D&D Unit 3 Flashcards

1
Q

What is the range for fitzpatrick skin types?

A

I to VI where I is super light and VI is super dark

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2
Q

What are the 2 types of melanin?

A

Eumelanin - black/bron

Pheomelanin - yellow/red-brown

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3
Q

What is the melanin distribution difference between light and dark skin?

A

Light - melanosomes are distributed in clusters above the nucleus
Dark - melanosomes are distributed individually throughout the cytoplasm

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4
Q

Which skin cells synthesize vitamin D?

A

Keratinocytes

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5
Q

Which skin cells provide immunologic protection?

A

Langerhans cells

I think they are the macrophages

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6
Q

Which skin glands lubricate the skin?

A

Sebaceous

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7
Q

Which skin glands create pheromones?

A

Apocrine glands

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8
Q

What are the 2 layers of the dermis? What is their connective tissue like?

A

Papillary - loose connective tissue

Reticular - dense connective tissue

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9
Q

What is the embryonic origin of melanocytes?

A

Neural crest

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10
Q

How many keratinocytes get melanin from each melanocyte?

A

30

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11
Q

How long does epidermis renewal take?

A

About 28 days

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12
Q

What causes epidermolysis bullosa symplex?

A

Congenital defects in keratin filaments 5 and 14

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13
Q

What are the 5 layers of the epidermis?

A
Stratum basalis
Stratum spinosum
Stratum granulosum
Stratum lucidum
Stratum corneum
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14
Q

What does filagrin do?

A

Cross-links keratin tonofilaments

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15
Q

What organs in the skin sense touch? Where are they located?

A

Meissner’s corpuscles

Papillary layer of the dermis

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16
Q

What organs in the skin sense touch, vibration, and pressure? Where are they located?

A

Pacinian corpuscles

Reticular layer of the dermis

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17
Q

Where are the blood vessels for thermoregulation located?

A

Reticular layer of the dermis

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18
Q

What are the 2 types of sweat glands?

A

Apocrine - in axillary, pubic, perianal regions

Eccrine - everywhere else

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19
Q

Downward projections of epidermis are called ________________ and interdigitate with the ______________ of the dermis

What are they for?

A

Epdermal rete
Dermal papillae
Increase strength of adherence and surface area between epidermis and dermis

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20
Q

Which collagen is most prevalent in the adult dermis?

A

Collage I

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21
Q

Which collagen is most prevalent in the fetal dermis?

A

Collagen II

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22
Q

Which collagen is most prevalent in the basement membrane?

A

Collagen IV

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23
Q

Which collagen attaches the epidermis and dermis?

A

Collagen VII

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24
Q

What is the structure of collagen?

A

3 chains arranged in an alpha helix

Striations at 68nm intervals. These are usually Gly-Pro-Hydroxyproline

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25
Q

What is an important cofactor required for extracellular assembly of collagen fibrils?

A

Vitamin C (ascorbic acid)

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26
Q

How do you tell microscopically if skin is from an old person or a sun-exposed site?

A

Presence of solar elastosis

They are basophilic

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27
Q

What happens to the skin in pseudoxanthoma elasticum?

A

Elastic fibers become enlarged, tangled, calcified

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28
Q

What 2 things is ground substance made of?

A

Hyaluronic acid
Dermatan sulfate

They are both glycosaminoglycans

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29
Q

What is auspitz sign?

A

In psoriasis, when scales are removed, pinpoint bleeding occurs

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30
Q

What causes leukocytoclastic vasculitis?

A

Immune complexes form and precipitate in vessel walls

  • > inflammation
  • > palpable purpura
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31
Q

What is itch n medical terms?

A

Pruritus

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32
Q

Where do nerves end in the skin:?

A

The dermoepidermal junction

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33
Q

What are the afferent nerves for pruritus?

A

Small, unmyelinated C fibers with a slow conduction rate

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34
Q

What do Pacinian corpuscles resemble?

What do Meissner’s corpuscles resemble?

A

Onion

Pinecone

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35
Q

What are the 2 types of hairs?

A

Terminal hairs

Vellus hairs

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36
Q

What are the 3 areas of a hair?

