Leukocoria ( or white pupillary reflex) is an abnormal white reflection from the eye.
Leukocoria is a medical sign for a number of several conditions.
- this presentation at annual conference of the Ophthalmic department, faculty of medicine - Al-Azhar University in association with DOS & EOS Cairo, Egypt January 2017
Leukocoria ( or white pupillary reflex) is an abnormal white reflection from the eye.
Leukocoria is a medical sign for a number of several conditions.
- this presentation at annual conference of the Ophthalmic department, faculty of medicine - Al-Azhar University in association with DOS & EOS Cairo, Egypt January 2017
The corneal diseases are one of the leading causes of blindness in the world. in most cases, these infections are preventable or treatable.
This seminar provides an overview of the anatomy and physiology of the cornea, as well as an overview of common conditions.
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
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
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
2. Outline
I. What is Herpes Zoster Ophthalmicus (HZO)?
II. Anatomy of CN V
III. Pathophysiology
IV. Risk of Ocular Involvement
V. Clinical Manifestation
VI. Management
3. I. What is Herpes Zoster Opthalmiscus
(HZO)?
❖ known as shingles/Zoster, is a viral disease
characterized by a painful skin rash in one or more
dermatome distributions of the fifth cranial nerve, shared
by the eye and orbit.
5. III. Pathophysiology
Following Primary infection of VZV
Dorsal Root of Sensory neural Ganglion
Dormant
Activated VZV
VZV specific cell mediated immunity
faded
Central
Nervous
System
Dermatologic
involvement
Optical system
Auditory
System
6. IV. Risk of Ocular Involvement
✤ Hutchinson Sign
✤ Age
✤ AIDS
8. V. Clinical Manifestation
. Vesicles
B. Confluent
crusting
Haemorrhagic
sh with
volvement of
oth the
phthalmic and
axillary nerve
D. Residual
Scarring
10. V. Clinical Manifestation
A. Dendritic epithelial lesions with tapered ends B. Nummular keratitis
C. Stromal Keratitis
11. V. Clinical Manifestation
C. Chronic Eye Diseases
❖ Neurotrophic keratitis 50% cases
❖ Scleritis patchy slceral atrophy
❖ Mucous plaque keratitis 5%, between 3rd and 6th month
❖ Lipid degeneration in eye with persistent severe nummular or disci form keratitis
❖ Lipid-filled granulomata under tarsal conjunctiva together with subconjunctival
scarring
❖ Eyelid scarring result in ptosis, cicatrices entropion and occasionally ectropion
12. V. Clinical Manifestation
A. Scleral atrophy B. Mucous Plaque Keratitis C. Lipid filled granuloma
Cicatricial entropion Cicatricial ectropion
13. V. Clinical Manifestation
D. Postherpetic Neuralgia
❖ Pain persist > 1 month after rash healed
❖ 75% of patient over 70 Yrs
❖ Pain (Constant or intermittent), worse at night and
aggravated by minor stimuli, touch and heat.
14. VI. Management
A. Acute Shingles
✦ Oral Aciclovir 800mg 5t/day for 7-10 days, start within 72 hours of onset
✦ Intravenous aciclovir 5-10mg/kg t.i.d is indicated for encephalits
✦ Other Oral antiviral agents Valaciclovir 1g tid, famiciclovir 500mg tid and
brivudine 125mg qd
✦ Systemic steroids (prednisone 40-60 mg daily)
✦ Symptomatic
Remember it’s contagious to get ChickenPox
15. VI. Management
B. Ocular Involvement
1. Conjunctival involvement: Cool compress and erythromycin ointment b.i.d
2. SPK: lubrication with preservative-free artificial tears q1-2h and ointment q.h.s
3. Corneal or conjunctival pseudodentrites: lubrication with preservative-free
artificial tears q1-2h, topical antivirals (e.g ganciclovir 0.15% or vidarabine 3% ointment) tid or aid
4. Immune stromal keratitis: topical steroid (prednisonelone acetate 1%) tapering over
months to years using weaker steroids and less than daily dosing
5. Uveitis (with or without immune stromal keratitis): Topical Steroid
(prednisolone acetate 1%) and cycloplegic (scopolamine o.25% bid) Treat increased IOP with
aggressive aqueous suppression; avoid prostaglandin analogues
16. VI. Management
B. Ocular Involvement
6. Neurotrophic Keratitis: treat mild epithelial defects with erythromycin ointment 4-8 times/days.
if corneal ulceration occurs, smears and cultures to rule out infection. If sterile, no response to ointment,
consider a bandage contact lens, tarsorrhaphy, amniotic membrane graft or conjunctival flap.
