Dermatology Flashcards
1
Q
Eccrine Glands
A
A type of sweat gland
opens directly onto skin
regulates body temperature through sweat
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
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
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
5
Q
Most common types of skin cancer arise from which skin layer?
A
Epidermis
Remember the layers by “Come Lets Get Sun Burnt”
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
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
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
9
Q
Acanthosis
A
abnormal thickness of epidermis (relative to the location on the body)
diffuse epidermal hyperplasia
10
Q
Invasive SCC
A
this means that the squamous cells have invaded based the basal membrane and into the dermis
11
Q
Hyperkeratosis
A
thickening of stratum corneum by abnormal keratin
often associated with a qualitative abnormality of the keratin
12
Q
Parakeratosis
A
Retention of nuclei in stratum corneum
normal in mucous membranes
13
Q
Hypergranulosis
A
Hyperplasia of stratum granulosum, usually caused by intense rubbing
14
Q
Papillomatosis
A
Hyperplasia and enlargement of contiguous dermal papillae leading to surface elevation
common wart
15
Q
Dyskeratosis
A
Abnormal keratinization occurring prematurely in cells below stratum granulosum
16
Q
Acantholysis
A
loss of intracellular connections causing loss of cohesion between keratinocytes
17
Q
Spongiosis
A
epidermal intracellular edema
18
Q
First Degree Burn
A
erythema, swelling
transitory, reversible
19
Q
Second Degree Burn
A
Blisters involving epidermis
Hair follicles, adenxa in dermis spared
20
Q
Third Degree Burn
A
Full-thickeness burns; massive necorsis of epidermis and parts of dermis, subcutis
cannot heal spontaneously
21
Q
Macule
A
flat, smaller than 2cm (ex. freckle)
22
Q
Patch
A
similar to macule but larger
flat >2cm
23
Q
Papule
A
slightly elevated, smaller than 1 cm
ex. eczema caused by allergy
24
Q
Nodule
A
similar to papule but greater than 1 cm
(slightly elevated)
ex. nevus
25
Tumor
nodule greater than 5 cm
26
Vesicle
fluid-filled elevation of epidermis
smaller than 1 cm
ex. herpesvirus lesion on the lip
27
Bulla
vesicle measuring more than 1 cm (ex. burns)
28
Pustule
vesicle filled with pus (ex. impetigo)
29
Ulcer
defect of the epidermis (ex. syphilitic chancre)
30
Crust
skin defect covered with coagulated plasma ("scab")
31
Scales
Keratin layers covering skin as flakes or sheets; can be scraped away
ex. psoriasis, seborrheic keratoiss
32
Squames
Large scales (ex. ichthyosis)
33
Excoritation
superficial skin defect caused by scratching
34
Fissure
sharp-edged defect extending deeper into dermis (ex. athlete's foot)
35
Orthokeratosis
hyperkeratosis with just keratin, no nuclei
36
Parakeratosis
hyperkeratosis with keratin and nuclei
37
Effects on skin from chronic sun exposure
hyperpigmentation
atrophy of epidermis
dermal connective tissue degeneration
38
Folliculitis
bacterial infection of the hair follicule
39
Acne vulgaris
infiltration and destruction of follicular epithelium by neutrophilic exudate
40
Where are fungal infections mc?
Keratin layer (dead tissues)
41
Verruca Vulgaris
Common Wart
| on microscope -- papillomatosis
42
Auspitz sign
seen with psoriasis
| bleeding points when scale is lifted from plaque d/t tortuous dilated vessels
43
What is the MC malignant skin tumor?
BCC
most commonly located on the FACE
44
What are telltale signs of skin cancer?
persistent, nonhealing ulcer
irregular shape
friable (crumbles), bleeds, multicolored
indurated (hardened) margins of an ulcer or tissue around it
45
Lentigo
macule or papule' pigmented but does not respond to sun
46
Junctional nevus
mole just in the epidermis
47
Compound nevus
mole in both epidermis and dermis layers
48
Clinical Warning Signs for Melanoma
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)
49
What is the most important prognostic factor in melanoma?
tumor thickness
50
Radial vs vertical growth phase of melanoma?
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
51
Onychogryphosis
hypertrophic nail
| related to trauma
52
Koilonychia
thin and spoon nail
| seen in Fe deficiency anemia
53
Onychomycosis
thicken, discolor, disfigure, and split nail, related to FUNGAL infection
54
Paronychia
soft tissue infection, pus formation around a fingernail
55
What is Impetigo?
superficial bacterial infection of the Epidermis
| typically caused by a mix of staph and strep
56
How do people get impetigo?
minor breaks in the skin
preexisting dermatoses
Bites
wounds, burns, ulcers
HIGHLY contagious amongst close contacts
57
What is nonbullous impetigo?
"Classic impetigo"
| Erythematous macules/papules that evolve into vesicles/pustules, rupture forming HONEY COLORED crusts
58
Where on the body is nonbullous impetigo most common?
face and extremities
59
Where on the body is bullous impetigo more common?
on the trunk and folds such as axillae
60
What is Ecthyma?
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
61
How do you dx impetigo?
Clinical dx
Microscope will help you determine if its staph or strep
```
Staph = clusters
Strep = chains
```
62
What is the treatment for impetigo?
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
63
What is Erysipelas?
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)
64
How does erysipelas present?
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
65
What is the treatment for erysipelas?
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)
66
How does the age distribution differ between cellulitis and erysipelas?
Erysipelas is bimodal (young and old)
| Cellulitis is MC in middle-aged, elderly, and immunocompromised
67
Pasteurella multocida
organism responsible for cellulitis secondary to dog or cat bites
68
IV Drug users are more likely to get cellulitis secondary to what bacteria?
