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Clinical Med I > Derm - Cellulitis, pemphigus & other - Exam 1 > Flashcards

Derm - Cellulitis, pemphigus & other - Exam 1 Flashcards

1
Q

What is lymphangitis?

A

Inflammation of lymphatic channels due to inflammation or infection
-Can present as tender, red streaks extending proximally

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2
Q

How can you effectively monitor changes in cellulitis in follow up visits?

A

Mark the borders to see how it has changed

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3
Q

What is folliculitis?

A

Inflammation of the hair follicle leading to pustules an papules.

  • Usually infectious (Staph aureus most common, or pseudomonas is common cause of hot tub cellulitis)
  • Itching and pain
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4
Q

What can folliculitis progress to?

A

A furuncle and a carbuncle/abscess

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5
Q

What is the treatment for staphylococcal folliculitis?

A
  • Usually self limited, but moderate, severe, or persistent need treatment
  • Topical antibiotics (mupirocin) or oral antibiotics (cephalexin)
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6
Q

What is the treatment for suspected MRSA folliculitis?

A

Sulfa, Clindamycin, or Doxycycline

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7
Q

What bacteria is responsible for gram negative folliculitis, or hot tub folliculitis?

A

Pseudomonas aeruginosa

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8
Q

What is the treatment for Gram negative folliculitis?

A
  • It is self limited and often resolves with good hygiene within one week.
  • Consider oral ciprofloxacin for severe cases
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9
Q

What are the 3 variants of impetigo?

A

Nonbullous, bulbous, and ecthyma impetigo

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10
Q

What is impetigo?

A

Contagious superficial bacterial infection. Occurs in children more than adults. Autoinoculation may result in satellite lesions

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11
Q

What is the most common form of impetigo?

A

Nonbullous

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12
Q

What is the presentation of nonbullous impetigo?

A

Papules -> vesicles -> pustules -> honey colored crusting

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13
Q

What is the presentation for bulbous impetigo?

A

Vesicles enlarge and form flaccid bulla

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14
Q

What is the presentation for ecthyma impetigo?

A

“Punched out” ulcers with overlying crust

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15
Q

What pathogen is responsible for bulbous and nonbullous impetigo?

A

S. Aureus

-MRSA is an uncommon cause

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16
Q

What is the pathogen responsible for ecthyma impetigo?

A

Strep bacteria

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17
Q

How is impetigo diagnosed?

A
  • Clinical diagnosis

- Culture and gram stain reveal gram-positive cocci staph aureus 95% of the time

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18
Q

How is mild bullous and nonbullous impetigo treated?

A

Topical antibiotics - Mupirocin

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19
Q

How is Moderate to severe bullous and nonbullous impetigo treated?

A

Oral antibiotics covering S. Aureus and streptococcal bacteria (Dicloxicillin, cephalexin)

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20
Q

How is ecthyma impetigo treated?

A

Always treated with oral antibiotics (Dicloxicillin, cephalexin)

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21
Q

What patient education should be given to patients with impetigo?

A

Hand washing and gently wash lesions

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22
Q

What are the 2 types of cellulitis?

A

Nonpurulent and purulent

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23
Q

What is cellulitis?

A

Diffuse, spreading superficial infection caused by B-hemolytic strep. Staph aureus (including MRSA) is less common

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24
Q

What are the nonpurulent cellulitis infections?

A

Cellulitis or erysipelas

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25
Q

What are the purulent cellulitis infections?

A

Abscess or purulent cellulitis

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26
Q

What are the symptoms of cellulitis or erysipelas?

A

Erythema, edema, warmth, and fever

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27
Q

What are the risk factors for cellulitis?

A

Skin trauma/inflammation, lymphedema, venous insufficiency, obesity, and immunosuppresion

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28
Q

What is Erysipelas?

A

A superficial skin infection caused by B-Hemolytic streptococci.

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29
Q

What is the presentation of Erysipelas?

A
  • Cheeks and lower extremities are most common
  • Tender, warm, and intensely erythematous with raised erythema. Sharply demarcated border.
  • Fever and chills are common
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30
Q

What is an abscess?

A

An enclosed collection of pus within a confined space.

-Most common cause is staph aureus

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31
Q

What is the presentation of an abscess?

A

Painful, fluctuant, erythematous nodule

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32
Q

How do you treat an abscess?

A

Incision and drainage (I&D) with culture and susceptibility testing. Possibly antibiotics (Trimethoprim-sulfamethaxazole, doxycycline, and clindamycin)

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33
Q

What is the treatment of Cellulitis?

A

Empiric coverage for beta-hemolytic streptococci and S. Aureus (Cephalexin PO or cefazolin IV)

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34
Q

What is the treatment for Erysipelas?

