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Clin med 1 > Dermatology -Jones > Flashcards

Dermatology -Jones Flashcards

1
Q

Erysipelas effects which layers of the skin?

A

Upper dermis and superficial lymphatics

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2
Q

Cellulitis effects which layers of the skin?

A

Deeper dermis and subcutaneous fat

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3
Q

Abscesses effect which layers of the skin?

A

Upper and deeper dermis

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4
Q

Which skin/soft tissue infection is observed in middle-aged and older adults?

A

Cellulitis

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5
Q

Which microbe commonly causes erysipelas?

A

Beta-hemolytic streptococci

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6
Q

Which microbe commonly causes cellulitis?

A

Beta-hemolytic strep and staphylococcus aureus including MRSA

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7
Q

Which microbe commonly causes a skin abscess?

A

Staph aureus

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8
Q

Acute onset of sx, clear demarcation-butterfly involvement of face are manifestations of what?

A

Erysipelas

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9
Q

Localized sx developing over days, indolent course with less distinct borders is what?

A

Cellulitis

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10
Q

Cellulitis can present with or without

A

Purulence (pus)

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11
Q

Erysipelas is what

A

Nonpurulent (no pus)

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12
Q

A skin abscess is a collection of

A

Pus within the dermis of subq space

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13
Q

Furuncle

A

Skin abscess can develop via infection of hair follicle

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14
Q

Carbuncle

A

Multiple hair follicle infection-leading to skin abscess

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15
Q

Regional adenopathy and surrounding induration happen with what?

A

Skin abscess

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16
Q

Diagnosis of erysipelas

A

Raised above level of surrounding skin, clear demarcations

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17
Q

LRINEC Score

A

Laboratory Risk Indicator for Necrotizing Fasciitis

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18
Q

A LRINEC score above what can rule in NF

A

6

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19
Q

Some complications of soft tissue infections include

A

NF, Bacteremia and sepsis, osteomyelitis, septic joint

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20
Q

What empiric therapy is used in a moderate purulent soft tissue infection? (Furuncle, carbuncle, abscess)

A

TMP/SMX (Bactrim) or Doxycycline

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21
Q

What empiric therapy can be used for a severe purulent soft tissue infection?

A

Vancomycin, daptomycin, linezolid, televancin, or ceftaroline

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22
Q

What is the proper treatment of a mild nonpurulent soft tissue infection? (Cellulitis, erysipelas)

A

Oral Rx! Like penicillin, cephalosporin, dicloxacillin, or clindamycin

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23
Q

What is the treatment for a moderate nonpurulent soft tissue infection?

A

IV Rx! Penicillin, Ceftriaxone, cefazolin, or clindamycin

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24
Q

How do you treat a severe nonpurulent soft tissue infection?

A

Surgical inspection/debriedment along with empiric Rx (Vanco plus piperacillin/tazobactam)

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25
Q

What is found most frequently in children ages 2-5?

A

Impetigo

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26
Q

What is primary impetigo?

A

Direct bacterial invasion of normal skin

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27
Q

What is secondary impetigo?

A

Infection is at the site of skin trauma

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28
Q

The most common form of impetigo

A

Non-bullous

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29
Q

Papules progress to vesicles surrounded by erythema in what?

A

Non-bullous impetigo

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30
Q

The papules in non-bullous impetigo form into what?

A

They breakdown and form thick golden crusts

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31
Q

Bullous impetigo

A

Vesicles enlarge to form flaccid bullae with clear fluid, leaves brown crust

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32
Q

What is ecthyma?

A

Ulcerative form of impetigo

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33
Q

“Punched-out” ulcers covered with yellow crusts are from what?

A

Ecthyma

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34
Q

What microbe causes impetigo?

A

Staph aureus, occasionally beta-hemolytic strep A

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35
Q

Microbe causing bullous impetigo

A

S.aureus strain that cleaves the superficial skin layer

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36
Q

Microbe causing ecthyma?

A

Group A beta-hemolytic strep pyogenes

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37
Q

What topical therapy is used for limited non-bullous and bullous impetigo?

A

Mupirocin and Retapamulin

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38
Q

What oral therapy is used for extensive impetigo and ecthyma?

A

Dicloxacillin and Cephalexin

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39
Q

What are hives, welts, and wheals?