Staph Aureus
69
If you are palpating a pt you suspect having cellulitis and you hear crunching, what pathogen should you be thinking about?
Clostridia
| Crepitant cellulitis
70
Haemophilus influenzae causing cellulitis commonly presents where on the body?
face and periorbital
71
What is the clinical manifestation of cellulitis?
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
72
What is lymphagitis?
```
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
```
73
For which pts with cellulitis should you cover for Pseudomonas aeruginosa?
penetrating trauma ("stepped on a nail")
immunocompromised
hospitalized
74
What is the treatment for Cellulitis?
Keflex
Augmentin (used for cat and dog bite - pasteurella)
Dicloxacillin
Clinda (MRSA)
Cipro (puncture wounds d/t covering pseudomonas)
75
When should you be suspecting MRSA for a pt with cellulitis?
(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
```
76
MRSA treatment
Oral:
- Bactrim DS (double strength)
- Doxycycline
- Clinda
- Linezolid
IV:
- Clinda
- Linezolid
- Vancomycin (not first line)
- Daptomycin
77
What is folliculitis?
Inflammation of the superficial or deep portion of the hair follicle
bacterial infection is MC cause
78
What is the MC bacteria responsible for folliculitis?
Staph Aureus
79
Hot Tub Folliculitis
pseudomonas aeruginosa
| rash presents 1-2 days after being in hot tub
80
Psuedofolliculitis barbae
"Razor bumps"
can occur over any shaved area
related to curved hair follicles, foreign-body type reaction
can be secondarily infected by staph aureus
81
What is a furuncle?
folliculitis that is deeper
| tender, nodules/abscesses (boils)
82
What is a carbuncle?
deeper folliculitis where the infections are interconnecting under the skin
several contiguous hair follicles
83
What is the treatment for Folliculitis?
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)
84
What is the treatment for Folliculitis?
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)
85
Acute Paronychia
acute infection caused by Staph Aureus of the nail fold
86
Chronic Paronychia
loss of cuticle, proximal nail fold becomes boggy, nail plate becomes irregular/discolored
87
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?
Cellulitis
treat with Augmentin
88
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?
folliculitis
treat with cipro to cover for psudomonas
89
What is pediculus humanus capitis?
Head louse
90
What is pdiculus humanus corporiss?
Body louse
91
What is phihirus pubis?
Crab or pubic louse
92
What is pediculosis?
Lice
93
What is the primary symptom of pediculosis and what causes it?
Itching due to an allergic reaction to louse saliva
94
What do you need to dx lice?
Must have at least one life louse
| Eggs (nits) does NOT confirm active infection unless they are "viable"
95
What is the treatment for head lice?
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
96
How do you treat crab lice?
Same as head lice
97
What diseases may be transmitted by body lice?
Typhus and trench fever
98
What is the treatment for body lice?
Wash entire body, topical treatment or oral ivermectin
99
What are the hallmark features of scabies?
Intense pruritic, papular rash with excoriations
Borrowing typical in hands and wrists
Typically the head and neck are spared
100
“Norwegian Scabies”
Crusted scabies
EXTREMELY contagious (primarily in older, immunocompromised, or homeless)
101
What is the treatment for scabies?
Permethrin
Lindane (risk of neurotoxicity)
Crotamiton
Oral Ivermectin
102
Cimex lectulrius
Bed bugs
103
What is the treatment for bed bugs?
```
Bites typically resolve within one or two weeks
Topical or oral steroids
Antihistamines
Eradication
-heating/steaming extermination
-laundering of linens
-vacuuming of furniture
```
104
Red, white, and blue sign
Seen with brown recluse spider bites
Red (peripheral erythema)
White (blanching)
Blue (violaceous center)
105
nits
pediculosis eggs
just the presence of eggs does not confirm dx because the shells might be empty
they must be viable
106
How do you tell the difference between head lice and dandruff?
dandruff should flake off while nits are attached to the shaft via protein
107
Where are you more likely to see head lice?
in the homeless
hair shafts
behind the ears and on the back of the neck
108
How to lice treatment drugs work?
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
109
What is the first line treatment for head lice?
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
110
A pt comes in with a pruritic papular rash that is more itchy at night, what should you be thinking?
Scabies
111
What is the key characteristic of scabies?
Burrowing
| typically in the webbed part of the hands and toes
112
Where are scabies rashes more commonly located?
Belt line
Buttocks
Genitalia
in between the fingers and toes
113
How do you instruct pts to treat their scabies?
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
114
How does treatment change for Norwegian scabies?
you do both topical and oral
115
Loxosceles reclusa
brown recluse spider
116
How do you treat a brown recluse spider bite?
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
117
What is the age of onset for pityriasis rosea?
adolescence through adults
| more common in spring and fall
118
What is pityriasis rosea?
```
often considered viral (but truly unknown)
falls under the class of papulosqaumous
```
119
What is the prodrome phase of pityriasis rosea?
HA
Malaise
mild constitutional sxs
120
What is the most common location on the body for pityriasis rosea?
the Herald patch - the trunk
| the exanthem that appears weeks later - trunk and proximal extremities
121
Herald Patch
```
that initial patch of
pityriasis rosea
single oval lesion 2-10cm in diameter
pink, salmon-red to erythematous
slightly raised, fine collarette scale
```
122
Exanthem
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
123
"Christmas Tree" distribution of a rash
Pityriasis rosea exanthem rash that follow langer's lines (cleavage lines of the body)
124
What is reverse pityriasis rosea?
when the lesions are on the extremities, sparing the trunk
125
What is atypical pityriasis?
