DERMATOLOGY

DR. MOHCEN AL. HAJ

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DR. MOHCEN AL. HAJ
 Index
Introduction ---------------------------------------------------------------------------------------------- 3

Skin Lesions ----------------------------------------------------------------------------------------------- 4

Skin Disorders
Papulo-Squamous Disorders------------------------------------------------------------------------ 5

Vesiculo-Bullous Disorders------------------------------------------------------------------------ 10

Pigmentation Disorders----------------------------------------------------------------------------- 12

Erythema-------------------------------------------------------------------------------------------------- 14

Eczema----------------------------------------------------------------------------------------------------- 16

Urticaria-------------------------------------------------------------------------------------------------- 20

Acne & Rosacea---------------------------------------------------------------------------------------- 21

Hair--------------------------------------------------------------------------------------------------------- 24

Genodermatosis---------------------------------------------------------------------------------------- 27

Skin Infections
Bacterial Skin Infections------------------------------------------------------------------------- 30

Viral Skin Infections-------------------------------------------------------------------------------- 34

Fungal Skin Infections------------------------------------------------------------------------------ 38

Parasitic Skin Infections-------------------------------------------------------------------------- 40

Mycobacterium Skin Infections---------------------------------------------------------------- 42

Sexual Transmitted Diseases------------------------------------------------------------------- 43

Skin Tumors
Skin Tumors--------------------------------------------------------------------------------------------- 46

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DR. MOHCEN AL. HAJ
 INTRODUCTION

- Structure of the Skin:

the skin has Three layers:
1- Epidermis. 2- Dermis. 3- Sub-Cutaneous Fat (Hypodermis).

 The Epidermis
It is Formed from Many layers of Closely Packed Cells arranged in Four layers:
1- Stratum Basale (Basal Cell Layer): It is a Single layer of Columnar or Cuboidal
Cells bounded Together by Desmosomes.

2- Stratum Spinosum (Prickle Cell Layer): Consists of Cuboidal, or Slightly

flattened Cells firmly bound Together by Spines and Desmosomes.

3- Stratum Granulosum (Granular Cell Layer): Consists of Three to Five layers of

flattened Polygonal Cells whose cytoplasm is filled with keratohyalin Granules.

4- Stratum Lucidum: It is a Translucent Layer, More apparent in Thick Skin.

5- Stratum Corneum (Corneal “Horny” Cell Layer): Consists of layers of flattened

Non Nucleated keratinized Cells whose cytoplasm is filled with keratin.
* All these cells differentiate from base to surface (from basal cell layer to Corneal cell layer)*

- Types of Cells in Epidermis:

1- Melanocyte; It is a Specialized Cell of the Epidermis found beneath or between the
Cells of the Stratum Basale and in the Hair follicles, Secretes Melanin ,
The Melanin is Responsible for Skin Color and Protective against U\V Light.

2- Keratinocyte; Present Mainly in Stratum Basale, Bounded by Desmosomes.

3- Langerhans cells; Found Mainly in Stratum Spinosum, They are Bone Marrow
Derived, Carried to the Skin by the Blood, they have a Significant Role in Immunological
Skin reactions (Macrophage of Skin) known as Antigen-Presenting Cells.

4- Merkles cells; Generally Present in the Thick Skin of Palm and Sole (Sensory Cells).

 The Dermis
This Part of the Skin Supports the Epidermis, it is Consists of:
1. Hair follicles. 2. Sweat glands.
3. Sebaceous glands: (Secrete Sebum to Prevent Dryness of Skin and Hair).
4. Rectus Pilli Muscle. 5. Blood Vessels and Nerves

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DR. MOHCEN AL. HAJ
  SKIN LESIONS

Primary skin lesions Secondary skin lesions

1. Flat Lesions: (No Elevation No Scale:
Depression) Two Types; Shedding of Dead keratin (Ex; Psoriasis).
 Macule : < 1cm Crust:

 Patch : > 1cm Dry Exudates (Ex; Post Bacterial infection).

Excoriation (Abrasion):
Or Scratch Mark (Ex; Pruritic Diseases).
2. Elevated Lesions: Could be;
Ulcer:
Solid Lesions: Fluid Lesions:
Discontinuous in Epidermis and Dermis,
- Papule: - Vesicle:
Healed with Scar (Ex; Venous Ulcer).
< 1cm (Ex; Wart). Papule Containing Erosion:
Serous Fluid Discontinuous in Epidermis Only Healed
- Plaque: (Ex; HSV). Without Scar (Ex; Bulla Eruption).
> 1cm No Depth Fissure:
(Ex; Psoriasis). - Pustule: Linear Cleft Discontinuous in Dermis.
Papule Containing Scar:
- Nodule: Pus Replacement of Normal Tissue by Fibrous
(Ex; Pyoderma). Tissue during process of Healing (The Scar
> 1cm With
Depth Could be Atrophic or Hypertrophic).
- Bulla (Blister): Lichnification:
Ex; Leishmaniasis.
> 1cm Diffuse Chronic Thickening of the Skin
(Ex; Pemphigus). Result from Chronic Rubbing or Scratching
3.Wheal:Firm Transient Edematous Plaque (Ex; Atopic Dermatitis).
with Pale Center (Present in Urticaria).

- Special skin lesions :

* Comedone: Deposition of Keratin material in Pilo-Sebaceous Hair Follicle Seen in Acne.
* Burrow: Tunnel in the Superficial Epidermis Caused by Scabies.
* Target Lesion: Also called “Iris lesion” Consists of 3 Zones; Dark or blistered Center,
Surrounded by Pale Zone, and the third Zone Consists of a Rim of Erythema Seen in
Erythema Multiform.
* Telangectasia: Small Dilated superficial Capillary that blanch by Pressure (Ex; Rosacea).
* Petechiae: Pin point Haemorrhage < 1cm
* Purpura: Small Extravasations of Blood of Small Blood Vessels in the Skin > 1cm
* Ecchymosis: Large Extravasations of Blood into the Skin.

How to Describe Skin Lesion

1- Say Single or Multiple… 2- Say Unilateral or Bilateral (if it was in Limb)… 3- Say The Color of the Lesion.
4- Say The Primary Lesion (Ex; Patch or Papule)... 5- Say The Color of the Base that Surround The Primary Lesion..
6- Say The Secondary Lesion That Cover or above The Primary Lesion (Ex; Covered with Scale or Covered with Crust)

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DR. MOHCEN AL. HAJ
 Papulo – Squamous Disorders
1- Psoriasis, 2- Lichen Planus, 3- Pityriasis Rosea, 4- Pityriasis Rubra Pilaris …

 Psoriasis: it is a Chronic, Relapsing, Inflammatory Skin Disorder with Strong

Genetically basis, affect 12% of Population Mainly young, M=F.
*According to Age Classified in to 2 Types:
Type1; Common in Young (20 – 40 years), related to HLACw6 with Strong F\H.
Type2; Common in Adult (50 – 60 years) rare with Mild F\H.
Psoriasis Common in Scandinavian populations and White Americans.

- Precipitating Factors of Psoriasis: “STD, SAMIH”

1- Stress.
2- Trauma: (Koebner phenomenon). *Koebner phenomenon is an Isomorphic lesion at
Site of Trauma (Scratching or Pressure after 10-14 days).

D\D of Koebner Phenomenon:

1. Psoriasis, 2. Lichen Planus, 3. Vitilligo, 4. Wart, 5. Molluscum contagiusum.
3- Drugs: Systemic Steroids, β-blockers, Anti-Malaria, Anti-Psychiatric, NSAID, Gold.
4- Sunlight: 15% of Cases (Sun Stroke).
5- Alcohol & Smoking.
6- Metabolic (Hypocalcaemia).
7- Infection: Post Streptococcal infection.
8- Hormonal: as in Pregnancy, Puberty.

Clinical Picture of Psoriasis:

Maculo-Papules, or Papules, or plaques, Dusky Red, Covered by White
Silvery Scales.

Removal of Scales Result in Pin point bleeding, This Sign Called

*Auspitz Sign*, It Confirms the Diagnosis of Psoriasis.

- Sites: Extensor Surfaces \ Elbow, Knee, Lumbo-Sacral joints \ Trunk, Palm, Sole, Scalp.

- Pathogenesis of Psoriasis: Infiltration of T-lymphocyte that secretes Interleukins (IL)

Cause hyper-Proliferation of keratinocytes through 4-5 days, it is Called;
Hyperkeratosis Acanthosis (Normal Transformation of Cells from basal layer to Corneal
layer Needs 28 days).

- Types of Psoriasis: (1). Psoriasis vulgaris, \ (2). Scalp psoriasis, \ (3). Nail psoriasis,\
(4). Guttate psoriasis, \ (5). Napkin psoriasis, \ (6). Psoriatic arthritis, \
(7). Psoriatic inverses, \ (8). Palmo-Planter psoriasis, \ (9). Erythrodermic psoriasis.
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DR. MOHCEN AL. HAJ
  Psoriasis Vulgaris: (Plaque Type)
It is the Most Common Type, Can affect any part, but it is More Distributed Over
Extensor Body Surfaces (Knee & Elbow joints).
-Typically Presented with Well Defined Circular or Oval Red Plaque Covered with
White Silvery Scales.
 Scalp Psoriasis:
Commonly occur at Hair lines and behind the Ears Causing Non Scaring Alopecia.
 Nail Psoriasis: It includes;
Pitting in Nail plate, Subungual Hyperkeratosis, Onycholysis, Oil Drop Sign.
 Guttate Psoriasis:
This Type is Proceeded by History of Upper Respiratory Tract Infection Secondary
to Group A- β-Haemolytic Streptococci, Common in individual younger than 30 Y
-Typically Presented with Small Pink Drop like Papules Covered with Fine Scales.
 Psoriatic Arthritis (Atrhropatic Psoriasis):  “Sever Type”
It is Sero-Negative Arthritis, Associated with HLAB27, Occur in Distal
inter-phalangeal joint More than Proximal inter-phalangeal joint.
Typically Presented with Red, Worm, Tender inflamed joint, Deformity, Dactylitis
 Psoriatic Inverses: “Flexural Type”
It affects Groin, Axilla, Sub Mammary, and Umbilicus.
Typically Presented with Erythematous Plaques lack of Scales, sometimes Fissure
 Palmo-Planter Psoriasis:
Affects the Palms and Soles, It is a Pustular Type Presented with Pustules.
 Erythrodermic Psoriasis:  “Sever Type”
This Type Caused by Irritated Psoriasis by intake of Tar, Dithranol, Systemic
Steroids, also Withdrawal of Topical Steroids,
It is life Treating Type Presented with Extensive Erythema of the Most Body
Surface with Fine Scales.
-This Type leads to;
Disturbance in Water and Electrolytes balance, High Cardiac Output (due to
increase Blood Supply of the Dermis), Hypo-proteinemia (Due to Extensive loss
of Keratin protein), Sever Hypothermia, V.D  Hypotension  Shock.

* Treatment of Erythrodermic Psoriasis:

- Admission to I.C.U.
- Worm the patient.
- Give I.V Fluids and Calcium.
- Give Anti Biotic.

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DR. MOHCEN AL. HAJ
 - Diagnosis of Psoriasis:
Plaque Psoriasis almost always Diagnosed Clinically by (Auspitz Sign), and Laboratory
investigations are Rarely indicated.
Skin Biopsy Used if Diagnosis doubt and to Exclude other D\D.
The Skin Biopsy Shows;
1. Acanthosis  Marked thickening of Epidermis.
2. Parakeratosis  Presence of Nuclei in Corneal layer.
3. Dilatation & Tortuosity of Capillary Dermis.

