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SD & AV Flashcards

1
Q

Def of Seborrheic Dermatitis

A
  • A common erythematous scaling eruption that is localized to the seborrheic sites.
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2
Q

Etiology of Seborrheic Dermatitis

A

Pityrosporum ovale may play a role.

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3
Q

Pathogenesis of Seborrheic Dermatitis

A
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4
Q

Prevalence of Seborrheic Dermatitis

A

eczematous form is estimated at 5%

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5
Q

Age affected by Seborrheic Dermatitis

A
  • Usually begins in adolescence (9-11 years) (with puberty) peak at age 40
  • Uncommon in preadolescent childhood (exclude t.capitis)
  • Infantile SD
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6
Q

which sex is more commnly affected by Seborrheic Dermatitis?

A

More common in males than females. (M > F)

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7
Q

what are sites of Seborrheic Dermatitis?

A
  • Scalp, behind ears, face
  • Pre-sternal and interscapular areas
  • flexures (umbilicus, axilla, infra-mammary, inguinal fold, perineum or anogenital crease.
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8
Q

Lesions of Seborrheic Dermatitis

A
  • Scalp
  • Ears
  • Eyebrows & Beard
  • Galbrous skin
  • Nasolabial fold
  • Eyelid margin
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9
Q

Scalp lesions of Seborrheic Dermatitis

A
  • Non inflammatory (dandruff) (pityriasis capitis)
  • Inflammatory (seborrheic eczema)
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10
Q

Shape of Non inflammatory
(dandruff) (pityriasis capitis) SD

A

Diffuse fine white (branny) or greasy scales

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11
Q

Characters of Non inflammatory
(dandruff) (pityriasis capitis) SD

A
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12
Q

what is the mildest form of SD?

A

Non inflammatory
(dandruff) (pityriasis capitis) SD

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13
Q

Characters of Inflammatory Scalp SD (seborrheic eczema)

A
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14
Q

SD in Ears

A
  • retro-auricular scaling, crusting and fissuring.
    Persistent non purulent otitis externa may occur.
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15
Q

SD in Eyebrows and beard

A

fine scaling

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16
Q

SD in Glabrous skin

A

diffuse redness.

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17
Q

SD in nasolabial fold

A

greasy scales.

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18
Q

SD in Eyelid margin

A

seborrheic blepharitis.

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19
Q

SD of facial skin

A
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20
Q

SD of trunk

A
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21
Q

Flexures (inverse SD) (axillae, groins, sub-mammary areas and umbilicus)

A

erythematous patches with maceration and oozing.

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22
Q

Types of inverse SD

A
  • Scaling Intertrigo
  • Non-Scaling Intertrigo
  • Crusted Fissures
  • Weeping Dermatitis
  • Sebopsoriasis
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23
Q

Scaling intertrigo

A
  • Sharply marginated erythema and greasy scaling
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24
Q

Non scaling intertrigo

A

May be erythema only

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25
Q

Weeping dermatilis

A
  • Due to sweating, secondary infection, and inappropriate treatment,
  • Erythema, maceration, oozing, crusting.
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26
Q

Sebopsoriasis

A
  • features of both psoriasis and SD.
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27
Q

Severity varies from mild dandruff to exfoliative erythroderma

A

..

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28
Q

Examples of Extensive SD

A
  • Erythrodermic: rare
  • HIV infection
  • Parkinson’s disease (with seborrhoea)
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29
Q

Adult SD

A
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30
Q

DDx of adult scalp SD

A
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31
Q

Introduction to TTT of SD

A
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32
Q

2 steps regimen in TTT of SD

A
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33
Q

Def of Infantile SD

A
  • SD inearly infancy due to stimulation of sebaceous glands by maternalandroge
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34
Q

Charachters of Infantile SD

A
  • simulates SD in adult, but the scaling on the scalp is thick forming yellowish heaped lesion (cradle cap).
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35
Q

Onset of Infantile SD

A
  • Begins 2-8 weeks after birth
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36
Q

Healing of Infantile SD

A
  • The lesions usually subside within 3-4 weeks.
  • May persist for several months
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37
Q

CP od Infantile SD

A
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38
Q

TTT of Infantile SD

A
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39
Q

DDx of Scaly scalp in prepubertal children

A
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40
Q

Def of Acne Vulgaris

A
  • Acne vulgaris is a chronic inflammatory disorder of the pilosebaceous apparatus, characterized by formation of comedones.
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41
Q

Pathogenesis of Acne Vulgaris

A

4 major factors (multifactorial disorder) are involved in the pathogenesis of acne in the genetically predisposed person.

