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FMED > derm > Flashcards

derm Flashcards

1
Q

Name the primary lesion.

A

Macula

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2
Q

This is a small spot that is not palpable & that is < 1 cm.

A

What is a macula?

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3
Q

What is a large spot that is not palpable & that is > 1 cm

A

A patch

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4
Q

Name the primary lesion.

A

Patch

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5
Q

What is a small superficial bump that is elevated & that is < 1 cm?

A

Papule

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6
Q

Name the primary lesion.

A

Papule

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7
Q

Name the primary lesion.

A

Plaque

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8
Q

What is a large superficial bump that is elevated & > 1 cm

A

Plaque

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9
Q

Name the primary lesion.

A

Nodule

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10
Q

What is a small bump with a significant deep component & is < 1 cm

A

Nodule

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11
Q

Name the primary lesion.

A

Tumour

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12
Q

What is a large bump with a significant deep component & is > 1 cm

A

Tumour

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13
Q

Name the primary lesion.

A

Vesicle

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14
Q

What is a small fluid-filled bubble that is usually superficial & that is < 0.5 cm

A

Vescile

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15
Q

Name the primary lesion.

A

Bulla(e)

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16
Q

What is a large fluid-filled bubble that is superficial or deep & that is > 0.5 cm

A

Bulla(e)

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17
Q

Name the primary lesion.

A

Pustule

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18
Q

What is pus containing bubble often categorized according to whether or not they are related to hair follicles

A

Pustule

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19
Q

Follicular pustule rash that is superficial, and generally multiple follicles

A

Folliculitis

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20
Q

Follicular pustule rash that is a deeper form of folliculitis.

A

Furuncle

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21
Q

A deeper follicular pustular rash that involves multiple follicles coalescing

A

Carbuncle

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22
Q

What may a nonfollicular pustule rash indicate, as opposed to a follicular rash.

A

Indicates systemic infection as opposed to local.

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23
Q

Name the primary lesion.

A

Cyst

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24
Q

What is a primary lesion?

A

Lesions that appear as a direct result of the pathologic process.

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25
Q

What is a secondary lesion?

A

Lesions that appear as a result of alteration or evolution of a primary lesion (e.g. rubbing, scratching, necrosis)

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26
Q

Name the secondary lesion.

A

Scale

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27
Q

What lesion is the accumulation or excess shedding of the stratum corneum?

A

Scale

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28
Q

What does a scale indicate?

A

It indicates that there is epidermal infolvment, specifically epidermal inflammation: i.e. psoriasis, tinea, eczema

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29
Q

Name the secondary lesion.

A

Crust.

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30
Q

What is a crust?

A

Crust is dried exudate (ie. blood, serum, pus) on the skin surface

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31
Q

Name the secondary lesion.

A

Excoriation

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32
Q

What is excoriation?

A

Excoriation is a loss of skin due to scratching or picking

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33
Q

Name the secondary lesion.

A

Lichenification

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34
Q

What is lichenification?

A

Lichenification is an increase in skin lines & creases from chronic rubbing

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35
Q

Name the secondary lesion.

A

Maceration

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36
Q

What is maceration?

A

Maceration is raw, wet tissue

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37
Q

Name the secondary lesion.

A

Fissure

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38
Q

What is a fissure?

A

A linear crack in the skin - often painful

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39
Q

Name the secondary lesion.

A

Erosion

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40
Q

What is an erosion?

A

An erosion is a superficial open wound with loss of epidermis or mucosa only

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41
Q

Name the secondary lesion.

A

Ulcer

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42
Q

What is an ulcer?

A

An ulcer is a deep open wound with partial or complete loss of the dermis or submucosa

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43
Q

Name the distinct lesion.

A

Wheal (Hive)

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44
Q

What is a wheal or hive?

A

A wheal or hive describes a short lived (< 24 hours), edematous, well circumscribed papule or plaque seen in urticaria

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45
Q

Name the distinct lesion.

A

Burrow.

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46
Q

What is a burrow.

A

A burrow is a small threadlike curvilinear papule that is virtually pathognomonic of scabies

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47
Q

Name the distinct lesion.

A

Comedome

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48
Q

Name the distinct lesion.

A

Atrophy

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49
Q

Name the distinct lesion.

A

Keloid

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50
Q

Distinguish keloid from hypertrophic scar.

A

A keloid overgrows the original wound boundaries and is chronic in nature
A hypertrophic scar on the other hand does not overgrow the wound boundaries

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51
Q

Name the distinct lesion.

A

Fibrosis / Sclerois

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52
Q

Name the distinct lesion.

A

Petechiae.

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53
Q

What does petechia, purpura, and ecchymosis describe?

A

Petechiae or purpura or ecchymosis describes red blood cells that are outside the vessel walls & areas are nonblanchable

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54
Q

Name the distinct lesion.

A

Telangiectasis

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55
Q

What is telangiectasis?

A

Telangiectasis describes dilated superficial dermal vessels

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56
Q

Name the distinct lesion.

A

Milium

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57
Q

What is a milium?

A

A milium is a small superficial cyst containing keratin (usually

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58
Q

What distinct lesion is striae an example of?

A

Atropy

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59
Q

Describe the lesions colour.

A

Erythematous

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60
Q

Describe the lesions colour.

A

Violaceous / Purpuric

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61
Q

Describe the lesions colour.

A

Blue-Grey

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62
Q

Describe the lesion’s colour.

A

Variegated - brown, blue-grey, black, hypopigmented.

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63
Q

Describe the lesion’s colour.

A

Hypopigmented

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64
Q

Describe the lesion’s colour.

A

Depigmented

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65
Q

Describe the lesion’s colour.

A

Yellow

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66
Q

Describe the lesion’s margin.

A

Well circumscribed, well demarcated

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67
Q

Describe the lesion’s margin.

A

Poorly circumscribed, poorly demarcated.

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68
Q

Describe the lesion’s shape.

A

Polygonal

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69
Q

Describe the lesion’s shape.

A

Targetoid. (e.g. erythema multiforme)

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70
Q

Describe the lesion’s shape.

A

Umbilicated (e.g. molluscum contagiosum)

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71
Q

Describe the lesion’ shape.

A

Serpiginous

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72
Q

Describe the lesion’s shape.

A

Verrucous

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73
Q

Descrie the lesion’s configuration.

A

Linear

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74
Q

Describe the lesion’s configuration.

A

Annular (forming a ring)

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75
Q

Describe the lesion’s configuration.

A

Arcuate (curved like a bow)

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76
Q

Describe the lesion’s configuration.

A

Polycyclic

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77
Q

Describe the lesion’s configuration.

A

Grouped

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78
Q

Describe the lesion’s configuration.

A

Zosteriform - Dermatomal

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79
Q

Describe the lesion’s configuration.

A

Reticulate (lacy-like pattern)

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80
Q

Name the 8 histological components of skin.

A
  1. Epidermis - epithelial layer (ectodermal origin)
  2. Dermis - CT layer (mesodermal origin)H
  3. Hair
  4. Sebaceous glands
  5. Sweat glands
  6. Vessels
  7. Nerves
  8. Hypodermis
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81
Q

Name the four physiological functions of the skin.

A
  1. Protection
    • UV light shield
    • injury
    • dehydration
    • microorganisms
  2. Sensation
    • touch
    • pressure
    • pain
    • temperature
  3. Thermoregulation
    • insulation against heat loss
    • heat loss by sweat and blood flow
  4. Metabolic
    • energy storage
    • Vit D syntehsis
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82
Q

The epidermal / dermal junction is irregular. What two regions interdigitate?

A

Dermal Papillae with epidermal Rete Ridges.

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83
Q

What kind of epithelium is the epidermis composed of?

A

Stratified, keratinizing squamous epithelium.

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84
Q

What are the four morphologic layers of the epidermis?

A
  1. Stratum basale
  2. Stratum spinosum
  3. Stratum granulosum
  4. Stratum corneum
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85
Q

Which layer of the epidermis is described as a single layer of mitotically active cuboidal cells?

A

Stratum basale.

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86
Q

Which layer of epidermis is described as an anucleate layer composed mostly of protein.

A

Stratum corneum.

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87
Q

Which layer of epidermis is described as the main living layer consisting of large polyhedral cells.

A

Stratum spinosum

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88
Q

Which layer of epidermis is described as 1-3 cells thick containing large keratohyaline granules.

A

Stratum granulosum.

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89
Q

What is the function of Stratum Corneum?

A

Main diffusion barrier.

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90
Q

In what layer of the epidermis do the cells flatten?

A

Stratum granulosum.

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91
Q

In what epidermal layer does most cellular maturation occur?

A

Stratum spinosum

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92
Q

What is the function of the Stratum basale?

A

Replicating immortal cells that give rise to other keratinocytes.

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93
Q

Name the four cell types within the epidermis

A
  1. Keratinocytes
  2. Melanoctyes
  3. Langerhans cells
  4. Merkel cells
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94
Q

Which epidermal cell relies on this structure to hold tightly to each other, and a hemi-desmosome to the basement membrane.

A

Keratinocyte.

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95
Q

Which epidermal cell is of neural crest origin?

A

Melanocyte

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96
Q

Which epidermal cell’s function is main melanin storage?

A

Keratinocyte

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97
Q

Which epidermal cell synthesizes melanosomes?

A

Melanocytes

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98
Q

Melanin is produces by the action of what enzyme?

A

Tyrosinase

(tyrosine –> DOPA –> dopaquinone –> melanin)

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99
Q

Which epidermal cell contains Birbeck granules, which are tennis racquet-shaped on EM?

