Dermatology Osmosis HY Pathology ATF - ATF

DERMATOLOGY
High-Yield
Notes
by
AfraTafreeh.com
PATHOLOGY
Table of contents
Burns and Frostbite 1
Actinic Keratosis 1
Burns 2
Burns Overview 4
Frostbite 6
Sunburn 8
Dermatitis and Eczema 10
Atopic Dermatitis (Eczema) 10
Contact Dermatitis 12
Seborrhoeic Dermatitis 14
Erythema Multiforme and Drug Eruption 16
Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis 18
Hair-Related Diseases 21
Alopecia Areata 21
Telogen Effluvium 22
Malignant Tumors 24
Basal Cell Carcinoma 25
Melanoma 26
Squamous Cell Carcinoma 29
Papulosquamous Disorders 32
Lichen Planus 32
Pityriasis Rosea 34
Psoriasis 35
Pigmentation Disorders 38
Albinism 39
Pityriasis Alba 40
Vitiligo 41
Skin and Soft Tissue Inflammation and Infections 43
Acne Vulgaris 44
Cellulitis 45
Erysipelas 47
Folliculitis 48
Table of contents
Hidradenitis Suppurativa 49
Impetigo 50
Necrotizing Fasciitis 51
Onchomycosis 54
Pressure Ulcer 56
Rosacea 57
Staphylococcal Scalded Skin Syndrome 58
Urticaria and Erythema Nodosum 59
Hereditary Angioedema 61
Urticaria (Hives) 62
Vesiculobullous Diseases 64
Bullous Pemphigoid 64
Epidermolysis Bullosa 65
Pemphigus Vulgaris 66
,
I
NOTES
NOTES
.
6
BURNS & FROSTBITE
GENERALLY,WHAT ARE THEY?
(
PATHOLOGY & CAUSES
)
O
O
O
)
• Clinical presentation
loss of skin function
Impaired thermoregulation
body heat
D_IA_GN_O_s,_s __
OTHER DIAGNOSTICS
• Damage to skin, underlying structures due
to overexposure to harmful conditions
• Burn/frostbite injury----.
(
O
----. loss of
Nature of exposure, appearance of
wound, depth of damage
Impaired fluid retention ----. large water,
protein losses from skin, affected tissues
(
Loss of microbial
risk of infection
MEDICATIONS
barrier function ----. high
T_R_E~_~_M_EN_T__
)
• Analgesia
(__ SI_G_NS_&_S_Y_M_PT_O_M_s_)
SURGERY
• Pain, erythema,
slough off
blistering,
• Debridement
skin layers
of dead tissue
ACTINIC l(ERATOSIS
osms.i"l/ e1e-linie_lce,-e1-losis
(
PATHOLOGY & CAUSES
• Repeated prolonged sun exposure ----. small,
ill-defined, rough, scaly patches of skin
• Once initial lesions develop, more may
follow without additional sun exposure
• UVB radiation ----. damage to keratinocytes
----. accumulation of oncogenic changes
(e.g. p53 gene mutation) ----. unchecked
proliferation of dysplastic keratinocvtes=precancerous lesion
RISI( FACTORS
• Fair-skinned individuals; facial distribution.
sun-exposed limbs; increased age;
immunosuppression; albinism; xeroderma
pigmentosum; human papillomavirus
(HPV)
infection
)
COMPLICATIONS
• Malignant transformation to squamous cell
carcinoma (0.03-20% likelihood)
(
SIGNS & SYMPTOMS
)
• Small, rough, scaly skin lesions
• Sandpaper-like
sensation felt on palpation
• lnduration, tenderness. bleeding----.
malignant transformation
possible
1
I
afratafreeh.com exclusive
(..____
D_IA_GN_O_SI_S
)
LAB RESULTS
• Skin biopsy
, Exclude malignancy
(
TR_E_AT_M_E_NT )
MEDICATIONS
• Topical pharmacotherapy: 5-Fluorouracil,
imiquimod, ingenol mebutate
Figure 1.1 The clinical appearance of an
actinic keratosis.
SURGERY
• Scraping,
excision
OTHER INTERVENTIONS
Prevention
• Avoid excessive sun exposure,
sunscreen
use
Dermatologic
• Cryotherapy (liquid nitrogen),
photodynamic therapy, electrodessication
Figure 1.2 The histological appearance
of actinic keratosis. There is full thickness
epidermal atypia with hyperchromatic basal
cells and nuclei in the stratum corneum
(parakeratosis).
BURNS
osms.i-l/\,u,-ns
(
PATHOLOGY & CAUSES
• Tissue destruction due to exposure
O Heat, electricity,
chemicals, radiation
• Burn injury -
)
• Cell survival favoured by moist
environment, aseptic conditions,
blood supply
good
TYPES
loss of skin function
• Impaired thermoregulation
heat
-
loss of body
• Contact with heat/heated objects, fluids
• Impaired fluid retention - large water,
protein losses from skin, affected tissues
• Loss of microbial barrier function risk of infection
Thermal burns
high
• > 44°C/lll.2°F
O
Proteins denature,
damage
break down -
cell
• Amount of tissue destruction determined
2
by temperature, duration ----> injury
diminishes outwards as heat disperses
around central site
• Zone of coagulation (ischemiaJ: area of
maximal damage; no remaining tissue
perfusfon-» irreversible cell damage---->
coagulative necrosis
• Zone of stasis (edematous): surrounds
coagulation area, microvascular sludging,
thrombosls=- decreased perfusion ---->
progressive tissue necrosis; cellular death
within 24-48 hours without treatment;
early intervention may save significant
amounts of tissue
• Zone of hyperemia: surrounds zone of
stasis; inflammation ----> vasodilation,
increased capillary permeability---->
erythema; tissues still vlable v- recovery
likely
n
O
O
O
Duration: longer duration ----> more tissue
damage
Pathway: current flowing through heart
----> lethal
Tissue resistance (pathway, depth
dependant): nerves < blood vessels<
muscle < skin < tendon < fat < bone
Radiation burns
• Excessive exposure to radiation
O
Ultraviolet (UV) light: sunlight most
common cause of radiation, superficial
burns
Ionizing radiation (e.g. radiation
therapy, X-rays, radioactive fallout):
skin effects vary from hair loss at 3Gy to
necrosis at 30Gy
O
Microwave burns
O
Chemical burns
• Exposure to corrosive substances (e.g.
acids, bases, oxidizing/reducing
agents,
solvents, alkylants, chemical weapons)
I
Frequency: very high frequencies ---->
tissue burning; doesn't penetrate deep
enough to affect heart
• Severity
O
Alkali> acid; warmer temperature;
greater volume, concentration,
contact duration; specific mechanism
of chemical action; degree of tissue
penetration
• Occur immediately on contact, may
continue to progress for some time
• May not be immediately
evident
• May diffuse to deeper structures without
initial damage to skin surface
Electrical burns
• Passage of electricity
rapid injury
through tissue
• Subdermal damage significantly
than superficial injury
c-
greater
• Extent of injury determined by
°` Current:
higher current-» increased
lethality/tissue damage
O
Voltage: higher voltage----> more
damage; higher voltage ----> dielectric
breakdown of skin ----> lowered
resistance, greater current flows
Figure 1.3 An adult male with superficial
partial thickness burns to the arms and torso,
secondary to sun overexposure.
3
I
RISI( FACTORS
• Complicated injury
O
Age (< 3, > 60), location (e.g. face, neck,
hands, feet, perineum), inhalational
injury, associated injuries (e.g. fractures),
comorbid disease (e.g. chronic renal
failure)
, Increased levels of catecholamines,
cortisol - hypermetabolism.
immunosuppression
• Additional
COMPLICATIONS
• Wound contracture/hypertrophic
infection
O
surface area - significant inflammatory
response - impaired organ perfusion
- gastrointestinal (GI) bleeding,
renal failure, progressive pulmonary
insufficiency
scarring,
Most common organisms: S. aureus, P.
aeruginosa, C. albicans
injury
, Singeing of airways - inflammation
eventual compromised airway
-
, Carbon monoxide inhalation
• Systemic effects of severe burns
O
Large burns> 30% of total body
Epidermis
Sensation intact - pain,
erythematous. blanchable.
hair follicles present
Extends into superficial
(papillary) dermis
Sensation intact - pain,
erythematous. forms
blisters containing clear
fluid, blanchable, hair
follicles present
Extends into deep
{reticular) dermis
Yellow/white, no sensation.
minor blanching, blisters.
some hair follicles still intact
Extends through
epidermis. dermis
No sensation, stiff leathery
eschar {black/ grey/white/
cherry red in colour). no hair
follicles, thrombosed
veins visible
Incomplete/months:
Re-epithelializes from wound
edge. grafting necessary to
replace dermal integrity,
limit scarring
Black/charred
Requires debridement/
amputation: skin flap for
coverage, does not
re-epithelialize. cannot graft
Injury to underlying
tissues (fat/muscle/bone)
5-10 days: no scarring,
heals completely
2-3 weeks: spontaneously
re-epithelializes
1-2 months: re-epitheliaizes.
hypertrophic scars common,
grafting recommended to
expedite healing
4
(
I
D_IA_GN_O_s,_s)
OTHER DIAGNOSTICS
•%of total body surface area (TBSA)
affected
O
O
O
Doesn't include areas with first degree/
superficial burns
Palm size estimation: size of individual's
hand print (palm, fingers) 1 % of TBSA
Wallace rule of nines: each major body
part assigned value corresponding to
approx. proportion of body surface area
American Burn Association severity
classification
• Minor
0
< 2% full thickness burn
0
< 10% TBSA (young/old < 5% TBSA)
• Moderate
0 2-5% full thickness
burn
0
O
10-20% TBSA (young/old 5-10%
TBSA)
high voltage injury, possible
inhalation injury, circumferential
comorbidities
burn,
(~~~~~~~~~~~~~~~~
TREATMENT
• Major
0 > 5% full thickness
burn
0
O
> 20% TBSA (young/old > 10% TBSA)
high voltage burn, known inhalation
injury, significant burns to face/joints/
hands/feet, associated injuries
)
OTHER INTERVENTIONS
Intravenous (IV) fluids
• Parkland formula
• Estimated IV fluid replacement
over initial 24 hours
• Volume required in 24 hours
(kg) x (% TBSA x 100)
required
= 4 x mass
• Half of requirement given over first eight
hours; remainder over following 16
hours
Wound care
• First degree: maintain moist skin barrier
with antimicrobial burn dressings
Figure 1.4 A full-thickness
the hand.
superficial
burn to
• Second degree: daily burn dressing change
with topical antimicrobial, leave blisters
intact unless circulation impaired/overlying
joint, inhibiting movement
• Deep second degree: prevention of sepsis
----. antibiotics
5
I
• Remove dead tissue
'Surgical debridement,
(bleeding) tissue
excise to viable
Chemical burn
• Remove contaminated
dry powder
clothing, brush off
• Irrigate with water for 1-2 hours under
low pressure; if elemental metal burn (e.g.
sodium, potassium, magnesium, lithium)
avoid exothermic reaction with water, soak
in mineral oil instead
• Acid
O Water irrigation,
followed by dilute
solution of sodium bicarbonate
Electrical burn
• De bride non-viable tissue, repeat every two
days
• Monitor for cardiac complications
Figure 1.5 A full thickness
aspect of the foot.
burn to the medial
FROSTBITE
osms.i-l/fTos-lbi-le
(
PATHOLOGY & CAUSES )
• Exposure to low temperatures for
significant periods of time. subsequent
rewarming - tissue damage
Freezing
• Temperatures < -4°C/24.8°F - formation
of ice crystals within tissues - damage to
cellular membranes, small blood vessels
• Cooling - vasoconstriction, impaired
circulation - further cooling, warm blood
unable to effectively perfuse freezing
extremities
capillaries - ischemia, inflammation.
coagulation - tissue death
blood
• Thawing - formation of blood clots in
small vessels
RISI( FACTORS
• Frequently exposed/thermally vulnerable
skin (e.g. hands, feet, face); occupational/
hobby exposure to low temperature
environments (e.g. winter sports
enthusiasts. military personnel); circulationimpairing disorders (e.g. Raynaud's
phenomenon,
diabetes). substance use (e.g.
smoking)
Thawing
COMPLICATIONS
• Rewarming - vasodilation - edema
• Poor blood flow through damaged
• Hypothermia,
compartment
syndrome
6
I
(__ S_IG_N_S_&_S_YM_P_T_O_MS
)
• Numbness prior to thawing
• White/bluish
discolouration
• Swelling/blistering
(
of skin
after treatment
D_IA_GN_o_s,_s
__
)
• Clinical presentation:
classification
physical assessment,
Figure 1.6 The clinical appearance of
frostbitten fingers.
