Block VIII, Week VII

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what is the difference between infective and reactive arthritis?: infective - inflammation of joint space caused by a microorganism
reactive - bacterial infection in one part of the body triggers arthritis in another joint
risk factors of infective and reactive arthritis?: *RA, DM
*AIDS or other immune suppression
*malignancy
*old age
*joint damage or abnormalities
which population is disseminated gonococcal disease commonly seen in?: young sexually active women
pathogenesis of infective arthritis?: bacteria can get to joint by hematogenous seeding or direct inoculation.
*PMNs enter joint in response. inflammation causes cellular damage and symptoms
top two bacteria involved in infective arthritis?: 1. Staph aureus
2. N. gonorrheae
bacteria involved in infective arthritis seen in: 1. diabetes pts? 2. arthroscopies 3. elderly: 1. Group B strep
2. Staph epi (coag. negative staph)
3. gram negative bacilli
describe the location and onset of non-gonococcal infective arthritis: location: typically monoarticular
acute onset
non-gonococcal infective arthritis is MC seen in what joint?: knee
what are the two distinct elements seen in gonococcal arthritis?: 1. early onset - bacteremia, fever, polyarthralgia, skin lesions
2. late onset - untreated pts will present later with monoarticular arthritis w/o skin lesions
what is the only definitive test for diagnosis of gonococcal arthritis?: culture of synovial fluid
in infective arthritis - if bacteria can't be cultured what can be done?: PCR
management of infective arthritis?: *drainage of synovial fluid
*Abx
which antibiotics would be prescribed for: 1. Staph 2. gonococcal 3. pseudomonas 4. MRSA: 1. nafcillin or oxacillin
2. ceftriaxone or cipro
3. ceftriaxone or cipro
4. Vancomycin
HLA that is associated with reactive arthritis susceptibility?: HLA-B27
(also seen in AI disorders)
Treatment of reactive arthritis?: manage symptoms
acute osteomyelitis is more common in which sex?: males
seasonal trend in acute osteomyelitis cases?: peak time is October (in N.America)
pathogenesis of acute osteomyelitis?: 1. adhesion (adhesins for ECM proteins are virulence factors)
2. glycocalyx aids in forming a biofilm. this enables evasion of host defenses and protection from Abx.
3. incr. levels of prostaglandin E2 stimulates bone resorption
4. pro-inflammatory cytokines cause damage
top two bacteria that cause acute osteomyelitis?: 1. Staph aureus
2. Streptococci (has ECM adhesins)
labs used to diagnose acute osteomyelitis?: culture from needle biopsies
ESR, C-reactive protein elevated
treatment for acute osteomyeliytis?: surgery may be req'd if pus is found in diagnostic specimen
*Abx. treatment for a minimum of 3wks
in acute osteomyelitis, which Abx would you prescribe for: 1. Staph aureus 2. MRSA 3. Streptococci 4. Peudomonas: 1. nafcillin or oxacillin
2. vancomycin
3. Pen G iv
4. Cipro
clinical s/s of chronic opsteomyelitis?: few systemic symptoms
*persistent pain and drainage through sinus tracts
*sometimes see neural complications when epidural abscesses occur
pathogenesis of chronic osteomyelitis?: primarily a result of injury, ocassionaly a result of acute osteomyelitis
*real problem is presence of pathogen and accompanying necrosis/inflammation.
