Week 11: Derm Flashcards
Any sore that does not heal within _______ weeks should be examined for the possibility of skin cancer.
Four
Part of screening for cancerous lesions is teaching your patient what to look for. What acronym is used for screening for lesions suspicious of melanoms?
Asymmetry
Border irregularity
Color (esp. black, blue)
Diameter >6mm
Evolving
What kind of things would you teach your patient to look for when screening for BCC?
Teach Your Patient What to Look For:
* Firm, flesh-coloured or slightly reddish bump, often with a pearly border and may have telangiectasia
* Whitish scar where there is no reason for scarring
* Sore or pimple-like growth that bleeds, crusts over, and then reappears
(Per weekly notes)
What kind of things would you teach your patient to look for when screening for Actinic Keratoses?
Teach your patient what to look for:
* Red, rough scaling spots
* Lesions that appear on sun-exposed areas such as the face, lips, ears, balding scalp, back of hand, forearm and leg.
* Usually people have a few at one time, and the spots may sting or itch
(Per weekly notes)
What kind of things would you teach your patient to look for when screening for Squamous Cell Carcinoma?
Teach your patient what to look for:
* Thickened, red scaly bumps, or wart like growths.
* An open sore or crusted skin
* Lesion with a central crater and rolled edges
* May grow quickly over a few weeks
* Small, red scaling patches most often seen on trunk or limbs
(per weekly notes)
What kind of things would you teach your patient to look for when screening for Bowels disease? What is Bowen’s disease?
SCC in situ
Teach Your Patient What to Look for:
* Bowen’s disease usually appears as a patch on the skin with clear edges and does not heal.
* Some people have more than 1 patch
* The patch may be:
o red or pink
o scaly or crusty
o flat or raised
o up to a few centimeters across
o itchy (but not all the time)
True or False: Experts haven’t recommended for or against routine skin cancer screening for adults at normal risk
True (see cit below)
Mass skin cancer screening of the entire population is unlikely to be beneficial, feasible, and/or cost-effective. (Up To date)
U.S. Preventive Services Task Force (2016). Screening for skin cancer: U.S. Preventive Services Task Force recommendation statement. JAMA, 316(4): 429–435. DOI:10.1001/jama.2016.8465. Accessed July 27, 2016.
Some guidelines (Canadian cancer society) suggest screening for skin cancer in high risk populations. How is screening done?
Up To Date recommends targeted screening of high risk groups, along with focused patient and provider education for warning signs. For patients at high risk of developing a melanoma, Up To Date suggests annual screening with TBSE (total body skin exam) by clinician with skin expertise.
Some guidelines suggest screening for skin cancer in high risk populations. What makes a patient high risk?
Risk factors
-Holy moly! (total nevus count >50, presence of large nevi
-Phx skin cancer
-Immunosuppression, esp. use of medications to suppress immune system (i.e., organ transplant recipients)
-very sun sensitive individuals and those with red hair phenotype (light skin pigmentation, red or blond hair, high density freckling, light eye color like green, hazel, blue)
-fhx melanoma in 1+ FDR or in more than one 2nd degree relative on same side.
-Specific to older adults- up to date suggest examination of white men 50+ as they are at increased risk of melanoma compared to other patients (sun exposed areas)
When prescribing a topical steroid medication, what factors must the provider consider?
Anatomic site
Patient preference
Rash attributes
Vehicle attributes
Which anatomic site would require a higher potency steroid- an acral site or an intertriginous area? Why?
Acral site.
Acral sites- palms and soles- very thick skin- absorb medications the least, can withstand a mid to high potency steroid.
Intertriginous sites- where skin folds touch- i.e., groin folds, axillae, gluteal cleft- thinner skin, often prone to moisture/ occlusion which can increase steroid absorption- a weak steroid is needed.
What is the best steroid vehicle (i.e., lotion, cream, ointment, etc.) is best used on hair bearing skin?