A

Infundibulum
Isthmus (from the sebaceous duct to insertion of arector pili)
Matrical area

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37
Q

What embryonic structure is the follicular unit derived from?

A

Primitive ectodermal germ

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38
Q

What are the lower, middle, and upper bulges of the primitive ectodermal germ for?

A

Lower - attachment for arrector pili
Middle - sebaceous gland
Upper - apocrine gland

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39
Q

What are the 3 growth phases hair can be in?

A

Anagen - growth
Telogen - resting
Catagen - transition between anagen and telogen

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40
Q

What 2 treatments are there for androgenic alopecia?

A

5-alpha-reductase inhibitor (blocks conversion of testosterone to 5-dihydrotestosterone
Minoxidil

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41
Q

What are the 3 parts of the eccrine gland?

A

Coiled secretory portion
Intradermal duct
Intraepidermal portion

From deep to surface

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42
Q

What neurotransmitter triggers sweating?

A

Acetylcholine

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43
Q

What part of the autonomic nervous system triggers sweating (sympathetic or parasympathetic)?

A

Sympathetic

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44
Q

Where are apoeccrine glands found?

A

Axilla

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45
Q

Albnism is due to a defect in the _________ gene in the melanin production pathway

A

Tyrosinase

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46
Q

Where are 3 places we get vitamin D from?

A

Sun exposure
Fish/figh liver oils
Egg yolks

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47
Q

What causes rickets?

A

Vitamin D deficiency

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48
Q

Which layer are skin stem cells located in?

A

Basal cell layer (stratum basalis)

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49
Q

Where in the skin are hemidesmosomes found?

A

They attach the basal cells to the basal lamina of the dermal-epidermal junction

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50
Q

What is bullous pemphigoid?

A

Autoimmune response to hemidesmosomes, causing the dermal-epidermal junction to separate -> subepidermal blisters

Antibodies to BP230 or BP180

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51
Q

What is epidermolysis bullosa?

A

Defect in laminin 5 -> blistering

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52
Q

What is dystrophic epidermolysis bullosa?

A

Defect in collagen VII -> scarring, flexion contractures

Autosomal recessive

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53
Q

What is pemphigus vulgaris?

A

An acquired autoimmune disease with antibodies to desmoglein 1 and desmoglein 3
-> flaccid bulla, intraepidermal blisters

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54
Q

What is epidermolysis bullosa simplex?

A

Genetic defects in keratin 5 and 14

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55
Q

What is the breakdown product of filaggrin?

A

Natural moisturizing factor. It binds water to keep the skin moist

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56
Q

What causes icthyosis vulgaris and atopic dermatitis?

A

Loss-of-function filaggrin mutations -> defective skin barrier function.
There are significantly reduced levels of natural moisturizing factor, so more water loss occurs

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57
Q

What are Merkel cells for? Where are they?

A

They are important for neural development and tactile sensation
They are small cells associated with nerve endings in the epidermis

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58
Q

Where is stratum lucidum located? What does it do?

A

In thick skin

It helps reduce friction and shear forces between the stratum corneum and stratum granulosum

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59
Q

What is are dermatologic terms for flat things (2)?

A

Macule - A flat area of color change 1 cm

Patch >1 cm

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60
Q

What are dermatologic terms for elevated things (3)?

A

Papule - 1cm. Width > thickness
Nodule - >1 cm
Plaque >2 cm

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61
Q

What is scale?

A

Excess stratum corneum
Can come as flakes or plates
Color is usually white or grey

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62
Q

What is crust?

A

Dried blood, serum, or purulent exudate that forms on the skin surface

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63
Q

What are dermatologic terms for fluid filled things?

A

Vesicle- 1cm filled with blood or fluid
Bulla >1 cm
Pustule filled with pus

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64
Q

What are the 2 types of bullas?

A

Tense

Flaccid

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65
Q

What are dermatologic terms for pus-filled things?

A

Pustile - >1 cm, circumscribed elevation

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66
Q

What defines an ulcer?

What 3 things further classify it

A

A circumscribed loss of epidermis and at least upper dermis

Depth
Edge
Tissue at base

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67
Q

What is an eschar?

A

A scab!

A black, adherent, thicky, dry crust

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68
Q

What is a dermatologic condition that is distributed following lymphatic vessels?

A

Lymphangitic

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69
Q

What is a dermatologic condition that is distributed on palms and soles?

A

Palmoplantar

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70
Q

What is a dermatologic condition that is distributed in regions with skin-skin contact that causes friction?

A

Intertriginous

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71
Q

What is a dermatologic condition that is distributed on skin overlaying muscles that flex joints?

A

Flexural

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72
Q

What are the collagen differences between the papillary and reticular dermis?

A

Papillary - thin collagen bundles

REticular - thick collagen bundles

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73
Q

Procollagen is synthesizes within fibroblasts and extracellularly and enzymatically cleaved into ____________

A

Tropocollagen

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74
Q

What is Ehlers-Danlos syndrome? What are 4 symptoms?

A
A group of diseases with messed up collagen synthesis
Hyperextensible skin
Hyperextensible joints
Fragile blood vessels
Poor wound healing
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75
Q

What is pseudoxanthoma elasticum? What are 4 symptoms?

A

Mutation in MDR gene
-> calcified, brittle elastic fibers

Plucked chicken skin
Systemic hypertension
Angioid streaks in retina
Arterial rupture (particuarly in eye)

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76
Q

Are there genetic diseases of ground substance?

A

No

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77
Q

Does the epidermis contain vasculature?

A

No

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78
Q

What are the 2 types of skin vessels?

A

Superficial and deep plexi

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79
Q

What are the 2 main differences between type A and C nerve fibers?

A

A - heavily myelinated, rpid conduction

C - unmyelinated, slow-conducting

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80
Q

What are the 4 subtypes of type A fibers?

A

A-alpha - proprioception and large motor units (largest)
A-beta - touch
A-gamma - spindle organs in muscle stretch receptors
A-delta - fast-localizing initial component of pain (smallest)

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81
Q

Does hair form from the outside in or inside out embryologically?

A

Outside in

The mesenchyme induces the overlying neuroecoderm to bud downwards

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82
Q

What is milaria?

A

Prickly heat

From blocked sweat ducts (the eccrine ones)

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83
Q

What is anhidrotic ectodermal dysplasia?

A

Mutant EDA gene
Abberant eccrine development
-> decreased sweating
-> poor temperature regulation

Also get other ectoderm problems like sparse hair and abnormal teeth

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84
Q

What is seborrheic dermatitis a more severe form of? What 4 things is it seen in?

A

Dandruff that can affect scalp, face, upper torso

Parkinson’s
Head trauma
HIV
Chronic neurologic conditions like cerebral palsy

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85
Q

What 4 skin problems are found in diabetes?

A

Acanthosis nigricans
Yellow skin
Brown patches on lower legs
Foot ulcers

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86
Q

What is the skin like in hyperthyroidism? (2)

A

Smooth, warm, moist

Pretibial myxedema

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87
Q

What is the skin like in hypothyroidism? (5)

A
Dry skin
Brittle nails
Sparse hair
Delayed wound healing
Puffy madarosis (loss of lateral third of eyebrow)
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88
Q

What is stasis dermatitis?

A

Chronic venous insufficiency of lower extremities with lower extremity edema

Often seen with other things due to venous insufficiency down there

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89
Q

What are the differences in morphology and location of inflammation between dermatitis and cellulitis?

A

Dermatitis has erythematous papules and thin plaques with scale
Cellulitis is warm, tender erythematous patches or plaques

Dermatitis is in the epidermis/dermis.
Cellulitis is in the dermis and subcutaneous tissues

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90
Q

How do you diagnose allergic contact dermatitis?

A

Patch testing

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91
Q

What is the most frequent dermatologic allergen?

A

Nickel sulfate

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92
Q

What is dermatitis also called?

A

Eczema

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93
Q

Where are venous stasis ulcers usually? What do they look like?

A

On medial lower leg just above ankle.

Red with yellow fibrinous base
Borders irregularly shaped
Can be purulent f infected

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94
Q

What is infantile atopic dermatitis?

A

Dry, red, scaly areas on the cheeks that become flushed w/ cold exposure

Usually under 5 years of age

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95
Q

What is the most common type of contact dermatitis?

A

Irritant contact dermatitis

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96
Q

What 3 things does allergic contact dermatitis require?

