Test 1 Flashcards

(157 cards)

1
Q

What are the 5 layers of epidermis, and what’s special about each?

A

Californians Love G-String Bikinis
Corneum: dead/dying cells
Lucidum: dead cells prominent in thick epidermis of palms and soles
Granulosum: waterfood, dense basophilic keratohyalin granules
Spinosum: bridged by desmosomes
Basale: keratinocytes, stem cells

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2
Q

What are the diseases found in the 5 layers of the epidermis?

A
Corneum: psoriasis and warts
Lucidum: none
Granulosum: warts
Spinosum: pemphigus vulgaris, squamous cell carcinoma, seborrheic keratosis
Basale: basal cell carcinoma
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3
Q

What are the 3 types of hair?

A

Languo: fine, downy, unpigmented hair on fetus
Vellus: fine/pale, replaces lanugo by birth, 2/3 of female hair, 1/10 of male hair, kids hair except eyebrows, eyelashes, scalp
Terminal: long/coarse/v pigmented, eyebrows, eyelashes, axillary/pubes after puberty, male facial, some hair on trunk and limbs

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4
Q

What are the 4 types of sensory nerves? and their roles?

A

Pacinian/lamella corpuscle: mechanoreceptor for pressure and vibration
Meissner’s/tactile corpuscle: light touch, highly sensitive
Nociceptors:
C-fibers: slow pain
A-delta: fast pain

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5
Q

What are the parts of the nail?

A

Outer: Paronychium, Eponychium, nail groove, Lanula
Nail bed
Nail fold
Nail root

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6
Q

What are the 5 ypes of cutaneous glands?

A

-Sudoriferous =
Merocine
Apocrine

  • Sebaceous
  • Ceruminous: modified apocrine, ear wax
  • Mammary: modified apocrine
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7
Q

Which embryological layers forms the integumentary sytem?

A

Ectoderm: Epithelium, assoc glands
Mesoderm: connective tissue of dermis and hypodermis

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8
Q

What is the Epidermis made of (material)?

What’s the Dermis made of (Material)?

A

Epidermis: keratin in intercellular networks connected by Desmosomes
Dermis: collagen I and III, in extracellular networks, made by fibroblasts

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9
Q

Walk through what connects epidermis to dermis (all the proteins)

A

Integrin-Laminin-Collagen IV in hexagonal lattice/net-Collagen VII-Collagen I and II of dermis

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10
Q

Differentiate Collagen and Keratin and Fibrillin (bonus, their disease assoc?)

A

Collagen: triple helix of glycine-proline-hydroxyproline (Ehler’s-Danlos)
Keratin: 2 coiled coils in antiparallel filaments (epidermolysis bullosa simplex)
Fibrillin: releases its bound TGF-beta w/tissue damage to increase cell/tissue growth (Marfan’s)

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11
Q

What are the 3 types of Epidermal Bullosa, and differentiate

A

Epidermolysis bullosa

1) Simplex: AD, most prevalent, affects cytoskeleton in basal and squamous cells, superficial/skin/nails/hair, can lead to muscular dystrophy and pyloric atresia
2) Junctional: AR, super rare, affects epidermis and BM, significant risk of congenital GU problems, can lead to pyloric atresia
3) Dysmorphic: affects BM and dermis

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12
Q

Differentiate pemphigus vulgaris, pemphigus foliaceus, and bullous pemphigoid in terms of etiology

A

1) Pemphigus vulgaris: AutoAb against desmoglein 3
2) Pemphigus foliaceus: AutoAb against desmoglein 1
3) Pemphigoid: AutoAb against Hemidesmosomes

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13
Q

Differentiate UVA and UVB rays

A

UVA: causes tAnning by oxidizing existing melanin, most of UV at sea level, present in all sunlight, penetrates glass and deep into dermis, targets basal cells
UVB: causes sun Burns, signals more melanin production, <5% of UV at sea level, only present at noon/high altitude/lower longitude, targets squamous cells, but still relevant risk factor for BCC, absorbed by DNA

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14
Q

How does Stratum Granulosum layer provide waterproofing?

A

Granules made mostly of Filaggrin
Filaggrin = histadine rich protein that binds to keratin in cytoskeleton
Skin drying signals Filaggrin degradation, releasing Histadine that helps retain H2o in skin
Histadine = Urocanic acid precursor, which signals skin moistening, immune suppression, and UV protection

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15
Q

Walk through mechanism of UV induced tanning

A

UV damages DNA in squamous cells
Basal cells upregulate p53
p53 bind to DNA as transcription factor, signaling expression of POMC
POMC cleaved to alpha-melanocyte stimulating hormone (alpha-MSH)
a-MSH binds to Melanocortin1 receptor on Melanocytes, GPCR
Melanocytes stimulated to make more melanin
Melanosomes move to surface

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16
Q

Differentiate Eumelanin and Pheomelanin

A

Eumelanin blocks UV

Pheomelanin is red/yellow, doesn’t block UV bc Europeans needed more sun to make VItD

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17
Q

What’s genetic cause of Xeroderma Pigmentosum?

A

XP caused by AR, loss of fx mutation of Nucleotide Excision Repair mechanisms

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18
Q

Skin is under what type of ANS control? What are the receptor types?

