2011-07-patho-head and neck disorders 2
TRANSCRIPT
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DISEASE OF THE EYES
ORBIT
PROPTOSIS
o Forward displacement of the
eyeo May result from any disease
process that increasesorbital contents
o Cornea may be exposedcausing corneal infection
o May be: axial (pushed
forward) or positional
THYROID OPHTHALMOPATHY(GRAVES DISEASE)
(Graves disease)o Accumulation of extracellular
matrix protein and variable
degree of fibrosis in therectus muscles
o Results in AXIAL PROPTOSIS
NEOPLASMSo
Capillary hemangiomao Lymphangioma
o Cavernous hemangioma:
encapsulated inadults
o Malignant lymphoma
o Metastatic tumour
EYELID
GLANDS OF THE EYELIDS & COMMONLY
ASSOCIATED PATHOLOGIC CONDITIONS
TYPE OF
GLAND
LOCATION PATHOLOG
YMeibomian
-sebaceous
- Upper and
lower tarsal
plates
- Open on
lid margin
-Chalazion
-Internal
hordeolum
Zeiss
-sebaceous
- lid margin
- open into
follicles of
the lashes
-External
hordeolum
Moll
-apocrine
- lid margin
- open into
follicles of
the lashes
-Ductal cysts
-Adenoma
Subject: PathologyTopic: Head and Neck 2Lecturer: Dra. Joan Pascual RodriguezDate of Lecture: July 28, 2011
Transcriptionist: Jak-statPages: S
Y
2011-2
012
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I. Inflammation
1.BLEPHARITIS
Obstruction of the drainagesystem of the sebaceousglands by chronicinflammation (lesscommonly by neoplasm) atthe eyelid margin
Chronic inflammation leadsto loss/ abnormalities ofeyelashes and thickened andulcerated lid margin
May cause cellulitis
Drainage: sebaceous
2.HORDEOLUM
EXTERNAL HORDEOLUM
i. Also: styeii. Purulent inflammation
of superficial sweat
and sebaceous glandsand hair follicle
iii. Causes abscessformation thennecrosis, spontaneousevacuation of theabscess
INTERNAL HORDEOLUM
i. Purulent inflammationof meibomian gland
ii. Produced byobstruction of themeibomian duct
associated with abacterial infection
iii. Resolution of abscessand healing areusually accompaniedby scarring
3.CHALAZION (LIPOGRANULOMA)
Results from blockage of theMeibomian duct or Gland ofZeiss. Then, Retention cystruptures formingLipogranulomatousinflammation
i. Meibomian Gland(deep chalazion)
ii. Gland of Zeiss(superficial chalazion)
Hard painless nodule
Extracellular accumulation of
fat with accompanyinggranulomatous response
Confluent series of focalgranulomas with smallmicroabscesses
Centered on a lipid globule4. XANTHELASMA
(Xanthelesma high cholesterol
symptom)
Intracellular accumulation offat (foam cells)
Soft yellow plaques
Lipid-laden histiocytesaround adnexal structure
II. NEOPLASMS
1. BASAL CELL CARCINOMA
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Most common malignanttumout of the eyelids
Lower lid inner canthus lateral canthus
Slow growing nodule or ulcer2. SEBACEOUS GLAND CARCINOMA
2nd most common malignancy ofthe eyelids
may mimic chalazion ordiffusely thicken the eyelids
CONJUNCTIVA
Zones:
1. palpebral conjunctiva
tightly tethered to the tarsus
non-keratinizing squamousepithelium
2. limbus
junction of sclera and cornea
contains epithelial stem cellscapable of differentiating intoconjunctival epithelium orcorneal epithelium
3. conjunctival fornix
pseudostratified columnar cells
rich in goblet cells conjunctival lymphoid
population4. bulbar conjunctivae
conjunctiva that covers thesurface of the eye
non-keratinizing stratifiedsquamous epithelium
I. INFLAMMATION
1. ACUTE CONJUNCTIVITIS
Edema, hyperemia, mucussecretions and exudation ofdegenerating epithelial cellsand inflammatory cells into theconjunctival sac accompaniedby tearing and lymphaticdilation
Ulceration
2. CHRONIC CONJUNCTIVITIS
Hyperplasia of the epithelium;increase in goblet cells
Stroma: papilla and follicleformation
Papilla formation: bactl,chlamydial, allergic cause
Follicle formation: viral cause
Keratinization or drying: vit a
deficiency Granulomas- sarcoidosis
Granulation tissue formation
3. CONJUNCTIVAL SCARRING
Chlamydia trachomatis, trauma,drug reactions, chemical burns,etc.