DIAGNOSTIC IMAGING
• Technetium (Tc)-99m
scan)/CT scan
scintigraphy (SPECT
• Assess salvageable tissue; earlier
debridement of nonviable soft tissue
• Perfusion/metabolic
imaging identifies
viable bone, tissue/location autoamputation
likely to occur
Superficial skin damage.
without ice crystal formation
Pallor, numbness. reverse
quickly on rewarming
Rapid recovery
Superficial skin damage
Central pallor. anesthesia
with surrounding edema
Skin surface may slough off.
damage not permanent
, full recovery
Full thickness skin injury
Within 24 hours after exposure:
large blisters containing clear
fluid form, surrounded by
edema. erythema
Blisters may form eschar -+
sloughs off to reveal healthy
granulation tissue ..... distal
tissues/nails rnav be destroyed
Full thickness skin injury,
may affect under tissues
Deeper than 2nd degree injury,
smaller blisters form ...., may
hemorrhage; skin forms black
eschar over weeks
Long term ulceration. lesions
on intermediate body parts-+
loss of function/autoamputation
Injury to underlying
tissues (fat/muscle/bone)
Complete tissue necrosis,
painless rewarming,
mummification occurs in
4-10 days
Sepsis likely, autoamputation
may occur over 1-2 months
7
I
activator, heparin for risk of amputation
, Blood vessel dilator: iloprost
, Sympatholytic drugs - counteract
peripheral vasoconstriction
, High risk of infection - antibiotic
prophylaxis (e.g. penicillin G)
SURGERY
• Debride dead tissue
• Escharotomy:
release restrictive eschars
• Fasciotomy: compartment
Figure 1.7 Toes three weeks following
bite.
syndrome
OTHER INTERVENTIONS
frost
General measures
(
T_R_E~_~_M_EN_T
__ )
MEDICATIONS
• Analgesia
Nonsteroidal anti-inflammatory
(NSAI Ds)/opioids
• Do not walk on frostbitten feet/rub
frostbitten hands (worse tissue damage)
• Avoid using stoves/fires to reheat insensate
limbs (avoid thermal damage)
Initial thawing
o
• Do not rewarm if possibility of refreezing
exists (worse tissue damage)
Initial thawing
drugs
• Temperature: immerse in 37-39°C/98.6102.20F agitated water; maintain steady
temperature
• Pharmacological adjuvants (severe cases,
grade 2+)
o Antithrombotics:
tissue plasminogen
• Duration: 10-30 min with povidone iodine/
chlorhexidine antiseptic
SUNBURN
osms.i"l/ sun\>u,-n
(
PATHOLOGY & CAUSES
• Radiation burn of living tissue due to
excessive exposure to UV radiation
o Burning may occur in 15 minutes of
sunlight exposure in high UV radiation
areas/seconds of non-shielded welding
arcs
)
, Within one hour mast cells degranulate
- release of histamine. serotonin, tumor
necrosis factor (TNF) - prostaglandin,
leukotriene synthesis - neutrophilic,
lymphocytic infiltrate - further
inflammation
• UV exposure - activation of genes
to produce melanin - absorbs UV
wavelength light - acts as photoprotectant
• UV light radiation overexposure
O
Initial direct DNA damage (formation
of thymine dimer) - activates cellular
response mechanisms - DNA repair/
inflammatory response, cell death via
apoptosis
RISIC FACTORS
• Outdoor work/sports, fair skin, very young/
old age, genetic defects in DNA repair, use
of photosensitizing medication
8
COMPLICATIONS
(
• Increased risk of skin cancers (e.g.
melanoma; basal-cell, squamous-cell
carcinoma)
(
SIGNS & SYMPTOMS
OTHER DIAGNOSTICS
)
• Clinical presentation (similar to thermal
burn)
, Superficial (first degree) ----. affects only
epidermis (erythematous)
• Initial erythema, heat given off by increased
blood flow to area due to vasodilation
• Pain proportional
• Blistering, swelling,
fever, chills
= Superficial partial
thickness (second
degree) ----. affects dermis (forms
blisters)
to severity of exposure
edema,
I
D_IA_GN_O_SI_S
)
peeling skin,
(
TREATMENT
)
MEDICATIONS
Analgesia
• hydrocortisone
cream, NSAIDs
OTHER INTERVENTIONS
• Protect burnt skin with loose fitting clothing
when outside to prevent further damage
Analgesia
• Cool baths/showers,
moisturizers
Figure 1.8 Desquamation
skin following sunburn.
(peeling)
of the
soothing skin
Prevention
• Avoid peak UV radiation intervals (10:00
AM to 4:00 PM), wear appropriate clothing
(e.g. long-sleeved shirts, long trousers,
wide-brimmed hats, sunglasses). broadspectrum sunscreen on any exposed skin
9
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afratafreeh.com exclusive
NOTES
r4
"
(
NOTES
DERMATITIS & ECZEMA
GENERALLY, WHAT ARE THEY?
PATHOLOGY & CAUSES
• Inflammatory
• Rash
, Appearance, distribution
skin damage
SIGNS & SYMPTOMS
• Rashes
O Pruritus
(itching),
(
OTHER DIAGNOSTICS
skin disorders
• Immune-mediated
(
)
)
(
T_R_EA_~_M_EN_T
__
)
MEDICATIONS
• Corticosteroids
• lmmunosuppressants
burning, pain
D_IA_GN_O_s,_s __
)
LAB RESULTS
• Skin biopsy, blood tests
ATOPIC DERMATITIS (ECZEMA)
osms.i"l/ o.-lopie-dermo..ltlis
(
PATHOLOGY & CAUSES
• Allergic. inflammatory skin condition
• Common for children; may affect adults
• Associated
O
with elevated
serum lgE levels
Atopy: predisposition to lgE antibody
release after trigger exposure
)
Type 4 hypersensitivity
• Primary immune
dysfunction
, T cell subset imbalance ---'> Th2
predominance
- increased
inflammatory cytokine production (IL-4,
5, 13) ---'> increased release of lgE from
plasma B-cells, recruitment of mast
cells, eosinophils
TYPES
RISI( FACTORS
Type 1 hypersensitivity
• Family history of atopy (eczema, asthma,
allergic rhinitis)
• Epidermal barrier dysfunction
O Skin
barrier defects (e.g. filaggrin
mutation) ---'> antigen entry---'>
inflammatory cytokines
• Environmental
allergen
sensitivities
• Loss of function mutation in filaggrin gene
(skin barrier function)
10
I
OTHER DIAGNOSTICS
• Higher incidence in urban populations,
high-income countries
• Morphology, distribution
• Low levels of early life exposure to
endotoxin (immunogenic component of
gram-negative bacteria)
of lesions
United Kingdom working group atopic
dermatitis criteria
• Mandatory
= Evidence of pruritic skin with rubbing/
COMPLICATIONS
scratching
• Skin infections
O
• 2::
Staphylococcus aureus common
commensal organism ---'> impetigo
three following criteria
= Skin crease involvement
(antecubital
fossa, popliteal fossae, neck, around
eyes, ankles)
• Eczema herpeticum
O
Rapid spread of herpes simplex virus on
affected skin
= History/first degree relative with
asthma/hay fever
• Social stigma, anxiety
= Dry skin in past year
• < two years old before symptoms arose
(not applicable to children < four years
old)
(__ s,_G_NS_&_S_Y_M_PT_O_M_s_)
= Visible dermatitis
• Acute
O Pruritic
erythematous papules, vesicles
with exudate, crusting
of flexural surfaces
(< four years old=-. examine cheeks,
forehead, outer aspects of extremities)
• Chronic
O
Dry, excoriated erythematous papules
with scaling; lichenification (hyperplasia)
• Dry skin
• Pruritus ---'> chronic scratching ---'> skin
thickening, increased infection risk
• Cutaneous hyperreactivity to environmental
antigens/stimuli
(e.g. stress)
• 0-2 years old
O
O
Erythematous, pruritic, scaly, crusted
lesions +/- vesicles, serous exudate
Extensor surfaces, cheeks, scalp
• 2-16 years old
O
°`
Lichenified
epidermis)
Figure 2.1 Atopic dermatitis affecting the
flexural surfaces of the forearms.
plaques (thickened
Flexural distribution (e.g. antecubital,
popliteal fossae); volar aspect of wrists,
ankles, neck
(
• Adults
O
°`
O
(
MEDICATIONS
Localized lichenified plaques
Flexural surface involvement
Uncommonly
• Control pruritus
involves face/neck/hands
D_IA_G_N_os_,s
LAB RESULTS
• Elevated level of Serum lgE
T_R_E~_;,-_M_EN_T
__
)
)
O
Antihistamines
O
Topical calcineurin inhibitors (tacrolimus
ointment, pimecrolimus cream)
O
Antibiotics to treat associated skin
infections
• Immune suppression
O Topical
---'> systemic corticosteroids
11
I
O
Topical calcineurin
O
inhibitors
Oral cyclosporine
O
Dupilumab (IL-4 receptor antagonist)
• Maintain skin hydration
O
O
OTHER INTERVENTIONS
• Reduce exposure to environmental
allergens
• Avoid triggers
O
Apply after bathing/hand
washing
Avoid lotions with high water/low oil
content (evaporation dries out skin,
triggers outbreak)
• Control pruritus
O
O
Thick, unscented creams with low water
content/ointments without water
Heat, low humidity
• Manage stress/anxiety
Prevent scratching; keep fingernails
short (esp. young children)
CONTACT DERMATITIS
osms.i"l/ eon-lo.e-l-de,-mo.-li-lis
(
PATHOLOGY & CAUSES )
• Inflammation of skin after contact exposure
to allergens/irritants
• Localized
• Exposure to foreign substance triggers
immune response
• Most common form: irritant contact
dermatitis
Allergic contact dermatitis
• Anacardiaceae family plants
O
O
O
CAUSES
• Exposure to irritant (irritation may be
mechanical/chemical/physical)
• Acute: strong irritant
• Chronic: recurring exposure to weak
irritant
• Detergents, surfactants, extreme pH,
organic solvents, water
• Altered epidermal barrier function: Fat
emulsion - defatting of dermal lipids cellular damage to epithelium - DNA
damage, transepidermal water loss
- cytotoxic cell damage - cytokine
release from keratinocytes - activation
of innate immunity
• Plants with spines/irritant
hairs
• Low humidity
• Skin loses moisture more easily
Poison ivy, poison oak, poison sumac
• Nickel,
fragrances,
dyes
Induction phase: immune system
primed for allergic response to antigen
Elicitation phase: contact allergens are
typically haptens - small, can cross
stratum corneum of skin to associate
with epidermal proteins - form
complete reactive antigen - dendritic
cells recognise antigen - internalise
antigen, transport to lymph nodes present to T lymphocytes - trigger
immune response - cell mediated
immune response (Type IV delayed
hypersensitivity) - memory cells
remain within skin. Future exposure
- triggers memory cells - immune
response (cytokines, chemokines, TNF,
lymphocytes, granulocytes migrate)
RISI( FACTORS
• Age
, Infants: highest risk
, > 65 years old: lowest risk
• Body site exposure
Difference in thickness of stratum
corneum, barrier function
O
n
Face, dorsum of hands, finger webs are
prone to irritation
• Atopy
12
°`
Chronically
impaired barrier function
(
• Occupational exposure
°`
Continuous moisture exposure, repeated
cycles of wet-to-dry from frequent
handwashing
MEDICATIONS
• Pruritus
, Calamine lotion
• Allergic contact dermatitis
O
• Mild topical
Occupation (health professionals,
chemical industry, beauticians,
hairdressers, machinists, construction)
corticosteroid
(hydrocortisone)
• Oral antihistamine
• Allergic contact dermatitis
O
Increases with age
, High potency topical corticosteroids
O
History of atopic dermatitis
= Oral corticosteroids
= Topical calcineurin
(
SIGNS & SYMPTOMS
• Erythematous rash (can develop
after exposure)
• Vesicles/bullae/wheals
site
• Glaze/parched/scaled
• Scaling,
I
T_R_E~_~_M_EN_T
)
)
occur at exposure
(tacrolimus/
= Systemic immunosuppression
(azathioprine,
cyclosporine)
s 72hrs
inhibitors
pimecrolimus)
mycophenolate
mofetil,
OTHER INTERVENTIONS
• Remove/avoid trigger
presentation
• Treat blistering
hyperkeratosis, fissuring
= Cold compress
• Avoid scratching
• Itching (favors allergic etiology); burning
(favors irritant)
• Retain moisture, protect skin
= Barrier cream (e.g. zinc oxide)
• Irritant contact dermatitis
= Mild acidic solutions
may neutralize
= Emollients
(e.g. acetic acid)
alkali irritants/vice versa
(e.g. Aquaphor)
= Gloves
• Allergic contact dermatitis
= Phototherapy
(narrow band UVB
radiation)
Figure 2.2 Contact dermatitis secondary to
poison ivy exposure.
(
D_IA_GN_o_s,_s __
)
OTHER DIAGNOSTICS
• History of possible
allergen
exposure to irritant/
• Patch allergen testing
13
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SEBORRHOEIC DERMATITIS
osmsJl/se boTThoeie-deTmo.·tJlis
(
PATHOLOGY & CAUSES )
• Sebaceous gland-centered
inflammation
skin
• Response to fungal antigens/irritants
• Chronidrelapsing
• Typically mild form of dermatitis
Distribution
• Areas containing significant
sebaceous glands
number of
, External ear, center of face, upper trunk,
areas where skin rubs together
• Scalp
= Infants: aka cradle cap; self-resolving
= Adults: aka dandruff
(pityriasis
sicca);
mildest form
CAUSES
= Fine, white scaliness without erythema
• Occurs in sites with greater density of
sebaceous glands
= Severe cases: inflammation;
• Not a disease of sebaceous glands, nor
increased sebum production
• Suspected connection to lipid-dependent
fungal genus Malassezia
O
Immune response to fungus
O
Local irritants produced by fungus
• Children
O
Nutritional deficiencies of biotin,
pyridoxine (vitamin 86), riboflavin
(vitamin 82)
+/- pruritus
patchy
orange plaques with yellow, oily scales
(pityriasis steatoides); may progress
to oozing/crusting fissures affecting
outer canal, concha of ear (vulnerable to
superinfection)
• Face
= Forehead, eyebrows, glabella, nasolabial
folds; may affect cheeks/malar area in
butterfly distribution
= Frequently
affects areas of facial hair
distribution
RISI( FACTORS
• Age (biphasic incidence: 2-12 months
of age to adolescence; adulthood: peaks
30s-40s)
• Hyperandrogenism
• Biological males > biological
females
• HIV
• Parkinson's
• Stress
• Cold, dry weather
• Sleep deprivation
• Poor general
health
(__ s,_G_NS_&_SY_M_PT_O_M_s_)
• Scaling erythematous
plaques
• Scales yellow, oily in appearance
Figure 2.3 Seborrhoeic dermatitis affecting
both nasal folds.
14
• Periocular
(
Blepharitis,
O
Yellow crusting between lashes
MEDICATIONS
Can occur in isolation/part
distribution
• Topical antifungals
°`
free margin redness
of larger
• Antifungal shampoo
• Trunk (five distinct patterns of distribution)
O
O
O
O
O
I
T_R_E~_~_M_EN_T
__
)
O
• Topical corticosteroids
Moist, skin-contact regions: axillae,
infra mammary folds, umbilicus,
genitocrural
• Topical calcineurin
inhibitors
• Oral antifungals
• Antiandrogens
Petaloid pattern: fine, scaling plaques
over sternum/interscapular
• Reserved for individuals for whom
feminization/male
infertility is
unproblematic
Annular/arcuate: round, scaly plaques,
may have hypopigmented central
clearing
Pityriasiform pattern: mimics pityriasis
rosea, 5-15mm oval, scaly lesions along
lines of skin tension
• Sexually-active, uterus-bearing people:
combine with contraception to avoid risk
to fetus
OTHER INTERVENTIONS
Psoriasiform pattern: large, rounded
erythematous plaques with thick scales
• Cradle cap
= Apply emollient
(
D_IA_GN_o_s,_s__
OTHER DIAGNOSTICS
• History, appearance,
distribution
)
(petroleum jelly,
vegetable oil, baby oil) to scalp overnight
to loosen scales - remove scales with
soft toothbrush
• Frequent shampooing with mild, nonmedicated baby shampoo - remove
scales with soft toothbrush
• Extensive/persistent
therapy
cases -
medical
• Topical
• Coal tar shampoo/ointment
15
I
NOTES
NOTES
r4
ERYTHEMA MULTIFORME &
DRUG ERUPTION
~
GENERALLY,WHAT ARE THEY?
(
PATHOLOGY & CAUSES
• Skin, mucous membrane
)
D_IA_GN_O_SI_S
__
)
LAB RESULTS
conditions
• Associated with medication
(
• Skin biopsy
use/infection
CAUSES
OTHER DIAGNOSTICS
• Exact mechanism unclear, severe immune
reaction against foreign antigen
• Clinical history
(
COMPLICATIONS
• Initial rash may -
epidermal layer loss
T_R_E~_~_M_EN_T
__
)
• Identify/remove/treat
infection
offending agent/
(__ SI_G_NS_&_S_Y_M_PT_O_M_s
)
• Desquamating
rash
skin, mucous membrane
ERYTHEMA MULTIFORME
• Type IV hypersensitivity
• Bacterial
O Hemolytic
Streptococci, Legionelfa,
Mycobacterium, Mycoplasma
pneumoniae, Neisseria meningitidis,
Pneumococcus, Salmonella,
Staphylococcus
CAUSES
• Parasitic
O Trichomonas,
Toxoplasma gondii
(
PATHOLOGY & CAUSES
• Immune-mediated,
condition
acute, self-limiting
• Suspected deposition of primarily lgMbound immune complexes in superficial
skin, oral mucous membranes
Infection (most)
• Viral
O
Herpes simplex
)
skin
Drugs (rarely)
• Non-steroidal anti-inflammatories
(NSAIDs), sulfonamides, phenytoin,
barbiturates, phenylbutazone,
penicillin,
allopurinol
primary cause
16
Physical factors
Erythema multiforme minor
• Sunlight, radiotherapy, cold
• Often herpes simplex
Autoimmune disease
• Involves skin (little/no mucous membrane
involvement)
• Vasculitides
• Favors skin of extremities, face
• Symmetrical circular lesions
Hematological malignancy
• Non-Hodgkin
metaplasia
I
lymphoma, leukemia,
myeloid
• Lesions become classic "target" lesions (red
border, small white center)
• Rash spreads towards body center
RISI( FACTORS
• < 20 years old
• j frequency in biological
(
Erythema multiforme major
• Often drug-related
males
SIGNS & SYMPTOMS
• "Multiforme" denotes wide associated
lesion variety
• Epidermal detachment/skin
progression
)
• Erythematous,
loss
confluent, bullous lesions
• Involves mucous membranes
• Nikolsky's sign (lightly rub skin with firm
object for few seconds - blister forms)
• Target lesions
O
Initially round erythematous papules dusky central area/blister, surrounded
by dark red inflammation, surrounded
by pale edematous ring, erythematous
region on periphery
• Pruritus in affected area
(
D_IA_G_N_os_,s
LAB RESULTS
• Biopsy to exclude other skin disorders
• Painful lesions
OTHER DIAGNOSTICS
• If severe
• Identify offending agent/infection
°`
Fever, weakness, malaise
)
• Identification: target lesions,
symmetrical distribution
C....___
T_R_E_AT_M_E_N_T _
__,,)
• Often self-resolving in 1-2 weeks
MEDICATIONS
• Control primary cause
, Treat/remove identifiable
causes
• Herpes simplex suspected: oral
acyclovir/valaciclovir/famciclovir
= Eliminate
possible offending drugs
Mild disease
• Topical corticosteroids
• Antihistamines
Figure 3.1 The abdomen of a child displaying
numerous target lesions in a case of
erythema multiforme.
Severe Disease
• Glucocorticoids
• In severe cases, prednisone considered
17
I
Recurrent disease
• Systemic antivirals
(up to 6 months)
• lmmunosuppression
if antivirals fail
STEVENS-J"OHNSON SYNDROME &
TOXIC EPIDERMAL NECROLYSIS
osms.i"l/ s-levens- johnson_s14ndTome
osms.i-l/-loxie-epideTmo.l-neeTol14sis
(
PATHOLOGY & CAUSES
• Same underlying
spectrum)
O
)
pathology (severity
Stevens-Johnson syndrome (lower end),
toxic epidermal necrolysis (upper end)
COMPLICATIONS
• Dehydration, sepsis, pneumonia, multiple
organ failure, renal tubular necrosis, acute
renal failure, phimosis, vaginal synechiae
(adhesions). inside eyelid-tissue scarring---->
corneal vascularisation ----> vision loss
• Severity, classification
O
Body surface involvement
• Severe mucocutaneous
epidermal detachment
%
reaction ---->
CAUSES
• Cytotoxic T cell mediated destruction of
keratinocytes expressing foreign antigen
Medications
• Most common
• Allopurinol, sulfa drugs (e.g. sulfonamide
antibiotics). lamotrigine. carbamazepine.
nevirapine, phenylbutazone, thiacetazone,
oxicam NSAIDS
Infections
• Mycoplasma pneumoniae most common
infective agent
RISI( FACTORS
• HIV/AIDS
• Systemic lupus erythematosus
• > 40 years old
• Genetic carbamazepine interaction
predisposition (HLA-8*15:02,
HLAA*31:01 alleles)
• j frequency in biological
Figure 3.2 An individual
Johnson syndrome.
with Stevens-
females
18
SIGNS & SYMPTOMS
(
)
Systemic
• Before skin eruptions
(
• Stevens-Johnson syndrome:<
involvement
occur
I
D_IA_GN_O_SI_S
)
10% skin
• SJS/TEN overlap: 10-30%
• Fever, sore throat, fatigue, cough
• Toxic epidermal necrolysis: > 30%
M ucocuta neous
• Burning eyes, skin
• Red-purple rnacules-« skin blisters epeels, forms painful raw areas
• Mucous membranes
crusts, erosions
(often)
---'>
painful
• Spontaneous ulceration of skin, mucous
membranes (often eyes/lips)
• Round ulcerating lesions
2.5cm/lin diameter)
O
• Skin biopsy
OTHER DIAGNOSTICS
• Clinical history, suspected
• Starts on trunk -e rest of body
• Conjunctivitis (often accompanied
purulent discharge)
LAB RESULTS
by
(approx.
Arise on face, trunk, arms, legs, soles of
feet (scalp spared)
• Nikolsky's sign
(
agents
T_R_E~_;,-_M_EN_T
)
MEDICATIONS
• Analgesics (non-opioid for non-severe,
opioids for severe pain)
• Antihistamines
• Intravenous immunoglobulin
Infection control
• Culture-specific
antibiotic
initiation
OTHER INTERVENTIONS
• Transfer to burn/intensive
care unit
• Fluid support
• Oral feeding, nasogastric tube
• Room temperature 30-32°C/86-90°F
(minimize heat loss)
Infection control
• Sterile handling
• Skin disinfection
= Antiseptic
solution
• 48 hourly skin, blood, indwelling
line culture
Figure 3.3 An individual with toxic epidermal
necrolysis ten days after the onset of
symptoms.
19
I
afratafreeh.com exclusive
EPIDERM~
·,,
Figure 3.4 A histological section of skin
demonstrating epidermal necrolysis. The
epidermis is detached from the dermis and
the keratinocytes have undergone necrosis.
This can be seen in erythema multiforma,
Stevens-Johnson syndrom and toxic
epidermal necrolysis.
20
I
NOTES
~
NOTES
_,
HAIR-RELATED DISEASES
GENERALLY,WHAT ARE THEY?
(
PATHOLOGY & CAUSES
)
(
D_IA_GN_o_s,_s __
• See individual
• Conditions affecting either total number of
hairs/thickness of hair on body
)
diseases
• Scalp most commonly affected
(
T_R_E_AT_M_E_N_T
)
(__ SI_G_NS_&_S_Y_M_PT_O_M_s
)
• See individual
diseases
• See individual diseases
ALOPECIA AREATA
osms.i"l/a.lo eeio.-o.Teo.-lo.
(
PATHOLOGY & CAUSES
• Chronic localized hair loss, generally
scalp; autoimmune-related
)
on
(
s,_G_NS_&_SY_M_PT_O_M_s
• Usually smooth, circular patches of hair
loss, but can be any shape
• May occur at any age, but> 30 years old in
most cases; lifetime prevalence 2%
• Can be accompanied by nail changes
O Nail
pitting, roughening/longitudinal
fissuring of nail plate
CAUSES
• Associated with other autoimmune
conditions
O Psoriasis,
vitiligo, thyroid disease
• Exact mechanism
O
unclear;
hypothesized
T cells release cytokines, chemokines normal hair cycle disrupted - hair loss
• Spontaneous regrowth of hair possible,
often within one year
)
(
D_IA_G_N_os_,s
)
LAB RESULTS
RISI( FACTORS
• Genetic
°` Close family members.
history of
autoimmune conditions
• Biopsy (unclear cases)
O
°`
Peribulbar lymphocytic inflammatory
infiltrates characteristic
Follicular edema, cellular necrosis,
microvesiculation,
pigment incontinence
21
I
OTHER DIAGNOSTICS
• Based on timeline of events, physical
examination (exclamation point hairs)
O
O
O
Short, broken hairs around area of hair
loss
Narrower proximal than distal end
Dermatoscope
spot
(
may make hairs easier to
T_R_EA_~_M_EN_T__
)
• Treatment unreliable, temporary; no cure
MEDICATIONS
• lntralesional steroid injections
triamcinolone acetonide
of
Figure 4.1 The clinical appearance of the
scalp in a case of alopecia areata.
• Topical agents including 5% minoxidil
solution/topical steroids
TELOGEN EFFLUVIUM
osmsJl/ -lelogen-effluvium
(
PATHOLOGY & CAUSES
)
• Periodic episodes of increased hair
thinning/shedding
due to altered follicle
growth cycle
O Occurs
during follicles' telogen (resting)
phase
(
OTHER DIAGNOSTICS
• Determine timeline of stressors, recent
events, drug/medication usage, course/
characteristics of hair loss
• Hair-pull test
O Grasp 50-60 hairs
CAUSES
O
O
• May be related to
O
Recent stressor (e.g. major illness/
surgery)
O
Drugs/toxins
O
Nutritional deficiencies
D_IA_GN_O_s,_s
__
)
(
---->
tug lightly
If> 6-10 hairs extracted, test= positive
Telogen hairs confirmed by microscopic
examination
T_R_EA_~_M_EN_T
__
)
• Sometimes self-correcting
(__ s,_G_NS_&_SY_M_PT_O_M_s_)
OTHER INTERVENTIONS
• Non-scarring, diffuse < 50% hair loss
• Nail changes
O Deep grooved lines running
from side to
side may be present
• Reduce stressors, improve diet, handle hair
carefully
22
I
Figure 4.2 The clinical appearance
nails in a case of telogen effluvium.
of the
23
I
NOTES
NOTES
II
..
.
MALIGNANT TUMORS
GENERALLY, WHAT ARE THEY?
(
PATHOLOGY & CAUSES
)
• Malignant cutaneous lesions due to
abnormal/uncontrolled growth of epithelial
cells
BRESLOW DEPTH AS
SURVIVAL PREDICTOR
BRESLOW DEPTH
S YEAR SURVIVAL
Jn situ
95-100%
< lmm
95-100%
1-2 mm
80-96%
2.1-4 mm
60-75%
(_~SI_G_NS_&~SY_M_P_TO_M_S~)
• ~ one multiple visible cutaneous tumors
• Melanoma can present noncutaneously
(e.g. ocular, mucosal)
(..____
D_IA_GN_O_s,_s __
LAB RESULTS
(..____
Histological analysis
• Confirms diagnosis,
grade
)
establishes
tumor
establishes
tumor
T_R_EA_:T_M_EN_T
__
)
MEDICATIONS
• lmmunomodulators
SURGERY
Biopsy
• Confirms diagnosis,
grade
• Surgical excision
• Electrodesiccation,
curettage of lesion
OTHER DIAGNOSTICS
OTHER INTERVENTIONS
• Dermatological
dermatoscope,
• Radiation therapy
examination with
TNM staging
• Breslow thickness
O Distance
of tumor cell from basal layer
of epidermis
24
I
BASAL-CELL CARCINOMA
osmsJl/\>o.so.1-eell_eo.Teinomo.
(
PATHOLOGY & CAUSES
)
CAUSES
• Most common type of skin cancer; emerges
from basal cells found in lower epidermis
• UV radiation: direct DNA damage
(pyrimidine dimers) - alters DNA structure
- mutations, carcinogenesis if tumor
suppressor gene involved
• Slow growing, can infiltrate surrounding
tissue, rarely metastasizes
• Gorlin syndrome: numerous basal cell
carcinomas due to mutation of PTCH1 gene
TYPES
RISI( FACTORS
Nodular
• Arsenic exposure; immunodeficiency;
fair
skin, albinism; xeroderma pigmentosum;
risk increases with age; high exposure to
UV radiation
• Pearly circular cystic pigmented nodule
Infiltrative
• Invades dermis
(__ s,_G_NS_&_SY_M_PT_O_M_s_)
Micronodular
• Solid white-coloured
lesion
• Presents on face, periocular,
sun-exposed areas)
Morpheaform
• Flat white-yellowish
waxy lesion
lesion
, Pearly elevated patch of skin
Superficial
• Erythematous
trunk
• Newly discovered
neck, scalp (i.e.
plaque, usually
on upper
• Does not heal within four weeks
• Dimpled at midpoint
• Grows slowly
• May bleed (esp. when poked/knocked)
• Painless, may itch
• Dilated blood vessels (telangiectasia)
• Ulcerated lesion
= Brown-black
pigmentation
in crater of
lesion
(
D_IA_GN_O_s,_s __
)
LAB RESULTS
Figure 5.1 The clinical appearance of a
basal-cell carcinoma on the nose of an elderly
individual. The tumor is nodular with central
ulceration and pearly borders.
