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111 Cards in this Set

  • Front
  • Back
BLEPHARITIS
VS
CHALAZION
VS
XANTHELASMA
BLEPHARITIS / sty / hordeolum
- inflamed EYELID

Foreign body granuloma of Meibomian gland
= CHALAZION
(NOT inflammation)

Yellow plaque made up of fatty macros on nasal eyelid
= XANTHELASMA
PINGEUCULA

VS

PTERYGIUM
BOTH ON CONJUNCTIVE 2' sun/UV damage

PINGUECULA =)
- most common
- nasal to coreno-scleral Limbus
- degen changes in collagen substantia propria
- Less aggressive
- NO vascularization


PTERYGIUM:
- VASCULARIZED
- conjunctival growth that grows traingularly & horizontally onto cornea
- insect wing
- same degen changes
LAYERS OF THE CORNEA

+ important features
+ what causes opacification of cornea (inherited vs acquired)
Shape & Transparency = most important
- cornea does MOST of the light focusing (NOT lens)

5 layers:
- Epithelium
- Bowman's layer
- Stroma(thick, carefully layered collagen sheets)
- Descemet's membrane
- Endothelial layer

INHERITED CORENAL DYSTROPHIES
- BL, symm
- defective enzyme system --> accum metabolites --> separate stromal layers

ACQUIRED:
- Vit A deficiency: thick, bubbly lesion at limbus of cornea
(bitot's spot)
- Severe = keratomalacia (soft cornea)
= india
ACUTE VS CHRONIC BACTERIAL CONJUNCTIVITIS

- organism
result?
ACUTE:
Hyperemia, edema, infiltration w/ Neutrophils & mononuclear cells
- conjunctival sac secretes PUS
- MCC: S. aureus, S. pneumo, Proteus mirabilis & H. aegyptius (pink eye)
- Scarring depends on amt of tissue destroyed
**Bowman's membrane does NOT regenerate**
**P. aeruginosa also a case = contact lens solutions

CHRONIC:
- usually infxn of lid margin
- same common causes; esp Proteus
Opthalmia neonatorum

- organism
- result
Severe, acute, pus-y conjunctivits
- Corneal ulceration --> scar --> blindness

causes:
n. gonorrhea
chlamydia
trachoma =(

- organism
- transmission
- result
- where?
Acute cicatrizing/scarring keratoconjunctivits

Chlamydia trachomatis (serotypes A B C)
- eye --> eye transmission & flies
- MCC blindness in world (africa, asia, middle east)

RESULT:
- Lymphoid follicles appear in conjunctiva & get red & edematous
+ cytoplasmic inclusions in conjunctiva
**Cicatrization: infiltrate replaced by granulation tissue & dense collagen
--> stratified squamous epithelium (NO goblet cells)
-->
A. trichiasis (inturned lashes)
B. Entropion (inturned lids)
C. symblepharon (fusion of lid margins
mycotic infxns

(not on cao's exams)

- organisms
- where?
- which pts?
tropica places

ASPERGILLUS & CANDIDA
- indolent & intractable corneal ulcerations or endophthalmitis
- Endopth only in immunosuppressed or steroid tx
viral infections of the eye

- who?
- what organisms?
- results?
NEONATES:
- CORNEA/keratitis = HSV2
--> also awful cerebritis

ADULTS: HSV-1
- asymptomatic plaques of epithelial cells
- actively replicating virus
--> ulcers & blindness
GLAUCOMA & EFFECTS OF ELEVATED IOP


**when ^ IOP < 3yo
--> BUPHTHALMOS (giant eyebals & big orbital bone)
GLAUCOMA = obstruction of aqueous humor drainage = ^ IOP

Acutely:
Corneal edema & irreversible endothelial damage

cHRONICALLY:
dEGENERATIVE "PANNUS" (Infiltration of limbus: fibrovasc tissue b/w Bowman's & epithelium)
- Cornea/sclera bulges at weak points
- Cupping of the optic disc (destruction of ganglions)
- Nasal displacement of retinal blood vessels
- Optic atrophy (loss of axons, gliosis, etc)
**Ganglion cell layer degenerations**
--> VISION LOSS


**outer retina (rods & cones) are spared until late bc separate blood supply = choroid plexus**
PRIMARY OPEN ANGLE GLAUCOMA

(chronic simple glaucoma)

- population
- clinical
- mech
MCC OF GLAUCOMA
2/3 white sw/ dz
- esp diabetics & myopic
1-3% of population > 40 yo
(but onset is usually 60s)

MAJOR Cause of blindness in USA

CLINICAL:
- Insidious onset; asymptomatic
- BILATERAL, but not nec same time
- LOSE PERIPHERAL VISION

mech
Increased resistance to the outflow around schlemm's canal
- access to ant. chamber is open
- trabecular meshwork is propbly weird; maybe 2' ^ IOP?
PRIMARY CLOSED/NARROW ANGLE GALUCOMA

- population
- clinical
- mech
YOUNGER ONSET than open angle
- middle aged-elderly
- Small eyes w/ large lens
- narrow ant. chamber angle

CLINICAL:
- SUDDEN ONSET, UL
- constricted/miosis = good; stretched iris; no occlusion
- Dilation/mydriasis = bad (iris obstrcuts flow)
- ocular pain, halos
- OCULAR EMERGENCY
**start hypotensive tx**
SECONDARY GLAUCOMA

- CAUSES
- MECH
- CLINICAL
- TX
PLUGGED DRAINAGE

Many causes - inflamm, hemorrhage, neovasculariztaion of iris adhesion

**Ant chamber angles/access is irrelevant
- can be open or closed

Trabecular meshwork is plugged w/ particulate matter

ASSC'D:
- LONG corticosteroid use
- fibrovascular adhesions bw iris & peripheral synechiae (post-thrombotic glaucoma)

**USUALLY UNILATERAL)
LENS PATHOLOGY

- CATARACTS
- presbyopia
LENS GROWS from equator THROUGHOUT LIFE
- loses compliance / zoom lens props as it gets thicker
- accums waste produces = opacification (cataracts)


PRESBYOPIA: middle aged vision
- removal of near pt of vision farther from eye
- lens remains oval & loses its elasticity
- CAN'T ACCOMMODATE
CATARACTS