A

Langerhans cells

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100
Q

What is the main function of Langerhans cells?

A

Antigen presenting cells

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101
Q

What epidermal layer are Langerhans cells located?

A

Spinous layer

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102
Q

Where in the epidermis are Merkel cells located?

A

Basal epidermis and hair follicle.

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103
Q

Which epidermal cell contains Neurosecretory granules?

A

Merkel cell

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104
Q

What is the main function of Merkel cells?

A

Sensory touch receptors

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105
Q

What are the two layers of dermis?

A

Papillary dermis and Reticular dermis

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106
Q

Which layer of dermis is immediately beneath epidermis?

A

Papillary dermis

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107
Q

What is the papillary layer of dermis made of?

A
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108
Q

What is the reticular dermis made of?

A

Thick type I collagen bundles, and thick elastic fibers

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109
Q

What is responsible for facial wrinkles?

A

Loss of elastic fibers in the papillary dermis

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110
Q

What layer in skin is responsible for thermal insulation?

A

Subcutis or Hypodermis composed of adipocytes

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111
Q

What structure separtes the papillary and reticular dermis?

A

Superficial dermal capillary plexus.

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112
Q

What structure is preset at the dermal subcutaneous junction?

A

Deep cutaneous plexus of larger vessels

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113
Q

Which four skin appendages form the pilosebacous unit?

A
  1. Hair follicle
  2. Sebacous gland
  3. Apocrine gland
  4. Arrector pili muscle
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114
Q

Lable the image.

A
  1. Hair shaft
  2. Follicular infudibulum
  3. Arrector pili muscle
  4. Follicular isthmus
  5. Follicular Bulge
  6. Hair Bulb
  7. Sebacous gland
  8. Eccrine gland
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115
Q

What is cutis anserina?

A

Goose bumps

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116
Q

What is described as the deepest of the hair follicle, with the appearance of basaloid epithelium and mesenchyme?

A

Hair bulb

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117
Q

What is the function of hair bulb?

A

Synthesize hair.

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118
Q

What is the bundle of spindle cells that attaches to the follicle at the bulge?

A

Arrector pili muscle?

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119
Q

What is the function of the Arector pili muscle?

A

Cutis anserina (goose bumps)

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120
Q

What is the function of the follicular bulge?

A

Stem cell reservoir

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121
Q

What is the superficial part of the hair follicle, above the opening of the sebaceous duct, called?

A

Follicular ifundibulum

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122
Q

What is the short section of hair follicle between the opening of the sebaceous duct and follicular bulge called?

A

Follicular isthmus

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123
Q

What kind of secretion do sebaceous glands undergo?

A

Holocrine (lysis of secretory cells)

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124
Q

What kind of secretion do apocrine glands undergo?

A

Apocrine (pinching off one end of the secretory cell)

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125
Q

What kind of secretion do Eccrine glands undergo?

A

Merocrine (secretion that is discharged without major damage to the secretory cells)

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126
Q

Which dermal gland appears as multivacuolated lipid laden cells?

A

Sebaceous

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127
Q

Which dermal gland appears as apical snouts

A

Apocrine

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128
Q

Which dermal gland appears with a tightly coiled intraepidermal duct

A

Eccrine

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129
Q

What is the function of the sebaceous gland

A

Lubricate hair

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130
Q

What is the function of the apocrine gland?

A

Scent glands in other mammals (pheromone?)

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131
Q

What is the function of the eccrine gland?

A

Temperature regulation - sweat

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132
Q

Which dermal gland is only found in the skin of the axilla, groin, genitalia, nipple and external ear and eyelid?

A

Apocrine

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133
Q

What is the tightly coiled intraepidermal duct of the eccrine gland called?

A

Acrosyringium

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134
Q

Which dermal gland does not connect with the surface via the follicular ostium, but rather connects directly with the epidermal surface?

A

Eccrine

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135
Q

What is the main product of sebaceous glands?

A

Sebum

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136
Q

What is the primary systemic control of sebum production?

A

Steroid hormones

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137
Q

What is the primary systemic control of eccrine glands?

A

Cholinergic sympathetic nerves

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138
Q

What is the primary systemic control of apocrine glands?

A

Adrenergic Sympathetic Nerves

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139
Q

What skin appendage is described as multilayered, onion-like structures?

A

Pacinian corpuscle

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140
Q

Where is a Pacinian corpuscle located?

A

Deep reticular dermis & subcutis adjacent to nerves

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141
Q

What is the function of Pacinian corpuscle?

A

Pressure and vibration receptors

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142
Q

What skin appendage is described as a rugby ball standing on its tip consisting of horizontally stacked fibers and spindle shaped nuclei?

A

Meissner’s corpuscle

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143
Q

Where is a Meissner’s corpuscle located?

A

Papillary dermis

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144
Q

What is the function of Meissner’s corpuscle?

A

Touch receptors

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145
Q

What skin appendage is described as one or more layers of uniform cuboidal cells arranged around a blood vessel in the deep reticular dermis?

A

Glomus body

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146
Q

What is the functio of a glomus body?

A

Regulate body temperature by controlling flow through direct arteriovenous shunts / anastomoses

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147
Q

Are hair follicles absent or present in thick skin?

A

Absent

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148
Q

Are specialized nerve end organs absent or present in thick skin?

A

Present

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149
Q

Are specialized nerve end organs absent or present in thin skin?

A

Absent

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150
Q

Are hair follicles absent or present in thin skin?

A

Present

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151
Q

Where is the highest density of eccrine glands?

A

Thick skin

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152
Q

Where are sebaceous glands absent?

A

Thick skin

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153
Q

Which form of UV does not reach earth’s surface significantly due to the ozone layer?

A

ultraviolet C

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154
Q

Which form of UV is the most carcinogenic band that reaches earth in significant quantity

A

ultraviolet B

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155
Q

Which form of UV directly damages DNA by causing strand breaks and nucleotide dimerization?

A

ultraviolet B

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156
Q

Which form of UV mainly produces vitamin D?

A

ultraviolet B

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157
Q

Which form of UV damages DNA indirectly by activating photosensitizers within the cell?

A

ultraviolet A

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158
Q

Which form of UV is a weak carcinogen by itself?

A

ultraviolet A

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159
Q

Which form of UV is an important cause of skin wrinkling?

A

ultraviolet A

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160
Q

Which kind(s) of skin carcinoma is associated with even low doses of UVB and childhood exposure increasing risk?

A

BCC and melanoma

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161
Q

Which kind(s) of skin carcinoma is associated with a cumulation of UV light based on large amount of exposure, as in outdoor workers, and active sport participants.

A

SCC

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162
Q

What are the two types of melanin, and which one - found commonly is in all racial groups - and more protective, as opposed to being found in red-heads.

A

Eumelanin & Phaeomelanin

Eumelanin

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163
Q

What is the most common type of skin cancer, that is locally invasive and rarely metastatic?

A

BCC

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164
Q

Which skin canner manifests most comony as a translucent nodule/plaque with telangiectasia, or later as an ulcer with a raised rolled edge?

A

BCC

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165
Q

Which skin cancer can have a slcerosing variant, and pigmented in darker skinned individuals?

A

BCC

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166
Q

What are the four treatment options for BCC?

A
  1. electrodessication and curettage
  2. simple surgical excision
  3. micrographic surgery
  4. radiation therapy
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167
Q

What is the precursor lesion - pink, scaling patch, limited to epidermis - that precedes SCC?

A

Actinic keratosis

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168
Q

What are the two treatment options for actinic keratoses?

A
  1. liquid nitrogen cryotherapy
  2. topical 5-Fluorouracil
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169
Q

Which skin cancer manifests as a clinically hard pink or white nodule, often surrounded by typical scaling, and can have systemic spread, particularly to lymph nodes?

A

SCC

170
Q

Which skin cancer can present intraorally as leukoplakia?

A

SCC

171
Q

What are the 2 treatment options for SCC?

A
  1. surgical excision
  2. radiation therapy
172
Q

What are the four ways that damaged melanocytes can manifest and what is there related malignancy?

A
  1. freckles (not malignant)
  2. nevi (not malignant - predicts melanoma risk)
  3. atypical nevi (pre-malignant)
  4. melanoma (malignant)
173
Q

What lesion is the result of an increased number / nest of melanocytes due to cell division?

A

Nevi

174
Q

What are the thre types of nevi, based on location?

A
  1. Junctional (dermal-epidermal junctional)
  2. Compound (epidermis and dermis)
  3. Dermal (entirely within dermis)
175
Q

What is the most significant predictor of melanoma risk?

A

Number of common Nevi (>100 nevi suggest melanoma risk of at least 1 in 10 - vs. 1:90)

176
Q

Define atypical nevi

A

Subset of nevi showing variation in edge and color, due to variable melanin production

177
Q

What are the ABCD’s of melanoma?

A

Asymmetry

Border

Color

Diameter

178
Q

Describe superficial spreading melanomas.

A

When nevi become melanomas.

Considerable variation in edge and color, like a very severely atypical nevus

179
Q

Describe nodular melanoma

A

Arises without obvious percursor lesion, rather than increasingly abnormal nevi

180
Q

Describe lentigo maligna melanoma.

A

Arises from expanding brown patch (lentigo maligna) from abnormal melanocytes extending along dermal-epidermal junction -often for years- similar etiology to SCC, 10% of melanomas.

181
Q

What is the primary treatment for melanoma?