A

Skin is under SNS control
Sweat glands that’re thermoregulatory are mACh
Stress sweat and Pilomotor muscles are alpha-adrenergic

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19
Q

Is sweat hyper, iso, or hypotonic?

A

Sweat is Hypotonic, salt is removed as fluid is secreted

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20
Q

Where is ‘shivering’ primary motor center? What happens when it activates?

A

Shivering command starts in Posterior Hypothalamus (dorsomedial, near wall of 3rd ventricle) after it senses cooling via Anterior Hypothalamus
Increases muscle tone
max shivering can increase body heat 4-5x normal

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21
Q

Walk through molecular pathway for non-shivering thermogenesis

A

In brown fat, SNS’s Epi/NE signals uncoupling of oxidative phsophorylation via mitochondrial uncoupling protein Therogenin
Heat released instead of ATP producted

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22
Q

Who has more brown fat, babies or adults?

A

Babies have more brown fat, can increase heat production 100%
Adults have little brown fat, can increase heat production 10-15%

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23
Q

How does thyroid help regulate heat? What disease can occur?

A

Anterior Hypothalamus-preoptic area senses cooling leads to TRH release
leads to Thyroxine release
activates uncoupling protein and increases cellular metabolism through body
extreme cold for weeks can lead to thryoid gland increases 20-40%
leads to goiters

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24
Q

How are fevers produced molecularly?