A

Urticaria

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40
Q

Urticaria can also be accompanied by what?

A

Angioedema

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41
Q

What is the duration of acute urticaria?

A

Less than 6 weeks

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42
Q

Chronic urticaria

A

Recurrent, with signs an symptoms recurring most days of the week for more than 6 weeks

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43
Q

Round oval vary in size 1 cm up to several

A

Urticaria

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44
Q

The angioedema in urticaria effects what parts of the body?

A

Lips, extremities, genitals

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45
Q

What mediates the reaction in urticaria?

A

Cutaneous mast cells in the superficial dermis

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46
Q

What is released by cutaneous mast cells in urticaria?

A

Histamine (itching) and vasodilator mediators (swelling)

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47
Q

What are some medications used to treat urticaria?

A 
H1 antihistamines (Diphenhydramine, chlopheniramine, hydroxyzine, cetirizine, loratadine, fexofenadine)
H2 antihistamines (Ranitidine, nizatidine, all end in -tidine)
Glucocorticoids (Prednisone)
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48
Q

A common benign soft-tissue neoplasm

A

Lipoma

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49
Q

What do lipomas consist of?

A

Mature fat cells, enclosed by a thin fibrous capsule

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50
Q

What is a benign soft tissue neoplasm that occurs mainly on the upper extremities and trunk?

A

Lipoma

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51
Q

A cutaneous cyst with a visible central punctum

A

Epidermal inclusion cyst

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52
Q

Skin colored dermal nodule

A

Epidermal inclusion cyst

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53
Q

Where are epidermal inclusion cysts commonly located

A

Face, scalp, neck, and trunk

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54
Q

What syndrome are epidermal inclusion cysts seen in?

A

Gardener Syndrome (hereditary condition)

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55
Q

Treatment of epidermal inclusion cyst?

A

Excision of cyst or incision and drainage

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56
Q

What’s the most common cutaneous disorder affecting adolescents and young adults

A

Acne

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57
Q

Acne is a disease of

A

Pilosebaceous follicles

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58
Q

What are the 4 factors of acne?

A
  1. Follicular hyperkeratinization
  2. Increased sebum production
  3. Cutibacterium acnes within the follicle
  4. Inflammation
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59
Q

What happens in prepuberty to the sebaceous glands?

A

They enlarge and sebum production increases

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60
Q

Sebum provides a growth medium for?

A

C.acnes

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61
Q

What provides an anaerobic lipid-rich environment for bacteria in acne?

A

Microcomedones

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62
Q

What is another name for a white-head?

A

Closed comedone

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63
Q

What is another name for a black-head?

A

Open comedone

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64
Q

What leads to inflammatory papules and nodules in acne?

A

Proinflammatory lipids and keratin

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65
Q

What can cause infantile acne?

A

Elevated levels of androgens produced by immature adrenal glands in girls and immature adrenal glands and testes in boys

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66
Q

What serum level rises as puberty approaches?

A

DHEA-S levels

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67
Q

DHEA-S is related to acne how?

A

Onset of acne correlates with high levels of DHEA-S, high levels found in prepubertal girls with acne

68
Q

What are some conditions where hyperandrogenism is seen?

A

PCOS, congenital adrenal hyperplasia, adrenal or ovarian tumors

69
Q

What can worsen acne?

A

Repetitive mechanical trauma like scrubbing; ruptures comedones and promotes inflammatory lesions

70
Q

Occlusion of pilosebaceous follicles leads to what?

A

Comedone formation

71
Q

What are some drug-induced causes of acne?

A

Glucocorticoids, phenytoin, lithium, isoniazid, iodides, bromides, androgens

72
Q

Can milk worsen acne?

A

Yes, increased levels of IGF are associated with consumption of milk. Hormones seem to exacerbate acne

73
Q

Is insulin resistance related to acne?

A

It can stimulate increased androgen production and is associated with increased serum levels of IGF

74
Q

What are the three classifications of acne?

A
  1. Comedones acne (noninflammatory)
  2. Inflammatory acne
  3. Modular acne
75
Q

What are some diagnostic tools for acne?

A

Endocrine fx, DHEA-S, total testosterone and free testosterone

76
Q

What can the rapid onset of acne suggest?