- what?
- risk factors
ATARACTS
accums waste produces = opacification
- accumulate fluid or disrupt matrix layering
- Yellow pigment: hydroxykynurenin glucoside (HKR-G)


risk factors:
Neonates: congenital rubella
Radiation: ionizing x-rays & UV light
- Corticosteroids **post. lens opacities*
- many other drugs
- Diabetes: no aldose reductase (sorbitol attracts water) --> sugar cataract
- HTN
- CHRONIC INTRAOCULAR DZ
UVEA

- COMPONENTS
- BOB: BLOOD-OCULAR BARRIER
UVEA = VASCULAR LAYERS + IRIS, CILIARBY BODY + CHOROID
- 2nd outermost layer (next o sclera)


BOB:
1. Blood-aqueous humor
- ciliary body & iris (tight jcts)

2. Blood-retinal : 2 levels
a.) retinal caps --> ganglions are non-fenestrated
b.) Bruch's membrane & pigmented epithelium = barrier
- zonulae occludens
- choroid caps are freely permeable
- supply rods/cones
UVEITIS

- what?
- clinical
Inflamed iris & ciliary body

- redy eye
- photophobia & blurred vision & pericorneal halo
- moderate pain
- dilated deep ciliary vessels
- ciliary flush
- constricted pupil / miosis

Post. cornea: leukocyte aggreg

Ant chamber:
- keratic precipitates settle (Hypopyon)
- increased protein seen w/ slit lamp (Flares)
anterior uveitis

- uncontrolled -->?
- genetics
- assciations
- pathology
NONSPECIFIC INFLAMM of anterior segment
- uncontrolled --> glaucoma
- adhesions block drainage

CAUSES:
- IDIOPATHIC: HLA-B27
- Autoimmune systemic diseases: many

PATH:
- Infiltration of iris & ciliary body w/ lymphocytes & plasma cells
--> leaked plasma proteins & inflamm cells into aqueous

ACUTE ONSET; OFTEN RECURS
SYMPATHETIC OPHTHALMITIS

- cuase
- mech
RARE IN USA NOW

1. penetrating ocular injury
2. Prolapse of uveal tissue (reveals hidden Ags 2 immune system)
3. Inflamm starts affecting OTHER eye
- usually 4-8 wk interval

TAKE THE PENETRATED EYE OUT!! (glass eye pts)
- granulomatous inflamm, affecting the choroid
--> sclera via emissary channels
- see multinucleated giant cells
SARCOIDOSIS OF THE EYE

- which area of eye?
1/4 - 1/3 of pts w/ sarcoidosis
- often presenting clincal manifestation

PREDILECTION FOR ANTERIOR SEGMENT FO THE EYE

**granulomatous rxn
PAPILLOEDEMA

- WHAT?
- EFFECTS?
SWELLING OF THE OPTIC DISC

= INCREASED ICP (2' focal lesion usu.)
Optic N. feels pressure & swells as it enters the CSF filled optic n. SHEATH

- Impaired axoplasm flow
- Dilated swollen axon
- impaired venous return --> 2' hemorrhage
RETINAL CHANGES

(NOT CAO'S EXAMS)
1. INTRA-RETINAL HEMORRHAGES
- flame shape

2. cotton-wool spots = microinfarcts of superficial n. fiber layer

3. Microanerurysm (retinal ischemia)

4. Drusen
- exudates from bruch's membrane
- formed by pigmented peithelium?

5. silver wiring: arteriolarsclerosis of retinal vessels
- walls replaced w/ hyaline
VASCULAR DISEASES OF THE EYE

DIABETIC RETINOPATHY
- FEATURES
- MECH
- COMPLICATIONS
1. Hyaline arteriosclerosis
2. Thickened capillary BM (glycosylation of BM)
3. Micoraneurysms (retinal ischemia)
4. Increased venous tortuosity

- as it progresses: cotton-wool spots, hard exudates, cystoid macular edema

complications:
NEOVASCULARIZATION
- new vessels suck
- 2' retinal ischemia --> angiogenic growth factors
= PROLIFERATIVE RETINOAPTHY

BLINDNESS!!
VASCULAR DISEASES OF THE EYE

- RETINOPATHY OF PREMATURITY
(RETROLENTAL FIBROPLASIA)

(ROP)

- WHY?
- COMPLICATIONS
PREMIES SUBJECTED TO SUSTAINED HYPEROXIA

HYPEROXIA: premature capillary closure in the eye
- Mesenchymal spindle cells don't migrate anteriorly from optic n. head
--> NO RETINAL VESSELS!

UH OH!
- Spindle cells proliferate & form A-V shunt (can arrest & partially regress =)
--> If progresses; capillary proliferation

NEW VESSELS SUCK
- Exudates
- hemorrhage
- SECONDARY DETACHMENT OF RETINA!! =(
HYPERTENSIVE RETINOPATHY

- FEATURES
FINDINGS RELATE TO SEVERITY OF HTN

1. Arteriolar narrowing
2. Flame shape hemorrhages (n. fiber layer)
3. Exudates (macular star)
4. Cotton wool spots (superficial retina)
5. Microaneurysms

6. A/V nicking = sclerosis in venous walls
7. Arterial sheathing: abnormal retinal arterioles = parallel white lines
- Copper wiring --> wilver wiring
INHERITIED RETINAL DEGENERATIONS

*also BL*

- RETINITIS PIGMENTOSA
Auto recessive

mech:
ATROPHY of pigmented epithelium in Posterior eye
- migration of pigment along attneuated blood vessels
= bone corpuscular pattern

*First = night-blindness (rods affected in post eye first)
- central vision aff'd 1st
- late: only stumpy cones left in fovea
MACULAR DEGENERATION

SENILE TYPE
- why?
- features
MOSTLY IN ELDERLY & BILATERAL
- peripheral retina is spared!
- CENTRAL VISION LOST

mech:
- Functional failure of pigmented epithelium
**accumulates all this crap bc cellular digestion is impaired**
--> extrusion of drusen & linear deposits on BRUCH'S membrane
--> becomes hydrophobic
- plastisizers deposit here in lipid deposits of b's membrane
RETINAL DETACHMENT