A

Fever = pyrogens create cytokines like IL1-1

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25
When does temp regulation start to fail, and what's the rate?
Temp retulation starts to fail at 94 degrees, and rate of heat production in each cell is depressed 2x for each 10 degree drop
26
What is frostbite?
Frostbite = ice crystals in cells that leads to permanent circulatory impairment and local tissue damage
27
How is Pruritis transmitted?
Pruritis: free nerve endings of unmyelinated C fibers to spinal cord's Anterolateral system
28
Differentiate Anterolateral vs Dorsalmedial systems of sensory transmission
Anteriolateral: pain, thermal, crude touch, tickle/itch, sexual, much slower and low spatial localization Dorsalmedial: touch localization and fine pressure gradations, vibratory, movement, joint sensation, much faster and high spatial localization
29
How do Estrogen and Testosterone affect the skin?
Estrogen: makes skin soft, smooth, more vascular, increased warmth and bleeding when cut Testosterone: makes skin thick, subQ tissue rugged, increased sebaceous gland activity
30
What cytokines do Keratinocytes secrete?
Keratinocytes: inflammatory = IL1, IL6, TNF-a bactericidal/static beta-defensins anti-inflammatory = IL10 and TGF-beta
31
What is the immune mediator for Pemphigus vulgaris? | What's its target antigen?
Pemphigus vulgaris: | IgG against Desmoglein 3
32
What is the immune mediator for Bullous pemphigoid | What's its target antigen?
Bullous pemphigoid: | IgG against hemidesmosome
33
What is the immune mediator for Dermatitis Herpetiformis? | What's its target antigen?
Dermatitis Herpetiformis: | IgA against epidermal transglutaminases
34
What is the immune mediator for Bechet's disease? | What's its target antigen?
Bechet's disease: | IgG against ANCA (antineutrophil cytoplasmic antibodies)
35
What is the immune mediator for SLE? | What's its target antigen?
SLE | IgG against dsDNA
36
What's the T-cell subtype and target antigen for Psoriasis?
Psoriasis: | Epidermal CD8 and Dermal Cd4, attacking unk
37
What's the T-cell subtype and target antigen for Atopic Dermatitis?
``` Atopic Dermatitis (eczema): CD4 attacking allergens on skin, unk what's inside ```
38
What's the T-cell subtype and target antigen for Allergic contact dermatitis?
Allergic contact dermatitis/hypersensitivity: | CD8 attacking Haptens = small molecules that elicit Type IV hypersensitivity rxn
39
What's the T-cell subtype and target antigen for Vitiligo?
Vitiligo: | CD8 attacking melanocyte autoantigens
40
What's the T-cell subtype and target antigen for Cutaneous Tcell Lymphoma?
Cutaneous Tcell lymphoma: | CD8, Ag independent
41
What causes SLE's malar rash? extremities/trunk rash? Chronic Discoid rash
Malar: Ig and/or compliment settle at dermal-epidermal junction extremities/trunk: Ab to Ro Ag Discoid: inflammation NOT Ab mediated
42
Describe pathology behind SJS and TEN
CD4 Th1 release inflammatory cytokines, induce macrophages and PMNs to destroy tissue CD4 Th2 cells release IL4 and IL5, stimulating eosinophils to cause inflammation and destruction CD8 cell kill via Fas-Fas ligand and releasing perforin granzymes
43
``` What are the HLA alleles that favor presentation of the following drugs to CD8 Tcells (causing drug-mediated skin toxicity)? Carbamazepine Phenytoin Abacavir Allopurinol ```
Carbamazepine: HLA-B 1502 (esp Asians) Phenytoin: HLA-B 5601 Abacavir: HLA-B 5701 Allopurinol: HLA-B 5801
44
``` Differentiate the following: • Creams • Foams • Gels • Lotions • Occlusive tapes • Ointments • Pastes • Powders • Shampoos • Solutions • Sprays ```
Cream: H2o + oil, can cause contact allergy Foam: Gel: thick polymer solvent, good for hairy Lotion: liquid w/medication suspension/dissolved in H20>oil, good for hairy Occlusive tapes Ointment: semi-solid, good for dry skin bc greasy/sticky/retains sweat (bad for weepy dermatitis) Pastes: Powders: base used to apply powders, powders can absorb secretion Shampoos: Solutions: Sprays:
45
What increases corticosteroid potency?
Steroid potency increases w/fluorinated chemical structure
46
Name low, moderate, high, and super high topical corticosteroids:
Low: Hydrocortisone Moderate: Triamcinolone High: Fluocinonide Super high: Clobetasol
47
How much is a finger-tip unit for topical drug use?
finger-trip = 0.5g, and 5mm wide (nozzle on the tube)
48
What is steroid rosacea?
ide effect commonly observed in fair-skinned people who already have rosacea. A typical example occurs when a person uses a very mild steroid on the face to counteract the facial flushing. This gives pleasing results, but tolerance develops, causing the person to use a higher strength steroid. At this point any attempt to cut down on the steroid application or stop altogether cause intense facial redness and pustules
49
Where do striae develop when using topical steroids?
Striae develop in groin and armpits, where there's skin-skin contact
50
Can use Wood's Lamp to aid in diagnosing what, and what will you see?
Tinea capitis: Microsporum will look blue-green Erythrasma: Corynebacterium will look coral-red Porphyria cutanea tarda: looks pink/orange-red
51
What do you see in a fungal culture, if there's a Dermatophyte?
Dermatophyte: | Yellow phenol indicator in media turns Red
52
What's the gold standard for skin cancer diagnosis?
BIOPSY
53
What gets a biopsy? What gets excisional? Excision/punch? Excision shave?
all suspected neoplastic lesions gets a biopsy! Including Bullous disorders! Excision: Erythema nodosum, Panniculitis Excision/punch: dysplastic nevi, malignant melanoma Excision/shave: actinic keratoses, BCC, Seborrheic keratosis, pyogenic granuloma, skin tags, SCC, warts
