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CMT-uno > Dermatology 2 > Flashcards

Dermatology 2 Flashcards

1
Q

Psoriasis

General

A

Chronic, immune-mediated disease with predominantly skin and joint manifestations.
Affects approximately 2% of the US population
Age of onset: 2 peaks
Ages 20-30 and ages 50-60
Strong genetic component with about 30% of patients having a first-degree relative with the disease

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2
Q

Psoriasis

Pathophysiology

A

Hyperproliferative state resulting in thick skin and excess scale
Skin proliferation is caused by cytokine release from immune cells
Exacerbation by environmental factors

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3
Q
A

Psoriasis

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4
Q

Psoriasis

Types and signs/phenom

A

Plaque - well-demarcated scaly, erythematous patches, papules, and plaques with overlying silvery-white scale
Most common form accounting for 80-90% of cases

Auspitz sign - bleeding after scale removal

Koebner phenomenon - lesions are induced by trauma to skin.

Inverse/Flexural
Guttate
Erythrodermic
Pustular

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5
Q

Psoriasis

important Hx questions

4

A

Are you taking any of these medications: systemic steroids, beta blockers, lithium, NSAIDs, antimalarials, interferons
Joint pain present?
Present in approximately 30% of patients and can lead to joint destruction if not appropriately managed.

Any cardiovascular risk factors?
Patients with psoriasis are at increased risk for cardiovascular disease

Any changes in your nails?
Can see nail pitting, onycholysis, subungual hyperkeratosis, and oil drop sign

Tobacco use? Alcohol consumption?
Both are risk factors and can contribute to symptoms

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6
Q
A

psoriasis

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7
Q

psoriasis

Topical Tx

A
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8
Q

Seborrheic dermatitis

general

A

Chronic, recurrent form of dermatitis occurring in areas rich with sebaceous glands.

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9
Q

Seborrheic dermatitis

Pathophysiology:

A

unclear
Increase sebaceous gland activity + hypersensitivity reaction to Malassezia furfur
Increase incidence in fall and winter months and with stress.
More pronounced in patients with neurologic diseases and HIV

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10
Q

Seborrheic dermatitis

Clinical Manifestations

A

Erythematous patches or plaques covered with fine whitish – yellow greasy scales.
Typically found on scalp, eyelids, beard, nasolabial folds, chest
May be associated with burning and pruritis

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11
Q

Seborrheic dermatitis

Dx

A

Clinical

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12
Q

Seborrheic dermatitis

Tx

A

Scalp: antifungal shampoo - Ketoconazole 2% or ciclopirox 1% BIW-TIW
+/- topical steroid if inflammation present
Face: topical antifungal agents +/- low potency topical steroid (hydrocortisone 2.5% cream qd-bid x 3-5 days)
Consider topical calcineurin inhibitor tacrolimus/pimecrolimus if needed for long term use.
Severe or refractory: oral antifungals

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13
Q

Pityriasis rosea

General

A

Etiology unknown - likely associated with viral infections
Common in older children and young adults
Increased incidence in spring and fall

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14
Q
A

Pityriasis rosea

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15
Q

Pityriasis rosea

Clin Man

A

Herald patch - solitary, salmon colored macular on the trunk has an initial lesion
Followed by a general exanthem 1 to 2 weeks later: smaller, very pruritic round to oval erythematous papules or thin plaques with a collarette of scale in a Christmas tree pattern
Confined to the trunk and proximal extremities

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16
Q

Pityriasis rosea

Tx

A

self limited, tends to resolve spontaneously in 4-6 weeks
Symptomatic treatment as needed
Topical corticosteroids – triamcinolone 0.1% cream QD-BID
Emollients

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17
Q
A

Pityriasis Rosea

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18
Q

Intertrigo

General

A

Inflammation of large skin folds - Inframammary fold, gluteal cleft, inguinal creases, and folds under pannus
Up to 10% of cases are complicated by Candida yeast colonization

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19
Q

Intertrigo

Clinical Manifestations

A

Classic symptom: burns more than it itches
Classic sign: satellite macules, papules, or pustules around erythema within the skin fold

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20
Q
A

Intertrigo

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21
Q

Intertrigo

Tx

A

Topical antifungals: miconazole, clotrimazole, econazole
Ketoconazole 2% cream bid to AA is most commonly prescribed in practice
Nystatin only works for Candida -typically results in incomplete resolution of symptoms
Topical anti-inflammatory: desonide ointment or hydrocortisone 1% ointment qd-bid for 1-2 weeks

