The document discusses various types of conjunctivitis including bacterial, viral, allergic, and infectious causes. It describes the anatomy of the conjunctiva and signs and symptoms of different types of conjunctival inflammation. Treatment options are provided for various conjunctival conditions such as bacterial, viral, membranous, and trachoma conjunctivitis.
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
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
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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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.
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
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
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.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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14. 14
Signs
-Congestion ( in
fornix)
-Papillae
-Purulent/MP
discharge
-Lid crusts
-Visual acuity usually
normal
15. 15
Treatment
Resolves in 10-14 days
Lab tests :Conjunctival swab/scraping
(severe, recurrent, non responsive infants)
Topical antibiotics and ointment HS
(Fluroquinolones, aminoglycosides)
Local hygiene
Avoid finger eye contact and instrument eye
contact
16. Accute Purulent conjunctivitis
Two forms: Adult purulent and ophthalmia
neonatorum
Commonest organism is Gonococci others
staph aureus and pneumococus
Clinical features
Stage of infilteration: 4-5 days . Painful
tender eyeball with red chemosed
conjunctiva. Lids are swollen with with
watery discharge. Preauricular nodes are
enlarged
16
17. Accute Purulent conjunctivitis
Stage of blenorrhoea: purulent thick
discharge
Stage of healing
Complications: corneal ulcer
Treatment:
Broad spectrum topical and systemic
antibiotics
Ocular Hygiene
17
19. Accute membranous
conjunctivitis
Causative org is corynebacterium diptheriae
Violent infl with fibrinous exudate with
membrane
Clinical features:
Stage of infilteration- swollen hard lids, red
chemosed conjunctiva with thick grey
membrane
scanty discharge with severe pain
19
20. Accute membranous
conjunctivitis
Stage of suppuration: Pain decrease with
soft lids. The membrane is sloughed with
copious discharge.
Stage of cicatrisation : healing with
cicatrisation, which may cause trichiasis
and xerosis
Complications
Corneal ulcer, symblepharon, trichiasis,
entropion and xerosis 20
22. Accute membranous
conjunctivitis
Treatment
Pencillin eye drops 1:10000/ml every half
hrly
Antidiptheric serum every hour
Broad spectrum antibiotics oint
Systemic : crystalline pencillin 5lac units IM
BD for 10 days
ADS 50000units IM stat 22
23. Pseudomembranous
conjunctivitis
Bacteria like low virulence C dipth,
staph,strept, N gonococci and H influnzae
Virus like H simplex and adenovirus
Chemical irritant like acid, ammonia, lime,
Agno3
Pathology : Fibrinous exudate on surface
which coagulate on surface as membrane
which can be peeled off underlying intact
epith 23
24. Chronic catarrhal conjunctivitis
Predisposing factors- Dust, foreign body,
seborrhoic scales, ref error etc
Organism – Staph aureus, G –ve like E coli,
klebsiella
Source:
untreated mucopurulentconjunctivitis, chr
dacryocystitis and URI
24
28. Trachoma
Chronic keratoconjunctivitis affecting supf
epithelium of the conjunctiva and cornea.
Mixed follicular and papilary response.
One of the leading cause of blindness
Etiology:
Chlamydia trachomatis .it is epitheliotopic
and produce inclusion bodies (HP bodies)
11 serotypes (A,B,Ba,C,D,E,F,G,H,J and K)
A,B,Ba,C assoc with hyperendemic
29. Trachoma
D-K assoc with paratrachoma or
oculogenital trachoma
Predisposition
Age no bar, more in females
Dry dusty weather and in poor class
Source: Discharge of affected person
Mode
Direct spread through contact
Vector -Flies 29
30. Trachoma
Fomites- towels, tonometers etc
Natural course: Accute stage in first decade
then inactive in second decade. The
sequelae occurs in 4th to 5th decade.
Symptoms- FB sensation, lacrimation,
mucoid discharge. If sec bacterial infection
then mucopurulent conjunctivitis .
