Derma Notes

Notes - Dermatology and Venerology
General Dermatology 3
Structure of the epidermis - anatomy and histology 3
Structure of the dermis and hypodermis - anatomy and histology 5
Skin appendages 7
Blood circulation and neurological structures in the skin 8
Oral and genital mucous - anatomy and histology 11
Keratinization 11
Melanogenesis 12
Physiology of skin. Protective, thermoregulatory, secretion, climinalogy and
immunological functions of skin 13
Maculous skin eruptions 13
Palpable skin eruptions 14
Exsudative skin eruptions 15
Skin eruptions due to interruption of skin surface 15
Discard skin eruptions. Skin eruptions due to variation of the number of skin elements 16
Major histopathological changes in epidermis 16
Major histopathological changes in dermis and hypodermis 18
External medicaments and the mechanism of action 19
Special dermatology 19
Dermatoses due to external factors (physical, chemical and biological) 19
Photodermatoses 21
Erythema exudative multiforme. erythema nodosum 22
Psoriasis vulgaris. Pityriasis rosea 23
Lincoln rubber planus 25
Bullous dermatoses (pemphigus, dermatitis herpetiformis, pemphigoid) 27
Urticaria. Oedema Quincke. Strophulus 29
Contact dermatitis. Professional dermatoses 31
Atopic dermatitis 32
Seborrheic dermatitis 32
Lupus erythematosus 33
Localizes sclerosis. Systemic sclerosis 35
Chronic venous insufficiency of lower legs 36
Disorders of the cutaneous melanocytes (hypochromia, vitiligo) 38
Disorders of the hair (alopecia areata, androgenetic alopecia, hypertrichosis) and nails 39
Disorders of the sebaceous glands (acne, seborrhoea, rosacea) 41
Nonmelanoma skin cancer (Basal cell carcinoma, squamous cell carcinoma).
Precancerosis 44
Malignant melanoma 46
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Viral infections. Classification. Herpes simplex. Herpes Zoster 47

Warts. Molluscum contagiosum . Condylomata accuminata 48
Bacterial infections (pyoderma). Etiology. Pathogenesis. Epidemiology. Classification. 50
Folliculitis. Furuncle. Carbuncle. Hidradenitis suppurativa 51
Impetigo. Erysipelas. Ecthyma 52
Cutaneous Tuberculosis and Tuberculosis skin diseases 53
Leprosy 55
Fungal infections: dermatophyte infections, pityriasis versicolor 56
Candida infections 58
Lyme disease 59
Venereal diseases 60
Venereal diseases: classification, epidemiology 60
Syphilis (etiology, pathogenesis, epidemiology) 60
Diagnosis of syphilis 61
Primary syphilis 63
Secondary syphilis 63
Tertiary syphilis 64
Congenital syphilis 65
Treatment of syphilis. Prognosis 66
Gonorrhea. Etiology. Mode of Transmission. Symptoms and course in the male.
Complications. Treatment 66
Gonorrhea. Etiology. Mode of transmission. Symptoms and course in the female.
Complications. Treatment 68
Gonorrhea. Etiology. Mode of Transmission. Symptoms and course in the children.
Complications. Treatment. 70
Nongonococcal urethritis. Chlamydiasis 70
Trichomoniasis. Chlamydiasis 71
Balanitis. Vulvitis 72
AIDS. Etiology. Epidemiology 73
AIDS. Skin and mucosal infections 74
Scabies. Pediculosis 75
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General Dermatology
1. Structure of the epidermis - anatomy and histology
Right, given we have an entire cycle about one organ, we should probably make sure we
know the anatomy quite well, so we’re going to waffle on a bit here!
The skin is composed of two main layers, the epidermis and the dermis, the hypodermis
(subepithelial layer) situated below. In this section we’ll consider the epidermis.
It is composed of keratinized, stratified squamous epithelium, made of four or five

histological layers. Areas of the body which are subject to severe wearing (e.g. hands and
feet) have five layers, while the rest of the body has four layers. These layers (from deep to
superficial) are:
- Stratum basale
- Stratum spinosum
- Stratum granulosum
- Stratum lucidum (only in five layer ‘thick’ skin)
- Stratum corneum
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Below we consider each layer in turn.
Stratum basale
This is the
deepest layerof the epidermal layer, and attaches the epidermis to the basal
lamina below via intertwining collagen fibers(the basement membrane). It is made of
cuboidal basal cells, a precursor of the keratinocytes of the epidermis. All of the cells of the
epithelium are formed in this layer and then ascend to fill the above layers. Two other
types of cells are found in this layer, these are the Merkel cell(which functions as a receptor
for touch) and melanocyte which produces the pigment melanin.
Stratum spinosum
So called because desmosomes now begin to link the cells(now known as
keratinocytes), binding them together, making them appear like the cells have spines.
This layer has 8-10 layers of keratinocytes within it along with langerhans cells, which
function as macrophages within the layer. The keratinocytes in the spinal layer begin the
process of keratin synthesis, and release a water-repelling glycolipid that helps prevent
water loss from the body.
Stratum granulosum
Given its name due to the grainy appearance as a result of increased keratin
composition compared to the spinal layer. The cells (3-5 deep) generate large amounts
of keratin and keratohyalin. The nucleus and other cell organs begin to degrade at this
point as the cells die, leaving behind keratin, keratohyalin, and cell membranes.
Stratum lucidum (hands and feet only)
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Thin layer of cells, only found on the soles of feet and palms of hands. These cells are
densely packed with eleiden, a clear protein which is rich in lipids, derived from keratohyalin.
It is the eleiden which gives them their transparent appearance, and therefore their name.
Stratum corneum
Most superficial layer of the epidermis, the increased keratinization of the cells gives it its
name, and there are usually 15-30 layers of cells. They are dead and dry which helps
prevent penetration of microbes and provides mechanical protection against
abrasion. The entire layer is replaced during a period of about 4 weeks.
The main functions of the epidermis are to provide a barrier to infection and regulate the
amount of water lost from the body. The word epidermis derives from epi meaning over
and derma meaning skin.
Within the epidermal layer there are areas of the epidermis where there are extensions
downwards between dermal papillae, these epidermal thickenings are known as Rete
ridges(or rete pegs). There is no blood supply of the epidermis itself, and it is nourished
almost exclusively by diffused oxygen from the surrounding air. Cells in the epidermal
layer are joined by adherens type cell junctions, formed by cadherins, to prevent
penetration by pathogens. The pushing of basal cells more superficially is thought to be due
to an elevation of extracellular calcium concentrations.
2. Structure of the dermis and hypodermis - anatomy and histology
The dermis contains all of the main appendagesthat we think of

with skin, it includes blood and lymph vessels, hair follicles and
sweat glands as well as others that will be considered in more detail
in question 3.
The dermis is made of two layers of connective tissue, the papillary

layer and the reticular layer. The papillary layer sits in between
the epithelial projections, forming the dermal papillae. The
reticular layer meanwhile, sits below this connecting the dermis
to the hypodermis.
Speaking more generally, we can say that the dermis has three
major types of cells (fibroblasts, macrophages and mast cells),
with a matrix comprised of collagen, elastin,
glycosaminoglycans and glycoproteins.
Let's now look at these the aforementioned layers:
Papillary layer
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Made of loose, areolar CT, meaning the collagen and elastin fibers of this layer forma
loose mesh. It projects into the stratum basale of the epidermis to form finger-like
dermal papillae. This layer consists of an abundance of small blood vesselsas well as
some adipocytes. Phagocytes, lymphatic capillaries, nerve fibers and Meissner
corpuscles(touch receptors) can also be found here.
Reticular layer
Composed of dense irregular CT,with rich vascularizationand a rich sensory and
sympathetic nerve supply. Reticular fibers appear net like due to meshwork of fibers. Elastin
fibers provide elasticity to the skin, enabling movement and flexibility of the skin.
Collagen fibers that extend into both the papillary layer and hypodermis provide
additional tensile strength. Collagen injections and Retin-A creams are targeted at this
layerand help to restore skin turgor either by introducing collagen externally or stimulating
blood flow and therefore improving repair of the dermis.
Hypodermis
Not technically part of the skin apparently, also known as the subcutaneous layeror
superficial fascia, this layer serves to connect the skin to the underlying fasciaof the
bones and muscles. It consists of well-vascularized, loose, areolar CT and adipose
tissue, which functions as a mode of fat storage, providing insulation and cushioning.
The hypodermis consists of fibroblasts, adipose cells and macrophages. Found within
the subcutaneous layer are free nerve endings, hair follicle roots, ruffini and pacinian
corpuscles, mast cells, bursae, and the glandular parts of some sweat glands(and all
of the mammary glands). In some areas fine, flat sheets of muscles also exist here, such as
in the scalp, face, hand, nipple and scrotum.
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3. Skin appendages
Appendages of skin include:

- Hair
- Nails
- Sweat glands
- Sebaceous glands
We’ll look at each below.
Hair
Hair is a keratinous filament growing out of a hair follicle that originates deep in the
dermis from a hair root. The anatomical parts of a hair are the hair shaft, inner root
sheath, outer root sheath, hair matrix, hair papilla and hair bulb. Associated with the
follicle is the Arrector pili muscle and sebaceous gland.
Hair texture is determined by the shape and structure of the hair cortex (the central element
of the hair shaft). Hair growth begins with the production of keratinocytes by the basal cells
of the hair bulb, which pushes the follicle towards the surface. External hair is completely
dead and composed entirely of keratin. Hair provides a sensory function along with
thermoregulation and communication. The arrector pili muscle will respond to the
sympathetic nervous system.
Nails
The nail bed is a specialised structure of the epidermisfound at the tips of fingers and
toes. The nail body is formed on the nail bed and protects the extremities. It is composed of
densely packed dead keratinocytes. The visible part of the nail bed (the pink bit) is rich in
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blood vessels making it appear pink, apart from the lunula region which consists of a thicker
layer of stratum corneum and so appear pailer.
Sweat glands
Sudoriferous glandsproduce sweat to cool the bodywhen the body is too warm. Sweat
glands develop from epidermal projections into the dermisand are classified as
merocrine glands(secretions are secreted by exocytosis through the duct without affecting
the cells of the gland. There are two types:
- Eccrine sweat glands - p roduce hypotonic sweat for thermoregulation, most
common on palms and soles and forehead. Coiled glands lying deep in dermis with
duct rising to a pore on the skin surface. Mostly composed of water, some salt,
antibodies, traces of metabolic waste and some antimicrobial peptide.
- Apocrine sweat gland- larger than their eccrine cousins, and lie deeper in the
dermis. These glands are found in the armpits and genital regions, the sweat is
hypertonic with increased organic compoundsthat make the sweat thicker and
subject to bacterial decomposition and subsequent smell - its release is under
nervous and hormonal control.
Sebaceous glands
These are a type of oil glandsfound all over the bodythat helps to keep the skin
lubricated and waterproof, most are associated with hair follicles. They generate
sebum, a mix of lipids, onto the skin. They are activated by hormonesthat do not
become active until puberty.
4. Blood circulation and neurological structures in the skin
Blood circulation
This part of the question is really asking about Arteriovenous Anastomosis, so that’s what
we’ll chat about! The skin has relatively low metabolic demandsand as such blood supply
doesn't need to be too high, but, the skin performs an important function in
thermoregulation, to do this it needs blood!? The bodies answer to this contradiction is
Arteriovenous anastomosis.
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These are low-resistance connectionsbetween the small arteries and small veinsthat
supply and drain the skin, these allow blood to go directly from the arterioles to the skin
without passing through capillaries(meaning there is no transport of nutrients). These
AVAs are under the control of the sympathetic nervous system, increases sympathetic
signals increase sphincter tone, therefore shutting off the AVAs, forcing blood
through the shallower capillaries, and allowing for loss of heat loss.
AVAs don’t exist everywhere in the skin, predominate in ‘thick’ skin

(aka apical skin) which is found on the palmar surface of the hand
and plantar surface of the foot. That’s why, when you get
nervous, your hands become all sweaty and read and hot (also
potentially lends some evidence to the whole ‘keeping your feet
warm’ when you’re ill! Shout out to the Bulgarian grandma’s!).
This will come up again when we get into some of the diseases, so
understand that there are three key elements in controlling AVAs:
Endothelium, Smooth muscle and nerve supply(obviously
nerves supply the smooth muscle).
Outside of AVAs it’s worth remembering that skin circulation is

effectively the product of a series of plexuses, these are the subfascial plexus, prefascial
plexus, subcutaneous plexus, subdermal plexus, dermal plexus and subepidermal
plexuses.
Neurological structures in the skin

1. Lamellar corpuscles (Pacinian corpuscles)
a. Detect rapid vibrations
b. Transient responses, but with large receptive fields.
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c. Found in the dermis (reticular layer)
2. Tactile corpuscles (Meissner corpuscles)
a. Detect light touch and adapt to changes in texture (low frequency vibrations)
b. Rapidly adapting receptor - small receptive fields with transient responses to
the onset and offset of stimulation
c. Found in upper dermis (papillary) but project into epidermis
3. Merkel nerve endings (Merkel's discs)
a. Detect sustained pressure
b. Slow Adapting type 1 receptor - small receptive fields
c. Found in the dermis (papillary layer)
4. Bulbous corpuscles (Ruffini endings)
a. Detect tension deep in skin and fascia
b. Slow adapting type 2 receptor - large receptive fields
c. Found in the dermis (reticular layer)
Additionally, the following are mechanoreceptors in slightly different contexts
5. Free nerve endings
a. Not true ‘receptors’ but these detect touch, pressure and stretching
b. Penetrate the dermis and end in the stratum granulosum of the epidermis
6. Hair follicle receptors
a. Receptors on the root of hair follicles detect movement in hair.
b. The hair follicle may be in the dermis or hypodermis
To sum up:
- Epidermal sensation
- Meissner corpuscles
- Free nerve ending
- Dermal sensation
- Papillary
- Meissiner corpscules
- Merkel's disc
- Free nerve endings
- Reticular
- Pacinian corpuscles
- Ruffini endings
- Hair follicle receptors
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5. Oral and genital mucous - anatomy and histology
Oral mucosa
Consists of stratified squamous epithelium supported by lamina propria. In the soft palate,
underside of the tongue, floor of the mouth, buccal surfaces and lips, the epithelium is not
keratinised, in other areas, such as the gums, hard palate and upper surface of the tongue,
the epithelium is keratinised.
Below the oral mucosa is a tough collagenous submucosal layer with accessory salivary
glands.
The oral tongue mucosa has small papillae that can be filiform, fungiform, folate or
circumvallate, along with taste buds present in a large number of circumvallate papillae and
in lesser numbers elsewhere.
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6. Keratinization
Keratinization is a cytoplasmic eventthat takes place in k eratinocytes that move through

the different layers of the epidermis to differentiate into corneocytes. It is a normal process
by which the cells of the stratum basale keratinized to become the cells of the stratum
corneum of the skin.
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Keratin is a family of proteins, and are encoded by 54 genes. We divide keratins into
primary keratins and secondary keratins(depending on if they are synthesized by the
epithelial cells regularly or more rarely). Keratin and associated filaments provide a scaffold
for epithelial cells and tissues to sustain mechanical stress, maintain structural integrity,
ensure mechanical resilienceand protect the cell from changes in pressure.
Within the skin there are two types of cell populations: progenitor and maturing
populations. The progenitor population consists of a stem cells and amplifying cells ,
after each division the daughter cells either enter the progenitor population again or
enter the maturing compartment. As cells enter the maturing compartment, the
keratinocyte undergoes differentiation and becomes committed to biochemical and
morphological changes. At the end of the differentiation process a dead cell filled with
densely packed protein contained within a toughened cell membrane is formed, when
it reaches the surface of the skin it is shed off in a process called desquamation. The time
for a cell to pass through the entire epithelium is the turnover time, this is 52-75 daysin the
skin.
Factors that affect the process of keratinocyte differentiation include:

