Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Derm > Test 1 > Flashcards

Test 1 Flashcards

You may prefer our related Brainscape-certified flashcards:
Dermatology Board Prep flashcards
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the parts of the nail?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 5 ypes of cutaneous glands?

A

-Sudoriferous =
Merocine
Apocrine

  • Sebaceous
  • Ceruminous: modified apocrine, ear wax
  • Mammary: modified apocrine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which embryological layers forms the integumentary sytem?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What’s genetic cause of Xeroderma Pigmentosum?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Is sweat hyper, iso, or hypotonic?

A

Sweat is Hypotonic, salt is removed as fluid is secreted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How are fevers produced molecularly?

A

Fever = pyrogens create cytokines like IL1-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

When does temp regulation start to fail, and what’s the rate?

A

Temp retulation starts to fail at 94 degrees, and rate of heat production in each cell is depressed 2x for each 10 degree drop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is frostbite?

A

Frostbite = ice crystals in cells that leads to permanent circulatory impairment and local tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How is Pruritis transmitted?

A

Pruritis: free nerve endings of unmyelinated C fibers to spinal cord’s Anterolateral system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Differentiate Anterolateral vs Dorsalmedial systems of sensory transmission

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How do Estrogen and Testosterone affect the skin?

A

Estrogen: makes skin soft, smooth, more vascular, increased warmth and bleeding when cut
Testosterone: makes skin thick, subQ tissue rugged, increased sebaceous gland activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What cytokines do Keratinocytes secrete?

A

Keratinocytes:
inflammatory = IL1, IL6, TNF-a
bactericidal/static beta-defensins
anti-inflammatory = IL10 and TGF-beta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the immune mediator for Pemphigus vulgaris?

What’s its target antigen?

A

Pemphigus vulgaris:

IgG against Desmoglein 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the immune mediator for Bullous pemphigoid

What’s its target antigen?

A

Bullous pemphigoid:

IgG against hemidesmosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the immune mediator for Dermatitis Herpetiformis?

What’s its target antigen?

A

Dermatitis Herpetiformis:

IgA against epidermal transglutaminases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the immune mediator for Bechet’s disease?

What’s its target antigen?

A

Bechet’s disease:

IgG against ANCA (antineutrophil cytoplasmic antibodies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the immune mediator for SLE?

What’s its target antigen?

A

SLE

IgG against dsDNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What’s the T-cell subtype and target antigen for Psoriasis?

A

Psoriasis:

Epidermal CD8 and Dermal Cd4, attacking unk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What’s the T-cell subtype and target antigen for Atopic Dermatitis?

A 
Atopic Dermatitis (eczema):
CD4 attacking allergens on skin, unk what's inside
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What’s the T-cell subtype and target antigen for Allergic contact dermatitis?

A

Allergic contact dermatitis/hypersensitivity:

CD8 attacking Haptens = small molecules that elicit Type IV hypersensitivity rxn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What’s the T-cell subtype and target antigen for Vitiligo?

A

Vitiligo:

CD8 attacking melanocyte autoantigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What’s the T-cell subtype and target antigen for Cutaneous Tcell Lymphoma?

A

Cutaneous Tcell lymphoma:

CD8, Ag independent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What causes SLE’s malar rash?
extremities/trunk rash?
Chronic Discoid rash

A

Malar: Ig and/or compliment settle at dermal-epidermal junction
extremities/trunk: Ab to Ro Ag
Discoid: inflammation NOT Ab mediated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Describe pathology behind SJS and TEN

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q 
What are the HLA alleles that favor presentation of the following drugs to CD8 Tcells (causing drug-mediated skin toxicity)?
Carbamazepine
Phenytoin
Abacavir
Allopurinol
A

Carbamazepine: HLA-B 1502 (esp Asians)
Phenytoin: HLA-B 5601
Abacavir: HLA-B 5701
Allopurinol: HLA-B 5801

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q 
Differentiate the following:
•     Creams
•     Foams
•     Gels
•     Lotions
•     Occlusive tapes
•     Ointments
•     Pastes
•     Powders
•     Shampoos
•     Solutions
•     Sprays
A

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:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What increases corticosteroid potency?

