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
2
Q
How can you effectively monitor changes in cellulitis in follow up visits?
A
Mark the borders to see how it has changed
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
4
Q
What can folliculitis progress to?
A
A furuncle and a carbuncle/abscess
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)
6
Q
What is the treatment for suspected MRSA folliculitis?
A
Sulfa, Clindamycin, or Doxycycline
7
Q
What bacteria is responsible for gram negative folliculitis, or hot tub folliculitis?
A
Pseudomonas aeruginosa
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
9
Q
What are the 3 variants of impetigo?
A
Nonbullous, bulbous, and ecthyma impetigo
10
Q
What is impetigo?
A
Contagious superficial bacterial infection. Occurs in children more than adults. Autoinoculation may result in satellite lesions
11
Q
What is the most common form of impetigo?
A
Nonbullous
12
Q
What is the presentation of nonbullous impetigo?
A
Papules -> vesicles -> pustules -> honey colored crusting
13
Q
What is the presentation for bulbous impetigo?
A
Vesicles enlarge and form flaccid bulla
14
Q
What is the presentation for ecthyma impetigo?
A
“Punched out” ulcers with overlying crust
15
Q
What pathogen is responsible for bulbous and nonbullous impetigo?
A
S. Aureus
-MRSA is an uncommon cause
16
Q
What is the pathogen responsible for ecthyma impetigo?
A
Strep bacteria
17
Q
How is impetigo diagnosed?
A
- Clinical diagnosis
- Culture and gram stain reveal gram-positive cocci staph aureus 95% of the time
18
Q
How is mild bullous and nonbullous impetigo treated?
A
Topical antibiotics - Mupirocin
19
Q
How is Moderate to severe bullous and nonbullous impetigo treated?
A
Oral antibiotics covering S. Aureus and streptococcal bacteria (Dicloxicillin, cephalexin)
20
Q
How is ecthyma impetigo treated?
A
Always treated with oral antibiotics (Dicloxicillin, cephalexin)
21
Q
What patient education should be given to patients with impetigo?
A
Hand washing and gently wash lesions
22
Q
What are the 2 types of cellulitis?
A
Nonpurulent and purulent
23
Q
What is cellulitis?
A
Diffuse, spreading superficial infection caused by B-hemolytic strep. Staph aureus (including MRSA) is less common
24
Q
What are the nonpurulent cellulitis infections?
A
Cellulitis or erysipelas
25
What are the purulent cellulitis infections?
Abscess or purulent cellulitis
26
What are the symptoms of cellulitis or erysipelas?
Erythema, edema, warmth, and fever
27
What are the risk factors for cellulitis?
Skin trauma/inflammation, lymphedema, venous insufficiency, obesity, and immunosuppresion
28
What is Erysipelas?
A superficial skin infection caused by B-Hemolytic streptococci.
29
What is the presentation of Erysipelas?
- Cheeks and lower extremities are most common
- Tender, warm, and intensely erythematous with raised erythema. Sharply demarcated border.
- Fever and chills are common
30
What is an abscess?
An enclosed collection of pus within a confined space.
| -Most common cause is staph aureus
31
What is the presentation of an abscess?
Painful, fluctuant, erythematous nodule
32
How do you treat an abscess?
Incision and drainage (I&D) with culture and susceptibility testing. Possibly antibiotics (Trimethoprim-sulfamethaxazole, doxycycline, and clindamycin)
33
What is the treatment of Cellulitis?
Empiric coverage for beta-hemolytic streptococci and S. Aureus (Cephalexin PO or cefazolin IV)
34
What is the treatment for Erysipelas?
Empiric treatment for B-Hemolytic strep, usually parenteral treatment (cefazolin, ceftriaxone)
35
What is the most common cause of abscess?
Staph aureus
36
What is purulent cellulitis treated with?
Empiric antibiotics with MRSA coverage (Trimethoprim-sulfamethoxazole, doxycycline, and clindamycin)
37
When would you treat an abscess with both I and D and antibiotics?
- Abscess is greater than 2 cm or there are multiple lesions
- Toxicity
- Extensive cellulitis
- immunosuppresion
- indwelling medical device
- High risk for transmission (Athlete, military)
38
What are the risk factors for MRSA?
Antibiotic use, invasive device, hospitalization, group settings, (Military, sports), chronic wounds, MRSA colonization, skin trauma (tattoo, IVDA)
39
How can MRSA be prevented?
Hand Hygiene, environmental cleaning, and contact precautions
40
What is the rule of thumb for cellulitis?
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
41
What does fluctuant mean?
When you press on an area and it feels fluid filled and it bounces back.
-It is “ripe”
42
What is the treatment for MRSA?
Antibiotics tailored to the C and S results and clinical circumstance.
-Oral antibiotics (Trimethoprim-sulfamethoxazole, doxycycline, and clindamycin)
43
When are IV antibiotics necessary for MRSA?
