Dermatology ✋🏻 Flashcards

1
Q

Basic structure of skin

A
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2
Q

Types of cells of epidermis

A
  • Keratinocytes
  • Dendritic
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3
Q

Layers of keratinocytes

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Keratinocytes are arranged in 5 layers from: below upward

❶ Basal cell layer (stratum basale).
❷ Prickle cell layer (stratum spinosum).
❸ Granular cell layer (stratum granulosum).
❹ Stratum lucidum.
❺ Horny layer (stratum corneum).

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4
Q

what are dendritic cells of epidermis?

A
  • Melanocytes
  • Langerhans
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5
Q

Site of Melanocytes

A

lie in between the basal cells

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6
Q

Function of Melanocytes

A
  • They form melanin from tyrosine under the effect of tyrosinase
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7
Q

Site of Langerhans cells

A
  • lie in between the prickle cells
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8
Q

Function of Langerhans cells

A
  • They act as macrophage & play important role in the immunological processes
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9
Q

Thickness of dermis

A
  • It is 15-40 times thicker than epidermis.
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10
Q

what does the dermis consist of?

A
  • Connective tissue fibers (collagen & elastic fibers)
  • Cells e.g., fibroblasts, mast cells & histocytes.
  • Ground substance

The epidermis is separated from the dermis by a basement membrane zone

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11
Q

what is the function of the dermis?

A
  • It acts as a framework and supports for blood and lymph vessels, nerves, hair follicles, sweat glands & sebaceous glands.
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12
Q

examples of skin appedages

A
  • Hair follicles
  • Sebaceous glands
  • Sweat glands
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13
Q

what does hair consist of?

A
  • dermal hair papilla.
  • hair matrix.
  • hair shaft.
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14
Q

what does a hair follicle undergo?

A
  • undergoes cycles of:
    growth (anagen), regression (catagen) rest (telogen)
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15
Q

what do hair shafts consist of?

A
  • largely consist of dead, terminally differentiated keratinocytes.
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16
Q

what are sebaceous glands associated with?

A
  • Associated with hair follicles (so not found at palms and soles)
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17
Q

Compare between types of sweat glands

A
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18
Q

what do nails consist of?

A
  • Nail plate.
  • Nail bed.
  • Nail folds.
  • Nail matrix.
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19
Q

Nail plate

A
  • is a fully keratinized structure.
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20
Q

Nail matrix

A
  • the germinative epithelium of nail matrix produces the plate.
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21
Q

Nail folds

A

are surrounding the plate proximally and laterally.

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22
Q

Nail bed

A
  • The structures upon which the nail rests is the nail bed.
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23
Q

what is nail growth rate?

A

fingernails: 3 mm/month

toenails: 1 mm/month

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24
Q

what are the functions of skin?

A
  • Protection
  • Heat regulation
  • Excretion
  • Vit D formation
  • Immunology
  • Sensations
  • Reflection of feeling
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25
Protection function of skin
26
heat regulation fuction of skin
- Skin is rich in blood vessels, through their constriction or dilatation heat loss is decreased or increased. - Evaporation of sweat. - Fat in subcutaneous tissue is poor conductor & prevents heat loss
27
**Reflection of internal feeling** function of skin
- Examples of feelings reflected by skin: fear, shame & anger.
28
Immunological function of skin
- Skin plays an important role in the immunological processes.
29
**Formation of Vit D** function of skin
- from ergosterol by ultraviolet rays
30
**Excretion through sweat** function of skin
Examples of which excreted by skin: NaCl, lactic acid, ammonia & some drugs.
31
**Perception of sensations** function of skin
Examples of sensations precipitated by skin: heat, cold, pain and touch.
32
hyperkeratosis
Increased thickness of the horny layer
33
Parakeratosis
- Immature keratinization resulting in retention of nuclei in the cells of the horny layer.
34
Acanthosis
Increased thickness of the prickle cell layer.
35
Spongiosis
- Intercellular oedema in the prickle cell layer
36
Acantholysis
- Loss of coherence between epidermal or epithelial cells.
37
compare between Primary acantholysis & Secondary acantholysis
38
Principles of dermatology diagnosis
- Preliminary History - Examination - Follow up history - Investigations
39
Preliminary history in dermatology
40
Examination in dermatology
- Skin examination must be done in good light. - It should involve oral mucous membrane, hair, nails and lymph nodes. - The following points should be noticed during examination. 1. Distribution 2. Configuration 3. Morphology of individual lesion
41
Types of distribution of the lesion
42
Types of Configuration of the eruption (Mode of arrangement of the lesions)
- Linear - Circinate - Polycyclic (geographic) - Grouped - Discrete - Dermatomal - Koebner phenomenon
43
examples of linear configuration
❶ Lichen planus ❷ Warts ❸ Psoriasis
44
examples of Circinate configuration
❶ Tinea circinata ❷ Pityriasis rosea ❸ Impetigo ❹ Psoriasis
45
examples of Polycyclic (geographic) configuration
❶ Psoriasis ❷ Urticarial
46
examples of Grouped configuration
❶ Warts ❷ Molluscum contagiosum ❸ Herpes simplex.
47
examples of Discrete configuration
- Chicken pox.
48
examples of Dermatomal configuration
❶ Herpes zoster ❷ Dermatomal vitiligo
49
Morphology of the individual lesion
50
examples of Koebner phenomenon configuration
Lesions appear in an area of trauma which is often linear as in: - Psoriasis - plane wart - lichen planus - vitiligo - Molluscum contagiosum.
51
Definition of patch
Macule > 1 cm
52
Definition of Macule
- Circumscribed area of change in skin color without change of its texture up to 0.5 cm in diameter
53
Examples of Macules and patches
54
Definition of **Nodule**
- Similar to papule but deeply seated and > 0.5 cm in diameter
55
How to diffrentiate between purpura and erythema?
56
Definition of **Papule**
- solid palpable elevated lesion up to 0.5 cm in diameter
57
Examples of **Papule**
- Lichen planus, psoriasis, warts, prurigo, molluscum contagiosum
58
Definition of **Plaque**
- Circumscribed area of abnormal skin formed by extension or coalescence of either papules or nodules.
59
Examples of **Nodule**
- Lupus vulgaris, Lepromatous leprosy.
60
Definition of **Cyst**
sac filled with expressible material either liquid or semisolid
61
On looking to a papule describe the following....
**Shape:** flat topped, dome shape, umbilicated, conical, polyangular. **Color:** Skin colored, red, violet, brown, white or yellow. **Surface:** Smooth, rough, scaly, crusty.
62
Examples of **Plaque**
Psoriasis, lupus vulgaris.
63
Examples of **Cyst**
Cystic acne
64
Definition of **Vesicle**
- Localized visible collection of fluid up to 0.5 cm in diameter.
65
Examples of **Vesicle**
- Herpes simplex. - Herpes zoster.
66
Definition of **Bulla**
- Localized visible collection of fluid > 0.5 cm in diameter.
67
Example of **Bulla**
- Bullous impetigo - Pemphigus
68
Definition of **Pustule**
- Localized visible collection of pus. (It may be 1ry lesion)
69
Examples of **Pustule**
- Pustular psoriasis - 2ry to bacterial infection of viral vesicle.
70
Definition of **Crust (scab)**
- Dried fluid (serum, blood. or pus) on the skin surface.
71
Definition of **Scale**
- Flat plate of horny layer formed by accumulation of excess keratin.
72
Characters of scales
- Scales may be dry or greasy, large or small. - It may occur in many inflammatory diseases such as seborrheic dermatitis or psoriasis
73
Definition of **Wheal**
- Evanescent elevated oedematous erythematous lesion. - Evanescent means that the lesion does not persist more than 48 hours.
74
Charaters of **Wheal**
- formed by dermal or dermal & hypodermal edema.
75
what is **Wheal** considered as?
- Wheal is the 1ry lesion of urticaria.
76
Definition of **Comedo**
Plug of keratin and sebum in a dilated pilosebaceous orifice.
77
Characters of **Comedo**
When the plug is Superficial ---> open (black) comedo. Deep ----> closed (white) comedo.
78
What is **Comedo** considered as?
- Comedo is the 1ry lesion of acne vulgaris.
79
Definition of **Burrow (Furrow)**
- Superficial tunnel in the skin caused by mite that appears as black dot at the end of the burrow.
80
Characters of **Burrow (Furrow)**
- It is tortuous, straight or S shaped skin coloured or grayish and 0.5-1.5 cm in length.
81
what is **Burrow (Furrow)** considered as?
- It is the 1ry lesion of scabies.
82
Definition of **Alopecia**
- Loss of hair from a normally hairy area.
83
Types of **Alopecia**
84
Definition of **Erosion**
85
Definition of **Ulcer**
86
Definition of **Excoriation**
87
Definition of **Fissure**
88
Definition of **Lichenfication**
89
Definition of **Atrophy**
90
Definition of **Sclerosis**
91
Definition of **Scar**
92
Types of scars
**Atrophic scar**: with thin and wrinkled skin. **Hypertrophic scar**: with elevated skin
93
Follow up history in dermatology
94
Investegations in dermatology
- Skin biopsy - Dermoscopy - fungus lesions (Wood's light, Culture, M/E) - Patch test - Oral provocation test
95
what is the most common procedure in dermatology investegations?
Skin biopsy
96
Dermoscopy
(epiluminescence) using dermoscope: - Dermoscopes have built-in illumination, and are applied to the skin surface to enhance visibility of subcorneal structures.
97
when is dermoscopy used in dermatology?
❶ Doubtful pigmented lesions ❷ Other lesions such as scabies burrows ❸ Many skin neoplasms
98
Investegations in cases of fungal lesions
- Wood's light - Culture - M/E
99
Culture in cases of fungal lesions
- On Sabouraud's agar media.
100
Microscopic examination in cases of fungl lesions
101
Patch test
102
Oral provocation test
103
what are the advantages of topical therapy in dermatology?
- Topical therapy plays a major role in dermatologic treatment. - It has many advantages, the most important of which is that: ❶ The active agent reaches the lesion directly and in a sufficient concentration ❷ slight or no systemic side effects.
104
Significance of Wood’s light in dermatology
105
Components of topical therapy
Any topical preparation consists of 2 components: ❶ Active agent: e.g., antibiotics, corticosteroids. ❷ Vehicle (base): Vehicles may have some therapeutic effects and sometimes may be used alone without the addition of active agent.
106
Liquid Vehicles
- Example: water, alcohol, Ca hydroxide & glycerin. They are used in the preparation of solutions, lotions, tinctures, paints, creams
107
Vehichles in topical therapy
- **Ideally a vehicle should be:** Non-toxic, non-irritant and non-allergic. - **Forms of Vehicles:** Liquids, powders, creams or ointments.
108
Powder Vehicles
- Usually applied to normal skin folds to reduce friction.
109
Creams
- Semisolid emulsion of oil in water. - They are used in subacute condition
110
Ointments
- Greasy base used for dry hyperkeratotic or lichenified skin disease
111
Gels
- Non-greasy transparent, semisolid emulsions that liquefy on contact with the skin, drying as a thin greaseless, non-staining film. - They are suitable for treating hairy areas
112
Uses of Topical Corticosteroids (TCS)
Topical corticosteroids are commonly prescribed for treatment of many skin diseases including: ❶ Atopic dermatitis ❷ Discoid eczema ❸ Contact dermatitis, seborrheic dermatitis ❹ Psoriasis ❺ Lichen planus ❻ DLE (discoid lupus erythematous) ❼ Vitiligo ❽ Alopecia areata, and many others.
113
Forms of Topical Corticosteroids (TCS)
Topical steroids are available in the form of: - Creams - Ointment - Lotion It can be mixed with salicylic acids, calcipotriene, antifungal, or antibiotics. Many OTC (over the counter preparations) are also available containing TCS, antifungal, and antibacterial.
114
Classification of Topical Corticosteroids (TCS)
115
Examples of Ultrapotent TCS
- Clobetasol propionate 0.05% [Dermovate ®]
116
Examples of Highly potent TCS
- Mometasone furoate 0.1% (Elocon , Elica) - Betamethasone dipropionate (Diprosone)
117
Examples of Moderately potent TCS
- Betamethasone valerate (Betnovate, Betaderm, Betaval)
118
Examples of Moderate/weekly potent TCS
- Hydrocortisone butyrate (Texacort) - Prednicarbate (Dermatop) - Alclometasone dipropionate 0.05% (perderm, weak) - **Hydrortisone acetate (the weakest TCS)**
119
Examples of Combination TCS
- Momenta (contain potent TCS) - Kenacomb, quadriderm, pandermal (contain moderately potent TCS) - Fucicort cream, Fusizon cream (contain moderately potent TCS) - Daktacort (contain hydrocortisone)
120
Side effects of TCS
121
Systemic side effects of TCS
- Growth retardation in children - Iatrogenic Cushing syndrome.
122
what causes side effects by TCS?
- **prolonged use** of more potent steroids especially on: Delicate skin including child skin (any site), face, flexures, and genitalia. - Even hydrocortisone acetate can produce skin atrophy with prolonged use especially on thin skin
123
Prescription of TCS
- TCS are used **once daily** in most of cases. - **Ultrapotent TCS and potent CS** should **not** be **prescribed** by **general practitioner**. - Any type of TCS should **not be prescribed without definite diagnosis**.
124
How does the skin protect itself?
1- Being a dry mechanical barrier. 2- Its acidity. 3- Sebum secretion.
125
What does staphylococci commonly attack?
commonly attack skin appendages. - hair follicles. - sweat glands - periungual tissues.
126
What does streptococci commonly attack?
skin proper
127
Dermal diseases caused by each type of bacteria
128
Definition of non-Bullous (Crusted) impetigo
- Impetigo is a contagious superficial pyogenic infection of the skin - It represents the most common bacterial skin infection in children.
129
Epidemiology (Age) of non-Bullous (Crusted) impetigo
All, but Children are most often affected
130
Etiology of non-Bullous (Crusted) impetigo
- Staphylococcus aureus, - Streptococcus pyogenes (group A B-hemolytic Streptococcus spp.) - or both
131
Predisposing factors for non-Bullous (Crusted) impetigo
1. Hot climate, high humidity, poor hygiene, overcrowding, skin trauma (minor abrasion), malnutrition. 2. Itchy skin diseases such as scabies, pediculosis, and atopic dermatitis. 3. Nasal carriers of S. aureus are at particular risk of developing impetigo.
132
Clinical picture of non-Bullous (Crusted) impetigo
- Shape & Color - Site - Systemic Manifestations - Complication
133
Shape and color of non-Bullous (Crusted) impetigo
Thin vesicles on erythematous base -> pustules rapidly rupture -> thick yellowish-brown crust
134
Site of non-Bullous (Crusted) impetigo
- face, scalp or anywhere except palms & soles
135
Systemic manifestations of non-Bullous (Crusted) impetigo
Fever & regional lymphadenitis in severe cases only
136
Complications of non-Bullous (Crusted) impetigo
- In the legs, thighs, and buttocks the lesion may form thick crust which if removed reveal a purulent irregular ulcer (ulcerative impetigo or ecthyma), that heals after few weeks with scarring - Glomerulonephritis in nephrogenic strains of streptococci
137
Healing (course) of non-Bullous (Crusted) impetigo
Spontaneous cure in 2-3 weeks or persist, The crust dries and separates leaving erythema without scar
138
Etiology of Bullous impetigo
- Staphylococcus aureus
139
Definition of Bullous impetigo
- Impetigo is a contagious superficial pyogenic infection of the skin - It represents the most common bacterial skin infection in children.
140
Epidemiology (age) of Bullous impetigo
All ages, especially newborn and young children
141
Predisposing factors for Bullous impetigo
1. Hot climate, high humidity, poor hygiene, overcrowding, skin trauma (minor abrasion), malnutrition. 2. Itchy skin diseases such as scabies, pediculosis, and atopic dermatitis. 3. Nasal carriers of S. aureus are at particular risk of developing impetigo.
142
Clinical picture for Bullous impetigo
- Shape & Color - Site - Systemic Manifestations - Complication
143
Shape and color of Bullous impetigo
Flaccid bullae (1-5 cm) persist for 2-3 days -> rupture "less rapidly" -> thin brownish crust
144
Site of Bullous impetigo
- Face, trunk buttocks, perineum, axillae & extremities (including palms and soles)
145
Systemic manifestations of Bullous impetigo
Regional adenitis is rare
146
Complications of Bullous impetigo
- Peripheral extension with central healing may give rise to circinate lesion (circinate impetigo)
147
Etiology of Ecthyma (Ulcerative “deep” impetigo)
- Strept (mainly) & staph
148
Healing (course) of Bullous impetigo
- Spontaneous cure in 2-3 weeks or persist. The crust dries and separates leaving erythema without scar
149
Clinical picture of Ecthyma (Ulcerative “deep” impetigo)
150
Treatment of impetigo
- Topical - Systemic antibiotic - Treatment of predisposing factors
151
Topical treatment of impetigo
for mild and localized infection. - Removal of the crust by olive oil. - Antiseptic lotion, e.g., K. permenganate. - Antibiotics, e.g., e.g., Mupirocin 2%, 2% fucidic acid, or neomycin- bacitracin,
152
Systemic antibiotics for treatment of impetigo
- **B-lactamase-resistant penicillin** (e.g.or dicloxacillin or amoxicillin/clavulinic acid) or flucloxacillin 1-1.5gm/d (infant, children 25-50mg/d) - **first-generation cephalosporin** (e.g. cephalexin or cefadroxil). - **Clindamycin or Azithromycin** if the patient is sensitive to penicillin. or erythromycin 1g/d (40mg/kg in infants and children)
153
Dose and indications of antibiotics in impetigo
- They are given for 7-10 days and are indicated in: 1. Extensive lesions. 2. Fever. 3. Regional lymphadenitis. 4. Bullous impetigo. 5. Nephrogenic strain of streptococcal impetigo
154
Treatment of predisposing factors in cases of impetigo
- When pediculosis is present, it should be treated topically after control of impetigo because pediculocidal drugs are toxic, so they are not applied on raw areas.
155
Compare between furunculosis (Boil) & carbuncle in terms of: - Definition - Organism - predisposing factors - Clinical picture
156
Predisposing factors for Furunculosis (Boil)
- Chronic S. aureus carriage (nasal and perianal colonization with S. aureus) - Diabetes mellitus - Seborrhea (increase secretion of sebaceous gland), obesity, poor hygiene, and malnutrition, anaemia. - Immunodeficiency states - Itchy dermatoses - Fatigue and emotional stress
157
Predisposing factors for carbuncles
- Diabetes mellitus. - Malnutrition. - Prolonged steroid therapy.
158
Healing of Furunculosis
- Heal with scar - In some patients, crops of lesions continue to develop for many months or years.
159
What are the complications of furuculosis?
**Cavernous sinus thrombosis, Septicemia, Pyemia** - Boils on the upper lip, bridge of the nose, and maxilla (danger triangle) may lead to cavernous sinus thrombosis if squeezed without incision.
160
Treatment of Furunculosis
161
Treatment of carbuncle
- Penicillinase resistant penicillin. - Surgical incision & drainage of pus.
162
Compare between erysipelas and cellulitis, in terms of: - Definition - How are bacteria reaches the wound? - Clinical picture
163
Treatment of erysipelas and cellulitis
1. **Rest and antipyretic** (usually paracetamol) with leg elevation. 2. **Penicillin** for 10-14 days is the drug of choice. - Aqueous penicilin C: for severe cases 600,000-2000,000 unt IV/6hr. - Oral penicillin: for mild cases 250-500 mg/6hr. For 10days. - Benzathine P: for rec. cases. 1,200,000 U. I.M/2-4ws for ms or ys - Erythromycin: 1-2 gm/day for 10 days. 3. **Erythromycin:** is an alternative therapy for those who are allergic to penicillin. 4. **Antibiotics** that covers both strept and staph are recommended in cellulitis (e.g. dicloxacillin, cephalexin, clindamycin, or combinations).
164
Definition of Streptococcal intertrigo
- Inflammation of skin areas between folds
165
Organism which causes Streptococcal intertrigo
- Group A streptococci
166
Age of Streptococcal intertrigo
- Usually affects infant and young children Obese adults may be also affected
167
Etiology & Site of Streptococcal intertrigo
- The condition is precipitated by continuous friction and irritation in moist, deep skin folds of the neck, axillae, antecubital and popliteal fossae, behind the ears, under the breast, groin, and natal cleft.
168
Differential diagnosis of Streptococcal intertrigo
- Simple intertrigo due to continuous friction in the deep moist fold. - Candida intertrigo (satellite lesions are characteristic) - Flexural psoriasis (characteristic scales) - Erythrasma. - Dermatophyte infection. - Seborrheic intertrigo
169
Clinical picture of Streptococcal intertrigo
- Sharply demarcated **(well-defined)**, intensely **erythematous patches** or thin plaques are observed - May occur in the depth of the affected flexure **especially behind the ears** - **Longitudinal painful fissure** at angle of skin folds, skin around is red, moist and may be crusted
170
Treatment of Streptococcal intertrigo
- Topical antiseptic. - Topical & systemic antibiotic.
171
Clinical picture of angular chelitis
172
Etiology, predisposing factors & treatment of angular cheilitis
173
Definition of erythrasma
- Chronic superficial infection of the skin caused by Corynebacterium minutissimum.
174
Predisposing factors for erythrasma
1- Warm humid climate. 2- Obesity. 3- Diabetes mellitus.
175
Epidemiology of erythrasma
- Affects adults > children.
176
Clinical picture of erythrasma
* Well-defined red brown or brown scaly patches. * Asymptomatic or itchy.
177
Sites of erythrasma
intertriginous areas e.g., groins, axillae, intergluteal clefts, sub mammary areas, or generalized covering the trunk & limbs.
178
Diagnosis of erythrasma
- Wood's light ---> Coral Red Fluorescence.
179
Differential diagnosis of erythrasma
180
Treatment of erythrasma
181
Epidemiology of tuberculosis of the skin
Infects 1/3 world population, since 1998 incidence is increasing due to - AIDS - Diabetes - Immune-Supressed patients - Drug resistance
182
What causes skin tuberculosis?
Mycobacterium tuberculosis
183
Characters of Mycobacterium tuberculosis
Non motile, aerobic, acid-fast bacillus (AFB)
184
Pathology of skin tuberculosis
- Organism gains access to macrophage, replicate then ingested by new macrophages and continue cycle >> Spread >> Specific Tissue reaction (granuloma) > chronicity
185
Mode of Infection by lupus vulgaris
186
Classification of skin tuberculosis
187
What is the most common form of skin tuberculosis?
Lupus vulgaris
188
Onset & Course of lupus vulgaris
- disease usually starts in childhood and progresses very slowly.
189
Lesions of **Lupus vulgaris**
- **Well-defined reddish-brown plaque** composed of **soft nodules that appear yellowish brown (apple jelly nodules)If pressed with a glass slide (Diascopy test)** - The lesion **enlarges slowly over years** with formation of **scar which may contain active nodules**. - The **scars are thick & contractile. (atrophic)**
190
Clinical picture of **Lupus vulgaris**
191
Sites of **Lupus vulgaris**
192
Course of **Lupus vulgaris**
progressive but spontaneous healing may occur.
193
Complications of **Lupus vulgaris**
194
Diagnosis of **Lupus vulgaris**
195
Treatment of **Lupus vulgaris**
196
Definition of **leprosy**
Chronic mycobacterial disease. - primarily affecting peripheral nerves - secondarily involving skin and other tissues
197
Mode of infection by **leprosy**
By Mycobacterium leprae - **Droplet infection** from the oronasal mucosa of patients having lepromatous leprosy. - Susceptible: Children > adults
198
Incubation period of **leprosy**
3-5 years
199
Classification of **leprosy**
Leprosy is classified into 3 types according to: ~ Clinical picture. ~ Histopathological examination of skin lesion. ~ Bacteriological examination of skin smear. ~ Lepromin test
200
What is lepromin test?
- It is an intradermal test using autoclaved lepromatous tissue as antigen.
201
Significance of lepromin test
- The test is positive in person having a high degree of immunity. - It is NOT of diagnostic value, but is valuable in assessment of the prognosis.
202
Types of leprosy
The 3 types of leprosy are: 1. Tuberculoid leprosy (T.T.). (paucibacillary) 2. Borderline leprosy (B.B.). (mullibacillary) 3. Lepromatous leprosy (L.L.). (mullibacillary)
203
Where does **Tuberculoid Leprosy (T.T)** develop?
- develops in persons with good immunity.
204
What tissues are affected in **Tuberculoid Leprosy (T.T)**?
- The skin and peripheral nerves are the only tissues affected.
205
Skin lesions in **Tuberculoid Leprosy (T.T)**
- **Solitary or few (1-5 in number)**. - **Well defined, dry, hairless**, insensitive erythematous or **hypopigmented patch or plaque**. - **Loss of sensation** starts by loss of light touch followed by temperature and finally deep touch. - The lesions occur **anywhere with exception of scalp, axillae, groins & perineum**.
206
where do skin lesions develop in **Tuberculoid Leprosy (T.T)**?
- The lesions occur **anywhere with exception of scalp, axillae, groins & perineum**.
207
Nerve and muscular lesions in **Tuberculoid Leprosy (T.T)**
- The disease may be **purely neural** showing **pain and swelling of the affected nerve.** - The **nerve becomes irregularly, thickened, beaded, tender** - The most frequent affected nerves are **ulnar, median, radial, great auricular and superficial peroneal.** - There are **atrophy of interosseous muscles of the hand, wasting of thenar & hypothenar eminences, contracture of the hands, foot drop & anaesthesia.** - **Repeated trauma and burns to the insensitive limbs** will result in **bone damage and resorption with subsequent mutilations**
208
Histopathology of **Tuberculoid Leprosy (T.T)**
tuberculoid infiltrate of Epithelioid cells & Lymphocytes
209
Bacteriology of **Tuberculoid Leprosy (T.T)**
- Lepra bacilli are absent from skin lesion.
210
Lepromin test of **Tuberculoid Leprosy (T.T)**
is strongly positive indicating high degree of cell mediated immunity
211
Where does **Lepromatous Leprosy (L.L)** Develop?
- develops in person with low immunity.
212
What tissues are affected in **Lepromatous Leprosy (L.L)**?
- skin, mucous membranes, eyes & testes are affected - Nerves affection is late.
213
Skin lesions in **Lepromatous Leprosy (L.L)**
- Consist of **symmetrically distributed multiple papules, nodules, plaques or rarely diffuse infiltration.** - lesions are **shiny erythematous, or of normal skin colour**. - **Hairs and sensations** over these lesions are **not impaired**. - **Exaggeration of the lines of the forehead** occurs, It becomes deeper as the skin thickened. - This, in addition to **thinning or loss of eyebrows** gives rise to a characteristic appearance **(leonine face)** - **Collapse of the nose** may result from septal perforation. - **Ear lobes** may become **thickened**.
214
Mucus membrane lesions in **Lepromatous Leprosy (L.L)**
- **papules and nodules** affecting lips, gums, palate, tongue, uvula & nasal mucosa. - Lesions of the **nasal mucosa** are associated with **epistaxis**.
215
Eye lesions in **Lepromatous Leprosy (L.L)**
Eyes may be involved resulting in - keratitis - iridocyclitis - iris atrophy.
216
Testicle lesions in **Lepromatous Leprosy (L.L)**
if involved will cause - sterility - impotence - gynaecomastia.
217
Histopathology of **Lepromatous Leprosy (L.L)**
dermis contains - foamy histiocytes with large number of leprae bacilli
218
Bacteriology of **Lepromatous Leprosy (L.L)**
Lepra bacilli are present in large number in: - skin lesion - nasal smear
219
Lepromin test result in **Lepromatous Leprosy (L.L)**
Negative
220
Definition of **Border line leprosy (B.B)**
- This type is immunologically unstable and usually evolves into one of the previous types.
221
Clinical picture of **Border line leprosy (B.B)**
- Lesions are intermediate in number between the two polar types. - The lesions are asymmetrically distributed and may take the form of nodules, plaques, annular lesions, and bizarre shaped bands. - Only the skin and nerves are affected.
222
Histopathology of **Border line leprosy (B.B)**
- mixture of lepromatous and tuberculoid changes.
223
Bacteriology of **Border line leprosy (B.B)**
- Lepra bacilli are present in lesions but are fewer in number than in L.L.
224
Lepromin test in **Border line leprosy (B.B)**
- weakly positive or negative.
225
Diagnosis of leprosy
226
Complications of leprosy
227
Treatment of leprosy
228
Types of fungal skin infections
229
What causes dermatophytosis (ringworm or tenia)?
- Dermatophytes
230
What causes superficial mycoses?
231
What causes candidiasis of skin and nails?
Candida species
232
Definition of Dermatophytosis
- **fungal infection of keratinous structures** (stratum corneum of skin, hair and nails) caused by a group of **keratinophilic filamentous fungi called dermatophytes**.
233
Incidence of the previous diseases
Common
234
Pathogenesis of Dermatophytosis
- Dermatophytes are keratinophilic fungi that grow only in dead keratinized tissue of stratum corneum of skin, within & around scalp hair and in nails **because they have keratinase enzyme that able to digest keratin.**
235
Mode of Transmission of Dermatophytosis
236
Etiology of Dermatophytosis
237
Classification of Dermatophytosis
- According to their usual habitat - According to site of infection - Clinically
238
Anthropophilic dermatophytosis
- Associated with humans only - Person to person through contaminated objects (clothes, combs, hats ,brushes and towels)
239
Classification of Dermatophytosis according to their usual Habitat
- Anthropophilic - Geophilic - Zoophilic
240
Organsims causing Anthropophilic dermatophytosis
- Scalp infections like M.audouinii & T.tonsurans. - Foot and nail infections like Epidermophyton &T.rubrum
241
Geophilic dermatophytosis
- Normally inhabit the soil. - Some species may cause infections in animals and man following contact with soil
242
Organisms causing Geophilic dermatophytosis
M.gypseum
243
Classification of dermatophytosis, according to the site of infection
- Agents of hair - Agents of skin - Agents of nails
244
Zoophilic Dermatophytosis
- Associated with animals, Transmitted directly to humans by close contact with animals. - Not from human to human
245
Organisms causing Zoophilic Dermatophytosis
1- microsporum canis (cats, dogs) 2- M.Equinium (hourses) 3- Trichophyton Verrucosum (cattle)
246
Agents of hair dermatophytosis
1. Trichophyton 2. Microsporum
247
Agents of skin dermatophytosis
1. Trichophyton 2. Microsporum 3. Epidermophyton
248
Agents of nail dermatophytosis
1. Trichophyton 2. Epidermophyton (rarely microsporum)
249
Clinical classification of dermatophytosis
250
What characterizes tinea capitis?
- Disease of children mainly, but it may affect adults also. - There are 4 types of tenia capitis
251
What characterizes T. Manum?
- Palms are diffusely dry, scaly & erythematous
252
What characterizes T. Corporis?
- Non hairy, smooth skin (trunk-back dorsum of hand)
253
What characterizes T.pedis?
Lesion: include fissures, scales, maceration in toe web &scaling of sole **(athlete's foot)**
254
What characterizes T.ungium?
- children mainly, may affect adults - Nails are thickened, discoloured, lusterless & broken. - Nail plate may separate from nail bed aka (onycholysis)
255
Sample used in diagnosis of dermatophytosis
- skin scrapping, nail scrapping or clipping, epilation of short length of affected hair.
256
Direct diagnosis of dermatophytosis
- Direct microscopy - Culture - Hair perforation test
257
Direct microscopy of dermatophytosis
258
Direct microscopy of hair in Dermatophytosis
259
Culture of Dermatophytosis
260
Stain for Dermatophytosis
Lactophenol cotton blue (LPCB)
261
Interpretation of hair perforation test
262
What does hair perforation test differentiate?
It may be helpful in differentiation of T. mentagrophytes from T. rubrum
263
Indirect diagnosis of Dermatophytosis
- molecular diagnosis - Serology
264
PCR diagnosis of dermatophytosis
PCR: detects fungal DNA frorn infected lesion. Also, species-specific primers are available.
265
Does Serology have a role in diagnosis of Dermatophytosis?
- No role of serology in diagnosis X X. (Because it's a localized infection)
266
Definition of wood’s light
267
Wood’s Light
268
Where do skin infections by candida occur?
- Skin infection usually occur on **sites that becomes abnormally moist warm area** as axilla, groin, submammary fold and toe clefts. - (In infant >>napkin dermatitis).
269
Clinical manifestations of skin infection by candida
270
Sites of nail infection by candida
- Usually finger or toe webs - Nail folds paronychia - Nail's onychia.
271
Clinical manifestations of nail infection by candida
272
Laboratory diagnosis of skin and nail infections caused by candida
273
Culture of candida
- Sabouraud's dextrose - CHROMagar Candida medium - Germ tube formation - Chlamydospores formation - Analytical profile index (API)
274
Culture of candida on SDA
- On Sabouraud's dextrose agar at 25 or 37"C for 2 days
275
Identification of growth of candida On SDA
276
CHROMagar candida Medium
277
Germ tube formation
278
Chlamydospores formation
279
analytical profile index (API)
280
Types of superficial mycoses
281
Definition of Pityriasis Versicolor
Superficial chronic infection of Stratum corneum
282
What causes hypopigmentation in Pityriasis Versicolor?
Discolouration is caused by inhibition of tyrosinase enzyme. (Used in melanin synthesis).
283
The diagnosis of Pityriasis Versicolor
10-30% KOH: clusters of round yeast cell along non branched hyphae **(spagetti & meat balls appearance)**
284
Etiology of Pityriasis Versicolor
- Malassezia furfur (Pityrosporum orbiculare) (Lipophilic yeast). - Present as normal flora in area rich in sebaceous gland.
285
Clinical picture of Pityriasis Versicolor
286
Etiology of T.Nigra
- hortae (Exophiala) wernekii (pigmented) - Frequent in tropical areas
287
Clinical picture of T.Nigra
288
Definition of T.Nigra
Brownish maculae on palms, fingers, face.
289
Site of Black Piedra
Fungal infection of the scalp hair
290
Diagnosis of T.Nigra
- Microscopic examination: Septate hyphae and yeast cells (brown in color) - Culture: black colonies.
291
Etiology of Black Piedra
Piedraia hortae
292
Frequency of Black Piedra
Frequent in tropical areas
293
Clinical picture of Black Piedra
294
Site of white Piedra
Fungal infection of facial, axillary or genital hair.
295
Etiology of white Piedra
trichosporon (yeast)
296
Frequency of white Piedra
- Frequent in tropical and temperate zones
297
Clinical picture of white Piedra
298
What is the most common pathogen of fungal infections of nails?
- Dermatophytes are the most common causative pathogen especially Trichophyton rubrum (about 70%). Other causes than dermatophytes include candida
299
Antifungal drugs
300
Absorption of **Amphotericin B**
- poorly absorbed from the GIT and is usually administered IV
301
Category of **Amphotericin B**
B
302
MOA of **Amphotericin B**
- Amphotericin B binds ergosterol in fungal cell membrane >> form pores in cell membrane >>>cell content leak out>>> cell death
303
Pharmacokinetics of **Amphotericin B**
304
Side effects of **Amphotericin B**
305
Forms of **Nystatin**
available as suspension, ointment, cream, powder and tablet (tablet for local use)
306
Uses of **Nystatin**
- only topically in Candida infections.
307
Other Uses of **Nystatin**
308
Side effects of **Nystatin**
- They include nausea and bitter taste. - Category A in pregnancy
309
Category of **Nystatin**
- Category A in pregnancy
310
Examples of Azoles
**Topical:** - Miconazole - Clotrimazole **Systemic:** - Ketoconazole - Fluconazole
311
Uses of Miconazole & Clotirazole
They are used topically for - Dermatophytic (tinea) - Candida infections.
312
Forms of Miconazole & Clotirazole
They are available as - cream, gel, lotion - solution, spray - vaginal pessary, etc. - Clotrimazole lozenge is also available.
313
Characters of **Ketoconazole**
- It is orally effective - Ketoconazole is the most toxic among azoles, but it is less toxic than amphotericin B.
314
Side effects of **Ketoconazole**
315
Administration of **Fluconazole**
For oral and i.v. administration
316
Indications for **Fluconazole**
Fluconazole is a drug of choice in - esophageal and - oropharyngeal candidiasis. A single oral dose usually eradicates vaginal candidiasis.
317
Drug interactions of azoles
- All azoles inhibit the hepatic CYP450 3A4 isoenzyme to varying degrees. - Patients on concomitant medications that are substrates for this isoenzyme may have increased concentrations and risk for toxicity (e.g warfarin).
318
Contraindications of azoles
- Azoles are considered teratogenic, and they should be avoided in pregnancy unless the potential benefit outweighs the risk to the fetus
319
Uses of **Terbinafine**
320
Side effects of **Terbinafine**
321
Side effects of **Griseofulvin**
disulfiram-like reaction
322
Uses of **Griseofulvin**
- Active only against dermatophytes (orally,not-topically) - by depositing in newly formed keratin and disrupting microtubule structure
323
MOA of **Echinocandins** (Caspofungin & other fungins)
Inhibit the synthesis of beta-1,2 glucan
324
Uses of **Echinocandins**
- A critical component of fungal cell walls (not membrane) - Back-up drugs given IV for disseminated and mucocutaneous Candida infections or invasive aspergillosis - Monitor liver function
325
What are the most commonly used antifungal drugs for oral candidiasis?
- Clotrimazole, nystatin and fluconazole
326
Antifungal drugs used in pregnancy
- Nystatin and amphotericin B can be used in pregnancy but azoles are better avoided
327
What are antifungal drugs used in systemic fungal infections?
Azoles, amphotericin B and caspofungin
328
Indication of Topical azoles
dermatophytes and candida
329
Indication of Amphotericin B
systemic fungal infection
330
Indication of Fluconazole
- esophageal &oropharyngeal candidiasis - vaginal candidiasis
331
Indication of Griseofulvin & Terbinafine
- dermatophytes only
332
Indication of Echinocandins
- Disseminated candidiasis - mucocutaneous candidiasis - Invasive aspergillosis
333
Indication of Nystatin
- candidal infection
334
Route of adminstration of Amphotericin B
IV infusion
335
Route of adminstration of Ketoconazole & griseofulvin
Oral
336
Route of adminstration of Fluconazole
Oral & IV
337
Route of adminstration of Echinocandins
IV
338
Superficial fungal infections
**Dermatophyte infections (Tinea):** Caused by one of the three genera of dermatophyte - microsporum - Trichophyton - Epidermophyton. **Pityriasis versicolor:** Caused by malassezia furfur which is the pathogenic form of normal skin flora pityrosporum orbiculare *(yeast-like)* **Candidiasis (moniliasis):** Caused by candida (*yeast* reproduce by budding)
339
Definition of dermatophyte infections
- These are fungi which have the ability to produce infection of the keratinized tissues as the skin, hair and nails.
340
Diagnosis of dermatophyte infections
341
Clinical types of **dermatophyte infections**
342
Mode of infection by **dermatophyte infections**
343
Definition of **T. Capitis**
- Dermatophyte infection of the scalp.
344
Clinical picture of **T. Capitis**
- Tinea capitis is mainly a disease of children, but it may affect adults.
345
Types of **T. Capitis**
There are 4 types of tinea capitis: - Scaly - Blak dot - Kerion (Inflammatory type) - Favus
346
# M.AC What causes **Scaly type of T.Capitis**?
- Microsporum audouinii & - Microsporum canis.
347
CP in **Scaly type of T.Capitis**
348
# T. TV What causes **Black dot T.Capitis**?
- Trichophyton tonsurans - Trichophyton violaceum.
349
CP of **Black dot T.Capitis**
350
What causes the presence of black dots in **Black dot T.Capitis**?
Due to breaking of hair shafts at the skin surface.
351
What causes **Kerion T.Capitis**?
animal fungi
352
Presentations of **Kerion T.Capitis**
There are two presentations: - Abcess like swelling - Well defined dull red plaque studded wit multiple pustules
353
CP of abcess-like swelling of kerion T.Capitis
354
What causes favus T.Capitis?
**Trichophyton schoenleinii**
355
CP of Favus T.Capitis
356
What is a **Scutulum**?
- A scutulum is a concave yellow crust surrounding the hair follicle opening and has a mousy odour
357
Diffrential diagnosis of **T.Capitis**
358
Preventive measures of **T.Capitis**
359
Treatment of **T.Capitis**
360
Mode of Infection by **T.Barbae**
- From man to man through infected towels or in the barber's shop. - Infected animals transmit infection to farmers.
361
Definition of **T.Barbae**
Dermatophyte infection of the beard and moustache areas of adult male.
362
CP of **T.Barbae**
363
DD of **T.Barbae**
364
TTT of **T.Barbae**
Similar to tinea capitis.
365
Definition of **T.Corporis**
- Tinea corporis is a dermatophyte infection of the (glabrous skin) of the trunk and extremities, excluding the hair, nails, palms, soles and groin.
366
Mode of infection by **T.Corporis**
1. Infected Person 2. Infected Animals (domestic animals) or soil-to-human spread. 3. Autoinoculation (from tinea capitis or pedis).)
367
CP of **T.Corporis**
368
Diagnosis of **T.Corporis**
- Scraping & M.E: scraping is done from the raised border of the lesion >>>> Spores & hyphae - Culture: on sabouraud's agar media
369
Def of **T.Cruris**
- Dermatophyte infection of the groins.
370
DD of **T.Corporis**
371
TTT of **T.Corporis**
372
Mode of infection by **T.Cruris**
- Auto inoculation. - Sharing cloths & towels.
373
Predisposing factors for **T.Cruris**
374
CP of **T.Cruris**
375
Diagnosis of **T.Cruris**
- Scraping,ME - culture
376
DD of **T.Cruris**
377
TTT of **T.Cruris**
Similar to T. Circinata
378
Def of **T.Pedis**
379
Predisposing factors for **T.Pedis**
1. Excessive use of water. 2. Hyperhidrosis. 3. Wearing occlusive shoes for long periods. 4. Hot weather. * All these conditions cause damage (maceration) of the skin and allow invasion and growth of dermatophytes.
380
What is the most common form of dermatophyte infections?
**Tinea Pedis**
381
CP of **T.Pedis**
3 types: - Interdigital T. pedis - Scaly hyperkeratotic type - Vesiculo-bullous type
382
Epidemiology of **T.Pedis**
Common in adults than children and in males than females.
383
What is the most common form of **T.Pedis**?
Interdigital T. pedis:
384
CP of **Interdigital T.Pedis**
385
CP of **Scaly Hyperkeratotic T.Pedis**
386
CP of **Vesiculo-Bullous T.Pedis**
387
Diagnosis of **T.Pedis**
- Scraping, ME - Culture
388
DD of **Interdigital T.Pedis**
389
DD of **Scaly Hyperkeratotic T.Pedis**
390
DD of **Vesiculo-Bullous T.pedis**
391
TTT of **T.Pedis**
392
Def of **T.Manum**
Dermatophyte infection of the palmar skin.
393
Mode of infection by **T.Manum**
1. Infected human 2. infected animal. 3. Auto inoculation (from tinea pedis).
394
Predisposing factors of **T.Manum**
- Trauma and maceration between fingers. - Poor peripheral circulation.
395
CP of **T.Manum**
396
DD of **T.Manum**
397
TTT of **T.Manum**
Similar to T.Pedis
398
Def of **Onchyomycosis (T.Unguium)**
- Onychomycosis is a fungal infection of the nails. - More than 50% of cases of nail dystrophy is due to onychomycosis
399
MOI by **Onchyomycosis (T.Unguium)**
- The fungus invades the nail plate from the lateral nail fold or from the free edge. - Nail infections may be the only manifestation of fungus disease in a patient or in greater majority of cases they are associated with other types of dermatophyte infection
400
What attributes to 50% of cases of nail dystrophy?
onychomycosis
401
Predisposing factors for **Onchyomycosis (T.Unguium)**
1- Trauma to the nail. 2. Poor peripheral circulation. 3. Old age, where the linear growth of nail is slow.
402
CP of **Onchyomycosis (T.Unguium)**
403
Diagnosis of **Onchyomycosis (T.Unguium)**
- Nail clipping is put in 5% KOH solution for 24 hours then examined under microscope for fungus - culture
404
DD of **Onchyomycosis (T.Unguium)**
405
TTT of **Onchyomycosis (T.Unguium)**
406
Topical antifungals for dermatophyte infections
407
Systemic antifungals for dermatophyte infections
408
Def of **Pityriasis Versicolor**
- Mild, Chronic superficial fungus infection of the horny layer of the skin caused by Malassezia furfur
409
What causes **Pityriasis Versicolor**?
**Malassezia furfur** (Pathogenic form of the normal skin flora, pityrosporum orbiculare).
410
Predisposing factors of **Pityriasis Versicolor**
411
Clinical picture of **Pityriasis Versicolor**
412
Epidemeology of **Pityriasis Versicolor**
Common skin disease, affecting adults more than children.
413
Site of **Pityriasis Versicolor**
- Any site however the commonest sites affected are **trunk, neck & upper arms**, Face is commonly affected in children
414
Diagnosis of **Pityriasis Versicolor**
415
Course of **Pityriasis Versicolor**
- Spontaneous remission may occur in winter & recurrence usually occurs in summer - Healing may occur with hypopigmented macules which may disappear spontaneously or persist indefinitely.
416
DDx of **Pityriasis Versicolor**
417
TTT of **Pityriasis Versicolor**
Topical & Systemic
418
Topical TTT of **Pityriasis Versicolor**
419
Systemic TTT of **Pityriasis Versicolor**
420
Def of **Candidiasis (Monaliasis)**
- Infection of the skin or mucous membranes by candida albicans.
421
What causes **Candidiasis (Monaliasis)**?
Candida albicans
422
Predisposing factors of **Candidiasis (Monaliasis)**
423
CP of **Cutaneous Candidiasis (Monaliasis)**
- Intertdigital candidiasis - Candidal intertrigo - Napkin candidiasis
424
Napkin Candidiasis
425
Candidal intertrigo
426
Interdigital candidiasis
427
Bacterial co-pathogen usually preset in the interdigital,intertrigenous types
..
428
Where is Candidal paronychia common?
- Common in housewives, cooks and those whose hands are frequently immersed in water.
429
CP of Candidal onychia
430
CP of Candidal paronychia
431
What are types of **Mucosal candidiasis**?
- Oral Candidiasis - Candidal vulvovaginitis - Candidal balanitis
432
Forms of **Oral candidiasis**
- oral thrush - Acute atrophic type - Chronic atrophic type (Denture stomatitis) - Chronic Hyperplastic leukoplakia -->Black hairy tongue - Angular Cheilitis (perleche) - Candidal Cheilitis
433
Oral thrush
434
Acute atrophic type of oral candidiasis
435
Chronic atrophy type (dentures stomatitis) of oral candidIasis
436
Angular cheilitis (Perleche)
437
Chronic hyperplastic type (candidal leukoplakia) & black, hairy tongue
438
Candidal cheilitis
439
CP of Candidal vulvovaginitis
440
CP of candidial balanitis
441
TTT of candida
- TTT of predisposing factors - Topical - Systemic
442
Topical TTT of Candida
443
Systemic TTT of Candida
444
What are viral skin diseases?
- Herpes Simplex. - Chicken pox. - Herpes Zoster. - Warts. - Molluscum contagiosum. - Pityriasis Rosea
445
What is the most common recurrent viral infection of skin and mucus membranes?
- Herpes Simplex
446
Etiology of **herpes simplex**
- H. virus type I: affects the skin and mucous membranes. - H. virus type II: affects the genitals.
447
Mode of infection by **herpes simplex**
Direct inoculation.
448
Characters of Primary **herpes simplex**
- Lesions are usually minimal or subclinical. - Develops in persons without pre-existing immunity to HSV - Severe cases occur in patients with immune defect, malignancy, malnutrition or atopic dermatitis.
449
CP of **herpes simplex**
- Two types are recognized primary and recurrent.
450
Lesions of primary **herpes simplex**
usually minimal or subclinical.
451
In what kind of people do primary lesion of **herpes simplex** Appear?
- Develops in persons without pre-existing immunity to HSV - Severe cases occur in patients with immune defect, malignancy, malnutrition or atopic dermatitis.
452
Incidence of **Gingivostomatitis**
- The commonest form - Most cases occur in infants and young children
453
CP of **Gingivostomatitis**
454
Lesion of **Gingivostomatitis**
- The gums are swollen, red and easily bleed. - Vesicles rupture forming white erosions with red areola on oral mucosa
455
Systemic manifestations of **Gingivostomatitis**
- High fever, malaise, dribbling, painful eating and foul breath
456
Site of **Gingivostomatitis**
457
LNs affection in **Gingivostomatitis**
- Regional LNs (Submental) are enlarged and tender
458
CP of **Keratoconjunctivits**
459
Course of **Gingivostomatitis**
- After 3-5 days fever subsides and complete recovery occurs in about 2 weeks
460
Lesions in **Keratoconjunctivits**
Conjunctivitis and keratitis - The eye lids are edematous - There may be vesicles on the surrounding skin
461
Site of **Keratoconjunctivits**
462
LNs affection in **Keratoconjunctivits**
Regional LNs (preauricular) are enlarged and tender
463
Complications of **Keratoconjunctivits**
It may cause corneal ulcer that leave scar which may result in impairment of vision. (Because it heals by fibrosis)
464
Incidence of **Inoculation HS**
- Commonly seen in dentists and nurses
465
Lesions in **Inoculation HS**
**Painful vesicles** - E.g., Herpetic whitlow: painful vesicles on fingertips that may be seen in young children, dentists and nurses (HSV1)
466
What is the clue to diagnosis in **Inoculation HS**?
Recurrences in the same location
467
Site of **Inoculation HS**
- Any site, but mainly on finger tips (classical site) - Inoculation may occur on the face, scalp and trunk in the form of multiple crops of vesicles on plaques of erythema and oedema.
468
What are Lesions of HS in **Eczema Herpeticum** complicated by?
Occasionally complicated by - bacterial superinfections or - systemic dissemination of HSV infection
469
Lesions of HS in **Eczema Herpeticum**
Lesion of H.S. may appear - on the top of atopic dermatitis or - may be generalized.
470
Lesions of primary infection by Gental HS?
- Vesicles which rapidly rupture forming erosions and painful white plaques on a red oedematous mucous membranes
471
Site of primary infection by Gental HS
- are seen in the genitals of both sex. - other sites include buttocks and perineum in both sexes - cervix in women.
472
LNs Affection in primary infection by Gental HS
- Inguinal lymph nodes are enlarged and tender.
473
Complication of primary infection by Gental HS
- Genital H.S. in homosexual suffering from AIDS may present with chronic perianal ulceration.
474
Latency of HS
- virus may remain hidden in a latent form within the sensory ganglion and sensory nerve which supply the infected area.
475
Reactivation of HS
- May occur without any reason(spontaneously), but may follow the following precipitating factors: 1. Fever: influenza, pneumonia, malaria & meningococcal meningitis. 2. R.T.I (resp tract infection) 3. Mechanical trauma. 4. Sun exposure. 5. Emotional stress.
476
CP of reactivated HS
477
Sites of Reactivated HS
- Usually **around orifices especially around the mouth.** - However, they can be situated anywhere on the body. - **2ry leukoderma** may develop in site of lesion. - A characteristic feature of the disease is that it is **recurrent with reappearance of the vesicles on or near the same site.**
478
Course of Reactivated HS
- The vesicles dry forming crust and healing occurs without scar within 7-10 days.
479
Complications of Reactivated HS
480
TTT of Reactivated HS
481
Etiology of **Chicken Pox (Varicella)**
- Varicella is the primary infection with varicella-zoster virus.
482
MOI by **Chicken Pox (Varicella)**
- Droplet infection from the nasopharynx (main route). - Direct contact with the vesicular fluid.
483
IP of **Chicken Pox (Varicella)**
10 - 20 days. *around from 2 wks to 3 wks*
484
Infectivity period of **Chicken Pox (Varicella)**
- 2 days before and 8 days after the rash onset (when all vesicles have been crusted).
485
CP of **Chicken Pox (Varicella)**
486
Ages affected by **Chicken Pox (Varicella)**
children more than adults.
487
Prodorma in **Chicken Pox (Varicella)**
- absent or 1-2 days of fever & malaise.
488
Lesions in **Chicken Pox (Varicella)**
489
Sites of **Chicken Pox (Varicella)**
- Trunk (centripetal), face, scalp and limbs. - Oral mucosa especially palate may contain vesicles.
490
**Chicken Pox (Varicella)** In Immunocomprimised patients
491
Diagnostic Criteria in **Chicken Pox (Varicella)**
1. Rapid onset. 2. Polymorphic lesions: The presence of lesions in all stages of development is a hallmark of varicella. 3. Centripetal distribution (more profuse on the trunk than extremities).
492
Complications of **Chicken Pox (Varicella)**
493
TTT of **Chicken Pox (Varicella)**
symptomatic TTT & Systemic Anticirals
494
Symtomatic TTT of **Chicken Pox (Varicella)**
Required for most children (immunocompetent) (no specific treatment) - Antipyretic for fever:(avoid salicylate). - Antihistamine for itching. - Antibiotic for secondary infection. - Topical antiseptic.
495
Systemic TTT of **Chicken Pox (Varicella)**
- Acyclovir or Valacyclovir (which must be given within 24-72 hours of onset of lesion).
496
Indications of Systemic TTT in **Chicken Pox (Varicella)**
- Immunocompromised patients . - Varicella in pregnant woman. - Severe varicella in immunocompetent children - Neonatal varicella (Acyclovir IV Infusion)
497
Prophylaxis from **Chicken Pox (Varicella)**
- Varicella-zoster immune globulin: immediate post exposure prophylaxis - Live attenuated varicella vaccine (Varivax®): routine vaccination (active immunity).
498
TTT of pregnant woman with **Chicken Pox (Varicella)**
- **IV acyclovir** * women who are not immune to varicella but are exposed may be treated with VZIG
499
Category of acyclovir
**Category B** - Safe in pregnancy(category B) Fetal risk not demonstrated in animal studies but there are no controlled studies in pregnant women, or animal reproduction studies have shown an adverse effect that was not confirmed in controlled studies in women during first trimester and there is no evidence of risk in later trimesters)
500
TTT of infant with **Chicken Pox (Varicella)**
- Infants whose mothers develop varicella 5 d. before delivery or 2 d. following delivery should receive VZIG after birth. - Infants who develop varicella during the first 2 w. of life should be treated with IV acyclovir.
501
Dose of VZIG in **Chicken Pox (Varicella)**
502
Def of **Herpes Zoster (shingles)**
- Acute condition characterized by grouped vesicles along course of sensory nerve.
503
Etiology of **Herpes Zoster (shingles)**
**Varicella zoster virus** - Latency: H.Z. results from reactivation of latent virus that persists in sensory ganglia after recovery from chicken pox.
504
Predisposing factors for **Herpes Zoster (shingles)**
HZ usually affects healthy persons, but it might be precipitated by one of the following: - Immunosuppressive states by disease as AIDS or drugs - Local trauma (to spinal cord)or pressure (usually trivial) - Radiotherapy - malignancy.
505
Is HZ a STD?
No
506
CP of **Herpes Zoster (shingles)**
- Fever, headache, malaise - Neuralgic pain : 1st symptom - Lesions - regional lymph nodes are tender and affected
507
Neurologic pain of **Herpes Zoster (shingles)**
- It is localized to areas supplied by one or more sensory nerves. - May precede eruption by 1 week - The severity of pain increases in old age & may be absent in children. (Pain is proportional to age)
508
Lesions in **Herpes Zoster (shingles)**
- A characteristic feature of the disease is that it is nearly always **unilateral** - Along the distribution of one or more of sensory nerves **(dermatomal distribution)** - The lesion appears in the form of **several groups of vesicles on an erythematous(red) base** arranged in a continuous or interrupted band. - The **early vesicles contain clear fluid**, but after few days the contents **become turbid** and **dry to form crust** which usually **separates within 2-4 weeks**. - **Edematous papules and plaques may precede the appearance of vesicles**, and **progression to pustules or bullae can occur**
509
Complications of **Herpes Zoster (shingles)**
510
Sites of lesions of **Herpes Zoster (shingles)**
- The most common sites affected are thoracic area followed by cervical, trigeminal (including ophthalmic branch) and lumbosacral areas.
511
Special types of **Herpes Zoster (shingles)**
* Abortive * Gangrenous * Haemorrhagic * An eruption of varicella with HZ
512
TTT of **Herpes Zoster (shingles)**
- Topical - Systemic - TTT of PHN
513
Topical TTT of **Herpes Zoster (shingles)**
- antiseptic, antibiotic.
514
Systemic TTT of **Herpes Zoster (shingles)**
- Must be given within 7 days after the onset of skin lesions. - Acyclovir, Famciclovir and Valacyclovir
515
Indications of Systemic TTT of **Herpes Zoster (shingles)**
- Patient older than 50 years. - Immunocompromised patients. - Ophthalmic zoster. - Ramsay Hunt syndrome. - Antibiotic: For neuralgic pain: (Tegretol 200-800mg/d, tryptizol 25-100mg/d, neurosurgical advice)
516
TTT of PHN
- Gabapentin (Neurontin® or pregabalin) - Tricyclic antidepressants (CA) as Amitriptyline (tryptizol 25-100mg/d) and nortriptyline. - Carbamazepine(Tegretol 200-800mg/d) - Other lines: lidocaine patches, narcotic analgesics, and nerve blocks + Neurosurgical advice
517
Def of **Pityriasis Rosea**
- Pityriasis rosea is an acute self-limiting skin disease, characterized by distinctive skin eruption.
518
Etiology of **Pityriasis Rosea**
May be viral
519
Epidemeology of **Pityriasis Rosea**
- More common in young adults (children & young adult) (power) - More common in autumn and spring.
520
Types of **Pityriasis Rosea**
- Classic - Special types
521
Manifestations of classic type of **Pityriasis Rosea**
522
Sites of the **Classic type of Pityriasis Rosea**
- trunk, neck & proximal parts of extremities. - However, involvement of the face and scalp is common especially in children.
523
Course of **Pityriasis Rosea**
- spontaneous remission usually occurs in 4-6 weeks with exception of some cases which persist for longer period. - Temporary hyper or hypopigmentation may follow resolution of the lesions.
524
Special types of **Pityriasis Rosea**
1. Abortive type: Herald patch is not followed by the secondary eruptions. 2. Inverted type: eruption is restricted to extremities and face with sparing of trunk. 3. Localized: one area 4. Generalized: trunk, extremities, face 5. Pityriasis circinate et marginate: few, large, ingroin or axilla, maybe confluent, persist for months
525
DDx of **Pityriasis Rosea**
526
TTT of **Pityriasis Rosea**
- Reassurance. - Avoid soap, hot bath and woolen clothing. - Antihistamines for itching. - Antipruritic topical agent or mild steroid for irritable lesions. - UVR.
527
Def of **Warts**
- Benign, usually self-regressing infectious new growth of the skin and adjacent mucous membranes caused by human papilloma virus (HPV).
528
Recurrence in **Warts**
- Recurrence is common even after treatment due to the presence of HPV DNA in the normal-appearing skin surrounding HPV-associated lesions.
529
MOI by **Warts**
530
Clinical types of **Warts**
1. Common warts (Verrucae vulgares) 2. Plane wart. 3. Plantar wart. 4. Filiform wart. 5. Digitiform wart. 6. Genital wart (Condyloma acuminatum).
531
Compare between Common & Plane warts
532
Lesions in **plantar (and palmar) warts**
533
Compare between Filiform & Digitiform warts
534
Sites of **plantar (and palmar) warts**
pressure areas of the soles or palms.
535
DDx of **plantar (and palmar) warts**
536
Def of **Genital warts (Condyloma accuminata)**
- Genital HPV is the most common STDs in western countries. - Nonsexual transmission is possible (during labor, autoinoculation or spread from nearby nongenital site). - In children, sexual abuse must be excluded.
537
Lesions in **Genital warts (Condyloma accuminata)**
- Begin as small elongated red soft papule, often pedunculated. - The papule enlarges in size and divides at its free margin into lobules giving malodorous cauliflower-like masses with dry surface. - Subclinical infection is common.
538
Sites of **Genital warts (Condyloma accuminata)**
- External genitalia and the perineum, perianally. - Lesions may extend into the vagina, cervix, urethra, or anal canal
539
Resolving of **Genital warts (Condyloma accuminata)**
- May resolve spontaneously but may persist in 10-30% of cases.
540
Oncogenic potential of HPV
- Persistent infection with HPV types with high oncogenic potential, is the major cause of cervical cancers and a subset of vaginal, vulvar, penile, anal and oropharyngeal neoplasias
541
DDx of **Genital warts (Condyloma accuminata)**
542
TTT of **Warts**
Because of the benign and self-limited nature of warts, aggressive treatments that cause scarring should be avoided especially in children - Electrocautery - Cryotherapy - Chemicalcautery - Others
543
Elctrocautery in **Warts**
- Used in painful and resistant warts, but carries risk of scarring. - NOT used in 1. plantar wart 2. larger wart more than 1cm 3. warts on the small joints of toes and fingers 4. large periungual warts (nail dystrophy).
544
Cryotherapy in TTT of **Warts**
- Using coz snow or liquid nitrogen, cause destruction by freezing
545
Chemical Cautery in TTT of **warts**
546
Other methods used in TTT of warts
547
TTT of **Anogenital wart**
548
TTT of **Planter wart**
Salicylic acid, if multiple use formalin
549
TTT of **Common wart**
Salicylic acid, Imiquimod
550
TTT of **Condyloma Accuminata**
Podophyllin, if resistant use interferon
551
TTT of **Plane wart**
Retinoic topical, Imiquimod
552
TTT of **Resistant & Multiple warts**
Levimizole
553
TTT of **Anogenital wart**
Imiquimod
554
Prevention of **Warts**
proactive vaccine for genital HPV infection
555
Def of **Mulluscum Contagiousm**
- Molluscum contagiosum is a pox virus skin infection caused by Molluscum Contagiosum virus (MCV) with characteristic shiny pearly-white umbilicated papules.
556
MOI by **Mulluscum Contagiousm**
- Contact with patient or contaminated objects - Auto inoculation.
557
CP of **Mulluscum Contagiousm**
558
Course of **Mulluscum Contagiousm**
- Spontaneous regression may occur in some lesions within 6-9 months.
559
Sites of **Mulluscum Contagiousm**
- Face, trunk, and genital areas are the sites of predilection. - However, any site may be affected.
560
TTT of **Mulluscum Contagiousm**
561
Classes of **Antiretroviral drugs**
- Nucleoside Reverse Transcriptase Inhibitors (NRTIs) - Non-nucleoside Reverse Transcriplase Inhibilors NNRTIs) - Protease Inhibitors (Pls)
562
MOA of **Nucleoside Reverse Transcriptase Inhibitors (RTIs)**
563
Examples of Nucleoside Reverse Transcriptase Inhibitors (RTIs)
**Nucleoside Reverse Transcriptase Inhibitors (NRTIs):** - Zidovudine [Azidothymidine (AZT)] **Other Nucleoside Reverse Transcriptase Inhibitors (NRTIs):** - Didanosine, Stavudine, Emtricitabine and Lamivudine
564
Uses of **Zidovudine [Azidothymidine (AZT)]**
565
AE of **Zidovudine [Azidothymidine (AZT)]**
**The common side effects:** - Bone marrow suppression, anaemia and neutropenia. **Initial stages of therapy commonly seen:** - Nausea, vomiting, abdominal discomfort, headache, and insomnia **Long-term therapy:** - May cause hepatotoxicity, myopathy with fatigue and lactic acidosis.
566
Uses of **Didanosine, Stavudine, Emtricitabine and Lamivudine**
- They are effective orally. - Lamivudine is a commonly used agent in antiretroviral therapy because of its efficacy and low toxicity.
567
AE of **Didanosine, Stavudine, Emtricitabine and Lamivudine**
1- peripheral neuritis 2- pancreatitis, gastrointestinal disturbances 3- lactic acidosis 4- skin rashes, etc.
568
Examples of **Non-nucleoside Reverse Transcriplase Inhibilors NNRTIs)**
Nevirapine & Efavirenz
569
MOA of **Non-nucleoside Reverse Transcriplase Inhibilors NNRTIs)**
570
AE of **Non-nucleoside Reverse Transcriplase Inhibilors NNRTIs)**
1- Skin rashes, pruritus. 2- Fever, nausea. 3- CNS disturbances like headache, confusion, insomnia, bad dreams, amnesia, etc.
571
Examples of **Protease Inhibitors (Pls)**
Lopinavir, Saquinavir, Ritonavir (navir)
572
MOA of **Protease Inhibitors (Pls)**
573
AE of **Protease Inhibitors (Pls)**
574
Drug interactions of **Protease Inhibitors (Pls)**
- Drug interactions are a common problem for PIs, because they potent inhibitors of CYP450 isoenzymes. - Drugs that rely on metabolism for their termination of action on CYP450 isoenzymes, may accumulate to toxic levels. **Examples of potentially dangerous interactions with PIs include excessive bleeding with warfarin**
575
Introduction to **Treatment of HIV Infection**
- Retroviruses contain RNA-dependent DNA polymerase (reverse transcriptase) enzyme. - They cause selective depletion of CD4 cells leading to a profound decrease in cell-mediated immunity. - Hence, the infected person is prone to severe opportunistic infections and lymphoid malignancies.
576
Objectives of anti-HIV therapy
577
Regimens in anti-HIV therapy
578
How require prophylactic therapy to HIV?
- Doctors, nurses, technicians and other healthcare workers who have had accidental exposure to HIV infection with surgical instruments, blood transfusion or needle-prick injury
579
Principles of anti-HIV therapy
580
The need of HIV PEP depens on ......
The need for postexposure prophylaxis (PEP) depends on 1. The degree of exposure to HIV (viral load) 2. The HIV status of the exposure source.
581
Basic & Expanded regimens in prophylaxis of HIV
582
Activity, Clinical Uses of **Acyclovir**
583
MOA of **Acyclovir**
- Monophosphorylated by viral thymidine kinase (K), - Then further bioactivated by host-cell kinases to the triphosphate - Acyclovir triphosphate is both a substrate for and inhibitor of viral polymerase when incorporated into the DNA molecule
584
AE of **Acyclovir**
- Minor with oral use - More obvious with IV - Crystalluria (maintain full hydration) and neurotoxicity (agitation, headache, confusion) - Acyclovir is not hematotoxic
585
MOA of **Ganciclovir**
Similar to that of acyclovir First phosphorylation step is viral-specific; involves : 1. thymidine kinase in HSV - phosphotransferase (UL97) in cytomegalovirus (CMV) - Triphosphate form inhibits viral DNA polymerase and causes chain termination
586
Activity, Clinical Uses of **Ganciclovir**
Of Ganciclovir - HSV, VZV, and CMV - Mostly used in prophylaxis and treatment of CMV infections, including retinitis, in AIDS and transplant
587
AE of **Ganciclovir**
- Dose-limiting hematotoxicity (leukopenia, thrombocytopenia), - Mucositis, fever, rash, crystalluria(maintain hydration); - Seizures in overdose
588
Def of **Scabies**
- Scabies is a contagious disease caused by a mite, the female Sarcoptes scabiei; which invade the epidermis and form a burrow.
589
MOI by **Scabies**
590
IP of **Scabies**
2 weeks- 2 months.
591
Pathogonomic lesions of **Scabies**
Burrows which may be present in a few or large numbers.
592
Lesion of **Scabies**
593
CP of **Scabies**
594
Distribution of lesions in **Scabies**
595
Difference of animal scabies from Human scabies
The difference from human scabies are: - Shorter I.P. - Self-limiting after eliminating the source of infection.
596
Sites of **Animal Scabies**
- localized or generalized according to the mode of exposure. Webs & genitalia are free.
597
Lesions of **Animal Scabies**
papules, wheals or papulovesicles with absence of burrows.
598
Transmission of **Animal Scabies**
not transmitted from human to human.
599
Scabies in infants and young children
- has Atypical distribution of lesions with involvement of scalp, face, neck, palms and soles.
600
Nodular scabies - Lesions - Sites - Cause
- Persistent reddish brown pruritic nodules may occur after treatment of scabies. - The sites of predilection are axillae, male genitalia, groins, umbilicus or anywhere. - These nodules represent hypersensitivity reaction to mites.
601
Scabies Incognito - Lesions - Distribution
- The lesions and the course are modified by the application of topical or systemic steroids. - Scabies has unusual extent and distribution.
602
What does **Crusted (Norwegian) scabies** represent?
- This type represents an abnormal host immune response to the mite.
603
Where is **Crusted (Norwegian) scabies** Seen?
- Mentally retarded. - Patients with poor cutaneous sensation - Patients with severe systemic diseases like leukemia and DM. - Patients with severe immunosuppression (e.g., AIDS).
604
CP of **Crusted (Norwegian) scabies**
- Large crusts on the hands and feet with subungual hyperkeratosis. - Erythematous scaly plaques occur on the face, neck, scalp and trunk and may become generalized. - Itching may be absent - The number of the invading mites may reach up to 2 millions, so these patients are highly contagious and may initiate epidemics of scabies.
605
Complications of **Scabies**
606
Diagnostic Criteria of **Scabies**
607
TTT of **Scabies**
- General Treatments - Topical Scabicides - Systemic Scabicidies
608
Topical Scabicides in TTT of **Scabies**
609
Systemic TTT of **Scabies**
610
Causes of persistent itching after treatment of scabies
611
Scabies in Bed-Ridden
- Like classic scabies but lesion is more common in the area with contact with bed
612
Scabies In Clean
- Difficulty to see the burrows due to frequent bathing.
613
Venereal Scabies
- Like classic scabies but NOT maybe sexually transmitted (In this case u must search for other venereal diseases)
614
DDx of **scabies**
* Popular urticaria * Eczema * Erythema multiform
615
General Measures During TTT of Scabies
- Boiling of cloths, bed linens, towels. - The mites cannot survive at temperature about 50°C for longer than 5min. - It cannot survive at room temperature in blanket or clothing for more than 2w - Treatment of all members of the family except in animal scabies. - Treatment of infested animals.
616
What is the drug of Choice in pregnant women with Scabies?
- The drug of choice is permethrin, with malathion as an alternative. - It is suggested that topical agents should be removed from the nipples before breast feeding, and then reapplied.
617
TTT of Nodular Scabies
1- Intralesional injection of steroid 2- Surgical excision.
618
Def of **Pediculosis**
- Pediculosis is caused by lice which are small gray-brown, blood sucking parasites
619
Eggs of Females **Pediculosis**
- Each female lays many eggs which appear as white nits firmly attached (cemented) to the hair shaft - Each nit hatches within a week.
620
CP of **Pediculosis**
621
Site of **Pediculosis**
- Pediculosis Capitis occurs on the hair of the scalp, mainly above the ears and occiput. - Beard and moustache may be infested.
622
MOI by **Pediculosis**
- Pediculosis capitis is communicated by direct contact, sharing hats, combs & brushes.
623
Epidemeology of **Pediculosis**
- Although the disease is more common in children, it may occur in adults
624
what is **Pediculosis** associated with?
- There is itching of the scalp this causes scratching with impetigo and cervical lymphadenopathy. - The general health may be impaired from septic absorption.
625
TTT of **Pediculosis**
626
Types of Pediculosis
- P. Capitis - P. Corporis - P. Pubis
627
Other names of Pediculosis pubis
(Crab lice, Pthirus pubis)
628
Def of Pediculosis pubis
- The pubic louse is sexually transmitted and is mostly found in young adults.
629
Sites of Pediculosis pubis
- Pubic lice infest the pubic and perineal hair - It may also infect the eye lashes
630
Lesions of Pediculosis pubis
- Crab lice cause severe itching in the pubic region with 2ry eczema and infection. - The lice firmly adhere to the base of hairs - They can be skin-coloured or mimic haemorrhagic crusts.
631
Def of **Urticaria**
- Urticaria is an acute skin disorder characterized by formation of wheals - It may be allergic or non-allergic.
632
what does Liberation of histamine and or other substances from the mast cells results from?
- From Allergic Reaction nearby the mast cells - From Non-Allergic Reaction, i.e., direct action of certain stimuli on mast cells.
633
Causes of **Urticaria**
634
CP of **Urticaria**
635
What is **Urticaria** associated with?
- Angioedema (diffuse swelling in certain areas of thin skin & loose SC tissue such as eye lids, lips, genitalia) may occur with wheals. - General symptoms may indicate involvement of internal organs such as 1. GIT (nausea, vomiting, dysphagia) 2. respiratory tract (hoarseness, wheezing and dyspnea).
636
What Characterizes **Urticaria**?
- Sudden appearance of itchy wheals that last from few hours up to 48 hours, then fade away (evanescent) and new lesions may appear, a feature distinguishing urticaria from other urticarial like lesions of the skin.
637
Course of **Urticaria**
- Acute urticaria: the lesions usually disappear within a few hours or days - Chronic urticaria: the disease persists for more than 6 weeks - Spontaneous improvement may occur even in absence of diagnosis or treatment.
638
Special Types of **Urticaria**
639
TTT of **Urticaria**
640
Def of **Papular Urticaria (Prurigo simplex)**
Hypersensitivity to insect bites such as fleas and mosquitoes.
641
CP of **Papular Urticaria (Prurigo simplex)**
642
Sites of **Papular Urticaria (Prurigo simplex)**
- The eruption occurs mainly on the limbs. - The trunk may show few lesions.
643
Epidemeology of **Papular Urticaria (Prurigo simplex)**
- It is frequently seen in children moving to new areas where mosquitoes prevail.
644
Prognosis of **Papular Urticaria (Prurigo simplex)**
645
Diagnosis of **Atopic Dermatitis**
**4 major criteria:** 1. pruritis 2. Typical morphology and distribution for age group 3. Chronic or chronically relapsing dermatitis 4. Personal or family history of atopy
646
TTT of **papular urticaria**
647
Def of **Atopic Dermatitis**
- AD is a **common chronic relapsing pruritic inflammatory skin disease** with a wide range of manifestations frequently associated with **personal or other family history other atopic diseases**
648
How id **atopy** Determined?
- Atopy is a **Genetically determined immune mediated disorder** in which there is an **increased liability to certain diseases**, e.g., asthma, allergic rhinitis, hay fever and atopic dermatitis.
649
CP of **Atopic Dermatitis**
- The cardinal symptom is pruritus. (itching) - Dry scaly skin - Crusted lesions on face, scalp, trunk & extremities - Lichenification (with chronic course)
650
Etiology of **Atopic Dermatitis**
Genetic defect in fillagerin gene leading to defective skin barrier
651
Causes of exacerbation of **Atopic Dermatitis**
- Emotional stress - Low humidity & Cold weather - Seasonal allergies, flowers pollen. - Cigarette smoke - Exposure to harsh detergents, soaps - Rough clothes, Synthetic fibres or wool - Dust, Animal fur or sand - Perfumes, Cosmetic products
652
Types of **Atopic Dermatitis**
1- Infantile atopic dermatitis. 2- Childhood atopic dermatitis. 3- Adulthood atopic dermatitis.
653
Lesion in **Infantile Atopic Dermatilis**
- Edematous Erythematous discrete & confluent papules. - Severe itching > Oozing & crusting plaques.
654
Course of **Infantile Atopic Dermatilis**
- About 50% of cases clear by the age of 2 years. - The remainder proceeds into childhood phase. - About 30-50% of infantile eczema subsequently develops asthma
655
Age of **Infantile Atopic Dermatilis**
2 months - 2 years
656
Sites of **Infantile Atopic Dermatilis**
The usually affected site: - The face, particularly the cheeks. - Scalp - Neck - Extensor aspects of the extremities - Trunk.
657
Age of **Childhood Atopic Dermatilis**
2-12 years
658
Lesion in **Childhood Atopic Dermatilis**
- The lesions are less exudative (i.e., dry skin) & tend to lichenify especially in the flexures (Flexural eczema, Besnier's prurigo)
659
Course of **Childhood Atopic Dermatitis**
- About 50% of cases may clear by the age 12 years - Otherwise, it changes into the adult phase.
660
Sites of **Childhood Atopic Dermatitis**
- Antecubital & popliteal fossae - Neck - Wrists - Ankles - Around the mouth & around the eyes. 1. Sometimes, only one site is involved. 2. may affect the extensors &
661
Prognosis of **Infantile & Childhood Atopic Dermatitis**
- This means that about 60%-75% of all cases of infantile and childhood AD go into remission by 12 years of age. (But in others, disease activity persists into adolescence & adulthood)
662
Age & Lesions of **Adult/Adolescent Atopic Dermatilis**
> 12 years - Similar to the childhood phase in showing areas of lichenification in the flexures
663
Course of **Adult/Adolescent Atopic Dermatilis**
- It is difficult to assess the prognosis in individual case. - It is worse if both parents are affected. (About 30-50% of infantile eczema subsequently develops asthma)
664
CP of **Childhood Atopic Dermatitis**
665
Pityriasis alba
666
Juvenile planter dermatosis
667
Prurigo of Hebra
668
Xerosis
669
CP of **Adult/Adolescent atopic dermatitis**
670
Regional variants of Atopic Dermatitis
671
Complications of **Atopic Dermatitis**
1- Bacterial infection. 2- Viral infections (warts and mollusca contagiosa). 3- Eczema herpeticum (herpes simplex viral infection of eczematous skin).
672
Diagnostic Criteria of **Atopic Dermatitis**
673
TTT of **Atopic Dermatitis**
- General Measures - Regular Emollient therapy - Topical Anti-inflammatory Therapy - Systemic therapy
674
General Measures of **Atopic Dermatitis**
- Avoid exposure to irritants, wool, synthetic cloths or other rough fabrics, dust mites. - Careful drug taking is advised particularly with penicillin, antitetantic serum and other drugs known to induce anaphylactic reaction.
675
Regular Emolient Therapy in **Atopic Dermatitis**
(ointment or water in oil creams): Basic line in treatment of all cases.
676
Systemic Therapy in **Atopic Dermatitis**
677
Topical Anti-Inflammatory therapy in **Atopic Dermatitis**
- Topical corticosteroids ointment: the main line - Topical calcineurin inhibitors (CIs) : Tacrolimus 0.03% and 0.1% ointment and pimicrolimus 1% cream. - Zinc oxid cream
678
Side effects of TCS
679
AE of **Pompholyx**
680
Def of **Pompholyx**
- Crops of severely Itchy, deeply seated vesicles on palms & soles. - Remission within 2 wks + Recur
681
TTT of **Pompholyx**
**Topical:** - Drying lotion. - Topical steroid. **Systemic:** - Antibiotic. - short course steroid.
682
What is **Pityriasis Alba**?
- It is a non-specific dermatitis characterized by oval or round dry scaly patches which subside with hypopigmentation.
683
Epidemeology of Pityriasis Alba
- It is more common in atopics but not confined to them. - It is mainly seen in children and young adults.
684
Site of Pityriasis Alba
- The face is the most frequently involved site. Other areas as the neck, arms & trunk may be involved.
685
Resolution of Pityriasis Alba
Most cases subside in few months. Recurrence may occur.
686
TTT of Pityriasis Alba
topical emollient.
687
Def of **Eczema**
- Eczema is a severe dermatitis (inflammation of the skin) characterized by itching, oozing & burning sensation.
688
Stages of **Eczema**
689
what induces **Eczema**?
induced by a wide range of external or internal factors.
690
Classification of **Eczema**
691
Def of **Contact Dermatitis**
- Contact dermatitis is an inflammatory skin disease induced by exposure to external injury; chemical or physical.
692
Cause of **Irritant Contact Dermatitis**
results from exposure of the skin to an irritant
693
Types of **Contact Dermatitis**
694
what is an **Irritant**?
- An agent that is capable of producing dermatitis on the first exposure
695
is **Irritant Contact Dermatitis** an immunulogical process?
No
696
what does the reaction of the skin to irritant depend on?
- The reaction of the skin to irritant depends on the potency of irritant - Strong irritants > acute eczema with vesiculation and even necrosis of the skin. - Repeated contact of Mild irritants → may cause subacute or chronic eczema. (Housewife eczema)
697
Examples of **irritants**
698
Is **Allergic contact dermatitis** an immunulogical process?
- It is an Immunological process - An eczematous rash develops after contact with an agent to which delayed hypersensitivity reaction has developed (Type IV Reaction).
699
What causes **Allergic contact dermatitis**?
- It results from exposure of the skin to a Sensitizer (contact allergen)
700
what is a **Sensitizer**?
- An agent that is Not capable of producing dermatitis on the first exposure but causes dermatitis after a latent period on further exposure.
701
Types of **Allergic contact dermatitis**
The dermatitis may be acute, subacute or chronic.
702
what causes Photoloxic CD?
- occur after activation of an irritant by UVR.
703
Examples of Sensitizers
704
Sites of Photoloxic CD
localized to areas of exposure
705
Examples of phototoxic agents
- Tar & psoralen paint, - Plants (phytophotodermatitis) - Phototoxic (Jelly fish) CD occur after activation of the irritant jelly fish secretion by UVR on coming out of water
706
what causes Photoallergic CD?
- occur after activation of a sensitizer by UVR
707
Examples of Photoallergic agent
- Perfumes - Cosmetics - Sunscreen.
708
what causes Infective Dermatitis?
- by micro-organism products.
709
CP of Infective Dermatitis
- erythema, pustules - oozing, crust - maybe dry & scaly
710
Sites of Infective Dermatitis
- Around discharging ear. - Wound, ulcer & sinuses. - Scalp in Pediculosis. - Trunk in scabies.
711
TTT of Infective Dermatitis
- Topical drying lotion: KMn04,saline. - Topical Abic-steroid combination - Systemic Abic.
712
Dx of **Contact Dermatitis**
713
Prevention of **Contact Dermatitis**
1. Avoid contact 2. Protect skin 3. Check early signs of dermatitis
714
TTT of **Contact Dermatitis**
715
Def of **Erythema Multiforme**
- Acute self- limited skin disease characterized by target or iris lesion.
716
Etiology of **Erythema Multiforme**
717
CP of **Erythema Multiforme minor**
718
TTT of **Erythema Multiforme**
1- Elimination of cause 2- Symptomatic and supportive 3- prevention (Recurrent cases): Oral acyclovir (400 mg twice daily for 6 months) to prevent recurrence of herpes associated E.M
719
CP **Erythema Multiforme Major**
720
Course of **Erythema Multiforme**
- E.M. usually fades within 2-4 weeks - E.M tends to recur (in 30% of cases)
721
Def of **Erythema Nodosum**
- Inflammation of subcutaneous fat (panniculitis) presents as an acute self-limited painful nodular erythematous eruption.
722
Etiology of **Erythema Nodosum**
723
CP of **Erythema Nodosum**
724
Course of **Erythema Nodosum**
- spontaneous resolution in about 2-6 weeks without residual scarring, - however, recurrence may occur
725
TTT of **Erythema Nodosum**
1- Treatment of the cause. 2- Bed rest and supportive bandages. 3- Non-steroidal anti-inflammatory drugs (NSAIDs) 4- potassium iodide for 2 weeks in severe cases
726
Def of **Drug Reactions**
- Drug reaction is harmful, unintended, response to drug in therapeutic dose.
727
Mechanism of **Drug Reactions**
- allergic or non-allergic
728
CP of **Drug Reactions**
The important forms of the drug eruptions include: - Severe life -threatening drug reactions - Other reactions
729
What are **Severe life -threatening drug reactions**?
730
Other forms of drug reactions
731
Urticaria **(Drug Reactions)**
732
Exanthematous rash **(Drug Reactions)**
733
Photosensetivity **(Drug Reactions)**
734
Acne-form eruption **(Drug Reactions)**
735
Pigmentation **(Drug Reactions)**
736
what are common drugs that cause Fixed drug eruption?
Sulfonamides, NSAIDs
737
Alopecia **(Drug Reactions)**
738
Characters of **Fixed drug eruption**
- recurs in the same sites each time the drug is administered.
739
CP of **Fixed drug eruption**
- Well-defined round or oval plaque of erythema & oedema. Bulla may develop on the top - Healed lesion is hyperpigmented (dark brown to violet)
740
Sites of **Fixed drug eruption**
- lips, anogenital area (glans penis), but can occur anywhere.
741
Dx of **drug reactions**
1- abrupt onset symmetric cutaneous eruption 2- History of drug intake. 3- De-challenge test: The eruption improves when the suspected drug is stopped. (clear in 2 weeks on withdrawal) 4- Re-challenge (oral provocation test)
742
TTT of drug reactions
- Elimination of the offending drug - Symptomatic treatment: 1. Antihistamines. 2. Topical steroid. 3. Systemic steroids in severe cases.
743
Epidermal Necrolysis
(Stevens-Johnson Syndrome & Toxic epidermal necrolysis)
744
Def of **Epidermal Necrolysis**
745
CP of **Epidermal Necrolysis**
746
Prodorma of **Epidermal Necrolysis**
of URT symptoms; High fever, painful skin and weakness.
747
Skin in **Epidermal Necrolysis**
- Erythematous and purpuric macules on trunk and proximal limbs → flaccid blisters → epidermal detachment and large confluent oozing erosions - Nikolsky sign is positive (firm sliding pressure on normal appearing skin → detachment of intact superficial epidermis)
748
Sites of **Epidermal Necrolysis**
mainly localized to face upper trunk, and hands
749
Mucous membrane affection in **Epidermal Necrolysis**
- Involvement in 90% of cases ( always at least two sites) - Erythema and painful erosions of buccal, ocular, and genital mucosa
750
Visceral involvment in **Epidermal Necrolysis**
is possible (pulmonary, GIT, renal)
751
Prognosis of **Epidermal Necrolysis**
- Mortality rate is up 25%. - Death may be due to sepsis, electrolyte imbalance or organ failure.
752
TTT of **Epidermal Necrolysis**
- Early(immediate) withdrawal of suspected drugs. - Rapid initiation of supportive care in intensive care burn unit
753
Def of **Pemphigus vulgaris**
- Autoimmune disease in which autoantibodies are formed against intercellular bridges of the prickle cell layer. - This results in acantholysis and formation of intraepidermal bullae
754
CP of **Pemphigus vulgaris**
755
Lesions in **Pemphigus vulgaris**
- Characterized by flaccid bullae arising upon normal skin and mucous membranes. - The bullae rupture easily leaving painful erosions & Crusts - Painful erosions on mucous membrane.
756
Incidence of **Pemphigus vulgaris**
Rare chronic disease, usually affects adults. (4-5th decades)
757
Complications of **Pemphigus vulgaris**
- Infection, fluid & electrolyte imbalance may result in death.
758
where can we find +ve nikolsky sign?
in STS-TEN & Pemphigus vulgaris
759
Sites of **Pemphigus vulgaris**
- commonly involved are scalp, intertriginous area and umbilicus, but in severe cases any site can be involved.
760
TTT of **Pemphigus vulgaris**
- Refer to dermatologist - Systemic steroids & immunosuppressive (cytotoxic) drugs.
761
Examples of Papulosquamous Diseases
- Psoriasis - Lichen Planus - DLE
762
Def of **Psoriasis**
- Psoriasis is a genetically determined common skin disease characterized by: chronic relapsing nature and variable clinical features.
763
Etiology of **Psoriasis**
764
Pathology of **Psoriasis**
765
Clinical types of **Psoriasis**
1- Psoriasis vulgaris. 2- Erythrodermic psoriasis 3- Pustular psoriasis. 4- Arthropathic psoriasis.
766
Koebner Phenomenon in **Psoriasis Vulgaris**
- Trauma to the apparently normal skin may elicit new psoriatic lesions.
767
Auspitz Sign in **Psoriasis Vulgaris**
- Removal of scales by scraping gives rise to small bleeding points which is pathognomonic for psoriasis
768
what is the most comn form of **Psoriasis Vulgaris**?
Plaque Psoriasis
769
Shape of **Plaque Psoriasis**
770
Color of **Plaque Psoriasis**
Salmon Pink Erythema
771
Covering of **Plaque Psoriasis**
Silvery white scales
772
Specific Charaters of **Plaque Psoriasis**
+ve Koebner phenomenon +ve Auspitz sign
773
Site of **Plaque Psoriasis**
- Elbows, knees and lower sacrum. - However, any site may be affected
774
Shape of **Scalp Psoriasis**
775
Specific Characters of **Scalp Psoriasis**
No hair loss
776
Sites of **Scalp Psoriasis**
Scalp
777
Shape of **Palms & Soles Psoriasis**
778
Color of **Palms & Soles Psoriasis**
Red
779
Covering of Color of **Palms & Soles Psoriasis**
Fine silvery scales
780
Sites of **Palms & Soles Psoriasis**
Palms & Soles
781
Shape of **Psoriasis of Nails**
782
Site of **Psoriasis of Nails**
Nails
783
Lesion in **Intertriginous Psoriasis**
784
Specific Characters of **Intertriginous Psoriasis**
- Itching is common & fissuring is often seen in the gluteal crease
785
Site of **Intertriginous Psoriasis**
Localized to groins, gluteal crease, axillae and sub-mammary areas
786
Lesion in **Mucosal Psoriasis**
787
Lesion in **Guttate Psoriasis**
788
Site of **Guttate Psoriasis**
trunk and proximal extremities
789
Incidence of **Guttate Psoriasis**
- Usually occurs in children and young adults following acute streptococcal infection
790
Course of **Guttate Psoriasis**
- The lesions may subside after about 6 weeks without treatment or change to plaque type
791
Erythrodermic Psoriasis
- The entire skin is red and covered with scales.
792
Pustular psoriasis
Macroscopic sterile pustules appear. - Localized to palms and soles. - Generalized pustular psoriasis.
793
Arthropathic psoriasis
Psoriasis associated with arthropathy.
794
Course of Psoriasis
The disease is usually chronic with remission and relapse.
795
TTT of **Psoriasis**
- Topical - Phototherapy - Systemic
796
Topical TTT of **Psoriasis**
- Steroids - Salicylic Acid - Tar - Calcipotriol (vitamin D analogue)
797
when is Tar Contraindicated in **Psoriasis**?
- Application on face, flexures & genitals. - Erythroderrnic and generalized pustular psoriasis. - Severe acne & folliculitis.
798
Steroids In TTT of **Psoriasis**
- Antimitotic & anti-inflammatory. (Topical, intralesional) - They are applied alone or in combination with salicylic acid. - Intralesional injection of steroid is used in localized small resistant lesion. - Also, it is used for nail psoriasis by injection in the nail fold. However.
799
Salicylic acid in TTT of **Psoriasis**
- Keratolytic agent which is used to remove the scales. It is usually used in combination with steroid, tar or anthralin.
800
Calcipotriol in TTT of **Psoriasis**
(vitamin D analogue) - It inhibits proliferation of keratinocytes. - It is applied twice daily with maximum dose of 100 gm weekly for 6 week - This drug may increase serum calcium.
801
Tar in TTT of **Psoriasis**
Antimitotic 2-5% tar ointment is applied at night, and then removed in the next day by mineral oil before exposure to UVB. (goekerman technique)
802
Phototherapy in TTT of **Psoriasis**
- UVB (broad band or narrow band) exposure 3 times weekly in mildly erythemogenic dose.
803
Systemic Therapy in TTT of **Psoriasis**
- Methotrexate. (given once weekly, hepatotoxic and myelotoxic) - PUVA (psoralen+ UVA). - Retinoids (acitretin), etretinate: teratogenic. - Cyclosporine: nephrotoxic. - Biologic therapy as TNFa blockers (as adalimumab, etanercept) and IL-17 antagonists (as sekicinumab)
804
Indications of Systemic Therspy in TTT of **Psoriasis**
should be used only by specialist in: - Extensive psoriasis vulgaris not responding to topical therapy. - Erythrodermic psoriasis. - Pustular psoriasis. - Arthropathic psoriasis
805
Why are Systemic corticosteroids absolutely contraindicated in psoriasis vulgaris?
Cause flare at withdrawl
806
Def of **Lichen Planus**
- a chronic sometimes acute disease of the skin and mucous membranes, with distinctive clinical and pathological features.
807
Pathology of **Lichen Planus**
808
Etiology of **Lichen Planus**
- Psychic stress is a predisposing factor. - Lichen planus may be more common among patients suffering from HCV.
809
Wickham's striae
The surface of the papule may show white fine dots and lines known as (Wickham's striae).
810
CP of **Lichen Planus**
811
what is the clsssic 1ry lesion of **Lichen Planus**?
- itchy flat topped, polygonal violaceous papules.
812
**Lichen Planus** Lesions in oral mucosa
813
**Lichen Planus** lesion in nail
814
**Lichen Planus** lesions in palms & soles
815
Sites of **Lichen Planus**
816
Clinical Varieties of **Lichen Planus**
817
Course of **Lichen Planus**
818
TTT of **Lichen Planus**
819
7 Characters starting with **P** for **Lichen Planus**
Papules Purple Polygonal (flat topped) Pruritic Peripheral extremities + oral Positive Koebner Pterygium in nail
820
Def of **Discoid lupus erythematosus (DLE)**
- Localized inflammatory skin disease characterized by plaques of erythema, scaling and atrophic scar.
821
what is the most common type of chronic cutaneous lupus?
**Discoid lupus erythematosus (DLE)**
822
Types of **Lupus erythematosus (LE)**
DLE & SLE
823
Predisposing factors for **Discoid lupus erythematosus (DLE)**
824
CP of **Discoid lupus erythematosus (DLE)**
825
Age & sex of **Discoid lupus erythematosus (DLE)**
adults 20-40 years. (4 decade) {Female: male = 2:1}
826
Sites of **Discoid lupus erythematosus (DLE)**
- Face especially the butterfly area, scalp, arms, legs, dorsum of hands and retro-auricular areas. - However, any site may be affected including oral mucosa. - Lesions on the scalp cause scarring alopecia.
827
Course of **Discoid lupus erythematosus (DLE)**
- Spontaneous regression may occur with or without scar. - Calcification - Spread to other area - In 6-6.5% of DLE patients they may change to SLE.
828
TTT of **Discoid lupus erythematosus (DLE)**
829
Systemic TTT of **Discoid lupus erythematosus (DLE)**
- Antimalarial drugs as hydroxychloroquine in cases not responding to topical steroid. - Prednisone 15 mg/d. - Etretinate
830
Lesions of **DLE**
831
Def of **Seborrheic Dermatitis**
- A common erythematous scaling eruption that is localized to the seborrheic sites.
832
Etiology of **Seborrheic Dermatitis**
Pityrosporum ovale may play a role.
833
Pathogenesis of **Seborrheic Dermatitis**
834
Prevalence of **Seborrheic Dermatitis**
eczematous form is estimated at 5%
835
Age affected by **Seborrheic Dermatitis**
- Usually begins in adolescence (9-11 years) (with puberty) peak at age 40 - Uncommon in preadolescent childhood (exclude t.capitis) - Infantile SD
836
which sex is more commnly affected by **Seborrheic Dermatitis**?
More common in males than females. (M > F)
837
what are sites of **Seborrheic Dermatitis**?
- Scalp, behind ears, face - Pre-sternal and interscapular areas - flexures (umbilicus, axilla, infra-mammary, inguinal fold, perineum or anogenital crease.
838
Lesions of **Seborrheic Dermatitis**
- Scalp - Ears - Eyebrows & Beard - Galbrous skin - Nasolabial fold - Eyelid margin
839
Shape of **Non inflammatory (dandruff) (pityriasis capitis) SD**
Diffuse fine white (branny) or greasy scales
840
Scalp lesions of **Seborrheic Dermatitis**
- Non inflammatory (dandruff) (pityriasis capitis) - Inflammatory (seborrheic eczema)
841
Characters of **Non inflammatory (dandruff) (pityriasis capitis) SD**
842
what is the mildest form of **SD**?
**Non inflammatory (dandruff) (pityriasis capitis) SD**
843
Characters of **Inflammatory Scalp SD (seborrheic eczema)**
844
SD in Ears
- retro-auricular scaling, crusting and fissuring. Persistent non purulent otitis externa may occur.
845
SD in Eyebrows and beard
fine scaling
846
SD in Glabrous skin
diffuse redness.
847
SD in nasolabial fold
greasy scales.
848
SD in Eyelid margin
seborrheic blepharitis.
849
Flexures (inverse SD) (axillae, groins, sub-mammary areas and umbilicus)
erythematous patches with maceration and oozing.
850
SD of facial skin
851
SD of trunk
852
Types of inverse SD
- Scaling Intertrigo - Non-Scaling Intertrigo - Crusted Fissures - Weeping Dermatitis - Sebopsoriasis
853
Scaling intertrigo
- Sharply marginated erythema and greasy scaling
854
Weeping dermatilis
- Due to sweating, secondary infection, and inappropriate treatment, - Erythema, maceration, oozing, crusting.
855
Non scaling intertrigo
**May be erythema only**
856
Sebopsoriasis
- features of both psoriasis and SD.
857
Examples of Extensive SD
- Erythrodermic: rare - HIV infection - Parkinson's disease (with seborrhoea)
858
Severity varies from mild dandruff to exfoliative erythroderma
..
859
DDx of adult scalp SD
860
Adult SD
861
Introduction to TTT of SD
862
2 steps regimen in TTT of SD
863
Def of **Infantile SD**
- SD inearly infancy due to stimulation of sebaceous glands by maternalandroge
864
Charachters of **Infantile SD**
- simulates SD in adult, but the scaling on the scalp is thick forming yellowish brown heaped lesion (cradle cap).
865
Onset of **Infantile SD**
- Begins 2-8 weeks after birth
866
Healing of **Infantile SD**
- The lesions usually subside within 3-4 weeks. - May persist for several months
867
CP od **Infantile SD**
868
TTT of **Infantile SD**
869
DDx of Scaly scalp in prepubertal children
870
Def of **Acne Vulgaris**
- Acne vulgaris is a chronic inflammatory disorder of the pilosebaceous apparatus, characterized by formation of comedones.
871
Pathogenesis of **Acne Vulgaris**
4 major factors (multifactorial disorder) are involved in the pathogenesis of acne in the genetically predisposed person. - Increased sebum secretion - Hyperkeratosis of pilosebaceous duct - Propionibacterium acne (P. acne) colonizes pilosebaceous duct - Inflammation
872
Increased sebum secreation **(Pathogenesis of Acne Vulgaris)**
- which may result from increased local synthesis of androgen in sebaceous glands or increased response to it.
873
Propionibacterium acne (P. acne) colonizes **(Pathogenesis of Acne Vulgaris)**
- Pilosebaceous duct and contributes in the formation of comedones and pustules.
874
Hyperkeratosis of pilosebaceous duct **(Pathogenesis of Acne Vulgaris)**
875
Inflammation **(Pathogenesis of Acne Vulgaris)**
initiated by P:acne
876
what causes Hyperkeratosis of pilosebaceous duct?
results from the irritant effect of excess sebum.
877
what does Obstruction of pilosebaceous duct result in?
result in comedones which consist of horny cells, sebum, and bacteria.
878
Types of comedoens according to level of obstruction
- If obstruction is deep: comedones are closed with narrow orifice (white head). - If obstruction is superficial: the comedones are open and have a patulous orifice (black head).
879
what does Propionibacterium acne (P. acne) colonize?
pilosebaceous duct
880
what initiates inflammation in Acne Vulgaris?
P. acne
881
what are Micro-comedones?
Invisible hyperkeratotic plug made of sebum and keratin in follicular canal
882
Excerbating factors of **Acne Vulgaris**
883
Lesions in **Acne Vulgaris**
884
Age of **Acne Vulgaris**
- Adolescence of both sexes. (12-24 years ) mainly - May start at 10 years and persist up 50 years
885
Characters of **Closed Comedones**
- Skin coloured - No visible follicular opening. - Often inconspicuous and require adequate lighting and stretching of the skin to be seen
886
Sites of **Acne Vulgaris**
face, back, chest and shoulders.
887
Classification of **Acne Vulgaris**
1- Mild acne: comedones with little or no papules. 2- Moderate acne: comedones, papules and pustules. 3- Severe acne: nodules and cysts predominate.
888
Course of **Acne Vulgaris**
889
TTT of **Acne Vulgaris**
890
Topical in TTT of **Acne Vulgaris**
- Comedolytic agents - Antibacterial agents
891
Comedolytic agents in TTT of **Acne Vulgaris**
892
what is cornerstone in acne ttt?
Topical retinoids
893
# AV = Acne Vulgaris Topical retinoids in TTT of AV
Retinoic acid (0.05-0.1%) is used in gradually increasing concentration
894
SE of Topical retinoids in TTT of AV
It may cause dryness & irritant dermatitis. (Most common side effect)
895
what are examples of Topical Retinoids?
896
Antibacterial agents in TTT of AV
897
Characters of Benzoyl peroxide (BPO) (2.5, 5, 10)%
- no resistance has mild comedolytic effect. - It may cause contact dermatitis.(irritant)
898
what are topical antibiotics used in TTT of AV?
erythromycin and clindamycin are effective in pustular lesions. (not alone)
899
Indication for topical TTT of AV
900
Systemic TTT of AV
- Antibiotics - Antiandrogens - Isotretinoin - Dapsone - Miscellanous therapy - TTT of scars
901
what is the systemic antibiotic of choice in acne?
- Doxycycline: 100mg/day is the antibiotic of choice in acne. - This dose is given until acne clears then dec. the dose gradually for 6 months - Erythromycin and Azithromycin are good alternatives. - clindamycin
902
MOA of antibiotics in systemic TTT of AV
- Reduce inflammation - Reduce P: acne population> reducing bacterial production of inflammatory factors as FFA - Intrinsic anti-inflammatory - Reduce PMN (poly morphonuclear leukocytes) migration
903
Indication of using of antiandroges on TTT of AV
used only in females with severe nodulocystic acne
904
Examples of antiandroges used in TTT of AV
1- contraceptive as Yasmin 2- Cyproterone acetate (with OCPs diane) 3- Spironolactone (K sparing diuretic but has antiandrogen effect)
905
Effects of isotretinoin used in systemic TTT of AV
- It decreases sebum secretion - Decrease P. acne. - Decrease follicular hyperkeratosis - has anti-inflammatory effect
906
AE of isotretinoin used in systemic TTT of AV
It is teratogenic drug with serious side effects, so it should be used only in severe acne and by highly experienced dermatologists.
907
Dapsone **Systemic TTT of AV**
Anti-inflammatory drug used in severe acne with special precautions.
908
Miscellaneous therapy **Systemic TTT of AV**
**Comedonae removal:** - If comedones are resistant **intralesional steroids:** - Triamcinolone acetonide (2-5 mg/ml) - Used for large inflammatory nodules/cysts
909
TTT of scars **Systemic TTT of AV**
- Dermabrasion, laser resurfacing, deeper chemical peels - Filler substances - Punch excision (ice-pick) scar
910
Treatment according to the severity of acne can be given as follow (overview)
911
Def of **Miliaria (Sweat rash)**
A disorder of the sweat duct in which obstruction of the sweat ducts at various levels occurs in association with excessive sweating >> sweat retention
912
Etiology of **Miliaria (Sweat rash)**
Common in: - Neonates: immature eccrine sweat ducts - Adults: living in hot humid condition **Resolve in cool environment**
913
Predisposing factors for **Miliaria (Sweat rash)**
1- Hot humid condition. 2- Excessive clothing. 3- Obesity. 4- Febrile illness.
914
Incidence of **Miliaria (Sweat rash)**
- The disease occurs in the tropics and subtropics - Affects persons of all ages and both sexes.
915
Site & Size of lesion of **Miliaria (Sweat rash)**
- Any site - Pin head size
916
Lesions of **Miliaria (Sweat rash)**
- The eruption consists of closely set red papules, vesicles - It is associated with itching, prickling, or burning sensation. - In infants the eruption may be generalized, and it may occur in any season depending on the habits of overclothing.
917
Complications of **Miliaria (Sweat rash)**
impetigo, folliculitis, and boils.
918
Types of **Miliaria (Sweat rash)**
919
TTT of **Miliaria (Sweat rash)**
920
Stages of Hair growth
921
Causes of hair loss
- Physiological - Pathological (Alopecia)
922
Definition of **Alopecia**
loss of hair from normally hairy area
923
Types of **Alopecia**
- Cicatricial or scarring alopecia (permanent) - non Cicatricial or nonscarring (transient)
924
Causes of Non-cicatricial alopecia
- Conginetal - Aquired
925
Aquired Causes of Non-cicatricial circuscribed (Patterned) alopecia
926
Aquired Causes of Non-cicatricial alopecia
- Circumscribed (Patterned) - Diffuse
927
Aquired Causes of Non-cicatricial Diffuse alopecia
928
Congenital causes of cicatricial alopecia
developmental defect
929
Aquired causes of cicatricial alopecia
930
Definition of **Alopecia Areata**
circumscribed non scarring hair loss with normal skin
931
Etiology of **Alopecia Areata**
932
CP of **Alopecia Areata**
933
Lesions in **Alopecia Areata**
- Circumscribed area of hair loss, nonscarring with normal skin - Positive exclamation mark! (tapered proximal end of the hair shaft) - May affect scalp, face or body hair
934
Clinical types of **Alopecia Areata**
935
Prognosis of **Alopecia Areata**
Bad prognosis in the following conditions: 1- Alopecia totalis, universalis and ophiasis 2- Alopecia areata with nail pitting 3- Alopecia areata in atopics
936
Associated features to **Alopecia Areata**
1- Nail pitting 2- Atopy (atopic dermatitis) 3- Vitiligo 4- Cataract
937
DDx of **Alopecia Areata**
938
TTT of **Alopecia Areata**
939
Causes of hyperpigmentation
940
Causes of Hypopigmentation
941
Casues of depigmentation
942
Def of **Vitiligo**
acquired idiopathic depigmentation (leukoderma) of the skin
943
Etiology of **Vitiligo**
944
Precipitataing factors for **Vitiligo**
1- Emotional stress 2- Sun burn 3- Physical trauma (Koebner's phenomenon)
945
CP of **Vitiligo**
- Milky white depigmented macules or patches affecting any area. - Hair and mucous membranes may be affected **Sites:** face, hand, feet. back are sires of predilection
946
Classification of Vitiligo
947
Prognosis of **Vitiligo**
1- Unpredictable 2- Stationary 3- Spontaneous re-pigmentation 4- Slowly progressive 5- Rapidly progressive
948
DDx of Vitiligo
1- Pityriasis alba 2- Pityriasis versicolor (hypopigmented type) 3- Post inflammatory hypopigmentation 4- Albinism 5- Post-burn and post-chemical depigmentation
949
TTT of **Vitiligo**