54
What's better for max cure rate, excision or Curretage and Electrodesiccation?
Excision!
55
How to differentiate b/w papule and plaque and nodule?
Papule <0.5cm, vesicle if clear fluid filled Plaque >0.5cm, bulla if fluid filled Nodule has DEPTH beneath skin, cyst if fluid filled
56
What are common drugs that cause Fixed Drug Eruptions? sxs?
Sulfonamides, NSAIDs, ASA, Tetracycline, laxatives, barbiturates Sxs: erythematous macules/edematous plaques, esp on lips/genitals, upper arm, thigh, tend to reoccur at same site w/re-exposure, chronically results in post-inflammatory hyperpigmentation
57
What's pathogenesis behind Fixed Drug Eruptions?
FDE: CD8 act as memory cells to incite next response
58
Differentiate nevus simplex and port wine stain sxs, tx?
Nevus simplex: congenital, erythematous macule, "Stork bite" or "salmon patch", esp on back of neck, glabellum, eyelids, fades within 1-2yrs Port Wine stain: Sturge-Weber syndrome (+seizures, leptomeningeal angiomas), "nevus flammeus", darker than nevus simplex, doesn't fade and may become thicker!
59
Pityriasis rosea sxs? tx plan?
Pityriasis rosea: maybe viral starts w/single macule "hearld patch", develops central clearing and peripheral scale (differentiates from secondary syphillis or guttate psoriasis, plus not on palms/soles) Looks like tinea corporis, but no fungal hyphae "christmas tree" configuration of many smaller lesions develop 1w-3mo after Resolves in 6w-months
60
Melasma sxs? associations?
Melasma = hyperpigmentated macules on face assoc: women, pregnancy, OCPs, cosmetics, dark skinned, worsened by sun exposure, photosensitizing drugs, thyroid dysufnction
61
Differentiate Ephelides, Simple Lentigines, and solar lentigines
Ephelides: freckles, same # melanocytes w/larger melanosomes, fades w/sun avoidance Simple Lentigines/Lentigo: increased # of melanocytes not in nests like mole/nevus, not limited to sun exposed areas, if peri-oral indicative of Peutz-Jegher's Solar Lentigines/Lentigo: increased melanin, 'age/liver spots' on sun-exposed skin, doesn't fade w/sun avoidance
62
Peutz-Jegher's syndrome presentation?
Peutz-Jegher's syndrome: AD pigmented macules on lips/hands/genitalia (aka Simple Lentigines), hamartomatous polyps in GI, increased risk of GI and BrCa
63
What's assoc w/cafe ole spots? and their sxs?
Neurfibromatosis Type 1 aka von Recklinghausen: AD, NF1 mutations, axillary freckling + CNS tumors, + 3 types w/different outcomes McCune-Albright Syndrome: GNAS mutation, mosaicsm, affects bones/skin/endocrine, polyostotic fibrous dysplasia Fanconi anemia: AR, most develop cancer, esp AML + bone marrow failure + endocrine problems
64
Differentiate Congenital vs Acquired Melanocytic nevi
Congenital = huge, esp bathing trunk distribution Acquired = benign neoplastic proliferation of melanocytes, increased # w/sun, rarely have malignant transformation Both have "nevus cells" = melanocytes in nests
65
Halo nevi sxs?
Halo nevi = pigmented, acquired nevi that loses pigmentation in periphery bc body mounts Tcell rxn against the melanocytes, BENIGN BUT DON'T BE FOOLED
66
What's 1 most prevalent effect observed in all types of albinism?
lack of melanin + adverse effects on vision
67
What's 1 enzyme that decreases inactivity in all 4 types of Oculocutaneous albinism?
Tyrosinase
68
What's 1 protein most implicated in Ocular albinism?
GPCR GPR143, needed for retinal development (ligand = Dopamine)
69
What're most severe vs most prevalent type of albinism?
``` OCA1A = most severe OCA1B = most prevalent ```
70
Differentiate Oculocutaneous vs Ocular Albinism?
OCA affects skin too, AR | OA only affects eyes, x-linked recessive
71
What's MOA of Nitisinone that helps pigment developing fetal mouse?
Nitisinone blocks alternative tyrosine processing pathway, forcing Tyrosine back towards Tyrosinase-DOPA-DOPAquinone...Eumelanin pathway
72
What's 1 a.a. precursor used to make monomeric building blocks for melanin? additional a.a. precursor needed to make Pheomelanin?
``` Tyrosine = building block Cysteine = addtl building block need to make Pheomelanin ```
73
Describe pathway to make melanin from dopamine?
Tyrosinee -> DOPA -> DOPAquinone, both via TYrosinase DOPAquinone can be linked to cystein to be make into Pheomelanin DOPAquinone can be made into Eumelanin
74
What are the melanin biosynthesis steps that're implicated in 5 types of albinism?
OCA1A/B have Tyrosinase mutations OCA2-4 have tyrosinase processing mutations: OCA2 has p-protein mutation OCA3 has Tyrosine related protein mutation OCA4 has Membrane ASsc Transport Protein mutation
75
Differentiate Eumelanin to Pheomelanin
``` Eumelanin = true black/brown that' protects from UV Pheomelanin = red/yellow, doesn't UV protect ```
76
How does UV signal an increase in melanin production?
UVB causes cell damage, activates p53, POMC transcription, cleavage into a-MSH, activates MC1R activates Adenylate cyclase converts ATP->cAMP activates PKA actiavtes CREB, Mitf as trasncription factor activated, Eumelanin made, melanosomes released to keratinocytes
77
What mutation assoc w/familial melanoma?
CDKN2A gene most commonly ID'd in familial forms of melanoma, Loss of tumor supression
78
What are 2 oncogene activations implicated w/Melanoma?
Oncogenes BRAF and NRAS
79
What are Stage III Melanoma adjuvant txs? MOA?
Melanoma Stage IIII Adjuvant txs: INFalpha2b: enhances dendritic cell immune response Nivolumab: PD1 inhibitor Ipilimmab: CTLA4 inhibitor Dabrafenib/Trametinib: BRAF/MEK blockers Talimogene laherparepvec: direct injection of HSV into tumor to cause lysis