A

Surgical management excised with 1-3 cm margin

182
Q

What does the risk of melanoma systemic spread correlate with?

A

Tumor thickness

183
Q

What is the indication for chemotherapy in melanoma and what is the prognosis?

A

Systemic involement, but response rate is low. 5-year survival with reginal lymph node - 60%, with distant metastes - 16%

184
Q

What is the definition of SPF?

A

Sun protective factor - the amount of light required to burn with sunscreen on divided by the amount without the sunscreen

185
Q

From the described pathology, name the condition:

(1) Inflammation in & around the hair follicles
(2) Excess collagen
(3) Plugging of the hair follicle by keratin

A

Acne

186
Q

From the described pathology, name the condition:

(1) Enlargement & pleomorphism of keratinocytes
(2) Sharply demarcated column of compact hyperkeratosis & parakeratosis
(3) Confinement of proliferation to epidermis
(4) Dermal inflammatory cells

A

Actinic Keratosis

187
Q

From the described pathology, name the condition:

(1) Peripheral palisading
(2) Rim of mucin
(3) Dermal nests of basaloid cells
(4) Intact epidermis

A

Basal Cell Carcinoma

188
Q

From the described pathology, name the condition:

  1. dermal eosinophils
  2. subepidermal cleft, with fluid accumulation
A

Bullous Pemphigoid

189
Q

From the described pathology, name the condition:

(1) Langerhans cells in the epidermis
(2) Lymphocytes in the epidermis
(3) Spongiosis
(4) Hyperkeratosis & parakeratosis
(5) Elongated rete ridges
(6) Lymphocytes surrounding dermal vessels

A

Eczema

190
Q

From the described pathology, name the condition:

(1) Nodule of dermal blood vessels

A

Hemangioma

191
Q

From the described pathology, name the condition:

(1) Necrosis of epidermal cells, sloughing
(2) Multinucleated keratinocyte
(3) Dermal inflammation

A

Herpes Simplex, Varicella - Zoster

192
Q

From the described pathology, name the condition:

(1) Band-like infiltrate of lymphocytes at the dermoepidermal junction
(2) Hypergranulosis
(3) Necrotic basal keratinocytes
(4) Hyperkeratosis

A

Lichen Planus

193
Q

From the described pathology, name the condition:

(1) Symmetry
(2) Nested pale slightly pigmented cells in the dermis

A

Melanocytic nevus

194
Q

From the described pathology, name the condition:

(1) Upward spread of pale cells above the basal layer of the epidermis
(2) Asymmetry
(3) Nested cells with pale slightly pigmented cytoplasm at the dermoepidermal junction
(4) Dermal inflammation
(5) Singly dispersed pale cells

A

Melanoma

195
Q

From the described pathology, name the condition:

(1) Suprabasal, intraepidermal bullae
(2) Superficial perivascular inflammatory infiltrate
(3) “Tombstoning” of basal keratinocytes
(4) Normal stratum corneum with basketweave appearance
(5) Acantholysis

A

Pemphigus vulgaris

196
Q

From the described pathology, name the condition:

(1) Patchy epidermal spongioses & lymphocytes
(2) Lymphocytes surrounding dermal vessels
(3) Extravasated red blood cells
(4) Patchy hyperkeratosis & parakeratosis

A

Pityriasis rosea

197
Q

From the described pathology, name the condition:

(1) Hyperkeratosis without parakeratosis
(2) Few inflammatory cells in the epidermis
(3) Numerous yeast & plump hyphae

A

Pityriasis versicolor / Tinea versicolor

198
Q

From the described pathology, name the condition:

(1) Hyperkeratosis & parakeratosis
(2) Neutrophils in the epidermis
(3) Thinning of the epidermis overlying the dermal papillae
(4) Vessels close to the epidermis
(5) Elongated rete ridges

A

Psoriasis

199
Q

From the described pathology, name the condition:

(1) Telangiectases
(2) Inflammation in & around the hair follicles

A

Rosacea

200
Q

From the described pathology, name the condition:

(1) Domed superficial aspect
(2) Melanin within tumour keratinocytes
(3) Sharply demarcated epidermal thickening
(4) “Cysts” containing keratin

A

Seborrheic keratosis

201
Q

From the described pathology, name the condition:

(1) Penetration of tumour epithelium into dermis
(2) Enlargement & pleomorphism of keratinocytes with abundant eosinophilic cytoplasm
(3) Hyperkeratosis

A

Squamous Cell carcinoma

202
Q

From the described pathology, name the condition:

(1) Sparse fine branching hyphae
(2) Numerous inflammatory cells in the epidermis
(3) Hyperkeratosis & parakeratosis

A

Tinea Corporis

203
Q

From the described pathology, name the condition:

(1) Serum in the stratum corneum
(2) Hyperkeratosis & parakeratosis
(3) Coarse keratohyaline granules & perinuclear vacuolation
(4) Papillomatosis

A

Verruca Vulgaris

204
Q

From the described pathology, name the condition:

(1) Intact epidermis
(2) Dermal proliferation of cells with round & angulated nuclei
(3) Thick collagen fibers
(4) Hemosiderin pigment
(5) Hemorrhage

A

Dermatofibroma

205
Q

What is the desribed method of specifmen aquisition:

Contains the full thickness of dermis, but not ideal for diagnosing melanoma

A

Punch biopsy

206
Q

What is the desribed method of specifmen aquisition:

Ideal for the one-step diagnosis and therapy of skin tumours

A

Excisional biopsy

207
Q

What is the desribed method of specifmen aquisition:

Results in a less consipicous scar than other biopsy methods

A

Shave biopsy

208
Q

What is the desribed method of specifmen aquisition:

Used specifically to obtain evidence of intraepidermal infections

A

Scrapings

209
Q

What is the desribed method of specifmen aquisition:

Most frequently combined with electrosurger

A

Curettage

210
Q

Name the five cardinal morpologic features of psoriasis.

A
  1. Plaque, raised lesions
  2. Well circumscribed margins
  3. Bright salmon red colour
  4. Silvery scale
  5. Symmetric distribution
211
Q

What lesion sites are common in psoriasis?

A

Extensor surfaces (elbows, knees)

Scalp, retroauricular, and ears

Palms and soles

Umbilicus

Glans Penis

Lumbar

Shins

Supragluteal

Nails - pitting, onycholysis

212
Q

Describe guttate psoriasis.

A

acute extensive eruption of small psoriatic papules over trunk and proximal extremities; usually in association with group A streptococcal infections, and may recur with each reinfection

213
Q

Describe inverse psoriasis

A

psoriasis occurring within flexural sites (i.e. axillae, groin, gluteal fold) will usually lack scale, and have a bright red, moist, macerated appearance

214
Q

Describe pustular psoriasis.

A

can be generalized (von Zumbusch) or localized (usually to the palms or soles); generalized pustular psoriasis is associated with fever, leukocytosis and can be life-threatening

215
Q

Describe erythrodermic psoriasis.

A

the entire body is affected and is red and scaly; prominent systemic complications

216
Q

Describe the pathology of psoriasis.

A
  • psoriasis is a chronic immunologic disease of the skin characterized by profound cutaneous inflammation and epidermal hyperproliferation
  • in psoriasis, it takes 3-4 days for a keratinocyte to transit from the basal layer to the surface where it is shed
  • key role for Th1 cells
217
Q

What phenomenon is seen, and what disease is it associated with?

A

Koebner phenomenon

Psoriasis aggragavation by tattoo

218
Q

Describe Psoriatic Arthritis

A

5-10% of patients with psoriasis will have psoriatic arthritis; seronegative (RF), association with HLA-B27

  • asymmetric peripheral joint involvement (most common)
  • symmetric peripheral joint involvement (resembles rheumatoid arthritis)
  • axial disease (resembles ankylosing spondylitis)
  • arthritis mutilans (uncommon)
219
Q

What are some of the systemic complications of generalized pustular or erythrodermic psoriasis?

A
  • fever, weight loss
  • congestive heart failure (due to increased cutaneous blood flow)
  • fluid/electrolyte imbalance
  • hypoalbuminemia, low iron, hyperuricemia
220
Q

What are the topical treatments used in psoriasis?

A

Glucocorticoids

Tars

Calcipotrial (Vit D derivative)

Anthralin

Taxarotene (retionoid, Vit A derivative)

Salicyclic acid

Calciurin inhibitor

221
Q

What systemic therapy is used in psoriasis?

A

Methotrexate

Acitretin (oral retinoid)

Cyclosporine

Phototherapy (UVB or Psoralen UVA)

222
Q

What is the intensely prurit inflammatory skin disorder Atopic dermatitis or “eczema” associated with?

A

Asthma, hayfever, allergic conjunctivitis

223
Q

Describe the pathogensis of Atopic dermatitis “eczema”

A
  • cutaneous inflammation mediated by Th2 cells (type 2 helper T cells producing Il-4 and IL-5)
  • elevated serum levels of IgE
  • impaired cutaneous barrier function (increased transepidermal water loss leads to dry skin)
  • skin colonization and infection by Staphylococcus aureus (the toxins of which may serve as superantigens to promote cutaneous inflammation)
  • diet factors rarely important
224
Q

Descibe the clinical symptoms and basic morphology of Atopic dermatitis “eczema”

A
  • pruritus is usually the most outstanding clinical feature
  • depending on the acuity of the skin disease there can be:
    • ill-defined erythema
    • tiny coalescing edematous papules or papulovesicles
    • excoriations
    • crusting (if secondarily infected)
    • xerosis (or dry, scaly skin)
  • depending on the acuity of the skin disease there can be:
    • lichenification
225
Q

What are the 3 phases of atopic dermatitis “eczema” and what are their clinical features?