  • Increased sebum secretion
  • Hyperkeratosis of pilosebaceous duct
  • Propionibacterium acne (P. acne) colonizes pilosebaceous duct
  • Propionibacterium acne (P. acne) colonizes pilosebaceous duct
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42
Q

Increased sebum secreation

(Pathogenesis of Acne Vulgaris)

A
  • which may result from increased local synthesis of androgen in sebaceous glands or increased response to it.
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43
Q

Hyperkeratosis of pilosebaceous duct (Pathogenesis of Acne Vulgaris)

A
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44
Q

Propionibacterium acne (P. acne) colonizes (Pathogenesis of Acne Vulgaris)

A
  • Pilosebaceous duct and contributes in the formation of comedones and pustules.
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45
Q

Inflammation
(Pathogenesis of Acne Vulgaris)

A

initiated by P:acne

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46
Q

what causes Hyperkeratosis of pilosebaceous duct?

A

results from the irritant effect of excess sebum.

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47
Q

what does Obstruction of pilosebaceous duct result in?

A

result in comedones which consist of horny cells, sebum, and bacteria.

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48
Q

Types of comedoens according to level of obstruction

A
  • If obstruction is deep: comedones are closed with narrow orifice (white head).
  • If obstruction is superficial: the comedones are open and have a patulous orifice (black head).
49
Q

what does Propionibacterium acne (P. acne) colonize?

A

pilosebaceous duct

50
Q

what initiates inflammation in Acne Vulgaris?

51
Q

what are Micro-comedones?

A

Invisible hyperkeratotic plug made of sebum and keratin in follicular canal

52
Q

Excerbating factors of Acne Vulgaris

53
Q

Age of Acne Vulgaris

A
  • Adolescence of both sexes. (12-24 years ) mainly
  • May start at 10 years and persist up 50 years
54
Q

Lesions in Acne Vulgaris

55
Q

Characters of Closed Comedones

A
  • Skin coloured
  • No visible follicular opening.
  • Often inconspicuous and require adequate lighting and stretching of the skin to be seen
56
Q

Classification of Acne Vulgaris

A

1- Mild acne: comedones with little or no papules.

2- Moderate acne: comedones, papules and pustules.

3- Severe acne: nodules and cysts predominate.

57
Q

Course of Acne Vulgaris

58
Q

Sites of Acne Vulgaris

A

face, back, chest and shoulders.

59
Q

TTT of Acne Vulgaris

60
Q

Topical in TTT of Acne Vulgaris

A
  • Comedolytic agents
  • Antibacterial agents
61
Q

Comedolytic agents in TTT of Acne Vulgaris

62
Q

what is cornerstone in acne ttt?

A

Topical retinoids

63
Q

AV = Acne Vulgaris

Topical retinoids in TTT of AV

A

Retinoic acid (0.05-0.1%) is used in gradually increasing concentration

64
Q

SE of Topical retinoids in TTT of AV

A

It may cause dryness & irritant dermatitis. (Most common side effect)

65
Q

what are examples of Topical Retinoids?

66
Q

Antibacterial agents in TTT of AV

67
Q

Characters of Benzoyl peroxide (BPO) (2.5, 5, 10)%

A
  • no resistance has mild comedolytic effect.
  • It may cause contact dermatitis.(irritant)
68
Q

what are topical antibiotics used in TTT of AV?

A

erythromycin and clindamycin are effective in pustular lesions. (not alone)

69
Q

Indication for topical TTT of AV

70
Q

Systemic TTT of AV

A
  • Antibiotics
  • Antiandrogens
  • Isotretinoin
  • Dapsone
  • Miscellanous therapy
  • TTT of scars
71
Q

what is the systemic antibiotic of choice in acne?

A
  • Doxycycline: 100mg/day is the antibiotic of choice in acne.
  • This dose is given until acne clears then dec. the dose gradually for 6 months
  • Erythromycin and Azithromycin are good alternatives.
  • clindamycin
72
Q

MOA of antibiotics in systemic TTT of AV

A
  • Reduce inflammation
  • Reduce P: acne population> reducing bacterial production of inflammatory factors as FFA
  • Intrinsic anti-inflammatory
  • Reduce PMN (poly morphonuclear leukocytes) migration
73
Q

Indication of using of antiandroges on TTT of AV

A

used only in females with severe nodulocystic acne

74
Q

Examples of antiandroges used in TTT of AV

A

1- contraceptive as Yasmin

2- Cyproterone acetate (with OCPs diane)

3- Spironolactone (K sparing diuretic but has
antiandrogen effect)

75
Q

Effects of isotretinoin used in systemic TTT of AV

A
  • It decreases sebum secretion
  • Decrease P. acne.
  • Decrease follicular hyperkeratosis
  • has anti-inflammatory effect
76
Q

AE of isotretinoin used in systemic TTT of AV

A

It is teratogenic drug with serious side effects, so it should be used only in severe acne and by highly experienced dermatologists.

77
Q

Dapsone Systemic TTT of AV

A

Anti-inflammatory drug used in severe acne with special precautions.