A

Steroid potency increases w/fluorinated chemical structure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Name low, moderate, high, and super high topical corticosteroids:

A

Low: Hydrocortisone
Moderate: Triamcinolone
High: Fluocinonide
Super high: Clobetasol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How much is a finger-tip unit for topical drug use?

A

finger-trip = 0.5g, and 5mm wide (nozzle on the tube)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is steroid rosacea?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Where do striae develop when using topical steroids?

A

Striae develop in groin and armpits, where there’s skin-skin contact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Can use Wood’s Lamp to aid in diagnosing what, and what will you see?

A

Tinea capitis: Microsporum will look blue-green
Erythrasma: Corynebacterium will look coral-red
Porphyria cutanea tarda: looks pink/orange-red

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What do you see in a fungal culture, if there’s a Dermatophyte?

A

Dermatophyte:

Yellow phenol indicator in media turns Red

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What’s the gold standard for skin cancer diagnosis?

A

BIOPSY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What gets a biopsy?
What gets excisional?
Excision/punch?
Excision shave?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What’s better for max cure rate, excision or Curretage and Electrodesiccation?

A

Excision!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How to differentiate b/w papule and plaque and nodule?

A

Papule <0.5cm, vesicle if clear fluid filled
Plaque >0.5cm, bulla if fluid filled
Nodule has DEPTH beneath skin, cyst if fluid filled

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What are common drugs that cause Fixed Drug Eruptions? sxs?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What’s pathogenesis behind Fixed Drug Eruptions?

A

FDE: CD8 act as memory cells to incite next response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Differentiate nevus simplex and port wine stain sxs, tx?

A

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!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Pityriasis rosea sxs? tx plan?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Melasma sxs? associations?

A

Melasma = hyperpigmentated macules on face
assoc: women, pregnancy, OCPs, cosmetics, dark skinned, worsened by sun exposure, photosensitizing drugs, thyroid dysufnction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Differentiate Ephelides, Simple Lentigines, and solar lentigines

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Peutz-Jegher’s syndrome presentation?

A

Peutz-Jegher’s syndrome: AD
pigmented macules on lips/hands/genitalia (aka Simple Lentigines), hamartomatous polyps in GI, increased risk of GI and BrCa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What’s assoc w/cafe ole spots? and their sxs?

A

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
Q

Differentiate Congenital vs Acquired Melanocytic nevi

A

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
Q

Halo nevi sxs?

A

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
Q

What’s 1 most prevalent effect observed in all types of albinism?

A

lack of melanin + adverse effects on vision

67
Q

What’s 1 enzyme that decreases inactivity in all 4 types of Oculocutaneous albinism?

A

Tyrosinase

68
Q

What’s 1 protein most implicated in Ocular albinism?

A

GPCR GPR143, needed for retinal development (ligand = Dopamine)

69
Q

What’re most severe vs most prevalent type of albinism?

A 
OCA1A = most severe
OCA1B = most prevalent
70
Q

Differentiate Oculocutaneous vs Ocular Albinism?

A

OCA affects skin too, AR

OA only affects eyes, x-linked recessive

71
Q

What’s MOA of Nitisinone that helps pigment developing fetal mouse?

A

Nitisinone blocks alternative tyrosine processing pathway, forcing Tyrosine back towards Tyrosinase-DOPA-DOPAquinone…Eumelanin pathway

72
Q

What’s 1 a.a. precursor used to make monomeric building blocks for melanin? additional a.a. precursor needed to make Pheomelanin?

A 
Tyrosine = building block
Cysteine = addtl building block need to make Pheomelanin
73
Q

Describe pathway to make melanin from dopamine?

A

Tyrosinee -> DOPA -> DOPAquinone, both via TYrosinase
DOPAquinone can be linked to cystein to be make into Pheomelanin
DOPAquinone can be made into Eumelanin

74
Q

What are the melanin biosynthesis steps that’re implicated in 5 types of albinism?

A

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
Q

Differentiate Eumelanin to Pheomelanin

A 
Eumelanin = true black/brown that' protects from UV
Pheomelanin = red/yellow, doesn't UV protect
76
Q

How does UV signal an increase in melanin production?