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
126
What are some of the DDx for pityriasis rosea?
lichen planus
erythema multiform
secondary syphilis
127
How do you dx pityriasis rosea?
clinically
| can use KOH prep or RPR to rule out fugal infection and syphilis
128
What is the treatment for pityriasis rosea?
symptomatic
antihistamines, calamine lotion, steroids
+/- UVB phototherapy
the rash will last for about 4-10 weeks
129
What is the epidemiology of lichen planus?
acute or chronic
more common in females
~1% of the population
30-60 years of age
130
What is the cause of lichen planus?
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
131
What are the 6 Ps of lichen planus?
```
Purple
Pruritic
Polygonal
Planar
Papules
Plaques
```
132
Where is lichen planus commonly found on the body?
```
flexor surfaces of the wrists, shins, lumbar, feet
genitalia
mouth
hair
nails
```
133
Koebner's Phenomenon
new lesions of lichen planus (and psoriasis) at the sight of trauma
134
Besides the 6 Ps, what does lichen planus look like? (looking for a commonly used descriptive term)
wickham striae
| white, lacy reticular pattern (especially oral lichen planus)
135
Pts with chronic oral lichen planus are at an increased risk for what?
SCC
136
What is the DDx for lichen planus?
```
drug induced
psoriasis
secondary syphilis
pityriasis roasea
lupus
```
137
What is the DDx for oral lichen planus?
candidiasis
leukoplakia
lupus
secondary syphilis
138
What types of drugs can cause lichen planus?
```
gold salts
BB
antimalaria pills
HCTZ
Furosemide
spironolactone
```
139
How is lichen planus dx?
clinical presentation + punch biopsy (punch typically done by dermatologist)
in the meantime start them on steroids (since it doesn't look fungal)
140
What is the treatment for lichen planus?
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
141
What is the prognosis of lichen planus?
majority of cutaneous LP spontaneously remit within 1-2 years
recurrences may occur
142
coin-shaped, disseminated, pruritic eczema lesions found on the extremities
nummular eczema
143
What is Tinea Corporis?
superficial fungal infection of the skin
typically from Trichophyton, Microsporum, Epidermophyton
T. RUBRUM MC
144
What are the risk factors for tinea corporis?
affects all ages
warm-hot environments
animals
contaminated soil
145
T. Rubrum
MC cause of tinea corporis
146
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
Tinea Corporis
147
Malassezia furfur
causes tinea versicolor
148
Well-demarcated macules/patches with fine scale
hypo-and hyperpigemention variable
MC on trunk
tinea versicolor
149
What does tinea versicolor look like on a KOH prep?
spaghetti and meatballs
150
What is the age group for acute guttate psoriasis?
children and adolescents
151
What is the rash distribution of acute guttate psoriasis?
mainly on the trunk
some on the face and scalp
usually spares palms and soles
152
What is associated with acute guttate psoriasis?
it is often precipitated by an acute strep infection
153
What does pityriasis mean?
scaling
154
Langer's Lines
Skin cleavage lines of the body that pityriasis rosea tends to follow (Christmas tree distribution)
155
What do you use KOH prep for?
to determine if a rash is fungal
| used in pityriasis to rule out fungal (since this rash looks fungal)
156
How does pityriasis rosea typically present?
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
157
at what point with pityriasis rosea would you get a skin biopsy?
if 3 months has passed and no improvement (maybe misdx)
158
What is the RPR test used for?
tests for syphilis
this is a do not miss dx
know when its on the ddx
-pityriasis rosea
159
If a pt comes in with lichen planus, what should you screen them for?
Hep C
| there is an association between these 2
160
If a pt has had a recent trauma and then presents with this papule like rash, what should you be thinking?
Lichen planus
| Koebner's Phenomenon
161
What age group is most common with erythema multiforme?
can occur in all ages but peaks between 20-40 years of age
| M > F
162
What is the MC etiology of erythema multiforme?
HSV
163
What drugs can cause erythema multiforme?
barbiturates, NSAIDs, PCNs, metformin, cipro, bupropion
even vaccines (diptheria -tetanus, hep B)
164
What is the prodrome for erythema multiforme?
Fever
malaise
myalgia
sore throat and cough if d/t mycoplasma
165
What is the typical presentation of erythema mutliforme?
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)
166
What is the difference between erythema mutliforme major and minor?
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
167
What is Nikolysky sign?
seen with major erythema multiforme
when you rub the skin it comes off
this is why you are worried about stevens-johnsons syndrome
168
What is the prognosis of erythema multiforme?
usually resolves spontaneously within 3-5 weeks
| may be recurrent (especially for those with recurrent HSV)
169
What is the treatment for erythema multiforme?
remove any offending drug
oral antihistamines and topical steroids for symptomatic relief
oral prednisone for severe cases
treat underlying etiology
- HSV: acyclovir
- Mycoplasma: macrolide
170
Where does secondary syphilis most commonly present on the body?
mucosal lesions
| palms and soles
171
What is atopy?
eczema, hay fever, asthma
sometimes we add ASA allergy
typically in the family hx
172
What is the cause of pityriasis (tinea) versicolor?
yeast infection
| overgrowth of the yeast on the body
173
What is the prevention for herpes zoster?
vaccine for those >60 years (~60% reduction)
174
What is the treatment for herpres zoster?
acyclovir within 72 hours of rash onset
| 5x/day for 7-10 days
175
Molluscum contagiosum
viral rash
caused by a pox virus
mostly in children or young adults
it's self limited for about 2 months
176
Verruca Vulgaris (HPV)
```
common wart (from HPV, just a different strand)
occurs weeks to months after skin to skin exposure
```
177
condylomata acuminata
anogenital warts
178
What is the treatment for HPV?
no treatment is curative
surgery is the most likely to be curative (and cheapest option)
QUIT SMOKING
179
How do you prevent HPV?
