skin Flashcards
common causes of rash
allergens, infections, collagen vascular disease, toxic, drugs, metabolic
life threatening rashes
anaphylaxis, angioedema, bacterial endocarditis, meningococcal meningitis, severe thrombocytopenia, Kawasaki syndrome, TSS, toxic epidermal necrolysis (TEN)
flat, non-palpable skin lesion
macule–>patch(>1cm)
elevated, firm circumscribed skin lesion
papule–>nodule(1-2cm)
elevated firm rough skin lesion (>1cm) flat top
plaque
elevated, irreg. shaped cutaneous edema
wheal
elevated, circumscribed, superficial, not into dermis, filled with serous fluid
vesicle–>bulla (>1cm)
like vesicle but pus
pustule
superficial dilated blood vessels
telangiectasia
1 cause: chronic etOH
allergic skin reaction
urticaria, hives
suspect bacterial endocarditis
Oslar nodes and Janeway lesions
if wet purpura in mouth worry about
severe thrombocytopenia (as low as 2000) infectious etiology
peds
Kawasaki
skin sloughs off, typ. medication related, tachy
toxic epidermal necrolysis (TEN)
also SJS w/ sulfa drugs
present w. purpura, fever, altered, neck stiffness
meningitis
K-OH prep
highlights fungal infection
basal cell carcinoma
- caucasians
- pearly white lesion, pt may scratch–>bleed
- slow growing tumor
- 30% lifetime risk M>F
BCC risk factors
-UV sunlight, tanning, chronic arsenic exposure, radiation, long term immunosuppr. tx (transplants)
BCC dx
- pearly/waxy translucent in light papule
- best obs. w/ stretched skin
- erythematous patch >6mm or non-healing ulcer in sun exposed areas
- shave or punch biopsy: bests of basaloid cells in dermis, sep. from adj stroma by thin clefts
BCC tx
- electrodessication and curettage: not able to histologically confirm complete removal
- surgical excision
- Mohs surgery: take out one slide at a time til histologically confirm no more BCC (imp. on face, lips, nose, etc)
BCC topical/non-surg tx
- 5-fluorouracil: pyrimidine antimetabolite, interferes w. DNA synthesis
- Imiquimod (Aldara): unknown mechanism, TLR7 agonist, induces cytokines (INF-a)
radiation therapy for BCC
typically avoided
used in pt. who are nonsurgical candidates
-admin. in 4+ fractions, limits side effects, gives normal skin time to heal while cancerous cells cannot repair themselves as quickly
benefits of radiation tx
-cosmetically sparing, noninvasive, painless, nonsurg. candidates
BCC follow up
monitor pt annually
metastatic basal cell
deeply invasive/large lesions >10cm2
- missed w. poor examination, altered elderly pts
- reg. lymph nodes, lungs, bones, skin, liver
- Vismodegib (Erivedge): Hedgehog pathway inhibitor
squamous cell carcinoma
non-healing ulcer/wart nodule
recurring, bleeding lesion, dry, scaly
dorsum of hand, arm, nose
-sun damage, fair skinned ind., transplant recipients
SCC risks
2nd most common
UV radiation, tanning, arsenic exposure, smoking, high fat/meat diet, immunesuppr (transplant >5 yrs, HIV, long term glucocorticoid use)
genetic risk factors for SCC
xeroderma pigmentosum, v. rare
epidermolysis bullosa
albinism
Fanconi’s anemia
other SCC risk factors
Chronic lymphocytic leukemia (CLL)
meds:
Voriconazole(longterm anti fungal)
BRAF inhibitors (Vemurafenib and Dabrafenib) used to tx metastatic melanoma, but do not stop, cut out SCC
Actinic Keratosis
-develops into SCC
-chronic sunlight exposure–>excess keratin buildup
-
SCC dx
complete skin and regional exam
-lymph node exam
biopsy
SCC tx
surgical excision
Mohs
electrodesiccation and curettage
radiation therapy: for non surg candidates, if extensive perineural or large nerve involvement, LN involvement
SCC follow up
every 3 mos w/ LN exam for 1 year, then every 6 mos thereafter
malignant melanoma
UV radiation exposure cutaneous acral: palms, soles mucosal ocular/uveal
inc. risk for malignant melanoma
- Irish/European, fair
- more freckles
- Fam Hx
ABCDE of malig mel
Asymmetric Borders-irregular Color-variations Diameter->pencil eraser Evolution-take pic to monitor changes
staging of malig mel
> 4 mm deep: systemic chemo (T4, metastatic)
- thickness, ulcerated or not
- regional LN
stage 1A-1B
wide excision
stage 1B (0.76-1mm)
wide excision +/- INF
stage III
LN dissection and INF
stage IV
systemic therapy (chemo)
wider margins do not have added benefit with tumor thickness
> 4mm (grow deeper)
sentinel LN biopsy if..
> 1mm depth
-less if high risk features: ulceration, elevated MR, regression signs, BT>=0.75 mm
complete LN dissection
radiation after
stereotactic radiosurgery
for brain metastases: hottest around lesions to spare rest of brain tissue
chemotherapy meds
Ipilimumab
Dabrafenib + trametinib
Pembrolizumab
Nivolumab
other chemo meds
Vemurafenib Dabrafenib Trametinib Imatinib Dacarbazine Temozolomide Alb-bound palitaxel IL-2 Dacarbazine or temozolomide-based combo Pacliltaxel Pacliltaxel/carboplatin
BRAF inhibitors
Vemurafenib, dabrafenib
-MAP kinase pathway inhib. (inhib. BRAF V600E)
SE: edema, HA, rash **SCC of skin! arthralgia
MEK inhibitors
Trametinib
-rev. and sel. inhib. mitogen-act EC kinase (MEK) downstream from BRAF (combine with BRAF inhibs.)
SE: *cardiomyopathy, rash, anemia, hemorrahge, liver inflamm.
CTLA-4 inhibitors
Ipilimumab
blocks CTLA-4, allows for enhanced T-cell activation and prolif
SE: (hyperactivates Imm. sys) colitis, dermatitis, hepatitis, hypophysitis, thyroiditis
Anti-PD-1 Monoclonal Ab
Nivolumab
Pembrolizumab
inhib. PD-1 activity by binding PD-1 rec. to block ligands PD-L1/2, releases PD-1 pathway med inhib of IR (anti tumor response)
SE: e-lyte abnormalities, cytopenia, rash
Ipilimumab
enables prolif of T cells thru CD28 or CTLA-4–>inc. signalling–>T-cell activation
- works in 10-15% pts
- takes 1-4 mos (diff. to monitor)
- may look worse on CAT scan after tx before gets better
50% BRAF mutations in
skin lesions, not as common in others
BRAF inhibitors (vemurafenib)
shuts down cascade of DNA replication