7. Retinitis, choroiditis, optic neuritis or cranial nerve palsy: Acyclovr 5-10
mg/kg i.v q8h for 1 week and prenisolone 60mg p.o for 3 days, then taper over 1 week. Management of
Acute retinal necrosis may require intraocular antivirales.
8. Increased IOP: maybe steroid response or secondary to
inflammation. if uveitis, increase frequency of steroid for a few days and use topical aqueous
suppressants eg. timolol 0.5% bid, brimonidine 0.2% tid or dorzolamide 2% tie. Oral carbonic anhydrase
inhibitors if IOP > 30mmhg. If IOP still increased but inflammation controlled, substitue fluorometholone
0.25%, rimexolone 1% or loteprednol 0.5% drops for prednisolone acetate and taper dose
17. References
✴Section 8, External Disease and Cornea. (2012-2013). The
American Association of Ophthalmology. page: 119-122
✴Kenski, J. Jack. MD, (2011). Clinical Ophthalmology: A
Systemic Approach, 7th Edition. Elsevier Saunders, UK.
page: 248-253
✴Ehlers, Justis, P.; Shah, Chirag, P. (2008). Will’s Eye
Manual, The Office and Emergency Room Diagnosis and
Treatment of Eye Diseases, 5th Edition. Lippincott Williams
& Wilkins
✴http://emedicine.medscape.com/article/1132465-overview
✴http://eyewiki.aao.org/Herpes_Zoster_Ophthalmicus
Editor's Notes
VZV is one of Human Herpes Virus (HHV).
There are 8 recognised of Human Herpes virus
Type 1: HSV1 (herpes Simplex virus 1): Infection above the waist (orofacial and ocular infection etc)
Type 2: HSV 2 (Herpes Simplelx virus 2): below the waist (genital infection)
Type 3: VZV (Varicella-Zoster Virus): Varicelle (Chicken pox) and herpes zoster (Shingle)
Type 4: EBV (Epstein-Barr Virus)
Type 5: CMV (Cytomegalovirus)
Type 6, 7: Rose-olovirus: Roseola infantum and encephalitis
Type 8: Associated with Kaposi sarcoma and HIV lymphomas.
CN V- largest and most complex of 12 CN, Mix nerve (Sensory and motor), supplies sensations to face, mucous membranes and other structure of head. motor for the muscles of mastication and contains proprioceptive fibbers.
Exit the brain by a large sensory root and smaller motor root coming out of the pons at its junction with middle cerebral peduncle. join gasserian gg in the meckel cave.
3 branches: Ophthalmic, maxillary and mandicular leave skull through 3 separate foramina: superior orbital fissure, foramen rotundum and foramen oval.
Ophthalmic V1 (Sensory) have 3 branches:
Frontal Nerve: Supraorbital nerve: upper lid, frontalis muscle, scalp
Supratrochlear nerve: conjunctiva, upper lid, forehead
Lacrimal nerve: receive branches of zygomatic nerve of maxillary: lacrimal glance Conjuntiva and apparelled
Nasocilliary: Anterior ethmoid : Frontal, anterior ethmoid sinuses
Branches to cilliary gg: anterior septum, nasal wall
Posterior ethmoid: Cornea, iris, cilliary body
2-3 long ciliary nerve: Posterior ethmoid sphenoid sinus
Maxillary V2 (Sensory) lower eyelid and cheek, the nares and upper lip, the upper teeth and gums, the nasal mucosa, the palate and roof of the pharynx, the maxillary, ethmoid and sphenoid sinuses and parts of the meninges.
3 branches: zygomatic, pterygopalatine and posterior superior alveolar nerves.
Maxillary V3 (Sensory & motor): Sensory: lowerlip, lower teeth, gums, chin and jaw, touch/position and pain/temperature sensations from the mouth.
9 branches: Recurrent meningeal nerve
Medial pterygoid nerve
Masseteric nerve
Deep temporal nerves
Lateral ptergoid nerve
Buccal nerve
Auriculotemporal nerve
Lingual nerve
Inferior alveolar nerve
VZV immunity faded due to aging, immunosuppressive therapy, psychological stress, or other factors.
CNS- Anterior horn lead to muscular weakness, Cranial nerve palsies, diaphragmatic paralysis, neurogenic bladder, and colonic pseudo obstruction, (Winder involvement) Guillain barre syndrome, transverse myelitis and myositis. Severely, Meningoencephalitis or encephalitis.
Dermatologic involvement- cutaneous rash
Optical System- (Ramsay Hunt syndrome, geniculate neuralgia, or herpes zoster auricularis) Vesicular eruptions may manifest on the pinna, tragus, or tympanic membrane or in the auditory canal, as well as anywhere in the facial nerve distribution. The patient may experience hearing impairment, nystagmus, vertigo, or a facial nerve palsy mimicking Bell palsy.
Hutchinson Sign: Involvement of Skin supplied by the external nasal nerve, a branch of the nasociliary nerve supplying the tip, side and root of the nose. The sign correlates strongly with ocular involvement although there is no correlation between the severity of the rash and the severity of ocular complications.
Age: frequently in the 6th and 7th decades. Elderly, sign & symptoms tend to be more severe and to be of longer duration.
AIDS: Shingles can be early indicator of HIV infection. The development of Shingles in children or young adults should be prompt a search for immunodeficiency or malignancy, though found in only a minority.
A Prodromal Phase: Precedes appearance of the rash. last 3-5 days and is characterised by tiredness, fever, malaise and headache. Symptoms on dermatome: superficial itching, tingling or burning sensation to a severe deep boring or lancing pain that is either constant or intermittent. Older patients with early severe pain and a larger area of involvement are at particular risk of postherpetic neuralgia.
Skin Lesions:
Rash respect midline- distinguishing Shingle from HSV
Erythematous areas with a maculopapular rash, may confused with cellulitis or contact dermatitis.
24H, groups of vesicles appear and these become confluent over 2-4 days
Rash does not affect the lower lid in HZO, but boggy odema of upper and lower eyelids is common.
Vesicles often pass through a pustular before they crust and dry after 2-3 weeks
Large, deep haemorrhage lesions are more common in immunodeifcient patients.
Lesion heal to leave residual skin destruction and depigmented scars.
Disseminated Zoster: May rarely develop in immunodeficiency or malignancy. The Patient becomes severely ill and the rash progresses to involve multiple dermatomes and multiple organ systems.
Conjunctivitis: associated with lid margin vesicles.
Episcleritis: occurs at onset of the rash and usually resolves spontaneously.
Scleritis & sclerokeratitis: uncommon, end of first week.
Acute Epithelial: 50% in 2 days of onset of rash, resolve spontaneously within a few days, characterised by dentritic lesions which are smaller and finer than herpes simplex and have a taper ends with terminal bulbs. Stained better with Rose Bengal than fluorescein.
Nummular: at site of epithelial lesions about 10 days after onset of the rash. Charaterised by fine granular sub epithelial deposits surrounded by a halo of stromal haze. Lesions fade in respond to steroids.
Stromal Keratitis: 5% of cases 3 weeks after onset of rash, respond to topical steroids, chronic need slow tapering.
Disciform keratitis: (immune-mediated endothelilits), less common than herpes simplex infection, may lead to cornea decompensation.
Anterior uveitis: 1/3 of patients with sectoral iris ischaemia and atrophy
Neurological complication: CN palsies ( CN3, 4 and 6), Optic neuritis (rare), CNS manifestation: encephalitis, cranial arteritis, guillain-barre syn.
Mucous Plaque keratits: sudden appearance of elevated mucous plaques that stain with rose bengal.
Systemic steroids used with antiviral. have moderate effect to reduce acute pain and accelerate skin healing but no effect on the incident or severity of postherpetic neuralgia.
Symptomatic: treatment of skin lesions is by drying, antisepsis and cold compresses.