A

An adrenal or ovarian tumor

77
Q

What is the treatment for follicular hyperkeratinization? (5)

A
  1. Topical retinoids
  2. Oral retinoids
  3. Azelaic acid
  4. Salicylic acid
  5. Hormonal therapies
78
Q

What is the treatment for increased sebum production? (2)

A
  1. Oral isotretinoin

2. Hormonal therapies

79
Q

What is the treatment for c. Acnes proliferation? (3)

A
  1. Benzoyl peroxide
  2. Topical and oral antibiotics
  3. Azelaic acid
80
Q

What is the treament for inflammation in acne? (4)

A
  1. Oral isotretinoin
  2. Oral tetracyclines
  3. Topical retinoids
  4. Azelaic acid
81
Q

Which acne symptoms can be treated with topical retinoids?

A

Follicular hyperkeratinization and inflammation

82
Q

What are some examples of topical retinoids?

A

Retin-A, Tretin-X, Atralin, Avita, Refissa, REnova, Adapalene, Tazaotene

83
Q

Which topical retinoid will you have to be careful of fish allergies?

A

Atralin

84
Q

When should topical retinoids be taken?

A

Once daily at bedtime, watch for sun sensitivity!!!

85
Q

What are some topical antimicrobials used to treat acne?

A

Benzoyl peroxide, Clindamycin, Erythromycin, Dapsone

86
Q

What is important to note about topical combination products (used for acne)?

A

Used once daily, may bleach hair or clothing

87
Q

What are some oral antibiotics used for acne?

A

Tetracycline, Doxycyline, Minocycline, Erythromycin, Trimethoprim-sulfamethoxazole, Azithromycin int. Dosing

88
Q

What hormonal agents are used to control acne?

A

Combination oral contraceptives and Spironolactone

89
Q

What oral retinoids are used to treat acne?

A

Isotretinoin, Accutane

90
Q

What acne symptoms can be treated with oral retinoid?

A

Follicular hyperkeratinization, increased sebum production, and inflammation

91
Q

How long can treatment take to work for acne?

A

4-6 weeks, may get worse before it gets better

92
Q

What is a common skin disorder localized primarily to the central face?

A

Rosacea

93
Q

What are the 4 main subtypes of rosacea?

A
  1. Erythematotelangiectatic
  2. Papulopustular
  3. Phymatous
  4. Ocular rosacea
94
Q

Who is most likely to get rosacea?

A

Celtic and Northern European origin, adults over 30, and females (except for phymatous form)

95
Q

What are some factors contributing to rosacea?

A

Vascular dysfx, UV damage, inflammatory rxns to cutaneous organisms, abnormalities in innate immunity

96
Q

What are clinical features of erythematotelangiectatic rosacea?

A

Persistent central erythema, flushing, enlarged cutaneous blood vessels, roughness and scaling

97
Q

Erythema congestivum

A

After an exacerbation of facial redness, return to baseline is slow (erythematotelangiectatic rosacea)

98
Q

What are the clinical features of papulopustular rosacea?

A

Papules and pustules present in central face, can be mistaken for acne although there are no comedones

99
Q

What are the clinical features of phymatous rosacea?

A

Exhibits tissue hypertrophy (thickened skin with irregular contours)
Commonly occurs in men, and involves the nose, chin, cheeks and forehead

100
Q

What are the clinical features of ocular rosacea?

A

Occurs in more than 50% of patients with rosacea

Conjunctival hyperemia, blepharitis, keratitis, lid margin teleangiectasias, abnormal tearing, chalazion, hordeolum

101
Q

What are some exacerbating factors to rosacea?

A

Extreme temps, sun, hot beverages, spicy food, alcohol, exercise, irritation from topical patterns, emotions (anger, rage, embarrassment), drugs (nicotinic acid, vasodilators), skin barrier disruption

102
Q

How do you diagnose rosacea?

A

Assessment is key, biopsies rarely indicated, no serologic studies useful

103
Q

How to manage erythematotelangiectatic rosacea?

A

First line: behavioral changes, sun protection, decrease alcohol
Second line: laser and light-base therapy
Rx: Topical Brimonidine and Oxymetazoline

104
Q

How to manage papulopustular rosacea?

A

Topical: metronidazole, azelaic acid, ivermectin
Oral: tetracycline, doxycycline, minocycline, isotretinoin

105
Q

How to manage ocular rosacea?