- Active metabolites of Vitamin D3 act as an autocrine pathway to decrease
keratinocyte proliferation and increase cell differentiation
- Epidermal growth factor has a mitogenic effect on the basal cells
- Keratinocyte growth factor is a powerful stimulus for epithelial cell proliferation
- High vitamin A cause the normally cornified epithelium to undergo mucous
metaplasia
In some cases hyperkeratosis can occur, this is the formation of a callus, when the skin is
continually subjected to mechanical stress, hyperemia occurs, stimulating proliferation of
epidermal cells while reducing desquamation. This has a protective function.
7. Melanogenesis
Melanogenesis is the process by which melanin is produced in melanosomes

(cytoplasmic organelles of melanocytes) by melanocytes. Melanocytes comprise 10% of
the cells in the basal layer, with another population of melanocytes in the hair follicle.
Melanin is synthesized from tyrosine, using the enzyme tyrosinase. Once produced the
melanin is packaged into the melanosomes which are then phagocytosed by
keratinocytesand moved to an area above the keratinocyte’s nucleus acting as a
protective shield from UV light. One melanocyte provides melanosomes for as many
as 30-40 keratinocytes. The purpose of melanogenesis is to protect the hypodermis from
damage by UV-B radiation, all melanin is black which allows it to absorb a majority of UV-B
light and block it from passing through the epidermis.
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All individuals have the same number of melanocytes, typically 1000-2000 per square
millimeter of skin, the difference comes in the number of melanosomes.
It is worth mentioning now what triggers this process of melanogenesis. When UV light hits
the keratinocyte there is stimulation of p53 which increases expression of POMC, a
precursor protein to alpha-melanocyte stimulating hormone (MSH). MSH can then
increase expression of enzymes and other proteins needed for the synthesis of
melanin and melanosomes. From here, the melanocytes can fuse with keratinocytes, and
allows for the transfer of melanosomes into keratinocytes, where the melanosomes
degranulate and release pigment into the keratinocyte.
8. Physiology of skin. Protective, thermoregulatory, secretion,

climinalogy and immunological functions of skin
Protective
Immunological
Epithelial cells at the interface between the skin and the environment are the first line of
defense as part of the innate (primary) immune system. Epithelial cells respond to the
environment using structures such as Toll-like receptors (TLR),
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9. Maculous skin eruptions
Macular lesions are changes in the colour of the skin, with no change in elevation. They can
be categorised as Macules (<0.5cm) or patches (>0.5cm).
The categories of macular skin lesions are:

- Lesions due to changes in blood vessels
- Hyperaemia
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- May be active or passive (red or blue)
- May be local (erythema) or generalised (erythroderma)
- Erythema may be due to mechanical, chemical or ionizing
factors causing inflammation
- Erythroderma may be due to psoriasis or atopic dermatitis
- Anaemica
- May be due to vasospasm or a congenital lack of blood vessels
(nevus anemicus)
- Telangiectasia
- May be congenital (nevus araneus, naevus vinosus) or acquired
(rosacea, sclerodermia progressiva, alcoholism, hepatic disorders,
secondary to topical corticosteroids)
- Haemorrhagica
- May be: Petechiae ((1-2mm), ecchymosis or haematoma
- Lesions due to changes in pigmentation

- Hyperchromia
- Due to melanin, carotenoids, hemosiderin, heavy metals, may be
congenital (lentigo, naevus pigmentosus, cafe au lait), acquired (sun
tan, linea fusca) or secondary (postlesional hyperpigmentation, lichen
rubber planus).
- Hypochromia
- May be congenital (albinism, nevus depigmentosus), acquired (vitiligo)
or secondary (leucoderma psoriatica)
- Other
- Exanthem
- Enanthem
- Erythroderma (diffuse reddening of the skin)
Based on the change in colour we can also identify some possible causes:
- Pale pink - urticaria
- Pink - dermatitis
- Red - angiomas
- Purple - Vasculitis
- Yellow - Xanthoma
- Brown - iMelasma, nevi
- Black - Nevus
- Blue - blue nevus
- White - vitiligo
10. Palpable skin eruptions
- Papula - <5mm in diameter, caused by increased thickening in epidermis and/or

dermis
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- E.g. lichen rubber planus, psoriasis
- Plaque - big flat papule
- E.g. psoriasis, eczema
- Nodules - localized thickness deep to the dermis
- E.g. lupus vulgaris, lepromas (leprosy)
- Urtica - transient papule or plaque caused by dermal edema
- E.g. nettle rash, hives, dermographism
- Lichenification - response of skin to chronic rubbing leading to thickening and
hyperpigmentation
- Eg. atopic dermatitis
- Vegatatio
- E.g. verruca vulgaris
- Hyperkeratosis (calluses)
- E.g. hyperkeratosis follicularis, diffusa etc
11. Exsudative skin eruptions
- Vesicule (<5mm with clear fluid)

- E.g. eczema acutum, herpes simplex or zoster)
- Bulla (>5mm)
- Mechanical trauma, pemphigus foliaceus, pemphigoid
- Pustule (fluid sits in dermal layer, often associated with hair follicles)
- Folliculitis, can be septic or aseptic
- Ecthyma (pustule with a necrotic base)
- Abscessus (purulent collection within tissue)
- Cyst (fluid in sac covered with epithelium)
12. Skin eruptions due to interruption of skin surface
- Erosio - Superficial damage of the epidermis or epithelium, heals without scar

- E.g. eczema acutum, pemphigus, bullous pemphigoid
- Excoriation - defect extending into the dermis, usually linear caused by scratching
- E.g. scabies, acne, neurodermitis, pathomania
- Fissura - linear split or defect, extending into dermis and often originating from an
orifice
- E.g fissura ani, eczema
- Fistula - tract lined with epithelium, often discharging secretion
- E.g. Tuberculosis cutis, actinomycosis
- Ulcer - chronic defect extending into dermis or subcutaneous tissue, develops as a
result of tissue necrosis and poor healing
- Ulcer venosum cruris
- Aphthae - small white painful ulceration on the mucous membrane with erythematous
border
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13. Discard skin eruptions. Skin eruptions due to variation of the

number of skin elements
Discuard skin eruptions

- Squama (scale) - visible aggregates of corneocytes
- E.g. psoriasis (white scales) dermatitis seborrhoica (yellowish scales),
ichthyosis (grey-black scales)
- Crusta (crust) - dried serum or exudate, often mixed with scale
- E.g. light yellow is serous exudate, yellow green is purulent, brown black is
hemorrhagic
- Eschara - localized dry necrosis of skin
- E.g. in disorders of blood circulation or chemical burns
- Comedone - black stopper in the canal of hair follicle
- E.g. acne
Skin eruptions due to variation in number of skin elements

- Atrophia - thinning of the skin with smoothing of surface
- Localised - lichen scleroatrophic, anetoderma, lipoatrophia
- Diffuse - atrophia senilis (old age), scleroderma progressiva
- Hypertrophia
- E.g. elephantiasis due to chronic inflammation
- Cicatrix (scar)
- May be raised, flat or atrophic
- Necrosis
- Dermatosclerosis - hardening and thickening of skin so it is less freely movable
14. Major histopathological changes in epidermis
Here we group the main histopathological changes that can be found in the epidermis.
Acanthosis (epidermal hyperplasia)

Thickening of the epidermis, can be categorised into flat, psoriasiform, papillomatous and
pseudocarcinomatous forms.
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Epidermal atrophy (epidermal hypoplasia)

Caused by a reduction of keratinocytes that leads to thinning of the epidermis.
Hyperkeratosis
The horny cell layer becomes abnormally thick, such as in psoriasis vulgaris, ichthyosis and
callus.
Parakeratosis
This is caused by incomplete keratinization with the nuclei remaining in the keratinocytes of
the horny cell layer.This occurs in inflammatory diseases such as psoriasis vulgaris or
tumour diseases.
Dyskeratosis
Occurs when some keratinocytes keratinize abnormally before they reach the horny cell
layer. These keratinocytes become apoptotic and necrotic, with intercellular bridges between
peripheral keratinocytes being lost and the cells becoming round. Often found in
inflammatory diseases and malignant tumors.
Hypergranulosis
Thickening of the granular cell layers to four or more layers from the normal 1-3 layers.
Found in lichen planus, viral warts and congenital ichthyosis
Granular degeneration, Epidermolytic hyperkeratosis

Numerous vacuolated cells containing large keratohyalin granules appear in the granular cell
layer and suprabasal cell layer. It is characteristic of bullous congenital ichthyosiform
erythroderma.
Intracellular edema
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Acantholysis
Dispersion of keratinocytes resulting from the dissociation of keratinocyte intercellular
adhesion (specifically desmosome failure). Intercellular spaces and blisters then form. Found
in diseases like warty dyskeratoma.
Blister
Can be intraepidermal or subepidermal depending on location.
Pustule
Exocytosis
This is infiltration of inflammatory cells and erythrocytes into the dermis, seen in epidermal
inflammatory diseases such as atopic dermatitis.
There are also some dermal-epidermal junction histological patterns to be aware of:
- Vacuolar degeneration
- Melanin synthesis abnormalities
15. Major histopathological changes in dermis

and hypodermis
Inflammatory cell infiltration

WBC and RBC infiltration into the dermal layer, there are several
patterns of infiltration including lichenoid infiltration, vasculitis,
and nodular infiltration. Most common causes are included in the
table below.
Granuloma
This is a thick aggregation of histiocytes that form focal chronic
infiltration. The macrophages in granulomas are known as
epithelioid cells. There are different types of granulomas
including Tuberculoid, Palisading, Suppurative and foreign-body
granulomas
Giant cell
This is a general term for cells that contain a large nucleus, there are different types that can
be identified that each have a different cause:
- Foreign-body giant cell
- Langhans giant cell (TB, sarcoidosis)
- Touton giant cell (juvenile xanthogranuloma and xanthoma)
Changes in connective tissue
Changes such as fibrosis and sclerosis are observed in the collagen fibers that sit below the
dermis. Changes most notable in cases of scleroderma and papillomatosis.
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Deposition of foreign substances

Include amyloids, mucins, calcium, hemosiderina, uric acid and hylian.
16. External medicaments and the mechanism of action
“If its dry, wet it, if its wet, dry it”. That is to say, in chronic dermatoses (psoriasis, atopic
dermatitis) use ointments, while creams are a good option for ‘wet’ dermatoses such as
acute contact dermatitis, and other blistering dermatoses.
The main two topical (external) medicaments are moisturizers and topical steroids.
Firstly, moisturizers, from most moist to least:

- Ointments - very good for ‘dry’ skin
- Cream - less oil than ointments
- Lotion - similar to cram, with more water and less oil
- Gel - transparent base that liquefies on contact with skin, but mildly drying
- Solution - base of water and/or alcohol, very drying, evaporates rapidly
- Foam and Powder
Moisturizers try and maintain and restore the barrier function of the skin which is commonly
damaged in many forms of dermatoses. Moisturizers should be applied liberally at least
twice a day, including immediately after bathing. At low concentrations of lactic acid and urea
act as moisturizers, while at higher concentrations they
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17. Internal medical treatment of skin diseases

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Special dermatology
1. Dermatoses due to external factors (physical, chemical and

biological)
Dermatoses is defined as a disease of the skin, especially one that does not cause
inflammation. This is distinct from dermatitis where inflammation is present. Lange’s uses
dermatoses as synonymous with rashes.
So with such a wide definition this is obviously quite unhelpful, nevertheless, let's take a look
at what the textbook says.
Common inflammatory dermatoses include:

- Drug rashes
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- Urticaria
- Contact dermatitis
- Seborrheic dermatitis
- Atopic dermatitis
However, this question is trying to get us to look at Physical, chemical and biological causes,
so let's do that.
Physical causes
- Heat injuries
- Thermal burns
- Electrical burns
- Miliaria
- Cold injuries
- Chilblains
- Frostbite
- Trench foot
Thermal burns
Can be divided into first, second, third and fourth degree burns. First degree burns cause
erythema due to congestion of superficial blood vessels, epidermal desquamation can then
occur. Second degree burns can be superficial or deep. The superficial form sees vesicles
and blebs with edema of superficial tissues, while the deep form sees injury to the dermis
and compromises blood flow to the skin, healing takes over a month and scaring occurs.
Third degree burns affect the full thickness of the epidermis and dermis. Skin appendages
are fully destroyed and there is no epithelium for regeneration. Fourth degree burns see the
destruction not only of the epidermis and dermis but also the subcutaneous fat
with any underlying tendons.
Estimate thermal burns based on the rule of nine. Each arm is 9%, the legs are
9% anterior and 9% posterior (18% in total) the abdomen is 3x9 (36%) and the
head/face is 9%.
Electrical burns
Can be divided into contact burns(small but deep, causing some necrosis of
underlying tissues) or flash burns(cover a large area, but are similar to surface
burns). Electrical burns are characterised by erythema ,edmea, bulla formation
and sloughing of necrotic epidermis.
Miliaria
Also known as a ‘sweat rash’, this is a disease characterised by small itchy
rashes due to sweat trapped under the skin by clogged sweat glands, it is most
common in hot and humid conditions (e.g. the tropics). Presents has a small erythematous
papular rash.
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Chilblains
Acute chilblain is the mildest form of cold injury, often affects toes and
fingers, it is the result of repeated acute vasoconstriction and it leads to chronic
tissue damage and inflammation. Individuals are genetically predisposed to the
development of chilblains, and it is considered and idiopathic disease. Patients
may present with blistering of the affected area, along with burning, itching,
dermatitis and erythema. Tx is simply to avoid extremities getting cold.
Frostbite
Frostbite is when soft tissue is frozen and locally deprived of blood supply. The frozen part is
painless and becomes pale and waxy. There are four stages:
1. Frostnip (with erythema)
2. Second degree - hyperemia, edema and blistering
3. Third degree - full thickness dermal loss with hemorrhagic bullae or waxy skin
4. Fourth degree - full thickness loss of entire part of the body
Trench foot
Results from prolonged exposure to cold, wet conditions without actual freezing, long term
tissue hypoxia leading to tissue damage.
Chemical causes
- Drug reactions
- Chemical irritants (often in a workplace setting) - always ask about work in history
….
2. Photodermatoses
Photo meaning light, dermatoses meaning skin disease, so these are a group of diseases
that are caused by exposure to sunlight. The most common group within this group is
Polymorphous light eruption (PMLE) diseases. This is a group of heterogeneous,
idiopathic, acquired, acute eruptionscharacterised by an abnormal reaction to UV rays.
PMLE incidence is between 10-23%, while the average age of patients is about 23. The
pathogenesis is thought to be a delayed-type hypersensitivity reaction to an
auto-antigen induced by UVR.
Lesions appear in spring or early summer within hours of exposure and persist for 7-10
days. The lesions are papular and papulovesicular, pink to red in colour, and generally
quite monomorphous. The pattern of rash is generally on the forearms, v area of the
neck, arms and chest, and sometimes the face.
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Dermatopathology shows edema of the epidermis, spongiosis, vesicle formation and
mild liquefaction degeneration of the basal layer with lymphocytic infiltrate of the
dermis. Diagnosis is generally clinical, although biopsy may be done to rule out LE.
Course of the disease is chronic and recurrent, management is taking beta-carotene three
times a day for 2 weeks prior to going into the sun, sun block is not very effective.
Other diseases in this category include:

- Phototoxic drug/chemical induced photosensitivity
- Solar urticaria (sunlight-induced whealing confined to exposed body sites)
- Photo-exacerbated dermatoses (acne, atopic eczema, lichen planus and others can
all be exacerbated by sunlight exposure).
3. Erythema exudative multiforme. erythema nodosum
Erythema multiforme
This is a mild, self-limiting, potentially recurring mucocutaneous inflammatory condition,
characterised by ‘target lesions’ that resemble a bull’s eye. These lesions erupt over
24-48 hours and last for 1-2 weeks, presenting in a symmetrical distribution of lesions over
the dorsal surfaces of the extensor extremitieswith minimal mucous membrane
involvement.
The most common etiology is infectious, including herpes simplex virus and
mycoplasma pneumoniae as the most common(other causes include hepatitis B,
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Epstein-Barr, cytomegalovirus). Can also be caused by some drugs include Sulfonamides,
phenytoin, barbiturates and penicillin.
Key diagnostic factors include a history of EM, along with the presence of target lesions (red
rim, clearance zone and central blister or erosion). The symmetry with the target lesions
should be enough to diagnose.
The disease can follow two main courses, designated EM minor and EM major. The minor
form has little or no mucous membrane involvement, with vesicles, but not bullae or
systemic symptoms. Such eruptions are usually limited to face and extremities. The severe
form is most often seen as a drug reaction with mucous membrane involvement,
severe bullous formation and wider systemic symptoms.
Management is control of herpes simplex using oral valaciclovir or famciclovir, in

severely ill patients, glucocorticoids can be given (50g prednisolone).
Erythema Nodosum
Erythema nodosum (EN) is an important and common acute inflammatory reaction
pattern of the subcutaneous fat, characterised by the appearance of painful nodules on
the lower legs, lesions are bright red and flat but nodular upon palpation, often occur
with fever and arthritis.
EN has a peak incidence at around 20-30 years, and is much more common in females
than males. The etiology is diverse, including bacterial, fungal, viral, drugs, malignancies
and autoimmune diseases.
The lesions are painful and tender, and usually present with systemic symptoms.
Nodules can be anywhere between 3-20 cm in size and are generally not sharply
marginated. The name best describes how they look and feel, erythema (red) and
nodosum (nodular).
Laboratory examination will show elevated ESR, CRP and WBC, imaging may be
required of the lungs to rule out sarcoidosis. In general EN spontaneously resolves
within 6 weeks, management is bed rest with compression bandage. Analgesics can be
given to manage pain, if severe than systemic glucocorticoids may be required.
4. Psoriasis vulgaris. Pityriasis rosea
Psoriasis Vulgaris
This is just psoriasis, the vularis bit is just to throw us off! It is a chronic condition with several
clinical presentations, and can vary from those with only a few localized plaques to
generalized skin involvement.
Classification:
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- Psoriasis vulgaris
- Acute guttate
- Chronic stable plaque
- Palmoplantar
- Inverse
- Psoriatic erythroderma
- Pustular psoriasis
- Pustular psoriasis of von Zumbusch
- Palmoplantar pustulosis
- Acrodermatitis continua
Most common onset is at 22 years of age, although can also have late presentation at an
average age of 55. Incidence is about2%in the west, equal incidence in males and
females.
There is a
genetic link, when one parent has psoriasis 8% of offspring develop, when both
parents have it, 41% of offspring develop it. It is thought the genetic predisposition
increases the likelihood of certain trigger factors causes psoriasis, triggers include
physical trauma, stress, drugs and alcohol ingestion.
Pathogenesis is as follows:
- Alteration of cell kinetics of keratinocyteswith a shortening of the cell cycle
resulting in 28 x the normal production of epidermal cells
- Abnormalities in the CD8+ T cells, which trigger an autoimmune inflammatory
reaction in the dermis, triggering epidermal changes (all psoriasis is a T cell
driven disease).
Clinical manifestation is in one of two types

- Acute guttate-Eruptive, inflammatory type with multiple small lesions and a
tendency towards spontaneous resolution(this is the rarer type, <2%)
- Salmon-pink papules up to 1cm with or without scales
- Often disseminated, generalized and mainly affects the trunk
- Chronic stable (plaque) psoriasiswhich is the majority of patients who have
chronic indolent lesions for months and years
- Dull-red plaques with loosely adherent, lamellar, silvery white scales are
present on the skin, plaques coalesce to form
polycyclic, geographic lesions
- Skull and anogenital type are the most pruritic
- Often symmetrical, with predilection for elbows, knees,
sacral gluteal region, scalp, and palm/soles, Nails
can also be affected
Dermatopathology shows overall thickening of the epidermis

(acanthosis)and thinning of the epidermis over the elongated
dermal papillae(the dermal papillae come closer to the epidermal
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surface). Increased mitosis of keratinocytes, fibroblasts and endothelial cells sees
parakeratotic hyperkeratosis(nucleus retained in stratum cornea).
Treatment for the plaque form is topical corticosteroid and/or topical vitamin D
analogue, phototherapy and methotrexate (IM) can also be added. If unsuccessful add
biological agent(infliximab) followed by oral retinoid. Treatment of guttate form is
phototherapy followed by methotrexate (IM) then oral retinoid.
Pityriasis rosea
This is a self limiting rash that affects those aged 10-43 years of age, most commonly in
spring and autumn, thought to be a result of human herpesvirus 6 and 7 reactivation.
The condition begins with a Herald patchthat occurs in 80% of patients on the trunk, this
plaque is 2-5 cm, salmen red and may be multiple. One or two weeks after this the
exanthem rash begins, this is a fine scaling papules and patches with marginal
collarette(marginal colour). The pattern is generally that of a ‘christmas tree’ patternwith
lesions usually confined to the trunk and proximal aspects of the arms and legs. The
condition is self limiting and spontaneous remission usually occurs within 6-12 weeks,
recurrences are rare.
Treatment is oral antihistamines for relief of pruritus, topical glucocorticoidsmay be

useful as well.
5. Lincoln rubber planus
Rubber planus (not sure what lincoln is doing getting involved) is an idiopathic
inflammatory disease that affects the skin, hair, nails and mucous membranes. It is
characterised by itchy, shiny, flat-topped violet papules and plaques that four the
extremities. The lesions are designated as the four P’s - papule, purple, polygonal and
pruritic.
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Age of onset is between 30-60, and is more common in femalesthan males. It is

idiopathic but cell-mediated immunity plays a major role. Drugs, metals or infection
result in alteration of cell-mediated immunity, can lead to an immunological reaction .
It is thought there might be HLA associated genetic susceptibilityas well that helps
explain the genetic element.
Onset is generally acute or insidious, and lesions can last months to years, being
asymptomatic or pruritic. Lesions are often in the wrists, lumbar regions, shins, scalp,
glans penis and mouth.
There are a number of variations of Rubber planus that can be distinguished clinically:
- Hypertrophic - large thick plaques that arise on the foot, dorsum of hands, and shins
- Atrophic - white-blueish, well demarcated papules and plaques with central atrophy
- Follicular - individual keratotic-follicular papules and plaques that lead to cicatricial
alopecia
- Vesicular - vesicular or bullous lesions may develop
- Pigmentosus - hyperpigmented, dark brown macules develop
- Actinicus - papular lesions in sun exposed sites
- Ulcerative
- Mucous membrane
Clinical findings can be confirmed by histopathology, dermatopathology shows

hyperkeratosis, increased granular layer, irregular acanthosis, liquefaction
degeneration of the basal cell layer and band like mononuclear infiltrate that hugs the
epidermis . Lesions also show Wickham’s striae, whitish lines visible in the papules under
magnification.
The condition usually persists for months, even years in some cases, especially the
hypertrophic form on shins and mouth that can last for years.
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Management is with topical glucocorticoids with occlusion for cutaneous lesions.
Cyclosporine, glucocorticoids and systemic retinoids can all be given systemically.
6. Bullous dermatoses (pemphigus, dermatitis herpetiformis,

pemphigoid)
Pemphigus
This is an autoimmune bullous disease of the skin and mucous membranes based on
acantholysis(loss of intercellular connections). There are two main types, Pemphigus
vulgaris (PV) and Pemphigus foliaceus (PF),PV is suprabasal, while PF is subcorneal .
Both PV and PF are rare, PV is more common in Jews and those of mediterranean descent,
while PF is more common in rural areas in Brazil. Age of onset is generally 40-60.
Pemphigus is an autoimmune disease with the loss of cell-to-cell adhesions in the

epidermis as a result of IgG antibodies which bind to desmogleins(PV affects
desmoglein 3, PF affects desmoglein 1).
Clinical manifestation:
- Pemphigus vulgaris- usually starts in the oral mucosa, then months later may
affect other parts of the skin. No pruritus but burning and painful erosions, painful
and tender mouth lesions may prevent eating. Vesicles and bullae with serous
content are easily ruptured. Nikolsky sign is present(dislodging of normal
epidermis by lateral finger pressure in the vicinity of lesions which leads to an
erosion). Most commonly affects scalp face, chest, axillae, groin and umbilicus
- Pemphigus foliaceus- No mucosal lesions, starts with scaly, crusted lesions
on an erythematous base. Lesions are commonly on face, scalp, upper chest and
abdomen.
(Both images below are Pemphigus vulgaris, image on the L shows what individual vesicle
look like, image on the R show what a confluence of these vesicles look like when ruptured).
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Dermatitis herpetiformis
This is a chronic recurrent intensely pruritic eruption occurring symmetrically on the
extremities and the trunk. The rash develops with tiny vesicles, papules and urticarial
plaques that are arranged in groups. Pathogenesis is due to IgA deposits in the skin,
patients have antibodies to transglutaminases that act as the autoantigen.
Clinical presentation is intense, episodic burning or stinging of the skin, symptoms

often precede appearance of skin lesions by about 12 hours. Patients have small bowel
malabsorption, although usually no systemic symptoms. Skin lesions are
erythematous papules or wheal-like plaques, tiny firm-topped vesicles which are
sometimes hemorrhagic and occasionally bullae. Typically affects extensor areas
(elbows, knees) and buttocks, and often very symmetrical.
Management is Dapsone (AB, sulfone) and Sulfapyridine. A gluten free diet may suppress
disease.
Pemphigoid
There are a number of pemphigoid variants, and the book divides them up into different
chapters, let's take a look.
Bullous pemphigoid - an autoimmune disease usually in elderly patients, pruritic

papular or urtical lesions develop with large tense bullae and subepidermal blisters
with eosinophils. Antigens are keratinocyte hemidesmosome proteins. Treatment is
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systemic prednisolone with or without azathioprine. Patients often go into permanent
remission and do not require further therapy, local recurrences can be controlled with topical
glucocorticoids.
Cicatricial pemphigoid - a rare disease of the elderly. Ocular involvement is common

here, often with unilateral or bilateral conjunctivitis with burning,
dryness and FB sensation. Blisters that rupture into erosions in
the conjunctiva, mouth, oropharynx and nasopharynx are
pathognomonic. Chronic involvement leads to scarring. Antigens
include BPAG1, BPAG2 and collagen type VII. Also known as
mucous membrane pemphigoid.
Pemphigoid Gestationis - a rare pruritic and polymorphic

inflammatory bullous dermatosis of pregnancy and postpartum period. Look for
extremely pruritic eruptions in the abdomen with sparing of the mucous membranes ,
it is a subepidermal blistering condition, with C3 depositions along the basement
membranezone with concomitant IgG deposition in 30% of patients. Manage with
Prednisolone.
7. Urticaria. Oedema Quincke. Strophulus
Urticaria. Oedema Quincke (Oedema quincke = angioedema)

Urticaria is composed of wheals (transient e dematous papules and plaques, usually
pruritic and due to edema of the papillary body), the wheals are superficial and well
defined. As a condition urticaria generally resolves within 24 hoursand leaves no residual
marking.
Angio-oedema on the other hand is swelling involving deeper layers of the subdermis
and occurs in association with urticaria in about 40% of cases, but can also occur in the
absence of urticaria.
Urticaria lasts less than 6 weeks and is often due to a hypersensitivity reaction to a
specific trigger, or an underlying viral infection.
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15-25% of the population may have urticaria/angioedema at some point in their lives, it can
be categorised as acute (<30 days) or chronic (>30 days).
Classification of urticaria is:

- Immunologic
- Physical
- Due to mast cell releasing agents
- Idiopathic
- Nonimmune contact urticaria
- vascular/connective tissue autoimmune disease
- Hereditary
Strophulus
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This is an eruption of red pimples on the face, neck and arms in early infancy. Can
occur with teething distress, also known as red gum and tooth rash.
8. Contact dermatitis. Professional dermatoses
Contact dermatitis is a generic term applied to acute or chronic inflammatory reactions

to substances that come into contact with the skin. It can be irritant contact dermatitis
(caused by a chemical irritant) or allergic contact dermatitis(caused by an allergen,
eliciting a type IV cell mediated hypersensitivity reaction). Below we consider both
Irritant and allergic contact dermatitis.
Irritant contact dermatitis

ICD is a localised diseasethat only affects the part of the skin that was exposed to
chemical or other physical agent. Most cases are caused by chronic cumulative exposure
to one or more irritants and most commonly the hands are affected.
Common irritants include soaps, detergents, acids and alkalis, industrial solvents, blants and
other substances such as fiberglass, wool and synthetics. ICD is the most common cause of
professional dermatoses, accounting for 80% of all such cases. Predisposing factors
include having fair skin, low temperature and low humidity.
Acute ICD is generally the result of direct cytotoxic damage to keratinocytes, while
chronic ICD is due to cell membrane disruption leading to skin barrier disruption.
Acute symptoms are burning, stinging and itching, with the development of lesions that
may range from erythema to vesiculation and caustic burn with necrosis. Lesions are
generally strongly demarcated in line with where the contact was.
Chronic symptoms are similar, although dryness generally precedes the erythema.
Allergic contact dermatitis

ACD is a classic, delayed, cell-mediated hypersensitivity reaction, this means
sensitization to the allergen must first occur, if it is a strong allergen this may take pace in a
week, a weak antigen may take years. Sensitized T-cells circulate in the blood and home
to wherever the antigen is presented, so all of the skin becomes hypersensitiveto the
allergen. .
Contact allergens can include metal salts, dyes, paints, and many other substances. Clinical
manifestation is eruption in a sensitized individual 48 hours after secondary contact
with the allergen. Repeated exposures lead to a crescendo reaction(worsening eruption),
symptoms are confined to the site of the exposure. The skin lesions are generally well
demarcated erythema with edema and papules or vesicles in the acute form, chronic
forms see plaques of lichenification of the epidermis. Diagnosed with patch testing and
treat by avoidance of the allergen.
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9. Atopic dermatitis
Atopic dermatitis is a synonym of eczema and atopic eczema, note the term atopy gives
us a clue about the pathogenesis here, indicating the auto immune, allergic element. It
can be acute, subacute or chronic relapsingand is very common in infancy and childhood
(20% prevalence). Has a strong genetic predisposition, it is thought that individuals have
genetic skin barrier disruption due to impaired filaggrin production. The condition can
be exacerbated in certain weather conditions, and certain clothings are a trigger (wool),
emotional stress also exacerbates the condition.
The pathogenesis of AD is around the interaction of skin barrier, genetic, environmental,

pharmacological and immunological factors. Type I (IgE mediated) hypersensitivity
reaction occurs as a result of the release of vasoactive substances from mast cells
and basophils that have been sensitized by the interaction of the antigen with IgE.
Acute inflammation is also associated with a predominance of interleukin 4 and 13
expression.
Patients present with dry skin, which causes the pruritus, which causes the scratching ,
leading to the itch-scratch-rash-itch-scratch cycle. Symptoms of allergy (atopy) may be
present such as allergic rhinitis or pharyngeal itching. Lesions will present with
erythematous patches, papules and plaques with or without scale, skin is edematous
and linear erosions due to scratching (excoriations) will occur. When the lesions
become chronic we will see lichenification. Atopic dermatitis has a predilection for the
flexures, front and sides of the neck, eyelids, forehead, face, wrists and hands and
feet.
Management is to avoid scratching, along with the use of emollients to try and moisten the
dry skin. Allergic workup is rarely helpful.
In acute cases:
- Wet dressing and topical glucocorticoids
- Hydroxyzine four times daily for the prurits
- Oral antibiotics
In chronic cases
- Hydration - oilated baths followed by use of emollients (e.g hydrated petroleum)
- Topical anti-inflammatory agents such as glucocorticoids
- Calcineurin inhibitors
- Oral antihistamines
10. Seborrheic dermatitis
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Seborrheic dermatitis is a very common chronic dermatitis characterised by redness
and scaling that occurs in regions where the sebaceous glands are most active(face,
scalp, presternal area sn body folds). It is a genetic disease, but more common in those
with parkinson's and immunosuppression.
Patients are commonly affected in infancy, puberty or between the ages 20-50. Patches
are red and pruritic with micaceous scales, commonly found on the scalp, glabella,
nasolabial fold, posterior auricular skin and anterior chest.
Lesions generally develop gradually, and some patients are worse in winter in dry,
indoor environments. Pruritus is variable, and often increased by perspiration. Classic
distributions include the face (the butterfly areas of the face), truink, body folds (axillae,
groins, anogenital region, submammary areas etc) and genitalia.
As well as the more common light greasy or white dry scaling on the face we can get scaling
from the head - namely dandruff.
Management
- Initial - scalp - use shampoos containing selenium sulfide, zinc pyrithione and/or tar.
- Face and trunk - ketoconazole shampoo (2%), glucocorticoid cream and
lotions
- Eyelids - removal of crusts with a cotton ball dipped in diluted baby shampoo -
apply 10% sodium sulfacetamide
- Infants (known as cradle cap) - ketoconazole shampoo 2%
- Systemic therapy - retinoic acid
- In all cases use emollients
11. Lupus erythematosus
Lupus erythematosus rages from life-threatening manifestations of acute systemic LE (SLE)

to exclusive skin involvement in chronic cutaneous LE (CCLE).
The main types of lupus that we should concern ourselves with are:
- Chilblain lupus
- Cold-induced plaques on fingers and toes
- Chronic cutaneous (discoid) lupus
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- Subacute cutaneous lupus erythematosus
- Acute systemic lupus
- Non-specific cutaneous lupus
Let us consider some of these in detail below.
Chronic cutaneous (discoid) lupus

Like SLE, is more common in women than men, although only twice as common. Only 5% of
cases will convert to SLE, but at least 25% of those with SLE with have discoid lupus
lesions at some point in their disease.
The primary lesion is an angular plaque with follicular plugging, central atrophy and
peripheral hyperpigmentation and erythema. The lesions often comes with pruritis or
burning, and lesions are generally on sun-exposed areas such as the upper chest,
face, arms, scalp and back. Lesions on the scalp may lead to a lopecia, and elsewhere
may leave a permanent hypo- or hyperpigmentation.
Discoid lupus can be hypertrophic, diffuse and tumid, the former being the most
common. ANA is present, but often at a lower titer, skin biopsy will show positive for
lupus band IgM, IgG and C3.
Management is topical steroids or calcineurin inhibitors, oral hydroxychloroquine can be

added for a more widespread disease.
Subacute cutaneous lupus

Again, more common in women than men, presence with sudden onset of figurate,
annular arcuate or psoriasiform lesions that are typically non scarring and non
atrophic in a photodistribution(face, neck, extensor arms). ANA again is often positive
,
and skin biopsy demonstrates positive lupus band test.
There are two types of skin lesions, the psoriasiform and the annular. The former with
sharply defined and delicate swelling, the latter with bright red annular lesions and central
regression, possibly with scaling.
50% of these patients will fulfil the criteria for SLE.
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Systemic lupus erythematosus

More common in women than men, strong genetic component, precipitating factors include
sunlight and certain drugs.
Lesions present for weeks in the acute form or months in the chronic form, with
pruritis, burning of skin, fatigue, fever, weight loss, malaise, arthralgia, abdominal
pain and CNS symptoms. In SLE skin symptoms are usually minimal, presenting with the
typical butterfly maculopapular rash. Raynaud’s symptoms are also common as well.
SLE is an antigen-driven immune mediated disease characterised by high affinity IgG

antibodies to double stranded DNA as well as nuclear proteins, due to T-cell
dysregulation of B-cells.
Patients will have a positive high titer ANAin more than 95% of cases, with anti-Sm and
rRNP antibodies characteristic of the disease, with leukopenia and anemia both also
common.
Management is systemic, with hydroxychloroquine, prednisolone, methotrexate, biological

agents and immunomodulators often indicated.
12. Localizes sclerosis. Systemic sclerosis
Localized sclerosis
Localised sclerosis (aka Localised scleroderma, aka morphea) is a localized and
circumscribed cutaneous sclerosis characterized by early colour change of the skin
to violet and later ivory, with hardening of the skin. The lesion may be solitary, linear,
generalized or along with atrophy of underlying structured, it is unrelated to the
systemic form.
It is a rare disease, most common in those between ages 20 and 50. Women are affected
three times more often than men, the etiology is unknown.
Classification:
- Circumscribed
- Macular
- Linear
- Frontoparietal
- Generalized morphea
- Pansclerotic (involves dermis, and subcutaneous tissue and muscle)
Dermatopathology shows epidermis appears normal to atrophic while dermis is

edematous with homogenous and eosinophilic collagen. It is this collagen that causes
the ‘sclerosis’.
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Systemic sclerosis
Scleroderma is a multisystem disorder characterised by inflammatory, vascular and
sclerotic changes of the skin and internal organs(especially the lungs, heart and GI).
There are two types:
- Limited systemic scleroderma (60%)
- Tends to have less severe internal organ involvement
- Diffuse systemic scleroderma
- More severe internal organ involvement - worse prognosis
Patients always present with skin sclerosis and a long history of Raynaud's(the
presence of Raynauds helps distinguish from the local form). Presentation is often that of
digital pain, coldness, stiffness of knees and fingers, heartburn, dysphagia,
constipation, diarrhea, abdominal bloating and malabsorption symptoms may also be
present.
Look out for painful ulcerations at the fingertips(rat bite necrosis), knuckles with pitted
white scars, and thinning of lips causing microstermia. Periorbital and lower limb
oedema might also be present.
The clinical course is determined by extent of vascular and fibrosing complications,

fibrosis can affect the lungs, heart and GI, while the vascular complications can cause
ischaemic digital ulcers, hypertensive crisis and pulmonary arterial hypertension. The
exact pathogenesis is unknown but thought to relate to vasculopathy, fibrosis and immune
system activation with autoimmunity.
Management is systemic glucocorticoids, with immunosuppressive drugs such as

cyclosporine and methotrexate. Additional therapy to limit complications such as renal
crisis, cardiac tamponade include ACE inhibitors and possibly dialysis.
13. Chronic venous insufficiency of lower legs
Chronic venous insufficiency results from a failure of centripetal return of venous blood
and increased capillary pressure, this results in edema, stasis, dermatitis,
hyperpigmentation and fibrosis of the skin and subcutaneous tissue .
Chronic venous insufficiency (CVI) is Commonly secondary to varicose veinswhich have

an incidence of ofsent at 30-50 years of age. The pathogenesis is relatively simple, the
damage the valves of the deep veins of the calf are incompeent at restricting backflow
of blood. Damaged communicating veins connecting deep and superficial veins also cause
CVI in that blood flows from deep veins to the superficial plexus. This causes fibrin to be
deposited in the extravascular space which then undergoes organization, causing
sclerosis and obliteration of the lymphatic and microvascular structure. This cycle then
repeats leading to ulceration secondary to stasis dermatitis.
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The clinical picture is that of heaviness of the legs, along with aching which is
aggravated by standing and relieved by walking. Shoes often feel tight by the end of the
day (due to swelling) and night cramps are present. The following staging system exists for
staging CVI:
- Clinical picture
- C0 no clinical signs to C6 active ulcer
- Anatomy
- As superficial, Ad deep, Ap perforans
- Etiology
- Ep primary, Es Secondary, Ec congenital
- Pathophysiology
- Pr reflux, Po obstruction, Pro, reflux + obstruction
The skin changes can be summarised as a number of separate phenomena:

- Varicose veins - dilated tortuous routes of superficial veins, may or may not be
associated with starburst phlebectasia
- Edema - improved in the morning after a night in the horizontal position
- Eczematous (stasis) dermatitis - classic eczematous dermatitis with inflammatory
papules, scaly and crusted erosions, with pigmentation and hemorrhages
- Atrophie Blanche - small white ivory depressed patches with hemosiderin pigmented
border
- Lipodermatosclerosis - inflammation, induration and pigmentation of the lower third of
the leg
- Ulceration - occurs in 30% of cases with a painful hyperalgesic microculer in an area
of atrophie blanche. Can develop into larger superficial or deep ulcers with defined
margin and necrotic base. Generally medial and above the ankles.
Examinations involve Doppler and dermatopathology. Management is the use of

compression dressings or stockings, avoid trauma in the area involved and use
topical glucocorticoids in cases of stasis dermatitis.
Note - Arterial vs Venous ulcers

- Venous ulcers medial > lateral, arterial ulcers lateral > medial
- Arterial usually at distal points such as toes, venous usually on the medial lower calf
- Arterial lesion is punched out with necrotic base while venous lesion is irregular, with
sloped borders and fibrotic necrotic base.
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Management of ulcers is with wet dressings.
14. Disorders of the cutaneous melanocytes (hypochromia, vitiligo)
Normal skin colour is composed of a mixture of four biochromes, these are reduced
hemoglobin, oxyhemoglobin, carotenoids, and melanin. The main determinant of skin
colour is melanin pigment, which gives us the three principal human skin colours: black,
brown and white.
Increased melanin in the epidermis is due to a state known as hypermelanosis, this is

either due to an increase in the number of melanocytes in the epidermis producing
increased level of melanin known asmelanocytic hypermelanosis (e.g. lentigo) or no
increased melanocyte number but an increase in melanin only known asmelanotic
hypermelanosis (e.g. melasma).Hypermelanosis can be genetic, hormonal or due to UVR.
Hypomelanosis is a decreased amount of melanin in the epidermis and reflects one of

two changes. A decrease in the production of melanin, known as melanopenic
hypomelanosis(e.g. albinism) or a decrease in the number of melanocytes known as
melanocytopenic hypomelanosis (e.g. vitiligo).
Vitiligo
Affects 1% of the population and can be a major psychological problem for brown or back
persons. May begin at any age but common between the age of 10 and 30. Has equal
prevalence among all races, but obviously more evident in those with darker skin. Has a
genetic component.
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Pathogenesis is one of three theories:
1. Autoimmune theoryholds that selected melanocytes are destroyed by certain
lymphocytes
2. Neurogenic hypothesisthat is based on an interaction of
the melanocyte and nerve cell
3. Self-destruct hypothesissuggests that melanocytes are
destroyed by toxic substance formed as part of normal
melanin biosynthesis.
Many patients attribute the onset of their vitiligo to physical

trauma (Koebner phenomenon), illness or emotional stress. The
skin lesions are macules or patches, and appear chalky white. It
commonly affects the face (mouth and eyes), genital region,
extensors of the knees, dorsum of the hands and feet and the
axillary regions. Where the white patches join up so there is no
normally pigmented skin remaining, we call this Universal vitiligo.
Associated with vitiligo is alopecia, and changes to the nails.

Management is sunscreens, cosmetic cover up and
repigmentation (with topical glucocorticoids).
Oculocutaneous Albinism
Mutations in the tyrosinase gene responsible for deficient tyrosinase activity in
melanocytes leads to albinism. Hair is white along with skin, eyes are red, with nystagmus
and reduction of visual activity. No treatment available, important to protect against skin
cancer.
Melasma
Greek for ‘black spot’, this is an acquired light or dark brown
hyperpigmentationthat occurs in exposed areas most often on the face
due to exposure to sunlight. Very common among persons with
constitutive brown skin taking contraceptive pills in sunny climates.
Hypochromia (aka hypopigmentation)

This is a postinflammatory phenomenonrelated to the loss of melanin.
Possible causes include pityriasis versicolour, atopic dermatitis,
psoriasis, guttate parapsoriasis and pityriasis lichenoides chronica.
Lupus, alopecia and others may also cause the condition.
15. Disorders of the hair (alopecia areata, androgenetic alopecia,

hypertrichosis) and nails
Firstly, a word or two about the hair follicle cycle, hair undergoes a life-long cyclic
transformation into three primary phages: anagen (the growth phase) telogen (the
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quiescence phase) and catagen (apoptosis driven phase between telogen and anagen
phase). Where a hair shaft is actively shed, we call this exogen.
For us to have a healthy head of hair we need more hair follicles in the Anagen phase, this is
determined by growth factors, hormones, stress and immunological and physical injury.
Androgenetic Alopecia
This can be noncicatricial alopecia, where there is no clinical sign of tissue inflammation,
scarring or atrophy, or cicatricial alopecia, where there is evidence of tissue destruction
and inflammation. The most common form of alopecia is nonscarring pattern hair loss .
Androgenic alopecia is characterised by progressive shortening of the anagen growth
phase with each hair cycle and increased telogen and catagen hair transformation. It
is thought this is due to stem cell factor(SCF) and insulin-like growth factor 1(IGF1)
being altered by dihydrotestosterone. The overexpression of androgen receptors seems
to facilitate this problem.
Alopecia areata
Alopecia areata is localized loss of hair in round or oval areas with no apparent
inflammationof the skin, it is a non-scarring form of alopecia meaning the hair follicle is
intact and the hair can regrow. The etiology is unknown but thought to be autoimmune in
origin due to its links with other autoimmune diseases. Most frequently affects young adults
but can occur at any age.
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This is a chronic organ-specific autoimmune disease, mediated by autoreactive T-cells
affecting hair follicles and nails. Follicular damage occurs in anagen followed by rapid
transformation to catagen and telogen then to dystrophic anagen status. Follicular
stem cell is spared however and the hair follicles are not destroyed.
Most commonly affects the scalp, beard, eyebrows, eyelashes and pubic hair can all be
affected. Based on the extent of damage we can categorise alopecia areata into four:
- Alopecia areata - solitary area of hair loss
- AA totalis - total loss of terminal scalp hair
- AA universalis - total loss of all hair
- Ophiasis - band like pattern of hair loss over periphery of scalp.
No treatment.
Hypertrichosis
Excess hair growth can occur in two ways:
- Hirsutism - hair growth in women at sites where hair is under androgen control
- Hypertrichosis - hair density or length beyond accepted limitis for age, race, sex
Hypertrichosis may be generalized or localized and may be acquired or congenital. The

hair may be lanugo (soft fine pigmented hair that covers the fetus), vellus (fine non
pigmented hair, unaffected by hormones) or terminal hair (thick found on scalp, beard,
axillae, pubic area, growth is influenced by hormones).
Nail disorders include

- Chronic paronychia - damage to nail cuticle leading to chronic dermatitis of proximal
nail fold and matrix (think of this as chronic inflammation of the nails)
- Onycholysis - detachment of nail from its bed at distal or lateral attachments
- Onychauxis - thickening of nail plate seen in the elderly
- Psychiatric disorders - repeated manipulation of nails leading to nail damage
Nails can also be affected by psoriasis, Lichen planus and alopecia areata.
16. Disorders of the sebaceous glands (acne, seborrhoea, rosacea)
Remember, sebaceous glands are microscopic endocrine glands that open into hair
follicles to secrete the oily matter called sebum, which lubricates the hair of skin.
Acne (Acne vulgaris)

Acne is an inflammation of the pilosebaceous unit and is an incredibly common
condition. It appears on the face, trunk and occasionally the buttocsk and is most
common in adolescents. Skin lesion presents as comedones, papulopustules, nodules
and cysts, and in the long term can last as pitted, depressed or hypertrophic scars.
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Acne is a multifactorial disease which has a genetic component. The pathogenesis is
follicular keratinization, androgens and Propionibacterium acnes. Follicular plugging
(comedones) prevents drainage of sebum, while androgens stimulate sebaceous
glands to produce more sebum. Bacterial piase then converts lipids to fatty acids and
produce proinflammatory mediators that lead to an inflammatory response. Certain
drugs can increase the symptoms as well, including lithium and glucocorticoids, while
emotional stress, occlusion and pressure on the skin can make symptoms worse.
A number of different lesions can form:

- Comedones - open (blackheads) or closed (white heads)
- Papules and papulopustules
- Nodules or cysts
Special forms of acne include neonatal acne, acne excoriee, acne mechanica, acne
conglobata, acne fulminans and topical acne.
Management
- Mild - use topical antibiotics (clindamycin and erythromycin) and benzyl peroxide gels
and topical retinoids
- Moderate - oral antibiotics add to the regime (Minocycline most effective)
- Severe acne - add systemic treatment with isotretinoin
Rosacea
This is a common chronic inflammatory disorder of the facial pilosebaceous units, it
occurs with increased reactivity of capillaries leading to flushing and telangiectasia.
Occurs ages 30-50, predominantly affects females of fair coloured skin.
Staging is as follows:
- Stage 1 - persistent erythema with telangiectasia
- Stage 2 - persistent erythema with telangiectasia, pules, and tiny pustules
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- Stage 3 - persistent deep erythema, dense telangiectasia, papules, pustules, nodues
and ‘solid’ edema of the central part of the face
The clinical manifestation is a history of episodic reddening of the face, acne may have
proceeded during adolescence but is not obligatory. The flushing red face is
pathognomonic, along with the telangiectasia and dusky-red papules and nodules. Red eyes
as a result of chronic blepharitis, conjunctivitis and episcleritis can also occur.
Management is the elimination of alcohol, along with topical metronidazole gel and topical
antibiotics.
Seborrhea
Also known as seborrhoeic dermatitis.
Seborrheic dermatitis is a very common chronic dermatitis characterised by redness and

scaling that occurs in regions where the sebaceous glands are most active (face, scalp,
presternal area sn body folds). It is a genetic disease, but more common in those with
parkinson's and immunosuppression.
Patients are commonly affected in infancy, puberty or between the ages 20-50. Patches are
red and pruritic with micaceous scales, commonly found on the scalp, glabella, nasolabial
fold, posterior auricular skin and anterior chest.
Lesions generally develop gradually, and some patients are worse in winter in dry, indoor
environments. Pruritus is variable, and often increased by perspiration. Classic distributions
include the face (the butterfly areas of the face), truink, body folds (axillae, groins, anogenital
region, submammary areas etc) and genitalia.
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As well as the more common light greasy or white dry scaling on the face we can get scaling
from the head - namely dandruff.
Management
- Initial - scalp - use shampoos containing selenium sulfide, zinc pyrithione and/or tar.
- Face and trunk - ketoconazole shampoo (2%), glucocorticoid cream and
lotions
- Eyelids - removal of crusts with a cotton ball dipped in diluted baby shampoo -
apply 10% sodium sulfacetamide
- Infants (known as cradle cap) - ketoconazole shampoo 2%
- Systemic therapy - retinoic acid
- In all cases use emollients
17. Nonmelanoma skin cancer (Basal cell carcinoma, squamous

cell carcinoma). Precancerosis
Basal cell carcinoma

BCC is the most common cancer in humans, it is the result of UVR damage, which causes
a PTCH gene mutationin many cases. It is most common in those over the age of 40,
and in males more than females.
There are five clinical types:

- Nodular BCC- papule or nodule, translucent or pearly. The skin is reddish with
smooth surface and telangiectasia
- Ulcerating BCC- has a central ulcer often covered with a crust and a rolled border
which is again translucent, pearly, smooth with telangiectasia
- Sclerosing (Morphoeic) BCC- appears as a small patch of morphea or a superficial

scar. Often ill defined and skin coloured
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- Superficial multicentric BCC- appears as thin plaques, pink or red in colour. Can
exhibit scaling and can give rise to nodular and ulcerating BCC.
- Pigmented BCC- may be brown to blue to black. Smooth, glistening surface, firm to
touch.
All BCCs histologically are similar, they are solid tumors consisting of proliferating
atypical basal cells, however have little anaplasia and infrequent mitosis. BCCs do not
metastasize, the tumours growth is dependent on its stroma, so when tumour cells
lodge at distant sites they are unable to multiply due to the absence of growth factors .
However problems may occur with BCC arising in the danger sites of the head as the tumour
may invade deeply, and cause destruction of muscle and bone.
Squamous Cell Carcinoma

Squamous cell carcinomas may be in situ or not, depending on if the growth is confined to
the epidermis or if it has invaded into the dermis. The in situ form is also
known as Bowen’s disease.
The greatest risk factor is exposure to UVR, although HPV is also a risk
factor. Those with immunosuppression are also at greater risk. Lesions
present as solitary or multiple macules, papules or plaques which may
be hyperkeratotic or scaling. There is generally a progressive process
from carcinoma in situ to a malignant SCC.
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Common sites are the helix of the year and the lower lip, along with the crown of the
head in bald individuals, the v of the neck, shins, back of the hands and forearms, and
groin.
SCC is a slowly evolving tumour, and any isolated keratotic or eroded papule or
plaque in a suspect patient that persists for over a month is considered a carcinoma
until proven otherwise. Occasionally, rapidly evolving invasive SCC can erupt within a few
weeks, with the rapid development of a painful tender lesions.
Diagnosis is with biopsy, the epidermis in SCC in situ with slow hyperkeratosis and
parakeratosis, with marked acanthosis and elongation and thickening of the rate ridges. In
the invasive SCC we will see infiltration of the epithelium into the dermis, through the
basement membrane. Greater differentiated tumors have a better long term prognosis.
18. Malignant melanoma
Melanomas have the highest rate of mortality of all dermatological cancers and they
are most common in younger patients. Key risk factors include a family history, being
fair skinned, having light hair or light eye colour, additionally, multiple melanocytic
naevi and a high freckle density all increase the risks of contracting malignant
melanoma .
Melanomas are asymmetric, ill-defined, pigmented lesions that are often found to
bleed or weep. Melanomas develop from melanocytes that sit just above the basement
membrane.
On examination look for the A-E of melanomas:

- A- Asymmetry
- B- Borders (irregular)
- C- Colour changes
- D- Diameter
- E- Elevation/evolution
- If the skin lesion changes rapidly then a melanoma should be suspected
Melanomas can be classified as follows:

- De novo
- Melanoma in situ
- Lentigo maligna melanoma
- Superficial spreading melanoma (70%)
- Mostly arises on the upper back, occurs as a slow growing lesion over
a period of 2 years
- Nodular melanoma (second in frequency)
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-Occurring largely in mid life, develops quite rapidly as a thick plaque or
exophytic, polypoid lesion
- Acral lentiginous melanoma
- Melanoma of mucous membranes
- Desmoplastic melanoma
- Melanoma arising from precursors
- Melanoma arising from dysplastic nevomelanocytic nevi (NMN)
- Melanoma arising from congenital NMN
- Melanoma arising from common NMN
There are a number of precursor lesions to melanomas that we should be aware of, they are
benign but have the potential to turn malignant. These include:
- Dysplastic melanocytic nevus - these are nevi that have different shapes compared
to others
- Congenital nevomelanocytic nevus - pigmented lesions present at birth that can
become malignant, this is true regardless of their size
- Common melanocytic nevi
Early detection of melanoma is vital for the effective removal and treatment of the patient.
19. Viral infections. Classification. Herpes simplex. Herpes Zoster
OK, i mean classification of viral infections, they can be viral or non-viral, just go with it!
Herpes simplex
HSV cause primary, latent and recurrent infections. HSV 1 primarily infects the oral
cavity, lips and perioral skin, while HSV 2 generally infects the genital area, although
HSV 1 is becoming a more common cause of genital herpes in young women.
Human herpes virus has a double-stranded DNAthat replicate within the nuclei of
infected cells. HSV infects mucocutaneous tissue after direct contact, or by way of
secretions (saliva in the case of HSV 1). The virus is transmitted via sensory nerves to
the ganglia where it may reside in a latent stage. Recurrent infections are caused by
reactivation of the virus which travels back to the skin or mucous membrane resulting
in an active infection, it is important to note that viral shedding may continue after the
infection has clinically resolved.
Patients with HSV 1may complain of fever blisters or cold sores on the lips or
periorbital area, while patients with genital herpes (HSV 2) may complain of pain or
tingling in the genital area during the prodrome and active phase.
The primary infection occurs3-7 days following infection

, this may be accompanied by
fever, malaise and lymphadenopathy. The primary skin lesion is that of vesicles, or small
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groups of vesicles,that progress to pustules and/or erosions that resolve in 1-2 weeks.
Recurrences are often triggered by stress or depressed immunity.
The presence of painful, grouped vesicles or erosions on the face or gential area is
usually enough for diagnosis. Management is not required in immunocompetent patients
with mild and limited orolabial HSV, however moderate to severe disease can be treated
with Acyclovir, Famiclovir or Valacyclovir.
Herpes Zoster
Herpes zoster (aka shingles) represents the reactivation of latent varicella (chicken pox)
infection. Herpes zoster beings with intense pain which may precede the eruption of
any cutaneous involvement by one or two days. Pruritus, tingling and tenderness may
also develop.
When the cutaneous eruption does occur, it presents as grouped vesicles within the
dermatome of the affected nerve, any area of the body may be affected, but it is most
commonly seen on the trunk and trigeminal (VI ophthalmic) nerve. Herpes zoster can
also affect other branches of the trigeminal, leading to erosions in the mouth, ears, pharynx
or larynx, while if it affects the facial nerve there may be involvement of the ear and or
tympanic membrane.
The rash usually resolves in 3-5 weeks, but symptoms may persist for longer. Diagnosis is
based on the clinical features of grouped painful vesicles within a dermatome. Management
should be with Acyclovir, Famciclovir or Valacyclovir and long management of pain.
Vaccination with live zoster vaccine may help reduce the risk of developing herpes zoster.
20. Warts. Molluscum contagiosum . Condylomata accuminata
Warts
Wars, Verrucae vulgaris, represent one of the most frequently seen viral
mucocutaneous infections. It most commonly found in children and
immunocompromised individuals. They are caused by H PV, a double stranded DNA
virus with over 100 genotypes, some of which are found on normal skin, others which are
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oncogenic (16, 18, 31, 33). The virus infects keratinocyte in the skin and mucous
membranes by direct skin-to-skin contact, or via floors etc.Warts often spontaneously
resolve after months, although ⅔ of patients will regress within 2 years.
Warts can develop on any skin or mucous membrane surface, most frequently affecting
hands, feet and genitalia, trauma may encourage inoculation with the virus. There are
a number of different clinical presentations of warts, these are:
- Verrucae vulgaris (common warts)
- Skin coloured, hyperkeratotic, exophytic dome shaped papules, may be linear
in configuration due to excoriation
- Verrucae plantaris (plantar warts)
- Verrucous or endophytic papules affect the plantar surface of the foot,
causing black or brown dots created by thrombosed capillaries
- Mosaic warts
- Verrucae planae
- Filiform warts
- Condylomata accuminata
- Genital or venereal warts
- These are sessile, smooth faced exophytic papillomas that may be skin
coloured, brown or whitish. Papilomas may be pedunculated or broad based,
sometimes coalescing into plaques.
Management of nongenital warts

- Salicylic acid topically
- Cryotherapy
- Surgical excision
Management of genital warts
- Imiquimod 5%
- 25% podophyllin in tincture of benzoin
- HPV vaccine
Molluscum contagiosum
A benign viral infection of the skin and mucous membrane that most commonly
affects children. Caused by a member of the pox virus group
, this double stranded DNA
virus is spread by direct skin-to-skin contact.
Small papules develop on the skin and sometimes on the genital mucous membranes,
usually within 2-7 weeks after contact with an infected individual. Lesions are typically
asymptomatic, but pruritus and inflammation can develop.
The lesions appear pearly and dome shaped. Management tricky as there is no single
therapy that is effective. Molluscum papules can be removed surgically using a skin
curette, or they can be incised with a needle or removed with cryotherapy.
Spontaneous resolution typically occurs in 6-9 months, but may take years.
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21. Bacterial infections (pyoderma). Etiology. Pathogenesis.

Epidemiology. Classification.
Pyoderma is an “archaic term” which means pus in the skin. It is commonly caused by
Staphylococcus aureus a nd group A streptococcus bacteria.
Staphylococci are common inhabitants of the skin and mucous membrane, they are
gram +ve and non-motile. Staphylococci can be categorised into two main groups,
coagulase +ve and coagulase -ve. Coagulase +ve include staph aureus and
saprophyticus, while -ve include s.epidermidis, s.hominis and s. Capitis. The most
important of these is Staphylococcus aureus.
While S.aureus is considered a perfectly normal bacteria in most people (15-40% of people
are healthy carriers of the bacteria), in cases where the barrier function of the skin is
impaired or the immune system is reduced, infections can occur. Once the bacteria
have invaded they are able to kill and survive within phagocytes, release toxins and
hide their antigens to prevent an immune reaction. Patients with atopic dermatitis,
psoriasis and other cutaneous diseases which interrupt the skins integrityare most
susceptible.
Meanwhile group a streptococcus usually colonizes the skin first and then the
nasopharynx, cutaneous production of toxins by the group can lead to diseases such
as toxic shock syndrome and scarlet fever.
Bacterial infections of the skin can be classified as skin and soft tissue infections (SSTI) and
acute bacterial skin and skin structure infections (ABSSSI). Examples are shown below:
- Skin and soft tissue infections
- Carbuncles
- Ecthyma
- Erythrasma
- Folliculitis
- Furuncles
- Impetigo
- Lymphadenitis
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- Minor cutaneous abscesses
- Acute bacterial skin and skin structure infections
- Cellulitis
- Erysipelas
- Lymphangitis
- Major cutaneous abscesses
- Necrotizing soft tissue infection
- Staphylococcal scalded skin syndrome
- Wound infections
22. Folliculitis. Furuncle. Carbuncle. Hidradenitis suppurativa
Folliculitis
Infectious folliculitis is an infection of a hair follicle, caused by s. aureus, pseudomonas
aeruginosa or gram negative bacteria. In rare cases it can also be due to viral or fungal
infections .
Folliculitis manifests as follicular papules, pustules, erosions or crusts at the follicular

infundibulum. The infection can extend the entire length of the follicle. It can
be a chronic disease, and lesions are generally non tender but may be
pruritic. The papule is confined to the hair follicle, with at times an
erythematous halo. Rupture of the pustules leads to superficial erosions
or crusts. Usually only a small portion of follicles in a region are affected.
Predisposing factors include shaving hair regions suchas the beard, axial or
legs, occlusion of hair bearing areas, topical glucocorticoid preparationand
systemic antibiotic use promotes growth of gram -ve bacteria.
Furuncle
A furuncle (boil) is an acute, deep-seated, red hot tender nodule or abscess
(boil) that evolves from staphylococcal folliculitis.
Carbuncle
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A carbuncle is a deeper infection composed of interconnecting abscesses usually
arising from several contiguous hair follicles. May be accompanied by low-grade fever
and malaise.
In effect, a boil is a deeper case of folliculitis while a carbuncle is a further continuation of

this, with multiple furuncles joining up. Etiology for all is S.aureus predominantly. Furuncles
and Carbuncles require treatment of incision and drainage plus systemic antimicrobial
therapy.
Give topical clindamycin for folliculitis and clindamycin for furuncles and carbuncles.
Hidradenitis suppurativa
Also known as acne inversa,this is a chronic suppurative disease of apocrine
gland-bearing skin. It generally involves the axillae, the anogenital region and rarely
the scalp. May be associated with severe nodulocystic acne.
Skin lesions are very tender, red inflammatory nodules/abscesses and may be
colonized by various infectious pathogens include s.aureus, streptococci, e.coli,
proteus and pseudomonas aeruginosa. Pathogenesis is keratinous plugging of the hair
folliclewhich causes dilation of the hair follicle and secondary plugging of the apocrine duct,
leading to inflammation, bacterial growth, rupture and then extension of suppuration and
ulceration.
Disease can be self-healing and mild, however some cases are progressively worse
and complications can include chronic pain, draining sinuses and scargin with
fistulas to urethra, bladder, and or rectum. Management is a combination of intralesional
glucocorticoids, surgery, oral antibiotics and isotretinoin.
23. Impetigo. Erysipelas. Ecthyma
Impetigo
Impetigo is caused by s.aureus (can be MRSA or MSSA), or beta-hemolytic
streptococcus group A. These bacteria generally access the skin through minor breaks,
often facial lesions secondary to dermatoses such as atopic dermatitis. Impetigo is a
superficial skin infection(ecthyma is the deeper form which we’ll talk about) and presents
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with erosion and crusts. The golden-yellow crusts are very typical for impetigo. Lesions
are scattered and discrete, without therapy lesions can become confluent.
Impetigo is highly contagiousand commonly passed between children when playing in

close proximity.
A rarer form of impetigo are bullous impetigo, blisters containing yellow fluid with
erythematous halo form.
Untreated lesions of impetigo become more extensive and

ecthyma, with adequate treatment with systemic antimicrobial treatment
based on sensitivity of organism, a complete recovery is made.
Erysipelas (Cellulitis)
Erysipelas is actually a less common type of cellulitis. Given there isn’t a
question in the syllabus about cellulitis, we’re going to talk about cellulitis
here and then mention erysipelas at the end.
Cellulitis is an acute infection of the dermis and subcutaneous tissue, and is a common
cause of hospitalisation. Most cases are caused by S.aureus and GAS, however in
some cases gram negative organisms can be to blame.
Risk factors include skin trauma or an underlying lesion such as a leg ulcer or fissured
toe webs. Chronic venous or arterial insufficiency, edema, surgery IV drug use and bites are
all significant risk factors as well.
Presentation is that of erythema, pain, warmth and edema, typically begins with acute
onset and surface crusts may develop. Systemic symptoms such as fever, malaise and
chills may also occur.
As mentioned erysipelas is a specific type of cellulitis, it is generally GAS in etiology, and

comes with a sharply defined red, edematous plaque, usually on the face or legs.
Ecthyma
Ecthyma is an uncommon variant of impetigo that initially presents as a typical
impetigo infection that then spreads deep into the dermis. It usually presents on the
lower legs with thick crusts overlying superficial ulcers, it is more common in
immunosuppressed patients and those with poor hygiene.
24. Cutaneous Tuberculosis and Tuberculosis skin diseases
Mycobacterium Tuberculosis is the causative agent of TB. It most commonly affects the
lungs, however can rarely affect the skin which is what we’re concerned with here.
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There are two main classificationsof cutaneous TB, Exogenous inoculationto skin, this
is where there is a direct mycobacterium tuberculosis infection into the skin forming a
tuberculous chancre, and endogenous spreadto the skin, where mycobacterium are
spread via the lymphatics and blood causing metastatic tuberculous abscess.
We can further divide the types of cutaneous TB as follows:

- TB verrucosa cutis- occurs after direct inoculation of TB into the skin of someone
who has never been previously infected. Presents as a purplish or brownish-red
warty growth. Lesions common on knees, elbows, hands, feet and buttocks. Lesions
persist for years but can clear without treatment
- Lupus vulgaris- This is a persistent and progressive form of cutaneous TB.
Presents with small sharply defined reddish-brown lesions with a gelatinous
consistency (called apple-jelly nodules). Lesions persist for years and can cause
disfigurement and are carcinogenic. Most lesions are on the head or neck.
- Scrofuloderma - skin lesions result from direct extension of underlying TB infection
of lymph nodes, bones or joints, associated with TB infection of the lungs. Creates a
firm painless lesion that eventually ulcerates. Most commonly occurs in the parotid,
submandibular and supraclavicular regions.
- Miliary TB- chronic TB infection that has spread from the primary infection to other
organs via the bloodstream. Skin lesions are small (millet-sized) red spots that
develop into ulcers and abscesses. More common in those with immunodeficiency
- Tuberculid - generalised exanthem in patients with a high degree of TB immunity
due to previous infection.
- Metastatic tuberculous abscess - a subcutaneous abscess, non-tender and ‘cold’.
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Treatment of TB is isoniazid + Rifampin along with ethambutol, streptomycin and

pyrazinamide in the initial phase of treatment.
25. Leprosy
Leprosy is a disease caused by Mycobacterium lepra, M.leprae is an obligate intracellular

acid-fast bacillus. It affects the skin and cutaneous nerves(schwann cell basal lamina).
Humans are the main reserve of M.lapae, with animals such as the wild armadillo and
mangabey monkeys naturally infected. Incidence rate peaks age 10-20 with prevalence
peaking at 30-50. Transmission is spread from person to person in respiratory droplets .
Leprosy is now a disease of the developing world, with very few cases in the developed
world. The clinical picture of leprosy depends on the specific type, the classifications have
been listed below:
- Tuberculoid (TL):localized skin involvement and/or peripheral nerve involvement,
few organisms
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- Lepromatous (LL):Generalized involvement including skin, upper respiratory
mucous membrane, reticuloendothelial system, adrenal glands and testes, all with
many bacilli
- Borderline (dimorphic):Has features of both TL and LL
- Indeterminate form
- Transitional form
The pathogenesis of leprosy depends on the host's ability to develop effective cell-mediated
immunity to the bacteria.M.leprae is able to invade and multiply in the peripheral
nerves, remaining subclinical, a picture that is common in areas where leprosy is
endemic.
Incubation period of leprosy is between 2-40 years(commonly 5-7), onset is insidious

and painless, first affecting the peripheral nervous systemwith persistent or recurrent
painful paresthesia and numbnesswithout any visible signs. At this point a macular rash
may appear, with blisters but a lack of awareness of trauma. Neural involvement leads to
muscle weakness and atrophy.
In the Tuberculoid form of leprosy, a few well defined hypopigmented hypoesthetic

macules appear with raised edges and varying in size. As time continues advanced
lesions become anesthetic and devoid of skin appendages.
Lepromatous leprosy sees skin coloured or erythematous papules/nodulesappear,

these nodules grow in size and begin to coalesce, often affecting the face and hairline .
Nerve involvement in this form of leprosy is more extensive, along with the
involvement of the upper respiratory tract and anterior chamber of the eye. If untreated
over a long period of time there is diffuse skin infiltration with multiple nodular lesions
and sensory loss throughout.
General findings show sensory neuropathy, plantar ulcers, secondary infections,

cranial nerve palsy and corneal damage in some cases. Once the disease is
symptomatic treatment is required, although 95% of those with M.leprae do not develop
the disease.
Leprosy can be managed with drugs, in the tuberculoid form give dapsone + rifampin, in
the lepromatous form give dapsone + rifampicin + clofazimine.
26. Fungal infections: dermatophyte infections, pityriasis versicolor
Dermatophytosis
Dermatophytes are a group of fungi capable of infecting nonviable keratinized structures
including stratum corneum, nails and hair. Spores can survive in human scales for up to
a year. We use the term Tinea + anatomical site to indicate infection with
dermatophytes, such as Tinea pedis.
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There are three genera of dermatophytes (dermatophyte literally means skin plants), these
are Trichophyton, Microsporum and Epdiermophyion. The most common species that
affect humans is Trichophyton rubrum- most common cause of epidermal
dermatophytosis and onychomycosis. Most common cause of dermatophytic folliculitis.
Children are susceptible to scalp infections (Tinea capitis), while young and older adults
have skin infections. Transmission is either via person to person contact, from animals or
least commonly from soili.
We can classify dermatophytes based on their ecology:

- Anthropophilic - person to person contact
- Zoophilia - animal to human contact
- Geophilic - environmental
We can also classify based on where the dermatophyte grows:

- Epidermal dermatophytosis
- Tinea facialis, tinea corporis, Tinea cruris, Tinea manus, Tinea pedis
- Dermatophytosis of nail apparatus
- Tinea unguium (aka onychomycosis)
- Dermatophytosis of hair follicle
- Tinea capitis, Tinea barbae
Dermatophytes all synthesize keratinases which digest keratin and sustain the
existence of the fugin in keratinized structures. Host factors that facilitate dermatophyte
infections include atopy, topical and systemic glucocorticoids, ichthyosis, sweating,
and high humidity.
The clinical presentation depends on the site of infection, immunological aspects of the host
and the species of fungus.
Treatment is systemic antifungals such as Terbinafine, Itraconazole, Fluconazole and

Ketoconazole. Below we consider some of the types of dermatophytosis in more detail:
- Tinea pedis
- Dermatophytic infection of the feet
- Presents with erythema, scaling, maceration and/or bulla formation
- Can cause breaks in integrity of epidermis allowing other bacteria to cause
soft tissue infection
- Aka athlete’s foot
- Tinea Manuum
- Chronic dermatophytosis of the hands
- Commonly unilateral, usually associated with tinea pedis
- Tinea Cruris
- Subacute or chronic dermatophytosis of upper thigh and adjacent inguinal
and pubic regions
- ‘Always’ associated with tinea pedis the source of the infection
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- Tinea capitis
- Dermatophytic trichomycosis on the scalp, predominantly in children
Pityriasis versicolor
Caused by a Malassezia yeast, this disease sees the discoloration of the skin due to
hypo or hyperpigmented macular lesions on seborrheic areas of the trunk. Most
common in adolescents in the summer months, commonly has a relapsing nature.
Treat with topical medicaments (zinc pyrithione shampoo).
27. Candida infections
So called Candidiasis (infection with yeast of candida species, most commonly Candida
albicans), candida infections can be mucosal, cutaneous or disseminated.
Cutaneous candidiasis
- Occurs in moist occluded sites
- Most patients have predisposing factors
- Types include
- Candidal intertrigo - pruritus, tenderness and pain. Pustules on erythematous
base become eroded and confluent. Commonly inframammary or
submammary
- Interdigitial - common in obese elderly
- Diaper dermatitis - irritability, discomfort with urination, defecation, changing
diapers. Erythema, edema with papular and pustular lesions.
- Occluded skin - under occlusive dressing (e.g. under a cast)
Treatment is with prevention (keep intertriginous areas dry and wash with benzoyl peroxide),
use topical antifungals (Nystatin, azole or imidazole cream), and oral antifungals (Nystatin or
Fluconazole).
Oropharyngeal candidiasis
- Oropharyngeal candidiasis occurs in individuals with immunocompromise
- Presents often asymptomatically, although burning or pain may occur when eating
spices/acidic food.
- Forms of oropharyngeal candidiasis include
- Pseudomembranous candidiasis
- Erythematous candidiasis
- Candidal leukoplakia
- Angular cheilitis
- Treat with Nystatin (topical) or fluconazole (systemic)
Genital candidiasis
- 20% of women have vaginal colonization by Candida
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- Most cases of candidiasis occur in healthy population, risk factors include HIV,
Diabetes, Hx of HB treatment.
- Presents with vulvitis/vulvovaginitis with erosions, edema and erythema
Chronic mucocutaneous candidiasis

- Characterised by persistent or recurrent candida infections of the oropharynx, skin
and or nail apparatus
- Is inherited, AD or sporadic, due to host defense defect
Disseminated candidiasis
- Fifth most common cause of nosocomial bloodstream infection
- RF include neutropenia, venous access catheters and hospitalization
- Candida enters the bloodstream having colonized venous access catheters or
penetrate the intestinal mucosa. Condidemia then seeds the skin and internal organs
(i.e. hepatosplenic candidiasis)
28. Lyme disease
Caused by the bacteria Borrelia burgdorferi, lyme disease is an infectious disease

transmitted by infected ticks of the genus ixodes ricinus. Common in the UK in parts of
Scotland and Wales, look out around summer and
autumn. .
The cycle starts with a blood meal by the tick which then
allows the spirochete b.burgdorferi it carries to invade
into the skin. Here the spirochaetes migrate
centrifugally producing an erythema migrans plaque
(‘bulls eye’)at the site of the bite. This is noted in about
80% of cases. At this stage, acute illness syndrome
(fever, chills, myalgia, headache, weakness and
photophobia) can occur.
Days to weeks after the tick bite secondary lesions can

occur. This includes cardiac manifestations(carditis, AV
nodal block), neurological manifestations (meningitis,
cranial neuritis, radiculoneuritis) and rheumatologic
manifestations(migratory musculoskeletal pain and
arthralgias). During this disseminated phase spirochaetes
can be found in all of the affected tissues.
The final stage is the chronic ‘late disseminated’ phase of the disease, where the patient
suffers from persistent arteritis, chronic encephalopathy or polyneuropathy and
acrodermatitismonths or years after the initial bite.
Treatment:
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- Known tick bite - single dose AB prophylaxis Doxycycline
- Erythema migrans - Doxycycline or Amoxicillin (Cefuroxime if indistinguishable from
cellulitis)
- Cardiac complications - doxycycline + temporary pacemaker
Venereal diseases
1. Venereal diseases: classification, epidemiology
Bacterial Viral
Syphilis (Treponema pallidum) Genital herpes

Gonorrhoea (Neisseiria gonorrhoeae) Anogenital warts
Chlamydia AIDS
Lymphogranuloma venereum Hepatitis B
Ulcus molle Molluscum contagiosum
Donovanosis
Mycoplasma hominis + Ureaplasma urealyticum
Nonspecific urogenital infections
Bacterial vaginosis
Lepra
Protozoa Mycotic
Trichomoniasis Candida sp
2. Syphilis (etiology, pathogenesis, epidemiology)
Overview + Etiology
Syphilis is a systemic chronic infection caused by the spirochete Treponema pallidum .
T.pallidum is a thin spirochete with 6-14 spirals, the only natural host is humans. There are
three subspecies that cause nonvenereal endemic syphilis (bejel, yaws and pinta). T.
pallidum is a gram negative highly motile bacteria and is unable to survive more than
a few days without a host. While it has a slow doubling time (>30 hours) it is highly
effective at avoiding the immune system.
Incidence is 30,000 cases annually and can be divided as a primary, secondary and tertiary
forms which we’ll consider in the questions below.
Transmission
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Transmitted by sexual contact and contact with infectious lesion(chancre, mucous
patch, condyloma latum or cutaneous lesions of secondary syphilis). Sixty percent of
sexual contacts of persons with primary and secondary syphilis results in infection.
Transmission can also be vertical from mother to fetus.
Rates of transmission are higher in those who have sex with men(60% of new cases),
while 20% of syphilis was due to oral sex alone.
Pathogenesis
The spirochetes pass through intact mucous membrane via microscopic abrasions in
the skin, from here to enter the lymphatics and blood within a few hours and produce
systemic infection and metastatic foci before the development of a primary lesion. The
spirochetes divide locally, with the resulting inflammatory response being known as a
chancre, this may be a single or multiple lesions.
Primary syphilis is the most contagious form of the disease, while later syphilis is
predominantly a vascular disease, secondary syphilis causes endarteritis and damage to
terminal arterioles resulting in inflammatory and necrotic changes.
3. Diagnosis of syphilis
Any patients with signs and symptoms of syphilis should undergo diagnostic testing, in
patients with asymptomatic infections, diagnosis relies on screening. A full history of sexual
activity is important when diagnosing syphilis, men who have sex with men, people infected
with HIV or other STIs, those with multiple sexual parters and sex workers are all at
increased risk.
Main diagnostic signs and symptoms for each stage of syphilis
Primary syphilis Look for solitary painless genital ulcer(chancre) in the anogenital or
cervix area. May not always be noticed and may heal spontaneously.
May also present with regional lymphadenopathy. Ulcer can also
be on the mouth where transmission is via oral sex.
Secondary syphilis Presents 4-8 weeks after primary infection . Presentation is diverse
and multi-system. May present with m alaise, fever, myalgia, fatigue
or arthralgia and generalised lymphadenopathy. Looks similar to a
viral illness. May also present with a generalised symmetrical
maculopapular diffuse rash, typically affecting the palmer hands
and planter feet as well as the trunk. Snail track linear ulcerations
on buccal mucosa and erosions on the genitalia may be
observed, along with flesh coloured wart like lesions in gential area
(condylomata lata)
Latent syphilis No clinical symptoms
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Tertiary syphilis Chronic end organ symptoms including neurosyphilis(ataxia, loss

of bladder and rectal control, areflexia, argyll-robertson pupils, dorsal
column loss, personality change, confusion, tremor etc),
cardiovascular syphilis(aortitis, aortic regurgitation, angina, cardiac
murmur), gummatous syphilis(organomegaly and infiltrative lesions
- gumma is a cutaneous skin lesions with a necrotic centre).
Congenital syphilis Intrauterine features include hydrops, increased risk of stillbirth

or neonatal death. Most clinical signs are not visible at birth but
develop within 3 months, including a highly infectious rhinitis(may
be purulent or blood-stained), hepatosplenomegaly,
glomerulonephritis, generalised lymphadenopathy, CNS
involvement and a neonatal skin rash. Necrotising funisitis
(inflammation of the umbilical cord) is almost diagnostic of congenital
syphilis and is usually found in preterm infants who are stillborn, or die
in the neonatal period. The umbilical cord appears as a ‘barber pole’.
Microscopic tests
Dark-field microscopy of the skin lesion can provide diagnosis but this is not practically
done outside of a specialist setting. In general the lesion is cleansed and abraded with a
gauze pad until serous exudate appears which is then collected onto a glass slide for
microscopic analysis. This sample allows for identification of T pallidum for immediate
diagnosis. A lesion is considered negative for T pallidum if microscopy is negative of three
different days.
Gummata in tertiary syphilis have few identifiable T pallidum organismsas such

dark-field microscopy must be performed, this is also the case for congenital syphilis when
analysing nasal secretions.
Serological tests
This is the most common method for diagnosing syphilis. There are Treponemal and
nontreponemal tests that can be performed, the most common approach is to use
treponemal test as the initial serological test followed by a non-treponemal test.
Treponemal tests include:

- Treponemal enzyme immunoassay (EIA)
- T. pallidum particle agglutination assay (TPPA)
- T pallidum haemagglutination assay (TPHA)
- Fluorescent antibody absorption (FTA-ABS)
- Immunocaputre assay (ICA)
Non-treponemal tests (measure IgG and IgM directed against cardiolipin-lecithin-cholesterol
antigen complex)
- Rapid plasma reagin test (RPR test, first choice)
- Venereal disease research laboratory test (VDRL test
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Note that in the treponemal tests, patients will remain positive for life, these tests cannot
distinguish an active infection compared to a past infection. Additionally, these tests will
show positive for yaws, pinta and bejel.
The non-treponemal tests are more effective for evaluating a quantitative measure of
disease activity (titre) and can be used to monitor treatment response.
Finally a line immunoassay serological test can be used to confirm syphilis infection
following initial serological treponemal testing.
4. Primary syphilis
Primary syphilis is characterised by the primary, button-like, painless ulcer that

developes at the site of infection, that is most commonly on the penis or vulva,
although can also be in the oral mucosa. The ulcer has a raised border with scanty
serous exudate which may be crusty, it is highly infectious. The lesion is a few
millimeters to 2cm in diameter. Histologically the chancre is characterised by mononuclear
leukocytic infiltration, it will heal spontaneously after a number of months.
Lymphadenopathy appears within 7 days, the nodes are discrete, firm, rubbery, nontender
and more commonly unilateral, this may last for months.
Treat with
IM benzathine penicillin G 2.4 million units single dose or doxycycline
100mg twice daily for 14 days
5. Secondary syphilis
Appears 2-6 months after primary infection, often 6-8 weeks after the healing of the
chancre, although in 15% of cases the chancre is still present when the second stage
occurs.
General clinical picture was covered above in ‘diagnosis’ section, but look for all the general
symptoms of a viral infection.
There are three important dermatological lesions in secondary syphilis to consider. The first
is the papulosquamous eruption, in this rash Macules and papules 0.5-1cm, round to oval,
pink brownish red appear in a symmetrical manner affecting the palms and soles of the
hands and feet as well as the trunk. On palpation the papules are firm. Secondly annular
plaques merging on the face, around the month are a common and significant feature.
Finally Condylomata lataare soft, flat-topped, moist, pink-tan papules and nodules most
commonly in the perineal area or around the mouth. These lesions are teaming with
T.pallidum.
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Non-dermatological changes include diffuse hair loss, causing patchy moth-eaten
alopecia on the scalp and beard areas, often with loss of eyelashes and lateral third of the
eyebrow. Mucous membranes may also undergo changes with small asymptomatic,
flat-topped, macules and papules covered by hyperkeratotic white to gray membrane in the
oral or genital mucosa.
40% of patients will have abnormal CSF findings with spirochetes in 30% of cases, liver
enzymes will commonly be raised with possible reduction in renal function due to immune
complex-mediated membranous glomerulonephritis.
The course of secondary syphilis is that of a relapsing remitting disease, with recurrent
eruptions appearing after month-long asymptomatic intervals.
Treatment is again IM benzyl penicillin or doxycycline.
6. Tertiary syphilis
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Again as mentioned above tertiary syphilis is an end stage organ disease, the most
significant and deadly consequences are not cutaneous, but here we will list the main clinical
manifestations.
Gumma
- Nodular or papulosquamous plaques that may ulceration and necrosis. These are
rapidly expanding destructive lesions. Commonly solitary and can affect any part of
the skin, although have a predilection for scalp, face, chest and calf.
Asymptomatic neurosyphilis
- 25% of patients with untreated ate latent syphilis, there is a lack of neurological
symptoms, however 20% of these progress to clinical neurosyphilis in 10 years
Meningeal syphilis
- Onset of symptoms generally <1 year after infection, causes headache, nausea, stiff
neck, cranial nerve palsies, seizures and changes in mental status
- Meningovascular syphilis is the later form of this disease, onset of symptoms is 5-10
years after initial infection and presents with subacute encephalitis prodrome followed
by stroke syndrome, it is a progressive vascular disease
General paresis
- Onset of symptoms 20 years after initial infection. PARESIS stands for Paresis,
Affect, Reflexes (hyperactive), Eye (Argyll Robertson pupils), Sensorium (illusions,
delusions, hallucinations), Intelect (reduced memory) and Speech
Tabes Dorsalis
- Onset of symptoms 20-30 years after initial infection. Patient becomes ataxic with
wide-based gait and foot slap, paresthesia, bladder disturbance, impotence,
areflexia, loss of position, deep pain and optic atrophy
Cardiovascular syphilis
- Results from endocarditis obliterans of vasa vasorum, occurs in 10% of late syphilitic
cases. Causes aoritis, aortic regurgitation, saccular aneurysm and coronary ostial
stenosis
Tertiary syphilis is now rare as most patients get treatment at some point, it is more
commonly found in patients with concomitant HIV.
Treatment
IM benzathine penicillin 2.4 million units once a week for three weeks.
7. Congenital syphilis
Congenital syphilis is passed down during gestation or intrapartumfrom the mother to

the fetus. Manifestations of the disease can be early or late.
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Early manifestations appear before the age of 2 years of age. The disease resembles
severe secondary syphilis that one might find in an adultwith Bullae and vesicles on
palms and soles, superficial desquamation, petechiae and papulosquamous lesions .
Highly infectious rhinitisoccurs in 23% of cases , while c
ondyloma latum(see above)
can also be found. Other symptoms include hepatosplenomegaly, jaundice,
lymphadenopathy, anemia, thrombocytopenia and leukocytosis. The early form is highly
infectious.
Late manifestations appear after 2 years of age. The late form is noninfectious and
similar to late acquired syphilis in adults. Cardiovascular syphilis, 8th nerve deafness,
recurrent arthropathy and bilateral knee effusions are all commonly seen symptoms .
Cutaneous presentations include interstitial keratitis and gummatous periostitis, causing
destructive lesions of nasal septum/palate. Neurosyphilis is also present, symptomatic in
25% and asymptomatic in 33%.
Untreated,
syphilis has a high chance of congenital transmission and carries a high
risk of miscarriages, premature births, stillbirth or neonatal death. Additionally, fetal
morphological diseases can present include saddle nose condition(depressed nasal
height due to collapse of bridge). Infants may also have notched incisor teeth, known as
Hutchinson’s teeth, something characteristic of congenital syphilis.
Note in general babies do not present with the primary syphilitic chancre.
If a mother is diagnosed with syphilis, and she is treated before the 16th week of
pregnancy, then vertical transmission can be prevented. The fetus is at greatest risk
when the mother is in the primary stage of the infection, in the secondary stage, the
mother can take treatment at any point before the birth of the child and she will massively
reduce the infants risk of congenital syphilis.
The CDC recommends procaine penicillin G, 50,000 U/kg dose IM in a single dose for
ten days for infants who are born to mothers with syphilis.
8. Treatment of syphilis. Prognosis
Have covered treatment in each section.
9. Gonorrhea. Etiology. Mode of Transmission. Symptoms and

course in the male. Complications. Treatment
Gonorrhea is an STI caused by Neisseria gonorrhoeae, a gram -ve diplococci bacteria

.
Humans are the only natural reservoir of the organism, and up to 40% of those with
gonorrhea have confluent C.trachomatis infection. Gonorrhea is the second most
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commonly reported bacterial STI(chlamydia is first). Commonly occurs in the young and
sexually active, symptomatic infection is more common in males.
Transmission is sexual, from a partner with or without symptoms. Sexxual activity may be
penetrative (either vaginal or anal) or oral.
Gonococcus has an affinity for columnar epithelium(stratified and squamous epithelium

are more resistant), the bacterium penetrates between epithelial cells causing a
submucosal inflammation with polymorphonuclear (PMN) leukocyte reaction with
resultant purulent discharge. The bacteria has the capacity to elude the immune system
by changing the outer membrane antigens through genomic plasticity. About 1% of
gonococcal infections can develop into disseminated infection, those strands of bacteria
that are more likely to develop into the disseminated form tend to cause little gneital
inflammation and there can be undetectable.
General symptoms that can occur in both men and women include rectal gonorrhea
causing mucopurulent dischargefrom the anus, gonococcal pharyngitisthat presents
almost identically to normal bacterial pharyngitis, and gonococcal conjunctivitisthat
can present with a thick white/yellow discharge(in such cases examination of the eyes
with a slit lamp is recommended so that infection of the cornea can be excluded).
Both men and women can also suffer from disseminated gonococcal infection (DGI).
This occurs when N. gonorrhoeae is left untreated but it only occurs in 1-3% of all
gonorrhea infections. Women are less likely to develop DGI than men. It commonly causes
skin (75%) and synovium (68%) infections, along with fever. Rarer complications include
endocarditis, meningitis, myocarditis and perihepatic abscess. Clinical findings include
papules that progress into hemorrhagic pustules, bullae, petechiae or necrotic lesions on the
extremities.
N.gonorrhoeae has no clinical serological test, Nucleac acid amplification testing
(NAAT) is generally the first line for diagnosis,this is preferable to culture in most
settings, especially where the patient is asymptomatic, due to better sensitivity. In
symptomatic patients, discharge can be sent for gram staining.
Symptoms in men
The most common presentation is purulent urethral discharge due to inflammation of
the penile urethra. This will lead to burning sensation during urination. Discharge with or
without burning occurs in half of all cases and is the most common symptom of the infection
Additional symptoms include tenderness and/or swelling of the epidermis however this
is quite uncommon.
The most common medical complication is inflammation of the epididymis, and an

increased risk of prostate cancer.
Diagnostic indicators in men is evidence of urethral infection and dysuria, combined this
is evidence enough of gonorrhea.
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First line treatment is IM ceftriaxone + oral azithromycin given together Doxycycline is
second line in those allergic to azithromycin.
10. Gonorrhea. Etiology. Mode of transmission. Symptoms and

course in the female. Complications. Treatment
Gonorrhea is an STI caused by Neisseria gonorrhoeae, a gram -ve diplococci bacteria .

Humans are the only natural reservoir of the organism, and up to 40% of those with
gonorrhea have confluent C.trachomatis infection. Gonorrhea is the second most
commonly reported bacterial STI(chlamydia is first). Commonly occurs in the young and
sexually active, symptomatic infection is more common in males.
Transmission is sexual, from a partner with or without symptoms. Sexxual activity may be
penetrative (either vaginal or anal) or oral.
Gonococcus has an affinity for columnar epithelium(stratified and squamous epithelium

are more resistant), the bacterium penetrates between epithelial cells causing a
submucosal inflammation with polymorphonuclear (PMN) leukocyte reaction with
resultant purulent discharge. The bacteria has the capacity to elude the immune system
by changing the outer membrane antigens through genomic plasticity. About 1% of
gonococcal infections can develop into disseminated infection, those strands of bacteria
that are more likely to develop into the disseminated form tend to cause little gneital
inflammation and there can be undetectable.
General symptoms that can occur in both men and women include rectal gonorrhea
causing mucopurulent dischargefrom the anus, gonococcal pharyngitisthat presents
almost identically to normal bacterial pharyngitis, and gonococcal conjunctivitisthat
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can present with a thick white/yellow discharge(in such cases examination of the eyes
with a slit lamp is recommended so that infection of the cornea can be excluded).
Both men and women can also suffer from disseminated gonococcal infection (DGI).
This occurs when N. gonorrhoeae is left untreated but it only occurs in 1-3% of all
gonorrhea infections. Women are less likely to develop DGI than men. It commonly causes
skin (75%) and synovium (68%) infections, along with fever. Rarer complications include
endocarditis, meningitis, myocarditis and perihepatic abscess. Clinical findings include
papules that progress into hemorrhagic pustules, bullae, petechiae or necrotic lesions on the
extremities.
N.gonorrhoeae has no clinical serological test, Nucleac acid amplification testing
(NAAT) is generally the first line for diagnosis,this is preferable to culture in most
settings, especially where the patient is asymptomatic, due to better sensitivity. In
symptomatic patients, discharge can be sent for gram staining.
Symptoms in women
Half of all women with gonorrhea are asymptomatic, the remaining experience vaginal
discharge, lower abdominal pain and/or pain with sexual intercause associated with
inflammation of the uterine cervix. M ucopurulent cervicitis is the classic sign of
gonorrhea infection in womenbut it is not common enough or specific enough for it to be
sufficient to make a diagnosis without supportive laboratory tests.
Complications in women include increased risk of ectopic pregnancy resulting from PID,
that can eventually cause infertility
.
Again treatment is IM ceftriaxone + oral azithromycin
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11. Gonorrhea. Etiology. Mode of Transmission. Symptoms and

course in the children. Complications. Treatment.
Neonates can transmit N.gonorrhoea if the mother has

an active gonorrhoea infection, and the infant is e xposed
to cervical exudate at birth. It presents as an acute
illness for 2-5 days after birth. The most severe
manifestations are ophthalmia neonatorum and sepsis,
which can include arteritis and meningitis. Less severe
manifestations include rhinitis, vaginitis and urethritis.
Ophthalmia neonaturm if left untreated can lead to severe
eye complications or disseminated infection.
In children, sexual abuse is the most frquent case of STIs(including gonococcal infection)
in pre-adolescent children. Anorectal and pharyngeal infection are common and
frequently asymptomatic in sexually abused children.
Neonates and children with gonorrhoea infections should be treated with IM/IV Ceftriaxone
(If child is >45kg use adult therapy).
12. Nongonococcal urethritis. Chlamydiasis
Nongonococcal urethritis = chlamydia urethritis (normally)! Chlamydia is four times as

common as gonococcal urethritisand the most common STI. Chlamydiasis is just a
silly term for Venereal chlamydiaso we’re not going to bother talking about that, just going
to talk about the STI chlamydia.
So chlamydia is a genuswith three prominent pathogenic species, C. trachomatis(causes

the urethritis we’re most concerned with along with other sexually transmitted chlamydial
diseases), C.pneumoniae(causes upper respiratory tract infections and pneumonia) and
C.psittaci(causes psittacosis).
Chlamydia is an obligate intracellular RNA bacteria, they are gram -veand are able to
survive within macrophages which act as the principal host.
Now lets look at sexutally and perinatally transmitted chlamydia specifically. It presents as
being asymptomatic or with urethritis in men (40-60% asymptomatic).The most
frequent symptoms are urethral discomfort(itching or pain) with urination and urethral
discharge(generally clear or cloudy but rarely purulent, use this to distinguish between
gonorrhoea and chlamydia). Chlamydia can spread from the urethra to the epididymis in
men(around 1%) causing testicular pain and scrotal erythema and oedema.
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In women an even greater percentage of cases are asymptomatic, those who are
symptomatic have symptoms mimicking a UTI, characterised by dysuria, frequency and
pyuria. Chlamydia should be suspected in women with pyuria but negative urine nitrate
or negative urine culture. Mild urethral discharge may be seen but is not common or
significant enough to be used diagnostically. Cervicitis is often caused by c.trachomatis,
with 50% of cases being due to the STI. Most women are asymptomatic, and symptoms
where present are mild and nonspecific, they include vaginal bleeding, dysuria and
dyspareunia. Chlamydia can spread from the cervix to the endometrium, fallopian
tubes or other pelvic organs causing Pelvic Inflammatory Disease (PID).
As well as causing genital infections,C.trachomatis can cause conjunctivitis(presents

with subacute or chronic unilateral conjunctival redness, mucoid or mucopurulent ocular
discharge, FB sensation and preauricular adenopathy) and oropharyngeal infection.
Neonates that are exposed to c.trachomatis during passage through the birth canal may
develop inclusion conjunctivitis(with cytoplasmic chlamydia inclusion bodies) or
pneumonia. Conjunctivitis usually develops 5-12 days after birth while pneumonia
usually occurs between 1-3 months of age.
Definitive diagnosis of chlamydia is with detection of the organism directly through

isolation of organism in cell culture. Due to the unspecific and sometimes
asymptomatic nature of chlamydia screening is recommended.
Treatment is with Tetracyclines or macrolides, usually doxycycline 100mg orally twice

daily for 7 days or azithromycin 1g in a single dose.
13. Trichomoniasis. Chlamydiasis
Trichomoniasis
Trichomonas vaginalis is a protozoa! It is one of the most common STIs worldwide with a
high incidence in those with multiple sexual partners and other STIs. T. vaginalis is a
flagellate with a tendency to multiply by binary fission on the epithelial surface of the
vagina or urethra as well as in vaginal or urethral secretions. No cyst form is known and
the trophozoites are killed by drying.
Trichomoniasis is one of the three common causes of vaginitis or vaginosis(along with

bacterial vaginosis and vulvovaginal candidiasis). It is characterised by a thin gray/yellow
frothy discharge, vulvovaginal erythema, ectovercial erythema(strawberry cervix) and a
positive whiff test(foul fishy odor). The incubation period is 5-28 days, and often
presents with irritation, dyspareunia, abdominal pain and dysuria. Men are carriers are
T.vaginals but are almost always asymptomatic, rarely it is associated with
epididymitis and superficial penile ulcerations.
Diagnosis is with direct observation of T.vaginalis on slide.
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Treatment is a single 2g oral dose of Tinidazole or metronidazole. Prevention is

condoms, a rare complication is PID. Infection during gestation may lead to fetal growth
retardation. Reinfection is common
Chlamydiasis
(see above)
14. Balanitis. Vulvitis
Balanitis
Balanoposthitis refers to inflammation of the glans penis and prepuce, it is a
descriptive term and not a diagnosis.Balantitis refers only to the inflammation of the
glans peins, as such Balanoposthitis cannot occur in circumcised men, however balanitis
can (although is rarer). There are many causes of Balanitis/Balanoposthitis which can
broadly be divided into inflammatory, infective and pre-cancerous.
Most common causes of balanoposthitis are:

- Inflammatory dermatoses (e.g. lichen sclerosus, eczema, psoriasis, lichen planus)
- Precancerous conditions (erythroplasia of Queyrat)
- STIs - Gonorrhoea, Candida
The penis presents with a persistent red, ovoid lesion on the glans, it often presents
with soreness, pruritus and dribbling of urine. Risk factors include congenital or
acquired dysfunctional foreskin, poor hygiene, over-washing and HPV along with
being uncircumcised.
Investigate with swab for microbiology(Gram stain and PCR) along with virology and
dark-field microscopy.
Management depends on the specific cause of the disease (e.g. atopic eczema see eczema
treatment).
Vulvitis
This is an inflammation of the vulva(including labia majora, minor, clitoris and introitus). It
may occur with vaginitis and vulvovaginitis.
Common causes of vulvitis are:

- Allergic reactionto perfumed toilet papers, vaginal sprays, shampoos, creams etc
- Irritations caused by yeast infections, chlorinated water, underwear, urine (in cases
where patient is wearing a diaper)
- Infections - vaginitis, genital herpes, viral and fungal infections
- Other - scabies, eczema, dermatitis, oral sex, diabetes
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Symptoms include itching, a burning sensation in the vulvar, vaginal discharge, cracks
on the vulva, erythema, bulla, squama, warts, dyspareunia and increased sensitivity
when wiping.
Diagnosis should include urine analysis, swabs and tests for STIs. Vulvitis is common
in children, especially caused by allergic dermatitis, contact dermatitis and lichen
sclerosus, as well as infectious causes.
15. AIDS. Etiology. Epidemiology
Autoimmune Deficiency Syndrome (AIDS) is a consequence of the Human

Immunodeficiency Virus (HIV).HIV is a virus that causes progressive quantitative and
qualitative deficiency of T helper cells. There are two forms of HIV, HIV 1 and HIV 2. HIV
1 is the main causative agent for HIV, HIV 2 causes diseases in western africa and other
focal locations.
Transmission of HIV is through sex, exposure to blood or blood products, perintal or
breast milk. There are approximately 34 million people living with HIV, 22.5 million in
sub-saharan africa. The condition was first recognised in 1981 in the US, since that point
80 million people had become infected, meaning 45 million dead, making it one of the
leading causes of death throughout the world.
HIV is a retrovirus, a member of the lentivirus genus. Important properties of the lentivirus
genus are:
- Spherical, 80-90 nm
- Single stranded RNA, linear, positive sense, genome is more complex than most
other retroviruses
- Has envelope, reverse transcriptase enzymes and proteases required for production
of infectious virus
- Replication is via reverse transcriptase that makes DNA copy from genomic RNA,
provirus DNA is template for viral RNA
Untreated HIV typically lasts a decade, stages include:

- Primary infection
- Dissemination of virus to lymphoid organs
- Clinical latency (may last as long as 10 years, high viral replication here, CD4
T-lymphocytes are major target of the virus)
- Elevated HIV expression
- Clinical disease
- Death
Clinical findings of HIV infection are nonspecific and include fatigue, rash, headache,
nausea and sweats. Autoimmune Disease syndrome(AIDS) which occurs as a result is
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characterised by pronounced suppressionof the immune system and development of a
wide number of opportunistic infections or neoplasia as a result.
16. AIDS. Skin and mucosal infections
Dermatological disorders are universal during the course of HIV disease, and the
diagnosis of certain cutaneous conditions warrants HIV sero testing. Such diseases include
Kaposi sarcoma, oral hairy leukoplakia, proximal subungual onychomycosis, bacillary
angiomatosis, eosinophilic folliculitis, chronic herpetic ulcers and any STI. Diseases
where consideration should be given for HIV include Herpes Zoster, molusscum
contagiosum, and candidiasis. Possible risk for HIV include diseases such as
lymphadenopathy, seborrheic dermatitis and aphthous ulcers.
Cutaneous Inflammatory disorders associated with HIV

- Seborrheic dermatitis
- Atopic dermatitis
- Prurigo nodularis
- Psoriasis
- Xerosis
- Eosinophilic folliculitis
- Pruritis
Opportunistic infections associated with HIV
- Molluscum contagiosum
- Varicella zoster virus infection
- Herpes simplex
- HOV
- S. aureus
- Mucosal candidiasis
- Dermatophytosis
Opportunistic neoplasms
- Kaposi sarcoma
- HPV induced dysplasia and invasive SCC
- Merkel cell carcinoma
- ‘Hodgkins and non-hodgkin's lymphoma
Below we list some of the different settings patients with HIV can have diseases:
- Acute HIV syndrome
- Exanthem (morbilliform rash with pink macules)
- Oropharyngeal lesions
- Genital lesions
- Ruritis and pruritic eruptions
- Eosinophilic folliculitis
- A chronic pruritic dermatitis, occurs with advanced HIV
- Papular pruritic eruption of HIV
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- Urticarial papules and noninfectious pustules found symmetrically on
extremities. Multiple excoriations, marked post-inflammatory
hyperpigmentation
- Often the initial presenting manifestation of HIV in developing nations
- Photosensitivity in HIV
- Idiopathic photosensitivity
- Oral hairy leukoplakia
- Caused by epstein barr virus, asymptomatic but stigmatization of HIV. A white
well demarcated plaque with corrugated texture is found on the lateral and
inferior surface of the tongue. Lesions do not rub off.
- Adverse cutaneous drug eruptions in HIV
- Incidence of drug eruptions are 100x more likely in those with HIV compared
to the general public. Rash generally appears exanthematous or morbilliform
17. Scabies. Pediculosis
Scabies
Scabies (S. scabiei var hominis) is an obligate human parasite that burrows into the
epidermis shortly after contact, to the depth of stratum granulosum, where it deposits
feces in tunnels. Females have a life span of 4-6 weeks and lay 40-50 eggs in their life,
approximately 3 eggs a day in burrows which then hatch in four days. Mites usually burrow
at night and lay eggs during the day,hatched larvae then migrate to the skin surface and
mature into adults, before copulation, and then the gravid female burrows back under the
stratum corneum and the male falls off. In classic scabies, approximately 10 females per
patient are present.
This is a major problem is less developed countries, especially the likes of south and central
america and bangladesh. Transmission is by skin-to-skin contactand via clothes or
bedding(mites can survive for 2 days outside of the body).
The pathogenesis is that of hypersensitivity of both immediate and delayed types. The
symptoms are pruritus, intense in nature, widespread and usually sparing the head and
neck. Itching often interferes with or prevents sleep. Rash ranges from no rash to
generalized erythroderma, scratching can often make the skin look like eczema.
Cutaneous findings show lesions at the site of mite infestation and secondary lesions
due to chronic rubbing and scratching. Intraepidermal burrows may also be visible.
Common distribution is areas with no hair follicles and where stratum corneum is soft
and thin i.e. interdigital webs of hands, wrists, shaft of penis, elbows, feet and buttocks.
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Diagnosis can be clinical or by microscopy.

Treatment is Permethrin 5% cream applied to all areas of the body. Lindane 1% location can
also be used.
Pediculosis
Pediculosis is a lice infestation. There are two main types that affect humans:
- Pediculosis capitis (head lice)
- Pediculosis pubis (crabs
Pediculosis capitis
This is infestation of the scalp by pediculus humanus capitis. These lice feed every 4-6
hours and move by grasping hairs close to the scalp, and can crawl 23 cm in one day. Lice
lay nits within 1-2mm of the scalp, which then hatch within 1 week. One female can lay
50-150 eggs in their 16 day lifetime . Lice are transmitted from hair to hair contact,
shared hats, caps, brushes etc, however they only survive a few hours off the scalp.
Symptoms are pruritus of the back and sides of the scalp, diagnosis is generally
clinical or through direct observation of the egg capsules (nits).Head Lice are almost
always confined to the scalp. Skin lesions do occur, papular urticaria on the neck are
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bite reactions, and secondary eczematous and excoriation lesions candevelpp on the
scalp. Such breaks in the skin lead to a risk of s. Aureus infection.
Treat with
Permethrin, malathion, pyrethrin or butoxide.
Pediculosis pubis
This is an infestation of hair bearing regions by the crab(public lice). They most
commonly inhabit the pubic regionbut can also affect the chest, axillae and upper
eyelashes. The lifespan is 14 days, and the females can lay 25 ova in this time. Nits
incubate for 7 days before nymphs hatch. Infestation is most common in young males,
transissin is during close physical contact such as sharing a bed.
Often asymptomatic, although may present with mild pruritus for months with
excoriation and secondary infections. Lice appear as brownish gray specks in hairy
areas. Skin lesions can develop, with papular urticaria(small erythematous papules) at
sites of feeding, especially periumbilical region.
Treatment is the same as with pediculosis capitis.
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Notes - Dermatology and Venerology

Viral infections. Classification. Herpes simplex. Herpes Zoster 47

1. Structure of the epidermis - anatomy and histology

It is composed of ​keratinized, stratified squamous epithelium, made of four or five

Below we consider each layer in turn.

Stratum lucidum (hands and feet only)

2. Structure of the dermis and hypodermis - anatomy and histology

The ​dermis contains all of the main appendages​that we think of

The dermis is made of two layers of connective tissue, the ​papillary

Let's now look at these the aforementioned layers:

Appendages of skin include:

We’ll look at each below.

4. Blood circulation and neurological structures in the skin

AVAs don’t exist everywhere in the skin, predominate in ​‘thick’ skin

Outside of AVAs it’s worth remembering that skin circulation is

Neurological structures in the skin

5. Oral and genital mucous - anatomy and histology

Keratinization is a ​cytoplasmic event​that takes place in k ​ eratinocytes ​that move through

Factors that affect the process of keratinocyte differentiation include:

Melanogenesis is the process by which melanin is produced in melanosomes

8. Physiology of skin. Protective, thermoregulatory, secretion,

9. Maculous skin eruptions

The categories of macular skin lesions are:

- Lesions due to changes in pigmentation

10. Palpable skin eruptions

- Papula - <5mm in diameter, caused by increased thickening in epidermis and/or

11. Exsudative skin eruptions

- Vesicule (<5mm with clear fluid)

12. Skin eruptions due to interruption of skin surface

- Erosio - Superficial damage of the epidermis or epithelium, heals without scar

13. Discard skin eruptions. Skin eruptions due to variation of the

Discuard skin eruptions

Skin eruptions due to variation in number of skin elements

14. Major histopathological changes in epidermis

Acanthosis (epidermal hyperplasia)

Epidermal atrophy (epidermal hypoplasia)

Granular degeneration, Epidermolytic hyperkeratosis

15. Major histopathological changes in dermis

Inflammatory cell infiltration

Deposition of foreign substances

16. External medicaments and the mechanism of action

Firstly, moisturizers, from most moist to least:

17. Internal medical treatment of skin diseases

1. Dermatoses due to external factors (physical, chemical and

Common inflammatory dermatoses include:

Other diseases in this category include:

3. Erythema exudative multiforme. erythema nodosum

Management is ​control of herpes simplex using oral valaciclovir or famciclovir​, in

4. Psoriasis vulgaris. Pityriasis rosea

Clinical manifestation is in one of two types

Dermatopathology shows overall ​thickening of the epidermis

Treatment is oral ​antihistamines for relief of pruritus, topical glucocorticoids​may be

5. Lincoln rubber planus

Age of onset is between 30-60​, and is ​more common in females​than males. It is

Clinical findings can be confirmed by histopathology, dermatopathology shows

6. Bullous dermatoses (pemphigus, dermatitis herpetiformis,

Pemphigus is an ​autoimmune disease with the loss of cell-to-cell adhesions in the

Clinical presentation is ​intense, episodic burning or stinging of the skin, symptoms

Bullous pemphigoid ​- an ​autoimmune ​disease usually in ​elderly patients, pruritic

Cicatricial pemphigoid ​- a rare disease of the elderly. ​Ocular involvement is common

It is composed of keratinized, stratified squamous epithelium, made of four or five

The dermis contains all of the main appendagesthat we think of

The dermis is made of two layers of connective tissue, the papillary

AVAs don’t exist everywhere in the skin, predominate in ‘thick’ skin

Keratinization is a cytoplasmic eventthat takes place in k eratinocytes that move through

Management is control of herpes simplex using oral valaciclovir or famciclovir, in

Dermatopathology shows overall thickening of the epidermis

Treatment is oral antihistamines for relief of pruritus, topical glucocorticoidsmay be

Age of onset is between 30-60, and is more common in femalesthan males. It is

Pemphigus is an autoimmune disease with the loss of cell-to-cell adhesions in the

Clinical presentation is intense, episodic burning or stinging of the skin, symptoms

Bullous pemphigoid - an autoimmune disease usually in elderly patients, pruritic

Cicatricial pemphigoid - a rare disease of the elderly. Ocular involvement is common

Pemphigoid Gestationis - a rare pruritic and polymorphic

Contact dermatitis is a generic term applied to acute or chronic inflammatory reactions

The pathogenesis of AD is around the interaction of skin barrier, genetic, environmental,

Management is topical steroids or calcineurin inhibitors, oral hydroxychloroquine can be

SLE is an antigen-driven immune mediated disease characterised by high affinity IgG

Dermatopathology shows epidermis appears normal to atrophic while dermis is

The clinical course is determined by extent of vascular and fibrosing complications,

Management is systemic glucocorticoids, with immunosuppressive drugs such as

Chronic venous insufficiency (CVI) is Commonly secondary to varicose veinswhich have

Increased melanin in the epidermis is due to a state known as hypermelanosis, this is

Hypomelanosis is a decreased amount of melanin in the epidermis and reflects one of

Many patients attribute the onset of their vitiligo to physical

Associated with vitiligo is alopecia, and changes to the nails.

Hypertrichosis may be generalized or localized and may be acquired or congenital. The

- Sclerosing (Morphoeic) BCC- appears as a small patch of morphea or a superficial

The primary infection occurs3-7 days following infection

Folliculitis manifests as follicular papules, pustules, erosions or crusts at the follicular

Impetigo is highly contagiousand commonly passed between children when playing in

Leprosy is a disease caused by Mycobacterium lepra, M.leprae is an obligate intracellular

Incubation period of leprosy is between 2-40 years(commonly 5-7), onset is insidious

In the Tuberculoid form of leprosy, a few well defined hypopigmented hypoesthetic

Lepromatous leprosy sees skin coloured or erythematous papules/nodulesappear,