Introduction To Dermatology pdf - All Lectures

Dermatology

Skin



Anatomy:

 It weighs about 4.5 kgs.
 It's surface area is 2 m

 Skin is composed of epidermis and dermis.
 The line separating between the 2 layers of the skin is called the dermo-epidermal junction.

Epidermis

 The basal cell layer (stratum basale) comes from the DEJ. These cells grow upward and form

another layer  called and  then  another layer  (Granulosum  and Malpegian)  above it and  then
the last layer, the stratified squamous cell layer (keratinocyte)the cells in BCL divide and
undergo  differentiation  and  form  keratohyaline  granules  and  then  begin  to  lose  organelles,
leading to the formation of dead cells containing keratin only Then this keratin undergoes
shedding.  This  process  is  programmed  and  it  takes  about  28  days  (from  the  BCL  to  the
shedding  phase).  Normally  the  shedding  of  keratin  is  insensible,  if  it  is  sensible, disease  is
suspected.

 With each 10 keratinocytes, there is an umbrella-like cellMelanocyteIt is the cells

responsible for pigmentation (melanin production). The number of melanocytes is the same
in all individuals. It is present in hair, skin, eye (retina), substantia nigra, etc.

 Melanocytes produce melaninit's (melanin) function is to protect the skin and the

underlying structures from the sun (UV light) by reflecting or absorbing the UV light (type
B& C) within the cell itself preventing it from passing towards the underlying structures.

 UV lightType A

Type B

Type C (Doesn’t pass through the Ozone layer)It is carcinogenic.

Dermis

 It contains:

1) Vasculature.
2) Fibroblastsproducing fibers (elastic & collagen)Function: recoiling of skin. With

aging, UV light damages the fibroblasts and fibersElastic and collagen fibers decrease
in the skin aging process (wrinkles).

3)  Sebaceous glandsproducing sebum.
4)  Sweat glandsApocrine sweat glands are located mostly in the axilla and groin.
5)  Hair follicles and arrector pili muscles. (hair is composed of keratin)
6)  Nerve endings.
7)

Nail

 It consists of:

1)  Nail plate is composed of keratin.
2)  Cuticle: The white area of the nail that is regarded as the nail matrix.
3)  Nail folds.
4)  Nail bed.

 Function:

1.  Protection.
2.  Thermal regulation.
3.  Appearance (organ of beauty).
4.  Vitamin D synthesis.
5.  Indicator of disease. (mirror of internal organs).
6.  Immunity, etc.

Language Of Dermatology

 In Dermatology, we do physical examination and then take history (ask questions related the

findings of the physical examination).

 Erythema Redness.
 MaculeAlteration in the skin's texture or color <0.5 cm.
 Patch Alteration in the skin's texture or color >0.5 cm.
 Papule Elevation in the skin <0.5 cm.
 Pluque Elevation in the skin >0.5 cm.
 Vesicle Papule containing clear fluid.
 Pustule Papule containing turbid fluid.
 Bullae Enlarged vesicle. If contains blood Haemorrhagic bullae.
 Fissure Loss of continuity of the skin.
 Crust Dry exudate.
 Scale ???? (Like the shedding of the keratin).

Acne



Types

 Acne vulgaris.
 Rosacia.



Acne vulgaris

 Definition:

It’s a self-limiting disease affecting the young age (from

puberty to 30 years),

occurring in the seborreic areas (face, chest, shoulder, upper back, gluteal region).

 Etiology:

1)  Genetic predisposition.
2)  Environmental factors.
3)  There 3 theories:

a. Internists noticed that the disease occurs in the young age (during puberty), there is

an increase in the levels of sex hormones (androgen)act on the sebaceous
glandsIncrease sebum secretion.

b. Microbiologists have noticed the presence of a pustule in the lesionprobyno

bacterium acnis which is a normal florathey noticed that this NF numbers are
increased in the lesion.

c. Pathologists have noticed that there is a narrowing in the opening of the sebaceous

glands in the lesionsebum exits with difficultyhyperkeratosis of the pilo-
sebaceous orifice.

 Clinical features & Complications:

Hyper secretion of sebum (seborrhea) + hyperkeratization blocking the pilo-sebaceous
orifice



Sebum contains cholesterol, FFA, etc



when this sebum accumulates in this

site  (there is no  way  out, because  the pilo-sebaceous duct is  blocked)Papule  will be
formed  (due  to  the  accumulation  of  sebum).  This  papule  is  called  comedon  (black  or
white.  If  the  accumulation  of  sebum  is  deep



white head {comedon}, but if it is

superficial



black head)



with further accumulation of sebum



it will rupture releasing

the contents inside the skin including FFA which will cause irritation and will provoke
an inflammatory reaction



ErythemapapulepustulecystScar

1) Erythema.
2) Papule (comedon).
3) Pustule.
4) Cyst.
5) Scarpitting scar (in acne), atrophic, hypertrophic, keloid.
6) PigmentationHyper or hypo.
7) Depression (mental scar).



Types

1) Acne vulgaris
2) Neonatal acneAndrogen H. from the mother through the placentastimulating the

sebaceous glands of the neonateAcne. (sebum acts in the 1

year of life due the maternal

androgen)

3) Childhood acneEarly puberty.
4) Acne medicamentosa Due to certain drugs (like steroids, CCP).
5) Post depilation acne Due to mechanical removal of the hair (sugar solution, waxing,

etc).

