Dermatology 1 Flashcards

1
Q

t

Macule

general and give an example

A

flat, non-palpable lesion
less than 1cm in size

e.g. freckle

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2
Q

Patch

A

Flat, non-palpable lesion
Greater than 1cm in size
Think macule, but bigger!

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3
Q

Papule

A

Raised, palpable, solid lesion that is a proliferation of cells in the epidermis and/or superficial dermis
Less than 1cm in size

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4
Q

Nodule

A

Raised, palpable, solid lesion
Deep seated- Located mid-deep dermis
Think papule, but deeper!

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5
Q

Pustule

A

variation of a papule (less than 1cm)
contains purulent fluid

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6
Q

Vesicle

General and example

A

variation on papule

Raised, circumscribed lesion
Contains clear to yellow-tinged serous fluid
Less than 1cm in size

e.g. HSV, Herpes Zoster, blister

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7
Q

Bulla

A

Raised, circumscribed lesion
Contains clear to yellow-tinged serous fluid
Greater than 1cm in size
Think vesicle, but larger!

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8
Q

Plaque

A

Raised, palpable flat-topped lesion
Can be formed by confluent papules
Greater than 1cm in size

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9
Q

Wheal

A

Localized edema
Variety of sizes, typically elevated - sometimes called papules and plaques
Transient, lasting <24 hours

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10
Q

Ulceration

A

full thickness loss of epidermal and dermal skin

graded by depth, can leak fluid or covered in hemorrhagic crust

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11
Q

Erosion

A

loss of superficial epidermis

think unhooded bulla

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12
Q

What is the difference between ulceration and erosion

A

erosion is surface level, an ulcer is deep.

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13
Q

Excoriation

A

superficial abrasion of the skin

typically result of scratching, rubbing, digging, squuezing of skin

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14
Q

Fissure

A

Vertical loss of epidermis extending through the epidermal and dermal skin

think deep cracks in the skin

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15
Q

Scales

A

Flakes or plates of compacted, desquamated layers or stratum corneum

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16
Q

Lichenification

A

Thickened, rough skin
Typically due to chronic inflammation and irritation

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17
Q

Woods Lamp Eval

A

use of black light for diagnosis

held 10-12 cm away

mostly for vitiligo and certain tinea infections

rarely used in practice

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18
Q

Microscopic eval

A

use a skin scrape (no blood should be drawn)

Potassium Hydroxide (KOH) or Mineral Oil Prep

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19
Q

KOH Microscopic Eval

A

useful for Dx fungal infections

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20
Q

Mineral Oil microscopic eval

A

useful for Dx of mites (scabies)

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21
Q

Bacterial Cultures are used for

A

used for open wounds, pustules, cystic, lesions, rashes.

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22
Q

Viral culture

A

consider if vesicles are present

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23
Q

most common injections, what are they used for?

A

intralesional corticosteroids

epidermal inclusion cysts, cystic acne lesions, and more

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24
Q

(EDC) Electrodessication and curettage
How deep, and commonly used for

A

Use of electrocautery and scraping with a curette that results in the destruction of a superficial skin lesion.