30
31. Trachoma
Conjunctival Signs
Congestion of tarsal and forniceal
conjunctiva
Conjunctival follicles- central part contain
histiocytes, lymphocytes and giant cells
(leber cell) ,cortex have lymphocytes and
periphery have blood vessels. P/o of
necrosis and leber cells differentiate
trachoma from other follicular conjunctivitis
31
32. Trachoma
Papillary hyperplasia
Conjunctival scarring, linear scar k.a Arlts
line
Concretions – dead epithelial cells with
inspissated mucous in glands of henle
Corneal signs:
Superficial keratitis
Heberts follicles
Pannus- Progressive or regressive 32
33. Trachoma
Corneal ulcer
Heberts pits
Corneal opacity
Grading
McCallan classification 1908
Stage 1- incipient or stage of infilteration.
Hyperemia of conjunctiva and immature
follicles 33
34. Trachoma
Stage 2- Established or florid. Mature
follicles, papilae and progressive pannus.
Stage 3- scarring of palpebral conjunctiva
Stage 4- Sequelae.
WHO classification 1987 (FISTO)
TF: Trachomatous infl-follicular- Five or
more follicle each 0.5mm or more on upper
tarsal conjunctiva. Deep tarsal vs visible
34
35. Trachoma
TI : Trachomatous infl intense- Inflamatory
thickening obscure more than half of deep
tarsal vessels
TS: scarring- white bands or sheets of
scarring
TT: Trachomatous trichiasis- atleast one
eyelash rubs cornea
CO: Opacity- partly obscuring pupil and
vision < 6/18 35
39. Trachoma
LAB Diagnosis
Conjunctival cytology- Geimsa stain show
PMN, plasma and leber cells
Inclusion bodies by geimsa, iodine stain or
imf stain
PCR
Isolation by yolk sac culture
39
40. Trachoma
Differential diagnosis
EKC - follicles in fornix, and lower
palpebral conjunctiva, assoc papilae and
pannus typical in trachoma.
VKC- large papilae with cobble stone
appearance.white ropy discharge
40
41. Trachoma
Management
Active trachoma
Topical antibiotic- 1%tetracycline or 1%
erythromycin ointment QID for 6 wks
followed by intermittent tt in endemic areas
Systemic –Tetracycline or erythromycin
250mgQID 3-4 wks
Doxycycline 100mgBID 3-4 wks or single
dose 1gm Azithromycin.
Combined therapy in severe cases
41
42. Trachoma
Treatment of sequelae
Concretions – removal
Trichiasis- epilation , electrolysis, cryolysis
Entropion – surgery
Xerosis – Artificial tears
Prophylaxis
Hygiene
SAFE and Blanket treatment 42
43. Adult Inclusion Conjunctivitis
Chlamydia Trachomatis serotype D-K
Source –urethritis in males and cervicitis in
female
Spread – contaminated fingers or pool
I/C- 4-12 days
Symptoms:
Mucopurulent discharge, hyperemia,
lacrimation, irritation and photophobia 43
44. Adult Inclusion Conjunctivitis
Signs :
Hperemia and follicular rx in lower fornix.
Mild supferficial keratitis
Preauricular lymphadenopathy,
If untreated leads to chr follicular
conjunctivitis
44
45. Adult Inclusion Conjunctivitis
Treatment :
Topical 1% tetracycline oint QID x6wks
Systemic Doxycycline 100 mg BIDx 2wks
Azithromycin 1g single dose
Prophylaxis – Treat the partner and
Hygiene.
45
47. Viral Conjunctivitis
Clinical types
Accute serous conjunctivitis
Accute haemorrhagic conjunctivitis
Accute follicular conjunctivitis
i. Adult inclusion conjunctivitis
ii. EKC conjunctivitis
iii. Pharyngoconjunctival fever
iv. New castle conjunctivitis
v. Accute herpetic
47
48. Viral Conjunctivitis
Accute serous conjunctivitis: mild infection
with follicular response.
C/F- mild congestion, watery discharge and
chemosis.
Treatment: self limiting.Broad spectrum
antibiotics to prevent second bacterial
infections.
48
49. Viral Conjunctivitis
Accute Haemorrhagic conjunctivitis:
Enterovirus 70 ,spread eye to hand contact
C/F- short incubation of 1-2 days
Pain, redness, watering, photophobia,
blurred vision and lid swelling
Signs- congestion, chemosis, haemorrhages
in bulbar conjunctiva, follicular hyperplasia,
lid edema and preauricular
lymphadenopathy, fine epith keratitis 49
51. Viral Conjunctivitis
Accute follicular conjunctivitis
Epidemic keratoconjunctivitis(EKC)
Occurs in epidemics and is assoc with
follicular rx.
Etiology – Adenovirus 8and 19
C/F-
i. First phase(serous) non spf hyperemia
watering and chemosis
ii. Follicles more marked in lower fornix
51
52. Viral Conjunctivitis
Treatment- supportive and prophylactic
antibiotics.
Pharyngoconjunctival fever
Adenovirus 3and 7
Primarily affects childrens and appear in
epidemic form
C/F- acc follicular rx with pharyngitis,fever
and preaur lymphadenopathy and supf
punctate keratitis
Treatment : supportive
52
54. Viral Conjunctivitis
Accute Herpetic conjunctivitis
Usually seen in childrens and adoloscents in
assoc with primary herpetic infection
Type 1 involves eyes and spread by kissing
Type 2 assoc with genital infection rarely
effects eyes
C/F- incubation 3-10 days
54
55. Viral Conjunctivitis
Typical form assoc with vesicles on face
and lids
Atypical without vesicles and resembles
EKC
Corneal involv rare but can occur as supff
punctate keratitis and dendritic ulcer
Treatment –self limiting but antiviral used
when there is corneal invilv
55
56. Ophthalmia Neonatorum
B/L inflamation of conjunctiva in infant
<30days old. Any watering in 1st wk should
arouse suspicion.
Etiology
Before birth- infected liquor in premature
ruptured membranes
Birth- infected birth canal. (Face present)
After birth- unhygienic delivery. Soiled
clothes,fingers or lochia 56
61. Ophthalmia Neonatorum
Curative treatment
Chemical is self limiting
Infected – saline lavage
Pencilin drops 5000- 10000U/ml every
minute for ½ hrly then every min ½ hrly
then ½ hrly till infection controled
If resistant other broad spectrum like
moxifloxacin, gatifloxacin
61
62. Ophthalmia Neonatorum
Systemic treatment
Ceftriaxone 75-100mg/kg IV/IM QID
Cefotaxime 100-150 mg/kg IV/IM BID
Crystaline Benzyl pencillin 50000 u to full
term and 20000u to premature IM BID for
3 days.
Neonatal incl conj- 1% tetracycline or 0.5
% erythromycin qid for 3wks.systemic
erythromycin 125mgorally QID x 3wks 62
63. Allergic conjunctivitis
Inflamation of conjunctiva due to allergic or
hypersenstivity rx which can be immediate
(humoral) or delayed (cellular)
Types
A. Simple allergic conjunctivitis
a) Hay fever
b) Seasonal allergic conjunctivitis(SAC)
c) Perenial allergic conjunctivitis (PAC) 63
64. Allergic conjunctivitis
B. Vernal keratoconjunctivitis(VKC)
C. Atopic keratoconjunctivitis(AKC)
D. Giant Papillary conjunctivitis(GPC)
E. Phylectunlar keratoconjunctivitis(PKC)
F. Contact dermatoconjunctivitis(CDC)
64
65. Allergic conjunctivitis
Simple allergic conjunctivitis
Hay fever- assoc with fever and allergic
conjunc. Allergens are grass, pollens and
animal dander.
SAC- response to seasonal allergens like
grass and pollens. Very common.
PAC- allergens like house dust and mite.
65
68. Allergic conjunctivitis
Treatment
Elimination of allergen if possible
Symptoms releif – vasoconstrictor like
Naphazoline.
Mast cell stablizer like sodium
cromoglycate
NSAIDS and topical antihitaminic and
systemic
Steroids
68
69. Allergic conjunctivitis
Vernal keratoconjunctivitis(VKC):
B//L self limiting allergic inflamation having
seasonal incidence.
Etiology – Grass pollens
Pathology
Conjunctival epithelial hyperplasia with
with infilt of eosinophils, plasma cells.
Vascular proliferation with increased
permeability. Hyaline changes in chronic 69
70. Allergic conjunctivitis
Symptoms
Marked itching, lacrimation with ropy
discharge and heaviness in lids.
Signs
Palpebral – flat topped papilae with cobble
stone pattern. Giant papilae > 1mm
Bulbar- dusky red congestion, tranta spots.
Cornea- punctate keratitis, shield’s ulcer,
plaques, subepithelial scarring. 70
71. 71
Palpebral type
Hyperaemia
Chemosis
Papillae( giant ) more
in superior fornix
size, flat topped
(cobblestone), sticky
and ropy discharge
72. 72
Bulbar type
Congestion
Oedematous/
thickened conjunctival
nodules
Discrete white
superficial spots
(trantas dots)
73. Allergic conjunctivitis
Pseudogerontoxon- cupid bow outline.
Keratoconus.
Clinical course- burn out 5-10 yrs
Treatment
Avoid allergen, cold sponging,
vasoconstrictors like naphazoline
NSAID- ketorolac tromethamine. Down
regulate cyclooxygenase 73
75. Allergic conjunctivitis
Treatment of papillae- supratarsal injection,
cryoapplications and surgical excision.
Keratopathy- mild steroid and antibiotic,
plaque removal , AMG transplantation.
75
76. Allergic conjunctivitis
Atopic keratoconjunctivitis (AKC)- Adult
equivalent of VKC and assoc with atopic
dermatitis. More in adult males.
Symptoms
Itching, mucoid discharge, dryness and
blurred vision.
Signs
Inflamed lid margins,hyperemia,
papilae,SPK,plaques and thinning of cornea76
78. Allergic conjunctivitis
Giant papillary conjunctivitis- inflamation of
conjunctiva with large papillae.
Etiology- localised allergic response to
deposited irritant e.g CL, suture, prosthesis.
Symptoms - itching, stringy discharge, CL
intolerance
Signs- large papilae >1mm and hyperemia.
Treatment – remove the cause and
antiallergics 78
79. Allergic conjunctivitis
Phylctenular conjunctivitis- nodular
inflamatory response of conjunctiva and
corneal epithelium to some endogenous
allergen.Delayed type 4 hypersenstivity to
tubercular or staphylococus protein or
parasites.
Predisposition- 3-15yr f, undernourished and
poor living conditions
79
80. Allergic conjunctivitis
Pathology
Stage of nodule- exudation and infilteration
of leucocytes into deeper layers.
Ulceration- necrosis at apex. Ulceration and
infilt by leucocytes,mast cells and plasma
cells
Granulation – Floor covered by granulation.
Healing – with minimal scar.
80
81. Allergic conjunctivitis
Symptoms- irritation and watering.
Clinical forms
a) Simple phylc conj- pink white nodule
which ulcerate and then heals
b) Necrotic PKC- large phylcten with
necrosis and ulceration lead to pustular
conj
c) Milliary – multiple phylctens.
81
82. Allergic conjunctivitis
Phylctenular keratitis
A. ulcerative
i. Sacrofulous- shallow marginal ulcer with
long axix parallel to limbus.Heals with no
opacity
ii. Fascicular ulcer- ulcer with parallel leash
of blood vs. Heals with band shaped
opacity.
iii. Milliary – multiple small ulcers
82
83. Allergic conjunctivitis
B. Diffuse infilterative keratitis- central
infilteration of cornea with rich vs from
limbus
Treatment - steroids and antibiotics,
cycloplegics
Treatment of cause e.g TB,tonsilitis etc
Improve general hygiene and nutrition
83
84. Allergic conjunctivitis
Contact Dermatoconjunctivitis
Allergic rx involv conjunctiva, skin of lids
with face.
Type 4 rx response to prolong contact with
chemicals/drugs e.g atropine, pencillin,
neomycin
Eczematous rx in area of skin with
hyperemia, papilae in fornix
Steroids and antibiotics 84
86. 86
Pterygium
Hot climate, Dryness and
exposure to sun
C/f: Conjunctival
overgrowth over the
cornea in triangular
fashion
Destruction of
Bowman’s membrane
and superficial corneal
lamellae
88. Pterygium
Elastotic hyaline degeneration of cornea.
Parts- head , neck and body.
Types
Progressive- vascular and fleshy with
infilterates in front of head
Regressive- thin atrophic,less vascular with
no infilterates.
88
91. For Any Queries and
Clarifications
Contact Dr. Bhavani Raina on Saturday
(21-11-2020), between 01:00 PM to 03:00
PM in Seminar Room of EYE Department.
91