A

Exposure of an allergen
Immune response
Development of memory T cells

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97
Q

3 risk factors for nckel sensitivity

A

Female
Young
Exposure

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98
Q

What 2 ointments often have sensitivity reactions?

A

Neomycin

Bacitracin

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99
Q

What is the usual time course for drug eruptions?

A

1-2 weeks after starting a new medication

Starts sooner if given a medication previously reacted to before

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100
Q

What type of immune hypersensitivity is urticaria?

A

Type I - mediated by IgE

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101
Q

What is nummular dermatitis caused by?

A

Excess use of soap and dry skin

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102
Q

What causes seborrheic dermatitis? (2)

A

A combination of overproduction of skin oil and irritation from yeast )malassezia furfur)

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103
Q

4 subtypes of psoriasis

A

Chronic plaque disease
Guttate
Erythroderma
Pustular psoriasis

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104
Q

2 comorbidities for psoriasis

A

Metabolic syndrome

Cardiovascular disease

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105
Q

How long does it take for a fingernail to grow out?

A

6 months

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106
Q

What is the diabetic rash on the shin?

A

Necrobiosis lipoidica

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107
Q

What are Janeway lesions?

A

Septic microemboli that cause bruises

108
Q

What are osler nodes?

A

Raised, red legions on hands and feet
Erythematous, painful vasculitis
Found in endocarditis

109
Q

What are Roth spots?

A

Retinal hemorrhages

110
Q

How do you get strep viridans in the blood?

A

Teeth - usually dental cleaning

111
Q

What happens in systemic scleroderma? (3)

A

Thickened skin (hands, mouth, esophagus, GI)
Raynaud’s
Pulmonary hypertension

112
Q

What happens in lichen planus? (4)

A

Purple, polygonal, pruritic papules
Lace-like white lines
Mucosal lesions
Nail involvement (like white lines there)

113
Q

What 3 things differentiate an expanding ulcer from a regular ulcer? How do you treat them?

A

Has a sharp drop-off edge
Not usually in places with bad circulation
More common in inflammatory disease

Treat with steroids, NOT antibiotics

114
Q

What are 2 nail discoloration findings where the tips turn red?

A

over half red - renal problems

less than half - cirrhosis, congestive heart failure

115
Q

What should are 6 dermatologic clues someone has cancer?

A

Erythema gyratum repens (whorly red marks)
Hypertrichosis languinosa acquisita (extra languo)
Tripe palms
Lesser trellat sign (explosive onset of multiple seborrheic keratoses)
Dermatomyositis
Sister Mary Joseph Node

116
Q

Where on the body are drug rashes?

A

Trunk, not extremities

117
Q

What are the pH differences between normal and pathogenic skin bacteria’s preferred environments.

A

Normal - acidic

Bad - neutral

118
Q

What are the 2 bacteria that cause impetigo?

A

Beta-hemolytic streptococci -> non-bullous impetigo

Staphylococcus aureus -> both non-bullous and bullous impetigo

119
Q

What is the food source for candida (2)?

A

Glucose

Serum

120
Q

What is the fancy-ass dermatologic term for skin tag?

A

Acrochordon

121
Q

What is a junctional nevi?

A

Nevus cells are at the dermal-epidermal junction just above the basement membrane zone of the epidermis

Not super elevated nevus

122
Q

Are fried-egg nevi malignant?

A

No but they are in people with increased risk of melanoma development

123
Q

What condition is basophilia seen in?

A

CML - chronic myeloid leukemia

124
Q

What is the definition of acute leukemia?

A

Neoplastic proliferation of blasts

They are >20% of the bone marrow

125
Q

What is a good way to test for ALL (acute lymphoblastic leukemia)

AML (acute myeloblastic leukemia) (2)

A

tdt positivity in nucleus

Myeloperoxidase and auer rod

126
Q

What are the 2 subtypes of ALL? Which is most common?

A

B-ALL (most common)

T-ALL

127
Q

What CDs are important in B-ALL?

A

CD10, CD19, CD20

128
Q

What are the 2 translocations commonly seen in B-ALLL?
Prognosis?
Patient population?

A

t(12;21) Good prognosis. Children

t(9;22) Poor prognosis. Adults. This is the Philadelphia chromosome

129
Q

What CDs are important in T-ALL?

A

2-8

No 10

130
Q

Which hematologic malignancy has increased risk for DIC?

A

acute promyelocytic leukemia

131
Q

What is a good way to test for acut emonocytic leukemia?

A

They don’t have myeloperoxidase

132
Q

How id impetigo most commonly acquired?

A

Person-to-person contact

133
Q

What is a rash on the cheeks with an indurated sharp border?

A

Erysipelas

134
Q

What fungus causes jock itch and athlete’s foot?

A

Epidermophyton

135
Q

What are the 3 common dermatophyte fungi? What do they eat?

A

Epidermophyton
Microsporum
Trichophyton

They eat keratin

136
Q

What is the most common dermatophyte?

A

Trichophyton

137
Q

What is a tinea infection that forms a plaque?

A

Kerion

138
Q

What happens if you treat a fungal skin infection with topical steroids?

A

It goes into the hair follicles, because steroids reduce immune response
Inflammed follicles - Majocchi’s granuloma
Must treat with systemic steroids now

139
Q

What does tinea look like with KOH?

A

Long, branching, septate hyphae

140
Q

What is candidiasis on the corners of the mouth?

A

Perleche

141
Q

What is candidiasis between the fingers?

A

Erosio interdigitalis blastomycetica chronica

142
Q

What does tinea versicolor eat?

A

Follicular lipids (which is why its patient population is post-pubertal)

143
Q

What fungal infection looks like spaghetti and meatballs with KOH?

A

Tinea versicolor

144
Q

What is Klippel-Trenaunay syndrome?

A

Overgrowth of an extremity covered by a large port wine stain
Becasue of vascular abnormalities

145
Q

What is the dermatologic dimple sign?

A

When you push in the sides, it indents

146
Q

What is seborrheic keratosis?

A

A benign tumor of the hair follicle

147
Q

Basal cell carcinomas arise from pluripotent cells due to mutations in the ___________ pathway

The most common mutant gene in this pathway is __________

A

Hedgehog

Patched 1

148
Q

What is the most common pre-malignant skin lesion?

A

Actinic keratoses

149
Q

The most important indicator of progress in melanoma is ________

A

Breslow depth

This is the maximal thickness of tumor invasion (mm)

150
Q

What is the Clarck level?

A

It describes how what layer of the skin a melanoma has penetrated

I (epidermis) to V (subcutis)

151
Q

Kaposi sarcoma is a cancer of _______

A

Endothelial cells

152
Q

How do the wavelengths of UVA and UVB compare?

A

UVA is longer wavelength

153
Q

3 types of DNA damage from UV radiation

A

Thymiine dimer
Pyrimidine-6-4 pyrimodone
Hydroxyguanosine

154
Q

What 3 ways things can move into the skin?

A

Passive diffusion
Active transport
Transport via appendageal structures like sweat glands and hair follicles

155
Q

What is the difference between and ointment and a cream?

A

Ointments are water in an oil emulsion

Creams are oil in a water emulsion

156
Q

How do glucocorticosteroids affect the NF-KB pathway?

A

They inhibit it, leading to reduction in transcription of cytokines, adhesion mlcs, inflammatory enzymes, and growth factors

157
Q

What 3 glucocorticosteroids do we care most about in derm?

A

In order of potency:
Hydrocortisone
Triamcinolone Acetonide
Clobetasol Propionate

158
Q

What is a disadvantage to an ointment?

A

Patients may dislike greasiness

May stain clothing

159
Q

What is a disadvantage to a cream?

A

Significant sensitization risk

160
Q

What is a disadvantage to a gel?

A

Significant sentitizaiton risk

Relatively high irritaion risk

161
Q

How many grams is a fingertip unit?

A

0.5

162
Q

How is potency of topical steroids evaluated?

A

Vasoconstrictor assays

163
Q

What are the 2 primary proinflammatory cytokines?

A

IL-1

IFN-Y

164
Q

What enzyme excises mutated DNA strands?

A

UVR ABC nuclease

165
Q

5 enzyme defenses against ROS in the epidermis

A
Peroxidase
Catalase
Superoxide dismutase
Glutathione reductase
Thioredoxin reductase
166
Q

The rate limiting enzyme in the melanin production pathway is ___________________

A

Tyrosinase

167
Q

What are 5 things UV light helps?