```
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
umbilicated papules
discrete, solid, skin-colored papules 3-5mm
describes what kind of skin problem?
Molluscum contagiosum
181
What is the treatment of verruca vulgaris?
chemically or physically burn it off or just wait because they are self limiting
educate the pt not to spread it around (contagious)
182
What is respiratory papillamatosis?
caused by vaginal birth when someone has HPV
| the infant inhaled the virus
183
How do you dx HPV?
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
When do you see post-adolescent acne?
83% of women have pre-menstrual flares
185
What is oral isotretinoin used to treat?
aka accutane
used for severe acne (6 months of treatment)
works by shrinking sebaceious glands and decrease sebum secretions
186
What topical agents can be prescribed for acne?
retinoids such as tretinoin, adapalene, tazoratene
187
What is the most mild form of acne?
comedonal acne
188
What is the worst form of acne?
nodulocystic
189
What is the treatment for pts with acne around their periods?
OCPs
spironolactone
(decrease sebum production)
190
What are the side effects of accutane?
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
What is rosacea?
facial flushing
inflammatory papulopustual eruption
unknown cause
chronic and relapsing
192
What is the classic form of rosacea?
papulopustual
erythematotalangiesctatic is central facial flushing (not classic)
193
What is phymatous?
Rosecea
| thickened and irregular surface of nose, chine, forehead, ears, eyelids
194
What treatements for rosecea help with the redness?
topical brimonidine and oxymetazoline
195
What is hidradenitis suppurativa?
follicular occlusive disease found in the skin folds
196
What is the epidemiology of hidradenitis supporativa?
rare
1-4%
onset: puberty - 40y/o
W > M
197
What is the pathogenesis of hidradenitis suppurativa?
hormones increase follicular epithelial hyperplasia that leads to nodule that can turn into an abscess
this can lead to comedones or scarring
198
What is stage 1 of hidradenitis suppurativa?
abscess formation without sinus tracts or scarring
199
What is stage 2 of hidradenitis suppurativa?
recurrent abscesses with sinus tracts, scarring
200
What is stage 3 of hidradenitis suppurativa?
diffuse involvement, multiple interconnected sinus tracts and abscesses
201
What is the treatment of hidradenitis suppurativa?
```
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
Anagen
growth phase of hair cycle
2-6 years
80-90% of hairs on normal scalp
203
Catagen
involutional phase of hair cycle
2-3 weeks
5-10% of hairs on normal scalp
204
Telogen
resting phase of hair cycle
2-3 months
1-3% of hairs on normal scalp
205
How many hairs is normal to loose a day?
100
206
Alopecia Areata
Chronic immune mediated disorders
target anagen hair follicles
non-scarring hair loss
very smooth round patch of skin
207
What is the age group for alopecia areata?
usually before the age of 30
| M = F
208
alopecia totalis
complete loss of scalp hair
209
alopecia universalis
loss of scalp and body hair
210
What is the treatment for alopecia areata?
intralesional corticosteriods (triamcinolone) injected into upper subQ of scalp
potent topical steroids
topical immunotherapy
211
What is telogen effluvium?
diffuse non-scarring alopecia
sometimes bitemporal hair loss
<50% hair loss, no balding occurs
212
What are the typical causes of telogen effluvium?
```
major surgery
serious illness
childbirth
protein or caloric malnutrition
thyroid disorders
drugs
emotional stress
```
213
What is the pathogenesis of telogen effluvium?
```
# of hairs in telogen phase increases
unknown why
```
214
What is the treatment for telogen effluvium?
removal or treatment of underlying cause
minoxidil is controversial
usually is self-limited in 6-12 months
215
What is androgenetic alopecia?
typically in men
| progressive loss of terminal hairs on anterior scalp, mid-scalp, temporal scalp
216
Malassezia
yeast that causes tinea versicolor
217
What is pityriasis alba?
small white scaly "patches" typically on the faces of kids after summer
218
Tinea capitis
infection of scalp hair
typically seen in children
caused by direct contact with an infected individual
pruritic
219
What is tinea corporis?
pruritic circular or oval, erythematous scaling plaque that usually has a central clearing and a raised border
220
What is tinea cruris?
fungal infection of the groin
221
What is tinea pedis?
fungal infection of the foot
| "athletes foot"
222
What is tinea unguium?
Fungal infection of the nail
| "onychomycosis"
223
What is the treatment for tinea capitis?
oral antifungals
| griseofulvin for 6-12 weeks
224
What is the treatment for tinea cruris?
topical antifungals
terbinafine PO
Itraconazole PO
225
What pathogen causes impetigo?
staph and strep
226
What is considered "classic impetigo?"
nonbullous impetigo
erythematous macules/papules that evolve into vesicles that rupture --> honey-colored crust
227
Where is classic impetigo more commonly located on the body?
face and extremities
228
Bulla
vesicle greater than 1 cm
229
Why might you prescribe clinamycin for impetgio and what are the possible side effects?
if you think the impetgio is MRSA
SE: C. Diff (so be cautious in older pts)
230
What is the likelihood that someone who is allergic to PCN will be allergic to cephalopsorins?
since PCNs and cephs are cousins there is a 10% chance that someone allergic to PCN will be allergic to cephs
231
What do you do if a pt has recurrent infections of impetigo?
do a nasal swab (MRSA likes to hang out in the nares)
treat with bactroban intransal
232
What is a potential complication of impetigo?
poststrep glomerulonephritis
233
What pathogen is most commonly responsible for erysipelas?
GAS - group A strep
234
"I went to bed last night fine and woke up this morning with the huge rash on face"
typical presentation of erysipelas
| very acute painful onset
235
How can you tell the difference between erysipelas and cellulitis?
