2011-07-PATHO-Head and Neck Disorders 2

8/6/2019 2011-07-PATHO-Head and Neck Disorders 2

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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!!!:)

2011-07-PATHO-Head and Neck Disorders 2

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Transcript of 2011-07-PATHO-Head and Neck Disorders 2