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CMT-uno > Dermatology 1 > Flashcards

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
Q

EDC Process (3 steps)

A
  1. Curette over lesion in all 4 directions
  2. Cauterize skinwith safety margin
  3. Repeat for total of 3 passes
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26
Q

Shave biopsy

A

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

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27
Q

Punch Biopsy

A

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

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28
Q

Excisional Biopsy

A

typically done by dermatologist/derm surgeon

the complete removal of a skin lesion w a margin surounding tissue taken to minimize recurrence

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29
Q

MOHS

A

Lower recurrence rate

done by derm surgeon

complete histologic analysis of the tumor margins while permitting the max conservation of tissue.

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30
Q

MOHS indicators (4)

A
  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
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31
Q

Patch Testing
What kind of sensitivity and how long does it take

A

used for contact sensitivity for allergens

testing Type IV Hypersensitivity rxn

requires large area of skin, takes 2-5 days

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32
Q

Cryotherapy

A

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.

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33
Q

does crytherapy require anesthetic

A

Does not require local anesthetic, is generally well tolerated, and requires minimal wound care after the procedure.

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34
Q

ABCDE

A

A- Asymmetry
B- Border
C- Color
D- Diameter
E- Evolving

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35
Q

Melanoma size

A

Melanomas are usually greater than 6 mm

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36
Q

Biopsy of pigmented lesion indications

6

A

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

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37
Q

Biopsy of pigmented lesion photos

A

take 2

one upclose and second at a distant for landmarks.

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38
Q

Biopsy- how much do you remove?

A

biopsy the entire lesion, unless very large in size

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39
Q

When should a melonoma biopsy be referred to a derm provider?

A

a basic rule for non-dermatology providers to follow is never do a superficial shave biopsy that you are considering for a possible melanoma

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40
Q

Lentigo

A

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.

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41
Q
A

Lentigo

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42
Q

Acanthosis nigricans clinical manifestation

A

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.

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43
Q

Acanthosis nigricans is associated with? (3)

A

Associated with insulin resistance – diabetes mellitus, metabolic syndrome, and polycystic ovarian syndrome.

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44
Q
A

Acanthosis nigricans

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45
Q

Melasma is also called?

A

Chloasma

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46
Q

Melasma or Chloasma clinical manifestation

A

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

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47
Q

Melasma or Chloasma is associated with?

A

Associated with hormonal changes, but it may occur idiopathically, with use of birth control pills or hormone replacement therapy

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48
Q

Melasma Tx

A

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

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49
Q

Hydroquinone should be reserved for what time of year?

A

for fall/winter months

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50
Q
A

Melasma / Chloasma

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51
Q
A

Seborrheic Keratosis (SK) (wisdom spots)

pigmented lesions

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52
Q

Seborrheic Keratosis (SK)

where is it commonly found, and what are the Clinical manifestations?

A

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.

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53
Q

Tx Seborrheic Keratosis (SK)

A

No treatment necessary

Can be symptomatically treated with cryotherapy - can recur with time.

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54
Q

MELANOCYTIC Nevi

A

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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55
Q
A

MELANOCYTIC Nevi

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56
Q

Congenital melanocytic nevi

A

tend to be the most prominent and persist throughout life

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57
Q

acquired melanocytic nevi

A

follow sun exposure, may fade away

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58
Q
A

MELANOCYTIC nevi

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59
Q
A

Atypical or dysplastic Nevi

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60
Q

Atypical or dysplastic Nevi

general and clin manifestations (5)

A

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

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61
Q

Atypical or dysplastic Nevi Tx

A

shave biopsy to determine atypia
then,
Mild DN: monitor for recurrence
Moderate, Severe DN - excision

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62
Q

Atypical or dysplastic Nevi

Spectrum of atypia

A

Mild —> Moderate —> Severe —> melanoma in situ —> malignant melanoma

63
Q

Blue nevus

General, Clin Mani, Tx

A

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
Q

Melanoma

epidemiology

ages, how common?

A

Lifetime risk of melanoma has increased
Affects all ages
The second most common cancer among young women ages 15-29

65
Q
A

Blue Nevus

66
Q

Melanoma

how does it develop?

A

Etiology:
Cumulative and prolonged UV exposure

67
Q

melanoma

What are risks of tanning bed?

A

Tanning bed use increased risk of melanoma by 75%
Especially risky if used before age 35 and risk increase with each exposure

68
Q

melanoma

risk factors

7

A

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

69
Q
A

melanoma

70
Q
A

melanoma

71
Q
A

basal cell carcinoma

72
Q

basal cell carcinoma

general and etiology

A

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
Q

basal cell carcinoma

risk factors

4

A

Fitzpatrick skin types 1 & 2
Severe actinic damage
Males > females
Immunosuppression

74
Q

basal cell carcinoma

types of clinical manifestations

2

A

Nodular BCC

Superficial BCC

75
Q

Nodular BCC
General

A

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
Q

superficial BCC Clin Man

A

Slightly scaly, “eczematous-like” macules, patches, or thin plaques with characteristic raised, pearly white rolled border
Pink to light red

77
Q
A

BCC

78
Q

melanoma

Clinical Manifestations

A

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
Q

melanoma

prognosis and prognosis factors

A

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
Q

when should you refer to derm?

A

If you suspect melanoma, refer to dermatology for biopsy

81
Q

melanoma

Main Tx

A

Dependent on Stage - based on Breslow’s depth, ulceration, lymph node involvement

Mainstay of treatment: Surgical excision with wide margins +/- lymph node biopsy

82
Q

melanoma

follow up

A

Seen by dermatology every 6 months for 10 years, then yearly for life
Annual eye examination
Annual complete physical examination

83
Q
A

BCC

84
Q
A

BCC, think malignant melanoma

85
Q
A

BCC that can easily be mistaken for excema

86
Q
A

BCC

87
Q
A

BCC

88
Q

BCC

Surgical Tx

A

Electrodessication and curettage
Excision
MOHS

89
Q

BCC

Non surgical Tx

A

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
Q

Squamous cell carcinoma

progression

A
91
Q

actinic keratosis

etiology

A

Etiology: cumulative and prolonged UV exposure resulting in genetic mutation of keratinocytes.

92
Q

Actinic Keratosis

Risk Factors (5)

A
  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
Q

Actinic Keratosis (AK)

Clin Man

A

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
Q
A

actinic keratosis

95
Q

AK

Tx types

2 types of therapy

A

There are several topical and procedural treatment options for AKs

Localized therapy

field therapy

96
Q

AK

localized therapy

A

Typically treated with cryotherapy

97
Q

AK

Field Therapy

A

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
Q

SCC in Situ / Bowen disease

Clin Man

A

(progress from AK)

well defined circumscribed pink to red patch or thin plaque with scaly/rough surface

99
Q

SCC in Situ / Bowen disease

Plan and Tx

A

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
Q
A

SCC in situ / bowen disease

101
Q
A

SCC

102
Q

SCC

how common & mortality?

A

Second most common dermatologic malignancy.
Increased mortality compared to basal cell carcinoma, due to a higher rate of metastasis

103
Q

SCC

etiology

A

Cell of origin: keratinocyte
Cumulative UV exposure is a major risk factor as it results in genetic alterations

104
Q

SCC

Risk factors

A

Most commonly occurs in fair skin individuals - think Fitzpatrick 1&2
Increase risk with tanning bed use
Chemical carcinogen exposure - arsenic

105
Q
A

SCC

106
Q

SCC

Tx
Standard, poor surgical candidates, non surgical candidates

A

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
Q

Urticaria

general
Type of sensitivity

A

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
Q

urticaria

common causes

A

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
Q

Urticaria

Clin Man

A

Trademark: ITCH!
Lesions appears over the course of minutes, enlarge, and then disappear within hours (rarely longer than 12 hours)
Blanch with pressure

110
Q

Urticaria

Tx

A

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
Q
A

Urticaria

112
Q
A

angioedema

113
Q

angioedema

general what type of rxn and what Med can initiate it?

A

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
Q

angioedema

ClinMan

A

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
Q

angioedema

Tx what about if it’s severe?

A

IV or oral glucocorticoids and 1st generation antihistamines
Epinephrine if severe

116
Q

Stevens-johnson Syndrome

AKA

A

Toxic Epidermal necrolysis

117
Q

Stevens-Johnson syndrome

general

A

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
Q

Stevens-Johnson syndrome

mortality rate

A

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
Q
A

Stevens-Johnson syndrome / Toxic Epidermal necrolysis

120
Q

Stevens-Johnson syndrome / Toxic Epidermal necrolysis

is associated with? and when does it happen?

A

Associated with medications, especially
Sulfa drugs, sulfasalazine
Allopurinol
Tetracyclines
Anticonvulsants
NSAIDS
(SATAN)

Typically begins within the first 8 weeks after drug initiation

121
Q

Stevens-Johnson syndrome

Clin Man

A

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
Q

SJS

Initial lesions

A

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
Q

SJS

mucous membrane involvement

A

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
Q
A

Stevens-Johnson Syndrome

125
Q

SJS/TEN

classification

A

SJS - less than10%
SJS/TEN - 10-30%
TEN - greater than 30%

126
Q

SJS / TEN

Tx

A

hospital admission to burn unit
Stop offending medication
Will require multidisciplinary care during admission

Therapies include IV corticosteroids, IVIG, cyclosporine, etanercept

127
Q

Erythema Multiforme

General, age group affected
Type of sensitivity

A

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
Q
A

Erythema Multiforme

129
Q

Erythema multiforme

Risk Factors

A

Infections: HSV, mycoplasma, S. pneumoniae
Medications: sulfa drugs, beta-lactams, phenytoin, phenobarbital, allopurinol
(PHABS)
Malignancy
Autoimmune
Idiopathic

130
Q

Erythema multiforme

Clinical Manifestations:

A

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
Q

erythema multiforme

minor vs major

A

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
Q

Erythema multiforme

Tx
Severe

A

Remove offending drugs, topical steroids, antihistamines, analgesics.

Systemic corticosteroids if severe.

Antibiotics if mycoplasma is inciting cause

133
Q

Brown recluse spider bite

general

A

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
Q

Brown rescluse bite

Clin Man

A

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
Q
A

Brown recluse spider bite

136
Q

Brown recluse spider bite

Tx

A

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
Q

Black widow

general

A

Black widow spider produces a neurotoxin
Characteristic right hourglass shape on the underside of its belly.

138
Q

black widow

Clinical Manifestations

A

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 appearanceblanched circular patch with erythematous perimeter and central punctum

139
Q

black widow

Tx

A

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
Q
A

black widow bite

141
Q
A

cellulitis

142
Q

cellulitis

general and agents

A

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
Q

cellulitis

risk factors

A

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
Q

cellulitis

clin man

A

Spreading erythematous, non-fluctuant, tender, poor-defined plaque
Tends to occur on lower extremities

145
Q

cellulitis

Tx

purulent vs not

A

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
Q

Erysipelas

general

A

Superficial cellulitis with marked dermal lymphatic involvement - causes edema
Main pathogen: Group A Streptococcus
Others: S. aureus, Haemophilus

147
Q

Erysipelas

Clin Man

A

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
Q
A

Erysipelas

reactive erythema

149
Q

Erysipelas

Tx

A

Empiric antibiotic therapy - penicillin V, amoxicillin, clindamycin, azithromycin
Elevation of involved area
Monitor patients closely

150
Q

Lymphangitis

general

A

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
Q

Lymphangitis

clin man

A

Red, tender streaks extending proximally from a site of cellulitis
May have lymphadenopathy or systemic symptoms such as fever and chills

152
Q
A

Lymphangitis

153
Q

Lymphangitis

Tx oral and IV
MRSA pal and IV

A

Oral: cephalexin, dicloxacillin. Erythromycin or Clindamycin if penicillin allergy
IV: cefazolin, ampicillin-sulbactam, ceftriaxone + Clindamycin

MRSA:
Oral: TMP-SMZ+cephalexin
IV: vancomycin

CMT-uno (54 decks)

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