- where?
- results
- reversible or irreversalbe?
WEAKT POINT: Attch of retina to choroid
- pigment epithelium on choroid
- 2 different fetal layers smashed together
- fluid separates the layers

RESULTS:
- outer retina (rods & cones) get fragmented
- eaten by pigment-laden macros
- diffuse edema of inner layers of retina

**changes are reversible if retina is restored WITHIN A FEW DAYS**
CAUSES OF RETINAL DETACHMENT

1. RHEGMATOGENOUS

2. EXUDATIVE

3. TRACTION
1. RHEGMATOGENOUS:
hold/rupture/rent + vitreous traction
- predispose: myopia, cataract sx, trauma
- low protein content = subretinal fluid (vitreous)

2. Exudative:
- leaked fluid from blood vessels
- Assc: uveitis, choroidal neoplasm, retinoblastoma
- high protein content of reitnal fluid (like plasma)

3. Traction: diabetic retinopathy
- fibrovascular proliferation w/in vitreous chamber
- also ROP, toxoplasma, post-thrombotic glaucoma,
MALINGANT MELANOMA OF THE EYE

- mech
- FEATURES
- SITE OF METASTASIS
RARE; but still most common 1' intra-ocular tumor

MOST COME FROM CHOROID
- post supratemporal quadrant
--> retinal detachment
= PAINLESS PROGRESSIVE UL LOSS OF VISION

also:
- massive necrosis - spont. endophthalmitis
- vitreous hemorrhage
- 2' glaucoma



UNIQUE from other melanomas: DOES NOT HAVE ACCESS TO LYMPAHTICS UNTIL EXTRA-OCULAR EXTN HAS OCCURED
--> LIVER = 1' SITE for hematogenous metastases


**GLASS EYE & HUGE LIVER**
RETINOBLASTOMA

- FEATRUES
- GENETICS
- ^ RISK
EMBRYONIC NEURONAL CELL tumor
- babies < 2yo (usu w/in 3 mo)
- usually UL // BL = inherited

FEATURES:
- leukocoria: white pupil
- NO red reflex or Cat's eye refelx
- Poor vision
- sPONTANEOUS HYPHEMA (RED, PAINFUL EYE)
- 2' Glaucoma

INHERITED = 7%
chrom 13q14
- mtt of Rb tumor suppressor gene

RISK OF
- other tumors
- osteogenic sarcoma
- ewing sarcoma
NEURONAL REGENERATION & DEGENERATION/DEATH
REGENERATION:
- Mature neurons do NOT replicate (G0)
- Need to stay in neural network
- NO neuronal regeneration (not really); only some functional rehab possible

DEGENERATION/DEATH
- Majority = apoptosis
- atrophy: deeply eosinophiliic
- Neuronophagia: neutros & macros eat dead neuron
- Chromatolysis = injury; central clearing & cytoplasmic swelling
- Wallerian Degen: loss of distal, amputated axon = fragmented myelin & dead soma
BLOOD BRAIN BARRIER

- MCCs of damaged BBB
1. Endothelial cells of capillaries
= MAIN BARRIER; tight junctions

2. Astrocytes: remove crap and induce formation of tight junctions
- attached to capillaries

3. Basement membrane

4. pericytes: macrophage origin

1. disruption of existing BBB
- trauma or toxicity
2. Neovascularization
- new vessels lack tight junctions
- tumors, abscess, hematoma
CSF FORMATION & DRAINAGE/FLOW


**saliva has amylase; CSF does NOT**
1. Choroid plexus (ependymal cells) make it in lateral ventricles
2. IV foramina of Monro
3. Thrid vENTRICLE
4. cerebral aqueduct of Sylvius
5. EXITS:
- 2 Lateral Luschka foramina
- 1 midline Magendie
6. Sub arachnoid space
7. Arachnoid granulations
8. Blood vessels?
CSF LEAKAGE

- HOW DO YOU KNOW IT'S CSF?
1. LOW PROTEIN (<1%)

2. Electrophoresis for transferrin
- csf = 2 isoforms
- plasma = only 1

3. NO amylase (saliva)
HYDROCEPHALUS

- COMMUNICATING TYPES

**Hydrocephalus = expansion of spaces containing CSF (ventricles or SAS**
- NOT in the parenchyma
1. Obstructive communicating hydrocephalus
- obstructed arachnoid granulations & SAS
ex// meningitis, SAH

2. Nonobstructive hydrocephalus
- Hypersecretion of CSF
- RARE CAUSE = Choroid plexus papilloma
- NOT on exams

3. Ex vacuo / Compensatory
- atrophy of CNS
- Alzheimer's / neurodegen diseases or periventricular infarcts

4. Normal pressure (normotensive)
- Increased ventricular size w/o increased intraventricular pressure OR atrophy
- DIG (dementia, incontinence, gait problems)
HYDROCEPHALUS

- NONCOMMUNICATING TYPES
Obstructive noncommunicating
- obstructed ventricular outflow
- Monro, Luschka, magendie, or sylvian aqueduct blocked

ex// brain tumors, abscesses, encephalitis, ventriculitis
CEREBRAL EDEMA


- why?
- what gets hurt?
CNS is deficient in lymphatics

- Excess fluid in the PARENCHYMA

1st hit = astrocyte --> downstream swelling
--> 2nd = neurons (brian anoxia)
- later = other cells

3 types: cytotoxic = intracellular; vasogenic & interstitial = extracellular
CEREBRAL EDEMA

- TYPES & DISTRIBUTION
1. CYTOTOXIC edema: intracellular
- cytoplasm has > osmotic P than ECS
- GRAY MATTER
(more cells here)
- hypoglycemia/hypoxia/toxin disrupts ATP production; NA/K ATPase nonfunctional

2. VASOGENIC edema:
- WHITE MATTER
(fewer capillaries to push out water)
- BBB is damaged / neovasc / ^ ICP

3. Intersitital edema
- PERIVENTRICULAR WHITE MATTER
- assc'd w/ ventricular enlargement (hydrocephalus)
- ^ IV pressure pushes fluid into brian tissue
INTRACRANIAL PRESSURE

- normal?
- increased ICP = results?
- assc with edema
NORMAL: 90-180 mmH2O - lying on side
- Increased = > 250

ICP caused by increased volume or solid
--> Systemic HTN

Mech of Systemic HTN:
1. ICP
2. Vascular compression
3. Decreased CBF
4. Cerebral ischemia
5. 2' HTN

**Brain edema can cause increased ICP --> edema --> ^ ICP
(VICIOUS CYCLE!!)
BRAIN HERNIATIONS

- cause
- types & clinical issues
Caused by increased pressure in one compartment pushing on adjoining compartment

types:
- sub-falcine: leg weakness/sensory loss
- trans-tentorial: CN 3 palsy, visual problems, ipsilateral hemiparesis, coma (RAS aff'd)
- Tonsillar: cardiac & resp centers depressed
BRAIN HERNIATIONS

- SUB-FALCINE
- TONSILLAR
1. SUB-FALCINE (under the falx cerebri - top of corpus callosum?)

