Pathogenesis Of Folliculitis

Question 1

Acne-form rashes

Answer 1

• pustules
• Folliculitis (inflammation of hair follicle)
• acne vulgaris (teenager) = only if you see comedones (black/whiteheads)
• rosacea

Question 2

Folliculitis

Answer 2

• superficial/ deep
• infectious/ non-infectious
• not diagnosis
• No comedones = not acne vulgaris
• pustule (pus filled papule)
• just because there is pus, does not mean infectious

Question 3

Causes of Folliculitis

Answer 3

Infectious
- small mite (demodex)
Non-infectious
- occlusive sunscreen/ Vaseline/ areas of frictions

Question 4

Definition Furuncle

Answer 4

Deep staph Folliculitis

Question 5

Definition furunculosis

Answer 5

Recurrent staph Folliculitis

Question 6

Definition carbuncle

Answer 6

Cluster of staph deep Folliculitis

Question 7

A. Pathogenesis of acne vulgaris

Answer 7

Early comedone
1. infundibulum (top part)
- hyperkeratosis (plug)
- corneocyte cohesiveness
2. Androgen stimulation of sebum secretion
Condition of hair follicle sebaceous unit
Teens = oil gland is more active - androgens, oil gland gets larger and secretes more oil in follicle

Question 8

B. Pathogenesis of acne vulgaris

Answer 8

Later comedone
1. Accumulation of shed keratin & sebum
2. Formation of whorled lamellar concretions
Plug blocks oil from going onto skin
Hair follicle gets inflamed = whitehead/ close comedone

Question 9

C. Pathogenesis of acne vulgaris

Answer 9

Inflammatory papule/ pustule
1. Cutibacterium (propionibacterium) acnes proliferation
2. Sebaceous lobule regression
3. Mild inflammation
Creates environment for normal commensal skin flora to proliferate
Immune response activated = inflammation
Develop a red papule
Neutrophil infiltration = pustule
Can become bigger/ burst/ cyst

Question 10

D. Pathogenesis of acne vulgaris

Answer 10

Nodule/cyst
1. Marked inflammation
2. Scarring

Question 11

4 key pathogenic factors of acne vulgaris

Answer 11

1. Keratinocytes & follicular proliferation
   +
2. Androgen driven sebum production
   Ductal obstruction
3. Proliferation of cutibacterium acnes
4. Inflammation
   Target for treatment = open hair follicle, decrease sebum production, decrease C acnes, anti-inflammatory

Question 12

Pathogenesis of Rosacea

Answer 12

Constellation of symptoms
Early = redness of cheeks/ nose, inflamed papules & pustules, redness around eye (ocular)
Dilated blood vessels = telangiectasia
Later = thickening of skin in all areas (nose = rhinophyma)
NB = blood vessel proliferation & redness
Sensitive skin = burning, stinging - cannot tolerate anything on skin (vascular hypersensitivity)

Question 13

2 pathways of rosacea

Answer 13

Inflammation & neurogenic (spices, stress, exercise, alcohol, heat)
UV light + demodex (skin mite) induces TLR 2 eliciting an immune response, anti microbial factors + innate immune system = inflammation & angiogenesis

Question 14

Triggers of rosacea

Answer 14

• inborn condition but exacerbated
• sun exposure
• emotional stress
• wind etc