80
What are Stage IV Melanoma Tx? MOA?
Melanoma Stage IV tx: INFalpha2b: enhances dentritic cell immune response Nivolumab, Pembrolizumab: PD1 inhibitor Ipilimumab: CTLA4 inhibitor Dabrafenib/Trametinib: BRAF/MEK blockers Vemurafenib/Cobimetinib: BRAF/MEK blockers Aldesleukin = IL2, stimulates cytokine cascade
81
What are Ipilimumab's ADEs?
Ipilimumab ADEs: | immune mediated enterocolitis/hepatitis/dermatitis/neuropathies/endocrinopathies
82
What are Nivolumab and Pembrolizumab's ADes?
Immune mediated problems, but less bad than Ipilimumab's
83
What's Ipilimumab's MOA?
Ipilimumab: blocks CTLA4, which normally turns off Tcells
84
What's Nivolumab and Pembrolizumab's MOA?
Nivolumab/Pembrolizumab: PD1 blocker (programmed death), allowing tumor specific Tcells to continue killing tumor cells
85
What's Vemurafenib / Cobimetinib and | Dabrafenib / Trametinib MOA?
``` Vemurafenib / Cobimetinib and Dabrafenib / Trametinib BRAF/MEK blockers BRAF mutations allow constitutive phosphorylation/activation of MEK/MAPK downstream MEK: protooncogene when mutated ```
86
What's Vemurafenib / Cobimetinib and | Dabrafenib / Trametinib ADEs?
``` BRAF-blockers: *Arthralgia CK Elevation *Cutaneous SCC Diarrhea *Photosensitivity *Pyrexia Skin rash / HFS MEK-blockers: CK Elevation Diarrhea *Edema *Lt Ventricular Dysfunction *Neuropsychiatric Sx *Retinopathy Skin rash / HFS (hand-foot syndrome) ```
87
How is Neurofibraomatosis1 inherited, what's it caused by? | What are the 2 forms?
NF1 d/t MF1 gene mutation that codes for Neurofibromin, AD inheritance 1 Cutaneous 2 Plexiform
88
How to dx and tx Neurofibromatosis1?
Dx 2+ of: • Six or more cafe-au-lait spots (> 5 mm prior to puberty and > 15 mm after puberty) 99% • Axillary or inguinal freckling 87 % • Two or more Lisch nodules (= iris hamartomas) 95 % • Two or more neurofibromas 75 % • One or more plexiform neurofibromas (almost exclusively seen in NF1) 30% • Optic pathway glioma (benign tumor derived from glial or “glue cell”) 15 % • Typical bony abnormality (i.e., pseudoarthrosis, sphenoid dysplasia) 5 % First-degree family relative with NF1 50 %
89
What does Neurofibromin do, esp in RAS/RAF/MEK/ERK pathway?
Neurofibromin normally downregulates RAS | Losing Neurfibromin's tumor suppressor activity, a loss of function that's AD bc of 2 hit model
90
Why do you see tumor clustering in segmental Neurofibromatosis1?
Mosaicism w/Somatic cell mutations
91
Differentiate cutaneous neurofibromas from plexiform neurofibromas
• cutaneous neurofibromas (at least 2) ○ benign tumors originating in the connective tissue of the nerve sheath in or under the skin ○ small tumors most prevalent on the trunk usually become apparent near puberty and increase as they age ○ Derived from non-myelinating Schwann Cell enveloping and supporting group of small nerve axons containing many cell types • plexiform neurofibroma (at least 1) ○ large tumors derived from nerves anywhere in body ○ may be present at birth ○ may become malignant (Malignant Peripheral Nerve Sheath Tumor MPNST) ○ Derived from multiple nerve sheath cells Forms “bag of worms” = a bulging, deformed, slowly growing vascularized, non-capsular, benign tumor that may become malignant (Pathognomic for NF1)
92
Differentiate Neurofibromatosis 1, 2, and Schwannomatosis
NF1: RASopathy, 100% have cafe-au-lait spots, 2 cutaneous and 1Plexiform neurofibromas, Lisch nodules, starts 0-10yo NF2: B/L Schwannomas, meningiomas, no Lisch nodules or neurofibramas, starts 18-24yo Schwannomatosis: Schwannomas in non-vestibular cranial nerves, starts 30-50yo
93
What's Neurofibromatosis 2 caused by, how does it present, how to dx?
d/t NF2 gene mutating the Neurofibromin2 (Merlin), intereferes w/cell-to-cell signaling Dx: sxs: B/L Vestibular Schwannomas (Schwann cells around 1 single axon) causing hearing loss, no Lisch nodules, no neurofibromas, can be meningiomas
94
What's Schwannomatosis caused by, how does it present, how to dx?
d/t SMARCB1 mutation, presents w/Schwannomas, chronic pain, numb/weak
95
common agents that cause photosensitivity?
* Drugs implicated in photosensitivity * Tetracycline * Ciprofloxacin * Diuretics (thiazide, furosemide) * Retinoids * NSAIDS * Musk ambrette, oil of bergamot (found in perfumes) * Agents found in some soaps and cosmetics
96
How does Dermatomyositis present? how to dx and tx?
○ Heliotrope rash - violaceous rash on eyelids ○ Gottron’s sign - erythematous plaques with scale on extensor surfaces of joints- hands, knees, elbows ○ Shawl sign and V sign - erythema over back of neck and V of chest. ○ Erythroderma - generalized Periungual erythema due to prominent capillary beds = red fingers ○ prox muscle weakness ○ may develop interstitial lung disease and mild myocarditis Dx: clinic/lab tests for Anti-Jo1 Tx: Glucocorticoids
97
Differentiate discoid lupus and SLE?
* Systemic lupus is an inflammatory disease affecting many organs, but including skin in the majority of patients * Discoid lupus is a variant with discoid lesions of the skin, W/O other systemic involvement, have 5-10% risk of developing systemic involvement later
98
What can cause post-inflammatory hyperpigmentation?
* Deposition of melanin in either the epidermis or dermis as a result of inflammatory stimulation of melanocytes. * Presents as brown discoloration in area with prior history of inflammation * May occur after trauma, infections, inflammatory skin conditions such as atopic dermatitis, acne, SLE and others. * More common in darker skinned individuals
99
What's tx of choice for vitiligo?