A

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
Q

What mutation assoc w/familial melanoma?

A

CDKN2A gene most commonly ID’d in familial forms of melanoma, Loss of tumor supression

78
Q

What are 2 oncogene activations implicated w/Melanoma?

A

Oncogenes BRAF and NRAS

79
Q

What are Stage III Melanoma adjuvant txs? MOA?

A

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
Q

What are Stage IV Melanoma Tx? MOA?

A

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
Q

What are Ipilimumab’s ADEs?

A

Ipilimumab ADEs:

immune mediated enterocolitis/hepatitis/dermatitis/neuropathies/endocrinopathies

82
Q

What are Nivolumab and Pembrolizumab’s ADes?

A

Immune mediated problems, but less bad than Ipilimumab’s

83
Q

What’s Ipilimumab’s MOA?

A

Ipilimumab: blocks CTLA4, which normally turns off Tcells

84
Q

What’s Nivolumab and Pembrolizumab’s MOA?

A

Nivolumab/Pembrolizumab: PD1 blocker (programmed death), allowing tumor specific Tcells to continue killing tumor cells

85
Q

What’s Vemurafenib / Cobimetinib and

Dabrafenib / Trametinib MOA?

A 
Vemurafenib / Cobimetinib and 
Dabrafenib / Trametinib
BRAF/MEK blockers
BRAF mutations allow constitutive phosphorylation/activation of MEK/MAPK downstream
MEK: protooncogene when mutated
86
Q

What’s Vemurafenib / Cobimetinib and

Dabrafenib / Trametinib ADEs?

A 
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
Q

How is Neurofibraomatosis1 inherited, what’s it caused by?

What are the 2 forms?

A

NF1 d/t MF1 gene mutation that codes for Neurofibromin, AD inheritance
1 Cutaneous
2 Plexiform

88
Q

How to dx and tx Neurofibromatosis1?

A

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
Q

What does Neurofibromin do, esp in RAS/RAF/MEK/ERK pathway?

A

Neurofibromin normally downregulates RAS

Losing Neurfibromin’s tumor suppressor activity, a loss of function that’s AD bc of 2 hit model

90
Q

Why do you see tumor clustering in segmental Neurofibromatosis1?

A

Mosaicism w/Somatic cell mutations

91
Q

Differentiate cutaneous neurofibromas from plexiform neurofibromas

A

• 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
Q

Differentiate Neurofibromatosis 1, 2, and Schwannomatosis

A

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
Q

What’s Neurofibromatosis 2 caused by, how does it present, how to dx?

A

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
Q

What’s Schwannomatosis caused by, how does it present, how to dx?

A

d/t SMARCB1 mutation, presents w/Schwannomas, chronic pain, numb/weak

95
Q

common agents that cause photosensitivity?

A
  • 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
Q

How does Dermatomyositis present? how to dx and tx?

A

○ 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
Q

Differentiate discoid lupus and SLE?

A
  • 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
Q

What can cause post-inflammatory hyperpigmentation?

A
  • 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
Q

What’s tx of choice for vitiligo?

A

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
Q

Why is the lab test for Dermatomyositis used?

A

Dermatomyositis test = anti-Jo1 bc it’s myositis specific Ab, directed against histidyl-tRNA synthetase which catalyzes histidine binding during protein synthesis

101
Q

How to differentiate Pityriasis alba from Vitiligo?

A

Pityriasis alba: lesions have indistinct borders, most ocmmon in kids, and cream colored (vs Vitiligo white), maybe assoc w/Atopic Dermatitis

102
Q

What’s presentation of Tuberous Sclerosis?

A 
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
Q

Differentiate 3 Dermatophytes

A

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
Q

Differentiate pyogenic granuloma and keratoacanthoma?

A

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
Q

What does granuloma annulare look like?

Who gets this?

A

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
Q

How to dx and tx Lyme disease?

A 
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
Q

What causes and sxs of Erythema nodosum?

Who gets it?

A 
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
108
Q

How to dx and tx Erythema nodosum?

A

Erythema nodosum
Dx: clinical
Tx: self-limited

109
Q

Differentiate common blue nevus to cellular blue venus

A

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)

110
Q

Describe seborrheic keratosis?

Tx?

A

Seborrheic keratosis
benign proliferation of keratinocytes in epidermis, >50yo, ‘stuck-on’ and greasy/warty/scaled
Tx: cosmetic removal

111
Q

What else presents w/acanthosis nigricans besides DM?

A

Acanthosis Nigricans assoc w/ DM, and

obesity, breast/bladder/colon/bile duct malignancies that have rapid onset

112
Q

Describe Verruca Vulgaris sxs

tx?

A

Verruca vulgaris: warts on hands

Tx: salicylic acid, liquid nitrogen, Bichloroacetic/trichloroacetic acid

113
Q

Differentiate Acrochordons, Molluscum, and Xanthelasma?

A 
Acrochordons = skin tags = benign, flesh colored, painless, pedunculated neoplasms
Molluscum = flesh colored umbilicated-centerd papules d/t poxvirus
Xanthelasma = cholesterol plaques on eyelids
114
Q

What’s the sign of Dermatofibroma?

clinical presentation?

A

Dermatofibroma:
“dimple sign” d/t fibroblastic nature
Presents as benign cutaneous nodule, more in women, lower legs, asymptomatic

115
Q

What are the 2 most common subtypes of cutaneous lymphoma, and differentiate?

A

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
Q

Describe Kaposi’s sarcoma, types, and tx?

A

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

117
Q

How does Lichen planus present?
assoc?
dx?
tx?

A

Lichen Planus:
chronic mucocutaneous disease of unk cause
Purple, Polygonal, Pruritic, Plaque, Planar
+Wickham striae, HepC, Koebner phenomenon
Dx: clinical, punch bx
Tx: corticosteroids

118
Q

What’s Koebner phenomenon

A

seen in psoriasis and other skin conditions, Koebner’s phenomenon is when lesions appear where they shouldn’t after traumatic injury

119
Q

What are cutaneous findings of sarcoidosis?

A

Sarcoidosis:

Lofgren’s syndrome = acute form of sarcoid, erythema nodosum + b/l hilar LAD, polyarthralgia/arthritis

120
Q

What’s presentation of psoriasis?

A

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

121
Q

How to dx and tx Psoriasis?

A

Psoriasis dx: clinical, famhx, skin bx

Tx: topicals

122
Q

What’s immunological etiology behind Psoriasis?

Differentiate cell mediated vs innate mechanisms

A

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

123
Q

Describe role of Treg cells in psoriasis

A

• 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

124
Q

Vit D3 agent names?
TI
PK
ADE

A

Calcitriol/Calcipotriene
TI: plaque psoriasis
PK: topical
ADE: burn/itchy/irritation/dry/erythematous skin, hypercalcemia

125
Q 
Retinoid agent names?
TI
PK
ADE
CI
A 
Acitretin/Tazarotene
TI: Severe intractable psoriasis, esp pustular forms
PK: oral
ADE: dry/itchy skin
CI: pregnancy
126
Q 
Immunosuppressant agent names for Psoriasis?
MOA?
TI
PK
ADE
A 
Tacrolimus/Pimecrolimus
MOA: inhibits calcineurin in Tcells
TI: Plaque and Inverse Psoriasis (and atopic dermatitis)
PK: topical
ADE: burn/warm/itchy skin
127
Q 
PDE4 Inhibitor agent for Psoriasis name?
MOA
TI
PK
ADE
Precautions
A

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

128
Q 
TNF inhibitor agents for Psoriasis name?
TI
PK
ADE
CI
A

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!

129
Q 
Cytokine blocker agents for Psoriasis names?
MOA?
TI
PK
ADE
CI
A

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!

130
Q

Differentiate Erythema multiforme major and minor

A

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

131
Q

Differentiate SJS and TEN

A

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

132
Q

What can cause TEN?

A

TEN usually drug induced (sulfa, pcn, allopurinol, dilantin, NSAIDs)

133
Q

Differentiate bullous pemphigoid and pemphigus vulgaris

A

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

134
Q

What does Nikolsky’s sign mean?