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
Where is erysipelas more commonly located on the body?
cheeks and ears
237
Why would you get imaging (Xray, MRI, CT) on a pt you suspect has cellulitis?
- to rule out osteomyelitis
| - if pt has periorobital cellulitis you want to see if they have proptosis and aggressively treat right away
238
You're in the ER with a pt who you suspect has cellulitis of the lower right calf. What will your discharge notes report?
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
What pathogen should you be thinking about with ciprofolxacin?
psuedomonas
240
What is the treatment for acute paronychia?
warm soaks
I and D
ABX
make sure their tetanus is up to date
241
What is the treatment for chronic paronychia?
encourage good nail hygiene
stop nail bitting
no ABX
242
Terms to describe the common wart?
Papillomatosis (microscopic term)
verruca vulgaris (HPV)
243
What is telangiectasia?
spider veins
| sometimes seen with BCC
244
How do you differentiate rosacea from acne?
rosacea doesn't have comedones and is more redness localized to the central part of the face (not usually on chest or back)
245
When should you be concerned about hyperandrogenism?
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
Which treatments are used to attack the follicular hyperkeratiniazation part of acne?
topical retinoids and isotretinoin
azelaic acid
salicylic acid
247
Which treatments are used to treat the increased sebum production part of acne?
```
oral isotretinoin
hormone therapies (OCP, spironolactone)
```
248
Which treatments are used to treat the P. Acnes proliferation part of acne?
Benzoyl Peroxide (BPO)
Topical antimicrobials
Oral ABX: doxy or minocycline (limited to 3 months)
Azelaic acid
249
Which treatments are used to treat the inflammation part of acne?
oral isotretinoin
oral ABX
Topical retinoids
azelaic acid
250
Hydroquinone plays what role in acne treatment?
post-inflammatory hyperpigmentation
| helps lighten dark spots
251
What treatments help with the rosacea bumps?
```
topical metronidazole
topical azelaic acid
sulfacetamide
topical acne meds
retinoids
ABX (targeting inflammation more than bacteria)
```
252
How can you tell rosacea from lupus?
both can be on the face
| lupus is more purple and has more demarcated borders
253
Alopecia universalis
a type of alopecia areata where there is loss of scalp and body hair including the eyelashes
254
What is the best treatment for onychomycosis?
Oral antifungals since topical antifungals take almost a year to work
255
Lichen Planus genital lesions are most commonly seen where?
glans penis
vulva/vagina
remember this may be associated with SCC --> long term follow up
256
Lichen Planus hair lesions if left untreated...
can result in scarring alopecia
257
Which lesions of lichen planus represent a more advanced lesion?
esophageal lesions
258
A pt comes in with oral lesions and body lesions, what should you be thinking?
lichen planus
| but also lupus!
259
What do you see on microscope with lichen planus?
hyperkeratosis
| both para and ortho
260
What is Nikolsky sign and when might it be positive?
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
Where is erythema multiforme commonly seen on the body?
the distal extremities moving proximally and the face
262
Risk factors of tinea corporis?
ringworm basically
warm-hot environments
animals
contaminated soil
263
Who is more likely to get mooluscum contagiosum?
children, sexually active adults, pts with HIV
264
What lesion is caused by pox virus?
molluscum contagiosum
265
How would you describe a molluscum contagiousm lesion?
discrete, solid, skin-colored papule 3-5mm on the chest
red halo regressing spontaneously
UMBILICATED papules
266
Condylomata acuminata
angogenital warts
267
How do you dx HPV?
acetic acid solution application with whitening of the lesions
268
Phthirus pubis
crab or pubic louse
269
Pediculus humans corprois
body lice
270
Which type of pediculosis run the risk of causing a systemic disease?
body lice
typhus and trench fever d/t louse feces (note even scabies runs this risk)
271
By the time a pt is scratching due to head lice, how long have they had the infestation?
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
Where are you likely to see nits are what do they look like?
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
Permethrin is used for what?
OTC treatment for head lice
274
How do you treat pediculus humansus capitus for a pregnant pt?
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
How does mayonnaise, olive oil, and vaseline work for head lice?
considered suffocating but what's really happening is that you are slowing them down enough to allow you to effectively comb them out
276
What must you keep in mind for anyone with crab lice?
that this is considered an STI and you should screen them for STIs
277
Ivermectin is used for what?
PO treatment for body lice and scabies
278
Why is dx body lice sometimes difficult?
body lice are only on the body when they are feeding
| so be sure to check clothing for fece marks
279
How long can scabies survive off the body?
4 days
280
How do you treat Norwegian scabies?
topical + oral drugs
| such as permethrin and ivermectin
281
Cimex lecturlrius
common bed bug
282
General characteristcs of drug induced rashes
symmetrically start on the trunk and move distally
283
Immediate reactions (drug-induced)
```
Occur less than 1 hr of the last administered dose
Type 1 hypersensitivity
Uritcaria
Angioedema
Anaphylaxis
```
284
Delayed reaction (drug-induced)
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
Which drug do we do allergy drug testing for?
PCN
286
What is the most important information in determining if a rash is medication-related?
TIMING
287
For exantheamtous drug eruptions, initiation of the medication is often ____days before the rash
7-10 days
288
What are risk factors for drug reactions?
```
Females
Prior history of drug reaction
Recurrent drug exposure
HLA type
Certain disease states (EBV, HIV)
```
289
Exanthematous Drug Eruption
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
Where are the greatest areas of steroid absorption on the body?
thin areas
eyelids, genitals, skin creases
use lower potency in these areas
291
Where are the least areas of steroid absorption on the body?
palms and soles
| require higher potency drugs
292
What are the characteristics and benefits of ointments?
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
What are the characteristics and benefits of creams?
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
What are the characteristics and benefits of gels?
```
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
What are the characteristics and benefits of lotions?
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
What are the 7 groups of topical steroid potency?
```
super potent (Group 1)
high (2 and 3)
medium (group 4)
lower - mid (group 5)
low (group 6)
least potent (group 7)
```
297
What conditions are treated with high potency steroids (group 1-2)?
```
alopecia areata
atopic dermatitis (only if resistant)
discoid lupus
lichen planus
nummular eczema (only if resistant)
hyperkeratotic eczema
psoriasis
```
298
What conditions are treated with medium potency steroids (group 3-5)?
anal inflammation
atopic dermatitis
nummular eczema
seborrheic dermatitis
299
What conditions are treated with low potency steroids (group 6-7)?
diaper dermatitis
| eyelid and facial dermatitis
300
What is the most common side effect of topical steroids?
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
Path of atopic dermatitis
genetic defect that disrupts skin barrier function making the skin more sensitive to irritants
302
What is the epidemiology of atopic dermatitis?
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
How does the rash distribution of atopic dermatitis differ between age?
children: face
older: flexor surfaces
304
What is a long term treatment to decrease skin infections d/t atopic dermatitis?
bleach baths
305
Exanthematous Drug Eruption
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
Fixed Drug Eruption
Solitary erythematous patch or plaque that will recur at the same site with re-exposure to the drug
307
What drugs are associated with fixed drug reaction?
```
Phenophthalein (laxatives)
Tetracyclines
Sulfa drugs
NSAIDs
Barbiturates
Food coloring (yellow)
```
308
Where are the common locations for fixed drug reaction rashes?
Mouth
Genitalia
Face
Acral areas
Remember this is one solitary lesion
309
What is the time of onset for fixed drug reactions?
30 minutes to 8 hours after ingesting the drug (for previously sensitized individuals)
310
What is the treatment of fixed drug reactions?
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
Drug-induced hypersensitivity syndrome
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
When are you going to stop all medications for a pt with a skin rash?
If you suspect DIHS and they’re basically on their way to the ICU
313
What is the treatment for DIHS?
Get Dermatology involved
Stop medications if severe
Start systemic steroids if severe (topical + antihistamines if moderate)
314
What medications can cause DIHS?
```
Allopurinol
ABX (sulfas, PCNs)
NSAIDs
AntiTB drugs
Anticonvulsants
AntiHIV drugs
```
315
What is the clinical course of DIHS?
typically starts 3 weeks post drug
```
macular exanthem
erythematous centrofacial swelling
fever, malaise
lymphadenopathy
>70% have eosinophilia
```
316
Epidermal Necrolysis Spectrum
A spectrum that includes SJS and TEN
317
What is the mortality rate of SJS/TEN?
SJS 5-12%
| TEN >20%
318
Which drugs have higher risk of SJS/TEN?
```
Sulfa ABX
Allopurinol
Tetracyclines
Anticonvulsants
NSAIDs
Nevirapine
Thiacetazone
```
(Mnemonic SATAN)
319
What is the time frame of SJS/TEN?
Clinically begins within 8 weeks after onset of drug exposure
320
What clinical findings do you see with SJS/TEN?
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
How do you determine the difference between SJS and TEN?
Based on the TBSA which is determined by counting ALL skin lesions, ruptured and unruptured blisters
322
For a pt you suspect has SJS/TENs which consults will you be contacting?
Derm
Ophthamology
Gynecology
323
SSSS
Staph Scalded Skin Syndrome
Infant disease most commonly
Staph bacteremia
324
Bright red confluent painful rash with large blisters. Sandpaper texture.
SSSS
325
What is the path behind SSSS?
Staph exfoliative exotoxin cleaves the desmoglein 1 complex
5% of all Staph Auerus strains produce this endotoxin
Spread person - person
326
What is the mortality rate of SSSS?
Infants 4%
| Older children/adults 60%
327
What is the prodrome for SSSS?
Fever
Sorethroat
Conjunctiviits
328
What is the time frame for SSSS?
Rash develops within 48 hours of prodrome
329
How do you differentiate SJS/TEN from SSSS?
Biopsy
SSSS - epidermal cleavage
SJS/TENS - subepidermal cleavage w/ epidermal necrosis
330
What is the treatment for SSSS?
Penicillinase-resistant PCN
- Nafcillin, oxacilin
- Vanco for MRSA
Wound care
Monitor fluid status
331
Pemphigus
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
What is the path behind pemphigus vulgaris?
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
What is the epi for pemphigus vulgaris?
Rare (0.1 per 100,000)
Higher risk in Ashkenazi jews, indian, mediterranean, middle east decent
Age 40-60 years
M = F
Genetics
334
Contributing factors of pemphigus?
Genetic -HLA class 2
Drugs - penicllamine, captopril, NSAIDs, cephs
Infections - Herpes, coxsackivirus
335
Clinical picture of pemphigus vulgaris
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
How do you dx pemphigus vulgaris?
Skin biopsy - intraepithelial seperation and acanthloysis
| “Tombstone” appearance d/t retention of keratinocytes
337
What is the treatment for Pemphigus vulgaris?
Corticosteroids
Immunosuppressive drugs -rituximab, sulfasalazine, methotrexate
IVIG
338
What is the difference between bullous pemphigoid?
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
What is necrotizing fasciitis?
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
What are risk factors for necrotizing fasciitis?
```
DM
immune compromised (CA, organ transplants)
Obesity
Surgery
Traumatic wounds
```
341
Necrotizing Fasciitis type 1
Polymicrobial
Anaerobes: one of (bacteroides, clostridium, peptostreptococcus)
PLUS
Facultative anaerobes (e. Coli, entrobacter, klebsiella, proteus)
342
Necrotizing Fasciitis type 2
```
Monomicrobial
GAS
Staph
MRSA
Vibro vulnificus
```
343
What is the presentation of necrotizing fasciitis?
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
What is the treatment for necrotizing fasciitis?
ABX
- carbapenems
- anaerobic coverage - clindmycin
- MRSA coverage (Vanco, linezolid)
NPO because they are going to the OR TODAY
345
Fournier Gangrene
Necrotizing fasciitis of the perineum or scrotum
346
What pathogens are responsible for fournier gangrene?
E. Coli (aerobe)
| Bacteroides (anaerobe)
347
What is the Epi of fournier gangrene?
80% have DM
Trauma to genitalia frequently associated
M > F
Age: 30-60 years
348
What is the path of fournier gangrene?
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
What is the treatment of fournier gangrene?
Fluid support
ABX (cover gram -, +, anaerobes, MRSA)
REMOVE DEAD TISSUE ASAP
+/- IVIG
350
What are complications of Fournier Gangrene?
```
Pain with erection (50%)
Genitial scarring
Impotence
Psych consideration
Extensive reconstruction needs
NSQIP mortality rate: 10%
```
351
Purpura fulminans
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
Protein C deficiency is associated with which type of skin disorder?
Pupura fulminans
353
Which infection is most commonly associated with purpura fulminans?
Neisseria meningococcal meningitis
354
What is the presentation of purpura fulminans?
7-10 day onset after infection
Starts DISTALLY symmetric
Systemically ill - fever, hypotension
355
What is the treatment for purpura fulminans?
```
Fluid management
ABX broad spectrum
DIC management
Heparin vs protein C concentrate
Remove dead tissue —typically amputation
```
356
For a pt with atopy, which part of the triad typically started first?
Atopic dermatitis when they were an infant
357
What is the most common treatment for atopic dermatitis?
Emollients (thicker form of lotion OTC)
358
What is the epi of atopic dermatitis?
Common. 11-19% prevalence
All cases start within the first decade of life
Only 5% of cases develop after 5 years of age
359
What is the lesion distribution by age for atopic dermatitis?
Infants: face
Older: flexor surfaces
360
What other skin condition might present with a pt who has atopic dermatitis and why?
Impetigo due to these pts having more staph on their skin
361
What are the characteristics of the rash for chronic atopic dermatitis?
Lichenification (leather like fibrosis d/t chronic scratching)
Hyperpigmentation (if active)
Depigmentation (overtime)
362
On your differential for atopic dermatitis is contact dermatitis. How can you tell these two apart?
Contact dermatitis (whether allergic or irritant) is always related to the location in which the pt was exposed
363
How can you tell scabies apart for atopic dermatitis?
Atopic dermatitis in infants is always on the face while scabies typically is seen on the trunk (belt line) and genitalia
364
How can you tell atopic dermatitis from seborrheic dermatitis?
Seborrheic dermatitis is commonly found in the nasolabial folds but has more flaking as opposed to the pustule appearance of atopic dermatitis
365
What is first line treatment for atopic dermatitis?
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
Rank in order from most potent to least potent vehicles of steroids
Ointment > cream > lotion
367
What are the major side effects of long term use of high dose steroids?
Skin atrophy!!
Telangiectasia
Striae
368
What is an appropriate long term treatment/prevention for atopic dermatitis?
Bleach baths
369
What determines potency of a topical steroid?
Vasoconstricitve effect
Grade 1 = most potent
Grade 7 = least potent
370
Super high potency topical steroids (group 1) are best for use where?
Palms and sole, hyperkeratotic lesions
Short term use - no longer than 3 weeks
371
How do you determine how much steroid to prescribe a pt?
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
Which steroids can be used for intralesional injections and for which conditions is this done?
Triamicinolone acetonide
Methylprednisone acetate
Hyperkeratotic lesions
Cystic acne
Keloids
373
Immediate reactions to drugs
Occur less than 1 hour after last administered dose
Type 1 hypersensitivity reaction
Urticaria
Angioedema
Anaphylaxis
374
Delayed reactions to drugs
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
What is angioedema?
Leaky blood vessels in the lower dermal layer caused by histamine release
376
Erythematous patch with central bulla
Fixed drug eruption
377
What is the path of psoriasis?
Autoimmune
Multifactorial (genes + environment)
HLA-Cw*0602
Bad MHC-1 receptor that the body sees as foreign and attacks
This results in hyperkeratosis
378
What do you see microscopically with psoriasis?
Acanthosis - “Test tubes in a row”
Hyperkaratosis with parakaratosis
379
Who gets psoriasis?
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
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.
Psoriasis
90% are plaque
Silvery scale unique to psoriasis
381
What is the most common ocular finding in psoriasis?
Blepharitis
Plaques forming at the glands that lead to the eye
Eyelid erythema, edema, and psoriatic plaques
382
What nail findings might you see with a psoriatic pt?
Onychodystrophy
Pitting
Fingernails > toenails
Does not respond well to tx
383
What is the time frame of psoriatic arthritis?
~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
How do you dx psoriasis?
Clinical dx
Unless its not the typical plaque psoriasis
Ddx
- syphilis
- pityriasis rosea
- pityriasis alba
- tine
- atopic dermatitis
385
What defines the difference between mild and severe psoriasis?
Mild: <5% of BSA
Severe: >5% of BSA
386
What are recommendations to help manage psoriasis for all forms and severity?
```
Daily sun exposure
Topical moisturizers
Sea bathing (order salt for salt baths at home)
Relaxation
Salicylic acid lotions
OTC “tar” preparations
```
387
What is the treatment for mild psoriasis?
