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111 Cards in this Set
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- 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 |
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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 |
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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 |
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RISK FACTORS OF BCC
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SIMILAR TO SCC
1. UV light 2. Irradiation 3. Arsenic 4. Coal-tar derivatives 5. Immunosupression** --> these people are MORE LIKELY TO HAVE SCC!!! |
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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 |
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XANTHOMAS
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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) |
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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) |
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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) |
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URTICARIA
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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) |
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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)** |
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LICHEN PLANUS
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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 |
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PEMPHIGUS VULGARIS
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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 |
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BULLOUS PEMPHIGOID
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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 |
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warts
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verruca vulgaris
- papillomatosis (and focal parakeratosis) - digitated epidermal hyperplasia - KOILOCYTOSIS - hyperganulosis NOT A NEOPLASM HPV 1 2 3 4 |
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molluscum contagiosum
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dome-shaped papules
- umbilicated w/ a central pore *self limited & resolve in 6-9 mon POXVIRUS kids: face/limb/trunk adult: sexual transmission |
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IMPETIGO
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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 |
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WHERE IS MELANIN NORMALLY PRESENT??
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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** |
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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 |
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define
- melanophores - nevus |
MELANOPHORE: PHAGOCYTIC CELL with melanin
nevus = mole/skin blemish |
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macule vs papule vs nodule
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MACULE: FLAT
- less than 5 mm? PAPULE: - Elevated < 1 cm NODULE: Larger; may be pedunculated |
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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 |
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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 |
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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 |
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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 |
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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 |
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FOUR TYPES OF MELANOMA
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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 |
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POSSIBLE PRECURSORS OF MELANOMA
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20% OF CAUSES:
- Dysplastic nevus - congenital nevus - xeroderma pigmentosum (DNA repair fail - stay outta the sun!) - Any nevus w/ junctional activity (^ risk) |
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MICROSCOPIC FEATURES OF MELANOMA
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S100 protein
HMB-45 Ab "great imitator" - Atypical large cells - many with nuceloli |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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TOBACCO SMOKING & LUNG CA
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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** |
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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. |
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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 |
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SYMPTOMS OF LUNG CA
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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 |
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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) |
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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 |
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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) |
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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 |