chronic osteomyelitis is more commonly seen in which bones?: long bones or vertebrae
treatment for chronic osteomyelitis?: parenteral antibiotics
(cipro is safe for just about every bug)
top 2 bacteria that infect prosthetic joints?: staph aureus (early onset infx)
staph epi (later onset infx)
which abx. is used prophylactically to prevent prosthetic joint infections?: 1st or 2nd generation cephalosporins
what is the MC vector borne disease in the US?: Lyme disease
causative agent of Lyme disease?: Borrelia burgdorferi (spirochete)
characteristic rash seen in early onset Lyme disease?: erythema migrans (target lesions)
how long after the tick bite does the erythema migrans show up?: median 7d
(range - few days to months)
early systemic symptoms seen in lyme disease?: malaise
fatigue
lethargy
H/A
fever chills
arthralgia, myalgia
skin lesions
pattern of symptom presentation seen in lyme?: relapsing/remitting
(characteristic of spirochete illness)
late systemic symptoms seen in lyme disease?: carditis (heart block, CHF)
cranial neuropathy
lyme meningitis
symptoms come and go over months then spontaneously resolve
characteristics seen in arthritis of Lyme disease?: typically occurs 6mo after EM
massive effusion
monoarthritis, commonly involves the knee
*attacks last for a few days to a few weeks over the course of years
chronic manifestations of lyme disease?: neurologic
chronic arthritis
chronic skin involvemetn
diagnosis of lyme disease?: *presence of EM
*western blot to confirm (look for antibody to spirochete)
management of lyme disease?: *doxycycline, amoxicillin (for early disease, arthritis or neurologic manifestations)
*ceftriaxone or Pen G (for lyme carditis)
*amox during pregnancy
3 types of clostridial soft tissue infections?: 1. simple wound contamination
2. anaerobic cellulitis
3. clostridial gas gangrene
simple wound contamination by clostridium is probably contained because of?: lack of devitalized tissue
when does clostridial cellulitis occur? pathogenesis?: when there is devitalized tissue for clostridial growth.
*gas is produced along fascial planes, but bacteremia and invasion of healthy tissue does not occur
treatment for clostridial cellulitis?: removal of affected tissue
three subtypes of clostridial gas gangrene?: 1. traumatic
2. spontaneous (non-traumatic)
3. recurrent (caused by C.perfringens)
what is the difference between clostridial gas gangrene and clostridial cellulitis?: cellulitis - no invasion of healthy tissue
gas gangrene - invasion of healthy living muscle
what is the MC form of clostridial gas gangrene?: traumatic
pathogenesis of traumatic gas gangrene?: develops when a deep, *penetrating injury compromises the blood supply and creates and anaerobic environment
*necrosis progresses within hours
MCC of clostridial gas gangrene?: C.perfringens
types of "trauma" that can cause traumatic gas gangrene?: *bowel & biliary tract surgery
*intramuscular epi injection
*illegal abortion, retained placenta
*missed abortion in postpartum patients
why is the histopathology "opposite" of that seen in Staph infections?: there is no strong inflammatory response that contains the infection (Clostridium suppresses the inflammatory and immune response)
function of the theta toxin seen in Clostridium?: destroys host tissues and inflammatory cells at the site of infection
*promotes dysregulation of leukocyte adhesive interactions with endothelial cells
function of the alpha toxin seen in clostridium?: may induce the shock seen in gangrene
*directly inhibits myocardial contractility, contributing to profound hypotension and reduction in CO
clinical findings in traumatic gas gangrene?: *severe pain
*skin may be pale then rapidly change to bronze then purplish-red
*affected area becomes tense and exquisitely tender
*gas is evident in the tissues
*systemic toxicity develops (tachycardia, fever, diaphoresis)
in gas gangrene, systemic toxicity can progress to?: shocsk and multiple organ failure
diagnosis of gas gangrene?: *crepitus in the soft tissue
*presence of clostridium
management of gas gangrene?: agressive debridement, repair of vascular supply
*Abx (preferably clindamycin)
*hyperbaric O2
spontaneous gas gangrene is caused by?: C. septicum
(aerotolerant)
spontaneous gas gangrene is seen in association with?: GI problems, colonic CA, surgery
leukemia
chemo/radiation therapy
AIDS
clinical s/s of spontaneous gas gangrene?: *bacteremia
*pain
*confusion, malaise
*swelling
*bullae filled with fluid. skin surrounding bullae is purplish
which has a higher mortality rate: traumatic gas gangrene or spontaneous gas gangrene?: spontaneous gas gangrene (67-100%)
tetanus presents as?, while botulism presents as?: tetanus - spastic contraction of muscle
botulism - flacid paralysis of muscle
action of the tetanus toxin?: toxin penetrates membrane of inhibitory interneuron, then blocks neuro-exocytosis by cleaving VAMP
*blocks inhibitory interneuron*
action of botulinum toxin?: inhibits the motor neurons at the NMJ
what is the cause of cercarial dermatitis "swimmer's itch"?: water-borne cerceriae
what is the cause of cutaneous larval migrans (creeping erruption)?: infective larvae of non-human hookworms
what is the most widespread ectoparasite of humans?: human follicle mite (Demodex follicularum)
*harmless*
how are chiggers contracted?: by walking into a "chigger island" outdoors.