Vitiligo tx of choice = Repigmentation w/topical corticosteroids (Fluticasone), immunomodulatorys, photochemotherapy, surgical autologous transplants of healthy melanocytes or application of psoralens and UVA exposure
100
Why is the lab test for Dermatomyositis used?
Dermatomyositis test = anti-Jo1 bc it's myositis specific Ab, directed against histidyl-tRNA synthetase which catalyzes histidine binding during protein synthesis
101
How to differentiate Pityriasis alba from Vitiligo?
Pityriasis alba: lesions have indistinct borders, most ocmmon in kids, and cream colored (vs Vitiligo white), maybe assoc w/Atopic Dermatitis
102
What's presentation of Tuberous Sclerosis?
``` Tuberous Sclerosis = Ash leaf macules seizures cortical tubers + facial angiofibromas brain/kidney/skin tumors + renal angiomyolipoma + cardiac rhabdomyoma + retinal hamartoma + adenoma sebaceum (red cheek papules) ```
103
Differentiate 3 Dermatophytes
Trichophyton: hair/skin/nail, Rt angle hyphae, endothrix infection, responsible for Onychomycoses Microsporum canis: hair/skin, spindle shaped thick walled hyphae, ectothrix infection, fluorescent blue-green under Wood's lamp Epidermophyton: skin/nail, smooth thin walled 2-4 cell macroconidia
104
Differentiate pyogenic granuloma and keratoacanthoma?
Pyogenic granuloma: benign vascular neoplasm, usually seen in kids/YA/preggos mouths, at trauma sites or w/exposure to drugs, friable and grows quickly Keratoacanthoma: domed papule w/keratin filled center, rapidly growing, occurs on hair-bearing sun-exposed areas, spontaneously resolves
105
What does granuloma annulare look like? | Who gets this?
Granuloma Annulare: looks like tinea corporis but w/o scale, usually on distal extremity, ropy border, central clearing More women, assoc w/diabetes and malignancy
106
How to dx and tx Lyme disease?
``` Lyme: Erythema migrans: occurs 1-2w after bite, slowly expands, maybe be multiple/warm, targetoid lesions may have systemic sxs Dx: clinical appearance Tx: amoxicillin or doxycycline ```
107
What causes and sxs of Erythema nodosum? | Who gets it?
``` Erythema Nodosum: etiology unk but ○ Streptococcal infection common, but also seen with fungal infections, tuberculosis ○ Sarcoidosis ○ Drugs-sulfonamides, OCPs ○ Pregnancy ○ Ulcerative colitis and Crohn’s ○ Bechet’s disease Lymphomas sxs: pretibial subQ nodules, erythematous/violaceous, painful, often fever/malaise/arthralgias precedes rash ```
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How to dx and tx Erythema nodosum?
Erythema nodosum Dx: clinical Tx: self-limited
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Differentiate common blue nevus to cellular blue venus
Common Blue Nevus: <1cm, hand/feet dorsum Cellular Blue Nevus: >1cm, scalp/butt/sacrum/face, more concern for melanoma Both: smooth papule of benign proliferation of dermal melanocytes, arises in teens-20s (NOT mongolian spot)
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Describe seborrheic keratosis? | Tx?
Seborrheic keratosis benign proliferation of keratinocytes in epidermis, >50yo, 'stuck-on' and greasy/warty/scaled Tx: cosmetic removal
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What else presents w/acanthosis nigricans besides DM?
Acanthosis Nigricans assoc w/ DM, and | obesity, breast/bladder/colon/bile duct malignancies that have rapid onset
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Describe Verruca Vulgaris sxs | tx?
Verruca vulgaris: warts on hands | Tx: salicylic acid, liquid nitrogen, Bichloroacetic/trichloroacetic acid
113
Differentiate Acrochordons, Molluscum, and Xanthelasma?
``` Acrochordons = skin tags = benign, flesh colored, painless, pedunculated neoplasms Molluscum = flesh colored umbilicated-centerd papules d/t poxvirus Xanthelasma = cholesterol plaques on eyelids ```
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What's the sign of Dermatofibroma? | clinical presentation?
Dermatofibroma: "dimple sign" d/t fibroblastic nature Presents as benign cutaneous nodule, more in women, lower legs, asymptomatic
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What are the 2 most common subtypes of cutaneous lymphoma, and differentiate?
Cutaneous lymphoma: M>F >50yo 1 Mycosis fungoides: patches of erythematous scaling plaques in non-sun exposed areas, bx non-diagnostic 2 Sezary syndrome: generalized erythrodema w/Sezary cells in blood (cerebriform nuclei), poor prognosis
116
Describe Kaposi's sarcoma, types, and tx?
Kaposi's sarcoma: HHV8 vascular tumor, 4 types, purple/red/brown plaques/nodules on extremities, face, oral mucosa may have GI/pulmonary lesions Tx: HAART if AIDS assoc, radiation therapy, IFN, chemo, cryo/surg if small
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How does Lichen planus present? assoc? dx? tx?
Lichen Planus: chronic mucocutaneous disease of unk cause Purple, Polygonal, Pruritic, Plaque, Planar +Wickham striae, HepC, Koebner phenomenon Dx: clinical, punch bx Tx: corticosteroids
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What's Koebner phenomenon
seen in psoriasis and other skin conditions, Koebner's phenomenon is when lesions appear where they shouldn't after traumatic injury
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What are cutaneous findings of sarcoidosis?
Sarcoidosis: | Lofgren's syndrome = acute form of sarcoid, erythema nodosum + b/l hilar LAD, polyarthralgia/arthritis
120
What's presentation of psoriasis?
Psoriasis: autoimmune salmon colored plaques w/silvery scale on extensor surfaces • 5 Types of psoriasis ○ Plaque psoriasis most common (typical salmon colored plaques w/silver scale) ○ Guttate psoriasis- sudden occurrence of many <1cm psoriatic lesions over the trunk, often following a streptococcal infection ○ Inverse psoriasis- affecting gluteal fold, inguinal folds, axillae ○ Pustular psoriasis- severe form ○ Erythrodermic • Psoriatic Nails ○ Nail involvement occurs in about half of all psoriasis patients, but can also be the sole manifestation in a minority of patients. • Psoriatic arthritis ○ Occurs in about 1/3 of patients with psoriasis ○ Often has nail involvement ○ May affect DIP joints only, or may mimic RA, or may affect SI joints and spine, Some forms are very destructive, Classic "pencil=in-cup" deformity of DIP on xray, Dactylitis = finer/toe inflammation, swells up into sausage tx: steroids
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How to dx and tx Psoriasis?
Psoriasis dx: clinical, famhx, skin bx | Tx: topicals
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What's immunological etiology behind Psoriasis? | Differentiate cell mediated vs innate mechanisms
Psoriasis immuno: Heat shock proteins (S100A12) released by keratinocytes TLR agonists stimulate dendritic and Langerhans cells chronic stimulation of adaptive immune response by exogenous Ags develops into chronic rxn w/o further outside activators d/t Treg inability to downregulate response
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Describe role of Treg cells in psoriasis
• TREG cells in peripheral blood and in skin lesions is increased • Positively correlated with disease activity • Function of TREG cells isolated from peripheral blood and skin is decreased • Effector T cells are more resistant to activity of TREG cells Mechanism: increased production of IL-6 at site of inflammation and upregulation of IL-6 receptors on effector lymphocytes
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Vit D3 agent names? TI PK ADE
Calcitriol/Calcipotriene TI: plaque psoriasis PK: topical ADE: burn/itchy/irritation/dry/erythematous skin, hypercalcemia
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``` Retinoid agent names? TI PK ADE CI ```
``` Acitretin/Tazarotene TI: Severe intractable psoriasis, esp pustular forms PK: oral ADE: dry/itchy skin CI: pregnancy ```
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``` Immunosuppressant agent names for Psoriasis? MOA? TI PK ADE ```
``` Tacrolimus/Pimecrolimus MOA: inhibits calcineurin in Tcells TI: Plaque and Inverse Psoriasis (and atopic dermatitis) PK: topical ADE: burn/warm/itchy skin ```
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``` PDE4 Inhibitor agent for Psoriasis name? MOA TI PK ADE Precautions ```
Apremilast MOA: blocking PDE4 increases cAMP which decreases inflammation TI: moderate to severe Plaque psoriasis, psoriatic arthritis PK: oral ADE: GI, HA precaustions: pts w/depression & wt loss
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``` TNF inhibitor agents for Psoriasis name? TI PK ADE CI ```
Etancercept and Infliximab TI: Plaque psoriasis and Psoriatic arthritis PK: SC ADE: serious infections (sepsis and pneumonia!) CI: other immunsuppressants bc will lead to sepsis, make sure they don't have TB!
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``` Cytokine blocker agents for Psoriasis names? MOA? TI PK ADE CI ```
Ustekinumab: IL12/23 block Secukinumb: IL17 block TI: Plaque psoriasis, psoriatic arthritis, ankylosing spondylitis PK: SC ADE: Nasopharyngitis, diarrhea CI: Hypersensitivity, make sure they don't have TB!
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Differentiate Erythema multiforme major and minor
EM Major: mucosal involved EM minor: no mocusa involved both EM: 90% triggered by infections, HSV most common and also mycoplasma, can be d/t drugs, target-like lesion, most spare palms/soles, usually 1-2w
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Differentiate SJS and TEN
SJS: immune rxn causes keratinocyte death, leading to epidermal separation from dermis, necrolysis, <10% body SA affected, prodrome of flu-like illness, 2-4w duration TEN: >30% of skin affected, (+) Nikolsky's sign
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What can cause TEN?
TEN usually drug induced (sulfa, pcn, allopurinol, dilantin, NSAIDs)
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Differentiate bullous pemphigoid and pemphigus vulgaris
Pemphigus vulgaris: IgG Type II hypersensitivity against desmosomes separating stratum spinosum from basale, net/reticular immunofluorescence, (+) Nikolsky sign, no scar, can be fatal, >50yo, no known cause Bullous Pemphigoid: IgG against hemidesmosomes separating basale from dermis, pruritic, tense bullae, (-) Nikolsky sign, scaring, linear immunofluorescence
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What does Nikolsky's sign mean?
(+) Nikolsky means damage is more superficial, causing skin to rupture when you touch the bullae
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How does Dermatitis herpetiformis present? Assoc? Dx? Tx?
Dermatitis herpetiformis: looks like herpes EM, but IgA mediated at papillary dermis and linked to Celiac disease Dx: bx w/immunofluorescence Tx: Dapsone
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What's another name for Dyshidrotic eczema?
Dyshidrotic eczema = acute palmoplantar eczema
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How does Dyshidrotic eczema present? exacerbating conditions? tx?
Dyshidrotic eczema = acute palmoplantar eczema dermatitis of hands/feet, deep seated vesicle/bullae on sides of fingers/feet, spreading to palms/soles assoc w/nickel or contact allergies tx: emollients and steroids
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How does rosacea present? | what are 4 types?
Rosacea = persistent erythema in central portion of face lasting at least 3mo • Erythematotelangiectatic- Most common, recurrent flushing of the central face, often triggered by sunlight, warm drinks/spicy foods, alcohol, exercise, hot showers, emotions or medications, Capillaries may become persistently dilated= telangiectasias. • Papulopustular- no comedos, but erythema of central face with small papules and pustules • Phymatous- skin thickening and nodularity in areas of nose, chin, ears or eyelids (usually nose= rhinophyma) • Ocular- blepharitis, conjunctivitis, conjunctival telangiectasias, burning and dryness.
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How does perioral dermatitis present? possible causes? tx?
Perioral dermatitis: papulopustular dermatitis around mouth sparing right around lips Maybe d/t: steroid use on face, hormones, OCPs, fluoride toothpastes, cosmetics... mostly seen in F 20-45yo Tx: topical Metornidazole/Erythromycin, oral Tetracycline, severe cases needs Isotretinoin
140
Differentiate pseudofolliculitis barbae and hot tub folliculitis?
pseudofolliculitis barbae: razor bumps, most commonly in black men, erythematous/hyperpigmented papules hot tub folliculitis: psuedomonas, common in swim suit covered areas
141
Describe miliaria in its various forms
Miliaria = heat rash, eccrine sweat glands become block and trap sweat under skin ○ Crystallina: most superficial-clear to white vesicles ○ Rubra: slightly deeper- erythematous papules/vesicles ○ Pustulosa: form of rubra with pustules ○ Profunda: deepest- flesh colored papules like goose bumps
142
What can you use Mupirocin for?
Mupirocin: TI: Impetigo and other minor skin infections, nasal application for MRSA, secondarily infected skin lesions like eczema
143
What Abx do you use for non-purulent cellulitis, moderate purulent cellulitis, and severe purulent cellulitis?
non-purulent cellulitis: beta-lactam like Cephaloxin or Dicloxacillin Moderate purulent cellulitis: Doxycycline or TMP-SMX Severe purulent cellulitis: Vancomycin, Daptomycin, Linezolid, Telavancin, Ceftaroline
144
What's the MOA for Bacitracin Polymixin B Colistin
Bacitracin: blocks lipid transport molecule in bacteria that carries building blocks of peptidoglycan bacterial cell wall outside cell membrane for construction Polymixin B: increases cell membrane permeability, works like soap, good for Gr(-) Colistin = Polymixin E: increases cell membrane permeability, works like soap, good for Gr(-)
145
Whats immunopathogenic mechanism behind Pemphigus vulgaris
Pemphigus vulgaris: HLA-DR4, and HLA-DR6 (MHC-II), IgG binds Desmoglein3
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Whats immunopathogenic mechanism behind Pemphigus foliaceus?
Pemphigus foliaceus: autoAb against Desmoglein1
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Whats immunopathogenic mechanism behind Paraneoplastic Pemphigus?
Paraneoplastic pemphigus: IgG in repsonse to neoplasms that bind keratinocytes, esp plakin proteins, Desmoglein 1/3
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Whats immunopathogenic mechanism behind Intraepidermal, Neutrophilic Dermatosis?
Intradermal, neutrophilic IgA Dermatosis: | IgA bound to keratinocytes that induces PMN infiltrate
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Whats immunopathogenic mechanism behind Bullous Pemphigoid?
Bullous pemphigoid: IgG and/or C3 deposits against hemidesmosomes
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Whats immunopathogenic mechanism behind Epidermolysis Bullous Acquisita? Sxs?
Epidermolysis bullous acquisita: HLA-DR2, IgG and compliment localized to dermal-epidermal junction against Type VII collagen Sxs: subepidermal blisters, assoc w/IBD and SLE
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Whats immunopathogenic mechanism behind Herpes Pemphigoid Gestationis? Sxs?
Pempigoid Gestationis: HLA-DR3/4, Ab and compliment for BP ag2, some women get anti-HLA Itchy, blistering disease of pregnancy
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Whats immunopathogenic mechanism behind Linear Bullous diseases? Sxs?
Linear Bullous diseases: Linear IgA at BM, and against LAD1 of Ladinin, an anchoring protein, and Type VII collagen No HLA assoc sxs: pruritic vesicles and papules
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Whats immunopathogenic mechanism behind Dermatitis herpetiformis? Sxs?
Dermatitis herpetiformis: HLA-B8, HLA-DR3, HLA-DQ2, w/IgA at dermal-epidermal junction itchy, small blisters on extensor surfaces, assoc w/Celiac
154
Which drugs for acne are at the following targets? Follicular hyperproliferation and abnormal desquamation Increased sebum production P acnes proflieration Inflammation
Follicular hyperproliferation and abnormal desquamation -topical retinoids, oral retinoids, benzoyl peroxide, azelaic acid Increased sebum production -OCP, Isotretinoin P acnes proliferation -Abx, benzoyl peroxide, azelaic acid Inflammation -Abx
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What are first line tx for mild, moderate, and severe acne?
Mild: benzoyl peroxide or topical retinoid +/- Abx Moderate: BP + Abx and/or Retinoid Severe: Abx + BP + Retinoid OR Isotretinoin
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What're 4 tx for Rosacea?
``` Rosacea tx 1 avoid trigger 2 topical/oral Metronidazol 3 Isoretinoin 4 Dermabrasion and tissue excision for rhinophyma rosacea ```
157
Oral Abx used to treat MRSA skin infection?
TMP-SMZ orally can treat MRSA skin infection | IV vancomycin, Tetracycline, Daptomycin, Linezolid, Cetarolene can treat systemic MRSA