Skin biopsy/histopathology
• Basal cells form clusters called islands with
peripheral palisading nuclei
25
I
(..____
T_R_EA_:l"_M_EN_T
)
MEDICATIONS
• Topical 5-fluorouracil/imiquimod
SURGERY
• Electrodesiccation,
curettage; complete
surgical excision; cryosurgery; Mohs
surgery
OTHER DIAGNOSTICS
Figure 5.2 The histological appearance
of a basal-cell carcinoma. Malignant darkstaining, basaloid cells infiltrate the dermis.
There is clefting at the junction between the
tumor and the dermis.
• Radiation, photodynamic therapy
OTHER DIAGNOSTICS
• Dermatoscopy
O Scattered
vascular pattern,
telangiectasias,
hemorrhage-ulceration,
hypopigmented areas with blue-grey
ovoid nests, red dots/globules
MELANOMA
osms.i"l/ me lo.nomo.
(
PATHOLOGY & CAUSES
)
• Malignant skin cancer, arises from
melanocytes
• Occurs most commonly on skin
O Rarely:
mouth, eyes, gastrointestinal
tract
(GI)
• Can arise from
O
Preexisting
O
De novo lump: nodular melanoma
dangerous)
mole
Variants
• Superficial
spreading melanoma
• Lentigo maligna
(most
Figure 5.3 A malignant melanoma
pigment production.
exhibiting
melanoma
• Nodular melanoma
• Acral lentiginous
melanoma
26
Growth phases
O
• Radial growth phase (< lmm thick)
O
Grows laterally along epidermis,
superficial dermis; does not spread
• Histopathological
grade
Rarely metastasizes; good prognosis if
detected
• Vertical growth phase (> lmm thick)
O
O
O
Grows deeper into dermis,
beyond
• Dermatological
dermatoscope
CAUSES
for tumor
in MC1R. CDKN2A,
examination
using
n
Classic melanoma: mnemonic
O
Nodular melanoma: mnemonic EFG
-,
• DNA damage caused by ultraviolet (UV)
light exposure (e.g. sun, tanning beds)
ABCDE
MNEMONIC: ABCDE
Appearance of classic
melanoma
Asymmetry
Border irregularities
RISI( FACTORS
Color variation
• lmmunosuppression
• Numerous
evaluation
OTHER DIAGNOSTICS
Invasive, able to metastasize through
lymph/blood vessels
• Genetic mutations
BRAF genes
I
See tables: American Joint Committee
on Cancer Guideline for TMN staging of
melanoma
Diameter: 6 mm
moles
Enlargement
• Family history of melanoma
• Syndromes
-,
Dysplastic nevus syndrome, xeroderma
pigmentosum, albinism, Gorlin
syndrome
• Exposure/overexposure to UV light (e.g.
sun, tanning beds)
'
O
O
Esp. if blistering/occurring early in life;
more common in people with fair skin
MNEMONIC: EFG
Appearance
melanoma
of nodular
Elevated
Firm to touch
Growing
COMPLICATIONS
• Metastazes most commonly to lymph
nodes, skin, subcutaneous tissue - lungs,
liver, brain
(__ s,_G_NS_&_S_Y_M_PT_O_M_s_)
• New skin lesion/change pre-existing lesion:
color, shape, size irregularities; ulcerations,
pruritus, bleeding
• Nausea, vomiting, loss of appetite, fatigue
(
D_IA_GN_o_s,_s__
LAB RESULTS
)
Figure 5.4 The clinical appearance of a
malignant melanoma. It is darkly pigmented
with an irregular border.
Full-thickness, sentinel node biopsy
• Tumor staging
27
I
PRIMARYTUMOR (T)
T CATEGORY
REGIONALLYMPHNODES (N)
TMICkNESS
N CATEGORY
TO: no evidence of
primary tumor
0
Tis (melanoma in situ)
N/A
Tl
slmm
T2
> 1-2 mm
T3
> 2-4 mm
T4
NO
No regional
metastases detected
Nl
1
N2
2-3
N3
2:4
>4mm
MO
No evidence of distant metastasis
N/A
Mla
Metastasis to skin, soft tissue
(e.g. muscle/nonregional lymph node)
Mla{O): ! LDH
Mla(l): I LDH
Mlb
Metastasis to lung
Mlb(O): ! LDH
Mlb(l): f LDH
Mlc
Metastasis to non-central nervous
system (CNS) visceral sites
Mlc(O): ! LDH
Mlc(l): I LDH
Mld
(
# OF TUMORINVOLVEDREGIONAL
LYMPHNODES
Metastasis to CNS
T_R_EA_:l"_M_EN_T__
MEDICATIONS
• lmmunotherapy
in case of metastases
)
M ld(O): no change
Mlb(l): l LDH
OTHER INTERVENTIONS
• Early detection for good prognosis
(depends directly on depth of invasion)
• Radiation/chemotherapy
metastases
in case of
SURGERY
• Surgical excision
O Wide margin
excision (l-3cm of normal
tissue depending on depth of invasion)
• Excision if sentinel
node biopsy is positive
28
I
Figure 5.5 The gross pathology of the heart
in a case of metastatic melanoma.
SQUAMOUS-CELL
CARCINOMA (SCC)
osms.tl:/ sq_uo.mous-cell_co.Y-cinomo.
(
PATHOLOGY & CAUSES
)
• Second most common type of skin cancer
• Epidermal keratinocytes acquire antiapoptotic properties ---> frequent mitosis
RISI( FACTORS
• lmmunosuppression,
chronic UV exposure,
fair skin, albinism, xeroderma pigmentosa,
tobacco use (increases risk of lip/oral SCC),
arsenic exposure (rare)
CAUSES
• UV radiation
(e.g. sun, tanning
beds)
• HPV infection
• Genetic mutations
O
Deletion of tumor progression
(Tpl2) gene
locus 2
• Preceding skin lesions (e.g. actinic keratosis,
other melanomas)
O Actinic keratosis:
precancerous skin
lesion; rough, scaly patch caused by
chronic, long-term sun exposure
• Bowen's disease (AKA squamous cell
carcinoma in situ)
Figure 5.6 An ulcerated squamous cell
carcinoma on the nose of a middle-aged
individual.
29
I
COMPLICATIONS
OTHER INTERVENTIONS
• Significant
• Chemotherapy,
therapy
risk of metastasis
radiotherapy,
photodynamic
C__s,_G_Ns_&_sv_M_PT_O_M_s_)
• Most commonly found on sun-exposed
areas (e.g. head, nose, neck)
• Small rough scaly nodule (slow growing)
O
PRIMARYTUMOR(T)
T CATEGORY
Nodule expands - center necroses
- evolves into ulcer covered by red
growing plaque - frequently scales,
easily bleeds
• Chronic
draining
C
Tis
Tl
sinuses
D_IA_GN_O_SI_S
__
)
DIAGNOSTIC IMAGING
T CRITERIA
Carcinoma in situ
< 2 cm in greatest
dimension
T2
2-4cm
T3
> 4an
T4
Tumor with gross
cortical bone/marrow/
sku II invasion
CT scan
• Assess surrounding tissue invasion (soft
tissue, bones, lymph nodes), metastasis
Dermatoscopy, excisional/incisional biopsy
of subcutaneous tissue
• Microscopic features: hyperkeratosis,
nuclear atypia
REGIONALLYMPH NODES (N)
N CATEGORY
# OF TUMORINVOLVEDREGIONAL
LYMPH NODES
• See tables: American Joint Committee
on Cancer Guideline for TMN staging of
cutaneous squamous-cell carcinoma
NO
No regional
metastases detected
MRI
Nl
1 ipsilateral node s 3 cm
• Evaluate vital structures (neural, vascular
invasions)
N2
1 ipsilateral node 3-6 cm
N3
Metastasis in lymph node
>6cm
(
T_R_E~_~_M_EN_T
__
)
MEDICATIONS
• Topical immunomodulators
SURGERY
• Surgical
M CATEGORY
excision
• Mohs surgery: microscopic procedure
removing thin layers of affected tissue,
examining under microscope until cancerfree tissue reached
• Electrodessication,
DISTANT METASTASIS(M)
ANATOMIC.SITE
MO
No evidence of
distant metastasis
Ml
Distant metastasis
curettage
30
I
Figure 5.7 The histological appearance of
well-differentiated
squamous cell carcinoma
of the skin. It is composed of polygonal cells
with eosinophilic cytoplasm which produce
keratin pearls.
31
I
NOTES
II
..
NOTES
.
PAPULOSQUAMOUS DISORDERS
GENERALLY, WHAT ARE THEY?
(
PATHOLOGY & CAUSES
)
O
O
Papule: circumscribed,
skin < lcm/0.39in
D_IA_GN_o_s,_s
)
OTHER DIAGNOSTICS
• Heterogeneous skin disorders; scaly
papules, plaques
O
(..____
• Rash patterns
solid elevation of
C..____
Plaque: broad papule/confluence of
papules 2:: lcm/0.39in
Scale: dry/greasy laminated masses of
keratin
T_R_EA_:T"_M_EN_T
)
• May spontaneously
resolve
MEDICATIONS
CAUSES
• Topical (e.g. corticosteroids), nonsteroidal
anti-inflammatory
drugs (NSAIDs),
antihistamines
• Inflammation
(
SIGNS & SYMPTOMS
• See individual
)
disorders
• lmmunosuppressants,
acitretin)
retinoids
(e.g.
OTHER INTERVENTIONS
• Phototherapy,
colloid baths
LICHEN PLANUS
osms.i"l/liehe n-plo.nus
(
PATHOLOGY & CAUSES
• Self-limiting
°`
• Chronic inflammation in mucosal leslons=squamous cell carcinoma
chronic dermatosis
• Multifactorial pathogenesis
O Environmental
tactors e- genetic
aberrations of immune system
°`
)
CDS+ T cells respond to altered
antigens in basal epidermidis/
dermoepidermal junction
Causal agent identified: lichenoid
reaction (e.g. drugs)
C.___s,_G_Ns_&_sY_M_PT_O_M_
)
• Shiny, flat-topped, pink-purple, polygonal
pa pules coalesce, form plaques with red
scales
• Wickham striae (pathognomonic)
, Interspersed grey-white lace-like
pattern of lines
32
• Symmetrical peripheral distribution, esp.
on flexural surfaces (e.g. wrists, elbows,
ankles, shins)
O
• Severe pruritus
• Koebner phenomenon
O
Skin lesions
induced by local trauma
OTHER DIAGNOSTICS
• Nail involvement
10% of individuals; subungual
thickening/hyperpigmentation,
thinning/
ridging/ grooving of nail plate, pterygium
formation, onycholysis
0
• Mucosal
O
O
O
• Skin biopsy
O
Rule out secondary malignancies
(...____
Asymptomatidburning
pain
Mostly bilateral,
T_R_E_AT_M_E_N_T __
)
sensation.severe
• Cutaneous lesions spontaneously resolve in
nine months, longer for mucosa I lesions
inner cheeks
O
Leaves area of hyperpigmentation
Various types may coexist; oral variant
of Wickham's striae, erosive/ulcerative,
papular, plaque-like,
atrophic, bullous
MEDICATIONS
Possible secondary Candida infections
• Reduce symptoms, shorten duration
• Esophageal
O
• Rash pattern distinctive at skin examination
involvement
• Oral mucosa
O
I
Basal keratinocytes degenerate,
appear like stratum spinosum cells
(squamatization)/undergo
necrosis,
become incorporated into inflamed
papillary dermis (Civatte bodies)
mucosa
• Antihistamines
Dysphagia/odynophagia
• Retinoids,
(pruritus),
corticosteroids
immunosuppressants
• Genital mucosa (glans penis, vulva/vagina)
O
Lower urinary tract symptoms,
dyspareunia, itching in individuals
are biologically female
'
OTHER INTERVENTIONS
who
• Occlusive dressings
• Phototherapy
O Ultraviolet
A radiation
MNEMONIC: G Ps
Clinical presentation of lichen
planus
Planar
Purple
Polygonal
Pruritic
Pa pules
Plaques
(
D_IA_GN_o_s,_s __
)
LAB RESULTS
• Typical microscopic
O
O
features
Acanthosis: epidermidis thickening
Interface dermatitis: continuous
infiltrate of lymphocytes along
dermoepidermal
junction sawtoothing {dermoepidermal
interface
with zig-zag contour)
Figure 6.1 Lesions on the shins of an
individual with lichen planus.
33
I
Figure 6.2 The histological appearance
of lichen planus. There is a lymphocytic
infiltrate at the junction between the dermis
and epidermis which is known as interface
dermatitis.
PITYRIASIS ROSEA
osms.i"l/ i-l14Tio.sis-Toseo.
(
PATHOLOGY & CAUSES
• Self-limiting
)
acute dermatosis
• Unknown etiology; may be viral in origin,
related to human herpesvirus 7 (HHV7)
• Trunk, neck, upper arms, thighs; "Christmas
tree" progression
, Across chest, then rib-line
• Pruritus
• Systemic
O Low-grade
fever, headache,
fatigue
nausea,
(__ SI_G_NS_&_S_Y_M_PT_O_M_s_)
• Upper respiratory tract infection may
precede rash
• "Herald patch"
O
°`
O
Solitary oval red plaque, usually located
on trunk
First skin lesion
Spreads with central clearing, fading in
2-10 days
• 1-2 weeks after herald patch, multiple
round/oval pink (white individuals of
European descent)/dark brown {black
individuals
of sub-Saharan African descent)
plaques with central scale appear
Figure 6.3 A herald patch is often seen at
the onset of pityriasis rosea. It is a slightly
raised, erythematous patch with superficial
scaling.
34
(..__ __
I
D_IA_GN_O_s,_s
__
)
LAS RESULTS
• Skin biopsy (rare)
• Microscopic
O
O
features
Dyskeratosis: abnormal premature
keratinization
Extravasated erythrocytes within dermal
papillae
OTHER DIAGNOSTICS
• Rash pattern
O Distinctive
at skin examination
(..__~~~~~~~~~~~~~~
TREATMENT
• May spontaneously
)
disappear in 6-8 weeks
Figure 6.4 The clinical appearance of
pityriasis rosea on the torso of an adult male.
MEDICATIONS
• Antihistamines
for pruritis
OTHER INTERVENTIONS
• May spontaneously
disappear in 6-8 weeks
• Colloid baths for pruritis
PSORIASIS
osmsJl/psoTio.sis
(
PATHOLOGY & CAUSES
• Chronic dermatosis
of skin, nails, joints
• Multifactorial pathogenesis
O Environmental
factors e- genetic
abnormalities of immune system
°`
CD4· THl, TH17, CDs+ T cells collect
in epidermis, secrete cytokines (e.g.
IFN-gamma, TNF-alpha, IL-17, IL22), growth ractors-« abnormal
microenvironment ("cytokine soup")
accelerates keratinocyte proliferation
----. defective keratinization, epidermal
thickening
• Unpredictable
progression
)
spontaneous remissions, sudden
exacerbations (e.g. may worsen in winterlack of sun, humidity)
O
Skin abrasion, infection, drugs (e.g.
lithium, beta blockers, chloroquine),
psychosocial stress e- exacerbations
• 10-15%
arthritis
of individuals
develop psoriatic
= Inflammatory
O
cells in joint tissue-»
synoviocyte proliferation
Surrounding connective tissue also
involved (e.g. enthesitis)
with
35
I
TYPES
joints of hands, feet most affected,
followed by sacroiliac bone, spine
• Plaque psoriasis, AKA vulgar psoriasis;
90%
, Fusiform swelling of digits (dactylitis);
aka "sausage digits"
• Guttate (eruptive), inverse (flexural),
pustular, erythrodermic
(
, Aggressive disease with joint damage,
malformations not common
)
SIGNS & SYMPTOMS
(
D_IA_GN_O_s,_s __
)
• Plaque
O
O
O
Pink, salmon-colored
papules/plaques
covered by loosely adherent silver-white
scales
Any area of body, esp. extensor surfaces
(e.g. knees, elbows). lumbosacral area,
scalp, glans penis
Itching is mild/absent
• Nail involvement
O
O
°`
O
Subungual
Yellow-brown discolorations
(resembling oil slicks)
of nail plate
separation of nail plate
Drop-like appearance, associated with
group A streptococcus
• Inverse (flexural)
Skin folds
• Pustular
Blisters filled with non-infectious
pus
• Erythrodermic
O
O
Total body inflammation, skin exfoliation,
severe itching, swelling, pain; ability to
regulate temperature, perform barrier
functions impaired; possibly fatal
May develop from any type (e.g.
plaque during corticosteroid rebound
phenomenon)
• Auspitz sign
O
Pinpoint bleeding appears when scale
removed
• Koebner phenomenon
°` Characteristic
skin lesions induced
local trauma
by
• Psoriatic arthritis
O
°`
O
Inflammatory arthritis: pain. red
overlying area. swelling, hot to touch
Frequently occurs after onset of rash
Asymmetric peripheral
in adjacent bone marrow and
LAB RESULTS
• Skin biopsy (rare)
• Acanthosis
, Epidermidis
O
O
• Erosive changes, "fluffy" periostitis,
presence of new bone formation
of nail plate
• Guttate (eruptive)
o
X-ray
• Inflammation
soft tissues
thickening
Onycholysis:
from bed
• For psoriatic arthritis
MRI
in 30% of individuals
Crumbling/ridging/pitting
DIAGNOSTIC IMAGING
oligoarthritis;
thickening
• Parakeratosis
, Keratinization (retention of nuclei in
stratum corneum)
• Neoangiogenesis with tortuous blood
vessels below stratum corneum
• Accumulation of neutrophils in superficial
epidermis (spongiform pustules), in stratum
corneum (Munro microabscesses)
• Clinical diagnosis
, Psoriasis features, clinical pattern of
joint involvement
• Confirmation
, Elevated inflammatory markers.
negative rheumatoid factor (RF). anticyclic citrullinated peptide antibody
(anti-CCP)
OTHER DIAGNOSTICS
• Rash pattern
, Distinctive
at skin examination
• Differentiation from rheumatoid arthritis
, Minority show polyarthritic pattern with
no skin lesions; note asymmetry, distal
interphalangeal
joint involvement, mild
joint destruction
36
(
I
T_R_E~_~_M_EN_T
)
• No definitive cure
• Avoid triggers
MEDICATIONS
• Topical corticosterotds-e
antiinflammatory, antiproliferative
• Vitamin D derivatives (calcipotriene,
calcipotriol) ----. limit keratinocyte
proliferation
• Anthralin----.
suppresses
proliferation
Figure 6.5 A large psoriatic plaque on the
upper limb.
• Combination therapy is most effective
(e.g. betamethasone dipropionate +
calcipotriene)
• Affected area > 10%, unsuccessful topical
treatment, involves face, hands, genitals
• lmmunosuppressant
O
Methotrexate,
• Systemic
O
cyclosporine
retinoids
Acitretirr-e
cytokines
inhibits pro-inflammatory
• Biologic therapy
O
Anti-TNF (infliximab, etanercept,
adalimumab), T-cells (alefacept), IL12/23 (ustekinumab)
• NSAIDs, immunosuppressant/biologic
therapy
°`
For psoriatic arthritis
OTHER INTERVENTIONS
• Topical
°` Coal
tar----. inhibits cellular mitotic
activity, proliferation
O
Moisturizers,
emollients
• Phototherapy
O
Ultraviolet
O
A radiation
Often combined with topical tar/
systemic acitretin/psoralen/methoxsalen
O
lmmunosuppressive,
antiproliferative
Figure 6.6 Psoriasis affecting the hand.
37
I
NOTES
r4
_,
NOTES
PIGMENTATION DISORDERS
GENERALLY, WHAT ARE THEY?
(
PATHOLOGY & CAUSES
)
(.._____
D_IA_GN_O_SI_S __
• Skin loses pigment,
becomes lighter/darker
LAB RESULTS
• Pigment-producing
cells (melanocytes)
• Skin biopsy
O
O
O
Expected number,
(melanin)
overproduce
pigment
Higher in number, produce expected
melanin
Destroyed, no melanin produced
CAUSES
• Autoimmune
destruction
disorders -
melanocyte
• Genetic testing
OTHER DIAGNOSTICS
• Dermatological physical examination
(e.g. dermoscopy)
(.._____
T_R_EA_~_M_EN_T
__
)
• Usually no cure
• Long periods of sun exposure
• Genetic mutations
MEDICATIONS
(__ s,_G_NS_&_SY_M_P_TO_M_s_)
• Changes in skin pigmentation
symptom
)
only
• Some disorders (esp. produced by sun
overexposure) heighten risk of skin cancer
• Topical medication
, Most respond to steroids
, Depigmentation agents effective for
hyperpigmentation disorders
SURGERY
• For some lesions
OTHER INTERVENTIONS
• Sun avoidance,
overexposure
if caused by ultraviolet
(UV)
38
I
ALBINISM
osmsJl/ e1l\>inism
(
PATHOLOGY & CAUSES
)
• Congenital condition; skin, eyes, hair
partially (hypomelanistic
albinism)/
completely (amelanistic albinism) devoid of
pigment
• Lack of pigment problems
O
(__ SI_G_NS_&_SY_M_PT_O_M_s_)
• Complete/partial
pigmentation
• Light yellow/white
of skin
hair
• Light eye colour
dermatological
Increased risk of sunburn,
absence
• Light blue (partial pigment production)
• Pink (complete absence
production)
skin cancer
of pigment
• Visual problems
TYPES
• Visual development in fetus highly
dependent on melanin production;
abnormal arrangements in optic nerves
fibres (e.g. abnormal optic chiasm)
Oculocutaneous albinism (OCA)
• Eyes, skin; possibly hair
• Autosomal
recessive transmission
O
• Seven different subtypes; OCAl, OCA2
most common
O
O
OCAl: defect in gene for enzyme
tyrosinase (TYR)
OCA2: defect in P gene (membrane
transporter, moves amino acid tyrosine)
• Rufous oculocutaneous
o
°`
O
albinism
Specific subtype of OCA
Common in people of sub-Saharan
African descent
O
(
Severe sensitivity
to light
Poor visual acuity due to foveal
hypoplasia
Amblyopia/nystagmus: poor
coordination between eye, brain
D_IA_GN_O_SI_S
__
)
LAB RESULTS
• Genetic testing
• Identify defective gene, allotype
Ocular albinism (OA)
• Only eyes
• OAl most common subtype (AKA
Nettleship-Falls
syndrome)
OX-linked
recessive inheritance
O
OTHER DIAGNOSTICS
• Physical examination
• Family history
Lack of pigment in retinal epithelium
CAUSES
• Hereditary/genetic
O Autosomal/X-linked
Recessive inheritance pattern - defect
leading to lack/absence of enzyme
in melanin synthesis pathway hypopigmentation/depigmentation
• Chediak-Higashi syndrome
O
O
Rare; malfunctions in lysosomal
trafficking regulator gene (CHSl/LYST)
39
I
afratafreeh.com exclusive
(
T_R_E~_~_M_EN_T
)
• No cure
SURGERY
• Manage strabismus,
nystagmus
OTHER INTERVENTIONS
• Lifestyle management
O
O
Avoid sunburn
Regular dermatological,
ophthalmological
check-ups
O
Visual rehabilitation
O
Glasses/contact
Figure 7.1 A baby with albinism.
lenses
PITYRIASIS ALBA
osmsJI:/ pi"l14Tio.sis-o.l\,o.
(
PATHOLOGY & CAUSES
• Common, irregularly hypopigmented skin
condition: slightly scaly patches, macules
)
COMPLIC ATIONS
• Benign
condition
(__ SI_G_NS_&_S_Y_M_PT_O_M_
O
Lesion diameter: 0.5-5cm/0.2-2in
O
Irregular borders
• Often asymptomatic,
Most common on face, neck, shoulders,
upper arms
May resolve spontaneously after
puberty
(
O
O
CAUSES
• Unknown etiology: eczema-related postinflammatory hypopigmentation
(possible
relation)
D_IA_GN_O_SI_S
__
)
OTHER DIAGNOSTICS
• Wood's lamp examination:
patches
• Microscopy:
(
RISI( FACTORS
may itch/burn
! melanocyte
hypomelanosis
number, size
T_R_E~_~_M_EN_T
• Atopy
MEDICATIONS
• Sun exposure
• Hydrocortisone (topical), calcineurin
inhibitors, emollients
• Frequent bathing
• Biologically
)
male
• Children/adolescents
> adults
40
I
VITILIGO
osmsJl/ vi-1:iligo
(
PATHOLOGY & CAUSES
• Pigmentation
lose pigment
)
disorder; parts of skin, hair
• Melanocytes destroyed ----. white patches of
depigmented skin
O
Sharp margins on depigmented
• May be autoimmune
patches
• Areas innervated
cord
by dorsal
roots of spinal
stable over time
• Can be associated with alopecia
• Symmetrical;
D_IA_GN_O_SI_S
)
• Rule out autoimmune/inflammatory
disorders
OTHER DIAGNOSTICS
• Ultraviolet light (Wood's lamp): lesions;
vitiligo turns blue
Non-segmental
appearance of new patches
• Multiple subtypes
Vitiligo universalis: most severe, almost
no pigmented skin remains
O
Generalized:
O
Focal: smaller,
O
Acrofacial:
O
Mucosal: only mucous membranes
most common
(
T_R_E~_~_M_EN_T
)
• No cure
localised patches
hands, face
MEDICATIONS
• Topical immune system suppressing
medication
• Glucocorticoids
CAUSES
• Autoimmune
destruction
• Patches grow over time (non-segmental
subtype)
(
Segmental
O
• Depigmented skin patches only symptom,
usually on extremities
condition
TYPES
• Unilateral;
(__ SI_G_NS_&_S_Y_M_PT_O_M_s_)
disorder
e-
melanocyte
• Calcineurin
inhibitors
OTHER INTERVENTIONS
RISI( FACTORS
• Ultraviolet
• Medical/family history of autoimmune
conditions
O Hashimoto's
thyroiditis
• Skin camouflage
O
Type I diabetes
O
Systemic lupus erythematosus
Celiac disease
°`
O
light therapy (phototherapy)
(e.g. makeup)
mellitus
Addison's disease
41
I
Figure 7.2 The clinical
affecting the hands.
appearance
of vitiligo
42
I
NOTES
,
NOTES
SklN s SOFT TISSUE
INFLAMMATION & INFECTIONS
,
•
GENERALLY,WHAT ARE THEY?
c
PATHOLOGY & CAUSES
)
c
DIAGNOSIS
• Inflammation of epidermis, dermis,
underlying tissues
LAB RESULTS
CAUSES
OTHER DIAGNOSTICS
• Infections, autoimmune response
• Mostly clinical,
RISI( FACTORS
c
• Impaired
• Tissue cultures,
skin barrier
)
Gram stain
based on presentation
TREATMENT
• Pressure
MEDICATIONS
• Friction
• Infections: antimicrobials
)
• Exposure to infectious agents
• lmmunosuppression
OTHER INTERVENTIONS
• Dressings, ointments
COMPLICATIONS
• Cryotherapy
• Infection
O Local
or systemic disease
c
SIGNS & SYMPTOMS
• See individual
• Curettage
)
disorders
43
I
ACNE VULGARIS
osms.i"l/ o.ene_ vu Igo.Tis
(
PATHOLOGY & CAUSES
)
• Common inflammatory skin disorder
affecting hair follicles, sebaceous glands
• May involve comedones,
cysts, scars
• Especially
O
O
papules,
affects individuals
pustules,
who are
Biologically male, with hormonal
disorders producing androgens
(e.g. polycystic ovarian syndrome),
adolescent
Symptoms decrease with age
TYPES
• Infection
, Follicle colonization by
Propionibacterium acnes
• Medications
O
Lithium, glucocorticoids,
steroids
anabolic
• Polycystic ovarian syndrome
• Stress
COMPLICATIONS
• Cosmetic
, Scars, hyperpigmentation,
pyogenic
granulomas, osteoma cutis
• Psychiatric
O
Low self esteem, depression
Mild
• Occasional, comedones, inflammatory
papules, pustules
Moderate
• Multiple
pustules,
nodules occur on trunk
Severe
• Cystic, large nodules predominant, with
persistent involvement of trunk; scarring
CAUSES
• Androgen stimulates sebaceous follicles
to overproduce sebum ----> follicles become
blocked
• Hyperkeratinization
of epithelium ---->
accumulation
----> follicular blocking ----> debris
accumulates further -e skin follicles rupture
• Propionibacterium acnes replicates
within follicle---->
releases lipase ----> sebum
converted to free fatty acids ----> release of
cytokines ----> inflammation
Figure 8.1 Acne vulgaris affecting the face of
an adolescent male.
RISI( FACTORS
• Genetic predisposition
• Oil-based
skin products
• Hormonal
imbalance
44
SIGNS & SYMPTOMS
(
)
• Papules, pustules, painful nodules (cysts)
on face, neck, chest, back
Mild to moderate
• Closed comedones
• Benzoyl peroxide, retinoid
• Erythema
• Add topical antibiotic (clindamycin) for
synergistic effect with benzoyl peroxide
(
D_IA_GN_O_SI_S
)
Severe
• Oral isotretinoin decreases sebum
production, bacterial proliferation,
inflammation
OTHER DIAGNOSTICS
• Clinical
I
• In case of comedonal acne, use azelaic
acid, salicylic acid as anti-inflammatory,
antibacterial,
antiproliferative agent
presentation
• Avoid using tetracycline due to sun
sensitivity
(
T_R_E~_~_M_EN_T
)
OTHER INTERVENTIONS
MEDICATIONS
• Clean skin with gentle agents
• Target sebum production, inflammation,
bacterial/follicular
proliferation
• Comedones
extraction
• Pigmentation
Mild
O
• Benzoyl peroxide treats Propionibacterium
acnes
O
• Add topical retinoids to prevent follicular
proliferation
O
Topical retinoid, azelaic acid, chemical
peels
Photodynamic treatment with lasers
(removes superficial layers of skin)
Dermabrasion
irritate skin)
(treatment of scars; may
CELLULITIS
osms.i-1:/eelluli-1:is
(
PATHOLOGY & CAUSES
)
O
O
• Non-necrotizing
inflammation of dermis,
subcutaneous tissue, typically caused
by streptococci (S. aureus, S. pyogenes);
usually unilateral
• Skin breach: trauma; dry, fissuring
skin; ulcers - bacteria invade skin,
subcutaneous tissue
• Common locations: face, legs; may affect
arms
• Other locations: causes vary
O
Orbital cellulitis: originates from trauma,
sinuses, hematogenous spread
O
Abdominal wall cellulitis: morbid obesity
causes bacteria to enter skin sores
Buccal cellulitis: spread from tooth
infection
Perianal cellulitis: affects all
demographics
TYPES
• Purulent
°` Furuncles
(inflamed follicles), carbuncles
(accumulation
of furuncles), abscesses,
cysts
• Non-purulent
O
Superficial cellulitis,
erysipelas
45
I
RISI( FACTORS
(..____
• Skin inflammation
Abrasion: wounds, eczema, radiation,
broken skin between toes
O
DIAGNOSTIC IMAGING
• Lowered immunity
Ultrasound
Diabetes mellitus, alcohol
older age
O
D_IA_GN_O_SI_S
)
abuse, HIV,
• Subcutaneous
fat separates into lobules
, Cobblestone
appearance
• Skin infection
Tinea, impetigo, varicella,
O
rash
• Edema
O Lymphatic
obstruction, venous
insufficiency
• Obesity
COMPLICATIONS
• Recurrence, abscess formation,
fasciitis, osteomyelitis, sepsis
(
necrotizing
)
SIGNS & SYMPTOMS
• Fever, chills
• Localized inflammation
O
Swelling
O
Warmth
LAB RESULTS
Erythema with unclear borders (contrast
to erysipelas-clear demarcations)
O
• Complete blood count (CBC)
, j inflammatory markers: j (-reactive
protein (CRP), l erythrocyte
sedimentation rate (ESR), t WBC count
• Wound, blood cultures
Often painful
O
• Enlarged lymph nodes
• Purulent cellulitis
infection
associated
Figure 8.2 An ultrasound scan of the right
lower limb demonstrating the cobblestone
appearance of subcutaneous
edema, in this
case secondary to cellulitis.
with S. aureus
= Identify
,.
..... .
. . . .•. j:'..
\
•
.
•
':
.
.. •..
..
I
.. ~· ! "·/
: ;:
•
•
"!
...
...
, .;
::·._
·:· . .' .
:....·\. :\J.'
.
i/-:·
,. ..
,
•
•
·...
,
J
. .:. .
.
',
.
(
...
. ~ ..
: y· .....
·,·
-.. ..· .·.:... .. . ."'
.. ';
. t.....:..·'" ", -'--"'
Figure 8.3 An individual
left leg.
,.'
.
with cellulitis
:
.
causative microbe
OTHER DIAGNOSTICS
• Clinical presentation
, Spreading inflammation
subcutaneous tissues
(
of skin/
T_R_E~_~_M_EN_T
)
MEDICATIONS
• Antibiotics: second generation penicillins,
first generation cephalosporins;
for MRSA
vancomycin
of the
OTHER INTERVENTIONS
• Immobilization,
elevation,
dressings
• Drain abscess
46
I
ERYSIPELAS
osms.i"l/ e,-14sipelo.s
(
PATHOLOGY & CAUSES
)
• Vesicles may be present; may be bright,
salmon red
• Acute, non-necrotizing infection of upper
dermis, superficial lymphatics; usually
unilateral
• Well-defined demarcation between normal,
infected tissue; non-purulent
• Usually caused by streptococci;
Streptococcus pyogenes
• Elevated, warm, painful rash called "forest
fire rash" (because it's reddest at border)
• Inflammation
lymphangitis
of regional lymph nodes,
in chronic infection
most often
RISI( FACTORS
• Very young/old age
• Breaks in skin
O
Abrasions, trauma, eczema, radiation,
bites
• Lowered immunity
O
Diabetes mellitus, alcohol
older age
abuse, HIV,
• Skin infection
O
Tinea, impetigo, varicella,
rash
• Edema
O Lymphatic
obstruction, venous
insufficiency
Figure 8.4 Erysipelas affecting the face of an
elderly individual.
• Obesity
COMPLICATIONS
• Lymphedema
drainage
(
due to impaired lymphatic
LAB RESULTS
• Necrosis
• Blood test
• If spread hematogenously to other areas
O Arthritis,
osteomyelitis, necrotizing
fasciitis, glomerulonephritis
(
SIGNS & SYMPTOMS
D_IA_G_N_OS_IS)
CBC: j CRP. l ESR, l WBCs;
antistreptolysin titer O shows
streptococcal involvement
• Wound, blood culture
°`
)
OTHER DIAGNOSTICS
• Initially, general infection symptoms
°` Fever,
chills, headache, fatigue
• Clinical presentation
• Lesions
O Mostly on legs,
but may be found on
face, arms, fingers. toes
47
I
(..____
T_R_E~_~_M_EN_T
)
MEDICATIONS
• Antibiotics: oral penicillins/macrolides,
vancomycin for MRSA, intravenous (IV)
route in severe infection
FOLLICULITIS
osms.l"l:/follieuli-1:is
(
PATHOLOGY & CAUSES )
• Hair follicle inflammation
usually infectious cause
(pyoderma),
COMPLICATIONS
• Recurrence
• Furunculosis
, Deep infection of hair follicle - evolves
into swollen nodule, may coalesce into
carbuncles
• May also be due to persistent trauma
(mechanical folliculitis)
• Pathogen enters hair follicle inflammatory inflammatory response infection causes a perifollicular infiltrate of
lymphocytes, neutrophils, macrophages pustule formation
(
SIGNS & SYMPTOMS
• Many small pustules, papules in areas of
hair growth (e.g. face, legs, arms, back)
O
CAUSES
O
• Bacterial
O S. aureus,
Pseudomonas aeruginosa
(hot-tub folliculitis)
• Viral
O
Gram-negative infections more common
on the face (areas of acne)
Methicillin resistant S. aureus (MRSA)
more common on the front trunk
• Does not appear in areas without hair
growth (palms of hands, soles of feet)
Tinea barbae
• Rarely
O Autoimmune;
O
Typical in groin, armpits
• Itching, redness: often tender
Herpes simplex virus (HSV)
• Fungal
O
)
• Sycosis vulgaris
O
oily skin in factory workers
Multiple pustules on chin, upper lip;
caused by S. aureus infection after
shaving
RISI( FACTORS
• Swimming pools, hot tubs
• Shaving against hair growth, tight
clothes causing friction. profuse sweating
(hyperhidrosis)
• Use of antibiotics,
corticosteroids
acne medication.
topical
• Upper respiratory
presence of S. aureus
(
D_IA_GN_O_SI_S
)
LAB RESULTS
• Gram stain, wound culture performed for
treatment-resistant
individuals
• Skin biopsy
, Differentiation from other skin disorders
in persistent folliculitis
48
I
OTHER DIAGNOSTICS
• History
O
Risk behavior/predisposition
• Clinical presentation
(
T_R_E~_~_M_EN_T__
)
MEDICATIONS
• Topical antibiotics: mupirocin, clindamycin
• Oral antibiotics: tetracycline,
O
Used in extensive
cephalosporin
involvement
• MRSA treatment: trimethoprim/
sulfamethoxazole,
clindamycin, tetracycline
• Fungal treatment: fluconazole,
Figure 8.5 The clinical
folliculitis.
appearance
of
itraconazole
• Viral treatment: acyclovir, valacyclovir,
famciclovir
OTHER INTERVENTIONS
• May resolve spontaneously
• Warm compress with antiseptic
use
• Loose fitting clothing; avoiding shaving
HIDRADENITIS SUPPURATIVA
osms.i"l/hid To.deni-lis-suppu To.-livo.
(
PATHOLOGY & CAUSES )
• Chronic, pus-producing
disorder
O
dermatological
AKA acne inversa
• Dysfunctional hair follicles/apocrine sweat
glands ---> pore clogging ---> inflammation --->
painful abscesses
CAUSES
RISI( FACTORS
• Obesity, tight clothes, smoking, deodorant
use, shaving
• More common for biologically-female
individuals
COMPLICATIONS
• Scarring, bacterial infection, interstitial
keratitis, sinus formation, fistula formation;
squamous cell carcinoma (chronic lesions);
depression
Environmental
• Skin/clothes friction, hormonal changes,
sweating, humidity
(__ SI_G_NS_&_S_Y_M_PT_O_M_s_)
Genetic
• Red inflamed areas, painful bumps that
drain with pus
• Apocrine gland dysfunction,
disorders
cellular
• Presence of double comedones
• Mostly in axilla, groin, under breasts
49
I
(..____
D_IA_GN_O_SI_S
)
OTHER DIAGNOSTICS
• Sartorius/Hurley's staging systems
(determines severity; guides treatment)
O
O
T_R_E~_~_M_EN_T
)
MEDICATIONS
Clinical presentation
O
(..____
Stage I: solitary/multiple isolated
abscess formation without scarring/
sinus tracts
Stage II: recurrent abscesses; lesions
may be single/multiple, widely
separated; sinus tract formation
Stage Ill: diffuse, regional involvement
across; multiple interconnected sinus
tracts, abscesses
• Corticosteroids, anti-androgen medication,
oral antibiotics, tumor necrosis factor (TNF)
inhibitors to ! inflammation
SURGERY
• Incision, drainage; sinus tract opening
OTHER INTERVENTIONS
• Clean affected area
• Laser treatments remove lesions, scarring
Behavioral
• Smoking cessation, weight loss
IMPETIGO
osms.i"l/hnpe-ligo
(
PATHOLOGY & CAUSES )
• Highly infectious skin infection; affects
superficial epidermis
°` Commonly
affects children
O
Skin-to-skin
COMPLICATIONS
• Cellulitis, poststreptococcal
glomerulonephritis
(
SIGNS & SYMPTOMS
spread possible
• Contact with carrier - pathogen enters
intact/non-intact skin - incubation lesion formation, spread over body through
scratching
• Commonly caused by S. aureus, S.
pyogenes
TYPES
• Nonbullous
• Nonbullous
, Most common
, Red bump - blister - blisters rupture,
ooze, form crusts - characteristic
yellow scab formation
• Bullous
O Bullae
on limbs, trunk
O
Not painful
O
Ruptured bullae become covered with
thin, brown crust
• Bullous
• Ecthyma
• Ecthyma
Deeper nonbullous
limbs
, Painful
O
RISI( FACTORS
• Higher incidence in warm, humid climates
• Eczema, HSV, diabetes mellitus,
malnutrition
)
O
impetigo appears on
Evolves into yellow scabs
• Fever (rare); blisters may be painful, itchy
• School, daycare
50
I
(-~~D_IA_G_N_OS_IS~~--)
LAS RESULTS
• Lesion culture
O
Identify pathogen, adjust treatment
OTHER DIAGNOSTICS
• History
• Physical
exam
(-~~TR_E_AT_M_E_N_T~
__ )
MEDICATIONS
• Topical antibiotic
• Penicillins
• In case of MRSA. use trimethoprim/
sulfamethoxazole
OTHER INTERVENTIONS
• Clean with antiseptic to prevent spreading
• Topical antibiotic
O
O
d
Figure 8.6 Impetigo on the back of the neck
of an adult male.
Penicillins
In case of MRSA use trimethoprim/
sulfamethoxazole
NECROTIZING FASCIITIS
osms.i"l/ neero-lizing_fo.seil"lis
( PATHOLOGY & CAUSES )
• Potentially
O
life-threatening
infection
Progressive destruction of deep soft
tissue (subcutaneous fat, muscle fascia)
• Bacteria spread via subcutaneous tissue
- release exotoxins - tissue destruction
spreads along fascial planes
TYPES
Type I: polymicrobia
l
• Causes: combination of aerobic, anaerobic
bacteria
O Most common
anaerobes: Bacteroides,
Clostridium, Peptostreptococcus
' Enterobacteriaceae: Escherichia coli,
Klebsiella, Proteus. Enterobacter
' Facultative anaerobic
streptococci
• Common sites
O Perineum
(Fournier's gangrene):
impaired gastrointestinal/urethral
mucosa I integrity - spreads to anterior
abdominal wall; gluteal muscles;
scrotum. penis (in biological male); labia
(in biological female)
°`
Cervical (head, neck): impaired
oropharynx mucosa (often related to
dental/odontogenic infection) - spreads
to face, neck, mediastinum
51
I
Type II: monomicrobial
(
• Causes: Group A Streptococcus,
other beta-hemolytic streptococci,
Staphylococcus aureus
)
SIGNS & SYMPTOMS
Overlying skin
• May appear normal initially
Type Ill: saltwater infection
• Later
, Warmth, erythema/violet/purple
(violaceous). woody induration,
necrosis
• Cause: Vibrio vulnificus
• Rare
Type IV: fungal infection
• Bullae; may fill with serosanguinous
• Subcutaneous
anaerobes)
RISI( FACTORS
• lmmunosuppression
HIV, diabetes, cirrhosis, corticosteroid
use
• Peripheral vascular disease
O
fluid
(if infection with
Systemic findings
• Pain
O Often out of proportion
to exam findings
• l pulse
• ! perfusion (motling, pallor, altered level of
• IV drug abuse
consciousness)
• Childbirth
• Exposure of open wound to fresh/salt
water, swimming pools, hot tubs
• Lemierre syndrome (septic
thrombophlebitis located in jugular
emphysema
• Fever
• Trauma
O Injury,
surgery
• Ludwig's angina (submandibular
infection)
edema,
region
• Hemodynamic
(..____
instability
(! BP)
D_IA_GN_O_SI_S
)
DIAGNOSTIC IMAGING
vein)
CT scan
COMPLICATIONS
• Shock
• Organ failure
• Potentially fatal
• Subcutaneous
planes
gas visualized in fascial
LAB RESULTS
Blood
• l WBCs, left shift; l creatine
phosphokinase;
! hemoglobin, l glucose, !
sodium
Urine
• Proteinuria
Gram stain, cultures of skin
• Debrided tissue identifies organism(s)
Figure 8.7 Necrotizing fasciitis on the left
leg. The dark areas represent progression to
necrosis.
OTHER DIAGNOSTICS
• Laboratory Risk Indicator for Necrotizing
Fasciitis (LRINEC) score
, Score = 6: j suspicion of necrotizing
fasciitis
, Score= 8: strongly predictive
52
I
Figure 8.9 A histological section of
subcutaneous tissue in a case of necrotizing
fasciitis showing an inflammatory infiltrate in
the fascia leading to necrosis.
(
T_R_E~_;,-_M_EN_T
__
)
MEDICATIONS
• Empiric IV antibiotics
°`
Figure 8.8 A CT scan in the coronal plane
demonstrating the presence of gas in the
fascia I planes of the leg, consistent with a
diagnosis of necrotizing fasciitis.
Carbapenem/beta-lactam-betalactamase inhibitor+ vancomycin/
linezolid + clindamycin
• Hemodynamic
°`
support
Fluids, vasopressors
SURGERY
• Direct surgical examination of skin,
subcutaneous tissue, fascia I planes, muscle
---. debridement of all devitalized, necrotic
tissue
• Fasciotomy
< 15
~ 15
0
< 15
0
1
2
15-25
> 25
> 13.5
11-13.5
< 11
c: 135
< 135
4
OTHER INTERVENTIONS
• Hyperbaric oxygen
0
1
2
0
2
s
1.6
> 1.6
0
2
s 180
0
> 180
1
53
I
ONYCHOMYCOSIS
osmsJl:/ on14ehom14eosis
(
PATHOLOGY & CAUSES )
• Chronic fungal infection
O
Nail bed, matrix, plate of toes/fingers
Mixed pattern
• Combination
of other types
RISI( FACTORS
• Infection spread by direct contact from
people. animals. soil, fomites (upholstery,
hairbrushes, hats)
• I age
• Causative agents
• Contributory/predisposing
O
O
O
• Biological
male>
• Communal
female
showers, swimming
pools
factors
Dermatophytes (tinea unguium): most
commonly Trichophyton rubrum
• I warmth, humidity
Nondermatophyte molds: Aspergillus
spp.
Yeasts: most commonly Candida
albicans
• Occupational
, Jobs that involve frequent hand
washing; dishwashers, housekeepers
• Occlusive footwear
• lmmunocompromised
state (HIV, diabetes)
• Dermatophyte hyphae penetrate stratum
corneum of skin, nails ----> manufacture
keratinolytic proteases ----> invade living cells
• Living with others affected by
onychomycosis
• Spores of nondermatophyte (e.g.
Aspergillus) lodge under nail/at lateral nail
folds ----> colonization, spread toward cuticle
Candida spp. ----> infect soft tissue around
nail, penetrate nail plate
COMPLICATIONS
• Chronic mucocutaneous
fungal infection
• Pain
• l risk of bacterial coinfection, cellulitis
• Nail disfigurement
TYPES
• Recurrence
Distal lateral subungual
• Initially affects distal corner of nail;
eventually spreads toward cuticle
• Most common
Proximal subungual
• Affects nail plate near cuticle; extends
distally
• Sign of severely immunocompromised
state
White superficial
• Affects nail surface; may spread to cover
entire nail
Endonyx
• Affects interior of nail plate
Total dystrophi
c
Figure 8.10 Onychomycosis of the toe nails.
• Nail plate is completely destroyed
54
)
SIGNS & SYMPTOMS
(
• Topical triazole
Yellow, brown, white discoloration;
subungual hyperkeratosis; mild
inflammation; onycholysis
, Efinaconazole
• Systemic
• Proximal subungual
O
, Terbinafine (dermatophyte infections);
itraconazole (yeast, non-dermatophyte
infections)
Diffuse patches/transverse striate of
white to yellow patches on nail plate
• Endonyx
O Discoloration,
• Coexisting tinea capitis
onycholysis
, Griseofulvin
• White superficial
O
I
T_R_E~_~_M_EN_T
)
MEDICATIONS
• Distal lateral subungual
O
(..____
• Keratolytic (urea)
Soft white spots on nail surface
, Reduces nail thickening
• Total dystrophic
°`
Keratotic debris on thick. rigid nail bed
• Other associated features
°`
°`
O
°`
• Nail removal in some cases (nail avulsion)
Coexisting tinea pedis infection
(common)
Chronic paronychia
inflammation)
SURGERY
(proximal/lateral
fold
Dermatophytoma (linear, yellow/white
band of dermatophyte hyphae)
OTHER INTERVENTIONS
• Laser (Nd:YAG)
• Photodynamic
therapy
Fungal melanonychia
(black/brown
discoloration; caused by pigmentproducing molds, fungi)
(..____
D_IA_GN_O_SI_S
)
LAB RESULTS
• Potassium hydroxide (KOH) microscopy
O
Identifies fungal elements (e.g. fungal
hyphae, pseudohyphae. yeast)
• Histopathological analysis
acid-Schiff (PAS) stain
O
using periodic
Identifies fungal elements
• Fungal culture (e.g. dermatophyte
mediu m/DTM)
O
test
Identifies organism
OTHER DIAGNOSTICS
• History, physical examination
characteristic findings
with
55
I
PRESSURE ULCER
osms.i"l/pTessuTe-u leer
(
PATHOLOGY & CAUSES
• Localized skin, underlying-tissue
o
)
injury
Caused by unrelieved pressure/pressure
in combination with friction, shearing
forces
• AKA bedsores/decubitus
• Blood flow diminishes
Pressure - ischemia - necrosis
• Bony prominences most commonly
affected
o
o
Sacrum,
heels, hips, elbows
RISI( FACTORS
o
Chronidacute disease (e.g. hip fracture,
stroke, Parkinson disease)
o
Central/peripheral
neural damage,
altered level of consciousness, advanced
age
• Reduced perfusion
o Atherosclerosis,
peripheral vascular
disease, hypotension, smoking
• Factors affecting skin structure
Malnutrition, protein deficiency, skin
moisture (incontinence, sweating)
• Diabetes mellitus
STAGING
• Stage I: nonblanchable
intact, localized
skin,
• Deep tissue injury: nonblanchable
erythema, skin separation; no skin
disruption
COMPLICATIONS
• Biofilm formation on wound inflammation - delayed healing
dehiscence
• Wound, bone, joint infection;
fistulas; gangrene
• Malignant
transformation
- wound
sepsis;
rare
(__ s,_G_NS_&_S_Y_M_PT_O_M_
• Reduced mobility
o
• Unstageable: iffilled with sloughed
scabs; diagnosis difficult
• Ulceration (skin in contact with underlying
surface)
• Fever, foul odor (if complicated
by infection)
• May be painful
(..____
D_IA_G_N_OS_IS)
LAB RESULTS
• Swab culture
, May help determine treatment in
healing-resistant
ulcers
OTHER DIAGNOSTICS
erythema; skin
• Stage II: partial thickness dermis loss: red
wound bed; serum-filled blister; no skin
sloughing
• Stage Ill: full thickness tissue loss; visible
subcutaneous fat; raised wound edges
(epibole); skin sloughs
• Stage IV: full thickness tissue loss; bone,
muscle, tendon exposed; raised wound
edges; skin sloughs/eschar formation
• Clinical presentation
(._____
T_R_E~_~_M_EN_T__
)
MEDICATIONS
• Topical sulfadiazine
cream
OTHER INTERVENTIONS
• Debridement
replacement,
of biofilm, dressing
negative pressure therapy
56
I
Prevention
• If bedridden, reposition at least every
two hours (reduces chance of ulcer
development)
• Use of special mattresses
ROSACEA
osmsJl/ resecee
(
PATHOLOGY & CAUSES
)
• Chronic inflammatory cutaneous disorder
O
O
Usually affects face (may extend to
neck, upper chest, ears)
Ocular involvement: dry, burning,
itching, foreign-body sensation
• Typical onset: 30-50 years
• Defining features
O
O
Persistent central facial erythema;
intensity may be intermittent
Phymatous changes (irregular,
nodular skin), usually affecting nose
(biologically-male
> biologically-female
individuals)
(__ SI_G_NS_&_S_Y_M_PT_O_M_s_)
• Telangiectasia
pustules
with erythema,
papules,
• Flushing
Characteristics of different types
• Papulopustular
O
Similar to acne, no comedones
• Phymatous
O
Thick oily skin; mostly on nose, in
biologically-male
individuals
• Ocular (common)
°` Conjunctivitis,
keratitis, tearing, burning,
telangiectasias
• Hyperactive vascular response, may extend
to eyes (ocular rosacea)
• Granulomatous
O Papules
around eyes, cheeks
• Triggered by warm weather, alcohol,
certain foods, sun, stress
• Pediatric (rare)
CAUSES
O
Never phymatous
• Neurogenic
O Pain,
neurologic symptoms
• Unknown
• May be innate immune system dysfunction;
response to bacteria, UV----> chronic
inflammation
(.._____
COMPLICATIONS
• History; clinical
findings
D_IA_GN_O_s,_s
__
)
OTHER DIAGNOSTICS
exam with characteristic
• Skin thickening, scarring, rhinophyma,
ocular rosacea (blepharitis)
(.._____
RISI( FACTORS
• Genetic predisposition
• More common in biologically-female
individuals, especially of Celtic/NorthernEuropean descent
T_R_E~_;,-_M_EN_T
__
)
MEDICATIONS
• Antibiotic
(topical metronidazole)
• Topical azelaic acid
• Oral doxycycline
57
I
OTHER 1NTERVENT10NS
• Avoid exacerbating factors (e.g. spicy food,
alcohol, sun, stress)
• Regular sunscreen
use
• Laser therapy
O
Telangiectasia
ablation
STAPHYLOCOCCAL SCALDED
Sl(IN SYNDROME (SSS)
osmsJl/SSS
(
PATHOLOGY & CAUSES
• Infectious, superficial
, Skin blistering,
)
skin disorder
desquamation
(
D_IA_GN_O_s,_s
__
)
D1AGNOSTIC IMAGING
Chest X-ray
• AKA Ritter's disease
• Check for pneumonia
lobar infiltrates
as infectious cause;
CAUSES
• S. aureus produces epidermolytic
exotoxin ----> enters skin ----> breaks down
desmosomes between cells ----> peeling skin
LAB RESULTS
Biopsy
COMPL1CATIONS
• Epidermal splitting in stratum granulosum
near skin surface
• Cellulitis,
Blood culture
sepsis
• S. aureus
RISI( FACTORS
• S. aureus infection
OTHER DIAGNOSTICS
• lmmunocompromised
state
• Immature renal function/kidney
• Affects children<
• Clinical presentation
disease
six years
(
T_R_EA_~_M_EN_T
__
)
MEDICAT10NS
(__ s,_G_NS_&_S_Y_M_PT_O_M_s_)
• Antibiotics
• Tender erythema with large desquamation
areas, moist patches
• Nikolsky sign: skin peels at gentle touch
• Fever, malaise, appetite loss
58
I
NOTES
,
NOTES
URTICARIA & ERYTHEMA
NODOSUM
,
•
GENERALLY, WHAT ARE THEY?
(
PATHOLOGY & CAUSES
)
• Vascular reaction of the skin triggered by
allergic reaction, irritation, or infection
• Range of dermatological
o
Erythema
o
Swelling
• Raised or flat lesions
• Physical examination
• Based on appearance
• Patch testing to confirm and determine the
allergy
• Can be acquired (e.g. medications),
associated with underlying illness (e.g.
malignancies,
autoimmune disorders), or
have genetic predisposition
SIGNS & SYMPTOMS
Urticaria, pruritus
(~~~D_IA_G_N_O_SI_S~
__ )
• Vasodilation, increased vascular
permeability - fluid leaks into interstitium
- swelling/edema
• Possible elicitation of hypersensitivity
reaction (immune system involved)
(
n
• Screening for autoimmune
etiologies
)
(~~~TR_E_AT_M_E_N_T~
__ )
• Identify/avoid triggers
• Address underlying
manifestations:
or neoplastic
• Symptomatic
cause
management
ERYTHEMA NODOSUM
osms.i-l/ eT14-lhemo.-nodosum
(
PATHOLOGY & CAUSES
)
• Acute skin eruption due to inflammation in
the subcutaneous adipose tissue
o Most common form of acute panniculitis
• Chronic or recurrent forms are rare but may
occur
• Presumably caused by a delayed
hypersensitivity type IV reaction to a variety
of antigens
CAUSES
• 30-50% unknown etiology
• Infections: Streptococcus spp., M.
tuberculosis complex, M. leprae, M.
pneumoniae, Yersinia spp., Histoplasma
capsulatum, Coccidioides immitis
• Autoimmune disorders: inflammatory
bowel disease, sarcoidosis, Behest's
disease, medium-vessel vasculitis
• Medications: sulfonamides, oral
contraceptives, amiodarone
59
I
afratafreeh.com exclusive
• Malignancies: hematological malignancies,
carcinoid tumours, pancreatic cancer
DIAGNOSTIC IMAGING
Chest X-ray
(
s,_G_NS_&_SY_M_PT_O_M_s_)
• Pre-eruptive
°`
• Additional evaluation
underlying cause
to determine the
phase
Fever, malaise,
and arthralgia
• Eruptions of red, painful, poorly defined
plaques and nodules, most commonly
located on shins, knees, arms, thighs, and
torso-« skin lesions gradually get softer
and smaller until they completely disappear
over the course of about two weeks
(..__ __
T_R_E~_~_M_EN_T__
)
MEDICATIONS
• Potassium iodide, corticosteroids and
colchicine can be used in severe refractory
cases
OTHER INTERVENTIONS
• Address underlying
cause
• Symptomatic management
, Bedrest, leg elevation, compressive
bandages, wet dressings, and
nonsteroidal anti-inflammatory
agents
Figure 9.1 A single area of erythema
nodosum.
(..____
D_IA_GN_O_s,_s)
• Observation of typical skin lesions
LAB RESULTS
• Biopsy in uncertain cases
• Additional evaluation to determine the
underlying cause
°` Complete
blood count, erythrocyte
sedimentation rate, antistreptolysin-0
titer, throat culture, urinalysis,
intradermal tuberculin test, venereal
disease research laboratory (VDRL), and
cultures, as appropriate
Figure 9.2 Erythema nodosum affecting the
shins; a common site for this disease.
60
I
HEREDITARY ANGIOEDEMA (HAE)
osms.i-l/heTecli"lo.T14-o.ngioecle
mo.
(
PATHOLOGY & CAUSES
)
• Small but important number of all cases of
angioedema
O
O
Increased vasodilation and vascular
permeability----> fluid leakage from deep
blood vessels ----> angioedema
Urticaria
• Attacks begin during childhood and
become increasingly frequent and severe
• Frequency of attacks differs greatly, varying
from weekly episodes to intervals longer
than a year; discrepancies can occur among
different individuals and at different times
in the same individual
and pruritus are not present
CAUSES
• Inherited in an autosomal dominant manner
involving mutation of genes associated
with Cl-inhibitor (CllNH) that inhibits the
complement pathway and is associated
with coagulation factor XII
O
O
Results in unregulated levels of
bradykinin and other vasoactive
substances ----> inflammation,
vasodilation, and cellular injury
Attack triggers may include minor
trauma, mood and temperature
changes, but often no obvious inciting
event can be established
Figure 9.3 Angioedema
of the lips.
(.____
D_IA_GN_O_SI_S
)
(__ SI_G_NS_&_S_Y_M_PT_O_M_s_)
DIAGNOSTIC IMAGING
• Recurrent attacks of angioedema
• Painless, nonpruritic, nonpitting swelling of
extremities, genitalia, buttocks, eyelids, lips,
tongue, larynx or gastrointestinal tract
Gastrointestinal tract-» nausea,
vomiting, intense colicky abdominal
pain, diarrhea, dehydration, and
intense exhaustion ----> mimics a surgical
emergency and unnecessary surgery
could be performed
O Larynx
----> life-threatening
airway
obstruction ----> without treatment, death
by asphyxia occurs in about 25%
• Tightness, tingling, or erythema
marginatum corresponding to the affected
area may precede the swelling
O
• Each episode usually resolves within 72
hours
• Imaging studies may be useful during
attacks of gastrointestinal edema
LAB RESULTS
• Complement
the system
(
testing to assess alterations in
T_R_E~_;,-_M_EN_T
__
)
MEDICATIONS
• Management of attacks
O Intravenous
Cl-inhibitor concentrates,
kallikrein inhibitors (ecallantide),
bradykinin B2 receptor antagonists
(icatibant) or, if those are unavailable,
fresh-frozen plasma as an alternative
61
I
• More than one episode in a month or high
risk of developing laryngeal edema - longterm prevention
O
°`
Danazol (an androgen that increases
levels of C4)
C 1-inhibitor
OTHER INTERVENTIONS
• Avoid specific stimuli that have previously
led to attacks
• Avoid medications associated with attacks
, ACE inhibitors;
estrogen
concentrates
medications
containing
URTICARIA (HIVES)
osms.i"l/uT-lieo:rio.
(
PATHOLOGY & CAUSES )
• Acute (< six weeks) or, rarely, chronic(>
weeks) skin eruption
six
• Acute form most common dermatologic
disorder seen in emergency department
O
Most often benign and self-limiting,
though may rarely progress to lifethreatening angioedema or anaphylactic
shock; strong tendency to recur
• Hypersensitivity reaction - mast cell
degranulation and release of inflammatory
mediators - increased vascular
permeability - fluid leakage from
superficial blood vessels - cutaneous
lesion
• Precipitants include psychological and
physical stress, cold or hot temperature,
pressure or vibration
• Physical urticaria is urticaria is induced by
an exogenous physical stimulus such as
scratching or firm stroking of the skin
, The most common type of physical
urticaria is called a dermatographism
(
SIGNS & SYMPTOMS
• Wheals: skin
itchy, burning
plaques with
margins and
O
O
TYPES
• Acute urticaria
O Single
lesions usually last less than 24
hours
Individual
)
eruption characterized by
or stinging, red, raised
well-defined
erythematous
pale centers
lesions
may coalesce
New lesions may appear as others
resolve
• Can occur anywhere, but common sites are
areas exposed to pressure (e.g., trunk, distal
extremities, ears)
• Chronic urticaria
O May last six weeks or more
CAUSES
• Assessment for potential causes includes
"5 ls"
O
Infection (bacterial/viral/fungal/parasitic)
O
Injection of a drug/insect venom
Inhaled substances (pollen, mold, dust)
O
O
Ingestion
of foods, drugs, chemicals
Internal disease process such as an
autoimmune disorder
• Vasculitis urticaria associated with
autoimmune and malignant diseases
O
Figure 9.4 Urticaria
of the forearm.
62
(
D_IA_GN_O_s,_s)
(
• Typically based on appearance
• Avoid triggers
• Patch testing to confirm and determine the
allergy
• Symptomatic
O
O
LAB RESULTS
• Complete blood count
• Erythrocyte sedimentation
• Thyroid-stimulating
thyroid disease)
• Autoimmune
O
rate
hormone
(rule out
I
T_R_E~_~_M_EN_T
)
management
Antihistamines
In severe cases, corticosteroids or
leukotriene inhibitors
Monoclonal antibodies and
immunosuppressants may be used in
refractory cases
screening
63
I
NOTES
II
..
NOTES
.
VESICULOBULLOUSDISEASES
GENERALLY, WHAT ARE THEY?
(
PATHOLOGY & CAUSES
)
(
D_IA_GN_O_SI_S
__
)
LAB RESULTS
• Chronic skin blistering diseases; associated
with underlying autoimmune, genetic
pathology
• Skin biopsy
• lmmunofluorescence
testing
• Destruction/malfunction
of structural,
anchoring proteins of skin
(
SIGNS & SYMPTOMS
)
T_R_EA_:l"_M_EN_T
__
)
MEDICATIONS
• Corticosteroids
• Skin blistering
• Mucosal
(
erosions pruritus
OTHER INTERVENTIONS
• Lifestyle modifications
BULLOUS PEMPHIGOID
osms.tl:/\,ullous-pemphigoid
(
PATHOLOGY & CAUSES
)
• Autoimmune skin disease; bubble-like
blisters
O Bulla= blister, pemphig- = bubble, oid= similar
• Chronic, relapsing, remitting, autoimmune
subepithelial
blistering disease
O
°`
Epithelial lesions
vulgaris)
(unlike pemphigus
Can affect mucous membranes
• Presents with cutaneous
erosions
bullae, mucosal
• Rare disease, most common autoimmune
blistering disorder
CAUSES
• Autoantibodies against hemidesmosomal
proteins
, Bullous pemphigoid antigen 2 (BPAg2)
, Collagen type XVII
• Autoantibodies may develop in response to
certain drugs/infections
• Autoantibody activation-« abnormal
lgG/complement deposition in basement
membrane zone ----> separation of dermis,
epidermis----> inflammatory reactlon-»
formation of blisters, inflammatory mucosal
erosions
RISIC FACTORS
• More common in individuals
> 60 years
64
(
(__ SI_G_NS_&_S_Y_M_PT_O_M_s
)
• Trunk, skin folds, extremities
• May exhibit prodromal
O
I
T_R_E~_~_M_EN_T
)
MEDICATIONS
most affected
• Topical/systemic
phase
corticosteroids
, Decrease blister formation, promote
blister healing, improve quality of life
Pruritic papular lesions, resemble
eczema
• Oral, ocular mucositis
• Blisters with inflammatory/noninflammatory
base
• Unlike pemphigus vulgaris, bullae tense,
difficult to rupture - negative Nikolsky sign
• After rupture, scarring uncommon
(
D_IA_GN_O_s,_s)
LAB RESULTS
• Histopathological
O
studies (confirm)
Skin biopsies, immunofluorescent
staining techniques
Figure 10.1 The histological appearance of
the skin in a case of bullous pemphigoid. In
contrast to pemphigus vulgaris, the bullae are
subepithelial. The bullae contain an infiltrate
of eosinophils.
• Complete blood count (CBC)
o
Eosinophilia
• i lgG antibodies
EPIDERMOLYSIS BULLOSA
osmsJl/ephieTmoh4sis-\,u llose1
(
PATHOLOGY & CAUSES
• Skin breakdown - blisters
O Epidermo= skin, lysis- = breakdown,
bullosa- = blistering
• Rare condition, inherited group of disorders;
blisters, erosions after minor skin trauma
due to fragility of epithelial tissue
• May also affect mucous membranes, nails
CAUSES
• Mutations in structural proteins of skin
responsible for tissue integrity
°` Keratin,
desmosomes, cell junctions,
intermediate filaments, etc.
O
disease
)
severity, clinical
presentation
RISI( FACTORS
• Genetic inheritance
(
SIGNS & SYMPTOMS
)
• Localized/systemic
• Skin blistering following minor trauma/
friction
• Nail dystrophy, loss (common)
• Oral lesions
Presence of some or all - determine
65
I
(
D_IA_GN_O_s,_s
__
)
LAB RESULTS
• Skin biopsy
• lmmunofluorescence
testing
OTHER DIAGNOSTICS
• Family history
(
T_R_E~_~_M_EN_T
__
)
• No specific therapy
Figure 10.2 The hands of an individual with
epidermolysis bullosa. Numerous consecutive
bullae have caused scarring and induration of
the skin. leading to contractures.
OTHER INTERVENTIONS
• Symptomatic care, wound care, infection
prophylaxis, pain management
PEMPHIGUS VULGARIS
osms.i"l/pemphigus-vulgC1Tis
(
PATHOLOGY & CAUSES
• Autoimmune, life-threatening
blistering
disorders of skin. mucous membranes
• Epithelial lesions
O
Unlike bullous pemphigoid, which
presents with subepithelial lesions
• Acantholysis: defining mechanism
(acanthus- = thorny, lysis- = breakdown)
O
Impaired adhesion between cells in
spinous layer of epidermis
CAUSES
• Autoantibodies
against desmoglein
• Autoantibody activation - attack of
adhesion molecules - breakdown of
intercellular adhesion - inflammatory
reaction - blister formation
)
(__ SI_G_NS_&_S_Y_M_PT_O_M_
• Oral mucosa (most common); can affect all
mucosal surfaces
• Nikolsky sign - blister ruptures with
pressure/friction
, Unlike bullous pemphigoid, where
blisters difficult to rupture
• Easily-eroding painful blisters over
erythematous skin
• No pruritus
(
D_IA_GN_O_s,_s
__
)
LAB RESULTS
• Skin biopsy
• lmmunofluorescent
staining
• Serum antibodies
RISI( FACTORS
• Adults
• Jewish people of Middle Eastern origin
66
(...____
T_R_E~_~_M_EN_T
I
)
MEDICATIONS
• Systemic steroids
• lmmunosuppressive
agents
Figure 10.3 A histological section of the
skin in a case of pemphigus vulgaris. There
is intraepidermal bu Ila formation in the
superficial epidermis and characteristic
tombstoning of the dermoepidermal junction.
67