difference between chiggers and scabies in regards to ectoparasitic activity?: chiggers - only larvae are ectoparasitic
scabies - all forms are ectoparasitic
what are the two stages of biphasic feeding in a tick?: 1. preparatory phase
2. the big sip
importance of the preparatory phase in tick feeding?: provides a "grace period" in the transmission of pathogens (ticks secrete toxins late in preparatory phase)
*pull tick out asap*
difference between the metamorphosis of lice and fleas?: lice - incomplete metamorphosis
fleas - complete metamorphosis
three type of fleas: 1. body louse (cootie) 2. head louse 3. pubic (crab) louse which is seen in the lower classes in the US?: body louse
three type of fleas: 1. body louse (cootie) 2. head louse 3. pubic (crab) louse which is commonly seen in children?: head louse
where are the eggs of lice (nits) laid?: in the hair shaft close to the skin
what is myiasis?: infestation of living flesh with maggots
4 ways in which myiasis is classified?: 1. cutaneous
2. nasopharyngeal
3. enteric
4. uro-genital
other name for atopic dermatitis?: eczema
pathogenesis of atopic dermatitis (eczema)?: IgE related, eliciting factors (ie. seafood, inhalants, dry skin)
atopic dermatitis (eczema) is often associated with?: asthma, rhinitis
three "stages" of atopic dermatitis (eczema)?: 1. infant stage (on extensor surfaces & face)
2. childhood stage (both areas)
3. adult stage (flexor areas, widespread, chronic)
stasis eczema is caused by?: impaired venous return (see lesions on lower legs and ankles)
treatment of choice for eczema?: wet dressing
two types of contact dermatitis?: 1. irritant (localized, nonimmunologic damage at the site of contact, can happen to anyone)
2. allergic - type IV hypersensitivity, itching spreads to periphery
treatment for contact dermatitis?: *remove offending agent
*drain larger vesicles
*wet dressing
*topical corticosteroid
*anti-histamine
when should patch testing be performed for allergic contact dermatitis?: at least 2 wks after dermatitis has resolved
what are some common drug allergens that cause drug erruptions?: antibiotics
pain relievers, NSAIDs
describe a fixed drug erruption: a lesion that recurs in the same location with rechallenge.
maculopapular erruption as a result of drug allergy must de differentiated from?: viral exanthem
(ie. measles)
Stevens-Johnson syndrome may progress to?: toxic epidermal necrolysis
(fatal 20-50%)
toxic epidermal necrolysis must be differentiated from?: SSSS (Staph Scalded Skin Syndrome) - severe staph infection
pathogenesis of urticaria?: *mast cell degranulation due to sensitization with IgE.
*leads to histamine release
*leads to dermal vascular hyperpermeability = edema
CAN ALSO BE DIRECTLY INDUCED BY CHEMICAL COMPUND OR PHYSICAL FACTORS
course of urticaria?: self-limited condition (individual lesions develop and regress w/i hours, new lesions evolve as old ones resolve)
treatment for urticaria?: anti-histamine
anti-itch lotion
type of urticaria precipated by rubbing or stroking the skin?: dermatographism
pathogenesis of erythema multiforme (EM)?: type III hypersensitivity rxn. most likely caused by drugs or in response to infection.