A
Psoriasis
Atopic dermatitis
Cutaneous T cell lymphoma
Mastocytosis
Vitiligo
168
Q

What is the most common malignancy in teh US?

A

Basal cell carcinoma

169
Q

What drug is used for basal cell carcinoma?

A

Vismodegib

170
Q

What skin condition often becomes skin cancer?

A
Actinic keratosis
(intraepidermal neoplasia)
171
Q

What is Bowen’s disease?

A

Squamous cell carcinoma in situ

172
Q

What is the gene most frequetly mutated in maloma?

A

BRAF

173
Q

Which layer are epidermal stem cells in?

A

Stratum basalis

174
Q

Where in the skin are desmosomes and hemidesmosomes?

A

Desmosomes connect epidermal cells

Hemidesmosomes connect the dermis and epidermis

175
Q

What is the differentce between atopic dermatitis and contact dermatitis?
What is their clinical presentation (5)

A

They are both pruritic, erythematous, oozing rashes with vesicles and edema

Atopic dermatitis is a type 1 hypersensitivity where the irritant is not known. The irritant is known in contact dermatitis

176
Q

What are 3 therapies for psoriasis?

A

Corticosteroids (topical)
UVA light - stops abnormal keratinocyte proliferation
Immune-modulating therapy

177
Q

What are the 5 P’s of the lichen planus signs?

A

Prutitic, planar, polygonal, purple papules

178
Q

What is the difference between pemphigus and pemphigoid?

A

Pemphigus - separation is in epidermis

Pemphigoid - separation of dermis and epidermis at the basement membrane

179
Q

What are 2 worse forms of erythema multiforme?

What is the main difference, besides being worse?

A

Steven Johnson
TEN (toxic epidermal necrolysis)

They have oral mucosa involvement

180
Q

What is the cause of erythema multiforme? What about Steven Johnson/TEN?

A

EM - herpes reaction most commonly but can also be autoimmune, drugs, or other pathogen

SJS is usually an adverse drug reaction

181
Q

Leser-Trelat sign is a sudden onset of multiple _______

A

Seborrheic keratosis

182
Q

What is the main genetic mutation (like on the molecular level) in basal cell carcinoma? What causes it?

A

Pyrimidine dimers

UVB

183
Q

What skin condition is the precursors to squamous cell carcinoma?

A

Actinic keratosis

184
Q

What are the 3 steps of mole growth?

A

Grow along the dermal-epidermal junction - junctional nevus
Extend down into nevus - compound nevus
Junctional component then disappears - intradermal nevus

185
Q

What is the most common complication of polycythemia vera?

A

Acute clotting event

186
Q

BCR-ABL always in ____________ and adult ____________ sometimes

A

CML

AML

187
Q

Which cytokine (?) suppresses immune responses and is released by Tregs?

A

TGF-B

188
Q

What cytokine is most responsible for the inflammatory reactions in the gut?

A

IL-6

189
Q

What 3 grains is gluten in?

A

Wheat
Rye
Barley

190
Q

What are Koch’s postulates showing that microbes cause specific diseases (4)

A
  1. Specific microbes are present regularly in characteristic lesions of the disease
  2. The specific microbes can be isolated and grown in vitro
  3. Injection of the cultured microbes into animals reproduces the disease seen in humans
  4. The specific microbes can be re-isolated from lesions of the disease in animals
191
Q

In a virus, what is the RNA strand that contains the translatable open reading frame that is ‘ribosome-ready’?

A

+ strand

192
Q

what is the eclipse period in viral infection?

A

Occurs after virus adsorption
When no infectious virus is detectable inside or outside the cell
This is because they have released their genomes into the cell

193
Q

What is the latent period in viral infection?

A

The period between initiation of infection to the release of new viruses from the cell

194
Q

What is the unique viral enzyme used to produce mRNA and replicate RNA?

A

RNA-dependent RNA polymerase

195
Q

What are the 2 ways packaging of the genome into the capsid occurs in icosahedral capsids? What about helical nucleocapsids?

