Dermatology Flashcards
1
Q
how much does the skin weight?
A
approximately 4 kg
2
Q
Surface area of skin
A
2 m2
3
Q
Function of skin
A
1) decoration 2) barrier 3) vitaminD synthesis 4) water homeostasis 5) thermoregulation 6) insulate/calorie reservoir 7) touch/sensation
4
Q
Fitzpatrick Skin Scale
A
way to categories skin types based on color and ability to sunburn
5
Q
Fitzpatrick 1
A
Red/blond hair, with blue/green eyes, white skin with lots of freckles, always sunburns and enver tans
6
Q
Fitzpatrick 2
A
Blond/brown hair, light to medium eyes, fair skin with some freckles, sunburns easily and minimally tans
7
Q
Fitzpatrick 3
A
Brown hair, medium to dark eyes, light brown skin, minimal freckles, sunburns initially, and tans gradually
8
Q
Fitzpatrick 4
A
Medium to dark hair, dark eyes, moderate brown skin, no freckles, minimal sunburn, tans well
9
Q
Fitzpatrick 5
A
dark hair and eyes, dark brown skin, no freckles, rarely sunburns, dark tan
10
Q
Fitzpatrick 6
A
dark hair and eyes, black skin, no freckles, never sunburns, always tan
11
Q
what gives our skin its color?
A
due to the type, size and distribution of melanosomes
12
Q
Eumelanin
A
brown to black pigment
13
Q
Pheomelanin
A
yellow to red-brown pigment; not as effect a eumelanin at blocking light
14
Q
Distribution of melanosomes in light skin
A
small melanosomes, distributed in clusters above nucleus of keratinocyte
15
Q
Distribution of melanosomes in dark skin
A
large melanosomes, distributed individually through cytoplasm of keratinoctye
16
Q
Albinism
A
defect in tyrosinase gene that is involved in melanin production
17
Q
Vitiligo
A
autoimmune response to melanocytes. It is acquired depigmentation so there is a complete lack of melanocytes. Most seen in periorificial and aural locations.
18
Q
Sources of Vitamin D
A
Sun exposure, fish, fish liver oil, egg yolks, fortified dairy, grains
19
Q
Vitamin D Deficiency
A
Rickets - weakened bones causing skeletal abnormalities
20
Q
How does Vitamin D get converted to active form in the skin?
A
Skin + UVB from the sunlight stimulates 7-dehydrocholesterol to convert to Cholecalciferol (Vit D3) in the skin.
21
Q
7-dehydrocholesterol
A
enzyme that when stimulated with by UBV is covered to cholecalciferol (Vitamin D3)
22
Q
what forms of Vitamin D do we get in our diet
A
Cholecalciferol (D3) and Ergocalciferol (D2), absorbed through intestines
23
Q
What happens to Vitamin D in the liver?
A
D2 and D3 are covered to Calcidiol (25-hydroxy)
24
Q
Calcidiol
A
25-hydroxy that is converted from Vitamin D3 and D2 in the liver and it transfered to the kidney
25
What happens to vitamin D in the kidney
it is converted to 1,25- dihydroxy Vitamin D (calcitrol) which is the active form.
26
Calcitrol
is the active form of vitamin D from the kidney, increases calcium absorption, PTH mediated bone resorption, decreases renal Ca2+ and phosphate excretion
27
Epidermis cell type
stratified squmaoue epithelial
28
Components of the dermis
Papillary Dermis: loose connective tissue just under epidermis; Reticular Dermis: dense connective tissue further down
29
Adnexal structures
Apocrine, eccrine gland, hair follicles, nails, subcutaneous fat
30
Where is thick skin found?
On palms and soles, hairless
31
Keratinocytes
Barrier layer in epidermis that synthesize keratin, the intracellular fibrous skin protein
32
Melanoctyes
pigment producing neural crest cells located on basal layer of epidermis near hair follicles; 1 melanocyte provides pigment to many more keratinocytes via dendritic branches
33
Melanin
pigment derived from tyrosine, packed in melanosomes. Protective of DNA and UV damage.
34
Langerhan Cells
Endogen presenting - cells of the immune response in the skin. There is a small number in the epidermal layer. Essentially Dendritic cells in epidermis that are BM derived
35
Merkel Cells
Never endings in epidermis, involved in neural development and tactile sensation; rarely become neoplastic and cause merkel cell carcinoma
36
How long is the life cycle of keratinocytes?
28 days!
37
What are the layers, form Bottom to Top of the epidermis?
Stratum basalis, Stratum Spinosum, Stratum Granulosm, Stratum Corneum
38
Stratum Basalis
deepest layer of the epidermis; single layer of columnar or cuboidal keratinocytes that are attached via hemidesmosomes to the basal lamina of dermal epidermal jungion; houses the stem cells of epidermis
39
What attaches the keratinocytes to basal lamina?
hemidesmosomes
40
Bullous Pemphigoid
autoimmune disease with Ab to BP230 or BP180 that attach Type XVII collage to make hemidesmosomes ineffective and lead to sub-epidermal blisters. Increased risk of infection. Occurs in older adults
41
Epidermolysis Bullosa
group of inherited disorders that results in blistering due to trauma at that sub epidermal junction. Two types: Junctional and Dystrophic
42
Junctional Epidermolysis Bullosa
Collagen XVII or Laminin 5 mutation; blistering disorder a subepidermal junction due to trauma/friction, improves with age
43
Dystrophic Epidermolysis Bullosa
mutation in Collagen VII which leads to psedosyndactylyl (mitten hand), flexion contractures, increased risk of squamous cell carcinoma, infection; recessive form is most severe.
44
Stratum Spinosum
Full of desmosomes that attach keratinocytes together (cell to cell adhesion)
45
Desmosomes
Cell to cell adhesion in stratum spinosum layer composed of intracellular Keratin Filaments (5 and 14) and Desmogleins
46
Pemphigus Vulgaris
autoAb to desmogelin 1 and 3 that produces flaccid bulla with intraepidermal blistering.
47
Epidermolysis Bullosa of the Stratus Spinosum layer?
Epidermolysis Bullosa Simplex; genetic defects in Keratin 5 and 14, generalized onset of blisters shortly after birth
48
Stratum Granulosum
2nd layer from the stop of the epidermis; cells start to loose their nuclei and keratohyalin granules contain filaggrin which cross links to form cornfield cell envelope, Contains lamellar bodies
49
Filaggrin
located in stratum granulosum of epidermis, is important for barrier formation
50
Lamellar bodies
located in stratum granulosum of epidermis, important for excretion of ceramics to form barrier
51
Stratum Lucidum
a layer seen only in thick skin, with no hair follicles. Cells no longer have nuclei or organelles. This layer helps reduced friction and shear forces
52
Stratum Corneum
Top most layer of the epidermis, with dead and desquamating keratinocytes. Breakdown of filaggrin forms Natural Moisturizing factor
53
Natural Mousturizing Factor
formed from the breakdown of filaggrin in the stratum corneum layer, binds to H20 to keep skin moist; levels decline with age.
54
What disorders arrise from loss of function of filaggrin?
Icthyosis Volgaris and Atopic Dermatitis
55
Small, light colored hair
Villous hair
56
Thicker hair
Terminal har
57
Allopecia Ariata
attack of hair follicles, can range form moderate to severe
58
Macule vs. Patch
both are flat areas of color change, macules are
59
Papule vs. Plaque
both are elevated bodies, Papules are
60
Nodule
firm and well-defined lesions that are dermal or subcutaneous >1 cm
61
Scale
excess stratum corneum, appears as white or gray flakes
62
Crust
dried blood, serum, or purulent exudate
63
Vesicles Vs. Bulla. vs pustule
Vesicle and bulla are both fluid filled, Vesicles is
64
Erythma vs. Erythroderma
Erythema is localized redness caused by increased blood flow; Erythroderma is generalized blanchable redness all over that is blanachable.
65
Telangiectasia
visible persistent dilation of superficial blood vessles
66
Ecchymoses
bruise, discoloration of skin or MM due to extravascular blood
67
Petichiae
tiny 1-2mm hemorrhages
68
Vasulitis
raised discoloration of palpable purport due to vascular inflammation and extravascular RBCs. can be red or violaceous
69
Atrophy vs Erosion
Atrophy is loss of epidermal, dermal or SC; Erosion, loss of epidermal or mucosal epithelium due to injury, denuding veiscle, bulla removal
70
Ulcer
Circumscribed loss of epidermis and at least some part of upper dermis; depth can extend to bone. Edge is clean or ragged. Tissue can be necrotic, purulent, healthy.
71
Fissure
deep linear crack found in thickened skin
72
Eschar
crust or scab that is black in color; due to trauma, infection, skin disease
73
Types of distribution of skin findings
Lyphagetic, dematomal, palmoplantar, photodistrubted
74
Intertriginous Distribution
skin surfaces that come into contact with eachother
75
Flexural Distrubition
overlapping muscles that flex joints
76
Dermatitis
Essential Eczema or inflammation of the skin
77
Types of Dermatitis
Stasis, Atopic, Irritant Contact, Allergic Contact, Drug erruptions, Psoriasis
78
Stasis Dermatitis is due to….
venous insufficiency of lower extremities that causes edema
79
Stasis Dermatitis looks like
dry, itchy, could be due to contact allergic due to topical application or irritant due to wound exudates
80
Complications of Stasis Dermatitis
stasis ulcers
81
Treatment of stasis ulcers
compression, elevation, exercise of calves, vascular surgery, topical steroids, avoid allergens
82
Major differences in Stasis Dermatitis vs. Cellulitis
Derm: causes erythmatous papules and plaques with scale that affect dermis and epidermis bilaterally! Cellulitis cases warm, tender erythematous patches or plaques to the dermis or subcutanoues regions Unilaterally
83
Atopic Determatitis
Due to a filaggrin mutation that is associated with Xeroxes and asthma and allergies. Most provolone in Children under 5; most often in flexture of joints like antecubital fossa, popliteal fossa, neck, wrist, ankle
84
Types of Atopic Dermatitis
Infantile, childhood, adulthood
85
Infantile Dermatitis
dry, red, scaly cheeks, flushed in gold.
86
Diagnosis of Atopic Dermatitis
Itchy skin with 3 or more of the follow: onset under 2 years; Hx of involvement in skin creases; Hx of asthma or hay fever; Hx of dry skin in last year; visible flexture eczema
87
Irritant Contact Dermatitis
Not immunologically mediated due to a single or repeated exposure of strong of weak irritants
88
Strong irritant
a small amount causes irritant contact dermatitis
89
Weak irritant
takes frequent exposure (large dose) to cause dermatitis, harmless by itself or single exposure
90
Allergic Contact Dermatitis
Contact exposure that initiates an immune response with memory T-cells; Delayed Type IV hypersensitivity. Small molecules penetrate the skin and elicits a TNFalpha and IL-1 cytokine release
91
What are the most common allergic contacts in Allergic contact dermatitis?
Nickel and balsam of Peru (fragrance)
92
Risk factors for nickel allergy?
female, young, pierced ears
93
Neomycin sulfate and bacitracin
allergens in topical antibiotic solutions
94
Ezcematous Eruptions
Drug eruptions; most common in adults due to use of drugs; being 7-14 days after beginning new med
95
Common drug eruption reactions occur with..
aminopenicillin, sulfonamide, cephalosporin, anticonvulsants, eallpurional
96
Treatment of drug eruptions
discontinue drug, topical steroids and antihistamine
97
Urticaria
hives, wheels (an immediate Type I hypersensitiviey_ by IgE due to physical and chemical triggers. the lesions last for less than 24 hours. Can be acute (6 weeks).
98
Nummular Dermatitis
Excess dry skin, red,scaly crusty patches most often seen on legs (somtimes arms and trunk) in Men over 50.
99
Treatment of nummular dermatitis
moisturizer, minimize soap, sometimes steroids
100
Suborrheic Dermatitis
sharply demarcated patches with pick or orange-yellow erythema seen in infancy or post-pubery when sebaceous glands are active. Most commonly seen on face, scalp, ears, and chest. Also known as Cradle Cap. Due to overproduction of skin oil and yeast irritation. Due to Malessazia Furfur.
101
Psoriasis
hyperproliferation of epidermis, elongation of rete ridges that occurs on the extensor surfaces. Often associated with a family history
102
Types of Psoriasis
Chronic Plaque disease, Guttate (strep throat), erythroderma, Pustular psorasis
103
Co-morbidities of psoriasis
Arthritis, Cardiovascular disease, anxiety, insulin resistance
104
Treatment of Psoriasis
Vitamin D3 analog, steroids, phototherapy, anti-T lymphocytes, Anti TNFalpha
105
what is the purpose of epidermal Rete?
