Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Y3R1 - DALR ✋🏻 > Dermatology ✋🏻 > Flashcards

Dermatology ✋🏻 Flashcards

1
Q

Basic structure of skin

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Types of cells of epidermis

A
  • Keratinocytes
  • Dendritic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Layers of keratinocytes

A

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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are dendritic cells of epidermis?

A
  • Melanocytes
  • Langerhans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Site of Melanocytes

A

lie in between the basal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Function of Melanocytes

A
  • They form melanin from tyrosine under the effect of tyrosinase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Site of Langerhans cells

A
  • lie in between the prickle cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Function of Langerhans cells

A
  • They act as macrophage & play important role in the immunological processes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Thickness of dermis

A
  • It is 15-40 times thicker than epidermis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

examples of skin appedages

A
  • Hair follicles
  • Sebaceous glands
  • Sweat glands
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what does hair consist of?

A
  • dermal hair papilla.
  • hair matrix.
  • hair shaft.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what does a hair follicle undergo?

A
  • undergoes cycles of:
    growth (anagen), regression (catagen) rest (telogen)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what do hair shafts consist of?

A
  • largely consist of dead, terminally differentiated keratinocytes.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are sebaceous glands associated with?

A
  • Associated with hair follicles (so not found at palms and soles)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Compare between types of sweat glands

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what do nails consist of?

A
  • Nail plate.
  • Nail bed.
  • Nail folds.
  • Nail matrix.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Nail plate

A
  • is a fully keratinized structure.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Nail matrix

A
  • the germinative epithelium of nail matrix produces the plate.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Nail folds

A

are surrounding the plate proximally and laterally.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Nail bed

A
  • The structures upon which the nail rests is the nail bed.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is nail growth rate?

A

fingernails: 3 mm/month

toenails: 1 mm/month

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the functions of skin?

A
  • Protection
  • Heat regulation
  • Excretion
  • Vit D formation
  • Immunology
  • Sensations
  • Reflection of feeling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Protection function of skin

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

heat regulation fuction of skin

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Reflection of internal feeling function of skin

A
  • Examples of feelings reflected by skin: fear, shame & anger.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Immunological function of skin

A
  • Skin plays an important role in the immunological processes.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Formation of Vit D function of skin

A
  • from ergosterol by ultraviolet rays
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Excretion through sweat function of skin

A

Examples of which excreted by skin: NaCl, lactic acid, ammonia & some drugs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Perception of sensations function of skin

A

Examples of sensations precipitated by skin: heat, cold, pain and touch.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

hyperkeratosis

A

Increased thickness of the horny layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Parakeratosis

A
  • Immature keratinization resulting in retention of nuclei in the cells of the horny layer.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Acanthosis

A

Increased thickness of the prickle cell layer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Spongiosis

A
  • Intercellular oedema in the prickle cell layer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Acantholysis

A
  • Loss of coherence between epidermal or epithelial cells.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

compare between Primary acantholysis & Secondary acantholysis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Principles of dermatology diagnosis

A
  • Preliminary History
  • Examination
  • Follow up history
  • Investigations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Preliminary history in dermatology

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Examination in dermatology

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Types of distribution of the lesion

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Types of Configuration of the eruption

(Mode of arrangement of the lesions)

A
  • Linear
  • Circinate
  • Polycyclic (geographic)
  • Grouped
  • Discrete
  • Dermatomal
  • Koebner phenomenon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

examples of linear configuration

A

❶ Lichen planus
❷ Warts
❸ Psoriasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

examples of Circinate configuration

A

❶ Tinea circinata
❷ Pityriasis rosea
❸ Impetigo
❹ Psoriasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

examples of Polycyclic (geographic) configuration

A

❶ Psoriasis
❷ Urticarial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

examples of Grouped configuration

A

❶ Warts
❷ Molluscum contagiosum
❸ Herpes simplex.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

examples of Discrete configuration

A
  • Chicken pox.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

examples of Dermatomal configuration

A

❶ Herpes zoster
❷ Dermatomal vitiligo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Morphology of the individual lesion

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

examples of Koebner phenomenon configuration

A

Lesions appear in an area of trauma which is often
linear as in:

  • Psoriasis
  • plane wart
  • lichen planus
  • vitiligo
  • Molluscum contagiosum.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Definition of patch

A

Macule > 1 cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Definition of Macule

A
  • Circumscribed area of change in skin color without change of its texture up to 0.5 cm in diameter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Examples of Macules and patches

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Definition of Nodule

A
  • Similar to papule but deeply seated and > 0.5 cm in diameter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How to diffrentiate between purpura and erythema?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Definition of Papule

A
  • solid palpable elevated lesion up to 0.5 cm in diameter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Examples of Papule

A
  • Lichen planus, psoriasis, warts, prurigo, molluscum contagiosum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Definition of Plaque

A
  • Circumscribed area of abnormal skin formed by extension or coalescence of either papules or nodules.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Examples of Nodule

A
  • Lupus vulgaris, Lepromatous leprosy.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Definition of Cyst

A

sac filled with expressible material either liquid or semisolid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

On looking to a papule describe the following….

A

Shape: flat topped, dome shape, umbilicated, conical, polyangular.

Color: Skin colored, red, violet, brown, white or yellow.

Surface: Smooth, rough, scaly, crusty.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Examples of Plaque

A

Psoriasis, lupus vulgaris.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Examples of Cyst

A

Cystic acne

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Definition of Vesicle

A
  • Localized visible collection of fluid up to 0.5 cm in diameter.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Examples of Vesicle

A
  • Herpes simplex.
  • Herpes zoster.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Definition of Bulla

A
  • Localized visible collection of fluid > 0.5 cm in diameter.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Example of Bulla

A
  • Bullous impetigo
  • Pemphigus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Definition of Pustule

A
  • Localized visible collection of pus.
    (It may be 1ry lesion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Examples of Pustule

A
  • Pustular psoriasis
  • 2ry to bacterial infection of viral vesicle.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Definition of Crust (scab)

A
  • Dried fluid (serum, blood. or pus) on the skin surface.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Definition of Scale

A
  • Flat plate of horny layer formed by accumulation of excess keratin.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Characters of scales

A
  • Scales may be dry or greasy, large or small.
  • It may occur in many inflammatory diseases such as
    seborrheic dermatitis or psoriasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Definition of Wheal

A
  • Evanescent elevated oedematous erythematous lesion.
  • Evanescent means that the lesion does not persist more than 48 hours.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Charaters of Wheal

A
  • formed by dermal or dermal & hypodermal edema.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

what is Wheal considered as?

A
  • Wheal is the 1ry lesion of urticaria.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Definition of Comedo

A

Plug of keratin and sebum in a dilated pilosebaceous orifice.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Characters of Comedo

A

When the plug is
Superficial —> open (black) comedo.
Deep —-> closed (white) comedo.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is Comedo considered as?

A
  • Comedo is the 1ry lesion of acne vulgaris.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Definition of Burrow (Furrow)

A
  • Superficial tunnel in the skin caused by mite that appears as black dot at the end of the burrow.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Characters of Burrow (Furrow)

A
  • It is tortuous, straight or S shaped
    skin coloured or grayish and 0.5-1.5 cm in length.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

what is Burrow (Furrow) considered as?

A
  • It is the 1ry lesion of scabies.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Definition of Alopecia

A
  • Loss of hair from a normally hairy area.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Types of Alopecia

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Definition of Erosion

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Definition of Ulcer

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Definition of Excoriation

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Definition of Fissure

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Definition of Lichenfication

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Definition of Atrophy

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Definition of Sclerosis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Definition of Scar

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Types of scars

A

Atrophic scar: with thin and wrinkled skin.

Hypertrophic scar: with elevated skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Follow up history in dermatology

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Investegations in dermatology

A
  • Skin biopsy
  • Dermoscopy
  • fungus lesions (Wood’s light, Culture, M/E)
  • Patch test
  • Oral provocation test
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

what is the most common procedure in dermatology investegations?

A

Skin biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Dermoscopy

A

(epiluminescence) using dermoscope:

  • Dermoscopes have built-in illumination, and are applied to the skin surface to enhance visibility of subcorneal structures.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

when is dermoscopy used in dermatology?

A

❶ Doubtful pigmented lesions
❷ Other lesions such as scabies burrows
❸ Many skin neoplasms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Investegations in cases of fungal lesions

A
  • Wood’s light
  • Culture
  • M/E
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Culture in cases of fungal lesions

A
  • On Sabouraud’s agar media.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Microscopic examination in cases of fungl lesions

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Patch test

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Oral provocation test

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

what are the advantages of topical therapy in dermatology?

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Significance of Wood’s light in dermatology

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Components of topical therapy

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Liquid Vehicles

A
  • Example: water, alcohol, Ca hydroxide & glycerin. They are used in the preparation of solutions, lotions, tinctures, paints, creams
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Vehichles in topical therapy

A
  • Ideally a vehicle should be: Non-toxic, non-irritant and non-allergic.
  • Forms of Vehicles: Liquids, powders, creams or ointments.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Powder Vehicles

A
  • Usually applied to normal skin folds to reduce friction.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Creams

A
  • Semisolid emulsion of oil in water.
  • They are used in subacute condition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Ointments

A
  • Greasy base used for dry hyperkeratotic or lichenified skin disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Gels

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Uses of Topical Corticosteroids (TCS)

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Forms of Topical Corticosteroids (TCS)

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Classification of Topical Corticosteroids (TCS)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Examples of Ultrapotent TCS

A
  • Clobetasol propionate 0.05% [Dermovate ®]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Examples of Highly potent TCS

A
  • Mometasone furoate 0.1% (Elocon , Elica)
  • Betamethasone dipropionate (Diprosone)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Examples of Moderately potent TCS

A
  • Betamethasone valerate (Betnovate, Betaderm, Betaval)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Examples of Moderate/weekly potent TCS

A
  • Hydrocortisone butyrate (Texacort)
  • Prednicarbate (Dermatop)
  • Alclometasone dipropionate 0.05% (perderm, weak)
  • Hydrortisone acetate (the weakest TCS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Examples of Combination TCS

A
  • Momenta (contain potent TCS)
  • Kenacomb, quadriderm, pandermal (contain moderately potent TCS)
  • Fucicort cream, Fusizon cream (contain moderately potent TCS)
  • Daktacort (contain hydrocortisone)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Side effects of TCS

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Systemic side effects of TCS

A
  • Growth retardation in children
  • Iatrogenic Cushing syndrome.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

what causes side effects by TCS?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Prescription of TCS

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

How does the skin protect itself?

A

1- Being a dry mechanical barrier.
2- Its acidity.
3- Sebum secretion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

What does staphylococci commonly attack?

A

commonly attack skin appendages.
- hair follicles.
- sweat glands
- periungual tissues.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

What does streptococci commonly attack?