6) Oil acneOccur in car mechanicsoil causes obstruction of the pilo-sebaceous orifices.
7) Rosacea



Treatment:

1) Includes topical & systemic.
2) Antibiotics 1

line of treatment.

3) Increased androgen levelAnti-androgen (like cemitidine, spirolactone, fenisteride, etc).
4) Heperkeratosiskeratolytic (salicylic acid, retinoid, etc).
5) Scar: PittingFiller.

Hypertrophickeratolytic.
Keloidresection & application of steroid (to prevent re-formation of keloid).
Hypopigmentationgive drugs that increase the pigmentation.
Hyperpigmentationgive drugs that decrease the pigmentation.

Psoriasis

 Definition:

 It is a chronic disease, occurring in old age, occurring in both genders, remission and

relapse and it is regarded as an autoimmune disease.

 Etiology:

1) Genetic factors.
2) Environmental factorsstress, D.M, infection, drugs (like beta blockers, gold, lithium),

sunlight, etc.

 Clinical features:

1)  Thickening of skin.
2)  Fissuring.
3)  Scaling.
4)  Papule & plaque.
5)  VasodilationhyperemiaErythema.
6)  Itching.

 Types:

1)  Localized or generalized (emergency condition).
2)  Psoriasis capitis.
3)  Frictural psoriasis.
4)  Pustular psoriasis.
5)  Palmer or planter psoriasis.
6)  Psoriasis of the nail.
7)  Gutet psoriasis. (caused by streptococcal infection)
8)  Etc.

 Treatment:

1)  Thickening of skinkeratolytic agents (topical & systemic).
2)  FissuringOintment (emollients).
3)  ErythemaSteroids (topical & systemic).
4)  InfectionAntibiotics.
5)  ItchingAntihistamines.
6)  Analgesia.
7)  Cytotoxic drug (methotrexate).
8)  Vit. A (acetritinenhance proliferation & differentiation)

When psoriasis is cured, it leads to post-inflamatory hypopigmentation, while lichen
planus leads to post-inflamatory hyperpigmentation.

Lichen planus

  Types: Generalized or localized.
  Same etiological factors.
  Same mechanism but here only papule and plaque are formed (no thickening and

fissuring).

 Both skin and mucous membranes are involved.
 The lesion is violate (no erythema)

Pyteriasis rosea

 It is an infection by Herpes virus type A

Pigmentary disorders

  Each 10 keratinocytes, there is 1 melanocyte.
  The number of melanocytes is fixed in all individuals.
  FunctionMelanin productionresponsible for pigmentation, absorption and reflection of UV

light type A & B (to prevent its passage into underlying structures. If it passesDamage to
fibroblasts (producing elasticresponsible for elasticity and collagenActs as a
cushion)Aging process. If it reaches the BCL may cause damage and lead to tumor
formation).

 Melanin is located in vesiclescalled melanosomes.

White

Black

Number of melanocytes

Same

Number of melanosomes

Less

Size of melanosomes

Smaller

Larger

Oxidation of melanin

Less

  Melanocytes are located in the skin, hair, retina, substantia nigra.
  Melanocytes activity decreases with age.
  Increased pigmentationHyperpigmentation.
  Decreased pigmentation Hypopigmentation.
  No pigmentationDepigmentation.

Hypopigmentation

 Vitiligo

 Definition:

It is an autoimmune disorder. Remission and relapse.

 Etiology:

1. Genetic factors.
2. Environmental factors. (i.e. stressful condition, infection, etc these factors stimulate

antibodies against the melanocytes)

 Clinical features:

1.  Hypopigmentation or depigmentation.
2.  Macule or patch.
3.  Mostly occurs at sites of friction (fingers, elbows, knees, eyes, ano-genital area, etc).

 Types:

1.  Generalized or localized vitiligo.
2.  Xosteriform vitiligo.
3.  Halo naevus vitiligo.
4.  Vitiligo of the hair.

 Complications:

1. Depression.

2.  Early aging process.
3.  Burning.
4.  Tanning.
5.  Tumor.

 Treatment:

1.  Genetic counseling.
2.  Immune modulationsteroids (topical & sysyemic), zinc sulphate, antioxidants.
3.  Psoralen and UV light exposure.
4.  Plastic surgery.
5.  Camouflage (dye or henna). (can be detected by Wood's light, the lesions will look

ivory in color).

6. If a pt. with 80% of his body is white and only some spots are blackDepigmentation

(bleaching agent).

 After being cured could lead to  Post-inflammatory hypo-pigmentation.

Hyperpigmentation

 Melasma

 Definition:????

 It is seen in the face.

 Etiology:

1. Genetic factors.
2. Environmental factors: Occupational (sun exposure), pregnancy (melanocyte

stimulating hormone), CCP, Post-inflammatory hyperpigmentation, drugs

 Types:

1. Localized or generalized.
2. Butterfly melasma.

 Treatment:

1.  Sun exposure sun screen.
2.  CCP avoid it and use other type of contraception.
3.  Bleaching agent (i.e. glutathione, etc). could be given topical, injection.
4.  Laser.
5.  Dermoabrasion.
6.  Peeling.
7.  Antioxidants, vitamins.

 Complications:

1. Depression.

By: Muthana Harith