Gels, lotions, shampoo, oil, foam
How does patient preference dictate vehicle?
Patient may be unwilling to use greasy cream- avoid ointment
What kinds of rash require a higher potency steroid?
-Thick, scaly skin
-Lichenified skin
-severe psoriasis
-rashes on palms, soles, scalp
-hyperkeratotic lesions (i.e., hyperkeratotic eczema)
-lichen planus/ scelrosus/ simplex
There are 7 “groups” of steroid potency. What group is the highest potency? Lowest?
Group 1= ULTRA high potency
Group 2, 3= high potency
Group 4,5= mid potency
Group 6,7= low potency
True or false: The vehicle by which a steroid is applied affects potency.
True!
Ointments are more potency compared with other vehicles.
True or false: The vehicle by which a steroid is applied can contribute to skin irritation
True- alcohol based solutions can be irritating on inflammed skin
Propylene glycol (found in many topicals) can sometimes cause irritant contact dermatitis
Jeremy has severe psoriasis. You instruct him to apply an ultra high potency steroid no more than ____ times daily
a) once
b) twice
c) three
d) four
Answer: B
Ultra high potency steroids should be limited to daily or BID.
How long will you instruct Jeremy to use his ultra high potency steroid for?
Less than 2-4 weeks
You can follow with a less potent agent if needed
What kind of adverse effects are we concerned about when using a topical steroid?
skin atrophy
acne
telangiectasia and irreversible striae with prolonged use
if on eyelids: glaucoma, cataracts
rarely: adrenal suppression, withdrawal reactions (more so a consideration with high potency and occlusive dressing/ young kids)
risk of OP apparently if high doses of group 3+ steroids
Rank from least to most occlusive:
Cream
Lotion
Ointment
Least: lotion
intermediate: cream
Most: ointment
What body areas would a lotion be good for?
axillae, groin
hair areas
acute weeping lesions
large areas
*may cause stinging, dryness
What body areas would a cream be good for
non acute/ wet lesions
intertriginous areas
cosmetically acceptable
does not hydrate as much as ointment
What body area would an ointment be good for?
Palms, soles
Anything with a dry/ scaly/ hyperkeratinized lesion
What is the best steroid of potency to use in the elderly?
Group 6 or 7 (low potency)
How frequently can you apply a low potency steroid?
BID- QID
True or false- It is better to start with a less potent steroid, and if the lesion does not respond adequately, increase potency.
False.
It is better to start treatment with amore potent corticosteroid rather than a mild, less effective one. As the disease becomes less severe, you may reduce the potency of the steroid molecule, The more acute and severe a disease, the more potent the drug should be.
Can you apply a steroid on eyelids?
yep but better make it a low potency (group 7) one!
beware risk of glaucoma, cataracts
Can you apply a steroid on the scrotum?
Yep! Again, group 6 or 7. Only slightly less absorptive than the eyelids.
Can you treat a patient with a topical steroid when they are taking an oral steroid?
Yes
I.e. lupus discoid lesions won’t resolve with oral steroid therapy and need topical steroid added
True or false: Healthy skin is a better barrier/ metabolizes the drug more than diseased skin, so as skin disease improves, absorption decreases substantially
True!
You prescribe a high potency steroid for a rash that you suspect is psoriasis. You reassess the patient a week later and the rash has spread. What do you do?
Reconsider your diagnosis. Both fungal and bacterial infections are made worse when treated with topical corticosteroids.
True or false- the patient should continue to apply steroid cream for at least 1 week after the skin lesion has cleared
False
STOP applying med when skin disease is cleared. Give pt specific parameters. Post inflammatory hyper/ hypopigmentation and residual erythema are expected, do not require treatment, and slowly resolve.