- Extensive involvement
- Toxicity
- rapid progression
- failed PO treatment
- immunocompromised
- infection near indwelling device
44
What are the two clinical manifestation of systemic lupus erythematosus (SLE)?
Discoid lupus and malar/butterfly rash
45
What is the presentation of discoid lupus?
Annular, erythematous, scaly plaques that occur mostly on sun exposed area (face, neck, scalp, and ears)
-Present in 15-30% of SLE patients
46
What is the presentation of a malar/butterfly rash?
Erythema on cheeks and bridge of nose. Nasolabial folds are spared
47
How is SLE diagnosed?
Labs- Autoimmune connective tissue disease work up
48
What is the treatment for SLE?
- Sun protection, smoking cessation
- Topical or intralesional steroids
- Hydroxychoroquine vs other systemic meds
- Consider possibility of Drug induced cutaneous lupus (diltiazem)
49
What is erythema multiforme (EM)?
Acute, immune mediated condition causing distinctive target like lesions
-major EM affects mucosa and minor EM does not
50
What is the most common cause of Erythema Multiforme (EM)?
Herpes simplex, but may be associated with other viral, bacterial, or fungal infections
51
How is EM diagnosed?
- Clinical diagnosis
- Labs (nonspecific elevated inflammatory markers (ESR) and leukocytosis)
- Biopsy if dx is uncertain
52
How is EM treated?
- 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
What are the best approaches for decolonization?
Chlorohexidine wash and mupirocin ointment intranasally, but the effectiveness of this is uncertain
54
What is dermatitis herpetiformis?
Uncommon autoimmune skin condition associated with gluten sensitivity (most have celiac disease)
55
What is the presentation of dermatitis herpetiformis?
Intensely pruritic papules and vesicles (“herpetiform pattern”) on forearm, knees, scalp, and buttocks
56
How is dermatitis herpetiformis diagnosed?
Serologic markers for celiac disease
| -Punch biopsy of perilesional skin and then do direct immunofluorescence (DIF), the gold standard
57
How is dermatitis herpetiformis treated?
Dapsone and gluten elimination
58
What is pemphigus?
A group of rare, autoimmune, life threatening, blistering disorders
59
What are the different types of pemphigus?
Pemphigus vulgaris, pemphigus foliaceus, IgA pemphigus, and paraneoplastic pemphigus
60
What is a herpetiform pattern?
Vesicles on an erythematous base
61
What is the etiology of pemphigus?
Autoimmune
- Antibodies cause acantholysis (separation of epidermal cells from each other) and blistering
- Genetics
- idiopathic
- Some cases are drug induced or environmental
62
What is the clinical presentation of pemphigus?
- 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
What is Nikolsky sign?
Gentle application of lateral pressure of an uninvolved area causes the superficial layer to slough off
64
How is pemphigus diagnosed?
- 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
How is pemphigus treated?
- 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
What is a pemphigoid?
A chronic autoimmune subepithelial blistering disorder
67
What are the two types of pemphigoid?
Bullous pemphigoid and mucous membrane pemphigoid
68
What is the clinical presentation of pemphigoid?
- 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
How is pemphigoid diagnosed?
Biopsy: Lesional (routine histological examination) and perilesional (direct immunofluorescence)
- Direct immunofluorescence is the gold standard
- Serology- indirect immunofluorescence (IIF) and ELISA
70
What is the treatment for pemphigoid?
- General skin care
- Topical and systemic corticosteroids
- Dermatology referral and immunosuppressive agents
71
Describe the progression of pemphigus.
Superficial separation -> intraepidermal acantholysis -> flaccid bulla that rupture easily -> infection -> death if not treated
72
Describe the progression of Pemphigoid?
Deep epidermal junction -> tense bulla that don’t rupture easily -> heal without scarring
73
What is melasma/Chloasma?
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
What is the “mask of pregnancy?”
Melasma or chloasma
75
What is the treatment for melasma?
If it is desired, skin lightening agents and chemical peels may be used.
-Encourage photoprotection
76
What is acanthodians nigricans?
-A common disorder associated with insulin resistance
77
What is the presentation of acanthosis Nigricans? What is the treatment?
Hyperpigmented, velvety plaques.
Treatment is to treat the underlying condition (obesity, DM)
78
What is hirsutism?
Male pattern hair growth in women
79
What causes Cushing syndrome?
Excess androgen/steroid hormone
80
What happens with Cushing Disease?
- It affects pilosebaceous unit
| - increased sebum, acne, andreogenic alopecia, hirsutism, atrophy, and striae
81
What causes Addison’s disease?
Adrenal insufficiency
82
What happens with Addison’s disease?
Hyperpigmentation to the gums, buccal mucosa, elbows, knees, palms, and genitalia
83
What are the effects of hyperthyroid?