A

Empiric treatment for B-Hemolytic strep, usually parenteral treatment (cefazolin, ceftriaxone)

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35
Q

What is the most common cause of abscess?

A

Staph aureus

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36
Q

What is purulent cellulitis treated with?

A

Empiric antibiotics with MRSA coverage (Trimethoprim-sulfamethoxazole, doxycycline, and clindamycin)

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37
Q

When would you treat an abscess with both I and D and antibiotics?

A
  • Abscess is greater than 2 cm or there are multiple lesions
  • Toxicity
  • Extensive cellulitis
  • immunosuppresion
  • indwelling medical device
  • High risk for transmission (Athlete, military)
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38
Q

What are the risk factors for MRSA?

A

Antibiotic use, invasive device, hospitalization, group settings, (Military, sports), chronic wounds, MRSA colonization, skin trauma (tattoo, IVDA)

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39
Q

How can MRSA be prevented?

A

Hand Hygiene, environmental cleaning, and contact precautions

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40
Q

What is the rule of thumb for cellulitis?

A

If there is no pus, it is most likely caused by Strep bacteria. If there is pus, it is most likely caused by S. Aureus

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41
Q

What does fluctuant mean?

A

When you press on an area and it feels fluid filled and it bounces back.
-It is “ripe”

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42
Q

What is the treatment for MRSA?

A

Antibiotics tailored to the C and S results and clinical circumstance.
-Oral antibiotics (Trimethoprim-sulfamethoxazole, doxycycline, and clindamycin)

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43
Q

When are IV antibiotics necessary for MRSA?

A
  • Extensive involvement
  • Toxicity
  • rapid progression
  • failed PO treatment
  • immunocompromised
  • infection near indwelling device
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44
Q

What are the two clinical manifestation of systemic lupus erythematosus (SLE)?

A

Discoid lupus and malar/butterfly rash

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45
Q

What is the presentation of discoid lupus?

A

Annular, erythematous, scaly plaques that occur mostly on sun exposed area (face, neck, scalp, and ears)
-Present in 15-30% of SLE patients

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46
Q

What is the presentation of a malar/butterfly rash?

A

Erythema on cheeks and bridge of nose. Nasolabial folds are spared

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47
Q

How is SLE diagnosed?

A

Labs- Autoimmune connective tissue disease work up

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48
Q

What is the treatment for SLE?

A
  • Sun protection, smoking cessation
  • Topical or intralesional steroids
  • Hydroxychoroquine vs other systemic meds
  • Consider possibility of Drug induced cutaneous lupus (diltiazem)
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49
Q

What is erythema multiforme (EM)?

A

Acute, immune mediated condition causing distinctive target like lesions
-major EM affects mucosa and minor EM does not

50
Q

What is the most common cause of Erythema Multiforme (EM)?

A

Herpes simplex, but may be associated with other viral, bacterial, or fungal infections

51
Q

How is EM diagnosed?

A
  • Clinical diagnosis
  • Labs (nonspecific elevated inflammatory markers (ESR) and leukocytosis)
  • Biopsy if dx is uncertain
52
Q

How is EM treated?

A
  • Mostly symptomatically and it is self limited for about 2 weeks
  • topical steroids, oral antihistamines, anesthetic mouthwash for symptomatic relief
  • Antivirals are NOT indicated for acute EM
  • Oral steroids only if severe
53
Q

What are the best approaches for decolonization?

A

Chlorohexidine wash and mupirocin ointment intranasally, but the effectiveness of this is uncertain

54
Q

What is dermatitis herpetiformis?

A

Uncommon autoimmune skin condition associated with gluten sensitivity (most have celiac disease)

55
Q

What is the presentation of dermatitis herpetiformis?

A

Intensely pruritic papules and vesicles (“herpetiform pattern”) on forearm, knees, scalp, and buttocks

56
Q

How is dermatitis herpetiformis diagnosed?

A

Serologic markers for celiac disease

-Punch biopsy of perilesional skin and then do direct immunofluorescence (DIF), the gold standard

57
Q

How is dermatitis herpetiformis treated?

A

Dapsone and gluten elimination

58
Q

What is pemphigus?

A

A group of rare, autoimmune, life threatening, blistering disorders

59
Q

What are the different types of pemphigus?

A

Pemphigus vulgaris, pemphigus foliaceus, IgA pemphigus, and paraneoplastic pemphigus

60
Q

What is a herpetiform pattern?

A

Vesicles on an erythematous base

61
Q

What is the etiology of pemphigus?

A

Autoimmune

  • Antibodies cause acantholysis (separation of epidermal cells from each other) and blistering
  • Genetics
  • idiopathic
  • Some cases are drug induced or environmental
62
Q

What is the clinical presentation of pemphigus?