common for carcinomas

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25
EDC Process (3 steps)
1. Curette over lesion in all 4 directions 2. Cauterize skinwith safety margin 3. Repeat for total of 3 passes
26
Shave biopsy
Used for superficial skin lesions to confirm diagnosis Does not include the full thickness of the skin No stitches required – the wound forms a scab that should heal in one to three weeks
27
Punch Biopsy
full thickness sample of the skin A disposable, round stainless steel blade is rotated through the skin Typically 3, 3.5, 4 mm punches are used Suture may be used to close a punch biopsy wound or control bleeding, but it’s not necessary with smaller biopsy diameters | 4 and larger typically need stitches
28
Excisional Biopsy
typically done by dermatologist/derm surgeon the complete removal of a skin lesion w a margin surounding tissue taken to minimize recurrence
29
MOHS
Lower recurrence rate done by derm surgeon complete histologic analysis of the tumor margins while permitting the max conservation of tissue.
30
MOHS indicators (4)
1. Location on face, nose, lips, ears, hands, scalp, groin 2. Aggressive malignancy subtypes: infiltrative, sclerosing, morpheaform, micronodular 3. large tumors or tumors with indistinct borders 4. recurrent tumors
31
Patch Testing What kind of sensitivity and how long does it take
used for contact sensitivity for allergens **testing Type IV Hypersensitivity rxn** requires large area of skin, takes 2-5 days
32
Cryotherapy
liquid nitrogen directly to the skin for short durations of time results in the cryo- destruction of the superficial layers of the skin. results in blister-like lesion initially that transform into an eschar that will be shed from the skin over a 2-4 week period.
33
does crytherapy require anesthetic
Does not require local anesthetic, is generally well tolerated, and requires minimal wound care after the procedure.
34
ABCDE
A- Asymmetry B- Border C- Color D- Diameter E- Evolving
35
Melanoma size
Melanomas are usually greater than 6 mm
36
Biopsy of pigmented lesion indications | 6
Consider biopsy if there are pigmentary changes, changes in border or diameter, bleeding, itching, a new lesion in a patient over 50 years of age, the ugly duckling sign
37
Biopsy of pigmented lesion photos
take 2 one upclose and second at a distant for landmarks.
38
Biopsy- how much do you remove?
biopsy the entire lesion, unless very large in size
39
When should a melonoma biopsy be referred to a derm provider?
**a basic rule for non-dermatology providers to follow is never do a superficial shave biopsy that you are considering for a possible melanoma**
40
Lentigo
freckles, sun spots, age spots benign, brown macules and patches typically found in sun exposed areas result of UV damage no Tx, use sunscreen to minimize appearance.
41
Lentigo
42
Acanthosis nigricans clinical manifestation
Clinical manifestations: velvety, hyperpigmented plaques on intertriginous areas, especially the neck and axillary regions. Associated with insulin resistance – diabetes mellitus, metabolic syndrome, and polycystic ovarian syndrome.
43
Acanthosis nigricans is associated with? (3)
Associated with insulin resistance – diabetes mellitus, metabolic syndrome, and polycystic ovarian syndrome.
44
Acanthosis nigricans
45
Melasma is also called?
Chloasma
46
Melasma or Chloasma clinical manifestation
Characterized by patchy light to dark brown hyperpigmentation of the face Usually affects women and may run in families Hyperpigmentation will worsen with exposure to UV light
47
Melasma or Chloasma is associated with?
Associated with hormonal changes, but it may occur idiopathically, with use of birth control pills or hormone replacement therapy
48
Melasma Tx
strict sun avoidance, use of SPF 30 to 50 daily. Hydroquinone 4% cream qd-bid to affected area up to one month at a time, can be repeated for a second month. Use of hydroquinone should be reserved for fall/winter months. Advise patients that hyperpigmentation can recur if area is exposed to UV
49
Hydroquinone should be reserved for what time of year?
for fall/winter months
50
Melasma / Chloasma
51
Seborrheic Keratosis (SK) (wisdom spots) | pigmented lesions
52
Seborrheic Keratosis (SK) | where is it commonly found, and what are the Clinical manifestations?
Most common benign epidermal skin growth Common in fair skin, elderly individuals, with a history of prolonged sun exposure. Clinical Manifestations: Well demarcated, round or oval, velvety, warty lesions with a greasy or “stuck“ appearance. Variety of colors from flesh colored to brown or black. May be scaly. Usually asymptomatic, but irritation due to friction may lead to pruritis, pain, or bleeding.
53
Tx Seborrheic Keratosis (SK)
No treatment necessary Can be symptomatically treated with cryotherapy - can recur with time.
54
MELANOCYTIC Nevi
A common benign skin lesion due to localized proliferation of melanocytes Can be present at birth (congenital) or appear later in life (acquired) e.g. mole more common in fair-skinned pts variety of presentations, colors,shapes, flat/raised, pink to black
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MELANOCYTIC Nevi
56
Congenital melanocytic nevi
tend to be the most prominent and persist throughout life
57
acquired melanocytic nevi
follow sun exposure, may fade away
58
MELANOCYTIC nevi
59
Atypical or dysplastic Nevi
60
Atypical or dysplastic Nevi | general and clin manifestations (5)
A melanocytic nevi with atypical features Clinical Manifestations Nevus with at least 3 of the following features Size >5mm Ill-defined or blurry borders Irregular margin —unusual shape Variety of colors within lesion Flat and bumpy components
61
Atypical or dysplastic Nevi Tx
shave biopsy to determine atypia then, Mild DN: monitor for recurrence Moderate, Severe DN - excision
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# Atypical or dysplastic Nevi Spectrum of atypia
Mild —> Moderate —> Severe —> melanoma in situ —> malignant melanoma
63
# Blue nevus General, Clin Mani, Tx
General Type of melanocytic nevus which are located deep within the dermis. Twice as common in women as in men More prevalent among Asian populations Can rarely form into melanoma Clinical Manifestations Solitary, bluish-grey, smooth-surfaced macule, papule, or plaque Treatment: observation
64
# Melanoma epidemiology | ages, how common?
Lifetime risk of melanoma has increased Affects all ages The second most common cancer among young women ages 15-29
65
Blue Nevus
66
# Melanoma how does it develop?
Etiology: Cumulative and prolonged UV exposure
67
# melanoma What are risks of tanning bed?
Tanning bed use increased risk of melanoma by 75% Especially risky if used before age 35 and risk increase with each exposure
68
# melanoma risk factors | 7
1.Increasing age 2.Fitzpatrick skin types 1&2 3.Greater than 25 acquired nevi 4.Atypical nevi 5.Immunosuppression 6.Personal or family history (1st degree relatives) of melanoma 7.UV exposure Severe blistering sunburns before puberty Indoor tanning
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melanoma
70
melanoma
71
basal cell carcinoma
72
# basal cell carcinoma general and etiology
General: Most common skin cancer Arises from the basal layer of the epidermis Locally invasive, metastasis is rare Etiology: Exposure to UV radiation induced DNA damage - think patients with significant sunburn history, tanning bed use
73
# basal cell carcinoma risk factors | 4
Fitzpatrick skin types 1 & 2 Severe actinic damage Males > females Immunosuppression
74
# basal cell carcinoma types of clinical manifestations | 2
Nodular BCC Superficial BCC
75
Nodular BCC General
raised, dome-shaped, papules with “rolled” borders and central depression/ulceration with overlying telangectasias Pink, white or flesh-colored Translucent, waxy, or pearly quality
76
superficial BCC Clin Man
Slightly scaly, “eczematous-like” macules, patches, or thin plaques with characteristic raised, pearly white rolled border Pink to light red
77
BCC
78
# melanoma Clinical Manifestations
Usually asymptomatic, pigmented papule, plaque, or nodule with any of the ABCDE features Can bleed, be eroded, or crusted History of changing appearance Most are de novo - arise from within an existing lesion Sun-exposed or non-sun-exposed areas
79