You diagnose Karen with stasis dermatitis. What potency of steroid do you prescribe?
a) group 1 ultra high potency
b) group 2/3 high potency
c) group 4/5 mid potency
d) group 6/7 low potency
c
(rx files)
You diagnose Jon with seborrheic dermatitis on his scalp. What potency of steroid do you prescribe?
a) group 1 ultra high potency
b) group 2/3 high potency
c) group 4/5 mid potency
d) group 6/7 low potency
c
(rx files)
You diagnose Janet with lichen sclerosus. What potency of steroid do you prescribe?
a) group 1 ultra high potency
b) group 2/3 high potency
c) group 4/5 mid potency
d) group 6/7 low potency
a
(rx files)
You diagnose Steve with psoriasis. What strength of steroid do you prescribe?
b
(rx files)
You diagnose Louise with atopic dermatitis. What strength of steroid do you prescribe?
a) group 1 ultra high potency
b) group 2/3 high potency
c) group 4/5 mid potency
d) group 6/7 low potency
c
What is psoriasis?
Chronic, inflammatory, immune mediated skin disorder with genetic base and environmental triggers
Describe the epidemiology of psoriasis
-peaks between 30-39 years and 50-69 years, but occurs in all ages
-no clear sex predilection
–2-3% of population, all races
-commonly family history (90% of cases)- typically genetic
-atopic people (highly allergic, ie asthma, allergies)
-triggers include stress, skin injury, anything immunosuppressant, infections (bacterial or viral), drugs (lithium, BB, antimalarials, NSAIDs, tetracyclines), low vit D,
What condition are associated with psoriasis?
Psoriasis is linked with many comorbidities include obesity, diabetes, metabolic syndrome, HTN, DM, Chron’s disease, liver/ kidney disease, psychiatric disease, local trauma, smoking, drinking, lithium, allopurinol, antimalarials, beta blockers
-Increases risk of malignancy 2 fold (lymphoma, non melanoma skin Ca, solid organ cancer)
What are the subtypes of psoriasis?
Plaque
Guttate
Pustular
Erythrodermic
Inverse (intertriginous)
Describe the stereotypic psoriasis lesion
Pink to red papules and plaques with white/ silvery scale
Pruritic
Well- demarcated
What is Auspitz sign?
Pin point bleeding when scale is removed, strongly indicates psoriasis
Fun clinical story!
I saw a pt in clinic with ? fungal infection, took skin scrapings for KOH prep, and noted pinpoint bleeding after scraping away the scale. I connected the dots and ID’d auspitz sign later when charting and researching on up to date. We started him on high potency steroids and it dramatically improved!
What nail findings are highly suggestive of psoriasis?
PITTING, nail whitening, friable nails, yellow spots, splinter hemorrhage, thickened nail beds, separation of distal end of nail plate from nail bed (onycholysis
Describe plaque psoriasis
- most common, 80-90% of cases
- Lesions: well-demarcated, thick, silvery, scaly, erythematous plaque surrounded by normal skin.
- Small erythematous papules enlarge and coalesce into larger lesions.
- Typically on face, scalp, elbows, knees and sites of trauma.
-often worse in winter due to lack of sun
Describe guttate psoriasis
- more common in young adults and children.
- Small, discrete, scattered round oval salmon pink/ red scaling papules all over trunk/extremities
-post strep pharyngitis infection.
-Can resolve in 6-12 months.
Describe erythrodermic psoriasis
-generalized erythema (>90% BAS) with fine desquamative scale on surface
-associated with arthralgia, pruritus, dehydration, electrolyte imbalance
-acute can be onset/ severe if drug induced (lithium, BB, NSAIDs, antimalarials or steroid withdrawal)
-can be chronic if poorly controlled psoriasis
Can be life threatening and requires immediate medical care
Describe pustular psoriasis
Sudden onset erythematous macules and papules which evolve rapidly into pustules
-Can be painful
-Can be generalized or localized
-patient usually has hx of psoriasis
-may occur with suden with drawal from steroid therapy
Describe inverse psoriasis
Erythematous plaques on flexural surfaces like axillae, inframmary folds, gluteal folds, inguinal folds; may be macerated/ moist
What is koebner phenomenon?