Shear strength
106
what is located in the dermis
hair glands, sweat glands, sebaceous glands, vessels, nerves
107
Papillary Dermis
Thin collagen bundles that locks with epidermal rete to increase strength and surface area
108
Reticular Dermis
thick collagen bundles with visible elastic fibers that cause reliance
109
what is the purpose of elastin?
located in reticular dermis provides resilience or springs back after distortion
110
Collagen Structure
Triple alpha helix that is made up of Gly- Porline- Hydroxyproline. There are a number of different types
111
Collagen I
most common in adult dermis, >85% of collagen in adults
112
Collagen III
fetal collagen
113
Collagen IV
collagen in basement membrane
114
Collagen VII
collagen in anchoring fibers
115
synthesis of Collagen
Procollagen is synthesized in fibroblasts and is excreted. Cleaved outside of fibroblasts convert it to tropocollagen where with the help of vitamin C, is cross linked to form final collagen network
116
Ground Substance
made up of glycosaminoglycans like hyaluronic acid and dreamt sulfate, fibronectins. This promotes diffusion of blood and other contents
117
Disorders of collagen production
1) Scurvy (Acquired) 2) Ehlers Danlos Syndrome (inherited)
118
Scurvy
Vitamin C deficiency causes decreased mature collagen production with signs and symptoms developing 1-3 months follow time of deficiency
119
Scurvy Signs and Symptoms
Keratotic plug, perifollicular hemorrhage, corkscrew hair, hemohorrhagic gingivitis, weakness, delayed wound healing
120
why is hemorrhage common in scurvy?
lack of collagen support for blood vessels
121
Ehlers Danlos Syndrome
inherited disorder in collagen formation
122
Ehlers Danlos Syndrome Signs/Symptoms
Hyper-extensible joints and skin, fragile blood vessels, poor wound healing, absent inferior labial and inguinal frenulum, Gorlin’s Sign, molluscoid pseudoturmors
123
Gorlin’s Sign
ability to touch tip of nose with tongue, sign of EDS
124
Mullucoid Pseudotumors
scar like nodules on knees, common in EDS
125
Elastin Disorders
Solar Eslastosis (acquired) and Psedoxanthoma Elasticum (inherited)
126
Solar Elastosis
an acquired disorder of elastase that is due to sun damage; ineffective remodeling and basophilic. Indicative of a persons age at biopsy
127
Pseudoxanthoma Elasticum
inherited disorder of elastin, due to mutation in MDR gene that causes brittle and calcified elastin.
128
Pesudoxanthoma elasticum signs/symptoms
Plucked chicken skin, systemic hypertension, angioid retina streaks, arterial rupture in eye
129
Ground Substance disorders
Restylane and NO congenital disorders
130
Restylane
a hyaluronic acid used a ground stubance filler to fill in wrinkles
131
Blood supply in the skin
Epidermis has no individual blood supply, so dermis must supply it with blood. Dermis has two levels of blood supply the Superficial plexus (supplies dermis) and the deep plexus
132
What diseases causes disorder capillary loops in the dermis blood supply?
Psorasis and verruca worts (disease with increased epidermal turnover)
133
Vascultis
inflammation of capillaries and venues that causes palpable purpura; due to drug hypersensitivity, infection, neoplasm, collagen vasculature diseases
134
Nerve supply in the dermis
Contain both Specialized and Free nerve endings
135
Type A nerves
heavily myelinated nerves with rapid salutatory conduction; involved in proprioception, touch, stretch, pain
136
Type C nerves
unmyelinated nerves with slow conduction; involved in dull, non-localized, diffuse sensation like temperature and pruritus
137
Meissner’s Corpuscles
Nerve receptors that look like leaves near Dermal-Epidermal junction that are used in find-touch sensation like in digits.
138
Pacinian Corpuscles
Nerve receptors that look like onions located deep in the dermis and are sensitive to pressure and vibrations, most prevalent in genitals
139
Hair Follicle Structure
Infundibulum: top most above/level with sebaceous duct; Isthmus: between sebaceous duct and arrector pili; lowest part is the bulb or the martial area
140
How are hair follicles formed during embryology?
Primitive edtodermal gland is induced by underlying dermal mesenchyme and forms 3 buldges. The lower budge mask up the attachment to arrector pili, middle budge forms sebaceous gland, upper part forms apocrine gland
141
hair cycle
Anagen, telogen, catagen, all random stages in which the hair is in
142
Anagen
growth stage of hair cycle; 85% of hairs are here, lasts for 3 years
143
Telogen
rest stage of hair cycle; 10-15% of hairs are here; lasts 3 months
144
Catagen
involution stage of hair cycle; 1-5% of hair is here; lasts 3 weeks
145
Androgenic hair loss
patterned baldness due to conversion of testosterone to dihydrotestosterone that leads to miniaturization of the hair follicles.
146
Treatment of Androgenic hair loss
Finasteride which blocks the DHT synthesis and moves follicles deeper and maintains the size of hair follicles. Dangerous in women, especially during menstrual years
147
Sebaceous glands
used to lubricate terminal hair
148
Acne
is due to pilosebaceous unit; abnormal follicular maturation which leads to a plugged follicle and overgrowth of P. Acnes which liberate Free Fatty Acids and/or ruptures follicles that leads to dermal inflammation.
149
Holocrine Gland
is a gland where secretion occurs of the entire cells. Example is Sebaceous gland where entire sebocyte is secreted to release its contents
150
Eccrine gland
sweat glands that are used in thermoregulation; most prevalent on forehand, upper lip, palms, and soles
151
Structure of eccrine gland
1) coiled secretory component deep in dermis 2) intradermal duct 3) acrosyringium (intraepidermal)
152
How is sweat released?
mediated by sympathetic Autonomic nervous system, but triggered by ACh (a parasympathetic Neurotransmitter)
153
Secretion from eccrine glands are…
watery and odorless
154
Merocrine
secretion of tiny vesicles like in eccrine glands
155
Acquired disorder of eccrine glands
heat shock, antipersperents
156
Miliaria
Aquired disorder of eccrine gland, blocked sweat ducts that cause heat rash
157
Anhidrotic Ectodermal Dysplasia
inherited eccrine disorder that is due to mutation in EDA gene, so that have decreased thermoregulation, decreased sweat, spare hair and malformed teeth
158
Apocrine Gland
located in axially and anogenital regions that release sialomucin. These are small and nonfiction until puberty
159
Sialomucin vs. eccrine secretion
stickier, but still odorless. Develops odor by contact with bacteria
160
Apocrine Secretion
secrets apex of cell to release contents
161
Apoeccrine Gland
hybrid sweat gland in axilla.