shrinkage of the conjunctiva
reduction in goblet cell number
eventually leads to:
o drying of eyes(xerophthalmia)
o corneal opacification
o ulceration
* TRACHOMA
epithelium undergoes markedhyperplasia
cytoplasm contain colonies ofelementary bodies
conjunctival and corneal inclusionbodies
edematous subepithelial tissue
infiltrated by inflammatory cells reactive proliferation of connective
tissue and fibrovascular repairscarring
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II. DEGENERATIVE LESIONS
1. PINGUECULA AND PTERYGIUM
Appear as submucosalelevations on the conjunctiva
Result from actinic damage andare therefore located in sun-exposed regions of theconjunctiva (interpalpebral
fissure)
PTERYGIUM
Submucosal growth of fibrovascular connective tissue thatmigrates onto the corneadissecting intothe plane occupiedby the bowmans membrane
Does not cross papillary axis
NO THREAT TO VISION
PINGUECULA
Elevated, yellowish-white (solarelastosis) area near the limbus
Does not invade the cornea but canresult in an uneven distribution ofthe tear film over the adjacentcornea
Dellen: saucer- like depression of
the cornea Actinic granuloma: inflammation of
pinguecula secondary to a foreignbody
o Granulomatous reaction
against elastotic collagen
III. NEOPLASMS
1. SQUAMOUS CELL CARCINOMA
Mild dysplasia carcinoma insitu
Conjunctival intraepithelialneoplasia (CIN)
2. MELANOCYTIC NEOPLASMS
Unilateral neoplasm
Middle-aged, fair complexion
Primary acquired melanosis
with atypia (Melanoma in situ) 50-90% of patients with
incompletely-treated melanosiswith atypia will developmelanoma
mortality rate: 25%
metastasis: parotid orsubmandibular gland
3. 3. CONJUNCTICAL NEVUS
CORNEA
EPITHELIUMo 5-6 layers of NK, squamous
epithelial cells
BOWMANS LAYERo Situated directly under the
basement membrane of theepithelium
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o Consists of collagen fibers
and muco-protein groundsubstance
o Cannot regenerate after
damage
STROMAo Forms 90% of the thickness
of the corneao
Devoid of blood vessels andlymphatics
DESCEMETS MEMBRANDEo True basement membrane
formed by cornealendothelium
o Thickness increases with age
o Can regenerate after
damage
ENDOTHELIUMo Derived from neural crest
cells and is not related tovascular endothelium
o Dissolution of the corneal
stroma
I. KERATITIS AND ULCERS
Dissolution of corneal stroma
1. EPITHELIAL EROSION ANDKERATITIS
Trauma, radiation, inflammation2. SUBEPITHELIAL KERATITIS
Epidermal keratoconjunctivitis,trachoma, leprosy
3. STROMAL/ INTERSTITIAL KERATITIS
Viral (herpes, EBV), bacterial(TB), syphilis, parasitic
4. ULCERATIVE KERATITIS
Destruction of cornealepithelium and bowmans layeroften followed by varyingdegrees of destruction of thestroma
Chronic corneal inflammation
Chronic herpes keratitis
Ulcerative Keratitis
ANTERIOR SEGMENT
o Cornea, anterior chamber,
posterior chamber, iris and lens
o Bounded anteriorly by cornea,
laterally by trabecular meshworkand posteriorly by iris
LENS
F
u n
c t
i o
n a
l
Anatomy (Recall)
Transparent biconvex disc
Avascular, no nerves
Closed epithelial system
Covered by the lens capsule whichis rich in type IV collagen andproteoglycans which totallyencloses the entire lens
Infoliates rather than exfoliates
With advancing age, proliferatesand becomes inwardly compacted.