- pushes cingulate gyrus beneath the falx
- Compressed ACAs --> Leg weakness/sensory loss

2. TONSILLAR:
- Pressure in posterior fossa
- Tonsils of cerebellum pushed through foramen magnum
- Cardiac & respiratory centers of b.s. depressed
--> DIE
BRAIN HERNIATIONS

- TRANS-TENTORIAL
Hippocampal/uncal
- Supra-tentorial pressure pushces uncal gyrus (temporal lobe) b/w tentorium & midbrain INTO posterior fossa

1. Compress CN 3 --> ipsi dilation & ocular movements

2. Compress PCAs = ischemia of visual areas of occipital cortex

3. Compressed contralat Peduncle
--> hemiparesis (ipsilateral to side of herniation)

4. Downward herniation of midbrain
--> Duret's hemorrhage
- impaired RAS
- lethargy -- > coma --> die
PATHOLOGY OF EXTERNAL EAR

- OTITIS EXTERNA
(org, complications?)
MCC = PSEUDOMONAS AERUGINOSA

- most cases = mild inflamm

complications:
1. malignant otitis externa (invasion)
2. Mastoiditis (osteomyelitis of the skull)
3. venous sinus thrombosis
4. meningitis / death
PATHOLOGY OF MIDDLE EAR

**middle ear connected to mastoid cavities & auditor tube **

- OTITIS MEDIA
- middle ear effusion mech
Type depends on infectious agent & changes in epitheliu & stuff

- can travel up from nasopharynx
- usually permeates through mastoid antrum into mastoid cells

acute: viral or bacterial or noninfectious obstruction
- viral can be nonsuppurative

**obstruction of the Eu-tube = MIDDLE EAR EFFUSION
- air can't enter = negative pressure
- Transudation of plasma & bleeding into middle ear
ACUTE VS CHRONIC SEROUS OTITIS MEDIA

- changes seen
- causes
- cholesterol granuloma
Same causes --> obstruction of Eu-tube
- flying or deep sea diving
NO PUS
- inflamm w/o bacterial invasion of middle ear


Acute type = VERY COMMON --> UL conductive hearing loss
- more often in kids

Chronis: inadequate ABX tx
- CA of nasopharynx can cause this
- UL effusion of ADULT ear
- Changes: Mucosal lining becomes secretory ( ^ sticky fluids)
- metaplasia of goblet cells
- can form cholesterol granuloma (cholesterol exudate stimulates foreign body rxn)
--> if big enough, can destroy tissue
--> Granulation tissue becomes fibrotis
--> COMPLETE obliteration of middle ear & mastoid
ACUTE VS CHRONIC SUPPURATIVE OTITIS MEDIA
+ PUS
- Same organisms: Strep pneumo & H. influenzae

ACUTE:
- sometimes can't cx bug
- eardrum can rupture & relieve pressure
- usually self-limiting
- invades through Eu-tube usually

CHRONIC: neglected or recurrent infxn
- inflamed mucosa / destruction of periosteum over ossicles
- PERMANENT perf of tympanic membrane or destroyed ossicles
- insidious, persistnent
**Painless otorrhea & hearing loss
- polyps can be seen (granulation tissue)
ACUTE MASTOIDITIS
infection of mastoid bone
- frequent before abx invented
- complication of acute OM

mastoid air cells fill w/ pus
--> thin osseous intercellular walls destroyed

--> can extend to brain / sinus thrombosis / cerebellar abscess / meninges
CHOLESTEATOMA

- NOT the same as cholesterol granuloma
- dangers
- what is it?
Expanding benign mass --> Pressure damage
- epithelial inclusion cyst
(mass of keratin from squamous epithelium of external ear canal --> middle ear via perf'd eardrum)
- post- acute/chronic OM
- can also be congenital

* can become infected & resistant to abx
- keratin shields it

DANGERS --> erosion of bone
- can destroy auditory ossicles, cn 7 , Labyrinth ( vestibular fxn)
OTOSCLEROSIS

- what?
- clinical
- who?
Ankylosis = Fusion of ossicle joints --> conductive hearing loss

- bONE DEPOSITION in annulus (around stapes footplate)

Auto dominant defect
- MCC conductive hearing loss in young-mid aged FEMALES
MENIERE'S DISEASE

- clinical
- pathology
= who?
TRIAD: TV'S
1. Tinnitus
2. Vertigo
3. Sensorineural hearing loss

pathology: Hydropic distention of endolymphatic system of cochlea

40s-50s; usually UL
- recovers bw attacks
- later permanent

tx: DECREASE FLUIDS
- low salt & diuretic

**pic: HUGE voluem of fluid in choclear duct
- vestibular membrane bulges into vestibular cavity & may perforate
LABYRINTHINE TOXICITY

- which agents?
- results?
DRUG-INDUCED damage of inner ear

Ototoxic SEs:
- Aminoglcyoside abx ****** (gentamicin)
- Diruetics
- antimalarials (quinine?)
- Nitrogen mustard
- salicylates
**esp labyrinth of embryo

*irrev damage 2 vestibular & cochlear sensory cells
VIRAL LABYRINTHITIS


- who?
-agents
PRENATAL INFXNS by cmv & rubella

- MUMPS = MCC of deafness among POST-NATAL infxn

= UL rapid hearing loss
ACOUSTIC TRAUMA

0 what's injured first?
NOISE-INDUCED hearing loss
- first world problem / occupational

earliest damage = external hair cells of organ of corti
--> deformation / swell/disintegrate of hair cells

progressive injury --> supporty cells
TUMORS OF INNER EAR

- results?
- MC
usually benign but LOCALLY destructive

- damage hearing, balance, & cn7

MC = Schwannoma, meningioma, & neurofibroma
(similar 2 cholestoma of middle ear)
benign epithelial tumors
1. Seborrheic Keratosis
- MC human neoplasm
- stuck on dark papules on head/neck/trunk