162
Axially Hyperhidrosis
focal excessive sweating, except during sleep. Treatment is botulinum toxin to prevent ACh release
163
Senile Cherry Angioma
Vascular tumor that occurs mostly in adults that leads to a bright red, smooth, papule on skin; mostly located on trunk
164
Treatment of Cherry Angiomas
Superficial Electrodessication, Liquid N2, Shave biopsy, pulse dye laser
165
Infantile Hemangioma
also called capillary or straberry hemangioma; is a benign endothelial neoplasm that can occur anywehere. Cells stain positive for GLUT-1, a placental vascular marker.
166
Onset of Infantile Hemangiomas
Could be born with it, or appear within first 2 months of life; grows rapidly for first few weeks and then involutes 10% each year. Most prevalence in girls, premature babies, and those with post-crionic villous sampling
167
Complications of infantile hemangioma
1) location: visual or airway interruptions 2) size 3) ulceration 4) Over 5 (visceral or CNS) 5) can cause systemic disease with Congestive heart fialure, Kasabach Merritt 6) Congential: PHACES
168
Kasabach-Merritt
Thromocytopenic Coagopathy - associated with infantile hemangiomas
169
PHACES
Posterior fossa abnormalities, hemangioma, arterial aorta abnormalities, cardiac, eye, and sternal defects - all complications of infantile hemangioma
170
Infantile hemangioma treatment
observation, local wound care, pulse dye laser, topic and systemic steroids, beta blockers
171
Port wine Stain
a capillary malformation within dermis that is lined by flat continuous endoethlium, NO GLUT-1 mutation, but somatic mutation in GNAQ. Presents as pink patch and can progress to purple with modularity.
172
Areas of port wine stain
trigeminal nerves, mid dorsal, lumobsacral, nape of neck
173
Age of onset for Port Wine Stain
present at birth and persists until adulthood
174
Klippel-Trenaunay Syndrome
complication of port wine stain; overgrowth of extremity covered with port wine. Complications of varicose veins, venous stasis, edema, ulceration
175
Sturge Weber Syndrome
Complication of Port Wine Stain; ocular and neurologic abnormalities - glaucoma, seizure, Developmental delay
176
Complications of Port Wine
Klippel-Trenaunay and Sturge weber
177
Treatment of Port Wine
Pulse dye laser to prevent thinking or darkening with time
178
nevus Sebaceous
hamartoma of sebaceous bland on face or scalp, appears papillomatous yellow-orange linear plaque with absent hairgrowht
179
Onset of Nevous Sebaceous
Rapid growth at puberty due to enlargement of sebaceous glands
180
Complications of Nevous Sebaceous
Neurological abnormalities (epidermal nevous syndrome) and potenital for epithelial neoplasm
181
Treatment of Nevus Sabeceous
Observation, surgical excision
182
Sebaceous Hyperplasia
Bengin tumor of sebaceous gland most prevent on face>trunk>extremities. Appears as a yellow-hits papule with central dull. Increased in frequency after middle age due to possible sun exposure
183
Treatment of Sebaceous hyperplasia
No treatment often; electrodessication, trichloroacetic acid, liquid N2, laser therapy
184
Acrochordon
also known as skin tags, or fibroepithelail polyps, benign skin grows that are soft, flesh colored (tan or brown) exophytic papules with narrow base. Occurs in areas of rubbling like neck, axially, inframammary
185
Acrochordon prevalence
1/4 of adults have these
186
Complications of Acrochordons
recurrent trauma or torsion
187
Treatment of Acrochordons
No treatment, snip excision, removal by cryosurgery with liquid N2, electrodessication
188
Dermatofibroma
Fibrous histiocytoma, a benign histiocytoma that appears as a brown, firm papule that has dimple sing when pinched. occurs most often on legs in adults
189
Complications of Dermatofibroma
large and enlarging may be malignant (dermatofibrosarcoma protuberans). can be painful or pruritus
190
Treatment of Dermatofibromas
no treatment, if necessary biopsy to rule out malignancy
191
Lipoma
Begnin adipose tumor that is soft to touch movable and painless, usually greater than 1 cm. Occurs in Adults, rare in children
192
Treatment of lipoma
not treatment often, sometimes surgical excision
193
Keloid scar
Overgrowth of granulation tissue. Early stage full of collagen III, later stage collage I. Firm, rubbery, shiny nodule that expands border of wound. Can be pink to dark brown in color.
194
Treatment of keloid scars
topical steroids, intralesional steroids, surgical excision (if prone to keloids, but not be beneficial), surgery +/- radiation
195
Seborrheic Keratosis
Branacle, benign tumor of hair follicle; a white, gray, brown of black exophytic papule that is sunk in. Can be smooth or verrucous, friable, and studied with small pits. Occurs on head, neck, or trunk
196
Types of Seborrheic Keratosis
1) dermatosis Papulos nigra (black and asians) 2) stucco keratosis (acral areas) 3) inflamed seborrheic keratosis 4) leser-Trelat: increased in size, number, and internal malignancies (adenocarcinoma of stomach)
197
Treatment of seborrheic keratosis
moisturizers (alpha-hydroxy-acids, lactic acid), cryosurgery, surgical removal
198
Nevocellular nevi
moles that can occurs in on any skin area or mucosal membranes. Increase in number with age of person.
199
Treatment of Nevocellular nevi
no treatment necessary; for atypical appearing/evolution: shave or punch biopsy and excision. DO not electrodissicate, cryotherapy, dermabrasion, or laser
200
Types of Nevocellular nevi
Intradermal, junctional, compound
201
Intradermal Nevus
Less than 6 mm papule or nodule, dome shaped, pedunulated cerebriform, located on head and neck
202
Junctional Nevis
1-5 mm macule, smooth surface, tan to brown/black. Can ben anywhere, common on plantar and palmar surfaces
203
Compound Nevus
varaible in size, papule or nodule, dome shpaed tan to brown to black, found on trunk and proximale extremities
204
Blue Nevus
Dermal proliferation of melanoctyes to produce abundant melanin, tyndall effect to have blue color
205
Blue Nevus onset
congenital; 1:3000 or acquired; common in asians or caucasians
206
Complications of blue nevus
malignancy is rare
207
Treatment of blue nevus
no treatment if unchanging, surgical removal, punch biopsy, excision
208
Congential Nevi
1mm to lauge, darkened patch with dark hair on step.. could be solitary or multiple on cutaneous surface.