EM is characterized by?: target lesions
what is a positive Auspitz sign associated with?: psoriasis vulgaris
(pinpoint bleeds when scale is removed)
what is the Koebner phenomenon?: new lesions that appear at a site of trauma, seen in psoriasis vulgaris
histologic characteristic of Psoriasis vulgaris?: Munro's microabscesses (aggregates of neutrophils in the epidermis)
treatment for psoriasis vulgaris?: MTX
systemic steroids
UVA, UVB light
topical preparations
suspected pathogenesis of lichen planus?: cell-mediated immune injury to basal cells
describe the course of lichen planus: self-limited
(lasts about 1-2 yrs)
what are the "4 Ps" seen in lichen planus?: Pruritic
Purple
Polygonal
Papules
what are Wickham striae?: white dots or lines that surround lesions seen in lichen planus
in lichen planus, what is seen upon immunoflourescence: globular immunoglobulin deposits at dermal/epidermal junction
pemphigous vulgaris is more common in which sex?: females=males
age of onset of pemphigous vulgaris?: 4th-6th decades
pathogenesis of pemphigous vulgaris?: AI disorder with separation between the epidermis and mucosal epithelium
what is the Nikolsky sign that is seen in pemphigous vulgaris?: application of pressure to an intact bulla causes the fluid to dissect laterally and the bulla to be extended
treatment for pemphigous vulgaris?: corticosteroids
immunosuppressive agents
treatment for lichen planus?: topical or systemic steroids
define acantholysis: separation of intercellular contact between keratinocytes
(seen in pemphigous vulgaris)
what pattern is seen upon immunoflourescence in pemphigous vulgaris?: fishnet patterns
(along membranes of keratinocytes throughout the epidermis)
bullous pemphigoid generally affects which age group?: elderly
pathogenesis of bullous pemphigoid?: AI disorder with separation in the dermoepidermal junction
is the Nikilsky sign + or - in a patient with bullous pemphigoid?: negative
in bullous pemphigoid what is seen upon immunoflourescence?: linear IgG and compliment deposition on the basement membrane
treatment for bullous pemphigoid?: cotricosteroids
immunosuppressant
which sex is dermatitis herpetiformis MC found in?: Males
which age is dermatitis herpetiformis MC found in?: 3rd-4th decade
pathogenesis of dermatitis herpetiformis?: AI - associated with specific HLA types
(seen in celiac disease)
treatment for dermatitis herpetiformis?: gluten-free diet
dapsone
which drug class often exacerbates dermatitis herpetiformans?: NSAIDs
in dermatitis herpetiformans, what is seen upon immunoflourescence?: IgA deposits in tips of dermal papillae
what type of hypersensitivity rxn. is dermatomyositis?: type III
dermatomyositis as associated with?: malignancy
what are Grottons papules?: papules that occur over the joint and along the sides of the fingers in dermatomyositis
symptoms of dermatomyositis?: photosensitivity
proximal skeletal muscle weakness
dysphagia
muscle atrophy
hallmark rash seen in dermatomyositis?: heliotrope rash (violet eyelids)
SLE is associated with what HLAs?: HLA-DR2 And DR3
rare genetic skin disease (dominant and recessive) with an unknown pathogenesis? *blisters are induced by minor trauma?: Epidermolysis bullosa
porphyrias are caused by a defect in which biosynthetic pathway?: heme
connection between excess porphyrin and blisters?: porphyrin absorbs UVA light, this activates porphyrin to produce peroxides, which cause blisters
actions of acetominophen: inihbits COX in CNS
(analgesic, antipyretic)
*weak peripheral inhibition of COX, therefore little to no anti-inflammatory effects
three indications for APAP?: 1. analgesia (mild pain)
2. fever
3. non-inflammatory musculoskeletal pain (ie. OA)
major adverse effect of APAP?: liver toxicity