A
  1. Infantile
    • facial, extensor distribution
  2. Childhood
    • tendency to xerosis
    • flexural distribution
    • more lichenification and excoriations
  3. Adult
    • improves with age, may remit
    • may primarily affect hands
226
Q

What is the treatment for atopic dermatitis “eczema”?

A
  • Avoid irritating factors
  • Aggressive restoration of the cutaneous permeability barrier with bland emollients and moisturizers
  • Topical glucocorticoids (creams or ointments)
  • Topical immunomodulators (tacrolimus, pimecrolimus)
  • Topical or systemic anti-staphylococcal antibiotics
  • Oral antihistamines
227
Q

What is allergic contact dermatitis?

A

type IV hypersensitivity to an allergen in contact with the skin (e.g. nickel allergy, poison ivy)

228
Q

What is irritant contact dermatitis?

A

contact of the skin with something that primarily causes direct local irritation

229
Q

Describe the pathogenesis of Seborrheic Dermatitis

A

Involves sebum production and Pityrosporum fungus

(fungus is lipophilic yeast that thrives on lipids in sebum - scaling and inflammation may be due to host reponse to increased fungi on skin)

230
Q

What are the clinical features of Seborrheic Dermatitis in adults

A
  • Dandruff
  • Ill-defined erythema
  • Greasy-appearing scale
  • Face distribution (glabella, eyelids, eybrows, nasolabial folds, nose, mustache/beard, ears)
  • Trunk (presternal, umbilicus)
231
Q

What are the clinical features of Seborrheic Dermatitis in infants?

A
232
Q

What are the associated disorders with seborrheic dermatitis?

A

Parkinson’s disease (and other neurologic disorders) - due to immobility of facial muscles

HIV infection - get a more resistant disease

233
Q

Name this greasy, scaly, erythematous lesion.

A

Seborrheic dermatitis

234
Q

What is a mild, common, self-limited eruption, that may be due to herpesvirus?

A

Pityriasis rosea

235
Q

Describe the clinical course of pityriasis rosea?

A

Evolves over 6-8 weeks, primarily in adolescents and young adults in spring and fall

  • herald “Patch” - solitary 2-6cm scaly plaque
  • eruption of multiple pauples with fine “collarette” scaling along rim of lesion
  • “T shirt and shorts”distribution
  • Pruritis variable
  • Recurrance uncommon
236
Q

What are the mimickers of Pityriasis rosea?

A

Secondary syphilis

Drug eruptions

237
Q

What is te treatment of Seborrheic dermatitis?

A
238
Q

What are the five clinical features of lichen planus?

A
  1. Papules (2-5mm)
  2. Pruritus (intense)
  3. Purple
  4. Polygonal
  5. Planer (flat-toppped)
  • Also may sow scale-like fine white lines on surface (Wickham’s striae)
239
Q

Where is the typical distribution of lichen planus lesions?

A

Flexor wrists and forearms, neck, thighs, shins, lumbar back, genitalia

Oral lesions common (with lacy white reticular lesions on buccal mucosa most common, may also become ulcerated)

240
Q

What is Dr. Lui’s #1 Rule?

A
241
Q

What are four common and distinctive drug reaction patterns?

A
  1. Urticaria
  2. Maculopapular / exanthematous / morbilliform (measles-like)
  3. Erythema multiform (target lesions, mucosal infolvement)
  4. Fixed drug eruption (localized plaques that recur at the same body site every time the patient is exposed to the offending systemic drug)
242
Q

What are the Skin infections that cause Vesicular and Vesicobullous Eruptions?

A
  • Herpes Simplex
  • Varicella
  • Herpes Zoster
  • Impetigo
  • Bullous insect bite reaction
  • Primary skin bullous disorder (eg. pemphigus)
243
Q

What are the clinical features of Herpes Simplex I and II

A

Grouped vesicles on an erythematous base

Most of adult population has been exposed

Virus can be shed without visible lesions

Persist in sensory ganglia leading to recurrent infections

Precipitated by UV, menses, fever, URTI, immunodeficiency

HSV-1 predominatly Labialis distribution

HSV-2 predominantly Urogenital distribution

244
Q

What are the clinical features of Varicella?

A

“Dewdrop on rose petal” distribution

Initially papules, which become vesiscles, which crust over

Christmas tree distribution due to hematogenous spread

Test with viral culture, Tzanck smear, or skin biopsy

245
Q

What are the clinical features of Herpes Zoster?

A

Prodrome of neuritic pain (days-weeks)

Acute vesicles then crusted papules

Unilateral dermatomal distribution

Grouped vesicles on erythematous base

Viral culture, Tzanck smear, or skin biopsy

246
Q

What are the identical histological changes seen in herpes simplex, varicella, and zoster on skin biopsy?

A

Tzanck smear shows multinucleated keratinocytes or acantholytic keratinocytes

247
Q

What are the clinical features of nonbullous impetigo?

A
  • Scaling honey crusted lesions
  • Group A Strep, or Staph aureus
  • Supericial infection
248
Q

What are the clinical features of bullous impetigo?

A
  • vesicles and bullae
  • clear or slightly yellow fluid
  • shallow erosions form if bullae break
  • caused by Staph aureus
249
Q

What are the clinical features of arthropod bites?

A

Grouped papeuls or vesicles

Multiple, close together bites “breakfast, lunch, dinner”

Pruritic / urticarial, painful papules

causes: mites, ticks, spiders, centipedes, millipedes, mosquitoes, black flies, sand flies, bedbugs, ants, bees, wasps, hornets, fleas

250
Q

What are the clinical features of bedbugs?

A

Erythematous papules, vesicles, nodules

Bugs are red-brown colour size of a ladybug

Nocturnal

Bites on body and head and neck area

251
Q

What are the infectious causes of follicular eruptions?

A
  1. Pityrosporum folliculitis
  2. Pseudomonas folliculitis
  3. Staphylococcal follicultis
  4. Acne
252
Q

How do you differentiate follicular eruptions?

A
  • hot tub exposure
  • distribution
  • presence of comodones, pauples, nodules and cysts (acne)
  • level of inflammation (pityrosporum has less)
  • KOH and cultures
253
Q

What are the clinical features of Pityrosporum folliculitis?

A

Monomorphous papules

Sweaty individual

KOH positive

254
Q

What are the clinical features of Pseudomonas folliculitis?

A

Hot tub exposure

Other proximal individuals affected

Inlammatory follicular-based papules and pustules

Culture positive

Self-limited

255
Q

What are the clinical features of staphylococcal folliculitis?

A

Inflammatory pustules

Gram stain and culture positive

256
Q

What is the infectious and inflammatory differential for annular and scaling eruptions?

A
  • Tinea corporis
  • Tinea versicolour
  • Secondary syphilis
  • Psoriasis
  • Nummular eczema
257
Q

How do you diagnose a scaling eruption? (4)

A
  • Scrape scaling edge for KOH and culture
  • Distribution – psoriasis symmetrical and extensor surfaces
  • Tinea versicolour non-inflammatory brown and white scaling patches
  • Tinea corporis few lesions with central clearing
258
Q

What are the clinical features of tinea corporis?

A

AKA ringworm

Annular scaling edge (ring-like)

Well demarcated plaque with central clearing

Single or multiple lesions

Assymetrical

Scrape edge for KOH and culture

Caused by Trichophyton rubrum and Microsporum canis

259
Q

What are the clinical features of Tinea versicolor, aka “pityriasis versicolor”

A

Well marginated round scaling brown or light macules

Common in young adults

risk factors: warm and humid climate, oil skin, hyperhidrosis

Psoitive KOH

Microscopy - scale + “spaghetti and meatballs” spores and hyphae

Malassezia furfur or Pityrosporum versicolor

260
Q

What are the clinical features of Secondary syphilis?

A

Widespread red-brown scaling papules

Involvement of palms and soles

2-6 months after primary infection

First eruption is macular, then papulosquamous, pustular, or acneiform

Condylomata lata - flat-topped papules in most areas (mouth and ano-genital)

Treponema pallidum

Dx with serology, or skin biopsy

261
Q

What are the infectious causes of papular eruptions? (3)

A
  • Verruca
  • Molluscum contagiosum
  • Insect bites
262
Q

How do you differentiate papules?

A
  • Central punctum + pearly apperance = molluscum
  • Often surrounding eczema = molluscum
  • Dull surface + capillary loops = verruca
  • Minimally elevated = verruca plana
  • Pruritic + grouped, also vesicular = insect bites
263
Q

What are te clinical features of Verruca vulgaris?

A

Firm, hyperkartotitc papules with clefted surface and vegetations

Red or brown dots caused by thrombosed capillary loops

HPV

Skin to skin transmittion

Breaks in stratum corneum to facilitate epidermal infection

Risk factors: immunocompromise, meat handlers

264
Q

What are the clinical features of Molluscum contagiosum?

A

Skin coloured umbilicated papules

Gentle pressure causes the central keratotic plug to extrude

Mollusca undergoing spontaneous regression may have an erthematous halo

Caused by a pox virus

Spread through skin to skin contact

Common in children and sexually active adults

Also seen in HIV

265
Q

What are the infectious and inflammtory causes of eczematous and pruritic eruptions? (4)

A

Scabies
Louse infestation
Insect bites
Eczema

266
Q

How do you differentiate pruritic eruptions? (4)

A
  • Scabies = burrows or nodules
  • Louse = no primary lesion
  • Insect bites = grouped
  • Atopic dermatitis = past history dry skin, hyper-linear palms, flexural dist.
267
Q

What are the clinical features of scabies

A

Widespread eruption

Nocturnal prurities

Due to hypersensitivy to mite Sarcoptes scabiei (can take 6 weeks post-exposure to develop)

Burrows: Serpiginous track with spot at end, scrape for Dx

Nodules: Red-brown nodules in axillary area and groin

Dx - mite, eggs, feces on microscopy, biopsy

Norwegian scabies - scabies in immunocomprosied, highly contagious, requires repeated treatment

268
Q

What are the clinical features of louse? AKA Pediculosis Corporis

A

Eczematous eruption

No primary lesions

Secondary infection common

Seen in crowded conditions, poverty

Etiology: pediculosis humanus humanus

Transmit infections: trench fever and epidemic typhus

Louse: look in seams of clothing for louse and nits

269
Q

What is the differential for scalp eruptions? (4)

A
  • Tinea capitis
  • Head lice
  • Psoriasis
  • Seborrheic dermatitis
270
Q

How do you differentiate scalp eruptions?

A
  • Pruritic? lice, nits or live louse confirm (nits adhere to hair shaft)
  • Tinea? KOH and culture of scale and hair
  • Well-marginated plaque erythematous = Psoriasis
  • Yellowish scale = seborrheic dermatitis
271
Q

What are te clinical features of Tinea capitis?

A

Infection of hair

Risk factors: contact with infected person, animal, fomites

Dx: Wood’s lamp exam: Microsporum display bright green fluorescence. KOH and cultures – scrape scale and some hairs

272
Q

What is a tinea capitis infection outside the hair shaft called and how will it present?

A

Ectothrix - partial alopecia with broken hair shafts

Microsporum spp.

273
Q

What is a tinea capitis infection within the hair shaft called and how will it present?

A

Endothrix

Black dot tinea capitis

hair breaks off near surface

Trichophyton spp.

274
Q

How will Kerion tinea capitis present?

A

Inflammtory mass with boggy plaques

275
Q

What are the clinical features of Pediculosis Capitis?

A

Scalp pruritis

Head lice and nits may be isible

Bite reactions - eczema, excoriation, lichenification

Pediculosis humanus capitisI

Transmitted via shared hats, brushes, head to head

276
Q

What are the infectious / inflammatory causes of intertrigo (body folds)? (4)

A
  • Tinea cruris
  • Candida
  • Erythrasma
  • Inverse psoriasis
277
Q

How do you differentiate causes of intertrigro? (4)

A
  • Scaling edge, feet involvement = tinea
  • Inflammatory with satellite pustules = candida
  • no scale, psoriasis elsewhere, recurrent = inverse psoriasis
  • brick red / coral red, fluorescence wit Wood’s light = erythrasma
278
Q

What are the clinical features of Tinea Cruris?

A

Well marginated scaling red plaques with central clearing

Papules and pustules may be present at margins

Inguinal region and on thighs

T. rubrum, T. mentagrophytes

Risk factors: warm weather, obesity, tight clothing, topical steroid use, male, tinea pedis or tinea unguium

KOH show hyphae

279
Q

What are the clinical features of Candida intertrigo?

A

Erythematous plaques with satellite papules and pustules

Found in moist environment

Risk factors: immunocompromised, topical steroid use, diabetic

Dx: Swab for gram stain and culture

280
Q

What are the clinical features of Erythrasma?

A

Sharply marginated patch

Prediliction for folds – toe web spaces, groin, axillae, intergluteal, inframammary

Etiology: Corynebacterium minutissimum

Epidemiology: adults, humid weather, obesity, tight clothes

Dx: coral red fluorescence on Wood’s light, bacterial culture positive for C. minutissimum, absence of fungi on KOH
281
Q

What are the clinical manifestations of Staph aureus? (8)

A
  • Impetigo
  • Ecthyma (ulcerative pyoderma of the skin - deeper from of impetigo extending into dermis)
  • Cellulitis
  • Folliculitis
  • Foruncles (boils)
  • Carbuncles
  • Abscesses
  • Staphylococcal Scalded skin
282
Q

What are the clinical features of cellulitis?

A

Skin infection extending into subcu. tissue

Painful firm area of erythema

Malaise, fever, chills may be present

May form bullae or undergo necrosis with epidermal sloughing

Common causes: Adults: Staph aureus, GAS, Children: Hib, Staph aureus, GAS

Ddx: DVT, stasis dermatitis, contact dermatitis, erysipelas

Risk factors: interdigital tinea, IVDU if arm, operative wound site

Diagnosis: clinical, wound cultures if exudative,

283
Q

What are the clinical features of furuncles (boils)?

A

Follicular infection spreads and involves the tissue around the hair follicle
Firm erythematous nodule (early)
Fluctuant erythematous nodule (later)
Very tender/painful
Sites: face, neck, axilla, buttocks, perineum, thighs
Course: red, tender nodule points → ruptures

284
Q

What are the clinical features of carbuncles?

A

Form as several furuncles connect subcutaneously
larger and deeper than furuncles
Sites: hair bearing skin, prefer back of the neck in males
Lesions drain through multiple sites to the skin surface
Diabetes predisposes to carbuncles

285
Q

What are the clinical features of abscesses?

A

Form when furuncles/carbuncles not treated adequately
Subcutaneous tissue liquefies, forms granulomatous “pus pocket”
Signs: tender, swollen areas of reddened skin, hot and tender to touch
Can progress via hematogenous or lymphatic spread → ultimately seed other end organs
Sepsis, pneumonia, arthritis, osteomyelitis and endocarditis can subsequently develop

286
Q

What are the clinical manifestations of HPV? (5)

A
  1. flat warts
  2. plantar warts
  3. verruca vulgaris
  4. periungal warts
  5. condylomata
287
Q

What are the clinical features of flat warts?

A

Verruca plana
Sharply defined flat skin coloured or brown papules; 1-2 mm thick
Ddx: seborrheic keratoses, skin tags
Hard to treat
Spread by shaving

288
Q

What are the clinical features of plantar warts?

A

Note multiple capillary loops – these distinguish warts from callus
Plantar warts are very common
Often acquired at swimming pool
Mosaic plantar warts

289
Q

What are the clinical features of condylomata?

A

Perianal condylomata due to HPV
Transmission primarily sexual
Etiology HPV 6 & 11 > 16, 18, 31, 35
HPV types 16, 18, 31, 35 associated with carcinoma
HPV vaccine should decrease incidence of infection
Ddx condylomata lata of secondary syphilis, seborrheic keratoses, skin tags
Diagnosis is clinical, biopsy can differentiate if clinically difficult

290
Q

What are the clinical manifestations of Tinea? (4)

A
  1. Tinea corporis
  2. Tinea capitis
  3. Tinea pedis
  4. Tinea unguium
291
Q

What are the clinical features of Tinea Unguium?

A

Thick yellow dystrophic toenails or fingernails
Toenails more often involved
Genetic predisposition
Often associated tinea pedis
Etiology: T. rubrum most common
DDx: psoriasis, traumatic changes
Dx: scrape under toenail for KOH and culture

292
Q

What are the clinical features of Tinea pedis?

A

Interdigital type: area has scaling, maceration and fissures. Often between 4th and 5th toes

Moccasin type: well marginated erythema with fine scale and hyperkeratosis
 Inflammatory or bullous type: vesicles filled with clear fluid
 Transmitted by walking barefoot on contaminated ground esp. swimming pool
 Etiology: Trichophyton, Microsporum, Epidermophyton
 Dx: hyphae on KOH, culture + for dermatophyte
 DDx: erythrasma, psoriasis, eczema
293
Q

What lesion sites are common in psoriasis?

A

Extensor surfaces (elbows, knees)

Scalp, retroauricular, and ears

Palms and soles

Umbilicus

Glans Penis

Lumbar

Shins

Supragluteal

Nails - pitting, onycholysis

294
Q

Describe guttate psoriasis.

A

acute extensive eruption of small psoriatic papules over trunk and proximal extremities; usually in association with group A streptococcal infections, and may recur with each reinfection

295
Q

Describe inverse psoriasis

A

psoriasis occurring within flexural sites (i.e. axillae, groin, gluteal fold) will usually lack scale, and have a bright red, moist, macerated appearance

296
Q

Describe pustular psoriasis.

A

can be generalized (von Zumbusch) or localized (usually to the palms or soles); generalized pustular psoriasis is associated with fever, leukocytosis and can be life-threatening

297
Q

Describe erythrodermic psoriasis.

A

the entire body is affected and is red and scaly; prominent systemic complications

298
Q

Describe the pathology of psoriasis.

A
  • psoriasis is a chronic immunologic disease of the skin characterized by profound cutaneous inflammation and epidermal hyperproliferation
  • in psoriasis, it takes 3-4 days for a keratinocyte to transit from the basal layer to the surface where it is shed
  • key role for Th1 cells
299
Q

What phenomenon is seen, and what disease is it associated with?

A

Koebner phenomenon

Psoriasis aggragavation by tattoo

300
Q

Describe Psoriatic Arthritis

A

5-10% of patients with psoriasis will have psoriatic arthritis; seronegative (RF), association with HLA-B27

  • asymmetric peripheral joint involvement (most common)
  • symmetric peripheral joint involvement (resembles rheumatoid arthritis)
  • axial disease (resembles ankylosing spondylitis)
  • arthritis mutilans (uncommon)
301
Q

What are some of the systemic complications of generalized pustular or erythrodermic psoriasis?

A
  • fever, weight loss
  • congestive heart failure (due to increased cutaneous blood flow)
  • fluid/electrolyte imbalance
  • hypoalbuminemia, low iron, hyperuricemia
302
Q

What are the topical treatments used in psoriasis?

A

Glucocorticoids

Tars

Calcipotrial (Vit D derivative)

Anthralin

Taxarotene (retionoid, Vit A derivative)

Salicyclic acid

Calciurin inhibitor

303
Q

What systemic therapy is used in psoriasis?

A

Methotrexate

Acitretin (oral retinoid)

Cyclosporine

Phototherapy (UVB or Psoralen UVA)

304
Q

What is the intensely prurit inflammatory skin disorder Atopic dermatitis or “eczema” associated with?

A

Asthma, hayfever, allergic conjunctivitis

305
Q

Describe the pathogensis of Atopic dermatitis “eczema”

A
  • cutaneous inflammation mediated by Th2 cells (type 2 helper T cells producing Il-4 and IL-5)
  • elevated serum levels of IgE
  • impaired cutaneous barrier function (increased transepidermal water loss leads to dry skin)
  • skin colonization and infection by Staphylococcus aureus (the toxins of which may serve as superantigens to promote cutaneous inflammation)
  • diet factors rarely important
306
Q

Descibe the clinical symptoms and basic morphology of Atopic dermatitis “eczema”

A
  • pruritus is usually the most outstanding clinical feature
  • depending on the acuity of the skin disease there can be:
    • ill-defined erythema
    • tiny coalescing edematous papules or papulovesicles
    • excoriations
    • crusting (if secondarily infected)
    • xerosis (or dry, scaly skin)
  • depending on the acuity of the skin disease there can be:
    • lichenification
307
Q

What are the 3 phases of atopic dermatitis “eczema” and what are their clinical features?

A
  1. Infantile
    • facial, extensor distribution
  2. Childhood
    • tendency to xerosis
    • flexural distribution
    • more lichenification and excoriations
  3. Adult
    • improves with age, may remit
    • may primarily affect hands
308
Q

What is the treatment for atopic dermatitis “eczema”?

A
  • Avoid irritating factors
  • Aggressive restoration of the cutaneous permeability barrier with bland emollients and moisturizers
  • Topical glucocorticoids (creams or ointments)
  • Topical immunomodulators (tacrolimus, pimecrolimus)
  • Topical or systemic anti-staphylococcal antibiotics
  • Oral antihistamines
309
Q

What is allergic contact dermatitis?

A

type IV hypersensitivity to an allergen in contact with the skin (e.g. nickel allergy, poison ivy)

310
Q

What is irritant contact dermatitis?

A

contact of the skin with something that primarily causes direct local irritation

311
Q

Describe the pathogenesis of Seborrheic Dermatitis

A

Involves sebum production and Pityrosporum fungus

(fungus is lipophilic yeast that thrives on lipids in sebum - scaling and inflammation may be due to host reponse to increased fungi on skin)

312
Q

What are the clinical features of Seborrheic Dermatitis in adults

A
  • Dandruff
  • Ill-defined erythema
  • Greasy-appearing scale
  • Face distribution (glabella, eyelids, eybrows, nasolabial folds, nose, mustache/beard, ears)
  • Trunk (presternal, umbilicus)
313
Q

What are the clinical features of Seborrheic Dermatitis in infants?

A
314
Q

What are the associated disorders with seborrheic dermatitis?

A

Parkinson’s disease (and other neurologic disorders) - due to immobility of facial muscles

HIV infection - get a more resistant disease

315
Q

Name this greasy, scaly, erythematous lesion.

A

Seborrheic dermatitis

316
Q

What is a mild, common, self-limited eruption, that may be due to herpesvirus?

A

Pityriasis rosea

317
Q

Describe the clinical course of pityriasis rosea?

A

Evolves over 6-8 weeks, primarily in adolescents and young adults in spring and fall

  • herald “Patch” - solitary 2-6cm scaly plaque
  • eruption of multiple pauples with fine “collarette” scaling along rim of lesion
  • “T shirt and shorts”distribution
  • Pruritis variable
  • Recurrance uncommon
318
Q

What are the mimickers of Pityriasis rosea?

A

Secondary syphilis

Drug eruptions

319
Q

What is te treatment of Seborrheic dermatitis?

A
320
Q

What are the five clinical features of lichen planus?

A
  1. Papules (2-5mm)
  2. Pruritus (intense)
  3. Purple
  4. Polygonal
  5. Planer (flat-toppped)
  • Also may sow scale-like fine white lines on surface (Wickham’s striae)
321
Q

Where is the typical distribution of lichen planus lesions?

A

Flexor wrists and forearms, neck, thighs, shins, lumbar back, genitalia

Oral lesions common (with lacy white reticular lesions on buccal mucosa most common, may also become ulcerated)

322
Q

What is Dr. Lui’s #1 Rule?

A
323
Q

What are four common and distinctive drug reaction patterns?

A
  1. Urticaria
  2. Maculopapular / exanthematous / morbilliform (measles-like)
  3. Erythema multiform (target lesions, mucosal infolvement)
  4. Fixed drug eruption (localized plaques that recur at the same body site every time the patient is exposed to the offending systemic drug)
324
Q

What are the Skin infections that cause Vesicular and Vesicobullous Eruptions?

A
  • Herpes Simplex
  • Varicella
  • Herpes Zoster
  • Impetigo
  • Bullous insect bite reaction
  • Primary skin bullous disorder (eg. pemphigus)
325
Q

What are the clinical features of Herpes Simplex I and II

A

Grouped vesicles on an erythematous base

Most of adult population has been exposed

Virus can be shed without visible lesions

Persist in sensory ganglia leading to recurrent infections

Precipitated by UV, menses, fever, URTI, immunodeficiency

HSV-1 predominatly Labialis distribution

HSV-2 predominantly Urogenital distribution

326
Q

What are the clinical features of Varicella?

A

“Dewdrop on rose petal” distribution

Initially papules, which become vesiscles, which crust over

Christmas tree distribution due to hematogenous spread

Test with viral culture, Tzanck smear, or skin biopsy

327
Q

What are the clinical features of Herpes Zoster?

A

Prodrome of neuritic pain (days-weeks)

Acute vesicles then crusted papules

Unilateral dermatomal distribution

Grouped vesicles on erythematous base

Viral culture, Tzanck smear, or skin biopsy

328
Q

What are the identical histological changes seen in herpes simplex, varicella, and zoster on skin biopsy?

A

Tzanck smear shows multinucleated keratinocytes or acantholytic keratinocytes

329
Q

What are the clinical features of nonbullous impetigo?

A
  • Scaling honey crusted lesions
  • Group A Strep, or Staph aureus
  • Supericial infection
330
Q

What are the clinical features of bullous impetigo?

A
  • vesicles and bullae
  • clear or slightly yellow fluid
  • shallow erosions form if bullae break
  • caused by Staph aureus
331
Q

What are the clinical features of arthropod bites?

A

Grouped papeuls or vesicles

Multiple, close together bites “breakfast, lunch, dinner”

Pruritic / urticarial, painful papules

causes: mites, ticks, spiders, centipedes, millipedes, mosquitoes, black flies, sand flies, bedbugs, ants, bees, wasps, hornets, fleas

332
Q

What are the clinical features of bedbugs?

A

Erythematous papules, vesicles, nodules

Bugs are red-brown colour size of a ladybug

Nocturnal

Bites on body and head and neck area

333
Q

What are the infectious causes of follicular eruptions?

A
  1. Pityrosporum folliculitis
  2. Pseudomonas folliculitis
  3. Staphylococcal follicultis
  4. Acne
334
Q

How do you differentiate follicular eruptions?

A
  • hot tub exposure
  • distribution
  • presence of comodones, pauples, nodules and cysts (acne)
  • level of inflammation (pityrosporum has less)
  • KOH and cultures
335
Q

What are the clinical features of Pityrosporum folliculitis?

A

Monomorphous papules

Sweaty individual

KOH positive

336
Q

What are the clinical features of Pseudomonas folliculitis?

A

Hot tub exposure

Other proximal individuals affected

Inlammatory follicular-based papules and pustules

Culture positive

Self-limited

337
Q

What are the clinical features of staphylococcal folliculitis?

A

Inflammatory pustules

Gram stain and culture positive

338
Q

What is the infectious and inflammatory differential for annular and scaling eruptions?

A
  • Tinea corporis
  • Tinea versicolour
  • Secondary syphilis
  • Psoriasis
  • Nummular eczema
339
Q

How do you diagnose a scaling eruption? (4)

A
  • Scrape scaling edge for KOH and culture
  • Distribution – psoriasis symmetrical and extensor surfaces
  • Tinea versicolour non-inflammatory brown and white scaling patches
  • Tinea corporis few lesions with central clearing
340
Q

What are the clinical features of tinea corporis?

A

AKA ringworm

Annular scaling edge (ring-like)

Well demarcated plaque with central clearing

Single or multiple lesions

Assymetrical

Scrape edge for KOH and culture

Caused by Trichophyton rubrum and Microsporum canis

341
Q

What are the clinical features of Tinea versicolor, aka “pityriasis versicolor”

A

Well marginated round scaling brown or light macules

Common in young adults

risk factors: warm and humid climate, oil skin, hyperhidrosis

Psoitive KOH

Microscopy - scale + “spaghetti and meatballs” spores and hyphae

Malassezia furfur or Pityrosporum versicolor

342
Q

What are the clinical features of Secondary syphilis?