2. Acanthosis Nigricans
- big velvety plaques in FOLDs of axilla & neck
- 50% underlying malignancy

3. Epithelial cyst
- Epidermal inclusion cyst
- MC cutaneous cyst
EPIDERMAL TUMORS
1. Actinic keratosis:
- like a SK but more yucky looking

2. Squamous cell carcinoma
- Headh/neck
- keratin pearl
- 2nd MC skin CA
- capable of metastasis

3. Basal cell carcinoma
- pearly raised, flesh colored papules
- MC CA in man; MC malignant skin CA
- very rarely metastasize
TUMORS OF THE DERMIS
1. BENIGN fibrous histiocytoma
(dermatofibroma)
- dimple sign
- fibrohistiocytic cells entrap preexisting collagen bundles

2. XANTHOMAS:
- Foam cells; hyperlipidemia
- any EXTENSOR surface & around eye
DERMAL VASCULAR TUMORS
1. Angiomas
- capillary: don't tx
- cavernous: liver, big vessels
- benign; doesn't metastasize

2. KAPOSI SARCOMA - HHV8
- classic (european): old mediterranean men
- african (endemic): younger males
- AIDS (epidemic): homosexuals
- Immunosuppresion
INFLAMM DERMATOSES

- acute vs chronic
ACUTE
1. Urticaria / hives
- NOT real inflamm; just allergic reaction?

CHRONIC:
1. Psoriasis: silvery plaques
- neutrophils in stratum corneum
- parakeratosis

2. Lichen Planus:
- Pruritic
- oral & genital involvement
- sawtoothing of rete ridges
- band of lymphocytes in upper dermis
BLISTERING / BULLOUS DISEASES
1. Pemphigus vulgaris
- flaccid bullae: face/scalp / chest, ORAL MUCOSA
- SUPRABASAL acantholysis
- Desmoglein 3 (cadherin)

2. Bullous Pemphigoid
- TENSE blisters w/ red base
- SUBepidermal blister
- lots eosinophils
- lower extremities
- BPAG1/2 adhesion proteins = antigens
DISORDERS OF EPIDERMAL APPENDAGES

- clinical
- histo
ACNE VULGARIS

CLINICAL:
- Adolescent Males
- on their FACE
- Comedones: black/white heads
(hair follicle is plugged with keratin
- Red papules, pustules, nodules, cysts
- SCARS occasionally

HISTO:
1. Comedone
- dilated follicular infundibulum
- keratin plug (open or closed)
2. Follicular pustule with or w/o rupture
3. INFLAMM RESPONSE
4. Cyst & sinus tract formation
5. DERMAL scarring

tx: high dose vit A
(accutane - cystic acne)
INFECTION & INFESTATION OF SKIN
1. Verruca vulgaris (warts
- HPV 1, 2, 3, 4
- MC in kids (hands, fingers, face)
- Koilocytes (halo around nuclei)
- NOT a neoplasm

2. Molluscum Contagiosum
- kids: face/limb/trunk
- adults: STD - genitals
- NOT a wart
- POXVIRUS
- epithelial cells have eosinophilic cytoplasmic inclusion bodies

3. IMPETIGO
- honey crusted lesions
- kids: MOIST FOLDS
- gram + cocci (staph / strep)
- superficial bacterial infxn
SEBORRHEIC KERATOSIS

- who/what/where?
- histo?
- prev
Mid-age/older Adults
- head/neck/trunk
- fleshy or dark papules
(look stuck on like enrique iglesias' mole)
- smooth to warty; 1mm - several cm

HISTO: BENIGN
- Acanthosis (squamoid & basaloid proliferation)
- Hyperkeratosis
- Papillomatosis
- Basal layer hyperpigmentation
- HORN PSEUDOCYSTS: islands of keratin
- infiltrating lymphs in Dermis & Epidermis

MC human neoplasm (benign)
- Can be sign of Leser-Trelat (Adenocarcinoma of GI tract)
acanthosis


vs.

hyperkeratosis

(layers of skin: basale, spinosum, licidum, granulosum, corneum)
diffuse epidermal hyperplasia
- thick stratum spinosum

SEEN IN:
- Sk
- Acanthosis nigricans?
- lichen planus

Hyperkeratosis: thickening of stratum corneum - keratinized layer
ACANTHOSIS NIGRICANS

- who/what/where
- histo
- associated with?
Blacks & Hispanics
(all races & ages affected tho)

Big velvety pigmented plaques
- in FOLDS of axilla & neck
- mucosal lesions too

HISTO:
- Hyperkeratosis
- Basal layer Hyperpigmentation
- thinned epidermis
- Papillomatosis
- Mild perivasc inflamm

ASSC'D with:
- Underlying malignancy (50%)
- obesity
- etc.
**prolonged growth factor simulation of keratinocytes & dermal fibroblasts
EPITHELIAL CYST
Epidermal inclusion cyst
- epidermis gets trapped
- keratin accumulates
--> rupture causes foreign body giant cell rxn & scarring

Solitary or multiple
- face / neck / torsa
- MC cutaneous cyst sent to path lab

HISTO:
- LINING = strat squamous
- Variably thick granular lyare
- loose, laminated keratin
ACTINIC KERATOSIS

**like a worse SK??**
- feels rough
Epidermal tumor
- Sun damaged skin

Small, red, keratotic (raised) lesion
- white/yellow brown scales
- astymptomatic or itchy/tender

HISTO:
- hyperkeratosis
(intermittent parakeratotic nuclei)
*** Keratinocyte ATYPIA along basal layer
- NO invasion (budding of basal layer cells)
- Perivascul inflamm
- SOLAR ELASTOSIS
(Dermal elastic tissue is blue, fragmented, hypertrophied 2' sum damage)