- Treatment of Psoriasis:

Local Treatment Systemic Treatment

1. Emolleint; Ex; Vaseline 1. PUVA; “Psoraline + UVA”
2. Keratolytic agent; Ex; Salicylic acid It is interfering with DNA Synthesis &
(2% - 5%) Ointment Decrease Cellular Proliferation.
3. Coal Tar; inhibit DNA Synthesis Patient take Psoraline tablet then
Decrease Mitotic Division  after 2Hours Expose to UVA “320 -
Decrease Cells Turnover. Can 400nm”.
be Used in Combination with U.V.B S\E of Psoraline; S\E of UVA;
Ray (it is called Goeckerman Regien). Hepato-toxicity. EarlyErythema,
S\E; Staining, inhibit DNA Replication. Nausea + Vomiting. Cataract,
Pigmentation.
4. Dithranol, also called (Anthraline); LateMalignancy
inhibit DNA Synthesis. Dithranol 2. Retinoid; “Vit A Derivatives ”
can be Used as; Paste (0.1% - Necessary for normal Keratinization
1%) or Ointment 4% S\E of Retinoid;
S\E; Staining, Highly Irritant. -Teratogenic (So you Should Stop the
drug 2 years, and then get Pregnant).
5. Vitamin D3 Analogues; Increase Ca it -Hyperlipidemia (So; Do Lipid Profile).
is Colorless odorless doesn’t Stain -Increase Liver Enzymes (So; Do LFT).
6. Topical Steroids. -Bone Marrow Suppression (Do CBC).
7. Topical Retinoids; Ex; Lazarotine Gel -Dryness of the Skin & Hair loss.
(0.1% – 0.5%). 3. Methotrexate;
S\E; Dryness of skin and Mucous Drug Of Choice for Psoriatic Arthritis.
Membrane, Hair loss, Mild Irritant. Once Per Week 10-25mg, Given with
Folic Acid (For; Megaloblastic Anemia).
8. Local U.V.B; S\E; Bone Marrow Suppression, Hepato-
Broad bond UVB290 - 320nm toxicity, Liver Cirrhosis.
Narrow bond311 - 319nm (Best). 4. Cyclosporine A; Immunosuppressant,
S\E; Carcinoma. inhibits Production of Interleukin-2.
S\E; Nephrotoxicity (So; Do RFT).
9. Tacrolimus. 5. Calcium.

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DR. MOHCEN AL. HAJ
  Lichen Planus: It is a Chronic Pruritic, Purple, Polygonal, Plane, Papule, or
Plaques, Covered with Fine Scales affect Skin, Mucous Membrane, and Nail.

- Aithiology; Unknown, (Positive Koebner Phenomenon), also May be Related to;

1. Infection;  HBV , HCV. 2. Drugs;  ACE.I , Diuretics , Cimitidine, Phenothiazine.
3. Immunological;  Thyroid Disease , Pemphegoid. 4. Genetic;  DR1.

Clinical Picture: Role of “P”

Pruritic, Purple, Polygonal, Plane, Papule, or Plaques, Covered with Fine Scales.
-Magnified lens on lesion Shows White lines Passing between Papule or Plaques
Called Wickhams Strea.

Nail change; Occur in 10% of Pt, Most commonly Change in Nail is a

Longitudinal Groove and bridge Called Pterygium.
Also There are; Subungual Hyperkeratosis, Onycholysis, Pitting, Koilonychias.

Lichen Planus Can involve the Scalp leading to Scarring Alopecia.

- Sites: Most Commonly found on Flexure Surfaces; Wrist, around Ankle\ Trunk,
Genitalia, and Mucous Membrane of the Mouth (Erosive Type; Pre-Malignant).

- Clinical Types of Lichen Planus:

1. Classical, \ 2. Atrophic, \ 3. Hypertrophic, \ 4. Erythrodermic, \ 5. Ulcerative, \
6. Linear, (Related to Koebner Phenomenon). \ 7. Follicular  Common in Scalp, \
8. Annular Common in Penis, \ 9. Actinic Type Common in face.

- Diagnosis of Lichen Planus:

In Most of Cases Lichen Planus Diagnosed Clinically.
Skin Biopsy; Shows T- Cell Infiltration in Upper Dermis, Hyper-Granlosis, Basal Cell
Layer Degeneration, with Saw-Teeth appearance, and Colloid Bodies.

If Lichen Planus Present in Mucous Membrane; Skin Biopsy is Mandatory to

take; To Exclude Malignancy.

- Treatment of Lichen Planus:

1. Topical Steroids
2. Anti Histamine
3. PUVA May be Used.

- In More Sever Cases Especially Scalp, Nail, and Mucous Membrane involvement, May
Need More intensive therapy like Systemic Steroids.
- In General Lichen Planus is a Self limiting disease usually within 8-12 Months.
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DR. MOHCEN AL. HAJ
  Pityriasis Rosea:
It is a Self Limited Erythematus Scaly, Itchy Disease.

- Athiology; Unknown, but May be Related to Viral infection.

Clinical Picture: Pink, Oval, Papules or Patches, Covered by Fine Scales.

Mother Lesion (Herald Patch);

It is an Erythematous, Itchy, Oval Patch, about 2-4cm, Healed without Scar,
appear few Days before the Eruption of Pitryasis Rosea.

- Site: Mainly Over the Trunk, also in the Thigh.

The lesion Tend to have their long Axes Parallel to the Ribs giving the lesion picture
Called  “Christmas Tree Distribution”.

-Diagnosis: Mainly Clinically.

- Treatment of Pityriasis Rosea: it is Self limited Disease between 6-8 weeks.

. Reassurance.
. Anti Histamine as Symptomatic Treatment.
. In Sever Cases Use Steroids.

 Pityriasis Rubra Pilaris:

it is Mild Itching Disease of Unknown Cause, affect Hair Follicles Causing
Follicular Hyperkeratosis.
May be Related to Vitamin A Deficiency.

- Sites: Mainly in Scalp, and Trunk.

- Treatment of Pityriasis Rubra Pilaris:

Local Treatment Systemic Treatment

1. Emollient. 1. Vitamin A & E.
2. Salicylic acid. 2. Oral Retinoids.
3. Coal Tar. 3. PUVA.

 Local and Systemic Steroids are Not effective her.

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DR. MOHCEN AL. HAJ
 Vesiculo - Bullous Disorders
Group of Disorders Characterized by Bullous “Blister” and\or Vesicle formation.

- Causes of Vesicles or Bullae: “ A. B. C. D. I “

1- Auto immune bullous Disease, Ex;(Pemphigus, Pemphigoid, Dermatitis Herpetiformis)
2- Burns.
3- Chemicals, Ex; (Strong Acids and Alkali).
4- Congenital, Ex; (Epidermolysis Bullosa).
5- Drugs, Ex; (Penicillin, Barbiturates, Sulphonamides).
6- Infection Bacterial Ex; (Impetigo, SSSS), Viral Ex; (HSV, HZV), FungalTinea Pedis

Pemphigus Vulgaris Bullous Pemphigoid Dermatitis Herpetiformis

Definition Chronic, Auto immune, Life Chronic, Auto immune, Not Chronic, Auto immune,
Threatening, Non Pruritic Life Threatening, Pruritic, Mild Intensely Pruritic, Painless (But
Painful, Bullae, affect Skin and Painless Bullae. Burning), Grouped Vesicles of
Mucous Membrane. Bullae are Large, Tense, Filled Symmetrical Distribution,
Bullae are Flaccid Easily rupture, with Blood Difficult to rupture, Associated with Caeliac Disease
-Positive Nikolsky Sign; -Negative Nikolsky Sign. (Gluten Sensitivity).
Nikolsky Sign; It is a
Sliding of Epidermis on
Dermis by Finger Pressure
on lesion leading to
Erosion of Normal &
Abnormal Skin.
Athiology Ab (IgG) attack Desmosomal Ab (IgG) attack Bullous Ab (IgA) attack Trans-
Protein (Desmoglein3) in Pemphigoid Antigen “BPA” Glutaminase in Skin & GIT
Epithelium Desmosomes That found in Hemi- leading to Activate Complement
Leading to Separation between desmosomes Chemotaxis & System Chemotaxis &
Desmosomes forming Blisters. attraction of Inflamm - Cells attraction of Inflamm - Cells
Site 50-70% Oral Lesion interferes 10-15% Oral Lesion. Extensor Surface of Elbow,
with Eating & Drinking. Also in; Trunk & Flexure Knee, and Shoulder.
Also in; Scalp, Face, Genitalia. Surface. Also in; Buttocks, and Face.
Age & 40 – 60 years old. 60 – 80 years old “Elderly”. 30 – 40 years old “young”.
Gender M=F M=F M > F “ 2:1”
General Very Bad, Good General Condition. Good General Condition.
Condition Dysphagia, Weight loss,
Weakness, Hoarseness of voice.
Diagnosis 1. Biopsy from involved Skin 1. Biopsy from involved Skin 1. Biopsy from involved Skin
Send to Histopathology Shows Send to Histopathology Send to Histopathology Shows
Intra-Epidermal Bollous Thin Shows Sub-Epidermal Sub-Epidermal Vesicles, with
Easily Rupture, No Blood, with Bullous, Tense, Turbid, with Inflammatory Cells
Acantholysis (keratinocyte float Blood at Basement “Neutrophilis + Esinophilis”.
free in Bullous). Membrane.
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DR. MOHCEN AL. HAJ
 2. Direct Immuno-fluorescence 2. Direct Immuno-fluorescence 2. Direct Immuno-fluorescence
Study, Study, Study,
Will Show Inter Cellular Will Show Deposition of IgG Will Show Deposition of IgA.
Deposition of IgG. on Basement Membrane. 3. Jejunal Biopsy,
3. Indirect Immuno- 3. Indirect Immuno- Will ShowSub-Total Villous
fluorescence Study, fluorescence Study, Atrophy.
Detect IgG by ELISA. Detect IgG in 70% in Serum.
4. Tzank Smear is Positive. 4. Tzank Smear is Negative. 4. Tzank Smear is Negative.
Treatment *Systemic Treatment: *Systemic Treatment: * 1\3 of Patient  Self Limiting.
1. Steroid; Start with Large Dose Steroid; But Small Dose. Gluten Free Diet.
then Decrease. *Local Treatment: Dapson; Testing Dose 100mg,
2. Immunosuppressive. Specific Care to Skin & Mouth Treatment Dose  25-50mg.
3. Plasma-phoresis. lesion by; - S\E of Dapson;
*Local Treatment: Potassium Permanganate + 1. Pancytopenia;
Specific Care to Skin & Mouth Topical Steroid Cream + “Haemolytic Anemia
lesion by; Topical Anti-Biotic + (Especially in pt with G.6.P.D.
Potassium Permanganate + Anti-Septic Mouth Wash. Deficiency)
Topical Steroid Cream + Topical + Leukopenia
Anti-Biotic + Anti-Septic Mouth + Thrombocytopenia”.
Wash. 2. Peripheral Neuropathy.
Sever Cases Treated Similar to 3. Hepatitis (Do LFT).
Sever Burns.

Epidermolysis Bullosa:
Large Group of Clinically Similar Desquamating Disease of Skin and Mucous Membrane
between Epithelium & Connective Tissue (Dermis).

Epidemolysis Bullosa is a part of Genetic Diseases known as “Geno-Dermatosis”.

- Types of Epidemolysis Bullosa:

1. Epidemolysis Bullosa Simplex: “Best Prognosis” Autosomal Dominant, Start in Early
Childhood (6-7 Months), Pathology in Epidermis, affect Nail and Hair without Scar.

2. Epidemolysis Bullosa Junctional: Autosomal Recessive, Start at Birth, Pathology in

Basement Membrane, affect Nail and Hair without Scar, also affect Mucous Membrane.

3. Epidemolysis Bullosa Dystrophica: “Worst Prognosis” Autosomal Dominant or

Autosomal Recessive, Start at Birth, Pathology in Basement Membrane Causing
Alteration of Collagen, affect Mucous Membrane, Teeth, Nail and Hair with Scar.

- Treatment of Epidermolysis Bullosa:

Symptomatic Treatment.

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DR. MOHCEN AL. HAJ
 Pigmentation Disorders
Include: Hypopigmented Disorders, Depigmented Disorders, Hyperpigmented Disorders.

- De-Pigmented Skin Disorder:

Vitiligo: It is an Acquired De-Pigmented Cutaneous Disorder Caused by Loss of
Melanocyte of Epidermis.
Most Common Age between 10 – 30 years old, “M = F”.

- Athiology: Unknown, But there are Pathogenic Theories;

1. Auto immune Theory; (Commonest) Presence of “Ab” against Melanocyte, associated
with Other Auto immune Diseases, (Ex; DM Type1, Addison Disease, Hypothyroidism).
2. Neurotoxic Theory; Present in certain Dermatomes neurotoxins Destruct Melanocyte.
3. Self Destruction; (Apoptosis).
4. Stress.

- Types of Vitiligo:

1. Local Vitiligo; Could be: 2. Diffuse Vitiligo; Could be:

 Acral; Found in Fingers, Lips.  Universal; Generalized
 Segmental  Common; (Vulgaris)
- Sites:
Hand, Wrist, Knee, Eyelid, Genitalia, around Mouth (Acrofacial), Over Bony Prominence.

Clinical Picture: Well Defined De-Pigmented Patches or Macules.

 Positive Koebner Phenomenon.