A

Widespread red-brown scaling papules

Involvement of palms and soles

2-6 months after primary infection

First eruption is macular, then papulosquamous, pustular, or acneiform

Condylomata lata - flat-topped papules in most areas (mouth and ano-genital)

Treponema pallidum

Dx with serology, or skin biopsy

343
Q

What are the infectious causes of papular eruptions? (3)

A
  • Verruca
  • Molluscum contagiosum
  • Insect bites
344
Q

How do you differentiate papules?

A
  • Central punctum + pearly apperance = molluscum
  • Often surrounding eczema = molluscum
  • Dull surface + capillary loops = verruca
  • Minimally elevated = verruca plana
  • Pruritic + grouped, also vesicular = insect bites
345
Q

What are te clinical features of Verruca vulgaris?

A

Firm, hyperkartotitc papules with clefted surface and vegetations

Red or brown dots caused by thrombosed capillary loops

HPV

Skin to skin transmittion

Breaks in stratum corneum to facilitate epidermal infection

Risk factors: immunocompromise, meat handlers

346
Q

What are the clinical features of Molluscum contagiosum?

A

Skin coloured umbilicated papules

Gentle pressure causes the central keratotic plug to extrude

Mollusca undergoing spontaneous regression may have an erthematous halo

Caused by a pox virus

Spread through skin to skin contact

Common in children and sexually active adults

Also seen in HIV

347
Q

What are the infectious and inflammtory causes of eczematous and pruritic eruptions? (4)

A

Scabies
Louse infestation
Insect bites
Eczema

348
Q

How do you differentiate pruritic eruptions? (4)

A
  • Scabies = burrows or nodules
  • Louse = no primary lesion
  • Insect bites = grouped
  • Atopic dermatitis = past history dry skin, hyper-linear palms, flexural dist.
349
Q

What are the clinical features of scabies

A

Widespread eruption

Nocturnal prurities

Due to hypersensitivy to mite Sarcoptes scabiei (can take 6 weeks post-exposure to develop)

Burrows: Serpiginous track with spot at end, scrape for Dx

Nodules: Red-brown nodules in axillary area and groin

Dx - mite, eggs, feces on microscopy, biopsy

Norwegian scabies - scabies in immunocomprosied, highly contagious, requires repeated treatment

350
Q

What are the clinical features of louse? AKA Pediculosis Corporis

A

Eczematous eruption

No primary lesions

Secondary infection common

Seen in crowded conditions, poverty

Etiology: pediculosis humanus humanus

Transmit infections: trench fever and epidemic typhus

Louse: look in seams of clothing for louse and nits

351
Q

What is the differential for scalp eruptions? (4)

A
  • Tinea capitis
  • Head lice
  • Psoriasis
  • Seborrheic dermatitis
352
Q

How do you differentiate scalp eruptions?

A
  • Pruritic? lice, nits or live louse confirm (nits adhere to hair shaft)
  • Tinea? KOH and culture of scale and hair
  • Well-marginated plaque erythematous = Psoriasis
  • Yellowish scale = seborrheic dermatitis
353
Q

What are te clinical features of Tinea capitis?

A

Infection of hair

Risk factors: contact with infected person, animal, fomites

Dx: Wood’s lamp exam: Microsporum display bright green fluorescence. KOH and cultures – scrape scale and some hairs

354
Q

What is a tinea capitis infection outside the hair shaft called and how will it present?

A

Ectothrix - partial alopecia with broken hair shafts

Microsporum spp.

355
Q

What is a tinea capitis infection within the hair shaft called and how will it present?

A

Endothrix

Black dot tinea capitis

hair breaks off near surface

Trichophyton spp.

356
Q

How will Kerion tinea capitis present?

A

Inflammtory mass with boggy plaques

357
Q

What are the clinical features of Pediculosis Capitis?

A

Scalp pruritis

Head lice and nits may be isible

Bite reactions - eczema, excoriation, lichenification

Pediculosis humanus capitisI

Transmitted via shared hats, brushes, head to head

358
Q

What are the infectious / inflammatory causes of intertrigo (body folds)? (4)

A
  • Tinea cruris
  • Candida
  • Erythrasma
  • Inverse psoriasis
359
Q

How do you differentiate causes of intertrigro? (4)

A
  • Scaling edge, feet involvement = tinea
  • Inflammatory with satellite pustules = candida
  • no scale, psoriasis elsewhere, recurrent = inverse psoriasis
  • brick red / coral red, fluorescence wit Wood’s light = erythrasma
360
Q

What are the clinical features of Tinea Cruris?

A

Well marginated scaling red plaques with central clearing

Papules and pustules may be present at margins

Inguinal region and on thighs

T. rubrum, T. mentagrophytes

Risk factors: warm weather, obesity, tight clothing, topical steroid use, male, tinea pedis or tinea unguium

KOH show hyphae

361
Q

What are the clinical features of Candida intertrigo?

A

Erythematous plaques with satellite papules and pustules

Found in moist environment

Risk factors: immunocompromised, topical steroid use, diabetic

Dx: Swab for gram stain and culture

362
Q

What are the clinical features of Erythrasma?

A

Sharply marginated patch

Prediliction for folds – toe web spaces, groin, axillae, intergluteal, inframammary

Etiology: Corynebacterium minutissimum

Epidemiology: adults, humid weather, obesity, tight clothes

Dx: coral red fluorescence on Wood’s light, bacterial culture positive for C. minutissimum, absence of fungi on KOH

363
Q

What are the clinical manifestations of Staph aureus? (8)

A
  • Impetigo
  • Ecthyma (ulcerative pyoderma of the skin - deeper from of impetigo extending into dermis)
  • Cellulitis
  • Folliculitis
  • Foruncles (boils)
  • Carbuncles
  • Abscesses
  • Staphylococcal Scalded skin
364
Q

What are the clinical features of cellulitis?

A

Skin infection extending into subcu. tissue

Painful firm area of erythema

Malaise, fever, chills may be present

May form bullae or undergo necrosis with epidermal sloughing

Common causes: Adults: Staph aureus, GAS, Children: Hib, Staph aureus, GAS

Ddx: DVT, stasis dermatitis, contact dermatitis, erysipelas

Risk factors: interdigital tinea, IVDU if arm, operative wound site

Diagnosis: clinical, wound cultures if exudative,

365
Q

What are the clinical features of furuncles (boils)?

A

Follicular infection spreads and involves the tissue around the hair follicle
Firm erythematous nodule (early)
Fluctuant erythematous nodule (later)
Very tender/painful
Sites: face, neck, axilla, buttocks, perineum, thighs
Course: red, tender nodule points → ruptures

366
Q

What are the clinical features of carbuncles?

A

Form as several furuncles connect subcutaneously
larger and deeper than furuncles
Sites: hair bearing skin, prefer back of the neck in males
Lesions drain through multiple sites to the skin surface
Diabetes predisposes to carbuncles

367
Q

What are the clinical features of abscesses?

A

Form when furuncles/carbuncles not treated adequately
Subcutaneous tissue liquefies, forms granulomatous “pus pocket”
Signs: tender, swollen areas of reddened skin, hot and tender to touch
Can progress via hematogenous or lymphatic spread → ultimately seed other end organs
Sepsis, pneumonia, arthritis, osteomyelitis and endocarditis can subsequently develop

368
Q

What are the clinical manifestations of HPV? (5)

A
  1. flat warts
  2. plantar warts
  3. verruca vulgaris
  4. periungal warts
  5. condylomata
369
Q

What are the clinical features of flat warts?

A

Verruca plana
Sharply defined flat skin coloured or brown papules; 1-2 mm thick
Ddx: seborrheic keratoses, skin tags
Hard to treat
Spread by shaving

370
Q

What are the clinical features of plantar warts?

A

Note multiple capillary loops – these distinguish warts from callus
Plantar warts are very common
Often acquired at swimming pool
Mosaic plantar warts

371
Q

What are the clinical features of condylomata?

A

Perianal condylomata due to HPV
Transmission primarily sexual
Etiology HPV 6 & 11 > 16, 18, 31, 35
HPV types 16, 18, 31, 35 associated with carcinoma
HPV vaccine should decrease incidence of infection
Ddx condylomata lata of secondary syphilis, seborrheic keratoses, skin tags
Diagnosis is clinical, biopsy can differentiate if clinically difficult

372
Q

What are the clinical manifestations of Tinea? (4)

A
  1. Tinea corporis
  2. Tinea capitis
  3. Tinea pedis
  4. Tinea unguium
373
Q

What are the clinical features of Tinea Unguium?

A

Thick yellow dystrophic toenails or fingernails
Toenails more often involved
Genetic predisposition
Often associated tinea pedis
Etiology: T. rubrum most common
DDx: psoriasis, traumatic changes
Dx: scrape under toenail for KOH and culture

374
Q

What are the clinical features of Tinea pedis?

A

Interdigital type: area has scaling, maceration and fissures. Often between 4th and 5th toes

Moccasin type: well marginated erythema with fine scale and hyperkeratosis

Inflammatory or bullous type: vesicles filled with clear fluid
Transmitted by walking barefoot on contaminated ground esp. swimming pool
Etiology: Trichophyton, Microsporum, Epidermophyton
Dx: hyphae on KOH, culture + for dermatophyte
DDx: erythrasma, psoriasis, eczema

375
Q

What is the following definition referring to?