what is the acute dose of APAP that, above which, increases risk of liver toxicity?: >7.5 g in adults
what is the chronic dose of APAP that, above which, increases risk of liver toxicity?: >4g/day
two populations that are at increased risk for liver toxicity caused by APAP?: alcoholics
those on CYP450 inducers
what is the antidote for an APAP overdose?: N-acetylcysteine
what is the only COX II inhibitor still on the market?: Celecoxib (Celebrex)
NSAIDs are COX inhibitors. what is the normal function of COX?: conversion of arachadonic acid to prostaglandins
how do prostaglandins mediated pain and inflammation?: *potent vasodilators
*act synergistically with inflammatory mediators
*sensitize pain receptors to histamine and bradykinin (lower pain threshold)
*potentiate spinal cord transmission of pain signals
COX-1 inhibitors inhibit the formation of what 2 inflammatory mediators?: prostacyclin
thromboxane A2
COX-2 inhibitors inhibit the formation of what 2 inflammatroy mediators?: prostaglandins I and E
which requires a higher dose: analgesia or anti-inflammatory effects?: anti-inflammatory
anti-inflammatory effects are mediated by inhibiting?: peripheral prostaglandins
antipyretic effects are mediated by inhibiting?: CNS prostaglandin synthesis
actions of ASA on platelets?: ireeversibly acetylates and inhibits platelet COX-1
*complete platelet inhibition for the life of the platelet (7-10d)
what is the FDA class warning on NSAIDs and Coxibs?: GI ulcers
most significant risk factor for GI adverse effects with NSAID use?: age >65 yrs.
(linear increase in risk)
what can be done to reduce NSAID GI toxicity?: *switch to COX 2 inhibitor or lower risk NSAID
*misoprostol
*PPI
pathogenesis of renal toxicity seen in NSAID use: NSAIDs inhibit renal PGI2 and PGE2. normally these regulate renal blood flow (renal vasodilators that increase renal bloodflow and H2O excretion)
BLOCKAGE BY NSAIDs REDUCES RENAL BLOOD FLOW LEADING TO TOXICITY
risk factors for renal toxicity induced by NSAIDs?: elderly
CHF
renal dysfx
cirrhosis/ascites
DM
Diuretic use
what are the two types of hypersensitivity rxns seen in NSAID use?: 1. respiratory (rhinitis, asthma, nasal polyps)
2. urticaria, angioneurotic edema, hypotension, shock, syncope
is there cross-sensitivity of hypersensitivity to other NSAIDs?: yes
(APAP is safe, though)
which is least likely to cause GI adverse effecs: COX-1 or COX-2 inhibitors?: COX-2 inhibitors
what do the following NSAIDs have in common? etodolac, nabumetone, meloxicam: traditional NSAIDs but relatively selective for COX-2
what is the MC used initial therapy in the treatment of RA?: MTX
(methotrexate)
MOA of MTX?: *competitively inhibits folic acid metabolism and DNA synthesis
*impairs function of inflammatory cells
serious toxicies associated with MTX?: *hepatic fibrosis, cirrhosis
*pulmonary fibrosis
*myelosuppression (leukopenia, anemia, thrombocytopenia)
monitoring tests that must be done with a pt on MTX?: CBC
LFTs
SCr
CXR
MOA of hydroxychloroquine (HCQ) in the treatment of RA?: (antimalarial)
suppresses lysosomal enzymes and inhibits IL release
adverse effect of HCQ?: retinal toxicity (rare and dose related)
MOA of sulfasalazine (SSZ) as a DMARD?: converted by colonic bacteria to 5-ASA and sulfapyridine
*anti-inflammatory and antibacterial
*impairs lymphocyte transformation
what is the role of TNF in RA?: promotes innapropriate inflammatory response
what is a recombinant soluble TNF receptor that binds & neutralizes TNF, therefore is used to treat RA?: etanercept (enbrel)
MOA of infliximab (remicade): monoclonal antibody to TNF, binds to and neutralizes circulating TNF
MOA of adalimumab?: recombinant IgG antibody specific to human TNF (binds to and neutralizes circulating TNF-a)
MOA of rituxumab?: anti-CD20 monoclonal antibody
(selectively depletes CD20+ B cells)