A
  • Mucosal involvement: oral cavity is most common
  • Flaccid bulla begin in oropharynx and may spread to skin (scalp, face, axilla, groin)
  • Positive Nikolsky sign
63
Q

What is Nikolsky sign?

A

Gentle application of lateral pressure of an uninvolved area causes the superficial layer to slough off

64
Q

How is pemphigus diagnosed?

A
  • Acantholysis is a hallmark finding (Nikolsky sign )
  • Biospy: lesional (routine histological exam) and perilesional (direct immunofluorescence) skin biopsy
  • Serology further supports diagnosis (IIF and ELISA to detect circulation antibodies)
65
Q

How is pemphigus treated?

A
  • Treatment is ALWAYS indicated
  • Urgent dermatology evaluation
  • Hospitalization if severe
  • Systemic corticosteroids, immunosuppressive agents are the mainstay
  • Oral lesions may need topical anesthesia (Lidocaine or triamcinolone)
  • Antibiotics for secondary infection (which is most common cause of death)
66
Q

What is a pemphigoid?

A

A chronic autoimmune subepithelial blistering disorder

67
Q

What are the two types of pemphigoid?

A

Bullous pemphigoid and mucous membrane pemphigoid

68
Q

What is the clinical presentation of pemphigoid?

A
  • prodrome lasts weeks to months with pruritic eczematous, popular, or urticaria skin lesions
  • Urticarial, erythematous plaques and tense bulla
  • Commonly on trunk and extremities
  • Possible mucosal involvement (Oral cavity, ocular conjunctiva, nose, pharynx, larynx, esophagus, anus, and genital)
69
Q

How is pemphigoid diagnosed?

A

Biopsy: Lesional (routine histological examination) and perilesional (direct immunofluorescence)

  • Direct immunofluorescence is the gold standard
  • Serology- indirect immunofluorescence (IIF) and ELISA
70
Q

What is the treatment for pemphigoid?

A
  • General skin care
  • Topical and systemic corticosteroids
  • Dermatology referral and immunosuppressive agents
71
Q

Describe the progression of pemphigus.

A

Superficial separation -> intraepidermal acantholysis -> flaccid bulla that rupture easily -> infection -> death if not treated

72
Q

Describe the progression of Pemphigoid?

A

Deep epidermal junction -> tense bulla that don’t rupture easily -> heal without scarring

73
Q

What is melasma/Chloasma?

A

Acquired hyperpigmentation of skin, usually in sun exposed areas of the face.

  • Can also present with oral contraceptive use
  • Frequently regresses within one year of delivery
74
Q

What is the “mask of pregnancy?”

A

Melasma or chloasma

75
Q

What is the treatment for melasma?

A

If it is desired, skin lightening agents and chemical peels may be used.
-Encourage photoprotection

76
Q

What is acanthodians nigricans?

A

-A common disorder associated with insulin resistance

77
Q

What is the presentation of acanthosis Nigricans? What is the treatment?

A

Hyperpigmented, velvety plaques.

Treatment is to treat the underlying condition (obesity, DM)

78
Q

What is hirsutism?

A

Male pattern hair growth in women

79
Q

What causes Cushing syndrome?

A

Excess androgen/steroid hormone

80
Q

What happens with Cushing Disease?

A
  • It affects pilosebaceous unit

- increased sebum, acne, andreogenic alopecia, hirsutism, atrophy, and striae

81
Q

What causes Addison’s disease?

A

Adrenal insufficiency

82
Q

What happens with Addison’s disease?

A

Hyperpigmentation to the gums, buccal mucosa, elbows, knees, palms, and genitalia

83
Q

What are the effects of hyperthyroid?

A
  • Warm, moist skin
  • pretibial myxedema and thyroid dermopathy (seen in less than 5% of patients with Graves’ disease)
  • Nonpitting, scaly, thickened skin. Orange peel appearance
84
Q

What effect does hypothyroid have on skin?

A

Cool, dry skin

85
Q

What is porphyria?

A

Metabolic disorders due to altered activity of enzymes in Heme Synthesis

86
Q

What is the most common type of porphyria?

A

Porphyria cutanea tarda (PCT)

87
Q

How does uroporphyrinogen decarboxylase (UROD) deficiency lead to porphyria?

A

UROD breaks down porphyrins so a deficiency in UROD leads to excess porphyrins

88
Q

What are the symptoms of porphyria?

A

Painless sub-epidermal blistering of skin on sub exposed areas, commonly on dorsum of hands, forearm, face, neck, and feet.
-Photosensitivity

89
Q

What is thought to cause porphyria?

A
  • 20% genetic contribution, 80% sporadic

- may be associated with tobacco she, EtOH, estrogens, liver disease, or hepatitis

90
Q

How is Porphyria Cutanea Tarda (PCT) diagnosed?