Chronic inflammatory conditions involving the pilosebacious units of the skin

A

Acneiform disorder

376
Q

What are the three types of pilosebacious units and what kind of hair are they associated with?

A
  1. Terminal follicles
    • Long hairs (scalp)
  2. Vellus follicles
    • Miniature hairs (arm)
  3. Sebaceous follicoles
    • No visible hair (most on face)
377
Q

What is the main type of follicle involved in acneiform disorders?

A

Sebaceous

378
Q

How is sebum produced by sebaceous glands?

A

Holocrine secretion - glandular cells degenerate and become secreted material

379
Q

What is the composition of sebum?

A

Triglyceride, cholesterol and cholesterol esters, wax esters and squalene.
Minor Ig A secretion role.

380
Q

What is the physiological function of sebum in humans?

A

No known function.

Possibly - hydration, antimicrobial, anti-oxidant

381
Q

What are the regulators of sebum production?

A

Androgens - increase production (peak levels at puberty)

Retinoids - inhibit sebum production, trigger sebocyte apoptosis

382
Q

What is the key definitive characteristic of acne vulgaris?

A

Presence of comodones

383
Q

Define comodone

A

Engorged follicular ostium - plugged hair follicles - by dead keratinocytes and sebum

384
Q

What are the four features of pathogenesis of Acne Vulgaris?

A
  1. Abnormal follicular keratinization
  2. “Over production” of sebum
  3. Over-growth of follicular bacterium, specifically Proprionibacterium acnes
  4. Inflammation
385
Q

List some common misconceptions about acne pathogenesis.

A

“Acne is worsened by chocolate and fatty foods.”
“Acne is caused by dirt and can be washed away.”
“Acne is due to poor hygiene.”
“Acne does not usually require treatment”
“Acne is caused by stress.”

386
Q

What are some proven acne exacerbaters (Hormonal, Meds, Hygiene, Diet)?

A

Hormonal - prementsrual flare, exogenous, endogenous excess syndromes

Medications - lithium, barbiturates, corticosteroids, environmental toxins

Hygiene - digital pressure, excessive cleaning, oily cosmetics, mechanical friction

Diet - excessive milk consumption

387
Q

Describe primary and secondary lesions of acne.

A

Primary

closed comodones (white heads) and open comodones (black heads) develop into inflammatory lesions

  • papules
  • pustules
  • cysts
  • nodules

Secondary

  • Scars
  • Post-inflammatory hyperpigmentation
388
Q

Define mild acne (for management purposes)

A

Mostly comedones

Few inflammatory lesions

No scars

389
Q

Define moderate acne (for management purposes)

A

Comedones

Numerous papules and pustles

Some scarring

No cysts or nodules

390
Q

Define severe acne (for management purposes)

A

Presence of cysts or nodules

Or

Papulo-pustular acne with significant scarring

391
Q

Describe the four treatment approaches to mild acne

A
  1. Hygienic advice:
    • gentle cleansing BID
    • avoid comedogenic face products,
    • salicylic acid and/or benzoyl peroxide based skin wash
  2. Treating comedones
    • topical retinoic acid creams or gels
    • surgical extraction
  3. Reducing sebum production
    • topical retinoic acids
  4. Decrease bacterial overgrowth
    • topical antibiotics
    • topical benzoyl peroxide
    • Topical azelaic acid
392
Q

Describe the six management approaches to moderate acne.

A
  1. Gentle skin cleansing (as per mild)
  2. Topical
    • antibiotics and anti-inflamm.
  3. Systemic antibiotics
    • Tetracyclines
    • Avoid erythromycin, clindamycin
  4. Systemic hormonal therapies
    • low dose estrogen plus
    • antiandrogen or 3rd gen. progestins
  5. Systemic isotretinoin (Acutane)
  6. Intra-lesional steroid injection (watch for dermal atrophy)
393
Q

Describe the three management approaches to severe acne.

A
  1. Limited role for topical
  2. Systemic anti-inflamm. antibiotics (tetracyclines)
  3. Systemic isotretinoin - most effective
394
Q

What is the MOA of Isotretinoin (acutane)

A

Inibits sebum production
causes sebaceous gland atrophy

395
Q

What are the transient side effects of Isotretinoin?

A

Teratogen

Depressive symptoms (controversial)

Dry skin

Decreased night vision

Arthralgia

Hyper-triglyceridemia

Elevated LFTs

Photosensitivy

Alopecia

396
Q

What are the considerations to starting systemic isotretinoin?

A

Informed consent

Contraceptive

Lab monitoring of ALT, fasting trigs, b-HCG

Stop tetracycline

Lipophilic - take with biggest meal

Manage xerosis, cheilitis

397
Q

What is the MOA of topical retinoic acids?

A

Comedolytic by improving desquamation of dead keratinocytes

Onset slow, therefore longterm

Can cause irritation and skin peeling

398
Q

What is the following definition referring to?

A cutaneous vascular and inflammatory disorder characterized by chronic facial flushing and erythema

A

Rosacea

399
Q

What are the epidemiologic trends of Rosacea?

A

More common in Caucasions than blacks and asians

More common in women

400
Q

While the pathogenesis is largely unknown, give some hypothetical factors.

A
  • genetic predisposition
  • microvascular dilatation
  • demodex flooculorum mites
  • UV light
  • Temp. shifts
  • topical steroids
  • alcohol
401
Q

What is the pathology of Rosacea?

A

Dilated capillaries

perifollicular inflammation

402
Q

What are the 5 clinical classifications of Rosacea?

A
  1. pre-rosacea
  2. subtype 1 - erythematotelangiectatic
  3. subtype 2 - papulopustular
  4. subtype 3 - phymatous
  5. subtype 4 - ocular
403
Q

What are the clinical features of Pre-rosacea?

A

“Blusher and flusher”

Transient erythema

most do not progress to clinical rosacea

404
Q

What are the clinical features of subtype 1 erythematotelangiectatic rosacea

A

Dilated capillaries

fixed facial erythema

405
Q

What are the five clinical features of subtype 2 papulo-pustular rosacea

A
  1. central facial erythema
  2. pustules
  3. papules
  4. fixed edema
  5. no comedones
406
Q

What is the clinical feature of phymatous rosacea

A

Hypertrophic changes of protuding structures

Nose - rhinophyma

Chin - gnathophyma

Eyelids - blepharophyma

Ears - otophyma

Forehead - metophyma

407
Q

What are the six clinical features of Ocular Rosacea?

A
  1. foreign body sensation
  2. burning or stinging, drynes, itching
  3. photophobia
  4. conjunctival telangiectasias
  5. periocular erythema
  6. possible keratitis and blindness
408
Q

What are the treatment principles for Pre-rosacea

A

No effective Tx

Avoid triggers (sun protection, cold compresses)

409
Q

What are the treatment principles for Erythematotelangectatic Rosacea

A

Erythema - no effective therapy, oral tetracyclines (mild to moderate), laser or intense pulsed light (moderate)

Telangectasia - vascular laser surgery, or intense pulse light

410
Q

What is the MOA of vascular laser and other light devices in Rosacea treatment?

A

Obliterates uperficial blood vessels

411
Q

What are the treatment principles for papulo-pustular rosacea

A

Topical therapies (anti-inflammatory?)

  • metronidazole
  • azelaic acid

Oral therapies (suppressive)

  • tetracyclines
  • isotretinoin (lower dose)
412
Q

What are the treatment principles for phymatous rosacea?

A
  • Oral tetracyclines
  • Oral isotretinoin
  • Surgical reconstruction
    • CO2 laser
    • Electric surgery
    • Reconstructive plastic surgery
413
Q

What are the treatment principles for Ocular Rosacea?

A

Topical steroid solutions

Oral tetracyclines

414
Q

What are the three childhood acne variants?

A
  • Nonatal - resolve spontaneously
  • Infantile - resolve spontaneously
  • Early onset acne vulgaris - may be associated with precocious puberty, treat acne
415
Q

What do these three highly inflammatory, nodular-cystic, interconnecting tract forming, scarring variants represent?

  1. Acne conglobata
  2. Dissecting cellulitis of the scalp
  3. Hidradenitis suppurativa (axillae, groin, perianal)
A

Follicular Occlusion Triad

416
Q

What are the treatment principles for Follicular Occlusion Triad?

A

Systemic antibiotics

Systemic isotretinoin

Surgical debridement / drainage

417
Q

What are the clinical features of Acne Fulminans

A

Acute febrile ulcerative acne

Young males

Sudden onset of papules, pustules on chest, back, and shoulders

Feber, arthralgias, anorexia, leukocytosis, focal lytic bone lesions

Treat with systemic isotretinoin

418
Q

What are the clinical features of Acne excoriee

A

Mild background acne

Self-inflicted excoriations

Therapy - supportive to stop excoriation

419
Q

What are the clinical features of Rosacea Conglobata

A

Similar to acne conglobata - except adult women

treat with systemic isotretinoin and prednisone

420
Q

What are the clinical features of steroid rosacea

A

Inflammatory papules and erythema associated with burning sensation following steroid use

Stop steroid

Treat with systemic tetracyclines

421
Q

What are the clinical features of Perioral dermatitis?

A

Typically females of childbearing age

Red papulopustules, no telangiectasia, no vasomotor flushing

Invovles nasolabial folds, perioral, periocular

Treat wit systemic tetracyclines

FMED (1 decks)

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