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Clin Med 2 > Dermatology > Flashcards

Dermatology Flashcards

1
Q

Eccrine Glands

A

A type of sweat gland
opens directly onto skin
regulates body temperature through sweat

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2
Q

Apocrine Glands

A 
A type of sweat gland 
opens directly into hair follicles 
found in axillae and anogenital areas 
becomes active during puberty, decrease in aging adult 
produce body odor
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3
Q

ABCDE Rule

A 
For nevi 
A - asymmetry 
B - borders (regular vs irregular) 
C - color (uniformity; tan, black, blue, red) 
D - diameter (>6mm) 
E - evolution or elevation
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4
Q

Secondary Skin Lesion

A

Later evolution or result of external trauma to the primary lesion

ex. 
Erosion 
Ulcer
Fissure 
Excoriation 
Atrophy 
Scaling 
Crusting
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5
Q

Most common types of skin cancer arise from which skin layer?

A

Epidermis

Remember the layers by “Come Lets Get Sun Burnt”

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6
Q

What are the two main cell types in epidermis?

A

Keratinocyte - (epithelial cells) starts out in the basal cell membrane and differentiates all the way to the corneum (dead cell layer) —keratinocyte carcinoma
Melanocyte - pigment cells - located in between the dermis and epidermis –melanoma

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7
Q

What is the difference between BCC and SCC?

A

Both types of keratinoctye carcinomas
Basal Cell Carcinoma - cancer originating from the stratum basale (or the basal cell layer)

Squamous Cell Carcinoma - cancer originating from corneum, lucidum, granulosum, or spinosum

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8
Q

Which type of skin cancer is most common?

A

Keratinocyte carcinomas (SCC, BCC) making up ~97% of skin cancer

melanoma makes up about 2% of skin cancer but is much more deadly

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9
Q

Acanthosis

A

abnormal thickness of epidermis (relative to the location on the body)

diffuse epidermal hyperplasia

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10
Q

Invasive SCC

A

this means that the squamous cells have invaded based the basal membrane and into the dermis

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11
Q

Hyperkeratosis

A

thickening of stratum corneum by abnormal keratin

often associated with a qualitative abnormality of the keratin

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12
Q

Parakeratosis

A

Retention of nuclei in stratum corneum

normal in mucous membranes

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13
Q

Hypergranulosis

A

Hyperplasia of stratum granulosum, usually caused by intense rubbing

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14
Q

Papillomatosis

A

Hyperplasia and enlargement of contiguous dermal papillae leading to surface elevation

common wart

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15
Q

Dyskeratosis

A

Abnormal keratinization occurring prematurely in cells below stratum granulosum

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16
Q

Acantholysis

A

loss of intracellular connections causing loss of cohesion between keratinocytes

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17
Q

Spongiosis

A

epidermal intracellular edema

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18
Q

First Degree Burn

A

erythema, swelling

transitory, reversible

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19
Q

Second Degree Burn

A

Blisters involving epidermis

Hair follicles, adenxa in dermis spared

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20
Q

Third Degree Burn

A

Full-thickeness burns; massive necorsis of epidermis and parts of dermis, subcutis
cannot heal spontaneously

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21
Q

Macule

A

flat, smaller than 2cm (ex. freckle)

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22
Q

Patch

A

similar to macule but larger

flat >2cm

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23
Q

Papule

A

slightly elevated, smaller than 1 cm

ex. eczema caused by allergy

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24
Q

Nodule

A

similar to papule but greater than 1 cm
(slightly elevated)

ex. nevus

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25
Q

Tumor

A

nodule greater than 5 cm

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26
Q

Vesicle

A

fluid-filled elevation of epidermis
smaller than 1 cm

ex. herpesvirus lesion on the lip

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27
Q

Bulla

A

vesicle measuring more than 1 cm (ex. burns)

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28
Q

Pustule

A

vesicle filled with pus (ex. impetigo)

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29
Q

Ulcer

A

defect of the epidermis (ex. syphilitic chancre)

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30
Q

Crust

A

skin defect covered with coagulated plasma (“scab”)

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31
Q

Scales

A

Keratin layers covering skin as flakes or sheets; can be scraped away
ex. psoriasis, seborrheic keratoiss

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32
Q

Squames

A

Large scales (ex. ichthyosis)

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33
Q

Excoritation

A

superficial skin defect caused by scratching

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34
Q

Fissure

A

sharp-edged defect extending deeper into dermis (ex. athlete’s foot)

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35
Q

Orthokeratosis

A

hyperkeratosis with just keratin, no nuclei

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36
Q

Parakeratosis

A

hyperkeratosis with keratin and nuclei

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37
Q

Effects on skin from chronic sun exposure

A

hyperpigmentation
atrophy of epidermis
dermal connective tissue degeneration

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38
Q

Folliculitis

A

bacterial infection of the hair follicule

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39
Q

Acne vulgaris

A

infiltration and destruction of follicular epithelium by neutrophilic exudate

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40
Q

Where are fungal infections mc?

A

Keratin layer (dead tissues)

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41
Q

Verruca Vulgaris

A

Common Wart

on microscope – papillomatosis

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42
Q

Auspitz sign

A

seen with psoriasis

bleeding points when scale is lifted from plaque d/t tortuous dilated vessels

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43
Q

What is the MC malignant skin tumor?

A

BCC

most commonly located on the FACE

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44
Q

What are telltale signs of skin cancer?

A

persistent, nonhealing ulcer
irregular shape
friable (crumbles), bleeds, multicolored
indurated (hardened) margins of an ulcer or tissue around it

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45
Q

Lentigo

A

macule or papule’ pigmented but does not respond to sun

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46
Q

Junctional nevus

A

mole just in the epidermis

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47
Q

Compound nevus

A

mole in both epidermis and dermis layers

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48
Q

Clinical Warning Signs for Melanoma

A

change in color, size, or shape of preexisting mole (typically >10mm)
itching or pain to nevus
new pigmented lesion developed in adult life
irregular notched borders
variegation of color (black, brown, red, blue, and gray)

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49
Q

What is the most important prognostic factor in melanoma?

A

tumor thickness

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50
Q

Radial vs vertical growth phase of melanoma?

A

Radial = (epidermis) tendency of melanoma cells to grow horizontally along the epidermis (no metastatic potential)

Vertical = (dermis) melanoma cells grow vertically in the deeper dermis with no maturation and acquire a metastatic potential

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51
Q

Onychogryphosis

A

hypertrophic nail

related to trauma

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52
Q

Koilonychia

A

thin and spoon nail

seen in Fe deficiency anemia

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53
Q

Onychomycosis

A

thicken, discolor, disfigure, and split nail, related to FUNGAL infection

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54
Q

Paronychia

A

soft tissue infection, pus formation around a fingernail

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55
Q

What is Impetigo?

A

superficial bacterial infection of the Epidermis

typically caused by a mix of staph and strep

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56
Q

How do people get impetigo?

A

minor breaks in the skin
preexisting dermatoses
Bites
wounds, burns, ulcers

HIGHLY contagious amongst close contacts

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57
Q

What is nonbullous impetigo?

A

“Classic impetigo”

Erythematous macules/papules that evolve into vesicles/pustules, rupture forming HONEY COLORED crusts

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58
Q

Where on the body is nonbullous impetigo most common?

A

face and extremities

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59
Q

Where on the body is bullous impetigo more common?

A

on the trunk and folds such as axillae

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60
Q

What is Ecthyma?

A

a type of impetigo that has extended into the dermis
the lesions are now coagulated and less honey-colored crusts
still considered a superficial infection since there is no systemic sxs

will heal with scarring

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61
Q

How do you dx impetigo?

A

Clinical dx
Microscope will help you determine if its staph or strep

Staph = clusters
Strep = chains
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62
Q

What is the treatment for impetigo?

A

think if you want to go topical or oral depending on the extent of spread of infection

Topical: Bactroban (Mupirocin) - covers MRSA too - 2% ointment
Retapamulin (Altabax) 1% ointment (less commonly used)

Oral: Cephalexin (Keflex) second gen that covers both gram - and +
Clindamycin (covers MRSA)
Staph only = dicloxacillin
Augmentin (Amoxicillin - Clavulanate) -big guns

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63
Q

What is Erysipelas?

A

soft tissue infection involving the dermis and subcutaneous tissue and superficial lymphatics (similar to cellulitis)
MC in young children and the elderly
MC caused by Group A Strep (GAS)

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64
Q

How does erysipelas present?

A

actue painful onset
edematous, red, warm plaques with clear borders
MC on cheeks and ears (can also be seen on extremities but less common)
fever, chills, regional lymphadenopathy

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65
Q

What is the treatment for erysipelas?