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22
Q

Intertrigo

Prevention

A

Keep the affected area dry, clean, and cool
Over-the-counter antifungal powders can be used as daily maintenance

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23
Q

KOH exam

A

This is the easiest and most effective method used to diagnose fungal infection of the hair, skin, and nails
KOH dissolves keratinocytes making it easier to see fungal hyphae
Proper technique interpretation requires training and experience

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24
Q

KOH exam

Procedural steps:

A

-Clean and moisten in the skin, typically with an alcohol swab
-Collect scale with a 15 blade
-Scrape over the skin, allowing scale to accumulate on the center of a glass slide
-Place coverslip atop scale
-Add one to two drops of KOH
-Microscopy: scan at a low power to locate cells, then study in detail for hyphae at 10X

General :

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25
Q

Tinea Capitis

General

A

Fungal infection of the scalp, involving the skin and hair.

Typically Trichophyton tonsurans or Microsporum canis

Typically affects children and immunocompromised individuals
Increased incidence in African Americans

Spread by contact - either by an infected individual or by fomites

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26
Q

Tinea Capitis

Risk factor

A

Poor hygiene

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27
Q

Tinea capitis

Clinical Manifestations

A

Patches of alopecia with black dots or scaly patches of hair loss, commonly with erythema and pruritus.
Kerion: characterized by the development of an inflammatory boggy edematous plaque with pustules, thick crusting, and/or drainage, with suppurative folliculitis. Painful and tender. Can lead to scarring.

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28
Q

Tinea capitis

Dx

A

clinical, can be confirmed with KOH or Wood’s Lamp
Definitive diagnosis: fungal culture.

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29
Q

Tinea capitis

Tx

A

1st line: oral griseofulvin
2nd line: oral terbinafine

Additional treatments:
Anti-fungal shampoos at least twice weekly - treat all household members with too
Avoid sharing hats, brushes/combs, hair clippers

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30
Q
A

Tinea corporis

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31
Q

Tinea corporis

General

A

Refers to dermatophytosis of the skin, usually affecting the trunk and limbs
Pathogen: Trichophyton rubrum or microsporum
Transmission is due to direct contact
Very common in pre-adolescent age individuals

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32
Q

Tinea corporis

Clinical Manifestations

A

Solitary or multiple erythematous, scaly, circular or oval plaques or patches with central clearing and well-defined raised borders that spread outward
Often pruritic

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33
Q

Tinea corporis

Dx

A

KOH prep – best initial test
Fungal culture can be performed for definitive diagnosis

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34
Q

Tinea Corporis

Tx

A

Topical antifungal – clotrimazole, ketoconazole, butenafine, terbinafine, ciclopirox - typically bid application x 1-3weeks
Oral if refractory: terbinafine

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35
Q

Tinea manuum

General

A

A dermatophyte infection of one or both hands
Typically Trichophyton species
Results from contact with an infected individual; from another site of infection, particularly the feet or groin; or contact with a fomite

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36
Q

Tinea manuum

Risk Factors

A

Manual laborers
Hyperhidrosis
Existing hand dermatitis

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37
Q

Tinea manuum

Clinical Manifestations:

A

Erythematous, scaly patch or plaque with a raised, well-defined border
Slow extending area of peeling, xerosis and mild pruritus
May have increased skin markings or vesicles/bullae

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38
Q

Tinea manuum

Dx and Tx

A

Best initial test: KOH
Definitive diagnosis: fungal culture

Topical anti-fungal agents
Oral terbinafine if refractory

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39
Q

Tinea cruris

General

A

Superficial fungal infection of the groin or inner thigh
Typically caused by Trichophyton rubrum

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40
Q
A

Tinea cruris

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41
Q

Tinea cruris

Risk Factors

A

Males
Copious sweating
Immunocompromised
Existing fungal infection like tinea pedis

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42
Q

Tinea Cruris

Clinical Manifestations

A

Hallmark : pruritus, annular, well-demarcated, hyperpigmented patches or plaques with diffuse erythema
May have vesicles
Typically spares the scrotum

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43
Q

Tinea Cruris

Dx

A

clinical
Best initial test: KOH
Definitive diagnosis: fungal culture

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44
Q

tinea cruris

Tx

A

Topical anti-fungals - clotrimazole, butenafine, terbinafine, Ketoconazole, ciclopirox

General measures: desiccant powders, avoidance of tight-fitting clothing, put socks on before underwear

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45
Q

Tinea pedis

general

A

The most common fungal infection seen in developed countries
Most commonly caused by the fungus Trichophyton rubrum
Public showers, gyms are common sources of infection from direct contact and breaks in the skin