besides RA, what is rituximab also used to treat?: B cell non-hodgkin's lymphoma
what is the least potent DMARD but has the least adverse effects?: hydrochloroquine (HCQ)
three medications used to treat ACUTE gout?: 1. NSAIDs
2. corticosteroids
3. colchicine
two classes of drugs that are used in the prophylaxis of recurrent gout attacks?: 1. uricosurics
2. inhibitors of uric acid synthesis
two uricosurics used in gout prophylaxis?: probenicid
sulfinpyrazone
MOA of colchicine?: unknown (not an analgesic)
*inhibits phagocytosis and migration of leukocytes in response to deposited uric acid crystals
*mitotic inhibitor
two serious adverse effects of colchicine?: pulmonary fibrosis
biliary cirrhosis
MOA of probenecid?: inhibits post-secretory renal proximal tubule reabsorption of Uric Acid
effects of probenecid on: 1. urinary excretion of uric acid 2. serum uric acid levels: 1. increases
2. decreases
probenecid has what important effect on the secretion of other drugs?: inhibits tubular secretion of other drugs (increases serum levels)
-penicillin, cephs, sulfas, indomethacin, MTX
T/F: probenecid is useful in acute gout attacks: FALSE
(prophylaxis only)
when initiating probenecid therapy, initial exacerbation of gout may be experienced. how can this be avoided?: colchicine or NSAIDs may be used prophylactically
adverse effects of probenecid?: uric acid stones
Heme - aplastic anemia, leukopenia
hypersensitivity (probenecid is a sulfa drug)
MOA of sulfinpyrazone?: uricosuric (inhibits reabsorption of uric acid in proximal tubule)
other action of sulfinpyrazone?: inhibits platelet aggregation
adverse effects of sulfinpyrazone?: GI
heme (rash, anemia, leukopenia, thrompocytopenia, aplastic anemia)
uric acid stones
MOA of allopurinol?: irreversible inhibition of xanthine oxidase - no uric acid formed
(reduces serum and urinary uric acid)
is allopurinol of benefit in acute attacks?: NO
adverse effects of allopurinol?: *may precipitate acute attack early in therapy
*pruritis, mild rash
*rare severe hypersensitivity syndrome
describe the rare, severe hypersensitivity sydrome seen with allopurinol administration?: *dose dependant, often in renal dysfx
*fever, eosinophilia, rash
*hepatic dysfx, renal failure
*vasculitis
DISCONTINUE at earliest signs (20% mortality rate)
effects of ASA on uric acid?: decreases uric acid renal excretion, increases serum uric acid
a cafe-au-lait spot os an example of what kind of skin lesion?: melanocytic nevi
what is lentigo?: melanocytic nevi (demarcated hyperpigmented macules)
*demarcated and hyperpigmented
*no predilection for sun exposed skin
significance of a giant congenital hairy nevi?: increased risk of melanoma (10-25%)
where is a spitz nevus MC found?: children
(frequently on face, light brown to red)
what is a nevus sebaceous: *preferentially on scalp
*hair absent
a nevus sebaceous is associated with an increased risk of?: BCC
(also may see CNS, skeletal abnormalities)
cysts are lined by?: epithelial cells
describe an epidermal cyst: (aka. sebaceous cyst)
*forms subcutaneous nodules, filled with keratin, most are acquired, stink if infected
a trichilemmal cyst has what origin?: hair sheath epithelium
which population is pilomatricoma MC seen in?: children
suborrheic keratosis is very common in what age group?: elderly
what is leser-trelat syndrome?: paraneoplastic (associated with visceral mignancy); see sudden development of many suborrheic keratoses with pruritis
appearance of suborrheic keratoses?: appear "stuck on"
variable size
rasied
two examples of precanceroses?: actinic keratosis
bowen's disease
what is actinic keratosis?: keratotic or erythematous patch seen on sun-exposed skin - may develop into SCC
what is Bowen's disease?: erythematous patch or plaque, clinically appears like eczema or psoriasis.