Development of skin disease in sites of truama. Occurs in psoriasis (and other disease like lichen planus, vitiligo)
Psoriatic arthritis is common in patients with psoriasis. What is the clinical presentation of psoriatic arthritis?
Joint pain, stiffness (morning), back pain
Tends to affect distal joints, DIPs
Asymmetric oligo arthritis in which <5 small joints/ large joints are affected
Can also present as symmetric polyarthritis (similar to and sometimes indistinguishable from RA)
Arthritis mutilans (destructive)
Spondyloarthropathy including sacroiliitis and spondylitis
Enthesitis
Dactylitis
How is psoriasis diagnosed?
Usually clinically
Skin biopsy for challenging cases (not usually necessary)
No labs to confirm
Genetic testing not used
What medications are used in the tx of psoriasis?
Emollients- reduce fissure formation
Topical corticosteroids- reduce scaling, thickness, redness
Topical vitamin D analogues (calcipotriene)- reduce keratinocyte hyperproliferation
Others- retinoids, calcineurin inhibitors
What potency of steroid is used in treatment of psoriasis?
Generally, a higher potency
Up To Date suggests Group 1 for short term control (except on face/ intertriginous regions)
What other treatments can be used in psoriasis?
Generally for moderate (3-10%) to severe (10% +) disease
Phototherapy
Systemic therapy- NSAIDs, methotrexate (severe disease), cyclosporin, acitretin (retinoid), DMARDs (TNF alpha inhibitors)
Name this lesion: common benign tumor of the epidermis formed from keratinocytes
Seborrheic keratosis
Where are SK’s found?
Scalp, face, neck, trunk of older adult
Usually on sun exposed regions of body
Spares palms and soles
How would you describe an SK?
Yellow or brown greasy “stuck on” macules or papules “smashed smartie”
What is the epidemiology of SKs?
Very common
69-100% caucasian males over the age of 50
Prevalence increases with age
M>F
Unusual in age <30
Risk factors: aging skin, UV exposure
How are SK’s diagnosed?
Clinical diagnosis
Biopsy only if uncertain
Ddx for SKs?
malignant melanoma (lentigo, nodular)
Melanocytic nevi
Pigmented BCC
Solar lentigo
Spreading pigmented AK
Management of SKs?
Only if desired for cosmetic purposes
Cryotherapy, electrodessication, shave excision
Follow up not needed unless looking infected
Management- sun protection
True or false: Seborrheic keratoses can be pre-malignant
False
What is the Leser- Trelat phenomenon? What can it indicate?
Sudden appearance of new SK’s (multiple lesions >5-10) may indicate internal malignancy
What is bullous pemphigoid?
autoimmune, subepidermal blistering disease
Who does bullous pemphigoid affect?
-mainly effecting older adults over the age of 60
-Often > 80 years of age, and mostly affects people over 50
-Rare in kids. Can occur in younger adults.
-F:M
-No racial preference
-More prevalent in older people with neurologic disease (parkinsons, dementia)
-Risk is greater in people with psoriasis, and it can be precipitated by treatment of psoriasis with phototherapy.
-Occasionally induced by drugs like furosemide, captopril, NSAIDs
Describe the patho of bullous pemphigoid
Autoimmune
Results from attack on basement membrane of epidermis by IgG antibodies and activated T lymphocytes
What is the clinical presentation of bullous pemphigoid?
prodrome of localized erythema or pruritic urticarial plaques that become more edematous and extensive (can be weeks to months)
develops into pruritic tense bullae (1-3 cm) on erythematous, urticarial, or non inflammatory base.
can affect mucous membranes
often symmetric and generalized
bullae rupture within 1 week leaving eroded base that heals without scarring
How to diagnosed bullous pemphigoid?
Often diagnosis is made clinically and confirmed with skin biopsy.
What is the treatment for bullous pemphigoid?
If severe and widespread, may need hospitalization. Risk of secondary skin infection. Potentially fatal disease.
Localized- high potency topical corticosteroids
Advanced/ generalized- oral corticosteroid (prednisone) plus dapsone or doxycycline
Treat itching- i.e., with hydroxyzine.
Takes about 6 weeks, and then steroids are tapered.
Assess for drug induced disease (can happen months to 1+year after starting inciting medication) and discontinue drug of concern
Referrals
-opthalmology if ocular involvement (itching, burning sensation in eyes or visual change)
-GI if esophageal involvement and dysphagia
-ENT if laryngeal, pharyngeal, nasal mucosa involvement (hoarse voice, nasal obstruction)
What is notalgia paresthetica
A form of cutaneous dysesthesia where itch and/or changed sensation arise in the areas of skin on the medial aspect of the shoulder blade on either side of the back
AKA thoracic cutaneous nerve entrapment syndrome
Patho of notalgia paresthetica
The nerves which supply sensation to the upper back emerge from the spinal cord (2nd to 6th thoracic segments) and run a long course up through the thick muscles of the back. They make a right-angled turn before reaching the skin. The nerves appear to be vulnerable to compression or traction. Partial compression, injury or nerve entrapment leads to the symptoms.
Initial injury to the nerve may include: back injury, herniated disc, herpes zoster, sunburn, myelopathy, small fiber neuropathy
S&S of notalgia paresthetica
Localized pruritis, unilateral to the skin medial to the scapular border on the mid or upper back
May have change in sensation to the area
May have reduced or absent sweating to the area
Cutaneous changes may occur but are secondary to scratching or rubbing the skin
What kind of cutaneous changes might you see in a patient with notalgia paresthetica (remember, these are secondary to scratching/rubbing and not the actual disease process)
Scratch marks
Hyperpigmentation
Hypopigmentation
Lichen simplex chronicus
Scarring
Diagnosis of notalgia paresthetica. What might you see on imaging?
I’m assuming is mostly a clinical diagnosis…
Radiology may demonstrate a degenerative vertebra or prolapsed disc in the area that corresponds to the nerve supply to the affected skin (the dermatome). In many cases, no abnormality is revealed.
Skin biopsy would be normal unless there is superimposed dermatitis
What is onychomycosis
fungal infection of the nail
Risk factors for onychomycosis
Older age
Other nail problems (psoriasis or trauma)
Peripheral vascular insufficiency
Hyperhidrosis
Immunosuppressed states (e.g., diabetes, HIV infection, immunosuppressive therapy)
Frequent public swimming pools
occupations requiring occlusive footwear (causes trauma)
1/3 of cases have presence of tinea pedis
What usually causes onychomycosis?
Dermatophytes, particularly Trichophyton rubrum, are the most common causes of onychomycosis
Rarely yeast (eg, Candida albicans) and nondermatophyte molds
What is the main concern for a patient with DM or who is immunocompromised and has onychomycosis?
In patients with diabetes or immunosuppression, these infected areas can serve as a reservoir of fungi that may cause reinfection or serve as a portal of entry for bacteria, leading to secondary bacterial infections such as cellulitis
S&S of onychomycosis
starts in 1-2 nails and spreads
most patients develop lifelong infection (unless treated)
yellow/ white nail plate
elevated due to accumulation of hyperkeratotic debris within the plate
brittle, thick nails
Can be painful
May disrupt surrounding skin and predispose to bacterial infection of surrounding area (paronychia –> cellulitis)
How do we diagnosis onychomycosis?
Up to Date & CPS recommends confirming presence of fungi prior to treatment because there are multiple conditions that can mimic OM
According to CPS: The current standard for diagnosis is a combination of fungal culture and microscopy
DO we need to treat onychomycosis in everyone? When might we treat?
No, don’t need to treat in everyone
History of repeated lower extremity cellulitis
DM or other risk factors for cellulitis (d/t risk of secondary bacterial infections with onychomycosis)
Immunosuppression
nail pain or discomfort
Patient desires treatment
T/F Treatment failure and disease recurrence are common in onychomycosis
True - ensure you tell your patients this before initiating treatment!
How can topical urea be helpful in treatment of onychomycosis
This is a curbsiders trick and not really included in other resources…
If a patient is bothered by the thickness of the nail, you can prescribe urea 40% ointment or cream, applied to the nail plate until desired thinness. Highly effective for patients who seek to have nails of normal thickness that they can then paint over.
Caution patient to keep off surrounding skin as can be irritating
How do we usually treat onychomycosis?
What are some non prescription options to try for mild infections?
Classic options: oral antifungals, topical antifungals, physical interventions (laser treatment, photodynamic therapy (PDT), and surgery
Other nonpharm options that can be helpful if infection just starting: mentholated ointment (Vick’s VapoRub), vinegar soaks, compounded thymol in alcohol, antifungal nail lacquers
**If severe, it seems like a lot of people just opt to get their nail removed!
When are topical antifungals helpful for treatment of onychomycosis?
Recommended for early/mild or limited cases, or if systemic tx contraindicated
Advantages of topical antifungals
negligible risk for serious adverse effects and drug interactions compared with systemic antifungal therapy
Disadvantages of topical antifungals
Often require long (many month) treatment, often not effective, recurrence common when stop tx
How long is the typical course of topical antifungals for onychomycosis
48 weeks
What can a patient do to possibly increase the efficacy of their topical antifungal?
Filing the upper surface of the thickened nail (vigorous debridement) may increase the extent of penetration for a topical preparation and may increase the likelihood for successful topical therapy
What medication is typically used for systemic tx of onychomycosis?
Terbinafine
** Oral terbinafine is considered the drug of choice for OM caused by dermatophytes based on its higher efficacy, tolerability and lower risk of drug interactions
Continuous dosing: Oral: 250 mg once daily for 6 weeks (fingernail) or 12 weeks (toenail).
Possible severe A/E of terbinafine?
can cause severe hepatotoxicity, severe cutaneous adverse reactions (such as SJS/TEN), thrombotic thrombocytopenic purpura and hemolytic-uremic syndrome. Can also cause prolonged taste & smell disturbances.
Common side effects of terbinafine
mild and transient headache, gastrointestinal symptoms (e.g., nausea, diarrhea, dyspepsia, abdominal pain), viral infections and skin rashes
Contraindications to terbinafine use
Hypersensitivity to terbinafine or any component of the formulation; chronic or active hepatic disease. Use in caution if renal impairment!
What monitoring is required for terbinafine use?
Obtain baseline and mid-treatment serum aminotransferase level
(and CBC seems to be sometimes recommended)
What is a digital mucus (myxoid) cyst? Where are they located? Is it a true cyst?
= a focal collection of mucin under the skin, and is commonly seen on the distal aspect of the fingers.
a shiny papule found at the end of a finger or toe, close to the nail.
It is called a pseudocyst because it is not surrounded by a capsule, unlike a true cyst. It is also called a myxoid cyst, a mucous cyst, a digital ganglion cyst, and a digital synovial cyst.
Will a myxoid cyst usually be plentiful or solitary? What colour?
Changes to nails associated?
It is usually a solitary lesion that is skin coloured to translucent
Jelly-like sticky fluid may be expressed from the pseudocyst (sometimes tinged with blood).
The corresponding nail can show a groove or structural changes as a pressure effect of the pseudocyst.
Osteoarthritis can accompany it, when it is regarded as a type of ganglion.
Tx of myxoid cyst.
Does it recur?
Treatments which may be successful for digital myxoid pseudocyst include:
Repeatedly pressing firmly on the cyst
Squeezing out its contents (make a hole with a sterile needle)
Cryotherapy (freezing)
Steroid injection
Sclerosant injection
Surgical removal.
Unfortunately, digital myxoid pseudocysts often recur, whatever treatment is used.