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46
Q

tinea pedis

Clinical Manifestations

A

Most common: Scaling and redness between the toes, maceration may be present
Look for “1 hand, 2 feet” syndrome
Moccasin: Chronic, hyperkeratotic type - sharply marginated scale, distributed along the lateral borders of the feet, heels, souls and is often associated with onychomycosis
Complete KOH prep to confirm diagnosis

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47
Q
A

tinea pedis

48
Q
A

tinea pedis

49
Q

tinea pedis

Tx

A

First line: allylamines - terbinafine, naftifine or butenafine cream qd-bid x 1-2 weeks
These are expensive!
Second line: imidazoles - clotrimazole, miconazole, Ketoconazole cream bid x 4-6 weeks
These are more commonly prescribed in practice!
Ciclopirox cream is my personal go-to treatment
Review hygiene practices with patients

50
Q

Tinea versicolor

general

A

Not caused by a dermatophyte - actually a colonization of a yeast, typically Malassezia furfur, that is a normal resident of the skin
Tends to onset during summer months

51
Q

Tinea versicolor

Morphology:

A

Called “versicolor “because it can be light, dark, or pink to tan

52
Q

Tinea versicolor

Clinical Manifestations
Diagnostic feature

A

Characterized by well-demarcated, hypopigmented or hyperpigmented macules, patches, occurring mostly on the trunk and arms
Macules will grow, coalesce and various shapes and sizes are obtained in an asymmetric distribution
Visible scale is often not present but when rubbed scale is readily seen this is a diagnostic feature of tinea versicolor

53
Q
A

Tinea versicolor

54
Q

Tinea versicolor

Dx

A

clinical, confirmed by KOH

55
Q

Tinea versicolor-furfur

Tx

3 kinds

A

Shampoos – apply for at least 5 minutes daily to the affected area

Imidazole creams: Ketoconazole cream, clotrimazole

Oral: fluconazole 300mg 1 dose per week x 2 weeks
Requires liver function studies due to risk of hepatotoxicity

56
Q

Sudden hair loss can be caused by

A

Alopecia areata
Telogen effluvium
Tinea capitis

57
Q

Gradual hair loss can be caused by

A

Androgenetic Alopecia
Trichotillomania

58
Q

Focal Hair loss agents

A

Alopecia areata
Androgenetic alopecia
Tinea capitis
Trichotillomania

59
Q

Diffuse hair loss agents

A

Telogen effluvium
Alopecia universalis
Iron deficiency anemia
Drug-induced hair loss

60
Q

Alopecia

PE

A

Examine the scalp for inflammation
Compare part width of the top of scalp with the back of scalp
Examine the entire scalp by making small parts in the hair
Note location and extent of hair thinning/loss
Perform a hair pull test and tug test

61
Q

Cicatrical baldness / Androgenetic Alopecia

General

A

An extremely common, genetically determined disorder characterized by the gradual conversion of terminal hairs into indeterminate and then finally vellus hairs

62
Q

Cicatrical baldness / Androgenetic Alopecia

Men vs women

A

Men: occurs in half of men by age 50
Frontal hairline recede, bitemporal thinning, then thinning on the top and crown

Women: occurs in half of women by their 80s
Unlike men, women tend to retain the shape of their hairline, but tend to go thin on the top and sides

63
Q

Androgenetic alopecia

Tx

A

Topical minoxidil 5% foam daily to the affected area
Reassure patients that it will take 6 to 12 months to see improvement or halt progression of hair loss
Oral finasteride or dustasteride daily

64
Q
A

Cicatrical baldness / Androgenetic Alopecia

65
Q
A

Androgenetic alopecia

66
Q

Telogen effluvium

general

A

Telogen effluvium results in faster cycling of the hair and loss of telogen hairs at the root
Often triggered by major stress to the body - think illnesses requiring hospitalization, pregnancy, surgery, significant mental stressors.
Usually resolves within 6 to 12 months of onset
Lasts longer for some people especially those with subtle changes in hormone levels, use of retinoids, cortisol, ferritin, vitamin D3, beta blockers, and general anesthetics as these are involved in hair cycle regulation

67
Q

Telogen effluvium

lab work up

A

Labs: TSH, T4, CBC, iron studies, vitamin D, possibly RPR

68
Q

what is the most common cause of female Telogen effluvium

A

Iron deficiency

69
Q

Telogen effluvium

Tx

A

Reassurance is the mainstay of treatment if there is no underlying cause as determined by labs
Tips for practice: most dermatology providers will recommend multivitamin supplementation and topical minoxidil to help stabilize hair loss if onset is relatively recent