78
Q

Miscellaneous therapy

Systemic TTT of AV

A

Comedonae removal:
- If comedones are resistant

intralesional steroids:
- Triamcinolone acetonide (2-5 mg/ml)
- Used for large inflammatory nodules/cysts

79
Q

TTT of scars

Systemic TTT of AV

A
  • Dermabrasion, laser resurfacing, deeper chemical peels
  • Filler substances
  • Punch excision (ice-pick) scar
80
Q

Treatment according to the severity of acne can be given as follow (overview)

81
Q

Def of Miliaria (Sweat rash)

A

A disorder of the sweat duct in which obstruction of the sweat ducts at various levels occurs in association with excessive sweating&raquo_space; sweat retention

82
Q

Etiology of Miliaria (Sweat rash)

A

Common in:
- Neonates: immature eccrine sweat ducts
- Adults: living in hot humid condition

Resolve in cool environment

83
Q

Predisposing factors for Miliaria (Sweat rash)

A

1- Hot humid condition.
2- Excessive clothing.
3- Obesity.
4- Febrile illness.

84
Q

Incidence of Miliaria (Sweat rash)

A
  • The disease occurs in the tropics and subtropics
  • Affects persons of all ages and both sexes.
85
Q

Site & Size of lesion of Miliaria (Sweat rash)

A
  • Any site
  • Pin head size
86
Q

Lesions of Miliaria (Sweat rash)

A
  • The eruption consists of closely set red papules, vesicles
  • It is associated with itching, prickling, or burning sensation.
  • In infants the eruption may be generalized,
    and it may occur in any season depending on the habits of overclothing.
87
Q

Complications of Miliaria (Sweat rash)

A

impetigo, folliculitis, and boils.

88
Q

Types of Miliaria (Sweat rash)

89
Q

TTT of Miliaria (Sweat rash)

90
Q

Stages of Hair growth

91
Q

Causes of hair loss

A
  • Physiological
  • Pathological (Alopecia)
92
Q

Definition of Alopecia

A

loss of hair from normally hairy area

93
Q

Types of Alopecia

A
  • Cicatricial or scarring alopecia (permanent)
  • non Cicatricial or nonscarring (transient)
94
Q

Causes of Non-cicatricial alopecia

A
  • Conginetal
  • Aquired
95
Q

Aquired Causes of Non-cicatricial circuscribed (Patterned) alopecia

96
Q

Aquired Causes of Non-cicatricial alopecia

A
  • Circumscribed (Patterned)
  • Diffuse
97
Q

Aquired Causes of Non-cicatricial Diffuse alopecia

98
Q

Congenital causes of cicatricial alopecia

A

developmental defect

99
Q

Aquired causes of cicatricial alopecia

100
Q

Definition of Alopecia Areata

A

circumscribed non scarring hair loss with normal skin

101
Q

Etiology of Alopecia Areata

102
Q

CP of Alopecia Areata

103
Q

Lesions in Alopecia Areata

A
  • Circumscribed area of hair loss, nonscarring with normal skin
  • Positive exclamation mark! (tapered proximal end of the hair shaft)
  • May affect scalp, face or body hair
104
Q

Clinical types of Alopecia Areata

105
Q

Prognosis of Alopecia Areata

A

Bad prognosis in the following conditions:
1- Alopecia totalis, universalis and ophiasis
2- Alopecia areata with nail pitting
3- Alopecia areata in atopics

106
Q

Associated features to Alopecia Areata

A

1- Nail pitting
2- Atopy (atopic dermatitis)
3- Vitiligo
4- Cataract

107
Q

DDx of Alopecia Areata

108
Q

TTT of Alopecia Areata

109
Q

Causes of hyperpigmentation

110
Q

Causes of Hypopigmentation

111
Q

Casues of depigmentation

112
Q

Def of Vitiligo

A

acquired idiopathic depigmentation (leukoderma) of the skin

113
Q

Etiology of Vitiligo

114
Q

Precipitataing factors for Vitiligo

A

1- Emotional stress
2- Sun burn
3- Physical trauma (Koebner’s phenomenon)

115
Q

CP of Vitiligo

A
  • Milky white depigmented macules or patches affecting any area.
  • Hair and mucous membranes may be affected

Sites: face, hand, feet. back are sires of predilection

116
Q

Classification of Vitiligo

117
Q

Prognosis of Vitiligo

A

1- Unpredictable
2- Stationary
3- Spontaneous re-pigmentation
4- Slowly progressive
5- Rapidly progressive

118
Q

DDx of Vitiligo

A

1- Pityriasis alba
2- Pityriasis versicolor (hypopigmented type)
3- Post inflammatory hypopigmentation
4- Albinism
5- Post-burn and post-chemical depigmentation

119
Q

TTT of Vitiligo

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