A

Lid scrubs, warm compresses, topical antibiotics (Ilotycin ointment), referral to ophthalmologist

106
Q

How to manage phymatous rosacea?

A

Oral isotretinoin in early disease and laser ablation/surgery in advanced disease

107
Q

Which skin disease is characterized by well-demarcated erythematous plaques with silver scales?

A

Psoriasis

108
Q

Prevalence of psoriasis tends to increase when?

A

When farther away from the equator

109
Q

What are the two peaks of age onset for psoriasis?

A

20-39 and 50-69 years

110
Q

What role does genetics play in psoriasis?

A

40% with family history have it, concordat among monozygotic twins

111
Q

Predisposing risk factors to psoriasis include

A

Smoking, obesity (increased proinflammatory cytokines), drugs, infections, alcohol, vitamind D deficiency

112
Q

Which drugs can be risk factors for psoriasis?

A

Beta blockers, lithium, antimalarials

113
Q

What types of infections can be risk factors for psoriasis?

A

Poststrep flares and HIV

114
Q

What is the pathophysiology behind psoriasis?

A

Complex immune-mediated disease

115
Q

Typical clinical findings of psoriasis

A

Scaling, induration and erythema, hyperproliferation and abnormal differentiation of the epidermis, inflammatory cell infiltrates, vascular dilitation

116
Q

What are the 6 clinical categories of psoriasis?

A
  1. Chronic plaque
  2. Guttate
  3. Pustular
  4. Erythrodermic
  5. Inverse
  6. Nail
117
Q

What is the most common variant of psoriasis?

A

Chronic plaque

118
Q

Chronic plaque manifestations

A

Symmetrically distributed, found on scalp, extensor elbows, knees, and gluteal cleft
May be asymptomatic but pruritis is common

119
Q

Guttate psoriasis manifestations

A

Abrupt appearance of multiple small psoriatic papules and plaques (usually less than 1 cm)
Strong association with recent infection (strep)

120
Q

Guttate psoriasis is most commonly found on what parts of the body?

A

Trunk and proximal extremities

121
Q

Which type of psoriasis can have life-threatening complications?

A

Pustular psoriasis

122
Q

What are the manifestations of pustular psoriasis?

A

Most severe variant (von Zumbusch type), acute onset wide-spread erythema, scaling and sheets of superficial pustules

123
Q

What is pustular psoriasis associated with?

A

Malaise, fever, diarrhea, leukocytosis, hypocalcemia

124
Q

Some possible causes of pustular psoriasis

A

Pregnancy, infection and withdrawal of glucocorticoids

125
Q

Which type of psoriasis is characterized by generalized erythema and scaling from head to toe?

A

Erythrodermic psoriasis

126
Q

Complications arising from erythrodermic psoriasis include

A

Related to loss of adequate barrier; electrolyte abnormalities

127
Q

Which areas of the body are affected by inverse psoriasis?

A

Inguinal, perineal, genital, intergluteal, axillary, inframammary

128
Q

Inverse psoriasis can sometimes be misdiagnosed as what?

A

Fungal or bacterial infection

129
Q

Patients with psoriatic arthritis are more likely to have

A

Nail psoriasis

130
Q

How to diagnose psoriasis

A

Family history, clinical exam, skin biopsy, no lab tests

131
Q

What is the management for mild to moderate psoriasis?

A

Emollients, topical corticosteroids, vitamin D analogs, topical retinoids, anthralin, tacrolimus or pimecrolimus (for face)

132
Q

Which topical corticosteroids can be used to treat mild to moderate psoriasis?

A

hydrocortisone, triamcinolone, fluocinonide, betamethasone diproprionate, clobetasol

133
Q

Which vitamin D analogs can be used for mild to moderate psoriasis?

A

Calcipotriol, calcitrol, tacalcitol, tar-t

134
Q

What is the management for moderate to severe psoriasis?

A

Phototherapy, systemic therapy, and biologics

135
Q

What are the options of phototherapy to treat psoriasis?

A

UVB alone or in combo with topical tar
Narrow band UVB in suberythemogenic doses
Home phototherapy machines ($$$)

136
Q

What systemic therapies are used to treat moderate to severe disease?

A

Methotrexate (folic acid antagonist)
Cyclosporine (t cell suppressor)
Apremilast (phosphodiesterase 4 inhibitor)

137
Q

What biologics are used to treat moderate to severe psoriasis?