A

skin proper

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Dermal diseases caused by each type of bacteria

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Definition of non-Bullous (Crusted) impetigo

A
  • Impetigo is a contagious superficial pyogenic infection of the skin
  • It represents the most common bacterial skin infection in children.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Epidemiology (Age) of non-Bullous (Crusted) impetigo

A

All, but Children are most often affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Etiology of non-Bullous (Crusted) impetigo

A
  • Staphylococcus aureus,
  • Streptococcus pyogenes (group A B-hemolytic Streptococcus spp.)
  • or both
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Predisposing factors for non-Bullous (Crusted) impetigo

A
  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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Clinical picture of non-Bullous (Crusted) impetigo

A
  • Shape & Color
  • Site
  • Systemic Manifestations
  • Complication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Shape and color of non-Bullous (Crusted) impetigo

A

Thin vesicles on erythematous base -> pustules rapidly rupture -> thick yellowish-brown crust

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Site of non-Bullous (Crusted) impetigo

A
  • face, scalp or anywhere except palms & soles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Systemic manifestations of non-Bullous (Crusted) impetigo

A

Fever & regional lymphadenitis in severe cases only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Complications of non-Bullous (Crusted) impetigo

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Healing (course) of non-Bullous (Crusted) impetigo

A

Spontaneous cure in 2-3 weeks or persist, The crust dries and separates leaving erythema without scar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Etiology of Bullous impetigo

A
  • Staphylococcus aureus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Definition of Bullous impetigo

A
  • Impetigo is a contagious superficial pyogenic infection of the skin
  • It represents the most common bacterial skin infection in children.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

Epidemiology (age) of Bullous impetigo

A

All ages, especially newborn and young children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

Predisposing factors for Bullous impetigo

A
  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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Clinical picture for Bullous impetigo

A
  • Shape & Color
  • Site
  • Systemic Manifestations
  • Complication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

Shape and color of Bullous impetigo

A

Flaccid bullae (1-5 cm) persist for 2-3 days -> rupture “less rapidly” -> thin brownish crust

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Site of Bullous impetigo

A
  • Face, trunk buttocks, perineum, axillae & extremities (including palms and soles)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

Systemic manifestations of Bullous impetigo

A

Regional adenitis is rare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Complications of Bullous impetigo

A
  • Peripheral extension with central healing may give rise to circinate lesion (circinate impetigo)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

Etiology of Ecthyma (Ulcerative “deep” impetigo)

A
  • Strept (mainly) & staph
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

Healing (course) of Bullous impetigo

A
  • Spontaneous cure in 2-3 weeks or persist. The crust dries and separates leaving erythema without scar
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

Clinical picture of Ecthyma (Ulcerative “deep” impetigo)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

Treatment of impetigo

A
  • Topical
  • Systemic antibiotic
  • Treatment of predisposing factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

Topical treatment of impetigo

A

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,
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

Systemic antibiotics for treatment of impetigo

A
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

Dose and indications of antibiotics in impetigo

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

Treatment of predisposing factors in cases of impetigo

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

Compare between furunculosis (Boil) & carbuncle in terms of:

  • Definition
  • Organism
  • predisposing factors
  • Clinical picture
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

Predisposing factors for Furunculosis (Boil)

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

Predisposing factors for carbuncles

A
  • Diabetes mellitus.
  • Malnutrition.
  • Prolonged steroid therapy.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

Healing of Furunculosis

A
  • Heal with scar
  • In some patients, crops of lesions continue to develop for many months or years.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

What are the complications of furuculosis?

A

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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

Treatment of Furunculosis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

Treatment of carbuncle

A
  • Penicillinase resistant penicillin.
  • Surgical incision & drainage of pus.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

Compare between erysipelas and cellulitis, in terms of:

  • Definition
  • How are bacteria reaches the wound?
  • Clinical picture
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

Treatment of erysipelas and cellulitis

A
  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).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

Definition of Streptococcal intertrigo

A
  • Inflammation of skin areas between folds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

Organism which causes Streptococcal intertrigo

A
  • Group A streptococci
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

Age of Streptococcal intertrigo

A
  • Usually affects infant and young children
    Obese adults may be also affected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

Etiology & Site of Streptococcal intertrigo

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

Differential diagnosis of Streptococcal intertrigo

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

Clinical picture of Streptococcal intertrigo

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

Treatment of Streptococcal intertrigo

A
  • Topical antiseptic.
  • Topical & systemic antibiotic.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

Clinical picture of angular chelitis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

Etiology, predisposing factors & treatment of angular cheilitis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

Definition of erythrasma

A
  • Chronic superficial infection of the skin caused by Corynebacterium minutissimum.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

Predisposing factors for erythrasma

A

1- Warm humid climate.
2- Obesity.
3- Diabetes mellitus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

Epidemiology of erythrasma

A
  • Affects adults > children.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

Clinical picture of erythrasma

A
  • Well-defined red brown or brown scaly patches.
  • Asymptomatic or itchy.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

Sites of erythrasma

A

intertriginous areas e.g., groins, axillae, intergluteal clefts, sub mammary areas, or generalized covering the trunk & limbs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

Diagnosis of erythrasma

A
  • Wood’s light —> Coral Red Fluorescence.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

Differential diagnosis of erythrasma

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

Treatment of erythrasma

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

Epidemiology of tuberculosis of the skin

A

Infects 1/3 world population, since 1998 incidence is increasing due to
- AIDS
- Diabetes
- Immune-Supressed patients
- Drug resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

What causes skin tuberculosis?

A

Mycobacterium tuberculosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

Characters of Mycobacterium tuberculosis

A

Non motile, aerobic, acid-fast bacillus (AFB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

Pathology of skin tuberculosis

A
  • Organism gains access to macrophage, replicate then ingested by new macrophages and continue cycle&raquo_space; Spread&raquo_space; Specific Tissue reaction (granuloma) > chronicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

Mode of Infection by lupus vulgaris

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

Classification of skin tuberculosis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

What is the most common form of skin tuberculosis?

A

Lupus vulgaris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

Onset & Course of lupus vulgaris

A
  • disease usually starts in childhood and progresses very slowly.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

Lesions of Lupus vulgaris

A
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

Clinical picture of Lupus vulgaris

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

Sites of Lupus vulgaris

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

Course of Lupus vulgaris

A

progressive but spontaneous healing may occur.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

Complications of Lupus vulgaris

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
194
Q

Diagnosis of Lupus vulgaris

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
195
Q

Treatment of Lupus vulgaris

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
196
Q

Definition of leprosy

A

Chronic mycobacterial disease.

  • primarily affecting peripheral nerves
  • secondarily involving skin and other tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
197
Q

Mode of infection by leprosy

A

By Mycobacterium leprae

  • Droplet infection from the oronasal mucosa of patients having lepromatous leprosy.
  • Susceptible: Children > adults
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
198
Q

Incubation period of leprosy

A

3-5 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
199
Q

Classification of leprosy

A

Leprosy is classified into 3 types according to:
~ Clinical picture.
~ Histopathological examination of skin lesion.
~ Bacteriological examination of skin smear.
~ Lepromin test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
200
Q

What is lepromin test?

A
  • It is an intradermal test using autoclaved lepromatous tissue as antigen.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
201
Q

Significance of lepromin test

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
202
Q

Types of leprosy

A

The 3 types of leprosy are:
1. Tuberculoid leprosy (T.T.). (paucibacillary)
2. Borderline leprosy (B.B.). (mullibacillary)
3. Lepromatous leprosy (L.L.). (mullibacillary)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
203
Q

Where does Tuberculoid Leprosy (T.T) develop?

A
  • develops in persons with good immunity.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
204
Q

What tissues are affected in Tuberculoid Leprosy (T.T)?

A
  • The skin and peripheral nerves are the only tissues affected.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
205
Q

Skin lesions in Tuberculoid Leprosy (T.T)

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
206
Q

where do skin lesions develop in Tuberculoid Leprosy (T.T)?

A
  • The lesions occur anywhere with exception of scalp, axillae, groins & perineum.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
207
Q

Nerve and muscular lesions in Tuberculoid Leprosy (T.T)

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
208
Q

Histopathology of Tuberculoid Leprosy (T.T)

A

tuberculoid infiltrate of Epithelioid cells & Lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
209
Q

Bacteriology of Tuberculoid Leprosy (T.T)

A
  • Lepra bacilli are absent from skin lesion.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
210
Q

Lepromin test of Tuberculoid Leprosy (T.T)

A

is strongly positive indicating high degree of cell mediated immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
211
Q

Where does Lepromatous Leprosy (L.L) Develop?

A
  • develops in person with low immunity.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
212
Q

What tissues are affected in Lepromatous Leprosy (L.L)?

A
  • skin, mucous membranes, eyes & testes are affected
  • Nerves affection is late.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
213
Q

Skin lesions in Lepromatous Leprosy (L.L)

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
214
Q

Mucus membrane lesions in Lepromatous Leprosy (L.L)

A
  • papules and nodules affecting lips, gums, palate, tongue, uvula & nasal mucosa.
  • Lesions of the nasal mucosa are associated with epistaxis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
215
Q

Eye lesions in Lepromatous Leprosy (L.L)

A

Eyes may be involved resulting in
- keratitis
- iridocyclitis
- iris atrophy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
216
Q

Testicle lesions in Lepromatous Leprosy (L.L)

A

if involved will cause
- sterility
- impotence
- gynaecomastia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
217
Q

Histopathology of Lepromatous Leprosy (L.L)

A

dermis contains
- foamy histiocytes with large number of leprae bacilli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
218
Q

Bacteriology of Lepromatous Leprosy (L.L)

A

Lepra bacilli are present in large number in:
- skin lesion
- nasal smear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
219
Q

Lepromin test result in Lepromatous Leprosy (L.L)

A

Negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
220
Q

Definition of Border line leprosy (B.B)

A
  • This type is immunologically unstable and usually evolves into one of the previous types.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
221
Q

Clinical picture of Border line leprosy (B.B)

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
222
Q

Histopathology of Border line leprosy (B.B)

A
  • mixture of lepromatous and tuberculoid changes.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
223
Q

Bacteriology of Border line leprosy (B.B)

A
  • Lepra bacilli are present in lesions but are fewer in number than in L.L.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
224
Q

Lepromin test in Border line leprosy (B.B)

A
  • weakly positive or negative.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
225
Q

Diagnosis of leprosy

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
226
Q

Complications of leprosy

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
227
Q

Treatment of leprosy

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
228
Q

Types of fungal skin infections

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
229
Q

What causes dermatophytosis (ringworm or tenia)?

A
  • Dermatophytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
230
Q

What causes superficial mycoses?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
231
Q

What causes candidiasis of skin and nails?

A

Candida species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
232
Q

Definition of Dermatophytosis

A
  • fungal infection of keratinous structures (stratum corneum of skin, hair and nails) caused by a group of keratinophilic filamentous fungi called dermatophytes.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
233
Q

Incidence of the previous diseases

A

Common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
234
Q

Pathogenesis of Dermatophytosis

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
235
Q

Mode of Transmission of Dermatophytosis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
236
Q

Etiology of Dermatophytosis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
237
Q

Classification of Dermatophytosis

A
  • According to their usual habitat
  • According to site of infection
  • Clinically
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
238
Q

Anthropophilic dermatophytosis

A
  • Associated with humans only
  • Person to person through contaminated objects (clothes, combs, hats ,brushes and towels)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
239
Q

Classification of Dermatophytosis according to their usual Habitat

A
  • Anthropophilic
  • Geophilic
  • Zoophilic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
240
Q

Organsims causing Anthropophilic dermatophytosis

A
  • Scalp infections like M.audouinii & T.tonsurans.
  • Foot and nail infections like Epidermophyton &T.rubrum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
241
Q

Geophilic dermatophytosis

A
  • Normally inhabit the soil.
  • Some species may cause infections in animals and man following contact with soil
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
242
Q

Organisms causing Geophilic dermatophytosis

A

M.gypseum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
243
Q

Classification of dermatophytosis, according to the site of infection

A
  • Agents of hair
  • Agents of skin
  • Agents of nails
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
244
Q

Zoophilic Dermatophytosis

A
  • Associated with animals, Transmitted directly to humans by close contact with animals.
  • Not from human to human
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
245
Q

Organisms causing Zoophilic Dermatophytosis

A

1- microsporum canis (cats, dogs)

2- M.Equinium (hourses)

3- Trichophyton Verrucosum (cattle)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
246
Q

Agents of hair dermatophytosis

A
  1. Trichophyton
  2. Microsporum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
247
Q

Agents of skin dermatophytosis

A
  1. Trichophyton
  2. Microsporum
  3. Epidermophyton
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
248
Q

Agents of nail dermatophytosis

A
  1. Trichophyton
  2. Epidermophyton
    (rarely microsporum)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
249
Q

Clinical classification of dermatophytosis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
250
Q

What characterizes tinea capitis?

A
  • Disease of children mainly, but it may affect adults also.
  • There are 4 types of tenia capitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
251
Q

What characterizes T. Manum?