This is accompanied byaccumulation of intracellular yellow
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pigment. Both decrease lighttransmission and decrease vision.
Components:o Lens capsule
o Subcapsular epithelium
o Lens substance (convex)
o Nucleus (central region)
1.)Cataract
> Lenticular opacities
Causes:
a. CongenitalFamilial cataract
Most are autosomaldominant; usuallybilateral
Secondary to
intrauterine
Infection (Rubella)
b. AcquiredSystemic disease
Galactosemia, DM,Wilsons disease(deficient in copper),atopic dermatitis
Drug induced
CorticosteroidsRadiation or trauma
Infrared radiationcauses exfoliation ofthe lens capsule
Other intraocular disorders
c. Physical and degenerativechanges
Liquefaction of thelens capsule
Proliferation andmigration of the
epithelium Degenereation and
atrophy of theepithelium
Rupture of the lenscapsule
Age- related Cataracts (senile
cataract)
No known cause; inelderly
3 types:o Cuneiform (in
the peripheralcortex)
o
Punctuateperinuclear ( inthe cortex nextto the nucleus)
o Culpuliform ( in
the posteriorcortex)
Secondary Cataracts
Intra-ocular disease
(cataracta complicate)o Uveitis,
malignantintraoculartumors,glaucoma,retinitispigmentosa
Trauma
Toxico Steroids
o Phenothiaznes,
allopurinolo Ergot poisoning
Endocrine/metabolico Galactosemia,
DM
HISTOLOGY: there is migration ofthe lining epithelium below orabove the lens, causingmetaplastic (metaplasia) changesin the lining epithelium
Treatment = removal of the Lensand replaced by a New Lens(Operation)
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2.) Glaucoma
Collection of the diseasecharacterized by distinctivechanges in the visual field and inthe cup of the optic nerve
Most are associated with elevated
intraocular pressure. Althoughsome with normal IOP it maydevelop characteristics optic nerveand visual field changes (normal orlow tension glaucoma)
Functional Anatomy (Recall)
Drainage
Aqueous Humor
Produced in theciliary process (ciliaryepithelium of the ciliary body)
Drains intocanal of Schlemm (whichultimately drains into thevenous network)
CC
increased intraocularpressure usually due to tissuechanges that reduce the removaloutflow or continuous production ofaqueous humor
symptoms includeheadaches and visual impairment
maybe due toinflammation, tumor, andcongenital or hereditary factors
damages the opticnerve loss of ganglion cells
thinning of the
retinal nerve fiber layer edematous corneawith formation of degenerativepannus
in infants and inchildren (elevated IOP)buphthalmos (diffuse enlargementof eye), megalocornea(enlargement of the cornea.
TYPES:1. Open angle
Glaucoma
angle appears openbut does notfunction properly intransportingaqueous humor outof eye, canal ispatent
the problem is infiltration, mostcommon in ageingindividuals
aqueous humor hascomplete access totrabecularmeshwork
elevated IOP resultsfrom increase
resistrance toaqueous flow inopen angle
a. PrimaryOAG- Most common form
b. Secondary OAG
Ciliary body Posterior chamber Pupil
Anterior Chamber Trabecular
meshworkCanal of Schlemm
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- Particulate matter
clogging the trabecular
meshwork
- Elevation on
pressure on the surface of
the eye (vascular
malformations, trauma)
2. Close angle Glaucoma/Angle Closure Glucoma
the eyes are smallerthan normal andhyperopic
surface of theperiphery of the irisis close to the innersurface of thetrabecular
meshwork, resultingin narrow or shallowanterior chamberangle
there is narrowing ofthe Canal ofSchlemm andtrabecularmeshwork bycontact with the iris
it is normallycomplicated byageing
a. Primary ACG
- papillary block
papillary margin of the
iris attaches to the
anterior surface of the
lens