A

outpt with oral ABX
remember you are doing broad spectrum to cover for both erysipelas and cellulitis

PCN (500mg every 6 hours)
Amoxicillin (500mg every 8 hours)
Keflex (250-500mg every 6 hours)

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66
Q

How does the age distribution differ between cellulitis and erysipelas?

A

Erysipelas is bimodal (young and old)

Cellulitis is MC in middle-aged, elderly, and immunocompromised

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67
Q

Pasteurella multocida

A

organism responsible for cellulitis secondary to dog or cat bites

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68
Q

IV Drug users are more likely to get cellulitis secondary to what bacteria?

A

Staph Aureus

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69
Q

If you are palpating a pt you suspect having cellulitis and you hear crunching, what pathogen should you be thinking about?

A

Clostridia

Crepitant cellulitis

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70
Q

Haemophilus influenzae causing cellulitis commonly presents where on the body?

A

face and periorbital

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71
Q

What is the clinical manifestation of cellulitis?

A

abrupt or gradual onset
swelling, erythema, tenderness, and warmth (may also have bulla, vesicles, necrosis)
Borders are rough and less defined - expanding
Lower extremities MC location
Fever, chills, malaise, anorexia, lymphadenopahty, lymphagitis

can lead to sepsis

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72
Q

What is lymphagitis?

A 
seen with cellulitis pts 
the red line showing the proximal spread of the infection 
this is a bad sign 
start on IV ABX right away 
this is a lymphatic spread
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73
Q

For which pts with cellulitis should you cover for Pseudomonas aeruginosa?

A

penetrating trauma (“stepped on a nail”)
immunocompromised
hospitalized

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74
Q

What is the treatment for Cellulitis?

A

Keflex
Augmentin (used for cat and dog bite - pasteurella)
Dicloxacillin
Clinda (MRSA)
Cipro (puncture wounds d/t covering pseudomonas)

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75
Q

When should you be suspecting MRSA for a pt with cellulitis?

A

(this is important because you would normally be treating with keflex but if you suspect MRSA you will change to clinda or something else)

Penetrating trauma 
IV Drug Users 
Abscess/Purulent Drainage 
Hx of MRSA
close contacts with MRSA pts
recent ABX use 
Hospitalization
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76
Q

MRSA treatment

A

Oral:

  • Bactrim DS (double strength)
  • Doxycycline
  • Clinda
  • Linezolid

IV:

  • Clinda
  • Linezolid
  • Vancomycin (not first line)
  • Daptomycin
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77
Q

What is folliculitis?

A

Inflammation of the superficial or deep portion of the hair follicle

bacterial infection is MC cause

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78
Q

What is the MC bacteria responsible for folliculitis?

A

Staph Aureus

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79
Q

Hot Tub Folliculitis

A

pseudomonas aeruginosa

rash presents 1-2 days after being in hot tub

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80
Q

Psuedofolliculitis barbae

A

“Razor bumps”
can occur over any shaved area
related to curved hair follicles, foreign-body type reaction

can be secondarily infected by staph aureus

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81
Q

What is a furuncle?

A

folliculitis that is deeper

tender, nodules/abscesses (boils)

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82
Q

What is a carbuncle?

A

deeper folliculitis where the infections are interconnecting under the skin
several contiguous hair follicles

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83
Q

What is the treatment for Folliculitis?

A

Topical:

  • Mupirocin (Bactroban) - covers MRSA
  • Retapamulin (Altabax)
Oral:
Keflex 
Augmentin (if you needed to bump it up) 
Bactrim DS (MRSA)
Doxy (MRSA)
Clinda (MRSA)

Cipro (psuedomonas - Hot tub)

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84
Q

What is the treatment for Folliculitis?

A

Topical: (if this is just one small location)

  • Mupirocin (Bactroban) - covers MRSA
  • Retapamulin (Altabax)
Oral:
Keflex 
Augmentin (if you needed to bump it up) 
Bactrim DS (MRSA)
Doxy (MRSA)
Clinda (MRSA)

Cipro (psuedomonas - Hot tub)

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85
Q

Acute Paronychia

A

acute infection caused by Staph Aureus of the nail fold

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86
Q

Chronic Paronychia

A

loss of cuticle, proximal nail fold becomes boggy, nail plate becomes irregular/discolored

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87
Q

A pt comes in with a red swollen, painful hand with some red streaking. After asking some questions you find out he has a new kitten. What do you think he has? How do you treat it?

A

Cellulitis

treat with Augmentin

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88
Q

A pt comes in with an itchy rash. After asking some questions you find out she was recently in a hot tub. What do you think she has and how would you treat?

A

folliculitis

treat with cipro to cover for psudomonas

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89
Q

What is pediculus humanus capitis?

A

Head louse

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90
Q

What is pdiculus humanus corporiss?

A

Body louse

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91
Q

What is phihirus pubis?

A

Crab or pubic louse

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92
Q

What is pediculosis?

A

Lice

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93
Q

What is the primary symptom of pediculosis and what causes it?

A

Itching due to an allergic reaction to louse saliva

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94
Q

What do you need to dx lice?

A

Must have at least one life louse

Eggs (nits) does NOT confirm active infection unless they are “viable”

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95
Q

What is the treatment for head lice?

A

Since developing embryos may survive initial topical treatment you must repeat a second course 7-10 days laters to kill newly hatched nymphs

Permethrin (Nix) 
Pyrethrin 
Malathion 
Benzyl Alcohol 
Ivermectin (topical and oral)

Other treatments might include shaving or suffocation with mayo or vaseline

Non-washable items should be sealed in plastic bags for 3-5 days

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96
Q

How do you treat crab lice?

A

Same as head lice

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97
Q

What diseases may be transmitted by body lice?

A

Typhus and trench fever

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98
Q

What is the treatment for body lice?

A

Wash entire body, topical treatment or oral ivermectin

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99
Q

What are the hallmark features of scabies?

A

Intense pruritic, papular rash with excoriations

Borrowing typical in hands and wrists
Typically the head and neck are spared

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100
Q

“Norwegian Scabies”

A

Crusted scabies

EXTREMELY contagious (primarily in older, immunocompromised, or homeless)

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101
Q

What is the treatment for scabies?

A

Permethrin
Lindane (risk of neurotoxicity)
Crotamiton
Oral Ivermectin

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102
Q

Cimex lectulrius

A

Bed bugs

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103
Q

What is the treatment for bed bugs?

A 
Bites typically resolve within one or two weeks 
Topical or oral steroids 
Antihistamines 
Eradication 
-heating/steaming extermination 
-laundering of linens 
-vacuuming of furniture
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104
Q

Red, white, and blue sign

A

Seen with brown recluse spider bites
Red (peripheral erythema)
White (blanching)
Blue (violaceous center)

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105
Q

nits

A

pediculosis eggs
just the presence of eggs does not confirm dx because the shells might be empty
they must be viable

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106
Q

How do you tell the difference between head lice and dandruff?

A

dandruff should flake off while nits are attached to the shaft via protein

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107
Q

Where are you more likely to see head lice?

A

in the homeless

hair shafts
behind the ears and on the back of the neck

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108
Q

How to lice treatment drugs work?

A

toxic to the louse nervous system

however this might not kill the nits so you will need to do a second treatment 7-10 days later

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109
Q

What is the first line treatment for head lice?

A

Nix (permethrin 1%) OTC
apply to dry hair for 10 minutes and then wash hair and comb to remove nits and lice
repeat in 7-10 days

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110
Q

A pt comes in with a pruritic papular rash that is more itchy at night, what should you be thinking?

A

Scabies

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111
Q

What is the key characteristic of scabies?

A

Burrowing

typically in the webbed part of the hands and toes

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112
Q

Where are scabies rashes more commonly located?

A

Belt line
Buttocks
Genitalia
in between the fingers and toes

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113
Q

How do you instruct pts to treat their scabies?

A

Permethrin 5% cream that is applied from the neck down after pt has showered
washed off after 14 hours and then reapplied again in 1 week

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114
Q

How does treatment change for Norwegian scabies?

A

you do both topical and oral

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115
Q

Loxosceles reclusa

A

brown recluse spider

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116
Q

How do you treat a brown recluse spider bite?

A

most bites can be treated with rest, ice, and elevation
make sure tetanus is up to date
pain meds
most importantly make sure wound is kept clean

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117
Q

What is the age of onset for pityriasis rosea?

A

adolescence through adults

more common in spring and fall

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118
Q

What is pityriasis rosea?

A 
often considered viral (but truly unknown) 
falls under the class of papulosqaumous
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119
Q

What is the prodrome phase of pityriasis rosea?

A

HA
Malaise
mild constitutional sxs

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120
Q

What is the most common location on the body for pityriasis rosea?