A
  • Palms are diffusely dry, scaly & erythematous
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
252
Q

What characterizes T. Corporis?

A
  • Non hairy, smooth skin (trunk-back dorsum of hand)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
253
Q

What characterizes T.pedis?

A

Lesion: include fissures, scales, maceration in toe web &scaling of sole (athlete’s foot)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
254
Q

What characterizes T.ungium?

A
  • children mainly, may affect adults
  • Nails are thickened, discoloured, lusterless & broken.
  • Nail plate may separate from nail bed aka (onycholysis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
255
Q

Sample used in diagnosis of dermatophytosis

A
  • skin scrapping, nail scrapping or clipping, epilation of short length of affected hair.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
256
Q

Direct diagnosis of dermatophytosis

A
  • Direct microscopy
  • Culture
  • Hair perforation test
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
257
Q

Direct microscopy of dermatophytosis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
258
Q

Direct microscopy of hair in Dermatophytosis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
259
Q

Culture of Dermatophytosis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
260
Q

Stain for Dermatophytosis

A

Lactophenol cotton blue (LPCB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
261
Q

Interpretation of hair perforation test

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
262
Q

What does hair perforation test differentiate?

A

It may be helpful in differentiation of T. mentagrophytes from T. rubrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
263
Q

Indirect diagnosis of Dermatophytosis

A
  • molecular diagnosis
  • Serology
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
264
Q

PCR diagnosis of dermatophytosis

A

PCR: detects fungal DNA frorn infected lesion.
Also, species-specific primers are available.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
265
Q

Does Serology have a role in diagnosis of Dermatophytosis?

A
  • No role of serology in diagnosis X X. (Because it’s a localized infection)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
266
Q

Definition of wood’s light

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
267
Q

Wood’s Light

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
268
Q

Where do skin infections by candida occur?

A
  • Skin infection usually occur on sites that becomes abnormally moist warm area as axilla, groin, submammary fold and toe clefts.
  • (In infant&raquo_space;napkin dermatitis).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
269
Q

Clinical manifestations of skin infection by candida

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
270
Q

Sites of nail infection by candida

A
  • Usually finger or toe webs
  • Nail folds paronychia
  • Nail’s onychia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
271
Q

Clinical manifestations of nail infection by candida

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
272
Q

Laboratory diagnosis of skin and nail infections caused by candida

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
273
Q

Culture of candida

A
  • Sabouraud’s dextrose
  • CHROMagar Candida medium
  • Germ tube formation
  • Chlamydospores formation
  • Analytical profile index (API)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
274
Q

Culture of candida on SDA

A
  • On Sabouraud’s dextrose agar at 25 or 37”C for 2 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
275
Q

Identification of growth of candida On SDA

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
276
Q

CHROMagar candida Medium

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
277
Q

Germ tube formation

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
278
Q

Chlamydospores formation

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
279
Q

analytical profile index (API)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
280
Q

Types of superficial mycoses

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
281
Q

Definition of Pityriasis Versicolor

A

Superficial chronic infection of Stratum corneum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
282
Q

What causes hypopigmentation in Pityriasis Versicolor?

A

Discolouration is caused by inhibition of tyrosinase enzyme. (Used in melanin synthesis).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
283
Q

The diagnosis of Pityriasis Versicolor

A

10-30% KOH: clusters of round yeast cell along non branched hyphae (spagetti & meat balls appearance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
284
Q

Etiology of Pityriasis Versicolor

A
  • Malassezia furfur (Pityrosporum orbiculare)
    (Lipophilic yeast).
  • Present as normal flora in area rich in sebaceous gland.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
285
Q

Clinical picture of Pityriasis Versicolor

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
286
Q

Etiology of T.Nigra

A
  • hortae (Exophiala)
    wernekii (pigmented)
  • Frequent in tropical areas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
287
Q

Clinical picture of T.Nigra

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
288
Q

Definition of T.Nigra

A

Brownish maculae on palms, fingers, face.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
289
Q

Site of Black Piedra

A

Fungal infection of the scalp hair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
290
Q

Diagnosis of T.Nigra

A
  • Microscopic examination: Septate hyphae and yeast cells (brown in color)
  • Culture: black colonies.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
291
Q

Etiology of Black Piedra

A

Piedraia hortae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
292
Q

Frequency of Black Piedra

A

Frequent in tropical areas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
293
Q

Clinical picture of Black Piedra

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
294
Q

Site of white Piedra

A

Fungal infection of facial, axillary or genital hair.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
295
Q

Etiology of white Piedra

A

trichosporon (yeast)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
296
Q

Frequency of white Piedra

A
  • Frequent in tropical and temperate zones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
297
Q

Clinical picture of white Piedra

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
298
Q

What is the most common pathogen of fungal infections of nails?

A
  • Dermatophytes are the most common causative pathogen especially Trichophyton rubrum (about 70%). Other causes than dermatophytes include candida
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
299
Q

Antifungal drugs

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
300
Q

Absorption of Amphotericin B

A
  • poorly absorbed from the GIT and is usually administered IV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
301
Q

Category of Amphotericin B

A

B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
302
Q

MOA of Amphotericin B

A
  • Amphotericin B binds ergosterol in fungal cell membrane&raquo_space; form pores in cell membrane&raquo_space;>cell content leak out»> cell death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
303
Q

Pharmacokinetics of Amphotericin B

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
304
Q

Side effects of Amphotericin B

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
305
Q

Forms of Nystatin

A

available as suspension, ointment, cream, powder and tablet (tablet for local use)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
306
Q

Uses of Nystatin

A
  • only topically in Candida infections.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
307
Q

Other Uses of Nystatin

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
308
Q

Side effects of Nystatin

A
  • They include nausea and bitter taste.
  • Category A in pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
309
Q

Category of Nystatin

A
  • Category A in pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
310
Q

Examples of Azoles

A

Topical:
- Miconazole
- Clotrimazole

Systemic:
- Ketoconazole
- Fluconazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
311
Q

Uses of Miconazole & Clotirazole

A

They are used topically for
- Dermatophytic (tinea)
- Candida infections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
312
Q

Forms of Miconazole & Clotirazole

A

They are available as
- cream, gel, lotion
- solution, spray
- vaginal pessary, etc.
- Clotrimazole lozenge is also available.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
313
Q

Characters of Ketoconazole

A
  • It is orally effective
  • Ketoconazole is the most toxic among azoles, but it is less toxic than amphotericin B.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
314
Q

Side effects of Ketoconazole

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
315
Q

Administration of Fluconazole

A

For oral and i.v. administration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
316
Q

Indications for Fluconazole

A

Fluconazole is a drug of choice in
- esophageal and
- oropharyngeal candidiasis.

A single oral dose usually eradicates vaginal candidiasis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
317
Q

Drug interactions of azoles

A
  • 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).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
318
Q

Contraindications of azoles

A
  • Azoles are considered teratogenic, and they should be avoided in pregnancy unless the potential benefit outweighs the risk to the fetus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
319
Q

Uses of Terbinafine

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
320
Q

Side effects of Terbinafine

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
321
Q

Side effects of Griseofulvin

A

disulfiram-like reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
322
Q

Uses of Griseofulvin

A
  • Active only against dermatophytes (orally,not-topically)
  • by depositing in newly formed keratin and disrupting microtubule structure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
323
Q

MOA of Echinocandins (Caspofungin & other fungins)

A

Inhibit the synthesis of beta-1,2 glucan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
324
Q

Uses of Echinocandins

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
325
Q

What are the most commonly used antifungal drugs for oral candidiasis?

A
  • Clotrimazole, nystatin and fluconazole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
326
Q

Antifungal drugs used in pregnancy

A
  • Nystatin and amphotericin B can be used in pregnancy but azoles are better avoided
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
327
Q

What are antifungal drugs used in systemic fungal infections?

A

Azoles, amphotericin B and caspofungin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
328
Q

Indication of Topical azoles

A

dermatophytes and candida

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
329
Q

Indication of Amphotericin B

A

systemic fungal infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
330
Q

Indication of Fluconazole

A
  • esophageal &oropharyngeal candidiasis
  • vaginal candidiasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
331
Q

Indication of Griseofulvin & Terbinafine

A
  • dermatophytes only
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
332
Q

Indication of Echinocandins

A
  • Disseminated candidiasis
  • mucocutaneous candidiasis
  • Invasive aspergillosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
333
Q

Indication of Nystatin

A
  • candidal infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
334
Q

Route of adminstration of Amphotericin B

A

IV infusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
335
Q

Route of adminstration of Ketoconazole & griseofulvin

A

Oral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
336
Q

Route of adminstration of Fluconazole

A

Oral & IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
337
Q

Route of adminstration of Echinocandins

A

IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
338
Q

Superficial fungal infections

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
339
Q

Definition of dermatophyte infections

A
  • These are fungi which have the ability to produce infection of the keratinized tissues as the skin, hair and nails.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
340
Q

Diagnosis of dermatophyte infections

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
341
Q

Clinical types of dermatophyte infections

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
342
Q

Mode of infection by dermatophyte infections

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
343
Q

Definition of T. Capitis

A
  • Dermatophyte infection of the scalp.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
344
Q

Clinical picture of T. Capitis

A
  • Tinea capitis is mainly a disease of children, but it may affect adults.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
345
Q

Types of T. Capitis

A

There are 4 types of tinea capitis:

  • Scaly
  • Blak dot
  • Kerion (Inflammatory type)
  • Favus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
346
Q

M.AC

What causes Scaly type of T.Capitis?

A
  • Microsporum audouinii &
  • Microsporum canis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
347
Q

CP in Scaly type of T.Capitis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
348
Q

T. TV

What causes Black dot T.Capitis?

A
  • Trichophyton tonsurans
  • Trichophyton violaceum.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
349
Q

CP of Black dot T.Capitis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
350
Q

What causes the presence of black dots in Black dot T.Capitis?

A

Due to breaking of hair shafts at the skin surface.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
351
Q

What causes Kerion T.Capitis?

A

animal fungi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
352
Q

Presentations of Kerion T.Capitis

A

There are two presentations:
- Abcess like swelling
- Well defined dull red plaque studded wit multiple pustules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
353
Q

CP of abcess-like swelling of kerion T.Capitis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
354
Q

What causes favus T.Capitis?

A

Trichophyton schoenleinii

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
355
Q

CP of Favus T.Capitis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
356
Q

What is a Scutulum?

A
  • A scutulum is a concave yellow crust surrounding the hair follicle opening and has a mousy odour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
357
Q

Diffrential diagnosis of T.Capitis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
358
Q

Preventive measures of T.Capitis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
359
Q

Treatment of T.Capitis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
360
Q

Mode of Infection by T.Barbae

A
  • From man to man through infected towels or in the barber’s shop.
  • Infected animals transmit infection to farmers.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
361
Q

Definition of T.Barbae

A

Dermatophyte infection of the beard and moustache areas of adult male.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
362
Q

CP of T.Barbae

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
363
Q

DD of T.Barbae

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
364
Q

TTT of T.Barbae

A

Similar to tinea capitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
365
Q

Definition of T.Corporis

A
  • Tinea corporis is a dermatophyte infection of the (glabrous skin) of the trunk and extremities, excluding the hair, nails, palms, soles and groin.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
366
Q

Mode of infection by T.Corporis

A
  1. Infected Person
  2. Infected Animals (domestic animals) or soil-to-human spread.
  3. Autoinoculation (from tinea capitis or pedis).)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
367
Q

CP of T.Corporis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
368
Q

Diagnosis of T.Corporis

A
  • Scraping & M.E: scraping is done from the raised border of the lesion&raquo_space;» Spores & hyphae
  • Culture: on sabouraud’s agar media
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
369
Q

Def of T.Cruris

A
  • Dermatophyte infection of the groins.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
370
Q

DD of T.Corporis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
371
Q

TTT of T.Corporis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
372
Q

Mode of infection by T.Cruris

A
  • Auto inoculation.
  • Sharing cloths & towels.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
373
Q

Predisposing factors for T.Cruris

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
374
Q

CP of T.Cruris

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
375
Q

Diagnosis of T.Cruris

A
  • Scraping,ME
  • culture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
376
Q

DD of T.Cruris

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
377
Q

TTT of T.Cruris

A

Similar to T. Circinata

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
378
Q

Def of T.Pedis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
379
Q

Predisposing factors for T.Pedis

A
  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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
380
Q

What is the most common form of dermatophyte infections?