A

The capsid assembles around the virus genome
The genome is fed into preformed capsids

The viral genome is coated with nucleocapsid protein during its synthesis

196
Q

What is viral tropism?

A

The fact that viruses infect some tissues and not others

Determined by access to tissue
Receptors
Expression of host genes required for virus infection and production of new progeny virus
Failure of host defences

197
Q

Are enveloped or non-enveloped viruses hardier?

A

Non-enveloped ones

198
Q

What is the difference between type I and II interferones?

A

Type I are made by infected cells

Type II are made by T and NK cells

199
Q

What are the 4 things used to classify viruses

A

Genetic material: DNA/RNA
Capsid: helical/icosahedral
Naked/enveloped
Size

200
Q

What is a spike in terms of viruses?

A

Virus-derived membrane-bound blycoproteins

201
Q

What is the difference between a virus-susceptible and permissive cell?

A

Susceptible has a functional receptor for the virus

Permissive has capacity to replicate the virus

202
Q

What is viremia?

A

The presence of viruses in the blood

203
Q

What is APOBEC3G?

A

A human protein that interferes with the replication of HIV by incorporating itself into virus particles and damaging the genetic material of the virus

204
Q

What is Vif?

A

An HIV protein that blocks APOBEC3G by

  1. binding to APOBEC3G
  2. Targeting APOBEC3G for destrution/elimination
205
Q

What Type I IFNs (2) do we care about? What Type II IFN (1)

A

IFN-A, IFN-B

IFN-Y

206
Q

What cells produce type II interferons?

A

T and NK cells

207
Q

Type I interferons regulate control genes through ______________
Type I interferons do this through __________

A

ISREs (interferon-stimulated response elements)

GAS (gamma activated site elements)

208
Q

Cells respond to interferons through receptor activation of _________ signalling

A

Jak/Stat

209
Q

What are 2 mediators of hte IFN-induced anti-viral state we care about? They reduce protein production ultimately.
What are they activated by?

A

PKR - a protein kinases that decreases protein synthesis by inactivating some translation initiation factors

OAS - activates a cellular ribonuclease that degrades mRNA

Both are activated by dsRNA

210
Q

How do drugs inhibit viral uncoating?

A

They block the virally-encoded H+ ion channel so that the pH change necessary for uncoating can’t occur

211
Q

What is the nucleic acid of choice for herpes?
What is their capsid-shape?
Are they envoloped?

A

dsDNA (linear)
Icosahedral capsid
Envelope

212
Q

What are the latentcy sites of the 3 herpes subfamilies?

A

Alpha - sensory ganglia
Beta - monocytes, lymphocytes
Gamma - B cells

213
Q

How is herpes assembled? How does it leave the nucleus.

A

Assembly occurs in the nucleus and capsids self-assemble
Then the virus gets its envelope from the Golgi
Then it leaves through exocytosis or lysis

214
Q

Which herpes is oral and which is genital?

A

HSV-1 -> orofacial/ocular lesions
HSV-2 -> genitals

Most commonly! Can actually be anywhere

215
Q

Are most primary HSV infections symptomatic?

A

No

216
Q

Where do latent HSV1 and HSV2 hang out?

A

1 - trigemnal ganglion

2 - sacral ganglion

217
Q

Where is herpetic whitlow? Where does it come from?

A

Fingers

Oral secretions

218
Q

Where is herpes keratitis?

A

Cornea

219
Q

At what point is chicken pox no longer infected?

A

When all the lesions are scabbed (about 7 days)

220
Q

Where does latent varicella zoster virus hang out?

A

Nerve ganglia associated with areas in which the virus was present in the skin

221
Q

Does varicella zoster exhibit asymptomatic viral shedding in normal hosts that experience reactivation?

A

No! It is the only herpesvirus that does not.

222
Q

What is the nucleic acid for influenza?

A

RNA

223
Q

What are the 2 types of drugs we use to treat influenza?

A

Matrix protein inhibitors - only for subtype A

Neuraminidase inhibitors - for both subtypes A and B

224
Q

What virus is the most common cause of bronchiolitis?

A

Respiratory syncytial virus

225
Q

What is the nucleic acid for RSV?

A

ssRNA

226
Q

What are F and G proteins for RSV?

A

F - fusion of viral envelope t host cell and membranes of infected cells (syncytia)
G - initial binding of virus to host cell

227
Q

What is the difference between pemphigus and pemphigoid?

A

Pemphigus - epidermal separation

Pempigoid - dermal-epidermal separation

228
Q

Proximal subungal white onchomycosis is associated with what other disease?

A

HIV

229
Q

Proximal subungal white onchomycosis is due to ________

A

Trichophyton infection

230
Q

Which dermatologic condition is on flexor surfaces? Which is on extensor surfaces?

A

Atopic dermatitis

Psoriasis

231
Q

In chicken pox, do lesions present at the same stage?

A

no

Lesions are in multiple stages in the same body regions

232
Q

Do shingles lesions cross the midline?

A

No

233
Q

Where does CMV establish latency?

A

Monocytes and lymphocytes

234
Q

Where does reactivated CMV shed?

A

Urine and saliva

235
Q

How does acyclovir help reduce influenza infection?

A

Blocks nucleic acid synthesis

Terminates DNA chains (may only be in herpes)

236
Q

Which drug blocks influenza nucleic acid synthesis?

A

Acyclovir

237
Q

What do amantadine and rimantadine do in influenza infections?

A

Prevent viral uncoating by blocking H+ channel formation, thus preventing pH change necessary for uncoating

238
Q

Which drugs (2) block influenza uncoating

A

Amantadine

Rimantidine

239
Q

What do zanamivir and oseltamivir do in influenza infections?

A

Prevent viral release from cells

240
Q

Which drugs (2) block influenza release from cells?

A

Zanamivir

Oseltamivir

241
Q

Neuraminidase inhibitors are most effective when started within _______ hours after symptom onset

A

48

242
Q

How is zanamivir administered?

A

Inhalation

243
Q

Which drug prevents the herpes virus family from attaching to cells?

A

Docosanol

244
Q

What does docosanol do?

A

Prevents herpes viral attachment to cells

245
Q

What 3 drugs inhibit herpes family viral DNA polymerase?

A

Acyclovir
Roscarnet
Ganciclovir

246
Q

What do acyclovir, roscarnet, and gancyclovi do?

A

Inhibit herpes viral DNA polymerase

247
Q

What is resistance to acyclovir usually from?

A

Reduction or loss of expression of viral tyrosine kinase

248
Q

What is the active form of vitamin D? What organ synthesizes it?

A

Calcitriol

Kidneys

249
Q

Which UVR converts 7-dehydrocholesterol to vitamin D3?

A

UVB

250
Q

What does the liver convert D2 and D3 to?

A

Calcidiol

251
Q

What is the difference between eclipse and latent phases of viral infection?

A

Eclipse - no viruses detectable becaseu they are being replicated
Latent - period from infection until viruses are detectable outside cells

252
Q

Cholera is _______ mediated
Pneumonia is _______cellular bacteria
TB is _____cellular bacteria

A

Toxin
Extra
Intra

253
Q

What are viral spikes?

A

Virally-encoded glycoproteins

254
Q

What is the nucleic acid for the herpes family?

A

dsDNA

255
Q

What is a holocrine gland? Which one is on the skin?

A

A holocrine gland excretes whole cells

Sebaceous gland

256
Q

What can you treat infantile hemangiomas with?

A

Beta blockers

257
Q

Kaposi’s sarcoma is a malignancy of _______

A

Melanocytes

258
Q

Malassazea furfur causes which 2 skin diseases?

A

Tinea versicolor

Seborrheic dermatitis

259
Q

What are the 2 types of empetigo and which bacteria causes each?

A

Bullous - staph

Nonbullous - strep

260
Q

What color is eumelanin?

A

Red/brown

261
Q

What is the nucleic acid for RSV and influenza?

A

ssRNA

262
Q

What is valacyclovir?

A

A prodrug of acyclovir that has better bioavailability

263
Q

How does acyclovir dose compare between VZV and HSV?

A

VZV is less sensitive and requires higher dose

264
Q

Within what time frame do you begin acyclovir treatment for stuff like shingles?

A
265
Q

What is a cell resistant to viral infection?

A

It does not have receptors to allow the virus entry

266
Q

What is FAMMM?

A

Familial atypical multiple mole melanoma