209
Complications of congenital nevi
head, neck, posterior midline, leptomeningeal melanocytosis could be increased risk of melanoma
210
Treatment of congenital nevi
elective surgical excision - controversial
211
Dysplastic Nevus
acquired melanocyte proliferation to have oval or irregular shape, color variation, indistinct margins with no size limits. Could appear to any skin area.
212
Complications of dysplastic nevi
melanoma, FAMM
213
FAMM
familial atypical moles and melanoma: melanoma in 1 or more 1st of 2ned degree relatives, numerous nevi
214
Treatment of Dyplastic nevi
mole mapping, total body photography, remove atypical
215
Cafe Au lait macules
subtle increase in melanocytes with increase melanin production on trunk and extremities. Associated with early childhood.
216
Complications of Cafe au Lait
Neurofibromatoosis: while with 6 mor more >5mm cafe au lait spots
217
Crowe’s Sign
child with six of more cafe au lait spots; sign of NF
218
Neurofibromas
soft, flesh colored papules with buttons hole sign, deep, form subcutaneous nodules.
219
Development of Neurofibromas
AD with variable expression, 50% sporadic mutation in NF-1 on Ch17
220
Diagnosis of NF
2 or more of the following: >6 café au lait macules; >2 neurofibromas; crow’s sign (axially, inguinal freckling); optic glioma; >2 lisch nodules; osseous lesion; first-degree relative with disorder
221
Proximal Subungual white Onychomycosis
white on the nail; associated with HIV due to trichophyton rubrum
222
Anagen Effluvium
loss of growing hair, most due to chemo
223
Telogen Effluvium
hair goes into resting cycle; may be due to medications and post-patrum
224
Intertrigo
irritant dermatitis
225
malassezia furfur
suborrheic dermatitis
226
Dermatomyositis
Photodistrubted violaceous poikiloderma that favors scalp and extensor skin sites. Heliotrope, samitz sign, Guttron’s papule, shawl sign
227
Heliotrope
eruption on upper eyelipds +/- periorbital edema
228
samitz sign
ragged cuticles
229
Guttron’s Papules
Lichenoid papules overlying knuckles, elbows, knees - dermatomyositis
230
Shawl sign
poikiloderma across back and shoulder
231
Tuberous Sclerosis
hypomelanotic macules, adenoma sebaceum, shagreen patch,
232
Pyoderma Gangrenosum
avoid surgery and debridement - oral and topical anti-inflammatory agents!
233
Pyoderma Gangrenosum associations
IBD, Arthritis, Monoclonal gammopathy, hematologic disorders
234
Lichen Planus
purple, polygonal pruritic papules with wickham’s striae
235
Wickham’s Striae
overlying lace-like patterns of white lines of surface
236
Lichen Planus Associations
Hepatits C
237
Ancanthosis Nigricans
velvety hyperpigmentation of intertriginous surfaces (sometimes extensor) Most foten nick, axillae, dorsal hands; due to stimulating epidermal keratinocyte and dermal fibroblast proliferation
238
Acanthosis Nigricans associations
AD, rare, onset in childhood; associated with DM,, Endocrinopathies (hyperandogren, cushings, PCOS) and really drugs
239
Acanthosis Nigricans and malignancy
many precede or accompany or follow internal cancer, due to malignancy of stomach, lunch, breast
240
Treatment of acanthuses nigricans
treatment of underlying disorder, keratolytics (ammonium lactate or urea cream)
241
Brick and Mortar model of the skin
in the stratum corneum, the bricks are the keratinocytes and the mortar is the lipids in the extracellular space
242
How do topical penetrate through the skin?
Passive diffusion, movement through channels or pores int he lacunar system, transported via apendegeal system like hair follicles
243
What drug factors influence topical absorption?
1) active drug concentration, molecular size, liophilicity, composition of vehicle
244
Molecular size and topicals
diffusion is inversely proportional to molecular size
245
Lipophilicity and topicals
lipophilic are more likely to permeate skin to get into lacunar region
246
Patient factors to topic use
complicance, barrier disruption, anatomical location, skin hydration, occlusion
247
What are potenital barrier disruptions in skin?
atopic dermatitis - in addition to the drug penetrating easily, so can infections
248
Anatomical locations that are very sensitive to topicals
face, jaw, scrotum, eyelids - must not use high potency steroids
249
Anatomical locations that are resistant to topicals
plantar surface
250
Skin hydration and topical penetration
good hydration equates to good penetration
251
Occlusion and topical penentration
use wet wraps to optimize absorption
252
what is the cross between a powder and a grease?
Protective paste
253
what is the cross between a powder and a liquid?
drying paste, gels, shake lotions and suspensions
254
what is the cross between a liquid and a grease?
ointments, creams, lotions
255
Cream
oil in water, moderate potency, some hydration, but less than ointments, significant sensitization and irritation risk, can be used on all body sites except macerations
256
Ointments
water in oil, strongest potency, hydrating, low sensitization and irritation risk. Use best on non-intertriginous sites - avoid face, hands groin. greasy and staining
257
Gels
alcohol based, drying. Strong potency, but significant sensitization and irritation risk. Best on oral and mucosal surfaces and scalp, avoid on fissures, erosions, macerated regions.
258
Lotions
powder in water (some oil in water), low potency, variability in drying. Avoid on fissures or erotions. Highest patient acceptance.
259
Foam
pressurized collection of gaseous bubbles in matrix, maximal delivery of active ingredient, strong potency, quick dry, use on hair bearing areas, avoid issues or erosions.
260
What topical is most potent?
Oinments, Gels, Foams
261
what topics are not very potent
lotions
262
What topicals have moderate potency
cream
263
which topicals are have greatest sensitization/irritation risk?
Cream, Gels
264
what do you consider when choosing a topical?
anatomic location, contact allergy/sensitization
265
A fingertip unit is how many grams?
0.5g
266
Face and neck, how many FTU?
2.5 FTU
267
Trunk - front and back FTU
7
268
One arm FTU
3
269
One hand - both sides FTU
1 FTU
270
One Leg FTU
6 FTU
271
One foot FTU
2 FTU
272
how much does 1 g of cream cover
10cm x 10cm area
273
how much does 1 g of ointment ocver
10% further than cream
274
how many grams is necessary to treat an adult man?
20g
275
Basic action of glucocorticoids
bind to cells and cause the release of HSP90 to dimerize and inhibit the transcription of NFkB to control inflammation and increase levels of IkB to inhibit NFkB directly.
276
Alternative Methods for antiinflammation to be used with steroids?
