Dermatology

Skin functions

- Regulates body temperature

- Prevents loss of essential body fluids, and penetration of toxic substances
- Protection of the body from harmful effects of the sun and radiation
- Excretes toxic substances with sweat
- Mechanical support
- Immunological function mediated by Langerhans cells
- Sensory organ for touch, heat, cold, socio-sexual and emotional sensations
- Vitamin D synthesis from its precursors under the effect of sunlight

Skin layers Lucidum appears only

in sole of foot & palms
➢ Epidermis: "Come Let Get Sun Burn" (from superficial to deeper)
- Stratum Corneum > Lucidum (thick skin) > Granulosum > Spinosum > Basale
➢ Dermis: (2 layers → papillary & reticular)
- CT, nerve endings, hair follicles, glands (sweat, sebaceous & apocrine), vessel (blood,
lymphatic)
➢ Hypodermis (subcutaneous tissue “SQ” or superficial fascia):
- Contains SQ fat mostly (but also has nerves, vessels that cross to & from the dermis)

Skin lesions: Bleeding under skin can be:

Petechiae → 1-2mm
➢ Primary skin lesions: Purpura → > 3mm
- Papule: Solid elevation of skin, <1 cm wide, well-circumscribed Ecchymosis → > 1-2cm
- Plaque (change of texture): Using diascopy test to differentiate
o Solid elevation of skin, >1 cm wide, usually well-circumscribed them from patch/macule → pressing
o When compared to a nodule, it is wider vs. higher nodule on them using glass slide; they are
- Macule: Flat skin discoloration <1 cm wide non-blanchable while patches are
- Patch: Flat skin discoloration > 1 cm wide blanchable (hidden with pressure)
- Nodule (collection of cells):
o Solid elevation of skin, with its height much more obvious than its width
o When histologically you find an epithelial lining around a cavity > cyst
- Blister: Fluid filled (not-pus) skin elevation // If < 1cm = vesicle, If > 1cm = bullae
- Pustule: Pus-containing skin elevation
- Wheal/hives: Rounded & flat topped transiently (24-48hrs) appearing papules &
plaques (resolve within 24 hours)
- Telengictasia: spider veins; enlargement of superficial blood vessels to the point of
being visible
Silvery-white
➢ Secondary lesions: they occur due to something/cause
→ psoriasis
- Erosion: Discontinuity of skin that only involves the epidermis/epithelium
- Ulcer: Discontinuity of skin that is deep enough to involve the dermis or below (it
heals with a scar, but if scar hypertrophied it is keloid)
- Crust: ruptured blister & secondary inf. > e.g. brownish in impetigo "dry exudates"
- Scale: laminated masses of keratin of the stratum corneum
Yellowish- - Lichenification: epidermal thickening visible as thickened skin
greasy → - Atrophy: loss of tissue, which can present with depressed or loose skin/wrinkling
seborrheic - Excoriations: linear abrasions 2ry to scratching // butterfly sign in the back
dermatitis
Erythroderma: intense and usually widespread reddening of the skin due to inflammatory
skin disease (>90%) – emergency – needs 2 skin biopsies
 When describing a skin lesion, use SAD mnemonic

S → size, shape & surface

A → arrangement (localized, generalized, linear, dermatomal, annular, serpiginous … etc.)
D → distribution = location (extensor, flexor, photo-distributive)

Rosacea:

➢ Chronic facial redness (forehead, nose, & cheeks), Caucasian women 30-50 yrs (most)
➢ Findings:
- Erythema, telangiectasia, papules, types (ocular, rhinophylum) (X comedones)
- Decrease by avoiding alcohol, hot drinks, extreme temp, & emotional stress
➢ Treatment:
- Topical metronidazole + tetracycline PO (maintenance), isotretinoin, laser
- Corticosteroids (PO or topical) are CI as they can cause flare up of the condition

Pityriasis rosea:

➢ Mostly < 10 yrs, associated with HHV-6, HHV-7

➢ Findings:
- Initially: single papulosquamous eruption "herald patch" that resemble ring worm
o Asymmetrical multiple erythematous annular lesion with scales "description"
- Then: generalized rash with multiple oval-shaped lesion "Christmas tree pattern"
- Pruritis, not contagious, mostly in trunk, upper limb, thigh (spares face, palm & sole)
➢ Treatment: spontaneous(6-8wks), antihistamine (for pruritis), steroids (if
symptomatic)

Acne vulgaris:

➢ Inflammation due to sebaceous follicles blockage by sebum > Propionibacterium acne

proliferation (aerobic bacteria), 2 peaks @ of age 12-24 & 30s-40s (neonatal @ 2-3wks)
➢ Risk factors: male gender, puberty(adolescent), Cushing syndrome, medication
➢ Classification:
- Non inflammatory: closed comedones (whitehead) or open comedones (blackhead)
- Inflammatory acne: pustule/papules (1ry lesion) > nodules to cyst to scar
➢ Pathogenesis:
- Ductal hyperkeratosis, colonization by P. acne
- Increase sebum excretion, inflammatory mediators release
➢ Variants: hidradenitis suppurativa, acne conglobata, pilonidal sinus, acne fulminans
➢ Treatment: " can takes 6 weeks to work & skin may worse before coming better"
- General: keep area clean, avoid promoting agents (specific make up & creams)
- Non inflammatory: mild (topical retinoid acitretin), severe (systemic isotretinoin)
o Hyperlipidemia & teratogenicity in oral retinoid (isotretinoin):
▪ All females should have 2 negative pregnancy tests before starting it
▪ Pt should use 2 birth control methods 1 month before & after treatment
▪ In severe acne in pregnancy use azelaic acid (isotretinoin is CI)
- Inflammatory:
o Mild (topical Abx erythromycin /clindamycin) severe (oral ABx: e.g. doxycycline)