70
Q

Alopecia areata

general

A

An autoimmune attack on hair follicles by lymphocytes - the hairs will fall out in well-defined patches
Associated with other autoimmune disorders, most commonly thyroid disease
Unpredictable course, but usually results without treatment in about six months
Regrowth can start with thin or white hairs

Focal and rapid

71
Q

Alopecia areata

lab work up

A

consider Thyroid panel

bc often associated with other autoimmune disorders like thyroid

72
Q

Alopecia areata

Tx

A

Intralesional triamcinolone injections 2.5 - 10 mg/mL every 4 to 6 weeks
ILK5 is most commonly used in practice
Topical steroids - start with potent or ultra-potent steroids
I recommend betamethasone valerate 0.01% foam or betamethasone dipropionate 0.05% lotion daily
Topical minoxidil 5% foam
If extensive - refer to dermatology

73
Q
A

Trichotillomania

74
Q

Trichotillomania

general and ClinMan

A

Caused by forceful pulling and removal of the hair
Clinical Manifestations
Different lengths of hair present within the patch
May also have black dots from short hairs
Lack scale or inflammation

75
Q

Trichotillomania

Tx

A

Screen for anxiety and depression
Behavioral interventions including habit reversal, self monitoring, competing reaction training, relaxation training, psychotherapy, hypnosis

Medical therapy: SSRIs - fluoxetine, sertraline, fluvoxamine

76
Q

Cherry angioma

general

A

A benign lesion formed due to abnormal mature capillary proliferation
Most commonly seen in middle-aged and older adults

77
Q

Cherry angioma

Clinical Manifestations

A

Cherry red to purple papules that may be flat topped or dome shaped
Blanch with pressure
Most commonly seen on the trunk
Tend to bleed profusely if they are traumatized

78
Q

Cherry angioma

DX and Tx

A

Diagnosis : clinical
Treatment: observation
Can be removed for cosmetic reasons with electrocauterization or laser therapy

79
Q
A

cherry angioma

80
Q
A

Pyogenic granuloma

81
Q

Pyogenic granuloma

General

A

Benign vascular tumor of the skin or mucous membranes, characterized by rapid growth and friable surface
Most common in children and young adults
Seen after hormonal changes, such as pregnancy, or after the initiation of new medication or chemotherapy

82
Q

Pyogenic granuloma

Clinical Manifestations

A

Solitary glistening, friable, bright red rapidly-growing nodule or papule that often bleeds after minor trauma or ulcerates
Found in arms, hands, legs or at sites of skin trauma

83
Q

Pyogenic granuloma

Dx and Tx

A

Diagnosis: biopsy
Treatment:
Excision with wound closure or curettage followed by electrocautery

84
Q
A

Kaposi Sarcoma

85
Q

Kaposi Sarcoma

general

A

Vascular cancer associated with Herpes virus 8 infection
Most commonly seen in immunosuppressed patients - HIV
Cutaneous KS typically seen on lower extremities, face, oral mucosa, genitalia

86
Q

Kaposi Sarcoma

Clin Man

A

Painless, non-pruritic pink, brown, erythematous or violaceous macules, papules or plaque-like nodules

87
Q

Kaposi Sarcoma

Dx and Tx

A

Diagnosis: biopsy
Management: refer to oncology
Chemotherapy, radiation
HIV- Antiretroviral therapy

88
Q

Stasis dermatitis

general

A

Inflammatory skin changes associated with chronic venous insufficiency

89
Q

Stasis dermatitis

Clin Man

A

Erythematous to brownish or dark purple hyperpigmented patches or plaques with eczematous features (scale, pruritis, weeping erosions and crusting)
Leg edema, increased leg circumference, variscosities are common - pulses are maintained

90
Q

Stasis dermatitis

Tx

A

management of underlying venous insufficiency
General measures: leg elevation, compression stockings, exercise
Gentle cleansing
Acute lesions: topical corticosteroids
Severe or refractory: oral prednisone

91
Q
A

Stasis dermatitis

92
Q
A

Stasis dermatitis

93
Q

Decubitus Ulcer

general

A

Pressure ulcer

Ulcers resulting from vertical pressure.
Commonly seen on bony prominences – sacrum, calcaneus, ischium