- 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
What effect does hypothyroid have on skin?
Cool, dry skin
85
What is porphyria?
Metabolic disorders due to altered activity of enzymes in Heme Synthesis
86
What is the most common type of porphyria?
Porphyria cutanea tarda (PCT)
87
How does uroporphyrinogen decarboxylase (UROD) deficiency lead to porphyria?
UROD breaks down porphyrins so a deficiency in UROD leads to excess porphyrins
88
What are the symptoms of porphyria?
Painless sub-epidermal blistering of skin on sub exposed areas, commonly on dorsum of hands, forearm, face, neck, and feet.
-Photosensitivity
89
What is thought to cause porphyria?
- 20% genetic contribution, 80% sporadic
| - may be associated with tobacco she, EtOH, estrogens, liver disease, or hepatitis
90
How is Porphyria Cutanea Tarda (PCT) diagnosed?
- Elevated serum and/or urinary porphyrins
| - elevated liver tests, increased iron stores, and iron deposition
91
How can PCT be prevented?
- Wearing sun-protective clothing
| - Sunscreen does not always help
92
What is the treatment for PCT?
- Discontinue or treat the potential cause
| - Phlebotomy (Iron depletion prevents formation of UROD inhibitor) and low dose hydroxychloroquine
93
What is a pressure ulcer?
Pressure induced injury over bony prominences, seen commonly on the sacrum and calcaneous
-released to immobility
94
What is the best treatment for a pressure ulcer?
Prevention
95
Describe a stage 1 Pressure injury.
Intact skin with localized erythema
96
Describe a stage 2 pressure injury.
Partial thickness skin loss with exposed dermis. Adipose is not visible, no eschar
97
Describe a stage 3 pressure injury.
```
Full thickness skin loss.
Adipose is visible.
Rolled edges.
Eschar may be visible.
Fascia, muscle, or bone are not exposed
```
98
Describe a stage 4 pressure injury.
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
What is eschar?
Dead tissue that eventually sloughs off healthy skin after an injury.
100
What are the general treatment recommendations for pressure injuries?
- Reduce or eliminate underlying contributing factors such as redistributing pressure
- Local wound care
- Treat infection if present
101
What is the recommended treatment for a stage 1 pressure injury?
Transparent film for protection
102
What is the recommended treatment for a stage 2 pressure injury?
Dressing that maintains moist wound environment (if there is no infection.)
Debridement is normally not necessary
103
What is the recommended treatment for a stage 3 & 4 pressure injury?
Debridement of necrotic tissue, appropriate dressing, and antibiotics
104
What are the 2 dermatologic findings associated with tick borne illnesses?
Erythema migrans and Rocky Mountain spotted fever
105
How can tick borne illnesses be prevented?
- 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
What is the proper way to remove a tick?
Grasp the tick as close to the skin surface with tweezers and pull straight up with steady pressure.
-No twisting, jerking, or crushing
107
How quickly is Lyme disease transmitted after tick bite?
2-3 days
108
What is erythema migrans also known as?
Lyme disease
109
What is the pathogenesis of Lyme disease?
Borrelia Burgdorferi
110
What is the clinical presentation of Erythema Migrans (Lyme disease)?
- Characteristic rash occurs 7-14 days after tick bite.
| - Slightly raised, warm, red with central clearing and Bulls eye appearance
111
What are the associated symptoms in the early stages of Erythema Migrans?
Fatigue, Headache, myalgia, arthralgia, and fever
112
What are the symptoms in the later stages of Erythema Migrans?
- cardiac, arthritis, and neurologic symptoms
| - If Bell’s palsy, consider Lyme in differential if in endemic areas
113
What is the treatment for Erythema migrans?
Usually doxycycline or Amoxicillin
114
What is the Lyme disease prophylaxis when the tick has been attached for greater than 36 hours?
Doxycycline 200mg single dose within 72 hours of removal.
115
What is the pathogenesis of Rocky Mountain spotted fever?
Rickettsia Rickettsia
116
When does the rash appear in Rocky Mountain spotted fever? What is the presentation of the rash?
- Within 3-5 days
| - Starts as a macular rash and turns into petechial lesions. Commonly on the ankles, wrists, and then trunk.
117
What percentage of patients with Rocky Mountain spotted fever do not get a rash? Why is this important?
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
Other than a rash, what are the symptoms of Rocky Mountain spotted fever?
Fever, HA, malaise, myalgia, arthritis, and nausea for 2-14 days after tick bite
119
How is Rocky Mountain Spotted fever diagnosed?
- Commonly a clinical diagnosis
| - Serology, though there may be a delay in antibody detection
120
What is the treatment for Rocky Mountain spotted fever?
- Empiric treatment based on clinical suspicion.
- Doxycycline
- Antibiotics have resulted in marked reduction in fatality rate