# melanoma prognosis and prognosis factors
Course and Prognosis High cure rates if diagnosed and treated early Prognostic Factors: Thickness or depth of tumor invasion - Breslow’s depth Survival decreases with increasing Breslow’s depth Ulceration = worse prognosis Involvement of lymph nodes or distant metastases have worse prognosis **If you suspect melanoma, refer to dermatology for biopsy**
80
when should you refer to derm?
If you suspect melanoma, refer to dermatology for biopsy
81
# melanoma Main Tx
Dependent on Stage - based on Breslow’s depth, ulceration, lymph node involvement Mainstay of treatment: Surgical excision with wide margins +/- lymph node biopsy
82
# melanoma follow up
Seen by dermatology every 6 months for 10 years, then yearly for life Annual eye examination Annual complete physical examination
83
BCC
84
BCC, think malignant melanoma
85
BCC that can easily be mistaken for excema
86
BCC
87
BCC
88
# BCC Surgical Tx
Electrodessication and curettage Excision MOHS
89
# BCC Non surgical Tx
reserved for superficial BCC or poor surgical candidate -Imiquimod 5% cream - weeknight application x 6 weeks to affected area -Fluorouracil 5% cream bid to affected area up to 12 weeks until response -Radiation
90
# Squamous cell carcinoma progression
91
# actinic keratosis etiology
Etiology: cumulative and prolonged UV exposure resulting in genetic mutation of keratinocytes.
92
# Actinic Keratosis Risk Factors (5)
1. Increasing age 2.fair skin, light eyes/hair - think Fitzpatrick skin types 1 & 2 3.Immunosuppression 4.Prior radiation history 5.Albinism **AKs have the potential to transform into squamous cell carcinoma over time**
93
# Actinic Keratosis (AK) Clin Man
Erythematous to tan, flat papule or thin plaque with a characteristic rough, gritty scale. **Feels like sandpaper.** Can present as a hypertrophic papule Located in sun exposed areas, typically on sun damaged skin. **Maybe tender to touch**
94
actinic keratosis
95
# AK Tx types | 2 types of therapy
There are several topical and procedural treatment options for AKs Localized therapy field therapy
96
# AK localized therapy
Typically treated with cryotherapy
97
# AK Field Therapy
Typically treated with topical 5-fluorouracil or imiquimod 5%cream 5-FU: twice daily application to affected area, typically treated for 2 to 4 weeks depending on treatment area, until erythematous, hemorrhagic crust formation. Imiquimod 5% cream MWF at night, typically treated for four weeks until erythematous, hemorrhagic crust formation. * better compliance due to once daily application, more tolerable for patients than 5-FU
98
# SCC in Situ / Bowen disease Clin Man
(progress from AK) well defined circumscribed pink to red patch or thin plaque with scaly/rough surface
99
# SCC in Situ / Bowen disease Plan and Tx
Plan: Biopsy - pathology will indicate that atypia is confined to the epidermis. Treatment Options: Cryotherapy, typically followed with either 5-fluorouracil or Imiquimod Electrodesiccation and curettage
100
SCC in situ / bowen disease
101
SCC
102
# SCC how common & mortality?
Second most common dermatologic malignancy. Increased mortality compared to basal cell carcinoma, due to a higher rate of metastasis
103
# SCC etiology
Cell of origin: keratinocyte Cumulative UV exposure is a major risk factor as it results in genetic alterations
104
# SCC Risk factors
Most commonly occurs in fair skin individuals - think Fitzpatrick 1&2 Increase risk with tanning bed use Chemical carcinogen exposure - arsenic
105
SCC
106
# SCC Tx Standard, poor surgical candidates, non surgical candidates
Treatment: medical and surgical treatment options Standard of care: surgical excision or MOHS Poor surgical candidates: radiation therapy Non-surgical candidates: Fluorouracil, imiquimod, and others
107
# Urticaria general Type of sensitivity
Vascular reaction of the upper epidermis characterized by wheals surrounded by a erythematous halo The mast cell is the major player in urticaria - release histamine Type 1 hypersensitivity reaction Think hives | Reactive Erythemas
108
# urticaria common causes
Idiopathic Infection Food reaction Drug reaction - penicillins, aspirin, NSAIDs (PAN) IV administration of blood products or contrast dye Physical causes: pressure cold/heat, water, sunlight, exercise, emotion Autoimmune
109
# Urticaria Clin Man
Trademark: ITCH! Lesions appears over the course of minutes, enlarge, and then disappear within hours (rarely longer than 12 hours) Blanch with pressure
110
# Urticaria Tx
First-line: 1st generation antihistamines (Benadryl, hydroxyzine) 1st generation antihistamines cause more sedation, require dose adjustment in children, elderly, renal or hepatic impairment, respiratory disease, BPH, glaucoma. Real-life: 2nd generation antihistamines are used more commonly
111
Urticaria
112
angioedema
113
# angioedema general what type of rxn and what Med can initiate it?
Can be caused by the same mechanisms as urticaria, but is located in the deep dermis and subcutaneous tissue Type 1 hypersensitivity reaction **Check for ACE - Inhibitor use!**
114
# angioedema ClinMan
Trademark swelling - most commonly affects the face (lips, cheeks, periorbital areas) or portion of an extremity Concerning if the tongue, pharynx, larynx, and bowels are affected May be painful or burning - usually not pruritic May last several days
115
# angioedema Tx what about if it’s severe?
IV or oral glucocorticoids and 1st generation antihistamines Epinephrine if severe
116
# Stevens-johnson Syndrome AKA
Toxic Epidermal necrolysis
117
# Stevens-Johnson syndrome general
Acute, life-threatening mucocutaneous reactions Characterized by extensive necrosis and detachment of the epidermis and/or mucosal surfaces Similar processes but differ in severity based on total body’s surface area involved
118
# Stevens-Johnson syndrome mortality rate
Mortality rate varies from 5-12% for SJS and >20% for TEN Increasing age, comorbidities, greater extent of skin involvement correlated with poor prognosis
119
Stevens-Johnson syndrome / Toxic Epidermal necrolysis
120
# Stevens-Johnson syndrome / Toxic Epidermal necrolysis is associated with? and when does it happen?
Associated with medications, especially Sulfa drugs, sulfasalazine Allopurinol Tetracyclines Anticonvulsants NSAIDS (SATAN) Typically begins within the first 8 weeks after drug initiation
121
# Stevens-Johnson syndrome Clin Man
Eruption is initially symmetric and distributed on the face, upper trunk, and proximal extremities Pain is a prominent symptom in skin lesions - signifies necrosis Lesions can rapidly extend to the rest of the body The epidermis, especially when necrotic, is easily detached at pressure points or by friction trauma revealing exposed, erythematous, sometimes oozing dermis.
122
# SJS Initial lesions
Initial lesions are characterized by erythematous, irregularly-shaped, dusky red to pruritic macules, which progressively coalesce and evolve to flaccid blisters, which spread with pressure and break easily
123
# SJS mucous membrane involvement
Mucous membranes involvement begins with erythema, follow by painful erosions of mouth, eyes, and genitals - ocular involvement can result in permanent ocular damage or blindness
124
Stevens-Johnson Syndrome
125
# SJS/TEN classification
SJS - less than10% SJS/TEN - 10-30% TEN - greater than 30%
126
# SJS / TEN Tx
hospital admission to burn unit Stop offending medication Will require multidisciplinary care during admission Therapies include IV corticosteroids, IVIG, cyclosporine, etanercept
127
# Erythema Multiforme General, age group affected Type of sensitivity
Type 4 hypersensitivity reaction of the skin following infectious exposure or medication exposure Most commonly affects young adults (20-40 years old) | reactive erythema
128
Erythema Multiforme
129
# Erythema multiforme Risk Factors
Infections: HSV, mycoplasma, S. pneumoniae Medications: sulfa drugs, beta-lactams, phenytoin, phenobarbital, allopurinol (PHABS) Malignancy Autoimmune Idiopathic
130
# Erythema multiforme Clinical Manifestations:
Hallmark: **target lesion** 3 components: dusky, central area or bulla; dark red inflammatory zone surrounded by a pale ring of edema ; erythematous halo on periphery Negative nikolsky sign
131
# erythema multiforme minor vs major
Minor: target lesions distributed on extremities with *no mucosal membrane involvement* Major:target lesions on extremities with central progression *with mucosal membrane involvement. No epidermal detachment*
132
# Erythema multiforme Tx Severe
Remove offending drugs, topical steroids, antihistamines, analgesics. Systemic corticosteroids if severe. Antibiotics if mycoplasma is inciting cause
133
