd ed (2008)
• Robbins : Pathologic Basis of Diseases – 8th ed (2012)
• Corticosteroids in ophthalmology- overview : DOS Times-
vol 12, no 8 ( 2007)
• Steroids & immunosuppressives in Ophth : Kerela Journal of
Ophthalmology – vol 18, no 3 (2006)
90. • Steroids for posterior segment : delivery systems &
indications : DOS Times – Vol 10, No 4 (2004)
• Intravitreal steroids in retinal disorders : DOS Times, vol
11, no 4 ( 2005)
• Corticosteroid implant for vascular occlusions : DJO - vol
22, no 2 (2011)
• www.fda.gov