Isotretinoin (Roaccutane) can be used for both inflammatory & non-inflammatory – needs LFT & lipid
profile before using as it raises liver enzymes & TG – most common side effect of it is dry skin &
most serious side effect is teratogenicity
 Irritant contact dermatitis Allergic contact dermatitis

Eczematic lesion → oozing + crust formation, No need for previous Requires previous exposure
exposure – not an – immune reaction – has
patient starts with itching then skin lesion appears immunologic reaction – does distant spread – not dose-
not spread – dose-related related – does not produce
Contact dermatitis: response – produce similar similar reaction if others
reaction if others exposed to exposed to same irritant
➢ Types: same irritant
- Irritant contact dermatitis: "80%" → burn symptoms
o Non immunological (no sensitization), appears soon after exposure, to any person
o Chemical or physical irritants (detergents, acids, frequent hand wash)
- Allergic contact dermatitis: "20%" → itching symptoms
o Type IV HSR, need sensitization (appear in the 2nd exposure), specific persons
o Examples of allergens: poison ivy, nickel (belt, phone, wristwatch), topical drugs
➢ Findings:
- In exposed areas, very pruritic, acute (erythematous papules & vesicles with oozing)
- Or chronic (thickening, crusting, scaling, lichenification)
➢ Diagnosis: clinically, patch test (to identify the allergen) in cases of:
- Doubt diagnosis, no response to treatment, rash reoccur
➢ Treatment: avoid allergen, emollients, topical or PO hydrocortisone

Atopic dermatitis (eczema):

Other features:
➢ Over-activity of mast cells (IgE), family history, mostly < 30 yrs, epidermal changes It is
Allergic shiners: ➢ Association: asthma & allergic rhinitis (food allergy doesn't exacerbate It) hypopigmented
periorbital ➢ Findings: pruritis & scratching, mostly in face, neck, & skin folds (flexors) while vitiligo is
hyperpigmentation ➢ Features: xerosis, Dennie-Morgan fold (periorbital), pityriasis alba (whitish spot, face) depigmented
➢ Complications: lichenification, 2ry inf. (staph), cataract & conjunctivitis, sweaty sock
Keratosis pilaris
➢ Treatment: Other
Atopic salute: - Skin care: keep skin moisturized (humidifier), avoid soap & wash cloth, wear cotton complications:

crease on nose - Medical:

Lichen simplex
o Corticosteroid: topical (betamethasone) if mild & oral (hydrocortisone) if severe chronicus
Hertoghe’s sign: o Topical anti-T cell:
loss of lateral 1/3 ▪ Long term control & help wean patient off steroids (tacrolimus/ pimecrolimus) 2ndry inf.
of eyebrows o Antihistamine: if mild (non-sedating- cetirizine or loratadine), if severe (doxepin) staph → impetigo
HSV → eczema
o Antibiotics: only in case of impetigo occur (e.g. cephalexin)
herpeticum
Discoid dermatitis (eczema) → common type, crust & oozing formation discoid in shape
Seborrheic dermatitis: Pigmentary
changes
➢ Hypersensitivity reaction to dermal inf. (e.g. Malassezia), affect infants (most), & adults
- Adult or sever form is triggered by: neurological disorder (e.g. Parkinson) or HIV inf.
➢ Exacerbation factors: anxiety, stress, hormonal factors
➢ Sites: scalp, hairline, behinds ears or in external ear canal, nasal folds, armpit, eyebrow
➢ Findings:
- Dandruff+/- hair loss, yellowish greasy scales on erythematous background, pruritis
➢ Treatment:
- Sun exposure & dandruff shampoo, topical ketoconazole, topical hydrocortisone

Erythema nodosum: "EN"

➢ F>M, young > elderly, self-limited (within weeks)

➢ Causes:
- Idiopathic, inf. (strept. pharyngitis (most), yersinia, fungal, syphilis, TB), conditions
(sarcoidosis, IBD, Bechet disease, pregnancy), drugs: OCP, sulfa, amiodarone, Abx
➢ Findings:
- Painful, red, subcutaneous, elevated nodules on ant. aspect of the tibia (bilateral)
- Less common in trunk & arms // +/- fever, malaise, & joint pain / no ulcer or drainage
➢ Diagnosis:
- X-rays (TB & sarcoidosis), anti-streptolysin O titer (Strept.), VDRL (syphilis), ESR, CBC, colonoscopy
➢ Treatment: treat underlying causes, if unknown: bed rest, leg raise, NSAIDs, K iodide
 Lichen planus: skin lesion has clean area around it