A

Entanercept, Infliximab, Adalimumab, Ustekinumab (-umab)

138
Q

What is a chronic immune-mediated disorder that targets active hair follicles causing hair loss?

A

Alopecia

139
Q

Commonly presents with discrete patches on the scalp

A

Alopecia

140
Q

What is alopecia areata?

A

Discrete patches of hair loss

141
Q

What is Alopecia totalis?

A

Hair loss of the entire scalp

142
Q

What is alopecia universalis?

A

Hair loss of hate entire body

143
Q

What is the pathophysiology behind alopecia?

A

T-cell mediated inflammation, inappropriate trigger of immune response against follicular antigens

144
Q

Does alopecia lead to the destruction of the hair follicle?

A

No

145
Q

What are some risk factors for alopecia?

A

Stress, drugs, infections, vitamin D definciency, genetics

146
Q

Alopecia develops over a period of what?

A

2-3 weeks

147
Q

What else can develop in patients with alopecia?

A

Nail abnormalities- onychorrhexis (longitudinal fissuring of nail plate)

148
Q

What are some associated diseases with alopecia?

A

Lupus, vitiligo, atopic dermatitis, thyroid disease, allergic rhinitis, psoriasis, Down syndrome, polyglandular autoimmune syndrome type 1

149
Q

50% of patients with alopecia will what?

A

Recover spontaneously in a year

150
Q

What can be a diagnostic tool when looking for alopecia?

A

Exclamation point hair at margins, skin biopsy, and peribulbar lymphatic inflammatory infiltrates surrounding the follicles

151
Q

For limited patchy hair loss what is the treatment?

A

Topical or intralesional corticosteroids (triamcinolone, betamethasone dipropionate)

152
Q

For extensive alopecia, what is the treatment?

A

Topical immunotherapy (DPCP, SADBE, DNCB)

153
Q

How is the topical immunotherapy dosed when treating extensive alopecia?

A

2% solution is applied first to desensitize the pt, 1-2 weeks later 0.01% applied to affected area 1/week titration get up to 2%

DC after 6 mo if no improvement

154
Q

What can be some second-line treatment for alopecia?

A

Minoxidil, Anthralin, and phototherapy

155
Q

Some examples of systemic therapies for alopecia

A

Oral glucocorticoids, sulfasalazine, methotrexate, cyclosporine, biologics

156
Q

What is hidradenitis suppurativa?

A

Hidros: sweat, Aden: glands

Chronic inflammatory skin condition, also known as acne inversa

157
Q

What population tend have hidradenitis suppurativa more?

A

African American women

158
Q

What is the patho behind hidradenitis suppurativa?

A

Plugging, rupture, and inflammation of follicle. Stimulates an immune response and leads to sinus tracts in the skin

159
Q

What are the most common sites of HS?

A

Axillae, inguinal, inner thigh, perianal, inframammary, buttocks, scrotum, vulva

160
Q

Hidradenitis suppurativa can be misdiagnosed as what?

A

Furunculosis or abscess

161
Q

What are the 3 stages of hidradenitis suppurativa?

A

1: abscess formation
2: recurrent abscess formation with sinus tract formation and scarring
3: diffuse involvement multiple interconnected sinus tracts

162
Q

What will be important to find in a clinical exam for a pt with hidradenitis suppurativa?

A 
Typical lesions (inflamed nodules, sinus tracts) in the typical locations (axillae, groin) with relapse and chronicity
Skin biopsy not necessary
163
Q

How can a pt prevent hidradenitis suppurativa?

A

Avoidance of skin trauma, stop smoking, weight management, chlorhexidine 1/week, emollients

164
Q

How can a pt in Hurley stage 1 (stage 1 of HS) manage it?

A

Topical clindamycin, intralesional corticosteroid (triamcinolone), punch debridement to evacuate inflammation, topical resorcinol (peel)

165
Q

What is the management for Hurley stage 2 of HS?

A

Oral tetracycline (many months), clindamycin and rifampin, oral retinoids, antiadrenergic therapies, punch biopsy of lesions

166
Q

What is the management of Hurley stage 3 of HS?

A

TNF-alpha inhibitors once weekly, systemic glucocorticoids (prednisone), cyclosporine, surgery

Clin med 1 (9 decks)

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