D\D of Vitiligo:
1. Post Traumatic,\ 2. Post Inflammatory ”Eczema”,\ 3. Pitryasis Versicolor,\
4. Pityriasis Alba,\ 5. Tuberculoid Leprosy,\ 6. Hypo-Pigmented Naevi.

- Diagnosis:
1. Clinically Mainly.
2. Woods Lamp  Milky White.
3. Blood Investigations; CBC  High Lymphocytes.

- Treatment of Vitiligo:
1. Reassurance.
2. Protect the Patient from Excessive Sun Exposure by Using Sun Screen.
3. Now Depend on the Type;

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DR. MOHCEN AL. HAJ
 Localized Type: Multiple diffuse Type:
1. Local Steroids. 1. PUVA (Psoraline + UVA).
2. Macrolide; Ex Tacrolimus. 2. Systemic Steroids  Used in Unstable
3. Cosmetic Camouflage; Cream Cover Active Vitiligo.
Color of the Skin “Especially in 3. Narrow bond UVB (290-300nm)  Good
Segmental Type”. in Non active Vitiligo.
4. Melanocyte Graft.
 If Patient had 90% of his body affected with Vitiligo;  Then Do
“De-Pigmentation” by Ethyl Ether Hydroquinone.

- Note;
*Leukoderma Decrease of Pigmentation leading to White Discoloration of Skin.

Genetic Causes of Leukoderma;

1. Albinism. \ 2. Phenyl-ketonuria. \ 3. Tuberus Sclerosis. \ 4. Piebaldism.

Albinism Vitiligo
Congenital Autosomal Recessive. Acquired.
Decrease of Tyrosinase Enzyme. Unknown Melanocyte Destruction.
Hypo-Pigmented areas. De-Pigmented areas.
Affect Skin, CNS. Eyes. Affect Skin Only.
C\P: White Hair, Iris, Nystagmus, Skin Malignancy No
Loss of Melanin Pigment. Loss of Melanocytes.
Generalized. Local.

- Hyper-Pigmented Skin Disorders:

Genetic Acquired (NSEM)

Post Traumatic.
Neuro-Fibromatosis.
Post Inflammatory, (Ex; Eczema, Acne,
Freckles. Lichen Planus).
Metabolic Diseases, Ex; Porphyria,
Xero-derma Pigmentosa. Kwashiorcor, Pellagra “Vit B3 Deficiency”.
Endocrine Diseases, Ex; Addison, Cushing,
Peutz-Jeghers Syndrome. Pituitary Tumor.
Systemic Diseases, Ex; Haemochromatosis,
Primary Biliary Cirrhosis, CRF.
Neoplasia, Ex; Malignant Melanoma,
naevi, Pigmented Basal Cell Carcinoma.
Others, Ex; Chloasma, Sun Ray.

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DR. MOHCEN AL. HAJ
 Erythema
Erythema is a Temporary Redness May be accompanied with Weakness, Sweating,
Pruritis, and Headache.
- Types of Erythema:
1- Erythema Nodosum. 2- Erythema Multiform. 3- Erythema Induratum.
4- Sweet Syndrome (Acute Febrile Neutrophilic Dermatosis) . 5- Erythema Annulare
Centrifugium (EAC). 7- Palmo-Planter Erythema. 6- Erythema Infectiosum (Fifth Disease).

*Erythema Multiform .VS. Erythema Nodosum:

Erythema Multiform Erythema Nodosum

Common affect Male & Female young, Middle Age (20-40). Common affect Female Adolescent & Young Age.
It has Poly Athiology (Many Causes): It has Poly Athiology (Many Causes):
1. Infection: 1. Infection
-Viral; Herpes Simplex Virus (Most Common), -Bacterial; Streptococci (Most Common),
Hepatitis B Virus, HIV, Measles, Mumps. TB, Mycoplasma, Salmonella, Shigella.
-Fungal; Histoplasmosis. -Fungal; Histoplasmosis.
-Bacterial; Mycoplasma. -Protozoal; Toxoplasmosis.

2. Drugs; OCP, Sulphonamides, Penicillin, Barbiturates. 2. Drugs; OCP, Sulphonamides, Gold.

3. Disease; SLE, Poly-arthritis Nodosa. 3. Disease; Sarcoidosis, Crhons Disease, Bahcet Disease.
4. Pregnancy. 4. Pregnancy.
5. Malignancy. 5. Malignancy.
6. Idiopathic. 6. Idiopathic.
Clinically: Two Types: Clinically:
Minor Type (Mild form) Major Type (Sever form) Firm, Tender, Bilateral, Nodules on Shine of Legs with
Bilateral Symmetrical Generalized Macules, Papules, Blurred border.
Red Macule, Papule, Bullae + Very ill Toxic Fever, No Ulcer But Hyper-Pigmentation.
Vesicle, Bullae with Malaise.
Target Lesion. Mucous Membrane is involved
known as; (Steven Johns
Syndrome) Investigation of Erythema Nodosum:
Affect Hand, Palm, Feet, Affect lips, Mouth, Cornea, -CBC; WBC Elevated.
Forearm, Legs. Conjunctiva, Genitalia. -ESR; High.
Has No Complication Complicated with; Pneumonia, -Throat Swab; ASO Titer.
Blindness, Renal & Liver -Chest X Ray.
Failure. -Tuberculin Test.
It is Self Limited (2-4 Need Admission,
Weeks) but can Treated Correct Fluid + Systemic
with; Local Steroids Steroids & Anti-Biotic.
Treatment: According to Type: Minor Topical Steroid Treatment: Bed Rest & Elevation of Legs
Major Type Systemic Steroid + Systemic Anti-Biotic. Cold Compression & NSAID (Indomethacin, Ibuprofen).

14
DR. MOHCEN AL. HAJ
 *Erythema Induratum .VS. Sweet’s Syndrome:

Erythema Induratum Sweet’s Syndrome

Affect Female Middle Age. Common in Female More than 30 Years Old (F>M).
Athiology: Athiology:
Uni-Athiology due to Hypersensitivity Associated with TB Hypersensitivity Reaction Type III.
(50% Post History of Pulmonary TB). (May Associated with Malignancy).
Course: Course:
Chronic Recurrent. More than 2 Months.
Clinically: Clinically:
Tender, Erythematous, Nodule on Lower Leg from Behind Dark Red, Slowly growing, Painful, Papule with Colored
Heals with Scar & Ulcer. Scales on Lower Limbs Back & Neck.
Investigation: Investigation:
ESR+CBC Elevated WBC, Chest X Ray + Skin Biopsy + PCR. ESR+CBC Elevated WBC Mainly Neutrophils.
Treatment: Treatment:
Bed Rest + Systemic Steroid for 2 Weeks. Topical Gucocorticoids Cream, Zink Lotion.
Anti TB for 9 Months. Systemic Prednisolone.

*Erythema Annulare Centrifugum (EAC):

Disease of Unknown Athiology, Common in Middle Age, Equal in Male & Female.

- Clinical picture:
Asymmetrical Elevation of Urticaria, Centrally Hyper-Pigmented with Arched Rings on
Trunk, Limbs, Gluteal Region + Itching.

- Treatment:
1. Anti Histamine  For Itching.
2. Anti Inflammatory  Steroid.

*Palmo-Planter Erythema (PPE):

Occurs in Thener & Hypothener of the Hands.

- Athiology:
1. Chronic Liver Disease.
2. Chronic Poly-arthritis.
3. DM.
4. Hyperthyroidism.

15
DR. MOHCEN AL. HAJ
 Eczema (Dermatitis)
Eczema is a Reaction pattern of Inflammatory Response of the Skin, Characterized by;
-Acute Stage: Characterized by Swelling, Erythema, Oozing, Vesiculation.
-Subacute Stage: Characterized by  Crusting.
-Chronic Stage: Characterized by  Hyper-Pigmentation, Scaling, Lichnefication.

Lichnefication is Characterized by; Thickening, Scaling, Hyper-Pigmentation, Excoriation

of Skin Mark Leading to Painful Fissure.
-Classification of Eczema (Dermatitis) According to Cause:
1- Exogenous Eczema (Dermatitis):
 Primary Irritant Dermatitis.
 Contact Allergic Dermatitis.
 Photo-Dermatitis.

2- Endogenous Eczema (Dermatitis):

 Atopic Dermatitis.
 Seborrhoeic Dermatitis.
 Discoid (Annular) Eczema.
 Stasis Dermatitis (Venous Ulcer).
 Asteatotic Dermatitis (Eczema Craquele).
 Pompholyx.
 Neuro Dermatitis (Lichen Simplex Chronicus).

Exogenous Dermatitis
1- Primary Irritant Dermatitis:
This Type Occurs Due to First Exposure.
According to the Irritant There are Two Types;
- Mild Irritantto Occur need long Contact, (House Wife Dermatitis, Napkin Dermatitis).
- Sever Irritantas Secondary Degree of Burns (Strong Acid & alkali, Corrosives).
It is Not Allergic Reaction; Because There is No Memory Cells.
-Treatment: Remove Irritant, Emollients (For Scales), Local Steroid (For inflammation),
Anti Histamine (For Itching), and May be Anti-Biotic (For Secondary Bacterial Infection).

2- Allergic Contact Dermatitis:

It is caused by Exposure to External Contact Allergens (Type4 Hypersensitivity Reaction).
Usually No Reaction in First Exposure to Allergy, But Repeated Exposure lead to
Eczematous Reaction by Memory Cells, Commonly Caused by Nickel, Rubber, Copper.

1st Exposure T Lymphocyte Produce Memory cell .. 2nd Exposure Memory cell Enhance Release HistamineVDInflammation
DxPatch Test To Differentiate Between Exogens & Endogens TxAvoid Allergens + Local Steroid (For Inflammation).

16
DR. MOHCEN AL. HAJ
 Endogenous Dermatitis
1- Atopic Dermatitis:
It is a Pruritic Disease that start in Early Infancy & associated with other Atopic Diseases
(Asthma, Allergic Rhinitis, Allergic Conjunctivitis).
- Athiology is Unknown, But There are a Positive Family History in Patient with Atopy.
-In 85% of Cases of Atopic Dermatitis Occurs In First year of life,
-In 95% Cases of Atopic Dermatitis Occurs Before age of 5 Years.

- Clinically Presented with:

-Xeosis (Dryness), Lichenification, Chronic Pruritis.
-Low Cell Mediated Immunity More Risk for Bacterial & Viral Infection.
-Slow Chemotactic of Neutrophils More Risk to Get Bacterial Infection.

In Atopic PtIncrease IgEDecrease Cell-Mediated ImmunitySlow Chemtaxis of NeutrophilsMore Susceptible to

InfectionDry Skin Due to Decrease of Sebaceous & Sweat GlandsChronic Pruritis Due to Low Itching Threshold.

- Types of Atopic Dermatitis According to Age:

Infantile Dermatitis Childhood Dermatitis Adult Dermatitis

Age 2 Months – 2 Years Old 2 Years – 12 Years old More Than 12 Years
Site Symmetrical Both Checks Common in Flexor Surface Any Where,
of Face, Scalp & Extensor as; Popletial Fossa, Cubital Scaly Erythematous
Surface. Fossa, Under Wrist. Lesion with Crust.
Any Patient With Atopic Dermatitis & Herpes Simplex Infection is an Emergency
Condition Needs Acyclovir Infusion. (This Condition Known as; Eczema Herpaticum).

- Diagnosis of Atopic Dermatitis:

Atopic Dermatitis Diagnosed by Triad; History + Examination + Investigation.
– History: Age, Site, Itching, Family History of Atopy (Asthma, Conjunctivitis, Rhinitis).
– Examination: By Atopic Criteria:-

Atopic Criteria:
1.Loss of Outer 1\3 of Eye Brows. 2.Thickening of Lower Eye Lid. 3.Extra Fold around
Eye (Demorgan Sign). 4.Dirty Neck Sign. 5.Waisting of Thener & Hypothener Muscles.
6.Palmar Creases More Visible (Thick). 7.Lichnification & Scratch Marks.
– investigation: CBC  High WBC, Mainly Esinophils + Blood  High IgE.

Complication of Atopic Dermatitis: Treatment of topic Dermatitis:

1. Secondary Bacterial infection. 1. Emollient Ex; Vaseline (For Skin Dryness).
2. Secondary Viral infection 2. Local or Systemic Steroid (For Inflammation).
3. Dry Skin. 3. Anti Histamine (For Itching).
4. Erythroderma Exfoliative. 4. Topical or Systemic Anti-Biotic (For Infection).

17
DR. MOHCEN AL. HAJ
 2- Seborrhoiec Dermatitis:
It is Occurs in Sites of Sebaceoous Glands in All Body Except; Palms, Soles, Lips.
More Common in Males (20-50 Years), Due to Androgen Control, (Can affect Infant).
- Predisposing Factors: Change in Humidity, Seasonal Variation, and Emotional Stress,
Also Related to Normal Skin Flora Lives in Hair Follicles Called Pityrosporum Ovale.

- Type of Seborrhoiec Dermatitis According to Age:

Infantile Adult (Relapsing & Remission)

Androgen From Mother Androgen Dependent
Site Scalp, Eye Brows, Napkin. Scalp, Eye Brows, Behind Ear.
Clinical Large Yellowish Scales, Diffuse Yellowish Scales, No itching,
Picture Worse in AIDS and Parkinson Disease.
- Diagnosis of Seborrhoiec Dermatitis:  Clinically
Greasy Yellow Scales in Scalp + Negative Family History

- Treatment of Seborrhoeic Dermatitis:  It is Self Limited Disease

. Topical Steroid (Anti-Inflammatory).
. Topical Anti-Fungal Cream or Shampoo.
. For Scalp  Ketocoazol + Steroids Lotion or Gel.

3- Descoid Eczema (Nummular Dermatitis):

It is a Chronic Relapsing Eczema, Presented with Scattered Coin Like, Mainly in Extensor
Surface of the Lower Limb & Dorsum of the Hand (Affect Children & Adult Equally).

- Clinically Presented with:

Well Defined Plaque on Erythematous base with Yellow Crust & Tiny Vesicle
Symmetrical as Mirror Image.

- Treatment of Discoid Ezcema:

Topical Steroid + Anti-Biotic as a Combination, Ex; Fucicort. (PUVA Used in Sever Cases).

4- Stasis Eczema (Gravitational Dermatitis):

Occurs Due to Chronic Venous Stasis, Commonly Associated with Varicose Veins.
Venous Stasis Deposition of Heamosedrine Pigment Mild DermatitisUlcer.
- Sites: In Lower Limb above Medial Mallulus. (Commonly in Obese Female Use OCP).
- Clinically Presented with: Erythema, Edema, Scaling, Oozing, Crusting, Pigmentation.

Complication of Stasis Eczema: Treatment of Stasis Eczema

1. Hyper-Pigmentation. 1. Prevention by Walking & Exercises.
2. Venous Ulcer. 2. Elevate the Foot Over Night + Compression Stocking.
3. Dermatitis around Ulcer. 3. Local Steroid Injection around ulcer.

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DR. MOHCEN AL. HAJ
 5- Asteatotic Dermatitis (Eczema Craquele):
It is Due to Extensive use of Soap That leads to Cracking, Fissuring & Dryness of the Skin.
Common in Elderly Due to Decrease of Lipid in Stratum Corneum (loss of Lubrication).

- Clinically Presented with:

Diffuse, Scaly, Plaque Mainly in Lower Limb, (Also in Forearm).

- Treatment:
. Emollient Cream (For Skin Dryness).
. Local Steroid (For Inflammation).
. Anti Histamine (For Itching).

6- Pompholyx (Dyshidrotic Eczema):

Intensely Itching Vesicle affecting Palm & Sole Associated with Sweating.

- Treatment:
. Topical Steroid (For Inflammation).
. Anti Histamine (For Itching).
. Systemic Anti-Biotic (For Secondary Bacterial infection).

7- Neurodermatitis (Lichen Simplex Chronicus):

Well Demarked area of Chronic Lichenified Skin Induced by Continuous Rubbing or
Stress.
- Clinically Presented with:
Simple Plaque on Lower Limb & Back of the Neck.
Sometimes Develop on Shin of Forearm Known as “Prurigo Nodularis”

- Treatment:
. Topical Steroid (For Inflammation).
. Anti Histamine (For Itching).

8- Exfoliative Dermatitis:
It is a Serious Condition of Dermatitis Because it Leads to Hypothermia.
25% Unknown Origin, But 15% Due to Malignancy.
Also Associated With Other Systemic Disease.

- Treatment:
. Worming the Patient.
. Systemic Steroid.

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DR. MOHCEN AL. HAJ
 Urticaria

Urticaria is Characterized by:

Itching & Transient Lesion Called“Wheal”, which Disappear without any work on Skin.

- Types of Urticaria:

-Acute Urticaria:
Less than 6 Weeks
Causes of Acute Urticaria: (In. Role)
1- Ingestion.
2- Injection of Penicillin.
3- Infestation (by Parasite Leading to Esinophilia).
4- Infection.
5- Insect Bite

-Chronic Urticaria:
More Than 6 Weeks
Cause  Idiopathic is the Most Common Cause.

- Treatment of Urticaria:
1- Hydrocortisone 50-100mg + Anti Histamine  Stabilize Mast Cell
2- Adrenaline Used Only in Acute Urticaria with Laryngeal Edema.

* NSAID & Aspirin are Contra-indicated in Case of Urticaria *

Side Effect of Steroid:

Local Steroid Side Effect: Systemic Steroid Side Effect:

1. Skin Atrophy. Cushing Syndrome Due to Prolonged Use
2. Stria. of Systemic Steroid:
3. Telangectasia. 1. Cataract.
4. Hypo & Hyper-Pigmentation. 2. Glaucoma.
5. Decrease Local Immunity  Risk of 3. DM.
Infection. 4. Hypertension.
5. Obesity.
6. Osteoporosis.
7. Hirsutism.
8. Acne.

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DR. MOHCEN AL. HAJ
 Acne
Acne is a Self Limiting Sub-acute Inflammation of Pilosebaceous Follicle Characterized
by Formation of Comedones, Mainly affect Aldocesent.

- Athiology: (Multifactorial)
1- Seborrhoic Activity: (No Acne between 2-6 Years; Because No Activity of Sebaceous Gland).
2- Genetic: Hereditary, Common in White Men.
3- Hormonal: Excess Androgen.
4- Bacterial Infection: Propionibacterium Acne (Anaerobic) + Staphylococcus Epidermidis
(Gram Negative) + Diphteroid  All of Those Multiply in Follicle Canal Leading to
Inflammation & Destruction of Follicular Wall.
5- Psychological: Stress increase Androgen.
6- Mechanical: By Occlusion Pressure on Skin (Ex: Cosmetics).
7- Drugs: Anti TB, Anti Epilepsy, Steroid, Sedative.

- Pathogenesis:
Androgen act on Sebaceous gland release Sebum Sebum is Breakdown by
Coryneabacteria into Free Fatty acid Free Fatty acid act as Chematactic Factor
Leading to Sterile Inflammation The Inflammation leads to Hyper-proliferation of
upper portion of Sebaceous duct + Hyperkeratosis Leading to Obstruction Causing
Formation of Dilated Chamber full with Sebum Known as Comedone.
If Follicle Open  Oxidation  Melanin Black Comedone.
If Not Open  Pulgging of Duct Deeply  White Comdone.

- Clinical Picture:
The Acne Presented in 4 Grades:

Grade 1 (Mild) Comedone Open & Close. “Non Inflammatory”.

Grade 2 (Moderate) Comedone + Papules & Postules. “Inflammatory”.
Grade 3 (Sever) Comedone + Nodules & Cysts (Nodulo-Cyst). “Inflammatory”.
Grade 4 (Advanced) Atrophic & Hypertrophic Scars.
- Sites: Early in  Face, Nose, Cheek …. Late in  Trunk.

- Types of Acne:
1. Acne Vulgaris (Commonest Type).
2. Infantile Acne.
3. Cosmetic Acne.
4. Excoriates Acne.
5. Drug Induced Acne + Steroid Induced Acne.
6. Acne Conglobata (Sever Type).
7. Acne Fulminans “Acute Febrile Ulcerative Acne” (Sever Type).
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DR. MOHCEN AL. HAJ
 * Acne Vulgaris:
It is the Commonest Type of Acne affecting Young adult 12-20 Years Old.
- Site  Face, Upper Chest, Upper Back, Shoulder.

- Precipitating Factors:
Stress, Menstruation, Hormonal Factors, Humidity, and Drugs.

- Complication:
1. Cosmetic, 2. Hyper-Pigmentation, 3. Secondary Bacterial Infection.

- Investigation:
No Special investigation Required,
But in Case of Sever Acne in Female + Hirsutism or Irregular Menses  Should be done
Hormonal Investigation & Ultra Sound For Adrenal glands & Ovaries to Exclude
Androgen Secreting Tumor + (PCO).
 If Pt takes OCP; She Should Stop it On Month, Then She Can Do Investigations.

- Treatment:
-Resolve Spontaneously at age of 25-30 Years Old.
-The Treatment Needs Cooperative Patient; Because take time from Months to Years.
-Reassurance & Remove the Precipitating Factors.
-Cleaning with Soap Not Irritant.
-Then According to Grade:
Grade 1 (Comedone) + Mild Grade 2 (Mild Papules + Pustules)Local Treatment.
Grade 3 (Nodulo-Cyst) + Sever Grade 2 (Sever Papules + Pustules)Systemic Treatment.

Local Treatment: Systemic Treatment:

1. Local Retinoid (Vit A Derivatives): Act as 1. Systemic Anti-Biotic:
Comedonolyitic, (Salicylic acid Can be Used in Oily Acne). -TetracyclineDecrease Free Fatty acid in Sebum.
Dose500-1000mg\Day\6 Weeks (on Empty Stomach).
2. Benzyl Peroxide: Anti-Bacterial Also Comedonolytic S\E: GIT Upset, Hepato-toxic, Staining of Teeth.
S\E of Benzyl Peroxide: C\I in Children; Because Irreversible Teeth Colorization.
Dryness, Erythema, Scaling, Contact Dermatitis. -Erythromycin is D.O.C in Pregnancy.
So Use Emollient with it. -If Azithromycin is used; you need to give it for 3 Days Then
Stop it For 10 Days, Then Use for 3 Then Stop 10.
3. Local Anti-Biotic: Erythromycin or Clindamycin at Day
or Combined with Benzyl Peroxide at Night. 2. Systemic Retinoid: Decrease Activity of Sebaceous
Gland Ex; Isotretinon, (Dose: 0.5-1mg\kg\12-16 Weeks).
4. Azelaic acid: (Natural Di-Carboxylic acid) 20%
Act on Inflammatory & Non Inflammatory Acne, Also 3. Hormonal Treatment: OCP.
Decrease Hyper-Pigmentation. 4. Intra-Lesion Steroid: For Deep Nodulo-Cyst.
5. Chemical Peeling: with Glycolic acid.

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DR. MOHCEN AL. HAJ
 - Other Types of Acne:

Infantile Acne: It is Self Limiting Occur during First Year of Life (3-12 Months), Common in Face.
Acne Excoriated: Common in Young Girls, Due to Direct Hand Face Contact.
Drug Induced Acne: It has No Comedone.
Steroid Induced Acne: Occur after 2 Weeks of Steroid use.

- Sever Types of Acne:

Acne Conglobata: Acne Fulminans:

Inflammatory Sever form of Comedone with large abscess, Affect Boys Mainly between 13-17
Cyst, Nodule Heals with Scar. It is Chronic, Un-Remitting Years Old, Usually Face Not involved.
Course, Commonly Seen in Face & Trunk, (M>F).
Clinical Nodulo-Cyst Acne Associated Fever, and Leukocytosis. Nodulo-Cyst, Ulcer, Asso- with Fever,
Picture Arthralgia, Myalgia and
Leukocytosis.
Complication 1. Emotional Disturbance, 2. Scarring & Keloid, Same
3. Squamose Cell Carcinoma.
Investigation CBCHigh WBC, Normocytic Normochromic Anaemia + CBCHigh WBC (>30,000), X-Ray at
Swab for Culture & Sensitivity. Site of Bone painOsteolytic Lesion.
Treatment Systemic Retinoid + Anti-Biotic + Steroid to Improve Systemic Retinoid + Anti-Biotic +
Inflammatory lesion More Fast. Steroid , (Also Intra-Lesion Steroid)

Rosacea
Chronic Inflammatory Acne form Disorder of Pilosebaceous Follicle Characterized by:
Papules, Pustules, Sebaceous gland Hyperplasia, Normal Sebum Production,
Telangiactasia (Dilated Dermal Blood Vessels), But NO Comedone.

Common in age between 30-50 Years Old, (F>M), Exacerbated by Sun Light.
- Site: Central Face Cross Distribution in Forehead, Cheeks, Chin.