A

(+) Nikolsky means damage is more superficial, causing skin to rupture when you touch the bullae

135
Q

How does Dermatitis herpetiformis present?
Assoc?
Dx?
Tx?

A

Dermatitis herpetiformis:
looks like herpes EM, but IgA mediated at papillary dermis and linked to Celiac disease
Dx: bx w/immunofluorescence
Tx: Dapsone

136
Q

What’s another name for Dyshidrotic eczema?

A

Dyshidrotic eczema = acute palmoplantar eczema

137
Q

How does Dyshidrotic eczema present?
exacerbating conditions?
tx?

A

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

138
Q

How does rosacea present?

what are 4 types?

A

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.

139
Q

How does perioral dermatitis present?
possible causes?
tx?

A

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
Q

Differentiate pseudofolliculitis barbae and hot tub folliculitis?

A

pseudofolliculitis barbae: razor bumps, most commonly in black men, erythematous/hyperpigmented papules
hot tub folliculitis: psuedomonas, common in swim suit covered areas

141
Q

Describe miliaria in its various forms

A

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
Q

What can you use Mupirocin for?

A

Mupirocin:
TI: Impetigo and other minor skin infections, nasal application for MRSA, secondarily infected skin lesions like eczema

143
Q

What Abx do you use for non-purulent cellulitis, moderate purulent cellulitis, and severe purulent cellulitis?

A

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
Q

What’s the MOA for
Bacitracin
Polymixin B
Colistin

A

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
Q

Whats immunopathogenic mechanism behind Pemphigus vulgaris

A

Pemphigus vulgaris: HLA-DR4, and HLA-DR6 (MHC-II), IgG binds Desmoglein3

146
Q

Whats immunopathogenic mechanism behind Pemphigus foliaceus?

A

Pemphigus foliaceus: autoAb against Desmoglein1

147
Q

Whats immunopathogenic mechanism behind Paraneoplastic Pemphigus?

A

Paraneoplastic pemphigus: IgG in repsonse to neoplasms that bind keratinocytes, esp plakin proteins, Desmoglein 1/3

148
Q

Whats immunopathogenic mechanism behind Intraepidermal, Neutrophilic Dermatosis?

A

Intradermal, neutrophilic IgA Dermatosis:

IgA bound to keratinocytes that induces PMN infiltrate

149
Q

Whats immunopathogenic mechanism behind Bullous Pemphigoid?

A

Bullous pemphigoid: IgG and/or C3 deposits against hemidesmosomes

150
Q

Whats immunopathogenic mechanism behind Epidermolysis Bullous Acquisita?
Sxs?

A

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

151
Q

Whats immunopathogenic mechanism behind Herpes Pemphigoid Gestationis?
Sxs?

A

Pempigoid Gestationis:
HLA-DR3/4, Ab and compliment for BP ag2, some women get anti-HLA
Itchy, blistering disease of pregnancy

152
Q

Whats immunopathogenic mechanism behind Linear Bullous diseases?
Sxs?

A

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

153
Q

Whats immunopathogenic mechanism behind Dermatitis herpetiformis?
Sxs?

A

Dermatitis herpetiformis:
HLA-B8, HLA-DR3, HLA-DQ2, w/IgA at dermal-epidermal junction
itchy, small blisters on extensor surfaces, assoc w/Celiac

154
Q

Which drugs for acne are at the following targets?
Follicular hyperproliferation and abnormal desquamation
Increased sebum production
P acnes proflieration
Inflammation

A

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

155
Q

What are first line tx for mild, moderate, and severe acne?

A

Mild: benzoyl peroxide or topical retinoid +/- Abx
Moderate: BP + Abx and/or Retinoid
Severe: Abx + BP + Retinoid OR Isotretinoin

156
Q

What’re 4 tx for Rosacea?

A 
Rosacea tx
1 avoid trigger
2 topical/oral Metronidazol
3 Isoretinoin
4 Dermabrasion and tissue excision for rhinophyma rosacea
157
Q

Oral Abx used to treat MRSA skin infection?

A

TMP-SMZ orally can treat MRSA skin infection

IV vancomycin, Tetracycline, Daptomycin, Linezolid, Cetarolene can treat systemic MRSA

Derm (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions