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NUNP547 Older Adult Theory > Week 11: Derm > Flashcards

Week 11: Derm Flashcards

1
Q

Any sore that does not heal within _______ weeks should be examined for the possibility of skin cancer.

A

Four

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2
Q

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?

A

Asymmetry
Border irregularity
Color (esp. black, blue)
Diameter >6mm
Evolving

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3
Q

What kind of things would you teach your patient to look for when screening for BCC?

A

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)

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4
Q

What kind of things would you teach your patient to look for when screening for Actinic Keratoses?

A

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)

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5
Q

What kind of things would you teach your patient to look for when screening for Squamous Cell Carcinoma?

A

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)

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6
Q

What kind of things would you teach your patient to look for when screening for Bowels disease? What is Bowen’s disease?

A

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)

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7
Q

True or False: Experts haven’t recommended for or against routine skin cancer screening for adults at normal risk

A

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.

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8
Q

Some guidelines (Canadian cancer society) suggest screening for skin cancer in high risk populations. How is screening done?

A

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.

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9
Q

Some guidelines suggest screening for skin cancer in high risk populations. What makes a patient high risk?

A

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)

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10
Q

When prescribing a topical steroid medication, what factors must the provider consider?

A

Anatomic site
Patient preference
Rash attributes
Vehicle attributes

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11
Q

Which anatomic site would require a higher potency steroid- an acral site or an intertriginous area? Why?

A

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.

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12
Q

What is the best steroid vehicle (i.e., lotion, cream, ointment, etc.) is best used on hair bearing skin?

A

Gels, lotions, shampoo, oil, foam

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13
Q

How does patient preference dictate vehicle?

A

Patient may be unwilling to use greasy cream- avoid ointment

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14
Q

What kinds of rash require a higher potency steroid?

A

-Thick, scaly skin
-Lichenified skin
-severe psoriasis
-rashes on palms, soles, scalp
-hyperkeratotic lesions (i.e., hyperkeratotic eczema)
-lichen planus/ scelrosus/ simplex

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15
Q

There are 7 “groups” of steroid potency. What group is the highest potency? Lowest?

A

Group 1= ULTRA high potency
Group 2, 3= high potency
Group 4,5= mid potency
Group 6,7= low potency

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16
Q

True or false: The vehicle by which a steroid is applied affects potency.

A

True!
Ointments are more potency compared with other vehicles.

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17
Q

True or false: The vehicle by which a steroid is applied can contribute to skin irritation

A

True- alcohol based solutions can be irritating on inflammed skin
Propylene glycol (found in many topicals) can sometimes cause irritant contact dermatitis

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18
Q

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

A

Answer: B
Ultra high potency steroids should be limited to daily or BID.

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19
Q

How long will you instruct Jeremy to use his ultra high potency steroid for?

A

Less than 2-4 weeks
You can follow with a less potent agent if needed

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20
Q

What kind of adverse effects are we concerned about when using a topical steroid?

A

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

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21
Q

Rank from least to most occlusive:
Cream
Lotion
Ointment

A

Least: lotion
intermediate: cream
Most: ointment

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22
Q

What body areas would a lotion be good for?

A

axillae, groin
hair areas
acute weeping lesions
large areas
*may cause stinging, dryness

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23
Q

What body areas would a cream be good for

A

non acute/ wet lesions
intertriginous areas
cosmetically acceptable
does not hydrate as much as ointment

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24
Q

What body area would an ointment be good for?

A

Palms, soles
Anything with a dry/ scaly/ hyperkeratinized lesion

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25
Q

What is the best steroid of potency to use in the elderly?

A

Group 6 or 7 (low potency)

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26
Q

How frequently can you apply a low potency steroid?

A

BID- QID

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27
Q

True or false- It is better to start with a less potent steroid, and if the lesion does not respond adequately, increase potency.

A

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.

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28
Q

Can you apply a steroid on eyelids?

A

yep but better make it a low potency (group 7) one!
beware risk of glaucoma, cataracts

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29
Q

Can you apply a steroid on the scrotum?

A

Yep! Again, group 6 or 7. Only slightly less absorptive than the eyelids.

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30
Q

Can you treat a patient with a topical steroid when they are taking an oral steroid?

A

Yes

I.e. lupus discoid lesions won’t resolve with oral steroid therapy and need topical steroid added

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31
Q

True or false: Healthy skin is a better barrier/ metabolizes the drug more than diseased skin, so as skin disease improves, absorption decreases substantially

A

True!

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32
Q

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?

A

Reconsider your diagnosis. Both fungal and bacterial infections are made worse when treated with topical corticosteroids.

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33
Q

True or false- the patient should continue to apply steroid cream for at least 1 week after the skin lesion has cleared

A

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.

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34
Q

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

A

c
(rx files)

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35
Q

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

A

c
(rx files)

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36
Q

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

a
(rx files)

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37
Q

You diagnose Steve with psoriasis. What strength of steroid do you prescribe?

A

b
(rx files)

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38
Q

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

A

c

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39
Q

What is psoriasis?

A

Chronic, inflammatory, immune mediated skin disorder with genetic base and environmental triggers

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40
Q

Describe the epidemiology of psoriasis

A

-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,

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41
Q

What condition are associated with psoriasis?

A

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)

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42
Q

What are the subtypes of psoriasis?

A

Plaque
Guttate
Pustular
Erythrodermic
Inverse (intertriginous)

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43
Q

Describe the stereotypic psoriasis lesion

A

Pink to red papules and plaques with white/ silvery scale
Pruritic
Well- demarcated

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44
Q

What is Auspitz sign?

A

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!

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45
Q

What nail findings are highly suggestive of psoriasis?

A

PITTING, nail whitening, friable nails, yellow spots, splinter hemorrhage, thickened nail beds, separation of distal end of nail plate from nail bed (onycholysis

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46
Q

Describe plaque psoriasis

A
  • 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
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47
Q

Describe guttate psoriasis

A
  • 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.
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48
Q

Describe erythrodermic psoriasis

A

-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

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49
Q

Describe pustular psoriasis

A

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

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50
Q

Describe inverse psoriasis

A

Erythematous plaques on flexural surfaces like axillae, inframmary folds, gluteal folds, inguinal folds; may be macerated/ moist

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51
Q

What is koebner phenomenon?

A

Development of skin disease in sites of truama. Occurs in psoriasis (and other disease like lichen planus, vitiligo)

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52
Q

Psoriatic arthritis is common in patients with psoriasis. What is the clinical presentation of psoriatic arthritis?

A

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

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53
Q

How is psoriasis diagnosed?

A

Usually clinically
Skin biopsy for challenging cases (not usually necessary)
No labs to confirm
Genetic testing not used

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54
Q

What medications are used in the tx of psoriasis?

A

Emollients- reduce fissure formation
Topical corticosteroids- reduce scaling, thickness, redness
Topical vitamin D analogues (calcipotriene)- reduce keratinocyte hyperproliferation
Others- retinoids, calcineurin inhibitors

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55
Q

What potency of steroid is used in treatment of psoriasis?

A

Generally, a higher potency
Up To Date suggests Group 1 for short term control (except on face/ intertriginous regions)

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56
Q

What other treatments can be used in psoriasis?

A

Generally for moderate (3-10%) to severe (10% +) disease
Phototherapy
Systemic therapy- NSAIDs, methotrexate (severe disease), cyclosporin, acitretin (retinoid), DMARDs (TNF alpha inhibitors)

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57
Q

Name this lesion: common benign tumor of the epidermis formed from keratinocytes

A

Seborrheic keratosis

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58
Q

Where are SK’s found?

A

Scalp, face, neck, trunk of older adult
Usually on sun exposed regions of body
Spares palms and soles

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59
Q

How would you describe an SK?

A

Yellow or brown greasy “stuck on” macules or papules “smashed smartie”

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60
Q

What is the epidemiology of SKs?

A

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

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61
Q

How are SK’s diagnosed?

A

Clinical diagnosis
Biopsy only if uncertain

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62
Q

Ddx for SKs?

A

malignant melanoma (lentigo, nodular)
Melanocytic nevi
Pigmented BCC
Solar lentigo
Spreading pigmented AK

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63
Q

Management of SKs?

A

Only if desired for cosmetic purposes
Cryotherapy, electrodessication, shave excision
Follow up not needed unless looking infected
Management- sun protection

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64
Q

True or false: Seborrheic keratoses can be pre-malignant

A

False

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65
Q

What is the Leser- Trelat phenomenon? What can it indicate?

A

Sudden appearance of new SK’s (multiple lesions >5-10) may indicate internal malignancy

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66
Q

What is bullous pemphigoid?

A

autoimmune, subepidermal blistering disease

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67
Q

Who does bullous pemphigoid affect?

A

-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

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68
Q

Describe the patho of bullous pemphigoid

A

Autoimmune
Results from attack on basement membrane of epidermis by IgG antibodies and activated T lymphocytes

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69
Q

What is the clinical presentation of bullous pemphigoid?

A

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

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70
Q

How to diagnosed bullous pemphigoid?

A

Often diagnosis is made clinically and confirmed with skin biopsy.

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71
Q

What is the treatment for bullous pemphigoid?

A

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)

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72
Q

What is notalgia paresthetica

A

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

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73
Q

Patho of notalgia paresthetica

A

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

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74
Q

S&S of notalgia paresthetica

A

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

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75
Q

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)

A

Scratch marks

Hyperpigmentation

Hypopigmentation

Lichen simplex chronicus

Scarring

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76
Q

Diagnosis of notalgia paresthetica. What might you see on imaging?

A

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

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77
Q

What is onychomycosis

A

fungal infection of the nail

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78
Q

Risk factors for onychomycosis

A

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

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79
Q

What usually causes onychomycosis?

A

Dermatophytes, particularly Trichophyton rubrum, are the most common causes of onychomycosis

Rarely yeast (eg, Candida albicans) and nondermatophyte molds

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80
Q

What is the main concern for a patient with DM or who is immunocompromised and has onychomycosis?

A

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

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81
Q

S&S of onychomycosis

A

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)

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82
Q

How do we diagnosis onychomycosis?

A

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

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83
Q

DO we need to treat onychomycosis in everyone? When might we treat?

A

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

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84
Q

T/F Treatment failure and disease recurrence are common in onychomycosis

A

True - ensure you tell your patients this before initiating treatment!

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85
Q

How can topical urea be helpful in treatment of onychomycosis

A

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

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86
Q

How do we usually treat onychomycosis?
What are some non prescription options to try for mild infections?

A

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!

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87
Q

When are topical antifungals helpful for treatment of onychomycosis?

A

Recommended for early/mild or limited cases, or if systemic tx contraindicated

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88
Q

Advantages of topical antifungals

A

negligible risk for serious adverse effects and drug interactions compared with systemic antifungal therapy

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89
Q

Disadvantages of topical antifungals

A

Often require long (many month) treatment, often not effective, recurrence common when stop tx

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90
Q

How long is the typical course of topical antifungals for onychomycosis

A

48 weeks

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91
Q

What can a patient do to possibly increase the efficacy of their topical antifungal?

A

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

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92
Q

What medication is typically used for systemic tx of onychomycosis?

A

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).

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93
Q

Possible severe A/E of terbinafine?

A

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.

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94
Q

Common side effects of terbinafine

A

mild and transient headache, gastrointestinal symptoms (e.g., nausea, diarrhea, dyspepsia, abdominal pain), viral infections and skin rashes

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95
Q

Contraindications to terbinafine use

A

Hypersensitivity to terbinafine or any component of the formulation; chronic or active hepatic disease. Use in caution if renal impairment!

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96
Q

What monitoring is required for terbinafine use?

A

Obtain baseline and mid-treatment serum aminotransferase level

(and CBC seems to be sometimes recommended)

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97
Q

What is a digital mucus (myxoid) cyst? Where are they located? Is it a true cyst?

A

= 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.

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98
Q

Will a myxoid cyst usually be plentiful or solitary? What colour?
Changes to nails associated?

A

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.

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99
Q

Tx of myxoid cyst.
Does it recur?

A

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.

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100
Q
A
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101
Q

What is Sebaceous Hyperplasia

A

= benign overgrowths of normal sebaceous oil glands that are usually found on the face

A form of benign hair follicle tumor

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102
Q

What is the typical anatomic distribution of sebaceous hyperplasia?

A

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).

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103
Q

Describe the appearance of sebaceous hyperplasia?

A

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

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104
Q

Who is more prone to sebaceous hyperplasia?

A

usually iodopathic

cyclosporine has been reported to cause diffuse lesions

Most often affects older people

More common in immunocompromised

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105
Q

Tx of sebaceous hyperplasia

A

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.

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106
Q

What is BCC
Where does it typically occur?

A

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

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107
Q

What is the main risk factor for BCC?

A

UV light -> mutation of tumor suppression genes and proto-oncogenes

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108
Q

Does BCC grow fast? Is it likely to met?

A

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

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109
Q

Describe BCC

A

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.

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110
Q

Is prevention of BCC possible? How do we do it?

A

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)

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111
Q

Treatment of BCC

A

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

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112
Q

What is THE most common cutaneous malignancy?

A

BCC

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113
Q

Is BCC dangerous?

A

It is neither life-threatening or trivial. Needs to be dealt with but slow moving

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114
Q

Does skin become thinner or thicker as we age?

A

Thinner

The dermis thins, producing translucent, paper-thin quality that is more susceptible to tearing.

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115
Q

Where does squamous cell carcinoma originate from?

A

From the epidermal keratinocytes.
Cutaneous invasive squamous cell carcinoma (SCC) generally arises within a actinic keratosis or within SCC in situ.

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116
Q

Where can squamous cell carcinoma develop?

A

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.

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117
Q

True or false-HPV virus is often related to most SCC in genital regions?

A

True!

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118
Q

Name some body locations where SCC is known to be most aggressive.

A

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.

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119
Q

Name some risk factors of squamous cell carcinoma.

A

Unprotected exposure to ultraviolet (UV) radiation from the sun or tanning beds.

Weakened immune system due to illness or certain immunosuppressive medications.

History of skin cancer including basal cell carcinoma (BCC).

Age over 50: Most SCCs appear in people over age 50.
Fair skin: People with fair skin are at an increased risk for SCC.

Gender: Men are more likely to develop SCC.
Sun-sensitive conditions including xeroderma pigmentosum.

Chronic infections and skin inflammation from burns, scars and other conditions.

Skin precancers including actinic keratosis.

History of human papilloma virus (HPV)

120
Q

What is Bowen’s disease?

A

Bowen’s disease or squamous cell carcinoma in situ usually presents as one or more slowly enlarging erythematous scaly plaques.

Histologically, atypical keratinocytes are found throughout the epidermis without invasion through the basement membrane.

121
Q

In SCC, is the upper lip or lower lip most commonly affected?

A

Lip cancer predominantly affects the lower lip. It particularly occurs in males chronically exposed to the sun and is more frequent in smokers.

122
Q

How does an SCC lesion look like (in fancy terms)?

A

SCC presents as an irregular keratinous nodule or a firm erythematous plaque, and frequently ulcerates.

Histologically, atypical keratinocytes proliferate within the dermis.

123
Q

What is a keratoacanthoma?

A

Keratoacanthomas are keratocytic epithelial tumors that clinically and histologically resemble squamous cell carcinoma (SCC).
It is controversial whether keratoacanthomas represent a subtype of well-differentiated cSCC or a separate entity.
Keratoacanthomas are usually found on actinically damaged skin.
Lesions typically exhibit rapid initial growth, manifesting as dome-shaped or crateriform nodules with a central keratotic core that develop within a few weeks.

124
Q

What is a Verrucous carcinoma?

A

Verrucous carcinoma is a rare variant of cSCC that presents with well-defined, exophytic, cauliflower-like growths that resemble large warts.

Most common locations are in the penis, scrotum, perianal region, oral mucosa, plantar foot.

125
Q

True or False-SCC can occur in the oral mucosa.

A

True!
Oral SCC usually presents as an ulcer, nodule, or indurated plaque involving the oral cavity.

The floor of the mouth and lateral or ventral tongue are the most common sites for these tumors.

Lesions may arise in sites of erythroplakia (premalignant, persistent, red patches in the oral cavity) or leukoplakia (oral, persistent, white plaques.

Oral SCC is often associated with a history of tobacco or heavy alcohol use.

126
Q

What is Marjolin’s ulcer?