- pressure build up inthe posterior chamber
- forward bowing of
the iris apposing it to the
trabecular meshwork
- lens epithelium may
be damaged by the
chronically elevated
pressure
b. Secondary ACG
- neovascular
glaucoma
- neovascular
membranes as a result of
injury or neoplasm,
closes the angle
- outflow of aqueous
humor is blocked
therefore there is an
increase in ICP
- lens epithelium may
be damaged by the
chronically elecated
pressure
3. Congenital or HereditaryGlaucoma
maybe secondary toinfectious disease i.eRubella
defective
development ofangle structures withabnormal insertionof ciliary musclefibers or trabecularbands
secondary glaucomais caused by iritis,iridocyclitis withpapillary adhesionsand angle block
UVEA
- made up of iris, ciliary body, choroid
-no lymphatics
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I. Uveitis = Inflammation of the Uvea
-may be Granulomatous or Non-
Granulomatous Uveitis
I. GRANULOMATOUS UVEITIS
-caused by Mycobacterium,Leprosy, HSV, Zoster, Blastomycosis,
Tryptococcosis, Candidiasis,
Toxoploscosis,
Oncocercasis
-Etiologic Agent = Bacteria, Fungi,
Parasites
**Histology:
o Epitheloid Cells
o Granulomatous Pattern of
Inflammation are seeno Lots of Lymphocytic
Infiltrates
II. NON-GRANULOMATOUS UVEITIS
-there is No Granuloma formation
-Histology: Polymorphonuclear
Cells are present
II. NEOPLASM
MELANOMA
-Origin of Melanoma = Melanocytes
-eyes are NOT spared by this
because it also contains Melanocytes
(there may also be Melanoma in the
Uvea)
-Melanoma may occur because
there are Melanocytes in the Uvea
-this is caused by the tendency of
Melanocytes to abnormally proliferate in
the eye
**Four Types of Melanoma in the
Uvea
1. Spindle-A Type
-presence of Cohesive Cells with
indistinct nucleoli and ill-defined,
scanty cytoplasm
-GOOD Prognosis
2. Spindle-B
-Cohesive Cells with a moreprominent Nucleoli and More
Cytoplasm
3. Epitheloid
-Poorly Cohesive and there is
abundant cytoplasm
-Epitheliod Like Cells are seen
-Rarest Type with Poor Prognosis
4. Mixed Type (most common)
-Mixed Type is the Most Common
Type
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-it is a Mixture of Spindle-B and
Epitheloid Types
RETINA AND VITREOUS
Functional Anatomy (recall)
Components of the Retina:1. Fovea Centralis
Depression in theMacula Lutea
2. Macula Lutea
Yellow pigmentedzone surrounding theFovea
3. Optic Disk Blind spot
Where the axons ofganglion celss exit
Lacks photoreceptors
( review the 10 layers of the retina)
I. Retinal Detachment
Separation of the neuro sensoryretina from the retinal pigmentlayer.
Emergency case
Causes:o Accumulation of fluid
beneath an intact neuronalretinao Traction bands in the
vitreous (DM, post traumatic)o Accumulation of fluidbeneath broken neuronal retina(vitreous traction)
Classification:o Rhegmatogenous (break in
the retina)
Full thickness retinaldefect associated withvitreous traction
When you haveposterior vitreousdetachment, the posteriorhyaloids does not separatecleanly from the internallimiting membrane of theretina and the vitreoushumor exerts traction retina
Eventually, theliquefied vitreous humorseeps throught the tear &insinulates between theneural retina and the retinalpigment epithelium.
Non-Rhegmatogeous(nobreak in the retina)
Detachment withourretinal break
Subretinal space isfilled with protein rich
exudates Macular diseasewhere there is significantexudation
o Malignant HPN
o Choroidal tumors
II. RETINAL VASCULAR DISEASE
1.)Retinopathy or Prematurity
(Retrolental Fibroplasia)
Bilateral; not present atbirth
Occurs in prematureinfants who have ahistory of oxygen therapy
Normally, nasal (ormedial) aspect of theretina is vascular and thetemporal (or lateral)aspect is incompletely
vascularized.
In premature or LBW infants
treated with oxygen, there is
hypoxia leading to
vasoconstriction of the immatureretinal blood vessels at the
temporal aspect
The area distal to the constricted
vessels become ischemic
Ischemia leads to increasesecretion of proangiogenicfactorsRetinal angiogenesis orneovascularizationOrganization of the avascular
retina into a contracting scar
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The detached retinal may bedrawn by fibrovasculartissue into a mass behindthe lens (hence also calledretrolental fibroplasia)
2.) Diabetes Mellitus
Stages:a. Background diabetic
retinopathy (BDR)/ preproliferative
loss of capillary pericyte
retinal capillarymicroaneurisms (RCM)
thickening of the retinalcapillary basementmembrane
A-V connection of shunts/collaterals
b. Diabetic or Exudativeretinopathy (wet)
Hard or waxyexudates
Macular edema
Microcysticdegeneration of the neuralretinal macule
Soft or cotton-woolspots
c. Proliferative Retinopathy
in respose to hypoxia,the retina producesangiogenic factorsneovascularization
Neovascularization isinitially intraretinal but later,it may break through the
internal limiting membraneand abut the vitreous
retinalneovascularization term isreserved forneovasculariation that hasbreached the internallimiting membrane
A neovascularmembrane may also form onthe iris surface contractsanterior synechiae (adhesionbetween the iris & trabecularnetwork) obstruction ofaqueous outflow
Glaucoma
3.) Hypertension
Thickening of the walls of
the retinal arterioles
Grading:
Grade I hypersensitive retinopathy (HR)
o Generalized narrowing of the
arteriolesGrade II HR
o Grade I + focal arteriolar
spasm
Grade III HR
o Grade II + hemorrhage and
exudateso Splinter hemorrhages, dot &
blot hemorrhagesGrade IV HR
o Grade III + optic disc edema
o Cotton wool spots
o Hard or waxy exudates
o Obliteration: choroidalinfarctsElshnigs spots
o Infarcts of nerve fiber layer
Axonal transport is
interrupted
Mitochondria accumulates at
ends of damaged axon
cystoids bodies
Histologically:o Thickenedretinal arterioleo Exudates
o Arteriolar
diameter reducedo Color blood
column appears lesssaturated (copper-wirelike)
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III. Age- related Macular
Degeneration( ARMD)
unknown etiology
Risk factors:
o Smoking
o Vascular pathology
Atherosclerosis
hypertension
Atrophic (dry) : Atrophy of retinalpigment epithelium
Exudative (wet):o Choroid neovascular
membrane(hallmark)
Vessel may leak
exudedorganized intomacular scars
diffuse vitreous
hemorrhage
***Arteriolosclerosis Grading:
Grade I = hyaline deposits beneath theintima & thickened media/adventitiathe arteries will become semiopaqueincrease light reflex
Grade II = grade I + arteriolar- venularcrossing defects
= arterioles share a commonadventitia with venules. When arteriolarwall thickens at areas where these 2vessels cross view of veins isobstructed
Grade III = grade II + copper wirearteriole
= when arteriole becomessufficiently opaque, reflected lightbecomes coppery
Grade IV = grade III + silver wireappearance
IV. RETINITIS PIGMENTOSA
inherited as either X-linked recessive,autosomal dominant and recessive
both rods and cones are lost to apoptosis,
in varying proportions
o loss of rods: night blindness and
constricted visual field
o loss of cones: central visual
acquity affected
retinal atrophy and constriction of retinal
vessel
optic nerve head atrophy
accumulation of retinal pigment around
the blood vessel
V. NEOPLASM
1. Retinoblastoma
most common primaryintraocular neoplasm of
the children (in adults:melanoma)
bilateral in 20-35%
growth pattern:o multifocal
spontaneous growthin more than 1 foci
o exophytic pattern
most grown towardsthe subneural retinal space& detaches neuronal retina
o endophytic pattern
grows toward thevitreous
Arise from photoreceptorprogenitor cells or from primitivestem cells that are capable ofdifferentiation along both neuronal &glial cell lines.