➢ Chronic inflammatory disease of unknown etiology (Th1?), affects adults mostly

➢ 5Ps: pruritis, polygonal, purple, flat-toped papules, plantar flat topped
White net-like
distribution on the
➢ Sites: wrist, shin, oral mucosa (whitish reticulate painless lesion), genitalia, nails Dorsal nail
inner cheek, known - If it was painful oral lesion +/- ulcers can indicate hepatitis C & at risk of SCC pterygium is
as Wickham striae ➢ Findings: Wickham`s striae, Koebner phenomena (psoriasis, vitiligo), Nails pterygium pathognomonic
(painful, itchy)
➢ Treatment: topical/intralesional CS, topical calcineurin inhibitor, phototherapy, oral
▪
CS t
e Epidermal: pemphigus vulgaris
n
e Blistering disease
Bullous pemphigoid:
t
(>50 yrs)
Epidermal-dermal junction: bullous pemphigoid
-
➢ Autoimmune,
l
i
mild form of PV, no malignant potential, elderly most, hemidesmosomes
➢ Findings:
k
e
- Multiple
d subepithelial blisters on ABD, groin, & extremities (not in mouth)
- Intact
i blisters (not easily rapture) & less inf., no nikolsky sign, Asboe-Hansen sign
s
➢ Diagnosis:
t biopsy with immunofluorescent
➢ Treatment:
r
i
prednisone (best initial), cyclophosphamide, ca or active vitamin D
b
u
Pemphigust
Vulgaris: (middle-age)
i
o
➢ Causes:
n
- Mostly
o autoimmune disease (IgG autoAb against desmosomes adhesion molecule)
n
- Ort drug-induced: ACE inhibitors, penicillamine, Phenobarbital, penicillin
➢ Malignant
h
e
potential:
- Non-Hodgkin
i lymphoma, chronic lymphocytic leukemia, Castleman disease
➢ Findings:
n
n
- Blisters
e that are easily rapture (becomes painful erosion), presence of Nikolsky sign
r
- Mostly
c starts in the mouth then generalized, more loss of fluid & risk of inf.
➢ Diagnosis:
h biopsy with immunofluorescent (auto-antibodies)
e
➢ Treatment:
e
- Prednisone,
k
,
azathioprine (wean off pt. from steroids), rituximab (anti-CD20), Ca
k
n SJS is considered the most
Drug reaction:
o severe form of EM
w
n
➢ Morbilliform
a rash > EM > SJS > TEN (from mild to severe) TEN is considered to be the
1. Erythema multiforme: "EM"
s
most severe form of SJS
W
Most common ➢ Causes:
i

cause is - Infection:
c
k
HSV inf. (HSV 1 > HSV 2) (recurrence) or mycoplasma pneumonia
following - (was
h related to) drugs (sulfa drugs (most), penicillin, phenytoin, allopurinol)
herpes simplex ➢ Findings:
a
m
virus infection - Erythematous
s macules/papules that resemble target lesion "Bull`s/iris eye lesion"
t
➢ Types:
r major or minor (depending on sub mucosal layers involvement)
Minor → <2 mucosal
EM mostly ➢ Treatment:
i
a membranes
acrofacial - If eHSV inf.: acyclovir (prevent recurrence & deterioration & as prophylaxis)
while SJS - Symptomatic:
(
i
prednisone, antihistamines (chlorpheniramine or loratadine) Major → >2 mucosal
involved t membranes
i
trunk, face & 2. Steven-Johnson
s
syndrome (SJS) & toxic epidermal necrolysis (TEN):
neck ➢ Causes:
p drug reaction: NSAIDS, Augmentin, allopurinol, penicillin, sulfa drugs
a
➢ Findings:
i " after 7-21 days of exposure"
- Skin involvement (+ 2 mucus membrane) (+/- skin peeling) if > 30% TEN, if <10% SJS
n
f
- Systemic:
u fever, dysphagia, renal failure, sepsis, respiratory epithelium sloughs out
- Signs:
l Asboe-Hansen (increase bullae size with pressure) & Nikolsky sign
,
➢ Complication:
i alopecia, scarring, high mortality rate
➢ Treatment:
t
c
ICU admit, aggressive rehydration, give IVIG, steroids, stop offending drug
h
y
)
 Skin cancer & pre-cancer lesions:

1. Actinic keratosis "solar keratosis” “AK":

➢ Premalignant lesion to SCC (low risk) due to cumulative prolonged sun exposure
➢ Mostly affect fair-skinned people, small rough scaly lesion on the face & hands (most)
➢ Biopsy is indicated if: lesion is hyperkeratotic, spontaneously bleed, or tender
➢ Treatment: sunscreen, scraping, cryotherapy, 5-FU cream, ablative laser technique

2. Basal cell carcinoma:

➢ Most common skin cancer (60-75%), from basal layer of epidermis, sun exposure is RF
Nodular basal ➢ Fair-skinned people, 3Ps (pearls, pink, papule), rare metastasis & recurrence
cell carcinoma ➢ Findings:
is the most - Raised smooth papules with rolled edges, +/- telangiectasia on the lesion surface
common type - In sun-exposed area (e.g. head (mostly nose) &neck, +/- central crusts
➢ Treatment: surgical excision via Mohs micrographic surgery (less loss of normal tissue)

3. Melanoma:
➢ Most aggressive (mostly to metastasize), high mortality rate (1st cause of death in skin
cancer), de novo or mole
➢ RF: sun exposure, Caucasian/red hair people, family history, multi moles, age
➢ Growth:
- Linear (initial) phase: lateral growth in the epidermis, good prognosis, no metastasis
- Vertical (late) phase: extends to reticular dermis or beyond, metastasis can occur
➢ Findings: " mostly found in the back"
- ABCDE: asymmetry, border irregular, color variation, diameter > 6 mm, elevation
(raised surface)/evolution (change in the color) // +/- bleeding & itching
- Benign form is rounded, even border, color evenly spread, & constant diameter
➢ Metastasis: lymph nodes & skin (59%), lung, (36%), brain (20%- cause of death)
➢ Diagnosis: full thickness biopsy (X shave biopsy), LN dissection, c-KIT /BRAF genes
➢ Treatment: surgical removal + interferon therapy + nivolumab (if brain metastasis)

4. Squamous cell carcinoma:

➢ 20% of skin cancer, from epidermal cells that are keratinizing, > risk of metastasis
➢ RF: sun exposure, AK, HPV inf., chronic skin damage (Marjolijn ulcer), IC, chemicals
➢ Findings: crusting ulcerated nodules or erosion // treatment: surgical removal
➢ Prognosis: excellent except if there is lymph node involvement

5. Kaposi sarcoma
➢ Caused by HHV-8, mostly in AIDS (sexual contact) or Mediterranean elderly
➢ Reddish/purplish lesion (vascular) that also can be found in GI tract & in the lungs
➢ Treatment:
- Treat AIDS via anti-retroviral, vincristine/interferon intra-lesion inj., chemotherapy

Seborrheic keratosis is the most common benign tumor

Miscellaneous condition:

1. Decubitus ulcers "pressure sores":

➢ Prolong pressure over the skin > ischemia > ulceration > necrosis, gangrene, inf.
➢ RF: immobilization (e.g. paraplegia), peripheral vascular disease, dementia, nursing
➢ Findings:
- Mostly found over bony prominence (sacrum, greater & ischial tuberosities -most)
- Can be necrotic or 2ry infected (cellulitis, sepsis, osteomyelitis)
➢ Staging:
- Stage I: intact skin, non-blanching erythema // stage II: partial skin thickness
- Stage III: reaches subcutaneous tissue // stage IV: reaches muscles, bones, joints
➢ Treatment:
- Prevention: turning pt. & changing his position every 2 hrs, special mattress & beds
- Local wound care, wet-to-dry dressing or local gel, surgical debridement, ABx if inf.

2. Seborrheic keratosis:
➢ Very common, mostly > 3o yrs & in elderly, hereditary (Autosomal Dominant)
➢ Not associated with sun exposure, most common benign skin tumor
➢ Findings:
- Slightly elevated plaques, hyper-pigmented, appear as "stuck on" the skin
- Found anywhere but mostly face & trunk, increase in number with time
➢ Treatment: not necessary but for cosmetic reasons: cryotherapy, surgery, or laser

3. Vitiligo:
➢ Acquired autoimmune → destruction of melanocytes by Th1
- Melanocytes are from neural crest & present in eyes, hair, skin, meninges & inner
ear (any of these sites can be affected in patient with vitiligo)
➢ Types: generalized, focal, segmental
➢ Findings: sharply demarcated patches of depigmented skin, mostly in the face
- Koebner phenomenon: appearance of skin lesion over lines of trauma
➢ Investigations: wood’s lamp, CBC, TFT, ANA, fasting blood glucose, ACTH
➢ Association: DM, hypothyroidism, pernicious anemia, Addison`s disease, SLE, RA
➢ Treatment: topical/systemic CS, topical calcineurin inhibitor, topical vitamin D analogs
& photo-chemotherapy (follicular re-pigmentation indicates pt. responsive to therapy)
➢ DDx: pityriasis alba in atopic dermatitis & tenia versicolor

4. Pityriasis Rubra Pilaris

➢ Very similar to psoriasis, but distinguishing features include:
- SMALLER SIZED plaques, but MORE WIDESPREAD, more ORANGE-LIKE COLOR
- Associated with ISLANDS OF SPARING
- It is PHOTOSENSITIVE (unlike psoriasis) > unresponsive/worsens with phototherapy
o Porphyria, lupus, dermatomyositis also is associated with photosensitive skin
➢ It is associated with increased COP secondary to widespread capillary vasodilation
➢ Management:
- Like psoriasis, BUT no phototherapy – avoid sun exposure
 5. Psoriasis: chronic non-contagious
Drugs mnemonic: ➢ Pathogenesis: immune (high Th1 cells), genetic predisposition + environmental trigger
- Triggers:
N → NSAIDs
o Stress, trauma, weather changes (better in summer & worsen in winter), smoking Normally cells
A → antimalarial
I → interferon
o Drugs (lithium, interferon, steroids, beta blocker), infection (group a sterpt., HIV) replicate every 28-
L → lithium ➢ Co-morbidities: depression, metabolic syndromes, IBD, heart attack 45 days, but in these
S → steroid ➢ Findings: patients, it happens
withdrawal - Well-demarcated erythematous papules/plaque, covered by silvery thick scales every 3 days, so
scales appear
systemic steroids - Auspitz’s sign (pinpoint bleeding after scaling), no pruritis, mostly in extensor
CI in psoriasis but
topical are fine
surface
- Koebner phenomenon / candle sign (it is confirmatory)
Appearing of - Woronoff’s ring (hypopigmentation around psoriatic plaque) → pathognomonic
skin lesions over ➢ Types: (either according to location or configuration)
lines of trauma - Pustular psoriasis (emergency)
DDx: vitiligo &
o Localized (palmoplantar pustulosis, acrodermatitis continua), or Generalized
Lichen planus o Pustules are sterile (other cause of sterile pustules? Drug-induced pustules)
- Psoriasis vulgaris (“common psoriasis”/non-pustular)
o Chronic plaque psoriasis (MC subtype ~ >90% in both adults & pediatrics)
▪ Scalp (most), extensors (elbow, knees), foot, hands, lower back, trunk, & nails
o Guttate psoriasis
▪ 2ry to inf. (group A strept. "pharyngitis") or other triggers (trauma/scratching)
▪ Pediatrics most // found mainly over the trunk, papules & scales "rain drops"
- Erythrodermic psoriasis (emergency) Appear moist &
▪ End point of any severe psoriasis, Medical emergency erythematous. Can
▪ Occurs when >90% of skin is involved with psoriatic lesions (erythematous) be mistaken with
fungal infection
o Inverse psoriasis: Involves the flexures (inframamillary, axilla, inguinal area)
(biopsy to confirm)
o Scalp psoriasis: confused with seborrheic dermatitis, psoriatic lesion in hairlines
o Nail psoriasis
▪ Bilateral limbs nail damage, Nail pitting (MC feature), splinter hemorrhage
▪ Onycholysis – separation of nail from nail-bed / (“oil spots” is pathognomonic)
If single nail: suspect onychomycosis (fungal infection of nail)
▪ Subungual hyperkeratosis: keratin buildup in the space created by onycholysis
▪ Beau’s lines: nail growth temporary cessation > deep grooved transverse lines
▪ Psoriatic arthritis (if pt. has nail psoriasis, he has more risk of it):
Part of the seronegative spondyloarthropathy, SAUSAGE DIGITS
Associated with involvement of the DIP and PIP (vs. RA)
➢ Treatment:
Before treating with
- Mild:
biologic treatment o Corticosteroid: 1st line drugs (e.g. betamethasone, triamcinolone)
(infliximab) check o Vit D derivatives: 1st line, mostly used in combination with CS, (e.g. calcipotriene)
PPD, HIV and o Calcineurin inhibitor: 2nd line, for inverse psoriasis or if face involved, (tacrolimus)
hepatitis o Coal tar: 2nd/3rd line, unpleasant odor, if used in combination > 80-90% remission
- Moderate: ultraviolet light, photo-chemotherapy, acitretin (S/E dyslipidemia)
- Severe: infliximab, methotrexate (hepatotoxic), cyclosporine (pregnancy, HTN risk)
Although cyclosporine is category C but it is preferable in pregnancy over other conventional drugs (acitretin, methotrexate ➔ both category X)

6. Pyoderma gangrenosum:
➢ Painful rapidly growing ulcers, gray-violate in color, peripheral rim of erythema
➢ Necrotic borders, mostly found in lower limbs, +/- purulent base
➢ Association: acute myelogenous leukemia & Inflammatory Bowel Disease
➢ Treatment: treat underlying disease, CS (systemic, intralesional or potent topical)
 7. Sarcoidosis:
➢ Granuloma formation in lungs (mostly), skin, liver, & spleen, idiopathic
➢ Skin findings: "maybe the 1st or only manifestation of the disease"
- Red-brown papule/plaque >yellowish with compression "diascopy"(the face mostly)
➢ Treatment: topical or IL: CS //oral: minocycline, methotrexate, tacrolimus

Allergic reaction: Wheals stay <24 hrs, if more

it is urticarial vasculitis

1. Urticaria (hives): wheals indicate urticaria until proven something else

Can be induced
➢ Skin reaction causes mast cells to release mediators, acute (<6 wks) or chronic (>6 wks)
by different
➢ Trigger factors: allergy (food, drugs (penicillin, ACEI), latex, pollen), pressure, cold/heat
stimuli:
➢ Findings: transient blanching erythematous wheals, very itching
➢ Treatment: "avoid triggers" // non-sedating H1 antihistamine (cetirizine)> sedating H1 Dermatographia;
anti histamine (doxepin) > ranitidine > immune-modulator (omalizumab) skin writing
Pressure urticaria
2. Angioedema: can continue for >24 hrs Cholinergic
➢ Can occur with urticaria & similar in mechanism to urticaria bur differs in: urticaria
Wheals &
- Occur in deeper tissue (sub-dermal), mostly due ACE inhibitors (appear after 1 wk) Cold urticaria
dyspnea
especially if there
➢ Hereditary angioedema: AD, due to C1 esterase inhibitor deficiency, recurrent Aquagenic
episodes urticaria
are angioedema
➢ Findings: (associated with
in face
polycythemia)
- Non-pitting puffy skin firm edema, if wheeze, SOB, low BP, or high HR > anaphylaxis
- Found mainly in the face (eyelids), lips & tongue, & hands (urticaria occur anywhere)
➢ Diagnosis: decrease in C2 & C4 complement & deficiency of C1 esterase inhibitor
➢ Complications: airways (life-threatening obstruction), GI (ABD pain, nausea & vomiting)
➢ Treatment:
- Acute: fresh frozen plasma > Ecallantide > Icatibant Hyperpigmentation
- Airways involvement: ensure airways protection 1 > SC epinephrine
st in face, MCC is UV
light
- Hereditary: C1 esterase inhibitor concentrate or recombinant C1 inhibitor conc.
- Long term: androgens (danazol, stanozolol) Others: pregnancy,
thyroid dysfunction
Alopecia: autoimmune, Th1 attacking hair follicles
Hair cycle: anagen (growth phase: 85%) – catagen (transition phase) – telogen (resting phase; hair fall) Terminal hair (adult) &
Hair fall history → generalized or localized / scarring or non-scarring (scarring → refer to dermatologist) vellus hair (prepubertal)

1. Androgenetic alopecia:
➢ Hair is sensitive to dihydrotestosterone (more localized)
➢ RX: topical minoxidil, finasteride (X 5-alpha reductase)(male), transplant (occipital hair) If block dots
2. Alopecia areata: present (not

IL CS:
➢ Description: bald clear patch, well defined, no scaring, +/- surrounded by broken hair clear patch) →
tenia capitis
intralesional ➢ Types: if <50%: localized, if >50%: totalis, if affect other body hair: universalis
(fungal)
corticosteroids ➢ Association: atopic dermatitis, vitiligo, any other autoimmune disease
➢ RX: potent topical or IL CS + immunosuppressant injection, minoxidil 5%
3. Telogen effluvium (comb with hair → telogen hair ↑ & anagen hair ↓):
S/E →
➢ Generalized non-scarring hair fall, causes: headache & hair
➢ Causes: surgery, post-delivery, stress, hypothyroidism, chemotherapy (3 months prior) loss aggravates
if pt. stop using
➢ Diffuse/extensive shedding or hair loss // treatment: treat the cause
4. Trichotillomania: Finasteride:
➢ Self-induced hair twirling/pulling, different lengths, psychological disorders or stress sexual
impotence in
Hair fall more than 200/day → hair pull test; +ve if more than 6 hair in around 40 pulled males &
feminization of
fetus in females
(FDA X)
Drug allergy: "occur within 1 month"

➢ Most common drugs: penicillin, NSAIDS, sulfa drugs (sulfonylurea, thiazide), insulin
➢ Systems involved:
- Dermatology: erosions (most common) e.g. urticaria, angioedema, EM, EN
- Pulmonary: asthma, pneumonitis // renal: interstitial nephritis, Nephrotic synd.
- Hematological: hemolytic anemia, thrombocytopenia, agranulocytosis
➢ Treatment: discontinue offending drug, antihistamine for symptoms

Food allergy:

➢ IgE mediated // most common food: eggs, peanuts, milk, tree nuts, shell fish, chocolate
➢ Findings:
- Skin (most common): pruritis, erythema, urticaria/angioedema
- GI (2nd): nausea, vomiting, ABD pain // anaphylaxis: respiratory, can be fatal
➢ Treatment: avoid offending agent, antihistamine, treat as anaphylaxis (if sever)

Insect sting allergy:

➢ Insects involved: yellow jackets, wasps, honeybees, hornets

➢ Reactions:
- Non-allergic: localized edema, redness, pain, & pruritis, for several hours
- Allergic: marked swelling & erythema, systemic S&S (malaise & nausea), days
o Can be confused with cellulitis
➢ Treatment: ice & oral antihistamine of mild, if sever treat as anaphylaxis

Anaphylaxis:

➢ Most severe form of allergy, type I IgE HSR, within sec to min, life-threatening
➢ Causes: food (most common), drugs, blood products, radio-contrast, latex
➢ Findings:
- Skin (most initial): rash, erythema, pruritis, urticaria, angioedema
- Respiratory: SOB & distress, wheezing // cardiac: hypotension, shock, arrhythmia
- GI: ABD pain, nausea,/vomiting, severe diarrhea // other: face/tongue/lips swelling
➢ Treatment:
- Maintain ABCs (intubation), immediate epinephrine, H1 & H2 antihistamine, CS
Infections:

1) Bacterial

1. Impetigo: "mainly in pediatrics

➢ Most superficial bacterial inf. (only epidermis), by staph. (1st), strept. (non-bullous)
➢ Findings: honey-colored crusting, (mouth), & draining of the skin, +/- bullous (S.
aureus)
➢ Treatment: "clean the wound with soap & remove the crusts by soaking"
- Mild (topical mupirocin/bacitracin), severe (PO dicloxacillin), MRSA (clindamycin)

2. Erysipelas:
➢ Deeper than impetigo as it involves the dermis & lymphatic, group A strept > staph.
➢ Predisposing factor: lymphatic obstruction, trauma, abscess, fungal inf., DM, & alcohol
➢ Findings:
- Well-demarcated, bright red, tender, swollen lesion mainly in lower limb & the face
- High grade fever & chills, leukocytosis
➢ Complication: sepsis, local spread, necrotizing fasciitis, GN (skin inf. doesn’t cause RH)
➢ Treatment:
- Mild: dicloxacillin > erythromycin (if penicillin allergic) > clindamycin (if MRSA) Needs RICE (rest,
- Severe (with fever): oxacillin > clindamycin (if allergic) > vancomycin (if MRSA) ice, compression
& elevation)
3. Necrotizing fasciitis:
➢ Life threatening inf. of deeper tissue, via strept. pyogenes or Clostridium perfringens
➢ RF: recent surgery, DM, IV drugs abuse, trauma
➢ Findings: pain out of proportion, fever, intense edema, violate or gray color
➢ Complications: sepsis, Toxic shock syndrome, thrombosis. discoloration, tissue necrosis
➢ Treatment: surgical debridement & broad-spectrum Antibiotics

4. Cellulitis:
➢ Skin & subcutaneous infection mostly due to group A strept. or S. aureus (gram –ve in
DM & IC) – deeper than erysipelas
➢ Routes:
- Skin break or trauma (strept.), wound, abscess, IV catheter (staph.),
- Water immersion (pseudomonas, vibrio), acute sinusitis (H. influenza)
➢ Association: DM ulcers, lymphedema, venous stasis disease
➢ Findings:
- Lesion is red, warm, tender, & swell, mainly in legs & arms (eye or face > worse)
➢ Diagnosis: inject sterile saline then take sample > culture (do Doppler to rule out DVT)
➢ Treatment:
- Mild: dicloxacillin > erythromycin (if penicillin allergic) > clindamycin (if MRSA) Needs RICE (rest,
- Severe (with fever): oxacillin > clindamycin (if allergic) > vancomycin (if MRSA) ice, compression
& elevation)
5. Scarlet fever (most common in 5-15 yrs)
➢ Bacterial illness by strept. featuring bright red rash that covers most of the body
▪ Rash begins on the face or neck and spreads to the trunk, arms and legs
▪ If pressure is applied to the reddened skin, it will turn pale
➢ Almost always accompanied by a Sore throat (URTI) and high fever
➢ Complications: can lead to rheumatic fever; heart problems & arthritis
➢ Findings → Strawberry tongue, Sand paper rash (feeling)
➢ Treatment: antibiotic covering gram +ve (erythromycin) for 2 wks, no need for topical
 6. Other bacterial infections: Caused by staph
➢ Infections that involves the hair follicles // treated with surgical, drainage, RICE Treated with
- Folliculitis: single follicle, either superficial or deep, erythema topical cream, soap
- Furuncles: single follicle involve the whole hair follicle, tender, small abscess, wash & antibiotic
Type of - Carbuncles: multiple follicles (several drainages opening), more abscess, in DM
impetigo ➢ Ecthyma: superficial dermis, S. pyogenes, ulceration with hemorrhagic crusting, in DM
but deeper ➢ Pseudomonas inf.: In ecthyma → Eschar:
- Ecthyma gangrenosum: piece of dead tissue
o Caused by pseudomonas mainly & opportunistic fungi, in IC & neutropenia that is cast off from
o Sign of bacteremia or septicemia, can be found in swimming pools the surface of the skin
o Red/purple macule or patch with central necrosis +/- hemorrhagic bullae
- Hoot-foot syndrome: Tender erythematous nodules on the heel
- Treatment:
o Superficial: 5% acetic acid soaks > topical ABx (gentamicin) > PO fluoroquinolone
o Severe or systemic: piperacillin/tazobactam or doripenem if penicillin allergic
➢ Erythrasma (MCQ):
- Corny. minutissimum, wood lamp (bright red), erythromycin + aluminum chloride
➢ Pitted keratolysis:
- Kytococcus/micrococcus sedentarius or Corynebacterium, same drugs for
erythrasma
- Multiple small crater @ pressure points of plantar surfaces, foul smell feet
➢ Leprosy:
- Mycobacterium leprae, Indian or Pakistani, slowly progressive,
- Granuloma that affected the nerves & skin, no sensation in the lesion
➢ Erythema marginatum:
- Circular rash with clear center, rheumatic heart (VS. Lyme disease), group A strept.
➢ Staphylococcal scalded skin syndrome (SSSS):
- Mostly in babies & children. Features fever, a rash & sometimes blisters
- Bacteria anywhere in body release toxin that cause scalding of skin
o Culture of bullae is negative; bacteria found elsewhere, not in skin
- Nikolsky sign is positive → putting pressure will shear off epidermis, found also in:
o Pemphigus vulgaris
o Toxic epidermal necrolysis

The great mimickers (for DDx) → THE 4S

SLE Sarcoidosis Syphilis (secondary) Scabies

2) Fungal:

• Tinea versicolor:
➢ Superficial fungal inf. (Malassezia group-normal flora), mostly in adolescence
➢ Findings:
- Well-demarcated lesion, mostly in trunk, hypo/hyperpigmented (can be
erythematous in white people), brown-to-white patches & macules
➢ Risk factors: hot/humid weather, oily skin, excessive sweating
➢ Diagnosis:
- KOH prep: "spaghetti & meatballs ", hyphae & yeast balls // yellow on wood lamp
➢ Treatment:
- Topical or oral antifungal that contain: selenium sulfide, or keto/fluconazole This is in clinic
Antifungal shampoo as prophylaxis because it is recurrent with hot/humid weather
In vitiligo they
appear chalky white
 • Candida
➢ Nappy rash can be due to many causes: erythrasma, irritant contact dermatitis or
fungal infection; if folds involved mostly is fungal infection not irritant dermatitis
➢ Skin lesion → well-demarcated erythematous with scalding, folds involved
- Presence of satellite region in candida, NOT in dermatophytes
- Scrotum involved while in dermatophytes scrotum is spared
➢ RF → DM, immunosuppression, obesity, poor hygiene, warm weather
➢ KOH → sausage-like pseudohyphae slings
➢ Treatment → topical antifungal or oral if severe

• Dermatophytes:
History of ➢ Superficial fungal inf. that affect coetaneous epithelium, nails, & hair Well-demarcated erythema,
contact with ➢ Three main species: trichophyton, microsporum, & Epidermophyton hypopigmented in the center
animals ➢ Types: “ring worm”
- Tinea corporis "ringworm": body/trunk, all age, pinkish annular lesion
- Tinea capitis: scalp, children, scaling + hair loss +/- pruritis Nails in psoriasis only distal
- Tinea unguium "onychomycosis": nails, elderly, thick opacified nail affected while in tinea it
- Tinea pedis "athlete foot": feet, young adult, scaling + erythema + pruritis can be lateral also
- Tinea cruris "jock itch": groin/inner thigh (spares scrotum), adult, scaling +
Pseudomonas infection →
erythema
green nails
➢ Diagnosis:
- Scraping & KOH preparation: best initial, visualize hyphae // culture: most accurate
Fungal in hair & - Wood lamp: differentiate species (if fluoresce microsporum, If not trichophyton)
nail must be
➢ Treatment:
treated with and
- Topical antifungal (ketoconazole, miconazole):
oral antifungal as
o All types except tinea capitis & unguium // ketoconazole can cause gynecomastia
topical is not
- Oral antifungal (terbinafine, itraconazole, Griseofulvin): for tinea capitis & unguium
beneficial
Herpes simplex virus = human herpes virus (HHV)
Herpetic lesions: group of
HHV-1 → herpes labialis (oral) HHV-2 → genital herpes
vesicles on an erythematous HHV-3 → chickenpox & shingles HHV-4 (Epstein-Barr virus; EBV) → infectious mononucleosis
background HHV-5 (Cytomegalovirus; CMV) → infectious mononucleosis
3) Viral:
HHV-6 & HHV-7 (Roseolovirus) → sixth disease (roseola infanatum), pityriasis rosea
HHV-8 → Kaposi’s sarcoma
• Herpes zoster (shingles):
Herpes virus ➢ Reactivation of varicella-zoster virus that remains dormant in dorsal root ganglia
other ➢ Occur in times of stress, inf. illness & only for those who had chickenpox (HHV-3)
complications: ➢ Mostly > 50 yrs (< 50 yrs if patient is immune-compromised "IC")
Eczema
➢ Contagious (if open vesicles present) for those who hadn`t had chickenpox or IC
herpeticum ➢ Findings: Does not
(monomorphic - Severe pain (1st) with rash (vesicles with erythema) in dermatomal distribution cross midline
punched-up o Vesicles are found in thorax (most), CNV distribution (V1 most), arms & legs
ulcers) ➢ Complication: postherpetic neuralgia, blindness, Ramsay hunt syndrome "deafness"
Erythema
➢ Treatment:
multiforme - Keep lesion clean & dry, analgesic (acetaminophen, aspirin, or codeine) Within first
(target lesion on - Antiviral: decrease the pain & duration, + risk of postherpetic neuralgia (acyclovir) 72 hours
palm & sole) - Live vaccine: reduce number of cases, severity & duration of postherpetic neuralgia
o Indicated for all patients > 60 yrs if there is no contraindication
Chickenpox in adults: generalized all over the body, polymorphous, must be treated
• Eczema herpeticum:
➢ Mostly with atopic dermatitis // do swap (tzanck smear> multinucleated giant cells)
➢ Causes: herpes simplex virus // treatment: systemic acyclovir
➢ Finding: monomorphic bulging ulcers on atopic dermatitis background, mouth mainly
 • Warts:
➢ Caused by human papilloma virus (HPV), transmitted via skin-skin contact or sexually
➢ Types:
- Common warts (verruca vulgaris): (HPV 1,2,4)
o Commonest type, found everywhere but mostly palms, fingers, elbow, knee
o Looks flesh-colored/whitish with hyper-keratotic surface
▪ Flat surface goes with skin tags rather than warts, mostly around the neck
- Flat warts (verruca plana): (HPV 3,10)
o Mainly in the chin/face, dorsum of hand, legs // hyperkeratotic, +/-flesh-colored
- Plantar warts (verruca plantaris): (HPV 1,2,4)
o Mainly in the plantar side of foot, flesh-colored with rough hyper-keratotic surface
o Differs from callus/corn in the color of the dots that appear → warts have small
black pinpoints in the center (due to blocked capillaries) while callus have white
dots
- Genital warts (condyloma acuminatum): (HPV 6,11, 16, 18) covered in the STD`s
o Female genital warts referred to Obs & Gyne to check for cervical cancer
➢ Findings:
- Mostly asymptomatic unless they bumped, +/- bleed & disfigure
- Plantar warts are painful mainly with walking or prolonged standing (pressure)
➢ Treatment:
Cryotherapy - Mostly spontaneously disappear in 1-2 yrs // 5-FU cream or retinoic acid: flat warts
kills the cell, not - Cryotherapy: freezing of the lesion with liquid nitrogen -200c, multiple sessions
the virus - Surgical excision or laser therapy // cryo S/E: pain, ulceration, secondary infection
Uses of cryo: warts, molluscum contagiosum, corns, skin tags
• Molluscum contagiosum:
➢ Self-limited viral inf. caused by poxvirus, common in sexually active young & child
➢ Transmitted via skin-skin contact (& sexually), highly contagious, child abuse??
➢ Findings: asymptomatic small papules with central umbilication, extensive in HIV +
➢ Treatment: spontaneous after 6-month, salicylic acid, podophyllin drops, cryotherapy

4) Protozoal & other infections:

1. Scabies: Female
➢ Caused by human skin mite sarcoptes scabiei var hominis that lies in stratum corneum
➢ Highly contagious: transmit via skin-skin or via towels, bed linens, clothes (6 wks IP)
➢ Pathogenesis:
- Mite will tunnel via epidermis, lays egg & deposit feces (scybala) > type IV HSR Feces cause
Mainly in
the itches
warm areas ➢ Sites: fingers, inter-digital (finger web space), wrist, elbow, genital area, ankle, feet
- Head, neck, palm & soles are spared except in infant, elderly, or IC
➢ Findings:
- Severe pruritis (mostly @ night & with hot shower) + scratching (lead to excoriation)
- Burrows: represent the tunnel of the mite, female mite if dark dot @ the end
- Eczematous plaque, crusted papules, & 2ry bacterial inf. can develop
➢ Norway scabies: severe form, whitish-slivery color
➢ Diagnosis:
- Look for burrows > scrap them (via scalpel) & visualize them > mite, egg or scybala
➢ Treatment:
- Wash all clothes, towels, & bed linen & put them to dry under the sun (or use dryer)
- Permethrin 5% cream or benzyl benzoate:
o DOC, cover all the body (head-toe), apply it @ night >wash it in morning (2 days)
o Treat also the close contact even if they don`t have pruritus
- Oral ivermectin or lindane: 2nd line in case permethrin isn`t available, CI or failed
o Lindane is CI in children < 2 yrs, pregnant lady, or lactating women (seizure risk)
- Topical CS & oral antihistamine: used mainly to treat pruritis
2. Erythema migrans:
➢ Associated with Lyme disease "spirochete borrelia burgdorferi"(transmit via ticks)
➢ Large, painless, well-demarcated, target shaped lesion // in thighs, groin, & axilla

3. Leishmaniases: parasite inf. transmitted via sand fly, in exposed areas (face mainly)

Pediatrics:

1. Henoch-Schoenlein purpura:
➢ Mainly in child > 10 yrs (not always), 1-2 wks after upper respiratory tract infection
➢ Painless palpable purpura in buttocks & lower limbs // other S&S: ABD pain, diarrhea
➢ Treatment: supportive (leg raise & NSAIDS), systemic CS (for rest of S&S e.g. arthritis)

2. Salmon patch: in the central of the face (goes), & nape area "stork bite" (persistent)
3. Facial port-wine stain: persistent red-pink patches & macules, present @ birth

5th disease → erythema infectiosum → slapped cheek (parvovirus B19)

Kawasaki disease → strawberry tongue – fever >5 days & lymphadenopathy – do echo