- Treatment:
Avoid Sun Light + Metronidazole Cream + Systemic Anti-Biotic + Systemic Retinoid.

Rosacea Acne
Limited in Face Face, Chest, Shoulder
Telangiectasia No Telangiectasia
No Comedone Comedone
Normal Sebum Production High Sebum Production
Age Between 30-50 Years Old Age Between 12-20 Years Old
Female > Male Male > Female

23
DR. MOHCEN AL. HAJ
 Hair
- Types of Hair:
1- Lanugo Hair: Fine, Long Hair Covering Fetus, Shed One Month after Birth.
2- Vellus Hair: Fine, Short, Un-Medullated Hair Covering much of the Body Surface.
3- Terminal Hair: Long, Coarse, Medullated Hair Seen in Scalp & Pubic region.

- Hair Growth Cycle (Phases of Follicular Activity):

1- Anagen  Active Phase of Hair Production (2-4 Days).
2- Catagen  Conversion from Active Growth to Resting Phase (1-2 Weeks).
3- Telogen  Resting Growth Phase (5-6 Weeks).

 Average Hair Number on Scalp  100,000 Hair.

 About 85% of Hair is Normally in Anagen & 15% in Telogen.

Alopecia (Hair Loss)

- Types & Causes of Alopecia:

Localized Alopecia Diffuse Alopecia

Non Scarring Scarring 1- Endocrine Disorders:
1- Alopecia Areata. 1- Inflammation: Hyperthyroidism, Hypothyroidism,
Lichen Planus, Bullous Hypoparathyroidism, Hypopituitarism.
2- Tractional Alopecia. Pemphegoid, Discoid Lupus,
Scleroderma, Sarcoidosis. 2- Drugs:
3- Hair Pulling Habit. Chemotherapy, Immuno-suppressant
2- Infection: Drugs (Cyclosporine), Cytotoxic Drugs
4- Trichotillomania. Bacterial Furuncle, Carbuncle, (Cyclophosphamide), Retinoid
Secondary Stage of Syphilis. (Excess Vit A), Anti-Coagulent (Heparin),
5- Non Inflammatory Colchicine.
Fungal Kerion, Favus.
Tinea Capitis.
Viral Herpes Zoster.
3- Diseases:
6- Male Pattern
Alopecia. 3- Genetic: SLE, Malnutrition, Stress.
Lamellar Ichthyosis.
Also: Scalp Psoriasis.
4- Physical:
Burns, Trauma, Chemical.

5- Malignancy.

24
DR. MOHCEN AL. HAJ
 * Alopecia Areata:
It is Recurrent, Non Scarring Type of Hair loss Due to Emotional & Psycological Stress.

- Patho-physiology:
Unknown, But Most accepted Hypothesis is T-Cell Auto-Immune Occur in Genetically
Susceptible Individual.
Can Occur in All Races and any Age, But Peak Age incidence appears in 15-29 Years Old.

- Clinical Picture:
- 20% Asymptomatic.
- 80% of Patient had Single Patch of Hair Loss, Smooth, Normal Colored or Slightly
Erythematous, NO Scales, NO Signs of Inflammation.

- Clinical Types of Alopecia Areata:

1- Alopecia Totalis Complete Loss of Scalp Hair.
2- Alopecia Universalis Loss of Hair All Over the Body.
3- Ophiasis Pattern Loss of Hair at Margin of Scalp “Behind Ear”, (Very Bad Prognosis).

Alopecia Areata may Associated with: Atopic Dermatitis, Vitiligo, DM Type I, Thyroid
Diseases, Down Syndrome, Mysthenia Gravis, Emotional & Psychological Disorders.

Bad Prognostic Feature of Alopecia Areata:

1- Alopecia Totalis or Universalis.
2- Ophiasis Pattern.
3- Nail Changes.
4- Young Patient before Puberty.
5- If Associated with Atopy or Down Syndrome.

- Treatment of Alopecia Areata:

1- Reassurance Because Spontaneous Remission is Common.
2- Topical Steroid or Intra-Lesion Steroid.
3- Tacrolimus.
4- Topical Immuno-Therapy.
5- Cyclosporin.
6- Dithranol.
7- PUVA May Used.
8- Minoxidil.

25
DR. MOHCEN AL. HAJ
 * Androgenic Alopecia:
It is Male Pattern Boldness, Can Occur in Female after Menopause.

- Causes:
1- Genetic.
2- Age: in Male 20-30 Years Old. In Female 40-50 Years Old.
3- Action of Androgen on Hair Follicles.

- Clinical Picture:
Start in Temporal area or Fronto-Temporal Then Crown.
Due to Reduction in Length of Anagen Phase (Hair Growth), The Hair Gradually become
Shorter & Finer  Then the Hair Do not Re-Grow & Hair Follicle Close Terminal Hair
Replaced by Vellus Hair.

- Treatment:
Topical Minoxidil Lotion.

Advantages of Minoxidil: Disadvantages of Minoxidil:

1- Reduction rate of Hair loss. 1- Expensive.
2- Need Long Time.
2- May Stimulate Growth of New Hair. 3- If Stopped; Newly Hair formed will be Lost.
4- Anti Androgen in Female.

* Tractional Alopecia:
Common Cause of Hair loss Due to Pulling Force.
Common in African & American Women.
Initially it is Reversible,; But Prolonged Becomes Permanent.

Hirsutism:
Excessive Growth of Thick Dark Hair in Location Where Hair growth in Female usually absent or Minimal (in Face,
Chest, Areola).
- Causes:
-Primary Idiopathic Familial Not Associated with Androgen Excess
-Secondary it includes:
Endocrine Causes; Poly Cystic Ovary (PCO), Ovarian Tumor, Congenital Adrenal Hyperplasia, Cushing Syndrome,
Acromegally, Hyper-Prolctenamia, Hypothyroidism. + Anorexia Nervosa
Drugs; Minoxidil, Steroid, D-Penicillamine, Phenytoin, Psoraline.

Hyper-trichosis:
Excessive Terminal Hair Growth in Non Androgenic Distribution.
- Caused Mainly by; Drugs (Ex; Cyclosporine + Phenytoin), Accompanying with Masculaizing Symptoms & Signs.

26
DR. MOHCEN AL. HAJ
 GENO-DERMATOSIS

Geno-Dermatosis are group of Inherited Genetic Skin Conditions. It Includes:

1- Ichthyosis.
2- Neurofibromatosis.
3- Xeroderma pigmentosa.
4- Epidermolysis Bullousa.

1- Ichthyosis
Group of Disorders which Present at Birth or in Early Childhood.
Characterized by Chronic, Generalized, Non Inflammatory, Scaling of Skin.
The Term Ichthyosis (Fish) Means Scaly appearance of Skin.

- Ichthyosis Vulgaris:
It is Autosomal Dominant.
Most Common Type  95%.
Appear in Early Childhood (Between 3 –12 Months), But the Skin look Normal at Birth.

Clinical Picture of Ichthyosis Vulgaris:

Fine Scales appear Mainly in Extensor Surface of Extremities & on the Trunk.
- Associated with Atopy.

*Treatment of Ichthyosis Vulgaris:

1- Lubricating Cream; (Ex 10% Urea Cream).
2- keratolytic Cream; (Ex 3-6% Salicylic acid).

- Lamellar Ichthyosis:
It is an Autosomal Recessive.
Appear at Birth Presented through Life.
The Newborn is born Encased with Colloid Membrane That Sheds in 10-14 Days Releave
Generalized Scaling with Redness of Skin

Clinical Picture of Lamellar Ichthyosis :

Fine Scales or Plate like (Fish Skin), Commonly in Flexure Surface.
 Also Presented with Scarring Alopecia, Ectropion, Bilateral Conjunctivitis, Small
Deformed Ears & Inflexible Digits.
 Also Presented with Nail Abnormality which Includes:
1- Dystrophy with Nail fold Inflammation.
2- Subungual Hyperkeratosis.
3- Long, Transverse Stippling.
4- The Nail grow 2-3 Times Faster Than Normal.

27
DR. MOHCEN AL. HAJ
 *Treatment of Lamellar Ichthyosis:
1- Emollients; (Ex Vaseline).
2- keratolytic Cream; (10 – 20% Urea Cream).
3- May Retinoid Used.

- X-Linked Ichthyosis:
It is The Second Common Type.
Seen at Birth or Immediately in Neonatal Period.
Caused by Decrease of Steroid Sulfatase Enzyme.

Clinical Picture of X-Linked Ichthyosis:

Large, Dark Brown, Adherent, Scales Commonly in Posterior of The Neck, Upper Trunk,
Extensor Surface (The Boy affected has a Dirty Face Appearance)
Also Presented with Corneal Opacity, Cryptorchidism occur in 20% of Patient.

*Treatment of X-Linked Ichthyosis:

1- Emollients; (Ex Vaseline).
2- keratolytic Cream; (10 – 20% Urea Cream).
3- May Retinoid Used.

- Acquired Ichthyosis:
This Type Associated with Various Systemic Disease, Auto-immune Disease, Malignancy ,
Drugs and HIV.

 Systemic Disease: Sarcoidosis, Leprosy, Chronic Renal Failure (CRF), Thyroid

Disease, Hyperparathyroidism.
 Auto-Immune Disease: Connective Tissue Disease as SLE, Dermatomyocytis.
 Malignancy: Lymphoma, Multiple Myeloma, Broncogenic Carcinoma, Kaposis
Sarcoma, Cancer Ovary & Cervix.
 Drugs: Cimetidine, Retinoid, Nicotinic acid, Clofazimine.

*Treatment of Acquired Ichthyosis:

-Treat the Underlying Causes.

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DR. MOHCEN AL. HAJ
 2- Neurofibromatosis (NF)
It is an Autosomal Dominant Disorder of Nervous System that Causes Tumors Grows
anywhere in or on the Body, Affect all Races and all Genders Equally.
There are 2 Types: Type1, Type2 (Type1 Most Important in Dermatology, Type2 is Rare).

Clinical Picture of Neurofibromatosis (CNAL):

1- Café-au-lait Spots are the Most Characteristic Feature of Disease, as they are present
in 100% Of Cases, (Café-au-lait Spots: are Multiple, Brown, Oval Macules and Patches).
2- Neurofibromas “Skin Tags”.
3- Armpit Freckling or Groin.
4- Leisch Nodules (Papules Present in Iris). 5- Plexiform Neurofibroma.

- Diagnosis: Clinically
But You Can Do Genetic Testing.

- Treatment of Neurofibromatosis:
No Cure Treatment for Neurofibromatosis, May Surgical.
Simple Excision, CO2 Laser ablation, or Electrocautary for Skin Tag.

3- Xeroderma Pigmentosa (XP)

It is an Autosomal Recessive Disorder Characterized by Photosensitivity (Sensitivity to
Sun Light) Due to Defect of Nucleotide Repair Enzyme (Endonuclease Enzyme).

Clinical Picture of Xeroderma Pigmentosa (XP):

1- Photosensitivity Increase risk of Skin Cancers (BCC, SCC).
2- Pigmented Freckles.
3- Dry & Scaly Skin + Irregular Dark Spots.

- Diagnosis: Mainly Clinically

But You Can do Genetic Testing.

- Treatment of Xeroderma Pigmntosa:

No Cure for Xeroderma Pigmentosa.
Avoid Exposure of Sun Light.

Note:
Tuberous Sclerosis: is a Rare AD, Multisystemic & Neuro-Cutaneous Genetic Disease Chatacterized By ASK:
Ash-leaf Spots(White Patches of Skin Due to lack of Melanine Visible at Birth), Shagreen Patch, Koenen Tumor.
Others: Café-au-lait Spots, Patches of White Hair (Koenen Tumor: Present around & Under Nails of Toes or Fingers).

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DR. MOHCEN AL. HAJ
 Skin Infections
Bacterial Skin Infection “Pyoderma”.
Viral Skin Infection.
Fungal Skin Infection.
Mycobacterium Skin Infection.
Parasitic Skin Infection “Infestation”.

Bacterial Skin Infection “Pyoderma”:

Pyodema Means Bacterial Infection of Skin Caused by Pus-Producing Bacteria like;
Staphylococcus & Streptococcus.
Bacterial Skin Infection “Pyoderma” Divided into  Primary & Secondary.

Primary Pyoderma: Commonly Caused by; Staphylococcus & Streptococcus;

Staphylococcus Infection: Streptococcus Infection:

1. Impetigo. 1. Impetigo.
2. Ecthyma. 2. Ecthyma.
3. Superficial Folliculitis. 3. Cellulitis.
4. Deep Folliculitis. 4. Erysipelas.
5. Staphylococcal Scalded Skin 5. Scarlet Fever; It is Caused by
Syndrome “SSSS”; It is Caused by Bacterial Toxins So it is Indirect
Bacterial Toxins So it is Indirect Infection.
Infection. 6. Erythema Nodosum.