A

Marjolin’s ulcer” is a term used to describe a rare type of cSCC arising in sites of chronic wounds or scars [13-15]. The malignant transformation is usually slow, with an average latency time of approximately 30 years.

initially present as an ulceration that fails to heal; nodules may develop as the lesion progresses. Other clinical signs include rolled or everted wound margins, excessive granulation tissue, rapid increase in size, and bleeding on touch.

Has poor prognosis.

126
Q

What are common treatments for SCC in situ or Bowen’s disease?

A

Squamous cell carcinoma in situ may be treated surgically. Other treatments include cryotherapy, 5-fluorouracil cream, imiquimod cream or photodynamic therapy (PDT).

127
Q

What is Lymphoepithelioma-like carcinoma of the skin?

A

A very rare, indolent, malignant skin tumor of epithelial origin, considered a variant of cSCC.

As a flesh-colored, firm nodule or plaque, most often located in the head and neck region.

Histopathologically, it shows islands of poorly differentiated epithelial cells with a dense lymphoid infiltrate, resembling undifferentiated nasopharyngeal carcinoma.

127
Q

What are common treatments for invasive SCC?

A

Invasive SCC is nearly always treated surgically. Wide margins are advisable for poorly differentiated or anaplastic tumours.
Some tumours are treated by radiotherapy, particularly when surgery is difficult or incomplete.

128
Q

What is stasis dermatitis.

A

A common, inflammatory dermatosis of the lower extremities occurring in patients with chronic venous insufficiency, often in association with varicose veins, dependent chronic edema, hyperpigmentation, lipodermatosclerosis, and ulcerations.

A late manifestation of chronic venous disease

129
Q

Name some risk factors of stasis dermatitis.

A

Age, family history of venous disease, female sex, standing occupation, obesity, and history of deep vein thrombosis. Heart failure and hypertension are aggravating factors.

130
Q

Describe the clinical presentation of stasis dermatitis?

A

Presents with erythematous, scaling, and eczematous patches or plaques on chronically edematous legs.

The medial ankle is most frequently and severely involved, although the skin changes may extend up to the knee and down to the foot.

Pruritus is variable but, when present, results in lichenification from chronic scratching or rubbing.

Hyperpigmentation due to dermal hemosiderin deposition and scaling are predominant features in chronic forms.

131
Q

What are some complications of stasis dermatitis?

A

-Higher frequency of contact dermatitis

-Superinfection-Staphylococcus aureus and Streptococcus pyogenes are the most frequent causes of superficial (impetiginization) or deep (cellulitis and erysipelas) superinfection of stasis dermatitis.

-Lipodermatosclerosis-The chronic phase is characterized by hyperpigmented and indurated skin that constricts the ankle region, giving the legs an appearance of an inverted champagne bottle.

-Acroangiodermatitis- “pseudo-Kaposi sarcoma,” is a rare, reactive, vasoproliferative disorder resembling Kaposi sarcoma that occurs on the lower limbs as a result of vascular hyperplasia secondary to hypostasis and elevated venous pressure

132
Q

What are some measures to help manage stasis dermatitis?

A

Pt can undertake lifestyle changes aimed at decreasing venous hypertension, reducing edema, and preventing venous ulcers. These include exercise, frequent walks, avoiding prolonged standing, leg elevation whenever possible, and weight loss.

Gentle skin cleansing with mild, fragrance-free liquid cleansers and frequent use of bland emollients are indicated for the symptomatic treatment of skin dryness and pruritus associated with mild or chronic stasis dermatitis.

Compression bandages or stockings

133
Q

Jerry comes in to see you because his legs are very itchy, are very erythematous and weepy. He needs a topical cortisone.

What potency would you give to help manage pruritis due to stasis dermatitis?

A

UptoDate suggests high or mid potency (group 3 and 4).
Can be applied to the affected skin once or twice daily for one to two weeks.

134
Q

What is rosacea, onset, and what are risk factors to having it?

A

Rosacea is a chronic inflammatory skin condition predominantly affecting the central face and most often starts between the age of 30–60 years, but can occur at any age.

Rosacea is common and is characterised by persistent facial redness. It typically has a relapsing and remitting course, with symptoms controlled by lifestyle measures, general skin care, medications, and procedural interventions.

Although rosacea can affect anyone, it is more common in with skin types most susceptible to sunburn (eg, individuals with lightly pigmented skin or skin phototypes I or II).

Women>men, but some studies suggests equal predisposition between sexes.

Adults males more predisposed to phymatous changes.

135
Q

Define these different terms used to describe lesion distribution:
Annular
Dermatomal
Grouped
Linear
Reticular

A

Annular - ringlike
Dermatomal - confined to a dermatome and abruptly stops at the midline
Grouped - clustered lesions (herpetiform)
Linear - arranged in a line (suggestive of external cause)
Reticular - netlike or meshlike (suggesting a process affecting the cutaneous vascular netowork)

136
Q

Differentiate a macule and a papule

A

Both macules and papules are <1cm in diameter. Papules are solid and raised, macules are flat (ie. just a color change).

If you close your eyes and you cannot feel a <1cm lesion’s presence then it is a macule

137
Q

What do you call primary lesions >1cm when they are raised? What about when they are flat ?

A

Plaque - Raised lesion > 1cm
Patch - flat, > 1 cm (a color change)

138
Q

Differentiate a nodule, pustule and cyst

A

Nodule - solid elevation of skin > 1 cm, usually extended into deeper skin layers (connective tissue/deep dermis/subcutis) (ex. cysts, lipomas, fibromas)

Pustule - small circumscribed raised lesion that contains pus (ex. bacterial infections, folliculitis)

Cyst - sac-like nodule that usually has an epithelial lining containing fluid or other debris

139
Q

Does skin become more moist or dry as we age?

A

Drier

Epidermal cells contain less moisture and change shape

Atrophy of eccrine, apocrine, and sebaceous glands causes dry skin.

140
Q

T/F our body’s ability to repair damage to the skin remains unchanged as we get older

A

False - DNA repair of damaged skin decreases

141
Q

Why does our skin become more susceptible to infection and irritation as we age?

A

The dermis becomes more permeable and less able to clear substances, so those substances accumulate and cause irritation.

The barrier function of the stratum corneum is reduced, increasing risk for injury and infection.

The significantly decreased number of Langerhans cells reduces the skin’s immune response.

142
Q

Wound healing decreases because of decreased ________ in both men and women, decreased blood flow, and slower rate of basal cell and fibroblast turnover

A

estrogen

143
Q

Why does the colour of our skin and hair change as we age?

A

There are fewer melanocytes; pigmentation becomes irregular, giving decreased protection from ultraviolet radiation and leading to greying of hair.

144
Q

Sensation in our skin _____ (increases/decreases) as we age

A

Decreases

Pressure and touch receptors and free nerve endings decrease in number, causing reduced sensory perception.

145
Q

Why are older adults less able to protect themselves from hypo/hyperthermia

A

With compromised temperature regulation, loss of cutaneous vasomotion, and decreased eccrine sweat production, there is an increased risk for heat stroke and hypothermia

146
Q

How do nails change as we age?

A

The nail plate thins, and nails are more brittle

147
Q

Health promotion stategies for skin health as we age?

A

Sun protection, sun protection, sun protection!

Avoid the sun when ultraviolet light is strongest (e.g., 10 a.m. to 3 p.m.), avoid sun tanning beds, seek shade, use sunscreen preparations, especially those containing ingredients such as PABA (para-aminobenzoic acid), and wear protective clothing

Do total body skin examinations routinely

148
Q

Is Actinic Keratosis (AK) lesions considered precancerous?

A

Yes

Up to 10% of AK, if left untreated, will develop into squamous cell carcinoma. Research has shown that people with AK have an increased risk of developing other types of skin cancer, including BCC and melanoma.

149
Q

Describe AK using SCALDA or 4 point dermatological description.

A
  • Red, rough scaling lesions, that can sting or be pruritic. Located on sun-exposed areas such as the face, lips, ears, balding scalp, back of hand, forearm and leg, grouped/clustered.
    -Gritty texture on palpation is a helpful diagnostic clue.
150
Q

Which epidermal cells does AK occupy?

A

Keratinocytes

151
Q

T/F: AK likes women who have dark skin complexions?

A

False - Multiple lesions are common in males with fair skin.

152
Q

AK is found along other signs of chronic sun exposure. What other skin descriptors describe breakdown of sun exposed skin.

A

uneven pigmentation, atrophy or thinning, and telangiectasias

153
Q

How does AK initially present?

A

Poorly defined area of redness or telangiectasia.

154
Q

How does AK develop?

A

Over time, the lesion becomes more defined and develops a thin, adherent, yellowish, or transparent scale.
-at this stage, easier to palpate than observe
-discrete sandpaper-like change in skin texture associated with minimal erythema.
-Presents most commonly as a 2- to 6-mm, erythematous, flat, rough, gritty or scaly, pink-purple papule.
-With time, the adherent scale becomes progressively thicker and yellow in color.
- Retained scale may form an elongated keratinous structure or a cutaneous horn.

155
Q

Advanced AK can be difficult to distinguish from which carcinoma?

A

squamous cell carcinoma - biopsy is required

156
Q

What does spreading pigmented AK mean?

A

describes AK with fine reticulated pigmentation and minimal scaling; they may mimic a solar lentigo or melanoma in situ.

Lentigo maligna (melanoma in situ) appears as a pigmented patch and occurs most frequently on sun-damaged skin; it may be confused with a spreading pigmented AK, and thus a biopsy may be required to establish the correct diagnosis.

157
Q

What is Actinic Cheilitis?

A

sun-induced keratinocyte atypia of the lower lip.

158
Q

What does Actinic Cheilitis look like? and are we concerned?

A
  • There is focal crusting and scaling along with blurring of the vermilion border, which appears whitish or gray.
  • Actinic lesions in this location can be quite subtle clinically and behave aggressively.
  • Like its cutaneous counterpart, actinic cheilitis may progress to overt squamous cell carcinoma of the lip.
159
Q

What areas of the body are most concerning for metastasis when AK is located?

A

lesions that develop on the ear, the scalp, or at the vermilion border of the lip are more likely to metastasize to SCC, compared to other skin sites (monitor and treat aggressively).

160
Q

How is AK treated?

A

AK are predominantly treated by cryotherapy.

They may also be treated with the following:

  • Keratolytic creams containing 10% urea, 2 to 4% salicylic acid or 10 to 15% lactic acid to reduce scaliness
  • 2 to 4 weeks of 5-fluorouracil cream applied once or twice daily
  • 4 to 16 weeks of imiquimod cream applied two or three times weekly
  • Photodynamic therapy
    • Patients with significant diffuse photodamage or multiple and recurrent lesions present difficult treatment problems.
  • Ingenol mebutate gel applied for 2-3 days
  • 3 months of topical diclofenac in hyaluran gel applied twice daily
  • Adequate sun avoidance with sun-protective clothing and sunscreens should be encouraged to limit further damage.
161
Q

How often do you follow up with a pt with AK?

A

The patient with multiple AK requires at least annual follow-up, if not more often for some patients who have more extensive sun damage.

  • Visible or detectable lesions represent a fraction of the total number of atypical keratinocytes actually present.
    • Most of the atypia are scattered within sun-damaged skin and below the level of clinical detection. Most certainly will develop more clinically apparent AK lesions over time.
  • It is well documented that patients with numerous AK have an increased risk for developing SCC over time.
162
Q

Patho description of chronic, pruritic, inflammatory skin condition: Epidermal barrier dysfunction, alterations in cell-mediated immune responses, IgE-mediated hypersensitivity, and environmental factors causes skin to be inflammed and irritated. What could this be?

A

Atopic Dermatitis (Eczema)

163
Q

What does Atopic mean?

A

sensitivity to allergens such as environmental (extreme weather changes, dust, pollen etc), animals (dogs, cats), food (dairy, wheat, nuts, fish), irritants (detergents, soaps, creams etc), and stress

164
Q

What is the difference between acute and chronic eczema?

A

Acute eczema is characterized by intensely pruritic, erythematous papules and vesicles with exudation and crusting, whereas subacute or chronic lesions present as dry, scaly, or excoriated erythematous papules.

165
Q

What are key descriptors of chronic eczema?

A

Skin thickening from chronic scratching (lichenification) and fissuring may develop over time

166
Q

Where is eczema normally noted on older adults?

A

flexure folds (elbows, wrists, and knees), hands, feet, eyes, face
*sparing groin and axillary

167
Q

What other specific skin conditions are associated features of atopic dermatitis?

A

vitiligo and alopecia areata.

168
Q

What is nummular eczema?

A

scaly, red, coin-shaped patches and plaques that often favors the lower extremities

169
Q

T/F: Person inherits atopic dermatitis or contact dermatitis?

A

True for atopic, not
contact dermatitis. contact occurs following exposure to an external factor that triggers a reaction

170
Q

T/F: Nummular eczema is common in children?

A

False - common in adults

171
Q

What are the differentials of Eczema?

A

Scabies, seborrheic dematitis, cutaneous t-cell lymphoma, psoriasis

172
Q

What should be considered in new onset eczema?

A

Scabies

173
Q

What is a good nonpharm treatment to help manage eczema?|

A

Moisturizers

■ Moisturizers work best when applied a few hours after topical steroids.
■ Application should continue for days or weeks after the inflammation has cleared.
■ Moisturizers are most effective when rubbed in well and applied directly after the skin is patted dry following a shower.

Controlling pruritis: tepid baths and emollients, wet dressings to soothe, habit reversal training (scratching), CBT.

  • Stress management and helping the client get restful, restorative sleep are important.
174
Q

Depending on location of flare up, what pharm treatment is recommended to help manage eczema?

A

Mild: low potency topical corticosteroid ointment (Hydrocortisone 2.5%) 1-2 times daily for up to 2 weeks.

Moderate: Medium to high potency topical corticosteroid (Mometasone 0.1%) 1-2 times daily for up to 2 weeks.

Topical calcineurin inhibitors (Tacrolimus 0.03%-0.1%) for moderate to severe eczema not controlled w/ topical steroid

Severe: High potency topical corticosteroids (Clobetasol 0.025-0.05%) 1-2 times a day for up to 2 weeks. Consider biologic agents, phototherapy, allergen immunotherapy

Topical anti-inflammatory therapy, oral antihistamines.

175
Q

What is intertrigo or intertriginous dermatitis?

A

common inflammatory condition of the skin folds characterized by moist erythema, malodor, weeping, pruritis and tenderness

176
Q

How does intertrigo develop?

A

from moisture and friction associated with an absence of air circulation in deep skin folds.
-Friction between adjacent skin surfaces leads to epidermal inflammation.
- Moisture and sweat accumulation further macerate the skin layers.

In addition, candidal or bacterial infection may initiate or aggravate intertrigo.

177
Q

Who is at risk for developing intertrigo?

A

*affects people of all ages, from infancy to advanced age.
*Most common in bedridden or debilitated older adults and infants because of immobility and minimal aeration of intertriginous areas

178
Q

What are the predisposing factors?

A

obesity, immunodeficiency (e.g., diabetes, HIV, prednisone), hot humid weather, poor hygiene, incontinence, tight-fitting clothing, hyperhidrosis (excessive sweating), frequent wet work involving hands (dishwashing), and use of topical steroids.

179
Q

What is a more common infection with intertrigo?

A

Candidal infection

180
Q

What is a hallmark clinical finding with intertrigo?

A

moist, red or red-brown, beefy, homogenous patch within skin folds.

181
Q

What is the most common site for intertrigo?

A

Groin is most comon site.

Other sites: axilla, inframammary skin, umbilicus, neck folds in infants, under the pannus and finger/toe web spaces

182
Q

Is there any discomfort with intertrigo?

A

Yes! Even though subtle onset, pts c/o pruritus, burning, tingling, and pain in the skin folds and flexural surfaces.

183
Q

What happens if intertrigo is not treated?

A

The erythematous patch can develop erosions, macerations, fissures, crust, and weeping from the site.

184
Q

How does bacterial intertrigo present?

A

Bacterial intertrigo tends to weep and is an intensely erythematous and a potentially tender lesion.

185
Q

How does candidal infection present?

A

satellite papules and pustules

186
Q

Whats the non pharm treatment for intertrigo?