A

the Herald patch - the trunk

the exanthem that appears weeks later - trunk and proximal extremities

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121
Q

Herald Patch

A 
that initial patch of 
 pityriasis rosea 
single oval lesion 2-10cm in diameter 
pink, salmon-red to erythematous 
slightly raised, fine collarette scale
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122
Q

Exanthem

A

In addition to the already present Herald rash, this new rash appears days to months later (typically 2 weeks later)

presents as a smaller lesion on the trunk/proximal extremities

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123
Q

“Christmas Tree” distribution of a rash

A

Pityriasis rosea exanthem rash that follow langer’s lines (cleavage lines of the body)

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124
Q

What is reverse pityriasis rosea?

A

when the lesions are on the extremities, sparing the trunk

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125
Q

What is atypical pityriasis?

A

herald patch may be absent or sole lesion
OR
multiple herald patches
OR
lesions may be present on face, neck, palsm and soles or unilateral
OR
vesicular, pustual, or urticarial variants

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126
Q

What are some of the DDx for pityriasis rosea?

A

lichen planus
erythema multiform
secondary syphilis

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127
Q

How do you dx pityriasis rosea?

A

clinically

can use KOH prep or RPR to rule out fugal infection and syphilis

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128
Q

What is the treatment for pityriasis rosea?

A

symptomatic
antihistamines, calamine lotion, steroids
+/- UVB phototherapy

the rash will last for about 4-10 weeks

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129
Q

What is the epidemiology of lichen planus?

A

acute or chronic
more common in females
~1% of the population
30-60 years of age

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130
Q

What is the cause of lichen planus?

A

idiopathic
however it can be associated with Hep C so screen pts with LP for HCV infection
can also be seen with drug reactions such as BB, HCTZ, ACEI, NSAIDs, antimalarial

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131
Q

What are the 6 Ps of lichen planus?

A 
Purple
Pruritic
Polygonal
Planar
Papules
Plaques
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132
Q

Where is lichen planus commonly found on the body?

A 
flexor surfaces of the wrists, shins, lumbar, feet
genitalia 
mouth 
hair
nails
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133
Q

Koebner’s Phenomenon

A

new lesions of lichen planus (and psoriasis) at the sight of trauma

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134
Q

Besides the 6 Ps, what does lichen planus look like? (looking for a commonly used descriptive term)

A

wickham striae

white, lacy reticular pattern (especially oral lichen planus)

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135
Q

Pts with chronic oral lichen planus are at an increased risk for what?

A

SCC

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136
Q

What is the DDx for lichen planus?

A 
drug induced
psoriasis 
secondary syphilis 
pityriasis roasea
lupus
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137
Q

What is the DDx for oral lichen planus?

A

candidiasis
leukoplakia
lupus
secondary syphilis

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138
Q

What types of drugs can cause lichen planus?

A 
gold salts
BB
antimalaria pills
HCTZ
Furosemide
spironolactone
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139
Q

How is lichen planus dx?

A

clinical presentation + punch biopsy (punch typically done by dermatologist)

in the meantime start them on steroids (since it doesn’t look fungal)

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140
Q

What is the treatment for lichen planus?

A

topical steroids if early and localized

  • Clobetasol (Temovate)
  • Bethamethason
  • Deproprionate (Diprolene)

intralesional injections of Tiamcinolone Acetonide (Kenalog) for resistant or hyperkeratotic lesions

Oral steroids for generalized lesions
-Prednisone for 4-6 weeks then taper for 4-6 weeks

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141
Q

What is the prognosis of lichen planus?

A

majority of cutaneous LP spontaneously remit within 1-2 years
recurrences may occur

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142
Q

coin-shaped, disseminated, pruritic eczema lesions found on the extremities

A

nummular eczema

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143
Q

What is Tinea Corporis?

A

superficial fungal infection of the skin
typically from Trichophyton, Microsporum, Epidermophyton

T. RUBRUM MC

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144
Q

What are the risk factors for tinea corporis?

A

affects all ages
warm-hot environments
animals
contaminated soil

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145
Q

T. Rubrum

A

MC cause of tinea corporis

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146
Q

Pruritic lesions typically begin as erythematous scaly plaques with central resolution that is annular in shape
might scale or crust due to inflammation in advancing border

A

Tinea Corporis

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147
Q

Malassezia furfur

A

causes tinea versicolor

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148
Q

Well-demarcated macules/patches with fine scale
hypo-and hyperpigemention variable
MC on trunk

A

tinea versicolor

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149
Q

What does tinea versicolor look like on a KOH prep?

A

spaghetti and meatballs

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150
Q

What is the age group for acute guttate psoriasis?

A

children and adolescents

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151
Q

What is the rash distribution of acute guttate psoriasis?

A

mainly on the trunk
some on the face and scalp
usually spares palms and soles

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152
Q

What is associated with acute guttate psoriasis?

A

it is often precipitated by an acute strep infection

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153
Q

What does pityriasis mean?

A

scaling

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154
Q

Langer’s Lines

A

Skin cleavage lines of the body that pityriasis rosea tends to follow (Christmas tree distribution)

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155
Q

What do you use KOH prep for?

A

to determine if a rash is fungal

used in pityriasis to rule out fungal (since this rash looks fungal)

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156
Q

How does pityriasis rosea typically present?

A

Might have a prodrome of HA and malaise
Herald Patch is the first and largest patch
about 2 weeks later they might have a full blown rash

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157
Q

at what point with pityriasis rosea would you get a skin biopsy?

A

if 3 months has passed and no improvement (maybe misdx)

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158
Q

What is the RPR test used for?

A

tests for syphilis
this is a do not miss dx
know when its on the ddx
-pityriasis rosea

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159
Q

If a pt comes in with lichen planus, what should you screen them for?

A

Hep C

there is an association between these 2

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160
Q

If a pt has had a recent trauma and then presents with this papule like rash, what should you be thinking?

A

Lichen planus

Koebner’s Phenomenon

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161
Q

What age group is most common with erythema multiforme?

A

can occur in all ages but peaks between 20-40 years of age

M > F

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162
Q

What is the MC etiology of erythema multiforme?

A

HSV

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163
Q

What drugs can cause erythema multiforme?

A

barbiturates, NSAIDs, PCNs, metformin, cipro, bupropion

even vaccines (diptheria -tetanus, hep B)

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164
Q

What is the prodrome for erythema multiforme?

A

Fever
malaise
myalgia
sore throat and cough if d/t mycoplasma

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165
Q

What is the typical presentation of erythema mutliforme?

A

might have a prodrome
starts benign acutely and evolve over days
have a dark center –> target lesion (round with 3 concentric zones)
typically starts distal and moves proximal
loves palms and soles (think about secondary syphilis and lichen planus) loves elbows and knees (so does psoriasis)

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166
Q

What is the difference between erythema mutliforme major and minor?

A

Major is more commonly d/t drug erruption (think about steven johnson syndrome)
major always has mucus membrane involvement

minor usually confined to extremities and face with classic target lesions with little to no mucous membrane involvement, usually associated with HSV outbreak

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167
Q

What is Nikolysky sign?

A

seen with major erythema multiforme
when you rub the skin it comes off
this is why you are worried about stevens-johnsons syndrome

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168
Q

What is the prognosis of erythema multiforme?

A

usually resolves spontaneously within 3-5 weeks

may be recurrent (especially for those with recurrent HSV)

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169
Q

What is the treatment for erythema multiforme?

A

remove any offending drug
oral antihistamines and topical steroids for symptomatic relief

oral prednisone for severe cases

treat underlying etiology

  • HSV: acyclovir
  • Mycoplasma: macrolide
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170
Q

Where does secondary syphilis most commonly present on the body?

A

mucosal lesions

palms and soles

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171
Q

What is atopy?

A

eczema, hay fever, asthma
sometimes we add ASA allergy
typically in the family hx

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172
Q

What is the cause of pityriasis (tinea) versicolor?

A

yeast infection

overgrowth of the yeast on the body

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173
Q

What is the prevention for herpes zoster?

A

vaccine for those >60 years (~60% reduction)

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174
Q

What is the treatment for herpres zoster?

A

acyclovir within 72 hours of rash onset

5x/day for 7-10 days

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175
Q

Molluscum contagiosum

A

viral rash
caused by a pox virus
mostly in children or young adults
it’s self limited for about 2 months

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176
Q

Verruca Vulgaris (HPV)

A 
common wart  (from HPV, just a different strand) 
occurs weeks to months after skin to skin exposure
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177
Q

condylomata acuminata

A

anogenital warts

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178
Q

What is the treatment for HPV?

A

no treatment is curative
surgery is the most likely to be curative (and cheapest option)

QUIT SMOKING

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179
Q

How do you prevent HPV?

A 
Gardasil vaccine 
protects against 9 different types 
-6 and 11
-16,18,31,33,45,52, and 58 
ideally administered before the individual has become sexually active
180
Q

umbilicated papules
discrete, solid, skin-colored papules 3-5mm
describes what kind of skin problem?

A

Molluscum contagiosum

181
Q

What is the treatment of verruca vulgaris?

A

chemically or physically burn it off or just wait because they are self limiting
educate the pt not to spread it around (contagious)

182
Q

What is respiratory papillamatosis?

A

caused by vaginal birth when someone has HPV

the infant inhaled the virus

183
Q

How do you dx HPV?

A

warts if its type 6 or 11
dysplasia of epithelial cells on pap smear (type 16 and 18)

application of acetic acid solution (vinegar) –> colposcopy (not sure how common this is)

184
Q

When do you see post-adolescent acne?

A

83% of women have pre-menstrual flares

185
Q

What is oral isotretinoin used to treat?

A

aka accutane
used for severe acne (6 months of treatment)

works by shrinking sebaceious glands and decrease sebum secretions

186
Q

What topical agents can be prescribed for acne?

A

retinoids such as tretinoin, adapalene, tazoratene

187
Q

What is the most mild form of acne?

A

comedonal acne

188
Q

What is the worst form of acne?

A

nodulocystic

189
Q

What is the treatment for pts with acne around their periods?

A

OCPs
spironolactone

(decrease sebum production)

190
Q

What are the side effects of accutane?

A

be sure this is monotherapy (no other acne meds)

  • dry skin and lips
  • photosensitivity
  • teratogenicity (iPLEDGE) –> must have monthly pregnancy tests
  • hypertriglyceridemia
  • hepatotoxicity
  • myalgia
  • Pysch effects
191
Q

What is rosacea?

A

facial flushing
inflammatory papulopustual eruption
unknown cause
chronic and relapsing

192
Q

What is the classic form of rosacea?

A

papulopustual

erythematotalangiesctatic is central facial flushing (not classic)

193
Q

What is phymatous?

A

Rosecea

thickened and irregular surface of nose, chine, forehead, ears, eyelids

194
Q

What treatements for rosecea help with the redness?

A

topical brimonidine and oxymetazoline

195
Q

What is hidradenitis suppurativa?

A

follicular occlusive disease found in the skin folds

196
Q

What is the epidemiology of hidradenitis supporativa?

A

rare
1-4%
onset: puberty - 40y/o
W > M

197
Q

What is the pathogenesis of hidradenitis suppurativa?

A

hormones increase follicular epithelial hyperplasia that leads to nodule that can turn into an abscess
this can lead to comedones or scarring

198
Q

What is stage 1 of hidradenitis suppurativa?

A

abscess formation without sinus tracts or scarring

199
Q

What is stage 2 of hidradenitis suppurativa?

A

recurrent abscesses with sinus tracts, scarring

200
Q

What is stage 3 of hidradenitis suppurativa?

A

diffuse involvement, multiple interconnected sinus tracts and abscesses

201
Q

What is the treatment of hidradenitis suppurativa?

A 
No cure
Lifestyle modification:
-avoid skin trauma (wear loose clothing) 
-daily gentle cleansing
-smoking cessation 
-no dairy

Mild:

  • topical treatment - CLINDA
  • punch debridement
  • intralesional corticosteroid injections
  • 7-10 day course of PO ABX (doxy)

Moderate:

  • PO ABX up to 3 months
  • spironolactone
  • punch debridment

Severe:

  • prednisone
  • humera
  • PO isotretinoin
202
Q

Anagen

A

growth phase of hair cycle
2-6 years
80-90% of hairs on normal scalp

203
Q

Catagen

A

involutional phase of hair cycle
2-3 weeks
5-10% of hairs on normal scalp

204
Q

Telogen

A

resting phase of hair cycle
2-3 months
1-3% of hairs on normal scalp

205
Q

How many hairs is normal to loose a day?

A

100

206
Q

Alopecia Areata

A

Chronic immune mediated disorders
target anagen hair follicles
non-scarring hair loss

very smooth round patch of skin

207
Q

What is the age group for alopecia areata?

A

usually before the age of 30

M = F

208
Q

alopecia totalis

A

complete loss of scalp hair

209
Q

alopecia universalis

A

loss of scalp and body hair

210
Q

What is the treatment for alopecia areata?

A

intralesional corticosteriods (triamcinolone) injected into upper subQ of scalp

potent topical steroids
topical immunotherapy

211
Q

What is telogen effluvium?

A

diffuse non-scarring alopecia
sometimes bitemporal hair loss
<50% hair loss, no balding occurs

212
Q

What are the typical causes of telogen effluvium?

A 
major surgery 
serious illness 
childbirth 
protein or caloric malnutrition 
thyroid disorders 
drugs 
emotional stress
213
Q

What is the pathogenesis of telogen effluvium?

A 
# of hairs in telogen phase increases
unknown why
214
Q

What is the treatment for telogen effluvium?

A

removal or treatment of underlying cause
minoxidil is controversial

usually is self-limited in 6-12 months

215
Q

What is androgenetic alopecia?

A

typically in men

progressive loss of terminal hairs on anterior scalp, mid-scalp, temporal scalp

216
Q

Malassezia

A

yeast that causes tinea versicolor

217
Q

What is pityriasis alba?

A

small white scaly “patches” typically on the faces of kids after summer

218
Q

Tinea capitis

A

infection of scalp hair
typically seen in children
caused by direct contact with an infected individual
pruritic

219
Q

What is tinea corporis?

A

pruritic circular or oval, erythematous scaling plaque that usually has a central clearing and a raised border

220
Q

What is tinea cruris?

A

fungal infection of the groin

221
Q

What is tinea pedis?

A

fungal infection of the foot

“athletes foot”

222
Q

What is tinea unguium?

A

Fungal infection of the nail

“onychomycosis”

223
Q

What is the treatment for tinea capitis?

A

oral antifungals

griseofulvin for 6-12 weeks

224
Q

What is the treatment for tinea cruris?

A

topical antifungals
terbinafine PO
Itraconazole PO

225
Q

What pathogen causes impetigo?

A

staph and strep

226
Q

What is considered “classic impetigo?”

A

nonbullous impetigo

erythematous macules/papules that evolve into vesicles that rupture –> honey-colored crust

227
Q

Where is classic impetigo more commonly located on the body?

A

face and extremities

228
Q

Bulla

A

vesicle greater than 1 cm

229
Q

Why might you prescribe clinamycin for impetgio and what are the possible side effects?

A

if you think the impetgio is MRSA

SE: C. Diff (so be cautious in older pts)

230
Q

What is the likelihood that someone who is allergic to PCN will be allergic to cephalopsorins?

A

since PCNs and cephs are cousins there is a 10% chance that someone allergic to PCN will be allergic to cephs

231
Q

What do you do if a pt has recurrent infections of impetigo?

A

do a nasal swab (MRSA likes to hang out in the nares)

treat with bactroban intransal

232
Q

What is a potential complication of impetigo?

A

poststrep glomerulonephritis

233
Q

What pathogen is most commonly responsible for erysipelas?

A

GAS - group A strep

234
Q

“I went to bed last night fine and woke up this morning with the huge rash on face”

A

typical presentation of erysipelas

very acute painful onset

235
Q

How can you tell the difference between erysipelas and cellulitis?

A

Erysipelas has very clear borders
acute onset
typically on the face

Cellulitis does not have clear borders and is less of an acute onset
can be anywhere on the body but lower extremities are more common

in some cases it will be hard to tell the difference between these two but you are going to treat it more broadly so you cover both

236
Q

Where is erysipelas more commonly located on the body?

A

cheeks and ears

237
Q

Why would you get imaging (Xray, MRI, CT) on a pt you suspect has cellulitis?

A
  • to rule out osteomyelitis

- if pt has periorobital cellulitis you want to see if they have proptosis and aggressively treat right away

238
Q

You’re in the ER with a pt who you suspect has cellulitis of the lower right calf. What will your discharge notes report?

A

first mark their leg with a skin marker around the rash so you can compare at a later date to see if it has improved
1) take kephlex (cephalexin)
2) elevate the leg
3) use Tylenol and warm compresses PRN
4) return in 2 days for wound check or set up a phone appointment to make sure the rash has improved
inform the pt that at first the rash might get worse due to the bacteria dying a releasing more toxins but that shortly after that it should improve

if the follow up will not be with you consider printing out their chart for the pt to give the next MD they see

239
Q

What pathogen should you be thinking about with ciprofolxacin?

A

psuedomonas

240
Q

What is the treatment for acute paronychia?

A

warm soaks
I and D
ABX
make sure their tetanus is up to date

241
Q

What is the treatment for chronic paronychia?

A

encourage good nail hygiene
stop nail bitting
no ABX

242
Q

Terms to describe the common wart?

A

Papillomatosis (microscopic term)

verruca vulgaris (HPV)

243
Q

What is telangiectasia?

A

spider veins

sometimes seen with BCC

244
Q

How do you differentiate rosacea from acne?

A

rosacea doesn’t have comedones and is more redness localized to the central part of the face (not usually on chest or back)

245
Q

When should you be concerned about hyperandrogenism?

A

it can be normal for women to get acnea around their periods, however if you see these other signs you should be concern (you want to rule out PCOS):

  • hair loss
  • irregular menses
  • infertility
  • abrupt onset of severe acne
  • cushingoid features
  • acne refractory to therapy
  • acanthosis nigricans
  • obesity
246
Q

Which treatments are used to attack the follicular hyperkeratiniazation part of acne?

A

topical retinoids and isotretinoin
azelaic acid
salicylic acid

247
Q

Which treatments are used to treat the increased sebum production part of acne?

A 
oral isotretinoin 
hormone therapies (OCP, spironolactone)
248
Q

Which treatments are used to treat the P. Acnes proliferation part of acne?

A

Benzoyl Peroxide (BPO)
Topical antimicrobials
Oral ABX: doxy or minocycline (limited to 3 months)
Azelaic acid

249
Q

Which treatments are used to treat the inflammation part of acne?

A

oral isotretinoin
oral ABX
Topical retinoids
azelaic acid

250
Q

Hydroquinone plays what role in acne treatment?

A

post-inflammatory hyperpigmentation

helps lighten dark spots

251
Q

What treatments help with the rosacea bumps?

A 
topical metronidazole
topical azelaic acid
sulfacetamide
topical acne meds
retinoids
ABX (targeting inflammation more than bacteria)
252
Q

How can you tell rosacea from lupus?

A

both can be on the face

lupus is more purple and has more demarcated borders

253
Q

Alopecia universalis

A

a type of alopecia areata where there is loss of scalp and body hair including the eyelashes

254
Q

What is the best treatment for onychomycosis?

A

Oral antifungals since topical antifungals take almost a year to work

255
Q

Lichen Planus genital lesions are most commonly seen where?

A

glans penis
vulva/vagina

remember this may be associated with SCC –> long term follow up

256
Q

Lichen Planus hair lesions if left untreated…

A

can result in scarring alopecia

257
Q

Which lesions of lichen planus represent a more advanced lesion?

A

esophageal lesions

258
Q

A pt comes in with oral lesions and body lesions, what should you be thinking?

A

lichen planus

but also lupus!

259
Q

What do you see on microscope with lichen planus?

A

hyperkeratosis

both para and ortho

260
Q

What is Nikolsky sign and when might it be positive?

A

its when you take a pencil eraser to the pts rash and gently twirl it back and forth. if a blister appears within minutes its a positive sign

seen often with Erythema multiforme major (typically d/t drug eruption)

261
Q

Where is erythema multiforme commonly seen on the body?

A

the distal extremities moving proximally and the face

262
Q

Risk factors of tinea corporis?

A

ringworm basically

warm-hot environments
animals
contaminated soil

263
Q

Who is more likely to get mooluscum contagiosum?

A

children, sexually active adults, pts with HIV

264
Q

What lesion is caused by pox virus?

A

molluscum contagiosum

265
Q

How would you describe a molluscum contagiousm lesion?

A

discrete, solid, skin-colored papule 3-5mm on the chest
red halo regressing spontaneously
UMBILICATED papules

266
Q

Condylomata acuminata

A

angogenital warts

267
Q

How do you dx HPV?

A

acetic acid solution application with whitening of the lesions

268
Q

Phthirus pubis

A

crab or pubic louse

269
Q

Pediculus humans corprois

A

body lice

270
Q

Which type of pediculosis run the risk of causing a systemic disease?

A

body lice

typhus and trench fever d/t louse feces (note even scabies runs this risk)

271
Q

By the time a pt is scratching due to head lice, how long have they had the infestation?

A

it takes 2-6 weeks to develop a reaction

the more times (# of times) you are exposed the shorter time it takes to mount a response

272
Q

Where are you likely to see nits are what do they look like?

A

close to the scalp on the shaft of the hair (they need the warmth of the head so they are close to the scalp) –they hold on using a protein matrix and do not easily flake off like dandruff would
brown colored indicates an active nit

273
Q

Permethrin is used for what?

A

OTC treatment for head lice

274
Q

How do you treat pediculus humansus capitus for a pregnant pt?

A

benzyl EtOH 5%

apply to dry hair for 10 minutes –wash hair – comb hair to remove nits and lice
repeat in 7-10 days

275
Q

How does mayonnaise, olive oil, and vaseline work for head lice?

A

considered suffocating but what’s really happening is that you are slowing them down enough to allow you to effectively comb them out

276
Q

What must you keep in mind for anyone with crab lice?

A

that this is considered an STI and you should screen them for STIs

277
Q

Ivermectin is used for what?

A

PO treatment for body lice and scabies

278
Q

Why is dx body lice sometimes difficult?

A

body lice are only on the body when they are feeding

so be sure to check clothing for fece marks

279
Q

How long can scabies survive off the body?

A

4 days

280
Q

How do you treat Norwegian scabies?

A

topical + oral drugs

such as permethrin and ivermectin

281
Q

Cimex lecturlrius

A

common bed bug

282
Q

General characteristcs of drug induced rashes

A

symmetrically start on the trunk and move distally

283
Q

Immediate reactions (drug-induced)

A 
Occur less than 1 hr of the last administered dose 
Type 1 hypersensitivity 
Uritcaria 
Angioedema 
Anaphylaxis
284
Q

Delayed reaction (drug-induced)

A

Occurring after 1 hour, but usually more than 6 hours and occasionally weeks to months after the start of administration
Exanthematous eruptions
Fixed drug eruption
Systemic reactions (DIHS, SJS, TEN)

285
Q

Which drug do we do allergy drug testing for?

A

PCN

286
Q

What is the most important information in determining if a rash is medication-related?

A

TIMING

287
Q

For exantheamtous drug eruptions, initiation of the medication is often ____days before the rash

A

7-10 days

288
Q

What are risk factors for drug reactions?

A 
Females 
Prior history of drug reaction 
Recurrent drug exposure 
HLA type 
Certain disease states (EBV, HIV)
289
Q

Exanthematous Drug Eruption

A

Most common of all cutaneous drug eruptions

Does not blister
Macularpapular
Pruritic +/- fever

Rash appears more than 2 days after drug has been started (commonly around day 8-11) will persist 2-3 days after stopping the drug

290
Q

Where are the greatest areas of steroid absorption on the body?

A

thin areas
eyelids, genitals, skin creases
use lower potency in these areas

291
Q

Where are the least areas of steroid absorption on the body?

A

palms and soles

require higher potency drugs

292
Q

What are the characteristics and benefits of ointments?

A

best for dry, thickened areas due to being oil based and helps trap in the water (moisturizer)

best for dry, non-hairy skin
avoid thin areas (face, armpits)

293
Q

What are the characteristics and benefits of creams?

A

water based with oil
less potent than ointments
easy to wash off
more cosmetically appealing
have preservatives (might cause side effects)
used for exudative types lesions and intertriginous areas

294
Q

What are the characteristics and benefits of gels?

A 
alcohol base with water and oil 
has drying effect
greaseless, transparent 
may be used on hair-bearing area 
will caused stinging to inflamed skin
295
Q

What are the characteristics and benefits of lotions?

A

powder in water (have pt shake the bottle)
least potent of topical steroids
good for large body areas (including hairy areas)
provide cooling, drying effect as they evaporate

296
Q

What are the 7 groups of topical steroid potency?

A 
super potent (Group 1)
high (2 and 3) 
medium (group 4) 
lower - mid (group 5) 
low (group 6) 
least potent (group 7)
297
Q

What conditions are treated with high potency steroids (group 1-2)?

A 
alopecia areata
atopic dermatitis (only if resistant) 
discoid lupus
lichen planus
nummular eczema (only if resistant)
hyperkeratotic eczema
psoriasis
298
Q

What conditions are treated with medium potency steroids (group 3-5)?

A

anal inflammation
atopic dermatitis
nummular eczema
seborrheic dermatitis

299
Q

What conditions are treated with low potency steroids (group 6-7)?

A

diaper dermatitis

eyelid and facial dermatitis

300
Q

What is the most common side effect of topical steroids?

A

skin atrophy

other side effects:

  • striae
  • easy bruising or tearing of the skin
  • telangiectasias
  • hypopigmentation
  • acneiform eruption, steroid - induced rosacea
  • cushing syndrome or hyperglycemia
  • glaucoma or cataracts
  • tachyphylaxis
301
Q

Path of atopic dermatitis

A

genetic defect that disrupts skin barrier function making the skin more sensitive to irritants

302
Q

What is the epidemiology of atopic dermatitis?

A

very common
11-19%
all cases start within first decade of life
only 5% of cases develop after 5 years of age
this is an infant/toddler disease

303
Q

How does the rash distribution of atopic dermatitis differ between age?

A

children: face
older: flexor surfaces

304
Q

What is a long term treatment to decrease skin infections d/t atopic dermatitis?

A

bleach baths

305
Q

Exanthematous Drug Eruption

A

Most common of all cutaneous drug eruptions

Does not blister
Macularpapular
Pruritic +/- fever

Rash appears more than 2 days after drug has been started (commonly around day 8-11) will persist 2-3 days after stopping the drug

306
Q

Fixed Drug Eruption

A

Solitary erythematous patch or plaque that will recur at the same site with re-exposure to the drug

307
Q

What drugs are associated with fixed drug reaction?

A 
Phenophthalein (laxatives) 
Tetracyclines
Sulfa drugs 
NSAIDs
Barbiturates 
Food coloring (yellow)
308
Q

Where are the common locations for fixed drug reaction rashes?

A

Mouth
Genitalia
Face
Acral areas

Remember this is one solitary lesion

309
Q

What is the time of onset for fixed drug reactions?

A

30 minutes to 8 hours after ingesting the drug (for previously sensitized individuals)

310
Q

What is the treatment of fixed drug reactions?

A

Lesions resolve days to weeks after the drug is discontinued

Non-eroded lesions can be treated with an antimicrobial ointment and a dressing until the site is reepithelized

Address pain

311
Q

Drug-induced hypersensitivity syndrome

A

Also known as drug reaction with eosinophilia and systemic symptoms (DRESS)

Skin eruption with systemic sxs and internal organ involvement (liver, kidney, heart)

Typical sxs: macular exanthema, erythematous centrofacial swelling, fever, malaise, lymphadenopathy, involvement of other organs

> 70% of pts have an eosinophilia

312
Q

When are you going to stop all medications for a pt with a skin rash?

A

If you suspect DIHS and they’re basically on their way to the ICU

313
Q

What is the treatment for DIHS?

A

Get Dermatology involved
Stop medications if severe
Start systemic steroids if severe (topical + antihistamines if moderate)

314
Q

What medications can cause DIHS?

A 
Allopurinol
ABX (sulfas, PCNs) 
NSAIDs
AntiTB drugs
Anticonvulsants 
AntiHIV drugs
315
Q

What is the clinical course of DIHS?

A

typically starts 3 weeks post drug

macular exanthem 
erythematous centrofacial swelling 
fever, malaise 
lymphadenopathy 
>70% have eosinophilia
316
Q

Epidermal Necrolysis Spectrum

A

A spectrum that includes SJS and TEN

317
Q

What is the mortality rate of SJS/TEN?

A

SJS 5-12%

TEN >20%

318
Q

Which drugs have higher risk of SJS/TEN?

A 
Sulfa ABX 
Allopurinol
Tetracyclines
Anticonvulsants 
NSAIDs
Nevirapine
Thiacetazone

(Mnemonic SATAN)

319
Q

What is the time frame of SJS/TEN?

A

Clinically begins within 8 weeks after onset of drug exposure

320
Q

What clinical findings do you see with SJS/TEN?

A

Fever
HA
Rhinitis
Myalgias
May precede the mucocuutaneous lesions by 1-3 days
Eruption is initially symmetric and distributed on the face, upper trunk, and proximal extremities
Rash can rapidly extend to the rest of the body
Erythematous, irregularly shaped, dusky red to purpuric macules (atypical targets) which coalesce

NIKOLSKY sign

321
Q

How do you determine the difference between SJS and TEN?

A

Based on the TBSA which is determined by counting ALL skin lesions, ruptured and unruptured blisters

322
Q

For a pt you suspect has SJS/TENs which consults will you be contacting?

A

Derm
Ophthamology
Gynecology

323
Q

SSSS

A

Staph Scalded Skin Syndrome

Infant disease most commonly
Staph bacteremia

324
Q

Bright red confluent painful rash with large blisters. Sandpaper texture.

A

SSSS

325
Q

What is the path behind SSSS?

A

Staph exfoliative exotoxin cleaves the desmoglein 1 complex
5% of all Staph Auerus strains produce this endotoxin

Spread person - person

326
Q

What is the mortality rate of SSSS?

A

Infants 4%

Older children/adults 60%

327
Q

What is the prodrome for SSSS?

A

Fever
Sorethroat
Conjunctiviits

328
Q

What is the time frame for SSSS?

A

Rash develops within 48 hours of prodrome

329
Q

How do you differentiate SJS/TEN from SSSS?

A

Biopsy

SSSS - epidermal cleavage

SJS/TENS - subepidermal cleavage w/ epidermal necrosis

330
Q

What is the treatment for SSSS?

A

Penicillinase-resistant PCN

  • Nafcillin, oxacilin
  • Vanco for MRSA

Wound care

Monitor fluid status

331
Q

Pemphigus

A

Bullous disease
Autoimmune disease

Painful, generalized flaccid blisters with mucosal involvement

Acute and chronic forms

Can be confused with SJS

4 types:

  • Pemphigus vulgaris (70%)
  • pemphigus foliaceus
  • IgA pemphigus
  • Paraneoplastic pemphigus
332
Q

What is the path behind pemphigus vulgaris?

A

Acanthloysis (loss of adhesion from keratinocyte to keratinocyte) results d/t circulating autoantibodies (IgG) against epithelial cell surface antigens (desmoglein 1 and 2) leading to intra epithelial cutaneous and mucosal lesions

333
Q

What is the epi for pemphigus vulgaris?

A

Rare (0.1 per 100,000)
Higher risk in Ashkenazi jews, indian, mediterranean, middle east decent

Age 40-60 years

M = F

Genetics

334
Q

Contributing factors of pemphigus?

A

Genetic -HLA class 2
Drugs - penicllamine, captopril, NSAIDs, cephs
Infections - Herpes, coxsackivirus

335
Q

Clinical picture of pemphigus vulgaris

A

usually starts with painful excoriated mouth blisters
can be months before cutaneous signs
flaccid irregular border and varying size blisters begin to form on normal appearing tissue
blisters usually coalesce and rupture easily
PAINFUL

336
Q

How do you dx pemphigus vulgaris?

A

Skin biopsy - intraepithelial seperation and acanthloysis

“Tombstone” appearance d/t retention of keratinocytes

337
Q

What is the treatment for Pemphigus vulgaris?

A

Corticosteroids
Immunosuppressive drugs -rituximab, sulfasalazine, methotrexate
IVIG

338
Q

What is the difference between bullous pemphigoid?

A

Both are autoimmune
Bullous pemphigoid is sub-epidermal blister while PV is intra-epidermal blistering

Bullous is less deadly and rarely involves mucous and higher age of onset (65-70)

Both are prone to relapse

339
Q

What is necrotizing fasciitis?

A

Invasive bacterial infection of the soft tissue and deep tissue invading the fat, fascia, and at times underlying muscle causing death of tissues

Bacteria spread occurs across fascial plane

340
Q

What are risk factors for necrotizing fasciitis?

A 
DM
immune compromised (CA, organ transplants)
Obesity 
Surgery 
Traumatic wounds
341
Q

Necrotizing Fasciitis type 1

A

Polymicrobial

Anaerobes: one of (bacteroides, clostridium, peptostreptococcus)
PLUS
Facultative anaerobes (e. Coli, entrobacter, klebsiella, proteus)

342
Q

Necrotizing Fasciitis type 2

A 
Monomicrobial 
GAS 
Staph 
MRSA
Vibro vulnificus
343
Q

What is the presentation of necrotizing fasciitis?

A

Fever
Intense pain (early on its out of proportion to PE findings)
Systemic toxicity
+/- site of introduction
Local edema, cerpitus
Skin abnormality, red, purple, or necrotic tissue
SPREADS RAPIDLY

344
Q

What is the treatment for necrotizing fasciitis?

A

ABX

  • carbapenems
  • anaerobic coverage - clindmycin
  • MRSA coverage (Vanco, linezolid)

NPO because they are going to the OR TODAY

345
Q

Fournier Gangrene

A

Necrotizing fasciitis of the perineum or scrotum

346
Q

What pathogens are responsible for fournier gangrene?

A

E. Coli (aerobe)

Bacteroides (anaerobe)

347
Q

What is the Epi of fournier gangrene?

A

80% have DM
Trauma to genitalia frequently associated
M > F
Age: 30-60 years

348
Q

What is the path of fournier gangrene?

A

Effects superficial and deep tissues of genitalia and perineum

Infection can originate from anorectum, urogenitalia tract, or skin of the genitalia

Can spread across the Colles fascia of the abdominal wall and Scarpa’s fascia of the inguinal area

349
Q

What is the treatment of fournier gangrene?

A

Fluid support
ABX (cover gram -, +, anaerobes, MRSA)
REMOVE DEAD TISSUE ASAP
+/- IVIG

350
Q

What are complications of Fournier Gangrene?

A 
Pain with erection (50%)
Genitial scarring 
Impotence 
Psych consideration 
Extensive reconstruction needs 
NSQIP mortality rate: 10%
351
Q

Purpura fulminans

A

Thrombotic disorder with purple hue enlarging lesions and necrotic distal digits caused by hemorrhagic skin necrosis and coagulation impairment rapidly leading to DIC

Idiopathic vs underlying infectious caused (meningococcal meningitis - Neisseria)

352
Q

Protein C deficiency is associated with which type of skin disorder?

A

Pupura fulminans

353
Q

Which infection is most commonly associated with purpura fulminans?

A

Neisseria meningococcal meningitis

354
Q

What is the presentation of purpura fulminans?

A

7-10 day onset after infection

Starts DISTALLY symmetric

Systemically ill - fever, hypotension

355
Q

What is the treatment for purpura fulminans?

A 
Fluid management 
ABX broad spectrum 
DIC management 
Heparin vs protein C concentrate 
Remove dead tissue —typically amputation
356
Q

For a pt with atopy, which part of the triad typically started first?

A

Atopic dermatitis when they were an infant

357
Q

What is the most common treatment for atopic dermatitis?

A

Emollients (thicker form of lotion OTC)

358
Q

What is the epi of atopic dermatitis?

A

Common. 11-19% prevalence

All cases start within the first decade of life

Only 5% of cases develop after 5 years of age

359
Q

What is the lesion distribution by age for atopic dermatitis?

A

Infants: face

Older: flexor surfaces

360
Q

What other skin condition might present with a pt who has atopic dermatitis and why?

A

Impetigo due to these pts having more staph on their skin

361
Q

What are the characteristics of the rash for chronic atopic dermatitis?

A

Lichenification (leather like fibrosis d/t chronic scratching)

Hyperpigmentation (if active)

Depigmentation (overtime)

362
Q

On your differential for atopic dermatitis is contact dermatitis. How can you tell these two apart?

A

Contact dermatitis (whether allergic or irritant) is always related to the location in which the pt was exposed

363
Q

How can you tell scabies apart for atopic dermatitis?

A

Atopic dermatitis in infants is always on the face while scabies typically is seen on the trunk (belt line) and genitalia

364
Q

How can you tell atopic dermatitis from seborrheic dermatitis?

A

Seborrheic dermatitis is commonly found in the nasolabial folds but has more flaking as opposed to the pustule appearance of atopic dermatitis

365
Q

What is first line treatment for atopic dermatitis?

A

Ideally using emollients often enough to decrease flare ups and thus the need for steroids

STEROIDs are first line treatment for flare-ups —mid potency (grade 5-7) apply 2-3 times a day

Second line - TCIs (Topical Calcineurin Inhibitors)

366
Q

Rank in order from most potent to least potent vehicles of steroids

A

Ointment > cream > lotion

367
Q

What are the major side effects of long term use of high dose steroids?

A

Skin atrophy!!
Telangiectasia
Striae

368
Q

What is an appropriate long term treatment/prevention for atopic dermatitis?

A

Bleach baths

369
Q

What determines potency of a topical steroid?

A

Vasoconstricitve effect

Grade 1 = most potent
Grade 7 = least potent

370
Q

Super high potency topical steroids (group 1) are best for use where?

A

Palms and sole, hyperkeratotic lesions

Short term use - no longer than 3 weeks

371
Q

How do you determine how much steroid to prescribe a pt?

A

You will be doing once or twice dosing daily
FTU - fingertip unit application method

1 fingertip unit = 0.5 grams
Multiply that by how many FTUs are needed to treat specific area (numbers given on a chart)
This will tell you how much is needed for 1 application

For ex.
0.5g x 7 FTUs needed for trunk = 3.5 gms needed per application
2 applications a day for 1 week = 49g tube needed

372
Q

Which steroids can be used for intralesional injections and for which conditions is this done?

A

Triamicinolone acetonide
Methylprednisone acetate

Hyperkeratotic lesions
Cystic acne
Keloids

373
Q

Immediate reactions to drugs

A

Occur less than 1 hour after last administered dose
Type 1 hypersensitivity reaction

Urticaria
Angioedema
Anaphylaxis

374
Q

Delayed reactions to drugs

A

Occurring after 1 hour but usually more than 6 hours and occasionally weeks to months after the start

  • exanthematous eruptions
  • fixed drug eruption
  • systemic reactions (DIHS, SJS, TEN)
375
Q

What is angioedema?

A

Leaky blood vessels in the lower dermal layer caused by histamine release

376
Q

Erythematous patch with central bulla

A

Fixed drug eruption

377
Q

What is the path of psoriasis?

A

Autoimmune
Multifactorial (genes + environment)

HLA-Cw*0602
Bad MHC-1 receptor that the body sees as foreign and attacks

This results in hyperkeratosis

378
Q

What do you see microscopically with psoriasis?

A

Acanthosis - “Test tubes in a row”

Hyperkaratosis with parakaratosis

379
Q

Who gets psoriasis?

A

2-3%

W > M (or is it that women are more likely to seek help?)

Onset 15 - 30 y/o (median age 28)

10-15% begin in children young than 10

380
Q

Erythematous scaly patches, plaques. Might be painful. Well defined round or oval plaques.
Symmetrically found on the extensor surfaces of arms, legs, scalp, buttocks, and trunk.

A

Psoriasis

90% are plaque

Silvery scale unique to psoriasis

381
Q

What is the most common ocular finding in psoriasis?

A

Blepharitis

Plaques forming at the glands that lead to the eye

Eyelid erythema, edema, and psoriatic plaques

382
Q

What nail findings might you see with a psoriatic pt?

A

Onychodystrophy

Pitting

Fingernails > toenails

Does not respond well to tx

383
Q

What is the time frame of psoriatic arthritis?

A

~12 years after onset of skin disease
This puts the onset to about 30-40 years of age
This is not typical for arthritis so it helps you narrow you ddx to psoriatic arthritis

If you treat it early you help prevent it from progressing to full blown arthritis

384
Q

How do you dx psoriasis?

A

Clinical dx

Unless its not the typical plaque psoriasis

Ddx

  • syphilis
  • pityriasis rosea
  • pityriasis alba
  • tine
  • atopic dermatitis
385
Q

What defines the difference between mild and severe psoriasis?

A

Mild: <5% of BSA

Severe: >5% of BSA

386
Q

What are recommendations to help manage psoriasis for all forms and severity?

A 
Daily sun exposure 
Topical moisturizers 
Sea bathing (order salt for salt baths at home) 
Relaxation 
Salicylic acid lotions
OTC “tar” preparations
387
Q

What is the treatment for mild psoriasis?

A

Topical steroids
Vitamin D analogs (calcipotriol, calcitriol)
Tazarotene (Tazorac)
Calcineurin inhibitors (tacrolimus, pimecrolimus)

Always consider PSYCH help for those that struggle with the social part or have genital plaques

388
Q

What is the treatment for severe psoriasis?

A

Severe (>5%)

Mainstay of treatment = systemic therapy +/- phototherapy

-methotrexate (immunosuppressant)
SE: bone marrow suppression
-Acitretin (retinoid) - particularly good for pustular or palmoplantar forms
SE: teratogen
-Cyclosporine (calcineurin inhibitor) - used for rapid relief, “crisis therapy”
-Apremilast (PDE4 inhibitor) —good for arthritis

389
Q

Cyclosporine is used for what?

A

Rapid relief, bridge therapy or “Crisis” therapy for severe psoriasis

SE: GI intolerance, renal impairment

390
Q

What other options do you have if a pt with severe psoriasis isn’t responding to topical + systemic meds?

A

Biologics - all injections

TNF-a inhibitor (Humira - Adalimumab - SC injections q2 weeks)
IL-12/IL-23 inhibitors
IL - 17 Inhibitors

On these injections for LIFE

$$$$$

Insurance will only cover it if you have exhausted every other option of psoriasis treatment

391
Q

Fitzpatrick Skin type 6

A

Black

Never burns, tans very easily

392
Q

Fitzpatrick skin type 1

A

White; very fair; red or blonde hair; blue eyes; freckles

Always burns, never tans

393
Q

What is the path of vitiligo?

A

Multifactorial disorder
Immune-mediated melanocyte destruction
Absence of melancytes within lesions
Must have some type of exposure before the disease starts (not sure what that exposure is but this isn’t seen at birth)
Associated with other autoimmune disorder

394
Q

Who gets vitiligo?

A 
It’s the most common depigmentation disorder 
1% of general population 
Family hx in 25 - 30% of pts 
Adults = children 
F = M

Age of onset typically ~10 years

Pts commonly have DM

395
Q

What are precipitating factors of vitiligo?

A

Usually nothing but sometimes:

Illness
Emotional stress
Sunburn

396
Q

How do you dx vitiligo?

A

Clinically

Might need woods lamp in fair skinned individuals —the lesions will illuminate

397
Q

What is the typical distribution of vitiligo?

A 
Neck, clavicle 
Arm pits 
Genitalia 
Fingertips 
Knees 
Feet

Might also see it at sites of “trauma” - Koebner’s Phenomenon

398
Q

What is the treatment for vitiligo?

A

Sun protection - SPF 50 min —need to protect from SCC, BCC
Cosmetic coverage
Topical steroids - Betamethasone (0.05%) - for actively growing lesions
Phototherapy - to kill off the expansion
Depigmentation
Surgical grafting (not a good option)

399
Q

Oculocutaneous albinism

A

Skin, hair, and eyes without melanin production

400
Q

What is the inheritance pattern of albinism?

A

Autosomal recessive

401
Q

What is the path of albinism?

A

Autosomal recessive

Mutation of tyrosinase - enzyme used in melanin production
Results in no melanin production

402
Q

What is the treatment of albinism?

A

Prevention of sun damage
SPF 50
UVR blocking clothes
Regular follow up with dermatology and ophthamology

403
Q

Solar lentigines

A

“Liver spots”

Localized proliferation of melanoctyes and melanization

Hperpigmented, well-circumscribed lesions

Sun exposed areas

Skin Types 1-3 most at risk

404
Q

What do you have to keep in mind when dx solar lentigines?

A

Must differentiate from actinic kertosis and lentigo maligna

  • premalignant condition
  • warning signs: rapid growth, pain, itching, bleeding, poor healing

Can be difficult to distinguish from early seborrheic keratosis

Solar lentigines will just show up over a few days and will stop growing …no pigmentation change, no growth, no elevation

If it does change be weary that this is no liver spots

405
Q

What is the treatment/prevention of solar lentigines?

A

Basically just make sure this isn’t precancerous

Albative therapies - chemical peels, cryotherpay, laster therapy
Topical theapies - hydroquinone, retinoids

Prevention: regular sunscreen use and limiting sun exposure

406
Q

Melasma

A

Progressive, macular, nonscaling hypermelanosis of sun-exposed areas (face)

Associated with:

  • pregnancy
  • oral contraceptive use
  • phenytoin

Skin types 4-6

407
Q

What is the treatment of melasma?

A

Hydroquinone 3% or 4%
Glycolic or Azelaic acid peel
Retinoids

Prevention:

  • sunscreen
  • discontinue oral contraceptive
408
Q

Freckles

A

Ephelides

Small 1-2mm sharply defined macular lesions, uniform color

Face, neck, chest, arms
Childhood onset
Fade in winter
Can be treated in same manner as lentigo if necessary

409
Q

Cafe-au-Lait macules

A 
Tan or brown macule 1-20 cm (HUGE)
Present at birth or early childhood 
10-30% of general population has isolated cafe-au-lait
Increase in melanin production 
Usually found on trunk 
IF >6 CAFE-AU-LAIT LESIONS:
Think about other underlying conditions (This can be a precursor) 
-fanconi anemia
-neurofibromatosis 
-tuberous sclerosis 
-albright syndrome
410
Q

Acanthosis Nigricans

A

Seen in DM or obese pts

Dark, hyperkeratosis streaks in skin folds:

  • neck
  • axilla
  • groin
  • body folds
411
Q

What is the treatment of acanthosis nigricans?

A

Treat the underlying condition

DM or weight loss

412
Q

Post-inflammatory hyperpigmentation

A

Irregular, dark pigmented macules and patches at site or previous injury or inflammation

  • acne
  • psoriasis
  • lichen planus
  • atopic dermatitis
  • contact dermatitis
  • trauma

All skin types
More obvious in 4-6 skin types

Lesions persist for months to years

Treatment: hydroquinone or azelaic acid

413
Q

Nevi

A 
Pigmented and no-pigmented tumors of the skin 
Contain nevus cells 
Any location on the body 
# increase with age 
Type/number genetically determined

Borders are regular and color even throughout lesion

414
Q

What is a mole?

A

A collection of nevus cells

415
Q

Keloids

A 
Overgrowth of fibrous tissue 
Extends beyond the site of injury 
Can also occur spontaneously 
Family hx, genetic predisposition 
4x more common in persons of afrobarribbean descent
416
Q

Where are the common sites of keloids?

A

Head, neck, chest, and arms

Can be painful, itchy, stingy

417
Q

What is the treatment for keloid?

A

Topical steroids - gels, locations, creams, ointments
Intralesional injections - kenalog, 5FU
Surgical excision

Recurrence is common

418
Q

What is the rule of thumb for hairs growing out of nevi?

A

If hairs grow out of nevi they are probably benign

419
Q

Epidermal cyst

A

“Balloon containing degraded skin contents”

Nodule with central pore (punctum)

Can originate from invagination of epidermis into the dermis or spontaneously

420
Q

What is the treatment for epidermal cyst?

A

Intralesions kenalog injection
Incision and drainage
Surgical excision

421
Q

Lipoma

A

Most common connective tissue tumor
Occurs most commonly in middle and later aged adults

F > M

Locations: back, chest, abdomen, neck

Cause - unknown
Asymptomatic

No treatment necessary - cosmetic surgery only reason usually

422
Q

What is the most common connective tissue tumor?

A

Lipoma

423
Q

Dermatofibroma

A 
Very common 
F > M 
Trauma may play a major role 
-insect bites 
-folliculitis 
-injury to the skin

Painless, slow growing

No treatment needed

Surgery is curative - cosmetic reasons

424
Q

Acronchordons

A

Skin tags

Soft tumors of normal skin

Location: neck, axillae, groin

Removal - cosmetic, irritation, and infection

425
Q

What is the treatment for skin tags?

A

(Aka acrochordons)

Electrodessication (destruction) or surgical excision

426
Q

Hemangioma

A

Vascular abnormalities

Not hereditary

Present at birth or develop in infancy

Can cause obstruction-eye, urogenital area, nose, mouth

Spontaneous involution may occur after a few years

Does not become cancerous

No treatment needed unless bleeding:

  • systemic steroids
  • arterial embolization
  • surgery
427
Q

Neurofibroma

A

Most common type of neural sheathe tumor

Nodular lesion located on the skin

Consider evaluation for neurofibromatosis

Neurofibromatosis

  • autosomal dominant
  • congenital and acquired tumors of CNS, skin, eyes, bones, endocrine glands, and Cafe au lait macules
428
Q

What is the most common type of neural sheath tumor?

A

Neruofibroma

429
Q

Actinic keratosis

A 
Precancerous lesions 
Red scaly plaques located on the skin 
Occur on sun exposed areas - face, ears, hands, scalp 
Common in fair skinned 
5-10% lesions become SCC
430
Q

What is the clinical sxs of actinic keratosis and how do you treat it?

A

Precancerous!

Tender, burny or itchy, or even no sxs

Tx:

  • cryosurgery
  • curettage
  • electrosurgery
  • topical chemotherapy
431
Q

What are the common locations for actinic keratosis?

A

Sun exposed areas - face, ears, hands, neck, scalp

432
Q

What are the malignant and precancerous lesions?

A

Actinic Keratosis
BCC
SCC
Malignant melanoma

433
Q

What is the most common type of skin cancer?

A

BCC

434
Q

Where are the common locations to find BCC?

A

Face and neck

435
Q

What are the clinical manifestations of BCC?

A

Translucent papule or lesions that will not heal

Become a large sore or ulcer that will not heal if untreated

Very rare metastasis

436
Q

What is the second most common type of skin cancer?

A

SCC

437
Q

What age group is more likely to get SCC?

A

Pts over 50

Can have a genetic tendency to develop lesions

438
Q

Malignant Melanoma

A

Most DEADLY form of skin cancer
Can metastasize to other organs
ABCDE rule of melanoma

439
Q

What are the 4 types of malignant melanoma?

A

Acral lentiginous
Nodular
Superficial spreading
Lentigo maligna

70% are superficial spreading type

440
Q

What is the treatment for malignant melanoma?

A

Same for all skin cancers

  • surgical excision
  • Mohs surgery
  • Electrodessication and curettage - not recommended
  • Cryosurgery - not recommended
  • Chemotheraperutic drugs - topical and oral
441
Q

“Test tubes in a row”

A

microscopic evaluation of PSORIASIS - epidermal acanthosis

442
Q

MC locations for psoriasis plaques?

A

extensor surfaces

443
Q

“beefy red”

A

intertrigo - candidiasis

444
Q

What is the treatment for intertrigo?

A

topical antifungals (clotrimazole, miconazole, nyastatin)
steroids
keep area dry

445
Q

Who gets intertrigo?

A

F > M
DM
Obese

located in the skin folds

446
Q

Tense bullae

A

bullous pemphigoid

treat with steroids

Clin Med 2 (13 decks)

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