# Brown recluse spider bite general
Most common in the midwestern and southwestern US The brown recluse spider has a violin pattern on it cephalothorax Venom is cytotoxic and hemolytic – local symptoms, can be necrotic, associated with a lack of severe systemic symptoms.
134
# Brown rescluse bite Clin Man
Burning sensation Typical progression: erythema at bite site for 3 to 4 hours, followed by *blanching* of the affected area, followed by a “red halo” (erythematous margin around the ischemic center) for 24 to 72 hours, followed by a hemorrhagic bulla that undergoes eschar formation May develop skin necrosis Systemic side effects: fever, chills, nausea, vomiting, or a morbilliform rash
135
Brown recluse spider bite
136
# Brown recluse spider bite Tx
Local wound care and pain control Most wounds heal spontaneously with adequate cleansing Pain control: NSAIDs are mostly commonly used, opioids if severe, refractory pain Necrosis: debridement once the lesion is well demarcated Antibiotics only if secondary infection present Tetanus vaccination if needed
137
# Black widow general
Black widow spider produces a neurotoxin Characteristic right hourglass shape on the underside of its belly.
138
# black widow Clinical Manifestations
Typical progression: localized pain at the bite site with the onset of systemic and neurologic symptoms within 30 minutes to 2 hours after bite Muscle pain is most common symptom, typically in the extremities, abdomen, or back Spasms and rigidity possible **Classic appearance**blanched circular patch with erythematous perimeter and central punctum
139
# black widow Tx
Usually self limited, tends to resolve within 1 to 3 days. Wound care and pain and spasm control Most wounds heal spontaneously with adequate cleansing Pain control: NSAIDs are mostly commonly used Muscle relaxants for spasm - benzodiazepines Antivenom - reserved for refractory symptoms. Tetanus vaccination if needed
140
black widow bite
141
cellulitis
142
# cellulitis general and agents
Results from an infection of the dermis that often begins with loss of integrity of the skin 80% of cases are caused by Gram - Positive organisms (Group A Strep) Staphylococcus aureus - IV drug use MRSA - purulent drainage present Pasteurella multiocida - animal bites
143
# cellulitis risk factors
Local trauma - insect/animal bite, laceration, abrasion, puncture wound Spread of a preceding or concurrent skin lesion - furuncle, ulcer Pre-existing skin infection due to compromised skin barrier Edema and impaired lymphatics in the affected area
144
# cellulitis clin man
Spreading erythematous, non-fluctuant, tender, poor-defined plaque Tends to occur on lower extremities
145
# cellulitis Tx | purulent vs not
Non-purulent cellulitis: Cephalexin, amoxicillin, amoxicillin- clavulanate (animal bites), or clindamycin Purulent cellulitis: Clindamycin, TMP/SMX, doxycycline + amoxicillin General measures - elevation of extremity, cool compresses
146
# Erysipelas general
Superficial cellulitis with marked dermal lymphatic involvement - causes edema Main pathogen: Group A Streptococcus Others: S. aureus, Haemophilus
147
# Erysipelas Clin Man
Usually affects face, lower extremities Painful, bright red erythematous, plaque-like edema with sharp margin May develop bullae Can be associated with high WBC count (>20,000/mcl) Can have associated fever, chills, headache, vomiting, joint pain
148
Erysipelas | reactive erythema
149
# Erysipelas Tx
Empiric antibiotic therapy - penicillin V, amoxicillin, clindamycin, azithromycin Elevation of involved area Monitor patients closely
150
# Lymphangitis general
Inflammation of lymphatic channels due to infectious or non infectious causes Pathogens include bacteria, viruses, fungi, and parasites - typically introduced through a skin wound or as a complication of a distal infection.
151
# Lymphangitis clin man
Red, tender streaks extending proximally from a site of cellulitis May have lymphadenopathy or systemic symptoms such as fever and chills
152
Lymphangitis
153
# Lymphangitis Tx oral and IV MRSA pal and IV
Oral: cephalexin, dicloxacillin. Erythromycin or Clindamycin if penicillin allergy IV: cefazolin, ampicillin-sulbactam, ceftriaxone + Clindamycin MRSA: Oral: TMP-SMZ+cephalexin IV: vancomycin