Morphology
o Gross Appearance = Nodulenear the Optic Tract
o necrosis
Histology:o Undifferentiated: Small
round cells withhyperchromaatic nuclei
o Differentiated: associated with
Flexner-Wintersteiner Rossettes
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and fleurettes (photosensory
differentiation)o Necrosis, dystrophic
calcificationo There is the presence of
Mitotic Figures**Flexner Wintersteimers Timer
=Retinoblastoma
-Microscopic Findings of
Retinoblastoma = Flower Like
-there is a Lumen with projections
-there are clusters of cuboidal cells
arranged around a central lumen.
Spread:o Local spread
o Extraocular extension
orbit & brain
Prognosis is affected by:o Histology
Abundant FWR 6xbetter prognosis thanif absent
Completelydifferentiated betterprognosis
o Choroidal invasion
poor prognosiso Optic nerve
involvement poorprognosiso Iris neovascularization
(can also lead to retinal
detachment) poorprognosiso Location and size
2. Retinal Lymphoma
(retinal lymphoma with leopard
furfur)
Systemic lymphoma uvea(commonly metastatic)
Primary retinal lymphoma involves neural retina & retinalpigmented epithelium
Diagnosis: presence of lymphomacells in vitreous.
OPTIC NERVE
1.) Papilledema
(papilledema Gr.1)
Edema of the head of theoptic nerve
Terminology:o Optic disc edema
non inflammatorycauses of swollenoptic nerve head
o Papillitis swollen
optic nerve head dueto inflammation
Causes:o Compression of
the nerve( neoplasms,glaucoma, malignantHPN)
Local spread-(anteriorly)
Vitreous & aqueous (posteriorly)
Subneural retinal space
ChoroidsSystemic circulationOptic nerveSubarachnoid space
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o Increase CSF
pressure surroundingthe nerve
Increase in pressurearound the nerve leads tovenous stasis at nerve head/block in axoplasmictransport nerve head
swelling
2.) Anterior Ischemic Optic
Neuropathy (AIOP)
Stroke of the optic nerve
Refers to the injury due toischemia/ infarction
Transient partial interruption ofblood flow to optic nervetransient loss of vision
Total infarction optic nerveinfarct
Causes:o Inflammation of vessels
supplying the optic nerve arteritic AION
o Embolic/ thrombotic event
non arteritic AION
*** END STAGE EYE ( Phthisis Bubi)
small(atrophic) & internallydisorganized eye
secondary to trauma, intraocularinflammation, chronic retinaldetachment
Morphology:o Ciliochoroidal effusion :
exudates/ blood in the spacebetween the ciliary body andsclera and the choroid andsclera.
o Cyclitic membrane:
membrane extending acrossthe eye from one aspect ofthe ciliary body to other
o Chronic retinal detachment
o Optic nerve atrophy
o Thickened sclera
o Hypotony (low IOP) is square
rather than round eye
**********END OFTRANSCRIPTION*********
Mga Pabati:
Congratulations batch 2014 dance crew
(Abi, Josh, Jake, Jhe, Jam, Jeff, Ica, Emily,
Trish, Ar-ar, Mike, Xands, Max, Lawrence,
Ace, Athena, Maebritt, Angela and me) for
winning the dance competition kahit
super late na tayo natatapos ng practice
nung last 2 days pero worth it naman.
Hahaha. I enjoyed dancing with you guys!
Thanks for the patience and for the effort!Hope to dance with you again. Salamat
din kay Pinay na matiyagang tumulong
gumawa ng props kasama yung uba pa.
pati yung mga naghawak ng box naming
while we are dancing. Salamat salamat!
2014 dance crew is the best! WHERE DO
WE GO? ON TOP OF THE WORLD!
Syempre san pa ba? Hehehe. Sa uulitin!
Sana makatulong itong tranx na ginawa
naming na super delayed na. good luck
sa mga exams natin. Kaya natin to, kapit
lang!
Hi 33.. belated happy bday Yldy..hi to me
cell group..my groupmates..all the yfc out
there! Congrats batch 2014..!!!! God
says..So whether you eat or drink, or
whatever you do, do everything for the glory
of God. 1 Corinthians 10:31
The eyes are the mirror of thesoul
Godbless BATCH 2014!!!:)