*represents SCC in situ*
SCC usually is seen in patients of: 1. which age? 2. skin tone? 3. sun exposure Hx?: 1. >50 yrs
2. light skin
3. prolonged sun exposure
metastatic potential of SCC?: relatively low
(except for lip, mouth)
basal cell carcinoma si MC seen in patients: 1. age 2. skin tone 3. sune xposure?: 1. >40 yrs
2. light skin
3. prolonged sun exposure
metastatic potential of basal cell carcinoma?: mets rare
(may locally invade)
characteristic histologic appearance of basal cell carcinoma?: palisading nuclei
infiltrating nests of neoplastic cells
characteristic gross appearance of basal cell carcinoma?: papule or nodule
translucent, pearly
small blood vessels visible
central ulcer common
a mesenchymal tumor that manifests as a soft SQ mobile mass that may be assymptomatic or painful and histologically resembles adipose tissue is called?: lipoma
which mesenchymal tumor resembles a "great big skin tag"?: soft fibroma
which patient population are dermatofibromas MC in?: middle age females
where on the body are dermatofibromas commonly seen?: extremities (esp. lower legs)
benign peripheral nerve tumor is called?: neurofibroma
cutaneous T cell lymphomas manifest as what 2 clinical syndromes?: mycosis fungioides
sezary syndrome
describe mycosis fungioides: many different clinical forms, see plaques, scaling
(mimics psoriasis, eczema, tinea)
*chronic, progressive over years*
describe sezary syndrome: erythoderma
pruritis
lymphadenopathy
alopecia
what is a juvenile xanthogranuloma?: yellow papule
often single, may be multiple
onset in infancy
is a juvenile xanthogranuloa benign or malignant?: benign
(often regresses in 6 mo to 2 yrs)
what is a merkel cell carcinoma?: neuroendocrine tumor (papule or nodule on head or neck)
*high recurrence rates
*tendency to produce early and aggressive metastasis
*mean age of onset 65 yrs old
four most common cancers to met to the skin?: breast
melanoma
lung
colon
what are the 2 most highly malignant skin tumors?: melanoma
merkel cell carcinoma
three MC sites of melanoma?: cutaneous (91.2)
ocular
mucosal
describe the connection between sun exposure and later melanoma?: high risk - blistering sunburn in childhood or adolescence (not necessarily related to cumulative lifetime exposure)
importance of family history in melanoma?: high risk w/ 1st degree relative
(dysplastic nevus syndrome is also hereditary)
what are the ABCDE criteria for evaluating a skin lesion?: A - asymmetry
B - borders
C - color
D - diameter (>6mm)
E - elevation, evolution
what type of biopsy is indicated for a lesion that is suspected melanoma?: excisional biopsy
3 in-situ (intraepidermal) forms of melanoma?: 1. superficial spreading melanoma in situ
2. acral lentiginous melanoma in situ
3. lentigo maligna
other name for lentigo maligna?: Hutchinsons freckle
where is superficial spreading melanoma in situ MC found?: horizontal/flat spread on upper back and lower legs
where is acral lentiginous melanoma in situ MC found?: hairless skin of palms, fingers, soles, toes
(lentigo like growth)

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