A
  • Elevated serum and/or urinary porphyrins

- elevated liver tests, increased iron stores, and iron deposition

91
Q

How can PCT be prevented?

A
  • Wearing sun-protective clothing

- Sunscreen does not always help

92
Q

What is the treatment for PCT?

A
  • Discontinue or treat the potential cause

- Phlebotomy (Iron depletion prevents formation of UROD inhibitor) and low dose hydroxychloroquine

93
Q

What is a pressure ulcer?

A

Pressure induced injury over bony prominences, seen commonly on the sacrum and calcaneous
-released to immobility

94
Q

What is the best treatment for a pressure ulcer?

A

Prevention

95
Q

Describe a stage 1 Pressure injury.

A

Intact skin with localized erythema

96
Q

Describe a stage 2 pressure injury.

A

Partial thickness skin loss with exposed dermis. Adipose is not visible, no eschar

97
Q

Describe a stage 3 pressure injury.

A 
Full thickness skin loss.
Adipose is visible.
Rolled edges.
Eschar may be visible.
Fascia, muscle, or bone are not exposed
98
Q

Describe a stage 4 pressure injury.

A

Full thickness skin and tissue loss with exposed muscle, tendon, bone, or other fascia.
Eschar and oiled edges common. Look for fistulas and tunneling

99
Q

What is eschar?

A

Dead tissue that eventually sloughs off healthy skin after an injury.

100
Q

What are the general treatment recommendations for pressure injuries?

A
  • Reduce or eliminate underlying contributing factors such as redistributing pressure
  • Local wound care
  • Treat infection if present
101
Q

What is the recommended treatment for a stage 1 pressure injury?

A

Transparent film for protection

102
Q

What is the recommended treatment for a stage 2 pressure injury?

A

Dressing that maintains moist wound environment (if there is no infection.)

Debridement is normally not necessary

103
Q

What is the recommended treatment for a stage 3 & 4 pressure injury?

A

Debridement of necrotic tissue, appropriate dressing, and antibiotics

104
Q

What are the 2 dermatologic findings associated with tick borne illnesses?

A

Erythema migrans and Rocky Mountain spotted fever

105
Q

How can tick borne illnesses be prevented?

A
  • tick repellants
  • long sleeves, pants, hat
  • Check for and promptly remove ticks after exposure
  • Bathe within 2 hours of exposure
  • Place clothes in dryer after outdoor activities
106
Q

What is the proper way to remove a tick?

A

Grasp the tick as close to the skin surface with tweezers and pull straight up with steady pressure.
-No twisting, jerking, or crushing

107
Q

How quickly is Lyme disease transmitted after tick bite?

A

2-3 days

108
Q

What is erythema migrans also known as?

A

Lyme disease

109
Q

What is the pathogenesis of Lyme disease?

A

Borrelia Burgdorferi

110
Q

What is the clinical presentation of Erythema Migrans (Lyme disease)?

A
  • Characteristic rash occurs 7-14 days after tick bite.

- Slightly raised, warm, red with central clearing and Bulls eye appearance

111
Q

What are the associated symptoms in the early stages of Erythema Migrans?

A

Fatigue, Headache, myalgia, arthralgia, and fever

112
Q

What are the symptoms in the later stages of Erythema Migrans?

A
  • cardiac, arthritis, and neurologic symptoms

- If Bell’s palsy, consider Lyme in differential if in endemic areas

113
Q

What is the treatment for Erythema migrans?

A

Usually doxycycline or Amoxicillin

114
Q

What is the Lyme disease prophylaxis when the tick has been attached for greater than 36 hours?

A

Doxycycline 200mg single dose within 72 hours of removal.

115
Q

What is the pathogenesis of Rocky Mountain spotted fever?

A

Rickettsia Rickettsia

116
Q

When does the rash appear in Rocky Mountain spotted fever? What is the presentation of the rash?

A
  • Within 3-5 days

- Starts as a macular rash and turns into petechial lesions. Commonly on the ankles, wrists, and then trunk.

117
Q

What percentage of patients with Rocky Mountain spotted fever do not get a rash? Why is this important?

A

10%. Rocky Mountain spotted fever can be lethal so don’t wait for a rash to appear before treating if you suspect this illness.

118
Q

Other than a rash, what are the symptoms of Rocky Mountain spotted fever?

A

Fever, HA, malaise, myalgia, arthritis, and nausea for 2-14 days after tick bite

119
Q

How is Rocky Mountain Spotted fever diagnosed?

A
  • Commonly a clinical diagnosis

- Serology, though there may be a delay in antibody detection

120
Q

What is the treatment for Rocky Mountain spotted fever?

A
  • Empiric treatment based on clinical suspicion.
  • Doxycycline
  • Antibiotics have resulted in marked reduction in fatality rate

Clinical Med I (24 decks)

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