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
What is the treatment for severe psoriasis?
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
Cyclosporine is used for what?
Rapid relief, bridge therapy or “Crisis” therapy for severe psoriasis
SE: GI intolerance, renal impairment
390
What other options do you have if a pt with severe psoriasis isn’t responding to topical + systemic meds?
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
Fitzpatrick Skin type 6
Black
| Never burns, tans very easily
392
Fitzpatrick skin type 1
White; very fair; red or blonde hair; blue eyes; freckles
Always burns, never tans
393
What is the path of vitiligo?
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
Who gets vitiligo?
```
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
What are precipitating factors of vitiligo?
Usually nothing but sometimes:
Illness
Emotional stress
Sunburn
396
How do you dx vitiligo?
Clinically
| Might need woods lamp in fair skinned individuals —the lesions will illuminate
397
What is the typical distribution of vitiligo?
```
Neck, clavicle
Arm pits
Genitalia
Fingertips
Knees
Feet
```
Might also see it at sites of “trauma” - Koebner’s Phenomenon
398
What is the treatment for vitiligo?
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
Oculocutaneous albinism
Skin, hair, and eyes without melanin production
400
What is the inheritance pattern of albinism?
Autosomal recessive
401
What is the path of albinism?
Autosomal recessive
Mutation of tyrosinase - enzyme used in melanin production
Results in no melanin production
402
What is the treatment of albinism?
Prevention of sun damage
SPF 50
UVR blocking clothes
Regular follow up with dermatology and ophthamology
403
Solar lentigines
“Liver spots”
Localized proliferation of melanoctyes and melanization
Hperpigmented, well-circumscribed lesions
Sun exposed areas
Skin Types 1-3 most at risk
404
What do you have to keep in mind when dx solar lentigines?
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
What is the treatment/prevention of solar lentigines?
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
Melasma
Progressive, macular, nonscaling hypermelanosis of sun-exposed areas (face)
Associated with:
- pregnancy
- oral contraceptive use
- phenytoin
Skin types 4-6
407
What is the treatment of melasma?
Hydroquinone 3% or 4%
Glycolic or Azelaic acid peel
Retinoids
Prevention:
- sunscreen
- discontinue oral contraceptive
408
Freckles
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
Cafe-au-Lait macules
```
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
Acanthosis Nigricans
Seen in DM or obese pts
Dark, hyperkeratosis streaks in skin folds:
- neck
- axilla
- groin
- body folds
411
What is the treatment of acanthosis nigricans?
Treat the underlying condition
| DM or weight loss
412
Post-inflammatory hyperpigmentation
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
Nevi
```
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
What is a mole?
A collection of nevus cells
415
Keloids
```
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
Where are the common sites of keloids?
Head, neck, chest, and arms
Can be painful, itchy, stingy
417
What is the treatment for keloid?
Topical steroids - gels, locations, creams, ointments
Intralesional injections - kenalog, 5FU
Surgical excision
Recurrence is common
418
What is the rule of thumb for hairs growing out of nevi?
If hairs grow out of nevi they are probably benign
419
Epidermal cyst
“Balloon containing degraded skin contents”
Nodule with central pore (punctum)
Can originate from invagination of epidermis into the dermis or spontaneously
420
What is the treatment for epidermal cyst?
Intralesions kenalog injection
Incision and drainage
Surgical excision
421
Lipoma
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
What is the most common connective tissue tumor?
Lipoma
423
Dermatofibroma
```
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
Acronchordons
Skin tags
Soft tumors of normal skin
Location: neck, axillae, groin
Removal - cosmetic, irritation, and infection
425
What is the treatment for skin tags?
(Aka acrochordons)
Electrodessication (destruction) or surgical excision
426
Hemangioma
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
Neurofibroma
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
What is the most common type of neural sheath tumor?
Neruofibroma
429
Actinic keratosis
```
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
What is the clinical sxs of actinic keratosis and how do you treat it?
Precancerous!
Tender, burny or itchy, or even no sxs
Tx:
- cryosurgery
- curettage
- electrosurgery
- topical chemotherapy
431
What are the common locations for actinic keratosis?
Sun exposed areas - face, ears, hands, neck, scalp
432
What are the malignant and precancerous lesions?
Actinic Keratosis
BCC
SCC
Malignant melanoma
433
What is the most common type of skin cancer?
BCC
434
Where are the common locations to find BCC?
Face and neck
435
What are the clinical manifestations of BCC?
Translucent papule or lesions that will not heal
Become a large sore or ulcer that will not heal if untreated
Very rare metastasis
436
What is the second most common type of skin cancer?
SCC
437
What age group is more likely to get SCC?
Pts over 50
Can have a genetic tendency to develop lesions
438
Malignant Melanoma
Most DEADLY form of skin cancer
Can metastasize to other organs
ABCDE rule of melanoma
439
What are the 4 types of malignant melanoma?
Acral lentiginous
Nodular
Superficial spreading
Lentigo maligna
70% are superficial spreading type
440
What is the treatment for malignant melanoma?
Same for all skin cancers
- surgical excision
- Mohs surgery
- Electrodessication and curettage - not recommended
- Cryosurgery - not recommended
- Chemotheraperutic drugs - topical and oral
441
"Test tubes in a row"
microscopic evaluation of PSORIASIS - epidermal acanthosis
442
MC locations for psoriasis plaques?
extensor surfaces
443
"beefy red"
intertrigo - candidiasis
444
What is the treatment for intertrigo?
topical antifungals (clotrimazole, miconazole, nyastatin)
steroids
keep area dry
445
Who gets intertrigo?
F > M
DM
Obese
located in the skin folds
446
Tense bullae
bullous pemphigoid
treat with steroids
