- Nails (“Ungals”):
o Composition:
▪ Plate of hardened and densely packed keratin (Protein)
o Functions:
▪ Protect distal phalanges of fingers and toes
▪ Aid in picking up objects
▪ Efficient natural weapon
o Structural Landmarks:
▪ Nail Plate:
• Fully keratinized structure
• Firmly attached to the nail bed
▪ Nail Bed: Skin underneath the nail
▪ Lunula: Proximal whitish half moon-shaped area on Nail Plate
▪ Cuticle: The dorsal part of the proximal nail fold
▪ Nail Matrix: Nail growth occurs From Here - by proliferation and differentiation of the nail matrix
▪ Paranychium: The Skin around the Nail
▪ Hyponychium: The area where the nail plate detaches from the digit
▪ Proxymal Nail Fold: The fold at the Proximal Edge of the nail (Covers ≈1/4 of the nail) ▪ Lateral Nail Folds: The folds of skin at the
Lateral Edges of the Nail
- Hair/The ‘Pilosebaceous Unit’:
o The Pilosebaceous Unit:
▪ Hair Shaft
▪ + Sebaceous/apocrine ducts empty into hair follicles
o Arrector Pili Muscle:
▪ Smooth Muscle
▪ Supplied by Adrenergic Nerves
▪ 🡪 Erection of the Hair during Cold/Emotional Stress (Goose-Bumps)
o 2 Types of Hair:
▪ Vellus:
• Fine, Short & Almost invisible
• (All over the body)
▪ Terminal:
• Thick, coloured & Visible
• (Scalp, beard, axilla, genital area)
o Hair Follicles Respond to Androgen:
▪ Pre-pubertal children don’t have Terminal Hair in Axilla/Genital Area/Facial Hair. ▪
During Puberty, hair grows in these areas
▪ With age, androgen stimulation decreases 🡪 Terminal Hair on scalp reverts from
Terminal to Vellus hair. (Hair follicles aren’t lost, but change to Vellus hair)
o Hair follicles undergo cycles of Growth, Resting and Shedding:
▪ Anagen (growing):
• Lasts 3 Years
, • Keratinocytes in the follicular bulb proliferate to form the hair shaft
▪ Catagen (Resting):
• Lasts 2 Weeks
• The keratinocytes and melanocytes undergo programmed cell death
▪ Telogen (Shedding):
• Last 3 Months
• Hair but does not grow.
• May Remain Anchored, or Be Shed.
• Following telogen a new growth cycle will begin (ie anagen)
o Hair Pigmentation:
▪ Colour of hair is determined by the melanocytes – actively pigmented only in Anagen. ▪
Absence of pigment 🡪white hair
▪ Diminished pigment 🡪grey hair
SAMPLE SKIN STRUCTURE QUESTIONS:
DERMATOLOGY Pathology:
Acne
- ACNE:
o What is it?:
③ Common Skin Condition in Teenagers (Although Can occur at any age)
③ Most Severe in Males
o Aetiology & Pathogenesis:
③ Genetic Basis (Familial)
ξ Chronic inflammation of the sebaceous glands
③ Abnormalities of the Pilosebaceous Unit:
ξ Blockage of the Sebaceous Duct ;By јKeratin Λ Duct Opening Ϳ
ξ Increased Sebum Production ;Often under influence of јAndrogen Ϳ
ξ ⮴ Bacterial Infection of the Pilosebaceous Unit (Proprionibacterium Acnes)
ξ ⮴ Rupture of the Sebaceous Duct
ξ ⮴ Inflammatory Effects.
③ NB: Combined Oral Contraceptives (Ie. With Progesterone) can contribute to Acne. ③ (IF
Severe, Damage to Dermis Occurs ⮴ Scarring. NB: Scarring is a FAILURE of the Doctor to
Adequately treat Acne)
o Presentation:
③ Wide Variation in Severity
③ Most often on Face, Upper Chest & Back.
③ **Presence of Comedones – Both Open (Blackheads) & Closed (Whiteheads)
ξ (NB: If no comedones are present, consider Differential Diagnoses)
o Composition:
▪ Plate of hardened and densely packed keratin (Protein)
o Functions:
▪ Protect distal phalanges of fingers and toes
▪ Aid in picking up objects
▪ Efficient natural weapon
o Structural Landmarks:
▪ Nail Plate:
• Fully keratinized structure
• Firmly attached to the nail bed
▪ Nail Bed: Skin underneath the nail
▪ Lunula: Proximal whitish half moon-shaped area on Nail Plate
▪ Cuticle: The dorsal part of the proximal nail fold
▪ Nail Matrix: Nail growth occurs From Here - by proliferation and differentiation of the nail matrix
▪ Paranychium: The Skin around the Nail
▪ Hyponychium: The area where the nail plate detaches from the digit
▪ Proxymal Nail Fold: The fold at the Proximal Edge of the nail (Covers ≈1/4 of the nail) ▪ Lateral Nail Folds: The folds of skin at the
Lateral Edges of the Nail
- Hair/The ‘Pilosebaceous Unit’:
o The Pilosebaceous Unit:
▪ Hair Shaft
▪ + Sebaceous/apocrine ducts empty into hair follicles
o Arrector Pili Muscle:
▪ Smooth Muscle
▪ Supplied by Adrenergic Nerves
▪ 🡪 Erection of the Hair during Cold/Emotional Stress (Goose-Bumps)
o 2 Types of Hair:
▪ Vellus:
• Fine, Short & Almost invisible
• (All over the body)
▪ Terminal:
• Thick, coloured & Visible
• (Scalp, beard, axilla, genital area)
o Hair Follicles Respond to Androgen:
▪ Pre-pubertal children don’t have Terminal Hair in Axilla/Genital Area/Facial Hair. ▪
During Puberty, hair grows in these areas
▪ With age, androgen stimulation decreases 🡪 Terminal Hair on scalp reverts from
Terminal to Vellus hair. (Hair follicles aren’t lost, but change to Vellus hair)
o Hair follicles undergo cycles of Growth, Resting and Shedding:
▪ Anagen (growing):
• Lasts 3 Years
, • Keratinocytes in the follicular bulb proliferate to form the hair shaft
▪ Catagen (Resting):
• Lasts 2 Weeks
• The keratinocytes and melanocytes undergo programmed cell death
▪ Telogen (Shedding):
• Last 3 Months
• Hair but does not grow.
• May Remain Anchored, or Be Shed.
• Following telogen a new growth cycle will begin (ie anagen)
o Hair Pigmentation:
▪ Colour of hair is determined by the melanocytes – actively pigmented only in Anagen. ▪
Absence of pigment 🡪white hair
▪ Diminished pigment 🡪grey hair
SAMPLE SKIN STRUCTURE QUESTIONS:
DERMATOLOGY Pathology:
Acne
- ACNE:
o What is it?:
③ Common Skin Condition in Teenagers (Although Can occur at any age)
③ Most Severe in Males
o Aetiology & Pathogenesis:
③ Genetic Basis (Familial)
ξ Chronic inflammation of the sebaceous glands
③ Abnormalities of the Pilosebaceous Unit:
ξ Blockage of the Sebaceous Duct ;By јKeratin Λ Duct Opening Ϳ
ξ Increased Sebum Production ;Often under influence of јAndrogen Ϳ
ξ ⮴ Bacterial Infection of the Pilosebaceous Unit (Proprionibacterium Acnes)
ξ ⮴ Rupture of the Sebaceous Duct
ξ ⮴ Inflammatory Effects.
③ NB: Combined Oral Contraceptives (Ie. With Progesterone) can contribute to Acne. ③ (IF
Severe, Damage to Dermis Occurs ⮴ Scarring. NB: Scarring is a FAILURE of the Doctor to
Adequately treat Acne)
o Presentation:
③ Wide Variation in Severity
③ Most often on Face, Upper Chest & Back.
③ **Presence of Comedones – Both Open (Blackheads) & Closed (Whiteheads)
ξ (NB: If no comedones are present, consider Differential Diagnoses)