Calcineriun inhibitors, Retinoid, Vitamin D analog
277
Calcineriun inhibitors
NF-ATn inhibition; good for use of dermatitis on groin
278
Retinoid
inihibits AP-1 transcription factor to be anti-inflammatory, but cant be used with Vitamin D analog
279
Vitamin D Analog- mechanism
inhibits AP-1 Transcirption factor to be anti-inflammatory
280
Classes of steroid
7 classes, 7 is least potent and 1 is most potent.
281
Hydrocortisone
class 7; low potency, good for children and adults with mild dermatits. Good for face, intertriginous areas, groin.
282
Triamcinolone
all purpose steroid, class 4; good for spongiotic dermatoses, trunk, extremities, long term use not recommended for face, intertriginous and groin regions
283
Clobetasol
high effectiivity and high potency steroid, high side effects, but good for severe dermatitis
284
Adverse affects of glucocorticoid use
skin atrophy, shiny, thinning, telangiectasia. if used long enough can cause systemic side effects like adrenal suppression, cushion’s growth retardation.
285
Which UV light has shortest wavelength?
UVC
286
why does UVC damage our skin?
it is absorbed by the upper and middle atmosphere
287
Results of UVB
sunburn, tan, formation of Vitamin D, eye damage, NMSC, DNA damage, immunosupression. Only penetrates the superficial tissue layer.
288
What tissues are affected by UVB?
superificial layers - keratinocytes, melanocytes, langerhans
289
Results of UV-A Damage
premature aging, loose skin, wrinkles, dark patches, DNA damage, ROS, Immunosuppression.
290
What tissues are affected by UVA?
dermis, everything above plus fibroblasts and connective tissue
291
Erythemal Action spectrum
carcinogenesis effectivenss of UV-B is much higher than at larger wavelengths
292
Direct results of UVR damage
1) Damage to DNA, RNA, lipids 2) pro-inflammatory response 3) Immunosupresive 4) induction of innate defense 5) induction of apoptosis 6) Vitamin D synthesis
293
DNA damage due to UVR
thymine dimers (UBV), primidine-6-4-pyromidone (UVB) and hydroxyguanosine (UVA)
294
what DNA damage is due to UVB?
thymine dimers and primidine-6-4-pyrimidone
295
what DNA damage is due to UVA?
Hydroxyguanosine
296
what UVR causes NMSC
UVB
297
What UVR causes melanoma?
UVB and UVA
298
What are the primary pro-inflammatory cytokines released with UVR?
IL-1 and TNF Alpha
299
What are secondary pro-inflammatory cytokines release with UVR?
IL-6, IL8, IL-10, GM-CSF
300
What are the lipid mediators (pro-inflammaotry) released with UVR?
PAF
301
What do mast cells release with UVR?
histamine
302
How does UVR lead to immunosuppression?
1) UVR decrease langerhan cell populations 2) inducted inhibitor cytokines like IL-10 and TH2 3) induces tolerance to Tregs and NKT 4) induces keratinocyte to release certain cytokines
303
UVR stimulates the keratinocyte to release..
Ci-Urocanic acid to activate mast or Bcells to make IL-10
304
what does PAF do with UVR stimulation?
stimulates release of prostaglandin E2 to lead to IL10 and IL-12 (Blocked) production
305
what are the skin’s defenses against UVR?
DNA repair, Activation of p53, Apoptosis of Cells with DNA damage, Defense against ROS, Melanin
306
XPC
recognizes DNA damage
307
XPB
incision and release DNA Damage
308
Incision and release of DNA damage is due to…
XPB, XPD, XPF, XPG
309
what is responsible for gap filling and ligation of DNA damage
PCNA, and DNA pol
310
what enzymes make DNA repair possible after UV damage
Recognition of DNA damage, incision and release of NT, Gap filing and ligation
311
what enzymes are responsible for defense against ROS?
peroxidase, catalse, superoxide dismutase, glutathione reductase, thioredoxin reductase
312
UVR and Melanin
UVR stimulates karatinocytes to signal for melanogensis, which produces ROS as a byproduct
313
Tyrosinase
rate limiting, involved in controlling pigmentation
314
tyrosinase related protein 2
regulates eumelanin production
315
Agouti signlaing peptide
Eumelanin production vs. phomelanin production
316
Photodermatoses
are mostly idiopathic, or due to DNA repair defects, chemical photosensitivity, photoaggrevated, Connective tissue disease
317
Disease with DNA repair defects
Xerderma Pigmentosum
318
Disease with Chemical photosensitivity
Drug induced, prophyria
319
Diseases that are photoaggrevated
psoriasis, atopic dermatitis
320
Connective tissue diseases with UVR sensitivity
Lupus erythematous, dermatomyositis, mixed connective tissue disease
321
Seborrheic Dermatitis - systemic diseases
Neurological disorders (PD), head trauma, PTSD, HIV
322
Skin Signs of HIV
Seborrheic Dermatitis, Proximal nail fungal infections, psoriasis
323
Velvet neck
acanthosis nigricans
324
Acanthosis Nigricans
velvet neck - a rare AD disorder, but associated with obesity, DM, insulin resistance, endocrinopathies, drugs, cancer (malignancy and adenocarcinoma)
325
Skin signs of Diabetes
brown patches over legs, thinning skin, ulcers, disseminated granuloma anulares (lots!)
326
Skin signs of Endocarditis
Splinter hemoorhages, Janeway lesions, Osler nodes, Roth spots in eyes, Strep viridian's from teeth
327
Janeway lesions
Bruiselike manifestations on hand - sign of endocarditis
328
Osler nodes
red, painful vascultiis - sign of endocarditis
329
PHACES skin signs
Hemangioma on face and neck, + associated cardiac problems
330
Ehler-Danos Skin signs
increased joint and skin elasticity, poor wound healing with large scars, increased ecchymoses
331
Marfan’s skin signs
habitus, decreased subcutaneous fat - stretchy skin.
332
Pulmonary Systemic Skin diseases
Scleroderma, Sarcoidosis
333
Scleroderma Skin manifestations
Thickened skin over fingers and hands, skin tightening over mouth, salt and peper changes, Raynoud’s sign
334
Raynoud’s Sign
fingers and toes feeling numb or tingling
335
Sarcoidosis skin manifestations
looks lik an inflammatory response, altitiude is protective Hyperpigmented plaques, erosive, ulcerated plaques, granulomatous reactions in tattoos, bilateral hilar lymphadenopathy.