94
Q

Decubitus Ulcer

Risk Factors

A

Elderly, immobilization, incontinence

95
Q
A

Decubitus ulcer

96
Q

Decubitus ulcer

stage 1 manifestation and tx

A

superficial, nonblanchable erythematous macule

preventive measures, wound protection

97
Q

Decubitus ulcer

stage 2 manifestation and tx

A

epidermal damage extending into the dermis. Resembles a bulla or abrasion

maintain a moist wound environment – hydrocolloids or hydrogels

98
Q

Decubitus ulcer

stage 3 manifestation and tx

A

Full thickness loss of the skin.
May extend into the subcutaneous layer

Wound cleansing, maintain a moist wound environment, debridement of necrotic tissue, and treatment of wound infection if necessary

99
Q

Decubitus ulcer

stage 4 manifestation and tx

A

Deepest. Extends beyond the fascia, into the muscle, tendon, or bone

Wound cleansing, maintain a moist wound environment, debridement of necrotic tissue, and treatment of wound infection if necessary

100
Q
A

Pyoderma gangrenosum

101
Q

Pyoderma gangrenosum

general

A

An auto-inflammatory ulcerative process mediated by an influx of neutrophils into the dermis
Typically triggered by trauma, surgical debridement, or attempts to graft an area

102
Q

Pyoderma gangrenosum

often misdiagnosed as

A

misdiagnosed as a spider bite or an infection and debridement occurs it will worsen the condition

103
Q

Pyoderma gangrenosum

associated with

A

Can be associated with inflammatory bowel disease, rheumatoid arthritis, hematologic conditions, arthritis, and malignancy

104
Q

Pyoderma gangrenosum

Clin Man

A

Begins as a small pustules that breaks down and rapidly expands forming an ulcer with an undermined violaceous border - tends to have a rapid progression
Satellite alterations may merge with the central larger ulcer
Can occur anywhere on the body
Can be very painful

105
Q

Pyoderma gangrenosum

Tx

A

refer to Dermatology - this is a DERMATOLOGIC EMERGENCY
Topical: Superpotent steroids, tacrolimus
Systemic: steroids, cyclosporine, tacrolimus, cellcept, thalidomide, TNF-inhibitors

106
Q

Drug eruptions

general

A

Acute or subacute adverse cutaneous reactions to a medicine
Most are hypersensitivity reactions
Majority or self-limited the offending drug is discontinued.

107
Q

drug eruptions

triggers

A

Antigen from foods, insect bites, environmental, exercise induced, and infections

108
Q

type 1 drug eruption

A

IgE-mediated

e.g. Urticaria, angioedema

slide 57 ppt2

109
Q

drug eruption

Morbilliform Drug Eruption

A

Most commonly occurs 5 to 14 days after initiation of a new medication or within one to two days in previously sensitized individuals
Type 4 T-cell mediated hypersensitivity reaction
Common medication: penicillin, sulfas, NSAIDs, allopurinol, anticonvulsants
(SAPAN)

110
Q

Morbilliform Drug Eruption
Clinical Manifestations

A

Characterized by erythematous macules or small papules after initiation of a medication
Generalized distribution that typically coalesce to form plaques, primarily involving the trunk and proximal extremities
May have mild systemic symptoms including low-grade fever, pruritus

111
Q

Morbilliform Drug Eruption

Tx

A

Stop attending medication
Oral antihistamines, +/- short course oral corticosteroids

112
Q
A

Morbilliform Drug Eruption

113
Q
A

Vitiligo

114
Q

Vitiligo

General

A

An acquired, chronic, depigmenting disorder of the skin, in which melanocytes are progressively lost
It is widely accepted that vitiligo is a result of autoimmune destruction of melanocytes
Appears in all races, all ages with ages 20-25 years most commonly affected, and both men and women appear to be equally affected
A familial component is present as more than 20 to 30% of affected individuals report vitiligo in a first or second-degree relative

115
Q

vitiligo

is associated with

A

Associated with several other disease states
Rheumatoid arthritis, insulin-dependent diabetes, B12 deficiency, SLE, alopecia areata, Addison disease, and other autoimmune dermatological conditions

116
Q

Vitiligo

Clin Man

A

Most common: complete loss of pigment in a single or multiple macules or patches of the skin with characteristic chalky or milky white coloration
Typically asymptomatic, but can be pruritic
Well defined with convex borders
Small patches may coalesce together merging into more complex shapes
Typically found in the sun exposed areas or in areas prone to repetitive trauma

117
Q

vitiligo

Tx

A

Topical potent corticosteroids have mixed results
New Janus Kinase inhibitor: Ruxolitinib (Opzelura) just FDA approved!

CMT-uno (54 decks)

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