**AKs are squamous cell carcinoma - in stu
--> 20% develop into invasive SCCa in 10 yrs
**similar to cervical CA (grading system)
SQUAMOUS CELL CARCINOMA
ELDERLY - Head/neck
- FAST GROWTH
- Overlying scale/crust
(frequently exudative)
- Fleshy/red nodule

HISTO:
- Keratin pearls
- Atypical epithelial cells invading the dermis

**2nd MC skin CA
- MCC is UV radiation
**CAPABLE OF METASTASIS
SQUAMOUS CELL CA RISK FACTORS
1. UV LIGHT
2. HPV
3. X RAYS
3. PUVA TX
BASAL CELL CARCINOMA
Fleshy, Pearly raised papules/nodules
- sun exposed site
- indurated; can bleed/ulcerate
(rodent ulcer)
*can be pigmented*

HISTO:
- Invasive nest/cords of basophilic cells ~ basal cells
(islands of basal cells)
- Nuclear palisading at edges of nests
- Peri-tumoral mucin production

**MC CA in man
**MC malignant skin CA
- VERY RARELY METASTASIZE =)
- cause local destruction mostly
RISK FACTORS OF BCC
SIMILAR TO SCC

1. UV light
2. Irradiation
3. Arsenic
4. Coal-tar derivatives
5. Immunosupression**
--> these people are MORE LIKELY TO HAVE SCC!!!
BENIGN FIBROUS HISTIOCYTOMA

(not a big deal)
Young, middle aged adults
- Papule/nodule
- Red/hyperpigmented
- Dimple sign (dimples when you push on it
- Can regress spontaneously

HISTO:
- Confined to dermis
- symmetric
- NOT encapsulated (but well demarcated)
- FIBROHISTIOCYTIC cells entrap pre-existingcollagen bundles
(looks like fried eggs)
- fascicles in storiform pattern ?

**unknown pathogenesis
- don't mistake this hyperpigmented tumor w/ melanocyte
XANTHOMAS
HYPERLIPIDEMIA
- yellow plaques made up of foam cells
- arranged interstitially bw collagen bundles
- few or no WBCs

EXTENSOR SURFACES & Eyelids

(eruptive type is on butt)
ANGIOMA

- CAPILLARY VS CAVERNOUS
Capillary: juvenile or strawberry hemangioma
- small vessels filled w/ RBCs
- DON'T TREAT (usually regress by 6 yo)
- HEAD & NECK


Cavernous hemangioma of liver
- larger, dilated vessels filled with RBCs

HISTO:
BENIGN PROLIFERATION of blood vessels
(does NOT metastasize)
KAPOSI SARCOMA

- classic vs african vs AIDS
- histo
- agent?
HHV 8

HISTO:
- Spindle cell infiltration
- Irregular, angled blood vessels with slit spaces containing RBCs
- 3 stages: patch/plaque/nodular

Classic = European
- > 50yo men, ashkenazic jews, mediterranean;
- lower ext

African: younger men

AIDS: homosexuals
- UPPER half of body
- small pink / purple lesions -> disseminated

Immunosuppresed (organ transplants)
URTICARIA
HIVES
- Transient ruptures
- PALPABLE red papules or wheals

*wax & wane w/o clinical residuum

- acute or chronic

histo:
edema w/ dilated lymphatics
(Not rEAL inflamm; just allergic rxn)
PSORIASIS

**HLA-B27: psoriasis & spondylitis
**parakeratosis: dying keratinocytes in s. corneum retain nuclei
CHRONIC INFLAMM DERMATOSIS

- Sharply circumscribed plaques
- SILVERY SCALES
- Scalp / Groin / Extensors / Nails

GENETIC:
- inherited (HLA-B13, HLA - BW17)
- 1% of population
- chronic; relapsing course
**increased epidermal turnover rate = acanthosis?

HISTO:
- Parakeratosis & hyperkeratosis
- Uniform elongation of rete ridges
- Dermal edema (dilated caps)
- Neutrophils in stratum corneum (Munro's microabscesses)**
LICHEN PLANUS
SUPER ITCHY
- pruritic
- violaceous polygonal papules
- oral & genital involvement common

HISTO:
- Band of lymphs in upper dermis (along rete ridges)
- Sawtoothing of rete
- Acanthosis
- Hypergranulosis
- Basal cell vacuolization (knock out cells)

**inflamm disorder of uncertain cause**

Lichenoid = band of lymphs in superficial dermis
PEMPHIGUS VULGARIS
FLACCID Bullae
- face/scalp/chest
- oral mucosa = 100%
- OLDER pts

hISTO:
- SUPRABASAL acantholysis
- hair follicles involved
- Chicken wire pattern (immunofluorescence of IgG & desmoglein 3 = cadherin)
- desmosomal cadherin is [ ]d in lower epidermis
BULLOUS PEMPHIGOID
ELDERLY pts
- Tense blisters w/ red bases
- intact blisters
- EXTREMITIES
- Mucosal surfaces SOMETIMES involved

HISTO:
- Subepidermal blister
- TONS of eosinophils
- NO necrosis of underlying skin
- Dense inflamm infiltration in papillary dermis

IgG & C3 at dermal-epidermal JCT
- intracellular/transmembrane Ags = BPAG1/2
- adhesion proteins
warts
verruca vulgaris

- papillomatosis
(and focal parakeratosis)
- digitated epidermal hyperplasia
- KOILOCYTOSIS
- hyperganulosis

NOT A NEOPLASM

HPV 1 2 3 4
molluscum contagiosum
dome-shaped papules
- umbilicated w/ a central pore

*self limited & resolve in 6-9 mon

POXVIRUS

kids: face/limb/trunk
adult: sexual transmission
IMPETIGO
HONEY CRUSTED LESIONS
- Bullae in bullous impetigo

MOIST FOLDS
- paranasal axilla, groin

histo:
- subcorneal pustule filled w/ neutrophils
- gram+ cocci found in pustule

STAPH OR STREP
WHERE IS MELANIN NORMALLY PRESENT??
Skin
Mucous membranes (basal layers)
Eye (retina, choroid, iris)

Brain: substantia nigra
Meninges

**melanin tumors of the skin are usually benign = nevi
**pigmented tumors can LOSE their melanin (amelanotic)

**MELANOCYTE = NEURAL CREST CELL**
HOW DO YOU MAKE MELANIN
(GENERAL)


albino vs. vitiligo
Tyrosine --> Tyrosinase --> dopa

dopa --> --> --> melanin

ALBINOS: lack tyrosinase
- increased risk of skin damage

VITILIGO: poss AI?
- skin DEpigmentation
define
- melanophores
- nevus
MELANOPHORE: PHAGOCYTIC CELL with melanin

nevus = mole/skin blemish
macule vs papule vs nodule
MACULE: FLAT
- less than 5 mm?

PAPULE:
- Elevated
< 1 cm

NODULE:
Larger; may be pedunculated
BENIGN MELANOCYTIC LESIONS

- non-neoplastic
- neoplastic
NON-NEOPLASTIC:
1. Freckle / Ephilid: sun deepens pigmentation
- basal cell layer hyperpigmented
- no acanthosis
2. Lentigo: adults (sun spots)
- does NOT deepen w/ sun exposure
- hyperpigmented basal layer + acanthosis

NEOPLASTIC:
NEVUS: benign melanocyte rests
(no dendritic processes)
a.) Junctional: macule @ derm/epiderm jct (basal layer)
b.) Intradermal: Papule/nodule
- within the dermis
c.) Compound: macule/papule
- feature of both jctal & intradermal
DEFINE:

- SPITZ NEVUS
- CONGENITAL NEVUS
- DYSPLASTIC
1. spitz nevus: Spindle & Epithelioid Nevus
- Benign mole
- Childhood/ adolescence
- Mimicks melanoma (FALSE ALARM!)

2. congenital nevus:
- frequently large (giant hairy nevus)
- CAN develop into melanoma

3. dysplastic nevus (clark's):
- may be PRECURSOR to melanoma
PREMALIGNANT MELNOCYTIC LESIONS

- dysplastic nevus syndrome
Too many melanocytes @ epiderm/derm jct
--> INFLAMM rxn

AFFECTS COVERED PORTION OF THE BODY
(unlike BCC & SCC & melanoma)
- back is usually involved
- family specific sites
- small dark macules noticed around 6yo
new ones can develop throughout adulthood

gross: macules can be > 5 mm w/ irregular outlines

micro:
- melanocytic pleomorphism
- hyperchromatism (dysplasia)
- underlying lymph inflamm & fibroplasia
MALIGNANT MELANOCYTIC LESIONS

- MELANOMA
(Location, s/s, growth phases)

**normal # of nevi = 20 / body
Location:
- sun exposed regions
- can also occur in deep soft tissues & retina

Mole w/ irreg borders; discoloration
(A, B, C, D)
- RECENT changes

Growth phases:
1. Radial: usually first; lateral spread
- exception = nodular melanoma
2. Vertical: invasion
RISK FACTORS OF MELANOMA

(WASP = White, affluent, sun sensitive and have Precursor moles)
MOST RISK:
- White skin
- Red hair
- Blue/grey eyes
- Nontanners (burn in sun)
- Childhood sunborn
- POSITIVE family hx

least risk = opposite things
FOUR TYPES OF MELANOMA
1. Lentigo malligna: Melanoma in-situ
- Superficial radial spread for a long time
- get big (> 6cm)
- INK STAIN
- GOOD PROG

2. Superficial Spreading melanoma
- Confluent atypical cell nests @ jct
- Major radial growth before & during vertical phase
- Get big ( <3cm) but not as big as lentigo maligna)

3. Nodular Melanoma: exception
- INVASIVE tumor
- very little radial growth
- poor prog

4. Acral Lentiginous:
- RARE
- Volar feet (92%) & hands, nails; mucosal
- Melanocyte BEGINS deep in the tissues
POSSIBLE PRECURSORS OF MELANOMA
20% OF CAUSES:
- Dysplastic nevus
- congenital nevus
- xeroderma pigmentosum (DNA repair fail - stay outta the sun!)
- Any nevus w/ junctional activity (^ risk)
MICROSCOPIC FEATURES OF MELANOMA
S100 protein
HMB-45 Ab

"great imitator"
- Atypical large cells
- many with nuceloli
PROGNOSIS
of melanoma
- different types of grading?
1. Clark's levels:
- vertical phase: depth of invasion

2. Breslow's Depths:
- invasion depth measured from granular layer
a.) < 1.0 mm = 80-95% 5 yr survival
b.) >1.0 mm = <50% survival
SUMMARY OF PROGNOSITC INDICATORS IN MELANOMA

WORST PROGNOSIS??
WORST PROG:
types: Nodular and Acro/lentiginous

1. Level: Clark's 4, 5
2. Depth: > 1.0 mm
3. Large size
4. High rate of mitoses
5. MALE GENDER
6. RARE LYMPHS (host response)
7. Stage: already metastatic
8. Surface: ulcerated


**best prognosis = lentigo maligna & opposites of above

**superficial spreading melanoma = int. prognosis
CLARK'S LEVELS OF MELANOMA GRADING

which leve is at epidermis / papillary dermi / reticular dermis/ sc fat
1. In situ: no vertical growth
- 100% cure if excised

2. Invasion into papillary dermis
- good prognosis

3. INVASIVE: breaking point
- fills papillary tumor
- forms a line @ beginning of reticular dermis
- thick 3's & thin 3s
- correlate w/ breslow's tumor depth

4. Invasive tumor in reticular dermis
- lesion depth > 0.75 mm

5. Invsaive tumor in SC tissue
- less than 10% 5 yr survival
Dermatitis herpetiformis:


STOP EATING _____???
Pt's with CELIAC DISEASE: gluten sensitive enteropathy

IgA Abs Form
--> ICs deposit in derm/epiderm JCTs
- IC initiate C' --> neutrophils come
--> toxic granulation (more neutros come)

**Vesicles form when basal layer is disrupted
--> rupture; encrust; scar
LOCATION:
Extensor surfaces of arms/legs
& BOOTY
Erythema Multiforme


**severe variant = toxic epidermal necrolysis
- worst variant = SJS (Mucosal surfaces)
HYPERSENSITIVITY skin rxn
- Drugs: sulfa
- Infxns: HSV
- malignancies; autoimmune

ONSET: teens - 20s

CLINICAL: Target lesions
- Pale red lesions w/ red border
- Center is very red
--> can progress to vesicle formation (which can coalesce)

MECHANISM:
- CD8+ cells at epiderm/derm JCT kill basal cells
--> acantholysis
- TONS of eosinophils
Dermatitis herpetiformis:


STOP EATING _____???
Pt's with CELIAC DISEASE: gluten sensitive enteropathy

IgA Abs Form
--> ICs deposit in derm/epiderm JCTs
- IC initiate C' --> neutrophils come
--> toxic granulation (more neutros come)

**Vesicles form when basal layer is disrupted
--> rupture; encrust; scar
LOCATION:
Extensor surfaces of arms/legs
& BOOTY
Erythema Multiforme


**severe variant = toxic epidermal necrolysis
- worst variant = SJS (Mucosal surfaces)
HYPERSENSITIVITY skin rxn
- Drugs: sulfa
- Infxns: HSV
- malignancies; autoimmune

ONSET: teens - 20s

CLINICAL: Target lesions
- Pale red lesions w/ red border
- Center is very red
--> can progress to vesicle formation (which can coalesce)

MECHANISM:
- CD8+ cells at epiderm/derm JCT kill basal cells
--> acantholysis
- TONS of eosinophils
BRONCHOGENIC LUNG CARCINOMA

- INCIDENCE
- AGE
- SEX
MCC CANCER DEATHS IN USA
- 35%: males; MC CA = prostate
- 20%: females; MC CA = BREAST

Peak incidence in early 60s

MALES: Squamous & small cell types

Nearly equal in adenocarcinoma


Previous M:F = 9;1
- NOW = 3:2
- increased incidence in females due to increased smoking
TOBACCO SMOKING & LUNG CA
MOST CLOSELY linked agent w/ bronchogenic carcinomas
- incidence is directly proportional
- Risk is proportional to amt smoked
- After cessation, risk decreases (baseline in 10 years)
- Second hand smoke & CA risk

CLINICAL:
- Metaplasia & dysplasia of bronchial epithelium

1.) Initiators: Polycyclic aromatic hydrocarbons
- cause DNA damage

2.) Promoters (phenol derivs)
- support tumor growth until they're self-sustainable

**humans are particularly sensitive to tobacco smoke**
OCCUPATIONAL/ENVIONRMENTAL EXPOSURES & LUNG CA

- radioactive
- metals
- asbestos
These risk factors are synergistic with SMOKING

RADIOACTIVE
4x ^ in uranium
Radon gas

ASBESTOS
^ 5X
^90X if also smoking
10-30 yr latent period
- mesothelioma

METALS: BANIC
- Beryllium, arsenic, nickel, iron, chromate

**AIR POLLUTION is NOT a risk factor on its own.
LOCATION OF LUNG TUMORS

- central / periph / diffuse
central: 75% of lung carcinomas
- SCC
- Small cell anaplastic
**can obscure tumor on CXR; but easy to access via bronchoscopy**

PERIPH:
- AdenoCA & large cell undifferentiated

DIFFUSE/MULTIFOCAL
- bronchioalveolar CA
SYMPTOMS OF LUNG CA
nonspecific

1.) Cough - bronchial irritation
2.) Hemoptysis (erosion/cavitation)
3.) Dyspnea
4.) Chest pain
5.) Weight loss

^ mucous production or ^ inflamm

*most are found incidentally on routine CXR

SECONDARY TO BRONCHIAL OBSTRUCTION
1. Emphysema (partial obstruction - ball valve)
2. Atelectasis (complete obstruction
3. Distal infxns (retains secretions)
- pneumonia: MCC death in lung CA
- abscess


SECONDARY TO DIRECT INVASION
1. malignant pleural effusion
2. SVC syndrome
- puffy upper arms & head
3. Pancoast tumor**
- brachial n. damage (atrophy of hand mm)
- horner's syn: ipsilat
4.) Recurrent laryngeal involvement
- hoarseness
PARANEOPLASTIC SYNDROMES

- ENDOCRINE
- NEUROMUSCULAR
- PULMONARY HYPERTROPHIC OSTEOARTHROPATHY
1.) ENDOCRINE
Small cell - ACTH, ADH
SCC - Parathormone
Carcinoid - 5-OH tyrptamine

Neuromuscular - usu w/ Small cell
- LES
- periph neuropathy, myopathy, leukoencephalopathy, cerebellar degen

PULMONARY HYPERTROPHIC OSTEOARTROPATHY
- clubbed nails
- dermatomyositis & polymyositis
- Migratory thrombophlebitis
(hypercoagulable state)
LOBAR PNEUMONIA

- presentation
- recovery
- classic organisms: S. pneumo & Klebsiella
Fills up alveoli and makes whole LOBE look SOLID
- fast spread
- exudative response

1.) Water or edema:
- fills alveoli w/ fluid
- few cells

2.) Red hepatization:
- Major capillary congestion
- Filled w/ RBCs & NEUTROs
- sheets of intra-alv neutros

3.) Grey heptization
- fibrin & macros

RECOVERY:
- minimal damage to alveoli
- return to normal fxn
- fibrin can organize into SCAR

Klebsiella is WORSE
- more damage, necrosis, scars
BRONCHOPNEUMONIA

- pattern
- population

**MORE COMMON THAN LOBAR PNEUMONIA**
LACKS WIDESPREAD SHEETS OF ALVEOLAR INFLAMM

DIFFUSE irregular foci inflamm
- centered around bronchioles/resp bronchioles
(bronchiolitis)

XRAY: multiple peri-bronchial foci of consolidation

WORSE THAN LOBAR
- more damage, necrosis, & scarring
- most assc'd with other types of bacterial infxns
- seen in terminally ill pts
(dependent/posterior lung fields)
SETTINGS OF PNEUMONIA

- Community acquired (typical vs atypical) vs nosocomial vs aspiration
CA:
non-hospitalized pts
immunocompetent
- Typical: bugs that cause normal presentation
- Atypical = walking pneumonia
(Mycoplasma, chlamydia, legionella)

NOSOCOMIAL
- acquired from health care facility
- decreased immunity
- scarier bugs


ASPIRATION
- people who aspirate
- usualy hospital, nursing home, etc.
- can be a multi-bug infxn due to gastric aspiration