336
Skin associations with Hepatitis B and C
Lichen planus, Vasculitis, Cryoglobliemia, Pruritius
337
Lichen Planus
purple, polygonal pruritic papules with Wickham's Straie. Associated with oral lesions (could be due to fillings) and Hep B And C
338
Wickham's Striae
overlying lace like pattern on Lichen Planus
339
Porhuria Cutanea Tarda skin manifestations
blistering lesions on hands with sun expsoure, hypertrichosis, and atrophic scars. Associated with hepatitis, deficiency of uroprohyinogen decarboxylase. Treatment is serial phlebotomy to decrease iron load
340
Hypertrichosis
excessive hair growth on face
341
Osler Webber Rendu
Vascular blebs in mouth, indicative of GI manifestations
342
Pyoderma Grangrinosum
lesions or pustules that form on an erythematous base that rapidly enlarge. Most commonly associated with Crohns or UV, arthritis, monoclonal gammopathy, hematological disorders (myelogenous leukemia, hairy cell leukemia). AVOID surgery or debridement.
343
Cullen’s Sign
sign of an abdominal bleed, pancreatitis, trauma
344
Grey Turner
ign of an abdominal bleed, pancreatitis, trauma
345
Chronic Iron Deficiency Skin manifestations
Koilonychia, hair loss, angular chelties
346
Koilonychia
spoon nails, associated with Fe def
347
Angular Cheilitis
inflammation of the corners of the mouth
348
Lindsay’s Sign
when 1/2 of the nail bet is white, sign of renal dysfunction
349
Terry’s Sign
when just the tip of the nail bed is red, sign of cirrhosis or CHF
350
Ectodermal Dysplasia skin signs
hair loss, nail changes, teeth malformation, no sweat glands
351
Systemic Lupus Erythematous Skin signs
Molar rash, Discoid Rash, Oral Ulcers, Photosenstiivty,
352
Systemic Lupus Erythematous signs
Molar, Discoid rash, Serositis, Oral unlcers, ANA+, Photosensitivity, blood disorders, renal involvement, arthritis, immunological, nuerological
353
Skin signs in lung cancer
Erythema Gryatum Repens, Hyptertrichosis Lanuginosa Acquisita
354
Erythema Gryatum Repens
wood grain appearance, associated with lung cancer
355
Hypertrichosis Languiosa Acquisita
Fuzzy face
356
Skin Signs associated with Adenocarcinoma/GI cancer
tripe palms
357
Leser Trellat Sign
multiple erruptive suberrohetic keratosis, sign of colon cancer
358
Dermatomyositis
shall like rash, that is associated with malignancies on reproductive organs
359
Sister Mary Joseph Node
papule nodule near umbilicus; sign of pancreatic or GI cancer
360
Where do drug rashes occur?
Most often on trunk, but also on palms, eye, mouth
361
Risk factors for Non-Melanoma SC
Fair skin, high UV exposure, Ionizing radiation, arsenic, polycyclic hydrocarbon, phototherapy, prior skin cancer, genetic skin ease, smoking
362
Smoking is a risk for what type of skin cancer
SCC
363
Which gender is most likely to get skin cancer?
Men
364
What type of UVR exposure causes SCC?
Total UVR
365
what type of UVR exposure causes BCC
intermittent exposure and sunburns
366
Types of Basal Cell Carcinomas
Superficial, Nodular, Infiltrative, Sclerosing/morpheaform
367
What types of BCC is most prevalent?
Nodular
368
Clinical Appearance of BCC
Flat, firm, pale or small pink, raised, very shiny, maybe areas of bleeding of abnormal vessels. Coulld have some crust or oozing
369
Pathophysiology of BCC
lower layer of epidermis (Basal layer) due to mutations in sonic hedgehog pathway.
370
Sonic Hedgehog pathway mutation in BCC
Mutation in PTCH1 which normally blocks Smoothed, a transcription factor that promotes tumor growth.
371
Growth/metastases pattern in BCC?
very slow growing, rarely metastesizes, can infiltrate into nearly areas if left untreated. Increased risk of other types of skin cancer
372
Treatment of BCC
Shaved biopsy, creams, burning, Moh’s Micrographic surgery. Vismedogib
373
Visbodegib
drug to inhibit SMO; used only on metastatic of inoperable cancer types.
374
Actinic Keratosis
premalignant skin lesion that develops into SCC (65%) or BCC (36%)
375
Actinic Kerotosis Appearance
intradermal neoplasia on areas of sun exposure; hyperatosis and erythmatous papules
376
Treatment of Actinic Kerotosis
Freezing, cream, photodynamic therapy, flurorescent light, sun protection
377
Squamous Cell Carcinoma location
near site of sun exposure - face,e ar, neck, lips, back, or in scars, ulcers, injury
378
Risk factors for SCC
immunosuppresion (transplant patients), UV damage, thermal injury, radiation, HPV, burns, chronic injury
379
SCC appearance
hyperkeratotic papule, variable size and thickness, flat, reddish patches that grow slowly
380
Clinical course of SCC
part of the epidermis, 03.-5% metastesize. most common sites occur to lymph nodes or dispant parts. More malignant than BCC, but not much.
381
SCC in situ
Bowen’s Disease, earliest form of SCC, only invaded into the epidermis. Appears scaly, reddish, with patches of crust. Due to too much sun exposure and HPV
382
Keratacanthoma
type of SCC with solitary lesion that growth rapidly over 6-8 weeks, crateriorn endophytic and exophytic nodules with keratin plug. Deep invasion in 10-20% of cases.
383
Invasive SCC
hyperkeratotic papule with variable size and thickness, found on sun damaged skin that mtastaes.
384
Transplant patients risk of skin cancer
Kaposis>SCC>BCC>melanoma
385
Factors for SCC
Age, Skin type, UV, Genetics, HPV (65-90% in SCC), level of immunosuppression (CD4, medications, Heart>kidney>liver)
386
Normal ratio vs translant ration risk of SCC to BCC
Norma: 1SCC:4BCC; Translplant 4SCC: 1BCC
387
Treatment of SCC
topical 5-flurouracil, topical imiquidmod, cryosurgery, electrodessication, excision, Moh’s micrographic surgery, radiation
388
Risk Factors of malignant melanoma
Middle age, history of melanoma, numbers common acquired nevi, history of blistering sunburns
389
Common areas of Malignant Melanoma for Africans
acral, mucosa
390
Common malignant melanoma areas for men and women?
men: back women: legs and back
391
Pathophysiology of Malignant melanoma
bening nevus with a BRAF mutation that activates MAPK. Mutations also in NRAS. Most arrive de novo, 30% are from a previous nevus.