A

Tinea Pedis

381
Q

CP of T.Pedis

A

3 types:

  • Interdigital T. pedis
  • Scaly hyperkeratotic type
  • Vesiculo-bullous type
382
Q

Epidemiology of T.Pedis

A

Common in adults than children and in males than females.

383
Q

What is the most common form of T.Pedis?

A

Interdigital T. pedis:

384
Q

CP of Interdigital T.Pedis

A
385
Q

CP of Scaly Hyperkeratotic T.Pedis

A
386
Q

CP of Vesiculo-Bullous T.Pedis

A
387
Q

Diagnosis of T.Pedis

A
  • Scraping, ME
  • Culture
388
Q

DD of Interdigital T.Pedis

A
389
Q

DD of Scaly Hyperkeratotic T.Pedis

A
390
Q

DD of Vesiculo-Bullous T.pedis

A
391
Q

TTT of T.Pedis

A
392
Q

Def of T.Manum

A

Dermatophyte infection of the palmar skin.

393
Q

Mode of infection by T.Manum

A
  1. Infected human
  2. infected animal.
  3. Auto inoculation (from tinea pedis).
394
Q

Predisposing factors of T.Manum

A
  • Trauma and maceration between fingers.
  • Poor peripheral circulation.
395
Q

CP of T.Manum

A
396
Q

DD of T.Manum

A
397
Q

TTT of T.Manum

A

Similar to T.Pedis

398
Q

Def of Onchyomycosis (T.Unguium)

A
  • Onychomycosis is a fungal infection of the nails.
  • More than 50% of cases of nail dystrophy is due to onychomycosis
399
Q

MOI by Onchyomycosis (T.Unguium)

A
  • 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
Q

What attributes to 50% of cases of nail dystrophy?

A

onychomycosis

401
Q

Predisposing factors for Onchyomycosis (T.Unguium)

A

1- Trauma to the nail.
2. Poor peripheral circulation.
3. Old age, where the linear growth of nail is slow.

402
Q

CP of Onchyomycosis (T.Unguium)

A
403
Q

Diagnosis of Onchyomycosis (T.Unguium)

A
  • Nail clipping is put in 5% KOH solution for 24 hours then examined under microscope for fungus
  • culture
404
Q

DD of Onchyomycosis (T.Unguium)

A
405
Q

TTT of Onchyomycosis (T.Unguium)

A
406
Q

Topical antifungals for dermatophyte infections

A
407
Q

Systemic antifungals for dermatophyte infections

A
408
Q

Def of Pityriasis Versicolor

A
  • Mild, Chronic superficial fungus infection of the horny layer of the skin caused by Malassezia furfur
409
Q

What causes Pityriasis Versicolor?

A

Malassezia furfur

(Pathogenic form of the normal skin flora, pityrosporum orbiculare).

410
Q

Predisposing factors of Pityriasis Versicolor

A
411
Q

Clinical picture of Pityriasis Versicolor

A
412
Q

Epidemeology of Pityriasis Versicolor

A

Common skin disease, affecting adults more than children.

413
Q

Site of Pityriasis Versicolor

A
  • Any site however the commonest sites affected are trunk, neck & upper arms, Face is commonly affected in children
414
Q

Diagnosis of Pityriasis Versicolor

A
415
Q

Course of Pityriasis Versicolor

A
  • 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
Q

DDx of Pityriasis Versicolor

A
417
Q

TTT of Pityriasis Versicolor

A

Topical & Systemic

418
Q

Topical TTT of Pityriasis Versicolor

A
419
Q

Systemic TTT of Pityriasis Versicolor

A
420
Q

Def of Candidiasis (Monaliasis)

A
  • Infection of the skin or mucous membranes by candida albicans.
421
Q

What causes Candidiasis (Monaliasis)?

A

Candida albicans

422
Q

Predisposing factors of Candidiasis (Monaliasis)

A
423
Q

CP of Cutaneous Candidiasis (Monaliasis)

A
  • Intertdigital candidiasis
  • Candidal intertrigo
  • Napkin candidiasis
424
Q

Napkin Candidiasis

A
425
Q

Candidal intertrigo

A
426
Q

Interdigital candidiasis

A
427
Q

Bacterial co-pathogen usually preset in the interdigital,intertrigenous types

A

..

428
Q

Where is Candidal paronychia common?

A
  • Common in housewives, cooks and those whose hands are frequently immersed in water.
429
Q

CP of Candidal onychia

A
430
Q

CP of Candidal paronychia

A
431
Q

What are types of Mucosal candidiasis?

A
  • Oral Candidiasis
  • Candidal vulvovaginitis
  • Candidal balanitis
432
Q

Forms of Oral candidiasis

A
  • oral thrush
  • Acute atrophic type
  • Chronic atrophic type (Denture stomatitis)
  • Chronic Hyperplastic leukoplakia –>Black hairy tongue
  • Angular Cheilitis (perleche)
  • Candidal Cheilitis
433
Q

Oral thrush

A
434
Q

Acute atrophic type of oral candidiasis

A
435
Q

Chronic atrophy type (dentures stomatitis) of oral candidIasis

A
436
Q

Angular cheilitis (Perleche)

A
437
Q

Chronic hyperplastic type (candidal leukoplakia) & black, hairy tongue

A
438
Q

Candidal cheilitis

A
439
Q

CP of Candidal vulvovaginitis

A
440
Q

CP of candidial balanitis

A
441
Q

TTT of candida

A
  • TTT of predisposing factors
  • Topical
  • Systemic
442
Q

Topical TTT of Candida

A
443
Q

Systemic TTT of Candida

A
444
Q

What are viral skin diseases?

A
  • Herpes Simplex.
  • Chicken pox.
  • Herpes Zoster.
  • Warts.
  • Molluscum contagiosum.
  • Pityriasis Rosea
445
Q

What is the most common recurrent viral infection of skin and mucus membranes?

A
  • Herpes Simplex
446
Q

Etiology of herpes simplex

A
  • H. virus type I: affects the skin and mucous membranes.
  • H. virus type II: affects the genitals.
447
Q

Mode of infection by herpes simplex

A

Direct inoculation.

448
Q

Characters of Primary herpes simplex

A
  • 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
Q

CP of herpes simplex

A
  • Two types are recognized primary and recurrent.
450
Q

Lesions of primary herpes simplex

A

usually minimal or subclinical.

451
Q

In what kind of people do primary lesion of herpes simplex Appear?

A
  • Develops in persons without pre-existing immunity to HSV
  • Severe cases occur in patients with immune defect, malignancy, malnutrition or atopic dermatitis.
452
Q

Incidence of Gingivostomatitis

A
  • The commonest form
  • Most cases occur in infants and young children
453
Q

CP of Gingivostomatitis

A
454
Q

Lesion of Gingivostomatitis

A
  • The gums are swollen, red and easily bleed.
  • Vesicles rupture forming white erosions with red areola on oral mucosa
455
Q

Systemic manifestations of Gingivostomatitis

A
  • High fever, malaise, dribbling, painful eating and foul breath
456
Q

Site of Gingivostomatitis

A
457
Q

LNs affection in Gingivostomatitis

A
  • Regional LNs (Submental) are enlarged and tender
458
Q

CP of Keratoconjunctivits

A
459
Q

Course of Gingivostomatitis

A
  • After 3-5 days fever subsides and complete recovery occurs in about 2 weeks
460
Q

Lesions in Keratoconjunctivits

A

Conjunctivitis and keratitis

  • The eye lids are edematous
  • There may be vesicles on the surrounding skin
461
Q

Site of Keratoconjunctivits

A
462
Q

LNs affection in Keratoconjunctivits

A

Regional LNs (preauricular) are enlarged and tender

463
Q

Complications of Keratoconjunctivits

A

It may cause corneal ulcer that leave scar which may result in impairment of vision. (Because it heals by fibrosis)

464
Q

Incidence of Inoculation HS

A
  • Commonly seen in dentists and nurses
465
Q

Lesions in Inoculation HS

A

Painful vesicles

  • E.g., Herpetic whitlow: painful vesicles on fingertips that may be seen in young children, dentists and nurses (HSV1)
466
Q

What is the clue to diagnosis in Inoculation HS?

A

Recurrences in the same location

467
Q

Site of Inoculation HS

A
  • 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
Q

What are Lesions of HS in Eczema Herpeticum complicated by?

A

Occasionally complicated by
- bacterial superinfections or
- systemic dissemination of HSV infection

469
Q

Lesions of HS in Eczema Herpeticum

A

Lesion of H.S. may appear

  • on the top of atopic dermatitis or
  • may be generalized.
470
Q

Lesions of primary infection by Gental HS?

A
  • Vesicles which rapidly rupture forming erosions and painful white plaques on a red oedematous mucous membranes
471
Q

Site of primary infection by Gental HS

A
  • are seen in the genitals of both sex.
  • other sites include buttocks and perineum in both sexes
  • cervix in women.
472
Q

LNs Affection in primary infection by Gental HS

A
  • Inguinal lymph nodes are enlarged and tender.
473
Q

Complication of primary infection by Gental HS

A
  • Genital H.S. in homosexual suffering from AIDS may present with chronic perianal ulceration.
474
Q

Latency of HS

A
  • virus may remain hidden in a latent form within the sensory ganglion and sensory nerve which supply the infected area.
475
Q

Reactivation of HS

A
  • 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
Q

CP of reactivated HS

A
477
Q

Sites of Reactivated HS

A
  • 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
Q

Course of Reactivated HS

A
  • The vesicles dry forming crust and healing occurs without scar within 7-10 days.
479
Q

Complications of Reactivated HS

A
480
Q

TTT of Reactivated HS

A
481
Q

Etiology of Chicken Pox (Varicella)

A
  • Varicella is the primary infection with varicella-zoster virus.
482
Q

MOI by Chicken Pox (Varicella)

A
  • Droplet infection from the nasopharynx (main route).
  • Direct contact with the vesicular fluid.
483
Q

IP of Chicken Pox (Varicella)

A

10 - 20 days. around from 2 wks to 3 wks

484
Q

Infectivity period of Chicken Pox (Varicella)

A
  • 2 days before and 8 days after the rash onset (when all vesicles have been crusted).
485
Q

CP of Chicken Pox (Varicella)

A
486
Q

Ages affected by Chicken Pox (Varicella)

A

children more than adults.