A

Remove causative factors:
- Minimize moisture and friction in skin folds
- Treatment of hyperhidrosis
- Weight loss if overweight
- Treatment of diabetes

  • Daily cleansing of skin folds with a mild cleanser and dryer (use a hair dryer on a cool setting)
  • Aeration of area when feasible
  • Daily use of drying powders
  • Use of absorbent material or clothing such as cotton or merino wool to separate skin folds
  • Barrier cream in areas that may contact urine/stool
187
Q

Pharmaceutical treatment for intertrigo?

A

Intertrigo infected by bacteria should be treated with topical (eg, mupirocin) or oral antibiotics (eg, penicillin); fungal infection treat with antifungal;
*1-2 times daily for 2-4wks

Low-potency topical steroids only if pruritic.
*Hydrocortisone 2.5% twice/day for one week, once/week for one week and then every second day for one week

188
Q

Differentiate a vesicle and a bulla

A

Vesicle - small circumscribed elevation of epidermis containing serous fluid, <1cm (small blisters) (ex. herpes infections, acute allergic contact dermatitis)

Bulla - circumscribed elevation of epidermis containing serous fluid, >1cm (large blister) (ex. autoimmune bullous disease such as pemphigus vulgaris, bullous pemphigoid

188
Q

What is another word for “old age spot” or “senile freckle”?

A

Solar Lentigo

189
Q

Describe a wheal. What are other names for this presentation?

A

Circumscribed, raised lesion of dermal edema (edematous papule or plaque) also known as hives or urticaria, typically last <24 hours

189
Q

Describe Solar Lentigo?

A

Common, benign, brown macules occurring on sun-exposed skin in whites and some Asians.

190
Q

Differentiate petechiae, purpura and ecchymoses

A

Petechiae- non-blanchable punctate foci of hemorrhage

Purpura- non-blanchable, raised and palpable

Ecchymoses - non-blanchable larger areas of purpura

190
Q

Is Solar lentigo the same as freckles?

A

No. Freckles appear in childhood and occur as an autosomal dominant trait.
*They are usually confined to the face, arms, and upper trunk; numerous and darken in response to sun exposure.
*red, tan, light brown macules (1–2 mm) with sharply defined borders.
*Freckles appear in early summer and usually fade by early winter.

Solar Lentigo increase in number and size with advancing age
*indicates sun damage d/t UVR
*2- to 20-mm oval macules, seen on a background of sun-damaged skin.
*skin-coloured, tan to dark brown or black; sometimes with scales
*persist year-round.
*most common: face, neck, upper chest, arms, back of hands

191
Q

Moving on to secondary features/lesions..

Differentiate erosions and ulceration

A

Erosions - loss of epidermis

Ulceration - loss of epidermis and part of the dermis

191
Q

Describe Solar Lentigo?

A

*2- to 20-mm oval macules, seen on a background of sun-damaged skin (years of sun exposure)
*skin-coloured, tan to dark brown or black; sometimes with scales
*persist year-round.
*most common: face, neck, upper chest, arms, back of hands

192
Q

Differentiate the secondary features of scale and crust

A

Scale - excess accumulation of “dead skin”/fragments of the stratum corneum

Crust - adherent, dried serum, exudate or blood on the skin (scab)

192
Q

Which complexion (fair or dark skinned) is more prone to solar lentigo?

A

Both - occur in light and dark skin
*more numerous in fair-skinned

193
Q

Differentiate the secondary features of lichenification and excoriation

A

Lichenification - thickening of the epidermis with accentuation of the normal skin lines (usually due to chronic rubbing/scratching)

Excoriation - Loss of epidermal integrity due to scratching

193
Q

What is solar lentigo hard to differentiate from?

A

melanoma

194
Q

This secondary feature is due to thinning of the skin (in the epidermis, dermis or sc fat)

A

atrophy

194
Q

Which skin cells are proliferated in solar lentigo?

A

melonocytes and accumulation of melanin within the skin cells (keratinocytes).

195
Q

Define the secondary features of scars and keloids

A

permanent fibrotic changes that result from damage extending into the dermis. Keloids extend beyond the borders of the original defect

195
Q

What the differentials for solar lentigo?

A

*Flat seborrheic keratoses
*Spreading pigmented actinic keratosis
*Lentigo maligna
- Lentigo maligna is an early form of melanoma in which the malignant cells are confined to the tissue of origin, the epidermis, hence it is often reported as [‘in situ’ melanoma]. It occurs in sun damaged skin so is generally found on the face or neck, particularly the nose and cheek. It grows slowly in diameter over 5 to 20 years or longer. [Dermnetz.org]
*Junctional nevus
*When numerous lentigines are present, consider the possibility of an associated syndrome, such as Peutz−Jeghers, LEOPARD, or NAME (LAMB)

196
Q

What does erythema indicate?

A

indicates vascular dilation, blanchable red or pink hue in skin - not a color

196
Q

How do we treat solar lentigo?

A

Monitor for any change.
Stable lesions do not require treatment

Cosmetic reasons there are creams, peels, and light cryosurgery (may cause depigmentation) that can help reduce pigmentation

Preventative measures include minimizing sun exposure and use of sunscreens, but this needs to start early in life.

197
Q

Which skin cancer is the worst skin cacner?

A

Melanoma!

197
Q

What am I: uncommon inflammatory disorder, producing ivory-white indurated plaques and scars in the genital skin

A

Lichen Sclerosus

198
Q

To differentiate benign lesions from melanoma use ABCDE, which stands for..

A

ABCDE: Asymmetry, borders, color, diameter, evolving

Asymmetry - of one side of the mole compared to the other

Border - irregularity - especially if ragged, notched or blurred

Color- variations - more than 2 colors, especially blue-black, white (loss of pigment due to regression), or red (inflammatory reaction to abnormal cells)

Diameter ≥ 6 mm (approx. the size of a pencil eraser)

Evolving - changing rapidly in size, symptoms, or morphology

198
Q

When is lichen sclerosus more common? Which sex does it favor more?

A

Lichen sclerosus can occur at any age but is more common in women older than 60 years and prepubertal girls between 8 and 13 years of age.
Women: Men 5/10:1

199
Q

What is the ugly duckling sign?

A

A way to detect suspicious lesions in a person with multiple nevi. A skin lesion that looks different from those surrounding it may be an important finding.

199
Q

What are the risk factors of Lichen sclerosus?

A

*family history (in 12%)
*associated with other autoimmune conditions such as thyroid disease, alopecia areata, pernicious anemia, vitiligo

200
Q

What other technique can aid in lesion identification in a trained clinician?

A

Dermoscopy - should be performed on all suspicious pigmented lesions as a first-line diagnostic support modality

200
Q

Is Lichen sclerosus an acute condition?

A

No.
chronic, progressive, relapsing

201
Q

How is melanoma definitively diagnosed?

A

Histopathological diagnosis.

UptoDate recommends: A complete full-thickness excisional biopsy of suspicious lesions with 1 to 3 mm margin of normal skin and extending to a depth to encompass the thickest portion of the lesion should be performed whenever possible. Partial incisional biopsy may be acceptable for very large lesions or for certain sites, including the face, palm or sole, ear, distal digit, or subungual lesions

201
Q

Since Lichen Sclerosus is uncommon, are we concerned then?

A

Yes, can evolve overtime into SCC - especiallly vulvar lichen sclerosus
*risk for SCC (2.1% after 5 years, 3.3% after 10 years, 6.7% after 20 years)

202
Q

Aside from ABCDE and ugly duckling, what are other important criteria for referral to derm for suspected melanoma?

A

A change in a long-standing mole; the development of a new, persistent skin lesion after puberty; a new, pigmented band in a nail; and any lesion growing under the nail

202
Q

What does lichen sclerosus look like?

A
  • ivory-white, flat topped, slightly raised papules with a faint-pink rim that coalesce into small oval plaques with a dull or glistening, smooth, white, atrophic, wrinkled surface.

might read: “polygonal papules and porcelain-white plaques, erosions and various degrees of sclerosus”.

203
Q

T/F: The majority of melanomas are initially detected by health care providers

A

False - the majority of melanomas are initially detected by patients themselves, but the melanomas detected by clinicians are thinner than those identified by patients

203
Q

In vulvar lichen Sclerosus, where is it more commonly located?

A

Mostly common to labia minora and majora, but may extend over the perineum (encircles the vagina) and around the anus in a keyhole fashion or hourglass shape

204
Q

What causes rosacea?

A

Is multifactorial:

Genetic susceptibility

Altered microbiome of the skin and gut

Dysregulation of the immune response may lead to excessive inflammation, vasodilation, lymphatic dilatation, and angiogenesis.