What is Sebaceous Hyperplasia
= benign overgrowths of normal sebaceous oil glands that are usually found on the face
A form of benign hair follicle tumor
What is the typical anatomic distribution of sebaceous hyperplasia?
They can be seen commonly on the face, vermilion lips and buccal mucosa (Fordyce spots), eyelids (meibomian glands), areola (Montgomery tubercles), and glans penis or clitoris (Tyson glands).
Describe the appearance of sebaceous hyperplasia?
yellow to flesh-colored appearance
Up to 3mm diameter
often associated central umbilication
Close inspection reveals a central hair follicle surrounded by yellowish lobules.
There are often prominent blood vessels, best seen using dermoscopy
Who is more prone to sebaceous hyperplasia?
usually iodopathic
cyclosporine has been reported to cause diffuse lesions
Most often affects older people
More common in immunocompromised
Tx of sebaceous hyperplasia
usually not required because they are typically asymptomatic
removal options include electrodesiccation, serial topical LN, or topical retinoids
When the lesions are severe, extensive or disfiguring, oral isotretinoin is effective in clearing lesions but these may recur when treatment is stopped.
In females, antiandrogens may help improve the appearance.
What is BCC
Where does it typically occur?
Skin cancer of the basal layer of keratinocytes in the epidermis
Mostly occurs on sun exposed areas of the body
70% on the face
Sometimes on chest/arms
What is the main risk factor for BCC?
UV light -> mutation of tumor suppression genes and proto-oncogenes
Does BCC grow fast? Is it likely to met?
Initial tumours are small and hard to detect
Lesions grow slowly over months to years
Metastasis is rare because tumors do not invade blood or lymph vessels
Describe BCC
Nodular variant (most common): typically a pearly white, almost translucent, dome-shaped papule with overlying telangiectasias
- Enlarges slowly, flattens centrally, or may develop raised rolled border
- Often bleed, erode, become crusted, ulcerate at the centre
Superficial BCC can resemble patch of eczema or psoriasis: circumscribed round or oval, red, scaling plaque. It can spreads peripherally, sometimes several centimeters. This is the least aggressive form. Most commonly on trunk or extremities
Sclerosing BCC may just look like scar tissue.
Pigmented BCC may look like melanoma.
Is prevention of BCC possible? How do we do it?
It’s key! Focus on prevention as there is approximately a 20-year delay between UV damage and BCC.
Avoid chronic direct sun exposure and especially overexposure (sun burn)
Treatment of BCC
Depends on location, size, tumor variant, patient’s concerns.
Completely remove the tumour to prevent reoccurrence at a later date.
Electrodesiccation (cure rate 92-96%)
Complete excision (preferred for non-facial, well-defined nodules; cure rate 90% at 5 years)
cryosurgery
Mohs surgery
Topical imiquimoid 5% for superficial BCC
What is THE most common cutaneous malignancy?
BCC
Is BCC dangerous?
It is neither life-threatening or trivial. Needs to be dealt with but slow moving
Does skin become thinner or thicker as we age?
Thinner
The dermis thins, producing translucent, paper-thin quality that is more susceptible to tearing.
Where does squamous cell carcinoma originate from?
From the epidermal keratinocytes.
Cutaneous invasive squamous cell carcinoma (SCC) generally arises within a actinic keratosis or within SCC in situ.
Where can squamous cell carcinoma develop?
Head, neck, trunk, extremities, oral mucosa, periungual skin, and anogenital areas.
Involvement of other areas, in particular the lower legs and anogenital region, is more common in people with darkly pigmented skin.
True or false-HPV virus is often related to most SCC in genital regions?
True!
Name some body locations where SCC is known to be most aggressive.
Tumors arising on the ear, preauricular surfaces, or at mucocutaneous interfaces (ie, lips, genitalia, and perianal area) tend to be more aggressive, with rates of metastasis estimated to range from 10 to 30 percent.