Secondary Pyoderma: It is Secondary to Pre-existing Skin Disease, Such as; Dermatitis,

Post Viral Skin Infection, Post Parasitic Skin Infection, Wounds, Ulcers.

- Predisposing Factors of Pyoderma:

1. Patient with Low Immunity, Such as; DM, AIDS.
2. Chronic Disease.
3. Chemotherapy.
4. Skin Diseases.

Most Common Areas to find Bacterial Infection in the Body are;

1. Around Nostril.
2. Moist Hairy area.

Best Anti-Biotic for Staphylococcus are Fluxacillin, Cloxacillin, Vavcomycin.

Best Anti-Biotic for Streptococcus is Penicillin, (If Pt Allergic; Give Erythromycin).

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DR. MOHCEN AL. HAJ
 * Impetigo
It is a Superficial Bacterial Infection affect Epidermis Caused by Staphylococcus &
Streptococcus affect Face & Extremities of Children.

Clinical Picture of Impetigo:

In the Beginning; Very Thin Walled Vesicle “Rapidly rupture” then Becomes;
Honey-Yellow, Colored Crust, Thin Easy Remove, Healing Without Scar.
- Sites: Face (around Nose, Mouth), and Extremities.

- Types of Impetigo:

Non Bullous Impetigo “Classical” Bullous Impetigo

-Also Known as Impetigo Vulgaris, -It is Caused by Staphylococcus.
It is Caused by Both Streptococcus &
Staphylococcus.
-Common in Children. -Present in All Ages.
-Mainly in Face “Peri Orifices” around -Mainly in Extremities.
Eyes, Nose, and Mouth.

- Complication of Impetigo:
1. Bacteremia. 2. Toxemia. 3. Abscess. 4. Erysipelas. 5. Cellulitis. 6. Lymphangitis \
Lymphadenitis. 7. Glumerulo-Nephritis; So you can do  Urine analysis & Culture, RFT.

- Treatment of Impetigo:
1. Remove Crust by  Potassium Permanganate.
2. Topical Anti-Biotic  Fusidic acid (Cream or Ointment).
3. In Sever Cases  Systemic Anti-Biotic.

* Ecthyma
It is a Deep Bacterial Infection affect Epidermis & Dermis Caused by Staphylococcus &
Streptococcus affect Mainly Thigh & Buttocks of Old.

Clinical Picture of Ecthyma:

Adherent Dark Crust with Ulcer below it Healing With Scar.
Usually associated with Fever and Enlargement of Lymph Nodes.
- Sites: Lower Limbs, Thigh, Buttocks, Legs.

- Treatment of Ecthyma:
1. Remove Crust by  Potassium Permanganate.
2. Topical Anti-Biotic  Fusidic acid (Cream or Ointment).
3. In Sever Cases  Systemic Anti-Biotic

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DR. MOHCEN AL. HAJ
 * Superficial Folliculitis
Inflammation of Hair Follicle Commonly Caused by Staphylococcus Auras, Common in
Children, affects Scalp, Limbs, Trunk, & Axilla.

Clinical Pictures of Superficial Folliculitis:

Small Pustules on Erythematous Base.
- Sites: Scalp, Limbs, Trunk, & Axilla.

- Treatment of Superficial Folliculitis:

Topical Anti-Biotic  Fucidine Ointment.

* Deep Folliculitis

Furuncle “Boil” Carbuncle Sycosis Barbae

Definition Acute infection of Multiple Communicating Also known as
Single Hair Follicle Hair Follicles in the Same “Pseudosycosis
Caused by area become deeply Barbae”
Staphylococcus Auras. infected with
Staphylococcus Auras.
Age Common in Adult Common in Middle and Common in Male
Male. Old Age. After Puberty.
Sites Face, Neck, Buttocks. Back of the Neck, Knee, Beard area.
and Groin region.
Clinical Tender, Red Nodule Tender, Red Nodule Pustules on
Pictures Discharging Pus from Discharging Pus through Erythematous
Single Opening, Multiple Openings, Indurated base.
Heals With Scar. Heals With Scar.
Treatment 1. Drainage of Abscess 1. Drainage of Abscess if Topical Anti-Biotic
if Large. Large.  Fucidine
2. Topical Anti-Biotic. 2. Topical Anti-Biotic.
3. Systemic Anti-Biotic. 3. Systemic Anti-Biotic.
Notes *When Furuncle Occur
in the Face at level *Predisposing Factors:
above upper Lip; It is -DM.
Very Serious; Because -Malnutrition.
Pass into Cavernous -Prolonged Steroids
Venous Sinus Therapy.
Causing Cavernous
Sinus Thrombosis.
*Furunculosis means
 Multiple Furuncles
Lesion in Different
areas.

32
DR. MOHCEN AL. HAJ
 * Cellulitis & *Erysipelas

Cellulitis Erysipelas
Definition Deep Skin infection in Superficial Skin infection in Dermis.
Subcutaneous Tissue.
Sites Common in Legs & Feet. Common in Face.
Clinical Dull Red, ill-defined border, Bright Red, Well-defined border Bulla.
Pictures Tender, Large area. Also associated with Fever & Malaise.
Cause Streptococcus, Staphylococcus, Caused by  Streptococcus.
H.Influenza in Children.
Management 1. Complete Bed Rest. 1. Complete Bed Rest.
2. Compress Stocks & Elevation 2. Compress Stocks & Elevation of the
of the Leg. Leg if Lesion was in the Leg.
3. Local & Systemic Anti-Biotic. 3. Local & Systemic Anti-Biotic.
4. Surgical Debridement. “Streptococcus-->Penicillin”
D\D Erysipelas, Insect Bite, DVT. Cellulitis, Dermatitis.
- Complication of Cellulitis & Erysipelas:
1. Subcutaneous Abscess, 2. Septicemia, 3. Lymphadenitis, 4. Osteomyelitis, 5. Nephritis.
If Both Cellulitis & Erysipelas not Treated Damage of Lymphatic System Lymph Edema

- Staphylococcal Scalded Skin Syndrome “SSSS”

Also known as Epidermolytic Toxica, Caused by Serotoxin from Staphylococcus Auras.
Serotoxin Lysis of Epidermis Blisters Separation of Epidermis Scalded Skin.

- Treatment of “SSSS”:
1. Good Personal Hygiene.
2. Local Treatment: Potassium Permanganate “for Crust” + Anti-Biotic Cream.
3. Systemic Treatment: Anti-Biotic “Staph Fluxacillin, Cloxacillin”.

* Erythrasma
Chronic Skin Lesion Caused by Coryneabacterium Minutissimus “Gram Positive Bacilli”.

Clinical Picture: Asymptomatic, Brown Red, Scaly Dry Patch, Irregular, well-Demarcated.
- Sites: Body Folds “Axilla, Submammary, Groin, Toe web Space between 4th & 5TH Finger”

- Diagnosis:
Woods Lamp  Coral Red Flurescence.

- Treatment of Erythrasma:
1. Anti-Biotic  Erythromycin.
2. Anti-Fungal  Topical Imidazole or Miconazole.
3. Benzyl Peroxide.

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DR. MOHCEN AL. HAJ
 Viral Skin Infection:
Common Viruses affecting Skin:
1. Herpes Simplex; Type1, Type2.
2. Herpes Zoster; 1ry Infection Varicella Zoster, 2ry Infection Herpes Zoster.
3. Pox Virus; Cause Molluscum Contagiosum + ORF.
4. Human Papilloma Virus; Cause Wart.

* Herpes Simplex Virus “HSV”

Caused by Herpes Virus Human, There are Two Types:

Type 1 HSV (Herpes Labials) Type 2 HSV (Genital Herpes)

Mode of Transmission: Mode of Transmission:
- Air Droplet, or Direct Contact with - Sexually.
Mucous Membrane. “Sexual Transmitted Disease” STD.

Clinical Pictures: Clinical Pictures:

- Primary Herpes Simplex; Multiple, Small Grouped, Painful, Vesicles
90% Asymptomatic Sub-Clinical on Erythematous base May Ulcerate.
10% Symptomatic 1.General Symptoms:
Fever, Anorexia, Headache, Malaise Site:
(FAHM), Tender Lymphadenopathy. External Genitalia in both Male & Female
“Cervix”.
 2.Specific Symptoms:
Clusters of Small Vesicles on Erythematous
base, Affect Skin and Mucous Membrane
of the Mouth.
If Eczematous Pt infected by Herpes
Simplex Virus, It is Sever Case Called
“Eczema Herpaticum” Common in
HIV Pt.

- Recurrent Herpes Simplex;

Clusters of Small Vesicles Proceeded by
Pain Itching, or Tingling or Burning
Sensation.
The lesion Persists few days and Subsides
Spontaneously.
No General Symptoms.

Trigger Factor of Recurrent HSV:

- Immune Suppression, Sun Light,
Stress, Psychological factors, Fever.
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DR. MOHCEN AL. HAJ
 - Complication of Herpes Simplex Virus:
1- Secondary Bacterial infection.
2- Erythema Multiform.
3- Eczema Herpaticum in patient with Atopic Dermatitis.
4- Cancer Cervix.
5- Corneal Ulcer & Opacity.
6- Herpes Encephalitis or Meningitis.
7- Dissemination of HSV Especially in immune-suppressant Pt and Children.
8- Herpatic Witlow; Inoculation of Virus from Pt to Tip of Finger of Medical Stuff.

- Diagnosis of Herpes Simplex Virus:  Usually Clinically

1. Tzank Smear: Scraping the floor of Vesicle then Stained with Wright Stain it will
Show Intra Cellular Inclusion Bodies.
2. Viral Culture from Vesicular fluid.
3. Polymerase Chain Reaction (PCR) to Detect Viral DNA.

- Treatment of Herpes Simplex Virus:

1. Topical Acyclovir “Zovirax Cream 5%” 5 Times \ Day \ 5 Days. (Role of 5)
2. Topical Anti-Biotic “Ointment” to Prevent Secondary Bacterial infection.

 Systemic Acyclovir Indicated in:

1. Immuno-compremised Patient.
2. Eczema Herpaticum.
3. Genital Herpes.
4. Neonatal Herpes.
Dose: Acyclovir Oral 200mg  5 Times \ Day \ One Week.
S\E of Acyclovir: GIT Upset, Hepato-toxicity, Renal-toxicity.

* Herpes Zoster “Shingles”

Acute Self limiting Vesicular Eruption Occurs in Dermatomal Distribution.
Caused by Varicella Zoster Virus.
The Initial infection with Varicella Zoster Causes Chicken pox which occurs in Children
and Young People, Then the Episode of Chicken Pox Resolve but the Virus Not
Eliminated; it Stays in Dorsal Root Ganglia of Spinal Cord, Then the Disease May
Reactivate again if the Patient has had Low Immunity or Stress Conditions.
Reactivation of the Virus Follow Dermatomal Distribution.

Initial infection with Varicella Zoster  Virus Hides in Dorsal Root Ganglia of
Spinal Cord  Reactivation of Virus follow Dermatomal distribution.
Dermatome:  Area of Skin Supplied by the Same Nerve Root.
35
DR. MOHCEN AL. HAJ
 Clinical Pictures of HZV:
Sever Pain, then after 2-3 Days Vesicles appear;
Grouped of Vesicles on Erythematous base within Dermatomal area following Nerve root
affect Single Dermatome (Unilateral).
- Sites: 50% Thoracic area, Abdomen, Ophthalmic branch of Trigeminal Nerve.

*If Nasociliary branch of Trigeminal Nerve affected; Patient develop Vesicles on Tip of
Nose, this Sign known as  Hutchinson’s Sign.
*Facial Nerve Palsy + Vesicles in External Ear Known as  Ramsy Hunt Syndrome.

- Complication of Herpes Zoster:

1- Secondary Bacterial infection.
2- Corneal Ulcer & Opacity..
3- Post Herpatic Neuralgia; (Persistent Sever Pain at Site of lesion, Occurs in 70% of Pt.
4- Post Herpatic Scar.
5- Dissemination of HSV Especially in Immune Suppressant Pt and Children.

- Treatment of Herpes Zoster:

1. Systemic Acyclovir “Zovirax” Orally  800mg  5 Times \ Day \ Week.
OR  I.V Acyclovir 5-10mg\ Kg every 8 Hours for Week.
2. Topical Anti-Biotic “Ointment” to Prevent Secondary Bacterial infection.
3. Analgesia + Vit B6,B12.

* Wart
It is a Benign Coetaneous Tumor Caused by Human Papilloma Virus (HPV).
“It is DNA Virus, More than 77 Types”. (Common in Children, Young, Adult).
- Mode of Transmission: by Direct or Indirect Contact.

1- Common Wart Multiple Papule, Skin Color, with Rough Treated by:
(Varruca Surface, and Hyperkeratosis, Which Can be Cryosurgery,
Vulgaris) Tender or Painless. (Cryotherapy).
They Can Occur at any part of the body But
Most Commonly Seen on Hands and Knees.
2- Plane Wart Flat or Slightly Elevated Flesh Color Papules Treated by:
(Flat Wart) that May be Smooth or Slightly Electrodessication &
(Varruca Plana) Hyperkeratotic. Curettage.
Common in face.
Common Seen in Children.
3- Planter Wart Papule Hyperkeratotic with Black dot in Treated by:
Planter Surface of the foot. Salicylic acid.
- Black dot Formed Due to Electrotherapy is
Thrombosed Blood Vessel. Painful here

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DR. MOHCEN AL. HAJ
 4- Filiform Wart Long Slender Growth Treated by:
Commonly Seen in Face around Lips, Electrodessication &
Eyelids, and Nose. Curettage.
5- Genital Wart Caused by HPV 6, 11, 16, 18 Treated by:
(Condyloma Affect Valva, Cervix, and Genital Tract Podophyllin.
acuminate) Pre-Cancerous Lesion (Cancer Cervix) C\I in Pregnancy
6- Mosaic Wart Hard Plaque Resist to Treatment.

- Treatment of Wart in General:

1. Salicylic acid.
2. Podophyllin; C\I in Pregnancy Teratogenic.
3. Electrodessication & Curettage
4. Cryosurgery; (Liquid Nitrogen(-196 C, is the Most Effective Method of Cryosurgery).
Liquid Nitrogen is Very Painful if Used in Planter Wart.

Planter Wart Callosity

Present anywhere in Planter area. Present only at Pressure area.
Painful on Side to Side Pressure. Painful on Vertical Pressure.
Black dot. No.
Scraping Lead to Pin-Point Bleeding. No

* Molluscum Conagiosum & *ORF

Molluscum Conagiosum ORF

Cause Pox Virus. Pox Virus.
Mode of Direct Contact & Sexually. Contact with infected Animals
Transmission (Cattles).
Common in Children. Common in Butchers.
Clinical Pink or Red, Dome shape Single or Multiple Flat Toped Papules
Picture Papules with Central & Pustules on Dorsum of Hands and
Umblicated or Punctum Contain Fingers, Erythematous in Color.
Cheesy material < 0.5cm.
Complication Secondary Bacterial infection. Lymphadenopathy & Erythema
Multiform.
Treatment Locally Removed by Curetage. Disappear Spontaneously after One
Also Cryotherapy by Liquid Month.
Nitrogen. Can use Topical Anti-Biotic.

37
DR. MOHCEN AL. HAJ
 Fungal Skin Infection “Dermatomycosis”:
Dermatomycosis Means Skin Disease Caused by Fungus.

Superficial Fungal Infection includes:

1. Dermatophytes  Trichophyte, Micosporum, Epidermophyte.
2. Yeasts  Malassezia Furfura , Candida.

> Dermatophytes: It includes:

1- Trichophyte  Affect Skin, Hair, and Nail.
2- Micosporum  Affect Skin and Hair.
3- Epidermophyte  Affect Only Skin.

Dermatophytosis: Means Fungal infection Caused by Dermatophytes.

* Trichophyte
This Type of Dermatophyte Cause Fungal Infection Known as; Tinea “Ring Worm”.
- Types of Tinea:

Types
Tinea Capitis Usually affects the Children less than 12 years, There are Two Types;
 Non inflammatory Tinea Capitis:  Patches of Hair loss Causing Non Scaring Alopecia.
The Hair shaft break Gives Black Dots appearance.

 Inflammatory Tinea Capitis: it has Two Pictures;

Kerion:  Boggy inflammatory Nodules or Plaques, Very Painful, Draining Pus from Multiple
Opening, Hairs Not break but Fallout Easy Leading to Scaring Alopecia.
Favus:  It is a Chronic infection appear as Thick, Yellow Cup shaped Crust Named “Scatula”
It has Smell Like Mouse Smell, Leading to Scaring Alopecia.

 Diagnosis:
1. Microscopic with KOH:
Collect Sample by Scraping Skin lesion & Put in Microscopic Slide with KOH 10-20%  If you see
Hyphea & Spores; that indicate Fungal Infection (NOTE: KOH for Favus Cause Air Bubbling).
2. Woods Lamp:
Green in Tinea Capitis.
Tinea Pedis Common in Toe web between 4th & 5th Toe, Common in Athletic People Also Diabetic Patient.
“Athletic Foot” Presented with Inter-Digital Whitish Maceration, Fissure, and Itching.
Tinea Corporis Single or Multiple Scaly Erythematous Plaque with sharp raised edges & Central Clearing.
Tinea Cruris Itchy, Erythematous, Scaly Plaques, Well-Demarcated Margin, Common in Athletic People.
Tinea Manuum Common in the Palm of the Hands.
Tinea Unguium Fungal Infection in Nail plate.
“Onychomycosis” Common in Diabetic Patient.

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DR. MOHCEN AL. HAJ
 - Treatment of Tinea:
1. Topical Anti-Fungal  Imadizoles Derivtices in form of Solution, Cream, Ointment.
Ketoconazole, Miconazole, Econazole Used forTinea pedis, Cruris, Corporis, Mannum.
2. Systemic Anti-Fungal  Grisofulvin 20mg \ kg \ Day for 6 Weeks “Given Orally with
Fatty Meal; because it is Fat Soluble Drug, Used for Tinea Capitis & Ungium.

S\E of Grisofulvin: GIT Upset, Hepato-toxicity, Headache, Increase risk of SLE, No Effect against Candidiasis.

* Pitryasis Versicolor
It is Superficial Cutaneous Fungal Infection Caused by Malassezia Furfura.

Clinical Picture: Non Tender, Unilateral or Bilateral, Single or Multiple, Hypopigmented

or Hyperpigmented, Macules or Patches Covered with Fine Scale, Mild Itching.
- Sites: Mainly around Scapula, Neck, Upper Shoulder, Chest, Back.

- Diagnosis:
1. Microscopy with KOH Hyphea & Spores in appearance Called; Spaghetti meat form.
2. Woods Lamp  Golden Yellow.

- Treatment of Pitryasis Versicolor:

1. Systemic Itrakonazole 100mg (OR Broad Spectrum Anti-Fungal  Fluconazol).
2. Nizoral Shampoo as Prophylactic Treatment.
3. Selenium Sulfate Shampoo 2% (SSS).
4. Salicylic acid 2.5%.

* Candida

Definition Candida Albicans is Normal Flora of GIT, Mouth, and Peri-anal Skin.
Predisposing DM, Patient with Low Immunity
Factors Obesity, Warm Moist areas.
Clinical Picture Satellite Distribution Lesion, Other according to the Type.
Types Oral Trush: White Membrane on Mucous Membrane, affect Chidren.
Intertrigon: Etythematous Patch in Satellite Disrtibutions Present in
Skin folds as; Axilla, Under Breast, Groin, Between Toes, affect Old age.
Genital Candidiasis: It is Sexual Transmitted Disease STD affect Male &
Female "M=F", (Female Complain from Vaginal Discharge + Itching).
Paronychia: affect Nail fold Common in Diabetic Patients.
 Acute Paronychia: it is Bacterial in Origin.
 Chronic Paronychia: it is Fungal in Origin.
Systemic Candidiasis: Common in GIT Problems, Dysphagia.
Treatment Nystatine (D.O.C), Amphetracin B injection, (Ketoconazole also Used).

39
DR. MOHCEN AL. HAJ
 Parasitic Skin Infection: “Infestation”
Cutaneous Parasitic Infestation includes:
1- Scabies.
2- Cutaneous Leishmaniasis.
3- Pediculosis.

* Scabies
Commonest Communicable Pruritic Parasitic Infection Caused by; Sarcoptus Scabie.
- Mode of Transmission:
1. Direct Contact.
2. Indirect Contact; Using of Common Towels, Clothes, Beds.
3. Sexually.
- Predisposing Factors:
Over Crowding, Poor Hygiene, Poverty.

Clinical Picture of Scabies:

Sever, Persistent, Itching Worse at Night and after Bathing.
Presented with Burrow in Stratum Corneum, also Scratch Marks (Excoriations) and May
Pustules; Due to Secondary Bacterial Infection.
Primary Skin Lesion Burrow
Secondary Skin Lesion Scratch Marks (Excoriations), and Pustules.

- Sites: Skin Folds; Inter-Digital Fold, Axillary Fold, Under Breast, Umbilicus, Genitalia,
Thigh, Gluteal region, Wrist, Elbow.
In Children; Mostly at Wrist. In Infant; Mostly in Face, Scalp, Palm, Sole.

- Complication of Scabies: “3S, PUC”

1- Secondary Bacterial Infection “Pyoderma”.
2- Spread to Community.
3- Scabio-Phobia “Even Try to Suicide”.
4- Pruritic Nodules.
5- Urticaria.
6- Chronic Scabies.

- Diagnosis: Mainly Clinically

- History of Itching Worsening at Night.
- Presence of Burrow at Site of Lesion.
- More than One of Family Member involved.
- Microscopic Examination Scraping from affected area KOH Mite, Feces, & Eggs.
- Therapeutic Test Give Treatment of Scabies; if Pt Respond; Test is Positive.
40
DR. MOHCEN AL. HAJ
 - Treatment of Scabies: (All Family Member Should be Treated “Mass Treatment”)
Start from Chin to Down word by Using Anti-Scabietic Drugs, 24 Hours \ 3 Days:
1. Sulfur Ointment; 2.5% Infant, 5% in Children, 10% in Adult, Following a Hot Bath.
2. Crotamitone; 10% “Eurax”. 3. Malathion; 0.5% 4. Permethrin; 5% (used in Children).
5. Gamma Benzene Hexachloride; 1% (C\I in Pregnancy & Children). 6. Benzyl Benzoate.

* Cutaneous Leishmaniasis “Oriented Sore”

Caused by Protozoa Called Leishmania Classified in to:
- Old World Leishmaniasis. - New World Leishmaniasis.
- Mode of infection Bite Vector Female Sand Fly Named Phlepothomus Papatazi.
- Animal Reservoir Rodents, Dogs. Common in; ‫ تاورغاء‬,‫ الخمس‬.‫ غريان‬,‫ ترهونة‬,‫جنزور‬

Clinical Picture: Start with Painless Red Nodule or Papule then Ulcerate
- Diagnosis: Mainly Clinically
1. Slit & Smear From Margin, Giemza Stain See Leishmaniasis Amastigoite.
2. Biopsy, Culture; NNN Media (Novy Mac, Neal, Nicolle) See Promastigoite.
3. Polymerase Chain Reaction (PCR). 4. Montenigro Test; (Not Done in Libya).

- Treatment of Cutaneous Leishmaiasis:

1. Sodium Stiboglyconate “Pentostam” Intra-Lesion Injection, Systemic Pentostam Given
Only inMultiple Nodules, Ear involvement, and Lymph Node Infiltration, (20mg\kg).

S\E of Pentostam: Nephritis, Hepatitis, ECG Change, So you Need to Do (R.F.T) (L.F.T) (ECG)
2. Cryotherapy.

* Pediculosis “Louse Infestation”

Pediculosis Capitis “Head Louse” Pediculosis Corporis “Body Louse” Pediculosis Pubis “Pubic Louse”
- More in School Children. - More in Homeless People. - Transmitted by Sexual Contact,
- Mostly found  Post-Auricular. - Mostly found in Clothes. lavatory Seats.
- Louse Present in Hair Nits. - Louse Take Blood Meal at Night. - Found in Pubic area, Axilla,
- C\P: Mainly Itching, - C\P: Hemorrhagic Spots, Thigh, Abdomen, Eye lashes.
Also Secondary Bacterial infection. Scratching due to Saliva of Louse. - C\P: Sever Itching.
Treatment of Pediculosis: 1. General Shaving of Hair, Disinfect of Clothes.
2. Topical Malathion, Benzyl Benzoate, Benzene Hexachlorid (C\I in Pregnancy, Lactating Mothers & Children).
3. Systemic Cotrimoxazole. 4. Anti-Biotic for Secondary Bacterial infection. 5. Treat Contacts Even Sexual Contacts
- Complication of Pediculosis:  Impetigo, Folliculitis, Lymphadenitis, Pigmentation.

Nits Dandruff
Size Equal Size. Different Size.
Shape Similar Shape. Different Shape.
Hair Adherent to Hair. Separates from Hair.

41
DR. MOHCEN AL. HAJ
 Mycobacterium Skin Infection:
1- Leprosy.
2- Cutaneous Tuberculosis.

* Leprosy
It is a Chronic Granulomatous Disease affect Skin & Peripheral Nervous System Caused
by  Mycobacterium Leprae.
M.Leprae is an Obligate Intracellular Acid Fast Bacilli, Its average Incubation is 2-3 Years.
- Types of Leprosy:

1- Tuberculoid Leprosy 2- Lepromatous Leprosy 3- Border line Leprosy

- Occur in Patient with - Occur in Patient with Low Immunity 10%. - It is Between Two Types.
Good Immunity 90%. - Affect Skin, Mucous Membrane, Internal - Affect Face, Trunk,
- Affect Skin & Peripheral Organs Extremities.
Nerve. Clinical Picture: Clinical Picture:
Clinical Picture: --Hypo-Pigmented or Erythematous Macules. --ill-Defined Macules.
--Hypo-Pigmented --Diffuse Nodular involvement of Face Usually --Normal Sensation.
Macules. loss of Lateral 1\3 of Eye brow giving --Normal Hair Growth.
--Loss of Sensation, (1st appearance of Leonine Face. --Normal Sweating.
loss Temperature). --Loss of Eye lashes + Alopecia
--Loss of Sweating (Dry --Nasal Septum Destruction + Nasal Discharge Fate: Disappear or
Skin). + Epistaxis. Change to Tuberculoid or
--Loss of Hair. --Mild Loss of Sensation But Normal Sweating. Lepromatous Leprosy.
--Also Bone, Eyes, Testis Involvement.
Diagnosis of Leprosy: Treatment of Leprosy:
1. Tissue Smear Testing: Obtain fluid from the lesion, 1. Dapson.
The fluid is Placed on Glass Slide and Stained by using 2. Rifampicin, One injection Stop Nasal Discharge.
Zeihl-Neelson Stain to look for Organisms. 3. Clofazamine.
2. Skin Biopsy. 3. Lepromin Test.

* Cutaneous Tuberculosis “TB of Skin”

1- Lupus Vulgaris 2- Scrofula 3- Warty TB

- Commonest TB of the Skin affect - Swelling of Lymph Nodes With Sinus - Painless, Warty Papule or Plaque
Exposed Parts as Face. Opening, Discharging Pus. Slowly Increase in Size, May Bleeds,
- C\P: Papule or Nodule Slowly - Usually in the Neck. Healing by Scar.
increase in Size with “Apple Jelly
Color” Healing by Scar. Treatment: - Affects anywhere of the body But
First Remove Lymph Nodes. Commonly in Hands & Fingers.
Treatment: First Remove the Scar - Give Anti TB Drugs for 9 Months.
Because it is Pre-Malignant Lesion.
- Give Anti TB Drugs for 9 Months.

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DR. MOHCEN AL. HAJ
 Sexual Transmitted Disease (STD) “VENEREAL DISEASE”
Caused by; Bacterial, Viral, Parasitic, Fungal.
Bacterial Sexual Transmitted Diseases are:

Genito-Ulcerative Bacterial Diseases Urethral Discharge Bacterial Diseases

1. Syphilis; Caused by  Treponema Pallidum. 1. Gonorrhea; Caused by  Neisseria
2. Chancroid; Caused by  Haemophilus Gonorrhea.
Ducreyi.
3. Lympho-Granuloma Venerium; Caused by 2. Non gonorrheal Urethritis; Caused by
 Chlamydia Trachomatis.  Chlamydia & Mycoplasma.

Viral Sexual Transmitted Diseases are:

1. Genital Herpes; Caused by  Herpes Simplex Virus Type2.

2. Genital Wart “Comdylomata Accuminata” Caused by  Human Papilloma Virus.
3. AIDS; Caused by  Human Immune Deficiency Virus “HIV”.
4. Molluscum Contagiosum; Caused by  Pox Virus.

Parasitic Sexual Transmitted Diseases are:

1. Scabies; Caused by  Sarcoptes Scabie Mite.

2. Pediculosis Pubis; Caused by  Pubic Louse.
3. Trichomoniasis; Caused by  Trichomonas Vaginalis.

Fungal Sexual Transmitted Disease is:

Genital Candidiasis; Caused by  Candida Albicans.

* Syphilis
It is Bacterial infection Caused by Spirochetes Bacteria Called “Treponema Pallidum”.

- Clinical Picture: Divided into 3 Stages;

1- Primary Stage, (Chancer).
2- Secondary Stage, (Condylomata Lata).
3- Tertiary Stage, (Gumma).

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DR. MOHCEN AL. HAJ
 Primary stage (Chancer) Secondary Stage Tertiary Stage (Gumma)
Definition - Occur at Site of Entry of - Start after One Months or - It appears within 2 Years
Organism. Two Months may with or from appearing of Chancer.
without Chancer.
- Chancer will appear - It is Due to Travel and - It is Due to Allergic Response
between; 9 Days and 90 Days Multiplication of Bacteria in to Organism.
“3 Months”. Blood.
Clinical - Start with Papule Covered by 1. Generalized Erythematous - Gumma in Skin:
picture Thin Skin, and then become Maculo-Papular Rash, It is Subcutaneous Lesion
Ulcer. Symmertical, Not itching, appear in form of Nodule or
- The Ulcer is Single, Painless, Brown Red “Coppery Color”. Grouped Nodules, that
Indurated base, Highly - Commonly affect Trunk, Ulcerate, (Nodulo-Ulcerative
Contagious. Extremities, Palm, Sole. Syphilis).

Also  Enlargement of Lymph 2. Some of Papules will be - The Gummatous Ulcer

Nodes ( Firm, Painless, Mobile) Enlarge in to Pink, Flat Toped Characterized by; Painless,
Plaque Called; Condylomata Punched out Edges. Dirty floor
Common Sites of Chancer; Lata, (Pathognomic). with Necrotic Sloughs, Not
Genitalia, Breast, Knee, Contagious, Heals with
index finger (can be Painful). 3. Non Scaring Alopecia Atrophic Scar.
Called Moth eaten Alopecia.
- Healing Spontaneously - Also Diffuse Reaction Occurs
Within 2-6 Weeks. 4. Painless, Grayish White, in CVS and CNS,
Patch in Mucous Membrane (Neurosyphilis).
Covered by Necrotic
membrane, Which May
Slough Leaving Ulcer Called
Snail Tract Ulcer.
Diagnosis 1. Dark Field Examination 1. Serology: 1. Serology.
(DFE): Diagnostic 100%. TPHA Test (Treponema
“Take Smear, Put it on Slide Pallidum Haemo- 2. Biopsy.
without Stain, Condense lens Agglutination)
and Close Light of Room; See
 Spiral Shape Organisms 2. VDR: (Venereal Disease
with “Rotator movement”. Research laboratory).

2. Serology Not Favor here;

because Ab Takes 2 Weeks to
appear.
Treatment Single Dose of Penzetine Penzetine Penicillin 2.4 Penzetine Penicillin 2.4 Mega
Penicillin 2.4 Mega unit IM. Mega unit IM \ One Weekly \ unit IM \ One Weekly \ for 3
for 3 Weeks. Weeks.
S\E of Penzetine Penicillin; Mild Fever + Rash + Headache + Joint Pain. “Result of Treponema Destruction”

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DR. MOHCEN AL. HAJ
 Chancer Chancroid
Caused by; Treponema Pallidum. Caused by; Haemophilus Ducreyi
“ Gram Negative Bacilli”.
Long Incubation Period  9-90 Days. Short Incubation Period  2-5 Days.
Single. Multiple.
Painless. Painful.
Hard. Soft.
Penicillin is Drug Of Choice. Ciprofloxacin, Erythromycin,
Cephalosporin (Penicillin is Not effective).

* Gonorrhea
It is Bacterial infection Caused by Neisseria Gonorrhea, ( Gram Negative Diplo-Cocci).
Affect Male & Female. (Male Urethra, Female Cervix).

- Clinical Picture:

Male: Female:
Presented with Muco-Purulent or About 50-75% Asymptomatic.
Purulent Urethral Discharge + Dysuria. Other Presented with Vaginal Discharge + Dysuria
Note: Adult Female Vagina Not affected; Because lined by Stratified Squamous Epith.
Female in Pre-Puberty Vagina Commonly affected; Because lined by Columnar Epith.

- Diagnosis:
1- Gram Stain Show Intra-Cellular Gram Negative Diplo-Cocci inside Neutrophils.
2- Culture: Put it in  Chocolate Agar  Shows Colonies of Organisms.

- Complication of Gonorrhea:
Pelvic Inflammatory Disease, Fibrosis & Adhesion of Fallopian Tube, Petitonitis.

- Treatment of Gonorrhea:
Single Dose of Ceftriaxone (Rocephin) \ IM 500mg.

Condylomata Lata Condylomata Acuminata

Caused by; Treponema Pallidum Caused by; Human Papilloma Virus
(Secondary Stage). (6-11 are Most Common)
(16-18-31-33-35 Most Important).
Flat Surface Plaques or Papules with Pedunculated
Sessile Base.
Hard Base Soft Base
Bleeds Difficulty. Bleeds Easley.
Not Pre-Cancerous. Pre-Cancerous.
Treated with Penicillin. Treated with Podophyllin, Cryotherapy.

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DR. MOHCEN AL. HAJ
 Skin Tumors
Benign Skin Tumors: Malignant Skin Tumors:
1- Benign Melanoma. 1- Malignant Melanoma.
2- Basal Cell Papilloma. 2- Basal Cell Carcinoma.
3- Squamous Cell Papilloma. 3- Squamous Cell Carcinoma.
- Malignant Tumors:

Malignant Melanoma Basal Cell Carcinoma Squamous Cell Carcinoma

Definition Malignant Tumor arises from Locally Malignant Tumor arises Malignant Tumor arises from
Epidermal Melanocyte. from Basal Layer of Epidermis. Keratinocyte of Epidermis.
Incidence Commonest Skin Tumor Causing Commonest Skin Tumor, Less Common,
Death, Male > Female (30-60 Y) Common in Male > 40 Years. Common in Male > 50 Years.
Predisposing -Sun Light; Most Common Cause.
Factors -Radiation. Same Same
-Pigmented Skin Lesion as; XP.
-Carcinogens as Tar, Wood Dust.
Pathology -Affect any Part of the Body -90% in Face (above line -Common in Sun Exposed area as
(Usually Face). Between Ear Lobule & Angle of Dorsum of Hand, Neck, Arms,
-Can Spread into Surrounding the Mouth. Upper Part of Face.
also has Lymphatic Spread. -Spread Only to Surrounding -Spread to Surrounding &
-Blood Metastasis is Very Rare. Structures. Lymphatic’s.
No Blood or Lymph Metastasis. -Blood Metastasis is Very Rare.
Clinical Raised ,Expanding, Pigmented Single Ulcer, Small, Oval, Single Ulcer, large, Irregular, with
Picture Skin Lesion. Rolled in Edges Called; Raised Everted Edges, Floor
Rodent Ulcer, Floor Covered Covered with Necrotic Tissue.
with Crust.
Diagnosis Biopsy & Histopathology. Biopsy Involving The Edges. Biopsy Involving The Edges.
Treatment -Surgical Excision with Wide Safe -Surgical Excision with Safe -Surgical Excision with Safe
Margin (5cm). Margin (> 2mm). Margin (1-2cm).
-Regional L.N Excision. -Radiotherapy. -Radiotherapy.
-If MetastasisChemotherapy. -Cryotherapy or Curretage. -Cryotherapy or Curretage.
Prognosis Bad Prognosis. If Early; Cure Rate 100%. Cure Rate 90%.

Criteria of Malignant Transformation of Benign Naevus:

Major Criteria: Minor Criteria:
1- Increase in Size > 5mm. 1- Ulceration & Bleeding.
2- Increase in Pigmentation. 2- Becomes Painful & Indurated.
3- Change in Shape. 3- Hard Enlarged Lymph Node.

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DR. MOHCEN AL. HAJ