Neurocutaneous mechanisms.

Impaired skin barrier.

Abnormalities of the innate immune system

204
Q

where is lichen sclerosus on men?

A

Penile lesions (balanitis xerotica obliterans) favor the glans and coronal sulcus but may extend to the shaft.

205
Q

What are the cutaneous features of rosacea?

A

Transient recurrent erythema, ie, flushing

Persistent centrofacial erythema

Telangiectasia

Facial skin other than in the nasal alar region

Lid margin telangiectases, conjunctival injection, and ocular irritation

Together often termed erythematotelangiectatic rosacea

Inflammatory papules and pustules (papulopustular)

Phymatous changes

Thickening of the skin due to hyperplasia/fibrosis of the sebaceous glands of the face. Most common area affected is the nose (termed rhinophyma)

burning or stinging sensations

cutaneous edema, and dryness

Refer to opthalmolohy if ocular manifestations are indentified.

205
Q

What are the symptoms r/t lichen sclerosus?

A

vulvar pruritus, burning, dyspareunia, and painful defecation (lead to constipation) which may have significantly detrimental effects on function and sexual health.
- interfere with daily activities and sleep

206
Q

In people with darker skin tones, what other clues should you look for when evaluating for rosacea?

A

Facial stinging or burning sensations, flushing, edema, dry-appearing skin, and papules and pustules, can aid with diagnosis of rosacea in patients with highly pigmented skin.

206
Q

T/F Lichen sclerosus only occurs anogenital?

A

False - can occur anywhere on the skin surface. Can also occur torso (front/back)

207
Q

How is rosacea diagnosed?

A

Usually a clinical diagnosis. Skin biopsy may be used in uncertainty.

**one diagnostic criterion or two major criteria to be fulfilled.

Diagnostic criteria:

-Persistent centrofacial erythema associated with periodic intensification by potential trigger factors
-Phymatous changes.

Major criteria

-(must occur in centrofacial distribution)
-Flushing/transient centrofacial erythema
-Inflammatory papules and pustules
-Telangiectasia — visible blood vessels (excluding nasal alar telangiectases, which are common in adults)
-Ocular rosacea (lid margin telangiectasia, blepharitis, keratitis/conjunctivitis/sclerokeratitis/anterior uveitis).

Minor features

-Burning sensation of the skin
-Stinging sensation of the skin
-Oedema
-Dry sensation of the skin

207
Q

What happens to the anogenital skin overtime with Lichen Sclerosus?

A

vulvar architecture is obliterated d/t longstanding erythema and edema; Mucocutaneous atrophy may lead to development of hemorrhagic bullae and erosions;

Men:
- Surface trauma leads to focal subepidermal hemorrhages and erosions.
- Atrophy leads to phimosis of the foreskin with pain on retraction of the foreskin or erection.
- The urethral meatus may become stenotic, and malignant degeneration may occur.

211
Q

What are some non-pharmacological recommendations for people with rosacea?

A

Encourage patients to record a symptom diary to aid the identification of triggers:

Common triggers include:
spicy food, hot/cold temperatures (hot baths), exercise, sun exposure, cosmetic products, medications (those that cause vasodilation), alcohol, fruits and vegetables, dairy, marinated meat products
Avoid the triggers identified.

General skincare advice:
-Moisturise frequently
-Use gentle over-the-counter cleansers
-Mild, synthetic detergent-based cleansers rather than traditional soaps due to risk of irritation
-Use physical sunscreens (ie, zinc oxide/titanium oxide) with SPF ≥ 30
-Avoid exfoliants
-Avoid alcohol-based topical products
-Avoid use of topical steroids as they may aggravate the condition
-Cosmetics with a green tint are useful to minimise the appearance of redness.

212
Q

Name some pharmacology treatments for rosacea.

A

Treatment depends on the individual’s cutaneous features.

*Transient erythema (flushing)
-Alpha-adrenergic agonists (topical brimonidine, topical oxymetazoline) — they are often used infrequently for special occasions only, as persistent use may result in rebound flushing on discontinuation
-Oral beta-blockers (carvedilol)
-Oral clonidine may reduce flushing

*Persistent erythema
-Alpha-adrenergic agonists (topical brimonidine, topical oxymetazoline, as above)
-Intense pulsed light therapy
-Vascular laser

*Inflammatory papules/pustules
Topical azelaic acid (for mild/moderate only)
Topical ivermectin
Topical metronidazole (for mild/moderate only)
Topical erythromycin
Oral tetracyclines (oxytetracycline, lymecycline, doxycycline)
Oral macrolides (erythromycin, azithromycin)
Oral metronidazole
Oral isotretinoin often at low dose (for refractory disease only)

*Telangiectasia
Electrodesiccation
Intense pulsed light therapy
Vascular laser
Neurogenic rosacea
Gabapentin
Amitriptyline
Oral beta-adrenergic blockers
Consideration of endoscopic sympathectomy

*Phyma
If clinically inflamed: doxycycline, isotretinoin
If clinically non-inflamed: physical modalities to remove excess tissue and reshape the structures (eg, ablative CO2 laser, erbium laser, radiofrequency, surgical debulking).

*Ocular rosacea-
General management
Increase dietary intake of omega-3 fatty acids
Warm compresses
Gentle eyelash/eyelid cleansing to express sebum trapped in the meibomian glands

First-line medical management (by opthalmology)
If mild-moderate: topical azithromycin/topical calcineurin inhibitors
If severe: azithromycin, doxycycline.

223
Q

Jessie, a 75 year-old patient, comes to the clinic to show you a a new skin lesion on her abdomen. On inspection, you a see a solitary firm red-purple papule, 0.5cm. You see other similar lesions scattered throughout her torso. She denies them being itchy, painful, or bleeding. What is your likely diagnosis?

A

A cherry angioma.

226
Q

What are cherry angiomas and who are prone to get them?

A

It is a true capillary haemangioma.

The angioma is composed of venules in a thickened papillary dermis. Collagen bundles may be prominent between the lobules.

Commonly diagnosed clinically. Benign.

Cherry angiomas markedly increase in number from about the age of 40, so it has been estimated that 75% of people over 75 years of age have them. But younger people can get them.

No differences in sex or race.
May be familial.

228
Q

Jessie would like some cherry angiomas removed, as they sometimes get caught when removing or putting on tops. What are some options?

A

Cryotherapy, electrosurgery, vascular laser.

230
Q

When would a cherry angioma be of concern?

A

It should be biopsied if you believe it may be something else, such as a nodular melanoma or amelanotic melanoma.

231
Q

What are the main complications we want to monitor for when managing someone with Lichen Sclerosis?

A

dyspareunia, urinary obstruction, constipation, secondary infection related to ulceration, secondary infection (candidiasis) as a consequence of treatment, steroid use, squamous cell carcinoma.

232
Q

If we are suspicious of SCC, what can we do?

A

punch biopsy

233
Q

What are the differentials of lichen sclerosus?

A
  • Morphea and lichen sclerosus are similar on the skin (rarely both conditions may be present in some patients, although the presence of mucosal lesions favors a single diagnosis of lichen sclerosus)
  • Lichen planus and pemphigus vulgaris (especially for erosive mucosal lesions)
  • Lichen simplex chronicus (vulvar involvement from scratching)
  • Allergic contact dermatitis (typically fragrance allergy from personal hygiene products or steroid allergy from prior treatment)
  • Extramammary Paget’s disease (should be considered for chronic anogenital itching with erosions)
  • Steroid-induced atrophy (can be confused with lichen sclerosus)
234
Q

What is lichen planus?

A

Lichen planus (LP) is an inflammatory disorder (T-cell mediated) of the skin and mucous membranes with no known cause. It appears as pruritic, violaceous papules and plaques most commonly found on the wrists, lower back, and ankles., but can be found anywhere.

The prevailing theory is that exposure to an exogenous agent such as a virus, drug, or contact allergen causes alteration of epidermal self-antigens and activation of cytotoxic CD8+ T cells.

235
Q

How can we treat lichen sclerous

A

Clobetasol propionate 0.05% ointment is effective for vaginal and penile disease in adults

0.05% clobetasol 1-2 times daily until remission achieved (typically 2-3 months) or daily for 4 weeks, every second day for 4 weeks and then twice/week for 4 weeks

236
Q

Who is prone to developing lichen planus?

A

Women > men at ratio of 1.5:1

Most cases develop between the ages of 30 and 60.

Maybe familial

237
Q

What maintenance therapy recommended for Lichen Sclerosus?

A

Yes:
topical corticosteroids 2-3 times/week even if asymptomatic (clobetasol or mometasone) adjust potency based on hyperkeratosis or presence of corticosteroid-induced atrophy

238
Q

What else can we tell our patients for Lichen Sclerosus?

A
  • Patients should used gentle cleansers such as Cetaphil and moisturize with a light moisturizer.
  • Women should avoid fragranced feminine hygiene products and scented toilet paper.
  • Ensure patients know which specific body surfaces to apply corticosteroids to
  • Teach monthly self-exam for signs of malignancy (hyperkeratotic plaques, erosions or ulcers that fail to improve with treatment within 2 weeks)

Longterm Follow up

239
Q

Name the 6 Ps of Lichen Planus.

A

6 Ps: purple, polygonal, planar, pruritic papules, and plaques.

240
Q

Describe the morphology of the most common type of lichen planus.

A

Lesions may have a shiny surface covered in fine white lines known as Wickham striae and are firm on palpation.
They may be seen as a few individual lesions, found scattered widely, grouped in plaques, or arranged in annular, linear, or actinic (sun-exposed) patterns.

Isomorphic response (i.e., Koebner phenomenon) can be seen in LP wherein new lesions arise in lines where scratching occurs, just as is seen in psoriasis.

The most common areas of involvement include the flexor wrists, dorsal hands, lower back, ankles, and shins.
Frequently a grayish-brown hyperpigmentation can be found after lesions resolve due to deposition of melanin in the superficial dermis

Other less common features:
Hypertrophic lichen planus can be a scaly and pruritic rash.

Atrophic lichen planus is a rare annular variant with an atrophic centre.

Reticular presents as asymptomatic white, lacy lines often seen on the bilateral buccal mucosa

Annular lichen planus describes the development of violaceous plaques with central clearing often involving penis, scrotum, and intertriginous areas.

Size ranges from pinpoint to larger than a centimetre.

241
Q

Pearls of Lichen Sclerosus!

A
  • Chronic vulvar itching in the absence of infection should raise the suspicion of lichen sclerosus.
  • Consider lichen sclerosus to be a precancerous condition requiring regular follow-up and biopsy of areas suspicious for malignant change.
242
Q

What may be some contributing factors to lichen planus?

A

Contributing factors to lichen planus may include:

Genetic predisposition

Physical and emotional stress

Injury to the skin; lichen planus often appears where the skin has been scratched or after surgery (koebnerisation)

Localised skin disease such as herpes zoster

Systemic viral infection, such as hepatitis C (which might modify self-antigens on the surface of basal keratinocytes)

Contact allergy, such as to metal fillings in oral lichen planus (rare) and colour photographic developers

Drugs; gold, quinine, quinidine, and others can cause a lichenoid rash.

Vit D deficiency

243
Q

Which subtype of LP is most common?

A

LP that involves the mucosal surfaces and frequently is the presenting site.

It is most commonly seen in the mouth but can be found on the lips, esophagus, glans penis, vulva, or vagina.

Other subtypes of Lichen Planus are:
Cutaneous lichen planus
Mucosal lichen planus
Lichen planopilaris
Lichen planus of the nails
Lichen planus pigmentosus
Lichenoid drug eruption.

244
Q

What are some complications of lichen planus?

A

Longstanding erosive lichen planus can result in true squamous cell carcinoma, most often in the mouth, vulva, or penis.

This should be suspected if there is an enlarging nodule or an ulcer with thickened edges.

Oesophageal lichen planus can cause dysphagia, strictures, and possibly squamous cell carcinoma.

245
Q

How is lichen planus diagnosed.

A

Is is diagnosed clinically, unless it is atypical or to look for cancer then you can do a biopsy.

246
Q

Lichen planus has many differentials. Name a few.

A

Psoriasis, lichen simplex, pityarisis rosea, tinea, lichen sclerosis , leukoplakia, candidiasis, bullous pemphigoid, SCC, lupus, onychomycosis, subacute cutaneous lupus erythematosus, discoid lupus erythematosus, pityriasis rosea, secondary syphilis

247
Q

What are some non-pharm interventions for lichen planus.

A

Avoid soaps and shower gels that will exacerbate scaling.
Use emollients regularly.
Sedating antihistamines may help troublesome nocturnal itch (caution in older adults).

248
Q

Jerry has lichen planus. Jerry asks you if this will ever go away.

A

Lichen planus can have a chronic remitting and relapsing course.
Cutaneous lichen planus tends to clear within a couple of years in most people, but post-inflammatory pigmentation may take years to subside.
Other subtypes may take longer or cause permanent scarring.

249
Q

Describe pharmacologic treatment for LP.

A

Goals of care is to manage pruritis.

Local treatments for the symptomatic cutaneous or mucosal disease are:

Potent topical corticosteroids (including steroid impregnated tape)
Topical calcineurin inhibitors, tacrolimus ointment, and pimecrolimus cream
Topical retinoids
Intralesional steroid injections.

Systemic treatment for widespread lichen planus or severe local disease often includes a 1- to 3-month course of systemic steroids (eg, prednisone), while commencing another agent from the following list:

Acitretin
Hydroxychloroquine
Methotrexate
Azathioprine
Mycophenolate mofetil
Phototherapy.
Antibiotics

Adalimubab has been used for oral LP.

250
Q

What are risk factors for melanoma?

A

Total nevus count above 50 and/or presence of large (atypical/dysplastic) nevi

Personal history of skin cancer

Immunosuppression - particularly chronic use of immunosuppressive medications such as those used by organ transplant recipients.

Sun-sensitive people and those with the red hair phenotype (light skin, red or blond hair, high-density freckling, light eye color)

Family history of melanoma

251
Q

What is suggested for melanoma screening for those at high risk?

A

Screening involves a full-body skin examination performed yearly by a clinician who has had appropriate training in the identification of melanoma (clinician examination) as well as education for patients about melanoma risk factors and advice to alert their clinician if self-examination detects changing moles or other suspicious skin lesions

252
Q

What are the components of the 4-point dermatologic description in Ham’s?

A

1 - anatomic distribution
2 - configuration
3 - primary lesion and color
4 - secondary change if present

253
Q

What is seborrheic dermatitis?

A

Chronic relapsing form of dermatitis occurring in areas rich in sebaceous glands

254
Q

Where does seborrheic dermatitis most often occur?

A

Areas rich in sebaceous glands (scalp, face, upper trunk, intertriginous areas)

255
Q

What is another name for the mildest and most common form of seborrheic dermatitis?

A

Dandruff - diffuse fine scaliness of the scalp without underlying erythema

256
Q

How do more severe forms of seborrheic dermatitis present?

A

Severe forms present with inflamed, erythematous plaques covered with yellowish, greasy scales

257
Q

What is the patho of seborrheic dermatitis?

A

Not fully understood. Possibility that is hormonally dependant, has a fungal component, is neurogenic, or may reflect a nutritional deficiency. Possible association with Malassezia spp (yeast)

Currently considered an inflammatory disorder that probably results from dysfunction of sebaceous glands

258
Q

How is a diagnosis of seborrheic dermatitis established?

A

Usually clinically based on appearance and location of the lesions. Can differentiate histologically if presentation is unclear.

259
Q

T/F: Recurrence is common with seborrheic dermatitis

A

True. This is a chronic condition that often requires repeated treatment or long-term maintenance therapy.

260
Q

Outline treatment of mild seborrheic dermatitis in adults.

A

Topical antifungal 1-2 times daily for 4 weeks. If no improvement at 4 weeks, add a low potency topical steroid 1-2 times daily for up to 2 weeks.

If improvement continue topical antifungal 1-2 times weekly to prevent relapse.

If no improvement with above, switch to a topical calcineurin inhibitor (tacrolimus ointment)

261
Q

Outline treatment of moderate to severe seborrheic dermatitis in adults

A

Start with both low potency topical corticosteroid and topical antifungal 1-2 times daily for 2 weeks.

Continue maintenance therapy with topical antifungal or calcineurin inhibitor 1-2 times/week to prevent relapse.

Second line: topical calcineurin inhibitor

Third line: systemic antifungal

262
Q

Does treatment differ if the condition is on the scalp?

A

Yes.

Mild cases: antifungal shampoo 2-3 times weekly. If no improvement at 4 weeks add high-potency topical corticosteroids (foam, lotion, spray or shampoo) once daily for up to 4 weeks.
Continue antifungal shampoo 1-2 times weekly to prevent relapse

Moderate-severe cases: go straight to antifungal shampoo and corticosteroids.
Second line after 4 weeks - systemic antifungal

263
Q

What causes shingles ?

A

Herpes zoster/shingles is caused by the reactivation of the varicella zoster virus (the chicken pox virus)

264
Q

What are risk factors for herpes zoster?

A

Immunosuppression (HIV, steroids, transplants), old age (most important risk factor, begins ~50yrs), autoimmune disorders (IBD, RA), F>M, occasionally associated with hematologic malignancy

265
Q

What is the typical presentation of herpes zoster?

A

Unilateral vesicular rash & neuritis. Dermatomal distribution, rash does not cross the midline.

266
Q

What is the usual time course for varicella zoster?

A
  • Dermatomal eruption occurs 3-5 d after pain and paresthesia of that dermatome
  • Within several days, grouped vesicles or bullae are the predominant manifestation
  • Within three to four days, the rash becomes pustular
  • In immunocompetent hosts, the lesions crust by 7 to 10 days and are no longer considered infectious
  • Painful, post herpetic neuralgia can last months
267
Q

What is Hutchinson’s sign?

A

Shingles on the tip of the nose - signifies ocular involvement
- shingles in this area involves the nasociliary branch of the ophthalmic branch of the trigeminal nerve (V1). Dangerous

268
Q

T/F: Shingles is contagious

A

True - kind of, people with shingles can spread VZV to people who have never had the virus or been vaccinated and this can cause chicken pox.

269
Q

How is shingles diagnosed?

A

usually based on the clinical presentation (ie, unilateral, usually painful, vesicular eruption with a well-defined dermatomal distribution).

Testing is available is diagnostic is uncertain - PCR, direct fluorescent antibody testing and viral culture

270
Q

Antivirals may be helpful in promoting healing of skin lesions, lessening severity/duration of acute neuritis and decreasing incidence/severity of chronic pain/postherpetic neuralgia

What is the cut off for when treatment should be initiated?

A

Antivirals recommended within 72 hours of rash starting. Can also be of benefit after 72 hours if all vesicles have not yet crusted

271
Q

What is the typical treatment selected for shingles?

A

Valacyclovir 1000 mg TID for 7 days

272
Q

What medications are recommended for pain relief with shingles?

A

Offer NSAIDs and/or acetaminophen. If pain is severe may require short acting opioid analgesics such as oxycodone. If pain is severe despite short acting opioid, can consider 10-14 day taper of oral prednisone. Last line - drugs like gabapentin.

UTD suggests against the routine use of adjunctive therapies, such as gabapentin, tricyclic antidepressants, or glucocorticoids. The clinical benefit of these agents in reducing the risk of acute neuritis has not been clearly demonstrated and there are significant risks associated with these medications.

273
Q

The shingrix vaccine is a two-dose series. Who is recommended to get this vaccine? How are the doses spaced?

A

Adults 50 years old and up

Second dose repeated 2-6 months after first.

274
Q

List risk factors for pressure ulcers

A

Immobility – neuromuscular disorders, frailty, post-surgical immobility, ADL dependence, bed rest

Impaired oxygenation status – COPD, HF, anemia

Sensory loss – spinal cord injury, neuropathy, CVA

Poor nutrition – inadequate intake of nutrients, dehydration, food insecurity, enteral/parenteral nutrition

Medical devices – CPAP, splints/casts, tracheostomy devices, nasal cannulas

Moisture/Incontinence – excess moisture on skin/skin folds

Cognitive impairment – difficulty expressing pain/discomfort

Comorbidity/Illness – edema, peripheral vascular disease, renal/liver disease, cancer, diabetes, autoimmune disease (increases risk of skin fragility)

Advanced age – skin fragility and bony prominences

Medications – NSAIDS, anti-neoplastics, systemic corticosteroids, anticoagulants, vasopressors can predispose to skin breakdown

Palliative status

Lifestyle – smoking, substance use

275
Q

What are the three factors which contribute to a pressure-induced injury?

A

Pressure - pressure to tissue exceeds arteriolar pressure, delivery of oxygen and nutrients is compromised, resulting in tissue hypoxia

Friction/Shear - deeper tissues (muscles and subcutaneous fat) are pulled one direction while the dermis and epidermis remain fixed due to contact with an external surface

Moisture - Skin that is exposed to moisture (perspiration, feces, urine) has decreased mechanical strength and decreased stratum corneum stiffness

276
Q

How long can it take for irreversible tissue damage to occur?

A

As little as two hours

277
Q

How long does it take a pressure injury to heal?

A

Depending on the severity of injury, healing may take weeks to months. Wounds may also be classified as chronic, non-healable

278
Q

Staging of pressure ulcers is based on the NPIAP Pressure Injury Staging System. Describe a stage 1 pressure injury

A

Skin intact, non-blanchable erythema, remains after relief of pressure

279
Q

Staging of pressure ulcers is based on the NPIAP Pressure Injury Staging System. Describe a stage 2 pressure injury

A

Blister or other break in dermis with partial thickness skin loss, with or without infection, sc fat is not visible

280
Q

Staging of pressure ulcers is based on the NPIAP Pressure Injury Staging System. Describe a stage 3 pressure injury

A

Full-thickness skin loss, with or without infection, sc fat may be visible, undermining and tunneling may be present

281
Q

Staging of pressure ulcers is based on the NPIAP Pressure Injury Staging System. Describe a stage 4 pressure injury

A

Full-thickness skin and tissue loss. Exposed or directly palpable fascia, muscle, tendon, ligament, cartilage or bone. With or without infection. Often includes undermining and tunneling

282
Q

Staging of pressure ulcers is based on the NPIAP Pressure Injury Staging System. Describe an unstageable pressure injury

A

Full thickness skin and tissue loss. Base of the ulcer is covered by slough or eschar

283
Q

Staging of pressure ulcers is based on the NPIAP Pressure Injury Staging System. Describe a deep tissue pressure injury.

A

Localized persistent, non-blanchable, discolored, but intact skin or blood-filled blister. Potential for deep tissue damage.

284
Q

What are some complications of pressure injuries?

A

Soft-tissue infection, sepsis, osteomyelitis

285
Q

What are some universal approaches to pressure wound care regardless of stage?

A

Initiate/maintain pressure injury prevention strategies based on Braden score

Manage risk factors/comorbidities
- Diabetes, PAD, venous insufficiency, neuropathy, incontinence
- Encourage smoking cessation

Nutrition

Pain relief

Consider patient concerns and goals of care

Treat infection

286
Q

Describe the appropriate wound care for a stage 1 pressure injury

A
  • Monitor twice daily
  • Do not cover with a dressing
287
Q

Describe wound care for a stage 2 pressure injury

A
  • Protective dry gauze for intact blister
  • Consider debridement of devitalized blister tissue
  • Non-adherent contact layer for open area or hydrophilic paste dressing (eg. Triad)
  • Protect from contamination (urine/feces)
288
Q

Describe wound care for a stage 3 pressure injury

A
  • Debride soft/boggy slough or eschar using the most appropriate method (autolytic, mechanical, sharp, etc.)
  • Fill/pack dead spaces, tunneling, undermining
  • Protect from contamination
289
Q

Describe wound care for a stage 4 pressure injury

A
  • Debride soft/boggy slough or eschar using the most appropriate method (autolytic, mechanical, sharp, etc.)
  • Contact layer for exposed fascia, muscle, tendon, bone, ligament, cartilage
  • Fill/pack dead spaces, tunneling, undermining
  • Protect from contamination
290
Q

Wound care for eschar

A

-Dry, stable eschar: keep it dry; paint with 10% povidone iodine daily or Q2days; protect from moisture; leave OTA or dry dressing
- Soft, boggy eschar or slough: debride with appropriate method; fill/pack dead spaces, tunneling, undermining; protect with cover dressing; restage once wound bed exposed

NUNP547 Older Adult Theory (10 decks)

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