487
Q

Prodorma in Chicken Pox (Varicella)

A
  • absent or 1-2 days of fever & malaise.
488
Q

Lesions in Chicken Pox (Varicella)

A
489
Q

Sites of Chicken Pox (Varicella)

A
  • Trunk (centripetal), face, scalp and limbs.
  • Oral mucosa especially palate may contain vesicles.
490
Q

Chicken Pox (Varicella) In Immunocomprimised patients

A
491
Q

Diagnostic Criteria in Chicken Pox (Varicella)

A
  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
Q

Complications of Chicken Pox (Varicella)

A
493
Q

TTT of Chicken Pox (Varicella)

A

symptomatic TTT & Systemic Anticirals

494
Q

Symtomatic TTT of Chicken Pox (Varicella)

A

Required for most children (immunocompetent) (no specific treatment)

  • Antipyretic for fever:(avoid salicylate).
  • Antihistamine for itching.
  • Antibiotic for secondary infection.
  • Topical antiseptic.
495
Q

Systemic TTT of Chicken Pox (Varicella)

A
  • Acyclovir or Valacyclovir (which must be given within
    24-72 hours of onset of lesion).
496
Q

Indications of Systemic TTT in Chicken Pox (Varicella)

A
  • Immunocompromised patients .
  • Varicella in pregnant woman.
  • Severe varicella in immunocompetent children
  • Neonatal varicella (Acyclovir IV Infusion)
497
Q

Prophylaxis from Chicken Pox (Varicella)

A
  • Varicella-zoster immune globulin: immediate post exposure prophylaxis
  • Live attenuated varicella vaccine (Varivax®): routine vaccination (active immunity).
498
Q

TTT of pregnant woman with Chicken Pox (Varicella)

A
  • IV acyclovir
  • women who are not immune to varicella but are exposed may be treated with VZIG
499
Q

Category of acyclovir

A

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
Q

TTT of infant with Chicken Pox (Varicella)

A
  • 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
Q

Dose of VZIG in Chicken Pox (Varicella)

A
502
Q

Def of Herpes Zoster (shingles)

A
  • Acute condition characterized by grouped vesicles along course of sensory nerve.
503
Q

Etiology of Herpes Zoster (shingles)

A

Varicella zoster virus

  • Latency: H.Z. results from reactivation of latent virus that persists in sensory ganglia after recovery from chicken pox.
504
Q

Predisposing factors for Herpes Zoster (shingles)

A

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
Q

Is HZ a STD?

A

No

506
Q

CP of Herpes Zoster (shingles)

A
  • Fever, headache, malaise
  • Neuralgic pain : 1st symptom
  • Lesions
  • regional lymph nodes are tender and affected
507
Q

Neurologic pain of Herpes Zoster (shingles)

A
  • 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
Q

Lesions in Herpes Zoster (shingles)

A
  • 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
Q

Complications of Herpes Zoster (shingles)

A
510
Q

Sites of lesions of Herpes Zoster (shingles)

A
  • The most common sites affected are thoracic area followed by cervical, trigeminal (including ophthalmic branch) and lumbosacral areas.
511
Q

Special types of Herpes Zoster (shingles)

A
  • Abortive
  • Gangrenous
  • Haemorrhagic
  • An eruption of varicella with HZ
512
Q

TTT of Herpes Zoster (shingles)

A
  • Topical
  • Systemic
  • TTT of PHN
513
Q

Topical TTT of Herpes Zoster (shingles)

A
  • antiseptic, antibiotic.
514
Q

Systemic TTT of Herpes Zoster (shingles)

A
  • Must be given within 7 days after the onset of skin lesions.
  • Acyclovir, Famciclovir and Valacyclovir
515
Q

Indications of Systemic TTT of Herpes Zoster (shingles)

A
  • 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
Q

TTT of PHN

A
  • 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
Q

Def of Pityriasis Rosea

A
  • Pityriasis rosea is an acute self-limiting skin disease, characterized by distinctive skin eruption.
518
Q

Etiology of Pityriasis Rosea

A

May be viral

519
Q

Epidemeology of Pityriasis Rosea

A
  • More common in young adults (children & young adult) (power)
  • More common in autumn and spring.
520
Q

Types of Pityriasis Rosea

A
  • Classic
  • Special types
521
Q

Manifestations of classic type of Pityriasis Rosea

A
522
Q

Sites of the Classic type of Pityriasis Rosea

A
  • trunk, neck & proximal parts of extremities.
  • However, involvement of the face and scalp is common especially in children.
523
Q

Course of Pityriasis Rosea

A
  • 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
Q

Special types of Pityriasis Rosea

A
  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
Q

DDx of Pityriasis Rosea

A
526
Q

TTT of Pityriasis Rosea

A
  • Reassurance.
  • Avoid soap, hot bath and woolen clothing.
  • Antihistamines for itching.
  • Antipruritic topical agent or mild steroid for irritable lesions.
  • UVR.
527
Q

Def of Warts

A
  • Benign, usually self-regressing infectious new growth of the skin and adjacent mucous membranes caused by human papilloma virus (HPV).
528
Q

Recurrence in Warts

A
  • Recurrence is common even after treatment due to the presence of HPV DNA in the normal-appearing skin surrounding HPV-associated lesions.
529
Q

MOI by Warts

A
530
Q

Clinical types of Warts

A
  1. Common warts (Verrucae vulgares)
  2. Plane wart.
  3. Plantar wart.
  4. Filiform wart.
  5. Digitiform wart.
  6. Genital wart (Condyloma acuminatum).
531
Q

Compare between Common & Plane warts

A
532
Q

Lesions in plantar (and palmar) warts

A
533
Q

Compare between Filiform & Digitiform warts

A
534
Q

Sites of plantar (and palmar) warts

A

pressure areas of the soles or palms.

535
Q

DDx of plantar (and palmar) warts

A
536
Q

Def of Genital warts (Condyloma accuminata)

A
  • 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
Q

Lesions in Genital warts (Condyloma accuminata)

A
  • 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
Q

Sites of Genital warts (Condyloma accuminata)

A
  • External genitalia and the perineum, perianally.
  • Lesions may extend into the vagina, cervix, urethra, or anal canal
539
Q

Resolving of Genital warts (Condyloma accuminata)

A
  • May resolve spontaneously but may persist in 10-30% of cases.
540
Q

Oncogenic potential of HPV

A
  • 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
Q

DDx of Genital warts (Condyloma accuminata)

A
542
Q

TTT of Warts

A

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
Q

Elctrocautery in Warts

A
  • 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
Q

Cryotherapy in TTT of Warts

A
  • Using coz snow or liquid nitrogen, cause destruction by freezing
545
Q

Chemical Cautery in TTT of warts

A
546
Q

Other methods used in TTT of warts

A
547
Q

TTT of Anogenital wart

A
548
Q

TTT of Planter wart

A

Salicylic acid, if multiple use formalin

549
Q

TTT of Common wart

A

Salicylic acid, Imiquimod

550
Q

TTT of Condyloma Accuminata

A

Podophyllin, if resistant use interferon

551
Q

TTT of Plane wart

A

Retinoic topical, Imiquimod

552
Q

TTT of Resistant & Multiple warts

A

Levimizole

553
Q

TTT of Anogenital wart

A

Imiquimod

554
Q

Prevention of Warts

A

proactive vaccine for genital HPV infection

555
Q

Def of Mulluscum Contagiousm

A
  • Molluscum contagiosum is a pox virus skin infection caused by Molluscum Contagiosum virus (MCV) with characteristic shiny pearly-white umbilicated papules.
556
Q

MOI by Mulluscum Contagiousm

A
  • Contact with patient or contaminated objects
  • Auto inoculation.
557
Q

CP of Mulluscum Contagiousm

A
558
Q

Course of Mulluscum Contagiousm

A
  • Spontaneous regression may occur in some lesions within 6-9 months.
559
Q

Sites of Mulluscum Contagiousm

A
  • Face, trunk, and genital areas are the sites of predilection.
  • However, any site may be affected.
560
Q

TTT of Mulluscum Contagiousm

A
561
Q

Classes of Antiretroviral drugs

A
  • Nucleoside Reverse Transcriptase Inhibitors (NRTIs)
  • Non-nucleoside Reverse Transcriplase Inhibilors NNRTIs)
  • Protease Inhibitors (Pls)
562
Q

MOA of Nucleoside Reverse Transcriptase Inhibitors (RTIs)

A
563
Q

Examples of Nucleoside Reverse Transcriptase Inhibitors (RTIs)

A

Nucleoside Reverse Transcriptase Inhibitors (NRTIs):
- Zidovudine [Azidothymidine (AZT)]

Other Nucleoside Reverse Transcriptase Inhibitors (NRTIs):
- Didanosine, Stavudine, Emtricitabine and Lamivudine

564
Q

Uses of Zidovudine [Azidothymidine (AZT)]

A
565
Q

AE of Zidovudine [Azidothymidine (AZT)]

A

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
Q

Uses of Didanosine, Stavudine, Emtricitabine and Lamivudine

A
  • They are effective orally.
  • Lamivudine is a commonly used agent in antiretroviral therapy because of its efficacy and low toxicity.
567
Q

AE of Didanosine, Stavudine, Emtricitabine and Lamivudine

A

1- peripheral neuritis
2- pancreatitis, gastrointestinal disturbances
3- lactic acidosis
4- skin rashes, etc.

568
Q

Examples of Non-nucleoside Reverse Transcriplase Inhibilors NNRTIs)

A

Nevirapine & Efavirenz

569
Q

MOA of Non-nucleoside Reverse Transcriplase Inhibilors NNRTIs)

A
570
Q

AE of Non-nucleoside Reverse Transcriplase Inhibilors NNRTIs)

A

1- Skin rashes, pruritus.

2- Fever, nausea.

3- CNS disturbances like headache, confusion, insomnia, bad dreams, amnesia, etc.

571
Q

Examples of Protease Inhibitors (Pls)

A

Lopinavir, Saquinavir, Ritonavir (navir)

572
Q

MOA of Protease Inhibitors (Pls)

A
573
Q

AE of Protease Inhibitors (Pls)

A
574
Q

Drug interactions of Protease Inhibitors (Pls)

A
  • 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
Q

Introduction to Treatment of HIV Infection

A
  • 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
Q

Objectives of anti-HIV therapy

A
577
Q

Regimens in anti-HIV therapy

A
578
Q

How require prophylactic therapy to HIV?

A
  • 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
Q

Principles of anti-HIV therapy

A
580
Q

The need of HIV PEP depens on ……

A

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
Q

Basic & Expanded regimens in prophylaxis of HIV

A
582
Q

Activity, Clinical Uses of Acyclovir

A
583
Q

MOA of Acyclovir

A
  • 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
Q

AE of Acyclovir

A
  • Minor with oral use
  • More obvious with IV
  • Crystalluria (maintain full hydration) and neurotoxicity (agitation, headache, confusion)
  • Acyclovir is not hematotoxic
585
Q

MOA of Ganciclovir

A

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
Q

Activity, Clinical Uses of Ganciclovir

A

Of Ganciclovir

  • HSV, VZV, and CMV
  • Mostly used in prophylaxis and treatment of CMV infections, including retinitis, in AIDS and transplant
587
Q

AE of Ganciclovir

A
  • Dose-limiting hematotoxicity (leukopenia, thrombocytopenia),
  • Mucositis, fever, rash, crystalluria(maintain hydration);
  • Seizures in overdose
588
Q

Def of Scabies

A
  • Scabies is a contagious disease caused by a mite, the female Sarcoptes scabiei; which invade the epidermis and form a burrow.
589
Q

MOI by Scabies

A
590
Q

IP of Scabies

A

2 weeks- 2 months.

591
Q

Pathogonomic lesions of Scabies

A

Burrows which may be present in a few or large numbers.

592
Q

Lesion of Scabies

A
593
Q

CP of Scabies

A
594
Q

Distribution of lesions in Scabies

A
595
Q

Difference of animal scabies from Human scabies

A

The difference from human scabies are:
- Shorter I.P.
- Self-limiting after eliminating the source of infection.

596
Q

Sites of Animal Scabies

A
  • localized or generalized according to the mode of exposure. Webs & genitalia are free.
597
Q

Lesions of Animal Scabies

A

papules, wheals or papulovesicles with absence of burrows.

598
Q

Transmission of Animal Scabies

A

not transmitted from human to human.

599
Q

Scabies in infants and young children

A
  • has Atypical distribution of lesions with involvement of scalp, face, neck, palms and soles.
600
Q

Nodular scabies

  • Lesions
  • Sites
  • Cause
A
  • 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
Q

Scabies Incognito
- Lesions
- Distribution

A
  • The lesions and the course are modified by the application of topical or systemic steroids.
  • Scabies has unusual extent and distribution.
602
Q

What does Crusted (Norwegian) scabies represent?

A
  • This type represents an abnormal host immune response to the mite.
603
Q

Where is Crusted (Norwegian) scabies Seen?

A
  • Mentally retarded.
  • Patients with poor cutaneous sensation
  • Patients with severe systemic diseases like leukemia and DM.
  • Patients with severe immunosuppression (e.g., AIDS).
604
Q

CP of Crusted (Norwegian) scabies

A
  • 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
Q

Complications of Scabies

A
606
Q

Diagnostic Criteria of Scabies

A
607
Q

TTT of Scabies

A
  • General Treatments
  • Topical Scabicides
  • Systemic Scabicidies
608
Q

Topical Scabicides in TTT of Scabies

A
609
Q

Systemic TTT of Scabies

A
610
Q

Causes of persistent itching after treatment of scabies

A
611
Q

Scabies in Bed-Ridden

A
  • Like classic scabies but lesion is more common in the area with contact with bed
612
Q

Scabies In Clean

A
  • Difficulty to see the burrows due to frequent bathing.
613
Q

Venereal Scabies

A
  • Like classic scabies but NOT maybe sexually transmitted (In this case u must search for other venereal diseases)
614
Q

DDx of scabies

A
  • Popular urticaria
  • Eczema
  • Erythema multiform
615
Q

General Measures During TTT of Scabies

A
  • 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
Q

What is the drug of Choice in pregnant women with Scabies?

A
  • 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
Q

TTT of Nodular Scabies

A

1- Intralesional injection of steroid
2- Surgical excision.

618
Q

Def of Pediculosis

A
  • Pediculosis is caused by lice which are small gray-brown, blood sucking parasites
619
Q

Eggs of Females

Pediculosis

A
  • Each female lays many eggs which appear as
    white nits firmly attached (cemented) to the hair shaft
  • Each nit hatches within a week.
620
Q

CP of Pediculosis

A
621
Q

Site of Pediculosis

A
  • Pediculosis Capitis occurs on the hair of the scalp, mainly above the ears and occiput.
  • Beard and moustache may be infested.
622
Q

MOI by Pediculosis

A
  • Pediculosis capitis is communicated by direct contact, sharing hats, combs & brushes.
623
Q

Epidemeology of Pediculosis

A
  • Although the disease is more common in children, it may occur in adults
624
Q

what is Pediculosis associated with?

A
  • There is itching of the scalp this causes scratching with impetigo and cervical lymphadenopathy.
  • The general health may be impaired from septic absorption.
625
Q

TTT of Pediculosis

A
626
Q

Types of Pediculosis

A
  • P. Capitis
  • P. Corporis
  • P. Pubis
627
Q

Other names of Pediculosis pubis

A

(Crab lice, Pthirus pubis)

628
Q

Def of Pediculosis pubis

A
  • The pubic louse is sexually transmitted and is mostly found in young adults.
629
Q

Sites of Pediculosis pubis

A
  • Pubic lice infest the pubic and perineal hair
  • It may also infect the eye lashes
630
Q

Lesions of Pediculosis pubis

A
  • 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
Q

Def of Urticaria

A
  • Urticaria is an acute skin disorder characterized by formation of wheals
  • It may be allergic or non-allergic.
632
Q

what does Liberation of histamine and or other substances from the mast cells results from?

A
  • From Allergic Reaction nearby the mast cells
  • From Non-Allergic Reaction, i.e., direct action of certain stimuli on mast cells.
633
Q

Causes of Urticaria

A
634
Q

CP of Urticaria

A
635
Q

What is Urticaria associated with?

A
  • 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
Q

What Characterizes Urticaria?

A
  • 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
Q

Course of Urticaria

A
  • 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
Q

Special Types of Urticaria

A
639
Q

TTT of Urticaria

A
640
Q

Def of Papular Urticaria (Prurigo simplex)

A

Hypersensitivity to insect bites such as fleas and mosquitoes.

641
Q

CP of Papular Urticaria (Prurigo simplex)

A
642
Q

Sites of Papular Urticaria (Prurigo simplex)

A
  • The eruption occurs mainly on the limbs.
  • The trunk may show few lesions.
643
Q

Epidemeology of Papular Urticaria (Prurigo simplex)

A
  • It is frequently seen in children moving to new areas where mosquitoes prevail.
644
Q

Prognosis of Papular Urticaria (Prurigo simplex)

A
645
Q

Diagnosis of Atopic Dermatitis

A

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
Q

TTT of papular urticaria

A
647
Q

Def of Atopic Dermatitis

A
  • 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
Q

How id atopy Determined?

A
  • 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
Q

CP of Atopic Dermatitis

A
  • The cardinal symptom is pruritus. (itching)
  • Dry scaly skin
  • Crusted lesions on face, scalp, trunk & extremities
  • Lichenification (with chronic course)
650
Q

Etiology of Atopic Dermatitis

A

Genetic defect in fillagerin gene leading to defective skin barrier

651
Q

Causes of exacerbation of Atopic Dermatitis

A
  • 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
Q

Types of Atopic Dermatitis

A

1- Infantile atopic dermatitis.
2- Childhood atopic dermatitis.
3- Adulthood atopic dermatitis.

653
Q

Lesion in Infantile Atopic Dermatilis

A
  • Edematous Erythematous discrete & confluent papules.
  • Severe itching > Oozing & crusting plaques.
654
Q

Course of Infantile Atopic Dermatilis

A
  • 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
Q

Age of Infantile Atopic Dermatilis

A

2 months - 2 years

656
Q

Sites of Infantile Atopic Dermatilis

A

The usually affected site:
- The face, particularly the cheeks.
- Scalp
- Neck
- Extensor aspects of the extremities
- Trunk.

657
Q

Age of Childhood Atopic Dermatilis

A

2-12 years

658
Q

Lesion in Childhood Atopic Dermatilis

A
  • The lesions are less exudative (i.e., dry skin) & tend to lichenify especially in the flexures (Flexural eczema, Besnier’s prurigo)
659
Q

Course of Childhood Atopic Dermatitis

A
  • About 50% of cases may clear by the age 12 years
  • Otherwise, it changes into the adult phase.
660
Q

Sites of Childhood Atopic Dermatitis

A
  • 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
Q

Prognosis of Infantile & Childhood Atopic Dermatitis

A
  • 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
Q

Age & Lesions of Adult/Adolescent Atopic Dermatilis

A

> 12 years

  • Similar to the childhood phase in showing areas of lichenification in the flexures
663
Q

Course of Adult/Adolescent Atopic Dermatilis

A
  • 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
Q

CP of Childhood Atopic Dermatitis

A
665
Q

Pityriasis alba

A
666
Q

Juvenile planter dermatosis

A
667
Q

Prurigo of Hebra

A
668
Q

Xerosis

A
669
Q

CP of Adult/Adolescent atopic dermatitis

A
670
Q

Regional variants of Atopic Dermatitis

A
671
Q

Complications of Atopic Dermatitis

A

1- Bacterial infection.

2- Viral infections (warts and mollusca contagiosa).

3- Eczema herpeticum (herpes simplex viral infection of eczematous skin).

672
Q

Diagnostic Criteria of Atopic Dermatitis

A
673
Q

TTT of Atopic Dermatitis

A
  • General Measures
  • Regular Emollient therapy
  • Topical Anti-inflammatory Therapy
  • Systemic therapy
674
Q

General Measures of Atopic Dermatitis

A
  • 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
Q

Regular Emolient Therapy in Atopic Dermatitis

A

(ointment or water in oil creams): Basic line in treatment of all cases.

676
Q

Systemic Therapy in Atopic Dermatitis

A
677
Q

Topical Anti-Inflammatory therapy in Atopic Dermatitis

A
  • 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
Q

Side effects of TCS

A
679
Q

AE of Pompholyx

A
680
Q

Def of Pompholyx

A
  • Crops of severely Itchy, deeply seated vesicles on palms & soles.
  • Remission within 2 wks + Recur
681
Q

TTT of Pompholyx

A

Topical:
- Drying lotion.
- Topical steroid.

Systemic:
- Antibiotic.
- short course steroid.

682
Q

What is Pityriasis Alba?

A
  • It is a non-specific dermatitis characterized by oval or round dry scaly patches which subside with hypopigmentation.
683
Q

Epidemeology of Pityriasis Alba

A
  • It is more common in atopics but not confined to them.
  • It is mainly seen in children and young adults.
684
Q

Site of Pityriasis Alba

A
  • The face is the most frequently involved site.
    Other areas as the neck, arms & trunk may be involved.
685
Q

Resolution of Pityriasis Alba

A

Most cases subside in few months. Recurrence may occur.

686
Q

TTT of Pityriasis Alba

A

topical emollient.

687
Q

Def of Eczema

A
  • Eczema is a severe dermatitis (inflammation of the skin) characterized by itching, oozing & burning sensation.
688
Q

Stages of Eczema

A
689
Q

what induces Eczema?

A

induced by a wide range of external or internal factors.

690
Q

Classification of Eczema

A
691
Q

Def of Contact Dermatitis

A
  • Contact dermatitis is an inflammatory skin disease induced by exposure to external injury; chemical or physical.
692
Q

Cause of Irritant Contact Dermatitis

A

results from exposure of the skin to an irritant

693
Q

Types of Contact Dermatitis

A
694
Q

what is an Irritant?

A
  • An agent that is capable of producing dermatitis on the first exposure
695
Q

is Irritant Contact Dermatitis an immunulogical process?

A

No

696
Q

what does the reaction of the skin to irritant depend on?

A
  • 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
Q

Examples of irritants

A
698
Q

Is Allergic contact dermatitis an immunulogical process?

A
  • 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
Q

What causes Allergic contact dermatitis?

A
  • It results from exposure of the skin to a Sensitizer (contact allergen)
700
Q

what is a Sensitizer?

A
  • An agent that is Not capable of producing dermatitis on the first exposure but causes dermatitis after a latent period on further exposure.
701
Q

Types of Allergic contact dermatitis

A

The dermatitis may be acute, subacute or chronic.

702
Q

what causes Photoloxic CD?

A
  • occur after activation of an irritant by UVR.
703
Q

Examples of Sensitizers

A
704
Q

Sites of Photoloxic CD

A

localized to areas of exposure

705
Q

Examples of phototoxic agents

A
  • 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
Q

what causes Photoallergic CD?

A
  • occur after activation of a sensitizer by UVR
707
Q

Examples of Photoallergic agent

A
  • Perfumes
  • Cosmetics
  • Sunscreen.
708
Q

what causes Infective Dermatitis?

A
  • by micro-organism products.
709
Q

CP of Infective Dermatitis

A
  • erythema, pustules
  • oozing, crust
  • maybe dry & scaly
710
Q

Sites of Infective Dermatitis

A
  • Around discharging ear.
  • Wound, ulcer & sinuses.
  • Scalp in Pediculosis.
  • Trunk in scabies.
711
Q

TTT of Infective Dermatitis

A
  • Topical drying lotion: KMn04,saline.
  • Topical Abic-steroid combination
  • Systemic Abic.
712
Q

Dx of Contact Dermatitis

A
713
Q

Prevention of Contact Dermatitis

A
  1. Avoid contact
  2. Protect skin
  3. Check early signs of dermatitis
714
Q

TTT of Contact Dermatitis

A
715
Q

Def of Erythema Multiforme

A
  • Acute self- limited skin disease characterized by target or iris lesion.
716
Q

Etiology of Erythema Multiforme

A
717
Q

CP of Erythema Multiforme minor

A
718
Q

TTT of Erythema Multiforme

A

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
Q

CP Erythema Multiforme Major

A
720
Q

Course of Erythema Multiforme

A
  • E.M. usually fades within 2-4 weeks
  • E.M tends to recur (in 30% of cases)
721
Q

Def of Erythema Nodosum

A
  • Inflammation of subcutaneous fat (panniculitis) presents as an acute self-limited painful nodular erythematous eruption.
722
Q

Etiology of Erythema Nodosum

A
723
Q

CP of Erythema Nodosum

A
724
Q

Course of Erythema Nodosum

A
  • spontaneous resolution in about 2-6 weeks
    without residual scarring,
  • however, recurrence may occur
725
Q

TTT of Erythema Nodosum

A

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
Q

Def of Drug Reactions

A
  • Drug reaction is harmful, unintended, response to drug in therapeutic dose.
727
Q

Mechanism of Drug Reactions

A
  • allergic or non-allergic
728
Q

CP of Drug Reactions

A

The important forms of the drug eruptions include:

  • Severe life -threatening drug reactions
  • Other reactions
729
Q

What are Severe life -threatening drug reactions?

A
730
Q

Other forms of drug reactions

A
731
Q

Urticaria

(Drug Reactions)

A
732
Q

Exanthematous rash

(Drug Reactions)

A
733
Q

Photosensetivity

(Drug Reactions)

A
734
Q

Acne-form eruption

(Drug Reactions)

A
735
Q

Pigmentation

(Drug Reactions)

A
736
Q

what are common drugs that cause Fixed drug eruption?

A

Sulfonamides, NSAIDs

737
Q

Alopecia

(Drug Reactions)

A
738
Q

Characters of Fixed drug eruption

A
  • recurs in the same sites each time the drug is administered.
739
Q

CP of Fixed drug eruption

A
  • Well-defined round or oval plaque of erythema & oedema. Bulla may develop on the top
  • Healed lesion is hyperpigmented (dark brown to violet)
740
Q

Sites of Fixed drug eruption

A
  • lips, anogenital area (glans penis), but can occur anywhere.
741
Q

Dx of drug reactions

A

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
Q

TTT of drug reactions

A
  • Elimination of the offending drug
  • Symptomatic treatment:
    1. Antihistamines.
    2. Topical steroid.
    3. Systemic steroids in severe cases.
743
Q

Epidermal Necrolysis

A

(Stevens-Johnson Syndrome & Toxic epidermal necrolysis)

744
Q

Def of Epidermal Necrolysis

A
745
Q

CP of Epidermal Necrolysis

A
746
Q

Prodorma of Epidermal Necrolysis

A

of URT symptoms; High fever, painful skin and weakness.

747
Q

Skin in Epidermal Necrolysis

A
  • 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
Q

Sites of Epidermal Necrolysis

A

mainly localized to face upper trunk, and hands

749
Q

Mucous membrane affection in Epidermal Necrolysis

A
  • Involvement in 90% of cases ( always at least two sites)
  • Erythema and painful erosions of buccal, ocular, and genital mucosa
750
Q

Visceral involvment in Epidermal Necrolysis

A

is possible (pulmonary, GIT, renal)

751
Q

Prognosis of Epidermal Necrolysis

A
  • Mortality rate is up 25%.
  • Death may be due to sepsis, electrolyte imbalance or organ failure.
752
Q

TTT of Epidermal Necrolysis

A
  • Early(immediate) withdrawal of suspected drugs.
  • Rapid initiation of supportive care in intensive care burn unit
753
Q

Def of Pemphigus vulgaris

A
  • 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
Q

CP of Pemphigus vulgaris

A
755
Q

Lesions in Pemphigus vulgaris

A
  • 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
Q

Incidence of Pemphigus vulgaris

A

Rare chronic disease, usually affects adults. (4-5th decades)

757
Q

Complications of Pemphigus vulgaris

A
  • Infection, fluid & electrolyte imbalance may result in death.
758
Q

where can we find +ve nikolsky sign?

A

in STS-TEN & Pemphigus vulgaris

759
Q

Sites of Pemphigus vulgaris

A
  • commonly involved are scalp, intertriginous area and umbilicus, but in severe cases any site can be involved.
760
Q

TTT of Pemphigus vulgaris

A
  • Refer to dermatologist
  • Systemic steroids & immunosuppressive (cytotoxic) drugs.
761
Q

Examples of Papulosquamous Diseases

A
  • Psoriasis
  • Lichen Planus
  • DLE
762
Q

Def of Psoriasis

A
  • Psoriasis is a genetically determined common skin disease characterized by: chronic relapsing nature and variable clinical features.
763
Q

Etiology of Psoriasis

A
764
Q

Pathology of Psoriasis

A
765
Q

Clinical types of Psoriasis

A

1- Psoriasis vulgaris.
2- Erythrodermic psoriasis
3- Pustular psoriasis.
4- Arthropathic psoriasis.

766
Q

Koebner Phenomenon in Psoriasis Vulgaris

A
  • Trauma to the apparently normal skin may elicit new psoriatic lesions.
767
Q

Auspitz Sign in Psoriasis Vulgaris

A
  • Removal of scales by scraping gives rise to small bleeding points which is pathognomonic for psoriasis
768
Q

what is the most comn form of Psoriasis Vulgaris?

A

Plaque Psoriasis

769
Q

Shape of Plaque Psoriasis

A
770
Q

Color of Plaque Psoriasis

A

Salmon Pink Erythema

771
Q

Covering of Plaque Psoriasis

A

Silvery white scales

772
Q

Specific Charaters of Plaque Psoriasis

A

+ve Koebner phenomenon
+ve Auspitz sign

773
Q

Site of Plaque Psoriasis

A
  • Elbows, knees and lower sacrum.
  • However, any site may be affected
774
Q

Shape of Scalp Psoriasis

A
775
Q

Specific Characters of Scalp Psoriasis

A

No hair loss

776
Q

Sites of Scalp Psoriasis

A

Scalp

777
Q

Shape of Palms & Soles Psoriasis

A
778
Q

Color of Palms & Soles Psoriasis

A

Red

779
Q

Covering of Color of Palms & Soles Psoriasis

A

Fine silvery scales

780
Q

Sites of Palms & Soles Psoriasis

A

Palms & Soles

781
Q

Shape of Psoriasis of Nails

A
782
Q

Site of Psoriasis of Nails

A

Nails

783
Q

Lesion in Intertriginous Psoriasis

A
784
Q

Specific Characters of Intertriginous Psoriasis

A
  • Itching is common & fissuring is often seen in the gluteal crease
785
Q

Site of Intertriginous Psoriasis

A

Localized to groins, gluteal crease, axillae and sub-mammary areas

786
Q

Lesion in Mucosal Psoriasis

A
787
Q

Lesion in Guttate Psoriasis

A
788
Q

Site of Guttate Psoriasis

A

trunk and proximal extremities

789
Q

Incidence of Guttate Psoriasis

A
  • Usually occurs in children and young adults following acute streptococcal infection
790
Q

Course of Guttate Psoriasis

A
  • The lesions may subside after about 6 weeks without treatment or change to plaque type
791
Q

Erythrodermic Psoriasis

A
  • The entire skin is red and covered with scales.
792
Q

Pustular psoriasis

A

Macroscopic sterile pustules appear.
- Localized to palms and soles.
- Generalized pustular psoriasis.

793
Q

Arthropathic psoriasis

A

Psoriasis associated with arthropathy.

794
Q

Course of Psoriasis

A

The disease is usually chronic with remission and relapse.

795
Q

TTT of Psoriasis

A
  • Topical
  • Phototherapy
  • Systemic
796
Q

Topical TTT of Psoriasis

A
  • Steroids
  • Salicylic Acid
  • Tar
  • Calcipotriol (vitamin D analogue)
797
Q

when is Tar Contraindicated in Psoriasis?

A
  • Application on face, flexures & genitals.
  • Erythroderrnic and generalized pustular psoriasis.
  • Severe acne & folliculitis.
798
Q

Steroids In TTT of Psoriasis

A
  • 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
Q

Salicylic acid in TTT of Psoriasis

A
  • Keratolytic agent which is used to remove the scales. It is usually used in combination with steroid, tar or anthralin.
800
Q

Calcipotriol in TTT of Psoriasis

A

(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
Q

Tar in TTT of Psoriasis

A

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
Q

Phototherapy in TTT of Psoriasis

A
  • UVB (broad band or narrow band) exposure 3 times weekly in mildly erythemogenic dose.
803
Q

Systemic Therapy in TTT of Psoriasis

A
  • 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
Q

Indications of Systemic Therspy in TTT of Psoriasis

A

should be used only by specialist in:

  • Extensive psoriasis vulgaris not responding to topical therapy.
  • Erythrodermic psoriasis.
  • Pustular psoriasis.
  • Arthropathic psoriasis
805
Q

Why are Systemic corticosteroids absolutely contraindicated in psoriasis vulgaris?

A

Cause flare at withdrawl

806
Q

Def of Lichen Planus

A
  • a chronic sometimes acute disease of the skin and mucous membranes, with distinctive clinical and pathological features.
807
Q

Pathology of Lichen Planus

A
808
Q

Etiology of Lichen Planus

A
  • Psychic stress is a predisposing factor.
  • Lichen planus may be more common among patients suffering from HCV.
809
Q

Wickham’s striae

A

The surface of the papule may show white fine dots and lines known as (Wickham’s striae).

810
Q

CP of Lichen Planus

A
811
Q

what is the clsssic 1ry lesion of Lichen Planus?

A
  • itchy flat topped, polygonal violaceous papules.
812
Q

Lichen Planus Lesions in oral mucosa

A
813
Q

Lichen Planus lesion in nail

A
814
Q

Lichen Planus lesions in palms & soles

A
815
Q

Sites of Lichen Planus

A
816
Q

Clinical Varieties of Lichen Planus

A
817
Q

Course of Lichen Planus

A
818
Q

TTT of Lichen Planus

A
819
Q

7 Characters starting with P for Lichen Planus

A

Papules
Purple
Polygonal (flat topped)
Pruritic
Peripheral extremities + oral
Positive Koebner
Pterygium in nail

820
Q

Def of Discoid lupus erythematosus (DLE)

A
  • Localized inflammatory skin disease characterized by plaques of erythema, scaling and atrophic scar.
821
Q

what is the most common type of chronic cutaneous lupus?

A

Discoid lupus erythematosus (DLE)

822
Q

Types of Lupus erythematosus (LE)

A

DLE & SLE

823
Q

Predisposing factors for Discoid lupus erythematosus (DLE)

A
824
Q

CP of Discoid lupus erythematosus (DLE)

A
825
Q

Age & sex of Discoid lupus erythematosus (DLE)

A

adults 20-40 years. (4 decade)
{Female: male = 2:1}

826
Q

Sites of Discoid lupus erythematosus (DLE)

A
  • 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
Q

Course of Discoid lupus erythematosus (DLE)

A
  • 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
Q

TTT of Discoid lupus erythematosus (DLE)

A
829
Q

Systemic TTT of Discoid lupus erythematosus (DLE)

A
  • Antimalarial drugs as hydroxychloroquine in cases not responding to topical steroid.
  • Prednisone 15 mg/d.
  • Etretinate
830
Q

Lesions of DLE

A
831
Q

Def of Seborrheic Dermatitis

A
  • A common erythematous scaling eruption that is localized to the seborrheic sites.
832
Q

Etiology of Seborrheic Dermatitis

A

Pityrosporum ovale may play a role.

833
Q

Pathogenesis of Seborrheic Dermatitis

A
834
Q

Prevalence of Seborrheic Dermatitis

A

eczematous form is estimated at 5%

835
Q

Age affected by Seborrheic Dermatitis

A
  • Usually begins in adolescence (9-11 years) (with puberty) peak at age 40
  • Uncommon in preadolescent childhood (exclude t.capitis)
  • Infantile SD
836
Q

which sex is more commnly affected by Seborrheic Dermatitis?

A

More common in males than females. (M > F)

837
Q

what are sites of Seborrheic Dermatitis?