392
Risk factors of melanoma
FAMM> sproadic dysplastic nevus syndrome > large congenital nevus > white skin, MM in first degree relative, immunosuppression, UV exposure, Tanning, fair skin
393
what is the increased risk of Malignant melanoma if using a tanning bed?
up 20% first time, 2% each time after
394
where does malignant melanoma metastasize?
draining lymph nodes, skin between primary site and notes, lung, liver, brain, GI
395
prevalance of malignant melanoma
increasing annually
396
types of malignant melanomas
superficial spreading, nodular, letigo maligna melanoma, acral letiginous
397
Clark's Level
rating for melanoma about how many layers the melanoma has spread. Not very indicative of prognosis
398
Breslow Depth
thickness of the invasion, most indicative for prognosis of malignant melanoma
399
Treatment of a
Excision with 1 cm margin with fascia
400
treamtnet of MM in situ
0.5 cm margins with subcutaneous tissue
401
treatment of MM >1 mm
1-2 cm margins with fascia and sentinal node biopsy
402
Vemuafenib
BRAF inhibitor, treatment of MM,
403
Trametinib or Cobimetinib
MEK inhibitor, used in combo with BRAF for MM
404
imatinib
Gleevec, cKIT inhibits
405
pembrolizumab
PD-1 inhibitors. Block the death receptor on Tcells to boost immune response in MM
406
Ipilimumab
CTLA-4 inhibitor. Blocks CTLA-4 to allow stronger immune response
407
Kapois's Sarcoma
endothelial malignancy of lymph or blood vessles trigger by HHV-8
408
Appearnce of Kaposis
on skin, musocal membranes (mouth) lymph nodes, lungs, GI, form purple, red, brown blotches on skin. Most often on legs and face.
409
Symptoms of kaposis
asymptomatic
410
Classical Kaposis
Mediterranean - elderly men on legs, ankles, soles of eet, slightly weaker immune system
411
Endemic Kaposis
lymphadeopathic, aggressive in Africa, young men, rapidly fatal. due to weakened immune system
412
Iatrognic Kaposi's
Transplant related due to immuneosuppression
413
Epidemic Kaposi's
AIDs associated
414
Treatment of Kaposi's Sarcoma
radiation, excision, INFalpha, chemo
415
Ages for Impetigo
most common in children, but all ages
416
Acquired by - impetigo
Staph, Strep, S. pyrogens due to direct contact more so than fomites
417
Predisposing factors for imeptigo
high humidity, cutaneous carriage, poor hygiene
418
Impetigo Contagiosa
Non-bullous impetigo of the face (sometimes extremities). One single erythematous macule + superficial blister that forms in multiple honey colored lesions. Variable lymphadenopathy. 5% associated with post-strep glomerulonephiritis
419
Non-Bollous - staph impetigo
Face of person of any age, secondary lesions due to injury or dermatitis, with yellow crust with variable erythema.
420
Bullous Impetigo
can occur anywhere with single superficial flaccid blister and layered pus that transforms into multiple blisters. Most often due to staph infection.
421
Scalded Skin Syndorme
Staph infection in children
422
Diagnosis of Impetigo
CP, culture, gram stain of crust/fluid, rarely skin biopsy
423
which impetigo is associated with glomerulonephritis?
Impetigo contagiosa
424
Cellulitis is acquired by..
bacterial infection of Beta-heylolytic strep, staph, H, influenza, through breaks in skin in elderly, immunocompromised, IV drug users, ulcers, post surg.
425
Erysipeals
St. Anthony's fire- cellulitis of the face. Appears as cliff border with non-pitting edema. Associated with pain, region lyphadenompathy. Rarely is there bullae, pustules or nerosis
426
Cellulitis
Located on extremities, ill defined, warmth, painful, lypthatic streaking, variable lymphadenopathy. Progresses to septicemia.
427
Diagnosis of Cellulti
CP, CBC with leukoctyosis, biopsy for edema and increased PMNS, not usually culture or gram staning
428
Dermatophytus
fungal infections due to contact with humans, animals, fomites and soil.
429
Trichophyton rubrum
cutaneous pathogen
430
Trichophyton mentagrophytes
tinea pedia
431
trichophyton tonsurans
tinea capitis
432
Microsporum canis
fluorescent tinea capitis
433
Epidermophyton fluccosum
tinea cruris
434
Scalp or hair fungal infections
tinea capitis with grey patch or black dots, associated with Kerion: abscess formation
435
Body fungal infections
Tinea corporis, occurs on glabrous skin (non hair bearing) Associated with Majoochi's Granuloma
436
Majoochi's Granuloma
follicular pus + Glanulomas associated with tinea corporis
437
Tinea Cruris
genital fungal infection
438
Onychomycosis
nail fungal infection
439
Candidasis Finections
Fungal infections on skin, MM
440
Predispoing factors to Candidasis
Diabetes, occlusion, corticosteroid, broad spectrum antibiotics
441
Food source of candidas
glucose and serum
442
Thrus
oral candidas infection
443
Perleche
Angular cheilitis or angles of mouth, candida infection
444
Erosio interdigalis Bastomyce
Interdigital candida infection
445
Tinea Versicolor
Melazzesi Furfur, occurs in post-Pubertal in warm/humid areas. most often occurs on cutaneous surfaces like the trunk. Has subtly scaly macules with patches. Mostly asymptomatic
446
Complications of Tinea Versicolor
Hypopigmented, Folicultiis: follicular papules.
447
Diagnosis of Tinea Versicolor
CP, KOH: spagetti and meatballs
448
What do Dermatophytus infections eat?
Keratin
449
what does candidas eat?
Glucose and serum
450
what does Tinea Versicolor eat?
Follicular Lipids
451
Scabies
Sarcropetes scabiei infection by direct contact which leads to interdigital, flextures, genitals or breast manifestations. Skin finginds: erythematous papules with burrows, scale, nodules. Pururitis that occurs at night or after bathing
452
Norwegian Scabies
massive hyperkeratosis in immunosuppressed people or with decreased sensation.
453
Scalp Lice
Pediculus Hamanus Va. Capitis
454
Body lice
pediculus hamanus var. corporis
455
Pubic Louse
Phthirus pubis
456
Head lice
scalp, post auricular, posterior neck, with nits. Lice are brown with six legs and difficult to find. Associated with intense puritus and erythymatous scale
457
Body lice
Only found on clothes similar appearnce to head, pruritus, erythemyatous papules and macules
458
Crab or pubic lice
Genital, eyelash, bear, axially found easily on hairy attachments causes pruritus
459
Diagnosis of scabies
mineral oil for scraping or skin biopsy