A
  • Scalp, behind ears, face
  • Pre-sternal and interscapular areas
  • flexures (umbilicus, axilla, infra-mammary, inguinal fold, perineum or anogenital crease.
838
Q

Lesions of Seborrheic Dermatitis

A
  • Scalp
  • Ears
  • Eyebrows & Beard
  • Galbrous skin
  • Nasolabial fold
  • Eyelid margin
839
Q

Shape of Non inflammatory
(dandruff) (pityriasis capitis) SD

A

Diffuse fine white (branny) or greasy scales

840
Q

Scalp lesions of Seborrheic Dermatitis

A
  • Non inflammatory (dandruff) (pityriasis capitis)
  • Inflammatory (seborrheic eczema)
841
Q

Characters of Non inflammatory
(dandruff) (pityriasis capitis) SD

A
842
Q

what is the mildest form of SD?

A

Non inflammatory
(dandruff) (pityriasis capitis) SD

843
Q

Characters of Inflammatory Scalp SD (seborrheic eczema)

A
844
Q

SD in Ears

A
  • retro-auricular scaling, crusting and fissuring.
    Persistent non purulent otitis externa may occur.
845
Q

SD in Eyebrows and beard

A

fine scaling

846
Q

SD in Glabrous skin

A

diffuse redness.

847
Q

SD in nasolabial fold

A

greasy scales.

848
Q

SD in Eyelid margin

A

seborrheic blepharitis.

849
Q

Flexures (inverse SD) (axillae, groins, sub-mammary areas and umbilicus)

A

erythematous patches with maceration and oozing.

850
Q

SD of facial skin

A
851
Q

SD of trunk

A
852
Q

Types of inverse SD

A
  • Scaling Intertrigo
  • Non-Scaling Intertrigo
  • Crusted Fissures
  • Weeping Dermatitis
  • Sebopsoriasis
853
Q

Scaling intertrigo

A
  • Sharply marginated erythema and greasy scaling
854
Q

Weeping dermatilis

A
  • Due to sweating, secondary infection, and inappropriate treatment,
  • Erythema, maceration, oozing, crusting.
855
Q

Non scaling intertrigo

A

May be erythema only

856
Q

Sebopsoriasis

A
  • features of both psoriasis and SD.
857
Q

Examples of Extensive SD

A
  • Erythrodermic: rare
  • HIV infection
  • Parkinson’s disease (with seborrhoea)
858
Q

Severity varies from mild dandruff to exfoliative erythroderma

A

..

859
Q

DDx of adult scalp SD

A
860
Q

Adult SD

A
861
Q

Introduction to TTT of SD

A
862
Q

2 steps regimen in TTT of SD

A
863
Q

Def of Infantile SD

A
  • SD inearly infancy due to stimulation of sebaceous glands by maternalandroge
864
Q

Charachters of Infantile SD

A
  • simulates SD in adult, but the scaling on the scalp is thick forming yellowish brown heaped lesion (cradle cap).
865
Q

Onset of Infantile SD

A
  • Begins 2-8 weeks after birth
866
Q

Healing of Infantile SD

A
  • The lesions usually subside within 3-4 weeks.
  • May persist for several months
867
Q

CP od Infantile SD

A
868
Q

TTT of Infantile SD

A
869
Q

DDx of Scaly scalp in prepubertal children

A
870
Q

Def of Acne Vulgaris

A
  • Acne vulgaris is a chronic inflammatory disorder of the pilosebaceous apparatus, characterized by formation of comedones.
871
Q

Pathogenesis of Acne Vulgaris

A

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
Q

Increased sebum secreation

(Pathogenesis of Acne Vulgaris)

A
  • which may result from increased local synthesis of androgen in sebaceous glands or increased response to it.
873
Q

Propionibacterium acne (P. acne) colonizes (Pathogenesis of Acne Vulgaris)

A
  • Pilosebaceous duct and contributes in the formation of comedones and pustules.
874
Q

Hyperkeratosis of pilosebaceous duct (Pathogenesis of Acne Vulgaris)

A
875
Q

Inflammation
(Pathogenesis of Acne Vulgaris)

A

initiated by P:acne

876
Q

what causes Hyperkeratosis of pilosebaceous duct?

A

results from the irritant effect of excess sebum.

877
Q

what does Obstruction of pilosebaceous duct result in?

A

result in comedones which consist of horny cells, sebum, and bacteria.

878
Q

Types of comedoens according to level of obstruction

A
  • 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
Q

what does Propionibacterium acne (P. acne) colonize?

A

pilosebaceous duct

880
Q

what initiates inflammation in Acne Vulgaris?

A

P. acne

881
Q

what are Micro-comedones?

A

Invisible hyperkeratotic plug made of sebum and keratin in follicular canal

882
Q

Excerbating factors of Acne Vulgaris

A
883
Q

Lesions in Acne Vulgaris

A
884
Q

Age of Acne Vulgaris

A
  • Adolescence of both sexes. (12-24 years ) mainly
  • May start at 10 years and persist up 50 years
885
Q

Characters of Closed Comedones

A
  • Skin coloured
  • No visible follicular opening.
  • Often inconspicuous and require adequate lighting and stretching of the skin to be seen
886
Q

Sites of Acne Vulgaris

A

face, back, chest and shoulders.

887
Q

Classification of Acne Vulgaris

A

1- Mild acne: comedones with little or no papules.

2- Moderate acne: comedones, papules and pustules.

3- Severe acne: nodules and cysts predominate.

888
Q

Course of Acne Vulgaris

A
889
Q

TTT of Acne Vulgaris

A
890
Q

Topical in TTT of Acne Vulgaris

A
  • Comedolytic agents
  • Antibacterial agents
891
Q

Comedolytic agents in TTT of Acne Vulgaris

A
892
Q

what is cornerstone in acne ttt?

A

Topical retinoids

893
Q

AV = Acne Vulgaris

Topical retinoids in TTT of AV

A

Retinoic acid (0.05-0.1%) is used in gradually increasing concentration

894
Q

SE of Topical retinoids in TTT of AV

A

It may cause dryness & irritant dermatitis. (Most common side effect)

895
Q

what are examples of Topical Retinoids?

A
896
Q

Antibacterial agents in TTT of AV

A
897
Q

Characters of Benzoyl peroxide (BPO) (2.5, 5, 10)%

A
  • no resistance has mild comedolytic effect.
  • It may cause contact dermatitis.(irritant)
898
Q

what are topical antibiotics used in TTT of AV?

A

erythromycin and clindamycin are effective in pustular lesions. (not alone)

899
Q

Indication for topical TTT of AV

A
900
Q

Systemic TTT of AV

A
  • Antibiotics
  • Antiandrogens
  • Isotretinoin
  • Dapsone
  • Miscellanous therapy
  • TTT of scars
901
Q

what is the systemic antibiotic of choice in acne?

A
  • 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
Q

MOA of antibiotics in systemic TTT of AV

A
  • Reduce inflammation
  • Reduce P: acne population> reducing bacterial production of inflammatory factors as FFA
  • Intrinsic anti-inflammatory
  • Reduce PMN (poly morphonuclear leukocytes) migration
903
Q

Indication of using of antiandroges on TTT of AV

A

used only in females with severe nodulocystic acne

904
Q

Examples of antiandroges used in TTT of AV

A

1- contraceptive as Yasmin

2- Cyproterone acetate (with OCPs diane)

3- Spironolactone (K sparing diuretic but has
antiandrogen effect)

905
Q

Effects of isotretinoin used in systemic TTT of AV

A
  • It decreases sebum secretion
  • Decrease P. acne.
  • Decrease follicular hyperkeratosis
  • has anti-inflammatory effect
906
Q

AE of isotretinoin used in systemic TTT of AV

A

It is teratogenic drug with serious side effects, so it should be used only in severe acne and by highly experienced dermatologists.

907
Q

Dapsone Systemic TTT of AV

A

Anti-inflammatory drug used in severe acne with special precautions.

908
Q

Miscellaneous therapy

Systemic TTT of AV

A

Comedonae removal:
- If comedones are resistant

intralesional steroids:
- Triamcinolone acetonide (2-5 mg/ml)
- Used for large inflammatory nodules/cysts

909
Q

TTT of scars

Systemic TTT of AV

A
  • Dermabrasion, laser resurfacing, deeper chemical peels
  • Filler substances
  • Punch excision (ice-pick) scar
910
Q

Treatment according to the severity of acne can be given as follow (overview)

A
911
Q

Def of Miliaria (Sweat rash)

A

A disorder of the sweat duct in which obstruction of the sweat ducts at various levels occurs in association with excessive sweating&raquo_space; sweat retention

912
Q

Etiology of Miliaria (Sweat rash)

A

Common in:
- Neonates: immature eccrine sweat ducts
- Adults: living in hot humid condition

Resolve in cool environment

913
Q

Predisposing factors for Miliaria (Sweat rash)

A

1- Hot humid condition.
2- Excessive clothing.
3- Obesity.
4- Febrile illness.

914
Q

Incidence of Miliaria (Sweat rash)

A
  • The disease occurs in the tropics and subtropics
  • Affects persons of all ages and both sexes.
915
Q

Site & Size of lesion of Miliaria (Sweat rash)

A
  • Any site
  • Pin head size
916
Q

Lesions of Miliaria (Sweat rash)

A
  • 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
Q

Complications of Miliaria (Sweat rash)

A

impetigo, folliculitis, and boils.

918
Q

Types of Miliaria (Sweat rash)

A
919
Q

TTT of Miliaria (Sweat rash)

A
920
Q

Stages of Hair growth

A
921
Q

Causes of hair loss

A
  • Physiological
  • Pathological (Alopecia)
922
Q

Definition of Alopecia

A

loss of hair from normally hairy area

923
Q

Types of Alopecia

A
  • Cicatricial or scarring alopecia (permanent)
  • non Cicatricial or nonscarring (transient)
924
Q

Causes of Non-cicatricial alopecia

A
  • Conginetal
  • Aquired
925
Q

Aquired Causes of Non-cicatricial circuscribed (Patterned) alopecia

A
926
Q

Aquired Causes of Non-cicatricial alopecia

A
  • Circumscribed (Patterned)
  • Diffuse
927
Q

Aquired Causes of Non-cicatricial Diffuse alopecia

A
928
Q

Congenital causes of cicatricial alopecia

A

developmental defect

929
Q

Aquired causes of cicatricial alopecia

A
930
Q

Definition of Alopecia Areata

A

circumscribed non scarring hair loss with normal skin

931
Q

Etiology of Alopecia Areata

A
932
Q

CP of Alopecia Areata

A
933
Q

Lesions in Alopecia Areata

A
  • 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
Q

Clinical types of Alopecia Areata

A
935
Q

Prognosis of Alopecia Areata

A

Bad prognosis in the following conditions:
1- Alopecia totalis, universalis and ophiasis
2- Alopecia areata with nail pitting
3- Alopecia areata in atopics

936
Q

Associated features to Alopecia Areata

A

1- Nail pitting
2- Atopy (atopic dermatitis)
3- Vitiligo
4- Cataract

937
Q

DDx of Alopecia Areata

A
938
Q

TTT of Alopecia Areata

A
939
Q

Causes of hyperpigmentation

A
940
Q

Causes of Hypopigmentation

A
941
Q

Casues of depigmentation

A
942
Q

Def of Vitiligo

A

acquired idiopathic depigmentation (leukoderma) of the skin

943
Q

Etiology of Vitiligo

A
944
Q

Precipitataing factors for Vitiligo

A

1- Emotional stress
2- Sun burn
3- Physical trauma (Koebner’s phenomenon)

945
Q

CP of Vitiligo

A
  • 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
Q

Classification of Vitiligo

A
947
Q

Prognosis of Vitiligo

A

1- Unpredictable
2- Stationary
3- Spontaneous re-pigmentation
4- Slowly progressive
5- Rapidly progressive

948
Q

DDx of Vitiligo

A

1- Pityriasis alba
2- Pityriasis versicolor (hypopigmented type)
3- Post inflammatory hypopigmentation
4- Albinism
5- Post-burn and post-chemical depigmentation

949
Q

TTT of Vitiligo

A

Y3R1 - DALR ✋🏻 (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions